PT	AU	BA	BE	GP	AF	BF	CA	TI	SO	SE	BS	LA	DT	CT	CY	CL	SP	HO	DE	ID	AB	C1	RP	EM	RI	OI	FU	FX	CR	NR	TC	Z9	U1	U2	PU	PI	PA	SN	EI	BN	J9	JI	PD	PY	VL	IS	PN	SU	SI	MA	BP	EP	AR	DI	D2	PG	WC	SC	GA	UT	PM
J	Dahl, ME; Dabbagh, K; Liggitt, D; Kim, S; Lewis, DB				Dahl, ME; Dabbagh, K; Liggitt, D; Kim, S; Lewis, DB			Viral-induced T helper type 1 responses enhance allergic disease by effects on lung dendritic cells	NATURE IMMUNOLOGY			English	Article							RESPIRATORY SYNCYTIAL VIRUS; EOSINOPHILIC AIRWAY INFLAMMATION; TH2 IMMUNE-RESPONSES; INFLUENZA-VIRUS; INTERFERON-GAMMA; ANTIGEN EXPOSURE; INFECTION; MICE; ASTHMA; SENSITIZATION	It is widely accepted that T helper type 1 (T(H)1) cytokines such as interferon-gamma(IFN-gamma) antagonize allergic diseases mediated by T(H)2 cytokines. The 'hygiene hypothesis' has also proposed that decreased childhood exposure to pathogen-derived T(H)1 cytokines may underlie the recent increased prevalence of asthma, a T(H)2-mediated disease. We show here that influenza A viral infection, which induces large amounts of intrapulmonary IFN-gamma production, unexpectedly enhanced later allergen-specific asthma and promoted dual allergen-specific T(H)1 and T(H)2 responses. Pulmonary dendritic cells obtained from the lung after viral clearance and resolution of acute inflammation conferred enhanced allergic disease and concurrent T(H)1 and T(H)2 immune responses, and these effects were dependent on IFN-gamma secreted during the acute viral infection. Thus, respiratory viral infection and the acute T(H)1 response can positively regulate T(H)2-dependent allergic pulmonary disease in vivo, at least in part, by altering pulmonary dendritic cell function.	Stanford Univ, Sch Med, Dept Pediat, Stanford, CA 94305 USA; Stanford Univ, Sch Med, Program Immunol, Stanford, CA 94305 USA; Univ Washington, Sch Med, Dept Comparat Med, Seattle, WA 98195 USA	Lewis, DB (reprint author), Stanford Univ, Sch Med, Dept Pediat, Stanford, CA 94305 USA.	dblewis@stanford.edu			NIAID NIH HHS [R01 AI 44699]		Brimnes MK, 2003, J EXP MED, V198, P133, DOI 10.1084/jem.20030266; Cella M, 2000, NAT IMMUNOL, V1, P305, DOI 10.1038/79747; CHERWINSKI HM, 1987, J EXP MED, V166, P1229, DOI 10.1084/jem.166.5.1229; COFFMAN RL, 1993, ADV IMMUNOL, V54, P229, DOI 10.1016/S0065-2776(08)60536-2; Dabbagh K, 2002, J IMMUNOL, V168, P4524; Dabbagh K, 2000, J IMMUNOL, V165, P3418; Doherty PC, 1997, IMMUNOL REV, V159, P105, DOI 10.1111/j.1600-065X.1997.tb01010.x; Doyle AG, 1999, J EXP MED, V190, P1081, DOI 10.1084/jem.190.8.1081; EICHELBERGER MC, 1991, J GEN VIROL, V72, P1695, DOI 10.1099/0022-1317-72-7-1695; Erb KJ, 1998, J EXP MED, V187, P561, DOI 10.1084/jem.187.4.561; FINKELMAN FD, 1990, ANNU REV IMMUNOL, V8, P303, DOI 10.1146/annurev.immunol.8.1.303; Gern JE, 2002, NAT REV IMMUNOL, V2, P132, DOI 10.1038/nri725; GRAHAM MB, 1993, J EXP MED, V178, P1725, DOI 10.1084/jem.178.5.1725; Hansen G, 1999, J CLIN INVEST, V103, P175, DOI 10.1172/JCI5155; Holgate ST, 1999, NATURE, V402, P2, DOI 10.1038/35037000; HUANG S, 1993, SCIENCE, V259, P1742, DOI 10.1126/science.8456301; Hussell T, 1996, J GEN VIROL, V77, P2447, DOI 10.1099/0022-1317-77-10-2447; Julia V, 2002, IMMUNITY, V16, P271, DOI 10.1016/S1074-7613(02)00276-5; Kamath AT, 2002, BLOOD, V100, P1734; KOLOPPSARDA MN, 1994, ANAT REC, V239, P150, DOI 10.1002/ar.1092390205; Krug N, 1996, AM J RESP CELL MOL, V14, P319; Kuchroo VK, 2003, NAT REV IMMUNOL, V3, P454, DOI 10.1038/nri1111; Lambrecht BN, 2000, J CLIN INVEST, V106, P551, DOI 10.1172/JCI8107; Lewis DB, 2002, CURR OPIN IMMUNOL, V14, P644, DOI 10.1016/S0952-7915(02)00388-6; Lloyd CM, 2001, ADV IMMUNOL, V77, P263, DOI 10.1016/S0065-2776(01)77019-8; Lyons AB, 2001, METHOD CELL BIOL, V63, P375; Magnan AO, 2000, AM J RESP CRIT CARE, V161, P1790; MARRACK P, 1983, J EXP MED, V158, P1635, DOI 10.1084/jem.158.5.1635; Martinez Fernando D, 2002, Paediatr Respir Rev, V3, P193, DOI 10.1016/S1526-0542(02)00188-4; MO XY, 1995, J VIROL, V69, P1288; Morel PA, 1998, CRIT REV IMMUNOL, V18, P275; MURPHY KM, 1990, SCIENCE, V250, P1720, DOI 10.1126/science.2125367; Randolph DA, 1999, J CLIN INVEST, V104, P1021, DOI 10.1172/JCI7631; Redd SC, 2002, ENVIRON HEALTH PERSP, V110, P557; Roman E, 2002, J EXP MED, V196, P957, DOI 10.1084/jem.20021052; Sampath D, 1999, J CLIN INVEST, V103, P1353, DOI 10.1172/JCI6130; SARAWAR SR, 1994, J IMMUNOL, V153, P1246; Schwarze J, 1999, J IMMUNOL, V163, P5729; Schwarze J, 1999, J IMMUNOL, V162, P4207; Schwarze J, 2002, EUR RESPIR J, V19, P341, DOI 10.1183/09031936.02.00254302; Schwarze J, 1999, J IMMUNOL, V162, P2997; Schwarze J, 1997, J CLIN INVEST, V100, P226, DOI 10.1172/JCI119516; ten Hacken NHT, 1998, EUR RESPIR J, V11, P312, DOI 10.1183/09031936.98.11020312; Trinchieri G, 2003, NAT REV IMMUNOL, V3, P133, DOI 10.1038/nri1001; Tsitoura DC, 2000, J IMMUNOL, V165, P3484; Wills-Karp M, 2001, NAT REV IMMUNOL, V1, P69, DOI 10.1038/35095579; Wohlleben G, 2003, J IMMUNOL, V170, P4601; Yamamoto N, 2000, EUR J IMMUNOL, V30, P316, DOI 10.1002/1521-4141(200001)30:1<316::AID-IMMU316>3.0.CO;2-0; Yamamoto N, 2001, J VIROL, V75, P499, DOI 10.1128/JVI.75.1.499-505.2001	49	152	158	0	0	NATURE PUBLISHING GROUP	NEW YORK	345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA	1529-2908			NAT IMMUNOL	Nat. Immunol.	MAR	2004	5	3					337	343		10.1038/ni1041		7	Immunology	Immunology	779ZV	WOS:000189344600017	14973436	
J	Tulic, MK; Fiset, PO; Christodoulopoulos, P; Vaillancourt, P; Desrosiers, M; Lavigne, F; Eiden, J; Hamid, Q				Tulic, MK; Fiset, PO; Christodoulopoulos, P; Vaillancourt, P; Desrosiers, M; Lavigne, F; Eiden, J; Hamid, Q			Amb a 1-immunostimulatory oligodeoxynucleotide conjugate immunotherapy decreases the nasal inflammatory response	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						amb a 1-immunostimulatory phosphorothioate; oligonucleotide conjugate; immunotherapy; rhinitis; ragweed	GRASS-POLLEN IMMUNOTHERAPY; MESSENGER-RNA; EOSINOPHILS; LYMPHOCYTES; EXPRESSION; ASTHMA; INCREASES; MUCOSA; DNA	Background: Amb a 1-immunostimulatory phosphorothioate oligonucleotide conjugate (AIC) is a novel immunotherapeutic compound consisting of purified Amb a 1 from short ragweed proteins covalently linked to an immunostimulatory phosphorothioate oligodeoxyribonucleotide. In sensitized animals AIC can stimulate an Amb a 1-specific T(H)1 response and decrease pulmonary reactivity to ragweed challenge. Clinical trials have documented reduced allergic response to AIC in comparison with licensed ragweed extract. Objectives: We sought to determine the in vivo effect,of shortcourse immunotherapy with AIC on eosinophilia and cytokine mRNA expression in the nasal mucosa of ragweed-sensitive patients. Methods: Ragweed-sensitive patients with allergic rhinitis were treated with 6 escalating doses of AIC (0.06-12 mug, n 28) or placebo (n = 29) at weekly intervals immediately before the 2001 ragweed season. Symptom scores and medication use were recorded for the 2001 and 2002 ragweed seasons for all patients. A subset of patients (12 receiving AIC and 7 receiving placebo) consented to have nasal biopsy specimens taken before immunization and before and after the first ragweed season. The preseason and postseason biopsy specimens were taken 24 hours after ragweed allergen challenge and compared with the initial unchallenged biopsy specimen to assess cytokine and inflammatory cell responses by using immunocytochemistry and in situ hybridization. Results: AIC was safe and well tolerated by all patients. There was no difference between the AIC and placebo groups in the number of allergen-induced major basic protein-, IL-4-, IL-5-, or IFN-gamma-positive cells in the mucosa in the first weeksafter AIC immunization. On rechallenge and rebiopsy after the end of the 2001 ragweed season, however, AIC-treated patients had a significantly reduced increase in eosinophils and IL-4 mRNA-positive cells and an increased number of IFN-gamma mRNA-positive cells compared with placebo-treated patients. No difference between treatment groups was observed in symptom scores or medication use during the first ragweed season. During the second ragweed season, however, there was a significant decrease in chest symptoms and a trend toward reduced nasal symptoms in the AIC-treated group. Conclusion: Short-course immunotherapy with AIC can modify the response of nasal mucosa to allergen challenge by increasing T(H)1 cytokine production and decreasing T(H)2 cytokine production and eosinophilia. This modification was not immediate but was observed 4 to 5 months after completion of immunotherapy and seasonal ragweed-pollen exposure. The T-cell subset shift after immunization and seasonal exposure was followed by evidence of clinical efficacy in the second ragweed season without additional AIC immunizations.	McGill Univ, Meakins Christie Labs, Montreal, PQ H2X 2P2, Canada; Univ Montreal, Ctr Hosp, Montreal, PQ, Canada; Dynavax Technol Corp, Berkeley, CA USA	Hamid, Q (reprint author), McGill Univ, Meakins Christie Labs, 3626 St Urbain St, Montreal, PQ H2X 2P2, Canada.		Tulic, Meri/P-6613-2016				CHRISTODOULOPOU.P, 2002, J ALLERGY CLIN IMMUN, V109, P973; Creticos PS, 2000, J ALLERGY CLIN IMMUN, V105, pS70, DOI 10.1016/S0091-6749(00)90645-6; Durham SR, 1999, NEW ENGL J MED, V341, P468, DOI 10.1056/NEJM199908123410702; Durham SR, 1996, J ALLERGY CLIN IMMUN, V97, P1356, DOI 10.1016/S0091-6749(96)70205-1; DURHAM SR, 1995, INT ARCH ALLERGY IMM, V107, P282; DURHAM SR, 1997, ARB P EHRLICH I BUND, V91, P33; FREW AJ, 1988, J IMMUNOL, V141, P4158; HAMID Q, 1987, P NATL ACAD SCI USA, V84, P6760, DOI 10.1073/pnas.84.19.6760; HAMID Q, 1991, J CLIN INVEST, V87, P1541, DOI 10.1172/JCI115166; Hamid QA, 1997, J ALLERGY CLIN IMMUN, V99, P254, DOI 10.1016/S0091-6749(97)70106-4; Marshall JD, 2001, J ALLERGY CLIN IMMUN, V108, P191, DOI 10.1067/mai.2001.116984; Nakamura Y, 1999, J ALLERGY CLIN IMMUN, V103, P215, DOI 10.1016/S0091-6749(99)70493-8; Santeliz JV, 2002, J ALLERGY CLIN IMMUN, V109, P455, DOI 10.1067/mai.2002.122156; Tighe H, 2000, J ALLERGY CLIN IMMUN, V106, P124, DOI 10.1067/mai.2000.107927; VARNEY VA, 1992, AM REV RESPIR DIS, V146, P170	15	152	170	0	3	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	FEB	2004	113	2					235	241		10.1016/j.jaci.2003.11.001		7	Allergy; Immunology	Allergy; Immunology	773EX	WOS:000188885700008	14767435	
J	Papadopoulos, NG; Stanciu, LA; Papi, A; Holgate, ST; Johnston, SL				Papadopoulos, NG; Stanciu, LA; Papi, A; Holgate, ST; Johnston, SL			A defective type 1 response to rhinovirus in atopic asthma	THORAX			English	Article							RESPIRATORY SYNCYTIAL VIRUS; COMMON COLD VIRUS; VIRAL-INFECTIONS; AIRWAYS INFLAMMATION; GAMMA PRODUCTION; NATURAL-KILLER; MESSENGER-RNA; OLD CHILDREN; T-CELLS; CYTOKINE	Background: Rhinoviruses (RVs) are the most frequent precipitants of the common cold and asthma exacerbations, but little is known about the immune response to these viruses and its potential implications in the pathogenesis of asthma. Methods: Peripheral blood mononuclear cells (PBMC) from patients with atopic asthma and normal subjects were exposed to live or inactivated RV preparations. Levels of interferon (IFN)gamma and interleukins IL-12, IL-10, IL-4, IL-5 and IL-13 were evaluated in the culture supernatants with specific immunoassays. Results: Exposure of PBMC to RVs induced the production of IFNgamma, IL-12, IL-10, and IL-13. Cells from asthmatic subjects produced significantly lower levels of IFNgamma and IL-12 and higher levels of IL-10 than normal subjects. IL-4 was induced only in the asthmatic group, while the IFNgamma/IL-4 ratio was more than three times lower in the asthmatic group. Conclusions: This evidence suggests that the immune response to RVs is not uniquely of a type 1 phenotype, as previously suggested. The type 1 response is defective in atopic asthmatic individuals, with a shift towards a type 2 phenotype in a way similar, but not identical, to their aberrant response to allergens. A defective type 1 immune response to RVs may be implicated in the pathogenesis of virus induced exacerbations of asthma.	Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Resp Med, Fac Med, London W2 1PG, England; Univ Southampton, Southampton Gen Hosp, Southampton SO16 6YD, Hants, England	Johnston, SL (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Resp Med, Fac Med, London W2 1PG, England.		Johnston, Sebastian/I-2423-2012; Papadopoulos, Nikolaos/L-8670-2013	Papadopoulos, Nikolaos/0000-0002-4448-3468; Papadopoulos, Nikolaos/0000-0002-2508-3872; PAPI, ALBERTO/0000-0002-6924-4500			ALWAN WH, 1994, J EXP MED, V179, P81, DOI 10.1084/jem.179.1.81; Borish L, 1997, J ALLERGY CLIN IMMUN, V99, P161, DOI 10.1016/S0091-6749(97)70090-3; Borish L, 1996, J ALLERGY CLIN IMMUN, V97, P1288, DOI 10.1016/S0091-6749(96)70197-5; CALHOUN WJ, 1994, J CLIN INVEST, V94, P2200, DOI 10.1172/JCI117581; Cousens LP, 1999, J EXP MED, V189, P1315, DOI 10.1084/jem.189.8.1315; COYLE AJ, 1995, J EXP MED, V181, P1229, DOI 10.1084/jem.181.3.1229; CRUMP CE, 1994, ANTIMICROB AGENTS CH, V38, P1425; Fischer JE, 1997, J VIROL, V71, P8672; FRAENKEL DJ, 1995, AM J RESP CRIT CARE, V151, P879; Gern JE, 1996, J IMMUNOL, V157, P1605; Gern JE, 1996, J IMMUNOL, V156, P621; Gern JE, 2000, AM J RESP CRIT CARE, V162, P2226; Grunberg K, 1999, CLIN EXP ALLERGY, V29, P65; HOFER F, 1994, P NATL ACAD SCI USA, V91, P1839, DOI 10.1073/pnas.91.5.1839; HSIA J, 1990, J INFECT DIS, V162, P591; Hussell T, 1996, J GEN VIROL, V77, P2447, DOI 10.1099/0022-1317-77-10-2447; JOHNSTON SL, 1995, BRIT MED J, V310, P1225; Johnston SL, 1997, J INFECT DIS, V175, P323; JOHNSTON SL, 1995, AM J RESP CRIT CARE, V152, P546; Johnston SL, 1995, DIAGNOSTIC PROCEDURE, P553; Kaur B, 1998, BRIT MED J, V316, P118; LEVANDOWSKI RA, 1986, J INFECT DIS, V153, P743; LEVANDOWSKI RA, 1991, J MED VIROL, V35, P116, DOI 10.1002/jmv.1890350208; Marone G, 1998, IMMUNOL TODAY, V19, P5, DOI 10.1016/S0167-5699(97)01187-0; McInnes E, 1998, RES VET SCI, V64, P163, DOI 10.1016/S0034-5288(98)90013-3; NICHOLSON KG, 1993, BRIT MED J, V307, P982; Orange JS, 1996, J IMMUNOL, V156, P1138; PANUSKA JR, 1995, J CLIN INVEST, V96, P2445, DOI 10.1172/JCI118302; Papadopoulos NG, 1999, J MED VIROL, V58, P100, DOI 10.1002/(SICI)1096-9071(199905)58:1<100::AID-JMV16>3.0.CO;2-D; PAPADOPOULOS NG, 1999, DIFFICULT ASTHMA, P183; Papi A, 1999, J BIOL CHEM, V274, P9707, DOI 10.1074/jbc.274.14.9707; Ramshaw IA, 1997, IMMUNOL REV, V159, P119, DOI 10.1111/j.1600-065X.1997.tb01011.x; Robinson DS, 1996, AM J RESP CELL MOL, V14, P113; Romagnani S, 1997, IMMUNOL TODAY, V18, P263, DOI 10.1016/S0167-5699(97)80019-9; SCOTT P, 1993, SCIENCE, V260, P496, DOI 10.1126/science.8097337; SUBAUSTE MC, 1995, J CLIN INVEST, V96, P549, DOI 10.1172/JCI118067; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; Wimalasundera SS, 1997, J INFECT DIS, V176, P755; Zhu Zhou, 1999, Journal of Clinical Investigation, V103, P779, DOI 10.1172/JCI5909	39	152	164	0	4	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	APR	2002	57	4					328	332		10.1136/thorax.57.4.328		5	Respiratory System	Respiratory System	541JJ	WOS:000174981200009	11923551	
J	McDuffie, HH; Pahwa, P; McLaughlin, JR; Spinelli, JJ; Fincham, S; Dosman, JA; Robson, D; Skinnider, LF; Choi, NW				McDuffie, HH; Pahwa, P; McLaughlin, JR; Spinelli, JJ; Fincham, S; Dosman, JA; Robson, D; Skinnider, LF; Choi, NW			Non-Hodgkin's lymphoma and specific pesticide exposures in men: Cross-Canada study of pesticides and health	CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION			English	Article							SOFT-TISSUE SARCOMA; MULTIPLE-MYELOMA; MALIGNANT-LYMPHOMA; CIGARETTE-SMOKING; CANCER MORTALITY; RISK-FACTORS; FARMERS; OCCUPATIONS; HERBICIDES; APPLIERS	Our objective in the study was to investigate the putative associations of specific pesticides with non-Hodgkin's Lymphoma [NHL; International Classification of Diseases, version 9 (ICD-9) 200, 202]. We conducted a Canadian multicenter population-based incident, case (n = 517)-control (n = 1506) study among men in a diversity of occupations using an initial postal questionnaire followed by a telephone interview for those reporting pesticide exposure of 10 h/year or more, and a 15% random sample of the remainder. Adjusted odds ratios (ORs) were computed using conditional logistic regression stratified by the matching variables of age and province of residence, and subsequently adjusted for statistically significant medical variables (history of measles, mumps, cancer, allergy desensitization treatment, and a positive history of cancer in first-degree relatives). We found that among major chemical classes of herbicides, the risk of NHL was statistically significantly increased by exposure to phenoxyherbicides [OR, 1.38; 95% confidence interval (CI), 1.06-1.81] and to dicamba (OR, 1.88; 95% Cl, 1.32-2.68). Exposure to carbamate (OR, 1.92; 95% CI, 1.22-3.04) and to organophosphorus insecticides (OR, 1.73; 95% Cl, 1.27-2.36), amide fungicides, and the fumigant carbon tetrachloride (OR, 2.42; 95% Cl, 1.19-5.14) statistically significantly increased risk. Among individual compounds, in multivariate analyses, the risk of NHL was statistically significantly increased by exposure to the herbicides 2,4-dichlorophenoxyacetic acid (2,4-D; OR, 1.32; 95% CL 1.01-1.73), mecoprop (OR, 2.33; 95% CI, 1.58-3.44), and dicamba (OR, 1.68; 95% CI, 1.00-2.81); to the insecticides malathion (OR, 1.83; 95% Cl, 1.31-2.55), 1,1,1-trichloro-2,2-bis (4-chlorophenyl) ethane (DDT), carbaryl (OR, 2.11; 95% CI, 1.21-3.69), aldrin, and lindane; and to the fungicides captan and sulfur compounds. In additional multivariate models, which included exposure to other major chemical classes or individual pesticides, personal antecedent cancer, a history of cancer among first-degree relatives, and exposure to mixtures containing dicamba (OR, 1.96; 95% CL 1.40-2.75) or to mecoprop (OR, 2.22; 95% CL 1.49-3.29) and to aldrin (OR, 3.42; 95% Cl, 1.18-9.95) were significant independent predictors of an increased risk for NHL, whereas a personal history of measles and of allergy desensitization treatments lowered the risk. We concluded that NHL was associated with specific pesticides after adjustment for other independent predictors.	Univ Saskatchewan, Ctr Agr Med, Saskatoon, SK S7N 0W8, Canada; Univ Toronto, Natl Canc Inst, Epidemiol Unit, Toronto, ON M5S 1A8, Canada; St Pauls Hosp, Ctr Hlth Evaluat & Outcome Sci, Vancouver, BC V6Z 1Y6, Canada; Alberta Canc Board, Div Epidemiol Prevent & Screening, Edmonton, AB T6G 1Z2, Canada; Allan Blair mem Ctr, Saskatchewan Canc Agcy, Regina, SK S4T 7TA, Canada; Univ Saskatchewan, Dept Pathol, Saskatoon, SK S7N 0W8, Canada; Manitoba Canc Treatment & Res Fdn, Winnipeg, MB R3E 0V9, Canada	McDuffie, HH (reprint author), Royal Univ Hosp, Ctr Agr Med, 103 Hosp Dr,POB 120, Saskatoon, SK S7N 0W8, Canada.		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Biomarkers Prev.	NOV	2001	10	11					1155	1163				9	Oncology; Public, Environmental & Occupational Health	Oncology; Public, Environmental & Occupational Health	492DX	WOS:000172154100007	11700263	
J	Wu, PS; Dupont, WD; Griffin, MR; Carroll, KN; Mitchel, EF; Gebretsadik, T; Hartert, TV				Wu, Pingsheng; Dupont, William D.; Griffin, Marie R.; Carroll, Kecia N.; Mitchel, Edward F.; Gebretsadik, Tebeb; Hartert, Tina V.			Evidence of a Causal Role of Winter Virus Infection during Infancy in Early Childhood Asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; respiratory winter virus infection; timing of birth	RESPIRATORY-SYNCYTIAL-VIRUS; VIRAL-INFECTIONS; LUNG-DISEASE; RISK-FACTORS; BRONCHIOLITIS; AGE; CHILDREN; ALLERGY; BIRTH; PATHOGENESIS	Rationale: Bronchiolitis during infancy is associated with an increased risk of childhood asthma. Whether winter viral infections cause asthma or are a manifestation of a predisposition to asthma development is unknown. Objectives: To study the relationship of winter virus infection during infancy and the development of childhood asthma. Methods: We studied over 95,000 infants born between 1995 and 2000 and followed through 2005 who were enrolled in the Tennessee Medicaid program from birth through early childhood to determine whether infant birth in relationship to the wintervirus peak alters the risk of developing early childhood asthma. Measurements and Main Results: Among 95,310 children studied during five winter virus seasons from birth through early childhood, the risk of developing asthma tracked with the timing of infant birth in relationship to the winter virus peak. Infant birth approximately 4 months before the winter virus peak carried the highest risk, with a 29% increase in odds of developing asthma compared with birth 12 months before the peak (adjusted odds ratio, 1.29; 95% confidence interval, 1.19-1.40). Infant age at the winter virus peak was comparable to or greater than other known risk factors for asthma. Conclusions: Timing of birth in relationship to winter virus season confers a differential and definable risk of developing early childhood asthma, establishing winter virus seasonality as a causal factor in asthma development. Delay of exposure or prevention of winter viral infection during early infancy could prevent asthma.	[Wu, Pingsheng; Hartert, Tina V.] Vanderbilt Univ, Sch Med, Div Allergy Pulm & Crit Care Med, Nashville, TN 37232 USA; [Wu, Pingsheng; Griffin, Marie R.; Hartert, Tina V.] Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37232 USA; [Wu, Pingsheng; Dupont, William D.; Gebretsadik, Tebeb] Vanderbilt Univ, Sch Med, Dept Biostat, Nashville, TN 37232 USA; [Griffin, Marie R.; Hartert, Tina V.] Vanderbilt Univ, Sch Med, Ctr Hlth Serv Res, Nashville, TN 37232 USA; [Griffin, Marie R.; Hartert, Tina V.] Vanderbilt Univ, Sch Med, Inst Med & Publ Hlth, Nashville, TN 37232 USA; [Dupont, William D.; Griffin, Marie R.; Mitchel, Edward F.] Vanderbilt Univ, Sch Med, Dept Prevent Med, Nashville, TN 37232 USA; [Carroll, Kecia N.] Vanderbilt Univ, Sch Med, Dept Pediat, Nashville, TN 37232 USA	Hartert, TV (reprint author), Vanderbilt Univ, Sch Med, Div Allergy Pulm & Crit Care Med, 6107 Med Ctr E, Nashville, TN 37232 USA.	tina.hartert@vanderbilt.edu	Dupont, William/I-4430-2012		NIH [U01 HL 072,471, F32 HL 086,048]; Thrasher Research Fund	Supported by research grants from NIH U01 HL 072,471 (T.V.H.), Thrasher Research Fund (P.W., T.V.H.), and NIH F32 HL 086,048 (P.W., T.V.H.).	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J. Respir. Crit. Care Med.	DEC 1	2008	178	11					1123	1129		10.1164/rccm.200804-579OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	378GO	WOS:000261309400005	18776151	
J	Bollinger, ME; Dahlquist, LM; Mudd, K; Sonntag, C; Dillinger, L; McKenna, K				Bollinger, ME; Dahlquist, LM; Mudd, K; Sonntag, C; Dillinger, L; McKenna, K			The impact of food allergy on the daily activities of children and their families	ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY			English	Article							QUALITY-OF-LIFE; PEANUT ALLERGY; POPULATION; PARENTS	Background: Food allergy affects a significant number of children, and its management requires considerable time and vigilance. Objective: To determine the impact of food allergy on the daily activities of food allergic children and their families. Methods: Caregivers of food allergic children from a university-based allergy practice completed a questionnaire that evaluated their perception of the impact of their child's food allergy on family activities. Results: Of the 87 families who completed the study, more than 60% of caregivers reported that food allergy significantly affected meal preparation and 49% or more indicated that food allergy affected family social activities. Forty-one percent of parents reported a significant impact on their stress levels and 34% reported that food allergy had an impact on school attendance, with 10% choosing to home school their children because of food allergy. The number of food allergies had a significant impact on activity scores, but the existence of comorbid conditions such as asthma and atopic dermatitis did not significantly affect the results. Conclusions: Food allergy has a significant effect on activities of families of food allergic children. Further study is needed to determine more detailed effects of food allergy on parent-child interactions and development.	Univ Maryland, Sch Med, Div Pediat Pulmonol Allergy, Baltimore, MD 21201 USA; Univ Maryland Baltimore Cty, Dept Psychol, Baltimore, MD 21228 USA	Bollinger, ME (reprint author), Univ Maryland, Sch Med, Div Pediat Pulmonol Allergy, Baltimore, MD 21201 USA.	mbolling@peds.umaryland.edu					Altschul AS, 2001, J ALLERGY CLIN IMMUN, V108, P468, DOI 10.1067/mai.2001.117794; AVERY NJ, 2003, PEDIATR ALLERGY IMMU, V12, P378; Bock SA, 2001, J ALLERGY CLIN IMMUN, V107, P191, DOI 10.1067/mai.2001.112031; Burks AW, 1998, J PEDIATR-US, V132, P132, DOI 10.1016/S0022-3476(98)70498-6; Cohen BL, 2004, J ALLERGY CLIN IMMUN, V114, P1159, DOI 10.1016/j.jaci.2004.08.007; CRNIC KA, 1990, CHILD DEV, V61, P1628, DOI 10.1111/j.1467-8624.1990.tb02889.x; DeVellis R. F., 2003, SCALE DEV THEORY APP; Joshi P, 2002, J ALLERGY CLIN IMMUN, V109, P1019, DOI 10.1067/mai.2002.123305; Juniper EF, 1998, J ALLERGY CLIN IMMUN, V101, P163; Landgraf JM, 1996, CHILD HLTH QUESTIONA; Nowak-Wegrzyn A, 2001, ARCH PEDIAT ADOL MED, V155, P790; Nunnally J. C., 1994, PSYCHOMETRIC THEORY; Parker JG, 1995, DEV PSYCHOPATHOL, V2, P96; Primeau MN, 2000, CLIN EXP ALLERGY, V30, P1135, DOI 10.1046/j.1365-2222.2000.00889.x; Sampson HA, 1996, ANNU REV NUTR, V16, P161, DOI 10.1146/annurev.nutr.16.1.161; Sicherer SH, 2001, ANN ALLERG ASTHMA IM, V87, P461; Stein REK, 2003, J DEV BEHAV PEDIATR, V24, P9; Wensing M, 2002, J ALLERGY CLIN IMMUN, V110, P915, DOI 10.1067/mai.2002.129235; Wood RA, 2003, PEDIATRICS, V111, P1631; Yocum MW, 1999, J ALLERGY CLIN IMMUN, V104, P452, DOI 10.1016/S0091-6749(99)70392-1	20	151	151	1	30	AMER COLL ALLERGY ASTHMA IMMUNOLOGY	ARLINGTON HTS	85 WEST ALGONQUIN RD SUITE 550, ARLINGTON HTS, IL 60005 USA	1081-1206			ANN ALLERG ASTHMA IM	Ann. Allergy Asthma Immunol.	MAR	2006	96	3					415	421				7	Allergy; Immunology	Allergy; Immunology	026XU	WOS:000236377400009	16597075	
J	Werfel, T; Breuer, K; Rueff, F; Przybilla, B; Worm, M; Grewe, M; Ruzicka, T; Brehler, R; Wolf, H; Schnitker, J; Kapp, A				Werfel, T; Breuer, K; Rueff, F; Przybilla, B; Worm, M; Grewe, M; Ruzicka, T; Brehler, R; Wolf, H; Schnitker, J; Kapp, A			Usefulness of specific immunotherapy in patients with atopic dermatitis and allergic sensitization to house dust mites: a multi-centre, randomized, dose-response study	ALLERGY			English	Article						atopic dermatitis; eczema; house dust mite; hyposensitization; specific immunotherapy	PATCH TEST; T-CELLS; HYPOSENSITIZATION; SKIN	Background: The effect of specific immunotherapy (SIT) on eczema in atopic dermatitis is not known. Therefore, a multi-centre, randomized dose-response trial, double-blind with respect to the efficacy of a biologically standardized depot house dust mite preparation was performed. Methods: Eighty-nine adults with a chronic course of atopic dermatitis, SCORAD >= 40 and allergic sensitization to house dust mites [CAP-FEIA >= 3] were included, of whom 51 completed the study. Subcutaneous SIT with a house dust mite preparation (Dermatophagoides pteronyssinus/D. farinae) applying maintenance doses of 20, 2000 and 20 000 SQ-U in weekly intervals for 1 year. The main outcome measures addressed the change of the SCORAD as average of the values after 9 and 12 months of SIT in comparison with the value at baseline. Results: The SCORAD declined in the three dose groups in a dose-dependent manner (P = 0.0368, Jonckheere-Terpstra test) and was significantly lower in the two high-dose groups (2000, 20000 SQ-U) compared with the low-dose group of 20 SQ-U (P = 0.0379, U-test) after 1 year of SIT. The use of topical corticosteroids was significantly reduced with higher doses (P = 0.0007, Mantel-Haenszel chi-square test). Conclusions: Allergen-SIT for 1 year with a house dust mite preparation is able to improve the eczema in patients with atopic dermatitis who are sensitized to house dust mite allergens and reduces the need for topical corticosteroids. SIT may be valuable in the treatment of this chronic skin disease.	Hannover Med Sch, Dept Dermatol & Allergol, D-30449 Hannover, Germany; Univ Munich, Clin & Polyclin Dermatol & Allergol, Munich, Germany; Humboldt Univ, Dept Dermatol & Allergol, Berlin, Germany; Univ Dusseldorf, Dept Dermatol, D-4000 Dusseldorf, Germany; Univ Hosp, Dept Dermatol, Munster, Germany; ALK SCHERAX Arzneimittel GmbH, Clin Res, Hamburg, Germany; Inst Angew Stat GmbH, Bielefeld, Germany	Werfel, T (reprint author), Hannover Med Sch, Dept Dermatol & Allergol, Ricklinger Str, D-30449 Hannover, Germany.						Di Prisco de Fuenmayor MC, 1979, BRIT J DERMATOL, V101, P697; Galli E, 1994, Allergol Immunopathol (Madr), V22, P18; Grewe M, 1998, IMMUNOL TODAY, V19, P359, DOI 10.1016/S0167-5699(98)01285-7; LEROY BP, 1993, J AM ACAD DERMATOL, V28, P232, DOI 10.1016/0190-9622(93)70033-P; Mastrandrea F, 2001, EXPERT OPIN INV DRUG, V10, P49, DOI 10.1517/13543784.10.1.49; MITCHELL EB, 1982, LANCET, V1, P127; Pacor Maria Luisa, 1994, Recenti Progressi in Medicina, V85, P273; RING J, 1982, BRIT J DERMATOL, V107, P597, DOI 10.1111/j.1365-2133.1982.tb00412.x; SAGER N, 1992, J ALLERGY CLIN IMMUN, V89, P801, DOI 10.1016/0091-6749(92)90434-4; SEIDENARI S, 1986, DERMATOLOGICA, V172, P229; STALDER JF, 1993, DERMATOLOGY, V186, P23; Trofimowicz A, 1995, Rocz Akad Med Bialymst, V40, P414; Werfel T, 1998, ALLERGY, V53, P731; Werfel T, 1996, J INVEST DERMATOL, V107, P871, DOI 10.1111/1523-1747.ep12331164; Zachariae H, 1985, Acta Derm Venereol Suppl (Stockh), V114, P48	15	151	158	0	9	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0105-4538			ALLERGY	Allergy	FEB	2006	61	2					202	205		10.1111/j.1398-9995.2006.00974.x		4	Allergy; Immunology	Allergy; Immunology	001XJ	WOS:000234575700009	16409197	
J	Ricciardolo, FLM				Ricciardolo, FLM			Multiple roles of nitric oxide in the airways	THORAX			English	Review							GUINEA-PIG TRACHEA; OBSTRUCTIVE PULMONARY-DISEASE; VASOACTIVE-INTESTINAL-PEPTIDE; VASCULAR SMOOTH-MUSCLE; EXHALED AIR; IN-VITRO; L-ARGININE; ASTHMATIC-PATIENTS; RELAXING FACTOR; MILD ASTHMA	Nitric oxide is endogenously released in the airways by nitric oxide synthase. Functionally, two isoforms of this enzyme exist: constitutive and inducible. The former seems to protect airways from excessive bronchoconstriction while the latter has a modulatory role in inflammatory disorders of the airways such as asthma. This review explores the physiological and pathophysiological role of endogenous nitric oxide in the airways, and the clinical aspects of monitoring nitric oxide in exhaled air of patients with respiratory disease.	Osped Riuniti Bergamo, Dept Resp Dis, I-24100 Bergamo, Italy	Ricciardolo, FLM (reprint author), Osped Riuniti Bergamo, Dept Resp Dis, Largo Barozzi 1, I-24100 Bergamo, Italy.						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J	Kharitonov, SA; Barnes, PJ				Kharitonov, Sergei A.; Barnes, Peter J.			Exhaled biomarkers	CHEST			English	Article						asthma; COPD; exhaled breath condensate; exhaled nitric oxide	NITRIC-OXIDE MEASUREMENTS; OBSTRUCTIVE PULMONARY-DISEASE; BREATH CONDENSATE; ASTHMA; COPD; LUNG; MARKERS; PROSTAGLANDINS; LEUKOTRIENES; AIR	Assessing airway and lung inflammation is important for investigating the underlying mechanisms of asthma and COPD. Yet these cannot be measured directly in clinical research and practice because of the difficulties in monitoring inflammation. Noninvasive monitoring may assist in early recognition of asthma and COPD, assessment of its severity, and response to treatment, especially during disease exacerbations. There is increasing evidence that breath analysis may have an important place in clinical management of asthma and COPD. The article reviews the role of current noninvasive measurements of exhaled gases, such as nitric oxide (NO), inflammatory markers in exhaled breath condensate (EBC), and exhaled breath temperature, as wen as novel methods in monitoring and management of asthma and COPD.	Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Royal Brompton & Natl Heart Hosp, London SW3 6LY, England	Kharitonov, SA (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Sect Airway Dis, Dovehouse St, London SW3 6LY, England.	s.kharitonov@imperial.ac.uk					ATS Workshop Proceedings, 2006, P AM THORAC SOC, V3, P131; Barnes PJ, 2006, AM J RESP CRIT CARE, V174, P6, DOI 10.1164/rccm.200510-1659PP; Biernacki WA, 2003, THORAX, V58, P294, DOI 10.1136/thorax.58.4.294; Brindicci C, 2005, EUR RESPIR J, V26, P52, DOI 10.1183/09031936.05.00125304; de Jongste J C, 2000, Paediatr Respir Rev, V1, P354; Dupont LJ, 2003, CHEST, V123, P751, DOI 10.1378/chest.123.3.751; Effros RM, 2003, AM J RESP CRIT CARE, V167, P91; Hunt JF, 2000, AM J RESP CRIT CARE, V161, P694; Jones SL, 2001, AM J RESP CRIT CARE, V164, P738; Kharitonov SA, 2001, AM J RESP CRIT CARE, V163, P1693; KHARITONOV SA, 1995, EUR RESPIR J, V8, P295, DOI 10.1183/09031936.95.08020295; Kharitonov SA, 2003, CURR ALLERGY ASTHM R, V3, P121, DOI 10.1007/s11882-003-0024-7; Kharitonov SA, 2004, SWISS MED WKLY, V134, P175; KHARITONOV SA, 1994, LANCET, V343, P133, DOI 10.1016/S0140-6736(94)90931-8; Kharitonov SA, 2003, EUR RESPIR J, V21, P433, DOI 10.1183/09031936.03.00066903; Kharitonov SA, 2002, THORAX, V57, P889, DOI 10.1136/thorax.57.10.889; Kharitonov SA, 1996, AM J RESP CRIT CARE, V153, pA799; Leung TF, 2005, THORAX, V60, P822, DOI 10.1136/thx.2004.039321; McCulloch M, 2006, INTEGR CANCER THER, V5, P30, DOI 10.1177/1534735405285096; Montuschi P, 2005, CLIN CHIM ACTA, V356, P22, DOI 10.1016/j.cccn.2005.01.012; Montuschi P, 2003, THORAX, V58, P585, DOI 10.1136/thorax.58.7.585; Montuschi P, 2002, J ALLERGY CLIN IMMUN, V109, P615, DOI 10.1067/mai.2002.122461; Montuschi P, 2005, THORAX, V60, P827, DOI 10.1136/thx.2004.035592; Paredi P, 2005, RESP RES, V6, DOI 10.1186/1465-9921-6-15; Smith AD, 2005, NEW ENGL J MED, V352, P2163, DOI 10.1056/NEJMoa043596; Van den Toorn LM, 2001, AM J RESP CRIT CARE, V164, P2107; van Straaten JFM, 1998, MODERN PATHOL, V11, P648	27	150	156	1	20	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	NOV	2006	130	5					1541	1546		10.1378/chest.130.5.1541		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	106OH	WOS:000242109800038	17099035	
J	Lai, CKW; de Guia, TS; Kim, YY; Kuo, SH; Mukhopadhyay, A; Soriano, JB; Trung, PL; Zhong, NS; Zainudin, N; Zainudin, BMZ				Lai, CKW; de Guia, TS; Kim, YY; Kuo, SH; Mukhopadhyay, A; Soriano, JB; Trung, PL; Zhong, NS; Zainudin, N; Zainudin, BMZ		Asthma Insights Reality Asia Pacif	Asthma control in the Asia-Pacific region: The asthma insights and reality in Asia-Pacific study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Asia; asthma epidemiology; asthma control; asthma management; inhaled corticosteroids	HONG-KONG; PREVALENCE; GUIDELINES; MANAGEMENT; EPIDEMIOLOGY; POPULATION; ISAAC	Background: Few data on asthma management are available for the Asia-Pacific region. Objective: This study examined asthma symptoms, health care use, and management in the Asia-Pacific region. Methods: We performed a cross-sectional survey, followed by administration of a questionnaire in a face-to-face setting in the respondents' homes in their language of choice. Urban centers in 8 areas were surveyed: China, Hong Kong, Korea, Malaysia, The Philippines, Singapore, Taiwan, and Vietnam. Results: A population sample of 3207 respondents with physician-diagnosed asthma was identified by screening 108,360 households. Daytime asthma symptoms were reported by 51.4% of respondents, and 44.3% reported sleep disturbance caused by asthma in the preceding 4 weeks. At least 2 in every 5 respondents (43.6%) had been hospitalized, attended a hospital emergency department, or made unscheduled emergency visits to other health care facilities for treatment of asthma during the previous 12 months. Overall, 15.3% of respondents reported that they had required admission to the hospital for asthma treatment. Asthma severity correlated with the frequencies of hospitalizations and emergency visits for asthma in the past year. Even in those patients with severe persistent asthma, 34.3% regarded their disease as being well or completely controlled. Current use of an inhaled corticosteroid was reported by only 13.6% of respondents, and 56.3% used quick-relief bronchodilators. Absence from school and work in the past year was reported by 36.5 % of children and 26.5 % of adults. Conclusion: As reported for other regions, current levels of asthma control in the Asia-Pacific region fall markedly short of goals specified in international guidelines for asthma management. (J Allergy Clin Immunol 2003; 111:263-8.).	Chinese Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China; Philippine Heart Ctr, Quezon City, Philippines; Seoul Natl Univ Hosp, Seoul 110744, South Korea; Natl Taiwan Univ Hosp, Taipei, Taiwan; Natl Univ Singapore Hosp, Singapore 117548, Singapore; GlaxoSmithKline Res & Dev Ltd, Worldwide Epidemiol, Greenford, Middx, England; Univ Med & Pharm, Ho Chi Minh City, Vietnam; Guangzhou Inst Resp Dis, Guangzhou, Peoples R China; Paediat Inst Hosp, Kuala Lumpur, Malaysia; Damansara Specialist Hosp, Petaling Jaya, Malaysia	Lai, CKW (reprint author), Room 1403,Tak Shing House,20 Voeux Rd Ctr, Hong Kong, Hong Kong, Peoples R China.			Soriano, Joan B/0000-0001-9740-2994			Adams RJ, 2002, J ALLERGY CLIN IMMUN, V110, P58, DOI 10.1067/mai.2002.125489; Asher MI, 1998, EUR RESPIR J, V12, P315; Beasley R., 2000, J ALLERGY CLIN IMMUN, V105, P466; Bousquet J, 1996, J ALLERGY CLIN IMMUN, V98, P514, DOI 10.1016/S0091-6749(96)70084-2; Choy DKL, 1999, CLIN EXP ALLERGY, V29, P84; Doerschug KC, 1999, AM J RESP CRIT CARE, V159, P1735; Enright PL, 1999, CHEST, V116, P603, DOI 10.1378/chest.116.3.603; FERRIS BG, 1978, AM REV RESPIR DIS, V118, P1; HE WQ, 2001, CHIN J TUBERC RESP D, V24, P444; Janson C, 1997, EUR RESPIR J, V10, P1795, DOI 10.1183/09031936.97.10081795; Kim YY, 1997, CLIN EXP ALLERGY, V27, P761, DOI 10.1046/j.1365-2222.1997.710839.x; Kish L, 1965, SURVEY SAMPLING; Lai CKW, 1996, CLIN EXP ALLERGY, V26, P5, DOI 10.1111/j.1365-2222.1996.tb00050.x; Legorreta AP, 1998, ARCH INTERN MED, V158, P457, DOI 10.1001/archinte.158.5.457; Leung R, 1997, EUR RESPIR J, V10, P354, DOI 10.1183/09031936.97.10020354; National Institutes of Health, 1995, NIH PUBL, V95-2754; Rabe KF, 2000, EUR RESPIR J, V16, P802, DOI 10.1183/09031936.00.16580200; Reid D, 2000, Respirology, V5, P281, DOI 10.1046/j.1440-1843.2000.00265.x; Taylor DM, 1999, CHEST, V116, P1638, DOI 10.1378/chest.116.6.1638; Woolcock A, 1998, Respirology, V3, P63, DOI 10.1111/j.1440-1843.1998.tb00098.x	20	150	180	0	8	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749	1097-6825		J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	FEB	2003	111	2					263	268		10.1067/mai.2003.30		6	Allergy; Immunology	Allergy; Immunology	644WF	WOS:000180942700007	12589343	
J	von Klot, S; Wolke, G; Tuch, T; Heinrich, J; Dockery, DW; Schwartz, J; Kreyling, WG; Wichmann, HE; Peters, A				von Klot, S; Wolke, G; Tuch, T; Heinrich, J; Dockery, DW; Schwartz, J; Kreyling, WG; Wichmann, HE; Peters, A			Increased asthma medication use in association with ambient fine and ultrafine particles	EUROPEAN RESPIRATORY JOURNAL			English	Article						asthma symptoms; inhaled beta(2)-agonists; inhaled corticosteroids; particulate air pollution; wheezing	PARTICULATE AIR-POLLUTION; PEAK EXPIRATORY FLOW; CHRONIC RESPIRATORY SYMPTOMS; TIME-SERIES; URBAN AIR; LONGITUDINAL DATA; PM10 POLLUTION; HEALTH; CHILDREN; MODELS	The association between particulate air pollution and asthma medication use and symptoms was assessed in a panel study of 53 adult asthmatics in Erfurt, Germany in winter 1996/1997. Number concentrations of ultrafine particles, 0.01-0.1 mum in diameter (NC0.01-0.1), mean 17,300.cm(-3), and mass concentrations of fine particles 0.01-2.5 mum in diameter (MC0.01-2.5), mean 30.3 mug.m(-3), were measured concurrently. They were not highly correlated (r=0.45). The associations between ambient particle concentrations and the prevalence of inhaled beta(2)-agonist, corticosteroid use and asthma symptoms, were analysed separately with logistic regression models, adjusting for trend, temperature, weekend, holidays, and first order autocorrelation of the error. Cumulative exposures over 14 days of ultrafine and fine particles were associated with corticosteroid use. beta(2)-agonist use was associated with 5-day mean NC0.01-0.1 and MC0.01-2.5. The prevalence of asthma symptoms was associated with ambient particle concentrations. The results suggest that reported asthma medication use and symptoms increase in association with particulate air pollution and gaseous pollutants such as nitrogen dioxide.	GSF, Natl Res Ctr Environm Hlth, Inst Epidemiol, D-85758 Neuherberg, Germany; Univ Munich, Inst Med Informat Biometry & Epidemiol, Chair Epidemiol, Munich, Germany; Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA; GSF, Natl Res Ctr Environm Hlth, Inst Inhalat Biol, D-85758 Neuherberg, Germany	von Klot, S (reprint author), GSF, Natl Res Ctr Environm Hlth, Inst Epidemiol, POB 1129, D-85758 Neuherberg, Germany.		Peters, Annette/A-6117-2011	Kreyling, Wolfgang/0000-0002-0702-6567			Boezen HM, 1999, LANCET, V353, P874, DOI 10.1016/S0140-6736(98)06311-9; Brumback BA, 2000, J AM STAT ASSOC, V95, P16; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; Delfino RJ, 1998, ENVIRON HEALTH PERSP, V106, P751, DOI 10.1289/ehp.98106751; DOCKERY DW, 1994, ANNU REV PUBL HEALTH, V15, P107, DOI 10.1146/annurev.pu.15.050194.000543; DUSSELDORP A, 1995, AM J RESP CRIT CARE, V152, P1932; Gielen MH, 1997, AM J RESP CRIT CARE, V155, P2105; Hiltermann TJN, 1998, EUR RESPIR J, V11, P686; Hoek G, 1998, EUR RESPIR J, V11, P1307, DOI 10.1183/09031936.98.11061307; Janssen NAH, 2000, J AIR WASTE MANAGE, V50, P1133; Katsouyanni K, 1996, J EPIDEMIOL COMMUN H, V50, pS12, DOI 10.1136/jech.50.Suppl_1.S12; LIANG KY, 1986, BIOMETRIKA, V73, P13, DOI 10.1093/biomet/73.1.13; Neukirch F, 1998, ARCH ENVIRON HEALTH, V53, P320; Pekkanen J, 1997, ENVIRON RES, V74, P24, DOI 10.1006/enrs.1997.3750; Penttinen P, 2001, EUR RESPIR J, V17, P428, DOI 10.1183/09031936.01.17304280; Peters A, 1997, ENVIRON HEALTH PERSP, V105, P430, DOI 10.1289/ehp.97105430; Peters A, 1997, EUR RESPIR J, V10, P872; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; POPE A, 1999, AIR POLLUTION HLTH, P673; POPE CA, 1991, AM REV RESPIR DIS, V144, P668; Pope CA, 2000, ENVIRON HEALTH PERSP, V108, P713, DOI 10.2307/3454408; POPE CA, 1992, AM REV RESPIR DIS, V145, P1123; POPE CA, 1996, AM J RESP CRIT CARE, V154, P229; Richter K, 1999, ALLERGOLOGIE, V22, P14; ROEMER W, 1993, AM REV RESPIR DIS, V147, P118; Roemer W, 1998, EUR RESPIR J, V12, P1354, DOI 10.1183/09031936.98.12061354; Roemer W, 2000, EUR RESPIR J, V15, P553, DOI 10.1034/j.1399-3003.2000.15.21.x; Roemer W, 2000, CLIN EXP ALLERGY, V30, P1067; Schwartz J, 1996, J AIR WASTE MANAGE, V46, P927, DOI 10.1080/10473289.1996.10467528; Schwartz J, 1999, ENVIRON HEALTH PERSP, V107, P339, DOI 10.2307/3434536; SCHWARTZ J, 1991, ENVIRON HEALTH PERSP, V90, P181, DOI 10.2307/3430866; SEATON A, 1995, LANCET, V345, P176, DOI 10.1016/S0140-6736(95)90173-6; SEGALA C, 1998, EUR RESPIR J, V11, P577; SILVERMAN F, 1992, ARCH ENVIRON HEALTH, V47, P51; Tiittanen P, 1999, EUR RESPIR J, V13, P266, DOI 10.1034/j.1399-3003.1999.13b08.x; Tuch T, 2000, ATMOS ENVIRON, V34, P139, DOI 10.1016/S1352-2310(99)00248-4; Tuch T, 1997, ATMOS ENVIRON, V31, P4193, DOI 10.1016/S1352-2310(97)00260-4; van der Zee SC, 1999, OCCUP ENVIRON MED, V56, P802; van der Zee SC, 2000, EUR RESPIR J, V15, P700, DOI 10.1034/j.1399-3003.2000.15d13.x; Wichmann HE, 2000, PHILOS T ROY SOC A, V358, P2751; Tuch T, 2000, RES REP HLTH EFF I, V98, P5; ZEGER SL, 1988, BIOMETRICS, V44, P1049, DOI 10.2307/2531734	42	150	151	0	13	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. 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J	DeMeo, MT; Mutlu, EA; Keshavarzian, A; Tobin, MC				DeMeo, MT; Mutlu, EA; Keshavarzian, A; Tobin, MC			Intestinal permeation and gastrointestinal disease	JOURNAL OF CLINICAL GASTROENTEROLOGY			English	Review						intestinal permeation; gastrointestinal disease; gastrointestinal tract	INFLAMMATORY-BOWEL-DISEASE; MULTIPLE ORGAN FAILURE; SEVERE ACUTE-PANCREATITIS; FIRST-DEGREE RELATIVES; 1ST DEGREE RELATIVES; COWS MILK ALLERGY; CROHNS-DISEASE; BACTERIAL TRANSLOCATION; CELIAC-DISEASE; INCREASED PERMEABILITY	The gastrointestinal tract constitutes one of the largest sites of exposure to the outside environment. The function of the gastrointestinal tract in monitoring and sealing the host interior from intruders is called the gut barrier. A variety of specific and nonspecific mechanisms are in operation to establish the host barrier: these include luminal mechanisms and digestive enzymes, the epithelial cells together with tight junctions in between them, and the gut immune system. Disruptions in the gut barrier follow injury from various causes including nonsteroidal anti-inflammatory drugs and oxidant stress, and involve mechanisms such as adenosine triphosphate depletion and damage to epithelial cell cytoskeletons that regulate tight junctions. Ample evidence links gut barrier dysfunction to multiorgan system failure in sepsis and immune dysregulation. Additionally, contribution of gut barrier dysfunction to gastrointestinal disease is an evolving concept and is the focus of this review. An overview of the evidence for the role of gut barrier dysfunction in disorders such as Crohn's disease, celiac disease. food allergy, acute pancreatitis, non-alcoholic fatty liver disease., and alcoholic liver disease is provided, together with critical insight into the implications of this evidence as a primary disease mechanism.	Rush Univ, Rush Presbyterian St Lukes Med Ctr, Div Gastroenterol & Nutr, Chicago, IL 60612 USA; Rush Univ, Rush Presbyterian St Lukes Med Ctr, Div Allergy & Immunol, Chicago, IL 60612 USA	DeMeo, MT (reprint author), Rush Univ, Rush Presbyterian St Lukes Med Ctr, Div Gastroenterol & Nutr, Profess Bldg,1725 W Harrison,Suite 206, Chicago, IL 60612 USA.						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Clin. Gastroenterol.	APR	2002	34	4					385	396		10.1097/00004836-200204000-00003		12	Gastroenterology & Hepatology	Gastroenterology & Hepatology	536RR	WOS:000174716100003	11907349	
J	Nafstad, P; Magnus, P; Gaarder, PI; Jaakkola, JJK				Nafstad, P; Magnus, P; Gaarder, PI; Jaakkola, JJK			Exposure to pets and atopy-related diseases in the first 4 years of life	ALLERGY			English	Article						allergic rhinitis; asthma; atopy; children; epidemiology; pets	RISK-FACTORS; RESPIRATORY HEALTH; FURRED PETS; HAY-FEVER; SENSITIZATION; ASTHMA; CHILDREN; ALLERGY; CAT; ENVIRONMENT	Background: It is still unclear how early-life exposure to pets is related to children's risk of developing atopy-related diseases. We estimated associations between early-life exposure to pets and atopy-related diseases at 0-4 years of life in a cohort of Norwegian children. Methods: A population-based cohort of 2531 children born in Oslo, Norway, was followed from birth to the age of 4 years. Information on early-life exposure to pets, a number of possible confounders, and atopy-related diseases was mainly collected by questionnaire. Results: In logistic regression analysis adjusting for potential confounders, the odds ratio for being exposed to pets in early life (reference category: not exposed) was, for bronchial obstruction at 0-2 years of life, 1.2 (95% confidence interval 0.9, 1.8); for asthma at the age of 4 years, 0.7 (0.5, 1.1); for allergic rhinitis at the age of 4 years, 0.6 (0.4, 1.0); and for atopic eczema at 0-6 months of life, 0.7 (0.5, 0.9). Conclusions: The results indicate that early-life exposure to pets or lifestyle factors associated with, exposure to pets reduce the risk of developing atopy-related diseases in early childhood. However, these findings might also be explained by selection for keeping pets.	Natl Publ Hlth Inst, Epidemiol Sect, Dept Populat Hlth Sci, N-0403 Oslo, Norway; Ulleval Univ Hosp, Dept Immunol & Transfus Med, Oslo, Norway; Nord Sch Publ Hlth, Gothenburg, Sweden	Nafstad, P (reprint author), Natl Publ Hlth Inst, Epidemiol Sect, Dept Populat Hlth Sci, POB 4404 Torshov, N-0403 Oslo, Norway.		Jaakkola, Jouni/G-4314-2012				ARSHAD SH, 1991, BRIT J CLIN PRACT, V45, P88; BRUNEKREEF B, 1992, INT J EPIDEMIOL, V21, P338, DOI 10.1093/ije/21.2.338; CHAPMAN MD, 1987, J ALLERGY CLIN IMMUN, V80, P184, DOI 10.1016/0091-6749(87)90128-X; Egmar AC, 1998, PEDIATR ALLERGY IMMU, V9, P31, DOI 10.1111/j.1399-3038.1998.tb00297.x; Frosh AC, 1999, CLIN EXP ALLERGY, V29, P457; Gordon S, 1997, CLIN EXP ALLERGY, V27, P479, DOI 10.1046/j.1365-2222.1997.d01-537.x; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; HONG CY, 1994, Q J MED, V87, P639; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Kleinert S, 2000, LANCET, V355, P1795, DOI 10.1016/S0140-6736(05)73062-2; KUEHR J, 1992, J ALLERGY CLIN IMMUN, V90, P358, DOI 10.1016/S0091-6749(05)80015-6; Munir AKM, 1997, J ALLERGY CLIN IMMUN, V100, P177, DOI 10.1016/S0091-6749(97)70221-5; MURRAY AB, 1983, J ALLERGY CLIN IMMUN, V72, P145, DOI 10.1016/0091-6749(83)90522-5; NAFSAD P, 1998, AM J RESP CRIT CARE, V157, P401; Nafstad P, 1999, PEDIATRICS, V103, P753, DOI 10.1542/peds.103.4.753; Nafstad P, 1996, EUR RESPIR J, V9, P2623, DOI 10.1183/09031936.96.09122623; Nafstad P, 1997, EPIDEMIOLOGY, V8, P293, DOI 10.1097/00001648-199705000-00011; Nafstad P, 2000, PEDIATRICS, V106, DOI 10.1542/peds.106.3.e38; POPP W, 1990, ALLERGY, V45, P75, DOI 10.1111/j.1398-9995.1990.tb01087.x; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Roost HP, 1999, J ALLERGY CLIN IMMUN, V104, P941, DOI 10.1016/S0091-6749(99)70072-2; STRACHAN DP, 1995, BRIT MED J, V311, P1053; Svanes C, 1999, J ALLERGY CLIN IMMUN, V103, P415, DOI 10.1016/S0091-6749(99)70465-3; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7	25	150	155	0	10	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	APR	2001	56	4					307	312		10.1034/j.1398-9995.2001.00881.x		6	Allergy; Immunology	Allergy; Immunology	415DR	WOS:000167706000007	11284797	
J	Tolbert, PE; Mulholland, JA; MacIntosh, DL; Xu, F; Daniels, D; Devine, OJ; Carlin, BP; Klein, M; Dorley, J; Butler, AJ; Nordenberg, DF; Frumkin, H; Ryan, PB; White, MC				Tolbert, PE; Mulholland, JA; MacIntosh, DL; Xu, F; Daniels, D; Devine, OJ; Carlin, BP; Klein, M; Dorley, J; Butler, AJ; Nordenberg, DF; Frumkin, H; Ryan, PB; White, MC			Air quality and pediatric emergency room visits for asthma in Atlanta, Georgia	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						air pollution; asthma; child; emergency service, hospital; ozone	HOSPITAL ADMISSIONS; RESPIRATORY HEALTH; CHILDHOOD ASTHMA; MEXICO-CITY; POLLUTION; OZONE	Pediatric emergency room visits for asthma were studied in relation to air quality indices in a spatio-temporal investigation of approximately 130,000 visits (similar to 6,000 for asthma) to the major emergency care centers in Atlanta, Georgia, during the summers of 1993-1995, Generalized estimating equations, logistic regression, and Bayesian models were fitted to the data. in logistic regression models comparing estimated exposures of asthma cases with those of the nonasthma patients, controlling for temporal and demographic covariates and using residential zip code to link patients to spatially resolved ozone levels, the estimated relative risk per 20 parts per billion (ppb) increase in the maximum 8-hour ozone level was 1.04 (p < 0.05). The estimated relative risk for particulate matter less than or equal to 10 mu m in aerodynamic diameter (PM10) was 1.04 per 15 mu g/m(3) (p < 0.05). Exposure-response trends (p < 0.01) were observed for ozone (>100 ppb vs. <50 ppb: odds ratio = 1.23, p = 0.003) and PM10 (>60 mu g/m(3) vs. <20 mu g/m(3): odds ratio = 1.26, p = 0.004). In models with ozone and PM10, both terms became nonsignificant because of collinearity of the variables (r = 0.75), The other analytical approaches yielded consistent findings. This study supports accumulating evidence regarding the relation of air pollution to childhood asthma exacerbation.	Emory Univ, Rollins Sch Publ Hlth, Atlanta, GA 30322 USA; Georgia Inst Technol, Sch Civil & Environm Engn, Atlanta, GA 30332 USA; Univ Georgia, Dept Environm Hlth Sci, Athens, GA 30602 USA; Ctr Dis Control & Prevent, Natl Ctr Environm Hlth, Cincinnati, OH USA; Emory Univ, Sch Med, Atlanta, GA USA	Tolbert, PE (reprint author), Emory Univ, Rollins Sch Publ Hlth, Atlanta, GA 30322 USA.		Ryan, P. Barry/A-7662-2009; White, Mary /C-9242-2012; Tolbert, Paige/A-5676-2015	White, Mary /0000-0002-9826-3962; Frumkin, Howard/0000-0001-7079-3534			Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; BATES DV, 1990, ENVIRON RES, V51, P51, DOI 10.1016/S0013-9351(05)80182-3; BESAG J, 1974, J ROY STAT SOC B MET, V36, P192; CARLIN BP, 1998, CASE STUDIES BAYESIA, V4, P303; CODY RP, 1992, ENVIRON RES, V58, P184, DOI 10.1016/S0013-9351(05)80214-2; CRESSIE N. A. C., 1991, STAT SPATIAL DATA; Gilks WR, 1996, MARKOV CHAIN MONTE C; Gold DR, 1999, EPIDEMIOLOGY, V10, P8, DOI 10.1097/00001648-199901000-00004; LIANG KY, 1986, BIOMETRIKA, V73, P13, DOI 10.1093/biomet/73.1.13; LINN W, 1994, AM J RESP CRIT CARE, V127, P51; Lipsett M, 1997, ENVIRON HEALTH PERSP, V105, P216, DOI 10.1289/ehp.97105216; MOLFINO NA, 1991, LANCET, V338, P199, DOI 10.1016/0140-6736(91)90346-Q; MULHOLLAND JA, 1998, J AIR WASTE MANAGE, V48, P174; Ponka A, 1996, J EPIDEMIOL COMMUN H, V50, pS59, DOI 10.1136/jech.50.Suppl_1.s59; POPE CA, 1991, AM REV RESPIR DIS, V144, P668; ROMIEU I, 1995, AM J EPIDEMIOL, V141, P546; Romieu I, 1996, AM J RESP CRIT CARE, V154, P300; SAS Institute Inc., 1989, SAS STAT US GUID VER, V2; Schouten JP, 1996, J EPIDEMIOL COMMUN H, V50, pS22, DOI 10.1136/jech.50.Suppl_1.s22; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; Stieb DM, 1996, ENVIRON HEALTH PERSP, V104, P1354, DOI 10.2307/3432974; THURSTON GD, 1992, J EXPO ANAL ENV EPID, V2, P429; WEISEL CP, 1995, ENVIRON HEALTH PERSP, V103, P97, DOI 10.2307/3432456; WHITE MC, 1994, ENVIRON RES, V65, P56, DOI 10.1006/enrs.1994.1021; *WHO, 1977, INT CLASS DIS MAN IN; 1993, MMWR MORB MORTAL WKL, V42, P301	26	150	152	0	11	OXFORD UNIV PRESS INC	CARY	JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA	0002-9262			AM J EPIDEMIOL	Am. J. Epidemiol.	APR 15	2000	151	8					798	810				13	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	303UR	WOS:000086443700009	10965977	
J	Grootendorst, DC; Gauw, SA; Verhoosel, RM; Sterk, PJ; Hospers, JJ; Bredenbroker, D; Bethke, TD; Hiemstra, PS; Rabe, KF				Grootendorst, Diana C.; Gauw, Stefanie A.; Verhoosel, Renate M.; Sterk, Peter J.; Hospers, Jeannette J.; Bredenbroeker, Dirk; Bethke, Thomas D.; Hiemstra, Pieter S.; Rabe, Klaus F.			Reduction in sputum neutrophil and eosinophil numbers by the PDE4 inhibitor roflumilast in patients with COPD	THORAX			English	Article							OBSTRUCTIVE PULMONARY-DISEASE; AIR-FLOW LIMITATION; PHOSPHODIESTERASE-4 INHIBITOR; LUNG-FUNCTION; SYSTEMIC INFLAMMATION; ASTHMA; METAANALYSIS; FLUTICASONE; PROPIONATE; MODULATION	Background: Roflumilast is a targeted oral once-daily administered phosphodiesterase 4 (PDE4) inhibitor with clinical efficacy in chronic obstructive pulmonary disease (COPD). Results from in vitro studies with roflumilast indicate that it has anti-inflammatory properties that may be applicable for the treatment of COPD. Methods: In a crossover study, 38 patients with COPD (mean (SD) age 63.1 (7.0) years, post-bronchodilator forced expiratory volume in 1 s (FEV1) 61.0 (12.6)% predicted) received 500 mu g roflumilast or placebo once daily for 4 weeks. Induced sputum samples were collected before and after 2 and 4 weeks of treatment. Differential and absolute cell counts were determined in whole sputum samples. Markers of inflammation were determined in sputum supernatants and blood. Spirometry was performed weekly. Results: Roflumilast significantly reduced the absolute number of neutrophils and eosinophils/g sputum compared with placebo by 35.5% (95% CI 15.6% to 50.7%; p = 0.002) and 50.0% (95% CI 26.8% to 65.8%; p<0.001), respectively. The relative proportion of sputum neutrophils and eosinophils was not affected by treatment (p>0.05). Levels of soluble interleukin-8, neutrophil elastase, eosinophil cationic protein and alpha(2)-macroglobulin in sputum and the release of tumour necrosis factor alpha from blood cells were significantly reduced by roflumilast compared with placebo treatment (p<0.05 for all). Post-bronchodilator FEV1 improved significantly during roflumilast compared with placebo treatment with a mean difference between treatments of 68.7 ml (95% CI 12.9 to 124.5; p = 0.018). Conclusion: PDE4 inhibition by roflumilast treatment for 4 weeks reduced the number of neutrophils and eosinophils, as well as soluble markers of neutrophilic and eosinophilic inflammatory activity in induced sputum samples of patients with COPD. This anti-inflammatory effect may in part explain the concomitant improvement in post-bronchodilator FEV1.	Leiden Univ, Med Ctr, Dept Pulmonol C3 P, NL-2300 RC Leiden, Netherlands; ALTANA Pharma AG, Constance, Germany	Grootendorst, DC (reprint author), Leiden Univ, Med Ctr, Dept Pulmonol C3 P, POB 9600, NL-2300 RC Leiden, Netherlands.	d.c.Grootendorst@lumc.nl					American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Barnes NC, 2006, AM J RESP CRIT CARE, V173, P736, DOI 10.1164/rccm.200508-1321OC; Bundschuh DS, 2001, J PHARMACOL EXP THER, V297, P280; Celli B, 2006, CHEST, V129, P5, DOI 10.1378/chest.129.1.5; Di Stefano A, 1998, AM J RESP CRIT CARE, V158, P1277; Di Stefano A, 2001, CLIN EXP ALLERGY, V31, P893, DOI 10.1046/j.1365-2222.2001.01098.x; Donaldson GC, 2005, CHEST, V128, P1995, DOI 10.1378/chest.128.4.1995; Essayan DM, 2001, J ALLERGY CLIN IMMUN, V108, P671; Faurschou M, 2003, MICROBES INFECT, V5, P1317, DOI 10.1016/j.micinf.2003.09.008; Fujimoto K, 1999, CHEST, V115, P697, DOI 10.1378/chest.115.3.697; Gamble E, 2003, AM J RESP CRIT CARE, V168, P976, DOI 10.1164/rccm.200212-1490OC; Gan WQ, 2004, THORAX, V59, P574, DOI 10.1136/thx.2003.019588; Gizycki MJ, 2002, THORAX, V57, P799, DOI 10.1136/thorax.57.9.799; Grootendorst DC, 2003, PULM PHARMACOL THER, V16, P115, DOI 10.1016/S1094-5539(02)00172-4; Grootendorst DC, 2003, PULM PHARMACOL THER, V16, P341, DOI 10.1016/S1094-5539(03)00090-7; Grootendorst DC, 1999, EUR RESPIR J, V13, P647, DOI 10.1183/09031936.99.13364799; GROOTENDORST DC, 2004, EUR RESP J S48, V24, pS306; Grootendorst Diana C, 2002, Curr Opin Allergy Clin Immunol, V2, P61, DOI 10.1097/00130832-200202000-00010; Hattotuwa KL, 2002, AM J RESP CRIT CARE, V165, P1592, DOI 10.1164/rccm.2105025; Hatzelmann A, 2001, J PHARMACOL EXP THER, V297, P267; Hogg JC, 2004, LANCET, V364, P709, DOI 10.1016/S0140-6736(04)16900-6; In 'T Veen J. C. C. M., 1996, European Respiratory Journal, V9, P2441, DOI 10.1183/09031936.96.09122441; Keatings VM, 1997, AM J RESP CRIT CARE, V155, P449; Keatings VM, 1996, AM J RESP CRIT CARE, V153, P530; Lipworth BJ, 2005, LANCET, V365, P167, DOI 10.1016/S0140-6736(05)17708-3; Moore TM, 1998, AM J PHYSIOL-LUNG C, V275, pL203; QUANJER PH, 1993, EUR RESPIR J, V6, P5; Rabe KF, 2005, LANCET, V366, P563, DOI 10.1016/S0140-6736(05)67100-0; Rabe KF, 2007, AM J RESP CRIT CARE, V176, P532, DOI 10.1164/rccm.200703-456SO; RIISE GC, 1994, EUR RESPIR J, V7, P1673, DOI 10.1183/09031936.94.07091673; Romano Suzanne J, 2005, Treat Respir Med, V4, P85, DOI 10.2165/00151829-200504020-00002; SCHOONBROOD DFM, 1994, AM J RESP CRIT CARE, V150, P1519; SIAFAKAS NM, 1995, EUR RESPIR J, V8, P1398, DOI 10.1183/09031936.95.08081398; Smits HH, 1998, CLIN EXP IMMUNOL, V111, P463; Sutherland ER, 2003, THORAX, V58, P937, DOI 10.1136/thorax.58.11.937; Suttorp N, 1996, LUNG, V174, P181; Van Rensen ELJ, 2002, AM J RESP CRIT CARE, V165, P1275, DOI 10.1164/rccm.2110092; Wollin L, 2006, PULM PHARMACOL THER, V19, P343, DOI 10.1016/j.pupt.2005.09.002; Wouters EF, 2002, CHEST, V121, P127	39	149	154	0	11	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	DEC	2007	62	12					1081	1087		10.1136/thx.2006.075937		7	Respiratory System	Respiratory System	235QV	WOS:000251250300019	17573446	
J	Alfven, T; Braun-Fahrlander, C; Brunekreef, B; von Mutius, E; Riedler, J; Scheynius, A; van Hage, M; Wickman, M; Benz, MR; Budde, J; Michels, KB; Schram, D; Ublagger, E; Waser, M; Pershagen, G				Alfven, T; Braun-Fahrlander, C; Brunekreef, B; von Mutius, E; Riedler, J; Scheynius, A; van Hage, M; Wickman, M; Benz, MR; Budde, J; Michels, KB; Schram, D; Ublagger, E; Waser, M; Pershagen, G		PARSIFAL Study Grp	Allergic diseases and atopic sensitization in children related to farming and anthroposophic lifestyle - the PARSIFAL study	ALLERGY			English	Article						asthma; environment; epidemiology; paediatrics; rhinitis	HOUSE-DUST ENDOTOXIN; HAY-FEVER; FARMERS CHILDREN; BIRTH COHORT; ASTHMA; EXPOSURE; PREVALENCE; CHILDHOOD; SCHOOLCHILDREN; SYMPTOMS	Background: The prevalence of allergic diseases has increased rapidly in recent decades, particularly in children. For adequate prevention it is important not only to identify risk factors, but also possible protective factors. The aim of this study was to compare the prevalence of allergic diseases and sensitization between farm children, children in anthroposophic families, and reference children, with the aim to identify factors that may protect against allergic disease. Methods: The study was of cross-sectional design and included 14 893 children, aged 5-13 years, from farm families, anthroposophic families (recruited from Steiner schools) and reference children in Austria, Germany, the Netherlands, Sweden and Switzerland. A detailed questionnaire was completed and allergen-specific IgE was measured in blood. Results: Growing up on a farm was found to have a protective effect against all outcomes studied, both self-reported, such as rhinoconjunctivitis, wheezing, atopic eczema and asthma and sensitization (allergen specific IgE >= 0.35 kU/l). The adjusted odds ratio (OR) for current rhinoconjunctivitis symptoms was 0.50 (95% confidence interval (CI) 0.38-0.65) and for atopic sensitization 0.53 (95% CI 0.42-0.67) for the farm children compared to their references. The prevalence of allergic symptoms and sensitization was also lower among Steiner school children compared to reference children, but the difference was less pronounced and not as consistent between countries, adjusted OR for current rhinoconjunctivitis symptoms was 0.69 (95% CI 0.56-0.86) and for atopic sensitization 0.73 (95% CI 0.58-0.92). Conclusions: This study indicates that growing up on a farm, and to a lesser extent leading an anthroposophic life style may confer protection from both sensitization and allergic diseases in childhood.	Karolinska Inst, Inst Environm Med, SE-17177 Stockholm, Sweden; Univ Basel, Inst Social & Prevent Med, Basel, Switzerland; Univ Utrecht, Inst Risk Assessment Sci, Utrecht, Netherlands; Dr Von Haunersche Kinderklin, Munich, Germany; Kinderspital Schwarzach, Schwarzach, Austria; Karolinska Hosp & Inst, Dept Med, Clin Allergy Res Unit, Stockholm, Sweden; Karolinska Univ Hosp, Dept Med, Allergy & Clin Immunol Unit, Stockholm, Sweden; Karolinska Hosp, Unit Environm Med, S-10401 Stockholm, Sweden; Harvard Univ, Brigham & Womens Hosp, Sch Med,Dept Epidemiol,Sch Publ Hlth, Obstet & Gynecol Epidemiol Ctr, Boston, MA 02115 USA; Childrens Hosp, Dept Paediat Pulmonol & Allergol, Salzburg, Austria	Alfven, T (reprint author), Karolinska Inst, Inst Environm Med, Box 210, SE-17177 Stockholm, Sweden.		van Hage, Marianne/A-9678-2017	van Hage, Marianne/0000-0003-3091-1596; Pershagen, Goran/0000-0002-9701-1130; brunekreef, bert/0000-0001-9908-0060; Alfven, Tobias/0000-0002-2328-3512			Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; Anderson HR, 2004, BRIT MED J, V328, P1052, DOI 10.1136/bmj.38057.583727.47; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Braun-Fahrlander C, 2003, CLIN EXP ALLERGY, V33, P409, DOI 10.1046/j.1365-2222.2003.01650.x; Braun-Fahrlander C, 2004, EUR RESPIR J, V23, P407, DOI 10.1183/09031936.04.00074004; BURNEY PGJ, 1990, BRIT MED J, V300, P1306; Filipiak B, 2001, CLIN EXP ALLERGY, V31, P1829, DOI 10.1046/j.1365-2222.2001.01246.x; Gehring U, 2002, AM J RESP CRIT CARE, V166, P939, DOI 10.1164/rccm.200203-256OC; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Janssen NAH, 2003, ENVIRON HEALTH PERSP, V111, P1512, DOI 10.1289/ehp.6243; Johansson SGO, 2004, J ALLERGY CLIN IMMUN, V113, P832, DOI 10.1016/j.jaci.2003.12.591; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Klintberg B, 2001, EUR RESPIR J, V17, P1151, DOI 10.1183/09031936.01.00027301; Lewis SA, 2000, CLIN EXP ALLERGY, V30, P153; Radon K, 2004, CLIN EXP ALLERGY, V34, P1178, DOI 10.1111/j.1365-2222.2004.02005.x; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Toelle BG, 2004, BRIT MED J, V328, P386, DOI 10.1136/bmj.328.7436.386; [Anonymous], 1997, EUR ALL WHIT PAP; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Hertzen LC, 2004, ALLERGY, V59, P124, DOI 10.1046/j.1398-9995.2003.00433.x; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; Wickman M, 2002, PEDIATR ALLERGY IMMU, V13, P11, DOI 10.1034/j.1399-3038.13.s.15.10.x	25	149	153	3	23	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0105-4538			ALLERGY	Allergy	APR	2006	61	4					414	421		10.1111/j.1398-9995.2005.00939.x		8	Allergy; Immunology	Allergy; Immunology	016BC	WOS:000235594500004	16512802	
J	Silva, GE; Sherrill, DL; Guerra, S; Barbee, RA				Silva, GE; Sherrill, DL; Guerra, S; Barbee, RA			Asthma as a risk factor for COPD in a longitudinal study	CHEST			English	Article						asthma; chronic bronchitis; COPD; pulmonary emphysema	MONOXIDE DIFFUSING-CAPACITY; AIR-FLOW OBSTRUCTION; SKIN-TEST REACTIVITY; RESPIRATORY SYMPTOMS; PULMONARY-FUNCTION; BRONCHIAL RESPONSIVENESS; POPULATION SAMPLE; LUNG-FUNCTION; SERUM IGE; FOLLOW-UP	Background: For several years, asthma and COPD have been regarded as distinct entities, with distinct clinical courses. However, despite distinctive physiologic features at the time of diagnosis, and different risk factors, the two diseases over time may develop features that are quite similar. Study objective: To evaluate the association between physician-diagnosed asthma and the subsequent development of COPD in a cohort of 3,099 adult subjects from Tucson, AZ. Design and methods: A prospective observational study. Participants completed up to 12 standard respiratory questionnaires and 11 spirometry lung function measurements over a period of 20 years. Survival curves (with time to development of COPD as the dependent variable) were compared between subjects with asthma and subjects without asthma at the initial survey. Results: Subjects with active asthma (n = 192) had significantly higher hazard ratios than inactive (n = 156) or nonasthmatic subjects (n = 2751) for acquiring COPD. As compared with nonasthmatics, active asthmatics had a 10-times-higher risk for acquiring symptoms of chronic bronchitis (95% confidence interval [CI], 4.94 to 20.25), 17-times-higher risk of receiving a diagnosis of emphysema (95% CI, 8.31 to 34.83), and 12.5-times-higher risk of fulfilling COPD criteria (95% CI, 6.84 to 22.84), even after adjusting for smoking history and other potential confounders. Conclusions: Physician-diagnosed asthma is significantly associated with an increased risk for CB, emphysema, and COPD.	Univ Arizona, Arizona Resp Ctr, Coll Med, Tucson, AZ 85724 USA	Sherrill, DL (reprint author), Univ Arizona, Arizona Resp Ctr, Coll Med, 1501 N Campbell Ave,POB 245073, Tucson, AZ 85724 USA.	duane@resp-sci.arizona.edu			NHLBI NIH HHS [HL10506-02]		American thoracic society, 1995, AM J RESP CRIT CARE, V152, pS77; BARBEE RA, 1976, ANN INTERN MED, V84, P129; BARBEE RA, 1997, EPIDEMIOLOGY NATURAL; Barnes PJ, 2000, CHEST, V117, P10; BURROWS B, 1989, NEW ENGL J MED, V320, P271, DOI 10.1056/NEJM198902023200502; BURROWS B, 1981, AM REV RESPIR DIS, V124, P523; CRAPO RO, 1981, AM REV RESPIR DIS, V123, P185; DEGOOIJER A, 1993, EUR RESPIR J, V6, P848; FANTA CH, 1989, J ASTHMA, V26, P87, DOI 10.3109/02770908909073237; Fletcher C, 1976, NATURAL HIST CHRONIC; Hudon C, 1997, ANN ALLERG ASTHMA IM, V78, P195; KNUDSON RJ, 1987, AM REV RESPIR DIS, V135, P805; Lange P, 1998, NEW ENGL J MED, V339, P1194, DOI 10.1056/NEJM199810223391703; LIEBERMA.J, 1969, NEW ENGL J MED, V281, P279, DOI 10.1056/NEJM196908072810601; Mannino DM, 2002, CHEST, V121, p121S, DOI 10.1378/chest.121.5_suppl.121S; National Asthma Education and Prevention Program, 1997, NIH PUBL, V97-4051; OCONNOR GT, 1995, AM J RESP CRIT CARE, V152, P87; Orie NGM, 1961, BRONCH INT S ASS NET; PEAT JK, 1987, EUR J RESPIR DIS, V70, P171; Reed CE, 1999, J ALLERGY CLIN IMMUN, V103, P539, DOI 10.1016/S0091-6749(99)70221-6; RENZETTI AD, 1986, AM REV RESPIR DIS, V133, P1205; RIJCKEN B, 1988, AM REV RESPIR DIS, V137, P826; RIJCKEN B, 1995, AM J RESP CRIT CARE, V151, P1377; Sherrill D, 2003, EUR RESPIR J, V21, P95, DOI 10.1183/09031936.03.00017103; SPARROW D, 1987, AM REV RESPIR DIS, V135, P1255; Ulrik CS, 1999, EUR RESPIR J, V14, P892, DOI 10.1034/j.1399-3003.1999.14d27.x; ULRIK CS, 1994, AM J RESP CRIT CARE, V150, P629; Vignola AM, 2000, J ALLERGY CLIN IMMUN, V105, P1041, DOI 10.1067/mai.2000.107195; VILLAR MTA, 1995, AM J RESP CRIT CARE, V151, P656; Vonk JM, 2003, THORAX, V58, P322, DOI 10.1136/thorax.58.4.322; World Health Organization, GOLD GLOB STRAT MAN; WOOLCOCK AJ, 1987, THORAX, V42, P361, DOI 10.1136/thx.42.5.361; Xu XP, 1997, LANCET, V350, P1431, DOI 10.1016/S0140-6736(97)10041-1; 1979, ANN REV RESP DIS, V119, P831	34	149	160	0	9	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	JUL	2004	126	1					59	65		10.1378/chest.126.1.59		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	841XP	WOS:000222965900013	15249443	
J	Berges-Gimeno, MP; Simon, RA; Stevenson, DD				Berges-Gimeno, MP; Simon, RA; Stevenson, DD			Long-term treatment with aspirin desensitization in asthmatic patients with aspirin-exacerbated respiratory disease	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						aspirin; asthma; rhinitis; desensitization; nonsteroidal anti-inflammatory drugs; aspirin desensitization treatment	RHINOSINUSITIS-ASTHMA; CHALLENGES	Background: Aspirin desensitization treatment is an option to decrease disease activity and reduce the need for systemic corticosteroids in patients with aspirin-exacerbated respiratory disease (AERD). Objective: This study was designed to determine whether the clinical courses of patients with AERD improved as early as 6 months after starting aspirin desensitization and to compare this with follow-up evaluations after at least a year. Methods: Between 1995 and 2000, 172 patients with AERD were admitted to our General Clinical Research Center, were desensitized to and treated with aspirin, were discharged to their home communities, and participated in follow-up interviews and written assessments of their clinical courses. Results: By the first 6 months of aspirin treatment, there were significant reductions in sinus infections and numbers of short courses of prednisone and improvements in sense of smell and general assessment of nasal-sinus and asthma symptoms (P <.0001). These results persisted for I to 5 years (P <.0001). Mean prednisone doses decreased from 10.8 mg/d to 8.1 and 3.6 mg/d at 6 months and greater than 1 year, respectively. Of the 172 patients, 24 (14%) discontinued aspirin treatment because of side effects, and 115 (67%) responded to aspirin treatment. After eliminating those who discontinued aspirin treatment because of side effects, the improvement rate was 115 (78%) of 148 patients. Of the 126 patients who completed a year or more of aspirin treatment, 110 (87%) experienced improvement. Conclusion: Aspirin desensitization followed by daily aspirin is efficacious by at least the first 6 months of treatment and continues to be effective for up to 5 years of follow-up.	Scripps Clin, La Jolla, CA 92037 USA; Scripps Res Inst, La Jolla, CA USA	Stevenson, DD (reprint author), Scripps Clin, 10666 N Torrey Rd, La Jolla, CA 92037 USA.				NCRR NIH HHS [M01RR00833]		CHIU JT, 1983, J ALLERGY CLIN IMMUN, V71, P560, DOI 10.1016/0091-6749(83)90437-2; Dahlen B, 1998, AM J RESP CRIT CARE, V157, P1187; Dahlen SE, 2002, AM J RESP CRIT CARE, V165, P9; Kennedy D W, 1992, Laryngoscope, V102, P1; Mastalerz L, 1997, ALLERGY, V52, P895, DOI 10.1111/j.1398-9995.1997.tb01248.x; McFadden EA, 1997, AM J RHINOL, V11, P263, DOI 10.2500/105065897781446702; Nakamura H, 1999, ACTA OTO-LARYNGOL, V119, P592; STEVENSON DD, 1988, NEW ENGL REG ALLERGY, V9, P135; STEVENSON DD, 1980, J ALLERGY CLIN IMMUN, V66, P82, DOI 10.1016/0091-6749(80)90143-8; STEVENSON DD, 1984, J ALLERGY CLIN IMMUN, V73, P500, DOI 10.1016/0091-6749(84)90361-0; Stevenson DD, 1996, J ALLERGY CLIN IMMUN, V98, P751, DOI 10.1016/S0091-6749(96)70123-9; Stevenson DD, 2001, ANN ALLERG ASTHMA IM, V87, P177; Stevenson DD, 1998, ALLERGY PRINCIPLES P, V2, P1225; Sweet JA, 1990, J ALLERGY CLIN IMMUN, V86, P59; Szczeklik A, 1999, J ALLERGY CLIN IMMUN, V104, P5, DOI 10.1016/S0091-6749(99)70106-5; Widal MF, 1922, PRESSE MED, V30, P189; ZEISS CR, 1976, J ALLERGY CLIN IMMUN, V57, P440, DOI 10.1016/0091-6749(76)90059-2; 1997, NIH PUBLICATION, V4051	18	149	153	1	3	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JAN	2003	111	1					180	186		10.1067/mai.2003.7		7	Allergy; Immunology	Allergy; Immunology	636PR	WOS:000180465500028	12532116	
J	Bucchieri, F; Puddicombe, SM; Lordan, JL; Richter, A; Buchanan, D; Wilson, SJ; Ward, J; Zummo, G; Howarth, PH; Djukanovic, R; Holgate, ST; Davies, DE				Bucchieri, F; Puddicombe, SM; Lordan, JL; Richter, A; Buchanan, D; Wilson, SJ; Ward, J; Zummo, G; Howarth, PH; Djukanovic, R; Holgate, ST; Davies, DE			Asthmatic bronchial epithelium is more susceptible to oxidant-induced apoptosis	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article							NONASTHMATIC SUBJECTS; FACTOR RECEPTOR; CELLS; AIRWAY; EXPRESSION; HYPERREACTIVITY; PROLIFERATION; ANTIOXIDANTS; INFLAMMATION; BIOPSIES	Abnormal apoptotic mechanisms are associated with disease pathogenesis. Because the asthmatic bronchial epithelium is characteristically damaged with loss of columnar epithelial cells, we postulated that this is due to unscheduled apoptosis. Using an antibody directed toward the caspase cleavage product of poly(ADP-ribose) polymerase, immunohistochemistry applied to endobronchial biopsies showed higher levels of staining in the bronchial epithelium of subjects with asthma as compared with normal control subjects (% epithelial staining [median (range) = 10.5 (1.4-24.5) versus 0.4 (0.0-9.7)]; P < 0.001). Because we were unable to determine whether this difference was due to ongoing inflammation in vivo, cultures of normal and asthmatic bronchial epithelial cells were used to study apoptosis in vitro. In complete growth medium, these cells showed no difference in their rate of proliferation or viability. However, cells from subjects with asthma were more susceptible to the apoptotic effects of H2O2 than cells from normal control subjects (% apoptotic cells = 32.2 [8.8-54.9] versus 14.3 [6.4-24.7]; P < 0.05), even though both were similarly affected by treatment with actinomycin D. These data indicate that the susceptibility of asthmatic bronchial epithelium to oxidants is greater than normal. This susceptibility may contribute to the rising trends in asthma associated with air pollution and diets low in antioxidants.	Southampton Gen Hosp, Brooke Labs, Sch Med, Southampton SO9 6YD, Hants, England; Univ Palermo, Human Anat Sect, Palermo, Italy	Davies, DE (reprint author), Southampton Gen Hosp, Brooke Labs, Sch Med, Level F,Mailpoint 888, Southampton SO9 6YD, Hants, England.		Bucchieri, Fabio/F-8877-2012; Davies, Donna/H-2993-2012	BUCCHIERI, Fabio/0000-0002-0209-8668			Benayoun L, 2001, AM J RESP CRIT CARE, V164, P1487; BRITTEN KM, 1993, BIOTECH HISTOCHEM, V68, P271, DOI 10.3109/10520299309105629; Caulin C, 1997, J CELL BIOL, V138, P1379, DOI 10.1083/jcb.138.6.1379; CHAGANI T, 2001, AM J RESP CRIT CARE, V163, pA739; DeRaeve HR, 1997, AM J PHYSIOL-LUNG C, V272, pL148; Devalia JL, 1999, INT ARCH ALLERGY IMM, V118, P437, DOI 10.1159/000024157; Druilhe A, 1998, AM J RESP CELL MOL, V19, P747; Erjefalt JS, 2000, AM J RESP CRIT CARE, V161, P2074; HATCH GE, 1995, AM J CLIN NUTR, V61, p625S; Hiltermann TJN, 1998, EUR RESPIR J, V11, P686; Holgate ST, 1999, NATURE, V402, pB2; Holgate ST, 2000, J ALLERGY CLIN IMMUN, V105, P193, DOI 10.1016/S0091-6749(00)90066-6; HURD SZ, 1991, J ALLERGY CLIN IMMUN, V88, P808; ILOWITE JS, 1989, AM REV RESPIR DIS, V139, P1139; JEFFERY PK, 1989, AM REV RESPIR DIS, V140, P1745; KAYANOKI Y, 1994, J BIOL CHEM, V269, P15488; Kelly FK, 1999, LANCET, V354, P482, DOI 10.1016/S0140-6736(99)01812-7; Knaapen M., 1999, PROMEGA NOTES, V72, P7; Martinez FD, 1999, LANCET S2, V354, pSII12; McDonald PP, 1999, J IMMUNOL, V163, P6164; MONTEFORT S, 1992, THORAX, V47, P499, DOI 10.1136/thx.47.7.499; Morcillo EJ, 1999, PHARMACOL RES, V40, P393, DOI 10.1006/phrs.1999.0549; *NAT I HLTH NAT HE, 1995, NIH PUBL; Ordonez C, 2000, AM J RESP CRIT CARE, V162, P2324; POSTMA DS, 1988, AM REV RESPIR DIS, V137, P57; Puddicombe SM, 2000, FASEB J, V14, P1362, DOI 10.1096/fj.14.10.1362; SCHRAUFSTATTER I, 1988, J CLIN INVEST, V82, P1040, DOI 10.1172/JCI113660; Schutte B, 2000, Prog Cell Cycle Res, V4, P207; SEDGWICK JB, 1992, J IMMUNOL, V149, P3710; Smith LJ, 1997, FREE RADICAL BIO MED, V22, P1301, DOI 10.1016/S0891-5849(96)00550-3; Trautmann A, 2000, J CLIN INVEST, V106, P25, DOI 10.1172/JCI9199; Uhal BD, 1998, AM J PHYSIOL-LUNG C, V275, pL1192; VERMES I, 1995, J IMMUNOL METHODS, V184, P39, DOI 10.1016/0022-1759(95)00072-I; Wallach D, 1999, ANNU REV IMMUNOL, V17, P331, DOI 10.1146/annurev.immunol.17.1.331; Wark P A, 2000, Respirology, V5, P51, DOI 10.1046/j.1440-1843.2000.00226.x; Wellington CL, 2000, CLIN GENET, V57, P1, DOI 10.1034/j.1399-0004.2000.570101.x; White SR, 2001, AM J RESP CELL MOL, V24, P282; Woolley KL, 1996, AM J RESP CRIT CARE, V154, P237	38	149	155	1	9	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1044-1549			AM J RESP CELL MOL	Am. J. Respir. Cell Mol. Biol.	AUG	2002	27	2					179	185				7	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	580XN	WOS:000177262200009	12151309	
J	Julia, V; Hessel, EM; Malherbe, L; Glaichenhaus, N; O'Garra, A; Coffman, RL				Julia, V; Hessel, EM; Malherbe, L; Glaichenhaus, N; O'Garra, A; Coffman, RL			A restricted subset of dendritic cells captures airborne antigens and remains able to activate specific T cells long after antigen exposure	IMMUNITY			English	Article							IN-VIVO; AIRWAY HYPERRESPONSIVENESS; IMMUNOLOGICAL-TOLERANCE; INHALED ANTIGEN; ATOPIC ASTHMA; MURINE MODEL; LYMPH-NODES; EXPRESSION; INDUCTION; LUNG	Mice sensitized for a Th2 response to Leishmania LACK antigen developed allergic airway inflammation upon exposure to LACK aerosol. Using multimers of I-A(d) molecules bound to a LACK peptide as probes, we tracked the migration of LACK-specific Th2 cells to the airways. Elevated numbers of LACK-specific Th2 cells remained in the airways for 5 weeks after the last aerosol. Substantial numbers of DC presenting LACK peptides were found in the airways, but not in other compartments, for up to 8 weeks after antigen exposure. These LACK-presenting airway DC expressed CD11c and CD11b as well as high levels of surface molecules involved in uptake and costimulation. Taken together, our results may explain the chronic Th2 airway inflammation characteristic of allergic asthma.	DNAX Res Inst Mol & Cellular Biol Inc, Res Inst, Dept Immunol, Palo Alto, CA 94304 USA; Univ Nice Sophia Antipolis, CNRS, Inst Pharmacol Mol & Cellulaire, F-06560 Valbonne, France	Julia, V (reprint author), DNAX Res Inst Mol & Cellular Biol Inc, Res Inst, Dept Immunol, 901 Calif Ave, Palo Alto, CA 94304 USA.	julia@ipmc.cnrs.fr; rcoffman@dvax.com		O'Garra, Anne/0000-0001-9845-6134			Asselin-Paturel C, 2001, NAT IMMUNOL, V2, P1144, DOI 10.1038/ni736; Blyth DI, 1998, AM J RESP CELL MOL, V19, P38; Busch DH, 1998, IMMUNITY, V8, P353, DOI 10.1016/S1074-7613(00)80540-3; Cohn L, 1998, J IMMUNOL, V161, P3813; Cohn L, 1997, J EXP MED, V186, P1737, DOI 10.1084/jem.186.10.1737; COYLE AJ, 1995, AM J RESP CELL MOL, V13, P54; Doherty PC, 1998, CURR OPIN MICROBIOL, V1, P419, DOI 10.1016/S1369-5274(98)80059-3; Foster PS, 1996, J EXP MED, V183, P195, DOI 10.1084/jem.183.1.195; GAVETT SH, 1994, AM J RESP CELL MOL, V10, P587; Grunig G, 1998, SCIENCE, V282, P2261, DOI 10.1126/science.282.5397.2261; Gutgemann I, 1998, IMMUNITY, V8, P667, DOI 10.1016/S1074-7613(00)80571-3; Hermans IF, 2000, J IMMUNOL, V164, P3095; HOLT PG, 1994, J IMMUNOL, V153, P256; Humbert M, 1999, IMMUNOL TODAY, V20, P528, DOI 10.1016/S0167-5699(99)01535-2; Hurst SD, 2001, J IMMUNOL, V166, P4922; INABA K, 1995, CELL IMMUNOL, V163, P148, DOI 10.1006/cimm.1995.1109; Inaba K, 1998, J EXP MED, V188, P2163, DOI 10.1084/jem.188.11.2163; Jenkins MK, 2001, ANNU REV IMMUNOL, V19, P23, DOI 10.1146/annurev.immunol.19.1.23; Julia V, 1996, SCIENCE, V274, P421, DOI 10.1126/science.274.5286.421; Kim SK, 2000, J IMMUNOL, V165, P7285; Knight SC, 1998, EUR J IMMUNOL, V28, P1636; Kronin V, 2000, INT IMMUNOL, V12, P731, DOI 10.1093/intimm/12.5.731; Leenen PJM, 1998, J IMMUNOL, V160, P2166; Liu CP, 2000, P NATL ACAD SCI USA, V97, P14596, DOI 10.1073/pnas.250390997; Malhotra V, 2000, J AM SOC ECHOCARDIOG, V13, P771, DOI 10.1067/mje.2000.106078; Mathew A, 2001, J EXP MED, V193, P1087, DOI 10.1084/jem.193.9.1087; McSorley SJ, 1997, IMMUNITY, V7, P401, DOI 10.1016/S1074-7613(00)80361-1; MOUGNEAU E, 1995, SCIENCE, V268, P563, DOI 10.1126/science.7725103; Nakano H, 2001, J EXP MED, V194, P1171, DOI 10.1084/jem.194.8.1171; Rees W, 1999, P NATL ACAD SCI USA, V96, P9781, DOI 10.1073/pnas.96.17.9781; Reinhardt RL, 2001, NATURE, V410, P101, DOI 10.1038/35065111; ROBINSON DS, 1992, NEW ENGL J MED, V326, P298, DOI 10.1056/NEJM199201303260504; Sallusto F, 1999, NATURE, V401, P708, DOI 10.1038/44385; SEDGWICK JD, 1985, IMMUNOLOGY, V56, P635; Seymour BWP, 1998, J EXP MED, V187, P721, DOI 10.1084/jem.187.5.721; Smith AL, 1999, J EXP MED, V189, P593, DOI 10.1084/jem.189.3.593; TAYLOR FGR, 1985, INT ARCH ALLER A IMM, V76, P243; Tsitoura DC, 1999, J IMMUNOL, V163, P2592; Vermaelen KY, 2001, J EXP MED, V193, P51; Wang J, 2000, BLOOD, V95, P2337; White DW, 1999, J IMMUNOL, V162, P980; WILLOUGHBY JB, 1977, J IMMUNOL, V119, P2137; Wills-Karp M, 1999, ANNU REV IMMUNOL, V17, P255, DOI 10.1146/annurev.immunol.17.1.255; XIA WJ, 1995, J EXP MED, V181, P1275, DOI 10.1084/jem.181.4.1275; Yamaguchi E, 1999, EUR RESPIR J, V13, P814, DOI 10.1034/j.1399-3003.1999.13d20.x	45	149	155	1	4	CELL PRESS	CAMBRIDGE	600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA	1074-7613			IMMUNITY	Immunity	FEB	2002	16	2					271	283		10.1016/S1074-7613(02)00276-5		13	Immunology	Immunology	524YC	WOS:000174039600010	11869687	
J	Patel, AM; Ryu, JH; Reed, CE				Patel, AM; Ryu, JH; Reed, CE			Hypersensitivity pneumonitis: Current concepts and future questions	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						hypersensitivity pneumonitis; immunopathogenesis; lymphocytes; antibody; cytokines; chemokines; adhesion molecules; causative agents; diagnosis; prognosis; high-resolution computed tomography; bronchoalveolar lavage; pathology	EXTRINSIC ALLERGIC ALVEOLITIS; BRONCHOALVEOLAR LAVAGE FLUID; PIGEON-BREEDERS DISEASE; IMMUNOLOGICAL LUNG-DISEASE; BIRD FANCIERS LUNG; MAST-CELL TRYPTASE; HIGH-RESOLUTION CT; ACUTE FARMERS LUNG; PULMONARY FIBROSIS; AIRWAY LESIONS	Hypersensitivity pneumonitis (extrinsic allergic alveolitis) caused by inhaled allergens can progress to disabling or even fatal end-stage lung disease. The only truly effective treatment is early recognition and control of exposure. Although patients produce antibody exuberantly, the immunopathogenesis involves cellular immunity-notably, CD8(+) cytotoxic lymphocytes, multinucleate giant cell granulomas, and ultimately interstitial fibrosis. Many causative agents have been recognized in occupational dusts or mists, but most current new cases arise from residential exposure to pet birds (pigeons and parakeets), contaminated humidifiers, and indoor molds. The symptoms and physical findings are nonspecific. Serum IgG containing high titers of specific antibody to the offending antigen is elevated, Pulmonary function tests show restrictive and diffusion defects with hypoxemia, especially after exercise. Occasionally, small airways disease causes obstruction. Radiographic changes vary according to the stage of the disease and are best evaluated by means of high-resolution computed tomography. In typical cases, the history of a known exposure and the presence of a characteristic interstitial lung disease with serologic confirmation of IgG antibody to the offending antigen suffice for diagnosis. In more obscure cases, observation of changes after a natural environmental exposure, bronchoalveolar lavage, and lung biopsy might be indicated. Among the many questions that remain are the following: What is the prevalence of hypersensitivity pneumonitis and how often is it the cause of chronic interstitial fibrosis? What is the long-term prognosis? Why do most individuals exposed to these antigens develop a vigorous antibody response whereas only a few develop the disease? How does exposure to endotoxin and cigarette smoking affect the disease? To answer these questions, standardized and validated clinical laboratory immunochemical tests are needed, in addition to a systematic approach to diagnosis, classification of disease severity, risk assessment, and management. This review is limited to the disease caused by airborne allergens and focuses on its immunopathogenesis, eliciting agents, clinical manifestations, diagnosis, management, and prognosis.	Mayo Clin, Dept Internal Med, Div Pulm & Crit Care Med, Rochester, MN 55905 USA; Mayo Clin, Dept Internal Med, Div Allerg Dis, Rochester, MN 55905 USA	Patel, AM (reprint author), Mayo Clin, Dept Internal Med, Div Pulm & Crit Care Med, Mayo Bldg E 18,200 1st St SW, Rochester, MN 55905 USA.						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Allergy Clin. Immunol.	NOV	2001	108	5					661	670				10	Allergy; Immunology	Allergy; Immunology	498RG	WOS:000172523800001	11692086	
J	Ip, S; Chung, M; Raman, G; Trikalinos, TA; Lau, J				Ip, Stanley; Chung, Mei; Raman, Gowri; Trikalinos, Thomas A.; Lau, Joseph			A Summary of the Agency for Healthcare Research and Quality's Evidence Report on Breastfeeding in Developed Countries	BREASTFEEDING MEDICINE			English	Article; Proceedings Paper	1st Annual Summit on Breastfeeding	JUN 11-12, 2009	Washington, DC				EPITHELIAL OVARIAN-CANCER; INFANT-DEATH-SYNDROME; ENVIRONMENTAL RISK-FACTORS; PROSPECTIVE BIRTH COHORT; ACUTE OTITIS-MEDIA; COGNITIVE-DEVELOPMENT; DIABETES-MELLITUS; REPRODUCTIVE FACTORS; CHILDHOOD LEUKEMIA; HIP FRACTURE	Objectives: This article summarizes the Agency for Healthcare Research and Quality's evidence report on the effects of breastfeeding on term infant and maternal health outcomes in developed countries. Evidence Report Data Sources: Medline, CINAHL, Cochrane Library, bibliographies of selected reviews, and suggestions from domain experts were surveyed. Searches were limited to English-language publications. Evidence Report Review Methods: Eligible comparisons examined the association between differential exposure to breastfeeding and health outcomes. We assessed 15 infant and six maternal outcomes. For four outcomes, we also updated previously published systematic reviews. For the rest of the outcomes, we either summarized previous systematic reviews or conducted new systematic reviews; randomized and non-randomized comparative trials, prospective cohorts, and case-control studies were included. Adjusted estimates were extracted from non-experimental designs. The studies were graded for methodological quality. We did not draw conclusions from poor quality studies. Evidence Report Results: We screened over 9,000 abstracts. Thirty-two primary studies on term infant health outcomes, 43 primary studies on maternal health outcomes, and 28 systematic reviews or meta-analyses that covered approximately 400 individual studies were included in this review. A history of breastfeeding was associated with a reduction in the risk of acute otitis media, nonspecific gastroenteritis, severe lower respiratory tract infections, atopic dermatitis, asthma (young children), obesity, type 1 and 2 diabetes, childhood leukemia, and sudden infant death syndrome. There was no relationship between breastfeeding in term infants and cognitive performance. There were insufficient good quality data to address the relationship between breastfeeding and cardiovascular diseases and infant mortality. For maternal outcomes, a history of lactation was associated with a reduced risk of type 2 diabetes, breast, and ovarian cancer. Early cessation of breastfeeding or no breastfeeding was associated with an increased risk of maternal postpartum depression. There was no relationship between a history of lactation and the risk of osteoporosis. The effect of breastfeeding in mothers on return-to-prepregnancy weight was negligible, and the effect of breastfeeding on postpartum weight loss was unclear. Evidence Report Conclusions: A history of breastfeeding is associated with a reduced risk of many diseases in infants and mothers. Future research would benefit from clearer selection criteria, definitions of breastfeeding exposure, and adjustment for potential confounders. Matched designs such as sibling analysis may provide a method to control for hereditary and household factors that are important in certain outcomes.	[Ip, Stanley; Chung, Mei; Raman, Gowri; Trikalinos, Thomas A.; Lau, Joseph] Tufts Med Ctr, Evidence Based Practice Ctr, Inst Clin Res & Hlth Policy Studies, Boston, MA 02111 USA	Ip, S (reprint author), Tufts Med Ctr, Evidence Based Practice Ctr, Inst Clin Res & Hlth Policy Studies, 800 Washington St, Boston, MA 02111 USA.	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Med.	OCT	2009	4			1			S17	S30		10.1089/bfm.2009.0050		14	Obstetrics & Gynecology; Pediatrics	Obstetrics & Gynecology; Pediatrics	585AW	WOS:000276797700007	19827919	
J	Jerrett, M; Shankardas, K; Berhane, K; Gauderman, WJ; Kunzli, N; Avol, E; Gilliland, F; Lurmann, F; Molitor, JN; Molitor, JT; Thomas, DC; Peters, J; McConnell, R				Jerrett, Michael; Shankardas, Ketan; Berhane, Kiros; Gauderman, W. James; Kunzli, Nino; Avol, Edward; Gilliland, Frank; Lurmann, Fred; Molitor, Jassy N.; Molitor, John T.; Thomas, Duncan C.; Peters, John; McConnell, Rob			Traffic-related air pollution and asthma onset in children: A prospective cohort study with individual exposure measurement	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; asthma onset; children; nitrogen dioxide; traffic	CHRONIC RESPIRATORY SYMPTOMS; CHILDHOOD ASTHMA; ALLERGIC RHINITIS; SCHOOL CHILDREN; PREVALENCE; HEALTH; QUESTIONNAIRE; COMMUNITY; AGE; EPIDEMIOLOGY	BACKGROUND: The question of whether air pollution contributes to asthma onset remains unresolved. OBJECTIVES: In this study, we assessed the association between asthma onset in children and traffic-related air pollution. METHODS: We selected a sample of 217 children from participants in the Southern California Children's Health Study, a prospective cohort designed to investigate associations between air pollution and respiratory health in children 10-18 years of age. Individual covariates and new asthma incidence (30 cases) were reported annually through questionnaires during 8 years of follow-up. Children had nitrogen dioxide monitors placed outside their home for 2 weeks in the summer and 2 weeks in the fall-winter season as a marker of traffic-related air pollution. We used multilevel Cox models to test the associations between asthma and air pollution. RESULTS: In models controlling for confounders, incident asthma was positively associated with traffic Pollution, with a hazard ratio (HR) of 1.29 [95% confidence interval (CI), 1.07-1.56] across the average within-community interquartille range of 6.2 ppb in annual residential NO(2). Using the total interquartile range for all measurements of 28.9 ppb increased the HR to 3.25 (95% CI, 1.35-7.85). CONCLUSIONS: In this cohort, markers of traffic-related air pollution were associated with the onset of asthma. The risks observed suggest that air pollution exposure contributes to new-onset asthma.	[Jerrett, Michael] Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA; [Shankardas, Ketan; Berhane, Kiros; Gauderman, W. James; Avol, Edward; Gilliland, Frank; Thomas, Duncan C.; Peters, John; McConnell, Rob] Univ So Calif, Dept Prevent Med, Keck Sch Med, Los Angeles, CA 90089 USA; [Kunzli, Nino] Ctr Res Environm Epidemiol CREAL, IMIM, Barcelona, Spain; [Lurmann, Fred] Sonoma Technol Inc, Petaluma, CA USA; [Molitor, Jassy N.; Molitor, John T.] Univ London Imperial Coll Sci Technol & Med, Dept Epidemiol & Publ Hlth, London, England	Jerrett, M (reprint author), Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, 140 Warren Hall, Berkeley, CA 94720 USA.	jerrett@berkeley.edu	Kunzli, Nino/F-7195-2014; Osborne, Nicholas/N-4915-2015	Kunzli, Nino/0000-0001-8360-080X; Osborne, Nicholas/0000-0002-6700-2284	National Institute of Environmental Health Sciences [5P30ES007048, 5P01ES011627, 5P01ES009581, 1R03ES014046]; U.S. Environmental Protection Agency [RD831861, R826708, R831845]; California Air Resources Board [94-331]; Hastings Foundation	This work was funded by the National Institute of Environmental Health Sciences (grants 5P30ES007048, 5P01ES011627, 5P01ES009581, and 1R03ES014046), the U.S. Environmental Protection Agency (grants RD831861, R826708, and R831845), California Air Resources Board contract 94-331, and the Hastings Foundation.	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OCT	2008	116	10					1433	1438		10.1289/ehp.10968		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	355TA	WOS:000259730100042	18941591	
J	Kull, I; Bergstrom, A; Lilja, G; Pershagen, G; Wickman, M				Kull, I.; Bergstrom, A.; Lilja, G.; Pershagen, G.; Wickman, M.			Fish consumption during the first year of life and development of allergic diseases during childhood	ALLERGY			English	Article						asthma; BAMSE; children; fish; sensitization	OIL SUPPLEMENTATION; BIRTH COHORT; FATTY-ACIDS; FOOD ALLERGY; ASTHMA RISK; CHILDREN; ATOPY; INFANTS; OMEGA-3-FATTY-ACIDS; PREVENTION	Background: Fish consumption during infancy has been regarded as a risk factor for allergic disease but later evidence suggests a protective role. However, methodological limitations in the studies make conclusions uncertain. The aim of this study was to assess the association between fish consumption during the first year of life and development of allergic diseases by age 4. Methods: A prospective birth cohort of 4089 new-born infants was followed for 4 years using parental questionnaires at ages 2 months, 1, 2 and 4 years to collect information on exposure and health effects. The response rate at 4 years was 90%. A clinical investigation was performed at age 4 years, which included blood sampling for analysis of specific IgE to common food and airborne allergens. Results: Parental allergic disease and onset of eczema or wheeze during the first year of life delayed introduction of fish in the child's diet. After exclusion of such children to avoid disease-related modification of exposure, regular fish consumption during the first year of life was associated with a reduced risk for allergic disease by age 4, ORadj 0.76 (95% CI 0.61-0.94) and sensitization, ORadj 0.76 (0.58-1.0). The reduced risk appeared most pronounced for multiple disease, ORadj 0.56 (0.35-0.89). IgE-sensitization to fish was only present among 18 of the 2614 children. Conclusion: Regular fish consumption before age 1 appears to be associated with a reduced risk of allergic disease and sensitization to food and inhalant allergens during the first 4 years of life.	Stockholm Cty Council, Stockholm, Sweden; Karolinska Inst, Natl Inst Environm Med, S-10401 Stockholm, Sweden; Childrens Hosp, Inst Sodersjukhuset, Karolinska Inst, Stockholm, Sweden	Kull, I (reprint author), Dept Occupat & Environm Med, Norrbacka 3rd Level, SE-17176 Stockholm, Sweden.			Pershagen, Goran/0000-0002-9701-1130; Kull, Inger/0000-0001-6096-3771			Barden AE, 2004, FREE RADICAL RES, V38, P233, DOI 10.1080/10715760310001656722; Black PN, 1997, EUR RESPIR J, V10, P6, DOI 10.1183/09031936.97.10010006; Bohme M, 2003, CLIN EXP ALLERGY, V33, P1226, DOI 10.1046/j.1365-2222.2003.01749.x; Calder PC, 2003, CLIN EXP ALLERGY, V33, P412, DOI 10.1046/j.1365-2222.2003.01633.x; Denburg JA, 2005, PEDIATR RES, V57, P276, DOI 10.1203/01.PDR.0000148279.72611.1D; Dunstan JA, 2003, J ALLERGY CLIN IMMUN, V112, P1178, DOI 10.1016/j.jaci.2003.09.009; Fogarty A, 2000, CLIN EXP ALLERGY, V30, P615, DOI 10.1046/j.1365-2222.2000.00766.x; FOUCARD T, 1995, ALLERGI OCH ASTMA BA; Hodge L, 1996, MED J AUSTRALIA, V164, P137; Hodge L, 1998, EUR RESPIR J, V11, P361, DOI 10.1183/09031936.98.11020361; Johansson SGO, 2004, J ALLERGY CLIN IMMUN, V113, P832, DOI 10.1016/j.jaci.2003.12.591; Kalantar-Zadeh K, 2004, MED HYPOTHESES, V62, P280, DOI 10.1016/j.mehy.2003.10.001; Kompauer I, 2004, EUR J MED RES, V9, P378; Mickleborough TD, 2003, AM J RESP CRIT CARE, V168, P1181, DOI 10.1164/rccm.200303-373OC; Nafstad P, 2003, J ASTHMA, V40, P343, DOI 10.1081/JAS-120018633; Oddy WH, 2004, J ASTHMA, V41, P319, DOI 10.1081/JAS-120026089; PEAT JK, 1992, EUR RESPIR J, V5, P921; Peat JK, 2004, J ALLERGY CLIN IMMUN, V114, P807, DOI 10.1016/j.jaci.2004.06.057; Roberts G, 2005, CLIN EXP ALLERGY, V35, P933, DOI 10.1111/j.1365-2222.2005.02280.x; Roehr CC, 2004, CLIN EXP ALLERGY, V34, P1534, DOI 10.1111/j.1365-2222.2004.02080.x; Simopoulos AP, 2002, J AM COLL NUTR, V21, P495; Simopoulos AP, 1999, AM J CLIN NUTR, V70, p560S; THIEN FCK, 1993, AM REV RESPIR DIS, V147, P1138; Wahn U, 2001, J ALLERGY CLIN IMMUN, V107, P567, DOI 10.1067/mai.2001.112943; Wickman M, 2003, ALLERGY, V58, P742, DOI 10.1034/j.1398-9995.2003.00078.x; Wickman M, 2004, ALLERGY, V59, P30, DOI 10.1111/j.1398-9995.2004.00572.x; Wickman M, 2002, PEDIATR ALLERGY IMMU, V13, P11, DOI 10.1034/j.1399-3038.13.s.15.10.x; Wickman M, 2005, ALLERGY, V60, P650, DOI 10.1111/j.1398-9995.2005.00764.x; Wijga AH, 2003, THORAX, V58, P567, DOI 10.1136/thorax.58.7.567; Woods RK, 2004, THORAX, V59, P105, DOI 10.1136/thorax.2003.009498; Zeiger RS, 2003, PEDIATRICS, V111, P1662	31	148	154	0	14	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0105-4538			ALLERGY	Allergy	AUG	2006	61	8					1009	1015		10.1111/j.1398-9995.2006.01115.x		7	Allergy; Immunology	Allergy; Immunology	061NZ	WOS:000238880600017	16867056	
J	Groskreutz, DJ; Monick, MM; Powers, LS; Yarovinsky, TO; Look, DC; Hunninghake, GW				Groskreutz, DJ; Monick, MM; Powers, LS; Yarovinsky, TO; Look, DC; Hunninghake, GW			Respiratory syncytial virus induces TLR3 protein and protein kinase R, leading to increased double-stranded RNA responsiveness in airway epithelial cells	JOURNAL OF IMMUNOLOGY			English	Article							NF-KAPPA-B; TOLL-LIKE RECEPTOR-3; DENDRITIC CELLS; ACTIVATION; PKR; EXPRESSION; LOCALIZATION; TRAFFICKING; RECOGNITION; CYTOKINES	Respiratory syncytial virus (RSV) preferentially infects airway epithelial cells, causing bronchiolitis, upper respiratory infections, asthma exacerbations, chronic obstructive pulmonary disease exacerbations, and pneumonia in immunocompromised hosts. A replication intermediate of RSV is dsRNA. This is an important ligand for both the innate immune receptor, TLR3, and protein kinase R (PKR). One known effect of RSV infection is the increased responsiveness of airway epithelial cells to subsequent bacterial ligands (i.e., LPS). In this study, we examined a possible role for RSV infection in increasing amounts and responsiveness of another TLR, TLR3. These studies demonstrate that RSV infection of A549 and human tracheobronchial epithelial cells increases the amounts of TLR3 and PKR in a time-dependent manner. This leads to increased NF-kappa B activity and production of the inflammatory cytokine IL-8 following a later exposure to dsRNA. Importantly, TLR3 was not detected on the cell surface at baseline but was detected on the cell surface after RSV infection. The data demonstrate that RSV, via an effect on TLR3 and PKR, sensitizes airway epithelial cells to subsequent dsRNA exposure. These findings are consistent with the hypothesis that RSV infection sensitizes the airway epithelium to subsequent viral and bacterial exposures by up-regulating TLRs and increasing their membrane localization.	Univ Iowa, Div Pulm Crit Care & Occupat Med, Roy J & Lucille A Carver Coll Med, Iowa City, IA 52242 USA; Univ Iowa, Div Pulm Crit Care & Occupat Med, Vet Adm Med Ctr, Iowa City, IA 52242 USA	Groskreutz, DJ (reprint author), Univ Iowa, Div Pulm Crit Care & Occupat Med, Roy J & Lucille A Carver Coll Med, 100 Eckstein Med Res Bldg, Iowa City, IA 52242 USA.	dayna-groskreutz@uiowa.edu			NCRR NIH HHS [RR00059]; NHLBI NIH HHS [HL-077431, HL-60316, K08 HL089392, R01 HL079901, R01 HL079901-05]		Akira S, 2001, NAT IMMUNOL, V2, P675, DOI 10.1038/90609; Akira S, 2001, ADV IMMUNOL, V78, P1, DOI 10.1016/S0065-2776(01)78001-7; Aksoy E, 2005, J BIOL CHEM, V280, P277, DOI 10.1074/jbc.M411223200; Aldallal N, 2002, AM J RESP CRIT CARE, V166, P1248, DOI 10.1164/rccm.200206-627OC; Alexopoulou L, 2001, NATURE, V413, P732, DOI 10.1038/35099560; Deb A, 2001, J IMMUNOL, V166, P6170; Demarchi F, 1999, J VIROL, V73, P7080; Ernst S, 2004, CELL MOL LIFE SCI, V61, P1684, DOI 10.1007/s00018-004-4116-x; Flaherty DM, 2002, J IMMUNOL, V168, P5675; FOTI M, 2004, NOVART FDN SYMP, V262, P141; Foti M, 2004, NOVART FDN SYMP, V262, P265; Foti Michelangelo, 2004, Novartis Found Symp, V262, P125; Funami K, 2004, INT IMMUNOL, V16, P1143, DOI 10.1093/intimm/dxh115; Gao ZH, 2003, J PHARMACOL EXP THER, V307, P870, DOI 10.1124/jpet.103.055525; Gil J, 2001, ONCOGENE, V20, P385, DOI 10.1038/sj.onc.1204109; Guillot L, 2005, J BIOL CHEM, V280, P5571, DOI 10.1074/jbc.M410592200; Hewson CA, 2005, J VIROL, V79, P12273, DOI 10.1128/JVI.79.19.12273-12279.2005; Jacobs BL, 1996, VIROLOGY, V219, P339, DOI 10.1006/viro.1996.0259; KINGSBURY D W, 1990, P945; KUMAR A, 1994, P NATL ACAD SCI USA, V91, P6288, DOI 10.1073/pnas.91.14.6288; Lund JM, 2004, P NATL ACAD SCI USA, V101, P5598, DOI 10.1073/pnas.0400937101; Martinez I, 2002, J GEN VIROL, V83, P1445, DOI 10.1099/vir.0.18337-0; Mastronarde JG, 1996, J INFECT DIS, V174, P262; Matsumoto M, 2002, BIOCHEM BIOPH RES CO, V293, P1364, DOI 10.1016/S0006-291X(02)00380-7; Matsumoto M, 2003, J IMMUNOL, V171, P3154; Ramaswamy M, 2004, AM J RESP CELL MOL, V30, P893, DOI 10.1165/rcmb.2003-0410OC; Rudd BD, 2005, J VIROL, V79, P3350, DOI 10.1128/JVI.79.6.3350-3357.2005; RUECKERT RR, 1990, VIROLOGY, V2, P507; Sarntinoranont M, 2003, J PHARM SCI, V92, P232, DOI 10.1002/jps.10280; Silva AM, 2004, J BIOL CHEM, V279, P37670, DOI 10.1074/jbc.M406554200; Spann KM, 2005, J VIROL, V79, P5353, DOI 10.1128/JVI.79.9.5353-5362.2005; Taddeo B, 2003, P NATL ACAD SCI USA, V100, P12408, DOI 10.1073/pnas.2034952100; Taylor DR, 1996, MOL CELL BIOL, V16, P6295; Tissari J, 2005, J IMMUNOL, V174, P4289; Ueta M, 2005, BIOCHEM BIOPH RES CO, V331, P285, DOI 10.1016/j.bbrc.2005.02.196; Vijay-Kumar M, 2005, J IMMUNOL, V174, P6322; Williams BRG, 1999, ONCOGENE, V18, P6112, DOI 10.1038/sj.onc.1203127	37	148	161	0	5	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	FEB 1	2006	176	3					1733	1740				8	Immunology	Immunology	004QF	WOS:000234766600052	16424203	
J	Robinson, DS; Campbell, DA; Durharm, SR; Pfeffer, J; Barnes, PJ; Chung, KF				Robinson, DS; Campbell, DA; Durharm, SR; Pfeffer, J; Barnes, PJ; Chung, KF		Asthma Allergy Research Grp of the	Systematic assessment of difficult-to-treat asthma	EUROPEAN RESPIRATORY JOURNAL			English	Article						adherence; diagnosis; psychiatry; severe asthma	AIR-FLOW LIMITATION; CLINICAL CHARACTERISTICS; RESISTANT ASTHMA; BRITTLE ASTHMA; MANAGEMENT; TRIAL	Five per cent of asthmatics remain symptomatic despite high-dose treatment. The aim of the study was to investigate how often such difficult-to-treat asthma is due to intractable asthma, misdiagnosis, non-adherence with therapy, or psychiatric problems. Difficult asthma was defined as persistence of symptoms despite treatment at step 4 of British guidelines or requirement for long-term oral glucocorticoids (step 5). One-hundred patients with a respiratory physician diagnosis of asthma were investigated in a single tertiary respiratory unit in an open and descriptive study. Twelve of the patients studied did not have asthma and a further seven had additional diagnoses. Of the remainder, 55 had an asthma diagnosis confirmed by demonstration of reversible airflow narrowing or peak flow variability, whilst 20 did not. Noncompliance with prednisolone therapy was more frequent in the 55 with confirmed asthma (nine of 18 prescribed oral prednisolone at a dose of greater than or equal to 15 mg(.)day(-1)) and was not detected in the "unconfirmed asthma" group. There were no other significant differences between these groups. A major psychiatric component was detected in 10 patients. Systematic evaluation of difficult asthma is useful as it can identify alternative or additional diagnoses, psychiatric illness or nonconcordance with therapy in a substantial proportion of cases (32% in the present series).	Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Upper Resp Med, Fac Med, London SW3 6LY, England; Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Thorac Med, Fac Med, London SW3 6LY, England; Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Allergy, Fac Med, London SW3 6LY, England; Royal Brompton & Harefield NHS Trust, London, England	Robinson, DS (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Allergy & Clin Immunol, Fac Med, Dovehouse St, London SW3 6LY, England.			Adcock, Ian/0000-0003-2101-8843; Chung, Kian Fan/0000-0001-7101-1426			ALEXANDER AG, 1992, LANCET, V339, P324, DOI 10.1016/0140-6736(92)91646-P; Ayres JG, 1998, THORAX, V53, P315; Barnes PJ, 1998, EUR RESPIR J, V12, P1209, DOI 10.1183/09031936.98.12051209; Bousquet J, 2001, J ALLERGY CLIN IMMUN, V108, p1s; British Thoracic Society, 1997, THORAX S1, V52, pS1, DOI DOI 10.1136/THX.52.2008.S1]; Carr DH, 1998, RESP MED, V92, P448, DOI 10.1016/S0954-6111(98)90290-6; Chan MTS, 1998, J ALLERGY CLIN IMMUN, V101, P594; Chung KF, 1999, EUR RESPIR J, V13, P1198; CORRIGAN CJ, 1991, AM REV RESPIR DIS, V144, P1016; Fireman P, 2000, ALLERGY ASTHMA PROC, V21, P45, DOI 10.2500/108854100778248935; GOLDBERG DP, 1976, BRIT J PSYCHIAT, V129, P61, DOI 10.1192/bjp.129.1.61; HIGGINS BG, 1989, AM REV RESPIR DIS, V140, P1368; Jatakanon A, 1999, AM J RESP CRIT CARE, V160, P1532; JONES PW, 1992, AM REV RESPIR DIS, V145, P1321; Miles JF, 1997, CLIN EXP ALLERGY, V27, P1151; Payne DNR, 2001, THORAX, V56, P345, DOI 10.1136/thorax.56.5.345; SHINER RJ, 1990, LANCET, V336, P137, DOI 10.1016/0140-6736(90)91659-X; Szefler SJ, 1997, EUR RESPIR J, V10, P1640, DOI 10.1183/09031936.97.10071640; ten Brinke A, 2001, AM J RESP CRIT CARE, V164, P744; Tunnicliffe WS, 1999, EUR RESPIR J, V13, P654, DOI 10.1183/09031936.99.13365499; WAREHAM NJ, 1993, THORAX, V48, P1117, DOI 10.1136/thx.48.11.1117; Wenzel SE, 1999, AM J RESP CRIT CARE, V160, P1001; [Anonymous], 2001, AM J RESP CRIT CARE, V162, P2341	23	148	154	0	2	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	SEP	2003	22	3					478	483		10.1183/09031936.03.00017003		6	Respiratory System	Respiratory System	721VP	WOS:000185339400016	14516138	
J	Kharitonov, SA; Barnes, PJ				Kharitonov, SA; Barnes, PJ			Clinical aspects of exhaled nitric oxide	EUROPEAN RESPIRATORY JOURNAL			English	Editorial Material						asthma; exhaled breath; isoprostanes; nitric oxide; noninvasive markers of airway; inflammation; S-nitrosothiols	OBSTRUCTIVE PULMONARY-DISEASE; LUNG-TRANSPLANT RECIPIENTS; CYSTIC-FIBROSIS; ASTHMATIC-PATIENTS; MILD ASTHMA; INDUCED SPUTUM; AIRWAY INFLAMMATION; OXIDATIVE STRESS; YOUNG-CHILDREN; OBLITERATIVE BRONCHIOLITIS	There has been intense research into the role nitric oxide (NO) plays in physiological and pathological mechanisms and its clinical significance in respiratory medicine, Elevated levels of exhaled levels of exhaled NO in asthma and other inflammatory lung diseases lead to many studies examining NO as potential markers of airway inflammation, enabling repeated noninvasive and standardized monitoring of airway inflammation. In airway inflammation, NO is not merely a marker but may have antiinflammatory and pro-inflammatory effects, Significant correlation has been found between exhaled NO and skin test scores in steroid naive asthmatic patients, allowing to discriminate patients with and without airway responsiveness. Exhaled NO is significantly elevated in acute asthma, or steroid-resistant severe asthma, or when the maintenance dose of inhaled steroids is reduced, and quickly reduced down to the levels in patients with stable asthma after steroid treatment. Exhaled NO has been successfully used to monitor anti-inflammatory treatment with inhaled corticosteroids in asthma, Exhaled NO is extremely sensitive and rapid marker of the dose-dependent effect of steroid treatment, or asthma deterioration, which is increased to any changes in lung function, provocative concentration causing a 20% fall in forced expiratory volume, sputum eosinophilia or asthma symptoms. Exhaled NO is not increased in stable chronic obstructive pulmonary disease (COPD), but patients with unstable COPD, or bronchiectasis have high NO levels. Exhaled and nasal NO are diagnostically low in cystic fibrosis and primary pulmonary dyskinesia. Analysis of exhaled air, including nitric oxide, is feasible and could provide a noninvasive method for use in monitoring and management of lung diseases.	Natl Heart & Lung Inst, Dept Thorac Med, Imperial Coll Sch Med, London SW3 6LY, England	Barnes, PJ (reprint author), Natl Heart & Lung Inst, Dept Thorac Med, Imperial Coll Sch Med, Dovehouse St, London SW3 6LY, England.						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Resp. J.	OCT	2000	16	4					781	792		10.1183/09031936.00.16478100		12	Respiratory System	Respiratory System	374ET	WOS:000165332000032	11106225	
J	Fisk, WJ				Fisk, WJ			Health and productivity gains from better indoor environments and their relationship with building energy efficiency	ANNUAL REVIEW OF ENERGY AND THE ENVIRONMENT			English	Review						economics; health; productivity	RESPIRATORY-TRACT INFECTIONS; OFFICE WORKERS; UNITED-STATES; TASK-PERFORMANCE; ALLERGIC DISEASE; ECONOMIC COSTS; ASTHMA; CHILDREN; SYMPTOMS; SATISFACTION	Theoretical considerations and empirical data suggest that existing technologies and procedures can improve indoor environments in a manner that significantly increases productivity and health. The existing literature contains moderate to strong evidence that characteristics of buildings and indoor environments significantly influence rates of communicable respiratory illness, allergy and asthma symptoms, sick building symptoms, and worker performance. Whereas there is considerable uncertainty in the estimates of the magnitudes of productivity gains that may be obtained by providing better indoor environments, the projected gains are very large. For the United States, the estimated potential annual savings and productivity gains are $6 to $14 billion from reduced respiratory disease, $1 to $4 billion from reduced allergies and asthma, $10 to $30 billion from reduced sick building syndrome symptoms, and $20 to $160 billion from direct improvements in worker performance that are unrelated to health. Productivity gains that are quantified and demonstrated could serve as a strong stimulus for energy efficiency measures that simultaneously improve the indoor environment.	Lawrence Berkeley Natl Lab, Indoor Environm Dept, Environm Energy Technol Div, Berkeley, CA 94720 USA	Fisk, WJ (reprint author), Lawrence Berkeley Natl Lab, Indoor Environm Dept, Environm Energy Technol Div, Berkeley, CA 94720 USA.						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Rev. Energ. Environ.		2000	25						537	566		10.1146/annurev.energy.25.1.537		30	Energy & Fuels; Engineering, Environmental	Energy & Fuels; Engineering	396EZ	WOS:000166624500016		
J	Willart, MAM; Deswarte, K; Pouliot, P; Braun, H; Beyaert, R; Lambrecht, BN; Hammad, H				Willart, Monique A. M.; Deswarte, Kim; Pouliot, Philippe; Braun, Harald; Beyaert, Rudi; Lambrecht, Bart N.; Hammad, Hamida			Interleukin-1 alpha controls allergic sensitization to inhaled house dust mite via the epithelial release of GM-CSF and IL-33	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article							THYMIC STROMAL LYMPHOPOIETIN; ADAPTIVE IMMUNE-RESPONSES; DENDRITIC CELL MATURATION; NF-KAPPA-B; T-CELLS; AIRWAY INFLAMMATION; TH2 RESPONSES; SEVERE ASTHMA; IN-VIVO; MICE	House dust mite (HDM) is one of the most common allergens worldwide. In this study, we have addressed the involvement of IL-1 in the interaction between HDM and the innate immune response driven by lung epithelial cells (ECs) and dendritic cells (DCs) that leads to asthma. Mice lacking IL-1R on radioresistant cells, but not hematopoietic cells, failed to mount a Th2 immune response and did not develop asthma to HDM. Experiments performed in vivo and in isolated air-liquid interface cultures of bronchial ECs showed that TLR4 signals induced the release of IL-1 alpha, which then acted in an autocrine manner to trigger the release of DC-attracting chemokines, GM-CSF, and IL-33. Consequently, allergic sensitization to HDM was abolished in vivo when IL-1 alpha, GM-CSF, or IL-33 was neutralized. Thymic stromal lymphopoietin (TSLP) became important only when high doses of allergen were administered. These findings put IL-1 alpha upstream in the cytokine cascade leading to epithelial and DC activation in response to inhaled HDM allergen.	[Willart, Monique A. M.; Deswarte, Kim; Pouliot, Philippe; Lambrecht, Bart N.; Hammad, Hamida] Univ Ghent VIB, Dept Mol Biomed Res, Lab Immunoregulat & Mucosal Immunol, B-9000 Ghent, Belgium; [Braun, Harald; Beyaert, Rudi] Univ Ghent VIB, Dept Mol Biomed Res, Unit Mol Signal Transduct Inflammat, B-9000 Ghent, Belgium; [Willart, Monique A. M.; Deswarte, Kim; Pouliot, Philippe; Lambrecht, Bart N.; Hammad, Hamida] Univ Ghent, Dept Resp Med, B-9000 Ghent, Belgium; [Braun, Harald; Beyaert, Rudi] Univ Ghent, Dept Biomed Mol Biol, B-9000 Ghent, Belgium; [Lambrecht, Bart N.] Erasmus MC, Dept Pulm Med, NL-3015 GE Rotterdam, Netherlands	Hammad, H (reprint author), Univ Ghent VIB, Dept Mol Biomed Res, Lab Immunoregulat & Mucosal Immunol, B-9000 Ghent, Belgium.	hamida.hammad@ugent.be	Beyaert, Rudi/B-2589-2009; Hammad, Hamida/J-9391-2015; Lambrecht, Bart/K-2484-2014	Hammad, Hamida/0000-0003-3762-8603; Lambrecht, Bart/0000-0003-4376-6834	Flemish Organization for Scientific Research (FWO); European Research Council; Ghent University; National Institutes of Health [5R21AI083690-02]; FWO	B.N. Lambrecht is a recipient of an Odysseus Grant of the Flemish Organization for Scientific Research (FWO) and a recipient of a European Research Council Consolidator grant and a Ghent University Multidisciplinary Research Partnership grant (Group-ID). H. Hammad and B.N. Lambrecht are supported by National Institutes of Health grant number 5R21AI083690-02. H. Hammad is a recipient of an FWO program grant. B.N. Lambrecht is a recipient of a GOA Concerted Research Initiative from Ghent University.	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Exp. Med.	JUL 30	2012	209	8					1505	1517		10.1084/jem.20112691		13	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	982BK	WOS:000307016500013	22802353	
J	Mackay, D; Haw, S; Ayres, JG; Fischbacher, C; Pell, JP				Mackay, Daniel; Haw, Sally; Ayres, Jon G.; Fischbacher, Colin; Pell, Jill P.			Smoke-free Legislation and Hospitalizations for Childhood Asthma.	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							ENVIRONMENTAL TOBACCO-SMOKE; CROSS-SECTIONAL SURVEY; SECONDHAND SMOKE; 2ND-HAND SMOKE; EXPOSURE; SCOTLAND; IMPLEMENTATION; CHILDREN; HEALTH	Background: Previous studies have shown that after the adoption of comprehensive smoke-free legislation, there is a reduction in respiratory symptoms among workers in bars. However, it is not known whether respiratory disease is also reduced among people who do not have occupational exposure to environmental tobacco smoke. The aim of our study was to determine whether the ban on smoking in public places in Scotland, which was initiated in March 2006, influenced the rate of hospital admissions for childhood asthma. Methods: Routine hospital administrative data were used to identify all hospital admissions for asthma in Scotland from January 2000 through October 2009 among children younger than 15 years of age. A negative binomial regression model was fitted, with adjustment for age group, sex, quintile of socioeconomic status, urban or rural residence, month, and year. Tests for interactions were also performed. Results: Before the legislation was implemented, admissions for asthma were increasing at a mean rate of 5.2% per year (95% confidence interval [CI], 3.9 to 6.6). After implementation of the legislation, there was a mean reduction in the rate of admissions of 18.2% per year relative to the rate on March 26, 2006 (95% CI, 14.7 to 21.8; P<0.001). The reduction was apparent among both preschool and school-age children. There were no significant interactions between hospital admissions for asthma and age group, sex, urban or rural residence, region, or quintile of socioeconomic status. Conclusions: In Scotland, passage of smoke-free legislation in 2006 was associated with a subsequent reduction in the rate of respiratory disease in populations other than those with occupational exposure to environmental tobacco smoke. (Funded by NHS Health Scotland.) N Engl J Med 2010;363:1139-45.	[Mackay, Daniel; Pell, Jill P.] Univ Glasgow, Sect Publ Hlth, Glasgow G12 8RZ, Lanark, Scotland; [Haw, Sally] Scottish Collaborat Publ Hlth Res Policy, Edinburgh, Midlothian, Scotland; [Ayres, Jon G.] Univ Birmingham, Inst Occupat & Environm Med, Birmingham, W Midlands, England; [Fischbacher, Colin] NHS Natl Serv, Informat Serv Div, Edinburgh, Midlothian, Scotland	Pell, JP (reprint author), Univ Glasgow, Sect Publ Hlth, Rm 305,1 Lilybank Gardens, Glasgow G12 8RZ, Lanark, Scotland.	j.pell@clinmed.gla.ac.uk			NHS Health Scotland	Supported by a project grant from NHS Health Scotland.	Akhtar PC, 2009, TOB CONTROL, V18, P409, DOI 10.1136/tc.2009.030627; Akhtar PC, 2007, BRIT MED J, V335, P545, DOI 10.1136/bmj.39311.550197.AE; Akhtar PC, 2010, J EPIDEMIOL COMMUN H, V64, P341, DOI 10.1136/jech.2008.084178; Anderson HR, 2007, THORAX, V62, P85, DOI 10.1136/thx.2006.066407; Ashley MJ, 1998, TOB CONTROL, V7, P61; Ayres JG, 2009, OCCUP ENVIRON MED, V66, P339, DOI 10.1136/oem.2008.040311; Baena-Cagnani CE, 2009, CURR OPIN ALLERGY CL, V9, P136, DOI 10.1097/ACI.0b013e3283294038; Black C., 2009, SCOTTISH SCH ADOLESC; Gergen PJ, 1998, PEDIATRICS, V101, part. no., DOI 10.1542/peds.101.2.e8; Haw SJ, 2007, BRIT MED J, V335, P549, DOI 10.1136/bmj.39315.670208.47; HERMAN PM, 2010, AM J PUBLIC HLT 0513; Meyers DG, 2009, J AM COLL CARDIOL, V54, P1902, DOI 10.1016/j.jacc.2009.10.004; Meyers DG, 2009, J AM COLL CARDIOL, V54, P1249, DOI 10.1016/j.jacc.2009.07.022; Naiman A, 2010, CAN MED ASSOC J, V182, P761, DOI 10.1503/cmaj.091130; Office of Environmental Health Hazard Assessment, 2005, HLTH EFF EXP ENV TOB; Pell JP, 2008, NEW ENGL J MED, V359, P482, DOI 10.1056/NEJMsa0706740; Scottish Government, 2009, SCOTL PEOPL ANN REP; Semple S, 2007, ANN OCCUP HYG, V51, P571, DOI 10.1093/annhyg/mem044; Semple S, 2007, TOB CONTROL, V16, P127, DOI 10.1136/tc.2006.018119; Vork KL, 2007, ENVIRON HEALTH PERSP, V115, P1394, DOI 10.1289/ehp.10155	20	147	155	0	13	MASSACHUSETTS MEDICAL SOC	WALTHAM	WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA	0028-4793			NEW ENGL J MED	N. Engl. J. Med.	SEP 16	2010	363	12					1139	1145		10.1056/NEJMoa1002861		7	Medicine, General & Internal	General & Internal Medicine	649TD	WOS:000281795800008	20843248	
J	Hackett, TL; Warner, SM; Stefanowicz, D; Shaheen, F; Pechkovsky, DV; Murray, LA; Argentieri, R; Kicic, A; Stick, SM; Bai, TR; Knight, DA				Hackett, Tillie-Louise; Warner, Stephanie Mary; Stefanowicz, Dorota; Shaheen, Furquan; Pechkovsky, Dmitri V.; Murray, Lynne A.; Argentieri, Rochelle; Kicic, Anthony; Stick, Stephen M.; Bai, Tony R.; Knight, Darryl A.			Induction of Epithelial-Mesenchymal Transition in Primary Airway Epithelial Cells from Patients with Asthma by Transforming Growth Factor-beta 1	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; epithelial-mesenchymal transition; transforming growth factor-beta 1; epithelium	GROWTH-FACTOR-BETA; RETICULAR BASEMENT-MEMBRANE; ACTIVATED PROTEIN-KINASE; PULMONARY-FIBROSIS; EXPRESSION; MOUSE; LUNG; SMAD; TRANSDIFFERENTIATION; TGF-BETA-1	Rationale Airway remodeling in asthma is associated with the accumulation of fibroblasts, the primary cell responsible for synthesis and secretion of extracellular matrix proteins. The process by which the number of fibroblasts increases in asthma is poorly understood, but epithelial-mesenchymal transition (EMT) may play a significant role. Objectives: To evaluate whether EMT occurs in primary airway epithelial cells (AECs), the mechanisms involved, and if this process is altered in asthmatic AECs. Methods: AECs were obtained from subjects with asthma (n = 8) and normal subjects without asthma (n = 10). Monolayer and air-liquid interface-AEC (ALI-AEC) cultures were treated with transforming growth factor (TGF)-beta 1 (10 ng/ml) for 72 hours and assayed for mesenchymal and epithelial markers using quantitative polymerase chain reaction, confocal microscopy, and immunoblot. The involvement of BMP-7, Smad3, and MAPK-mediated signaling were also evaluated. Measurements and Main Results: TGF-beta 1-induced EMT in AEC monolayers derived from subjects with asthma and normal donors. EMT was characterized by changes in cell morphology, increased expression of mesenchymal markers EDA-fibronectin, vimentin, alpha-smooth muscle actin, and collagen-1, and loss of epithelial markers E-cadherin and zonular occludin-1. Inhibition of TGF-beta 1-induced signaling with Smad3-inhibiting siRNA or TGF-beta 1-neutralizing antibodies prevented and reversed EMT, respectively, whereas BMP-7 had no effect. In ALI-AEC cultures derived from normal subjects, EMT was confined to basally situated cells, whereas in asthmatic ALI-AEC cultures EMT was widespread throughout the epithelium. Conclusions: TGF-beta 1 induces EMT in a Smad3-dependent manner in primary AECs. However, in asthmatic-derived ALI-AEC cultures, the number of cells undergoing EMT is greater. These findings support the hypothesis that epithelial repair in asthmatic airways is dysregulated.	[Hackett, Tillie-Louise; Warner, Stephanie Mary; Stefanowicz, Dorota; Shaheen, Furquan; Pechkovsky, Dmitri V.; Bai, Tony R.; Knight, Darryl A.] St Pauls Hosp, James Hogg iCAPTURE Ctr Cardiovasc & Pulm Res, Vancouver, BC V6Z 1Y6, Canada; [Hackett, Tillie-Louise; Pechkovsky, Dmitri V.; Knight, Darryl A.] Univ British Columbia, Dept Anesthesiol Pharmacol & Therapeut, Vancouver, BC V5Z 1M9, Canada; [Murray, Lynne A.; Argentieri, Rochelle] Centocor Ltd, Dept Immunobiol, Radnor, PA USA; [Kicic, Anthony; Stick, Stephen M.] Princess Margaret Hosp Children, Dept Resp Med, Perth, WA, Australia; [Kicic, Anthony; Stick, Stephen M.] Univ Western Australia, Sch Pediat & Child Hlth, Nedlands, WA 6009, Australia; [Stick, Stephen M.] Telethon Inst Child Hlth Res, Subiaco, WA, Australia	Hackett, TL (reprint author), St Pauls Hosp, James Hogg iCAPTURE Ctr Cardiovasc & Pulm Dis, 1081 Burrard St, Vancouver, BC V6Z 1Y6, Canada.	thackett@mrl.ubc.ca	Stick, Stephen/O-5683-2014	Pechkovsky, Dmitri/0000-0001-8908-3444	Thomas Abraham at The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research; Departments of Pathology and Laboratory Medicine; The University of British Columbia-St. Paul's Hospital, Vancouver, British Columbia, Canada	Images were generated with the help of Thomas Abraham at The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, Departments of Pathology and Laboratory Medicine, The University of British Columbia-St. Paul's Hospital, Vancouver, British Columbia, Canada. The imaging facility is CFI funded.	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J	Murcray, CE; Lewinger, JP; Gauderman, WJ				Murcray, Cassandra E.; Lewinger, Juan Pablo; Gauderman, W. James			Gene-Environment Interaction in Genome-Wide Association Studies	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article							BREAST-CANCER; AIR-POLLUTION; SUSCEPTIBILITY; RISK; ASTHMA; LOCI; REPLICATION; CHILDREN; SMOKING	It is a commonly held belief that most complex diseases (e.g., diabetes, asthma, cancer) are affected in part by interactions between genes and environmental factors. However, investigators conducting genome-wide association studies typically test for only the marginal effects of each genetic marker on disease. In this paper, the authors propose an efficient and easily implemented 2-step analysis of genome-wide association study data aimed at identifying genes involved in a gene-environment interaction. The procedure complements screening for marginal genetic effects and thus has the potential to uncover new genetic signals that have not been identified previously.	[Murcray, Cassandra E.; Lewinger, Juan Pablo; Gauderman, W. James] Univ So Calif, Dept Prevent Med, Los Angeles, CA 90089 USA	Murcray, CE (reprint author), Univ So Calif, Dept Prevent Med, 1540 Alcazar St,CHP 222F, Los Angeles, CA 90089 USA.	murcray@usc.edu			NHGRI NIH HHS [P50 HG 002790-02, P50 HG002790]; NHLBI NIH HHS [5R01HL087680, 5R01HL61768, 5R01HL76647, R01 HL061768, R01 HL076647, R01 HL087680]; NIEHS NIH HHS [P01 ES009581, 5P01ES009581, 5P01ES011627, 5P30ES007048, 5R01ES014447, 5R01ES014708, P01 ES011627, P30 ES007048, R01 ES014447, R01 ES014708, T32 ES013678]; ORD VA [RD831861]; PHS HHS [R826708]		BENJAMINI Y, 1995, J ROY STAT SOC B MET, V57, P289; Browning BL, 2007, GENET EPIDEMIOL, V31, P365, DOI 10.1002/gepi.20216; Clayton D, 2001, LANCET, V358, P1356, DOI 10.1016/S0140-6736(01)06418-2; Easton DF, 2007, NATURE, V447, P1087, DOI 10.1038/nature05887; Gauderman WJ, 2007, LANCET, V369, P571, DOI 10.1016/S0140-6736(07)60037-3; Gauderman WJ, 2004, NEW ENGL J MED, V351, P1057, DOI 10.1056/NEJMoa040610; Gauderman WJ, 2002, AM J EPIDEMIOL, V155, P478, DOI 10.1093/aje/155.5.478; Gauderman WJ, 2005, EPIDEMIOLOGY, V16, P737, DOI 10.1097/01.ede.00001813087.51440.75; Hunter DJ, 2007, NAT GENET, V39, P870, DOI 10.1038/ng2075; Ito H, 2004, CARCINOGENESIS, V25, P1395, DOI 10.1093/carcin/bgh153; Khoury MJ, 1996, AM J EPIDEMIOL, V144, P207; Kraft P, 2007, HUM HERED, V63, P111, DOI 10.1159/000099183; McConnell R, 2002, LANCET, V359, P386, DOI 10.1016/S0140-6736(02)07597-9; McConnell R, 1999, ENVIRON HEALTH PERSP, V107, P757, DOI 10.2307/3434662; Millstein J, 2006, AM J HUM GENET, V78, P15, DOI 10.1086/498850; PIEGORSCH WW, 1994, STAT MED, V13, P153, DOI 10.1002/sim.4780130206; RISCH N, 1996, SCIENCE, V273, P1517; Saxena R, 2007, SCIENCE, V316, P1331, DOI 10.1126/science.1142358; Scott LJ, 2007, SCIENCE, V316, P1341, DOI 10.1126/science.1142382; Stern MC, 2002, CANCER EPIDEM BIOMAR, V11, P1004; Van Steen K, 2005, NAT GENET, V37, P683, DOI 10.1038/ng1582; van der Vaart A. W., 1998, ASYMPTOTIC STAT; Zeggini E, 2007, SCIENCE, V316, P1336, DOI 10.1126/science.1142364; Zhao JY, 2006, GENETICS, V174, P1529, DOI 10.1534/genetics.106.060491	24	147	154	2	12	OXFORD UNIV PRESS INC	CARY	JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA	0002-9262			AM J EPIDEMIOL	Am. J. Epidemiol.	JAN 15	2009	169	2					219	226		10.1093/aje/kwn353		8	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	395IQ	WOS:000262518200013	19022827	
J	D'Amato, G; Liccardi, G; D'Amato, M; Holgate, S				D'Amato, G; Liccardi, G; D'Amato, M; Holgate, S			Environmental risk factors and allergic bronchial asthma	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review						air pollution; bronchial asthma; pollen allergy; respiratory allergy; thunderstorm-associated asthma; urban air pollution	OUTDOOR AIR-POLLUTION; THUNDERSTORM-ASSOCIATED ASTHMA; RESPIRATORY HEALTH SURVEY; DIESEL EXHAUST PARTICLES; FINE-PARTICULATE MATTER; GRASS-POLLEN ALLERGEN; PPM NITROGEN-DIOXIDE; OZONE EXPOSURE; PULMONARY-FUNCTION; SULFUR-DIOXIDE	The prevalence of allergic respiratory diseases such as bronchial asthma has increased in recent years, especially in industrialized countries. A change in the genetic predisposition is an unlikely cause of the increase in allergic diseases because genetic changes in a population require several generations. Consequently, this increase may be explained by changes in environmental factors, including indoor and outdoor air pollution. Over the past two decades, there has been increasing interest in studies of air pollution and its effects on human health. Although the role played by outdoor pollutants in allergic sensitization of the airways has yet to be clarified, a body of evidence suggests that urbanization, with its high levels of vehicle emissions, and a westernized lifestyle are linked to the rising frequency of respiratory allergic diseases observed in most industrialized countries, and there is considerable evidence that asthmatic persons are at increased risk of developing asthma exacerbations with exposure to ozone, nitrogen dioxide, sulphur dioxide and inhalable particulate matter. However, it is not easy to evaluate the impact of air pollution on the timing of asthma exacerbations and on the prevalence of asthma in general. As concentrations of airborne allergens and air pollutants are frequently increased contemporaneously, an enhanced IgE-mediated response to aeroallergens and enhanced airway inflammation could account for the increasing frequency of allergic respiratory allergy and bronchial asthma. Pollinosis is frequently used to study the interrelationship between air pollution and respiratory allergy. Climatic factors (temperature, wind speed, humidity, thunderstorms, etc) can affect both components (biological and chemical) of this interaction. By attaching to the surface of pollen grains and of plant-derived particles of paucimicronic size, pollutants could modify not only the morphology of these antigen-carrying agents but also their allergenic potential. In addition, by inducing airway inflammation, which increases airway permeability, pollutants overcome the mucosal barrier and could be able to 'prime' allergen-induced responses. There are also observations that a thunderstorm occurring during pollen season can induce severe asthma attacks in pollinosis patients. After rupture by thunderstorm, pollen grains may release part of their cytoplasmic content, including inhalable, allergen-carrying paucimicronic particles.	High Special Hosp A Cardarelli, Div Pneumol Allergol, Dept Chest Dis, I-80121 Naples, Italy; Southampton Gen Hosp, Resp Cell & Mol Biol Res Div, Southampton SO9 4XY, Hants, England	D'Amato, G (reprint author), High Special Hosp A Cardarelli, Div Pneumol Allergol, Dept Chest Dis, Via Rione Sirignano 10, I-80121 Naples, Italy.	gdamato@qubisoft.it	D'Amato, Maria/H-3074-2012	D'Amato, Maria/0000-0002-5906-5701			ACEVES M, 1991, J ALLERGY CLIN IMMUN, V88, P124, DOI 10.1016/0091-6749(91)90309-C; ADAMS WC, 1983, J APPL PHYSIOL, V55, P805; *AM THOR SOC, 1996, HLTH EFFECTS OUTDO 2, V153, P477; *AMB IT, 2001, RAPP STAT PAES; Anderson M, 1994, J AEROSOL SCI, V25, P567; ANTO JM, 1993, NEW ENGL J MED, V329, P1760, DOI 10.1056/NEJM199312093292402; ANTO JM, 1989, NEW ENGL J MED, V320, P1097, DOI 10.1056/NEJM198904273201701; Atkinson RW, 1999, EUR RESPIR J, V13, P257, DOI 10.1183/09031936.99.13225799; Ball BA, 1996, J ALLERGY CLIN IMMUN, V98, P563, DOI 10.1016/S0091-6749(96)70090-8; BALMES JR, 1987, AM REV RESPIR DIS, V136, P1117; BALMES JR, 1993, ENVIRON HEALTH PERSP, V101, P219, DOI 10.2307/3431683; Balmes J. 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J	van Strien, RT; Engel, R; Holst, O; Bufe, A; Eder, W; Waser, M; Braun-Fahrlander, C; Riedler, J; Nowak, D; von Mutius, E				van Strien, RT; Engel, R; Holst, O; Bufe, A; Eder, W; Waser, M; Braun-Fahrlander, C; Riedler, J; Nowak, D; von Mutius, E		ALEX Study Team	Microbial exposure of rural school children, as assessed by levels of N-acetyl-muramic acid in mattress dust, and its association with respiratory health	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						farming; allergy; asthma; peptidoglycan; muramic acid; microbial exposure; hygiene hypothesis	TANDEM MASS-SPECTROMETRY; ALLERGIC SENSITIZATION; ENDOTOXIN LEVELS; HAY-FEVER; FARMERS CHILDREN; ASTHMA; ENVIRONMENTS; AGE; DETERMINANTS; COMMUNITY	Background: Endotoxin exposure has been shown to be associated with a decreased prevalence of atopic sensitization and symptoms. Yet endotoxin represents only a part of the indoor microbial exposure. Muramic acid, a constituent of peptidoglycan, is present in gram-negative and gram-positive bacteria in the environment and may therefore serve as an additional marker of microbial exposure. Objective: To study the factors determining the level of indoor exposure to muramic acid/peptidoglycan, as well as its potential association with respiratory health. Methods: In 553 farm and nonfarm school children from Austria, Switzerland, and Germany, mattress dust muramic acid concentrations were determined, and health was assessed by using IgE measurements and questionnaire information. Results: The muramic acid concentration was found to be significantly higher in dust from farm children's mattresses than in dust from nonfarm children's mattresses (157 vs 131 ng/mg). Children with higher mattress dust muramic acid concentrations had a significantly lower prevalence of wheezing (odds ratio of highest vs lowest tertile of muramic acid concentration, 0.3; 95 % CI, 0.1-0.9), regardless of farming status and endotoxin exposure. The association for asthma was similar, and no association was found with atopic sensitization. Conclusion: Next to endotoxin, muramic acid provides us with an independent marker of microbial exposure. Unlike endotoxin, muramic acid was inversely associated with wheezing rather than with atopic sensitization.	Univ Munich, Childrens Hosp, D-8000 Munich, Germany; Res Ctr Borstel, Div Struct Biochem, Leibniz Ctr Med & Biol Sci, Borstel, Germany; Ruhr Univ Bochum, Dept Expt Pneumol, D-4630 Bochum, Germany; Arizona Resp Ctr, Tucson, AZ USA; Inst Social & Prevent Med, Basel, Switzerland; Childrens Hosp, Salzburg, Austria; Inst Occupat & Environm Med, Munich, Germany	von Mutius, E (reprint author), Von Haunersche Kinderklin, Lindwurmstr 4, D-80337 Munich, Germany.	erika.von.mutius@med.uni-muenchen.de					BLACK GE, 1994, ANAL CHEM, V66, P4171, DOI 10.1021/ac00095a010; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Gehring U, 2002, AM J RESP CRIT CARE, V166, P939, DOI 10.1164/rccm.200203-256OC; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Gereda JE, 2001, J ALLERGY CLIN IMMUN, V107, P790, DOI 10.1067/mai.2001.115245; Heine H, 2003, INT ARCH ALLERGY IMM, V130, P180, DOI 10.1159/000069517; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; HEUMANN D, 1994, INFECT IMMUN, V62, P2715; Krahmer M, 1998, AM IND HYG ASSOC J, V59, P524, DOI 10.1202/0002-8894(1998)059<0524:TAVABL>2.0.CO;2; Kramer U, 1999, LANCET, V353, P450, DOI 10.1016/S0140-6736(98)06329-6; Laitinen S, 2001, ANN AGR ENV MED, V8, P213; Lauener RP, 2002, LANCET, V360, P465, DOI 10.1016/S0140-6736(02)09641-1; Liu LJS, 2000, J AIR WASTE MANAGE, V50, P1957, DOI 10.1080/10473289.2000.10464225; Matricardi PM, 2000, BRIT MED J, V320, P412, DOI 10.1136/bmj.320.7232.412; Matricardi PM, 2000, CLIN EXP ALLERGY, V30, P1506, DOI 10.1046/j.1365-2222.2000.00994.x; MIELNICZUK Z, 1995, J CHROMATOGR B, V670, P167, DOI 10.1016/0378-4347(95)00152-9; Ownby DR, 2002, JAMA-J AM MED ASSOC, V288, P963, DOI 10.1001/jama.288.8.963; Pearce N, 2000, THORAX, V55, P424, DOI 10.1136/thorax.55.5.424; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Saraf A, 1999, INDOOR AIR, V9, P219, DOI 10.1111/j.1600-0668.1999.00002.x; Sebastian A, 2003, APPL ENVIRON MICROB, V69, P3103, DOI 10.1128/AEM.69.6.3103-3109.2003; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Strachan DP, 2000, THORAX S1, V55, pS2; VONMUTIUS E, 1994, BRIT MED J, V308, P692; Waser M, 2004, CLIN EXP ALLERGY, V34, P389, DOI 10.1111/j.1365-2222.2004.01873.x; WEIDEMANN B, 1994, INFECT IMMUN, V62, P4709; Wickens K, 2003, INDOOR AIR, V13, P128, DOI 10.1034/j.1600-0668.2003.00187.x; Zhiping Wang, 1996, American Journal of Respiratory and Critical Care Medicine, V154, P1261	30	147	149	2	14	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	MAY	2004	113	5					860	867		10.1016/j.jaci.2004.01.078		8	Allergy; Immunology	Allergy; Immunology	818UC	WOS:000221269000007	15131567	
J	Bernard, A; Carbonnelle, S; Michel, O; Higuet, S; de Burbure, C; Buchet, JP; Hermans, C; Dumont, X; Doyle, I				Bernard, A; Carbonnelle, S; Michel, O; Higuet, S; de Burbure, C; Buchet, JP; Hermans, C; Dumont, X; Doyle, I			Lung hyperpermeability and asthma prevalence in schoolchildren: unexpected associations with the attendance at indoor chlorinated swimming pools	OCCUPATIONAL AND ENVIRONMENTAL MEDICINE			English	Article							CLARA CELL PROTEIN; RESPIRATORY SYMPTOMS; BRONCHIAL RESPONSIVENESS; NITROGEN TRICHLORIDE; SERUM; CHILDREN; CC16; DISINFECTANT; SWIMMERS; SMOKERS	Aims: To study whether exposure to nitrogen trichloride in indoor chlorinated pools may affect the respiratory epithelium of children and increase the risk of some lung diseases such as asthma. Methods: In 226 healthy children, serum surfactant associated proteins A and B (SP-A and SP-B), 16 kDa Clara cell protein (CC 16), and IgE were measured. Lung specific proteins were measured in the serum of 16 children and 13 adults before and after exposure to NCl3, in an indoor chlorinated pool. Relations between pool attendance and asthma prevalence were studied in 1881 children. Asthma was screened with the exercise induced bronchoconstriction test (EIB). Results: Pool attendance was the most consistent predictor of lung epithelium permeability. A positive dose-effect relation was found with cumulated pool attendance and serum SP-A and SP-B. Serum IgE. was unrelated to pool attendance, but correlated positively with lung hyperpermeability as assessed by serum SP-B. Changes in serum levels of lung proteins were reproduced in children and adults attending an indoor pool. Serum SP-A and SP-B were already significantly increased after one hour on the pool side without swimming. Positive EIB and total asthma prevalence were significantly correlated with cumulated pool attendance indices. Conclusions: Regular attendance at chlorinated pools by Young children is associated with an exposure dependent increase in lung epithelium permeability and increase in the risk of developing asthma especially in association with other risk factors. We therefore postulate that the increasing exposure of children to chlorination products in indoor pools might be an important cause of the rising incidence of childhood asthma and allergic diseases in industrialised countries. Further epidemiological studies should be undertaken to test this hypothesis.	Univ Catholique Louvain, Fac Med, Ind Toxicol Unit, B-1200 Brussels, Belgium; Free Univ Brussels, St Pierre Univ Hosp, Clin Allergol & Resp Dis, B-1000 Brussels, Belgium; Flinders Univ S Australia, Dept Human Physiol, Sch Med, Adelaide, SA 5001, Australia; Flinders Univ S Australia, Dept Crit Care Med, Sch Med, Adelaide, SA 5001, Australia	Bernard, A (reprint author), Univ Catholique Louvain, Toxicol Unit, 30-54 Clos Chapelle Aux Champs, B-1200 Brussels, Belgium.		BERNARD, Alfred/A-6511-2010	BERNARD, Alfred/0000-0003-3171-3743; michel, olivier/0000-0002-1528-1277			BARBEE SJ, 1983, AM IND HYG ASSOC J, V44, P145, DOI 10.1202/0002-8894(1983)044<0145:AITONT>2.3.CO;2; BATES DV, 1995, ENVIRON HEALTH PERSP, V103, P243, DOI 10.2307/3432380; Belsley D., 1980, REGRESSION DIAGNOSTI; BERNARD A, 1992, LANCET, V339, P1620, DOI 10.1016/0140-6736(92)91891-B; Boezen HM, 1999, LANCET, V353, P874, DOI 10.1016/S0140-6736(98)06311-9; Broeckaert F, 1999, LANCET, V353, P900, DOI 10.1016/S0140-6736(99)00540-1; Broeckaert F, 2000, CLIN EXP ALLERGY, V30, P469; BURNEY PGJ, 1989, EUR RESPIR J, V2, P940; DESCHAMPS D, 1994, CHEST, V105, P1895, DOI 10.1378/chest.105.6.1895; DOYLE IR, 1995, AM J RESP CRIT CARE, V152, P307; Doyle IR, 1997, AM J RESP CRIT CARE, V156, P1217; *EPA, 1994, CHLOR; ERNST P, 1995, AM J RESP CRIT CARE, V152, P570; Fjellbirkeland Lars, 1995, Tidsskrift for den Norske Laegeforening, V115, P2051; GAGNAIRE F, 1994, J APPL TOXICOL, V14, P405, DOI 10.1002/jat.2550140604; Helenius IJ, 1998, ALLERGY, V53, P346, DOI 10.1111/j.1398-9995.1998.tb03904.x; Hermans C, 1999, AM J RESP CRIT CARE, V159, P646; Hermans C, 1998, CLIN CHIM ACTA, V272, P101, DOI 10.1016/S0009-8981(98)00006-0; Hermans C, 1998, EUR RESPIR J, V11, P801, DOI 10.1183/09031936.98.11040801; HERY M, 1995, ANN OCCUP HYG, V39, P437; JESSEN HJ, 1988, Z GESAMTE HYG, V34, P248; JONES A, 1994, THORAX, V49, P757, DOI 10.1136/thx.49.8.757; Karnak I, 1996, CLIN PEDIATR, V35, P471, DOI 10.1177/000992289603500908; Laing IA, 2000, AM J RESP CRIT CARE, V161, P124; MARTINEZ TT, 1995, J TOXICOL-CLIN TOXIC, V33, P349; Massin N, 1998, OCCUP ENVIRON MED, V55, P258; MCFADDEN ER, 1994, NEW ENGL J MED, V330, P1362, DOI 10.1056/NEJM199405123301907; MUSTCHIN CP, 1979, THORAX, V34, P682, DOI 10.1136/thx.34.5.682; NAKAMURA TY, 1995, J CELL BIOL, V131, P509, DOI 10.1083/jcb.131.2.509; Nelson H S, 1998, Clin Cornerstone, V1, P57; Newman D J, 1994, Kidney Int Suppl, V47, pS20; PENNY PT, 1983, BRIT MED J, V287, P461; Potts J, 1996, SPORTS MED, V21, P256, DOI 10.2165/00007256-199621040-00002; Preller L, 1996, EUR RESPIR J, V9, P1407, DOI 10.1183/09031936.96.09071407; Priftanji A, 2001, LANCET, V358, P1426, DOI 10.1016/S0140-6736(01)06521-7; Ring PC, 2000, CLIN EXP ALLERGY, V30, P1085; Robin M, 2002, EUR RESPIR J, V20, P1152, DOI 10.1183/09031936.02.02042001; SCHRAUFSTATTER IU, 1990, J CLIN INVEST, V85, P554, DOI 10.1172/JCI114472; SCHULLERLEVIS G, 1994, ADV EXP MED BIOL, V35, P931; Shijubo N, 1997, EUR RESPIR J, V10, P1108, DOI 10.1183/09031936.97.10051108; Stewart G A, 1993, Pediatr Allergy Immunol, V4, P163, DOI 10.1111/j.1399-3038.1993.tb00087.x; Tanen DA, 1999, NEW ENGL J MED, V341, P848, DOI 10.1056/NEJM199909093411115; TATSUMI T, 1994, AM J PHYSIOL-HEART C, V267, pH1597; WATT SJ, 1991, UNDERSEA BIOMED RES, V18, P347; WHO, 2000, GUID SAF RECR WAT EN, V2	45	147	152	1	16	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	1351-0711			OCCUP ENVIRON MED	Occup. Environ. Med.	JUN	2003	60	6					385	394		10.1136/oem.60.6.385		10	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	683LJ	WOS:000183149900002	12771389	
J	Leigh, R; Ellis, R; Wattie, J; Southam, DS; de Hoogh, M; Gauldie, J; O'Byrne, PM; Inman, MD				Leigh, R; Ellis, R; Wattie, J; Southam, DS; de Hoogh, M; Gauldie, J; O'Byrne, PM; Inman, MD			Dysfunction and remodeling of the mouse airway persist after resolution of acute allergen-induced airway inflammation	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article							OBSTRUCTIVE PULMONARY-DISEASE; MILD ASTHMA; SUBEPITHELIAL FIBROSIS; INDUCED INCREASE; MURINE MODEL; HYPERRESPONSIVENESS; RESPONSIVENESS; HYPERREACTIVITY; METHACHOLINE; EOSINOPHILIA	The mechanisms underlying airway hyperresponsiveness remain unclear, although airway inflammation and remodeling are likely important contributing factors. We hypothesized that airway physiology would differ between mice subjected to brief or chronic allergen exposure, and that these differences would be associated with characteristic inflammatory markers and indices of airway remodeling. BALB/c mice were sensitized to ovalbumin and studied at several time points following brief or chronic allergen challenge protocols. By measuring airway responses to methacholine, we demonstrated increases in maximal inducible bronchoconstriction that persisted for 8 wk following either brief or chronic allergen challenge; we also observed increases in airway reactivity, although it was only in chronically challenged mice that these changes persisted beyond the resolution of allergen-induced inflammation. Using airway morphometry, we further demonstrated that increases in maximal bronchoconstriction were associated with increases in airway contractile tissue in both models, and that chronic, but not brief, allergen challenge resulted in subepithelial fibrosis. Our observations that different aspects of sustained airway dysfunction and remodeling persist beyond the resolution of acute inflammatory events support the concept that remodeling occurs as a consequence of allergic airway inflammation, and that these structural changes contribute independently to the persistence of airway hyperresponsiveness.	Firestone Inst Resp Hlth, St Josephs Healthcare, Dept Med, Hamilton, ON L8N 4A6, Canada; McMaster Univ, Ctr Gene Therapeut, Dept Pathol, Hamilton, ON L8N 4A6, Canada	Inman, MD (reprint author), Firestone Inst Resp Hlth, St Josephs Healthcare, Dept Med, 50 Charlton Ave E, Hamilton, ON L8N 4A6, Canada.			O'Byrne, Paul/0000-0003-0979-281X			Boulet L P, 1998, Can Respir J, V5, P16; Boulet LP, 2000, AM J RESP CRIT CARE, V162, P1308; Boulet LP, 1997, CHEST, V112, P45, DOI 10.1378/chest.112.1.45; BOUSQUET J, 1990, NEW ENGL J MED, V323, P1033, DOI 10.1056/NEJM199010113231505; BROWN RH, 1995, J APPL PHYSIOL, V79, P1242; BRUSASCO V, 1990, J APPL PHYSIOL, V69, P2209; Busse W, 1999, AM J RESP CRIT CARE, V160, P1035; Busse WW, 2001, NEW ENGL J MED, V344, P350; CARROLL N, 1993, AM REV RESPIR DIS, V147, P405; Chetta A, 1997, CHEST, V111, P852, DOI 10.1378/chest.111.4.852; Cockcroft DW, 1997, ASTHMA, P1253; Corry DB, 1996, J EXP MED, V183, P109, DOI 10.1084/jem.183.1.109; DJUKANOVIC R, 1990, AM REV RESPIR DIS, V142, P434; DJUKANOVIC R, 1992, AM REV RESPIR DIS, V145, P669; Elias JA, 1999, J CLIN INVEST, V104, P1001, DOI 10.1172/JCI8124; Fish JE, 1999, J ALLERGY CLIN IMMUN, V104, P509, DOI 10.1016/S0091-6749(99)70315-5; Foster PS, 1996, J EXP MED, V183, P195, DOI 10.1084/jem.183.1.195; GAVETT SH, 1995, J EXP MED, V182, P1527, DOI 10.1084/jem.182.5.1527; Grunig G, 1998, SCIENCE, V282, P2261, DOI 10.1126/science.282.5397.2261; Hogan SP, 1998, J IMMUNOL, V161, P1501; Inman MD, 1999, AM J RESP CELL MOL, V21, P473; Inman MD, 1998, J ALLERGY CLIN IMMUN, V101, P342; JEFFERY PK, 1989, AM REV RESPIR DIS, V140, P1745; JEFFERY PK, 1992, AM REV RESPIR DIS, V145, P890; KUWANO K, 1993, AM REV RESPIR DIS, V148, P1220; LAMBERT RK, 1993, J APPL PHYSIOL, V74, P2771; Laprise C, 1999, EUR RESPIR J, V14, P63, DOI 10.1034/j.1399-3003.1999.14a12.x; Leckie MJ, 2000, LANCET, V356, P2144, DOI 10.1016/S0140-6736(00)03496-6; Lotvall J, 1998, THORAX, V53, P419; Ohno I, 1997, AM J RESP CELL MOL, V16, P212; Palmans E, 2000, AM J RESP CRIT CARE, V161, P627; RENZ H, 1992, J ALLERGY CLIN IMMUN, V89, P1127, DOI 10.1016/0091-6749(92)90296-E; ROCHE WR, 1989, LANCET, V1, P520; Shapiro SD, 1999, AM J RESP CELL MOL, V20, P1100; Sont JK, 1999, AM J RESP CRIT CARE, V159, P1043; Temelkovski J, 1998, THORAX, V53, P849; Trifilieff A, 2000, AM J PHYSIOL-LUNG C, V279, pL1120; Vignola AM, 2000, J ALLERGY CLIN IMMUN, V105, P1041, DOI 10.1067/mai.2000.107195; Volgyesi GA, 2000, J APPL PHYSIOL, V89, P413; Wang J, 1998, J CLIN INVEST, V102, P1132, DOI 10.1172/JCI2686; WARDLAW AJ, 1988, AM REV RESPIR DIS, V137, P62; Webb DC, 2000, J IMMUNOL, V165, P108; WIGGS BR, 1992, AM REV RESPIR DIS, V145, P1251; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; [Anonymous], NIH PUBLICATION	45	147	161	0	2	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1044-1549			AM J RESP CELL MOL	Am. J. Respir. Cell Mol. Biol.	NOV	2002	27	5					526	535		10.1165/rcmb.2002-0048OC		10	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	614KW	WOS:000179189000002	12397011	
J	Bergmann, RL; Diepgen, TL; Kuss, O; Bergmann, KE; Kujat, J; Dudenhausen, JW; Wahn, U				Bergmann, RL; Diepgen, TL; Kuss, O; Bergmann, KE; Kujat, J; Dudenhausen, JW; Wahn, U		MAS-Study Grp	Breastfeeding duration is a risk factor for atopic eczema	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						atopic eczema; children; breastfeeding	COWS MILK ALLERGY; BREAST-FED INFANTS; DISEASE; CHILDHOOD; PROTEINS; EXPOSURE; IGE; AGE	Background The results of numerous studies on the influence of breastfeeding in the prevention of atopic disorders are often contradictory. One of the most important problems is confounding by other lifestyle factors. Objective The aim of the present study was to analyse the effect of any breastfeeding duration on the prevalence of atopic eczema in the first seven years of life taking into account other risk factors. Methods In an observational birth cohort study 1314 infants born in 1990 were followed-up for seven years. At 3, 6, 12, 18, 24 months and every year thereafter, parents were interviewed and filled in questionnaires, children were examined and blood was taken for in vitro allergy tests. Generalized Estimation Equations (GEE)-models were used to model risk factors for the prevalence of atopic eczema and for confounder adjustment Results Breastfeeding was carried out for longer if at least one parent had eczema, the mother was older, did not smoke in pregnancy, and the family had a high social status. The prevalence of atopic eczema in the first seven years increased with each year of age (OR 1.05; 95% CI 1.01-1.09 for each year), with each additional month of breastfeeding (1.03; 1.00-1.06 for each additional month), with a history of parental atopic eczema (2.06; 1.38-3.08), and if other atopic signs and symptoms appeared, especially specific sensitization (1.53; 1.25-1.88), and asthma (1.41; 1.07-1.85). Although breastfeeding should be recommended for all infants, it does not prevent eczema in children with a genetic risk. Conclusion Parental eczema is the major risk factor for eczema. But in this study, each month of breastfeeding also increased the risk.	Univ Hosp Rudolf Virchow, Charite, Dept Obstet, D-13353 Berlin, Germany; Univ Hosp Rudolf Virchow, Charite, Dept Pediat, D-13353 Berlin, Germany; Univ Heidelberg, Dept Clin Soc Med, D-6900 Heidelberg, Germany; Robert Koch Inst, D-1000 Berlin, Germany	Bergmann, RL (reprint author), Univ Hosp Rudolf Virchow, Charite, Dept Obstet, Augustenburger Pl 1, D-13353 Berlin, Germany.			Kuss, Oliver/0000-0003-3301-5869			Bergmann R L, 1994, Pediatr Allergy Immunol, V5, P19, DOI 10.1111/j.1399-3038.1994.tb00343.x; Bergmann R L, 1993, Pediatr Allergy Immunol, V4, P130, DOI 10.1111/j.1399-3038.1993.tb00081.x; Bergmann RL, 2000, CLIN EXP ALLERGY, V30, P1740, DOI 10.1046/j.1365-2222.2000.00927.x; Bergmann RL, 1998, CLIN EXP ALLERGY, V28, P965; BERGMANN RL, 1994, MONATSSCHR KINDERH, V142, P412; BJORKSTEN B, 1999, ALLERGY CLIN IMMUNOL, V104, P119; Bottcher MF, 2000, PEDIATR RES, V47, P157; Cantisani A, 1997, FEBS LETT, V412, P515, DOI 10.1016/S0014-5793(97)00828-4; de Jong MH, 1998, ARCH DIS CHILD, V79, P126; deBoissieu D, 1997, ACTA PAEDIATR, V86, P1042; Duchen K, 1998, PEDIATR RES, V44, P478, DOI 10.1203/00006450-199810000-00003; Golding J, 1987, Paediatr Perinat Epidemiol, V1, P67, DOI 10.1111/j.1365-3016.1987.tb00091.x; Grulee CG, 1936, J PEDIATR-US, V9, P223, DOI 10.1016/S0022-3476(36)80058-4; Hanifin JM, 1980, ACTA DERM-VENEREOL S, V92, P44; HATTEVIG G, 1989, CLIN EXP ALLERGY, V19, P27, DOI 10.1111/j.1365-2222.1989.tb02339.x; HOST A, 1988, ACTA PAEDIATR SCAND, V77, P663, DOI 10.1111/j.1651-2227.1988.tb10727.x; HOWIE PW, 1990, BRIT MED J, V300, P11; Isolauri E, 1999, J PEDIATR-US, V134, P27, DOI 10.1016/S0022-3476(99)70368-9; JACOBSSON I, 1991, EUR J CLIN NUTR S1, V45, P29; Jarvinen KM, 2000, PEDIATR RES, V48, P457; Kalliomaki M, 1999, J ALLERGY CLIN IMMUN, V104, P1251, DOI 10.1016/S0091-6749(99)70021-7; KILSHAW PJ, 1984, INT ARCH ALLER A IMM, V75, P8; KOLETZKO B, 1999, PADIATRISCHE ALLERGO, P148; KRAMER MS, 1988, J PEDIATR-US, V112, P181, DOI 10.1016/S0022-3476(88)80054-4; Kramer MS, 2001, JAMA-J AM MED ASSOC, V285, P413, DOI 10.1001/jama.285.4.413; LINDFORS ATB, 1992, ALLERGY, V47, P207, DOI 10.1111/j.1398-9995.1992.tb00652.x; Saarinen KM, 1999, J ALLERGY CLIN IMMUN, V104, P457, DOI 10.1016/S0091-6749(99)70393-3; Saarinen KM, 2000, CLIN EXP ALLERGY, V30, P400, DOI 10.1046/j.1365-2222.2000.00732.x; TAYLOR B, 1983, J EPIDEMIOL COMMUN H, V37, P95, DOI 10.1136/jech.37.2.95; WILLIAMS HC, 1994, BRIT MED J, V308, P1132; Wright AL, 1999, J ALLERGY CLIN IMMUN, V104, P589, DOI 10.1016/S0091-6749(99)70328-3; Ziegler A, 1998, BIOMETRICAL J, V40, P115, DOI 10.1002/(SICI)1521-4036(199806)40:2<115::AID-BIMJ115>3.0.CO;2-6	32	147	152	2	11	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	FEB	2002	32	2					205	209		10.1046/j.1365-2222.2002.01274.x		5	Allergy; Immunology	Allergy; Immunology	537PM	WOS:000174767800011	11929483	
J	Phipatanakul, W; Eggleston, PA; Wright, EC; Wood, RA				Phipatanakul, W; Eggleston, PA; Wright, EC; Wood, RA		Natl Cooperative Inner City Asthma	Mouse allergen. II. The relationship of mouse allergen exposure to mouse sensitization and asthma morbidity in inner-city children with asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						mouse allergen; indoor allergens; inner-city asthma; sensitization; asthma morbidity	DER-P-I; MITE; RISK; CHILDHOOD; CAT	Background: Although mouse allergen is known to cause occupational asthma in laboratory workers, its potential significance in home environments has never been studied. Objective: This study was designed to define the prevalence of mouse sensitivity and its relationship to mouse allergen exposure and disease activity in inner-city children with asthma, Methods: A subset Of 499 subjects from the National Cooperative Inner-City Asthma Study had dust samples adequate for mouse allergen analysis, as well as valid puncture skin test (PST) results, Data were analyzed to relate mouse allergen exposure and other risk factors to mouse sensitization and asthma morbidity, Results: Eighty-nine (18%) of the 499 children had a positive mouse skin test response, Children whose homes had mouse allergen levels above the median (1.60 mug/g) in the kitchen had a significantly higher rate of mouse sensitization (23% vs 11%, P = .007). Atopy was also significantly related to mouse sensitization, with 40% of those with more than 4 positive PST responses having mouse sensitivity compared with 4% of those with no other positive PST responses (P < .0001). When atopy and exposure were considered together, 53% of those with more than 4 positive PST responses and allergen levels above the median had a positive PST response to mouse allergen compared with 22% of those with more than 4 positive PST responses and allergen levels below the median (P < .0001). The relationship among mouse allergen exposure, sensitization, and any measures of asthma morbidity was not statistically significant, Conclusions: Mouse allergen may be an important indoor allergen in inner-city children with asthma, with exposure and atopy contributing to mouse sensitization.	Harvard Univ, Sch Med, Childrens Hosp, Dept Pediat,Div Allergy & Immunol, Boston, MA USA; Johns Hopkins Univ, Sch Med, Dept Pediat, Div Allergy & Immunol, Baltimore, MD USA; New England Res Inst, Watertown, MA 02172 USA; Albert Einstein Sch Med, Bronx, NY USA; Childrens Mem Hosp, Chicago, IL 60614 USA; Cook Cty Hosp, Chicago, IL 60612 USA; Rainbow Babies & Childrens Hosp, Cleveland, OH 44106 USA; Henry Ford Hosp, Detroit, MI 48202 USA; Wayne State Univ, Med Ctr, Detroit, MI 48202 USA; Mt Sinai Sch Med, New York, NY USA; Washington Univ, Sch Med, St Louis, MO USA; St Louis Univ, Sch Med, St Louis, MO USA; Howard Univ, Washington, DC 20059 USA; NIAID, Program Off, Bethesda, MD 20892 USA; Ctr Occupat Environm Hlth, Irvine, CA USA; New England Res Inst, Watertown, MA 02172 USA	Wood, RA (reprint author), Johns Hopkins Hosp, CMSC 1102,600 N Wolfe St, Baltimore, MD 21287 USA.				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J	Friedberg, MW; Schneider, EC; Rosenthal, MB; Volpp, KG; Werner, RM				Friedberg, Mark W.; Schneider, Eric C.; Rosenthal, Meredith B.; Volpp, Kevin G.; Werner, Rachel M.			Association Between Participation in a Multipayer Medical Home Intervention and Changes in Quality, Utilization, and Costs of Care	JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION			English	Article							LONGITUDINAL DATA-ANALYSIS; STRUCTURAL CAPABILITIES; TRANSFORMATION; EFFICIENCY; MODELS; TRIAL; WILL	IMPORTANCE Interventions to transform primary care practices into medical homes are increasingly common, but their effectiveness in improving quality and containing costs is unclear. OBJECTIVE To measure associations between participation in the Southeastern Pennsylvania Chronic Care Initiative, one of the earliest and largest multipayer medical home pilots conducted in the United States, and changes in the quality, utilization, and costs of care. DESIGN, SETTING, AND PARTICIPANTS Thirty-two volunteering primary care practices participated in the pilot (conducted from June 1, 2008, to May 31, 2011). We surveyed pilot practices to compare their structural capabilities at the pilot's beginning and end. Using claims data from 4 participating health plans, we compared changes (in each year, relative to before the intervention) in the quality, utilization, and costs of care delivered to 64 243 patients who were attributed to pilot practices and 55 959 patients attributed to 29 comparison practices (selected for size, specialty, and location similar to pilot practices) using a difference-in-differences design. EXPOSURES Pilot practices received disease registries and technical assistance and could earn bonus payments for achieving patient-centered medical home recognition by the National Committee for Quality Assurance (NCQA). MAIN OUTCOMES AND MEASURES Practice structural capabilities; performance on 11 quality measures for diabetes, asthma, and preventive care; utilization of hospital, emergency department, and ambulatory care; standardized costs of care. RESULTS Pilot practices successfully achieved NCQA recognition and adopted new structural capabilities such as registries to identify patients overdue for chronic disease services. Pilot participation was associated with statistically significantly greater performance improvement, relative to comparison practices, on 1 of 11 investigated quality measures: nephropathy screening in diabetes (adjusted performance of 82.7% vs 71.7% by year 3, P<.001). Pilot participation was not associated with statistically significant changes in utilization or costs of care. Pilot practices accumulated average bonuses of $92 000 per primary care physician during the 3-year intervention. CONCLUSIONS AND RELEVANCE A multipayer medical home pilot, in which participating practices adopted new structural capabilities and received NCQA certification, was associated with limited improvements in quality and was not associated with reductions in utilization of hospital, emergency department, or ambulatory care services or total costs over 3 years. These findings suggest that medical home interventions may need further refinement.	[Friedberg, Mark W.; Schneider, Eric C.] RAND Corp, Boston, MA USA; [Friedberg, Mark W.; Schneider, Eric C.] Brigham & Womens Hosp, Div Gen Internal Med, Boston, MA 02115 USA; [Friedberg, Mark W.; Schneider, Eric C.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA; [Schneider, Eric C.; Rosenthal, Meredith B.] Harvard Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA 02115 USA; [Volpp, Kevin G.; Werner, Rachel M.] Philadelphia VA Med Ctr, Ctr Hlth Equ Res & Promot, Philadelphia, PA USA; [Volpp, Kevin G.] Univ Penn, Perelman Sch Med, Ctr Hlth Incent & Behav Econ, Philadelphia, PA 19104 USA; [Volpp, Kevin G.; Werner, Rachel M.] Univ Penn, Div Gen Internal Med, Perelman Sch Med, Philadelphia, PA 19104 USA; [Volpp, Kevin G.] Wharton Business Sch, Dept Hlth Care Management, Philadelphia, PA USA; [Volpp, Kevin G.] Penn Med Ctr Hlth Care Innovat, Philadelphia, PA USA	Friedberg, MW (reprint author), 20 Pk Plaza,Ste 920, Boston, MA 02116 USA.	mfriedbe@rand.org		Rosenthal, Meredith/0000-0003-3410-0184; Schneider, Eric/0000-0002-1132-5084	Commonwealth Fund; Aetna	This study was sponsored by the Commonwealth Fund and Aetna.	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Am. Med. Assoc.	FEB 26	2014	311	8					815	825		10.1001/jama.2014.353		11	Medicine, General & Internal	General & Internal Medicine	AB4XQ	WOS:000331793700021	24570245	
J	Pulendran, B; Artis, D				Pulendran, Bali; Artis, David			New Paradigms in Type 2 Immunity	SCIENCE			English	Review							T-HELPER-CELL; THYMIC STROMAL LYMPHOPOIETIN; ANTIGEN-PRESENTING CELLS; DUST MITE ALLERGEN; RESPONSES IN-VIVO; DENDRITIC CELLS; EPITHELIAL-CELLS; INNATE IMMUNITY; IL-4 PRODUCTION; LYMPHOID-CELLS	Nearly half of the world's population harbors helminth infections or suffers from allergic disorders. A common feature of this population is the so-called "type 2 immune response," which confers protection against helminths, but also promotes pathologic responses associated with allergic inflammation. However, the mechanisms that initiate and control type 2 responses remain enigmatic. Recent advances have revealed a role for the innate immune system in orchestrating type 2 responses against a bewildering array of stimuli, from nanometer-sized allergens to 20-meter-long helminth parasites. Here, we review these advances and suggest that the human immune system has evolved multiple mechanisms of sensing such stimuli, from recognition of molecular patterns via innate immune receptors to detecting metabolic changes and tissue damage caused by these stimuli.	[Pulendran, Bali] Yerkes Natl Primate Res Ctr, Emory Vaccine Ctr, Dept Pathol, Atlanta, GA 30329 USA; [Artis, David] Univ Penn, Perelman Sch Med, Dept Microbiol, Philadelphia, PA 19104 USA; [Artis, David] Univ Penn, Perelman Sch Med, Inst Immunol, Philadelphia, PA 19104 USA	Pulendran, B (reprint author), Yerkes Natl Primate Res Ctr, Emory Vaccine Ctr, Dept Pathol, 954 Gatewood Rd, Atlanta, GA 30329 USA.	bpulend@emory.edu; dartis@mail.med.upenn.edu			NIH [U19AI090023, HHSN266200700006C, U54AI057157, R37AI48638, R37DK057665, U19AI057266, N01 AI50025, AI061570, AI087990, AI074878, AI083480, AI095466, AI095608]; Bill and Melinda Gates Foundation; Burroughs Wellcome Fund in Pathogenesis of Infectious Disease Award	Research in the Pulendran lab is supported by the NIH (grants U19AI090023, HHSN266200700006C, U54AI057157, R37AI48638, R37DK057665, U19AI057266, and N01 AI50025 to B.P.) and the Bill and Melinda Gates Foundation. Research in the Artis lab is supported by the NIH (grants AI061570, AI087990, AI074878, AI083480, AI095466, and AI095608 to D.A.) and the Burroughs Wellcome Fund Investigator in Pathogenesis of Infectious Disease Award (D.A.). We sincerely apologize to our colleagues that, owing to limitations of space, we were unable to cite many relevant references.	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J	Nordling, E; Berglind, N; Melen, E; Emenius, G; Hallberg, J; Nyberg, F; Pershagen, G; Svartengren, M; Wickman, M; Bellander, T				Nordling, Emma; Berglind, Niklas; Melen, Erik; Emenius, Gunnel; Hallberg, Jenny; Nyberg, Fredrik; Pershagen, Goeran; Svartengren, Magnus; Wickman, Magnus; Bellander, Tom			Traffic-related air pollution and childhood respiratory symptoms, function and allergies	EPIDEMIOLOGY			English	Article							LONG-TERM EXPOSURE; LUNG-FUNCTION GROWTH; 3 EUROPEAN AREAS; NITROGEN-DIOXIDE; PULMONARY-FUNCTION; BIRTH COHORT; CHILDREN; HEALTH; ASTHMA; SCHOOLCHILDREN	Background: Urban air pollution can trigger asthma symptoms in children, but there is conflicting evidence on effects of long-term exposure on lung function, onset of airway disease and allergic sensitization. Methods: The spatial distribution of nitrogen oxides from traffic (traffic-NOx) and inhalable particulate matter from traffic (traffic-PM10) in the study area was assessed with emission databases and dispersion modeling. Estimated levels were used to assign first-year exposure levels for children in a prospective birth cohort (n = 4089), by linking to geocoded home addresses. Parents in 4 Swedish municipalities provided questionnaire data on symptoms and exposures when the children were 2 months and 1, 2, and 4-year-old. At 4 years, 73% of the children underwent clinical examination including peak expiratory flow and specific IgE measurements. Results: Exposure to air pollution from traffic during the first year of life was associated with an excess risk of persistent wheezing (odds ratio [OR] for 44 mu g/m(3) [5th-95th percentile] difference in traffic-NO, = 1.60; 95% confidence interval [Cl] = 1.09-2.36). Similar results were found for sensitization (measured as specific IgE) to inhalant allergens, especially pollen (OR for traffic-NO, = 1.67; 95% CI = 1.10-2.53), at the age of 4 years. Traffic-related air pollution exposure during the first year of life was also associated with lower lung function at 4 years of age. Results were similar using traffic-NOx and traffic-PM10 as indicators. Conclusions: Exposure to moderate levels of locally emitted air pollution from traffic early in life appears to influence the development of airway disease and sensitization in preschool children.	[Bellander, Tom] Karolinska Hosp, Stockholm Cty Council, Dept Environm & Occupat Hlth, SE-17176 Stockholm, Sweden; [Berglind, Niklas; Melen, Erik; Nyberg, Fredrik; Pershagen, Goeran; Wickman, Magnus; Bellander, Tom] Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; [Melen, Erik; Hallberg, Jenny; Wickman, Magnus] Karolinska Inst, Ctr Allergy Res, Stockholm, Sweden; [Melen, Erik] Karolinska Univ Hosp, Astrid Lindgren Childrens Hosp, Stockholm, Sweden; [Hallberg, Jenny; Svartengren, Magnus] Karolinska Inst, Dept Publ Hlth Sci, Stockholm, Sweden; [Nyberg, Fredrik] AstraZeneca R&D, Molndal, Sweden	Bellander, T (reprint author), Karolinska Hosp, Stockholm Cty Council, Dept Environm & Occupat Hlth, Norrbacka 3rd Floor, SE-17176 Stockholm, Sweden.	tom.bellander@sll.se					Baldi I, 1999, EUR RESPIR J, V14, P132, DOI 10.1034/j.1399-3003.1999.14a22.x; Bellander T, 2001, ENVIRON HEALTH PERSP, V109, P633, DOI 10.2307/3455039; Boezen HM, 1999, LANCET, V353, P874, DOI 10.1016/S0140-6736(98)06311-9; Brauer M, 2002, AM J RESP CRIT CARE, V166, P1092, DOI 10.1164/rccm.200108-007OC; BraunFahrlander C, 1997, AM J RESP CRIT CARE, V155, P1042; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; DOCKERY DW, 1989, AM REV RESPIR DIS, V139, P587; Emenius G, 2003, OCCUP ENVIRON MED, V60, P876, DOI 10.1136/oem.60.11.876; Franze T, 2005, ENVIRON SCI TECHNOL, V39, P1673, DOI 10.1021/es0488737; Gauderman WJ, 2004, NEW ENGL J MED, V351, P1057, DOI 10.1056/NEJMoa040610; Gidhagen L, 2004, ATMOS ENVIRON, V38, P2029, DOI 10.1016/j.atmosenv.2004.02.014; Hallberg J, 2006, ACTA PAEDIATR, V95, P1191, DOI 10.1080/08035250600584794; Hoek G, 2002, ATMOS ENVIRON, V36, P4077, DOI 10.1016/S1352-2310(02)00297-2; Horak F, 2002, EUR RESPIR J, V19, P838, DOI 10.1183/09031936.02.00512001; Janssen NAH, 2003, ENVIRON HEALTH PERSP, V111, P1512, DOI 10.1289/ehp.6243; Jedrychowski W, 1999, ENVIRON HEALTH PERSP, V107, P669, DOI 10.2307/3434460; JOHANSSON C, 1999, PUBLICATION, V41; Kramer U, 2000, EPIDEMIOLOGY, V11, P64, DOI 10.1097/00001648-200001000-00014; Lannero E, 2002, PEDIATR ALLERGY IMMU, V13, P182, DOI 10.1034/j.1399-3038.2002.01055.x; LANTMATERIVERKE, 1996, IATORT 2000; Lewne M, 2004, SCI TOTAL ENVIRON, V332, P217, DOI 10.1016/j.scitotenv.2004.04.014; Llewellin P, 2002, RESPIROLOGY, V7, P333, DOI 10.1046/j.1440-1843.2002.00417.x; Magnus P, 1998, INT J EPIDEMIOL, V27, P995, DOI 10.1093/ije/27.6.995; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; McConnell R, 2006, ENVIRON HEALTH PERSP, V114, P766, DOI 10.1289/ehp.8594; Melen E, 2004, CLIN EXP ALLERGY, V34, P839, DOI 10.1111/j.1365-2222.2004.01957.x; Miyabara Y, 1998, INT ARCH ALLERGY IMM, V116, P124, DOI 10.1159/000023935; Morgenstern V, 2007, OCCUP ENVIRON MED, V64, P8, DOI 10.1136/oem.2006.028241; Motta AC, 2006, INT ARCH ALLERGY IMM, V139, P294, DOI 10.1159/000091600; *NAT, 2005, 5519 SWED ENV PROT A; NEAS LM, 1991, AM J EPIDEMIOL, V134, P204; Penard-Morand C, 2005, CLIN EXP ALLERGY, V35, P1279, DOI 10.1111/j.1365-2222.2005.02336.x; Pershagen G, 1995, INT J EPIDEMIOL, V24, P1147, DOI 10.1093/ije/24.6.1147; Raizenne M, 1996, ENVIRON HEALTH PERSP, V104, P506, DOI 10.2307/3432991; Rosenlund M, 2006, EPIDEMIOLOGY, V17, P383, DOI 10.1097/01.ede.0000219722.25569.0f; Schildcrout JS, 2006, AM J EPIDEMIOL, V164, P505, DOI 10.1093/aje/kwj225; SCHWARTZ J, 1989, ENVIRON RES, V50, P309, DOI 10.1016/S0013-9351(89)80012-X; Shima M, 2003, J EPIDEMIOL, V13, P108; *SLB AN, 2007, AIR STOCKH ANN REP 2; Sydbom A, 2001, EUR RESPIR J, V17, P733, DOI 10.1183/09031936.01.17407330; Takano H, 1997, AM J RESP CRIT CARE, V156, P36; 1989, OCCUPATIONS POPULATI	42	146	150	5	41	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	1044-3983			EPIDEMIOLOGY	Epidemiology	MAY	2008	19	3					401	408		10.1097/EDE.0b013e31816alce3		8	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	293DF	WOS:000255314400010	18379426	
J	Williams, H; Flohr, C				Williams, Hywel; Flohr, Carsten			How epidemiology has challenged 3 prevailing concepts about atopic dermatitis	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						atopy; atopic march; eczema; hygiene	ECZEMA; SENSITIZATION; CHILDREN; ALLERGY; ASTHMA; ASSOCIATION; PREVALENCE; DISEASES; SCHOOLCHILDREN; RHINITIS	We challenge 3 prevailing concepts in understanding atopic dermatitis using data from epidemiologic studies. First, we show that although atopy is associated with atopic dermatitis to some degree, its importance is not likely to be a simple cause-and-effect relationship, especially at a population level. Our epidemiologic data do not exclude a contributory role for IgE-mediated immunologic processes, especially in those with existing and severe disease. Second, evidence is presented that does not support a straightforward inverse relationship between infections and atopic dermatitis risk. A link, if present, is likely to be more complex, depending critically on the timing and type of infectious exposure. Third, recent evidence suggests that the risk of subsequent childhood asthma is not increased in children with early atopic dermatitis who are not also early wheezers, suggesting a comanifestation of phenotypes rather than a progressive atopic march. Collectively, these observations underline the importance of epidemiologic studies conducted at a population level to gain a more balanced understanding of the enigma of atopic dermatitis.	Univ Nottingham, Ctr Evidence Based Dermatol, Nottingham NG7 2NR, England	Williams, H (reprint author), Univ Nottingham, Ctr Evidence Based Dermatol, Kings Meadow Campus,Room A103,Lenton Lane, Nottingham NG7 2NR, England.	hywel.williams@nottingham.ac.uk					Arshad SH, 2002, CLIN EXP ALLERGY, V32, P843, DOI 10.1046/j.1365-2222.2002.01378.x; Bergmann RL, 1998, CLIN EXP ALLERGY, V28, P965; BIEBER T, 2005, J ALLERGY CLIN IMMUN, V117, P378; Bjorksten B, 2001, J ALLERGY CLIN IMMUN, V108, P516; Boguniewicz M, 2006, J ALLERGY CLIN IMMUN, V117, pS475, DOI 10.1016/j.jaci.2005.10.018; Chatila TA, 2005, J ALLERGY CLIN IMMUN, V116, P949, DOI 10.1016/j.jaci.2005.08.047; Cookson W, 2004, NAT REV IMMUNOL, V4, P978, DOI 10.1038/nri1500; Cooper PJ, 2004, PARASITE IMMUNOL, V26, P455, DOI 10.1111/j.0141-9838.2004.00728.x; Flohr C, 2005, Br J Dermatol, V152, P202, DOI 10.1111/j.1365-2133.2004.06436.x; Flohr C, 2004, J ALLERGY CLIN IMMUN, V114, P150, DOI 10.1016/j.jaci.2004.04.027; FLOHR C, 2005, J ALLERGY CLIN IMMUN, V117, P378; HATTEVIG G, 1987, ACTA PAEDIATR SCAND, V76, P349, DOI 10.1111/j.1651-2227.1987.tb10473.x; Hesselmar B, 2001, PEDIATR ALLERGY IMMU, V12, P208, DOI 10.1034/j.1399-3038.2001.012004208.x; Illi S, 2004, J ALLERGY CLIN IMMUN, V113, P925, DOI 10.1016/j.jaci.2004.01.778; Johansson SGO, 2004, J ALLERGY CLIN IMMUN, V113, P832, DOI 10.1016/j.jaci.2003.12.591; Leung DYM, 2003, LANCET, V361, P151, DOI 10.1016/S0140-6736(03)12193-9; LEUNG R, 1994, THORAX, V49, P1205, DOI 10.1136/thx.49.12.1205; Mohrenschlager M, 2006, BRIT J DERMATOL, V154, P505, DOI 10.1111/j.1365-2133.2005.07042.x; Mortz CG, 2003, ACTA DERM-VENEREOL, V83, P194, DOI 10.1080/00015550310007201; Novak N, 2003, J ALLERGY CLIN IMMUN, V112, P252, DOI 10.1067/mai.2003.1595; Palmer CNA, 2006, NAT GENET, V38, P441, DOI 10.1038/ng1767; Perkin MR, 2004, PEDIATR ALLERGY IMMU, V15, P221, DOI 10.1111/j.1399-3038.2004.00160.x; Ring J, 2001, J AM ACAD DERMATOL, V45, P49; Ronmark E, 2003, PEDIATR ALLERGY IMMU, V14, P91, DOI 10.1034/j.1399-3038.2003.00042.x; Schafer T, 2000, BRIT J DERMATOL, V143, P992, DOI 10.1046/j.1365-2133.2000.03832.x; Schafer T, 1999, J ALLERGY CLIN IMMUN, V104, P1280, DOI 10.1016/S0091-6749(99)70025-4; Sicherer SH, 2005, J ALLERGY CLIN IMMUN, V116, P153, DOI 10.1016/j.jaci.2005.03.017; Soto-Quiros ME, 2002, PEDIATR PULM, V33, P237, DOI 10.1002/ppul.10070; Spergel Jonathan M., 2003, Journal of Allergy and Clinical Immunology, V112, pS118, DOI 10.1016/j.jaci.2003.09.033; STRACHAN DP, 1989, BRIT MED J, V299, P1259; STRACHAN DP, 2000, ATOPIC DERMATITIS EP, P221, DOI 10.1017/CBO9780511545771.019; Warner JO, 2001, J ALLERGY CLIN IMMUN, V108, P929, DOI 10.1067/mai.2001.120015; Williams HC, 2005, J ALLERGY CLIN IMMUN, V116, P1064, DOI 10.1016/j.jaci.2005.08.026; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P383, DOI 10.1111/j.1365-2133.1994.tb08530.x; Williams HC, 2000, ATOPIC DERMATITIS EP, P41, DOI 10.1017/CBO9780511545771.005; Williams HC, 2000, ATOPIC DERMATITIS EP, V1st, P3, DOI 10.1017/CBO9780511545771.003; WILLIAMS HC, 2006, IN PRESS ARCH DERMAT; Yemaneberhan H, 2004, CLIN EXP ALLERGY, V34, P779, DOI 10.1111/j.1365-2222.2004.01946.x	38	146	156	1	9	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUL	2006	118	1					209	213		10.1016/j.jaci.2006.04.043		5	Allergy; Immunology	Allergy; Immunology	065UH	WOS:000239184800025	16815157	
J	Ono, SJ; Nakamura, T; Miyazaki, D; Ohbayashi, M; Dawson, M; Toda, M				Ono, SJ; Nakamura, T; Miyazaki, D; Ohbayashi, M; Dawson, M; Toda, M			Chemokines: Roles in leukocyte development, trafficking, and effector function	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						chemokines; receptors; allergy; asthma; signal transduction	HUMAN MAST-CELLS; MACROPHAGE INFLAMMATORY PROTEIN-1-ALPHA; EOTAXIN RECEPTOR CCR3; CD4(+) T-CELLS; FC-EPSILON-RI; LATE-PHASE; DENDRITIC CELLS; IN-VIVO; ALLERGIC CONJUNCTIVITIS; NEUTROPHIL MIGRATION	Chemokines, representing a large superfamily of 8- to 15-kd proteins, were originally discovered through their ability to recruit various cell types into sites of inflammation. It is now clear that these molecules play a much wider role in immune homeostasis, playing key roles in driving the maturation, homing, and activation of leukocytes. In this review we analyze the roles chemokines play in the development, recruitment, and activation of leukocytes. Because signaling from the receptors drives these processes, signal transduction from chemokine receptors will also be reviewed. Taken together, we highlight the various points at which chemokines contribute to allergic inflammation and at which their targeting might contribute to new therapies for type I hypersensitivity reactions.	UCL, Univ London, Inst Ophthalmol, Dept Immunol, London EC1V 9EL, England; UCL, Univ London, Inst Child Hlth, Dept Immunol, London EC1V 9EL, England; Moorfields Eye Hosp, London, England	Ono, SJ (reprint author), UCL, Univ London, Inst Ophthalmol, Dept Immunol, 11-43 Bath St, London EC1V 9EL, England.						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Allergy Clin. Immunol.	JUN	2003	111	6					1185	1199		10.1067/mai.2003.1594		15	Allergy; Immunology	Allergy; Immunology	688FZ	WOS:000183424700002	12789214	
J	Reed, CE; Milton, DK				Reed, CE; Milton, DK			Endotoxin-stimulated innate immunity: A contributing factor for asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						airway inflammation; asthma; cell biology; chronic obstructive pulmonary disease; endotoxin; eosinophils; environmental exposure neutrophils; tolerance	TUMOR-NECROSIS-FACTOR; ACUTE LUNG INJURY; NF-KAPPA-B; CAUSES BRONCHIAL HYPERRESPONSIVENESS; RESOLUTION COMPUTED-TOMOGRAPHY; DOSE-RESPONSE RELATIONSHIPS; PLATELET-ACTIVATING-FACTOR; PROTEIN-TYROSINE KINASE; COTTON TEXTILE WORKERS; TNF-ALPHA PRODUCTION	Exposure to airborne endotoxin in infancy may protect against asthma by promoting enhanced T(H)1 response and tolerance to allergens. On the other hand, later in life, it adversely affects patients with asthma. Endotoxin binding to receptors on macrophages and other cells generates IL-12, which inhibits IgE responses. It also generates cytokines like IL-1, TNF-alpha, and IL-8, which cause inflammation. These signal transduction pathways resemble those leading to the generation of cytokines, such as IL-4, IL-13, and IL-5, which are responsible for the inflammation of IgE-mediated allergic disease. The main difference seems to be that endotoxin recruits neutrophils, but IgE recruits eosinophils, and the details of the tissue injury from these granulocytes differ. Sources of airborne endotoxin include many agricultural dusts, aerosols from contaminated water in many industrial plants, contaminated heating and air-conditioning systems, mist-generating humidifiers, and damp or water-damaged homes. Acute inhalation of high concentrations of endotoxin can cause fever, cough, and dyspnea. Chronic inhalation of lesser amounts causes chronic bronchitis and emphysema and is associated with airway hyperresponsiveness. Airborne endotoxin adversely affects patients with asthma in 3 ways: (1) by increasing the severity of the airway inflammation; (2) by increasing the susceptibility to rhinovirus-induced colds; and (3) by causing chronic bronchitis and emphysema with development of irreversible airway obstruction after chronic exposure of adults. The most effective management is mitigating exposure. The potential of drug treatments requires further clinical investigation.	Mayo Clin, Allerg Dis Res Lab, Rochester, MN USA; Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA	Reed, CE (reprint author), POB 158, Boulder Jct, WI 54512 USA.		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Allergy Clin. Immunol.	AUG	2001	108	2					157	166		10.1067/mai.2001.116862		10	Allergy; Immunology	Allergy; Immunology	465HY	WOS:000170584600001	11496229	
J	Bernard, SM; Samet, JM; Grambsch, A; Ebi, KL; Romieu, I				Bernard, SM; Samet, JM; Grambsch, A; Ebi, KL; Romieu, I			The potential impacts of climate variability and change on air pollution-related health effects in the United States	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; climate change; criteria air pollutants; global warming; ozone; particulate matter	SOUTHERN CALIFORNIA COMMUNITIES; OBSTRUCTIVE PULMONARY-DISEASE; 0.12 PPM OZONE; HOSPITAL ADMISSIONS; NITROGEN-DIOXIDE; RESPIRATORY MORBIDITY; EXERCISING CHILDREN; CHRONIC EXPOSURE; DIFFERING LEVELS; UCLA POPULATION	Climate change may affect exposures to air pollutants by affecting weather, anthropogenic emissions, and biogenic emissions and by changing the distribution and types of airborne allergens. Local temperature, precipitation, clouds, atmospheric water vapor. wind speed, and wind direction influence atmospheric chemical processes, and interactions occur between local and global-scale environments. If the climate becomes warmer and more variable, air quality is likely to be affected. However, the specific types of change (i.e., local, regional, or global), the direction of change in a particular location (i.e., positive or negative), and the magnitude of change in air quality that may be attributable to climate change are a matter of speculation, based on extrapolating present understanding to future scenarios. There is already extensive evidence on the health effects of air pollution. Ground-level ozone can exacerbate chronic respiratory diseases and cause short-term reductions in lung function. Exposure to particulate matter can aggravate chronic respiratory and cardiovascular diseases, alter host defenses, damage lung tissue, lead to premature death, and possibly contribute to cancer. Health effects of exposures to carbon monoxide, sulfur dioxide, and nitrogen dioxide can include reduced work capacity, aggravation of existing cardiovascular diseases, effects on pulmonary function, respiratory illnesses, lung irritation, and alterations in the lung's defense systems. Adaptations to climate change should include ensuring responsiveness of air quality protection programs to changing pollution levels. Research needs include basic atmospheric science work on the association between weather and air pollutants; improving air pollution models and their linkage with climate change scenarios; and closing gaps in the understanding of exposure patterns and health effects.	Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD 21205 USA; Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Epidemiol, Baltimore, MD USA; US EPA, Off Res & Dev, Washington, DC 20460 USA; EPRI, Palo Alto, CA USA; US Ctr Dis Control & Prevent, Natl Ctr Environm Hlth, Atlanta, GA USA	Bernard, SM (reprint author), Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Environm Hlth Sci, 615 N Wolfe St,Room 7041, Baltimore, MD 21205 USA.						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J	Kool, M; Willart, MAM; van Nimwegen, M; Bergen, I; Pouliot, P; Virchow, JC; Rogers, N; Osorio, F; Reis e Sousa, C; Hammad, H; Lambrecht, BN				Kool, Mirjam; Willart, Monique A. M.; van Nimwegen, Menno; Bergen, Ingrid; Pouliot, Philippe; Virchow, J. Christian; Rogers, Neil; Osorio, Fabiola; Reis e Sousa, Caetano; Hammad, Hamida; Lambrecht, Bart N.			An Unexpected Role for Uric Acid as an Inducer of T Helper 2 Cell Immunity to Inhaled Antigens and Inflammatory Mediator of Allergic Asthma	IMMUNITY			English	Article							HOUSE-DUST MITE; INDUCED NEUTROPHIL ACTIVATION; MONOSODIUM URATE CRYSTALS; HELPER TYPE-2 RESPONSE; CD4(+) T-CELLS; DENDRITIC CELLS; AIRWAY INFLAMMATION; NALP3 INFLAMMASOME; XANTHINE-OXIDASE; ADAPTIVE IMMUNITY	Although deposition of uric acid (UA) crystals is known as the cause of gout, it is unclear whether UA plays a role in other inflammatory diseases. We here have shown that UA is released in the airways of allergen-challenged asthmatic patients and mice, where it was necessary for mounting T helper 2 (Th2) cell immunity, airway eosinophilia, and bronchial hyperreactivity to inhaled harmless proteins and clinically relevant house dust mite allergen. Conversely, administration of UA crystals together with protein antigen was sufficient to promote Th2 cell immunity and features of asthma. The adjuvant effects of UA did not require the inflammasome (NIrp3, Pycard) or the interleukin-1 (Myd88, IL-1r) axis. UA crystals promoted Th2 cell immunity by activating dendritic cells through spleen tyrosine kinase and PI3-kinase delta signaling. These findings provide further molecular insight into Th2 cell development and identify UA as an essential initiator and amplifier of allergic inflammation.	[Kool, Mirjam; Willart, Monique A. M.; Pouliot, Philippe; Lambrecht, Bart N.] Univ Ghent, Dept Resp Dis, Lab Immunoregulat & Mucosal Immunol, B-9000 Ghent, Belgium; [Hammad, Hamida] Univ Ghent, Dynam Imaging Unit, B-9000 Ghent, Belgium; [Kool, Mirjam; van Nimwegen, Menno; Bergen, Ingrid; Lambrecht, Bart N.] Erasmus Univ, Med Ctr, Dept Pulm Med, NL-3015 Rotterdam, Netherlands; [Kool, Mirjam] VIB, Dept Mol Biomed Res, B-9052 Ghent, Belgium; [Virchow, J. Christian] Univ Hosp Rostock, Dept Pulm Med, D-18057 Rostock, Germany; [Rogers, Neil; Osorio, Fabiola; Reis e Sousa, Caetano] Canc Res UK, Immunobiol Lab, London Res Inst, Lincolns Inn Fields Labs, London WC2A 3LY, England	Hammad, H (reprint author), Univ Ghent, Dept Resp Dis, Lab Immunoregulat & Mucosal Immunol, B-9000 Ghent, Belgium.	hamida.hammad@ugent.be; bartiambrecht@ugent.be	Osorio, Fabiola/H-4529-2014; Hammad, Hamida/J-9391-2015; Lambrecht, Bart/K-2484-2014	Osorio, Fabiola/0000-0001-5306-7856; Hammad, Hamida/0000-0003-3762-8603; Lambrecht, Bart/0000-0003-4376-6834; Reis e Sousa, Caetano/0000-0001-7392-2119	Marie-Curie Intereuropean Fellowship; Flemish Organization for Scientific Research (FWO); European Research Council; Ghent University; NIH [R21]	M.K. is a recipient of a Marie-Curie Intereuropean Fellowship. B.N.L. is a recipient of an Odysseus Grant of the Flemish Organization for Scientific Research (FWO), a European Research Council starting grant, a Concerted Research Initiative Grant (GOA) of Ghent University, and a Multidisciplinary Research Platform (MRP) Grant of Ghent University. H.H. and B.N.L. are the recipients of an NIH grant (R21) and a University of Ghent 4-year project grant. We thank B. Ryffel, B. Vanhaesebroeck, T. De Smedt, and J. Tschopp for provision of mice.	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J	Gibson, PG; McDonald, VM; Marks, GB				Gibson, Peter G.; McDonald, Vanessa M.; Marks, Guy B.			Asthma in older adults	LANCET			English	Review							OBSTRUCTIVE PULMONARY-DISEASE; RANDOMIZED CONTROLLED-TRIALS; AIR-FLOW OBSTRUCTION; DRY POWDER INHALERS; QUALITY-OF-CARE; SMOKING-CESSATION; ELDERLY-PATIENTS; GERIATRIC ASSESSMENT; COMORBID CONDITIONS; PRACTICE GUIDELINES	Asthma in older people is common and is characterised by underdiagnosis and undertreatment. Ageing is associated with unique issues that modify expression, recognition, and treatment of the disease. In particular, asthma and chronic obstructive pulmonary disease (COPD) both overlap and converge in older people. This concurrence, together with absence of precise diagnostic methods, makes diagnosis complex. A multidimensional assessment that addresses airway problems, comorbidities, risk factors, and management skills will draw attention to key needs for intervention. Increased attention to the complications of asthma and obstructive airway disease in older people is needed, specifically to develop effective systems of care, appropriate clinical practice guidelines, and a research agenda that delivers improved health outcomes.	[Gibson, Peter G.; McDonald, Vanessa M.; Marks, Guy B.] Univ Newcastle, Fac Hlth, Sch Med & Publ Hlth, Callaghan, NSW 2308, Australia; [McDonald, Vanessa M.] Univ Newcastle, Fac Hlth, Sch Nursing & Midwifery, Callaghan, NSW 2308, Australia; [Gibson, Peter G.; McDonald, Vanessa M.] John Hunter Hosp, Hunter Med Res Inst, Dept Resp & Sleep Med, New Lambton, NSW, Australia; [Gibson, Peter G.; Marks, Guy B.] Woolcock Inst Med Res, Sydney, NSW, Australia; [Marks, Guy B.] Liverpool Hosp, Dept Resp Med, Sydney, NSW, Australia; [Marks, Guy B.] Univ New S Wales, S Western Sydney Clin Sch, Sydney, NSW, Australia	Gibson, PG (reprint author), Univ Newcastle, Fac Hlth, Sch Med & Publ Hlth, Callaghan, NSW 2308, Australia.	peter.gibson@newcastle.edu.au			NHMRC; AstraZeneca; Boehringer Ingelheim; GlaxoSmithKline; Novartis; Pharmaxis; National Health and Medical Research Council (NHMRC) Centre for Respiratory and Sleep Medicine; Australian Department of Health and Ageing through the Australian Institute of Health and Welfare	PGG holds an NHMRC Practitioner Fellowship. He has participated in educational symposia funded by AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline and Novartis, and has participated in studies funded by Pharmaxis and GlaxoSmithKline. VMM is supported by the National Health and Medical Research Council (NHMRC) Centre for Respiratory and Sleep Medicine. She has also received honorariums for participation in educational meetings from AstraZeneca and Novartis. G BM is on an advisory board for Novartis and has given lectures at educational seminars sponsored by AstraZeneca and Boehringer Ingelheim. He has undertaken contract research for GlaxoSmithKline. The Australian Centre for Asthma Monitoring, of which he is Director, is funded by the Australian Department of Health and Ageing through the Australian Institute of Health and Welfare. He is the recipient of a Practitioner Fellowship from the Australian National Health and Medical Research Council.	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J	Katz, Y; Rajuan, N; Goldberg, MR; Eisenberg, E; Heyman, E; Cohen, A; Leshno, M				Katz, Yitzhak; Rajuan, Nelly; Goldberg, Michael R.; Eisenberg, Eli; Heyman, Eli; Cohen, Adi; Leshno, Moshe			Early exposure to cow's milk protein is protective against IgE-mediated cow's milk protein allergy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						IgE-mediated cow's milk allergy; soy allergy; breast-feeding; skin prick test; oral challenge	KOALA BIRTH COHORT; FOOD CHALLENGES; PEANUT ALLERGY; INFANTS; IMMEDIATE; CHILDREN; AGE; HYPERSENSITIVITY; CONSUMPTION; CHILDHOOD	Background: The diversity in the perceived prevalence, recovery, and risk factors for cow's milk allergy (CMA) necessitated a large-scale, population-based prospective study. Objective: We sought to determine the prevalence, cross-reactivity with soy allergy, and risk factors for the development of CMA. Methods: In a prospective study the feeding history of 13,019 infants was obtained by means of telephone interview (95.8%) or questionnaire (4.2%). Infants with probable adverse reactions to milk were examined, skin prick tested, and challenged orally. Results: Ninety-eight percent of the cohort participated in the study. The cumulative incidence for IgE-mediated CMA was 0.5% (66/13,019 patients). The mean age of cow's milk protein (CMP) introduction was significantly different (P<.001) between the healthy infants (61.6 +/- 92.5 days) and those with IgE-mediated CMA (116.1 +/- 64.9 days). Only 0.05% of the infants who were started on regular CMP formula within the first 14 days versus 1.75% who were started on formula between the ages of 105 and 194 days had IgE-mediated CMA (P<.001). The odds ratio was 19.3 (95% CI, 6.0-62.1) for development of IgE-mediated CMA among infants with exposure to CMP at the age of 15 days or more (P<.001). Sixty-four patients with IgE-mediated CMA tolerated soy, and none had a proved allergy to soy. Conclusions: IgE-mediated CMA is much less common than generally reported. Early exposure to CMP as a supplement to breast-feeding might promote tolerance. Finally, soy is a reasonable feeding alternative in patients with IgE-mediated CMA. (J Allergy Clin Immunol 2010;126:77-82.)	[Katz, Yitzhak; Goldberg, Michael R.; Cohen, Adi] Assaf Harofeh Med Ctr, Inst Allergy & Immunol, IL-70300 Zerifin, Israel; [Heyman, Eli] Assaf Harofeh Med Ctr, Dept Neonatol, IL-70300 Zerifin, Israel; [Katz, Yitzhak; Rajuan, Nelly] Tel Aviv Univ, Sackler Fac Med, Dept Pediat, IL-69978 Tel Aviv, Israel; [Eisenberg, Eli] Tel Aviv Univ, Raymond & Beverly Sackler Sch Phys & Astron, IL-69978 Tel Aviv, Israel; [Leshno, Moshe] Tel Aviv Univ, Fac Management, IL-69978 Tel Aviv, Israel	Katz, Y (reprint author), Assaf Harofeh Med Ctr, Inst Allergy & Immunol, IL-70300 Zerifin, Israel.	ykatz49@gmail.com	Eisenberg, Eli/D-2587-2009	Eisenberg, Eli/0000-0001-8681-3202	Israel Dairy Board	Supported by the Israel Dairy Board.	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Allergy Clin. Immunol.	JUL	2010	126	1					77	82		10.1016/j.jaci.2010.04.020		6	Allergy; Immunology	Allergy; Immunology	627SE	WOS:000280061800014	20541249	
J	Chen, G; Korfhagen, TR; Xu, Y; Kitzmiller, J; Wert, SE; Maeda, Y; Gregorieff, A; Clevers, H; Whitsett, JA				Chen, Gang; Korfhagen, Thomas R.; Xu, Yan; Kitzmiller, Joseph; Wert, Susan E.; Maeda, Yutaka; Gregorieff, Alexander; Clevers, Hans; Whitsett, Jeffrey A.			SPDEF is required for mouse pulmonary goblet cell differentiation and regulates a network of genes associated with mucus production	JOURNAL OF CLINICAL INVESTIGATION			English	Article							BRONCHIAL EPITHELIAL-CELLS; TRANSCRIPTION FACTOR; HUMAN AIRWAY; LUNG MORPHOGENESIS; MUCIN BIOSYNTHESIS; EXPRESSION; RECEPTOR; ASTHMA; GROWTH; IL-13	Various acute and chronic inflammatory stimuli increase the number and activity of pulmonary mucus-producing goblet cells, and goblet cell hyperplasia and excess mucus production are central to the pathogenesis of chronic pulmonary diseases. However, little is known about the transcriptional programs that regulate goblet cell differentiation. Here, we show that SAM-pointed domain-containing Ets-like factor (SPDEF) controls a transcriptional program critical for pulmonary goblet cell differentiation in mice. Initial cell-lineage-tracing analysis identified nonciliated secretory epithelial cells, known as Clara cells, as the progenitors of goblet cells induced by pulmonary allergen exposure in vivo. Furthermore, in vivo expression of SPDEF in Clara cells caused rapid and reversible goblet cell differentiation in the absence of cell proliferation. This was associated with enhanced expression of genes regulating goblet cell differentiation and protein glycosylation, including forkhead box A3 (Foxa3), anterior gradient 2 (Agr2), and glucosaminyl. (N-acetyl) transferase 3, mucin type (Gcnt3). Consistent with these findings, levels of SPDEF and FOXA3 were increased in mouse goblet cells after sensitization with pulmonary allergen, and the proteins were colocalized in goblet cells lining the airways of patients with chronic lung diseases. Deletion of the mouse Spdef gene resulted in the absence of goblet cells in tracheal/laryngeal submucosal glands and in the conducting airway epithelium after pulmonary allergen exposure in vivo. These data show that SPDEF plays a critical role in regulating a transcriptional network mediating the goblet cell differentiation and mucus hyperproduction associated with chronic pulmonary disorders.	[Chen, Gang; Korfhagen, Thomas R.; Xu, Yan; Kitzmiller, Joseph; Wert, Susan E.; Maeda, Yutaka; Whitsett, Jeffrey A.] Cincinnati Childrens Hosp, Med Ctr, Div Pulm Biol, Perinatal Inst, Cincinnati, OH 45229 USA; [Chen, Gang; Korfhagen, Thomas R.; Xu, Yan; Kitzmiller, Joseph; Wert, Susan E.; Maeda, Yutaka; Whitsett, Jeffrey A.] Univ Cincinnati, Sch Med, Cincinnati, OH USA; [Gregorieff, Alexander; Clevers, Hans] Netherlands Inst Dev Biol, Utrecht, Netherlands	Whitsett, JA (reprint author), Cincinnati Childrens Hosp, Med Ctr, Div Pulm Biol, Perinatal Inst, MLC 7029,3333 Burner Ave, Cincinnati, OH 45229 USA.	jeff.whitsett@cchmc.org			NIH [HL090156, HL095580]	The authors acknowledge support from Ann Maher for preparation of the manuscript; the Morphology Core in the Division of Pulmonary Biology at Cincinnati Children's Hospital Medical Center; Michael Mucenski, Michael Bruno, and Angela Keiser for technical support; and Johannes C.M. van der Loo, Punam Malik, and Anusha Sridharan for assistance with lentiviral vectors. Grant support was provided by the NIH to J.A. Whitsett (HL090156 and HL095580) and T.R. Korfhagen (HL095580).	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J	Brackbill, RM; Hadler, JL; DiGrande, L; Ekenga, CC; Farfel, MR; Friedman, S; Perlman, SE; Stellman, SD; Walker, DJ; Wu, D; Yu, SC; Thorpe, LE				Brackbill, Robert M.; Hadler, James L.; DiGrande, Laura; Ekenga, Christine C.; Farfel, Mark R.; Friedman, Stephen; Perlman, Sharon E.; Stellman, Steven D.; Walker, Deborah J.; Wu, David; Yu, Shengchao; Thorpe, Lorna E.			Asthma and Posttraumatic Stress Symptoms 5 to 6 Years Following Exposure to the World Trade Center Terrorist Attack	JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION			English	Article							NEW-YORK-CITY; CENTER HEALTH REGISTRY; DISASTER VICTIMS SPEAK; 11 SEPTEMBER 2001; PSYCHOMETRIC PROPERTIES; RESPIRATORY SYMPTOMS; RECOVERY WORKERS; PTSD CHECKLIST; RISK-FACTORS; CENTER SITE	Context The World Trade Center Health Registry provides a unique opportunity to examine long-term health effects of a large-scale disaster. Objective To examine risk factors for new asthma diagnoses and event-related post-traumatic stress (PTS) symptoms among exposed adults 5 to 6 years following exposure to the September 11, 2001, World Trade Center (WTC) terrorist attack. Design, Setting, and Participants Longitudinal cohort study with wave 1 (W1) enrollment of 71 437 adults in 2003-2004, including rescue/recovery worker, lower Manhattan resident, lower Manhattan office worker, and passersby eligibility groups; 46 322 adults (68%) completed the wave 2 (W2) survey in 2006-2007. Main Outcome Measures Self-reported diagnosed asthma following September 11; event-related current PTS symptoms indicative of probable posttraumatic stress disorder (PTSD), assessed using the PTSD Checklist (cutoff score >= 44). Results Of W2 participants with no stated asthma history, 10.2% (95% confidence interval [CI], 9.9%-10.5%) reported new asthma diagnoses postevent. Intense dust cloud exposure on September 11 was a major contributor to new asthma diagnoses for all eligibility groups: for example, 19.1% vs 9.6% in those without exposure among rescue/recovery workers (adjusted odds ratio, 1.5 [ 95% CI, 1.4-1.7]). Asthma risk was highest among rescue/recovery workers on the WTC pile on September 11 (20.5% [ 95% CI, 19.0%-22.0%]). Persistent risks included working longer at the WTC site, not evacuating homes, and experiencing a heavy layer of dust in home or office. Of participants with no PTSD history, 23.8% ( 95% CI, 23.4%-24.2%) reported PTS symptoms at either W1(14.3%) or W2 (19.1%). Nearly 10% ( 9.6% [ 95% CI, 9.3%-9.8%]) had PTS symptoms at both surveys, 4.7% ( 95% CI, 4.5%-4.9%) had PTS symptoms at W1 only, and 9.5% ( 95% CI, 9.3%-9.8%) had PTS symptoms at W2 only. At W2, passersby had the highest rate of PTS symptoms (23.2% [ 95% CI, 21.4%-25.0%]). Event-related loss of spouse or job was associated with PTS symptoms at W2. Conclusion Acute and prolonged exposures were both associated with a large burden of asthma and PTS symptoms 5 to 6 years after the September 11 WTC attack. JAMA. 2009;302(5):502-516 www.jama.com	[Hadler, James L.; DiGrande, Laura; Ekenga, Christine C.; Farfel, Mark R.; Friedman, Stephen; Perlman, Sharon E.; Stellman, Steven D.; Walker, Deborah J.; Wu, David; Yu, Shengchao; Thorpe, Lorna E.] New York City Dept Hlth & Mental Hyg, New York, NY 10013 USA; [Brackbill, Robert M.] Ctr Dis Control & Prevent, Agcy Tox Subst & Dis Registry, Atlanta, GA USA; [Stellman, Steven D.] Columbia Univ, Dept Epidemiol, Mailman Sch Publ Hlth, New York, NY USA	Thorpe, LE (reprint author), New York City Dept Hlth & Mental Hyg, 125 Worth St,Room 315, New York, NY 10013 USA.	lthorpe@health.nyc.gov			Agency for Toxic Substances and Disease Registry (ATSDR) of the Centers for Disease Control and Prevention (CDC) [U50/ATU272750]; National Center for Environmental Health (NCEH); New York City Department of Health and Mental Hygiene (NYCDOHMH)	This study was supported by Cooperative Agreement U50/ATU272750 from the Agency for Toxic Substances and Disease Registry (ATSDR) of the Centers for Disease Control and Prevention (CDC), which included support from the National Center for Environmental Health (NCEH), and by the New York City Department of Health and Mental Hygiene (NYCDOHMH).	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Am. Med. Assoc.	AUG 5	2009	302	5					502	516				15	Medicine, General & Internal	General & Internal Medicine	479DS	WOS:000268640500015	19654385	
J	Morgenstern, V; Zutavern, A; Cyrys, J; Brockow, I; Gehring, U; Koletzko, S; Bauer, CP; Reinhardt, D; Wichmann, HE; Heinrich, J				Morgenstern, V.; Zutavern, A.; Cyrys, J.; Brockow, I.; Gehring, U.; Koletzko, S.; Bauer, C. P.; Reinhardt, D.; Wichmann, H-Erich; Heinrich, J.			Respiratory health and individual estimated exposure to traffic-related air pollutants in a cohort of young children	OCCUPATIONAL AND ENVIRONMENTAL MEDICINE			English	Article							PARTICULATE MATTER; PRESCHOOL-CHILDREN; ATOPIC-DERMATITIS; NITROGEN-DIOXIDE; BIRTH COHORT; POLLUTION; ASTHMA; SYMPTOMS; ASSOCIATION; GIS	Objectives: To estimate long-term exposure to traffic-related air pollutants on an individual basis and to assess adverse health effects using a combination of air pollution measurement data, data from geographical information systems (GIS) and questionnaire data. Methods: 40 measurement sites in the city of Munich, Germany were selected at which to collect particulate matter with a 50% cut-off aerodynamic diameter of 2.5 mm (PM2.5) and to measure PM2.5 absorbance and nitrogen dioxide (NO2). A pool of GIS variables (information about street length, household and population density and land use) was collected for the Munich metropolitan area and was used in multiple linear regression models to predict traffic-related air pollutants. These models were also applied to the birth addresses of two birth cohorts (German Infant Nutritional Intervention Study (GINI) and Influence of Life-style factors on the development of the Immune System and Allergies in East and West Germany (LISA)) in the Munich metropolitan area. Associations between air pollution concentrations at birth address and 1-year and 2-year incidences of respiratory symptoms were analysed. Results: The following means for the estimated exposures to PM2.5, PM2.5 absorbance and NO2 were obtained: 12.8 mu g/m(3), 1.7 x 10(-5) m(-1) and 35.3 mu g/m(3), respectively. Adjusted odds ratios (ORs) for wheezing, cough without infection, dry cough at night, bronchial asthma, bronchitis and respiratory infections indicated positive associations with traffic-related air pollutants. After controlling for individual confounders, significant associations were found between the pollutant PM2.5 and sneezing, runny/stuffed nose during the first year of life (OR 1.16, 95% confidence interval 1.01 to 1.34) Similar effects were observed for the second year of life. These findings are similar to those from our previous analysis that were restricted to a subcohort in Munich city. The extended study also showed significant effects for sneezing, running/stuffed nose. Additionally, significant associations were found between NO2 and dry cough at night (or bronchitis) during the first year of life. The variable "living close to major roads'' (< 50 m), which was not analysed for the previous inner city cohort with birth addresses in the city of Munich, turned out to increase the risk of wheezing and asthmatic/spastic/obstructive bronchitis. Conclusions: Effects on asthma and hay fever are subject to confirmation at older ages, when these outcomes can be more validly assessed.	GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, D-85764 Neuherberg, Germany; Univ Munich, Inst Med Data Management Biometr & Epidemiol, Munich, Germany; Kinderklin & Kinderpoliklin Dr Haunerschen Kinder, Munich, Germany; Univ Augsburg, WZU, Ctr Environm Sci, D-8900 Augsburg, Germany; Tech Univ Munich, Kinderklin & Poliklin, D-8000 Munich, Germany; Univ Utrecht, Inst Risk Assessment Sci, Utrecht, Netherlands	Heinrich, J (reprint author), GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, Ingolstaedter Landstr 1, D-85764 Neuherberg, Germany.	joachim.heinrich@gsf.de	Mavoa, Suzanne/B-5372-2010; Cyrys, Josef/B-5359-2014; Wang, Linden/M-6617-2014	Cyrys, Josef/0000-0002-2105-8696; Gehring, Ulrike/0000-0003-3612-5780			Brauer M, 2003, EPIDEMIOLOGY, V14, P228, DOI 10.1097/00001648-200303000-00019; Brauer M, 2002, AM J RESP CRIT CARE, V166, P1092, DOI 10.1164/rccm.200108-007OC; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; BRAUNFAHRLANDER C, 1992, AM REV RESPIR DIS, V145, P42; Briggs DJ, 1997, INT J GEOGR INF SCI, V11, P699, DOI 10.1080/136588197242158; Briggs DJ, 2000, SCI TOTAL ENVIRON, V253, P151, DOI 10.1016/S0048-9697(00)00429-0; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; Ciccone G, 1998, OCCUP ENVIRON MED, V55, P771; Cyrys J, 2005, ENVIRON HEALTH PERSP, V113, P987, DOI 10.1289/ehp.7662; Cyrys J, 2003, J EXPO ANAL ENV EPID, V13, P134, DOI 10.1038/sj.jea.7500262; Cyrys J, 2000, SCI TOTAL ENVIRON, V250, P51, DOI 10.1016/S0048-9697(00)00361-2; Duhme H, 1996, EPIDEMIOLOGY, V7, P578, DOI 10.1097/00001648-199611000-00003; EDWARDS J, 1994, ARCH ENVIRON HEALTH, V49, P223; Gehring U, 2002, EUR RESPIR J, V19, P690, DOI 10.1183/09031936.02.01182001; Gordian ME, 2006, J EXPO SCI ENV EPID, V16, P49, DOI 10.1038/sj.jea.7500436; Han KS, 2004, REMOTE SENS ENVIRON, V92, P52, DOI 10.1016/j.rse.2004.05.005; Heinrich J, 2005, OCCUP ENVIRON MED, V62, P517, DOI 10.1136/oem.2004.016766; Hirsch T, 1999, EUR RESPIR J, V14, P669, DOI 10.1034/j.1399-3003.1999.14c29.x; Hochadel M, 2006, ATMOS ENVIRON, V40, P542, DOI 10.1016/j.atmosenv.2005.09.067; Hoek G, 2002, ATMOS ENVIRON, V36, P4077, DOI 10.1016/S1352-2310(02)00297-2; Hoek G, 2002, LANCET, V360, P1203, DOI 10.1016/S0140-6736(02)11280-3; Jerrett M, 2005, EPIDEMIOLOGY, V16, P727, DOI 10.1097/01.ede.0000181630.15826.7d; Kuehni CE, 2006, INT J EPIDEMIOL, V35, P779, DOI 10.1093/ije/dyl022; Kunzli N, 2000, LANCET, V356, P795, DOI 10.1016/S0140-6736(00)02653-2; *LAND MUNCH, 2006, STAT AMT; Laubereau B, 2004, J PEDIATR-US, V144, P602, DOI 10.1016/j.jpeds.2003.12.029; Livingstone AE, 1996, BRIT MED J, V312, P676; Masson V, 2003, J CLIMATE, V16, P1261, DOI 10.1175/1520-0442-16.9.1261; McConnell R, 2006, ENVIRON HEALTH PERSP, V114, P766, DOI 10.1289/ehp.8594; Monn C, 2001, ATMOS ENVIRON, V35, P1, DOI 10.1016/S1352-2310(00)00330-7; Oosterlee A, 1996, OCCUP ENVIRON MED, V53, P241; ROEMER W, 1993, AM REV RESPIR DIS, V147, P118; Schikowski T, 2005, RESP RES, V6, DOI 10.1186/1465-9921-6-152; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; Weiland SK, 2004, EUR RESPIR J, V24, P406, DOI 10.1183/09031936.04.00090303; WHO, 2005, WHO AIR QUAL GUID GL; Wilkinson P, 1999, THORAX, V54, P1070; WJST M, 1993, BRIT MED J, V307, P596; Zutavern A, 2006, PEDIATRICS, V117, P401, DOI 10.1542/peds.2004-2521	39	145	149	6	40	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	1351-0711			OCCUP ENVIRON MED	Occup. Environ. Med.	JAN	2007	64	1					8	16		10.1136/oem.2006.028241		9	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	119VT	WOS:000243043100006	16912084	
J	Cates, EC; Fattouh, R; Wattie, J; Inman, MD; Goncharova, S; Coyle, AJ; Gutierrez-Ramos, JC; Jordana, M				Cates, EC; Fattouh, R; Wattie, J; Inman, MD; Goncharova, S; Coyle, AJ; Gutierrez-Ramos, JC; Jordana, M			Intranasal exposure of mice to house dust mite elicits allergic airway inflammation via a GM-CSF-mediated mechanism	JOURNAL OF IMMUNOLOGY			English	Article							COLONY-STIMULATING FACTOR; EPITHELIAL-CELLS; INHALED ANTIGEN; T-CELL; SENSITIZED MICE; IGE RESPONSES; MODEL; HYPERRESPONSIVENESS; EOSINOPHILIA; OVALBUMIN	It is now well established that passive exposure to inhaled OVA leads to a state of immunological tolerance. Therefore, to elicit allergic sensitization, researchers have been compelled to devise alternative strategies, such as the systemic delivery of OVA in the context of powerful adjuvants, which are alien to the way humans are exposed and sensitized to allergens. The objectives of these studies were to investigate immune-inflammatory responses to intranasal delivery of a purified house dust mite (HDM) extract and to evaluate the role of GM-CSF in this process. HDM was delivered to BALB/c mice daily for 10 days. After the last exposure, mice were killed, bronchoalveolar lavage was performed, and samples were obtained. Expression/production of Th2-associated molecules in the lymph nodes, lung, and spleen were evaluated by real-time quantitative PCR and ELISA, respectively. Using this exposure protocol, exposure to HDM alone generated Th2 sensitization based on the expression/production of Th2 effector molecules and airway eosinophilic inflammation. Flow cytometric analysis demonstrated expansion and activation of APCs in the lung and an influx of activated Th2 effector cells. Moreover, this inflammation was accompanied by airways hyper-responsiveness and a robust memory-driven immune response. Finally, administration of anti-GM-CSF-neutralizing Abs markedly reduced immune-inflammatory responses in both lung and spleen. Thus, intranasal delivery of HDM results in Th2 sensitization and airway eosinophilic inflammation that appear to be mediated, at least in part, by endogenous GM-CSF production.	McMaster Univ, Dept Pathol & Mol Med, Ctr Gene Therapeut, Div Resp Dis & Allergy, W Hamilton, ON L8S 3Z5, Canada; St Josephs Healthcare, Firestone Inst Resp Hlth, Hamilton, ON, Canada; Millennium Pharmaceut, Cambridge, MA 02139 USA	Jordana, M (reprint author), McMaster Univ, Dept Pathol & Mol Med, Ctr Gene Therapeut, Div Resp Dis & Allergy, HSC-4H21,1200 Main St, W Hamilton, ON L8S 3Z5, Canada.	jordanam@mcmaster.ca					Asokananthan N, 2002, J IMMUNOL, V169, P4572; Duez C, 1996, EUR J IMMUNOL, V26, P1088, DOI 10.1002/eji.1830260520; Gajewska BU, 2001, J CLIN INVEST, V108, P577, DOI 10.1172/JCI12627; GORDON MY, 1987, NATURE, V326, P403, DOI 10.1038/326403a0; Herz U, 1998, J INVEST DERMATOL, V110, P224, DOI 10.1046/j.1523-1747.1998.00119.x; Hewitt CRA, 1998, ALLERGY, V53, P60; HOLT PG, 1981, IMMUNOLOGY, V42, P409; HOYNE GF, 1993, J EXP MED, V178, P1783, DOI 10.1084/jem.178.5.1783; Hoyne GF, 2000, AM J RESP CRIT CARE, V162, pS169; Hsiue TR, 1997, INT ARCH ALLERGY IMM, V112, P295; Inman MD, 1999, AM J RESP CELL MOL, V21, P473; King C, 1998, J IMMUNOL, V161, P3645; Lee YL, 2001, HUM GENE THER, V12, P2065, DOI 10.1089/10430340152677412; Leigh R, 2002, AM J RESP CELL MOL, V27, P526, DOI 10.1165/rcmb.2002-0048OC; Lohning M, 1998, P NATL ACAD SCI USA, V95, P6930, DOI 10.1073/pnas.95.12.6930; MCMENAMIN C, 1994, SCIENCE, V265, P1869, DOI 10.1126/science.7916481; Neeno T, 1996, J IMMUNOL, V156, P3191; OBrien RM, 1996, IMMUNOL CELL BIOL, V74, P174, DOI 10.1038/icb.1996.24; OBRIEN RM, 1992, J ALLERGY CLIN IMMUN, V89, P1021, DOI 10.1016/0091-6749(92)90225-Q; Ritz SA, 2002, AM J RESP CELL MOL, V27, P428, DOI 10.1165/rcmb.4824; Ritz SA, 2002, TRENDS IMMUNOL, V23, P396, DOI 10.1016/S1471-4906(02)02278-0; Seymour BWP, 1998, J EXP MED, V187, P721, DOI 10.1084/jem.187.5.721; Soumelis V, 2002, NAT IMMUNOL, V3, P673, DOI 10.1038/ni805; Stampfli MR, 1998, J CLIN INVEST, V102, P1704, DOI 10.1172/JCI4160; Sun G, 2001, J IMMUNOL, V167, P1014; Swirski FK, 2002, CLIN EXP ALLERGY, V32, P411, DOI 10.1046/j.1365-2222.2002.01291.x; Swirski FK, 2002, J IMMUNOL, V169, P3499; Tategaki A, 2002, INT ARCH ALLERGY IMM, V129, P204, DOI 10.1159/000066774; Tournoy KG, 2000, CLIN EXP ALLERGY, V30, P79; Volgyesi GA, 2000, J APPL PHYSIOL, V89, P413	30	145	153	0	12	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	NOV 15	2004	173	10					6384	6392				9	Immunology	Immunology	869QL	WOS:000224999000058	15528378	
J	Vander Leek, TK; Liu, AH; Stefanski, K; Blacker, B; Bock, SA				Vander Leek, TK; Liu, AH; Stefanski, K; Blacker, B; Bock, SA			The natural history of peanut allergy in young children and its association with serum peanut-specific IgE	JOURNAL OF PEDIATRICS			English	Article							COW MILK ALLERGY; FOOD CHALLENGES; CLINICAL COURSE; DOUBLE-BLIND; NUT ALLERGY; SKIN-TESTS; HYPERSENSITIVITY; ANAPHYLAXIS; ADOLESCENTS; INFANTS	Objectives: To observe the nature and frequency of adverse reactions caused by accidental peanut exposure in young children with clinical peanut hypersensitivity and to determine the value of serum peanut-specific IgE levels during follow-up. Study design: Eighty-three children with clinical peanut hypersensitivity diagnosed before their fourth birthdays were contacted yearly to track adverse peanut reactions. Serum peanut-specific IgE levels were determined in 51 of 83 subjects. Results: Fifty-eight percent (31/53) of subjects followed up for 5 years experienced adverse reactions from accidental peanut exposure, Regardless of the nature of their initial reaction, the majority with subsequent reactions (52%, 31/60) experienced potentially life-threatening symptoms. The group with isolated skin symptoms (11/51, 22%) had lower serum peanut-specific IgE levels than the group with respiratory and/or gastrointestinal symptoms (40/51, 78%) (median: 1.25 kU(A)/L vs 11.65 kU(A)/L, P = .004, Wilcoxon rank sums test). Despite this, there was no threshold level below which only skin symptoms appeared to occur. Four selected subjects had negative double-blind placebo-controlled food challenge responses to peanuts during follow-up. Conclusions: The majority of children with clinical peanut hypersensitivity followed up for 5 years will have adverse reactions from accidental peanut exposure. Symptoms experienced during subsequent adverse peanut reactions may not be consistent with symptoms reported during initial reactions. Therefore proper education regarding peanut avoidance land treatment of adverse reactions is necessary in all cases of clinical peanut hypersensitivity. Young children who are allergic to peanuts can lose clinical hypersensitivity.	Natl Jewish Med & Res Ctr, Dept Pediat, Denver, CO 80206 USA; Univ Colorado, Hlth Sci Ctr, Denver, CO USA	Bock, SA (reprint author), Natl Jewish Med & Res Ctr, Dept Pediat, 1400 Jackson St,Rm J211, Denver, CO 80206 USA.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	NCRR NIH HHS [M 01 RR00051]		BECK MS, 1990, MEAS SCI TECHNOL, V1, P561, DOI 10.1088/0957-0233/1/7/004; BISHOP JM, 1990, J PEDIATR-US, V116, P862, DOI 10.1016/S0022-3476(05)80641-9; BOCK SA, 1989, J ALLERGY CLIN IMMUN, V83, P900, DOI 10.1016/0091-6749(89)90103-6; BOCK SA, 1978, J ALLERGY CLIN IMMUN, V62, P327, DOI 10.1016/0091-6749(78)90132-X; BOCK SA, 1978, CLIN ALLERGY, V8, P559, DOI 10.1111/j.1365-2222.1978.tb01509.x; BOCK SA, 1988, J ALLERGY CLIN IMMUN, V82, P986; DANNAEUS A, 1981, CLIN ALLERGY, V11, P533, DOI 10.1111/j.1365-2222.1981.tb02171.x; Eigenmann PA, 1998, PEDIATR ALLERGY IMMU, V9, P186, DOI 10.1111/j.1399-3038.1998.tb00371.x; Ewan PW, 1996, BRIT MED J, V312, P1074; HOST A, 1990, ALLERGY, V45, P587, DOI 10.1111/j.1398-9995.1990.tb00944.x; Hourihane JO, 1996, BRIT MED J, V313, P518; Hourihane JO, 1997, CLIN EXP ALLERGY, V27, P634, DOI 10.1046/j.1365-2222.1997.d01-559.x; Hourihane JO, 1998, BRIT MED J, V316, P1271; KEMP SF, 1995, ARCH INTERN MED, V155, P1749, DOI 10.1001/archinte.155.16.1749; Pumphrey RSH, 1996, CLIN EXP ALLERGY, V26, P1364, DOI 10.1046/j.1365-2222.1996.d01-297.x; SAMPSON HA, 1984, J ALLERGY CLIN IMMUN, V74, P26, DOI 10.1016/0091-6749(84)90083-6; SAMPSON HA, 1985, J PEDIATR-US, V107, P669, DOI 10.1016/S0022-3476(85)80390-5; Sampson HA, 1997, J ALLERGY CLIN IMMUN, V100, P444; SAMPSON HA, 1992, NEW ENGL J MED, V327, P380, DOI 10.1056/NEJM199208063270603; Sicherer SH, 1999, J ALLERGY CLIN IMMUN, V103, P559, DOI 10.1016/S0091-6749(99)70224-1; Sicherer S.H., 1998, PEDIATRICS, V102, P6; Tariq SM, 1996, BRIT MED J, V313, P514; YUNGINGER JW, 1988, JAMA-J AM MED ASSOC, V260, P1450, DOI 10.1001/jama.260.10.1450	23	145	147	0	4	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0022-3476	1097-6833		J PEDIATR-US	J. Pediatr.	DEC	2000	137	6					749	755		10.1067/mpd.2000.109376		7	Pediatrics	Pediatrics	383HD	WOS:000165876300005	11113829	
J	Douwes, J; Zuidhof, A; Doekes, G; van der Zee, S; Wouters, I; Boezen, HM; Brunekreef, B				Douwes, J; Zuidhof, A; Doekes, G; van der Zee, S; Wouters, I; Boezen, HM; Brunekreef, B			(1 -> 3)-beta-D-glucan and endotoxin in house dust and peak flow variability in children	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							RESPIRATORY SYMPTOMS; HOME DAMPNESS; AIRWAYS INFLAMMATION; ASTHMATIC SYMPTOMS; CHILDHOOD ASTHMA; MITE ALLERGEN; EXPOSURE; HEALTH; MOLDS; ENVIRONMENTS	House dust-associated bacterial endotoxins have been shown to be associated with asthma severity, and a similar role has been suggested for fungal (1-->3)-beta-D-glucans. In this study the relation between these agents and peak expiratory flow (PEF) variability was investigated in 148 children 7 to 11 yr of age of whom 50% had self- or parent-reported chronic respiratory symptoms. All children self-monitored twice daily their PEF for a period of 16 wk. Dust samples were collected from mattresses and from living room and bedroom floors, and endotoxin and (1-->3)-beta-D-glucan were measured in dust extracts. The relations with mean daily PEF variability (Ampl%mean) were investigated by linear regression analysis, adjusting for dust mite allergen levels, presence of pets, and type of floor cover. In unadjusted analyses the levels of both endotoxin and (1-->3)-beta-D-glucan per square meter of living room floor were significantly associated with PEF-variability (but not when expressed per gram of sampled dust), particularly in atopic children with asthma symptoms. Adjusted analyses showed the same association for (1-->3)-beta-D-glucan but not for endotoxin. Although no associations were found with microbial agent levels in bedroom floor or mattress dust, high levels of (1-->3)-beta-D-glucan in living room floor dust apparently increase PEF variability in asthmatic children.	Univ Wageningen & Res Ctr, Environm & Occupat Hlth Grp, NL-6700 AE Wageningen, Netherlands; Univ Groningen, Dept Epidemiol, Groningen, Netherlands; Wellington Sch Med, Wellington Asthma Res Grp, Wellington, New Zealand	Doekes, G (reprint author), Univ Wageningen & Res Ctr, Environm & Occupat Hlth Grp, POB 238, NL-6700 AE Wageningen, Netherlands.			brunekreef, bert/0000-0001-9908-0060; Douwes, Jeroen/0000-0003-3599-4036			Andriessen JW, 1998, CLIN EXP ALLERGY, V28, P1191; *BIBLE, LEVITICUS, V14; BJORNSSON E, 1995, CLIN EXP ALLERGY, V25, P423, DOI 10.1111/j.1365-2222.1995.tb01073.x; BLACKLEY CH, 1873, HAY FEVER EXPT RES C; BRUNEKREEF B, 1989, AM REV RESPIR DIS, V140, P1363; CASTELLAN RM, 1987, NEW ENGL J MED, V317, P605, DOI 10.1056/NEJM198709033171005; COLOFF MJ, 1992, CLIN EXP ALLERGY   S, V22, P1; DALES RE, 1991, AM J EPIDEMIOL, V134, P196; Douwes J, 1999, J ALLERGY CLIN IMMUN, V103, P494, DOI 10.1016/S0091-6749(99)70476-8; DOUWES J, 1995, APPL ENVIRON MICROB, V61, P1763; Douwes J, 1996, APPL ENVIRON MICROB, V62, P3176; FLOYER SJ, 1726, TREATISE ASTHMA; FOGELMARK B, 1994, INT J EXP PATHOL, V75, P85; JAAKKOLA JJK, 1993, J EXPO ANAL ENV EPID, V3, P129; Jalaludin B, 1998, J ALLERGY CLIN IMMUN, V102, P382, DOI 10.1016/S0091-6749(98)70124-1; MICHEL O, 1991, CLIN EXP ALLERGY, V21, P441, DOI 10.1111/j.1365-2222.1991.tb01684.x; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; Milton DK, 1997, AM IND HYG ASSOC J, V58, P861; Peat JK, 1998, ALLERGY, V53, P120, DOI 10.1111/j.1398-9995.1998.tb03859.x; QUACKENBOSS JJ, 1991, AM REV RESPIR DIS, V143, P323; Rizzo MC, 1997, PEDIATR ALLERGY IMMU, V8, P121; ROEMER W, 1998, EUR RESPIR REV, V8, P4; Rylander R, 1997, MEDIAT INFLAMM, V6, P275, DOI 10.1080/09629359791613; SMID T, 1992, AM REV RESPIR DIS, V146, P1474; Stone BA, 1992, CHEM BIOL 1 3 BETA G; STRACHAN DP, 1989, J EPIDEMIOL COMMUN H, V43, P7, DOI 10.1136/jech.43.1.7; STRACHAN DP, 1990, THORAX, V45, P382, DOI 10.1136/thx.45.5.382; STRACHAN DP, 1988, BRIT MED J, V297, P1223; Thorn J, 1998, AM J IND MED, V33, P463; Thorn J, 1998, AM J RESP CRIT CARE, V157, P1798; Ulmer AJ, 1997, INT J OCCUP ENV HEAL, V3, pS8; VANSTRIEN RT, 1994, CLIN EXP ALLERGY, V24, P843; Verhoeff AP, 1997, ANN ALLERG ASTHMA IM, V78, P544; VERHOEFF AP, 1994, CLIN EXP ALLERGY, V24, P1061, DOI 10.1111/j.1365-2222.1994.tb02744.x; VERHOEFF AP, 1995, AM J EPIDEMIOL, V141, P103; WAEGEMAEKERS M, 1989, ALLERGY, V44, P192, DOI 10.1111/j.1398-9995.1989.tb02261.x; ZOCK JP, 1994, EUR RESPIR J, V7, P1254, DOI 10.1183/09031936.94.07071254; 1850, NATURE, V2, P199	38	145	146	2	6	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	OCT	2000	162	4					1348	1354				7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	364RD	WOS:000089905900027	11029343	
J	Kerstjens, HAM; Disse, B; Schroder-Babo, W; Bantje, TA; Gahlemann, M; Sigmund, R; Engel, M; van Noord, JA				Kerstjens, Huib A. M.; Disse, Bernd; Schroeder-Babo, Winfried; Bantje, Theo A.; Gahlemann, Martina; Sigmund, Ralf; Engel, Michael; van Noord, Jan A.			Tiotropium improves lung function in patients with severe uncontrolled asthma: A randomized controlled trial	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Asthma; severe uncontrolled asthma; randomized controlled trial; anticholinergics; tiotropium	OBSTRUCTIVE PULMONARY-DISEASE; COPD PATIENTS; BROMIDE; ADULTS; EFFICACY	Background: Some patients with severe asthma remain symptomatic and obstructed despite maximal recommended treatment. Tiotropium, a long-acting inhaled anticholinergic agent, might be an effective bronchodilator in such patients. Objective: We sought to compare the efficacy and safety of 2 doses of tiotropium (5 and 10 mu g daily) administered through the Respimat inhaler with placebo as add-on therapy in patients with uncontrolled severe asthma (Asthma Control Questionnaire score, >= 1.5; postbronchodilator FEV(1), <= 80% of predicted value) despite maintenance treatment with at least a high-dose inhaled corticosteroid plus a long-acting beta(2)-agonist. Methods: This was a randomized, double-blind, crossover study with three 8-week treatment periods. The primary end point was peak FEV(1) at the end of each treatment period. Results: Of 107 randomized patients (54% female patients; mean, 55 years of age; postbronchodilator FEV(1), 65% of predicted value), 100 completed all periods. Peak FEV(1) was significantly higher with 5 mu g (difference, 139 mL; 95% CI, 96181 mL) and 10 mu g (difference, 170 mL; 95% CI, 128-213 mL) of tiotropium than with placebo (both P < .0001). There was no significant difference between the active doses. Trough FEV(1) at the end of the dosing interval was higher with tiotropium (5 mg: 86 mL [95% CI, 41-132 mL]; 10 mg: 113 mL [95% CI, 67-159 mL]; both P < .0004). Daily home peak expiratory flow measurements were higher with both tiotropium doses. There were no significant differences in asthma-related health status or symptoms. Adverse events were balanced across groups except for dry mouth, which was more common on 10 mu g of tiotropium. Conclusion: The addition of once-daily tiotropium to asthma treatment, including a high-dose inhaled corticosteroid plus a long-acting beta(2)-agonist, significantly improves lung function over 24 hours in patients with inadequately controlled, severe, persistent asthma. (J Allergy Clin Immunol 2011;128:308-14.)	[Kerstjens, Huib A. M.] Univ Groningen, Dept Pulmonol, Univ Med Ctr Groningen, NL-9700 RB Groningen, Netherlands; [Disse, Bernd; Gahlemann, Martina; Sigmund, Ralf; Engel, Michael] Boehringer Ingelheim Pharma GmbH & Co KG, Biberach, Germany; [Schroeder-Babo, Winfried] Krankenhaus Gelnhausen, Gelnhausen, Germany; [Bantje, Theo A.] Amphia Ziekenhuis, Dept Pulmonol, Breda, Netherlands; [van Noord, Jan A.] Atrium Med Ctr, Dept Pulmonol, Heerlen, Netherlands	Kerstjens, HAM (reprint author), Univ Groningen, Dept Pulmonol, Univ Med Ctr Groningen, Postbox 30-001, NL-9700 RB Groningen, Netherlands.	h.a.m.kerstjens@long.umcg.nl			Boehringer Ingelheim; Pfizer; Chiesi; Novartis; GlaxoSmithKline	H. A. M. Kerstjens receives research support from Boehringer Ingelheim and Pfizer and has consulted with Boehringer Ingelheim. J. A. van Noord receives research support from Boehringer Ingelheim, Chiesi, Novartis, and GlaxoSmithKline. The rest of the authors have declared that they have no conflict of interest.	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Allergy Clin. Immunol.	AUG	2011	128	2					308	314		10.1016/j.jaci.2011.04.039		7	Allergy; Immunology	Allergy; Immunology	799IQ	WOS:000293280800009	21636120	
J	Fens, N; Zwinderman, AH; van der Schee, MP; de Nijs, SB; Dijkers, E; Roldaan, AC; Cheung, D; Bel, EH; Sterk, PJ				Fens, Niki; Zwinderman, Aeilko H.; van der Schee, Marc P.; de Nijs, Selma B.; Dijkers, Erica; Roldaan, Albert C.; Cheung, David; Bel, Elisabeth H.; Sterk, Peter J.			Exhaled Breath Profiling Enables Discrimination of Chronic Obstructive Pulmonary Disease and Asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						biomarkers; diagnosis; electronic nose; exhaled breath; volatile organic compounds	ELECTRONIC NOSE; LUNG-CANCER; SYSTEMIC INFLAMMATION; GLOBAL STRATEGY; COPD; AIR; SIMILARITIES; BIOMARKERS; PROTEOMICS; MECHANISMS	Rationale Chronic obstructive pulmonary disease (COPD) and asthma can exhibit overlapping clinical features. Exhaled air contains volatile organic compounds (VOCs) that may qualify as noninvasive biomarkers. VOC profiles can be assessed using integrative analysis by electronic nose, resulting in exhaled molecular fingerprints (breathprints). Objectives: We hypothesized that breathprints by electronic nose can discriminate patients with COPD and asthma. Methods: Ninety subjects participated in a cross-sectional study: 30 patients with COPD (age, 61.6+/-9.3 years; FEV1, 1.72+/-0.69 L), 20 patients with asthma (age, 35.4+/-15.1 years; FEV1, 3.32+/-0.86 L), 20 nonsmoking control subjects (age, 56.7+/-9.3 years; FEV1, 3.44+/-0.76 L), and 20 smoking control subjects (age, 56.1+/-5.9 years; FEV1, 3.58+/-0.78). After 5 minutes of tidal breathing through an inspiratory VOC filter, an expiratory vital capacity was collected in a Tedlar bag and sampled by electronic nose. Breathprints were analyzed by discriminant analysis on principal component reduction resulting in cross-validated accuracy values (accuracy). Repeatability and reproducibility were assessed by measuring samples in duplicate by two devices. Measurements and Main Results: Breathprints from patients with asthma were separated from patients with COPD (accuracy 96%; P < 0.001), from nonsmoking control subjects (accuracy, 95%; P < 0.001), and from smoking control subjects (accuracy, 92.5%; P < 0.001). Exhaled breath profiles of patients with COPD partially overlapped with those of asymptomatic smokers (accuracy, 66%; P = 0.006). Measurements were repeatable and reproducible. Conclusions: Molecular profiling of exhaled air can distinguish patients with COPD and asthma and control subjects. Our data demonstrate a potential of electronic noses in the differential diagnosis of obstructive airway diseases and in the risk assessment in asymptomatic smokers. Clinical trial registered with www.trialregister.nI (NTR 1282).	[Fens, Niki; van der Schee, Marc P.; de Nijs, Selma B.; Dijkers, Erica; Bel, Elisabeth H.; Sterk, Peter J.] Univ Amsterdam, Dept Resp Med, Acad Med Ctr, NL-1100 DE Amsterdam, Netherlands; [Roldaan, Albert C.] Haga Teaching Hosp Leyweg, Dept Pulm Dis, The Hague, Netherlands; [Cheung, David] Albert Schweitzer Hosp, Dept Resp Med, Dordrecht, Netherlands	Fens, N (reprint author), Univ Amsterdam, Dept Resp Med, Acad Med Ctr, F5-260,POB 22700, NL-1100 DE Amsterdam, Netherlands.	N.Fens@amc.nl			Netherlands Asthma Foundation [3.2.06.17]	Supported by Netherlands Asthma Foundation grant no. 3.2.06.17.	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J. Respir. Crit. Care Med.	DEC 1	2009	180	11					1076	1082		10.1164/rccm.200906-0939OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	523WA	WOS:000272104100008	19713445	
J	Scadding, GK; Durlham, SR; Mirakian, R; Jones, NS; Leech, SC; Farooque, S; Ryan, D; Walker, SM; Clark, AT; Dixon, TA; Jolles, SRA; Siddique, N; Cullinan, P; Howarth, PH; Nasser, SM				Scadding, G. K.; Durlham, S. R.; Mirakian, R.; Jones, N. S.; Leech, S. C.; Farooque, S.; Ryan, D.; Walker, S. M.; Clark, A. T.; Dixon, T. A.; Jolles, S. R. A.; Siddique, N.; Cullinan, P.; Howarth, P. H.; Nasser, S. M.			BSACI guidelines for the management of allergic and non-allergic rhinitis	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review						allergen; allergy; antihistamine; anti-leukotriene; aspirin; asthma; BSACI; cat allergen; child; corticosteroid; cromoglicate; decongestant; guideline; house dust mite; IgE; immunotherapy; ipratropium bromide; lactation; nitric oxide; occupational; pregnancy; rhinitis; rhinosinusitis; sinusitis; skin prick test; sublingual immunotherapy; surgery	AQUEOUS NASAL SPRAY; LEUKOTRIENE RECEPTOR ANTAGONISTS; RANDOMIZED CONTROLLED-TRIAL; SUBLINGUAL-SWALLOW IMMUNOTHERAPY; PLACEBO-CONTROLLED EVALUATION; GRASS-POLLEN IMMUNOTHERAPY; CONTROLLED CLINICAL-TRIAL; HEALTH-CARE WORKERS; QUALITY-OF-LIFE; DOUBLE-BLIND	This guidance for the management of patients with allergic and non-allergic rhinitis has been prepared by the Standards of Care Committee (SOCC) of the British Society for Allergy and Clinical Immunology (BSACI). The guideline is based on evidence as well as on expert opinion and is for use by both adult physicians and paediatricians practicing in allergy. The recommendations are evidence graded. During the development of these guidelines, all BSACI members were included in the consultation process using a web-based system. Their comments and suggestions were carefully considered by the SOCC. Where evidence was lacking, consensus was reached by the experts on the committee. Included in this guideline are clinical classification of rhinitis, aetiology, diagnosis, investigations and management including subcutaneous and sublingual immunotherapy. There are also special sections for children, co-morbid associations and pregnancy. Finally, we have made recommendations for potential areas of future research.	[Mirakian, R.; Clark, A. T.; Nasser, S. M.] Univ Cambridge, NHS Fdn Trust, Allergy Clin, Cambridge, England; [Scadding, G. K.] Royal Natl Throat Nose & Ear Hosp, London WC1X 8DA, England; [Durlham, S. R.] Imperial Coll NHLI, Dept Upper Resp Med, London, England; [Jones, N. S.] Queens Med Ctr, Dept Otorhinolaryngol Head & Neck Surg, Nottingham NG7 2UH, England; [Leech, S. C.] Kings Coll Hosp London, Dept Child Hlth, London, England; [Farooque, S.] Guys Hosp, Dept Asthma Allergy & Resp Med, London SE1 9RT, England; [Ryan, D.] Univ Aberdeen, Dept Gen Practice & Primary Care, Aberdeen, Scotland; [Walker, S. M.] The Athenaeum, Educ Hlth, Warwick, England; [Dixon, T. A.] Royal Liverpool & Broadgreen Univ Hosp, NHS Trust, Liverpool, Merseyside, England; [Jolles, S. R. 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Exp. Allergy	JAN	2008	38	1					19	42		10.1111/j.1365-2222.2007.02888.x		24	Allergy; Immunology	Allergy; Immunology	253QS	WOS:000252533300003	18081563	
J	Poole, JA; Barriga, K; Leung, DYM; Hoffman, M; Eisenbarth, GS; Rewers, M; Norris, JM				Poole, JA; Barriga, K; Leung, DYM; Hoffman, M; Eisenbarth, GS; Rewers, M; Norris, JM			Timing of initial exposure to cereal grains and the risk of wheat allergy	PEDIATRICS			English	Article						food allergy; wheat; solid-food exposure and introduction (timing); infant diet	FOOD ALLERGY; ATOPIC SENSITIZATION; MUCOSAL IMMUNITY; CELIAC-DISEASE; FOLLOW-UP; AUTOIMMUNITY; PREVENTION; CHILDREN; ASTHMA; HYPERSENSITIVITY	OBJECTIVE. Early exposure to solid foods in infancy has been associated with the development of allergy. The aim of this study was to examine the association between cereal-grain exposures (wheat, barley, rye, oats) in the infant diet and development of wheat allergy. METHODS. A total of 1612 children were enrolled at birth and followed to the mean age of 4.7 years. Questionnaire data and dietary exposures were obtained at 3, 6, 9, 15, and 24 months and annually thereafter. The main outcome measure was parent report of wheat allergy. Children with celiac disease autoimmunity detected by tissue transglutaminase autoantibodies were excluded. Wheat-specific immunoglobulin E levels on children reported to have wheat allergy were obtained. RESULTS. Sixteen children (1%) reported wheat allergy. Children who were first exposed to cereals after 6 months of age had an increased risk of wheat allergy compared with children first exposed to cereals before 6 months of age ( after controlling for confounders including a family history of allergic disorders and history of food allergy before 6 months of age). All 4 children with detectable wheat-specific immunoglobulin E were first exposed to cereal grains after 6 months. A first-degree relative with asthma, eczema, or hives was also independently associated with an increased risk of wheat-allergy development. CONCLUSIONS. Delaying initial exposure to cereal grains until after 6 months may increase the risk of developing wheat allergy. These results do not support delaying introduction of cereal grains for the protection of food allergy.	Univ Colorado, Dept Prevent Med & Biometr, Denver, CO 80262 USA; Univ Colorado, Dept Biometr, Denver, CO 80262 USA; Univ Colorado, Barbara Davis Ctr Childhood Diabet, Denver, CO 80262 USA; Hlth Sci Ctr, Denver, CO 80262 USA; Natl Jewish Med & Res Ctr, Dept Med, Div Clin Immunol & Allergy, Denver, CO USA; Natl Jewish Med & Res Ctr, Dept Pediat, Div Clin Immunol & Allergy, Denver, CO USA	Norris, JM (reprint author), Univ Colorado, Dept Prevent Med & Biometr, 4200 E 9th Ave,Box B119, Denver, CO 80262 USA.	jill.norris@uchsc.edu			NCRR NIH HHS [M01RR00069]; NIDDK NIH HHS [DK32493, DK50979, P30 DK 57516, R01-DK49654]		Baker SS, 2000, PEDIATRICS, V106, P346; Bjorksten B, 2005, CURR OPIN ALLERGY CL, V5, P249; Bjorksten B, 2004, CLIN REV ALLERG IMMU, V26, P129, DOI 10.1385/CRIAI:26:3:129; FALTHMAGNUSSON K, 1992, J ALLERGY CLIN IMMUN, V89, P709, DOI 10.1016/0091-6749(92)90378-F; FERGUSSON DM, 1990, PEDIATRICS, V86, P541; Fleischer DM, 2004, J ALLERGY CLIN IMMUN, V114, P1195, DOI 10.1016/j.jaci.2004.08.035; Friedman NJ, 2005, J ALLERGY CLIN IMMUN, V115, P1238, DOI 10.1016/j.jaci.2005.01.069; Gartner LM, 2005, PEDIATRICS, V115, P496, DOI 10.1542/peds.2004-2491; Host A, 1999, ARCH DIS CHILD, V81, P80; Illi S, 2001, J ALLERGY CLIN IMMUN, V108, P709, DOI 10.1067/mai.2001.118786; Ivarsson A, 2002, AM J CLIN NUTR, V75, P914; Jarvinen KM, 2003, CLIN EXP ALLERGY, V33, P1060, DOI 10.1046/j.1365-2222.2003.01741.x; JONES SM, 1995, J ALLERGY CLIN IMMUN, V96, P341, DOI 10.1016/S0091-6749(95)70053-6; Kajosaari M, 1991, Adv Exp Med Biol, V310, P453; KLEINMAN RE, 2004, PEDIAT NUTR HDB, P103; Mayer L, 2003, PEDIATRICS, V111, P1595; Norris JM, 2005, JAMA-J AM MED ASSOC, V293, P2343, DOI 10.1001/jama.293.19.2343; Norris JM, 2003, JAMA-J AM MED ASSOC, V290, P1713, DOI 10.1001/jama.290.13.1713; Rewers M, 1996, DIABETOLOGIA, V39, P807, DOI 10.1007/s001250050514; ROEHR CC, 2001, J ALLERGY CLIN IMMUN, V10, P7548; Sampson HA, 2005, J ALLERGY CLIN IMMUN, V115, P139, DOI 10.1016/j.jaci.2004.11.003; Sampson HA, 2004, J ALLERGY CLIN IMMUN, V113, P805, DOI 10.1016/j.jaci.2004.03.014; Sicherer SH, 2004, J ALLERGY CLIN IMMUN, V114, P118, DOI 10.1016/j.jaci.2004.03.056; Sudo N, 1997, J IMMUNOL, V159, P1739; ZEIGER RS, 1995, J ALLERGY CLIN IMMUN, V95, P1179, DOI 10.1016/S0091-6749(95)70074-9; Zutavern A, 2006, PEDIATRICS, V117, P401, DOI 10.1542/peds.2004-2521; Zutavern A, 2004, ARCH DIS CHILD, V89, P303, DOI 10.1136/adc.2002.025353	27	144	154	0	13	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	JUN	2006	117	6					2175	2182		10.1542/peds.2005-1803		8	Pediatrics	Pediatrics	048XE	WOS:000237979000038	16740862	
J	Jaakkola, JJK; Gissler, M				Jaakkola, JJK; Gissler, M			Maternal smoking in pregnancy, fetal development, and childhood asthma	AMERICAN JOURNAL OF PUBLIC HEALTH			English	Article							ENVIRONMENTAL TOBACCO-SMOKE; LOW-BIRTH-WEIGHT; FAMILY HISTORY; LUNG-FUNCTION; RESPIRATORY-FUNCTION; PARENTAL SMOKING; CHILDREN; INFANTS; HEALTH; LIFE	Objectives. We examined the relationships among maternal smoking in pregnancy, fetal development, and the risk of asthma in childhood. Methods. We conducted a population-based cohort study, where all 58841 singleton births were followed for 7 years using nationwide registries. Results. Maternal smoking increased the risk of asthma (adjusted odds ratio = 1.35; 95% confidence interval = 1.13, 1.62 for high exposure). Low birthweight and preterm delivery increased the risk of asthma at the age of 7, whereas being small for gestational age did not. Conclusions. Maternal smoking in pregnancy increases the risk of asthma during the first 7 years of life, and only a small fraction of the effect seems to be mediated through fetal growth. (Am J Public Health. 2004;94:136-140).	Univ Birmingham, Inst Occupat Hlth, Birmingham B15 2TT, W Midlands, England; Univ Helsinki, Dept Publ Hlth, Helsinki, Finland; Natl Res & Dev Ctr Welf & Hlth, Helsinki, Finland	Jaakkola, JJK (reprint author), Univ Birmingham, Inst Occupat Hlth, Birmingham B15 2TT, W Midlands, England.	j.jaakkola@bham.ac.uk	Jaakkola, Jouni/G-4314-2012				Carlsen KCL, 1997, EUR RESPIR J, V10, P1774; Gilliland FD, 2001, AM J RESP CRIT CARE, V163, P429; Gissler M, 1998, PAEDIATR PERINAT EP, V12, P437; GISSLER M, 1995, SCAND J SOC MED, V23, P75; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; HANRAHAN JP, 1992, AM REV RESPIR DIS, V145, P1129; Hoo AF, 1998, AM J RESP CRIT CARE, V158, P700; Infante-Rivard C, 1999, AM J EPIDEMIOL, V150, P528; Jaakkola JJK, 2002, SCAND J WORK ENV HEA, V28, P71; KRAMER MS, 1987, B WORLD HEALTH ORGAN, V65, P663; London SJ, 2001, EPIDEMIOLOGY, V12, P577, DOI 10.1097/00001648-200109000-00019; Milner AD, 1999, ARCH DIS CHILD, V80, pF8; Nafstad P, 1997, EPIDEMIOLOGY, V8, P293, DOI 10.1097/00001648-199705000-00011; Pihkala J, 1989, Duodecim, V105, P1540; Steffensen FH, 2000, EPIDEMIOLOGY, V11, P185, DOI 10.1097/00001648-200003000-00018; Stick SM, 1996, LANCET, V348, P1060, DOI 10.1016/S0140-6736(96)04446-7; Strachan DP, 1998, THORAX, V53, P204; World Health Organization, 1980, INT CLASS DIS; YOUNG S, 1991, NEW ENGL J MED, V324, P1168, DOI 10.1056/NEJM199104253241704	19	144	147	0	10	AMER PUBLIC HEALTH ASSOC INC	WASHINGTON	1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 USA	0090-0036			AM J PUBLIC HEALTH	Am. J. Public Health	JAN	2004	94	1					136	140		10.2105/AJPH.94.1.136		5	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	762CL	WOS:000187952700035	14713711	
J	Fusco, D; Forastiere, F; Michelozzi, P; Spadea, T; Ostro, B; Arca, M; Perucci, CA				Fusco, D; Forastiere, F; Michelozzi, P; Spadea, T; Ostro, B; Arca, M; Perucci, CA			Air pollution and hospital admissions for respiratory conditions in Rome, Italy	EUROPEAN RESPIRATORY JOURNAL			English	Article						air pollution; hospital admissions; respiratory disease; time-series	OBSTRUCTIVE PULMONARY-DISEASE; MINNEAPOLIS ST-PAUL; URBAN AIR; EUROPEAN CITIES; APHEA PROJECT; TIME-SERIES; ASTHMA; ASSOCIATION; EMERGENCY; LONDON	Most of the evidence regarding the association between particulate air pollution and emergency room visits or hospital admissions for respiratory conditions and asthma comes from the USA. European time-series analyses have suggested that gaseous air pollutants are important determinants of acute hospitalization for respiratory conditions, at least as important as particulate mass. The association between daily mean levels of suspended particles and gaseous pollutants (sulphur dioxide, nitrogen dioxide, carbon monoxide, ozone) was examined. The daily emergency hospital admissions for respiratory conditions in the metropolitan area of Rome during 1995 - 1997,were also recorded. Daily counts of hospital admissions for total respiratory conditions (43 admissions .day(-1)), acute respiratory infections including pneumonia (18.day(-1)), chronic obstructive pulmonary disease (COPD) (13.day(-1)), and asthma (4.5.day(-1)) among residents of all ages and among children (0-14 yrs) were analysed, The generalized additive models included spline smooth functions of the day of study, mean temperature, mean humidity, influenza epidemics, and indicator variables for day of the week and holidays, Total respiratory admissions were significantly associated with same-da, level of NO2 (2.5%, increase per interquartile range (IQR) change, 22.3 mug.m(-3)) and CO (2.8% increase per IQR, 1.5 mg.m(-3)). No effect was found for particulate matter and SO2, whereas O-3 was associated with admissions only among children (lag 1, 5.5%, increase per IQR, 23.9 mug.m(3)). The effect of NO2 was stronger on acute respirator!, infections (lag 0, 4.0% increase) and on asthma among children (lag 1, 10.7% increase). The admissions for all ages for asthma and CORD were associated only with same-day level of CO (5.5% and 4.3% increase, respectively). Multipollutant models confirmed the role of CO on all respiratory admissions, including asthma and COPD, and that of NO2 on acute respiratory infections, Among children, O-3 remained a strong indicator of acute respiratory infections, Carbon monoxide and photochetnical pollutants (nitrogen dioxide, ozone) appear to he determinants of acute respiratory conditions in Rome, Since carbon monoxide and nitrogen dioxide are good indicators of combustion products from traffic related sources, the detected effect may be due to unmeasured fine and ultrafine particles.	Agcy Publ Hlth, I-00198 Rome, Italy; Calif Environm Protect Agcy, Oakland, CA USA	Forastiere, F (reprint author), Agcy Publ Hlth, Lazio Reg,Via Santa Costanza 53, I-00198 Rome, Italy.		Michelozzi, Paola/J-8608-2016; Forastiere, Francesco/J-9067-2016; Fusco, Danilo/K-1383-2016; Spadea, Teresa/K-4991-2016	Michelozzi, Paola/0000-0002-1646-2555; Forastiere, Francesco/0000-0002-9162-5684; Fusco, Danilo/0000-0003-1759-5621; Spadea, Teresa/0000-0002-0771-0545			Anderson HR, 1998, THORAX, V53, P842; Anderson HR, 1997, EUR RESPIR J, V10, P1064, DOI 10.1183/09031936.97.10051064; Atkinson RW, 1999, EUR RESPIR J, V13, P257, DOI 10.1183/09031936.99.13225799; Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; BATES DV, 1987, ENVIRON RES, V43, P317, DOI 10.1016/S0013-9351(87)80032-4; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Becker S, 1999, J TOXICOL ENV HEAL A, V57, P445, DOI 10.1080/009841099157539; Brook JR, 1997, J AIR WASTE MANAGE, V47, P2; BURNETT RT, 1995, AM J EPIDEMIOL, V142, P15; Burnett RT, 1997, ENVIRON RES, V72, P24, DOI 10.1006/enrs.1996.3685; Burnett RT, 1997, ENVIRON HEALTH PERSP, V105, P614, DOI 10.1289/ehp.97105614; Chauhan A. J., 1998, Reviews on Environmental Health, V13, P73; CHAUHAN AJ, 1992, AM J RESP CRIT CARE, V159, pA699; D'Innocenzio F, 1998, ANN CHIM-ROME, V88, P281; DOCKERY DW, 1994, ANNU REV PUBL HEALTH, V15, P107, DOI 10.1146/annurev.pu.15.050194.000543; EPA (Environmental Protection Agency), 1996, EPA600P95001; Hagen JA, 2000, EPIDEMIOLOGY, V11, P136, DOI 10.1097/00001648-200003000-00009; Hajat S, 1999, THORAX, V54, P597; Hastie T, 1990, GEN ADDITIVE MODELS; Katsouyanni K, 1996, J EPIDEMIOL COMMUN H, V50, pS12, DOI 10.1136/jech.50.Suppl_1.S12; Michelozzi P, 1998, OCCUP ENVIRON MED, V55, P605; Moolgavkar SH, 1997, EPIDEMIOLOGY, V8, P364, DOI 10.1097/00001648-199707000-00003; Morgan G, 1998, AM J PUBLIC HEALTH, V88, P1761, DOI 10.2105/AJPH.88.12.1761; Norris G, 1999, ENVIRON HEALTH PERSP, V107, P489, DOI 10.2307/3434632; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Pitard A, 1997, STAT MED, V16, P527, DOI 10.1002/(SICI)1097-0258(19970315)16:5<527::AID-SIM429>3.0.CO;2-C; Poloniecki JD, 1997, OCCUP ENVIRON MED, V54, P535; PONKA A, 1991, ARCH ENVIRON HEALTH, V46, P262; Schwartz J, 1999, EPIDEMIOLOGY, V10, P17, DOI 10.1097/00001648-199901000-00005; SCHWARTZ J, 1994, ARCH ENVIRON HEALTH, V49, P366; Schwartz J, 1996, EPIDEMIOLOGY, V7, P20, DOI 10.1097/00001648-199601000-00005; SCHWARTZ J, 1994, AM J RESP CRIT CARE, V150, P648; SCHWARTZ J, 1994, AM J EPIDEMIOL, V139, P589; Sheppard L, 1999, EPIDEMIOLOGY, V10, P23, DOI 10.1097/00001648-199901000-00006; Spix C, 1998, ARCH ENVIRON HEALTH, V53, P54; Sunyer J, 1997, THORAX, V52, P760; SUNYER J, 1991, AM J EPIDEMIOL, V134, P277; Tenias JM, 1998, OCCUP ENVIRON MED, V55, P541; Thom SR, 1997, CHEM RES TOXICOL, V10, P1023, DOI 10.1021/tx970041h	39	144	146	0	24	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146, WEST ST, STE 2.4 HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	JUN	2001	17	6					1143	1150		10.1183/09031936.01.00005501		8	Respiratory System	Respiratory System	454HT	WOS:000169967700015	11491157	
J	Harding, SM; Guzzo, MR; Richter, JE				Harding, SM; Guzzo, MR; Richter, JE			The prevalence of gastroesophageal reflux in asthma patients without reflux symptoms	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article; Proceedings Paper	Digestive Disease Week / 98th American-Gastroenterology-Association Meeting	MAY 11-14, 1997	WASHINGTON, D.C.	Amer Gastroenterol Assoc			PLACEBO-CONTROLLED CROSSOVER; LOWER ESOPHAGEAL SPHINCTER; CHRONIC COUGH; DOUBLE-BLIND; OMEPRAZOLE; THERAPY; DISEASE; DIAGNOSIS; PRESSURE	Gastroesophageal reflux is a potential trigger of asthma that may be clinically silent. This study examines the prevalence of gastroesophageal reflux in asthma patients without reflux symptoms. This prospective cohort study evaluated 26 patients with stable asthma without reflux symptoms using esophageal manometry and 24-h esophageal pH testing. Gastroesophageal reflux was considered present if esophageal acid contact times were abnormal. Demographic variables were analyzed to determine if they predicted the presence of gastroesophageal reflux, Asthma patients with asymptomatic gastroesophageal reflux were compared with 30 age-matched asthma patients with symptomatic gastroesophageal reflux. The prevalence of abnormal 24-h esophageal pH tests in asthma patients without reflux symptoms was 62% (16 of 26), Demographic variables did not predict abnormal 24-h esophageal pH tests in asthma patients with asymptomatic gastroesophageal reflux. Asthma patients with asymptomatic gastroesophageal reflux had higher amounts of proximal esophageal acid exposure (p < 0.05) compared with asthma patients with symptomatic gastroesophageal reflux. Because demographic variables do not predict abnormal 24-h esophageal pH tests in asthma patients without reflux symptoms, 24-h esophageal pH testing is required. This study suggests that gastroesophageal reflux is present in asthma patients, even in the absence of esophageal symptoms.	Univ Alabama, Div Pulm Allergy & Crit Care Med, Dept Med, Birmingham, AL 35294 USA; Cleveland Clin Fdn, Dept Gastroenterol, Cleveland, OH 44195 USA	Harding, SM (reprint author), Univ Alabama, Div Pulm Allergy & Crit Care Med, Dept Med, 215 Tinsley Harrison Tower,1900 Univ Blvd, Birmingham, AL 35294 USA.				NHLBI NIH HHS [HL03633]		American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P225, DOI DOI 10.1164/AJRCCM/136.1.225; Boeree MJ, 1998, EUR RESPIR J, V11, P1070, DOI 10.1183/09031936.98.11051070; DALTON CB, 1987, ESOPHAGEAL MOTILITY, P35; DEVAULT KR, 1995, ARCH INTERN MED, V155, P2165; Field SK, 1996, CHEST, V109, P316, DOI 10.1378/chest.109.2.316; Field SK, 1999, CHEST, V116, P766, DOI 10.1378/chest.116.3.766; Field SK, 1998, CHEST, V114, P275, DOI 10.1378/chest.114.1.275; GARCIAPULIDO J, 1990, CHEST, V98, P806, DOI 10.1378/chest.98.4.806; Hamamoto J, 1997, J APPL PHYSIOL, V82, P738; Harding SM, 1996, AM J MED, V100, P395, DOI 10.1016/S0002-9343(97)89514-9; Harding SM, 1999, J ALLERGY CLIN IMMUN, V104, P251, DOI 10.1016/S0091-6749(99)70360-X; Harding SM, 1997, CHEST, V111, P1389, DOI 10.1378/chest.111.5.1389; Harding SM, 1999, CHEST, V115, P654, DOI 10.1378/chest.115.3.654; HOLMES PW, 1978, THORAX, V33, P394, DOI 10.1136/thx.33.3.394; IRWIN RS, 1993, CHEST, V103, P1662, DOI 10.1378/chest.103.6.1662; JAMIESON JR, 1992, AM J GASTROENTEROL, V87, P1102; Kahrilas PJ, 1996, GASTROENTEROLOGY, V110, P1982, DOI 10.1053/gast.1996.1101982; Kiljander TO, 1999, CHEST, V116, P1257, DOI 10.1378/chest.116.5.1257; LAM HGT, 1994, DIGEST DIS SCI, V39, P402, DOI 10.1007/BF02090215; LARRAIN A, 1991, CHEST, V99, P1330, DOI 10.1378/chest.99.6.1330; Matthews DE, 1996, USING UNDERSTANDING; MEIER JH, 1994, DIGEST DIS SCI, V39, P2127, DOI 10.1007/BF02090360; MITTAL RK, 1988, J CLIN INVEST, V81, P1182, DOI 10.1172/JCI113433; Mittal RK, 1997, NEW ENGL J MED, V336, P924; RICHTER JE, 1992, DIGEST DIS SCI, V37, P849, DOI 10.1007/BF01300382; ROUSSOS C, 1982, NEW ENGL J MED, V307, P786, DOI 10.1056/NEJM198209233071304; SCHNATZ PF, 1996, AM J GASTROENTEROL, V91, P715; SHEFFER LA, 1991, US DEP HHS PUBLICATI; SINCLAIR JW, 1991, AMBULATORY ESOPHAGEA, P23; SONTAG SJ, 1990, GASTROENTEROLOGY, V99, P613; STEIN MR, 1980, ANN ALLERGY, V45, P238; TASHKIN DP, 1992, AM REV RESPIR DIS, V145, P301; Teichtahl H, 1996, AUST NZ J MED, V26, P671, DOI 10.1111/j.1445-5994.1996.tb02938.x; Vaezi MF, 1997, SOUTHERN MED J, V90, P305, DOI 10.1097/00007611-199703000-00008	35	144	148	0	2	AMER LUNG ASSOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	JUL	2000	162	1					34	39				6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	333JH	WOS:000088126800007	10903216	
J	Akdis, M; Akdis, CA				Akdis, Muebeccel; Akdis, Cezmi A.			Mechanisms of allergen-specific immunotherapy: Multiple suppressor factors at work in immune tolerance to allergens	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Regulatory T cells; immunotherapy; IgE; T cells; IL-10; TGF-beta; allergen immunotherapy; T helper cells; immune tolerance; IgE; IgG; T cells; B cells; mast cells; basophils; eosinophils	REGULATORY T-CELLS; IMMUNOLOGY/PRACTALL CONSENSUS REPORT; EOSINOPHIL CATIONIC PROTEIN; GRASS-POLLEN IMMUNOTHERAPY; TRANSCRIPTION FACTOR FOXP3; TOLL-LIKE RECEPTORS; HOUSE-DUST MITES; SUBLINGUAL IMMUNOTHERAPY; TGF-BETA; ASTHMATIC-CHILDREN	Allergen-specific immunotherapy (AIT) has been used for more than 100 years as a desensitizing therapy for IgE-mediated allergic diseases and represents a potentially curative way of treatment. The mechanisms of action of AIT include the induction of very early desensitization of mast cells and basophils; generation of regulatory T and regulatory B (Breg) cell responses; regulation of IgE and IgG(4); decreases in numbers and activity of eosinophils and mast cells in mucosal allergic tissues; and decreases in the activity of basophils in circulation. Skewing of allergen-specific effector T and effector B cells to a regulatory phenotype appears as a key event in the course of AIT and normal immune response to allergens. Recently, inducible IL-10-secreting Breg cells were also demonstrated to contribute to allergen tolerance through suppression of effector T cells and selective induction of IgG4 isotype antibodies. Allergen-specific regulatory T and Breg cells orchestrate a general immunoregulatory activity, which can be summarized as suppression of cytokines from inflammatory dendritic cells; suppression of effector T(H)1, T(H)2, and T(H)17 cells; suppression of allergen-specific IgE and induction of IgG(4); and suppression of migration of mast cells, basophils, eosinophils, and effector T cells to tissues. A detailed knowledge of the mechanisms of AIT is not only important in designing the prevention and treatment of allergic diseases but might also find applications in the treatment of autoimmune diseases, organ transplantation, chronic infection, and cancer.	[Akdis, Muebeccel; Akdis, Cezmi A.] Univ Zurich, Swiss Inst Allergy & Asthma Res SIAF, CH-8006 Zurich, Switzerland	Akdis, M (reprint author), Swiss Inst Allergy & Asthma Res SIAF, Obere Str 22, CH-7270 Davos, Switzerland.	akdism@siaf.uzh.ch; akdisac@siaf.uzh.ch			Swiss National Foundation [320030_140772, 320030_132899]; Christine Kuhne Center for Allergy Research and Education (CK-CARE); European 7th frame work project MeDALL: Mechanisms of the Development of Allergy [261357]; European 7th frame work project PREDICTA: Post-Infectious Immune Reprogramming and Its Association with Persistence and Chronicity of Respiratory Allergic Diseases [260895]	The authors' laboratories are supported by the Swiss National Foundation grants 320030_140772 and 320030_132899 and the Christine Kuhne Center for Allergy Research and Education (CK-CARE), European 7th frame work projects MeDALL: Mechanisms of the Development of Allergy (no. 261357), and PREDICTA: Post-Infectious Immune Reprogramming and Its Association with Persistence and Chronicity of Respiratory Allergic Diseases (no. 260895).	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Allergy Clin. Immunol.	MAR	2014	133	3					621	631		10.1016/j.jaci.2013.12.1088		11	Allergy; Immunology	Allergy; Immunology	AC3EK	WOS:000332397600002	24581429	
J	Wolterink, RGJK; KleinJan, A; van Nimwegen, M; Bergen, I; de Bruijn, M; Levani, Y; Hendriks, RW				Wolterink, Roel G. J. Klein; KleinJan, Alex; van Nimwegen, Menno; Bergen, Ingrid; de Bruijn, Marjolein; Levani, Yelvi; Hendriks, Rudi W.			Pulmonary innate lymphoid cells are major producers of IL-5 and IL-13 in murine models of allergic asthma	EUROPEAN JOURNAL OF IMMUNOLOGY			English	Article						Asthma; Cytokines; House dust mite; Innate immunity; Innate lymphoid cells	ROR-GAMMA-T; AIRWAY HYPERREACTIVITY; ADAPTIVE IMMUNITY; IN-VIVO; DENDRITIC CELLS; TYPE-2 IMMUNITY; NKP46(+) CELLS; LUNG; INFLAMMATION; CYTOKINE	Allergic asthma is characterized by chronic airway inflammation and hyperreactivity and is thought to be mediated by an adaptive T helper-2 (Th2) cell-type immune response. Here, we demonstrate that type 2 pulmonary innate lymphoid cells (ILC2s) significantly contribute to production of the key cytokines IL-5 and IL-13 in experimental asthma. In naive mice, lineage-marker negative ILC2s expressing IL-7Ra, CD25, Sca-1, and T1/ST2(IL-33R) were present in lungs and mediastinal lymph nodes (MedLNs), but not in broncho-alveolar lavage (BAL) fluid. Upon intranasal administration of IL-25 or IL-33, an asthma phenotype was induced, whereby ILC2s accumulated in lungs, MedLNs, and BAL fluid. After IL-25 and IL-33 administration, ILC2s constituted similar to 50 and similar to 80% of IL-5+/IL-13+ cells in lung and BAL, respectively. Also in house dust mite-induced or ovalbumin-induced allergic asthma, the ILC2 population in lung and BAL fluid increased significantly in size and ILC2s were a major source of IL-5 or IL-13. Particularly in OVA-induced asthma, the contribution of ILC2s to the total population of intracellular IL-5+ and IL-13+ cells in the lung was in the same range as found for Th2 cells. We conclude that both ILC2s and Th2 cells produce large amounts of IL-5 and IL-13 that contribute to allergic airway inflammation.	[Wolterink, Roel G. J. Klein; KleinJan, Alex; van Nimwegen, Menno; Bergen, Ingrid; de Bruijn, Marjolein; Levani, Yelvi; Hendriks, Rudi W.] Erasmus MC, Dept Pulm Med, Rotterdam, Netherlands; [Wolterink, Roel G. J. Klein] Inst Pasteur, Dept Immunol, Innate Immun Unit, F-75724 Paris, France; [Wolterink, Roel G. J. Klein] Inst Pasteur, INSERM U668, Paris, France; [Wolterink, Roel G. J. Klein] Univ Paris Diderot, Paris, France	Hendriks, RW (reprint author), Erasmus MC, Dept Pulm Med, Rotterdam, Netherlands.	r.hendriks@erasmusmc.nl		Levani, Yelvi/0000-0002-8291-6842	Ligue Nationale Contre le Cancer (LNCC), France	We thank Bart Lambrecht, Mirjam Kool, Tom Cupedo and Ferry Cornelissen (Erasmus MC Rotterdam) and James Di Santo (Institut Pasteur, Paris) for valuable discussions regarding this research. We thank Bjorn Clausen, Christian Wohn, Tom Cupedo, Ferry Cornelissen, Kim van der Weerd, Odilia Corneth and Erik Lubberts for providing various mouse strains. RKW is supported by a scholarship from the Ligue Nationale Contre le Cancer (LNCC), France.	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J. Immunol.	MAY	2012	42	5					1106	1116		10.1002/eji.201142018		11	Immunology	Immunology	932VD	WOS:000303317700008	22539286	
J	Commins, SP; James, HR; Kelly, LA; Pochan, SL; Workman, LJ; Perzanowski, MS; Kocan, KM; Fahy, JV; Nganga, LW; Ronmark, E; Cooper, PJ; Platts-Mills, TAE				Commins, Scott P.; James, Hayley R.; Kelly, Libby A.; Pochan, Shawna L.; Workman, Lisa J.; Perzanowski, Matthew S.; Kocan, Katherine M.; Fahy, John V.; Nganga, Lucy W.; Ronmark, Eva; Cooper, Philip J.; Platts-Mills, Thomas A. E.			The relevance of tick bites to the production of IgE antibodies to the mammalian oligosaccharide galactose-alpha-1,3-galactose	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Ticks; anaphylaxis; oligosaccharide; alpha-gal; IgE antibody to CCD	AMBLYOMMA-AMERICANUM ACARI; UNITED-STATES; COLORECTAL-CANCER; INDOOR ALLERGEN; ACUTE ASTHMA; CETUXIMAB; ANAPHYLAXIS; HUMANS; RISK; SENSITIZATION	Background: In 2009, we reported a novel form of delayed anaphylaxis to red meat that is related to serum IgE antibodies to the oligosaccharide galactose-alpha-1,3-galactose (alpha-gal). Most of these patients had tolerated meat for many years previously. The implication is that some exposure in adult life had stimulated the production of these IgE antibodies. Objectives: We sought to investigate possible causes of this IgE antibody response, focusing on evidence related to tick bites, which are common in the region where these reactions occur. Methods: Serum assays were carried out with biotinylated proteins and extracts bound to a streptavidin ImmunoCAP. Results: Prospective studies on IgE antibodies in 3 subjects after tick bites showed an increase in levels of IgE to alpha-gal of 20fold or greater. Other evidence included (1) a strong correlation between histories of tick bites and levels of IgE to alpha-gal (chi(2) = 26.8, P < .001), (2) evidence that these IgE antibodies are common in areas where the tick Amblyomma americanum is common, and (3) a significant correlation between IgE antibodies to alpha-gal and IgE antibodies to proteins derived from A americanum (r(s) = 0.75, P < .001). Conclusion: The results presented here provide evidence that tick bites are a cause, possibly the only cause, of IgE specific for alpha-gal in this area of the United States. Both the number of subjects becoming sensitized and the titer of IgE antibodies to alpha-gal are striking. Here we report the first example of a response to an ectoparasite giving rise to an important form of food allergy. (J Allergy Clin Immunol 2011;127:1286-93.)	[Commins, Scott P.; James, Hayley R.; Kelly, Libby A.; Pochan, Shawna L.; Workman, Lisa J.; Platts-Mills, Thomas A. E.] Univ Virginia Hlth Syst, Asthma & Allerg Dis Ctr, Charlottesville, VA 22908 USA; [Perzanowski, Matthew S.] Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA; [Kocan, Katherine M.] Oklahoma State Univ, Ctr Vet Hlth Sci, Stillwater, OK 74078 USA; [Fahy, John V.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA; [Nganga, Lucy W.] Kenya Med Res Inst KEMRI, Ctr Resp Dis, Nairobi, Kenya; [Ronmark, Eva] Umea Univ, Dept Publ Hlth & Clin Med, Umea, Sweden; [Cooper, Philip J.] Univ San Francisco Quito, Cumbaya, Quito, Ecuador; [Cooper, Philip J.] Univ Liverpool Liverpool Sch Trop Med, Liverpool, Merseyside, England	Platts-Mills, TAE (reprint author), Univ Virginia Hlth Syst, Asthma & Allerg Dis Ctr, POB 801355, Charlottesville, VA 22908 USA.	tap2z@virginia.edu			National Institutes of Health [RO1 AI-20565, AI-AADCRC-U19-070364, K08 AI085190, R21 AI087985]; Wellcome Trust [072405/Z/03/Z]; Phadia; NIH	Supported by National Institutes of Health grant RO1 AI-20565, AI-AADCRC-U19-070364, K08 AI085190, R21 AI087985, and the Wellcome Trust 072405/Z/03/Z (to P. J. C.).; Disclosure of potential conflict of interest: S. P. Commins is a volunteer committee member for the American Association of Allergy, Asthma & Immunology (AAAAI) and the American College of Allergy, Asthma & Immunology and is an author for Up to Date. M. S. Perzanowski receives research support from the National Institutes of Health (NIH) and is a member of the AAAAI. J. V. Fahy receives research support from the NIH. P. J. Cooper receives research support from Wellcome Trust. T. A. E. Platts-Mills receives research support from Phadia and the NIH and has a patent on an assay. The rest of the authors have declared that they have no conflict of interest.	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Allergy Clin. Immunol.	MAY	2011	127	5					1286	U310		10.1016/j.jaci.2011.02.019		14	Allergy; Immunology	Allergy; Immunology	756NG	WOS:000290018600025	21453959	
J	Lamprecht, B; McBurnie, MA; Vollmer, WM; Gudmundsson, G; Welte, T; Nizankowska-Mogilnicka, E; Studnicka, M; Bateman, E; Anto, JM; Burney, P; Mannino, DM; Buist, SA				Lamprecht, Bernd; McBurnie, Mary Ann; Vollmer, William M.; Gudmundsson, Gunnar; Welte, Tobias; Nizankowska-Mogilnicka, Ewa; Studnicka, Michael; Bateman, Eric; Anto, Josep M.; Burney, Peter; Mannino, David M.; Buist, Sonia A.		BOLD Collaborative Res Grp	COPD in Never Smokers Results From the Population-Based Burden of Obstructive Lung Disease Study	CHEST			English	Article							NUTRITION EXAMINATION SURVEY; ENVIRONMENTAL TOBACCO-SMOKE; AIR-FLOW OBSTRUCTION; 3RD NATIONAL-HEALTH; PULMONARY-DISEASE; GRAIN DUST; GENDER-DIFFERENCES; PASSIVE SMOKING; BIOMASS SMOKE; US POPULATION	Background: Never smokers comprise a substantial proportion of patients with COPD. Their characteristics and possible risk factors in this population are not yet well defined. Methods: We analyzed data from 14 countries that participated in the international, population-based Burden of Obstructive Lung Disease (BOLD) study. Participants were aged >= 40 years and completed postbronchodilator spirometry testing plus questionnaires about respiratory symptoms, health status, and exposure to COPD risk factors. A diagnosis of COPD was based on the postbronchodilator FEV1/FVC ratio, according to current GOLD (Global Initiative for Obstructive Lung Disease) guidelines. In addition to this, the lower limit of normal (LLN) was evaluated as an alternative threshold for the FEV1/FVC ratio. Results: Among 4,291 never smokers, 6.6% met criteria for mild (GOLD stage I) COPD, and 5.6% met criteria for moderate to very severe (GOLD stage II+) COPD. Although never smokers were less likely to have COPD and had less severe COPD than ever smokers, never smokers nonetheless comprised 23.3% (240/1,031) of those classified with GOLD stage II+ COPD. This proportion was similar, 20.5% (171/832), even when the LLN was used as a threshold for the FEV1/FVC ratio. Predictors of COPD in never smokers include age, education, occupational exposure, childhood respiratory diseases, and BMI alterations. Conclusion: This multicenter international study confirms previous evidence that never smokers comprise a substantial proportion of individuals with COPD. Our data suggest that, in addition to increased age, a prior diagnosis of asthma and, among women, lower education levels are associated with an increased risk for COPD among never smokers. CHEST 2011; 139(4):752-763	[Lamprecht, Bernd; Studnicka, Michael] Paracelsus Med Univ, Dept Pulm Med, A-5020 Salzburg, Austria; [Buist, Sonia A.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA; [McBurnie, Mary Ann; Vollmer, William M.] Kaiser Permanente Ctr Hlth Res, Portland, OR USA; [Gudmundsson, Gunnar] Landspitali Univ Hosp, Dept Resp Med Allergy & Sleep, Reykjavik, Iceland; [Welte, Tobias] Hannover Med Sch, Dept Resp Med, Hannover, Germany; [Nizankowska-Mogilnicka, Ewa] Jagiellonian Univ, Sch Med, Dept Med, Krakow, Poland; [Bateman, Eric] Univ Cape Town, ZA-7925 Cape Town, South Africa; [Anto, Josep M.] Ctr Res Environm Epidemiol, Barcelona, Spain; [Burney, Peter] Kings Coll London, Dept Publ Hlth Sci, London WC2R 2LS, England; [Mannino, David M.] Univ Kentucky, Lexington, KY USA	Lamprecht, B (reprint author), Paracelsus Med Univ, Dept Pulm Med, Mullner Hauptstr 48, A-5020 Salzburg, Austria.	b.lamprecht@salk.at	Gudmundsson, Gunnar/F-1974-2013; Anto, J/H-2676-2014	Gudmundsson, Gunnar/0000-0002-7251-8322; Anto, J/0000-0002-4736-8529; Mannino, David/0000-0003-3646-7828	ALTANA; Aventis; AstraZeneca; Boehringer-Ingleheim; Chiesi; GlaxoSmithKline; Merck; Novartis; Pfizer Inc; Schering-Plough; Sunovion Pharmaceuticals Inc; University of Kentucky; Schering Plough; Sepracor; AstraZeneca, Spain	The BOLD initiative was funded in part by unrestricted educational grants to the operations center from ALTANA. Aventis, AstraZeneca, Boehringer-Ingleheim, Chiesi, GlaxoSmithKline, Merck, Novartis, Pfizer Inc, Schering-Plough, Sunovion Pharmaceuticals Inc, and the University of Kentucky.; The authors have reported to CHEST the following conflicts of interest: Dr McBurnie received funding for the BOLD study operations center and/or other research from unrestricted educational grants from GlaxoSmithKline, Pfizer, Boehringer Ingelheim, AstraZeneca, ALTANA, Novartis, Merck, Chiesi, Schering Plough, and Sepracor. Dr Vollmer has served on ad hoc advisory boards for Merck and Co; has participated in COPD workshops funded by Merck and GlaxoSmithKline; mid is director of the Burden of Obstructive Lung Disease (BOLD) Operations Center, for which funding includes unrestricted educational grants to the Kaiser Permanente Center for Health Research from Boehringer Ingelheim, Pfizer, ALTANA, GlaxoSmithKline, AstraZeneca, Novartis, Chiesi, and Merck. Dr Auto has received an educational grant from AstraZeneca, Spain. Dr Mannino has received research funding from GlaxoSmithKline, Pfizer, and Novartis. He has served as a speaker, advisor, or consultant for AstraZeneca, MAP Dey, Seprecor, Boehringer-Ingelheim, GlaxoSmithKline, Pfizer, and Novartis. He has also served as an expert witness in active and passive smoking cases. Dr Buist is a member of Advisory Boards for AstraZeneca, GlaxoSmithKline, Merck, and Novartis and has received unrestricted educational grants to the BOLD Operations Center from Chiesi, Boehringer Ingelheim, Pfizer, Novartis, GlaxoSmithKline, Sepracor, and Merck. Drs Lamprecht, Gudmundsson, Welte, Nizankowska-Mogilnicka, Studnicka, Bateman, and Burney have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.	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J	Poon, AH; Laprise, C; Lemire, M; Montpetit, A; Sinnett, D; Schurr, E; Hudson, TJ				Poon, AH; Laprise, C; Lemire, M; Montpetit, A; Sinnett, D; Schurr, E; Hudson, TJ			Association of vitamin D receptor genetic variants with susceptibility to asthma and atopy	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						genetic predisposition; polymorphism; vitamin D receptor	FAMILY-BASED TESTS; 1,25-DIHYDROXYVITAMIN D-3; CHEMOKINE RECEPTOR; ONSET ASTHMA; BONE-DENSITY; POLYMORPHISM; TUBERCULOSIS; ALLELES; DISEASE; PROGRESSION	Genome scans for asthma have identified suggestive or significant linkages on 17 different chromosomes, including chromosome 12, region q13-23, housing the vitamin D receptor (VDR) gene. Through interaction with VDR, 1,25-dihydroxyvitamin D3 mediates numerous biological activities, such as regulation of helper T-cell development and subsequent cytokine secretion profiles. Variants of the VDR have been found to be associated with immune-mediated diseases that are characterized by an imbalance in helper T-cell development, such as Crohn's disease and tuberculosis. The VDR, hence, is a good candidate to be investigated for association with asthma, which is characterized by enhanced helper T-cell type 2 activity. Here, we examined VDR genetic variants in an asthma family-based cohort from Quebec. We report six variants to be strongly associated with asthma and four with atopy (0.0005 less than or equal to p less than or equal to 0.05). Analysis of the linkage disequilibrium pattern and haplotypes also revealed significant association with both phenotypes (0.0004 less than or equal to p less than or equal to 0.01). The findings have been replicated by another research team in a second but not in a third cohort. These results identify VDR variants as genetic risk factors for asthma/atopy and implicate a non-human leukocyte antigen immunoregulatory molecule in the pathogenesis of asthma and atopy.	McGill Univ, Montreal, PQ H3A 1A4, Canada; Genome Quebec Innovat Ctr, Montreal, PQ H3A 1A4, Canada; McGill Univ, Ctr Hlth, McGill Ctr Study Host Resistance, Inst Res, Montreal, PQ, Canada; Univ Quebec, Chicoutimi, PQ, Canada; Univ Montreal, Chicoutimi Hosp, Community Genom Med Ctr, Chicoutimi, PQ, Canada	Hudson, TJ (reprint author), McGill Univ, 740 Penfield Ave,Room 7105, Montreal, PQ H3A 1A4, Canada.	tom.hudson@mcgill.ca	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Abecasis GR, 2002, NAT GENET, V30, P97, DOI 10.1038/ng786; ALROY I, 1995, MOL CELL BIOL, V15, P5789; Barber Y, 2001, J INFECT DIS, V184, P1279, DOI 10.1086/324000; Becker Y, 2004, VIRUS GENES, V28, P5, DOI 10.1023/B:VIRU.0000012260.32578.72; Bell PA, 2002, BIOTECHNIQUES, P70; Bell PA, 2002, BIOTECHNIQUES S, P74; Bell PA, 2002, BIOTECHNIQUES S, P76; BELL PA, 2002, BIOTECHNIQUES S, P77; Bellamy R, 1999, J INFECT DIS, V179, P721, DOI 10.1086/314614; Boonstra A, 2001, J IMMUNOL, V167, P4974; Camargo CA, 1999, ARCH INTERN MED, V159, P2582, DOI 10.1001/archinte.159.21.2582; Cantorna MT, 2000, ARCH BIOCHEM BIOPHYS, V377, P135, DOI 10.1006/abbi.2000.1765; Cantorna MT, 1998, J IMMUNOL, V160, P5314; Carling T, 1998, J CLIN ENDOCR METAB, V83, P2255, DOI 10.1210/jc.83.7.2255; Chang TJ, 2000, CLIN ENDOCRINOL, V52, P575, DOI 10.1046/j.1365-2265.2000.00985.x; Cherniack R, 1999, CONTROL CLIN TRIALS, V20, P91; Crofts LA, 1998, P NATL ACAD SCI USA, V95, P10529, DOI 10.1073/pnas.95.18.10529; Engert JC, 2002, DIABETES, V51, P1629, DOI 10.2337/diabetes.51.5.1629; Fassbender WJ, 2002, HORM METAB RES, V34, P330, DOI 10.1055/s-2002-33262; Gabriel SB, 2002, SCIENCE, V296, P2225, DOI 10.1126/science.1069424; Haussler MR, 1998, J BONE MINER RES, V13, P325, DOI 10.1359/jbmr.1998.13.3.325; HAUSSLER MR, 1997, J ENDOCRINOL, V154, P57; Hizawa N, 2002, AM J RESP CRIT CARE, V166, P686, DOI 10.1164/rccm.2002020090OC; Holick MF, 2003, J CELL BIOCHEM, V88, P296, DOI 10.1002/jcb.10338; Horvath S, 2004, GENET EPIDEMIOL, V26, P61, DOI 10.1002/gepi.10295; Hudson TJ, 2003, NAT GENET, V33, P439, DOI 10.1038/ng0403-439; Ioannidis JPA, 2003, TRENDS MOL MED, V9, P135, DOI 10.1016/S1471-4914(03)00030-3; Kraichely Dennis M., 1998, Frontiers in Bioscience, V3, pD821; Laird NM, 2000, GENET EPIDEMIOL, V19, P36; Laitinen T, 2004, SCIENCE, V304, P300, DOI 10.1126/science.1090010; Lake SL, 2000, AM J HUM GENET, V67, P1515, DOI 10.1086/316895; LEMIRE JM, 1995, J NUTR, V125, pS1704; LEMIRE JM, 1995, J STEROID BIOCHEM, V53, P599, DOI 10.1016/0960-0760(95)00106-A; LEWONTIN RC, 1988, GENETICS, V120, P849; Liu Wei, 2003, Zhonghua Liu Xing Bing Xue Za Zhi, V24, P389; Lohmueller KE, 2003, NAT GENET, V33, P177, DOI 10.1038/ng1071; Lorentzon M, 2000, J CLIN ENDOCR METAB, V85, P1666, DOI 10.1210/jc.85.4.1666; McDermott MF, 1997, DIABETOLOGIA, V40, P971, DOI 10.1007/s001250050776; MORRISON NA, 1994, NATURE, V367, P284, DOI 10.1038/367284a0; MORRISON NA, 1992, P NATL ACAD SCI USA, V89, P6665, DOI 10.1073/pnas.89.15.6665; Motohashi Y, 2003, J CLIN ENDOCR METAB, V88, P3137, DOI 10.1210/jc.2002-021881; Noguchi E, 2002, AM J RESP CRIT CARE, V166, P43, DOI 10.1164/rccm.2110052; Ofori H, 2004, SCAND J INFECT DIS, V36, P46, DOI 10.1080/00365540310017087; Pani MA, 2000, DIABETES, V49, P504, DOI 10.2337/diabetes.49.3.504; POON A, 2003, AM J HUM GENET, V73, pS385; RABY BA, IN PRESS AM J RESP C; Roy S, 1999, J INFECT DIS, V179, P187, DOI 10.1086/314536; Sainz J, 1997, NEW ENGL J MED, V337, P77, DOI 10.1056/NEJM199707103370202; Selvaraj P, 2000, INDIAN J MED RES, V111, P172; Simmons JD, 2000, GUT, V47, P211, DOI 10.1136/gut.47.2.211; Szefler S, 2000, NEW ENGL J MED, V343, P1054; Taylor JA, 1996, CANCER RES, V56, P4108; Van Eerdewegh P, 2002, NATURE, V418, P426, DOI 10.1038/nature00878; Verbeek W, 1997, BIOCHEM BIOPH RES CO, V238, P77, DOI 10.1006/bbrc.1997.7239; Wilkinson RJ, 2000, LANCET, V355, P618, DOI 10.1016/S0140-6736(99)02301-6; Wong HL, 2003, CARCINOGENESIS, V24, P1091, DOI 10.1093/carcin/bgg059; [Anonymous], 1987, AM REV RESP DIS, V136, P225	57	143	151	11	28	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	NOV 1	2004	170	9					967	973		10.1164/rccm.200403-412oc		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	865YJ	WOS:000224739800010	15282199	
J	Aaron, SD; Fergusson, D; Dent, R; Chen, Y; Vandemheen, KL; Dales, RE				Aaron, SD; Fergusson, D; Dent, R; Chen, Y; Vandemheen, KL; Dales, RE			Effect of weight reduction on respiratory function and airway reactivity in obese women	CHEST			English	Article						asthma; obesity; pulmonary function	ASTHMA; HEALTH	Background: Population-based studies have documented an association between obesity and an increased prevalence of asthma in women. Methods: We prospectively studied 58 obese women with a body mass index of > 30 kg/m(2), 24 of whom had asthma, who were enrolled in an intensive 6-month weight loss program to determine whether loss of body mass would be correlated with improvements in bronchial reactivity, lung function, and disease-specific health status. Results: Patients lost air average of 20 kg over the 6-month period. For every 10% relative loss of weight, the FVC improved by 92 mL (p = 0.05) and the FEV1 improved by 73 mL (p = 0.04), however, bronchial reactivity did not significantly change with weight loss (p = 0.23). Patients who lost > 13% of their pretreatment weight experienced improvements in FEV1 (p = 0.01), FVC (p = 0.02), and total lung capacity (p = 0.05) compared to patients in the lowest quartile who failed to lose significant amounts of weight. Neither group experienced any significant change in methacholine responsiveness (p = 0.57). Patients who completed the 6-month weight loss program experienced improvements in respiratory health status, irrespective of weight loss. Conclusion: We concluded that weight loss can improve lung function in obese women, however, the improvements appear to be independent of changes in airway reactivity.	Univ Ottawa, Dept Med, Ottawa, ON, Canada; Univ Ottawa, Ottawa Hlth Res Inst, Ottawa, ON, Canada; Univ Ottawa, Dept Epidemiol & Community Med, Ottawa, ON, Canada	Aaron, SD (reprint author), Ottawa Gen Hosp, Div Resp Med, Gen Campus,Room 1812F,501 Smyth Rd, Ottawa, ON K1H 8L6, Canada.	saaron@ottawahospital.on.ca		Aaron, Shawn/0000-0002-4762-3542			BARR RG, 2001, CHEST, V120, P1434; Beckett WS, 2001, AM J RESP CRIT CARE, V164, P2045; BOUSHEY HA, 1980, AM REV RESPIR DIS, V121, P389; Chen Y, 1999, AM J EPIDEMIOL, V150, P255; Chen Y, 2001, RESP MED, V95, P13, DOI 10.1053/rmed.2000.0961; COCKCROFT DW, 1977, CLIN ALLERGY, V7, P235, DOI 10.1111/j.1365-2222.1977.tb01448.x; Crapo RO, 2000, AM J RESP CRIT CARE, V161, P309; Dent RM, 2002, OBES RES, V10, P651, DOI 10.1038/oby.2002.88; JONES PW, 1992, AM REV RESPIR DIS, V145, P1321; Jones PW, 1997, AM J RESP CRIT CARE, V155, P1283; Lau DCW, 1999, CAN MED ASSOC J, V160, P503; NAIMARK A, 1960, J APPL PHYSIOL, V15, P377; Schachter LM, 2001, THORAX, V56, P4, DOI 10.1136/thorax.56.1.4; Shaheen SO, 1999, THORAX, V54, P396; SHARP JT, 1980, CLIN CHEST MED, V1, P103; SHARP JT, 1964, J CLIN INVEST, V43, P728, DOI 10.1172/JCI104957; Stenius-Aarniala B, 2000, BRIT MED J, V320, P827, DOI 10.1136/bmj.320.7238.827	17	143	153	1	7	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	JUN	2004	125	6					2046	2052		10.1378/chest.125.6.2046		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	832FQ	WOS:000222253100017	15189920	
J	Dahlen, I; Janson, C				Dahlen, I; Janson, C			Anxiety and depression are related to the outcome of emergency treatment in patients with obstructive pulmonary disease	CHEST			English	Article						anxiety; asthma; COPD; depression; emergency treatment; relapse	AIR-FLOW OBSTRUCTION; NEAR-FATAL ASTHMA; HOSPITAL ANXIETY; RISK-FACTORS; LUNG-DISEASE; SCALE; MORBIDITY; SYMPTOMS; LIFE; BREATHLESSNESS	Study objectives: To investigate whether psychological factors predict outcome after emergency treatment for obstructive pulmonary disease. Setting: Emergency department at a university hospital. Patients: Forty-three patients presenting with exacerbation of asthma or COPD. Intervention: The patients received emergency treatment and were followed up for 4 weeks. Measurement: Spirometry, blood sampling, pulse oximetry, breathing rate, pulse rate, and dyspnea score was measured before and during emergency treatment. The psychological status was assessed using the hospital anxiety and depression (HAD) scale questionnaire at the end of the follow-up period. Results: Anxiety and/or depression was found in 17 patients (40%). Of these patients, nine patients (53%) were admitted to hospital or had a relapse within 1 month, compared with five patients (19%) in the group without anxiety and/or depression (p < 0.05). Among patients who relapsed within 1 month (n = 14), the HAD total score was 12.4 +/- 5.9 compared with 8.6 +/- 5.1 (mean +/- SD) among the patients without a relapse (p < 0.05). After making adjustments for age, gender, atopic status, treatment, and pack-years, the significant association between treatment failure and anxiety and/or depression still remained. Conclusion: Our study indicates that anxiety and depression are related to the outcome of emergency treatment in patients with obstructive pulmonary disease. Further studies should be conducted evaluating the effect of treatment of anxiety and depression in patients with recurrent exacerbations of asthma and COPD.	Univ Uppsala Hosp, Dept Med Sci Resp Med & Allergol, SE-75185 Uppsala, Sweden	Dahlen, I (reprint author), Univ Uppsala Hosp, Dept Lung Med & Allergol, SE-75185 Uppsala, Sweden.						BENJAMIN S, 1977, J PSYCHOSOM RES, V21, P463, DOI 10.1016/0022-3999(77)90069-1; BURDON JGW, 1982, AM REV RESPIR DIS, V126, P825; CAMPBELL DA, 1995, THORAX, V50, P254, DOI 10.1136/thx.50.3.254; Centanni S, 2000, RESP MED, V94, P742, DOI 10.1053/rmed.1999.0766; Chetta A, 1998, AM J RESP CRIT CARE, V157, P116; Dahlen I, 1999, RESP MED, V93, P744, DOI 10.1016/S0954-6111(99)90043-4; DALES RE, 1995, THORAX, V50, P520, DOI 10.1136/thx.50.5.520; DEAL EC, 1979, J APPL PHYSIOL, V46, P476; EMERMAN CL, 1995, ANN EMERG MED, V26, P6, DOI 10.1016/S0196-0644(95)70230-X; *EUR COMM COAL STE, 1983, CLIN RESPIR PHYSL, V19, pS22; GUYATT GH, 1987, BRIT J DIS CHEST, V81, P45, DOI 10.1016/0007-0971(87)90107-0; Harrison BDW, 1998, THORAX, V53, P519; Innes NJ, 1998, J ROY COLL PHYS LOND, V32, P430; ISOAHO R, 1995, PSYCHOL REP, V76, P287; JANSON C, 1994, AM J RESP CRIT CARE, V149, P930; Joseph KS, 1996, BMJ-BRIT MED J, V312, P79; KELLNER R, 1987, J PSYCHOSOM RES, V31, P575, DOI 10.1016/0022-3999(87)90036-5; LEWIN B, 1992, LANCET, V339, P1036, DOI 10.1016/0140-6736(92)90547-G; Lisspers J, 1997, ACTA PSYCHIAT SCAND, V96, P281, DOI 10.1111/j.1600-0447.1997.tb10164.x; MAHLER DA, 1987, AM REV RESPIR DIS, V135, P1229; MASUDA M, 1966, J PSYCHOSOM RES, V10, P255, DOI 10.1016/0022-3999(66)90092-4; Miles JF, 1997, CLIN EXP ALLERGY, V27, P1151; MOOREY S, 1991, BRIT J PSYCHIAT, V158, P255, DOI 10.1192/bjp.158.2.255; MURATA GH, 1989, ANN EMERG MED, V18, P501, DOI 10.1016/S0196-0644(89)80833-9; PEACH H, 1981, THORAX, V36, P585, DOI 10.1136/thx.36.8.585; PICADO C, 1989, J ASTHMA, V26, P231, DOI 10.3109/02770908909073254; RYAN G, 1991, AUST NZ J MED, V21, P681, DOI 10.1111/j.1445-5994.1991.tb01370.x; Schmaling KB, 1998, J ASTHMA, V35, P631, DOI 10.3109/02770909809048965; SILVERMAN M, 1988, AM REV RESPIR DIS, V137, P206; STEHR DE, 1991, ANN EMERG MED, V20, P1113, DOI 10.1016/S0196-0644(05)81386-1; TAL A, 1976, PSYCHOSOM MED, V38, P190; WAREHAM NJ, 1993, THORAX, V48, P1117, DOI 10.1136/thx.48.11.1117; WILKINSON MJB, 1988, J ROY COLL GEN PRACT, V38, P311; WOLKOVE N, 1989, CHEST, V96, P1247, DOI 10.1378/chest.96.6.1247; YAMAMOTO H, 1987, RESPIRATION, V52, P42; YELLOWLEES PM, 1987, MED J AUSTRALIA, V146, P305; YELLOWLEES PM, 1989, CHEST, V95, P1298, DOI 10.1378/chest.95.6.1298; Yohannes AM, 2000, INT J GERIATR PSYCH, V15, P1090, DOI 10.1002/1099-1166(200012)15:12<1090::AID-GPS249>3.0.CO;2-L; ZIGMOND AS, 1983, ACTA PSYCHIAT SCAND, V67, P361, DOI 10.1111/j.1600-0447.1983.tb09716.x	39	143	153	0	6	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	NOV	2002	122	5					1633	1637		10.1378/chest.122.5.1633		5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	617TH	WOS:000179376600026	12426264	
J	Lordan, JL; Bucchieri, F; Richter, A; Konstantinidis, A; Holloway, JW; Thornber, M; Puddicombe, SM; Buchanan, D; Wilson, SJ; Djukanovic, R; Holgate, ST; Davies, DE				Lordan, JL; Bucchieri, F; Richter, A; Konstantinidis, A; Holloway, JW; Thornber, M; Puddicombe, SM; Buchanan, D; Wilson, SJ; Djukanovic, R; Holgate, ST; Davies, DE			Cooperative effects of Th2 cytokines and allergen on normal and asthmatic bronchial epithelial cells	JOURNAL OF IMMUNOLOGY			English	Article							DIESEL EXHAUST PARTICLES; IN-VITRO; INFLAMMATORY CYTOKINE; NONASTHMATIC SUBJECTS; GENETIC-VARIANTS; ILE50VAL VARIANT; IL-4 RECEPTOR; SOCS PROTEINS; IGE SYNTHESIS; EXPRESSION	In sensitized individuals, exposure to allergens such as Dermatophagoides pteronyssinus (Der p) causes Th2 polarization and release of cytokines, including IL-4 and IL-13. Because Der p extracts also have direct effects on epithelial cells, we hypothesized that allergen augments the effects of Th2 cytokines by promoting mediator release from the bronchial epithelium in allergic asthma. To test our hypothesis, primary bronchial epithelial cultures were grown from bronchial brushings of normal and atopic asthmatic subjects. RT-PCR showed that each culture expressed IL-4Ralpha, common gamma-chain, and IL-13Ralpha(1), as well as IL-13Ralpha(2), which negatively regulates IL-13 signaling; FACS analysis confirmed IL-13Ralpha(2) protein expression. Exposure of epithelial cultures to either Der p extracts, TNF-alpha, IL-4, or IL-13 enhanced GM-CSF and IL-8 release, and this was partially suppressible by corticosteroids. Simultaneous exposure of the epithelial cultures to IL-4 or IL-13 together with Der p resulted in a further increase in cytokine release, which was at least additive. Release of TGF-alpha was also increased by TNF-a and combinations of IL-4, IL-13, and Der p; however, this stimulation was only significant in the asthma-derived cultures. These data suggest that, in an allergic environment, Th2 cytokines and allergen have the potential to sustain airway inflammation through a cooperative effect on cytokine release by the bronchial epithelium. Our novel finding that IL-4, IL-13, and allergen enhance release of TGF-a, a ligand for the epidermal growth factor receptor that stimulates fibroblast proliferation and goblet cell differentiation, provides a potential link between allergen exposure, Th2 cytokines, and airway remodelling in asthma.	Southampton Gen Hosp, Resp Cell & Mol Biol Div 810, Sch Med, Southampton SO16 6YD, Hants, England	Davies, DE (reprint author), Southampton Gen Hosp, Resp Cell & Mol Biol Div 810, Sch Med, Southampton SO16 6YD, Hants, England.		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Immunol.	JUL 1	2002	169	1					407	414				8	Immunology	Immunology	565GA	WOS:000176360400052	12077271	
J	Strickland, I; Kisich, K; Hauk, PJ; Vottero, A; Chrousos, GP; Klemm, DJ; Leung, DYM				Strickland, I; Kisich, K; Hauk, PJ; Vottero, A; Chrousos, GP; Klemm, DJ; Leung, DYM			High constitutive glucocorticoid receptor beta in human neutrophils enables them to reduce their spontaneous rate of cell death in response to corticosteroids	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article						neutrophils; glucocorticoid insensitivity; glucocorticoid receptor; interleukin 8; inflammation	STREPTOLYSIN-O; APOPTOSIS; ISOFORM; EXPRESSION; BINDING; DEXAMETHASONE; INFLAMMATION; SPECIFICITY; ASTHMA	Neutrophils are markedly less sensitive to glucocorticoids than T cells, making it difficult to control inflammation in neutrophil-mediated diseases. Development of new antiinflammatory strategies for such diseases would be aided by an understanding of mechanisms underlying differential steroid responsiveness. Two protein isoforms of the human glucocorticoid receptor (GR) exist, GR alpha and GR beta, which arise from alternative splicing of the GR pre-mRNA primary transcripts. GR beta does not bind glucocorticoids and is an inhibitor of GR alpha activity. Relative amounts of these two GRs can therefore determine the level of glucocorticoid sensitivity. In this study, human neutrophils and peripheral blood mononuclear cells (PBMCs) were studied to determine the relative amounts of each GR isoform. The mean fluorescence intensity (MFI) using immunofluorescence analysis for GR alpha was 475 +/- 62 and 985 +/- 107 for PBMCs and neutrophils, respectively. For GR beta, the MFI was 350 +/- 60 and 1,389 +/- 143 for PBMCs and neutrophils, respectively (P < 0.05). After interleukin (IL)-8 stimulation of neutrophils, there was a statistically significant increase in intensity of GR<beta> staining to 2,497 +/- 140 (P < 0.05). No change in GR<alpha> expression was observed. This inversion of the GR alpha /GR beta ratio in human neutrophils compared with PBMCs was confirmed by quantitative Western analysis. Increased GR beta mRNA expression in neutrophils at baseline, and after IL-8 exposure, was observed using RNA dot blot analysis. Increased levels of GR alpha /GR beta heterodimers were found in neutrophils as compared with PBMCs using coimmunoprecipitation/Western analysis. Transfection of mouse neutrophils, which do not contain GR beta, resulted in a significant reduction in the rate of cell death when treated with dexamethasone. We conclude that high constitutive expression of GR beta by human neutrophils may provide a mechanism by which these cells escape glucocorticoid-induced cell death. Moreover, upregulation of this GR by proinflammatory cytokines such as IL-8 further enhances their survival in the presence of glucocorticoids during inflammation.	Natl Jewish Med Res Ctr, Dept Pediat, Denver, CO 80206 USA; Natl Jewish Med Res Ctr, Dept Med, Denver, CO 80206 USA; Univ Colorado, Hlth Sci Ctr, Dept Pediat, Denver, CO 80262 USA; NICHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA	Leung, DYM (reprint author), Natl Jewish Med Res Ctr, Dept Pediat, 1400 Jackson St, Denver, CO 80206 USA.				NCRR NIH HHS [M01 RR000051, MO1 RR00051]; NHLBI NIH HHS [HL34303, HL36577, HL37260, P01 HL034303, P01 HL036577, R37 HL037260]; NIAMS NIH HHS [AR41256, R01 AR041256]		BAMBERGER CM, 1995, J CLIN INVEST, V95, P2435, DOI 10.1172/JCI117943; BLOOM JW, 1999, IMMUNOLOGY ALLERGY C, P653; Brogan IJ, 1999, MOL CELL ENDOCRINOL, V157, P95, DOI 10.1016/S0303-7207(99)00156-2; Broughton CM, 1997, LEUKEMIA, V11, P1435, DOI 10.1038/sj.leu.2400774; CHU P, 1994, ARCH DERMATOL, V130, P1278, DOI 10.1001/archderm.130.10.1278; COBLE BI, 1988, INT ARCH ALLER A IMM, V55, P398; Cox G, 1997, J LEUKOCYTE BIOL, V61, P224; deCastro M, 1996, MOL MED, V2, P597; deLange P, 1997, MOL ENDOCRINOL, V11, P1156, DOI 10.1210/me.11.8.1156; Di Baldassarre A, 2000, CELL MOL BIOL, V46, P153; ENCIO IJ, 1991, J BIOL CHEM, V266, P7182; GIGUERE V, 1986, CELL, V46, P645, DOI 10.1016/0092-8674(86)90339-9; Hecht K, 1997, J BIOL CHEM, V272, P26659, DOI 10.1074/jbc.272.42.26659; Jatakanon A, 1999, AM J RESP CRIT CARE, V160, P1532; Kato T, 1995, NAT IMMUN, V14, P198; Leung DYM, 1997, J EXP MED, V186, P1567, DOI 10.1084/jem.186.9.1567; Liles WC, 1996, J EXP MED, V184, P429, DOI 10.1084/jem.184.2.429; MEIER F, 1989, Skin Pharmacology, V2, P61; Modarress KJ, 1997, J BIOL CHEM, V272, P23986, DOI 10.1074/jbc.272.38.23986; Negoescu A, 1998, BIOMED PHARMACOTHER, V52, P252, DOI 10.1016/S0753-3322(98)80010-3; Oakley RH, 1996, J BIOL CHEM, V271, P9550; Oakley RH, 1999, J BIOL CHEM, V274, P27857, DOI 10.1074/jbc.274.39.27857; Otto C, 1997, J BIOL CHEM, V272, P26665, DOI 10.1074/jbc.272.42.26665; Reichardt HM, 1998, CELL, V93, P531, DOI 10.1016/S0092-8674(00)81183-6; Sala A, 1999, J BIOL CHEM, V274, P28264, DOI 10.1074/jbc.274.40.28264; Schleimer RP, 1990, AM REV RESPIR DIS S, V141, pS59; SPILLER DG, 1995, ANTISENSE RES DEV, V5, P13; Starkebaum G, 1997, Curr Opin Hematol, V4, P196; Wenzel SE, 1997, AM J RESP CRIT CARE, V156, P737	29	143	149	2	2	ROCKEFELLER UNIV PRESS	NEW YORK	1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA	0022-1007			J EXP MED	J. Exp. Med.	MAR 5	2001	193	5					585	593		10.1084/jem.193.5.585		9	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	411WN	WOS:000167522500005	11238589	
J	Fagan, KA; McMurtry, IF; Rodman, DM				Fagan, KA; McMurtry, IF; Rodman, DM			Role of endothelin-1 in lung disease	RESPIRATORY RESEARCH			English	Review						asthma; endothelin; fibrosis; inflammation; pulmonary hypertension	BRONCHOALVEOLAR LAVAGE FLUID; OBSTRUCTIVE PULMONARY-DISEASE; RESPIRATORY-DISTRESS-SYNDROME; BRONCHIAL EPITHELIAL-CELLS; PERFUSED RAT LUNGS; COLLAGEN GEL CONTRACTION; GUINEA-PIG PULMONARY; AIR-FLOW OBSTRUCTION; SMOOTH-MUSCLE CELLS; PLASMA ENDOTHELIN-1	Endothelin-1 (ET-1) is a 21 amino acid peptide with diverse biological activity that has been implicated in numerous diseases. ET-1 is a potent mitogen regulator of smooth muscle tone, and inflammatory mediator that may play a key role in diseases of the airways, pulmonary circulation, and inflammatory lung diseases, both acute and chronic. This review will focus on the biology of ET-1 and its role in lung disease.	Univ Colorado, Hlth Sci Ctr, Div Pulm Sci & Crit Care Med, Cardiovasc Pulm Res Lab, Denver, CO 80262 USA	Fagan, KA (reprint author), Univ Colorado, Hlth Sci Ctr, Div Pulm Sci & Crit Care Med, Cardiovasc Pulm Res Lab, 4200 E 9th Ave,B-133, Denver, CO 80262 USA.	karen.fagan@uchsc.edu					Aarnio P, 1996, SCAND J THORAC CARD, V30, P113, DOI 10.3109/14017439609107255; ABRAHAM DJ, 1997, AM J PATHOL, V151, P81; ACKERMAN V, 1995, J ALLERGY CLIN IMMUN, V96, P618, DOI 10.1016/S0091-6749(95)70260-1; Aguirre JI, 2000, AM J PHYSIOL-LUNG C, V278, pL981; Ahmed SI, 2000, AM J RESP CELL MOL, V22, P422; Alanen K, 2000, HISTOPATHOLOGY, V36, P161; ALBERTINE KH, 1999, CHEST, V116, P1015; Ali H, 2000, GUT, V47, P685, DOI 10.1136/gut.47.5.685; ALLISON RC, 1990, J APPL PHYSIOL, V69, P597; AOKI T, 1994, ANN ALLERGY, V73, P365; ARAI H, 1990, NATURE, V348, P730, DOI 10.1038/348730a0; ARINAMI T, 1991, AM J HUM GENET, V48, P990; ASAKURA H, 1992, AM J HEMATOL, V41, P71, DOI 10.1002/ajh.2830410202; Aversa CR, 1997, AM J PHYSIOL-LUNG C, V273, pL848; 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Res.		2001	2	2					90	101		10.1186/rr44		12	Respiratory System	Respiratory System	443UZ	WOS:000169361200007	11686871	
J	Chapman, MD; Pomes, A; Breiteneder, H; Ferreira, F				Chapman, Martin D.; Pomes, Anna; Breiteneder, Heimo; Ferreira, Fatima			Nomenclature and structural biology of allergens	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergen; nomenclature; IgE; asthma; protein families; allergic disease; protein structure; biologic function	BIRCH POLLEN ALLERGEN; DUST-MITE ALLERGENS; SEED STORAGE PROTEINS; PLANT FOOD ALLERGENS; CRYSTAL-STRUCTURE; CROSS-REACTIVITY; CAT ALLERGEN; BINDING; COCKROACH; IMMUNOTHERAPY	Purified allergens are named using the systematic nomenclature of the Allergen Nomenclature Sub-Committee of the World Health Organization and International Union of Immunological Societies. The system uses abbreviated Linnean genus and species names and an Arabic number to indicate the chronology of allergen purification. Most major allergens from mites, animal dander, pollens, insects, and foods have been cloned, and more than 40 three-dimensional allergen structures are in the Protein Database. Allergens are derived from proteins with a variety of biologic functions, including proteases, ligand-binding proteins, structural proteins, pathogenesis-related proteins, lipid transfer proteins, profilins, and calcium-binding proteins. Biologic function, such as the proteolytic enzyme allergens of dust mites, might directly influence the development of IgE responses and might initiate inflammatory responses in the lung that are associated with asthma. Intrinsic structural or biologic properties might also influence the extent to which allergens persist in indoor and outdoor environments or retain their allergenicity in the digestive tract. Analyses of the protein family database suggest that the universe of allergens comprises more than 120 distinct protein families. Structural biology and proteomics define recombinant allergen targets for diagnostic and therapeutic purposes and identify motifs, patterns, and structures of immunologic significance.	INDOOR Biotechnol Inc, Charlottesville, VA 22903 USA; Med Univ Vienna, Vienna, Austria; Salzburg Univ, Christian Doppler Lab Allergy Diag & Therapy, A-5020 Salzburg, Austria	Chapman, MD (reprint author), INDOOR Biotechnol Inc, 1216 Harris St, Charlottesville, VA 22903 USA.	mdc@inbio.com	Ferreira, Fatima/E-4889-2011	Ferreira, Fatima/0000-0003-0989-2335; Pomes, Anna/0000-0002-8729-1829			Agea E, 2005, J EXP MED, V202, P295, DOI 10.1084/jem.20050773; Arruda LK, 2001, J ALLERGY CLIN IMMUN, V107, P419, DOI 10.1067/mai.2001.112854; Asokananthan N, 2002, J IMMUNOL, V169, P4572; BOCSKEI Z, 1992, NATURE, V360, P186, DOI 10.1038/360186a0; Breiteneder H, 2004, J ALLERGY CLIN IMMUN, V113, P821, DOI 10.1016/j.jaci.2004.01.079; BREITENEDER H, 2006, DETECTING ALLERGENS, P37; Chapman MD, 2000, J ALLERGY CLIN IMMUN, V106, P409; CHAPMAN MD, 2003, ALLERGENS ALLERGEN I, P51; Cosgrove DJ, 2000, NATURE, V407, P321, DOI 10.1038/35030000; Creticos PS, 2006, NEW ENGL J MED, V355, P1445, DOI 10.1056/NEJMoa052916; Czerwinski EW, 2005, J BIOL CHEM, V280, P3740, DOI 10.1074/jbc.M409655200; de Halleux S, 2006, J ALLERGY CLIN IMMUN, V117, P571, DOI 10.1016/j.jaci.2005.11.032; Dunwell JM, 2000, MICROBIOL MOL BIOL R, V64, P153, DOI 10.1128/MMBR.64.1.153-179.2000; Fan Y, 2005, INSECT MOL BIOL, V14, P45, DOI 10.1111/j.1365-2583.2004.00530.x; Ferreira F, 2004, ALLERGY, V59, P243, DOI 10.1046/j.1398-9995.2003.00407.x; Ferreira F, 2004, ADV IMMUNOL, V84, P79, DOI 10.1016/S0065-2776(04)84003-3; Ferreira F, 1996, J EXP MED, V183, P599, DOI 10.1084/jem.183.2.599; Gadermaier G, 2004, CURR ALLERGY ASTHM R, V4, P391, DOI 10.1007/s11882-004-0090-5; Gruber A, 2004, J BIOL CHEM, V279, P28475, DOI 10.1074/jbc.M400993200; Gustchina A, 2005, J MOL BIOL, V348, P433, DOI 10.1016/j.jmb.2005.02.062; Ivanciuc O, 2003, NUCLEIC ACIDS RES, V31, P359, DOI 10.1093/nar/gkg010; Jenkins JA, 2005, J ALLERGY CLIN IMMUN, V115, P163, DOI 10.1016/j.jaci.2004.10.026; Jutel M, 2005, J ALLERGY CLIN IMMUN, V116, P608, DOI 10.1016/j.jaci.2005.06.004; Kaiser L, 2003, J BIOL CHEM, V278, P37730, DOI 10.1074/jbc.M304740200; KING TP, 1994, INT ARCH ALLERGY IMM, V105, P224; KING TP, 1994, B WORLD HEALTH ORGAN, V72, P797; KING TP, 1995, ALLERGY, V50, P765, DOI 10.1111/j.1398-9995.1995.tb01222.x; KREIS M, 1985, J MOL BIOL, V183, P499, DOI 10.1016/0022-2836(85)90017-8; Markovic-Housley Z, 2003, J MOL BIOL, V325, P123, DOI 10.1016/S0022-2836(02)01197-X; MARSH DG, 1986, B WORLD HEALTH ORGAN, V64, P767; Marsh D, 1975, ANTIGENS, V3, P271; Meno K, 2005, J IMMUNOL, V175, P3835; Piboonpocanun S, 2006, CLIN EXP ALLERGY, V36, P510, DOI 10.1111/j.1365-2222.2006.02464.x; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; Radauer C, 2006, J ALLERGY CLIN IMMUN, V117, P141, DOI 10.1016/j.jaci.2005.09.010; Schenk MF, 2006, BMC GENOMICS, V7, DOI 10.1186/1471-2164-7-168; Sharma S, 2003, CLIN EXP ALLERGY, V33, P163, DOI 10.1046/j.1365-2222.2003.01605.x; Smith AM, 2001, J ALLERGY CLIN IMMUN, V107, P977, DOI 10.1067/mai.2001.115629; Smith WA, 2001, J ALLERGY CLIN IMMUN, V107, P985, DOI 10.1067/mai.2001.114652; Tinghino R, 2002, J ALLERGY CLIN IMMUN, V109, P314, DOI 10.1067/mai.2002.121528; Valenta R, 1998, INT ARCH ALLERGY IMM, V117, P160, DOI 10.1159/000024005; Vieths S, 2002, ANN NY ACAD SCI, V964, P47; Wopfner N, 2005, INT ARCH ALLERGY IMM, V138, P337, DOI 10.1159/000089188; Wunschmann S, 2005, J ALLERGY CLIN IMMUN, V116, P140, DOI 10.1016/j.jaci.2005.04.024	44	142	150	0	19	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	FEB	2007	119	2					414	420		10.1016/j.jaci.2006.11.001		7	Allergy; Immunology	Allergy; Immunology	137YB	WOS:000244327900020	17166572	
J	Jackson, LE				Jackson, LE			The relationship of urban design to human health and condition	LANDSCAPE AND URBAN PLANNING			English	Article						ecological design; public health; social capital	LYME-DISEASE; RISK; ENVIRONMENT; COMMUNITY; PEOPLE; HOME	The population of the United States of America is currently experiencing increased illness from dispersed and synergistic causes. Many of the acute insults of the past have receded due to centralized health care and regulatory action. However, chronic ailments including asthma and allergies, animal-transmitted diseases, obesity, diabetes, heart disease, and depression are on the rise. These diverse illnesses join with forest fragmentation, stream degradation, wetlands destruction, and the concomitant loss of native species to suggest detrimental contributions from the built environment. This paper surveys the state of the science on the impacts of urban design on human health and well-being. Drawing primarily on recent peer-reviewed literature in a broad array of health, planning, and environmental fields, it outlines the influence of design at three spatial scales on aspects of physical and mental health, and social and cultural vibrancy. Selected ecological effects are also discussed to illustrate shared associations with urbanization. While causal chains are generally complex and not always completely understood, sufficient evidence exists to reveal urban design as a powerful tool for improving human condition. Solutions are discussed at the personal and professional level, emphasizing cross-disciplinary collaboration in urban planning and design, and the participation of residents in shaping their living environment. At the parcel scale, greenery and access to it visually and physically are the principal keys to health. These elements must be incorporated into relatively high-density neighborhood designs that include public buildings, open space, mixed land use, and pedestrian walkways to increase physical exercise and enhance civic life. Finally, neighborhoods must be embedded in existing urban infrastructure to provide larger cultural and business opportunities and reduce reliance on the automobile. Further research is recommended to strengthen the associations between design and health. Increased communication on this subject is also necessary between design and health practitioners and their clients and colleagues. (C) 2002 Elsevier Science B.V. All rights reserved.	US EPA, Natl Hlth & Environm Effects Res Lab, Off Res & Dev, Res Triangle Pk, NC 27711 USA	Jackson, LE (reprint author), US EPA, Natl Hlth & Environm Effects Res Lab, Off Res & Dev, Res Triangle Pk, NC 27711 USA.		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J	McKeever, TM; Lewis, SA; Smith, C; Hubbard, R				McKeever, TM; Lewis, SA; Smith, C; Hubbard, R			The importance of prenatal exposures on the development of allergic disease - A birth cohort study using the West Midlands General Practice Database	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; epidemiology; hay fever; eczema; perinatal exposures	CORD BLOOD; HAY-FEVER; ATOPIC DISORDERS; ASTHMATIC WOMEN; EARLY-CHILDHOOD; FAMILY-SIZE; NEW-ZEALAND; IN-UTERO; RISK; INFECTIONS	The etiology of allergic disease is not understood, but a decreased exposure to infection may play an important role. There are few published data on the impact of change in microbial exposure during pregnancy on the child's risk of developing allergic disease. Using a birth cohort of 24,690 children, derived from the West Midlands General Practice Research Database, we investigated a number of perinatal exposures on the incidence of asthma, eczema, and hay fever. Our findings suggest that exposure to antibiotics in utero is associated with an increased risk of asthma in a dose-related manner (more than two courses of antibiotics compared wit ne adjusted hazard ratio [HR] 1.68; 95% confidence interval [CI], 1.51-1.87), and similar associations are present for eczema (adjust HR 1.17; 95% CI, 1.06-1.29) and hay fever (adjusted HR 1.56; 95% CI, 1.22-2.01). Exposure to a range of infections in utero was also associated with a small increased risk of developing allergic disease. Strong protective effects of older siblings on the incidence of allergy are present within this cohort, but previous pregnancies that did not result in a live birth were not protective. Our findings suggest that exposure to antibiotics and to infections in utero is a potentially important risk factor in the development of allergic disease.	Univ Nottingham, Div Resp Med, Nottingham NG7 2RD, England	McKeever, TM (reprint author), City Hosp, Div Resp Med, Clin Sci Bldg,Hucknall Rd, Nottingham NG5 1PB, England.		Research Datalink, Clinical Practice/H-2477-2013; CPRD, CPRD/B-9594-2017	McKeever, Tricia/0000-0003-0914-0416			Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; Annesi-Maesano I, 2001, ALLERGY, V56, P491, DOI 10.1034/j.1398-9995.2001.056006491.x; Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; BELL IR, 1991, PSYCHOTHER PSYCHOSOM, V55, P24; Bodner C, 1998, THORAX, V53, P28; Demissie K, 1998, AM J RESP CRIT CARE, V158, P1091; Droste JHJ, 2000, CLIN EXP ALLERGY, V30, P1547; Gustafsson P A, 1997, Pediatr Pulmonol Suppl, V16, P262; *JOINT FORM COMM, 2001, BRIT NAT FORM; Karmaus W, 2001, AM J EPIDEMIOL, V154, P909, DOI 10.1093/aje/154.10.909; Klinnert MD, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.4.e69; Liu SL, 2001, AM J OBSTET GYNECOL, V184, P90, DOI 10.1067/mob.2001.108073; McKeever TM, 2002, J ALLERGY CLIN IMMUN, V109, P43, DOI 10.1067/mai.2002.121016; MCKEEVER TM, 2001, THORAX, V56, P458; MICHEL FB, 1980, J ALLERGY CLIN IMMUN, V65, P422, DOI 10.1016/0091-6749(80)90234-1; Mrazek DA, 1999, PEDIATR PULM, V27, P85, DOI 10.1002/(SICI)1099-0496(199902)27:2<85::AID-PPUL4>3.0.CO;2-B; Nafstad P, 2000, J ALLERGY CLIN IMMUN, V106, P867, DOI 10.1067/mai.2000.110558; NASR S, 1981, J AFFECT DISORDERS, V3, P291, DOI 10.1016/0165-0327(81)90030-6; OSSOFSKY HJ, 1976, COMPR PSYCHIAT, V17, P335, DOI 10.1016/0010-440X(76)90008-0; Pekkanen J, 1999, ACTA PAEDIATR, V88, P710; Rusconi F, 1999, AM J RESP CRIT CARE, V160, P1617; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Strachan DP, 1996, ARCH DIS CHILD, V74, P422; Strachan DP, 2000, THORAX S1, V55, pS2; SUGERMAN AA, 1982, ANN ALLERGY, V48, P166; Sunyer J, 2001, CLIN EXP ALLERGY, V31, P1352, DOI 10.1046/j.1365-2222.2001.01187.x; Timonen M, 2001, AM J MED GENET, V105, P216, DOI 10.1002/ajmg.1199; von Mutius E, 1999, EUR RESPIR J, V14, P4, DOI 10.1034/j.1399-3003.1999.14a03.x; Wamboldt MZ, 1996, J AM ACAD CHILD PSY, V35, P1042, DOI 10.1097/00004583-199608000-00015; Wamboldt MZ, 2000, AM J MED GENET, V96, P146, DOI 10.1002/(SICI)1096-8628(20000403)96:2<146::AID-AJMG4>3.0.CO;2-J; Wen SW, 2001, ANN EPIDEMIOL, V11, P7, DOI 10.1016/S1047-2797(00)00077-6; Wickens K, 1999, J ALLERGY CLIN IMMUN, V104, P554, DOI 10.1016/S0091-6749(99)70323-4; Wickens KL, 1999, EPIDEMIOLOGY, V10, P699, DOI 10.1097/00001648-199911000-00009; Wright RJ, 2002, AM J RESP CRIT CARE, V165, P358; Wright RJ, 1999, AM J RESP CRIT CARE, V159, pA103; Xu B, 1999, ALLERGY, V54, P829, DOI 10.1034/j.1398-9995.1999.00117.x; Xu BZ, 1999, INT J EPIDEMIOL, V28, P723, DOI 10.1093/ije/28.4.723	37	142	145	6	12	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	SEP 15	2002	166	6					827	832		10.1164/rccm.200202-158OC		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	594AU	WOS:000178027300011	12231492	
J	Pedotti, R; Mitchell, D; Wedemeyer, J; Karpuj, M; Chabas, D; Hattab, EM; Tsai, M; Galli, SJ; Steinman, L				Pedotti, R; Mitchell, D; Wedemeyer, J; Karpuj, M; Chabas, D; Hattab, EM; Tsai, M; Galli, SJ; Steinman, L			An unexpected version of horror autotoxicus: anaphylactic shock to a self peptide	NATURE IMMUNOLOGY			English	Article							MYELIN BASIC-PROTEIN; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MAST-CELL DEGRANULATION; CENTRAL-NERVOUS-SYSTEM; TUMOR-NECROSIS-FACTOR; FC-GAMMA-RIII; MULTIPLE-SCLEROSIS; T-CELLS; PROTEOLIPID PROTEIN	EAE can refer either to experimental autoimmune encephalomyelitis or experimental allergic encephalomyelitis. Although EAE is classically a prototypicT helper I (THI) cell-mediated autoimmune disease, it can also be induced by T(H)2 cells. Characteristically, the most severe manifestation of allergy, anaphylaxis, is associated with exposure to a foreign antigen that is often derived from medication, insect venom or food. We report here that, after self-tolerance to myelin is destroyed, anaphylaxis may be triggered by a self-antigen, in this case a myelin peptide. "Horror autotoxicus", which was initially described by Ehrlich, may not only include autoimmunity to self, it may also encompass immediate hypersensitivity to self, which leads to shock and rapid death.	Stanford Univ, Med Ctr, Dept Neurol & Neurol Sci, Stanford, CA 94305 USA; Stanford Univ, Med Ctr, Dept Pathol, Stanford, CA 94305 USA; Univ Milan, IRCCS Osped Maggiore Policlin, Inst Clin Neurol, Milan, Italy	Steinman, L (reprint author), Stanford Univ, Med Ctr, Dept Neurol & Neurol Sci, Stanford, CA 94305 USA.		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J	Bitton, A; Martin, C; Landon, BE				Bitton, Asaf; Martin, Carina; Landon, Bruce E.			A Nationwide Survey of Patient Centered Medical Home Demonstration Projects	JOURNAL OF GENERAL INTERNAL MEDICINE			English	Article						primary care; physician payment; health reform	CHRONIC CARE MODEL; COMMUNITY-HEALTH CENTERS; QUALITY IMPROVEMENT; INTERNAL-MEDICINE; OUTCOMES; DISEASE; ASTHMA	The patient centered medical home has received considerable attention as a potential way to improve primary care quality and limit cost growth. Little information exists that systematically compares PCMH pilot projects across the country. Cross-sectional key-informant interviews. Leaders from existing PCMH demonstration projects with external payment reform. We used a semi-structured interview tool with the following domains: project history, organization and participants, practice requirements and selection process, medical home recognition, payment structure, practice transformation, and evaluation design. A total of 26 demonstrations in 18 states were interviewed. Current demonstrations include over 14,000 physicians caring for nearly 5 million patients. A majority of demonstrations are single payer, and most utilize a three component payment model (traditional fee for service, per person per month fixed payments, and bonus performance payments). The median incremental revenue per physician per year was $22,834 (range $720 to $91,146). Two major practice transformation models were identified-consultative and implementation of the chronic care model. A majority of demonstrations did not have well-developed evaluation plans. Current PCMH demonstration projects with external payment reform include large numbers of patients and physicians as well as a wide spectrum of implementation models. Key questions exist around the adequacy of current payment mechanisms and evaluation plans as public and policy interest in the PCMH model grows.	[Bitton, Asaf; Martin, Carina; Landon, Bruce E.] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA; [Bitton, Asaf] Brigham & Womens Hosp, Div Gen Med, Boston, MA 02115 USA; [Landon, Bruce E.] Beth Israel Deaconess Med Ctr, Div Gen Med & Primary Care, Boston, MA 02215 USA	Landon, BE (reprint author), Harvard Univ, Sch Med, Dept Hlth Care Policy, 180 Longwood Ave, Boston, MA 02115 USA.	landon@hcp.med.harvard.edu			Agency for Health Care Research and Quality; Commonwealth Fund; The American Board of Internal Medicine Foundation; Health Resources and Services Administration of the Department of Health and Human Services [T32HP10251]	The authors would like to thank all of the survey respondents for their willingness to participate in the study. This study was funded in part by grants from the Agency for Health Care Research and Quality, the Commonwealth Fund, and The American Board of Internal Medicine Foundation. Dr. Bitton is supported by grant number T32HP10251 from the Health Resources and Services Administration of the Department of Health and Human Services to support the Harvard Medical School Fellowship in General Medicine and Primary Care. The study contents are solely the responsibility of the authors and do not necessarily represent the official views of the Department of Health and Human Services.	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Gen. Intern. Med.	JUN	2010	25	6					584	592		10.1007/s11606-010-1262-8		9	Health Care Sciences & Services; Medicine, General & Internal	Health Care Sciences & Services; General & Internal Medicine	596UY	WOS:000277712200020	20467907	
J	Rothenberg, ME				Rothenberg, Marc E.			Biology and Treatment of Eosinophilic Esophagitis	GASTROENTEROLOGY			English	Review							GASTROESOPHAGEAL-REFLUX DISEASE; ANTI-IL-5 MEPOLIZUMAB THERAPY; MAJOR BASIC-PROTEIN; CELIAC-DISEASE; FOOD ALLERGY; SKIN PRICK; CLINICAL-FEATURES; CATIONIC PROTEIN; PATCH TESTS; T-CELLS	Eosinophilic esophagitis is a recently recognized but expanding disorder characterized by antigen-driven eosinophil accumulation in the esophagus. Symptoms frequently mimic those of gastroesophageal reflux disease, but the diseases are distinct in their histopathology, gene expression signature, response to therapy, hereditary risk, and association with allergies. The pathogenesis of eosinophilic esophagitis involves environmental and genetic factors, particularly food antigens and expression level of the eosinophil chemoattractant eotaxin-3, respectively. Analyses of gene expression signatures and animal models have indicated the importance of adaptive T-cell immunity that involves interleukin-5 and interleukin-13-induced esophageal epithelial cell responses. Symptoms, dysregulation of esophageal gene expression, and pathology are largely reversible following reduced exposure to specific food antigens as well as anti-inflammatory therapy, but chronic treatment is necessary to prevent relapse. Therefore, eosinophilic esophagitis is a disease with unique features that include chronic esophagitis, atopy, immune sensitization to oral antigens, reversibility, and familial association.	Univ Cincinnati, Div Allergy & Immunol, Cincinnati Childrens Hosp, Dept Pediat,Med Ctr,Coll Med, Cincinnati, OH 45229 USA	Rothenberg, ME (reprint author), Univ Cincinnati, Div Allergy & Immunol, Cincinnati Childrens Hosp, Dept Pediat,Med Ctr,Coll Med, 3333 Burnet Ave, Cincinnati, OH 45229 USA.	rothenberg@cchmc.org			NIAID NIH HHS [U19 AI070235, R01 AI045898, R01 AI05780, R01 AI057803, R01 AI080581, R01 AI45898]; NIDDK NIH HHS [P30 DK078392, R01 DK067255, R01 DK076893]		Aceves SS, 2007, J ALLERGY CLIN IMMUN, V119, P206, DOI 10.1016/j.jaci.2006.10.016; Aceves SS, 2005, J ALLERGY CLIN IMMUN, V116, P705, DOI 10.1016/j.jaci.2005.05.011; Akei HS, 2005, GASTROENTEROLOGY, V129, P985, DOI 10.1053/j.gastro.2005.06.027; Almansa C, 2009, AM J GASTROENTEROL, V104, P828, DOI 10.1038/ajg.2008.169; Assa'ad A, 2005, ANN ALLERG ASTHMA IM, V95, P309; Assa'ad AH, 2007, J ALLERGY CLIN IMMUN, V119, P731, DOI 10.1016/j.jaci.2006.10.044; ATTWOOD SEA, 1993, DIGEST DIS SCI, V38, P109, DOI 10.1007/BF01296781; Attwood SEA, 2003, GUT, V52, P181, DOI 10.1136/gut.52.2.181; 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J	Zanation, AM; Carrau, RL; Snyderman, CH; Germanwala, AV; Gardner, PA; Prevedello, DM; Kassam, AB				Zanation, Adam M.; Carrau, Ricardo L.; Snyderman, Carl H.; Germanwala, Anand V.; Gardner, Paul A.; Prevedello, Daniel M.; Kassam, Amin B.			Nasoseptal flap reconstruction of high flow intraoperative cerebral spinal fluid leaks during endoscopic skull base surgery	AMERICAN JOURNAL OF RHINOLOGY & ALLERGY			English	Article						CSF leak; endoscopic; meningioma; nasoseptal flap; prognosis; reconstruction; sinonasal tumor; skull base; vascularized flap		Background: Over the past 10 years, significant anatomic, technical, and instrumentation advances have facilitated the exposure and resection of intradural lesions via a fully endoscopic expanded endonasal approach (EEA). The vascularized nasoseptal flap (based on the posterior nasoseptal artery) has become our primary endoscopic reconstructive technique. The goals of this study are to prospectively evaluate the nasoseptal flap and high-risk cerebral spinal fluid (CSF) leak variables. Methods: Prospective evaluation was performed of EEA patients with intraoperative high-flow leaks (either a cistern or ventricle open to nasal cavity during tumor dissection) who underwent nasoseptal flap reconstruction. Results: Seventy consecutive nasoseptal flaps for high-flow intraoperative leaks were evaluated prospectively by the primary author. Twelve risk factors were then graded at the time of the operations and correlated to CSF leak outcomes. The overall postoperative CSF leak rate was 5.7% (4/70). All four postoperative leaks were successfully managed with endoscopic repair and CSF diversion. A multivariate analysis of all 12 risk factors is detailed. Pediatric patients, large dural defects, and radiation therapy were noted to be factors in reconstructive failure. One flap death occurred in a patient with prior surgery and proton therapy, this leak was managed with a temporoparietal flap and endonasal repair. Conclusion: The nasoseptal flap is an excellent anterior skull base reconstructive technique. Patients with high-flow intraoperative CSF leaks had a 94% successful reconstruction rate. Patients with skull base proton radiation therapy are at higher risk for flap failure and preparation for nonradiated tissue reconstruction should be discussed with the patient. (Am J Rhinol Allergy 23, 518-521, 2009; doi: 10.2500/ajra.2009.23.3378)	[Zanation, Adam M.] Univ N Carolina, Dept Otolaryngol Head & Neck Surg, Chapel Hill, NC 27599 USA; [Germanwala, Anand V.] Univ N Carolina, Dept Neurol Surg, Chapel Hill, NC 27599 USA; [Carrau, Ricardo L.; Snyderman, Carl H.] Univ Pittsburgh, Med Ctr, Dept Otolaryngol Head & Neck Surg, Pittsburgh, PA USA; [Carrau, Ricardo L.; Snyderman, Carl H.; Gardner, Paul A.; Prevedello, Daniel M.; Kassam, Amin B.] Univ Pittsburgh, Med Ctr, Dept Neurol Surg, Pittsburgh, PA USA	Zanation, AM (reprint author), Univ N Carolina, Dept Otolaryngol Head & Neck Surg, CB 7070,Phys Off Bldg,Manning Dr, Chapel Hill, NC 27599 USA.	azanatio@med.unc.edu					Fortes FSG, 2007, LARYNGOSCOPE, V117, P1329, DOI 10.1097/mlg.0b013e318062111f; Fortes FSG, 2007, LARYNGOSCOPE, V117, P970, DOI 10.1097/MLG.0b013e3180471482; Hadad G, 2006, LARYNGOSCOPE, V116, P1882, DOI 10.1097/01.mlg.0000234933.37779.c4; Harvey RJ, 2008, AM J RHINOL, V22, P516, DOI 10.2500/ajr.2008.22.3223; Kassam Amin, 2005, Neurosurg Focus, V19, pE4; Kassam Amin, 2005, Neurosurg Focus, V19, pE3; Kassam AB, 2008, NEUROSURGERY, V63, P44, DOI 10.1227/01.NEU.0000297074.13423.F5; Nicolai P, 2008, AM J RHINOL, V22, P308, DOI 10.2500/ajr.2008.22.3170; Pinheiro-Neto CD, 2007, LARYNGOSCOPE, V117, P1560, DOI 10.1097/MLG.0b013e31806db514; Shah RN, 2009, LARYNGOSCOPE, V119, P1067, DOI 10.1002/lary.20216; Zanation AM, 2009, LARYNGOSCOPE, V119, P13, DOI 10.1002/lary.20022	11	141	149	0	3	OCEAN SIDE PUBLICATIONS INC	PROVIDENCE	95 PITMAN ST, PROVIDENCE, RI 02906 USA	1945-8924			AMJ RHINOL ALLERGY	Am. J. Rhinol. Allergy	SEP-OCT	2009	23	5					518	521		10.2500/ajra.2009.23.3378		4	Otorhinolaryngology	Otorhinolaryngology	503KS	WOS:000270533800013	19807986	
J	Simons, FER; Frew, AJ; Ansotegui, IJ; Bochner, BS; Golden, DBK; Finkelman, FD; Leung, DYM; Lotvall, J; Marone, G; Metcalfe, DD; Muller, U; Rosenwasser, LJ; Sampson, HA; Schwartz, LB; van Hage, M; Walls, AF				Simons, F. Estelle R.; Frew, Anthony J.; Ansotegui, Ignacio J.; Bochner, Bruce S.; Golden, David B. K.; Finkelman, Fred D.; Leung, Donald Y. M.; Lotvall, Jan; Marone, Gianni; Metcalfe, Dean D.; Mueller, Ulrich; Rosenwasser, Lanny J.; Sampson, Hugh A.; Schwartz, Lawrence B.; van Hage, Marianne; Walls, Andrew F.			Risk assessment in anaphylaxis: Current and future approaches	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						anaphylaxis; mast cell; basophil; IgE; Fc epsilon RI; histamine; tryptase; most cell carboxypeptidase; allergens; insect venom allergy; food allergy	HYMENOPTERA VENOM ALLERGY; INSECT-STING CHALLENGE; HUMAN MAST-CELLS; FC-EPSILON-RI; BASOPHIL ACTIVATION TEST; PEANUT ALLERGY; FOOD ALLERGY; IN-VITRO; SKIN PRICK; FATAL REACTIONS	Risk assessment of individuals with anaphylaxis is currently hampered by lack of (1) an optimal and readily available laboratory test to confirm the clinical diagnosis of an anaphylaxis episode and (2) an optimal method of distinguishing allergen-sensitized individuals who are clinically tolerant from those at risk for anaphylaxis episodes after exposure to the relevant allergen. Our objectives were to review the effector mechanisms involved in the pathophysiology of anaphylaxis; to explore the possibility of developing an optimal laboratory test to confirm the diagnosis of an anaphylaxis episode, and the possibility of improving methods to distinguish allergen sensitization from clinical reactivity; and to develop a research agenda for risk assessment in anaphylaxis. Researchers from the American Academy of Allergy, Asthma & Immunology and the European Academy of Allergology and Clinical Immunology held a PRACTALL (Practical Allergy) meeting to discuss these objectives. New approaches being investigated to support the clinical diagnosis of anaphylaxis include serial measurements of total tryptase in serum during an anaphylaxis episode, and measurement of baseline total tryptase levels after the episode. Greater availability of the test for mature beta-tryptase, a more specific mast cell activation marker for anaphylaxis than total tryptase, is needed. Measurement of chymase, mast cell carboxypeptidase A3, platelet-activating factor, and other mast cell products may prove to be useful. Consideration should be given to measuring a panel of mediators from mast cells and basophils. New approaches being investigated to help distinguish sensitized individuals at minimum or no risk from those at increased risk of developing anaphylaxis include measurement of the ratio of allergen-specific IgE to total IgE, determination of IgE directed at specific allergenic epitopes, measurement of basophil activation markers by using flow cytometry, and assessment of allergen-specific cytokine responses. Algorithms have been developed for risk assessment of individuals with anaphylaxis, along with a research agenda for studies that could lead to an improved ability to confirm the clinical diagnosis of anaphylaxis and to identify allergen-sensitized individuals who are at increased risk of anaphylaxis.	Univ Manitoba, Dept Pediat & Child Hlth, Dept Immunol, Winnipeg, MB R3T 2N2, Canada; Brighton Gen Hosp, Dept Resp Med, Brighton, E Sussex, England; Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA; Royal Hosp, Belfast, Antrim, North Ireland; Univ Cincinnati, Coll Med, Div Immunol, Cincinnati, OH 45221 USA; Natl Jewish Med & Res Ctr, Dept Pediat, Denver, CO 80206 USA; Dept Resp Med & Allergol, Gothenburg, Sweden; Univ Naples Federico 2, Div Clin Immunol & Allergy, Naples, Italy; NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA; Univ Bern, Inselspital, Med Klin, CH-3010 Bern, Switzerland; Childrens Mercy Hosp & Clin, Dept Pediat, Kansas City, MO 64108 USA; Mt Sinai Sch Med, Dept Pediat & Biomed Sci, New York, NY 10029 USA; Virginia Commonwealth Univ, Div Rheumatol Allergy & Immunol, Richmond, VA 23284 USA; Karolinska Inst & Univ Hosp, Dept Med Clin Immunol & Allergy, Stockholm, Sweden; Southampton Gen Hosp, Immunopharmacol Grp, Southampton, Hants, England	Simons, FER (reprint author), 820 Sherbrook St, Winnipeg, MB R3A 1R9, Canada.	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Allergy Clin. Immunol.	JUL	2007	120	1		S			S2	S24		10.1016/j.jaci.2007.05.001		23	Allergy; Immunology	Allergy; Immunology	193KY	WOS:000248274100002	17602945	
J	Kohl, J; Baelder, R; Lewkowich, IP; Pandey, MK; Hawlisch, H; Wang, LH; Best, J; Herman, NS; Sproles, AA; Zwirner, J; Whitsett, JA; Gerard, C; Sfyroera, G; Lambris, JD; Wills-Karp, M				Kohl, J; Baelder, R; Lewkowich, IP; Pandey, MK; Hawlisch, H; Wang, LH; Best, J; Herman, NS; Sproles, AA; Zwirner, J; Whitsett, JA; Gerard, C; Sfyroera, G; Lambris, JD; Wills-Karp, M			A regulatory role for the C5a anaphylatoxin in, type 2 immunity in asthma	JOURNAL OF CLINICAL INVESTIGATION			English	Article							INDUCED AIRWAY HYPERRESPONSIVENESS; PLASMACYTOID DENDRITIC CELLS; ISCHEMIA-REPERFUSION INJURY; TH2 EFFECTOR FUNCTIONS; GENOME-WIDE SEARCH; ALLERGIC-ASTHMA; INHALED ANTIGEN; CUTTING EDGE; IN-VIVO; C3A ANAPHYLATOXIN	Complement component 5 (CS) has been described as either promoting or protecting against airway hyper-responsiveness (AHR):in experimental allergic asthma, suggesting pleomorphic effects of C5. Here we report that local pharmacological targeting of the C5a receptor (C5aR) prior to initial allergen sensitization in murine models of inhalation tolerance or allergic asthma resulted in either induction or marked enhancement of Th2-polarized immune responses, airway inflammation, and AHR. Importantly, C5aR-deficient mice exhibited a similar, increased allergic phenotype. Pulmonary allergen exposure in CSaR-targeted mice resulted in increased sensitization and accumulation of CD4(+)CD69(+) T cells associated with a marked increase in pulmonary myeloid, but not plasmacytoid, DC numbers. Pulmonary DCs from C5aR-targeted mice produced large amounts of CC chemokine ligand 17 (CCL17) and CCL22 ex vivo, suggesting a negative impact of C5aR signaling on pulmonary homing of Th2 cells. In contrast, C5aR targeting in sensitized mice led to suppressed airway inflammation and AHR but was still associated with enhanced production of Th2 effector cytokines. These data suggest a dual role for C5a in allergic asthma, i.e., protection from the development of maladaptive type 2 immune responses during allergen sensitization at the DC/T cell interface but enhancement of airway inflammation and AHR in an established inflammatory environment.	Childrens Hosp, Med Ctr, Div Mol Immunol, Cincinnati, OH 45229 USA; Childrens Hosp, Med Ctr, Div Immunobiol, Cincinnati, OH 45229 USA; Univ Cincinnati, Coll Med, Cincinnati, OH USA; Univ Gottingen, Dept Immunol, D-3400 Gottingen, Germany; Childrens Hosp, Med Ctr, Div Pulm Biol, Cincinnati, OH 45229 USA; Univ Cincinnati, Coll Med, Cincinnati, OH USA; Harvard Univ, Childrens Hosp, Sch Med, Ina Sue Perlmutter Lab, Boston, MA 02115 USA; Univ Penn, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA	Kohl, J (reprint author), Childrens Hosp Res Fdn, Div Mol Immunol, MLC 7021, Cincinnati, OH 45229 USA.	joerg.koehl@chmcc.org	Koehl, Joerg/C-8531-2011	Koehl, Joerg/0000-0003-1121-3178; Lambris, John/0000-0002-9370-5776	NHLBI NIH HHS [R01 HL067736, R01-HL67736]; NIAID NIH HHS [R01 AI057839, R01-AI057839]		Abe K, 2001, KIDNEY INT, V60, P137, DOI 10.1046/j.1523-1755.2001.00780.x; Abe M, 2001, J IMMUNOL, V167, P4651; Akbari O, 2001, NAT IMMUNOL, V2, P725, DOI 10.1038/90667; Baelder R, 2005, J IMMUNOL, V174, P783; Bautsch W, 2000, J IMMUNOL, V165, P5401; BITO LZ, 1977, SCIENCE, V196, P83, DOI 10.1126/science.557238; Brimnes MK, 2003, J EXP MED, V198, P133, DOI 10.1084/jem.20030266; Cates EC, 2004, J IMMUNOL, V173, P6384; Colonna M, 2004, NAT IMMUNOL, V5, P1219, DOI 10.1038/ni1141; Colten H. 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Clin. Invest.	MAR	2006	116	3					783	796		10.1172/JCI26582		14	Medicine, Research & Experimental	Research & Experimental Medicine	019RL	WOS:000235854300030	16511606	
J	Kumar, RK; Foster, PS				Kumar, RK; Foster, PS			Modeling allergic asthma in mice - Pitfalls and opportunities	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Review							INDUCED AIRWAY HYPERREACTIVITY; ANTIGEN-INDUCED EOSINOPHIL; GOBLET CELL HYPERPLASIA; MURINE MODEL; MOUSE MODELS; BRONCHIAL HYPERRESPONSIVENESS; TRANSGENIC MICE; LUNG DAMAGE; T-CELLS; IMMUNOLOGICAL-TOLERANCE	Studies in murine experimental models have contributed greatly to understanding the mechanisms of allergic inflammation underlying asthma. However, models involving short-term high-level exposure of sensitized animals to antigen have significant limitations for investigating the pathogenesis of the lesions of chronic asthma. Modeling chronic asthma is problematic, because long-term antigenic challenge often triggers widespread pulmonary parenchymal inflammation or leads to eventual downregulation of inflammation and airway hyperreactivity. We have developed an improved murine model in which animals are exposed to low mass concentrations of aerosolized antigen for 6-8 wk. The mice exhibit airway-specific acute-on-chronic inflammation and changes of airway wall remodeling as seen in human asthma, together with hyperreactivity to a cholinergic agonist which can be specifically attributed to airway disease. This more realistic model of asthma offers a number of opportunities for investigation of pathogenetic mechanisms and novel therapeutic agents.	Univ New S Wales, Dept Pathol, Sydney, NSW 2052, Australia; Australian Natl Univ, John Curtin Sch Med Res, Div Biochem & Mol Biol, Canberra, ACT 2601, Australia	Kumar, RK (reprint author), Univ New S Wales, Dept Pathol, Sydney, NSW 2052, Australia.		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J. Respir. Cell Mol. Biol.	SEP	2002	27	3					267	272		10.1165/rcmb.F248		6	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	590EZ	WOS:000177806500001	12204888	
J	Vahter, M; Berglund, M; Akesson, A; Liden, C				Vahter, M; Berglund, M; Akesson, A; Liden, C			Metals and women's health	ENVIRONMENTAL RESEARCH			English	Review							BLOOD LEAD LEVELS; ENVIRONMENTAL CADMIUM EXPOSURE; JAPANESE GENERAL-POPULATION; NUTRIENT-SUFFICIENT DIET; DRINKING-WATER; COGNITIVE FUNCTION; POSTMENOPAUSAL WOMEN; CONTACT-DERMATITIS; OSTEOBLASTIC CELLS; MERCURY EXPOSURE	There is a lack of information concerning whether environmental-related health effects are more or less prevalent or manifested differently in women compared to men. Previously, most research in the area of toxicology and environmental and occupational health involved male subjects. The present work aims at reviewing exposure and health effects of cadmium, nickel, lead, mercury, and arsenic manifested differently in women than in men. The gender difference in exposure to nickel results in a much higher prevalence of nickel allergy and hand eczema in women than in men. The internal cadmium dose is generally higher in women than in men, due to a higher gastrointestinal absorption at low iron stores. This was probably one major reason why Itai-itai disease was mainly a woman's disease. Yet, data are sparse regarding the risk for women relative to men to develop cadmium-induced kidney damage in populations exposed to low levels of cadmium. Lead is accumulated mainly in bone and increased endogenous lead exposure has been demonstrated in women during periods of increased bone turnover, e.g., menopause. Both lead and mercury exposure in pregnant women has to be kept low in order to prevent neurodevelopment effects in the developing fetus and child. Limited data indicate that women are more affected than men following exposure to methylmercury at adult age, while males seem to be more sensitive to exposure during early development. Regarding arsenic, some data indicate gender differences in the biotransformation by methylation, possibly also in susceptibility to certain arsenic-related cancers. Obviously, gender-related differences in exposure and health effects caused by metals are highly neglected research areas, which need considerable focus in the future. (C) 2002 Elsevier Science (USA).	Karolinska Inst, Inst Environm Med, Div Met & Hlth, SE-17177 Stockholm, Sweden; Karolinska Inst, Dept Med, Stockholm, Sweden; Stockholm Cty Council, Stockholm, Sweden	Vahter, M (reprint author), Karolinska Inst, Inst Environm Med, Div Met & Hlth, Box 210, SE-17177 Stockholm, Sweden.			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Res.	MAR	2002	88	3					145	155		10.1006/enrs.2002.4338		11	Environmental Sciences; Public, Environmental & Occupational Health	Environmental Sciences & Ecology; Public, Environmental & Occupational Health	552NM	WOS:000175626500002	12051792	
J	Ring, J; Kramer, U; Schafer, T; Behrendt, H				Ring, J; Kramer, U; Schafer, T; Behrendt, H			Why are allergies increasing?	CURRENT OPINION IN IMMUNOLOGY			English	Review							HOUSE-DUST MITE; IMMUNOGLOBULIN-E; AIR-POLLUTION; ATOPIC ECZEMA; HAY-FEVER; LIFE-STYLE; CHILDREN; ASTHMA; PREVALENCE; CHILDHOOD	The incidence of atopic allergy is increasing in certain 'Western' countries but this remains unexplained. Various hypotheses with differing amounts of evidence and/or relevance have been assessed, including increased awareness of the diseases, improved diagnostics, genetic susceptibility, psycho-social influences, allergen exposure, decreased immune-system stimulation, underlying disease, anti-allergic therapy and pollution.	Tech Univ Munich, Dept Dermatol & Allergy Biederstein, D-80802 Munich, Germany; Med Inst Umwelthyg, D-40225 Dusseldorf, Germany; Neuherberg Tech Univ Munich, GSF, Natl Res Ctr Environm & Hlth, Div Environm Dermatol & Allergy, D-80802 Munich, Germany	Ring, J (reprint author), Tech Univ Munich, Dept Dermatol & Allergy Biederstein, Biedersteiner Str 29, D-80802 Munich, Germany.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; BEHRENDT H, 1992, INT ARCH ALLERGY IMM, V99, P425; Behrendt H, 1995, PROG ALLER CLIN IMM, V3, P83; Behrendt H, 1993, ALLERGO J, V3, P31; BEHRENDT H, 2000, NATL COUNCIL ENV ISS; BEHRENDT H, 2001, ALLERGY CLIN IMMUNOL, V13, P127; Bjorksten B, 1999, CLIN EXP ALLERGY, V29, P342; Blumenthal M, 1997, GENETICS ALLERGY AST; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; BURR ML, 1993, EPIDEMIOLOGY ALLERGI; Coca AF, 1923, J IMMUNOL, V8, P163; COOKSON WOCM, 1989, LANCET, V1, P1292; CUSTOVIC A, 1994, CLIN EXP ALLERGY, V24, P1164; DiazSanchez D, 1997, ALLERGY, V52, P52; Diepgen T, 2000, ATOPIC DERMATITIS EP, P96, DOI 10.1017/CBO9780511545771.009; GASSNERBACHMANN M, 2000, DEUT MED WOCHENSCHR, V125, P923; Heinrich J, 1999, Eur J Med Res, V4, P107; Heinrich J, 1998, AM J PUBLIC HEALTH, V88, P1319, DOI 10.2105/AJPH.88.9.1319; Hirsch T, 1999, EUR RESPIR J, V14, P669, DOI 10.1034/j.1399-3003.1999.14c29.x; Holgate ST, 1999, NATURE, V402, pB2; Holt PG, 2000, LANCET, V356, P1699, DOI 10.1016/S0140-6736(00)03198-6; ILLI S, 2001, ALLERGY CLIN IMMUNOL, V13, P99, DOI 10.1027/0838-1925.13.3.99; JUTEL M, 2001, IN PRESS NATURE; Kramer U, 2000, EPIDEMIOLOGY, V11, P64, DOI 10.1097/00001648-200001000-00014; Kramer U, 1999, LANCET, V353, P450, DOI 10.1016/S0140-6736(98)06329-6; Kramer U, 1999, INT J EPIDEMIOL, V28, P865, DOI 10.1093/ije/28.5.865; KRAMER U, 1997, AIR POLLUTION EPIDEM, V8; KUEHR J, 1992, J ALLERGY CLIN IMMUN, V90, P358, DOI 10.1016/S0091-6749(05)80015-6; LARRICK JW, 1983, J ALLERGY CLIN IMMUN, V71, P184, DOI 10.1016/0091-6749(83)90097-0; LESOUEF P, 2000, ACI INT S, V1, P43; MARTINEZ FD, 1988, AM REV RESPIR DIS, V138, P518; Matricardi PM, 1998, J ALLERGY CLIN IMMUN, V101, P439, DOI 10.1016/S0091-6749(98)70350-1; Matsuda H, 1997, INT IMMUNOL, V9, P461, DOI 10.1093/intimm/9.3.461; MURANAKA M, 1986, J ALLERGY CLIN IMMUN, V77, P616, DOI 10.1016/0091-6749(86)90355-6; Olesen AB, 2001, LANCET, V357, P1749, DOI 10.1016/S0140-6736(00)04896-0; Platts-Mills TAE, 2001, INT ARCH ALLERGY IMM, V124, P126, DOI 10.1159/000053689; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; RING J, 1985, HAUTARZT, V36, P470; Ring J, 1997, INT ARCH ALLERGY IMM, V113, P7; Schafer T, 1996, ALLERGY, V51, P532; Schafer T, 1997, J AM ACAD DERMATOL, V36, P550, DOI 10.1016/S0190-9622(97)70242-1; SCHNYDER U. W., 1960, ACTA GENET ET STATIST MED, V10, P1; Schultz Larsen F, 1993, Monogr Allergy, V31, P9; Shaheen SO, 1996, LANCET, V347, P1792, DOI 10.1016/S0140-6736(96)91617-7; Shirakawa T, 1997, SCIENCE, V275, P77, DOI 10.1126/science.275.5296.77; SIGURS N, 1995, PEDIATRICS, V95, P500; Simons E, 1994, ANCESTORS ALLERGY; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; STRACHAN DP, 1989, BRIT MED J, V299, P1259; SUZUKI KK, 2001, INT ARCH ALLERGY IMM, V124, P113; TAYLOR B, 1984, LANCET, V2, P1255; VARJONEN E, 1992, ALLERGY, V47, P243, DOI 10.1111/j.1398-9995.1992.tb00657.x; VONMUTIUS E, 1992, BRIT MED J, V305, P1395; VONMUTIUS E, 1994, BRIT MED J, V308, P692; Wahn U, 2000, SPECIAL REPORT ALLER; Warner JO, 1998, PEDIATR ALLERGY IMMU, V9, P116; Wichmann H, 1995, ALLERGOL J, V6, P315; WICKMAN M, 1994, CLIN EXP ALLERGY, V24, P109, DOI 10.1111/j.1365-2222.1994.tb00205.x; Williams HC, 2000, ATOPIC DERMATITIS EP; WOOLCOCK AJ, 2000, ACI INT S, V1, P53; WUTHRICH B, 1989, INT ARCH ALLER A IMM, V90, P3; 1997, EUROPEAN ALLERGY WHI	64	141	148	2	23	CURRENT BIOLOGY LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0952-7915			CURR OPIN IMMUNOL	Curr. Opin. Immunol.	DEC	2001	13	6					701	708		10.1016/S0952-7915(01)00282-5		8	Immunology	Immunology	486BB	WOS:000171797600012	11677093	
J	Chapman, MD; Smith, AM; Vailes, LD; Arruda, LK; Dhanaraj, V; Pomes, A				Chapman, MD; Smith, AM; Vailes, LD; Arruda, LK; Dhanaraj, V; Pomes, A			Recombinant allergens for diagnosis and therapy of allergic disease	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						recombinant allergens; mites; animal allergens; allergy diagnostics; allergy therapeutics; asthma; allergy vaccines; allergen immunotherapy	HOUSE-DUST-MITE; DER-P-I; CROSS-REACTIVE ALLERGEN; HIGH-LEVEL EXPRESSION; IGE-BINDING; PICHIA-PASTORIS; MOLECULAR-CLONING; MAJOR ALLERGEN; X-RAY; DERMATOPHAGOIDES-PTERONYSSINUS	Many of the problems associated with using natural allergenic products for allergy diagnosis and treatment can be overcome with use of genetically engineered recombinant allergens. Over the past 10 years, the most important allergens from mites, pollens, animal dander, insects, and foods have been cloned, sequenced, and expressed. In many cases the three-dimensional allergen structure has been determined and B-cell and T-cell epitopes have been mapped. These studies show that allergens have diverse biologic functions (they may be enzymes, enzyme inhibitors, lipocalins, or structural proteins) and that as a rule the allergen function is unrelated to its ability to cause IgE antibody responses, High-level expression systems have been developed to produce recombinant allergens in bacteria, yeast, or insect cells. Recombinant allergens show comparable IgE antibody binding to their natural counterparts (where available) and show excellent reactivity on skin testing and in in vitro diagnostic tests. Cocktails of recombinant allergens can be formulated with predetermined and uniform allergen levels, which could replace natural allergens and result in the development of innovative, patient-based tests for allergy diagnosis. Recombinant allergens also offer the exciting possibility of developing new forms of allergen immunotherapy, including the use of hypoallergens, allergens coupled to IgE suppressive adjuvants, and peptide-based therapies. The production of recombinant allergens as defined molecular entities makes it feasible to consider the possibility of developing prophylactic allergen vaccines. The introduction of recombinant allergens in research and in clinical trials should lead to significant improvements in allergy diagnosis and treatment.	Univ Virginia, Asthma & Allerg Dis Ctr, Dept Internal Med, Charlottesville, VA 22908 USA; USP, Fac Med Ribeirao Preto, Dept Microbiol Immunol & Parasitol, Ribeirao Preto, Brazil; Univ Cambridge, Dept Biochem, Cambridge CB2 1QW, England	Chapman, MD (reprint author), Univ Virginia, Asthma & Allerg Dis Ctr, Dept Internal Med, Box 801355, Charlottesville, VA 22908 USA.		Arruda, L. Karla /D-5845-2013; Osborne, Nicholas/N-4915-2015	Arruda, L. 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Allergy Clin. Immunol.	SEP	2000	106	3					409	418				10	Allergy; Immunology	Allergy; Immunology	356YN	WOS:000089471900001	10984358	
J	Yokouchi, Y; Nukaga, Y; Shibasaki, M; Noguchi, E; Kimura, K; Ito, S; Nishihara, M; Yamakawa-Kobayashi, K; Takeda, K; Imoto, N; Ichikawa, K; Matsui, A; Hamaguchi, H; Arinami, T				Yokouchi, Y; Nukaga, Y; Shibasaki, M; Noguchi, E; Kimura, K; Ito, S; Nishihara, M; Yamakawa-Kobayashi, K; Takeda, K; Imoto, N; Ichikawa, K; Matsui, A; Hamaguchi, H; Arinami, T			Significant evidence for linkage of mite-sensitive childhood asthma to chromosome 5q31-q33 near the interleukin 12 B locus by a genome-wide search in Japanese families	GENOMICS			English	Article							TOTAL SERUM IGE; IL-4 GENE-EXPRESSION; BRONCHIAL HYPERRESPONSIVENESS; UNDERLYING ASTHMA; ALLERGIC-ASTHMA; RELATIVE RISKS; MAJOR GENE; NF-Y; MARKERS; RESPONSIVENESS	Childhood-onset asthma is frequently found in association with atopy. Although asthmatic children may develop IgE antibodies against variety of allergens, asthma is associated primarily with allergy to house-dust mites, molds, or other allergens. In this study, me conducted a genome-wide linkage search in 47 Japanese families (197 members) with more than two mite-sensitive atopic asthmatics (65 affected sib-pairs) using 398 markers. Multipoint linkage analysis was carried out for atopic asthma as a qualitative trait using the MAPMAKER/SIB program. We observed signficant evidence for linkage with maximum lod scores (MLS) of 4.8 near the interleukin 12 B gene locus on chromosome 5q31-q33. In addition, suggestive evidence on 4q35 with MLS = 2.7 and on 13q11 with MLS = 2.4 was obtained. The other possible linkage regions included 6p22-p21.3 (MLS = 2.1), 12q21-q23 (MILS = 1.9), and 13q14.1-q14.3 (MLS = 2.0). Many of the linkage loci suggested in this study were at or close to those suggested by genome-wide studies for asthma in Caucasian populations. The present study suggests the contribution of the interleukin 12 B gene or nearby gene(s) to mite-sensitive atopic asthma and a considerable number of genetic variants common across Caucasians and Japanese populations contributing to asthma, although the relative importance of various variants may differ between the groups. (C) 2000 Academic Press.	Univ Tsukuba, Inst Basic Med Sci, Dept Med Genet, Tsukuba, Ibaraki 3058575, Japan; Univ Tsukuba, Inst Clin Med, Dept Pediat, Tsukuba, Ibaraki 3058575, Japan; Univ Tsukuba, Inst Clin Med, Dept Dermatol, Tsukuba, Ibaraki 3058575, Japan	Arinami, T (reprint author), Univ Tsukuba, Inst Basic Med Sci, Dept Med Genet, Tsukuba, Ibaraki 3058575, Japan.		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J	Martinez, FD; Vercelli, D				Martinez, Fernando D.; Vercelli, Donata			Asthma	LANCET			English	Article							INNATE LYMPHOID-CELLS; MILD PERSISTENT ASTHMA; REGULATORY T-CELLS; INTERMITTENT INHALED CORTICOSTEROIDS; RANDOMIZED CONTROLLED-TRIAL; PLACEBO-CONTROLLED TRIAL; GENOME-WIDE ASSOCIATION; ACTING BETA-AGONISTS; STEP-UP THERAPY; CHILDHOOD ASTHMA	Asthma is a heterogeneous group of conditions that result in recurrent, reversible bronchial obstruction. Although the disease can start at any age, the first symptoms occur during childhood in most cases. Asthma has a strong genetic component, and genome-wide association studies have identified variations in several genes that slightly increase the risk of disease. Asthma is often associated with increased susceptibility to infection with rhinoviruses and with changes in the composition of microbial communities colonising the airways, but whether these changes are a cause or consequence of the disease is unknown. There is currently no proven prevention strategy; however, the finding that exposure to microbial products in early life, particularly in farming environments, seems to be protective against asthma offers hope that surrogates of such exposure could be used to prevent the disease. Genetic and immunological studies point to defective responses of lung resident cells, especially those associated with the mucosal epithelium, as crucial elements in the pathogenesis of asthma. Inhaled corticosteroids continue to be the mainstay for the treatment of mild and moderate asthma, but limited adherence to daily inhaled medication is a major obstacle to the success of such therapy. Severe asthma that is refractory to usual treatment continues to be a challenge, but new biological therapies, such as humanised antibodies against IgE, interleukin 5, and interleukin 13, off er hope to improve the quality of life and long-term prognosis of severe asthmatics with specific molecular phenotypes.	[Martinez, Fernando D.; Vercelli, Donata] Univ Arizona, Arizona Resp Ctr, Tucson, AZ 85724 USA; [Martinez, Fernando D.; Vercelli, Donata] Univ Arizona, Inst BIO5, Tucson, AZ 85724 USA	Martinez, FD (reprint author), Univ Arizona, Arizona Resp Ctr, 1501 N Campbell, Tucson, AZ 85724 USA.	fernando@arc.arizona.edu			US National Heart, Lung, and Blood Institute; US National Institute of Allergy and Infectious Diseases	The authors were funded by grants from the US National Heart, Lung, and Blood Institute and the US National Institute of Allergy and Infectious Diseases.	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J	Meijboom, WB; Mollet, NR; Van Mieghem, CAG; Kluin, J; Weustink, AC; Pugliese, F; Vourvouri, E; Cademartiri, F; Bogers, AJJC; Krestin, GP; de Feyter, PJ				Meijboom, Willem B.; Mollet, Nico R.; Van Mieghem, Carlos A. G.; Kluin, Jolanda; Weustink, Annick C.; Pugliese, Francesca; Vourvouri, Eleni; Cademartiri, Filippo; Bogers, Ad J. J. C.; Krestin, Gabriel P.; de Feyter, Pim J.			Pre-operative computed tomography coronary anglography to detect significant coronary artery disease in patients referred for cardiac valve surgery	JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY			English	Article							VALVULAR HEART-DISEASE; PRACTICE GUIDELINES COMMITTEE; ASSOCIATION TASK-FORCE; AORTIC-STENOSIS; RADIATION-EXPOSURE; ANGINA-PECTORIS; ANGIOGRAPHY; ACCURACY; CT; QUANTIFICATION	OBJECTIVES We studied the diagnostic performance of 64-slice computed tomography coronary angiography (CTCA) to rule out or detect significant coronary stenosis in patients referred for valve surgery. BACKGROUND Invasive conventional coronary angiography (CCA) is recommended in most patients scheduled for valve surgery. METHODS During a 6-month period, 145 patients were prospectively identified from a consecutive patient population scheduled for valve surgery. Thirty-five patients were excluded because of CTCA criteria: irregular heart rhythm (n = 26), impaired renal function (n = 5), and known contrast allergy (n = 4). General exclusion criteria were: hospitalization in community hospital (n = 4), no need for CCA (n = 4), previous coronary artery bypass surgery (n = 1), or percutaneous coronary intervention (n = 4). Of the remaining 97 patients, 27 denied written informed consent. Thus, the study population comprised 70 patients (49 male, 21 female;, mean age 63 +/- 11 years). RESULTS Prevalence of significant coronary artery disease, defined as having at least 1 >= 50% stenosis per patient, was 25.7%. Beta-blockers were administered in 71%, and 64% received lorazepam. The mean heart rate dropped from 72.5 +/- 12.4 to 59.5 +/- 7.5 beats/min. The mean scan time was 12.8 +/- 1.3 s. On a per-patient analysis, the sensitivity, specificity, and positive and negative predictive values were: 100% (18 of 18; 95% confidence interval [CI] 78 to 100), 92% (48 of 52; 95% CI 81 to 98), 82% (18 of 22; 95% CI 59 to 94), and 100% (48 of 48; 95% CI 91 to 100), respectively. CONCLUSIONS The diagnostic accuracy of 64-slice CTCA for ruling out the presence of significant coronary stenoses in patients undergoing valve surgery is excellent and allows CTCA implementation as a gatekeeper for invasive CCA in these patients.	Erasmus Med Ctr, Dept Cardiol, Thoraxctr, NL-3015 GD Rotterdam, Netherlands; Erasmus Med Ctr, Dept Radiol, Thoraxctr, NL-3015 GD Rotterdam, Netherlands; Erasmus Med Ctr, Dept Cardiothorac Surg, Thoraxctr, NL-3015 GD Rotterdam, Netherlands	de Feyter, PJ (reprint author), Erasmus Med Ctr, Dept Cardiol & Radiol, Thoraxctr, Room BA 589,Dr Molewaterpl 40, NL-3015 GD Rotterdam, Netherlands.	p.j.defeyter@erasmusmc.nl	Cademartiri, Filippo/H-7336-2015	Cademartiri, Filippo/0000-0002-0579-3279			Achenbach S, 2006, EUR J RADIOL, V57, P331, DOI 10.1016/j.ejrad.2005.12.017; AGATSTON AS, 1990, J AM COLL CARDIOL, V15, P827; ALEXOPOULOS D, 1993, ANGIOLOGY, V44, P707, DOI 10.1177/000331979304400906; Austen WG, 1975, CIRCULATION S4, V51, P5; Bonow RO, 1998, CIRCULATION, V98, P1949; Coles DR, 2006, J AM COLL CARDIOL, V47, P1840, DOI 10.1016/j.jacc.2005.11.078; Flohr TG, 2006, EUR RADIOL, V16, P256, DOI 10.1007/s00330-005-2919-2; Gilard M, 2006, J AM COLL CARDIOL, V47, P2020, DOI 10.1016/j.jacc.2005.11.085; GREEN SJ, 1985, AM J CARDIOL, V55, P1063, DOI 10.1016/0002-9149(85)90747-7; Hausleiter J, 2006, CIRCULATION, V113, P1305, DOI 10.1161/CIRCULATIONAHA.105.602490; Jakobs TF, 2002, EUR RADIOL, V12, P1081, DOI 10.1007/s00330-001-1278-x; KETTUNEN R, 1992, AM J CARDIOL, V69, P1442, DOI 10.1016/0002-9149(92)90898-9; KUPARI M, 1992, AM J CARDIOL, V70, P635, DOI 10.1016/0002-9149(92)90204-C; Leber AW, 2005, J AM COLL CARDIOL, V46, P147, DOI 10.1016/j.jacc.2005.03.071; Leschka S, 2005, EUR HEART J, V26, P1482, DOI 10.1093/eurheartj/ehi261; LUND O, 1990, J THORAC CARDIOV SUR, V100, P327; Lung B, 1993, J HEART VALVE DIS, V2, P430; LYTLE B W, 1991, Cardiology Clinics, V9, P301; Mollet NR, 2005, CIRCULATION, V112, P2318, DOI 10.1161/CIRCULATIONAHA.105.533471; MULLANY CJ, 1987, J AM COLL CARDIOL, V10, P66; OLOFSSON BO, 1985, ACTA MED SCAND, V218, P365; Raff GL, 2005, J AM COLL CARDIOL, V46, P552, DOI 10.1016/j.jacc.2005.05.056; RAMSDALE DR, 1984, EUR HEART J, V5, P716; RASK P, 1994, J NUCL MED, V35, P983; SAMUELS B, 1995, J AM COLL CARDIOL, V25, P99, DOI 10.1016/0735-1097(94)00317-J; Scanlon PJ, 1999, J AM COLL CARDIOL, V33, P1756, DOI 10.1016/S0735-1097(99)00126-6; Trabold T, 2003, ROFO-FORTSCHR RONTG, V175, P1051; VANDEPLAS A, 1988, AM J CARDIOL, V62, P117, DOI 10.1016/0002-9149(88)91375-6; Vogl TJ, 2002, RADIOLOGY, V223, P212, DOI 10.1148/radiol.2231010515	29	140	144	0	1	ELSEVIER SCIENCE INC	NEW YORK	360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA	0735-1097			J AM COLL CARDIOL	J. Am. Coll. Cardiol.	OCT 17	2006	48	8					1658	1665		10.1016/j.jacc.2006.06.054		8	Cardiac & Cardiovascular Systems	Cardiovascular System & Cardiology	096ZC	WOS:000241414600022	17045904	
J	Schaumann, F; Borm, PJA; Herbrich, A; Knoch, J; Pitz, M; Schins, RPF; Luettig, B; Hohlfeld, JM; Heinrich, J; Krug, N				Schaumann, F; Borm, PJA; Herbrich, A; Knoch, J; Pitz, M; Schins, RPF; Luettig, B; Hohlfeld, JM; Heinrich, J; Krug, N			Metal-rich ambient particles (Particulate Matter(2.5)) cause airway inflammation in healthy subjects	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						air pollution; bronchoscopy; monocytes; oxidants	RESPIRATORY SYMPTOMS; EAST-GERMANY; POLLUTION; LUNG; CHILDREN; DISEASE; PM2.5; INSTILLATION; PHENOTYPE; ENDOTOXIN	Epidemiologic studies have shown an increased prevalence of allergic asthma in children living in a German smelter area (Hettstedt) compared with a cohort who live in a nonindustrialized area (Zerbst). However, it is not known whether ambient particles (particulate matter(2.5) [PM2.5]) from these areas induce distinct lung inflammation, which might be an explanation for this difference. Therefore, 100 mug of PM2.5 suspensions, collected simultaneously in the two areas, were instilled through a bronchoscope into contralateral lung segments of 12 healthy volunteers. PM2.5 from both Hettstedt and Zerbst increased the number of leukocytes in the bronchoalveolar lavage performed 24 hours later. PM2.5 from Hettstedt, but not Zerbst, induced a significant influx of monocytes (Hettstedt: 7.0% vs. Zerbst: 4.3%) without influencing the expression of surface activation markers on monocytes and alveolar macrophages. Oxidant radical generation of bronchoalveolar lavage cells and cytokine concentration (interieukin-6 and tumor necrosis factor-alpha) in bronchoalveolar lavage fluid was significantly increased after instillation of Hettstedt PM2.5. We conclude that environmentally relevant concentrations of PM2.5 from the smelter area induced distinct airway inflammation in healthy subjects with a selective influx of monocytes and increased generation of oxidant radicals. The higher concentration of transition metals in PM2.5 from Hettstedt might be responsible for this increased inflammation.	Fraunhofer Inst Toxicol & Expt Med, D-30625 Hannover, Germany; Inst Umweltmed Forsch, Dusseldorf, Germany; GSF Natl Res Ctr Environm & Hlth, Inst Epidemiol, Neuherberg, Germany	Krug, N (reprint author), Fraunhofer Inst Toxicol & Expt Med, Nikolai Fuchs Str 1, D-30625 Hannover, Germany.	krug@item.fraunhofer.de					Adamson IYR, 2000, TOXICOL APPL PHARM, V166, P111, DOI 10.1006/taap.2000.8955; Erpenbeck VJ, 2004, AM J RESP CRIT CARE, V169, P578, DOI 10.1164/rccm.200301-104OC; Frye C, 2003, ENVIRON HEALTH PERSP, V111, P383, DOI 10.1289/ehp.5355; GAIL DB, 1991, AM REV RESPIR DIS, V144, P1414; Gavett SH, 2003, ENVIRON HEALTH PERSP, V111, P1471, DOI 10.1289/ehp.6300; Ghio AJ, 2001, AM J RESP CRIT CARE, V164, P704; Gong H, 2003, INHAL TOXICOL, V15, P305, DOI 10.1080/08958370390168300; Harder SD, 2001, ENVIRON HEALTH PERSP, V109, P599, DOI 10.2307/3454676; Heinrich J, 1999, ENVIRON HEALTH PERSP, V107, P53, DOI 10.2307/3434289; Heinrich J, 2002, EUR RESPIR J, V19, P1040, DOI 10.1183/09031936.02.00261802; Heinrich J, 2003, ATMOS ENVIRON, V37, P3659, DOI 10.1016/S1352-2310(03)00467-9; Heinrich J, 2002, EPIDEMIOLOGY, V13, P394, DOI 10.1097/01.EDE.00000016977.59359.B6; Heinrich J, 2000, AM J RESP CRIT CARE, V161, P1930; Krombach F, 1996, EUR RESPIR J, V9, P984, DOI 10.1183/09031936.96.09050984; Lensmar C, 1999, CLIN EXP ALLERGY, V29, P1632, DOI 10.1046/j.1365-2222.1999.00757.x; Maus U, 2001, AM J PHYSIOL-LUNG C, V280, pL58; Meyer I, 2003, INT J HYG ENVIR HEAL, V206, P181, DOI 10.1078/1438-4639-00207; O'Grady NP, 2001, AM J RESP CRIT CARE, V163, P1591; POPE CA, 1991, AM REV RESPIR DIS, V144, P668; POPE CA, 1989, AM J PUBLIC HEALTH, V79, P623, DOI 10.2105/AJPH.79.5.623; SCHAUMANN F, 2000, AM J RESP CRIT CARE, V169, pA278; Shi TM, 2003, J ENVIRON MONITOR, V5, P550, DOI 10.1039/b303928p	22	140	151	2	27	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	OCT 15	2004	170	8					898	903		10.1164/rccm.200403-423OC		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	861GT	WOS:000224404800014	15229099	
J	Peat, JK; Mihrshahi, S; Kemp, AS; Marks, GB; Tovey, ER; Webb, K; Mellis, CM; Leeder, SR				Peat, JK; Mihrshahi, S; Kemp, AS; Marks, GB; Tovey, ER; Webb, K; Mellis, CM; Leeder, SR		Childhood Asthma Study Team	Three-year outcomes of dietary fatty acid modification and house dust mite reduction in the Childhood Asthma Prevention Study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergen avoidance; allergy; asthma; atopy; omega-3 fatty acids; house dust mite; primary prevention	RESPIRATORY SYMPTOMS; RANDOMIZED TRIAL; HIGH-RISK; FISH-OIL; ATOPY; COUGH; INTERVENTION; AVOIDANCE; PREGNANCY; INFANTS	Background: Two factors thought to influence the risk of asthma are the promoting effect of sensitization to house dust mites and the preventive effect of increased omega-3 fatty acids. Although house dust mite allergen avoidance has been used as a preventive strategy in several trials, the effect of omega-3 fatty acid supplementation in the primary prevention of asthma and allergic disease is not known. Objective: To measure the effects of dietary supplementation with omega-3 fatty acids and house dust mite allergen avoidance in children with a family history of asthma. Methods: A total of 616 children at high risk of asthma were enrolled antenatally in a randomized controlled trial, and 526 children remained in the trial at age 3 years. The outcomes were symptoms of allergic disease and allergen sensitization. Results: There was a significant 10.0% (95% CI, 3.7-16.4) reduction in the prevalence of cough in atopic children in the active diet group (P = .003; number needed to treat, 10) but a negligible 1.1 % (95 % CI, -7.1 to 9.5) reduction cough among nonatopic children. There was a 7.2% (95% CI, 10.11-14.3) reduction in sensitization to house dust mite in the active allergen avoidance group (P = .05; number needed to treat, 14). No significant differences in wheeze were found with either intervention. Conclusion: These results suggest that our interventions, designed to be used in simple public health campaigns, may have a role in preventing the development of allergic sensitization and airways disease in early childhood. This offers the prospect of reducing allergic disease in later life.	Univ Sydney, Discipline Paediat & Child Hlth, Childrens Hosp, Westmead Clin Sch, Sydney, NSW 2006, Australia; Childrens Hosp, Clin Epidemiol Unit, Westmead, NSW 2145, Australia; Woolcock Inst Med Res, Camperdown, NSW, Australia; Cooperat Res Ctr Asthma, Camperdown, NSW, Australia; Univ Sydney, Sch Publ Hlth, Sydney, NSW 2006, Australia; Univ Sydney, Sch Mol & Microbial Biosci, Sydney, NSW 2006, Australia; Univ Sydney, Fac Med, Sydney, NSW 2006, Australia	Mihrshahi, S (reprint author), Childrens Hosp, Clin Epidemiol Unit, Locked Bag 4001, Westmead, NSW 2145, Australia.	seemann@chw.edu.au	Mihrshahi, Seema/A-9877-2009; Osborne, Nicholas/N-4915-2015; Tovey, Euan/G-8604-2017	Mihrshahi, Seema/0000-0001-6567-9884; Osborne, Nicholas/0000-0002-6700-2284; Tovey, Euan/0000-0002-1802-7266			Arntzen KJ, 1998, PROSTAG OTH LIPID M, V56, P183, DOI 10.1016/S0090-6980(98)00048-3; Arshad SH, 2003, THORAX, V58, P489, DOI 10.1136/thorax.58.6.489; CALDER PC, 1908, CLIN EXP ALLERG, V33, P412; Chan-Yeung M, 2000, ARCH PEDIAT ADOL MED, V154, P657; Chang AB, 1999, ARCH DIS CHILD, V80, P211; COLERIDGE HM, 1976, NATURE, V264, P451, DOI 10.1038/264451a0; Custovic A, 2001, LANCET, V358, P188, DOI 10.1016/S0140-6736(01)05406-X; Dunstan JA, 2003, CLIN EXP ALLERGY, V33, P442, DOI 10.1046/j.1365-2222.2003.01590.x; Ewart HS, 2002, J NUTR, V132, P1149; Faniran AO, 1998, ARCH DIS CHILD, V79, P411; Gore Claudia, 2003, Paediatr Respir Rev, V4, P213, DOI 10.1016/S1526-0542(03)00055-1; Haby MM, 2001, THORAX, V56, P589, DOI 10.1136/thorax.56.8.589; HALMERBAUER G, 2002, PEDIAT ALLERGY I S15, V3, P47; Hodge L, 1996, MED J AUSTRALIA, V164, P137; Koopman LP, 2002, AM J RESP CRIT CARE, V166, P307, DOI 10.1164/rccm.2106026; Mantzioris E, 2000, AM J CLIN NUTR, V72, P42; Martinez FD, 1999, ALLERGY, V54, P24, DOI 10.1111/j.1398-9995.1999.tb04384.x; Mihrshahi S, 2003, J ALLERGY CLIN IMMUN, V111, P162, DOI 10.1067/mai.2003.36; Mihrshahi S, 2003, ALLERGY, V58, P784, DOI 10.1034/j.1398-9995.2003.00194.x; Mihrshahi S, 2001, CONTROL CLIN TRIALS, V22, P333, DOI 10.1016/S0197-2456(01)00112-X; National Asthma Council Australia, 2002, ASTHM MAN HDB; Oddy WH, 2004, J ASTHMA, V41, P319, DOI 10.1081/JAS-120026089; PEAT JK, 1990, J ALLERGY CLIN IMMUN, V85, P65, DOI 10.1016/0091-6749(90)90223-Q; Ponsonby AL, 2002, J CLIN EPIDEMIOL, V55, P556, DOI 10.1016/S0895-4356(01)00519-4; Raatz SK, 2001, J NUTR, V131, P231; SCHWARTZ J, 1990, AM J EPIDEMIOL, V132, P67; SCHWARTZ J, 2000, AM J CLIN NUTR S, V71, P393; Sears MR, 2003, NEW ENGL J MED, V349, P1414, DOI 10.1056/NEJMoa022363; SHAHAR E, 1994, NEW ENGL J MED, V331, P228, DOI 10.1056/NEJM199407283310403; STONE R, 1992, J APPL PHYSIOL, V73, P649; Warner JO, 1998, PEDIATR PULM, V25, P1	31	140	147	1	6	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	OCT	2004	114	4					807	813		10.1016/j.jaci.2004.06.057		7	Allergy; Immunology	Allergy; Immunology	861SO	WOS:000224439100013	15480319	
J	Ferreira, F; Hawranek, T; Gruber, P; Wopfner, N; Mari, A				Ferreira, F; Hawranek, T; Gruber, P; Wopfner, N; Mari, A			Allergic cross-reactivity: from gene to the clinic	ALLERGY			English	Review						allergen structure; allergenicity; arthropod allergens; cross-reactive carbohydrate determinant; cross-reactivity; food allergens; immunoglobulin E antibodies; insect venom allergens; latex allergens; pollen allergens	IGE-BINDING EPITOPES; GRASS-POLLEN ALLERGEN; HOUSE-DUST MITE; BET V 1; CONTROLLED FOOD CHALLENGE; MAJOR CHERRY ALLERGEN; LATEX-FRUIT SYNDROME; COWS MILK ALLERGY; BIRD-EGG SYNDROME; PEANUT ALLERGY	A large number of allergenic proteins have now their complete cDNA sequences determined and in some cases also the 3D structures. It turned out that most allergens could be grouped into a small number of structural protein families, regardless of their biological source. Structural similarity among proteins from diverse sources is the molecular basis of allergic cross-reactivity. The clinical relevance of immunoglobulin E (IgE) cross-reactivity seems to be influenced by a number of factors including the immune response against the allergen, exposure and the allergen. As individuals are exposed to a variable number of allergenic sources bearing homologous molecules, the exact nature of the antigenic structure inducing the primary IgE immune response cannot be easily defined. In general, the 'cross-reactivity' term should be limited to defined clinical manifestations showing reactivity to a source without previous exposure. 'Co-recognition', including by definition 'cross-reactivity', could be used to describe the large majority of the IgE reactivity where co-exposure to a number of sources bearing homologous molecules do not allow unequivocal identification of the sensitizing molecule. The analysis of reactivity clusters in diagnosis allows the interpretation of the patient's reactivity profile as a result of the sensitization process, which often begins with exposure to a single allergenic molecule.	Salzburg Univ, Inst Genet & Allgemeine Biol, Dept Genet & Gen Biol, A-5020 Salzburg, Austria; Landeskliniken Salzburg, Dept Dermatol, Salzburg, Austria; Natl Hlth Serv, Allergy Unit, Rome, Italy	Ferreira, F (reprint author), Salzburg Univ, Inst Genet & Allgemeine Biol, Dept Genet & Gen Biol, Hellbrunnerstr 34, A-5020 Salzburg, Austria.		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J	Mcmillan, SJ; Lloyd, CM				Mcmillan, SJ; Lloyd, CM			Prolonged allergen challenge in mice leads to persistent airway remodelling	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						airway remodelling; allergic airway inflammation; asthma; eosinophils; Th2 cytokines	BRONCHIAL EPITHELIAL-CELLS; MOUSE ASTHMA MODEL; GROWTH-FACTOR-BETA; MURINE MODEL; SUBEPITHELIAL FIBROSIS; INTERFERON-GAMMA; TRANSFORMING GROWTH-FACTOR-BETA-1; GENE-EXPRESSION; ATOPIC ASTHMA; IN-VITRO	Background Inflammatory infiltrates, airway hyper-responsiveness, goblet cell hyperplasia and subepithelial thickening are characteristic of chronic asthma. Current animal models of allergen-induced airway inflammation generally concentrate on the acute inflammation following allergen exposure and fail to mimic all of these features. Objective The aim of this study was to use a murine model of prolonged allergen-induced airway inflammation in order to characterize the cells and molecules involved in the ensuing airway remodelling. Moreover, we investigated whether remodelling persists in the absence of continued allergen challenge. Methods Acute pulmonary eosinophilia and airways hyper-reactivity were induced after six serial allergen challenges in sensitized mice (acute phase). Mice were subsequently challenged three times a week with ovalbumin (OVA) (chronic phase) up to day 55. To investigate the persistence of pathology, one group of mice were left for another 4 weeks without further allergen challenge (day 80). Results The extended OVA challenge protocol caused significant airway remodelling, which was absent in the acute phase. Specifically, remodelling was characterized by deposition of collagen as well as airway smooth muscle and goblet cell hyperplasia. Importantly, these airway changes, together with tissue eosinophilia were sustained in the absence of further allergen challenge. Examination of cytokines revealed a dramatic up-regulation of IL-4 and tumour growth factor-beta1 during the chronic phase. Interestingly, while IL-4 levels were significantly increased during the chronic phase, levels of IL-13 fell. Levels of the Th1-associated cytokine IFN-gamma also increased during the chronic phase. Conclusion In conclusion, we have demonstrated that prolonged allergen challenge results in persistent airway wall remodelling.	Univ London Imperial Coll Sci Technol & Med, Fac Med, Leukocyte Biol Sect, Div Biomed Sci, London SW7 2AZ, England	Lloyd, CM (reprint author), Univ London Imperial Coll Sci Technol & Med, Fac Med, Leukocyte Biol Sect, Div Biomed Sci, London SW7 2AZ, England.	c.lloyd@imperial.ac.uk			Wellcome Trust [087618, 057704]		Blyth DI, 2000, AM J RESP CELL MOL, V23, P241; Blyth DI, 1996, AM J RESP CELL MOL, V14, P425; Bousquet J, 2000, AM J RESP CRIT CARE, V161, P1720; BREWSTER CEP, 1990, AM J RESP CELL MOL, V3, P507; Busse W, 1999, AM J RESP CRIT CARE, V160, P1035; CEMBRZYNSKANOWAK M, 1993, AM REV RESPIR DIS, V147, P291; CHAKIR J, 2003, ALLERGY CLIN IMMUNOL, V111, P1293; CORRIGAN CJ, 1990, AM REV RESPIR DIS, V141, P970; Doucet C, 1998, J CLIN INVEST, V101, P2129, DOI 10.1172/JCI741; Dunhill M, 1969, THORAX, V24, P176; Elias JA, 1999, J CLIN INVEST, V104, P1001, DOI 10.1172/JCI8124; Flood-Page P, 2003, J CLIN INVEST, V112, P1029, DOI 10.1172/JCI200317974; Foster PS, 1996, J EXP MED, V183, P195, DOI 10.1084/jem.183.1.195; Gharaee-Kermani M, 2001, CYTOKINE, V15, P138, DOI 10.1006/cyto.2001.0903; Grootendorst DC, 2001, CLIN EXP ALLERGY, V31, P400, DOI 10.1046/j.1365-2222.2001.01022.x; Grunig G, 1998, SCIENCE, V282, P2261, DOI 10.1126/science.282.5397.2261; Hamelmann E, 1997, AM J RESP CRIT CARE, V156, P766; HARTNELL A, 1993, IMMUNOLOGY, V80, P281; Henderson WR, 2002, AM J RESP CRIT CARE, V165, P108; Hoshino M, 1998, THORAX, V53, P21; Huaux F, 2003, J IMMUNOL, V170, P2083; JEFFERY PK, 1989, AM REV RESPIR DIS, V140, P1745; Lee CG, 2001, J EXP MED, V194, P809, DOI 10.1084/jem.194.6.809; Lee JJ, 1997, J EXP MED, V185, P2143, DOI 10.1084/jem.185.12.2143; Leigh R, 2002, AM J RESP CELL MOL, V27, P526, DOI 10.1165/rcmb.2002-0048OC; Lloyd CM, 2001, J IMMUNOL, V166, P2033; Lloyd CM, 2001, ADV IMMUNOL, V77, P263, DOI 10.1016/S0065-2776(01)77019-8; Magnan A, 1997, CLIN EXP ALLERGY, V27, P389; McKenzie ANJ, 2000, PHARMACOL THERAPEUT, V88, P143, DOI 10.1016/S0163-7258(00)00088-7; Minshall EM, 1997, AM J RESP CELL MOL, V17, P326; Moir LM, 2003, AM J PHYSIOL-LUNG C, V284, pL148, DOI 10.1152/ajplung.00105.2002; Ohno I, 1996, AM J RESP CELL MOL, V15, P404; Rankin JA, 1996, P NATL ACAD SCI USA, V93, P7821, DOI 10.1073/pnas.93.15.7821; Redington AE, 1997, AM J RESP CRIT CARE, V156, P642; Renauld JC, 2001, J CLIN PATHOL, V54, P577, DOI 10.1136/jcp.54.8.577; Richter A, 2001, AM J RESP CELL MOL, V25, P385; ROCHE WR, 1989, LANCET, V1, P520; Sempowski GD, 1996, J CELL PHYSIOL, V167, P290, DOI 10.1002/(SICI)1097-4652(199605)167:2<290::AID-JCP13>3.0.CO;2-C; Tanaka H, 2001, INFLAMM RES, V50, P616, DOI 10.1007/PL00000243; Tang WL, 1996, J CLIN INVEST, V98, P2845, DOI 10.1172/JCI119113; Temann UA, 1998, J EXP MED, V188, P1307, DOI 10.1084/jem.188.7.1307; Temelkovski J, 1998, THORAX, V53, P849; Vignola AM, 1997, AM J RESP CRIT CARE, V156, P591; WANNER A, 1990, CHEST S, V97, P11; Wen FQ, 2002, AM J RESP CELL MOL, V26, P484; Wenzel SE, 2002, J IMMUNOL, V169, P4613; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; Zhang SL, 1999, LAB INVEST, V79, P395; Zhu Zhou, 1999, Journal of Clinical Investigation, V103, P779, DOI 10.1172/JCI5909	49	140	151	0	3	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	MAR	2004	34	3					497	507		10.1111/j.1365-2222.2004.01895.x		11	Allergy; Immunology	Allergy; Immunology	801LY	WOS:000220098600025	15005746	
J	Pronovost, P; Weast, B; Schwarz, M; Wyskiel, RM; Prow, D; Milanovich, SN; Berenholtz, S; Dorman, T; Lipsett, P				Pronovost, P; Weast, B; Schwarz, M; Wyskiel, RM; Prow, D; Milanovich, SN; Berenholtz, S; Dorman, T; Lipsett, P			Medication reconciliation: A practical tool to reduce the risk of medication errors	JOURNAL OF CRITICAL CARE			English	Article							ACUTE MYOCARDIAL-INFARCTION; HOSPITALIZED-PATIENTS; EVENTS; DISEASE	Preventable adverse drug events are associated with one out of five injuries or deaths. Estimates reveal that 46% of medication errors occur on admission or discharge from a clinical unit/hospital when patient orders are written. This study was performed to reduce medication errors in patient's discharge orders through a reconciliation process in an adult surgical intensive care unit (ICU). A discharge survey was implemented as part of the medication reconciliation process. The admitting nurse initiated the survey within 24 hours of ICU admission and the charge nurse completed the survey on discharge. Baseline data were obtained through a random sampling of 10% of discharges in first 2 weeks of the study (July 2001-May 2002). Medical and anesthesia records were reviewed, allergies and home medications verified with patient/family and findings compared with orders at time of ICU discharge. Baseline data revealed that 31 of 33 (94%) patients had orders changed. By week 24, nearly all medication errors in discharge orders were eliminated. In conclusion, use of the discharge survey in this medication reconciliation process resulted in a dramatic drop in medications errors for patients discharged from an ICU. The survey is now a part of our electronic medical record and used in 4 adult ICUs and 2 medicine floors. (C) 2003 Elsevier Inc. All rights reserved.	Johns Hopkins Univ, Dept Anesthesiol & Crit Care Med Surg, Baltimore, MD USA	Pronovost, P (reprint author), 901 S Bond St,Suite 318, Baltimore, MD 21231 USA.						*AHA, 2003, HEART STROK FACTS 20; Agency for Healthcare Research and Quality (AHRQ), 2002, TRANSL RES PRACT RED; Bates DW, 1997, JAMA-J AM MED ASSOC, V277, P307, DOI 10.1001/jama.277.4.307; Boersma E, 2001, JAMA-J AM MED ASSOC, V285, P1865, DOI 10.1001/jama.285.14.1865; Braunstein J B, 2001, Cardiol Rev, V9, P96, DOI 10.1097/00045415-200103000-00008; FROLKIS J, 1999, CIRCULATION, V95, P851; KOHN L, 1999, MTO ERR IS HUMAN BUI; Langley G, 1996, IMPROVEMENT GUIDE PR; LEAPE LL, 1991, NEW ENGL J MED, V324, P377, DOI 10.1056/NEJM199102073240605; MANGANO D, 1997, NEW ENGL J MED, V335, P1713; Newby LK, 2000, NEW ENGL J MED, V342, P749, DOI 10.1056/NEJM200003163421101; *NTSB, 2002, WE ARE ALL SAF NTSB; PILOTE L, 1995, NEW ENGL J MED, V333, P565, DOI 10.1056/NEJM199508313330907; Reason J, 2000, BRIT MED J, V320, P786; SEXTON JB, 2001, P 11 INT S AV PSYCH; Smith SC, 2001, CIRCULATION, V104, P1577, DOI 10.1161/hc3801.097475; Sueta CA, 1999, AM J CARDIOL, V83, P1303, DOI 10.1016/S0002-9149(99)00117-4	17	140	145	5	22	W B SAUNDERS CO	PHILADELPHIA	INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA	0883-9441			J CRIT CARE	J. Crit. Care	DEC	2003	18	4					201	205		10.1016/S0883-9441(03)00108-4		5	Critical Care Medicine	General & Internal Medicine	759BG	WOS:000187717500001	14691892	
J	Utell, MJ; Frampton, MW				Utell, MJ; Frampton, MW			Acute health effects of ambient air pollution: The ultrafine particle hypothesis	JOURNAL OF AEROSOL MEDICINE-DEPOSITION CLEARANCE AND EFFECTS IN THE LUNG			English	Article; Proceedings Paper	12th International Congress of the Internatioanl-Society-for-Aerosols-in-Medicine (ISAM)	JUN 12-16, 1999	VIENNA, AUSTRIA	Int Soc Aerosols Med		air pollution; particulate matter; ultrafine particles	MORTALITY	A strong and consistent association has been observed between adjusted mortality rates and ambient particle concentration. The strongest associations are seen for respiratory and cardiac deaths, particularly among the elderly. Particulate air pollution is also associated with asthma exacerbations, increased respiratory symptoms, decreased lung function, increased medication use, and increased hospital admissions. The U.S. Environmental Protection Agency (EPA) has recently promulgated a new national ambient air quality standard for fine particles, and yet the mechanisms for health effects at such low particle mass concentrations remain unclear. Hypotheses to identify the responsible particles have focused on particle acidity, particle content of transition metals, bioaerosols, and ultrafine particles. Because ultrafine particles are efficiently deposited in the respiratory tract and may be important in initiating airway inflammation, we have initiated clinical studies with ultrafine carbon particles in healthy subjects. These studies examine the role of ultrafines in: (1) the induction of airway inflammation; (2) expression of leukocyte and endothelial adhesion molecules in blood; (3) the alteration of blood coagulability; and (4) alteration in cardiac electrical activity. These events could lead to exacerbation of underlying cardiorespiratory disease. For example, airway inflammation may activate endothelium and circulating leukocytes, and induce a systemic acute phase response with transient hypercoagulability; this could explain the epidemiologic linkages between pollutant exposures and cardiovascular events. These approaches should be useful in identifying mechanisms for pollutant-induced respiratory and systemic effects, and in providing data for determining appropriate air quality standards.	Univ Rochester, Med Ctr, Dept Med, Pulm Unit, Rochester, NY 14642 USA	Utell, MJ (reprint author), Univ Rochester, Med Ctr, Dept Med, Pulm Unit, Box 692,601 Elmwood Ave, Rochester, NY 14642 USA.						Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; BOSCIA JA, 2000, AM J RESP CRIT CARE, V161, pA239; BRAND P, 1991, ATMOS ENVIRON A-GEN, V25, P581, DOI 10.1016/0960-1686(91)90055-C; BRAND P, 1992, ATMOS ENVIRON A-GEN, V26, P2541; CAMPEN MJ, 1997, AM J RESP CRIT CARE, V155, pA247; COLOME SD, 1992, ATMOS ENVIRON A-GEN, V26, P2173, DOI 10.1016/0960-1686(92)90405-A; FRAMPTON MW, 2000, PARTICLE LUNG INTERA, P653; FRAMPTON MW, 2000, AM J RESP CRIT CARE, V161, pA257; Godleski J. J., 2000, 91 HLTH EFF I; International Committee on Radiological Protection, 1994, HUM RESP TRACT MOD R; Lioy PJ, 1999, J AIR WASTE MANAGE, V49, P200, DOI 10.1080/10473289.1999.10463789; LUKACS NW, 1995, AM J RESP CELL MOL, V13, P1; Mauderly J, 1998, ATMOSPHERIC OBSERVATIONS: HELPING BUILD THE SCIENTIFIC BASIS FOR DECISIONS RELATED TO AIRBORNE PARTICULATE MATTER, P9; *NAT RES COUNC, 1998, RES PRIOR AIRB PART, V1, P44; OBERDORSTER G, 1995, INHAL TOXICOL, V7, P111, DOI 10.3109/08958379509014275; Oberdorster G, 1994, ANN OCCUP HYG     S1, V38, P295; Peters A, 1997, LANCET, V349, P1582, DOI 10.1016/S0140-6736(97)01211-7; PETERS A, 1998, AM J RESP CRIT CARE, V157, P880; Petersen LJ, 1997, NEPHROL DIAL TRANSPL, V12, P1376, DOI 10.1093/ndt/12.7.1376; Riesenfeld E, 2000, INHAL TOXICOL, V12, P83, DOI 10.1080/08958378.2000.11463201; Salmi M, 1997, ADV IMMUNOL, V64, P139, DOI 10.1016/S0065-2776(08)60889-5; SEATON A, 1995, LANCET, V345, P176, DOI 10.1016/S0140-6736(95)90173-6	22	140	145	2	29	MARY ANN LIEBERT INC PUBL	LARCHMONT	2 MADISON AVENUE, LARCHMONT, NY 10538 USA	0894-2684			J AEROSOL MED	J. Aerosol Med.-Depos. Clear. Eff. Lung	WIN	2000	13	4					355	359		10.1089/jam.2000.13.355		5	Public, Environmental & Occupational Health; Respiratory System	Public, Environmental & Occupational Health; Respiratory System	395UH	WOS:000166599300005	11262441	
J	Hofmann, AM; Scurlock, AM; Jones, SM; Palmer, KP; Lokhnygina, Y; Steele, PH; Kamilaris, J; Burks, AW				Hofmann, Alison M.; Scurlock, Amy M.; Jones, Stacie M.; Palmer, Kricia P.; Lokhnygina, Yuliya; Steele, Pamela H.; Kamilaris, Janet; Burks, A. Wesley			Safety of a peanut oral immunotherapy protocol in children with peanut allergy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Peanut; food allergy; oral immunotherapy	TREE NUT ALLERGY; ANAPHYLACTIC REACTIONS; TOLERANCE INDUCTION; EGG ALLERGY; FOOD; DESENSITIZATION	Background: Oral immunotherapy (OIT) offers a promising therapeutic option for peanut allergy. Given that during OIT an allergic patient ingests an allergen that could potentially cause a serious reaction, the safety of OIT is of particular concern. Objective: The purpose of this study was to examine safety during the initial escalation day, buildup phase, and home dosing phase in subjects enrolled in a peanut OIT study. Methods: Skin, upper respiratory tract, chest, and abdominal symptoms were recorded with initial escalation day and buildup phase dosings. Subjects also maintained daily diaries detailing symptoms after each home dosing. A statistical analysis of these data was performed. Results: Twenty of 28 patients completed all phases of the study. During the initial escalation day, upper respiratory tract (79%) and abdominal (68%) symptoms were the most likely symptoms experienced. The risk of mild wheezing during the initial escalation day was 18%. The probability of having any symptoms after a buildup phase dose was 46%, with a risk of 29% for upper respiratory tract symptoms and 24% for skin symptoms. The risk of reaction with any home dose was 3.5%. Upper respiratory tract (1.2%) and skin (1.1%) symptoms were the most likely after home doses. Treatment was given with 0.7% of home doses. Two subjects received epinephrine after I home dose each. Conclusions: Subjects were more likely to have significant allergic symptoms during the initial escalation day when they were in a closely monitored setting than during other phases of the study. Allergic reactions with home doses were rare. (J Allergy Clin Immunol 2009;124:286-91.)	[Hofmann, Alison M.; Steele, Pamela H.; Kamilaris, Janet; Burks, A. Wesley] Duke Univ, Med Ctr, Div Allergy & Immunol, Dept Pediat, Durham, NC 27710 USA; [Scurlock, Amy M.; Jones, Stacie M.; Palmer, Kricia P.] Univ Arkansas, Dept Pediat, Div Allergy & Immunol, Little Rock, AR 72204 USA; [Lokhnygina, Yuliya] Duke Univ, Dept Biostat & Bioinformat, Durham, NC 27706 USA	Burks, AW (reprint author), Duke Univ, Med Ctr, Div Allergy & Immunol, Dept Pediat, Box 2644, Durham, NC 27710 USA.	wesley.burks@duke.edu			Food Allergy and Anaphylaxis Network; Gerber Foundation; Food Allergy Project; Dorothy and Frank Robins Family Foundation; National Center for Research Resources (NCRR) [1 UL 1 RR024128-01]; National Institutes of Health (NIH); NIH Roadmap for Medical Research	Supported by the Food Allergy and Anaphylaxis Network, the Gerber Foundation, the Food Allergy Project, and the Dorothy and Frank Robins Family Foundation. The project described was supported by grant no. 1 UL 1 RR024128-01 from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH) and NIH Roadmap for Medical Research, and its contents are solely the responsibility of the authors and do not necessarily represent the official view of NCRR or NIH.	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Allergy Clin. Immunol.	AUG	2009	124	2					286	291		10.1016/j.jaci.2009.03.045		6	Allergy; Immunology	Allergy; Immunology	482CD	WOS:000268860400015	19477496	
J	Joubert, E; Gelderblom, WCA; Louw, A; de Beer, D				Joubert, E.; Gelderblom, W. C. A.; Louw, A.; de Beer, D.			South African herbal teas: Aspalathus linearis, Cyclopia spp. and Athrixia phylicoides-A review	JOURNAL OF ETHNOPHARMACOLOGY			English	Review						Anticarcinogenic; Antioxidant; Bush tea; Chemical composition; Honeybush; Phyto-oestrogenic; Polyphenols; Rooibos	CAMELLIA-SINENSIS TEAS; ANTIOXIDANT ACTIVITY RELATIONSHIPS; BATCH EXTRACTION CONDITIONS; MAJOR PHENOLIC-COMPOUNDS; FIXED-BED EXTRACTION; ROOIBOS TEA; HONEYBUSH TEA; AQUEOUS EXTRACTS; BUSH TEA; IN-VITRO	Rooibos (Aspalathus linearis (Brum.f) Dahlg.) and honeybush (Cyclopia Vent. species) are popular indigenous South African herbal teas enjoyed for their taste and aroma. Traditional medicinal uses of rooibos in South Africa include alleviation of infantile colic, allergies, asthma and dermatological problems, while a decoction of honeybush was used as a restorative and as an expectorant in chronic catarrh and pulmonary tuberculosis. Traditional medicinal uses of Athrixia phylicoides DC., or bush tea, another indigenous South African plant with very limited localised use as herbal tea, include treatment of boils, acne, infected wounds and infected throats. Currently rooibos and honeybush are produced for the herbal tea market, while bush tea has potential for commercialisation. A summary of the historical and modern uses, botany, distribution, industry and chemical composition of these herbal teas is presented. A comprehensive discussion of in vitro, ex vivo and in vivo biological properties, required to expand their applications as nutraceutical and cosmeceutical products, is included, with the main emphasis on rooibos. Future research needs include more comprehensive chemical characterisation of extracts, identification of marker compounds for extract standardisation and quality control, bioavailability and identification of bio-markers of dietary exposure, investigation of possible herb-drug interactions and plant improvement with regards to composition and bioactivity. (C) 2008 Elsevier Ireland Ltd. All rights reserved.	[Joubert, E.; de Beer, D.] ARC Infruitec Nietvoorbij, Post Harvest & Wine Technol Div, ZA-7599 Stellenbosch, South Africa; [Joubert, E.] Univ Stellenbosch, Dept Food Sci, ZA-7602 Matieland, South Africa; [Gelderblom, W. C. A.] MRC, PROMEC Unit, ZA-7505 Bellville, South Africa; [Gelderblom, W. C. A.; Louw, A.] Univ Stellenbosch, Dept Biochem, ZA-7602 Matieland, South Africa	Joubert, E (reprint author), ARC Infruitec Nietvoorbij, Post Harvest & Wine Technol Div, Private Bag X5026, ZA-7599 Stellenbosch, South Africa.	joubertL@arc.agric.za	Louw, Ann/A-7620-2012	Louw, Ann/0000-0002-1021-6732; De Beer, Dalene/0000-0002-3680-142X; Joubert, Elizabeth/0000-0002-9717-9769			Adlercreutz H, 1997, ANN MED, V29, P95; AKAIKE T, 1995, J AGR FOOD CHEM, V43, P1864, DOI 10.1021/jf00055a021; Almajano MP, 2008, FOOD CHEM, V108, P55, DOI 10.1016/j.foodchem.2007.10.040; AMIN A, 2007, RECENT PAT ANTI-CANC, V2, P1; Araya H. 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W., 2002, SA Patent, Patent No. [2002/2802, 20022802]; 2006, S AFRICAN FOOD REV, V33, P24; 2005, FOODNAVIGATOR E 1201; 1991, ROOIBOS TEA BOARD AN; 2008, ATHRIXIA; 1994, ROOIBOS, P4; 1967, ROOIBOS TEA BOARD AN	211	139	146	3	29	ELSEVIER IRELAND LTD	CLARE	ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND	0378-8741			J ETHNOPHARMACOL	J. Ethnopharmacol.	OCT 28	2008	119	3					376	412		10.1016/j.jep.2008.06.014		37	Plant Sciences; Chemistry, Medicinal; Integrative & Complementary Medicine; Pharmacology & Pharmacy	Plant Sciences; Pharmacology & Pharmacy; Integrative & Complementary Medicine	372LU	WOS:000260903900006	18621121	
J	Kolarik, B; Naydenov, K; Larsson, M; Bornehag, CG; Sundell, J				Kolarik, Barbara; Naydenov, Kiril; Larsson, Malin; Bornehag, Carl-Gustaf; Sundell, Jan			The association between phthalates in dust and allergic diseases among Bulgarian children	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						allergy; asthma; children; DEHP; phthalates	IN-HOUSE DUST; INTERIOR SURFACE MATERIALS; DI(2-ETHYLHEXYL) PHTHALATE; PRESCHOOL-CHILDREN; YOUNG-CHILDREN; INDOOR AIR; ASTHMA; SYMPTOMS; EXPOSURE; POPULATION	BACKGROUND: Recent studies have identified associations between the concentration of phthalates in indoor dust and allergic symptoms in the airways, nose, and skin. OBJECTIVES: Our goal was to investigate the associations between allergic symptoms in children and the concentration of phthalate esters in settled dust collected from children's homes in Sofia and Burgas, Bulgaria. METHODS: Dust samples from the child's bedroom were collected. A total of 102 children (2-7 Years of age) had symptoms of wheezing, rhinitis, and/or eczema in preceding 12 months (cases), and 82 were nonsymptomatic (controls). The dust samples were analyzed for their content of dimethyl phthalate (DMP), diethyl phthalate (DEP), di-n-butyl phthalate (DnBP), butyl benzyl phthalate (BBzP), di(2-ethylhexyl) phthalate (DEHP), and di-n-octyl phthalate (DnOP). RESULTS: A higher concentration of DEHP was found in homes of case children than in those of controls (1.24 vs. 0.86 mg/g dust). The concentration of DEHP was significantly associated with wheezing in the preceding 12 months (p = 0.035) as reported by parents. We found a dose-response relationship between DEHP concentration and case status and between DEHP concentration and wheezing in the preceding 12 months. CONCLUSIONS: This study shows an association between concentration of DEHP in indoor dust and wheezing among preschool children in Bulgaria.	[Kolarik, Barbara] Silesian Tech Univ, Fac Environm Engn & Energy, ISE, OWiTO, PL-44100 Gliwice, Poland; [Kolarik, Barbara] Tech Univ Denmark, Dept Mech Engn, Int Ctr Indoor Environm & Energy, DK-2800 Lyngby, Denmark; [Naydenov, Kiril] Birch & Krogboe AS, Virum, Denmark; [Bornehag, Carl-Gustaf] SP Tech Res Inst Sweden, Boras, Sweden	Kolarik, B (reprint author), Silesian Tech Univ, Fac Environm Engn & Energy, ISE, OWiTO, Konarskiego 18, PL-44100 Gliwice, Poland.	bf@mek.dtu.dk	Sundell, Jan/B-2857-2012				Adibi JJ, 2003, ENVIRON HEALTH PERSP, V111, P1719, DOI 10.1289/ehp.6235; Asher MI, 1998, EUR RESPIR J, V12, P315; ASHER MI, 2006, LANCET, V368, P783; Becker K, 2004, INT J HYG ENVIR HEAL, V207, P409, DOI 10.1078/1438-4639-00309; Blount BC, 2000, ENVIRON HEALTH PERSP, V108, P979, DOI 10.1289/ehp.00108979; Bornehag CG, 2006, SCAND J PUBLIC HEALT, V34, P534, DOI 10.1080/14034940600607467; Bornehag CG, 2005, INDOOR AIR, V15, P48, DOI 10.1111/j.1600-0668.2005.00306.x; Bornehag CG, 2005, ENVIRON HEALTH PERSP, V113, P1399, DOI 10.1289/ehp.7809; Bornehag CG, 2004, ENVIRON HEALTH PERSP, V112, P1393, DOI 10.1289/ehp.7187; Brasche S, 2005, INT J HYG ENVIR HEAL, V208, P247, DOI 10.1016/j.ijheh.2005.03.003; Butte W, 2001, GEFAHRST REINHALT L, V61, P19; CALAFAT A, 2004, PEDIATRICS, V113, P429; Chalubinski M, 2006, ALLERGY, V61, P1326, DOI 10.1111/j.1398-9995.2006.01135.x; Clausen PA, 2003, J CHROMATOGR A, V986, P179, DOI 10.1016/S0021-9673(02)02007-1; Fromme H, 2004, INDOOR AIR, V14, P188, DOI 10.1046/j.1600-0668.2003.00223.x; Glue C, 2005, BASIC CLIN PHARMACOL, V96, P140, DOI 10.1111/j.1742-7843.2005.pto960208.x; Green R, 2005, ENVIRON HEALTH PERSP, V113, P1222, DOI 10.1289/chp.7932; *ISAAC, 1998, ISAAC PHAS 2; Jaakkola JJK, 1999, AM J PUBLIC HEALTH, V89, P188, DOI 10.2105/AJPH.89.2.188; Jaakkola JJK, 2000, AM J PUBLIC HEALTH, V90, P797, DOI 10.2105/AJPH.90.5.797; Jaakkola JJK, 2006, AM J EPIDEMIOL, V164, P742, DOI 10.1093/aje/kwj249; KERSTEN W, 2003, REINHALTUNG LUFT, V63, P85; Koch HM, 2005, INT ARCH OCC ENV HEA, V78, P223, DOI 10.1007/s00420-004-0570-x; Koch HM, 2003, INT J HYG ENVIR HEAL, V206, P77, DOI 10.1078/1438-4639-00205; Larsen ST, 2007, TOXICOLOGY, V235, P119, DOI 10.1016/j.tox.2007.03.010; Lee MH, 2004, INT ARCH ALLERGY IMM, V134, P213, DOI 10.1159/000078768; Naydenov K., 2005, P 10 INT C IND ARI Q, P3574; Naydenov K G, 2007, THESIS TU DENMARK LY; Nielsen GD, 2007, INDOOR AIR, V17, P236, DOI 10.1111/j.1600-0668.2006.00468.x; Oie L, 1997, ENVIRON HEALTH PERSP, V105, P972; Platts-Mills TAE, 2005, ALLERGY, V60, P25, DOI 10.1111/j.1398-9995.2005.00854.x; POHNER A, 1997, UMWELT GESUNDHEIT, V2, P1; Rudel RA, 2003, ENVIRON SCI TECHNOL, V37, P4543, DOI 10.1021/es0264596; STRACHAN DP, 1989, BRIT MED J, V299, P1259; World Health Organization (WHO), 2003, CHILDR RISK MAIN HLT; Wormuth M, 2006, RISK ANAL, V26, P803, DOI 10.1111/j.1539-6924.2006.00770.x	36	139	150	4	61	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	JAN	2008	116	1					98	103		10.1289/ehp.10498		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	248GZ	WOS:000252142100031	18197306	
J	Brugge, D; Durant, JL; Rioux, C				Brugge, Doug; Durant, John L.; Rioux, Christine			Near-highway pollutants in motor vehicle exhaust: A review of epidemiologic evidence of cardiac and pulmonary health risks	ENVIRONMENTAL HEALTH			English	Review							PARTICULATE AIR-POLLUTION; HEART-RATE-VARIABILITY; LONG-TERM EXPOSURE; CHRONIC RESPIRATORY SYMPTOMS; LUNG-CANCER; ULTRAFINE PARTICLES; SUBMICROMETER PARTICLES; CHILDHOOD ASTHMA; SCHOOL-CHILDREN; URBAN AIR	There is growing evidence of a distinct set of freshly-emitted air pollutants downwind from major highways, motorways, and freeways that include elevated levels of ultrafine particulates (UFP), black carbon (BC), oxides of nitrogen (NOx), and carbon monoxide (CO). People living or otherwise spending substantial time within about 200 m of highways are exposed to these pollutants more so than persons living at a greater distance, even compared to living on busy urban streets. Evidence of the health hazards of these pollutants arises from studies that assess proximity to highways, actual exposure to the pollutants, or both. Taken as a whole, the health studies show elevated risk for development of asthma and reduced lung function in children who live near major highways. Studies of particulate matter (PM) that show associations with cardiac and pulmonary mortality also appear to indicate increasing risk as smaller geographic areas are studied, suggesting localized sources that likely include major highways. Although less work has tested the association between lung cancer and highways, the existing studies suggest an association as well. While the evidence is substantial for a link between near-highway exposures and adverse health outcomes, considerable work remains to understand the exact nature and magnitude of the risks.			dbrugge@aol.com; john.durant@tufts.edu; Christine.rioux@tufts.edu	Durant, John/F-2424-2017	Durant, John/0000-0002-7016-1622	NIEHS NIH HHS [R01 ES015462]		Adar SD, 2007, EPIDEMIOLOGY, V18, P95, DOI 10.1097/01.ede.0000249409.81050.46; *AM HOUS SURV US, 2003, H15003 AM HOUS SURV; Beeson WL, 1998, ENVIRON HEALTH PERSP, V106, P813, DOI 10.1289/ehp.98106813; Biggeri A, 1996, ENVIRON HEALTH PERSP, V104, P750, DOI 10.2307/3433221; Brauer M, 2007, EUR RESPIR J, V29, P879, DOI 10.1183/09031936.00083406; Brauer M, 2003, EPIDEMIOLOGY, V14, P228, DOI 10.1097/00001648-200303000-00019; Brook RD, 2004, CIRCULATION, V109, P2655, DOI 10.1161/01.CIR.0000128587.30041.C8; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; Brunekreef B, 2002, LANCET, V360, P1233, DOI 10.1016/S0140-6736(02)11274-8; Chambers L A, 1976, AIR POLLUTION, V1; Chan CC, 2004, ENVIRON HEALTH PERSP, V112, P1063, DOI 10.1289/chp.6897; Choi KS, 1997, ARCH ENVIRON HEALTH, V52, P160; Chuang KJ, 2005, ENVIRON HEALTH PERSP, V113, P1693, DOI 10.1289/ehp.8145; Delfino RJ, 2005, ENVIRON HEALTH PERSP, V113, P934, DOI 10.1289/ehp.7938; Delfino RJ, 2004, ENVIRON HEALTH PERSP, V112, P932, DOI 10.1289/ehp.6815; DOCKERY DW, 1993, NEW ENGL J MED, V329, P1753, DOI 10.1056/NEJM199312093292401; English P, 1999, ENVIRON HEALTH PERSP, V107, P761, DOI 10.2307/3434663; Finkelstein MM, 2005, J EPIDEMIOL COMMUN H, V59, P481, DOI 10.1136/jech.2004.026203; Fischer PH, 2000, ATMOS ENVIRON, V34, P3713, DOI 10.1016/S1352-2310(00)00067-4; Gauderman WJ, 2007, LANCET, V369, P571, DOI 10.1016/S0140-6736(07)60037-3; Gauderman WJ, 2000, AM J RESP CRIT CARE, V162, P1383; Gauderman WJ, 2004, NEW ENGL J MED, V351, P1057, DOI 10.1056/NEJMoa040610; Gauderman WJ, 2005, EPIDEMIOLOGY, V16, P737, DOI 10.1097/01.ede.00001813087.51440.75; Graedel T. 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S. Environmental Protection Agency, 2004, AIR QUAL CRIT PART M; U. S. Environmental Protection Agency, 2002, HLTH ASS DOC DIES EN; van der Zee SC, 1999, OCCUP ENVIRON MED, V56, P802; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; Venn A, 2005, OCCUP ENVIRON MED, V62, P376, DOI 10.1136/oem.2004.017228; Venn A, 2000, OCCUP ENVIRON MED, V57, P152, DOI 10.1136/oem.57.3.152; Venn AJ, 2001, AM J RESP CRIT CARE, V164, P2177, DOI 10.1164/rccm2106126; Vineis P, 2006, INT J CANCER, V119, P169, DOI 10.1002/ijc.21801; Vinzents PS, 2005, ENVIRON HEALTH PERSP, V113, P1485, DOI 10.1289/ehp.7562; Visser O, 2004, CANCER CAUSE CONTROL, V15, P331, DOI 10.1023/B:CACO.0000027480.32494.a3; WALDRON G, 1995, J PUBLIC HEALTH MED, V17, P85; Wheeler A, 2006, ENVIRON HEALTH PERSP, V114, P560, DOI 10.1289/ehp.8337; WJST M, 1993, BRIT MED J, V307, P596; Zhang KM, 2004, ATMOS ENVIRON, V38, P6655, DOI 10.1016/j.atmosenv.2004.06.044; Zhu YF, 2002, J AIR WASTE MANAGE, V52, P1032; Zhu YF, 2002, ATMOS ENVIRON, V36, P4323, DOI 10.1016/S1352-2310(02)00354-0	91	139	144	6	68	BIOMED CENTRAL LTD	LONDON	236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND	1476-069X			ENVIRON HEALTH-GLOB	Environ. Health	AUG 9	2007	6								23	10.1186/1476-069X-6-23		12	Environmental Sciences; Public, Environmental & Occupational Health	Environmental Sciences & Ecology; Public, Environmental & Occupational Health	208EA	WOS:000249301400001	17688699	
J	Clougherty, JE; Levy, JI; Kubzansky, LD; Ryan, PB; Suglia, SF; Canner, MJ; Wright, RJ				Clougherty, Jane E.; Levy, Jonathan I.; Kubzansky, Laura D.; Ryan, P. Barry; Suglia, Shakira Franco; Canner, Marina Jacobson; Wright, Rosalind J.			Synergistic effects of traffic-related air pollution and exposure to violence on urban asthma etiology	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						childhood asthma; exposure to violence (ETV); geographic information systems (GIS); intraurban variability; nitrogen dioxide (NO2); social-environmental synergy; stress	COMMUNITY VIOLENCE; ENVIRONMENTAL JUSTICE; HEALTH DISPARITIES; STRESS REACTIVITY; CHILDHOOD ASTHMA; LUNG-FUNCTION; BIRTH-COHORT; CHILDREN; ASSOCIATION; SYMPTOMS	BACKGROUND: Disproportionate-life stress and consequent physiologic alteration (i.e., immune dysregulation) has been proposed as a major pathway linking socioeconomic position, environmental exposures, and health disparities. Asthma, for example, disproportionately affects lower-income urban communities, where air pollution and social stressors may be elevated. OBJECTIVES: We aimed to examine the role of exposure to violence (ETV), as a chronic stressor, in altering susceptibility to traffic-related air pollution in asthma etiology. METHODS: We developed geographic information systems (GIS)-based models to retrospectively estimate residential exposures to traffic-related pollution for 413 children in a community-based pregnancy cohort, recruited in East Boston, Massachusetts, between 1987 and 1993, using monthly nitrogen dioxide measurements for 13 sites over 18 years. We merged pollution estimates with questionnaire data on lifetime ETV and examined the effects of both on childhood asthma etiology. RESULTS: Correcting for potential confounders, we found an elevated risk of asthma with a 1-SD (4.3 ppb) increase in NO2 exposure solely among children with above-median ETV [odds ratio (OR) = 1.63; 95% confidence interval (0), 1.14-2-33)]. Among children always living in the same community, with lesser exposure measurement error, this association was magnified (OR = 2.40; 95% Cl, 1.48-3.88). Of multiple exposure periods, year-of-diagnosis NO2 was most predictive of asthma, outcomes. CONCLUSIONS: We found an association between traffic-related air pollution and asthma solely among urban children exposed to violence. Future studies should consider socially patterned susceptibility, common spatial distributions of social and physical environmental factors, and potential synergies among these. Prospective assessment of physical and social exposures may help determine causal pathways and critical exposure periods.	Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02215 USA; Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Boston, MA 02215 USA; Emory Univ, Rollins Sch Publ Hlth, Dept Environm Hlth, Atlanta, GA 30322 USA; Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02215 USA; Harvard Univ, Sch Med, Boston, MA 02215 USA; Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA	Clougherty, JE (reprint author), Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Landmark Ctr Room 404,POB 15677, Boston, MA 02215 USA.	jcloughe@hsph.harvard.edu	Levy, Jonathan/A-9102-2008; Ryan, P. 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Health Perspect.	AUG	2007	115	8					1140	1146		10.1289/ehp.9863		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	197CO	WOS:000248531400026	17687439	
J	Saxon, A; Diaz-Sanchez, D				Saxon, A; Diaz-Sanchez, D			Air pollution and allergy: you are what you breathe	NATURE IMMUNOLOGY			English	Editorial Material							S-TRANSFERASE M1; OZONE EXPOSURE; POLYMORPHISMS; CHALLENGE; RESPONSES; CHILDREN; ASTHMA; CELLS	How does air pollution affect asthma and allergic rhinitis? Particulate and gaseous pollution drive proallergic inflammation through the generation of oxidative stress, which is regulated by individual genetic susceptibility.	Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Clin Immunol,Hart & Louis Lab, Los Angeles, CA 90095 USA	Saxon, A (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Clin Immunol,Hart & Louis Lab, Los Angeles, CA 90095 USA.	ddiazsa@mednet.ucla.edu					Bayley JP, 2004, GENES IMMUN, V5, P315, DOI 10.1038/sj.gene.6364055; Bernstein JA, 2004, J ALLERGY CLIN IMMUN, V114, P1116, DOI 10.1016/j.jaci.2004.08.030; Chen LL, 2004, CHEST, V125, P2328, DOI 10.1378/chest.125.6.2328; David GL, 2003, AM J RESP CRIT CARE, V168, P1199, DOI 10.1164/rccm.200305-684OC; Diaz-Sanchez D, 1999, J ALLERGY CLIN IMMUN, V104, P1183; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; Fahy O, 2002, J IMMUNOL, V168, P5912; Gilliland FD, 2002, AM J RESP CRIT CARE, V166, P457, DOI 10.1164/rccm.2112064; Gilliland FD, 2004, LANCET, V363, P119, DOI 10.1016/S0140-6736(03)15262-2; Heinrich Joachim, 2004, Curr Opin Allergy Clin Immunol, V4, P341, DOI 10.1097/00130832-200410000-00003; Hollingsworth JW, 2004, AM J RESP CRIT CARE, V170, P126, DOI 10.1164/rccm.200311-1499OC; Kleeberger SR, 2000, AM J RESP CELL MOL, V22, P620; LONDON SJ, 1995, J NATL CANCER I, V87, P1246, DOI 10.1093/jnci/87.16.1246; Romieu I, 2004, THORAX, V59, P8; Shore SA, 2001, AM J RESP CRIT CARE, V164, P602; Takizawa Hajime, 2004, Curr Opin Allergy Clin Immunol, V4, P355, DOI 10.1097/00130832-200410000-00005; Todokoro M, 2004, INFLAMMATION, V28, P105, DOI 10.1023/B:IFLA.0000033026.91221.ed; U. S. EPA, 1997, NAT AIR POLL EM TREN; Xiao GG, 2003, J BIOL CHEM, V278, P50781, DOI 10.1074/jbc.M306423200; YANG IA, 2004, AM J RESP CRIT CARE, V171, P171	20	139	145	1	13	NATURE PUBLISHING GROUP	NEW YORK	345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA	1529-2908			NAT IMMUNOL	Nat. Immunol.	MAR	2005	6	3					223	226		10.1038/ni0305-223		4	Immunology	Immunology	899AN	WOS:000227117400002	15716966	
J	Arshad, SH; Kurukulaaratchy, RJ; Fenn, M; Matthews, S				Arshad, SH; Kurukulaaratchy, RJ; Fenn, M; Matthews, S			Early life risk factors for current wheeze, asthma, and bronchial hyperresponsiveness at 10 years of age	CHEST			English	Article						atopy; bronchial hyperresponsiveness; childhood asthma; risk factors; wheezing	AUSTRALIAN SCHOOLCHILDREN; ENVIRONMENTAL-FACTORS; RESPIRATORY SYMPTOMS; ALLERGIC DISORDERS; PARENTAL SMOKING; 2 POPULATIONS; BIRTH COHORT; NEW-ZEALAND; CHILDREN; PREVALENCE	Study objectives: We sought to identify early life factors (ie, first 4 years) associated with wheeze, asthma, and bronchial hyperresponsiveness (BHR) at age 10 years, comparing their relative influence for these conditions. Methods: Children were seen at birth, and at 1, 2, 4, and 10 years of age in a whole-population birth cohort study (1,456 subjects). Information was collected prospectively on genetic and environmental risk factors. Skin-prick testing was performed at 4 years of age. Current wheeze (in the last 12 months) and currently diagnosed asthma (CDA) [ie, current wheeze and ever-diagnosed asthmatic subject] were recorded at 10 years of age when BHR was measured at bronchial challenge. Independent significant risk factors for these outcomes were identified by logistic regression. Results: Independent significance for current wheeze occurred with maternal asthma (odds ratio [OR], 2.08; 95% confidence interval [CI], 1.27 to 3.41) and paternal asthma (OR,. 2.12; 95% CI 1.29 to 3.51), recurrent chest infections at 2 years (OR, 3.98; 95% CI, 2.36 to 6.70), atopy at 4 years of age (OR, 3.69; 95% CI, 2.36 to 5.76), eczema at 4 years of age (OR, 2.15; 95% CI, 1.24 to 3.73), and parental smoking at 4 years of age (OR, 2.18; 95% CI, 1.25 to 3.81). For CDA, significant factors were maternal asthma (OR, 2.26; 95% CI, 1.24 to 3.73), paternal asthma (OR, 2.30; 95% CI, 1.17 to 4.52), and sibling asthma (OR, 2.00; 95% CI, 1.16 to 3.43), recurrent chest infections at I year of age (OR, 2.67; 95% CI, 1.12 to 6.40) and 2 years of age (OR, 4.11; 95% CI, 2.06 to S. IS), atopy at 4 years of age (OR, 7.22; 95% CI, 4.13 to 12.62), parental smoking at I year of age (OR, 1.99; 95% CI, 1.15 to 3.45), and male gender (OR, 1.72; 95% CI, 1.01 to 2.95). For BHR, atopy at 4 years of age (OR, 5.38; 95% CI, 3.06 to 9.47) and high social class at birth (OR, 2.03; 95% CI, 1.16 to 3.53) proved to be significant. Conclusions: Asthmatic heredity, predisposition to early life atopy, plus early passive smoke exposure and recurrent chest infections are important influences for the occurrence of wheeze and asthma at 10 years of age. BHR at 10 years of age has a narrower risk profile, suggesting that factors influencing wheezing symptom expression may differ from those predisposing the patient to BHR.	St Marys Hosp, David Hide Asthma & Allergy Res Ctr, Newport, Wight, England	Arshad, SH (reprint author), Univ Hosp N Staffordshire, Dept Resp Med, Newcastle Rd, Stoke On Trent ST4 6QG, Staffs, England.	sha@soton.ac.uk					Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; Apelberg BJ, 2001, J ALLERGY CLIN IMMUN, V107, P455, DOI 10.1067/mai.2001.113240; ARSHAD SH, 1992, J ALLERGY CLIN IMMUN, V90, P235, DOI 10.1016/0091-6749(92)90077-F; ARSHAD SH, 1993, CLIN EXP ALLERGY, V23, P504, DOI 10.1111/j.1365-2222.1993.tb03238.x; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; BURNEY PGJ, 1990, BRIT MED J, V300, P1306; BURR M L, 1989, Archives of Disease in Childhood, V64, P1452; CLIFFORD RD, 1987, ARCH DIS CHILD, V62, P66; CRANE J, 1989, J ALLERGY CLIN IMMUN, V84, P768, DOI 10.1016/0091-6749(89)90307-2; Crapo RO, 2000, AM J RESP CRIT CARE, V161, P309; DUFF AL, 1994, AM J RESP CRIT CARE, V149, P365; FORASTIERE F, 1994, AM J RESP CRIT CARE, V149, P365; Halken Susanne, 2003, Paediatr Respir Rev, V4, P128, DOI 10.1016/S1526-0542(03)00026-5; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Hide DW, 1996, PEDIATR ALLERGY IMMU, V7, P117, DOI 10.1111/j.1399-3038.1996.tb00410.x; Kurukulaaratchy RJ, 2003, J ALLERGY CLIN IMMUN, V112, P311, DOI 10.1067/mai.2003.1623; KURUKULAARATCHY RJ, 2002, RESP MED, V96, P162; Lau Susanne, 2002, Paediatr Respir Rev, V3, P265, DOI 10.1016/S1526-0542(02)00189-6; LEE DA, 1983, BRIT MED J, V286, P1256; Lemanske RF, 2003, J PEDIATR-US, V142, pS3, DOI 10.1067/mpd.2003.19; MARTINEZ FD, 1988, AM REV RESPIR DIS, V138, P518; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; MARTINEZ FD, 1994, THORAX, V49, P1189, DOI 10.1136/thx.49.12.1189; Oddy WH, 1999, BRIT MED J, V319, P815; PEAT JK, 1987, CLIN ALLERGY, V17, P283, DOI 10.1111/j.1365-2222.1987.tb02016.x; PEAT JK, 1994, BRIT MED J, V308, P1591; POSTMA DS, 1995, NEW ENGL J MED, V333, P894, DOI 10.1056/NEJM199510053331402; SALOME CM, 1987, CLIN ALLERGY, V17, P271, DOI 10.1111/j.1365-2222.1987.tb02015.x; Sarafino EP, 2000, PEDIATR ALLERGY IMMU, V11, P80, DOI 10.1034/j.1399-3038.2000.00065.x; SEARS MR, 1986, THORAX, V41, P283, DOI 10.1136/thx.41.4.283; Sears MR, 1996, ARCH DIS CHILD, V75, P392; SEARS MR, 1991, NEW ENGL J MED, V325, P1067, DOI 10.1056/NEJM199110103251504; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; Stein R, 1999, LANCET, V354, P541, DOI 10.1016/S0140-6736(98)10321-5; Stein RT, 1999, AM J EPIDEMIOL, V149, P1030; Tariq SM, 1998, J ALLERGY CLIN IMMUN, V101, P587; Van Asperen P P, 1994, Pediatr Allergy Immunol, V5, P178; vonMutius E, 1996, AM J RESP CRIT CARE, V153, P1266; VONMUTIUS E, 2000, AM J RESP CRIT CARE, V161, P1563	39	139	147	0	9	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	FEB	2005	127	2					502	508		10.1378/chest.127.2.502		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	898LV	WOS:000227079200018	15705988	
J	Dannenberg, AL; Jackson, RJ; Frumkin, H; Schieber, RA; Pratt, M; Kochtitzky, C; Tilson, HH				Dannenberg, AL; Jackson, RJ; Frumkin, H; Schieber, RA; Pratt, M; Kochtitzky, C; Tilson, HH			The impact of community design and land-use choices on public health: A scientific research agenda	AMERICAN JOURNAL OF PUBLIC HEALTH			English	Article							OUTDOOR AIR-POLLUTION; PHYSICAL-ACTIVITY; BUILT ENVIRONMENT; CHILDREN; TRENDS; SPRAWL; ASTHMA	The design of a community's built environment influences the physical and mental health of its residents. Because few studies have investigated this relationship, the Centers for Disease Control and Prevention hosted a workshop in May 2002 to help develop a scientific research agenda on these issues. Workshop participants' areas of expertise included physical activity, injury prevention, air pollution, water quality, urban planning, transportation, architecture, epidemiology, land use, mental health, social capital, housing, and social marketing. This report describes the 37 questions in the resulting research agenda. The next steps are to define priorities and obtain resources. The proposed research will help identify the best practices for designing new communities and revitalizing old ones in ways that promote physical and mental health.	CDC, Div Emergency & Environm Hlth Serv, Natl Ctr Environm Hlth, Atlanta, GA 30341 USA; Emory Univ, Rollins Sch Publ Hlth, Dept Environm & Occupat Hlth, Atlanta, GA 30322 USA; CDC, Natl Ctr Injury Prevent & Control, Atlanta, GA 30341 USA; CDC, Natl Ctr Chron Dis Prevent & Hlth Promot, Atlanta, GA 30341 USA; CDC, Natl Ctr Birth Defects & Dev Disabil, Atlanta, GA 30341 USA; Univ N Carolina, Sch Publ Hlth, Chapel Hill, NC 27515 USA	Dannenberg, AL (reprint author), CDC, Div Emergency & Environm Hlth Serv, Natl Ctr Environm Hlth, 4770 Buford Hwy,Mail Stop F-30, Atlanta, GA 30341 USA.						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J	Pearce, N; Douwes, J; Beasley, R				Pearce, N; Douwes, J; Beasley, R			Is allergen exposure the major primary cause of asthma?	THORAX			English	Review						asthma; allergen; childhood exposure; atopy	DUST MITE ALLERGEN; PAPUA-NEW-GUINEA; INNER-CITY CHILDREN; DER-P-I; RESPIRATORY SYMPTOMS; CHILDHOOD ASTHMA; RISK-FACTORS; LOS-ALAMOS; NEW-MEXICO; PREVALENCE	In recent decades a number of authors have argued that allergen exposure is the major primary cause of asthma, and that the global increases in asthma prevalence are due to increases in exposure to aeroallergens. We have assessed the epidemiological evidence in support of this hypothesis. No longitudinal studies were identified in which allergen exposure during infancy in a random population sample has been related to asthma risk after the age of six years. Two studies have been conducted in selected populations chosen on the basis of a family history of asthma or allergy; one study found a nonstatistically significant association whereas the other study found no association. Many of the identified prevalence studies in children showed negative associations between allergen exposure and current asthma, and the weighted averages of the population attributable risks in children were 4% for Der p 1, 11% for Fel d 1, -4% for Bla g 2, and 6% for Can f 1. There was little change in these estimates in studies in which children whose parents had adopted allergen avoidance measures were excluded. Furthermore, evidence from population studies is equivocal and provides little consistent evidence that allergen exposure is associated with the prevalence of asthma at the population level. Population-based cohort studies are clearly required, but currently available evidence does not indicate that allergen exposure is a major risk factor for the primary causation of asthma in children.	Wellington Sch Med, Wellington Asthma Res Grp, Wellington, New Zealand	Pearce, N (reprint author), Wellington Sch Med, Wellington Asthma Res Grp, POB 7343, Wellington, New Zealand.			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J	Guilliams, M; Bruhns, P; Saeys, Y; Hammad, H; Lambrecht, BN				Guilliams, Martin; Bruhns, Pierre; Saeys, Yvan; Hammad, Hamida; Lambrecht, Bart N.			The function of Fc gamma receptors in dendritic cells and macrophages	NATURE REVIEWS IMMUNOLOGY			English	Review							CYTOPLASMIC DOMAIN HETEROGENEITY; ANTIBODY-DEPENDENT ENHANCEMENT; DENGUE HEMORRHAGIC-FEVER; IGG IMMUNE-COMPLEXES; RII-MEDIATED UPTAKE; DUST MITE ALLERGEN; CD8(+) T-CELLS; ANTIGEN PRESENTATION; IN-VIVO; CROSS-PRESENTATION	Dendritic cells (DCs) and macrophages use various receptors to recognize foreign antigens and to receive feedback control from adaptive immune cells. Although it was long believed that all immunoglobutin Fc receptors are universally expressed by phagocytes, recent findings indicate that only monocyte-derived DCs and macrophages express high levels of activating Fc receptors for IgG (Fc gamma Rs), whereas conventional and plasmacytoid DCs express the inhibitory Fc gamma R. In this Review, we discuss how the uptake, processing and presentation of antigens by DCs and macrophages is influenced by Fc gamma R recognition of innmunoglobulins and immune complexes in the steady state and during inflammation.	[Guilliams, Martin; Saeys, Yvan; Hammad, Hamida; Lambrecht, Bart N.] VIB Inflammat Res Ctr, Immunoregulat Lab, B-9052 Ghent, Belgium; [Guilliams, Martin; Saeys, Yvan; Hammad, Hamida; Lambrecht, Bart N.] Univ Ghent, Dept Resp Med, B-9000 Ghent, Belgium; [Bruhns, Pierre] Inst Pasteur, Dept Immunol, Lab Anticorps Therapie & Pathol, F-75015 Paris, France; [Bruhns, Pierre] Inst Natl Sante & Rech Med, U760, F-75015 Paris, France; [Lambrecht, Bart N.] Erasmus Univ, Med Ctr, Dept Pulm Med, Rotterdam, Netherlands	Guilliams, M (reprint author), VIB Inflammat Res Ctr, Immunoregulat Lab, B-9052 Ghent, Belgium.	martin.guilliams@irc.vib-ugent.be; bart.lambrecht@irc.vib-ugent.be	Bruhns, Pierre/F-5567-2013; Saeys, Yvan/C-1311-2009; Lambrecht, Bart/K-2484-2014	Bruhns, Pierre/0000-0002-4709-8936; Saeys, Yvan/0000-0002-0415-1506; Lambrecht, Bart/0000-0003-4376-6834			Akilesh S, 2004, J CLIN INVEST, V113, P1328, DOI 10.1172/JCI200418838; Akiyama K, 2003, J IMMUNOL, V170, P1641; Amigorena S, 1999, IMMUNOL REV, V172, P279, DOI 10.1111/j.1600-065X.1999.tb01372.x; 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Rev. Immunol.	FEB	2014	14	2					94	108		10.1038/nri3582		15	Immunology	Immunology	AA3VI	WOS:000331022400012	24445665	
J	Caliskan, M; Bochkov, YA; Kreiner-Moller, E; Bonnelykke, K; Stein, MM; Du, GX; Bisgaard, H; Jackson, DJ; Gern, JE; Lemanske, RF; Nicolae, DL; Ober, C				Caliskan, Minal; Bochkov, Yury A.; Kreiner-Moller, Eskil; Bonnelykke, Klaus; Stein, Michelle M.; Du, Gaixin; Bisgaard, Hans; Jackson, Daniel J.; Gern, James E.; Lemanske, Robert F., Jr.; Nicolae, Dan L.; Ober, Carole			Rhinovirus Wheezing Illness and Genetic Risk of Childhood-Onset Asthma	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							GASDERMIN-LIKE GSDML; 17Q21 VARIANTS; SMOKE EXPOSURE; EXPRESSION; ORMDL3; ASSOCIATION; EXACERBATIONS; INFECTIONS; CHILDREN; DISEASE	BACKGROUND Both genetic variation at the 17q21 locus and virus-induced respiratory wheezing illnesses are associated with the development of asthma. Our aim was to determine the effects of these two factors on the risk of asthma in the Childhood Origins of Asthma (COAST) and the Copenhagen Prospective Study on Asthma in Childhood (COPSAC) birth cohorts. METHODS We tested genotypes at the 17q21 locus for associations with asthma and with human rhinovirus (HRV) and respiratory syncytial virus (RSV) wheezing illnesses and tested for interactions between 17q21 genotypes and HRV and RSV wheezing illnesses with respect to the risk of asthma. Finally, we examined genotype-specific expression of 17q21 genes in unstimulated and HRV-stimulated peripheral-blood mononuclear cells (PBMCs). RESULTS The 17q21 variants were associated with HRV wheezing illnesses in early life, but not with RSV wheezing illnesses. The associations of 17q21 variants with asthma were restricted to children who had had HRV wheezing illnesses, resulting in a significant interaction effect with respect to the risk of asthma. Moreover, the expression levels of ORMDL3 and of GSDMB were significantly increased in HRV-stimulated PBMCs, as compared with unstimulated PBMCs. The expression of these genes was associated with 17q21 variants in both conditions, although the increase with exposure to HRV was not genotype-specific. CONCLUSIONS Variants at the 17q21 locus were associated with asthma in children who had had HRV wheezing illnesses and with expression of two genes at this locus. The expression levels of both genes increased in response to HRV stimulation, although the relative increase was not associated with the 17q21 genotypes. (Funded by the National Institutes of Health.)	[Caliskan, Minal; Stein, Michelle M.; Du, Gaixin; Nicolae, Dan L.; Ober, Carole] Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA; [Nicolae, Dan L.] Univ Chicago, Dept Med, Chicago, IL 60637 USA; [Nicolae, Dan L.] Univ Chicago, Dept Stat, Chicago, IL 60637 USA; [Ober, Carole] Univ Chicago, Dept Obstet & Gynecol, Chicago, IL 60637 USA; [Bochkov, Yury A.; Jackson, Daniel J.; Gern, James E.; Lemanske, Robert F., Jr.] Univ Wisconsin, Dept Pediat, Madison, WI USA; [Lemanske, Robert F., Jr.] Univ Wisconsin, Dept Med, Madison, WI USA; [Kreiner-Moller, Eskil; Bonnelykke, Klaus; Bisgaard, Hans] Univ Copenhagen, Fac Hlth Sci, Gentofte, Denmark; [Kreiner-Moller, Eskil; Bonnelykke, Klaus; Bisgaard, Hans] Copenhagen Univ Hosp, Danish Pediat Asthma Ctr, Gentofte, Denmark	Caliskan, M (reprint author), Univ Chicago, Dept Human Genet, 920 E 58th St, Chicago, IL 60637 USA.	caliskan@uchicago.edu; c-ober@genetics.uchicago.edu	Du, Gaixin/M-9901-2014; Bisgaard, Hans/N-4761-2016	Du, Gaixin/0000-0002-4616-7725; Bisgaard, Hans/0000-0003-4131-7592; Bochkov, Yury/0000-0003-2618-4496; Kreiner, Eskil/0000-0003-1204-2438	National Institutes of Health [HL070831, AI070503]; KL2 from the National Institutes of Health [UL1TR00042]; Lundbeck Foundation; Danish Council for Strategic Research; Danish Pediatric Asthma Center	Funded by the National Institutes of Health.; Supported by grants (HL070831 and AI070503) from the National Institutes of Health. Dr. Jackson was supported by KL2 grant UL1TR000427 from the National Institutes of Health. The Lundbeck Foundation, Danish Council for Strategic Research, and Danish Pediatric Asthma Center provided the core funding for the COPSAC research unit.	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Engl. J. Med.	APR 11	2013	368	15					1398	1407		10.1056/NEJMoa1211592		10	Medicine, General & Internal	General & Internal Medicine	122QT	WOS:000317333600007	23534543	
S	Lambrecht, BN; Hammad, H		Paul, WE		Lambrecht, Bart N.; Hammad, Hamida			Lung Dendritic Cells in Respiratory Viral Infection and Asthma: From Protection to Immunopathology	ANNUAL REVIEW OF IMMUNOLOGY, VOL 30	Annual Review of Immunology		English	Review; Book Chapter						dendritic cells; virus; asthma; allergy	ALLERGIC AIRWAY INFLAMMATION; HOUSE-DUST MITE; CD8(+) T-CELL; THYMIC STROMAL LYMPHOPOIETIN; INFLUENZA-VIRUS INFECTION; AMBIENT PARTICULATE MATTER; HELPER TYPE-2 RESPONSE; BLOOD MONOCYTE SUBSETS; BRONCHIAL LYMPH-NODE; EPITHELIAL-CELLS	Lung dendritic cells (DCs) bridge innate and adaptive immunity, and depending on context, they also induce a Th1, Th2, or Th17 response to optimally clear infectious threats. Conversely, lung DCs can also mount maladaptive Th2 immune responses to harmless allergens and, in this way, contribute to immunopathology. It is now clear that the various aspects of DC biology can be understood only if we take into account the functional specializations of different DC subsets that are present in the lung in homeostasis or are attracted to the lung as part of the inflammatory response to inhaled noxious stimuli. Lung DCs are heavily influenced by the nearby epithelial cells, and a model is emerging whereby direct communication between DCs and epithelial cells determines the outcome of the pulmonary immuneresponse. Here, we have approached DC biology from the perspective of viral infection and allergy to illustrate these emerging concepts.	[Lambrecht, Bart N.; Hammad, Hamida] Univ Ghent VIB, Lab Immunoregulat & Mucosal Immunol, Dept Mol Biomed Res, B-9052 Ghent, Belgium; [Lambrecht, Bart N.] Ghent Univ Hosp, Dept Resp Med, B-9000 Ghent, Belgium; [Lambrecht, Bart N.] Erasmus Univ, Med Ctr, Dept Pulm Med, NL-3015 CE Rotterdam, Netherlands	Lambrecht, BN (reprint author), Univ Ghent VIB, Lab Immunoregulat & Mucosal Immunol, Dept Mol Biomed Res, B-9052 Ghent, Belgium.	bart.lambrecht@ugent.be; hamida.hammad@ugent.be	Hammad, Hamida/J-9391-2015; Lambrecht, Bart/K-2484-2014	Hammad, Hamida/0000-0003-3762-8603; Lambrecht, Bart/0000-0003-4376-6834			Akbari O, 2001, NAT IMMUNOL, V2, P725, DOI 10.1038/90667; Akbari O, 2002, NAT MED, V8, P1024, DOI 10.1038/nm745; Ballesteros-Tato A, 2010, NAT IMMUNOL, V11, P216, DOI 10.1038/ni.1838; Barrett NA, 2011, J EXP MED, V208, P593, DOI 10.1084/jem.20100793; Barrett NA, 2009, J IMMUNOL, V182, P1119; Beaty SR, 2007, J IMMUNOL, V178, P1882; Beauchamp NM, 2010, J VIROL, V84, P10191, DOI 10.1128/JVI.00892-10; 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Rev. Immunol.		2012	30						243	270		10.1146/annurev-immunol-020711-075021		28	Immunology	Immunology	BAH94	WOS:000304198100011	22224777	
J	Carlsen, KH; Anderson, SD; Bjermer, L; Bonini, S; Brusasco, V; Canonica, W; Cummiskey, J; Delgado, L; Del Giacco, SR; Drobnic, F; Haahtela, T; Larsson, K; Palange, P; Popov, T; van Cauwenberge, P				Carlsen, K. H.; Anderson, S. D.; Bjermer, L.; Bonini, S.; Brusasco, V.; Canonica, W.; Cummiskey, J.; Delgado, L.; Del Giacco, S. R.; Drobnic, F.; Haahtela, T.; Larsson, K.; Palange, P.; Popov, T.; van Cauwenberge, P.			Exercise-induced asthma, respiratory and allergic disorders in elite athletes: epidemiology, mechanisms and diagnosis: Part I of the report from the Joint Task Force of the European Respiratory Society (ERS) and the European Academy of Allergy and Clinical Immunology (EAACI) in cooperation with GA(2)LEN	ALLERGY			English	Review						asthma; allergy; bronchial responsiveness; sports; exercise-induced asthma	CROSS-COUNTRY SKIERS; HYPERVENTILATION-INDUCED ASTHMA; ICE HOCKEY PLAYERS; BRONCHIAL RESPONSIVENESS; INDUCED BRONCHOSPASM; INDUCED BRONCHOCONSTRICTION; AIRWAY INFLAMMATION; INDUCED ANAPHYLAXIS; COLD-AIR; INDUCED HYPOXEMIA	Aims: To analyze the changes in the prevalence of asthma, bronchial hyperresponsiveness (BHR) and allergies in elite athletes over the past years, to review the specific pathogenetic features of these conditions and to make recommendations for their diagnosis. Mehtods: The Task Force reviewed present literature by searching Medline up to November 2006 for relevant papers by the search words: asthma, bronchial responsiveness, EIB, athletes and sports. Sign criteria were used to assess level of evidence and grades of recommendation. Results: The problems of sports-related asthma and allergy are outlined. Epidemiological evidence for an increased prevalence of asthma and BHR among competitive athletes, especially in endurance sports, is provided. The mechanisms for development of asthma and bronchial hyperresponsiveness in athletes are outlined. Criteria are given for the diagnosis of asthma and exercise induced asthma in the athlete. Conclusions: The prevalence of asthma and bronchial hyperresponsiveness is markedly increased in athletes, especially within endurance sports. Environmental factors often contribute. Recommendations for the diagnosis of asthma in athletes are outlined.	[Carlsen, K. H.] Univ Oslo, Rikshosp, Fac Med, Dept Paediat,Med Ctr, NO-0791 Oslo, Norway; [Carlsen, K. H.] Norwegian Sch Sport Sci, Oslo, Norway; [Anderson, S. D.] Royal Prince Alfred Hosp, Dept Resp Med, Camperdown, NSW 2050, Australia; [Bjermer, L.] Univ Lund Hosp, Dept Resp Med & Allergol, S-22185 Lund, Sweden; [Bonini, S.] CNR, Inst Neurobiol & Mol Med, Rome, Italy; [Bonini, S.] Univ Naples 2, Naples, Italy; [Brusasco, V.] Univ Genoa, Dipartimento Med Interna, Genoa, Italy; [Canonica, W.] Univ Genoa, Dept Internal Med, I-16126 Genoa, Italy; [Cummiskey, J.] Blackrock Clin, Dublin, Ireland; [Delgado, L.] Univ Porto, Serv & Lab Imunol, Fac Med, Hosp S Joao, P-4100 Oporto, Portugal; [Del Giacco, S. 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J	Thompson, C; Powrie, F				Thompson, C; Powrie, F			Regulatory T cells	CURRENT OPINION IN PHARMACOLOGY			English	Review							TRANSCRIPTION FACTOR FOXP3; IN-VIVO; TGF-BETA; CUTTING EDGE; DENDRITIC CELLS; DEPENDENT MECHANISMS; SUPPRESSOR FUNCTION; IMMUNE PATHOLOGY; CD4(+)CD25(+); CD25(+)	Regulatory T (T-R) cells are a subset of T cells that function to control immune responses. Different populations of T-R cells have been described, including thymically derived CD4(+)CD25(+) T-R cells and TO cells induced in the periphery through exposure to antigen. A transcription factor, Foxp3, has been identified that is essential for CD4(+)CD25(+) T-R cell development and function. There is now evidence that transforming growth factor-beta might play a role in this pathway. CD4(+)CD25(+) T-R cells proliferate extensively in vivo in an antigen-specific manner, and can respond to both self and foreign peptides. By suppressing excessive immune responses, T-R cells play a key role in the maintenance of self-tolerance, thus preventing autoimmune disease, as well as inhibiting harmful inflammatory diseases such as asthma and inflammatory bowel disease.	Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England	Powrie, F (reprint author), Univ Oxford, Sir William Dunn Sch Pathol, S Parks Rd, Oxford OX1 3RE, England.	fiona.powrie@pathology.oxford.ac.uk					Aluvihare VR, 2004, NAT IMMUNOL, V5, P266, DOI 10.1038/ni1037; Annacker O, 2001, J IMMUNOL, V166, P3008; Belghith M, 2003, NAT MED, V9, P1202, DOI 10.1038/nm924; Belkaid Y, 2002, NATURE, V420, P502, DOI 10.1038/nature01152; Bruder D, 2004, EUR J IMMUNOL, V34, P623, DOI 10.1002/eji.200324799; Caramalho I, 2003, J EXP MED, V197, P403, DOI 10.1084/jem.20021633; Chen WJ, 2003, J EXP MED, V198, P1875, DOI 10.1084/jem.20030152; Cobbold SP, 2004, J IMMUNOL, V172, P6003; Cong YZ, 2002, J IMMUNOL, V169, P6112; Cozzo C, 2003, J IMMUNOL, V171, P5678; Fallarino F, 2003, NAT IMMUNOL, V4, P1206, DOI 10.1038/ni1003; Fantini MC, 2004, J IMMUNOL, V172, P5149; Fisson S, 2003, J EXP MED, V198, P737, DOI 10.1084/jem.20030686; Fontenot JD, 2003, NAT IMMUNOL, V4, P330, DOI 10.1038/ni904; Foussat A, 2003, J IMMUNOL, V171, P5018; Gavin M, 2003, CURR OPIN IMMUNOL, V15, P690, DOI 10.1016/j.coi.2003.09.011; Gorelik L, 2002, NAT REV IMMUNOL, V2, P46, DOI 10.1038/nri704; Graca L, 2002, J EXP MED, V195, P1641, DOI 10.1084/jem.20012097; Green EA, 2003, P NATL ACAD SCI USA, V100, P10878, DOI 10.1073/pnas.1834400100; Grohmann U, 2003, TRENDS IMMUNOL, V24, P242, DOI 10.1016/S1471-4906(03)00072-3; Hesse M, 2004, J IMMUNOL, V172, P3157; Higgins SC, 2003, J IMMUNOL, V171, P3119; Hisaeda H, 2004, NAT MED, V10, P29, DOI 10.1038/nm975; Hori S, 2002, EUR J IMMUNOL, V32, P1282, DOI 10.1002/1521-4141(200205)32:5<1282::AID-IMMU1282>3.0.CO;2-#; Hori S, 2003, SCIENCE, V299, P1057, DOI 10.1126/science.1079490; Huehn J, 2004, J EXP MED, V199, P303, DOI 10.1084/jem.20031562; Jonuleit H, 2002, J EXP MED, V196, P255, DOI 10.1084/jem.20020394; Jordan MS, 2001, NAT IMMUNOL, V2, P301, DOI 10.1038/86302; Khattri R, 2003, NAT IMMUNOL, V4, P337, DOI 10.1038/ni909; Klein L, 2003, P NATL ACAD SCI USA, V100, P8886, DOI 10.1073/pnas.1533365100; Kriegel MA, 2004, J EXP MED, V199, P1285, DOI 10.1084/jem.20032158; Kullberg MC, 2002, J EXP MED, V196, P505, DOI 10.1084/jem.20020556; Lin CH, 2003, EUR J IMMUNOL, V33, P626, DOI 10.1002/eji.200323570; Liu HY, 2003, J IMMUNOL, V171, P5012; Malek TR, 2003, J LEUKOCYTE BIOL, V74, P961, DOI 10.1189/jlb.0603272; Maloy KJ, 2001, NAT IMMUNOL, V2, P816, DOI 10.1038/ni0901-816; Maloy KJ, 2003, J EXP MED, V197, P111, DOI 10.1084/jem.20021345; Mamura M, 2004, BLOOD, V103, P4594, DOI 10.1182/blood-2003-08-2897; Mills KHG, 2004, SEMIN IMMUNOL, V16, P107, DOI 10.1016/j.smim.2003.12.006; Mottet C, 2003, J IMMUNOL, V170, P3939; Nakamura K, 2001, J EXP MED, V194, P629, DOI 10.1084/jem.194.5.629; Nakamura K, 2004, J IMMUNOL, V172, P834; Oldenhove G, 2003, J EXP MED, V198, P259, DOI 10.1084/jem.20030654; Pasare C, 2003, SCIENCE, V299, P1033, DOI 10.1126/science.1078231; Peng YF, 2004, P NATL ACAD SCI USA, V101, P4572, DOI 10.1073/pnas.0400810101; Piccirillo CA, 2004, SEMIN IMMUNOL, V16, P81, DOI 10.1016/j.smim.2003.12.003; Piccirillo CA, 2002, J EXP MED, V196, P237, DOI 10.1084/jem.20020590; Piccirillo CA, 2001, J IMMUNOL, V167, P1137; Ramsdell F, 2003, CURR OPIN IMMUNOL, V15, P718, DOI 10.1016/j.coli.2003.09.008; Roncarolo MG, 2001, IMMUNOL REV, V182, P68, DOI 10.1034/j.1600-065X.2001.1820105.x; Sakaguchi S, 2001, IMMUNOL REV, V182, P18, DOI 10.1034/j.1600-065X.2001.1820102.x; Seddon B, 2000, IMMUNOL TODAY, V21, P95, DOI 10.1016/S0167-5699(99)01559-5; Singh B, 2001, IMMUNOL REV, V182, P190, DOI 10.1034/j.1600-065X.2001.1820115.x; Sundstedt A, 2003, J IMMUNOL, V170, P1240; Suvas S, 2003, J EXP MED, V198, P889, DOI 10.1084/jem.20030171; Tang QZ, 2003, J IMMUNOL, V171, P3348; Tone M, 2003, P NATL ACAD SCI USA, V100, P15059, DOI 10.1073/pnas.2334901100; Uraushihara K, 2003, J IMMUNOL, V171, P708; Vieira PL, 2004, J IMMUNOL, V172, P5986; Viglietta V, 2004, J EXP MED, V199, P971, DOI 10.1084/jem.20031579; Wakkach A, 2003, IMMUNITY, V18, P605, DOI 10.1016/S1074-7613(03)00113-4; Walker LSK, 2003, J EXP MED, V198, P249, DOI 10.1084/jem.20030315; Walker MR, 2003, J CLIN INVEST, V112, P1437, DOI 10.1172/JCI200319441; Wood KJ, 2003, NAT REV IMMUNOL, V3, P199, DOI 10.1038/nri1027; Yamazaki S, 2003, J EXP MED, V198, P235, DOI 10.1081/jem.20030422; Zheng SG, 2004, J IMMUNOL, V172, P5213	66	138	156	0	1	ELSEVIER SCI LTD	OXFORD	THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND	1471-4892			CURR OPIN PHARMACOL	Curr. Opin. Pharmacol.	AUG	2004	4	4					408	414		10.1016/j.coph.2004.05.001		7	Pharmacology & Pharmacy	Pharmacology & Pharmacy	846LC	WOS:000223316000017	15251137	
J	de Marco, R; Accordini, S; Cerveri, I; Corsico, A; Sunyer, J; Neukirch, F; Kunzli, N; Leynaert, B; Janson, C; Gislason, T; Vermeire, P; Svanes, C; Anto, JM; Burney, P				de Marco, R; Accordini, S; Cerveri, I; Corsico, A; Sunyer, J; Neukirch, F; Kunzli, N; Leynaert, B; Janson, C; Gislason, T; Vermeire, P; Svanes, C; Anto, JM; Burney, P		European Community Resp Hlth Surve	An international survey of chronic obstructive pulmonary disease in young adults according to GOLD stages	THORAX			English	Article							RESPIRATORY-HEALTH-SURVEY; AIR-FLOW OBSTRUCTION; GENDER-DIFFERENCES; SMOKING-HABITS; UNITED-STATES; COPD; MORTALITY; ASTHMA	Background: The recently published GOLD guidelines provide a new system for staging chronic obstructive pulmonary disease (COPD) from mild (stage I) to very severe (stage IV) and introduce a stage 0 (chronic cough and phlegm without airflow obstruction) that includes subjects "at risk" of developing the disease. Methods: In order to assess the prevalence of GOLD stages of COPD in high income countries and to evaluate their association with the known risk factors for airflow obstruction, data from the European Community Respiratory Health Survey on more than 18 000 young adults (20-44 years) were analysed. Results: The overall prevalence was 11.8% (95% CI 11.3 to 12.3) for stage 0, 2.5% (95% CI 2.2 to 2.7) for stage I, and 1.1% (95% CI 1.0 to 1.3) for stages II-III. Moderate to heavy smoking (greater than or equal to15 pack years) was significantly associated with both stage 0 (relative risk ratio (RRR) = 4.15; 95% CI 3.55 to 4.84) and stages I+ (RRR = 4.09; 95% CI 3.17 to 5.26), while subjects with stages I+ COPD had a higher likelihood of giving up smoking (RRR = 1.39; 95% CI 1.04 to 1.86) than those with GOLD stage 0 (RRR = 1.05; 95% CI 0.86 to 1.27). Environmental tobacco smoke had the same degree of positive association in both groups. Respiratory infections in childhood and low socioeconomic class were significantly and homogeneously associated with both groups, whereas occupational exposure was significantly associated only with stage 0. All the GOLD stages showed a significantly higher percentage of healthcare resource users than healthy subjects (p < 0.001), with no difference between stage 0 and COPD. Conclusions: A considerable percentage of young adults already suffered from COPD. GOLD stage 0 was characterised by the presence of the same risk factors as COPD and by the same high demand for medical assistance.	Univ Verona, Ist Biol 2, Dipartimento Med & Sanita Pubbl, Sez Epidemiol & Stat Med,Unit Epidemiol & Med Sta, I-37134 Verona, Italy; Univ Pavia, IRCCS Policlin S Matteo, Div Resp Dis, I-27100 Pavia, Italy; Inst Municipal Invest Med, Resp & Environm Hlth Res Unit, E-08003 Barcelona, Spain; INSERM, U408, Paris, France; Univ So Calif, Keck Sch Med, Div Occupat & Eniviron Hlth, Los Angeles, CA USA; Univ Basel, Inst Social & Prevent Med, Basel, Switzerland; Uppsala Univ, Dept Med Sci Resp Med & Allergol, Uppsala, Sweden; Univ Hosp, Dept Allergy & Resp Med, Reykjavik, Iceland; Univ Antwerp, Dept Resp Med, B-2020 Antwerp, Belgium; Univ Bergen, Dept Thorac Med, Bergen, Norway; Univ Pompeu Fabra, Dept Expt & Hlth Sci, Barcelona, Spain; Univ London Kings Coll, Dept Publ Hlth Sci, London WC2R 2LS, England	de Marco, R (reprint author), Univ Verona, Ist Biol 2, Dipartimento Med & Sanita Pubbl, Sez Epidemiol & Stat Med,Unit Epidemiol & Med Sta, Str Grazie 8, I-37134 Verona, Italy.	roberto.demarco@univr.it	de Marco, Roberto/A-5470-2008; SESM, SESM/C-1440-2008; bucca, caterina/C-9886-2009; Kunzli, Nino/F-7195-2014; Anto, J/H-2676-2014; Sunyer, J/G-6909-2014	bucca, caterina/0000-0002-9941-9236; Kunzli, Nino/0000-0001-8360-080X; Anto, J/0000-0002-4736-8529; Sunyer, J/0000-0002-2602-4110; Corsico, Angelo Guido/0000-0002-8716-4694			Becklake MR, 2000, THORAX, V55, P629; BUIST AS, 1994, TXB RESP MED, P1959; Burney P, 1997, J ALLERGY CLIN IMMUN, V99, P314, DOI 10.1016/S0091-6749(97)70048-4; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; Calverley PMA, 2000, CHEST, V117, p365S, DOI 10.1378/chest.117.5_suppl_2.365S; Cerveri I, 2003, EUR RESPIR J, V22, P413, DOI 10.1183/09031936.03.00121103; Cerveri I, 2001, EUR RESPIR J, V18, P85, DOI 10.1183/09031936.01.00087101; CERVERII, 2003, AM J RESP CRIT CARE, V167, P936; Coultas DB, 2001, AM J RESP CRIT CARE, V164, P372; DEMARCO R, 1994, EUR RESPIR J, V7, P2139, DOI 10.1183/09031936.94.07122139; Fabbri LM, 2003, AM J RESP CRIT CARE, V167, P418, DOI 10.1164/rccm.200203-183OC; FEINLEIB M, 1989, AM REV RESPIR DIS, V140, pS9; Hosmer W.D., 1989, APPL LOGISTIC REGRES; Janson C, 1997, EUR RESPIR J, V10, P1795, DOI 10.1183/09031936.97.10081795; Jarvis D, 2002, EUR RESPIR J, V20, P1071, DOI 10.1183/09031936.02.00046802; Medical Research Council, 1976, RESP SYMPT QUEST; *NHLBI, 2003, NHLBI WHO WORKSH APR; Quanjer PH, 1993, EUR RESPIR J S, V16, P5, DOI 10.1183/09041950.005s1693; RENNARD S, 2002, EUR RESPIR J, V20, P793; Snider GL, 2003, AM J RESP CRIT CARE, V167, P678, DOI 10.1164/rccm.200203-204PP; Sobradillo Pena Victor, 2000, Chest, V118, P981; THOM TJ, 1989, AM REV RESPIR DIS, V140, pS27; Vestbo J, 2002, AM J RESP CRIT CARE, V166, P329, DOI 10.1164/rccm.2112048; XU X, 1994, EUR RESPIR J, V7, P1056	24	138	138	1	8	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	FEB 1	2004	59	2					120	125		10.1136/thorax.2003.011163		6	Respiratory System	Respiratory System	770UY	WOS:000188750200010	14760151	
J	Heinrich, J; Bolte, G; Holscher, B; Douwes, J; Lehmann, I; Fahlbusch, B; Bischof, W; Weiss, M; Borte, M; Wichmann, HE				Heinrich, J; Bolte, G; Holscher, B; Douwes, J; Lehmann, I; Fahlbusch, B; Bischof, W; Weiss, M; Borte, M; Wichmann, HE		LISA study grp	Allergens and endotoxin on mothers' mattresses and total immunoglobulin E in cord blood of neonates	EUROPEAN RESPIRATORY JOURNAL			English	Article						cat allergen; cord blood immunoglobulin E; endotoxin; house dust; mite allergen; prenatal exposures	HOUSE-DUST ENDOTOXIN; HUMAN IMMUNE-SYSTEM; EARLY-LIFE; ENVIRONMENTAL ALLERGENS; PRENATAL SENSITIZATION; ASTHMA; EXPOSURE; RESPONSES; PREGNANCY; GESTATION	The current authors examined whether mite and cat allergen and bacterial endotoxin levels in dust of the mothers' mattresses were associated with cord blood immunoglobulin (Ig)E (CB-IgE) levels in newborns. Data from 1,332 term and normal weight neonates, from an ongoing birth cohort study, Influences of life-style related factors on the immune system and the development of allergies in childhood (LISA), with complete information on exposure to biocontaminants in mattress dust and CB-IgE were analysed. Two thirds of CB-IgE were undetectable (<0.35 kU(.)L(-1)). Thus, 0.35 and 0.45 kU(.)L(-1) (4th quartile) were chosen as cut-offs. Nonparametric smoothing (generalised additive models) showed statistically significant confounder-adjusted associations between elevated CB-IgE levels (greater than or equal to0.45 kU(.)L(-1)) and log-transformed exposures to cat (linear), mite (inverse u-shaped), and endotoxin (u-shaped). After adjustment for covariables, elevated CB-IgE levels (logistic regression using the 1st-4th quartiles of exposure) were positively associated with high cat-allergen exposure and medium exposure to mite allergen, but were inversely associated with exposure to endotoxin. The associations were similar, but somewhat weaker, when 0.35 kU(.)L(-1) was used as cut-off. These results, showing an association between prenatal allergen and endotoxin exposures and immunoglobulin E production, suggest that the development of foetal immune responses may be affected.	GSF, Inst Epidemiol, Natl Res Ctr Environm & Hlth, D-85764 Neuherberg, Germany; Univ Utrecht, Div Environm & Occupat Hlth, IRAS, Utrecht, Netherlands; Leipzig Halle Ltd, Dept Human Exposure Res & Epidemiol, UFZ, Leipzig, Germany; Univ Jena, Inst Clin Immunol, D-6900 Jena, Germany; Univ Jena, Dept Indoor Climatol Ark, Erfurt, Germany; Univ Munich, Dr Von Haunersches Kinderspital, Munich, Germany; Univ Leipzig, Dept Paediat, Leipzig, Germany	Heinrich, J (reprint author), GSF, Inst Epidemiol, Natl Res Ctr Environm & Hlth, Inglostaeder Landstr 1, D-85764 Neuherberg, Germany.	Joachim.Heinrich@gsf.de		Douwes, Jeroen/0000-0003-3599-4036			Bergmann RL, 1997, CLIN EXP ALLERGY, V27, P752, DOI 10.1046/j.1365-2222.1997.310899.x; Fahlbusch B, 1999, ALLERGY, V54, P1215, DOI 10.1034/j.1398-9995.1999.00196.x; Gehring U, 2001, J ALLERGY CLIN IMMUN, V108, P847, DOI 10.1067/mai.2001.119026; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Gern JE, 1999, J CLIN INVEST, V104, P837, DOI 10.1172/JCI8272; Hastie T, 1990, GEN ADDITIVE MODELS; Heinrich J, 2001, CLIN EXP ALLERGY, V31, P1839, DOI 10.1046/j.1365-2222.2001.01220.x; Herz U, 2000, AM J RESP CRIT CARE, V162, pS62; Holloway JA, 2000, LANCET, V356, P1900, DOI 10.1016/S0140-6736(00)03265-7; Holt PG, 2000, ALLERGY, V55, P688, DOI 10.1034/j.1398-9995.2000.00118.x; Jones AC, 1996, PEDIATR ALLERGY IMMU, V7, P109, DOI 10.1111/j.1399-3038.1996.tb00117.x; Jones CA, 2000, ALLERGY, V55, P2, DOI 10.1034/j.1398-9995.2000.00109.x; King CL, 1998, J IMMUNOL, V160, P3578; Liu AH, 2002, J ALLERGY CLIN IMMUN, V109, P379, DOI 10.1067/mai.2002.122157; Martinez FD, 1999, LANCET, V354, pSII12; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; Ownby DR, 1996, PEDIATR ALLERGY IMMU, V7, P125, DOI 10.1111/j.1399-3038.1996.tb00119.x; Palfi M, 1998, AM J REPROD IMMUNOL, V39, P24; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; Prescott SL, 2000, ALLERGY, V55, P470; Prescott SL, 1998, J IMMUNOL, V160, P4730; Reed CE, 2001, J ALLERGY CLIN IMMUN, V108, P157, DOI 10.1067/mai.2001.116862; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Sacks G, 1999, IMMUNOL TODAY, V20, P114, DOI 10.1016/S0167-5699(98)01393-0; Szepfalusi Z, 2000, PEDIATR RES, V48, P404; Szepfalusi Z, 2000, J ALLERGY CLIN IMMUN, V106, P530; Tulic MK, 2000, AM J RESP CELL MOL, V22, P604; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; Wan GH, 2000, CLIN EXP ALLERGY, V30, P426; Warner JA, 1998, CLIN EXP ALLERGY, V28, P35; Warner JA, 1996, PEDIATR ALLERGY IMMU, V7, P98, DOI 10.1111/j.1399-3038.1996.tb00406.x	32	138	138	0	3	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	SEP	2002	20	3					617	623		10.1183/09031936.02.02322001		7	Respiratory System	Respiratory System	596VL	WOS:000178187100018	12358337	
J	Vernooy, JHJ; Dentener, MA; van Suylen, RJ; Buurman, WA; Wouters, EFM				Vernooy, JHJ; Dentener, MA; van Suylen, RJ; Buurman, WA; Wouters, EFM			Long-term intratracheal lipopolysaccharide exposure in mice results in chronic lung inflammation and persistent pathology	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article							OBSTRUCTIVE PULMONARY-DISEASE; TRANSGENIC MICE; AIRWAY INFLAMMATION; CELL HYPERPLASIA; CIGARETTE-SMOKE; COTTON DUST; GRAIN DUST; ENDOTOXIN; EXPRESSION; EMPHYSEMA	Lipopolysaccharide (LPS), a major proinflammatory glycolipid component of the gram-negative bacterial cell wall, is one of the agents ubiquitously present as contaminant on airborne particles, including air pollution, organic dusts, and cigarette smoke. Chronic exposure to significant levels of LPS is reported to be associated with the development and/or progression of many types of lung diseases, including asthma, chronic bronchitis, and progressive irreversible airflow obstruction, that are all characterized by chronic inflammatory processes in the lung. In the present study, pathologic effects of long-term LPS exposure to the lung were investigated in detail. To this end, a murine model in which mice were exposed to repeated intratracheal instillation of Escherichia coli LPS was developed. We show that long-term LPS instillation in mice results in persistent chronic pulmonary inflammation, characterized by peribronchial and perivascular lymphocytic aggregates (CD4(+), CD8(+), and CD19(+)), parenchymal accumulation of macrophages and CD8+ T cells, and altered cytokine expression. Furthermore, airway and alveolar alterations such as mucus cell metaplasia, airway wall thickening, and irreversible alveolar enlargement accompanied the chronic inflammatory response. Interestingly, the observed inflammatory and pathologic changes mimic changes observed in human subjects with chronic inflammatory lung diseases, especially chronic obstructive pulmonary disease (COPD), suggesting that this murine model could be applicable to dissect the role of inflammation in the pathogenesis of these disease conditions.	Univ Hosp Maastricht, Dept Pulmonol, Dept Pathol, NL-6202 AZ Maastricht, Netherlands; Maastricht Univ, Nutr & Toxicol Res Inst Maastricht, Dept Pulmonol, Maastricht, Netherlands; Maastricht Univ, Nutr & Toxicol Res Inst Maastricht, Dept Gen Surg, Maastricht, Netherlands	Vernooy, JHJ (reprint author), Univ Hosp Maastricht, Dept Pulmonol, Dept Pathol, POB 5800, NL-6202 AZ Maastricht, Netherlands.						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J. Respir. Cell Mol. Biol.	JAN	2002	26	1					152	159				8	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	510YX	WOS:000173236100020	11751215	
J	Gereda, JE; Klinnert, MD; Price, MR; Leung, DYM; Liu, AH				Gereda, JE; Klinnert, MD; Price, MR; Leung, DYM; Liu, AH			Metropolitan home living conditions associated with indoor endotoxin levels	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergy; asthma; prevention; infants; endotoxin; house dust; allergen; animal; cat; dog; air conditioning	IN-HOUSE DUST; HAY-FEVER; ENVIRONMENTAL ENDOTOXIN; BACTERIAL-ENDOTOXIN; INHALED ENDOTOXIN; COTTON DUST; ASTHMA; EXPOSURE; CHILDREN; ALLERGEN	Background: Household endotoxin exposure in allergy and asthma has been gaining attention for its dual potential to exacerbate these conditions in individuals with established disease and to abrogate atopy before disease onset. Objective: We sought to better understand the home environmental and Lifestyle factors influencing house dust endotoxin levels, Methods: From the homes of 86 infants with wheeze in metropolitan Denver, Colorado, house dust endotoxin (detected with a standardized Limulus Amebocyte Lysate assay) and common indoor allergen (Fel d 1, Can f 1, Her p 1, Her f 1, and Bla g 1) contents were quantified. Comprehensive home environment and lifestyle questionnaires were completed during home visits by trained study staff and parents. Results: House dust endotoxin levels were associated with only 2 home environmental features: animals in the home and the presence of central air conditioning. The strongest positive associations were found with animals in the home, Interestingly,the homes without cats or other animals revealed a negative correlation between house dust Fel d 1 and endotoxin (P = .03), Central air conditioning, especially during months of typical use, was associated with lower house dust endotoxin levels, No significant associations between house dust endotoxin levels and home dampness, number of household inhabitants or young children, cleaning frequency, or presence of tobacco smokers in the home were found, Conclusions: Indoor endotoxin exposure can be increased by the presence of animals in the home and decreased with central air conditioning, In some homes without animals, where allergen exposure adequate for sensitization still occurs, there are lower levels of house dust endotoxin, Therefore in homes without animals, factors that influence allergen and endotoxin levels in house dust probably differ, Households with detectable allergen levels but low endotoxin levels may provide a predisposing environment for animal allergen sensitization.	Natl Jewish Med & Res Ctr, Div Pediat Allergy & Immunol, Denver, CO 80206 USA; Univ Colorado, Hlth Sci Ctr, Dept Pediat, Denver, CO 80262 USA; Natl Jewish Med & Res Ctr, Div Pediat Behav Hlth, Denver, CO USA	Liu, AH (reprint author), Natl Jewish Med & Res Ctr, Div Pediat Allergy & Immunol, 1400 Jackson St,K1023, Denver, CO 80206 USA.				NCRR NIH HHS [M01-RR00051]; NHLBI NIH HHS [HL-36577]; NIAID NIH HHS [R18AI41137]		Almqvist C, 1999, J ALLERGY CLIN IMMUN, V103, P1012, DOI 10.1016/S0091-6749(99)70172-7; Andriessen JW, 1998, CLIN EXP ALLERGY, V28, P1191; Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; CASTELLAN RM, 1987, NEW ENGL J MED, V317, P605, DOI 10.1056/NEJM198709033171005; Chan-Yeung M, 1999, CLIN EXP ALLERGY, V29, P762; Chun D T, 2000, Appl Occup Environ Hyg, V15, P152; DANDREA A, 1992, J EXP MED, V176, P1387, DOI 10.1084/jem.176.5.1387; DONHAM K, 1989, BRIT J IND MED, V46, P31; Douwes J, 2000, AM J RESP CRIT CARE, V162, P1348; Dubin W, 1996, AM J PHYSIOL-LUNG C, V270, pL736; Duchaine C, 1999, AM IND HYG ASSOC J, V60, P89, DOI 10.1080/00028899908984426; Eldridge MW, 2000, J ALLERGY CLIN IMMUN, V105, P475, DOI 10.1067/mai.2000.104552; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Gereda JE, 2000, JAMA-J AM MED ASSOC, V284, P1652, DOI 10.1001/jama.284.13.1652; Hamilton RG, 1997, METHODS, V13, P53, DOI 10.1006/meth.1997.0495; Hasday JD, 1999, CHEST, V115, P829, DOI 10.1378/chest.115.3.829; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; KORSGAARD J, 1983, ALLERGY, V38, P85, DOI 10.1111/j.1398-9995.1983.tb01591.x; KUEHR J, 1994, CLIN EXP ALLERGY, V24, P229, DOI 10.1111/j.1365-2222.1994.tb00224.x; LE JM, 1986, J IMMUNOL, V136, P4525; Matricardi PM, 1998, J ALLERGY CLIN IMMUN, V101, P439, DOI 10.1016/S0091-6749(98)70350-1; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; MICHEL O, 1989, J APPL PHYSIOL, V66, P1059; MICHEL O, 1991, ANN ALLERGY, V66, P39; Milton DK, 1997, AM IND HYG ASSOC J, V58, P861; Mitchell H, 1997, PEDIATR PULM, V24, P237; Nicolai T, 1998, THORAX, V53, P1035; OLENCHOCK SA, 1992, SCAND J WORK ENV HEA, V18, P58; Park JH, 2000, ENVIRON HEALTH PERSP, V108, P1023, DOI 10.2307/3434953; Peden DB, 1999, J ALLERGY CLIN IMMUN, V104, P388, DOI 10.1016/S0091-6749(99)70383-0; Perzanowski MS, 1999, J ALLERGY CLIN IMMUN, V103, P1018, DOI 10.1016/S0091-6749(99)70173-9; PLATT SD, 1989, BRIT MED J, V298, P1673; Ponsonby AL, 1999, THORAX, V54, P664; Quinn PJ, 1994, CLIN VET MICROBIOLOG; REIIJONEN TM, 2000, PEDIATRICS, V106, P1406; Rizzo MC, 1997, PEDIATR ALLERGY IMMU, V8, P121; RYLANDER R, 1985, AM REV RESPIR DIS, V131, P209; SCHWARTZ J, 1990, AM REV RESPIR DIS, V142, P555; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Svanes C, 1999, J ALLERGY CLIN IMMUN, V103, P415, DOI 10.1016/S0091-6749(99)70465-3; THELIN A, 1984, EUR J RESPIR DIS, V65, P266; WEISS K, 1992, CHEST, V6, pS362; Wickens K, 1999, J ALLERGY CLIN IMMUN, V104, P554, DOI 10.1016/S0091-6749(99)70323-4	43	138	139	2	8	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. 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J	Arruda, LK; Vailes, LD; Ferriani, VPL; Santos, BR; Pomes, A; Chapman, MD				Arruda, LK; Vailes, LD; Ferriani, VPL; Santos, BR; Pomes, A; Chapman, MD			Cockroach allergens and asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article; Proceedings Paper	Annual Meeting of the American-Academy-of-Allergy-Asthma-and-Immunology	MAR, 2000	SAN DIEGO, CALIFORNIA	Amer Acad Allergy Asthma & Immunol		cockroach; asthma; indoor allergens; public health; risk factors; environment	HOUSE-DUST MITE; IMMUNOSTIMULATORY DNA-SEQUENCES; INNER-CITY CHILDREN; HIGH-LEVEL EXPRESSION; AMERICAN COCKROACH; RISK-FACTORS; AIRWAY HYPERRESPONSIVENESS; BLATTELLA-GERMANICA; INHALANT ALLERGENS; SHRIMP ALLERGEN	Asthma and allergy are the most common diseases associated with cockroach infestation of houses in the United States and other parts of the world. Sensitization and exposure to cockroach allergens is associated with increased asthma morbidity in the United States, especially among lower socioeconomic groups, including African American and Hispanic populations. Exposure to cockroach allergens in the first 3 months of life has been associated with repeated wheezing and asthma. The principal domestic cockroach species are Blattella germanica and Periplaneta americana. Both species produce several potent allergens, including Bla g 2 (inactive aspartic proteinase), Bla g 4 (calycin), Bla g 5 (glutathione-S-transferase), the group 1 cross-reactive allergens Bla g 1 and Per a 1, and tropomyosin. Structural homology between tropomyosins from cockroaches, mites, and shrimp may explain clinical cases of the oral allergy syndrome. The 3-dimensional structures of several cockroach allergens are known, and biologically active recombinant allergens have been produced in high-level expression vectors. The use of recombinant cockroach allergens should allow mechanisms of cockroach-induced asthma to be investigated and may lead to the development of new approaches to asthma treatment. Environmental allergen measurements of Bla g 1 and Bla g 2 have allowed exposure levels that cause allergic sensitization to be established. Abatement studies have shown that a sustained decrease in cockroach allergen levels is difficult but can be accomplished by professional application of insecticides, together with rigorous household cleaning. Cockroach asthma is an important public health problem that affects patients who are the least likely to be compliant with treatment with asthma medications or environmental control. Patient education, improvements in the housing stock, and improvements in environmental and immunologic treatment strategies are likely to be the most successful approaches to reduce the prevalence of cockroach-induced asthma.	Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Pediat, BR-14049 Ribeirao Preto, Brazil; Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Cell & Mol Biol, BR-14049 Ribeirao Preto, Brazil; Univ Virginia, Asthma & Allerg Dis Ctr, Charlottesville, VA USA	Chapman, MD (reprint author), UVA Hlth Syst, Asthma & Allerg Dis Ctr, POB 801355, Charlottesville, VA 22908 USA.		Arruda, L. Karla /D-5845-2013; Ferriani, Virginia/E-2209-2012	Arruda, L. 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J	Boulet, LP; Turcotte, H; Laviolette, M; Naud, F; Bernier, MC; Martel, S; Chakir, J				Boulet, LP; Turcotte, H; Laviolette, M; Naud, F; Bernier, MC; Martel, S; Chakir, J			Airway hyperresponsiveness, inflammation, and subepithelial collagen deposition in recently diagnosed versus long-standing mild asthma - Influence of inhaled corticosteroids	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							NONASTHMATIC SUBJECTS; OCCUPATIONAL ASTHMA; ALLERGIC RHINITIS; TERM TREATMENT; BUDESONIDE; METHACHOLINE; EXPRESSION; CESSATION; STEROIDS; EXPOSURE	This study aimed at documenting airway inflammation and subepithelial collagen deposition in patients using only inhaled beta(2)-agonists with either recently diagnosed asthma (RDA: less than or equal to 2 yr, n = 16) or long-standing asthma (LSA: greater than or equal to 13 yr, n = 16) and at the influence of an intense inhaled corticosteroid (ICS) treatment on these parameters, in relation to changes in airway responsiveness. Patients had a methacholine inhalation test and a bronchoscopy with bronchial biopsies before and after an 8-wk treatment with inhaled fluticasone propionate (FP), 1,000 mu g/day. Baseline FEV1 (mean +/- SEM) was normal and similar in both groups (RDA: 98.1 +/- 2.7, LSA: 94.5 +/- 4.6%). Geometric mean methacholine PC20 was lower in LSA than in RDA (0.44 versus 3.37 mg/ml) at baseline and improved similarly by 1.85 and 1.86 double concentrations with FP treatment. PC20 normalized (greater than or equal to 16 mg/ml) in five patients with RDA and two patients with LSA. Baseline mean bronchial cell counts (per mm(2) connective tissue surface) for CD3(+), CD4(+), CD8(+), CD25(+), EG1(+), CD45ro(+), and AA1(+) cells were similar in both groups. With FP, EG1(+) (p < 0.001), EG2(+) (p = 0.018), and AA1(+) counts (p = 0.009) decreased significantly in both groups while CD45ro(+) (p = 0.02) counts decreased only in LSA. Baseline type 1 and type 3 collagen deposition underneath the basement membrane was similar in RDA and LSA and did not change significantly after FP. This study shows that recent compared to long-standing mild asthma is associated with a similar degree of airway inflammation and subepithelial fibrosis, and a similar improvement in airway hyperresponsiveness after 8 wk on high-dose ICS. It also indicates that once asthma becomes symptomatic, airway responsiveness cannot normalize in most subjects over such a time period, even with a high dose of ICS.	Univ Laval, Hop Laval, Inst Cardiol & Pneumol, St Foy, PQ G1V 4G5, Canada	Boulet, LP (reprint author), Univ Laval, Hop Laval, Inst Cardiol & Pneumol, 2725 Chemin St Foy, St Foy, PQ G1V 4G5, Canada.						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J	Mauroy, B; Filoche, M; Weibel, ER; Sapoval, B				Mauroy, B; Filoche, M; Weibel, ER; Sapoval, B			An optimal bronchial tree may be dangerous	NATURE			English	Article							MODEL	The geometry and dimensions of branched structures such as blood vessels or airways are important factors in determining the efficiency of physiological processes. It has been shown that fractal trees can be space filling(1) and can ensure minimal dissipation(2-4). The bronchial tree of most mammalian lungs is a good example of an efficient distribution system with an approximate fractal structure(5,6). Here we present a study of the compatibility between physical optimization and physiological robustness in the design of the human bronchial tree. We show that this physical optimization is critical in the sense that small variations in the geometry can induce very large variations in the net air flux. Maximum physical efficiency therefore cannot be a sufficient criterion for the physiological design of bronchial trees. Rather, the design of bronchial trees must be provided with a safety factor and the capacity for regulating airway calibre. Paradoxically, our results suggest that bronchial malfunction related to asthma is a necessary consequence of the optimized efficiency of the tree structure.	Ecole Normale Super, Ctr Math & Leurs Applicat, F-94235 Cachan, France; Ecole Polytech, CNRS, Phys Mat Condensee Lab, F-91128 Palaiseau, France; Univ Bern, Dept Anat, CH-3000 Bern, Switzerland	Ecole Normale Super, Ctr Math & Leurs Applicat, F-94235 Cachan, France.	Bernard.Sapoval@polytechnique.fr		FILOCHE, Marcel/0000-0001-8637-3016			Bejan A., 2000, SHAPE STRUCTURE ENG; Brown J.H., 2000, SCALING BIOL; Hess WR, 1914, ARCH ANAT PHYSL, P1; Hoppeler H, 2003, MED SCI SPORT EXER, V35, P95, DOI 10.1249/01.MSS.0000043292.99104.12; Kitaoka H, 1999, J APPL PHYSIOL, V87, P2207; Mandelbrot B. B., 1982, FRACTAL GEOMETRY NAT; Mauroy B, 2003, PHYS REV LETT, V90, DOI 10.1103/PhysRevLett.90.148101; Murray CD, 1926, P NATL ACAD SCI USA, V12, P207, DOI 10.1073/pnas.12.3.207; NELSON TR, 1988, IEEE T MED IMAGING, V7, P321, DOI 10.1109/42.14515; Que CL, 2001, J APPL PHYSIOL, V91, P1131; Sapoval B, 2002, P NATL ACAD SCI USA, V99, P10411, DOI 10.1073/pnas.122352499; Sapoval B., 1997, UNIVERSALITES FRACTA; Weibel E, 1963, MORPHOMETRY HUMAN LU; Weibel ER, 2000, SYMMORPHOSIS; Weibel E. R., 1984, PATHWAY OXYGEN; Weibel E. R., 1997, LUNG SCI FDN, V1, P1061; WEST BJ, 1986, J APPL PHYSIOL, V60, P1089; West GB, 1997, SCIENCE, V276, P122, DOI 10.1126/science.276.5309.122; Wilber RL, 2000, MED SCI SPORT EXER, V32, P732, DOI 10.1097/00005768-200004000-00003	19	137	145	1	13	NATURE PUBLISHING GROUP	LONDON	MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND	0028-0836	1476-4687		NATURE	Nature	FEB 12	2004	427	6975					633	636		10.1038/nature02287		4	Multidisciplinary Sciences	Science & Technology - Other Topics	773AJ	WOS:000188875300041	14961120	
J	Prather, M; Gauss, M; Berntsen, T; Isaksen, I; Sundet, J; Bey, I; Brasseur, G; Dentener, F; Derwent, R; Stevenson, D; Grenfell, L; Hauglustaine, D; Horowitz, L; Jacob, D; Mickley, L; Lawrence, M; von Kuhlmann, R; Muller, JF; Pitari, G; Rogers, H; Johnson, M; Pyle, J; Law, K; van Weele, M; Wild, O				Prather, M; Gauss, M; Berntsen, T; Isaksen, I; Sundet, J; Bey, I; Brasseur, G; Dentener, F; Derwent, R; Stevenson, D; Grenfell, L; Hauglustaine, D; Horowitz, L; Jacob, D; Mickley, L; Lawrence, M; von Kuhlmann, R; Muller, JF; Pitari, G; Rogers, H; Johnson, M; Pyle, J; Law, K; van Weele, M; Wild, O			Fresh air in the 21st century?	GEOPHYSICAL RESEARCH LETTERS			English	Article							TROPOSPHERIC OZONE; INTERCONTINENTAL TRANSPORT; POLLUTION; ASTHMA; POLLUTANTS; EXPOSURE; HEALTH	Ozone is an air quality problem today for much of the world's population. Regions can exceed the ozone air quality standards (AQS) through a combination of local emissions, meteorology favoring pollution episodes, and the clean-air baseline levels of ozone upon which pollution builds. The IPCC 2001 assessment studied a range of global emission scenarios and found that all but one projects increases in global tropospheric ozone during the 21st century. By 2030, near-surface increases over much of the northern hemisphere are estimated to be about 5 ppb (+2 to +7 ppb over the range of scenarios). By 2100 the two more extreme scenarios project baseline ozone increases of >20 ppb, while the other four scenarios give changes of -4 to +10 ppb. Even modest increases in the background abundance of tropospheric ozone might defeat current AQS strategies. The larger increases, however, would gravely threaten both urban and rural air quality over most of the northern hemisphere.	Univ Calif Irvine, Dept Earth Syst Sci, Irvine, CA 92697 USA; Univ Oslo, Inst Geofys, N-0315 Oslo, Norway; Swiss Fed Inst Technol, CH-1015 Lausanne, Switzerland; Max Planck Inst Meteorol, D-20146 Hamburg, Germany; Commiss European Communities, Joint Res Ctr, Inst Environm, I-21020 Ispra, Italy; Hadley Ctr, UK Met Off, Bracknell, Berks, England; CEA, CNRS, Inst Pierre Simon Laplace, F-91198 Gif Sur Yvette, France; NOAA, Geophys Fluid Dynam Lab, Princeton, NJ USA; Harvard Univ, Dept Earth & Planetary Sci, Cambridge, MD USA; Max Planck Inst Chem, D-55128 Mainz, Germany; Inst Aeron Spatiale Belgique, B-1180 Brussels, Belgium; Univ Aquila, Dipartimento Fis, I-67010 Laquila, Italy; Univ Cambridge, Ctr Atmospher Sci, Cambridge CB2 1EW, England; Royal Netherlands Meteorol Inst, NL-3730 AE De Bilt, Netherlands; Frontier Res Syst Global Change, Yokohama, Kanagawa, Japan	Prather, M (reprint author), Univ Calif Irvine, Dept Earth Syst Sci, Irvine, CA 92697 USA.		Wild, Oliver/A-4909-2009; Stevenson, David/C-8089-2012; Mickley, Loretta/D-2021-2012; Pfister, Gabriele/A-9349-2008; Horowitz, Larry/D-8048-2014	Wild, Oliver/0000-0002-6227-7035; Stevenson, David/0000-0002-4745-5673; Mickley, Loretta/0000-0002-7859-3470; Horowitz, Larry/0000-0002-5886-3314; Pitari, Giovanni/0000-0001-7051-9578			Brasseur GP, 1998, GEOPHYS RES LETT, V25, P3807, DOI 10.1029/1998GL900013; Desqueyroux H, 2002, ENVIRON RES, V89, P29, DOI 10.1006/enrs.2002.4357; *EEA, 2002, 9 EEA, P73; Emberson LD, 2001, WATER AIR SOIL POLL, V130, P107, DOI 10.1023/A:1012251503358; Fiore AM, 2002, GEOPHYS RES LETT, V29, DOI 10.1029/2002GL015601; Gupta ML, 1998, GEOPHYS RES LETT, V25, P3931, DOI 10.1029/1998GL900099; HAAGENSMIT AJ, 1952, IND ENG CHEM, V44, P1342, DOI 10.1021/ie50510a045; Jensen SS, 2001, INT J VEHICLE DES, V27, P195, DOI 10.1504/IJVD.2001.001964; Johnson CE, 2001, GEOPHYS RES LETT, V28, P1723, DOI 10.1029/2000GL011996; Li Q., 2002, J GEOPHYS RES, V107, DOI [10.1029/2001JD001422, DOI 10.1029/2001JD001422]; Mauzerall DL, 2001, ANNU REV ENERG ENV, V26, P237, DOI 10.1146/annurev.energy.26.1.237; Morrison GC, 2002, ENVIRON SCI TECHNOL, V36, P2185, DOI 10.1021/es0113089; Mortimer KM, 2002, EUR RESPIR J, V19, P699, DOI 10.1183/09031936.02.00247102; Nakicenovic N. J., 2000, SPECIAL REPORT EMISS; Oksanen E, 2001, ATMOS ENVIRON, V35, P5245, DOI 10.1016/S1352-2310(01)00346-6; Peden DB, 2001, ANN ALLERG ASTHMA IM, V87, P12; Penner J. E., 2001, CLIMATE CHANGE 2001, P289; Prather M, 2001, CLIMATE CHANGE 2001, P239; Tarrason L, 1998, TELLUS B, V50, P331, DOI 10.1034/j.1600-0889.1998.t01-3-00002.x; Taylor GE, 2001, HUM ECOL RISK ASSESS, V7, P1183, DOI 10.1080/20018091094934; Wild O, 2001, J GEOPHYS RES-ATMOS, V106, P27729, DOI 10.1029/2000JD000123	21	137	146	1	15	AMER GEOPHYSICAL UNION	WASHINGTON	2000 FLORIDA AVE NW, WASHINGTON, DC 20009 USA	0094-8276			GEOPHYS RES LETT	Geophys. Res. Lett.	JAN 31	2003	30	2							1100	10.1029/2002GL016285		4	Geosciences, Multidisciplinary	Geology	678YB	WOS:000182893300006		
J	Celedon, JC; Litonjua, AA; Ryan, L; Platts-Mills, T; Weiss, ST; Gold, DR				Celedon, JC; Litonjua, AA; Ryan, L; Platts-Mills, T; Weiss, ST; Gold, DR			Exposure to cat allergen, maternal history of asthma, and wheezing in first 5 years of life	LANCET			English	Article							CHILDREN; ATOPY	We looked for an association between early exposure to pets and asthma and wheezing in children whose mothers or fathers did or did not have a history of asthma. We followed up 448 children, who had at least one parent with a history of atopy, from birth to 5 years. Among children whose mothers had no history of asthma, exposure to a cat or a Fel d 1 concentration of at least 8 mug/g at the age of 2-3 months was associated with a reduced risk of wheezing between the ages of 1 and 5 years. However, among children whose mothers did have a history of asthma, such exposures were associated with an increased risk of wheezing at or after the age of 3 years. There was no association between wheezing and exposure to dog or dog allergen, and the father's allergy status had no effect on the relation between childhood wheezing and cat exposure.	Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA; Univ Virginia, Dept Med, Ctr Asthma & Allergy, Charlottesville, VA USA; Harvard Sch Publ Hlth, Boston, MA 02115 USA	Celedon, JC (reprint author), Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA.		Ryan, Louise/A-4562-2009	Ryan, Louise/0000-0001-5957-2490	NHLBI NIH HHS [KO1 HL04370-01A1]; NIEHS NIH HHS [ES35786]		Celedon JC, 1999, PEDIATRICS, V104, P495, DOI 10.1542/peds.104.3.495; Kitch BT, 2000, ENVIRON HEALTH PERSP, V108, P301, DOI 10.2307/3454347; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; Remes ST, 2001, J ALLERGY CLIN IMMUN, V108, P509, DOI 10.1067/mai.2001.117797; THERNEAU TM, 2000, MODELING SURVIVAL DA, P185	5	137	142	2	8	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	SEP 7	2002	360	9335					781	782		10.1016/S0140-6736(02)09906-3		2	Medicine, General & Internal	General & Internal Medicine	592HX	WOS:000177933000022	12241839	
J	Antczak, A; Montuschi, P; Kharitonov, S; Gorski, P; Barnes, PJ				Antczak, A; Montuschi, P; Kharitonov, S; Gorski, P; Barnes, PJ			Increased exhaled cysteinyl-leukotrienes and 8-isoprostane in aspirin-induced asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						aspirin-induced asthma; cysteinyl-leukotrienes; exhaled breath condensate; 8-isoprostane; prostaglandin E-2	SENSITIVE ASTHMATICS; OXIDATIVE STRESS; URINARY LEUKOTRIENE-E4; BRONCHIAL PROVOCATION; INTOLERANT ASTHMA; EPITHELIAL-CELLS; ARACHIDONIC-ACID; C-4 SYNTHASE; IN-VIVO; CONDENSATE	The pathogenesis of aspirin-induced asthma (AIA) has not yet been clearly elucidated, although eicosanoid metabolites appear to play an important role. We hypothesized that levels of eicosanolds in exhaled air condensate are abnormal in patients with AIA and that they change in patients receiving steroid therapy. We measured cysteinyl-leukotrienes (cys-LTs), prostaglandin E-2 (PGE(2)), and leukotriene B-4 (LTB4), and also 8-isoprostane as a marker of oxidative stress, by enzyme immunoassay in exhaled breath condensate from patients with AIA (17 steroid naive; mean age, 41 +/- 23 years; FEV1, 63%pred), 26 patients with aspirin-tolerant asthma (ATA) (11 steroid naive; mean age, 47 +/- 18 years; FEV1, 69%pred), and 16 healthy subjects (mean age, 45 +/- 17 years; FEV1, 93%pred). Cys-LTs were significantly higher in steroid-naive patients with Al compared with steroid-naive patients with ATA and healthy subjects (152.3 +/- 30.4 and 36.6 +/- 7.1 versus 19.4 +/- 2.8 pg/ml; p < 0.05 and p < 0.05, respectively). Steroid-naive patients with AIA also had higher levels of 8-isoprostane than normal subjects (131.8 +/- 31.0 versus 21.9 +/- 4.5 pg/ml; p < 0.05). There were significantly lower levels of both cys-LTs and 8-isoprostanes in steroid-treated patients with AIA. There was no difference in either the PGE(2) or LTB4 level between the patient groups. This is the first study to show that cys-LTs and 8-isoprostanes are elevated in expired breath condensate of steroid-naive patients with AIA, and that cys-LTs are decreased in steroid-treated patients. Exhaled PGE(2) levels are not reduced, so that it is unlikely that a deficiency of PGE(2) is an important mechanism, whereas exhaled LT84 levels are unchanged, indicating an abnormality beyond 5-lipoxygenase.	Med Univ Lodz, Dept Pneumol & Allergol, PL-50153 Lodz, Poland; Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Thorac Med, London, England	Antczak, A (reprint author), Med Univ Lodz, Dept Pneumol & Allergol, Kopcinskiego Str 22, PL-50153 Lodz, Poland.			MONTUSCHI, Paolo/0000-0001-5589-1750			Aksoy MO, 1999, J ALLERGY CLIN IMMUN, V103, P1081, DOI 10.1016/S0091-6749(99)70183-1; Antczak A, 2000, RESP MED, V94, P416, DOI 10.1053/rmed.1999.0801; Antczak A, 1997, EUR RESPIR J, V10, P1231; Bochenek G, 1996, ALLERGY, V51, P16, DOI 10.1111/j.1398-9995.1996.tb04544.x; BOZEMAN PM, 1990, J IMMUNOL METHODS, V126, P125, DOI 10.1016/0022-1759(90)90020-V; CHRISTIE PE, 1991, AM REV RESPIR DIS, V143, P1025; CHRISTIE PE, 1991, AM REV RESPIR DIS, V49, P749; COCKCROFT DW, 1985, ANN ALLERGY, V55, P527; Cowburn AS, 1998, J CLIN INVEST, V101, P834, DOI 10.1172/JCI620; Crocker IC, 1997, ANN ALLERG ASTHMA IM, V78, P497; DAHLEN B, 1993, EUR RESPIR J, V6, P1018; Dekker JW, 1997, CLIN EXP ALLERGY, V27, P574, DOI 10.1046/j.1365-2222.1997.540848.x; Dworski R, 1999, AM J RESP CRIT CARE, V160, P1947; DWORSKI R, 1994, AM J RESP CRIT CARE, V149, P953; HAM EA, 1983, P NATL ACAD SCI-BIOL, V80, P4349, DOI 10.1073/pnas.80.14.4349; Hanazawa T, 2000, AM J RESP CRIT CARE, V162, P1273; ISRAEL E, 1993, AM REV RESPIR DIS, V148, P1447; Jakobsson PJ, 1999, P NATL ACAD SCI USA, V96, P7220, DOI 10.1073/pnas.96.13.7220; Kowalski ML, 2000, AM J RESP CRIT CARE, V161, P391; KUMLIN M, 1992, AM REV RESPIR DIS, V146, P96; Lindsay MA, 1998, J IMMUNOL, V160, P4526; Montuschi P, 2000, THORAX, V55, P205, DOI 10.1136/thorax.55.3.205; Montuschi P, 1999, AM J RESP CRIT CARE, V160, P216; Montuschi P, 2000, AM J RESP CRIT CARE, V162, P1175; MURRAY JJ, 1998, AM J RESP CRITICA S3, V157, pA872; Nizankowska E, 2000, EUR RESPIR J, V15, P863, DOI 10.1034/j.1399-3003.2000.15e09.x; OSHAUGHNESSY KM, 1993, AM REV RESPIR DIS, V147, P1472; Picado C, 1999, AM J RESP CRIT CARE, V160, P291; PICADO C, 1992, AM REV RESPIR DIS, V145, P65; Pratico D, 1996, J BIOL CHEM, V271, P8919; Roberts LJ, 2000, FREE RADICAL BIO MED, V28, P505, DOI 10.1016/S0891-5849(99)00264-6; SAMTER M, 1968, ANN INTERN MED, V68, P975; Sanak M, 2000, AM J RESP CELL MOL, V23, P290; Schafer D, 1999, EUR RESPIR J, V13, P638, DOI 10.1183/09031936.99.13363899; SEBALDT RJ, 1990, P NATL ACAD SCI USA, V87, P6974, DOI 10.1073/pnas.87.18.6974; SEDGWICK JB, 1990, AM REV RESPIR DIS, V142, P120; SERHAN CN, 1982, BIOCHEM BIOPH RES CO, V107, P1006, DOI 10.1016/0006-291X(82)90622-2; Sestini P, 1996, AM J RESP CRIT CARE, V153, P572; SHINDO K, 1994, CHEST, V105, P1038, DOI 10.1378/chest.105.4.1038; SLADEK K, 1994, AM J RESP CRIT CARE, V149, P940; SMITH CM, 1992, EUR RESPIR J, V5, P693; Szczeklik A, 1999, J ALLERGY CLIN IMMUN, V104, P5, DOI 10.1016/S0091-6749(99)70106-5; Szczeklik A., 1992, P548; Szczeklik A, 1996, AM J RESP CRIT CARE, V154, P1608; SZCZEKLIK A, 1988, CLIN ALLERGY, V18, P15, DOI 10.1111/j.1365-2222.1988.tb02838.x; Szczeklik A, 2000, EUR RESPIR J, V16, P432, DOI 10.1034/j.1399-3003.2000.016003432.x; Takagi A, 1996, J BIOCHEM-TOKYO, V119, P979	47	137	142	0	5	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	AUG 1	2002	166	3					301	306		10.1164/rccm.2101021		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	580QV	WOS:000177246000011	12153961	
J	Wickman, M; Kull, I; Pershagen, G; Nordvall, SL				Wickman, M; Kull, I; Pershagen, G; Nordvall, SL			The BAMSE Project: presentation of a prospective longitudinal birth cohort study	PEDIATRIC ALLERGY AND IMMUNOLOGY			English	Article; Proceedings Paper	Congress of the European-Academy-of-Allergy-and-Clinical-Immunology	JUN, 2001	BERLIN, GERMANY	European Acad Allergy & Clin Immunol				The aims of this prospective and longitudinal project are to establish crucial risk factors for asthma and other allergic diseases in childhood, and to study factors of importance for prognosis at already established allergic disease. Socio-economic factors, such as inequality in health, are also to be addressed. The project started in February 1994. To reach sufficient power, 4,000 children had to be included. In November 1996, this number was reached (4,093). Inclusion in the study was made at 3-4 months of age. At that time, and before induction of allergic disease/asthma of the child, a questionnaire focused on exposure, genetics and socio-economic factors was answered. Settled dust was sampled for later analysis of furred animal and mite allergens. When the children were aged both 1 and 2 years, their parents were asked to fill in new questionnaires focusing on respiratory and allergic (skin, gastrointestinal) symptoms, but also key variables of exposure. Cases with asthma are identified and, for every case, two matched controls drawn. During the following winter, the homes of cases and controls were investigated and the temperature, indoor humidity, air change rate and NO2 measured. Two hundred cases (5%) were expected to be identified during the first 2 years of the children's lives. Some 479 homes have now been investigated and 97.7% of the original 4,093 children still remain in the cohort. The 2-year symptom follow-up ended in November 1998. The 4-year follow-up started on 1 September 1998 and was planned to be finished in June 2000. Questionnaires (allergic and respiratory symptoms, key variables of exposure at home and day care) are sent out to all 4,093 families. All children are invited for examination, lung function tests (PEF, flow-volume, MVV and oxygen clearance) and physical performance. Blood is taken from all children (20 ml). Allergy screening is performed and specific IgE examined. Blood cells will be frozen to allow for later DNA extraction. In subsets (children with any allergic and/or respiratory manifestation and controls), markers of inflammation in blood and urine will be examined, as well as eosinophils in nasal smear. Interviews are carried out to assess the severity of asthma, type/periodicity of health care given, asthma medication and parental sick leave when appropriate. As a separate project, financed by the EU, outdoor pollution as risk factors for asthma and allergies are to be studied within the BAMSE cohort. A follow-up of 8-9 years is underway.	Stockholm Cty Council, Dept Environm Hlth, Stockholm, Sweden; Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; Karolinska Inst, Sachs Childrens Hosp, Inst Sodersjukhuset, Stockholm, Sweden; Uppsala Univ, Dept Womens & Childrens Hlth, Uppsala, Sweden	Wickman, M (reprint author), Karolinska Hosp, Dept Environm Hlth, Norrbacka Bldg,Level 3, SE-17176 Stockholm, Sweden.							0	137	137	1	16	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0905-6157			PEDIATR ALLERGY IMMU	Pediatr. Allergy Immunol.		2002	13			15			11	13		10.1034/j.1399-3038.13.s.15.10.x		3	Allergy; Immunology; Pediatrics	Allergy; Immunology; Pediatrics	638KW	WOS:000180571000003	12688617	
J	Leynaert, B; Neukirch, C; Jarvis, D; Chinn, S; Burney, P; Neukirch, F				Leynaert, B; Neukirch, C; Jarvis, D; Chinn, S; Burney, P; Neukirch, F		European Comm Resp Hlth Survey	Does living on a farm during childhood protect against asthma, allergic rhinitis, and atopy in adulthood?	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; allergic rhinitis; immunologic sensitization; farm; epidemiologic studies	RESPIRATORY-HEALTH-SURVEY; HAY-FEVER; INTESTINAL MICROFLORA; FAMILY-SIZE; CHILDREN; SENSITIZATION; PREVALENCE; COMMUNITY; EXPOSURE; RISK	Recent studies of children suggest that factors encountered in a farm environment might protect against the development of allergy. However, it remains uncertain whether living on a farm in childhood is associated with a decreased risk of atopic diseases in adulthood. We analyzed data from 6,251 randomly selected adults 20 to 44 yr of age participating in the European Community Respiratory Health Survey (ECRHS). Subjects answered a detailed questionnaire and underwent specific IgE measurements to five allergens. After adjustment for potential confounders, including pet exposure in childhood, number of siblings, severe respiratory infection in childhood, and parental history of allergy, living on a farm in childhood was associated with a reduced risk of atopic sensitization in adulthood (OR = 0.76, Cl 95% = 0.60-0.97). Compared with other adults, those who had lived on a farm as a child were less frequently sensitized to cat (OR = 0.63, Cl 95% = 0.41-0.96) and to Timothy grass (OR = 0.68, Cl 95% = 0.50-0.94), and were at lower risk of having nasal symptoms in the presence of pollen (OR = 0.80, Cl 95% = 0.64-1.02). The protective effect of farming environment in childhood observed in this population-based sample of young adults provides evidence in favor of the hypothesis that environmental factors encountered in childhood may have a lifelong protective effect against the development of allergy.	Univ Paris 07, INSERM U408, F-75870 Paris 18, France; Kings Coll London, Dept Publ Hlth Sci, London WC2R 2LS, England	Leynaert, B (reprint author), Univ Paris 07, INSERM U408, BP 416, F-75870 Paris 18, France.	leynaert@bichat.inserm.fr	Jarvis, Deborah/E-6494-2011; bucca, caterina/C-9886-2009	bucca, caterina/0000-0002-9941-9236	NCRR NIH HHS [2 S07 RR05521-28]		Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; Bjorksten B, 1999, CLIN EXP ALLERGY, V29, P342; Bodner C, 1998, THORAX, V53, P28; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Burney P, 1996, EUR RESPIR J, V9, P687; Burney P, 1997, J ALLERGY CLIN IMMUN, V99, P314, DOI 10.1016/S0091-6749(97)70048-4; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; Ernst P, 2000, AM J RESP CRIT CARE, V161, P1563; Gassner-Bachmann M, 2000, DEUT MED WOCHENSCHR, V125, P924, DOI 10.1055/s-2000-6778; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Heinrich J, 1998, ALLERGY, V53, P89, DOI 10.1111/j.1398-9995.1998.tb03779.x; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Holt PG, 1999, ALLERGY, V54, P12, DOI 10.1111/j.1398-9995.1999.tb04382.x; Illi S, 2001, BRIT MED J, V322, P390, DOI 10.1136/bmj.322.7283.390; Jarvis D, 1997, CLIN EXP ALLERGY, V27, P240; Kalliomaki M, 2001, LANCET, V357, P1076, DOI 10.1016/S0140-6736(00)04259-8; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Kramer U, 1999, LANCET, V353, P450, DOI 10.1016/S0140-6736(98)06329-6; Majamaa H, 1997, J ALLERGY CLIN IMMUN, V99, P179, DOI 10.1016/S0091-6749(97)70093-9; Martinez FD, 1999, LANCET S2, V354, pSII12; Matricardi PM, 2000, BRIT MED J, V320, P412, DOI 10.1136/bmj.320.7232.412; Matricardi PM, 1998, J ALLERGY CLIN IMMUN, V101, P439, DOI 10.1016/S0091-6749(98)70350-1; Nafstad P, 2001, ALLERGY, V56, P307, DOI 10.1034/j.1398-9995.2001.00881.x; Pearce N, 1999, THORAX, V54, P268; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Roost HP, 1999, J ALLERGY CLIN IMMUN, V104, P941, DOI 10.1016/S0091-6749(99)70072-2; Sepp E, 1997, ACTA PAEDIATR, V86, P956, DOI 10.1111/j.1651-2227.1997.tb15178.x; Strachan David P., 2000, Thorax, V55, pS2, DOI 10.1136/thorax.55.suppl_1.S2; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Sudo N, 1997, J IMMUNOL, V159, P1739; Svanes C, 1999, J ALLERGY CLIN IMMUN, V103, P415, DOI 10.1016/S0091-6749(99)70465-3; Upton MN, 2000, BRIT MED J, V321, P88, DOI 10.1136/bmj.321.7253.88; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; VONMUTIUS E, 1994, BRIT MED J, V308, P692	37	137	140	0	12	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	NOV 15	2001	164	10					1829	1834				6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	502TK	WOS:000172758700017	11734431	
J	Herrick, CA; MacLeod, H; Glusac, E; Tigelaar, RE; Bottomly, K				Herrick, CA; MacLeod, H; Glusac, E; Tigelaar, RE; Bottomly, K			Th2 responses induced by epicutaneous or inhalational protein exposure are differentially dependent on IL-4	JOURNAL OF CLINICAL INVESTIGATION			English	Article							CD4+ T-CELLS; INTERLEUKIN-4-DEFICIENT MICE; NIPPOSTRONGYLUS-BRASILIENSIS; EOSINOPHILIC INFLAMMATION; IL-4-DEFICIENT MICE; AIRWAY INFLAMMATION; AEROSOLIZED ANTIGEN; CYTOKINE RESPONSES; ATOPIC-DERMATITIS; TRANSGENIC MICE	Atopic individuals are predisposed to mounting vigorous Th2-type immune responses to environmental allergens. To determine the factors responsible, animal models that closely mimic natural modes of allergen exposure should prove most informative. Therefore, we investigated the role of IL-4, a known Th2-promoting cytokine, in generation of Th2 responses after exposure of either the skin or airway to soluble protein. Compared with wild-type (WT) mice, IL-4-deficient (IL-4(-/-)) mice showed markedly impaired Th2 activation after primary exposure to inhaled ovalbumin (OVA), with decreased OVA-specific IgG1 and IgE, and significantly fewer eosinophils in bronchoalveolar lavage (BAL) fluid after airway challenge. In contrast, IL-4(-/-) mice initially exposed to epicutaneous (e.c.) OVA mounted Th2 responses equivalent to responses in WT mice, with high numbers of eosinophils in BAL fluid. Because Th2 responses were not induced by e.c. OVA exposure in Stat6(-/-) mice (mice lacking signal transducer and activator of transcription 6), the role of IL-13 was tested. In vivo depletion of IL-13 prevented Th2 responses induced by e.c. OVA exposure in IL-4(-/-) mice. These data demonstrate a marked difference in the IL-4 dependence of Th2 responses generated at two anatomic sites of natural allergen encounter and identify the skin as a particularly potent site for Th2 sensitization.	Yale Univ, Sch Med, Dept Dermatol, New Haven, CT 06520 USA; Yale Univ, Sch Med, Immunobiol Sect, New Haven, CT 06520 USA; Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06520 USA	Herrick, CA (reprint author), Yale Univ, Sch Med, Dept Dermatol, 333 Cedar St,POB 208059, New Haven, CT 06520 USA.				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J	Zwiener, C; Richardson, SD; De Marini, DM; Grummt, T; Glauner, T; Frimmel, FH				Zwiener, Christian; Richardson, Susan D.; De Marini, David M.; Grummt, Tamara; Glauner, Thomas; Frimmel, Fritz H.			Drowning in disinfection byproducts? Assessing swimming pool water	ENVIRONMENTAL SCIENCE & TECHNOLOGY			English	Review							DRINKING-WATER; MUTATION SPECTRA; BIRTH-WEIGHT; TRIHALOMETHANE CONCENTRATIONS; LIQUID-CHROMATOGRAPHY; RESPIRATORY SYMPTOMS; NITROGEN TRICHLORIDE; CHEMICAL-IONIZATION; MASS-SPECTROMETRY; SALMONELLA TA100	Disinfection is mandatory for swimming pools: public pools are usually disinfected by gaseous chlorine or sodium hypochlorite and cartridge filters; home pools typically use stabilized chlorine. These methods produce a variety of disinfection byproducts (DBPs), such as trihalomethanes (THMs), which are regulated carcinogenic DBPs in drinking water that have been detected in the blood and breath of swimmers and of nonswimmers at indoor pools. Also produced are halogenated acetic acids (HAAs) and haloketones, which irritate the eyes, skin, and mucous membranes; trichloramine, which is linked with swimming-pool-associated asthma; and halogenated derivatives of UV sun screens, some of which show endocrine effects. Precursors of DBPs include human body substances, chemicals used in cosmetics and sun screens, and natural organic matter. Analytical research has focused also on the identification of an additional portion of unknown DBPs using gas chromatography (GC)/mass spectrometry (MS) and liquid chromatography (LC)/MS/MS with derivatization. Children swimmers have an increased risk of developing asthma and infections of the respiratory tract and ear. A 1.6-2.0-fold increased risk for bladder cancer has been associated with swimming or showering/bathing with chlorinated water. Bladder cancer risk from THM exposure (all routes combined) was greatest among those with the GSTT1-1 gene. This suggests a mechanism involving distribution of THMs to the bladder by dermal/inhalation exposure and activation there by GSTT1-1 to mutagens. DBPs may be reduced by engineering and behavioral means, such as applying new oxidation and filtration methods, reducing bromide and iodide in the source water, increasing air circulation in indoor pools, and assuring the cleanliness of swimmers. The positive health effects gained by swimming can be increased by reducing the potential adverse health risks.	Univ Karlsruhe, Engler Bunte Inst, D-7500 Karlsruhe, Germany; US EPA, Natl Exposure Res Lab, Athens, GA 30613 USA; US EPA, Div Environm Carcinogenesis, Res Triangle Pk, NC 27711 USA; Fed Environm Agcy, Bad Elster, Germany	Zwiener, C (reprint author), Univ Karlsruhe, Engler Bunte Inst, D-7500 Karlsruhe, Germany.	christian.zwiener@ciw.uni-karlsruhe.de					AGGAZZOTTI G, 1986, WATER RES, V20, P959, DOI 10.1016/0043-1354(86)90036-9; AGGAZZOTTI G, 1990, ARCH ENVIRON HEALTH, V45, P175; AGGAZZOTTI G, 1993, ARCH ENVIRON HEALTH, V48, P250; Aggazzotti G, 1998, SCI TOTAL ENVIRON, V217, P155, DOI 10.1016/S0048-9697(98)00174-0; AGGAZZOTTI G, 2004, J WATER HEALTH, P1; Backer LC, 2000, J EXPO ANAL ENV EPID, V10, P321, DOI 10.1038/sj.jea.7500098; BEECH JA, 1980, AM J PUBLIC HEALTH, V70, P79, DOI 10.2105/AJPH.70.1.79; Bernard A, 2005, TOXICOL APPL PHARM, V206, P185, DOI 10.1016/j.taap.2004.10.022; Bernard A, 2003, OCCUP ENVIRON MED, V60, P385, DOI 10.1136/oem.60.6.385; CANTOR KP, 2006, EPIDEMIOLOGY SS150, V17; Carbonnelle S, 2002, BIOMARKERS, V7, P464, DOI 10.1080/13547500210166612; *CDCP, HLTH SWIMM; Chu H, 2002, OCCUP ENVIRON MED, V59, P243, DOI 10.1136/oem.59.4.243; *CRANF U, 2002, 3 INT C POOL WAT QUA; DEMARINI DM, 1994, MUTAGENESIS, V9, P429, DOI 10.1093/mutage/9.5.429; DeMarini DM, 1995, ENVIRON MOL MUTAGEN, V26, P270, DOI 10.1002/em.2850260403; DeMarini DM, 1997, ENVIRON MOL MUTAGEN, V30, P440, DOI 10.1002/(SICI)1098-2280(1997)30:4<440::AID-EM9>3.0.CO;2-M; *DIN, 2000, 19643 DIN; ERDINGER L, 1990, FORUM STADTE HYG, V41, P185; Fantuzzi G, 2001, SCI TOTAL ENVIRON, V264, P257, DOI 10.1016/S0048-9697(00)00722-1; Frimmel F. 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Sci. Technol.	JAN 15	2007	41	2					363	372		10.1021/es062367v		10	Engineering, Environmental; Environmental Sciences	Engineering; Environmental Sciences & Ecology	124RS	WOS:000243388200010	17310693	
J	Calder, PC; Krauss-Etschmann, S; de Jong, EC; Dupont, C; Frick, JS; Frokiaer, H; Heinrich, J; Garn, H; Koletzko, S; Lack, G; Mattelio, G; Renz, H; Sangild, PT; Schrezenmeir, J; Stulnig, TM; Thymann, T; Wold, AE; Koletzko, B				Calder, Philip C.; Krauss-Etschmann, Susanne; de Jong, Esther C.; Dupont, Christophe; Frick, Julia-Stefanie; Frokiaer, Hanne; Heinrich, Joachim; Garn, Holger; Koletzko, Sibylle; Lack, Gideon; Mattelio, Gianluca; Renz, Harald; Sangild, Per T.; Schrezenmeir, Juergen; Stulnig, Thomas M.; Thymann, Thomas; Wold, Agnes E.; Koletzko, Berthold			Early nutrition and immunity - progress and perspectives	BRITISH JOURNAL OF NUTRITION			English	Review						immunity; infection; allergy; asthma; atopic disease; lymphocyte; dendritic cell; cytokine; inflammation; probiotic; polyunsaturated fatty acid	POLYUNSATURATED FATTY-ACIDS; FISH-OIL SUPPLEMENTATION; CHILDHOOD ASTHMA PREVENTION; GUT EPITHELIAL MONOLAYERS; PLACEBO-CONTROLLED TRIAL; REGULATORY T-CELLS; ATOPIC DISEASE; ALLERGIC SENSITIZATION; DENDRITIC CELLS; DOUBLE-BLIND	The immune system exists to protect the host against pathogenic organisms and highly complex pathways of recognition, response, elimination and memory have evolved in order to fulfil this role. The immune system also acts to ensure tolerance to 'self', to food and other environmental components, and to commensal bacteria. A breakdown in the tolerogenic pathways can also lead to inflammatory diseases. The prevalence of inflammatory diseases, including atopic disorders, has increased over the last 60 years. The development of tolerance is the result of active immune mechanisms and both development and maintenance of tolerance are lifelong processes which start very early in life, even prenatally. Profound immunologic changes occur during pregnancy, involving a polarization of T helper (Th) cells towards a dominance of Th2 and regulatory T cell effector responses in both mother and fetus. This situation is important to maintain pregnancy through avoidance of the rejection of the immunologically incompatible fetus. During the third trimester of human pregnancy, fetal T cells are able to mount antigen-specific responses to environmental and food-derived antigens and antigen-specific T cells are detectable in cord blood in virtually all newborns indicating in utero sensitization. If the neonatal immune system is not able to down-regulate the pre-existing Th2 dominance effectively then an allergic phenotype may develop. Changes occur at, and soon after, birth in order that the immune system of the neonate becomes competent and functional and that the gut becomes colonized with bacteria. Exposure to bacteria during birth and from the mother's skin and the provision of immunologic factors in breast milk are amongst the key events that promote maturation of the infant's gut and gut-associated and systemic immune systems. The introduction of formula and of solid foods exposes the infant to novel food antigens and also affects the gut flora. Nutrition may be the source of antigens to which the immune system must become tolerant, provide factors, including nutrients, that themselves might modulate immune maturation and responses, and provide factors that influence intestinal flora, which in turn will affect antigen exposure, immune maturation and immune responses. Through these mechanisms it is possible that nutrition early in life might affect later immune competence, the ability to mount an appropriate immune response upon infection, the ability to develop a tolerogenic response to 'self' and to benign environmental antigens, and the development of immunologic disorders. A Workshop held in February 2006 considered recent findings in the areas of oral tolerance, routes of sensitization to allergens and factors affecting the development of atopic disease; factors influencing the maturation of dendritic cells and the development of regulatory T cells; the influence of gut microflora on immunity, allergic sensitization and infectious disease; the role of nutrition in preventing necrotizing enterocolitis in an animal model of preterm birth; and the role of PUFA of different classes in influencing immune responses and in shaping the development of atopic disease. This report summarizes the content of the lectures and the subsequent discussions.	Univ Southampton, Sch Med, Inst Human Nutr, Southampton SO16 7PX, Hants, England; Univ Munich, Dr Von Haunerschen Kinderspital, Clin Cooperat Grp Pediat Immune Regulat, D-80337 Munich, Germany; GSF, Natl Res Ctr Environm & Hlth, D-85758 Neuherberg, Germany; Univ Amsterdam, Acad Med Ctr, NL-1105 AZ Amsterdam, Netherlands; Univ Amsterdam, Dept Cell Biol & Histol, NL-1105 AZ Amsterdam, Netherlands; Univ Paris 05, Hop St Vincent de Paul, Dept Pediat Gastroenterol, F-75014 Paris, France; Univ Paris 05, Hop St Vincent de Paul, Nutr Unit, F-75014 Paris, France; Univ Tubingen, Dept Med Microbiol & Hyg, D-72076 Tubingen, Germany; Tech Univ Denmark, Bioctr, DK-2800 Lyngby, Denmark; GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, D-85758 Neuherberg, Germany; Univ Marburg, Dept Clin Chem & Mol Diagnost, Cent Lab, D-35043 Marburg, Germany; Univ Munich, Dr Von Haunerschen Kinderspital, Div Gastroenterol, D-80337 Munich, Germany; Univ London Imperial Coll Sci Technol & Med, St Marys Hosp, London W2 1NY, England; European Inst Oncol, Dept Expt Oncol, I-20141 Milan, Italy; Royal Vet & Agr Univ, Dept Human Nutr, DK-1958 Frederiksberg, Denmark; Fed Res Ctr Nutr & Food, Inst Physiol & Biochem Nutr, D-24103 Kiel, Germany; Univ Vienna, Dept Internal Med 3, Clin Div Endocrinol & Metab, A-1090 Vienna, Austria; Gothenburg Univ, Sahlgrenska Acad, Dept Clin Bacteriol, S-41346 Gothenburg, Sweden; Univ Munich, Dr Von Haunerschen Kinderspital, Div Metab Dis & Nutr Med, D-80337 Munich, Germany	Calder, PC (reprint author), Univ Southampton, Sch Med, Inst Human Nutr, Bassett Crescent E, Southampton SO16 7PX, Hants, England.	pcc@soton.ac.uk	Perez , Claudio Alejandro/F-8310-2010; Wold, Agnes/M-6310-2013; Calder, Philip/E-9739-2013; Wilkinson, Stuart/C-2802-2013; Osborne, Nicholas/N-4915-2015	Perez , Claudio Alejandro/0000-0001-9688-184X; Calder, Philip/0000-0002-6038-710X; Osborne, Nicholas/0000-0002-6700-2284; Wold, Agnes/0000-0001-9196-5040			ADLERBERTH I, 2005, PEDIATR RES, V59, P96; Ahrne S, 2005, MICROBES INFECT, V7, P1256, DOI 10.1016/j.micinf.2005.04.011; Akerblom H K, 1985, Acta Paediatr Scand Suppl, V318, P49; Alfven T, 2006, ALLERGY, V61, P414, DOI 10.1111/j.1398-9995.2005.00939.x; Autenrieth IB, 1997, GUT, V41, P793; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; Bagga D, 2003, P NATL ACAD SCI USA, V100, P1751, DOI 10.1073/pnas.0334211100; Barnes KC, 2006, J ALLERGY CLIN IMMUN, V117, P243, DOI 10.1016/j.jaci.2005.11.030; Bergonzelli GE, 2005, DIGESTION, V72, P57, DOI 10.1159/000087638; Bjerke T, 1994, Pediatr Allergy Immunol, V5, P88, DOI 10.1111/j.1399-3038.1994.tb00223.x; Bjornvad CR, 2005, AM J PHYSIOL-REG I, V289, pR1212, DOI 10.1152/ajpregu.00776.2004; Black FT, 1989, TRAVEL MED, V7, P333; Black PN, 1997, EUR RESPIR J, V10, P6, DOI 10.1183/09031936.97.10010006; Bluestone JA, 2003, NAT REV IMMUNOL, V3, P253, DOI 10.1038/nri1032; Blumer N, 2005, CLIN EXP ALLERGY, V35, P397, DOI 10.1111/j.1365-2222.2005.02184.x; Bolte G, 2005, ANN EPIDEMIOL, V15, P207, DOI 10.1016/j.annepidem.2004.04.004; Bolte G, 2001, AM J RESP CRIT CARE, V163, P277; Borchers AT, 2005, J ASTHMA, V42, P225, DOI 10.1081/JAS-200051302; Braback L, 2001, PEDIATR ALLERGY IMMU, V12, P4, DOI 10.1034/j.1399-3038.2001.012001004.x; Braun-Fahrlander C, 2000, PEDIATR ALLERGY IMMU, V11, P19, DOI 10.1034/j.1399-3038.2000.00505.x; Broughton KS, 1997, AM J CLIN NUTR, V65, P1011; Calder P C, 1992, Mediators Inflamm, V1, P107, DOI 10.1155/S0962935192000188; CALDER PC, 1994, BIOCHEM J, V300, P509; CALDER PC, 1992, CLIN SCI, V82, P695; CALDER PC, 1991, INT J BIOCHEM, V23, P579; Calder PC, 2006, AM J CLIN NUTR, V83, p1505S; Calder PC, 2000, PEDIATR ALLERGY IMMU, V11, P29, DOI 10.1034/j.1399-3038.2000.00508.x; Calder PC, 2003, CLIN EXP ALLERGY, V33, P412, DOI 10.1046/j.1365-2222.2003.01633.x; Calder PC, 2002, BRIT J NUTR, V87, pS31, DOI [10.1079/BJN2001455, 10.1079/BJN2001482]; Calder PC, 2001, NUTR RES, V21, P309, DOI 10.1016/S0271-5317(00)00287-6; Calder P. 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Zeyda M, 2002, J BIOL CHEM, V277, P28418, DOI 10.1074/jbc.M203343200; Zeyda M, 2003, J IMMUNOL, V170, P6033; Zirngibl A, 2002, PEDIATR ALLERGY IMMU, V13, P394, DOI 10.1034/j.1399-3038.2002.01110.x	144	136	144	4	55	CAMBRIDGE UNIV PRESS	CAMBRIDGE	EDINBURGH BLDG, SHAFTESBURY RD, CB2 2RU CAMBRIDGE, ENGLAND	0007-1145			BRIT J NUTR	Br. J. Nutr.	OCT	2006	96	4					774	790		10.1079/BJN20061917		17	Nutrition & Dietetics	Nutrition & Dietetics	089GB	WOS:000240867300022	17010239	
J	Belanger, K; Beckett, W; Triche, E; Bracken, MB; Holford, T; Ren, P; McSharry, JE; Gold, DR; Platts-Mills, TAE; Leaderer, BP				Belanger, K; Beckett, W; Triche, E; Bracken, MB; Holford, T; Ren, P; McSharry, JE; Gold, DR; Platts-Mills, TAE; Leaderer, BP			Symptoms of wheeze and persistent cough in the first year of life: Associations with indoor allergens, air contaminants, and maternal history of asthma	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						allergens; cockroaches; cough; dust; fungi; infant; nitrogen dioxide; respiratory sounds	INFANT RESPIRATORY SYMPTOMS; HOUSE-DUST MITE; CHILDHOOD ASTHMA; NITROGEN-DIOXIDE; PARENTAL SMOKING; UNITED-STATES; CHILDREN; EXPOSURE; RISK; PREDICTORS	In a cohort of 849 infants with an asthmatic sibling, the authors examined the relations of exposure to allergens (dust mite, cockroach, cat, and dog), nitrogen dioxide, and mold with symptoms of wheeze and persistent cough in the first year of life (1998-2000). Among infants whose mothers had physician-diagnosed asthma, neither dust mite allergen nor dog allergen was associated with either symptom. Exposure to cockroach allergen (Bla g 1 at greater than or equal to2 U/g) modestly increased the risk for wheeze (odds ratio (OR)=1.87, 95% confidence interval (CI): 0.94, 3.71), and exposure to cat allergen modestly decreased the risk (OR=0.60, 95% CI: 0.35, 1.03). Among infants of mothers with no asthma history, exposure to gas stoves (OR=1.50, 95% CI: 1.05, 2.15) and wood-burning stoves (OR=2.09, 95% CI: 1.12, 3.91) increased the risk of persistent cough. Similarly, measured nitrogen dioxide concentration was associated with persistent cough (OR=1.21, 95% CI: 1.05, 1.40). Persistent mold affected both infants of mothers with asthma (for wheeze, OR=2.27, 95% CI: 1.27, 4.07; for cough, OR=1.83, 95% CI: 1.04, 3.22) and infants of mothers without asthma (for cough, OR=1.55, 95% CI: 1.04, 2.31). Reported exposure was confirmed by an association of measured fungi with wheeze (OR=1.23, 95% CI: 1.01, 1.49). This appears to have been the first study to measure all of these home exposures (indoor allergens, nitrogen dioxide, fungi) and to prospectively measure the frequency of infant wheeze and persistent cough.	Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06520 USA; Univ Rochester, Sch Med & Dent, Dept Environm Med, Occupat Med Div, Rochester, NY USA; Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA; Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Pulm, Boston, MA USA; Univ Virginia, Med Ctr, Dept Med, Div Allergy & Immunol, Charlottesville, VA USA	Belanger, K (reprint author), Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, 60 Coll St,POB 208034, New Haven, CT 06520 USA.		Triche, Elizabeth/I-4986-2014; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	NIEHS NIH HHS [ES05410, ES07456]		BJORKSTEN B, 1987, CLIN REV ALLERG, V5, P339; Bosken CH, 2000, AM J RESP CRIT CARE, V161, P1810; BRUNEKREEF B, 1992, INT J EPIDEMIOL, V21, P338, DOI 10.1093/ije/21.2.338; BURR ML, 1993, ARCH DIS CHILD, V68, P724; *COMM ASTHM IND AI, 2000, CLEAN AIR ASTHM IND; Csonka P, 2000, PEDIATR ALLERGY IMMU, V11, P225, DOI 10.1034/j.1399-3038.2000.00088.x; Eggleston PA, 1999, ENVIRON HEALTH PERSP, V107, P439; Gent JF, 2002, ENVIRON HEALTH PERSP, V110, pA781; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; HASSELBLAD V, 1992, J AIR WASTE MANAGE, V42, P662; Illi S, 2001, J ALLERGY CLIN IMMUN, V108, P709, DOI 10.1067/mai.2001.118786; INGRAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449, DOI 10.1016/S0091-6749(95)70286-5; KELLY YJ, 1995, THORAX, V50, P525, DOI 10.1136/thx.50.5.525; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; Leaderer BP, 1997, J PHARM PHARMACOL, V49, P39; Leaderer BP, 2002, ENVIRON HEALTH PERSP, V110, P419; Litonjua AA, 1998, AM J RESP CRIT CARE, V158, P176; Mannino DM, 1998, MMWR-MORBID MORTAL W, V47, P1; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Ortega AN, 2001, ANN ALLERG ASTHMA IM, V86, P405; PALMES ED, 1976, AM IND HYG ASSOC J, V37, P570, DOI 10.1080/0002889768507522; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Peat JK, 1998, ALLERGY, V53, P120, DOI 10.1111/j.1398-9995.1998.tb03859.x; PEDREIRA FA, 1985, PEDIATRICS, V75, P594; Pershagen G, 1995, INT J EPIDEMIOL, V24, P1147, DOI 10.1093/ije/24.6.1147; PLATTSMILLS TA, 1997, J ALLERGY CLIN IMMUN, V97, P1079; Rosenstreich DL, 1997, NEW ENGL J MED, V336, P1356, DOI 10.1056/NEJM199705083361904; ROWNTREE S, 1987, J ALLERGY CLIN IMMUN, V80, P622, DOI 10.1016/0091-6749(87)90017-0; Samet J M, 1993, Res Rep Health Eff Inst, P1; SCHWARTZ J, 1990, AM REV RESPIR DIS, V142, P555; Sears MR, 1996, ARCH DIS CHILD, V75, P392; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; Stein RT, 1999, AM J EPIDEMIOL, V149, P1030; Strachan DP, 1998, THORAX, V53, P204; Tager IB, 1998, AM J RESP CRIT CARE, V158, P349; Triche EW, 2002, AM J RESP CRIT CARE, V166, P1105, DOI 10.1164/rccm.2202014; vanStrien RT, 1996, EUR RESPIR J, V9, P926, DOI 10.1183/09031936.96.09050926; Verhoeff AP, 1997, ANN ALLERG ASTHMA IM, V78, P544; WEITZMAN M, 1990, PEDIATRICS, V85, P505; WEITZMAN M, 1990, AM J DIS CHILD, V144, P1189; ZEIGER RS, 1985, J ALLERGY CLIN IMMUN, V75, P633, DOI 10.1016/0091-6749(85)90086-7	41	136	139	2	8	OXFORD UNIV PRESS INC	CARY	JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA	0002-9262			AM J EPIDEMIOL	Am. J. Epidemiol.	AUG 1	2003	158	3					195	202		10.1093/aje/kwg148		8	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	707RF	WOS:000184523100001	12882940	
J	Mihrshahi, S; Peat, JK; Marks, GB; Mellis, CM; Tovey, ER; Webb, K; Britton, WJ; Leeder, SR				Mihrshahi, S; Peat, JK; Marks, GB; Mellis, CM; Tovey, ER; Webb, K; Britton, WJ; Leeder, SR		CAPS Team	Eighteen-month outcomes of house dust mite avoidance and dietary fatty acid modification in the Childhood Asthma Prevention Study (CAPS)	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergen avoidance; asthma; atopy; fatty acids; house dust mite; primary prevention	RANDOMIZED TRIAL; EARLY-LIFE; PREGNANCY; INFANCY	Background: Observational studies have linked house dust mite (HDM) exposure and dietary fatty acid intake with asthma in childhood. However, definitive evidence of their role in the etiology of asthma requires a randomized controlled trial. Objective: We hypothesized that the incidence of asthma and allergy in high-risk children would be reduced by avoidance of HDM allergens, supplementation with omega-3 fatty acids, or the combination of these strategies. We present the results of an interim analysis reporting outcomes assessed at 18 months. Methods: A total of 616 pregnant women were randomized to an HDM avoidance intervention, comprising the use of impermeable mattress covers and an acaricide or control and the use of an oil supplement, margarines, and cooking oils containing high levels of omega-3 fatty acids or control. Atopic status was measured by skin prick testing. Symptoms, diagnoses, and medication histories were elicited by means of parental interviews. Results: The diet intervention resulted in a 9.8% absolute reduction (95% CI, 1.5-18.1; P =.02) in the prevalence of any wheeze and a 7.8% absolute reduction (95% CI, 0.5-15.1, P =.04) in prevalence of wheeze of >1 week, but it had no effect on serum IgE, atopy, or doctors' diagnosis of asthma. The HDM avoidance intervention did not affect these outcomes but was associated with a lower use of oral steroids. Conclusion: Increasing dietary omega-3 fatty acids might have a beneficial effect on the prevalence of wheeze during the first 18 months of life. Follow-up to age 5 years, when the effect of the interventions on asthma risk will be assessed, is underway.	Childrens Hosp, Clin Epidemiol Unit, Westmead, NSW 2145, Australia; Univ Sydney, Fac Med, Sydney, NSW 2006, Australia; Univ Sydney, Dept Med, Sydney, NSW 2006, Australia; Univ Sydney, Centenary Inst Canc Med & Cell Biol, Sydney, NSW 2006, Australia; Univ Sydney, Dept Biochem, Sydney, NSW 2006, Australia; Cooperat Res Ctr Asthma, Camperdown, NSW, Australia; Univ Sydney, Woolcock Inst Med Res, Sydney, NSW 2006, Australia; Univ Sydney, Dept Child Hlth & Paediat, Sydney, NSW 2006, Australia	Mihrshahi, S (reprint author), Childrens Hosp, Clin Epidemiol Unit, Locked Bag 4001, Westmead, NSW 2145, Australia.		Mihrshahi, Seema/A-9877-2009; Tovey, Euan/G-8604-2017	Mihrshahi, Seema/0000-0001-6567-9884; Tovey, Euan/0000-0002-1802-7266			ARSHAD SH, 1992, LANCET, V339, P1493, DOI 10.1016/0140-6736(92)91260-F; Chan-Yeung M, 2000, ARCH PEDIAT ADOL MED, V154, P657; Custovic A, 2001, LANCET, V358, P188, DOI 10.1016/S0140-6736(01)05406-X; Custovic A, 2000, J ALLERGY CLIN IMMUN, V105, P252, DOI 10.1016/S0091-6749(00)90073-3; Hide DW, 1996, ALLERGY, V51, P89, DOI 10.1111/j.1398-9995.1996.tb04563.x; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Mihrshahi S, 2002, RESPIROLOGY, V7, P147, DOI 10.1046/j.1440-1843.2002.00384.x; Mihrshahi S, 2001, CONTROL CLIN TRIALS, V22, P333, DOI 10.1016/S0197-2456(01)00112-X; MIHRSHAHI S, 2003, IN PRESS ALLERGY; PEAT JK, 1992, EUR RESPIR J, V5, P921; Peat JK, 1999, J ALLERGY CLIN IMMUN, V103, P1, DOI 10.1016/S0091-6749(99)70517-8; Peat JK, 1996, AM J RESP CRIT CARE, V153, P141; Rhodes HL, 2002, AM J RESP CRIT CARE, V165, P176; Sherriff A, 2001, INT J EPIDEMIOL, V30, P1473, DOI 10.1093/ije/30.6.1473; VANASPEREN PP, 1984, J ALLERGY CLIN IMMUN, V73, P381, DOI 10.1016/0091-6749(84)90412-3; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P383, DOI 10.1111/j.1365-2133.1994.tb08530.x	16	136	142	0	3	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JAN	2003	111	1					162	168		10.1067/mai.2003.36		7	Allergy; Immunology	Allergy; Immunology	636PR	WOS:000180465500025	12532113	
J	Zock, JP; Jarvis, D; Luczynska, C; Sunyer, J; Burney, P				Zock, JP; Jarvis, D; Luczynska, C; Sunyer, J; Burney, P		European Community Resp Hlth Surv	Housing characteristics, reported mold exposure, and asthma in the European Community Respiratory Health Survey	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; housing; dampness; mold; carpeting; European Community Respiratory Health Survey	HOME DAMPNESS; DUST MITES; FUNGAL PROPAGULES; INDOOR AIR; SYMPTOMS; ADULTS; CHILDREN; (1->3)-BETA-D-GLUCAN; INFECTIONS; ALLERGENS	Background: The effects of home dampness and mold exposure on adult asthma are not clear. Objective: We aimed to investigate the associations between housing characteristics related to dampness, mold exposure, and house dust mite levels and adult asthma in 38 study centers from the European Community Respiratory Health Survey. Methods: Data about the present home, heating and ventilation systems, double glazing, floor covers, recent water damage, and mold exposure were obtained by means of an interviewer-led questionnaire. The associations between these factors and asthma, as defined on the basis of symptoms in the last year, and of bronchial responsiveness, as determined with methacholine challenge, were evaluated. Odds ratios (ORs) were obtained by using random-effects meta-analyses adjusted within study centers for sex, age group, and smoking status. Results: Fitted carpets and rugs in the bedroom were related to fewer asthma symptoms and bronchial responsiveness (OR range, 0.69-0.91). This effect was consistent across centers and more pronounced among house dust mite-sensitized individuals. Reported mold exposure in the last year was associated with asthma symptoms and bronchial responsiveness (OR range, 1.14-1.44). This effect was homogeneous among centers and stronger in subjects sensitized to Cladosporium species. In centers with a higher prevalence of asthma, the prevalence of reported indoor mold exposure was also high. This association was observed for reported mold exposure by asthmatic subjects (Spearman r(s) = 0.46), as well as reported mold exposure by nonasthmatic subjects (r(s) = 0.54). Reported mold exposure was highest in older houses with recent water damage. Conclusion: We conclude that indoor mold growth has an adverse effect on adult asthma.	Municipal Inst Med Res, Resp & Environm Hlth Res Unit, E-08003 Barcelona, Spain; Kings Coll London, Dept Publ Hlth Sci, London WC2R 2LS, England	Zock, JP (reprint author), Municipal Inst Med Res, Resp & Environm Hlth Res Unit, Dr Aiguader 80, E-08003 Barcelona, Spain.		Jarvis, Deborah/E-6494-2011; Sanchez-Ramos, Jose Luis/G-1259-2011; Sunyer, J/G-6909-2014	Sanchez-Ramos, Jose Luis/0000-0001-7187-9989; Sunyer, J/0000-0002-2602-4110; ROMANO, Canzio/0000-0001-5294-9793; Abramson, Michael/0000-0002-9954-0538; Soriano, Joan B/0000-0001-9740-2994	NCRR NIH HHS [2SO7 RR 05521-28]		ARMSTRONG BG, 1990, AM J EPIDEMIOL, V132, P1176; BJORNSSON E, 1995, CLIN EXP ALLERGY, V25, P423, DOI 10.1111/j.1365-2222.1995.tb01073.x; BRUNEKREEF B, 1992, ALLERGY, V47, P498, DOI 10.1111/j.1398-9995.1992.tb00672.x; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; Dales RE, 1997, INT J EPIDEMIOL, V26, P120, DOI 10.1093/ije/26.1.120; DALES RE, 1991, AM REV RESPIR DIS, V143, P505; Delfino RJ, 1997, ENVIRON HEALTH PERSP, V105, P622; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; Dharmage S, 2001, AM J RESP CRIT CARE, V164, P65; Douwes J, 2000, AM J RESP CRIT CARE, V162, P1348; Douwes J, 1999, J ALLERGY CLIN IMMUN, V103, P494, DOI 10.1016/S0091-6749(99)70476-8; Evans J, 2000, J EPIDEMIOL COMMUN H, V54, P677, DOI 10.1136/jech.54.9.677; Garrett MH, 1998, CLIN EXP ALLERGY, V28, P459; Gehring U, 2001, EUR RESPIR J, V18, P555, DOI 10.1183/09031936.01.00096801; Gereda JE, 2001, J ALLERGY CLIN IMMUN, V107, P790, DOI 10.1067/mai.2001.115245; Janson C, 2001, EUR RESPIR J, V18, P598, DOI 10.1183/09031936.01.00205801; Kilpelainen M, 2001, THORAX, V56, P462, DOI 10.1136/thorax.56.6.462; Koch A, 2000, ALLERGY, V55, P176, DOI 10.1034/j.1398-9995.2000.00233.x; LINTNER TJ, 1993, J ALLERGY CLIN IMMUN, V91, P862, DOI 10.1016/0091-6749(93)90343-E; Norback D, 1999, INT J TUBERC LUNG D, V3, P368; Pirhonen I, 1996, EUR RESPIR J, V9, P2618, DOI 10.1183/09031936.96.09122618; PLATT SD, 1989, BRIT MED J, V298, P1673; Ren P, 2001, ALLERGY, V56, P419, DOI 10.1034/j.1398-9995.2001.056005419.x; Roca J, 1998, EUR RESPIR J, V11, P1354, DOI 10.1183/09031936.98.11061354; Rylander R, 1997, MEDIAT INFLAMM, V6, P275, DOI 10.1080/09629359791613; VANSTRIEN RT, 1994, CLIN EXP ALLERGY, V24, P843; Verhoeff AP, 1997, ANN ALLERG ASTHMA IM, V78, P544; VERHOEFF AP, 1994, CLIN EXP ALLERGY, V24, P1061, DOI 10.1111/j.1365-2222.1994.tb02744.x; VERHOEFF AP, 1994, ALLERGY, V49, P540, DOI 10.1111/j.1398-9995.1994.tb01126.x; VERHOEFF AP, 1995, AM J EPIDEMIOL, V141, P103; Williamson IJ, 1997, THORAX, V52, P229	31	136	138	0	14	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	AUG	2002	110	2					285	292	UNSP 1/81/126383	10.1067/mai.2002.126383		8	Allergy; Immunology	Allergy; Immunology	585DY	WOS:000177509800014	12170270	
J	Koppelman, GH; Stine, OC; Xu, JF; Howard, TD; Zheng, SQL; Kauffman, HF; Bleecker, ER; Meyers, DA; Postma, DS				Koppelman, GH; Stine, OC; Xu, JF; Howard, TD; Zheng, SQL; Kauffman, HF; Bleecker, ER; Meyers, DA; Postma, DS			Genome-wide search for atopy susceptibility genes in Dutch families with asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						genetics of atopy; asthma; specific IgE; eosinophils; genoine-wide search	LINKAGE ANALYSIS; CHROMOSOME 5Q31-Q33; MITE SENSITIZATION; FOUNDER POPULATION; UNDERLYING ASTHMA; ALLERGY; MARKERS; SCREEN; LOCUS; HYPERRESPONSIVENESS	Background: Atopy is a phenotype associated with asthma that has a heritable component. However, the role of atopy-susceptibility genes in the development and expression of asthma and allergic disorders is not understood. Objective: We sought to study the familial aggregation and co-occurrence of atopic phenotypes within family members of patients with asthma and to identify chromosomal regions that may contain genes that regulate different atopic phenotypes. Methods: In 200 families (n = 1174) ascertained through a proband with asthma, genome-wide screen and linkage analysis was performed for the following atopic phenotypes: (1) specific IgE to common aeroallergens (Phadiatop assay); (2) specific IgE to Der p 1; (3) positive skin test responses to house dust mite; (4) positive skin test responses to 1 or more of 16 allergens; and (5) peripheral blood eosinophils. Results were compared with the linkage results for total serum IgE levels. Results: There was clear familial aggregation of atopy. A high total serum IgE level in combination with a positive Phadiatop result or a normal total IgE level in combination with a negative Phadiatop result was found in 56.1% of the probands and 66.9% of the offspring. Several chromosomal regions that showed evidence for linkage to an atopic phenotype (ie, 2q, 6p, 7q, and 13q) also showed evidence of linkage with total serum IgE (Xu et al. Am J Hum Genet 2000;67:1163-73). Specific regions of interest for atopic traits were also detected on chromosomes 11q, 17q, and 22q. Conclusions: Atopic phenotypes show familial aggregation, although family members may differ in expression of atopy. Specific chromosomal regions appear to be important in susceptibility to different phenotypes of atopic responsiveness.	Beatrixoord, Dept Pulm Rehabil, Haren, Netherlands; Univ Groningen Hosp, Dept Pulmonol, Groningen, Netherlands; Univ Groningen Hosp, Dept Allergol, Groningen, Netherlands; Univ Maryland, Sch Med, Dept Epidemiol & Prevent Med, Baltimore, MD 21201 USA; Wake Forest Univ, Sch Med, Ctr Human Genomics, Winston Salem, NC 27109 USA	Postma, DS (reprint author), Univ Groningen, Dept Pulmonol, POB 30-001, NL-9700 RB Groningen, Netherlands.				NCRR NIH HHS [1 P41 RR03655]; NHLBI NIH HHS [R01HL48341, R01HL66393]		Almasy L, 1998, AM J HUM GENET, V62, P1198, DOI 10.1086/301844; Amelung PJ, 1998, CLIN EXP ALLERGY, V28, P397; Barnes KC, 1996, GENOMICS, V37, P41, DOI 10.1006/geno.1996.0518; Burney PGJ, 1997, ASTHMA, P35; Clarke JR, 2000, AM J RESP CRIT CARE, V162, P2188; COOKSON WOCM, 1989, LANCET, V1, P1292; Daniels SE, 1996, NATURE, V383, P247, DOI 10.1038/383247a0; Dizier MH, 2000, AM J RESP CRIT CARE, V162, P1812; Fryer AA, 2000, GENES IMMUN, V1, P509, DOI 10.1038/sj.gene.6363717; Kay AB, 2001, NEW ENGL J MED, V344, P30; Kjellman NIM, 1999, PEDIATR ALLERGY IMMU, V10, P11; Kong A, 1997, AM J HUM GENET, V61, P1179, DOI 10.1086/301592; KOPPELMAN GH, 2000, ASTHMA, P146; Kruglyak L, 1996, AM J HUM GENET, V58, P1347; Kurz T, 2000, J ALLERGY CLIN IMMUN, V106, P925, DOI 10.1067/mai.2000.110557; Laitinen T, 2001, NAT GENET, V28, P87, DOI 10.1038/ng0501-87; LANDER E, 1995, NAT GENET, V11, P241, DOI 10.1038/ng1195-241; Lee YA, 2000, NAT GENET, V26, P470, DOI 10.1038/82625; MARSHALL E, 1994, SCIENCE, V264, P1524, DOI 10.1126/science.8202702; Martinez FD, 1998, AM J RESP CRIT CARE, V158, P1739; Nickel RG, 2000, J IMMUNOL, V164, P1612; Noguchi E, 1997, AM J RESP CRIT CARE, V156, P1390; Ober C, 2000, AM J HUM GENET, V67, P1154, DOI 10.1016/S0002-9297(07)62946-2; Palmer LJ, 2000, AM J RESP CRIT CARE, V161, P1836; Panhuysen CIM, 1998, AM J RESP CRIT CARE, V157, P1734; POSTMA DS, 1995, NEW ENGL J MED, V333, P894, DOI 10.1056/NEJM199510053331402; Strauch K, 2000, AM J HUM GENET, V66, P1945, DOI 10.1086/302911; VANCAMP G, 1997, TRENDS GENET, V13, P82; Wilkinson J, 1998, GENOMICS, V53, P251, DOI 10.1006/geno.1998.5485; Wjst M, 1999, GENOMICS, V58, P1, DOI 10.1006/geno.1999.5806; Woolcock AJ, 1997, CIBA F SYMP, V206, P122; Xu JF, 2001, AM J HUM GENET, V68, P1437, DOI 10.1086/320589; Xu JF, 2000, AM J HUM GENET, V67, P1163, DOI 10.1086/321190; Yokouchi Y, 2000, GENOMICS, V66, P152, DOI 10.1006/geno.2000.6201	34	136	143	1	2	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	MAR	2002	109	3					498	506		10.1067/mai.2002.122235		9	Allergy; Immunology	Allergy; Immunology	534KW	WOS:000174586400018	11897998	
J	Haby, MM; Peat, JK; Marks, GB; Woolcock, AJ; Leeder, SR				Haby, MM; Peat, JK; Marks, GB; Woolcock, AJ; Leeder, SR			Asthma in preschool children: prevalence and risk factors	THORAX			English	Article						asthma; prevalence; risk factors; preschool children	HOUSE-DUST MITE; CHILDHOOD ASTHMA; ATOPIC DISEASE; ALLERGEN AVOIDANCE; FAMILY-SIZE; HAY-FEVER; ASSOCIATION; AGE; SENSITIVITY; SEVERITY	Background-The prevalence of asthma in children has increased in many countries over recent years. To plan effective interventions to reverse this trend we need a better understanding of the risk factors for asthma in early life. This study was undertaken to measure the prevalence of, and risk factors for, asthma in preschool children. Methods-Parents of children aged 3-5 years living in two cities (Lismore, n=383; Wagga Wagga, n=591) in New South Wales, Australia were surveyed by questionnaire to ascertain the presence of asthma and various proposed risk factors for asthma in their children. Recent asthma was defined as ever having been diagnosed with asthma and having cough or wheeze in the last 12 months and having used an asthma medication in the last 12 months. Atopy was measured by skin prick tests to six common allergens. Results-The prevalence of recent asthma was 22% in Lismore and 18% in Wagga Wagga. Factors which increased the risk of recent asthma were: atopy (odds ratio (OR) 2.35, 95% CI 1.49 to 3.72), having a parent with a history of asthma (OR 2.05, 95% CI 1.34 to 3.16), having had a serious respiratory infection in the first 2 years of life (OR 1.93, 95% CI 1.25 to 2.99), and a high dietary intake of polyunsaturated fats (OR 2.03, 95% CI 1.15 to 3.60). Breast feeding (OR 0.41, 95% CI 0.22 to 0.74) and having three or more older siblings (OR 0.16, 95% CI 0.04 to 0.71) decreased the risk of recent asthma. Conclusions-Of the factors tested, those that have the greatest potential to be modified to reduce the risk of asthma are breast feeding and consumption of polyunsaturated fats.	Royal Childrens Hosp, Ctr Community Child Hlth, Parkville, Vic 3052, Australia; Univ Sydney, Dept Paediat & Child Hlth, Sydney, NSW 2006, Australia; Univ Sydney, Inst Resp Med, Sydney, NSW 2006, Australia; Univ Sydney, Fac Med, Sydney, NSW 2006, Australia	Haby, MM (reprint author), Royal Childrens Hosp, Ctr Community Child Hlth, Flemington Rd, Parkville, Vic 3052, Australia.						Altman DG, 1992, PRACTICAL STAT MED R; Armitage P., 1994, STAT METHODS MED RES; *AUSTR BUR STAT, 1991, 43640 AUSTR BUR STAT; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Black PN, 1997, EUR RESPIR J, V10, P6, DOI 10.1183/09031936.97.10010006; CHINN S, 1991, THORAX, V46, P454, DOI 10.1136/thx.46.6.454; Haby MM, 2000, PEDIATR PULM, V30, P377, DOI 10.1002/1099-0496(200011)30:5<377::AID-PPUL3>3.0.CO;2-3; Hide DW, 1996, ALLERGY, V51, P89, DOI 10.1111/j.1398-9995.1996.tb04563.x; HODGE L, 1994, AUST NZ J MED, V24, P727, DOI 10.1111/j.1445-5994.1994.tb01793.x; Jarvis D, 1997, CLIN EXP ALLERGY, V27, P240; KIRSHNER B, 1990, J CLIN EPIDEMIOL, V43, P765, DOI 10.1016/0895-4356(90)90236-I; Kleinbaum D, 1982, EPIDEMIOLOGICAL RES; LEWIS S, 1995, EUR RESPIR J, V8, P349, DOI 10.1183/09031936.95.08030349; LUCAS A, 1990, BRIT MED J, V300, P837; LUYT DK, 1993, BRIT MED J, V306, P1386; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; MARTINEZ FD, 1994, THORAX, V49, P1189, DOI 10.1136/thx.49.12.1189; MERRETT TG, 1988, ANN ALLERGY, V61, P13; Moffatt MF, 1998, CLIN EXP ALLERGY, V28, P56; Oddy WH, 1999, BRIT MED J, V319, P815; PEAT JK, 1994, AUST NZ J MED, V24, P270, DOI 10.1111/j.1445-5994.1994.tb02171.x; PEAT JK, 1994, BRIT MED J, V308, P1591; PEAT JK, 1991, CLIN EXP ALLERGY, V21, P573, DOI 10.1111/j.1365-2222.1991.tb00849.x; PEAT JK, 1995, MED J AUSTRALIA, V163, P22; Pepys J., 1975, BRIT J HOSP MED, V14, P412; Ponsonby AL, 1998, ARCH DIS CHILD, V79, P328; ROBERTSON CF, 1991, BRIT MED J, V302, P116; Rona RJ, 1997, J ALLERGY CLIN IMMUN, V99, P454, DOI 10.1016/S0091-6749(97)70070-8; SCHWARTZ J, 1990, AM REV RESPIR DIS, V142, P555; SEARS MR, 1989, CLIN EXP ALLERGY, V19, P419, DOI 10.1111/j.1365-2222.1989.tb02408.x; STRACHAN DP, 1989, BRIT MED J, V299, P1259; VONMUTIUS E, 1994, BRIT MED J, V308, P692; WRIGHT AL, 1995, ARCH PEDIAT ADOL MED, V149, P758; ZEIGER RS, 1989, J ALLERGY CLIN IMMUN, V84, P72, DOI 10.1016/0091-6749(89)90181-4	34	136	139	3	9	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	AUG	2001	56	8					589	595		10.1136/thorax.56.8.589		7	Respiratory System	Respiratory System	456XF	WOS:000170107500003	11462059	
J	Marrie, TJ				Marrie, TJ			Community-acquired pneumonia in the elderly	CLINICAL INFECTIOUS DISEASES			English	Review							RESISTANT STREPTOCOCCUS-PNEUMONIAE; INITIAL ANTIMICROBIAL THERAPY; RESPIRATORY-TRACT INFECTIONS; NURSING-HOME RESIDENTS; TERM-CARE FACILITIES; RISK-FACTORS; HOSPITALIZED-PATIENTS; PENICILLIN-RESISTANT; RANDOMIZED TRIAL; REQUIRING HOSPITALIZATION	Pneumonia in the elderly is a common and serious problem with a clinical presentation that can differ from that in younger patients. Older patients with pneumonia complain of significantly fewer symptoms than do younger patients, and delirium commonly occurs. Indeed, delirium may be the only manifestation of pneumonia in this group of patients. Alcoholism, asthma, immunosuppression, and age >70 years are risk factors for community-acquired pneumonia in the elderly. Among nursing home residents, the following are risk factors for pneumonia: advanced age, male sex, difficulty in swallowing, inability to take oral medications, profound disability, bedridden state, and urinary incontinence. Streptococcus pneumoniae is the most common cause of pneumonia among the elderly Aspiration pneumonia is underdiagnosed in this group of patients, and tuberculosis always should be considered. In this population an etiologic diagnosis is rarely available when antimicrobial therapy must be instituted. Use of the guidelines for treatment of pneumonia issued by the Infectious Diseases Society of America, with modification for treatment in the nursing home setting, is recommended.	Univ Alberta, Dept Med, Edmonton, AB, Canada	Marrie, TJ (reprint author), 2F130 WMC,8440 112 St, Edmonton, AB T6G 2B7, Canada.						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Infect. Dis.	OCT	2000	31	4					1066	1078		10.1086/318124		13	Immunology; Infectious Diseases; Microbiology	Immunology; Infectious Diseases; Microbiology	375EU	WOS:000165387200031	11049791	
J	Ostrom, QT; Bauchet, L; Davis, FG; Deltour, I; Fisher, JL; Langer, CE; Pekmezci, M; Schwartzbaum, JA; Turner, MC; Walsh, KM; Wrensch, MR; Barnholtz-Sloan, JS				Ostrom, Quinn T.; Bauchet, Luc; Davis, Faith G.; Deltour, Isabelle; Fisher, James L.; Langer, Chelsea Eastman; Pekmezci, Melike; Schwartzbaum, Judith A.; Turner, Michelle C.; Walsh, Kyle M.; Wrensch, Margaret R.; Barnholtz-Sloan, Jill S.			The epidemiology of glioma in adults: a "state of the science" review	NEURO-ONCOLOGY			English	Article						brain tumors; epidemiology; genome-wide association studies; glioma; risk factors	CENTRAL-NERVOUS-SYSTEM; UPPER MIDWEST HEALTH; MAGNETIC-FIELD EXPOSURE; HIGH-GRADE GLIOMA; MOBILE PHONE USE; SINGLE-NUCLEOTIDE POLYMORPHISMS; INTEGRATED GENOMIC ANALYSIS; CHILDHOOD-CANCER SURVIVOR; OCCUPATIONAL RISK-FACTORS; POPULATION-BASED ANALYSIS	Gliomas are the most common primary intracranial tumor, representing 81% of malignant brain tumors. Although relatively rare, they cause significant mortality and morbidity. Glioblastoma, the most common glioma histology (similar to 45% of all gliomas), has a 5-year relative survival of similar to 5%. A small portion of these tumors are caused by Mendelian disorders, including neurofibromatosis, tuberous sclerosis, and Li-Fraumeni syndrome. Genomic analyses of glioma have also produced new evidence about risk and prognosis. Recently discovered biomarkers that indicate improved survival include O-6-methylguanine-DNA methyltransferase methylation, isocitrate dehydrogenase mutation, and a glioma cytosine-phosphate-guanine island methylator phenotype. Genome-wide association studies have identified heritable risk alleles within 7 genes that are associated with increased risk of glioma. Many risk factors have been examined as potential contributors to glioma risk. Most significantly, these include an increase in risk by exposure to ionizing radiation and a decrease in risk by history of allergies or atopic disease(s). The potential influence of occupational exposures and cellular phones has also been examined, with inconclusive results. We provide a "state of the science" review of current research into causes and risk factors for gliomas in adults.	[Ostrom, Quinn T.; Barnholtz-Sloan, Jill S.] Case Western Reserve Univ, Case Comprehens Canc Ctr, Sch Med, Cleveland, OH 44106 USA; [Bauchet, Luc] CHU Montpellier, Montpellier 5, France; [Bauchet, Luc] INSERM, Montpellier 5, France; [Davis, Faith G.] Univ Alberta, Sch Publ Hlth, Edmonton Clin Hlth Acad 3 300, Edmonton, AB, Canada; [Deltour, Isabelle] Int Agcy Res Canc, F-69372 Lyon 8, France; [Fisher, James L.] Ohio State Univ, James Canc Hosp, Columbus, OH 43210 USA; [Fisher, James L.] Ohio State Univ, Solove Res Inst, Columbus, OH 43210 USA; [Langer, Chelsea Eastman; Turner, Michelle C.] Ctr Res Environm Epidemiol, Barcelona, Spain; [Langer, Chelsea Eastman; Turner, Michelle C.] Univ Pompeu Fabra, Barcelona, Spain; [Langer, Chelsea Eastman; Turner, Michelle C.] CIBER Epidemiol & Salud Publ, Barcelona, Spain; [Pekmezci, Melike] Univ Calif San Francisco, Sch Med, Dept Pathol, San Francisco, CA 94143 USA; [Schwartzbaum, Judith A.] Ohio State Univ, Coll Publ Hlth, Dept Epidemiol, Columbus, OH 43210 USA; [Turner, Michelle C.] Univ Ottawa, Inst Populat Hlth, McLaughlin Ctr Populat Hlth Risk Assessment, Ottawa, ON, Canada; [Walsh, Kyle M.; Wrensch, Margaret R.] Univ Calif San Francisco, Sch Med, Dept Neurol Surg, San Francisco, CA USA	Barnholtz-Sloan, JS (reprint author), Case Western Reserve Univ, Case Comprehens Canc Ctr, Sch Med, 11100 Euclid Ave,Wearn 152, Cleveland, OH 44106 USA.	jsb42@case.edu	Fisher, James/F-4996-2012; Schwartzbaum, Judith/A-9022-2016		NCI NIH HHS [P50 CA097257, P30 CA043703]		Amirian E, 2010, NEURO-ONCOLOGY, V12, P444, DOI 10.1093/neuonc/nop057; Amirian ES, 2013, CANCER EPIDEMIOL, V37, P908, DOI 10.1016/j.canep.2013.08.004; Arita H, 2013, ACTA NEUROPATHOL, V126, P267, DOI 10.1007/s00401-013-1141-6; Arora RS, 2010, EUR J CANCER, V46, P1607, DOI 10.1016/j.ejca.2010.02.007; Arora RS, 2009, NEURO-ONCOLOGY, V11, P403, DOI 10.1215/15228517-2008-097; Arrigo RT, 2012, J NEURO-ONCOL, V106, P627, DOI 10.1007/s11060-011-0702-6; Baan R, 2011, LANCET ONCOL, V12, P624, DOI 10.1016/S1470-2045(11)70147-4; 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J	Tatham, AS; Shewry, PR				Tatham, A. S.; Shewry, P. R.			Allergens in wheat and related cereals	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review						allergy; cereals; wheat	EXERCISE-INDUCED ANAPHYLAXIS; ALPHA-AMYLASE-INHIBITOR; LIPID TRANSFER PROTEIN; CONTROLLED FOOD CHALLENGE; IGE-BINDING EPITOPE; ASPERGILLUS-DERIVED ENZYMES; BAKERS ASTHMA DISEASE; LOW-MOLECULAR-WEIGHT; MAJOR ALLERGEN; OMEGA-5 GLIADIN	Wheat is one of the major crops grown, processed and consumed by humankind and is associated with both intolerances (notably coeliac disease) and allergies. Two types of allergy are particularly well characterized. The first is bakers' asthma, which results from the inhalation of flour and dust during grain processing. Although a number of wheat proteins have been shown to bind IgE from patients with bakers' asthma, there is no doubt a well-characterized group of inhibitors of alpha-amylase (also called chloroform methanol soluble, or CM, proteins) are the major components responsible for this syndrome. The second well-characterized form of allergy to wheat proteins is wheat-dependent exercise-induced anaphylaxis (WDEIA), with the omega(5)-gliadins (part of the gluten protein fraction) being the major group of proteins which are responsible. Other forms of food allergy have also been reported, with the proteins responsible including gluten proteins, CM proteins and non-specific lipid transfer proteins. Processing of wheat and of related cereals (barley and rye, which may contain related allergens) may lead to decreased allergenicity while genetic engineering technology offers opportunities to eliminate allergens by suppressing gene expression.	[Tatham, A. 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Exp. Allergy	NOV	2008	38	11					1712	1726		10.1111/j.1365-2222.2008.03101.x		15	Allergy; Immunology	Allergy; Immunology	364KH	WOS:000260334100005	18823308	
J	Mosen, DM; Schatz, M; Magid, DJ; Carnargo, CA				Mosen, David M.; Schatz, Michael; Magid, David J.; Carnargo, Carlos A., Jr.			The relationship between obesity and asthma severity and control in adults	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; quality of life; obesity; hospitalization; inhaled; corticosleroids	BODY-MASS INDEX; QUALITY-OF-LIFE; HEALTH-CARE UTILIZATION; WEIGHT-REDUCTION; ASSOCIATION; PREVALENCE; OVERWEIGHT; TRENDS; WOMEN	Background: The association of obesity with asthma outcomes is not well understood. Objective: The objective of this study was to examine the association of obesity, as represented by a body mass index (BMI) of greater than 30 kg/m(2), with quality-of-life scores, asthma control problems, and asthma-related hospitalizations. Methods: The study followed a cross-sectional design. Questionnaires were completed at home by a random sample of 1113 members of a large integrated health care organization who were 35 years of age or older with health care use suggestive of active asthma. Outcomes included the mini-Asthma Quality of Life Questionnaire, the Asthma Therapy Assessment Questionnaire, and self-reported asthma-related hospitalization. Several other factors known to influence asthma outcomes also were collected: demographics, smoking status, oral corticosteroid use in the past month, evidence of gastroesophageal reflux disease, and inhaled corticosteroid use in the past month. Multiple logistic regression models were used to measure the association of BMI status with outcomes. Results: Even after adjusting for demographics, smoking status, oral corticosteroid use, evidence of gastroesophageal reflux disease, and inhaled corticosteroid use, obese adults were more likely than those with normal BMIs (<25 k g/m(2)) to report poor asthma-specific quality of life (odds ratio [OR], 2.8; 95% Cl, 1.6-4.9), poor asthma control (OR, 2.7; 95% Cl, 1.7-4.3), and a history of asthma-related hospitalizations (OR, 4.6; 95% Cl, 1.4-14.4). Conclusions: Our findings suggest that obesity is associated with worse asthma outcomes, especially an increased risk of asthma related hospitalizations.	[Schatz, Michael] Kaiser Permanente, Dept Allergy, San Diego, CA USA; [Magid, David J.] Kaiser Permanente, Clin Res Unit, Denver, CO USA; [Carnargo, Carlos A., Jr.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA; [Mosen, David M.] Kaiser Permanente, Ctr Hlth Res, Portland, OR USA	Mosen, DM (reprint author), Kaiser Permanente NW, Ctr Hlth Res, 3800 N Interstate Ave, Portland, OR USA.	david.m.mosen@kpchr.org			National Institutes of Health; Research Foundations; AstraZeneca; Critical Therapeutics; GlaxoSmithKline; Merck; Novartis; Respironics	M. Schatz has consulting arrangements with GlaxoSmithKline and has received research support from GlaxoSmithKline and Merck. C. A. Camargo has consulting arrangements with AstraZeneca, Novartis, and Critical Therapeutics; is on the advisory board for Dey, Genentech. GlaxoSmithKline. Merck, Novartis, and Schering-Plough: is on the speakers bureau for AstraZeneca, GlaxoSmithKline, and Merck: and has received research support from the National Institutes of Health, Research Foundations. AstraZeneca. Critical Therapeutics. GlaxoSmithKline. Merck. Novartis. and Respironics. The rest of the authors have declared that they have no conflict of interest.	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Allergy Clin. Immunol.	SEP	2008	122	3					507	511		10.1016/j.jaci.2008.06.024		5	Allergy; Immunology	Allergy; Immunology	348TW	WOS:000259234000010	18774387	
J	Shea, KM; Truckner, RT; Weber, RW; Peden, DB				Shea, Katherine M.; Truckner, Robert T.; Weber, Richard W.; Peden, David B.			Climate change and allergic disease	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						climate change; global warming; pollen; air pollution; ozone; allergic rhinitis; asthma; mitigation; adaptation; prevention	RAGWEED AMBROSIA-ARTEMISIIFOLIA; PARTICULATE AIR-POLLUTION; ELEVATED ATMOSPHERIC CO2; DIESEL EXHAUST PARTICLES; ASTHMATIC-CHILDREN; MEXICO-CITY; NITROGEN-DIOXIDE; CHILDHOOD ASTHMA; OZONE EXPOSURE; AMBIENT OZONE	Climate change is potentially the largest global threat to human health ever encountered. The earth is warming, the warming is accelerating, and human actions are largely responsible. If current emissions and land use trends continue unchecked, the next generations will face more injury, disease, and death related to natural disasters and heat waves, higher rates of climate-related infections, and wide-spread malnutrition, as well as more allergic and air pollution-related morbidity and mortality. This review highlights links between global climate change and anticipated increases in prevalence and severity of asthma and related allergic disease mediated through worsening ambient air pollution and altered local and regional pollen production. The pattern of change will vary regionally depending on latitude, altitude, rainfall and storms, land-use patterns, urbanization, transportation, and energy production. The magnitude of climate change and related increases in allergic disease will be affected by how aggressively greenhouse gas mitigation strategies are pursued, but at best an average warming of I to 2 degrees C is certain this century. Thus, anticipation of a higher allergic disease burden will affect clinical practice as well as public health planning. A number of practical primary and secondary prevention strategies are suggested at the end of the review to assist in meeting this unprecedented public health challenge.	[Shea, Katherine M.] Univ N Carolina, Inst Environm, Sch Publ Hlth, Dept Mat & Child Health, Chapel Hill, NC 27599 USA; [Peden, David B.] Univ N Carolina, Dept Pediat, Chapel Hill, NC 27599 USA; [Truckner, Robert T.] US Environm Protect Agcy, Natl Hlth & Environm Effects Lab, NHEERL Human Res Protocol Off, Res Triangle Pk, NC USA; [Weber, Richard W.] Univ Colorado, Natl Jewish Med & Res Ctr, Dept Med, Hlth Sci Ctr, Boulder, CO 80309 USA	Shea, KM (reprint author), Univ N Carolina, Inst Environm, Sch Publ Hlth, Dept Mat & Child Health, 111 Miller Hall,Campus Box 1105, Chapel Hill, NC 27599 USA.	kshea@email.unc.edu	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			*AQI, 2007, AQI ED TOOLK WEATH; Aw J, 2003, J GEOPHYS RES-ATMOS, V108, DOI 10.1029/2002JD002688; Barck C, 2005, ENVIRON RES, V97, P58, DOI 10.1016/j.envres.2004.02.009; BARNES PJ, 1994, POSTGRAD MED J, V70, P319; Bates DV, 2005, EPIDEMIOLOGY, V16, P427, DOI 10.1097/01.ede.0000165793.71278.ec; Beggs PJ, 2004, CLIN EXP ALLERGY, V34, P1507, DOI 10.1111/j.1365-2222.2004.02061.x; 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Allergy Clin. Immunol.	SEP	2008	122	3					443	453		10.1016/j.jaci.2008.06.032		11	Allergy; Immunology	Allergy; Immunology	348TW	WOS:000259234000001	18774380	
J	Soar, J; Pumphrey, R; Cant, A; Clarke, S; Corbett, A; Dawson, P; Ewan, P; Foex, B; Gabbott, D; Griffiths, M; Hall, J; Harper, N; Jewkes, F; Maconochie, I; Mitchell, S; Nasser, S; Nolan, J; Rylance, G; Sheikh, A; Unsworth, DJ; Warrell, D				Soar, Jasmeet; Pumphrey, Richard; Cant, Andrew; Clarke, Sue; Corbett, Allison; Dawson, Peter; Ewan, Pamela; Foex, Bernard; Gabbott, David; Griffiths, Matt; Hall, Judith; Harper, Nigel; Jewkes, Fiona; Maconochie, Ian; Mitchell, Sarah; Nasser, Shuaib; Nolan, Jerry; Rylance, George; Sheikh, Aziz; Unsworth, David Joseph; Warrell, David		Working Grp Resuscitat Council UK	Emergency treatment of anaphylactic reactions - Guidelines for healthcare providers	RESUSCITATION			English	Article						anaphylactic reactions; treatment	RESUSCITATION-COUNCIL GUIDELINES; EPINEPHRINE ABSORPTION; ALLERGIC REACTIONS; LIFE-SUPPORT; MANAGEMENT; CHILDREN; SHOCK; ADRENALINE; EPIDEMIOLOGY; VASOPRESSIN	The UK incidence of anaphylactic reactions is increasing. Patients who have an anaphylactic reaction have life-threatening airway and, or breathing and, or circulation problems usually associated with skin or mucosal changes. Patients having an anaphylactic reaction should be treated using the Airway, Breathing, Circulation, Disability, Exposure (ABCDE) approach. Anaphylactic reactions are not easy to study with randomised controlled trials. There are, however, systematic reviews of the available evidence and a wealth of clinical experience to help formulate guidelines. The exact treatment will depend on the patient's location, the equipment and drugs available, and the skills of those treating the anaphylactic reaction. Early treatment with intramuscular adrenaline is the treatment of choice for patients having an anaphylactic reaction. Despite previous guidelines, there is still confusion about the indications, dose and route of adrenaline. Intravenous adrenaline must only be used in certain specialist settings and only by those skilled and experienced in its use. All those who are suspected of having had an anaphylactic reaction should be referred to a specialist in allergy. Individuals who are at high risk of an anaphylactic reaction should carry an adrenaline auto-injector and receive training and support in its use. There is a need for further research about the diagnosis, treatment and prevention of anaphylactic reactions. (C) 2008 Resuscitation Council (UK). Published by Elsevier Ireland Ltd.	[Soar, Jasmeet; Unsworth, David Joseph] Southmead Gen Hosp, N Bristol NHS Trust, Bristol BS10 5NB, Avon, England; [Pumphrey, Richard] Cent Manchester & Manchester Childrens Hosp, Manchester M13 9WL, Lancs, England; [Cant, Andrew] Newcastle Gen Hosp, Newcastle Upon Tyne NE4 6BE, Tyne & Wear, England; [Clarke, Sue] Community Hlth Clin, Royston SG8 6HH, Herts, England; [Corbett, Allison] Royal Pharmaceut Soc GB, British Natl Formulary, London SE1 7JN, England; [Ewan, Pamela] Univ Cambridge, NHS Fdn Trust, Cambridge CB2 0QQ, England; [Foex, Bernard] Manchester Royal Infirm, Manchester M13 9WL, Lancs, England; [Gabbott, David] Gloucestershire Royal Hosp, Gloucester GL1 3NN, England; [Griffiths, Matt] Royal Coll Nursing UK, London W1G 0RN, England; [Hall, Judith] Cardiff Univ, Dept Anaesthet & Intens Care Med, Cardiff CF14 4XN, S Glam, Wales; [Harper, Nigel] Manchester Royal Infirm, Anaesthet React Clin, Manchester M13 9WL, Lancs, England; [Jewkes, Fiona] Ambulance Serv Assoc, London SE1 8RT, England; [Maconochie, Ian] St Marys Hosp NHS Trust, London W2 1NY, England; [Nasser, Shuaib] Univ Cambridge, NHS Fdn Trust, Cambridge CB2 0QQ, England; [Nolan, Jerry] Royal United Hosp, Bath BA1 3NG, Avon, England; [Rylance, George] Royal Victoria Infirm, Newcastle Upon Tyne NE1 4LP, Tyne & Wear, England; [Sheikh, Aziz] Univ Edinburgh, Gen Practice Sect Div Community Hlth Sci, Edinburgh EH8 9DX, Midlothian, Scotland; [Warrell, David] John Radcliffe Hosp, Oxford OX3 9DU, England	Soar, J (reprint author), Southmead Gen Hosp, N Bristol NHS Trust, Bristol BS10 5NB, Avon, England.	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J	Samet, J; Krewski, D				Samet, Jonathan; Krewski, Daniel			Health effects associated with exposure to ambient air pollution	JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES			English	Article; Proceedings Paper	Conference on Strategies for Clean Air and Health	NOV 05-07, 2003	Rome, ITALY	NERAM			LONG-TERM EXPOSURE; AMERICAN-CANCER-SOCIETY; ALL-CAUSE MORTALITY; HARVARD 6 CITIES; PARTICULATE MATTER; TIME-SERIES; RESPIRATORY-DISEASES; CANADIAN CITIES; CASE-CROSSOVER; ASTHMA HOSPITALIZATION	The World Health Organization has identified ambient air pollution as a high public health priority, based on estimates of air pollution related death and disability-adjusted life years derived in its Global Burden of Disease initiative. The NERAM Colloquium Series on Health and Air Quality was initiated to strengthen the linkage between scientists, policymakers, and other stakeholders by reviewing the current state of science, identifying policy-relevant gaps and uncertainties in the scientific evidence, and proposing a path forward for research and policy to improve air quality and public health. The objective of this paper is to review the current state of science addressing the impacts of air pollution on human health. The paper is one of four background papers prepared for the 2003 NERAM/AirNet Conference on Strategies for Clean Air and Health, the third meeting in the international Colloquium Series. The review is based on the framework and findings of the U. S. National Research Committee (NRC) on Research Priorities for Airborne Particulate Matter and addresses key questions underlying air quality risk management policy decisions.	Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA; Univ Ottawa, McLaughlin Ctr Populat Hlth Risk Assessment, Ottawa, ON K1N 6N5, Canada	Samet, J (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, 615 N Wolfe St,Suite W6041, Baltimore, MD 21205 USA.	jsamet@jhsph.edu					Abbey DE, 1999, AM J RESP CRIT CARE, V159, P373; Anderson HR, 2003, EUR RESPIR J, V21, p39S, DOI 10.1183/09031936.03.00402203; Atkinson RW, 2001, AM J RESP CRIT CARE, V164, P1860; Brook RD, 2002, CIRCULATION, V105, P1534, DOI 10.1161/01.CIR.0000013838.94747.64; Brunekreef B, 2003, J TOXICOL ENV HEAL A, V66, P1723, DOI 10.1080/15287390390211720; BURNETT RT, 1995, AM J EPIDEMIOL, V142, P15; Burnett RT, 1999, ARCH ENVIRON HEALTH, V54, P130; Burnett RT, 1997, ENVIRON RES, V72, P24, DOI 10.1006/enrs.1996.3685; Burnett RT, 1997, EPIDEMIOLOGY, V8, P162, DOI 10.1097/00001648-199703000-00007; Burnett RT, 2001, AM J EPIDEMIOL, V153, P444, DOI 10.1093/aje/153.5.444; Burnett RT, 2000, INHAL TOXICOL, V12, P15, DOI 10.1080/089583700750019495; Cakmak S, 2003, J TOXICOL ENV HEAL A, V66, P1811, DOI 10.1080/15287390390212053; Calderon-Garciduenas L, 2003, PEDIATR PULM, V36, P148, DOI 10.1002/ppul.10338; *CAN WID STAND DEV, 1999, COMP BEN INF; Chang LT, 2003, J TOXICOL ENV HEAL A, V66, P1825, DOI 10.1080/15287390390212099; Clancy L, 2002, LANCET, V360, P1210, DOI 10.1016/S0140-6736(02)11281-5; Cohen A. 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Toxicol. Env. Health Part A	FEB 1	2007	70	3-4					227	242		10.1080/15287390600884644		16	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	141FC	WOS:000244562800007	17365585	
J	Zimmermann, G				Zimmermann, Gisbert			Review on safety of the entomopathogenic fungus Metarhizium anisopliae	BIOCONTROL SCIENCE AND TECHNOLOGY			English	Review						Metarhizium anisopliae; occurrence; host range; toxins; environmental fate; safety; side-effects	VAR. ACRIDUM DEUTEROMYCOTINA; GROUND-DWELLING ARTHROPODS; BEETLE MELIGETHES-AENEUS; INSECT PATHOGENIC FUNGI; MYCOTOXIN DESTRUXIN-E; LEGUME FLOWER THRIPS; VIRUS-LIKE PARTICLES; BEAUVERIA-BASSIANA; ENTOMOGENOUS FUNGI; METARRHIZIUM-ANISOPLIAE	The entomopathogenic fungus Metarhizium anisopliae (Metschn.) Sorokin is widely used for biocontrol of pest insects, and many commercial products are on the market or under development. The aim of this review is to summarise all relevant safety data of this fungus, which are necessary for the commercialisation and registration process. The review contains the following sections: (1) identity, (2) biological properties (history, natural occurrence and geographical distribution, host range, mode of action, production of metabolites/toxins, effect of environmental factors), (3) methods to determine and quantify residues, (4) fate and behaviour in the environment (mobility and persistence in air, water and soil), (5) effects on non-target organisms (microorganisms, plants, soil organisms, aquatic organisms, predators, parasitoids, honey bees, earth worms, etc.), (6) effects on vertebrates (fish, amphibia, reptiles, and birds), and (7) effects on mammals and human health (allergy, pathogenicity/toxicity). On the basis of the presented knowledge, M. anisopliae is considered to be safe with minimal risks to vertebrates, humans and the environment.	Inst Biol Control, Fed Biol Res Ctr Agr & Forestry, D-64287 Darmstadt, Germany	Zimmermann, G (reprint author), Inst Biol Control, Fed Biol Res Ctr Agr & Forestry, Heinrichstr 243, D-64287 Darmstadt, Germany.	gisbert.zimmermanng@gmx.net					Alves RT, 1998, CROP PROT, V17, P675, DOI 10.1016/S0261-2194(98)00074-X; Alves SB, 1996, J APPL ENTOMOL, V120, P559; ALVES SB, 1984, J APPL ENTOMOL, V97, P127; Amiri B, 1999, BIOCONTROL SCI TECHN, V9, P487, DOI 10.1080/09583159929451; Amiri-Besheli B, 2000, MYCOL RES, V104, P447, DOI 10.1017/S095375629900146X; Arthurs S, 2003, BIOL CONTROL, V26, P333, DOI 10.1016/S1049-9644(02)00166-4; Asensio L., 2003, Spanish Journal of Agricultural Research, V1, P37; Peveling R., 1999, IOBC WPRS B, V22, P2; Austwick PKC., 1980, ECOLOGICAL B STOCKHO, V31, P91; BAATH E, 1991, MYCOL RES, V95, P1140; Barbieri RT, 2005, J INVEST ALLERG CLIN, V15, P131; Barker CW, 1998, NEW ZEAL J ECOL, V22, P189; BATEMAN RP, 1993, ANN APPL BIOL, V122, P145, DOI 10.1111/j.1744-7348.1993.tb04022.x; BEILHARZ VC, 1982, T BRIT MYCOL SOC, V79, P507; BIDOCHKA MJ, 1994, CURR GENET, V25, P107, DOI 10.1007/BF00309534; Bidochka MJ, 2000, MYCOL RES, V104, P1094, DOI 10.1017/S0953756299002403; Bidochka MJ, 1998, CAN J BOT, V76, P1198; BIDOCHKA MJ, 2005, INSECT FUNGAL ASS, P3; Bischoff JF, 2006, MYCOLOGIA, V98, P737, DOI 10.3852/mycologia.98.5.737; Bogo MR, 1996, MYCOL RES, V100, P1468; BOUCIAS DG, 1998, PRINCIPLES INSECT PA, P568; Braga GUL, 2001, J INVERTEBR PATHOL, V78, P98, DOI 10.1006/jipa.2001.5048; Braga GUL, 2001, MYCOL RES, V105, P874, DOI 10.1017/S0953756201004270; Braga GUL, 2001, PHOTOCHEM PHOTOBIOL, V74, P734, DOI 10.1562/0031-8655(2001)074<0734:BSUAUR>2.0.CO;2; Broza M, 2001, PEDOBIOLOGIA, V45, P523, DOI 10.1078/0031-4056-00104; BUCHWALDT L, 1992, PLANT PATHOL, V41, P55, DOI 10.1111/j.1365-3059.1992.tb02316.x; BUDAVARI S, 1996, MERCK INDEX, P472; Burges HD, 1981, MICROBIAL CONTROL PE, P737; Burgner D, 1998, J CLIN MICROBIOL, V36, P1146; Butt T. 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Technol.		2007	17	9-10					879	920		10.1080/09583150701593963		42	Biotechnology & Applied Microbiology; Entomology	Biotechnology & Applied Microbiology; Entomology	249ST	WOS:000252250700001		
J	Montagnoli, C; Fallarino, F; Gaziano, R; Bozza, S; Bellocchio, S; Zelante, T; Kurup, WP; Pitzurra, L; Puccetti, P; Romani, L				Montagnoli, C; Fallarino, F; Gaziano, R; Bozza, S; Bellocchio, S; Zelante, T; Kurup, WP; Pitzurra, L; Puccetti, P; Romani, L			Immunity and tolerance to Aspergillus involve functionally distinct regulatory T cells and tryptophan catabolism	JOURNAL OF IMMUNOLOGY			English	Article							INDUCED AIRWAY HYPERREACTIVITY; DENDRITIC CELLS; INDOLEAMINE 2,3-DIOXYGENASE; EXPERIMENTAL ASTHMA; CANDIDA-ALBICANS; INHALED ANTIGEN; MURINE MODEL; TGF-BETA; IN-VIVO; FUMIGATUS	The inherent resistance to diseases caused by Aspergillus fumigatus suggests the occurrence of regulatory mechanisms that provide the host with adequate defense without necessarily eliminating the fungus or causing unacceptable levels of host damage. In this study, we show that a division of labor occurs between functionally distinct regulatory T cells (Treg) that are coordinately activated by a CD28/B-7-dependent costimulatory pathway after exposure of mice to Aspergillus conidia. Early in infection, inflammation is controlled by the expansion, activation and local recruitment of CD4(+)CD25(+) Treg capable of suppressing neutrophils through the combined actions of IL-10 and CTLA-4 on indoleamine 2,3-dioxygenase. The levels of IFN-gamma produced in this early phase set the subsequent adaptive stage by conditioning the indoleamine 2,3-dioxygenase-dependent tolerogenic program of dendritic cells and the subsequent activation and expansion of tolerogenic Treg, which produce IL-10 and TGF-beta, inhibit Th2 cells, and prevent allergy to the fungus. The coordinate activation of Treg may, however, be subverted by the fungus, as germinating conidia are capable of interfering with anti-inflammatory and tolerogenic Treg programs. Thus, regulation is an essential component of the host response in infection and allergy to the fungus, and its manipulation may allow the pathogen to overcome host resistance and promote disease.	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J	Ek, KH; Morrison, GM; Rauch, S				Ek, KH; Morrison, GM; Rauch, S			Environmental routes for platinum group elements to biological materials - a review	SCIENCE OF THE TOTAL ENVIRONMENT			English	Article; Proceedings Paper	7th International Symposium on Highway and Urban Pollution	MAY, 2002	Inst Quimic Sarria, Barcelona, SPAIN		Inst Quimic Sarria	platinum; palladium; rhodium; PGE; biological material; transformation; mobility; speciation; bioavailability; uptake	PLASMA-MASS SPECTROMETRY; AUTOMOBILE CATALYTIC-CONVERTERS; MAGNETIC-SECTOR FIELD; AIRBORNE PARTICULATE MATTER; SIZE-EXCLUSION CHROMATOGRAPHY; URBAN ROAD DUST; GROUP-METALS; ICP-MS; CONTACT-DERMATITIS; PRECIOUS METALS	The increased use of platinum group elements (PGE) in automobile catalysts has led to concern over potential environmental and biological accumulation. Platinum (Pt), palladium (Pd) and rhodium (Rh) concentrations have increased in the environment since the introduction of automobile catalysts. This review summarises current knowledge concerning the environmental mobility, speciation and bioavailability of Pt, Pd and Rh. The greater proportion of PGE emissions is from automobile catalysts, in the form of nanometer-sized catalyst particles, which deposit on roadside surfaces, as evidenced in samples of road dust, grass and soil. In soil, PGE can be transformed into more mobile species through complexation with organic matter and can be solubilised in low pH rainwater. There are indications that environmentally formed Pd species are more soluble and hence more mobile in the environment than Rh and Pt. PGE can reach waterbodies through stormwater transport and deposition in sediments. Besides external contamination of grass close to roads, internal PGE uptake has been observed for plants growing on soil contaminated with automobile catalyst PGE. Fine particles of PGE were also detected on the surface of feathers sampled from passerines and raptors in their natural habitat, and internal organs of these birds also contained PGE. Uptake has been observed in sediment-dwelling invertebrates, and laboratory studies have shown an uptake of PGE in eel and fish exposed to water containing road dust. The available evidence indicates that the PGE, especially Pd, are transported to biological materials through deposition in roots by binding to sulphur-rich low molecular weight species in plants. PGE uptake to exposed animals have uptake rates in the following order: Pd>Pt>Rh. The liver and kidney accumulate the highest levels of PGE, especially Pd. Urinary Pd and Rh, but not Pt, levels are correlated with traffic intensity. Dental alloys may lead to elevated urinary Pt levels. Platinum is a well-known allergen and Pd also shows a strong sensitisation potential. (C) 2004 Elsevier B.V. All rights reserved.	Chalmers Univ Technol, Water Environm Transport, SE-41296 Gothenburg, Sweden; MIT, RM Parsons Lab 48 108, Cambridge, MA 02139 USA	Ek, KH (reprint author), Chalmers Univ Technol, Water Environm Transport, SE-41296 Gothenburg, Sweden.	kristine.ek@wet.chalmers.se		Rauch, Sebastien/0000-0003-3636-0684			ALT F, 1993, FRESEN J ANAL CHEM, V346, P693, DOI 10.1007/BF00321274; Alt F, 2002, ANAL LETT, V35, P1349, DOI [10.1081/AL-120006671, 10.1081/AL-12000671]; Artelt S, 1999, SCI TOTAL ENVIRON, V228, P219, DOI 10.1016/S0048-9697(99)00049-2; Barany E, 2002, SCI TOTAL ENVIRON, V286, P129, DOI 10.1016/S0048-9697(01)00970-6; Barany E, 2002, TOXICOL LETT, V134, P177, DOI 10.1016/S0378-4274(02)00187-X; Barbante C, 2001, ENVIRON SCI TECHNOL, V35, P835, DOI 10.1021/es000146y; Barefoot RR, 1997, ENVIRON SCI TECHNOL, V31, P309, DOI 10.1021/es960712i; Becker JS, 2000, FRESEN J ANAL CHEM, V368, P490, DOI 10.1007/s002160000539; BEDELLO PG, 1987, CONTACT DERMATITIS, V17, P111, DOI 10.1111/j.1600-0536.1987.tb02674.x; 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Total Environ.	DEC 1	2004	334				SI		21	38		10.1016/j.scitotenv.2004.04.027		18	Environmental Sciences	Environmental Sciences & Ecology	873QN	WOS:000225295900005	15504490	
J	Cyrys, J; Heinrich, J; Hoek, G; Meliefste, K; Lewne, M; Gehring, U; Bellander, T; Fischer, P; Van Vliet, P; Brauer, M; Wichmann, HE; Brunekreef, B				Cyrys, J; Heinrich, J; Hoek, G; Meliefste, K; Lewne, M; Gehring, U; Bellander, T; Fischer, P; Van Vliet, P; Brauer, M; Wichmann, HE; Brunekreef, B			Comparison between different traffic-related particle indicators: Elemental. carbon (EC), PM2.5 mass, and absorbance	JOURNAL OF EXPOSURE ANALYSIS AND ENVIRONMENTAL EPIDEMIOLOGY			English	Article						traffic-related pollutants; particles; PM10; PM2.5; absorbance; EC	CHRONIC RESPIRATORY SYMPTOMS; DIESEL EXHAUST PARTICLES; PARTICULATE MATTER; AIR-POLLUTION; SPATIAL VARIABILITY; DAILY MORTALITY; CHILDREN; HEALTH; SMOKE; PM10	Here we compare PM2.5 (particles with aerodynamic diameter less than 2.5 mum) mass and filter absorbance measurements with elemental carbon (EC) concentrations measured in parallel at the same site as well as collocated PM2.5 and PM10 (particles with aerodynamic diameter less than 10 mum) mass and absorbance measurements. The data were collected within the Traffic-Related Air Pollution on Childhood Asthma (TRAPCA) study in Germany, The Netherlands and Sweden. The study was designed to assess the health impact of spatial contrasts in long-term average concentrations. The measurement sites were distributed between background and traffic locations. Annual EC and PM2.5 absorbance measurements were at traffic sites on average 43-84% and 26-76% higher, respectively, compared to urban background sites. The contrast for PM2.5 mass measurements was lower (8-35%). The smaller contrast observed for PM2.5 mass in comparison with PM2.5 absorbance and EC documents that PM2.5 mass underestimates exposure contrasts related to motorized traffic emissions. The correlation between PM10 and PM2.5 was high, documenting that most of the spatial variation of PM10 was because of PM2.5. The measurement of PM2.5 absorbance was highly correlated with EC measurements and suggests that absorbance can be used as a simple, inexpensive and non-destructive method. to estimate motorized traffic-related particulate air pollution. The EC/absorbance relation differed between countries and site type (background/traffic), supporting the need for site-specific calibrations of the simple absorbance method. While the ratio between PM2.5 and PM10 mass ranged from 0.54 to 0.68, the ratio of PM2.5 absorbance and PM10 absorbance was 0.96-0.97, indicating that PM2.5 absorbance captures nearly all of the particle absorbance.	GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, D-85764 Neuherberg, Germany; Univ Munich, Inst Med Data Management Biometr & Epidemiol, Chair Epidemiol, Munich, Germany; Univ Utrecht, Inst Risk Assessment Sci, Environm & Occupat Hlth Unit, Utrecht, Netherlands; Stockholm Cty Council, Dept Environm Hlth, Stockholm, Sweden; Natl Inst Publ Hlth & Environm, Lab Exposure Assessment & Environm Epidemiol, Bilthoven, Netherlands; Univ British Columbia, Sch Occupat & Environm Hyg, Vancouver, BC V5Z 1M9, Canada	Cyrys, J (reprint author), GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, Ingolstaedter Landstr 1, D-85764 Neuherberg, Germany.		Cyrys, Josef/B-5359-2014; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; brunekreef, bert/0000-0001-9908-0060; Cyrys, Josef/0000-0002-2105-8696; Gehring, Ulrike/0000-0003-3612-5780; Brauer, Michael/0000-0002-9103-9343			BAYRAM H, 1998, J RESP CELL MOL BIOL, V18, P441; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; CHOW JC, 1995, J AIR WASTE MANAGE, V45, P320; Ciccone G, 1998, OCCUP ENVIRON MED, V55, P771; COUNTANT B, EPA454R01008 OFF AIR; Cyrys J, 1998, J EXPO ANAL ENV EPID, V8, P447; DELUMYEA RG, 1980, ATMOS ENVIRON, V14, P647, DOI 10.1016/0004-6981(80)90047-5; DiazSanchez D, 1997, ALLERGY, V52, P52; Duhme H, 1996, EPIDEMIOLOGY, V7, P578, DOI 10.1097/00001648-199611000-00003; English P, 1999, ENVIRON HEALTH PERSP, V107, P761, DOI 10.2307/3434663; FISCHER A, 1997, SCHRIFTENREIHE UMWEL, V80; Fischer PH, 2000, ATMOS ENVIRON, V34, P3713, DOI 10.1016/S1352-2310(00)00067-4; Gray HA, 1998, ATMOS ENVIRON, V32, P3805; HAMILTON RS, 1991, ATMOS ENVIRON A-GEN, V25, P715, DOI 10.1016/0960-1686(91)90070-N; Hies T, 2000, ATMOS ENVIRON, V34, P3495, DOI 10.1016/S1352-2310(00)00146-1; Hoek G, 1997, ATMOS ENVIRON, V31, P3609, DOI 10.1016/S1352-2310(97)00158-1; Hoek G, 1997, ATMOS ENVIRON, V31, P3341, DOI 10.1016/S1352-2310(97)00150-7; Hoek G, 2002, ATMOS ENVIRON, V36, P4077, DOI 10.1016/S1352-2310(02)00297-2; HORVATH H, 1993, ATMOS ENVIRON A-GEN, V27, P293, DOI 10.1016/0960-1686(93)90104-7; *ISO, 1993, 98351993 ISO INT ORG; Janssen NAH, 2001, ATMOS ENVIRON, V35, P3875, DOI 10.1016/S1352-2310(01)00144-3; Janssen NAH, 1997, ATMOS ENVIRON, V31, P1185, DOI 10.1016/S1352-2310(96)00291-9; KEEBER G, 1990, ATMOSPHERIC ENV A, V24, P2795; Kinney PL, 2000, ENVIRON HEALTH PERSP, V108, P213, DOI 10.2307/3454436; Kramer U, 2000, EPIDEMIOLOGY, V11, P64, DOI 10.1097/00001648-200001000-00014; Laden F, 2000, ENVIRON HEALTH PERSP, V108, P941, DOI 10.2307/3435052; MARPLE VA, 1987, JAPCA J AIR WASTE MA, V37, P1303; Monn C, 1997, ATMOS ENVIRON, V31, P2243, DOI 10.1016/S1352-2310(97)00030-7; NAKAI S, 1995, J EXPO ANAL ENV EPID, V5, P125; Nielsen T, 1996, ATMOS ENVIRON, V30, P3481, DOI 10.1016/1352-2310(96)00096-9; Nyberg F, 2000, EPIDEMIOLOGY, V11, P487, DOI 10.1097/00001648-200009000-00002; OECD, 1964, METH MEAS AIR POLL; Oosterlee A, 1996, OCCUP ENVIRON MED, V53, P241; Penttinen P, 2000, ATMOS ENVIRON, V34, P2581, DOI 10.1016/S1352-2310(99)00491-4; Schmid H, 2001, ATMOS ENVIRON, V35, P2111, DOI 10.1016/S1352-2310(00)00493-3; Schwartz J, 1996, J AIR WASTE MANAGE, V46, P927, DOI 10.1080/10473289.1996.10467528; Tolocka MP, 2001, AEROSOL SCI TECH, V34, P88; Ulrich E., 1992, J AEROSOL SCI S23, V1, pS925; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; *VDI, 1996, VER DTSCH ING 1, V2465; Weiland Stephan K., 1994, Annals of Epidemiology, V4, P243; WJST M, 1993, BRIT MED J, V307, P596; WOLFF GT, 1985, ATMOS ENVIRON, V19, P305, DOI 10.1016/0004-6981(85)90098-8	43	135	136	3	41	NATURE PUBLISHING GROUP	NEW YORK	345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA	1053-4245			J EXPO ANAL ENV EPID	J. Expo. Anal. Environ. Epidemiol.	MAR	2003	13	2					134	143		10.1038/sj.jea.7500262		10	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	676HD	WOS:000182744500005	12679793	
J	Cataldo, D; Munaut, C; Noel, A; Frankenne, F; Bartsch, P; Foidart, JM; Louis, R				Cataldo, D; Munaut, C; Noel, A; Frankenne, F; Bartsch, P; Foidart, JM; Louis, R			MMP-2-and MMP-9-linked gelatinolytic activity in the sputum from patients with asthma and chronic obstructive pulmonary disease	INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY			English	Article						asthma; COPD; matrix metalloproteinases; MMP-9; TIMP-1	BRONCHOALVEOLAR LAVAGE FLUID; AIR-FLOW OBSTRUCTION; TISSUE INHIBITOR; IV COLLAGENASE; MATRIX METALLOPROTEINASES; ALVEOLAR MACROPHAGES; CHRONIC-BRONCHITIS; PROGELATINASE-A; SMOOTH-MUSCLE; INFLAMMATION	Background: The course of asthma and chronic obstructive pulmonary disease (COPD) is associated with bronchial morphological changes. Metalloproteinases are thought to play a role in these structural changes. Methods: We studied the gelatinolytic activity present in the induced sputum from 20 patients with asthma, 20 with COPD and 19 healthy controls. The assessment of gelatinolytic activity was performed by quantitative zymography, and gelatinolytic species were identified by Western blot analysis. Tissue inhibitor of metalloproteinase-l (TIMP-1) was detected by reverse zymography and ELISA. Results: From zymography, we found significantly higher gelatinolytic activity linked to pro-matrix metalloproteinase-9 (pro-MMP-9) in the sputum from asthmatics (p < 0.0001) and COPD patients (p < 0.0001) compared to the control group. Furthermore, the activated form of MMP-9 (85 kD) was found in the sputum from 60% of asthmatics and 85% of COPD patients, but was absent in that of control subjects (p < 0.0001). Importantly, although less frequently detectable than pro-MMP-9, pro-MMP-2 (72 kD) was found more frequently in asthmatics (50%) than in control subjects (5%) (p < 0.005). We also described two unusual gelatinolytic species of 45 and 120 kD and showed that they derived from MMP-9 according to their ability to bind gelatin and anti-MMP-9 antibody. Levels of TIMP-1 were higher in asthmatics (p < 0.05) and COPD patients (p < 0.05) than in controls. Conclusion: Asthmatics and COPD patients display an increased gelatinolytic activity linked to MMP-2 and MMP-9 and higher levels of TIMP-1 in their sputum. Copyright (C) 2000 S. Karger AG, Basel.	Univ Liege, Dept Pneumol, Liege, Belgium; Univ Liege, Dept Biol Tumor & Dev, Liege, Belgium	Cataldo, D (reprint author), CHU Sart Tilman, Dept Pneumol, B-4000 Liege, Belgium.			Noel, Agnes/0000-0002-7670-6179; Cataldo, Didier/0000-0002-3079-7941			American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P225, DOI DOI 10.1164/AJRCCM/136.1.225; Bigg HF, 1997, J BIOL CHEM, V272, P15496, DOI 10.1074/jbc.272.24.15496; Bosse M, 1999, AM J RESP CRIT CARE, V159, P596; BOUSQUET J, 1992, ALLERGY, V47, P3, DOI 10.1111/j.1398-9995.1992.tb02242.x; BOUSQUET J, 1990, NEW ENGL J MED, V323, P1033, DOI 10.1056/NEJM199010113231505; CATALDO D, 1998, AM J RESP CRIT CARE, V157, pA502; COLLIER IE, 1992, J BIOL CHEM, V267, P6776; Culpitt SV, 1999, AM J RESP CRIT CARE, V160, P1635; Dahlen B, 1999, THORAX, V54, P590; Devy L, 1997, BIOCHEM BIOPH RES CO, V238, P842, DOI 10.1006/bbrc.1997.7398; DJUKANOVIC R, 1990, AM REV RESPIR DIS, V142, P434; DUNNILL MS, 1960, J CLIN PATHOL, V13, P27, DOI 10.1136/jcp.13.1.27; Edwards DR, 1996, INT J OBES RELAT MET, V20, P9; Elias JA, 1999, J CLIN INVEST, V104, P1001, DOI 10.1172/JCI8124; Finlay GA, 1997, AM J RESP CRIT CARE, V156, P240; FLETCHER C, 1977, BRIT MED J, V1, P1645; GOLDBERG GI, 1992, J BIOL CHEM, V267, P4583; HEUSSEN C, 1980, ANAL BIOCHEM, V102, P196, DOI 10.1016/0003-2697(80)90338-3; Hoshino M, 1999, J ALLERGY CLIN IMMUN, V104, P356, DOI 10.1016/S0091-6749(99)70379-9; Hoshino M, 1998, J ALLERGY CLIN IMMUN, V102, P783, DOI 10.1016/S0091-6749(98)70018-1; HUHTALA P, 1991, J BIOL CHEM, V266, P16485; JEFFERY PK, 1994, AM J RESP CRIT CARE, V150, pS6; Johnson S, 1999, AM J PHYSIOL-LUNG C, V277, pL1109; Kips JC, 1998, EUR RESPIR J, V11, p9S; Kumagai K, 1999, J IMMUNOL, V162, P4212; LACOSTE JY, 1993, J ALLERGY CLIN IMMUN, V92, P537, DOI 10.1016/0091-6749(93)90078-T; Lange P, 1998, NEW ENGL J MED, V339, P1194, DOI 10.1056/NEJM199810223391703; Lemjabbar H, 1999, AM J RESP CRIT CARE, V159, P1298; Mautino G, 1999, AM J RESP CRIT CARE, V160, P324; Mautino G, 1997, AM J RESP CELL MOL, V17, P583; Nagase H, 1997, BIOL CHEM, V378, P151; Naureckas ET, 1999, AM J RESP CRIT CARE, V160, P2062; Noel A, 1997, INVAS METAST, V17, P221; REMACLE AG, 1995, PROTEIN EXPRES PURIF, V6, P417, DOI 10.1006/prep.1995.1056; Shapiro SD, 1998, CURR OPIN CELL BIOL, V10, P602, DOI 10.1016/S0955-0674(98)80035-5; Vignola AM, 1998, AM J RESP CRIT CARE, V158, P1945	36	135	145	0	2	KARGER	BASEL	ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND	1018-2438			INT ARCH ALLERGY IMM	Int. Arch. Allergy Immunol.	NOV	2000	123	3					259	267		10.1159/000024452		9	Allergy; Immunology	Allergy; Immunology	379VF	WOS:000165663000010	11112863	
J	Johansen, JD; Menne, T; Christophersen, J; Kaaber, K; Veien, N				Johansen, JD; Menne, T; Christophersen, J; Kaaber, K; Veien, N			Changes in the pattern of sensitization to common contact allergens in Denmark between 1985-86 and 1997-98, with a special view to the effect of preventive strategies	BRITISH JOURNAL OF DERMATOLOGY			English	Article						chromate; contact allergy; Denmark; fragrance mix; nickel; patch testing	PATCH TEST; DERMATITIS; CEMENT	The objective of the present study is to describe any changes in the prevalence of sensitization to common contact allergens in patch-tested patients over a 12-year period, Attention is given to possible effects of preventive strategics introduced in Denmark regarding nickel and chromate sensitization during that period, and particular areas of concern are identified. Members of the Danish Contact Dermatitis Group collected patch-test results from consecutive eczema patients as well as information about exposures and demographic variables over a 6-month period in 1985-86. The investigation was repeated in 1997-98 in the same clinics, at the same time of year, using identical methods and patch-test substances, including nickel sulphate 5%, potassium dichromate 0.5% and fragrance mix 8%. Nickel was the most common contact allergen in both study periods, followed by the fragrance mix. In children 0-18 years of age, the frequency of nickel allergy decreased from 24.8% in the first study period to 9.2% in the second study period (P < 0.0008), Fragrance mix allergy doubled in frequency from 4.1% in 1985-86 to 9.9% in 1997-98, an increase that affected all age groups. Contact allergy to potassium dichromate decreased significantly from 3.0% in the first period to 1.2% in the second period (P = 0.001). The decrease was seen in both sexes and was most pronounced among those of working age, No other significant changes were found in the frequency of sensitization to common allergens over the 12-year observation period.	Univ Copenhagen, Gentofte Hosp, Dept Dermatol, DK-2900 Copenhagen, Denmark; Dermatol Clin, DK-2830 Virum, Denmark; Dermatol Clin, DK-7400 Herning, Denmark; Dermatol Clin, Aalborg, Denmark	Johansen, JD (reprint author), Univ Copenhagen, Gentofte Hosp, Dept Dermatol, DK-2900 Copenhagen, Denmark.						Andersen K. E., 1995, TXB CONTACT DERMATIT, P421; AVNSTORP C, 1992, ACTA DERM-VENER    S, V179, P2; BUCKLEY DA, IN PRESS BR J DERMAT; BUTLER H, 1993, POUCHERS PERFUMES CO, V3, P639; CHRISTOPHERSEN J, 1989, CONTACT DERMATITIS, V21, P291, DOI 10.1111/j.1600-0536.1989.tb04746.x; *DAN MIN ENV SAT O, 1991, 854 DAN MIN ENV STAT; *DAN WORK ENV SERV, 1983, 661 DAN WORK ENV SER; *INT FRAGR ASS, 1974, COD PRACT GUID PER B; IRVINE C, 1994, OCCUP MED-OXFORD, V44, P17, DOI 10.1093/occmed/44.1.17; Johansen JD, 1997, ACTA DERM-VENEREOL, V77, P149; Johansen JD, 1996, BRIT J DERMATOL, V135, P419, DOI 10.1111/j.1365-2133.1996.tb01506.x; LIM JTE, 1992, CONTACT DERMATITIS, V26, P321; Marks JG, 1998, J AM ACAD DERMATOL, V38, P911, DOI 10.1016/S0190-9622(98)70587-0; Menne T, 1996, ANN CLIN LAB SCI, V26, P133; NIELSEN NH, 1992, ACTA DERM-VENEREOL, V72, P456; Olsavszky R, 1998, CONTACT DERMATITIS, V38, P329, DOI 10.1111/j.1600-0536.1998.tb05768.x; ROTHENBORG HW, 1968, ARCH DERMATOL, V97, P417, DOI 10.1001/archderm.97.4.417; Somogyi LP, 1996, CHEM IND-LONDON, P170; Uter W, 1998, EUR J DERMATOL, V8, P36; WILKINSON DS, 1970, ACTA DERM-VENEREOL, V50, P287; Zachariae COC, 1996, CONTACT DERMATITIS, V35, P83, DOI 10.1111/j.1600-0536.1996.tb02295.x	21	135	137	1	4	BLACKWELL SCIENCE LTD	OXFORD	P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND	0007-0963			BRIT J DERMATOL	Br. J. Dermatol.	MAR	2000	142	3					490	495		10.1046/j.1365-2133.2000.03362.x		6	Dermatology	Dermatology	296GP	WOS:000086016300016	10735956	
J	Jackson, DJ; Sykes, A; Mallia, P; Johnston, SL				Jackson, David J.; Sykes, Annemarie; Mallia, Patrick; Johnston, Sebastian L.			Asthma exacerbations: Origin, effect, and prevention	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Asthma; asthma exacerbations; viral infection; virus; allergy; allergen; pollutant; bacteria	BRONCHIAL EPITHELIAL-CELLS; VIRUS-INDUCED ASTHMA; BUDESONIDE/FORMOTEROL COMBINATION THERAPY; PLACEBO-CONTROLLED TRIAL; SEVERE PERSISTENT ASTHMA; INDOOR NITROGEN-DIOXIDE; SEVERE ALLERGIC-ASTHMA; NECROSIS-FACTOR-ALPHA; INNER-CITY CHILDREN; HUMAN RHINOVIRUS C	Asthma is the most common chronic respiratory disease, affecting up to 10% of adults and 30% of children in the Western world. Despite advances in asthma management, acute exacerbations continue to occur and impose considerable morbidity on patients and constitute a major burden on health care resources. Respiratory tract viruses have emerged as the most frequent triggers for exacerbations in both children and adults; however, the mechanisms underlying these remain poorly understood. More recently, it has become increasingly clear that interactions might exist between viruses and other triggers, increasing the likelihood of an exacerbation. In this article we begin with an overview of the health, economic, and social burden that exacerbations of asthma carry with them. This is followed by a review of the pathogenesis of asthma exacerbations, highlighting the various triggers responsible and multiple interactions that exist between them. The final section first addresses what preventative measures are currently available for asthma exacerbations and subsequently examines which of the new treatments in development might lessen the burden of exacerbations in the future. (J Allergy Clin Immunol 2011;128:1165-74.)	[Johnston, Sebastian L.] Univ London Imperial Coll Sci Technol & Med, Dept Resp Med, Natl Heart & Lung Inst, Wright Fleming Inst Infect & Immun, London W2 1PG, England; [Jackson, David J.; Sykes, Annemarie; Mallia, Patrick; Johnston, Sebastian L.] Univ London Imperial Coll Sci Technol & Med, MRC & Asthma UK Ctr Allerg Mech Asthma, London W2 1PG, England; [Jackson, David J.; Sykes, Annemarie; Mallia, Patrick; Johnston, Sebastian L.] Ctr Resp Infect, London, England; [Jackson, David J.; Sykes, Annemarie; Mallia, Patrick; Johnston, Sebastian L.] Imperial Coll Healthcare NHS Trust, London, England	Johnston, SL (reprint author), Univ London Imperial Coll Sci Technol & Med, Dept Resp Med, Natl Heart & Lung Inst, Wright Fleming Inst Infect & Immun, Norfolk Pl, London W2 1PG, England.	s.johnston@imperial.ac.uk	Johnston, Sebastian/I-2423-2012		MRC [G0601236]; MRC Centre [G1000758]; Predicta FP7 Collaborative Project [260895]; Wellcome Trust; ERC [233015]; National Institutes of Health Research; Asthma UK	Supported in part by MRC project grant G0601236, MRC Centre grant G1000758, the Predicta FP7 Collaborative Project grant 260895, and the Wellcome Trust-sponsored Centre for Respiratory Infection (CRI). D.J.J. is supported by ERC FP7 Advanced grant 233015 (to S.L.J.), A.S. is supported by an MRC Clinical Training Fellowship, A.S. and P.M. are National Institutes of Health Research Clinical Lecturers, and S.L.J. holds the Asthma UK Clinical Chair (CH1155).; S.L. Johnston is a consultant for AstraZeneca, Centocor, and Sanofi-Pasteur; is a consultant for and shareholder in Synairgen; has received research support from the European Research Council, Medical Research Council Clinical Training Fellowship, National Institutes of Health Research, Asthma UK, Medical Research Council, Predicta FP7 Collaborative Project, and the Wellcome Trust-sponsored Centre for Respiratory Infection. The rest of the authors declare that they have no relevant conflicts of interest.	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Allergy Clin. Immunol.	DEC	2011	128	6					1165	1174		10.1016/j.jaci.2011.10.024		10	Allergy; Immunology	Allergy; Immunology	865WX	WOS:000298342700003	22133317	
J	Zosky, GR; Sly, PD				Zosky, G. R.; Sly, P. D.			Animal models of asthma	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review						animal; asthma; model	ALLERGEN-INDUCED AIRWAY; HOUSE-DUST MITE; ANTIGEN-INDUCED BRONCHOCONSTRICTION; LATE-PHASE BRONCHOCONSTRICTION; RESPIRATORY SYSTEM MECHANICS; BROWN-NORWAY RAT; MOUSE MODEL; T-CELLS; BRONCHIAL RESPONSIVENESS; LUNG INFLAMMATION	Animal models of asthma are a tool that allows studies to be conducted in the setting of an intact immune and respiratory system. These models have highlighted the importance of T-helper type 2 driven allergic responses in the progression of asthma and have been useful in the identification of potential drug targets for interventions involving allergic pathways. However, a number of drugs that have been shown to have some efficacy in animal models of asthma have shown little clinical benefit in human asthmatics. This may be due to a number of factors including the species of animal chosen and the methods used to induce an asthmatic phenotype in animals that do not normally develop a disease that could be characterized as asthma. The range of animal models available is vast, with the most popular models being rodents (inbred mice and rats) and guinea-pigs, which have the benefit of being easy to handle and being relatively cost effective compared with other models that are available. The recent advances in transgenic technology and the development of species-specific probes, particularly in mice, have allowed detailed mechanistic studies to be conducted. Despite these advances in technology, there are a number of issues with current animal models of asthma that must be recognized including the disparity in immunology and anatomy between these species and humans, the requirement for adjuvant during senitization in most models, the acute nature of the allergic response that is induced and the use of adult animals as the primary disease model. Some larger animal models using sheep and dogs have been developed that may address some of these issues but they also have different biology from humans in many ways and are extremely costly, with very few probes available for characterizing allergic responses in the airway in these species. As research in this area continues to expand, the relative merits and limitations of each model must be defined and understood in order to evaluate the information that is obtained from these models and to extrapolate these findings to humans so that effective drug therapies can be developed. Despite these issues, animal models have been, and will continue to be, vital in understanding the mechanisms that are involved in the development and progression of asthma.	Telethon Inst Child Hlth Res, Div Clin Sci, Subiaco, WA 6008, Australia; Univ Western Australia, Ctr Child Hlth Res, Crawley, WA, Australia	Zosky, GR (reprint author), Telethon Inst Child Hlth Res, Div Clin Sci, 100 Roberts Rd, Subiaco, WA 6008, Australia.	graemez@ichr.uwa.edu.au	Sly, Peter/F-1486-2010; Zosky, Graeme/B-2048-2014	Sly, Peter/0000-0001-6305-2201; Zosky, Graeme/0000-0001-9039-0302			ABRAHAM W M, 1989, Pulmonary Pharmacology, V2, P33, DOI 10.1016/S0952-0600(89)80007-9; ABRAHAM WM, 1988, AM REV RESPIR DIS, V138, P1565; ABRAHAM WM, 1983, AM REV RESPIR DIS, V128, P839; ABRAHAM WM, 1995, EUR RESPIR REV, V5, P211; Adler A, 2004, J APPL PHYSIOL, V97, P286, DOI 10.1152/japplphysiol.00821.2003; Anderson GG, 1998, ARCH DIS CHILD, V78, P488; ANDREW DK, 1984, INT ARCH ALLER A IMM, V75, P208; Aoshiba K, 2004, CLIN REV ALLERG IMMU, V27, P35, DOI 10.1385/CRIAI:27:1:035; Babu KS, 2001, CLIN EXP ALLERGY, V31, P182, DOI 10.1046/j.1365-2222.2001.01058.x; Barnes PJ, 2006, EUR RESPIR J, V27, P413, DOI 10.1183/09031936.06.00125404; 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D., 2006, ALLERGY CLIN IMMUNOL, V18, P76, DOI 10.1027/0838-1925.18.2.76	154	134	138	1	23	WILEY-BLACKWELL	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	JUL	2007	37	7					973	988		10.1111/j.1365-2222.2007.02740.x		16	Allergy; Immunology	Allergy; Immunology	180WQ	WOS:000247398300004	17581191	
J	de Lange, EE; Altes, TA; Patrie, JT; Gaare, JD; Knake, JJ; Mugler, JP; Platts-Mills, TA				de lange, Eduard E.; Altes, Talissa A.; Patrie, James T.; Gaare, John D.; Knake, Jeffrey J.; Mugler, John P., III; Platts-Mills, Thomas A.			Evaluation of asthma with hyperpolarized helium-3 MRI - Correlation with clinical severity and spirometry	CHEST			English	Article						airflow obstruction; airway; asthma; bronchial activity; hyperpolarized gases; hyperpolarized helium-3; MRI; pulmonary function test; spirometry; ventilation defect	LUNG-TRANSPLANT RECIPIENTS; PULMONARY-FUNCTION TESTS; MAGNETIC-RESONANCE; CYSTIC-FIBROSIS; SMALL AIRWAYS; AIR SPACES; GAS; ABNORMALITIES; VENTILATION; VOLUMES	Background: Accurate characterization of asthma severity is difficult due to the variability of symptoms. Hyperpolarized helium-3 MRI ((HHeMR)-He-3) is a new technique in which the airspaces are visualized, depicting regions with airflow obstruction as "ventilation defects." The objective of this study was to compare the extent of (HHeMR)-He-3 ventilation defects with measures of asthma severity and spirometry. Methods: Patients with a physician diagnosis of asthma and normal control subjects underwent (HHeMR)-He-3. For each person, the number and size of ventilation defects were scored and the average number of ventilation defects per slice (VDS) was calculated. The correlations of the imaging findings with measures of asthma severity and spirometry were determined. Results: There were 58 patients with asthma (mild-intermittent, n = 13; mild-persistent, n = 13; moderate-persistent, n = 20; and severe-persistent, n = 12) and 18 control subjects. Mean +/- SE VDS for asthmatics was significantly greater than for control subjects (0.99 +/- 0.15 vs; 0.26 +/- 0.22, p = 0.004). Among asthmatics, VDS was significantly higher for the group with moderate-persistent and severe-persistent disease than for the group with mild-intermittent and mild-persistent disease (1.37 +/- 0.24 vs 0.53 +/- 0.12, p < 0.001). VDS correlated significantly with FEV1/FVC (r = -0.51, p = 0.002), forced expiratory flow between 25% and 75% from the beginning of FVC (FEF25-75%) percentage of predicted for height, sex, and race (%predicted) [r = -0.50, p = 0.001], and FEV1 %predicted (r = -0.40, p = 0.002), but not with FVC %predicted (r = -0.26, p = 0.057) and peak expiratory flow %predicted (r = -0.16, p = 0.231). Many asthmatics had an elevated VDS, but their spirometric indexes, except FEF25%-75%, were normal. Most ventilation defects were < 3 cm in size for all asthmatics. In the group of patients with moderate-to-severe persistant asthma, there were more defects >= 3 cm than in the group with mild-intermittent and mild-persistent disease (p = 0.021). Conclusions: Regional changes of airflow obstruction in asthmatics depicted by (HHeMR)-He-3 correlate with measures of asthma severity and spirometry.	Univ Virginia, Dept Radiol, Charlottesville, VA USA; Univ Virginia, Dept Hlth Evaluat Sci, Charlottesville, VA USA; Univ Virginia, Dept Internal Med, Div Asthma Allergy & Immunol, Charlottesville, VA USA	de Lange, EE (reprint author), Univ Virginia Hlth Sci Syst, Dept Radiol, HSC 800170, Charlottesville, VA 22908 USA.	delange@virginia.edu	Mugler, John/B-9432-2013	Mugler, John/0000-0002-4140-308X	NHLBI NIH HHS [HL66479]		AGNEW JE, 1984, CLIN SCI, V66, P525; Altes TA, 2001, J MAGN RESON IMAGING, V13, P378, DOI 10.1002/jmri.1054; ALTES TA, 2002, P RSNA 88 M, P347; American Thoracic Society, 1991, AM REV RESPIR DIS, V144, P1202, DOI 10.1164/ajrccm/144.5.1202; BATTISTON JJ, 2005, P RSNA 91 M, P241; COSIO M, 1978, NEW ENGL J MED, V298, P1277, DOI 10.1056/NEJM197806082982303; de Lange EE, 1999, RADIOLOGY, V210, P851; DELANGE EE, 2003, P 89 SCI ASS ANN M R, P525; Donnelly LF, 1999, RADIOLOGY, V212, P885; Fonseca-Guedes CHF, 2003, PEDIATR PULM, V36, P49, DOI 10.1002/ppul.10309; GAARE J, 2004, P 90 SCI ASS ANN M R, P514; Gono H, 2003, EUR RESPIR J, V22, P965, DOI 10.1183/09031936.03.00085302; Guenther D, 2000, NMR BIOMED, V13, P182, DOI 10.1002/1099-1492(200006)13:4<182::AID-NBM642>3.0.CO;2-N; Hamid Q, 1997, J ALLERGY CLIN IMMUN, V100, P44; Heaney LG, 2005, LANCET, V365, P974, DOI 10.1016/S0140-6736(05)71087-4; HODSON ME, 1974, THORAX, V29, P296, DOI 10.1136/thx.29.3.296; Israel E, 2004, LANCET, V364, P1505, DOI 10.1016/S0140-6736(04)17273-5; JAMES AL, 1989, AM REV RESPIR DIS, V139, P242; Kauczor HU, 1996, RADIOLOGY, V201, P564; Kavuru MS, 1999, CLIN CHEST MED, V20, P153, DOI 10.1016/S0272-5231(05)70133-7; KNUDSON RJ, 1983, AM REV RESPIR DIS, V127, P725; MacFall JR, 1996, RADIOLOGY, V200, P553; McAdams HP, 1999, AM J ROENTGENOL, V173, P955; Mentore K, 2005, ACAD RADIOL, V12, P1423, DOI 10.1016/j.acra.2005.07.008; MIDDLETON H, 1995, MAGNET RESON MED, V33, P271, DOI 10.1002/mrm.1910330219; Miller LA, 2005, CLIN EXP ALLERGY, V35, P894, DOI 10.1111/j.1365-2222.2005.02271.x; Mitsunobu F, 2003, EUR RESPIR J, V22, P106, DOI 10.1183/09031936.03.00081702; MITSUNOBU F, 2002, THORAX, V57, P851; Mugler JP, 1997, MAGNET RESON MED, V37, P809, DOI 10.1002/mrm.1910370602; National Asthma Education and Prevention Program, 1997, PUBL NAT ASTHM ED PR; Paganin F, 1996, AM J RESP CRIT CARE, V153, P110; PETHERAM IS, 1981, CLIN RADIOL, V32, P281, DOI 10.1016/S0009-9260(81)80039-6; Petty TL, 2001, CLIN CHEST MED, V22, P845, DOI 10.1016/S0272-5231(05)70070-8; Salerno M, 2002, RADIOLOGY, V222, P252; Samee S, 2003, J ALLERGY CLIN IMMUN, V111, P1205, DOI 10.1067/mai.2003.1544; Swift AJ, 2005, EUR J RADIOL, V54, P352, DOI 10.1016/j.ejrad.2004.08.002; van Beek EJR, 2004, J MAGN RESON IMAGING, V20, P540, DOI 10.1002/jmri.20154; VERNON P, 1986, EUR J NUCL MED, V12, P16, DOI 10.1007/BF00638789; Woodhouse N, 2005, J MAGN RESON IMAGING, V21, P365, DOI 10.1002/jmri.20290; Zaporozhan J, 2004, CHEST, V125, P173, DOI 10.1378/chest.125.1.173	40	134	137	2	7	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	OCT	2006	130	4					1055	1062		10.1378/chest.130.4.1055		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	094UX	WOS:000241265700022	17035438	
J	Gurney, JG; McPheeters, ML; Davis, MM				Gurney, James G.; McPheeters, Melissa L.; Davis, Matthew M.			Parental report of health conditions and health care use among children with and without autism - National Survey of Children's Health	ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE			English	Article							SPECTRUM DISORDERS; GASTROINTESTINAL DISORDERS; TUBEROUS SCLEROSIS; MEDICAL CONDITIONS; PREVALENCE TRENDS; ASPERGER-SYNDROME; ABNORMALITIES; EPILEPSY; DISABILITIES; INDIVIDUALS	Objective: To compare parent-reported prevalence of health conditions and health care use between children with and without autism. Design: Cross-sectional analysis of the 2003 to 2004 National Survey of Children's Health. Setting: Population-based sample across the United States. Participants: More than 100 000 parents. The main exposure was "autism" (not further defined), from response to the question: "Has a doctor or health professional ever told you that your child has autism?" Main Outcome Measures: Medical and mental health conditions and measures of health care use. Results: Autism prevalence among children aged 3 to 17 years was 53 per 10 000 (95% confidence interval, 45-61 per 10 000), equating to a national estimate of 324 000 children (95% confidence interval, 274 000-375 000 children). Children with autism had a significantly (P <.001) higher prevalence of depression or anxiety problems (38.9% vs 4.2%) and behavioral or conduct problems (58.9% vs 5.2%) than children without autism. Respiratory, food, and skin allergies were reported by parents more often for children with autism, with food allergies having the strongest relative difference between the groups (odds ratio, 4.5; 95% confidence interval, 3.0-7.0). Children with autism had significantly (P <.001) higher mean physician visits over 12 months for preventive care, nonemergency care, and hospital emergency care, and were far more likely than children without autism to receive physical, occupational, or speech therapy (76.0% vs 6.3%), to need treatment or counseling for an emotional, developmental, or behavioral problem (75.4% vs 7.0%), and, among those taking a prescribed medication, to be using a medication long-term (51.4% vs 14.5%). Conclusion: We found markedly higher reports of concurrent conditions and health care use associated with childhood autism in this study.	Univ Michigan, Dept Pediat, Child Hlth Evaluat & Res Unit, Ann Arbor, MI 48109 USA; Univ Michigan, Gerald R Ford Sch Publ Policy, Div Gen Internal Med, Ann Arbor, MI 48109 USA	Gurney, JG (reprint author), Univ Michigan, Dept Pediat, Child Hlth Evaluat & Res Unit, 300 N Ingalls St,Room 6E02, Ann Arbor, MI 48109 USA.	jamegurn@umich.edu					*AM AC PED, 2002, PEDIATRICS, V7, P1221; *AM AC PED COUNC C, 2005, PEDIATRICS, V116, P1268; American Psychiatric Association, 1994, DIAGN STAT MAN MENT; Baker P, 1998, J AUTISM DEV DISORD, V28, P279, DOI 10.1023/A:1026004501631; Barton M, 1998, J AUTISM DEV DISORD, V28, P273, DOI 10.1023/A:1026052417561; Black C, 2002, BRIT MED J, V325, P419, DOI 10.1136/bmj.325.7361.419; Canitano R, 2005, J CHILD NEUROL, V20, P27, DOI 10.1177/08830738050200010401; Castillo M, 2005, ACAD RADIOL, V12, P533, DOI 10.1016/j.acra.2005.02.012; Cooley WC, 2004, CURR OPIN PEDIATR, V16, P689, DOI 10.1097/01.mop.0000146440.79293.5b; Danielsson S, 2005, EPILEPSIA, V46, P918, DOI 10.1111/j.1528-1167.2005.57504.x; Duan N, 1983, J EC BUSINESS STATIS, V1, P115; Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508; Ghaziuddin M, 1998, J INTELL DISABIL RES, V42, P279; Ghaziuddin M, 2002, J AUTISM DEV DISORD, V32, P299, DOI 10.1023/A:1016330802348; GHAZLUDDIN M, 2005, MENTAL HLTH ASPECTS, P109; Gillberg C, 2000, ACTA PSYCHIAT SCAND, V102, P321, DOI 10.1034/j.1600-0447.2000.102005321.x; Gillberg C, 1996, DEV MED CHILD NEUROL, V38, P191; GILLBERG IC, 1994, DEV MED CHILD NEUROL, V36, P50; Goldstein S, 2004, J AUTISM DEV DISORD, V34, P329, DOI 10.1023/B:JADD.0000029554.46570.68; Gurney JG, 2003, ARCH PEDIAT ADOL MED, V157, P622, DOI 10.1001/archpedi.157.7.622; Harrison J, 2004, J AUTISM DEV DISORD, V34, P727, DOI 10.1007/s10803-004-5293-z; Hastings RP, 2005, RES DEV DISABIL, V26, P456, DOI 10.1016/j.ridd.2004.10.003; Horvath K, 2002, CURR OPIN PEDIATR, V14, P583, DOI 10.1097/01.MOP.0000030221.71203.46; Kielinen M, 2004, AUTISM, V8, P49, DOI 10.1177/1362361304040638; Kuddo T, 2003, CURR OPIN PEDIATR, V15, P339, DOI 10.1097/00008480-200306000-00020; LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145; Malow BA, 2004, MENT RETARD DEV D R, V10, P122, DOI 10.1002/mrdd.20023; Molloy CA, 2003, AUTISM, V7, P165, DOI 10.1177/1362361303007002004; *NCHS, 2004, HLTH US 2004 CHARTB; Newschaffer CJ, 2005, PEDIATRICS, V115, pE277, DOI 10.1542/peds.2004-1958; ONeill M, 1997, J AUTISM DEV DISORD, V27, P283, DOI 10.1023/A:1025850431170; RUTTER M, 1994, J CHILD PSYCHOL PSYC, V35, P311, DOI 10.1111/j.1469-7610.1994.tb01164.x; RUTTER M, 1983, J CHILD PSYCHOL PSYC, V24, P513, DOI 10.1111/j.1469-7610.1983.tb00129.x; Sturm H, 2004, DEV MED CHILD NEUROL, V46, P444, DOI 10.1017/S0012162204000738; Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49	35	134	134	2	21	AMER MEDICAL ASSOC	CHICAGO	515 N STATE ST, CHICAGO, IL 60610-0946 USA	1072-4710			ARCH PEDIAT ADOL MED	Arch. Pediatr. Adolesc. Med.	AUG	2006	160	8					825	830		10.1001/archpedi.160.8.825		6	Pediatrics	Pediatrics	071BX	WOS:000239573400010	16894082	
J	Greinacher, A; Lubenow, N; Eichler, P				Greinacher, A; Lubenow, N; Eichler, P			Anaphylactic and anaphylactoid reactions associated with lepirudin in patients with heparin-induced thrombocytopenia	CIRCULATION			English	Article						hirudin; antibodies; anticoagulants; shock, anaphylactic	RECOMBINANT HIRUDIN; ANTIHIRUDIN ANTIBODIES; CLINICAL-RELEVANCE; R-HIRUDIN; ANTICOAGULATION; IGE	Background - Lepirudin (Refludan) is a hirudin derivative. It is a direct thrombin inhibitor obtained by recombinant technology from the medicinal leech and is approved for treatment of heparin-induced thrombocytopenia complicated by thrombosis. Because 3 cases of fatal anaphylaxis possibly associated with use of lepirudin have been reported, we initiated an investigation of putative lepirudin-associated anaphylaxis. Methods and Results - Aided by the manufacturer (Schering AG, Berlin, Germany), we used the lepirudin study databases to identify all patients in whom possible anaphylaxis/severe allergy was recorded from 1994 to September 2002. The 26 possible cases identified were reviewed independently by 2 investigators. After excluding patients with mild skin reactions, reactions likely caused by concomitant medications, poorly documented cases, and reactions that did not correspond temporally with lepirudin use, there remained 9 patients judged to have had severe anaphylaxis in close temporal association with lepirudin. All reactions occurred within minutes of intravenous lepirudin administration, with 4 fatal outcomes (3 acute cardiorespiratory arrests, 1 hypotension-induced myocardial infarction). In these 4 cases, a previous uneventful treatment course with lepirudin was identified (1 to 12 weeks earlier). We recorded high-titer IgG-anti-lepirudin antibodies in an additional patient with anaphylaxis. Because lepirudin has been used in approximate to35 000 patients, the risk of anaphylaxis is approximate to0.015% (5 of 32 500) on first exposure and 0.16% (4 of 2500) in reexposed patients (7.5% estimated reexposures). Conclusion - Lepirudin can cause fatal anaphylaxis, particularly in patients who are treated within 3 months of a previous exposure. The overall risk/benefit assessment of lepirudin as a treatment for heparin-induced thrombocytopenia remains favorable.	Univ Greifswald, Inst Immunol & Transfus Med, D-17489 Greifswald, Germany; Berlex Inc, Wayne, NJ 07470 USA	Greinacher, A (reprint author), Univ Greifswald, Inst Immunol & Transfus Med, Klinikum Sauerbruchstr, D-17489 Greifswald, Germany.						Bircher AJ, 1996, J ALLERGY CLIN IMMUN, V98, P994, DOI 10.1016/S0091-6749(96)80018-2; CLOSE P, 1994, CORONARY ARTERY DIS, V5, P943; Eichler P, 2000, BLOOD, V96, P2373; Greinacher A, 2003, BLOOD, V101, P2617, DOI 10.1182/blood-2002-04-1055; Greinacher A, 1999, CIRCULATION, V100, P587; Greinacher A, 1999, CIRCULATION, V99, P73; Greinacher A, 2001, CIRCULATION, V103, P1479; Harenberg J, 2000, BRIT J HAEMATOL, V108, P528; Huhle G, 1999, BRIT J HAEMATOL, V106, P195; KRAFT D, 1982, ALLERGY, V37, P481, DOI 10.1111/j.1398-9995.1982.tb02331.x; PROEBSTLE TM, 1995, J ALLERGY CLIN IMMUN, V95, P1059, DOI 10.1016/S0091-6749(95)70111-7; Song XH, 1999, CIRCULATION, V100, P1528; Warkentin TE, 1998, THROMB HAEMOSTASIS, V79, P1; WEISS ME, 1989, NEW ENGL J MED, V320, P886, DOI 10.1056/NEJM198904063201402	14	134	138	1	1	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	0009-7322			CIRCULATION	Circulation	OCT 28	2003	108	17					2062	2065		10.1161/01.CIR.0000096056.37269.14		4	Cardiac & Cardiovascular Systems; Peripheral Vascular Disease	Cardiovascular System & Cardiology	736TT	WOS:000186189800006	14568897	
J	Skoner, DP; Rachelefsky, GS; Meltzer, EO; Chervinsky, P; Morris, RM; Seltzer, JM; Storms, WW; Wood, RA				Skoner, DP; Rachelefsky, GS; Meltzer, EO; Chervinsky, P; Morris, RM; Seltzer, JM; Storms, WW; Wood, RA			Detection of growth suppression in children during treatment with intranasal beclomethasone dipropionate	PEDIATRICS			English	Article						beclomethasone dipropionate; intranasal corticosteroids; growth; allergic rhinitis; pediatric	ADRENAL AXIS SUPPRESSION; ALLERGIC RHINITIS; THERAPEUTIC EFFICACY; PREPUBERTAL CHILDREN; ASTHMATIC-CHILDREN; SHORT-TERM; BUDESONIDE; GLUCOCORTICOSTEROIDS; CORTICOSTEROIDS; PLACEBO	Objective. Intranasal beclomethasone dipropionate (BDP) has generally been considered to have no systemic activity at recommended doses, but the potential for long-term effects on growth has not previously been evaluated. This study was undertaken to assess the effects of 1 year of treatment with intranasal BDP on growth in children. Study Design. In this double-blind, randomized, parallel- group study, 100 prepubertal children 6 to 9 years old with perennial allergic rhinitis were treated with aqueous BDP 168 mu g twice daily (n = 51) or placebo (n = 49) for 1 year. Subjects' baseline heights were required to be between the 5th and 95th percentile, and skeletal age as determined by left wrist radiograph was required to be within 2 years of chronological age. Washout periods for medications known to affect growth, including other forms of corticosteroids, were established, and these medications were prohibited during the study. However, short courses of oral prednisolone lasting no more than 7 days, and short courses of dermatologic corticosteroids lasting no more than 10 days, were allowed. Height was measured with a stadiometer after 1, 2, 4, 6, 8, 10, and 12 months of treatment. The hypothalamic-pituitary-adrenocortical axis was assessed by measurements of 8 AM basal cortisol concentrations and response to .25 mg cosyntropin stimulation. The primary safety parameter was the rate of change in standing height. Statistical analyses were based on all randomized subjects who received at least 1 dose of medication (intent-to-treat principle). The rate of change in standing height was analyzed for all subjects who entered the study and for those completing the full 12 months of treatment (n = 80). The rate of change in standing height over the 1-year study was calculated as the slope of a linear regression line fitted to each subject's height measurements over time. Because there was a statistically significant between-group difference in standing height at baseline, an analysis of covariance was performed for all analyses of standing height data. Results. Of the 100 subjects enrolled, 90 completed the study. The 2 treatment groups were generally comparable at baseline; however, at baseline, mean age and mean height were significantly greater in the BDP treatment group that the in placebo treatment group. In both analyses, overall growth rate was significantly slower in BDP-treated subjects than placebo-treated subjects. The mean change in standing height after 1 year was 5.0 cm in the BDP-treated subjects compared with 5.9 cm in the placebo-treated subjects. The difference in growth rates was evident as early as the 1-month treatment visit, suggesting that the effect on growth occurred initially. The growth-suppressive effect of BDP remained consistent across all age and gender subgroups, and among subjects with and without a previous history of corticosteroid use. Use of additional exogenous corticosteroids during the study was similar in both groups and did not affect the results. Because there was a baseline imbalance in height, a supplemental analysis of the differences in prestudy growth rates was performed. This analysis found no baseline imbalance in prestudy growth rates. To determine whether the difference in growth rates during the study could be attributed to preexisting growth rates, a z score analysis was performed. The heights of both groups were normalized at baseline and at the end of the study using the US National Center for Health Statistics data for mean and standard deviations of height. This analysis confirmed that the difference in growth rates between the 2 groups was primarily attributable to the treatment rather than to any preexisting difference in growth. Additional analyses confirmed that the results were not influenced by outlier values. No significant between-group difference were found in the hypothalamic-pituitary-adrenocortical axis assessments. No unusual adverse events were observed. No evidence of other systemic effects of BDP was found, including analysis for fluid and electrolyte imbalances; alterations in protein, lipid, or carbohydrate metabolism; alterations in formed elements in blood; and alterations in differential white blood cell counts, including eosinophils. Conclusions. Additional study is warranted to define the clinical relevance of these findings. This study suggests, however, that intranasal BDP may slow growth rate in children without suppressing basal 6 AM cortisol concentrations or the response to cosyntropin stimulation, which are commonly used clinically to test for adrenal suppression. The effect on final height is unknown. Alterative explantations for the finding of drug-induced growth suppression, including the possibility that the results were affected by either differences in height and age at baseline between the 2 groups or by outlier values, were discounted upon additional analysis. The results of this study were considered by the Food and Drug Administration in the development of recently proposed new class labeling for all inhaled and intranasal corticosteroids, which states that these agents may cause a reduction in growth velocity in pediatric patients (see reference 21). However, both the Food and Drug Administration and several professional bodies in the United States concur that, depending on disease severity, the benefits of intranasal corticosteroid therapy may outweigh the risks (see reference 22). Because the effect, if any, on final height in not known, the height of children receiving long-term therapy should be monitored periodically during treatment, and should be plotted on a growth or growth-velocity chart to monitor for growth suppression. To minimize the risks of systemic corticosteroid exposure, including growth suppresson, dose-reduction strategies should be considered. For patients who concomitantly receive exogenous corticosteroids via other routes for other conditions, such as inhaled corticosteroids for asthma, clinicians should consider the total corticosteroid exposure and titrate each patient to the lowest effective dose. Clinicians should also consider each medication's potential for systemic effects when selecting among the various available corticosteroids.	Childrens Hosp, Pittsburgh, PA 15231 USA; Allergy Res Fdn, Los Angeles, CA USA; Allergy & Asthma Med Grp & Res Ctr, San Diego, CA USA; New England Res Ctr, N Dartmouth, MA USA; Park Nicollet Med Ctr, Minneapolis, MN USA; Clin Res Inst, San Diego, CA USA; Asthma & Allergy Associates, Colorado Springs, CO USA; Pediat Consultants, Lutherville Timonium, MD USA	Skoner, DP (reprint author), Childrens Hosp, 3705 5th Ave, Pittsburgh, PA 15231 USA.						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J	Sorkness, RL; Bleecker, ER; Busse, WW; Calhoun, WJ; Castro, M; Chung, KF; Curran-Everett, D; Erzurum, SC; Gaston, BM; Israel, E; Jarjour, NN; Moore, WC; Peters, SP; Teague, WG; Wenzel, SE				Sorkness, Ronald L.; Bleecker, Eugene R.; Busse, William W.; Calhoun, William J.; Castro, Mario; Chung, Kian Fan; Curran-Everett, Douglas; Erzurum, Serpil C.; Gaston, Benjamin M.; Israel, Elliot; Jarjour, Nizar N.; Moore, Wendy C.; Peters, Stephen P.; Teague, W. Gerald; Wenzel, Sally E.		Natl Heart Lung Blood Inst Severe	Lung function in adults with stable but severe asthma: air trapping and incomplete reversal of obstruction with bronchodilation	JOURNAL OF APPLIED PHYSIOLOGY			English	Article						airway closure; difficult asthma; fixed obstruction	CHRONIC PERSISTENT ASTHMA; ELASTIC RECOIL; NOCTURNAL ASTHMA; FLOW OBSTRUCTION; RESEARCH-PROGRAM; REFERENCE VALUES; RESIDUAL VOLUME; EXPIRATORY FLOW; SMOOTH-MUSCLE; DISTAL LUNG	Five to ten percent of asthma cases are poorly controlled chronically and refractory to treatment, and these severe cases account for disproportionate asthma-associated morbidity, mortality, and health care utilization. While persons with severe asthma tend to have more airway obstruction, it is not known whether they represent the severe tail of a unimodal asthma population, or a severe asthma phenotype. We hypothesized that severe asthma has a characteristic physiology of airway obstruction, and we evaluated spirometry, lung volumes, and reversibility during a stable interval in 287 severe and 382 nonsevere asthma subjects from the National Heart, Lung, and Blood Institute Severe Asthma Research Program. We partitioned airway obstruction into components of air trapping [indicated by forced vital capacity (FVC)] and airflow limitation [indicated by forced expiratory volume in 1 s (FEV1)/FVC]. Severe asthma had prominent air trapping, evident as reduced FVC over the entire range of FEV1/FVC. This pattern was confirmed with measures of residual lung volume/total lung capacity (TLC) in a subgroup. In contrast, nonsevere asthma did not exhibit prominent air trapping, even at FEV1/FVC <75% predicted. Air trapping also was associated with increases in TLC and functional reserve capacity. After maximal bronchodilation, FEV1 reversed similarly from baseline in severe and nonsevere asthma, but the severe asthma classification was an independent predictor of residual reduction in FEV1 after maximal bronchodilation. An increase in FVC accounted for most of the reversal of FEV1 when baseline FEV1 was <60% predicted. We conclude that air trapping is a characteristic feature of the severe asthma population, suggesting that there is a pathological process associated with severe asthma that makes airways more vulnerable to this component.	[Sorkness, Ronald L.; Busse, William W.; Jarjour, Nizar N.] Univ Wisconsin, Madison, WI 53705 USA; [Bleecker, Eugene R.; Moore, Wendy C.; Peters, Stephen P.] Wake Forest Univ, Winston Salem, NC 27109 USA; [Calhoun, William J.] Univ Pittsburgh, Pittsburgh, PA USA; [Calhoun, William J.] Univ Texas Galveston, Med Branch, Galveston, TX 77550 USA; [Castro, Mario] Washington Univ, St Louis, MO USA; [Chung, Kian Fan] Univ London Imperial Coll Sci Technol & Med, London, England; [Curran-Everett, Douglas; Wenzel, Sally E.] Natl Jewish Med & Res Ctr, Denver, CO USA; [Erzurum, Serpil C.] Cleveland Clin, Cleveland, OH 44106 USA; [Gaston, Benjamin M.] Univ Virginia, Charlottesville, VA USA; [Israel, Elliot] Brigham & Womens Hosp, Boston, MA 02115 USA; [Teague, W. Gerald] Emory Univ, Atlanta, GA 30322 USA	Sorkness, RL (reprint author), Univ Wisconsin, 777 Highland Ave, Madison, WI 53705 USA.	rlsorkne@wisc.edu		Chung, Kian Fan/0000-0001-7101-1426	NCATS NIH HHS [UL1 TR000005]; NCRR NIH HHS [M01-RR-007122-14, M01-RR-018390, M01-RR-03186]; NHLBI NIH HHS [HL-69116, HL-69130, HL-69149, HL-69155, HL-69167, HL-69170, HL-69174, HL-69349]		Abraham B, 2003, EUR RESPIR J, V22, P470, DOI 10.1183/09031936.03.00261903; American Thoracic Society, 1991, AM REV RESPIR DIS, V144, P1202, DOI 10.1164/ajrccm/144.5.1202; American Thoracic Society, 2000, AM J RESP CRIT CARE, V162, P2341, DOI DOI 10.1164/AJRCCM.162.6.ATS9-00; Brown RH, 2006, J APPL PHYSIOL, V101, P30, DOI 10.1152/japplphysiol.01190.2005; Bumbacea D, 2004, EUR RESPIR J, V24, P122, DOI 10.1183/09031936.04.00077803; Cassino C, 2000, AM J RESP CRIT CARE, V162, P1423; Cockcroft DW, 2006, J ALLERGY CLIN IMMUN, V117, P1244, DOI 10.1016/j.jaci.2006.02.038; Crapo RO, 2000, AM J RESP CRIT CARE, V161, P309; de Lange EE, 2006, CHEST, V130, P1055, DOI 10.1378/chest.130.4.1055; DING DJ, 1987, J APPL PHYSIOL, V62, P1324; Fitzpatrick AM, 2006, J ALLERGY CLIN IMMUN, V118, P1218, DOI 10.1016/j.jaci.2006.08.019; Gelb AF, 2000, AM J RESP CRIT CARE, V162, P1778; Gelb AF, 2002, CHEST, V121, P715, DOI 10.1378/chest.121.3.715; Gibbons WJ, 1996, AM J RESP CRIT CARE, V153, P582; GOLD WM, 1967, J APPL PHYSIOL, V23, P433; Hankinson JL, 1999, AM J RESP CRIT CARE, V159, P179; Hill MJ, 1997, J APPL PHYSIOL, V82, P233; In't Veen CCM, 2000, AM J RESP CRIT CARE, V161, P1902; Irvin CG, 2000, AM J RESP CRIT CARE, V161, P50; Jarjour NN, 1999, AM J RESP CRIT CARE, V160, P336; Kaminsky DA, 2000, AM J RESP CRIT CARE, V162, P179; KAMM RD, 1989, RESP PHYSIOL, V75, P141, DOI 10.1016/0034-5687(89)90059-5; King GG, 1998, AM J RESP CRIT CARE, V158, P1900; Kraft M, 2001, AM J RESP CRIT CARE, V163, P1551; LEITH DE, 1967, J APPL PHYSIOL, V23, P221; Lutchen KR, 2001, AM J RESP CRIT CARE, V164, P207; Mackay LG, 2003, ACCREDIT QUAL ASSUR, V8, P191, DOI 10.1007/s00769-003-0622-z; Macklem PT, 1996, AM J RESP CRIT CARE, V153, P83; Mauad T, 2004, AM J RESP CRIT CARE, V170, P857, DOI 10.1164/rccm.200403-305OC; MCCARTHY DS, 1980, THORAX, V35, P298, DOI 10.1136/thx.35.4.298; MEAD J, 1967, J APPL PHYSIOL, V22, P95; Miller MK, 2005, J ALLERGY CLIN IMMUN, V116, P990, DOI 10.1016/j.jaci.2005.08.018; Miller MR, 2005, EUR RESPIR J, V26, P319, DOI 10.1183/09031936.05.00034805; Moore WC, 2006, J ALLERGY CLIN IMMUN, V117, P487, DOI 10.1016/j.jaci.2006.01.033; Moore WC, 2007, J ALLERGY CLIN IMMUN, V119, P405, DOI 10.1016/j.jaci.2006.11.639; Pellegrino R, 2005, EUR RESPIR J, V26, P948, DOI 10.1183/09031936.05.00035205; PRIDE NB, 1967, J APPL PHYSIOL, V23, P646; Sont JK, 1999, AM J RESP CRIT CARE, V159, P1043; STOCKS J, 1995, EUR RESPIR J, V8, P492, DOI 10.1183/09031936.95.08030492; STREK ME, 2001, AM J RESP CRIT CARE, V164, P744; Verbanck S, 2003, J APPL PHYSIOL, V94, P1380, DOI 10.1152/japplphysiol.00588.2002; Wagers S, 2004, J APPL PHYSIOL, V96, P2019, DOI 10.1152/japplphysiol.00924.2003; Wagers SS, 2004, J CLIN INVEST, V114, P104, DOI 10.1172/JC1200419569; WAGNER EM, 1990, AM REV RESPIR DIS, V141, P584; Wanger J, 2005, EUR RESPIR J, V26, P511, DOI 10.1183/09031936.05.00035005; WEMPE JB, 1992, J ALLERGY CLIN IMMUN, V89, P679, DOI 10.1016/0091-6749(92)90374-B; Wenzel S, 2005, AM J RESP CRIT CARE, V172, P149, DOI 10.1164/rccm.200409-1181PP; Wenzel SE, 2007, J ALLERGY CLIN IMMUN, V119, P14, DOI 10.1016/j.jaci.2006.10.025; Wenzel SE, 1999, AM J RESP CRIT CARE, V160, P1001; Wenzel SE, 1997, AM J RESP CRIT CARE, V156, P737; WOOLCOCK AJ, 1968, AM REV RESPIR DIS, V98, P788	51	133	137	0	6	AMER PHYSIOLOGICAL SOC	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	8750-7587			J APPL PHYSIOL	J. Appl. Physiol.	FEB	2008	104	2					394	403		10.1152/japplphysiol.00329.2007		10	Physiology; Sport Sciences	Physiology; Sport Sciences	260PO	WOS:000253022500010	17991792	
J	Camargo, CA; Clark, S; Kaplan, MS; Lieberman, P; Wood, RA				Camargo, Carlos A., Jr.; Clark, Sunday; Kaplan, Michael S.; Lieberman, Philip; Wood, Robert A.			Regional differences in EpiPen prescriptions in the United States: The potential role of vitamin D	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						anaphylaxis; epidemiology; EpiPen; vitamin D	REGULATORY T-CELLS; SUN EXPOSURE; ANAPHYLAXIS; EPIDEMIOLOGY; POPULATION; ALLERGY; MELANOMA; CHILDREN; RISK; D-3	Background: The epidemiology of anaphylaxis is uncertain, especially its geographic distribution. Objective: To address this deficit, we examined regional rates of EpiPen prescriptions in the United States. Methods: EpiPen prescriptions in 2004 were obtained for all 50 states and Washington, DC, from NDCHealth, Pharmaceutical Audit Suite (Alpharetta, Ga). Data included the number of total filled prescriptions, including refills, and the actual number of EpiPens prescribed. Several data sets were used to obtain state-specific populations, as well as multiple demographic, health, and weather characteristics. State population was used to calculate the average number of prescriptions written per person. Results: Overall, there were 1,511,534 EpiPen prescriptions filled during 2004. These prescriptions accounted for 2,495,188 EpiPens. On average, there were 5.71 EpiPens prescribed per 1000 persons. Massachusetts had the highest number of prescriptions per 1000 persons (11.8), whereas Hawaii had the lowest (2.7). In addition to state-to-state variation, there was an obvious regional difference: New England (Connecticut, Rhode Island, Massachusetts, Vermont, New Hampshire, Maine) had the highest values, with 8 to 12 EpiPen prescriptions per 1000 persons, whereas the southern states (between and including California and Mississippi) had only 3 prescriptions per 1000 persons. The New England finding persisted even when controlling for all available factors (eg, population demographic characteristics, number of health care providers, prescriptions for other medications). Conclusion: A strong north-south gradient was observed for the prescription of EpiPens in the United States, with the highest rates found in New England. Clinical implications: The regional differences in EpiPen prescribing may provide important etiologic clues (vitamin D status) and merit further investigation.	Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr D Receptor Activat Res, Boston, MA 02114 USA; Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA; Kaiser Permanente, Dept Allergy, Los Angeles, CA USA; Univ Tennessee, Coll Med, Memphis, TN 38163 USA; Johns Hopkins Med Ctr, Dept Pediat, Div Pediat Allergy & Immunol, Baltimore, MD USA	Camargo, CA (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr D Receptor Activat Res, 326 Cambridge St,Suite 410, Boston, MA 02114 USA.	ccamargo@partners.org	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Annesi-Maesano I, 2002, PEDIATR RES, V52, P3, DOI 10.1023/01.PDR/0000017228.29635.EF; Bohlke K, 2004, J ALLERGY CLIN IMMUN, V113, P536, DOI 10.1016/j.jaci.2003.11.033; Brown SJ, 2006, ANN PHARMACOTHER, V40, P1158, DOI 10.1345/aph.1G513; Camargo CA, 2007, AM J CLIN NUTR, V85, P788; Cantorna MT, 2004, AM J CLIN NUTR, V80, p1717S; Centers for Disease Control and Prevention, 2006, BEH RISK FACT SURV S; Estelle F, 2006, J ALLERGY CLIN IMMUN, V117, P367, DOI 10.1016/j.jaci.2005.12.002; Gregori S, 2002, DIABETES, V51, P1367, DOI 10.2337/diabetes.51.5.1367; Griffin MD, 2003, ANNU REV NUTR, V23, P117, DOI 10.1146/annurev.nutr.23.011702.073114; Gupta R, 2004, CLIN EXP ALLERGY, V34, P520, DOI 10.1111/j.1365-2222.2004.1935.x; Hernan MA, 1999, NEUROLOGY, V53, P1711; Hollis BW, 2005, J NUTR, V135, P317; Ivry GB, 2006, DERMATOL SURG, V32, P481, DOI 10.1111/j.1524-4725.2006.32101.x; Jemal A, 2004, CA-CANCER J CLIN, V54, P8; Lieberman P, 2006, ANN ALLERG ASTHMA IM, V97, P596; Lin R, 2004, BIOESSAYS, V26, P21, DOI 10.1002/bies.10368; MEEHAN MA, 1992, CELL IMMUNOL, V140, P400, DOI 10.1016/0008-8749(92)90206-5; Neugut AI, 2001, ARCH INTERN MED, V161, P15, DOI 10.1001/archinte.161.1.15; Oliveria SA, 2006, ARCH DIS CHILD, V91, P131, DOI 10.1136/adc.2005.086918; Peng MM, 2004, ARCH INTERN MED, V164, P317, DOI 10.1001/archinte.164.3.317; Pichler J, 2002, PEDIATR RES, V52, P12, DOI 10.1023/01.PDR.0000017267.23950.48; Feldman D, 2005, VITAMIN D: VOLS 1 AND 2, 2ND EDITION, P1; Schwartz RH, 2005, NAT IMMUNOL, V6, P327, DOI 10.1038/ni1184; Simons FER, 2002, J ALLERGY CLIN IMMUN, V110, P647, DOI 10.1067/mai.2002.127860; Thomas MK, 1998, NEW ENGL J MED, V338, P777, DOI 10.1056/NEJM199803193381201; WEBB AR, 1988, J CLIN ENDOCR METAB, V67, P373; Yocum MW, 1999, J ALLERGY CLIN IMMUN, V104, P452, DOI 10.1016/S0091-6749(99)70392-1; 2006, US CENSUS BUREAU WEB; 2006, NOAA WEB SITE	29	133	135	1	7	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749	1097-6825		J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUL	2007	120	1					131	136		10.1016/j.jaci.2007.03.049		6	Allergy; Immunology	Allergy; Immunology	190NS	WOS:000248066400019	17559916	
J	Kozyrskyj, AL; Ernst, P; Becker, AB				Kozyrskyj, Anita L.; Ernst, Pierre; Becker, Allan B.			Increased risk of childhood asthma from antibiotic use in early life	CHEST			English	Article						antibacterial agents; asthma; child; infant	INTESTINAL MICROFLORA; ATOPIC-DERMATITIS; 1ST YEAR; ALLERGIC DISEASE; ORAL ANTIBIOTICS; SWEDISH INFANTS; BIRTH COHORT; SCHOOL-AGE; CHILDREN; EXPOSURE	Background: To address the major methodological issues of reverse causation and selection bias in epidemiologic studies of antibiotic use in early life and the development of asthma, we undertook a cohort study of this association in a complete population of children. Methods: Using the health-care and prescription databases of Manitoba, Canada, this longitudinal study assessed the association between antibiotic prescription use during the first year of life and asthma at age 7 years in a 1995 birth cohort of 13,116 children. Results: Independent of well-known asthma risk factors, asthma was significantly more likely to develop in children who had received antibiotics in the first year of life at age 7 years. The association with asthma was observed for antibiotic use in non-respiratory tract infections (adjusted odds ratio [OR], 1.86; 95% confidence interval [CI], 1.02 to 3.37). The risk of asthma was highest in children receiving more than four courses of antibiotics (adjusted OR, 1.46; 95% CI, 1.14 to 1.88), especially among rural children, and in the absence of maternal asthma or a dog in the birth year. Broad-spectrum (BS) cephalosporin use was more common in these sub-populations of children. Conclusions: Antibiotic use in early life was associated with the development of childhood asthma, a risk that may be reduced by avoiding the use of BS cephalosporins.	Univ Manitoba, Fac Pharm, Winnipeg, MB R3T 2N2, Canada; Royal Victoria Hosp, Div Clin Epidemiol, Montreal, PQ H3A 1A1, Canada; Univ Manitoba, Fac Med, Dept Pediat & Child Hlth, Winnipeg, MB, Canada	Kozyrskyj, AL (reprint author), 210 Pharm Bldg, Winnipeg, MB R3T 2N2, Canada.	kozyrsk@cc.umanitoba.ca					Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Bennet R, 2002, INFECTION, V30, P158, DOI 10.1007/s15010-002-2140-z; BENNET R, 1991, SCAND J INFECT DIS, V23, P63, DOI 10.3109/00365549109023376; Bjorksten B, 2001, J ALLERGY CLIN IMMUN, V108, P516; Bjorksten B, 1999, CLIN EXP ALLERGY, V29, P342; Bohme M, 2002, ACTA DERM-VENEREOL, V82, P98, DOI 10.1080/00015550252948112; Bonnemaison E, 2003, BIOL NEONATE, V84, P304, DOI 10.1159/000073639; Bottcher MF, 2000, CLIN EXP ALLERGY, V30, P1590; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Celedon JC, 2004, CLIN EXP ALLERGY, V34, P1011, DOI 10.1111/j.1365-2222.2004.01994.x; Celedon JC, 2002, AM J RESP CRIT CARE, V166, P72, DOI 10.1164/rccm.2109074; Cohet C, 2004, J EPIDEMIOL COMMUN H, V58, P852, DOI 10.1136/jech.2003.019182; Droste JHJ, 2000, CLIN EXP ALLERGY, V30, P1547; Edlund C, 2000, J ANTIMICROB CHEMOTH, V46, P41, DOI 10.1093/jac/46.suppl_1.41; Ernst P, 2000, AM J RESP CRIT CARE, V161, P1563; Farooqi IS, 1998, THORAX, V53, P927; Illi S, 2001, BRIT MED J, V322, P390, DOI 10.1136/bmj.322.7283.390; Johnson CC, 2005, J ALLERGY CLIN IMMUN, V115, P1218, DOI 10.1016/j.jaci.2005.04.020; Kalliomaki M, 2003, LANCET, V361, P1869, DOI 10.1016/S0140-6736(03)13490-3; Kalliomaki M, 2001, J ALLERGY CLIN IMMUN, V107, P129, DOI 10.1067/mai.2001.111237; Kozyrskyj AL, 2004, CAN MED ASSOC J, V171, P133, DOI 10.1503/cmaj.1031630; Kozyrskyj AL, 1998, ANN PHARMACOTHER, V32, P1152, DOI 10.1345/aph.18117; KOZYRSKYJ AL, 2005, J ALLERGY CLIN IMMUN, V115, P173; KOZYRSKYJ AL, 2005, ALLERGY ASTHMA CLIN, V1, P108; Liu AH, 2003, J ALLERGY CLIN IMMUN, V111, P471, DOI 10.1067/mai.2003.172; Macpherson AJ, 2004, NAT REV IMMUNOL, V4, P478, DOI 10.1038/nri1373; MANFREDA J, 1993, CHEST, V103, P151, DOI 10.1378/chest.103.1.151; Marra F, 2006, CHEST, V129, P610, DOI 10.1378/chest.129.3.610; MARTINEZ F, 1999, LANCET S2, V354, P112; Masoli M, 2004, ALLERGY, V59, P469, DOI 10.1111/j.1398-9995.2004.00526.x; Mattes J, 1999, CLIN EXP ALLERGY, V29, P729; McCaig LF, 2002, JAMA-J AM MED ASSOC, V287, P3096, DOI 10.1001/jama.287.23.3096; McKeever TM, 2002, J ALLERGY CLIN IMMUN, V109, P43, DOI 10.1067/mai.2002.121016; Merchant JA, 2005, ENVIRON HEALTH PERSP, V113, P350, DOI 10.1289/ehp.7240; Noverr MC, 2005, CLIN EXP ALLERGY, V35, P1511, DOI 10.1111/j.1365-2222.2005.02379.x; Noverr MC, 2005, INFECT IMMUN, V73, P30, DOI 10.1128/IAI.73.1.30-38.2005; Oyama N, 2001, J ALLERGY CLIN IMMUN, V107, P153, DOI 10.1067/mai.2001.111142; Palmer CNA, 2006, NAT GENET, V38, P441, DOI 10.1038/ng1767; Pekkanen J, 1999, EUR RESPIR J, V14, P951, DOI 10.1034/j.1399-3003.1999.14d37.x; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; Remes ST, 2001, J ALLERGY CLIN IMMUN, V108, P509, DOI 10.1067/mai.2001.117797; Robinson JR, 1997, MED CARE, V35, P932, DOI 10.1097/00005650-199709000-00006; Schumann A, 2005, PHYSIOL GENOMICS, V23, P235, DOI 10.1152/physiolgenomics.00057.2005; Sepp E, 1997, ACTA PAEDIATR, V86, P956, DOI 10.1111/j.1651-2227.1997.tb15178.x; Thomas M, 2006, PEDIATR ALLERGY IMMU, V17, P184, DOI 10.1111/j.1399-3038.2006.00389.x; von Mutius E, 2004, J ALLERGY CLIN IMMUN, V113, P373, DOI 10.1016/j.jaci.2003.12.040; von Mutius E, 1999, EUR RESPIR J, V14, P4, DOI 10.1034/j.1399-3003.1999.14a03.x; Voor T, 2005, CLIN EXP ALLERGY, V35, P153, DOI 10.1111/j.1365-2222.2005.02157.x; Weiss KB, 2001, J ALLERGY CLIN IMMUN, V107, P3, DOI 10.1067/mai.2001.112262; Wickens K, 1999, CLIN EXP ALLERGY, V29, P766	50	133	152	2	19	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	JUN	2007	131	6					1753	1759		10.1378/chest.06-3008		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	180CD	WOS:000247336600023	17413050	
J	von Mutius, E				von Mutius, Erika			Allergies, infections and the hygiene hypothesis - The epidemiological evidence	IMMUNOBIOLOGY			English	Article						hygiene hypothesis; epidemiology; allergy; infection	EARLY BCG VACCINATION; SCHOOL-AGE-CHILDREN; DAY-CARE ATTENDANCE; ATOPIC DISEASE; BIRTH COHORT; EARLY-LIFE; FARMERS CHILDREN; EARLY-CHILDHOOD; HAY-FEVER; 1ST YEAR	The 'hygiene hypothesis' was first proposed by Strachan in 1989 suggesting that infections and unhygienic contact with older siblings or through other exposures may confer protection from the development of allergic illnesses. This hypothesis has evolved in various ways exploring the role of overt viral and bacterial infections, the significance of environmental exposure to microbial compounds, and their effect on underlying responses of innate and adaptive immunity. So far a truly unifying concept is still lacking, but various pieces of a complex interplay between a host's immune response, characteristics of the invading microorganism, the level and variety of the environmental exposure, and the interactions between a genetic background and a range of exposures become apparent. All these pieces eventually assemble to the clinical presentation of a complex syndrome namely of asthma and allergic illnesses. Even if today practical implications cannot directly be deduced from these findings, there is great potential for the development of novel preventive and therapeutic strategies in the future based on the concepts of the 'hygiene hypothesis'. (C) 2007 Elsevier GmbH. All rights reserved.	Univ Munich, Childrens Hosp, D-80337 Munich, Germany	von Mutius, E (reprint author), Univ Munich, Childrens Hosp, Lindwurmstr 4, D-80337 Munich, Germany.	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J	Eduard, W; Douwes, J; Omenaas, E; Heederik, D				Eduard, W; Douwes, J; Omenaas, E; Heederik, D			Do farming exposures cause or prevent asthma? Results from a study of adult Norwegian farmers	THORAX			English	Article							RESPIRATORY SYMPTOMS; DANISH FARMERS; HAY-FEVER; ALLERGIC SENSITIZATION; OCCUPATIONAL EXPOSURE; CHRONIC-BRONCHITIS; CHILDREN; PREVALENCE; ENDOTOXIN; DUST	Background: A protective effect of endotoxin exposure on atopy and asthma in farmers' children has been postulated. Studies of adult farmers have shown conflicting results but often lack exposure data. The prevalence of asthma in farmers with different exposure levels to microbial agents and irritant gases was compared. Methods: Atopy was defined as a positive response to multiple radioallergosorbent tests (RAST) with a panel of 10 common respiratory allergens, and asthma was ascertained by a questionnaire using a stratified sample (n = 2169) of a farming population from south-eastern Norway. Exposure of farmers to total dust, fungal spores, bacteria, endotoxins, and ammonia was assessed by exposure measurements. Results: The prevalence of asthma was 3.7% for physician diagnosed asthma and 2.7% for current asthma. The prevalence of atopy was 14%, but most asthmatic subjects were non-atopic (80%). Compared with farmers without livestock, ( 1) asthma was significantly higher in cattle farmers (ORadj 1.8, 95% CI 1.1 to 2.8) and pig farmers (ORadj 1.6, 95% CI 1.0 to 2.5), (2) non-atopic asthma was significantly higher in pig farmers (ORadj 2.0, 95% CI 1.2 to 3.3) and in farmers with two or more types of livestock (ORadj 1.9, 95% CI 1.1 to 3.3), and ( 3) atopic asthma was less common in farmers with two or more types of livestock (ORadj 0.32, 95% CI 0.11 to 0.97). Exposure to endotoxins, fungal spores, and ammonia was positively associated with non-atopic asthma and negatively associated with atopic asthma. No associations were found with atopy. Conclusions: Exposure to endotoxins and fungal spores appears to have a protective effect on atopic asthma but may induce non-atopic asthma in farmers.	Natl Inst Occupat Hlth, N-0033 Oslo, Norway; Univ Utrecht, Inst Risk Assessment Sci, NL-3508 TC Utrecht, Netherlands; Massey Univ, Ctr Publ Hlth Res, Wellington, New Zealand; Univ Bergen, Inst Med, N-5020 Bergen, Norway	Eduard, W (reprint author), Natl Inst Occupat Hlth, POB 8149, N-0033 Oslo, Norway.	wijnand.eduard@stami.no		Douwes, Jeroen/0000-0003-3599-4036			BAKKE P, 1990, SCAND J WORK ENV HEA, V16, P195; BAKKE P, 1991, EUR RESPIR J, V4, P273; BLAINEY AD, 1988, THORAX, V43, P697, DOI 10.1136/thx.43.9.697; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Court CS, 2002, THORAX, V57, P951, DOI 10.1136/thorax.57.11.951; Douwes J, 2002, THORAX, V57, P86, DOI 10.1136/thorax.57.1.86; DOUWES J, 1995, APPL ENVIRON MICROB, V61, P1763; Douwes J, 2002, THORAX, V57, P643, DOI 10.1136/thorax.57.7.643; Downs SH, 2001, CLIN EXP ALLERGY, V31, P570, DOI 10.1046/j.1365-2222.2001.01070.x; Eduard W, 2001, OCCUP ENVIRON MED, V58, P113, DOI 10.1136/oem.58.2.113; Eduard W, 1988, ANN OCCUP HYG, V32, P447; EDUARD W, 1999, NOR J EPIDEMIOL, V142, P43; Fishwick D, 1997, OCCUP ENVIRON MED, V54, P301; HAMSTEN MV, 1987, CLIN EXP ALLERGY, V17, P417; Heldal K, 1996, ANN OCCUP HYG, V40, P437, DOI 10.1016/0003-4878(95)00089-5; IVERSEN M, 1988, THORAX, V43, P872, DOI 10.1136/thx.43.11.872; IVERSEN M, 1990, ALLERGY, V45, P347, DOI 10.1111/j.1398-9995.1990.tb00510.x; Klintberg B, 2001, EUR RESPIR J, V17, P1151, DOI 10.1183/09031936.01.00027301; Martinez FD, 1999, LANCET S2, V354, pSII12; Melbostad E, 1997, SCAND J WORK ENV HEA, V23, P271; Melbostad E, 2001, AM J IND MED, V39, P209, DOI 10.1002/1097-0274(200102)39:2<209::AID-AJIM1008>3.0.CO;2-5; OMENAAS E, 1994, CLIN EXP ALLERGY, V24, P530, DOI 10.1111/j.1365-2222.1994.tb00950.x; Omland O, 1999, EUR RESPIR J, V13, P31, DOI 10.1183/09031936.99.13103199; Portengen L, 2002, CLIN EXP ALLERGY, V32, P247, DOI 10.1046/j.1365-2222.2002.01310.x; Preller L, 1995, SCAND J WORK ENV HEA, V21, P504; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Steenland K, 2000, SCAND J WORK ENV HEA, V26, P37; Toren K, 1996, OCCUP ENVIRON MED, V53, P757; TOREN K, 1991, BRIT J IND MED, V48, P323; Vogelzang PFJ, 1999, EUR RESPIR J, V13, P187, DOI 10.1034/j.1399-3003.1999.13a34.x; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, J ALLERGY CLIN IMMUN, V105, P9, DOI 10.1016/S0091-6749(00)90171-4	33	133	135	0	9	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	MAY 1	2004	59	5					381	386		10.1136/thx.2004.013326		6	Respiratory System	Respiratory System	815WQ	WOS:000221072800007	15115863	
J	Ryu, JH; Myers, J; Swenson, SJ				Ryu, JH; Myers, J; Swenson, SJ			Bronchiolar disorders	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Review						bronchiolitis; bronchiolitis obliterans; organizing pneumonia	INTERSTITIAL LUNG-DISEASE; OBLITERANS ORGANIZING PNEUMONIA; HIGH-RESOLUTION CT; LANGERHANS-CELL HISTIOCYTOSIS; IDIOPATHIC PULMONARY FIBROSIS; RESPIRATORY SYNCYTIAL VIRUS; SMALL AIRWAYS DISEASES; AIR-FLOW OBSTRUCTION; THIN-SECTION CT; DIFFUSE PANBRONCHIOLITIS	Bronchiolar abnormalities are relatively common and occur in a variety of clinical settings. Various histopathologic patterns of bronchiolar injury have been described and have led to confusing nomenclature with redundant and overlapping terms. Some histopathologic patterns of bronchiolar disease may be relatively unique to a specific clinical context but others are nonspecific with respect to either etiology or pathogenesis. Herein, we present a scheme separating (1) those disorders in which the bronchiolar disease is the predominant abnormality (primary bronchiolar disorders) from (2) parenchymal disorders with prominent bronchiolar involvement and (3) bronchiolar involvement in large airway diseases. Primary bronchiolar disorders include constrictive bronchiolitis (obliterative bronchiolitis, bronchiolitis obliterans), acute bronchiolitis, diffuse panbronchiolitis, respiratory bronchiolitis, mineral dust airway disease, follicular bronchiolitis, and a few other rare variants. Prominent bronchiolar involvement may be seen in several interstitial lung diseases, including hypersensitivity pneumonitis, respiratory bronchiolitis-associated interstitial lung disease, cryptogenic organizing pneumonia (idiopathic bronchiolitis obliterans organizing pneumonia), and pulmonary Langerhans' cell histiocytosis. Large airway diseases that commonly involve bronchioles include bronchiectasis, asthma, and chronic obstructive pulmonary disease. The clinical relevance of a bronchiolar lesion is best determined by identifying the underlying histopathologic pattern and assessing the correlative clinico-physiologic-radiologic context.	Mayo Clin, Div Pulm & Crit Care Med, Rochester, MN 55905 USA; Mayo Clin, Dept Lab Med & Pathol, Rochester, MN 55905 USA; Mayo Clin, Dept Radiol, Rochester, MN 55905 USA	Ryu, JH (reprint author), Mayo Clin, Div Pulm & Crit Care Med, Desk E 18,200 1st St SW, Rochester, MN 55905 USA.						AGUAYO SM, 1992, NEW ENGL J MED, V327, P1285, DOI 10.1056/NEJM199210293271806; AKIRA M, 1989, RADIOLOGY, V171, P117; American Thoracic Society European Respiratory Society. 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Vassallo R, 2000, NEW ENGL J MED, V342, P1969, DOI 10.1056/NEJM200006293422607; Wang JS, 2000, HISTOPATHOLOGY, V37, P402, DOI 10.1046/j.1365-2559.2000.00990.x; WELLS AU, 1993, CLIN CHEST MED, V14, P655; Wells AU, 2001, SEM RESP CRIT CARE M, V22, P449, DOI 10.1055/s-2001-17387; WILCOX P, 1987, CHEST, V92, P18, DOI 10.1378/chest.92.1.18; WRIGHT JL, 1992, AM REV RESPIR DIS, V146, P240; WRIGHT JL, 1993, CLIN CHEST MED, V14, P635; Yanagihara K, 2001, INT J ANTIMICROB AG, V18, pS83; Yousem SA, 1997, MODERN PATHOL, V10, P864; YOUSEM SA, 1985, HUM PATHOL, V16, P700, DOI 10.1016/S0046-8177(85)80155-6; Yousem SA, 2002, MODERN PATHOL, V15, P1148, DOI 10.1097/01.MP.0000037309.04985.B4; YOUSEM SA, 1989, MAYO CLIN PROC, V64, P1373; YOUSEM SA, 1989, TRANSPLANTATION, V47, P893, DOI 10.1097/00007890-198905000-00030	164	133	156	0	6	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	DEC 1	2003	168	11					1277	1292		10.1164/rccm.200301.053SO		16	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	747KU	WOS:000186804300008	14644923	
J	Gilbert, NL; Woodhouse, S; Stieb, DM; Brook, JR				Gilbert, NL; Woodhouse, S; Stieb, DM; Brook, JR			Ambient nitrogen dioxide and distance from a major highway	SCIENCE OF THE TOTAL ENVIRONMENT			English	Article						air pollution; nitrogen dioxide; NO2; passive monitoring; traffic	AIR-POLLUTION; ASTHMA; MOTORWAYS	The primary objective of this pilot study was to measure the variation of ambient nitrogen dioxide (NO2) concentration with increasing distance from a major highway in Montreal, Canada, in order to assess the validity of distance from the roadways as a surrogate for exposure to traffic-related air pollution in epidemiologic studies. A total of 31 two-sided Ogawa(TM) passive samplers (using triethanolamine-impregnated filters as an absorbent) were installed for 7 days in groups of two or three along an axis perpendicular to a major highway where traffic density exceeds 100 000 vehicles/day. Distances ranged from 0 to 1310 m from the highway. Concentrations of NO2 ranged from 11.9 to 29.3 ppb, and decreased significantly with increasing logarithmic distance from the highway (P < 0.0001). Concentrations of NO2 were also significantly lower upwind than downwind relative to the highway (P= 0.0012). These findings indicate that distance from highways may be a valid surrogate for traffic-related air pollution. (C) 2003 Elsevier Science B.V. All rights reserved.	Hlth Canada, Air Hlth Effects Div, Ottawa, ON K1A 0L2, Canada; Environm Canada, Ctr Atmospher Res Expt, Egbert, ON, Canada; Environm Canada, Meteorol Serv Canada, Toronto, ON, Canada	Gilbert, NL (reprint author), Hlth Canada, Air Hlth Effects Div, 7th Floor,275 Slater St,PL 3807B, Ottawa, ON K1A 0L2, Canada.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Gilbert, Nicolas/0000-0001-6985-8046			Briggs DJ, 1997, INT J GEOGR INF SCI, V11, P699, DOI 10.1080/136588197242158; Briggs DJ, 2000, SCI TOTAL ENVIRON, V253, P151, DOI 10.1016/S0048-9697(00)00429-0; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; English P, 1999, ENVIRON HEALTH PERSP, V107, P761, DOI 10.2307/3434663; *GOV QUEB, 1996, DEB CIRC JOURN MOYEN; Hoek G, 2002, LANCET, V360, P1203, DOI 10.1016/S0140-6736(02)11280-3; LIARD R, 1999, ENVIRON RES, V81, P331; Livingstone AE, 1996, BRIT MED J, V312, P676; PALMES ED, 1976, AM IND HYG ASSOC J, V37, P570, DOI 10.1080/0002889768507522; RODES CE, 1981, ATMOS ENVIRON, V15, P243, DOI 10.1016/0004-6981(81)90024-X; Roorda-Knape MC, 1999, SCI TOTAL ENVIRON, V235, P339, DOI 10.1016/S0048-9697(99)00217-X; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; World Health Organization, 1997, ENV HLTH CRIT, V188; Wilkinson P, 1999, THORAX, V54, P1070	14	133	136	3	14	ELSEVIER SCIENCE BV	AMSTERDAM	PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS	0048-9697			SCI TOTAL ENVIRON	Sci. Total Environ.	AUG 1	2003	312	1-3					43	46		10.1016/S0048-9697(03)00228-6		4	Environmental Sciences	Environmental Sciences & Ecology	708TH	WOS:000184585100005	12873397	
J	Hoek, G; Meliefste, K; Cyrys, J; Lewne, M; Bellander, T; Brauer, M; Fischer, P; Gehring, U; Heinrich, J; van Vliet, P; Brunekreef, B				Hoek, G; Meliefste, K; Cyrys, J; Lewne, M; Bellander, T; Brauer, M; Fischer, P; Gehring, U; Heinrich, J; van Vliet, P; Brunekreef, B			Spatial variability of fine particle concentrations in three European areas	ATMOSPHERIC ENVIRONMENT			English	Article						PM2.5; diesel; soot; traffic; exposure	URBAN AIR-POLLUTION; PARTICULATE MATTER; NITROGEN-DIOXIDE; BLACK SMOKE; RURAL SITES; EXPOSURE; CHILDREN; INDOOR; PM10; NETHERLANDS	Epidemiological studies of long-term air pollution effects have been hampered by difficulties in characterizing the spatial variation in air pollution. We conducted a study to assess the risk of long-term exposure to traffic-related air pollution for the development of inhalant allergy and asthma in children in Stockholm county, Munich and the Netherlands. Exposure to traffic-related air pollution was assessed through a 1-year monitoring program and regression modeling using exposure indicators. This paper documents the performance of the exposure monitoring strategy and the spatial variation of ambient particle concentrations. We measured the ambient concentration of PM2.5 and the reflectance of PM2.5 filters ('soot') at 40-42 sites representative of different exposure conditions of the three study populations. Each site was measured during four 14-day average sampling periods spread over one year (spring 1999 to summer 2000). In each study area, a continuous measurement site was operated to remove potential bias due to temporal variation. The selected approach was an efficient method to characterize spatial differences in annual average concentration between a large number of sites in each study area. Adjustment with data from the continuous measurement site improved the precision of the calculated annual averages, especially for PM2.5. Annual average PM2.5 concentrations ranged from 11 to 20 mug/m(3) in Munich, from 8 to 16 mug/m(3) in Stockholm and from 14 to 26 mug/m(3) in the Netherlands. Larger spatial contrasts were found for the absorption coefficient of PM2.5. PM2.5 concentrations were on average 17-18% higher at traffic sites than at urban background sites, but PM2.5 absorption coefficients at traffic sites were between 31% and 55% increased above background. This suggests that spatial variation of traffic-related air pollution may be underestimated if PM2.5 only is measured. (C) 2002 Elsevier Science Ltd. All rights reserved.	Univ Utrecht, Inst Risk Assessment Sci, Environm & Occupat Hlth Unit, NL-3508 TD Utrecht, Netherlands; GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, Neuherberg, Germany; Stockholm Cty Council, Dept Environm Hlth, Stockholm, Sweden; Karolinska Inst, Inst Environm Med, Stockholm, Sweden; Natl Inst Publ Hlth & Environm, Lab Exposure Assessment & Environm Epidemiol, NL-3720 BA Bilthoven, Netherlands	Hoek, G (reprint author), Univ Utrecht, Inst Risk Assessment Sci, Environm & Occupat Hlth Unit, POB 80-176, NL-3508 TD Utrecht, Netherlands.		Cyrys, Josef/B-5359-2014	brunekreef, bert/0000-0001-9908-0060; Gehring, Ulrike/0000-0003-3612-5780; Cyrys, Josef/0000-0002-2105-8696; Brauer, Michael/0000-0002-9103-9343			Bellander T, 2001, ENVIRON HEALTH PERSP, V109, P633, DOI 10.2307/3455039; Bernard NL, 1997, J EXPO ANAL ENV EPID, V7, P165; Briggs DJ, 1997, INT J GEOGR INF SCI, V11, P699, DOI 10.1080/136588197242158; BRUNEKREEF B, 1995, ENVIRON HEALTH PERSP, V103, P3, DOI 10.2307/3432443; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; Burton RM, 1996, ENVIRON SCI TECHNOL, V30, P400, DOI 10.1021/es950030f; Cyrys J, 1998, J EXPO ANAL ENV EPID, V8, P447; Fischer PH, 2000, ATMOS ENVIRON, V34, P3713, DOI 10.1016/S1352-2310(00)00067-4; Hering S, 1999, J AIR WASTE MANAGE, V49, P725, DOI 10.1080/10473289.1999.10463843; Hoek G, 1997, ATMOS ENVIRON, V31, P3609, DOI 10.1016/S1352-2310(97)00158-1; Hoek G, 2000, J AIR WASTE MANAGE, V50, P1380, DOI 10.1080/10473289.2000.10464182; Hoek G., 2001, RISK ASSESSMENT EXPO; Janssen NAH, 2001, ATMOS ENVIRON, V35, P3875, DOI 10.1016/S1352-2310(01)00144-3; Janssen NAH, 1997, ATMOS ENVIRON, V31, P1185, DOI 10.1016/S1352-2310(96)00291-9; Janssen NAH, 2000, J AIR WASTE MANAGE, V50, P1133; Kinney PL, 2000, ENVIRON HEALTH PERSP, V108, P213, DOI 10.2307/3454436; Lebret E, 2000, ATMOS ENVIRON, V34, P177, DOI 10.1016/S1352-2310(99)00292-7; MARPLE VA, 1987, JAPCA J AIR WASTE MA, V37, P1303; MONN C, 1995, ATMOS ENVIRON, V29, P2565, DOI 10.1016/1352-2310(95)94999-U; Monn C, 2001, ATMOS ENVIRON, V35, P1, DOI 10.1016/S1352-2310(00)00330-7; Nyberg F, 2000, EPIDEMIOLOGY, V11, P487, DOI 10.1097/00001648-200009000-00002; Raaschou-Nielsen O, 2000, J EXPO ANAL ENV EPID, V10, P4, DOI 10.1038/sj.jea.7500070; Roemer WH, 2001, ENVIRON HEALTH PERSP, V109, P151, DOI 10.2307/3434768; Roosli M, 2000, J AIR WASTE MANAGE, V50, P1115, DOI 10.1080/10473289.2000.10464161; Roosli M, 2001, ATMOS ENVIRON, V35, P3701, DOI 10.1016/S1352-2310(00)00511-2; Van der Zee SC, 1998, ATMOS ENVIRON, V32, P3717, DOI 10.1016/S1352-2310(98)00094-6; Weiland Stephan K., 1994, Annals of Epidemiology, V4, P243; WJST M, 1993, BRIT MED J, V307, P596	28	133	133	4	30	PERGAMON-ELSEVIER SCIENCE LTD	OXFORD	THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND	1352-2310			ATMOS ENVIRON	Atmos. Environ.	SEP	2002	36	25					4077	4088	PII S1352-2310(02)00297-2	10.1016/S1352-2310(02)00297-2		12	Environmental Sciences; Meteorology & Atmospheric Sciences	Environmental Sciences & Ecology; Meteorology & Atmospheric Sciences	601XB	WOS:000178473100007		
J	Pandya, RJ; Solomon, G; Kinner, A; Balmes, JR				Pandya, RJ; Solomon, G; Kinner, A; Balmes, JR			Diesel exhaust and asthma: Hypotheses and molecular mechanisms of action	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Review						air pollution; allergy; asthma; diesel exhaust; immunology; irritant; particulate matter; respiratory	BRONCHIAL EPITHELIAL-CELLS; PARTICULATE AIR-POLLUTION; IGE ANTIBODY-PRODUCTION; EMERGENCY ROOM VISITS; SHORT-TERM EXPOSURE; ACTIVITY IN-VITRO; ADJUVANT ACTIVITY; CYTOKINE PRODUCTION; CHILDHOOD ASTHMA; NITROGEN-DIOXIDE	Several components of air pollution have been linked to asthma. In addition to the well-studied critera air pollutants, such as nitrogen dioxide, sulfur dioxide, and ozone, diesel exhaust and diesel exhaust particles (DEPs) also appear to play a role in respiratory and allergic diseases. Diesel exhaust is composed of vapors, gases, and fine particles emitted by diesel-fueled compression-ignition engines. DEPs can act as nonspecific airway irritants at relatively high levels. At lower levels, DEPs promote release of specific cytokines, chemokines, immunoglobulins, and oxidants in the upper and lower airway. Release of these mediators of the allergic and inflammatory response initiates a cascade that can culminate in airway inflammation, mucus secretion, serum leakage into the air-ways, and bronchial smooth muscle contraction. DEPs also may promote expression of the T(H)2 immunologic response phenotype that has been associated with asthma and allergic disease. DEPs appear to have greater immunologic effects in the presence of environmental allergens than they do a-lone. This immunologic evidence may help explain the epidemiologic studies indicating that children living along major trucking thoroughfares are at increased risk for asthmatic and allergic symptoms and a-re more likely to have objective evidence of respiratory dysfunction.	Univ Calif San Francisco, Div Occupat & Environm Med, San Francisco, CA 94143 USA; San Francisco Gen Hosp, San Francisco, CA 94110 USA; Natl Resources Def Council, San Francisco, CA USA	Balmes, JR (reprint author), Univ Calif San Francisco, Div Occupat & Environm Med, POB 0843, San Francisco, CA 94143 USA.				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FEB	2002	110			1			103	112				10	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	538BV	WOS:000174794900011	11834468	
J	Radulovic, S; Wilson, D; Calderon, M; Durham, S				Radulovic, S.; Wilson, D.; Calderon, M.; Durham, S.			Systematic reviews of sublingual immunotherapy (SLIT)	ALLERGY			English	Review						allergic rhinitis; immunotherapy; systematic review	PLACEBO-CONTROLLED TRIAL; GRASS ALLERGEN TABLETS; RANDOMIZED CONTROLLED-TRIAL; HOUSE-DUST-MITE; STANDARDIZED 5-GRASS-POLLEN EXTRACT; PARIETARIA-JUDAICA EXTRACT; DOUBLE-BLIND; SWALLOW IMMUNOTHERAPY; POLLEN EXTRACT; CLINICAL-EFFICACY	P>Allergic rhinitis is common worldwide, with significant morbidity and impact on quality of life. In patients who don't respond adequately to anti-allergic drugs. Subcutaneous allergen immunotherapy is effective although requires specialist administration. Sublingual immunotherapy may represent an effective and safer alternative. This Cochrane systematic review is an update of one published in 2003. We searched Cochrane ENT Group Trials Register, Central, PubMed, EMBASE, CINAHL, Web of Science, Biosis Previews, Cambridge Scientific Abstarcts, mRCT and additional sources. We included randomised, double-blind, placebo- controlled trials of sublingual immunotherapy in adults and children. Two authors selected studies and assessed them for quality. Data were put into RevMan 5.0 for a statistical analysis. We used standardised mean difference (SMD), with a random effect model to combine data. Sixty studies were included, with 49 suitable for meta-analysis. We found significant reductions in symptoms (SMD -0.49; 95%CI (-0.64 to -0.34, P < 0.00001)) and medication requirements (SMD -0.32; 95%CI (-0.43 to -0.21, P < 0.00001)) compared with placebo. None of the trials reported severe systemic reactions, anaphylaxis or use of Adrenaline. This updated review reinforces the conclusion of the original 2003 Cochrane Review that sublingual immunotherapy is effective for allergic rhinitis and appears a safe route of administration.	[Durham, S.] Royal Brompton Hosp, Imperial Coll NHLI, Dept Allergy & Resp Med, London SW3 6LY, England; [Radulovic, S.] Kings Coll London, London WC2R 2LS, England; [Wilson, D.] Univ Hosp Birmingham NHS Trust, Selly Oak Hosp, Birmingham, W Midlands, England	Durham, S (reprint author), Royal Brompton Hosp, Imperial Coll NHLI, Dept Allergy & Resp Med, London SW3 6LY, England.	s.durham@imperial.ac.uk			ALK Abello; Horsholm Denmark	SR Durham has received lecture and consultancy fees and research funding via Imperial College from ALK Abello, Horsholm Denmark, a manufacturer of allergy vaccines. Moises Calderon has received lecture fees from ALK Abello, Horsholm Denmark, a manufacturer of allergy vaccines.	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J	Bedoret, D; Wallemacq, H; Marichal, T; Desmet, C; Calvo, FQ; Henry, E; Closset, R; Dewals, B; Thielen, C; Gustin, P; de Leval, L; Van Rooijen, N; Le Moine, A; Vanderplasschen, A; Cataldo, D; Drion, PV; Moser, M; Lekeux, P; Bureau, F				Bedoret, Denis; Wallemacq, Hugues; Marichal, Thomas; Desmet, Christophe; Calvo, Florence Quesada; Henry, Emmanuelle; Closset, Rodrigue; Dewals, Benjamin; Thielen, Caroline; Gustin, Pascal; de Leval, Laurence; Van Rooijen, Nico; Le Moine, Alain; Vanderplasschen, Alain; Cataldo, Didier; Drion, Pierre-Vincent; Moser, Muriel; Lekeux, Pierre; Bureau, Fabrice			Lung interstitial macrophages alter dendritic cell functions to prevent airway allergy in mice	JOURNAL OF CLINICAL INVESTIGATION			English	Article							RESPIRATORY SYNCYTIAL VIRUS; COLONY-STIMULATING FACTOR; HOUSE-DUST ENDOTOXIN; ALVEOLAR MACROPHAGES; IN-VIVO; INHALED ANTIGEN; IMMUNE-RESPONSES; PERITONEAL-MACROPHAGES; CYTOKINE PRODUCTION; IL-12 PRODUCTION	The respiratory tract is continuously exposed to both innocuous airborne antigens and immunostimulatory molecules of microbial origin, such as LPS. At low concentrations, airborne LPS can induce a lung DC-driven Th2 cell response to harmless inhaled antigens, thereby promoting allergic asthma. However, only a small fraction of people exposed to environmental LIPS develop allergic asthma. What prevents most people from mounting a lung DC-driven Th2 response upon exposure to LPS is not understood. Here we have shown that lung interstitial macrophages (IMs), a cell population with no previously described in vivo function, prevent induction of a Th2 response in mice challenged with LPS and an experimental harmless airborne antigen. IMs, but not alveolar macrophages, were found to produce high levels of IL-10 and to inhibit LPS-induced maturation and migration of DCs loaded with the experimental harmless airborne antigen in an IL-10-dependent manner. We further demonstrated that specific in vivo elimination of IMs led to overt asthmatic reactions to innocuous airborne antigens inhaled with low doses of LPS. This study has revealed a crucial role for IMs in maintaining immune homeostasis in the respiratory tract and provides an explanation for the paradox that although airborne LPS has the ability to promote the induction of Th2 responses by lung DCs, it does not provoke airway allergy under normal conditions.	[Bedoret, Denis; Wallemacq, Hugues; Marichal, Thomas; Desmet, Christophe; Closset, Rodrigue; Lekeux, Pierre; Bureau, Fabrice] Univ Liege, Lab Cellular & Mol Physiol, GIGA Res, B-4000 Liege, Belgium; [Calvo, Florence Quesada; Cataldo, Didier] CHU Liege, Lab Biol Tumors & Dev, GIGA Res, Liege, Belgium; [Henry, Emmanuelle; Moser, Muriel] Univ Libre Bruxelles, Inst Mol Biol & Med, Physiol Anim Lab, Gosselies, Belgium; [Dewals, Benjamin; Vanderplasschen, Alain] Univ Liege, Fac Vet Med, Lab Immunol & Vaccinol, B-4000 Liege, Belgium; [Thielen, Caroline; de Leval, Laurence] CHU Liege, Pathol Lab, GIGA Res, Liege, Belgium; [Gustin, Pascal] Univ Liege, Fac Vet Med, Dept Funct Sci, B-4000 Liege, Belgium; [Van Rooijen, Nico] Vrije Univ Amsterdam, Med Ctr, Fac Med, Dept Mol Cell Biol, Amsterdam, Netherlands; [Le Moine, Alain] Univ Libre Bruxelles, Inst Med Immunol, Gosselies, Belgium; [Drion, Pierre-Vincent] Univ Liege, Anim Facil B23, B-4000 Liege, Belgium	Bureau, F (reprint author), Univ Liege, Lab Cellular & Mol Physiol, GIGA Res, Ave Hop,Batiment B34, B-4000 Liege, Belgium.	fabrice.bureau@ulg.ac.be		Cataldo, Didier/0000-0002-3079-7941	Fonds National de la Recherche Scientifique (FNRS; Belgium; Mandat d'Impulsion Scientifique); Fonds de la Recherche Scientifique Medicale (FRSM; Belgium); Belgian Programme on Interuniversity Attraction Poles (IUAP)	We thank Kris Thielemans for providing recombinant murine GM-CSF; Sandrine Florquin for providing Tlr4<SUP>-/-</SUP> mice; Sandra Ormenese and the Cell Imaging and Flow Cytometry GIGA Technological Platform for FACS analysis; and Ilham Sbai, Cedric Francois, and Fabrice Jaspar for excellent technical and secretarial assistance. Clodronate (Cl<INF>2</INF>MDP) was a gift of Roche Diagnostics GmbH. The Laboratory of Cellular and Molecular Physiology is supported by grants from the Fonds National de la Recherche Scientifique (FNRS; Belgium; Mandat d'Impulsion Scientifique), by the Fonds de la Recherche Scientifique Medicale (FRSM; Belgium), by the Belgian Programme on Interuniversity Attraction Poles (IUAP; FEDIMMUNE) initiated by the Belgian State (Belgian Science Policy), and by an Action de Recherche Concertee de la Communaute Francaise de Belgique. D. Bedoret and T. Marichal are research fellows, C. Desmet is a postdoctoral researcher, and M. Moser is a research director at the FNRS.	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Clin. Invest.	DEC	2009	119	12					3723	3738		10.1172/JCI39717		16	Medicine, Research & Experimental	Research & Experimental Medicine	527SI	WOS:000272386400021	19907079	
J	Brockow, K; Romano, A; Aberer, W; Bircher, AJ; Barbaud, A; Bonadonna, P; Faria, E; Kanny, G; Lerch, M; Pichler, WJ; Ring, J; Cernadas, JR; Tomaz, E; Demoly, P; Christiansen, C				Brockow, K.; Romano, A.; Aberer, W.; Bircher, A. J.; Barbaud, A.; Bonadonna, P.; Faria, E.; Kanny, G.; Lerch, M.; Pichler, W. J.; Ring, J.; Cernadas, J. Rodrigues; Tomaz, E.; Demoly, P.; Christiansen, C.		European Network Drug Allergy; EAACI Interest Grp Drug	Skin testing in patients with hypersensitivity reactions to iodinated contrast media - a European multicenter study	ALLERGY			English	Article						contrast media; hypersensitivity; skin tests	DRUG HYPERSENSITIVITY; ANAPHYLAXIS; IMMEDIATE; ALLERGY; GUIDELINES; PROTOCOL; RISK	Iodinated contrast media cause both immediate and nonimmediate hypersensitivity reactions. The aim of this prospective study was to determine the specificity and sensitivity of skin tests in patients who have experienced such reactions. Skin prick, intradermal and patch tests with a series of contrast media were conducted in 220 patients with either immediate or nonimmediate reaction. Positive skin tests were defined according to internationally accepted guidelines. Seventy-one never-exposed subjects and 11 subjects who had tolerated contrast medium exposure, served as negative controls. Skin test specificity was 96-100%. For tests conducted within the time period from 2 to 6 months after the reaction, up to 50% of immediate reactors and up to 47% of nonimmediate reactors were skin test positive. For immediate reactors, the intradermal tests were the most sensitive, whereas delayed intradermal tests in combination with patch tests were needed for optimal sensitivity in nonimmediate reactors. Contrast medium cross-reactivity was more common in the nonimmediate than in the immediate group. Interestingly, 49% of immediate and 52% of nonimmediate symptoms occurred in previously unexposed patients. Many of these patients were skin test positive, indicating that they were already sensitized at the time of first contrast medium exposure. These data suggest that at least 50% of hypersensitivity reactions to contrast media are caused by an immunological mechanism. Skin testing appears to be a useful tool for diagnosis of contrast medium allergy and may play an important role in selection of a safe product in previous reactors.	[Brockow, K.; Ring, J.] Tech Univ Munich, Dept Dermatol & Allergol Biederstein, Div Environm Dermatol & Allergol, Helmholtz Zentrum Munchen, D-80802 Munich, Germany; [Aberer, W.] Med Univ Graz, Dept Dermatol, Graz, Austria; [Bircher, A. J.] Univ Basel Hosp, Dept Dermatol, Allergy Unit, CH-4031 Basel, Switzerland; [Romano, A.] CI Columbus, Allergy Unit, Rome, Italy; [Romano, A.] IRCCS Oasi Maria SS, Troina, Italy; [Barbaud, A.] Univ Hosp, Dept Dermatol, Fournier Hosp, Nancy, France; [Bonadonna, P.] Verona Hosp, Allergy Unit, Verona, Italy; [Faria, E.] Coimbra Univ Hosp, Immunoallergol Dept, Coimbra, Portugal; [Kanny, G.] Univ Hosp, Dept Internal Med Clin Immunol & Allergy, Cent Hosp, Nancy, France; [Lerch, M.; Pichler, W. J.] Univ Bern, Inselspital, Clin Rheumatol & Clin Immunol Allergol, CH-3010 Bern, Switzerland; [Cernadas, J. Rodrigues] Univ Hosp S Joao, Dept Allergy & Clin Immunol, Oporto, Portugal; [Tomaz, E.] Hosp S Bernardo, Setubal, Portugal; [Demoly, P.] Univ Hosp Montpellier, Hop Arnaud de Villeneuve, INSERM, Montpellier, France; [Christiansen, C.] GE Healthcare, Res & Dev, Oslo, Norway	Brockow, K (reprint author), Tech Univ Munich, Dept Dermatol & Allergol Biederstein, Div Environm Dermatol & Allergol, Helmholtz Zentrum Munchen, Biedersteiner Str 29, D-80802 Munich, Germany.			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J	Terashima, A; Watarai, H; Inoue, S; Sekine, E; Nakagawa, R; Hase, K; Iwamura, C; Nakajima, H; Nakayama, T; Taniguchi, M				Terashima, Asuka; Watarai, Hiroshi; Inoue, Sayo; Sekine, Etsuko; Nakagawa, Ryusuke; Hase, Koji; Iwamura, Chiaki; Nakajima, Hiroshi; Nakayama, Toshinori; Taniguchi, Masaru			A novel subset of mouse NKT cells bearing the IL-17 receptor B responds to IL-25 and contributes to airway hyperreactivity	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article							KILLER T-CELLS; IN-VIVO; ALLERGIC-ASTHMA; TH2 RESPONSES; ACTIVATION; IDENTIFICATION; POPULATION; EXPRESSION; LUNG; HYPERRESPONSIVENESS	Airway hypersensitive reaction (AHR) is an animal model for asthma, which is caused or enhanced by environmental factors such as allergen exposure. However, the precise mechanisms that drive AHR remain unclear. We identified a novel subset of natural killer T (NKT) cells that expresses the interleukin 17 receptor B (IL-17RB) for IL-25 (also known as IL-17E) and is essential for the induction of AHR. IL-17RB is preferentially expressed on a fraction of CD4(+) NKT cells but not on other splenic leukocyte populations tested. IL-17RB(+) CD4(+) NKT cells produce predominantly IL-13 and Th2 chemokines upon stimulation with IL-25 in vitro. IL-17RB(+) NKT cells were detected in the lung, and depletion of IL-17RB(+) NKT cells by IL-17RB(-)specific monoclonal antibodies or NKT cell deficient J alpha 18(-/-) mice failed to develop IL-25-dependent AHR. Cell transfer of IL-17RB(+) but not IL-17RB(-) NKT cells into J alpha 18(-/-) mice also successfully reconstituted AHR induction. These results strongly suggest that IL-17RB(+) CD4(+) NKT cells play a crucial role in the pathogenesis of asthma.	[Terashima, Asuka; Watarai, Hiroshi; Inoue, Sayo; Sekine, Etsuko; Nakagawa, Ryusuke; Taniguchi, Masaru] RIKEN, Res Ctr Allergy & Immunol, Lab Immune Regulat, Tsurumi Ku, Kanagawa 2300045, Japan; [Hase, Koji] RIKEN, Res Ctr Allergy & Immunol, Lab Epithelial Immunobiol, Tsurumi Ku, Kanagawa 2300045, Japan; [Iwamura, Chiaki; Nakayama, Toshinori] Chiba Univ, Dept Immunol, Chuo Ku, Chiba 2608670, Japan; [Nakajima, Hiroshi] Chiba Univ, Dept Mol Genet, Grad Sch Med, Chuo Ku, Chiba 2608670, Japan	Watarai, H (reprint author), RIKEN, Res Ctr Allergy & Immunol, Lab Immune Regulat, Tsurumi Ku, Kanagawa 2300045, Japan.	hwatarai@rcai.riken.jp	Watarai, Hiroshi/G-9894-2012; Taniguchi, Masaru/N-7932-2015; Nakayama, Toshinori/E-1067-2017	Watarai, Hiroshi/0000-0003-1511-2593; Taniguchi, Masaru/0000-0001-7821-7179; Nakayama, Toshinori/0000-0002-1434-2007			Akbari O, 2003, NAT MED, V9, P582, DOI 10.1038/nm851; Ballantyne SJ, 2007, J ALLERGY CLIN IMMUN, V120, P1324, DOI 10.1016/j.jaci.2007.07.051; Brigl M, 2003, NAT IMMUNOL, V4, P1230, DOI 10.1038/ni1002; Coquet JM, 2008, P NATL ACAD SCI USA, V105, P11287, DOI 10.1073/pnas.0801631105; Crowe NY, 2005, J EXP MED, V202, P1279, DOI 10.1084/jem.20050953; Cui JQ, 1997, SCIENCE, V278, P1623, DOI 10.1126/science.278.5343.1623; Fallon PG, 2006, J EXP MED, V203, P1105, DOI 10.1084/jem.20051615; Fallon PG, 2002, IMMUNITY, V17, P7, DOI 10.1016/S1074-7613(02)00332-1; Fort MM, 2001, IMMUNITY, V15, P985, DOI 10.1016/S1074-7613(01)00243-6; Harada M, 2006, J EXP MED, V203, P2929, DOI 10.1084/jem.20062206; Hizawa N, 2006, CLIN EXP ALLERGY, V36, P1109, DOI 10.1111/j.1365-2222.2006.02550.x; Hurst SD, 2002, J IMMUNOL, V169, P443; Ikeda K, 2003, BLOOD, V101, P3594, DOI 10.1182/blood-2002-09-2817; Jamieson AM, 2002, IMMUNITY, V17, P19, DOI 10.1016/S1074-7613(02)00333-3; Johnston B, 2003, J IMMUNOL, V171, P2960; Kim MR, 2002, BLOOD, V100, P2330, DOI 10.1182/blood-2002-01-0012; Letuve S, 2006, J ALLERGY CLIN IMMUN, V117, P590, DOI 10.1016/j.jaci.2005.10.025; Meyer EH, 2006, P NATL ACAD SCI USA, V103, P2782, DOI 10.1073/pnas.0510282103; Meyer EH, 2007, J IMMUNOL, V179, P4661; Michel ML, 2007, J EXP MED, V204, P995, DOI 10.1084/jem.20061551; Moseley TA, 2003, CYTOKINE GROWTH F R, V14, P155, DOI 10.1016/S1359-6101(03)00002-9; Pan GH, 2001, J IMMUNOL, V167, P6559; Pichavant M, 2008, J EXP MED, V205, P385, DOI 10.1084/jem.20071507; Rachitskaya AV, 2008, J IMMUNOL, V180, P5167; Rahman MS, 2006, J IMMUNOL, V177, P4064; Tamachi T, 2006, J ALLERGY CLIN IMMUN, V118, P606, DOI 10.1016/j.jaci.2006.04.051; Taniguchi M, 2003, ANNU REV IMMUNOL, V21, P483, DOI 10.1146/annurev.ummunol.21.120601.141057; Umetsu DT, 2006, IMMUNOL REV, V212, P238, DOI 10.1111/j.0105-2896.2006.00413.x; Watarai H, 2008, NAT PROTOC, V3, P70, DOI 10.1038/nprot.2007.515; Wills-Karp M, 1999, ANNU REV IMMUNOL, V17, P255, DOI 10.1146/annurev.immunol.17.1.255; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258	31	132	137	1	5	ROCKEFELLER UNIV PRESS	NEW YORK	1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA	0022-1007			J EXP MED	J. Exp. Med.	NOV 24	2008	205	12					2727	U29		10.1084/jem.20080698		10	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	378BE	WOS:000261295300007	19015310	
J	Sundell, J				Sundell, J			On the history of indoor air quality and health	INDOOR AIR			English	Article						IAQ; health; allergy; indoor environments; dampness; ventilation	SYNDROME SBS SYMPTOMS; SCIENTIFIC EVIDENCE; ENVIRONMENTS; VENTILATION; BUILDINGS; EXPOSURE; PRODUCTIVITY; ASSOCIATIONS; DAMPNESS; OFFICE	Indoor air is a dominant exposure for humans. More that half of the body's intake during a lifetime is air inhaled in the home. Thus, most illnesses related to environmental exposures stem from indoor air exposure. Indoor air was believed to be a major environmental factor for more than a hundred years, from the start of the hygienic revolution, around 1850, until outdoor environmental issues entered the scene, and became dominant around 1960. Main environmental issues today are outdoor air quality, energy use, and sustainable buildings, but not indoor air quality (IAQ). But, there is mounting evidence that exposure to IAQ is the cause of excessive morbidity and mortality. In developing regions indoor unvented burning of biomass for cooking is the cause of at least 2,000,000 deaths a year (mainly women and children), and in the developed world IAQ is a main cause of allergies, other hypersensitivity reactions, airway infections, and cancers. Cancer of the lungs is related to indoor radon and ETS exposure. Allergies, airway infections and sick building syndrome are associated with, e.g., "dampness", a low ventilation rate, and plasticizers. In the future more emphasis must be given to IAQ and health issues.	Tech Univ Denmark, Int Ctr Indoor Environm & Energy, DK-2800 Lyngby, Denmark	Sundell, J (reprint author), Tech Univ Denmark, Int Ctr Indoor Environm & Energy, Niels Koppels Alle,Bldg 402, DK-2800 Lyngby, Denmark.	jas@mek.dtu.dk	Sundell, Jan/B-2857-2012				Ahlbom A, 1998, INDOOR AIR, V8, P219, DOI 10.1111/j.1600-0668.1998.00003.x; Andersson K, 1997, INDOOR AIR, V7, P78, DOI 10.1111/j.1600-0668.1997.t01-2-00002.x; Bornehag CG, 2001, INDOOR AIR, V11, P72; Bornehag CG, 2004, INDOOR AIR, V14, P59, DOI 10.1111/j.1600-0668.2004.00274.x; BORNEHAG CG, 2004, IN PRESS INDOOR AIR; Carnelly D, 1887, PHILOS T R SOC B, V178, P61; Fang L, 1999, INDOOR AIR, V9, P193, DOI 10.1111/j.1600-0668.1999.t01-1-00006.x; FANGER PO, 1988, ENERG BUILDINGS, V12, P7, DOI 10.1016/0378-7788(88)90052-7; FANGER PO, 1988, ENERG BUILDINGS, V12, P1, DOI 10.1016/0378-7788(88)90051-5; FANGER PO, 1992, EURO CH ENV, V4, P59; Schneider T, 2003, INDOOR AIR, V13, P38, DOI 10.1034/j.1600-0668.2003.02025.x; SMITH KR, 2003, P HLTH BUILDINGS, V1, P118; SUNDELL J, 1995, ALLERGY, V50, P106; Sundell J., 1993, INDOOR AIR, V3, P82, DOI 10.1111/j.1600-0668.1993.t01-2-00003.x; SUNDELL J, 1994, INDOOR AIR S, V2; Sundell J., 1999, INDOOR ENV HLTH; van Odijk J, 2003, ALLERGY, V58, P833, DOI 10.1034/j.1398-9995.2003.00264.x; Wargocki P, 2000, INDOOR AIR, V10, P222, DOI 10.1034/j.1600-0668.2000.010004222.x; Wargocki P, 2002, INDOOR AIR, V12, P113, DOI 10.1034/j.1600-0668.2002.01145.x; Wargocki P, 1999, INDOOR AIR, V9, P165, DOI 10.1111/j.1600-0668.1999.t01-1-00003.x; Weschler CJ, 2000, INDOOR AIR, V10, P92, DOI 10.1034/j.1600-0668.2000.010002092.x; Weschler CJ, 2000, INDOOR AIR, V10, P269, DOI 10.1034/j.1600-0668.2000.010004269.x	22	132	148	6	64	WILEY-BLACKWELL	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0905-6947			INDOOR AIR	Indoor Air	AUG	2004	14			7			51	58		10.1111/j.1600-0668.2004.00273.x		8	Construction & Building Technology; Engineering, Environmental; Public, Environmental & Occupational Health	Construction & Building Technology; Engineering; Public, Environmental & Occupational Health	850DF	WOS:000223590700007	15330772	
J	McParland, BE; Macklem, PT; Pare, PD				McParland, BE; Macklem, PT; Pare, PD			Airway wall remodeling: friend or foe?	JOURNAL OF APPLIED PHYSIOLOGY			English	Review						asthma; pathophysiology; smooth muscle	SMOOTH-MUSCLE CELLS; OBSTRUCTIVE PULMONARY-DISEASE; BRONCHIAL BASEMENT-MEMBRANE; DOSE-RESPONSE CURVE; FATAL ASTHMA; SUBEPITHELIAL FIBROSIS; DEEP INSPIRATION; MILD ASTHMA; INDUCED BRONCHOCONSTRICTION; LENGTH OSCILLATION	Airway wall remodeling is well documented for asthmatic airways and is believed to result from chronic and/or short-term exposure to inflammatory stimuli. Airway wall remodeling can contribute to airway narrowing as well as to the airway hyperresponsiveness, which is a characteristic abnormality in asthma. However, the potential for airway narrowing could be much worse if it were not for some of the protective effects of remodeling that may help to limit airway narrowing in asthmatic patients. This minireview discusses the evidence for airway wall remodeling and its effects, friend and/or foe, on airway narrowing in asthmatic patients.	Univ British Columbia, McDonald Res Labs, iCAPTURE Ctr, St Pauls Hosp, Vancouver, BC V6Z 1Y6, Canada; McGill Univ, Div Resp, Montreal, PQ H2X 2P2, Canada; McGill Univ, Meakins Christie Labs, Montreal, PQ H2X 2P2, Canada	Pare, PD (reprint author), Univ British Columbia, McDonald Res Labs, iCAPTURE Ctr, St Pauls Hosp, Burrard Bldg,1081 Burrard St, Vancouver, BC V6Z 1Y6, Canada.		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Appl. Physiol.	JUL	2003	95	1					426	434		10.1152/japplphysiol.00159.2003		9	Physiology; Sport Sciences	Physiology; Sport Sciences	687AY	WOS:000183354700052	12794101	
J	Centeno, JA; Mullick, FG; Martinez, L; Page, NP; Gibb, H; Longfellow, D; Thompson, C; Ladich, ER				Centeno, JA; Mullick, FG; Martinez, L; Page, NP; Gibb, H; Longfellow, D; Thompson, C; Ladich, ER			Pathology related to chronic arsenic exposure	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article; Proceedings Paper	3rd International Meeting on the Molecular Mechanisms of Metal Toxicity and Carcinogenicity	SEP 02-06, 2001	STINTINO, ITALY			angiosarcoma; arsenic; Bowen disease; hepatocellular carcinoma; hepatoportal sclerosis; hyperkeratosis; liver; noncirrhotic portal fibrosis; squamous cell carcinoma	IDIOPATHIC PORTAL-HYPERTENSION; DRINKING-WATER; WELL WATER; MORTALITY; ANGIOSARCOMA; PREVALENCE; ARGENTINA; DISEASES	Millions now suffer the effects of chronic arseniasis related to environmental arsenic exposure. The biological mechanisms responsible for arsenic-induced toxicity and especially chronic effects, including cancer, are not well known. The U.S. Armed Forces Institute of Pathology (AFIP) is participating in an international research effort to improve this understanding by the development of the International Tissue and Tumor Repository for Chronic Arsenosis (ITTRCA). The ITTRCA obtains, archives, and makes available for research purposes, tissues from subjects exposed to arsenic. We provide here a short overview of arsenic-induced pathology, briefly describe arsenic-induced lesions in the skin and liver, and present five case reports from the ITTRCA. Arsenic-induced skin pathology includes hyperkeratosis, pigmentation changes, Bowen disease, squamous cell carcinoma, and basal cell carcinomas. A unique spectrum of skin lesions, known as arsenical keratosis, is rather characteristic of chronic arseniasis. Bowen disease, or squamous cell carcinoma in situ of the skin, has been well documented as a consequence of arsenical exposure. A spectrum of liver lesions has also been attributed to chronic arseniasis. Of these, hepatocellular carcinoma, angiosarcoma, cirrhosis, and hepatoportal sclerosis have been associated with arsenic exposure. We present case reports that relate to these health conditions, namely, squamous cell carcinoma, basal cell carcinoma, and Bowen disease of the skin and hepatocellular carcinoma and angiosarcoma of the liver. Four patients had been treated with arsenical medications for such conditions as asthma, psoriasis, and syphilis, and one case occurred in a boy chronically exposed to arsenic in drinking water.	Armed Forces Inst Pathol, Div Biophys Toxicol, Washington, DC 20306 USA; US EPA, Washington, DC 20460 USA; Natl Canc Inst, Bethesda, MD USA; Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA	Centeno, JA (reprint author), Armed Forces Inst Pathol, Div Biophys Toxicol, Washington, DC 20306 USA.						Biggs ML, 1998, SCIENCE, V281, P785; Centeno J.A., 2000, ARSENIC INDUCED LESI, P46; Chen Chien-Jen, 1994, V27, P109; CHEN CJ, 1990, CANCER RES, V50, P5470; CHEN CJ, 1995, HYPERTENSION, V25, P53; Chen CJ, 1996, ARTERIOSCL THROM VAS, V16, P504; DATTA DV, 1979, GUT, V20, P378, DOI 10.1136/gut.20.5.378; Duenas C, 1998, J CLIN GASTROENTEROL, V26, P303, DOI 10.1097/00004836-199806000-00019; Falk H, 1981, Am J Ind Med, V2, P43, DOI 10.1002/ajim.4700020108; HOOD RD, 1977, ENVIRON HEALTH PERSP, V19, P219; Hopenhayn-Rich C, 1998, INT J EPIDEMIOL, V27, P561, DOI 10.1093/ije/27.4.561; HopenhaynRich C, 1996, EPIDEMIOLOGY, V7, P117, DOI 10.1097/00001648-199603000-00003; LAI MS, 1994, AM J EPIDEMIOL, V139, P484; LEONARD A, 1980, MUTAT RES, V75, P49, DOI 10.1016/0165-1110(80)90027-5; Maloney ME, 1996, DERMATOL SURG, V22, P301; Mazumder DNG, 1999, ARSENIC EXPOSURE AND HEALTH EFFECTS, P335, DOI 10.1016/B978-008043648-7/50037-6; National Research Council, 2001, ARS DRINK WAT 2001 U; NESHIWAT LF, 1992, AM J MED, V93, P219, DOI 10.1016/0002-9343(92)90054-F; NEVENS F, 1990, J HEPATOL, V11, P80, DOI 10.1016/0168-8278(90)90276-W; NORDSTROM S, 1978, HEREDITAS, V88, P51; OKUDA K, 1989, ADV LIVER DIS, P79; PAGE NP, 2000, METALS BIOL MED, V6, P759; REGELSON W, 1968, CANCER, V21, P514, DOI 10.1002/1097-0142(196803)21:3<514::AID-CNCR2820210323>3.0.CO;2-Z; Roth F., 1957, GERMAN MED MONTHLY, V2, P172; Tsai SM, 1999, ARCH ENVIRON HEALTH, V54, P186; WU MM, 1989, AM J EPIDEMIOL, V130, P1123	26	132	137	4	9	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	OCT	2002	110			5			883	886				4	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	612FQ	WOS:000179064200042	12426152	
J	Anderson, SD; Argyros, GJ; Magnussen, H; Holzer, K				Anderson, SD; Argyros, GJ; Magnussen, H; Holzer, K			Provocation by eucapnic voluntary hyperpnoea to identify exercise induced bronchoconstriction	BRITISH JOURNAL OF SPORTS MEDICINE			English	Article						hyperpnoea; bronchial provocation; exercise	THERMALLY-INDUCED ASTHMA; COLD-AIR; BRONCHOPROVOCATION TECHNIQUE; INDUCED BRONCHOSPASM; DRY AIR; HYPERVENTILATION; CHALLENGE; RESPONSIVENESS; REACTIVITY; CHILDREN	The International Olympic Committee Medical Commission (IOC-MC) requires notification for use of a beta (2) agonist at the Winter Olympic Games in Salt Lake City. This notification will be required seven days before the event and must be accompanied by objective evidence that justifies the need to use one. The IOC-MC has expressed the viewpoint that, at present, eucapnic voluntary hyperpnoea (EVH) is the optimal laboratory challenge to confirm that an athlete has exercise induced bronchoconstriction (EIB). The EVH test recommended was specifically designed to identify EIB. EVH has been performed in thousands of subjects in both the laboratory and the field. The test requires the subject to hyperventilate dry air containing 5% carbon dioxide at room temperature for six minutes at a target ventilation of 30 times the subject's forced expiratory volume in one second (FEV1). The test conditions can be modified to simulate the conditions that give the athlete their symptoms with exercise. A reduction in FEV1 of 10% or more of the value before the test is considered positive.	Royal Prince Alfred Hosp, Dept Resp Med, Camperdown, NSW 2050, Australia; Krankenhaus Grosshansdorf, Ctr Pneumol & Thorac Surg, D-22927 Grosshansdorf, Germany; Walter Reed Hlth Care Syst, Walter Reed Army Med Ctr, Washington, DC 20307 USA; Alfred Hosp, Dept Immunol & Asthma, Prahran, Vic 3052, Australia	Anderson, SD (reprint author), Royal Prince Alfred Hosp, Dept Resp Med, Level 9 Page Chest Pavil, Camperdown, NSW 2050, Australia.			Anderson, Sandra/0000-0002-6308-8770			American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Anderson SD, 2000, J ALLERGY CLIN IMMUN, V106, P419, DOI 10.1067/mai.2000.108914; Anderson SD, 2000, J ALLERGY CLIN IMMUN, V106, P453; Anderson SD, 2001, MED SCI SPORT EXER, V33, P893, DOI 10.1097/00005768-200106000-00007; ANDERSON SD, 2001, RESPIROLOGY, V6, pA10; ARGYROS GJ, 1995, CHEST, V108, P419, DOI 10.1378/chest.108.2.419; Argyros GJ, 1996, CHEST, V109, P1520, DOI 10.1378/chest.109.6.1520; ASSOUFI BK, 1986, B EUR PHYSIOPATH RES, V22, P349; BANNER AS, 1984, NEW ENGL J MED, V311, P883, DOI 10.1056/NEJM198410043111404; Brannan JD, 1998, AM J RESP CRIT CARE, V158, P1120; DEAL EC, 1980, AM REV RESPIR DIS, V121, P621; DEAL EC, 1979, J APPL PHYSIOL, V46, P476; Dwyer TM, 1997, AM J PHYSIOL-LUNG C, V272, pL1121; ELIASSON AH, 1992, CHEST, V102, P347, DOI 10.1378/chest.102.2.347; FINNERTY JP, 1992, EUR RESPIR J, V5, P323; HURWITZ KM, 1995, CHEST, V108, P1240, DOI 10.1378/chest.108.5.1240; ISRAEL E, 1990, NEW ENGL J MED, V323, P1740, DOI 10.1056/NEJM199012203232505; Mannix ET, 1999, CHEST, V115, P649, DOI 10.1378/chest.115.3.649; McFadden ER, 1999, AM J RESP CRIT CARE, V160, P221; MCFADDEN ER, 1986, J CLIN INVEST, V78, P18, DOI 10.1172/JCI112549; NICOLAI T, 1993, AM REV RESPIR DIS, V147, P565; NOWAK D, 1992, EUR J CLIN PHARMACOL, V43, P591, DOI 10.1007/BF02284956; PHILLIPS YY, 1985, AM REV RESPIR DIS, V131, P31; ROACH JM, 1994, CHEST, V105, P667, DOI 10.1378/chest.105.3.667; Rundell KW, 2000, MED SCI SPORT EXER, V32, P309, DOI 10.1097/00005768-200002000-00010; Rundell KW, 2001, MED SCI SPORT EXER, V33, P208; VATHENEN AS, 1991, THORAX, V46, P811, DOI 10.1136/thx.46.11.811; WEISS ST, 1984, AM REV RESPIR DIS, V129, P898; WILBER RL, 2000, IN PRESS MED SCI SPO; ZACH M, 1984, PEDIATR RES, V18, P469, DOI 10.1203/00006450-198405000-00016	30	132	135	0	7	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0306-3674			BRIT J SPORT MED	Br. J. Sports Med.	OCT	2001	35	5					344	347		10.1136/bjsm.35.5.344		4	Sport Sciences	Sport Sciences	479FR	WOS:000171394800019	11579071	
J	Karjalainen, A; Kurppa, K; Martikainen, R; Klaukka, T; Karjalainen, J				Karjalainen, A; Kurppa, K; Martikainen, R; Klaukka, T; Karjalainen, J			Work is related to a substantial portion of adult-onset asthma incidence in the Finnish population	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; occupational medicine; risk; incidence; population	OCCUPATIONAL ASTHMA; BRONCHIAL-ASTHMA; SMOKING; EXPOSURES; RISK; FINLAND	There are no population-based follow-up studies to estimate the fraction of asthma incidence that is attributable to work. In Finland, individuals with clinically well-established persistent asthma are registered for reimbursement of medication from the national health insurance scheme. We combined, at an individual level, these data with the population census data of 1985, 1990, and 1995 to estimate the attributable fraction of work in adult-onset persistent asthma. Our follow-up study covered the entire 25- to 59-yr-old employed population of Finland in 1986-1998. Relative risks (RR) for occupational categories were estimated in comparison to those employed in administrative work. There were 49,575 incident cases of asthma. The attributable fraction of occupation was 29% (95% CI 25-33%) for men and 17% (95% CI 15-19%) for women. The risk was increased especially in agricultural work, manufacturing work, and service work. In addition to already established risk occupations of occupational asthma, such as food and beverage work, the analysis identified a large number of occupations with significant excess of asthma incidence. The results indicate that the impact of occupational factors in the inception of adult-onset persistent asthma, and consequently the potential for prevention, is much larger and more widely spread than generally assumed.	Finnish Inst Occupat Hlth, Dept Epidemiol & Biostat, FIN-00250 Helsinki, Finland; Social Insurance Inst, SF-00381 Helsinki, Finland; Tampere Univ Hosp, Dept Resp Med, Tampere, Finland	Karjalainen, A (reprint author), Finnish Inst Occupat Hlth, Dept Epidemiol & Biostat, Topeliuksenkatu 41 aA, FIN-00250 Helsinki, Finland.						Arinen S, 1998, MAIN FINDINGS FINNIS, P5; Blanc PD, 1999, AM J MED, V107, P580, DOI 10.1016/S0002-9343(99)00307-1; Flodin U, 1996, SCAND J WORK ENV HEA, V22, P451; FLODIN U, 1995, EPIDEMIOLOGY, V6, P503, DOI 10.1097/00001648-199509000-00007; Haahtela T, 1998, THORAX, V53, P1005; HELAKORPI S, 1999, PUBLICATION NATL PUB, pB19; Johnson AR, 2000, AM J RESP CRIT CARE, V162, P2058; Karjalainen A., 1998, European Respiratory Journal, V12, p76s; Karjalainen A, 2000, AM J IND MED, V37, P451, DOI 10.1002/(SICI)1097-0274(200005)37:5<451::AID-AJIM1>3.0.CO;2-U; Kogevinas M, 1996, AM J RESP CRIT CARE, V154, P137; Kogevinas M, 1999, LANCET, V353, P1750, DOI 10.1016/S0140-6736(98)07397-8; Melbostad E, 1998, SCAND J WORK ENV HEA, V24, P262; Meredith S, 1996, THORAX, V51, P435, DOI 10.1136/thx.51.4.435; Milton DK, 1998, AM J IND MED, V33, P1, DOI 10.1002/(SICI)1097-0274(199801)33:1<1::AID-AJIM1>3.0.CO;2-2; NG TP, 1994, AM J IND MED, V25, P709, DOI 10.1002/ajim.4700250510; Pekkanen J, 1999, EUR RESPIR J, V14, P951, DOI 10.1034/j.1399-3003.1999.14d37.x; Reijula K, 1996, CHEST, V110, P58, DOI 10.1378/chest.110.1.58; ROTHMAN KJ, 1997, MODER EPIDEMIOLOGY; Sears MR, 1997, LANCET, V350, P1; Siroux V, 2000, EUR RESPIR J, V15, P470, DOI 10.1034/j.1399-3003.2000.15.08.x; Toren K, 1999, EUR RESPIR J, V13, P496, DOI 10.1183/09031936.99.13349699; TROISI RJ, 1995, CHEST, V108, P1557, DOI 10.1378/chest.108.6.1557; Venables KM, 1997, LANCET, V349, P1465, DOI 10.1016/S0140-6736(96)07219-4; VESTERINEN E, 1988, THORAX, V43, P534, DOI 10.1136/thx.43.7.534; XU XP, 1993, CHEST, V104, P1364, DOI 10.1378/chest.104.5.1364	25	132	134	0	6	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	AUG 15	2001	164	4					565	568				4	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	469LL	WOS:000170816900011	11520716	
J	Ostro, B; Lipsett, M; Mann, J; Braxton-Owens, H; White, M				Ostro, B; Lipsett, M; Mann, J; Braxton-Owens, H; White, M			Air pollution and exacerbation of asthma in African-American children in Los Angeles	EPIDEMIOLOGY			English	Article						air pollution; asthma; children; race; particulate matter; fungi; pollens; environmental exposure	EMERGENCY ROOM VISITS; RESPIRATORY HEALTH; CHILDHOOD ASTHMA; OZONE EXPOSURE; PM10 POLLUTION; ACID AEROSOLS; SYMPTOMS; SEVERITY; ADMISSIONS; CALIFORNIA	Significant increases in asthma morbidity and mortality in the United States have occurred since the 1970s, particularly among African-Americans. Exposure to various environmental factors, including air pollutants and allergens, has been suggested as a partial explanation of these trends. To examine relations between several air pollutants and asthma exacerbation in African Americans, we recruited a panel of 138 children in central Los Angeles. We recorded daily data on respiratory symptoms and medication use for 13 weeks and examined these data in conjunction with data on ozone (O-3) nitrogen dioxide (NO2), particulate matter (PM10 and PM2.5), meteorological variables, pollens, and molds. Using generalized estimating equations, we found associations between respiratory symptom occurrence and several environmental factors. For example, new episodes of cough were associated with exposure to PM10 (OR = 1.25; 95% CI = 1.12-1.39; interquartile range [IQR] = 17 mug/m(3), 24-hour average), PM2.5 (OR = 1.10; 95% CI = 1.03-1.18; IQR = 30 mug/m(3), 12-hour average), NO2, and the molds Cladosporium and Alternaria, but not with exposure to O-3 or pollen. The factors PM10 and O-3 were associated with the use of extra asthma medication. For this population several bioaerosols and air pollutants had effects that may be clinically significant.	Calif Off Environm Hlth Hazard Assessment, Air Pollut Epidemiol Unit, Oakland, CA 94612 USA; Univ Calif San Francisco, Sch Med, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA; Calif Publ Hlth Inst, Berkeley, CA USA; Ctr Dis Control & Prevent, Natl Ctr Environm Hlth, Air Pollut Resp Hlth Branch, Atlanta, GA USA	Ostro, B (reprint author), Calif Off Environm Hlth Hazard Assessment, Air Pollut Epidemiol Unit, 1515 Clay St,16th Floor, Oakland, CA 94612 USA.		White, Mary /C-9242-2012	White, Mary /0000-0002-9826-3962	PHS HHS [U60/CCU908048-03-1]		BURNETT RT, 1994, ENVIRON RES, V65, P172, DOI 10.1006/enrs.1994.1030; Delfino RJ, 1998, ENVIRON HEALTH PERSP, V106, P751, DOI 10.1289/ehp.98106751; Delfino RJ, 1997, ENVIRON HEALTH PERSP, V105, P622; Delfino RJ, 1996, AM J RESP CRIT CARE, V154, P633; Gielen MH, 1997, AM J RESP CRIT CARE, V155, P2105; Gong H, 1997, ARCH ENVIRON HEALTH, V52, P34; KAUFFMAN HF, 1995, AM J RESP CRIT CARE, V151, P2109; LIANG KY, 1986, BIOMETRIKA, V73, P13, DOI 10.1093/biomet/73.1.13; Lipsett M, 1997, ENVIRON HEALTH PERSP, V105, P216, DOI 10.1289/ehp.97105216; Mannino DM, 1998, MMWR-MORBID MORTAL W, V47, P1; McConnell R, 1999, ENVIRON HEALTH PERSP, V107, P757, DOI 10.2307/3434662; Hallaren MT, 1991, NEW ENGL J MED, V324, P359; OSTRO BD, 1991, AM J PUBLIC HEALTH, V81, P694, DOI 10.2105/AJPH.81.6.694; OSTRO BD, 1995, INHAL TOXICOL, V7, P711, DOI 10.3109/08958379509014475; POPE CA, 1991, AM REV RESPIR DIS, V144, P668; POPE CA, 1992, AM REV RESPIR DIS, V145, P1123; ROEMER W, 1993, AM REV RESPIR DIS, V147, P118; Romieu I, 1997, ARCH ENVIRON HEALTH, V52, P368; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; Sheppard L, 1999, EPIDEMIOLOGY, V10, P23, DOI 10.1097/00001648-199901000-00006; SLY RM, 1988, ANN ALLERGY, V60, P433; TARGONSKI PV, 1995, J ALLERGY CLIN IMMUN, V95, P955, DOI 10.1016/S0091-6749(95)70095-1; Thurston GD, 1997, AM J RESP CRIT CARE, V155, P654; THURSTON GD, 1994, ENVIRON RES, V65, P271, DOI 10.1006/enrs.1994.1037; WEISS KB, 1990, JAMA-J AM MED ASSOC, V264, P1683, DOI 10.1001/jama.264.13.1683; WHITE MC, 1994, ENVIRON RES, V65, P56, DOI 10.1006/enrs.1994.1021; WHITTEMORE AS, 1980, AM J PUBLIC HEALTH, V70, P687, DOI 10.2105/AJPH.70.7.687; WISSOW LS, 1988, AM J PUBLIC HEALTH, V78, P777, DOI 10.2105/AJPH.78.7.777	28	132	140	1	25	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	1044-3983			EPIDEMIOLOGY	Epidemiology	MAR	2001	12	2					200	208		10.1097/00001648-200103000-00012		9	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	405CJ	WOS:000167139400012	11246581	
J	Custovic, A; Simpson, BM; Simpson, A; Hallam, C; Craven, M; Brutsche, M; Woodcock, A				Custovic, A; Simpson, BM; Simpson, A; Hallam, C; Craven, M; Brutsche, M; Woodcock, A			Manchester Asthma and Allergy Study: Low-allergen environment can be achieved and maintained during pregnancy and in early life	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						primary prevention; dust mite; avoidance; atopy; asthma	HOUSE-DUST MITE; RISK FACTOR; P-I; SENSITIZATION; AVOIDANCE; CHILDHOOD; EXPOSURE; INFANCY; POPULATION; DISORDERS	Background: Early exposure to dust mite allergens may be critical for primary sensitization. Reducing exposure may offer a realistic chance for primary prevention of sensitization and asthma, but it is essential to implement measures that can achieve and maintain the low-allergen environment. Objective: Our purpose was to assess the effectiveness of mite allergen avoidance measures in achieving and maintaining a low-allergen environment during pregnancy and in the first year of life. Methods: The Manchester Asthma and Allergy Study is a prospective, prenatally randomized study that follows the development of asthma and atopy in a cohort of infants at high risk (both parents atopic) who are randomly allocated to full mite allergen avoidance or to a normal regimen. Avoidance measures comprise (1) mite-proof covers (mattress, pillow, and quilt) for parental bed, (2) high-filtration vacuum cleaner, (3) vinyl flooring in infant's bedroom, (4) new crib and portable crib mattresses encased in mite-proof material, (5) benzyl benzoate (Acarosan) applied on carpets and soft furniture, (6) bed linens washed in hot water weekly, and (7) washable soft toys. Dust samples from the parental bed, bedroom floor, living room floor, infant's mattress, and nursery floor were collected between the 10th and 14th weeks of pregnancy, immediately after birth, and then at age 6 months and 1 year, and Der p 1 levels were determined by mAb-based ELISA. Results: Recovered Der p 1 from maternal mattress was reduced by 97.25% (95% confidence interval [CI] 95.25%-98.41%) during the second and third trimesters of pregnancy, with the effect persisting for 6 months (98% reduction, 95% CI 97.258-99.1%) and 12 months (97.6% reduction, 95% CI 95.7%-98.6%) after the birth (active vs control, P <.000001). Total Der p 1 from bedroom floor in the active group was reduced by 53.7% (95 % CI 25.7%-71.2%) in samples collected within 4 weeks of the child's birth, with the percentage reduction being 62.8% (95 % CI 39.3%-77.2%) at 6 months and 26.5% (95% CI-24% to 57.1%) at 1 year (active compared vs control, P <.007). Der p 1 levels in crib mattress and nursery floor in the active group were extremely low (crib mattresses geometric mean [95% CI] 2.3 ng [1.6-3.4] at birth, 6.8 ng [4.5-10] at age 6 months, and 15.6 ng [9.8-24.8] at age 1 year [active vs control, P =.001]; nursery 1 ng [0.9-1.1] at birth, 1.7 ng [1.2-2.5] at age 6 months, and 2 ng [1.3-3.5] at age 1 year [active vs control, P <.00001]). The total amount of allergen recovered at age 1 year was 29-fold (95% CI 15.1- to 56.7-fold) higher in the control group than in the active group. Conclusions: The avoidance measures used in this study achieved and maintained a low mite allergen environment during pregnancy and in the first year of life in homes of infants at risk of atopy.	Wythenshawe Hosp, North West Lung Ctr, Manchester M23 9LT, Lancs, England	Custovic, A (reprint author), Wythenshawe Hosp, North West Lung Ctr, Southmoor Rd, Manchester M23 9LT, Lancs, England.		Custovic, Adnan/A-2435-2012	Custovic, Adnan/0000-0001-5218-7071; Woodcock, Ashley/0000-0002-5428-8578; Simpson, Angela/0000-0003-2733-6666			ARSHAD SH, 1992, LANCET, V339, P1493, DOI 10.1016/0140-6736(92)91260-F; Asher MI, 1998, EUR RESPIR J, V12, P315; BJORKSTEN F, 1980, CLIN ALLERGY, V10, P581; BROWN T, 1994, IRISH UNIV REV, V24, P38; Custovic A, 1998, THORAX, V53, P63; Hide DW, 1996, ALLERGY, V51, P89, DOI 10.1111/j.1398-9995.1996.tb04563.x; Hill DJ, 1997, J ALLERGY CLIN IMMUN, V99, P323, DOI 10.1016/S0091-6749(97)70049-6; Holt PG, 1997, THORAX, V52, P1; Jones CA, 1998, CLIN EXP ALLERGY, V28, P655; Leung R, 1997, J ALLERGY CLIN IMMUN, V99, P594, DOI 10.1016/S0091-6749(97)70018-6; LUCZYNSKA CM, 1989, J IMMUNOL METHODS, V118, P227, DOI 10.1016/0022-1759(89)90010-0; Munir AKM, 1997, J ALLERGY CLIN IMMUN, V100, P177, DOI 10.1016/S0091-6749(97)70221-5; *NAT ASTHM CAMP, 1999, NAT ASTHM AUD 1999 2; OWEN S, 1990, LANCET, V335, P396, DOI 10.1016/0140-6736(90)90219-U; Peat JK, 1999, J ALLERGY CLIN IMMUN, V103, P1, DOI 10.1016/S0091-6749(99)70517-8; Peat JK, 1996, AM J RESP CRIT CARE, V153, P141; Platts-Mills Thomas A. 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FEB	2000	105	2	1				252	258		10.1016/S0091-6749(00)90073-3		7	Allergy; Immunology	Allergy; Immunology	285RQ	WOS:000085402200008	10669844	
J	Bel, EH; Sousa, A; Fleming, L; Bush, A; Chung, KF; Versnel, J; Wagener, AH; Wagers, SS; Sterk, PJ; Compton, CH				Bel, Elisabeth H.; Sousa, Ana; Fleming, Louise; Bush, Andrew; Chung, K. Fan; Versnel, Jennifer; Wagener, Ariane H.; Wagers, Scott S.; Sterk, Peter J.; Compton, Chris H.		Unbiased Biomarkers Prediction	Diagnosis and definition of severe refractory asthma: an international consensus statement from the Innovative Medicine Initiative (IMI)	THORAX			English	Review							TO-TREAT ASTHMA; RANDOMIZED CONTROLLED-TRIAL; AIR-FLOW LIMITATION; LUNG-FUNCTION; SPUTUM EOSINOPHILIA; RESEARCH-PROGRAM; CLINICAL CHARACTERISTICS; INHALED CORTICOSTEROIDS; GASTROESOPHAGEAL-REFLUX; OCCUPATIONAL ASTHMA	Patients with severe refractory asthma pose a major healthcare problem. Over the last decade it has become increasingly clear that, for the development of new targeted therapies, there is an urgent need for further characterisation and classification of these patients. The Unbiased Biomarkers for the Prediction of Respiratory Disease Outcomes (U-BIOPRED) consortium is a pan-European public-private collaboration funded by the European Commission Innovative Medicines Initiative of the European Union. U-BIOPRED aims to subphenotype patients with severe refractory asthma by using an innovative systems biology approach. This paper presents the U-BIOPRED international consensus on the definition and diagnosis of severe asthma, aligning the latest concepts in adults as well as in children. The consensus is based on existing recommendations up to 2010 and will be used for the selection of patients for the upcoming U-BIOPRED study. It includes the differentiation between 'problematic', 'difficult' and 'severe refractory' asthma, and provides a systematic algorithmic approach to the evaluation of patients presenting with chronic severe asthma symptoms for use in clinical research and specialised care.	[Bel, Elisabeth H.; Wagener, Ariane H.; Sterk, Peter J.] Univ Amsterdam, Dept Resp Med, Acad Med Ctr, NL-1105 AZ Amsterdam, Netherlands; [Sousa, Ana] GlaxoSmithKline Inc, Stevenage, Herts, England; [Fleming, Louise] Univ London Imperial Coll Sci Technol & Med, Clin Trials & Evaluat Unit, London, England; [Bush, Andrew] Royal Brompton Hosp, Dept Paediat Resp Med, London SW3 6LY, England; [Chung, K. Fan] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London, England; [Versnel, Jennifer] Asthma UK, London, England; [Wagers, Scott S.] BioSci Consulting, Maasmechelen, Belgium; [Compton, Chris H.] EFPIA Headquarters, EFPIA, Brussels, Belgium	Bel, EH (reprint author), Univ Amsterdam, Dept Resp Med, Acad Med Ctr, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands.	e.h.bel@amc.uva.nl	Bisgaard, Hans/N-4761-2016	Bisgaard, Hans/0000-0003-4131-7592; Chung, Kian Fan/0000-0001-7101-1426; Djukanovic, Ratko/0000-0001-6039-5612	European Commission Innovative Medicine Initiative [IMI_Call_2008_1_12]	This report was supported by grants from the European Commission Innovative Medicine Initiative Understanding Severe Asthma, IMI_Call_2008_1_12; final protocol available at http://www.imi.europa.eu/.	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J	Reilly, JJ; Kelly, J				Reilly, J. J.; Kelly, J.			Long-term impact of overweight and obesity in childhood and adolescence on morbidity and premature mortality in adulthood: systematic review	INTERNATIONAL JOURNAL OF OBESITY			English	Review						overweight; child; BMI; morbidity	BODY-MASS INDEX; CORONARY-HEART-DISEASE; CARDIOVASCULAR RISK-FACTORS; YOUNG ADULTHOOD; FOLLOW-UP; BLOOD-PRESSURE; BREAST-CANCER; LIFE-COURSE; MIDDLE-AGE; SUBSEQUENT MORTALITY	Background and objective: The last systematic review on the health consequences of child and adolescent obesity found little evidence on consequences for adult health. The present study aimed to summarize evidence on the long-term impact of child and adolescent obesity for premature mortality and physical morbidity in adulthood. Methods: Systematic review with evidence searched from January 2002 to June 2010. Studies were included if they contained a measure of overweight and/or obesity between birth and 18 years (exposure measure) and premature mortality and physical morbidity (outcome) in adulthood. Results: Five eligible studies examined associations between overweight and/or obesity, and premature mortality: 4/5 found significantly increased risk of premature mortality with child and adolescent overweight or obesity. All 11 studies with cardiometabolic morbidity as outcomes reported that overweight and obesity were associated with significantly increased risk of later cardiometabolic morbidity (diabetes, hypertension, ischaemic heart disease, and stroke) in adult life, with hazard ratios ranging from 1.1-5.1. Nine studies examined associations of child or adolescent overweight and obesity with other adult morbidity: studies of cancer morbidity were inconsistent; child and adolescent overweight and obesity were associated with significantly increased risk of later disability pension, asthma, and polycystic ovary syndrome symptoms. Conclusions: A relatively large and fairly consistent body of evidence now demonstrates that overweight and obesity in childhood and adolescence have adverse consequences on premature mortality and physical morbidity in adulthood. International Journal of Obesity (2011) 35, 891-898; doi: 10.1038/ijo.2010.222; published online 26 October 2010	[Reilly, J. J.] Univ Glasgow, Yorkhill Hosp, Fac Med, Glasgow G3 8SJ, Lanark, Scotland; [Kelly, J.] NHS QIS, Scottish Intercollegiate Guidelines Network, Glasgow, Lanark, Scotland	Reilly, JJ (reprint author), Univ Glasgow, Yorkhill Hosp, Fac Med, Glasgow G3 8SJ, Lanark, Scotland.	jjr2y@clinmed.gla.ac.uk	Sriwisit, Sukhumaphorn/G-1405-2011		Scottish Funding Council	This work was funded by Scottish Funding Council.	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J. Obes.	JUL	2011	35	7					891	898		10.1038/ijo.2010.222		8	Endocrinology & Metabolism; Nutrition & Dietetics	Endocrinology & Metabolism; Nutrition & Dietetics	791DB	WOS:000292641300002		
J	Vocanson, M; Hennino, A; Rozieres, A; Poyet, G; Nicolas, JF				Vocanson, M.; Hennino, A.; Rozieres, A.; Poyet, G.; Nicolas, J. -F.			Effector and regulatory mechanisms in allergic contact dermatitis	ALLERGY			English	Review						allergic contact dermatitis; CD4+regulatory T cells; CD8+effector T cells; haptens; mast cells	CD8(+) T-CELLS; DELAYED-TYPE HYPERSENSITIVITY; LANGERIN(+) DENDRITIC CELLS; EPIDERMAL LANGERHANS CELLS; MAJOR HISTOCOMPATIBILITY COMPLEX; CUTANEOUS LYMPHOCYTE ANTIGEN; IN-VIVO; IMMUNE-RESPONSES; INFLAMMATORY RESPONSES; SKIN SENSITIZATION	Allergic contact dermatitis (ACD), one of the commonest occupational diseases, is a T-cell-mediated skin inflammation caused by repeated skin exposure to contact allergens, i.e. nonprotein chemicals called haptens. Allergic contact dermatitis, also referred to as contact hypersensitivity, is mediated by CD8+ T cells, which are primed in lymphoid organs during the sensitization phase and are recruited in the skin upon re-exposure to the hapten. Subsets of CD4+ T cells endowed with suppressive activity are responsible for both the down-regulation of eczema in allergic patients and the prevention of priming to haptens in nonallergic individuals. Therefore, ACD should be considered as a breakdown of the skin immune tolerance to haptens. Recent advances in the pathophysiology of ACD have demonstrated the important role of skin innate immunity in the sensitization process and have revisited the dogma that Langerhans cells are mandatory for CD8+ T-cell priming. They have also introduced mast cells as a pivotal actor in the magnitude of the inflammatory reaction. Finally, the most recent studies address the nature, the mode and the site of action of the regulatory T cells that control the skin inflammation with the aim of developing new strategies of tolerance induction in allergic patients.	[Vocanson, M.] INSERM, IFR BioSci Lyon Gerland 128, U851, F-69365 Lyon, France; [Vocanson, M.; Hennino, A.; Rozieres, A.; Poyet, G.; Nicolas, J. -F.] Univ Lyon 1, Fac Med Lyon Sud, F-69365 Lyon, France; [Vocanson, M.; Hennino, A.; Rozieres, A.; Poyet, G.; Nicolas, J. -F.] Univ Lyon, IFR128, Lyon, France; [Nicolas, J. -F.] Hosp Civils Lyon, Lyon, France	Vocanson, M (reprint author), INSERM, IFR BioSci Lyon Gerland 128, U851, 21 Av Tony Garnier, F-69365 Lyon, France.		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Immunology	Allergy; Immunology	516CT	WOS:000271520000001	19839974	
J	Burks, AW; Laubach, S; Jones, SM				Burks, A. Wesley; Laubach, Susan; Jones, Stacie M.			Oral tolerance, food allergy, and immunotherapy: Implications for future treatment	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						immune tolerance; immunotherapy; food allergy; food hypersensitivity; T cells; TGF-beta; clonal anergy; forkhead box P3 protein; sublingual immunotherapy; oral immunotherapy	REGULATORY T-CELLS; COWS MILK ALLERGY; GROWTH-FACTOR-BETA; QUALITY-OF-LIFE; PEANUT ALLERGY; TGF-BETA; ACTIVE SUPPRESSION; IMMUNE-RESPONSES; SMALL-INTESTINE; MURINE MODEL	The lumen of the gastrointestinal tract is exposed daily to an array of dietary proteins. The vast majority of proteins are tolerated through suppression of cellular or Immoral responses, a process known as oral tolerance. However, in approximately 6% of children and 4% of adults in the United States, tolerance to a given dietary antigen either is not established or breaks down, resulting in food hypersensitivity. Although food allergies can result in sudden and life-threatening symptoms, their prevalence is remarkably low considering the complexities of the gut-associated mucosal system. Suppression involves signaling by an array of nonprofessional antigen-presenting cells, dendritic cells, and regulatory T cells, as well as lymphocyte anergy or deletion. Several factors, including antigen properties, route of exposure, and genetics and age of the host, contribute to the development of oral tolerance. Although the current standard of care for patients with food allergies is based on avoidance of the trigger, increased understanding of the mechanisms involved in tolerance has shifted focus of treatment and prevention toward inducing tolerance. Data from early-phase clinical trials suggest both sublingual and oral immunotherapy are effective in reducing sensitivity to allergens. In this article we review the mechanisms of tolerance, discuss aberrations in oral tolerance, and provide information on novel prevention and treatment paradigms for food allergy.	[Burks, A. Wesley; Laubach, Susan] Duke Univ, Med Ctr, Div Allergy & Immunol, Dept Pediat, Durham, NC 27710 USA; [Jones, Stacie M.] Univ Arkansas Med Sci, Div Allergy & Immunol, Dept Pediat, Little Rock, AR 72205 USA; [Jones, Stacie M.] Arkansas Childrens Hosp, Little Rock, AR USA	Burks, AW (reprint author), Duke Univ, Med Ctr, Div Allergy & Immunol, Dept Pediat, Durham, NC 27710 USA.	wesley.burks@duke.edu					Appleman LJ, 2003, IMMUNOL REV, V192, P161, DOI 10.1034/j.1600-065X.2003.00009.x; Barone KS, 2000, CELL IMMUNOL, V199, P65, DOI 10.1006/cimm.1999.1603; BARONE KS, 1995, CELL IMMUNOL, V163, P19, DOI 10.1006/cimm.1995.1094; Bennett CL, 2001, NAT GENET, V27, P20; Beyer K, 2005, J ALLERGY CLIN IMMUN, V116, P704, DOI 10.1016/j.jaci.2005.05.007; Beyer K, 2002, J ALLERGY CLIN IMMUN, V109, P707, DOI 10.1067/mai.2002.122503; BLAND PW, 1986, IMMUNOLOGY, V58, P9; Buchanan AD, 2007, J ALLERGY CLIN IMMUN, V119, P199, DOI 10.1016/j.jaci.2006.09.016; CHASE MW, 1946, P SOC EXP BIOL MED, V61, P257; Chatchatee P, 2001, CLIN EXP ALLERGY, V31, P1256, DOI 10.1046/j.1365-2222.2001.01167.x; Chehade M, 2005, J ALLERGY CLIN IMMUN, V115, P3, DOI 10.1016/j.jaci.2004.11.008; Chen WJ, 1998, J EXP MED, V188, P1849, DOI 10.1084/jem.188.10.1849; CHEN YH, 1995, J IMMUNOL, V155, P910; CHEN YH, 1995, NATURE, V376, P177, DOI 10.1038/376177a0; Cohen BL, 2004, J ALLERGY CLIN IMMUN, V114, P1159, DOI 10.1016/j.jaci.2004.08.007; Dakin R, 1929, AM J MED SCI, V4, P98; Enrique E, 2005, J ALLERGY CLIN IMMUN, V116, P1073, DOI 10.1016/j.jaci.2005.08.027; Fadok VA, 1998, J CLIN INVEST, V101, P890, DOI 10.1172/JCI1112; Faria AMC, 2005, IMMUNOL REV, V206, P232, DOI 10.1111/j.0105-2896.2005.00280.x; Fontenot JD, 2003, NAT IMMUNOL, V4, P330, DOI 10.1038/ni904; Freire-de-Lima CG, 2000, NATURE, V403, P199, DOI 10.1038/35003208; FRIEDMAN A, 1994, P NATL ACAD SCI USA, V91, P6688, DOI 10.1073/pnas.91.14.6688; GARSIDE P, 1995, INT IMMUNOL, V7, P501, DOI 10.1093/intimm/7.3.501; *IMM TOL NETW, LEAP STUD; Iwasaki A, 2004, NAT IMMUNOL, V5, P987, DOI 10.1038/ni1112; Karlsson MR, 2004, J EXP MED, V199, P1679, DOI 10.1084/jem.20032121; Kawai T, 2006, CELL DEATH DIFFER, V13, P816, DOI 10.1038/sj.cdd.4401850; Khattri R, 2003, NAT IMMUNOL, V4, P337, DOI 10.1038/ni909; Kopper RA, 2005, INT ARCH ALLERGY IMM, V136, P16, DOI 10.1159/000082580; Kraehenbuhl J P, 1992, Trends Cell Biol, V2, P170, DOI 10.1016/0962-8924(92)90036-M; Lack G, 2003, NEW ENGL J MED, V348, P977, DOI 10.1056/NEJMoa013536; Lemaitre B, 1996, CELL, V86, P973, DOI 10.1016/S0092-8674(00)80172-5; Levy Y, 2003, ALLERGY, V58, P1206, DOI 10.1046/j.1398-9995.2003.00307.x; Li XM, 1999, J IMMUNOL, V162, P3045; Li XM, 2003, J ALLERGY CLIN IMMUN, V112, P159, DOI 10.1067/mai.2003.1622; Longo G, 2008, J ALLERGY CLIN IMMUN, V121, P343, DOI 10.1016/j.jaci.2007.10.029; Marth T, 1998, ANN NY ACAD SCI, V859, P290, DOI 10.1111/j.1749-6632.1998.tb11148.x; MASON DW, 1981, NATURE, V293, P150, DOI 10.1038/293150a0; Medzhitov R, 1997, NATURE, V388, P394; Meglio P, 2004, ALLERGY, V59, P980, DOI 10.1111/j.1398-9995.2004.00542.x; Menezes JD, 2003, INT IMMUNOL, V15, P447, DOI 10.1093/intimm/dxg043; MICHAEL JG, 1989, IMMUNOL INVEST, V18, P1049, DOI 10.3109/08820138909030606; Morafo V, 2003, J ALLERGY CLIN IMMUN, V111, P1122, DOI 10.1067/mai.2003.1463; Nakamura K, 2001, J EXP MED, V194, P629, DOI 10.1084/jem.194.5.629; Nelson HS, 1997, J ALLERGY CLIN IMMUN, V99, P744, DOI 10.1016/S0091-6749(97)80006-1; Ostroukhova M, 2004, J CLIN INVEST, V114, P28, DOI 10.1172/JC1200420509; Patriarca G, 2003, ALIMENT PHARM THERAP, V17, P459, DOI 10.1046/j.0269-2813.2003.01468.x; Piccirillo CA, 2002, J EXP MED, V196, P237, DOI 10.1084/jem.20020590; Primeau MN, 2000, CLIN EXP ALLERGY, V30, P1135, DOI 10.1046/j.1365-2222.2000.00889.x; Rolinck-Werninghaus C, 2005, ALLERGY, V60, P1320, DOI 10.1111/j.1398-9995.2005.00882.x; SCOTT H, 1980, SCAND J IMMUNOL, V12, P77, DOI 10.1111/j.1365-3083.1980.tb00043.x; Shreffler WG, 2006, J IMMUNOL, V177, P3677; Sicherer SH, 2007, J ALLERGY CLIN IMMUN, V120, P491, DOI 10.1016/j.jaci.2007.07.015; Sicherer SH, 2006, J ALLERGY CLIN IMMUN, V117, pS470, DOI 10.1016/j.jaci.2005.05.048; Sicherer SH, 2001, ANN ALLERG ASTHMA IM, V87, P461; Staden U, 2007, ALLERGY, V62, P1261, DOI 10.1111/j.1398-9995.2007.01501.x; Strid J, 2005, CLIN EXP ALLERGY, V35, P757, DOI 10.1111/j.1365-2222.2005.02260.x; STROBEL S, 1984, PEDIATR RES, V18, P588, DOI 10.1203/00006450-198407000-00004; Torgerson TR, 2007, GASTROENTEROLOGY, V132, P1705, DOI 10.1053/j.gastro.2007.02.044; Wells HG, 1911, J INFECT DIS, V9, P147; Yocum MW, 1999, J ALLERGY CLIN IMMUN, V104, P452, DOI 10.1016/S0091-6749(99)70392-1	61	131	140	4	24	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUN	2008	121	6					1344	1350		10.1016/j.jaci.2008.02.037		7	Allergy; Immunology	Allergy; Immunology	313WW	WOS:000256771700007	18410959	
J	Jansen, KL; Larson, TV; Koenig, JQ; Mar, TF; Fields, C; Stewart, J; Lippmann, M				Jansen, KL; Larson, TV; Koenig, JQ; Mar, TF; Fields, C; Stewart, J; Lippmann, M			Associations between health effects and particulate matter and black carbon in subjects with respiratory disease	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; black carbon; chronic obstructive pulmonary disease; fractional exhaled nitric oxide; panel study; particulate matter	EXHALED NITRIC-OXIDE; OBSTRUCTIVE PULMONARY-DISEASE; AMBIENT AIR-POLLUTION; SHORT-TERM EXPOSURE; SOURCE APPORTIONMENT; ULTRAFINE PARTICLES; ASTHMATIC-CHILDREN; OXYGEN-SATURATION; FINE PARTICLES; LUNG-FUNCTION	We measured fractional exhaled nitric oxide (FENO), spirometry, blood pressure, oxygen saturation of the blood (SaO(2)), and pulse rate in 16 older subjects with asthma or chronic obstructive pulmonary disease (COPD) in Seattle, Washington. Data were collected daily for 12 days. We simultaneously collected PM10 and PM2.5 (particulate matter <= 10 mu m or <= 2.5 mu m, respectively) filter samples at a central outdoor site, as well as outside and inside the subjects' homes. Personal PM10 filter samples were also collected. All filters were analyzed for mass and light absorbance. We analyzed within-subject associations between health outcomes and air pollution metrics using a linear mixed-effects model with random intercept, controlling for age, ambient relative humidity, and ambient temperature. For the 7 subjects with asthma, a 10 mu g/m(3) increase in 24-hr average outdoor PM10 and PM2.5 was associated with a 5.9 [95% confidence interval (CI), 2.9-8.9] and 4.2 ppb (95% CI, 1.3-7.1) increase in FENO, respectively. A 1 mu g/m(3) increase in outdoor, indoor, and personal black carbon (BC) was associated with increases in FENO of 2.3 ppb (95% Cl, 1.1-3.6), 4.0 ppb (95% CI, 2.0-5.9), and 1.2 ppb (95% Cl, 0.2-2.2), respectively. No significant association was found between PM or BC measures and changes in spirometry, blood pressure, pulse rate, or SaO(2) in these subjects. Results from this study indicate that FENO may be a more sensitive market of PM exposure than traditional health outcomes and that particle-associated BC is useful for examining associations between primary combustion constituents of PM and health outcomes.	Univ Washington, Sch Publ Hlth & Community Med, Dept Environm & Occupat Hlth Sci, Seattle, WA 98195 USA; NYU, Sch Med, Tuxedo Pk, NY USA	Koenig, JQ (reprint author), Univ Washington, Sch Publ Hlth & Community Med, Dept Environm & Occupat Hlth Sci, Box 357234, Seattle, WA 98195 USA.	jkoenig@u.washington.edu			NIEHS NIH HHS [ES 07033, P30 ES007033]		Adamkiewicz G, 2004, THORAX, V59, P204, DOI 10.1136/thorax.2003.006445; ALLEN R, 2001, J AIR WASTE MANAGE, V51, P1651; Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; Brauer M, 2001, J EXPO ANAL ENV EPID, V11, P490, DOI 10.1038/sj.jea.7500195; Brunekreef B., 2005, RES REP HLTH EFF I, V127, P1; CONNY JM, 2002, J GEOPHYS RES, P107; Crapo RO, 1995, AM J RESP CRIT CARE, V152, P1107; DeMeo DL, 2004, AM J RESP CRIT CARE, V170, P383, DOI 10.1164/rccm.200402-244OC; Deykin A, 1998, AM J RESP CRIT CARE, V157, P769; Dockery DW, 2001, ENVIRON HEALTH PERSP, V109, P483, DOI 10.2307/3454657; Fischer PH, 2002, INT ARCH OCC ENV HEA, V75, P348, DOI 10.1007/s00420-002-0320-x; Gan WQ, 2004, THORAX, V59, P574, DOI 10.1136/thx.2003.019588; Gauderman WJ, 2004, NEW ENGL J MED, V351, P1057, DOI 10.1056/NEJMoa040610; Gielen MH, 1997, AM J RESP CRIT CARE, V155, P2105; Gold DR, 2005, ENVIRON HEALTH PERSP, V113, P883, DOI 10.1289/ehp.7737; Gong Jr H, 2003, RES REP HLTH EFF I, V118; Hobbs PV, 2003, J GEOPHYS RES-ATMOS, V108, DOI 10.1029/2002JD002352; Ibald-Mulli A, 2001, AM J PUBLIC HEALTH, V91, P571, DOI 10.2105/AJPH.91.4.571; Jobsis Q, 1999, EUR RESPIR J, V13, P1406; Jones SL, 2002, EUR RESPIR J, V20, P601, DOI 10.1183/09031936.02.00285302; KHARITONOV SA, 1995, AM J RESP CRIT CARE, V152, P609; Kim JJ, 2004, AM J RESP CRIT CARE, V170, P520, DOI 10.1164/rccm.200403-2810C; KOENIG JQ, 1993, ENVIRON RES, V63, P26, DOI 10.1006/enrs.1993.1123; Koenig JQ, 2003, ENVIRON HEALTH PERSP, V111, P1625, DOI 10.1289/ehp.6160; Larson T, 2004, J AIR WASTE MANAGE, V54, P1175; Li XY, 1996, THORAX, V51, P1216, DOI 10.1136/thx.51.12.1216; LIN C, 1973, APPL OPTICS, V12, P1356, DOI 10.1364/AO.12.001356; Linn WS, 1999, J AIR WASTE MANAGE, V49, P108; Liu LJS, 2003, ENVIRON HEALTH PERSP, V111, P909, DOI 10.1289/ehp.6011; Liu LJS, 2002, ENVIRON SCI TECHNOL, V36, P2977, DOI 10.1021/es0112644; Mar TF, 2005, EPIDEMIOLOGY, V16, P681, DOI 10.1097/01.ede.0000173037.83211.d6; Martin LD, 1997, ENVIRON HEALTH PERSP, V105, P1301, DOI 10.2307/3433551; Maykut NN, 2003, ENVIRON SCI TECHNOL, V37, P5135, DOI 10.1021/es030370y; Mayol-Bracero OL, 2002, J GEOPHYS RES-ATMOS, V107, DOI 10.1029/2001JD000522; Maziak W, 1998, AM J RESP CRIT CARE, V157, P998; Newson EJ, 2000, J OCCUP ENVIRON MED, V42, P270, DOI 10.1097/00043764-200003000-00007; Nightingale JA, 1999, THORAX, V54, P1061; O'Neill MS, 2005, CIRCULATION, V111, P2913, DOI 10.1161/CIRCULATIONAHA.104.517110; Olin AC, 2001, RESP MED, V95, P491, DOI 10.1053/rmed.2001.1076; Pekkanen J, 1997, ENVIRON RES, V74, P24, DOI 10.1006/enrs.1997.3750; Peters A, 1999, AM J EPIDEMIOL, V150, P1094; Peters A, 2000, EPIDEMIOLOGY, V11, P11, DOI 10.1097/00001648-200001000-00005; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Piacentini GL, 2002, PEDIATR ALLERGY IMMU, V13, P137, DOI 10.1034/j.1399-3038.2002.00072.x; Pietropaoli AP, 2004, INHAL TOXICOL, V16, P59, DOI 10.1080/08958370490443079; Pope CA, 1999, AM J RESP CRIT CARE, V159, P365; POPE CA, 1999, ENVIRON HEALTH PERSP, V107, P567, DOI 10.2307/3434399; Posfai M, 2004, J GEOPHYS RES-ATMOS, V109, DOI 10.1029/2003JD004169; Romieu I, 1996, AM J RESP CRIT CARE, V154, P300; Salvi S, 1999, AM J RESP CRIT CARE, V159, P702; Schwartz J, 2000, EPIDEMIOLOGY, V11, P6, DOI 10.1097/00001648-200001000-00004; Shepherd MD, 1999, DIFFER GEOM APPL, V10, P1, DOI 10.1016/S0926-2245(98)00025-4; SLAUGHTER JC, 2004, J EXPO ANAL ENV EPID, V9, P1; Slutsky AS, 1999, AM J RESP CRIT CARE, V160, P2104; Steerenberg PA, 1999, EUR RESPIR J, V13, P334, DOI 10.1034/j.1399-3003.1999.13b19.x; Tunnicliffe WS, 2003, OCCUP ENVIRON MED, V60, DOI 10.1136/oem.60.11.e15; U.S. EPA, 2004, 600P99002ABF US EPA; Van Amsterdam JGC, 1999, ARCH ENVIRON HEALTH, V54, P331; Yu OC, 2000, ENVIRON HEALTH PERSP, V108, P1209, DOI 10.2307/3434835	59	131	139	2	56	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765	1552-9924		ENVIRON HEALTH PERSP	Environ. Health Perspect.	DEC	2005	113	12					1741	1746		10.1289/ehp.8153		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	989ZP	WOS:000233713200046	16330357	
J	Kabesch, M; Hoefler, C; Carr, D; Leupold, W; Weiland, SK; von Mutius, E				Kabesch, M; Hoefler, C; Carr, D; Leupold, W; Weiland, SK; von Mutius, E			Glutathione S transferase deficiency and passive smoking increase childhood asthma	THORAX			English	Article							ENVIRONMENTAL TOBACCO-SMOKE; PARENTAL SMOKING; SPIROMETRIC INDEXES; LUNG-FUNCTION; CHILDREN; POLYMORPHISMS; M1; PREVALENCE; GENOTYPES; GENE	Background: It has been suggested that the genetically determined deficiency of glutathione S transferase (GST) enzymes involved in the detoxification of environmental tobacco smoke (ETS) components may contribute to the development of asthma. Methods: A large population of German schoolchildren (n = 3054) was genotyped for deficiencies of the GST isoforms M1 and T1. The association between GSTM1 and GSTT1 genotypes and asthma as well as atopy was investigated with respect to current and in utero ETS exposure. Results: In children lacking the GSTM1 allele who were exposed to current ETS the risk for current asthma (OR 5.5, 95% CI 1.6 to 18.6) and asthma symptoms such as wheeze ever (OR 2.8, 95% CI 1.3 to 6.0), current wheezing (OR 4.7, 95% CI 1.8 to 12.6) and shortness of breath (OR 8.9, 95% CI 2.1 to 38.4) was higher than in GSTM1 positive individuals without ETS exposure. Hints of an interaction between ETS exposure and GSTM1 deficiency were identified. In utero smoke exposure in GSTT1 deficient children was associated with significant decrements in lung function compared with GSTT1 positive children not exposed to ETS. Conclusions: GSTM1 and GSTT1 deficiency may increase the adverse health effects of in utero and current smoke exposure.	Univ Munich, Childrens Univ Hosp, D-80337 Munich, Germany; Univ Childrens Hosp Dresden, Dresden, Germany; Univ Ulm, Inst Epidemiol, D-89069 Ulm, Germany	Kabesch, M (reprint author), Univ Munich, Childrens Univ Hosp, Lindwurmstr 4, D-80337 Munich, Germany.	Kabesch@med.uni-muenchen.de	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Alexandrov K, 2002, CARCINOGENESIS, V23, P1969, DOI 10.1093/carcin/23.12.1969; Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Botto LD, 2001, AM J EPIDEMIOL, V153, P1016, DOI 10.1093/aje/153.10.1016; Chen CL, 1996, PHARMACOGENETICS, V6, P187, DOI 10.1097/00008571-199604000-00005; COOK DG, 1993, THORAX, V48, P14, DOI 10.1136/thx.48.1.14; Cook DG, 1999, THORAX, V54, P357; Cook DG, 1997, THORAX, V52, P1081; Cook DG, 1998, THORAX, V53, P884; Gilliland FD, 2002, AM J RESP CRIT CARE, V166, P457, DOI 10.1164/rccm.2112064; Gilliland FD, 2002, AM J RESP CRIT CARE, V166, P710, DOI 10.1164/rccm.2112065; Gilliland FD, 2004, LANCET, V363, P119, DOI 10.1016/S0140-6736(03)15262-2; Ivaschenko TE, 2002, J MOL MED-JMM, V80, P39, DOI 10.1007/s001090100274; Kabesch M, 2003, J ALLERGY CLIN IMMUN, V111, P813, DOI 10.1067/mai.2003.1336; Lazarus R, 2002, IMMUNOL REV, V190, P9, DOI 10.1034/j.1600-065X.2002.19002.x; LOFROTH G, 1989, MUTAT RES, V222, P73, DOI 10.1016/0165-1218(89)90021-9; Menegon A, 1998, LANCET, V352, P1344, DOI 10.1016/S0140-6736(98)03453-9; Oddoze C, 1999, CLIN CHEM, V45, P505; Ollikainen T, 1998, ENVIRON MOL MUTAGEN, V31, P311, DOI 10.1002/(SICI)1098-2280(1998)31:4<311::AID-EM2>3.0.CO;2-L; Reiner A, 2003, BIOINFORMATICS, V19, P368, DOI 10.1093/bioinformatics/btf877; Ryberg D, 1997, CARCINOGENESIS, V18, P1285, DOI 10.1093/carcin/18.7.1285; Sheehan D, 2001, BIOCHEM J, V360, P1, DOI 10.1042/0264-6021:3600001; VANPOPPEL G, 1992, CARCINOGENESIS, V13, P303, DOI 10.1093/carcin/13.2.303; von Ehrenstein OS, 2002, EUR RESPIR J, V19, P1099, DOI 10.1183/09031936.02.00104302; Weiland SK, 1999, EUR RESPIR J, V14, P862, DOI 10.1034/j.1399-3003.1999.14d23.x	25	131	133	0	5	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	JUL	2004	59	7					569	573		10.1136/thx.2003.016667		5	Respiratory System	Respiratory System	833IC	WOS:000222329600007	15223862	
J	Bachrach, VRG; Schwarz, E; Bachrach, LR				Bachrach, VRG; Schwarz, E; Bachrach, LR			Breastfeeding and the risk of hospitalization for respiratory disease in infancy - A meta-analysis	ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE			English	Article							SYNCYTIAL VIRUS-INFECTION; BREAST-FEEDING DEFINITIONS; PARENTAL SMOKING; PASSIVE SMOKING; ATOPIC DISEASE; ASTHMA; CHILDREN; BRONCHIOLITIS; ILLNESS; ASSOCIATION	Objective: To examine breastfeeding and the risk of hospitalization for lower respiratory tract disease in healthy full-term infants with access to modern medical care. Data Sources: MEDLINE, personal communication with researchers, the OVID databases, Dissertation Abstracts Online, and BIOSIS. Study Selection: The titles, abstracts, and text of studies from developed countries were explored for breastfeeding exposure measures and lower respiratory tract disease hospitalization rates. For summary statistics, we required 3 inclusion criteria: (1) a feeding contrast of a minimum of 2 months of exclusive breastfeeding (no formula supplementation) vs no breastfeeding and (2) study populations that excluded sick, low birth weight or premature infants and (3) reflected affluent regions; 27% of studies met these criteria. Data Extraction: We abstracted data from all relevant reports. Data Synthesis: Data from all primary material (33 studies) indicated a protective association between breastfeeding and the risk of respiratory disease hospitalization. Nine studies met all inclusion criteria, and 7 cohort studies were pooled. The feeding contrasts in these 7 studies were 4 or more months of exclusive breastfeeding vs no breastfeeding. The summary relative risk (95% confidence interval) was 0.28 (0.14-0.54), using a random-effects model. This effect remained stable and statistically significant after adjusting for the effects of smoking or socioeconomic status. Conclusion: Among generally healthy infants in developed nations, more than a tripling in severe respiratory tract illnesses resulting in hospitalizations was noted for infants who were not breastfed compared with those who were exclusively breastfed for 4 months.	Univ Calif San Francisco, Div Gen Internal Med, San Francisco, CA 94143 USA; Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA	Bachrach, VRG (reprint author), Oak Hill Ave, Palo Alto, CA 94306 USA.			Schwarz, Eleanor Bimla/0000-0002-9912-8236			*ABB LAB ROSS PROD, ROSS MOTH SURV; ANDERSON LJ, 1988, PEDIATRICS, V82, P300; AVERY ME, 1994, PEDIAT MED, P286; Ball TM, 1999, PEDIATRICS, V103, P870; BAUCHNER H, 1986, JAMA-J AM MED ASSOC, V256, P887, DOI 10.1001/jama.256.7.887; BEAUDRY M, 1995, J PEDIATR-US, V126, P191, DOI 10.1016/S0022-3476(95)70544-9; Beck Laurie F, 2002, MMWR Surveill Summ, V51, P1; Lopez Bravo IM, 1997, REV PANAM SALUD PUBL, V1, P9; Bulkow LR, 2002, PEDIATRICS, V109, P210, DOI 10.1542/peds.109.2.210; Busse W W, 1999, Can Respir J, V6, P97; Busse WW, 2001, NEW ENGL J MED, V344, P350; CARLSEN KH, 1987, PEDIATR PULM, V3, P153, DOI 10.1002/ppul.1950030308; Cesar JA, 1999, BRIT MED J, V318, P1316; CHEN Y, 1989, CHEST, V95, P1004, DOI 10.1378/chest.95.5.1004; CHEN Y, 1988, PEDIATRICS, V81, P58; Coffin CJ, 1997, CONTRACEPTION, V55, P323, DOI 10.1016/S0010-7824(97)00039-5; COOK RJ, 1995, BRIT MED J, V310, P452; CULLINAN TR, 1983, ARCH DIS CHILD, V58, P423; CUNNINGHAM AS, 1979, J PEDIATR-US, V95, P685, DOI 10.1016/S0022-3476(79)80711-8; Dell S, 2001, ARCH PEDIAT ADOL MED, V155, P1261; *DEP HLTH HUM SERV, 2001, DHHS PUBL, P211; DEWEY KG, 1995, J PEDIATR-US, V126, P696, DOI 10.1016/S0022-3476(95)70395-0; DOWNHAM MAPS, 1976, BRIT MED J, V2, P274; ELLESTADSAYED J, 1979, CAN MED ASSOC J, V120, P295; ELLIS AA, 1991, WHY ARE PRESCHOOL CH, P14; *EUR LONG STUD PRE, 1989, PAEDIATR PERINAT EP, V3, P460; FALLOT ME, 1980, PEDIATRICS, V65, P1121; FERGUSSON DM, 1981, AUST PAEDIATR J, V17, P191; FRANK AL, 1982, PEDIATRICS, V70, P239; Gartner LM, 1997, PEDIATRICS, V100, P1035; Gern JE, 2000, J ALLERGY CLIN IMMUN, V106, P201; Golding J, 1997, EARLY HUM DEV, V49, pS105, DOI 10.1016/S0378-3782(97)00056-X; Goldman AS, 1997, CURR TOP MICROBIOL, V222, P205; Haby MM, 2001, THORAX, V56, P589, DOI 10.1136/thorax.56.8.589; HALL CB, 1984, J PEDIATR-US, V105, P358, DOI 10.1016/S0022-3476(84)80005-0; Hanson LA, 2000, ACTA PAEDIATR, V89, P252, DOI 10.1080/080352500750028339; Hawkes JS, 1999, PEDIATR RES, V45, P648, DOI 10.1203/00006450-199905010-00006; HEILMAN CA, 1990, J INFECT DIS, V161, P402; Henderson L, 2000, BRIT MED J, V321, P1196, DOI 10.1136/bmj.321.7270.1196; Hoey C, 1997, AM J MANAG C, V3, P861; Howard TS, 2000, J PEDIATR-US, V137, P227, DOI 10.1067/mpd.2000.107525; HOWIE PW, 1990, BRIT MED J, V300, P11; *I MED, 1985, NEW VACC DEV EST PRI, V2; JIN C, 1993, J PEDIATR-US, V123, P553, DOI 10.1016/S0022-3476(05)80949-7; KAUFMAN HS, 1976, ANN ALLERGY, V37, P410; KOVAR MG, 1984, PEDIATRICS, V74, P615; KRAMER MS, 1988, J PEDIATR-US, V112, P181, DOI 10.1016/S0022-3476(88)80054-4; Kramer MS, 2001, JAMA-J AM MED ASSOC, V285, P413, DOI 10.1001/jama.285.4.413; LABBOK M, 1990, STUD FAMILY PLANN, V21, P226, DOI 10.2307/1966617; LEVENTHAL JM, 1986, PEDIATRICS, V78, P896; MOK JYQ, 1982, BRIT MED J, V285, P333; Nafstad P, 1996, EUR RESPIR J, V9, P2623, DOI 10.1183/09031936.96.09122623; Oddy WH, 1999, BRIT MED J, V319, P815; *OFF WOM HLTH, 2000, BREASTF HHS BLUEPR A; OGSTON SA, 1987, J EPIDEMIOL COMMUN H, V41, P21, DOI 10.1136/jech.41.1.21; Pabst HF, 1997, ACTA PAEDIATR, V86, P1291, DOI 10.1111/j.1651-2227.1997.tb14900.x; Perlstein PH, 2000, ARCH PEDIAT ADOL MED, V154, P1001; PETITTI DB, 2000, MONOGRAPHS EPIDEMIOL, P101; PISACANE A, 1994, ACTA PAEDIATR, V83, P714, DOI 10.1111/j.1651-2227.1994.tb13125.x; PULLAN CR, 1980, BRIT MED J, V281, P1034; RYLANDER E, 1995, EPIDEMIOLOGY, V6, P289, DOI 10.1097/00001648-199505000-00017; SAARINEN UM, 1995, LANCET, V346, P1065, DOI 10.1016/S0140-6736(95)91742-X; Shay DK, 1999, JAMA-J AM MED ASSOC, V282, P1440, DOI 10.1001/jama.282.15.1440; SIGURS N, 1995, PEDIATRICS, V95, P500; Sigurs N, 2000, AM J RESP CRIT CARE, V161, P1501; SLY R, 2000, NELSON TXB PEDIAT, P666; Smith DH, 1997, AM J RESP CRIT CARE, V156, P787; Spencer N, 1996, ARCH DIS CHILD, V74, P50; *STAT CORP, 1999, STAT TECHN B REPR, V8; TAYLOR B, 1982, LANCET, V1, P1227; Weiss KB, 1992, CHEST, V101, P362; [Anonymous], 1994, LANCET, V344, P1239	72	131	142	0	9	AMER MEDICAL ASSOC	CHICAGO	515 N STATE ST, CHICAGO, IL 60610 USA	1072-4710			ARCH PEDIAT ADOL MED	Arch. Pediatr. Adolesc. Med.	MAR	2003	157	3					237	243				7	Pediatrics	Pediatrics	653KX	WOS:000181435300007	12622672	
J	Janson, C; Chinn, S; Jarvis, D; Zock, JP; Toren, K; Burney, P				Janson, C; Chinn, S; Jarvis, D; Zock, JP; Toren, K; Burney, P		European Community Resp Hlth Surv	Effect of passive smoking on respiratory symptoms, bronchial responsiveness, lung function, and total serum IgE in the European Community Respiratory Health Survey: a cross-sectional study	LANCET			English	Article							ENVIRONMENTAL TOBACCO-SMOKE; PULMONARY-FUNCTION; PARENTAL SMOKING; ASTHMA; EXPOSURE; ADULTS; SENSITIZATION; POPULATION; WOMEN; HYPERRESPONSIVENESS	Background Passive smoking is widespread, and environmental tobacco smoke contains many potent respiratory irritants. This analysis aimed to estimate the effect of passive smoking on respiratory symptoms, bronchial responsiveness, lung function, and total serum IgE in the European Community Respiratory Health Survey. Methods This analysis included data from 7882 adults (age 20-48 years) who had never smoked, from 36 centres in.16 countries. Information on passive smoking, respiratory symptoms, asthma, and allergic rhinitis was gathered through a structured interview. Spirometry and methacholine challenge were carried out, and total and specific IgE were measured. The effect of passive smoking was estimated by means of logistic and multiple linear regression for each country and combined across countries by random-effects meta-analysis. Findings In 12 of the 36 centres, more than half the participants were regularly involuntarily exposed to tobacco smoke. The prevalence of passive smoking in the workplace varied from 2.5% in Uppsala, Sweden, to 53.8% in Galdalkao, Spain. Passive smoking was significantly associated with nocturnal chest tightness (odds ratio 1.28 [95% CI 1.02 to 1.60]), nocturnal breathlessness (1.30 [1.01 to 1.67]), breathlessness after activity (1.25 [1.07 to 1.47]), and increased bronchial responsiveness (effect -0.18 [-0.30 to -0.05]). Passive smoking in the workplace was significantly associated with all types of respiratory symptoms and current asthma (odds ratio 1.90 [95% CI 0.90 to 2.88]). No significant association was found between passive smoking and total serum IgE. Interpretation Passive smoking is common but the prevalence varies widely between different countries, Passive smoking increased the likelihood of experiencing respiratory symptoms and was associated with increased bronchial responsiveness. Decreasing involuntary exposure to tobacco smoke in the community, especially in workplaces, is likely to improve respiratory health.	Uppsala Univ, Akad Sjukhuset, Dept Med Sci Resp Med & Allergol, Uppsala, Sweden; Univ London Kings Coll, Dept Publ Hlth Sci, London WC2R 2LS, England; IMIM, Resp & Environm Hlth Res Unit, Barcelona, Spain; Sahlgrens Univ Hosp, Sect Occupat & Environm Hlth, S-41345 Gothenburg, Sweden; Sahlgrens Univ Hosp, Sect Allergol, S-41345 Gothenburg, Sweden	Janson, C (reprint author), Akad Sjukhuset, Dept Resp Med, SE-75185 Uppsala, Sweden.		Jarvis, Deborah/E-6494-2011; Jarvis, Martin/B-1034-2008	Jarvis, Martin/0000-0001-9238-8038			Blanc PD, 1999, AM J RESP CRIT CARE, V160, P2028; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; CARREY IM, 1999, EPIDEMIOLOGY, V10, P319; Chinn S, 1997, EUR RESPIR J, V10, P2495, DOI 10.1183/09031936.97.10112495; Chinn S, 1999, EUR RESPIR J, V14, P876, DOI 10.1034/j.1399-3003.1999.14d25.x; Cook DG, 1999, THORAX, V54, P357; Corrao M, 2000, TOBACCO CONTROL COUN; Coultas DB, 1998, THORAX, V53, P381; DELFINO RJ, 1993, EUR RESPIR J, V6, P1104; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; European Community for Coal and Steel, 1983, CLIN RESP PHYS S5, V19, P22; Frette C, 1996, AM J EPIDEMIOL, V143, P757; GREER JR, 1993, J OCCUP ENVIRON MED, V35, P909, DOI 10.1097/00043764-199309000-00014; Jarvis D, 1999, J ALLERGY CLIN IMMUN, V104, P934, DOI 10.1016/S0091-6749(99)70071-0; Kogevinas M, 1999, LANCET, V353, P1750, DOI 10.1016/S0140-6736(98)07397-8; LEUENBERGER P, 1994, AM J RESP CRIT CARE, V150, P1222; Leynaert B, 1997, AM J RESP CRIT CARE, V156, P1413; MASJEDI MR, 1990, THORAX, V45, P27, DOI 10.1136/thx.45.1.27; MENON P, 1992, J ALLERGY CLIN IMMUN, V89, P560, DOI 10.1016/0091-6749(92)90323-T; OLIVIERI M, IN PRESS ARCH ENV HL; Oryszczyn MP, 2000, AM J RESP CRIT CARE, V161, P1241; Piitulainen E, 1998, THORAX, V53, P939; Pirkle JL, 1996, JAMA-J AM MED ASSOC, V275, P1233; Plaschke PP, 2000, AM J RESP CRIT CARE, V162, P920; RANDO RJ, 1992, AM IND HYG ASSOC J, V53, P699, DOI 10.1202/0002-8894(1992)053<0699:AOMMOE>2.0.CO;2; RIBOLI E, 1990, CANCER CAUSE CONTROL, V1, P243, DOI 10.1007/BF00117476; ROBBINS AS, 1993, INT J EPIDEMIOL, V22, P809, DOI 10.1093/ije/22.5.809; Roca J, 1998, EUR RESPIR J, V11, P1354, DOI 10.1183/09031936.98.11061354; Sapigni T, 1998, EUR RESPIR J, V11, P278, DOI 10.1183/09031936.98.11020278; STANKUS RP, 1988, J ALLERGY CLIN IMMUN, V82, P331, DOI 10.1016/0091-6749(88)90003-6; Strachan DP, 1998, THORAX, V53, P117; Sunyer J, 1997, THORAX, V52, P235; Thorn J, 2001, ALLERGY, V56, P287, DOI 10.1034/j.1398-9995.2001.00805.x; XU XP, 1995, AM J RESP CRIT CARE, V151, P41	34	131	132	0	5	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	DEC 22	2001	358	9299					2103	2109		10.1016/S0140-6736(01)07214-2		7	Medicine, General & Internal	General & Internal Medicine	505GV	WOS:000172905800007	11784622	
J	Dennekamp, M; Howarth, S; Dick, CAJ; Cherrie, JW; Donaldson, K; Seaton, A				Dennekamp, M; Howarth, S; Dick, CAJ; Cherrie, JW; Donaldson, K; Seaton, A			Ultrafine particles and nitrogen oxides generated by gas and electric cooking	OCCUPATIONAL AND ENVIRONMENTAL MEDICINE			English	Article						cooking fuels; nitrogen oxides; ultrafine particles	PARTICULATE AIR-POLLUTION; PERSONAL EXPOSURE; RESPIRATORY SYMPTOMS; DIOXIDE EXPOSURE; LUNG-CANCER; PULMONARY TOXICITY; INHALED ALLERGEN; PM10 POLLUTION; CHILDREN; HEALTH	Objectives - To measure the concentrations of particles less than 100 nm diameter and of oxides of nitrogen generated by cooking with gas and electricity, to comment on possible hazards to health in poorly ventilated kitchens. Methods - Experiments with gas and electric rings, grills, and ovens were used to compare different cooking procedures. Nitrogen oxides (NO,) were measured by a chemiluminescent ML9841A NO, analyser. A TSI 3934 scanning mobility particle sizer was used to measure average number concentration and size distribution of aerosols in the size range 10-500 nm. Results-High concentrations of particles are generated by gas combustion, by frying, and by cooking of fatty foods. Electric rings and grills may also generate particles from their surfaces. In experiments where gas burning was the most important source of particles, most particles were in the size range 15-40 nm. When bacon was fried on the gas or electric rings the particles were of larger diameter, in the size range 50-100 nm. The smaller particles generated during experiments grew in size with time because of coagulation. Substantial concentrations of NO, were generated during cooking on gas; four rings for 15 minutes produced 5 minute peaks of about 1000 ppb nitrogen dioxide and about 2000 ppb nitric oxide. Conclusions - Cooking in a poorly ventilated kitchen may give rise to potentially toxic concentrations of numbers of particles. Very high concentrations of oxides of nitrogen may also be generated by gas cooking, and with no extraction and poor ventilation, may reach concentrations at which adverse health effects may be expected. Although respiratory effects of exposure to NO, might be anticipated, recent epidemiology suggests that cardiac effects cannot be excluded, and further investigation of this is desirable.	Univ Aberdeen, Sch Med, Dept Environm & Occupat Med, Aberdeen AB25 2ZD, Scotland; Napier Univ, Sch Life Sci, Edinburgh EH10 5DT, Midlothian, Scotland	Seaton, A (reprint author), Univ Aberdeen, Sch Med, Dept Environm & Occupat Med, Foresterhill, Aberdeen AB25 2ZD, Scotland.		Cherrie, John/A-4879-2008	Cherrie, John/0000-0001-8901-6890			Abt E, 2000, ENVIRON HEALTH PERSP, V108, P35, DOI 10.2307/3454293; Anderson HR, 1998, THORAX, V53, P842; Berry RW, 1996, INDOOR AIR QUALITY 1; Chao CYH, 2000, BUILD ENVIRON, V35, P545, DOI 10.1016/S0360-1323(99)00040-2; Chiang TA, 1999, ENVIRON RES, V81, P18, DOI 10.1006/enrs.1998.3876; Cyrys J, 2000, SCI TOTAL ENVIRON, V250, P51, DOI 10.1016/S0048-9697(00)00361-2; Dick CAJ, 2001, OCCUP ENVIRON MED, V58, P208, DOI 10.1136/oem.58.3.208; Dimitroulopoulou C, 2001, ATMOS ENVIRON, V35, P269, DOI 10.1016/S1352-2310(00)00176-X; DOCKERY DW, 1994, ANNU REV PUBL HEALTH, V15, P107, DOI 10.1146/annurev.pu.15.050194.000543; DONALDSON K, 1998, MECH LUNG INJURY CAU, V10, P21; Farrow A, 1997, ARCH ENVIRON HEALTH, V52, P189; FERIN J, 1990, J AEROSOL SCI, V21, P381, DOI 10.1016/0021-8502(90)90064-5; FERIN J, 1992, AM J RESP CELL MOL, V6, P535; GAO YT, 1987, INT J CANCER, V40, P604, DOI 10.1002/ijc.2910400505; Garrett MH, 1998, AM J RESP CRIT CARE, V158, P891; Hajat S, 1999, THORAX, V54, P597; Jarvis D, 1998, EUR RESPIR J, V11, P651; Jarvis D, 1996, LANCET, V347, P426, DOI 10.1016/S0140-6736(96)90009-4; Ko YC, 1997, INT J EPIDEMIOL, V26, P24, DOI 10.1093/ije/26.1.24; Ko YC, 2000, AM J EPIDEMIOL, V151, P140; Levy JI, 1998, J AIR WASTE MANAGE, V48, P553, DOI 10.1080/10473289.1998.10463704; Li S, 1994, Arch Environ Health, V49, P119; MELIA RJW, 1977, BRIT MED J, V2, P149; OSUNSANYA T, 2000, OCCUP ENVIRON MED, V58, P154; Ozkaynak H, 1996, J EXPO ANAL ENV EPID, V6, P57; Pekkanen J, 1997, ENVIRON RES, V74, P24, DOI 10.1006/enrs.1997.3750; Peters A, 2000, EPIDEMIOLOGY, V11, P11, DOI 10.1097/00001648-200001000-00005; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Pilotto LS, 1997, INT J EPIDEMIOL, V26, P788, DOI 10.1093/ije/26.4.788; POPE CA, 1991, AM REV RESPIR DIS, V144, P668; POPE CA, 1992, AM REV RESPIR DIS, V145, P1123; QUACKENBOSS JJ, 1986, ENVIRON SCI TECHNOL, V20, P775, DOI 10.1021/es00150a003; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; SEATON A, 1995, LANCET, V345, P176, DOI 10.1016/S0140-6736(95)90173-6; Siegmann K., 1996, J AEROSOL SCI, V27, pS493, DOI DOI 10.1016/0021-8502(96)00319-9; SPEIZER FE, 1980, AM REV RESPIR DIS, V121, P3; SPENGLER J, 1994, J AIR WASTE MANAGE, V44, P39; Strand V, 1997, AM J RESP CRIT CARE, V155, P881; Touloumi G, 1997, AM J EPIDEMIOL, V146, P177; TUNNICLIFFE WS, 1994, LANCET, V344, P1733, DOI 10.1016/S0140-6736(94)92886-X; VOLKMER RE, 1995, J PAEDIATR CHILD H, V31, P116, DOI 10.1111/j.1440-1754.1995.tb00758.x; Wallace L, 2000, Appl Occup Environ Hyg, V15, P39, DOI 10.1080/104732200301836; WARE JH, 1984, AM REV RESPIR DIS, V129, P366; WARHEIT DB, 1990, EXP MOL PATHOL, V52, P309, DOI 10.1016/0014-4800(90)90072-L; Willeke K., 1993, AEROSOL MEASUREMENT; Wu PF, 1999, ENVIRON RES, V80, P122, DOI 10.1006/enrs.1997.3798	46	131	136	9	31	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	1351-0711			OCCUP ENVIRON MED	Occup. Environ. Med.	AUG	2001	58	8					511	516		10.1136/oem.58.8.511		6	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	454ZY	WOS:000170002900004	11452045	
J	Kroes, R; Galli, C; Munro, I; Schilter, B; Tran, LA; Walker, R; Wurtzen, G				Kroes, R; Galli, C; Munro, I; Schilter, B; Tran, LA; Walker, R; Wurtzen, G			Threshold of toxicological concern for chemical substances present in the diet: A practical tool for assessing the need for toxicity testing	FOOD AND CHEMICAL TOXICOLOGY			English	Review						threshold; toxicological endpoints; structural alerts; NOEL	DEVELOPMENTAL NEUROTOXICITY EVALUATION; CARCINOGENIC POTENCY DATABASE; ACOUSTIC STARTLE RESPONSE; NONCANCER RISK ASSESSMENT; ESTROGEN-RECEPTOR-BETA; PERINATAL PCB EXPOSURE; BREAST-CANCER CELLS; SPRAGUE-DAWLEY RATS; FEMALE B6C3F1 MICE; PRENATAL EXPOSURE	The de,minimis concept acknowledges a human exposure threshold value for chemicals below which there is no significant risk to human health. It is the underlying principle for the US Food and Drug Administration (FDA) regulation on substances used in food-contact articles. Further to this, the principle of Threshold of Toxicological Concern (TTC) has been developed and is now used by the joint FAO/WHO Expert Committee on Food Additives (JECFA) in their evaluations. Establishing an accepted TTC would benefit consumers, industry and regulators, since it would preclude extensive toxicity evaluations when Lumen intakes are below such threshold, and direct considerable time and cost resources towards testing substances with the highest potential risk to human health. It was questioned, however, whether specific endpoints that may potentially give rise to low-dose effects would be covered by such threshold. In this review., the possibility of defining a TTC for chemical substances present in the diet was examined for general toxicity endpoints (including carcinogenicity), as well as for specific endpoints, namely neurotoxicity and developmental neurotoxicity, immunotoxicity and developmental toxicity. For each of these endpoints, a database of specific no-observed-effect levels (NOELs) was compiled by screening oral toxicity studies. The substances recorded in each specific database were selected on the basis of their demonstrated adverse effects. For the neurotoxicity and developmental neurotoxicity databases, it was intended to cover all classes of compounds reported to hare tither a demonstrated neurotoxic or developmentally neurotoxic effect, or at least, on a biochemical or pharmacological basis were considered to have a potential for displaying such effects. For the immunotoxicity endpoint, it was ensured that only immunotoxicants were included in the database by selecting most of the substances from the Luster er al. database, provided that they satisfied the criteria for immunotoxicity defined by Luster. For the developmental toxicity database, substances were selected from the Munro ct nl. database that contained the lowest NOELs retrieved from the literature for more than 600 compounds. After screening these, substances shelving any effect which could point to developmental toxicity as broadly defined by the US EPA (1986) were recorded in the database. Additionally., endocrine toxicity and allergenicity, were addressed as two separate cases, using different approaches and methodology. The distributions of NOELs for the neurotoxicity, developmental neurotoxicity and developmental toxicity endpoints were compared with the distribution of NOELs for non-specific carcinogenic endpoints. As the immunotoxicity database was too limited to draw such a distribution of immune NOELs, the immunotoxicity endpoint,vas evaluated by comparing immune NOELs (or LOELs-lowest-observed-effect levels-when NOELs were not available),vith non-immune NOELs (or LOELs), in order to compare the sensitivity of this endpoint with non-specific endpoints. A different methodology was adopted for the evaluation of the endocrine toxicity endpoint since data currently available do not permit the establishment of a clear causal link between endocrine active chemicals and adverse effects in humans. Therefore, this endpoint was analysed by estimating the human exposure to oestrogenic environmental chemicals and evaluating their potential impact on human health, based on their contribution to the overall exposure, and their estrogenic potency relative to endogenous hormones. The allergenicity endpoint was not analysed as such. It was addressed in a separate section because this issue is not relevant to the overall population but rather to subsets of susceptible individuals, and allergic risks are usually controlled by other means (i.e, labelling) than the Threshold of Toxicological Concern approach. However, as several researchers are currently examining the existence of a threshold in allergy, the possibility of determining threshold doses for food allergens was put into perspective, and the likelihood for chemical substances to induce allergy at dietary relevant doses was discussed. The analysis indicated that, within the limitation of the databases, developmental neurotoxicity and developmental toxicity were not more sensitive than other non-specific endpoints. Although the cumulative distribution of NOELs for neurotoxic compounds was significantly loner than those for other non-cancer endpoints, these substances were accommodated within the TTC of 1.5 mu g/person/day. Furthermore, the analysis demonstrated that none of the specific non-cancer endpoints evaluated in the present study was more sensitive than cancer and, that a TTC of 1.5 mu g/person/day based on cancer endpoints provides an adequate margin of safety. Analysis of the immunotoxicity database should that for the group of immunotoxicants examined here, the specific immunotoxic endpoint was not more sensitive than other endpoints. In other words, the distribution of immunotoxic NOELs for these compounds did not appear to differ from the distribution of nonspecific endpoints NOELs for the same compounds. The dietary intakes of environmental oestrogenic chemicals were estimated and their oestrogenic potencies were compared with that of endogenous hormones, in order to assess their impact on human health. The results are in line with scientific data obtained so far, suggesting that estrogenic compounds of anthropogenic origin, in comparison with endogenous hormones, possess only little hormonal activity lilts phytoestrogens. Results of animal studies do not suggest that hormonal effects are to be expected from the rather lon concentrations found in foods. More data are necessary to determine threshold doses for food allergens. However, provided that numerous criteria need to be satisfied before sensitization occurs, it is unlikely that small molecules used in little amounts in foods would induce such reactions. On the basis of the present analysis, which was conducted using conservative assumptions at each step of the procedure (i.e. in data compilation and data analysis), and continually adopting a "worst case" perspective, it can be concluded that a Threshold of Toxicological Concern of 1.5 mu g/person/day provides adequate safety assurance. Chemical substances present in the diet that are consumed at levels below this threshold pose no appreciable risk. Moreover, for compounds which do not possess structural alerts for genotoxicity and carcinogenicity, further analysis mag indicate that a higher Threshold of Toxicological Concern mag he appropriate. (C) 2000 Elsevier in Science Ltd. All rights reserved.	ILSI Europe, B-1200 Brussels, Belgium; Univ Utrecht, Fac Vet Med, RITOX, NL-3508 TD Utrecht, Netherlands; Univ Milan, Inst Pharmacol Sci, I-20133 Milan, Italy; CanTox Inc, Mississauga, ON L5N 2XN, Canada; Nestec Ltd, Nestle Res Ctr, CH-1000 Lausanne, Switzerland; Univ Surrey, Sch Biol Sci, Guildford GU2 5XH, Surrey, England; Coca Cola, Nord & No Eurasia Div, DK-2600 Glostrup, Denmark	Tran, LA (reprint author), ILSI Europe, Ave E Mounier 83,Box 6, B-1200 Brussels, Belgium.						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Wise LD, 1997, NEUROTOXICOL TERATOL, V19, P315, DOI 10.1016/S0892-0362(97)00002-0; WISE LD, 1994, FOOD CHEM TOXICOL, V32, P239, DOI 10.1016/0278-6915(94)90196-1; WOLFF MS, 1993, J NATL CANCER I, V85, P648, DOI 10.1093/jnci/85.8.648; WUTHRICH B, 1995, P 16 EUR C ALL CLIN, P859; YANG RSH, 1984, FUND APPL TOXICOL, V4, P539, DOI 10.1016/0272-0590(84)90043-5; Yu TX, 1997, BRAIN RES, V747, P195, DOI 10.1016/S0006-8993(96)01181-X; Ziegler J, 1997, J NATL CANCER I, V89, P1186; 1968, EVALUATION CARCINOGE, V2; 1986, TOXICOLOGY APPL PHAR, V82, P19; 1991, NEUROTOXICITY 83; 1986, AM CYANAMID; 1984, TOXICOLOGIST, V4, P179; 1991, NEUROTOXICITY 81; 1968, EVALUATION CARCINOGE, V1; 1980, AM CYANAMID; 1991, NEUROTOXICITY 82	267	131	140	2	24	PERGAMON-ELSEVIER SCIENCE LTD	OXFORD	THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND	0278-6915			FOOD CHEM TOXICOL	Food Chem. Toxicol.	FEB-MAR	2000	38	2-3					255	312		10.1016/S0278-6915(99)00120-9		58	Food Science & Technology; Toxicology	Food Science & Technology; Toxicology	308BC	WOS:000086687800012	10717364	
J	Palmans, E; Kips, JC; Pauwels, RA				Palmans, E; Kips, JC; Pauwels, RA			Prolonged allergen exposure induces structural airway changes in sensitized rats	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							SMOOTH-MUSCLE CELLS; BROWN-NORWAY RATS; CHRONIC-BRONCHITIS; ANTIGEN CHALLENGE; ASTHMA; EXPRESSION; FIBRONECTIN; RESPONSIVENESS; PROLIFERATION; METHACHOLINE	The pathogenesis and functional consequences of airway remodeling in asthma remain to be fully established. In the present study we evaluated the effect of prolonged allergen exposure on airway function and structure in rats. Sensitized Brown Norway rats were repeatedly exposed for periods of 2 4, or 12 wk to aerosolized ovalbumin (OA) or phosphate-buffered saline (PBS). OA exposure induced a persistent increase in OA-specific serum IgE and in the number of peribronchial eosinophils. After 2 wk of OA exposure, airway histology revealed goblet-cell hyperplasia, an increase in bromodeoxyuridine-positive cells in airway epithelium, increased fibronectin deposition, and a thickening of the airway inner wall area. This coincided with airway hyperresponsiveness (AHR) to aerosolized carbachol. After OA exposure for 12 wk, increased fibronectin (p < 0.05 versus PBS) and collagen deposition (p < 0.05 versus PBS) were observed in the submucosa. After 12 wk of exposure, neither total nor inner wall area or airway responsiveness to carbachol were any longer significantly different from those of PBS-exposed animals. In conclusion, prolonged OA exposure in rats induces structural airway changes that bear similarities to airway remodeling in asthma. The study data further indicate that depending on the extent and distribution of remodeling, changes in the extracellular matrix can enhance or protect against AHR.	State Univ Ghent Hosp, Dept Resp Dis, B-9000 Ghent, Belgium	Palmans, E (reprint author), State Univ Ghent Hosp, Dept Resp Dis, De Pintelaan 185, B-9000 Ghent, Belgium.						BAI A, 1994, J APPL PHYSIOL, V77, P1011; BELLOFIORE S, 1988, J APPL PHYSIOL, V65, P1642; Blyth DI, 1996, AM J RESP CELL MOL, V14, P425; BRAMLEY AM, 1995, AM J RESP CRIT CARE, V152, P1513; Cairns JA, 1996, J IMMUNOL, V156, P275; CASSCELLS W, 1990, AM J PATHOL, V137, P801; Cohen MD, 1997, AM J RESP CELL MOL, V16, P85; COHEN P, 1995, AM J PHYSIOL-LUNG C, V269, pL151; EBINA M, 1993, AM REV RESPIR DIS, V148, P720; ELWOOD W, 1991, J ALLERGY CLIN IMMUN, V88, P951, DOI 10.1016/0091-6749(91)90253-K; GILLERY P, 1986, EXP CELL RES, V167, P29, DOI 10.1016/0014-4827(86)90201-6; GLASSBERG MK, 1994, AM J RESP CELL MOL, V10, P316; HACKZU A, 1994, AM J RESP CRIT CARE, V150, P23; Hirst SJ, 1996, EUR RESPIR J, V9, P808, DOI 10.1183/09031936.96.09040808; JAMES AL, 1989, AM REV RESPIR DIS, V139, P242; JEFFERY PK, 1989, AM REV RESPIR DIS, V140, P1745; KIPS JC, 1992, AM REV RESPIR DIS, V145, P1306; Laitinen A, 1997, AM J RESP CRIT CARE, V156, P951; LAMBERT RK, 1994, J APPL PHYSIOL, V77, P1206; LAMBERT RK, 1993, J APPL PHYSIOL, V74, P2771; Li X, 1997, AM J RESP CRIT CARE, V156, P229; Macklem PT, 1996, AM J RESP CRIT CARE, V153, P83; McKay S, 1998, AM J RESP CELL MOL, V18, P823; MORENO RH, 1986, AM REV RESPIR DIS, V133, P1171; PANETTIERI RA, 1990, AM J PHYSIOL, V259, pL365; Panettieri Reynold Jr., 1998, American Journal of Physiology, V274, pL417; RAGHOW R, 1994, FASEB J, V8, P823; ROCHE WR, 1989, LANCET, V1, P520; SAPIENZA S, 1991, AM REV RESPIR DIS, V144, P423; STEWART AG, 1995, AM J RESP CELL MOL, V12, P110; TAKIZAWA T, 1971, AM REV RESPIR DIS, V104, P331; Temelkovski J, 1998, THORAX, V53, P849; Vignola AM, 1998, AM J RESP CRIT CARE, V158, P1945; WELCH MP, 1990, J CELL BIOL, V110, P133, DOI 10.1083/jcb.110.1.133; Wiggs BR, 1997, J APPL PHYSIOL, V83, P1814; ZHANG ZH, 1995, P NATL ACAD SCI USA, V92, P6161, DOI 10.1073/pnas.92.13.6161	36	131	170	0	3	AMER LUNG ASSOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	FEB	2000	161	2					627	635				9	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	285ED	WOS:000085376000046	10673209	
J	Wootton, R				Wootton, Richard			Twenty years of telemedicine in chronic disease management - an evidence synthesis	JOURNAL OF TELEMEDICINE AND TELECARE			English	Article							OBSTRUCTIVE PULMONARY-DISEASE; CONGESTIVE-HEART-FAILURE; OF-THE-LITERATURE; HOME TELEHEALTH; DIABETES MANAGEMENT; METAANALYSIS; CARE; INTERVENTIONS; SUPPORT; BURDEN	A literature review was conducted to obtain a high-level view of the value of telemedicine in the management of five common chronic diseases (asthma, COPD, diabetes, heart failure, hypertension). A total of 141 randomised controlled trials (RCTs) was identified, in which 148 telemedicine interventions of various kinds had been tested in a total of 37,695 patients. The value of each intervention was categorised in terms of the outcomes specified by the investigators in that trial, i.e. no attempt was made to extract a common outcome from all studies, as would be required for a conventional meta-analysis. Summarizing the value of these interventions shows, first, that most studies have reported positive effects (n = 108), and almost none have reported negative effects (n = 2). This suggests publication bias. Second, there were no significant differences between the chronic diseases, i.e. telemedicine seems equally effective (or ineffective) in the diseases studied. Third, most studies have been relatively short-term (median duration 6 months). It seems unlikely that in a chronic disease, any intervention can have much effect unless applied for a long period. Finally, there have been very few studies of cost-effectiveness. Thus the evidence base for the value of telemedicine in managing chronic diseases is on the whole weak and contradictory.	Univ Hosp N Norway, Norwegian Ctr Integrated Care & Telemed, N-9038 Tromso, Norway	Wootton, R (reprint author), Univ Hosp N Norway, Norwegian Ctr Integrated Care & Telemed, POB 6060, N-9038 Tromso, Norway.	r_wootton@pobox.com	Wootton, Richard/F-7609-2014	Wootton, Richard/0000-0002-2666-3596			AbuDagga A, 2010, TELEMED J E-HEALTH, V16, P830, DOI 10.1089/tmj.2010.0015; Bartoli L, 2009, TELEMED J E-HEALTH, V15, P877, DOI 10.1089/tmj.2009.0044; Bolton C.E., 2010, J EVAL CLIN PRACT, V17, P1216; Chaudhry SI, 2007, J CARD FAIL, V13, P56, DOI 10.1016/j.cardfail.2006.09.001; Chaudhry SI, 2010, NEW ENGL J MED, V363, P2301, DOI 10.1056/NEJMoa1010029; Clark RA, 2007, BRIT MED J, V334, P942, DOI 10.1136/bmj.39156.536968.55; Clarke M, 2011, J TELEMED TELECARE, V17, P7, DOI 10.1258/jtt.2010.100113; Costa BM, 2009, BMC FAM PRACT, V10, DOI 10.1186/1471-2296-10-72; Dang S, 2009, TELEMED J E-HEALTH, V15, P783, DOI 10.1089/tmj.2009.0028; Darkins A, 2008, TELEMED J E-HEALTH, V14, P1118, DOI 10.1089/tmj.2008.0021; Druss BG, 2001, HEALTH AFFAIR, V20, P233, DOI 10.1377/hlthaff.20.6.233; Farmer A, 2005, DIABETIC MED, V22, P1372, DOI 10.1111/j.1464-5491.2005.01627.x; Freidlin B, 2008, CLIN CANCER RES, V14, P4368, DOI 10.1158/1078-0432.CCR-08-0325; Hebert PL, 2008, ANN INTERN MED, V149, P540; Inglis SC, 2010, COCHRANE DB SYST REV, V8; Jaana M, 2009, AM J MANAG CARE, V15, P313; Koehler F, 2011, CIRCULATION, V123, P1873, DOI 10.1161/CIRCULATIONAHA.111.018473; Lopez AD, 2006, LANCET, V367, P1747, DOI 10.1016/S0140-6736(06)68770-9; Louis AA, 2003, EUR J HEART FAIL, V5, P583, DOI 10.1016/S1388-9842(03)00160-0; Martinez A, 2006, J TELEMED TELECARE, V12, P234, DOI 10.1258/135763306777889109; McLEan S., 2010, COCHRANE DB SYST REV, V10; McLean S, 2011, COCHRANE DB SYST REV, V7, P1; Ouwens M, 2005, INT J QUAL HEALTH C, V17, P141, DOI 10.1093/intqhc/mzi016; Polisena J, 2009, DIABETES OBES METAB, V11, P913, DOI 10.1111/j.1463-1326.2009.01057.x; Polisena J, 2010, J TELEMED TELECARE, V16, P120, DOI 10.1258/jtt.2009.090812; Polisena J, 2010, J TELEMED TELECARE, V16, P68, DOI 10.1258/jtt.2009.090406; Seto E, 2008, TELEMED J E-HEALTH, V14, P679, DOI 10.1089/tmj.2007.0114; Shea S, 2009, J AM MED INFORM ASSN, V16, P446, DOI 10.1197/jamia.M3157; Shulman RM, 2010, INT J PEDIAT ENDOCRI; Sterne JAC, 2011, BRIT MED J, V343, DOI 10.1136/bmj.d4002; Sutherland D, 2009, J CLIN NURS, V18, P2978, DOI 10.1111/j.1365-2702.2009.02900.x; Verhoeven Fenne, 2010, J Diabetes Sci Technol, V4, P666; Verhoeven F, 2007, J MED INTERNET RES, V9, DOI 10.2196/jmir.9.5.e37; Wootton R, 2003, BEST PRACTICES BEHAV, VII, P1	34	130	131	3	41	ROYAL SOC MEDICINE PRESS LTD	LONDON	1 WIMPOLE STREET, LONDON W1G 0AE, ENGLAND	1357-633X			J TELEMED TELECARE	J. Telemed. Telecare		2012	18	4					211	220		10.1258/jtt.2012.120219		10	Health Care Sciences & Services	Health Care Sciences & Services	969HK	WOS:000306046100007	22674020	
J	Liu, L; Poon, R; Chen, L; Frescura, AM; Montuschi, P; Ciabattoni, G; Wheeler, A; Dales, R				Liu, Ling; Poon, Raymond; Chen, Li; Frescura, Anna-Maria; Montuschi, Paolo; Ciabattoni, Giovanni; Wheeler, Amanda; Dales, Robert			Acute Effects of Air Pollution on Pulmonary Function, Airway Inflammation, and Oxidative Stress in Asthmatic Children	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; asthma; children; exhaled breath condensate; inflammation; oxidative stress; pulmonary function	EXHALED BREATH CONDENSATE; NITRIC-OXIDE; THIOBARBITURIC-ACID; LIPID-PEROXIDATION; PARTICULATE MATTER; RESPIRATORY HEALTH; EPITHELIAL INJURY; IN-VIVO; EXPOSURE; 8-ISOPROSTANE	BACKGROUND: Air pollution is associated with respiratory symptoms, lung function decrements, and hospitalizations. However, there is little information about the influence of air pollution on lung injury. OBJECTIVE: In this study we investigated acute effects of air pollution on pulmonary function and airway oxidative stress and inflammation in asthmatic children. METHODS: We studied 182 children with asthma, 9-14 years of age, for 4 weeks. Daily ambient concentrations of sulfur dioxide, nitrogen dioxide, ozone, and particulate matter <= 2.5 mu m in aerodynamic diameter (PM(2.5)) were monitored from two stations. Once a week we measured spirometry and fractional exhaled nitric oxide (Fe(NO)), and determined thiobarbituric acid reactive substances (TBARS) and 8-isoprostane-two oxidative stress markers-and interieukin-6 (IL-6) in breath condensate. We tested associations using mixed-effects regression models, adjusting for confounding variables. RESULTS: Interquartile-range increases in 3-day average SO(2) (5.4 ppb), NO(2) (6.8 ppb), and PM(2.5) (5.4 mu g/m(3)) were associated with decreases in forced expiratory flow between 25% and 75% of forced vital capacity, with changes being -3.1% [95% confidence interval (CI), -5.8 to -0.3), -2.8% (95% CI, -4.8 to -0.8), and -3.0% (95% CI, -4.7 to -1.2), respectively. SO(2), NO(2), and PM(2.5) were associated with increases in TBARS, with changes being 36.2% (95% CI, 15.7 to 57.2), 21.8% (95% CI, 8.2 to 36.0), and 24.8% (95% CI, 10.8 to 39.4), respectively. Risk estimates appear to be larger in children not taking corticosteroids than in children taking corticosteroids. O(3) (5.3 ppb) was not associated with health end points. Fe(NO), 8-isoprostane, and IL-6 were not associated with air pollutants. CONCLUSION: Air pollution may increase airway oxidative stress and decrease small airway function of asthmatic children. Inhaled corticosteroids may reduce oxidative stress and improve airway function.	[Liu, Ling; Poon, Raymond; Chen, Li; Frescura, Anna-Maria; Wheeler, Amanda; Dales, Robert] Hlth Canada, Healthy Environm & Consumer Safety Branch, Ottawa, ON K1A 0K9, Canada; [Montuschi, Paolo; Ciabattoni, Giovanni] Univ Cattolica Sacro Cuore, Fac Med, Dept Pharmacol, I-00168 Rome, Italy	Liu, L (reprint author), Hlth Canada, Healthy Environm & Consumer Safety Branch, AL 4903B,269 Laurier Ave, Ottawa, ON K1A 0K9, Canada.	ling_liu@hc-sc.gc.ca		MONTUSCHI, Paolo/0000-0001-5589-1750; Wheeler, Amanda/0000-0001-9288-8163	Canada-the United States Border Air Quality Strategy	This study was funded by the Canada-the United States Border Air Quality Strategy.	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Health Perspect.	APR	2009	117	4					668	674		10.1289/ehp11813		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	426JQ	WOS:000264704500044	19440509	
J	Beckerman, B; Jerrett, M; Brook, JR; Verma, DK; Arain, MA; Finkelstein, MM				Beckerman, Bernardo; Jerrett, Michael; Brook, Jeffrey R.; Verma, Dave K.; Arain, Muhammad A.; Finkelstein, Murray M.			Correlation of nitrogen dioxide with other traffic pollutants near a major expressway	ATMOSPHERIC ENVIRONMENT			English	Article						traffic; air pollution; NO2; VOC; fine particulate matter; ultrafine particles; Toronto; distance decay	AIR-POLLUTION; ULTRAFINE PARTICLES; PM2.5 CONCENTRATIONS; HIGHWAY; INDOOR; ROAD; EXPOSURE; CHILDREN; OUTDOOR; ASTHMA	Objectives: This study addresses three objectives: (1) to assess the correlation of NO2 to other ambient pollutants measured with passive samplers; (2) to explore peak traffic particulate matter air pollution correlations with passively measured NO2; and (3) to pilot an advanced mobile air pollution laboratory to supply supplementary information on correlations between NO2 and other air pollutants. Methods: Active and passive monitoring was conducted at two transects perpendicular to an expressway with nearly 400,000 vehicles per day. NO2, NOx, O-3, VOCs, fine-particles and ultrafine particles were measured at increasing distance away from the expressway. The measurement equipment included Ogawa, TraceAir and 3 M organic vapor monitors (OVM-3500) passive samplers, and an array of active measurement equipment: Dust-Trak and P-Trak monitors, chemoluminescent analyzer, aethalometer, tapered element oscillating microbalance, Grimm condensation particle counter, and an lonicon analytik proton transfer reaction mass spectrometer. Results: Levels of NO2 were observed to decay with increasing distance from the expressway, declining to background levels by 300 m. Moderate to high correlations were observed between passive NO2 measurements and passive NOx, O-3 (r similar to 0.60-0.86). The correlations with active PM measurements made with Dust-Trak and P-Trak monitors were in the range 0.64-0.78; correlations between NO2 and VOCs were more variable. Active measurements of NO2 and PM2.5, ultrafine particles, O-3 and black carbon, had high correlations (r similar to 0.7-0.96). Discussion: The variability of many traffic-related pollutants around an expressway is characterized well by passive measurements of NO2. Further research is needed to assess whether these relationships hold in different traffic and land-use environments. (c) 2007 Elsevier Ltd. All rights reserved.	[Beckerman, Bernardo] Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA; [Jerrett, Michael] Univ Calif Berkeley, Berkeley, CA 94720 USA; [Jerrett, Michael] Univ So Calif, Los Angeles, CA 90089 USA; [Verma, Dave K.; Arain, Muhammad A.; Finkelstein, Murray M.] McMaster Univ, Hamilton, ON L8S 4L8, Canada	Beckerman, B (reprint author), Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, 140 Warren Hall 7360, Berkeley, CA 94720 USA.	beckerman@berkeley.edu		Arain, M. 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Environ.	JAN	2008	42	2					275	290		10.1016/j.atmosenv.2007.09.042		16	Environmental Sciences; Meteorology & Atmospheric Sciences	Environmental Sciences & Ecology; Meteorology & Atmospheric Sciences	261OD	WOS:000253088300006		
J	Cruz, AA; Popov, T; Pawankar, R; Annesi-Maesano, I; Fokkens, W; Kemp, J; Ohta, K; Price, D; Bousquet, J				Cruz, A. A.; Popov, T.; Pawankar, R.; Annesi-Maesano, I.; Fokkens, W.; Kemp, J.; Ohta, K.; Price, D.; Bousquet, J.		ARIA Initiative Sci Comm	Common characteristics of upper and lower airways in rhinitis and asthma: ARIA update, in collaboration with GA(2)LEN	ALLERGY			English	Review						allergy; asthma; atopy; review; rhinitis	SEASONAL ALLERGIC RHINITIS; EXHALED NITRIC-OXIDE; INDEPENDENT RISK-FACTOR; PRIMARY-SCHOOL CHILDREN; ADULT-ONSET ASTHMA; QUALITY-OF-LIFE; IN-HOUSE DUST; HAY-FEVER; BRONCHIAL HYPERRESPONSIVENESS; ATOPIC ECZEMA	This update aimed to review the new evidence available to support or refute prior Allergic Rhinitis and its Impact on Asthma (ARIA) statements. A Medline search of publications between 2000 and 2005 was conducted, with articles selected by experts. New evidence supports previous ARIA statements, such as: (i) allergic rhinitis (AR) is a risk factor for asthma; (ii) patients with persistent rhinitis should be evaluated for asthma; (iii) most patients with asthma have rhinitis; (iv) a combined strategy should be used to treat the airways and (v) in low- to middle-income countries, a different strategy may be needed. The increased risk of asthma has also been found among sufferers from non-AR. Recent reports show AR is a global problem. Many studies demonstrated parallel increasing prevalence of asthma and rhinitis, but in regions of highest prevalence, it may be reaching a plateau. Factors associated with a reduced risk of asthma and AR have been identified, confirming previous findings of protection related to exposure to infections. Treatment of rhinitis with intranasal glucocorticosteroids, antihistamines, leukotriene antagonists or immunotherapy may reduce morbidity because of asthma. To take advantage of the paradigm of unified airways, there is a need to rationalize diagnosis and treatment to optimize management.	Univ Fed Bahia, Sch Med, CNPq, Programme Control Asthma & Allerg Rhinitis, Salvador, BA, Brazil; Med Univ Sofia, Clin Ctr Allergol, Sofia, Bulgaria; Nippon Med Coll, Dept Otolaryngol, Div Rhinol & Allergy, Tokyo 113, Japan; INSERM, Paris, France; Univ Amsterdam, Acad Med Ctr, Dept Otorhinolaryngol, NL-1105 AZ Amsterdam, Netherlands; Univ Calif San Diego, Sch Med, Dept Pediat, San Diego, CA 92103 USA; Univ Tokyo, Dept Otolaryngol, Tokyo 113, Japan; Univ Aberdeen, Foresterhill Hlth Ctr, Dept Gen Practice & Primary Care, Aberdeen, Scotland; Univ Hosp, INSERM, Montpellier, France	Cruz, AA (reprint author), Univ Fed Bahia, Sch Med, CNPq, Programme Control Asthma & Allerg Rhinitis, Salvador, BA, Brazil.		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Venn AJ, 2001, AM J RESP CRIT CARE, V164, P1660; Vignola AM, 2004, ALLERGY, V59, P709, DOI 10.1111/j.1398-9995.2004.00550.x; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, THORAX, V55, P449, DOI 10.1136/thorax.55.6.449; Walker SM, 2001, J ALLERGY CLIN IMMUN, V107, P87, DOI 10.1067/mai.2001.112027; Walusiak J, 2004, ALLERGY, V59, P1294, DOI 10.1111/j.1398-9995.2004.00560.x; Walusiak J, 2004, ALLERGY, V59, P442, DOI 10.1111/j.1398-9995.2003.00418.x; Walusiak Jolanta, 2004, Int J Occup Med Environ Health, V17, P433; Wang XS, 2004, ARCH DIS CHILD, V89, P423, DOI 10.1136/adc.2003.031112; Waser M, 2005, ALLERGY, V60, P177, DOI 10.1111/j.1398-9995.2004.00645.x; Watelet JB, 2004, AM J RHINOL, V18, P267; Watelet JB, 2004, ALLERGY, V59, P54, DOI 10.1046/j.1398-9995.2003.00364.x; Weiland SK, 2004, OCCUP ENVIRON MED, V61, P609, DOI 10.1136/oem.2002.006809; Wilson AM, 2004, AM J MED, V116, P338, DOI 10.1016/j.amjmed.2003.10.030; Wilson AM, 2001, CLIN EXP ALLERGY, V31, P616, DOI 10.1046/j.1365-2222.2001.01088.x; Wilson AM, 2005, CLIN EXP ALLERGY, V35, P39, DOI 10.1111/j.1365-2222.2004.02072.x; Wilson DR, 2005, ALLERGY, V60, P4, DOI 10.1111/j.1398-9995.2005.00699.x; Wong TW, 2004, ARCH DIS CHILD, V89, P631, DOI 10.1136/adc.2003.030601; Woszczek G, 2002, EUR RESPIR J, V20, P79, DOI 10.1183/09031936.02.01002001; Yan DC, 2005, ANN ALLERG ASTHMA IM, V95, P579; Yu Jui-Huan, 2005, Journal of Microbiology Immunology and Infection, V38, P123; Zanolin ME, 2004, ALLERGY, V59, P306, DOI 10.1046/j.1398-9995.2003.00391.x	196	130	138	0	8	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0105-4538			ALLERGY	Allergy	NOV	2007	62			84			1	41		10.1111/j.1398-9995.2007.01551.x		41	Allergy; Immunology	Allergy; Immunology	218VL	WOS:000250043200001	17924930	
J	Chan-Yeung, M; Ferguson, A; Watson, W; Dimich-Ward, H; Rousseau, R; Lilley, M; DyBuncio, A; Becker, A				Chan-Yeung, M; Ferguson, A; Watson, W; Dimich-Ward, H; Rousseau, R; Lilley, M; DyBuncio, A; Becker, A			The Canadian childhood asthma primary prevention study: Outcomes at 7 years of age	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Editorial Material						asthma; primary prevention	FATTY-ACID MODIFICATION; ALLERGEN AVOIDANCE; BRONCHIAL HYPERRESPONSIVENESS; HOUSE-DUST; INFANCY; CHILDREN; REACTIVITY; SYMPTOMS; ATOPY	Background: Avoidance of any one of the individual risk factors associated with childhood asthma has not been successful in preventing its development. Objective: The purpose of this study is to determine the effectiveness of a multifaceted intervention program for the primary prevention of asthma in high-risk infants at 7 years of age. Methods: Five hundred forty-five high-risk infants with an immediate family history of asthma and allergies were prospectively randomized into intervention or control groups prenatally. Intervention measures introduced before birth and during the first year of life included avoidance of house dust, pets, and environmental tobacco smoke and encouragement of breast-feeding with delayed introduction of solid foods. Assessment of outcomes at 7 years consisted of examination by pediatric allergists, methacboline inhalation tests, and allergy skin tests. Results: At 7 years, 469 of the 545 children were contacted, and 380 returned for further assessment. The prevalence of pediatric allergist-diagnosed asthma was significantly lower in the intervention group than in the control group (14.9% vs 23.0%; adjusted risk ratio, 0.44; 95% CI, 0.25-0.79). The prevalence of allergic rhinitis, atopic dermatitis, atopy (defined as positive skin test reactions to any common allergen), and bronchial hyperresponsiveness (defined as the provocative concentration of methacholine that induced a 20% decrease in FEV1 from a postsaline value of less than 7.8 mg/mL) were not significantly different between the 2 groups. The prevalence of asthma (defined as wheeze without colds and the presence of bronchial hyperresponsiveness) was also significantly lower in the intervention group compared with the control group (12.9% vs 25.0%; adjusted risk ratio, 0.39; 95% CI, 0.22-0.71).	Univ British Columbia, Dept Med, Div Resp, Occupat & Environm Lung Dis Unit, Vancouver, BC V5Z 3J5, Canada; Univ British Columbia, Dept Pediat, Div Allergy, Vancouver, BC V5Z 3J5, Canada; Univ Manitoba, Manitoba Inst Child Hlth, Sect Allergy & Clin Immunol, Dept Pediat & Child Hlth, Winnipeg, MB R3T 2N2, Canada	Chan-Yeung, M (reprint author), Univ British Columbia, Dept Med, Div Resp, Occupat & Environm Lung Dis Unit, 2775 Heather St, Vancouver, BC V5Z 3J5, Canada.	myeung@interchange.ubc.ca					ARSHAD SH, 1992, LANCET, V339, P1493, DOI 10.1016/0140-6736(92)91260-F; Arshad SH, 2003, THORAX, V58, P489, DOI 10.1136/thorax.58.6.489; Becker A, 2004, J ALLERGY CLIN IMMUN, V113, P650, DOI 10.1016/j.jaci.2004.01.754; Chan-Yeung M, 2002, ANN ALLERG ASTHMA IM, V88, P52; Chan-Yeung M, 2000, ARCH PEDIAT ADOL MED, V154, P657; COCKCROFT DW, 1977, CLIN ALLERGY, V7, P235, DOI 10.1111/j.1365-2222.1977.tb01448.x; Custovic A, 2001, LANCET, V358, P188, DOI 10.1016/S0140-6736(01)05406-X; Ernst P, 2002, EUR RESPIR J, V20, P635, DOI 10.1183/09031936.02.00962002; Godfrey S, 1999, EUR RESPIR J, V14, P659, DOI 10.1034/j.1399-3003.1999.14c28.x; HIDE DW, 1994, J ALLERGY CLIN IMMUN, V93, P842, DOI 10.1016/0091-6749(94)90375-1; Hide DW, 1996, ALLERGY, V51, P89, DOI 10.1111/j.1398-9995.1996.tb04563.x; Horak F, 2004, CLIN EXP ALLERGY, V34, P1220, DOI 10.1111/j.1365-2222.2004.02024.x; *ISAAC COORD COMM, 1992, MAN INT STUD ASTHM A; Kurukulaaratchy RJ, 2003, J ALLERGY CLIN IMMUN, V112, P311, DOI 10.1067/mai.2003.1623; Mihrshahi S, 2003, J ALLERGY CLIN IMMUN, V111, P162, DOI 10.1067/mai.2003.36; PATTEMORE PK, 1990, AM REV RESPIR DIS, V142, P549; Peat JK, 2004, J ALLERGY CLIN IMMUN, V114, P807, DOI 10.1016/j.jaci.2004.06.057	17	130	135	0	2	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUL	2005	116	1					49	55		10.1016/j.jaci.2005.03.029		7	Allergy; Immunology	Allergy; Immunology	017IC	WOS:000235686300007	15990772	
J	Cenci, E; Mencacci, A; Bacci, A; Bistoni, F; Kurup, VP; Romani, L				Cenci, E; Mencacci, A; Bacci, A; Bistoni, F; Kurup, VP; Romani, L			T cell vaccination in mice with invasive pulmonary aspergillosis	JOURNAL OF IMMUNOLOGY			English	Article							ALLERGIC BRONCHOPULMONARY ASPERGILLOSIS; CHRONIC GRANULOMATOUS-DISEASE; HUMAN-IMMUNODEFICIENCY-VIRUS; CANDIDA-ALBICANS INFECTION; LUNG DENDRITIC CELLS; HOST-DEFENSE; MURINE ASPERGILLOSIS; ANTIFUNGAL ACTIVITY; MUCOSAL IMMUNITY; MAJOR ALLERGEN	Aspergillus fumigatus, an opportunistic fungal pathogen, is responsible for multiple airway diseases of an allergic and a nonallergic nature. In a murine model of invasive pulmonary aspergillosis, resistance is associated with a decreased lung inflammatory pathology and the occurrence of an IL-12-dependent Th1-type reactivity that are both impaired by IL-4, In the present study we assess the ability of Aspergillus crude culture filtrate Ags and the recombinant allergen Asp f 2 to induce protective antifungal responses in mice with invasive pulmonary aspergillosis, Similar to what occurred upon nasal exposure to viable A. fumigatus conidia, treatment of immunocompetent mice with Aspergillus crude culture filtrate Ags resulted in the development of local and peripheral protective Th1 memory responses, mediated by Ag-specific CD4(+) T cells producing IFN-gamma and IL-2 capable of conferring protection upon adoptive transfer to naive recipients. Protective Th1 responses could not be observed in mice deficient of IFN-gamma or IL-12 and did not occur in response to Asp f 2, which, on the contrary, elicited high level production of inhibitory IL-4. The results show that Ags of Aspergillus exist with the ability to induce both Th1- and Th2-type reactivity during infection, a finding that suggests a possible mechanism through which potentially protective immune responses are inhibited in mice with the infection. However, the occurrence of Th1-mediated resistance upon vaccination with Aspergillus crude culture filtrate Ags, suggests the existence of fungal Ags useful as a candidate vaccine against invasive pulmonary aspergillosis.	Univ Perugia, Dept Expt Med & Biochem Sci, Microbiol Sect, I-06122 Perugia, Italy; Med Coll Wisconsin, Div Allergy Immunol, Milwaukee, WI 53295 USA; Vet Affairs Med Ctr, Milwaukee, WI 53295 USA	Romani, L (reprint author), Univ Perugia, Dept Expt Med & Biochem Sci, Microbiol Sect, Via Giochetto, I-06122 Perugia, Italy.				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Immunol.	JUL 1	2000	165	1					381	388				8	Immunology	Immunology	327WH	WOS:000087816800050	10861075	
J	Hansen, G; Jin, SLC; Umetsu, DT; Conti, M				Hansen, G; Jin, SLC; Umetsu, DT; Conti, M			Absence of muscarinic cholinergic airway responses in mice deficient in the cyclic nucleotide phosphodiesterase PDE4D	PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA			English	Article							BETA(2)-ADRENERGIC RECEPTOR; SELECTIVE-INHIBITION; ATOPIC-DERMATITIS; SMOOTH-MUSCLE; RAT-BRAIN; T-CELLS; AMP; IDENTIFICATION; ACTIVATION; ASTHMA	Muscarinic cholinergic signaling plays an essential role in the control of the normal airway functions and in the development of pulmonary pathologies including asthma. In this paper we demonstrate that the airways of mice deficient in a cAMP-specific phosphodiesterase (PDE4D) are no longer responsive to cholinergic stimulation. Airway hyperreactivity that follows exposure to antigen was also abolished in PDE4D(-/-) mice, despite an apparently normal lung inflammatory infiltration. The loss of cholinergic responsiveness was specific to the airway, not observed in the heart, and was associated with a loss of signaling through muscarinic receptors with an inability to decrease cAMP accumulation. These findings demonstrate that the PDE4D gene plays an essential role in cAMP homeostasis and cholinergic stimulation of the airway, and in the development of hyperreactivity. In view of the therapeutic potentials of PDE4 inhibitors, our findings provide the rationale for novel strategies that target a single PDE isoenzyme.	Stanford Univ, Sch Med, Dept Obstet & Gynecol, Div Reprod Biol, Stanford, CA 94305 USA; Stanford Univ, Sch Med, Dept Pediat, Div Immunol & Transplantat Biol, Stanford, CA 94305 USA	Conti, M (reprint author), Stanford Univ, Sch Med, Dept Obstet & Gynecol, Div Reprod Biol, Stanford, CA 94305 USA.				NIAID NIH HHS [R01 AI026322, R01 AI26322]; NICHD NIH HHS [R01 HD020788, R01 HD20788]		BARNES PJ, 1995, EUR RESPIR J, V8, P457, DOI 10.1183/09031936.95.08030457; BEAVO JA, 1995, PHYSIOL REV, V75, P725; BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1006/abio.1976.9999; BUXTON ILO, 1985, J BIOL CHEM, V260, P6733; CHAN SC, 1993, J ALLERGY CLIN IMMUN, V91, P1179, DOI 10.1016/0091-6749(93)90321-6; CLAYBERGER C, 1983, J EXP MED, V157, P1906, DOI 10.1084/jem.157.6.1906; CONTI M, 1995, ENDOCR REV, V16, P370, DOI 10.1210/er.16.3.370; CONTI M, 1982, ENDOCRINOLOGY, V110, P1189; Conti M, 1999, Prog Nucleic Acid Res Mol Biol, V63, P1; Costello RW, 1998, THORAX, V53, P613; Eglen RM, 1996, PHARMACOL TOXICOL, V78, P59; ENGELS P, 1994, FEBS LETT, V350, P291, DOI 10.1016/0014-5793(94)00788-8; ERNEUX C, 1985, MOL CELL ENDOCRINOL, V43, P123, DOI 10.1016/0303-7207(85)90075-9; Fuhrmann M, 1999, AM J RESP CELL MOL, V20, P292; Gantner F, 1997, J ALLERGY CLIN IMMUN, V100, P527; GREEN SA, 1994, BIOCHEMISTRY-US, V33, P9414, DOI 10.1021/bi00198a006; Hamelmann E, 1997, AM J RESP CRIT CARE, V156, P766; HANIFIN JM, 1995, J INVEST DERMATOL, V105, pS84, DOI 10.1111/1523-1747.ep12316116; HARDEN TK, 1985, ADV CYCLIC NUCL PROT, V19, P207; HARGREAVE FE, 1981, J ALLERGY CLIN IMMUN, V68, P347, DOI 10.1016/0091-6749(81)90132-9; HARPER JF, 1975, J CYCLIC NUCL PROT, V1, P207; Holgate ST, 1997, NAT GENET, V15, P227, DOI 10.1038/ng0397-227; Houslay MD, 1998, ADV PHARMACOL, V44, P225, DOI 10.1016/S1054-3589(08)60128-3; HULME EC, 1990, ANNU REV PHARMACOL, V30, P633, DOI 10.1146/annurev.pa.30.040190.003221; Iona S, 1998, MOL PHARMACOL, V53, P23; Jin SLC, 1998, J BIOL CHEM, V273, P19672, DOI 10.1074/jbc.273.31.19672; Jin SLC, 1999, P NATL ACAD SCI USA, V96, P11998, DOI 10.1073/pnas.96.21.11998; LEVITT RC, 1989, J APPL PHYSIOL, V67, P1125; Lim J, 1999, J BIOL CHEM, V274, P19677, DOI 10.1074/jbc.274.28.19677; Macaulay AE, 1998, J IMMUNOL, V160, P1694; MAEDA A, 1988, FEBS LETT, V239, P339, DOI 10.1016/0014-5793(88)80947-5; Nagase T, 1998, AM J RESP CRIT CARE, V157, P560; Shirakawa T, 1997, SCIENCE, V275, P77, DOI 10.1126/science.275.5296.77; Stengel PW, 2000, J PHARMACOL EXP THER, V292, P877; Takahashi M, 1999, J NEUROSCI, V19, P610; TANNER LI, 1986, MOL PHARMACOL, V29, P455; TENOR H, 1999, ANTIINFLAMMATORY DRU, P87; THOMPSON WJ, 1971, BIOCHEMISTRY-US, V10, P311; TOMLINSON PR, 1995, BIOCHEM PHARMACOL, V49, P1809, DOI 10.1016/0006-2952(94)00532-Q; TORPHY TJ, 1990, MOL PHARMACOL, V37, P206; Torphy TJ, 1998, AM J RESP CRIT CARE, V157, P351; TURKI J, 1995, J CLIN INVEST, V95, P1635, DOI 10.1172/JCI117838; Wess J, 1996, CRIT REV NEUROBIOL, V10, P69; Zaagsma J, 1997, LIFE SCI, V60, P1061, DOI 10.1016/S0024-3205(97)00048-9	44	130	133	0	1	NATL ACAD SCIENCES	WASHINGTON	2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA	0027-8424			P NATL ACAD SCI USA	Proc. Natl. Acad. Sci. U. S. A.	JUN 6	2000	97	12					6751	6756		10.1073/pnas.97.12.6751		6	Multidisciplinary Sciences	Science & Technology - Other Topics	322UA	WOS:000087526300093	10841571	
J	Karlberg, AT; Bergstrom, MA; Borje, A; Luthman, K; Nilsson, JLG				Karlberg, Ann-Therese; Bergstrom, Moa Andresen; Borje, Anna; Luthman, Kristina; Nilsson, J. Lars G.			Allergic contact dermatitis-formation, structural requirements, and reactivity of skin sensitizers	CHEMICAL RESEARCH IN TOXICOLOGY			English	Review							LYMPH-NODE ASSAY; OXIDIZED D-LIMONENE; MECHANISTIC APPLICABILITY DOMAINS; HEPATIC CYTOCHROME-P450 ENZYMES; HUMAN DENDRITIC CELLS; IN-VITRO; GUINEA-PIG; 15-HYDROPEROXYABIETIC ACID; OXIDATION-PRODUCTS; P-PHENYLENEDIAMINE	Contact allergy is caused by a wide range of chemicals after skin contact. Its clinical manifestation, allergic contact dermatitis (ACD), is developed upon repeated contact with the allergen. This perspective focuses on two areas that have yielded new useful information during the last 20 years: (i) structure-activity relationship (SAR) studies of contact allergy based on the concept of hapten-protein binding and (ii) mechanistic investigations regarding activation of nonsensitizing compounds to contact allergens by air oxidation or skin metabolism. The second area is more thoroughly reviewed since the full Picture has previously not been published. Prediction of the sensitizing capacity of a chemical is important to avoid outbreaks of ACD in the population. Much research has been devoted to the development of in vitro and in silico predictive testing methods. Today, no method exists that is sensitive enough to detect weak allergens and that is robust enough to be used for routine screening. To cause sensitization, a chemical C, must bind to macromolecules (proteins) in the skin, Expert systems containing information about the relationship between the chemical structure and the ability of chemicals to haptenate proteins are available. However, few designed SAR studies based on mechanistic investigations of prohaptens have been published. Many compounds are not allergenic themselves but are activated in the skin (e.g., metabolically) or before skin contact (e.g., via air oxidation) to form skin sensitizers. Thus, more basic research is needed on the chemical reactions involved in the antigen formation and the immunological mechanisms. The clinical importance of air oxidation to activate nonallergenic compounds has been demonstrated. Oxidized fragrance terpenes, in contrast to the pure terpenes, gave positive patch test reactions in consecutive dermatitis patients as frequently as the most common standard allergens. This shows the importance of using compounds to which people are exposed when screening for ACD in dermatology clinics.	[Karlberg, Ann-Therese; Bergstrom, Moa Andresen; Borje, Anna; Luthman, Kristina; Nilsson, J. 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K., 2001, ALLERGIC CONTACT DER, P89; Sosted H, 2004, CONTACT DERMATITIS, V51, P241, DOI 10.1111/j.0105-1873.2004.00440.x; Stanley LA, 2005, TOXICOLOGY, V210, P147, DOI 10.1016/j.tox.2005.01.019; Tang XJ, 2002, BIOMED ENVIRON SCI, V15, P113; Testa B, 2005, CHEM BIODIVERS, V2, P872, DOI 10.1002/cbdv.200590064; Van den Broeke LT, 1999, IMMUNOLOGY, V96, P578; Vandebriel Rob J, 2005, Toxicol Appl Pharmacol, V207, P142, DOI 10.1016/j.taap.2005.01.054; Vohr H-W, 2005, ARCH TOXICOL, V79, P721, DOI 10.1007/s00204-005-0005-9; Volkel W, 1999, TOXICOL SCI, V47, P144, DOI 10.1093/toxsci/47.2.144; Wahlberg JE, 2006, CONTACT DERMATITIS, P366; Wallenhammar LM, 2004, J INVEST DERMATOL, V122, P1381, DOI 10.1111/j.0022-202X.2004.22604.x; White IR, 2006, CLIN EXP DERMATOL, V31, P724, DOI 10.1111/j.1365-2230.2006.02226.x; White JML, 2006, CLIN EXP ALLERGY, V36, P1289, DOI 10.1111/j.1365-2222.2006.02561.x; WIDMARK G, 1975, SVENSK KEM TIDSKR, V69, P175; Wright Z. M., 2001, International Journal of Cosmetic Science, V23, P75, DOI 10.1046/j.1467-2494.2001.00066.x	175	129	132	1	23	AMER CHEMICAL SOC	WASHINGTON	1155 16TH ST, NW, WASHINGTON, DC 20036 USA	0893-228X			CHEM RES TOXICOL	Chem. Res. Toxicol.	JAN	2008	21	1					53	69		10.1021/tx7002239		17	Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology	Pharmacology & Pharmacy; Chemistry; Toxicology	254KJ	WOS:000252585200006	18052130	
J	Bai, TR; Vonk, JM; Postma, DS; Boezen, HM				Bai, T. R.; Vonk, J. M.; Postma, D. S.; Boezen, H. M.			Severe exacerbations predict excess lung function decline in asthma	EUROPEAN RESPIRATORY JOURNAL			English	Article						airways remodelling; exacerbations; prognosis; treatment of asthma	AIR-FLOW OBSTRUCTION; FOLLOW-UP; GENERAL-POPULATION; CORTICOSTEROIDS; POLYMORPHISMS; LIMITATION; DISEASE; ADULTS	Severe asthma exacerbations are periods of intense airway inflammation that have been hypothesised to contribute to structural changes in the airways. If so, accelerated lung function decline over time should be more prevalent in adult patients with asthma who have frequent exacerbations than those without, but to date this has not been demonstrated. A cohort study was performed in order to investigate the effect of severe exacerbations on the progression of airway obstruction in 93 nonsmoking asthmatics with moderate-to-severe disease prior to treatment with inhaled corticosteroids. Subjects were followed for >= 5 yrs (median follow-up 11 yrs). In total, 56 (60.2%) subjects experienced at least one severe exacerbation (median rate 0.10.yr(-1)). Oral corticosteroid use and more severe airway obstruction at baseline were associated with a higher exacerbation rate. Independent of these variables, asthma patients with frequent exacerbations had a significantly larger annual decline in forced expiratory volume in one second (FEV1; median difference (95% confidence interval) 16.9 (1.5-32.2) mL.yr(-1)). Exacerbation rate significantly predicted an excess decline in FEV1, such that one severe exacerbation per year was associated with a 30.2 mL greater annual decline in FEV1. These data support the hypothesis that exacerbations, indicating intermittent periods of worsening airway inflammation, are associated with excess lung function decline in asthma.	Univ British Columbia, St Pauls Hosp, Div Resp, James Hogg Capture Ctr, Vancouver, BC V6Z 1Y6, Canada; Univ Groningen, Univ Med Ctr Groningen, Dept Epidemiol, Groningen, Netherlands; Univ Groningen, Univ Med Ctr Groningen, Dept Pulmonol, Groningen, Netherlands	Bai, TR (reprint author), Univ British Columbia, St Pauls Hosp, Div Resp, James Hogg Capture Ctr, Rm 166,1081 Burrard St, Vancouver, BC V6Z 1Y6, Canada.	tbai@mrl.ubc.ca					Apostol GG, 2002, AM J RESP CRIT CARE, V166, P166, DOI 10.1164/rccm.2007035; Bai TR, 2005, CLIN SCI, V108, P463; Bumbacea D, 2004, EUR RESPIR J, V24, P122, DOI 10.1183/09031936.04.00077803; Dijkstra A, 2006, THORAX, V61, P105, DOI 10.1136/thx.2004.039271; Donaldson GC, 2002, THORAX, V57, P847, DOI 10.1136/thorax.57.10.847; *GINA, NAT I HLTH PUBL; Jongepier H, 2004, CLIN EXP ALLERGY, V34, P757, DOI 10.1111/j.1365-2222.2004.01938.x; Lange P, 1998, NEW ENGL J MED, V339, P1194, DOI 10.1056/NEJM199810223391703; Linden A, 2005, EUR RESPIR J, V25, P159, DOI 10.1183/09031936.04.00032904; Oshita Y, 2003, THORAX, V58, P757, DOI 10.1136/thorax.58.9.757; Panizza JA, 2006, INTERN MED J, V36, P773, DOI 10.1111/j.1445-5994.2006.01214.x; Pauwels Romain A, 2004, Proc Am Thorac Soc, V1, P73, DOI 10.1513/pats.2306024; PEAT JK, 1987, EUR J RESPIR DIS, V70, P171; Prescott E, 1997, THORAX, V52, P287; Reddel H, 1999, LANCET, V353, P364, DOI 10.1016/S0140-6736(98)06128-5; Reddel HK, 2005, THORAX, V60, P164, DOI 10.1136/thx.2004.030437; Shute JK, 1997, INT ARCH ALLERGY IMM, V113, P366; ten Brinke A, 2004, AM J RESP CRIT CARE, V170, P601, DOI 10.1164/rccm.200404-440OC; ten Brinke A, 2001, AM J RESP CRIT CARE, V164, P744; Ulrik CS, 1999, EUR RESPIR J, V14, P892, DOI 10.1034/j.1399-3003.1999.14d27.x; van Diemen CC, 2005, AM J RESP CRIT CARE, V172, P329, DOI 10.1164/rccm.200411-1486OC; Vonk JM, 2003, THORAX, V58, P322, DOI 10.1136/thorax.58.4.322	22	129	132	0	2	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	SEP	2007	30	3					452	456		10.1183/09031936.00165106		5	Respiratory System	Respiratory System	211FM	WOS:000249509700010	17537763	
J	Delfino, RJ; Quintana, PJE; Floro, J; Gastanaga, VM; Samimi, BS; Kleinman, MT; Liu, LJS; Bufalino, C; Wu, CF; McLaren, CE				Delfino, RJ; Quintana, PJE; Floro, J; Gastanaga, VM; Samimi, BS; Kleinman, MT; Liu, LJS; Bufalino, C; Wu, CF; McLaren, CE			Association of FEV1 in asthmatic children with personal and microenvironmental exposure to airborne particulate matter	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; epidemiology; forced expiratory volume; longitudinal data analysis; nitrogen dioxide; ozone; panel study; particulate air pollution	ANTIINFLAMMATORY MEDICATION USE; AMBIENT AIR-POLLUTION; INNER-CITY CHILDREN; RESPIRATORY HEALTH; SYMPTOM SEVERITY; PARTICLES; INDOOR; TIME; CALIFORNIA; POLLUTANTS	Exposure to particulate matter (PM) air pollution has been shown to exacerbate children's asthma, but the exposure sources and temporal characteristics are still under study. Children's exposure to PM is likely to involve both combustion-related ambient PM and PM related to a child's activity in various indoor and outdoor microenvironments. Among 19 children with asthma, 9-17 years of age, we examined the relationship of temporal changes in percent predicted forced expiratory volume in 1 sec (FEV1) to personal continuous PM exposure and to 24-hr average gravimetric PM mass measured at home and central sites. Subjects were followed for 2 weeks during either the fall of 1999 or the spring of 2000, in a southern California region affected by transported air pollution. FEV1 was measured by subjects in the morning, afternoon, and evening. Exposure measurements included continuous PM using a passive nephelometer carried by subjects; indoor, outdoor home, and central-site 24-hr gravimetric PM2.5 (PM of aerodynamic diameter < 2.5 mum) and PM10; and central-site hourly PM10, nitrogen dioxide, and ozone. Data were analyzed with linear mixed models controlling for within-subject autocorrelation, FEV1 maneuver time, and exposure period. We found inverse associations of FEV1 with increasing PM exposure during the 24 hr before the FEV1 maneuver and with increasing multiday PM averages. Deficits in percent predicted FEV1 (95% confidence interval) for given PM interquartile ranges measured during the preceding 24-hr were as follows: 128 mug/m(3) 1-hr maximum personal PM, -6.0% (-10.5 to -1.4); 30 mug/m(3) 24-hr average personal PM, -5.9% (-10.8 to -1.0); 6.7 mug/m(3) indoor home PM2.5, -1.6% (-2.8 to -0.4); 16 mug/m(3) indoor home PM10, -2.1% (-3.7 to -0.4); 7.1 mug/m(3) outdoor home PM2.5, -1-1% (-2.4 to 0.1); and 7.5 mug/m(3) central-site P-M2.5, -0.7% (-1.9 to 0.4). Stronger associations were found for multiday moving averages of PM for both personal and stationary-site PM. Stronger associations with personal PM were found in boys allergic to indoor allergens. FEV1 was weakly associated with NO2 but not with O-3. Results suggest mixed respiratory effects of PM in asthmatic children from both ambient background exposures and personal exposures in various microenvironments.	Univ Calif Irvine, Coll Med, Dept Med, Div Epidemiol, Irvine, CA 92697 USA; San Diego State Univ, Grad Sch Publ Hlth, Div Occupat & Environm Hlth, San Diego, CA 92182 USA; Univ Calif Irvine, Coll Med, Dept Community & Environm Med, Irvine, CA 92717 USA; Univ Washington, Dept Environm & Occupat Hlth Sci, Seattle, WA 98195 USA	Delfino, RJ (reprint author), Univ Calif Irvine, Coll Med, Dept Med, Div Epidemiol, 224 Irvine Hall, Irvine, CA 92697 USA.	rdelfino@uci.edu		Wu, Chang-fu/0000-0003-2244-1934	NIEHS NIH HHS [ES 06214]		Allen G, 1997, J AIR WASTE MANAGE, V47, P682; Allen R, 2003, ENVIRON SCI TECHNOL, V37, P3484, DOI 10.1021/es021007e; American Thoracic Society, 1991, AM REV RESPIR DIS, V144, P1202, DOI 10.1164/ajrccm/144.5.1202; Custovic A, 1999, PEDIATR ALLERGY IMMU, V10, P258, DOI 10.1034/j.1399-3038.1999.00050.x; Delfino RJ, 1998, ENVIRON HEALTH PERSP, V106, P751, DOI 10.1289/ehp.98106751; Delfino RJ, 2003, ENVIRON HEALTH PERSP, V111, P647, DOI 10.1289/ehp.5992; Delfino RJ, 2002, ENVIRON HEALTH PERSP, V110, pA607; Diggle P, 2002, ANAL LONGITUDINAL DA; Gielen MH, 1997, AM J RESP CRIT CARE, V155, P2105; Hankinson JL, 1999, AM J RESP CRIT CARE, V159, P179; HERING S, 1997, ATMOS ENVIRON, V3, P1; Hopke PK, 2003, ATMOS ENVIRON, V37, P3289, DOI 10.1016/S1352-2310(03)00331-5; Howard-Reed C, 2000, J AIR WASTE MANAGE, V50, P1125; Just J, 2002, EUR RESPIR J, V20, P899, DOI 10.1183/09031936.02.00236902; Koenig JQ, 2003, ENVIRON HEALTH PERSP, V111, P1625, DOI 10.1289/ehp.6160; LARSON T, IN PRESS J AIR WASTE; Lee K, 1999, J AIR WASTE MANAGE, V49, P1238, DOI 10.1080/10473289.1999.10463913; Lin M, 2004, AM J EPIDEMIOL, V159, P294, DOI 10.1093/aje/kwh043; Lipfert FW, 1999, J AIR WASTE MANAGE, V49, P182; Littell R., 1996, SAS SYSTEM MIXED MOD; Liu LJS, 1997, ENVIRON HEALTH PERSP, V105, P58, DOI 10.1289/ehp.9710558; Liu LJS, 2003, ENVIRON HEALTH PERSP, V111, P909, DOI 10.1289/ehp.6011; Liu LJS, 2002, ENVIRON SCI TECHNOL, V36, P2977, DOI 10.1021/es0112644; McBride SJ, 1999, J EXPO ANAL ENV EPID, V9, P602, DOI 10.1038/sj.jea.7500057; Morawska L, 1999, ATMOS ENVIRON, V33, P4401, DOI 10.1016/S1352-2310(99)00217-4; Mortimer KM, 2002, EUR RESPIR J, V19, P699, DOI 10.1183/09031936.02.00247102; Mortimer KM, 2000, AM J RESP CRIT CARE, V162, P1838; National Research Council, 1998, RES PRIOR AIRB PART; Ostro B, 2001, EPIDEMIOLOGY, V12, P200, DOI 10.1097/00001648-200103000-00012; Ozkaynak H, 1996, J EXPO ANAL ENV EPID, V6, P57; Pekkanen J, 1997, ENVIRON RES, V74, P24, DOI 10.1006/enrs.1997.3750; Peters A, 1997, ENVIRON HEALTH PERSP, V105, P430, DOI 10.1289/ehp.97105430; Peters A, 1997, EUR RESPIR J, V10, P872; Peters JM, 1999, AM J RESP CRIT CARE, V159, P768; Quintana PJE, 2000, J EXPO ANAL ENV EPID, V10, P437, DOI 10.1038/sj.jea.7500105; Quintana PJE, 2001, ENVIRON RES, V87, P199, DOI 10.1006/enrs.2001.4304; Richards LW, 1999, ATMOS ENVIRON, V33, P4787, DOI 10.1016/S1352-2310(99)00267-8; Roemer W, 1999, OCCUP ENVIRON MED, V56, P86; Roemer W, 2000, CLIN EXP ALLERGY, V30, P1067; Romieu I, 1996, AM J RESP CRIT CARE, V154, P300; Segala C, 1998, EUR RESPIR J, V11, P677; Slaughter JC, 2003, ANN ALLERG ASTHMA IM, V91, P346; THOMAS A, 1994, ATMOS ENVIRON, V28, P935, DOI 10.1016/1352-2310(94)90251-8; Thurston GD, 1997, AM J RESP CRIT CARE, V155, P654; Timonen KL, 1997, AM J RESP CRIT CARE, V156, P546; *US EPA, 1990, NAT AIR QUAL EM TREN; Vedal S, 1998, AM J RESP CRIT CARE, V157, P1034; von Klot S, 2002, EUR RESPIR J, V20, P691, DOI 10.1183/09031936.02.01402001; WU CF, IN PESS J EXPO ANAL; YAKOVLEVA E, 1999, ENVIRON SCI TECHNOL, V33, P3845; Yu OC, 2000, ENVIRON HEALTH PERSP, V108, P1209, DOI 10.2307/3434835	51	129	135	2	19	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	JUN	2004	112	8					932	941		10.1289/ehp.6815		10	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	829BO	WOS:000222018200046	15175185	
J	Ameille, J; Pauli, G; Calastreng-Crinquand, A; Vervloet, D; Iwatsubo, Y; Popin, E; Bayeux-Dunglas, MC; Kopferschmitt-Kubler, MC; Arnaud, G; Bergeret, A; Blaumeiser, M; de Blay, F; Boitel, L; Bonnin, C; Brochard, P; Brun, J; Cabal, C; Cador, B; Caillaud, D; Cantineau, A; Chazenfus, J; Choudat, D; Conso, F; Costes, S; Couot, M; Curtes, JP; Dalphin, JC; Danaud, D; Danjou, P; Delemott, B; Deschamps, F; Dewitte, JD; Didier, A; Dhivert-Donnadieu, H; Doutrellot-Philippon, C; Dufresne-Benetti, F; Dumont, D; Dupas, D; Faucon, D; Fumery, JL; Gabrillargues, D; Garnier, R; Godard, P; Grudzien, F; Hemery, JM; Javelaud, B; Lasfargues, G; Leleu, B; Letourneux, M; Libert, B; Loriot, J; Martin, F; Michel, MP; Nisse, C; Paris, C; Pairon, JC; Penneau-Fontbonne, D; Perdrix, A; Petiet, G; de Santi, PP; Robin, H; Saadjian, M; Smolik, HJ; Soulat, JM; Tarin, C; Terracol, D; Tessier-Cotte, C; de Lara, JMT				Ameille, J; Pauli, G; Calastreng-Crinquand, A; Vervloet, D; Iwatsubo, Y; Popin, E; Bayeux-Dunglas, MC; Kopferschmitt-Kubler, MC; Arnaud, G; Bergeret, A; Blaumeiser, M; de Blay, F; Boitel, L; Bonnin, C; Brochard, P; Brun, J; Cabal, C; Cador, B; Caillaud, D; Cantineau, A; Chazenfus, J; Choudat, D; Conso, F; Costes, S; Couot, M; Curtes, JP; Dalphin, JC; Danaud, D; Danjou, P; Delemott, B; Deschamps, F; Dewitte, JD; Didier, A; Dhivert-Donnadieu, H; Doutrellot-Philippon, C; Dufresne-Benetti, F; Dumont, D; Dupas, D; Faucon, D; Fumery, JL; Gabrillargues, D; Garnier, R; Godard, P; Grudzien, F; Hemery, JM; Javelaud, B; Lasfargues, G; Leleu, B; Letourneux, M; Libert, B; Loriot, J; Martin, F; Michel, MP; Nisse, C; Paris, C; Pairon, JC; Penneau-Fontbonne, D; Perdrix, A; Petiet, G; de Santi, PP; Robin, H; Saadjian, M; Smolik, HJ; Soulat, JM; Tarin, C; Terracol, D; Tessier-Cotte, C; de Lara, JMT			Reported incidence of occupational asthma in France, 1996-99: the ONAP programme	OCCUPATIONAL AND ENVIRONMENTAL MEDICINE			English	Article							WORK-RELATED ASTHMA; RESPIRATORY-DISEASES; UNITED-KINGDOM; SURVEILLANCE SYSTEM; POPULATION; RISK; EXPOSURES; FINLAND; CANADA	Aims: To estimate the general and specific incidence of occupational asthma in France in 1996-99; and to describe the distribution of cases by age, sex, suspected causal agents, and occupation. Methods: New cases of occupational asthma were collected by a national surveillance programme, based on voluntary reporting, named Observatoire National des Asthmes Professionnels (ONAP), involving a network of occupational and chest physicians. For each case, the reporting form included information on age, sex, location of workplace, occupation, suspected causal agent, and methods of diagnosis. Estimates of the working population, used to calculate incidence rates by age, sex, region, and occupation, were obtained from the Institut National de la Statistique et des Etudes Economiques (INSEE) and from the French Securite Sociale statistics. Results: In 1996-99, 2178 cases of occupational asthma were reported to the ONAP, giving a mean annual rate of 24/million. Rates in men were higher than rates in women (27/million versus 19/million). The highest rate was observed in the 15-29 years age group (30/million). The most frequently incriminated agents were flour (20.3%), isocyanates (14.1%), latex (7.2%), aldehyde (5.9%), persulphate salts (5.8%), and wood dusts (3.7%). The highest risks of occupational asthma were found in bakers and pastry makers (683/million), car painters (326/million), hairdressers (308/million), and Wood workers (218/million). Conclusion: Despite likely underreporting, the number of cases of occupational asthma reported to the ONAP was approximately twice the number of compensated cases over the same period. The relevance of the programme is confirmed by the reproducibility of the results year after year, and its consistency with other surveillance programmes. The ONAP programme is useful for the identification of targets for primary prevention.	Inst Interuniv Med Travail Paris Ile France, F-75270 Paris 06, France; Soc Pneumol Langue Francaise, F-75006 Paris, France	Ameille, J (reprint author), Hop Ray Poincare, Unite Pathol Profess & Sante Travail, 104 Bd Raymond Poincare, F-92380 Garches, France.		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Environ. Med.	FEB	2003	60	2					136	141		10.1136/oem.60.2.136		6	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	641MF	WOS:000180748000011	12554842	
J	Lehtimaki, L; Kankaanranta, H; Saarelainen, S; Hahtola, P; Jarvenpaa, R; Koivula, T; Turjanmaa, V; Moilanen, E				Lehtimaki, L; Kankaanranta, H; Saarelainen, S; Hahtola, P; Jarvenpaa, R; Koivula, T; Turjanmaa, V; Moilanen, E			Extended exhaled NO measurement differentiates between alveolar and bronchial inflammation	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							POTENT OXIDANT PEROXYNITRITE; NITRIC-OXIDE; ASTHMATIC-PATIENTS; PULMONARY-FUNCTION; LOWER AIRWAYS; METHACHOLINE; INDUCTION; FIBROSIS; SYNTHASE; AIR	Lower respiratory tract inflammation can be detected by measuring exhaled nitric oxide (NO) concentration at a single exhalation flow rate, but this does not differentiate between alveolar and bronchial NO production. We assessed alveolar NO concentration and bronchial NO flux with an extended method of measuring exhaled NO at several exhalation flow rates in 40 patients with asthma, 17 patients with alveolitis, and 57 healthy control subjects. Bronchial NO flux was higher in asthma (2.5 +/- 0.3 nl/s, p < 0.001) than in alveolitis (0.7 +/- 0.1 nl/s) and healthy control subjects (0.7 + 0.1 nl/s). Alveolar NO concentration was higher in alveolitis (4.1 +/- 0.3 ppb, p < 0.001) than in asthma (1.1 +/- 0.2 ppb) and healthy control subjects (1.1 +/- 0.1 ppb). In asthma, bronchial NO flux correlated with serum level of eosinophil protein X (EPX) (r = 0.60, p < 0.001) and bronchial hyperresponsiveness (r = 0.55, p < 0.001). In alveolitis, alveolar NO concentration correlated inversely with pulmonary diffusing capacity (r = -0.55, p = 0.022) and pulmonary restriction. Glucocorticoid treatment or allergen avoidance normalized bronchial NO flux in asthma and decreased alveolar NO concentration toward normal in alveolitis. In conclusion, extended exhaled NO measurement can be used to separately assess alveolar and bronchial inflammation and to assess disease activity/severity in asthma and alveolitis.	Univ Tampere, Sch Med, Immunopharmacol Res Grp, FIN-33014 Tampere, Finland; Tampere Univ Hosp, Dept Clin Chem, FIN-33521 Tampere, Finland; Tampere Univ Hosp, Dept Resp Med, Tampere, Finland; Tampere Univ Hosp, Dept Radiol, Tampere, Finland; Tampere Univ Hosp, Dept Clin Physiol, Tampere, Finland	Moilanen, E (reprint author), Univ Tampere, Sch Med, Immunopharmacol Res Grp, FIN-33014 Tampere, Finland.			Kankaanranta, Hannu/0000-0001-5258-0906			Altman DG, 1991, PRACTICAL STAT MED R; ALVING K, 1993, EUR RESPIR J, V6, P1368; American Thoracic Society, 2000, AM J RESP CRIT CARE, V161, P646; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P2185; BORLAND CDR, 1989, EUR RESPIR J, V2, P56; CHINET T, 1990, THORAX, V45, P675, DOI 10.1136/thx.45.9.675; Gabbay E, 1999, AM J RESP CRIT CARE, V160, P2093; HAMID Q, 1993, LANCET, V342, P1510, DOI 10.1016/S0140-6736(05)80083-2; Hogman M, 2000, RESP MED, V94, P985, DOI 10.1053/rmed.2000.0872; Hogman M, 1999, AM J RESP CRIT CARE, V159, pA862; HOGMAN M, 2000, EUR RESPIR J, V16, pS443; Hyde RW, 1997, J APPL PHYSIOL, V82, P1290; KHARITONOV SA, 1994, LANCET, V343, P133, DOI 10.1016/S0140-6736(94)90931-8; Koller DY, 1999, CLIN EXP ALLERGY, V29, P786; Kraft M, 1996, AM J RESP CRIT CARE, V154, P1505; Lehtimaki L, 2000, ANN MED, V32, P417, DOI 10.3109/07853890008995949; Moilanen E, 1999, INFLAMMATION BASIC P, P787; NIEMINEN MM, 1992, CHEST, V102, P1537, DOI 10.1378/chest.102.5.1537; OCONNOR G, 1987, AM REV RESPIR DIS, V136, P1412; Paredi P, 1999, CHEST, V115, P1352, DOI 10.1378/chest.115.5.1352; Saleh D, 1998, FASEB J, V12, P929; Saleh D, 1997, AM J RESP CRIT CARE, V155, P1763; Silkoff PE, 2000, AM J RESP CRIT CARE, V161, P1218; Silkoff PE, 2000, CLIN CHEST MED, V21, P345, DOI 10.1016/S0272-5231(05)70271-9; Slutsky AS, 1999, AM J RESP CRIT CARE, V160, P2104; Sont JK, 1996, THORAX, V51, P496, DOI 10.1136/thx.51.5.496; TERHO EO, 1986, AM J IND MED, V10, P329, DOI 10.1002/ajim.4700100333; Tsoukias NM, 1998, J APPL PHYSIOL, V85, P653; Viljanen A A, 1982, Scand J Clin Lab Invest Suppl, V159, P21	29	129	130	0	1	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	JUN	2001	163	7					1557	1561				5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	443JE	WOS:000169337400013	11401873	
J	Ren, P; Jankun, TM; Belanger, K; Bracken, MB; Leaderer, BP				Ren, P; Jankun, TM; Belanger, K; Bracken, MB; Leaderer, BP			The relation between fungal propagules in indoor air and home characteristics	ALLERGY			English	Article						fungal propagules; house characteristics; indoor air; seasonal variation	MOLDS; PREVALENCE; DAMPNESS; DUST	Background: Questionnaires are commonly used in epidemiologic studies to obtain information about house characteristics in order to predict the household aeroallergen exposure levels. However, the reliability of the predictions made with the questionnaires has not been evaluated. To address this issue, we compared objectively measured fungal propagules including the most frequently isolated mold genera (i.e., Alternaria, Aspergillus, Cladosporium, Penicillium, etc.) in a large sample of homes and compared these measured values to the questionnaire-determined household characteristics. Methods: As part of a prospective cohort study on the relation between residential allergen exposure and development of asthma in neonates, fungal air samples were collected from infant bedrooms and main living areas in 1000 homes in the Northeast USA, from December 1996 to January 1999. A Burkard portable air sampler was used in combination with DG-18 and MEA agars. A questionnaire was used to obtain information on host and house characteristics that may have an impact on the presence of fungal propagules in the air. This included information on observation of moisture problems (e.g., water leakage or damage, and mold or mildew growth), ventilation and heating facilities, building age and type, number of occupants, annual household income, presence of pets and pests, cleaning regimens, etc. Results: The number of CFU/m(3) air collected on MEA was significantly higher than on DG-18 (means, respectively, 1033.5 and 846.0 CFU/m(3)) (P < 0.0005). However, there was no significant difference between the numbers of CFU/m(3) air collected from the main living area and from the infant bedroom. There was only a very weak relationship between the house characteristics, as described by questionnaire, and the presence of fungal propagules in indoor air. Only the temperature, relative humidity, season, and cats inside homes had a statistically significant impact on the presence of fungal propagules in indoor air. Conclusions: The presence of fungal propagules in indoor air cannot be reliably predicted by home characteristics. Actual measurements are required for fungal exposure assessment, and the use of only;one medium to collect samples in one location in a home might be adequate to represent residential levels of fungi in indoor air.	Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, Div Environm Hlth Sci, New Haven, CT 06510 USA	Ren, P (reprint author), NYSDOH, Wadsworth Ctr Labs & Res, David Axelrod Inst, 120 New Scotland Ave, Albany, NY 12208 USA.				NIEHS NIH HHS [ES/07456]		Blackley CH, 1873, EXPT RES CAUSES NATU; *COMM EUR COMM, 1994, 12 CEC; DALES RE, 1991, AM REV RESPIR DIS, V143, P505; DALES RE, 1991, AM J EPIDEMIOL, V134, P196; DAmato G, 1997, ALLERGY, V52, P711, DOI 10.1111/j.1398-9995.1997.tb01227.x; Feinberg S, 1935, WISC MED J, V34, P254; GRAVESEN S, 1979, ALLERGY, V34, P135, DOI 10.1111/j.1398-9995.1979.tb01562.x; PLATT SD, 1989, BRIT MED J, V298, P1673; PRINCE H, 1934, TEX J MED, V30, P340; Ren P, 1999, J EXPO ANAL ENV EPID, V9, P560, DOI 10.1038/sj.jea.7500061; RUSSELL C, 1999, INDOOR AIR S, V4, P934; VERHOEFF AP, 1995, AM J EPIDEMIOL, V141, P103; VERHOEFF AP, 1994, AIR QUAL MG, V2, P129; VONDERWERFF P, 1958, MOLD FUNGI BRONCHIAL	14	129	135	0	12	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	MAY	2001	56	5					419	424		10.1034/j.1398-9995.2001.056005419.x		6	Allergy; Immunology	Allergy; Immunology	437BW	WOS:000168971200008	11350305	
J	Campbell, JJ; Brightling, CE; Symon, FA; Qin, S; Murphy, KE; Hodge, M; Andrew, DP; Wu, LJ; Butcher, EC; Wardlaw, AJ				Campbell, JJ; Brightling, CE; Symon, FA; Qin, S; Murphy, KE; Hodge, M; Andrew, DP; Wu, LJ; Butcher, EC; Wardlaw, AJ			Expression of chemokine receptors by lung T cells from normal and asthmatic subjects	JOURNAL OF IMMUNOLOGY			English	Article							CHEMOATTRACTANT RECEPTORS; DIFFERENTIAL EXPRESSION; ATOPIC ASTHMA; LYMPHOCYTES; RECOGNITION; PULMONARY; BIOLOGY	The lung is an important tertiary lymphoid organ with constant trafficking of T cells through the lung in both health and disease. T cell migration is controlled by a combination of adhesion receptors and chemokines expressed on vascular endothelium and in the tissue, often in an organ-specific manner. This leads to selective accumulation of different T cell subsets, a process called lymphocyte homing. There is evidence for a distinct lung-homing pathway, but no specific lung-homing receptors have been described. We analyzed the chemokine receptor profile of lung T cells to determine the extent to which lung T cells shared homing pathways with other organs such as the gut and skin. In addition, we compared expression of receptors in normal and asthmatic individuals to determine whether different pathways were used in health and disease, We observed that lung T cells expressed a profile of chemokine and adhesion receptors distinct from that of gut- and skin-homing T cells although no chemokine receptor specific for the lung was found. In particular, lung T cells expressed CCR5 and CXCR3, but not CeR9 or cutaneous lymphocyte Ag, and only low levels of CCR4 and alpha (4)beta (7). No differences were observed between lung T cells from normal vs asthmatic subjects. This study provides added support far the concept of a lung-homing pathway separate from other mucosal organs such as the gut and suggests that the chemokine pathways that control T cell migration in normal homeostasis and Th2-type inflammatory responses are similar.	Univ Leicester, Sch Med, Inst Lung Hlth, Leicester, Leics, England; Univ Leicester, Sch Med, Div Resp Med, Leicester, Leics, England; Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA; Childrens Hosp, Div Transfus Med, Boston, MA 02115 USA; Stanford Univ, Sch Med, Dept Pathol, Lab Immunol & Vasc Biol, Stanford, CA 94305 USA; Stanford Univ, Sch Med, Dept Med, Ctr Digest Dis, Stanford, CA 94305 USA; Vet Affairs Palo Alto Healthcare Syst, Ctr Mol Biol & Med, Palo Alto, CA 94304 USA; Millenium Pharmaceut, Cambridge, MA 02142 USA	Wardlaw, AJ (reprint author), Glenfield Gen Hosp, Groby Rd, Leicester LE3 9QP, Leics, England.				NIAID NIH HHS [AI46784, AI47822]; NIGMS NIH HHS [GM37734]		Abitorabi MA, 1996, J IMMUNOL, V156, P3111; AZZAWI M, 1990, AM REV RESPIR DIS, V142, P1407; BARGATZE RF, 1995, IMMUNITY, V3, P99, DOI 10.1016/1074-7613(95)90162-0; Brandtzaeg P, 1999, MUCOSAL IMMUNOLOGY, P439; Butcher EC, 1999, ADV IMMUNOL, V72, P209, DOI 10.1016/S0065-2776(08)60022-X; BUTCHER EC, 1991, CELL, V67, P1033, DOI 10.1016/0092-8674(91)90279-8; Campbell JJ, 1996, J CELL BIOL, V134, P255, DOI 10.1083/jcb.134.1.255; Campbell JJ, 1998, J CELL BIOL, V141, P1053, DOI 10.1083/jcb.141.4.1053; Campbell JJ, 2000, CURR OPIN IMMUNOL, V12, P336, DOI 10.1016/S0952-7915(00)00096-0; Campbell JJ, 1999, NATURE, V400, P776, DOI 10.1038/23495; CURTIS JL, 1995, AM J RESP CELL MOL, V12, P520; Cyster JG, 1999, SCIENCE, V286, P2098, DOI 10.1126/science.286.5447.2098; ERLE DJ, 1994, AM J RESP CELL MOL, V10, P237; Homey B, 2000, J IMMUNOL, V164, P3465; Jarmin DI, 2000, J IMMUNOL, V164, P3460; Krug N, 1996, AM J RESP CELL MOL, V14, P319; Kunkel EJ, 2000, J EXP MED, V192, P761, DOI 10.1084/jem.192.5.761; Luster AD, 1998, NEW ENGL J MED, V338, P436; Morales J, 1999, P NATL ACAD SCI USA, V96, P14470, DOI 10.1073/pnas.96.25.14470; MURPHY PM, 1994, ANNU REV IMMUNOL, V12, P593, DOI 10.1146/annurev.immunol.12.1.593; PICKER LJ, 1994, EUR J IMMUNOL, V24, P1269, DOI 10.1002/eji.1830240605; Read S, 2000, J EXP MED, V192, P295, DOI 10.1084/jem.192.2.295; ROBINSON DS, 1992, NEW ENGL J MED, V326, P298, DOI 10.1056/NEJM199201303260504; Rossi D, 2000, ANNU REV IMMUNOL, V18, P217, DOI 10.1146/annurev.immunol.18.1.217; Sallusto F, 2000, ANNU REV IMMUNOL, V18, P593, DOI 10.1146/annurev.immunol.18.1.593; Sauty A, 1999, J IMMUNOL, V162, P3549; Teraki Y, 1997, J IMMUNOL, V159, P6018; WANG W, 2000, J BIOL CHEM; Zabel BA, 1999, J EXP MED, V190, P1241, DOI 10.1084/jem.190.9.1241; Zlotnik A, 2000, IMMUNITY, V12, P121, DOI 10.1016/S1074-7613(00)80165-X	30	129	134	3	5	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	FEB 15	2001	166	4					2842	2848				7	Immunology	Immunology	400QA	WOS:000166882000086	11160352	
J	Ahmed, SR				Ahmed, SR			The immune system as a potential target for environmental estrogens (endocrine disrupters): a new emerging field	TOXICOLOGY			English	Review						immune; autoimmune; estrogens; environmental estrogens; endocrine disrupters; allergies	ADULT MALE-RATS; LUPUS-ERYTHEMATOSUS; SEX-HORMONES; AUTOIMMUNE-DISEASES; POLYCHLORINATED-BIPHENYLS; ORGANOCHLORINE COMPOUNDS; AUTOANTIBODY PRODUCTION; CYTOKINE PRODUCTION; MURINE SPLENOCYTES; GONADAL-STEROIDS	It is now well known that natural (17 beta-estradiol) and synthetic (e.g. diethylstilbestrol) estrogens not only affect the reproductive system, but also markedly influence the immune system. Recently, a new class of estrogens that is abundant in the environment (in industrial chemicals, pesticides, and surfactants) has been recognized. Some of these estrogenic chemicals (which are a large subgroup of endocrine disrupters) have also been shown to influence the immune system. This review assimilates growing evidence in wildlife, laboratory animals and to a limited extent in humans, which suggests that environmental chemicals may also affect the immune system. Further studies are needed to ascertain the immunological consequences of exposure to environmental estrogens, especially in humans. At the present time, it is not known whether the human immune system responds to a low dose of environmental estrogens or if environmental estrogens influence certain subsets of human populations, rather than the general population. Conceivably, an alteration of the immune system by environmental estrogens could affect the individuals' ability to mount well-regulated immune responses to microbial and vaccine antigens, allergens, self and tumor antigens. Possible changes in the immune system must be investigated routinely in toxicity studies. A comprehensive mechanistic understanding of potential immunomodulatory chemicals is needed. 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J	Masopust, D; Schenkel, JM				Masopust, David; Schenkel, Jason M.			The integration of T cell migration, differentiation and function	NATURE REVIEWS IMMUNOLOGY			English	Review							CHEMOKINE RECEPTOR CCR7; CD103(+) DENDRITIC CELLS; LYMPH-NODES; CUTTING EDGE; IN-VIVO; RESIDENT MEMORY; ANTIGEN PRESENTATION; PERIPHERAL-TISSUES; HOMING RECEPTOR; L-SELECTIN	T cells function locally. Accordingly, T cells' recognition of antigen, their subsequent activation and differentiation, and their role in the processes of infection control, tumour eradication, autoimmunity, allergy and alloreactivity are intrinsically coupled with migration. Recent discoveries revise our understanding of the regulation and patterns of T cell trafficking and reveal limitations in current paradigms. Here, we review classic and emerging concepts, highlight the challenge of integrating new observations with existing T cell classification schemes and summarize the heuristic framework provided by viewing T cell differentiation and function first through the prism of migration.	[Masopust, David; Schenkel, Jason M.] Univ Minnesota, Sch Med, Dept Microbiol, Ctr Immunol, Minneapolis, MN 55455 USA	Masopust, D (reprint author), Univ Minnesota, Sch Med, Dept Microbiol, Ctr Immunol, Minneapolis, MN 55455 USA.	masopust@umn.edu			US National Institutes of Health (NIH) [R01AI084913-01]; NIH [T32AI007313]; Office Of The Director, NIH [DP2OD006467]	The authors thank V. Vezys and S. Jameson (University of Minnesota) for helpful discussion. This study was supported by US National Institutes of Health (NIH) grant R01AI084913-01 (to D.M.), NIH grant T32AI007313 (to J.M.S.) and the Office Of The Director, NIH, under Award Number DP2OD006467 (to D.M.). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.	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J	Nygaard, UC; Hansen, JS; Samuelsen, M; Alberg, T; Marioara, CD; Lovik, M				Nygaard, Unni C.; Hansen, Jitka S.; Samuelsen, Mari; Alberg, Torunn; Marioara, Calin D.; Lovik, Martinus			Single-Walled and Multi-Walled Carbon Nanotubes Promote Allergic Immune Responses in Mice	TOXICOLOGICAL SCIENCES			English	Article						carbon nanotubes; adjuvant effect; airway inflammation; allergy; mice; IgE	DIESEL EXHAUST PARTICLES; AIRWAY INFLAMMATION; ADJUVANT ACTIVITY; ULTRAFINE PARTICLES; RESPIRATORY HEALTH; FINE PARTICLES; IGE PRODUCTION; SENSITIZATION; TOXICITY; ANTIGEN	The adjuvant effect of particles on allergic immune responses has been shown to increase with decreasing particle size and increasing particle surface area. Like ultrafine particles, carbon nanotubes (CNTs) have nano-sized dimensions and a large relative surface area and might thus increase allergic responses. Therefore, we examined whether single-walled (sw) and multi-walled (mw) CNTs have the capacity to promote allergic responses in mice, first in an sc injection model and thereafter in an intranasal model. Balb/cA mice were exposed to three doses of swCNT, mwCNT, as well as ultrafine carbon black particles (ufCBPs, Printex90) during sensitization with the allergen ovalbumin (OVA). Five days after an OVA booster, OVA-specific IgE, IgG1, and IgG2a antibodies in serum and the numbers of inflammatory cells and cytokine levels in bronchoalveolar lavage fluid (BALF) were determined. Furthermore, ex vivo OVA-induced cytokine release from mediastinal lymph node (MLN) cells was measured. In separate experiments, differential cell counts were determined in BALF 24 h after a single intranasal exposure to the particles in the absence of allergen. We demonstrate that both swCNT and mwCNT together with OVA strongly increased serum levels of OVA-specific IgE, the number of eosinophils in BALF, and the secretion of Th2-associated cytokines in the MLN. On the other hand, only mwCNT and ufCBP with OVA increased IgG2a levels, neutrophil cell numbers, and tumor necrosis factor-alpha and monocyte chemoattractant protein-1 levels in BALF, as well as the acute influx of neutrophils after exposure to the particles alone. This study demonstrates that CNTs promote allergic responses in mice.	[Nygaard, Unni C.; Hansen, Jitka S.; Samuelsen, Mari; Alberg, Torunn; Lovik, Martinus] Norwegian Inst Publ Hlth, Div Environm Med, NO-0403 Oslo, Norway; [Hansen, Jitka S.] Natl Res Ctr Working Environm, DK-2100 Copenhagen, Denmark; [Marioara, Calin D.] SINTEF Mat & Chem, NO-7465 Trondheim, Norway; [Lovik, Martinus] Norwegian Univ Sci & Technol, Fac Med, Dept Canc Res & Mol Med, NO-7489 Trondheim, Norway	Nygaard, UC (reprint author), Norwegian Inst Publ Hlth, Div Environm Med, POB 4404 Nydalen,Lovisenbergata 8, NO-0403 Oslo, Norway.	unni.cecilie.nygaard@fhi.no					Annesi-Maesano I, 2007, RESP MED, V101, P1721, DOI 10.1016/j.rmed.2007.02.022; Bang JJ, 2004, J NANOSCI NANOTECHNO, V4, P716, DOI 10.1166/jnn.2004.095; Brunauer S, 1938, J AM CHEM SOC, V60, P309, DOI 10.1021/ja01269a023; Buford Mary C, 2007, Part Fibre Toxicol, V4, P6, DOI 10.1186/1743-8977-4-6; de Haar C, 2006, CLIN EXP ALLERGY, V36, P1469, DOI 10.1111/j.1365-2222.2006.02586.x; de Haar C, 2005, TOXICOL SCI, V87, P409, DOI 10.1093/toxsci/kfi255; DEHAAR C, 2008, J ALLERGY CLIN IMMUN, V101, P1246; Dutta D, 2007, TOXICOL SCI, V100, P303, DOI 10.1093/toxsci/kfm217; Granum B, 2002, TOXICOL SCI, V65, P7, DOI 10.1093/toxsci/65.1.7; Granum B, 2000, INHAL TOXICOL, V12, P365, DOI 10.1080/08958378.2000.11463247; Hansen SF, 2008, ECOTOXICOLOGY, V17, P438, DOI [10.1007/s10646-008-0210-4, 10.1007/s00787-008-0686-8]; Inoue K, 2005, RESP RES, V6, DOI 10.1186/1465-9921-6-106; Kagan VE, 2006, TOXICOL LETT, V165, P88, DOI 10.1016/j.toxlet.2006.02.001; Lam CW, 2004, TOXICOL SCI, V77, P126, DOI 10.1093/toxsci/kfg243; Lovik M, 1997, TOXICOLOGY, V121, P165, DOI 10.1016/S0300-483X(97)00075-9; Lovik M, 2007, METHODS, V41, P72, DOI 10.1016/j.ymeth.2006.07.014; Mercer RR, 2008, AM J PHYSIOL-LUNG C, V294, pL87, DOI 10.1152/ajplung.00186.2007; Morgenstern V, 2008, AM J RESP CRIT CARE, V177, P1331, DOI 10.1164/rccm.200701-036OC; Muller J, 2005, TOXICOL APPL PHARM, V207, P221, DOI 10.1016/j.taap.2005.01.008; Muller J, 2008, CHEM RES TOXICOL, V21, P1698, DOI 10.1021/tx800101p; Murr L E, 2006, Int J Environ Res Public Health, V3, P48, DOI 10.3390/ijerph2006030007; Nygaard UC, 2004, TOXICOL SCI, V82, P515, DOI 10.1093/toxsci/kfh287; Ormstad H, 1998, TOXICOLOGY, V129, P227, DOI 10.1016/S0300-483X(98)00079-1; Parnia S, 2002, ALLERGY, V57, P1111, DOI 10.1034/j.1398-9995.2002.02167.x; Penttinen P, 2001, EUR RESPIR J, V17, P428, DOI 10.1183/09031936.01.17304280; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Pope CA, 2006, J AIR WASTE MANAGE, V56, P709; Powers KW, 2007, NANOTOXICOLOGY, V1, P42, DOI 10.1080/17435390701314902; Renwick LC, 2004, OCCUP ENVIRON MED, V61, P442, DOI 10.1136/oem.2003.008227; Ryman-Rasmussen JP, 2009, AM J RESP CELL MOL, V40, P349, DOI 10.1165/rcmb.2008-0276OC; Salvador-Morales C, 2006, MOL IMMUNOL, V43, P193, DOI 10.1016/j.molimm.2005.02.006; SAMUELSEN M, SCAND J IMM IN PRESS; Sato Y, 2005, MOL BIOSYST, V1, P176, DOI 10.1039/b502429c; Schwartz J, 2000, EPIDEMIOLOGY, V11, P6, DOI 10.1097/00001648-200001000-00004; Service RF, 2004, SCIENCE, V304, P1732, DOI 10.1126/science.304.5678.1732; Shvedova AA, 2008, AM J PHYSIOL-LUNG C, V295, pL552, DOI 10.1152/ajplung.90287.2008; Stern ST, 2008, TOXICOL SCI, V101, P4, DOI 10.1093/toxsci/kfm169; Takano H, 1997, AM J RESP CRIT CARE, V156, P36; Van den Broeck W, 2006, J IMMUNOL METHODS, V312, P12, DOI 10.1016/j.jim.2006.01.022; Wan JX, 2007, INHAL TOXICOL, V19, P177, DOI 10.1080/08958370701496145; Wick P, 2007, TOXICOL LETT, V168, P121, DOI 10.1016/j.toxlet.2006.08.019	41	128	134	2	19	OXFORD UNIV PRESS	OXFORD	GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND	1096-6080			TOXICOL SCI	Toxicol. Sci.	MAY	2009	109	1					113	123		10.1093/toxsci/kfp057		11	Toxicology	Toxicology	441AQ	WOS:000265742100014	19293371	
J	Sjogren, YM; Jenmalm, MC; Bottcher, MF; Bjorksten, B; Sverremark-Ekstrom, E				Sjogren, Y. M.; Jenmalm, M. C.; Bottcher, M. F.; Bjorksten, B.; Sverremark-Ekstrom, E.			Altered early infant gut microbiota in children developing allergy up to 5 years of age	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergy; bifidobacteria; Clostridium difficile; endotoxin; Fel d 1; gut microbiota; infant; lactobacilli; siblings	PLACEBO-CONTROLLED TRIAL; SPECIES-SPECIFIC PRIMERS; REAL-TIME PCR; SWEDISH INFANTS; ATOPIC ECZEMA; INTESTINAL BIFIDOBACTERIA; FECAL MICROBIOTA; ENDOTOXIN LEVELS; RIBOSOMAL-RNA; HOUSE-DUST	Early colonization with bifidobacteria and lactobacilli is postulated to protect children from allergy, while Clostridium (C.) difficile colonization might be associated with allergic disease. Previous studies of infant gut microbiota in relation to subsequent allergy development have mostly employed culture-dependent techniques, studied genera of bacteria and the follow-up period was limited to 2 years. To relate gut microbiota in early infancy, notably bifidobacteria and lactobacilli at species level, to allergy development during the first 5 years of life and study if environmental factors influence the early infant gut microbiota. Fecal samples were collected at 1 week, 1 month and 2 months after birth from 47 Swedish infants, followed prospectively to 5 years of age. Bacterial DNA was analysed with real-time PCR and related to allergy development, family size as well as endotoxin and Fel d 1 levels in house dust samples. Primers binding to C. difficile, four species of bifidobacteria, two lactobacilli groups and Bacteroides fragilis were used. Children regarded as allergic manifested allergic symptoms and were skin prick test positive during their first 5 years while non-allergic children were neither. Children who developed allergy were significantly less often colonized with lactobacilli group I (Lactobacillus (L.) rhamnosus, L. casei, L. paracasei), Bifidobacterium adolescentis and C. difficile during their first 2 months. Infants colonized with several Bifidobacterium species had been exposed to higher amounts of endotoxin and grew up in larger families than infants harbouring few species. A more diverse gut microbiota early in life might prevent allergy development and may be related to the previously suggested inverse relationship between allergy, family size and endotoxin exposure. Cite this as: Y. M. Sjogren, M. C. Jenmalm, M. F. Bottcher, B. BjorkstEn and E. Sverremark-Ekstrom, Clinical & Experimental Allergy, 2009 (39) 518-526.	[Sjogren, Y. M.] Stockholm Univ, Wenner Gren Inst, Dept Immunol, Arrhenius Lab Nat Sci F5, S-10691 Stockholm, Sweden; [Jenmalm, M. C.; Bottcher, M. F.] Linkoping Univ, Fac Hlth Sci, Dept Clin & Expt Med, Div Paediat, Linkoping, Sweden; [Bjorksten, B.] Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden	Sjogren, YM (reprint author), Stockholm Univ, Wenner Gren Inst, Dept Immunol, Arrhenius Lab Nat Sci F5, Svante Arrhenius Vag 16-18, S-10691 Stockholm, Sweden.	ylva.sjogren@imun.su.se	Jenmalm, Maria/C-9679-2009; Sverremark-Ekstrom, Eva/A-2305-2016	Jenmalm, Maria/0000-0002-2117-5366; Sverremark-Ekstrom, Eva/0000-0001-6271-8681	Ekhaga foundation; Cancer and Allergy foundation; Mjolkdroppen; Magnus Bergvall foundation,; Swedish Research Council [57X-15160-05-2, 74X-20146-01-2]; National Swedish Association against Allergic Diseases; National Heart and Lung Association; Swedish Foundation for Health Care Sciences and Allergy Research	This work was supported by the Ekhaga foundation, the Cancer and Allergy foundation, Mjolkdroppen, the Magnus Bergvall foundation, the Swedish Research Council (57X-15160-05-2 and 74X-20146-01-2), the National Swedish Association against Allergic Diseases, the National Heart and Lung Association, and the Swedish Foundation for Health Care Sciences and Allergy Research.	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Exp. Allergy	APR	2009	39	4					518	526		10.1111/j.1365-2222.2008.03156.x		9	Allergy; Immunology	Allergy; Immunology	418YA	WOS:000264184800010	19220322	
J	de Jongste, JC; Carraro, S; Hop, WC; Baraldi, E				de Jongste, Johan C.; Carraro, Silvia; Hop, Wim C.; Baraldi, Eugenio		CHARISM Study Grp	Daily Telemonitoring of Exhaled Nitric Oxide and Symptoms in the Treatment of Childhood Asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						airway inflammation; inhaled corticosteroid; symptom-free days; lung function; telemedicine	RANDOMIZED CONTROLLED-TRIAL; CHILDREN; EXACERBATIONS; GUIDE; MANAGEMENT	Rationale Asthma treatment might improve when inhaled steroids are titrated on airway inflammation. Fractional exhaled nitric oxide (FE(NO0.05)), a marker of eosinophilic airway inflammation, can be measured at home. Objectives: We assessed daily FE(NO0.05) telemonitoring in the management of childhood asthma. Methods: Children with atopic asthma (n = 151) were randomly assigned to two groups: FE(NO0.05) Plus symptom monitoring, or monitoring of symptoms only. All patients scored asthma symptoms in an electronic diary over 30 weeks; 77 received a portable nitric oxide (NO) analyzer. Data were transmitted daily to the coordinating centers. Patients were phoned every 3 weeks and their steroid dose was adapted according to FE(NO0.05) and symptoms, or according to symptoms. Children were seen at 3, 12, 21, and 30 weeks for examination and lung function testing. The primary end point was the proportion of symptom-free days in the last 12 study weeks. Measurements and Main Results: Telemonitoring was feasible with reliable FE(NO0.05) data for 86% of days, and valid diary entries for 79% of days. Both groups showed an increase in symptom-free days, improvement of FEV(1) and quality of life, and a reduction in steroid dose. None of the changes from baseline differed between groups. The difference in symptom-free days over the last 12 weeks was 0.3% (P = 0.95; 95% confidence interval, -10 to 11%). There was a trend for fewer exacerbations in the FE(NO0.05) group. Conclusions: Thirty weeks of daily FENO(0.05) and symptom telemonitoring was associated with improved asthma control and a lower steroid dose. We found no added value of daily FENO(0.05) monitoring compared with daily symptom monitoring only.	[de Jongste, Johan C.] Erasmus Univ, Med Ctr, Sophia Childrens Hosp, Div Pediat Resp Med,Dept Pediat, NL-3000 CB Rotterdam, Netherlands; [Carraro, Silvia; Baraldi, Eugenio] Univ Padua, Dept Pediat, Unit Allergy & Resp Med, Padua, Italy; [Hop, Wim C.] Erasmus Univ, Med Ctr, Dept Biostat, NL-3000 CB Rotterdam, Netherlands	de Jongste, JC (reprint author), Erasmus Univ, Med Ctr, Sophia Childrens Hosp, Div Pediat Resp Med,Dept Pediat, POB 2060, NL-3000 CB Rotterdam, Netherlands.	j.c.dejongste@erasmusmc.nl		BARALDI, EUGENIO/0000-0002-1829-3652; MARSEGLIA, GIAN LUIGI/0000-0003-3662-0159			American Thoracic Society, 2005, AM J RESP CRIT CARE, V171, P912, DOI DOI 10.1164/RCCM.200406-710ST.PUBMED:15817806; Buchvald F, 2005, J ALLERGY CLIN IMMUN, V115, P1130, DOI 10.1016/j.jaci.2005.03.020; de Jongste JC, 2005, EUR RESPIR J, V26, P379, DOI 10.1183/09031936.05.00080705; DEJONGSTE JC, 2008, AM J RESP CRIT CARE, V177, pA992; Fritsch M, 2006, PEDIATR PULM, V41, P855, DOI 10.1002/ppul.20455; Gelb AF, 2006, CHEST, V129, P1492, DOI 10.1378/chest.129.6.1492; Green RH, 2002, LANCET, V360, P1715, DOI 10.1016/S0140-6736(02)11679-5; Haldar P, 2008, AM J RESP CRIT CARE, V178, P218, DOI [10.1164/rccm.200711-1754OC, 10.1164/rccm.200711-17540C]; Juniper EF, 1996, QUAL LIFE RES, V5, P27, DOI 10.1007/BF00435966; Pijnenburg MW, 2006, PEDIATR ALLERGY IMMU, V17, P189, DOI 10.1111/j.1399-3038.2006.00394.x; Pijnenburg MW, 2005, THORAX, V60, P215, DOI 10.1136/thx.2004.023374; Pijnenburg MW, 2005, AM J RESP CRIT CARE, V172, P831, DOI 10.1164/rccm.200503-458OC; Pijnenburg MWH, 2005, CLIN EXP ALLERGY, V35, P920, DOI 10.1111/j.1365-2222.2005.02279.x; Rabe KF, 2004, J ALLERGY CLIN IMMUN, V114, P40, DOI 10.1016/j.jaci.2004.04.042; Reddel H, 1999, LANCET, V353, P364, DOI 10.1016/S0140-6736(98)06128-5; Shaw DE, 2007, AM J RESP CRIT CARE, V176, P231, DOI 10.1164/rccm.200610-14270C; Smith AD, 2005, NEW ENGL J MED, V352, P2163, DOI 10.1056/NEJMoa043596; Sont JK, 1999, AM J RESP CRIT CARE, V159, P1043; Taylor DR, 2006, THORAX, V61, P817, DOI 10.1136/thx.2005.056093; Zacharasiewicz A, 2005, AM J RESP CRIT CARE, V171, P1077, DOI 10.1164/rccm.200409-1242OC	20	128	130	0	2	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	JAN 15	2009	179	2					93	97		10.1164/rccm.200807-1010OC		5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	394PC	WOS:000262458000005	18931330	
J	Gunthorpe, MJ; Szallasi, A				Gunthorpe, Martin J.; Szallasi, Arpad			Peripheral TRPV1 receptors as targets for drug development: New molecules and mechanisms	CURRENT PHARMACEUTICAL DESIGN			English	Review							GENE-RELATED PEPTIDE; SENSORY NERVE DESENSITIZATION; HUMAN EPIDERMAL-KERATINOCYTES; ACID-INDUCED COLITIS; OBESE ZUCKER RATS; VANILLOID RECEPTOR-1; CAPSAICIN RECEPTOR; POTENTIAL VANILLOID-1; EPITHELIAL-CELLS; SUBSTANCE-P	Based on the painful effects of exposure to capsaicin, TRPV1 ( transient receptor potential vanilloid subfamily member 1) localization is most readily associated with peripheral sensory neurons, however, TRPV1 is now known to be expressed, albeit at lower levels, in the spinal cord, brain and a wide-range of non-neuronal cells. The latter includes epithelial cells ( e. g. keratinocytes, urothelium, gastric epithelial cells, enterocytes, and pneumocytes) through vascular endothelium and cells of the immune system ( e. g. T-cells and mast cells) to smooth muscle, fibroblasts and hepatocytes. Despite extensive research, the physiological function of TRPV1 in the brain and in non-neuronal tissues remains elusive. The preliminary results are exciting, but many are unconfirmed and/ or contradictory. As yet, studies with TRPV1 knock-out mice have proven unhelpful in clarifying such biological roles. Now that a range of potent and selective TRPV1 antagonists are available in this rapidly expanding research field, further understanding of the biological roles of TRPV1 throughout the body is within reach. In this article, we will summarize the known roles of peripheral TRPV1 receptors in physiology and disease and review the current perspectives for the therapeutic potential of TRPV1 agonists and antagonists in the treatment of a wide range of conditions such as pain, cancer, migraine, chronic cough, asthma, rectal hypersensitivity, inflammatory bowel disease, obesity, overactive bladder and diabetes. New applications of targeting central TRPV1 receptors are reviewed in the accompanying article by Starowicz et al. ( in this issue).	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Pharm. Design	JAN	2008	14	1					32	41				10	Pharmacology & Pharmacy	Pharmacology & Pharmacy	274XT	WOS:000254036800004	18220816	
J	Bachert, C; Bousquet, J; Canonica, GW; Durham, SR; Klimek, L; Mullol, J; Van Cauwenberge, PB; Van Hammee, G				Bachert, C; Bousquet, J; Canonica, GW; Durham, SR; Klimek, L; Mullol, J; Van Cauwenberge, PB; Van Hammee, G		XPERT Study Grp	Levocetirizine improves quality of life and reduces costs in long-term management of persistent allergic rhinitis	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						ARIA; persistent allergic rhinitis; health-related quality of life; levocetirizine; long-term therapy; pharmacoeconomics	HISTAMINE-INDUCED WHEAL; HEALTH-STATUS; DOUBLE-BLIND; CETIRIZINE; ASTHMA; RHINOCONJUNCTIVITIS; QUESTIONNAIRE; EPIDEMIOLOGY; LORATADINE; VOLUNTEERS	Background: Allergic Rhinitis and its Impact on Asthma in collaboration with the World Health Organization initiative reclassified allergic rhinitis, like asthma, by duration and severity. The Xyzal in Persistent Rhinitis Trial is the first large, long-term clinical trial studying patients with persistent rhinitis as defined by Allergic Rhinitis and its Impact on Asthma. Objectives: Two primary objectives were defined: comparison of the Rhinoconjunctivitis Quality of Life Questionnaire overall score and Total 5 Symptoms Score (rhinorrhea, sneezing, nasal congestion, and nasal and ocular pruritus) over a period of 4 weeks between levocetirizine 5 mg and placebo. Secondary endpoints included similar evaluations at 1 week and 3, 4.5, and 6 months, summary scores for a general health status questionnaire (Medical Outcomes Survey Short Form 36), a pharmacoeconomic assessment, comorbidities, and a safety evaluation. Methods: The Xyzal in Persistent Rhinitis Trial was a 6-month double-blind, placebo-controlled, multicenter, multinational trial in 551 patients. Adults with persistent rhinitis sensitized to both grass pollen and house dust mite were randomized to receive levocetirizine 5 mg/d or placebo. Results: A total of 421 patients completed the full study. Levocetirizine significantly improved both the Rhinoconjunctivitis Quality of Life Questionnaire overall score and the Total 5 Symptoms Score from week 1 to 6 months (all P values < .001). Medical Outcomes Survey Short Form 36 summary scores were also improved in the levocetirizine group compared with the placebo group. Treatment cessation because of lack of effect, comorbidities, and overall costs of disease, and comorbidities per working patient per month (E160.27 vs E108.18) were lower in the levocetirizine group. Conclusion: Levocetirizine was shown to improve quality of life and symptoms and to decrease the overall costs of the disease over the 6-month treatment period.	State Univ Ghent Hosp, Dept Otorhinolaryngol, B-9000 Ghent, Belgium	Bachert, C (reprint author), State Univ Ghent Hosp, Dept Otorhinolaryngol, Pintelaan 185, B-9000 Ghent, Belgium.	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J	Noakes, PS; Holt, PG; Prescott, SL				Noakes, PS; Holt, PG; Prescott, SL			Maternal smoking in pregnancy alters neonatal cytokine responses	ALLERGY			English	Article						allergens; cord blood; cytokines; pregnancy; smoking	BLOOD MONONUCLEAR-CELLS; INTERFERON-GAMMA PRODUCTION; CORD-BLOOD; PARENTAL SMOKING; ALLERGIC SENSITIZATION; SERUM IGE; BRONCHIAL RESPONSIVENESS; SUBSEQUENT DEVELOPMENT; RESPIRATORY-FUNCTION; 9-YEAR-OLD CHILDREN	Background: Maternal cigarette smoking in pregnancy is an important, common and avoidable exposure that has been linked with elevated cord blood ( CB) immunoglobulin E levels and subsequent asthma and allergic disease in childhood. Despite this, there is still very little information about the immunological effects of maternal smoking on the fetus. Methods: This aim of this study was to compare cord blood mononuclear cell (CBMC) cytokine responses to allergens [ ovalbumin ( OVA) or house dust mite (HDM)] and mitogens [ concanavalin A ( ConA) or phytohemaglutinen (PHA)] in neonates whose mothers smoked throughout pregnancy ( n = 17) with responses of neonates whose mothers never smoked ( n = 40). Cell cultures were stimulated for 24 h and supernatants collected for cytokine detection by enzyme-linked immunosorbent assay [ interleukin (IL)-13, IL-6, interferon (IFN) gamma and IL-10]. Cell pellets were also collected for cytokine mRNA detection (IL-5, IL-9, IFNgamma). Results: Maternal smoking in pregnancy was associated with significantly higher neonatal T helper type 2 (IL-13 protein) responses to both HDM ( P = 0.01) and OVA ( P = 0.035). These effects remained statistically significant after allowing for confounding factors, including the effects of maternal atopy. Similar trends were also seen for IL-9mRNA, IL-5mRNA and IL-6 responses, although these were not statistically significant. Although IFNgamma mRNA responses to PHA ( P = 0.015) and ConA ( P = 0.025) were lower if mothers smoked in pregnancy, there were no differences in neonatal (Th1) IFNgamma protein responses to allergens or mitogens. Conclusions: These findings indicate that maternal cigarette smoking can modify aspects of fetal immune function and highlight the need for further studies in this area.	Univ Western Australia, Princess Margaret Hosp Children, Sch Paediat & Child Hlth, Perth, WA 6840, Australia; Telethon Inst Child Hlth Res, Div Cell Biol, Perth, WA, Australia	Prescott, SL (reprint author), Univ Western Australia, Princess Margaret Hosp Children, Sch Paediat & Child Hlth, GPO Box D184, Perth, WA 6840, Australia.		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J	Kips, JC; Anderson, GP; Fredberg, JJ; Herz, U; Inman, MD; Jordana, M; Kemeny, DM; Lotvall, J; Pauwels, RA; Plopper, CG; Schmidt, D; Sterk, PJ; Van Oosterhout, AJM; Vargaftig, BB; Chung, KF				Kips, JC; Anderson, GP; Fredberg, JJ; Herz, U; Inman, MD; Jordana, M; Kemeny, DM; Lotvall, J; Pauwels, RA; Plopper, CG; Schmidt, D; Sterk, PJ; Van Oosterhout, AJM; Vargaftig, BB; Chung, KF			Murine models of asthma	EUROPEAN RESPIRATORY JOURNAL			English	Article						airway reactivity; asthma; in vivo models; murine	AIRWAY SMOOTH-MUSCLE; CD4(+) T-CELLS; PASSIVE SENSITIZATION; IGE RESPONSES; ALLERGEN; MICE; RESPONSIVENESS; EXPOSURE; MOUSE; INFLAMMATION	In vivo animal models can offer valuable information on several aspects of asthma pathogenesis and treatment. The mouse is increasingly used in these models, mainly because this species allows for the application in vivo of a broad range of immunological tools, including gene deletion technology. Mice, therefore, seem particularly useful to further elucidate factors influencing the response to inhaled allergens. Examples include: the role of immunoregulatory mechanisms that protect against T-helper cell type 2 cell development; the trafficking of T-cells; and the contribution of the innate immunity. However, as for other animal species, murine models also have limitations. Mice do not spontaneously develop asthma and no model mimics the entire asthma phenotype. Instead, mice should be used to model specific traits of the human disease. The present task force report draws attention to specific aspects of lung structure and function that need to be borne in mind when developing such models and interpreting the results. In particular, efforts should be made to develop models that mimic the lung function changes characteristic of asthma as closely as possible. A large section of this report is therefore devoted to an overview of airway function and its measurement in mice.	State Univ Ghent Hosp, Dept Med Genet, B-9000 Ghent, Belgium	Kips, JC (reprint author), State Univ Ghent Hosp, Dept Med Genet, De Pintelaan 185, B-9000 Ghent, Belgium.		Vargaftig, Bernardo Boris/C-3323-2013	Lotvall, Jan/0000-0001-9195-9249; Chung, Kian Fan/0000-0001-7101-1426			Akbari O, 2002, NAT MED, V8, P1024, DOI 10.1038/nm745; Blyth DI, 2000, AM J RESP CELL MOL, V23, P241; BRUSASCO V, 1989, J APPL PHYSIOL, V66, P1190; Drazen JM, 1999, ANNU REV PHYSIOL, V61, P593, DOI 10.1146/annurev.physiol.61.1.593; Duez C, 2000, AM J RESP CRIT CARE, V161, P200; Duguet A, 2000, AM J RESP CRIT CARE, V161, P839; Evans MJ, 1999, AM J RESP CELL MOL, V21, P655; Fredberg JJ, 1997, AM J RESP CRIT CARE, V156, P1752; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Goldmann WH, 1998, EXP CELL RES, V239, P235, DOI 10.1006/excr.1997.3915; Hamelmann E, 1997, AM J RESP CRIT CARE, V156, P766; Held HD, 1999, BRIT J PHARMACOL, V126, P1191, DOI 10.1038/sj.bjp.0702394; Herz U, 1999, EUR J IMMUNOL, V29, P1021, DOI 10.1002/(SICI)1521-4141(199903)29:03<1021::AID-IMMU1021>3.0.CO;2-3; Hofstra CL, 1998, J IMMUNOL, V161, P5054; Holmes BJ, 1997, EUR J IMMUNOL, V27, P2657, DOI 10.1002/eji.1830271027; HOLT PG, 1981, IMMUNOLOGY, V42, P409; in 't Veen Johannes C. 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Resp. J.	AUG	2003	22	2					374	382		10.1183/09031936.03.00026403		9	Respiratory System	Respiratory System	713NU	WOS:000184865400033	12952276	
J	Werler, MM; Sheehan, JE; Mitchell, AA				Werler, MM; Sheehan, JE; Mitchell, AA			Maternal medication use and risks of gastroschisis and small intestinal atresia	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						gastroschisis; intestinal atresia; medicine; pregnancy	VASCULAR DISRUPTION; EXPOSURE; DEFECTS	Gastroschisis and small intestinal atresia (SIA) are birth defects that are thought to arise from vascular disruption of fetal mesenteric vessels. Previous studies of gastroschisis have suggested that risk is increased for maternal use of vasoactive over-the-counter medications, including specific analgesics and decongestants. This retrospective study evaluated the relation between maternal use of cough/cold/analgesic medications and risks of gastroschisis and SIA. From 1995 to 1999, the mothers of 206 gastroschisis cases, 126 SIA cases, and 798 controls in the United States and Canada were interviewed about medication use and illnesses. Risks of gastroschisis were elevated for use of aspirin (odds ratio = 2.7, 95% confidence interval: 1.2, 5.9), pseudoephedrine (odds ratio = 1.8, 95% confidence interval: 1.0, 3.2), acetaminophen (odds ratio = 1.5, 95% confidence interval: 1.1, 2.2), and pseudoephedrine combined with acetaminophen (odds ratio = 4.2, 95% confidence interval: 1.9, 9.2). Risks of SIA were increased for any use of pseudoephedrine (odds ratio = 2.0, 95% confidence interval: 1.0, 4.0) and for use of pseudoephedrine in combination with acetaminophen (odds ratio = 3.0, 95% confidence interval: 1.1, 8.0). Reported fever, upper respiratory infection, and allergy were not associated with risks of either defect. These findings add more evidence that aspirin use in early pregnancy increases risk of gastroschisis. Although pseudoephedrine has previously been shown to increase gastroschisis risk, findings of this study raise questions about interactions between medications and possible confounding by underlying illness.	Boston Univ, Sch Publ Hlth, Slone Epidemiol Unit, Brookline, MA 02446 USA	Werler, MM (reprint author), Boston Univ, Sch Publ Hlth, Slone Epidemiol Unit, 1371 Beacon St, Brookline, MA 02446 USA.						DRONGOWSKI R A, 1991, Fetal Diagnosis and Therapy, V6, P14; GOLDBAUM G, 1990, TERATOLOGY, V42, P397, DOI 10.1002/tera.1420420408; GOODMAN GA, 1996, PHRM BASIS THERAPEUT; HOYME HE, 1990, PEDIATRICS, V85, P743; HOYME HE, 1981, J PEDIATR-US, V98, P228, DOI 10.1016/S0022-3476(81)80640-3; LOUW JH, 1955, LANCET, V2, P1065; Lynberg M, 1992, TERATOLOGY, V45, P453; MARTIN ML, 1992, TERATOLOGY, V45, P647, DOI 10.1002/tera.1420450609; MartinezFrias ML, 1997, TERATOLOGY, V56, P241, DOI 10.1002/(SICI)1096-9926(199710)56:4<241::AID-TERA2>3.0.CO;2-1; Penman DG, 1998, BRIT J OBSTET GYNAEC, V105, P328, DOI 10.1111/j.1471-0528.1998.tb10095.x; Szabo KT, 1989, CONGENITAL MALFORMAT; Torfs CP, 1996, TERATOLOGY, V54, P84, DOI 10.1002/(SICI)1096-9926(199606)54:2<84::AID-TERA4>3.0.CO;2-4; VANALLEN MI, 1981, PEDIATR ANN, V10, P219; WERLER MM, 1992, TERATOLOGY, V45, P361, DOI 10.1002/tera.1420450407	14	128	136	1	9	OXFORD UNIV PRESS INC	CARY	JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA	0002-9262			AM J EPIDEMIOL	Am. J. Epidemiol.	JAN 1	2002	155	1					26	31		10.1093/aje/155.1.26		6	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	509GC	WOS:000173137100005	11772781	
J	von Berg, A; Filipiak-Pittroff, B; Kraemer, U; Link, E; Bollrath, C; Brockow, I; Koletzko, S; Armin, G; Heinrich, J; Wichmann, HE; Bauer, CP; Reinhardt, D; Berdel, D				von Berg, Andrea; Filipiak-Pittroff, Birgit; Kraemer, Ursula; Link, Elke; Bollrath, Christina; Brockow, Inken; Koletzko, Sibylle; Gruebl, Armin; Heinrich, Joachim; Wichmann, H. -Erich; Bauer, Carl-P.; Reinhardt, Dietrich; Berdel, Dietrich		GINIplus study grp	Preventive effect of hydrolyzed infant formulas persists until age 6 years: Long-term results from the German Infant Nutritional Intervention Study (GINI)	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						birth cohort; long-term allergy prevention; hydrolysates; double-blind randomized trial	FOOD-ALLERGEN AVOIDANCE; DIETARY PREVENTION; CHILDHOOD ASTHMA; SMALL CHILDREN; RECOMMENDATIONS; DISEASE; ATOPY; PROPHYLAXIS; COMMITTEE; EXPOSURE	Background: The long-term effect of nutritional intervention with hydrolyzed infant formulas on allergy development has not been sufficiently evaluated. Objective: We performed a follow-up of the German Infant Nutritional Intervention study until 6 years of life to investigate the long-term allergy-preventive effect of 3 hydrolyzed infant formulas compared with cow's milk formula (CMF) in a randomized, double-blind trial. Methods: Between 1995 and 1998, 2252 newborns with atopic heredity were randomly assigned at birth to receive one of 4 blinded formulas: partially or extensively hydrolyzed whey formula, extensively hydrolyzed casein formula, or CMF as milk substitute for the first 4 months when breast-feeding was insufficient. The cohort was followed from birth until 6 years of age with yearly questionnaires. Outcomes were physician-diagnosed allergic diseases (atopic dermatitis, food allergy, allergic urticaria, asthma, and hay fever/allergic rhinitis). Log-binomial regression modeled with generalized estimation equations was used for the statistical analysis. Results: In the intent-to-treat analysis the relative risk of a physician's diagnosis of allergic manifestation (AM) compared with CMF was 0.82 (95% CI, 0.70-0.96) for partially hydrolyzed whey formula, 0.90 (95% CI, 0.78-1.04) for extensively hydrolyzed whey formula, and 0.80 (95% CI, 0.69-0.93) for extensively hydrolyzed casein formula. The corresponding figures for atopic eczema were 0.79 (95% CI, 0.64-0.97), 0.92 (95% CI, 0.76-1.11), and 0.71 (95% CI, 0.58-0.88), respectively. In the per-protocol analysis all effects were stronger and significant. No significant effect on other AMs was found. Conclusion: The data confirm a long-term allergy-preventive effect of hydrolyzed infant formulas on AM and atopic eczema until 6 years of age.	[von Berg, Andrea; Filipiak-Pittroff, Birgit; Bollrath, Christina; Berdel, Dietrich] Marien Hosp, Dept Pediat, Wesel, Germany; [Kraemer, Ursula; Link, Elke] Univ Dusseldorf, Inst Umweltmed Forschung, Dusseldorf, Germany; [Brockow, Inken; Heinrich, Joachim; Wichmann, H. -Erich] German Res Ctr Environm Hlth GmbH, Helmholtz Zentrum Munchen, Inst Epidemiol, Neuherberg, Germany; [Koletzko, Sibylle; Reinhardt, Dietrich] Univ Munich, Dr Von Haunerschen Kinderspital, D-80337 Munich, Germany; [Brockow, Inken; Gruebl, Armin; Bauer, Carl-P.] Tech Univ Munich, Dept Pediat, D-8000 Munich, Germany; [Bauer, Carl-P.] LVA Oberbayern, Munich, Germany; [Wichmann, H. -Erich] Univ Munich, Inst Med Data Management Biometr & Epidemiol, Munich, Germany	von Berg, A (reprint author), Marien Hosp, Dept Pediat, Pastor Janssen Str 8-38, Wesel, Germany.	vonberg@marien-hospital-wesel.de					American Academy of Pediatrics Committee on Nutrition, 2000, PEDIATRICS, V106, P236; Arshad SH, 2007, J ALLERGY CLIN IMMUN, V119, P307, DOI 10.1016/j.jaci.2006.12.621; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Brand PLP, 2007, PEDIAT ALLERG IMM-UK, V18, P475, DOI 10.1111/j.1399-3038.200700541.x; Chan-Yeung M, 2005, J ALLERGY CLIN IMMUN, V116, P49, DOI 10.1016/j.jaci.2005.03.029; Diggle P, 2002, ANAL LONGITUDINAL DA; Filipiak B, 2007, J PEDIATR-US, V151, P352, DOI 10.1016/j.jpeds.2007.05.01; Halken S, 2000, PEDIATR ALLERGY IMMU, V11, P149, DOI 10.1034/j.1399-3038.2000.00081.x; Hays T, 2005, ARCH PEDIAT ADOL MED, V159, P810, DOI 10.1001/archpedi.159.9.810; Holt PG, 2005, J ALLERGY CLIN IMMUN, V116, P16, DOI 10.1016/j.jaci.2005.04.017; Host A, 1999, ARCH DIS CHILD, V81, P80; Johansson SGO, 2004, J ALLERGY CLIN IMMUN, V113, P832, DOI 10.1016/j.jaci.2003.12.591; Kleinbaum DG, 1982, EPIDEMIOLOGIC RES PR; KUEHR J, 1994, J ALLERGY CLIN IMMUN, V94, P44, DOI 10.1016/0091-6749(94)90070-1; Muraro A, 2004, PEDIATR ALLERGY IMMU, V15, P103, DOI 10.1046/j.1399-3038.2003.00129.x; Muraro A, 2004, PEDIATR ALLERGY IMMU, V15, P291, DOI 10.1111/j.1399-3038.2004.00127.x; Oldaeus G, 1997, ARCH DIS CHILD, V77, P4; Osborn D. A., 2003, COCHRANE DB SYST REV, DOI DOI 10.1002/14651858.CD003664; Schoetzau A, 2002, ARCH DIS CHILD, V86, P180, DOI 10.1136/adc.86.3.180; Schoetzau A, 2001, EUR J PEDIATR, V160, P323, DOI 10.1007/PL00008442; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; van Schayck OCP, 2007, J ALLERGY CLIN IMMUN, V119, P1323, DOI 10.1016/j.jaci.2007.02.024; VANDENPLAS Y, 1995, EUR J PEDIATR, V154, P488, DOI 10.1007/s004310050330; von Berg A, 2003, J ALLERGY CLIN IMMUN, V111, P533, DOI 10.1067/mai.2003.101; von Berg A, 2007, J ALLERGY CLIN IMMUN, V119, P718, DOI 10.1016/j.jaci.2006.11.017; Wahn U, 2001, J ALLERGY CLIN IMMUN, V107, P567, DOI 10.1067/mai.2001.112943; Zeiger RS, 2003, PEDIATRICS, V111, P1662; ZEIGER RS, 1989, J ALLERGY CLIN IMMUN, V84, P72, DOI 10.1016/0091-6749(89)90181-4	28	127	135	0	11	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUN	2008	121	6					1442	1447		10.1016/j.jaci.2008.04.021		6	Allergy; Immunology	Allergy; Immunology	313WW	WOS:000256771700021	18539195	
J	Chen, E; Miller, GE				Chen, Edith; Miller, Gregory E.			Stress and inflammation in exacerbations of asthma	BRAIN BEHAVIOR AND IMMUNITY			English	Review						stress; asthma; cytokines; glucocorticoids; autonomic nervous system	PSYCHOLOGICAL STRESS; CHILDHOOD ASTHMA; SOCIOECONOMIC-STATUS; CYTOKINE PROFILES; COMMON COLD; EXPRESSION; CHILDREN; ATOPY; SUSCEPTIBILITY; ADOLESCENTS	In this mini-review, we outline a model depicting the immunologic mechanisms by which psychological stress can exacerbate clinical symptoms in patients with asthma. This model highlights the importance of both social and physical exposures in the exacerbation of asthma symptoms. The basic premise of the model is that psychological stress operates by altering the magnitude of the airway inflammatory response that irritants, allergens, and infections bring about in persons with asthma. The biological pathways for how stress amplifies the immune response to asthma triggers include the hypothalamic-pituitary-adrenal (HPA) axis, the sympathetic-adrenal-medullary (SAM) axis, and the sympathetic (SNS) and parasympathetic (PNS) arms of the autonomic nervous system. Empirical evidence for this model is reviewed, and conclusions and future research directions are discussed. (C) 2007 Elsevier Inc. All rights reserved.	Univ British Columbia, Dept Psychol, Vancouver, BC V6T 1Z4, Canada	Chen, E (reprint author), Univ British Columbia, Dept Psychol, 2136 W Mall, Vancouver, BC V6T 1Z4, Canada.	echen@psych.ubc.ca	Osborne, Nicholas/N-4915-2015; Vollrath, Margarete/G-1297-2011	Osborne, Nicholas/0000-0002-6700-2284; 	NHLBI NIH HHS [HL073975, R01 HL073975, R01 HL073975-01A2, R01 HL073975-02, R01 HL073975-03]		Andrulis DP, 1998, ANN INTERN MED, V129, P412; Busse WW, 2001, NEW ENGL J MED, V344, P350; Chen E, 2006, J ALLERGY CLIN IMMUN, V117, P1014, DOI 10.1016/j.jaci.2006.01.036; Chen E, 2003, PSYCHOSOM MED, V65, P984, DOI 10.1097/01.PSY.0000097340.54195.3C; Cohen S, 1999, PSYCHOSOM MED, V61, P175; COHEN S, 1991, NEW ENGL J MED, V325, P606, DOI 10.1056/NEJM199108293250903; Cohen S, 1998, HEALTH PSYCHOL, V17, P214, DOI 10.1037//0278-6133.17.3.214; Cohen S, 1995, MEASURING STRESS GUI, P3; Dickerson SS, 2004, PSYCHOL BULL, V130, P355, DOI 10.1037/0033-2909.130.3.355; Holtzman MJ, 2002, PHYSIOL REV, V82, P19; Jaakkola JJK, 2001, ENVIRON HEALTH PERSP, V109, P579, DOI 10.2307/3455031; Kang DH, 2001, RES NURS HEALTH, V24, P245, DOI 10.1002/nur.1027; Kang DH, 1997, J INTERF CYTOK RES, V17, P481, DOI 10.1089/jir.1997.17.481; LAZARUS RS, 1984, STRES APPRAISAL COPI; LEHRER PM, 1993, J ASTHMA, V30, P5, DOI 10.3109/02770909309066375; Liu LY, 2002, AM J RESP CRIT CARE, V165, P1062, DOI 10.1164/rccm.2109065; Marshall GD, 2000, ALLERGY ASTHMA PROC, V21, P241, DOI 10.2500/108854100778248917; MILLER BD, 1994, J AM ACAD CHILD PSY, V33, P1236, DOI 10.1097/00004583-199411000-00004; Miller GE, 2006, P NATL ACAD SCI USA, V103, P5496, DOI 10.1073/pnas.0506312103; Miller GE, 2002, HEALTH PSYCHOL, V21, P531, DOI 10.1037//0278-6133.21.6.531; Miller GE, 2007, PSYCHOL BULL, V133, P25, DOI 10.1037/0033-2909.133.1.25; Nelson HS, 1999, J ALLERGY CLIN IMMUN, V104, P775; Ober C, 2006, GENES IMMUN, V7, P95, DOI 10.1038/sj.gene.6364284; Sandberg S, 2000, LANCET, V356, P982, DOI 10.1016/S0140-6736(00)02715-X; Segerstrom SC, 2004, PSYCHOL BULL, V130, P601, DOI 10.1037/0033-2909.130.4.601; Sigurs N, 2005, AM J RESP CRIT CARE, V171, P137, DOI 10.1164/rccm.200406-730OC; Smith A, 2001, PSYCHONEUROENDOCRINO, V26, P411, DOI 10.1016/S0306-4530(00)00063-9; Wright RJ, 2005, CURR OPIN ALLERGY CL, V5, P23, DOI 10.1097/00130832-200502000-00006; Wright RJ, 1998, THORAX, V53, P1066; Wright RJ, 2004, J ALLERGY CLIN IMMUN, V113, P1051, DOI 10.1016/j.jaci.2004.03.032; WRIGHT RJ, 2005, J ALLERGY CLIN IMMUN, V116, P130	31	127	132	4	14	ACADEMIC PRESS INC ELSEVIER SCIENCE	SAN DIEGO	525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA	0889-1591			BRAIN BEHAV IMMUN	Brain Behav. Immun.	NOV	2007	21	8					993	999		10.1016/j.bbi.2007.03.009		7	Immunology; Neurosciences	Immunology; Neurosciences & Neurology	227NV	WOS:000250664300001	17493786	
J	Strickland, DH; Stumbles, PA; Zosky, GR; Subrata, LS; Thomas, JA; Turner, DJ; Sly, PD; Holt, PG				Strickland, Deborah H.; Stumbles, Philip A.; Zosky, Graeme R.; Subrata, Lily S.; Thomas, Jenny A.; Turner, Debra J.; Sly, Peter D.; Holt, Patrick G.			Reversal of airway hyperresponsiveness by induction of airway mucosal CD4(+) CD25(+) regulatory T cells	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article							DENDRITIC CELLS; INHALED ANTIGEN; RESPIRATORY-TRACT; ASTHMATIC REACTIONS; IGE RESPONSES; IN-VIVO; ALLERGEN; HYPERREACTIVITY; INFLAMMATION; SUPPRESSION	An important feature of atopic asthma is the T cell-driven late phase reaction involving transient bronchoconstriction followed by development of airways hyperresponsiveness (AHR). Using a unique rat asthma model we recently showed that the onset and duration of the aeroallergen-induced airway mucosal T cell activation response in sensitized rats is determined by the kinetics of functional maturation of resident airway mucosal dendritic cells (AMDCs) mediated by cognate interactions with CD4(+) T helper memory cells. The study below extends these investigations to chronic aeroallergen exposure. We demonstrate that prevention of ensuing cycles of T cell activation and resultant AHR during chronic exposure of sensitized rats to allergen aerosols is mediated by CD4(+) CD25(+) Foxp3(+) LAG3(+) CTLA(+) CD45RC(+) T cells which appear in the airway mucosa and regional lymph nodes within 24 h of initiation of exposure, and inhibit subsequent Th-mediated upregulation of AMDC functions. These cells exhibit potent regulatory T (T reg) cell activity in both in vivo and ex vivo assay systems. The maintenance of protective T reg activity is absolutely dependent on continuing allergen stimulation, as interruption of exposure leads to waning of T reg activity and reemergence of sensitivity to aeroallergen exposure manifesting as AMDC/T cell upregulation and resurgence of T helper 2 cytokine expression, airways eosinophilia, and AHR.	Univ Western Australia, Telethon Inst Child Hlth, Fac Med & Dent, Perth, WA 6008, Australia; Univ Western Australia, Ctr Child Hlth Res, Fac Med & Dent, Perth, WA 6008, Australia	Holt, PG (reprint author), Univ Western Australia, Telethon Inst Child Hlth, Fac Med & Dent, Perth, WA 6008, Australia.	patrick@ichr.uwa.edu.au	Sly, Peter/F-1486-2010; Holt, Patrick/H-1548-2011; Zosky, Graeme/B-2048-2014	Sly, Peter/0000-0001-6305-2201; Holt, Patrick/0000-0003-1193-0935; Zosky, Graeme/0000-0001-9039-0302			Akbari O, 2002, NAT MED, V8, P1024, DOI 10.1038/nm745; Akdis M, 2004, J EXP MED, V199, P1567, DOI 10.1084/jem.20032058; Busse WW, 2001, NEW ENGL J MED, V344, P350; Cederbom L, 2000, EUR J IMMUNOL, V30, P1538, DOI 10.1002/1521-4141(200006)30:6<1538::AID-IMMU1538>3.0.CO;2-X; de Heer HJ, 2004, J EXP MED, V200, P89, DOI 10.1084/jem.20040035; Haselden BM, 1999, J EXP MED, V189, P1885, DOI 10.1084/jem.189.12.1885; Hawrylowicz CM, 2005, NAT REV IMMUNOL, V5, P271, DOI 10.1038/nri1589; HOLT PG, 1989, CLIN EXP ALLERGY, V19, P597, DOI 10.1111/j.1365-2222.1989.tb02752.x; HOLT PG, 1981, IMMUNOLOGY, V42, P409; Huang CT, 2004, IMMUNITY, V21, P503, DOI 10.1016/j.immuni.2004.08.010; Huh JC, 2003, J EXP MED, V198, P19, DOI 10.1084/jem.20021328; Karagiannidis C, 2004, J ALLERGY CLIN IMMUN, V114, P1425, DOI 10.1016/j.jaci.2004.07.014; Kearley J, 2005, J EXP MED, V202, P1539, DOI 10.1084/jem.20051166; Lewkowich IP, 2005, J EXP MED, V202, P1549, DOI 10.1084/jem.20051506; Mannie MD, 2004, CELL IMMUNOL, V230, P33, DOI 10.1016/j.cellimm.2004.08.005; MCMENAMIN C, 1994, SCIENCE, V265, P1869, DOI 10.1126/science.7916481; MCMENAMIN C, 1993, J EXP MED, V178, P889, DOI 10.1084/jem.178.3.889; McWilliam AS, 1996, J EXP MED, V184, P2429, DOI 10.1084/jem.184.6.2429; Ostroukhova M, 2004, J CLIN INVEST, V114, P28, DOI 10.1172/JC1200420509; Petak F, 1997, J APPL PHYSIOL, V82, P1479; PLATTSMILLS TAE, 1995, PROGR ALLERGY CLIN I, P90; Read S, 2000, J EXP MED, V192, P295, DOI 10.1084/jem.192.2.295; SCHONHEGRAD MA, 1991, J EXP MED, V173, P1345, DOI 10.1084/jem.173.6.1345; Stock P, 2004, NAT IMMUNOL, V5, P1149, DOI 10.1038/ni1122; Stumbles PA, 1998, J EXP MED, V188, P2019, DOI 10.1084/jem.188.11.2019; Tadokoro CE, 2006, J EXP MED, V203, P505, DOI 10.1084/jem.20050783; Tang QJY, 2005, NAT IMMUNOL, V7, P83; Umetsu DT, 2003, J ALLERGY CLIN IMMUN, V112, P480, DOI 10.1067/mai.2003.1717; Van Rijt LS, 2005, CLIN EXP ALLERGY, V35, P1125, DOI 10.1111/j.1365-2222.2005.02321.x; vanHalteren AG, 1997, J IMMUNOL, V159, P3009; von Garnier C, 2005, J IMMUNOL, V175, P1609; Wilson MS, 2005, J EXP MED, V202, P1199, DOI 10.1084/jem.20042572; Woolcock AJ, 1995, ALLERGY, V50, P935, DOI 10.1111/j.1398-9995.1995.tb02504.x; Zuany-Amorim C, 2002, NAT MED, V8, P625, DOI 10.1038/nm0602-625	34	127	140	0	6	ROCKEFELLER UNIV PRESS	NEW YORK	1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA	0022-1007			J EXP MED	J. Exp. Med.	NOV 27	2006	203	12					2649	2660		10.1084/jem.20060155		12	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	109WG	WOS:000242339700008	17088431	
J	Wagers, S; Lundblad, LKA; Ekman, M; Irvin, CG; Bates, JHT				Wagers, S; Lundblad, LKA; Ekman, M; Irvin, CG; Bates, JHT			The allergic mouse model of asthma: normal smooth muscle in an abnormal lung?	JOURNAL OF APPLIED PHYSIOLOGY			English	Article						inflammation; lung impedance; resistance; elastance; mucosal thickening	RESPIRATORY SYSTEM MECHANICS; ACUTE PULMONARY RESPONSE; INTRAVENOUS HISTAMINE; FORCED-OSCILLATIONS; AIRWAY-CLOSURE; VENTILATION DISTRIBUTION; FREQUENCY-DEPENDENCE; ASYMPTOMATIC ASTHMA; TEMPORAL DYNAMICS; TISSUE MECHANICS	Mice with allergically inflamed airways are widely used as animal models of asthma, but their relevance for human asthma is not understood. We, therefore, examined the time course of changes in respiratory input impedance during induced bronchoconstriction in BALB/c mice sensitized and challenged with ovalbumin. Our results indicate that bronchoconstriction in mice is accompanied by complete closure of substantial regions of the lung and that closure increases markedly when the lungs are allergically inflamed. With the aid of an anatomically accurate computational model of the mouse lung, we show that the hyperresponsiveness of mice with allergically inflamed airways can be explained entirely by a thickening of the airway mucosa and an increased propensity of the airways to close, without the involvement of any increase in the degree of airway smooth muscle shortening. This has implications for the pathophysiology of asthma and suggests that at least some types of asthma may benefit from therapies aimed at manipulating surface tension at the air-liquid interface in the lungs.	Univ Vermont, Dept Med, Vermont Lung Ctr, Burlington, VT 05405 USA; Lund Univ, Dept Physiol Sci, SE-22184 Lund, Sweden	Bates, JHT (reprint author), HSRF 228,149 Beaumont Ave, Burlington, VT 05405 USA.	jason.h.bates@uvm.edu			NCRR NIH HHS [P20 RR-15557]; NHLBI NIH HHS [R01 HL-67273]		BALASSY Z, 1995, J APPL PHYSIOL, V78, P875; BATES JHT, 1993, J APPL PHYSIOL, V75, P405; BATES JHT, 1990, J APPL PHYSIOL, V69, P995; BATES JHT, 1994, J APPL PHYSIOL, V76, P616; Bates JHT, 1997, J APPL PHYSIOL, V82, P55; Black LD, 2003, J APPL PHYSIOL, V95, P511, DOI 10.1152/japplphysiol.01114.2002; Brusasco V, 2003, J APPL PHYSIOL, V95, P1305, DOI 10.1152/japplphysiol.00001.2003; CHEN B, 2003, AM J RESP CRIT CARE, V167, pA882; Evans KLJ, 2003, J APPL PHYSIOL, V94, P245, DOI 10.1152/japplphysiol.00593.2002; Fredberg JJ, 1997, AM J RESP CRIT CARE, V156, P1752; Fredberg JJ, 1996, J APPL PHYSIOL, V81, P2703; FREDBERG JJ, 1993, J APPL PHYSIOL, V74, P1387; GAVER DP, 1990, J APPL PHYSIOL, V69, P74; Gillis HL, 1999, ANN BIOMED ENG, V27, P14, DOI 10.1114/1.161; Gillis HL, 1999, J APPL PHYSIOL, V86, P2001; Gomes RFM, 2000, J APPL PHYSIOL, V89, P908; Gomes RFM, 2002, RESP PHYSIOL NEUROBI, V130, P317, DOI 10.1016/S0034-5687(02)00017-8; Gunst SJ, 2001, J APPL PHYSIOL, V90, P741; Hamelmann E, 1999, AM J RESP CELL MOL, V21, P480; HANTOS Z, 1992, J APPL PHYSIOL, V72, P168; HORSFIELD K, 1982, J APPL PHYSIOL, V52, P21; Jensen A, 2001, J APPL PHYSIOL, V91, P506; KAMINSKY DA, 1995, AM J RESP CRIT CARE, V152, P1784; Kaminsky DA, 2003, CHEST, V123, p363S, DOI 10.1378/chest.123.3_suppl.363S; Kaminsky DA, 2000, AM J RESP CRIT CARE, V162, P179; King GG, 1998, AM J RESP CRIT CARE, V158, P1900; Kraft M, 2001, AM J RESP CRIT CARE, V163, P1551; Kumar RK, 2002, AM J RESP CELL MOL, V27, P267, DOI 10.1165/rcmb.F248; Lauzon AM, 2000, J APPL PHYSIOL, V89, P2023; Leigh R, 2002, AM J RESP CELL MOL, V27, P526, DOI 10.1165/rcmb.2002-0048OC; LUDWIG MS, 1994, J APPL PHYSIOL, V77, P2029; Lundblad LKA, 2002, J APPL PHYSIOL, V93, P1198, DOI 10.1152/japplphysiol.00080.2002; Lutchen KR, 1996, J APPL PHYSIOL, V80, P1841; Lutchen KR, 1996, J APPL PHYSIOL, V80, P1696; Lutchen KR, 1997, J APPL PHYSIOL, V83, P1192; Macklem PT, 1996, AM J RESP CRIT CARE, V153, P83; MACKLEM PT, 1987, CHEST, V91, pS189, DOI 10.1378/chest.91.6.189S; MCCARTHY D, 1973, AM REV RESPIR DIS, V107, P559; MISHIMA M, 1994, J APPL PHYSIOL, V77, P2140; MORENO RH, 1986, AM REV RESPIR DIS, V133, P1171; MORENO RH, 1993, J APPL PHYSIOL, V75, P738; NAURECKAS ET, 1994, J APPL PHYSIOL, V76, P1372; OKAZAWA M, 1995, J APPL PHYSIOL, V78, P608; OTIS DR, 1993, J APPL PHYSIOL, V75, P1323; PERUN ML, 1995, J APPL PHYSIOL, V79, P1717; Petak F, 1997, J APPL PHYSIOL, V82, P1479; Samee S, 2003, J ALLERGY CLIN IMMUN, V111, P1205, DOI 10.1067/mai.2003.1544; SIEGLER D, 1976, AM REV RESPIR DIS, V114, P123; SIMILOWSKI T, 1991, EUR RESPIR J, V4, P353; Thorpe CW, 1997, J APPL PHYSIOL, V82, P1616; Tomioka S, 2002, J APPL PHYSIOL, V93, P263, DOI 10.1152/japplphysiol.01129.2001; WIGGS BR, 1990, J APPL PHYSIOL, V69, P849	52	127	131	0	5	AMER PHYSIOLOGICAL SOC	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	8750-7587			J APPL PHYSIOL	J. Appl. Physiol.	JUN	2004	96	6					2019	2027		10.1152/japplphysiol.00924.2003		9	Physiology; Sport Sciences	Physiology; Sport Sciences	819EJ	WOS:000221296600002	14660507	
J	Mapp, CE; Fryer, AA; De Marzo, N; Pozzato, V; Padoan, M; Boschetto, P; Strange, RC; Hemmingsen, A; Spiteri, MA				Mapp, CE; Fryer, AA; De Marzo, N; Pozzato, V; Padoan, M; Boschetto, P; Strange, RC; Hemmingsen, A; Spiteri, MA			Glutathione S-transferase GSTP1 is a susceptibility gene for occupational asthma induced by isocyanates	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						isocyanates; occupational asthma; airway hyperresponsiveness; genetic markers	TOLUENE DIISOCYANATE TDI; SENSITIZED SUBJECTS; OXIDATIVE STRESS; INFLAMMATION; ASSOCIATION; HYPERRESPONSIVENESS; IDENTIFICATION; LOCALIZATION; POLYMORPHISM; RESPONSES	Background: Polymorphism at the pi class glutathione-S-transferase locus (GSTP1) is associated with allergen-induced asthma and related phenotypes. Objective: We sought to determine whether GSTP1 polymorphism influences susceptibility to asthma induced by toluene diisocyanate (TDI). Methods: The role of GSTP1 was assessed in 131 workers exposed to TDI, 92 with TDI-induced asthma and 39 asymptomatic subjects. The phenotype of the disease was characterized by using detailed clinical history, lung volumes, airway responsiveness to methacholine, and airway responsiveness to TDI. GST genotypes were determined by using PCR-based assays. Results: In patients exposed to TDI for 10 or more years, the frequency of the GSTP1 Val/Val genotype was lower in subjects who had asthma (odds ratio, 0.23; 95% confidence interval, 0.05-1.13; P = .074). Similarly, the frequency of this genotype was significantly lower in subjects with evidence of moderate-to-severe airway hyperresponsiveness to methacholine compared with the frequency in subjects with normal or mild hyperresponsiveness (P = .033). Conclusion: These data suggest that homozygosity for the GSTP1*Val allele confers protection against TDI-induced asthma and airway hyperresponsiveness. This view is supported by the finding that the protective effect increases in proportion to the duration of exposure to TDI.	Univ Ferrara, Dept Clin & Expt Med, Sect Occupat Med, I-44100 Ferrara, Italy; N Staffordshire Hosp Trust, Stoke On Trent, Staffs, England; Keele Univ, Stoke On Trent, Staffs, England; Univ Padua, Dept Environm Med & Publ Hlth, Sect Occupat Med, Padua, Italy	Mapp, CE (reprint author), Dipartimento Med Clin & Sperimentale, Sez Igiene & Med Lavoro, Via Fossato Mortara 64-B, I-44100 Ferrara, Italy.			Fryer, Anthony/0000-0001-8678-0404			ANTTILA S, 1993, CANCER RES, V53, P5643; BARNES PJ, 1990, FREE RADICAL BIO MED, V9, P235, DOI 10.1016/0891-5849(90)90034-G; BIGNON JS, 1994, AM J RESP CRIT CARE, V149, P71; BOARD PG, 1989, ANN HUM GENET, V53, P205, DOI 10.1111/j.1469-1809.1989.tb01786.x; CHANYEUNG M, 1994, EUR RESPIR J, V7, P346, DOI 10.1183/09031936.94.07020346; *COMM COMM EUR, 1971, TABL REF EX SPIR; Fryer AA, 2000, AM J RESP CRIT CARE, V161, P1437; Harries LW, 1997, CARCINOGENESIS, V18, P641, DOI 10.1093/carcin/18.4.641; HAYES JD, 1995, FREE RADICAL RES, V22, P193, DOI 10.3109/10715769509147539; Hemmingsen A, 2001, RESPIR RES, V2, P250; KLEINBAUM DG, 1982, EPIDEMIOLOGIC RES PR, P438; MAESTRELLI P, 1994, CLIN EXP ALLERGY, V24, P29, DOI 10.1111/j.1365-2222.1994.tb00913.x; MALO JL, 1992, J ALLERGY CLIN IMMUN, V90, P937, DOI 10.1016/0091-6749(92)90466-F; MAPP CE, 1986, EUR J RESPIR DIS, V69, P276; Mapp CE, 1997, AM J RESP CRIT CARE, V156, pS139; Mapp CE, 2000, CLIN EXP ALLERGY, V30, P651; MAPP CE, 1988, EUR RESPIR J, V1, P273; MAPP CE, 1988, AM REV RESPIR DIS, V137, P1326; MAPP CE, 1985, J ALLERGY CLIN IMMUN, V75, P568, DOI 10.1016/0091-6749(85)90031-4; MAPP CE, 1999, EUROPEAN RESP MONOGR, V11, P255; Mattey DL, 1999, ANN RHEUM DIS, V58, P164, DOI 10.1136/ard.58.3.164; Piirila P, 2001, PHARMACOGENETICS, V11, P437, DOI 10.1097/00008571-200107000-00007; Postma DS, 2000, AM J RESP CRIT CARE, V162, pS118; Rahman I, 2000, EUR RESPIR J, V16, P534, DOI 10.1034/j.1399-3003.2000.016003534.x; ROWE D, 1997, BIOCHEM J, V235, P481; SAETTA M, 1992, AM REV RESPIR DIS, V145, P160; SAETTA M, 1992, AM REV RESPIR DIS, V145, P169; Spiteri MA, 2000, ALLERGY, V55, P15, DOI 10.1034/j.1398-9995.2000.00502.x; ZOCCA E, 1990, J APPL PHYSIOL, V68, P1576	29	127	133	0	1	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	MAY	2002	109	5					867	872		10.1067/mai.2002.123234		6	Allergy; Immunology	Allergy; Immunology	553QW	WOS:000175687800019	11994713	
J	von Mutius, E; Pearce, N; Beasley, R; Cheng, S; von Ehrenstein, O; Bjorksten, B; Weiland, S				von Mutius, E; Pearce, N; Beasley, R; Cheng, S; von Ehrenstein, O; Bjorksten, B; Weiland, S		ISAAC Steering Comm	International patterns of tuberculosis and the prevalence of symptoms of asthma, rhinitis, and eczema	THORAX			English	Article						tuberculosis; atopy; asthma	CHILDHOOD ISAAC; IMMUNE-RESPONSE; CHILDREN; ALLERGIES; INFECTION; ASSOCIATION; WORLDWIDE; ATOPY; MICE	Background-An ecological analysis was conducted of the relationship between tuberculosis notification rates and the prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and atopic eczema in 85 centres from 23 countries in which standardised data are available. These essentially comprised countries in Europe as well as the USA, Canada, Australia, and New Zealand. Methods-Tuberculosis notification rates were obtained from the World Health Organization. Data on the prevalence of symptoms of asthma, rhinitis, and eczema in 235 477 children aged 13-14 years were based on the responses to the written and video questionnaires from the International Study of Asthma and Allergies in Childhood (ISAAC). The analysis was adjusted for gross national product (GNP) as an estimate of the level of affluence. Results-Tuberculosis notification rates were significantly inversely associated with the lifetime prevalence of wheeze and asthma and the 12 month period prevalence of wheeze at rest as assessed by the video questionnaire. An increase in the tuberculosis notification rates of 25 per 100 000 was associated with an absolute decrease in the prevalence of wheeze ever of 4.7%. Symptoms of allergic rhinoconjunctivitis in the past 12 months were inversely associated with tuberculosis notification rates, but there were no other significant associations with other ISAAC questions on allergic rhinoconjunctivitis or atopic eczema. Conclusions-These findings are consistent with recent experimental evidence which suggests that exposure to Mycobacterium tuberculosis may reduce the risk of developing asthma.	Univ Munich, Childrens Hosp, Klinikum Innenstadt, D-8000 Munich, Germany; Univ Otago, Wellington Sch Med, Wellington, New Zealand; Linkoping Univ Hosp, S-58185 Linkoping, Sweden; Univ Munster, Inst Epidemiol & Social Med, D-4400 Munster, Germany	von Mutius, E (reprint author), Klinikum Innenstadt, Haunersche Kinderklin, Linwurmstr 4, D-80337 Munich, Germany.		Clayton, Tadd/B-7914-2009; Ellwood, Philippa/G-7555-2015	Ellwood, Philippa/0000-0002-1994-4023; Beasley, Richard/0000-0003-0337-406X			Anderson HR, 1997, CIBA F SYMP, V206, P190; Asher MI, 1998, EUR RESPIR J, V12, P315; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; BraunFahrlander C, 1997, PEDIATR ALLERGY IMMU, V8, P75, DOI 10.1111/j.1399-3038.1997.tb00147.x; Cauthen G. M., 1988, ANN RISK TUBERCULOUS; Cookson WOCM, 1997, SCIENCE, V275, P41, DOI 10.1126/science.275.5296.41; COPELAND KT, 1977, AM J EPIDEMIOL, V105, P488; Erb KJ, 1998, J EXP MED, V187, P561, DOI 10.1084/jem.187.4.561; Fearon DT, 1996, SCIENCE, V272, P50, DOI 10.1126/science.272.5258.50; HILMAN BC, 1993, PEDIAT RESP DIS DIAN, P311; Hopkin JM, 1997, CURR OPIN IMMUNOL, V9, P788, DOI 10.1016/S0952-7915(97)80179-3; MARTINEZ FD, 1994, THORAX, V49, P1189, DOI 10.1136/thx.49.12.1189; Matricardi PM, 1998, J ALLERGY CLIN IMMUN, V101, P439, DOI 10.1016/S0091-6749(98)70350-1; Morgenstern H, 1998, MODERN EPIDEMIOLOGY, P459; NOVMARK A, 1975, ACTA DERM-VENEREOL, V55, P181; ORME IM, 1993, J INFECT DIS, V167, P1481; Rothman KJ, 1998, MODERN EPIDEMIOLOGY, V2nd, P115; Schluger NW, 1998, AM J RESP CRIT CARE, V157, P679; SHAW R, 1995, INT J EPIDEMIOL, V24, P597, DOI 10.1093/ije/24.3.597; SHAW RA, 1992, CLIN EXP ALLERGY, V22, P562; Shirakawa T, 1997, SCIENCE, V275, P77, DOI 10.1126/science.275.5296.77; SPORIK R, 1995, AM J RESP CRIT CARE, V151, P1388; Strachan DP, 1997, PEDIATR ALLERGY IMMU, V8, P161, DOI 10.1111/j.1399-3038.1997.tb00156.x; Strannegard IL, 1998, ALLERGY, V53, P249, DOI 10.1111/j.1398-9995.1998.tb03884.x; STYBLO K, 1981, Bulletin of the International Union Against Tuberculosis, V56, P118; United Nations Development Programme, 1994, HUM DEV REP; Wang CC, 1998, IMMUNOLOGY, V93, P307; World Health Organization, 1996, TUB GLOB EM CAS NOT; WILLIAMS H, 2000, IN PRESS J ALLERGY C; Woolcock AJ, 1997, CIBA F SYMP, V206, P122	31	127	130	0	6	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	JUN	2000	55	6					449	453		10.1136/thorax.55.6.449		5	Respiratory System	Respiratory System	319WP	WOS:000087367100004	10817790	
J	Thorburn, AN; Macia, L; Mackay, CR				Thorburn, Alison N.; Macia, Laurence; Mackay, Charles R.			Diet, Metabolites, and "Western-Lifestyle" Inflammatory Diseases	IMMUNITY			English	Review							CHAIN FATTY-ACIDS; REGULATORY T-CELLS; PROTEIN-COUPLED RECEPTOR; GERMINATED BARLEY FOODSTUFF; GUT MICROBIOTA; ULCERATIVE-COLITIS; IMMUNE-RESPONSES; BOWEL-DISEASE; DEACETYLASE INHIBITION; AIRWAY INFLAMMATION	One explanation for the increased incidence of allergies, asthma, and even some autoimmune diseases has been the hygiene hypothesis. However, recent studies also highlight an important role for diet and bacterial metabolites in controlling various immune pathways, including gut and immune homeostasis, regulatory T cell biology, and inflammation. Dietary-related metabolites engage "metabolite-sensing'' G-protein-coupled receptors, such as GPR43, GPR41, GPR109A, GPR120, and GPR35. These receptors are expressed on immune cells and some gut epithelial cells and generally mediate a direct anti-inflammatory effect. Insufficient intake of "healthy foodstuffs'' adversely affects the production of bacterial metabolites. These metabolites and those derived directly from food drive beneficial downstream effects on immune pathways. We propose that insufficient exposure to dietary and bacterial metabolites might underlie the development of inflammatory disorders in Western countries. This review highlights what is currently known about diet, metabolites, and their associated immune pathways in relation to the development of inflammatory disease.	[Thorburn, Alison N.; Macia, Laurence; Mackay, Charles R.] Monash Univ, Dept Immunol, Clayton, Vic 3800, Australia	Mackay, CR (reprint author), Monash Univ, Dept Immunol, Clayton, Vic 3800, Australia.	charles.mackay@monash.edu	Mackay, Charles/A-9673-2008	Mackay, Charles/0000-0002-6338-7340	Australian National Health and Medical Research Council; Australian Research Council; CRC for Asthma and Airways	We have been supported by Australian National Health and Medical Research Council, the Australian Research Council, and the CRC for Asthma and Airways.	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J	Edwards, TM; Myers, JP				Edwards, Thea M.; Myers, John Peterson			Environmental exposures and gene regulation in disease etiology	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Review						chemicals; disease risk; DNA methylation; drug resistance; endocrine disruption; environment; fetal origins of adult disease; gene expression; gene regulation; susceptibility	DIESEL EXHAUST PARTICLES; ACTIVATOR MESSENGER-RNA; AIRWAY EPITHELIAL-CELLS; PRIMORDIAL GERM-CELLS; SMOOTH-MUSCLE-CELLS; PARKINSONS-DISEASE; PROSTATE-CANCER; ALPHA-SYNUCLEIN; 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN TCDD; ESCHERICHIA-COLI	OBJECTIVE: Health or disease is shaped for all individuals by interactions between their genes and environment. Exactly how the environment changes gene expression and how this can lead to disease are being explored in a fruitful new approach to environmental health research, representative studies of which are reviewed here. DATA SOURCES: We searched Web of Science and references of relevant publications to understand the diversity of gene regulatory mechanisms affected by environmental exposures with disease implications. DATA SYNTHESIS: Pharmaceuticals, pesticides, air pollutants, industrial chemicals, heavy metals, hormones, nutrition, and behavior can change gene expression through a broad array of gene regulatory mechanisms. Mechanisms include regulation of gene translocation, histone modifications, DNA methylation, DNA repair, transcription, RNA stability, alternative RNA splicing, protein degradation, gene copy number, and transposon activation. Furthermore, chemically induced changes in gene regulation are associated with serious and complex human diseases, including cancer, diabetes and obesity, infertility, respiratory diseases, allergies, and neurodegenerative disorders such as Parkinson and Alzheimer diseases. One of the best-studied areas of gene regulation is epigenetics, especially DNA methylation. Our examples of environmentally induced changes in DNA methylation are presented in the context of early development, when methylation patterns are initially laid down. This approach highlights the potential role for altered DNA methylation in fetal origins of adult disease and inheritance of acquired genetic change. CONCLUSIONS: The reviewed studies indicate that genetic predisposition for disease is best predicted in the context of environmental exposures. Second, the genetic mechanisms investigated in these studies offer new avenues for risk assessment research. Finally, we are likely to witness dramatic improvements in human health, and reductions in medical costs, if environmental pollution is decreased.	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Health Perspect.	SEP	2007	115	9					1264	1270		10.1289/ehp.9951		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	206RM	WOS:000249200600020	17805414	
J	Ege, MJ; Frei, R; Bieli, C; Schram-Bijkerk, D; Waser, M; Benz, MR; Weiss, G; Nyberg, F; van Hage, M; Pershagen, G; Brunekreef, B; Riedler, J; Lauener, R; Braun-Fahrlander, C; von Mutius, E				Ege, Markus Johannes; Frei, Remo; Bieli, Christian; Schram-Bijkerk, Dieneke; Waser, Marco; Benz, Marcus R.; Weiss, Gertraud; Nyberg, Fredrik; van Hage, Marianne; Pershagen, Goeran; Brunekreef, Bert; Riedler, Josef; Lauener, Roger; Braun-Fahrlaender, Charlotte; von Mutius, Erika		PARSIFAL Study team	Not all farming environments protect against the development of asthma and wheeze in children	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; wheeze; atopic sensitization; farming; microbial components	SCHOOL-AGE-CHILDREN; ALLERGIC DISEASES; FARMERS CHILDREN; HAY-FEVER; ATOPIC SENSITIZATION; LIFE-STYLE; HOUSE DUST; PREVALENCE; EXPOSURE; DEOXYNIVALENOL	Background: In recent years, studies have shown a protective effect of being raised in a farm environment on the development of hay fever and atopic sensitization. Inconsistent data on the relation of farming to asthma and wheeze have raised some doubt about a true protective effect. Objective: We sought to study the differential effects of farm-associated exposures on specific asthma-related health outcomes. Methods: The cross-sectional Prevention of Allergy Risk Factors for Sensitization in Children Related to Farming and Anthroposophic Lifestyle study included 8263 school-age children from rural areas in 5 European countries. Information on farm-related exposures and health outcomes was obtained by using questionnaires. In subsamples allergen-specific IgE and RNA expression of CD14 and Toll-like receptor genes were measured, and dust from children's mattresses was evaluated for microbial components. Results: Inverse relations with a diagnosis of asthma were found for pig keeping (odds ratio [OR], 0.57; 95% CI, 0.38-0.86), farm milk consumption (OR, 0.77; 95% CI, 0.60-0.99), frequent stay in animal sheds (OR, 0.71; 95% CI, 0.54-0.95), child's involvement in haying (OR, 0.56; 95% CI, 0.38-0.81), and use of silage (OR, 0.55; 95% CI, 0.31-0.98; for nonatopic asthma) and in Germany for agriculture (OR, 0.34; 95% CI, 0.22-0.53). Protective factors were related with higher expression levels of genes of the innate immunity. Potential risk factors for asthma and wheeze were also identified in the farm milieu. Levels of endotoxin and extracellular polysaccharides were related to the health outcomes independently of the farm exposures. Conclusions: The protective effect of being raised in a farm environment was ascribed to distinct exposures. Clinical implications: The development of atopic sensitization and atopic and nonatopic asthma is most likely determined by different environmental factors, possibly reflecting distinct pathomechanisms.	Univ Munich, Childrens Hosp, D-8000 Munich, Germany; Univ Basel, Inst Social & Prevent Med, CH-4003 Basel, Switzerland; Univ Utrecht, Med Ctr, Inst Risk Assessment Sci, NL-3508 TC Utrecht, Netherlands; Univ Utrecht, Med Ctr, Julius Ctr Hlth Sci & Primary Care, NL-3508 TC Utrecht, Netherlands; Childrens Hosp, Salzburg, Austria; AstraZeneca R&D, Molndal, Sweden; Karolinska Inst, Dept Med, Clin Immunol & Allergy Unit, Stockholm, Sweden; Univ Hosp, Stockholm, Sweden; Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; Childrens Hosp, Stockholm, Sweden	Ege, MJ (reprint author), Univ Munich, Dr Von Haunerschen Kinderspital, Lindwurmstr 4, D-803371 Munich, Germany.	markus.ege@med.uni-muenchen.de	Osborne, Nicholas/N-4915-2015; Lauener, Roger/O-8612-2016; van Hage, Marianne/A-9678-2017	Osborne, Nicholas/0000-0002-6700-2284; Lauener, Roger/0000-0002-8412-606X; van Hage, Marianne/0000-0003-3091-1596; Pershagen, Goran/0000-0002-9701-1130; brunekreef, bert/0000-0001-9908-0060; Ege, Markus/0000-0001-6643-3923; von Mutius, Erika/0000-0002-8893-4515			Adler A, 2005, J ALLERGY CLIN IMMUN, V115, P67, DOI 10.1016/j.jaci.2004.10.008; Alfven T, 2006, ALLERGY, V61, P414, DOI 10.1111/j.1398-9995.2005.00939.x; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Barnes M, 2001, CLIN EXP ALLERGY, V31, P1822, DOI 10.1046/j.1365-2222.2001.01240.x; Bondy GS, 2000, J TOXICOL ENV HEAL B, V3, P109, DOI 10.1080/109374000281113; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; CHAMBLESS LE, 1985, COMMUN STAT-THEOR M, V14, P1377, DOI 10.1080/03610928508828982; Chew GL, 2001, INDOOR AIR, V11, P171, DOI 10.1034/j.1600-0668.2001.011003171.x; Chrischilles E, 2004, J ALLERGY CLIN IMMUN, V113, P66, DOI 10.1016/j.jaci.2003.09.037; D'Agostino RB, 1998, STAT MED, V17, P2265, DOI 10.1002/(SICI)1097-0258(19981015)17:19<2265::AID-SIM918>3.0.CO;2-B; Downs SH, 2001, CLIN EXP ALLERGY, V31, P570, DOI 10.1046/j.1365-2222.2001.01070.x; Ege MJ, 2006, J ALLERGY CLIN IMMUN, V117, P817, DOI 10.1016/j.jaci.2005.12.1307; Ernst P, 2000, AM J RESP CRIT CARE, V161, P1563; Filipiak B, 2001, CLIN EXP ALLERGY, V31, P1829, DOI 10.1046/j.1365-2222.2001.01246.x; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Klintberg B, 2001, EUR RESPIR J, V17, P1151, DOI 10.1183/09031936.01.00027301; Leynaert B, 2001, AM J RESP CRIT CARE, V164, P1829; Merchant JA, 2005, ENVIRON HEALTH PERSP, V113, P350, DOI 10.1289/ehp.7240; Pestka J, 2006, TOXICOL SCI, V92, P445, DOI 10.1093/toxsci/kfl012; Pestka JJ, 2005, J TOXICOL ENV HEAL B, V8, P39, DOI 10.1080/10937400590889458; Pestka JJ, 2004, TOXICOL LETT, V153, P61, DOI 10.1016/j.toxlet.2004.04.023; Portengen L, 2002, CLIN EXP ALLERGY, V32, P247, DOI 10.1046/j.1365-2222.2002.01310.x; Radon K, 2003, OCCUP ENVIRON MED, V60, P770, DOI 10.1136/oem.60.10.770; Remes ST, 2005, CLIN EXP ALLERGY, V35, P160, DOI 10.1111/j.1365-2222.2005.02172.x; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Roussel S, 2005, ANN AGR ENV MED, V12, P217; Roussel S, 2004, OCCUP ENVIRON MED, V61; Schneweis I, 2000, APPL ENVIRON MICROB, V66, P3639, DOI 10.1128/AEM.66.8.3639-3641.2000; Schollenberger M, 2006, MYCOPATHOLOGIA, V161, P43, DOI 10.1007/s11046-005-0199-7; Schram D, 2005, ALLERGY, V60, P611, DOI 10.1111/j.1398-9995.2005.00748.x; Schram-Bijkerk D, 2005, CLIN EXP ALLERGY, V35, P1272, DOI 10.1111/j.1365-2222.2005.02339.x; Shaheen SO, 1996, LANCET, V347, P1792, DOI 10.1016/S0140-6736(96)91617-7; van Strien RT, 2004, J ALLERGY CLIN IMMUN, V113, P860, DOI 10.1016/j.jaci.2004.01.078; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; Wagner M, 2005, J VET MED B, V52, P278, DOI 10.1111/j.1439-0450.2005.00866.x; Waser M, 2004, CLIN EXP ALLERGY, V34, P389, DOI 10.1111/j.1365-2222.2004.01873.x; WASER M, 2007, IN PRESS ALLERGY; Wickens K, 2002, ALLERGY, V57, P1171, DOI 10.1034/j.1398-9995.2002.t01-1-23644.x; Yeung VP, 1998, J IMMUNOL, V161, P4146	41	126	127	4	21	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	MAY	2007	119	5					1140	1147		10.1016/j.jaci.2007.01.037		8	Allergy; Immunology	Allergy; Immunology	167CB	WOS:000246427200014	17349684	
J	Sampson, MA; Munoz-Furlong, A; Sicherer, SH				Sampson, MA; Munoz-Furlong, A; Sicherer, SH			Risk-taking and coping strategies of adolescents and young adults with food allergy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						food allergy; adolescent; risk taking	DIAL TELEPHONE SURVEY; TREE NUT ALLERGY; ANAPHYLACTIC REACTIONS; PREVALENCE; CHILDREN; PEANUT	Background: Fatal food-allergic reactions are most common among adolescents and young adults. Objective: To gain insight toward devising interventions, we queried risk-taking behaviors and coping strategies of persons age 13 to 21 years with food allergy. Methods: We used an Internet-based anonymous questionnaire devised on the basis of data from focus groups. Results: Participants (174 subjects; 49% male; mean age, 16 years) reported the following: 75% had peanut allergy, 75% had 2 or more food allergies, and 87% had been prescribed self-injectable epinephrine. Regarding risk taking, 61% reported that they "always" carry self-injectable epinephrine, but frequencies varied according to activities: traveling (94%), restaurants (81%), friends' homes (67%), school dance (61%), wearing tight clothes (53%), and sports (43%). Fifty-four percent indicated purposefully ingesting a potentially unsafe food. Willingness to eat a food labeled "may contain" an allergen was reported by 42%. Twenty-nine participants were designated at high risk because they did not always carry epinephrine and ate foods that "may contain" allergens. The high-risk group, compared with the rest of the participants (P < .05), felt less "concern" about and "different" because of their allergy and had more recent reactions. The high-risk group was not distinguishable (P = not significant) by age, sex, or number or severity of reactions. Participants variably (60%) tell their friends about their allergy, but 68% believe education of their friends would make living with food allergy easier. Conclusions: A significant number of teens with food allergy admit to risk taking that varies by social circumstances and perceived risks. The results imply that education of teenagers and, importantly, those around them during social activities might reduce risk taking and its consequences. Clinical implications: Our survey of adolescents and young adults with food allergy revealed risk-taking behaviors that vary by social circumstances and perceived risks, indicating that education of teenagers and their peers might reduce risk taking and its consequences.	Mt Sinai Sch Med, Elliot & Roslyn Jaffe Food Allergy Inst, Div Allergy & Immuonl, Dept Pediat, New York, NY USA; Food Allergy & Anaphylaxis Network, Fairfax, VA USA	Sicherer, SH (reprint author), Mt Sinai Hosp, Div Allergy Immunol, Jaffe Food Allergy Inst, Box 1198,1 Gustave L Levy Pl, New York, NY 10029 USA.	scott.sicherer@mssm.edu					Bock SA, 2001, J ALLERGY CLIN IMMUN, V107, P191, DOI 10.1067/mai.2001.112031; Kim JS, 2005, J ALLERGY CLIN IMMUN, V116, P164, DOI 10.1016/j.jaci.2005.03.039; Noone S. A., 2003, Journal of Allergy and Clinical Immunology, V111, pS133, DOI 10.1016/S0091-6749(03)80417-7; Pereira B, 2005, J ALLERGY CLIN IMMUN, V116, P884, DOI 10.1016/j.jaci.2005.05.047; Rolison MR, 2002, ADOLESCENCE, V37, P585; SAMPSON HA, 1992, NEW ENGL J MED, V327, P380, DOI 10.1056/NEJM199208063270603; Sampson HA, 2004, J ALLERGY CLIN IMMUN, V113, P805, DOI 10.1016/j.jaci.2004.03.014; Sampson Hugh A, 2006, J Allergy Clin Immunol, V117, P391, DOI 10.1016/j.jaci.2005.12.1303; Sicherer SH, 2005, J ALLERGY CLIN IMMUN, V115, P575, DOI 10.1016/j.jaci.2004.12.1122; Sicherer SH, 2004, J ALLERGY CLIN IMMUN, V114, P159, DOI 10.1016/j.jaci.2004.04.018; Sicherer SH, 2003, J ALLERGY CLIN IMMUN, V112, P1203, DOI 10.1016/S0091-6749(03)02026-8; Sicherer SH, 1999, J ALLERGY CLIN IMMUN, V103, P559, DOI 10.1016/S0091-6749(99)70224-1; Yocum MW, 1999, J ALLERGY CLIN IMMUN, V104, P452, DOI 10.1016/S0091-6749(99)70392-1	13	126	126	0	22	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUN	2006	117	6					1440	1445		10.1016/j.jaci.2006.03.009		6	Allergy; Immunology	Allergy; Immunology	053UX	WOS:000238332300037	16751011	
J	Baker, BS				Baker, BS			The role of microorganisms in atopic dermatitis	CLINICAL AND EXPERIMENTAL IMMUNOLOGY			English	Review							STAPHYLOCOCCAL-ENTEROTOXIN-B; LYMPHOCYTE-ASSOCIATED ANTIGEN; T-CELLS; ANTIMICROBIAL PEPTIDES; HYGIENE HYPOTHESIS; PITYROSPORUM-OVALE; CROHNS-DISEASE; BACTERIAL SUPERANTIGENS; MALASSEZIA-FURFUR; STRATUM-CORNEUM	Atopic dermatitis (AD) is a common, fluctuating skin disease that is often associated with atopic conditions such as asthma and IgE-mediated food allergy and whose skin lesions are characterized by a Th-2 cell-mediated response to environmental antigens. The increasing prevalence and severity of atopic diseases including AD over the last three decades has been attributed to decreased exposure to microorganisms during early life, which may result in an altered Th-1/Th-2-balance and/or reduced T cell regulation of the immune response. Patients with AD exhibit defects in innate and acquired immune responses resulting in a heightened susceptibility to bacterial, fungal and viral infections, most notably colonization by S. aureus. Toxins produced by S. aureus exacerbate disease activity by both the induction of toxin-specific IgE and the activation of various cell types including Th-2 cells, eosinophils and keratinocytes. Allergens expressed by the yeast Malazessia furfur, a component of normal skin flora, have also been implicated in disease pathogenesis in a subset of AD patients. Microorganisms play an influential role in AD pathogenesis, interacting with disease susceptibility genes to cause initiation and/or exacerbation of disease activity.			drbsbaker@aol.com					Ahmad-Nejad P, 2004, J ALLERGY CLIN IMMUN, V113, P565, DOI 10.1016/j.jaci.2003.12.583; ALMOHANA F, 1993, J ALLERGY CLIN IMMUN, V92, P575; Arikawa J, 2002, J INVEST DERMATOL, V119, P433, DOI 10.1046/j.1523-1747.2002.01846.x; Aspres Nicholas, 2004, Australas J Dermatol, V45, P199, DOI 10.1111/j.1440-0960.2004.00097.x; BELEW PW, 1980, MYCOPATHOLOGIA, V70, P187, DOI 10.1007/BF00443030; BIRAGYN A, 2002, SCIENCE, V298, P10255; Bjorksten B, 2001, J ALLERGY CLIN IMMUN, V108, P516; BREDIUS RGM, 1993, J IMMUNOL, V151, P1463; BROBERG A, 1992, ACTA DERM-VENEREOL, V72, P187; Buentke E, 2003, APMIS, V111, P789, DOI 10.1034/j.1600-0463.2003.11107810.x; Cho SH, 2001, J INVEST DERMATOL, V116, P658, DOI 10.1046/j.0022-202x.2001.01331.x; Cookson WOCM, 2001, NAT GENET, V27, P372, DOI 10.1038/86867; Cox HE, 1998, BRIT J DERMATOL, V138, P182; 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Exp. Immunol.	APR	2006	144	1					1	9		10.1111/j.1365-2249.2005.02980.x		9	Immunology	Immunology	021YT	WOS:000236022500001	16542358	
J	Shaheen, SO; Newson, RB; Henderson, AJ; Headley, JE; Stratton, FD; Jones, RW; Strachan, DP				Shaheen, SO; Newson, RB; Henderson, AJ; Headley, JE; Stratton, FD; Jones, RW; Strachan, DP		ALSPAC Study Team	Prenatal paracetamol exposure and risk of asthma and elevated immunoglobulin E in childhood	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						asthma; birth cohort; fetal; IgE; paracetamol (acetaminophen); pregnancy; prenatal; wheezing	GLUTATHIONE-S-TRANSFERASE; NORMAL-CHILDREN; HUMAN-FETAL; ACETAMINOPHEN; PREGNANCY; RAT; MOUSE; CELLS; LUNG; COMPLICATIONS	Background We recently found that paracetamol (acetaminophen) use in late pregnancy was associated with an increased risk of early wheezing in the offspring. Objective To see whether use of paracetamol in late pregnancy is associated with an increased risk of asthma, wheezing and other atopic outcomes in the child at school age. Methods In the population-based Avon Longitudinal Study of Parents and Children, we measured associations of paracetamol and aspirin use in late pregnancy (20-32 weeks) with asthma, hayfever, eczema (n=8511) and wheezing (8381) in the offspring at 69-81 months, and with atopy (positive skin prick test to Dermatophagoides pteronyssinus, cat or grass, n=6527) and blood total IgE (n=5148) at 7 years. We used logistic and linear regression to analyse binary outcomes and log-transformed IgE, respectively, controlling for potential confounders. Results Use of paracetamol, but not aspirin, in late pregnancy was positively associated with asthma (odds ratios (ORs), comparing children whose mothers took paracetamol 'sometimes' and 'most days/daily' with those whose mothers never took it, 1.22 (95% confidence interval (CI): 1.06-1.41) and 1.62 (95% CI: 0.86-3.04), respectively; P trend=0.0037), wheezing (ORs 1.20 (95% CI: 1.02-1.40) and 1.86 (95% CI: 0.98-3.55), respectively; P trend=0.011), and total IgE (geometric mean ratios 1.14 (95% CI: 1.03-1.26) and 1.52 (95% CI: 0.98-2.38), respectively; P trend=0.0034), but not hayfever, eczema or skin test positivity. The proportion of asthma attributable to paracetamol use in late pregnancy, assuming a causal relation, was 7%. Conclusion: Paracetamol exposure in late gestation may cause asthma, wheezing and elevated IgE in children of school age.	Univ London Kings Coll, Guys Kings & St Thomas Sch Med, Dept Publ Hlth Sci, London SE1 3QD, England; Univ Bristol, Inst Child Hlth, Unit Paediat & Perinatal Epidemiol, Bristol, Avon, England; Univ London St Georges Hosp, Sch Med, Dept Community Hlth Sci, London SW17 0RE, England	Shaheen, SO (reprint author), Univ London Kings Coll, Guys Kings & St Thomas Sch Med, Dept Publ Hlth Sci, Capital House ,42 Weston St, London SE1 3QD, England.	seif.shaheen@kcl.ac.uk		Henderson, Alexander John/0000-0001-9650-231X			Annesi-Maesano I, 2001, ALLERGY, V56, P491, DOI 10.1034/j.1398-9995.2001.056006491.x; CHEN TC, 1990, ARCH NEUROL-CHICAGO, V47, P1227; CHEN TS, 1990, DRUG METAB DISPOS, V18, P882; COSSAR D, 1990, BIOCHIM BIOPHYS ACTA, V1037, P221, DOI 10.1016/0167-4838(90)90171-B; Dimova S, 2000, BIOCHEM PHARMACOL, V59, P1467, DOI 10.1016/S0006-2952(00)00257-4; FRYER AA, 1986, BIOCHIM BIOPHYS ACTA, V883, P448, DOI 10.1016/0304-4165(86)90283-7; Gilliland FD, 2001, AM J RESP CRIT CARE, V163, P429; Golding J, 2001, PAEDIATR PERINAT EP, V15, P74; GREENLAND S, 1993, BIOMETRICS, V49, P865, DOI 10.2307/2532206; Gregory A, 1999, CLIN EXP ALLERGY, V29, P330; HART SGE, 1995, FUND APPL TOXICOL, V24, P260, DOI 10.1006/faat.1995.1029; JEFFERY EH, 1988, TOXICOL APPL PHARM, V93, P452, DOI 10.1016/0041-008X(88)90048-8; Leadbitter P, 1999, THORAX, V54, P905; LEVY G, 1975, PEDIATRICS, V55, P895; McKeever TM, 2002, AM J RESP CRIT CARE, V166, P827, DOI 10.1164/rccm.200202-158OC; MICHELI L, 1994, ENVIRON HEALTH PERSP, V102, P63; Mumford SE, 1999, ARCH DIS CHILD, V81, pF228; Mumford SE, 1999, ARCH DIS CHILD, V81, pF146; Nafstad P, 2000, J ALLERGY CLIN IMMUN, V106, P867, DOI 10.1067/mai.2000.110558; Newson RB, 2000, EUR RESPIR J, V16, P817, DOI 10.1183/09031936.00.16581700; Peterson JD, 1998, P NATL ACAD SCI USA, V95, P3071, DOI 10.1073/pnas.95.6.3071; PLACKE ME, 1987, TOXICOL PATHOL, V15, P381; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; ROLLINS DE, 1979, SCIENCE, V205, P1414, DOI 10.1126/science.38505; SEARS MR, 1991, NEW ENGL J MED, V325, P1067, DOI 10.1056/NEJM199110103251504; Shaheen SO, 2000, THORAX, V55, P266, DOI 10.1136/thorax.55.4.266; Shaheen SO, 2002, THORAX, V57, P958, DOI 10.1136/thorax.57.11.958; StataCorp, 2003, STAT STAT SOFTW REL; Strachan DP, 1996, BRIT MED J, V312, P1195; Terwindt GM, 2000, NEUROLOGY, V55, P624; Whitekus MJ, 2002, J IMMUNOL, V168, P2560; Wu Z, 2004, CLIN EXP IMMUNOL, V135, P194, DOI 10.1111/j.1365-2249.2004.02372.x; Wu Z, 2001, INT IMMUNOL, V13, P297, DOI 10.1093/intimm/13.3.297; Xu B, 1999, ALLERGY, V54, P829, DOI 10.1034/j.1398-9995.1999.00117.x; Xu BZ, 1999, INT J EPIDEMIOL, V28, P723, DOI 10.1093/ije/28.4.723	35	126	129	2	14	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	JAN	2005	35	1					18	25		10.1111/j.1365-2222.2005.02151.x		8	Allergy; Immunology	Allergy; Immunology	887ZH	WOS:000226343500004	15649261	
J	Gern, JE; Reardon, CL; Hoffjan, S; Nicolae, D; Li, ZH; Roberg, KA; Neaville, WA; Carlson-Dakes, K; Adler, K; Hamilton, R; Anderson, E; Gilbertson-White, S; Tisler, C; DaSilva, D; Anklam, K; Mikus, LD; Rosenthal, LA; Ober, C; Gangnon, R; Lemanske, RF				Gern, JE; Reardon, CL; Hoffjan, S; Nicolae, D; Li, ZH; Roberg, KA; Neaville, WA; Carlson-Dakes, K; Adler, K; Hamilton, R; Anderson, E; Gilbertson-White, S; Tisler, C; DaSilva, D; Anklam, K; Mikus, LD; Rosenthal, LA; Ober, C; Gangnon, R; Lemanske, RF			Effects of dog ownership and genotype on immune development and atopy in infancy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Interleukin-10; hypersensitivity; dogs; cats; children; Interleukin-13; allergy; cytokines; CD14; atopic dermatitis	MODIFIED TH2 RESPONSE; ALLERGIC SENSITIZATION; DENDRITIC CELLS; EARLY EXPOSURE; CAT ALLERGEN; RISK-FACTORS; SCHOOL-AGE; EARLY-LIFE; 1ST YEAR; ASTHMA	Background: Exposure to furred pets might confer protection against the development of allergic sensitization through a mechanism that is incompletely understood. Objective: The objective of this study was to determine the effects of pet exposure and genotype on immunologic development and the incidence of atopic markers and diseases in the first year of life. Methods: Pet exposure in the home was compared with cytokine secretion patterns (mitogen-stimulated mononuclear cells at birth and age 1 year) and indicators of atopy (allergen-specific and total IgE, eosinophilia, food allergy, atopic dermatitis) in 285 infants. Interactions with genotype at the CD14 locus were also evaluated in the data analyses. Results: Exposure to dogs was associated with reduced allergen sensitization (19% vs 33%, P =.020) and atopic dermatitis (30% vs 51%, P < .001). The risk for atopic dermatitis was further influenced by genotype at the CD14 locus (P =.006), even after adjusting for exposure to dogs (P =.003). Furthermore, infants with the genotype -159TT were less likely to develop atopic dermatitis if they were exposed to a dog (5% vs 43%, P =.04). Last, dog exposure was associated with increased IL-10 (117 vs 79 pg/mL, P =.002) and IL-13 (280 vs 226 pg/mL, P =.013) responses at age 1 year. Conclusions: Having a dog in infancy is associated with higher IL-10 and IL-13 cytokine secretion profiles and reduced allergic sensitization and atopic dermatitis. These findings suggest that postnatal exposure to dogs can influence immune development in a genotype-specific fashion and thereby attenuate the development of atopy in at-risk children.	Univ Wisconsin, Dept Pediat, Madison, WI USA; Univ Wisconsin, Dept Biostat & Med Informat, Madison, WI USA; Univ Wisconsin, Dept Med, Madison, WI USA; Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA; Univ Chicago, Dept Stat, Chicago, IL 60637 USA	Gern, JE (reprint author), K4-918 CSC,600 Highland Ave, Madison, WI 53792 USA.		Rosenthal, Louis/A-8868-2008		NCRR NIH HHS [2 M01 RR03186-16]; NHLBI NIH HHS [P01 HL70831-01, 1R01HL61879-01]		Akbari O, 2001, NAT IMMUNOL, V2, P725, DOI 10.1038/90667; Akbari O, 2002, NAT MED, V8, P1024, DOI 10.1038/nm745; Apter AJ, 2003, J ALLERGY CLIN IMMUN, V111, P938, DOI 10.1067/mai.2003.1417; ARSHAD SH, 1991, BRIT J CLIN PRACT, V45, P88; Blahnik MJ, 2001, PEDIATR RES, V50, P726, DOI 10.1203/00006450-200112000-00016; Braback L, 2001, PEDIATR ALLERGY IMMU, V12, P4, DOI 10.1034/j.1399-3038.2001.012001004.x; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Celedon JC, 2002, LANCET, V360, P781, DOI 10.1016/S0140-6736(02)09906-3; Custovic A, 2001, LANCET, V358, P188, DOI 10.1016/S0140-6736(01)05406-X; DESJARDINS A, 1993, J ALLERGY CLIN IMMUN, V91, P979, DOI 10.1016/0091-6749(93)90210-7; ENK AH, 1994, J EXP MED, V179, P1397, DOI 10.1084/jem.179.4.1397; Freund RJ, 1997, STAT METHODS; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Gereda JE, 2000, JAMA-J AM MED ASSOC, V284, P1652, DOI 10.1001/jama.284.13.1652; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Jeannin P, 1998, J IMMUNOL, V160, P3555; KUEHR J, 1992, J ALLERGY CLIN IMMUN, V90, P358, DOI 10.1016/S0091-6749(05)80015-6; Langrish CL, 2002, CLIN EXP IMMUNOL, V128, P118, DOI 10.1046/j.1365-2249.2002.01817.x; Lemanske RF, 2002, PEDIATR ALLERGY IMMU, V13, P38, DOI 10.1034/j.1399-3038.13.s.15.8.x; LINDFORS A, 1995, ARCH DIS CHILD, V73, P408; Mirel DB, 2002, DIABETES, V51, P3336, DOI 10.2337/diabetes.51.11.3336; Nafstad P, 2001, ALLERGY, V56, P307, DOI 10.1034/j.1398-9995.2001.00881.x; Neaville WA, 2003, J ALLERGY CLIN IMMUN, V112, P740, DOI 10.1067/mai.2003.1716; Nickel R, 1997, J ALLERGY CLIN IMMUN, V99, P613, DOI 10.1016/S0091-6749(97)70021-6; Ownby DR, 2002, JAMA-J AM MED ASSOC, V288, P963, DOI 10.1001/jama.288.8.963; Pagano M., 2000, PRINCIPLES BIOSTATIS; Park JH, 2001, ENVIRON HEALTH PERSP, V109, P859, DOI 10.2307/3454831; Perzanowski MS, 2002, AM J RESP CRIT CARE, V166, P696, DOI 10.1164/rccm.2201035; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; Platts-Mills TAE, 2001, INT ARCH ALLERGY IMM, V124, P126, DOI 10.1159/000053689; Remes ST, 2001, J ALLERGY CLIN IMMUN, V108, P509, DOI 10.1067/mai.2001.117797; Roost HP, 1999, J ALLERGY CLIN IMMUN, V104, P941, DOI 10.1016/S0091-6749(99)70072-2; Strachan David P., 2000, Thorax, V55, pS2, DOI 10.1136/thorax.55.suppl_1.S2; Svanes C, 1999, J ALLERGY CLIN IMMUN, V103, P415, DOI 10.1016/S0091-6749(99)70465-3; van den Biggelaar AHJ, 2000, LANCET, V356, P1723, DOI 10.1016/S0140-6736(00)03206-2; Vercelli D, 2003, CLIN EXP ALLERGY, V33, P153, DOI 10.1046/j.1365-2222.2003.01606.x; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7	37	126	126	1	8	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	FEB	2004	113	2					307	314		10.1016/j.jaci.2003.11.017		8	Allergy; Immunology	Allergy; Immunology	773EX	WOS:000188885700020	14767447	
J	D'Amato, G; Liccardi, G; D'Amato, M; Cazzola, M				D'Amato, G; Liccardi, G; D'Amato, M; Cazzola, M			Outdoor air pollution, climatic changes and allergic bronchial asthma	EUROPEAN RESPIRATORY JOURNAL			English	Review						air pollution; bronchial asthma; pollen allergy; respiratory allergy; urban air pollution	THUNDERSTORM-ASSOCIATED ASTHMA; DIESEL EXHAUST PARTICLES; PPM NITROGEN-DIOXIDE; OZONE EXPOSURE; PULMONARY-FUNCTION; GRASS-POLLEN; PARTICULATE MATTER; SULFUR-DIOXIDE; RESPIRATORY RESPONSES; NONASTHMATIC SUBJECTS	Both the prevalence and severity of respiratory allergic diseases such as bronchial asthma have increased in recent years. Among the factors implicated in this "epidemic" are indoor and outdoor airborne pollutants. Urbanisation with its high levels of vehicle emissions and Westernised lifestyle parallels the increase in respiratory allergy in most industrialised countries, and people who live in urban areas tend to be more affected by the disease than those of rural areas. In atopic subjects, exposure to air pollution increases airway responsiveness to aeroallergens. Pollen is a good model with which to study the interrelationship between air pollution and respiratory allergic diseases. Biological aerosols carrying antigenic proteins, such as pollen grains or plant-derived paucimicronic components, can produce allergic symptoms. By adhering to the surface of these airborne allergenic agents, air pollutants could modify their antigenic properties. Several factors influence this interaction, i.e., type of air pollutant, plant species, nutrient balance, climatic factors, degree of airway sensitisation and hyperresponsiveness of exposed subjects. However, the airway mucosal damage and the impaired mucociliary clearance induced by air pollution may facilitate the penetration and the access of inhaled allergens to the cells of the immune system, and so promote airway sensitisation. As a consequence, an enhanced immunoglobulin E-mediated response to aeroallergens and enhanced airway inflammation favoured by air pollution could account for the increasing prevalence of allergic respiratory diseases in urban areas.	Azienda Osped Alta Specialita A Cardarelli, Div Pneumol & Allergol, Naples, Italy; Azienda Osped Alta Specialita A Cardarelli, Dept Chest Dis, Naples, Italy	D'Amato, G (reprint author), Hosp A Cardarelli, Div Pneumol & Allergol, Via Rione Sirignano 10, I-80121 Naples, Italy.		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N., 1995, European Respiratory Journal, V8, p500S; White MC, 1997, AM J EPIDEMIOL, V145, P432; WHITE MC, 1994, ENVIRON RES, V65, P56, DOI 10.1006/enrs.1994.1021; WHITTEMORE AS, 1980, AM J PUBLIC HEALTH, V70, P687, DOI 10.2105/AJPH.70.7.687; WILSON AF, 1973, NEW ENGL J MED, V288, P1056, DOI 10.1056/NEJM197305172882006; WJST M, 1993, BRIT MED J, V307, P596; Woolcock AJ, 1997, CIBA F SYMP, V206, P122; YANAI M, 1990, J APPL PHYSIOL, V68, P2267; 2001, AMBIENTE ITALIA 2000	162	126	130	5	22	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	SEP	2002	20	3					763	776		10.1183/09031936.02.00401402		14	Respiratory System	Respiratory System	596VL	WOS:000178187100038	12358357	
J	Almqvist, C; Wickman, M; Perfetti, L; Berglind, N; Renstrom, A; Hedren, M; Larsson, K; Hedlin, G; Malmberg, P				Almqvist, C; Wickman, M; Perfetti, L; Berglind, N; Renstrom, A; Hedren, M; Larsson, K; Hedlin, G; Malmberg, P			Worsening of asthma in children allergic to cats, after indirect exposure to cat at school	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							PEAK EXPIRATORY FLOW; DAY-CARE-CENTERS; DOG CAN-F-1; SYMPTOMS; SENSITIZATION; FEL-D-1; DUST; MITE; HYPERRESPONSIVENESS; ENVIRONMENT	Exposure to cat allergen at school might exacerbate symptoms in asthmatic children with cat allergy. To study this, we identified 410 children, 6-12 yr of age, who were being treated for asthma (inhaled steroids and beta -agonists), were allergic to cats, and had no Eat at home. Peak expiratory flow (PEF), asthma symptoms, medication, fever and/or sore throat, and contact with furred pets were recorded twice daily during the last week of summer holidays and the second and third weeks of school. The number of cat owners in each class was recorded. Ninety-two children with asthma reported no contact with furred pets. Among these, children who attended classes with > 18% (median value) cat owners reported significantly decreased PEF, more days with asthma symptoms, and increased use of medication after school started. Those in classes with less than or equal to 18% cat owners reported no change. Children in classes with many cat owners ran a 9-fold increased risk of exacerbated asthma after school start compared with children in classes with few cat owners, after adjusting for age, sex, and fever and/or sore throat. Thus, asthma symptoms, PEF, and the use of asthma medication in children with cat allergy may be affected by indirect cat exposure at school.	Karolinska Hosp, Dept Environm Hlth, S-17176 Stockholm, Sweden; Fdn Salvatore Maugeri, Ist Sci Pavia, Clin Lavoro & Riabilitazione, IRCCS, Pavia, Italy; Natl Inst Working Life, Stockholm, Sweden; Karolinska Inst, Inst Environm Med, Stockholm, Sweden; Karolinska Inst, Sachs Childrens Hosp, Stockholm, Sweden; Karolinska Inst, Dept Woman & Child Hlth, Astrid Lindgren Childrens Hosp, Stockholm, Sweden	Almqvist, C (reprint author), Karolinska Hosp, Dept Environm Hlth, Norrbacka Bldg,3rd Floor, S-17176 Stockholm, Sweden.						Almqvist C, 1999, J ALLERGY CLIN IMMUN, V103, P1012, DOI 10.1016/S0091-6749(99)70172-7; Brand PLP, 1997, EUR RESPIR J, V10, P1242, DOI 10.1183/09031936.97.10061242; BRUNEKREEF B, 1992, INT J EPIDEMIOL, V21, P338, DOI 10.1093/ije/21.2.338; BURGE PS, 1982, EUR J RESPIR DIS, V63, P47; *COLL STAT, 1999, STAT US GUID REL 6, P256; Custovic A, 1996, CLIN EXP ALLERGY, V26, P1246, DOI 10.1046/j.1365-2222.1996.d01-278.x; Dreborg S, 1989, ALLERGY S10, V44, P1; ENBERG RN, 1993, ANN ALLERGY, V70, P471; HIGGINS BG, 1992, AM REV RESPIR DIS, V145, P588; Hollander A, 1998, EUR RESPIR J, V11, P929, DOI 10.1183/09031936.98.11040929; IHRE E, 1993, CLIN EXP ALLERGY, V23, P298, DOI 10.1111/j.1365-2222.1993.tb00326.x; INGRAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449, DOI 10.1016/S0091-6749(95)70286-5; Johnston SL, 1996, AM J RESP CRIT CARE, V154, P654; MUNIR AKM, 1995, CLIN EXP ALLERGY, V25, P119, DOI 10.1111/j.1365-2222.1995.tb01016.x; Noertjojo K, 1999, J ALLERGY CLIN IMMUN, V103, P60, DOI 10.1016/S0091-6749(99)70526-9; Patchett K, 1997, J ALLERGY CLIN IMMUN, V100, P755, DOI 10.1016/S0091-6749(97)70269-0; Perzanowski MS, 1999, J ALLERGY CLIN IMMUN, V103, P1018, DOI 10.1016/S0091-6749(99)70173-9; Plaschke P, 1999, J ALLERGY CLIN IMMUN, V104, P58, DOI 10.1016/S0091-6749(99)70114-4; Plaschke P, 1999, ALLERGY, V54, P843, DOI 10.1034/j.1398-9995.1999.00162.x; Quanjer PH, 1997, PEDIATR PULM, V24, P2, DOI 10.1002/(SICI)1099-0496(199707)24:1<2::AID-PPUL2>3.3.CO;2-U; Reddel HK, 1998, EUR RESPIR J, V12, P309, DOI 10.1183/09031936.98.12020309; ROEMER W, 1998, EUR RESPIR REV, V8, P4; Smedje G, 1997, CLIN EXP ALLERGY, V27, P1270, DOI 10.1111/j.1365-2222.1997.tb01171.x; Sporik R, 1999, THORAX, V54, P675; Sterk PJ, 1999, EUR RESPIR J, V14, P1435, DOI 10.1183/09031936.99.14614359; STORR J, 1989, ARCH DIS CHILD, V64, P103; Sulakvelidze I, 1998, EUR RESPIR J, V11, P821, DOI 10.1183/09031936.98.11040821; Warner JO, 1998, PEDIATR PULM, V25, P1; Wickman M, 1999, CLIN EXP ALLERGY, V29, P626	29	126	127	0	1	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	MAR	2001	163	3					694	698				5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	419HW	WOS:000167944100021	11254526	
J	Arkwright, PD; David, TJ				Arkwright, PD; David, TJ			Intradermal administration of a killed Mycobacterium vaccae suspension (SRL 172) is associated with improvement in atopic dermatitis in children with moderate-to-severe disease	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Mycobacterium vaccae; atopic dermatitis; atopy; T(H)2	ALLERGIC DISEASE; BCG VACCINATION; DENDRITIC CELLS; INFECTION; IMMUNOTHERAPY; TUBERCULOSIS; LYMPHOCYTES; OVALBUMIN; ASTHMA; TRIAL	Background: Although a doubling in the prevalence of atopic disease, including atopic dermatitis, in the Western world over the last few generations has been paralleled by a marked reduction in infectious diseases, especially tuberculosis, it is unclear whether this increase in atopy is causally related to reduced exposure to mycobacteria. Objectives: The aim of this study was to determine whether administration of mycobacterial antigens to atopic individuals might ameliorate their disease. Methods: Forty-one children aged 5 to 18 years with moderate-to-severe atopic dermatitis were enrolled in a randomized, double-blind, placebo-controlled trial, where they were given either one intradermal injection of killed Mycobacterium vaccae (SRL 172) or buffer solution (placebo). Changes in skin surface area affected by dermatitis and dermatitis severity score were assessed before treatment and at 1 and 3 months after treatment. Results: Children treated with SRL 172 showed a mean 48% (95% CI, 32%-65%) reduction in surface area affected by dermatitis compared with a mean 4% (95% CI, -29% to 22%) reduction for the placebo group (P < .001) and a median 68% (interquartile range, 46%-85%) reduction in dermatitis severity score compared with 18% (interquartile range, -2% to 34%) for the placebo group (P < .01) at 3 months after treatment. There were no untoward effects of the treatment, apart from a local reaction in 13 of the 21 children, which occurred 1 month after SRL 172 administration and settled spontaneously. Conclusion: SRL 172 was associated with an improvement in the severity of the dermatitis in children with moderate-to-severe disease.	Univ Manchester, Booth Hall Childrens Hosp, Acad Unit Child Hlth, Manchester M9 7AA, Lancs, England	Arkwright, PD (reprint author), Univ Manchester, Booth Hall Childrens Hosp, Acad Unit Child Hlth, Charlestown Rd, Manchester M9 7AA, Lancs, England.		Arkwright, Peter/C-5149-2012				Alm JS, 1997, LANCET, V350, P400, DOI 10.1016/S0140-6736(97)02207-1; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; BerthJones J, 1996, BRIT J DERMATOL, V135, P25, DOI 10.1111/j.1365-2133.1996.tb00706.x; Cookson WOCM, 1997, SCIENCE, V275, P41, DOI 10.1126/science.275.5296.41; DAVID TJ, 1984, BRIT J DERMATOL, V111, P597, DOI 10.1111/j.1365-2133.1984.tb06630.x; Hart DNJ, 1997, BLOOD, V90, P3245; Holgate ST, 2000, J ALLERGY CLIN IMMUN, V105, P193, DOI 10.1016/S0091-6749(00)90066-6; Hrouda D, 1998, BRIT J UROL, V82, P568; Johnson D, 1999, VACCINE, V17, P2583, DOI 10.1016/S0264-410X(99)00055-9; Leung DYM, 2000, J ALLERGY CLIN IMMUN, V105, P860, DOI 10.1067/mai.2000.106484; Maraveyas A, 1999, ANN ONCOL, V10, P817, DOI 10.1023/A:1008307821189; Romagnani S, 2000, J ALLERGY CLIN IMMUN, V105, P399, DOI 10.1067/mai.2000.104575; Schaible UE, 2000, J IMMUNOL, V164, P4843; Shirakawa T, 1997, SCIENCE, V275, P77, DOI 10.1126/science.275.5296.77; Stead WW, 1997, CLIN CHEST MED, V18, P65, DOI 10.1016/S0272-5231(05)70356-7; Strannegard IL, 1998, ALLERGY, V53, P249, DOI 10.1111/j.1398-9995.1998.tb03884.x; Tocque K, 1998, AM J RESP CRIT CARE, V158, P484; Tukenmez F, 1999, PEDIATR ALLERGY IMMU, V10, P107, DOI 10.1034/j.1399-3038.1999.00029.x; von Mutius E, 2000, J ALLERGY CLIN IMMUN, V105, P9, DOI 10.1016/S0091-6749(00)90171-4; Wang CC, 1998, IMMUNOLOGY, V93, P307	20	126	127	0	6	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	MAR	2001	107	3					531	534		10.1067/mai.20001.113081		4	Allergy; Immunology	Allergy; Immunology	416RE	WOS:000167793300017	11240956	
J	Van Schoor, J; Joos, GF; Pauwels, RA				Van Schoor, J; Joos, GF; Pauwels, RA			Indirect bronchial hyperresponsiveness in asthma: mechanisms pharmacology and implications for clinical research	EUROPEAN RESPIRATORY JOURNAL			English	Review						adenosine challenge; airway inflammation; asthma; bronchial challenges; bronchial hyperresponsiveness; exercise challenge	EXERCISE-INDUCED ASTHMA; NEBULIZED DISTILLED WATER; METABISULFITE-INDUCED BRONCHOCONSTRICTION; BRADYKININ-INDUCED BRONCHOCONSTRICTION; SALINE-INDUCED BRONCHOCONSTRICTION; PROPRANOLOL-INDUCED BRONCHOCONSTRICTION; NEUTRAL ENDOPEPTIDASE INHIBITOR; A-INDUCED BRONCHOCONSTRICTION; METHACHOLINE-INDUCED BRONCHOCONSTRICTION; ADENOSINE-INDUCED BRONCHOCONSTRICTION	Bronchial hyperresponsiveness (BHR), an abnormal increase in airflow limitation following the exposure to a stimulus, is an important pathophysiological characteristic of bronchial asthma. Because of heterogeneity of the airway response to different stimuli, the latter have been divided into direct and indirect stimuli. Direct stimuli cause airflow limitation by a direct action on the effector cells involved in the airflow limitation, while indirect stimuli exert their action essentially on inflammatory and neuronal cells that act as an intermediary between the stimulus and the effector cells. This manuscript reviews the clinical and experimental studies on the mechanisms involved in indirect BHR in patients with asthma. Pharmacological stimuli (adenosine, tachykinins, bradykinin, sodium metabisulphite/sulphur dioxide, and propranolol) as well as physical stimuli (exercise, nonisotonic aerosols, and isocapnic hyperventilation) are discussed. The results of the different direct and indirect bronchial challenge tests are only weakly correlated and are therefore not mutually interchangeable. Limited available data (studies on the effects of allergen avoidance and inhaled corticosteroids) suggest that indirectly acting bronchial stimuli (especially adenosine) might better reflect the degree of airway inflammation than directly acting stimuli. It remains to be established whether monitoring of indirect BHR as a surrogate marker of inflammation tin addition to symptoms and lung function) is of clinical relevance to the long-term management of asthmatic patients. This seems to be the case for the direct stimulus methacholine. More work needs to be performed to find out whether, indirect stimuli are more suitable in asthma monitoring than direct ones. Recommendations on the application of indirect challenges in clinical practice and research will shortly be available from the European Respiratory Society Task Force.	State Univ Ghent Hosp, Dept Resp Dis, B-9000 Ghent, Belgium	Joos, GF (reprint author), State Univ Ghent Hosp, Dept Resp Dis, 7K12 IE,De Pintelaan 185, B-9000 Ghent, Belgium.						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Resp. J.	SEP	2000	16	3					514	533		10.1034/j.1399-3003.2000.016003514.x		20	Respiratory System	Respiratory System	359RH	WOS:000089625500026	11028670	
J	Rundell, KW; Wilber, RL; Szmedra, L; Jenkinson, DM; Mayers, LB; Im, J				Rundell, KW; Wilber, RL; Szmedra, L; Jenkinson, DM; Mayers, LB; Im, J			Exercise-induced asthma screening of elite athletes: field versus laboratory exercise challenge	MEDICINE AND SCIENCE IN SPORTS AND EXERCISE			English	Article						bronchospasm; athlete; exercise; cold; pulmonary function test	CROSS-COUNTRY SKIERS; INDUCED BRONCHOSPASM; COLD-AIR; FIGURE SKATERS; RESPONSIVENESS; INHALATION; HYPERPNEA; DIAGNOSIS; EXPOSURE; SEVERITY	Purpose: The purpose of this study was to compare a laboratory based exercise challenge (LBC) to a field based exercise challenge (FBC) for pulmonary function test (PFT) exercise-induced asthma (EIA) screening of elite athletes. Methods: Twenty-three elite cold weather athletes (14 men, 9 women) PFT positive for EIA (FBC screened) served as subjects. Twenty-three gender and sport matched Controls (nonasthmatics) were randomly selected to establish PFT reference values for normal elite athletes. Before FBC, athletes completed a medical history questionnaire for EIA symptoms. FBC evaluations consisted of baseline spirometry, actual or simulated competition, and 5, 10, and 15 min postexercise spirometry. PFT positive athletes were evaluated in the laboratory using an exercise challenge simulating race intensity (ambient conditions: 21 degrees C, 60% relative humidity). PFT procedures were identical to FBC. Results: 91%, of PFT positive and 48% of PFT normal athletes reported at least one symptom of EIA, with postrace cough most frequent. Baseline spirometry was the same for PFT positives and normal controls. Lower limit reference range (MN - 2 SD) of FEV1 for controls suggests that postexercise decrements of greater than similar to-7% indicate abnormal airway response in this population. Exercise time duration did not effect bronchial reactivity; 78% of FBC PFT positives; were PFT normal post-LBC. Conclusion: Self-reported symptoms by elite athletes are not reliable in identifying EIA. Reference range criterion for FEV1 decrement in the elite athlete postexercise contrasts current recommended guidelines. Moreover, a large number of false negatives may occur in this population if EIA screening is performed with inadequate exercise and environmental stress.	United States Olymp Comm Lake Placid, Sport Sci & Technol Div, Lake Placid, NY 12946 USA	Rundell, KW (reprint author), United States Olymp Comm Lake Placid, Sport Sci & Technol Div, Lake Placid, NY 12946 USA.						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O., 1999, Medicine and Science in Sports and Exercise, V31, pS99, DOI 10.1097/00005768-199905001-00335; Tikkanen Heikki Iikka Helenius, 1996, Medicine and Science in Sports and Exercise, V28, pS90; VOY RO, 1986, MED SCI SPORT EXER, V18, P328, DOI 10.1249/00005768-198606000-00013; WARREN JB, 1984, CLIN SCI, V66, P79; Weiler JM, 1998, J ALLERGY CLIN IMMUN, V102, P722, DOI 10.1016/S0091-6749(98)70010-7; WILBER RL, IN PRESS MED SCI SPO	38	126	129	0	8	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	0195-9131			MED SCI SPORT EXER	Med. Sci. Sports Exerc.	FEB	2000	32	2					309	316		10.1097/00005768-200002000-00010		8	Sport Sciences	Sport Sciences	283TG	WOS:000085291400010	10694112	
J	Paunio, M; Heinonen, OP; Virtanen, M; Leinikki, P; Patja, A; Peltola, H				Paunio, M; Heinonen, OP; Virtanen, M; Leinikki, P; Patja, A; Peltola, H			Measles history and atopic diseases - A population-based cross-sectional study	JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION			English	Article							VACCINATION PROGRAM; ASTHMA; INFECTIONS; CHILDHOOD; RUBELLA; FINLAND; MUMPS; CHILDREN; SIZE	Context Many recent cross-sectional studies have suggested that lack of early exposure to communicable diseases, including measles, in affluent countries may have increased rates of atopic disease. Objective To study the association between natural measles infection and atopy, Design and Setting Cross-sectional nationwide study in Finland using data gathered between November 1, 1982, and June 30, 1986. Subjects A total of 547 910 individuals aged 14 months to 19 years who at the time of measles-mumps-rubella (MMR) vaccination had relevant information collected on the occurrence of measles and allergic rhinitis, eczema, and asthma. Main Outcome Measures Lifetime occurrence of atopic manifestations in subjects who had had measles compared with those who had not, expressed as age-specific and age-adjusted prevalence ratios. Results The age-adjusted prevalence ratio of atopic manifestations among those who had had measles (n = 20 690) compared with those who had not (n = 527 220) was 1.32 (95% confidence interval [CI], 1.27-1.36) for eczema, 1.41 (95% CI, 1.33-1.49) for rhinitis, and 1.67 (95% CI, 1.54-1.79) for asthma. The positive association between measles and atopy was evident at all ages, in both urban and rural dwellers, and among subjects with many or few contacts at home or in day care. Conclusions Based on our data, measles and atopy occur more frequently together than expected, which does not support the hypothesis that experiencing natural measles infection offers protection against atopic disease.	Univ Helsinki, Dept Publ Hlth, Helsinki, Finland; Assoc Local & Reg Author, Dept Hosp Serv, Helsinki, Finland; Natl Publ Hlth Inst, Dept Infect Dis, Helsinki, Finland; Univ Helsinki, Cent Hosp, Hosp Children & Adolescents, Helsinki, Finland	Paunio, M (reprint author), Minist Social Affairs & Hlth, POB 267, Helsinki 00171, Finland.						Allen JE, 1997, IMMUNOL TODAY, V18, P387, DOI 10.1016/S0167-5699(97)01102-X; Bodner C, 1998, THORAX, V53, P28; Campbell DE, 1996, LANCET, V348, P825, DOI 10.1016/S0140-6736(05)65244-0; *CENTR STAT OFF FI, 1987, STAT YB FINL 1987; Cookson WOCM, 1997, SCIENCE, V275, P41, DOI 10.1126/science.275.5296.41; FOX JP, 1971, AM J EPIDEMIOL, V94, P179; GREENLAND S, 1985, BIOMETRICS, V41, P55, DOI 10.2307/2530643; Hayney M S, 1998, Int J Infect Dis, V2, P143, DOI 10.1016/S1201-9712(98)90116-3; Holgate ST, 1997, NAT GENET, V15, P227, DOI 10.1038/ng0397-227; HOLT PG, 1994, LANCET, V344, P456, DOI 10.1016/S0140-6736(94)91776-0; Kramer U, 1999, LANCET, V353, P450, DOI 10.1016/S0140-6736(98)06329-6; LOUHIALA PJ, 1995, AM J PUBLIC HEALTH, V85, P1109, DOI 10.2105/AJPH.85.8_Pt_1.1109; MARTINEZ FD, 1994, THORAX, V49, P1189, DOI 10.1136/thx.49.12.1189; Matricardi PM, 1997, BRIT MED J, V314, P999; PAUNIO M, 1991, AM J EPIDEMIOL, V133, P1152; PELTOLA H, 1994, NEW ENGL J MED, V331, P1397, DOI 10.1056/NEJM199411243312101; PELTOLA H, 1986, LANCET, V1, P137; Shaheen SO, 1996, LANCET, V347, P1792, DOI 10.1016/S0140-6736(96)91617-7; Shirakawa T, 1997, SCIENCE, V275, P77, DOI 10.1126/science.275.5296.77; Soothill JF, 1996, LANCET, V348, P825, DOI 10.1016/S0140-6736(05)65245-2; STRACHAN DP, 1989, BRIT MED J, V299, P1259; VONMUTIUS E, 1994, BRIT MED J, V308, P692	22	126	130	1	3	AMER MEDICAL ASSOC	CHICAGO	515 N STATE ST, CHICAGO, IL 60610 USA	0098-7484			JAMA-J AM MED ASSOC	JAMA-J. Am. Med. Assoc.	JAN 19	2000	283	3					343	346		10.1001/jama.283.3.343		4	Medicine, General & Internal	General & Internal Medicine	273WM	WOS:000084732400025	10647796	
J	Ryman-Rasmussen, JP; Tewksbury, EW; Moss, OR; Cesta, MF; Wong, BA; Bonner, JC				Ryman-Rasmussen, Jessica P.; Tewksbury, Earl W.; Moss, Owen R.; Cesta, Mark F.; Wong, Brian A.; Bonner, James C.			Inhaled Multiwalled Carbon Nanotubes Potentiate Airway Fibrosis in Murine Allergic Asthma	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article						carbon nanotubes; asthma; fibrosis; lung	INTRATRACHEAL INSTILLATION; PULMONARY TOXICITY; MICE; PARTICLES; INTERLEUKIN-13; FIBROBLASTS; DEPOSITION; RESPONSES; EXPOSURE	Carbon nanotubes are gaining increasing attention due to possible health risks from occupational or environmental exposures. This study tested the hypothesis that inhaled multiwalled carbon nanotubes (MWCNT) would increase airway fibrosis in mice with allergic asthma. Normal and ovalbumin-sensitized mice were exposed to a MWCNT aerosol (100 mg/m(3)) or saline aerosol for 6 hours. Lung injury, inflammation, and fibrosis were examined by histopathology, clinical chemistry, ELISA, or RT-PCR for cytokines/chemokines, growth factors, and Collagen at 1 and 14 days after inhalation. Inhaled MWCNT were distributed throughout the lung and found in macrophages by light microscopy, but were also evident in epithelial cells by electron microscopy. Quantitative morphometry showed significant airway fibrosis at 14 days in mice that received a combination of ovalbumin and MWCNT, but not in mice that received ovalbumin or MWCNT only. Ovalbumin-sensitized mice that did not inhale MWCNT had elevated levels IL-13 and transforming growth factor (TGF)-beta 1 in lung lavage fluid, but not platelet-derived growth factor (PDGF)-AA. In contrast, unsensitized mice that inhaled MWCNT had elevated PDGF-AA, but not increased levels of TGF-beta 1 and IL-13. This suggested that airway fibrosis resulting from combined ovalbumin sensitization and MWCNT inhalation requires PDGF, a potent fibroblast mitogen, and TGF-beta 1, which stimulates Collagen production. Combined ovalbumin sensitization and MWCNT inhalation also synergistically increased IL-5 mRNA levels, which could further contribute to airway fibrosis. These data indicate that inhaled MWCNT require pre-existing inflammation to cause airway fibrosis. Our findings suggest that individuals with pre-existing allergic inflammation may be susceptible to airway fibrosis from inhaled MWCNT.	[Ryman-Rasmussen, Jessica P.; Cesta, Mark F.; Bonner, James C.] N Carolina State Univ, Dept Environm & Mol Toxicol, Raleigh, NC 27695 USA; [Ryman-Rasmussen, Jessica P.; Tewksbury, Earl W.; Moss, Owen R.; Cesta, Mark F.; Wong, Brian A.; Bonner, James C.] Hamner Inst Hlth Sci, Res Triangle Pk, NC USA; [Cesta, Mark F.] Natl Inst Environm Hlth Sci, Cellular & Mol Pathol Branch, Res Triangle Pk, NC USA	Bonner, JC (reprint author), N Carolina State Univ, Dept Environm & Mol Toxicol, Box 7633, Raleigh, NC 27695 USA.	james_bonner@ncsu.edu			The American Chemistry Council's Long Range Research Initiative; The Intramural Research Program of the National Institutes of Health; National Institute of the Environmental Health Sciences; North Carolina State University's College of Agricultural and Life Sciences	This study was funded by The American Chemistry Council's Long Range Research Initiative provided to The Hamner Institutes for Health Sciences, The Intramural Research Program of the National Institutes of Health, National Institute of the Environmental Health Sciences, and North Carolina State University's College of Agricultural and Life Sciences.	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J. Respir. Cell Mol. Biol.	MAR	2009	40	3					349	358		10.1165/rcmb.2008-0276OC		10	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	412PC	WOS:000263735700012	18787175	
J	Busacker, A; Newell, JD; Keefe, T; Hoffman, EA; Granroth, JC; Castro, M; Fain, S; Wenzel, S				Busacker, Ashley; Newell, John D., Jr.; Keefe, Thomas; Hoffman, Eric A.; Granroth, Janice Cook; Castro, Mario; Fain, Sean; Wenzel, Sally			A Multivariate Analysis of Risk Factors for the Air-Trapping Asthmatic Phenotype as Measured by Quantitative CT Analysis	CHEST			English	Article						air trapping; asthma; atopy; neutrophils; quantitative CT	OBSTRUCTIVE PULMONARY-DISEASE; VOLUME REDUCTION SURGERY; COMPUTED-TOMOGRAPHY; OBJECTIVE QUANTIFICATION; LUNG DENSITOMETRY; HUMAN NEUTROPHILS; FLOW OBSTRUCTION; ALLERGIC-ASTHMA; EMPHYSEMA; DENSITY	Background: Patients with severe asthma have increased physiologically measured air trapping; however, a study using CT measures of air trapping has not been performed. This study was designed to address two hypotheses: (1) air trapping measured by multidetector CT (MDCT) quantitative methodology would be a predictor of a more severe asthma phenotype; and (2) historical, clinical, allergic, or inflammatory risk factors could be identified via multivariate analysis. Methods: MDCT scanning of a subset of Severe Asthma Research Program subjects ,vas performed at functional residual capacity. Air trapping was defined as >= 9.66% of the lung tissue < - 850 Hounsfield units (HU). Subjects classified as having air trapping were then compared to subjects without air trapping on clinical and demographic factors using both univariate and multivariate statistical analyses. Results: Subjects with air trapping were significantly more likely to have a history of asthma-related hospitalizations, ICU visits, and/or mechanical ventilation.. Duration of asthma a (odds ratio [OR], 1.42; 95% confidence interval [CI], 1.08 to 1.87), history pneumonia (OR, 8.55; 95% CI, 2.07 to 35.26), high levels of airway neutrophils (OR, 8.67; 95% CI, 2.05 to 36.57), airflow obstruction (FEN(1)/FVC) OR, 1.61; 95% CI, 1.21 to 2.14], and atopy (OR, 11.54; 95% CI, 1.97 to 67.70) were identified as independent risk factors associated with the air-trapping phenotype. Conclusions: Quantitative CT-determined air trapping in asthmatic subjects identifies a group of individuals it high risk for severe disease. Several independent risk factors for the presence of this phenotype were identified: perhaps most interestingly, history of Pneumonia, neutrophilic inflammation, and atopy. (CHEST 2009; 135:48-56)	[Busacker, Ashley; Keefe, Thomas] Colorado State Univ, Dept Environm & Radiol Hlth Sci, Ft Collins, CO 80523 USA; [Newell, John D., Jr.] Natl Jewish Med & Res Ctr, Div Radiol, Denver, CO USA; [Hoffman, Eric A.; Granroth, Janice Cook] Univ Iowa, Dept Radiol, Carver Coll Med, Iowa City, IA 52242 USA; [Castro, Mario] Washington Univ, Sch Med, Div Pulm & Crit Care Med, St Louis, MO USA; [Fain, Sean] Univ Wisconsin, Madison, WI USA; [Wenzel, Sally] Univ Pittsburgh, Med Ctr, Div Pulm Allergy & Crit Care Med, Pittsburgh, PA USA	Busacker, A (reprint author), Colorado State Univ, Dept Environm & Radiol Hlth Sci, Campus Delivery 1681, Ft Collins, CO 80523 USA.	Ashley.Busacker@colostate.edu	Fain, Sean/K-4260-2016	Fain, Sean/0000-0001-5461-0646	National Institutes of Health [HL69149, HL64368, HL69349, HL69170, HL-69155, HL69174, HL69130, HL69167, HL69116, HL69174-05]	Grant support was provided by National Institutes of Health HL69149, HL64368, HL69349, HL69170, HL-69155, HL69174, HL69130. HL69167, HL69116, and HL69174-05.	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W., 2000, APPL LOGISTIC REGRES; Hu SY, 2001, IEEE T MED IMAGING, V20, P490, DOI 10.1109/42.929615; Huda W, 2007, AM J ROENTGENOL, V188, P540, DOI 10.2214/AJR.06.0101; Jain N, 2005, PEDIATR PULM, V40, P211, DOI 10.1002/ppul.20215; Johnson JL, 1998, RADIOLOGY, V206, P95; Lee JH, 2006, J ASTHMA, V43, P179, DOI 10.1080/02770900600566405; LILES WC, 1995, BLOOD, V86, P3181; Madani A, 2006, RADIOLOGY, V238, P1036, DOI 10.1148/radiol.2382042196; Martinez FJ, 2006, AM J RESP CRIT CARE, V173, P1326, DOI 10.1164/rccm.200510-1677OC; Mauad T, 2004, AM J RESP CRIT CARE, V170, P857, DOI 10.1164/rccm.200403-305OC; Mauad Thais, 1999, American Journal of Respiratory and Critical Care Medicine, V160, P968; Mergo PJ, 1998, AM J ROENTGENOL, V170, P1355; MINIATI M, 1995, AM J RESP CRIT CARE, V151, P1359; Miranda C, 2004, J ALLERGY CLIN IMMUN, V113, P101, DOI 10.1016/j.jaci.2003.10.041; Mitsunobu F, 2001, THORAX, V56, P851, DOI 10.1136/thorax.56.11.851; Moore WC, 2007, J ALLERGY CLIN IMMUN, V119, P405, DOI 10.1016/j.jaci.2006.11.639; MULLER NL, 1988, CHEST, V94, P782, DOI 10.1378/chest.94.4.782; Newell J D Jr, 2004, Eur Respir J, V23, P769, DOI 10.1183/09031936.04.00026504; NEWMAN KB, 1994, CHEST, V106, P105, DOI 10.1378/chest.106.1.105; Paganin F, 1996, AM J RESP CRIT CARE, V153, P110; Pham DN, 2003, ANN ALLERG ASTHMA IM, V90, P72; Sorkness RL, 2008, J APPL PHYSIOL, V104, P394, DOI 10.1152/japplphysiol.00329.2007; Szczeklik A, 2003, J ALLERGY CLIN IMMUN, V111, P913, DOI 10.1067/mai.2003.1487; Talbot TR, 2005, NEW ENGL J MED, V352, P2082, DOI 10.1056/NEJMoa044113; ten Brinke A, 2002, J ALLERGY CLIN IMMUN, V109, P621, DOI 10.1067/mai.2002.122458; van Beek EJR, 2008, CLIN CHEST MED, V29, P195, DOI 10.1016/j.ccm.2007.12.003; VIRCHOW JC, 1992, AM REV RESPIR DIS, V146, P604; Walamies MA, 1998, CLIN PHYSIOL, V18, P49; Wenzel SE, 1999, AM J RESP CRIT CARE, V160, P1001; Wenzel S, 2000, AM J RESP CRIT CARE, V162, P2341	51	125	130	0	2	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	JAN	2009	135	1					48	56		10.1378/chest.08-0049		9	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	392LN	WOS:000262304300011	18689585	
J	Prescott, SL; Smith, P; Tang, M; Palmer, DJ; Sinn, J; Huntley, SJ; Cormack, B; Heine, RG; Gibson, RA; Makrides, M				Prescott, Susan L.; Smith, Peter; Tang, Mimi; Palmer, Debra J.; Sinn, John; Huntley, Sophie J.; Cormack, Barbara; Heine, Ralf G.; Gibson, Robert A.; Makrides, Maria			The importance of early complementary feeding in the development of oral tolerance: Concerns and controversies	PEDIATRIC ALLERGY AND IMMUNOLOGY			English	Article						infant feeding; weaning practices; allergy prevention; growth and development	BREAST-FED INFANTS; PROSPECTIVE BIRTH COHORT; SOLID FOOD INTRODUCTION; ALLERGIC DISEASE; CHILDHOOD ECZEMA; CELIAC-DISEASE; NEW-ZEALAND; FOLLOW-UP; PREVENTION; RISK	Rising rates of food allergies in early childhood reflect increasing failure of early immune tolerance mechanisms. There is mounting concern that the current recommended practice of delaying complementary foods until 6 months of age may increase, rather than decrease, the risk of immune disorders. Tolerance to food allergens appears to be driven by regular, early exposure to these proteins during a 'critical early window' of development. Although the timing of this window is not clear in humans, current evidence suggests that this is most likely to be between 4 and 6 months of life and that delayed exposure beyond this period may increase the risk of food allergy, coeliac disease and islet cell autoimmunity. There is also evidence that other factors such as favourable colonization and continued breastfeeding promote tolerance and have protective effects during this period when complementary feeding is initiated. This discussion paper explores the basis for concern over the current recommendation to delay complementary foods as an approach to preventing allergic disease. It will also examine the growing case for introducing complementary foods from around 4 months of age and maintaining breastfeeding during this early feeding period, for at least 6 months if possible.	[Prescott, Susan L.] Univ Western Australia, Princess Margaret Hosp, Sch Paediat & Child Hlth Res, Perth, WA 6001, Australia; [Smith, Peter] Bond Univ, Sch Med, Gold Coast, Qld, Australia; [Tang, Mimi] Royal Childrens Hosp, Dept Allergy & Immunol, Parkville, Vic 3052, Australia; [Palmer, Debra J.; Makrides, Maria] Womens & Childrens Hlth Res Inst, Children Youth & Womens Hlth Serv, Adelaide, SA, Australia; [Sinn, John] Royal N Shore Hosp, Dept Neonatol, St Leonards, NSW 2065, Australia; [Huntley, Sophie J.] Flinders Univ S Australia, Dept Nutr & Dietet, Adelaide, SA, Australia; [Cormack, Barbara] Auckland City Hosp, Nutr Serv, Auckland, New Zealand; [Heine, Ralf G.] Royal Childrens Hosp, Dept Gastroenterol & Clin Nutr, Parkville, Vic 3052, Australia; [Gibson, Robert A.] Univ Adelaide, Sch Agr Food & Wine, Adelaide, SA, Australia	Prescott, SL (reprint author), Univ Western Australia, Princess Margaret Hosp, Sch Paediat & Child Hlth Res, POB D184, Perth, WA 6001, Australia.	sprescott@meddent.uwa.edu.au	Palmer, Debra /L-8554-2013; Makrides, Maria/B-6392-2014; Prescott, Susan/H-5665-2014	Makrides, Maria/0000-0003-3832-541X; Cormack, Barbara/0000-0003-2329-8287; Gibson, Robert/0000-0002-8750-525X			Arshad SH, 2007, J ALLERGY CLIN IMMUN, V119, P307, DOI 10.1016/j.jaci.2006.12.621; Baker SS, 2000, PEDIATRICS, V106, P346; Chan-Yeung M, 2005, J ALLERGY CLIN IMMUN, V116, P49, DOI 10.1016/j.jaci.2005.03.029; Chantry CJ, 2007, BREASTFEED MED, V2, P63, DOI 10.1089/bfm.2007.0002; Exl BM, 2000, EUR J NUTR, V39, P145, DOI 10.1007/s003940070018; FERGUSSON DM, 1990, PEDIATRICS, V86, P541; FERGUSSON DM, 1982, J EPIDEMIOL COMMUN H, V36, P118, DOI 10.1136/jech.36.2.118; Filipiak B, 2007, J PEDIATR-US, V151, P352, DOI 10.1016/j.jpeds.2007.05.01; Fiocchi A, 2006, ANN ALLERG ASTHMA IM, V97, P10; FORSYTH JS, 1993, BRIT MED J, V306, P1572; Halken S, 1996, PEDIATR ALLERGY IMMU, V7, P102, DOI 10.1111/j.1399-3038.1996.tb00407.x; Host A, 1999, ARCH DIS CHILD, V81, P80; Hourihane JO, 2007, J ALLERGY CLIN IMMUN, V119, P1197, DOI 10.1016/j.jaci.2006.12.670; Ivarsson A, 2002, AM J CLIN NUTR, V75, P914; KAJOSAARI M, 1983, ACTA PAEDIATR SCAND, V72, P411, DOI 10.1111/j.1651-2227.1983.tb09738.x; Kajosaari M, 1991, Adv Exp Med Biol, V310, P453; Kramer MS, 2004, ADV EXP MED BIOL, V554, P63; Kramer MS, 2000, ADV EXP MED BIOL, V478, P327; Lanigan JA, 2001, EUR J CLIN NUTR, V55, P309, DOI 10.1038/sj.ejcn.1601168; Mihrshahi S, 2007, CLIN EXP ALLERGY, V37, P671, DOI 10.1111/j.1365-2222.2007.02696.x; Munns C, 2006, MED J AUSTRALIA, V185, P268; Norris JM, 2005, JAMA-J AM MED ASSOC, V293, P2343, DOI 10.1001/jama.293.19.2343; Norris JM, 2003, JAMA-J AM MED ASSOC, V290, P1713, DOI 10.1001/jama.290.13.1713; POLOUS LM, 2007, J ALLERGY CLIN IMMUN, V120, P878; Poole JA, 2006, PEDIATRICS, V117, P2175, DOI 10.1542/peds.2005-1803; Prescott SL, 2005, MED J AUSTRALIA, V182, P464; Sicherer SH, 2003, J ALLERGY CLIN IMMUN, V112, P1203, DOI 10.1016/S0091-6749(03)02026-8; Skeaff SA, 2005, NUTRITION, V21, P325, DOI 10.1016/j.nut.2004.07.004; Sudo N, 1997, J IMMUNOL, V159, P1739; Tarini BA, 2006, ARCH PEDIAT ADOL MED, V160, P502, DOI 10.1001/archpedi.160.5.502; WALRAVENS PA, 1992, LANCET, V340, P683, DOI 10.1016/0140-6736(92)92229-9; *WHO DEP NUTR HLTH, 2001, OPT DUR EXCL BREASTF; ZEIGER R, 1995, J ALLERGY CLIN IMMUN, V96, P1179; Zutavern A, 2006, PEDIATRICS, V117, P401, DOI 10.1542/peds.2004-2521	34	125	132	5	21	WILEY-BLACKWELL	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0905-6157			PEDIAT ALLERG IMM-UK	Pediatr. Allergy Immunol.	AUG	2008	19	5					375	380		10.1111/j.1399-3038.2008.00718.x		6	Allergy; Immunology; Pediatrics	Allergy; Immunology; Pediatrics	325EI	WOS:000257570900001	18266825	
J	Liu, J; Ballaney, M; Al-Alem, U; Quan, C; Jin, X; Perera, F; Chen, LC; Miller, RL				Liu, Jinming; Ballaney, Manisha; Al-Alem, Umaima; Quan, Chunli; Jin, Ximei; Perera, Frederica; Chen, Lung-Chi; Miller, Rachel L.			Combined inhaled diesel exhaust particles and allergen exposure alter methylation of T helper genes and IgE production In vivo	TOXICOLOGICAL SCIENCES			English	Article						environmental exposure; respiratory sensitization; cytokines; inhalation toxicology; epigenetic modification.	IFN-GAMMA GENE; CELL DIFFERENTIATION; TH2 DIFFERENTIATION; AIR-POLLUTION; EXPRESSION; PROMOTER; CPG; DEMETHYLATION; TRANSCRIPTION; ENVIRONMENT	Changes in methylation of CpG sites at the interleukin (IL)-4 and interferon (IFN)-gamma promoters are associated with T helper (Th) 2 polarization in vitro. No previous studies have examined whether air pollution or allergen exposure alters methylation of these two genes in vivo. We hypothesized that diesel exhaust particles (DEP) would induce hypermethylation of the IFN-gamma promoter and hypomethylation of IL-4 in CD4(+) T cells among mice sensitized to the fungus allergen Aspergillus fumigatus. We also hypothesized that DEP-induced methylation changes would affect immunoglobulin (Ig) E regulation. BALB/c mice were exposed to a 3-week course of inhaled DEP exposure while undergoing intranasal sensitization to A. fumigatus. Purified DNA from splenic CD4(+) cells underwent bisulfite treatment, PCR amplification, and pyrosequencing. Sera IgE levels were compared with methylation levels at several CpG sites in the IL-4 and IFN-gamma promoter. Total IgE production was increased following intranasal sensitization A. fumigatus. IgE production was augmented further following combined exposure to A. fumigatus and DEP exposure. Inhaled DEP exposure and intranasal A. fumigatus induced hypermethylation at CpG(-45), CpG(-53), CpG(-205) sites of the IFN-gamma promoter and hypomethylation at CpG(-408) of the IL-4 promoter. Altered methylation of promoters of both genes was correlated significantly with changes in IgE levels. This study is the first to demonstrate that inhaled environmental exposures influence methylation of Th genes in vivo, supporting a new paradigm in asthma pathogenesis.	[Liu, Jinming; Ballaney, Manisha; Al-Alem, Umaima; Miller, Rachel L.] Columbia Univ Coll Phys & Surg, Dept Med, Div Pulm Allergy & Crit Care Med, New York, NY 10032 USA; [Quan, Chunli; Jin, Ximei; Chen, Lung-Chi] NYU, Tuxedo Pk, NY 10987 USA; [Perera, Frederica] Columbia Univ, Joseph L Mailman Sch Publ Hlth, New York, NY 10032 USA	Miller, RL (reprint author), Columbia Univ Coll Phys & Surg, Dept Med, Div Pulm Allergy & Crit Care Med, PH8C,630 W 168th St, New York, NY 10032 USA.	rlm14@columbia.edu	Cjem, Lung-Chi/H-5030-2012	Chen, Lung Chi/0000-0003-1154-2107	NIEHS NIH HHS [P30 ES000260, 1R21ES013063, ES00260, P01 ES009600, P01ES09600, R01 ES015495, R01ES015495, R21 ES013063, R21 ES013063-01, R21 ES013063-02, R21 ES013063-03]		Agarwal S, 1998, IMMUNITY, V9, P765, DOI 10.1016/S1074-7613(00)80642-1; Ansel KM, 2006, ANNU REV IMMUNOL, V24, P607, DOI 10.1146/annurev.immunol.23.021704.115821; Ansel KM, 2003, NAT IMMUNOL, V4, P616, DOI 10.1038/ni0703-616; Anway MD, 2005, SCIENCE, V308, P1466, DOI 10.1126/science.1108190; Belinsky SA, 2002, CARCINOGENESIS, V23, P335, DOI 10.1093/carcin/23.2.335; Bommel H, 2000, J ALLERGY CLIN IMMUN, V105, P796, DOI 10.1067/mai.2000.105124; Brauer M, 2002, AM J RESP CRIT CARE, V166, P1092, DOI 10.1164/rccm.200108-007OC; COMB M, 1990, NUCLEIC ACIDS RES, V18, P3975, DOI 10.1093/nar/18.13.3975; Dupont JM, 2004, ANAL BIOCHEM, V333, P119, DOI 10.1016/j.ab.2004.05.007; Fujieda S, 1998, AM J RESP CELL MOL, V19, P507; Gehring U, 2002, EUR RESPIR J, V19, P690, DOI 10.1183/09031936.02.01182001; Gilmour P.S., 2003, AM J PHYSIOL-LUNG C, V284, P533; Grunig G, 1997, J EXP MED, V185, P1089, DOI 10.1084/jem.185.6.1089; Jones B, 2006, EMBO J, V25, P2443, DOI 10.1038/sj.emboj.7601148; Kersh EN, 2006, J IMMUNOL, V176, P4083; Lee DU, 2002, IMMUNITY, V16, P649, DOI 10.1016/S1074-7613(02)00314-X; McDonald JD, 2004, AEROSOL SCI TECH, V38, P62, DOI 10.1080/02786820490247623; Miller RL, 1999, AM J PUBLIC HEALTH, V89, P819, DOI 10.2105/AJPH.89.6.819; MOSMANN TR, 1986, J IMMUNOL, V136, P2348; Padilla J, 2005, J IMMUNOL, V174, P8097; Thompson SL, 2001, TOXICOL LETT, V120, P143, DOI 10.1016/S0378-4274(01)00292-2; Tost J, 2007, NAT PROTOC, V2, P2265, DOI 10.1038/nprot.2007.314; Tykocinski LO, 2005, J BIOL CHEM, V280, P28177, DOI 10.1074/jbc.M502038200; VENN AJ, 2001, AM J RESP CRIT CARE, V164, P2217; Vickaryous N, 2005, REPROD FERT DEVELOP, V17, P335, DOI 10.1071/RD04133; White GP, 2002, J IMMUNOL, V168, P2820; White GP, 2006, PEDIATR ALLERGY IMMU, V17, P557, DOI 10.1111/j.1399-3038.2006.00465.x; Whitehead GS, 2003, AM J PHYSIOL-LUNG C, V285, pL32, DOI 10.1152/ajplung.00390.2002; Yano S, 2003, J IMMUNOL, V171, P2510; YE JP, 1994, J BIOL CHEM, V269, P25728; YOUNG HA, 1994, J IMMUNOL, V153, P3603; Zimmermann N, 2003, J CLIN INVEST, V111, P1863, DOI 10.1172/JCI200317912	32	125	135	0	10	OXFORD UNIV PRESS	OXFORD	GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND	1096-6080			TOXICOL SCI	Toxicol. Sci.	MAR	2008	102	1					76	81		10.1093/toxsci/kfm290		6	Toxicology	Toxicology	260PY	WOS:000253023600007	18042818	
J	Celedon, JC; Milton, DK; Ramsey, CD; Litonjua, AA; Ryan, L; Platts-Mills, TAE; Gold, DR				Celedon, Juan C.; Milton, Donald K.; Ramsey, Clare D.; Litonjua, Augusto A.; Ryan, Louise; Platts-Mills, Thomas A. E.; Gold, Diane R.			Exposure to dust mite allergen and endotoxin in early life and asthma and atopy in childhood	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						endotoxin; dust mite; wheeze; atopy; asthma	DAY-CARE ATTENDANCE; HOUSE-DUST; 1ST YEAR; LIMULUS ASSAY; P-I; CHILDREN; WHEEZE; RISK; HISTORY; INFANCY	Background: There has been no longitudinal study of the relation between concurrent exposure to dust mite allergen and endotoxin in early life and asthma and atopy at school age. Objectives: To examine the relation between exposure to dust mite allergen and endotoxin at age 2 to 3 months and asthma, wheeze, and atopy in high-risk children. Methods: Birth cohort study of 440 children with parental history of atopy in the Boston metropolitan area. Results: In multivariate analyses, early exposure to high levels of dust mite allergen (>= 10 mu g/g) was associated with increased risks of asthma at age 7 years (odds ratio [OR], 3.0; 95% CI, 1.1-7.9) and late-onset wheeze (OR, 5.0; 95% Cl, 1.5-16.4). Exposure to endotoxin levels above the lowest quartile at age 2 to 3 months was associated with reduced odds of atopy at school age (OR, 0.5; 95% CI, 0.2-0.9). In contrast with its inverse association with atopy, endotoxin exposure in early life was associated with an increased risk of any wheeze between ages I and 7 years that did not change significantly with time (hazard ratio for each quartile increment in endotoxin levels, 1.23; 95% CI, 1.07-1.43). Conclusion: Among children at risk of atopy, early exposure to high levels of dust mite allergen is associated with increased risks of asthma and late-onset wheeze. In these children, endotoxin exposure is associated with a reduced risk of atopy but an increased risk of wheeze. Clinical implications: Early endotoxin exposure may be a protective factor against atopy but a risk factor for wheeze in high-risk children.	Channing Labs, Boston, MA 02115 USA; Brigham & Womens Hosp, Div Pulm & Crit Care Med, Boston, MA 02115 USA; Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA; Univ Massachusetts, Sch Hlth & Environm, Dept Work Environm, Lowell, MA USA; Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA; Dana Farber Canc Inst, Boston, MA 02115 USA; Univ Virginia, Dept Med, Asthma & Allergy Ctr, Charlottesville, VA 22903 USA	Celedon, JC (reprint author), Channing Labs, 181 Longwood Ave, Boston, MA 02115 USA.	juan.celedon@channing.harvard.edu	Ryan, Louise/A-4562-2009; Milton, Donald/G-3286-2010; Mac Sharry, John/B-5509-2011	Ryan, Louise/0000-0001-5957-2490; Milton, Donald/0000-0002-0550-7834; Mac Sharry, John/0000-0002-9528-6261; Litonjua, Augusto/0000-0003-0422-5875	NHLBI NIH HHS [R01 HL073373, HL04370, HL073373, HL079966, K01 HL004370, R01 HL079966]; NIAID NIH HHS [R01 AI035786, R01 AI035786-10]; NIEHS NIH HHS [ES07036, ES35786, R01 ES007036, R56 ES007036]		Abraham JH, 2005, J ALLERGY CLIN IMMUN, V116, P431, DOI 10.1016/j.jaci.2005.05.015; Andersen P.K., 1982, ANN STAT, V10, P1110; Arshad SH, 2003, THORAX, V58, P489, DOI 10.1136/thorax.58.6.489; Bolte G, 2003, CLIN EXP ALLERGY, V33, P770, DOI 10.1046/j.1365-2222.2003.01665.x; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Brussee JE, 2005, J ALLERGY CLIN IMMUN, V115, P946, DOI 10.1016/j.jaci.2005.02.035; Celedon JC, 1999, PEDIATRICS, V104, P495, DOI 10.1542/peds.104.3.495; Celedon JC, 2004, CLIN EXP ALLERGY, V34, P1011, DOI 10.1111/j.1365-2222.2004.01994.x; Celedon JC, 2003, AM J RESP CRIT CARE, V167, P1239, DOI 10.1164/rccm.200209-1063OC; Celedon JC, 2002, PEDIATRICS, V110, DOI 10.1542/peds.110.6.e77; Chew GL, 1998, AM J RESP CRIT CARE, V157, P1536; Cullinan P, 2004, THORAX, V59, P855, DOI 10.1136/thx.2003.019877; FERRIS BG, 1978, AM REV RESPIR DIS, V118, P1; Gehring U, 2001, J ALLERGY CLIN IMMUN, V108, P847, DOI 10.1067/mai.2001.119026; Gehring U, 2002, AM J RESP CRIT CARE, V166, P939, DOI 10.1164/rccm.200203-256OC; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; Johnson CC, 2004, J ALLERGY CLIN IMMUN, V114, P105, DOI 10.1016/j.jaci.2004.04.007; Kitch BT, 2000, ENVIRON HEALTH PERSP, V108, P301, DOI 10.2307/3454347; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; LE JM, 1986, J IMMUNOL, V136, P4525; Litonjua AA, 2002, J ALLERGY CLIN IMMUN, V110, P736, DOI 10.1067/mai.2002.128948; Litonjua AA, 1998, AM J RESP CRIT CARE, V158, P176; LUCZYNSKA CM, 1989, J IMMUNOL METHODS, V118, P227, DOI 10.1016/0022-1759(89)90010-0; Marks GB, 2006, J ALLERGY CLIN IMMUN, V118, P53, DOI 10.1016/j.jaci.2006.04.004; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Michel O, 2003, J ENDOTOXIN RES, V9, P293, DOI 10.1179/096805103225002539; Milton DK, 1997, AM IND HYG ASSOC J, V58, P861; MILTON DK, 1992, ENVIRON RES, V57, P212, DOI 10.1016/S0013-9351(05)80081-7; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Perzanowski MS, 2006, J ALLERGY CLIN IMMUN, V117, P1082, DOI 10.1016/j.jaci.2005.12.1348; Phipatanakul W, 2004, PEDIATRICS, V114, P13, DOI 10.1542/peds.114.1.13; Polk S, 2004, AM J RESP CRIT CARE, V170, P273, DOI 10.1164/rccm.200310-1348OC; Raby BA, 2004, PEDIATRICS, V114, pE327, DOI 10.1542/peds.2003-0838-L; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; THERNEAU TM, 2000, MODELING SURVIVAL DA, P185; Thorne PS, 2005, AM J RESP CRIT CARE, V172, P1371, DOI 10.1164/rccm.200505-758OC; Wahl SM, 2004, CURR OPIN IMMUNOL, V16, P768, DOI 10.1016/j.coi.2004.09.006	38	125	131	1	4	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUL	2007	120	1					144	149		10.1016/j.jaci.2007.03.037		6	Allergy; Immunology	Allergy; Immunology	190NS	WOS:000248066400021	17507083	
J	Izbicki, G; Chavko, R; Banauch, GI; Weiden, MD; Berger, KI; Aldrich, TK; Hall, C; Kelly, KJ; Prezant, DJ				Izbicki, Gabriel; Chavko, Robert; Banauch, Gisela I.; Weiden, Michael D.; Berger, Kenneth I.; Aldrich, Thomas K.; Hall, Charles; Kelly, Kerry J.; Prezant, David J.			World Trade Center "sarcoid-like" granulomatous pulmonary disease in New York city fire department rescue workers	CHEST			English	Article						airway hyperreactivity; asthma; emergency medical services workers; firefighters; granulomatous pneumonitis; sarcoidosis; World Trade Center	BRONCHIAL HYPERREACTIVITY; AIRWAY HYPERREACTIVITY; CENTER COLLAPSE; RISK-FACTORS; CENTER SITE; FIREFIGHTERS; EXPOSURE; PNEUMONITIS; ASSOCIATION; INVOLVEMENT	Background: Previous reports suggest that sarcoidosis occurs with abnormally high frequency in firefighters. We sought to determine whether exposure to World Trade Center (WTC) "dust" during the collapse and rescue/recovery effort increased the incidence of sarcoidosis or "sarcoid-like" granulomatous pulmonary disease (SLGPD). Methods: During the 5 years after the WTC disaster, enrollees in the Fire Department of New York (FDNY) WTC monitoring and treatment programs who had chest radiograph findings suggestive of sarcoidosis underwent evaluation, including the following: chest CT imaging, pulmonary function, provocative challenge, and biopsy. Annual incidence rates were compared to the 15 years before the WTC disaster. Results: After WTC dust exposure, pathologic evidence consistent with new-onset sarcoidosis was found in 26 patients: all 26 patients had intrathoracic adenopathy, and 6 patients (23%) had extrathoracic disease. Thirteen patients were identified during the first year after WTC dust exposure (incidence rate, 86/100,000), and 13 patients were identified during the next 4 years (average annual incidence rate, 22/100,000; as compared to 15/100,000 during the 15 years before the WTC disaster). Eighteen of 26 patients (69%) had findings consistent with asthma. Eight of 21 patients (38%) agreeing to challenge testing had airway hyperreactivity (AHR), findings not seen in FDNY sarcoidosis patients before the WTC disaster. Conclusion: After the WTC disaster, the incidence of sarcoidosis or SLGPD was increased among FDNY rescue workers. This new information about the early onset of WTC-SLGPD and its association with asthma/AHR has important public health consequences for disease prevention, early detection, and treatment following environmental/occupational exposures.	New York City Fire Dept, Off Med Affairs, Brooklyn, NY 11201 USA; Montefiore Med Ctr, Albert Einstein Coll Med, Div Pulm, Bronx, NY 10467 USA; Shaare Zedek Med Ctr, Pulm Inst, IL-91000 Jerusalem, Israel; Ben Gurion Univ Negev, IL-84105 Beer Sheva, Israel; NYU, Coll Med, Div Pulm, New York, NY USA; Albert Einstein Coll Med, Bronx, NY 10467 USA	Prezant, DJ (reprint author), New York City Fire Dept, Off Med Affairs, Room 4w-1, Brooklyn, NY 11201 USA.	prezand@fdny.nyc.gov		Berger, Kenneth/0000-0003-4879-6071			American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P1299, DOI 10.1164/ajrccm/136.5.1299; American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P1285, DOI 10.1164/ajrccm/136.5.1285; Armbruster C, 1996, LANCET, V348, P690, DOI 10.1016/S0140-6736(05)65119-7; Banauch GI, 2005, CURR OPIN PULM MED, V11, P160, DOI 10.1097/01.mcp.0000151716.96241.0a; Banauch GI, 2003, AM J RESP CRIT CARE, V168, P54, DOI 10.1164/rccm.200211-1329OC; Banauch GI, 2006, AM J RESP CRIT CARE, V174, P312, DOI 10.1164/rccm.200511-1736OC; Barnard J, 2005, J OCCUP ENVIRON MED, V47, P226, DOI 10.1097/01.jom.0000155711.88781.91; Baughman RP, 2001, AM J RESP CRIT CARE, V164, P1885; BECHTEL JJ, 1981, AM REV RESPIR DIS, V124, P759; Crapo RO, 2000, AM J RESP CRIT CARE, V161, P309; DEPALMA A, 2006, NY TIMES        1026; Drent M, 2000, RESP MED, V94, P815, DOI 10.1053/rmed.2000.0827; Duval-Morin G, 2001, Rev Pneumol Clin, V57, P28; EDMONSTONE WM, 1998, THORAX, V43, P342; Gorham ED, 2004, CHEST, V126, P1431, DOI 10.1378/chest.126.5.1431; Hankinson JL, 1999, AM J RESP CRIT CARE, V159, P179; Herbert R, 2006, ENVIRON HEALTH PERSP, V114, P1853, DOI 10.1289/ehp.9592; Hunninghake GW, 1999, AM J RESP CRIT CARE, V160, P736; Judson MA, 1999, SARCOIDOSIS VASC DIF, V16, P75; Kajdasz DK, 2001, ANN EPIDEMIOL, V11, P111, DOI 10.1016/S1047-2797(00)00179-4; KERN DG, 1993, AM REV RESPIR DIS, V148, P974; Klimczak A, 2000, Pneumonol Alergol Pol, V68, P273; Kreider ME, 2005, CHEST, V128, P207, DOI 10.1378/chest.128.1.207; Lioy PJ, 2002, ENVIRON HEALTH PERSP, V110, P703; MACEIRA JMP, 1984, AM J CLIN PATHOL, V81, P563; Mann JM, 2005, AM J IND MED, V48, P225, DOI 10.1002/ajim.20196; MARCIAS S, 1994, SARCOIDOSIS, V11, P118; Meloni M, 1988, Recenti Prog Med, V79, P179; *NAT I OCC SAF HLT, 1997, MMWR-MORBID MORTAL W, V46, P539; Newman L S, 1998, Semin Respir Infect, V13, P212; Newman LS, 2004, AM J RESP CRIT CARE, V170, P1324, DOI 10.1164/rccm.200402-2490C; Nowak D, 1990, Pneumologie, V44 Suppl 1, P572; OHRN MB, 1995, RESPIRATION, V62, P136; OLAFSSON M, 1985, THORAX, V40, P51, DOI 10.1136/thx.40.1.51; PRESAS FM, 1986, ANN NY ACAD SCI, V465, P523, DOI 10.1111/j.1749-6632.1986.tb18529.x; Prezant DJ, 2002, NEW ENGL J MED, V347, P806, DOI 10.1056/NEJMoa021300; Prezant DJ, 1999, CHEST, V116, P1183, DOI 10.1378/chest.116.5.1183; Rafnsson V, 1998, OCCUP ENVIRON MED, V55, P657; Rom WN, 2002, AM J RESP CRIT CARE, V166, P797, DOI 10.1164/rccm.200206-576OC; Safirstein BH, 2003, CHEST, V123, P301, DOI 10.1378/chest.123.1.301; SCADDING JG, 1961, BRIT MED J, V4, P1165; SHAPIRO GG, 1989, PROVOCATIVE CHALLENG, P405; Shorr AF, 2001, CHEST, V120, P881, DOI 10.1378/chest.120.3.881; Williams W J, 1989, Sarcoidosis, V6, P111; WINTERBAUER RH, 1973, ANN INTERN MED, V78, P65	46	125	130	0	4	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	MAY	2007	131	5					1414	1423		10.1378/chest.06-2114		10	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	168SQ	WOS:000246544700024	17400664	
J	Eder, W; Klimecki, W; Yu, LZ; von Mutius, E; Riedler, J; Braun-Fahrlander, C; Nowak, D; Martinez, FD				Eder, W; Klimecki, W; Yu, LZ; von Mutius, E; Riedler, J; Braun-Fahrlander, C; Nowak, D; Martinez, FD		ALEX Study Team	Opposite effects of CD14/-260 on serum IgE levels in children raised in different environments	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						serium IgE; CD14/-260; microbial exposure; gene-environment interaction	PROMOTER POLYMORPHISM; CD14 PROMOTER; C-159T POLYMORPHISM; ENDOTOXIN LEVELS; MATTRESS DUST; SOLUBLE CD14; ASTHMA; GENE; ASSOCIATION; EXPOSURE	Background: Most complex diseases are the result of interactions between polymorphisms in the genome and environmental exposures. Objective: We sought to investigate the previously reported association between a polymorphism in the promoter region of CD14 (CD14/-260C -> T) and serum IgE levels in relation to the environment to which children are exposed. Methods: In 624 children living in 2 rural communities in Europe, we compared total and specific serum IgE levels between the genotypes of CD14/-260 in relation to exposure to animals and in relation to house dust endotoxin. Results: We found that the C allele of CD14/-260 was associated with higher levels of both total and specific serum IgE to aeroallergens in children with regular contact with pets, whereas an association in the opposite direction was found in children with regular contact with stable animals. This modifying effect of animal exposure was not explained by levels of house dust endotoxin. However, in children with high levels of house dust endotoxin, the C allele was associated with less specific IgE, independently from animal exposure. Conclusion: Because CD14 is a pattern recognition receptor for microbial molecules, the results suggest that the type and concentrations of such molecules present in the environment strongly determine the direction of the association between CD14/-260 and serum markers of atopy.	Univ Arizona, Arizona Resp Ctr, Innate Immun Program Genom Applicat, Tucson, AZ 85724 USA; Univ Munich, Dr von Hauner Childrens Hosp, Munich, Germany; Childrens Hosp, Salzburg, Austria; Univ Basel, Inst Social & Prevent Med, Basel, Switzerland; Univ Munich, Inst & Outpatient Clin Occupat & Environm Med, Munich, Germany	Martinez, FD (reprint author), Univ Arizona, Arizona Resp Ctr, Innate Immun Program Genom Applicat, 1501 N Campbell Ave,POB 245030, Tucson, AZ 85724 USA.	fernando@arc.arizona.edu		von Mutius, Erika/0000-0002-8893-4515	NHLBI NIH HHS [HL66800, HL67672]		AMELUNG PJ, 2000, AM J RESP CRIT CARE, V161, pA927; Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Dziarski R, 2003, CELL MOL LIFE SCI, V60, P1793, DOI 10.1007/s00018-003-3019-6; Eisenbarth SC, 2002, J EXP MED, V196, P1645, DOI 10.1084/jem.20021340; Gao PS, 1999, CLIN GENET, V56, P164; Gehring U, 2004, INDOOR AIR, V14, P284, DOI 10.1111/j.1600-0668.2004.00244.x; Gern JE, 2004, J ALLERGY CLIN IMMUN, V113, P307, DOI 10.1016/j.jaci.2003.11.017; Heumann D, 2002, CLIN CHIM ACTA, V323, P59, DOI 10.1016/S0009-8981(02)00180-8; Hirschhorn JN, 2002, GENET MED, V4, P45, DOI 10.1097/00125817-200203000-00002; HOLLANDER A, 1993, AM IND HYG ASSOC J, V54, P647, DOI 10.1202/0002-8894(1993)054<0647:IAEITA>2.0.CO;2; Kabesch M, 2004, ALLERGY, V59, P520, DOI 10.1111/j.1398-9995.2004.00439.x; Karhukorpi J, 2002, CLIN EXP IMMUNOL, V128, P326, DOI 10.1046/j.1365-2249.2002.01837.x; Kedda MA, 2005, THORAX, V60, P211, DOI 10.1136/thx.2004.028449; Koppelman GH, 2001, AM J RESP CRIT CARE, V163, P965; Leung TF, 2003, PEDIATR ALLERGY IMMU, V14, P255, DOI 10.1034/j.1399-3038.2003.00048.x; LeVan TD, 2001, J IMMUNOL, V167, P5838; LEWONTIN RC, 1994, AM J HUM GENET, V26, P400; Lotz S, 2004, J LEUKOCYTE BIOL, V75, P467, DOI 10.1189/jlb.0803360; Obana N, 2002, SCAND J GASTROENTERO, V37, P699, DOI 10.1080/00365520212504; Ober C, 2000, AM J HUM GENET, V67, P1154, DOI 10.1016/S0002-9297(07)62946-2; Remold SK, 2004, NAT GENET, V36, P423, DOI 10.1038/ng1324; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; SCHLICHTING CD, 1998, PHENOTYPIC EVOLUTION, P51; Schmitz G, 2002, CURR OPIN LIPIDOL, V13, P513, DOI 10.1097/00041433-200210000-00007; Sengler C, 2003, CLIN EXP ALLERGY, V33, P166, DOI 10.1046/j.1365-2222.2003.01549.x; van Strien RT, 2004, J ALLERGY CLIN IMMUN, V113, P860, DOI 10.1016/j.jaci.2004.01.078; Vercelli D, 2003, CLIN EXP ALLERGY, V33, P153, DOI 10.1046/j.1365-2222.2003.01606.x; Waser M, 2004, CLIN EXP ALLERGY, V34, P389, DOI 10.1111/j.1365-2222.2004.01873.x; 2003, LANCET, V361, P357	30	125	126	0	8	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	SEP	2005	116	3					601	607		10.1016/j.jaci.2005.05.003		7	Allergy; Immunology	Allergy; Immunology	017IE	WOS:000235686500020	16159630	
J	Leigh, R; Ellis, R; Wattlie, JN; Hirota, JA; Matthaei, KI; Foster, PS; O'Byrne, PM; Inman, MD				Leigh, R; Ellis, R; Wattlie, JN; Hirota, JA; Matthaei, KI; Foster, PS; O'Byrne, PM; Inman, MD			Type 2 cytokines in the pathogenesis of sustained airway dysfunction and airway remodeling in mice	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						allergic disease; asthma; interleukin-4; interleukin-5; interleukin-13	OBSTRUCTIVE PULMONARY-DISEASE; ALLERGEN-INDUCED INCREASE; MURINE MODEL; CHRONIC ASTHMA; MILD ASTHMA; DEFICIENT MICE; LUNG DAMAGE; MOUSE MODEL; INFLAMMATION; HYPERREACTIVITY	The mechanisms underlying airway hyperresponsiveness remain unclear, although airway inflammation and remodeling likely play important roles. We have observed sustained airway hyperreactivity and airway remodeling occurring in mice after chronic allergen exposure and persisting beyond resolution of allergen-induced inflammation. The aim of this study was to delineate mechanisms involved in allergen-induced airway hyperreactivity and airway remodeling and to examine evidence for a causal association between airway remodeling and sustained airway hyperreactivity. Wild-type (WT) and interleukin (IL)-4-, IL-5-, and IL-13-deficient (-/-) mice were sensitized and studied 4 weeks after chronic allergen exposure. By measuring airway responsiveness and airway morphometry, we demonstrated that WT mice developed sustained airway hyperreactivity and aspects of airway remodeling after chronic allergen exposure. Both IL-4(-/-) and IL-13(-/-) mice were protected from developing sustained airway hyperreactivity and aspects of airway remodeling. In contrast, IL-5(-/-) mice developed sustained airway hyperreactivity and aspects of airway remodeling similar to that seen in WT mice. Our results confirm that IL-4 and IL-13, but not IL-5, are critical for the development of sustained airway hyperreactivity and airway remodeling after allergen exposure.	McMaster Univ, Dept Med, Firestone Inst Resp Hlth, Hamilton, ON L8S 4L8, Canada; Australian Natl Univ, John Curtin Sch Med Res, Div Mol Biosci, Canberra, ACT 2601, Australia	Inman, MD (reprint author), St Josephs Healthcare, Firestone Inst Resp Hlth, 50 Charlton Ave E, Hamilton, ON L8N 4A6, Canada.	inmanma@mcmaster.ca	Klaus, Matthaei/D-8691-2011; Foster, Paul/G-5057-2013	O'Byrne, Paul/0000-0003-0979-281X			Boulet L P, 1998, Can Respir J, V5, P16; Boulet L P, 2000, Can Respir J, V7, P239; Boulet LP, 2000, AM J RESP CRIT CARE, V162, P1308; Bradford-Hill A., 1965, P ROY SOC MED, P295; BRUSASCO V, 1990, J APPL PHYSIOL, V69, P2209; BRUSSELLE GG, 1994, CLIN EXP ALLERGY, V24, P73, DOI 10.1111/j.1365-2222.1994.tb00920.x; Busse W, 1999, AM J RESP CRIT CARE, V160, P1035; Busse WW, 2001, NEW ENGL J MED, V344, P350; CARROLL N, 1993, AM REV RESPIR DIS, V147, P405; Cockcroft DW, 1997, ASTHMA, P1253; CORRIGAN CJ, 1992, IMMUNOL TODAY, V13, P501, DOI 10.1016/0167-5699(92)90026-4; Corry DB, 1996, J EXP MED, V183, P109, DOI 10.1084/jem.183.1.109; Corry DB, 1998, MOL MED, V4, P344; DJUKANOVIC R, 1990, AM REV RESPIR DIS, V142, P434; DJUKANOVIC R, 1992, AM REV RESPIR DIS, V145, P669; Elias JA, 1999, J CLIN INVEST, V104, P1001, DOI 10.1172/JCI8124; Ellis R, 2003, LAB INVEST, V83, P1285, DOI 10.1097/01.LAB.0000087586.25982.B5; Foster PS, 2000, LAB INVEST, V80, P655; Foster PS, 2002, LAB INVEST, V82, P455; Foster PS, 1996, J EXP MED, V183, P195, DOI 10.1084/jem.183.1.195; Gavett SH, 1997, AM J PHYSIOL-LUNG C, V272, pL253; Grunig G, 1998, SCIENCE, V282, P2261, DOI 10.1126/science.282.5397.2261; Hamelmann E, 1997, AM J RESP CELL MOL, V16, P674; HEGELE RG, 1995, AM J RESP CRIT CARE, V151, P1659; Hogaboam CM, 2000, AM J PATHOL, V156, P723, DOI 10.1016/S0002-9440(10)64775-X; Hogan SP, 1997, J CLIN INVEST, V99, P1329, DOI 10.1172/JCI119292; Inman MD, 1999, AM J RESP CELL MOL, V21, P473; James AL, 2002, AM J RESP CRIT CARE, V166, P1590, DOI 10.1164/rccm.2108069; JEFFERY PK, 1989, AM REV RESPIR DIS, V140, P1745; JEFFERY PK, 1992, AM REV RESPIR DIS, V145, P890; Kopf M, 1996, IMMUNITY, V4, P15, DOI 10.1016/S1074-7613(00)80294-0; Kumar RK, 2002, CLIN EXP ALLERGY, V32, P1104, DOI 10.1046/j.1365-2222.2002.01420.x; Kuperman DA, 2002, NAT MED, V8, P885, DOI 10.1038/nm734; KUWANO K, 1993, AM REV RESPIR DIS, V148, P1220; LAMBERT RK, 1993, J APPL PHYSIOL, V74, P2771; Laprise C, 1999, EUR RESPIR J, V14, P63, DOI 10.1034/j.1399-3003.1999.14a12.x; Leigh R, 2002, AM J RESP CELL MOL, V27, P526, DOI 10.1165/rcmb.2002-0048OC; LEIGH R, 2003, AM J RESP CRIT CARE, V167, pA494; McKenzie GJ, 1998, IMMUNITY, V9, P423, DOI 10.1016/S1074-7613(00)80625-1; Palmans E, 2000, AM J RESP CRIT CARE, V161, P627; Persson CGA, 2002, AM J RESP CRIT CARE, V166, P6, DOI 10.1164/rccm.2204001; RENZ H, 1992, J ALLERGY CLIN IMMUN, V89, P1127, DOI 10.1016/0091-6749(92)90296-E; ROCHE WR, 1989, LANCET, V1, P520; Sont JK, 1999, AM J RESP CRIT CARE, V159, P1043; Tanaka H, 2001, INFLAMM RES, V50, P616, DOI 10.1007/PL00000243; Temelkovski J, 1998, THORAX, V53, P849; Trifilieff A, 2000, AM J PHYSIOL-LUNG C, V279, pL1120; Vignola AM, 2000, J ALLERGY CLIN IMMUN, V105, P1041, DOI 10.1067/mai.2000.107195; Volgyesi GA, 2000, J APPL PHYSIOL, V89, P413; WARDLAW AJ, 1988, AM REV RESPIR DIS, V137, P62; Webb DC, 2000, J IMMUNOL, V165, P108; WIGGS BR, 1992, AM REV RESPIR DIS, V145, P1251; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; Yang M, 2001, AM J RESP CELL MOL, V25, P522; Zhu Z, 2002, J IMMUNOL, V168, P2953; Zhu Zhou, 1999, Journal of Clinical Investigation, V103, P779, DOI 10.1172/JCI5909	56	125	133	0	0	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	APR 1	2004	169	7					860	867		10.1164/rccm.200305-706OC		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	807IB	WOS:000220494100019	14701709	
J	Zhang, JF; Smith, KR				Zhang, JF; Smith, KR			Indoor air pollution: a global health concern	BRITISH MEDICAL BULLETIN			English	Article							VOLATILE ORGANIC-COMPOUNDS; ENVIRONMENTAL TOBACCO-SMOKE; SICK BUILDING SYNDROME; DEVELOPING-COUNTRIES; PASSIVE SMOKING; PARENTAL SMOKING; LUNG-CANCER; EXPOSURE; CHILDREN; OZONE	Indoor air pollution is ubiquitous, and takes many forms, ranging from smoke emitted from solid fuel combustion, especially in households in developing countries, to complex mixtures of volatile and semi-volatile organic compounds present in modern buildings. This paper reviews sources of, and health risks associated with, various indoor chemical pollutants, from a historical and global perspective. Health effects are presented for individual compounds or pollutant mixtures based on real-world exposure situations. Health risks from indoor air pollution are likely to be greatest in cities in developing countries, especially where risks associated with solid fuel combustion coincide with risk associated with modern buildings. Everyday exposure to multiple chemicals, most of which are present indoors, may contribute to increasing prevalence of asthma, autism, childhood cancer, medically unexplained symptoms, and perhaps other illnesses. Given that tobacco consumption and synthetic chemical usage will not be declining at least in the near future, concerns about indoor air pollution may be expected to remain.	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J	van Ree, R				van Ree, R			Carbohydrate epitopes and their relevance for the diagnosis and treatment of allergic diseases	INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY			English	Review						IgE; carbohydrate epitopes; recombinant allergens; diagnostic tests; immunotherapy	YEAST PICHIA-PASTORIS; BASOPHIL HISTAMINE-RELEASE; AEGYPTI SALIVARY ALLERGEN; O-GLYCOSYLATION CODES; IGE CROSS-REACTIVITY; DUST MITE ALLERGEN; RECOMBINANT ALLERGENS; ESCHERICHIA-COLI; BIRCH POLLEN; DENDRITIC CELLS	Allergenicity of plant and invertebrate N-glycans has been shown to be caused by the presence of two typical nonmammalian substitutions: an alpha(1,3)-fucose linked to the proximal N-acetylglucosamine and a beta(1,2)-xylose linked to the core mannose. IgE antibodies against these carbohydrate structures are induced upon exposure to pollen or after insect stings, and result in extensive cross-reactivity to plant and invertebrate foods. These cross-reactive IgE antibodies have been shown to possess variable degrees of biological activity, but have never been convincingly shown to induce clinical food allergy. The most likely explanation for this lack of clinical relevance has to be sought in a combination of epitope valency and antibody affinity. In diagnostic tests, these antibodies are at the basis of many false-positive test results for food allergy. Recombinant technologies offer the possibility to produce allergens that do not carry IgE-binding glycans. Whether their absence or presence is of importance for the application of recombinant allergens in immunotherapy is still largely unknown. Copyright (C) 2002 S. Karger AG, Basel.	Sanquin Res, CLB, Dept Immunopathol, NL-1006 AD Amsterdam, Netherlands	van Ree, R (reprint author), Sanquin Res, CLB, Dept Immunopathol, POB 9190, NL-1006 AD Amsterdam, Netherlands.						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Arch. Allergy Immunol.	NOV	2002	129	3					189	197		10.1159/000066770		9	Allergy; Immunology	Allergy; Immunology	625EC	WOS:000179803100002	12444315	
J	Gilliland, FD; Gauderman, WJ; Vora, H; Rappaport, E; Dubeau, L				Gilliland, FD; Gauderman, WJ; Vora, H; Rappaport, E; Dubeau, L			Effects of Glutathione-S-Transferase M1, T1, and P1 on childhood lung function growth	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						glutathione-S-transferase; FEV; children; polymorphism; growth	OBSTRUCTIVE PULMONARY-DISEASE; SOUTHERN CALIFORNIA COMMUNITIES; OXIDATIVE STRESS; AIR-POLLUTION; RESPIRATORY SYMPTOMS; MATERNAL SMOKING; SUPERGENE FAMILY; DIFFERING LEVELS; BIRTH-WEIGHT; CHILDREN	The effects of glutathione-S-transferase (GST) M1, GSTT1, and GSTP1 genotypes on lung function growth were investigated in 1,940 children enrolled in the Children's Health Study as fourth graders (aged 8-11 years) in two cohorts during 1993 and 1996 and were followed annually over a 4-year period. Genotypes for GSTM1 and GSTT1 and GSTP1 codon 105variants (ile105 and val105)were determined using DNA from buccal cell specimens. We used two-level regression models to estimate the effects of GSTM1, GSTT1, and GSTP1 genotypes on the adjusted annual average lung function growth. GSTM1 null was associated with deficits in annual growth rates for FVC (-0.21%; 95% confidence interval [Cl], -0.40, 0.03) and FEV1, (-0.27%; 95% Cl, -0.50, -0.04). Children who were homozygous for the GSTP1 val105 allele had slower lung function growth (FVC -0.35%; 95% Cl, -0.62, -0.07; and FEV1 -0.34%; 95% Cl, -0.68, 0.00) than children with one or more ile105 alleles. Children with asthma who were homozygous for the GSTP1 val105 allele had substantially larger deficits in FVC, IFEVI, and maximal mid-expiratory flow than children without asthma. The deficits in FVC and FEV1 growth associated with both GSTM1 null and the GSTP1 val105 allele were largest and were statistically significant in non-Hispanic white children. We conclude that GSTM1 and GSTP1 genotypes are associated with lung function growth in school children.	Univ So Calif, Dept Prevent Med, Keck Sch Med, Los Angeles, CA 90033 USA; Univ So Calif, Dept Pathol, Keck Sch Med, Los Angeles, CA 90033 USA	Gilliland, FD (reprint author), Univ So Calif, Dept Prevent Med, Keck Sch Med, 1540 Alcazar St,CHP 236, Los Angeles, CA 90033 USA.				NHLBI NIH HHS [5 R01HL61768]; NIEHS NIH HHS [2P30ES07048, 1P50ES09581]		American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P1285, DOI 10.1164/ajrccm/136.5.1285; Baranova H, 1997, HUM GENET, V99, P822, DOI 10.1007/s004390050455; BARKER DJP, 1991, BRIT MED J, V303, P671; Barnes PJ, 2000, NEW ENGL J MED, V343, P269, DOI 10.1056/NEJM200007273430407; Berhane K, 2000, AM J RESP CRIT CARE, V162, P1723; BURROWS B, 1980, AM REV RESPIR DIS, V122, P813; Chen Y, 1999, THORAX, V54, P818; Chen Y, 1999, GENET EPIDEMIOL, V16, P95, DOI 10.1002/(SICI)1098-2272(1999)16:1<95::AID-GEPI8>3.3.CO;2-Y; Cook DG, 1998, THORAX, V53, P884; Dezateux C, 1997, BRIT MED BULL, V53, P40; EBIKRYSTON KL, 1988, J CLIN EPIDEMIOL, V41, P251, DOI 10.1016/0895-4356(88)90129-1; Forsberg L, 2001, ARCH BIOCHEM BIOPHYS, V389, P84, DOI 10.1006/abbi.2001.2295; Fryer AA, 2000, AM J RESP CRIT CARE, V161, P1437; Garte S, 2001, CANCER EPIDEM BIOMAR, V10, P1239; Gauderman WJ, 2000, AM J RESP CRIT CARE, V162, P1383; Geisler SA, 2001, AM J EPIDEMIOL, V154, P95, DOI 10.1093/aje/154.2.95; Gilliland FD, 2000, THORAX, V55, P271, DOI 10.1136/thorax.55.4.271; Gilliland FD, 1999, ENVIRON HEALTH PERSP, V107, P403; GOLD DR, 1989, AM REV RESPIR DIS, V140, P877; Greene LS, 1999, NUTRITION, V15, P899, DOI 10.1016/S0899-9007(99)00209-9; Harrison DJ, 1997, HUM EXP TOXICOL, V16, P356; Hayes JD, 1995, CRIT REV BIOCHEM MOL, V30, P445, DOI 10.3109/10409239509083491; HAYES JD, 1995, FREE RADICAL RES, V22, P193, DOI 10.3109/10715769509147539; Hayes JD, 2000, PHARMACOLOGY, V61, P154, DOI 10.1159/000028396; Hemmingsen A, 2001, Respir Res, V2, P255, DOI 10.1186/rr64; Hole DJ, 1996, BRIT MED J, V313, P711; Ishii T, 1999, THORAX, V54, P693; KAUFFMANN F, 1989, AM J EPIDEMIOL, V129, P1289; Koyama H, 1998, THORAX, V53, pS10; MacNee W, 2000, CHEST, V117, p303S, DOI 10.1378/chest.117.5_suppl_1.303S-a; Peterhans E, 1997, J NUTR, V127, pS962; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; Peters JM, 1999, AM J RESP CRIT CARE, V159, P768; Sandford AJ, 2001, AM J RESP CRIT CARE, V163, P469; Sandford AJ, 2000, CLIN CHEST MED, V21, P633, DOI 10.1016/S0272-5231(05)70173-8; SAS Institute, 2001, SAS STAT US GUID VER; Schunemann HJ, 1997, AM J EPIDEMIOL, V146, P939; Schwarz KB, 1996, FREE RADICAL BIO MED, V21, P641, DOI 10.1016/0891-5849(96)00131-1; SHAHEEN SO, 1994, AM J RESP CRIT CARE, V149, P616; SHAHEEN SO, 1995, AM J RESP CRIT CARE, V151, P1649; SHERRILL DL, 1991, AM REV RESPIR DIS, V144, P17; SILVERMAN EK, 2001, FOUND S, V234, P45; Strange RC, 2001, MUTAT RES-FUND MOL M, V482, P21, DOI 10.1016/S0027-5107(01)00206-8; Szefler S, 2000, NEW ENGL J MED, V343, P1054; TAGER IB, 1988, AM REV RESPIR DIS, V138, P837; TAGER IB, 1983, NEW ENGL J MED, V309, P699, DOI 10.1056/NEJM198309223091204; Wjst M, 1998, PEDIATR ALLERGY IMMU, V9, P80, DOI 10.1111/j.1399-3038.1998.tb00308.x; WOODHOUSE G, 1995, MLN USERS GUIDE	48	125	127	0	2	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	SEP 1	2002	166	5					710	716		10.1164/rccm.2112065		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	588ZZ	WOS:000177734100018	12204870	
J	Mannino, DM; Homa, DM; Redd, SC				Mannino, DM; Homa, DM; Redd, SC			Involuntary smoking and asthma severity in children - Data from the Third National Health and Nutrition Examination Survey	CHEST			English	Article						asthma; children; tobacco smoke pollution	ENVIRONMENTAL TOBACCO-SMOKE; PASSIVE SMOKING; PARENTAL SMOKING; RESPIRATORY HEALTH; CHILDHOOD ASTHMA; UNITED-STATES; US POPULATION; EXPOSURE; COTININE	Study objectives: We sought to determine the indicators of asthma severity among children in the United States with high and low levels of tobacco smoke exposure. Design: Cross-sectional study. Setting: Nationally representative survey of participants in the Third National Health and Nutrition Examination Survey (from 1988 to 1994). Participants. Five hundred twenty-three children with physician-diagnosed asthma. Measurements and results: We stratified the study participants into tertiles on the basis of serum levels of cotinine (a metabolite of nicotine that indicates tobacco smoke exposure). We used logistic and linear regression modeling, adjusting for known covariates, to determine the effect of high environmental tobacco smoke exposure on the following outcomes: asthma severity (determined using reported symptom and respiratory illness frequency); lung function; physician P visits; and school absence. Among our study sample, 78.6% of children had mild asthma, 6.8% of children bad moderate asthma, and 14.6% of children had severe asthma. Asthmatic children with high levels of smoke exposure, compared with those with low levels of exposure, were more likely to have moderate or severe asthma (odds ratio, 2.7 95% confidence interval [CI], 1.1 to 6.8) and decreased lung function, with a mean FEV1 decrement of 213 mL or 8.1% (95% CI, -14.7 to - 3.5). Conclusions: Involuntary smoke exposure is associated with increased asthma severity and worsened lung function in a nationally representative group of US children with asthma.	CDCP, Natl Ctr Environm Hlth, Div Environm Hazards & Hlth Effects, Air Pollut & Resp Hlth Branch, Atlanta, GA 30333 USA	Mannino, DM (reprint author), CDCP, Natl Ctr Environm Hlth, Div Environm Hazards & Hlth Effects, Air Pollut & Resp Hlth Branch, 1600 Clifton Rd,MS E-17, Atlanta, GA 30333 USA.			Mannino, David/0000-0003-3646-7828			Abulhosn RS, 1997, ARCH PEDIAT ADOL MED, V151, P135; AZIZI BHO, 1990, PEDIATR PULM, V9, P24, DOI 10.1002/ppul.1950090106; Benowitz NL, 1996, EPIDEMIOL REV, V18, P188; CHILMONCZYK BA, 1993, NEW ENGL J MED, V328, P1665, DOI 10.1056/NEJM199306103282303; Cook DG, 1999, THORAX, V54, P357; Cunningham J, 1996, AM J RESP CRIT CARE, V153, P218; Eggleston PA, 1998, PEDIATRICS, V101, P349, DOI 10.1542/peds.101.3.349; EVANS D, 1987, AM REV RESPIR DIS, V135, P567; Fielder HMP, 1999, ARCH DIS CHILD, V80, P253; FORASTIERE F, 1992, INT J EPIDEMIOL, V21, P66, DOI 10.1093/ije/21.1.66; Gergen PJ, 1998, PEDIATRICS, V101, part. no., DOI 10.1542/peds.101.2.e8; Halterman JS, 2000, PEDIATRICS, V105, P272; Hankinson JL, 1999, AM J RESP CRIT CARE, V159, P179; INFANTERIVARD C, 1993, AM J EPIDEMIOL, V137, P834; Kohler E, 1999, HUM EXP TOXICOL, V18, P212, DOI 10.1191/096032799678839932; Mannino DM, 1998, MMWR-MORBID MORTAL W, V47, P1; Mannino DM, 2001, ARCH PEDIAT ADOL MED, V155, P36; MURRAY AB, 1988, CHEST, V94, P701, DOI 10.1378/chest.94.4.701; National Center for Health Statistics, 1994, VITAL HLTH STAT, V1, P1; Oddoze C, 1999, CLIN CHEM, V45, P505; Osborne ML, 1999, CHEST, V115, P85, DOI 10.1378/chest.115.1.85; Pirkle JL, 1996, JAMA-J AM MED ASSOC, V275, P1233; *SAS I, 1990, SAS VERS 6; SCHULMAN R, 2002, BUCUVALAS RES ASTHMA; Shah B., 1996, SUDAAN USERS MANUAL; SHEFFER AL, 1993, MED CARE, V31, pMS20; SHERRILL DL, 1992, AM REV RESPIR DIS, V145, P1136; Strachan DP, 1998, THORAX, V53, P204; [Anonymous], 1987, AM REV RESP DIS, V136, P1285	29	125	127	0	1	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	AUG	2002	122	2					409	415		10.1378/chest.122.2.409		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	584CJ	WOS:000177449400009	12171810	
J	Zanobetti, A; Schwartz, J; Gold, D				Zanobetti, A; Schwartz, J; Gold, D			Are there sensitive subgroups for the effects of airborne particles?	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						effect modification; hospital admissions; particulate air pollution	PARTICULATE AIR-POLLUTION; CLINICAL COMORBIDITY INDEX; EMERGENCY ROOM VISITS; FLY-ASH PARTICLES; HOSPITAL ADMISSIONS; TIME-SERIES; RESPIRATORY-DISEASE; ADMINISTRATIVE DATA; EUROPEAN CITIES; APHEA PROJECT	Recent studies have shown that particulate air pollution is a risk factor for hospitalization for heart and lung disease; however, little is known about what subpopulations are most sensitive to this pollutant. We analyzed Medicare hospital admissions for heart disease, chronic obstructive pulmonary disorders (COPD) and pneumonia in Chicago, Cook County, Illinois, between 1985 and 1994. We examined whether previous admissions or secondary diagnoses for selected conditions predisposed persons to having a greater risk from air pollution. We also considered effect modification by age, sex, and race. We found that the air-pollution-associated increase in hospital admissions for cardiovascular diseases was almost doubled in subjects with concurrent respiratory infections. The risk was also increased by a previous admission for conduction disorders. For COPD and pneumonia admissions, diagnosis of conduction disorders or dysrhythmias increased the risk of particulate matter < 10 mu m in aerodynamic diameter (PM10)-associated admissions. Persons with asthma had twice the risk of a PM10-associated pneumonia admission and persons with heart failure had twice the risk of PM10-induced COPD admissions. The PM10 effect did not vary by sex, age, and race. These results suggest that patients with acute respiratory infections or defects in the electrical control of the heart are a risk group for particulate matter effects.	Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Environm Epidemiol Program, Boston, MA 02115 USA; Harvard Univ, Sch Med, Dept Med, Channing Lab, Boston, MA USA; Brigham & Womens Hosp, Boston, MA 02115 USA	Zanobetti, A (reprint author), Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Environm Epidemiol Program, 665 Huntington Ave, Boston, MA 02115 USA.				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J., 2000, 91 HLTH EFF I; Gold DR, 2000, CIRCULATION, V101, P1267; GOLESKI JJ, 1996, AM J RESP CRIT CARE, V153, pA15; Gordon T, 1998, TOXICOL LETT, V96-7, P285, DOI 10.1016/S0378-4274(98)00084-8; Hallstrom AP, 1996, CIRCULATION, V93, P2019; HAMADA K, 1999, AM J RESP CRIT CAR A, V28; Hastie T, 1990, GEN ADDITIVE MODELS; Hoek G, 1999, EPIDEMIOLOGY, V10, pS177; Katsouyanni K, 1997, BMJ-BRIT MED J, V314, P1658; KODAVENTI UP, 1998, AM J RESP CRIT CARE, V157, pA260; Lambert AL, 1999, AM J RESP CRIT CARE, V159, pA26; Liao DP, 1999, ENVIRON HEALTH PERSP, V107, P521, DOI 10.2307/3434393; Librero J, 1999, J CLIN EPIDEMIOL, V52, P171, DOI 10.1016/S0895-4356(98)00160-7; MALENKA DJ, 1994, J CLIN EPIDEMIOL, V47, P1027, DOI 10.1016/0895-4356(94)90118-X; Matsui K, 1996, J GEN INTERN MED, V11, P262, DOI 10.1007/BF02598265; MONANE M, 1996, ARCH NEUROL-CHICAGO, V53, P848; National Research Council, 1998, RES PRIOR AIRB PART; NEHLS GJ, 1973, JAPCA J AIR WASTE MA, V23, P180; Norris G, 1999, ENVIRON HEALTH PERSP, V107, P489, DOI 10.2307/3434632; Peters A, 1999, EPIDEMIOLOGY, V10, pS177; Peters A, 2000, EPIDEMIOLOGY, V11, P11, DOI 10.1097/00001648-200001000-00005; Peters A, 1997, LANCET, V349, P1582, DOI 10.1016/S0140-6736(97)01211-7; Pope CA, 1999, AM HEART J, V138, P890, DOI 10.1016/S0002-8703(99)70014-1; POPE CA, 1991, AM REV RESPIR DIS, V144, P668; POPE CA, 1989, AM J PUBLIC HEALTH, V79, P623, DOI 10.2105/AJPH.79.5.623; POPE CA, 1995, INHAL TOXICOL, V7, P1, DOI 10.3109/08958379509014267; ROMANO PS, 1993, J CLIN EPIDEMIOL, V46, P1075, DOI 10.1016/0895-4356(93)90103-8; Rossi G, 1999, ARCH ENVIRON HEALTH, V54, P158; SALDIVA PHN, 1995, ARCH ENVIRON HEALTH, V50, P159; Salvi S, 1999, AM J RESP CRIT CARE, V159, P702; Samet J. M., 1995, PARTICULATE AIR POLL; Schwartz J, 1999, EPIDEMIOLOGY, V10, P17, DOI 10.1097/00001648-199901000-00005; Schwartz J, 2000, EPIDEMIOLOGY, V11, P320, DOI 10.1097/00001648-200005000-00016; SCHWARTZ J, 1994, ARCH ENVIRON HEALTH, V49, P366; SCHWARTZ J, 1995, THORAX, V50, P531, DOI 10.1136/thx.50.5.531; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; SCHWARTZ J, 1994, ENVIRON RES, V64, P36, DOI 10.1006/enrs.1994.1005; SCHWARTZ J, 1994, AM J RESP CRIT CARE, V150, P648; SCHWARTZ J, 1992, AM REV RESPIR DIS, V145, P600; SCHWARTZ J, 1994, AM J EPIDEMIOL, V139, P589; SCHWARTZ J, 1994, ENVIRON RES, V64, P26, DOI 10.1006/enrs.1994.1004; Schwartz J, 1997, EPIDEMIOLOGY, V8, P371, DOI 10.1097/00001648-199707000-00004; SCHWARTZ J, 1994, INT BIOM SOC 17 INT, P55; Sunyer J, 2000, AM J EPIDEMIOL, V151, P50; TAN WC, 1997, AM J RESP CRIT CARE, V155, P1441; THURSTON GD, 1994, ENVIRON RES, V65, P271, DOI 10.1006/enrs.1994.1037; Watkinson WP, 1998, TOXICOL SCI, V41, P209, DOI 10.1093/toxsci/41.2.209; WATKINSON WP, 1998, AM J RESP CRIT CARE, V157, pA150; Zeger SL, 2000, ENVIRON HEALTH PERSP, V108, P419, DOI 10.2307/3454382; ZELIKOFF JT, 1999, P 3 C PART AIR POLL	64	125	138	3	12	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	SEP	2000	108	9					841	845		10.1289/ehp.00108841		5	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	360BW	WOS:000089647400021	11017888	
J	Kankaanranta, H; Lindsay, MA; Giembycz, MA; Zhang, XZ; Moilanen, E; Barnes, PJ				Kankaanranta, H; Lindsay, MA; Giembycz, MA; Zhang, XZ; Moilanen, E; Barnes, PJ			Delayed eosinophil apoptosis in asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						albuterol; apoptosis; asthma; eosinophil; fenoterol; GM-CSF; IL-5; salmeterol	HUMAN-BLOOD EOSINOPHILS; PROGRAMMED CELL-DEATH; IN-VITRO; GM-CSF; SURVIVAL; MACROPHAGES; ALBUTEROL; AGONISTS; PROLONG; IL-5	Background: Eosinophilic inflammation of the airways is a key characteristic of asthma, A defect in apoptosis might contribute to the chronic tissue eosinophilia associated with asthma. Objective: Our purpose was to examine whether the rate of apoptosis differs between peripheral blood eosinophils from asthmatic patients and healthy volunteers, Methods: Peripheral blood was obtained from volunteers with asthma and from control volunteers. Eosinophils were isolated by CD16-negative selection to >99% purity and were cultured for 48 hours, The number of apoptotic eosinophils in the culture was assessed by flow cytometric analysis of relative DNA content in propidium iodide-stained cells. Eosinophil apoptosis is expressed as apoptosis index (number of apoptotic cells/total number of cells). Results: Eosinophils From asthmatic patients not taking steroid medication survived longer (apoptosis index 0.25) than those of healthy control subjects (apoptosis index 0.40, P < .05). In contrast, the rate of apoptosis in eosinophils from patients concurrently taking steroids (apoptosis index 0.46) is higher than that of those not using steroids (P < .01) and not different from that of healthy subjects. To assess whether endogenous IL-3, IL-5, and CM-CSF production contributes to the delayed eosinophil apoptosis, the effects of the corresponding neutralizing antibodies were studied on eosinophil longevity. Neutralization of GM-CSF, but not of IL-3 or IL-5, increased slightly but significantly (P < .01) the rate of apoptosis in eosinophils obtained from patients with asthma, To assess whether beta(2)-agonist medication could contribute to the observed differences, we determined the in vitro effects of albuterol, Fenoterol, and salmeterol on eosinophil apoptosis, All beta(2)-agonists inhibited eosinophil apoptosis by 12% to 19%, A possibility existed that a prior in vivo exposure to IL-5, GM-CSF, or beta(2)-agonists would explain the observed difference. To study this, eosinophils were incubated with GM-CSF, IL-5, and albuterol for 2 to 3 hours, followed by washout of the added compounds, and were subsequently cultured for 48 hours. However, an exposure to GM-CSF (7 pmol/L) or IL-5 (10 pmol/L) for 15 to 180 minutes was not a sufficient signal to prevent eosinophil apoptosis, In contrast, exposure to albuterol (100 nmol/L) for 120 minutes was sufficient to induce a significant (P < .05) decrease in eosinophil apoptosis, Conclusions: The results suggest that eosinophil apoptosis is delayed in asthma, This delay may be partly explained by production of GM-CSF, The in vitro effects of beta(2)-agonists suggest that beta(2)-agonist use might contribute to the prolonged eosinophil survival through inhibition of apoptosis and thus may worsen eosinophilia in asthmatic patients, Use of inhaled glucocorticoids seems to totally reverse the delayed eosinophil apoptosis in asthma.	Univ London Imperial Coll Sci Technol & Med, Sch Med, Natl Heart & Lung Inst, Dept Thorac Med, London SW3 6LY, England; Tampere Univ, Sch Med, FIN-33101 Tampere, Finland; Tampere Univ Hosp, Dept Resp Med, Tampere, Finland; Tampere Univ Hosp, Dept Clin Chem, FIN-33521 Tampere, Finland	Barnes, PJ (reprint author), Univ London Imperial Coll Sci Technol & Med, Sch Med, Natl Heart & Lung Inst, Dept Thorac Med, Dovehouse St, London SW3 6LY, England.			Kankaanranta, Hannu/0000-0001-5258-0906			Adkins JC, 1997, DRUGS, V54, P331, DOI 10.2165/00003495-199754020-00011; Druilhe A, 1998, AM J RESP CELL MOL, V19, P747; Evans DJ, 1996, EUR RESPIR J, V9, P703, DOI 10.1183/09031936.96.09040703; Gauvreau GM, 1997, AM J RESP CRIT CARE, V156, P1738; Giembycz MA, 1999, PHARMACOL REV, V51, P213; Hallsworth MP, 1996, BRIT J PHARMACOL, V117, P79; HANSEL TT, 1989, J IMMUNOL METHODS, V122, P97, DOI 10.1016/0022-1759(89)90339-6; Haslett C, 1997, BRIT MED BULL, V53, P669; HOCHHAUS G, 1992, INT J CLIN PHARM TH, V30, P342; JONKMAN JHG, 1986, ARZNEIMITTEL-FORSCH, V36-2, P1133; Kankaanranta H, 1999, J PHARMACOL EXP THER, V290, P621; KANKAANRANTA H, IN PRESS METHODS MOL; MURPHY S, 1997, NIH PUBL; NICOLETTI I, 1991, J IMMUNOL METHODS, V139, P271, DOI 10.1016/0022-1759(91)90198-O; Nielson CP, 1998, AM J RESP CRIT CARE, V157, P184; Peacock CD, 1999, J ALLERGY CLIN IMMUN, V104, P153, DOI 10.1016/S0091-6749(99)70127-2; POWELL ML, 1986, J CLIN PHARMACOL, V26, P643; SCHLEIMER RP, 1994, J ALLERGY CLIN IMMUN, V94, P1202, DOI 10.1016/0091-6749(94)90333-6; Simon HU, 1997, J IMMUNOL, V158, P3902; SPITZER WO, 1992, NEW ENGL J MED, V326, P501, DOI 10.1056/NEJM199202203260801; SPRY CJF, 1993, IMMUNOPHARMACOLOGY E, P1; STERN M, 1992, J IMMUNOL, V148, P3543; TAI PC, 1991, CLIN EXP IMMUNOL, V85, P312; Vignola AM, 1999, J ALLERGY CLIN IMMUN, V103, P563, DOI 10.1016/S0091-6749(99)70225-3; Walsh GM, 1997, CLIN EXP ALLERGY, V27, P482, DOI 10.1046/j.1365-2222.1997.d01-532.x; Wedi B, 1997, J ALLERGY CLIN IMMUN, V100, P536; Woolley KL, 1996, AM J RESP CRIT CARE, V154, P237; YAMAGUCHI Y, 1991, BLOOD, V78, P2542	28	125	140	0	0	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUL	2000	106	1	1				77	83				7	Allergy; Immunology	Allergy; Immunology	337ZH	WOS:000088393300011	10887309	
J	Kurup, VP; Shen, HD; Banerjee, B				Kurup, VP; Shen, HD; Banerjee, B			Respiratory fungal allergy	MICROBES AND INFECTION			English	Review						fungal allergens; IgE antibody; recombinant allergens; ELISA; Western blot	ASPERGILLUS-FUMIGATUS ALLERGENS; ALKALINE SERINE PROTEINASE; MAJOR ALLERGEN; BRONCHOPULMONARY ASPERGILLOSIS; CLADOSPORIUM-HERBARUM; MOLD ALLERGY; ALTERNARIA-ALTERNATA; PENICILLIUM-CITRINUM; ASTHMATIC-PATIENTS; IMMUNE-RESPONSES	Fungal allergy including allergic rhinitis, conjunctivitis, bronchial asthma, and allergic bronchopulmonary mycoses results from exposure to spores. In this review are have dealt with the common allergenic fungi and allergens, immunopathogenesis, diagnostic assays, and the possible control of allergy in the future based on epitope-specific immunotherapy and vaccination. (C) 2000 Editions scientifiques et medicales Elsevier SAS.	Med Coll Wisconsin, Dept Pediat, Milwaukee, WI 53226 USA; Vet Affairs Med Ctr, Milwaukee, WI USA; Vet Gen Hosp Taipei, Dept Med Res & Educ, Taipei 11217, Taiwan	Kurup, VP (reprint author), Med Coll Wisconsin, Dept Pediat, 8701 Watertown Plank Rd, Milwaukee, WI 53226 USA.				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JUL	2000	2	9					1101	1110		10.1016/S1286-4579(00)01264-8		10	Immunology; Infectious Diseases; Microbiology	Immunology; Infectious Diseases; Microbiology	353PG	WOS:000089284200013	10967290	
J	Bisgaard, H; Simpson, A; Palmer, CNA; Bonnelykke, K; Mclean, I; Mukhopadhyay, S; Pipper, CB; Halkjaer, LB; Lipworth, B; Hankinson, J; Woodcock, A; Custovic, A				Bisgaard, Hans; Simpson, Angela; Palmer, Colin N. A.; Bonnelykke, Klaus; Mclean, Irwin; Mukhopadhyay, Somnath; Pipper, Christian B.; Halkjaer, Liselotte B.; Lipworth, Brian; Hankinson, Jenny; Woodcock, Ashley; Custovic, Adnan			Gene-environment interaction in the onset of eczema in infancy: Filaggrin loss-of-function mutations enhanced by neonatal cat exposure	PLOS MEDICINE			English	Article							ATOPIC-DERMATITIS; ICHTHYOSIS VULGARIS; CHILDHOOD ASTHMA; BIRTH COHORT; RISK; LIFE; SENSITIZATION; PREDISPOSE; DIAGNOSIS; ALLERGENS	Background Loss-of-function variants in the gene encoding filaggrin (FLG) are major determinants of eczema. We hypothesized that weakening of the physical barrier in FLG-deficient individuals may potentiate the effect of environmental exposures. Therefore, we investigated whether there is an interaction between FLG loss-of-function mutations with environmental exposures ( pets and dust mites) in relation to the development of eczema. Methods and Findings We used data obtained in early life in a high-risk birth cohort in Denmark and replicated the findings in an unselected birth cohort in the United Kingdom. Primary outcome was age of onset of eczema; environmental exposures included pet ownership and mite and pet allergen levels. In Copenhagen (n = 379), FLG mutation increased the risk of eczema during the first year of life ( hazard ratio [HR] 2.26, 95% confidence interval [CI] 1.27-4.00, p = 0.005), with a further increase in risk related to cat exposure at birth amongst children with FLG mutation (HR 11.11, 95% CI 3.79-32.60, p < 0.0001); dog exposure was moderately protective (HR 0.49, 95% CI 0.24-1.01, p = 0.05), but not related to FLG genotype. In Manchester ( n 503) an independent and significant association of the development of eczema by age 12 mo with FLG genotype was confirmed (HR 1.95, 95% CI 1.13-3.36, p = 0.02). In addition, the risk increased because of the interaction of cat ownership at birth and FLG genotype (HR 3.82, 95% CI 1.35-10.81, p = 0.01), with no significant effect of the interaction with dog ownership (HR 0.59, 95% CI 0.16-2.20, p = 0.43). Mite-allergen had no effects in either cohort. The observed effects were independent of sensitisation. Conclusions We have demonstrated a significant interaction between FLG loss-of-function main mutations (501x and 2282del4) and cat ownership at birth on the development of early-life eczema in two independent birth cohorts. Our data suggest that cat but not dog ownership substantially increases the risk of eczema within the first year of life in children with FLG loss-of-function variants, but not amongst those without. FLG-deficient individuals may need to avoid cats but not dogs in early life.	[Bisgaard, Hans; Bonnelykke, Klaus; Pipper, Christian B.; Halkjaer, Liselotte B.] Univ Hosp Gentofte, Danish Paediat Asthma Ctr, Copenhagen, Denmark; [Simpson, Angela; Hankinson, Jenny; Woodcock, Ashley; Custovic, Adnan] Univ S Manchester Hosp, Natl Hlth Serv Fdn Trust, Sch Translat Med, Manchester M20 8LR, Lancs, England; [Palmer, Colin N. A.; Mclean, Irwin] Univ Dundee, Populat Pharmacogenet Grp, Biomed Res Ctr, Ninewells Hosp, Dundee, Scotland; [Palmer, Colin N. A.; Mclean, Irwin] Univ Dundee, Sch Med, Dundee, Scotland; [Mukhopadhyay, Somnath] Royal Alexandra Hosp Children, Brighton, E Sussex, England; [Mukhopadhyay, Somnath] Sussex Med Sch, Brighton, E Sussex, England; [Lipworth, Brian] Univ Dundee, Asthma & Allergy Res Grp, Div Med & Therapeut, Ninewells Hosp, Dundee DD1 4HN, Scotland; [Lipworth, Brian] Univ Dundee, Sch Med, Dundee DD1 4HN, Scotland	Bisgaard, H (reprint author), Univ Hosp Gentofte, Danish Paediat Asthma Ctr, Copenhagen, Denmark.	bisgaard@copsac.com	Palmer, Colin/C-7053-2008; Kronow, Joern/B-1054-2011; Custovic, Adnan/A-2435-2012; Bisgaard, Hans/N-4761-2016	Palmer, Colin/0000-0002-6415-6560; Custovic, Adnan/0000-0001-5218-7071; Bisgaard, Hans/0000-0003-4131-7592; McLean, William Henry Irwin/0000-0001-5539-5757; Woodcock, Ashley/0000-0002-5428-8578; Simpson, Angela/0000-0003-2733-6666; Pipper, Christian Bressen/0000-0003-0261-616X			Almqvist C, 2003, J ALLERGY CLIN IMMUN, V111, P800, DOI 10.1067/mai.2003.1334; Bisgaard H, 2004, ANN ALLERG ASTHMA IM, V93, P381; Bisgaard H, 2006, NEW ENGL J MED, V354, P1998, DOI 10.1056/NEJMoa054692; Bisgaard H, 2007, NEW ENGL J MED, V357, P1487, DOI 10.1056/NEJMoa052632; Custovic A, 2002, PEDIATR ALLERGY IMMU, V13, P32, DOI 10.1034/j.1399-3038.13.s.15.3.x; Custovic Adnan, 2004, Pediatr Pulmonol Suppl, V26, P12; Halkjaer LB, 2006, ARCH DERMATOL, V142, P561, DOI 10.1001/archderm.142.5.561; HANIFIN JM, 1980, ACTA DERM-VENEREOL, P44; Kim JL, 2005, INDOOR AIR, V15, P170, DOI 10.1111/j.1600-0668.2005.00334.x; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; Marenholz I, 2006, J ALLERGY CLIN IMMUN, V118, P866, DOI 10.1016/j.jaci.2006.07.026; Ownby DR, 2002, JAMA-J AM MED ASSOC, V288, P963, DOI 10.1001/jama.288.8.963; Paganelli R, 1998, ALLERGY, V53, P763; Palmer CNA, 2006, NAT GENET, V38, P441, DOI 10.1038/ng1767; Sandilands A, 2007, NAT GENET, V39, P650, DOI 10.1038/ng2020; Smith FJD, 2006, NAT GENET, V38, P337, DOI 10.1038/ng1743; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; Weidinger S, 2006, J ALLERGY CLIN IMMUN, V118, P214, DOI 10.1016/j.jaci.2006.05.004; Weidinger S, 2007, J INVEST DERMATOL, V127, P724, DOI 10.1038/sj.jid.5700630; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P397, DOI 10.1111/j.1365-2133.1994.tb08531.x	20	124	125	2	12	PUBLIC LIBRARY SCIENCE	SAN FRANCISCO	1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA	1549-1676			PLOS MED	PLos Med.	JUN	2008	5	6							e131	10.1371/journal.pmed.0050131		6	Medicine, General & Internal	General & Internal Medicine	318QB	WOS:000257105600018	18578563	
J	Krishnamoorthy, N; Oriss, TB; Paglia, M; Fei, MJ; Yarlagadda, M; Vanhaesebroeck, B; Ray, A; Ray, P				Krishnamoorthy, Nandini; Oriss, Timothy B.; Paglia, Melissa; Fei, Mingjian; Yarlagadda, Manohar; Vanhaesebroeck, Bart; Ray, Anuradha; Ray, Prabir			Activation of c-Kit in dendritic cells regulates T helper cell differentiation and allergic asthma	NATURE MEDICINE			English	Article							TRANSCRIPTION FACTOR GATA-3; BOUND TGF-BETA; AIRWAY INFLAMMATION; MAST-CELLS; PROTO-ONCOGENE; CHOLERA-TOXIN; GROWTH-FACTOR; W-LOCUS; EXPRESSION; RESPONSES	Dendritic cells ( DCs) are integral to the differentiation of T helper cells into T helper type 1 T(H)1, T(H)2 and T(H)17 subsets. Interleukin-6 ( IL-6) plays an important part in regulating these three arms of the immune response by limiting the T(H)1 response and promoting the T(H)2 and T(H)17 responses. In this study, we investigated pathways in DCs that promote IL-6 production. We show that the allergen house dust mite ( HDM) or the mucosal adjuvant cholera toxin promotes cell surface expression of c-Kit and its ligand, stem cell factor ( SCF), on DCs. This dual upregulation of c-Kit and SCF results in sustained signaling downstream of c-Kit, promoting IL-6 secretion. Intranasal administration of antigen into c-Kit-mutant mice or neutralization of IL-6 in cultures established from the lung-draining lymph nodes of immunized wild-type mice blunted the T(H)2 and T(H)17 responses. DCs lacking functional c-Kit or those unable to express membrane-bound SCF secreted lower amounts of IL- 6 in response to HDM or cholera toxin. DCs expressing nonfunctional c-Kit were unable to induce a robust T(H)2 or T(H)17 response and elicited diminished allergic airway inflammation when adoptively transferred into mice. Expression of the Notch ligand Jagged-2, which has been associated with T(H)2 differentiation, was blunted in DCs from c-Kit-mutant mice. c-Kit upregulation was specifically induced by T(H)2- and T(H)17-skewing stimuli, as the T(H)1-inducing adjuvant, CpG oligodeoxynucleotide, did not promote either c-Kit or Jagged-2 expression. DCs generated from mice expressing a catalytically inactive form of the p110 delta subunit of phosphatidylinositol-3 ( PI3) kinase ( p110(D910A)) secreted lower amounts of IL-6 upon stimulation with cholera toxin. Collectively, these results highlight the importance of the c-Kit-PI3 kinase-IL-6 signaling axis in DCs in regulating T cell responses.	[Krishnamoorthy, Nandini; Oriss, Timothy B.; Paglia, Melissa; Fei, Mingjian; Yarlagadda, Manohar; Ray, Anuradha; Ray, Prabir] Univ Pittsburgh, Sch Med, Div Pulm Allergy & Crit Care Med, Dept Med, Pittsburgh, PA 15213 USA; [Krishnamoorthy, Nandini; Ray, Anuradha; Ray, Prabir] Univ Pittsburgh, Sch Med, Dept Immunol, Pittsburgh, PA 15213 USA; [Vanhaesebroeck, Bart] Queen Mary Univ London, Ctr Cell Signalling, Inst Canc, Barts & London Queen Marys Sch Med & Dent, London EC1M 6BQ, England	Ray, A (reprint author), Univ Pittsburgh, Sch Med, Div Pulm Allergy & Crit Care Med, Dept Med, 3459 5th Ave, Pittsburgh, PA 15213 USA.	raya@pitt.edu; rayp@pitt.edu			NHLBI NIH HHS [HL 060207, HL 069810, HL 077430, HL 084932, P50 HL084932, R01 HL060207, R01 HL069810, R01 HL077430]; NIAID NIH HHS [AI 048927, R01 AI048927]		Acosta-Rodriguez EV, 2007, NAT IMMUNOL, V8, P942, DOI 10.1038/ni1496; Ali K, 2004, NATURE, V431, P1007, DOI 10.1038/nature02991; Amsen D, 2004, CELL, V117, P515, DOI 10.1016/S0092-8674(04)00451-9; Amsen D, 2007, IMMUNITY, V27, P89, DOI 10.1016/j.immuni.2007.05.021; Arora M, 2006, P NATL ACAD SCI USA, V103, P7777, DOI 10.1073/pnas.0508492103; Bagley KC, 2002, INFECT IMMUN, V70, P5533, DOI 10.1128/IAI.70.10.5533-5539.2002; Bettelli E, 2006, NATURE, V441, P235, DOI 10.1038/nature04753; Borg C, 2004, J CLIN INVEST, V114, P379, DOI 10.1172/jci20041102; BRANNAN CI, 1991, P NATL ACAD SCI USA, V88, P4671, DOI 10.1073/pnas.88.11.4671; Braun MC, 1999, J EXP MED, V189, P541, DOI 10.1084/jem.189.3.541; Cates EC, 2004, J IMMUNOL, V173, P6384; CHABOT B, 1988, NATURE, V335, P88, DOI 10.1038/335088a0; Chatterjea D, 2005, IMMUNOL LETT, V99, P122, DOI 10.1016/j.imlet.2005.02.015; Chen L, 2006, J IMMUNOL, V177, P2373; Crackower MA, 2002, CELL, V110, P737, DOI 10.1016/S0092-8674(02)00969-8; Das J, 2001, NAT IMMUNOL, V2, P45, DOI 10.1038/83158; Dodge IL, 2003, J IMMUNOL, V170, P4457; Fang TC, 2007, IMMUNITY, V27, P100, DOI 10.1016/j.immuni.2007.04.018; FLANAGAN JG, 1991, CELL, V64, P1025, DOI 10.1016/0092-8674(91)90326-T; FRANKE TF, 1995, CELL, V81, P727, DOI 10.1016/0092-8674(95)90534-0; Fukao T, 2002, NAT IMMUNOL, V3, P875, DOI 10.1038/ni825; GEISSLER EN, 1988, CELL, V55, P185, DOI 10.1016/0092-8674(88)90020-7; Happel KI, 2005, J EXP MED, V202, P761, DOI 10.1084/jem.20050193; Harrington LE, 2005, NAT IMMUNOL, V6, P1123, DOI 10.1038/ni1254; Houde C, 2004, BLOOD, V104, P3697, DOI 10.1182/blood-2003-12-4114; Illi S, 2006, LANCET, V368, P763, DOI 10.1016/S0140-6736(06)69286-6; Ivanov II, 2006, CELL, V126, P1121, DOI 10.1016/j.cell.2006.07.035; Kalesnikoff J, 2006, P NATL ACAD SCI USA, V103, P2659, DOI 10.1073/pnas.0511191103; Kapsenberg ML, 2003, NAT REV IMMUNOL, V3, P984, DOI 10.1038/nri1246; Kolls JK, 2004, IMMUNITY, V21, P467, DOI 10.1016/j.immuni.2004.08.018; Lukacs NW, 1996, J IMMUNOL, V156, P3945; Luty WH, 2007, J IMMUNOL, V179, P819; MIYAZAWA K, 1995, BLOOD, V85, P641; Okkenhaug K, 2002, SCIENCE, V297, P1031; Oriss TB, 2005, J IMMUNOL, V174, P854; Ostroukhova M, 2006, J CLIN INVEST, V116, P996, DOI 10.1127/JCI26490; Ostroukhova M, 2004, J CLIN INVEST, V114, P28, DOI 10.1172/JC1200420509; Park H, 2005, NAT IMMUNOL, V6, P1133, DOI 10.1038/ni1261; QIU F, 1988, EMBO J, V7, P1003; Rincon M, 1997, J EXP MED, V185, P461, DOI 10.1084/jem.185.3.461; Schulz O, 2000, IMMUNITY, V13, P453, DOI 10.1016/S1074-7613(00)00045-5; SERVE H, 1995, EMBO J, V14, P473; Szabo SJ, 2000, CELL, V100, P655, DOI 10.1016/S0092-8674(00)80702-3; Veldhoen M, 2006, IMMUNITY, V24, P179, DOI 10.1016/j.immuni.2006.01.001; YEE NS, 1993, J BIOL CHEM, V268, P14189; Zhang DH, 1999, IMMUNITY, V11, P473, DOI 10.1016/S1074-7613(00)80122-3; Zhang DH, 1997, J BIOL CHEM, V272, P21597, DOI 10.1074/jbc.272.34.21597; Zheng WP, 1997, CELL, V89, P587, DOI 10.1016/S0092-8674(00)80240-8; Zhu JF, 2004, NAT IMMUNOL, V5, P1157, DOI 10.1038/ni1128	49	124	127	0	10	NATURE PUBLISHING GROUP	NEW YORK	75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA	1078-8956			NAT MED	Nat. Med.	MAY	2008	14	5					565	573		10.1038/nm1766		9	Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental	Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine	298IQ	WOS:000255681800038	18454155	
J	Bousquet, J; Annesi-Maesano, I; Carat, F; Leger, D; Rugina, M; Pribil, C; El Hasnaoui, A; Chanal, I				Bousquet, J; Annesi-Maesano, I; Carat, F; Leger, D; Rugina, M; Pribil, C; El Hasnaoui, A; Chanal, I			Characteristics of intermittent and persistent allergic rhinitis: DREAMS study group	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergy; ARIA; asthma; rhinitis	SKIN PRICK TESTS; PERENNIAL RHINITIS; ASTHMA; POPULATION; POLLEN; VALIDATION; ADULTS; ATOPY; QUESTIONNAIRE; HETEROGENEITY	Background In the Allergic Rhinitis and its Impact on Asthma ( ARIA) classification, intermittent and persistent rhinitis were proposed to replace seasonal and perennial allergic rhinitis (AR). Aim To better understand the ARIA classification of rhinitis. Methods A cross-sectional study was carried out in 591 patients consulting ENT or allergy specialists for AR and 502 control subjects. The diagnosis of AR was based on a score for allergic rhinitis (SFAR) >= 7. Patients were classified according to the four ARIA classes ( mild intermittent, mild persistent, moderate/severe intermittent and moderate/severe persistent). Allergen sensitization (skin prick tests (SPTs) or specific IgE) and co- morbidities were examined according to the ARIA classes. Results Ten percent of patients had mild intermittent rhinitis, 14% mild persistent rhinitis, 17% moderate/severe intermittent rhinitis and 59% moderate/severe persistent rhinitis. Most patients with intermittent rhinitis had a pollen sensitivity, but 5% had a single house dust mite (HDM) sensitization. Over 50% of patients with persistent rhinitis were allergic to pollens or HDM. Asthma was present in 24% of rhinitis patients and in only 2% of the control population ( P < 0.0001). Patients with moderate/severe persistent rhinitis had the highest asthma prevalence (33%). Discussion Intermittent and persistent rhinitis are not synonymous of seasonal and perennial rhinitis. Most patients consulting specialists have severe rhinitis. Asthma prevalence increases with duration and severity of rhinitis supporting the ARIA major recommendation that patients with persistent rhinitis should be evaluated for asthma.	CHU Montpellier, Clin Malad Resp, Hop Arnaud de Villeneuve, F-34295 Montpellier, France; INSERM U454, Montpellier, France; INSERM U472, Villejuif, France; Hop Cochin, F-75674 Paris, France; Hop Hotel Dieu, Paris, France; Hop Intercommunal Creteil, Creteil, France; GSK, Marly Le Roi, France	Bousquet, J (reprint author), CHU Montpellier, Clin Malad Resp, Hop Arnaud de Villeneuve, F-34295 Montpellier, France.	jean.bousquet@wanadoo.fr	Annesi-Maesano, Isabella/D-9173-2016				Annesi-Maesano I, 2002, ALLERGY, V57, P107, DOI 10.1034/j.1398-9995.2002.1o3170.x; BOUSQUET J, 1993, ALLERGY, V48, P183, DOI 10.1111/j.1398-9995.1993.tb00711.x; BOUSQUET J, 1982, ALLERGY, V37, P397, DOI 10.1111/j.1398-9995.1982.tb02318.x; BOUSQUET J, 2002, ALLERGY, V58, P841; Bousquet J, 2001, J ALLERGY CLIN IMMUN, V108, P147, DOI DOI 10.1067/MAI.2001.118891; BraunFahrlander C, 1997, PEDIATR ALLERGY IMMU, V8, P75, DOI 10.1111/j.1399-3038.1997.tb00147.x; BUCHOLTZ GA, 1991, ANN ALLERGY, V67, P534; CHANAL I, 1988, J ALLERGY CLIN IMMUN, V82, P878, DOI 10.1016/0091-6749(88)90093-0; Ciprandi G, 1995, J ALLERGY CLIN IMMUN, V96, P971, DOI 10.1016/S0091-6749(95)70235-0; D'Amato G, 1998, ALLERGY, V53, P567, DOI 10.1111/j.1398-9995.1998.tb03932.x; DAMATO G, 1992, ALLERGY, V47, P443, DOI 10.1111/j.1398-9995.1992.tb00661.x; Demoly P, 2003, ALLERGY, V58, P672, DOI 10.1034/j.1398-9995.2003.t01-1-00202.x; Dykewicz MS, 1998, ANN ALLERG ASTHMA IM, V81, P478, DOI 10.1016/S1081-1206(10)63155-9; International Consensus Report on Diagnosis and Management of Rhinitis, 1994, ALLERGY S, V49, P1; Kilpelainen M, 2001, ALLERGY, V56, P377, DOI 10.1034/j.1398-9995.2001.056005377.x; Lagier B, 1995, J ALLERGY CLIN IMMUN, V96, P932, DOI 10.1016/S0091-6749(95)70231-8; Leynaert B, 1997, AM J RESP CRIT CARE, V156, P1413; Leynaert N, 2004, J ALLERGY CLIN IMMUN, V113, P86, DOI 10.1016/j.jaci.2003.10.010; Lockey RF, 2001, J ALLERGY CLIN IMMUN, V108, P497; Pariente PD, 1997, PHARMACOECONOMICS, V12, P585; PENE J, 1994, IMMUNOLOGY, V81, P58; PEPYS J, 1973, CLIN ALLERGY, V3, P491, DOI 10.1111/j.1365-2222.1973.tb03057.x; PEPYS J, 1994, ALLERGY, V49, P397, DOI 10.1111/j.1398-9995.1994.tb00830.x; PLATTSMILLS TAE, 1987, J ALLERGY CLIN IMMUN, V79, P781, DOI 10.1016/0091-6749(87)90211-9; Ricca V, 2000, J ALLERGY CLIN IMMUN, V105, P54, DOI 10.1016/S0091-6749(00)90177-5; Rudin A, 2001, ALLERGY, V56, P1042, DOI 10.1034/j.1398-9995.2001.00991.x; SIBBALD B, 1991, THORAX, V46, P895, DOI 10.1136/thx.46.12.895; Tschopp JM, 1998, ALLERGY, V53, P608, DOI 10.1111/j.1398-9995.1998.tb03937.x; van Cauwenberge P, 2000, ALLERGY, V55, P116, DOI 10.1034/j.1398-9995.2000.00526.x; Wood RA, 1999, J ALLERGY CLIN IMMUN, V103, P773, DOI 10.1016/S0091-6749(99)70419-7	30	124	125	1	6	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	JUN	2005	35	6					728	732		10.1111/j.1365-2222.2005.02274.x		5	Allergy; Immunology	Allergy; Immunology	937WG	WOS:000229956100009	15969662	
J	Douwes, J				Douwes, J			(1 -> 3)-beta-D-glucans and respiratory health: a review of the scientific evidence	INDOOR AIR			English	Article						(1 -> 3)-beta-D-glucan; review; respiratory health; fungi; damp; epidemiology	UPPER AIRWAY INFLAMMATION; IN-HOUSE DUST; WORK-RELATED SYMPTOMS; MOLD EXPOSURE; PULMONARY INFLAMMATION; PERSONAL EXPOSURES; ALLERGIC RESPONSE; WASTE COLLECTORS; CYTOKINE RELEASE; SOLUBLE GLUCAN	(1 -> 3)-beta-D-glucan are non-allergenic structural cell wall components of most fungi that have been suggested to play a causal role in the development of respiratory symptoms associated with indoor fungal exposure. This review describes the currently available epidemiological literature on health effects of (1 -> 3)-beta-D-glucan, focusing on atopy, airway inflammation and symptoms, asthma, and lung function. In addition to population studies, studies in human volunteers experimentally exposed to (1 -> 3)-beta-D-glucan are described as well as relevant animal studies. Furthermore, the review discusses exposure assessment methods, the potential for exposure control and it concludes with identifying research needs. The observational and experimental studies reviewed suggested some association between (1 -> 3)-beta-D-glucan exposure, airway inflammation and symptoms, however, results were mixed and specific symptoms and potential underlying inflammatory mechanisms associated with exposure could not be identified. Large observational studies using well validated exposure assessment methods are needed to further our knowledge regarding the potential health effects of indoor (1 -> 3)-beta-D-glucan exposure.	Massey Univ, Ctr Publ Hlth Res, Palmerston North, New Zealand	Douwes, J (reprint author), Private Box 756, Wellington, New Zealand.	j.douwes@massey.ac.nz		Douwes, Jeroen/0000-0003-3599-4036			ADACHI Y, 1994, BIOL PHARM BULL, V17, P1554; AKETAGAWA J, 1993, J BIOCHEM-TOKYO, V113, P683; Beijer L, 2003, EUR RESPIR J, V21, P317, DOI 10.1183/09031936.03.00283603; Beijer L, 2002, MEDIAT INFLAMM, V11, P149, DOI 10.1080/09622935020138181; Black PN, 2000, ALLERGY, V55, P501, DOI 10.1034/j.1398-9995.2000.00293.x; Bonlokke JH, 2004, INT ARCH OCC ENV HEA, V77, P136, DOI 10.1007/s00420-003-0479-9; BOWERS GJ, 1986, INT J IMMUNOPHARMACO, V8, P313, DOI 10.1016/0192-0561(86)90113-X; COOK JA, 1980, CIRC SHOCK, V7, P225; DILUZIO NR, 1979, J RETICULOENDOTH SOC, V26, P67; Douwes J, 2000, AM J RESP CRIT CARE, V162, P1348; Douwes J, 2003, ANN OCCUP HYG, V47, P187, DOI 10.1093/annhyg/meg032; Douwes J, 2000, AM J IND MED, V37, P459, DOI 10.1002/(SICI)1097-0274(200005)37:5<459::AID-AJIM2>3.0.CO;2-J; Douwes J, 2003, AM J EPIDEMIOL, V158, P203, DOI 10.1093/aje/kwg149; Douwes J, 1998, INDOOR AIR, V8, P255, DOI 10.1111/j.1600-0668.1998.00006.x; Douwes J, 1996, APPL ENVIRON MICROB, V62, P3176; Eduard W, 2001, OCCUP ENVIRON MED, V58, P113, DOI 10.1136/oem.58.2.113; FOGELMARK B, 1992, AGENTS ACTIONS, V35, P50, DOI 10.1007/BF01990951; FOGELMARK B, 1994, INT J EXP PATHOL, V75, P85; Fogelmark B, 2001, MEDIAT INFLAMM, V10, P13, DOI 10.1080/09629350151073748; Fogelmark B, 1997, INDOOR BUILT ENVIRON, V6, P291, DOI 10.1177/1420326X9700600506; Foto M, 2004, ANAL BIOANAL CHEM, V379, P156, DOI 10.1007/s00216-004-2583-4; Gehring U, 2001, ENVIRON HEALTH PERSP, V109, P139, DOI 10.2307/3434766; Gladding T, 2003, AM J IND MED, V43, P584, DOI 10.1002/ajim.10220; Halonen M, 1997, AM J RESP CRIT CARE, V155, P1356; Heldal KK, 2003, EUR RESPIR J, V21, P641, DOI 10.1183/09031936.03.00059702; Heldal KK, 2003, OCCUP ENVIRON MED, V60, P444, DOI 10.1136/oem.60.6.444; Institute of Medicine (US) Committee on Damp Indoor Spaces and Health, 2004, DAMP IND SPAC HLTH; Institute of Medicine, 2000, CLEAR AIR ASTHM IND; Instanes C, 2004, CLIN EXP ALLERGY, V34, P1634, DOI 10.1111/j.1365-2222.2004.02076.x; KLIS FM, 1994, YEAST, V10, P851, DOI 10.1002/yea.320100702; Korpi A, 2003, MEDIAT INFLAMM, V12, P139, DOI 10.1080/0962935031000134851; Kruger T, 2004, CYTOKINE, V25, P73, DOI 10.1016/j.cyto.2003.10.001; Lebron F, 2003, J BIOL CHEM, V278, P25001, DOI 10.1074/jbc.M301426200; Mandryk J, 1999, AM J IND MED, V35, P481, DOI 10.1002/(SICI)1097-0274(199905)35:5<481::AID-AJIM5>3.0.CO;2-N; Mandryk J, 2000, ANN OCCUP HYG, V44, P281; Milton DK, 2001, APPL ENVIRON MICROB, V67, P5420, DOI 10.1128/AEM.67.12.5420-5424.2001; Ormstad H, 2000, J TOXICOL ENV HEAL A, V61, P55, DOI 10.1080/00984100050116780; Peat JK, 1998, ALLERGY, V53, P120, DOI 10.1111/j.1398-9995.1998.tb03859.x; RAMANI M, 1988, CLIN IMMUNOL, V81, P696; Rylander R, 1997, ARCH ENVIRON HEALTH, V52, P281; Rylander R, 1998, MEDIAT INFLAMM, V7, P105; Rylander R, 1998, AM J RESP CRIT CARE, V158, P1685; Rylander R, 2000, TOXICOLOGY, V152, P47, DOI 10.1016/S0300-483X(00)00291-2; Rylander R, 1999, EUR RESPIR J, V13, P1151, DOI 10.1034/j.1399-3003.1999.13e35.x; RYLANDER R, 1996, INDOOR BUILT ENVIRON, V5, P106, DOI 10.1177/1420326X9600500206; [Anonymous], 1994, INDOOR ENVIRON, DOI DOI 10.1177/1420326X9400300311; Rylander R, 1992, INDOOR ENVIRON, V1, P263, DOI 10.1177/1420326X9200100502; SAITO K, 1992, CHEM PHARM BULL, V40, P1227; Sigsgaard T, 2000, EUR RESPIR J, V16, P140, DOI 10.1034/j.1399-3003.2000.16a25.x; Stone BA, 1992, CHEM BIOL 1 3 BETA G; Thorn J, 1998, AM J IND MED, V33, P463; Thorn J, 1998, AM J RESP CRIT CARE, V157, P1798; Thorn J, 2001, MEDIAT INFLAMM, V10, P173; Wan GH, 1999, ARCH ENVIRON HEALTH, V54, P172; Williams DL, 1997, MEDIAT INFLAMM, V6, P247, DOI 10.1080/09629359791550; Wouters IM, 2002, OCCUP ENVIRON MED, V59, P106, DOI 10.1136/oem.59.2.106; Wouters IM, 2000, APPL ENVIRON MICROB, V66, P627, DOI 10.1128/AEM.66.2.627-631.2000; Young SH, 2003, J TOXICOL ENV HEAL A, V66, P551, DOI 10.1080/15287390390156281; Young SH, 2003, J TOXICOL ENV HEAL A, V66, P25, DOI 10.1080/152873903901557232; Young SH, 2002, TOXICOL APPL PHARM, V178, P172, DOI 10.1006/taap.2001.9332; Young SH, 2001, J TOXICOL ENV HEAL A, V64, P311, DOI 10.1080/152873901316981303; ZHANG K, 1994, J CELL BIOCHEM, V56, P225, DOI 10.1002/jcb.240560217; Zock JP, 2002, J ALLERGY CLIN IMMUN, V110, P285, DOI 10.1067/mai.2002.126383; Zureik M, 2002, BRIT MED J, V325, P411, DOI 10.1136/bmj.325.7361.411	64	124	131	2	15	BLACKWELL MUNKSGAARD	FREDERIKSBERG C	1 ROSENORNS ALLE, DK-1970 FREDERIKSBERG C, DENMARK	0905-6947			INDOOR AIR	Indoor Air	JUN	2005	15	3					160	169		10.1111/j.1600-0668.2005.00333.x		10	Construction & Building Technology; Engineering, Environmental; Public, Environmental & Occupational Health	Construction & Building Technology; Engineering; Public, Environmental & Occupational Health	921GF	WOS:000228751500003	15865616	
J	Banauch, GI; Alleyne, D; Sanchez, R; Olender, K; Cohen, HW; Weiden, M; Kelly, KJ; Prezant, DJ				Banauch, GI; Alleyne, D; Sanchez, R; Olender, K; Cohen, HW; Weiden, M; Kelly, KJ; Prezant, DJ			Persistent hyperreactivity and reactive airway dysfunction in firefighters at the World Trade Center	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						inorganic particulate matter; nonspecific bronchial hyperreactivity; reactive airways dysfunction syndrome; firefighters; World Trade Center collapse	DOSE-RESPONSE CURVES; BRONCHIAL RESPONSIVENESS; OCCUPATIONAL ASTHMA; FOLLOW-UP; HEALTH CONSEQUENCES; POPULATION-SAMPLE; SMOKE-INHALATION; SYNDROME RADS; LUNG-FUNCTION; EXPOSURE	New York City Fire Department rescue workers experienced massive exposure to airborne particulates at the World Trade Center site. Aims of this longitudinal study were to (1) determine if bronchial hyperreactivity was present, persistent, and independently associated with exposure intensity, (2) identify objective measures shortly after the collapse that would predict persistent hyperreactivity and a diagnosis of reactive airways dysfunction 6 months post-collapse. A representative sample of 179 rescue workers stratified by exposure intensity (high, moderate, and control) without current smoking or prior respiratory disease was enrolled. Highly exposed workers arrived within 2 hours of collapse, moderately exposed workers arrived later on Days 1-2; control subjects were not exposed. Hyperreactivity at 1, 3, and 6 months post-collapse was associated with exposure intensity, independent of ex-smoking and airflow obstruction. Six months post-collapse, highly exposed workers were 6.8 times more likely than moderately exposed workers and control subjects to be hyperreactive (95% confidence interval, 1.8-25.2; p = 0.004), and hyperreactivity persisted in 55% of those hyperreactive at I and/or 3 months. In highly exposed subjects, hyperreactivity 1 or 3 months post-collapse was the sole predictor for reactive airways dysfunction (p = 0.021). In conclusion, development and persistence of hyperreactivity and reactive airways dysfunction were strongly and independently associated with exposure intensity. Hyperreactivity shortly post-collapse predicted reactive airways dysfunction at 6 months in highly exposed workers; this has important implications for disaster management.	Montefiore Med Ctr, Div Pulm, Bronx, NY 10467 USA; Albert Einstein Coll Med, Dept Epidemiol & Social Med, Bronx, NY 10467 USA; New York City Fire Dept, Bur Hlth Sci, Brooklyn, NY USA; NYU, Sch Med, Div Pulm, New York, NY USA	Prezant, DJ (reprint author), Montefiore Med Ctr, Div Pulm, Centennial 423, Bronx, NY 10467 USA.			Cohen, Hillel/0000-0002-4524-0898	NIOSH CDC HHS [R01-OH07350]; ODCDC CDC HHS [U1Q/CCU221158-01]		Abul AT, 2001, ANN ALLERG ASTHMA IM, V86, P465; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Bardana EJ, 1999, ANN ALLERG ASTHMA IM, V83, P583, DOI 10.1016/S1081-1206(10)62876-1; BAXTER PJ, 1983, ARCH ENVIRON HEALTH, V38, P138; BECKETT WS, 1997, BRIT MED J, V314, P338; BLANC PD, 1993, CHEST, V103, P1699, DOI 10.1378/chest.103.6.1699; Bourbeau J, 1996, EUR RESPIR J, V9, P1470, DOI 10.1183/09031936.96.09071470; BROOKS SM, 1985, CHEST, V88, P376, DOI 10.1378/chest.88.3.376; Chen LC, 2002, LANCET, V360, pS37, DOI 10.1016/S0140-6736(02)11814-9; CHIA KS, 1990, BRIT J IND MED, V47, P524; CONE JE, 1994, CHEST, V106, P500, DOI 10.1378/chest.106.2.500; Crapo RO, 2000, AM J RESP CRIT CARE, V161, P309; ERNST P, 1989, THORAX, V44, P116, DOI 10.1136/thx.44.2.116; Fagan J, 2002, MMWR-MORBID MORTAL W, V51, P781; FIREMAN E, IN PRESS AM J RESP C; Ghio AJ, 2001, AM J RESP CRIT CARE, V164, P704; Ghio AJ, 2000, AM J RESP CRIT CARE, V162, P981; Hodgins P, 1998, AM J RESP CRIT CARE, V157, P1390; HUGEL DW, 1998, J LAB CLIN MED, V111, P684; KERN DG, 1991, AM REV RESPIR DIS, V144, P1058; KINSELLA J, 1991, LANCET, V337, P595, DOI 10.1016/0140-6736(91)91650-J; KNUDSON RJ, 1983, AM REV RESPIR DIS, V127, P725; KREMER AM, 1994, AM J IND MED, V26, P655, DOI 10.1002/ajim.4700260508; Laprise C, 1997, AM J RESP CRIT CARE, V156, P403; Lemiere C, 1996, MED CLIN N AM, V80, P749, DOI 10.1016/S0025-7125(05)70466-1; Leroyer C, 1998, OCCUP ENVIRON MED, V55, P356; Lioy PJ, 2002, ENVIRON HEALTH PERSP, V110, P703; MALO JL, 1988, AM REV RESPIR DIS, V138, P807; McKinney K, 2002, MMWR-MORBID MORTAL W, V51, P453; Mochizuki H, 2000, PEDIATRICS, V106, P1442, DOI 10.1542/peds.106.6.1442; Nightingale JA, 2000, AM J RESP CRIT CARE, V162, P161; OCONNOR G, 1987, AM REV RESPIR DIS, V136, P1412; Perfetti L, 1998, CHEST, V114, P398, DOI 10.1378/chest.114.2.398; Piirila PL, 1996, SCAND J WORK ENV HEA, V22, P191; Prezant DJ, 2002, NEW ENGL J MED, V347, P806, DOI 10.1056/NEJMoa021300; PROMISLOFF RA, 1990, CHEST, V98, P928, DOI 10.1378/chest.98.4.928; RIJCKEN B, 1987, AM REV RESPIR DIS, V136, P62; RIJCKEN B, 1993, AM REV RESPIR DIS, V147, P1447; RIJCKEN B, 1993, EUR RESPIR J, V6, P617; Rom WN, 2002, AM J RESP CRIT CARE, V166, P797, DOI 10.1164/rccm.200206-576OC; SARIC M, 1991, BRIT J IND MED, V48, P653; SHERMAN CB, 1989, AM REV RESPIR DIS, V140, P185; Stephenson J, 2002, JAMA-J AM MED ASSOC, V288, P1219, DOI 10.1001/jama.288.10.1219; Tarlo SM, 2000, OCCUP MED, V15, P471; TATTERSFIELD AE, 1985, AIRWAY RESPONSIVENES, P94; Townsend MC, 2000, J OCCUP ENVIRON MED, V42, P228, DOI 10.1097/00043764-200003000-00003; Verlato G, 1996, EUR RESPIR J, V9, P506, DOI 10.1183/09031936.96.09030506; Vijayan VK, 1996, EUR RESPIR J, V9, P1977, DOI 10.1183/09031936.96.09101977	48	124	124	0	6	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	JUL 1	2003	168	1					54	62		10.1164/rccm.200211-1329OC		9	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	695HH	WOS:000183824700008	12615613	
J	Helenius, I; Rytila, P; Sarna, S; Lumme, A; Helenius, M; Remes, V; Haahtela, T				Helenius, I; Rytila, P; Sarna, S; Lumme, A; Helenius, M; Remes, V; Haahtela, T			Effect of continuing or finishing high-level sports on airway inflammation, bronchial hyperresponsiveness, and asthma: A 5-year prospective follow-up study of 42 highly trained swimmers	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; athletes; airway inflammation; bronchial hyperresponsiveness; swimming; sports medicine	CROSS-COUNTRY SKIERS; INDUCED SPUTUM; PREVALENCE; RESPONSIVENESS; EXPOSURE; RISK	Background: Mild eosinophilic airway inflammation and bronchial hyperresponsiveness-ie, mild asthma-have been shown to affect a high proportion of endurance athletes. The persistence of airway inflammation, bronchial hyperresponsiveness, and asthma in this population is not known, however, inasmuch as follow-up studies of athletes' asthma have not been performed. Objective: The purpose of this study was to investigate effect of finishing high-level sports on airway inflammation, bronchial hyperresponsiveness, and asthma. Methods: Forty-two elite competitive swimmers, most of them from the Finnish national team (37/42; 88%), were followed for 5 years in a prospective manner. All of the swimmers completed questionnaires and underwent resting spirometry, histamine challenge testing, and skin prick tests at baseline and at follow-up. Twenty-nine swimmers (69%) also gave induced sputum samples on both occasions. Sixteen (38%) of the swimmers had continued their competitive careers during follow-up (active swimmers), but 26 (62%) had stopped competing more than 3 months before the follow-up examination (past swimmers). Results: Bronchial responsiveness was increased in 7 (44%) of the 16 active swimmers at baseline and in 8 (50%) of the 16 active swimmers at follow-up; it was increased in 8 (31%) of the 26 past swimmers at baseline and in 3 (12%) of the 26 past swimmers at follow-up (McNemar test, P = .025). The difference in the change in bronchial hyperresponsiveness between the study groups was significant (likelihood ratio test, P = .023). Current asthma (defined as bronchial hyperresponsiveness and exercise-induced bronchial symptoms monthly) was observed in 5 (31%) of the active swimmers at baseline and in 7 (44%) of the active swimmers at follow-up; of the past swimmers, it occurred in 6 (23%) at baseline and in 1 (4%) at follow-up (McNemar test, P = .025). The difference in the change in current asthma between the study groups was significant (likelihood ratio test, P = .0040). The sputum differential cell counts of eosinophils and lymphocytes increased significantly during the follow-up period in the active swimmers (Wilcoxon signed rank sum test; P = .033 and P = .0029, respectively); in the past swimmers, the sputum differential cell counts of eosinophils tended to decrease during the follow-up period (P = .17), whereas the differential cell counts of lymphocytes did not change significantly. The changes in the sputum differential cell counts of eosinophils between the study groups differed significantly (Mann-Whitney U test, P = .019). Conclusion: In swimmers who had stopped high-level training, bronchial hyperresponsiveness and asthma attenuated or even disappeared. Mild eosinophilic airway inflammation was aggravated among highly trained swimmers who remained active during the 5-year follow-up. Our results suggest that athletes' asthma is partly reversible and that it may develop during and subside after an active sports career.	Univ Helsinki, Cent Hosp, Div Allergy, Helsinki, Finland; Univ Helsinki, Dept Publ Hlth, Helsinki, Finland	Helenius, I (reprint author), Arhipanpolku 8 B A, FIN-00420 Helsinki, Finland.			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Allergy Clin. Immunol.	JUN	2002	109	6					962	968		10.1067/mai.2002.124769		7	Allergy; Immunology	Allergy; Immunology	566RU	WOS:000176442700011	12063525	
J	Chan, E; Zhan, CL; Homer, CJ				Chan, E; Zhan, CL; Homer, CJ			Health care use and costs for children with attention-deficit/hyperactivity disorder - National estimates front the Medical Expenditure Panel Survey	ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE			English	Article; Proceedings Paper	Annual Meeting of the Academy-for-Health-Services-Research-and-Health-Policy	JUN   11, 2001	ATLANTA, GEORGIA	Acad Hlth Serv Res & Hlth Policy			DEFICIT HYPERACTIVITY DISORDER; COUNTY-WIDE SAMPLE; PSYCHOSOCIAL PROBLEMS; ASTHMA; IDENTIFICATION; ADOLESCENTS; MANAGEMENT; PATTERNS; CRITERIA	Context: Although attention-deficit/hyperactivity disorder (ADHD) is a highly prevalent chronic condition of childhood, little is known about patterns of health care use and associated expenditures. Objective: To compare health care use and costs among children with ADHD, children with asthma, and the general pediatric population. Design and Setting: The 1996 Medical Expenditure Panel Survey, a nationally representative household survey. Participants: All 5439 children aged 5 to 20 years from the 1996 Medical Expenditure Panel Survey were included in this analysis. Children who had ADHD, asthma,d or neither (general population) were identified from Into-national Classification of Diseases, Ninth Revision, Clinical Modification codes and prescription records. Main Outcome Measures: Mean health care use (outpatient visits, emergency department visits, hospital stays, home health visit days, and prescriptions) and associated expenditures. Results: We identified 105 children with ADHD, 322 with asthma, and 4052 with neither diagnosis. Children with ADHD had significantly higher mean total health care costs ($1151) compared with children with asthma ($1091 P<.05) and the general population ($712 P<.001). After adjusting for age, Sex, race, household income, access to care, parent education, and martial Status, excess total costs were $479 for children with ADHD (P<.001) and $437 for children with asthma (P<.01). Conclusions: Overall costs of care for children with ADHD are comparable to costs for children with asthma and significantly greater than for the general pediatric Population, Specific types of health care use and the sources of expenditures differ between children with ADHD and children with asthma. Because much ADHD-related care occurs within school and mental health settings, these figures likely underestimate the true costs of caring for children with this condition.	Childrens Hosp, Hlth Serv Res, Div Gen Pediat, Boston, MA 02115 USA; Agcy Healthcare Res & Qual, Rockville, MD USA	Chan, E (reprint author), Childrens Hosp, Hlth Serv Res, Div Gen Pediat, 300 Longwood Ave,LO-240, Boston, MA 02115 USA.				BHP HRSA HHS [T32 PE10018]		BARKLEY RA, 1991, J AM ACAD CHILD PSY, V30, P752, DOI 10.1097/00004583-199109000-00009; Barkley RA, 1996, PEDIATRICS, V98, P1089; Camp BW, 1997, ARCH PEDIAT ADOL MED, V151, P78; Cohen J., 1997, DESIGN METHODS MED E; DiScala C, 1998, PEDIATRICS, V102, P1415, DOI 10.1542/peds.102.6.1415; Donahue JG, 1997, J ASTHMA, V34, P273, DOI 10.3109/02770909709067217; GOLDBERG ID, 1984, PEDIATRICS, V73, P278; Guevara J, 2001, PEDIATRICS, V108, P71, DOI 10.1542/peds.108.1.71; Haggerty RJ, 1975, CHILD HLTH COMMUNITY; HORWITZ SM, 1992, PEDIATRICS, V89, P480; Jensen PS, 1999, ARCH GEN PSYCHIAT, V56, P1073; KELLEHER K, 2001, TEN ECON NEUROSCI, V3, P60; Kelleher KJ, 2000, PEDIATRICS, V105, P1313, DOI 10.1542/peds.105.6.1313; Korn EL, 1999, ANAL HLTH SURVEYS; Leibson CL, 2001, JAMA-J AM MED ASSOC, V285, P60, DOI 10.1001/jama.285.1.60; Lozano P, 1997, PEDIATRICS, V99, P757, DOI 10.1542/peds.99.6.757; Lozano P, 1999, J ALLERGY CLIN IMMUN, V104, P957; OSBORNE ML, 1995, J CLIN EPIDEMIOL, V48, P1393, DOI 10.1016/0895-4356(95)00065-8; Safer DJ, 1996, PEDIATRICS, V98, P1084; Shah B. V., 1997, SUDAAN USERS MANUAL; SHARP L, 1992, PEDIATRICS, V89, P619; SZATMARI P, 1989, J CHILD PSYCHOL PSYC, V30, P205, DOI 10.1111/j.1469-7610.1989.tb00235.x; Szatmari P., 1992, CHILD ADOL PSYCH CL, P361; *US DHHS, 1988, INT CLASS DIS 9 REV; Wasserman RC, 1999, PEDIATRICS, V103, DOI 10.1542/peds.103.3.e38; Wolraich ML, 1996, J AM ACAD CHILD PSY, V35, P319, DOI 10.1097/00004583-199603000-00013; Wolraich ML, 1998, J DEV BEHAV PEDIATR, V19, P162, DOI 10.1097/00004703-199806000-00003	27	124	125	2	5	AMER MEDICAL ASSOC	CHICAGO	515 N STATE ST, CHICAGO, IL 60610 USA	1072-4710			ARCH PEDIAT ADOL MED	Arch. Pediatr. Adolesc. Med.	MAY	2002	156	5					504	511				8	Pediatrics	Pediatrics	548RC	WOS:000175402100018	11980558	
J	Leaderer, BP; Belanger, K; Triche, E; Holford, T; Gold, DR; Kim, Y; Jankun, T; Ren, P; McSharry, JE; Plattsmills, TAE; Chapman, MD; Bracken, MB				Leaderer, BP; Belanger, K; Triche, E; Holford, T; Gold, DR; Kim, Y; Jankun, T; Ren, P; McSharry, JE; Plattsmills, TAE; Chapman, MD; Bracken, MB			Dust mite, cockroach, cat, and dog allergen concentrations in homes of asthmatic children in the northeastern United States: Impact of socioeconomic factors and population density	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						aeroallergens; asthma; cats; cockroaches; dogs; dust mites; indoor air; socioeconomic factors	INNER-CITY CHILDREN; MONOCLONAL-ANTIBODIES; INDOOR ALLERGENS; PUERTO-RICAN; RISK-FACTORS; EXPOSURE; PREVALENCE; MORTALITY; SENSITIZATION; MORBIDITY	Home exposures to aeroallergens are an important environmental factor in allergic sensitization and in the development and exacerbation of asthma. We assessed variations in home concentrations of dust Mite, cock-roach, cat, and dog allergens in dust collected in the main living areas of asthmatics' homes by family income, mother's education, dwelling type, population density, household population density, and ethnicity in Connecticut and south-central Massachusetts. Dust samples were collected at the time of home interview in 999 homes as part of an ongoing longitudinal birth cohort study of 1,002 infants and their asthmatic siblings. The analysis employed lower arid upper cut points for group 1 dust mite (greater than or equal to2.0 mug/g and greater than or equal to10 mug/g), cockroach (greater than or equal to1.0 U/g and greater than or equal to4.0 U/g), cat (greater than or equal to1.0 mug/g and greater than or equal to8.0 ug/g), and dog (greater than or equal to2.0 mug/g and 10.0 mug/g) allergens. Subject residences were geocoded to assess population density from the U.S. Census, and multiple logistic regression was used to control for confounding, The portion of homes at the lower cut point for dust mite, cockroach, cat, and dog allergens were 46.9%, 24.9%, 42.2%, and 35.6%, respectively; the upper cut point for each of the allergens was reached in 22.4%, 13.4%, 21.0%, and 22.9% of the homes, respectively. In all, 86.0% of the homes had at least one allergen at the lower cut point, and 58.0% had at least one allergen at the upper cut point. Forty-nine percent of the homes had two or more allergens at the lower cut point, and 19.7% had two or more allergens at the upper cut point. Higher education of the mother, higher household income, living in a single-family home in a less densely populated area with fewer people per room, and being a white household were associated with elevated dust mite, cat, and dog allergens and low cockroach allergen. In contrast, low income, living in a multifamily home in a high population density area with a higher occupancy rate per room, and being a Hispanic or black household were associated with elevated cockroach allergens and low concentrations of dust mite, cat, and dog allergens. Although the presence of an individual allergen is more likely associated with one or more socioeconomic or ethnic factors, most homes typically have multiple allergen burdens in excess of concentrations thought to be associated with sensitization and exacerbation of asthma. Mite and cockroach allergens have distinct and opposite associations with socioeconomic factors and population density.	Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06520 USA; Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA; Harvard Univ, Sch Med, Bostons Beth Israel Hosp, Div Pulm, Boston, MA 02115 USA; Univ Virginia, Med Ctr, Dept Med, Div Allergy & Immunol, Charlottesville, VA USA	Leaderer, BP (reprint author), Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, 60 Coll St,POB 208034, New Haven, CT 06520 USA.		Triche, Elizabeth/I-4986-2014		NIEHS NIH HHS [ES05410, ES07456]		Beckett WS, 1996, AM J RESP CRIT CARE, V154, P894; CAIL RS, 1992, J PEDIATR, V121, P862; CARR W, 1992, AM J PUBLIC HEALTH, V82, P59, DOI 10.2105/AJPH.82.1.59; CARTERPOKRAS OD, 1993, AM J PUBLIC HEALTH, V83, P580, DOI 10.2105/AJPH.83.4.580; CHANYEUNG M, 1995, AM J RESP CRIT CARE, V152, P1805; Chew GL, 1999, ALLERGY, V54, P1058, DOI 10.1034/j.1398-9995.1999.00003.x; COULTAS DB, 1994, AM J RESP CRIT CARE, V149, pS93; Eggleston PA, 1999, ENVIRON HEALTH PERSP, V107, P439; Eggleston PA, 1998, J ALLERGY CLIN IMMUN, V102, P563, DOI 10.1016/S0091-6749(98)70272-6; EVANS R, 1992, CHEST, V101, pS368; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; *GEOL INC, 1990, CENS CD PLUS MAPS 19; GERGEN PJ, 1992, AM REV RESPIR DIS, V146, P823; GERGEN PJ, 1990, JAMA-J AM MED ASSOC, V264, P1688, DOI 10.1001/jama.264.13.1688; GERGEN PJ, 1988, PEDIATRICS, V81, P1; GOLD DR, 1993, AM REV RESPIR DIS, V148, P10; INGRAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449, DOI 10.1016/S0091-6749(95)70286-5; Kitch BT, 2000, ENVIRON HEALTH PERSP, V108, P301, DOI 10.2307/3454347; LANG DM, 1994, NEW ENGL J MED, V331, P1542, DOI 10.1056/NEJM199412083312302; LUCZZYNSKA CM, 1989, J IMMUNOL METHODS, V118, P277; Mannino DM, 1998, MMWR-MORBID MORTAL W, V47, P1; OVSYANNIKOVA IG, 1994, J ALLERGY CLIN IMMUN, V94, P537, DOI 10.1016/0091-6749(94)90211-9; PERSKY VW, 1998, ANN ALLERG ASTHMA IM, V81, P226; PLATTSMILLS TA, 1997, J ALLERGY CLIN IMMUN, V97, P1079; PLATTSMILLS TAE, 1989, J ALLERGY CLIN IMMUN, V83, P416, DOI 10.1016/0091-6749(89)90128-0; POLLART SM, 1991, J ALLERGY CLIN IMMUN, V87, P511, DOI 10.1016/0091-6749(91)90010-L; RAPPAPORT S, 1998, MMWR-MORBID MORTAL W, V47, P1022; Ray NF, 1998, CHEST, V113, P1277, DOI 10.1378/chest.113.5.1277; Rosenstreich DL, 1997, NEW ENGL J MED, V336, P1356, DOI 10.1056/NEJM199705083361904; SAS/STAT User's guide, 1990, SAS STAT US GUID, V1; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; WEISS KB, 1990, JAMA-J AM MED ASSOC, V264, P1683, DOI 10.1001/jama.264.13.1683; WEISS KB, 1993, ANNU REV PUBL HEALTH, V14, P491, DOI 10.1146/annurev.pu.14.050193.002423; WEISS KB, 1990, CHEST, V98, pS179, DOI 10.1378/chest.98.5_Supplement.179S; WEISS ST, 1993, J ASTHMA, V30, P329, DOI 10.3109/02770909309056738; WEITZMAN M, 1992, JAMA-J AM MED ASSOC, V268, P2673, DOI 10.1001/jama.268.19.2673; WEITZMAN M, 1990, AM J DIS CHILD, V144, P1189	37	124	128	1	5	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	APR	2002	110	4					419	425				7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	541GB	WOS:000174975900031	11940461	
J	Apelberg, BJ; Aoki, Y; Jaakkola, JJK				Apelberg, BJ; Aoki, Y; Jaakkola, JJK			Systematic review: Exposure to pets and risk of asthma and asthma-like symptoms	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						pets; asthma; wheeze; domestic animal; meta-analysis; selection bias	RESPIRATORY SYMPTOMS; CHILDHOOD ASTHMA; HOME-ENVIRONMENT; ATOPIC SENSITIZATION; CHILDREN; PREVALENCE; ALLERGY; CAT; ASSOCIATION; MORBIDITY	Background: Studies of exposure to pets and risk of asthma have yielded conflicting results. Objectives: We performed a systematic review to synthesize the evidence of the effect of exposure to pets in the home on the risk of asthma and asthma-related symptoms. We also assessed differences between the studies as sources of heterogeneity of the results. Methods: We conducted a MEDLINE search (until the end of 1999) using the following boolean search command: (asthma[all] OR wheez*[all]) AND (domestic animal*[all] OR pets[all]). The outcome was limited to either diagnosis of asthma or the symptom of wheezing, The exposure of interest was domestic animals in the home, Appropriate temporal relationship was defined as present in studies with either pet keeping within the first 2 years of life, in the past, or exposure to pets preceding the outcome. Results: Thirty-two of the 217 retrieved articles fulfilled the eligibility criteria. Inappropriate time sequence of the exposure and outcome information was an important source of heterogeneity and an indication of potential selection bias. Therefore we analyzed studies focusing on early exposure or ensuring appropriate temporal sequence. The pooled risk estimates for both asthma (fixed-effects odds ratio, 1.11; 95% CI, 0.98-1.25; heterogeneity, P = .04; random-effects odds ratio, 1.09; 95% CI, 0.89-1.34) and wheezing (fixed-effects odds ratio, 1.19; 95% CI, 1.05-1.35; heterogeneity, P = .03; random-effects odds ratio, 1.17; 95% CI, 0.95-1.44) indicated a small effect, which was limited to studies with a median study population age of over 6 years (fixed-effects odds ratio, 1.19; 95% CI, 1.02-1.40; heterogeneity, P = .04; random-effects odds ratio, 1.15; 95% CI, 0.86-1.56; fixed-effects odds ratio, 1.29; 95% CI, 1.12-1.48; heterogeneity, P = .31). In younger children the harmful effect disappeared for wheezing (odds ratio, 0.80; 95% CI, 0.59-1.08; P = .38). Conclusion: Exposure to pets appears to increase the risk of asthma and wheezing in older children. The observed lower risk among exposed than among unexposed young children is consistent with a protective effect in this age, group but could also be explained by selection bias.	Johns Hopkins Sch Hyg & Publ Hlth, Dept Epidemiol, Baltimore, MD USA; Johns Hopkins Sch Hyg & Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD USA	Jaakkola, JJK (reprint author), Nord Sch Publ Hlth, Environm Hlth Program, POB 12133, SE-40242 Gothenburg, Sweden.		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Allergy Clin. Immunol.	MAR	2001	107	3					455	460		10.1067/mai.2001.113240		6	Allergy; Immunology	Allergy; Immunology	416RE	WOS:000167793300006	11240945	
J	Mannino, DM; Moorman, JE; Kingsley, B; Rose, D; Repace, J				Mannino, DM; Moorman, JE; Kingsley, B; Rose, D; Repace, J			Health effects related to environmental tobacco smoke exposure in children in the United States - Data from the Third National Health and Nutrition Examination Survey	ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE			English	Article							PARENTAL SMOKING; PASSIVE SMOKING; COTININE; PARTICULATE; POLLUTION; WORKPLACE; CHILDHOOD; ASTHMA	Objective: To determine the effects of prenatal. and postnatal smoke exposure on the respiratory health of children in the United States. Design: Nationally representative cross-sectional survey, including questionnaire information, measurements of serum cotinine (a metabolite of nicotine), and pulmonary function measurement, of 5400 US children. Setting and Participants: Children aged 4 to 16 years in the Third National Health and Nutrition Examination Survey, October 25, 1988, to October 15, 1994. Methods: We stratified the study participants into tertiles, on the basis of serum cotinine levels, and used logistic and linear regression modeling, adjusting for known covariates, to determine the effect of high environmental tobacco smoke (ETS) exposure (on the basis of a high cotinine level) on outcomes such as the prevalence of current asthma, the prevalence of frequent wheezing, school absence, and lung function. For children aged 4 to 11 years, we also determined the effect of prenatal maternal smoking on these outcomes. Results: We observed effects of ETS exposure in all age groups, although the effects varied between age groups. Among all children significant effects associated with high cotinine levels were for wheezing apart from cold in the past year (odds ratio [OR], 1.8; 95% confidence interval [CI], 1.1-2.8); 6 or more days of school absence in the past year (OR, 2.0; 95% CI, 1.4-2.8); and lung function decrements in the forced expiratory volume in 1 second (mean change, -1.8%; 95% CI, -3.2% to -0.4%) and the maximal midexpiratory flow (mean change, -5.9%; 95% CI, -8.1% to -3.4%). Although current and ever asthma were not significantly associated with high cotinine levels in the overall group (OR, 1.5; 95% CI, 0.8-2.7, and OR, 1.3; 95% CI, 0.8-2.2, respectively), they were increased significantly among 4- to 6-year-old children (OR, 5.3; 95% CI, 2.2-12.7, and OR, 2.3; 95% CI, 1.1-5.1, respectively). Conclusions: We investigated recent ETS exposures as important predictors of respiratory health outcomes in children 4 years and older. Environmental tobacco smoke exposure affects children of all ages, although the exact effects may vary between age groups.	Ctr Dis Control & Prevent, Air Pollut & Resp Hlth Branch, Div Environm Hazards & Hlth Effects, Natl Ctr Environm Hlth, Atlanta, GA 30333 USA; Ctr Dis Control, Ctr Chron Dis Prevent & Hlth Promot, Epidemiol Branch, Off Smoking & Hlth, Atlanta, GA 30333 USA; Ctr Dis Control & Prevent, Off Vital & Hlth Stat, Natl Ctr Hlth Stat, Washington, DC USA; Repace Associates, Bowie, MD USA	Mannino, DM (reprint author), Ctr Dis Control & Prevent, Air Pollut & Resp Hlth Branch, Div Environm Hazards & Hlth Effects, Natl Ctr Environm Hlth, 1600 Clifton Rd,MS E-17, Atlanta, GA 30333 USA.			Mannino, David/0000-0003-3646-7828			American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P1285, DOI 10.1164/ajrccm/136.5.1285; Benowitz NL, 1996, EPIDEMIOL REV, V18, P188; California Environmental Protection Agency, 1997, TOB CONTROL, V6, P346; Caraballo RS, 1998, JAMA-J AM MED ASSOC, V280, P135, DOI 10.1001/jama.280.2.135; Cook DG, 1999, THORAX, V54, P357; Cook DG, 1997, THORAX, V52, P1081; Cook DG, 1998, THORAX, V53, P884; DOCKERY DW, 1994, ANNU REV PUBL HEALTH, V15, P107, DOI 10.1146/annurev.pu.15.050194.000543; Gergen PJ, 1998, PEDIATRICS, V101, part. no., DOI 10.1542/peds.101.2.e8; Gold DR, 1999, EPIDEMIOLOGY, V10, P8, DOI 10.1097/00001648-199901000-00004; Klepeis NE, 1999, J EXPO ANAL ENV EPID, V9, P622, DOI 10.1038/sj.jea.7500065; Mannino D M, 1996, Tob Control, V5, P13, DOI 10.1136/tc.5.1.13; Pirkle JL, 1996, JAMA-J AM MED ASSOC, V275, P1233; POPE CA, 1992, AM REV RESPIR DIS, V145, P1123; Repace JL, 1998, RISK ANAL, V18, P71, DOI 10.1111/j.1539-6924.1998.tb00917.x; REPACE JL, 1993, RISK ANAL, V13, P463, DOI 10.1111/j.1539-6924.1993.tb00747.x; SAS Institute Inc, 1990, SAS LANG REF VERS 6; Shah B. V., 1997, SUDAAN USERS MANUAL; Strachan DP, 1997, THORAX, V52, P905; Strachan DP, 1998, THORAX, V53, P204; Theunissen NCM, 1998, QUAL LIFE RES, V7, P387, DOI 10.1023/A:1008801802877; [Anonymous], 1994, VITAL HLTH STAT 1, V1, P1	22	124	129	0	1	AMER MEDICAL ASSOC	CHICAGO	515 N STATE ST, CHICAGO, IL 60610 USA	1072-4710			ARCH PEDIAT ADOL MED	Arch. Pediatr. Adolesc. Med.	JAN	2001	155	1					36	41				6	Pediatrics	Pediatrics	389RU	WOS:000166252200007	11177060	
J	Tournoy, KG; Kips, JC; Schou, C; Pauwels, RA				Tournoy, KG; Kips, JC; Schou, C; Pauwels, RA			Airway eosinophilia is not a requirement for allergen-induced airway hyperresponsiveness	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						airway hyperresponsiveness; Der p 1; eosinophil; house dust mite; immunoglobulin E	CELL-DEFICIENT MICE; DUST MITE ALLERGEN; DER-P-I; T-CELLS; DERMATOPHAGOIDES-PTERONYSSINUS; BRONCHIAL HYPERREACTIVITY; MURINE MODEL; GUINEA-PIGS; INFLAMMATION; ASTHMA	Background House dust mites (HDMs) are the major source of perennial allergens causing human allergic asthma. Animal models mimicking as closely as possible the allergic features observed in human asthma are therefore interesting tools for studying the immunological and pathophysiological mechanisms involved. Especially the role of eosinophils and allergen-specific immunoglobulin (Ig) E in the pathophysiology of airway hyperresponsiveness (AHR) remains a subject of intense debate. Objective To develop a mouse model of allergic airway inflammation and hyperresponsiveness based on the use of purified house dust mite allergen (Der p 1) as clinical relevant allergen. Furthermore, we studied the effects of low dose allergen exposure on the airway eosinophilia and AHR. Methods On day 0, C57B1/6 mice were immunized with purified Der p 1 intraperitoneally. From day 14-20, the mice were exposed daily to a 30-min aerosol of different concentrations of house dust mite extract. Results Mice, actively immunized with Der p 1 and subsequently exposed to HDM aerosols, developed AHR, eosinophil infiltration of the airways and allergen-specific IgE. Moreover, lowering the concentration of the HDM aerosol also induced AHR and IgE without apparent eosinophil influx into the airways. Der p 1-sensitized mice exposed to PBS produced IgE, but did not show AHR or eosinophil influx. Conclusion This in vivo model of HDM-induced allergic airway changes suggests that AHR is not related to either eosinophil influx or allergen-specific serum IgE, thereby reducing the importance of these factors as essential elements for allergic AHR.	State Univ Ghent Hosp, Dept Resp Dis, B-9000 Ghent, Belgium; ALK, Horsholm, Denmark	Tournoy, KG (reprint author), State Univ Ghent Hosp, Dept Resp Dis, Pintelaan 185,7 K12 IE, B-9000 Ghent, Belgium.						BUIJS J, 1995, AM J RESP CRIT CARE, V151, P873; CHUNG KF, 1995, EUR RESPIR REV, V5, P184; Corry DB, 1996, J EXP MED, V183, P109, DOI 10.1084/jem.183.1.109; Coyle AJ, 1998, EUR J IMMUNOL, V28, P2640, DOI 10.1002/(SICI)1521-4141(199809)28:09<2640::AID-IMMU2640>3.0.CO;2-X; CURTIS JL, 1991, J CLIN INVEST, V88, P1244, DOI 10.1172/JCI115428; DAVIS PB, 1995, AM J RESP CELL MOL, V12, P367; DeSanctis GT, 1997, NAT MED, V3, P460, DOI 10.1038/nm0497-460; Drazen JM, 1996, J EXP MED, V183, P1, DOI 10.1084/jem.183.1.1; Duez C, 1996, EUR J IMMUNOL, V26, P1088, DOI 10.1002/eji.1830260520; GARSSEN J, 1993, AM REV RESPIR DIS, V147, P307; Hessel EM, 1997, AM J RESP CELL MOL, V16, P325; Hogan SP, 1998, J IMMUNOL, V161, P1501; Hogan SP, 1998, AM J RESP CRIT CARE, V157, P210; Hsiue TR, 1997, INT ARCH ALLERGY IMM, V112, P295; ISHII A, 1989, INT ARCH ALLER A IMM, V89, P400; Kips JC, 1996, AM J RESP CRIT CARE, V153, P535; KIPS JC, 1997, CLIN ASTHMA REV, V1, P45; Korsgren M, 1997, J EXP MED, V185, P885, DOI 10.1084/jem.185.5.885; KUNG TT, 1994, INT ARCH ALLERGY IMM, V105, P83; LACK C, 1995, AM J RESP CRIT CARE, V152, P1765; Lee YL, 1999, SCAND J IMMUNOL, V49, P229; Lefort J, 1996, J ALLERGY CLIN IMMUN, V97, P788, DOI 10.1016/S0091-6749(96)80157-6; LIND P, 1985, J ALLERGY CLIN IMMUN, V76, P753, DOI 10.1016/0091-6749(85)90682-7; Matsubara S, 1998, INT ARCH ALLERGY IMM, V116, P67, DOI 10.1159/000023927; Mehlhop PD, 1997, P NATL ACAD SCI USA, V94, P1344, DOI 10.1073/pnas.94.4.1344; MILLS TAP, 1997, J ALLERGY CLIN IMMUN, V100, pS2; *NAT HEART LUNG BL, 1995, NHLBI PUBL; Oshiba A, 1996, J CLIN INVEST, V97, P1398, DOI 10.1172/JCI118560; Persson CGA, 1997, TRENDS PHARMACOL SCI, V18, P465; RENZ H, 1995, INT ARCH ALLERGY IMM, V106, P46; SPORIK R, 1992, CLIN EXP ALLERGY, V22, P897, DOI 10.1111/j.1365-2222.1992.tb02062.x; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; STEWART GA, 1987, INT ARCH ALLER A IMM, V83, P44; Takeda K, 1997, J EXP MED, V186, P449, DOI 10.1084/jem.186.3.449; TOVEY ER, 1981, NATURE, V289, P592, DOI 10.1038/289592a0; Yasue M, 1998, LAB ANIM SCI, V48, P346; Zhang Y, 1997, AM J RESP CRIT CARE, V155, P661; Zuany-Amorim C, 1998, SCIENCE, V280, P1265, DOI 10.1126/science.280.5367.1265	38	124	133	2	5	BLACKWELL SCIENCE LTD	OXFORD	P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	JAN	2000	30	1					79	85				7	Allergy; Immunology	Allergy; Immunology	286RN	WOS:000085459400012	10606934	
J	Lambrecht, BN; Hammad, H				Lambrecht, Bart N.; Hammad, Hamida			The role of dendritic and epithelial cells as master regulators of allergic airway inflammation	LANCET			English	Review							HOUSE-DUST MITE; THYMIC STROMAL LYMPHOPOIETIN; RESPIRATORY SYNCYTIAL VIRUS; CD4(+) T-CELLS; IMMUNE-RESPONSES; INHALED ANTIGEN; CIGARETTE-SMOKE; LYMPH-NODES; IN-VIVO; EXPERIMENTAL ASTHMA	Lung dendritic cells bridge innate and adaptive immunity, integrating a variety of stimuli from allergens, microbial colonisation, environmental pollution, and innate immune cells into a signal for T lymphocytes of the adaptive immune system. Dendritic cells have a pivotal role in the activation of T helper (Th) 2 cells and allergic inflammation. Lung dendritic cells can also prevent harmful immune responses to innocuous inhaled antigens via induction of regulatory T cells or Th1 cells. In our Review, we discuss how understanding the biology of dendritic cells is crucial for understanding the interaction between allergens, the environment, and genetics, and focus on how dendritic cells conspire with airway epithelial cells and innate pro-Th2 cells to cause allergic sensitisation and asthma.	[Lambrecht, Bart N.; Hammad, Hamida] Ghent Univ Hosp, Dept Pulm Med, Lab Immunoregulat & Mucosal Immunol, B-9000 Ghent, Belgium	Lambrecht, BN (reprint author), Ghent Univ Hosp, Dept Pulm Med, Lab Immunoregulat & Mucosal Immunol, De Pintelaan 185, B-9000 Ghent, Belgium.	bart.lambrecht@ugent.be	Hammad, Hamida/J-9391-2015; Lambrecht, Bart/K-2484-2014	Hammad, Hamida/0000-0003-3762-8603; Lambrecht, Bart/0000-0003-4376-6834			Adam E, 2010, EUR J IMMUNOL, V40, P1995, DOI 10.1002/eji.200939913; Bachem A, 2010, J EXP MED, V207, P1273, DOI 10.1084/jem.20100348; Banchereau J, 1998, NATURE, V392, P245, DOI 10.1038/32588; Barrett NA, 2009, IMMUNITY, V31, P425, DOI 10.1016/j.immuni.2009.08.014; Barrett NA, 2009, J IMMUNOL, V182, P1119; Beaty SR, 2007, J IMMUNOL, V178, P1882; BENSASSON SZ, 1990, P NATL ACAD SCI USA, V87, P1421, DOI 10.1073/pnas.87.4.1421; Boldogh I, 2005, J CLIN INVEST, V115, P2169, DOI 10.1172/JCI24422; CONSTANT S, 1995, J EXP MED, V182, P1591, DOI 10.1084/jem.182.5.1591; de Haar C, 2008, J ALLERGY CLIN IMMUN, V121, P1246, DOI 10.1016/j.jaci.2008.01.010; 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J	Heinzerling, L; Frew, AJ; Bindslev-Jensen, C; Bonini, S; Bousquet, J; Bresciani, M; Carlsen, KH; Cauwenberge, P; Darsow, U; Fokkens, WJ; Haahtela, T; van Hoecke, H; Jessberger, B; Kowalski, ML; Kopp, T; Lahoz, CN; Lodrup Carlsen, KC; Papadopoulos, NG; Ring, J; Schmid-Grendelmeier, P; Vignola, AM; Wohrl, S; Zuberbier, T				Heinzerling, L; Frew, AJ; Bindslev-Jensen, C; Bonini, S; Bousquet, J; Bresciani, M; Carlsen, KH; Cauwenberge, P; Darsow, U; Fokkens, WJ; Haahtela, T; van Hoecke, H; Jessberger, B; Kowalski, ML; Kopp, T; Lahoz, CN; Lodrup Carlsen, KC; Papadopoulos, NG; Ring, J; Schmid-Grendelmeier, P; Vignola, AM; Wohrl, S; Zuberbier, T			Standard skin prick testing and sensitization to inhalant allergens across Europe - a survey from the GA(2)LEN network	ALLERGY			English	Article						European network; inhalant allergens; standard skin prick testing	RESPIRATORY-HEALTH-SURVEY; BRONCHIAL HYPERRESPONSIVENESS; INDIVIDUAL ALLERGENS; COPENHAGEN ALLERGY; COMMON ALLERGENS; SCHOOL-CHILDREN; TEST REACTIVITY; ATOPIC ECZEMA; YOUNG-ADULTS; HAY-FEVER	Skin prick testing (SPT) is the standard method for diagnosing allergic sensitization but is to some extent performed differently in clinical centres across Europe. There would be advantages in harmonizing the standard panels of allergens used in different European countries, both for clinical purposes and for research, especially with increasing mobility within Europe and current trends in botany and agriculture. As well as improving diagnostic accuracy, this would allow better comparison of research findings in European allergy centres. We have compared the different SPT procedures operating in 29 allergy centres within the Global Allergy and Asthma European Network (GA(2)LEN). Standard SPT is performed similarly in all centres, e.g. using commercial extracts, evaluation after 15-20 min exposure with positive results defined as a wheal > 3 mm diameter. The perennial allergens included in the standard SPT panel of inhalant allergens are largely similar (e.g. cat: pricked in all centres; dog: 26 of 29 centres and Dermatophagoides pteronyssinus: 28 of 29 centres) but the choice of pollen allergens vary considerably, reflecting different exposure and sensitization rates for regional inhalant allergens. This overview may serve as reference for the practising doctor and suggests a GA(2)LEN Pan-European core SPT panel.	Charite Univ Med Berlin, Dept Dermatol & Allergy, Allergy Ctr Charite, D-10117 Berlin, Germany; Univ Southampton, Southampton Gen Hosp, Infect Inflammat & Repair Div, Southampton, Hants, England; Odense Univ Hosp, Dept Dermatol, DK-5000 Odense, Denmark; Odense Univ Hosp, Allergy Ctr, DK-5000 Odense, Denmark; CNR, Rome, Italy; INSERM, Paris, France; Univ Oslo, Natl Hosp, Voksentoppen BKL, Oslo, Norway; State Univ Ghent Hosp, Dept Otorhinolaryngol, B-9000 Ghent, Belgium; Tech Univ Munich, Dept Dermatol & Allergy Biederstein, Div Environm Dermatol & Allergy GSF, D-8000 Munich, Germany; Univ Amsterdam, Acad Med Ctr, Dept Otorhinolaryngol, NL-1105 AZ Amsterdam, Netherlands; Univ Helsinki, Cent Hosp, Helsinki, Finland; Med Univ Lodz, Dept Allergy & Clin Immunol, Lodz, Poland; Med Univ Vienna, Vienna, Austria; Univ Autonoma Madrid, Fdn Jimenez Diaz, ImmunoAllergy Dept, Madrid, Spain; Ullevaal Univ Hosp, Dept Pediat, Oslo, Norway; NKUA, Dept Allergy, Pediat Clin 2, Athens, Greece; Univ Zurich Hosp, Dept Dermatol, CH-8091 Zurich, Switzerland; Univ Palermo, CNR, Inst Internal Med & Pneumol, Palermo, Italy; CNR, IBIM, Palermo, Italy	Zuberbier, T (reprint author), Charite Univ Med Berlin, Dept Dermatol & Allergy, Allergy Ctr Charite, Schumannstr 20-21, D-10117 Berlin, Germany.		Bindslev-Jensen, Carsten/H-1877-2011; Wohrl, Stefan/B-6954-2013	Bindslev-Jensen, Carsten/0000-0002-8940-038X; Papadopoulos, Nikolaos/0000-0002-2508-3872; Wohrl, Stefan/0000-0002-6324-0007; Bonini, Sergio/0000-0003-0079-3031			AAS K, 1972, ACTA ALLERGOL, V27, P439; Anderson HR, 2004, BRIT MED J, V328, P1052, DOI 10.1136/bmj.38057.583727.47; Anyo G, 2002, CLIN EXP ALLERGY, V32, P361, DOI 10.1046/j.1365-2222.2002.01254.x; Arshad SH, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.2.e33; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Bernstein IL, 1995, ANN ALLERG ASTHMA IM, V75, P543; Bjornsson E, 1996, ANN ALLERG ASTHMA IM, V77, P327; Bousquet J, 2004, ALLERGY, V59, P1, DOI 10.1111/j.1398-9995.2004.00425.x; Bousquet PJ, 2005, ALLERGY, V60, P407, DOI 10.1111/j.1398-9995.2004.00667.x; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; BURR ML, 1994, INT J EPIDEMIOL, V23, P341, DOI 10.1093/ije/23.2.341; CANONICA GW, 1989, ALLERGY, V44, P1, DOI 10.1111/j.1398-9995.1989.tb00438.x; Carlsen KCL, 2002, ALLERGY, V57, P529, DOI 10.1034/j.1398-9995.2002.13305.x; Chinn S, 1999, EUR RESPIR J, V14, P876, DOI 10.1034/j.1399-3003.1999.14d25.x; Del Giacco SG, 2004, ALLERGY, V59, P575, DOI 10.1111/j.1398-9995.2004.00478.x; DREBORG S, 1989, J AM ACAD DERMATOL, V21, P820, DOI 10.1016/S0190-9622(89)70256-5; Droste JHJ, 1996, J ALLERGY CLIN IMMUN, V97, P922, DOI 10.1016/S0091-6749(96)80066-2; EAACI, 1993, ALLERGY, V48, P48; Gislason T, 2002, CHEST, V121, P158, DOI 10.1378/chest.121.1.158; HAAHTELA T, 1980, ALLERGY, V35, P425, DOI 10.1111/j.1398-9995.1980.tb01789.x; Janson C, 2001, EUR RESPIR J, V18, P598, DOI 10.1183/09031936.01.00205801; Jarvis D, 2002, EUR RESPIR J, V20, P1071, DOI 10.1183/09031936.02.00046802; Kauffmann F, 1999, CLIN EXP ALLERGY, V29, P17; Krouse JH, 2003, OTOLARYNG HEAD NECK, V129, pS33, DOI 10.1016/S0194-5998(03)01398-6; Linneberg A, 2000, ALLERGY, V55, P767, DOI 10.1034/j.1398-9995.2000.00672.x; Linneberg A, 2001, CLIN EXP ALLERGY, V31, P1409, DOI 10.1046/j.1365-2222.2001.01178.x; Mortz CG, 2003, ACTA DERM-VENEREOL, V83, P194, DOI 10.1080/00015550310007201; Piette V, 2002, ALLERGY, V57, P940, DOI 10.1034/j.1398-9995.2002.23536.x; Plaschke P, 1999, J ALLERGY CLIN IMMUN, V104, P58, DOI 10.1016/S0091-6749(99)70114-4; Plaschke P, 1999, ALLERGY, V54, P843, DOI 10.1034/j.1398-9995.1999.00162.x; Plaschke P, 1996, ALLERGY, V51, P461, DOI 10.1111/j.1398-9995.1996.tb04652.x; Priftanji AV, 1999, ALLERGY, V54, P1042, DOI 10.1034/j.1398-9995.1999.00108.x; Rhodius R, 2002, ANN ALLERG ASTHMA IM, V88, P374; Ronchetti R, 2003, PEDIATR ALLERGY IMMU, V14, P201, DOI 10.1034/j.1399-3038.2003.00027.x; Saraclar Y, 1997, RESP MED, V91, P461; Sastre J, 1996, ALLERGY, V51, P582; Schafer T, 1996, ALLERGY, V51, P532; SIBBALD B, 1990, BRIT J GEN PRACT, V40, P338; Sunyer J, 2000, INT J EPIDEMIOL, V29, P125, DOI 10.1093/ije/29.1.125; van Amsterdam JGC, 2003, CLIN EXP ALLERGY, V33, P187, DOI 10.1046/j.1365-2222.2003.01597.x; van Ree Ronald, 2004, Allergy, V59, P571; van Ree R, 2003, ARB P EHRLICH I BUND, V94, P70; Vartiainen E, 2002, J ALLERGY CLIN IMMUN, V109, P643, DOI 10.1067/mai.2002.123307; von Mutius E, 1998, LANCET, V351, P862, DOI 10.1016/S0140-6736(97)10100-3; Wieringa MH, 2001, CLIN EXP ALLERGY, V31, P1553, DOI 10.1046/j.1365-2222.2001.01188.x; Wuthrich B, 2001, Ther Umsch, V58, P253, DOI 10.1024/0040-5930.58.5.253; Zuberbier T, 2004, ALLERGY, V59, P338, DOI 10.1046/j.1398-9995.2003.00403.x; Zureik M, 2002, BRIT MED J, V325, P411, DOI 10.1136/bmj.325.7361.411	49	123	123	1	5	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0105-4538			ALLERGY	Allergy	OCT	2005	60	10					1287	1300		10.1111/j.1398-9995.2005.00895.x		14	Allergy; Immunology	Allergy; Immunology	960BS	WOS:000231565800011	16134996	
J	Koenig, JQ; Mar, TF; Allen, RW; Jansen, K; Lumley, T; Sullivan, JH; Trenga, CA; Larson, TV; Liu, LJS				Koenig, JQ; Mar, TF; Allen, RW; Jansen, K; Lumley, T; Sullivan, JH; Trenga, CA; Larson, TV; Liu, LJS			Pulmonary effects of indoor- and outdoor-generated particles in children with asthma	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						ambient air pollution; asthma; exhaled nitric oxide; infiltration; PM2.5	EXHALED NITRIC-OXIDE; ANTIINFLAMMATORY MEDICATION USE; PARTICULATE AIR-POLLUTION; HOSPITAL ADMISSIONS; RESPIRATORY SYMPTOMS; LUNG-FUNCTION; ASSOCIATION; EXPOSURE; MATTER; SEATTLE	Most particulate matter (PM) health effects studies use outdoor (ambient) PM as a surrogate for personal exposure. However, people spend most of their time indoors exposed to a combination of indoor-generated particles and ambient particles that have infiltrated. Thus, it is important to investigate the differential health effects of indoor- and ambient-generated particles. We combined our recently adapted recursive model and a predictive model for estimating infiltration efficiency to separate personal exposure (L) to PM2.5 (PM with aerodynamic diameter <= 2.5 pm) into its indoor-generated (E-ig) and ambient-generated (E-ag) components for 19 children with asthma. We then compared E-ig and E-ag to changes in exhaled nitric oxide (eNO), a marker of airway inflammation. Based on the recursive model with a sample size of eight children, E-ag was marginally associated with increases in eNO [5.6 ppb per 10-mu g/m(3) increase in PM2.5; 95% confidence interval (CI), -0.6 to 11.9; p = 0.08]. E-ig was not associated with eNO (-0.19 ppb change per 10 mu g/m(3)). Our predictive model allowed us to estimate E-ag and E-ig for all 19 children. For those combined estimates, only E-ag was significantly associated with an increase in eNO (E-ag: 5.0 ppb per 10-mu g/m(3) increase in PM2.5; 95% CI, 0.3 to 9.7; p = 0.04; E-ig: 3.3 ppb per 10-mu g/m(3) increase in PM2.5; 95% CI, -1.1 to 7.7; p = 0.15). Effects were seen only in children who were not using corticosteroid therapy. We conclude that the ambient-generated component of PM2.5 exposure is consistently associated with increases in eNO, and the indoor-generated component is less strongly associated with eNO.	Univ Washington, Dept Environm Hlth & Occupat Sci, Seattle, WA 98195 USA; Univ Washington, Dept Biostat, Seattle, WA 98195 USA; Univ Washington, Dept Civil & Environm Engn, Seattle, WA 98195 USA	Koenig, JQ (reprint author), Univ Washington, Dept Environm Hlth, Box 357234,Room F5614,1705 NE Pacific, Seattle, WA 98195 USA.	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Health Perspect.	APR	2005	113	4					499	503		10.1289/ehp.7511		5	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	913NO	WOS:000228158900052	15811822	
J	Brockow, K; Christiansen, C; Kanny, G; Clement, O; Barbaud, A; Bircher, A; DeWachter, P; Gueant, JL; Gueant, RMR; Mouton-Faivre, C; Ring, J; Romano, A; Sainte-Laudy, J; Demoly, P; Pichler, WJ				Brockow, K; Christiansen, C; Kanny, G; Clement, O; Barbaud, A; Bircher, A; DeWachter, P; Gueant, JL; Gueant, RMR; Mouton-Faivre, C; Ring, J; Romano, A; Sainte-Laudy, J; Demoly, P; Pichler, WJ		ENDA; EAACI Interest Grp Drug Hypersensi	Management of hypersensitivity reactions to iodinated contrast media	ALLERGY			English	Editorial Material						contrast media; diagnosis; immediate reaction; nonimmediate reaction; premedication; skin tests	DELAYED ADVERSE-REACTIONS; LATE-TYPE ALLERGY; ANAPHYLACTOID REACTION; RADIOCONTRAST MEDIUM; INVITRO HISTAMINE; DRUG-REACTIONS; SKIN-TESTS; AGENTS; PREMEDICATION; FREQUENCY	All iodinated contrast media (CM) are known to cause both immediate (less than or equal to1 h) and nonimmediate (>1 h) hypersensitivity reactions. Although for most immediate reactions an allergic hypersensitivity cannot be demonstrated, recent studies indicate that the severe immediate reactions may be IgE-mediated, while most of the nonimmediate exanthematous skin reactions, appear to be T-cell mediated. Patients who experience such hypersensitivity reactions are therefore advised to undergo an allergologic evaluation. Several investigators have found skin testing to be useful in confirming a CM allergy, especially in patients with nonimmediate skin eruptions. If a patient with confirmed allergy to a CM needs a new CM exposure, a skin test negative CM should be chosen and premedication may be tried. However, none of these precautional measures is a guarantee against a repeat reaction. More research focusing on pathomechanisms, diagnostic testing and premedication is therefore clearly needed in order to prevent CM-induced hypersensitivity reactions in the future.	Klin & Poliklin Dermatol & Allergol Biederstein, Munich, Germany; Amersham Hlth AS, Res & Dev, Oslo, Norway; Univ Hosp, Cent Hosp, Dept Internal Med Clin Immunol & Allergy, Nancy, France; Hosp Europeen G Pompidou, Serv Radiol, Paris, France; Fournier Hosp, Dept Dermatol, Nancy, France; Univ Hosp, Dept Dermatol, Allergy Unit, Basel, Switzerland; Cent Hosp, Dept Anesthesie Reanimat, Nancy, France; Fac Med Nancy, Lab Pathol Cellulaire & Mol Nutr, Nancy, France; UCSC, Allergy Unit, Dept Internal Med & Geriatr, Rome, Italy; IRCCS, Oasi Maria SS, Troina, Italy; Lab Immunol & Allergol, Paris, France; Hop Arnaud Villeneuve, INSERM, U454, Montpellier, France; Univ Bern, Inselspital, Clin Rheumatol & Clin Immunol Allergol, CH-3010 Bern, Switzerland	Brockow, K (reprint author), Tech Univ Munich, Dept Dermatol & Allergy Biederstein, Biedersteiner Str 29, D-80802 Munich, Germany.		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SWEENEY MJ, 1983, J ALLERGY CLIN IMMUN, V71, P147, DOI 10.1016/0091-6749(83)90360-3; Vernassiere C, 2004, CONTACT DERMATITIS, V50, P359, DOI 10.1111/j.0105-1873.2004.00367.x; WAKKERSGARRITSEN BG, 1976, ANN ALLERGY, V36, P122; Watanabe H, 1999, DERMATOLOGY, V198, P291, DOI 10.1159/000018133; Webb JAW, 2003, EUR RADIOL, V13, P181, DOI 10.1007/s00330-002-1650-5; WITTEN DM, 1973, AM J ROENTGENOL, V119, P832; WOLF GL, 1991, INVEST RADIOL, V26, P404, DOI 10.1097/00004424-199105000-00003; WOLF GL, 1989, AM J ROENTGENOL, V152, P939; YAMAGUCHI K, 1991, RADIOLOGY, V178, P363; Yamauchi Ritsuko, 1997, Journal of Dermatology (Tokyo), V24, P243; Yasuda R, 1998, INVEST RADIOL, V33, P1, DOI 10.1097/00004424-199801000-00001; YOCUM MW, 1978, J ALLERGY CLIN IMMUN, V62, P309, DOI 10.1016/0091-6749(78)90163-X; YOSHIKAWA H, 1992, RADIOLOGY, V183, P737	80	123	130	0	7	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	FEB	2005	60	2					150	158		10.1111/j.1398-9995.2005.00745.x		9	Allergy; Immunology	Allergy; Immunology	887VF	WOS:000226332900004	15647034	
J	Copenhaver, CC; Gern, JE; Li, ZH; Shult, PA; Rosenthal, LA; Mikus, LD; Kirk, CJ; Roberg, KA; Anderson, EL; Tisler, CJ; DaSilva, DF; Hiemke, HJ; Gentile, K; Gangnon, RE; Lemanske, RF				Copenhaver, CC; Gern, JE; Li, ZH; Shult, PA; Rosenthal, LA; Mikus, LD; Kirk, CJ; Roberg, KA; Anderson, EL; Tisler, CJ; DaSilva, DF; Hiemke, HJ; Gentile, K; Gangnon, RE; Lemanske, RF			Cytokine response patterns, exposure to viruses, and respiratory infections in the first year of life	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						interferon-gamma; respiratory syncytial virus; daycare; sibling	DAY-CARE ATTENDANCE; INTERFERON-GAMMA; SYNCYTIAL VIRUS; AIRWAY INFLAMMATION; TRACT ILLNESS; ASTHMA; CHILDREN; RATS; BRONCHIOLITIS; INFANCY	Daycare attendance and siblings are associated with viral-induced wheezing in children. Preexisting immunologic factors may influence the expression of viral infections in infancy, and in turn, recurrent infections may influence the development of immune responses. A total of 285 children were enrolled in the Childhood Origins of Asthma Project at birth and followed for at least 1 year. Cord blood and 1-year mononuclear cells were stimulated with phytohemagglutinin, and cytokine-response profiles were measured by enzyme-linked immunosorbent assay. Nasal lavage was performed for moderate to severe respiratory illnesses. Daycare attendance and/or siblings significantly increased the likelihood of contracting respiratory syncytial virus (1.5-1.6-fold increase) and rhinovirus (1.8-2.1-fold increase), and increased the risk of rhinovirus-induced wheezing (14-18% vs. 2%, p = 0.011). Cord blood IFN-gamma responses were inversely related to the frequency of viral respiratory infections (r(s) = -0.11, p = 0.05), and more significant for subjects with high exposure to other children (r(s) = -0.27, p = 0.028). The interval change in infantile IFN-gamma responses correlated positively with the frequency of viral infections in infancy (r(s) = 0.12, p = 0.047). These data suggest that neonatal IFN-gamma responses may influence antiviral activity, or may represent a marker of antiviral immunity maturation. Conversely, the frequency of viral infections in infancy can influence IFN-gamma responses.	Univ Wisconsin, Dept Pediat, Madison, WI USA; Univ Wisconsin, Dept Biostat & Med Informat, Madison, WI USA; Univ Wisconsin, Dept Med, Madison, WI USA; Univ Wisconsin, Wisconsin State Lab Hyg, Madison, WI 53706 USA	Copenhaver, CC (reprint author), Univ Wisconsin Hosp, K4-910,600 Highland Ave, Madison, WI 53792 USA.	cc.copenhaver@hosp.wisc.edu	Rosenthal, Louis/A-8868-2008		NHLBI NIH HHS [1R01HL61879-01, 1P01HL70831-01]		Aldous MB, 1996, AM J EPIDEMIOL, V143, P423; Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; Boehm U, 1997, ANNU REV IMMUNOL, V15, P749, DOI 10.1146/annurev.immunol.15.1.749; BONDESTAM M, 1984, ACTA PAEDIATR SCAND, V73, P197, DOI 10.1111/j.1651-2227.1984.tb09928.x; Celedon JC, 2003, AM J RESP CRIT CARE, V167, P1239, DOI 10.1164/rccm.200209-1063OC; Cho JY, 2001, J ALLERGY CLIN IMMUN, V108, P697, DOI 10.1067/mai.2001.119918; Choi EH, 2002, J INFECT DIS, V186, P1207, DOI 10.1086/344310; DaSilva D. F., 2003, Journal of Allergy and Clinical Immunology, V111, pS188, DOI 10.1016/S0091-6749(03)80639-5; Dorman SE, 1999, J PEDIATR-US, V135, P640, DOI 10.1016/S0022-3476(99)70064-8; Gern JE, 2002, PEDIATR ALLERGY IMMU, V13, P386, DOI 10.1034/j.1399-3038.2002.01093.x; Gern JE, 2004, J ALLERGY CLIN IMMUN, V113, P307, DOI 10.1016/j.jaci.2003.11.017; Guerra S, 2004, AM J RESP CRIT CARE, V169, P70, DOI 10.1164/rccm.200304-499OC; HOLBERG CJ, 1993, PEDIATRICS, V91, P885; Hull J, 2000, THORAX, V55, P1023, DOI 10.1136/thorax.55.12.1023; Hull J, 2003, J INFECT DIS, V188, P904, DOI 10.1086/377587; IRELAND DC, 1993, J MED VIROL, V40, P96, DOI 10.1002/jmv.1890400204; Kumar A, 1997, AM J RESP CRIT CARE, V155, P130; Lemanske RF, 2002, PEDIATR ALLERGY IMMU, V13, P38, DOI 10.1034/j.1399-3038.13.s.15.8.x; Lemanske RF, 2003, J PEDIATR-US, V142, pS3, DOI 10.1067/mpd.2003.19; Mikus LD, 2001, AM J RESP CELL MOL, V24, P74; Neaville WA, 2003, J ALLERGY CLIN IMMUN, V112, P740, DOI 10.1067/mai.2003.1716; Nja F, 2003, ARCH DIS CHILD, V88, P566, DOI 10.1136/adc.88.7.566; Roberg K. A., 2003, Journal of Allergy and Clinical Immunology, V111, pS345, DOI 10.1016/S0091-6749(03)81270-8; Rusconi F, 1999, AM J RESP CRIT CARE, V160, P1617; Sorkness RL, 1999, AM J RESP CRIT CARE, V160, P705; Strachan DP, 1996, ARCH DIS CHILD, V74, P422; TZONEVA M, 1988, CLIN GENET, V33, P454; Uhl EW, 1996, AM J RESP CRIT CARE, V154, P1834; VONMUTIUS E, 1994, BRIT MED J, V308, P692	29	123	126	1	7	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	JUL 15	2004	170	2					175	180		10.1164/rccm.200312-1647OC		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	837NU	WOS:000222643000014	15087299	
J	Bumbacea, D; Campbell, D; Nguyen, L; Carr, D; Barnes, PJ; Robinson, D; Chung, KF				Bumbacea, D; Campbell, D; Nguyen, L; Carr, D; Barnes, PJ; Robinson, D; Chung, KF			Parameters associated with persistent airflow obstruction in chronic severe asthma	EUROPEAN RESPIRATORY JOURNAL			English	Article						airway remodelling; airway thickening; eosinophils; severe asthma	QUALITY-OF-LIFE; RESOLUTION COMPUTED-TOMOGRAPHY; HEALTH-STATUS; INHALED BUDESONIDE; DISEASE SEVERITY; WALL THICKNESS; NITRIC-OXIDE; MILD ASTHMA; INFLAMMATION; LUNGS	The significance of severe airflow obstruction in severe asthma is unclear. The current study determined whether severe airflow obstruction is related to inflammatory or structural changes in the airways. Patients with severe asthma from a tertiary referral clinic were divided into two groups according to their postbronchodilator forced expiratory volume in one second (FEV1): severe persistent airflow limitation (FEV1 <50% predicted; group S; n=37) and no obstruction (FEV1 >80% pred; group N; n=29). Smoking history, atopic status, lung function tests, exhaled NO, blood eosinophil count, quality of life scores using St George's Respiratory Questionnaire and high resolution computed tomography (HRCT) of the lungs were assessed. Patients from group S were older and had longer disease duration. There was no difference in smoking history, atopic status, hospital admissions, quality of life scores and amount of treatment with inhaled or oral corticosteroids. Exhaled NO and peripheral blood eosinophils were higher in group S (21.0+/-2.4 versus 12.8+/-2.3 ppb; 0.41+/-0.06 versus 0.15+/-0.03x10(9)cells(.)L(-1), respectively). HRCT scores for bronchial wall thickening and dilatation were higher in group S with no differences in air trapping. Peripheral blood eosinophilia and bronchial wall thickening on HRCT scan were the only parameters significantly and independently associated with persistent airflow obstruction. Patients with severe asthma and irreversible airflow obstruction had longer disease duration, a greater inflammatory process and more high resolution computed tomography airway abnormalities suggestive of airway remodelling, despite being on similar treatments and experiencing equivalent impairment in quality of life.	Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW3 6LY, England; Univ Med Farm Carol Davila, Inst Natl Pneumol, Clin Pneumol, Bucharest, Romania	Chung, KF (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dovehouse St, London SW3 6LY, England.	f.chung@imperial.ac.uk		Chung, Kian Fan/0000-0001-7101-1426			American Thoracic Society, 2000, AM J RESP CRIT CARE, V162, P2341, DOI DOI 10.1164/AJRCCM.162.6.ATS9-00; Ayres JG, 1998, THORAX, V53, P315; Barley EA, 1998, RESP MED, V92, P1207, DOI 10.1016/S0954-6111(98)90423-1; Barley EA, 1999, EUR RESPIR J, V14, P591, DOI 10.1034/j.1399-3003.1999.14c18.x; BOULET LP, 1995, AM J RESP CRIT CARE, V152, P865; BOUSQUET J, 1990, NEW ENGL J MED, V323, P1033, DOI 10.1056/NEJM199010113231505; Busse W, 1999, AM J RESP CRIT CARE, V160, P1035; Carr DH, 1998, RESP MED, V92, P448, DOI 10.1016/S0954-6111(98)90290-6; Chung KF, 1999, EUR RESPIR J, V13, P1198; Godard P, 2002, EUR RESPIR J, V19, P61, DOI 10.1183/09031936.02.00232001; HIGGINS BG, 1989, AM REV RESPIR DIS, V140, P1368; Jatakanon A, 1999, AM J RESP CRIT CARE, V160, P1532; Jatakanon A, 1999, THORAX, V54, P108; JONES PW, 1992, AM REV RESPIR DIS, V145, P1321; JUNIPER EF, 1992, THORAX, V47, P76, DOI 10.1136/thx.47.2.76; Juniper EF, 2001, EUR RESPIR J, V18, P38, DOI 10.1183/09031936.01.00088301; KHARITONOV SA, 1994, LANCET, V343, P133, DOI 10.1016/S0140-6736(94)90931-8; Kraft M, 1996, AM J RESP CRIT CARE, V154, P1505; Lange P, 1998, NEW ENGL J MED, V339, P1194, DOI 10.1056/NEJM199810223391703; Lim S, 1999, AM J RESP CRIT CARE, V159, P22; LYNCH DA, 1993, RADIOLOGY, V188, P829; Minshall EM, 1997, AM J RESP CELL MOL, V17, P326; Moy ML, 2001, AM J RESP CRIT CARE, V163, P924; Niimi A, 2000, AM J RESP CRIT CARE, V162, P1518; Paganin F, 1996, AM J RESP CRIT CARE, V153, P110; PAGANIN F, 1992, AM REV RESPIR DIS, V146, P1084; Park CS, 1997, RADIOLOGY, V203, P361; Quanjer P H, 1993, Eur Respir J Suppl, V16, P85; Redington AE, 1997, THORAX, V52, P310; Robinson DS, 2003, EUR RESPIR J, V22, P478, DOI 10.1183/09031936.03.00017003; Stirling RG, 1998, THORAX, V53, P1030; ten Brinke A, 2001, AM J RESP CRIT CARE, V164, P744; ULRIK CS, 1995, CLIN EXP ALLERGY, V25, P820, DOI 10.1111/j.1365-2222.1995.tb00024.x; Wenzel SE, 1999, AM J RESP CRIT CARE, V160, P1001; Wenzel SE, 1997, AM J RESP CRIT CARE, V156, P737	35	123	129	0	3	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	JUL	2004	24	1					122	128		10.1183/09031936.04.00077803		7	Respiratory System	Respiratory System	839FR	WOS:000222769400020	15293614	
J	Shinagawa, K; Kojima, M				Shinagawa, K; Kojima, M			Mouse model of airway remodeling - Strain differences	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; eosinophil; airway hyperresponsiveness; A/J mouse	SMOOTH-MUSCLE; CHRONIC EXPOSURE; MURINE MODEL; FATAL ASTHMA; INBRED MICE; INFLAMMATION; HYPERRESPONSIVENESS; EPITHELIUM; ANTIGEN; RESPONSIVENESS	We found that continuous eosinophilic inflammation after repeated antigen instillation into the nose was observed only in A/J mice, not in three other strains. Histologic analysis of tissues from A/J mice revealed features typical of airway remodeling, i.e., airway wall thickening and increased Collagen depositions were observed after 12 weeks' antigen exposure. Persistent airway hyperresponsiveness (AHR) was observed in chronically antigen-exposed A/J mice. Eosinophilic inflammation, Collagen deposition, and airway wall thickening were all less marked in BALB/c mice than in A/J mice, and no AHR was observed in the former strain. In C57BL/6 and C3H/HeJ mice, eosinophilic inflammation, airway wall thickening, and AHR were not observed at all, although slightly increase Collagen deposition was observed. Thus, we found that these changes were strain-dependent. On the other hand, in A/J mice inhalational antigen challenge after ovalbumin/alum immunization led only to a transient increase in eosinophils and to less airway wall thickening, indicating the importance of the protocol used. Use of A/J mice and giving antigen by instillation via the nose is to be recommended for studies of the mechanisms underlying asthma. In particular, useful qualitative and quantitative information relating to the structural and histologic changes in the lungs may be obtainable using this model.	Kissei Pharmaceut Co Ltd, Pharmacol Lab, Nagano 3998304, Japan	Shinagawa, K (reprint author), Kissei Pharmaceut Co Ltd, Pharmacol Lab, 4365-1 Kashiwabara, Nagano 3998304, Japan.						AIKAWA T, 1992, CHEST, V101, P916, DOI 10.1378/chest.101.4.916; Akbari O, 2001, NAT IMMUNOL, V2, P725, DOI 10.1038/90667; BAI A, 1994, J APPL PHYSIOL, V77, P1011; Barnes KC, 1998, IMMUNOL TODAY, V19, P325, DOI 10.1016/S0167-5699(97)01241-3; Bento AM, 1998, ALLERGY ASTHMA PROC, V19, P353, DOI 10.2500/108854198778612672; Black JL, 2001, AM J RESP CRIT CARE, V164, pS63; Bousquet J, 2000, AM J RESP CRIT CARE, V161, P1720; BOUSQUET J, 1990, NEW ENGL J MED, V323, P1033, DOI 10.1056/NEJM199010113231505; Brewer JP, 1999, AM J RESP CRIT CARE, V160, P1150; CARROLL N, 1993, AM REV RESPIR DIS, V147, P405; CUTZ E, 1978, HISTOPATHOLOGY, V2, P407, DOI 10.1111/j.1365-2559.1978.tb01735.x; Doull IJM, 1996, AM J RESP CRIT CARE, V153, P1280; Duguet A, 2000, AM J RESP CRIT CARE, V161, P839; DUNNILL MS, 1969, THORAX, V24, P176, DOI 10.1136/thx.24.2.176; DUNNILL MS, 1960, J CLIN PATHOL, V13, P27, DOI 10.1136/jcp.13.1.27; Ewart SL, 2000, AM J RESP CELL MOL, V23, P537; Fahy JV, 2001, AM J RESP CRIT CARE, V164, pS46; HIRANO T, 1988, INT ARCH ALLER A IMM, V85, P47; JAMES AL, 1989, AM REV RESPIR DIS, V139, P242; Jeffery PK, 2001, AM J RESP CRIT CARE, V164, pS28; Johnson PRA, 2001, AM J RESP CRIT CARE, V164, P474; Kumar RK, 2002, AM J RESP CELL MOL, V27, P267, DOI 10.1165/rcmb.F248; LAITINEN LA, 1985, AM REV RESPIR DIS, V131, P599; Lloyd CM, 2001, ADV IMMUNOL, V77, P263, DOI 10.1016/S0065-2776(01)77019-8; McDonald DM, 2001, AM J RESP CRIT CARE, V164, pS39; MONTEFORT S, 1993, CLIN EXP ALLERGY, V23, P185, DOI 10.1111/j.1365-2222.1993.tb00880.x; NAGATANI Y, 1986, YAKUGAKU ZASSHI, V106, P41; Ohta K, 1999, J ALLERGY CLIN IMMUN, V104, P1024; Orsida BE, 2001, AM J RESP CRIT CARE, V164, P117; Redington AE, 2000, CLIN EXP ALLERGY, V30, P42; SAETTA M, 1991, AM REV RESPIR DIS, V143, P138; Shinagawa K, 2000, J IMMUNOL METHODS, V237, P65, DOI 10.1016/S0022-1759(00)00134-4; Shinagawa K, 2003, INT ARCH ALLERGY IMM, V130, P150, DOI 10.1159/000069005; Swirski FK, 2002, J IMMUNOL, V169, P3499; Temelkovski J, 1998, THORAX, V53, P849; Weiner HL, 1997, IMMUNOL TODAY, V18, P335, DOI 10.1016/S0167-5699(97)01053-0; Wilson JW, 1997, CLIN EXP ALLERGY, V27, P363; Yasue M, 1998, LAB ANIM SCI, V48, P346; Yiamouyiannis CA, 1999, AM J PATHOL, V154, P1911, DOI 10.1016/S0002-9440(10)65449-1	39	123	130	0	5	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	OCT 15	2003	168	8					959	967		10.1164/rccm.200210-1188OC		9	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	731JY	WOS:000185881600009	12857720	
J	Jahn-Schmid, B; Harwanegg, C; Hiller, R; Bohle, B; Ebner, C; Scheiner, O; Mueller, MW				Jahn-Schmid, B; Harwanegg, C; Hiller, R; Bohle, B; Ebner, C; Scheiner, O; Mueller, MW			Allergen microarray: comparison of microarray using recombinant allergens with conventional diagnostic methods to detect allergen-specific serum immunoglobulin E	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						IgE; microarray technology; recombinant allergen; Type I allergy	GRASS PHLEUM-PRATENSE; POLLEN ALLERGEN; MAJOR ALLERGEN; PROTEIN MICROARRAYS; IGE; IMMUNOASSAYS; DISEASES; THERAPY; CLONING; GENE	Background The availability of recombinant allergens and recent advances in biochip technology led to the development of a novel test system for the detection of allergen-specific IgE. Objective To test the performance of this allergen microarray in a serological analytical study. Methods Standard allergens contained in grass pollen (Phl p 1, Phl p 2, Phl p 5 and Phl p 6) and tree pollen ( Bet v 1 and Bet v 2) were used as a model system. The detection of allergen-specific serum IgE using microarrays was compared with standard test systems: CAP/RAST and an in-house ELISA. In order to test the analytical sensitivity of the assays, geometric dilutions of a serum pool containing high levels of pollen-specific IgE from allergic individuals were tested in each system. To assess the analytical specificity, the sera of 51 patients with presumptive allergic symptoms were collected before diagnosis. Thereafter, the results for grass/tree-pollen-specific IgE were compared. Results The microarray has a good dynamic range similar to the CAP/RAST system. Microarray and ELISA showed comparable analytical sensitivity exceeding the CAP/RAST system. With respect to the analytical specificity, no significant cross-reactivity of the allergens was observed. For two of the allergens tested, weak positive signals were detected in the microarray test system, whereas they were not detectable by CAP/ RAST. Conclusion A good correlation of presently used methods to detect serum IgE and the novel microarray test system was observed. As a next step, a careful validation of this method for a multitude of allergens and a thorough clinical evaluation has to be provided. Microarray testing of allergen-specific IgE can be presumed to be the method of choice for a prospective component-resolved diagnosis of Type I allergy, and the basis for the design and monitoring of a patient-tailored specific immunotherapy in the future.	Univ Vienna, Inst Pathophysiol, A-1090 Vienna, Austria; VBC GENOMICS Biosci Res GmbH, Vienna, Austria	Scheiner, O (reprint author), Univ Vienna, Inst Pathophysiol, AKH-3Q,Wahringer Gurtel 18-20, A-1090 Vienna, Austria.						Avseenko NV, 2002, ANAL CHEM, V74, P927, DOI 10.1021/ac010970k; Breiteneder H, 2001, INT ARCH ALLERGY IMM, V124, P48, DOI 10.1159/000053665; BREITENEDER H, 1989, EMBO J, V8, P1935; DOLECEK C, 1993, FEBS LETT, V335, P299, DOI 10.1016/0014-5793(93)80406-K; Haab B., 2001, GENOME BIOL, V2; Hiller R, 2002, FASEB J, V16, P414, DOI 10.1096/fj.01-0711fje; Joos TO, 2002, CURR OPIN CHEM BIOL, V6, P76, DOI 10.1016/S1367-5931(01)00289-7; Joos TO, 2000, ELECTROPHORESIS, V21, P2641, DOI 10.1002/1522-2683(20000701)21:13<2641::AID-ELPS2641>3.3.CO;2-X; Kazemi-Shirazi L, 2002, INT ARCH ALLERGY IMM, V127, P259, DOI 10.1159/000057742; Kim TE, 2002, EXP MOL MED, V34, P152; LAFFER S, 1994, J ALLERGY CLIN IMMUN, V94, P689, DOI 10.1016/0091-6749(94)90176-7; Lueking A, 1999, ANAL BIOCHEM, V270, P103, DOI 10.1006/abio.1999.4063; Lundberg M, 2001, ALLERGY, V56, P794, DOI 10.1034/j.1398-9995.2001.056008794.x; MacBeath G, 2000, SCIENCE, V289, P1760; Mezzasoma L, 2002, CLIN CHEM, V48, P121; Monzavi-Karbassi B, 2002, TRENDS BIOTECHNOL, V20, P207, DOI 10.1016/S0167-7799(02)01940-6; Robinson WH, 2002, NAT MED, V8, P295, DOI 10.1038/nm0302-295; SCHEINER O, 1995, ALLERGY, V50, P384, DOI 10.1111/j.1398-9995.1995.tb01167.x; Schmid-Grendelmeier P, 2001, INT ARCH ALLERGY IMM, V125, P96, DOI 10.1159/000053803; Schweitzer B, 2000, P NATL ACAD SCI USA, V97, P10113, DOI 10.1073/pnas.170237197; Suck R, 2002, ALLERGY, V57, P821, DOI 10.1034/j.1398-9995.2002.23705.x; VALENTA R, 1991, SCIENCE, V253, P557, DOI 10.1126/science.1857985; Valenta R, 1995, CURR OPIN IMMUNOL, V7, P751, DOI 10.1016/0952-7915(95)80043-3; VALENTA R, 1992, INT ARCH ALLERGY IMM, V97, P287; Valenta R, 1999, CLIN EXP ALLERGY, V29, P896; VRTALA S, 1993, J IMMUNOL, V151, P4773; Vrtala S, 1999, J IMMUNOL, V163, P5489	27	123	132	0	12	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	OCT	2003	33	10					1443	1449		10.1046/j.1365-2222.2003.01784.x		7	Allergy; Immunology	Allergy; Immunology	727KN	WOS:000185657300019	14519153	
J	Kull, I; Wickman, M; Lilja, G; Nordvall, SL; Pershagen, G				Kull, I; Wickman, M; Lilja, G; Nordvall, SL; Pershagen, G			Breast feeding and allergic diseases in infants - a prospective birth cohort study	ARCHIVES OF DISEASE IN CHILDHOOD			English	Article							AGE 6; ASTHMA; CHILDREN; CHILDHOOD; EXPOSURE; SENSITIZATION; PREDICTORS; RISK; OLD	Aims: To investigate the effect of breast feeding on allergic disease in infants up to 2 years of age. Methods: A birth cohort of 4089 infants was followed prospectively in Stockholm, Sweden. Information about various exposures was obtained by parental questionnaires when the infants were 2 months old, and about allergic symptoms and feeding at 1 and 2 years of age. Duration of exclusive and partial breast feeding was assessed separately. Symptom related definitions of various allergic diseases were used. Odds ratios (OR) and 95% confidence intervals (CI) were estimated in a multiple logistic regression model. Adjustments were made for potential confounders. Results: Children exclusively breast fed during four months or more exhibited less asthma (7.7% v 12%, ORadj 0.7, 95% CI 0.5 to 0.8), less atopic dermatitis (24% v 27%, ORadj = 0.8, 95% CI 0.7 to 1.0), and less suspected allergic rhinitis (6.5% v 9%, ORadj = 0.7, 95% CI 0.5 to 1.0) by 2 years of age. There was a significant risk reduction for asthma related to partial breast feeding during six months or more (ORadj = 0.7, 95% CI 0.5 to 0.9). Three or more of five possible allergic disorders-asthma, suspected allergic rhinitis, atopic dermatitis, food allergy related symptoms, and suspected allergic respiratory symptoms after exposure to pets or pollen-were found in 6.5% of the children. Exclusive breast feeding prevented children from having multiple allergic disease (ORadj = 0.7, 95% CI 0.5 to 0.9) during the first two years of life. Conclusion: Exclusive breast feeding seems to have a preventive effect on the early development of allergic disease-that is, asthma, atopic dermatitis, and suspected allergic rhinitis, up to 2 years of age. This protective effect was also evident for multiple allergic disease.	Stockholm Cty Council, Dept Environm Hlth, Stockholm, Sweden; Karolinska Inst, Sachs Childrens Hosp, Inst Sodersjukhuset, Stockholm, Sweden; Uppsala Univ, Dept Womens & Childrens Hlth, Uppsala, Sweden; Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden	Wickman, M (reprint author), Karolinska Hosp, Dept Environm Hlth, Norrbacka Bldg,Level 3, SE-17176 Stockholm, Sweden.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Bergmann RL, 1998, CLIN EXP ALLERGY, V28, P965; BURR ML, 1993, ARCH DIS CHILD, V68, P724; Csonka P, 2000, PEDIATR ALLERGY IMMU, V11, P225, DOI 10.1034/j.1399-3038.2000.00088.x; Foucard T, 2000, ACTA PAEDIATR, V89, P71, DOI 10.1080/080352500750027439; Gdalevich M, 2001, J PEDIATR-US, V139, P261, DOI 10.1067/mpd.2001.117006; HOST A, 1988, ACTA PAEDIATR SCAND, V77, P663, DOI 10.1111/j.1651-2227.1988.tb10727.x; KRAMER, 1988, J PEDIAT, V112, P81; Lannero E, 2002, PEDIATR ALLERGY IMMU, V13, P182, DOI 10.1034/j.1399-3038.2002.01055.x; LEWIS S, 1995, EUR RESPIR J, V8, P349, DOI 10.1183/09031936.95.08030349; MCCONNOCHIE KM, 1986, PEDIATR PULM, V2, P260, DOI 10.1002/ppul.1950020503; Melen E, 2001, ALLERGY, V56, P646, DOI 10.1034/j.1398-9995.2001.00387.x; Oddy WH, 1999, BRIT MED J, V319, P815; Pearce N, 2000, THORAX, V55, P424, DOI 10.1136/thorax.55.5.424; Peat JK, 1998, CLIN EXP ALLERGY, V28, P261; Pershagen G, 1997, ALLERGY, V52, P1045, DOI 10.1111/j.1398-9995.1997.tb00174.x; RYLANDER E, 1993, EUR J EPIDEMIOL, V9, P517; SAARINEN UM, 1995, LANCET, V346, P1065, DOI 10.1016/S0140-6736(95)91742-X; SAVILAHTI E, 1987, ARCH DIS CHILD, V62, P269; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; Tariq SM, 1998, J ALLERGY CLIN IMMUN, V101, P587; VANDENPLAS Y, 1997, ACTA PAEDIATR SCAND, V86, P283; WICKMAN M, 1991, J ALLERGY CLIN IMMUN, V88, P89, DOI 10.1016/0091-6749(91)90305-8; WICKMAN M, 1992, PEDIATRIC ALLERGY IM, V3, P128, DOI 10.1111/j.1399-3038.1992.tb00036.x; WJST M, 1992, MONATSSCHR KINDERH, V140, P769; WRIGHT AL, 1995, ARCH PEDIAT ADOL MED, V149, P758; Wright AL, 2001, THORAX, V56, P192, DOI 10.1136/thorax.56.3.192	26	123	132	3	13	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0003-9888			ARCH DIS CHILD	Arch. Dis. Child.	DEC	2002	87	6					478	481		10.1136/adc.87.6.478		4	Pediatrics	Pediatrics	622PJ	WOS:000179655200007	12456543	
J	Pochard, P; Gosset, P; Grangette, C; Andre, C; Tonnel, AB; Pestel, J; Mercenier, A				Pochard, P; Gosset, P; Grangette, C; Andre, C; Tonnel, AB; Pestel, J; Mercenier, A			Lactic acid bacteria inhibit T(H)2 cytokine production by mononuclear cells from allergic patients	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergy; type 2 cytokine; lactic acid bacteria; immunomodulation; superantigen; dust mite	INTERLEUKIN-12 IL-12; PROBIOTICS; LACTOBACILLI; CHILDHOOD; RESPONSES; MICE	Background: Among factors potentially involved in the increased prevalence of allergic diseases, modification of the intestinal bacteria flora or lack of bacterial stimulation during childhood has been proposed. Lactic acid bacteria (LAB) present in fermented foods or belonging to the natural intestinal microflora were shown to exert beneficial effects on human health. Recent reports have indicated their capacity to reduce allergic symptoms. Objective: The purpose of this investigation was to determine the effect of LAB on the production of type 2 cytokines, which characterize allergic diseases. Methods: PBMCs from patients allergic to house dust mite versus those from healthy donors were stimulated for 48 hours with the related Dermatophagoides pteronyssinus allergen or with a staphylococcal superantigen. The effect of LAB preincubation was assessed by measuring the type 2 cytokine production by means of specific ELISA. Results: The tested gram-positive LAB were shown to inhibit the secretion of T(H)2 cytokines (IL-4 and IL-5). This effect was dose dependent and was observed irrespective of the LAB strain used. No significant inhibition was induced by the control, gram-negative Escherichia coli TG1. Interestingly, LAB reduced the T(H)2 cytokine production from allergic PBMCs specifically restimulated with the related allergen. The inhibition mechanism was shown to be dependent on antigen-presenting cells (ie, monocytes) and on the involvement of IL-12 and IFN-gamma. Conclusion: The tested LAB strains were demonstrated to exhibit an anti-T(H)2 activity, and thus different, strains of this family might be useful in the prevention of allergic diseases.	Inst Pasteur, INSERM U 416, F-59019 Lille, France; Inst Biol, Lab Bacteriol Ecosyst, Lille, France; Stallergenes SA, Antony, France	Pestel, J (reprint author), Inst Pasteur, INSERM U 416, 1 Rue Prof Calmette,BP 425,IFR 17, F-59019 Lille, France.						Bengmark S, 2001, CURR OPIN CLIN NUTR, V4, P571, DOI 10.1097/00075197-200111000-00019; Bjorksten B, 1999, CLIN EXP ALLERGY, V29, P342; Bjorksten B, 1997, CLIN REV ALLERG IMMU, V15, P125, DOI 10.1007/BF02826583; Bjorksten B, 1999, ALLERGY, V54, P17, DOI 10.1111/j.1398-9995.1999.tb04383.x; Cameron SB, 2001, EUR CYTOKINE NETW, V12, P210; Drouault S, 2001, VET RES, V32, P101, DOI 10.1051/vetres:2001115; Fooks LJ, 1999, INT DAIRY J, V9, P53, DOI 10.1016/S0958-6946(99)00044-8; Hessle C, 2000, INFECT IMMUN, V68, P3581, DOI 10.1128/IAI.68.6.3581-3586.2000; Holt PG, 1997, PEDIATR ALLERGY IMMU, V8, P53, DOI 10.1111/j.1399-3038.1997.tb00145.x; Isolauri E, 2000, CLIN EXP ALLERGY, V30, P1604, DOI 10.1046/j.1365-2222.2000.00943.x; Julge K, 1997, ACTA PAEDIATR, V86, P1188, DOI 10.1111/j.1651-2227.1997.tb14842.x; Kalliomaki M, 2001, LANCET, V357, P1076, DOI 10.1016/S0140-6736(00)04259-8; Kopp-Hoolihan L, 2001, J AM DIET ASSOC, V101, P229, DOI 10.1016/S0002-8223(01)00060-8; Lee YK, 2000, APPL ENVIRON MICROB, V66, P3692, DOI 10.1128/AEM.66.9.3692-3697.2000; Maassen CBM, 1998, VET QUART, V20, pS81; Marteau PR, 2001, AM J CLIN NUTR, V73, p430S; MARTINEZ FD, 1999, LANCET S2, V354; Matsuzaki T, 2000, IMMUNOL CELL BIOL, V78, P67, DOI 10.1046/j.1440-1711.2000.00887.x; Matsuzaki T, 1998, J DAIRY SCI, V81, P48; Miettinen M, 2000, J IMMUNOL, V164, P3733; Miettinen M, 1998, INFECT IMMUN, V66, P6058; Muller-Alouf H., 1999, Immunology Letters, V69, P33; Murch SH, 2001, LANCET, V357, P1057, DOI 10.1016/S0140-6736(00)04305-1; Murosaki S, 1998, J ALLERGY CLIN IMMUN, V102, P57, DOI 10.1016/S0091-6749(98)70055-7; Ouwehand AC, 1999, INT DAIRY J, V9, P43, DOI 10.1016/S0958-6946(99)00043-6; Robinson DS, 1996, CHEM IMMUNOL, V63, P187; Shida K, 1998, INT ARCH ALLERGY IMM, V115, P278, DOI 10.1159/000069458	27	123	130	0	3	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	OCT	2002	110	4					617	623		10.1067/mai.2002.128528		7	Allergy; Immunology	Allergy; Immunology	602JJ	WOS:000178501900013	12373271	
J	Rhodes, HL; Sporik, R; Thomas, P; Holgate, ST; Cogswell, JJ				Rhodes, HL; Sporik, R; Thomas, P; Holgate, ST; Cogswell, JJ			Early life risk factors for adult asthma: A birth cohort study of subjects at risk	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; atopy; bronchial hyperresponsiveness; food allergen; aeroallergen; risk factors	ALLERGIC AIRWAY DISEASE; DUST MITE ALLERGEN; SERUM IGE; CHILDHOOD ASTHMA; LUNG-FUNCTION; CHILDREN; ATOPY; EXPOSURE; AGE; RESPONSIVENESS	Background: Prediction of adult asthma is important, and early prevention strategies should be targeted at those most at risk. Identifying high-risk children at an early age, however, is currently difficult. Objective: We sought to determine those factors present in early life that predict an increased risk of adult asthma. Methods: A prospective cohort study of subjects at risk of asthma and atopy was undertaken in Poole, England. One hundred babies of atopic parents were recruited at birth. During the first 5 years of life, subjects were recalled annually, all respiratory events were reported, and skin prick tests and total serum IgE measurements were performed. At 11 and 22 years, bronchial hyperresponsiveness was also measured. Seventy-three subjects were followed up at 5 years, 67 at 11 years, and 63 at 22 years. Results: Twenty-three (37%) adult subjects reported wheezing within the previous 12 months. Fifteen (25%) of these subjects showed signs of bronchial hyperresponsiveness and were regarded as asthmatic. Wheezing before the age of 2 years occurred in 28% and was not significantly related to adult asthma (odds ratio, 0.3; 95% CI, 0.03-1.7; P =.19). A positive skin prick test response to hen's egg, cow's milk, or both in the first year was independently predictive of adult asthma (odds ratio, 10.7; 95% CI, 2.1-55.1; P =.001; sensitivity, 57%; specificity, 89%). Conclusion: Prediction of adult asthma remains difficult. In this study of subjects at risk of atopy, skin sensitivity to hen's egg or cow's milk in the first year was predictive of adult asthma.	Poole Hosp, Dept Paediat, Poole, Dorset, England; Bournemouth Univ, Poole Hosp, Dorset Res & Dev Support Unit, Bournemouth, Dorset, England; Dept Univ Med, Southampton, Hants, England	Rhodes, HL (reprint author), Southampton Gen Hosp, Room EG228,Mail Point 43,Tremona Rd, Southampton SO16 6YD, Hants, England.			Thomas, Peter/0000-0003-2478-4324			Bergmann RL, 1997, CLIN EXP ALLERGY, V27, P752, DOI 10.1046/j.1365-2222.1997.310899.x; Bergmann RL, 1998, CLIN EXP ALLERGY, V28, P965; BRITTEN N, 1987, BRIT MED J, V294, P1317; BURROWS B, 1989, NEW ENGL J MED, V320, P271, DOI 10.1056/NEJM198902023200502; CHAPMAN MD, 1980, J IMMUNOL, V125, P587; Clough JB, 1999, AM J RESP CRIT CARE, V160, P1473; Cook DG, 1999, THORAX, V54, P357; *CYTEL SOFTW CORP, 1999, LOGX 4 WIND LOG REGR; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Hide DW, 1996, ALLERGY, V51, P89, DOI 10.1111/j.1398-9995.1996.tb04563.x; Hijazi N, 2000, THORAX, V55, P775, DOI 10.1136/thorax.55.9.775; HORN MEC, 1979, THORAX, V34, P23, DOI 10.1136/thx.34.1.23; Kulig M, 1998, PEDIAT ALLERG IMM-UK, V9, P61, DOI 10.1111/j.1399-3038.1998.tb00305.x; Leadbitter P, 1999, THORAX, V54, P905; LEWIS S, 1995, EUR RESPIR J, V8, P349, DOI 10.1183/09031936.95.08030349; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; MARTINEZ FD, 1988, NEW ENGL J MED, V319, P1112, DOI 10.1056/NEJM198810273191702; NICKEL R, 1999, J ALLERGY CLIN IMMUN, V5, P613; Oddy WH, 1999, BRIT MED J, V319, P815; PATTEMORE PK, 1992, CLIN EXP ALLERGY, V22, P325, DOI 10.1111/j.1365-2222.1992.tb03094.x; Rasanen M, 2000, THORAX, V55, P25, DOI 10.1136/thorax.55.1.25; RONMARK E, 2000, EUR RESP J S31, V16, pS515; RONNA RJ, 1993, THORAX, V48, P21; SEARS MR, 1991, NEW ENGL J MED, V325, P1067, DOI 10.1056/NEJM199110103251504; Shaheen SO, 1999, THORAX, V54, P396; SIGURS N, 1994, J ALLERGY CLIN IMMUN, V94, P757, DOI 10.1016/0091-6749(94)90184-8; SPORIK R, 1991, ARCH DIS CHILD, V66, P1050; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; STROPE GL, 1991, AM REV RESPIR DIS, V144, P655; TOVEY ER, 1981, AM REV RESPIR DIS, V124, P630; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 1999, EUR RESPIR J, V14, P4, DOI 10.1034/j.1399-3003.1999.14a03.x; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; Warner JO, 1998, PEDIATR ALLERGY IMMU, V9, P116; Warner JO, 1998, CLIN EXP ALLERGY, V28, P71; WILSON NM, 1992, ARCH DIS CHILD, V22, P325; YAN K, 1983, THORAX, V38, P760, DOI 10.1136/thx.38.10.760; ZEIGER RS, 1995, J ALLERGY CLIN IMMUN, V95, P1179, DOI 10.1016/S0091-6749(95)70074-9	38	123	126	0	4	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	NOV	2001	108	5					720	725		10.1067/mai.2001.119151		6	Allergy; Immunology	Allergy; Immunology	498RG	WOS:000172523800010	11692095	
J	Klinnert, MD; Nelson, HS; Price, MR; Adinoff, AD; Leung, DYM; Mrazek, DA				Klinnert, MD; Nelson, HS; Price, MR; Adinoff, AD; Leung, DYM; Mrazek, DA			Onset and persistence of childhood asthma: Predictors from infancy	PEDIATRICS			English	Article						pediatric asthma; parenting; IgE allergy; psychosocial problems; risk; respiratory illness	RISK-FACTORS; NATURAL-HISTORY; CORD BLOOD; CHILDREN; STRESS; IGE; MOTHERS; HYPERRESPONSIVENESS; SENSITIZATION; RESPONSES	family history of asthma, asthma onset by 3 years of age was found previously to be positively associated with variables from the first year of life, including elevated total immunoglobulin E (IgE), frequent respiratory infections, and parenting difficulties. We followed this cohort of genetically at-risk children to investigate the relationship between factors assessed in infancy and asthma, allergy, and psychological status at school age. Methods. A cohort of 150 children who were at risk for developing asthma were identified prenatally on the basis of the mothers' having asthma. For 28 children, the father had asthma as well, putting them at bilateral genetic risk. Families primarily were middle and upper middle class Caucasians. Parents came to the clinic during the third trimester of pregnancy for assessments of medical and psychosocial functioning. A home visit took place when the infant was 3 weeks old, when parenting risk was assessed before the onset of any asthma symptoms. Parenting difficulties included problems with infant caregiving as well as components of maternal functioning, such as postpartum depression and inadequate marital support. Blood was drawn for serum IgE at 6 months of age. Parents and offspring subsequently came to the clinic multiple times, with the last clinic visit during the child's sixth year. Follow-up at age 6 involved a clinic visit for allergy and psychosocial evaluations, consisting of interviews and a behavior questionnaire. Seventy-seven children received the allergy and psychosocial evaluation, 26 received the psychosocial evaluation in the clinic, and 30 families received telephone interviews and mailed in questionnaires. Additional monitoring of families by telephone and mail was maintained over the next 2 years, until the children were 8, to ensure accurate characterization of the course of illness. Comprehensive medical records were obtained and reviewed for all health care contacts. Children were designated as having asthma when there was documentation in medical records of physician-diagnosed asthma, observed wheezing, and/or prescription of asthma medications during the time period when the child was between 6 and 8 years of age. Parental reports of the occurrence of asthma corroborated the medical record data. Results. Data regarding asthma status were available for 145 children through 8 years of age. Forty (28%) of the children manifested asthma between 6 and 8 years of age. Among variables previously reported to predict asthma onset by age 3, 3 proved to have significant univariate relationships with asthma between ages 6 and 8: elevated IgE levels measured when the children were 6 months of age, global ratings of parenting difficulties measured when infants were 3 weeks old, and higher numbers of respiratory infections in the first year of life. Among these offspring of mothers with asthma, paternal asthma showed a significant association with asthma between ages 6 and 8. Eczema in the first year was not significantly related to later asthma. Multiple logistic regression showed that the model that best predicted asthma at ages 6 to 8 from infancy variables included 2 main effects. The adjusted odds ratio for 6-month IgE was 2.15 (1.51, 3.05) and for parenting difficulties was 2.07 (1.15, 3.71). Although socioeconomic status (SES) was not associated with asthma at ages 6 to 8, families of lower SES were more likely to be rated as having parenting difficulties early in the child's life. The mothers of lower SES breastfed for a shorter period of time and were more likely to smoke during their infant's first year. There were more respiratory infections during the first year of life among infants whose mother was rated as having more parenting difficulties. Mothers who reported smoking breastfed their infants for a shorter length of time. Male gender was significantly associated with higher IgE levels when infants were 6 months of age. Laboratory testing was completed for 77 children at age 6. Total serum IgE levels were significantly higher for the children with asthma between ages 6 and 8. Skin-prick testing showed that the children with asthma had significantly more positive skin test reactions than did the children without asthma. Psychosocial interview data at 6 years of age were available for 103 families, and behavioral questionnaires were available for 133 families. On the basis of 6-year interviews, children with asthma were rated as being at greater psychological risk than were the children without asthma. Mothers' Child Behavior Checklist (CBCL) ratings of their children's behavior indicated higher internalizing scores for the children with asthma as compared with the children without asthma. Like the 6-month IgE, 6-year IgE was higher for boys. IgE levels measured at 6 months of age were significantly correlated with 6-year IgE levels. Parenting difficulties measured at 3 weeks were significantly correlated with 6-year measures of maternal depression, CBCL Internalizing score, and Child Psychological Risk (CPR) score. There also were significant correlations among the psychosocial variables assessed when the children were 6 years of age; maternal depression was significantly associated with child CBCL Internalizing score and CPR score, and the last 2 also were significantly correlated. Multiple logistic regression showed that 2 concurrently measured variables entered the model showing the strongest associations with asthma at ages 6 to 8. The adjusted odds ratio for CPR score was 3.21 (1.29-7.96) and for 6-year IgE was 1.71 (1.04-2.80). Conclusions. This study of the natural history of childhood asthma focused on the development of asthma into the school-age years in a genetically at-risk group of children. The relationships between biological and psychosocial variables in the first year and school-age asthma support the formulation of asthma as beginning early in life, with the developing immune system interacting with environmental influences. The data provide support for the possible contribution of psychosocial factors to asthma onset and persistence into childhood.	Natl Jewish Med & Res Ctr, Denver, CO 80206 USA; Colorado Allergy & Asthma Ctr, Littleton, CO USA; Mayo Clin, Rochester, MN USA	Klinnert, MD (reprint author), Natl Jewish Med & Res Ctr, 1400 Jackson St, Denver, CO 80206 USA.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	NCRR NIH HHS [M01 RR00051]; NHLBI NIH HHS [HL-36577, R01HL53584]		Achenbach TM, 1991, MANUAL CHILD BEHAV C; ARSHAD SH, 1992, J ALLERGY CLIN IMMUN, V90, P235, DOI 10.1016/0091-6749(92)90077-F; Braun-Fahrlander C, 1998, PEDIATR PULM, V25, P159, DOI 10.1002/(SICI)1099-0496(199803)25:3<159::AID-PPUL5>3.0.CO;2-H; BUSSE WW, 1995, AM J RESP CRIT CARE, V151, P249; Chilcoat HD, 1997, J AM ACAD CHILD PSY, V36, P971, DOI 10.1097/00004583-199707000-00020; COGSWELL JJ, 1987, ARCH DIS CHILD, V62, P338; COHEN S, 1991, NEW ENGL J MED, V325, P606, DOI 10.1056/NEJM199108293250903; DeGarmo DS, 1999, CHILD DEV, V70, P1231, DOI 10.1111/1467-8624.00089; GERGEN PJ, 1988, PEDIATRICS, V81, P1; GLEZEN WP, 1998, RSV ASTHMA IS THERE, P1; Gunnar MR, 1998, PREV MED, V27, P208, DOI 10.1006/pmed.1998.0276; GUNNAR MR, 1992, PEDIATRICS, V90, P491; GUNNAR MR, 1989, DEV PSYCHOL, V25, P355, DOI 10.1037//0012-1649.25.3.355; HERBERT TB, 1993, PSYCHOSOM MED, V55, P364; HERRSCHER RF, 1992, J CLIN INVEST, V90, P596, DOI 10.1172/JCI115898; Hoek G, 1999, INT J EPIDEMIOL, V28, P293, DOI 10.1093/ije/28.2.293; Holgate ST, 1997, LANCET, V350, P5; Hollingshead A. 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J	Tang, CB; Inman, MD; van Rooijen, N; Yang, PC; Shen, HH; Matsumoto, K; O'Byrne, PM				Tang, CB; Inman, MD; van Rooijen, N; Yang, PC; Shen, HH; Matsumoto, K; O'Byrne, PM			Th type 1-stimulating activity of lung macrophages inhibits Th2-mediated allergic airway inflammation by an IFN-gamma-dependent mechanism	JOURNAL OF IMMUNOLOGY			English	Article							ANTIGEN-PRESENTING CELLS; DENDRITIC CELLS; ALVEOLAR MACROPHAGES; IMMUNE-RESPONSES; IL-12 PRODUCTION; INHALED ANTIGEN; DOWN-REGULATION; MICE; INDUCTION; ASTHMA	In the mucosal immune system, resident dendritic cells are specialized for priming Th2-polarized immunity, whereas the Ag-presenting activity of macrophages has been linked with the development of Th1 phenotype. As an immune switch toward Th1 can protect against Th2-mediated allergic response, this study investigated the capacity of lung macrophages to stimulate Th1 responses during the secondary exposure to inhaled allergen, thereby suppressing Th2-mediated allergic airway inflammation in a murine model of allergic asthma. Following airway macrophage depletion in OVA-sensitized mice, lung T cells defaulted to a phenotype that produced less Th1 (IFN-gamma) and more Th2 (IL-4 and IL-5) cytokines, leading to more severe airway hyperreactivity and inflammation after intranasal Ag challenge. After OVA pulsing and adoptive transfer, lung macrophages selectively promoted a Th1 response in Ag-sensitized recipients and did not induce pulmonary eosinophilia. By contrast, OVA pulsing and adoptive transfer of a lung cell preparation, consisting of dendritic cells, B cells, and macrophages, promoted a Th2 response with an associated inflammatory response that was suppressed when macrophages were present and pretreated with IFN-gamma, but exacerbated when macrophages were depleted before IFN-gamma treatment. In addition, Th1-promoting activity of lung macrophages was not related to the autocrine production of IL-12p40. These results suggest that the Th1-promoting APC activity may be an inherent property of the lung macrophage population, and may play an important role, upon stimulation by IFN-gamma, in antagonizing an ongoing Th2 immunity and Th2-dependent allergic responses.	McMaster Univ, Dept Med, Asthma Res Grp, Hamilton, ON, Canada; Vrije Univ Amsterdam, Fac Med, Dept Cell Biol & Immunol, Amsterdam, Netherlands	O'Byrne, PM (reprint author), St Josephs Hosp, Firestone Reg Chest & Allergy Clin, 50 Charlton Ave E, Hamilton, ON, Canada.			O'Byrne, Paul/0000-0003-0979-281X			Ahuja SS, 1998, J IMMUNOL, V161, P868; Ashkar S, 2000, SCIENCE, V287, P860, DOI 10.1126/science.287.5454.860; Bingisser RM, 1998, J IMMUNOL, V160, P5729; Borish L, 1997, J ALLERGY CLIN IMMUN, V99, P161, DOI 10.1016/S0091-6749(97)70090-3; BREWER JM, 1994, CLIN EXP IMMUNOL, V97, P164; BRUSSELLE G, 1995, AM J RESP CELL MOL, V12, P254; Chattergoon MA, 1998, J IMMUNOL, V160, P5707; DeKruyff R, 1998, J IMMUNOL, V160, P2231; DEKRUYFF RH, 1995, J IMMUNOL, V154, P2578; Desmedt M, 1998, J IMMUNOL, V160, P5300; FINKELMAN FD, 1994, J EXP MED, V179, P1563, DOI 10.1084/jem.179.5.1563; GAJEWSKI TF, 1991, J IMMUNOL, V146, P1750; GERMANN T, 1995, INT IMMUNOL, V7, P1649, DOI 10.1093/intimm/7.10.1649; Gracie JA, 1999, J CLIN INVEST, V104, P1393, DOI 10.1172/JCI7317; GUBLER U, 1991, P NATL ACAD SCI USA, V88, P4143, DOI 10.1073/pnas.88.10.4143; Heufler C, 1996, EUR J IMMUNOL, V26, P659, DOI 10.1002/eji.1830260323; HOLT PG, 1993, J EXP MED, V177, P397, DOI 10.1084/jem.177.2.397; Holtzman MJ, 1996, AM J RESP CELL MOL, V14, P316; HSIEH CS, 1993, SCIENCE, V260, P547, DOI 10.1126/science.8097338; Humbert M, 1996, AM J RESP CRIT CARE, V154, P1497; Inman MD, 1999, AM J RESP CELL MOL, V21, P473; Jun HS, 1999, J EXP MED, V189, P347, DOI 10.1084/jem.189.2.347; Koch F, 1996, J EXP MED, V184, P741, DOI 10.1084/jem.184.2.741; Korsgren M, 1997, J EXP MED, V185, P885, DOI 10.1084/jem.185.5.885; Lambrecht BN, 1998, J IMMUNOL, V160, P4090; Lee JS, 1997, J FOOD DRUG ANAL, V5, P185; Lee SC, 1999, J IMMUNOL, V162, P6867; Li XM, 1998, J IMMUNOL, V160, P1378; Marinaro M, 1999, J IMMUNOL, V162, P114; MARSHALL JD, 1995, J IMMUNOL, V155, P111; Masten BJ, 1999, J IMMUNOL, V162, P1310; Masten BJ, 1997, AM J RESP CELL MOL, V16, P335; Munn DH, 1999, J EXP MED, V189, P1363, DOI 10.1084/jem.189.9.1363; Nabeshima S, 1999, INFECT IMMUN, V67, P3221; Salez L, 2000, J LEUKOCYTE BIOL, V67, P545; SALLUSTO F, 1994, J EXP MED, V179, P1109, DOI 10.1084/jem.179.4.1109; SEDER RA, 1994, ANNU REV IMMUNOL, V12, P635, DOI 10.1146/annurev.immunol.12.1.635; Stumbles PA, 1998, J EXP MED, V188, P2019, DOI 10.1084/jem.188.11.2019; Takeuchi M, 1998, J IMMUNOL, V160, P1589; Tang C, 1997, EUR RESPIR J, V10, P624; Tang CB, 1998, AM J RESP CRIT CARE, V157, P1120; Tang CB, 1998, J ALLERGY CLIN IMMUN, V102, P368, DOI 10.1016/S0091-6749(98)70122-8; TRINCHIERI G, 1995, ANNU REV IMMUNOL, V13, P251, DOI 10.1146/annurev.immunol.13.1.251; Tsuyuki S, 1997, J EXP MED, V185, P1671, DOI 10.1084/jem.185.9.1671; Underhill DM, 1999, J EXP MED, V190, P1909, DOI 10.1084/jem.190.12.1909; vanRooijen N, 1996, J IMMUNOL METHODS, V193, P93, DOI 10.1016/0022-1759(96)00056-7; VANROOIJEN N, 1994, J IMMUNOL METHODS, V174, P83; Wijburg OLC, 1997, J VIROL, V71, P9450; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; WYNN TA, 1995, J IMMUNOL, V154, P3999	50	123	131	0	4	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	FEB 1	2001	166	3					1471	1481				11	Immunology	Immunology	396EE	WOS:000166622700008	11160186	
J	Halken, S; Hansen, KS; Jacobsen, HP; Estmann, A; Faelling, AE; Hansen, LG; Kier, SR; Lassen, K; Lintrup, M; Mortensen, S; Ibsen, KK; Osterballe, O; Host, A				Halken, S; Hansen, KS; Jacobsen, HP; Estmann, A; Faelling, AE; Hansen, LG; Kier, SR; Lassen, K; Lintrup, M; Mortensen, S; Ibsen, KK; Osterballe, O; Host, A			Comparison of a partially hydrolyzed infant formula with two extensively hydrolyzed formulas for allergy prevention: A prospective, randomized study	PEDIATRIC ALLERGY AND IMMUNOLOGY			English	Article						hypoallergenic infant formula; protein hydrolysates; allergy prevention; cow's milk allergy; pediatric	HIGH-RISK INFANTS; PARTIAL WHEY HYDROLYSATE; COW MILK FORMULAS; ATOPIC DISEASE; FOLLOW-UP; AVOIDANCE; PROPHYLAXIS; SOY; AGE; DISORDERS	The aim of this study was to compare the allergy-preventive effect of a partially hydrolyzed formula with two extensively hydrolyzed formulas, in infants with a high risk for development of allergic disease. High-risk infants from four Danish centres were included in the period from June 1994 to July 1995. Five-hundred and ninety-five high-risk infants were identified. Nigh-risk infants were defined as having biparental atopy, or a single atopic first-degree relative combined with cord blood immunoglobulin E (IgE) greater than or equal to 0.3 kU/l, At birth all infants were randomized to one of three different blinded formulas. All mothers had unrestricted diets during pregnancy and lactation and were encouraged to breast-feed exclusively. If breastfeeding was insufficient, one of the three formulas, according to randomization, was given during the first 4 months. It was recommended not to introduce cow's milk, cow's milk products, and solid foods until the age of 4 months. After the age of 4 months a normal unrestricted diet and conventional cow's milk-based formula were given when needed. All infants were followed-up prospectively with interview and physical examination at the age of 6, 12, and 18 months, and if any possible atopic symptoms were reported. If food allergy was suspected, controlled elimination/challenge procedures were performed in a hospital setting. Of 550 infants included in the study, 514 were seen at all visits and 36 were excluded owing to noncompliance. Of 478 infants who completed the study, 232 were exclusively breast-fed, 79 received an extensively hydrolyzed casein formula (Nutramigen), 82 an extensively hydrolyzed whey formula (Profylac), and 85 a partially hydrolyzed whey formula (Nan WA), during the first 4 months of life. These four groups were identical in regard to atopic predisposition, cord blood IgE, birthplace, and gender. Exclusively breastfed children were exposed less to tobacco smoke and pets at home and belonged to higher social classes, whereas the three formula groups were identical concerning environmental factors. The frequency of breast-feeding was high; only eight (2%) children were not breast-fed at all. The three formula groups were identical in regard to duration of breast-feeding: and age at introduction of formula and solid foods. No significant differences were found in the three groups of infants receiving formula milk regarding the cumulative incidence of atopic dermatitis or respiratory symptoms. The cumulative incidence of parental-reported cow's milk allergy was significantly higher in children fed partially hydrolyzed formula (Nan HA) compared with extensively hydrolyzed formula (Nutramigen or Profylac) at 12 and 18 months (NanHA, 7.1%; Nutramigen, 2.5%; Profylac, 0%; p = 0.033). The cumulative incidence of confirmed cow's milk allergy was 1.3% (three of 232) in exclusively breast-fed infants, 0.6% tone of 161) in infants fed extensively hydrolyzed formula (Nutramigen or Profylac), and 4.7% (four of 85) in infants fed partially hydrolyzed formula (Nan HA). Partially hydrolyzed formula was found to be less effective than extensively hydrolyzed formula in preventing cow's milk allergy, 0.6% vs. 4.7% (p = 0.05), but because of the small number of cases the results should be interpreted with caution. Compared with other similar studies the frequency of atopic symptoms was low, even though the dietetic intervention did not include either maternal diet during lactation or dietary restrictions to the children after the age of 3 months.	Sonderborg Hosp, Dept Paediat, DK-6400 Sonderborg, Denmark; Glostrup Univ Hosp, Glostrup, Denmark; Odense Univ Hosp, DK-5000 Odense, Denmark; Viborg Hosp, Viborg, Denmark	Halken, S (reprint author), Sonderborg Hosp, Dept Paediat, DK-6400 Sonderborg, Denmark.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			ARSHAD SH, 1992, LANCET, V339, P1493, DOI 10.1016/0140-6736(92)91260-F; Businco L, 1993, Pediatr Allergy Immunol, V4, P101, DOI 10.1111/j.1399-3038.1993.tb00077.x; CHANDRA RK, 1989, BMJ-BRIT MED J, V299, P228; CHANDRA RK, 1991, ANN ALLERGY, V67, P129; CHANDRA RK, 1989, ANN ALLERGY, V63, P102; Chandra RK, 1997, J PEDIATR GASTR NUTR, V24, P380, DOI 10.1097/00005176-199704000-00005; CHANDRA RK, 1985, CLIN ALLERGY, V15, P517, DOI 10.1111/j.1365-2222.1985.tb02304.x; Halken S, 1993, Pediatr Allergy Immunol, V4, P173, DOI 10.1111/j.1399-3038.1993.tb00088.x; HALKEN S, 1992, ALLERGY, V47, P545, DOI 10.1111/j.1398-9995.1992.tb00680.x; Halken S, 1995, ALLERGY S, V26, P49; HIDE DW, 1994, J ALLERGY CLIN IMMUN, V93, P842, DOI 10.1016/0091-6749(94)90375-1; Hide DW, 1996, ALLERGY, V51, P89, DOI 10.1111/j.1398-9995.1996.tb04563.x; Hollis S, 1999, BRIT MED J, V319, P670; HOST A, 1990, CLIN EXP ALLERGY, V45, P547; LUCAS A, 1990, BRIT MED J, V300, P837; MAKINENKILJUNEN S, 1993, CLIN EXP ALLERGY, V23, P287, DOI 10.1111/j.1365-2222.1993.tb00324.x; Marini A, 1996, ACTA PAEDIATR, V85, P1, DOI 10.1111/j.1651-2227.1996.tb14267.x; MISKELLY FG, 1988, ARCH DIS CHILD, V63, P388; Niggemann B, 1994, Pediatr Allergy Immunol, V5, P11, DOI 10.1111/j.1399-3038.1994.tb00212.x; Oldaeus G, 1997, ARCH DIS CHILD, V77, P4; OLDAEUS G, 1991, PEDIATR ALLERGY IMMU, V4, P156; RAGNO V, 1993, EUR J PEDIATR, V152, P760, DOI 10.1007/BF01953996; SAARINEN UM, 1995, LANCET, V346, P1065, DOI 10.1016/S0140-6736(95)91742-X; VANDENPLAS Y, 1992, ANN ALLERGY, V68, P419; VANDENPLAS Y, 1995, EUR J PEDIATR, V154, P488, DOI 10.1007/s004310050330; VANDENPLAS Y, 1988, EUR J PEDIATR, V148, P274, DOI 10.1007/BF00441420; ZEIGER RS, 1995, J ALLERGY CLIN IMMUN, V95, P1179, DOI 10.1016/S0091-6749(95)70074-9; ZEIGER RS, 1989, J ALLERGY CLIN IMMUN, V84, P72, DOI 10.1016/0091-6749(89)90181-4; Zeiger R, 1992, PEDIATR ALLERGY IMMU, V3, P110, DOI 10.1111/j.1399-3038.1992.tb00035.x	29	123	130	1	12	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0905-6157			PEDIATR ALLERGY IMMU	Pediatr. Allergy Immunol.	AUG	2000	11	3					149	161		10.1034/j.1399-3038.2000.00081.x		13	Allergy; Immunology; Pediatrics	Allergy; Immunology; Pediatrics	349UA	WOS:000089062900005	10981524	
J	Sanak, M; Levy, BD; Clish, CB; Chiang, N; Gronert, K; Mastalerz, L; Serhan, CN; Szczeklik, A				Sanak, M; Levy, BD; Clish, CB; Chiang, N; Gronert, K; Mastalerz, L; Serhan, CN; Szczeklik, A			Aspirin-tolerant asthmatics generate more lipoxins than aspirin-intolerant asthmatics	EUROPEAN RESPIRATORY JOURNAL			English	Article						anti-inflammatory mediators; aspirin-intolerant asthma; cysteinyl-leukotrienes; lipoxins	SENSITIVE ASTHMATICS; BRONCHIAL BIOPSIES; NASAL POLYPS; LEUKOTRIENE-E4; INHIBITION; RESPONSES; SYNTHASE; FLUIDS; ACID; ATL	Asthma is characterized by chronic airway inflammation resulting from overproduction of pro-inflammatory mediators, such as leukotrienes (LT), The authors questioned the biosynthetic capacity of asthmatic patients for lipoxins (LX) and 15-epimer lipoxins (15-epi-LX), endogenous regulators of inflammatory responses that inhibit pro-inflammatory events, Levels of LXA(4), 15-epi-LXA(4) and LTC4 were determined in 14 clinically characterized aspirin-intolerant asthmatics (AIA), 11 aspirin-tolerant asthmatics (ATh) and eight healthy volunteers using a stimulated whole blood protocol, Both LXA(4) and 15-epi-LXA(4) were generated in whole blood activated by the divalent cation ionophore, A23187, Higher levels of LXA(4) were produced in ATA than either AIA or healthy volunteers, Exposure of AIA whole blood to interleukin-3 prior to A23187 did not elevate their reduced capacity to generate LXA(4). Generation of a bronchoconstrictor, LTC4, was similar in both AIA and ATA, Consequently, the ratio of LXA(4):LTC4 quantitatively favoured the bronchoconstrictor for AIA and differed from both ATA and healthy subjects. In addition, the capacity for 15-epi-LXA(4) generation was also diminished in AIA, since whole blood stimulated in the presence of aspirin gave increased levels only in samples from ATA, The present results indicate that asthmatics possess the capacity to generate both lipoxins and 15-epimer-lipoxins, but aspirin-intolerant asthmatics display a lower biosynthetic capacity than aspirin-tolerant asthmatics for these potentially protective lipid mediators. This previously unappreciated, diminished capacity for lipoxin formation by aspirin-intolerant asthmatic patients may contribute to their more severe clinical phenotype, and represents a novel paradigm for the development of chronic inflammatory disorders.	Harvard Univ, Brigham & Womens Hosp, Sch Med,Ctr Expt Therapeut & Reperfus, Dept Anesthesiol Perioperat & Pain Med, Boston, MA 02115 USA; Jagiellonian Univ, Sch Med, Dept Med, Krakow, Poland	Serhan, CN (reprint author), Harvard Univ, Brigham & Womens Hosp, Sch Med,Ctr Expt Therapeut & Reperfus, Dept Anesthesiol Perioperat & Pain Med, Thorn Bldg Med Res,Room 724,75 Francis St, Boston, MA 02115 USA.		Sanak, Marek/A-2115-2008	Sanak, Marek/0000-0001-7635-8103	NHLBI NIH HHS [HL56383, K08-HL03788]; NIGMS NIH HHS [GM-38765]		Chiang N, 1998, J PHARMACOL EXP THER, V287, P779; CHRISTIE PE, 1992, AM REV RESPIR DIS, V145, P1281; CLARIA J, 1995, P NATL ACAD SCI USA, V92, P9475, DOI 10.1073/pnas.92.21.9475; Cowburn AS, 1998, J CLIN INVEST, V101, P834, DOI 10.1172/JCI620; Dahlen B, 1998, AM J RESP CRIT CARE, V157, P1187; DAHLEN SE, 1991, LIPOXYGENASES THEIR, P235; Drazen JM, 1999, NEW ENGL J MED, V340, P197; EDENIUS C, 1990, FEBS LETT, V272, P25, DOI 10.1016/0014-5793(90)80440-T; Gavett SH, 1999, J CLIN INVEST, V104, P721, DOI 10.1172/JCI6890; ISRAEL E, 1993, AM REV RESPIR DIS, V148, P1447; KOWALSKI ML, 1993, J ALLERGY CLIN IMMUN, V91, P580, DOI 10.1016/0091-6749(93)90264-G; KUMLIN M, 1992, AM REV RESPIR DIS, V146, P96; LAITINEN LA, 1993, LANCET, V341, P989, DOI 10.1016/0140-6736(93)91073-U; LEE TH, 1991, BIOCHEM BIOPH RES CO, V180, P1416, DOI 10.1016/S0006-291X(05)81354-3; LEE TH, 1990, AM REV RESPIR DIS, V141, P1453; LEVY BD, 1993, LIPIDS, V28, P1047, DOI 10.1007/BF02537069; LEVY BD, 1999, LIPID 2 MESSENGERS, P83; Miura K, 1998, J ALLERGY CLIN IMMUN, V102, P512, DOI 10.1016/S0091-6749(98)70142-3; Nasser SMS, 1996, AM J RESP CRIT CARE, V153, P90; ORTOLANI C, 1987, ANN ALLERGY, V59, P106; Picado C, 1999, AM J RESP CRIT CARE, V160, P291; SAMTER M, 1968, ANN INTERN MED, V68, P975; SAMUELSSON B, 1987, SCIENCE, V237, P1171, DOI 10.1126/science.2820055; Serhan CN, 1996, FASEB J, V10, P1147; Serhan CN, 1997, PROSTAGLANDINS, V53, P107, DOI 10.1016/S0090-6980(97)00001-4; Szczeklik A, 1999, J ALLERGY CLIN IMMUN, V104, P5, DOI 10.1016/S0091-6749(99)70106-5; Szczeklik A, 1996, AM J RESP CRIT CARE, V154, P1608; Takano T, 1997, J EXP MED, V185, P1693, DOI 10.1084/jem.185.9.1693; Young JM, 1996, INFLAMM RES, V45, P246, DOI 10.1007/BF02259611	29	123	128	0	4	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0903-1936			EUR RESPIR J	Eur. Resp. J.	JUL	2000	16	1					44	49		10.1034/j.1399-3003.2000.16a08.x		6	Respiratory System	Respiratory System	335UE	WOS:000088262500008	10933083	
J	Lack, G				Lack, Gideon			Update on risk factors for food allergy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Food allergy; risk factors; filaggrin; genetics; dual-allergen-exposure hypothesis	ORAL TOLERANCE INDUCTION; OF-FUNCTION MUTATIONS; PEANUT ALLERGY; ATOPIC-DERMATITIS; UNITED-STATES; GENE POLYMORPHISMS; FUNCTION VARIANTS; EARLY-CHILDHOOD; MATERNAL DIET; NUT ALLERGY	Despite efforts to prevent food allergy (FA) in children, IgE-mediated FAs are increasing in westernized countries. Previous preventive strategies, such as prolonged exclusive breast-feeding and delayed weaning onto solid foods, have recently been called into question. The present review considers possible risk factors and theories for the development of FA. An alternative hypothesis is proposed, suggesting that early cutaneous exposure to food protein through a disrupted skin barrier leads to allergic sensitization and that early oral exposure to food allergen induces tolerance. Novel interventional strategies to prevent the development of FA are also discussed. (J Allergy Clin Immunol 2012;129:1187-97.)	Kings Coll London, St Thomas Hosp, Guys & St Thomas NHS Fdn Trust, MRC Asthma UK Ctr Allerg Mech Asthma,Childrens Al, London SE1 7EH, England	Lack, G (reprint author), Kings Coll London, St Thomas Hosp, Guys & St Thomas NHS Fdn Trust, MRC Asthma UK Ctr Allerg Mech Asthma,Childrens Al, Westminster Bridge Rd, London SE1 7EH, England.	gideon.lack@kcl.ac.uk	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	Medical Research Council [G1000758, MC_G1001205]		Alberto EJC, 2008, PEDIAT ALLERG IMM-UK, V19, P716, DOI 10.1111/j.1399-3038.2007.00709.x; Allan K, 2010, CLIN EXP ALLERGY, V40, P370, DOI 10.1111/j.1365-2222.2009.03413.x; Amoli MM, 2002, GENES IMMUN, V3, P220, DOI 10.1038/sj.gene.6363872; Anandan C, 2009, ALLERGY, V64, P840, DOI 10.1111/j.1398-9995.2009.02042.x; Arshad SH, 2007, J ALLERGY CLIN IMMUN, V119, P307, DOI 10.1016/j.jaci.2006.12.621; Bager P, 2008, CLIN EXP ALLERGY, V38, P634, DOI 10.1111/j.1365-2222.2008.02939.x; Baker SS, 2000, PEDIATRICS, V106, P346; Bergmann RL, 2002, CLIN EXP ALLERGY, V32, P205, DOI 10.1046/j.1365-2222.2002.01274.x; 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Allergy Clin. Immunol.	MAY	2012	129	5					1187	1197		10.1016/j.jaci.2012.02.036		11	Allergy; Immunology	Allergy; Immunology	934CG	WOS:000303418000002	22464642	
J	Calderon, MA; Simons, FER; Malling, HJ; Lockey, RF; Moingeon, P; Demoly, P				Calderon, M. A.; Simons, F. E. R.; Malling, H. -J.; Lockey, R. F.; Moingeon, P.; Demoly, P.			Sublingual allergen immunotherapy: mode of action and its relationship with the safety profile	ALLERGY			English	Review						allergen immunotherapy; mucosal; safety; subcutaneous; sublingual	SYSTEMIC REACTIONS; DOUBLE-DUMMY; DOUBLE-BLIND; ANAPHYLAXIS; RHINITIS; ORGANIZATION; ASTHMA; EFFICACY; INJECTIONS; FREQUENCY	Allergen immunotherapy reorients inappropriate immune responses in allergic patients. Sublingual allergen immunotherapy (SLIT) has been approved, notably in the European Union, as an effective alternative to subcutaneous allergen immunotherapy (SCIT) for allergic rhinitis patients. Compared with SCIT, SLIT has a better safety profile. This is possibly because oral antigen-presenting cells (mostly Langerhans and myeloid dendritic cells) exhibit a tolerogenic phenotype, despite constant exposure to danger signals from food and microbes. This reduces the induction of pro-inflammatory immune responses leading to systemic allergic reactions. Oral tissues contain relatively few mast cells and eosinophils (mostly located in submucosal areas) and, in comparison with subcutaneous tissue, are less likely to give rise to anaphylactic reactions. SLIT-associated immune responses include the induction of circulating, allergen-specific Th1 and regulatory CD4+ T cells, leading to clinical tolerance. Although 4075% of patients receiving SLIT experience mild, transient local reactions in the oral mucosa, these primary reactions rarely necessitate dose reduction or treatment interruption. We discuss 11 published case reports of anaphylaxis (all nonfatal) diagnosed according to the World Allergy Organization criteria and relate this figure to the approximately 1 billion SLIT doses administered worldwide since 2000. Anaphylaxis risk factors associated with SCIT and/or SLIT should be characterized further.	[Calderon, M. A.] Imperial College NHLI, Sect Allergy & Clin Immunol, Royal Brompton Hosp, London, England; [Simons, F. E. R.] Univ Manitoba, Dept Pediat & Child Hlth, Dept Immunol, Winnipeg, MB R3T 2N2, Canada; [Malling, H. -J.] Copenhagen Univ Hosp, Allergy Clin, Copenhagen, Denmark; [Lockey, R. F.] Univ S Florida, Coll Med, Div Allergy & Immunol, Tampa, FL USA; [Moingeon, P.] Stallergenes SA, Dept Res & Dev, Antony, France; [Demoly, P.] Univ Hosp Montpellier, Hop Arnaud Villeneuve, INSERM, Allergy Div,Pneumol Dept,U657, Montpellier, France	Calderon, MA (reprint author), Imperial College NHLI, Sect Allergy & Clin Immunol, Royal Brompton Hosp, Dovehouse St, London, England.	m.calderon@imperial.ac.uk			ALK-Abello; Stallergenes; Allergopharma	Moises Calderon has received consulting fees, honoraria for lectures and/or research funding from ALK-Abello and Stallergenes. F. Estelle R. Simons is on the Anaphylaxis Advisory Boards for ALK-Abello, Dey and Sanofi Aventis. Hans-Jorgen Malling has received consulting fees, honoraria for lectures and/or research funding from Allergopharma, ALK-Abello & Stallergenes. Richard F. Lockey consults with Merck-Schering, ALK and Dey. Philippe Moingeon is an employee of Stallergenes. Pascal Demoly is a consultant and a speaker for Stallergenes, ALK and Therabel and was a speaker for Schering-Plough-MSD, Astra Zeneca and GlaxoSmithKline.	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J	D'Amato, G; Cecchi, L; D'Amato, M; Liccardi, G				D'Amato, G.; Cecchi, L.; D'Amato, M.; Liccardi, G.			Urban Air Pollution and Climate Change as Environmental Risk Factors of Respiratory Allergy: An Update	JOURNAL OF INVESTIGATIONAL ALLERGOLOGY AND CLINICAL IMMUNOLOGY			English	Review						Air pollution; Allergy; Allergic asthma; Bronchial asthma; Climate change; Environmental diseases; Airway hyperreactivity; Pollen allergy; Respiratory allergy; Urban air pollution; Hypersensitivity	LUNG-FUNCTION GROWTH; SOUTHERN CALIFORNIA CHILDREN; CASE-CROSSOVER ANALYSIS; HEAT-RELATED MORTALITY; PARTICULATE MATTER; CHILDHOOD ASTHMA; SCHOOL-CHILDREN; BRONCHIAL-ASTHMA; EUROPEAN CITIES; POLLEN ALLERGY	The incidence of allergic respiratory diseases and bronchial asthma appears to be increasing worldwide, and people living in urban areas more frequently experience these conditions than those living in rural areas. One of the several causes of the rise in morbidity associated with allergic respiratory diseases is the increased presence of outdoor air pollutants resulting from more intense energy consumption and exhaust emissions from cars and other vehicles. Urban air pollution is now a serious public health hazard. Laboratory studies confirm epidemiologic evidence that air pollution adversely affects lung function in asthmatics. Damage to airway mucous membranes and impaired mucociliary clearance caused by air pollution may facilitate access of inhaled allergens to the cells of the immune system, thus promoting sensitization of the airway. Consequently, a more severe immunoglobulin (Ig) E-mediated response to aeroallergens and airway inflammation could account for increasing prevalence of allergic respiratory diseases in polluted urban areas. The most abundant components of urban air pollution in urban areas with high levels of vehicle traffic are airborne particulate matter, nitrogen dioxide, and ozone. In addition, the earth's temperature is increasing, mainly as a result of anthropogenic factors (eg, fossil fuel combustion and greenhouse gas emissions from energy supply, transport, industry, and agriculture), and climate change alters the concentration and distribution of air pollutants and interferes with the seasonal presence of allergenic pollens in the atmosphere by prolonging these periods.	[D'Amato, G.; Liccardi, G.] High Specialty Hosp A Cardarelli, Dept Resp Dis, Div Pneumol & Allergol, I-80121 Naples, Italy; [Cecchi, L.] Allergy Clin, Florence, Italy; [Cecchi, L.] Univ Florence, Interdepartmental Ctr Bioclimatol, Florence, Italy; [D'Amato, M.] High Specialty Hosp V Monaldi, Dept Resp Dis, Div PheumoTisiol, Naples, Italy	D'Amato, G (reprint author), High Specialty Hosp A Cardarelli, Dept Resp Dis, Div Pneumol & Allergol, Via Rione Sirignano 10, I-80121 Naples, Italy.	gdamato@qubisoft.it	D'Amato, Maria/H-3074-2012; Osborne, Nicholas/N-4915-2015	D'Amato, Maria/0000-0002-5906-5701; Osborne, Nicholas/0000-0002-6700-2284			Andersen ZJ, 2008, THORAX, V63, P710, DOI 10.1136/thx.2007.085480; Annesi-Maesano I, 2007, RESP MED, V101, P1721, DOI 10.1016/j.rmed.2007.02.022; ANTO JM, 2002, MONOGRAPH EUROPEAN R, P108; Asher MI, 1998, EUR RESPIR J, V12, P315; Atkinson RW, 1999, EUR RESPIR J, V13, P257, DOI 10.1183/09031936.99.13225799; Ayres JG, 2009, EUR RESPIR J, V34, P295, DOI 10.1183/09031936.00003409; Baccini M, 2008, EPIDEMIOLOGY, V19, P711, DOI 10.1097/EDE.0b013e318176bfcd; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Beggs PJ, 2004, CLIN EXP ALLERGY, V34, P1507, DOI 10.1111/j.1365-2222.2004.02061.x; Boezen HM, 1999, LANCET, V353, P874, DOI 10.1016/S0140-6736(98)06311-9; BOUSQUET J, 1993, CLIN EXP ALLERGY, V23, P484; Brauer M, 2002, AM J RESP CRIT CARE, V166, P1092, DOI 10.1164/rccm.200108-007OC; Burney P, 1996, EUR RESPIR J, V9, P687; BURR M L, 1989, Archives of Disease in Childhood, V64, P1452; Celenza A, 1996, BRIT MED J, V312, P604; Ciccone G, 1998, OCCUP ENVIRON MED, V55, P771; Curtis Luke, 2006, Environ Int, V32, P815, DOI 10.1016/j.envint.2006.03.012; D'Amato G, 2008, CLIN EXP ALLERGY, V38, P1264, DOI 10.1111/j.1365-2222.2008.03033.x; D'Amato G, 2007, ALLERGY, V62, P976, DOI 10.1111/j.1398-9995.2007.01393.x; D'Amato G, 2007, ALLERGY, V62, P11, DOI 10.1111/j.1398-9995.2006.01271.x; D'Amato G, 2005, CLIN EXP ALLERGY, V35, P1113, DOI 10.1111/j.1365-2222.2005.02328.x; D'Amato G, 2002, EUR RESPIR J, V20, P763, DOI 10.1183/09031936.02.00401402; D'Amato G., 2008, Allergy and allergic diseases. 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Invest. Allergol. Clin. Immunol.		2010	20	2					95	102				8	Allergy; Immunology	Allergy; Immunology	590SM	WOS:000277247900001	20461963	
J	Lin, S; Luo, M; Walker, RJ; Liu, X; Hwang, SA; Chinery, R				Lin, Shao; Luo, Ming; Walker, Randi J.; Liu, Xiu; Hwang, Syni-An; Chinery, Robert			Extreme High Temperatures and Hospital Admissions for Respiratory and Cardiovascular Diseases	EPIDEMIOLOGY			English	Article							HEAT-RELATED MORTALITY; AMBIENT-TEMPERATURE; AIR-POLLUTION; EUROPEAN CITIES; UNITED-STATES; TIME-SERIES; MORBIDITY; CITY; WAVE; HUMIDITY	Background: Although the association of high temperatures with mortality is well-documented, the association with morbidity has seldom been examined. We assessed the potential impact of hot weather on hospital admissions due to cardiovascular and respiratory diseases in New York City. We also explored whether the weather-disease relationship varies with socio-demographic variables. Method: We investigated effects of temperature and humidity on health by linking the daily cardiovascular and respiratory hospitalization counts with meteorologic conditions during summer, 1991-2004. We used daily mean temperature, mean apparent temperature, and 3-day moving average of apparent temperature as the exposure indicators. Threshold effects for health risks of meteorologic conditions were assessed by log-linear threshold models, after controlling for ozone, day of week, holidays, and long-term trend. Stratified analyses were used to evaluate temperature-demographic interactions. Results: For all 3 exposure indicators, each degree C above the threshold of the temperature-health effect curve (29 degrees C-36 degrees C) was associated with a 2.7%-3.1% increase in same-day hospitalizations due to respiratory diseases, and an increase of 1.4%-3.6% in lagged hospitalizations due to cardiovascular diseases. These increases for respiratory admissions were greater for Hispanic persons (6.1%/degrees C) and the elderly (4.7%/degrees C). At high temperatures, admission rates increased for chronic airway obstruction, asthma, ischemic heart disease, and cardiac dysrhythmias, but decreased for hypertension and heart failure. Conclusions: Extreme high temperature appears to increase hospital admissions for cardiovascular and respiratory disorders in New York City. Elderly and Hispanic residents may be particularly vulnerable to the temperature effects on respiratory illnesses.	[Lin, Shao] New York State Dept Hlth, Bur Environm & Occupat Epidemiol, Ctr Environm Hlth, Troy, NY 12180 USA; [Chinery, Robert] New York State Off Attorney Gen, Albany, NY USA	Lin, S (reprint author), New York State Dept Hlth, Bur Environm & Occupat Epidemiol, Ctr Environm Hlth, 547 River St,Room 200, Troy, NY 12180 USA.	sxl05@health.state.ny.us	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Lin, Shao/0000-0002-5535-7504	National Environmental Public Health Tracking Program, Centers for Disease Control and Prevention; National Science Foundation;  [5U38EH000184]	Supported in part by grants from the National Environmental Public Health Tracking Program, Centers for Disease Control and Prevention (5U38EH000184). The National Center for Atmospheric Research (NCAR) (see Acknowledgments) is supported by grants from the National Science Foundation.	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J	Marwick, JA; Caramori, G; Stevenson, CS; Casolari, P; Jazrawi, E; Barnes, PJ; Ito, K; Adcock, IM; Kirkham, PA; Papi, A				Marwick, John A.; Caramori, Gaetano; Stevenson, Christopher S.; Casolari, Paolo; Jazrawi, Elen; Barnes, Peter J.; Ito, Kazuhiro; Adcock, Ian M.; Kirkham, Paul A.; Papi, Alberto			Inhibition of PI3K delta Restores Glucocorticoid Function in Smoking-induced Airway Inflammation in Mice	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						inflammation; histone deacetylase; chromatin; oxidative stress	OBSTRUCTIVE PULMONARY-DISEASE; HISTONE DEACETYLASE ACTIVITY; PHOSPHOINOSITIDE 3-KINASE; GENE-EXPRESSION; RECEPTOR; ACTIVATION; ASTHMA; THEOPHYLLINE; P110-DELTA; PATHOGENESIS	Rationale. There is an increasing prevalence of reduced responsiveness to glucocorticoid therapy in severe asthma and chronic obstructive pulmonary disease (COPD). The molecular mechanism of this remains unknown. Recent studies have shown that histone deacetylase activity, which is critical to glucocorticoid function, is altered by oxidant stress and may be involved in the development of glucocorticoid insensitivity. Objectives: To determine the role of phosphoinositol-3-kinase (PI3K) in the development of cigarette smoke-induced glucocorticoid insensitivity. Methods: Wild-type, PI3K gamma knock-out and PI3K delta kinase dead knock-in transgenic mice were used in a model of cigarette smoke-induced glucocorticoid insensitivity. Peripheral lung tissue was obtained from six healthy nonsmokers, nine smokers with normal lung function, and eight patients with COPD. Measurements and Main Results: In vitro oxidative stress activates PI3K and induced a relative glucocorticoid resistance, which is restored by PI3K inhibition. In vivo, cigarette smoke exposure in mice increased tyrosine nitration of histone deacetylase 2 in the lung, correlating with reduced histone deacetylase 2 activity and reduced glucocorticoid function. Histone deacetylase 2 activity and the antiinflammatory effects of glucocorticoids were restored in PI3K delta kinase dead knock-in but not PI3K gamma knock-out smoke-exposed mice compared with wild type mice, correlating with reduced histone deacetylase 2 tyrosine nitration. Glucocorticoid receptor expression was significantly reduced in smoke-exposed mice, in smokers with normal lung function, and in patients with COPD. Conclusions: These data show that therapeutic inhibition of PI3K delta may restore glucocorticoid function in oxidative stress-induced glucocorticoid insensitivity.	[Marwick, John A.; Jazrawi, Elen; Barnes, Peter J.; Ito, Kazuhiro; Adcock, Ian M.; Kirkham, Paul A.] Univ London Imperial Coll Sci Technol & Med, Airways Dis Sect, Natl Heart & Lung Inst, London SW3 6LY, England; [Marwick, John A.; Stevenson, Christopher S.; Kirkham, Paul A.; Papi, Alberto] Novartis Inst Biomed Res, Resp Dis Area, Horsham, W Sussex, England; [Marwick, John A.; Caramori, Gaetano; Casolari, Paolo] Univ Ferrara, Ctr Ric Asma, I-44100 Ferrara, Italy; [Marwick, John A.; Caramori, Gaetano; Casolari, Paolo] Univ Ferrara, BPCO, I-44100 Ferrara, Italy	Marwick, JA (reprint author), Univ London Imperial Coll Sci Technol & Med, Airways Dis Sect, Natl Heart & Lung Inst, Dovehouse St, London SW3 6LY, England.	j.marwick@imperial.ac.uk		PAPI, ALBERTO/0000-0002-6924-4500	Novartis Institute for Biomedical Research	Supported by Novartis Institute for Biomedical Research	Ali K, 2004, NATURE, V431, P1007, DOI 10.1038/nature02991; Barnes PJ, 2008, NAT REV IMMUNOL, V8, P183, DOI 10.1038/nri2254; Bonneau O, 2006, AM J PHYSIOL-LUNG C, V290, pL1036, DOI 10.1152/ajplung.00422.2005; Ciencewicki J, 2008, J ALLERGY CLIN IMMUN, V122, P456, DOI 10.1016/j.jaci.2008.08.004; Condliffe AM, 2005, BLOOD, V106, P1432, DOI 10.1182/blood-2005-03-0944; Cosio BG, 2004, J EXP MED, V200, P689, DOI 10.1084/jem.20040416; Foukas LC, 2002, J BIOL CHEM, V277, P37124, DOI 10.1074/jbc.M202101200; Galasinski SC, 2002, J BIOL CHEM, V277, P19618, DOI 10.1074/jbc.M201174200; Glass CK, 2006, NAT REV IMMUNOL, V6, P44, DOI 10.1038/nri1748; Goleva E, 2006, AM J RESP CRIT CARE, V173, P607, DOI 10.1164/rccm.200507-1046OC; GRUMMELLI SM, 2007, AM J RESP CRIT CARE, V175, pA684; Hew M, 2006, AM J RESP CRIT CARE, V174, P134, DOI 10.1164/rccm.200512-1930OC; Hirsch E, 2000, SCIENCE, V287, P1049, DOI 10.1126/science.287.5455.1049; Ito K, 2006, J EXP MED, V203, P7, DOI 10.1084/jem.20050466; Ito K, 2005, NEW ENGL J MED, V352, P1967, DOI 10.1056/NEJMoa041892; Ito K, 2004, BIOCHEM BIOPH RES CO, V315, P240, DOI 10.1016/j.bbrc.2004.01.046; Ito K, 2002, P NATL ACAD SCI USA, V99, P8921, DOI 10.1073/pnas.132556899; Ito K., 2001, FASEB Journal, V15, P1110; Leclerc O, 2006, EUR RESPIR J, V27, P1102, DOI 10.1183/09031936.06.00076905; Lee KS, 2006, FASEB J, V20, P455, DOI 10.1096/fj.05-5045com; MacNee W, 2007, CLIN CHEST MED, V28, P479, DOI 10.1016/j.ccm.2007.06.008; MARWICK J, 2007, AM J RESP CRIT CARE, V175, pA696; Marwick JA, 2004, AM J RESP CELL MOL, V31, P633, DOI 10.1165/rcmb.2004-0006OC; MARWICK JA, 2008, AM J RESP CRIT CARE, V177, pA333; Morris A, 2008, J PHARMACOL EXP THER, V327, P851, DOI 10.1124/jpet.108.140848; Mostefai HA, 2008, J IMMUNOL, V180, P5028; Okkenhaug K, 2003, NAT REV IMMUNOL, V3, P317, DOI 10.1038/nri1056; Okkenhaug K, 2002, SCIENCE, V297, P1031; Puri KD, 2004, BLOOD, V103, P3448, DOI 10.1182/blood-2003-05-1667; Rabe KF, 2007, AM J RESP CRIT CARE, V176, P532, DOI 10.1164/rccm.200703-456SO; Reichardt HM, 1998, CELL, V93, P531, DOI 10.1016/S0092-8674(00)81183-6; Rommel C, 2007, NAT REV IMMUNOL, V7, P191, DOI 10.1038/nri2036; Sasaki T, 2000, SCIENCE, V287, P1040, DOI 10.1126/science.287.5455.1040; Stevenson CS, 2005, AM J PHYSIOL-LUNG C, V288, pL514, DOI 10.1152/ajplung.00317.2004; Varani K, 2006, AM J RESP CRIT CARE, V173, P398, DOI 10.1164/rccm.200506-869OC	35	122	133	12	19	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	APR 1	2009	179	7					542	548		10.1164/rccm.200810-1570OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	425UU	WOS:000264663700006	19164702	
J	Bateson, TF; Schwartz, J				Bateson, Thomas F.; Schwartz, Joel			Children's response to air pollutants	JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES			English	Article							ENVIRONMENTAL TOBACCO-SMOKE; LOW-BIRTH-WEIGHT; POSTNEONATAL INFANT-MORTALITY; SOUTHERN CALIFORNIA CHILDREN; CHRONIC RESPIRATORY SYMPTOMS; DIESEL EXHAUST PARTICLES; CROSS-SECTIONAL AREA; PARTICULATE MATTER; LUNG-FUNCTION; AMERICAN CHILDREN	It is important to focus on children with respect to air pollution because (1) their lungs are not completely developed, (2) they can have greater exposures than adults, and (3) those exposures can deliver higher doses of different composition that may remain in the lung for greater duration. The undeveloped lung is more vulnerable to assault and less able to fully repair itself when injury disrupts morphogenesis. Children spend more time outside, where concentrations of combustion-generated air pollution are generally higher. Children have higher baseline ventilation rates and are more physically active than adults, thus exposing their lungs to more air pollution. Nasal breathing in adults reduces some pollution concentrations, but children are more typically mouth-breathers - suggesting that the composition of the exposure mixture at the alveolar level may be different. Finally, higher ventilation rates and mouth-breathing may pull air pollutants deeper into children's lungs, thereby making clearance slower and more difficult. Children also have immature immune systems, which plays a significant role in asthma. The observed consequences of early life exposure to adverse levels of air pollutants include diminished lung function and increased susceptibility to acute respiratory illness and asthma. Exposure to diesel exhaust, in particular, is an area of concern for multiple endpoints, and deserves further research.	[Bateson, Thomas F.] US EPA, NCEA, Off Res & Dev, Washington, DC 20460 USA; [Schwartz, Joel] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA; [Schwartz, Joel] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA; [Schwartz, Joel] Harvard Univ, Brigham & Womens Hosp, Sch Med, Channing Lab, Boston, MA 02115 USA	Bateson, TF (reprint author), US EPA, NCEA, Off Res & Dev, 1200 Penn Ave NW,Mail Code 8623D, Washington, DC 20460 USA.	bateson.thomas@epa.gov					Ahluwalia IB, 1997, AM J EPIDEMIOL, V146, P42; ANDERSON H.R., 1999, AIR POLLUTION HLTH, P461, DOI 10.1016/B978-012352335-8/50096-X; Arcus-Arth A, 2007, RISK ANAL, V27, P97, DOI 10.1111/j.1539-6924.2006.00862.x; Avol EL, 2001, AM J RESP CRIT CARE, V164, P2067; Barnett AG, 2005, AM J RESP CRIT CARE, V171, P1272, DOI 10.1164/rccm.200411-1586OC; Bayer-Oglesby L, 2005, ENVIRON HEALTH PERSP, V113, P1632, DOI 10.1289/ehp.8159; Bennett WD, 2003, J APPL PHYSIOL, V95, P497, DOI 10.1152/japplphysiol.00718.2002; BOBAK M, 1992, LANCET, V340, P1010, DOI 10.1016/0140-6736(92)93017-H; Bobak M, 1999, OCCUP ENVIRON MED, V56, P539; Bobak M, 2000, ENVIRON HEALTH PERSP, V108, P173, DOI 10.2307/3454517; Bobak M, 2001, EPIDEMIOLOGY, V12, P358, DOI 10.1097/00001648-200105000-00018; BraunFahrlander C, 1997, AM J RESP CRIT CARE, V155, P1042; Broeckaert F, 2000, ENVIRON HEALTH PERSP, V108, P533, DOI 10.2307/3454615; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; BURRI PH, 1984, ANNU REV PHYSIOL, V46, P617, DOI 10.1146/annurev.ph.46.030184.003153; BURRI P., 1997, LUNG GROWTH DEV, P1; Chay KY, 2003, Q J ECON, V118, P1121, DOI 10.1162/00335530360698513; Dejin-Karlsson E, 1998, AM J PUBLIC HEALTH, V88, P1523, DOI 10.2105/AJPH.88.10.1523; Dejmek J, 1999, ENVIRON HEALTH PERSP, V107, P475, DOI 10.2307/3434630; Dejmek J, 2002, ENVIRON HEALTH PERSP, V110, P601; Diaz-Sanchez D, 2003, CURR ALLERGY ASTHM R, V3, P146, DOI 10.1007/s11882-003-0027-4; Diaz-Sanchez D, 1999, J ALLERGY CLIN IMMUN, V104, P1183; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; DOCKERY DW, 1989, AM REV RESPIR DIS, V139, P587; Dockery DW, 1996, ENVIRON HEALTH PERSP, V104, P500, DOI 10.2307/3432990; DUNNILL M. 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Toxicol. Env. Health Part A		2008	71	3					238	243		10.1080/15287390701598234		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	251AA	WOS:000252341400008	18097949	
J	Douwes, J; van Strien, R; Doekes, G; Smit, J; Kerkhof, M; Gerritsen, J; Postma, D; Travier, N; Brunekreef, B				Douwes, J; van Strien, R; Doekes, G; Smit, J; Kerkhof, M; Gerritsen, J; Postma, D; Travier, N; Brunekreef, B			Does early indoor microbial exposure reduce the risk of asthma? The Prevention and Incidence of Asthma and Mite Allergy birth cohort study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; allergy; endotoxin; (1 -> 3)-beta-D-glucan; hygiene hypothesis; infant cohort study	HOUSE-DUST ENDOTOXIN; CHILDREN; ATOPY; SENSITIZATION; INFANCY; LIFE; POLYMORPHISM; WHEEZE; AIRWAY; CD14	Background: Exposure to microbial agents might inhibit the development of atopy and asthma. Objective: We measured the association between microbial exposure assessed at 3 months and the development of atopic sensitization and doctor-diagnosed (DD) asthma and wheeze in the first 4 years in a birth cohort study of children with atopic mothers. Methods: Endotoxin, fungal (1 -> 3)-beta-D-glucans, extracellular polysaccharides from the genera Penicillium and Aspergillus (EPS-Pen/Asp), and dust on living room floors were measured at 3 months of age. Serum IgE levels against common allergens were determined at 1 and 4 years, and questionnaire information about respiratory morbidity was collected yearly. Results: Microbial levels in mattresses were low and not associated with serum IgE levels, DD asthma, and wheeze. Floor levels of biocontaminants and dust, on the other hand, were inversely associated with DD asthma, being most pronounced for endotoxin (odds ratio [OR], 0.40; 95% CI, 0.210.77) and EPS-Pen/Asp (OR, 0.42; 95% CI, 0.18-0.99). Mutual adjustment for other exposures did not significantly after the results for endotoxin and only moderately affected the results for EPS-Pen/Asp. Persistent wheeze was also consistently less common in the high-exposure group, being significant only for EPS-PenlAsp (OR, 0.37; 95% CI, 0.15-0.96). Transient wheeze and wheeze in the past 12 months were also reduced, but effects were smaller and not significant. Relationships with serum-specific IgE levels, which could only be assessed in 41% at age 4 years, were less pronounced and statistically significant only for EPS-Pen/Asp. Conclusions: Early exposure to common microbial contaminants, including fungal agents, might protect against asthma. Clinical implications: Microbial exposure in early life might protect against asthma and might constitute a novel target for prevention.	Univ Utrecht, Inst Risk Assessment Sci, NL-3508 TD Utrecht, Netherlands; Massey Univ, Ctr Publ Hlth Res, Wellington, New Zealand; Municipal Hlth Serv, Dept Environm Med, Amsterdam, Netherlands; Natl Inst Publ Hlth & Environm, RIVM, Bilthoven, Netherlands; Univ Groningen, Beatrix Childrens Hosp, Groningen, Netherlands; Univ Groningen, Med Ctr, Dept Epidemiol, Groningen, Netherlands; Univ Groningen, Med Ctr, Dept Pulm Med, Groningen, Netherlands; Erasmus Univ, Sophia Childrens Hosp, Dept Pediat, Rotterdam, Netherlands; Univ Utrecht, Med Ctr, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands	Brunekreef, B (reprint author), Univ Utrecht, Inst Risk Assessment Sci, POB 80178, NL-3508 TD Utrecht, Netherlands.	B.Brunekreef@iras.uu.nl	Kerkhof, Marjan/A-8846-2008	brunekreef, bert/0000-0001-9908-0060; Douwes, Jeroen/0000-0003-3599-4036			ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Bottcher MF, 2003, CLIN EXP ALLERGY, V33, P295, DOI 10.1046/j.1365-2222.2003.01562.x; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Brunekreef B, 2002, PEDIAT ALLERG IMM-UK, V13, P55, DOI 10.1034/j.1399-3038.13.s.15.1.x; Brussee JE, 2005, J ALLERGY CLIN IMMUN, V115, P946, DOI 10.1016/j.jaci.2005.02.035; Brussee JE, 2005, EUR RESPIR J, V25, P455, DOI 10.1183/09031936.05.00079604; Douwes J, 2000, AM J RESP CRIT CARE, V162, P1348; Douwes J, 2002, THORAX, V57, P86, DOI 10.1136/thorax.57.1.86; Douwes J, 1999, J ALLERGY CLIN IMMUN, V103, P494, DOI 10.1016/S0091-6749(99)70476-8; DOUWES J, 1995, APPL ENVIRON MICROB, V61, P1763; Douwes J, 1996, APPL ENVIRON MICROB, V62, P3176; Gehring U, 2001, J ALLERGY CLIN IMMUN, V108, P847, DOI 10.1067/mai.2001.119026; Gehring U, 2002, AM J RESP CRIT CARE, V166, P939, DOI 10.1164/rccm.200203-256OC; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Hastie T, 1990, GEN ADDITIVE MODELS; Institute of Medicine (US) Committee on Damp Indoor Spaces and Health, 2004, DAMP IND SPAC HLTH; Jain VV, 2004, EXPERT OPIN BIOL TH, V4, P1533, DOI 10.1517/14712598.4.9.1533; Kabesch M, 2004, ALLERGY, V59, P520, DOI 10.1111/j.1398-9995.2004.00439.x; Lakwijk N, 1998, CLIN EXP ALLERGY, V28, P454; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Romagnani S, 2004, IMMUNOLOGY, V112, P352, DOI 10.1111/j.1365-2567.2004.01925.x; Singh J, 2005, J ALLERGY CLIN IMMUN, V115, P330, DOI 10.1016/j.jaci.2004.11.021; van Strien RT, 2004, J ALLERGY CLIN IMMUN, V113, P860, DOI 10.1016/j.jaci.2004.01.078; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; Watanabe J, 2003, J BIOL CHEM, V278, P42361, DOI 10.1074/jbc.M307752200; Woo JG, 2003, J ALLERGY CLIN IMMUN, V112, P438, DOI 10.1067/mai.2003.1634; Zambelli-Weiner A, 2005, J ALLERGY CLIN IMMUN, V115, P1203, DOI 10.1016/j.jaci.2005.03.001	30	122	124	2	12	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	MAY	2006	117	5					1067	1073		10.1016/j.jaci.2006.02.002		7	Allergy; Immunology	Allergy; Immunology	041EM	WOS:000237436300014	16675334	
J	Geppetti, P; Materazzi, S; Nicolettl, P				Geppetti, P; Materazzi, S; Nicolettl, P			The transient receptor potential vanilloid 1: Role in airway inflammation and disease	EUROPEAN JOURNAL OF PHARMACOLOGY			English	Review						transient receptor potential vanilloid 1; cough; asthma exacerbation; acidic media	GENE-RELATED PEPTIDE; NERVE GROWTH-FACTOR; OBSTRUCTIVE PULMONARY-DISEASE; DEPENDENT PROTEIN-KINASE; SENSITIVE SENSORY NERVES; CAPSAICIN RECEPTOR; GUINEA-PIG; ACTIVATED RECEPTOR-2; EPITHELIAL-CELLS; URINARY-BLADDER	The transient receptor potential vanilloid 1 (TRPV1) is air excitatory cation channel, rather selectively expressed in a subpopulation of nociceptive, primary sensory neurons that promote neurogenic inflammation via neuropeptide release. TRPV1 is activated by noxious temperature, low extracellular pH and diverse lipid derivatives, and is uniquely sensitive to vanilloid molecules, including capsaicin. TRPV1 expression and sensitivity is highly regulated by diverse G protein-coupled and tyrosine kinase receptors. Other exogenous or endogenous chemical agents, including reactive oxygen species, ethanol and hydrogen sulphide sensitize/activate TRPV1. In the airways, TRPV1 agonists; cause cough, bronchoconstriction, microvascular leakage, hyperreactivity and hypersecretion. Patients with asthma and chronic obstructive pulmonary disease are more sensitive to the tussive effect of TRPV1 agonists and TRPV1 activation may contribute to respiratory symptoms caused by acidic media present in the airways during asthma exacerbation, gastroesophageal reflux induced asthma or in other conditions. TRPV1 antagonists may be useful in the treatment of these diseases. (c) 2005 Elsevier B.V. All rights reserved.	Univ Florence, Clin Pharmacol Unit, Dept Crit Care Med & Surg, I-50139 Florence, Italy; Univ Ferrara, Ctr Excellence Study Inflammat, I-44100 Ferrara, Italy	Geppetti, P (reprint author), Univ Florence, Clin Pharmacol Unit, Dept Crit Care Med & Surg, Viale Pieraccini 6, I-50139 Florence, Italy.	pierangelo.geppetti@unifi.it					Agopyan N, 2004, AM J PHYSIOL-LUNG C, V286, pL563, DOI 10.1152/ajplung.00299.2003; Agopyan N, 2003, TOXICOL APPL PHARM, V192, P21, DOI 10.1016/S0041-008X(03)00259-X; Amadesi S, 2004, J NEUROSCI, V24, P4300, DOI 10.1523/JNEUROSCI.5679-03.2004; Amadesi S, 2001, AM J RESP CRIT CARE, V163, P1206; Baluk P, 1996, EXP LUNG RES, V22, P409, DOI 10.3109/01902149609046032; BARNES PJ, 1986, LANCET, V1, P242; Basu S, 2005, P NATL ACAD SCI USA, V102, P5120, DOI 10.1073/pnas.0407780102; Bertrand C, 1996, TRENDS PHARMACOL SCI, V17, P255, DOI 10.1016/0165-6147(96)10027-4; BEVAN S, 1995, J NEUROSCI, V15, P4918; BEVAN S, 1994, TRENDS NEUROSCI, V17, P509, DOI 10.1016/0166-2236(94)90149-X; 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J. Pharmacol.	MAR 8	2006	533	1-3					207	214		10.1016/j.ejphar.2005.12.063		8	Pharmacology & Pharmacy	Pharmacology & Pharmacy	025KS	WOS:000236265400020	16464449	
J	Ryan, PH; LeMasters, G; Biagini, J; Bernstein, D; Grinshpun, SA; Shukla, R; Wilson, K; Villareal, M; Burkle, J; Lockey, J				Ryan, PH; LeMasters, G; Biagini, J; Bernstein, D; Grinshpun, SA; Shukla, R; Wilson, K; Villareal, M; Burkle, J; Lockey, J			Is it traffic type, volume, or distance? Wheezing in infants living near truck and bus traffic	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						diesel; traffic; truck; bus; wheezing; geographic information system; infants	DIESEL EXHAUST PARTICLES; CHRONIC RESPIRATORY SYMPTOMS; AIR-POLLUTION; BRONCHIAL HYPERRESPONSIVENESS; PARTICULATE MATTER; CYTOKINE PRODUCTION; VEHICLE EMISSIONS; CHILDHOOD ASTHMA; FINE PARTICLES; URBAN AIR	Background: Previous studies of air pollution have not examined the association between exposure to varying types, distance, and amounts of traffic and wheezing in very young infants. Objective: We sought to determine the relationship between types of traffic, traffic volume, and distance and wheezing among infants less than 1 year of age. Methods: A geographic information system and a classification scheme were developed to categorize infants enrolled in the study as living near moving truck and bus traffic (highway > 50 miles per hour, > 1000 trucks daily, < 400 m), stop-and-go truck and bus traffic (< 50 miles per hour, < 100 m), or unexposed and not residing near either. Symptom data were based on health questionnaires administered to parents when the infants were 6 months of age and monthly health diaries. Results: Infants living very near (< 100 m) stop-and-go bus and truck traffic had a significantly increased prevalence of wheezing (adjusted odds ratio, 2.50; 95% CI, 1.15-5.42) when compared with unexposed infants. The prevalence of wheezing among nonwhite infants was at least twice that of white infants, regardless of exposure. Infants living less than 400 m from a high volume of moving traffic, however, did not have an increased prevalence of wheezing. Conclusion: These results suggest that the distance from and type of traffic exposures are more significant risk factors than traffic volume for wheezing in early infancy.	Univ Cincinnati, Dept Environm Hlth, Cincinnati, OH 45267 USA; Univ Cincinnati, Div Immunol, Dept Internal Med, Cincinnati, OH 45267 USA	Ryan, PH (reprint author), Univ Cincinnati, Dept Environm Hlth, Cincinnati, OH 45267 USA.	ryanph@email.uc.edu	Ryan, Patrick /L-7062-2015		NIEHS NIH HHS [ES11170, ES10957]		Arshad SH, 2005, CHEST, V127, P502, DOI 10.1378/chest.127.2.502; Brauer M, 2001, ENVIRON HEALTH PERSP, V109, P1039, DOI 10.2307/3454959; Brauer M, 2002, AM J RESP CRIT CARE, V166, P1092, DOI 10.1164/rccm.200108-007OC; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; Ciccone G, 1998, OCCUP ENVIRON MED, V55, P771; DiazSanchez D, 1996, J ALLERGY CLIN IMMUN, V98, P114, DOI 10.1016/S0091-6749(96)70233-6; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; El-Sharif N, 2003, CLIN EXP ALLERGY, V33, P176, DOI 10.1046/j.1365-2222.2003.01598.x; Fujieda S, 1998, AM J RESP CELL MOL, V19, P507; FUJIMAKI H, 1994, TOXICOLOGY, V92, P261, DOI 10.1016/0300-483X(94)90182-1; Grant EN, 2000, AM J PUBLIC HEALTH, V90, P1923, DOI 10.2105/AJPH.90.12.1923; Hirsch T, 1999, EUR RESPIR J, V14, P669, DOI 10.1034/j.1399-3003.1999.14c29.x; Jalaludin BB, 2004, ENVIRON RES, V95, P32, DOI 10.1016/S0013-9351(03)00038-0; Janssen NAH, 2003, ENVIRON HEALTH PERSP, V111, P1512, DOI 10.1289/ehp.6243; Jenkins MA, 1996, INT J EPIDEMIOL, V25, P609, DOI 10.1093/ije/25.3.609; Joseph CLM, 2000, CHEST, V117, P1336, DOI 10.1378/chest.117.5.1336; Knox RB, 1997, CLIN EXP ALLERGY, V27, P246; LEMASTERS GK, 2003, AM THOR SOC INT C MA; Li N, 2003, ENVIRON HEALTH PERSP, V111, P455, DOI 10.1289/ehp.6000; Lin S, 2002, ENVIRON RES, V88, P73, DOI 10.1006/enrs.2001.4303; London SJ, 2001, EPIDEMIOLOGY, V12, P577, DOI 10.1097/00001648-200109000-00019; Norris G, 1999, ENVIRON HEALTH PERSP, V107, P489, DOI 10.2307/3434632; Ormstad H, 2000, TOXICOLOGY, V152, P53, DOI 10.1016/S0300-483X(00)00292-4; Pandya RJ, 2002, ENVIRON HEALTH PERSP, V110, P103; Peden DB, 2005, J ALLERGY CLIN IMMUN, V115, P213, DOI 10.1016/j.jaci.2004.12.003; Peden DB, 2000, ENVIRON HEALTH PERSP, V108, P475, DOI 10.2307/3454539; Penttinen P, 2001, EUR RESPIR J, V17, P428, DOI 10.1183/09031936.01.17304280; Pino P, 2004, EPIDEMIOLOGY, V15, P702, DOI 10.1097/01.ede.0000142153.28496.d0; Reponen T, 2003, J ENVIRON MONITOR, V5, P557, DOI 10.1039/b303557c; Riedl M, 2005, J ALLERGY CLIN IMMUN, V115, P221, DOI 10.1016/j.jaci.2004.11.047; Schwartz J, 2000, EPIDEMIOLOGY, V11, P6, DOI 10.1097/00001648-200001000-00004; Shah SD, 2004, ENVIRON SCI TECHNOL, V38, P2544, DOI 10.1021/es0350583; Sherriff A, 2001, INT J EPIDEMIOL, V30, P1473, DOI 10.1093/ije/30.6.1473; Shima M, 2003, J EPIDEMIOL, V13, P108; Shima M, 2002, ARCH ENVIRON HEALTH, V57, P529; Simon PA, 2003, J ASTHMA, V40, P535, DOI 10.1081/JAS-120018788; SOLOMON G, 2001, COALITION CLEAN AIR; Taussig LM, 2003, J ALLERGY CLIN IMMUN, V111, P661, DOI 10.1067/mai.2003.162; Tong HY, 2000, J AIR WASTE MANAGE, V50, P543; Unal A, 2004, J AIR WASTE MANAGE, V54, P130; *US EPA, HLTH ASS DOC DIES EN; van der Zee SC, 1999, OCCUP ENVIRON MED, V56, P802; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; Venn AJ, 2001, AM J RESP CRIT CARE, V164, P2177, DOI 10.1164/rccm2106126; Wilkinson P, 1999, THORAX, V54, P1070	45	122	123	0	11	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	AUG	2005	116	2					279	284		10.1016/j.jaci.2005.014		6	Allergy; Immunology	Allergy; Immunology	017ID	WOS:000235686400006	16083780	
J	Weidinger, S; Klopp, N; Rummler, L; Wagenpfeil, S; Novak, N; Baurecht, HJ; Groer, W; Darsow, U; Heinrich, J; Gauger, A; Schafer, T; Jakob, T; Behrendt, H; Wichmann, HE; Ring, J; Illig, T				Weidinger, S; Klopp, N; Rummler, L; Wagenpfeil, S; Novak, N; Baurecht, HJ; Groer, W; Darsow, U; Heinrich, J; Gauger, A; Schafer, T; Jakob, T; Behrendt, H; Wichmann, HE; Ring, J; Illig, T			Association of NOD1 polymorphisms with atopic eczema and related phenotypes	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						atopic eczema; asthma; allergic rhinoconjunctivitis; IgE; CARD4; NOD1; SNP; haplotype; association	RESPIRATORY-HEALTH-SURVEY; HOUSE-DUST ENDOTOXIN; TOLL-LIKE RECEPTOR-2; CROHNS-DISEASE; LINKAGE DISEQUILIBRIUM; HYGIENE HYPOTHESIS; INNATE IMMUNITY; CELIAC-DISEASE; ASTHMA; CHILDREN	Background: Interactions with microbial pathogens are crucial for the maturation of the immune system. The nucleotide-binding oligomerization domain protein 1 (NOD1) is a cytosolic receptor sensing a muropeptide found mostly in gram-negative bacterial peptidoglycans. NOD1 is located on chromosome 7p14-p15, a region that has been linked with atopy. Recently, polymorphisms of the closely related NOD2 have been associated with atopy-related traits. Objectives: Within a large population-based cohort of German adults (n = 1417), a case-control population for atopic eczema (n = 454), and a large cohort of parent-offspring trios for atopic eczema (189 trios), we evaluated 11 NOD1 polymorphisms for associations with atopic phenotypes. Methods: Subjects were phenotyped by standardized questionnaires and interviews, skin examination, and serum IgE measurements. Genotyping was performed by using matrix-assisted laser desorption ionization-time of flight mass spectrometry. Results: Analyses revealed significant association of one NOD1 haplotype with atopic eczema in the population-based cohort (P = .004) and the case-control population (P = .003). Another NOD1 haplotype was associated with decreased total IgE (P = .008). In addition, significant associations with total serum IgE levels were observed for polymorphisms rs2907748 (P = .006), rs2907749 (P = .012), and rs2075822 (P = .018). These polymorphisms were significantly associated with atopic eczema and asthma in the family-based association analyses (P = .001-043). Seven polymorphisms showed significant transmission distortion for total IgE levels (P values < .0001-.029). Conclusion: These data indicate that genetic variants within NOD1 are important determinants of atopy susceptibility.	Tech Univ Munich, Dept Dermatol & Allergy, D-80802 Munich, Germany; GSF, Inst Epidemiol, Natl Res Ctr Environm & Hlth, Neuherberg, Germany; Tech Univ Munich, Inst Med Stat & Epidemiol, D-80802 Munich, Germany; Univ Bonn, Dept Dermatol & Allergy, D-5300 Bonn, Germany; Med Univ Lubeck, Inst Social Med, Lubeck, Germany; Tech Univ Munich, Div Environm Dermatol & Allergy, GSF, D-80802 Munich, Germany; Tech Univ Munich, ZAUM Ctr Allergy & Environm, D-80802 Munich, Germany	Weidinger, S (reprint author), Tech Univ Munich, Dept Dermatol & Allergy, Biedersteiner St 29, D-80802 Munich, Germany.	weidinger@lrz.turn.de	Weidinger, Stephan/C-8461-2011; Jakob, Thilo/J-1621-2012; Baurecht, Hansjoerg/C-4035-2013				Abecasis GR, 2000, EUR J HUM GENET, V8, P545, DOI 10.1038/sj.ejhg.5200494; Ahmad-Nejad P, 2004, J ALLERGY CLIN IMMUN, V113, P565, DOI 10.1016/j.jaci.2003.12.583; Athman R, 2004, CURR OPIN MICROBIOL, V7, P25, DOI 10.1016/j.mib.2003.12.013; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Bouchier-Hayes L, 2002, EMBO REP, V3, P616, DOI 10.1093/embo-reports/kvf1391; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; Ciacci C, 2004, J ALLERGY CLIN IMMUN, V113, P1199, DOI 10.1016/j.jaci.2004.03.012; Eder W, 2004, J ALLERGY CLIN IMMUN, V113, P482, DOI 10.1016/j.jaci.2003.12.374; Eder Waltraud, 2004, Curr Opin Allergy Clin Immunol, V4, P113, DOI 10.1097/00130832-200404000-00008; EXCOFFIER L, 1995, MOL BIOL EVOL, V12, P921; Gabriel SB, 2002, SCIENCE, V296, P2225, DOI 10.1126/science.1069424; Gehring U, 2002, AM J RESP CRIT CARE, V166, P939, DOI 10.1164/rccm.200203-256OC; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Girardin SE, 2003, SCIENCE, V300, P1584, DOI 10.1126/science.1084677; Hampe J, 2002, LANCET, V359, P1661, DOI 10.1016/S0140-6736(02)08590-2; Heine H, 2003, INT ARCH ALLERGY IMM, V130, P180, DOI 10.1159/000069517; Holt PG, 2002, EUR RESPIR J, V19, P538, DOI 10.1183/09031936.02.00229302; Homma T, 2004, AM J RESP CELL MOL, V31, P463, DOI 10.1165/rcmb.2004-0161OC; Hugot JP, 2001, NATURE, V411, P599, DOI 10.1038/35079107; Illig T, 2003, DIABETES, V52, P2861, DOI 10.2337/diabetes.52.11.2861; Inohara N, 2000, J BIOL CHEM, V275, P27823; INOHARA N, 2001, NAT REV IMMUNOL, V3, P371; Jarvis D, 1999, J ALLERGY CLIN IMMUN, V104, P934, DOI 10.1016/S0091-6749(99)70071-0; Kabesch M, 2003, J ALLERGY CLIN IMMUN, V111, P813, DOI 10.1067/mai.2003.1336; Kero J, 2001, J ALLERGY CLIN IMMUN, V108, P781, DOI 10.1067/mai.2001.119557; Laitinen T, 2001, NAT GENET, V28, P87, DOI 10.1038/ng0501-87; Lazarus R, 2002, IMMUNOL REV, V190, P9, DOI 10.1034/j.1600-065X.2002.19002.x; Leung DYM, 2003, CURR OPIN IMMUNOL, V15, P634, DOI 10.1016/j.coi.2003.09.009; Martinez FD, 1999, LANCET, V354, pSII12; Matsubara M, 2004, FEBS LETT, V566, P195, DOI 10.1016/j.febslet.2004.04.028; O'Connell JR, 1998, AM J HUM GENET, V63, P259, DOI 10.1086/301904; Ogura Y, 2001, NATURE, V411, P603, DOI 10.1038/35079114; Palmer LJ, 2000, AM J RESP CRIT CARE, V161, P1836; Powrie F, 2003, SCIENCE, V299, P1030, DOI 10.1126/science.1082031; Romagnani S, 2004, IMMUNOLOGY, V112, P352, DOI 10.1111/j.1365-2567.2004.01925.x; Simpson CR, 2002, CLIN EXP ALLERGY, V32, P37, DOI 10.1046/j.0022-0477.2001.01250.x; Slatkin M, 1996, HEREDITY, V76, P377, DOI 10.1038/hdy.1996.55; SPIELMAN RS, 1993, AM J HUM GENET, V52, P506; Stene LC, 2001, LANCET, V357, P607, DOI 10.1016/S0140-6736(00)04067-8; Travassos LH, 2004, EMBO REP, V5, P1000, DOI 10.1038/sj.embor.7400248; van Strien RT, 2004, J ALLERGY CLIN IMMUN, V113, P860, DOI 10.1016/j.jaci.2004.01.078; Wallin J, 1996, DEVELOPMENT, V122, P23; Weidinger S, 2004, J MED GENET, V41, P658, DOI 10.1136/jmg.2004.020263; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P383, DOI 10.1111/j.1365-2133.1994.tb08530.x; Yazdanbakhsh M, 2002, SCIENCE, V296, P490, DOI 10.1126/science.296.5567.490; Yoo NJ, 2002, BIOCHEM BIOPH RES CO, V299, P652, DOI 10.1016/S0006-291X(02)02714-6	48	122	127	1	5	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUL	2005	116	1					177	184		10.1016/j.jaci.2005.02.034		8	Allergy; Immunology	Allergy; Immunology	017IC	WOS:000235686300027	15990792	
J	Lowe, LA; Simpson, A; Woodcock, A; Morris, J; Murray, CS; Custovic, A				Lowe, LA; Simpson, A; Woodcock, A; Morris, J; Murray, CS; Custovic, A		NAC Manchester Asthma All	Wheeze phenotypes and lung function in preschool children	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						dry air challenge; lung function; specific airway resistance; wheeze phenotypes	COLD-AIR CHALLENGE; RESPIRATORY SYMPTOMS; BRONCHIAL RESPONSIVENESS; MANCHESTER ASTHMA; HEALTHY-CHILDREN; YOUNG-CHILDREN; EARLY-LIFE; INFANTS; CHILDHOOD; ADULT	Distinct phenotypes can be identified in childhood wheezing illness. Within the context of a birth cohort study, we investigated the association between preschool lung function and phenotypes of wheeze. From parentally reported history of wheeze (interviewer-administered questionnaire, age 3 and 5 years), children were classified as never wheezers, transient early wheezers, late-onset wheezers, or persistent wheezers. Lung function (specific airway resistance [sRaw]; kPa/second) was assessed at age 3 (n = 463) and 5 years (n = 690). Persistent wheezers had markedly poorer lung function compared with other groups. In children who had wheezed by age 3, the risk of persistent wheeze increased with increased sRaw (odds ratio [OR] 5.2, 95% confidence interval [CI] 1.3-22.0; p = 0.02). In a multivariate model, increasing sRaw (OR 5.5, 95% CI 1.2-25.9; p = 0.03) and the child's sensitization (OR 2.8, 95% CI 1.3-5.8; p = 0.008) were significant independent predictors of persistent wheezing. We found no association between lung function at age 3 and late-onset wheeze in children who had not wheezed previously (OR 0.6, 95% CI 0.07-5.3; p = 0.64). In conclusion, poor lung function at age 3 predicted the subsequent persistence of symptoms in children who had wheezed within the first 3 years, but was not associated with the onset of wheeze after age 3 in children who had not wheezed previously.	Wythenshawe Hosp, NW Lung Ctr, Manchester M23 9LT, Lancs, England; Wythenshawe Hosp, Dept Med Stat, Manchester M23 9LT, Lancs, England	Custovic, A (reprint author), Wythenshawe Hosp, NW Lung Ctr, Manchester M23 9LT, Lancs, England.	a.custovic@man.ac.uk	Custovic, Adnan/A-2435-2012	Custovic, Adnan/0000-0001-5218-7071; Woodcock, Ashley/0000-0002-5428-8578; Simpson, Angela/0000-0003-2733-6666			BRUSSCE JE, 2004, AM J RESP CRIT CARE, V169, P1262; BUHR W, 1990, PEDIATR PULM, V8, P23, DOI 10.1002/ppul.1950080108; BURROWS B, 1992, J ALLERGY CLIN IMMUN, V90, P376, DOI 10.1016/S0091-6749(05)80018-1; Clough JB, 1999, AM J RESP CRIT CARE, V160, P1473; Crenesse D, 2001, PEDIATR PULM, V32, P56, DOI 10.1002/ppul.1089; Custovic A, 2002, PEDIATR ALLERGY IMMU, V13, P32, DOI 10.1034/j.1399-3038.13.s.15.3.x; Custovic A, 2001, LANCET, V358, P188, DOI 10.1016/S0140-6736(01)05406-X; Custovic A, 2000, J ALLERGY CLIN IMMUN, V105, P252, DOI 10.1016/S0091-6749(00)90073-3; Dab I, 1976, Pediatr Res, V10, P998; Delacourt C, 2001, AM J RESP CRIT CARE, V164, P1382; Dezateux C, 1999, AM J RESP CRIT CARE, V159, P403; Dezateux C, 1997, BRIT MED BULL, V53, P40; Dezateux C, 2001, THORAX, V56, P680, DOI 10.1136/thorax.56.9.680; Eigen H, 2001, AM J RESP CRIT CARE, V163, P619; Klug B, 1997, EUR RESPIR J, V10, P1599, DOI 10.1183/09031936.97.10071599; Kurukulaaratchy RJ, 2003, CLIN EXP ALLERGY, V33, P573, DOI 10.1046/j.1365-2222.2003.01657.x; Lowe L, 2002, LANCET, V359, P1904, DOI 10.1016/S0140-6736(02)08781-0; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; MARTINEZ FD, 1988, NEW ENGL J MED, V319, P1112, DOI 10.1056/NEJM198810273191702; Murray CS, 2002, THORAX, V57, P388, DOI 10.1136/thorax.57.5.388; Nielsen KG, 2000, AM J RESP CRIT CARE, V161, P1805; Nielsen KG, 2001, AM J RESP CRIT CARE, V164, P554; Nystad W, 2002, THORAX, V57, P1021, DOI 10.1136/thorax.57.12.1021; Palmer LJ, 2001, AM J RESP CRIT CARE, V163, P37; Phelan PD, 2002, J ALLERGY CLIN IMMUN, V109, P189, DOI 10.1067/mai.2001.120951; Rasmussen F, 2002, AM J RESP CRIT CARE, V165, P1480, DOI 10.1164/rccm.2108009; Stick S, 2000, THORAX, V55, P587, DOI 10.1136/thorax.55.7.587; Turner SW, 2004, AM J RESP CRIT CARE, V169, P921, DOI 10.1164/rccm.200307-891OC; Turner SW, 2002, AM J RESP CRIT CARE, V165, P1294, DOI 10.1164/rccm.200110-018OC; Vilozni D, 2001, AM J RESP CRIT CARE, V164, P2200, DOI 10.1164/rccm2101002; von Mutius E, 2001, THORAX, V56, P153, DOI 10.1136/thorax.56.2.153; WOODCOCK A, 2004, AM J RESP CRIT CARE, V170, P4333; ZACH M, 1984, PEDIATR RES, V18, P469, DOI 10.1203/00006450-198405000-00016	33	122	124	0	4	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	FEB 1	2005	171	3					231	237		10.1164/rccm.200406-695OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	891MY	WOS:000226586400007	15502115	
J	Helenius, I; Haahtela, T				Helenius, I; Haahtela, T			Allergy and asthma in elite summer sport athletes	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; athletes; bronchial hyperresponsiveness; chlorine derivatives; maximal exercise capacity; sports medicine; summer events; swimming	EXERCISE-INDUCED BRONCHOSPASM; CROSS-COUNTRY SKIERS; COLD-AIR; INDUCED BRONCHOCONSTRICTION; BRONCHIAL RESPONSIVENESS; FIGURE SKATERS; MILD ASTHMA; CHILDREN; EXPOSURE; SWIMMERS	Exercise may increase ventilation up to 200 L/min for short periods of time in speed and power athletes, and for longer periods in endurance athletes, such as long-distance runners and swimmers. Therefore highly trained athletes are repeatedly and strongly exposed to cold air during winter training and to many pollen allergens in spring and summer. Competitive swimmers inhale and microaspirate large amounts of air that floats above the water surface, which means exposure to chlorine derivatives from swimming pool disinfectants. In the summer Olympic Games, 4% to 15% of the athletes showed evidence of asthma or used anti-asthmatic medication. Asthma is most commonly found in endurance events, such as cycling, swimming, or long-distance running. The risk of asthma is especially increased among competitive swimmers, of which 36% to 79% show bronchial hyperresponsiveness to methacholine or histamine. The risk of asthma is closely associated with atopy and its severity among athletes. A few studies have investigated occurrence of exercise-induced bronchospasm among highly trained athletes, The occurrences of exercise-induced bronchospasm vary from 3% to 35% and depend on testing environment, type of exercise used, and athlete population tested. Mild eosinophilic airway inflammation has been shown to affect elite swimmers and cross-country skiers. This eosinophilic inflammation correlates with clinical parameters (ie, exercise-induced bronchial symptoms and bronchial hyperresponsiveness). Athletes commonly use antiasthmatic medication to treat their exercise-induced bronchial symptoms. However, controlled studies on their long-term effects on bronchial hyperresponsiveness and airway inflammation in the athletes are lacking. Follow-up studies on asthma in athletes are also lacking. What will happen to bronchial hyperresponsiveness and airway inflammation after discontinuation of competitional career is unclear. In the future, follow-up studies on bronchial responsiveness and airway inflammation, as well as controlled studies on both short- and long-term effects of antiasthmatic drugs in the athletes are needed.	Univ Helsinki, Cent Hosp, Skin & Allergy Hosp, Dept Allergol, Helsinki, Finland; Paijat Hame Cent Hosp, Lahti, Finland	Helenius, I (reprint author), Ohjaajantie 3A 4, Helsinki 00400, Finland.						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Allergy Clin. Immunol.	SEP	2000	106	3					444	452		10.1067/mai.2000.107749		9	Allergy; Immunology	Allergy; Immunology	356YN	WOS:000089471900005	10984362	
J	Arrieta, MC; Stiemsma, LT; Dimitriu, PA; Thorson, L; Russell, S; Yurist-Doutsch, S; Kuzeljevic, B; Gold, MJ; Britton, HM; Lefebvre, DL; Subbarao, P; Mandhane, P; Becker, A; McNagny, KM; Sears, MR; Kollmann, T; Mohn, WW; Turvey, SE; Finlay, BB				Arrieta, Marie-Claire; Stiemsma, Leah T.; Dimitriu, Pedro A.; Thorson, Lisa; Russell, Shannon; Yurist-Doutsch, Sophie; Kuzeljevic, Boris; Gold, Matthew J.; Britton, Heidi M.; Lefebvre, Diana L.; Subbarao, Padmaja; Mandhane, Piush; Becker, Allan; McNagny, Kelly M.; Sears, Malcolm R.; Kollmann, Tobias; Mohn, William W.; Turvey, Stuart E.; Finlay, B. Brett		CHILD Study Investigators	Early infancy microbial and metabolic alterations affect risk of childhood asthma	SCIENCE TRANSLATIONAL MEDICINE			English	Article							LONGITUDINAL DEVELOPMENT CHILD; NUCLEAR-MAGNETIC-RESONANCE; EARLY-LIFE; INTESTINAL MICROBIOTA; ANTIBIOTIC EXPOSURE; ALLERGIC-ASTHMA; GUT MICROBIOTA; YOUNG-CHILDREN; BIRTH COHORT; DISEASE	Asthma is the most prevalent pediatric chronic disease and affects more than 300 million people worldwide. Recent evidence in mice has identified a "critical window" early in life where gut microbial changes (dysbiosis) are most influential in experimental asthma. However, current research has yet to establish whether these changes precede or are involved in human asthma. We compared the gut microbiota of 319 subjects enrolled in the Canadian Healthy Infant Longitudinal Development (CHILD) Study, and show that infants at risk of asthma exhibited transient gut microbial dysbiosis during the first 100 days of life. The relative abundance of the bacterial genera Lachnospira, Veillonella, Faecalibacterium, and Rothia was significantly decreased in children at risk of asthma. This reduction in bacterial taxa was accompanied by reduced levels of fecal acetate and dysregulation of enterohepatic metabolites. Inoculation of germ-free mice with these four bacterial taxa ameliorated airway inflammation in their adult progeny, demonstrating a causal role of these bacterial taxa in averting asthma development. These results enhance the potential for future microbe-based diagnostics and therapies, potentially in the form of probiotics, to prevent the development of asthma and other related allergic diseases in children.	[Arrieta, Marie-Claire; Thorson, Lisa; Russell, Shannon; Yurist-Doutsch, Sophie; Britton, Heidi M.; Finlay, B. Brett] Univ British Columbia, Michael Smith Labs, Vancouver, BC V6T 1Z4, Canada; [Arrieta, Marie-Claire; Stiemsma, Leah T.; Dimitriu, Pedro A.; Russell, Shannon; Yurist-Doutsch, Sophie; Mohn, William W.; Finlay, B. Brett] Univ British Columbia, Dept Microbiol & Immunol, Vancouver, BC V6T 1Z3, Canada; [Kuzeljevic, Boris; Kollmann, Tobias; Turvey, Stuart E.] Child & Family Res Inst, Vancouver, BC V4Z 4H4, Canada; [Kuzeljevic, Boris; Kollmann, Tobias; Turvey, Stuart E.] BC Childrens Hosp, Vancouver, BC V4Z 4H4, Canada; [Gold, Matthew J.; McNagny, Kelly M.] Univ British Columbia, Biomed Res Ctr, Vancouver, BC V6T 1Z3, Canada; [Lefebvre, Diana L.; Sears, Malcolm R.] McMaster Univ, Dept Med, Hamilton, ON L8S 4L8, Canada; [Subbarao, Padmaja] Univ Toronto, Dept Pediat, Toronto, ON M5S 2J7, Canada; [Subbarao, Padmaja] Hosp Sick Children, Toronto, ON M5G 1X8, Canada; [Mandhane, Piush] Univ Alberta, Dept Pediat, Edmonton, AB T6G 2R3, Canada; [Mandhane, Piush] Univ Alberta, Sch Publ Hlth, Edmonton, AB T6G 2R3, Canada; [Becker, Allan] Univ Manitoba, Dept Pediat & Child Hlth, Winnipeg, MB R3T 2N2, Canada; [Kollmann, Tobias; Turvey, Stuart E.] Univ British Columbia, Dept Pediat, Vancouver, BC V6T 1Z4, Canada; [Finlay, B. Brett] Univ British Columbia, Dept Biochem & Mol Biol, Vancouver, BC V6T 1Z4, Canada	Turvey, SE (reprint author), Child & Family Res Inst, Vancouver, BC V4Z 4H4, Canada.	sturvey@cw.bc.ca; bfinlay@mail.ubc.ca		Kuzeljevic, Boris/0000-0003-4712-9867; Tang, Patrick/0000-0003-1583-5484	Canadian Institutes of Health Research (CIHR) [CHM-94316, CMF 108029]; CIHR; Allergy, Genes and Environment (AllerGen) Network of the Centres of Excellence (NCE); Health Canada; Environment Canada; Canada Mortgage and Housing Corporation; Childhood Asthma Foundation; University of British Columbia; Tula Foundation; Aubrey J. Tingle Professorship in Pediatric Immunology	Funding: This research was supported by the Canadian Institutes of Health Research (CIHR; grants CHM-94316 and CMF 108029). The CIHR and the Allergy, Genes and Environment (AllerGen) Network of the Centres of Excellence (NCE) provided core funding for CHILD. Additional support for the CHILD Study has been provided by Health Canada, Environment Canada, Canada Mortgage and Housing Corporation, and the Childhood Asthma Foundation. L.T.S. is supported by the University of British Columbia Four Year Fellowship. A grant from the Tula Foundation to the Centre for Microbial Diversity and Evolution supported the work of P.A.D. S.E.T. holds the Aubrey J. Tingle Professorship in Pediatric Immunology and is a clinical scholar of the Michael Smith Foundation for Health Research.	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J	Oliphant, CJ; Hwang, YY; Walker, JA; Salimi, M; Wong, SH; Brewer, JM; Englezakis, A; Barlow, JL; Hams, E; Scanlon, ST; Ogg, GS; Fallon, PG; McKenzie, ANJ				Oliphant, Christopher J.; Hwang, You Yi; Walker, Jennifer A.; Salimi, Maryam; Wong, See Heng; Brewer, James M.; Englezakis, Alexandros; Barlow, Jillian L.; Hams, Emily; Scanlon, Seth T.; Ogg, Graham S.; Fallon, Padraic G.; McKenzie, Andrew N. J.			MHCII-Mediated Dialog between Group 2 Innate Lymphoid Cells and CD4(+) T Cells Potentiates Type 2 Immunity and Promotes Parasitic Helminth Expulsion	IMMUNITY			English	Article							ALLERGIC LUNG INFLAMMATION; DUST-MITE ALLERGEN; DENDRITIC CELLS; IN-VIVO; ADAPTIVE IMMUNITY; CYSTEINE PROTEASE; ANTIBODY-RESPONSE; TH2 RESPONSES; IL-4; EXPRESSION	Group 2 innate lymphoid cells (ILC2s) release interleukin-13 (IL-13) during protective immunity to helminth infection and detrimentally during allergy and asthma. Using two mouse models to deplete ILC2s in vivo, we demonstrate that T helper 2 (Th2) cell responses are impaired in the absence of ILC2s. We show that MHCII-expressing ILC2s interact with antigen-specific T cells to instigate a dialog in which IL-2 production from T cells promotes ILC2 proliferation and IL-13 production. Deletion of MHCII renders IL-13-expressing ILC2s incapable of efficiently inducing Nippostrongylus brasiliensis expulsion. Thus, during transition to adaptive T cell-mediated immunity, the ILC2 and T cell crosstalk contributes to their mutual maintenance, expansion and cytokine production. This interaction appears to augment dendritic-cell-induced T cell activation and identifies a previously unappreciated pathway in the regulation of type-2 immunity.	[Oliphant, Christopher J.; Hwang, You Yi; Walker, Jennifer A.; Wong, See Heng; Englezakis, Alexandros; Barlow, Jillian L.; Scanlon, Seth T.; McKenzie, Andrew N. J.] MRC, Mol Biol Lab, Cambridge CB2 0QH, England; [Salimi, Maryam; Ogg, Graham S.] Univ Oxford, John Radcliffe Hosp, NIHR Biomed Res Ctr, MRC Human Immunol Unit, Oxford OX3 9DS, England; [Hams, Emily; Fallon, Padraic G.] Trinity Coll Dublin, Trinity Biomed Sci Inst, Dublin 2, Ireland; [Fallon, Padraic G.] Our Ladys Childrens Hosp, Natl Childrens Res Ctr, Dublin 12, Ireland; [Fallon, Padraic G.] Trinity Coll Dublin, Inst Mol Med, Dublin 2, Ireland; [Brewer, James M.] Univ Pl, GRBC, Inst Infect Immun & Inflammat, Glasgow G12 8TA, Lanark, Scotland	McKenzie, ANJ (reprint author), MRC, Mol Biol Lab, Francis Crick Ave, Cambridge CB2 0QH, England.	anm@mrc-lmb.cam.ac.uk	Brewer, James/A-7186-2010	Brewer, James/0000-0001-7933-0915; Scanlon, Seth Thomas/0000-0002-1792-6382; Fallon, Padraic/0000-0002-8401-7293; Hams, Emily/0000-0002-9745-3246	American Asthma Foundation; UK-MRC; Wellcome Trust [100963/Z/13/Z]; A-STAR; Science Foundation Ireland; National Children's Research Centre; NIHR Biomedical Research Centre Programme; Janssen Research and Development	We thank the Ares staff for their technical assistance. We also thank A. Betz for providing MHCII-deficient mice. This work was supported by the American Asthma Foundation (A.N.J.M.), UK-MRC (A.N.J.M., G.S.O.), Wellcome Trust (grant number 100963/Z/13/Z) (A.N.J.M.), A-STAR (Y.Y.H.), Science Foundation Ireland and National Children's Research Centre (P.G.F.), and NIHR Biomedical Research Centre Programme (G.S.O.). A.N.J.M. and G.S.O. have research grant funding from Janssen Research and Development.	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J	Hamilos, DL				Hamilos, Daniel L.			Chronic rhinosinusitis: Epidemiology and medical management	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						Rhinosinusitis; sinusitis; nasal polyposis; epidemiology; medical management; treatment	ENDOSCOPIC SINUS SURGERY; ALLERGIC FUNGAL RHINOSINUSITIS; PLACEBO-CONTROLLED TRIAL; CHRONIC HYPERPLASTIC SINUSITIS; MESSENGER-RNA EXPRESSION; AQUEOUS NASAL SPRAY; QUALITY-OF-LIFE; DOUBLE-BLIND; ASPIRIN DESENSITIZATION; MUCOCILIARY CLEARANCE	Chronic rhinosinusitis (CRS) affects 12.5% of the US population. On epidemiologic grounds, some association has been found between CRS prevalence and air pollution, active cigarette smoking, secondhand smoke exposure, perennial allergic rhinitis, and gastroesophageal reflux. The majority of pediatric and adult patients with CRS are immune competent. Data on genetic associations with CRS are still sparse. Current consensus definitions subclassify CRS into CRS without nasal polyposis (CRSsNP), CRS with nasal polyposis (CRSwNP), and allergic fungal rhinosinusitis (AFRS). Evaluation and medical management of CRS has been the subject of several recent consensus reports. The highest level of evidence for treatment for CRSsNP exists for saline lavage, intranasal steroids, and long-term macrolide antibiotics. The highest level of evidence for treatment of CRSwNP exists for intranasal steroids, systemic glucocorticoids, and topical steroid irrigations. Aspirin desensitization is beneficial for patients with aspirin-intolerant CRSwNP. Sinus surgery followed by use of systemic steroids is recommended for AFRS. Other modalities of treatment, such as antibiotics for patients with purulent infection and antifungal drugs for patients with AFRS, are potentially useful despite a lack of evidence from controlled treatment trials. The various modalities of medical treatment are reviewed in the context of recent consensus documents and the author's personal experience. (J Allergy Clin Immunol 2011; 128:693-707.)	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Allergy Clin. Immunol.	OCT	2011	128	4					693	709		10.1016/j.jaci.2011.08.004		17	Allergy; Immunology	Allergy; Immunology	841UA	WOS:000296538100001	21890184	
J	Gregory, LG; Lloyd, CM				Gregory, Lisa G.; Lloyd, Clare M.			Orchestrating house dust mite-associated allergy in the lung	TRENDS IN IMMUNOLOGY			English	Review							PROTEASE-ACTIVATED RECEPTOR-2; THYMIC STROMAL LYMPHOPOIETIN; ADAPTIVE IMMUNE-RESPONSES; GROWTH-FACTOR RECEPTOR; DENDRITIC CELLS; AIRWAY INFLAMMATION; DERMATOPHAGOIDES-PTERONYSSINUS; T-CELL; STRUCTURAL BIOLOGY; NLRP3 INFLAMMASOME	House dust mites (HDM; Dermatophagoides sp.) are one of the commonest aeroallergens worldwide and up to 85% of asthmatics are typically HDM allergic. Allergenicity is associated both with the mites themselves and with ligands derived from mite-associated bacterial and fungal products. Murine models of allergic airways disease for asthma research have recently switched from the use of surrogate allergen ovalbumin together with adjuvant to use of the HDM extract. This has accelerated understanding of how adaptive and innate immunity generate downstream pathology. We review the myriad ways in which HDM allergic responses are orchestrated. Understanding the molecular pathways that elicit HDM-associated pathology is likely to reveal novel targets for therapeutic intervention.	[Gregory, Lisa G.; Lloyd, Clare M.] Univ London Imperial Coll Sci Technol & Med, Leukocyte Biol Sect, Natl Heart & Lung Inst, Fac Med, London SW7 2AZ, England	Lloyd, CM (reprint author), Univ London Imperial Coll Sci Technol & Med, Leukocyte Biol Sect, Natl Heart & Lung Inst, Fac Med, London SW7 2AZ, England.	c.1loyd@imperial.ac.uk		Lloyd, Clare/0000-0001-8977-6726	Medical Research Council [G1000758]; Wellcome Trust [087618]		Abramson MJ, 2010, COCHRANE DB SYST REV, V8, DOI DOI 10.1002/14651858.CD001186.PUB2; Adams M.N., 2011, PHARMACOL THERAPEUT, V13, P248; Akdis CA, 2009, J ALLERGY CLIN IMMUN, V123, P735, DOI 10.1016/j.jaci.2009.02.030; Akers IA, 2000, AM J PHYSIOL-LUNG C, V278, pL193; Angkasekwinai P, 2007, J EXP MED, V204, P1509, DOI 10.1084/jem.20061675; Barrett NA, 2011, J EXP MED, V208, P593, DOI 10.1084/jem.20100793; Barrett NA, 2009, J IMMUNOL, V182, P1119; Bhure UN, 2009, ANN NUCL MED, V23, P549, DOI 10.1007/s12149-009-0275-z; Blumberga G, 2011, ALLERGY, V66, P178, DOI 10.1111/j.1398-9995.2010.02451.x; 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J	Subrata, LS; Bizzintino, J; Mamessier, E; Bosco, A; McKenna, KL; Wikstrom, ME; Goldblatt, J; Sly, PD; Hales, BJ; Thomas, WR; Laing, IA; LeSouef, PN; Holt, PG				Subrata, Lily S.; Bizzintino, Joelene; Mamessier, Emilie; Bosco, Anthony; McKenna, Katherine L.; Wikstroem, Matthew E.; Goldblatt, Jack; Sly, Peter D.; Hales, Belinda J.; Thomas, Wayne R.; Laing, Ingrid A.; LeSouef, Peter N.; Holt, Patrick G.			Interactions between Innate Antiviral and Atopic Immunoinflammatory Pathways Precipitate and Sustain Asthma Exacerbations in Children	JOURNAL OF IMMUNOLOGY			English	Article							FC-EPSILON-RI; ALLERGIC AIRWAY INFLAMMATION; KILLER T-CELLS; DENDRITIC CELLS; RESPIRATORY-TRACT; VIRAL-INFECTION; HOSPITAL ADMISSIONS; IMMUNE-RESPONSE; VIRUS-INFECTION; EXPRESSION	Severe asthma exacerbations in children requiring hospitalization are typically associated with viral infection and occur almost exclusively among atopics, but the significance of these comorbidities is unknown. We hypothesized that underlying interactions between immunoinflammatory pathways related to responses to aeroallergen and virus are involved, and that evidence of these interactions is detectable in circulating cells during exacerbations. To address this hypothesis we used a genomics-based approach involving profiling of PBMC subpopulations collected during exacerbation vs convalescence by microarray and flow cytometry. We demonstrate that circulating T cells manifest the postactivated "exhausted" phenotype during exacerbations, whereas monocyte/dendritic cell populations display up-regulated CCR2 expression accompanied by phenotypic changes that have strong potential for enhancing local inflammation after their recruitment to the atopic lung. Notably, up-regulation of Fc epsilon R1, which is known to markedly amplify capacity for allergen uptake/presentation to Th2 effector cells via IgE-mediated allergen capture, and secondarily programming of IL-4/IL-13-dependent IL-13R(+) alternatively activated macrophages that have been demonstrated in experimental settings to be a potent source of autocrine IL-13 production. We additionally show that this disease-associated activation profile can be reproduced in vitro by cytokine exposure of atopic monocytes, and furthermore that IFN-alpha can exert both positive and negative roles in the process. Our findings suggest that respiratory viral infection in atopic children may initiate an atopy-dependent cascade that amplifies and sustains airway inflammation initiated by innate antiviral immunity via harnessing underlying atopy-associated mechanisms. These interactions may account for the unique susceptibility of atopics to severe viral-induced asthma exacerbations. The Journal of Immunology, 2009, 183: 2793-2800.	Telethon Inst Child Hlth Res, Perth, WA, Australia; Univ Western Australia, Fac Med & Dent, Ctr Child Hlth Res, Perth, WA 6009, Australia	Holt, PG (reprint author), Telethon Inst Child Hlth Res, Div Cell Biol, POB 855, Perth, WA 6872, Australia.	patrick@ichr.uwa.edu.au	Sly, Peter/F-1486-2010; Hales, Belinda/C-3858-2013; Laing, Ingrid/I-7092-2013; Bizzintino, Joelene/H-8840-2014; Bizzintino, Joelene/C-8665-2016; Holt, Patrick/H-1548-2011	Sly, Peter/0000-0001-6305-2201; Hales, Belinda/0000-0003-2193-3996; Laing, Ingrid/0000-0002-1641-9899; Holt, Patrick/0000-0003-1193-0935	National Health and Medical Research Council of Australia; The Australian Respiratory Council Ann Woolcock Research Fellowship	This work was funded by National Health and Medical Research Council of Australia. I.A.L. is supported by The Australian Respiratory Council Ann Woolcock Research Fellowship.	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Immunol.	AUG 15	2009	183	4					2793	2800		10.4049/jimmunol.0900695		8	Immunology	Immunology	482RN	WOS:000268906500068	19620293	
J	Garn, H; Renz, H				Garn, Holger; Renz, Harald			Epidemiological and immunological evidence for the hygiene hypothesis	IMMUNOBIOLOGY			English	Review						hygiene hypothesis; allergy; T cell responses; innate immunity	TOLL-LIKE RECEPTORS; REGULATORY T-CELLS; PATTERN-RECOGNITION RECEPTOR; ALLERGIC AIRWAY DISEASE; INNATE IMMUNE-SYSTEM; LACTIC-ACID BACTERIA; DENDRITIC CELLS; MURINE MODEL; INTESTINAL MICROFLORA; ATOPIC-DERMATITIS	Allergic diseases are inflammatory disorders that develop on the basis of complex gene-environment interactions. The prevalence of allergies is steadily increasing and seems to be associated with modern lifestyle. Therefore, it was hypothesized that high living standards and hygienic conditions are correlated with an increased risk for the development of an allergic disease. This so-called "hygiene hypothesis" states that due to reduced exposure to microbial components, the proposed allergy-preventing potential of these factors is no more present in sufficient qualities and/or quantities, which leads to an imbalance of the immune system with a predisposition to the development of allergic disorders. Meanwhile, several epidemiological studies were conducted supporting this concept and generating novel ideas for the underlying mechanisms that were then followed up by use of well-defined animal models and human studies. The current view of cellular and molecular mechanisms responsible for these phenomena includes changes in the fine balancing of T helper cell 1 (Th1), Th2 and regulatory T cell (Treg) responses which are triggered by altered or missing innate immune cell activation. In fact, proper activation of cells of the innate immune system via their so-called pattern recognition receptors has been demonstrated to play a crucial role in early shaping of the immune system and suppression of the development of Th2-driven allergic immune responses. These processes start already in utero and prenatal as well as early postnatal developmental stages seem to represent a certain "window of opportunity" for allergy-preventing environmental influences. (C) 2007 Elsevier GmbH. All rights reserved.	Univ Marburg, Fac Med, Dept Clin Chem & Mol Diagnost, Biomed Res Ctr, D-35043 Marburg, Germany	Garn, H (reprint author), Univ Marburg, Fac Med, Dept Clin Chem & Mol Diagnost, Biomed Res Ctr, Hans Meerwein Str 2, D-35043 Marburg, Germany.	garn@staff.uni-marburg.de					Aaby P, 2000, CLIN EXP ALLERGY, V30, P644, DOI 10.1046/j.1365-2222.2000.00803.x; ADLERBERTH I, 1991, ACTA PAEDIATR SCAND, V80, P602, DOI 10.1111/j.1651-2227.1991.tb11917.x; Ahmad-Nejad P, 2004, J ALLERGY CLIN IMMUN, V113, P565, DOI 10.1016/j.jaci.2003.12.583; Akbari O, 2005, CURR ALLERGY ASTHM R, V5, P56, DOI 10.1007/s11882-005-0055-3; Alm JS, 1998, ALLERGY, V53, P537, DOI 10.1111/j.1398-9995.1998.tb04093.x; Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; Asher MI, 2006, LANCET, V368, P733, DOI 10.1016/S0140-6736(06)69283-0; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; Banerjee B, 2004, INFECT IMMUN, V72, P6087, DOI 10.1128/IAI.72.10.6087-6094.2004; Barlan IB, 2005, CURR OPIN ALLERGY CL, V5, P552, DOI 10.1097/01.all.0000191238.20632.e2; 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J	Hengge, UR; Currie, BJ; Jager, G; Lupi, O; Schwartz, RA				Hengge, Ulrich R.; Currie, Bart J.; Jaeger, Gerold; Lupi, Omar; Schwartz, Robert A.			Scabies: a ubiquitous neglected skin disease	LANCET INFECTIOUS DISEASES			English	Review							CRUSTED NORWEGIAN SCABIES; HOUSE-DUST MITE; TEA TREE OIL; SARCOPTES-SCABIEI; DERMATOPHAGOIDES-PTERONYSSINUS; ORAL IVERMECTIN; IN-VITRO; NOSOCOMIAL OUTBREAK; NORTHERN AUSTRALIA; EPIDEMIC SCABIES	Scabies has been a scourge among human beings for thousands of years. Its worldwide occurrence with epidemics during war, famine, and overcrowding is responsible for an estimated 300 million people currently infested. Scabies refers to the various skin lesions produced by female mites, and their eggs and scybala that are deposited in the epidermis, leading to delayed-type hypersensitivity reaction. Recent immunological findings such as cross-reactivity with house dust mite allergens and an altered T-helper-1/T-helper-2 pattern contribute to a better understanding of the pathomechanism. Furthermore, progress in molecular biology and cloning of relevant antigens could enable the development of a diagnostic ELISA system and candidate vaccines in the near future. Typical and atypical clinical presentations with pruritus as a hallmark of scabies occur in young, pregnant, immunocompromised, and elderly patients and include bullous and crusted (Norwegian) manifestations as well as those masked by steroid use (scabies incognito). This article reviews scabies management strategies in developed countries and resource-poor communities as well as typical complications, including the emergence of resistance and drug-related adverse events. Other problems such as post-scabies eczema and reinfestation, and newer treatments such as ivermectin are also discussed.	Univ Dusseldorf, Dept Dermatol, D-40225 Dusseldorf, Germany; Charles Darwin Univ, Menzles Sch Hlth Res, Darwin, NT, Australia; Royal Darwin Hosp, No Terr Clin Sch, Darwin, NT, Australia; Ikonda HOsp, Njombe, Tanzania; Fed Univ State Rio de Janiero, Rio De Janeiro, Brazil; Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Dermatol, Newark, NJ 07103 USA	Hengge, UR (reprint author), Univ Dusseldorf, Dept Dermatol, Moorenstr 5, D-40225 Dusseldorf, Germany.	ulrich.hengge@uni-duesseldorf.de					Adedayo O, 2003, POSTGRAD MED J, V79, P341, DOI 10.1136/pmj.79.932.341; Adjei O, 1997, E AFR MED J, V74, P729; ALEXANDER JO, 1984, ARTHROPODS HUMAN SKI, P227; Almeida Hiram Larangeira de Jr, 2005, J Am Acad Dermatol, V53, P357; Antony R, 1982, Indian J Public Health, V26, P108; Arlian LG, 2004, J MED ENTOMOL, V41, P74, DOI 10.1603/0022-2585-41.1.74; ARLIAN LG, 1995, AM J TROP MED HYG, V52, P539; ARLIAN LG, 1991, J INVEST DERMATOL, V96, P349, DOI 10.1111/1523-1747.ep12465257; AUBIN F, 1995, NEW ENGL J MED, V332, P612, DOI 10.1056/NEJM199503023320917; Austad Steven N., 1997, ILAR J, V38, P137; Badiaga S, 2005, EUR J DERMATOL, V15, P382; Barkwell R, 1997, LANCET, V349, P1144, DOI 10.1016/S0140-6736(05)63020-6; Birrell G, 2000, LANCET, V356, P1084, DOI 10.1016/S0140-6736(00)02739-2; Blas M, 2005, AM J TROP MED HYG, V72, P855; Boix V, 1997, INFECT CONT HOSP EP, V18, P677; BOWEN R, 1951, South Med J, V44, P836; BURGESS I, 1994, ADV PARASIT, V33, P235, DOI 10.1016/S0065-308X(08)60414-5; BURKHART CG, 1983, ANN INTERN MED, V98, P498; CABRERA R, 1993, SEMIN DERMATOL, V12, P15; Cargill CF, 1997, VET PARASITOL, V70, P191, DOI 10.1016/S0304-4017(96)01137-5; Carson CF, 2006, CLIN MICROBIOL REV, V19, P50, DOI 10.1128/CMR.19.1.50-62.2006; Chosidow O, 2000, LANCET, V355, P819, DOI 10.1016/S0140-6736(99)09458-1; Chouela EN, 1999, ARCH DERMATOL, V135, P651, DOI 10.1001/archderm.135.6.651; CHRISTOPHERSEN J, 1978, ARCH DERMATOL, V114, P747, DOI 10.1001/archderm.114.5.747; Coleman CI, 2005, PHARMACOTHERAPY, V25, P448, DOI 10.1592/phco.25.3.448.61596; Corbett EL, 1996, GENITOURIN MED, V72, P115; COSKEY RJ, 1979, ARCH DERMATOL, V115, P109; Currie B, 1997, LANCET, V350, P1551, DOI 10.1016/S0140-6736(05)63983-9; Currie B J, 2000, Australas J Dermatol, V41, P139, DOI 10.1046/j.1440-0960.2000.00417.x; Currie BJ, 2004, CLIN INFECT DIS, V39, pE8, DOI 10.1086/421776; CURRIE BJ, 1994, MED J AUSTRALIA, V161, P636; Davies J E, 1983, Arch Dermatol, V119, P142; del Giudice P, 1999, ARCH DERMATOL, V135, P705, DOI 10.1001/archderm.135.6.705; Dent JA, 1997, EMBO J, V16, P5867, DOI 10.1093/emboj/16.19.5867; Dougall A, 2005, AM J TROP MED HYG, V73, P977; Dourmishev A, 1998, J EUR ACAD DERMATOL, V11, P247, DOI 10.1016/S0926-9959(98)00075-0; Dourmishev AL, 2005, INT J DERMATOL, V44, P981, DOI 10.1111/j.1365-4632.2004.02253.x; Dourmishev AL, 1998, INT J DERMATOL, V37, P231; ESTES SA, 1993, SEMIN DERMATOL, V12, P26; ESTES SA, 1993, SEMIN DERMATOL, V12, P34; FAIN A, 1978, INT J DERMATOL, V17, P20, DOI 10.1111/j.1365-4362.1978.tb06040.x; FALK ES, 1981, ALLERGY, V36, P233, DOI 10.1111/j.1398-9995.1981.tb01568.x; FALK ES, 1980, BRIT J DERMATOL, V103, P283, DOI 10.1111/j.1365-2133.1980.tb07245.x; Fischer K, 2003, AM J TROP MED HYG, V68, P61; Gardon J, 1997, LANCET, V350, P18, DOI 10.1016/S0140-6736(96)11094-1; GEORGHIOU GP, 1990, ACS SYM SER, V421, P18; GLAZIOU P, 1993, TROP MED PARASITOL, V44, P331; GLOVER R, 1987, J AM ACAD DERMATOL, V16, P396, DOI 10.1016/S0190-9622(87)80145-7; HAAG ML, 1993, GERIATRICS, V48, P45; HENDERSON CA, 1992, TROP DOCT, V22, P165; Henderson CA, 1996, INT J DERMATOL, V35, P640, DOI 10.1111/j.1365-4362.1996.tb03688.x; HERNANDEZPEREZ E, 1983, J AM ACAD DERMATOL, V8, P121, DOI 10.1016/S0190-9622(83)80285-0; Heukelbach J, 2004, B WORLD HEALTH ORGAN, V82, P563; Heukelbach J, 2003, TROP MED INT HEALTH, V8, P368, DOI 10.1046/j.1365-3156.2003.01038.x; Heukelbach Jörg, 2003, Cad. 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Dis.	DEC	2006	6	12					769	779		10.1016/S1473-3099(06)70654-5		11	Infectious Diseases	Infectious Diseases	110JV	WOS:000242375500019	17123897	
J	Rolinck-Werninghaus, C; Staden, U; Mehl, A; Hamelmann, E; Beyer, K; Niggemann, B				Rolinck-Werninghaus, C; Staden, U; Mehl, A; Hamelmann, E; Beyer, K; Niggemann, B			Specific oral tolerance induction with food in children: transient or persistent effect on food allergy?	ALLERGY			English	Article						children; food allergy; specific oral tolerance induction		Background: The standard treatment of food allergy is elimination of the incriminated food from the diet. Specific oral tolerance induction (SOTI) seems to be a promising approach for a causal treatment; however, it is unclear whether the tolerance achieved is transient or persistent. We report on a subset of three patients of a larger ongoing study who were treated successfully with SOTI treatment, but experienced a secondary loss of tolerance after a period of allergen avoidance. Methods: The patients suffered from IgE-mediated allergy either to cow's milk (CM) (patient A) or hen's egg (HE) (patients B and C), confirmed by double-blind, placebo-controlled food challenge (DBPCFC). SOTI treatment was performed at home on a daily basis until tolerance to a maximum of 250 ml CM or 4.5 g lyophilized HE protein was achieved. The daily maintenance dose was 100 ml CM or 2.5 g HE protein. Results: Patients A, B and C reached tolerance to the maximum dose after 37, 41 and 52 weeks, respectively. According to the protocol, patients A and B performed a strict secondary elimination diet for 2 months prior to a follow-up DBPCFC after a maintenance phase of 27 and 39 weeks, respectively. Patient C discontinued treatment for 2 days after 4 weeks on the maintenance dose. Despite previous tolerance, on re-exposure to the allergen all patients experienced moderate systemic allergic reactions. Conclusions: We conclude that SOTI can induce transient tolerance in food allergy, but does not necessarily lead to its permanent abrogation. Regular allergen intake seems necessary to maintain the established tolerance.	Humboldt Univ, Childrens Hosp Charite, Dept Pediat Pneumol & Immunol, D-13353 Berlin, Germany	Niggemann, B (reprint author), Humboldt Univ, Childrens Hosp Charite, Dept Pediat Pneumol & Immunol, Augustenburger Pl 1, D-13353 Berlin, Germany.						Eigenmann PA, 2003, ALLERGY, V58, P1217, DOI 10.1046/j.1398-9995.2003.00303.x; Fleischer DM, 2004, J ALLERGY CLIN IMMUN, V114, P1195, DOI 10.1016/j.jaci.2004.08.035; Meglio P, 2004, ALLERGY, V59, P980, DOI 10.1111/j.1398-9995.2004.00542.x; Niggemann B, 1999, CLIN EXP ALLERGY, V29, P91; Patriarca G, 2003, ALIMENT PHARM THERAP, V17, P459, DOI 10.1046/j.0269-2813.2003.01468.x	5	121	124	0	2	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0105-4538			ALLERGY	Allergy	OCT	2005	60	10					1320	1322		10.1111/j.1398-9995.2005.00882.x		3	Allergy; Immunology	Allergy; Immunology	960BS	WOS:000231565800016	16135001	
J	Schmid-Grendelmeier, P; Fluckiger, S; Disch, R; Trautmann, A; Wuthrich, B; Blaser, K; Scheynius, A; Crameri, R				Schmid-Grendelmeier, P; Fluckiger, S; Disch, R; Trautmann, A; Wuthrich, B; Blaser, K; Scheynius, A; Crameri, R			IgE-mediated and T cell-mediated autoimmunity against manganese superoxide dismutase in atopic dermatitis	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						autoallergy; Aspergillus fumigatus; atopic dermatitis; atopy; fungi; Malassezia sympodialis; intrinsic type; nonatopic eczema; recombinant allergens	ALLERGIC BRONCHOPULMONARY ASPERGILLOSIS; FUMIGATUS ALLERGENS; PATCH TEST; MALASSEZIA; DISEASE; AUTOANTIBODIES; ITRACONAZOLE; REACTIVITY; RESPONSES; CLONING	Background: Autoreactivity of patients with atopic dermatitis (AD) to human proteins has been postulated as a decisive pathogenetic factor for AD. Objective: In this study, it was investigated whether the stress-inducible enzyme manganese superoxide dismutase (MnSOD) of human and fungal origin might act as an autoallergen in atopic dermatitis. Methods: Patients with AD (n = 69; mean SCORAD [SCORing Atopic Dermatitis], 27) and other inflammatory skin diseases as well as with inhalant allergies were investigated. The presence of specific IgE against recombinant MnSOD of fungal and human origin and the fungal extracts of Aspergillus fumigatus and Malassezia sympodialis was measured by CAP, ELISA, skin prick test, and in subset of patients also by atopy patch tests (APTs) and PBMC proliferation assays. Cross-reactivity between allergens was determined by CAP inhibition. The presence of MnSOD in human skin in various inflammatory skin conditions was investigated by immunohistochemistry. Results: Specific IgE antibodies against human MnSOD correlating with the disease activity were found in 29 out of 67 patients with AD. The human protein was able to induce in vitro T-cell reactivity and eczematous reactions in APT in MnSOD-sensitized patients with AD. MnSOD was upregulated in various inflammatory skin reactions and APT skin specimens. Cosensitization to structurally related and cross-reacting fungal MnSOD and the skin-colonizing yeast M sympodialis was observed in all patients sensitized against human MnSOD. Conclusion: Human MnSOD may play a role as an autoallergen in a subset of patients with AD, including nonatopic eczema. By molecular mimicry leading to cross-reactivity such sensitization might be induced primarily by exposure to environmental fungal MnSOD of M sympodialis.	Univ Zurich Hosp, Dept Dermatol, Allergy Unit, CH-8091 Zurich, Switzerland; Swiss Inst Allergy & Asthma Res, CH-7270 Davos, Switzerland; BioVisioN Schweiz AG, Davos, Switzerland; Alexanderhaus Klin, Davos, Switzerland; Karolinska Hosp & Inst, Dept Med, Unit Clin Allergy Res, Stockholm, Sweden	Schmid-Grendelmeier, P (reprint author), Univ Zurich Hosp, Dept Dermatol, Allergy Unit, Gloriastr 31, CH-8091 Zurich, Switzerland.	peter.schmid@usz.ch					Andersson A, 2004, EUR J BIOCHEM, V271, P1885, DOI 10.1111/j.1432-1033.2004.04098.x; Crameri R, 1998, INT IMMUNOL, V10, P1211, DOI 10.1093/intimm/10.8.1211; Crameri R, 1996, J EXP MED, V184, P265, DOI 10.1084/jem.184.1.265; DARSOW U, 1995, J ALLERGY CLIN IMMUN, V95, P677, DOI 10.1016/S0091-6749(95)70172-9; Fluckiger S, 2002, J IMMUNOL, V168, P1267; Hanifin JM, 1980, ACTA DERM-VENEREOL S, V92, P44; Hemmann S, 1998, EUR J IMMUNOL, V28, P1155, DOI 10.1002/(SICI)1521-4141(199804)28:04<1155::AID-IMMU1155>3.3.CO;2-Y; Hemmann S, 1999, J ALLERGY CLIN IMMUN, V104, P601, DOI 10.1016/S0091-6749(99)70330-1; HIROSE K, 1993, FASEB J, V7, P361; Hofer MF, 1999, J INVEST DERMATOL, V112, P171, DOI 10.1046/j.1523-1747.1999.00492.x; Ikezawa Z, 2004, EUR J DERMATOL, V14, P400; JANSSEN YMW, 1993, LAB INVEST, V69, P261; Johansson SGO, 2004, J ALLERGY CLIN IMMUN, V113, P832, DOI 10.1016/j.jaci.2003.12.591; Kinaciyan T, 2002, J ALLERGY CLIN IMMUN, V109, P717, DOI 10.1067/mai.2002.123303; Leung DYM, 2003, LANCET, V361, P151, DOI 10.1016/S0140-6736(03)12193-9; Linder MT, 2000, CLIN EXP ALLERGY, V30, P122, DOI 10.1046/j.1365-2222.2000.00702.x; Lintu P, 2001, ALLERGY, V56, P512, DOI 10.1034/j.1398-9995.2001.056006512.x; MacMillan-Crow LA, 2001, FREE RADICAL RES, V34, P325, DOI 10.1080/10715760100300281; Mayer C, 1999, J EXP MED, V189, P1507, DOI 10.1084/jem.189.9.1507; Mayer C, 1997, INT ARCH ALLERGY IMM, V113, P213; Nakabayashi A, 2000, MED MYCOL, V38, P337, DOI 10.1080/714030958; Novak N, 2003, J ALLERGY CLIN IMMUN, V112, P252, DOI 10.1067/mai.2003.1595; Ochs RL, 2000, J ALLERGY CLIN IMMUN, V105, P1211, DOI 10.1067/mai.2000.107039; Omata N, 2001, LIFE SCI, V69, P223, DOI 10.1016/S0024-3205(01)01124-9; Ong PY, 2002, NEW ENGL J MED, V347, P1151, DOI 10.1056/NEJMoa021481; Patterson R, 2000, CHEST, V118, P7, DOI 10.1378/chest.118.1.7; Poswig A, 1999, J INVEST DERMATOL, V112, P13, DOI 10.1046/j.1523-1747.1999.00465.x; Scheynius A, 2002, INT ARCH ALLERGY IMM, V127, P161, DOI 10.1159/000053860; Schmid P, 2001, ALLERGY, V56, P841, DOI 10.1034/j.1398-9995.2001.00144.x; SCHMIDGRENDELMEIER, 2001, INT ARCH ALLERGY IMM, V125, P96; Svejgaard EI, 2004, J EUR ACAD DERMATOL, V18, P445, DOI 10.1111/j.1468-3083.2004.00963.x; Trautmann A, 2000, J CLIN INVEST, V106, P25, DOI 10.1172/JCI9199; Trautmann A, 2001, TRENDS IMMUNOL, V22, P530, DOI 10.1016/S1471-4906(01)02004-X; Valenta R, 2000, J ALLERGY CLIN IMMUN, V105, P432, DOI 10.1067/mai.2000.104783; Valenta R, 1998, J INVEST DERMATOL, V111, P1178, DOI 10.1046/j.1523-1747.1998.00413.x; Werfel T, 1998, ALLERGY, V53, P731; [Anonymous], 1992, ALLERGY, V47, P1; 1993, CONSENSUS REPORT EUR, V186, P23	38	121	128	0	4	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	MAY	2005	115	5					1068	1075		10.1016/j.jaci.2005.01.065		8	Allergy; Immunology	Allergy; Immunology	925LR	WOS:000229055100026	15867868	
J	Miller, RL; Garfinkel, R; Horton, M; Camann, D; Pereral, FP; Whyatt, RM; Kinney, PL				Miller, RL; Garfinkel, R; Horton, M; Camann, D; Pereral, FP; Whyatt, RM; Kinney, PL			Polycyclic aromatic hydrocarbons, environmental tobacco smoke, and respiratory symptoms in an inner-city birth cohort	CHEST			English	Article						asthma; environmental tobacco smoke; polycyclic aromatic hydrocarbons	DIESEL EXHAUST PARTICLES; CIGARETTE-SMOKE; LUNG-FUNCTION; AIR-POLLUTION; EXPOSURE; ALLERGEN; CHALLENGE; MICE; IGE; PARTICULATE	Study objectives: Several studies have found associations between diesel exposure, respiratory symptoms, and/or impaired pulmonary function. We hypothesized that prenatal exposure to airborne polycyclic aromatic hydrocarbons (PAH), important components of diesel exhaust and other combustion sources, may be associated with respiratory symptoms in young children. We also hypothesized that exposure to environmental tobacco smoke (ETS) may worsen symptoms beyond that observed to be associated with PAH alone. Design/participants: To test our hypotheses, we recruited 303 pregnant women from northern Manhattan believed to be at high risk for exposure to both PAH and ETS, collected 48-h personal PAH exposure measurements, and monitored their children prospectively. Results: By 12 months of age, more cough and wheeze were reported in children exposed to prenatal PAH in concert with ETS postnatally (PAH X ETS interaction odds ratios [ORs], 1.41 [p < 0.01] and 1.29 [p < 0.05], respectively). By 24 months, difficulty breathing and probable asthma were reported more frequently among children exposed to prenatal PAH and ETS postnatally (PAR X ETS ORs, 1.54 and 1.64, respectively [p < 0.05]). Conclusions: Our results suggest that early exposure to airborne PAH and ETS can lead to increased respiratory symptoms and probable asthma by age 12 to 24 months. Interventions to lower the risk of respiratory disease in young children living in the inner city may need to address the importance of multiple environmental exposures.	Columbia Univ, Coll Phys & Surg, Dept Med, Div Pulm Allergy Crit Care Med, New York, NY USA; Columbia Univ, Mailman Sch Publ Hlth, Columbia Ctr Childrens Environm Hlth, New York, NY USA; Columbia Univ, Mailman Sch Publ Hlth, Dept Environm Hlth Sci, New York, NY USA; SW Res Inst, Dept Analyt & Environm Chem, San Antonio, TX USA	Miller, RL (reprint author), 630 168th St, New York, NY 10032 USA.	rlm14@columbia.edu	Kinney, Patrick/H-7914-2012		NCRR NIH HHS [M01 RR000645, RR 00645]; NIEHS NIH HHS [R01 ES008977, 5R01 ES 08977, P01 ES009600, P01 ES009600-060005, P01 ES009600-070005, P01 ES009600-080005, P01 ES009600-090005, P30 ES 09089, P30 ES009089, P501 ES 09600, R01 ES 012468, R01 ES 11115 8, R01 ES012468]		BARKER DJP, 1989, LANCET, V2, P577; Bernert JT, 2000, J ANAL TOXICOL, V24, P333; Bommel H, 2000, J ALLERGY CLIN IMMUN, V105, P796, DOI 10.1067/mai.2000.105124; CHURCH DF, 1985, ENVIRON HEALTH PERSP, V64, P111; COULTAS DB, 1989, AM J EPIDEMIOL, V130, P338; Dempsey D, 2002, J PHARMACOL EXP THER, V301, P594, DOI 10.1124/jpet.301.2.594; DiazSanchez D, 1997, ALLERGY, V52, P52; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; DOCKERY DW, 1989, AM REV RESPIR DIS, V139, P587; Fujieda S, 1998, AM J RESP CELL MOL, V19, P507; Gehring U, 2002, EUR RESPIR J, V19, P690, DOI 10.1183/09031936.02.01182001; Georgiadis P, 2001, CARCINOGENESIS, V22, P1447, DOI 10.1093/carcin/22.9.1447; Gilliland FD, 2000, THORAX, V55, P271, DOI 10.1136/thorax.55.4.271; Hamada K, 2003, J IMMUNOL, V170, P1683; HAMADA K, 2003, AM J RESP CRIT CARE, V167, pA942; Harrod KS, 2003, AM J RESP CELL MOL, V28, P451, DOI 10.1165/rcmb.2002-0100OC; Heo Y, 2001, TOXICOLOGY, V159, P143, DOI 10.1016/S0300-483X(00)00418-2; Kanoh T, 1996, J Clin Lab Immunol, V48, P133; Li YF, 2000, AM J RESP CRIT CARE, V162, P2097; Lum S, 2001, AM J RESP CRIT CARE, V164, P2078; Lux AL, 2000, ARCH DIS CHILD, V83, P307, DOI 10.1136/adc.83.4.307; MENON P, 1992, J ALLERGY CLIN IMMUN, V89, P560, DOI 10.1016/0091-6749(92)90323-T; Northridge ME, 1999, AM J PUBLIC HEALTH, V89, P998, DOI 10.2105/AJPH.89.7.998; Ohta K, 1999, J ALLERGY CLIN IMMUN, V104, P1024; Ormstad H, 2000, TOXICOLOGY, V152, P53, DOI 10.1016/S0300-483X(00)00292-4; Pandya RJ, 2002, ENVIRON HEALTH PERSP, V110, P103; Perera FP, 2003, ENVIRON HEALTH PERSP, V111, P201, DOI 10.1289/ehp.5742; Perera FP, 1998, AM J EPIDEMIOL, V147, P309; Perera FP, 2002, ENVIRON HEALTH PERSP, V110, P197; RAUH V, 2002, ENV HLTH PERSPECT, V10, P323; ROMAGNANI, 1998, ALLERGY S, V46, P12; Rudell B, 1996, OCCUP ENVIRON MED, V53, P658; Salvi SS, 2000, AM J RESP CRIT CARE, V161, P550; Takano H, 1997, AM J RESP CRIT CARE, V156, P36; United Church of Christ. Commission for Racial Justice, 1987, TOX WAST RAC US NAT; WHITEKUS MJ, 2002, THE J IMMUNOL, V168, P2560; Wyler C, 2000, EPIDEMIOLOGY, V11, P450, DOI 10.1097/00001648-200007000-00015; Yu M, 2002, TOXICOL SCI, V65, P99, DOI 10.1093/toxsci/65.1.99	38	121	129	6	18	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	OCT	2004	126	4					1071	1078		10.1378/chest.126.4.1071		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	864ZY	WOS:000224673100017	15486366	
J	Rana, JS; Mittleman, MA; Sheikh, J; Hu, FB; Manson, JE; Colditz, GA; Speizer, FE; Barr, RG; Camargo, CA				Rana, JS; Mittleman, MA; Sheikh, J; Hu, FB; Manson, JE; Colditz, GA; Speizer, FE; Barr, RG; Camargo, CA			Chronic obstructive pulmonary disease, asthma, and risk of type 2 diabetes in women	DIABETES CARE			English	Article							TUMOR-NECROSIS-FACTOR; C-REACTIVE PROTEIN; INSULIN-RESISTANCE; OXIDATIVE STRESS; GENE-TRANSCRIPTION; LUNG-FUNCTION; TNF-ALPHA; MELLITUS; WEIGHT; COHORT	OBJECTIVE - Inflammation plays a key role in chronic obstructive pulmonary disease (COPD) and asthma. Increasing evidence points toward a role of inflammation in the pathogenesis of type 2 diabetes. We wanted to determine the relation of COPD and asthma with the development of type 2 diabetes. RESEARCH DESIGN AND METHODS - The Nurses' Health Study is a prospective cohort study. From 1988-1996, 103,614 female nurses were asked biennially about a physician diagnosis of emphysema, chronic bronchitis, asthma, and diabetes. RESULTS - During 8 years of follow-up, we documented a total of 2,959 new cases of type 2 diabetes. The risk of type 2 diabetes was significantly higher for patients with COPD than those without (multivariate relative risk 1.8, 95% CI 1.1-2.8). By contrast, the risk of type 2 diabetes among asthmatic patients was not increased (1.0, 0.8-1.2). The asthma results remained non-significant even when we evaluated diabetes risk by duration of asthma exposure. CONCLUSIONS - Our findings suggest that COPD may be a risk factor for developing type 2 diabetes. Differences in the inflammation and cytokine profile between COPD and asthma might explain why COPD, but not asthma, is associated with increased risk of type 2 diabetes.	Beth Israel Deaconess Med Ctr, Div Cardiol, Dept Med, Boston, MA USA; Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA; Beth Israel Deaconess Med Ctr, Div Allergy & Inflammat, Dept Med, Boston, MA USA; Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA; Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med, Boston, MA USA; Harvard Univ, Brigham & Womens Hosp, Div Prevent Med, Dept Med,Med Sch, Boston, MA USA; Columbia Presbyterian Med Ctr, Dept Med, Div Gen Med, New York, NY USA; Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA USA	Camargo, CA (reprint author), Channing Labs, 181 Longwood Ave, Boston, MA 02115 USA.	ccamargo@partners.org	Colditz, Graham/A-3963-2009	Colditz, Graham/0000-0002-7307-0291	NCI NIH HHS [R01 CA87969]; NHLBI NIH HHS [R01 HL63841, T32 HL07374, T32 HL07427]; NIDDK NIH HHS [R01 DK58845]		Anto JM, 2001, EUR RESPIR J, V17, P982, DOI 10.1183/09031936.01.17509820; Barnes Peter J., 2000, Chest, V117, p10S, DOI 10.1378/chest.117.2_suppl.10S; Barnes PJ, 2000, NEW ENGL J MED, V343, P269, DOI 10.1056/NEJM200007273430407; Barr RG, 2002, AM J EPIDEMIOL, V155, P965, DOI 10.1093/aje/155.10.965; Blackburn D, 2002, J GEN INTERN MED, V17, P717, DOI 10.1046/j.1525-1497.2002.10649.x; Camargo CA, 1999, ARCH INTERN MED, V159, P2582, DOI 10.1001/archinte.159.21.2582; CHAN JM, 1994, DIABETES CARE, V17, P961, DOI 10.2337/diacare.17.9.961; Chung K. F., 2007, EUR RESPIR J, V34, p50s, DOI DOI 10.1183/09031936.01.00229701); Congleton J, 1999, P NUTR SOC, V58, P321, DOI 10.1017/S0029665199000439; Coultas DB, 2001, AM J RESP CRIT CARE, V164, P372; CREUTZBERG EC, 2004, EUR RESP J S46, V22, pS76; Delaunay F, 1997, J CLIN INVEST, V100, P2094, DOI 10.1172/JCI119743; Eid AA, 2001, AM J RESP CRIT CARE, V164, P1414; Engstrom G, 2003, J INTERN MED, V253, P574, DOI 10.1046/j.1365-2796.2003.01138.x; Engstrom G, 2002, DIABETIC MED, V19, P167, DOI 10.1046/j.1464-5491.2002.00652.x; Festa A, 2002, DIABETES, V51, P1131, DOI 10.2337/diabetes.51.4.1131; Gavin JR, 1997, DIABETES CARE, V20, P1183; Grimble RF, 2002, CURR OPIN CLIN NUTR, V5, P551, DOI 10.1097/00075197-200209000-00015; GURWITZ JH, 1994, ARCH INTERN MED, V154, P97, DOI 10.1001/archinte.154.1.97; HARRIS M, 1979, DIABETES, V28, P1039; Hjalmarsen A, 1996, DIABETES METAB, V22, P37; Hotamisligil GS, 1999, J INTERN MED, V245, P621, DOI 10.1046/j.1365-2796.1999.00490.x; HOTAMISLIGIL GS, 1994, P NATL ACAD SCI USA, V91, P4854, DOI 10.1073/pnas.91.11.4854; Hu FB, 2004, DIABETES, V53, P693, DOI 10.2337/diabetes.53.3.693; Hu FB, 2001, NEW ENGL J MED, V345, P790, DOI 10.1056/NEJMoa010492; JAKOBSSON P, 1995, CLIN PHYSIOL, V15, P319, DOI 10.1111/j.1475-097X.1995.tb00522.x; JAKOBSSON P, 1995, CLIN PHYSIOL, V15, P547, DOI 10.1111/j.1475-097X.1995.tb00543.x; Lazarus R, 1998, EUR RESPIR J, V12, P641, DOI 10.1183/09031936.98.12030641; Mador MJ, 2002, AM J RESP CRIT CARE, V166, P787, DOI 10.1164/rccm.2206003; Majori M, 1999, J ALLERGY CLIN IMMUN, V103, P458, DOI 10.1016/S0091-6749(99)70471-9; Mannino DM, 2003, AM J MED, V114, P758, DOI 10.1016/S0002-9343(03)00185-2; MANSON JE, 1991, LANCET, V338, P774, DOI 10.1016/0140-6736(91)90664-B; Pauwels R A, 2001, Respir Care, V46, P798; Pitsiou G, 2002, RESP MED, V96, P594, DOI 10.1053/rmed.2002.1322; Pradhan AD, 2001, JAMA-J AM MED ASSOC, V286, P327, DOI 10.1001/jama.286.3.327; Rahman I, 2002, MOL CELL BIOCHEM, V234, P239, DOI 10.1023/A:1015905010086; Rahman I, 2003, J BIOCHEM MOL BIOL, V36, P95; Renauld JC, 2001, J CLIN PATHOL, V54, P577, DOI 10.1136/jcp.54.8.577; RIMM EB, 1993, AM J PUBLIC HEALTH, V83, P211, DOI 10.2105/AJPH.83.2.211; Rosen P, 2001, DIABETES METAB RES, V17, P189, DOI 10.1002/dmrr.196; Schols A M W J, 2003, Eur Respir J Suppl, V46, p81s; Schols AMWJ, 1996, THORAX, V51, P819, DOI 10.1136/thx.51.8.819; Spranger J, 2003, DIABETES, V52, P812, DOI 10.2337/diabetes.52.3.812; Takabatake N, 2000, AM J RESP CRIT CARE, V161, P1179; Thorand B, 2003, ARCH INTERN MED, V163, P93, DOI 10.1001/archinte.163.1.93; Vermeeren MAP, 1997, EUR RESPIR J, V10, P2264, DOI 10.1183/09031936.97.10102264; Wouters EFM, 2002, THORAX, V57, P1067, DOI 10.1136/thorax.57.12.1067	47	121	132	1	4	AMER DIABETES ASSOC	ALEXANDRIA	1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA	0149-5992			DIABETES CARE	Diabetes Care	OCT	2004	27	10					2478	2484		10.2337/diacare.27.10.2478		7	Endocrinology & Metabolism	Endocrinology & Metabolism	857KQ	WOS:000224115700030	15451919	
J	Wallace, LA; Mitchell, H; O'Connor, GT; Neas, L; Lippmann, M; Kattan, M; Koenig, J; Stout, JW; Vaughn, BJ; Wallace, D; Walter, M; Adams, K; Liu, LJS				Wallace, LA; Mitchell, H; O'Connor, GT; Neas, L; Lippmann, M; Kattan, M; Koenig, J; Stout, JW; Vaughn, BJ; Wallace, D; Walter, M; Adams, K; Liu, LJS			Particle concentrations in inner-city homes of children with asthma: The effect of smoking, cooking, and outdoor pollution	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						continuous monitors; environmental tobacco smoke; gravimetric measurements; indoor air; MIE pDR; optical scattering; PM10; PM2.5	PARTICULATE AIR-POLLUTION; PERSONAL EXPOSURE; FINE PARTICLES; HOSPITAL ADMISSIONS; AIRBORNE PARTICLES; INDOOR; SEATTLE; BALTIMORE; MATTER; EPIDEMIOLOGY	inner-city children have high rates of asthma. Exposures to particles, including allergens, may cause or exacerbate asthma symptoms. As part of an epidemiologic study of inner-city children with asthma, continuous (10-min average) measurements of particle concentrations were made for 2-week periods in 294 homes drawn from seven cities. Measurements were made using an optical scattering device that is most sensitive to fine particles. The concentrations recorded by these devices were corrected to agree with colocated outdoor gravimetric PM2.5 monitors. Indoor concentrations in the homes averaged 27.7 (standard deviation = 35.9) mug/m(3), compared with concurrent outdoor concentrations of 13.6 (7.5) mug/m(3). A multivariate model indicated that outdoor particles penetrated indoors with an efficiency of 0.48 and were therefore responsible for only 25% of the mean indoor concentration. The major indoor source was smoking, which elevated indoor concentrations by 37 mug/m(3) in the 10 1 homes with smokers. Other significant sources included frying, smoky cooking events, use of incense, and apartment housing, although the increases due to these events ranged only from 3 to 6 mug/m(3). The 10-min averaging time allowed calculation of an average diurnal variation, showing large increases in the evening due to smoking and smaller increases at meal times due to cooking. Most of the observed variance in indoor concentrations was day to day, with roughly similar contributions to the variance from visit to visit and home to home within a city and only a small contribution made by variance among cities. The small variation among cities and the similarity across cities of the observed indoor air particle distributions suggest that sources of indoor concentrations do not vary considerably from one city to the next, and thus that simple models can predict indoor air concentrations in cities having only outdoor measurements.	US EPA, Reston, VA 20191 USA; Rho Inc, Chapel Hill, NC USA; Boston Univ, Boston, MA 02215 USA; US EPA, Res Triangle Pk, NC 27711 USA; NYU, Sch Med, Tuxedo Pk, NY 10987 USA; Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA; Univ Washington, Seattle, WA 98195 USA; NIAID, Bethesda, MD 20892 USA	Wallace, LA (reprint author), US EPA, 11568 Woodhollow Ct, Reston, VA 20191 USA.		Neas, Lucas/J-9378-2012; Wallace, Lance/K-7264-2013	O'Connor, George/0000-0002-6476-3926; Wallace, Lance/0000-0002-6635-2303	NIAID NIH HHS [AI-39789, AI-39761, AI-39769, AI-39776, AI-39785, AI-39900, AI-39901, AI-39902]		BAHADORI T, IN PRESS J EXPO ANAL; Crain EF, 2002, ENVIRON HEALTH PERSP, V110, P939; DOCKERY DW, 1981, JAPCA J AIR WASTE MA, V31, P153; HIGHSMITH VR, 1988, ENVIRON SCI TECHNOL, V22, P1109, DOI 10.1021/es00174a019; Howard-Reed C, 2000, J AIR WASTE MANAGE, V50, P1125; Janssen NAH, 1999, ARCH ENVIRON HEALTH, V54, P95; Janssen NAH, 1998, AM J EPIDEMIOL, V147, P537; Janssen NAH, 1997, OCCUP ENVIRON MED, V54, P888; Jetter JJ, 2002, SCI TOTAL ENVIRON, V295, P51, DOI 10.1016/S0048-9697(02)00043-8; Kattan M, 1997, PEDIATR PULM, V24, P253, DOI 10.1002/(SICI)1099-0496(199710)24:4<253::AID-PPUL4>3.0.CO;2-L; KELLY TJ, 2001, 5083 GAS RES I; KLEPEIS N, 1995, 68017325 US EPA; Lin M, 2002, ENVIRON HEALTH PERSP, V110, P575; LIOY PJ, 1990, ATMOS ENVIRON B-URB, V24, P57, DOI 10.1016/0957-1272(90)90010-R; Liu LJS, 2003, ENVIRON HEALTH PERSP, V111, P909, DOI 10.1289/ehp.6011; Liu LJS, 2002, ENVIRON SCI TECHNOL, V36, P2977, DOI 10.1021/es0112644; Long CM, 2001, ENVIRON HEALTH PERSP, V109, P1019, DOI 10.2307/3454956; *MIE, 1998, 8A MIE; Norris G, 1999, ENVIRON HEALTH PERSP, V107, P489, DOI 10.2307/3434632; Ott W, 2000, J AIR WASTE MANAGE, V50, P1390; Ozkaynak H, 1996, J EXPO ANAL ENV EPID, V6, P57; PELLIZZARI ED, 1993, PARTICLE TOTAL EXPOS, V1; Peters A, 1997, EUR RESPIR J, V10, P872; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Pope CA, 2000, ENVIRON HEALTH PERSP, V108, P713, DOI 10.2307/3454408; Quintana PJE, 2001, ENVIRON RES, V87, P199, DOI 10.1006/enrs.2001.4304; ROJASBRACHO L, 2000, SCI TOTAL ENVIRON, V287, P249; Sarnat JA, 2000, J AIR WASTE MANAGE, V50, P1184; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; SCHWARTZ J, 1994, ENVIRON RES, V64, P36, DOI 10.1006/enrs.1994.1005; Schwartz J, 2000, EPIDEMIOLOGY, V11, P6, DOI 10.1097/00001648-200001000-00004; SHELDON LS, 1989, 736CONBCS85 NEW YORK; Sheppard L, 1999, EPIDEMIOLOGY, V10, P23, DOI 10.1097/00001648-199901000-00006; Sioutas C, 2000, ATMOS ENVIRON, V34, P4829, DOI 10.1016/S1352-2310(00)00244-2; SPENGLER JD, 1981, ATMOS ENVIRON, V15, P23, DOI 10.1016/0004-6981(81)90121-9; *US EPA, 2002, 600P99002AC2V EPA; *US EPA, 1996, 600P95001AFCF3V EPA; EPA U.S., 2001, NAT AIR QUAL EM TREN; WALLACE LA, 2002, J AIR WASTE MANAGE, V52, P174; WALLACE LA, 2000, APPL OCCUP ENV HYG, V15, P1; WALLACE LA, 2002, ANN M INT SOC EXP AN; Williams R, 2000, ATMOS ENVIRON, V34, P4193, DOI 10.1016/S1352-2310(00)00209-0; Wilson AL, 1996, J EXPO ANAL ENV EPID, V6, P311; Yu OC, 2000, ENVIRON HEALTH PERSP, V108, P1209, DOI 10.2307/3434835; Zanobetti A, 2000, ENVIRON HEALTH PERSP, V108, P1071, DOI 10.2307/3434961; 1997, FED REG, V62, P57	46	121	124	5	33	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	JUL	2003	111	9					1265	1272		10.1289/ehp.6135		8	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	715VH	WOS:000184992700041	12842784	
J	Holzer, K; Anderson, SD; Douglass, J				Holzer, K; Anderson, SD; Douglass, J			Exercise in elite summer athletes: Challenges for diagnosis	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; eucapnic hyperpnea; elite athletes; methacholine challenge	EUCAPNIC VOLUNTARY HYPERVENTILATION; INDUCED ASTHMA; BRONCHIAL RESPONSIVENESS; INDUCED BRONCHOSPASM; HYPERTONIC SALINE; REACTIVITY; CHILDREN; METHACHOLINE; PROVOCATION; SALBUTAMOL	Background: There is a high prevalence of asthma and exercise-induced bronchoconstriction (EIB) in elite athletes when the diagnosis is based on symptoms and medication use. Objective measurements are now required by some sporting bodies to support a diagnosis of asthma or EIB to justify use of beta-agonists. Such measurements could include bronchial provocation with methacholine, with eucapnic voluntary hyperpnea (EVH) of dry air (a surrogate for exercise), or both. Objective: The aim of the study was to investigate the relationship between asthma symptoms and responses to methacholine and the EVH challenge in a group of unselected elite summer-sport athletes. The outcome would be to inform practitioners of a suitable objective approach to identifying those with asthma and EIB. Methods: Fifty elite summer-sport athletes with or without asthma were recruited from sporting teams and sports medicine centers throughout Melbourne, Australia. All subjects completed a respiratory questionnaire and, on separate days, underwent a bronchoprovocation challenge test with methacholine and EVH. Results: Forty-two subjects reported one or more respiratory symptoms in the past year, 9 had positive methacholine challenge results (mean PD20 of 1.69 +/- 2.05 mumol), and 25 had posit e EVH challenge results (mean fall in FEV1 of 25.4% +/- 15%). Although all subjects with positive methacholine challenge results had positive EVH challenge results, methacholine had a negative predictive value of only 61% and a sensitivity of 36% for identifying those responsive to EVH. Conclusion: These findings suggest that the pathogenesis of EIB in elite athletes might be different from that of asthma, and as such, neither symptoms nor the methacholine challenge test should be used exclusively for identifying EIB.	Alfred Hosp, Dept Allergy Asthma & Clin Immunol, Prahran, Vic 3181, Australia; Monash Univ, Prahran, Vic, Australia; Royal Prince Alfred Hosp, Dept Resp Med, Camperdown, NSW 2050, Australia	Holzer, K (reprint author), Alfred Hosp, Dept Allergy Asthma & Clin Immunol, Prahran, Vic 3181, Australia.			Anderson, Sandra/0000-0002-6308-8770			ABRAMSON MJ, 1990, THORAX, V45, P924, DOI 10.1136/thx.45.12.924; Anderson SD, 2001, MED SCI SPORT EXER, V33, P893, DOI 10.1097/00005768-200106000-00007; Anderson SD, 2001, BRIT J SPORT MED, V35, P344, DOI 10.1136/bjsm.35.5.344; ARGYROS GJ, 1995, CHEST, V108, P419, DOI 10.1378/chest.108.2.419; BACKER V, 1992, CLIN EXP ALLERGY, V22, P741, DOI 10.1111/j.1365-2222.1992.tb02813.x; BARNES NC, 1984, THORAX, V39, P500, DOI 10.1136/thx.39.7.500; Brannan JD, 1998, AM J RESP CRIT CARE, V158, P1120; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; DAHLEN SE, 1980, NATURE, V288, P484, DOI 10.1038/288484a0; ELIASSON AH, 1992, CHEST, V102, P347, DOI 10.1378/chest.102.2.347; Eliasson AH, 1999, CHEST, V115, P608, DOI 10.1378/chest.115.3.608; Gravetter F. J., 2000, STAT BEHAV SCI; HABY MM, 1995, EUR RESPIR J, V8, P729; HURWITZ KM, 1995, CHEST, V108, P1240, DOI 10.1378/chest.108.5.1240; *INT OL MED COMM, 2002, BER 2 ADR AG OL WINT; Mannix ET, 1999, CHEST, V115, P649, DOI 10.1378/chest.115.3.649; PATTEMORE PK, 1990, AM REV RESPIR DIS, V142, P549; PHILLIPS YY, 1985, AM REV RESPIR DIS, V131, P31; PIPER PJ, 1984, PHYSIOL REV, V64, P744; Quanjer PH, 1993, EUR RESPIR J, V6, P16; RICE SG, 1985, ANN ALLERGY, V55, P790; RIEDLER J, 1994, AM J RESP CRIT CARE, V150, P1632; Rundell KW, 2000, MED SCI SPORT EXER, V32, P309, DOI 10.1097/00005768-200002000-00010; Rundell KW, 2001, MED SCI SPORT EXER, V33, P208; RUPP NT, 1992, AM J DIS CHILD, V146, P941; SEARS MR, 1986, THORAX, V41, P283, DOI 10.1136/thx.41.4.283; SMITH CM, 1990, EUR RESPIR J, V3, P144; SMITH CM, 1989, EUR RESPIR J, V2, P36; SMITH LJ, 1985, AM REV RESPIR DIS, V131, P369; TOELLE BG, 1992, AM REV RESPIR DIS, V146, P633; van Baak MA, 2000, MED SCI SPORT EXER, V32, P1300, DOI 10.1097/00005768-200007000-00018; van Grunsven PM, 1999, THORAX, V54, P316; VATHENEN AS, 1991, THORAX, V46, P811, DOI 10.1136/thx.46.11.811; Weiler JM, 1998, J ALLERGY CLIN IMMUN, V102, P722, DOI 10.1016/S0091-6749(98)70010-7; YAN K, 1983, THORAX, V38, P760, DOI 10.1136/thx.38.10.760	35	121	126	2	3	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	SEP	2002	110	3					374	380		10.1067/mai.2002.127784		7	Allergy; Immunology	Allergy; Immunology	592KM	WOS:000177936900005	12209082	
J	Thickett, KM; McCoach, JS; Gerber, JM; Sadhra, S; Burge, PS				Thickett, KM; McCoach, JS; Gerber, JM; Sadhra, S; Burge, PS			Occupational asthma caused by chloramines in indoor swimming-pool air	EUROPEAN RESPIRATORY JOURNAL			English	Article						bronchial provocation test; nitrogen trichloride; occupational asthma; peak expiratory flow; swimming pool	BRONCHIAL RESPONSIVENESS; WORKERS	The first series of three workers who developed occupational asthma following exposure to airborne chloramines in indoor chlorinated swimming pools is reported. Health problems of swimmers in indoor pools have traditionally been attributed to the chlorine in the water. Chlorine reacts with bodily proteins to form chloramines; the most volatile and prevalent in the air above swimming pools is nitrogen trichloride. Two lifeguards and one swimming teacher with symptoms suggestive of occupational asthma kept 2-hourly measurements of peak expiratory flow at home and at work, analysed using the occupational asthma system (OASYS) plotter, and/or had specific bronchial challenge testing to nitrogen trichloride, or a workplace challenge. Air measurement in one of the pools showed the nitrogen trichloride levels to be 0.1-0.57 mg.m(-3), which was similar to other studies. Two workers had peak expiratory flow measurements showing occupational asthma (OASYS-2 scores 2.88 and 3.8), both had a positive specific challenge to nitrogen trichloride at 0.5 mg.m(-3) with negative challenges to chlorine released from sodium hypochlorite. The third worker had a positive workplace challenge. Swimming-pool asthma due to airborne nitrogen trichloride can occur in workers who do not enter the water because of this chloramine. The air above indoor swimming pools therefore needs to be assessed and managed as carefully as the water.	Birmingham Heartlands Hosp, Dept Resp Med, Occupat Lung Dis Unit, Birmingham B5 5SS, W Midlands, England; Inst Natl Rech & Secur, F-54501 Vandoeuvre Les Nancy, France; Univ Birmingham, Inst Occupat Hlth, Birmingham B15 2TT, W Midlands, England	Thickett, KM (reprint author), Birmingham Heartlands Hosp, Dept Resp Med, Occupat Lung Dis Unit, Bordesley Green E, Birmingham B5 5SS, W Midlands, England.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			BURGE PS, 1982, EUR J RESPIR DIS, V63, P91; Gannon PFG, 1996, THORAX, V51, P484, DOI 10.1136/thx.51.5.484; Hailin G, 1990, ANAL CHIM ACTA, V237, P149; HERY M, 1995, ANN OCCUP HYG, V39, P427, DOI 10.1016/0003-4878(95)00013-5; HOLZWARTH G, 1984, WATER RES, V18, P1421, DOI 10.1016/0043-1354(84)90012-5; LAHL U, 1981, WATER RES, V15, P803, DOI 10.1016/0043-1354(81)90133-0; Massin N, 1998, OCCUP ENVIRON MED, V55, P258; MCCOACH JS, 1999, INDOOR AIR, V4, P459; POTTS JE, 1994, THESIS U BRIT COLOMB; Quanjer P. H., 1993, EUR RESP J S16, V6, p5S; TCHOBANOGLOUS G, 1991, WASTEWATER ENG TREAT, P332; YAN K, 1983, THORAX, V38, P760, DOI 10.1136/thx.38.10.760	12	121	121	3	13	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	MAY	2002	19	5					827	832		10.1183/09031936.02.00232802		6	Respiratory System	Respiratory System	553AP	WOS:000175653600008	12030720	
J	Jeebhay, MF; Robins, TG; Lehrer, SB; Lopata, AL				Jeebhay, MF; Robins, TG; Lehrer, SB; Lopata, AL			Occupational seafood allergy: a review	OCCUPATIONAL AND ENVIRONMENTAL MEDICINE			English	Review						occupational seafood allergy; occupational asthma; protein contact dermatitis	PROTEIN CONTACT-DERMATITIS; FISH PROCESSING-INDUSTRY; HUMAN EPIDERMAL KERATIN; HYPERSENSITIVITY REACTIONS; RESPIRATORY SYMPTOMS; URTICARIA SYNDROME; SKIN TEMPERATURE; MAJOR ALLERGEN; IGE; ASTHMA	Background-Recent years have seen increased levels of production and consumption of seafood, leading to more frequent reporting of allergic reactions in occupational and domestic settings. This review focuses on occupational allergy in the fishing and seafood processing industry. Review-Workers involved in either manual or automated processing of crabs' prawns, mussels, fish, and fishmeal production are commonly exposed to various constituents of seafood. Aerosolisation of seafood and cooking fluid during processing are potential occupational situations that could result in sensitisation through inhalation. There is great variability of aerosol exposure within and among various jobs with reported allergen concentrations ranging from 0.001 to 5.061(mug/m(3)). Occupational dermal exposure occurs as a result of unprotected handling of seafood and its byproducts. Occupational allergies have been reported in workers exposed to arthropods (crustaceans), molluscs, pisces (bony fish) and other agents derived from seafood. The prevalence of occupational asthma ranges from 7% to 36%, and for occupational protein contact dermatitis, from 3% to 11%. These health outcomes are mainly due to high molecular weight proteins in seafood causing an IgE mediated response. Cross reactivity between various species within a major seafood grouping also occurs. Limited evidence from dose-response relations indicate that development of symptoms is related to duration or intensity of exposure. The evidence for atopy as a risk factor for occupational sensitisation and asthma is supportive, whereas evidence for cigarette smoking is limited. Disruption of the intact skin barrier seems to be an important added risk factor for occupational protein contact dermatitis. Conclusion-The range of allergic disease associated with occupational exposure to crab is well characterised, whereas for other seafood agents the evidence is somewhat limited. There is a need for further epidemiological studies to better characterise this risk. More detailed characterisation of specific protein antigens in aerosols and associated establishment of dose-response relations for acute and chronic exposure to seafood; the respective roles of skin contact and inhalational exposure in allergic sensitisation and cross reactivity; and the contribution of host associated factors in the development of occupational seafood allergies are important areas for future research.	Univ Cape Town, Dept Publ Hlth, Occupat & Environm Hlth Res Unit, ZA-7925 Observatory, South Africa; Univ Michigan, Dept Environm Hlth Sci, Ann Arbor, MI 48109 USA; Tulane Univ, Med Ctr, Dept Med, New Orleans, LA USA; Groote Schuur Hosp, Dept Immunol, Allergol Unit, ZA-7925 Cape Town, South Africa	Jeebhay, MF (reprint author), Univ Cape Town, Dept Publ Hlth, Occupat & Environm Hlth Res Unit, Room 1111C,1st Floor,Anat Bldg,Anzio Rd, ZA-7925 Observatory, South Africa.		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Environ. Med.	SEP	2001	58	9					553	562		10.1136/oem.58.9.553		10	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	464UQ	WOS:000170550500001	11511741	
J	Nordenhall, C; Pourazar, J; Ledin, MC; Levin, JO; Sandstrom, T; Adelroth, E				Nordenhall, C; Pourazar, J; Ledin, MC; Levin, JO; Sandstrom, T; Adelroth, E			Diesel exhaust enhances airway responsiveness in asthmatic subjects	EUROPEAN RESPIRATORY JOURNAL			English	Article						asthma; airway responsiveness; diesel exhaust; induced sputum	EMERGENCY ROOM VISITS; INDUCED SPUTUM; NITROGEN-DIOXIDE; DAILY MORTALITY; POLLUTION; EXPOSURE; PARTICLES; INFLAMMATION; MICE; CHILDREN	Particulate matter (PM) pollution has been associated with negative health effects, including exacerbations of asthma following exposure to PM peaks. The aim of the present study was to investigate the effects of short-term exposure to diesel exhaust (DE) in asthmatics, by specifically addressing the effects on airway hyperresponsiveness, lung function and airway inflammation. Fourteen nonsmoking, atopic asthmatics with stable disease, on continuous treatment with inhaled corticosteroids, were included. All were hyperresponsive to methacholine. Each subject was exposed to DE (particles with a 50% cut-off aerodynamic diameter of 10 mum (PM10) 300 mug(.)m(-3)) and air during Ih on two separate occasions. Lung function was measured before and immediately after the exposures. Sputum induction was performed 6 h, and methacholine inhalation test 24 h, after each exposure. Exposure to DE was associated with a significant increase in the degree of hyperresponsiveness, as compared to after air, of 0.97 doubling concentrations at 24 h after exposure (p < 0.001). DE also induced a significant increase in airway resistance (p = 0.004) and in sputum levels of interleukin (IL)-6 (p = 0.048). No changes were detected in sputum levels of methyl-histamine, eosinophil cationic protein, myeloperoxidase and IL-8. This study indicated that short-term exposure to diesel exhaust, equal to high ambient levels of particulate matter, is associated with adverse effects in asthmatic airways, even in the presence of inhaled corticosteroid therapy. The increase in airway responsiveness may provide an important link to epidemiological findings exacerbations of asthma following exposure to particulate matter.	Umea Univ Hosp, Dept Resp Med & Allergy, S-90185 Umea, Sweden; Inst Working Life, Dept Occupat Chem, Umea, Sweden	Adelroth, E (reprint author), Umea Univ Hosp, Dept Resp Med & Allergy, S-90185 Umea, Sweden.						*AIRB PART EXP GRO, 1999, SOURC APP AIRB PART, P157; BARRY CC, 1994, ENVIRONMENT, V36, P5; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; JORRES R, 1991, LUNG, V169, P77, DOI 10.1007/BF02714145; JUNIPER EF, 1994, HISTAMINE METACHOLIN; Knox RB, 1997, CLIN EXP ALLERGY, V27, P246; Lipsett M, 1997, ENVIRON HEALTH PERSP, V105, P216, DOI 10.1289/ehp.97105216; Miyabara Y, 1998, INT ARCH ALLERGY IMM, V116, P124, DOI 10.1159/000023935; Nordenhall C, 2000, EUR RESPIR J, V15, P1046, DOI 10.1034/j.1399-3003.2000.01512.x; OBYRNE PM, 1987, AM REV RESPIR DIS, V136, P740; Peters A, 1997, EUR RESPIR J, V10, P872; PIN I, 1992, THORAX, V47, P25, DOI 10.1136/thx.47.1.25; Pizzichini E, 1996, AM J RESP CRIT CARE, V154, P308; POPE CA, 1992, ARCH ENVIRON HEALTH, V47, P211; POPE CA, 1992, AM REV RESPIR DIS, V145, P1123; ROGER LJ, 1990, TOXICOL IND HEALTH, V6, P155; Romieu I, 1996, AM J RESP CRIT CARE, V154, P300; RUDELL B, 1994, INT ARCH OCC ENV HEA, V66, P77, DOI 10.1007/BF00383361; Rudell B, 1999, OCCUP ENVIRON MED, V56, P527; Rudell B, 1990, J AEROSOL SCI     S1, V21, P411; RYAN G, 1981, J ALLERGY CLIN IMMUN, V67, P156, DOI 10.1016/0091-6749(81)90012-9; Sagai M, 1996, FREE RADICAL BIO MED, V21, P199, DOI 10.1016/0891-5849(96)00032-9; Salvi S, 1999, AM J RESP CRIT CARE, V159, P702; Salvi SS, 2000, AM J RESP CRIT CARE, V161, P550; Schwartz J, 1996, EPIDEMIOLOGY, V7, P20, DOI 10.1097/00001648-199601000-00005; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; SCHWARTZ J, 1994, ENVIRON RES, V64, P36, DOI 10.1006/enrs.1994.1005; Steerenberg PA, 1998, EXP LUNG RES, V24, P85; Strand V, 1996, EUR RESPIR J, V9, P733, DOI 10.1183/09031936.96.09040733; Takano H, 1998, IMMUNOPHARM IMMUNOT, V20, P329, DOI 10.3109/08923979809038548; Takano H, 1998, TOXICOL APPL PHARM, V150, P328, DOI 10.1006/taap.1998.8437; Takano H, 1997, AM J RESP CRIT CARE, V156, P36; Vedal S, 1998, AM J RESP CRIT CARE, V157, P1034	33	121	122	1	12	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146, WEST ST, STE 2.4 HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	MAY	2001	17	5					909	915		10.1183/09031936.01.17509090		7	Respiratory System	Respiratory System	458RU	WOS:000170209000013	11488325	
J	Shukla, A; Timblin, C; BeruBe, K; Gordon, T; McKinney, W; Driscoll, K; Vacek, P; Mossman, BT				Shukla, A; Timblin, C; BeruBe, K; Gordon, T; McKinney, W; Driscoll, K; Vacek, P; Mossman, BT			Inhaled particulate matter causes expression of nuclear factor (NF)-kappa B-related genes and oxidant-dependent NF-kappa B activation in vitro	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article							NECROSIS-FACTOR-ALPHA; TRACHEAL EPITHELIAL-CELLS; DNA-BINDING ACTIVITY; AIR-POLLUTION; ALVEOLAR MACROPHAGES; RAT LUNG; C-JUN; ASBESTOS; ASTHMA; GENERATION	High levels of ambient air pollution are associated with exacerbation of asthma and respiratory morbidity, yet little is known concerning the mechanisms of inflammation and toxicity by components of inhaled particulate matter (PM), Brief inhalation of PM2.5 (particles of an aerodynamic diameter of <2.5 microns) (300 mu g/m(3) air for 6 h followed by a period of 24 h in clean air) by either C3H/HeJ or C57/BL6 mice caused significant (P less than or equal to 0.05) increases in steady-state messenger RNA (mRNA) levels of a number of nuclear factor (NF)-kappa B-associated and/or -regulated genes, including tumor necrosis factor-alpha and -beta, interleukin-6, interferon-gamma, and transforming growth factor-beta. Lung mRNA levels of lymphotoxin-beta and macrophage migration inhibitory factor were unchanged. In murine C10 alveolar cells and an NF-kappa B-luciferase reporter cell line, exposure to PM2.5 at noncytotoxic concentrations resulted in increases in transcriptional activation of NF-kappa B-dependent gene expression which were inhibited in the presence of catalase. Early and persistent increases in intracellular oxidants, as measured by flow cytometry and cell imaging using the oxidant probe 2'-7'-dichlorofluoroscin diacetate, were observed in epithelial cells exposed to PM2.5, and ultrafine carbon black particles. Studies here are the first to show NF-kappa B-related inflammatory and cytokine gene expression after inhalation of PM2.5 and oxidant-dependent induction of NF-kappa B activity by PM2.5 in pulmonary epithelial cells.	Univ Vermont, Coll Med, Dept Pathol, Burlington, VT 05405 USA; Univ Vermont, Dept Biostat, Burlington, VT 05405 USA; Univ Wales Coll Cardiff, Sch Biosci, Cardiff CF1 1XL, S Glam, Wales; NYU, Inst Environm Med, Sch Med, Tuxedo Park, NY 10987 USA; Procter & Gamble Co, Cardiovasc Res, Mason, OH USA	Mossman, BT (reprint author), Univ Vermont, Coll Med, Dept Pathol, Med Alumni BLdg, Burlington, VT 05405 USA.				NHLBI NIH HHS [HL39469]; NIEHS NIH HHS [ES06499, R01ES/HL09213]		Abbey DE, 1999, AM J RESP CRIT CARE, V159, P373; Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; Becker S, 1996, TOXICOL APPL PHARM, V141, P637, DOI 10.1006/taap.1996.0330; CATALANO PB, 1999, AM J RESP CRIT CARE, V159, pA29; CEMBRZYNSKANOWAK M, 1993, AM REV RESPIR DIS, V147, P291; Cheshire JL, 1997, MOL CELL BIOL, V17, P6746; Choi AMK, 1996, AM J PHYSIOL-LUNG C, V271, pL383; Cohen AJ, 1995, ENVIRON HEALTH PERSP, V103, P219, DOI 10.2307/3432314; Donaldson K, 1997, ENVIRON HEALTH PERSP, V105, P1285, DOI 10.2307/3433548; Donnelly SC, 1997, NAT MED, V3, P320, DOI 10.1038/nm0397-320; Gamble JF, 1998, ENVIRON HEALTH PERSP, V106, P535, DOI 10.1289/ehp.98106535; Gordon T, 1999, INHAL TOXICOL, V11, P71, DOI 10.1080/089583799197276; Grabowski GM, 1999, TOXICOL APPL PHARM, V156, P170, DOI 10.1006/taap.1999.8642; HALLSWORTH MP, 1994, EUR RESPIR J, V7, P1096; Hart LA, 1998, AM J RESP CRIT CARE, V158, P1585; JANSSEN YMW, 1995, P NATL ACAD SCI USA, V92, P8458, DOI 10.1073/pnas.92.18.8458; Janssen YMW, 1997, AM J PATHOL, V151, P389; Jimenez LA, 1997, AM J PHYSIOL-LUNG C, V273, pL1029; Kadiiska MB, 1997, CHEM RES TOXICOL, V10, P1104, DOI 10.1021/tx970049r; Keatings VM, 1996, AM J RESP CRIT CARE, V153, P530; Kennedy T, 1998, AM J RESP CELL MOL, V19, P366; KLEEBERGER SR, 1990, AM J PHYSIOL, V258, pL313; Ledbetter A, 1999, AM J RESP CRIT CARE, V159, pA29; Malkinson AM, 1997, TOXICOLOGY, V123, P53, DOI 10.1016/S0300-483X(97)00108-X; Mossman BT, 1998, AM J RESP CRIT CARE, V157, P1666; PHAN SH, 1992, J IMMUNOL, V149, P103; Quay JL, 1998, AM J RESP CELL MOL, V19, P98; QUINLAN TR, 1994, AM J RESP CRIT CARE, V150, P200; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; SEATON A, 1995, LANCET, V345, P176, DOI 10.1016/S0140-6736(95)90173-6; Smith KR, 1997, CHEM RES TOXICOL, V10, P828, DOI 10.1021/tx960164m; Timblin C, 1998, CANCER RES, V58, P4543; TIMBLIN CR, 1995, CANCER RES, V55, P2723	33	121	135	4	24	AMER LUNG ASSOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019 USA	1044-1549			AM J RESP CELL MOL	Am. J. Respir. Cell Mol. Biol.	AUG	2000	23	2					182	187				6	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	344FW	WOS:000088749400011	10919984	
J	Chan-Yeung, M; Manfreda, J; Dimich-Ward, H; Ferguson, A; Watson, W; Becker, A				Chan-Yeung, M; Manfreda, J; Dimich-Ward, H; Ferguson, A; Watson, W; Becker, A			A randomized controlled study on the effectiveness of a multifaceted intervention program in the primary prevention of asthma in high-risk infants	ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE			English	Article							ALLERGEN AVOIDANCE; FOLLOW-UP; AGE; MITE; DIET; LIFE	Background: The prevalence of asthma has increased in developed countries in the past 2 decades. The effectiveness of intervention measures on the primary prevention of asthma has not been well studied. Objective: To assess the effectiveness of a multifaceted intervention program in the primary prevention of asthma in high-risk infants (in this study, infants are defined as persons from birth to the age of 1 year). Design: Prospective, prenatally randomized, controlled study with follow-up through the age of 1 year. Setting: University hospital-based settings at 2 Canadian centers: Vancouver, British Columbia, and Winnipeg, Manitoba. Participants: A total of 545 high-risk infants (at least 1 first-degree relative with asthma or 2 first-degree relatives with other IgE-mediated allergic diseases) identified before birth. Interventions: Avoidance of house dust mite and pet allergens and environmental tobacco smoke, encouragement of breastfeeding, and supplementation with a partially hydrolyzed formula. Main Outcome Measures: Probable or possible asthma, rhinitis without apparent colds, and a prick skin test result positive for common inhalant allergens. Results: Thirty-eight (15.1%) of the 251 infants available for assessment in the intervention group and 49 (20.2%) of the 242 infants available for assessment in the control group fulfilled the criteria for possible or probable asthma (adjusted relative risk, 0.66; 90% confidence interval, 0.44-0.98). Also, 16.7% of the infants in the intervention group and 27.3% of the infants in the control group developed rhinitis without colds (adjusted relative risk, 0.51; 90% confidence interval, 0.35-0.74). The incidence of positive skin test results to 1 or more inhalant allergens was similar in both groups (4.4% in the intervention group and 4.6% in the control group). Conclusions: Our multifaceted intervention program resulted in a modest but significant (P = .04) reduction in the risk of possible or probable asthma and rhinitis without apparent colds at the age of 12 months in high-risk infants. In the absence of a validated definition of asthma at the age of 12 months, follow-up studies are needed to determine the effectiveness of the intervention program in the primary prevention of asthma in high-risk infants.	Univ British Columbia, Dept Med, Div Resp, Occupat & Environm Lung Dis Unit, Vancouver, BC, Canada; Univ British Columbia, Dept Paediat, Div Allergy, Vancouver, BC, Canada; Univ Manitoba, Dept Med, Winnipeg, MB, Canada; Univ Manitoba, Dept Community Hlth Sci, Winnipeg, MB R3T 2N2, Canada; Univ Manitoba, Dept Paediat & Child Hlth, Allergy & Clin Immunol Sect, Winnipeg, MB, Canada	Chan-Yeung, M (reprint author), Univ Hong Kong, Queen Mary Hosp, Dept Med, Room 418,Professorial Block, Hong Kong, Hong Kong, Peoples R China.						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E., 1997, Journal of Allergy and Clinical Immunology, V100, pS1; SAARINEN UM, 1995, LANCET, V346, P1065, DOI 10.1016/S0140-6736(95)91742-X; Sears MR, 1997, LANCET, V350, P1015, DOI 10.1016/S0140-6736(97)01468-2; Szepfalusi Z, 1997, CLIN EXP ALLERGY, V27, P28, DOI 10.1046/j.1365-2222.1997.d01-417.x; UPHAM JW, 1995, CLIN EXP ALLERGY, V25, P634, DOI 10.1111/j.1365-2222.1995.tb01111.x; WEISS KB, 1992, NEW ENGL J MED, V326, P862, DOI 10.1056/NEJM199203263261304; ZEIGER RS, 1995, J ALLERGY CLIN IMMUN, V95, P1179, DOI 10.1016/S0091-6749(95)70074-9	24	121	124	0	2	AMER MEDICAL ASSOC	CHICAGO	515 N STATE ST, CHICAGO, IL 60610 USA	1072-4710			ARCH PEDIAT ADOL MED	Arch. Pediatr. Adolesc. Med.	JUL	2000	154	7					657	663				7	Pediatrics	Pediatrics	332LE	WOS:000088075100003	10891016	
J	Martin, SF; Esser, PR; Weber, FC; Jakob, T; Freudenberg, MA; Schmidt, M; Goebeler, M				Martin, S. F.; Esser, P. R.; Weber, F. C.; Jakob, T.; Freudenberg, M. A.; Schmidt, M.; Goebeler, M.			Mechanisms of chemical-induced innate immunity in allergic contact dermatitis	ALLERGY			English	Review						contact dermatitis; inflammation; innate immunity; NOD-like receptor; Toll-like receptor	NF-KAPPA-B; TOLL-LIKE RECEPTORS; CELL-LINE THP-1; LYMPH-NODE ASSAY; CD8 T-CELLS; IN-VITRO; REACTIVE OXYGEN; DENDRITIC CELLS; SKIN SENSITIZERS; GENE-EXPRESSION	Allergic contact dermatitis (ACD) is one of the most prevalent occupational skin diseases and causes severe and long-lasting health problems in the case of chronification. It is initiated by an innate inflammatory immune response to skin contact with low molecular weight chemicals that results in the priming of chemical-specific, skin-homing CD8(+) Tc1/Tc17 and CD4(+) Th1/Th17 cells. Following this sensitization step, T lymphocytes infiltrate the inflamed skin upon challenge with the same chemical. The T cells then exert cytotoxic function and secrete inflammatory mediators to produce an eczematous skin reaction. The recent characterization of the mechanisms underlying the innate inflammatory response has revealed that contact allergens activate innate effector mechanisms and signalling pathways that are also involved in anti-infectious immunity. This emerging analogy implies infection as a potential trigger or amplifier of the sensitization to contact allergens. Moreover, new mechanistic insights into the induction of ACD identify potential targets for preventive and therapeutic intervention. We summarize here the latest findings in this area of research.	[Martin, S. F.; Esser, P. R.; Weber, F. C.; Jakob, T.] Univ Med Ctr Freiburg, Allergy Res Grp, Dept Dermatol, D-79104 Freiburg, Germany; [Weber, F. C.] Univ Freiburg, Fac Biol, D-7800 Freiburg, Germany; [Freudenberg, M. A.] Max Planck Inst Immunbiol & Epigenet, Freiburg, Germany; [Schmidt, M.; Goebeler, M.] Univ Giessen, Dept Dermatol, Giessen, Germany	Martin, SF (reprint author), Univ Med Ctr Freiburg, Allergy Res Grp, Dept Dermatol, Hauptstr 7, D-79104 Freiburg, Germany.	stefan.martin@uniklinik-freiburg.de	Esser, Philipp/F-6849-2011; Jakob, Thilo/J-1621-2012; Goebeler, Matthias/F-7118-2013; Schmidt, Marc/E-8821-2010	Schmidt, Marc/0000-0002-8643-1615			Ade N, 2009, TOXICOL SCI, V107, P451, DOI 10.1093/toxsci/kfn243; Aeby P, 2010, TOXICOL IN VITRO, V24, P1465, DOI 10.1016/j.tiv.2010.07.005; Antonopoulos C, 2001, J Immunol, V166, P3672; Antonopoulos C, 2008, J LEUKOCYTE BIOL, V83, P361, DOI 10.1189/jlb.0604352; Arthur JC, 2010, J IMMUNOL, V185, P4515, DOI 10.4049/jimmunol.1002227; Artik S, 1999, J IMMUNOL, V163, P1143; Ashikaga T, 2010, ATLA-ALTERN LAB ANIM, V38, P275; Babelova A, 2009, J BIOL CHEM, V284, P24035, DOI 10.1074/jbc.M109.014266; Basketter DA, 2007, CONTACT DERMATITIS, V57, P70, DOI 10.1111/j.1600-0536.2007.01141.x; 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J	Po, JYT; FitzGerald, JM; Carlsten, C				Po, June Y. T.; FitzGerald, J. Mark; Carlsten, Chris			Respiratory disease associated with solid biomass fuel exposure in rural women and children: systematic review and meta-analysis	THORAX			English	Article							INDOOR AIR-POLLUTION; CHRONIC-BRONCHITIS; RISK-FACTORS; DEVELOPING-COUNTRIES; PULMONARY-DISEASE; INDIAN CHILDREN; LUNG-FUNCTION; HEALTH; SMOKE; INFECTIONS	Background Numerous studies with varying associations between domestic use of solid biomass fuels (wood, dung, crop residue, charcoal) and respiratory diseases have been reported. Objective To present the current data systematically associating use of biomass fuels with respiratory outcomes in rural women and children. Methods Systematic searches were conducted in 13 electronic databases. Data were abstracted from original articles that satisfied selection criteria for meta-analyses. Publication bias and heterogeneity of samples were tested. Studies with common diagnoses were analysed using random-effect models. Results A total of 2717 studies were identified. Fifty-one studies were selected for data extraction and 25 studies were suitable for meta-analysis. The overall pooled ORs indicate significant associations with acute respiratory infection in children (OR 3.53, 95% CI 1.94 to 6.43), chronic bronchitis in women (OR 2.52, 95% CI 1.88 to 3.38) and chronic obstructive pulmonary disease in women (OR 2.40, 95% CI 1.47 to 3.93). In contrast, no significant association with asthma in children or women was noted. Conclusion Biomass fuel exposure is associated with diverse respiratory diseases in rural populations. Concerted efforts in improving stove design and lowering exposure to smoke emission may reduce respiratory disease associated with biomass fuel exposure.	[Po, June Y. T.; FitzGerald, J. Mark; Carlsten, Chris] Univ British Columbia, Dept Med, Vancouver, BC V5Z 1M9, Canada	Carlsten, C (reprint author), Univ British Columbia, Vancouver Gen Hosp, Dept Med, 7th Floor,2775 Laurel St, Vancouver, BC V5Z 1M9, Canada.	chris.carlsten@vch.ca			Department of Medicine, University of British Columbia	Funding Department of Medicine, University of British Columbia.	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J	Thyssen, JP; Johansen, JD; Linneberg, A; Menne, T				Thyssen, Jacob P.; Johansen, Jeanne D.; Linneberg, Allan; Menne, Torkil			The epidemiology of hand eczema in the general population - prevalence and main findings	CONTACT DERMATITIS			English	Review						general population; hand eczema; hand dermatitis; nickel allergy; public health; regulation	IRRITANT CONTACT-DERMATITIS; ODENSE ADOLESCENCE COHORT; SECONDARY-SCHOOL PUPILS; 15-YEAR FOLLOW-UP; NICKEL ALLERGY; ATOPIC-DERMATITIS; INDUSTRIAL-CITY; SKIN EXPOSURE; FILAGGRIN MUTATIONS; SWEDISH POPULATION	Numerous studies have investigated the prevalence and risk factors of hand eczema in the general population. These studies are of high value as they tend to be less biased than studies using clinical populations and as they are important for healthcare decision makers when they allocate resources. This study aimed to review the epidemiology of hand eczema in the general population. Literature was examined using Pubmed-Medline, Biosis, Science Citation Index, and dermatology text books. On the basis of studies performed between 1964 and 2007, the point prevalence of hand eczema was around 4%, the 1-year prevalence nearly 10%, whereas the lifetime prevalence reached 15%. Based on seven studies, the median incidence rate of hand eczema was 5.5 cases/1000 person-years (women = 9.6 and men = 4.0). A high incidence rate was associated with female sex, contact allergy, atopic dermatitis, and wet work. Atopic dermatitis was the single most important risk factor for hand eczema. Hand eczema resulted in medical consultations in 70%, sick leave (> 7 days) in about 20%, and job change in about 10%. Mean sick time was longer among those with allergic hand eczema than those with atopic and irritant hand eczema. Moderate to severe extension of hand eczema was the strongest risk factor for persistence of hand eczema. Other risk factors included early onset of hand eczema and childhood eczema. The aetiology of hand eczema is multifactorial and includes environmental as well as genetic factors. Future studies should focus on unresolved areas of hand eczema, for example, genetic predisposition.	[Thyssen, Jacob P.; Johansen, Jeanne D.] Univ Copenhagen, Natl Allergy Res Ctr, Dept Dermatoloallergol, Gentofte Hosp, DK-2900 Hellerup, Denmark; [Linneberg, Allan] Univ Copenhagen, Glostrup Hosp, Res Ctr Prevent & Hlth, DK-2900 Hellerup, Denmark; [Menne, Torkil] Gentofte Univ Hosp, Dept Dermatoallergol, Gentofte, Denmark	Thyssen, JP (reprint author), Univ Copenhagen, Natl Allergy Res Ctr, Dept Dermatoloallergol, Gentofte Hosp, Niels Andersens Vej 65, DK-2900 Hellerup, Denmark.	jacpth01@geh.regionh.dk			Horslev Foundation	The study was funded by the Horslev Foundation.	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Thyssen JP, 2009, J AM ACAD DERMATOL, V61, P799, DOI 10.1016/j.jaad.2009.03.030; Thyssen JP, 2008, DERMATITIS, V19, P303, DOI 10.2310/6620.2008.08022; Thyssen JP, 2009, NEW ENGL J MED, V360, P2259, DOI 10.1056/NEJMc0809293; THYSSEN JP, BRIT J DERMATOL; Williams H, 1999, J ALLERGY CLIN IMMUN, V103, P125, DOI 10.1016/S0091-6749(99)70536-1; Yngveson M, 1998, ACTA DERM-VENEREOL, V78, P371; Yngveson M, 1997, ACTA DERM-VENEREOL, V77, P455; Yngveson M, 2000, BRIT J DERMATOL, V142, P485, DOI 10.1046/j.1365-2133.2000.03361.x	92	120	121	3	20	WILEY-BLACKWELL PUBLISHING, INC	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0105-1873			CONTACT DERMATITIS	Contact Dermatitis		2010	62	2					75	87				13	Allergy; Dermatology	Allergy; Dermatology	550XQ	WOS:000274167800002	20136890	
J	Condorelli, P; Shin, HW; Aledia, AS; Silkoff, PE; George, SC				Condorelli, Peter; Shin, Hye-Won; Aledia, Anna S.; Silkoff, Philip E.; George, Steven C.			A simple technique to characterize proximal and peripheral nitric oxide exchange using constant flow exhalations and an axial diffusion model	JOURNAL OF APPLIED PHYSIOLOGY			English	Article						model; airway; alveolar	RESPIRATORY-TRACT; EXHALED AIR; BREATH-HOLD; ASTHMA; ALVEOLAR; IMPACT; DYNAMICS; HUMANS; LUNGS; NO	The most common technique employed to describe pulmonary gas exchange of nitric oxide (NO) combines multiple constant flow exhalations with a two-compartment model (2CM) that neglects 1) the trumpet shape (increasing surface area per unit volume) of the airway tree and 2) gas phase axial diffusion of NO. However, recent evidence suggests that these features of the lungs are important determinants of NO exchange. The goal of this study is to present an algorithm that characterizes NO exchange using multiple constant flow exhalations and a model that considers the trumpet shape of the airway tree and axial diffusion (model TMAD). Solution of the diffusion equation for the TMAD for exhalation flows > 100 ml/s can be reduced to the same linear relationship between the NO elimination rate and the flow; however, the interpretation of the slope and the intercept depend on the model. We tested the TMAD in healthy subjects (n = 8) using commonly used and easily performed exhalation flows (100, 150, 200, and 250 ml/s). Compared with the 2CM, estimates (mean +/- SD) from the TMAD for the maximum airway flux are statistically higher (J'aw(NO) = 770 +/- 470 compared with 440 +/- 270 pl/s), whereas estimates for the steady-state alveolar concentration are statistically lower (CA(NO) = 0.66 +/- 0.98 compared with 1.2 +/- 0.80 parts/billion). Furthermore, CANO from the TMAD is not different from zero. We conclude that proximal (airways) NO production is larger than previously predicted with the 2CM and that peripheral (respiratory bronchioles and alveoli) NO is near zero in healthy subjects.	Univ Calif Irvine, Dept Biomed Engn, Irvine, CA 92697 USA; Univ Calif Irvine, Dept Chem Engn & Mat Sci, Irvine, CA 92697 USA; Univ Calif Irvine, Dept Med, Div Pulm & Crit Care, Irvine, CA 92697 USA; Drexel Univ, Philadelphia, PA 19104 USA	George, SC (reprint author), Univ Calif Irvine, Dept Biomed Engn, 3120 Nat Sci 2, Irvine, CA 92697 USA.	scgeorge@uci.edu	George, Steven/K-9359-2015	George, Steven/0000-0003-2263-1914	NCRR NIH HHS [RR-00827]; NHLBI NIH HHS [HL-070645]		ALVING K, 1993, EUR RESPIR J, V6, P1368; American Thoracic Society, 2005, AM J RESP CRIT CARE, V171, P912, DOI DOI 10.1164/RCCM.200406-710ST.PUBMED:15817806; Barnes PJ, 1996, THORAX, V51, P233, DOI 10.1136/thx.51.3.233; Berkman N, 2005, THORAX, V60, P383, DOI 10.1136/thx.2004.031104; BOUHUYS A, 1987, AM PHYSL SOC, P699; Condorelli P, 2004, J APPL PHYSIOL, V96, P1832, DOI 10.1152/japplphysiol.01157.2003; Dupont LJ, 2003, CHEST, V123, P751, DOI 10.1378/chest.123.3.751; Gelb AF, 2004, AM J RESP CRIT CARE, V170, P737, DOI 10.1164/rccm.200403-408OC; George SC, 2004, J APPL PHYSIOL, V96, P831, DOI 10.1152/japplphysiol.00950.2003; Girgis RE, 2002, AM J RESP CRIT CARE, V165, P1587, DOI 10.1164/rccm.2104003; GUSTAFSSON LE, 1991, BIOCHEM BIOPH RES CO, V181, P852, DOI 10.1016/0006-291X(91)91268-H; HANNA LM, 1986, J BIOMECH ENG-T ASME, V108, P12; Hogman M, 2000, RESP MED, V94, P985, DOI 10.1053/rmed.2000.0872; Hogman M, 1997, ACTA PHYSIOL SCAND, V159, P345, DOI 10.1046/j.1365-201X.1997.00101.x; Hogman M, 2002, RESP MED, V96, P24, DOI 10.1053/rmed.2001.1204; Lehtimaki L, 2000, ANN MED, V32, P417, DOI 10.3109/07853890008995949; Lehtimaki L, 2001, AM J RESP CRIT CARE, V163, P1557; Pietropaoli AP, 1999, J APPL PHYSIOL, V87, P1532; Pijnenburg MW, 2005, THORAX, V60, P215, DOI 10.1136/thx.2004.023374; Rottier BL, 2005, J APPL PHYSIOL, V99, P378, DOI 10.1152/japplphysiol.00163.2005; Shin HW, 2006, J APPL PHYSIOL, V100, P623, DOI 10.1152/japplphysiol.00008.2005; Shin HW, 2005, J APPL PHYSIOL, V98, P1869, DOI 10.1152/japplphysiol.01002.2004; Shin HW, 2004, J APPL PHYSIOL, V97, P874, DOI 10.1152/japplphysiol.01297.2003; Shin HW, 2004, J APPL PHYSIOL, V96, P65, DOI 10.1152/japplphysiol.00575.2003; Shin HW, 2003, MED SCI SPORT EXER, V35, P995, DOI 10.1249/01.MSS.0000072247.46963.CD; Shin HW, 2002, J APPL PHYSIOL, V93, P2070, DOI 10.1152/japplphysiol.00129.2002; Shin HW, 2002, AM J RESP CRIT CARE, V165, P349; Shin HW, 2001, J APPL PHYSIOL, V91, P2173; Silkoff PE, 2000, AM J RESP CRIT CARE, V161, P1218; Silkoff PE, 1997, AM J RESP CRIT CARE, V155, P260; Smith AD, 2005, NEW ENGL J MED, V352, P2163, DOI 10.1056/NEJMoa043596; Tsoukias NM, 1998, J APPL PHYSIOL, V85, P653; Tsoukias NM, 1998, J APPL PHYSIOL, V85, P642; Tsoukias NM, 2001, J APPL PHYSIOL, V91, P477; Van Muylem A, 2003, J APPL PHYSIOL, V94, P119, DOI 10.1152/japplphysiol.00044.2002; Weibel E, 1963, MORPHOMETRY HUMAN LU	36	120	121	0	2	AMER PHYSIOLOGICAL SOC	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	8750-7587			J APPL PHYSIOL	J. Appl. Physiol.	JAN	2007	102	1					417	425		10.1152/japplphysiol.00533.2006		9	Physiology; Sport Sciences	Physiology; Sport Sciences	127QB	WOS:000243600300057	16888048	
J	Balali-Mood, M; Hefazi, M				Balali-Mood, Mahdi; Hefazi, Mehrdad			Comparison of early and late toxic effects of sulfur mustard in Iranian veterans	BASIC & CLINICAL PHARMACOLOGY & TOXICOLOGY			English	Review							CHEMICAL WARFARE AGENTS; RESPIRATORY-TRACT; GAS INHALATION; COMPLICATIONS; EXPOSURE; INJURY; WEAPONS; WORKERS; CANCER	Sulfur mustard is an alkylating agent that reacts with ocular, respiratory, cutaneous, and bone marrow tissues, resulting in early and late toxic effects. We compare these effects based on the experience in Iranian veterans exposed to the agent during the Iran-Iraq conflict (1983-88). The first clinical manifestations of sulfur mustard poisoning occurred in the eyes with a sensation of grittiness, lacrimation, photophobia, blepharospasm, and corneal ulceration. Respiratory effects appeared as rhinorhea, laryngitis, tracheobronchitis, and dyspnoea. Skin lesions varied from erythema to bullous necrotization. Initial leukocytosis and lymphopenia returned to normal within four weeks in recovered patients, but marked cytopenia with bone marrow failure occurred in fatal cases. Late toxic effects of sulfur mustard were most commonly found in lungs, skin and eyes. Main respiratory complications were chronic obstructive pulmonary disease, bronchiectasis, asthma, large airway narrowing, and pulmonary fibrosis. Late skin lesions were hyperpigmentation, dry skin, atrophy, and hypopigmentation. Fifteen of the severely intoxicated patients were diagnosed with delayed keratitis, having corneal vascularization, thinning, and epithelial defect. Respiratory complications exacerbated over time, while cutaneous and ocular lesions decreased or remained constant. Both the severity and frequency of bronchiectatic lesions increased during long-term follow-up. The only deteriorating cutaneous complication was dry skin. The maximum incidence of delayed kaeratitis was observed 15 to 20 years after initial exposure. Being suggested as the main cause ofassociated with malignancies and recurrent infections, natural killer cells were significantly lower 16 to 20 years after intoxication.	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Pharmacol. Toxicol.	OCT	2006	99	4					273	282		10.1111/j.1742-7843.2006.pto_429.x		10	Pharmacology & Pharmacy; Toxicology	Pharmacology & Pharmacy; Toxicology	094LB	WOS:000241239800001	17040211	
J	Shannon, MW; Best, D; Binns, HJ; Johnson, CL; Kim, JJ; Mazur, LJ; Reynolds, DW; Roberts, JR; Weil, WB; Balk, SJ; Miller, M; Shea, KM; Lipsett, M; Johnson, RH; Linet, M; Rogan, W; Spire, P				Shannon, MW; Best, D; Binns, HJ; Johnson, CL; Kim, JJ; Mazur, LJ; Reynolds, DW; Roberts, JR; Weil, WB; Balk, SJ; Miller, M; Shea, KM; Lipsett, M; Johnson, RH; Linet, M; Rogan, W; Spire, P		Comm Environm Hlth	Ambient air pollution: Health hazards to children	PEDIATRICS			English	Article						air pollution; adverse effects; children; asthma; environmental health	LOW-BIRTH-WEIGHT; SOUTHERN CALIFORNIA CHILDREN; RESPIRATORY HOSPITAL ADMISSIONS; AFRICAN-AMERICAN CHILDREN; DIESEL EXHAUST PARTICLES; MOTOR-VEHICLE EXHAUST; EMERGENCY-ROOM VISITS; LUNG-FUNCTION GROWTH; PULMONARY-FUNCTION; DAILY MORTALITY	Ambient (outdoor) air pollution is now recognized as an important problem, both nationally and worldwide. Our scientific understanding of the spectrum of health effects of air pollution has increased, and numerous studies are finding important health effects from air pollution at levels once considered safe. Children and infants are among the most susceptible to many of the air pollutants. In addition to associations between air pollution and respiratory symptoms, asthma exacerbations, and asthma hospitalizations, recent studies have found links between air pollution and preterm birth, infant mortality, deficits in lung growth, and possibly, development of asthma. This policy statement summarizes the recent literature linking ambient air pollution to adverse health outcomes in children and includes a perspective on the current regulatory process. The statement provides advice to pediatricians on how to integrate issues regarding air quality and health into patient education and children's environmental health advocacy and concludes with recommendations to the government on promotion of effective air-pollution policies to ensure protection of children's health.	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J	Shore, SA; Rivera-Sanchez, YM; Schwartzman, IN; Johnston, RA				Shore, SA; Rivera-Sanchez, YM; Schwartzman, IN; Johnston, RA			Responses to ozone are increased in obese mice	JOURNAL OF APPLIED PHYSIOLOGY			English	Article						inflammation; polymorphonuclear leukocytes; pulmonary mechanics; leptin	TUMOR-NECROSIS-FACTOR; BODY-MASS INDEX; INDUCED AIRWAY HYPERRESPONSIVENESS; EMERGENCY ROOM VISITS; INSULIN-RESISTANCE; WEIGHT-REDUCTION; OXIDATIVE STRESS; LEPTIN RECEPTOR; FACTOR-ALPHA; ASTHMA	Epidemiological data indicate an increased incidence of asthma in overweight adults and children. Ozone (O-3) is a common trigger for asthma. Accordingly, the purpose of this study was to compare O-3-induced airway hyperresponsiveness and airway inflammation in lean, wild-type (C57BL/6J) mice and mice that are obese as a consequence of a genetic defect in the gene encoding the satiety hormone leptin (ob/ob mice). The ob/ob mice eat excessively and weighed more than twice as much as age- and gender-matched wild-type mice. Airway responsiveness to intravenous methacholine was measured by forced oscillation. In air-exposed controls, baseline pulmonary resistance was greater, and the dose of methacholine required to double pulmonary resistance was lower in ob/ob than wild-type mice. Exposure to O-3 (2 parts/million for 3 h) caused AHR and airway inflammation in both groups of mice, but responses to O-3 were enhanced in ob/ob compared with wild-type mice. Administration of exogenous leptin did not reverse the enhanced inflammatory response observed in ob/ob mice, but augmented airway inflammation in wild-type mice. The inhaled dose of O-3 per gram of lung tissue was greater in ob/ob than wild-type mice. Our results indicate that O-3-induced airway responses are enhanced in ob/ob mice and suggest that inhaled O-3 dose may be one factor contributing to this difference, but other aspects of the obese phenotype may also contribute. Our results also indicate that the hormone leptin, which is increased in the obese, has the capacity to increase airway inflammation.	Harvard Univ, Sch Publ Hlth, Physiol Program, Boston, MA 02115 USA	Shore, SA (reprint author), Harvard Univ, Sch Publ Hlth, Physiol Program, 665 Huntington Ave, Boston, MA 02115 USA.				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J	Liu, LJS; Box, M; Kalman, D; Kaufman, J; Koenig, J; Larson, T; Lumley, T; Sheppard, L; Wallace, L				Liu, LJS; Box, M; Kalman, D; Kaufman, J; Koenig, J; Larson, T; Lumley, T; Sheppard, L; Wallace, L			Exposure assessment of particulate matter for susceptible populations in Seattle	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; CHD; COPD; infiltration efficiency; longitudinal correlation; personal cloud; PM2.5; wood smoke	OBSTRUCTIVE PULMONARY-DISEASE; PERSONAL EXPOSURE; AIR-POLLUTION; OUTDOOR CONCENTRATIONS; FINE PARTICLES; EPIDEMIOLOGY-EXPOSURE; COARSE PARTICLES; CASE-CROSSOVER; INDOOR; AMBIENT	In this article we present results from a 2-year comprehensive exposure assessment study that examined the particulate matter (PM) exposures and health effects in 108 individuals with and without chronic obstructive pulmonary disease (COPD), coronary heart disease (CHD), and asthma. The average personal exposures to PM with aerodynamic diameters < 2.5 mum (PM2.5) were similar to the average outdoor PM2.5 concentrations but significantly higher than the average indoor concentrations. Personal PM2.5 exposures in our study groups were lower than those reported in other panel studies of susceptible populations. Indoor and outdoor PM2.5, PM10 (PM with aerodynamic diameters < 10 mum), and the ratio of PM2.5 to PM10 were significantly higher during the heating season. The increase in outdoor PM10 in winter was primarily due to an increase in the PM2.5 fraction. A similar seasonal variation was found for personal PM2.5. The high-risk subjects in our study engaged in an equal amount of dust-generating activities compared with the healthy elderly subjects. The children in the study experienced the highest indoor PM2.5 and PM10 concentrations. Personal PM2.5 exposures varied by study group, with elderly healthy and CHD subjects having the lowest exposures and asthmatic children having the highest exposures. Within study groups, the PM2.5 exposure varied depending on residence because of different particle infiltration efficiencies. Although we found a wide range of longitudinal correlations between central-site and personal PM2.5 measurements, the longitudinal r is closely related to the particle infiltration efficiency. PM2.5 exposures among the COPD and CHD subjects can be predicted with relatively good power with a microenvironmental model composed of three microenvironments. The prediction power is the lowest for the asthmatic children.	Univ Washington, Dept Environm & Occupat Hlth Sci, Seattle, WA 98195 USA; Univ Washington, Dept Civil & Environm Engn, Seattle, WA 98195 USA; Univ Washington, Dept Biostat, Seattle, WA 98195 USA; US EPA, Reston, VA USA	Liu, LJS (reprint author), Univ Washington, Dept Environm & Occupat Hlth Sci, Box 354695, Seattle, WA 98195 USA.		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Health Perspect.	JUN	2003	111	7					909	918		10.1289/ehp.6011		10	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	689ND	WOS:000183498900028	12782491	
J	Cataldo, DD; Tournoy, KG; Vermaelen, K; Munaut, C; Foidart, JM; Louis, R; Noel, A; Pauwels, RA				Cataldo, DD; Tournoy, KG; Vermaelen, K; Munaut, C; Foidart, JM; Louis, R; Noel, A; Pauwels, RA			Matrix metalloproteinase-9 deficiency impairs cellular infiltration and bronchial hyperresponsiveness during allergen-induced airway inflammation	AMERICAN JOURNAL OF PATHOLOGY			English	Article							BROWN-NORWAY RATS; GELATINASE-B; TISSUE INHIBITOR; BRONCHOALVEOLAR LAVAGE; ENDOTHELIAL-CELLS; HUMAN-NEUTROPHILS; MAST-CELLS; T-CELL; ASTHMA; ACTIVATION	We investigated the specific role of matrix metalloproteinase (MMP)-9 in allergic asthma using a murine model of allergen-induced airway inflammation and airway hyperresponsiveness in MMP-9(-/-) mice and their corresponding wild-type (WT) littermates. After a single intraperitoneal sensitization to ovalbumin, the mice were exposed daily either to ovalbumin (1%) or phosphate-buffered saline aerosols from days 14 to 21. Significantly less peribronchial mononuclear cell infiltration of the airways and less lymphocytes in the bronchoalveolar lavage fluid were detected in challenged MMP-9(-/-) as compared to WT mice. In contrast, comparable numbers of bronchoalveolar lavage fluid eosinophils; were observed in both genotypes. After allergen exposure, the WT mice developed a significant airway hyperresponsiveness to carbachol whereas the MMP-9(-/-) mice failed to do so. Allergen exposure induced an increase of MMP-9-related gelatinolytic activity in WT lung extracts. Quantitative reverse transcriptase-polymerase chain reaction showed increased mRNA levels of MMP-12, MMP-14, and urokinase-type plasminogen activator after allergen exposure in the lung extracts of WT mice but not in MMP-9-deficient mice. in contrast, the expression of tissue inhibitor of metalloproteinases-1 was enhanced after allergen exposure in both groups. We conclude that MMP-9 plays a key role in the development of airway inflammation after allergenexposure.	Univ Liege, Dept Resp Dis, Liege, Belgium; Univ Liege, Lab Biol Tumours & Dev, Liege, Belgium; State Univ Ghent Hosp, Dept Resp Dis, B-9000 Ghent, Belgium	Cataldo, DD (reprint author), CHU Sart Tilman, B-4000 Liege, Belgium.			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J. Pathol.	AUG	2002	161	2					491	498		10.1016/S0002-9440(10)64205-8		8	Pathology	Pathology	582DQ	WOS:000177334800018	12163374	
J	Jensen, CS; Lisby, S; Baadsgaard, O; Volund, A; Menne, T				Jensen, CS; Lisby, S; Baadsgaard, O; Volund, A; Menne, T			Decrease in nickel sensitization in a Danish schoolgirl population with ears pierced after implementation of a nickel-exposure regulation	BRITISH JOURNAL OF DERMATOLOGY			English	Article						contact allergy; Denmark; exposure regulation; nickel; patch test	ORTHODONTIC TREATMENT; IMMUNE TOLERANCE; ALLERGY; CONTACT; INDUCTION; DENMARK; ATOPY	Background To reduce the skin nickel exposure of the population the Danish Ministry of Environment issued a regulation that was implemented in 1992, and the European Union countries have recently adopted an expanded regulation. Objectives The aim of our combined patch testing and questionnaire investigation of girls in public schools and high schools/production schools was to evaluate whether the regulation has had an impact on the prevalence of nickel sensitization. Methods To find a group of girls with cars pierced mainly after implementation of the nickel-exposure regulation in Denmark, girls were recruited from the fifth and sixth grade in 12 public schools (the public school group). After the public school level almost all girls from a public school population continue their education in high schools or other schools such as production schools or technical schools. Therefore, to find girls demographically similar to the public school girls but older, and with ears pierced before implementation of the regulation, girls from seven high schools and two production schools were recruited (the high school group). Four hundred and twenty-seven girls in the public school group (mean age 12.4 years, range 10-14) and 534 in the high school group (mean age 18.8 years, range 17-22) participated. All participants filled out a questionnaire concerning ear piercing, use of oral braces and former patch testing for nickel sensitivity. Three hundred and five girls (71.4%) in the public school group and 275 (51.5%) in the high school group were patch tested or had been tested previously and the results of these tests were included in the study. The relation between the frequency of nickel sensitization and the various factors that might influence the prevalence of nickel sensitization was evaluated by multivariate logistic regression analysis. The investigation was conducted from March 1999 to March 2000. Results The study showed that both increasing age and having ears pierced before 1992 enhanced the prevalence of nickel sensitization. We found that 17.1% of the girls in the high school group demonstrated a positive patch test reaction to nickel. In contrast, the prevalence of nickel sensitization in the public school group was only 3.9%. Comparing girls with and without pierced ears, the prevalence of nickel sensitization was significantly higher in girls with ears pierced before, but not after, 1992 (odds ratio 3.34 and 1.20, respectively). Only in the high school group was there a tendency that wearing oral braces before ear piercing had a protective effect on nickel sensitization, but this did not reach statistical significance. Conclusions As we found an effect of ear piercing before but not after 1992, this study strongly suggests that implementation of the nickel-exposure regulation in 1992 in Denmark has had the intended effect of protecting the female population from becoming allergic to nickel.	Univ Copenhagen, Gentofte Hosp, Dept Dermatol, DK-2900 Hellerup, Denmark; Novo Nordisk AS, Dept Biostat, DK-2880 Bagsvaerd, Denmark	Jensen, CS (reprint author), Univ Copenhagen, Gentofte Hosp, Dept Dermatol, Niels Andersensvej 65, DK-2900 Hellerup, Denmark.						BOSS A, 1982, CONTACT DERMATITIS, V8, P211, DOI 10.1111/j.1600-0536.1982.tb04191.x; Danish Ministry of Environment, 1991, 854 DAN MIN ENV; *DAN MIN ENV EN, 2000, 24 DAN MIN ENV EN; Devos SA, 2001, CONTACT DERMATITIS, V44, P273, DOI 10.1034/j.1600-0536.2001.440503.x; DOTTERUD LK, 1994, CONTACT DERMATITIS, V31, P308, DOI 10.1111/j.1600-0536.1994.tb02025.x; EMMETT EA, 1988, J AM ACAD DERMATOL, V19, P314, DOI 10.1016/S0190-9622(88)70178-4; *INT CONT DERM RES, 1984, EUR STAND SER ICDRG, V11, P63; Johansen JD, 2000, BRIT J DERMATOL, V142, P490, DOI 10.1046/j.1365-2133.2000.03362.x; KANERVA L, 1988, CONTACT DERMATITIS, V18, P10, DOI 10.1111/j.1600-0536.1988.tb05482.x; Kerosuo H, 1996, AM J ORTHOD DENTOFAC, V109, P148, DOI 10.1016/S0889-5406(96)70175-0; LARSSONSTYMNE B, 1985, CONTACT DERMATITIS, V13, P289, DOI 10.1111/j.1600-0536.1985.tb02580.x; MCDONAGH AJG, 1992, BRIT J DERMATOL, V126, P16, DOI 10.1111/j.1365-2133.1992.tb08396.x; Menne T, 1996, ANN CLIN LAB SCI, V26, P133; MENNE T, 1990, CONTACT DERMATITIS, V23, P57, DOI 10.1111/j.1600-0536.1990.tb00093.x; Menne T., 1989, NICKEL SKIN IMMUNOLO, P109; MOERTZ CG, 1999, THESIS U SO DENMARK; NIELSEN NH, 1993, CONTACT DERMATITIS, V29, P16; Nielsen NH, 2001, ACTA DERM-VENEREOL, V81, P31, DOI 10.1080/000155501750208155; STAERKJAER L, 1990, EUR J ORTHODONT, V12, P284; TODD DJ, 1989, ULSTER MED J, V58, P168; VANHOOGSTRATEN IMW, 1992, J INVEST DERMATOL, V99, P608, DOI 10.1111/1523-1747.ep12668010; VANHOOGSTRATEN IMW, 1993, J INVEST DERMATOL, V101, P26, DOI 10.1111/1523-1747.ep12358502; VANHOOGSTRATEN IMW, 1991, CLIN EXP IMMUNOL, V85, P441; VANHOOGSTRATEN IMW, 1994, J INVEST DERMATOL, V102, P80, DOI 10.1111/1523-1747.ep12371736; WAHLBERG JE, 2001, TXB CONTACT DERMATIT, P438	25	120	121	0	1	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0007-0963			BRIT J DERMATOL	Br. J. Dermatol.	APR	2002	146	4					636	642		10.1046/j.1365-2133.2002.04666.x		7	Dermatology	Dermatology	559HG	WOS:000176020300014	11966696	
J	Mortimer, KM; Neas, LM; Dockery, DW; Redline, S; Tager, IB				Mortimer, KM; Neas, LM; Dockery, DW; Redline, S; Tager, IB			The effect of air pollution on inner-city children with asthma	EUROPEAN RESPIRATORY JOURNAL			English	Article						air pollution; asthma; generalized estimating equations; inner-city; mixed linear models	RESPIRATORY-FUNCTION; AMBIENT OZONE; MEXICO-CITY; PARTICULATE; ASSOCIATION; REANALYSIS; RESPONSES; HEALTH	The effect of daily ambient air pollution was examined within a cohort of 846 asthmatic children residing in eight urban areas of the USA, using data from the National Cooperative Inner-City, Asthma Study. Daily air pollution concentrations were extracted from the Aerometric Information Retrieval System database from the Environment Protection Agency in the USA. Mixed linear models and generalized estimating equation models were used to evaluate the effects of several air pollutants (ozone, sulphur dioxide (SOD, nitrogen dioxide (NO2) and particles with a 50% cut-off aerodynamic diameter of 10 mum (PM10) on peak expiratory flow rate (PEFR) and symptoms in 846 children with a history of asthma (ages 4-9 yrs). None of the pollutants were associated with evening PEFR or symptom reports. Only ozone was associated with declines in morning %, PEFR (0.59% decline (95%, confidence interval (CI) 0.13-1.05%,) per interquartile range (IQR) increase in 5-day average ozone). In single pollutant models, each pollutant was associated with an increased incidence of morning symptoms: (odds ratio (OR)=1.16 (95%, Cl 1.02-1.30) per IQR increase in 4-day average ozone, OR=1.32 (95% CI 1.03-1.70) per IQR increase in 2-day average SO2, OR=1.48 (95% CI 1.02-2.16) per IQR increase in 6-day average NO2 and OR=1.26 (95% CI 1.0 1.59) per IQR increase in 2-day average PM10. This longitudinal analysis supports previous time-series findings that at levels below current USA air-quality standards, summer-air pollution is significantly related to symptoms and decreased pulmonary function among children with asthma.	Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA; US EPA, Epidemiol & Biomarkers Branch, Natl Hlth & Environm Effects Res Lab, Human Studies Div, Chapel Hill, NC USA; Harvard Univ, Sch Publ Hlth, Dept Epidemiol & Environm Hlth, Boston, MA 02115 USA; Case Western Reserve Univ, Rainbow Babies & Childrens Hosp, Dept Pediat, Cleveland, OH 44106 USA; Univ Calif Berkeley, Dept Publ Hlth Biol & Epidemiol, Berkeley, CA 94720 USA	Mortimer, KM (reprint author), Univ Calif Berkeley, Sch Publ Hlth, 1918 Univ Ave, Berkeley, CA 94720 USA.		Neas, Lucas/J-9378-2012		NIAID NIH HHS [AI-15105, AI-30752, AI-30756, AI-30772, AI-30773, AI-30777, AI-30779, AI30780, U01 AI-30751]		AVOL EL, 1998, 82 HLTH EFF I; BALMES JR, 1993, ENVIRON HEALTH PERSP, V101, P219, DOI 10.2307/3431683; Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; Chatfield C., 1996, ANAL TIME SERIES; Delfino RJ, 1998, ENVIRON HEALTH PERSP, V106, P751, DOI 10.1289/ehp.98106751; Diggle P. J., 1994, ANAL LONGITUDINAL DA; FRISCHER TM, 1993, AM REV RESPIR DIS, V148, P961; Gielen MH, 1997, AM J RESP CRIT CARE, V155, P2105; Gold DR, 1999, EPIDEMIOLOGY, V10, P8, DOI 10.1097/00001648-199901000-00004; Hoek G, 1998, EUR RESPIR J, V11, P1307, DOI 10.1183/09031936.98.11061307; Kimber Ian, 1998, Toxicology Letters (Shannon), V102-103, P301, DOI 10.1016/S0378-4274(98)00320-8; Kinney PL, 1996, ENVIRON HEALTH PERSP, V104, P170, DOI 10.2307/3432785; KINNEY PL, 1998, 98 HLTH EFF I; Littell R., 1996, SAS SYSTEM MIXED MOD; Mitchell H, 1997, PEDIATR PULM, V24, P237; Mortimer KM, 2000, AM J RESP CRIT CARE, V162, P1838; National Heart Lung and Blood Institute, 1997, NIH PUB; NEAS LM, 1995, AM J EPIDEMIOL, V141, P111; OSTRO BD, 1991, AM J PUBLIC HEALTH, V81, P694, DOI 10.2105/AJPH.81.6.694; Peters A, 1997, ENVIRON HEALTH PERSP, V105, P430, DOI 10.1289/ehp.97105430; Redline S, 1996, PEDIATR PULM, V21, P203; Roemer W, 2000, CLIN EXP ALLERGY, V30, P1067; Romieu I, 1996, AM J RESP CRIT CARE, V154, P300; Scannell C, 1996, AM J RESP CRIT CARE, V154, P24; SCHWARTZ J, 1994, AM J RESP CRIT CARE, V150, P1234; SPEKTOR DM, 1991, ENVIRON RES, V55, P107, DOI 10.1016/S0013-9351(05)80167-7; TAGER IB, 1998, 81 HLTH EFF I; Thurston GD, 1997, AM J RESP CRIT CARE, V155, P654; WHITE MC, 1994, ENVIRON RES, V65, P56, DOI 10.1006/enrs.1994.1021; [Anonymous], 1997, FED REG, V62	30	120	123	0	15	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	APR	2002	19	4					699	705		10.1183/09031936.02.00247102		7	Respiratory System	Respiratory System	541RB	WOS:000174996600018	11999000	
J	Rodriguez, MA; Winkleby, MA; Ahn, D; Sundquist, J; Kraemer, HC				Rodriguez, MA; Winkleby, MA; Ahn, D; Sundquist, J; Kraemer, HC			Identification of population subgroups of children and adolescents with high asthma prevalence - Findings from the Third National Health and Nutrition Examination Survey	ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE			English	Article							BODY-MASS INDEX; CHILDHOOD ASTHMA; UNITED-STATES; RISK-FACTORS; RESPIRATORY ILLNESS; PARENTAL SMOKING; PUERTO-RICAN; ENVIRONMENTAL EXPOSURES; PASSIVE SMOKING; YOUNG-ADULTS	Objectives: To provide national estimates of asthma prevalence in African-American, Mexican American and white (non-Latino) children and adolescents using several common definitions; to evaluate familial, sociodemographic, and environmental risk factors that are independently associated with current asthma in children and to identify subgroups at particular risk for current asthma using 2 complementary data analytic approaches. Design: Cross-sectional study, using the Third National Health and Nutrition Examination Survey, 1988-1994. Setting: Eighty-nine mobile examination centers in the United States. Participants: Twelve thousand three hundred eighty-eight African American, Mexican American, and white (non-Latino) children and adolescents, aged 2 months through 16 years, selected from a systematic random, population-based, nationally representative sample. Main Outcome Measure: Current asthma, defined by caregivers who reported that their child currently had doctor-diagnosed asthma. Results: The overall prevalence of current asthma was 6.7% (95% confidence interval [CI], 5.6-7.8). Odds ratios for current asthma from the multiple regression analysis were 4.00 (95% CI, 2.90-5.52) for children with a parental history of asthma or hay fever, 1.94 (95% CI, 1.09-3.46) for children with body mass index (calculated as weight in kilograms divided by the square of height in meters) greater than or equal to the 85th percentile, and 1.64 (95% CI, 1.20-2.26) for children of African American ethnicity. African American and Mexican American children showed a consistent prevalence of current asthma across age while white children showed an increase in prevalence with age. The 2 highest-risk subgroups identified by the signal detection analysis were composed of children with a parental history of asthma or hay fever who were 10 years or older with a body mass index greater than or equal to the 85th percentile (31.0% current asthma), and children with a parental history who were 10 years or younger and of African American ethnicity (15.6% current asthma). Conclusions: The findings from this analysis show a strong independent association between obesity and current asthma in children and adolescents, and confirm previous reports of a parental history of asthma or hay fever and African American ethnicity as additional important risk factors.	Univ Calif San Francisco, Dept Family & Community Med, San Francisco, CA 94143 USA; Stanford Univ, Sch Med, Stanford Ctr Res Dis Prevent, Dept Med, Palo Alto, CA 94304 USA; Stanford Univ, Sch Med, Dept Psychiat, Palo Alto, CA 94304 USA	Rodriguez, MA (reprint author), Univ Calif Los Angeles, Sch Med, Dept Family Med, 924 Westwood Blvd,Suite 725, Los Angeles, CA 90024 USA.		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Pediatr. Adolesc. Med.	MAR	2002	156	3					269	275				7	Pediatrics	Pediatrics	528XK	WOS:000174270000012	11876672	
J	Nielsen, KG; Bisgaard, H				Nielsen, KG; Bisgaard, H			Discriminative capacity of bronchodilator response measured with three different lung function techniques in asthmatic and healthy children aged 2 to 5 years	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						healthy children; preschool children; bronchodilator responsiveness; lung function tests	AIRWAY-RESISTANCE; INTERRUPTER TECHNIQUE; OSCILLATION TECHNIQUE; PRESCHOOL-CHILDREN; YOUNG-CHILDREN; COLD-AIR; PLETHYSMOGRAPHY; REVERSIBILITY; CHALLENGE	The primary aim of this study was to quantify and compare bronchodilator responsiveness in healthy and asthmatic children aged 2 to 5 yr. The secondary aim of the study was to compare discriminative capacity (i.e., sensitivity, specificity, and predictive values of the reversibility test for the diagnosis of asthma) for each of the lung function tests applied in the study. Specific airway resistance (sRaw) as measured by whole-body plethysmography, respiratory resistance as measured with the interrupter technique (Rint), and respiratory resistance and reactance at 5 Hz (Rrs5, Xrs5, respectively) as measured with the impulse oscillation technique were assessed before and 20 min after inhalation of terbutaline from a pressurized metered-dose inhaler via a metal spacer by 92 children (37 healthy controls and 55 asthmatic subjects). The study of healthy children followed a randomized, double-blind, crossover design, whereas the study of asthmatic children was open. Baseline lung function was significantly decreased in asthmatic children as compared with healthy control subjects as reflected by all techniques used in the study. sRaw, Rint, and Rrs5, but not Xrs5, improved significantly with terbutaline as compared with placebo in healthy control subjects. Lung function Improved to a significantly greater extent in asthmatic children than in control subjects as reflected by all methods. sRaw provided the best discriminative power of such a bronchodilator response, with a sensitivity of 66% and specificity of 81% at the cutoff level of a 25% decrease in sRaw after bronchodilator administration. In conclusion, bronchodilator response measured by sRaw allows a separation of asthmatic from healthy young children. This may help define asthma in this clinically difficult-to-manage group of young wheezy children. The sensitivity and specificity of the other methods used in the study were less than those of sRaw.	Univ Copenhagen Hosp, Dept Pediat 5003, Rigshosp, DK-2100 Copenhagen, Denmark	Bisgaard, H (reprint author), Univ Copenhagen Hosp, Dept Pediat 5003, Rigshosp, DK-2100 Copenhagen, Denmark.		Kronow, Joern/B-1054-2011	Bisgaard, Hans/0000-0003-4131-7592			American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P1285, DOI 10.1164/ajrccm/136.5.1285; BIBI H, 1991, PEDIATR PULM, V10, P244, DOI 10.1002/ppul.1950100404; Bisgaard H, 2000, AM J RESP CRIT CARE, V162, P187; Bisgaard H, 1995, EUR RESPIR J, V8, P2067, DOI 10.1183/09031936.95.08122067; BLAND JM, 1986, LANCET, V1, P307; Bridge PD, 1999, EUR RESPIR J, V13, P792, DOI 10.1034/j.1399-3003.1999.13d16.x; CASAN P, 1983, B EUR PHYSIOPATH RES, V19, P567; DALES RE, 1988, AM REV RESPIR DIS, V138, P317; DEMEDTS M, 1990, EUR RESPIR J, V3, P1084; EKWO EE, 1983, AM REV RESPIR DIS, V127, P108; Hellinckx J, 1998, EUR RESPIR J, V12, P438, DOI 10.1183/09031936.98.12020438; Klug B, 1998, PEDIATR PULM, V25, P322, DOI 10.1002/(SICI)1099-0496(199805)25:5<322::AID-PPUL6>3.0.CO;2-K; Klug B, 1999, EUR RESPIR J, V14, P1185, DOI 10.1183/09031936.99.14511859; Klug B, 1996, PEDIATR PULM, V21, P290; Klug B, 1997, EUR RESPIR J, V10, P1599, DOI 10.1183/09031936.97.10071599; Nielsen KG, 2000, AM J RESP CRIT CARE, V162, P1500; Nielsen KG, 2000, AM J RESP CRIT CARE, V161, P1805; VANNOORD JA, 1994, AM J RESP CRIT CARE, V150, P551; WAALKENS HJ, 1993, EUR RESPIR J, V6, P645; Warner JO, 1998, PEDIATR PULM, V25, P1	20	120	130	1	8	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	AUG 15	2001	164	4					554	559				6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	469LL	WOS:000170816900009	11520714	
J	Marogna, M; Spadolini, I; Massolo, A; Canonica, GW; Passalacqua, G				Marogna, Maurizio; Spadolini, Igino; Massolo, Alessandro; Canonica, Giorgio Walter; Passalacqua, Giovanni			Long-lasting effects of sublingual immunotherapy according to its duration: A 15-year prospective study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Sublingual immunotherapy; allergic rhinitis; long-lasting effect; house dust mite	GRASS-POLLEN IMMUNOTHERAPY; RANDOMIZED CONTROLLED-TRIAL; TERM CLINICAL-EFFICACY; HOUSE-DUST MITE; RESPIRATORY ALLERGY; IMMUNOGLOBULIN-E; POSITION PAPER; FOLLOW-UP; ASTHMA; CHILDREN	Background: Data on the long-term effects of sublingual immunotherapy (SLIT) are sparse, and the optimal duration of treatment is a matter of debate. Objective: We sought to prospectively evaluate the long-term effect of SLIT given for 3, 4, or 5 years and to compare the effect of those different durations. Methods: In this prospective open controlled study we followed up patients with respiratory allergy who were monosensitized to mites for 15 years. The subjects were divided in 4 groups receiving drug therapy alone or SLIT for 3, 4, or 5 years. Clinical scores, skin sensitizations, methacholine reactivity, and nasal eosinophil counts were evaluated every year during the winter months. The clinical effect was considered to persist until clinical scores remained at less than 50% of the baseline value, and then patients underwent another course of SLIT. Results: Seventy-eight patients were enrolled, and 59 completed the study. In the 12 control subjects no relevant change in clinical scores was seen throughout the study. In the patients receiving SLIT for 3 years, the clinical benefit persisted for 7 years. In those receiving immunotherapy for 4 or 5 years, the clinical benefit persisted for 8 years. New sensitizations occurred in all the control subjects over 15 years and in less than a quarter of the patients receiving SLIT (21%, 12%, and 11%, respectively). The second course of vaccination induced a benefit more rapidly than the first course. The behavior of bronchial hyperreactivity and nasal eosinophils paralleled the clinical score. Conclusion: Under the present conditions, it can be suggested that a 4-year duration of SLIT is the optimal choice because it induces a long-lasting clinical improvement similar to that seen with a 5-year course and greater than that of a 3-year vaccination. (J Allergy Clin Immunol 2010;126:969-75.)	[Marogna, Maurizio] Macchi Hosp Fdn, Pneumol Unit, Varese, Italy; [Spadolini, Igino] Anallergo, Dept Med, Florence, Italy; [Massolo, Alessandro] Univ Calgary, Fac Vet Med, Dept Ecosyst & Publ Hlth, Calgary, AB T2N 1N4, Canada; [Canonica, Giorgio Walter; Passalacqua, Giovanni] Univ Genoa, DIMI, I-16126 Genoa, Italy	Passalacqua, G (reprint author), Padiglione Maragliano, Dept Internal Med, Lgo R Benzi 10, I-16132 Genoa, Italy.	passalacqua@unige.it	Massolo, Alessandro/I-3437-2012		ARMIA (Associazione Ricerca Malattie Immunologiche e Allergiche)	Supported in part by ARMIA (Associazione Ricerca Malattie Immunologiche e Allergiche).	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Allergy Clin. Immunol.	NOV	2010	126	5					969	975		10.1016/j.jaci.2010.08.030		7	Allergy; Immunology	Allergy; Immunology	674HB	WOS:000283727100012	20934206	
J	Barrett, NA; Maekawa, A; Rahman, OM; Austen, KF; Kanaoka, Y				Barrett, Nora A.; Maekawa, Akiko; Rahman, Opu M.; Austen, K. Frank; Kanaoka, Yoshihide			Dectin-2 Recognition of House Dust Mite Triggers Cysteinyl Leukotriene Generation by Dendritic Cells	JOURNAL OF IMMUNOLOGY			English	Article							C-TYPE LECTIN; MANSONI EGG ANTIGENS; ALLERGIC AIRWAY INFLAMMATION; ARACHIDONIC-ACID CASCADE; RECEPTOR GAMMA-CHAIN; MOUSE BONE-MARROW; HUMAN MAST-CELLS; SCHISTOSOMA-MANSONI; DC-SIGN; PATTERN-RECOGNITION	House dust mites are a significant source of airborne allergen worldwide, but there is little understanding of how they so potently generate allergic inflammation. We found that extracts from the house dust mites Dermatophagoides farinae (Df) and Dermatophagoides pteronyssinus and from the mold Aspergillus fumigatus stimulated a rapid and robust production of cysteinyl leukotrienes (cys-LTs), proinflammatory lipid mediators, from mouse bone marrow-derived dendritic cells (BMDCs). Con A affinity chromatography of the Df extract revealed that the relevant ligand is a glycan(s), suggesting stimulation via a dendritic cell (DC) lectin receptor. Cys-LT production in BMDCs from wild-type mice was inhibited by spleen tyrosine kinase (Syk) inhibitors and was abolished in BMDCs from FcR gamma(-/-) mice, implicating either Dectin-2 or DC immunoactivating receptor. Transfection of each receptor in bone marrow-derived mast cells revealed that only Dectin-2 mediates cys-LT production by Df, Dermatophagoides pteronyssinus, and Aspergillus famigatus. Lentiviral knockdown of Dectin-2 in BMDCs attenuated Df extract-elicited cys-LT generation, thereby identifying Dectin-2 as the receptor. Lung CD11c(+) cells, but not peritoneal or alveolar macrophages, also generated cys-LTs in response to Df. These findings place Dectin-2 among the C-type lectin receptors that activate arachidonic acid metabolism and identify the Dectin-2/FcR gamma/Syk/cys-LT axis as a novel mechanism by which three potent indoor allergens may activate innate immune cells to promote allergic inflammation. The Journal of Immunology, 2009, 182: 1119-1128.	[Kanaoka, Yoshihide] Brigham & Womens Hosp, Div Rheumatol Allergy & Immunol, Boston, MA 02115 USA; Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA	Kanaoka, Y (reprint author), Brigham & Womens Hosp, Div Rheumatol Allergy & Immunol, Smith Bldg,Room 626C,1 Jimmy Fund Way, Boston, MA 02115 USA.	ykanaoka@rics.bwh.harvard.edu			National Institutes of Health [AI-07306, AI-31599, AI-52353, HL-36110, HL-82695]	This work was supported by National Institutes of Health Grants AI-07306, AI-31599, AI-52353, HL-36110, and HL-82695. N.A.B. is supported by an American Academy of Allergy, Asthma, and Immunology/Altana grant for advanced fellows-in-training and the Joycelyn C. Austen Fund for the Career Development of Women Physician Scientists.	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Immunol.	JAN 15	2009	182	2					1119	1128				10	Immunology	Immunology	393RO	WOS:000262390600041	19124755	
J	Slama, R; Morgenstern, V; Cyrys, J; Zutavern, A; Herbarth, O; Wichmann, HE; Heinrich, J				Slama, Remy; Morgenstern, Verena; Cyrys, Josef; Zutavern, Anne; Herbarth, Olf; Wichmann, Heinz-Erich; Heinrich, Joachim		LISA Study Group	Traffic-related atmospheric pollutants levels during pregnancy and offspring's term birth weight: a study relying on a land-use regression exposure model	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						atmospheric pollution; birth weight; diesel soot; environment; geographic information system; intrauterine growth restriction; particulate matter; pregnancy; reproduction; road traffic; sensitivity analysis	PARTICULATE AIR-POLLUTION; POLYCYCLIC AROMATIC-HYDROCARBONS; LOS-ANGELES-COUNTY; FETAL-GROWTH; RESPIRATORY HEALTH; ORGANIC-COMPOUNDS; MATERNAL SMOKING; FINE PARTICLES; DNA-DAMAGE; OUTCOMES	BACKGROUND: Some studies have suggested that particulate matter (PM) levels during pregnancy may be associated with birth weight. Road traffic is a major source of fine PM (PM with aerodynamic diameter < 2.5 mu m; PM(2.5)). OBJECTIVE: We determined to characterize the influence of maternal exposure to atmospheric pollutants due to road traffic and urban activities on offspring term birth weight. METHODS: Women from a birth cohort [the LISA (Influences of Lifestyle Related Factors on the Human Immune System and Development of Allergies in Children) cohort] who delivered a non-premature baby with a birth weight > 2,500 g in Munich metropolitan area were included. We assessed PM(2.5), PM(2.5) absorbance (which depends on the blackness of PM(2.5), a marker of traffic-related air pollution), and nitrogen dioxide levels using a land-use regression model, taking into account the type and length of roads, population density, land coverage around the home address, and temporal variations in pollution during pregnancy. Using Poisson regression, we estimated prevalence ratios (PR) of birth weight < 3,000 g, adjusted for gestational duration, sex, maternal smoking, height, weight, and education. RESULTS: Exposure was defined for 1,0 16 births. Taking the lowest quartile of exposure during pregnancy as a reference, the PR of birth weight < 3,000 g associated with the highest quartile was 1.7 for PM(2.5) [95% confidence interval (CI), 1.2-2.7], 1.8 for PM(2.5) absorbance (95% Cl, 1.1-2.7), and 1.2 for NO(2) (95% Cl, 0.7-1.7). The PR associated with an increase of 1 mu g/m(3) in PM(2.5) levels was 1. 13 (95% Cl, 1.00-1.29). CONCLUSION: Increases in PM(2.5) levels and PM(2.5) absorbance were associated with decreases in term birth weight. Traffic-related air pollutants may have adverse effects on birth weight.	GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, Neuherberg, Germany; INSERM, Inst Natl Sante Rech Med, UMR822, Le Kremlin Bicetre, France; INED, Inst Natl Etud Demog, Paris, France; Univ Paris Sud, F-94275 Le Kremlin Bicetre, France; Univ Augsburg, Ctr Environm Sci, WZU, Augsburg, Germany; Kinderklin & Kinderpoliklin Dr V Haunerschen Kind, Munich, Germany; UFZ Umwelt Forsch Zentrum, Leipzig, Germany; Univ Leipzig, Fac Med, Leipzig, Germany; Univ Munich, Inst Med Data Management Biometr & Epidemiol, Munich, Germany	Slama, R (reprint author), GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, Neuherberg, Germany.	slama@vjf.inserm.fr	Cyrys, Josef/B-5359-2014; Slama, Remy/M-1755-2013	Slama, Remy/0000-0002-8980-8529; Cyrys, Josef/0000-0002-2105-8696			Albuquerque CA, 2004, EARLY HUM DEV, V80, P31, DOI 10.1016/j.earlhumdev.2004.05.004; Archibong AE, 2002, REPROD TOXICOL, V16, P801, DOI 10.1016/S0890-6238(02)00058-8; Basu R, 2004, J EXPO ANAL ENV EPID, V14, P391, DOI 10.1038/sj.jea.7500336; Bell ML, 2007, ENVIRON HEALTH PERSP, V115, P1118, DOI 10.1289/ehp.9759; Bobak M, 2000, ENVIRON HEALTH PERSP, V108, P173, DOI 10.2307/3454517; Brauer M, 2003, EPIDEMIOLOGY, V14, P228, DOI 10.1097/00001648-200303000-00019; Brook RD, 2005, CURR HYPERTENS REP, V7, P427, DOI 10.1007/s11906-005-0037-9; Brunekreef B., 2005, 127 HLTH EFF I; Choi H, 2006, ENVIRON HEALTH PERSP, V114, P1744, DOI 10.1289/ehp.8982; Council Directive, 1999, OFFICIAL J EUROPEA L, V163, P0041; Cyrys J, 2005, ENVIRON HEALTH PERSP, V113, P987, DOI 10.1289/ehp.7662; Cyrys J, 2003, J EXPO ANAL ENV EPID, V13, P134, DOI 10.1038/sj.jea.7500262; Cyrys J, 2000, SCI TOTAL ENVIRON, V250, P51, DOI 10.1016/S0048-9697(00)00361-2; Dejmek J, 1999, ENVIRON HEALTH PERSP, V107, P475, DOI 10.2307/3434630; Dejmek J, 2000, ENVIRON HEALTH PERSP, V108, P1159, DOI 10.2307/3434828; Dubowsky SD, 2006, ENVIRON HEALTH PERSP, V114, P992, DOI 10.1289/ehp.8469; Efron B., 1993, INTRO BOOTSTRAP; Gehrig R, 2003, ATMOS ENVIRON, V37, P2571, DOI 10.1016/S1352-2310(03)00221-8; Gehring U, 2002, EUR RESPIR J, V19, P690, DOI 10.1183/09031936.02.01182001; Glinianaia SV, 2004, EPIDEMIOLOGY, V15, P36, DOI 10.1097/01.ede.0000101023.41844.ac; Gomiscek B, 2004, ATMOS ENVIRON, V38, P3917, DOI 10.1016/j.atmosenv.2004.03.056; Greenland S, 2004, AM J EPIDEMIOL, V160, P301, DOI 10.1093/aje/kwh221; HANSTEEN IL, 1998, J OCCUP ENV HLTH, V4, P63; Harrell F. E., 2001, REGRESSION MODELING; Hoek G, 2002, ATMOS ENVIRON, V36, P4077, DOI 10.1016/S1352-2310(02)00297-2; Infante-Rivard C, 2006, EPIDEMIOLOGY, V17, P38, DOI 10.1097/01.ede.0000187669.34003.b1; Janssen NAH, 2001, ATMOS ENVIRON, V35, P3875, DOI 10.1016/S1352-2310(01)00144-3; Jedrychowski W, 2004, ENVIRON HEALTH PERSP, V112, P1398, DOI 10.1289/ehp.7065; Kaaja RJ, 2005, JAMA-J AM MED ASSOC, V294, P2751, DOI 10.1001/jama.294.21.2751; Kanaka-Gantenbein C, 2003, ANN NY ACAD SCI, V997, P150, DOI 10.1196/annals.1290.017; Kinney PL, 2000, ENVIRON HEALTH PERSP, V108, P213, DOI 10.2307/3454436; KLEEMAN MJ, 1999, ENVIRON SCI TECHNOL, V33, P3518; Kreyling WG, 2002, J TOXICOL ENV HEAL A, V65, P1513, DOI 10.1080/00984100290071649; Krzyzanowski M., 2005, HLTH EFFECTS TRANSPO; Lash TL, 2003, EPIDEMIOLOGY, V14, P451, DOI 10.1097/01.EDE.0000071419.41011.cf; Lewis C, 2006, AM J EPIDEMIOL, V163, P38, DOI 10.1093/aje/kwj009; Lloyd AC, 2001, J AIR WASTE MANAGE, V51, P809; Miozzo M, 2002, BIOL NEONATE, V81, P217, DOI 10.1159/000056752; MONN C, 1995, ATMOS ENVIRON, V29, P2565, DOI 10.1016/1352-2310(95)94999-U; Morgenstern V, 2007, OCCUP ENVIRON MED, V64, P8, DOI 10.1136/oem.2006.028241; National Center for Environmental Assessment, 2004, AIR QUAL CRIT PART M; Nieuwenhuijsen M, 2006, ENVIRON INT, V32, P996, DOI 10.1016/j.envint.2006.06.015; Parker JD, 2005, PEDIATRICS, V115, P121, DOI 10.1542/peds.2004-0889; Peduzzi P, 1996, J CLIN EPIDEMIOL, V49, P1373, DOI 10.1016/S0895-4356(96)00236-3; Perera FP, 2005, ENVIRON HEALTH PERSP, V113, P1062, DOI 10.1289/ehp.7908; Perera FP, 2004, ENVIRON HEALTH PERSP, V112, P1133, DOI 10.1289/ehp.6833; Perera FP, 2004, ENVIRON HEALTH PERSP, V112, P626, DOI 10.1289/ehp.6617; Perera FP, 1998, AM J EPIDEMIOL, V147, P309; Peters A, 1997, LANCET, V349, P1582, DOI 10.1016/S0140-6736(97)01211-7; Pope CA, 2006, J AIR WASTE MANAGE, V56, P709; *REG VON, 2004, LUFTR STADT MUNCH BA; Roemer WH, 2001, ENVIRON HEALTH PERSP, V109, P151, DOI 10.2307/3434768; Schauer JJ, 1999, ENVIRON SCI TECHNOL, V33, P1578, DOI 10.1021/es980081n; Schauer JJ, 2002, ENVIRON SCI TECHNOL, V36, P1169, DOI 10.1021/es0108077; Slama R, 2005, REV EPIDEMIOL SANTE, V53, p2S65; Spiegelman D, 2005, AM J EPIDEMIOL, V162, P199, DOI 10.1093/aje/kwi188; Sram RJ, 2005, ENVIRON HEALTH PERSP, V113, P375, DOI 10.1289/ehp.6362; Takeda Y, 2004, J VIRAL HEPATITIS, V11, P33, DOI 10.1046/j.1365-2893.2003.00472.x; Tsukue N, 2002, INHAL TOXICOL, V14, P635, DOI 10.1080/08958370290084548; Vittinghoff E, 2007, AM J EPIDEMIOL, V165, P710, DOI 10.1093/aje/kwk052; Whyatt RM, 1998, ENVIRON HEALTH PERSP, V106, P821, DOI 10.2307/3434196; Wilhelm M, 2005, ENVIRON HEALTH PERSP, V113, P1212, DOI 10.1289/ehp.7751; Wilhelm M, 2003, ENVIRON HEALTH PERSP, V111, P207, DOI 10.1289/ehp.5688; Yoshida Seiichi, 2006, Environmental Sciences, V13, P139; Zdravkovic T, 2005, PLACENTA, V26, pS81, DOI 10.1016/j.placenta.2005.02.003	65	119	122	1	33	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	SEP	2007	115	9					1283	1292		10.1289/ehp.10047		10	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	206RM	WOS:000249200600023	17805417	
J	Litonjua, AA; Rifas-Shiman, SL; Ly, NP; Tantisira, KG; Rich-Edwards, JW; Camargo, CA; Weiss, ST; Gillman, MW; Gold, DR				Litonjua, Augusto A.; Rifas-Shiman, Sheryl L.; Ly, Ngoc P.; Tantisira, Kelan G.; Rich-Edwards, Janet W.; Camargo, Carlos A., Jr.; Weiss, Scott T.; Gillman, Matthew W.; Gold, Diane R.			Maternal antioxidant intake in pregnancy and wheezing illnesses in children at 2 y of age	AMERICAN JOURNAL OF CLINICAL NUTRITION			English	Article						asthma; diet; antioxidants; eczema; childhood; wheezing	ALLERGIC RHINITIS; CHILDHOOD ASTHMA; BLOOD-PRESSURE; HAY-FEVER; NATIONAL-HEALTH; DIETARY FACTORS; UNITED-STATES; LUNG-FUNCTION; T-CELLS; RISK	Background: Low intakes of dietary antioxidants may contribute to increases in asthma and allergy. Objective: We investigated the association of maternal total intakes (foods + supplements) of 10 antioxidant nutrients during pregnancy with wheezing and eczema in 2-y-old children. Design: Subjects were 1290 mother-child pairs in an ongoing cohort study. Maternal dietary and supplement intakes were assessed by using a validated food-frequency questionnaire administered in the first and second trimesters. Antioxidant nutrient intakes were calculated. and the mean for each nutrient was considered to be the exposure during pregnancy. The outcomes of interest were any wheezing by the child during either the first or second year of life, recurrent wheezing in both years, and eczema in either the first or second year. Results: No association was observed between maternal total intake of any antioxidant nutrient and eczema. In multivariate logistic regression models, the highest quartile compared with the lowest quartile of maternal total intakes of vitamin E [odds ratio (OR): 0.70; 95% Cl: 0.48,1.03] and zinc (OR: 0.59; 95% Cl: 0.41, 0.88) was inversely associated with any wheezing at 2 y of age (P for trend = 0.06 and 0.01 over quartiles of intake for vitamin E and zinc, respectively). Similar results were obtained for recurrent wheezing at 2 y of age with vitamin E (OR: 0.49; 95% Cl: 0.27, 0.90) and zinc (OR: 0.49; 95% Cl: 0.27. 0.87) (P for trend = 0.05 and 0.06 over quartiles of intake for vitamin E and zinc, respectively). Conclusion: Our results suggest that higher maternal total intakes of antioxidants during pregnancy may decrease the risks for wheezing illnesses in early childhood.	Brigham & Womens Hosp, Channing Lab, Dept Med, Boston, MA 02115 USA; Beth Israel Deaconess Med Ctr, Div Pulm & Crit Care Med, Boston, MA 02215 USA; Massachusetts Gen Hosp, Div Pediat Pulm Med, Boston, MA 02114 USA; Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA; Harvard Univ, Sch Med, Dept Ambulatory Care & Prevent, Boston, MA 02115 USA; Harvard Pilgrim Hlth Care, Boston, MA USA; Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA	Litonjua, AA (reprint author), Brigham & Womens Hosp, Channing Lab, Dept Med, 181 Longwood Ave, Boston, MA 02115 USA.	augusto.litonjua@channing.harvard.edu			NHLBI NIH HHS [HL61907, HL64925, K24 HL068041, K24 HL068041-03, R01 HL061907, R01 HL061907-03, R01 HL064925, R01 HL064925-03]; NIAID NIH HHS [AI35786, R01 AI035786, R56 AI035786]; NICHD NIH HHS [R37 HD034568, HD34568, R01 HD034568, R01 HD034568-03]		ACOG Committee on Practice Bulletins, 2003, OBSTET GYNECOL, V102, P203; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Braback L, 2004, CLIN EXP ALLERGY, V34, P38, DOI 10.1111/j.1365-2222.2004.01841.x; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Braun-Fahrlander C, 2004, EUR RESPIR J, V23, P407, DOI 10.1183/09031936.04.00074004; Carter ER, 2005, ANN ALLERG ASTHMA IM, V94, P634; Castro-Rodriguez JA, 2000, AM J RESP CRIT CARE, V162, P1403; Cook DG, 1997, THORAX, V52, P628; Cunningham-Rundles S, 2005, J ALLERGY CLIN IMMUN, V115, P1119, DOI 10.1016/j.jaci.2005.04.036; Devereux G, 2005, J ALLERGY CLIN IMMUN, V115, P1109, DOI 10.1016/j.jaci.2004.12.11.39; Devereux G, 2002, CLIN EXP ALLERGY, V32, P43, DOI 10.1046/j.0022-0477.2001.01267.x; DITORO R, 1987, ACTA PAEDIATR SCAND, V76, P612; Farchi S, 2003, EUR RESPIR J, V22, P772, DOI 10.1183/09031936.03.00006703; Fawzi WW, 2004, ANN EPIDEMIOL, V14, P754, DOI 10.1016/j.annepidem.2004.03.001; Forastiere F, 2000, THORAX, V55, P283, DOI 10.1136/thorax.55.4.283; Fowles ER, 2004, JOGNN-J OBST GYN NEO, V33, P809, DOI 10.1177/0884217504270599; Gilliland FD, 2003, AM J EPIDEMIOL, V158, P576, DOI 10.1093/aje/kwg181; Gillman MW, 2004, CIRCULATION, V110, P1990, DOI 10.1161/01.CIR.0000143199.93495.96; Gillman MW, 2004, J PEDIATR-US, V144, P240, DOI 10.1016/j.jpeds.2003.10.064; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; Ho E, 2004, J NUTR BIOCHEM, V15, P572, DOI 10.1016/j.jnutbio.2004.07.005; Hu FB, 1997, NEW ENGL J MED, V337, P1491, DOI 10.1056/NEJM199711203372102; Huh SY, 2005, INT J EPIDEMIOL, V34, P378, DOI 10.1093/ije/dyh373; *I MED FOOD NUTR B, 2000, PAN DIET ANT REL COM; *I MED FOOD NUTR B, 1990, COMM NUTR STAT DUR P; Kadrabova J, 1996, J TRACE ELEM MED BIO, V10, P50; King JC, 2000, AM J CLIN NUTR, V71, p1334S; Lara M, 2002, PEDIATRICS, V109, P919, DOI 10.1542/peds.109.5.919; Latvala J, 2005, BRIT MED J, V330, P1186, DOI 10.1136/bmj.38448.603921.AF; LEWIS S, 1995, EUR RESPIR J, V8, P349, DOI 10.1183/09031936.95.08030349; Li-Weber M, 2002, EUR J IMMUNOL, V32, P2401, DOI 10.1002/1521-4141(200209)32:9<2401::AID-IMMU2401>3.0.CO;2-S; Litonjua AA, 1999, PEDIATR PULM, V28, P394, DOI 10.1002/(SICI)1099-0496(199912)28:6<394::AID-PPUL2>3.0.CO;2-6; Litonjua AA, 1998, AM J RESP CRIT CARE, V158, P176; Litonjua A. 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J. Clin. Nutr.	OCT	2006	84	4					903	911				9	Nutrition & Dietetics	Nutrition & Dietetics	093AX	WOS:000241140700030	17023719	
J	Jowsey, IR; Basketter, DA; Westmoreland, C; Kimber, I				Jowsey, Ian R.; Basketter, David A.; Westmoreland, Carl; Kimber, Ian			A future approach to measuring relative skin sensitising potency: a proposal	JOURNAL OF APPLIED TOXICOLOGY			English	Article						skin; sensitisation; allergy; in vitro; in silico	LYMPH-NODE ASSAY; EPIDERMAL LANGERHANS CELLS; HUMAN DENDRITIC CELLS; NECROSIS-FACTOR-ALPHA; VITRO PRIMARY SENSITIZATION; SURFACE-MARKER EXPRESSION; MESSENGER-RNA EXPRESSION; IN-VITRO; CONTACT SENSITIZERS; ICCVAM EVALUATION	Current approaches to skin sensitisation risk assessment are dependent upon the availability of information regarding two fundamental parameters. Firstly, data relating to the relative skin sensitising potency of the chemical, and secondly, information regarding likely conditions of human exposure. During the past two decades, much has been achieved in terms of refining methods capable of informing these parameters. For example, the development of the local lymph node assay (LLNA) has made it possible to predict skin sensitising hazard, and to determine relative skin sensitising potency, in a way that was not possible previously. Taken together with accurate information about predicted exposure, such potency data can be used to facilitate the derivation of effective risk assessments. However, although the LLNA provides an integrated assessment of skin sensitising activity, it does require the use of experimental animals and there is growing enthusiasm for designing robust alternative approaches that will reduce or obviate that need. Progress is being made in defining alternative experimental strategies that avoid animal use, but it is clear that accurate characterisation of skin sensitisation hazards will require the effective integration of various sources of information. For this reason, we exemplify here one possible approach that, in theory, provides a framework for not only the identification of skin sensitising chemicals, but also the estimation of relative sensitising potency. This paradigm depends upon development of an understanding of the various biological, biochemical and chemical factors that impact on the allergenic properties of chemicals and the acquisition of skin sensitisation, and an ability to measure these in vitro. Copyright (c) 2006 John Wiley & Sons, Ltd.	Unilever Safety & Environm Assurance Ctr, Sharnbrook MK44 1LQ, Beds, England; Syngenta Cent Toxicol Lab, Macclesfield SK10 4TJ, Cheshire, England	Jowsey, IR (reprint author), Unilever Safety & Environm Assurance Ctr, Colworth House, Sharnbrook MK44 1LQ, Beds, England.	ian.jowsey@unilever.com					Aiba S, 1997, EUR J IMMUNOL, V27, P3031, DOI 10.1002/eji.1830271141; Aiba S, 2000, IMMUNOLOGY, V101, P68, DOI 10.1046/j.1365-2567.2000.00087.x; Ashikaga T, 2002, TOXICOL IN VITRO, V16, P711, DOI 10.1016/S0887-2333(02)00060-7; AZAM P, 2005, IN PRESS TOXICOL APP; BARRATT MD, 1992, CONTACT DERMATITIS, V27, P98, DOI 10.1111/j.1600-0536.1992.tb05217.x; Basketter DA, 2000, CONTACT DERMATITIS, V42, P344, DOI 10.1034/j.1600-0536.2000.042006344.x; Basketter DA, 2002, FOOD CHEM TOXICOL, V40, P593, DOI 10.1016/S0278-6915(01)00130-2; Basketter DA, 2001, TRENDS PHARMACOL SCI, V22, P264, DOI 10.1016/S0165-6147(00)01704-1; BASKETTER DA, 1992, ACTA DERM-VENEREOL, V72, P264; Chapuis F, 1997, EUR J IMMUNOL, V27, P431, DOI 10.1002/eji.1830270213; Coutant KD, 1999, TOXICOL SCI, V48, P74, DOI 10.1093/toxsci/48.1.74; Cumberbatch M, 2001, IMMUNOLOGY, V102, P323, DOI 10.1046/j.1365-2567.2001.01187.x; Cumberbatch M, 1997, IMMUNOLOGY, V92, P388, DOI 10.1046/j.1365-2567.1997.00360.x; Dean JH, 2001, REGUL TOXICOL PHARM, V34, P258, DOI 10.1006/rtph.2001.1497; Dearman RJ, 1998, J APPL TOXICOL, V18, P281, DOI 10.1002/(SICI)1099-1263(199807/08)18:4<281::AID-JAT506>3.0.CO;2-4; Degwert J, 1997, TOXICOL IN VITRO, V11, P613, DOI 10.1016/S0887-2333(97)00053-2; DUPUIS G, 1982, ALLERGIC CONTACT DER; ENK AH, 1992, P NATL ACAD SCI USA, V89, P1398, DOI 10.1073/pnas.89.4.1398; Felter SP, 2003, REGUL TOXICOL PHARM, V37, P1, DOI 10.1016/S0273-2300(02)00021-1; Gerberick G F, 2001, Am J Contact Dermat, V12, P156, DOI 10.1053/ajcd.2001.23926; Gerberick GF, 2004, TOXICOL SCI, V81, P332, DOI 10.1093/toxsci/kfh213; GERBERICK GF, 1992, FUND APPL TOXICOL, V19, P438, DOI 10.1016/0272-0590(92)90183-I; Haneke KE, 2001, REGUL TOXICOL PHARM, V34, P274, DOI 10.1006/rtph.2001.1498; HAUSER C, 1988, P NATL ACAD SCI USA, V85, P5625, DOI 10.1073/pnas.85.15.5625; Hulette BC, 2005, TOXICOL APPL PHARM, V209, P159, DOI 10.1016/j.taap.2005.03.019; Hulette BC, 2002, TOXICOL APPL PHARM, V182, P226, DOI 10.1006/taap.2002.9447; Kimber I, 2003, FOOD CHEM TOXICOL, V41, P1799, DOI 10.1016/S0278-6915(03)00223-0; Kimber I, 2002, CONTACT DERMATITIS, V47, P315, DOI 10.1034/j.1600-0536.2002.470601.x; Kimber I, 2001, TOXICOL IN VITRO, V15, P307, DOI 10.1016/S0887-2333(01)00027-3; KIMBER I, 1992, TOXICOL APPL PHARM, V117, P137, DOI 10.1016/0041-008X(92)90230-P; KIMBER I, 1992, FOOD CHEM TOXICOL, V30, P165, DOI 10.1016/0278-6915(92)90153-C; KIMBER I, 1991, FOOD CHEM TOXICOL, V29, P125, DOI 10.1016/0278-6915(91)90167-6; Kimber I, 1997, HUM ECOL RISK ASSESS, V3, P385; Krasteva M, 1996, CLIN EXP ALLERGY, V26, P563, DOI 10.1046/j.1365-2222.1996.d01-342.x; MAURER T, 1994, TOXICOLOGY, V93, P47, DOI 10.1016/0300-483X(94)90195-3; MOULON C, 1993, IMMUNOLOGY, V80, P373; Patlewicz G, 2001, CONTACT DERMATITIS, V44, P331, DOI 10.1034/j.1600-0536.2001.044006331.x; Patlewicz GY, 2004, CONTACT DERMATITIS, V50, P91, DOI 10.1111/j.0105-1873.2004.00322.x; Patlewicz GY, 2002, CONTACT DERMATITIS, V47, P219, DOI 10.1034/j.1600-0536.2002.470406.x; Pichowski JS, 2001, J APPL TOXICOL, V21, P115, DOI 10.1002/jat.742; Pichowski JS, 2000, TOXICOL IN VITRO, V14, P351, DOI 10.1016/S0887-2333(00)00030-8; POTTS RO, 1992, PHARMACEUT RES, V9, P663, DOI 10.1023/A:1015810312465; Reutter K, 1997, TOXICOL IN VITRO, V11, P619, DOI 10.1016/S0887-2333(97)00048-9; Roberts DW, 2000, CONTACT DERMATITIS, V42, P154, DOI 10.1034/j.1600-0536.2000.042003154.x; Rougier N, 2000, TOXICOLOGY, V145, P73, DOI 10.1016/S0300-483X(99)00222-X; Rustemeyer T, 2003, EXP DERMATOL, V12, P682, DOI 10.1034/j.1600-0625.2003.00077.x; Sailstad DM, 2001, REGUL TOXICOL PHARM, V34, P249, DOI 10.1006/rtph.2001.1496; SALLUSTO F, 1994, J EXP MED, V179, P1109, DOI 10.1084/jem.179.4.1109; SMITH CK, 2001, ALLERGIC CONTACT DER; Steiling W, 2001, FOOD CHEM TOXICOL, V39, P293, DOI 10.1016/S0278-6915(00)00147-2; Tuschl H, 2001, TOXICOL IN VITRO, V15, P327, DOI 10.1016/S0887-2333(01)00030-3; Warbrick EV, 1999, J APPL TOXICOL, V19, P255, DOI 10.1002/(SICI)1099-1263(199907/08)19:4<255::AID-JAT573>3.0.CO;2-S; Yoshida Y, 2003, TOXICOL IN VITRO, V17, P221, DOI 10.1016/S0887-2333(03)00006-7	53	119	119	0	2	JOHN WILEY & SONS LTD	CHICHESTER	THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND	0260-437X			J APPL TOXICOL	J. Appl. Toxicol.	JUL-AUG	2006	26	4					341	350		10.1002/jat.1146		10	Toxicology	Toxicology	066KF	WOS:000239227600007	16773645	
J	Pitchford, SC; Momi, S; Giannini, S; Casali, L; Spina, D; Page, CP; Gresele, P				Pitchford, SC; Momi, S; Giannini, S; Casali, L; Spina, D; Page, CP; Gresele, P			Platelet P-selectin is required for pulmonary eosinophil and lymphocyte recruitment in a murine model of allergic inflammation	BLOOD			English	Article							PLATELET/POLYMORPHONUCLEAR LEUKOCYTE INTERACTION; ENDOTHELIUM IN-VIVO; GLYCOPROTEIN LIGAND-1; BRONCHIAL-ASTHMA; DEFICIENT MICE; WHOLE-BLOOD; CROSS-TALK; ADHESION; BETA(2)-INTEGRIN; CD11B/CD18	Platelets are necessary for lung leukocyte recruitment in a murine model of allergic inflammation, and platelet-leukocyte aggregates are formed in circulating blood of patients with asthma after allergen exposure. However, it is unknown how platelets induce pulmonary leukocyte recruitment in asthma. Here, we have investigated the importance of platelet adhesion molecule expression on pulmonary eosinophil and lymphocyte recruitment and on leukocyte CD11b and very late antigen (VLA)-4 expression in mice. Pulmonary leukocyte recruitment in platelet-depleted mice (sensitized and exposed to ovalbumin) transfused with fixed, unstimulated platelets (FUSPs) was abolished, whereas transfusion with platelets stimulated and fixed (FSPs), expressing P-selectin and P-selectin glycoprotein ligand-1 (PSGL-1), restored eosinophil and lymphocyte recruitment. Transfusion with platelets from P-selectin-deficient mice, or with FSPs stimulated in the presence of a blocking anti-P-selectin antibody, were unable to restore pulmonary leukocyte recruitment. Flow cytometric analysis revealed increased expression of CD11b and VLA-4 on leukocytes attached to platelets after allergen exposure, and CD11b expression on leukocytes was suppressed in thrombocytopenic mice but was restored with the transfusion of FSPs, but not FUSPs, a phenomenon concurrent with the formation of platelet-leukocyte complexes. P-selectin expression on the surfaces of platelets is a major requirement for pulmonary eosinophil and lymphocyte recruitment, allowing circulating platelets to bind to and stimulate leukocytes for endothelial attachment. (C) 2005 by The American Society of Hematology.	Univ Perugia, Dept Internal Med, Div Internal & Cardiovasc Med, I-06126 Perugia, Italy; Kings Coll London, Sackler Inst Pulm Pharmacol, GKT Sch Biomed Sci, London WC2R 2LS, England; Univ Perugia, Pneumatol Unit, Terni, Italy	Gresele, P (reprint author), Univ Perugia, Dept Internal Med, Div Internal & Cardiovasc Med, Via E dal Pozzo, I-06126 Perugia, Italy.	grespa@unipg.it	Gresele, Paolo/F-6775-2013	Gresele, Paolo/0000-0001-5365-8445; Spina, Domenico/0000-0002-6815-1564			BARNES PJ, 1992, J INTERN MED, V231, P453; BECK MR, 1980, BIORHEOLOGY, V17, P455; Blanks JE, 1998, EUR J IMMUNOL, V28, P433, DOI 10.1002/(SICI)1521-4141(199802)28:02<433::AID-IMMU433>3.0.CO;2-U; Broide DH, 1998, AM J RESP CELL MOL, V18, P218; BRUIJNEADMIRAAL LG, 1992, BLOOD, V80, P134; Burger PC, 2003, BLOOD, V101, P2661, DOI 10.1182/blood-2002-07-2209; Cerletti C, 1999, THROMB HAEMOSTASIS, V82, P787; DeSanctis GT, 1997, J APPL PHYSIOL, V83, P681; Diacovo TG, 1996, BLOOD, V88, P146; Diacovo TG, 1996, SCIENCE, V273, P252, DOI 10.1126/science.273.5272.252; DONATI MB, 2002, PLATELETS THROMBOTIC, P824, DOI 409862349,12,1; Evangelista V, 1999, BLOOD, V93, P876; Evangelista V, 1996, BLOOD, V88, P4183; FRENETTE PS, 1995, P NATL ACAD SCI USA, V92, P7450, DOI 10.1073/pnas.92.16.7450; GOLDSMITH HL, 1981, BIORHEOLOGY, V18, P531; GRESELE P, 1982, NEW ENGL J MED, V306, P549; GRESELE P, 1993, J ALLERGY CLIN IMMUN, V91, P894, DOI 10.1016/0091-6749(93)90347-I; Huo YQ, 2003, NAT MED, V9, P61, DOI 10.1038/nm810; Jawien J, 2002, POL J PHARMACOL, V54, P157; JEFFERY PK, 1989, AM REV RESPIR DIS, V140, P1745; Jia GQ, 1999, INT IMMUNOL, V11, P1, DOI 10.1093/intimm/11.1.1; KARPATKIN S, 1981, ANN INTERN MED, V95, P636; Katayama T, 2000, CIRC RES, V86, P1031; Konstantopoulos K, 1998, CIRCULATION, V98, P873; LEY K, 1995, J EXP MED, V181, P669, DOI 10.1084/jem.181.2.669; Massberg S, 2002, J EXP MED, V196, P887, DOI 10.1084/jem.20012044; MAYADAS TN, 1993, CELL, V74, P541, DOI 10.1016/0092-8674(93)80055-J; Moritani C, 1998, CHEST, V113, P452, DOI 10.1378/chest.113.2.452; Peters MJ, 1999, BRIT J HAEMATOL, V106, P391, DOI 10.1046/j.1365-2141.1999.01553.x; Pitchford SC, 2004, BLOOD, V103, P639, DOI 10.1182/blood-2003-05-1707; Pitchford SC, 2003, J ALLERGY CLIN IMMUN, V112, P109, DOI 10.1067/mai.2003.1514; RINDER HM, 1991, BLOOD, V78, P1730; Schmidtke DW, 2000, J CELL BIOL, V149, P719, DOI 10.1083/jcb.149.3.719; Schober A, 2002, CIRCULATION, V106, P1523, DOI 10.1161/01.CIR.0000028590.02477.6F; Singbartl K, 2001, FASEB J, V15, P2337, DOI 10.1096/fj.01-0199com; Sullivan PJ, 2000, RESPIRATION, V67, P514, DOI 10.1159/000067466; TANGELDER GJ, 1982, MICROVASC RES, V23, P214, DOI 10.1016/0026-2862(82)90066-8; Teixeira MM, 1998, J IMMUNOL, V161, P2516; Theoret JF, 2001, J PHARMACOL EXP THER, V298, P658; Ulfman LH, 2003, AM J RESP CELL MOL, V28, P512, DOI 10.1165/rcmb.4806; YAMAMOTO H, 1993, J ALLERGY CLIN IMMUN, V91, P79, DOI 10.1016/0091-6749(93)90299-U	41	119	122	3	5	AMER SOC HEMATOLOGY	WASHINGTON	1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA	0006-4971			BLOOD	Blood	MAR 1	2005	105	5					2074	2081		10.1182/blood-2004-06-2282		8	Hematology	Hematology	901UU	WOS:000227308400042	15528309	
J	Noverr, MC; Noggle, RM; Toews, GB; Huffnagle, GB				Noverr, MC; Noggle, RM; Toews, GB; Huffnagle, GB			Role of antibiotics and fungal microbiota in driving pulmonary allergic responses	INFECTION AND IMMUNITY			English	Article							ORAL TOLERANCE INDUCTION; REGULATORY T-CELLS; BRONCHOPULMONARY ASPERGILLOSIS; CANDIDA-ALBICANS; MURINE MODEL; AIRWAY HYPERREACTIVITY; LYMPHOKINE PRODUCTION; PROSTAGLANDIN D-2; EARLY-CHILDHOOD; PEYERS-PATCHES	Over the past four decades, there has been a significant increase in allergy and asthma in westernized countries, which correlates with alterations in fecal microbiota (microflora) and widespread use of antibiotics (the "hygiene hypothesis"). Antibiotics also lead to overgrowth of the yeast Candida albicans, which can secrete potent prostaglandin-like immune response modulators. We have developed a mouse model of antibiotic-induced microbiota disruption that includes stable increases in gastrointestinal (GI) enteric bacteria and GI Candida levels with no introduction of microbes into the lungs. Mice are treated for 5 days with cefoperazone in the drinking water, followed by a single oral gavage of C albicans. This results in alterations of GI bacterial populations and increased yeast numbers in the GI microbiota for at least 2 to 3 weeks and can drive the development of a CD4 T-cell-mediated allergic airway response to subsequent mold spore (Aspergillus fumigatus) exposure in immunocompetent mice without previous systemic antigen priming. The allergic response in the lungs is characterized by increased levels of eosinophils, mast cells, interleukin-5 (IL-5), IL-13, gamma interferon, immunoglobulin E, and mucus-secreting cells. In the absence of antibiotics, mice exposed to Aspergillus spores do not develop an allergic response in the airways. This study provides the first experimental evidence to support a role for antibiotics and fungal microbiota in promoting the development of allergic airway disease. In addition, these studies also highlight the concept that events in distal mucosal sites such as the GI tract can play an important role in regulating immune responses in the lungs.	Univ Michigan, Sch Med, Dept Internal Med, Div Pulm & Crit Care Med, Ann Arbor, MI 48109 USA; Univ Michigan, Sch Med, Dept Microbiol & Immunol, Ann Arbor, MI 48109 USA	Huffnagle, GB (reprint author), Univ Michigan, Sch Med, Dept Internal Med, Div Pulm & Crit Care Med, Ann Arbor, MI 48109 USA.	ghuff@umich.edu			NHLBI NIH HHS [R01 HL065912, 2T32HL007749-11, R01-HL65912, T32 HL007749]; NIAID NIH HHS [R01 AI059201, R01-AI059201]		Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; Angeli V, 2001, J EXP MED, V193, P1135, DOI 10.1084/jem.193.10.1135; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; BETZ M, 1991, J IMMUNOL, V146, P108; Bjorksten B, 2001, J ALLERGY CLIN IMMUN, V108, P516; Blease K, 2001, J IMMUNOL, V166, P5219; Bottcher MF, 2000, CLIN EXP ALLERGY, V30, P1590; Calderone RA, 2001, CANDIDA CANDIDIASIS; Chung Y, 2002, IMMUNOBIOLOGY, V206, P408, DOI 10.1078/0171-2985-00190; Constant SL, 2000, EUR J IMMUNOL, V30, P840, DOI 10.1002/1521-4141(200003)30:3<840::AID-IMMU840>3.3.CO;2-C; 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Umetsu DT, 2002, NAT IMMUNOL, V3, P715, DOI 10.1038/ni0802-715; VILLA ML, 1991, INT J IMMUNOPHARMACO, V13, P1099, DOI 10.1016/0192-0561(91)90161-Y; Whitacre CC, 1996, ANN NY ACAD SCI, V778, P217, DOI 10.1111/j.1749-6632.1996.tb21130.x; Wickens K, 1999, CLIN EXP ALLERGY, V29, P766; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; Wills-Karp M, 2001, NAT REV IMMUNOL, V1, P69, DOI 10.1038/35095579; Wjst M, 2001, EUR J MED RES, V6, P263; Wu XM, 1998, EUR J IMMUNOL, V28, P134, DOI 10.1002/(SICI)1521-4141(199801)28:01<134::AID-IMMU134>3.0.CO;2-3; Yamanaka T, 2003, J IMMUNOL, V170, P816; Zhang XM, 2001, J IMMUNOL, V167, P4245	71	119	132	0	13	AMER SOC MICROBIOLOGY	WASHINGTON	1752 N ST NW, WASHINGTON, DC 20036-2904 USA	0019-9567			INFECT IMMUN	Infect. Immun.	SEP	2004	72	9					4996	5003		10.1128/IAI.72.9.4996-5003.2004		8	Immunology; Infectious Diseases	Immunology; Infectious Diseases	849ZM	WOS:000223580400008	15321991	
J	Naisbitt, DJ; Farrell, J; Wong, G; Depta, JPH; Dodd, CC; Hopkins, JE; Gibney, CA; Chadwick, DW; Pickler, WJ; Pirmohamed, M; Park, BK				Naisbitt, DJ; Farrell, J; Wong, G; Depta, JPH; Dodd, CC; Hopkins, JE; Gibney, CA; Chadwick, DW; Pickler, WJ; Pirmohamed, M; Park, BK			Characterization of drug-specific T cells in lamotrigine hypersensitivity	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						lamotrigine; anticonvulsant hypersensitivity; T cells; antigen processing; cytokines; chemokines; T-cell receptors	TOXIC EPIDERMAL NECROLYSIS; LYMPHOCYTE-TRANSFORMATION TEST; REACTIVE METABOLITES; COVALENT BINDING; IN-VITRO; CARBAMAZEPINE; RECOGNITION; SULFAMETHOXAZOLE; CLONES; SKIN	Background: Lamotrigine is associated with hypersensitivity reactions, which are most commonly characterized by skin rash. An immune etiology has been postulated, though the nature of this is unclear. Objectives: The aim of this study was to characterize the role of T cells in lamotrigine hypersensitivity. Methods: A lymphocyte transformation test was performed on 4 hypersensitive patients. Lymphocytes from 3 of 4 lamotrigine-hypersensitive patients proliferated when stimulated with lamotrigine. T-cell clones were generated from one patient to further characterize the nature of the T-cell involvement. Cells were characterized in terms of their phenotype, functionality, and mechanisms of antigen presentation and cytotoxicity. Results: Of the 44 drug-specific T-cell clones generated, most were CD4(+) with occasional CD8(+) cells. All clones expressed the up T-cell receptor; several Vbeta 5.1(+) or 9(+) T-cell clones were generated. All clones also expressed the skin-homing receptor cutaneous lymphocyte antigen. Lamotrigine-stimulated T cells were cytotoxic and secreted perforin, IFN-gamma, IL-5, and macrophage inflammatory protein la, macrophage inflammatory protein 1beta, RANTES, and I-309. Lamotrigine was present on HLA-DR and HLA-DQ by antigen-presenting cells in the absence of drug metabolism and processing. The T-cell receptor of certain clones could accommodate analogs of lamotrigine, but no cross-reactivity was seen with other anticonvulsants. Conclusions: Our data provide evidence that T cells are involved in the pathogenesis of some lamotrigine-hypersensitivity reactions. The identification of drug-specific cells that express cutaneous lymphocyte antigen and type 1 cytokines after T-cell receptor activation is consistent with the clinical symptoms. Furthermore, identification of large numbers of Vbeta 5.1(+) T cells suggests that polymorphisms within T-cell receptor genes might act as determinants of susceptibility. (J Allergy Clin Immunol 2003;111:1393-1403.).	Univ Liverpool, Dept Pharmacol & Therapeut, Liverpool L69 3GE, Merseyside, England; Univ Liverpool, Dept Dermatol, Liverpool L69 3GE, Merseyside, England; Univ Bern, Inselspital, Clin Rheumatol & Clin Immunol Allergol, Bern, Switzerland; Univ Liverpool, Dept Neurol Sci, Liverpool L69 3BX, Merseyside, England	Naisbitt, DJ (reprint author), Univ Liverpool, Dept Pharmacol & Therapeut, Sherrington Bldg,Ashton St,POB 147, Liverpool L69 3GE, Merseyside, England.		Pirmohamed, Munir/H-6004-2011	Pirmohamed, Munir/0000-0002-7534-7266			Blanca M, 2000, ALLERGY, V55, P998, DOI 10.1034/j.1398-9995.2000.00628.x; Bocquet H, 1996, SEMIN CUTAN MED SURG, V15, P250, DOI 10.1016/S1085-5629(96)80038-1; Britschgi M, 2001, J CLIN INVEST, V107, P1433, DOI 10.1172/JCI12118; Brown KL, 1999, DEV MED CHILD NEUROL, V41, P267, DOI 10.1017/S0012162299000560; BRUNNER KT, 1968, IMMUNOLOGY, V14, P181; Dorner BG, 2002, P NATL ACAD SCI USA, V99, P6181, DOI 10.1073/pnas.092141999; FRIEDMANN PS, 1994, ARCH DERMATOL, V130, P598, DOI 10.1001/archderm.130.5.598; Gonzalez F. 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Allergy Clin. Immunol.	JUN	2003	111	6					1393	1403		10.1067/mai.2003.1507		11	Allergy; Immunology	Allergy; Immunology	688FZ	WOS:000183424700032	12789244	
J	Vonk, JM; Jongepier, H; Panhuysen, CIM; Schouten, JP; Bleecker, ER; Postma, DS				Vonk, JM; Jongepier, H; Panhuysen, CIM; Schouten, JP; Bleecker, ER; Postma, DS			Risk factors associated with the presence of irreversible airflow limitation and reduced transfer coefficient in patients with asthma after 26 years of follow up	THORAX			English	Article							AIR-FLOW OBSTRUCTION; LUNG-FUNCTION; RESPIRATORY SYMPTOMS; PULMONARY-FUNCTION; BRONCHIAL-ASTHMA; DECLINE; CHILDHOOD; ADULTS; HYPERRESPONSIVENESS; PERSISTENCE	Background: Childhood asthma is generally believed to be a disorder with a good prognosis. However, some asthmatics develop irreversible airway obstruction, probably as a result of airway remodelling. Methods: After 21-33 years, 228 adults (aged 13-44 years at baseline) with a history of asthma were re-examined to assess risk factors for the development of irreversible airway obstruction (IAO, forced expiratory volume in 1 second (FEV1) <80% predicted and reversibility <9% predicted) and a reduced postbronchodilator transfer coefficient (carbon monoxide transfer factor/alveolar volume, <80% predicted), both characteristics of COPD. Results: At follow up, 41% did not have airway obstruction (NAO), 43% had reversible airway obstruction (RAO), and 16% had IAO; 23% had a reduced transfer coefficient. Patients with RAO had asthma-like characteristics (wheezing, asthma attacks, bronchial hyperresponsiveness (BHR)) while patients with IAO had COPD-like symptoms (cough, phlegm, dyspnoea) at follow up. The development of IAO is determined by a lower FEV1, less reversibility of airway obstruction and, surprisingly, less severe BHR at initial screening. Eighty percent of the patients with asthma who used anti-inflammatory medication still had airway obstruction, but IAO developed less frequently. Smoking was associated with a reduced transfer coefficient but not with the development of IAO. Female sex was associated with a reduced transfer coefficient, whereas corticosteroid use was not. Conclusions: Although IAO and a low transfer coefficient are both characteristics of COPD, they represent distinct entities in adult asthmatics in terms of symptomatology, aetiology, and probably in therapeutic approaches and disease prevention.	Univ Groningen Hosp, Dept Pulmonol, NL-9713 GZ Groningen, Netherlands; Univ Groningen, Dept Epidemiol & Stat, NL-9700 AB Groningen, Netherlands; Beatrixoord Hosp, Haren, Netherlands; Boston Univ, Sch Med, Boston, MA 02118 USA; Boston Univ, Sch Publ Hlth, Boston, MA 02118 USA; Univ Maryland, Baltimore, MD 21201 USA	Postma, DS (reprint author), Univ Groningen Hosp, Dept Pulmonol, Hanzepl 1, NL-9713 GZ Groningen, Netherlands.						Committee on Diagnostic Standards for Nontuberculous Respiratory Diseases American Thoracic Society, 1962, AM REV RESPIR DIS, V85, P762; American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P225, DOI DOI 10.1164/AJRCCM/136.1.225; Backman KS, 1997, CHEST, V112, P1234, DOI 10.1378/chest.112.5.1234; BOOYNOORD H, 1957, INT ARCH ALLER A IMM, V10, P321; BOULET LP, 1994, CHEST, V105, P1024, DOI 10.1378/chest.105.4.1024; BROWN PJ, 1984, THORAX, V39, P131, DOI 10.1136/thx.39.2.131; DEGOOIJER A, 1993, EUR RESPIR J, V6, P848; Elias JA, 2000, AM J RESP CRIT CARE, V161, pS168; FINUCANE KE, 1985, MED J AUSTRALIA, V142, P602; GERRITSEN J, 1989, AM REV RESPIR DIS, V140, P1325; Grol MH, 1999, AM J RESP CRIT CARE, V160, P1830; Hudon C, 1997, ANN ALLERG ASTHMA IM, V78, P195; Lange P, 1998, NEW ENGL J MED, V339, P1194, DOI 10.1056/NEJM199810223391703; LYNCH DA, 1993, RADIOLOGY, V188, P829; Panhuysen CIM, 1997, AM J RESP CRIT CARE, V155, P1267; PEAT JK, 1987, EUR J RESPIR DIS, V70, P171; ROORDA RJ, 1994, J ALLERGY CLIN IMMUN, V93, P575, DOI 10.1016/S0091-6749(94)70069-9; ROORDA RJ, 1993, AM REV RESPIR DIS, V148, P1490; ROORDA RJ, 2001, PEDIATR PULM, V18, P99; SAKAI F, 1987, J COMPUT ASSIST TOMO, V11, P963, DOI 10.1097/00004728-198711000-00007; SELROOS O, 1995, CHEST, V108, P1228, DOI 10.1378/chest.108.5.1228; Ulrik CS, 1999, EUR RESPIR J, V14, P892, DOI 10.1034/j.1399-3003.1999.14d27.x; ULRIK CS, 1994, AM J RESP CRIT CARE, V150, P629; VANBORK EL, 1978, THESIS RIJKSUNIVERSI; Vignola AM, 2000, J ALLERGY CLIN IMMUN, V105, P1041, DOI 10.1067/mai.2000.107195; XU X, 1994, EUR RESPIR J, V7, P1056	26	119	127	0	3	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	APR	2003	58	4					322	327		10.1136/thorax.58.4.322		6	Respiratory System	Respiratory System	666BT	WOS:000182156300010	12668795	
J	Platts-Mills, TAE				Platts-Mills, TAE			The role of immunoglobulin E in allergy and asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						pathophysiology; asthma; allergy; IgE; allergic cascade	HOUSE-DUST MITE; SKIN-TEST REACTIVITY; FC-EPSILON-RI; MAST-CELLS; SERUM IGE; AIRWAY RESPONSIVENESS; ATOPIC-DERMATITIS; CHILDHOOD ASTHMA; EARLY EXPOSURE; CHILDREN	it has been nearly a century since the first suggestion that a soluble factor in plasma or serum might be responsible for the symptoms of allergic disease and asthma, and more than 30 yr since immunoglobulin E (IgE) was identified as the key molecule in mediating what are now described as type 1 hypersensitivity reactions (allergic asthma, allergic rhinitis, food allergy, atopic dermatitis, some forms of drug allergy, and insect sting allergy). Since that time, many of the details of the inflammatory cascade underlying allergy and asthma have been elucidated, and IgE is now known to play a key upstream role. The goals of this report are to review the cellular and molecular events set in motion by IgE and to examine the evidence for its participation in both the immediate allergic response and the late-phase or chronic inflammatory response in the skin and lungs.	Univ Virginia, Med Ctr, Div Allergy & Immunol, Charlottesville, VA 22908 USA	Platts-Mills, TAE (reprint author), Univ Virginia, Med Ctr, Div Allergy & Immunol, Box 225, Charlottesville, VA 22908 USA.				NIAID NIH HHS [AI-20565, P01-AI50989]		Borish LC, 1999, AM J RESP CRIT CARE, V160, P1816; BRADDING P, 1992, J EXP MED, V176, P1381, DOI 10.1084/jem.176.5.1381; BURROWS B, 1989, NEW ENGL J MED, V320, P271, DOI 10.1056/NEJM198902023200502; BUSSE WW, 1995, AM J RESP CRIT CARE, V152, P388; Chang TW, 2000, NAT BIOTECHNOL, V18, P157, DOI 10.1038/72601; Fahy J V, 2000, Curr Opin Pulm Med, V6, P15, DOI 10.1097/00063198-200001000-00004; Haselden BM, 1999, J EXP MED, V189, P1885, DOI 10.1084/jem.189.12.1885; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; ISHIZAKA K, 1966, J IMMUNOL, V97, P75; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; MITCHELL EB, 1986, BRIT J DERMATOL, V114, P65, DOI 10.1111/j.1365-2133.1986.tb02780.x; MITCHELL EB, 1984, J INVEST DERMATOL, V83, P290, DOI 10.1111/1523-1747.ep12340423; Oettgen HC, 1999, J CLIN INVEST, V104, P829, DOI 10.1172/JCI8205; Patalano F, 1999, ALLERGY, V54, P103; Pearlman DS, 1999, J ALLERGY CLIN IMMUN, V104, pS132; Peat JK, 1999, J ALLERGY CLIN IMMUN, V103, P1, DOI 10.1016/S0091-6749(99)70517-8; Peat JK, 1996, AM J RESP CRIT CARE, V153, P141; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; Platts-Mills TAE, 2000, J ALLERGY CLIN IMMUN, V106, P441; Platts-Mills TAE, 2000, J ALLERGY CLIN IMMUN, V106, P787, DOI 10.1067/mai.2000.110548; PRESTA L, 1994, J BIOL CHEM, V269, P26368; Rajakulasingam K, 1997, J ALLERGY CLIN IMMUN, V100, P78; RAWLE FC, 1984, J IMMUNOL, V133, P195; Ronmark E, 1999, ALLERGY, V54, P926, DOI 10.1034/j.1398-9995.1999.00044.x; SEARS MR, 1991, NEW ENGL J MED, V325, P1067, DOI 10.1056/NEJM199110103251504; Smith AM, 1998, J ALLERGY CLIN IMMUN, V101, P423; Sporik R, 1999, THORAX, V54, P675; SPORIK R, 1995, AM J RESP CRIT CARE, V151, P1388; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; Squillace SP, 1997, AM J RESP CRIT CARE, V156, P1760; SUNYER J, 1995, J ALLERGY CLIN IMMUN, V95, P699, DOI 10.1016/S0091-6749(95)70175-3; Ward GW, 1999, J ALLERGY CLIN IMMUN, V104, P541, DOI 10.1016/S0091-6749(99)70321-0; Williams CMM, 2000, J ALLERGY CLIN IMMUN, V105, P847, DOI 10.1067/mai.2000.106485; Woodfolk JA, 2000, J IMMUNOL, V165, P4379; Yamaguchi M, 1997, J EXP MED, V185, P663, DOI 10.1084/jem.185.4.663	35	119	124	1	15	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	OCT 15	2001	164	8		S			S1	S5				5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	497DV	WOS:000172438200001	11704610	
J	Rastogi, SC; Heydorn, S; Johansen, JD; Basketter, DA				Rastogi, SC; Heydorn, S; Johansen, JD; Basketter, DA			Fragrance chemicals in domestic and occupational products	CONTACT DERMATITIS			English	Article						fragrance chemicals; domestic and occupational products; chemical analysis; fragrance mix (FM)	CONTACT ALLERGY; PATCH TEST; CONSTITUENTS; MIX; DERMATITIS; DEODORANTS; COSMETICS; PERFUMES	Epidemiological studies have described an increasing prevalence of fragrance allergy and indicated an association with hand eczema. 59 domestic and occupational products intended for hand exposure were subjected to gas chromatography-mass spectrometric (GC-MS) analyses to test the hypothesis that fragrance chemicals known to have the potential to cause contact allergy but not included in fragrance mix (FM) may be common ingredients in these products. A quantitative analysis of 19 selected fragrances was performed by GC-MS. Further analysis of GC-MS data revealed the presence of 43 other fragrance chemicals/groups of fragrance chemicals in the products investigated. Among the 19 target substances the most commonly detected were limonene in 78%, linalool in 61% and citronellol in 47% of the products investigated. The FM ingredients were present in these products with the following frequencies: oak moss (evernic acid methylester) 2%, cinnamic, alcohol 2%, cinnamic aldehyde (cinnamal) 3%, isoeugenol 5%, alpha -amylcinnamic aldehyde (amyl cinnamal) 8%, hydroxycitronellal 12%, eugenol 27%, and geraniol 41%. Thus, the chemical analyses of domestic and occupational products indicates that investigation of potential contact allergy related to these products types should consider fragrance allergens additional to those in the FM, since these may occur with high frequency. (C) Munksgaard, 2001.	Natl Environm Res Inst, Dept Environm Chem, DK-4000 Roskilde, Denmark; Univ Copenhagen, Gentofte Hosp, Dept Dermatol, DK-1168 Copenhagen, Denmark; Unilever Res, SEAC Toxicol, Sharnbrook, Beds, England	Rastogi, SC (reprint author), Natl Environm Res Inst, Dept Environm Chem, Frederiksborgvej 399,POB 358, DK-4000 Roskilde, Denmark.						Buckley DA, 2000, CONTACT DERMATITIS, V43, P304; CHRISTOPHERSEN J, 1989, CONTACT DERMATITIS, V21, P291, DOI 10.1111/j.1600-0536.1989.tb04746.x; EU Scientific Committee on Cosmetic and Non-Food Products Intended for Consumers, 1999, FRAGR ALL CONS REV P; FROSCH PJ, 1995, CONTACT DERMATITIS, V33, P333, DOI 10.1111/j.1600-0536.1995.tb02048.x; JOHANSEN JD, 1995, CONTACT DERMATITIS, V32, P18, DOI 10.1111/j.1600-0536.1995.tb00834.x; Johansen JD, 1997, ACTA DERM-VENEREOL, V77, P149; Johansen JD, 1996, BRIT J DERMATOL, V135, P419, DOI 10.1111/j.1365-2133.1996.tb01506.x; Johansen JD, 1996, CONTACT DERMATITIS, V34, P106, DOI 10.1111/j.1600-0536.1996.tb02139.x; KARLBERG AT, 1991, ANN OCCUP HYG, V35, P419, DOI 10.1093/annhyg/35.4.419; Opdyke DJL, 1975, FD COSMET TOXCOL S, V13, P825; Rastogi SC, 1998, CONTACT DERMATITIS, V39, P293, DOI 10.1111/j.1600-0536.1998.tb05944.x; Rastogi SC, 1998, CONTACT DERMATITIS, V38, P29, DOI 10.1111/j.1600-0536.1998.tb05633.x; RASTOGI SC, 1995, HRC-J HIGH RES CHROM, V18, P653; Rastogi SC, 1999, CONTACT DERMATITIS, V41, P84; SCHNUCH A, 1993, DERMATOS BER UMWELT, V41, P60	15	119	121	3	24	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-1873			CONTACT DERMATITIS	Contact Dermatitis	OCT	2001	45	4					221	225		10.1034/j.1600-0536.2001.450406.x		5	Allergy; Dermatology	Allergy; Dermatology	481WY	WOS:000171544500006	11683833	
J	Hammad, H; Charbonnier, AS; Duez, C; Jacquet, A; Stewart, GA; Tonnel, AB; Pestel, J				Hammad, H; Charbonnier, AS; Duez, C; Jacquet, A; Stewart, GA; Tonnel, AB; Pestel, J			Th2 polarization by Der p 1-pulsed monocyte-derived dendritic cells is due to the allergic status of the donors	BLOOD			English	Article							DUST MITE ALLERGEN; COSTIMULATORY MOLECULES; INTERLEUKIN (IL)-12; ATOPIC-DERMATITIS; LANGERHANS CELLS; DOWN-REGULATION; UP-REGULATION; IGE SYNTHESIS; CLASS-II; T-CELLS	The polarization of the immune response toward a Th2 or a Th1 profile can be mediated by dendritic cells (DCs) following antigen presentation and interaction with T cells. Costimulatory molecules such as CD80 and CD86 expressed by DCs, the polarizing cytokine environment during DC-T-cell interaction, and also the nature of the antigen are critical in the orientation of the immune response. In this study, the effect of the cysteine protease Der p 1, one of the major allergens of the house dust mite Dermatophagoides, pteronyssinus, on these different parameters was evaluated comparatively on monocyte-derived DCs obtained from healthy donors, from pollen-sensitive patients, or from patients sensitive to Dermatophagoides pteronyssinus. Results showed that Der p 1 induced an increase in CD86 expression only on DCs from house dust mite-sensitive patients. This was also associated with a higher capacity to induce T-cell proliferation, a rapid increase in the production of proinflammatory cytokines, tumor necrosis factor-alpha and interleukin (IL)-1 beta, and the type 2 cytokine IL-10. No changes in the release of IL-12 p70 were induced by Der p 1. Finally, purified T cells from house dust mite-sensitive patients stimulated by autologous Der p 1-pulsed DCs preferentially produced IL-4 rather than interferon-gamma. These effects were abolished ih the presence of the inactive precursor of Der p 1 (ProDer p 1). Taken together, these data suggest that DCs from house dust mite-sensitive patients, in contrast to DCs from healthy donors and from pollen-sensitive patients, exposed to Der p 1 play a pivotal role in the enhancement of the Th2 response associated with the allergic reaction developed in response to house dust mite exposure.	Inst Pasteur, INSERM, U416, F-59019 Lille, France; Free Univ Brussels, Dept Appl Genet, Gosselies, Belgium; Univ Western Australia, Dept Microbiol, Nedlands, WA 6009, Australia; CHRU Lille, Hop A Calmette, Dept Pneumol, Lille, France	Pestel, J (reprint author), Inst Pasteur, INSERM, U416, 1 Rue Professeur Calmette,BP-245, F-59019 Lille, France.		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NW SUITE 200, WASHINGTON, DC 20036 USA	0006-4971			BLOOD	Blood	AUG 15	2001	98	4					1135	1141		10.1182/blood.V98.4.1135		7	Hematology	Hematology	461KU	WOS:000170364100034	11493462	
J	Gao, Y; Nish, SA; Jiang, RY; Hou, L; Licona-Limon, P; Weinstein, JS; Zhao, HY; Medzhitov, R				Gao, Yan; Nish, Simone A.; Jiang, Ruoyi; Hou, Lin; Licona-Limon, Paula; Weinstein, Jason S.; Zhao, Hongyu; Medzhitov, Ruslan			Control of T Helper 2 Responses by Transcription Factor IRF4-Dependent Dendritic Cells	IMMUNITY			English	Article							INTERFERON REGULATORY FACTOR-4; DUST MITE ALLERGEN; IN-VIVO; TYPE-2 IMMUNITY; CONTACT HYPERSENSITIVITY; LYMPH-NODES; T-CELLS; DIFFERENTIATION; EXPRESSION; SPECIFICATION	CD4(+) T cell differentiation is regulated by specialized antigen-presenting cells. Dendritic cells (DCs) produce cytokines that promote naive CD4(+) T cell differentiation into T helper 1 (Th1), Th17, and inducible T regulatory (iTreg) cells. However, the initiation of Th2 cell responses remains poorly understood, although it is likely that more than one mechanism might be involved. Here we have defined a specific DC subset that is involved in Th2 cell differentiation in vivo in response to a protease allergen, as well as infection with Nippostrongylus brasiliensis. We have demonstrated that this subset is controlled by the transcription factor interferon regulatory factor 4 (IRF4), which is required for their differentiation and Th2 cell-inducing function. IRF4 is known to control Th2 cell differentiation and Th2 cell-associated suppressing function in Treg cells. Our finding suggests that IRF4 also plays a role in DCs where it controls the initiation of Th2 cell responses.	[Gao, Yan; Nish, Simone A.; Licona-Limon, Paula; Weinstein, Jason S.; Medzhitov, Ruslan] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT 06520 USA; [Gao, Yan] Yale Univ, Sch Med, Dept Cell Biol, New Haven, CT 06520 USA; [Jiang, Ruoyi] Yale Univ, Dept Mol Cellular & Dev Biol, New Haven, CT 06520 USA; [Hou, Lin] Yale Univ, Sch Publ Hlth, Dept Biostat, New Haven, CT 06520 USA; [Medzhitov, Ruslan] Yale Univ, Sch Med, Howard Hughes Med Inst, New Haven, CT 06520 USA	Medzhitov, R (reprint author), Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT 06520 USA.	ruslan.medzhitov@yale.edu			National Institutes of Health [RO1 AI08977, 5RO1 AI055502, R37 AI046688]; Howard Hughes Medical Institute	We would like to thank A. Iwasaki, Y. Kumamoto, U. Klein, B. Reizis, L. Chen, and A. Pernis for providing reagents. This study was supported by a grant from the National Institutes of Health (RO1 AI08977, 5RO1 AI055502, and R37 AI046688) and the Howard Hughes Medical Institute.	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J	van Nimwegen, FA; Penders, J; Stobberingh, EE; Postma, DS; Koppelman, GH; Kerkhof, M; Reijmerink, NE; Dompeling, E; van den Brandt, PA; Ferreira, I; Mommers, M; Thijs, C				van Nimwegen, Frederika A.; Penders, John; Stobberingh, Ellen E.; Postma, Dirkje S.; Koppelman, Gerard H.; Kerkhof, Marjan; Reijmerink, Naomi E.; Dompeling, Edward; van den Brandt, Piet A.; Ferreira, Isabel; Mommers, Monique; Thijs, Carel			Mode and place of delivery, gastrointestinal microbiota, and their influence on asthma and atopy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Mode of delivery; cesarean section; hospital delivery; gastrointestinal microbiota composition; wheeze; eczema; asthma; atopy; mediation analysis; cohort study; KOALA study	KOALA BIRTH COHORT; INTESTINAL MICROFLORA; CESAREAN-SECTION; FECAL MICROFLORA; CHILDHOOD; ALLERGY; CHILDREN; INFANTS; RISK; GUT	Background: Both gastrointestinal microbiota composition and cesarean section have been linked to atopic manifestations. However, results are inconsistent, and the hypothesized intermediate role of the microbiota in the association between birth mode and atopic manifestations has not been studied yet. Objectives: We sought to investigate the relationship between microbiota composition, mode and place of delivery, and atopic manifestations. Methods: The Child, Parent and Health: Lifestyle and Genetic Constitution Birth Cohort Study included data on birth characteristics, lifestyle factors, and atopic manifestations collected through repeated questionnaires from birth until age 7 years. Fecal samples were collected at age 1 month (n = 1176) to determine microbiota composition, and blood samples were collected at ages 1 (n = 921), 2 (n = 822), and 6 to 7 (n = 384) years to determine specific IgE levels. Results: Colonization by Clostridium difficile at age 1 month was associated with wheeze and eczema throughout the first 6 to 7 years of life and with asthma at age 6 to 7 years. Vaginal home delivery compared with vaginal hospital delivery was associated with a decreased risk of eczema, sensitization to food allergens, and asthma. After stratification for parental history of atopy, the decreased risk of sensitization to food allergens (adjusted odds ratio, 0.52; 95% CI, 0.35-0.77) and asthma (adjusted odds ratio, 0.47; 95% CI, 0.29-0.77) among vaginally home-born infants was only found for children with atopic parents. Mediation analysis showed that the effects of mode and place of delivery on atopic outcomes were mediated by C difficile colonization. Conclusion: Mode and place of delivery affect the gastrointestinal microbiota composition, which subsequently influences the risk of atopic manifestations. (J Allergy Clin Immunol 2011;128:948-55.)	[van Nimwegen, Frederika A.; Penders, John; Mommers, Monique; Thijs, Carel] Maastricht Univ, Dept Epidemiol, CAPHRI Sch Publ Hlth & Primary Care, Med Ctr, NL-6200 MD Maastricht, Netherlands; [Penders, John; Stobberingh, Ellen E.] Maastricht Univ, Dept Med Microbiol, CAPHRI Sch Publ Hlth & Primary Care, Med Ctr, NL-6200 MD Maastricht, Netherlands; [Dompeling, Edward] Maastricht Univ, Dept Pediat Pulmonol, CAPHRI Sch Publ Hlth & Primary Care, Med Ctr, NL-6200 MD Maastricht, Netherlands; [Ferreira, Isabel] Maastricht Univ, Dept Clin Epidemiol & Med Technol Assessment, CAPHRI Sch Publ Hlth & Primary Care, Med Ctr, NL-6200 MD Maastricht, Netherlands; [Ferreira, Isabel] Maastricht Univ, Dept Internal Med, CAPHRI Sch Publ Hlth & Primary Care, Med Ctr, NL-6200 MD Maastricht, Netherlands; [Postma, Dirkje S.; Reijmerink, Naomi E.] Univ Groningen, Beatrix Childrens Hosp, Dept Pulmonol, NL-9700 AB Groningen, Netherlands; [Koppelman, Gerard H.] Univ Groningen, Beatrix Childrens Hosp, Dept Pediat Pulmonol & Pediat Allergol, NL-9700 AB Groningen, Netherlands; [Kerkhof, Marjan] Univ Groningen, Univ Med Ctr Groningen, Dept Epidemiol, NL-9700 AB Groningen, Netherlands; [Reijmerink, Naomi E.] Univ Groningen, Univ Med Ctr Groningen, Beatrix Childrens Hosp, NL-9700 AB Groningen, Netherlands; [van den Brandt, Piet A.] Maastricht Univ, Dept Epidemiol, Sch Oncol & Dev Biol GROW, Med Ctr, NL-6200 MD Maastricht, Netherlands	Penders, J (reprint author), Maastricht Univ, Dept Epidemiol, CAPHRI Sch Publ Hlth & Primary Care, Med Ctr, POB 616, NL-6200 MD Maastricht, Netherlands.	j.penders@maastrichtuniversity.nl	Ferreira, Isabel/B-6033-2008	Ferreira, Isabel/0000-0003-1434-0607	Netherlands Asthma Foundation [3.2.07.022, 3.2.03.48]; Stichting Astma Bestrijding; Dutch Biobanking and Biomolecular Resources Infrastructure (BBMRI-NL); Topinstitute Pharma; GlaxoSmithKline; AstraZeneca	Supported by the Netherlands Asthma Foundation (grant no. 3.2.07.022&3.2.03.48), the Stichting Astma Bestrijding, and the Dutch Biobanking and Biomolecular Resources Infrastructure (BBMRI-NL).; Disclosure of potential conflict of interest: D. S. Postma has consultant arrangements with Nycomed and has received research support from Topinstitute Pharma and AstraZeneca. G. H. Koppelman has received honoraria and research support from GlaxoSmithKline. C. Thijs has received research support from the Netherlands Asthma Foundation. The rest of the authors have declared that they have no conflict of interest.	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Allergy Clin. Immunol.	NOV	2011	128	5					948	U371		10.1016/j.jaci.2011.07.027		11	Allergy; Immunology	Allergy; Immunology	842FJ	WOS:000296578200005	21872915	
J	Ziska, L; Knowlton, K; Rogers, C; Dalan, D; Tierney, N; Elder, MA; Filley, W; Shropshire, J; Ford, LB; Hedberg, C; Fleetwood, P; Hovanky, KT; Kavanaugh, T; Fulford, G; Vrtis, RF; Patz, JA; Portnoy, J; Coates, F; Bielory, L; Frenz, D				Ziska, Lewis; Knowlton, Kim; Rogers, Christine; Dalan, Dan; Tierney, Nicole; Elder, Mary Ann; Filley, Warren; Shropshire, Jeanne; Ford, Linda B.; Hedberg, Curtis; Fleetwood, Pamela; Hovanky, Kim T.; Kavanaugh, Tony; Fulford, George; Vrtis, Rose F.; Patz, Jonathan A.; Portnoy, Jay; Coates, Frances; Bielory, Leonard; Frenz, David			Recent warming by latitude associated with increased length of ragweed pollen season in central North America	PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA			English	Article						aerobiology; allergies; global warming	AMBROSIA-ARTEMISIIFOLIA L.; CLIMATE-CHANGE; COMMON RAGWEED; PUBLIC-HEALTH; UNITED-STATES; AEROALLERGENS; ALLERGY; URBANIZATION; TEMPERATURES; COUNTS	A fundamental aspect of climate change is the potential shifts in flowering phenology and pollen initiation associated with milder winters and warmer seasonal air temperature. Earlier floral anthesis has been suggested, in turn, to have a role in human disease by increasing time of exposure to pollen that causes allergic rhinitis and related asthma. However, earlier floral initiation does not necessarily alter the temporal duration of the pollen season, and, to date, no consistent continental trend in pollen season length has been demonstrated. Here we report that duration of the ragweed (Ambrosia spp.) pollen season has been increasing in recent decades as a function of latitude in North America. Latitudinal effects on increasing season length were associated primarily with a delay in first frost of the fall season and lengthening of the frost free period. Overall, these data indicate a significant increase in the length of the ragweed pollen season by as much as 13-27 d at latitudes above similar to 44 degrees N since 1995. This is consistent with recent Intergovernmental Panel on Climate Change projections regarding enhanced warming as a function of latitude. If similar warming trends accompany long-term climate change, greater exposure times to seasonal allergens may occur with subsequent effects on public health.	[Ziska, Lewis] ARS, Crop Syst & Global Change Lab, USDA, Beltsville, MD 20705 USA; [Knowlton, Kim] Columbia Univ, Mailman Sch Publ Hlth, Hlth & Environm Program, Nat Resources Def Council, New York, NY 10032 USA; [Knowlton, Kim] Columbia Univ, Mailman Sch Publ Hlth, Dept Environm Hlth Sci, New York, NY 10032 USA; [Rogers, Christine] Univ Massachusetts, Amherst, MA 01003 USA; [Dalan, Dan] Allergy & Asthma Care Ctr, Fargo, ND 58103 USA; [Tierney, Nicole; Elder, Mary Ann] Allergy & Asthma Specialists, Minneapolis, MN 55402 USA; [Filley, Warren; Shropshire, Jeanne] Oklahoma Allergy & Asthma Clin, Oklahoma City, OK 73104 USA; [Ford, Linda B.] Ctr Asthma & Allergy, Omaha, NE 68123 USA; [Hedberg, Curtis; Fleetwood, Pamela] Hedberg Allergy & Asthma Ctr, Rogers, AR 72758 USA; [Hovanky, Kim T.] Allergy & Asthma Ctr Georgetown, Georgetown, TX 78628 USA; [Kavanaugh, Tony; Fulford, George] Allergy Associates, La Crosse, WI 54602 USA; [Vrtis, Rose F.; Patz, Jonathan A.] Univ Wisconsin, Nelson Inst Environm Studies, Madison, WI 53706 USA; [Vrtis, Rose F.; Patz, Jonathan A.] Univ Wisconsin, Dept Populat Hlth Sci, Madison, WI 53706 USA; [Portnoy, Jay] Univ Missouri, Sch Med, Childrens Mercy Hosp, Sect Allergy Asthma & Immunol, Kansas City, MO 64108 USA; [Coates, Frances] Aerobiol Res Labs, Nepean, ON K2E 7Y5, Canada; [Bielory, Leonard] Rutgers State Univ, Ctr Environm Predict, New Brunswick, NJ 08901 USA; [Frenz, David] HealthE Care Syst, St Paul, MN 55102 USA	Ziska, L (reprint author), ARS, Crop Syst & Global Change Lab, USDA, Beltsville, MD 20705 USA.	l.ziska@ars.usda.gov	Rogers, Christine/A-2189-2008; Knowlton, Kim/A-7159-2012; Osborne, Nicholas/N-4915-2015	Rogers, Christine/0000-0003-0887-9606; Osborne, Nicholas/0000-0002-6700-2284			[Anonymous], ASTHM IMM; *ARB DAY FDN, 2006, ZON CHANG USDA PLANT; Ariano R, 2010, ANN ALLERG ASTHMA IM, V104, P215, DOI 10.1016/j.anai.2009.12.005; Beggs PJ, 2004, CLIN EXP ALLERGY, V34, P1507, DOI 10.1111/j.1365-2222.2004.02061.x; *CDCP, 2005, ALL HAYF; CHAPMAN JA, 1986, GRANA, V25, P235; Cleland EE, 2007, TRENDS ECOL EVOL, V22, P357, DOI 10.1016/j.tree.2007.04.003; Clot Bernard, 2003, Aerobiologia, V19, P227, DOI 10.1023/B:AERO.0000006572.53105.17; Dahl A., 1996, AEROBIOLOGIA, V12, P97, DOI DOI 10.1007/BF02248133; Deen W, 1998, WEED SCI, V46, P561; Dvorin DJ, 2001, ANN ALLERG ASTHMA IM, V87, P394; Emberlin J, 2002, INT J BIOMETEOROL, V46, P159, DOI 10.1007/s00484-002-0139-x; Emberlin J, 1997, GRANA, V36, P29; EMBERLIN J, 1994, ALLERGY, V49, P15, DOI 10.1111/j.1398-9995.1994.tb04233.x; ENVIRONMENT CANADA, 2011, NAT CLIM DAT INF ARC; Frenz DA, 1999, ANN ALLERG ASTHMA IM, V83, P341, DOI 10.1016/S1081-1206(10)62828-1; Frenz DA, 2001, ANN ALLERG ASTHMA IM, V86, P150; GERGEN PJ, 1987, J ALLERGY CLIN IMMUN, V80, P669, DOI 10.1016/0091-6749(87)90286-7; Hansen J, 2006, P NATL ACAD SCI USA, V103, P14288, DOI 10.1073/pnas.0606291103; *INT PAN CLIM CHAN, 2007, CLIM CHANG 2007 PHYS; Rodriguez-Rajo FJ, 2010, AEROBIOLOGIA, V26, P1, DOI 10.1007/s10453-009-9138-2; Kosisky SE, 1997, ANN ALLERG ASTHMA IM, V78, P381; Levetin E, 2008, CURR ALLERGY ASTHM R, V8, P418, DOI 10.1007/s11882-008-0081-z; Miller-Rushing AJ, 2008, TREE PHYSIOL, V28, P659; Rogers CA, 2006, ENVIRON HEALTH PERSP, V114, P865, DOI 10.1289/ehp.8549; Shea KM, 2008, J ALLERGY CLIN IMMUN, V122, P443, DOI 10.1016/j.jaci.2008.06.032; *US EPA, 2008, EPA600R06164F; Van Vliet AJH, 2002, INT J CLIMATOL, V22, P1757, DOI 10.1002/joc.820; Wayne P, 2002, ANN ALLERG ASTHMA IM, V88, P279; Wodehouse R, 1971, HAYFEVER PLANTS; Yang Y, 2010, COMPUT ELECTRON AGR, V71, P77, DOI 10.1016/j.compag.2009.12.006; Yli-Panula E, 2009, INT J ENV RES PUB HE, V6, P1706, DOI 10.3390/ijerph6061706; Ziska LH, 2000, AUST J PLANT PHYSIOL, V27, P893, DOI 10.1071/PP00032; Ziska LH, 2003, J ALLERGY CLIN IMMUN, V111, P290, DOI 10.1067/mai.2003.53	34	118	120	2	57	NATL ACAD SCIENCES	WASHINGTON	2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA	0027-8424			P NATL ACAD SCI USA	Proc. Natl. Acad. Sci. U. S. A.	MAR 8	2011	108	10					4248	4251		10.1073/pnas.1014107108		4	Multidisciplinary Sciences	Science & Technology - Other Topics	731PA	WOS:000288120400079	21368130	
J	Barber, D; de la Torre, F; Feo, F; Florido, F; Guardia, P; Moreno, C; Quiralte, J; Lombardero, M; Villalba, M; Salcedo, G; Rodriguez, R				Barber, D.; de la Torre, F.; Feo, F.; Florido, F.; Guardia, P.; Moreno, C.; Quiralte, J.; Lombardero, M.; Villalba, M.; Salcedo, G.; Rodriguez, R.			Understanding patient sensitization profiles in complex pollen areas: a molecular epidemiological study	ALLERGY			English	Article						allergens; environment; epidemiology; food allergens; pollen	OLEA-EUROPAEA POLLEN; CROSS-REACTIVITY; RELEVANT ALLERGENS; MAJOR ALLERGENS; PURIFICATION; EXPRESSION; MARKER; NOMENCLATURE; PATTERNS; OLE-E-1	Background: Allergy diagnosis in patients exposed to multiple pollen species is complex and misdiagnosis is often a cause for unsuccessful specific immunotherapy. Objective: We studied the sensitization profile of individual allergens (major, minor and pan-allergens) in pollen-sensitized patients in a region with high exposure to olive pollen by investigating the influence of minor allergens on allergic disease and the association between pan- and minor allergen sensitizations. Methods: A panel of 13 purified allergens, which included the most relevant allergens in the area, as well as minor olive allergens and pan-allergens, were screened using a high-capacity technology (ADVIA-Centaur((R))) in 891 patients. Results: Olive allergy as measured by specific IgE to Ole e 1 was the leading pollinosis in the area. The minor olive allergens Ole e 7 and Ole e 9 were markers of more severe allergic illness. Profilin sensitization was associated mainly with grass allergy, the second most prevalent pollinosis. Salsola kali pollen allergy was the third most common cause of pollinosis in the area. The prevalence of sensitization to the peach allergen Pru p 3, a nonspecific lipid-transfer protein, was notable. Conclusion: Epidemiological analysis by component-resolved diagnosis is a new method, which elucidates the interaction between allergen exposure gradient and patient sensitization. High exposure leads to differential sensitization profiles some of which are associated with more severe allergic conditions. Profilin sensitization, related mainly to grass pollinosis, was a marker of more severe grass pollen sensitization.	[Barber, D.; Lombardero, M.] ALK Abello, Dept ID, E-28037 Madrid, Spain; [de la Torre, F.] ALK Abello, Med Mkt, E-28037 Madrid, Spain; [Feo, F.] Gen Hosp, Serv Alergia, Ciudad Real, Spain; [Florido, F.] Hosp Clin, Serv Alergia, Granada, Spain; [Guardia, P.] Hosp Virgen Macarena, Serv Alergia, Seville, Spain; [Moreno, C.] Hosp Reina Sofia, Serv Alergia, Cordoba, Spain; [Quiralte, J.] Hosp Ciudad Jaen, Serv Alergia, Jaen, Spain; [Villalba, M.; Rodriguez, R.] Univ Complutense, Dept Bioquim & Biol Mol, Fac Ciencias Quim, E-28040 Madrid, Spain; [Salcedo, G.] Univ Politecn Madrid, Unidad Bioquim, Dept Biotecnol, ETS Ingn Agron, Madrid, Spain	Barber, D (reprint author), ALK Abello, Dept ID, C Miguel Fleta 19, E-28037 Madrid, Spain.		IBIS, ALERGICAS/C-1733-2016; RODRIGUEZ, ROSALIA/K-4993-2014	RODRIGUEZ, ROSALIA/0000-0002-4280-3691	ALK-Abello. S. A (Madrid, Spain)	We thank the EXPO study group for their excellent work, and the participating investigators from the following hospitals and private allergy practices: Hospital Perpetuo Socorro ( Albacete), Dr M. Barcelo (Almeria), Hospital de Don Benito, Hospital Infanta Cristina and Hospital de Merida (Badajoz), Hospital de Caceres, Hospital de Coria and Hospital de Navalmoral de la Mata (Caceres), Hospital de Jerez, Dr D. Gutierrez and Clinica Dr Lobaton (Cadiz), Hospital General (Castellon), Hospital del Carmen and Dr P. Mur (Ciudad Real), Hospital Reina Sofia (Cordoba), Hospital Clinico and Clinica ALERGOMEDIC (Granada), Hospital Clinico Virgen de la Cinta and Dr Arias Irigoyen (Huelva), Hospital Ciudad Jaen (Jaen), Hospital Carlos Haya (Malaga), Hospital de Lorca, Hospital Morales Messeguer and Hospital Virgen Arrixaca (Murcia), Clinica Santa Isabel, Hospital El Tomillar, Hospital Virgen Macarena and Hospital Virgen del Rocio (Sevilla), Dr R. Guspi, Hospital San Pau i Sta. Tecla and Hospital Virgen de la Cinta (Tarragona), Hospital Talavera and Hospital Virgen del Valle (Toledo) and Hospital de Xativa (Valencia). We thank Ms Linda Puebla and K. Shashok for language revision of the manuscript, and Ms Carmen Barrio for expert secretarial assistance. This trial was supported by ALK-Abello. S. A (Madrid, Spain).	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J	von Leupoldt, A; Sommer, T; Kegat, S; Baumann, HJ; Klose, H; Dahme, B; Buchel, C				von Leupoldt, Andreas; Sommer, Tobias; Kegat, Sarah; Baumann, Hans Joerg; Klose, Hans; Dahme, Bernhard; Buechel, Christian			The unpleasantness of perceived dyspnea is processed in the anterior insula and amygdala	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						brain; dyspnea; emotions; magnetic resonance imaging; perception	OBSTRUCTIVE PULMONARY-DISEASE; POSITRON-EMISSION-TOMOGRAPHY; AFFECTIVE DIMENSION; INTEROCEPTIVE AWARENESS; AIR HUNGER; BRAIN; PAIN; PERCEPTION; EXERCISE; ASTHMA	Rationale: The subjective perception of dyspnea, which is an impairing symptom in various cardiopulmonary diseases, consists of sensory (intensity) and affective aspects (unpleasantness). However, little is known about the cortical processing of the perception of dyspnea. Objectives: To investigate the cortical areas associated with the processing of the affective unpleasantness of perceived dyspnea. Methods: Brain imaging study using functional magnetic resonance imaging in 14 healthy volunteers. Measurements and Main Results: Dyspnea was induced by inspiratory resistive loaded breathing with concomitant positive and negative emotional stimulation by viewing standardized emotional picture series. The blood oxygen level-dependent contrast was measured as an index of local neuronal activity while respiration was continuously monitored. Negative emotional stimulation during loaded breathing was associated with higher unpleasantness of perceived dyspnea when compared with loaded breathing with concomitant positive emotional stimulation (P < 0.05). The levels of intensity of perceived dyspnea, respiratory responses, and load magnitude were similar between both conditions. Higher unpleasantness of dyspnea was associated with neuronal activations in the limbic system-that is, in the right anterior insula and in the right amygdala (respective Z values = 3.93 and 3.15; P < 0.05). Conclusions: The results of the present brain imaging study suggest that the unpleasantness of subjectively perceived dyspnea is processed in the right human anterior insula and amygdala.	[von Leupoldt, Andreas; Kegat, Sarah; Dahme, Bernhard] Univ Hamburg, Dept Psychol, D-20146 Hamburg, Germany; [von Leupoldt, Andreas; Sommer, Tobias; Buechel, Christian] Univ Med Ctr Hamburg Eppendorf, Dept Syst Neurosci Neuroimage Nord, Hamburg, Germany; [Baumann, Hans Joerg; Klose, Hans] Univ Med Ctr Hamburg Eppendorf, Dept Pneumol, Hamburg, Germany	von Leupoldt, A (reprint author), Univ Hamburg, Dept Psychol, Von Melle Pk 5, D-20146 Hamburg, Germany.	andreas.vonleupoldt@uni-hamburg.de	Frank, David/E-8213-2012				Augustine JR, 1996, BRAIN RES REV, V22, P229, DOI 10.1016/S0165-0173(96)00011-2; Banzett RB, 2000, NEUROREPORT, V11, P2117, DOI 10.1097/00001756-200007140-00012; Banzett RB, 2000, AM J RESP CRIT CARE, V162, P1178; Banzett RB, 2001, APS B, V11, P1; BERTHIER M, 1988, ANN NEUROL, V24, P41, DOI 10.1002/ana.410240109; Bingel U, 2002, PAIN, V99, P313, DOI 10.1016/S0304-3959(02)00157-4; Buchel C, 1998, NEURON, V20, P947, DOI 10.1016/S0896-6273(00)80476-6; CarrieriKohlman V, 1996, CHEST, V110, P1526, DOI 10.1378/chest.110.6.1526; CORFIELD DR, 1995, J PHYSIOL-LONDON, V488, P77; Craig AD, 2002, NAT REV NEUROSCI, V3, P655, DOI 10.1038/nrn894; Critchley HD, 2004, NAT NEUROSCI, V7, P189, DOI 10.1038/nn1176; Center for the Study of Emotion and Attention (CSEA-NIMH), 1999, INT AFF PICT SYST; Davenport PW, 1995, REGULATION BREATHING, P365; De Peuter S, 2004, CLIN PSYCHOL REV, V24, P557, DOI 10.1016/j.cpr.2004.05.001; De Peuter S, 2007, RESP MED, V101, P925, DOI 10.1016/j.rmed.2006.09.018; Evans KC, 2002, J NEUROPHYSIOL, V88, P1500, DOI 10.1152/jn.00957.2001; Farrell MJ, 2006, P NATL ACAD SCI USA, V103, P2416, DOI 10.1073/pnas.0511019103; Fink GR, 1996, J APPL PHYSIOL, V81, P1295; Friston K., 1995, HUMAN BRAIN MAPPING, P165, DOI DOI 10.1002/HBM.460030303; Giardino ND, 2007, COMPR PSYCHIAT, V48, P103, DOI 10.1016/j.comppsych.2006.11.001; Grant S, 1999, CHEST, V116, P1208, DOI 10.1378/chest.116.5.1208; Greenspan JD, 1999, PAIN, V81, P273, DOI 10.1016/S0304-3959(99)00021-4; Guz A, 1997, RESP PHYSIOL, V109, P197, DOI 10.1016/S0034-5687(97)00050-9; KILLIAN KJ, 1982, J APPL PHYSIOL, V52, P578; Lavietes MH, 2000, AM J RESP CRIT CARE, V161, P737; LEHRER PM, 1993, J PSYCHOSOM RES, V37, P515, DOI 10.1016/0022-3999(93)90007-3; Liotti M, 2001, P NATL ACAD SCI USA, V98, P2035, DOI 10.1073/pnas.98.4.2035; Meek PM, 2003, HEART LUNG, V32, P335, DOI 10.1016/S0147-9563(03)00100-6; Meek PM, 1999, AM J RESP CRIT CARE, V159, P321; MUZA SR, 1990, AM REV RESPIR DIS, V141, P909; O'Donnell Denis E, 2007, Proc Am Thorac Soc, V4, P145, DOI 10.1513/pats.200611-159CC; OGAWA S, 1990, MAGNET RESON MED, V14, P68, DOI 10.1002/mrm.1910140108; Peiffer C, 2001, AM J RESP CRIT CARE, V163, P951; Phan KL, 2002, NEUROIMAGE, V16, P331, DOI 10.1006/nimg.2002.1087; Pollatos O, 2005, COGNITIVE BRAIN RES, V25, P948, DOI 10.1016/j.cogbrainres.2005.09.019; Price DD, 2000, SCIENCE, V288, P1769, DOI 10.1126/science.288.5472.1769; Reiman EM, 1997, AM J PSYCHIAT, V154, P918; SCANO G, 2006, CURR OPIN PULM MED, V12, P8; Schreckenberger M, 2005, NEUROLOGY, V64, P1175; Small DM, 2003, NEURON, V39, P701, DOI 10.1016/S0896-6273(03)00467-7; Tataranni PA, 1999, P NATL ACAD SCI USA, V96, P4569, DOI 10.1073/pnas.96.8.4569; Thornton JM, 2001, J PHYSIOL-LONDON, V533, P823, DOI 10.1111/j.1469-7793.2001.00823.x; Tzourio-Mazoyer N, 2002, NEUROIMAGE, V15, P273, DOI 10.1006/nimg.2001.0978; von Leupoldt A, 2005, CHEST, V128, P3345, DOI 10.1378/chest.128.5.3345; von Leupoldt A, 2005, CHEST, V128, P345, DOI 10.1378/chest.128.1.345; von Leupoldt A, 2007, CHEST, V132, P1506, DOI 10.1378/chest.07-1245; von Leupoldt A, 2007, CHEST, V132, P141, DOI 10.1378/chest.07-0103; von Leupoldt A, 2007, RESP MED, V101, P839, DOI 10.1016/j.rmed.2006.06.033; von Leupoldt A, 2007, RESP MED, V101, P411, DOI 10.1016/j.rmed.2006.06.011; Von Leupoldt A, 2006, PSYCHOPHYSIOLOGY, V43, P641, DOI 10.1111/j.1469-8986.2006.00453.x; Von Leupoldt A, 2006, PSYCHOPHYSIOLOGY, V43, P382, DOI 10.1111/j.1469-8986.2006.00415.x; WILSON RC, 1991, CLIN SCI, V80, P65; WITTCHEN HU, 1997, SKID 1 STRUCTURED CL	53	118	120	2	9	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	MAY 1	2008	177	9					1026	1032		10.1164/rccm.200712-18210C		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	295PJ	WOS:000255486100017	18263796	
J	Pajno, GB; Caminiti, L; Vita, D; Barberio, G; Salzano, G; Lombardo, F; Canonica, GW; Passalacqua, G				Pajno, Giovanni B.; Caminiti, Lucia; Vita, Daniela; Barberio, Giovanni; Salzano, Giuseppina; Lombardo, Fortunato; Canonica, Giorgio Walter; Passalacqua, Giovanni			Sublingual immunotherapy in mite-sensitized children with atopic dermatitis: A randomized, double-blind, placebo-controlled study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						atopic dermatitis; house dust mites; sublingual immunotherapy	ALLERGIC RHINITIS; CONSENSUS REPORT; EFFICACY; ASTHMA; STANDARDIZATION; MULTICENTER; TRIALS	Background: Atopic dermatitis often has an allergic component, and immunotherapy may therefore prove beneficial. Objective: To assess the effect of sublingual immunotherapy (SLIT) in children with atopic dermatitis. Methods: Children age 5 to 16 years with atopic dermatitis (Scoring Atopic Dermatitis [SCORAD] > 7) and sensitization to dust mites alone, without food allergy or chronic asthma, were enrolled in a randomized, double-blind, placebo-controlled study and stratified according to disease severity. SLIT or placebo was given for 18 months in addition to standard therapy. SCORAD, visual analog scale, and rescue medication consumption were recorded at 3-month intervals. Results: Fifty-six children were enrolled, and 28 were allocated to SLIT. Forty-eight completed the study, with 2 dropouts in the active and 6 in the placebo group. The difference from baseline in the SCORAD was significant (P = .025) between the 2 groups starting from month 9. Similarly, there was a significant reduction in the use of medications only in the active group. A trend toward significance was seen for the visual analog score only in the active group versus baseline (P = .07). A significant difference in the considered parameters was found only in patients with a mild-moderate disease, whereas severe patients had only a marginal benefit. SLIT had to be discontinued in 2 patients because of exacerbation of dermatitis. Conclusion: Sublingual immunotherapy to dust mite improves mild-moderate atopic dermatitis. Clinical implications: Sublingual immunotherapy may represent an additional therapeutic tool for the treatment of extrinsic atopic dermatitis in properly selected children.	Univ Genoa, Dept Internal Med, I-16132 Genoa, Italy; Univ Messina, Dept Pediat, Allergy Unit, I-98100 Messina, Italy	Passalacqua, G (reprint author), Univ Genoa, Dept Internal Med, Padiglione Maragliano,Lgo R Benzi 10, I-16132 Genoa, Italy.	passalacqua@unige.it					Akdis CA, 2006, J ALLERGY CLIN IMMUN, V118, P152, DOI 10.1016/j.jaci.2006.03.045; Bindslev-Jensen C, 2001, ALLERGY, V56, P75, DOI 10.1034/j.1398-9995.2001.00922.x; BOCK SA, 1988, J ALLERGY CLIN IMMUN, V82, P986; Boguniewicz M, 2006, J ALLERGY CLIN IMMUN, V118, P40, DOI 10.1016/j.jaci.2006.04.044; Bousquet J, 2001, J ALLERGY CLIN IMMUN, V108, pS147, DOI 10.1067/mai.2001.118891; Bussmann C, 2006, J ALLERGY CLIN IMMUN, V118, P1292, DOI 10.1016/j.jaci.2006.07.054; Calamita Z, 2006, ALLERGY, V61, P1162, DOI 10.1111/j.1395-9995.2006.01205.x; CHAI H, 1975, J ALLERGY CLIN IMMUN, V56, P323, DOI 10.1016/0091-6749(75)90107-4; Fonacier L, 2006, ANN ALLERG ASTHMA IM, V97, P117; Galli E, 1994, Allergol Immunopathol (Madr), V22, P18; GLOVER MT, 1992, CLIN EXP ALLERGY, V22, P440, DOI 10.1111/j.1365-2222.1992.tb00145.x; Johansson SGO, 2004, J ALLERGY CLIN IMMUN, V113, P832, DOI 10.1016/j.jaci.2003.12.591; LEROY BP, 1993, J AM ACAD DERMATOL, V28, P232, DOI 10.1016/0190-9622(93)70033-P; Leung DYM, 2004, J CLIN INVEST, V113, P651, DOI 10.1172/JCI200421060; Lue KH, 2006, PEDIATR ALLERGY IMMU, V17, P408, DOI 10.1111/j.1399-3038.2006.00443.x; Mastrandrea F, 2000, Allergol Immunopathol (Madr), V28, P54; Niu CK, 2006, RESP MED, V100, P1374, DOI 10.1016/j.rmed.2005.11.016; NOWAK N, 2003, J ALLERGY CLIN IM S6, V112, pS128; Pacor Maria Luisa, 1994, Recenti Progressi in Medicina, V85, P273; Pajno GB, 2003, PEDIATR ALLERGY IMMU, V14, P292, DOI 10.1034/j.1399-3038.2003.00060.x; Passalacqua G, 2006, CURR OPIN ALLERGY CL, V6, P449, DOI 10.1097/01.all.0000246617.41871.40; Penagos M, 2006, ANN ALLERG ASTHMA IM, V97, P141; Petrova S, 2001, Zh Mikrobiol Epidemiol Immunobiol, V1, P33; PLATTSMILLS TAE, 1983, CLIN EXP DERMATOL, V8, P233, DOI 10.1111/j.1365-2230.1983.tb01776.x; Rienzo VD, 2005, CLIN EXP ALLERGY, V35, P560, DOI 10.1111/j.1365-2222.2005.02219.x; Scalabrin DMF, 1999, J ALLERGY CLIN IMMUN, V104, P1273, DOI 10.1016/S0091-6749(99)70024-2; STALDER JF, 1993, DERMATOLOGY, V186, P23; Till SJ, 2004, J ALLERGY CLIN IMMUN, V113, P1025, DOI 10.1016/j.jaci.2004.03.024; Werfel T, 2006, ALLERGY, V61, P202, DOI 10.1111/j.1398-9995.2006.00974.x; Werfel T, 1998, ALLERGY, V53, P731	30	118	121	0	3	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUL	2007	120	1					164	170		10.1016/j.jaci.2007.04.008		7	Allergy; Immunology	Allergy; Immunology	190NS	WOS:000248066400024	17543376	
J	Romieu, I; Torrent, M; Garcia-Esteban, R; Ferrer, C; Ribas-Fito, N; Anto, JM; Sunyer, J				Romieu, I.; Torrent, M.; Garcia-Esteban, R.; Ferrer, C.; Ribas-Fito, N.; Anto, J. M.; Sunyer, J.			Maternal fish intake during pregnancy and atopy and asthma in infancy	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						asthma; atopy; children; fish intake; n-3 PUFA; pregnancy	POLYUNSATURATED FATTY-ACIDS; OIL SUPPLEMENTATION; ALLERGIC DISEASE; IMMUNOGLOBULIN-A; CONTROLLED-TRIAL; HIGH-RISK; CHILDHOOD; CONSUMPTION; RESPONSES; LIFE	Background: There is growing evidence that n-3 fatty acids have anti-inflammatory properties and may modulate immune response. Dietary intake of these nutrients during pregnancy could play a role in the risk of asthma and atopy in the offspring. Methods: Using data from a cohort of women (n=462) enrolled during pregnancy and whose offspring were followed up to 6 years, we evaluated the impact of fish consumption during pregnancy on the incidence of atopy and asthma. Dietary intake was assessed by food frequency questionnaire (42 items) applied by an interviewer. Results: Thirty-four percent of infants had a medical diagnosis of eczema at age 1 year, 14.3% of the children were atopic [based on skin prick test (SPT) at 6 years], and 5.7% had atopic wheeze at age 6 years. After adjusting for potential confounding factors, fish intake during pregnancy was protective against the risk of eczema at age 1 year, a positive SPT for house dust mite at age 6 years and atopic wheeze at age 6 years [odds ratio (OR)=0.73 95% confidence interval (CI) 0.55-0.98, OR=0.68, 95% CI 0.46-1.01 and OR=0.55, 95% CI 0.31-0.96, respectively]. For an increase in fish intake from once per week to 2.5 times per week, the risk of eczema at age 1 year decreased by 37%, and the risk of positive SPT at age 6 years by 35%. Stratification by breastfeeding showed that fish intake was significantly related to a decrease risk in persistent wheeze among non-breastfed children (P for interaction < 0.05). No protective effect was observed among breastfed children. Conclusion: Our data suggest a protective effect of fish intake during pregnancy on the risk of atopy-related outcomes.	Inst Nacl Salud Publ, Cuernavaca 62508, Morelos, Mexico; IB SALUT, Area Salud Menorca, Menorca, Spain; Inst Municipal Invest Med, CREAL, E-08003 Barcelona, Spain; Univ Pompeu Fabra, Barcelona, Spain	Romieu, I (reprint author), Inst Nacl Salud Publ, 655 Avenida Univ, Col Santa Maria Ahuacatitlan, Cuernavaca 62508, Morelos, Mexico.	iromieu@correo.insp.mx	Sunyer, J/G-6909-2014	Sunyer, J/0000-0002-2602-4110			Barden AE, 2004, FREE RADICAL RES, V38, P233, DOI 10.1080/10715760310001656722; Basagana X, 2002, PEDIATR ALLERGY IMMU, V13, P412, DOI 10.1034/j.1399-3038.2002.02081.x; Bingham SA, 2001, PUBLIC HEALTH NUTR, V4, P847, DOI 10.1079/PHN2000102; Calder PC, 2006, CURR OPIN CLIN NUTR, V9, P77, DOI 10.1097/01.mco.0000214562.14074.fa; Calder PC, 2006, CLIN EXP ALLERGY, V36, P138, DOI 10.1111/j.1365-2222.2006.02433.x; Calder PC, 2002, BRIT J NUTR, V87, pS31, DOI [10.1079/BJN2001455, 10.1079/BJN2001482]; Calder P, 2002, BR J NUTR, V88, P165; Calvani M, 2006, PEDIATR ALLERGY IMMU, V17, P94, DOI 10.1111/j.1399-3038.2005.00367.x; Duchen K, 2001, ALLERGY, V56, P587, DOI 10.1034/j.1398-9995.2001.00040.x; Duchen K, 2000, PEDIATR ALLERGY IMMU, V11, P29, DOI 10.1034/j.1399-3038.2000.00052.x; Dunstan JA, 2004, CLIN EXP ALLERGY, V34, P1237, DOI 10.1111/j.1365-2222.2004.02028.x; Dunstan JA, 2003, J ALLERGY CLIN IMMUN, V112, P1178, DOI 10.1016/j.jaci.2003.09.009; Friedman NJ, 2005, J ALLERGY CLIN IMMUN, V115, P1238, DOI 10.1016/j.jaci.2005.01.069; Hastie T, 1990, GEN ADDITIVE MODELS; Hughes DA, 1997, CLIN EXP IMMUNOL, V110, P516, DOI 10.1046/j.1365-2249.1997.4351455.x; James M.J., 2000, AM J CLIN NUTR S, V71, P343; Jones AC, 1996, PEDIATR ALLERGY IMMU, V7, P109, DOI 10.1111/j.1399-3038.1996.tb00117.x; Jones P. 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Exp. Allergy	APR	2007	37	4					518	525		10.1111/j.1365-2222.2007.02685.x		8	Allergy; Immunology	Allergy; Immunology	152XM	WOS:000245395600008	17430348	
J	Kitagaki, K; Businga, TR; Racila, D; Elliott, DE; Weinstock, JV; Kline, JN				Kitagaki, Kunihiko; Businga, Thomas R.; Racila, Doina; Elliott, David E.; Weinstock, Joel V.; Kline, Joel N.			Intestinal helminths protect in a murine model of asthma	JOURNAL OF IMMUNOLOGY			English	Article							REGULATORY T-CELLS; INDUCED AIRWAY INFLAMMATION; CYTOKINE PRODUCTION; INTERLEUKIN-10-DEFICIENT MICE; CPG OLIGODEOXYNUCLEOTIDES; ALLERGIC SENSITIZATION; INVERSE ASSOCIATION; HYGIENE HYPOTHESIS; TH2 RESPONSES; HAY-FEVER	Underdeveloped nations are relatively protected from the worldwide asthma epidemic; the hygiene hypothesis suggests this is due to suppression of Th2-mediated inflammation by increased exposure to pathogens and their products. Although microbial exposures can promote Th2-suppressing Th1 responses, even Th2-skewing infections, such as helminths, appear to suppress atopy, suggesting an alternate explanation for these observations. To investigate whether induction of regulatory responses by helminths may counter allergic inflammation, we examined the effects of helminth infection in a murine model of atopic asthma. We chose Heligosomoides polygyrus, a gastrointestinal nematode, as the experimental helminth; this worm does not enter the lung in its life cycle. We found that H. polygyrus infection suppressed allergen-induced airway eosinophilia, bronchial hyperreactivity, and in vitro allergen-recall Th2 responses in an IL-10-dependent manner; total and OVA-specific IgE, however, were increased by worm infection. Finally, helminth-infected mice were protected against eosinophilic inflammation induced by adoptive transfer of OVA-stimulated CD4(+) cells, and transfer of cells from helminth-infected/OVA-exposed mice suppressed OVA-induced eosinophilic inflammation, suggesting a role for regulatory cells. Increased CD4(+)CD25(+)Foxp3(+) cells were found in thoracic lymph nodes of helminth-infected/OVA-exposed mice. Helminthic colonization appears to protect against asthma and atopic disorders; the regulatory cytokine, IL-10, may be a critical player.	Univ Iowa, Carver Coll Med, Dept Med, Iowa City, IA 52242 USA	Kline, JN (reprint author), Univ Iowa Hosp & Clin, C33GH,200 Hawkins Dr, Iowa City, IA 52242 USA.	joel-kline@uiowa.edu			NHLBI NIH HHS [HL079447, HL079448, HL59324]; NIEHS NIH HHS [ES05605]		Ameredes BT, 2005, J IMMUNOL, V175, P1206; Araujo MI, 2000, INT ARCH ALLERGY IMM, V123, P145, DOI 10.1159/000024433; Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; BATES JHT, 1992, J APPL PHYSIOL, V72, P46; Beasley R, 2000, J ALLERGY CLIN IMMUN, V105, pS466, DOI 10.1016/S0091-6749(00)90044-7; Berg DJ, 1996, J CLIN INVEST, V98, P1010, DOI 10.1172/JCI118861; Edwards LJ, 2004, MULT SCLER, V10, P575, DOI 10.1191/1352458504ms1087oa; Elliott DE, 2004, EUR J IMMUNOL, V34, P2690, DOI 10.1002/eji.200324833; Elliott DE, 2000, FASEB J, V14, P1848, DOI 10.1096/fj.99-0885hyp; Erb KJ, 1998, J EXP MED, V187, P561, DOI 10.1084/jem.187.4.561; Finkelman FD, 1997, ANNU REV IMMUNOL, V15, P505, DOI 10.1146/annurev.immunol.15.1.505; FIORENTINO DF, 1991, J IMMUNOL, V147, P3815; FIORENTINO DF, 1991, J IMMUNOL, V146, P3444; Fox JG, 2000, NAT MED, V6, P536, DOI 10.1038/75015; GODFREY R C, 1975, Clinical Allergy, V5, P201, DOI 10.1111/j.1365-2222.1975.tb01853.x; Groux H, 1997, NATURE, V389, P737; Grunig G, 1997, J EXP MED, V185, P1089, DOI 10.1084/jem.185.6.1089; Herz U, 1998, J ALLERGY CLIN IMMUN, V102, P867, DOI 10.1016/S0091-6749(98)70030-2; Justice JP, 2001, AM J PHYSIOL-LUNG C, V280, pL363; Kay AB, 1996, ANN NY ACAD SCI, V796, P1, DOI 10.1111/j.1749-6632.1996.tb32561.x; Kitagaki K, 2002, CLIN DIAGN LAB IMMUN, V9, P1260, DOI 10.1128/CDLI.9.6.1260-1269.2002; Kline JN, 1999, J ALLERGY CLIN IMMUN, V104, P1258; MacDonald AJ, 2002, J INFECT DIS, V185, P720, DOI 10.1086/339340; Makela MJ, 2002, AM J RESP CRIT CARE, V165, P824, DOI 10.1164/rccm.2105062; Makela MJ, 2000, P NATL ACAD SCI USA, V97, P6007, DOI 10.1073/pnas.100118997; MASTERS S, 1985, EPIDEMIOL REV, V7, P49; McGuirk P, 2002, TRENDS IMMUNOL, V23, P450, DOI 10.1016/S1471-4906(02)02288-3; MERRETT TG, 1976, CLIN ALLERGY, V6, P131, DOI 10.1111/j.1365-2222.1976.tb01890.x; MOSMANN TR, 1986, J IMMUNOL, V136, P2348; Nyan OA, 2001, CLIN EXP ALLERGY, V31, P1672, DOI 10.1046/j.1365-2222.2001.00987.x; Pelosi U, 2005, ALLERGY, V60, P626, DOI 10.1111/j.1398-9995.2005.00747.x; ROBINSON M, 1989, PARASITOLOGY, V98, P115; SCHUESSLER TF, 1995, IEEE T BIO-MED ENG, V42, P860, DOI 10.1109/10.412653; Scrivener S, 2001, LANCET, V358, P1493, DOI 10.1016/S0140-6736(01)06579-5; Shi HN, 1998, J IMMUNOL, V160, P2449; Stene LC, 2001, LANCET, V357, P607, DOI 10.1016/S0140-6736(00)04067-8; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Tomioka S, 2002, J APPL PHYSIOL, V93, P263, DOI 10.1152/japplphysiol.01129.2001; Tournoy KG, 2000, CLIN EXP ALLERGY, V30, P775; van den Biggelaar AHJ, 2000, LANCET, V356, P1723, DOI 10.1016/S0140-6736(00)03206-2; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; Wills-Karp M, 2001, NAT REV IMMUNOL, V1, P69, DOI 10.1038/35095579; Wilson MS, 2006, CHEM IMMUNOL ALLERGY, V90, P176; Wilson MS, 2005, J EXP MED, V202, P1199, DOI 10.1084/jem.20042572; Wohlleben G, 2004, INT IMMUNOL, V16, P585, DOI 10.1093/intimm/dxh062; Yang X, 2000, EUR J IMMUNOL, V30, P382, DOI 10.1002/1521-4141(200002)30:2<382::AID-IMMU382>3.3.CO;2-C; Yazdanbakhsh M, 2002, SCIENCE, V296, P490, DOI 10.1126/science.296.5567.490; Yazdanbakhsh M, 2001, TRENDS IMMUNOL, V22, P372, DOI 10.1016/S1471-4906(01)01958-5; Yemaneberhan H, 1997, LANCET, V350, P85, DOI 10.1016/S0140-6736(97)01151-3; Zuany-Amorim C, 2002, NAT MED, V8, P625, DOI 10.1038/nm0602-625	50	118	125	1	15	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	AUG 1	2006	177	3					1628	1635				8	Immunology	Immunology	065DT	WOS:000239140300037	16849471	
J	Bel, EH				Bel, EH			Clinical phenotypes of asthma	CURRENT OPINION IN PULMONARY MEDICINE			English	Article						phenotypes; childhood asthma; adult-onset asthma; severe asthma	ASPIRIN-INDUCED ASTHMA; ADULT-ONSET ASTHMA; NEAR-FATAL ASTHMA; AIR-FLOW LIMITATION; CHLAMYDIA-PNEUMONIAE; OCCUPATIONAL ASTHMA; RISK-FACTORS; FOLLOW-UP; BRONCHIAL RESPONSIVENESS; ALLERGIC SENSITIZATION	Purpose of review Asthma is a phenotypically heterogeneous disorder and, over the years, many different clinical subtypes of asthma have been described. A precise definition of asthma phenotypes is now becoming more and more important, not only for a better understanding of pathophysiologic mechanisms, but in particular to ascertain the specific genes associated with these phenotypes. Recent findings In children, three asthma phenotypes are now well defined: transient infant wheezing, nonatopic wheezing of the toddler, and IgE-mediated wheezing/asthma. Recently, a fourth phenotype, late-onset childhood asthma has been added to this list. In adults, asthma persisting from childhood into adulthood should be distinguished from asthma starting in adulthood. The phenotypes of adult-onset asthma are still poorly defined. Until now, phenotypic classification has been based primarily on etiologic factors (eg, aspirin sensitivity, persistent respiratory infections, occupational factors, or toxic exposures) or clinical characteristics of the disease (eg, mild, severe, brittle, near fatal, with fixed airflow obstruction, steroid resistant). Novel noninvasive techniques to assess the type and severity of airway inflammation and dysfunction are increasingly used to identify better the different phenotypes. Summary The classic phenotype of IgE-mediated asthma starting in childhood is now clearly defined. However, many other phenotypes of asthma in childhood as well in adulthood are being recognized. In particular, asthma starting in adulthood and noneosinophilic asthma constitute an important part of the adult asthma population, and are,still poorly defined. A precise definition of these asthma phenotypes is urgently needed because they are likely to be associated with different genotypes, responses to treatment, and prognoses.	Leiden Univ, Ctr Med, Dept Pulm Dis, NL-2300 RC Leiden, Netherlands	Bel, EH (reprint author), Leiden Univ, Ctr Med, Dept Pulm Dis, POB 9600,C3P, NL-2300 RC Leiden, Netherlands.	e.h.d.bel@lumc.nl					Antczak A, 2002, AM J RESP CRIT CARE, V166, P301, DOI 10.1164/rccm.2101021; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; Balmes J, 2003, AM J RESP CRIT CARE, V167, P787, DOI 10.1164/rccm.167.5.787; BARDANA EJ, 2003, ALLERGY CLIN IMMU S2, V111, pS530; Benayoun L, 2003, AM J RESP CRIT CARE, V167, P1360, DOI 10.1164/rccm.200209-1030OC; Berges-Gimeno MP, 2003, ANN ALLERG ASTHMA IM, V90, P338; BETSOU F, 2003, DIAGN LAB IMMUNOL, V10, P446; Bisgaard H, 2003, AM J RESP CRIT CARE, V167, P379, DOI 10.1164/rccm.200207-747OC; Bochenek G, 2003, J ALLERGY CLIN IMMUN, V111, P743, DOI 10.1067/mai.2003.1387; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Castro M, 2002, CHEST, V121, P1394, DOI 10.1378/chest.121.5.1394; Celedon JC, 2002, LANCET, V360, P781, DOI 10.1016/S0140-6736(02)09906-3; 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Litonjua AA, 2002, J ALLERGY CLIN IMMUN, V110, P736, DOI 10.1067/mai.2002.128948; Liu Q, 2003, ANN ALLERG ASTHMA IM, V90, P35; Mallia P, 2002, ALLERGY, V57, P1118, DOI 10.1034/j.1398-9995.2002.02169.x; Mapp CE, 2002, J ALLERGY CLIN IMMUN, V109, P867, DOI 10.1067/mai.2002.123234; Marks GB, 2003, J ALLERGY CLIN IMMUN, V111, P541, DOI 10.1067/mai.2003.171; Martin JG, 2003, AM J RESP CRIT CARE, V168, P568, DOI 10.1164/rccm.200201-021OC; Martinez FD, 2003, PEDIATR INFECT DIS J, V22, pS76, DOI 10.1097/00006454-200302001-00011; Martinez FD, 2002, PEDIATRICS, V109, P362; Matricardi PM, 2002, J ALLERGY CLIN IMMUN, V110, P381, DOI 10.1067/mai.2002.126658; Mitchell I, 2002, CHEST, V121, P1407, DOI 10.1378/chest.121.5.1407; Morahan G, 2002, LANCET, V360, P455, DOI 10.1016/S0140-6736(02)09676-9; Namazy JA, 2002, ANN ALLERG ASTHMA IM, V89, P542; NEWMANTAYLOR AJ, 2003, ANN ALLERG ASTHMA IM, V90, P24; Ownby DR, 2002, JAMA-J AM MED ASSOC, V288, P963, DOI 10.1001/jama.288.8.963; Phelan PD, 2002, J ALLERGY CLIN IMMUN, V109, P189, DOI 10.1067/mai.2001.120951; Picado C, 2003, ALLERGY, V58, P122, DOI 10.1034/j.1398-9995.2003.23792.x; Pierzchalska M, 2003, J ALLERGY CLIN IMMUN, V111, P1041, DOI 10.1067/mai.2003.1491; Platts-Mills TAE, 2002, JAMA-J AM MED ASSOC, V288, P1012, DOI 10.1001/jama.288.8.1012; Prezant DJ, 2002, NEW ENGL J MED, V347, P806, DOI 10.1056/NEJMoa021300; RACKEMANN FM, 1947, AM J MED, V3, P601, DOI 10.1016/0002-9343(47)90204-0; Sousa AR, 2002, NEW ENGL J MED, V347, P1493, DOI 10.1056/NEJMoa013508; Strachan DP, 1996, BRIT MED J, V312, P1195; Szczeklik A, 2003, J ALLERGY CLIN IMMUN, V111, P913, DOI 10.1067/mai.2003.1487; Tarlo SA, 2003, ANN ALLERG ASTHMA IM, V90, P19; Taussig LM, 2003, J ALLERGY CLIN IMMUN, V111, P661, DOI 10.1067/mai.2003.162; ten Brinke A, 2001, J ALLERGY CLIN IMMUN, V107, P449, DOI 10.1067/mai.2001.113047; Thickett KM, 2002, EUR RESPIR J, V19, P827, DOI 10.1183/09031936.02.00232802; Toren K, 2002, RESP MED, V96, P635, DOI 10.1053/rmed.2002.1319; Vandenplas O, 2003, EUR RESPIR J, V21, P706, DOI 10.1183/09031936.03.00113303; Vignola AM, 2003, CHEST, V123, p417S, DOI 10.1378/chest.123.3_suppl.417S-a; Vonk JM, 2003, THORAX, V58, P322, DOI 10.1136/thorax.58.4.322; Wenzel S, 2003, CHEST, V123, p405S, DOI 10.1378/chest.123.3_suppl.405S-a; Wenzel SE, 1999, AM J RESP CRIT CARE, V160, P1001; Wikman H, 2002, PHARMACOGENETICS, V12, P227, DOI 10.1097/00008571-200204000-00007; Yao TC, 2003, J ALLERGY CLIN IMMUN, V111, P1285, DOI 10.1067/mai.2003.1506; Yazdanbakhsh M, 2002, SCIENCE, V296, P490, DOI 10.1126/science.296.5567.490	76	118	129	3	13	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	1070-5287			CURR OPIN PULM MED	Curr. Opin. Pulm. Med.	JAN	2004	10	1					44	50		10.1097/00063198-200401000-00008		7	Respiratory System	Respiratory System	773EY	WOS:000188885800007	14749605	
J	Delfino, RJ; Gong, H; Linn, WS; Pellizzari, ED; Hu, Y				Delfino, RJ; Gong, H; Linn, WS; Pellizzari, ED; Hu, Y			Asthma symptoms in Hispanic children and daily ambient exposures to toxic and criteria air pollutants	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						environmental air pollutants; hydrocarbons; longitudinal studies; nitrogen dioxide; ozone; statistical models; sulfur dioxide; vehicle emissions	PEAK EXPIRATORY FLOW; VOLATILE ORGANIC-COMPOUNDS; ANTIINFLAMMATORY MEDICATION USE; INNER-CITY CHILDREN; RESPIRATORY HEALTH; ULTRAFINE PARTICLES; FORMALDEHYDE EXPOSURE; FINE PARTICLES; LUNG-FUNCTION; LOS-ANGELES	Although acute adverse effects on asthma have been frequently found for the U.S. Environmental Protection Agency's principal criteria air pollutants, there is little epidemiologic information on specific hydrocarbons from toxic emission sources. We conducted a panel study of 22 Hispanic children with asthma who were 10-16 years old and living in a Los Angeles community with high traffic density. Subjects filled out symptom diaries daily for up to 3 months (November 1999 through January 2000). Pollutants included ambient hourly values of ozone, nitrogen dioxide, Sulfur dioxide, and carbon monoxide and 24-hr values of volatile organic compounds (VOCs), particulate matter with aerodynamic diameter <10 &mu;m (PM10), and elemental carbon (EC) and organic carbon (OC) PM10 fractions. Asthma symptom severity was regressed on pollutants using generalized estimating equations, and peak expiratory flow (PEF) was regressed on pollutants using mixed models. We found positive associations of symptoms with criteria air pollutants (O-3, NO2, SO2, PM10),, EC-OC, and VOCs (benzene, ethylbenzene, formaldehyde, acetaldehyde, acetone, 1,3-butadiene, tetrachloroethylene, toluene, m,p-xylene, and o-xylene). Selected adjusted odds ratios for bothersome or more severe asthma symptoms from interquartile range increases in pollutants were, for 1.4 ppb 8-hr NO2, 1.27 [95% confidence interval (Cl), 1.05-1-54]; 1.00 ppb benzene, 1.23 (95% Cl, 1.02-1.48); 3.16 ppb formaldehyde, 1.37 (95% CI, 1.04-1.80); 37 &mu;g/m(3) PM,0, 1.45 (95% Cl, 1.11-1.90); 2.91 &mu;g/m(3) EC, 1.85 (95% Cl, 1.11-3.08); and 4.64 &mu;g/m(3) OC, 1.88 (95% CI, 1.12-3.17). Two-pollutant models of EC or OC with PM10 showed little change in odds ratios for EC (to 1.83) or OC (to 1.89), but PM10 decreased from 1.45 to 1.0. There were no significant associations with PEF. Findings support the view that air toxics in the pollutant mix from traffic and industrial sources may have adverse effects on asthma in children.	Univ Calif Irvine, Coll Med, Dept Med, Div Epidemiol, Irvine, CA 92697 USA; Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA USA; Los Amigos Res & Educ Inst, Environm Hlth Serv, Downey, CA USA; Res Triangle Inst, Exposure Anal Res Program, Res Triangle Pk, NC 27709 USA	Delfino, RJ (reprint author), Univ Calif Irvine, Coll Med, Dept Med, Div Epidemiol, 224 Irvine Hall, Irvine, CA 92697 USA.				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Health Perspect.	APR	2003	111	4					647	656		10.1289/ehp.5992		10	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	665WM	WOS:000182144300059	12676630	
J	Litonjua, AA; Milton, DK; Celedon, JC; Ryan, L; Weiss, ST; Gold, DR				Litonjua, AA; Milton, DK; Celedon, JC; Ryan, L; Weiss, ST; Gold, DR			A longitudinal analysis of wheezing in young children: The independent effects of early life exposure to house dust endotoxin, allergens, and pets	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						endotoxin; allergens; domestic animals; wheeze; asthma	HAY-FEVER; ASTHMA; RISK; SENSITIZATION; ATOPY; INHALATION; COMMUNITY; DECREASES; COCKROACH; RESPONSES	Background: It has been postulated that exposure to bacterial endotoxins and animals early in life might confer protection against the development of asthma and allergies. Objective: We investigated the longitudinal effects of exposure to house dust endotoxin (HDE), allergen levels, and the presence of a dog in the home on wheezing in young children over a 4-year period. Methods: Two hundred twenty-six children younger than 5 years were followed for 4 years. Endotoxin and allergen levels were measured from house dust collected at baseline. Longitudinal associations were investigated by using a proportional hazards technique that allowed for multiple outcomes per subject. Results: Exposure to high concentrations of HDE of greater than the median level was associated with an increased risk for wheezing over the period of observation (multivariate relative risk, 1.52; 95% CI, 1.07-2.14), but this risk rapidly decreased over time (P for trend = .005). Exposure to cockroach allergen was associated with increased risk for wheezing, whereas exposure to cat allergen and the presence of a dog in the home were both associated with decreased risk for wheezing. The risks associated with cockroach allergen, cat allergen, and dog did not change over the period of observation. Conclusion: The negative associations between exposures to dogs and cat allergen and wheeze appear to be independent of the effects of endotoxin and suggest that separate mechanisms might mediate the effects of HDE exposure and pet exposure on the developing immune system.	Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA; Beth Israel Deaconess Med Ctr, Div Pulm & Crit Care Med, Boston, MA 02215 USA; Harvard Univ, Sch Med, Boston, MA 02115 USA; Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA; Dana Farber Canc Inst, Boston, MA 02115 USA	Litonjua, AA (reprint author), Channing Labs, 181 Longwood Ave, Boston, MA 02115 USA.		Milton, Donald/G-3286-2010; Ryan, Louise/A-4562-2009	Milton, Donald/0000-0002-0550-7834; Ryan, Louise/0000-0001-5957-2490; Litonjua, Augusto/0000-0003-0422-5875	NHLBI NIH HHS [K08 HL-03870]; NIAID NIH HHS [R01 AI/EHS-35786]; NIEHS NIH HHS [R01 ES-07036]		Abbas AK, 1996, NATURE, V383, P787, DOI 10.1038/383787a0; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Chew GL, 1998, AM J RESP CRIT CARE, V157, P1536; DANDREA A, 1992, J EXP MED, V176, P1387, DOI 10.1084/jem.176.5.1387; FITCH FW, 1993, ANNU REV IMMUNOL, V11, P29, DOI 10.1146/annurev.immunol.11.1.29; Gehring U, 2001, J ALLERGY CLIN IMMUN, V108, P847, DOI 10.1067/mai.2001.119026; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Jagielo PJ, 1996, CHEST, V110, P263, DOI 10.1378/chest.110.1.263; Keman S, 1998, INT ARCH OCC ENV HEA, V71, P131, DOI 10.1007/s004200050260; LE JM, 1986, J IMMUNOL, V136, P4525; Litonjua AA, 2001, J ALLERGY CLIN IMMUN, V107, P41, DOI 10.1067/mai.2001.111143; Litonjua AA, 1998, AM J RESP CRIT CARE, V158, P176; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Martinez FD, 1999, LANCET S2, V354, pSII12; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; MICHEL O, 1989, J APPL PHYSIOL, V66, P1059; Milton DK, 1997, AM IND HYG ASSOC J, V58, P861; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; PLATTSMILLS TAE, 1992, J ALLERGY CLIN IMMUN, V89, P1046, DOI 10.1016/0091-6749(92)90228-T; POLLART SM, 1989, J ALLERGY CLIN IMMUN, V83, P875, DOI 10.1016/0091-6749(89)90100-0; Remes ST, 2001, J ALLERGY CLIN IMMUN, V108, P509, DOI 10.1067/mai.2001.117797; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; ROSNER B, 1995, FUNDAMENTALS BIOSTAT, P443; RYLANDER R, 1989, AM REV RESPIR DIS, V140, P981; Silva JRL, 2000, TOXICOLOGY, V152, P31; Svanes C, 1999, J ALLERGY CLIN IMMUN, V103, P415, DOI 10.1016/S0091-6749(99)70465-3; THERNEAU TM, 2000, MODELING SURVIVAL DA, P185; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230	33	118	118	0	4	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	NOV	2002	110	5					736	742		10.1067/mai.2002.128948		7	Allergy; Immunology	Allergy; Immunology	612NN	WOS:000179082500008	12417882	
J	Takuma, K; Phuagphong, P; Lee, E; Mori, K; Baba, A; Matsuda, T				Takuma, K; Phuagphong, P; Lee, E; Mori, K; Baba, A; Matsuda, T			Anti-apoptotic effect of cGMP in cultured astrocytes - Inhibition by cGMP-dependent protein kinase of mitochondrial permeable transition pore	JOURNAL OF BIOLOGICAL CHEMISTRY			English	Article							PROGRAMMED CELL-DEATH; CYTOCHROME-C RELEASE; NITRIC-OXIDE; RAT ASTROCYTES; NA+-CA2+ EXCHANGER; REPERFUSION INJURY; CYCLOSPORINE-A; INNER MEMBRANE; PC12 CELLS; ACTIVATION	Reperfusion of cultured astrocytes with normal medium after exposure to H2O2-containing medium causes apoptosis. We have recently shown that ibudilast, which has been used for bronchial asthma and cerebrovascular disorders, attenuated the H2O2-induced apoptosis of astrocytes via the cGMP signaling pathway. This study examines the mechanism underlying the protective effect of cGMP. The membrane-permeable cGMP analog dibutyryl-cGMP attenuated the H2O2-induced decrease in cell viability, DNA ladder formation, nuclear condensation, reduction of the mitochondrial membrane potential, cytochrome c release from mitochondria, and caspase-3 activation in cultured astrocytes. These effects of dibutyryl-cGMP were almost completely inhibited by the cGMP-dependent protein kinase (PKG) inhibitor KT5823. In isolated rat brain mitochondria, cGMP in the presence of cytosolic extract from astrocytes inhibited the mitochondrial permeability transition pore (PTP) as determined by monitoring Ca2+-induced mitochondrial swelling. This ability of the cytosolic extract was inactivated by heat treatment and was mimicked by exogenous PKG. The effect of cGMP on the mitochondrial swelling was blocked by KT5823. The PTP inhibitors cyclosporin A and bongkrekic acid prevented the H2O2-induced decrease in cell viability and caspase-3 activation. These findings demonstrate that cGMP inhibits the mitochondrial PTP via the activation of PKG, and the prevention of mitochondrial dysfunction contributes to its anti-apoptotic effect.	Osaka Univ, Grad Sch Pharmaceut Sci, Lab Med Pharmacol, Suita, Osaka 5650871, Japan; Osaka Univ, Grad Sch Pharmaceut Sci, Lab Mol Neuropharmacol, Suita, Osaka 5650871, Japan; Kobe Gakuin Univ, Fac Pharmaceut Sci, Dept Analyt Chem, Kobe, Hyogo 6512180, Japan; Kobe Gakuin Univ, Fac Pharmaceut Sci, Dept Pharmacol, Kobe, Hyogo 6512180, Japan; Kobe Gakuin Univ, High Technol Res Ctr, Kobe, Hyogo 6512180, Japan	Matsuda, T (reprint author), Osaka Univ, Grad Sch Pharmaceut Sci, Lab Med Pharmacol, 1-6 Yamadaoka, Suita, Osaka 5650871, Japan.						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Biol. Chem.	DEC 21	2001	276	51					48093	48099		10.1074/jbc.M108622200		7	Biochemistry & Molecular Biology	Biochemistry & Molecular Biology	505QL	WOS:000172927000049	11677240	
J	Penttinen, P; Timonen, KL; Tiittanen, P; Mirme, A; Ruuskanen, J; Pekkanen, J				Penttinen, P; Timonen, KL; Tiittanen, P; Mirme, A; Ruuskanen, J; Pekkanen, J			Number concentration and size of particles in urban air: Effects on spirometric lung function in adult asthmatic subjects	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; asthma; FVC; FEV1; particles; particle size; peak expiratory flow rate; PEFR; spirometry	RESPIRATORY HEALTH; ULTRAFINE PARTICLES; CYTOKINE PRODUCTION; FINE PARTICLES; POLLUTION; CHILDREN; PM10; MORTALITY; ASSOCIATION; ATMOSPHERE	Daily variations in ambient particulate air pollution are associated with variations in respiratory lung Function. It has been suggested that the effects of particulate matter may be due to particles in the ultrafine (0.01-0.1 mum) size range. Be-cause previous studies on ultrafine particles only used self-monitored peak expiratory now rate (PEFR), we assessed the associations between particle mars and number concentrations in several size ranges measured at a central site and measured (biweekly) spirometric lung function among a group of 54 adult asthmatics (n = 495 measurements). We also compared results to daily morning, afternoon, and evening PEFR measurements done at home (n = 7,672-8,110 measurements), The median (maximum) 24 hr number concentrations were 14,500/cm(3) (46,500/cm(3)) ultrafine particles and 800/cm(3) (2,800/cm3) accumulation mode (0.1-1 mum) particles. The median (maximum) mass concentration of PM2.5 (particulate matter <2.5 <mu>m) and PM10 (particulate matter <10 <mu>m in aerodynamic diameter) were 8.4 mug/m(3) (38.3 mug/m(3)) and 13.5 mug/m(3) (73.7 mug/m(3)), respectively. The number of accumulation mode particles was consistently inversely associated with PEFR in spirometry. Inverse, but nonsignificant, associations were observed with ultrafine particles, and no associations were observed with large particles (PM10). Compared to the effect estimates for self-monitored PEFR, the effect estimates for spirometric PEFR tended to be larger. The standard errors were also larger, probably due to the lower number of spirometric measurements. The present results support the need to monitor the particle number and size distributions in urban air in addition to mass.	Natl Publ Hlth Inst, Environm Epidemiol Unit, Kuopio 70701, Finland; Univ Tartu, Inst Environm Phys, EE-50090 Tartu, Estonia; Univ Kuopio, Dept Environm Sci, FIN-70211 Kuopio, Finland	Pekkanen, J (reprint author), Natl Publ Hlth Inst, Environm Epidemiol Unit, POB 95, Kuopio 70701, Finland.						Becker S, 1996, TOXICOL APPL PHARM, V141, P637, DOI 10.1006/taap.1996.0330; Carter JD, 1997, TOXICOL APPL PHARM, V146, P180, DOI 10.1006/taap.1997.8254; DOCKERY DW, 1994, ANNU REV PUBL HEALTH, V15, P107, DOI 10.1146/annurev.pu.15.050194.000543; DOCKERY DW, 1993, NEW ENGL J MED, V329, P1753, DOI 10.1056/NEJM199312093292401; DUSSELDORP A, 1995, AM J RESP CRIT CARE, V152, P1932; Harrison RM, 1999, ATMOS ENVIRON, V33, P309, DOI 10.1016/S1352-2310(98)00164-2; HOEK G, 1994, ENVIRON RES, V64, P136, DOI 10.1006/enrs.1994.1012; Hosiokangas J, 1999, ATMOS ENVIRON, V33, P3821, DOI 10.1016/S1352-2310(98)00400-2; Hughes LS, 1998, ENVIRON SCI TECHNOL, V32, P1153, DOI 10.1021/es970280r; KOENIG JQ, 1993, ENVIRON RES, V63, P26, DOI 10.1006/enrs.1993.1123; Neas LM, 1999, EPIDEMIOLOGY, V10, P550, DOI 10.1097/00001648-199909000-00015; OBERDORSTER G, 1995, INHAL TOXICOL, V7, P111, DOI 10.3109/08958379509014275; Pekkanen J, 1997, ENVIRON RES, V74, P24, DOI 10.1006/enrs.1997.3750; PENTTINEN P, IN PRESS EUR RESP J; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; POPE CA, 1991, AM REV RESPIR DIS, V144, P668; Roemer W, 2000, EUR RESPIR J, V15, P553, DOI 10.1034/j.1399-3003.2000.15.21.x; Salvi S, 1999, AM J RESP CRIT CARE, V159, P702; SCHLESINGER RB, 1994, ENVIRON RES, V65, P69, DOI 10.1006/enrs.1994.1022; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; Schwartz J, 1999, ENVIRON HEALTH PERSP, V107, P339, DOI 10.2307/3434536; Tiittanen P, 1999, EUR RESPIR J, V13, P266, DOI 10.1034/j.1399-3003.1999.13b08.x; Timonen KL, 1997, AM J RESP CRIT CARE, V156, P546; TIMONEN KL, UNPUB; Vallius MJ, 2000, ENVIRON SCI TECHNOL, V34, P1919, DOI 10.1021/es990603e; VANDERZEE S, 1999, THESIS U WAGENINGEN; Vedal S, 1997, J AIR WASTE MANAGE, V47, P551; 1997, FINNISH POLLEN B, V22; [Anonymous], 1987, AM REV RESP DIS, V136, P1285	29	118	125	2	20	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	APR	2001	109	4					319	323		10.2307/3454889		5	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	427NZ	WOS:000168413600020	11335178	
J	Palmer, LJ; Rye, PJ; Gibson, NA; Burton, PR; Landau, LI; LeSouef, PN				Palmer, LJ; Rye, PJ; Gibson, NA; Burton, PR; Landau, LI; LeSouef, PN			Airway responsiveness in early infancy predicts asthma, lung function, and respiratory symptoms by school age	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							BRONCHIAL HYPERRESPONSIVENESS; SUBSEQUENT DEVELOPMENT; EARLY-CHILDHOOD; FAMILY HISTORY; RISK-FACTORS; CHILDREN; SMOKING; LIFE; POPULATION; INFLAMMATION	Asthma is the most common chronic childhood disease in developed nations. Little is known about the relationship between airway responsiveness in infancy and the development of asthma later in life. The relationship of airway responsiveness at 1 mo with asthma, atopy, lower respiratory symptoms, and lung function at 6 yr of age was investigated prospectively in 95 white children from a randomly ascertained birth cohort. Baseline spirometry, airway responsiveness to histamine, and skin reactivity to common allergens were assessed at the age of 1 mo and 6 yr. Total serum immunoglobulin E (IgE) was measured from cord blood and at 6 yr. Brood eosinophil counts were measured at 6 yr only. Family, symptom, and exposure histories at both time points were derived from questionnaire data. Independently of the other factors assessed, increased airway responsiveness at 1 mo was significantly associated with the following parameters measured at six yr: decreased FEV1 (p < 0.001); decreased FVC (p < 0.001); physician-diagnosed asthma (p < 0.001); and lower respiratory tract symptoms (p < 0.05). None of the other physiologic factors measured in infancy showed such consistent associations with important clinical and physiologic outcomes at age 6. These data suggest that airway responsiveness in early life defines a functional state that is associated with abnormal airway function, lower respiratory symptoms, and the emergence of asthma by 6 yr of age.	Univ Western Australia, Dept Paediat, Perth, WA 6009, Australia; TVW Telethon Inst Child Hlth Res, Div Populat Sci, Genet Epidemiol Unit, Perth, WA, Australia	Palmer, LJ (reprint author), Brigham & Womens Hosp, Channing Lab, 181 Longwood Ave, Boston, MA 02115 USA.		Palmer, Lyle/K-3196-2014; Burton, Paul/H-7527-2016	Palmer, Lyle/0000-0002-1628-3055; 			American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P1285, DOI 10.1164/ajrccm/136.5.1285; BJORKSTEN B, 1994, ALLERGY, V49, P400, DOI 10.1111/j.1398-9995.1994.tb00831.x; BORRES MP, 1995, J ALLERGY CLIN IMMUN, V95, P694, DOI 10.1016/S0091-6749(95)70174-5; Burr ML, 1997, CLIN EXP ALLERGY, V27, P1247; Carlsen KH, 1997, PEDIATR ALLERGY IMMU, V8, P40; CLARKE JR, 1992, ARCH DIS CHILD, V67, P1454; Daly LE, 1991, INTERPRETATION USES; GELLER DE, 1988, PEDIATR PULM, V4, P90, DOI 10.1002/ppul.1950040206; HABY MM, 1994, PEDIATR PULM, V18, P323, DOI 10.1002/ppul.1950180510; The International Study of Asthma and Allergies in Childhood (ISAAC) Steering Committee, 1998, LANCET, V351, P1125; Janson C, 1997, EUR RESPIR J, V10, P1795, DOI 10.1183/09031936.97.10081795; KNUDSON RJ, 1983, AM REV RESPIR DIS, V127, P725; LESOUEF PN, 1989, AM REV RESPIR DIS, V139, P62; Lombardi E, 1997, AM J RESP CRIT CARE, V156, P1863; Ludviksdottir D, 2000, ALLERGY, V55, P259, DOI 10.1034/j.1398-9995.2000.00252.x; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; MARTINEZ FD, 1995, AM J RESP CRIT CARE, V151, P1644; Martinez FD, 1998, J ALLERGY CLIN IMMUN, V102, P915, DOI 10.1016/S0091-6749(98)70328-8; McCullagh P., 1989, GEN LINEAR MODELS; MONTGOMERY GL, 1990, AM REV RESPIR DIS, V142, P1372; MORGAN WJ, 1992, PEDIATR CLIN N AM, V39, P1185; OCONNOR G, 1987, AM REV RESPIR DIS, V136, P1412; PATTEMORE PK, 1993, CLIN EXP ALLERGY, V23, P886, DOI 10.1111/j.1365-2222.1993.tb00273.x; PEAT JK, 1989, CLIN EXP ALLERGY, V19, P299, DOI 10.1111/j.1365-2222.1989.tb02387.x; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; Sandford A, 1996, AM J RESP CRIT CARE, V153, P1749; SANTING RE, 1994, J ALLERGY CLIN IMMUN, V93, P1021, DOI 10.1016/S0091-6749(94)70051-6; SPEIGHT ANP, 1978, BRIT MED J, V2, P331; Stick SM, 1996, LANCET, V348, P1060, DOI 10.1016/S0140-6736(96)04446-7; STICK SM, 1991, AM REV RESPIR DIS, V144, P1012; TAGER IB, 1993, AM REV RESPIR DIS, V147, P811; TAGER IB, 1987, AM REV RESPIR DIS, V136, P1366; Warner JA, 1998, CLIN EXP ALLERGY, V28, P35; Warner JO, 1998, PEDIATR ALLERGY IMMU, V9, P56, DOI 10.1111/j.1399-3038.1998.tb00304.x; WEISS ST, 1984, AM REV RESPIR DIS, V129, P898; Wright A L, 1998, Eur Respir J Suppl, V27, p17s; YAN K, 1983, THORAX, V38, P760, DOI 10.1136/thx.38.10.760; YOUNG S, 1991, NEW ENGL J MED, V324, P1168, DOI 10.1056/NEJM199104253241704	38	118	124	0	0	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	JAN	2001	163	1					37	42				6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	394TV	WOS:000166540100012	11208623	
J	Turner, MC; Krewski, D; Pope, CA; Chen, Y; Gapstur, SM; Thun, MJ				Turner, Michelle C.; Krewski, Daniel; Pope, C. Arden, III; Chen, Yue; Gapstur, Susan M.; Thun, Michael J.			Long-term Ambient Fine Particulate Matter Air Pollution and Lung Cancer in a Large Cohort of Never-Smokers	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						fine particulate matter air pollution; lung neoplasms; never-smokers; asthma; pulmonary disease, chronic obstructive	OBSTRUCTIVE PULMONARY-DISEASE; OXIDATIVE DAMAGE; HEALTH IMPACTS; NORWEGIAN MEN; FOLLOW-UP; MORTALITY; RISK; ASSOCIATION; EXPOSURE; INTERVENTIONS	Rationale: There is compelling evidence that acute and chronic exposure to ambient fine particulate matter (PM2.5) air pollution increases cardiopulmonary mortality. However, the role of PM2.5 in the etiology of lung cancer is less clear, particularly at concentrations that prevail in developed countries and in never-smokers. Objectives: This study examined the association between mean long-term ambient PM2.5 concentrations and lung cancer mortality among 188,699 lifelong never-smokers drawn from the nearly 1.2 million Cancer Prevention Study-II participants enrolled by the American Cancer Society in 1982 and followed prospectively through 2008. Methods: Mean metropolitan statistical area PM2.5 concentrations were determined for each participant based on central monitoring data. Cox proportional hazards regression models were used to estimate multivariate adjusted hazard ratios and 95% confidence intervals for lung cancer mortality in relation to PM2.5. Measurements and Main Results: A total of 1,100 lung cancer deaths were observed during the 26-year follow-up period. Each 10 mu g/m(3) increase in PM2.5 concentrations was associated with a 15-27% increase in lung cancer mortality. The association between PM2.5 and lung cancer mortality was similar in men and women and across categories of attained age and educational attainment, but was stronger in those with a normal body mass index and a history of chronic lung disease at enrollment (P < 0.05). Conclusions: The present findings strengthen the evidence that ambient concentrations of PM2.5 measured in recent decades are associated with small but measurable increases in lung cancer mortality.	[Turner, Michelle C.; Krewski, Daniel] Univ Ottawa, McLaughlin Ctr Populat Hlth Risk Assessment, Inst Populat Hlth, Ottawa, ON K1N 6N5, Canada; [Turner, Michelle C.] Univ Ottawa, Fac Grad & Postdoctoral Studies, Ottawa, ON K1N 6N5, Canada; [Krewski, Daniel; Chen, Yue] Univ Ottawa, Fac Med, Dept Epidemiol & Community Med, Ottawa, ON K1N 6N5, Canada; [Pope, C. Arden, III] Brigham Young Univ, Dept Econ, Provo, UT 84602 USA; [Krewski, Daniel] Risk Sci Int, Ottawa, ON, Canada; [Gapstur, Susan M.; Thun, Michael J.] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA	Turner, MC (reprint author), Univ Ottawa, McLaughlin Ctr Populat Hlth Risk Assessment, Inst Populat Hlth, 1 Stewart St,Room 313, Ottawa, ON K1N 6N5, Canada.	mturner@uottawa.ca			Canadian Institutes of Health Research	Supported by Canada Graduate Scholarship from the Canadian Institutes of Health Research (M. C. T.). D. K. is the Natural Sciences and Engineering Research Council Chair in Risk Science at the University of Ottawa.	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J. Respir. Crit. Care Med.	DEC 15	2011	184	12					1374	1381		10.1164/rccm.201106-1011OC		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	863AF	WOS:000298134500014	21980033	
J	Nohynek, GJ; Antignac, E; Re, T; Toutain, H				Nohynek, Gerhard J.; Antignac, Eric; Re, Thomas; Toutain, Herve			Safety assessment of personal care products/cosmetics and their ingredients	TOXICOLOGY AND APPLIED PHARMACOLOGY			English	Review						Safety assessment; Personal care products; Cosmetic ingredients; Hair dyes; Ultraviolet filters; Threshold of toxicological concern; Nanoparticles	PERMANENT HAIR-DYES; VITRO PERCUTANEOUS-ABSORPTION; TOXICOLOGICAL CONCERN TTC; NATURAL FLAVOR COMPLEXES; BLADDER-CANCER RISK; HUMAN HEALTH-RISK; PARA-PHENYLENEDIAMINE; IN-VITRO; AROMATIC-AMINES; STRATUM-CORNEUM	We attempt to review the safety assessment of personal care products (PCP) and ingredients that are representative and pose complex safety issues. PCP are generally applied to human skin and mainly produce local exposure, although skin penetration or use in the oral cavity, on the face, lips, eyes and mucosa may also produce human systemic exposure. In the EU, US and Japan, the safety of PCP is regulated under cosmetic and/or drug regulations. Oxidative hair dyes contain arylamines, the most chemically reactive ingredients of PCP. Although arylamines have an allergic potential, taking into account the high number of consumers exposed, the incidence and prevalence of hair dye allergy appears to be low and stable. A recent (2001) epidemiology study suggested an association of oxidative hair dye use and increased bladder cancer risk in consumers, although this was not confirmed by subsequent or previous epidemiologic investigations. The results of genetic toxicity, carcinogenicity and reproductive toxicity studies Suggest that modern hair dyes and their ingredients pose no genotoxic, carcinogenic or reproductive risk. Recent reports suggest that arylamines contained in oxidative hair dyes are N-acetylated in human or mammalian skin resulting in systemic exposure to traces of detoxified, i.e. non-genotoxic, metabolites, whereas human hepatocytes were unable to transform hair dye arylamines to potentially carcinogenic metabolites. An expert panel of the International Agency on Research of Cancer (IARC) concluded that there is no evidence for a causal association of hair dye exposure with an elevated cancer risk in consumers. Ultraviolet filters have important benefits by protecting the consumer against adverse effects of UV radiation; these substances undergo a stringent safety evaluation under current international regulations prior to their marketing. Concerns were also raised about the safety of solid nanoparticles in PCP, mainly TiO(2) and ZnO in Sunscreens. However, current evidence suggests that these particles are non-toxic, do not penetrate into or through normal or compromised human skin and, therefore, pose no risk to human health. The increasing use of natural plant ingredients in personal care products raised new safety issues that require novel approaches to their safety evaluation similar to those of plant-derived food ingredients. For example, the Threshold of Toxicological Concern (TTC) is a promising tool to assess the safety of substances present at trace levels as well as minor ingredients of plant-derived substances. The potential human systemic exposure to PCP ingredients is increasingly estimated on the basis of in vitro skin penetration data. However, new evidence suggests that the in vitro test may overestimate human systemic exposure to PCP ingredients due to the absence of metabolism in cadaver skin or misclassification of skin residues that, in vivo, remain in the stratum corneum or hair follicle openings, i.e. outside the living skin. Overall, today's safety assessment of PCP and their ingredients is not only based on science, but also on their respective regulatory status as well as other issues, such as the ethics of animal testing. Nevertheless, the record shows that today's PCP are safe and offer multiple benefits to quality of life and health of the consumer. In the interest of all stakeholders, consumers, regulatory bodies and producers, there is an urgent need for an international harmonization on the status and safety requirements of these products and their ingredients. (C) 2009 Elsevier Inc. Al rights reserved.	[Nohynek, Gerhard J.; Antignac, Eric; Toutain, Herve] LOREAL R&D, Global Safety Evaluat, F-92600 Asnieres, France; [Re, Thomas] LOreal USA, Res & Dev, Clark, NJ 07066 USA	Nohynek, GJ (reprint author), LOREAL R&D, Global Safety Evaluat, 25-29 Quai Aulagnier, F-92600 Asnieres, France.	gnohynec@rd.loreal.com					Aeby P, 2009, J INVEST DERMATOL, V129, P99, DOI 10.1038/jid.2008.209; Allemann IB, 2009, INT J DERMATOL, V48, P923, DOI 10.1111/j.1365-4632.2009.04081.x; AMES BN, 1975, P NATL ACAD SCI USA, V72, P2423, DOI 10.1073/pnas.72.6.2423; ASHBY J, 1991, MUTAT RES, V257, P229, DOI 10.1016/0165-1110(91)90003-E; Axmon A, 2009, OCCUP ENVIRON MED, V66, P198, DOI 10.1136/oem.2008.039784; Baan R, 2008, LANCET ONCOL, V9, P322, DOI 10.1016/S1470-2045(08)70089-5; BABISH JG, 1991, J TOXICOL ENV HEALTH, V34, P197; BACHTHOMSEN M, 1993, PHOTODERMATOL PHOTO, V9, P242; Bando H, 1997, J PHARM SCI, V86, P759, DOI 10.1021/js960408n; Barlow SM, 2002, FOOD CHEM TOXICOL, V40, P145, DOI 10.1016/S0278-6915(01)00117-X; 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J	Favrot, C; Steffan, J; Seewald, W; Picco, F				Favrot, Claude; Steffan, Jean; Seewald, Wolfgang; Picco, Federicca			A prospective study on the clinical features of chronic canine atopic dermatitis and its diagnosis	VETERINARY DERMATOLOGY			English	Article							ACVD TASK-FORCE; FOOD SENSITIVITY; CRITERIA; DOGS; ALLERGY; MANIFESTATIONS; POPULATION; PREVALENCE; VALIDATION; ETIOLOGY	Canine atopic dermatitis (CAD) is a multifaceted disease associated with exposure to various offending agents such as environmental and food allergens. The diagnosis of this condition is difficult because none of the typical signs are pathognomonic. Sets of criteria have been proposed but are mainly used to include dogs in clinical studies. The goals of the present study were to characterize the clinical features and signs of a large population of dogs with CAD, to identify which of these characteristics could be different in food-induced atopic dermatitis (FIAD) and non-food-induced atopic dermatitis (NFIAD) and to develop criteria for the diagnosis of this condition. Using simulated annealing, selected criteria were tested on a large and geographically widespread population of pruritic dogs. The study first described the signalment, history and clinical features of a large population of CAD dogs, compared FIAD and NFIAD dogs and confirmed that both conditions are clinically indistinguishable. Correlations of numerous clinical features with the diagnosis of CAD are subsequently calculated, and two sets of criteria associated with sensitivity and specificity ranging from 80% to 85% and from 79% to 85%, respectively, are proposed. It is finally demonstrated that these new sets of criteria provide better sensitivity and specificity, when compared to Willemse and Prelaud criteria. These criteria can be applied to both FIAD and NFIAD dogs.	[Favrot, Claude; Picco, Federicca] Univ Zurich, Clin Small Anim Internal Med, Vetsuisse Fac, Zurich, Switzerland; [Steffan, Jean; Seewald, Wolfgang] Novartis Anim Hlth, Basel, Switzerland	Favrot, C (reprint author), Univ Zurich, Clin Small Anim Internal Med, Vetsuisse Fac, Zurich, Switzerland.	cfavrot@vetclinics.unizh.ch			Novartis Animal Health, Basel, Switzerland	The study was funded by Novartis Animal Health, Basel, Switzerland.	Chesney CJ, 2002, J SMALL ANIM PRACT, V43, P203, DOI 10.1111/j.1748-5827.2002.tb00058.x; Chesney CJ, 2001, VET REC, V148, P445; DeBoer DJ, 2001, VET IMMUNOL IMMUNOP, V81, P271, DOI 10.1016/S0165-2427(01)00312-9; Denis Serge, 1994, Medecin Veterinaire du Quebec, V24, P11; Denis Serge, 1994, Medecin Veterinaire du Quebec, V24, P15; Fraser MA, 2008, J SMALL ANIM PRACT, V49, P128, DOI 10.1111/j.1748-5827.2007.00439.x; Griffin CE, 2001, VET IMMUNOL IMMUNOP, V81, P255, DOI 10.1016/S0165-2427(01)00346-4; HALLIWELL RE, 1971, VET REC, V89, P209; Halliwell R, 2006, VET IMMUNOL IMMUNOP, V114, P207, DOI 10.1016/j.vetimm.2006.08.013; HANIFIN JM, 1980, ACTA DERM-VENEREOL, P44; KIRKPATRICK S, 1983, SCIENCE, V220, P671, DOI 10.1126/science.220.4598.671; Nesbitt GH, 2003, VET DERMATOL, V14, P67, DOI 10.1046/j.1365-3164.2003.00328.x; NESBITT GH, 1984, COMP CONT EDUC PRACT, V6, P73; NESBITT GH, 1978, J AM VET MED ASSOC, V172, P55; Nodtvedt A, 2006, VET REC, V159, P241; Olivry T, 2001, VET IMMUNOL IMMUNOP, V81, P219, DOI 10.1016/S0165-2427(01)00311-7; Olivry T, 2007, VET DERMATOL, V18, P390, DOI 10.1111/j.1365-3164.2007.00625.x; Picco F, 2008, VET DERMATOL, V19, P150, DOI 10.1111/j.1365-3164.2008.00669.x; Prelaud P, 1998, REV MED VET-TOULOUSE, V149, P1057; Saridomichelakis MN, 2007, VET DERMATOL, V18, P341, DOI 10.1111/j.1365-3164.2007.00619.x; SCOTT DW, 1981, J AM ANIM HOSP ASSOC, V17, P89; Sousa CA, 2001, VET IMMUNOL IMMUNOP, V81, P153, DOI 10.1016/S0165-2427(01)00297-5; Tarpataki N, 2006, ACTA VET HUNG, V54, P353, DOI 10.1556/AVet.54.2006.3.6; Verlinden A, 2006, CRIT REV FOOD SCI, V46, P259, DOI 10.1080/10408390591001117; WILLEMSE A, 1983, RES VET SCI, V34, P261; WILLEMSE T, 1986, J SMALL ANIM PRACT, V27, P771, DOI 10.1111/j.1748-5827.1986.tb02119.x; Williams HC, 1996, LANCET, V348, P1391, DOI 10.1016/S0140-6736(05)65466-9; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P397, DOI 10.1111/j.1365-2133.1994.tb08531.x; Williams HC, 2005, NEW ENGL J MED, V352, P2314, DOI 10.1056/NEJMcp042803; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P406, DOI 10.1111/j.1365-2133.1994.tb08532.x; Williams HC, 1996, BRIT J DERMATOL, V135, P12; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P383, DOI 10.1111/j.1365-2133.1994.tb08530.x; Zur G, 2002, VET DERMATOL, V13, P89, DOI 10.1046/j.1365-3164.2002.00285.x	33	117	117	5	37	WILEY-BLACKWELL PUBLISHING, INC	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0959-4493			VET DERMATOL	Vet. Dermatol.	FEB	2010	21	1					23	30		10.1111/j.1365-3164.2009.00758.x		8	Dermatology; Veterinary Sciences	Dermatology; Veterinary Sciences	551CR	WOS:000274183900003	20187911	
J	Moshammer, H; Hoek, G; Luttmann-Gibson, H; Neuberger, MA; Antova, T; Gehring, U; Hruba, F; Pattenclen, S; Rudnai, P; Slachtova, H; Zlotkowska, R; Fletcher, T				Moshammer, H; Hoek, G; Luttmann-Gibson, H; Neuberger, MA; Antova, T; Gehring, U; Hruba, F; Pattenclen, S; Rudnai, P; Slachtova, H; Zlotkowska, R; Fletcher, T			Parental smoking and lung function in children - An international study	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						child; passive smoking; pregnancy; spirometry; tobacco	ENVIRONMENTAL TOBACCO-SMOKE; MATERNAL SMOKING; IN-UTERO; RESPIRATORY SYMPTOMS; AIR-POLLUTION; RISK-FACTORS; EXPOSURE; ASTHMA; CHILDHOOD; HEALTH	Rationale: Both prenatal and postnatal passive smoking have been linked with respiratory symptoms and asthma in childhood. Their differential contributions to lung function growth in the general children's population are less clear. Objective: To study the relative impact of pre- and postnatal exposure on respiratory functions of primary school children in a wide range of geographic settings, we analyzed flow and volume data of more than 20,000 children (aged 6-12 yr) from nine countries in Europe and North America. Methods: Exposure information had been obtained by comparable questionnaires, and spirometry followed a protocol of the American Thoracic Society/European Respiratory Society. Linear and logistic regressions were used, controlling for individual risk factors and study area. Heterogeneity between study-specific results and mean effects were estimated using meta-analytic tools. Main Results: Smoking during pregnancy was associated with decreases in lung function parameters between -1% (FEV1) and -6% maximal expiratory flow at 25% of vital capacity left (MEF25). A 4% lower maximal midexpiratory flow (MMEF) corresponded to a 40% increase in the risk of poor lung function (MMEF < 75% of expected). Associations with current passive smoking were weaker though still measurable, with effects ranging from -0.5% (FEV1) to -2% maximal expiratory flow (MEF50). Conclusions: Considering the high number of children exposed to maternal smoking in utero and the even higher number exposed to passive smoking after birth, this risk factor for reduced lung function growth remains a serious pediatric and public health issue.	Med Univ Vienna, Inst Environm Hlth, ZPH, Vienna, Austria; Univ Utrecht, Inst Risk Assessment Sci, Utrecht, Netherlands; Natl Ctr Publ Hlth Protect, Environm Hlth Unit, Sofia, Bulgaria; Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA; GSF, Natl Res ctr Environm & Hlth, Inst Epidemiol, Neuherberg, Germany; Reg Author Publ Hlth, Dept Hlth Stat & Informat, Banska Bystrica, Slovakia; London Sch Hyg & Trop Med, Publ & Environm Hlth Res Unit, London WC1, England; Jozef Fodor Natl Ctr Publ Hlth, Natl Inst Environm Hlth, Budapest, Hungary; Inst Publ Hlth, Ostrava, Czech Republic; Inst Occupat Med & Environm Hlth, Dept Epidemiol, Sosnowiec, Poland	Neuberger, MA (reprint author), Kinderspitalgasse 15, A-1095 Vienna, Austria.	manfred.neuberger@univie.ac.at	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Neuberger, Manfred/0000-0002-8994-378X; Gehring, Ulrike/0000-0003-3612-5780			American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P1286; Apostol GG, 2002, AM J RESP CRIT CARE, V166, P166, DOI 10.1164/rccm.2007035; Cook DG, 1998, THORAX, V53, P884; Corbo GM, 1996, AM J RESP CRIT CARE, V154, P695; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; European Respiratory Society, 1993, EUR RESPIR J, V16, P1; Gehring U, 2006, EUR RESPIR J, V27, P95, DOI 10.1183/09031936.06.00017205; Gilliland FD, 2000, THORAX, V55, P271, DOI 10.1136/thorax.55.4.271; Gilliland FD, 2002, AM J RESP CRIT CARE, V166, P457, DOI 10.1164/rccm.2112064; Gilliland FD, 2003, AM J RESP CRIT CARE, V167, P917, DOI 10.1164/rccm.200206-616OC; Grol MH, 1999, AM J RESP CRIT CARE, V160, P1830; Heinrich J, 1999, ENVIRON HEALTH PERSP, V107, P53, DOI 10.2307/3434289; Janssen NAH, 2003, ENVIRON HEALTH PERSP, V111, P1512, DOI 10.1289/ehp.6243; Kooi EMW, 2004, PEDIATR PULM, V38, P419, DOI 10.1002/ppul.20093; Kunzli N, 2000, EUR RESPIR J, V15, P131; Leonardi GS, 2002, EUR RESPIR J, V20, P890, DOI 10.1183/09031936.02.00260802; Li YF, 2000, AM J RESP CRIT CARE, V162, P2097; Lodrup Carlsen K C, 1997, Eur Respir J, V10, P1774, DOI 10.1183/09031936.97.10081774; Luttmann H, 1997, Pneumologie, V51, P47; Mannino DM, 2001, ARCH PEDIAT ADOL MED, V155, P36; Morgan WJ, 1998, AM J RESP CRIT CARE, V158, P689; Moshammer H, 2004, INT J HYG ENVIR HEAL, V207, P337, DOI 10.1078/1438-4639-00299; Neuberger M, 2002, ATMOS ENVIRON, V36, P1733, DOI 10.1016/S1352-2310(02)00179-6; Neuberger M., 1994, PNEUMOLOGIE, V48, P175; Raizenne M, 1996, ENVIRON HEALTH PERSP, V104, P506, DOI 10.2307/3432991; Rasmussen F, 2002, AM J RESP CRIT CARE, V165, P1480, DOI 10.1164/rccm.2108009; Rizzi M, 2004, CHEST, V125, P1387, DOI 10.1378/chest.125.4.1387; ROSE G, 1990, BRIT MED J, V301, P1031; Skorge TD, 2005, AM J RESP CRIT CARE, V172, P61, DOI 10.1164/rccm.200409-1158OC; Upton MN, 2004, AM J RESP CRIT CARE, V169, P479, DOI 10.1164/rccm.200211-1357OC; VONEHRENSTEIN OS, 2002, EUR RESPIR J, V12, P1099; Wenten M, 2005, AM J RESP CRIT CARE, V172, P1563, DOI 10.1164/rccm.200506-4900C; ZAPLETAL A, 1969, J APPL PHYSIOL, V26, P308; Zlotkowska R, 2005, EUR J EPIDEMIOL, V20, P719, DOI 10.1007/s10654-005-0033-z	34	117	126	0	9	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	JUN 1	2006	173	11					1255	1263		10.1164/rccm.200510-1552OC		9	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	049BJ	WOS:000237990100014	16484675	
J	Taylor, SL; Hefle, SL; Bindslev-Jensen, C; Atkins, FM; Andre, C; Bruijnzeel-Koomen, C; Burks, AW; Bush, RK; Ebisawa, M; Eigenmann, PA; Host, A; Hourihane, JO; Isolauri, E; Hill, DJ; Knulst, A; Lack, G; Sampson, HA; Moneret-Vautrin, DA; Rance, F; Vadas, PA; Yunginger, JW; Zeiger, RS; Salminen, JW; Madsen, C; Abbott, P				Taylor, SL; Hefle, SL; Bindslev-Jensen, C; Atkins, FM; Andre, C; Bruijnzeel-Koomen, C; Burks, AW; Bush, RK; Ebisawa, M; Eigenmann, PA; Host, A; Hourihane, JO; Isolauri, E; Hill, DJ; Knulst, A; Lack, G; Sampson, HA; Moneret-Vautrin, DA; Rance, F; Vadas, PA; Yunginger, JW; Zeiger, RS; Salminen, JW; Madsen, C; Abbott, P			A consensus protocol for the determination of the threshold doses for allergenic foods: how much is too much?	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergy; clinical trial; DBPCFC; exposure; food; threshold; risk assessment	CASEIN HYDROLYSATE FORMULA; DOUBLE-BLIND; IGE CONCENTRATIONS; ATOPIC-DERMATITIS; PEANUT ALLERGY; EGG ALLERGY; COW MILK; CHALLENGES; HYPERSENSITIVITY; IDENTIFICATION	Background While the ingestion of small amounts of an offending food can elicit adverse reactions in individuals with IgE-mediated food allergies, little information is known regarding these threshold doses for specific allergenic foods. While low-dose challenge trials have been conducted on an appreciable number of allergic individuals, a variety of different clinical protocols were used making the estimation of the threshold dose very difficult. Objective A roundtable conference was convened to develop a consensus clinical protocol for low-dose challenge trials for the estimation of threshold doses for specific allergenic foods. Methods In May 2002, 20 clinical allergists and other interested parties were invited to participate in a roundtable conference to develop consensus of the key elements of a clinical protocol for low-dose challenge trials. Results A consensus protocol was developed. Patients with convincing histories of food allergies and supporting diagnostic evidence including past challenge trials or high CAP-RAST scores can be enrolled in low-dose challenge trials. Care must be taken with younger patients to assure that they have not outgrown their food allergy. An approach was developed for the medication status of patients entering such trials. Challenge materials must be standardized, for example, partially defatted peanut flour composed of equal amounts of the three major varieties of peanuts (Florunner, Virginia, Spanish). Challenge materials must be appropriately blinded with sensory evaluation used to confirm the adequacy of blinding. A double-blind, placebo-controlled design should be used for low-dose challenge trials. Low-dose challenge trials would begin at doses of 10 mug of the allergenic food and would continue with doses of 100 mug and 1 mg followed by specific higher doses up to 100 mg depending upon the expert judgement of the physician; even higher doses might be applied to assure that the patient is indeed reactive to the particular food. A 30-min time interval would be used between doses, and reactive doses would be expressed as both discrete and cumulative doses. The goal of each challenge would be to develop objective symptoms; trials should not be discontinued on the basis of subjective symptoms only. Statistically, a minimum of 29 patients would be enrolled in low-dose challenge trials for each allergenic food because 0 reactors out of 29 patients at a particular dose allow the conclusion that there is 95% certainty that 90% of allergic individuals will not react to that dose. Conclusion A consensus protocol was developed. Using this protocol, it will be possible to estimate threshold doses for allergenic foods, the lowest amount that elicits mild, objective symptoms in highly sensitive individuals.	Univ Nebraska, Food Allergy Res & Resource Program, Lincoln, NE 68583 USA; Odense Univ Hosp, Dept Dermatol, DK-5000 Odense, Denmark; Natl Jewish Med & Res Ctr, Denver, CO USA; Stallergenes, Antony, France; Univ Med Ctr, Dept Dermatol Allergol, Utrecht, Netherlands; Arkansas Childrens Hosp, Little Rock, AR 72202 USA; Univ Wisconsin Hosp & Clin, William S Middleton Mem Vet Adm Hosp, Madison, WI 53792 USA; Natl Sagamihara Hosp, Kanagawa, Japan; Hop Enfants, Geneva, Switzerland; Odense Univ Hosp, Dept Pediat, DK-5000 Odense, Denmark; Univ Southampton, Southampton, Hants, England; Univ Turku, Dept Pediat, Turku, Finland; Royal Childrens Hosp, Parkville, Vic 3052, Australia; St Marys Hosp, London, England; CUNY Mt Sinai Sch Med, New York, NY 10029 USA; Univ Hosp, Dept Internal Med Clin Immunol & Allergol, Nancy, France; Hop Enfants, Dept Allergol, Toulouse, France; Wellesley Cent Hosp, Toronto, ON, Canada; Mayo Clin, Rochester, MN USA; Kaiser Permanente Med Ctr, San Diego, CA USA; Hlth Prod & Foods Branch, Chem Hlth Hazard Assessment Div, Ottawa, ON, Canada; Danish Vet & Food Adm, Soborg, Denmark; Food Stand Australia New Zealand, Canberra, ACT, Australia	Taylor, SL (reprint author), Univ Nebraska, Food Allergy Res & Resource Program, 143 Food Ind Bldg, Lincoln, NE 68583 USA.	staylor2@unl.edu	Bindslev-Jensen, Carsten/H-1877-2011; Osborne, Nicholas/N-4915-2015; Eigenmann, Philippe/A-6569-2017	Bindslev-Jensen, Carsten/0000-0002-8940-038X; Osborne, Nicholas/0000-0002-6700-2284; Eigenmann, Philippe/0000-0003-1738-1826			*AM AC PED SUBC NU, 1990, INF FORM ALL DIS REP; ANET J, 1985, INT ARCH ALLER A IMM, V77, P363; BERNHISELBROADBENT J, 1992, J ALLERGY CLIN IMMUN, V89, P730, DOI 10.1016/0091-6749(92)90381-B; Betschel S. 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Exp. Allergy	MAY	2004	34	5					689	695		10.1111/j.1365-2222.2004.1886.x		7	Allergy; Immunology	Allergy; Immunology	820PN	WOS:000221401900005	15144458	
J	Ricciardolo, FLM; Gaston, B; Hunt, J				Ricciardolo, FLM; Gaston, B; Hunt, J			Acid stress in the pathology of asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						airway pH; gastroesophageal reflux; tachykinins; capsaicin; exhaled breath condensate; acid; asthma; chronic obstructive pulmonary disease; cough; bronchoconstriction	EXHALED BREATH CONDENSATE; INDUCED AIRWAY HYPERRESPONSIVENESS; TACHYKININ RECEPTOR ANTAGONISTS; GUINEA-PIGS; CITRIC-ACID; INDUCED BRONCHOCONSTRICTION; NITRIC-OXIDE; GASTROESOPHAGEAL-REFLUX; CYSTIC-FIBROSIS; INDUCED COUGH	Although alteration of airway pH may serve an innate host defense capacity, it also is implicated in the pathophysiology of obstructive airway diseases. Acid-induced asthma appears in association with gastroesophageal reflux after accidental inhalation of acid (fog, pollution, and workplace exposure) and in the presence of altered airway pH homeostasis. Endogenous and exogenous exposures to acids evoke cough, bronchoconstriction, airway hyperreactivity, microvascular leakage, and heightened production of mucous, fluid, and nitric oxide. Abnormal acidity of the airways is reflected in exhaled breath assays. The intimate mechanisms of acid-induced airway obstruction are dependent on activation of capsaicin-sensitive sensory nerves. Protons activate these nerves with the subsequent release of tachykinins (major mediators of this pathway) that, in conjunction with kinins, nitric oxide, oxygen radicals, and proteases, modulate diverse aspects of airway dysfunction and inflammation. The recognition that acid stress might initiate or exacerbate airway obstructive symptomatology has prompted the consideration of new therapies targeting pH homeostasis.	Univ Virginia, Div Pediat Resp Med, Hlth Syst, Charlottesville, VA 22908 USA; G Gaslini Inst Children, Unit Resp Dis, Genoa, Italy	Hunt, J (reprint author), Univ Virginia, Div Pediat Resp Med, Hlth Syst, Box 800386, Charlottesville, VA 22908 USA.						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KLEBANOFF SJ, 1993, FREE RADICAL BIO MED, V14, P351, DOI 10.1016/0891-5849(93)90084-8; Kohrogi H, 2001, AM J MED, V111, P25, DOI 10.1016/S0002-9343(01)00859-2; KopferschmittKubler MC, 1996, REV MAL RESPIR, V13, P421; Kostikas K, 2002, AM J RESP CRIT CARE, V165, P1364, DOI 10.1164/rccm.200111-068OC; Kruk-Zagajewska A, 1976, Otolaryngol Pol, V30, P479; Lai YL, 1999, BRIT J PHARMACOL, V126, P778, DOI 10.1038/sj.bjp.0702352; LALLOO UG, 1995, J APPL PHYSIOL, V79, P1082; Lardner A, 2001, J LEUKOCYTE BIOL, V69, P522; Leblebicioglu B, 1999, INFECT IMMUN, V67, P2019; Lee KH, 1998, CRIT CARE MED, V26, P2042, DOI 10.1097/00003246-199812000-00038; Lee LY, 2001, J APPL PHYSIOL, V91, P1318; Long R, 1999, ANTIMICROB AGENTS CH, V43, P403; Lopes FDTQS, 2002, J APPL PHYSIOL, V93, P842, DOI 10.1152/japplphysiol.00013.2002; Lopez DH, 1999, IMMUNOLOGY, V98, P450, DOI 10.1046/j.1365-2567.1999.00884.x; LOU YP, 1991, ACTA PHYSIOL SCAND, V142, P191, DOI 10.1111/j.1748-1716.1991.tb09147.x; MAGGI CA, 1995, PHYSIOL REV, V75, P277; Maggi CA, 1997, TRENDS PHARMACOL SCI, V18, P351, DOI 10.1016/S0165-6147(97)01107-3; MARTLING CR, 1988, ANESTHESIOLOGY, V68, P350, DOI 10.1097/00000542-198803000-00005; McShane D, 2003, EUR RESPIR J, V21, P37, DOI 10.1183/09031936.03.00027603; Metheny NA, 1999, NURS RES, V48, P189, DOI 10.1097/00006199-199907000-00001; Mishra A, 2001, J CLIN INVEST, V107, P83, DOI 10.1172/JCI10224; Nader-Djalal N, 1998, ANESTH ANALG, V87, P127, DOI 10.1097/00000539-199807000-00028; NAHAS GG, 1971, P SOC EXP BIOL MED, V138, P350; NEAS LM, 1995, AM J EPIDEMIOL, V141, P111; NGAMTRAKULPANIT L, 2003, AM J RESP CRIT CARE, V167, pA446; NUUTINEN J, 1993, J OTOLARYNGOL, V22, P79; Ohrui T, 1997, CHEST, V111, P454, DOI 10.1378/chest.111.2.454; PALMER LB, 1986, AM REV RESPIR DIS, V133, P784; RABINOVITCH M, 1980, J RETICULOENDOTH SOC, V27, P189; Rahman I, 1996, AM J RESP CRIT CARE, V154, P1055; RATNER S, 1992, CELL IMMUNOL, V139, P399, DOI 10.1016/0008-8749(92)90081-Y; REGOLI D, 1994, PHARMACOL REV, V46, P551; Ricciardolo FLM, 1999, AM J RESP CRIT CARE, V159, P557; Ricciardolo FLM, 2001, AM J MED, V111, P18, DOI 10.1016/S0002-9343(01)00816-6; ROTSTEIN OD, 1988, J SURG RES, V45, P298, DOI 10.1016/0022-4804(88)90079-0; SATOH H, 1993, EUR J PHARMACOL, V236, P367, DOI 10.1016/0014-2999(93)90473-U; Song YL, 2003, J GEN PHYSIOL, V122, P511, DOI 10.1085/jgp.200308866; Tate S, 2002, THORAX, V57, P926, DOI 10.1136/thorax.57.11.926; Teramoto S, 2003, CHEST, V123, P524, DOI 10.1378/chest.123.2.524; Trevani AS, 1999, J IMMUNOL, V162, P4849; Vaughan J, 2003, EUR RESPIR J, V22, P889, DOI 10.1183/09031936.03.00038803; Vincent D, 1997, EUR RESPIR J, V10, P2255, DOI 10.1183/09031936.97.10102255; Wadsworth SJ, 1997, AM J PHYSIOL-LUNG C, V273, pL427; Yasumitsu R, 1996, EUR J PHARMACOL, V300, P215, DOI 10.1016/0014-2999(95)00881-0; ZIGMOND SH, 1981, J IMMUNOL, V126, P478	98	117	122	0	9	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749	1097-6825		J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	APR	2004	113	4					610	619		10.1016/j.jaci.2003.12.034		10	Allergy; Immunology	Allergy; Immunology	814DY	WOS:000220956600005	15100663	
J	McConnell, R; Berhane, K; Gilliland, F; Molitor, J; Thomas, D; Lurmann, F; Avol, E; Gauderman, WJ; Peters, JM				McConnell, R; Berhane, K; Gilliland, F; Molitor, J; Thomas, D; Lurmann, F; Avol, E; Gauderman, WJ; Peters, JM			Prospective study of air pollution and bronchitic symptoms in children with asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; epidemiology; air pollution; child; particulate matter	SOUTHERN CALIFORNIA CHILDREN; DIESEL EXHAUST PARTICLES; LUNG-FUNCTION GROWTH; RESPIRATORY HEALTH; ORGANIC AEROSOL; INHALABLE PARTICLES; PERSONAL EXPOSURE; NITROGEN-DIOXIDE; ASSOCIATION; ADMISSIONS	The relationship of bronchitic symptoms to ambient particulate matter and to particulate elemental and organic carbon (OC), nitrogen dioxide (NO2), and other gaseous pollutants was examined in a cohort of children with asthma in 12 Southern California communities. Symptoms, assessed yearly by questionnaire from 1996 to 1999, were associated with the yearly variability of particulate matter with aerodynamic diameter less than 2.5 mum (odds ratio [OR] 1.09/mug/m(3); 95% confidence interval [CI] 1.01-1.17), OC (OR 1.41/mug/m(3); 95% CI 1.12-1.78), NO2 (OR 1.07/ppb; 95% CI 1.02-1.13), and ozone (OR 1.06/ppb; 95% Cl 1.00-1.12). The ORs associated with yearly within-community variability in air pollution were larger than the effect of the between-community 4-year average concentrations. In two pollutant models, the effects of yearly variation in OC and NO2 were only modestly reduced by adjusting for other pollutants, except in a model containing both OC and NO2; the effects of all other pollutants were reduced after adjusting for OC or NO2. We conclude that OC and NO2 deserve greater attention as potential causes of the chronic symptoms of bronchitis in children with asthma and that previous cross-sectional studies may have underestimated the risks associated with air pollution.	Univ So Calif, Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA; Sonoma Technol Inc, Petaluma, CA USA	McConnell, R (reprint author), Univ So Calif, Sch Med, Dept Prevent Med, 1540 Alcazar St,CHP 236, Los Angeles, CA 90033 USA.				NHLBI NIH HHS [5 R01 HL61768-04]; NIEHS NIH HHS [1 P01 ES11627-01, 5 P01 ES09581-05, 5 P30 ES07048-07]		Atkinson RW, 2001, AM J RESP CRIT CARE, V164, P1860; Bascom R, 1996, AM J RESP CRIT CARE, V153, P477; BATES DV, 1995, ENVIRON HEALTH PERSP, V103, P243, DOI 10.2307/3432380; Bonvallot V, 2001, AM J RESP CELL MOL, V25, P515; BraunFahrlander C, 1997, AM J RESP CRIT CARE, V155, P1042; Casillas AM, 1999, ANN ALLERG ASTHMA IM, V83, P624, DOI 10.1016/S1081-1206(10)62884-0; Chauhan AJ, 1999, AM J RESP CRIT CARE, V159, pA699; Delfino RJ, 1998, ENVIRON HEALTH PERSP, V106, P751, DOI 10.1289/ehp.98106751; Delfino RJ, 1996, AM J RESP CRIT CARE, V154, P633; DIGGLE PJ, 1994, ANAL LONGITUDIANAL D; DOCKERY DW, 1994, ANNU REV PUBL HEALTH, V15, P107, DOI 10.1146/annurev.pu.15.050194.000543; DOCKERY DW, 1989, AM REV RESPIR DIS, V139, P587; Dockery DW, 1996, ENVIRON HEALTH PERSP, V104, P500, DOI 10.2307/3432990; Gauderman WJ, 2000, AM J RESP CRIT CARE, V162, P1383; Gauderman WJ, 2002, AM J RESP CRIT CARE, V166, P76, DOI 10.1164/rccm.2111021; Hashimoto KI, 2001, AM J RESP CRIT CARE, V164, P1957; Heagerty PJ, 2000, STAT SCI, V15, P1; Heinrich J, 2000, AM J RESP CRIT CARE, V161, P1930; Hirsch T, 1999, EUR RESPIR J, V14, P669, DOI 10.1034/j.1399-3003.1999.14c29.x; Hiura TS, 1999, J IMMUNOL, V163, P5582; Jedrychowski W, 1998, EUR RESPIR J, V11, P1312, DOI 10.1183/09031936.98.11061312; KOREN HS, 1995, ENVIRON HEALTH PERSP, V103, P235, DOI 10.2307/3432379; Li N, 2002, INHAL TOXICOL, V14, P459, DOI 10.1080/089583701753678571; Lierl MB, 2003, ANN ALLERG ASTHMA IM, V90, P28; Linaker CH, 2000, THORAX, V55, P930, DOI 10.1136/thorax.55.11.930; MANCHESTER JB, 2001, DETERMINATION ELEM B; McArdle W, 1996, EXERCISE PHYSL ENERG; McConnell R, 2002, LANCET, V359, P386, DOI 10.1016/S0140-6736(02)07597-9; McConnell R, 1999, ENVIRON HEALTH PERSP, V107, P757, DOI 10.2307/3434662; McConnell R, 2002, EPIDEMIOLOGY, V13, pS148; *NIOSH, 1999, NIOSH MAN AN METH; *NIOSH, 1996, EL CARB DIES EXH NIO; Norris G, 1999, ENVIRON HEALTH PERSP, V107, P489, DOI 10.2307/3434632; PETERS J, 1997, EPIDEMIOLOGIC INVEST; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; POPE CA, 1991, AM REV RESPIR DIS, V144, P668; POPE CA, 1991, ARCH ENVIRON HEALTH, V46, P90; Romieu I, 1996, AM J RESP CRIT CARE, V154, P300; SALMON LG, 2000, ORGANIC ELEMENTAL CA; *SAS I INC, 1999, SAS STAT VERS 8 02 M; SCHAUER J, 1996, ATMOS ENVIRON, V22, P3837; Strader R, 1999, ATMOS ENVIRON, V33, P4849, DOI 10.1016/S1352-2310(99)00310-6; Sydbom A, 2001, EUR RESPIR J, V17, P733, DOI 10.1183/09031936.01.17407330; TURPIN BJ, 1991, ATMOS ENVIRON A-GEN, V25, P207, DOI 10.1016/0960-1686(91)90291-E; TURPIN BJ, 1995, ATMOS ENVIRON, V29, P3527, DOI 10.1016/1352-2310(94)00276-Q; Vedal S, 1998, AM J RESP CRIT CARE, V157, P1034; VERHEIJ T, 1995, SCAND J PRIM HEALTH, V13, P8, DOI 10.3109/02813439508996728; Yu OC, 2000, ENVIRON HEALTH PERSP, V108, P1209, DOI 10.2307/3434835	48	117	120	3	8	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	OCT 1	2003	168	7					790	797		10.1164/rccm.200304-466OC		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	726QZ	WOS:000185611700010	12893648	
J	Hansel, TT; Kharitonov, SA; Donnelly, LE; Erin, EM; Currie, MG; Moore, WM; Manning, PT; Recker, DP; Barnes, PJ				Hansel, TT; Kharitonov, SA; Donnelly, LE; Erin, EM; Currie, MG; Moore, WM; Manning, PT; Recker, DP; Barnes, PJ			A selective inhibitor of inducible nitric oxide synthase inhibits exhaled breath nitric oxide in healthy volunteers and asthmatics	FASEB JOURNAL			English	Article						respiratory; pharmacology; tolerability	OBSTRUCTIVE PULMONARY-DISEASE; INOS INHIBITOR; AIRWAYS; LUNG; MICE; AIR; BRONCHODILATOR; NITROTYROSINE; PEROXYNITRITE; INFLAMMATION	The inducible isoenzyme of nitric oxide synthase (iNOS) generates nitric oxide (NO) in inflammatory diseases such as asthma. The prodrug L-N-6-(1-iminoethyl)lysine 5-tetrazole amide (SC-51) is rapidly converted in vivo to the active metabolite L-N-6-(1-iminoethyl)lysine (L-NIL). Initially, we performed in vitro experiments in human primary airway epithelial cells to demonstrate that L-NIL causes inhibition of iNOS. In a randomized double-blind placebo-controlled crossover trial, SC-51 was administered as a single oral dose (20 or 200 mg) in separate cohorts of healthy volunteers (two groups of n=12) and mild asthmatic patients (two groups of n=12). SC-51 (200 mg) reduced exhaled breath NO levels to <2 ppb in both healthy volunteers (P<0.001) and mild asthmatics (P<0.001) within 15 min, representing >90% inhibition of baseline levels of NO in asthmatic patients, with the effects lasting at least 72 h. There were no significant effects on blood pressure, pulse rate, or respiratory function (FEV1). This study demonstrates that an inhibitor of iNOS produces marked inhibition of exhaled breath NO in normal and asthmatic subjects without producing the side effects observed following the systemic administration of non-selective NOS inhibitors, and thus provides support for the potential use of iNOS inhibitors to treat a range of inflammatory clinical disorders.	Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Clin Studies Unit, London, England; Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Thorac Med, London, England; Pharmacia Corp, Skokie, IL USA; Pharmacia Corp, St Louis, MO USA	Hansel, TT (reprint author), Royal Brompton Hosp, NHLI Clin Studies Unit, London SW3 6HP, England.	t.hansel@imperial.ac.uk					Alderton WK, 2001, BIOCHEM J, V357, P593, DOI 10.1042/0264-6021:3570593; ALVING K, 1993, EUR RESPIR J, V6, P1368; Amin Ashok R., 1999, Current Opinion in Rheumatology, V11, P202, DOI 10.1097/00002281-199905000-00009; Ashina M, 1999, LANCET, V353, P287, DOI 10.1016/S0140-6736(98)01079-4; Ashutosh K, 2000, THORAX, V55, P109, DOI 10.1136/thorax.55.2.109; Barnes PJ, 2000, NEW ENGL J MED, V343, P269, DOI 10.1056/NEJM200007273430407; BELVISI MG, 1992, EUR J PHARMACOL, V210, P221, DOI 10.1016/0014-2999(92)90676-U; BRYNE J, 2001, BR J CARDIOL, V8, P570; Clini E, 1998, THORAX, V53, P881; CONNOR JR, 1995, EUR J PHARMACOL, V273, P15, DOI 10.1016/0014-2999(94)00672-T; Corradi M, 1999, THORAX, V54, P572; Donnelly LE, 2001, AM J RESP CELL MOL, V24, P295; Dworski R, 2000, THORAX, V55, pS51, DOI 10.1136/thorax.55.suppl_2.S51; Gomez FP, 1998, EUR RESPIR J, V12, P865, DOI 10.1183/09031936.98.12040865; Hallinan EA, 2002, J MED CHEM, V45, P1686, DOI 10.1021/jm010420e; Hanazawa T, 2000, AM J RESP CRIT CARE, V162, P1273; Hart CM, 1999, CHEST, V115, P1407, DOI 10.1378/chest.115.5.1407; Hickey MJ, 2001, CLIN SCI, V100, P1, DOI 10.1042/CS20000135; Hobbs AJ, 1999, ANNU REV PHARMACOL, V39, P191, DOI 10.1146/annurev.pharmtox.39.1.191; HUANG PL, 1995, NATURE, V377, P239, DOI 10.1038/377239a0; Ichinose M, 2000, AM J RESP CRIT CARE, V162, P701; Kaminsky DA, 1999, J ALLERGY CLIN IMMUN, V104, P747; Kharitonov S, 1997, EUR RESPIR J, V10, P1683, DOI 10.1183/09031936.97.10071683; Kharitonov SA, 2001, AM J RESP CRIT CARE, V163, P1693; KHARITONOV SA, 1994, LANCET, V343, P133, DOI 10.1016/S0140-6736(94)90931-8; Koarai A, 2000, PULM PHARMACOL THER, V13, P267, DOI 10.1006/pupt.2000.0254; KUO HP, 1992, EUR J PHARMACOL, V221, P385; Leckie MJ, 2000, EXPERT OPIN INV DRUG, V9, P3; Lipton AJ, 2001, NATURE, V413, P171, DOI 10.1038/35093117; Lopez-Jaramillo P, 1998, LANCET, V351, P1176, DOI 10.1016/S0140-6736(05)79119-4; Maziak W, 1998, AM J RESP CRIT CARE, V157, P998; MISKO TP, 1993, ANAL BIOCHEM, V214, P1; MONCADA S, 1989, BIOCHEM PHARMACOL, V38, P1709, DOI 10.1016/0006-2952(89)90403-6; Moncada S, 1999, J ROY SOC MED, V92, P164; Moore WM, 1996, J MED CHEM, V39, P669, DOI 10.1021/jm950766n; Perner A, 1999, ALIMENT PHARM THERAP, V13, P135; Ricciardolo FLM, 1996, LANCET, V348, P374, DOI 10.1016/S0140-6736(96)04450-9; RITTER J, 2001, BR J CARDIOL, V8, P564; Rutgers SR, 1999, THORAX, V54, P576; Sadeghi-Hashjin G, 1998, CLIN EXP ALLERGY, V28, P1464; Saleh D, 1998, FASEB J, V12, P929; Salvemini D, 1996, BRIT J PHARMACOL, V118, P829; SALVEMINI D, 1995, J CLIN INVEST, V96, P301, DOI 10.1172/JCI118035; Shah AM, 2000, PHARMACOL THERAPEUT, V86, P49, DOI 10.1016/S0163-7258(99)00072-8; Singh S, 1997, EUR RESPIR J, V10, P699; Slutsky AS, 1999, AM J RESP CRIT CARE, V160, P2104; Stirling RG, 1998, THORAX, V53, P1030; Szabo C, 1999, SHOCK, V12, P1, DOI 10.1097/00024382-199907000-00001; Taylor DA, 1998, AM J RESP CRIT CARE, V158, P99; Thomsen LL, 1998, CLIN NEUROSCI, V5, P28; Torreilles J, 2001, FRONT BIOSCI, V6, pD1161, DOI 10.2741/Torreill; Trifilieff A, 2000, J IMMUNOL, V165, P1526; Tulic MK, 2000, EUR RESPIR J, V15, P870, DOI 10.1183/09031936.00.15587000; VALLANCE P, 1989, LANCET, V2, P997; WARD JK, 1995, AM J RESP CELL MOL, V13, P175; Weinberger B, 1999, PHARMACOL THERAPEUT, V84, P401, DOI 10.1016/S0163-7258(99)00044-3; Xiong YL, 1999, J IMMUNOL, V162, P445; YATES DH, 1995, AM J RESP CRIT CARE, V152, P892; Yates DH, 1996, AM J RESP CRIT CARE, V154, P247	59	117	122	0	6	FEDERATION AMER SOC EXP BIOL	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA	0892-6638			FASEB J	Faseb J.	MAY	2003	17	8					1298	+		10.1096/fj.02-0633fje		20	Biochemistry & Molecular Biology; Biology; Cell Biology	Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology	683TE	WOS:000183165000030	12738811	
J	Raby, BA; Klimecki, WT; Laprise, C; Renaud, Y; Faith, J; Lemire, M; Greenwood, C; Weiland, KM; Lange, C; Palmer, LJ; Lazarus, R; Vercelli, D; Kwiatkowski, DJ; Silverman, EK; Martinez, FD; Hudson, TJ; Weiss, ST				Raby, BA; Klimecki, WT; Laprise, C; Renaud, Y; Faith, J; Lemire, M; Greenwood, C; Weiland, KM; Lange, C; Palmer, LJ; Lazarus, R; Vercelli, D; Kwiatkowski, DJ; Silverman, EK; Martinez, FD; Hudson, TJ; Weiss, ST			Polymorphisms in toll-like receptor 4 are not associated with asthma or atopy-related phenotypes	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; genetics; polymorphism; toll-like receptor 4; genetic association	SINGLE-NUCLEOTIDE POLYMORPHISMS; HOUSE-DUST ENDOTOXIN; LINKAGE DISEQUILIBRIUM; BACTERIAL LIPOPOLYSACCHARIDE; HAPLOTYPE STRUCTURE; UNIFIED APPROACH; CD14 GENE; POPULATION; TLR4; MUTATIONS	Toll-like receptor 4 (TLR4) is the principal receptor for bacterial endotoxin recognition, and functional variants in the gene confer endotoxin-hyporesponsiveness in humans. Furthermore, there is evidence that endotoxin exposure during early life is protective against the development of atopy and asthma, although this relationship remains poorly understood. It is therefore possible that genetic variation in the TLR4 locus contributes to asthma susceptibility. In this study we characterize the genetic diversity in the TLR4 locus and test for association between the common genetic variants and asthma-related phenotypes. In a cohort of 90 ethnically diverse subjects, we resequenced the TLR4 locus and identified a total of 29 single nucleotide polymorphisms. We assessed five common polymorphisms for evidence of association with asthma in two large family-based cohorts: a heterogeneous North American cohort (589 families), and a more homogenous population from northeastern Quebec, Canada (167 families). Using the transmission-disequilibrum test, we found no evidence of association for any of the polymorphisms tested, including two functional variants. Furthermore, we found no evidence for association between the TLR4 variants and four quantitative intermediate asthma- and atopy-related phenotypes. Based on these results, we found no evidence that genetic variation in TLR4 contributes to asthma susceptibility.	Harvard Univ, Channing Lab, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA; Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA; Brigham & Womens Hosp, Div Hematol, Boston, MA 02115 USA; Harvard Univ, Partners Ctr Genet & Genomics, Boston, MA 02115 USA; Univ Arizona, Arizona Resp Ctr, Tucson, AZ USA; Univ Montreal, Chicoutimi Hosp, Community Genomic Med Ctr, Montreal, PQ, Canada; Univ Quebec, Chicoutimi, PQ, Canada; McGill Univ, Ctr Hlth, Montreal Genome Ctr, Dept Human Genet, Montreal, PQ H3A 2T5, Canada; McGill Univ, Ctr Hlth, Montreal Genome Ctr, Dept Med, Montreal, PQ H3A 2T5, Canada; McGill Univ, Ctr Hlth, Res Inst, Montreal, PQ H3A 2T5, Canada	Raby, BA (reprint author), Harvard Univ, Channing Lab, Brigham & Womens Hosp, Sch Med, 181 Longwood Ave, Boston, MA 02115 USA.	benjamin.raby@channing.harvard.edu	Palmer, Lyle/K-3196-2014	Palmer, Lyle/0000-0002-1628-3055; lazarus, ross/0000-0003-3939-1961	NHLBI NIH HHS [1 U01 HL66795-01, 2 T32 HL07427-22, N01HR-16049, P01 HL67664]		Aderem A, 2000, NATURE, V406, P782, DOI 10.1038/35021228; American thoracic society (ATS), 1979, AM REV RESPIR DIS, V119, P831; Arbour NC, 2000, NAT GENET, V25, P187; Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Cherniack R, 1999, CONTROL CLIN TRIALS, V20, P91; Clark AG, 1998, AM J HUM GENET, V63, P595, DOI 10.1086/301977; Clayton D, 1999, AM J HUM GENET, V65, P1170, DOI 10.1086/302577; Daly MJ, 2001, NAT GENET, V29, P229, DOI 10.1038/ng1001-229; Drysdale CM, 2000, P NATL ACAD SCI USA, V97, P10483, DOI 10.1073/pnas.97.19.10483; Ewing B, 1998, GENOME RES, V8, P175; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Gordon D, 1998, GENOME RES, V8, P195; GUO SW, 1992, BIOMETRICS, V48, P361, DOI 10.2307/2532296; Hakonarson H, 2001, AM J RESP CRIT CARE, V164, P2036; HEYER E, 1995, AM J HUM GENET, V56, P970; HILL W G, 1968, Theoretical and Applied Genetics, V38, P226, DOI 10.1007/BF01245622; HILL WG, 1974, HEREDITY, V33, P229, DOI 10.1038/hdy.1974.89; HOLLAND PM, 1991, P NATL ACAD SCI USA, V88, P7276, DOI 10.1073/pnas.88.16.7276; Hollox EJ, 2001, AM J HUM GENET, V68, P160, DOI 10.1086/316924; Juniper EF, 1994, HISTAMINE METHACHOLI; Kiechl S, 2002, NEW ENGL J MED, V347, P185, DOI 10.1056/NEJMoa012673; Kline JN, 1999, AM J RESP CRIT CARE, V160, P297; Koppelman GH, 2001, AM J RESP CRIT CARE, V163, P965; Kruglyak L, 2001, NAT GENET, V27, P234, DOI 10.1038/85776; Labuda M, 1996, AM J HUM GENET, V59, P633; Laird NM, 2000, GENET EPIDEMIOL, V19, pS36, DOI 10.1002/1098-2272(2000)19:1+<::AID-GEPI6>3.0.CO;2-M; Laitinen T, 2001, NAT GENET, V28, P87, DOI 10.1038/ng0501-87; Lange C, 2002, GENET EPIDEMIOL, V23, P165, DOI 10.1002/gepi.0209; Lazarus R, 2002, GENOMICS, V80, P223, DOI 10.1006/geno.2002.6820; Lien E, 2000, J CLIN INVEST, V105, P497, DOI 10.1172/JCI8541; Lindblad-Toh K, 2000, NAT GENET, V24, P381, DOI 10.1038/74215; Lorenz E, 2002, ARCH INTERN MED, V162, P1028, DOI 10.1001/archinte.162.9.1028; Lorenz E, 2001, AM J PHYSIOL-LUNG C, V281, pL1106; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; Michel O, 1997, AM J RESP CRIT CARE, V156, P1157; Nickerson DA, 2001, METH MOL B, V175, P29; O'Connell JR, 1998, AM J HUM GENET, V63, P259, DOI 10.1086/301904; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Platts-Mills TAE, 2001, AM J RESP CRIT CARE, V164, P1107; Poltorak A, 1998, SCIENCE, V282, P2085, DOI 10.1126/science.282.5396.2085; Rabinowitz D, 2000, HUM HERED, V50, P211, DOI 10.1159/000022918; Schneider S, 2000, SOFTWARE POPULATION; Schwartz DA, 2001, AM J RESP CRIT CARE, V163, P305; Smirnova I, 2001, GENETICS, V158, P1657; SPIELMAN RS, 1993, AM J HUM GENET, V52, P506; Stephens M, 2001, AM J HUM GENET, V68, P978, DOI 10.1086/319501; STEPHENS M, 2001, PHASE; Strachan DP, 1996, ARCH DIS CHILD, V74, P422; Szefler S, 2000, NEW ENGL J MED, V343, P1054; Tulic MK, 2000, AM J RESP CELL MOL, V22, P604; von Mutius E, 2001, AM J RESP CRIT CARE, V164, P1106; VONMUTIUS E, 1999, PEDIAT ASTHMAED; Wjst M, 1998, BIOINFORMATICS, V14, P827, DOI 10.1093/bioinformatics/14.9.827; 1987, AM REV RESPIR DIS, V136, P225	54	117	125	0	4	AMER THORACIC SOC	NEW YORK	61 BROADWAY, FL 4, NEW YORK, NY 10006 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	DEC 1	2002	166	11					1449	1456		10.1164/rrcm.200207-634OC		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	621LT	WOS:000179590900009	12406828	
J	Crain, EF; Walter, M; O'Connor, GT; Mitchell, H; Gruchalla, RS; Kattan, M; Malindzak, GS; Enright, P; Evans, R; Morgan, W; Stout, JW				Crain, EF; Walter, M; O'Connor, GT; Mitchell, H; Gruchalla, RS; Kattan, M; Malindzak, GS; Enright, P; Evans, R; Morgan, W; Stout, JW			Home and allergic characteristics of children with asthma in seven US urban communities and design of an environmental intervention: The Inner-City Asthma Study	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						environmental intervention; home environmental characteristics; inner-city children; pediatric asthma	RISK-FACTORS; CHILDHOOD ASTHMA; PASSIVE SMOKING; VACUUM-CLEANERS; DOG ALLERGEN; EXPOSURE; SENSITIZATION; EFFICIENCY; MORBIDITY; HEALTH	Most published environmental remediation interventions have been directed at single allergens and have employed demanding strategies; few have been performed in the homes of inner-city children disproportionately burdened by asthma. Our objective was a) to describe the allergen sensitivities, environmental tobacco smoke (ETS) exposure, and home environmental characteristics of a national sample of inner-city children with moderate to severe asthma and b) to develop and implement a multifaceted, home-based comprehensive intervention to reduce home allergens and ETS, tailored to the specific sensitization and exposure profiles of those children. Allergen skin testing and a home evaluation were performed to determine the presence of ETS and factors known to be associated with increased indoor allergen levels. Based on published remediation techniques, a home environmental intervention, organized into modules, each addressing one of five specific allergen groups or ETS, was designed. Of 994 allergic children from seven U.S. urban communities, 937 successfully completed baseline interviews and home allergen surveys and were enrolled. More than 50% of children had positive skin tests to three or more allergen groups. Cockroaches were reported in 58% of homes, wall-to-wall carpeting in the child's bedroom in 55%, a smoker in 48%, mice or rats in 40%, and furry pets in 28%. More than 60% of enrolled families received four or more modules, and between 94% and 98% of all modules were completed. We conclude that most inner-city children with moderate to severe asthma are sensitized to multiple indoor allergens and that environmental factors known to be associated with asthma severity are commonly present in their homes. The intervention developed for the Inner-City Asthma Study employs accepted methods to address an array of allergens and ETS exposure while ensuring that the intervention is tailored to the specific sensitization profiles and home characteristics of these children.	Albert Einstein Coll Med, Jacobi Med Ctr, Dept Pediat Emergency Med, Bronx, NY 10467 USA; Rho Inc, Chapel Hill, NC USA; Boston Univ, Sch Med, Boston, MA 02118 USA; Univ Texas, SW Med Sch, Dept Med, Dallas, TX 75230 USA; Mt Sinai Sch Med, Dept Pediat, New York, NY USA; NIEHS, Res Triangle Pk, NC 27709 USA; Univ Arizona, Resp Sci Ctr, Tucson, AZ USA; Northwestern Univ, Sch Med, Dept Pediat, Chicago, IL 60611 USA; Northwestern Univ, Sch Med, Dept Med, Chicago, IL 60611 USA; Univ Washington, Sch Med, Dept Pediat, Seattle, WA 98195 USA	Crain, EF (reprint author), 1W20 Jacobi Hosp, 1400 Pelham Pkwy, Bronx, NY 10461 USA.			O'Connor, George/0000-0002-6476-3926	NIAID NIH HHS [AI-39900, AI-39761, AI-39769, AI-39776, AI-39901, AI-39902, AI39785, AI39789]		Arshad SH, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.2.e33; BANDURA A, 1977, PSYCHOL REV, V84, P191, DOI 10.1037/0033-295X.84.2.191; BANDURA A, 1986, SOCIAL FDN THOUGHT A; Bandura A., 1986, SOCIAL LEARNING THEO; BUSH RK, 2001, J ALLERGY CLIN IMM S, V107, P403; CALL RS, 1992, J PEDIATR-US, V121, P862, DOI 10.1016/S0022-3476(05)80329-4; CHILMONCZYK BA, 1993, NEW ENGL J MED, V328, P1665, DOI 10.1056/NEJM199306103282303; Clark NM, 1998, HDB HLTH BEHAV CHANG, P5; Dales RE, 1997, INT J EPIDEMIOL, V26, P120, DOI 10.1093/ije/26.1.120; Eggleston PA, 1998, J ALLERGY CLIN IMMUN, V102, P563, DOI 10.1016/S0091-6749(98)70272-6; EHRLICH R, 1992, AM REV RESPIR DIS, V145, P594; Ehrlich RI, 1996, AM J RESP CRIT CARE, V154, P681; Elder JP, 1999, AM J PREV MED, V17, P275, DOI 10.1016/S0749-3797(99)00094-X; FORASTIERE F, 1994, AM J RESP CRIT CARE, V149, P365; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; Green R, 1999, ALLERGY, V54, P484, DOI 10.1034/j.1398-9995.1999.00029.x; Halonen M, 1997, AM J RESP CRIT CARE, V155, P1356; Horak F, 1995, Wien Med Wochenschr, V145, P1; *I MED CLEAR AIR, 2000, ASTHM IND EXP; Jones JA, 2001, PATIENT EDUC COUNS, V42, P67, DOI 10.1016/S0738-3991(00)00102-6; KANG BC, 1993, J ALLERGY CLIN IMMUN, V92, P802, DOI 10.1016/0091-6749(93)90057-M; Kattan M, 1997, PEDIATR PULM, V24, P253, DOI 10.1002/(SICI)1099-0496(199710)24:4<253::AID-PPUL4>3.0.CO;2-L; Lioy PJ, 1999, J AIR WASTE MANAGE, V49, P200, DOI 10.1080/10473289.1999.10463789; Maier WC, 1997, ENVIRON HEALTH PERSP, V105, P208, DOI 10.1289/ehp.97105208; Mannino DM, 1998, MMWR-MORBID MORTAL W, V47, P1; MARTINEZ FD, 1992, PEDIATRICS, V89, P21; Nelson HS, 1998, J ALLERGY CLIN IMMUN, V101, P153; National Institutes of Health, 1997, NIH PUBL; Phipatanakul W, 2000, J ALLERGY CLIN IMMUN, V106, P1075; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; Platts-Mills TAE, 2000, J ALLERGY CLIN IMMUN, V106, P787, DOI 10.1067/mai.2000.110548; Popplewell EJ, 2000, PEDIATR ALLERGY IMMU, V11, P142, DOI 10.1034/j.1399-3038.2000.00058.x; Rosenstreich DL, 1997, NEW ENGL J MED, V336, P1356, DOI 10.1056/NEJM199705083361904; Slezak JA, 1998, J ASTHMA, V35, P203, DOI 10.3109/02770909809068208; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; Strachan DP, 1998, THORAX, V53, P204; STRACHAN DP, 1988, BRIT MED J, V297, P1223; *US BUR CENS, 2000, CENS 2000 SUMM TAP F; van der Heide S, 1999, J ALLERGY CLIN IMMUN, V104, P447, DOI 10.1016/S0091-6749(99)70391-X	39	117	118	4	13	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	SEP	2002	110	9					939	945				7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	591RJ	WOS:000177893800037	12204830	
J	Besnard, AG; Togbe, D; Guillou, N; Erard, F; Quesniaux, V; Ryffel, B				Besnard, Anne-Gaelle; Togbe, Dieudonnee; Guillou, Noelline; Erard, Francois; Quesniaux, Valerie; Ryffel, Bernhard			IL-33-activated dendritic cells are critical for allergic airway inflammation	EUROPEAN JOURNAL OF IMMUNOLOGY			English	Article						Allergy; Cytokines; DC; IL-33; Lung inflammation	IL-1-LIKE CYTOKINE IL-33; T-CELLS; HUMAN EOSINOPHILS; HUMAN BASOPHILS; ST2 RECEPTOR; MURINE MODEL; MAST-CELLS; TH2 CELLS; IN-VIVO; ASTHMA	IL-33, a new member of the IL-1 family cytokine, is involved in Th2-type responses in a wide range of diseases and signals through the ST2 receptor expressed on many immune cells. Since the effects of IL-33 on DCs remain controversial, we investigated the ability of IL-33 to modulate DC functions in vitro and in vivo. Here, we report that IL-33 activates myeloid DCs to produce IL-6, IL-1 beta, TNF, CCL17 and to express high levels of CD40, CD80 OX40L and CCR7. Importantly, IL-33-activated DCs prime naive lymphocytes to produce the Th2 cytokines IL-5 and IL-13, but not IL-4. In vivo, IL-33 exposure induces DC recruitment and activation in the lung. Using an OVA-induced allergic lung inflammation model, we demonstrate that the reduced airway inflammation in ST2-deficient mice correlates with the failure in DC activation and migration to the draining LN. Finally, we show that adoptive transfer of IL-33-activated DCs exacerbates lung inflammation in a DC-driven model of allergic airway inflammation. These data demonstrate for the first time that IL-33 activates DCs during antigen presentation and thereby drives a Th2-type response in allergic lung inflammation.	[Besnard, Anne-Gaelle; Togbe, Dieudonnee; Guillou, Noelline; Erard, Francois; Quesniaux, Valerie; Ryffel, Bernhard] Univ Orleans, F-45071 Orleans 2, France; [Besnard, Anne-Gaelle; Togbe, Dieudonnee; Guillou, Noelline; Erard, Francois; Quesniaux, Valerie; Ryffel, Bernhard] CNRS, UMR 6218, F-45071 Orleans, France; [Togbe, Dieudonnee] Artimmune SAS, Ctr Innovat, Orleans, France	Ryffel, B (reprint author), Univ Orleans, 3B Rue Ferollerie, F-45071 Orleans 2, France.	bryffel@cnrs-orleans.fr			EFIS; "Agence Nationale pour la Recherche'' (ANR) [2007 MIME-103-02]; "Fondation pour la Recherche Medicale'' (FRM) [DAL 2007 0822007]; "Fond europeen de developpement regional'' (FEDER) [1575-32168]	We thank Professor Eddy Liew for critical reading and comments. We are grateful to the EFIS for financial support allowing a fruitful collaboration with Eddy Liew's group. This work was supported by the "Agence Nationale pour la Recherche'' (ANR 2007 MIME-103-02), the "Fondation pour la Recherche Medicale'' (FRM allergy DAL 2007 0822007), the "Fond europeen de developpement regional'' (FEDER Asthme 1575-32168).	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V., 2008, Expert Reviews in Molecular Medicine, V10, P1, DOI 10.1017/S1462399408000707; Sims JE, 2010, NAT REV IMMUNOL, V10, P89, DOI 10.1038/nri2691; Smith DE, 2009, CLIN EXP ALLERGY, V40, P200; Smithgall MD, 2008, INT IMMUNOL, V20, P1019, DOI 10.1093/intimm/dxn060; Suzukawa M, 2008, LAB INVEST, V88, P1245, DOI 10.1038/labinvest.2008.82; Suzukawa M, 2008, J IMMUNOL, V181, P5981; Townsend MJ, 2000, J EXP MED, V191, P1069, DOI 10.1084/jem.191.6.1069; Turnquist HR, 2009, EUR J IMMUNOL, V39, P3292, DOI 10.1002/eji.200940026; van Rijt LS, 2004, J IMMUNOL METHODS, V288, P111, DOI 10.1016/j.jim.2004.03.004; VanOosterhout AJM, 1997, AM J RESP CELL MOL, V17, P386; Woerly G, 2003, J EXP MED, V198, P411, DOI 10.1084/jem.20021384; Xu D, 1998, J EXP MED, V187, P787, DOI 10.1084/jem.187.5.787	44	116	121	0	12	WILEY-BLACKWELL	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0014-2980			EUR J IMMUNOL	Eur. J. Immunol.	JUN	2011	41	6					1675	1686		10.1002/eji.201041033		12	Immunology	Immunology	776TB	WOS:000291559700018	21469105	
J	Vally, H; Misso, NLA; Madan, V				Vally, H.; Misso, N. L. A.; Madan, V.			Clinical effects of sulphite additives	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review							METABISULFITE-INDUCED BRONCHOCONSTRICTION; DIOXIDE-INDUCED BRONCHOCONSTRICTION; ALLERGIC CONTACT-DERMATITIS; CHRONIC CHILDHOOD ASTHMA; SODIUM METABISULFITE; SULFUR-DIOXIDE; OCCUPATIONAL ASTHMA; BRONCHIAL HYPERREACTIVITY; BRONCHODILATOR SOLUTIONS; INHALED METABISULFITE	P>Sulphites are widely used as preservative and antioxidant additives in the food and pharmaceutical industries. Topical, oral or parenteral exposure to sulphites has been reported to induce a range of adverse clinical effects in sensitive individuals, ranging from dermatitis, urticaria, flushing, hypotension, abdominal pain and diarrhoea to life-threatening anaphylactic and asthmatic reactions. Exposure to the sulphites arises mainly from the consumption of foods and drinks that contain these additives; however, exposure may also occur through the use of pharmaceutical products, as well as in occupational settings. While contact sensitivity to sulphite additives in topical medications is increasingly being recognized, skin reactions also occur after ingestion of or parenteral exposure to sulphites. Most studies report a 3-10% prevalence of sulphite sensitivity among asthmatic subjects following ingestion of these additives. However, the severity of these reactions varies, and steroid-dependent asthmatics, those with marked airway hyperresponsiveness, and children with chronic asthma, appear to be at greater risk. In addition to episodic and acute symptoms, sulphites may also contribute to chronic skin and respiratory symptoms. To date, the mechanisms underlying sulphite sensitivity remain unclear, although a number of potential mechanisms have been proposed. Physicians should be aware of the range of clinical manifestations of sulphite sensitivity, as well as the potential sources of exposure. Minor modifications to diet or behaviour lead to excellent clinical outcomes for sulphite-sensitive individuals.	[Vally, H.] Australian Natl Univ, Natl Ctr Epidemiol & Populat Hlth, ANU Coll Med & Hlth Sci, Canberra, ACT 0200, Australia; [Misso, N. L. A.] Univ Western Australia, Ctr Asthma Allergy & Resp Res, Lung Inst Western Australia Inc, Perth, WA 6009, Australia; [Madan, V.] Salford Royal NHS Fdn Trust, Dermatol Ctr, Manchester, Lancs, England	Vally, H (reprint author), Australian Natl Univ, Natl Ctr Epidemiol & Populat Hlth, ANU Coll Med & Hlth Sci, GPO Box 4, Canberra, ACT 0200, Australia.	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Exp. Allergy	NOV	2009	39	11					1643	1651		10.1111/j.1365-2222.2009.03362.x		9	Allergy; Immunology	Allergy; Immunology	509FY	WOS:000271001600005	19775253	
J	Nials, AT; Uddin, S				Nials, Anthony T.; Uddin, Sorif			Mouse models of allergic asthma: acute and chronic allergen challenge	DISEASE MODELS & MECHANISMS			English	Article							INHIBITS AIRWAY INFLAMMATION; SEVERE PERSISTENT ASTHMA; SOLUBLE IL-4 RECEPTOR; MURINE MODEL; BRONCHIAL HYPERRESPONSIVENESS; PULMONARY INFLAMMATION; MONOCLONAL-ANTIBODY; ATOPIC ASTHMA; PHOSPHODIESTERASE-4 INHIBITOR; CYSTEINYL-LEUKOTRIENES	Asthma is defined as a chronic inflammatory disease of the airways; however, the underlying physiological and immunological processes are not fully understood. Animal models have been used to elucidate asthma pathophysiology, and to identify and evaluate novel therapeutic targets. Several recent review articles (Epstein, 2004; Lloyd, 2007; Boyce and Austen, 2005; Zosky and Sly, 2007) have discussed the potential value of these models. Allergen challenge models reproduce many features of clinical asthma and have been widely used by investigators; however, the majority involve acute allergen challenge procedures. It is recognised that asthma is a chronic inflammatory disease resulting from continued or intermittent allergen exposure, usually via inhalation, and there has been a recent focus on developing chronic allergen exposure models, predominantly in mice. Here, we review the acute and chronic exposure mouse models, and consider their potential role and impact in the field of asthma research.	[Nials, Anthony T.; Uddin, Sorif] GlaxoSmithKline Med Res Ctr, Resp Ctr Excellence Drug Discovery, Stevenage SG1 2NY, Herts, England	Nials, AT (reprint author), GlaxoSmithKline Med Res Ctr, Resp Ctr Excellence Drug Discovery, Gunnels Wood Rd, Stevenage SG1 2NY, Herts, England.	tony.t.nials@gsk.com					ALEXANDER AG, 1992, LANCET, V339, P324, DOI 10.1016/0140-6736(92)91646-P; Bartlett NW, 2008, NAT MED, V14, P199, DOI 10.1038/nm1713; Blyth DI, 2000, AM J RESP CELL MOL, V23, P241; Blyth DI, 1996, AM J RESP CELL MOL, V14, P425; Borish LC, 2001, J ALLERGY CLIN IMMUN, V107, P963, DOI 10.1067/mai.2001.115624; Borish LC, 1999, AM J RESP CRIT CARE, V160, P1816; Bousquet J, 2000, AM J RESP CRIT CARE, V161, P1720; Boyce JA, 2005, J EXP MED, V201, P1869, DOI 10.1084/jem.20050584; Busse W, 2001, J ALLERGY CLIN IMMUN, V108, P184, DOI 10.1067/mai.2001.117880; CARROLL N, 1993, AM REV RESPIR DIS, V147, P405; Cho JY, 2004, J CLIN INVEST, V113, P551, DOI 10.1172/JCI200419133; Choi IW, 2005, J ALLERGY CLIN IMMUN, V116, P537, DOI 10.1016/j.jaci.2005.05.034; 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Model. Mech.	NOV-DEC	2008	1	4-5					213	220		10.1242/dmm.000323		8	Cell Biology; Pathology	Cell Biology; Pathology	474AK	WOS:000268254400010	19093027	
J	Arbes, SJ; Gergen, PJ; Vaughn, B; Zeldin, DC				Arbes, Samuel J., Jr.; Gergen, Peter J.; Vaughn, Ben; Zeldin, Darryl C.			Asthma cases attributable to atopy: Results from the third national health and nutrition examination survey	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergens; allergic sensitization; allergy skin test; asthma; atopy; epidemiology; NHANES III; skin prick test; survey	HOUSE-DUST MITE; COMMON ALLERGENS; CAT ALLERGEN; ASSOCIATION; SENSITIZATION; POPULATION; EXPOSURE; ADOLESCENTS; REACTIVITY; CHILDHOOD	Background: The percentage of asthma cases attributable to atopy is the subject of debate. Objectives: The objectives were to estimate the percentage of asthma cases in the US population attributable to atopy and to examine associations between allergen-specific skin tests and asthma. Methods: Data were obtained from the Third National Health and Nutrition Examination Survey, in which subjects age 6 to 59 years were skin tested with 10 allergens. Atopy was defined as at least 1 positive allergen-specific test. Doctor-diagnosed current asthma was assessed by questionnaire. Results: In the United States, 56.3% of the asthma cases were attributable to atopy, and that percentage was greater among males than females, among persons in the highest education category than in lower education categories, and among persons living in highly populated metropolitan areas than in all other areas. Each allergen-specific test was strongly associated with asthma before adjustment (odds ratios varied from 2.1 to 4.5); however, after adjustment by all the allergens, only tests to cat, Alternaria, white oak, and perennial rye were independently associated with asthma. Perennial rye was inversely associated with asthma. Of the 10 allergens, a positive response to cat accounted for the highest percentage of asthma cases (29.3%). Conclusion: About half of the current asthma cases in the US population represented by the Third National Health and Nutrition Examination Survey were attributable to atopy. Some allergen-specific skin tests were not independently associated with asthma. Clinical implications: If atopy could be prevented or reversed, or its effect on asthma blocked, then a large percentage of asthma cases in the US population could be prevented.	NIEHS, Lab Resp Biol, Div Intramural Res, NIH, Res Triangle Pk, NC 27709 USA; NIAID, Div Allergy Immunol & Transplantat, NIH, Bethesda, MD 20892 USA; Rho Inc, Chapel Hill, NC USA	Zeldin, DC (reprint author), NIEHS, Lab Resp Biol, Div Intramural Res, NIH, POB 12233,MD D2-01, Res Triangle Pk, NC 27709 USA.	zeldin@niehs.nih.gov			Intramural NIH HHS [Z01 ES025041-10]		Arbes SJ, 2005, J ALLERGY CLIN IMMUN, V116, P377, DOI 10.1016/j.jaci.2005.05.017; Arbes SJ, 2004, J ALLERGY CLIN IMMUN, V114, P111, DOI 10.1016/j.jaci.2004.04.036; Arshad SH, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.2.e33; BURROWS B, 1989, NEW ENGL J MED, V320, P271, DOI 10.1056/NEJM198902023200502; Cohn RD, 2006, ENVIRON HEALTH PERSP, V114, P522, DOI 10.1289/ehp.8561; GERGEN PJ, 1992, J ALLERGY CLIN IMMUN, V90, P579, DOI 10.1016/0091-6749(92)90130-T; Jaakkola MS, 2006, J ALLERGY CLIN IMMUN, V117, P642, DOI 10.1016/j.jaci.2005.11.003; Judkins D. R., 1990, J OFF STAT, V6, P223; Lanphear BP, 2001, PEDIATRICS, V107, DOI 10.1542/peds.107.6.e98; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; MIETTINE.OS, 1974, AM J EPIDEMIOL, V99, P325; *NAT CTR HLTH STA, 1986, PUBL US DAT TAP DOC; Pearce N, 1999, THORAX, V54, P268; Plaschke P, 1999, J ALLERGY CLIN IMMUN, V104, P58, DOI 10.1016/S0091-6749(99)70114-4; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; Ponsonby AL, 2002, CHEST, V121, P135, DOI 10.1378/chest.121.1.135; Rothman K., 1986, MODERN EPIDEMIOLOGY; Sood A, 2006, THORAX, V61, P300, DOI 10.1136/thx.2004.031468; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; Squillace SP, 1997, AM J RESP CRIT CARE, V156, P1760; Sunyer J, 2004, J ALLERGY CLIN IMMUN, V114, P1033, DOI 10.1016/j.jaci.2004.05.072; VONMUTIUS E, 2007, P AM THORAC SOC, V4, P217	22	116	117	1	2	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	NOV	2007	120	5					1139	1145		10.1016/j.jaci.2007.07.056		7	Allergy; Immunology	Allergy; Immunology	231TZ	WOS:000250973400024	17889931	
J	Chan, PC; Xia, QS; Fu, PP				Chan, Po-Chuen; Xia, Qingsu; Fu, Peter P.			Ginkgo biloba leave extract: Biological, medicinal, and toxicological effects	JOURNAL OF ENVIRONMENTAL SCIENCE AND HEALTH PART C-ENVIRONMENTAL CARCINOGENESIS & ECOTOXICOLOGY REVIEWS			English	Review						Gingko biloba leave extract; biological and toxicological effects; ginkgolidc; quercetin	HERB-DRUG INTERACTIONS; INDUCED NEURONAL DEATH; GLOBAL BRAIN ISCHEMIA; EGB 761 PROTECTS; DNA-DAMAGE; INDUCED NEPHROTOXICITY; INDUCED TOXICITY; NITRIC-OXIDE; IN-VITRO; CYTOCHROME-P450 PHENOTYPES	Ginkgo biloba leave extract is among the most widely sold herbal dietary supplements in the United States. Its purported biological effects include: scavenging free radical; lowering oxidative stress; reducing neural damages, reducing platelets aggregation; anti-inflammation; anti-tumor activities; and anti-aging. Clinically, it has been prescribed to treat CNS disorders such as Alzheimer's disease and cognitive deficits. It exerts allergy and changes in bleeding time. While its mutagenicity or carcinogenic activity has not been reported, its components, quercetin, kaempferol and rutin have been shown to be genotoxic. There are no standards or guidelines regulating the constituent components of Ginkgo biloba leave extract nor are exposure limits imposed. Safety evaluation of Ginkgo biloba leave extract is being conducted by the U.S. National Toxicology Program.	[Chan, Po-Chuen] NIEHS, Res Triangle Pk, NC 27709 USA; [Xia, Qingsu; Fu, Peter P.] Natl Ctr Toxicol Res, Jefferson, AR 72079 USA	Chan, PC (reprint author), NIEHS, Res Triangle Pk, Res Triangle Pk, NC 27709 USA.	chanp@niehs.nih.gov					Agha AM, 2001, J EXP CLIN CANC RES, V20, P39; Ahlemeyer B, 2003, PHARMACOPSYCHIATRY, V36, pS8; Al-Yahya AA, 2006, J ETHNOPHARMACOL, V107, P222, DOI 10.1016/j.jep.2006.03.014; AMBROSE AM, 1952, J AM PHARM ASSOC SCI, V41, P119; Antognoni F, 2004, ATLA-ALTERN LAB ANIM, V32, P79; Arenz A, 1996, PLANTA MED, V62, P548, DOI 10.1055/s-2006-957967; ATZORI C, 1993, ANTIMICROB AGENTS CH, V37, P1492; Bastianetto S, 2000, EUR J NEUROSCI, V12, P1882, DOI 10.1046/j.1460-9568.2000.00069.x; Bastianetto S, 2000, J NEUROCHEM, V74, P2268, DOI 10.1046/j.1471-4159.2000.0742268.x; Bastianetto S, 2002, NEUROBIOL AGING, V23, P891, DOI 10.1016/S0197-4580(02)00024-6; Bastianetto S, 2002, CELL MOL BIOL, V48, P693; Bent S, 2005, J GEN INTERN MED, V20, P657, DOI 10.1111/j.1525-1497.2005.0121.x; BENZI G, 1995, FREE RADICAL BIO MED, V19, P77, DOI 10.1016/0891-5849(94)00244-E; BHATTACHARYA RK, 1988, CANCER LETT, V39, P85, DOI 10.1016/0304-3835(88)90043-2; *BIOT U, 1998, PEG GINKG BIL; Boersma MG, 2000, CHEM RES TOXICOL, V13, P185, DOI 10.1021/tx990161k; Boots AW, 2005, BIOCHEM BIOPH RES CO, V338, P923, DOI 10.1016/j.bbrc.2005.10.031; Boots AW, 2005, FEBS LETT, V579, P677, DOI 10.1016/j.febslet.2004.12.044; BRAQUET P, 1991, J ETHNOPHARMACOL, V32, P135, DOI 10.1016/0378-8741(91)90111-P; BRAQUET P, 1987, Drugs of the Future, V12, P643; Bressler R, 2005, GERIATRICS, V60, P30; BROWN DJ, 1996, NARD J           MAY, P41; BROWN S, 1983, EXPERIENTIA, V39, P198, DOI 10.1007/BF01958898; CARIA H, 1995, MUTAT RES-GENET TOX, V343, P85, DOI 10.1016/0165-1218(95)90075-6; CARVER JH, 1983, MUTAT RES, V113, P45, DOI 10.1016/0165-1161(83)90240-6; Celik I, 2005, BASIC CLIN PHARMACOL, V97, P325, DOI 10.1111/j.1742-7843.2005.pto_153.x; Chandrasekaran K, 2003, PHARMACOPSYCHIATRY, V36, pS89; Chandrasekaran K, 2002, CELL MOL BIOL, V48, P663; Chermat R, 1997, PHARMACOL BIOCHEM BE, V56, P333, DOI 10.1016/S0091-3057(96)00298-5; Choi JY, 2005, ANALOG INTEGR CIRC S, V43, P5, DOI 10.1007/s10470-005-6566-y; Christen Y., 2000, AM J CLIN NUTR, V71, P621; Cohen-Salmon C, 1997, J PHYSIOLOGY-PARIS, V91, P291, DOI 10.1016/S0928-4257(97)82409-6; Coskun O, 2005, J APPL TOXICOL, V25, P8, DOI 10.1002/jat.1002; CREBELLI R, 1987, FOOD CHEM TOXICOL, V25, P9, DOI 10.1016/0278-6915(87)90301-2; CROOM EM, 1995, DRUG TOPICS      NOV, P84; da Silva J, 2002, FOOD CHEM TOXICOL, V40, P941, DOI 10.1016/S0278-6915(02)00015-7; Daba MH, 2002, PHARMACOL RES, V45, P461, DOI 10.1006/phrs.2002.0985; Dajas F, 2003, NEUROTOX RES, V5, P425; DeFeudis F. 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Environ. Sci. Health Pt. C-Environ. Carcinog. Ecotoxicol. Rev.		2007	25	3					211	244		10.1080/10590500701569414		34	Oncology; Environmental Sciences; Toxicology	Oncology; Environmental Sciences & Ecology; Toxicology	264DD	WOS:000253264800002	17763047	
J	Delfino, RJ; Staimer, N; Gillen, D; Tjoa, T; Sioutas, C; Fung, K; George, SC; Kleinman, MT				Delfino, Ralph J.; Staimer, Norbert; Gillen, Dan; Tjoa, Thomas; Sioutas, Constantinos; Fung, Kochy; George, Steven C.; Kleinman, Michael T.			Personal and ambient air pollution is associated with increased exhaled nitric oxide in children with asthma	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; epidemiology; exhaled nitric oxide; longitudinal data analysis; nitrogen dioxide; ozone; panel study; particulate air pollution	ANTIINFLAMMATORY MEDICATION USE; PARTICULATE-MATTER; NITROGEN-DIOXIDE; HEALTHY-SUBJECTS; EXPOSURE; SYMPTOMS; FLOW; PARTICLES; MONTELUKAST; POPULATION	BACKGROUND: Research has shown associations between pediatric asthma outcomes and airborne particulate matter (PM). The importance of particle components remains to be determined. METHODS: We followed a panel of 45 schoolchildren with persistent asthma living in Southern California. Subjects were monitored over 10 days with offline fractional exhaled nitric oxide (FENO), a biomarker of airway inflammation. Personal active sampler exposures included continuous particulate matter < 2.5 mu m in aerodynamic diameter (PM2.5), 24-hr PM2.5 elemental and organic carbon (EC, OC), and 24-hr nitrogen dioxide. Ambient exposures included PM2.5, PM2.5 EC and OC, and NO2. Data were analyzed with mixed models controlling for personal temperature, humidity and 10-day period. RESULTS: The strongest positive associations were between FENO and 2-day average pollutant concentrations. Per interquartile range pollutant increase, these were: for 24 mu g/m(3) personal PM2.5, 1.1 ppb F-ENO [95% confidence interval (CI), 0.1-1.9]; for 0.6 mu g/m(3) personal EC, 0.7 ppb FENO (95% CI, 0.3-1.1); for 17 ppb personal NO2, 1.6 ppb FENO (95% CI, 0.4-2.8). Larger associations were found for ambient EC and smaller associations for ambient NO2. Ambient PM2.5 and personal and ambient OC were significant only in subjects taking inhaled corticosteroids (ICS) alone. Subjects taking both ICS and antileukotrienes showed no significant associations. Distributed lag models showed personal PM2.5 in the preceding 5 hr was associated with F-ENO. In two-pollutant models, the most robust associations were for personal and ambient EC and NO2, and for personal but not ambient PM2.5. CONCLUSION: PM associations with airway inflammation in asthmatics may be missed using ambient particle mass, which may not sufficiently represent causal pollutant components from fossil fuel combustion.	Univ Calif Irvine, Sch Med, Dept Med, Div Epidemiol, Irvine, CA 92617 USA; Univ Calif Irvine, Dept Stat, Irvine, CA USA; Univ Calif Irvine, Dept Biomed Engn, Irvine, CA USA; Univ Calif Irvine, Sch Med, Dept Community & Environm Med, Irvine, CA 92717 USA; Univ So Calif, Dept Civil & Environm Engn, Sch Engn, Los Angeles, CA USA; AtmAA Inc, Calabasas, CA USA	Delfino, RJ (reprint author), Univ Calif Irvine, Sch Med, Dept Med, Div Epidemiol, 100 Theory,Suite 100, Irvine, CA 92617 USA.	rdelfino@uci.edu	Wang, Linden/M-6617-2014; George, Steven/K-9359-2015	George, Steven/0000-0003-2263-1914	NIEHS NIH HHS [ES11615, R01 ES011615]		Adamkiewicz G, 2004, THORAX, V59, P204, DOI 10.1136/thorax.2003.006445; American Thoracic Society, 2005, AM J RESP CRIT CARE, V171, P912, DOI DOI 10.1164/RCCM.200406-710ST.PUBMED:15817806; Buchvald F, 2005, J ALLERGY CLIN IMMUN, V115, P1130, DOI 10.1016/j.jaci.2005.03.020; Chakrabarti B, 2004, ATMOS ENVIRON, V38, P3329, DOI 10.1016/j.atmosenv.2004.03.007; Delfino RJ, 1998, ENVIRON HEALTH PERSP, V106, P751, DOI 10.1289/ehp.98106751; Delfino RJ, 2002, ENVIRON HEALTH PERSP, V110, P573; Delfino RJ, 2004, ENVIRON HEALTH PERSP, V112, P932, DOI 10.1289/ehp.6815; Delfino RJ, 2003, ENVIRON HEALTH PERSP, V111, P647, DOI 10.1289/ehp.5992; Delfino RJ, 2002, ENVIRON HEALTH PERSP, V110, pA607; Diggle P, 2002, ANAL LONGITUDINAL DA; Ebelt ST, 2005, EPIDEMIOLOGY, V16, P396, DOI 10.1097/01.ede.0000158918.57071.3e; Fabbri LM, 1998, AM J RESP CRIT CARE, V157, pS195; Fine PM, 2004, ENVIRON SCI TECHNOL, V38, P1296, DOI 10.1021/es0348389; Fischer PH, 2002, INT ARCH OCC ENV HEA, V75, P348, DOI 10.1007/s00420-002-0320-x; Fung K, 2002, J AIR WASTE MANAGE, V52, P1333; Gent JF, 2003, JAMA-J AM MED ASSOC, V290, P1859, DOI 10.1001/jama.290.14.1859; GONG H, 2001, CHEST, V19, P402; Hamid Qutayba, 2003, Journal of Allergy and Clinical Immunology, V111, pS5, DOI 10.1067/mai.2003.22; Hankinson JL, 1999, AM J RESP CRIT CARE, V159, P179; Jansen KL, 2005, ENVIRON HEALTH PERSP, V113, P1741, DOI 10.1289/ehp.8153; Jobsis Q, 2001, THORAX, V56, P285, DOI 10.1136/thorax.56.4.285; Jones SL, 2001, AM J RESP CRIT CARE, V164, P738; Kim JJ, 2004, AM J RESP CRIT CARE, V170, P520, DOI 10.1164/rccm.200403-2810C; Koenig JQ, 2005, ENVIRON HEALTH PERSP, V113, P499, DOI 10.1289/ehp.7511; Koenig JQ, 2003, ENVIRON HEALTH PERSP, V111, P1625, DOI 10.1289/ehp.6160; Kroesbergen A, 1999, EUR RESPIR J, V14, P871, DOI 10.1034/j.1399-3003.1999.14d24.x; Lewis TC, 2005, ENVIRON HEALTH PERSP, V113, P1068, DOI 10.1289/ehp.7533; Li N, 2003, CLIN IMMUNOL, V109, P250, DOI 10.1016/j.clim.2003.08.006; Linn WS, 2004, ARCH ENVIRON HEALTH, V59, P385, DOI 10.3200/AEOH.59.8.385-391; Lipworth BJ, 1999, LANCET, V353, P57, DOI 10.1016/S0140-6736(98)09019-9; Mar TF, 2005, ENVIRON HEALTH PERSP, V113, P1791, DOI 10.1289/ehp.7883; Mortimer KM, 2000, AM J RESP CRIT CARE, V162, P1838; *NAT I OCC SAF HLH, 1994, DHHS PUBL; Persinger RL, 2002, MOL CELL BIOCHEM, V234, P71, DOI 10.1023/A:1015973530559; Rabinovitch N, 2006, AM J RESP CRIT CARE, V173, P1098, DOI 10.1164/rccm.200509-1393OC; Rabinovitch N, 2005, J ALLERGY CLIN IMMUN, V116, P1053, DOI 10.1016/j.jaci.2005.08.045; Roorda-Knape MC, 1999, SCI TOTAL ENVIRON, V235, P339, DOI 10.1016/S0048-9697(99)00217-X; Rundell KW, 2005, INHAL TOXICOL, V17, P99, DOI 10.1080/08958370590899479; Schauer JJ, 2002, ENVIRON SCI TECHNOL, V36, P1169, DOI 10.1021/es0108077; Schwartz J, 2000, EPIDEMIOLOGY, V11, P320, DOI 10.1097/00001648-200005000-00016; Sheppard L, 2005, J EXPO ANAL ENV EPID, V15, P366, DOI 10.1038/sj.jea.7500413; Sioutas C, 2005, ENVIRON HEALTH PERSP, V113, P947, DOI 10.1289/ehp.7939; Staimer N, 2005, ANAL BIOANAL CHEM, V383, P955, DOI 10.1007/s00216-005-0086-6; Steerenberg PA, 2003, INT ARCH ALLERGY IMM, V131, P127, DOI 10.1159/000070928; Steerenberg PA, 2001, ARCH ENVIRON HEALTH, V56, P167; Van Amsterdam JGC, 1999, ARCH ENVIRON HEALTH, V54, P331; Molenberghs G, 2001, LINEAR MIXED MODELS; Zeidler MR, 2004, CURR OPIN PULM MED, V10, P31, DOI 10.1097/00063198-200401000-00006; Zeiger RS, 2006, J ALLERGY CLIN IMMUN, V117, P45, DOI 10.1016/j.jaci.2005.10.012	49	116	117	3	52	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	NOV	2006	114	11					1736	1743		10.1289/ehp.9141		8	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	102OS	WOS:000241822300036	17107861	
J	Marra, F; Lynd, L; Coombes, M; Richardson, K; Legal, M; FitzGerald, JM; Marra, CA				Marra, F; Lynd, L; Coombes, M; Richardson, K; Legal, M; FitzGerald, JM; Marra, CA			Does antibiotic exposure during infancy lead to development of asthma? A systematic review and metaanalysis	CHEST			English	Review						antibiotics; childhood asthma; pediatrics	EARLY-CHILDHOOD; ALLERGIC DISEASE; BIRTH COHORT; INFECTIOUS-DISEASES; 1ST YEAR; RISK; PREVALENCE; LIFE; RHINITIS; DATABASE	Objectives: To determine the association between antibiotic exposure in the first year of life and the development of childhood asthma. Design: Metaanalysis of observational studies retrieved through systematic search of all available electronic data sources. Studies included in the metaanalyses were those with populations exposed to one or more courses of antibiotics during the first year of life, and asthma diagnosis was defined as diagnosis by a physician between the age of 1 to 18 years. Setting: Retrospective and prospective studies published in the English-language literature from 1966 to present. Results: Eight studies (four prospective and four retrospective) examined the association between exposure to at least one course of antibiotics and development of childhood asthma. The total number of subjects for the analysis comparing exposure to at least one antibiotic to no exposure in the first year of life was 12,082 children and 1,817 asthma cases. In the dose-response analysis, we included data from a total of 27,167 children and 3,392 asthma cases. The pooled odds ratio (OR) for the eight studies was 2.05 (95% confidence interval [CI], 1.41 to 2.99). The association was significantly stronger in the retrospective studies (OR, 2.82; 95% CI, 2.07 to 3.85) than the prospective studies (OR, 1.12; 95% CI, 0.88 to 1.42). Five of the eight studies examined whether the association was related to the number of courses of antibiotics taken in the first year of life. The overall OR for the dose-response analysis was 1.16 (95% CI, 1.05 to 1.28) for each additional course of antibiotics; however, this association was not significantly stronger in the retrospective studies (OR, 1.37; 95% CI, 1.18 to 1.60) relative to the prospective studies (OR, 1.07; 95% CI, 0.95 to 1.20). Conclusions: Exposure to at least one course of antibiotics in the first year of life appears to be a risk factor for the development of childhood asthma. Because of the limitations of the studies conducted to date, additional large-scale, prospective studies are needed to confirm this potential association.	Univ British Columbia, Hlth Econ Program, Ctr Clin Epidemiol & Evaluat, Vancouver Coastal Hlth Res Inst,Fac Pharmaceut Sc, Vancouver, BC V5Z 1L8, Canada; Univ British Columbia, Ctr Dis Control, Ctr Clin Epidemiol & Evaluat, Fac Med, Vancouver, BC V5Z 1L8, Canada	Marra, CA (reprint author), Univ British Columbia, Hlth Econ Program, Ctr Clin Epidemiol & Evaluat, Vancouver Coastal Hlth Res Inst,Fac Pharmaceut Sc, 828 W 10th Ave, Vancouver, BC V5Z 1L8, Canada.	carlo.marra@ubc.ca					Adams PF, 1999, VITAL HLTH STAT, V10, P1; ANDERSON HR, 1994, BRIT MED J, V308, P1600; BERLIN JA, 1993, EPIDEMIOLOGY, V4, P218, DOI 10.1097/00001648-199305000-00005; BURR M L, 1989, Archives of Disease in Childhood, V64, P1452; Celedon JC, 2004, CLIN EXP ALLERGY, V34, P1011, DOI 10.1111/j.1365-2222.2004.01994.x; Celedon JC, 2002, AM J RESP CRIT CARE, V166, P72, DOI 10.1164/rccm.2109074; Cohet C, 2004, J EPIDEMIOL COMMUN H, V58, P852, DOI 10.1136/jech.2003.019182; Cullinan P, 2004, THORAX, V59, P11; Downs SH, 1998, J EPIDEMIOL COMMUN H, V52, P377; Droste JHJ, 2000, CLIN EXP ALLERGY, V30, P1547; Farooqi IS, 1998, THORAX, V53, P927; GALBRAITH RF, 1988, STAT MED, V7, P889, DOI 10.1002/sim.4780070807; Holt PG, 1997, PEDIATR ALLERGY IMMU, V8, P53, DOI 10.1111/j.1399-3038.1997.tb00145.x; Illi S, 2001, BRIT MED J, V322, P390, DOI 10.1136/bmj.322.7283.390; JOHNSON CC, 2003, EPIDEMIOLOGY, V15, pS88; LABBE KA, 1987, ANN INTERN MED, V107, P224; Light R. J., 1984, SUMMING SCI REVIEWIN; Martinez FD, 1999, LANCET S2, V354, pSII12; McKeever TM, 2002, J ALLERGY CLIN IMMUN, V109, P43, DOI 10.1067/mai.2002.121016; McKeever TM, 2002, AM J RESP CRIT CARE, V166, P827, DOI 10.1164/rccm.200202-158OC; Nyquist AC, 1998, JAMA-J AM MED ASSOC, V279, P875, DOI 10.1001/jama.279.11.875; ROBERTSON CF, 1991, BRIT MED J, V302, P1116; Schappert SM, 1992, ADV DATA, P1; Thomas M, 2003, THORAX, V58, P67; *US CENS BUR, 1997, WHOS MIND KIDS CHILD; von Mutius E, 1999, EUR RESPIR J, V14, P4, DOI 10.1034/j.1399-3003.1999.14a03.x; Wickens K, 1999, CLIN EXP ALLERGY, V29, P766; Wjst M, 2001, EUR J MED RES, V6, P263; 1995, MMWR MORB MORTAL WKL, V44, P609	29	116	122	0	7	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	MAR	2006	129	3					610	618		10.1378/chest.129.3.610		9	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	027GY	WOS:000236404200018	16537858	
J	Boman, BC; Forsberg, AB; Jarvholm, BG				Boman, BC; Forsberg, AB; Jarvholm, BG			Adverse health effects from ambient air pollution in relation to residential wood combustion in modern society	SCANDINAVIAN JOURNAL OF WORK ENVIRONMENT & HEALTH			English	Review						air pollution; asthma; biomass combustion; epidemiology; particulate matter; review; short-term exposure; wood smoke	FINE PARTICULATE MATTER; EMERGENCY ROOM VISITS; SANTA-CLARA COUNTY; SOURCE APPORTIONMENT; ORGANIC-COMPOUNDS; DAILY MORTALITY; ASTHMA; CHILDREN; PARTICLES; SEATTLE	This is a review of the adverse health effects of ambient air pollution in relation to residential wood combustion in modem society. From a literature search of PubMed, nine relevant studies were identified. All of them focused on the effects of short-term exposure such as asthma, respiratory symptoms, daily mortality, and lung function. Substantial quantitative information was only found for acute asthma in relation to particulate matter with an aerodynamic diameter of <10 mum. In comparison with the present general estimations for ambient particulate matter and adverse health effects, the relative risks were even stronger in the studies in which residential wood combustion was considered a major source of particulate matter. Thus there seems to be no reason to assume that the effects of particulate matter in areas polluted by wood smoke are weaker than elsewhere.	Umea Univ, SE-90187 Umea, Sweden	Boman, BC (reprint author), Umea Univ, SE-90187 Umea, Sweden.						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L, 1999, AIR POLLUTION HLTH, P749, DOI 10.1016/B978-012352335-8/50108-3; MUHLBAIERDASCH J, 1982, ENVIRON SCI TECHNOL, V16, P639; NORDIN A, 1998, ASHES PARTICULATE EM, P119; Norris G, 1999, ENVIRON HEALTH PERSP, V107, P489, DOI 10.2307/3434632; Pope CA, 2000, AEROSOL SCI TECH, V32, P4, DOI 10.1080/027868200303885; Pope CA, 2002, JAMA-J AM MED ASSOC, V287, P1132, DOI 10.1001/jama.287.9.1132; Pope III CAD, 1999, AIR POLLUTION HLTH, P673; Purvis CR, 2000, ENVIRON SCI TECHNOL, V34, P1653, DOI 10.1021/es981006f; RAMDAHL T, 1983, NATURE, V306, P580, DOI 10.1038/306580a0; RAU JA, 1989, AEROSOL SCI TECH, V10, P181, DOI 10.1080/02786828908959233; Reddy A., 1996, ENERGY RIO PROSPECTS; Samet JM, 2000, NEW ENGL J MED, V343, P1742, DOI 10.1056/NEJM200012143432401; Schauer JJ, 2001, ENVIRON SCI TECHNOL, V35, P1716, DOI 10.1021/es001331e; Schauer JJ, 1996, ATMOS ENVIRON, V30, P3837, DOI 10.1016/1352-2310(96)00085-4; SCHLESINGER RB, 1999, AIR POLLUTION HLTH, P485; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; Sheppard L, 1999, EPIDEMIOLOGY, V10, P23, DOI 10.1097/00001648-199901000-00006; Smith KR, 2000, THORAX, V55, P518, DOI 10.1136/thorax.55.6.518; TORNQVIST M, 1994, ENVIRON HEALTH PERSP, V102, P173, DOI 10.2307/3431949; [Anonymous], 2000, 454R00002 USEPA; Valmari T, 1999, ENERG FUEL, V13, P390, DOI 10.1021/ef9800866; Vedal S, 1998, AM J RESP CRIT CARE, V157, P1034; WHO, 2000, GUID AIR QUAL; WIESER U, 2001, P 1 WORLD C EXH BIOM, P805; Yu OC, 2000, ENVIRON HEALTH PERSP, V108, P1209, DOI 10.2307/3434835; Zelikoff JT, 2002, J TOXICOL ENV HEAL B, V5, P269, DOI 10.1080/10937400290070062	60	116	117	0	27	SCAND J WORK ENV HEALTH	HELSINKI	TOPELIUKSENKATU 41A, SF-00250 HELSINKI, FINLAND	0355-3140			SCAND J WORK ENV HEA	Scand. J. Work Environ. Health	AUG	2003	29	4					251	260				10	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	711XH	WOS:000184766000002	12934718	
J	Chew, GL; Rogers, C; Burge, HA; Muilenberg, ML; Gold, DR				Chew, GL; Rogers, C; Burge, HA; Muilenberg, ML; Gold, DR			Dustborne and airborne fungal propagules represent a different spectrum of fungi with differing relations to home characteristics	ALLERGY			English	Article						air sampling; dust sampling; fungi; home characteristics; mold	IN-HOUSE DUST; RESIDENTIAL CHARACTERISTICS; RESPIRATORY SYMPTOMS; INDOOR ENVIRONMENT; DOMESTIC INTERIORS; EXPOSURE; HEALTH; CHILDREN; ASTHMA; PREVALENCE	Background: Exposure to fungi is often assessed by culturing floor dust or air samples. Our objective was to evaluate the relationships between dustborne and airborne fungi and to identify factors that modify these relationships. Methods: From November 1994 to September 1996 sequential duplicate 45-l air samples were collected in bedrooms of 496 homes in the Boston area, using a Burkard culture plate sampler. After air sampling, bedroom floors were sampled with a vacuum cleaner that was modified to collect dust in a cellulose extraction thimble. Dust was sieved, and the fine dust was dilution-plated onto DG-18 media. Results: Concentrations of total culturable fungi per gram of bedroom-floor dust were correlated weakly, but significantly, with those of indoor air (r = 0.13, P < 0.05). Concentrations of some individual taxa in the dust and indoor air were also weakly associated. Adjusting for the concentrations of fungi in outdoor air, dustborne fungal concentrations were positively associated with those in indoor air for the taxa Cladosporium and Penicillium , but not for total fungi. The indoor air fungal levels were often predicted by different covariates to those predicting fungal levels in dust. The type of housing (house or apartment) and the presence of carpeting were often predictive factors for dust fungi. In contrast, outdoor fungal levels were often predictive of the indoor air fungal levels. Conclusions: Because our data do not indicate a strong overall relationship between culturable fungi in dust and indoor air, the results from these two methods (dust and air sampling) likely represent different types of potential fungal exposures to residents. It may be essential to collect both air and dust samples, as well as information on housing characteristics, as indicators for fungal exposure.	Columbia Univ, Mailman Sch Publ Hlth, Dept Environm Hlth Sci, New York, NY 10032 USA; Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA; Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA	Chew, GL (reprint author), Columbia Univ, Mailman Sch Publ Hlth, Dept Environm Hlth Sci, 60 Haven Ave B-1, New York, NY 10032 USA.		Rogers, Christine/A-2189-2008	Rogers, Christine/0000-0003-0887-9606	NHLBI NIH HHS [HL-07427]; NIAID NIH HHS [AI-35786]		*AM C GOV IND HYG, 1998, BIOAER ASS CONTR; ANDERSEN AA, 1958, J BACTERIOL, V76, P471; *ASTM, 1990, E33784 ASTM; BEAUMONT F, 1984, ANN ALLERGY, V53, P486; Beguin H, 1996, AEROBIOLOGIA, V12, P113, DOI 10.1007/BF02248135; BJORNSSON E, 1995, CLIN EXP ALLERGY, V25, P423, DOI 10.1111/j.1365-2222.1995.tb01073.x; BURGE H, 1990, J ALLERGY CLIN IMMUN, V86, P687, DOI 10.1016/S0091-6749(05)80170-8; BURGE HA, 1995, OCCUP MED, V10, P27; Chew GL, 1999, ALLERGY, V54, P1058, DOI 10.1034/j.1398-9995.1999.00003.x; DALES RE, 1991, AM REV RESPIR DIS, V143, P505; Delfino RJ, 1997, ENVIRON HEALTH PERSP, V105, P622; Dillon HK, 1999, ENVIRON HEALTH PERSP, V107, P473; Douwes J, 1999, J ALLERGY CLIN IMMUN, V103, P494, DOI 10.1016/S0091-6749(99)70476-8; Douwes J, 1996, APPL ENVIRON MICROB, V62, P3176; Garrett MH, 1998, CLIN EXP ALLERGY, V28, P459; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; GRAVESEN S, 1978, ALLERGY, V33, P268, DOI 10.1111/j.1398-9995.1978.tb01547.x; Halonen M, 1997, AM J RESP CRIT CARE, V155, P1356; HORNER WE, 1995, CLIN MICROBIOL REV, V8, P161; *I MED DIV HLTH PR, 2000, CLEAR AIR ASTHM IND; Johansson SGO, 2001, ALLERGY, V56, P813, DOI 10.1034/j.1398-9995.2001.t01-1-00001.x; Koch A, 2000, ALLERGY, V55, P176, DOI 10.1034/j.1398-9995.2000.00233.x; Li DW, 1995, MYCOPATHOLOGIA, V131, P149, DOI 10.1007/BF01102894; Malloch DW., 1981, MOULDS THEIR ISOLATI; Miller JD, 1997, AM IND HYG ASSOC J, V58, P39; OHOLLAREN MT, 1991, NEW ENGL J MED, V324, P359, DOI 10.1056/NEJM199102073240602; PASANEN AL, 1991, ATMOS ENVIRON A-GEN, V25, P459, DOI 10.1016/0960-1686(91)90316-Y; PASANEN AL, 1992, ATMOS ENVIRON B-URB, V26, P121, DOI 10.1016/0957-1272(92)90044-S; PEAT JK, 1993, CLIN EXP ALLERGY, V23, P812, DOI 10.1111/j.1365-2222.1993.tb00258.x; Peat JK, 1998, ALLERGY, V53, P120, DOI 10.1111/j.1398-9995.1998.tb03859.x; Ren P, 2001, ALLERGY, V56, P419, DOI 10.1034/j.1398-9995.2001.056005419.x; Rylander R, 1992, INDOOR ENVIRON, V1, P263, DOI 10.1177/1420326X9200100502; SCHAEFFER N, 1953, J ALLERGY, V23, P348; SOLOMON WR, 1975, J ALLERGY CLIN IMMUN, V56, P235, DOI 10.1016/0091-6749(75)90095-0; SPORIK RB, 1993, CLIN EXP ALLERGY, V23, P326, DOI 10.1111/j.1365-2222.1993.tb00330.x; STRACHAN DP, 1990, THORAX, V45, P382, DOI 10.1136/thx.45.5.382; SU HJ, 1992, APPL ENVIRON MICROB, V58, P181; Su HJJ, 2001, ARCH ENVIRON HEALTH, V56, P144; SWAEBLY MA, 1953, J ALLERGY, V23, P370; Verhoeff AP, 1997, ANN ALLERG ASTHMA IM, V78, P544; VERHOEFF AP, 1994, ALLERGY, V49, P540, DOI 10.1111/j.1398-9995.1994.tb01126.x; von Arx J. A., 1970, GENERA FUNGI SPORULA	42	116	117	0	10	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	JAN	2003	58	1					13	20		10.1034/j.1398-9995.2003.00013.x		8	Allergy; Immunology	Allergy; Immunology	643GJ	WOS:000180853300004	12580801	
J	Becker, S; Fenton, MJ; Soukup, JM				Becker, S; Fenton, MJ; Soukup, JM			Involvement of microbial components and toll-like receptors 2 and 4 in cytokine responses to air pollution particles	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article							ALVEOLAR MACROPHAGE RESPONSES; EMERGENCY ROOM VISITS; TNF-ALPHA; RESPIRATORY ILLNESSES; INSOLUBLE COMPONENTS; SIGNAL-TRANSDUCTION; CUTTING EDGE; IN-VITRO; LIPOPOLYSACCHARIDE; ENDOTOXIN	Inhalation of particulate matter (PM) may result in exacerbation of inflammatory airways disease, including asthma. Results from this laboratory have shown that the coarse inhalable particle fraction (PM2.5-10) is responsible for most of the PM effects on human airway macrophages (AM), including induction of cytokine production. Endotoxins associated with these particles account for a large part of their potency, as activity of PM can be inhibited by polymixin B and an activating moiety bound by lipopolysaccharide (LPS)-binding protein (LBP). The hypothesis behind the present study was that not only particle-bound LPS, but also Gram-negative (Gram-) and Gram-positive (Gram+) bacteria are responsible for PM-induced stimulation of AM, and therefore that PM are likely to activate receptors involved in recognition of microbes. Low level contamination of model pollution particles with environmental Staphyloccocus, Streptococcus, and Pseudomonas species was found to confer cytokine-inducing activity on inactive particles. Only one Gram- bacterium was sufficient for significant stimulatation of 100 AM, whereas at least three times more Gram+ bacteria were required for a similar level of response. Cytokine responses induced by PM as well as Gram+ and Gram- bacteria were inhibited by anti-CD14 antibody and required the presence of LBP-containing serum. The involvement of Toll-like receptor (TLR) 2 and 4 in recognition of PMZ.,o was investigated in transfected Chinese hamster ovary cells expressing CD14 and TLR2 or TLR4. TLR4 was found to be involved in PM2.5-10 and Pseudomonas-induced activation, whereas TLR2 activation was induced by both Gram+ and Gram- bacteria and by PM. The synthetic lipid A analog E5531 fully inhibited the response to purified LPS and partially inhibited the response to PM and Pseudomonas. In contrast, E5531 had no effect on the response to Staphylococcus. Taken together, these results implicate microbial components as important players in AM-dependent inflammatory responses to PM.	US EPA, Natl Hlth & Environm Effect Res Lab, Res Triangle Pk, NC 27711 USA; Boston Univ, Sch Med, Ctr Pulm, Boston, MA 02118 USA	Becker, S (reprint author), Human Studies Facil, EPA Bldg,104 Mason Farm Rd, Chapel Hill, NC 27599 USA.						Atkinson RW, 1999, ARCH ENVIRON HEALTH, V54, P398; Becker S, 1996, TOXICOL APPL PHARM, V141, P637, DOI 10.1006/taap.1996.0330; BOVALLIUS A, 1978, APPL ENVIRON MICROB, V35, P847; Chow JC, 1999, J BIOL CHEM, V274, P10689, DOI 10.1074/jbc.274.16.10689; Daniels AU, 2000, J BIOMED MATER RES, V49, P469, DOI 10.1002/(SICI)1097-4636(20000315)49:4<469::AID-JBM5>3.0.CO;2-A; Delfino RJ, 1997, AM J RESP CRIT CARE, V155, P568; Delude RL, 1998, J IMMUNOL, V161, P3001; Garcia JEL, 1999, MEDIAT INFLAMM, V8, P43; Ghio A. J. B. 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J. Respir. Cell Mol. Biol.	NOV	2002	27	5					611	618		10.1165/rcmb.4868		8	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	614KW	WOS:000179189000012	12397021	
J	Lin, S; Munsie, JP; Hwang, SA; Fitzgerald, E; Cayo, MR				Lin, S; Munsie, JP; Hwang, SA; Fitzgerald, E; Cayo, MR			Childhood asthma hospitalization and residential exposure to state route traffic	ENVIRONMENTAL RESEARCH			English	Article						asthma hospitalization; childhood asthma; traffic; automobile exhaust	RESPIRATORY HEALTH; AIR-POLLUTION; ADJUVANT ACTIVITY; CHILDREN; EXHAUST; ADMISSIONS; PARTICLES; ADULTS; ROADS; MICE	This study investigated whether pediatric hospitalization for asthma was related to living near a road with heavy traffic. In this case-control study, cases (N=417) consisted of white children aged 0-14 years who were admitted for asthma and who resided in Erie County, New York, excluding the city of Buffalo. Controls (N=461) were children in the same age range admitted during the same time period for nonrespiratory diseases. Subjects' residential addresses were linked to traffic information provided by the New York State Department of Transportation. After adjustments for age and poverty level were made, children hospitalized for asthma were more likely to live on roads with the highest tertile of vehicle miles traveled (VMT) (odds ratio (OR): 1.93, 95% confidence interval (CI): 1.13-3.29) within 200 m and were more likely to have trucks and trailers passing by within 200m of their residence (OR=1.43, 95% CI: 1.03-1.99) compared to controls. However, childhood asthma hospitalization was not significantly associated with residential distance from state roads, annual VMT within 500m, or whether trucks or trailers passed by within 500m. This study suggests that exposure to high volumes of traffic/trucks within 200m of homes contributes to childhood asthma hospitalizations. (C) 2002 Elsevier Science (USA).	New York State Dept Hlth, Bur Environm & Occupat Epidemiol, Troy, NY 12180 USA	Lin, S (reprint author), New York State Dept Hlth, Bur Environm & Occupat Epidemiol, Troy, NY 12180 USA.		Fitzgerald, Edward/F-4087-2010; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Lin, Shao/0000-0002-5535-7504			Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; COLLEY JRT, 1973, BRIT MED J, V3, P195; DOCKERY DW, 1989, AM REV RESPIR DIS, V139, P587; EDWARDS J, 1994, ARCH ENVIRON HEALTH, V49, P223; *GEOGR DAT TECHN I, 1995, MATCHM 2000 2 1 WIND; Heinrich J, 1999, ENVIRON HEALTH PERSP, V107, P53, DOI 10.2307/3434289; HILDEMANN LM, 1991, AEROSOL SCI TECH, V14, P138, DOI 10.1080/02786829108959478; Lin S, 1999, J ASTHMA, V36, P241; LINN W S, 1986, Toxicology and Industrial Health, V2, P99; LINN WS, 1983, AM REV RESPIR DIS, V289, P235; Livingstone AE, 1996, BRIT MED J, V312, P676; LUNN JE, 1967, BRIT J PREV SOC MED, V21, P7; *MAIL SOFTW, 1995, MAIL PLUS 4 US MAN; *MAP CORP, 1998, MAP PROF US GUID; MARTIN AE, 1964, P ROY SOC MED, V57, P969; MURANAKA M, 1986, J ALLERGY CLIN IMMUN, V77, P616, DOI 10.1016/0091-6749(86)90355-6; NITTA H, 1993, ARCH ENVIRON HEALTH, V48, P53; *NY STAT DEP TRANS, 1994, HIGHW SUFF RAT; ONO M, 1989, J JAPAN SOC AIR POLL, V24, P90; Oosterlee A, 1996, OCCUP ENVIRON MED, V53, P241; OREHEK J, 1986, J CLIN INVEST, V56, P301; Pershagen G, 1995, INT J EPIDEMIOL, V24, P1147, DOI 10.1093/ije/24.6.1147; POPE CA, 1991, ARCH ENVIRON HEALTH, V46, P90; Rijnders E, 2001, ENVIRON HEALTH PERSP, V109, P411, DOI 10.2307/3434789; TAKAFUJI S, 1987, J ALLERGY CLIN IMMUN, V79, P639, DOI 10.1016/S0091-6749(87)80161-6; *US BUR CENS, 1993, 185 CURR POP REP P60; WARE JH, 1986, AM REV RESPIR DIS, V133, P834; Weiland Stephan K., 1994, Annals of Epidemiology, V4, P243; World Health Organization/United Nations Environment Programme, 1992, URB AIR POLL MEG WOR; WJST M, 1993, BRIT MED J, V307, P596	30	116	122	0	23	ACADEMIC PRESS INC ELSEVIER SCIENCE	SAN DIEGO	525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA	0013-9351			ENVIRON RES	Environ. Res.	FEB	2002	88	2					73	81		10.1006/enrs.2001.4303		9	Environmental Sciences; Public, Environmental & Occupational Health	Environmental Sciences & Ecology; Public, Environmental & Occupational Health	536LG	WOS:000174701100001	11908931	
J	Laumbach, RJ; Kipen, HM				Laumbach, Robert J.; Kipen, Howard M.			Respiratory health effects of air pollution: Update on biomass smoke and traffic pollution	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Biomass; traffic; chronic obstructive pulmonary disease; asthma; air pollutants; particulate matter	OBSTRUCTIVE PULMONARY-DISEASE; DIESEL EXHAUST PARTICLES; ENVIRONMENTAL RISK-FACTORS; LONG-TERM EXPOSURE; AMBIENT AIR; LOS-ANGELES; SOLID-FUEL; STREPTOCOCCUS-PNEUMONIAE; DEVELOPING-COUNTRIES; ULTRAFINE PARTICLES	Mounting evidence suggests that air pollution contributes to the large global burden of respiratory and allergic diseases, including asthma, chronic obstructive pulmonary disease, pneumonia, and possibly tuberculosis. Although associations between air pollution and respiratory disease are complex, recent epidemiologic studies have led to an increased recognition of the emerging importance of traffic-related air pollution in both developed and less-developed countries, as well as the continued importance of emissions from domestic fires burning biomass fuels, primarily in the less-developed world. Emissions from these sources lead to personal exposures to complex mixtures of air pollutants that change rapidly in space and time because of varying emission rates, distances from source, ventilation rates, and other factors. Although the high degree of variability in personal exposure to pollutants from these sources remains a challenge, newer methods for measuring and modeling these exposures are beginning to unravel complex associations with asthma and other respiratory tract diseases. These studies indicate that air pollution from these sources is a major preventable cause of increased incidence and exacerbation of respiratory disease. Physicians can help to reduce the risk of adverse respiratory effects of exposure to biomass and traffic air pollutants by promoting awareness and supporting individual and community-level interventions. (J Allergy Clin Immunol 2012; 129: 3-11.)	[Kipen, Howard M.] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, EOHSI, Piscataway, NJ 08854 USA; Rutgers State Univ, Piscataway, NJ USA	Kipen, HM (reprint author), Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, EOHSI, 170 Frelinghuysen Rd, Piscataway, NJ 08854 USA.	kipen@eohsi.rutgers.edu			National Institute of Environmental Health Sciences [P30 ES005022]; US Environmental Protection Agency STAR [RD 83457901]	Supported in part by National Institute of Environmental Health Sciences grant P30 ES005022 and US Environmental Protection Agency STAR Grant RD 83457901.	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Zuurbier M, 2009, ENVIRON HEALTH-GLOB, V8, DOI 10.1186/1476-069X-8-48	92	115	118	6	77	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JAN	2012	129	1					3	13		10.1016/j.jaci.2011.11.021		11	Allergy; Immunology	Allergy; Immunology	869XT	WOS:000298634000002	22196520	
J	Gill, MA; Bajwa, G; George, TA; Dong, CC; Dougherty, II; Jiang, N; Gan, VN; Gruchalla, RS				Gill, Michelle A.; Bajwa, Gagan; George, Tiffany A.; Dong, Caroline C.; Dougherty, Irene I.; Jiang, Nan; Gan, Vanthaya N.; Gruchalla, Rebecca S.			Counterregulation between the Fc epsilon RI Pathway and Antiviral Responses in Human Plasmacytoid Dendritic Cells	JOURNAL OF IMMUNOLOGY			English	Article							INTERFERON-PRODUCING CELLS; ANTIGEN-PRESENTING CELLS; TOLL-LIKE RECEPTOR-9; ATOPIC-DERMATITIS; ASTHMA; VIRUS; EXPRESSION; IMMUNITY; ALPHA; IGE	Plasmacytoid dendritic cells (pDCs) play essential roles in directing immune responses. These cells may be particularly important in determining the nature of immune responses to viral infections in patients with allergic asthma as well those with other atopic diseases. The purposes of this study were 1) to compare the functional capacity of pDCs in patients with one type of allergic disorder, allergic asthma, and controls; 2) to determine whether IgE cross-linking affects antiviral responses of influenza-exposed pDCs; and 3) to determine whether evidence of counterregulation of Fc epsilon RIa and IFN-alpha pathways exists in these cells. pDC function was assessed in a subset of asthma patients and in controls by measuring IFN-alpha production after exposure of purified pDCs to influenza viruses. Fc epsilon RIa expression on pDCs was determined by flow cytometry in blood samples from patients with allergic asthma and controls. pDCs from patients with asthma secreted significantly less IFN-alpha upon exposure to influenza A (572 versus 2815; p = 0.03), and secretion was inversely correlated with serum IgE levels. Moreover, IgE cross-linking prior to viral challenge resulted in 1) abrogation of the influenza-induced pDC IFN-alpha response; 2) diminished influenza and gardiquimod-induced TLR-7 upregulation in pDCs; and 3) interruption of influenza-induced upregulation of pDC maturation/ costimulatory molecules. In addition, exposure to influenza and gardiquimod resulted in upregulation of TLR-7, with concomitant downregulation of Fc epsilon RIa expression in pDCs. These data suggest that counterregulation of Fc epsilon RI and TLR-7 pathways exists in pDCs, and that IgE cross-linking impairs pDC antiviral responses. The Journal of Immunology, 2010, 184: 5999-6006.	[Gill, Michelle A.; George, Tiffany A.; Dong, Caroline C.; Dougherty, Irene I.; Jiang, Nan; Gruchalla, Rebecca S.] Univ Texas SW Med Ctr Dallas, Div Allergy & Immunol, Dept Internal Med, Dallas, TX 75290 USA; [Gill, Michelle A.; Bajwa, Gagan] Univ Texas SW Med Ctr Dallas, Div Pediat Infect Dis, Dallas, TX 75290 USA; [Gill, Michelle A.; Bajwa, Gagan] Univ Texas SW Med Ctr Dallas, Div Pulm Vasc Biol, Dallas, TX 75290 USA; [Gan, Vanthaya N.] Univ Texas SW Med Ctr Dallas, Div Gen Pediat, Dept Pediat, Dallas, TX 75290 USA; Childrens Med Ctr Dallas, Dallas, TX 75290 USA	Gill, MA (reprint author), Univ Texas SW Med Ctr Dallas, Dept Pediat, Room F3-202,5323 Harry Hines Blvd, Dallas, TX 75390 USA.	michelle.gill@utsouthwestern.edu			Exxon Mobil Corporation; National Institutes of Health, National Institute of Allergy and Infectious Diseases [5 RO1 AI049570]	This work was supported by grants from Exxon Mobil Corporation (to M. G. and R. G.) and the National Institutes of Health, National Institute of Allergy and Infectious Diseases (no. 5 RO1 AI049570, to R. G.).	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Immunol.	JUN 1	2010	184	11					5999	6006		10.4049/jimmunol.0901194		8	Immunology	Immunology	606PP	WOS:000278439600011	20410486	
J	Renz-Polster, H; David, MR; Buist, AS; Vollmer, WM; O'Connor, EA; Frazier, EA; Wall, MA				Renz-Polster, H; David, MR; Buist, AS; Vollmer, WM; O'Connor, EA; Frazier, EA; Wall, MA			Caesarean section delivery and the risk of allergic disorders in childhood	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergic rhinoconjunctivitis; asthma; atopic dermatitis; atopy; allergy; Caesarean section; intestinal flora; intestinal microbes; risk of allergic disorders	PLACEBO-CONTROLLED TRIAL; HAY-FEVER; ATOPIC DISEASE; BACTERIAL-FLORA; ASTHMA; CHILDREN; MODE; LIFE; INTERLEUKIN-10; COMPLICATIONS	Background The composition of the intestinal flora in young children, if unfavourable, may increase the susceptibility to allergic disorders. Beneficial intestinal microbes originate from the maternal vaginal tract and thus are more likely to be transferred during vaginal births than during Caesarean sections (C-sections). Objective To determine whether children born by C-section have a different risk of allergic disorders compared with those delivered vaginally. We also tested the hypothesis that the risk of allergic disorders is highest for children born after 'repeat C-sections'. Methods A retrospective cohort study of 8953 children aged 3-10 years. Children diagnosed with allergic rhinoconjunctivitis (AR), asthma, atopic dermatitis (AD), or food allergies were identified from the Kaiser Permanente Northwest Region electronic records. The children's sex, birth weight, birth order, postnatal exposure to antibiotics as well as the mothers' age, ethnicity, education, marital status, smoking status during pregnancy, and use of asthma or hayfever medications were identified through the mothers' medical records or through the Oregon Birth Registry. Results The risk of being diagnosed with AR was significantly higher in the children born by C-section than in those delivered vaginally: adjusted odds ratio (OR)=1.37%, 95% confidence interval (CI)=1.14-1.63. Delivery by C-section was also associated with the subsequent diagnosis of asthma (OR=1.24%, 95% CI=1.01-1.53); this association was gender specific, with a positive association restricted to girls (OR for asthma in girls: OR=1.53%, 95% CI=1.11-2.10; in boys: OR=1.08%, 95% CI=0.81-1.43). There was no significant association between mode of delivery and AD. If children born in a 'repeat C-section' were considered separately the risk of being diagnosed with AR increased further (OR=1.78%, 95% CI=1.34-2.37). The same increase was noted for asthma in girls (OR=1.83%, 95% CI=1.13-2.97) but not in boys. Conclusion Caesarean sections may be associated with an increased risk of developing AR in childhood.	Oregon Hlth Sci Univ, Portland, OR 97201 USA; Kaiser Permanente Ctr Hlth Res, Portland, OR USA	Renz-Polster, H (reprint author), Rohrmoos 10, D-88267 Vogt, Germany.	renzpoh@pol.net	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; ANNIBALE DJ, 1995, ARCH PEDIAT ADOL MED, V149, P862; Bager P, 2003, J ALLERGY CLIN IMMUN, V111, P51, DOI 10.1067/mai.2003.34; Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; Bjorksten B, 1999, CLIN EXP ALLERGY, V29, P342; Bjorksten B, 1999, J ALLERGY CLIN IMMUN, V104, P1119; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Butland BK, 1997, BRIT MED J, V315, P717; Chapman DJ, 1999, J AM DIET ASSOC, V99, P450, DOI 10.1016/S0002-8223(99)00109-1; Demissie K, 1998, AM J RESP CRIT CARE, V158, P1091; DiMatteo MR, 1996, HEALTH PSYCHOL, V15, P303; Gronlund MM, 1999, CLIN EXP IMMUNOL, V116, P521; Gronlund MM, 1999, J PEDIATR GASTR NUTR, V28, P19, DOI 10.1097/00005176-199901000-00007; Guarner F, 2003, LANCET, V361, P512, DOI 10.1016/S0140-6736(03)12489-0; Hakansson S, 2003, CLIN EXP ALLERGY, V33, P757, DOI 10.1046/j.1365-2222.2003.01667.x; HALL MA, 1990, ARCH DIS CHILD, V65, P185; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Illi S, 2004, J ALLERGY CLIN IMMUN, V113, P925, DOI 10.1016/j.jaci.2004.01.778; JENKINS MA, 1994, BRIT MED J, V309, P90; Kalliomaki M, 2003, LANCET, V361, P1869, DOI 10.1016/S0140-6736(03)13490-3; Kalliomaki M, 2001, LANCET, V357, P1076, DOI 10.1016/S0140-6736(00)04259-8; Kero J, 2002, PEDIATR RES, V52, P6, DOI 10.1023/01.PDR.0000017263.01840.F0; Laubereau B, 2004, ARCH DIS CHILD, V89, P993, DOI 10.1136/adc.2003.043265; Leung GM, 2002, OBSTET GYNECOL, V99, P785, DOI 10.1016/S0029-7844(02)01940-3; Maitra A, 2004, CLIN EXP ALLERGY, V34, P1349, DOI 10.1111/j.1365-2222.2004.02048.x; Martinez F D, 1999, Lancet, V354 Suppl 2, pSII12, DOI 10.1016/S0140-6736(99)90437-3; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; MARTINEZ FD, 1994, THORAX, V49, P1189, DOI 10.1136/thx.49.12.1189; McKeever TM, 2002, J ALLERGY CLIN IMMUN, V109, P800, DOI 10.1067/mai.2002.124046; Nafstad P, 2000, J ALLERGY CLIN IMMUN, V106, P867, DOI 10.1067/mai.2000.110558; Negele K, 2004, PEDIAT ALLERG IMM-UK, V15, P48, DOI 10.1046/j.0905-6157.2003.00101.x; Pearce N, 1999, THORAX, V54, P268; Pessi T, 2000, CLIN EXP ALLERGY, V30, P1804, DOI 10.1046/j.1365-2222.2000.00948.x; ROTIMI VO, 1981, J MED MICROBIOL, V14, P51; Salminen S, 2004, GUT, V53, P1388, DOI 10.1136/gut.2004.041640; Sears MR, 2002, LANCET, V360, P901, DOI 10.1016/S0140-6736(02)11025-7; Smith GCS, 2004, ARCH DIS CHILD, V89, P956, DOI 10.1136/adc.2003.045971; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Strachan DP, 1996, ARCH DIS CHILD, V74, P422; Sudo N, 1997, J IMMUNOL, V159, P1739; van den Biggelaar AHJ, 2000, LANCET, V356, P1723, DOI 10.1016/S0140-6736(00)03206-2; Wahn U, 2001, J ALLERGY CLIN IMMUN, V107, P567, DOI 10.1067/mai.2001.112943; Wills-Karp M, 2001, NAT REV IMMUNOL, V1, P69, DOI 10.1038/35095579; Withers NJ, 1998, AM J RESP CRIT CARE, V158, P352; Xu B, 2001, J ALLERGY CLIN IMMUN, V107, P732; Xu BZ, 2000, J ASTHMA, V37, P589, DOI 10.3109/02770900009090814; [Anonymous], 1993, MMWR MORB MORTAL WKL, V42, P285	48	115	127	1	22	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	NOV	2005	35	11					1466	1472		10.1111/j.1365-2222.2005.02356.x		7	Allergy; Immunology	Allergy; Immunology	982NR	WOS:000233169400009	16297144	
J	Sicherer, SH				Sicherer, SH			Food protein-induced enterocolitis syndrome: Case presentations and management lessons	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						food allergy; food protein-induced enterocolitis syndrome	COWS MILK ALLERGY; EPITHELIAL BARRIER FUNCTION; NECROSIS-FACTOR-ALPHA; ATOPY PATCH TEST; GASTROINTESTINAL MANIFESTATIONS; CLINICAL-FEATURES; SKIN PRICK; TNF-ALPHA; INFANTS; SOY	Enterocolitis induced in infants by cow's milk and/or soy protein has been recognized for decades. Symptoms typically begin in the first month of life in association with failure to thrive and may progress to acidemia and shock. Symptoms resolve after the causal protein is removed from the diet but recur with a characteristic symptom pattern on re-exposure. Approximately 2 hours after reintroduction of the protein, vomiting ensues, followed by an elevation of the peripheral blood polymorphonuclear leukocyte count, diarrhea, and possibly lethargy and hypotension. The disorder is generally not associated with detectable food-specific IgE antibody. There are increasing reports of additional causal foods, prolonged clinical courses, and onset outside of early infancy, leading to description of a food protein-induced enterocolitis syndrome. The disorder poses numerous diagnostic and therapeutic challenges. The purpose of this report is to delineate the characteristic clinical features and review the possible pathophysiologic basis to frame a rational strategy toward management.	Mt Sinai Sch Med, Dept Pediat, Elliot & Roslyn Jaffe Food Allergy Inst, Div Allergy & Immunol, New York, NY USA	Sicherer, SH (reprint author), Mt Sinai Hosp, Jaffe Food Allergy Inst, Div Allergy Immunol, Box 1198,1 Gustave L Levy Pl, New York, NY 10029 USA.	scott.sicherer@mssm.edu					Benlounes N, 1996, J ALLERGY CLIN IMMUN, V98, P781, DOI 10.1016/S0091-6749(96)70127-6; Benlounes N, 1999, J ALLERGY CLIN IMMUN, V104, P863; BOCK SA, 1988, J ALLERGY CLIN IMMUN, V82, P986; Burks A W, 1994, Pediatr Allergy Immunol, V5, P40, DOI 10.1111/j.1399-3038.1994.tb00217.x; Busse PJ, 2000, J ALLERGY CLIN IMMUN, V105, pS129, DOI 10.1016/S0091-6749(00)90815-7; Chung HL, 2002, J ALLERGY CLIN IMMUN, V109, P150, DOI 10.1067/mai.2002.120562; COELLORAMIREZ P, 1984, J PEDIATR GASTR NUTR, V3, P215, DOI 10.1097/00005176-198403000-00008; de Boissieu D, 2003, J PEDIATR-US, V142, P203, DOI 10.1067/mpd.2003.92; FONTAINE JL, 1975, ARCH DIS CHILD, V50, P357; GOLDMAN H, 1986, AM J SURG PATHOL, V10, P75, DOI 10.1097/00000478-198602000-00001; GRYBOSKI JD, 1967, PEDIATRICS, V40, P354; HALPIN TC, 1977, J PEDIATR-US, V91, P404, DOI 10.1016/S0022-3476(77)81308-5; HEYMAN M, 1994, GASTROENTEROLOGY, V106, P1514; HILL DJ, 1986, J PEDIATR-US, V109, P270, DOI 10.1016/S0022-3476(86)80384-5; Hoffman KM, 1997, J ALLERGY CLIN IMMUN, V99, P360, DOI 10.1016/S0091-6749(97)70054-X; Isolauri E, 1996, J ALLERGY CLIN IMMUN, V97, P9, DOI 10.1016/S0091-6749(96)70277-4; Jarvinen KM, 1999, J PEDIATR-US, V135, P506, DOI 10.1016/S0022-3476(99)70175-7; JENKINS HR, 1984, ARCH DIS CHILD, V59, P326; Kapel N, 1999, CLIN CHEM LAB MED, V37, P29, DOI 10.1515/CCLM.1999.004; KELSO JM, 1993, J ALLERGY CLIN IMMUN, V92, P909, DOI 10.1016/0091-6749(93)90069-R; Levy Y, 2003, PEDIATR ALLERGY IMMU, V14, P325, DOI 10.1034/j.1399-3038.2003.00039.x; Lin XP, 2002, J ALLERGY CLIN IMMUN, V109, P879, DOI 10.1067/mai.2002.123238; Majamaa H, 2001, CLIN EXP ALLERGY, V31, P590, DOI 10.1046/j.1365-2222.2001.01035.x; MCDONALD PJ, 1984, PEDIATR RES, V18, P751, DOI 10.1203/00006450-198408000-00016; MURRAY KF, 1993, J PEDIATR-US, V122, P90, DOI 10.1016/S0022-3476(05)83495-X; Nowak-Wegrzyn A, 2003, PEDIATRICS, V111, P829, DOI 10.1542/peds.111.4.829; Perackis K, 2003, J ALLERGY CLIN IMMUN, V112, P625, DOI 10.1067/mai.2003.1656; Planchon S, 1999, J CELL PHYSIOL, V181, P55, DOI 10.1002/(SICI)1097-4652(199910)181:1<55::AID-JCP6>3.0.CO;2-M; PLANCHON SM, 1994, J IMMUNOL, V153, P5730; POWELL G K, 1986, Comprehensive Therapy, V12, P28; POWELL GK, 1978, J PEDIATR-US, V93, P553, DOI 10.1016/S0022-3476(78)80887-7; POWELL GK, 1976, J PEDIATR-US, V88, P840, DOI 10.1016/S0022-3476(76)81128-6; Rubin MI, 1940, AM J MED SCI, V200, P385, DOI 10.1097/00000441-194009000-00014; Sampson HA, 2000, J PEDIATR GASTR NUTR, V30, pS87, DOI 10.1097/00005176-200001001-00013; Sampson Hugh A., 2003, Journal of Allergy and Clinical Immunology, V111, pS540; Sicherer SH., 2000, J PEDIAT GASTROENT S, V30, P45; Sicherer SH, 2003, PEDIATRICS, V111, P1609; Sicherer SH, 1998, J PEDIATR-US, V133, P214, DOI 10.1016/S0022-3476(98)70222-7; Sicherer SH, 1999, PEDIATR ALLERGY IMMU, V10, P226, DOI 10.1034/j.1399-3038.1999.00040.x; Spergel JM, 2002, J ALLERGY CLIN IMMUN, V109, P363, DOI 10.1067/mai.2002.121458; Untersmayr E, 2003, J ALLERGY CLIN IMMUN, V112, P616, DOI 10.1016/mai.2003.1681; VANDENPLAS Y, 1994, J PEDIATR GASTR NUTR, V19, P240, DOI 10.1097/00005176-199408000-00016; VANSICKLE GJ, 1985, GASTROENTEROLOGY, V88, P1915; VITORIA JC, 1982, ARCH DIS CHILD, V57, P44	44	115	120	0	3	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JAN	2005	115	1					149	156		10.1016/j.jaci.2004.09.033		8	Allergy; Immunology	Allergy; Immunology	886XS	WOS:000226267000022	15637562	
J	Terreehorst, I; Hak, E; Oosting, AJ; Tempels-Pavlica, Z; de Monchy, JGR; Bruijnzeel-Koomen, CAFM; Aalberse, RC; Gerth van Wijk, R				Terreehorst, I; Hak, E; Oosting, AJ; Tempels-Pavlica, Z; de Monchy, JGR; Bruijnzeel-Koomen, CAFM; Aalberse, RC; Gerth van Wijk, R			Evaluation of impermeable covers for bedding in patients with allergic rhinitis	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							HOUSE-DUST-MITE; PERENNIAL RHINITIS; INTRANASAL CAPSAICIN; MATTRESS ENCASINGS; ASTHMATIC-PATIENTS; AVOIDANCE MEASURES; ATOPIC-DERMATITIS; CUTOFF VALUES; DOUBLE-BLIND; CHILDREN	Background: Encasing bedding in impermeable covers reduces exposure to house-dust mites, but the clinical benefit of this intervention as part of mite-avoidance measures for patients with allergic rhinitis is not known. We performed a multicenter, randomized, placebo-controlled trial of one year of use of impermeable bedding covers in the bedrooms of patients with rhinitis who were sensitized to house-dust mites to determine the effects on the signs and symptoms of disease. Methods: Three participating university medical centers enrolled 279 patients with allergic rhinitis who were randomly assigned to receive impermeable or non-impermeable (control) covers for their mattress, pillow, and duvet or blanket. At the start of the study, all participants received information on general allergen-avoidance measures. The severity of rhinitis was measured on a rhinitis-specific visual-analogue scale and by means of a daily symptom score and nasal allergen provocation testing. We also measured the concentrations of Dermatophagoides pteronyssinus (Der p1) and D. farinae (Der f 1) in dust from patients' mattresses, bedroom floors, and living-room floors at base line and after 12 months as a measure of the efficacy of the intervention. Results: A total of 232 patients completed the study. There was a significant reduction in Der p1 and Der f 1 concentrations in the mattresses of the impermeable-cover group, whereas there was no significant reduction in the control group. However, there was no significant effect on the clinical outcome measures. Analyses of subgroups defined according to age, level of exposure, type and severity of sensitization, or characteristics of the patient's home had similar results. Conclusions: Mite-proof bedding covers, as part of a structured allergy-control program, reduced the level of exposure to mite allergens. Despite the success of the intervention, this single avoidance measure did not lead to a significant improvement of clinical symptoms in patients with allergic rhinitis.	Erasmus Med Ctr, Dept Allergol, NL-3015 GD Rotterdam, Netherlands; Albert Scheitzer Hosp, Dept Internal Med, Dordrecht, Netherlands; Univ Utrecht, Med Ctr, Dept Dermatol, Utrecht, Netherlands; Univ Groningen Hosp, Dept Allergol, Groningen, Netherlands; Sanquin Res, Dept Immunopathol, Amsterdam, Netherlands; Univ Utrecht, Med Ctr, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands	Gerth van Wijk, R (reprint author), Erasmus Med Ctr, Dept Allergol, Dr Molewaterplein 40, NL-3015 GD Rotterdam, Netherlands.			Terreehorst, Ingrid/0000-0002-3264-2740			Ad Hoc Working group on environmental allergens and asthma, 1999, J ALLERGY CLIN IMMUN, V103, P203; *AM AC ALL ASTHM I, 2001, ALL REP 2000; BEAUMONT F, 1985, ALLERGY, V40, P181, DOI 10.1111/j.1398-9995.1985.tb00214.x; Blom HM, 1997, CLIN EXP ALLERGY, V27, P796, DOI 10.1046/j.1365-2222.1997.670842.x; Bousquet J, 2001, J ALLERGY CLIN IMMUN, V108, pS147, DOI 10.1067/mai.2001.118891; Casale TB, 2001, JAMA-J AM MED ASSOC, V286, P2956, DOI 10.1001/jama.286.23.2956; Cloosterman SGM, 1999, CLIN EXP ALLERGY, V29, P1336, DOI 10.1046/j.1365-2222.1999.00627.x; de Graaf-in 't Veld T, 1995, Ann Allergy Asthma Immunol, V75, P261; De Lucca SD, 2000, J ALLERGY CLIN IMMUN, V106, P874, DOI 10.1067/mai.2000.110804; deGraafintVeld C, 1997, THORAX, V52, P143; Durham SR, 1999, NEW ENGL J MED, V341, P468, DOI 10.1056/NEJM199908123410702; EHNERT B, 1992, J ALLERGY CLIN IMMUN, V90, P135, DOI 10.1016/S0091-6749(06)80024-2; Frederick JM, 1997, EUR RESPIR J, V10, P361, DOI 10.1183/09031936.97.10020361; Gotzsche PC, 2001, COCHRANE DB SYST REV, V3; Herman D, 1997, INT J PEDIATR OTORHI, V39, P1, DOI 10.1016/S0165-5876(96)01457-7; International Consensus Report on the diagnosis and management of rhinitis, 1994, ALLERGY S19, V49, P1; Koepke JW, 1999, ALLERGY ASTHMA PROC, V20, P337; LEBEL B, 1988, J ALLERGY CLIN IMMUN, V82, P869, DOI 10.1016/0091-6749(88)90092-9; Malm L, 2000, RHINOLOGY, V38, P1; MARKS GB, 1995, J ALLERGY CLIN IMMUN, V96, P441, DOI 10.1016/S0091-6749(95)70285-7; Moon JS, 1999, YONSEI MED J, V40, P238; NIEMEIJER NR, 1993, ALLERGY, V48, P491, DOI 10.1111/j.1398-9995.1993.tb01104.x; NIEMEIJER NR, 1993, ALLERGY, V48, P498, DOI 10.1111/j.1398-9995.1993.tb01105.x; Oosting AJ, 2002, J ALLERGY CLIN IMMUN, V110, P500, DOI 10.1067/mai.2002.126791; Sheikh A, 2001, COCHRANE DB SYST REV, V4; Terreehorst I, 2002, CLIN EXP ALLERGY, V32, P1160, DOI 10.1046/j.1365-2745.2002.01461.x; van Cauwenberge P, 2000, ALLERGY, V55, P116, DOI 10.1034/j.1398-9995.2000.00526.x; van Strien RT, 2002, ENVIRON HEALTH PERSP, V110, pA693; Van Wijk RG, 2000, CLIN EXP ALLERGY, V30, P1792, DOI 10.1046/j.1365-2222.2000.00920.x; vanderHeide S, 1997, ALLERGY, V52, P921; Vanlaar CH, 2000, J ALLERGY CLIN IMMUN, V105, P1130, DOI 10.1067/mai.2000.106213; VANREE R, 1994, ALLERGY, V49, P254; VARNEY VA, 1991, BRIT MED J, V302, P265; Weiss KB, 2001, J ALLERGY CLIN IMMUN, V107, P3, DOI 10.1067/mai.2001.112262	34	115	122	0	7	MASSACHUSETTS MEDICAL SOC/NEJM	WALTHAM	WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA	0028-4793			NEW ENGL J MED	N. Engl. J. Med.	JUL 17	2003	349	3					237	246		10.1056/NEJMoa023171		10	Medicine, General & Internal	General & Internal Medicine	701KA	WOS:000184165700007	12867607	
J	Leikauf, GD				Leikauf, GD			Hazardous air pollutants and asthma	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Review						acrolein; aldehydes; asthma; cadmium; chromium; formaldehyde; hazardous air pollutants; metals; nickel; ozone; particulate matter; urban air toxics	VOLATILE ORGANIC-COMPOUNDS; DIESEL EXHAUST PARTICLES; ENVIRONMENTAL TOBACCO-SMOKE; INDUCED OCCUPATIONAL ASTHMA; HYDROGEN-SULFIDE EXPOSURE; TOLUENE DIISOCYANATE TDI; MOLECULAR-WEIGHT AGENTS; QUANTITATIVE TRAIT LOCI; EMERGENCY ROOM VISITS; HUMAN-SERUM-ALBUMIN	Asthma has a high prevalence in the United States, and persons with asthma may be at added risk from the adverse effects of hazardous air pollutants (HAPs). Complex mixtures (fine particulate matter and tobacco smoke) have been associated with respiratory symptoms and hospital admissions for asthma. The toxic ingredients of these mixtures are HAPs, but whether ambient HAP exposures. can induce asthma remains unclear. Certain HAPs are occupational asthmagens, whereas others may act as adjuncts during sensitization. HAPs may exacerbate asthma because, once sensitized, individuals can respond to remarkably low concentrations, and irritants lower the bronchoconstrictive threshold to respiratory antigens. Adverse responses after ambient exposures to complex mixtures often occur at concentrations below those producing effects in controlled human exposures to a single compound. In addition, certain HAPs that have been associated with asthma in occupational settings may interact with criteria pollutants in ambient air to exacerbate asthma. Based on these observations and past experience with 188 HAPs, a list of 19 compounds that could have the highest impact on the induction or exacerbation of asthma was developed. Nine additional compounds were identified that might exacerbate asthma based on their irritancy, respirability, or ability to react with biological macromolecules. Although the ambient levels of these 28 compounds are largely unknown, estimated exposures from emissions inventories and limited air monitoring suggest that aldehydes (especially acrolein and formaldehyde) and metals (especially nickel and chromium compounds) may have possible health risk indices sufficient for additional attention. Recommendations for research are presented regarding exposure monitoring and evaluation of biologic mechanisms controlling how these substances induce and exacerbate asthma. Key words: acrolein, aldehydes, asthma, cadmium, chromium, formaldehyde, hazardous air pollutants, metals, nickel, ozone, particulate matter, urban air toxics.	Univ Cincinnati, Ctr Environm Genet, Dept Environm Hlth, Cincinnati, OH 45267 USA; Univ Cincinnati, Ctr Environm Genet, Dept Pulm & Crit Care Med, Cincinnati, OH 45267 USA	Leikauf, GD (reprint author), Univ Cincinnati, Ctr Environm Genet, Dept Environm Hlth, POB 670056, Cincinnati, OH 45267 USA.				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Health Perspect.	AUG	2002	110			4			505	526				22	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	586ER	WOS:000177572100003	12194881	
J	Lima, MT; Wilson, D; Pitkin, L; Roberts, A; Nouri-Aria, K; Jacobson, M; Walker, S; Durham, S				Lima, MT; Wilson, D; Pitkin, L; Roberts, A; Nouri-Aria, K; Jacobson, M; Walker, S; Durham, S			Grass pollen sublingual immunotherapy for seasonal rhinoconjunctivitis: a randomized controlled trial	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						antibodies; cytokines; hayfever; inummohistochemistry; immunotherapy; rhinoconjunctivitis; sublingual	PLACEBO-CONTROLLED TRIAL; STANDARDIZED 5-GRASS-POLLEN EXTRACT; PARIETARIA-JUDAICA EXTRACT; HOUSE-DUST-MITE; DOUBLE-BLIND; SWALLOW IMMUNOTHERAPY; CLINICAL EFFICACY; INDUCED RHINITIS; DENDRITIC CELLS; ORAL-MUCOSA	Background Previous studies suggest that sublingual immunotherapy (SLIT) represents a safer alternative to injection immunotherapy but equivalent efficacy is yet to be confirmed. Objective To evaluate the efficacy and safety of SLIT in grass pollen-induced seasonal rhinoconjunctivitis. Methods A randomized, placebo-controlled trial in 56 adults over 18 months. Outcome measures included diary scores of seasonal symptoms and medication use, overall assessments, conjunctival and intradermal provocation tests and serum antibody measurements. To investigate possible mechanisms, sublingual biopsies were taken for measurement of local T cells, antigen-presenting cells and IL-12 mRNA expression. Results There were no significant differences between the mimunotherapy (IT) and placebo groups for diary symptom scores (P = 0.48) or rescue medication (P = 0.19). The patients' overall assessment of hayfever severity compared with previous years showed a highly significant improvement in favour of the IT group (P < 0.02). After treatment the late skin response was smaller (P = 0.003) and the ratio of serum allergen-specific IgG4/IgE was higher (P = 0.05) in the IT group. Both of these variables correlated with the clinical response to SLIT. There were no differences between groups in either the sublingual epithelium or lamina propria for numbers of CD3(+) cells (epithelium: P = 0.9. lamina propria: P = 0.2), CD1a(+) cells (P = 0.3, P = 0.25), CD68(+) cells (P = 0.9 P = 1.0) or IL-12 mRNA(+) cells (P = 0.6, P = 0.4). Local side-effects were minor and there were no serious treatment-related adverse events. Conclusion Grass pollen sublingual immunotherapy was well tolerated. Although there was no significant change in diary scores, the improvement in overall assessments, which correlated with inhibition of the late skin response and increases in serum IgG4: IgE ratio, indicates the need for larger, dose-ranging studies.	Natl Heart & Lung Inst, Imperial Coll Sci Technol & Med, Fac Med, Upper Resp Med, London SW3 6LY, England; Royal Brompton & Harefield Hosp NHS Trust, London, England	Durham, S (reprint author), Natl Heart & Lung Inst, Imperial Coll Sci Technol & Med, Fac Med, Upper Resp Med, Dovehouse St, London SW3 6LY, England.		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Exp. Allergy	APR	2002	32	4					507	514		10.1046/j.0954-7894.2002.01327.x		8	Allergy; Immunology	Allergy; Immunology	546HX	WOS:000175269600005	11972594	
J	Van den Berge, M; Kerstjens, HAM; Meijer, RJ; De Reus, DM; Koeter, GH; Kauffman, HF; Postma, DS				Van den Berge, M; Kerstjens, HAM; Meijer, RJ; De Reus, DM; Koeter, GH; Kauffman, HF; Postma, DS			Corticosteroid-induced improvement in the PC20 of adenosine monophosphate is more closely associated with reduction in airway inflammation than improvement in the PC20 of methacholine	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						adenosine 5 '-monophosphate; hyperresponsiveness; inflammation; asthma; sputum	BRONCHIAL BIOPSY SPECIMENS; NITRIC-OXIDE; INDUCED BRONCHOCONSTRICTION; INHALED BUDESONIDE; ASTHMATIC-PATIENTS; ATOPIC ASTHMA; EXHALED AIR; MILD ASTHMA; MAST-CELLS; HYPERRESPONSIVENESS	It has been suggested in cross-sectional studies that provocation with adenosine 5'-monophosphate (AMP) more closely reflects the inflammatory process in asthma than does provocation with methacholine or histamine. We investigated whether the steroid-induced improvement in the provocative concentration of AMP producing a 20% decline in FEV1 (PC20 AMP) is more closely associated with the concomitant reduction in airway inflammation than is the improvement in PC20 methacholine. In 120 asthmatic patients, we measured PC20 methacholine and PC20 AMP as well as sputum induction and nitric oxide (NO) in exhaled air before and after 2 weeks of treatment with corticosteroids. Improvement in PC20 AMP was solely related to reduction in airway inflammation (i.e., change in the number of sputum eosinophils, lymphocytes, epithelial cells, and concentration of NO in exhaled air). In contrast, improvement in PC20 methacholine was related to both reduction in airway inflammation (i.e., change in the number of sputum eosinophils and lymphocytes) and increase in FEV1 %predicted. The total explained variance of the improvement in bronchial hyperresponsiveness was greater for AMP than for methacholine (36% versus 22%, respectively). We conclude that PC20 AMP is more sensitive to changes in acute airway inflammation than is PC20 methacholine, further reinforcing the notion that PC20 AMP can be a useful tool for monitoring the effects of antilnflammatory therapy.	Univ Groningen Hosp, Dept Pulmonol, Groningen, Netherlands; Univ Groningen Hosp, Dept Allergol, Groningen, Netherlands	Postma, DS (reprint author), Univ Groningen Hosp, Dept Pulm Dis, Hanzeplein 1, NL-9700 RB Groningen, Netherlands.		van den berge, maarten/D-3990-2013				AALBERS R, 1993, EUR RESPIR J, V6, P840; Alvarez MJ, 2000, ALLERGY, V55, P355, DOI 10.1034/j.1398-9995.2000.00312.x; ALVING K, 1993, EUR RESPIR J, V6, P1368; Baraldi E, 1999, AM J RESP CRIT CARE, V159, P262; BEASLEY R, 1989, AM REV RESPIR DIS, V139, P806; Bousquet J, 1996, AM J RESP CRIT CARE, V153, P1648; BRADLEY BL, 1991, J ALLERGY CLIN IMMUN, V88, P661, DOI 10.1016/0091-6749(91)90160-P; Busse W, 1999, AM J RESP CRIT CARE, V160, P1035; Busse WW, 1998, J ALLERGY CLIN IMMUN, V102, pS17, DOI 10.1016/S0091-6749(98)70002-8; Chetta A, 1996, AM J RESP CRIT CARE, V153, P910; COCKCROFT DW, 1977, CLIN ALLERGY, V7, P235, DOI 10.1111/j.1365-2222.1977.tb01448.x; Crimi E, 1998, AM J RESP CRIT CARE, V157, P4; CRIMI N, 1992, EUR RESPIR J, V5, P560; FAHY JV, 1993, AM REV RESPIR DIS, V147, P1126; FINNEY MJB, 1985, BRIT J PHARMACOL, V85, P29; Fish JE, 1999, J ALLERGY CLIN IMMUN, V104, P509, DOI 10.1016/S0091-6749(99)70315-5; Gauvreau GM, 2000, AM J RESP CRIT CARE, V161, P1473; GRATZIOU C, 1992, AM REV RESPIR DIS, V145, P1259; Holgate ST, 2000, J ALLERGY CLIN IMMUN, V105, P193, DOI 10.1016/S0091-6749(00)90066-6; Hoshino M, 1998, J ALLERGY CLIN IMMUN, V102, P783, DOI 10.1016/S0091-6749(98)70018-1; Ichinose M, 2000, EUR RESPIR J, V15, P248, DOI 10.1034/j.1399-3003.2000.15b05.x; In 'T Veen J. C. C. M., 1996, European Respiratory Journal, V9, P2441, DOI 10.1183/09031936.96.09122441; Jeffery PK, 1996, EUR RESPIR J, V9, P1583, DOI 10.1183/09031936.96.09081583; KERSTJENS HAM, 1992, NEW ENGL J MED, V327, P1413, DOI 10.1056/NEJM199211123272003; Kharitonov SA, 1996, AM J RESP CRIT CARE, V153, P454; Kidney JC, 1996, AM J RESP CRIT CARE, V153, P540; Lemiere C, 2001, J ALLERGY CLIN IMMUN, V107, pS36; Lim S, 1999, AM J RESP CRIT CARE, V159, P22; Meijer RJ, 1999, THORAX, V54, P894; OCONNOR BJ, 1992, AM REV RESPIR DIS, V146, P560; OOSTERHOFF Y, 1993, J ALLERGY CLIN IMMUN, V92, P773, DOI 10.1016/0091-6749(93)90023-9; PAUWELS RA, 1987, AM REV RESPIR DIS, V136, P374; PHILLIPS GD, 1987, THORAX, V42, P939, DOI 10.1136/thx.42.12.939; PHILLIPS GD, 1990, AM REV RESPIR DIS, V141, P9; POLOSA R, 1995, AM J RESP CRIT CARE, V151, P624; Quanjer PH, 1993, EUR RESPIR J S, V16, P5, DOI 10.1183/09041950.005s1693; Sont JK, 1996, THORAX, V51, P496, DOI 10.1136/thx.51.5.496; Van dn Berge M, 2001, AM J RESP CRIT CARE, V163, P1546; WAALKENS JH, 1993, EUR RESPIR J, V6, P652; Weersink EJM, 1997, AM J RESP CRIT CARE, V155, P1241	40	115	119	0	2	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	OCT 1	2001	164	7					1127	1132				6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	489VM	WOS:000172013200012	11673197	
J	Radon, K; Danuser, B; Iversen, M; Jorres, R; Monso, E; Opravil, U; Weber, C; Donham, KJ; Nowak, D				Radon, K; Danuser, B; Iversen, M; Jorres, R; Monso, E; Opravil, U; Weber, C; Donham, KJ; Nowak, D			Respiratory symptoms in European animal farmers	EUROPEAN RESPIRATORY JOURNAL			English	Article						animal confinement houses; ECRHS; pig farmers; poultry farmers	CHRONIC-BRONCHITIS; DAIRY FARMERS; LUNG-FUNCTION; HAY-FEVER; SENSITIZATION; ASTHMA; DUST; PREVALENCE; POPULATION; COMMUNITY	Farmers are known to be at high risk for the development of occupational airway disease. The aim of this European study was to determine which airway symptoms predominate in different types of animal farmers (cattle, pigs, poultry, sheep) and to compare the prevalence of symptoms to the general population. A total of 6,156 randomly selected animal farmers in Denmark, Germany (Schleswig-Holstein, Niedersachsen), Switzerland, and Spain completed a questionnaire on respiratory symptoms and farming characteristics in 1995-1997. The prevalence of general respiratory symptoms was compared to the results of the European Community Respiratory Health Survey (ECRHS) obtained in the same regions. Pig farmers were at highest risk for the development of work-related symptoms. A significant dose-response relationship between daily hours worked inside animal houses and symptoms was established for pig and poultry farmers. Additionally, self-reported nasal allergies (odds ratio (95% confidence interval): 3.92 (3.26-4.71)) and nasal irritation during work (3.98 (3.35-4.73)) were shown to be associated with the development of chronic phlegm. The prevalence of wheezing, shortness of breath, asthma and nasal allergies was significantly lower among all farmers in the age group 20-44 yrs than among the general population. However, the prevalence of usually bringing up phlegm in winter among farmers was significantly higher than in the general population (9.4 (8.3-10.5%) versus 7.5 (6.5-8.5%)). Individual factors have been shown to be related to the prevalence of chronic phlegm among farmers. Additionally, this study could support the hypothesis that farming could be negatively related to allergic diseases.	Univ Munich, Inst & Poliklin Arbeits & Umweltmed, Munich, Germany; ETH Zurich, Inst Hyg & Arbeitsphysiol, Zurich, Switzerland; Aarhus Kommune Hosp, DK-8000 Aarhus, Denmark; Zentrum Pneumol & Thoraxchirurg, Grosshansdorf, Germany; Hosp Germans Trias & Pujol, Badalona, Spain; Zentrum Arbeitsbedingte Erkankungen, Brunsbuttel, Germany; Univ Iowa, Coll Med, Dept Prevent Med & Environm Hlth, Iowa City, IA 52242 USA	Radon, K (reprint author), Univ Munich, Inst Occupat & Environm Med, Ziemssenstr 1, D-80336 Munich, Germany.						Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Burney P, 1996, EUR RESPIR J, V9, P687; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; DALPHIN JC, 1989, CHEST, V95, P1244, DOI 10.1378/chest.95.6.1244; DALPHIN JCH, 1993, CHEST, V103, P417, DOI 10.1378/chest.103.2.417; DUTKIEWICZ J, IN PRESS PREVENTION; IVERSEN M, 1988, THORAX, V43, P872, DOI 10.1136/thx.43.11.872; Kimbell-Dunn M, 1999, AM J IND MED, V35, P51, DOI 10.1002/(SICI)1097-0274(199901)35:1<51::AID-AJIM7>3.0.CO;2-F; Kogevinas M, 1999, LANCET, V353, P1750, DOI 10.1016/S0140-6736(98)07397-8; Melbostad E, 1997, SCAND J WORK ENV HEA, V23, P271; Melbostad E, 1998, SCAND J WORK ENV HEA, V24, P262; Monso E, 2000, AM J RESP CRIT CARE, V162, P1246; MULLER S, 1986, AM J IND MED, V10, P281, DOI 10.1002/ajim.4700100313; NOWAK D, 1994, ANN AGR ENV MED, V1, P81; PRELLER L, 1995, OCCUP ENVIRON MED, V52, P654; Radon K, 2000, ALLERGY, V55, P219, DOI 10.1034/j.1398-9995.2000.00461.x; RASKANDERSEN A, 1989, BRIT J IND MED, V46, P233; RYLANDER R, 1990, AM J IND MED, V17, P121; Schenker MB, 1998, AM J RESP CRIT CARE, V158, pS1; STELLMAN SD, 1988, AM J IND MED, V13, P43, DOI 10.1002/ajim.4700130104; Takai H, 1998, J AGR ENG RES, V70, P59, DOI 10.1006/jaer.1997.0280; Terho E O, 1987, Eur J Respir Dis Suppl, V152, P19; TERHO EO, 1990, AM J IND MED, V18, P269, DOI 10.1002/ajim.4700180305; VOHLONEN I, 1987, EUR J RESPIR DIS, V71, P175; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187	25	115	118	0	5	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146, WEST ST, STE 2.4 HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	APR	2001	17	4					747	754		10.1183/09031936.01.17407470		8	Respiratory System	Respiratory System	438JT	WOS:000169050400027	11401073	
J	Paredi, P; Kharitonov, SA; Barnes, PJ				Paredi, P; Kharitonov, SA; Barnes, PJ			Elevation of exhaled ethane concentration in asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							SMOOTH-MUSCLE CELLS; LIPID-PEROXIDATION; NITRIC-OXIDE; BRONCHIAL HYPERRESPONSIVENESS; OXIDATIVE STRESS; OXYGEN; GLUCOCORTICOIDS; EXHALATION; METHYLPREDNISOLONE; INFLAMMATION	Ethane is a product of lipid peroxidation as a result of oxidative stress and can be detected in the exhaled air. Oxidative stress plays a role in the pathogenesis of asthma. We measured exhaled ethane in 26 asthmatic subjects (mean age +/- SEM, 38 +/- 8 yr; 15 male, FEV1 60 +/- 4%) and compared it with exhaled nitric oxide (NO) measured by chemiluminescence, a noninvasive marker of oxidative stress and inflammation. Exhaled ethane was collected during a flow- and pressure-controlled exhalation into a reservoir discarding dead space air contaminated with ambient air. A sample of the expired air was analyzed by chromatography. Exhaled ethane levels were elevated in asthma patients not receiving steroid (n = 12, 2.06 +/- 0.30 ppb) compared with steroid-treated patients (n = 14, 0.79 +/- 0.70 ppb, p < 0.01) and to 14 nonsmoking control subjects (0.88 +/- 0.09 ppb, p < 0.05). In patients not receiving steroid treatment there was a positive correlation between exhaled ethane and NO (r = 0.55, p < 0.05) and air trapping assessed by the ratio of residual volume to total lung capacity (RV/TLC) (r = 0.60, p < 0.05). In addition, untreated patients with FEV1 < 60% predicted value had higher concentrations of ethane (2.86 +/- 0.37 ppb) compared with less obstructed patients (FEV1 > 60%, 1.26 +/- 0.12 ppb, p < 0.05). NO concentrations were higher in patients not on steroid treatment (14.7 +/- 1.7 ppb) than in steroid-treated patients (8.6 +/- 0.5 ppb, p < 0.05). Exhaled ethane is elevated in asthma, reduced in steroid-treated patients, and correlates with NO and airway obstruction. It may be a useful noninvasive marker of oxidative stress.	Natl Heart & Lung Inst, Dept Thorac Med, Imperial Coll Sch Sci Technol & Med, London SW3 6LY, England	Barnes, PJ (reprint author), Natl Heart & Lung Inst, Dept Thorac Med, Imperial Coll Sch Sci Technol & Med, Dovehouse St, London SW3 6LY, England.						Antczak A, 1997, EUR RESPIR J, V10, P1235, DOI 10.1183/09031936.97.10061235; AULIK I. V., 1966, BYUL EKSP BIOL MED, V62, P115; BARNES PJ, 1990, FREE RADICAL BIO MED, V9, P235, DOI 10.1016/0891-5849(90)90034-G; BARNES PJ, 1989, J ALLERGY CLIN IMMUN, V83, P1013, DOI 10.1016/0091-6749(89)90441-7; BRAUGHLER JM, 1985, J NEUROCHEM, V44, P1282, DOI 10.1111/j.1471-4159.1985.tb08755.x; CHIARA O, 1991, CRIT CARE MED, V19, P260, DOI 10.1097/00003246-199102000-00023; Enright PL, 1994, AM J RESP CRIT CAR S, V149, P9; HABIB MP, 1989, J APPL PHYSIOL, V66, P1268; HABIB MP, 1995, AM J RESP CRIT CARE, V151, P1368; Inoue H, 1999, LUNG, V177, P53, DOI 10.1007/PL00007627; JEEJEEBHOY KN, 1991, FREE RADICAL BIO MED, V10, P191, DOI 10.1016/0891-5849(91)90075-E; JOSEPH BZ, 1993, INFLAMMATION, V17, P361, DOI 10.1007/BF00918997; Katsuyama K, 1999, ENDOCRINOLOGY, V140, P2183, DOI 10.1210/en.140.5.2183; KAZUI M, 1992, FREE RADICAL BIO MED, V13, P509, DOI 10.1016/0891-5849(92)90145-7; Keatings VM, 1997, AM J RESP CRIT CARE, V155, P542; KHARITONOV SA, 1994, LANCET, V343, P133, DOI 10.1016/S0140-6736(94)90931-8; KINNULA VL, 1995, LAB INVEST, V73, P3; KNEEPKENS CMF, 1994, FREE RADICAL BIO MED, V17, P127; KOUNO T, 1994, JPN J PHARMACOL, V64, P163, DOI 10.1254/jjp.64.163; Kraft M, 1999, EUR RESPIR J, V14, P1403, DOI 10.1183/09031936.99.14614039; LETTERON P, 1993, GUT, V34, P409, DOI 10.1136/gut.34.3.409; Marumo T, 1998, HYPERTENSION, V32, P1083; Montuschi P, 1999, AM J RESP CRIT CARE, V160, P216; Morrison D, 1999, AM J RESP CRIT CARE, V159, P473; NATHAN C, 1994, J BIOL CHEM, V269, P13725; NEIJENS HJ, 1984, AM REV RESPIR DIS, V130, P744; Olopade CO, 1997, CHEST, V111, P862, DOI 10.1378/chest.111.4.862; Paredi P, 1998, THORAX, V53, P775; Rahman I, 1996, AM J RESP CRIT CARE, V154, P1055; STANBROOK MB, 1995, CHEST, V107, P992, DOI 10.1378/chest.107.4.992; TOSHNIWAL PK, 1992, NEUROCHEM RES, V17, P205, DOI 10.1007/BF00966801; Ulrik CS, 1999, EUR RESPIR J, V13, P904, DOI 10.1034/j.1399-3003.1999.13d35.x; VACHIER I, 1994, EUR RESPIR J, V7, P1585, DOI 10.1183/09031936.94.07091585; ZARLING EJ, 1987, CLIN CHEM, V33, P140; [Anonymous], 1987, AM REV RESP DIS, V136, P225	35	115	116	1	12	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	OCT	2000	162	4					1450	1454				5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	364RD	WOS:000089905900044	11029360	
J	Huby, RDJ; Dearman, RJ; Kimber, I				Huby, RDJ; Dearman, RJ; Kimber, I			Why are some proteins allergens?	TOXICOLOGICAL SCIENCES			English	Review						allergenicity; epitopes; proteins; simulated gastric fluid (SGF)	ALTERED PEPTIDE LIGANDS; HOUSE-DUST MITE; T-CELL CLONES; SITE-DIRECTED MUTAGENESIS; ANTIGEN-SPECIFIC IGE; NORWAY RAT MODEL; DER-P-I; DENDRITIC CELLS; MANNOSE RECEPTOR; MAJOR ALLERGEN	The ability of certain proteins to induce an allergic response in susceptible individuals is well established. Symptoms can range from mild erythema or rhinitis, to acute, and possibly fatal, anaphylactic shock. Because such allergic responses require complex interactions between the protein and the immune system, they are notoriously difficult to predict. Nevertheless, it is clear that some proteins are intrinsically more allergenic than others. The challenge for toxicologists is to identify those characteristics that confer on proteins the potential to induce allergic sensitization and allergic disease. Here, we first consider the potential contribution that individual epitopes may make to the allergenicity of a protein. These are the minimal peptide units within proteins that can be recognized by the immune system and are a fundamental requirement for all immune responses, including those resulting in allergic sensitization. It appears that allergens must necessarily contain B-cell epitopes to which immunoglobulin E (IgE) can bind, and T-cell epitopes capable of inducing a type 2 T-lymphocyte response. Nevertheless, it appears doubtful that the presence of appropriate epitopes alone is sufficient to endow a protein with allergenic potential. We therefore consider also the contribution that other features and characteristics of proteins may make to their overall allergenicity. In particular, we consider the effects that resistance to proteolysis, post-translational glycosylation, and enzymatic activity may have. It appears that relative stability in simulated gastric fluid (SGF) sometimes correlates with allergenic activity. However, this is not universally true, and it is known that there are protein allergens, such as some of those associated with oral allergy syndrome, that are unstable. Nevertheless, if stability in SGF is associated with the intrinsic allergenicity of many proteins irrespective of the route of exposure, then this may reflect some more fundamental property of proteins, and possibly their stability in other biologic matrices and/or to intracellular proteases. Post-translational modification appears generally to enhance allergenicity, perhaps by increasing uptake and detection of the protein by the immune system. Some enzymatic activities also enhance allergenicity through what appear to be several different mechanisms, including nonspecific activation of cells participating in the immunologic response. Overall, it appears likely that many factors can contribute to the overall allergenicity of any given protein. Some, such as the presence of epitopes with allergenic potential, may be essential. Others, such as the glycosylation status, resistance to proteolysis, and enzymatic activity, may play a subsidiary but nevertheless critically important role. By better defining the limits within which these factors operate, we can hope to gain a better understanding of the fundamental origins of protein allergenicity, and therefore be in a position to identify and characterize the hazards and risks of allergic disease associated with novel proteins.	AstraZeneca, Safety Assessment, Macclesfield SK10 4TG, Cheshire, England; AstraZeneca Cent Toxicol Lab, Macclesfield SK10 4TJ, Cheshire, England	Huby, RDJ (reprint author), AstraZeneca, Safety Assessment, Alderley Pk, Macclesfield SK10 4TG, Cheshire, England.						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Sci.	JUN	2000	55	2					235	246		10.1093/toxsci/55.2.235		12	Toxicology	Toxicology	319JT	WOS:000087338300002	10828254	
J	Dodson, RE; Nishioka, M; Standley, LJ; Perovich, LJ; Brody, JG; Rudel, RA				Dodson, Robin E.; Nishioka, Marcia; Standley, Laurel J.; Perovich, Laura J.; Brody, Julia Green; Rudel, Ruthann A.			Endocrine Disruptors and Asthma-Associated Chemicals in Consumer Products	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Review						alkylphenols; asthma; bisphenol A; consumer products; cyclosiloxane; endocrine disruptors; fragrance compounds; parabens; phthalates; UV filters	POLYBROMINATED DIPHENYL ETHERS; PRENATAL PHTHALATE EXPOSURE; PERSONAL CARE PRODUCTS; SPRAGUE-DAWLEY RAT; OCCUPATIONAL ASTHMA; COSMETIC PRODUCTS; POLYCYCLIC MUSKS; BISPHENOL-A; UV FILTERS; INDOOR AIR	BACKGROUND: Laboratory and human studies raise concerns about endocrine disruption and asthma resulting from exposure to chemicals in consumer products. Limited labeling or testing information is available to evaluate products as exposure sources. OBJECTIVES: We analytically quantified endocrine disruptors and asthma-related chemicals in a range of cosmetics, personal care products, cleaners, sunscreens, and vinyl products. We also evaluated whether product labels provide information that can be used to select products without these chemicals. METHODS: We selected 213 commercial products representing 50 product types. We tested 42 composited samples of high-market-share products, and we tested 43 alternative products identified using criteria expected to minimize target compounds. Analytes included parabens, phthalates, bisphenol A (BPA), triclosan, ethanolamines, alkylphenols, fragrances, glycol ethers, cyclosiloxanes, and ultraviolet (UV) filters. RESULTS: We detected 55 compounds, indicating a wide range of exposures from common products. Vinyl products contained > 10% bis(2-ethylhexyl) phthalate (DEHP) and could be an important source of DEHP in homes. In other products, the highest concentrations and numbers of detects were in the fragranced products (e.g., perfume, air fresheners, and dryer sheets) and in sunscreens. Some products that did not contain the well-known endocrine-disrupting phthalates contained other less-studied phthalates (dicyclohexyl phthalate, diisononyl phthalate, and di-n-propyl phthalate; also endocrine-disrupting compounds), suggesting a substitution. Many detected chemicals were not listed on product labels. CONCLUSIONS: Common products contain complex mixtures of EDCs and asthma-related compounds. Toxicological studies of these mixtures are needed to understand their biological activity. Regarding epidemiology, our findings raise concern about potential confounding from co-occurring chemicals and misclassification due to variability in product composition. Consumers should be able to avoid some target chemicals-synthetic fragrances, BPA, and regulated active ingredients-using purchasing criteria. More complete product labeling would enable consumers to avoid the rest of the target chemicals.	[Dodson, Robin E.; Standley, Laurel J.; Perovich, Laura J.; Brody, Julia Green; Rudel, Ruthann A.] Silent Spring Inst, Newton, MA 02458 USA; [Nishioka, Marcia] Battelle Mem Inst, Columbus, OH 43201 USA; [Standley, Laurel J.] Clear Current LLC, Belmont, CA USA	Dodson, RE (reprint author), Silent Spring Inst, 29 Crafts St, Newton, MA 02458 USA.	dodson@silentspring.org			Goldman Fund; Hurricane Voices Breast Cancer Foundation; Centers for Disease Control and Prevention [1 R01 EH000632-01]	This work was funded by the Goldman Fund, the Hurricane Voices Breast Cancer Foundation, and a grant from the Centers for Disease Control and Prevention (1 R01 EH000632-01).	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Health Perspect.	JUL	2012	120	7					935	943		10.1289/ehp.1104052		9	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	969DG	WOS:000306035300016	22398195	
J	Kim, HY; Chang, YJ; Subramanian, S; Lee, HH; Albacker, LA; Matangkasombut, P; Savage, PB; McKenzie, ANJ; Smith, DE; Rottman, JB; DeKruyff, RH; Umetsu, DT				Kim, Hye Young; Chang, Ya-Jen; Subramanian, Srividya; Lee, Hyun-Hee; Albacker, Lee A.; Matangkasombut, Ponpan; Savage, Paul B.; McKenzie, Andrew N. J.; Smith, Dirk E.; Rottman, James B.; DeKruyff, Rosemarie H.; Umetsu, Dale T.			Innate lymphoid cells responding to IL-33 mediate airway hyperreactivity independently of adaptive immunity	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Innate; natural killer T; natural helper cells; T(H)2; IL-33; IL-13; glycolipid; asthma	KILLER T-CELLS; INVARIANT NKT CELLS; IN-VIVO; RHEUMATOID-ARTHRITIS; EXPERIMENTAL ASTHMA; TYPE-2 IMMUNITY; INFLAMMATION; RECEPTOR; EXPRESSION; RESPONSES	Background: Asthma has been considered an immunologic disease mediated by T(H)2 cells and adaptive immunity. However, clinical and experimental observations suggest that additional pathways might regulate asthma, particularly in its nonallergic forms, such as asthma associated with air pollution, stress, obesity, and infection. Objectives: Our goal was to understand T(H)2 cell-independent conditions that might lead to airway hyperreactivity (AHR), a cardinal feature of asthma. Methods: We examined a murine model of experimental asthma in which AHR was induced with glycolipid antigens, which activate natural killer T (NKT) cells. Results: In this model AHR developed rapidly when mice were treated with NKT cell-activating glycolipid antigens, even in the absence of conventional CD4(+) T cells. The activated NKT cells directly induced alveolar macrophages to produce IL-33, which in turn activated NKT cells, as well as natural helper cells, a newly described non-T, non-B, innate lymphoid cell type, to increase production of IL-13. Surprisingly, this glycolipid-induced AHR pathway required not only IL-13 but also IL-33 and its receptor, ST2, because it was blocked by an anti-ST2 mAb and was greatly reduced in ST2(-/-) mice. When adoptively transferred into IL-13(-/-) mice, both wild-type natural helper cells and NKT cells were sufficient for the development of glycolipid-induced AHR. Conclusion: Because plant pollens, house dust, and some bacteria contain glycolipids that can directly activate NKT cells, these studies suggest that AHR and asthma can fully develop or be greatly enhanced through innate immune mechanisms involving IL-33, natural helper cells, and NKT cells. (J Allergy Clin Immunol 2012;129:216-27.)	[Kim, Hye Young; Chang, Ya-Jen; Subramanian, Srividya; Lee, Hyun-Hee; Albacker, Lee A.; Matangkasombut, Ponpan; DeKruyff, Rosemarie H.; Umetsu, Dale T.] Harvard Univ, Sch Med, Childrens Hosp, Div Immunol & Allergy, Boston, MA 02115 USA; [Savage, Paul B.] Brigham Young Univ, Dept Chem & Biochem, Provo, UT 84602 USA; [McKenzie, Andrew N. J.] MRC Lab Mol Biol, Cambridge, England; [Smith, Dirk E.] Amgen Inc, Dept Inflammat Res, Seattle, WA USA; [Rottman, James B.] Amgen Inc, Dept Pathol, Cambridge, MA USA	Umetsu, DT (reprint author), Harvard Univ, Sch Med, Childrens Hosp, Karp Labs,Div Immunol, Rm 10127,1 Blackfan Circle, Boston, MA 02115 USA.	dale.umetsu@childrens.harvard.edu			National Institutes of Health; Amgen, Inc.	P. B. Savage has received research support from the National Institutes of Health. J. B. Rottman is employed by and has received research support from Amgen, Inc. The rest of the authors declare that they have no relevant conflicts of interest.	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Allergy Clin. Immunol.	JAN	2012	129	1					216	U319		10.1016/j.jaci.2011.10.036		18	Allergy; Immunology	Allergy; Immunology	869XT	WOS:000298634000028	22119406	
J	Strickland, MJ; Darrow, LA; Klein, M; Flanders, WD; Sarnat, JA; Waller, LA; Sarnat, SE; Mulholland, JA; Tolbert, PE				Strickland, Matthew J.; Darrow, Lyndsey A.; Klein, Mitchel; Flanders, W. Dana; Sarnat, Jeremy A.; Waller, Lance A.; Sarnat, Stefanie E.; Mulholland, James A.; Tolbert, Paige E.			Short-term Associations between Ambient Air Pollutants and Pediatric Asthma Emergency Department Visits	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						ambient particulate matter, asthma; minors; ozone	SOUTHEASTERN UNITED-STATES; CASE-CROSSOVER ANALYSES; FINE PARTICULATE MATTER; TIME-SERIES METHODS; SOURCE APPORTIONMENT; SPATIAL VARIABILITY; REFERENT SELECTION; AEROSOL RESEARCH; ORGANIC-CARBON; DAILY DEATHS	Rationale: Certain outdoor air pollutants cause asthma exacerbations in children. To advance understanding of these relationships, further characterization of the dose-response and pollutant lag effects are needed, as are investigations of pollutant species beyond the commonly measured criteria pollutants. Objectives: Investigate short-term associations between ambient air pollutant concentrations and emergency department visits for pediatric asthma. Methods: Daily counts of emergency department visits for asthma or wheeze among children aged 5 to 17 years were collected from 41 Metropolitan Atlanta hospitals during 1993-2004 (n = 91,386 visits). Ambient concentrations of gaseous pollutants and speciated particulate matter were available from stationary monitors during this time period Rate ratios for the warm season (May to October) and cold season (November to April) were estimated using Poisson generalized linear models in the framework of a case-crossover analysis Measurements and Main Results: Both ozone and primary pollutants from traffic sources were associated with emergency department visits for asthma or wheeze; evidence for independent effects of ozone and primary pollutants from traffic sources were observed in multipollutant models. These associations tended to be of the highest magnitude for concentrations on the day of the emergency department visit and were present at relatively low ambient concentrations. Conclusions. Even at relatively low ambient concentrations, ozone and primary pollutants from traffic sources independently contributed to the burden of emergency department visits for pediatric asthma	[Strickland, Matthew J.; Darrow, Lyndsey A.; Klein, Mitchel; Sarnat, Jeremy A.; Sarnat, Stefanie E.; Tolbert, Paige E.] Emory Univ, Rollins Sch Publ Hlth, Dept Environm Hlth, Atlanta, GA 30322 USA; [Flanders, W. Dana] Emory Univ, Rollins Sch Publ Hlth, Dept Epidemiol, Atlanta, GA 30322 USA; [Waller, Lance A.] Emory Univ, Rollins Sch Publ Hlth, Dept Biostat & Bioinformat, Atlanta, GA 30322 USA; [Mulholland, James A.] Georgia Inst Technol, Sch Civil & Environm Engn, Atlanta, GA 30332 USA	Strickland, MJ (reprint author), Dept Environm & Occupat Hlth, 1518 Clifton Rd NE, Atlanta, GA 30322 USA.		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J. Respir. Crit. Care Med.	AUG 1	2010	182	3					307	316		10.1164/rccm.200908-1201OC		10	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	635ZP	WOS:000280697400005	20378732	
J	Martin, SF; Dudda, JC; Bachtanian, E; Lembo, A; Liller, S; Durr, C; Heimesaat, MM; Bereswill, S; Fejer, G; Vassileva, R; Jakob, T; Freudenberg, N; Termeer, CC; Johner, C; Galanos, C; Freudenberg, MA				Martin, Stefan F.; Dudda, Jan C.; Bachtanian, Eva; Lembo, Annalisa; Liller, Stefanie; Duerr, Christoph; Heimesaat, Markus M.; Bereswill, Stefan; Fejer, Gyoergy; Vassileva, Ralitsa; Jakob, Thilo; Freudenberg, Nikolaus; Termeer, Christian C.; Johner, Caroline; Galanos, Chris; Freudenberg, Marina A.			Toll-like receptor and IL-12 signaling control susceptibility to contact hypersensitivity	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article							ACTIVATED PROTEIN-KINASE; CD8(+) T-CELLS; DENDRITIC CELLS; IFN-ALPHA; IMMUNE-RESPONSES; CUTTING EDGE; FLUORESCEIN ISOTHIOCYANATE; SENSITIZER TRINITROPHENYL; MEDIATED INHIBITION; C57BL/10SCCR MICE	Allergic contact hypersensitivity (CHS) is a T cell-mediated inflammatory skin disease. Interleukin (IL)-12 is considered to be important in the generation of the allergen-specific T cell response. Loss of IL-12 function in IL-12R beta 2-deficient mice, however, did not ameliorate the allergic immune response, suggesting alternate IL-12-independent pathways in the induction of CHS. Because exposure to contact allergens always takes place in the presence of microbial skin flora, we investigated the potential role of Toll-like receptors (TLRs) in the induction of CHS. Using mice deficient in TLR4, the receptor for bacterial lipopolysaccharide (LPS), IL-12 receptor (R) beta 2, or both, we show that the concomitant absence of TLR4 and IL-12R beta 2, but not the absence of TLR4 or IL-12R beta 2 alone, prevented DC-mediated sensitization, generation of effector T cells, and the subsequent CHS response to 2,4,6-trinitro-1-chlorobenzene (TNCB), oxazolone, and fluorescein isothiocyanate. Introduction of the TLR4 transgene into the TLR4/IL-12R beta 2 mutant restored the CHS inducibility, showing a requirement for TLR4 in IL-12-independent CHS induction. Furthermore, the concomitant absence of TLR2 and TLR4 prevented the induction of CHS to TNCB in IL-12-competent mice. Finally, CHS was inducible in germ-free wild-type and IL-12R beta 2-deficient mice, but not in germ-free TLR4/IL-12R beta 2 double deficient mice, suggesting that the necessary TLR activation may proceed via endogenous ligands.	[Martin, Stefan F.; Dudda, Jan C.; Bachtanian, Eva; Liller, Stefanie; Duerr, Christoph; Jakob, Thilo; Termeer, Christian C.] Univ Med Ctr Freiburg, Allergy Res Grp, Dept Dermatol, D-79104 Freiburg, Germany; [Lembo, Annalisa; Fejer, Gyoergy; Vassileva, Ralitsa; Johner, Caroline; Galanos, Chris; Freudenberg, Marina A.] Max Planck Inst Immunobiol, D-79108 Freiburg, Germany; [Heimesaat, Markus M.; Bereswill, Stefan] Charite Univ Med Berlin, Inst Microbiol & Hyg, D-13353 Berlin, Germany; [Freudenberg, Nikolaus] Univ Med Ctr Freiburg, Inst Pathol, D-79106 Freiburg, Germany	Martin, SF (reprint author), Univ Med Ctr Freiburg, Allergy Res Grp, Dept Dermatol, D-79104 Freiburg, Germany.	stefan.martin@uniklinik-freiburg.de; freudenberg@immunbio.mpg.de	Fejer, Gyorgy/D-5080-2011; Jakob, Thilo/J-1621-2012		Deutsche Forschungsgemeinschaft [DFG SP1110-FR 448/4-3, SFB633/A7]; Forschungskommission der Medizinischen Fakultat; Fritz-Thyssen-Stiftung [Az.: 10.05.2.194]	The study was supported in part by a grant of the Deutsche Forschungsgemeinschaft (DFG SP1110-FR 448/4-3) to M. A. Freudenberg and by a grant of the Forschungskommission der Medizinischen Fakultat, University Medical Center Freiburg, to S. F. Martin. M. M. Heimesaat and S. Bereswill were financed by the Fritz-Thyssen-Stiftung (Az.: 10.05.2.194) and by the Deutsche Forschungsgemeinschaft (SFB633/A7), respectively.	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Exp. Med.	SEP 1	2008	205	9					2151	2162		10.1084/jem.20070509		12	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	354RI	WOS:000259656300019	18725520	
J	Pilette, C; Nouri-Aria, KT; Jacobson, MR; Wilcock, LK; Detry, B; Walker, SM; Francis, JN; Durham, SR				Pilette, Charles; Nouri-Aria, Kayhan T.; Jacobson, Mikila R.; Wilcock, Louisa K.; Detry, Bruno; Walker, Samantha M.; Francis, James N.; Durham, Stephen R.			Grass pollen immunotherapy induces an allergen-specific IgA2 antibody response associated with mucosal TGF-beta expression	JOURNAL OF IMMUNOLOGY			English	Article							GROWTH-FACTOR-BETA; MESSENGER-RNA EXPRESSION; T-CELL DIFFERENTIATION; VENOM IMMUNOTHERAPY; DENDRITIC CELLS; B-CELLS; IGG ANTIBODIES; SECRETORY IGA; HOUSE-DUST; INTERLEUKIN-10	Allergen immunotherapy (IT) has long-term efficacy in IgE-mediated allergic rhinitis and asthma. IT has been shown to modify lymphocyte responses to allergen, inducing IL-10 production and IgG Abs. In contrast, a putative role for IgA and local TGF-beta-producing cells remains to be determined. In 44 patients with seasonal rhinitis/asthma, serum IgA1, IgA2, and polymeric (J chain-containing) Abs to the major allergen Phi p 5 were determined by ELISA before and after a 2-year double-blind trial of grass pollen (Phleum pratense) injection IT. Nasal TGF-beta expression was assessed by in situ hybridization. Sera from five IT patients were fractionated for functional analysis of the effects of IgA and IgG Abs on IL-10 production by blood monocytes and allergen-IgE binding to B cells. Serum Phi p 5-specific IgA2 Abs increased after a 2-year treatment (similar to 8-fold increase, p = 0.002) in contrast to IgA1. Increases in polymeric Abs to Phi p 5 (similar to 2-fold increase,p = 0.02) and in nasal TGF-beta mRNA (p = 0.05) were also observed, and TGF-beta mRNA correlated with serum Phi p 5 IgA2 (r = 0.61,p = 0.009). Post-IT IgA fractions triggered IL-10 secretion by monocytes while not inhibiting allergen-IgE binding to B cells as observed with IgG fractions. This study shows for the first time that the IgA response to IT is selective for IgA2, correlates with increased local TGF-beta expression, and induces monocyte IL-10 expression, suggesting that IgA Abs could thereby contribute to the tolerance developed in IT-treated allergic patients.	Imperial Coll Sch Med, Natl Heart & Lung Inst, Allergy & Clin Immunol Sect, London, England; Univ Louvain, Unit Pneumol, Brussels, Belgium	Durham, SR (reprint author), Imperial Coll Sch Med, Natl Heart & Lung Inst, Allergy & Clin Immunol Sect, Dovehouse St, London, England.	s.durham@imperial.ac.uk	James, Louisa/C-9831-2010; Walker, Samantha/B-9740-2013	James, Louisa/0000-0002-2252-4636; Walker, Samantha/0000-0001-5503-8258	Medical Research Council [G0601303]		AALBERSE RC, 1983, J IMMUNOL, V130, P722; Aghayan-Ugurluoglu R, 2000, J ALLERGY CLIN IMMUN, V105, P803, DOI 10.1067/mai.2000.104782; Akbari O, 2001, NAT IMMUNOL, V2, P725, DOI 10.1038/90667; Akdis CA, 1998, J CLIN INVEST, V102, P98, DOI 10.1172/JCI2250; Akoum H, 1996, IMMUNOLOGY, V87, P593, DOI 10.1046/j.1365-2567.1996.506585.x; Allavena P, 1998, EUR J IMMUNOL, V28, P359, DOI 10.1002/(SICI)1521-4141(199801)28:01<359::AID-IMMU359>3.0.CO;2-4; Bahceciler NN, 2005, INT ARCH ALLERGY IMM, V136, P287, DOI 10.1159/000083956; Bellinghausen I, 1997, EUR J IMMUNOL, V27, P1131, DOI 10.1002/eji.1830270513; Benson M, 2003, ALLERGY, V58, P386, DOI 10.1034/j.1398-9995.2003.00113.x; Bousquet J, 1998, J ALLERGY CLIN IMMUN, V102, P558, DOI 10.1016/S0091-6749(98)70271-4; CHALLACOMBE SJ, 1980, J EXP MED, V152, P1459, DOI 10.1084/jem.152.6.1459; Chen CH, 2003, J EXP MED, V197, P1689, DOI 10.1084/jem.20021170; COFFMAN RL, 1989, J EXP MED, V170, P1039, DOI 10.1084/jem.170.3.1039; DELACROIX DL, 1986, MOL IMMUNOL, V23, P367, DOI 10.1016/0161-5890(86)90134-3; Fayette J, 1997, J EXP MED, V185, P1909, DOI 10.1084/jem.185.11.1909; FLANAGAN JG, 1984, CELL, V36, P681, DOI 10.1016/0092-8674(84)90348-9; Francis JN, 2003, J ALLERGY CLIN IMMUN, V111, P1255, DOI 10.1067/mai.2003.1570; Geissmann F, 2001, J IMMUNOL, V166, P346; GEORGITIS JW, 1985, J ALLERGY CLIN IMMUN, V75, P496, DOI 10.1016/S0091-6749(85)80023-3; Goerdt S, 1999, IMMUNITY, V10, P137, DOI 10.1016/S1074-7613(00)80014-X; Gorelik L, 2000, IMMUNITY, V12, P171, DOI 10.1016/S1074-7613(00)80170-3; Heystek HC, 2002, J IMMUNOL, V168, P102; Jutel M, 2003, EUR J IMMUNOL, V33, P1205, DOI 10.1002/eji.200322919; JUTEL M, 1995, J IMMUNOL, V154, P4187; KITANI A, 1994, J IMMUNOL, V153, P1466; LICHTENSTEIN LM, 1968, J IMMUNOL, V101, P317; MALEFYT RD, 1991, J EXP MED, V174, P915; MCHUGH SM, 1995, CLIN EXP ALLERGY, V25, P828, DOI 10.1111/j.1365-2222.1995.tb00025.x; Nasser SMS, 2001, EUR J IMMUNOL, V31, P3704, DOI 10.1002/1521-4141(200112)31:12<3704::AID-IMMU3704>3.0.CO;2-3; Nouri-Aria KT, 2004, J IMMUNOL, V172, P3252; Pilette C, 2003, AM J RESP CELL MOL, V28, P485, DOI 10.1165/rcmb.4913; Pilette Charles, 2004, Proc Am Thorac Soc, V1, P125, DOI 10.1513/pats.2306032; PLATTSMILLS TAE, 1976, J CLIN INVEST, V57, P1041, DOI 10.1172/JCI108346; Reisinger J, 2005, J ALLERGY CLIN IMMUN, V116, P347, DOI 10.1016/j.jaci.2005.04.003; Robertson AKL, 2003, J CLIN INVEST, V112, P1342, DOI 10.1172/JCI200318607; Savolainen J, 2004, CLIN EXP ALLERGY, V34, P413, DOI 10.1111/j.1365-2222.2004.01823.x; Schmidt-Weber CB, 2004, CURR OPIN IMMUNOL, V16, P709, DOI 10.1016/j.coi.2004.09.008; Schwarze J, 1998, AM J RESP CRIT CARE, V158, P519; SECRIST H, 1993, J EXP MED, V178, P2123, DOI 10.1084/jem.178.6.2123; STOKES CR, 1974, LANCET, V2, P485; Sutterwala FS, 1998, J EXP MED, V188, P217, DOI 10.1084/jem.188.1.217; TAUDORF E, 1994, ALLERGY, V49, P760, DOI 10.1111/j.1398-9995.1994.tb02099.x; TAYLOR B, 1973, LANCET, V2, P111; van der Boog PJM, 2002, J IMMUNOL, V168, P1252; van Neerven RJJ, 1999, J IMMUNOL, V163, P2944; VanRee R, 1997, CLIN EXP ALLERGY, V27, P68, DOI 10.1046/j.1365-2222.1997.d01-416.x; VARNEY VA, 1993, J CLIN INVEST, V92, P644, DOI 10.1172/JCI116633; Wachholz PA, 2003, J ALLERGY CLIN IMMUN, V112, P915, DOI [10.1067/mai.2003.1770, 10.1016/S0091-6749(03)02022-0]; Walker SM, 2001, J ALLERGY CLIN IMMUN, V107, P87, DOI 10.1067/mai.2001.112027; Wilson DR, 2001, CLIN EXP ALLERGY, V31, P1705, DOI 10.1046/j.1365-2222.2001.01231.x; WOLF HM, 1994, PEDIATR RES, V36, P235, DOI 10.1203/00006450-199408000-00016; Woof JM, 2005, IMMUNOL REV, V206, P64, DOI 10.1111/j.0105-2896.2005.00290.x	52	114	124	0	1	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	APR 1	2007	178	7					4658	4666				9	Immunology	Immunology	150EB	WOS:000245197300075	17372025	
J	Steinbuch, M; Youket, TE; Cohen, S				Steinbuch, M; Youket, TE; Cohen, S			Oral glucocorticoid use is associated with an increased risk of fracture	OSTEOPOROSIS INTERNATIONAL			English	Article; Proceedings Paper	World Congress on Osteoporosis	JUN 15-18, 2000	CHICAGO, IL			epidemiology; fracture; oral glucocorticoids; osteoporosis	LOW-DOSE CORTICOSTEROIDS; RHEUMATOID-ARTHRITIS PATIENTS; BONE-MINERAL DENSITY; INDUCED OSTEOPOROSIS; VERTEBRAL FRACTURES; INDUCED OSTEOPENIA; THERAPY; ASTHMA; MASS; SPINE	Oral glucocorticoids (GCs) are widely used and despite their adverse effects on bone mineral density, the risk of sustaining osteoporotic fractures is not well addressed. The objective of this retrospective, cohort study was to assess fracture risk in patients exposed to oral GCs. Patients from an administrative claims database who were prescribed oral GCs and were enrolled 1 year before and 1 year after the initial oral GC claim were matched with a comparison population on age, sex, and date of first claim. Measurements of exposure included amount, duration, and pattern of oral GC use. The osteoporosis-related risk of fracture was based on the ratio of hazard functions estimated using a Cox proportional hazards model. The adjusted relative risk (RR) estimates (and 95% CI) for fractures were hip 1.87 (95% CI, 1.2 to 2.9), vertebral 2.92 (95% CI, 2.0 to 4.3), wrist/forearm 1.03 (95% CI, 0.8 to 1.4), nonvertebral 1.68 (95% CI, 1.5 to 1.9), any fracture 1.75 (95% CI, 1.6 to 1.9). A dose dependence of fracture risk was observed for hip, vertebral, nonvertebral, and any fractures. Long duration and continuous pattern of GC use demonstrated a significant 5-fold increased risk of hip and 5.9-fold increased risk of vertebral fracture. The combined effect of higher dose, longer duration, and continuous pattern further increased RR estimates to 7-fold for hip and 17-fold for vertebral fractures. This study confirms previous observations that suggest oral GCs have a rapid deleterious effect on trabecular-rich bone. The emerging relationship between amount, duration, and pattern of oral GC exposure and fracture risk should be considered in clinical practice and managed care settings to avoid the debilitating effects of fractures in patients.	Procter & Gamble Co, Hlth Care Res Ctr, Mason, OH 45040 USA; St Paul Ramsey Med Ctr, Dept Rheumatol, Dallas, TX 75235 USA	Steinbuch, M (reprint author), Procter & Gamble Co, Hlth Care Res Ctr, 8700 Mason Montgomery Rd, Mason, OH 45040 USA.	Steinbuch.m@pg.com					ADINOFF AD, 1983, NEW ENGL J MED, V309, P265, DOI 10.1056/NEJM198308043090502; ALS OS, 1985, ARTHRITIS RHEUM, V28, P369, DOI 10.1002/art.1780280403; Buckley L, 2001, ARTHRITIS RHEUM, V44, P1496; BUCKLEY LM, 1995, J RHEUMATOL, V22, P1055; BUTLER RC, 1991, BRIT J RHEUMATOL, V30, P86; COOPER C, 1995, ANN RHEUM DIS, V54, P49, DOI 10.1136/ard.54.1.49; DEDEUXCHAISNES CN, 1984, ADV EXP MED BIOL, V171, P209; DYKMAN TR, 1985, ARTHRITIS RHEUM, V28, P361, DOI 10.1002/art.1780280402; GARTON MJ, 1993, ARTHRITIS RHEUM, V36, P222; GREENBERGER PA, 1982, CLIN ALLERGY, V12, P363, DOI 10.1111/j.1365-2222.1982.tb02540.x; HAHN TJ, 1979, J CLIN INVEST, V64, P655, DOI 10.1172/JCI109506; HOOYMAN JR, 1984, ARTHRITIS RHEUM, V27, P1353, DOI 10.1002/art.1780271205; LAAN RFJM, 1993, ANN INTERN MED, V119, P963; LAAN RFJM, 1992, BRIT J RHEUMATOL, V31, P91; LEMS WF, 1995, CLIN EXP RHEUMATOL, V13, P293; LUENGO M, 1991, THORAX, V46, P803, DOI 10.1136/thx.46.11.803; MICHEL BA, 1993, J RHEUMATOL, V20, P1666; Naganathan V, 2000, ARCH INTERN MED, V160, P2917, DOI 10.1001/archinte.160.19.2917; Ramsey-Goldman R, 1999, ARTHRITIS RHEUM, V42, P882, DOI 10.1002/1529-0131(199905)42:5<882::AID-ANR6>3.0.CO;2-C; REID DM, 1986, BRIT MED J, V293, P1463; REID IR, 1992, J BONE MINER RES, V7, P1221; RUEGSEGGER P, 1983, EUR J CLIN PHARMACOL, V25, P615, DOI 10.1007/BF00542348; SAMBROOK P, 1990, J BONE MINER RES, V5, P1211; SAMBROOK PN, 1987, ARTHRITIS RHEUM, V30, P721, DOI 10.1002/art.1780300701; van Staa TP, 2002, OSTEOPOROSIS INT, V13, P777; van Staa TP, 2002, ARTHRITIS RHEUM, V46, pS585; Van Staa TP, 2000, J BONE MINER RES, V15, P993, DOI 10.1359/jbmr.2000.15.6.993; VERSTRAETEN A, 1986, ANN RHEUM DIS, V45, P852, DOI 10.1136/ard.45.10.852	28	114	130	0	1	SPRINGER-VERLAG LONDON LTD	GODALMING	SWEETAPPLE HOUSE CATTESHALL ROAD, GODALMING GU7 3DJ, SURREY, ENGLAND	0937-941X			OSTEOPOROSIS INT	Osteoporosis Int.	APR	2004	15	4					323	328		10.1007/s00198-003-1548-3		6	Endocrinology & Metabolism	Endocrinology & Metabolism	808HP	WOS:000220560500010	14762652	
J	Akdis, M; Trautmann, A; Klunker, S; Daigle, I; Kucuksezer, UC; Deglmann, W; Disch, R; Blaser, K; Akdis, CA				Akdis, M; Trautmann, A; Klunker, S; Daigle, I; Kucuksezer, UC; Deglmann, W; Disch, R; Blaser, K; Akdis, CA			T helper (Th) 2 predominance in atopic diseases is due to preferential apoptosis of circulating memory/effector Th1 cells	FASEB JOURNAL			English	Article						activation-induced cell death; atopic dermatitis; cytokines; T cells; Th1/Th2	LYMPHOCYTE-ASSOCIATED ANTIGEN; ACTIVATION-INDUCED APOPTOSIS; FAS-MEDIATED APOPTOSIS; SIGNALING COMPLEX; HECA-452 EPITOPE; IN-VIVO; DERMATITIS; DEATH; EXPRESSION; SKIN	T cells constitute a large population of cellular infiltrate in atopic/allergic inflammation and a dysregulated, Th2-biased peripheral immune response appears to be an important pathogenetic factor. In atopic dermatitis, circulating cutaneous lymphocyte-associated antigen-bearing (CLA(+)) CD45RO(+) T cells with skin-specific homing property represent an activated memory/effector T cell subset. They express high levels of Fas and Fas ligand and undergo activation-induced apoptosis. The freshly purified (CLA(+)) CD45RO(+) T cells of atopic individuals display distinct features of in vivo-triggered apoptosis such as procaspase degradation and active caspase-8 formation. In particular, the Th1 compartment of activated memory/effector T cells selectively undergoes activation-induced cell death, skewing the immune response toward surviving Th2 cells in atopic dermatitis patients. The apoptosis of circulating memory/effector T cells was confined to atopic individuals whereas non-atopic patients such as psoriasis, intrinsic-type asthma, contact dermatitis, intrinsic type of atopic dermatitis, bee venom allergic patients, and healthy controls showed no evidence for enhanced T cell apoptosis in vivo. These results define a novel mechanism for peripheral Th2 response in atopic diseases.	Swiss Inst Allergy & Asthma Res, CH-7270 Davos, Switzerland; Istanbul Univ, Expt Med Res Inst, TR-34280 Istanbul, Turkey; Clin Dermatol & Allergy, CH-7270 Davos, Switzerland	Akdis, CA (reprint author), Swiss Inst Allergy & Asthma Res, Obere Str 22, CH-7270 Davos, Switzerland.	akdism@siaf.unizh.ch					ABERNATHYCARVER KJ, 1995, J CLIN INVEST, V95, P913, DOI 10.1172/JCI117743; Akdis CA, 2000, CURR OPIN IMMUNOL, V12, P641, DOI 10.1016/S0952-7915(00)00156-4; Akdis CA, 1999, J INVEST DERMATOL, V113, P628, DOI 10.1046/j.1523-1747.1999.00720.x; Akdis CA, 2000, FASEB J, V14, P1666; Akdis M, 1997, J IMMUNOL, V159, P4611; Akdis M, 1999, J IMMUNOL, V163, P466; Akdis M, 2000, EUR J IMMUNOL, V30, P3533, DOI 10.1002/1521-4141(2000012)30:12<3533::AID-IMMU3533>3.0.CO;2-5; BABI LFS, 1995, J EXP MED, V181, P1935; Belaud-Rotureau MA, 1999, CELL DEATH DIFFER, V6, P788, DOI 10.1038/sj.cdd.4400552; BRUNNER T, 1995, NATURE, V373, P441, DOI 10.1038/373441a0; CLOARK EA, 1995, SCIENCE, V268, P233; Dalton DK, 2000, J EXP MED, V192, P117, DOI 10.1084/jem.192.1.117; DHEIN J, 1995, NATURE, V373, P438, DOI 10.1038/373438a0; Enari M, 1996, NATURE, V380, P723, DOI 10.1038/380723a0; Finotto S, 2002, SCIENCE, V295, P336, DOI 10.1126/science.1065544; FRISCH SM, 1994, J CELL BIOL, V124, P619, DOI 10.1083/jcb.124.4.619; GAVRIELI Y, 1992, J CELL BIOL, V119, P493, DOI 10.1083/jcb.119.3.493; GREEN DR, 1994, CURR OPIN IMMUNOL, V6, P476, DOI 10.1016/0952-7915(94)90130-9; Grewe M, 1998, IMMUNOL TODAY, V19, P359, DOI 10.1016/S0167-5699(98)01285-7; Hanifin JM, 1980, ACTA DERM-VENEREOL S, V92, P44; Hunger RE, 1999, BRIT J DERMATOL, V141, P565; Jutel M, 2001, NATURE, V413, P420, DOI 10.1038/35096564; KOOPMAN G, 1994, BLOOD, V84, P1415; Ledru E, 1998, J IMMUNOL, V160, P3194; LI WC, 2000, J IMMUNOL, V164, P1193; LIU Y, 1990, Journal of Experimental Medicine, V172, P1735, DOI 10.1084/jem.172.6.1735; LYNCH DH, 1995, IMMUNOL TODAY, V16, P569, DOI 10.1016/0167-5699(95)80079-4; MARTIN SJ, 1995, CELL, V82, P349, DOI 10.1016/0092-8674(95)90422-0; Medema JP, 1997, EMBO J, V16, P2794, DOI 10.1093/emboj/16.10.2794; MEREDITH JE, 1993, MOL BIOL CELL, V4, P953; MULLER G, 1994, J CLIN INVEST, V94, P1799, DOI 10.1172/JCI117528; Muller U, 1998, J ALLERGY CLIN IMMUN, V101, P747, DOI 10.1016/S0091-6749(98)70402-6; Muzio M, 1996, CELL, V85, P817, DOI 10.1016/S0092-8674(00)81266-0; Ng TTC, 1997, J IMMUNOL, V158, P2984; Norris DA, 1997, APOPTOSIS, V2, P136, DOI 10.1023/A:1026456229688; PICKER LJ, 1990, AM J PATHOL, V136, P1053; ROBINSON DS, 1992, NEW ENGL J MED, V326, P298, DOI 10.1056/NEJM199201303260504; RUOSLAHTI E, 1987, SCIENCE, V238, P491, DOI 10.1126/science.2821619; Salmon M, 1997, J CLIN INVEST, V99, P439, DOI 10.1172/JCI119178; Scaffidi C, 1999, CURR OPIN IMMUNOL, V11, P277, DOI 10.1016/S0952-7915(99)80045-4; SHYRTE J, 1995, NATURE, V373, P444; Stoll S, 1998, EUR J IMMUNOL, V28, P3231, DOI 10.1002/(SICI)1521-4141(199810)28:10<3231::AID-IMMU3231>3.0.CO;2-Q; Thepen T, 1996, J ALLERGY CLIN IMMUN, V97, P828, DOI 10.1016/S0091-6749(96)80161-8; THOMPSON CB, 1995, SCIENCE, V267, P1456, DOI 10.1126/science.7878464; Trautmann A, 2000, J CLIN INVEST, V106, P25, DOI 10.1172/JCI9199; Trautmann A, 2002, J ALLERGY CLIN IMMUN, V109, P329, DOI 10.1067/mai.2002.121460; Trautmann A, 2001, TRENDS IMMUNOL, V22, P530, DOI 10.1016/S1471-4906(01)02004-X; Varadhachary AS, 1999, J IMMUNOL, V163, P4772; VARNEY VA, 1993, J CLIN INVEST, V92, P644, DOI 10.1172/JCI116633; VERCELLI D, 1989, J EXP MED, V169, P1295, DOI 10.1084/jem.169.4.1295; WALKER C, 1992, AM REV RESPIR DIS, V146, P109; Wu CY, 2002, NAT IMMUNOL, V3, P852, DOI 10.1038/ni832; Yawalkar N, 2000, EUR J IMMUNOL, V30, P491, DOI 10.1002/1521-4141(200002)30:2<491::AID-IMMU491>3.3.CO;2-8; Zeuner A, 1999, CELL DEATH DIFFER, V6, P1075, DOI 10.1038/sj.cdd.4400596; Zhang XH, 1997, J EXP MED, V185, P1837, DOI 10.1084/jem.185.10.1837	55	114	121	0	8	FEDERATION AMER SOC EXP BIOL	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA	0892-6638			FASEB J	Faseb J.	JUN	2003	17	9					1026	1035		10.1096/fj.02-1070com		10	Biochemistry & Molecular Biology; Biology; Cell Biology	Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology	695EK	WOS:000183818000006	12773485	
J	Shaheen, SO; Newson, RB; Sherriff, A; Henderson, AJ; Heron, JE; Burney, PGJ; Golding, J				Shaheen, SO; Newson, RB; Sherriff, A; Henderson, AJ; Heron, JE; Burney, PGJ; Golding, J		ALSPAC Study Team	Paracetamol use in pregnancy and wheezing in early childhood	THORAX			English	Article							GLUTATHIONE S-TRANSFERASE; ATOPIC DISEASE; RISK-FACTORS; HUMAN-FETAL; ASTHMA; ACETAMINOPHEN; LUNG; CHILDREN; MOUSE; LIFE	Background: We recently reported links between frequent paracetamol (acetaminophen) use and wheezing and asthma in adults and children, but data are lacking on possible effects of prenatal exposure on wheezing in early childhood. Methods: In the population based Avon Longitudinal Study of Parents and Children (ALSPAC) women were asked twice during pregnancy (at 18-20 weeks and 32 weeks) about their usage of paracetamol and aspirin. Six months after birth, and at yearly intervals thereafter, mothers were asked about wheezing and eczema symptoms in their child. The effects of paracetamol and aspirin use in pregnancy on the risk in the offspring of wheezing at 30-42 months (n=9400) and eczema at 18-30 months (n=10 2 16) and on their risk of different wheezing patterns (defined by presence or absence of wheezing at <6 months and at 30-42 months) were examined. Results: Paracetamol was taken frequently (most days/daily) by only 1% of women. After controlling for potential confounders, frequent paracetamol use in late pregnancy (20-32 weeks), but not in early pregnancy (<18-20 weeks), was associated with an increased risk of wheezing in the offspring at 30-42 months (adjusted odds ratio (OR) compared with no use 2.10 (95% Cl 1.30 to 3.41); p=0.003), particularly if wheezing started before 6 months (OR 2.34 (95% Cl 1.24 to 4.40); P=0.008). Assuming a causal relation, only about 1% of wheezing at 30-42 months was attributable to this exposure. Frequent paracetomol use in pregnancy was not associated with an increased risk of eczema. Frequent aspirin use in pregnancy was associated with an increased risk of wheezing only at <6 months. Conclusions: Frequent use of paracetamol in late pregnancy may increase the risk of wheezing in the offspring, although such an effect could explain only about 1% of the population prevalence of wheezing in early childhood.	Kings Coll London, Guys Kings & St Thomas Sch Med, Dept Publ Hlth Sci, London SE1 3QD, England; Univ Bristol, Inst Child Hlth, Unit Paediat & Perinatal Epidemiol, Bristol BS8 1TQ, Avon, England	Shaheen, SO (reprint author), Kings Coll London, Guys Kings & St Thomas Sch Med, Dept Publ Hlth Sci, Capital House,42 Weston St, London SE1 3QD, England.	seif.shaheen@kcl.ac.uk	Heron, Jon/D-5884-2011	Heron, Jon/0000-0001-6199-5644; Henderson, Alexander John/0000-0001-9650-231X			Barker D. J. 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J	Bergner, A; Sanderson, MJ				Bergner, A; Sanderson, MJ			Acetylcholine-induced calcium signaling and contraction of airway smooth muscle cells in lung slices	JOURNAL OF GENERAL PHYSIOLOGY			English	Article						asthma; hyper-reactivity; confocal microscopy; Ca2+ oscillations; frequency modulation	INDIVIDUAL AIRWAYS; RESPONSIVENESS; HETEROGENEITY; METHACHOLINE; TRANSDUCTION; RAT; OSCILLATIONS; RESPONSES; EXPLANTS; CHANNELS	The Ca2+ signaling and contractility of airway smooth Muscle cells (SMCs) were investigated with confocal microscopy in murine lung slices (similar to75-mum thick) that maintained the in situ organization of the airways and the contractility of the SMCs for at least 5 d. 10-500 nM acetylcholine (ACH) induced a contraction of the air- way lumen and a transient increase in [Ca2+], in individual SMCs that subsequently declined to initiate multiple intracellular Ca2+ oscillations. These Ca2+ oscillations spread as Ca2+ waves through the SMCs at similar to48 mum/s. The magnitude of the airway contraction, the initial Ca2+ transient, and the frequency of the subsequent Ca2+ oscillations were all concentration-dependent. In a Ca2+-free solution, ACH induced a similar Ca2+ response, except that the Ca2+ oscillations ceased after 1-1.5 min. Incubation with thapsigargin, xestospongin, or ryanodine inhibited the ACH-induced Ca2+ signaling. A comparison of airway contraction with the ACH-induced Ca2+ response of the SMCs revealed that the onset of airway contraction correlated with the initial Ca2+ transient, and that sustained airway contraction correlated with the occurrence of the Ca2+ oscillations. Buffering intracellular Ca2+ with BATIA prohibited Ca2+ signaling and airway contraction, indicating a Ca2+-dependent pathway. Cessation of the Ca2+ oscillations, induced by ACH-esterase, halothane, or the absence of extracellular Ca2+ resulted in a relaxation of the airways The concentration dependence of the airway contraction matched the concentration dependeuce of the increased frequency of the Ca2+ oscillations. These results indicate that Ca2+ oscillations, induced by ACH in murine bronchial SMCs, are generated by Ca2+ release from the SR involving IPs and ryanodine receptors, and are required to maintain airway contraction.	Univ Massachusetts, Sch Med, Dept Physiol, Worcester, MA 01655 USA	Sanderson, MJ (reprint author), Univ Massachusetts, Sch Med, Dept Physiol, 55 Lake Ave, Worcester, MA 01655 USA.				NHLBI NIH HHS [HL49288]		Berridge MJ, 2000, NAT REV MOL CELL BIO, V1, P11, DOI 10.1038/35036035; Bootman MD, 2001, SEMIN CELL DEV BIOL, V12, P3, DOI 10.1006/scdb.2000.0211; DANDURAND RJ, 1994, AM J RESP CRIT CARE, V149, P1499; DANDURAND RJ, 1993, J APPL PHYSIOL, V75, P364; DIVIRGILIO F, 1990, CELL CALCIUM, V11, P57, DOI 10.1016/0143-4160(90)90059-4; Duguet A, 2000, AM J RESP CRIT CARE, V161, P839; Hall IP, 2000, EUR RESPIR J, V15, P1120, DOI 10.1034/j.1399-3003.2000.01523.x; HALL IP, 1995, AM J PHYSIOL-LUNG C, V268, pL1; Held HD, 1999, BRIT J PHARMACOL, V126, P1191, DOI 10.1038/sj.bjp.0702394; KUROSAWA H, 1995, J APPL PHYSIOL, V79, P41; Liu XB, 1996, J PHARMACOL EXP THER, V276, P178; Martin C, 1996, EUR RESPIR J, V9, P2479, DOI 10.1183/09031936.96.09122479; Martin C, 2000, EUR RESPIR J, V16, P316, DOI 10.1034/j.1399-3003.2000.16b21.x; Martin C, 2001, AM J RESP CELL MOL, V24, P139; Martin JG, 2000, EUR RESPIR J, V16, P349, DOI 10.1034/j.1399-3003.2000.16b25.x; Minshall E, 1997, CAN J PHYSIOL PHARM, V75, P911, DOI 10.1139/cjpp-75-7-911; Pabelick CM, 2001, ANESTHESIOLOGY, V95, P207, DOI 10.1097/00000542-200107000-00032; Pabelick CM, 2001, J APPL PHYSIOL, V91, P488; Pfitzer G, 2001, J APPL PHYSIOL, V91, P497; PLACKE ME, 1987, TOXICOL APPL PHARM, V90, P284, DOI 10.1016/0041-008X(87)90336-X; Prakash YS, 2000, CELL CALCIUM, V27, P153, DOI 10.1054/ceca.1999.0106; Prakash YS, 1997, AM J PHYSIOL-CELL PH, V272, pC966; Salerno FG, 1996, BRIT J PHARMACOL, V118, P734; SANDERSON MJ, 2002, IN PRESS METHODS ENZ; Savineau JP, 2000, NEWS PHYSIOL SCI, V15, P50; SHIEH CC, 1991, J PHARMACOL EXP THER, V256, P141; Sieck GC, 1997, CAN J PHYSIOL PHARM, V75, P878, DOI 10.1139/cjpp-75-7-878; Sims SM, 1996, AM J PHYSIOL-LUNG C, V271, pL300; Somlyo AP, 2000, J PHYSIOL-LONDON, V522, P177, DOI 10.1111/j.1469-7793.2000.t01-2-00177.x; Tulic MK, 1999, THORAX, V54, P531; WIDDOP S, 1993, AM J RESP CELL MOL, V9, P541; Wohlsen A, 2001, AM J RESP CRIT CARE, V163, P1462	32	114	115	0	7	ROCKEFELLER UNIV PRESS	NEW YORK	1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA	0022-1295			J GEN PHYSIOL	J. Gen. Physiol.	FEB	2002	119	2					187	198		10.1085/jgp.119.2.187		12	Physiology	Physiology	561LL	WOS:000176142100006	11815668	
J	Kimber, I; Basketter, DA; Gerberick, GF; Dearman, RJ				Kimber, I; Basketter, DA; Gerberick, GF; Dearman, RJ			Allergic contact dermatitis	INTERNATIONAL IMMUNOPHARMACOLOGY			English	Review						allergic contact dermatitis; skin sensitization; hazard identification; risk assessment; Langerhans cells; T lymphocytes	LYMPH-NODE ASSAY; CD8(+) T-CELLS; CYTOKINE SECRETION PROFILES; SKIN SENSITIZATION RISK; CHEMICAL ALLERGENS; EFFECTOR CD8(+); LANGERHANS CELLS; CD4(+); MICE; HYPERSENSITIVITY	Allergic contact dermatitis (ACD) is a common occupational and environmental health issue. In common with other forms of allergy the disease progresses in two stages; an initial phase during which sensitization is acquired, followed later (after subsequent exposure to the same chemical allergen) by elicitation of a cutaneous inflammatory reaction. The development of skin sensitization is associated with, and requires, the activation and clonal expansion of allergen responsive T lymphocytes and it is these cells that orchestrate the cutaneous allergic reaction. In recent years, much has been: learned of the characteristics of immune responses to skin sensitizing chemicals and of the roles played by dendritic cells, cytokines and chemokines. Some of the more interesting cellular and molecular mechanisms are reviewed briefly in this article. A more detailed appreciation of responses induced by chemical allergens has in turn facilitated the design of novel approaches to the toxicological evaluation of skin sensitization. Real progress has been made, not only in the development of improved methods for hazard identification and characterization, but also in the application of new paradigms for risk assessment. The newer methods now available and the opportunities that exist for further advances are considered. Finally, progress has been made in the characterization of skin sensitization in humans and in the clinical management of ACD. This article seeks to consider skin sensitization and ACD in holistic fashion, bridging experimental observations with clinical disease and basic mechanisms with practical toxicology. (C) 2002 Elsevier Science B.V. All rights reserved.	Syngenta Cent Toxicol Lab, Macclesfield SK10 4TJ, Cheshire, England; Unilever Res Labs Colworth, SEAC Toxicol Unit, Sharnbrook MK44 1LQ, Beds, England; Procter & Gamble Co, Miami Valley Labs, Cincinnati, OH 45253 USA	Kimber, I (reprint author), Syngenta Cent Toxicol Lab, Alderley Pk, Macclesfield SK10 4TJ, Cheshire, England.						Andersen K.E., 1985, CONTACT ALLERGY PRED; BARRATT MD, 1996, TOXICOLOGY CONTACT H, P75; Basketter D. 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Immunopharmacol.	FEB	2002	2	2-3					201	211		10.1016/S1567-5769(01)00173-4		11	Immunology; Pharmacology & Pharmacy	Immunology; Pharmacology & Pharmacy	513DA	WOS:000173361600006	11811925	
J	Diaz-Sanchez, D; Penichet-Garcia, M; Saxon, A				Diaz-Sanchez, D; Penichet-Garcia, M; Saxon, A			Diesel exhaust particles directly induce activated mast cells to degranulate and increase histamine levels and symptom severity	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergy; pollution; mediators; clinical outcomes; hypersensitivity	IN-VIVO; IGE PRODUCTION; CYTOKINE PRODUCTION; MERCURIC-CHLORIDE; RAGWEED ALLERGEN; MESSENGER-RNA; DRY AIR; RELEASE; CHALLENGE; IL-4	Background: The ability of combustion products, such as diesel exhaust particles (DEPs), to modulate the immune system has now been firmly established. DEPs can synergize with allergen at the human upper respiratory mucosa to enhance allergen-specific IgE production, initiate a T(H)2 cytokine environment, and even promote primary allergic sensitization. Experiments suggest that these effects result from the initial activation of mast cells to produce IL-4. Objective: We sought to demonstrate that in vivo mast cell activation by DEPs plus allergen will also affect the release of classic mast cell mediators and consequently enhance the immediate-phase response. Methods: Dust mite-sensitive subjects were challenged intranasally with allergen, and symptom scores and histamine levels in nasal wash samples were compared after prechallenge with 0.3 mg of DEPs, Results: If the subjects were first sprayed with DEPs, mean symptom scores rose from 3.7 to 9.9; additionally, only one fifth of the amount of intranasal dust mite allergen was required to induce clinical symptoms. DEPs alone had no effect. The changes in symptoms correlated with histamine levels measured in nasal lavage specimens from these subjects, Although challenge with DEPs alone did not induce histamine release, challenge with both DEPs and allergen resulted in 3-fold higher histamine concentrations than those seen with allergen alone. In contrast, carbon black particles (elemental carbon devoid of chemicals) had no effect. The role of chemicals was confirmed because degranulation of a murine mast cell fine by Fc epsilon RI cross-linking was increased significantly (by 72%) by the soluble organic chemicals extracted from DEPs. Conclusions: Overall, these results suggest that exposure to DEPs can enhance the severity of clinical symptoms to allergen by enhancing mast cell degranulation.	Univ Calif Los Angeles, Sch Med, Hart & Louise Lyon Lab, Div Clin Immunol Allergy,Dept Med, Los Angeles, CA 90095 USA; Univ Calif Los Angeles, Sch Med, Jonsson Comprehens Canc Ctr Inst, Los Angeles, CA 90095 USA; Univ Calif Los Angeles, Sch Med, Inst Mol Biol, Los Angeles, CA 90095 USA	Diaz-Sanchez, D (reprint author), Univ Calif Los Angeles, Sch Med, Ctr Hlth Sci 52 175, Div Clin Immunol Allergy,Dept Med, Los Angeles, CA 90095 USA.				NIAID NIH HHS [AI-15251, AI-34567]		Beasley R., 2000, J ALLERGY CLIN IMMUN, V105, P466; BENHAMOU M, 1990, P NATL ACAD SCI USA, V87, P5327, DOI 10.1073/pnas.87.14.5327; *CENS TRANSP, 1995, US BUR CENS PUBL; CHURCH MK, 1983, BRIT J PHARMACOL, V80, P719; Dastych J, 1999, J ALLERGY CLIN IMMUN, V103, P1108, DOI 10.1016/S0091-6749(99)70186-7; Diaz-Sanchez D, 1999, CLIN IMMUNOL, V90, P313, DOI 10.1006/clim.1998.4676; Diaz-Sanchez D, 1999, J ALLERGY CLIN IMMUN, V104, P1183; DiazSanchez D, 1996, J ALLERGY CLIN IMMUN, V98, P114, DOI 10.1016/S0091-6749(96)70233-6; DIAZSANCHEZ D, 1994, J CLIN INVEST, V94, P1417, DOI 10.1172/JCI117478; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; DIAZSANCHEZ D, 2000, IMMUNOLOGY, V101, P1; *FED HIGHW ADM, 1995, US DEP TRANSP PUBL; Fujieda S, 1998, CLIN CANCER RES, V4, P1583; Hiura TS, 1999, J IMMUNOL, V163, P5582; HUGHES PJ, 1984, BIOCHEM PHARMACOL, V33, P384; Kittelson DB, 1998, J AEROSOL SCI, V29, P575, DOI 10.1016/S0021-8502(97)10037-4; Kumagai Y, 1997, FREE RADICAL BIO MED, V22, P479, DOI 10.1016/S0891-5849(96)00341-3; Lovik M, 1997, TOXICOLOGY, V121, P165, DOI 10.1016/S0300-483X(97)00075-9; Matsuoka T, 2000, SCIENCE, V287, P2013, DOI 10.1126/science.287.5460.2013; MIYABARA Y, 1998, AM J RESP CRIT CARE, V157, P1; MURANAKA M, 1986, J ALLERGY CLIN IMMUN, V79, P639; Nel AE, 1998, J ALLERGY CLIN IMMUN, V102, P539, DOI 10.1016/S0091-6749(98)70269-6; Ng D, 1998, J IMMUNOL, V161, P942; OCHEL M, 1991, J IMMUNOL, V146, P3006; PLAUT M, 1989, NATURE, V339, P64, DOI 10.1038/339064a0; Polosa R, 1999, THORAX, V54, P230; PROUD D, 1992, J ALLERGY CLIN IMMUN, V89, P1098, DOI 10.1016/0091-6749(92)90293-B; PROUVOSTDANON A, 1981, J IMMUNOL, V126, P699; Salvi S, 1999, AM J RESP CRIT CARE, V159, P702; Saneyoshi K, 1997, INT ARCH ALLERGY IMM, V114, P237; SCHWARTZ LB, 1979, J IMMUNOL, V123, P1445; Suzuki Takahito, 1993, Japanese Journal of Allergology, V42, P963; Terada N, 1999, CLIN EXP ALLERGY, V29, P52; TOGIAS A, 1990, AM REV RESPIR DIS, V141, P1428; TOGIAS A, 1987, J ALLERGY CLIN IMMUN, V79, P699; Toru H, 1998, J ALLERGY CLIN IMMUN, V102, P491, DOI 10.1016/S0091-6749(98)70140-X; Tsien A, 1997, TOXICOL APPL PHARM, V142, P256, DOI 10.1006/taap.1996.8063; Wang M, 1999, CLIN IMMUNOL, V90, P47, DOI 10.1006/clim.1998.4628	38	114	117	2	9	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	DEC	2000	106	6					1140	1146		10.1067/mai.2000.111144		7	Allergy; Immunology	Allergy; Immunology	384ER	WOS:000165930300017	11112898	
J	Phipatanakul, W; Eggleston, PA; Wright, EC; Wood, RA				Phipatanakul, W; Eggleston, PA; Wright, EC; Wood, RA		Natl Cooperative Inner City Asthma	Mouse allergen. I. The prevalence of mouse allergen in inner-city homes	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						mouse allergen; indoor allergens; inner-city asthma; sensitization	COCKROACH ALLERGEN; HOUSE DUST; ASTHMA; CHILDREN; EXPOSURE; MITE; SENSITIZATION; CAT	Background: Although mouse allergen is a well-defined cause of IgE-mediated hypersensitivity in occupational settings, it has not been web studied in the general population. Objective: We sought to determine the prevalence of mouse allergen in inner-city homes. Methods: A subset of 608 homes from the National Cooperative Inner-City Asthma Study population had dust samples adequate for analysis of mouse allergen. In addition, data regarding the demographics and housing of the subjects were related to the mouse allergen levels. Results: Ninety-five percent of all homes had detectable mouse allergen (Mus m 1) in at least one room, with the highest levels found in kitchens (kitchen: range, 0-618 mug/g; median, 1.60 mug/g; bedroom: range, 0-294 mug/g; median, 0.52 mug/g; television-living room: range, 0-203 mug/g; median, 0.57 mug/g). By city, 100% of the kitchens in Baltimore had detectable mouse allergen, with the lowest percentage (74%) in Cleveland Mouse allergen levels correlated among rooms (R = 0.65-0.75). Forty-nine percent of the homes had reported problems with mice within the last year, and 29% of the homes had evidence of mice in one or more rooms on home inspection and had higher levels of mouse allergen (P = .0001). Higher allergen levels were also associated with evidence of cockroach infestation in any room (P = .006), None of the other subject or housing demographics evaluated were associated with a higher prevalence or level of mouse allergen. Conclusions: We conclude that mouse allergen is widely distributed in inner-city homes and that cockroach infestation is associated with high mouse allergen levels.	Harvard Univ, Sch Med, Childrens Hosp, Dept Pediat,Div Allergy & Immunol, Boston, MA USA; Johns Hopkins Univ, Sch Med, Dept Pediat, Div Allergy & Immunol, Baltimore, MD 21205 USA; New England Res Inst, Watertown, MA 02172 USA	Wood, RA (reprint author), Johns Hopkins Hosp, CMSC 1102,600 N Wolfe St, Baltimore, MD 21287 USA.				NIAID NIH HHS [AI07007]; NIEHS NIH HHS [ES09606]		BIRKHEAD G, 1989, J ALLERGY CLIN IMMUN, V84, P484, DOI 10.1016/0091-6749(89)90361-8; Bush RK, 1998, J ALLERGY CLIN IMMUN, V102, P99, DOI 10.1016/S0091-6749(98)70060-0; CALL RS, 1992, J PEDIATR, V121, P362; Eggleston PA, 1998, J ALLERGY CLIN IMMUN, V102, P563, DOI 10.1016/S0091-6749(98)70272-6; Evans R, 1987, CHEST S, V91, P65; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; Gergen PJ, 1999, J ALLERGY CLIN IMMUN, V103, P501, DOI 10.1016/S0091-6749(99)70477-X; GOTTLIEB DJ, 1995, CHEST, V108, P28, DOI 10.1378/chest.108.1.28; INGRAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449, DOI 10.1016/S0091-6749(95)70286-5; Kattan M, 1997, PEDIATR PULM, V24, P253, DOI 10.1002/(SICI)1099-0496(199710)24:4<253::AID-PPUL4>3.0.CO;2-L; Mitchell H, 1997, PEDIATR PULM, V24, P237; MURRAY AB, 1983, PEDIATRICS, V71, P418; OHMAN JL, 1994, J ALLERGY CLIN IMMUN, V94, P810, DOI 10.1016/0091-6749(94)90147-3; Rosenstreich DL, 1997, NEW ENGL J MED, V336, P1356, DOI 10.1056/NEJM199705083361904; SWANSON MC, 1985, J ALLERGY CLIN IMMUN, V76, P724, DOI 10.1016/0091-6749(85)90678-5; Wade S, 1997, PEDIATR PULM, V24, P263, DOI 10.1002/(SICI)1099-0496(199710)24:4<263::AID-PPUL5>3.0.CO;2-L; WALSHAW MJ, 1986, Q J MED, V58, P199; WOOD RA, 1988, AM REV RESPIR DIS, V137, P358	18	114	114	1	1	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	DEC	2000	106	6					1070	1074				5	Allergy; Immunology	Allergy; Immunology	384ER	WOS:000165930300007	11112888	
J	Trifilieff, A; El-Hashim, A; Bertrand, C				Trifilieff, A; El-Hashim, A; Bertrand, C			Time course of inflammatory and remodeling events in a murine model of asthma: effect of steroid treatment	AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY			English	Article						airway hyperreactivity; dexamethasone; eosinophils	SUBEPITHELIAL FIBROSIS; AIRWAY INFLAMMATION; BRONCHIAL-ASTHMA; SMOOTH-MUSCLE; ALLERGEN; RESPONSIVENESS; HYPERRESPONSIVENESS; HYPERREACTIVITY; RESPONSES; EXPOSURE	The kinetics of airway inflammation and remodeling processes following ovalbumin aerosol challenge in sensitized BALB/c mice was studied. Mice were exposed to either single or five ovalbumin challenges over 5 days. In both protocols, time-dependent increases in bronchoalveolar lavage (BAL) cellular fibronectin, neutrophils and eosinophils were observed. The kinetics of these events were similar in both protocols; however, the magnitude of the response was much greater following repeated challenges. BAL protein levels and lymphocyte numbers were increased only following repeated challenges, whereas interleukin (IL)-5 and IL-4 were increased in both protocols. Histological analysis revealed a time-dependent increase in epithelial cell proliferation and in mucus-producing epithelial cells. Proliferation of alveolar cells was observed only following repeated challenges. Airway hyperreactivity was observed in both protocols but was much greater following repeated challenges. Pretreatment with dexamethasone fully inhibited the inflammatory response and airway hyperreactivity but only partially inhibited the remodeling process. These data suggest that glucocorticoids, although potent anti-inflammatory agents, may not be potent in reducing the lung remodeling process associated with asthma.	Novartis Horsham Res Ctr, Horsham RH12 5AB, W Sussex, England	Trifilieff, A (reprint author), Novartis Horsham Res Ctr, Wimblehurst Rd, Horsham RH12 5AB, W Sussex, England.						AYERS MM, 1988, EUR RESPIR J, V1, P58; BREWSTER CEP, 1990, AM J RESP CELL MOL, V3, P507; COCKCROFT DW, 1987, J ALLERGY CLIN IMMUN, V79, P734, DOI 10.1016/0091-6749(87)90204-1; COYLE AJ, 1995, AM J RESP CELL MOL, V13, P54; DJUKANOVIC R, 1990, AM REV RESPIR DIS, V142, P434; Gillis HL, 1999, J APPL PHYSIOL, V86, P2001; Haile S, 1999, EUR RESPIR J, V13, P961, DOI 10.1034/j.1399-3003.1999.13e06.x; Hamelmann E, 1997, AM J RESP CRIT CARE, V156, P766; Hogan SP, 1998, J IMMUNOL, V161, P1501; HOSSAIN S, 1973, AM REV RESPIR DIS, V107, P99; JAMES AL, 1989, AM REV RESPIR DIS, V139, P242; JEFFERY PK, 1989, AM REV RESPIR DIS, V140, P1745; Laitinen A, 1997, AM J RESP CRIT CARE, V156, P951; LAMBERT RK, 1993, J APPL PHYSIOL, V74, P2771; LEDERMANN F, 1991, J IMMUNOL METHODS, V141, P263, DOI 10.1016/0022-1759(91)90153-7; MACKLEM PT, 1987, CHEST, V91, pS189, DOI 10.1378/chest.91.6.189S; Olivieri D, 1997, AM J RESP CRIT CARE, V155, P1864; PADRID P, 1995, AM J RESP CRIT CARE, V151, P184; Panettieri Reynold Jr., 1998, American Journal of Physiology, V274, pL417; RENNARD SI, 1980, ANAL BIOCHEM, V104, P205, DOI 10.1016/0003-2697(80)90300-0; ROCHE WR, 1989, LANCET, V1, P520; Salmon M, 1999, EUR RESPIR J, V14, P633, DOI 10.1034/j.1399-3003.1999.14c25.x; STEWART AG, 1993, TRENDS PHARMACOL SCI, V14, P275, DOI 10.1016/0165-6147(93)90130-C; TANIZAKI Y, 1993, J ASTHMA, V30, P257, DOI 10.3109/02770909309054525; Temelkovski J, 1998, THORAX, V53, P849; TRIGG CJ, 1994, AM J RESP CRIT CARE, V150, P17; WIGGS BR, 1992, AM REV RESPIR DIS, V145, P1251	27	114	119	0	6	AMER PHYSIOLOGICAL SOC	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	1040-0605			AM J PHYSIOL-LUNG C	Am. J. Physiol.-Lung Cell. Mol. Physiol.	DEC	2000	279	6					L1120	L1128				9	Physiology; Respiratory System	Physiology; Respiratory System	375GY	WOS:000165392200013	11076802	
J	Kennedy, SM; Le Moual, N; Choudat, D; Kauffmann, F				Kennedy, SM; Le Moual, N; Choudat, D; Kauffmann, F			Development of an asthma specific job exposure matrix and its application in the epidemiological study of genetics and environment in asthma (EGEA)	OCCUPATIONAL AND ENVIRONMENTAL MEDICINE			English	Article						job exposure matrix; asthma; occupational exposure; epidemiological methods; case-control	OCCUPATIONAL CASE-CONTROL; WORK HISTORIES; INFORMATION; RELIABILITY; ZUTPHEN; COHORT; ATOPY	Objectives-To develop a method suitable for estimating exposure risks in population studies of asthma from job titles and international codes, by combining a new job exposure matrix (JEM) with the expert judgement approach. The method was applied in the French epidemiological study of the genetics and environment in asthma (EGEA). Methods-The JEM contains 22 exposure groups including 18 high risk groups based on known risk factors for occupational asthma, divided into high molecular weight agents, low molecular weight agents, and mixed environments. After applying the JEM to job codes, exposure estimates for each subject were reevaluated by examining job title texts. Three high risk exposure estimates for asthma were compared: firstly, applying the JEM to original codes (from different coders in each study centre); secondly, applying the JEM to revised codes (from one experienced coder); and thirdly, after reviewing JEM exposure estimates in the light of job title texts. Results-The study comprised 173 cases with asthma and 285 controls (age 18-65). Odds ratios (ORs) for asthma for high risk jobs were 1.0 (95% confidence interval (95% CI) 0.6 to 1.7), applying the JEM to original codes; 1.4 (95% CI 0.8 to 2.3), applying the JEM to revised codes; and 1.7 (95% CI 1.1 to 2.7), applying the JEM and subsequently re-evaluating exposure estimates from job title texts. Asthma ORs were 1.4 (95% CI 0.6 to 2.9) for high molecular weight agents, 2.3 (95% CI 1.2 to 4.4) for low molecular weight agents, and 2.1 (95% CI 0.9 to 5.2) for mixed environments. Conclusions-This asthma JEM, when enhanced by expert re-evaluation of exposure estimates from job title texts, may be a useful tool in general population studies of asthma. In this study, a 1.7-fold increase in prevalence odds of high risk exposures was found among asthmatic workers compared with controls, with risk magnitude varying for different classes of exposure.	Univ British Columbia, Sch Occupat & Environm Hyg, Vancouver, BC V6T 1Z3, Canada; INSERM U472, Villejuif, France; Hop Cochin, Serv Pathol Profess, Paris, France	Kennedy, SM (reprint author), Univ British Columbia, Sch Occupat & Environm Hyg, 2206 E Mall, Vancouver, BC V6T 1Z3, Canada.		LeMoual, Nicole/R-8976-2016	LeMoual, Nicole/0000-0002-2723-5569			Benke G, 1997, INT J EPIDEMIOL, V26, P635, DOI 10.1093/ije/26.3.635; BOUYER J, 1993, AM J EPIDEMIOL, V137, P472; BOUYER J, 1993, INT J EPIDEMIOL, V22, pS65; Brower PS, 1998, AM J EPIDEMIOL, V148, P920; Chan-Yeung M., 1993, ASTHMA WORKPLACE, P595; DUBROW R, 1987, AM J IND MED, V11, P329, DOI 10.1002/ajim.4700110309; Fishwick D, 1997, OCCUP ENVIRON MED, V54, P301; Hedman J, 1998, RESP MED, V92, P32, DOI 10.1016/S0954-6111(98)90029-4; HEEDERIK D, 1989, INT J EPIDEMIOL, V18, P382, DOI 10.1093/ije/18.2.382; Hoar S, 1983, J Toxicol Clin Toxicol, V21, P9; HSAIRI M, 1992, INT J EPIDEMIOL, V21, P972, DOI 10.1093/ije/21.5.972; *INT LAB ORG, 1991, INT LAB ORG INT STAN; Kauffmann F, 1999, CLIN EXP ALLERGY, V29, P17; Kauffmann F, 1997, AM J RESP CRIT CARE, V156, pS123; KAUPPINEN TP, 1992, SCAND J WORK ENV HEA, V18, P105; Kogevinas M, 1996, AM J RESP CRIT CARE, V154, P137; Kogevinas M, 1999, LANCET, V353, P1750, DOI 10.1016/S0140-6736(98)07397-8; KROMHOUT H, 1992, AM J EPIDEMIOL, V136, P698; Le Moual N, 2000, OCCUP ENVIRON MED, V57, P126, DOI 10.1136/oem.57.2.126; NG TP, 1994, AM J IND MED, V25, P709, DOI 10.1002/ajim.4700250510; PANNETT B, 1985, BRIT J IND MED, V42, P777; ROSENBERG CR, 1993, BRIT J IND MED, V50, P822; SIEMIATYCKI J, 1989, AM J EPIDEMIOL, V130, P1236; STEWART WF, 1994, AM J IND MED, V26, P297, DOI 10.1002/ajim.4700260304; Toren K, 1999, INT J TUBERC LUNG D, V3, P192	25	114	115	1	4	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	1351-0711			OCCUP ENVIRON MED	Occup. Environ. Med.	SEP	2000	57	9					635	641		10.1136/oem.57.9.635		7	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	345KK	WOS:000088815000009	10935945	
J	Guarnieri, M; Balmes, JR				Guarnieri, Michael; Balmes, John R.			Outdoor air pollution and asthma	LANCET			English	Article							DIESEL EXHAUST PARTICLES; TOBACCO-SMOKE EXPOSURE; EMERGENCY-DEPARTMENT VISITS; AMBIENT PARTICULATE MATTER; NITROGEN-DIOXIDE EXPOSURE; EXHALED NITRIC-OXIDE; NEW-YORK-CITY; CHILDHOOD ASTHMA; LUNG-FUNCTION; OXIDATIVE STRESS	Traffic and power generation are the main sources of urban air pollution. The idea that outdoor air pollution can cause exacerbations of pre-existing asthma is supported by an evidence base that has been accumulating for several decades, with several studies suggesting a contribution to new-onset asthma as well. In this Series paper, we discuss the effects of particulate matter (PM), gaseous pollutants (ozone, nitrogen dioxide, and sulphur dioxide), and mixed traffic-related air pollution. We focus on clinical studies, both epidemiological and experimental, published in the previous 5 years. From a mechanistic perspective, air pollutants probably cause oxidative injury to the airways, leading to inflammation, remodelling, and increased risk of sensitisation. Although several pollutants have been linked to new-onset asthma, the strength of the evidence is variable. We also discuss clinical implications, policy issues, and research gaps relevant to air pollution and asthma.	[Guarnieri, Michael; Balmes, John R.] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA; [Guarnieri, Michael; Balmes, John R.] Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA	Balmes, JR (reprint author), Univ Calif San Francisco, Box 0843, San Francisco, CA 94143 USA.	jbalmes@medsfgh.ucsf.edu			NHLBI NIH HHS [T32 HL007185]		Acciani TH, 2013, CLIN EXP ALLERGY, V43, P1406, DOI 10.1111/cea.12200; Adams C, 2009, J ENVIRON MONITOR, V11, P1331, DOI 10.1039/b903841h; Akinbami LJ, 2010, ENVIRON RES, V110, P294, DOI 10.1016/j.envres.2010.01.001; Anderson HR, 2013, AIR QUAL ATMOS HLTH, V6, P47, DOI 10.1007/s11869-011-0144-5; Anderson HR, 2013, AIR QUAL ATMOS HLTH, V6, P57, DOI 10.1007/s11869-011-0145-4; ARIS RM, 1993, AM REV RESPIR DIS, V148, P1363; Balmes JR, 2014, RESPIR MED SER, V7, P383, DOI 10.1007/978-1-4614-8417-2_22; Balmes JR, 2009, J ALLERGY CLIN IMMUN, V123, P626, DOI 10.1016/j.jaci.2008.10.062; Barck C, 2002, RESP MED, V96, P907, DOI 10.1053/rmed.2002.1374; 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J	Lin, SY; Erekosima, N; Kim, JM; Ramanathan, M; Suarez-Cuervo, C; Chelladurai, Y; Ward, D; Segal, JB				Lin, Sandra Y.; Erekosima, Nkiruka; Kim, Julia M.; Ramanathan, Murugappan; Suarez-Cuervo, Catalina; Chelladurai, Yohalakshmi; Ward, Darcy; Segal, Jodi B.			Sublingual Immunotherapy for the Treatment of Allergic Rhinoconjunctivitis and Asthma A Systematic Review	JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION			English	Review							PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND PLACEBO; RANDOMIZED CONTROLLED-TRIAL; GRASS-POLLEN EXTRACT; HOUSE-DUST-MITE; PARIETARIA-JUDAICA EXTRACT; JAPANESE CEDAR POLLINOSIS; QUALITY-OF-LIFE; SWALLOW IMMUNOTHERAPY; RESPIRATORY ALLERGY	Importance Allergic rhinitis affects up to 40% of the US population. To desensitize allergic individuals, subcutaneous injection immunotherapy or sublingual immunotherapy may be administered. In the United States, sublingual immunotherapy is not approved by the Food and Drug Administration. However, some US physicians use aqueous allergens, off-label, for sublingual desensitization. Objective To systematically review the effectiveness and safety of aqueous sublingual immunotherapy for allergic rhinoconjunctivitis and asthma. Evidence Acquisition The databases of MEDLINE, EMBASE, LILACS, and the Cochrane Central Register of Controlled Trials were searched through December 22, 2012. English-language randomized controlled trials were included if they compared sublingual immunotherapy with placebo, pharmacotherapy, or other sublingual immunotherapy regimens and reported clinical outcomes. Studies of sublingual immunotherapy that are unavailable in the United States and for which a related immunotherapy is unavailable in the United States were excluded. Paired reviewers selected articles and extracted the data. The strength of the evidence for each comparison and outcome was graded based on the risk of bias (scored on allocation, concealment of intervention, incomplete data, sponsor company involvement, and other bias), consistency, magnitude of effect, and the directness of the evidence. Results Sixty-three studies with 5131 participants met the inclusion criteria. Participants' ages ranged from 4 to 74 years. Twenty studies (n=1814 patients) enrolled only children. The risk of bias was medium in 43 studies (68%). Strong evidence supports that sublingual immunotherapy improves asthma symptoms, with 8 of 13 studies reporting greater than40% improvement vs the comparator. Moderate evidence supports that sublingual immunotherapy use decreases rhinitis or rhinoconjunctivitis symptoms, with 9 of 36 studies demonstrating greater than 40% improvement vs the comparator. Medication use for asthma and allergies decreased by more than 40% in 16 of 41 studies of sublingual immunotherapy with moderate grade evidence. Moderate evidence supports that sublingual immunotherapy improves conjunctivitis symptoms (13 studies), combined symptom and medication scores (20 studies), and disease-specific quality of life (8 studies). Local reactions were frequent, but anaphylaxis was not reported. Conclusions and Relevance The overall evidence provides a moderate grade level of evidence to support the effectiveness of sublingual immunotherapy for the treatment of allergic rhinitis and asthma, but high-quality studies are still needed to answer questions regarding optimal dosing strategies. There were limitations in the standardization of adverse events reporting, but no life-threatening adverse events were noted in this review. JAMA. 2013; 309(12): 1278-1288 www.jama.com	[Kim, Julia M.] Johns Hopkins Univ, Sch Med, Div Gen Pediat & Adolescent Med, Baltimore, MD 21287 USA; [Lin, Sandra Y.; Ramanathan, Murugappan] Johns Hopkins Univ, Sch Med, Dept Otolaryngol Head & Neck Surg, Baltimore, MD 21287 USA; [Erekosima, Nkiruka; Suarez-Cuervo, Catalina; Chelladurai, Yohalakshmi; Ward, Darcy; Segal, Jodi B.] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21287 USA; [Kim, Julia M.] Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21287 USA	Lin, SY (reprint author), Johns Hopkins Univ, Sch Med, 601 N Caroline St,Ste 6254, Baltimore, MD 21287 USA.	slin30@jhmi.edu	Segal, Jodi/A-2863-2009	Segal, Jodi/0000-0003-3978-9662	Agency for Healthcare Research and Quality (AHRQ) [HHSA 290 2007 10061]; Johns Hopkins University Evidence-based Practice Center [HHSA 290 2007 10061 I]	This study was funded by grant HHSA 290 2007 10061 I from the Agency for Healthcare Research and Quality (AHRQ) and is based on research conducted at the Johns Hopkins University Evidence-based Practice Center under contract HHSA 290 2007 10061 I.	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Am. Med. Assoc.	MAR 27	2013	309	12					1278	1288		10.1001/jama.2013.2049		11	Medicine, General & Internal	General & Internal Medicine	112WO	WOS:000316625200028	23532243	
J	Rosenblum, MD; Gratz, IK; Paw, JS; Lee, K; Marshak-Rothstein, A; Abbas, AK				Rosenblum, Michael D.; Gratz, Iris K.; Paw, Jonathan S.; Lee, Karen; Marshak-Rothstein, Ann; Abbas, Abul K.			Response to self antigen imprints regulatory memory in tissues	NATURE			English	Article							T-CELLS; IN-VIVO; EXPRESSION; AUTOANTIGEN; HOMEOSTASIS; AUTOIMMUNE; DEPLETION; DISEASES; MICE	Immune homeostasis in tissues is achieved through a delicate balance between pathogenic T-cell responses directed at tissue-specific antigens and the ability of the tissue to inhibit these responses. The mechanisms by which tissues and the immune system communicate to establish and maintain immune homeostasis are currently unknown. Clinical evidence suggests that chronic or repeated exposure to self antigen within tissues leads to an attenuation of pathological autoimmune responses, possibly as a means to mitigate inflammatory damage and preserve function. Many human organ-specific autoimmune diseases are characterized by the initial presentation of the disease being the most severe, with subsequent flares being of lesser severity and duration(1). In fact, these diseases often spontaneously resolve, despite persistent tissue autoantigen expression(2). In the practice of antigen-specific immunotherapy, allergens or self antigens are repeatedly injected in the skin, with a diminution of the inflammatory response occurring after each successive exposure(3). Although these findings indicate that tissues acquire the ability to attenuate autoimmune reactions upon repeated responses to antigens, the mechanism by which this occurs is unknown. Here we show that upon expression of self antigen in a peripheral tissue, thymus-derived regulatory T cells (T-reg cells) become activated, proliferate and differentiate into more potent suppressors, which mediate resolution of organ-specific autoimmunity in mice. After resolution of the inflammatory response, activated T-reg cells are maintained in the target tissue and are primed to attenuate subsequent autoimmune reactions when antigen is re-expressed. Thus, T-reg cells function to confer 'regulatory memory' to the target tissue. These findings provide a framework for understanding how T-reg cells respond when exposed to self antigen in peripheral tissues and offer mechanistic insight into how tissues regulate autoimmunity.	[Gratz, Iris K.; Paw, Jonathan S.; Abbas, Abul K.] Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94143 USA; [Rosenblum, Michael D.; Paw, Jonathan S.] Univ Calif San Francisco, Dept Dermatol, San Francisco, CA 94115 USA; [Lee, Karen] Columbia Univ, Dept Pediat, Med Ctr, New York, NY 10032 USA; [Marshak-Rothstein, Ann] Univ Massachusetts, Div Rheumatol, Dept Med, Worcester, MA 01655 USA	Abbas, AK (reprint author), Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94143 USA.	Abul.Abbas@ucsf.edu	Gratz, Iris /L-6267-2015	Gratz, Iris /0000-0001-7470-7277	Dermatology Foundation; UCSF Department of Dermatology; NIH [P01 AI35297, R01 AI73656, U19 AI56388, AR055634]; Scleroderma Research Foundation; Austrian Science Fund (FWF) [J2997-B13]	We thank C. Benetiz for assistance with animal husbandry, S. Isakson for genotyping, S.-w. Jiang and M. Lee for cell sorting, and K. Ravid and G. Martin for derivation of TRE-TGO transgenic mice. We thank S. Ziegler, Benaroya Research Institute, for transgenic mice. M. D. R. is supported by a Dermatology Foundation Career Development Award and the UCSF Department of Dermatology. This work was partially funded through NIH grants P01 AI35297, R01 AI73656 and U19 AI56388 (to A. K. A.); NIH grant AR055634 to (A.M.-R.); and the Scleroderma Research Foundation (A.M.-R.). I. K. G. is supported by an Erwin Schroedinger Fellowship from the Austrian Science Fund (FWF), J2997-B13.	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J	Thyssen, JP; Menne, T				Thyssen, Jacob P.; Menne, Torkil			Metal Allergy-A Review on Exposures, Penetration, Genetics, Prevalence, and Clinical Implications	CHEMICAL RESEARCH IN TOXICOLOGY			English	Review							OCCUPATIONAL CONTACT-DERMATITIS; UNSELECTED DANISH POPULATION; PATCH TEST CONCENTRATIONS; GOLD SODIUM THIOSULFATE; TOTAL HIP-ARTHROPLASTY; IN-STENT RESTENOSIS; NICKEL ALLERGY; ON-METAL; ORTHOPEDIC IMPLANTS; FERROUS SULFATE	The prevalence of metal allergy is high in the general population, and it is estimated that up to 17% of women and 3% of men are allergic to nickel and that 1-3% are allergic to cobalt and chromium. Among dermatitis patients, the prevalence of metal allergy is even higher. Metal allergy is mainly an environmental disorder although null Mutations in the filaggrin gene complex were recently found to be associated with nickel allergy and dermatitis. Environmental metal exposures include jewelry, buttons, clothing fasteners, dental restorations, mobile phones, and leather. Although consumer exposure is responsible for most cases of metal allergy, the importance Of Occupational metal exposure remains present and should always be taken into consideration when one interprets allergic patch test reactions to metals. Traditionally, nickel, cobalt, and chromium have been the most important contact allergens. However, recently, gold and palladium have drawn much attention as the prevalence of contact allergy to these metals is high. Palladium allergy is mainly a result of cross-sensitization to nickel, whereas gold allergy is rarely clinically relevant when one takes its high prevalence into account. The epidemiology of metal allergy has recently changed in Europe as nickel allergy among ear-pierced Danish women has decreased following regulatory intervention oil nickel release from consumer products. In the United States, the prevalence of nickel allergy is still increasing, which may be explained by the absence of regulation. The prevalence of chromium allergy is increasing in the United States, Singapore, and Denmark among dermatitis patients. This increase is significantly associated with leather exposure in Denmark. Metal allergy may result in allergic contact dermatitis and systemic allergic (contact) dematitis. Furthermore, metal allergy has been associated with device failure following insertion of intracoronary stents, hip and knee prostheses, as well as other implants. This area is in need of more research.	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Res. Toxicol.	FEB	2010	23	2					309	318		10.1021/tx9002726		10	Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology	Pharmacology & Pharmacy; Chemistry; Toxicology	555QU	WOS:000274529400003	19831422	
J	Cookson, H; Granell, R; Joinson, C; Ben-Shlomo, Y; Henderson, AJ				Cookson, Hannah; Granell, Raquel; Joinson, Carol; Ben-Shlomo, Yoav; Henderson, A. John			Mothers' anxiety during pregnancy is associated with asthma in their children	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Anxiety; pregnancy; prenatal programming; asthma; child	DAY-CARE ATTENDANCE; MATERNAL ANTENATAL ANXIETY; POSTNATAL DEPRESSION; COMORBID ANXIETY; INCREASED RISK; BIRTH-COHORT; EARLY-LIFE; STRESS; DISORDERS; CHILDHOOD	Background: Maternal stress in early life has been associated with the development of asthma in children, although it is unclear whether there are any critical periods of exposure. The association of asthma with prenatal exposure to maternal stress has not been reported. Objective: We tested whether prenatal and postnatal anxiety and/or depression in pregnant women predicted the risk of their offspring developing asthma in childhood. Methods: The Avon Longitudinal Study of Parents and Children is a population-based birth cohort recruited during pregnancy. Data were available on maternal anxiety scores and asthma at age 71/2 years in 5810 children. Anxiety was assessed at 18 and 32 weeks of gestation by using the validated Crown-Crisp Experiential Index. Asthma was defined at age 71/2 years as doctor-diagnosed asthma with current symptoms or treatment in the previous 12 months. Multivariable logistic regression was used to determine the association of prenatal anxiety with asthma (odds ratio; 95% CI). Results: Independent of postnatal anxiety and adjusted for a number of likely confounders, there was a higher likelihood of asthma at age 71/2 years (odds ratio, 1.64; 95% CI, 1.25-2.17) in children of mothers in the highest compared with lowest quartile of anxiety scores at 32 weeks of gestation, with evidence for a dose-response (P value for trend <0.001). Conclusions: Maternal anxiety symptoms as an indicator of stress during fetal life may program the development of asthma during childhood. (J Allergy Clin Immunol 2009;123:847-853.)	[Henderson, A. John] Univ Bristol, ALSPAC, Dept Community Based Med, Bristol BS8 2BN, Avon, England; [Cookson, Hannah] Sir Charles Gairdner Hosp, Dept Internal Med, Perth, WA, Australia; [Granell, Raquel; Ben-Shlomo, Yoav] Univ Bristol, Dept Social Med, Bristol BS8 2BN, Avon, England	Henderson, AJ (reprint author), Univ Bristol, ALSPAC, Dept Community Based Med, Oakfield House,Oakfield Grove, Bristol BS8 2BN, Avon, England.	a.j.henderson@bris.ac.uk		Henderson, Alexander John/0000-0001-9650-231X	UK Medical Research Council; Wellcome Trust; University of Bristol; Asthma UK	The UK Medical Research Council, the Wellcome Trust, and the University of Bristol provide core support for the Avon Longitudinal Study of Parents and Children. R.G. wits supported by a project grant from Asthma UK.	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Allergy Clin. Immunol.	APR	2009	123	4					847	853		10.1016/j.jaci.2009.01.042		7	Allergy; Immunology	Allergy; Immunology	431JW	WOS:000265058600010	19348924	
J	Makita, H; Nasuhara, Y; Nagai, K; Ito, Y; Hasegawa, M; Betsuyaku, T; Onodera, Y; Hizawa, N; Nishimura, M				Makita, Hironi; Nasuhara, Yasuyuki; Nagai, Katsura; Ito, Yoko; Hasegawa, Masaru; Betsuyaku, Tomoko; Onodera, Yuya; Hizawa, Nobuyuki; Nishimura, Masaharu		Hokkaido COPD Cohort Study Grp	Characterisation of phenotypes based on severity of emphysema in chronic obstructive pulmonary disease	THORAX			English	Article							AIR-FLOW LIMITATION; BRONCHOALVEOLAR LAVAGE FLUID; BRONCHODILATOR RESPONSE; SUBCLINICAL EMPHYSEMA; SMALL AIRWAYS; BODY-WEIGHT; COPD; HEALTH; MORTALITY; CAPACITY	Background: Airflow limitation in chronic obstructive pulmonary disease ( COPD) is caused by a mixture of small airway disease and emphysema, the relative contributions of which may vary among patients. Phenotypes of COPD classified purely based on severity of emphysema are not well defined and may be different from the classic phenotypes of "pink puffers'' and "blue bloaters''. Methods: To characterise clinical phenotypes based on severity of emphysema, 274 subjects with COPD were recruited, excluding those with physician-diagnosed bronchial asthma. For all subjects a detailed interview of disease history and symptoms, quality of life (QOL) measurement, blood sampling, pulmonary function tests before and after inhalation of salbutamol (0.4 mg) and high- resolution CT scanning were performed. Results: Severity of emphysema visually evaluated varied widely even among subjects with the same stage of disease. No significant differences were noted among three groups of subjects classified by severity of emphysema in age, smoking history, chronic bronchitis symptoms, blood eosinophil count, serum IgE level or bronchodilator response. However, subjects with severe emphysema had significantly lower body mass index (BMI) and poorer QOL scores, evaluated using St George's Respiratory Questionnaire (SGRQ), than those with no/mild emphysema (mean ( SD) BMI 21.2 (0.5) vs 23.5 (0.3) kg/m(2), respectively; SGRQ total score 40 (3) vs 28 (2), respectively; p < 0.001 for both). These characteristics held true even if subjects with the same degree of airflow limitation were chosen. Conclusions: The severity of emphysema varies widely even in patients with the same stage of COPD, and chronic bronchitis symptoms are equally distributed irrespective of emphysema severity. Patients with the phenotype in which emphysema predominates have lower BMI and poorer health-related QOL.	Hokkaido Univ, Sch Med, Dept Med 1, Kita Ku, Sapporo, Hokkaido 0608638, Japan	Nishimura, M (reprint author), Hokkaido Univ, Sch Med, Dept Med 1, Kita Ku, N-15 W-7, Sapporo, Hokkaido 0608638, Japan.	ma-nishi@med.hokudai.ac.jp	Nasuhara, Yasuyuki/G-1647-2012; Nishimura, Masaharu/A-4062-2012	Nishimura, Masaharu/0000-0002-6456-4361			*AM THOR SOC, 2004, STAND DIAGN MAN SUBJ; American thoracic society, 1995, AM J RESP CRIT CARE, V152, pS77; Anthonisen NR, 2005, EUR RESPIR J, V26, P45, DOI 10.1183/09031936.05.00102604; ANTHONISEN NR, 1986, AM REV RESPIR DIS, V133, P814; Anthonisen NR, 1989, AM REV RESPIR DIS, V140, pS95; Betsuyaku T, 1999, AM J RESP CRIT CARE, V159, P1985; [Anonymous], 2006, CHEST; BURROWS B, 1966, LANCET, V1, P830; Calverley PMA, 2003, THORAX, V58, P659, DOI 10.1136/thorax.58.8.659; Celli BR, 2004, EUR RESPIR J, V23, P932, DOI 10.1183/09031936.04.00014304; Celli BR, 2004, NEW ENGL J MED, V350, P1005, DOI 10.1056/NEJMoa021322; Ciba Guest Symposium, 1959, THORAX, V14, P286; *COMM PULM PHYSL J, 2004, GUID PULM FUNCT TEST; Domingo-Salvany A, 2002, AM J RESP CRIT CARE, V166, P680, DOI 10.1164/rccm.2112043; FILLEY GF, 1968, AM J MED, V44, P26, DOI 10.1016/0002-9343(68)90234-9; Fukuchi Y, 2004, RESPIROLOGY, V9, P458, DOI 10.1111/j.1440-1843.2004.00637.x; GELB AF, 1993, AM REV RESPIR DIS, V147, P1157; Gelb AF, 1996, CHEST, V109, P353, DOI 10.1378/chest.109.2.353; GODDARD PR, 1982, CLIN RADIOL, V33, P379, DOI 10.1016/S0009-9260(82)80301-2; Global Initiative for Chronic Obstructive Lung Disease (GOLD), 2003, GLOB STRAT DIAGN MAN; GOULD GA, 1991, EUR RESPIR J, V4, P141; Hasegawa M, 2006, AM J RESP CRIT CARE, V173, P1309, DOI 10.1164/rccm.200601-037OC; HOGG JC, 1968, NEW ENGL J MED, V278, P1355, DOI 10.1056/NEJM196806202782501; HOGG JC, 1994, THORAX, V49, P473, DOI 10.1136/thx.49.5.473; Hogg JC, 2004, NEW ENGL J MED, V350, P2645, DOI 10.1056/NEJMoa032158; Hogg JC, 2004, LANCET, V364, P709, DOI 10.1016/S0140-6736(04)16900-6; *JAP RESP SOC, 2004, COPD GUID DIAGN TREA; JONES PW, 1992, AM REV RESPIR DIS, V145, P1321; Lopez AD, 1998, NAT MED, V4, P1241, DOI 10.1038/3218; Marti S, 2006, EUR RESPIR J, V27, P689, DOI 10.1183/09031936.06.00076405; NETTER F, 1979, CIBA COLLECTION MED; Nishimura K, 2002, CHEST, V121, P1434, DOI 10.1378/chest.121.5.1434; Takabatake N, 2005, AM J RESP CRIT CARE, V172, P1097, DOI 10.1164/rccm.200503-319OC; Thurlbeck W M, 1982, Eur J Respir Dis Suppl, V121, P9; WRIGHT JL, 1984, AM REV RESPIR DIS, V129, P989; YANAI M, 1992, J APPL PHYSIOL, V72, P1016; YOSHIOKA A, 1995, AM J RESP CRIT CARE, V152, P2127	37	113	118	0	4	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	NOV	2007	62	11					932	937		10.1136/thx.2006.072777		6	Respiratory System	Respiratory System	224SU	WOS:000250467500005	17573447	
J	Park, KS; Korfhagen, TR; Bruno, MD; Kitzmiller, JA; Wan, HJ; Wert, SE; Hershey, GKK; Chen, G; Whitsett, JA				Park, Kwon-Sik; Korfhagen, Thomas R.; Bruno, Michael D.; Kitzmiller, Joseph A.; Wan, Huajing; Wert, Susan E.; Hershey, Gurjit K. Khurana; Chen, Gang; Whitsett, Jeffrey A.			SPDEF regulates goblet cell hyperplasia in the airway epithelium	JOURNAL OF CLINICAL INVESTIGATION			English	Article							TRANSCRIPTION FACTOR-I; SURFACTANT PROTEIN-C; SP-A GENE; RESPIRATORY EPITHELIUM; MOUSE LUNG; TRANSGENIC MICE; ETS-DOMAIN; EXPRESSION; DIFFERENTIATION; FACTOR-1	Goblet cell hyperplasia and mucous hypersecretion contribute to the pathogenesis of chronic pulmonary diseases including cystic fibrosis, asthma, and chronic obstructive pulmonary disease. In the present work, mouse SAM pointed domain-containing ETS transcription factor (SPDEF) mRNA and protein were detected in subsets of epithelial cells lining the trachea, bronchi, and tracheal glands. SPDEF interacted with the C-terminal domain of thyroid transcription factor 1, activating transcription of genes expressed selectively in airway epithelial cells, including Sftpa, Scgb1a1, Foxj1, and Sox17. Expression of Spdef in the respiratory epithelium of adult transgenic mice caused goblet cell hyperplasia, inducing both acidic and neutral mucins in vivo, and stainined for both acidic and neutral mucins in vivo. SPDEF expression was increased at sites of goblet cell hyperplasia caused by IL-13 and dust mite allergen in a process that was dependent upon STAT-6. SPDEF was induced following intratracheal allergen exposure and after Th2 cytokine stimulation and was sufficient to cause goblet cell differentiation of Clara cells in vivo.	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J	Wright, RJ				Wright, RJ			Stress and atopic disorders	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						asthma; atopy; psychological stress; oxidative stress; psychoneuroimmunology; genetics	PSYCHOSOCIAL STRESS; GENETIC-VARIATION; MATERNAL STRESS; BIRTH-COHORT; EXPOSURE; DISEASE; INFANCY; ASTHMA; MODEL; PSYCHONEUROIMMUNOLOGY	Evidence linking psychological stress to the expression of asthma and atopy continues to grow. Examining the underlying molecular mechanisms linking stress to asthma and other allergic phenomena is an active area of research. Evidence is reviewed for the influence of stress on neuroimmunoregulation and oxidative stress pathways, which, in turn, may affect biological hypersensitivity to environmental stimuli characteristic of atopic disorders. Critical periods of development, including in utero environment, are underscored. The role of genetics and gene-by-environment interactions is also discussed.	Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med, Cambridge, MA 02138 USA; Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Cambridge, MA 02138 USA	Wright, RJ (reprint author), Channing Labs, 181 Longwood Ave, Boston, MA 02115 USA.	rosalind.wright@channing.harvard.edu	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	NHLBI NIH HHS [R01 HL64108, U01 HL072494]; NIEHS NIH HHS [R01 ES10932]		Barker D J, 2001, Med Health Care Philos, V4, P31, DOI 10.1023/A:1009934412988; BENEDIKTSSON R, 1993, LANCET, V341, P339, DOI 10.1016/0140-6736(93)90138-7; Bienenstock J, 2003, AUTONOMIC NEUROIMMUN; Bonham AC, 2004, PULM PHARMACOL THER, V17, P69; Buske-Kirschbaum A, 2004, PSYCHONEUROENDOCRINO, V29, P705, DOI 10.1016/S0306-4530(03)00100-8; Chen CY, 2003, J APPL PHYSIOL, V94, P819, DOI 10.1152/japplphysiol.00552.2002; Chen CY, 2001, J ALLERGY CLIN IMMUN, V108, P557; Child F, 2003, RESP MED, V97, P1247, DOI 10.1016/S0954-6111(03)00250-6; Chrousos GP, 1996, AM J RESP CRIT CARE, V154, pS39; Chrousos GP, 1998, ANN NY ACAD SCI, V851, P311, DOI 10.1111/j.1749-6632.1998.tb09006.x; CHROUSOS GP, 1996, AM J RESP CRIT CARE, V154, pS44; Cohen S, 1996, ANNU REV PSYCHOL, V47, P113, DOI 10.1146/annurev.psych.47.1.113; Cohen S, 2003, BRAIN BEHAV IMMUN, V17, P407, DOI 10.1016/S0889-1591(03)00110-7; Cohen S, 1998, HEALTH PSYCHOL, V17, P214, DOI 10.1037//0278-6133.17.3.214; Cohen S, 1995, MEASURING STRESS GUI, P3; Dantzer R, 2004, BRAIN BEHAV IMMUN, V18, P1, DOI 10.1016/bbi.2003.09.008; Donaldson K, 2000, Respir Res, V1, P12, DOI 10.1186/rr5; Essex MJ, 2002, BIOL PSYCHIAT, V52, P776, DOI 10.1016/S0006-3223(02)01553-6; Fukata J, 1993, J ENDOCRINOL INVEST, V16, P141; Glosli H, 2002, FASEB J, V16, P1450, DOI 10.1096/fj.01-0948fje.; Gluckman PD, 2005, EARLY HUM DEV, V81, P51, DOI 10.1016/j.earlhumdev.2004.10.003; Hoffjan S, 2004, J ALLERGY CLIN IMMUN, V113, P511, DOI 10.1016/j.jaci.2003.10.044; Kelley KW, 2004, BRAIN BEHAV IMMUN, V18, P95, DOI 10.1016/j.bbi.2003.10.003; Lazarus R. S., 1984, STRESS APPRAISAL COP; McEwen BS, 1998, NEW ENGL J MED, V338, P171; Meaney MJ, 2005, TRENDS NEUROSCI, V28, P456, DOI 10.1016/j.tins.2005.07.006; Miller GE, 2002, HEALTH PSYCHOL, V21, P531, DOI 10.1037//0278-6133.21.6.531; Osler W, 1892, PRINCIPLES PRACTICE; Pike JL, 1997, PSYCHOSOM MED, V59, P447; Rich EL, 2005, AM J PHYSIOL-REG I, V288, pR1628, DOI 10.1152/ajpregu.00484.2004; Seckl JR, 1997, STEROIDS, V62, P89, DOI 10.1016/S0039-128X(96)00165-1; SHANKS N, 2001, J CLIN INVEST, V108, P1667; Spiteri MA, 2000, ALLERGY, V55, P15, DOI 10.1034/j.1398-9995.2000.00502.x; STEWART PM, 1995, J CLIN ENDOCR METAB, V80, P885, DOI 10.1210/jc.80.3.885; Theoharides TC, 2004, TRENDS PHARMACOL SCI, V25, P563, DOI 10.1016/j.tips.2004.09.007; Tracey KJ, 2002, NATURE, V420, P853, DOI 10.1038/nature01321; UNDEM BJ, 2000, J ALLERGY CLIN IMMUN, V106, P213; von Hertzen LC, 2002, J ALLERGY CLIN IMMUN, V109, P923, DOI 10.1067/mai.2002.124776; Wamboldt MZ, 2003, J ALLERGY CLIN IMMUN, V111, P509, DOI 10.1067/mai.2003.140; WELBERG L, 2001, J NEUROENDOCRINOL, V17, P113; Wright RJ, 1998, THORAX, V53, P1066; Wright RJ, 2004, J ALLERGY CLIN IMMUN, V113, P1051, DOI 10.1016/j.jaci.2004.03.032; Wright RJ, 2002, AM J RESP CRIT CARE, V165, P358; WRIGHT RJ, 2004, CURR OPIN ALLERGY CL, V5, P23; Wu Z, 2004, CLIN EXP IMMUNOL, V135, P194, DOI 10.1111/j.1365-2249.2004.02372.x; Wust S, 2004, ANN NY ACAD SCI, V1032, P52, DOI 10.1196/annals.1314.005; Wust S, 2004, J CLIN ENDOCR METAB, V89, P565, DOI 10.1210/jc.2003-031148; Zhou JF, 2000, BIOMED ENVIRON SCI, V13, P44	48	113	119	1	8	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	DEC	2005	116	6					1301	1306		10.1016/j.jaci.2005.09.050		6	Allergy; Immunology	Allergy; Immunology	017IJ	WOS:000235687000022	16337463	
J	Lau, S; Illi, S; Platts-Mills, TAE; Riposo, D; Nickel, R; Gruber, C; Niggemann, B; Wahn, U				Lau, S; Illi, S; Platts-Mills, TAE; Riposo, D; Nickel, R; Gruber, C; Niggemann, B; Wahn, U		Multicentre Allergy Study Grp	Longitudinal study on the relationship between cat allergen and endotoxin exposure, sensitization, cat-specific IgG and development of asthma in childhood - report of the German Multicentre Allergy Study (MAS 90)	ALLERGY			English	Article						cat allergen exposure; childhood asthma; sensitization and immunoglobulin G antibodies to cat	MODIFIED TH2 RESPONSE; HOUSE-DUST; ATOPIC SENSITIZATION; PET OWNERSHIP; BIRTH COHORT; EARLY-LIFE; HAY-FEVER; CHILDREN; RISK; DISORDERS	Background: Controversial data have emerged regarding the question whether cat exposure in childhood favours or decreases the risk of sensitization and allergic airway disease. In a prospective birth-cohort study, we assessed the association between longitudinal cat allergen exposure, sensitization (immunoglobulin E, IgE), IgG antibody (ab) levels to cat and the development of asthma in children up to the age of 10 years. Methods: Of 1314 newborn infants enrolled in five German cities in 1990, follow-up data at age 10 years were available for 750 children. Assessments included yearly measurements of specific serum IgE to cat and at age 6 and 18 months, 3, 4 and 10 years measurement of cat allergen Fel d 1 in house dust samples. Additionally, Fel d 1-specific IgG ab were determined in 378 serum samples of 207 children. Endotoxin exposure in mattress dust was measured in a subgroup of 153 children at age 10 years. From age 4 years on, International Study of Asthma and Allergy in Childhood (ISAAC) questionnaires were completed yearly in order to assess the prevalence of wheeze and asthma. Results: Serum IgG-levels to cat showed a large variation, however, intraindividually values showed rather constant concentration over a longer time period. The IgG levels at school-age correlated with cat allergen exposure during the first 2 years of life. Specific IgE to cat was clearly associated with wheeze ever, current wheeze and bronchial hyperresponsiveness (BHR), this was also observed for children with specific IgE ab to cat (&GT; 0.35 kU/l) plus IgG levels above 125 U/ml. A large percentage of very highly exposed children showed high IgG but no IgE responses to cat, however, not all highly exposed children were found to be protected from sensitization. Children with IgG but without IgE ab to cat showed the lowest prevalence of wheeze ever and current wheeze despite high cat allergen exposure, however, this trend did not achieve significance. While homes of cat owners showed higher Fel d 1 concentrations than homes without cats, homes of cat owners were not found to have higher endotoxin levels in carpet dust samples than homes without cats. Conclusions: We could confirm that high cat allergen exposure in a cohort with lower community prevalence of cats is associated with higher serum IgG and IgE levels to cat in schoolchildren. Sensitization to cat allergen (IgE) is a risk factor for childhood asthma. While exposure to cat allergen during infancy is associated with sensitization (IgE), only in the very highly exposed children the likelihood of sensitization (IgE) is decreased and high IgG levels to cat without IgE were associated with low risk of wheeze. However, cat-specific IgG ab levels did not protect children with IgE-mediated sensitization from wheeze.	Charite Univ Med Berlin, Dept Pediat Pneumol & Immunol, D-13353 Berlin, Germany; Univ Childrens Hosp von Hauner, Munich, Germany; Univ Virginia, Asthma & Allerg Dis Ctr, Charlottesville, VA USA	Lau, S (reprint author), Charite Univ Med Berlin, Dept Pediat Pneumol & Immunol, Univ Childrens Hosp Charite Campus, D-13353 Berlin, Germany.						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J	Strid, J; Hourihane, J; Kimber, I; Callard, R; Strobel, S				Strid, J; Hourihane, J; Kimber, I; Callard, R; Strobel, S			Epicutaneous exposure to peanut protein prevents oral tolerance and enhances allergic sensitization	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						epicutaneous sensitization; food allergy; IgE; oral tolerance; peanut; skin	FOOD ALLERGY; ATOPIC-DERMATITIS; TH2 RESPONSES; MURINE MODEL; PREVALENCE; ANTIGEN; IMMUNIZATION; MECHANISMS; CHILDREN; DISEASES	Food allergies are an important cause of life-threatening hypersensitivity reactions. Oral tolerance can be considered the default immune response to dietary antigens, with immune deviation resulting in allergic sensitization. However, primary sensitization to food allergens may not solely be through the gastrointestinal mucosa, as strong T-helper type 2 (Th2)-biased immunity can result from exposure to protein allergens on barrier-disrupted skin. The purpose of this study was to examine whether exposure to allergens through the skin may interfere with the normal development of oral tolerance and promote allergic sensitization to food proteins. Female BALB/c mice were exposed epicutaneously to peanut protein and induction of systemic oral tolerance through high dose feeds of peanut protein was subsequently assessed. Other mice were rendered tolerant prior to epicutaneous peanut exposure. Sensitivity to peanut was determined by assessing delayed-type hypersensitivity, proliferative, cytokine and antibody responses. Epicutaneous exposure to peanut protein induced potent Th2-type immunity with high levels of IL-4 and serum IgE. Primary skin exposure prevented the subsequent induction of oral tolerance to peanut in an antigen-specific manner. Upon oral challenge, mice became further sensitized and developed strong peanut-specific IL-4 and IgE responses. Furthermore, animals with existing tolerance to peanut were partly sensitized following epicutaneous exposure. Epicutaneous exposure to peanut protein can prevent induction of oral tolerance, and may even modify existing tolerance to peanut. Epidermal exposure to protein allergens selectively drives Th2-type responses, and as such may promote sensitization to food proteins upon gastrointestinal exposure.	UCL, Inst Child Hlth, Immunobiol Unit, London WC1N 1EH, England; Univ Southampton, Div Infect Inflammat & Repair, Southampton, Hants, England; Syngenta, Cent Toxicol Lab, Macclesfield, Cheshire, England; Peninsula Postgrad Hlth Inst, Plymouth, Devon, England	Strid, J (reprint author), UCL, Inst Child Hlth, Immunobiol Unit, 30 Guilford St, London WC1N 1EH, England.	j.strid@ich.ucl.ac.uk	Callard, Robin/C-5682-2008; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Strid, Jessica/0000-0003-3690-2201			Armitage P., 1971, STAT METHODS MED RES; Bilsborough J, 2002, IMMUNOLOGY, V106, P139, DOI 10.1046/j.1365-2567.2002.01445.x; Bock SA, 2001, J ALLERGY CLIN IMMUN, V107, P191, DOI 10.1067/mai.2001.112031; Cochet O, 1998, IMMUNOLOGICAL TECHNI; Crespo JF, 2003, ALLERGY, V58, P98, DOI 10.1034/j.1398-9995.2003.02170.x; deJong EC, 1996, J ALLERGY CLIN IMMUN, V98, P73, DOI 10.1016/S0091-6749(96)70228-2; Garside P, 2001, SEMIN IMMUNOL, V13, P177, DOI 10.1006/smim.2001.0310; Grundy J, 2002, J ALLERGY CLIN IMMUN, V110, P784, DOI 10.1067/mai.2002.128802; Hachem JP, 2003, J INVEST DERMATOL, V121, P345, DOI 10.1046/j.1523-1747.2003.12365.x; Herrick CA, 2000, J CLIN INVEST, V105, P765, DOI 10.1172/JCI8624; Herrick CA, 2003, J IMMUNOL, V170, P2488; Hourihane JO, 1996, BRIT MED J, V313, P518; Hsieh KY, 2003, CLIN EXP ALLERGY, V33, P1067, DOI 10.1046/j.1365-2222.2003.01724.x; Kagan RS, 2003, J ALLERGY CLIN IMMUN, V112, P1223, DOI 10.1016/j.jaci.2003.09.026; Lack G, 2003, NEW ENGL J MED, V348, P977, DOI 10.1056/NEJMoa013536; Leung DYM, 2003, NEW ENGL J MED, V348, P986, DOI 10.1056/NEJMoa022613; Leung DYM, 2003, LANCET, V361, P151, DOI 10.1016/S0140-6736(03)12193-9; Li XM, 2000, J ALLERGY CLIN IMMUN, V106, P150, DOI 10.1067/mai.2000.107395; Li XM, 1999, J IMMUNOL, V162, P3045; Novak Natalija, 2003, Journal of Allergy and Clinical Immunology, V112, pS128, DOI 10.1016/j.jaci.2003.09.032; Perry TT, 2004, J ALLERGY CLIN IMMUN, V113, P973, DOI 10.1016/j.jaci.2004.02.035; Roy K, 1999, NAT MED, V5, P387; Sampson HA, 2004, J ALLERGY CLIN IMMUN, V113, P805, DOI 10.1016/j.jaci.2004.03.014; Schleimer RP, 2000, J ALLERGY CLIN IMMUN, V106, pS191; Sicherer SH, 1999, J ALLERGY CLIN IMMUN, V104, pS114, DOI 10.1016/S0091-6749(99)70053-9; Sicherer SH, 2003, J ALLERGY CLIN IMMUN, V112, P1203, DOI 10.1016/S0091-6749(03)02026-8; Spergel JM, 1998, J CLIN INVEST, V101, P1614, DOI 10.1172/JCI1647; Strid J, 2004, EUR J IMMUNOL, V34, P2100, DOI 10.1002/eji.200324843; Strid J, 2004, IMMUNOLOGY, V113, P293, DOI 10.1111/j.1365-2567.2004.01989.x; STRID J, 2005, IN PRESS CURR DRUG T; Strobel S, 1998, IMMUNOL TODAY, V19, P173, DOI 10.1016/S0167-5699(97)01239-5; Wang L F, 1996, J Immunol, V156, P4077; Warner RR, 2003, J INVEST DERMATOL, V120, P275, DOI 10.1046/j.1523-1747.2003.12046.x; Weiner HL, 1997, IMMUNOL TODAY, V18, P335, DOI 10.1016/S0167-5699(97)01053-0; Werfel T, 2001, ALLERGY, V56, P98, DOI 10.1034/j.1398-9995.2001.00929.x; Wollenberg A, 2000, CLIN EXP DERMATOL, V25, P530, DOI 10.1046/j.1365-2230.2000.00699.x	36	113	116	0	5	WILEY-BLACKWELL	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	JUN	2005	35	6					757	766		10.1111/j.1365-2222.2005.02260.x		10	Allergy; Immunology	Allergy; Immunology	937WG	WOS:000229956100014	15969667	
J	Borkow, G; Gabbay, J				Borkow, G; Gabbay, J			Putting copper into action: copper-impregnated products with potent biocidal activities	FASEB JOURNAL			English	Article						HIV-1; filters; fabrics; dust mites; athlete's foot	METAL-IONS; INTRAUTERINE-DEVICES; BLOOD-TRANSFUSION; MARATHON RUNNERS; PLASMA-MEMBRANE; TINEA-PEDIS; VIRUS; INACTIVATION; MECHANISMS; HIV-1	Copper ions, either alone or in copper complexes, have been used for centuries to disinfect liquids, solids, and human tissue. Today copper is used as a water purifier, algaecide, fungicide, nematocide, molluscicide, and antibacterial and antifouling agent. Copper also displays potent antiviral activity. We hypothesized that introducing copper into clothing, bedding, and other articles would provide them with biocidal properties. A durable platform technology has been developed that introduces copper into cotton fibers, latex, and other polymeric materials. This study demonstrates the broad-spectrum antimicrobial ( antibacterial, antiviral, antifungal) and antimite activities of copper-impregnated fibers and polyester products. This technology enabled the production of antiviral gloves and filters (which deactivate HIV-1 and other viruses), antibacterial self-sterilizing fabrics (which kill antibiotic-resistant bacteria, including methicillin-resistant Staphylococcus aureus and vancomycin-resistant Enterococci), antifungal socks (which alleviate symptoms of athlete's foot), and anti-dust mite mattress covers (which reduce mite-related allergies). These products did not have skin-sensitizing properties, as determined by guine pig maximization and rabbit skin irritation tests. Our study demonstrates the potential use of copper in new applications. These applications address medical issues of the greatest importance, such as viral transmissions; nosocomial, or healthcare-associated, infections; and the spread of antibiotic-resistant bacteria.	Cupron Inc, New York, NY 10165 USA	Borkow, G (reprint author), Hameyasdim 44, IL-76910 Kfar Gibton, Israel.	gadi@cupron.com					AUGER P, 1993, MYCOSES, V36, P35; Avery SV, 1995, BIOCHEM J, V312, P811; Biggerstaff BJ, 2002, TRANSFUSION, V42, P1019, DOI 10.1046/j.1537-2995.2002.00167.x; Bilian X, 2002, BEST PRACT RES CL OB, V16, P155, DOI 10.1053/beog.2002.0267; Borkow G, 1997, BIOCHEMISTRY-US, V36, P3179, DOI 10.1021/bi9624696; Brunton SA, 1999, HOSP PRACT, V34, P67; CERVANTES C, 1994, FEMS MICROBIOL REV, V14, P121; Cooney JJ, 1999, METHOD ENZYMOL, V310, P637; COONEY TE, 1995, INFECT CONT HOSP EP, V16, P444; CORONEL D, 2000, REANIMATION, V9, P86; CORONEL D, 2001, REANIMATION S, V10, P43; Dollwet HH, 2001, TRACE ELEM MED, V2, P80; *FDA, 2003, MIN SAF EFF METH RED; Fowler MG, 2002, J ACQ IMMUN DEF SYND, V30, P230, DOI 10.1097/01.QAI.0000018364.28828.14; FRASER WD, 2001, 211 INCRA HUNT RES C, P43; Goodnough LT, 2003, LANCET, V361, P161, DOI 10.1016/S0140-6736(03)12195-2; HAZEL JR, 1990, PROG LIPID RES, V29, P167, DOI 10.1016/0163-7827(90)90002-3; Hellstern P, 2002, THROMB RES, V107, pS3, DOI 10.1016/S0049-3848(02)00145-7; Hess C, 2002, LANCET, V359, P2230, DOI 10.1016/S0140-6736(02)09291-7; Hostynek Jurij J, 2003, Rev Environ Health, V18, P153; Hubacher D, 2001, NEW ENGL J MED, V345, P561, DOI 10.1056/NEJMoa010438; International Diabetes Federation, 2000, DIAB ATL; JORDAN FTW, 1971, VET REC, V89, P609; KARLSTROM AR, 1991, P NATL ACAD SCI USA, V88, P5552, DOI 10.1073/pnas.88.13.5552; Kim JH, 2000, ARCH BIOCHEM BIOPHYS, V382, P72, DOI 10.1006/abbi.2000.1996; KIMPTON J, 1992, J VIROL, V66, P2232; Lacroix C, 2002, J EUR ACAD DERMATOL, V16, P139, DOI 10.1046/j.1468-3083.2002.00400.x; LOUDER M, 1999, HIV PROTOCOLS, P23; MAGNUSSON B, 1980, CONTACT DERMATITIS, V6, P46, DOI 10.1111/j.1600-0536.1980.tb03894.x; MASCOLA JR, 1999, HIV PROTOCOLS, P317; OHSUMI Y, 1988, J BACTERIOL, V170, P2676; Pena MMO, 1999, J NUTR, V129, P1251; Redd SC, 2002, ENVIRON HEALTH PERSP, V110, P557; ROBINSON MK, 1989, FOOD CHEM TOXICOL, V27, P479, DOI 10.1016/0278-6915(89)90036-7; RODRIGUEZMONTELONGO L, 1993, BIOCHIM BIOPHYS ACTA, V1144, P77, DOI 10.1016/0005-2728(93)90033-C; Sagripanti JL, 1996, AIDS RES HUM RETROV, V12, P333, DOI 10.1089/aid.1996.12.333; Sagripanti JL, 1997, ANTIMICROB AGENTS CH, V41, P812; SAGRIPANTI JL, 1993, APPL ENVIRON MICROB, V59, P4374; Silver S, 1996, GENE, V179, P9, DOI 10.1016/S0378-1119(96)00323-X; SKONER DP, 2000, J ALLERGY CLIN IMMUN, V100, pS2; Snyder E L, 2001, Hematology Am Soc Hematol Educ Program, P433; Spencer RC, 1994, INTENSIVE CARE ME S4, V20, P2; STOHS SJ, 1995, FREE RADICAL BIO MED, V18, P321, DOI 10.1016/0891-5849(94)00159-H; Stout JE, 1998, INFECT CONT HOSP EP, V19, P911; Strong DM, 2002, TRENDS MOL MED, V8, P355, DOI 10.1016/S1471-4914(02)02361-4; UEDA K, 1980, CHEM-BIOL INTERACT, V29, P145, DOI 10.1016/0009-2797(80)90029-0; Weber DJ, 2001, DISINFECTION STERILI, P415; Yahaya M.T., 2001, 48 INT COPP RES ASS; Youssefian T, 2002, BLOOD, V99, P4021, DOI 10.1182/blood-2001-12-0191; TAL M, 1999, Patent No. 5871816; 2002, DRUG THER B, V40, P67	51	113	121	6	51	FEDERATION AMER SOC EXP BIOL	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA	0892-6638			FASEB J	Faseb J.	SEP	2004	18	12					1728	+		10.1096/fj.04-2029fje		19	Biochemistry & Molecular Biology; Biology; Cell Biology	Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology	859DQ	WOS:000224243200042	15345689	
J	Strid, J; Hourihane, J; Kimber, I; Callard, R; Strobel, S				Strid, J; Hourihane, J; Kimber, I; Callard, R; Strobel, S			Disruption of the stratum corneum allows potent epicutaneous immunization with protein antigens resulting in a dominant systemic Th2 response	EUROPEAN JOURNAL OF IMMUNOLOGY			English	Article						skin; Th1/Th2 cells; allergy; Langerhans cells; vaccination	TUMOR-NECROSIS-FACTOR; DENDRITIC CELLS; LANGERHANS CELLS; PEANUT ALLERGY; AEROSOLIZED ANTIGEN; ATOPIC-DERMATITIS; IGE PRODUCTION; FOOD ALLERGY; FACTOR-ALPHA; BARE SKIN	The skin is an important immunological organ with an outer protective layer, the stratum corneum forming a barrier between the skin-associated lymphoid tissue and the environment. We show that gently removing the stratum corneum with adhesive tape permits potent epicutaneous immunization to protein antigens. IL-4 secretion by T cells from draining lymph nodes and high levels of specific IgE and IgG1 with no IgG2a showed that the immune responses induced following epicutaneous antigen exposure are strongly Th2 biased. Similar responses were obtained With different antigens and mouse strains. In contrast, subcutaneous immunization with antigen delivery into the dermis was less potent and gave predominantly Th1 responses. Removal of the stratum corneum increased expression of MHC class II, CD86, CD40, CD54 and CD11c on Langerhans cells, but did not cause them to migrate. Rapid migration from epidermis to draining lymph node was obtained, however, by exposure to antigen after removal of the stratum corneum, suggesting that maturation and migration of Langerhans cells are independently regulated events. These results suggest that antigen presentation by Langerhans cells gives predominantly Th2 responses. This may provide an explanation for allergic sensitization to some antigens. It may also be a useful non-invasive, non-adjuvant-dependent method of vaccination.	UCL, Inst Child Hlth, Immunobiol Unit, London WC1N 1EH, England; Southampton Univ Hosp NHS Trust, Wellcome Trust Clin Res Facil, Southampton, Hants, England; Syngenta, Cent Toxicol Lab, Macclesfield, Cheshire, England	Strid, J (reprint author), UCL, Inst Child Hlth, Immunobiol Unit, 30 Guilford St, London WC1N 1EH, England.	j.strid@ich.ucl.ac.uk	Callard, Robin/C-5682-2008	Strid, Jessica/0000-0003-3690-2201			Banchereau J, 1998, NATURE, V392, P245, DOI 10.1038/32588; Beignon AS, 2002, IMMUNOLOGY, V105, P204, DOI 10.1046/j.0019-2805.2001.01357.x; Beignon AS, 2001, IMMUNOLOGY, V102, P344, DOI 10.1046/j.1365-2567.2001.01183.x; Cochet O, 1998, IMMUNOLOGICAL TECHNI; Cumberbatch M, 2001, IMMUNOLOGY, V102, P323, DOI 10.1046/j.1365-2567.2001.01187.x; Cumberbatch M, 1997, IMMUNOLOGY, V92, P388, DOI 10.1046/j.1365-2567.1997.00360.x; Darsow U, 1996, BRIT J DERMATOL, V135, P182, DOI 10.1111/j.1365-2133.1996.tb01144.x; deJong EC, 1996, J ALLERGY CLIN IMMUN, V98, P73, DOI 10.1016/S0091-6749(96)70228-2; Elbe-Burger A, 2002, J INVEST DERMATOL, V118, P767, DOI 10.1046/j.1523-1747.2002.01753.x; ELIAS PM, 1991, ADV LIPID RES, V24, P1; Finkelman FD, 1996, J IMMUNOL, V157, P1406; Geissmann F, 2002, J EXP MED, V196, P417, DOI 10.1084/jem.20020018; Glenn GM, 1998, NATURE, V391, P851, DOI 10.1038/36014; HAUSER C, 1989, EUR J IMMUNOL, V19, P245, DOI 10.1002/eji.1830190205; Herrick CA, 2000, J CLIN INVEST, V105, P765, DOI 10.1172/JCI8624; Herrick CA, 2003, J IMMUNOL, V170, P2488; Hourihane JO, 1996, BRIT MED J, V313, P518; Kimber I, 2000, BRIT J DERMATOL, V142, P401, DOI 10.1046/j.1365-2133.2000.03349.x; Kondo H, 1998, EUR J IMMUNOL, V28, P769, DOI 10.1002/(SICI)1521-4141(199803)28:03<769::AID-IMMU769>3.0.CO;2-H; Lack G, 2003, NEW ENGL J MED, V348, P977, DOI 10.1056/NEJMoa013536; Luft T, 2002, BLOOD, V100, P1362, DOI 10.1182/blood-2001-12-0360; Lutz MB, 1996, EUR J IMMUNOL, V26, P586, DOI 10.1002/eji.1830260313; Matsui K, 2002, CLIN EXP ALLERGY, V32, P783, DOI 10.1046/j.1365-2222.2002.01357.x; Maurer D, 2001, DENDRITIC CELLS, P35, DOI 10.1016/B978-012455851-9/50044-4; MCMENAMIN C, 1994, SCIENCE, V265, P1869, DOI 10.1126/science.7916481; Nelde A, 2001, INT ARCH ALLERGY IMM, V124, P461, DOI 10.1159/000053781; NICKOLOFF BJ, 1994, J AM ACAD DERMATOL, V30, P535; NICKOLOFF BJ, 1994, CLIN IMMUNOL IMMUNOP, V73, P63, DOI 10.1006/clin.1994.1170; Nishijima T, 1997, J INVEST DERMATOL, V109, P175, DOI 10.1111/1523-1747.ep12319282; RENZ H, 1992, J ALLERGY CLIN IMMUN, V89, P1127, DOI 10.1016/0091-6749(92)90296-E; ROAKE JA, 1995, J EXP MED, V181, P2237, DOI 10.1084/jem.181.6.2237; Sampson HA, 1999, J ALLERGY CLIN IMMUN, V103, P717, DOI 10.1016/S0091-6749(99)70411-2; Scandella E, 2002, BLOOD, V100, P1354, DOI 10.1182/blood-2002-11-0017; Sicherer SH, 1999, J ALLERGY CLIN IMMUN, V104, pS114, DOI 10.1016/S0091-6749(99)70053-9; Spergel JM, 1998, J CLIN INVEST, V101, P1614, DOI 10.1172/JCI1647; Stumbles PA, 1998, J EXP MED, V188, P2019, DOI 10.1084/jem.188.11.2019; Viney JL, 1998, J IMMUNOL, V160, P5815; Wang L F, 1996, J Immunol, V156, P4077; Werfel T, 2001, ALLERGY, V56, P98, DOI 10.1034/j.1398-9995.2001.00929.x; Williamson E, 1999, J IMMUNOL, V163, P3668; Wollenberg A, 2000, CLIN EXP DERMATOL, V25, P530, DOI 10.1046/j.1365-2230.2000.00699.x; WOOD LC, 1992, J CLIN INVEST, V90, P482, DOI 10.1172/JCI115884	42	113	117	0	2	WILEY-BLACKWELL	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0014-2980			EUR J IMMUNOL	Eur. J. Immunol.	AUG	2004	34	8					2100	2109		10.1002/eji.200324843		10	Immunology	Immunology	844RR	WOS:000223177800005	15259007	
J	Myou, S; Leff, AR; Myo, S; Boetticher, E; Tong, JK; Meliton, AY; Liu, J; Munoz, NM; Zhu, XD				Myou, S; Leff, AR; Myo, S; Boetticher, E; Tong, JK; Meliton, AY; Liu, J; Munoz, NM; Zhu, XD			Blockade of inflammation and airway hyperresponsiveness in immune-sensitized mice by dominant-negative phosphoinositide 3-kinase-TAT	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article						allergy; cytokines; eosinophils; lung; inflammation	FC-EPSILON-RI; IN-VIVO; HUMAN EOSINOPHILS; PHOSPHATIDYLINOSITOL 3-KINASE; BRONCHIAL RESPONSIVENESS; GENE-EXPRESSION; GUINEA-PIGS; MAST-CELLS; B-CELLS; ASTHMA	Phosphoinositide 3-kinase (PI3K) is thought to contribute to the pathogenesis of asthma by effecting the recruitment, activation, and apoptosis of inflammatory cells. We examined the role of class IA PI3K in antigen-induced air-way inflammation and hyperresponsiveness by i.p. administration into mice of Deltap85 protein, a dominant negative form of the class IA PI3K regulatory subunit, p85alpha, which was fused to HIV-TAT (TAT-Deltap85). Intraperitoneal administration of TXT-Deltap85 caused time-dependent transduction into blood leukocytes, and inhibited activated phosphorylation of protein kinase B (PKB), a downstream target of PI3K, in lung tissues in mice receiving intranasal FMLP. Antigen challenge elicited pulmonary infiltration of lymphocytes, eosinophils and neutrophils, increase in mucus-containing epithelial cells, and airway hyperresponsiveness to methacholine. Except for modest airway neutrophilia, these effects all were blocked by treatment with 3-10 mg/kg of TAT-Deltap85. There was also significant reduction in IL-5 and IL-4 secretion into the BAL. Intranasal administration of IL-5 caused eosinophil migration into the air-way lumen, which was attenuated by systemic pretreatment with TAT-Deltap85. We conclude that PI3K has a regulatory role in Th2-cell cytokine secretion, airway inflammation, and air-way hyperresponsiveness in mice.	Univ Chicago, Dept Med, Pulm & Crit Care Med Sect, Chicago, IL 60637 USA; Univ Chicago, Dept Neurobiol & Physiol, Chicago, IL 60637 USA; Univ Chicago, Comm Mol Med, Chicago, IL 60637 USA; Univ Chicago, Comm Clin Pharmacol, Chicago, IL 60637 USA; Univ Chicago, Comm Cell Physiol, Chicago, IL 60637 USA	Leff, AR (reprint author), Univ Chicago, Dept Med, Pulm & Crit Care Med Sect, 5841 S Maryland Ave, Chicago, IL 60637 USA.	aleff@medicine.bsd.uchicago.edu			NHLBI NIH HHS [HL-46368, HL-56399, P50 HL056399, R01 HL046368]; NIAID NIH HHS [AI-52109, K08 AI052109]		ARCARO A, 1993, BIOCHEM J, V296, P297; BOCHNER BS, 1994, ANNU REV IMMUNOL, V12, P295; BONSER RW, 1991, BRIT J PHARMACOL, V103, P1237; Bracke M, 2000, J LEUKOCYTE BIOL, V68, P655; Chou MM, 1998, CURR BIOL, V8, P1069, DOI 10.1016/S0960-9822(98)70444-0; COFFMAN RL, 1986, J IMMUNOL, V136, P4538; CROSS MJ, 1995, J BIOL CHEM, V270, P25352; CUSS FM, 1986, LANCET, V2, P189; Dabbagh K, 1999, J IMMUNOL, V162, P6233; DHAND R, 1994, EMBO J, V13, P511; Duguet A, 2000, AM J RESP CRIT CARE, V161, P839; Dunzendorfer S, 1998, J LEUKOCYTE BIOL, V64, P828; Evans DJ, 1999, AM J PHYSIOL-LUNG C, V277, pL233; Ezeamuzie CI, 2001, AM J RESP CRIT CARE, V164, P1633; Ford JG, 2001, J IMMUNOL, V167, P1769; Foster PS, 1996, J EXP MED, V183, P195, DOI 10.1084/jem.183.1.195; Fruman DA, 2000, NAT GENET, V26, P379; Fruman DA, 1999, SCIENCE, V283, P393, DOI 10.1126/science.283.5400.393; Fujitani Y, 2003, AM J RESP CRIT CARE, V167, P193, DOI 10.1164/rccm.200205-455OC; Fukao T, 2002, NAT IMMUNOL, V3, P295, DOI 10.1038/ni768; Fukao T, 2002, NAT IMMUNOL, V3, P875, DOI 10.1038/ni825; Hall DJ, 2001, BLOOD, V98, P2014, DOI 10.1182/blood.V98.7.2014; HAMID Q, 1991, J CLIN INVEST, V87, P1541, DOI 10.1172/JCI115166; HSIEH CS, 1992, P NATL ACAD SCI USA, V89, P6065, DOI 10.1073/pnas.89.13.6065; Humbles AA, 2000, NATURE, V406, P998; KOTANI K, 1994, EMBO J, V13, P2313; Krymskaya VP, 1999, AM J PHYSIOL-LUNG C, V277, pL65; Kwak YG, 2003, J CLIN INVEST, V111, P1083, DOI 10.1172/JCI200316440; Le Good JA, 1998, SCIENCE, V281, P2042, DOI 10.1126/science.281.5385.2042; Lefort J, 1996, J CLIN INVEST, V97, P1117, DOI 10.1172/JCI118505; Mathur M, 1999, AM J RESP CRIT CARE, V159, P580; MAUSER PJ, 1995, AM J RESP CRIT CARE, V152, P467; MOSER R, 1992, J IMMUNOL, V149, P1432; Myou S, 2002, J IMMUNOL, V169, P2670; Nagahara H, 1998, NAT MED, V4, P1449, DOI 10.1038/4042; Page K, 1999, J BIOL CHEM, V274, P22065, DOI 10.1074/jbc.274.31.22065; Palframan RT, 1998, J EXP MED, V188, P1621, DOI 10.1084/jem.188.9.1621; Pawankar R, 1997, J CLIN INVEST, V99, P1492, DOI 10.1172/JCI119311; Powell N, 2001, J ALLERGY CLIN IMMUN, V108, P915, DOI 10.1067/mai.2001.119742; RABE KF, 1994, AM J PHYSIOL, V267, pL326; ROBINSON D, 1993, AM REV RESPIR DIS, V148, P401; Sasaki T, 2000, SCIENCE, V287, P1040, DOI 10.1126/science.287.5455.1040; Schwarze SR, 1999, SCIENCE, V285, P1569, DOI 10.1126/science.285.5433.1569; SEDER RA, 1992, J EXP MED, V176, P1091, DOI 10.1084/jem.176.4.1091; Smith AJ, 2001, J BIOL CHEM, V276, P17213, DOI 10.1074/jbc.M100417200; Strek ME, 1996, AM J PHYSIOL-LUNG C, V270, pL133; Vachier I, 1997, AM J RESP CRIT CARE, V155, P1211; WEISS JW, 1982, SCIENCE, V216, P196, DOI 10.1126/science.7063880; WHITE SR, 1993, J CLIN INVEST, V91, P2118, DOI 10.1172/JCI116436; WHITMAN M, 1988, NATURE, V332, P644, DOI 10.1038/332644a0; Zhu XD, 2002, J LEUKOCYTE BIOL, V72, P1046	51	113	126	0	3	ROCKEFELLER UNIV PRESS	NEW YORK	1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA	0022-1007			J EXP MED	J. Exp. Med.	NOV 17	2003	198	10					1573	1582		10.1084/jem.20030298		10	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	748CX	WOS:000186845600012	14623911	
J	Lehrer, P; Feldman, J; Giardino, N; Song, HS; Schmaling, K				Lehrer, P; Feldman, J; Giardino, N; Song, HS; Schmaling, K			Psychological aspects of asthma	JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY			English	Review							PEAK EXPIRATORY FLOW; NEAR-FATAL ASTHMA; SELF-MANAGEMENT PROGRAM; RESPIRATORY SINUS ARRHYTHMIA; INSPIRATORY RESISTIVE LOADS; LIFE-THREATENING ASTHMA; VOCAL CORD DYSFUNCTION; INNER-CITY CHILDREN; RANDOMIZED CONTROLLED-TRIAL; HEALTH BELIEF MODEL	Asthma can be affected by stress, anxiety, sadness, and suggestion, as well as by environmental irritants or allergens, exercise, and infection. It also is associated with an elevated prevalence of anxiety and depressive disorders. Asthma and these psychological states and traits may mutually potentiate each other through direct psychophysiological mediation, nonadherence to medical regimen, exposure to asthma triggers, and inaccuracy of asthma symptom perception. Defensiveness is associated with inaccurate perception of airway resistance and stress-related bronchoconstriction. Asthma education programs that teach about the nature of the disease, medications, and trigger avoidance tend to reduce asthma morbidity. Other promising psychological interventions as adjuncts to medical treatment include training in symptom perception, stress management, hypnosis, yoga, and several biofeedback procedures.	Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Psychiat, Piscataway, NJ 08854 USA; Rutgers State Univ, Dept Psychol, Piscataway, NJ 08855 USA; Univ Texas, Dept Hlth Sci, El Paso, TX 79968 USA	Lehrer, P (reprint author), Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Psychiat, 671 Hoes Lane, Piscataway, NJ 08854 USA.	lehrer@umdnj.edu	Schmaling, Karen/F-5217-2011	Schmaling, Karen/0000-0003-2085-134X	NHLBI NIH HHS [R01 HL058805-03, R01 HL58805]; NIMH NIH HHS [R21 MH058196-03, R21MH58196A]		ABDULWADUD O, 1997, PATIENT EDUC COUNS, V39, P253; Adams S, 1997, SOC SCI MED, V45, P189, DOI 10.1016/S0277-9536(96)00333-4; Afari N, 2001, J CLIN PSYCHOL MED S, V8, P245, DOI 10.1023/A:1011912712262; Affleck G, 2000, PSYCHOSOM MED, V62, P61; Ajzen I., 1985, ACTION CONTROL COGNI, P1; Apter AJ, 1997, J ALLERGY CLIN IMMUN, V99, P605, DOI 10.1016/S0091-6749(97)70020-4; Apter AJ, 1998, AM J RESP CRIT CARE, V157, P1810; Apter AJ, 2001, ANN ALLERG ASTHMA IM, V86, P421; ARNTZ A, 1994, PAIN, V56, P307, DOI 10.1016/0304-3959(94)90169-4; 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Consult. Clin. Psychol.	JUN	2002	70	3					691	711		10.1037//0022-006X.70.3.691		21	Psychology, Clinical	Psychology	562LJ	WOS:000176198000016	12090377	
J	Downs, SH; Mitakakis, TZ; Marks, GB; Car, NG; Belousova, EG; Leuppi, JD; Xuan, W; Downie, SR; Tobias, A; Peat, JK				Downs, SH; Mitakakis, TZ; Marks, GB; Car, NG; Belousova, EG; Leuppi, JD; Xuan, W; Downie, SR; Tobias, A; Peat, JK			Clinical importance of Alternaria exposure in children	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						Alternaria; airway responsiveness; asthma; fungi; children	BRONCHIAL RESPONSIVENESS; ALLERGIC SENSITIZATION; LONGITUDINAL DATA; CHILDHOOD ASTHMA; CLIMATIC REGIONS; ALT-I; POPULATION; SEVERITY; OUTDOOR; SPORE	The fungus Alternaria is known to be allergenic and is one of the most common fungi worldwide. We investigated the extent to which exposure to Alternaria increases the severity of asthma. We undertook a prospective cohort study in Australia of 399 school children who had positive skin tests to one or more aeroallergens. Airway responsiveness to histamine, wheeze, and bronchodilator use in 1 mo was measured five times between 1997 and 1999. Airway hyperresponsiveness was defined as PD20FEV1 = 3.9 mu mol histamine. Airborne concentrations of Alternaria spores were measured throughout the study, and mean daily concentrations over 1 mo ranged from 2.2 to 307.7 spores/m(3) of ambient air. Using generalized estimating equations, we found that airway responsiveness, wheeze, and bronchodilator use increased significantly in association with increased spore concentrations and that the increase in airway responsiveness was greater in children sensitized to Alternarxia than in other children (p = 0.01). The odds ratio for airway hyperresponsiveness in children sensitized to Alternaria was 1.26 (95% CI, 1.14 to 1.39) after an increase in mean exposure of 100 spore/m(3)/d over 1 mo. These results suggest that Alternaria allergens contribute to severe asthma in regions where exposure to the fungus is high.	Univ Sydney, Inst Resp Med, Sydney, NSW, Australia; Univ Sydney, Sch Biol Sci, Sydney, NSW, Australia; Charles Sturt Univ, Sch Biomed Sci, Wagga Wagga, NSW, Australia; New Childrens Hosp, Clin Epidemiol Unit, Westmead, NSW, Australia; Hosp Santa Cruz & San Pablo, Dept Clin Epidemiol & Publ Hlth, Barcelona, Spain	Downs, SH (reprint author), Inst Resp Med, POB M77,Missenden Rd Post Off, Camperdown, NSW 2050, Australia.		Downs, Sara/D-8478-2011	Downs, Sara/0000-0003-1044-3182			AGARWAL MK, 1983, J ALLERGY CLIN IMMUN, V72, P40, DOI 10.1016/0091-6749(83)90050-7; Armstrong B.K., 1995, PRINCIPLES EXPOSURE; Barnes C, 2000, ANN ALLERG ASTHMA IM, V84, P47, DOI 10.1016/S1081-1206(10)62740-8; Bass D, 1997, GRANA, V36, P293; BOULET LP, 1983, J ALLERGY CLIN IMMUN, V71, P399, DOI 10.1016/0091-6749(83)90069-6; CALVO MA, 1980, MYCOPATHOLOGIA, V71, P89, DOI 10.1007/BF00440614; Chelkowski J, 1992, ALTERNARIA BIOL PLAN; DAMATO G, 1995, ALLERGY, V50, P870, DOI 10.1111/j.1398-9995.1995.tb02492.x; Delfino RJ, 1997, ENVIRON HEALTH PERSP, V105, P622; FADEL R, 1992, ANN ALLERGY, V69, P329; GERGEN PJ, 1992, J ALLERGY CLIN IMMUN, V90, P579, DOI 10.1016/0091-6749(92)90130-T; Halonen M, 1997, AM J RESP CRIT CARE, V155, P1356; HATCH M, 1993, ENVIRON HEALTH PERSP, V101, P49, DOI 10.2307/3431659; HJELMROOS M, 1993, GRANA, V32, P40; HORNER WE, 1995, CLIN MICROBIOL REV, V8, P161; JUNIPER EF, 1990, AM REV RESPIR DIS, V142, P832; KAUFFMAN HF, 1995, AM J RESP CRIT CARE, V151, P2109; LICORISH K, 1985, J ALLERGY CLIN IMMUN, V76, P819, DOI 10.1016/0091-6749(85)90755-9; Mitakakis T, 1997, AEROBIOLOGIA, V13, P83, DOI 10.1007/BF02694423; Mitakakis TZ, 2000, GRANA, V39, P141; Mitakakis TZ, 2000, CLIN EXP ALLERGY, V30, P1733, DOI 10.1046/j.1365-2222.2000.00966.x; Neukirch C, 1999, J ALLERGY CLIN IMMUN, V103, P709, DOI 10.1016/S0091-6749(99)70247-2; OCONNOR G, 1987, AM REV RESPIR DIS, V136, P1412; OHOLLAREN MT, 1991, NEW ENGL J MED, V324, P359, DOI 10.1056/NEJM199102073240602; PEAT JK, 1991, AM REV RESPIR DIS, V144, P663; PEAT JK, 1993, CLIN EXP ALLERGY, V23, P812, DOI 10.1111/j.1365-2222.1993.tb00258.x; PEAT JK, 1995, MED J AUSTRALIA, V163, P22; Pepys J., 1975, BRIT J HOSP MED, V14, P412; PLATTSMILLS TAE, 1982, LANCET, V2, P675; QUANJER PH, 1995, PEDIATR PULM, V19, P135, DOI 10.1002/ppul.1950190209; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; SNELLER MR, 1981, ANN ALLERGY, V46, P30; Sont JK, 1996, THORAX, V51, P496, DOI 10.1136/thx.51.5.496; SRIVASTAVA AK, 1992, GRANA, V31, P61; Takahashi T, 1997, MYCOPATHOLOGIA, V139, P23, DOI 10.1023/A:1006831111595; TOELLE BG, 1992, AM REV RESPIR DIS, V146, P633; Ulrik CS, 1999, EUR RESPIR J, V13, P904, DOI 10.1034/j.1399-3003.1999.13d35.x; USHERWOOD TP, 1990, ARCH DIS CHILD, V65, P779; YAN K, 1983, THORAX, V38, P760, DOI 10.1136/thx.38.10.760; YUNGINGER JW, 1980, J ALLERGY CLIN IMMUN, V66, P138, DOI 10.1016/0091-6749(80)90061-5; ZEGER SL, 1988, BIOMETRICS, V44, P1049, DOI 10.2307/2531734; ZEGER SL, 1986, BIOMETRICS, V42, P121, DOI 10.2307/2531248	42	113	117	0	5	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	AUG 1	2001	164	3					455	459				5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	466NG	WOS:000170651200022	11500349	
J	Johnson, PRA; Black, JL; Carlin, S; Ge, Q; Underwood, PA				Johnson, PRA; Black, JL; Carlin, S; Ge, Q; Underwood, PA			The production of extracellular matrix proteins by human passively sensitized airway smooth-muscle cells in culture - The effect of beclomethasone	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							SUBEPITHELIAL FIBROSIS; ALTERED RESPONSIVENESS; FIBRONECTIN EXPRESSION; BRONCHIAL-ASTHMA; ADHESION; PROLIFERATION; DEXAMETHASONE; ANTIBODIES; INHIBITION; COLLAGEN	Airway remodeling is a key feature of persistent asthma. Part of the remodeling process involves the laying down of extracellular matrix (ECM) proteins within the airways. In this study we compared the production of ECM proteins by human airway smooth-muscle (ASM) cells in culture after exposure to 10% serum from an asthmatic individual or 10% serum from a nonasthmatic individual with or without beclomethasone (0.01 to 100 nM). Enzyme-linked immunosorbent assays were done with antibodies to human fibronectin; perlecan; elastin; the laminin beta (1), gamma (1), beta (2), alpha (1), chains; thrombospondin; chondroitin sulfate; collagen types I, III, IV, and V; versican; and decorin. Serum from the asthmatic individual, when compared with that from the nonasthmatic individual, caused a significant increase in the production of fibronectin, perlecan, laminin gamma (1), and chondroitin sulfate. Beclomethasone caused a significant reduction in the number of cells exposed to serum from either the asthmatic or nonasthmatic individual, but did not reverse the increase in ECM protein induced by the former. These results suggest an interaction between the ASM and the allergic process that may alter components of the airway wall in asthma, and that corticosteroids may not prevent the fibrosis induced by resident cells within the airways.	Univ Sydney, Dept Pharmacol, Sydney, NSW 2006, Australia; CSIRO Mol Sci, N Ryde, NSW, Australia	Johnson, PRA (reprint author), Univ Sydney, Dept Pharmacol, Sydney, NSW 2006, Australia.		Black, Judith/C-6559-2008; Ge, Qi/D-3988-2013				AKIYAMA SK, 1989, J CELL BIOL, V109, P863, DOI 10.1083/jcb.109.2.863; BARNES PJ, 1990, AM REV RESPIR DIS S, V141, P70; Black JL, 2000, AM J RESP CRIT CARE, V161, pS207; BOUSQUET J, 1992, ALLERGY, V47, P3, DOI 10.1111/j.1398-9995.1992.tb02242.x; BREWSTER CEP, 1990, AM J RESP CELL MOL, V3, P507; Carlin S, 1999, AM J PHYSIOL-LUNG C, V276, pL506; Dunsmore SE, 1996, AM J PHYSIOL-LUNG C, V270, pL215; EBINA M, 1993, AM REV RESPIR DIS, V148, P720; ERLE DJ, 1992, AM J RESP CELL MOL, V6, P459; Fernandes D, 1999, AM J RESP CELL MOL, V21, P77; GOSPODAROWICZ D, 1981, J CELL PHYSIOL, V109, P69, DOI 10.1002/jcp.1041090109; Hakonarson H, 1998, P NATL ACAD SCI USA, V95, P5257, DOI 10.1073/pnas.95.9.5257; Hakonarson H, 1999, J CLIN INVEST, V103, P1077, DOI 10.1172/JCI5809; Hakonarson H, 1997, J CLIN INVEST, V99, P117, DOI 10.1172/JCI119122; HIRST SJ, 1997, AM J RESP CRIT CARE, V155, pA371; JEFFERY PK, 1992, AM REV RESPIR DIS, V145, P890; John M, 1997, J IMMUNOL, V158, P1841; Kylmaniemi M, 1996, J DENT RES, V75, P919; Laitinen A, 1997, AM J RESP CRIT CARE, V156, P951; LAITINEN LA, 1995, INT ARCH ALLERGY IMM, V107, P215; Laitinen LA, 1996, J ALLERGY CLIN IMMUN, V98, pS3, DOI 10.1016/S0091-6749(96)80122-9; NAKAMURA Y, 1995, AM J PHYSIOL-LUNG C, V269, pL377; Naureckas ET, 1999, AM J RESP CRIT CARE, V160, P2062; Rabe KF, 1998, AM J RESP CRIT CARE, V157, P1429; Roberts C R, 1998, Can Respir J, V5, P48; ROCHE WR, 1989, LANCET, V1, P520; SCHLEIMER RP, 1990, AM REV RESPIR DIS, V141, pS59; SCHLEIMER RP, 1987, AM REV RESPIR DIS, V135, P562; Schramm CM, 1996, BRIT J PHARMACOL, V119, P807; Shiels IA, 1996, INFLAMMATION, V20, P373, DOI 10.1007/BF01486740; Shiels IA, 1999, INFLAMMATION, V23, P321; STEWART AG, 1995, AM J RESP CELL MOL, V12, P110; Underwood PA, 1998, ATHEROSCLEROSIS, V141, P141, DOI 10.1016/S0021-9150(98)00164-6; UNDERWOOD PA, 1992, J CELL SCI, V102, P833; UOTILA P, 1986, ACTA DERM-VENEREOL, V66, P381; Vigano T, 1997, AM J RESP CRIT CARE, V155, P864; Vignola AM, 1997, AM J RESP CRIT CARE, V156, P591	37	113	123	0	1	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	DEC	2000	162	6					2145	2151				7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	381ZV	WOS:000165794700031	11112129	
J	Letuve, S; Kozhich, A; Arouche, N; Grandsaigne, M; Reed, J; Dombret, MC; Kiener, PA; Aubier, M; Coyle, AJ; Pretolani, M				Letuve, Severine; Kozhich, Alexander; Arouche, Nassim; Grandsaigne, Martine; Reed, Jennifer; Dombret, Marie-Christine; Kiener, Peter A.; Aubier, Michel; Coyle, Anthony J.; Pretolani, Marina			YKL-40 is elevated in patients with chronic obstructive pulmonary disease and activates alveolar macrophages	JOURNAL OF IMMUNOLOGY			English	Article							SERUM YKL-40; STIMULATES PROLIFERATION; CHITINASE FAMILY; SEVERE ASTHMA; PROTEIN; LUNG; INFLAMMATION; COLLAGEN; HC-GP39; DIFFERENTIATION	YKL-40 is a chitin-binding protein that is elevated in patients with various inflammatory conditions associated with ongoing remodeling. We investigated whether the levels of YKL-40 were up-regulated in the circulation and the airways of patients with chronic obstructive pulmonary disease (COPD), and whether it promoted the production of inflammatory mediators from macrophages. Serum, bronchoalveolar lavage (BAL), bronchial biopsies, lung tissue specimens, and alveolar macrophages from never-smokers (n = 15), smokers without COPD (n = 20), and smokers with COPD (n = 30) were assessed for YKL-40 levels and immunolocalization. In addition, YKL-40-induced mediator release from alveolar macrophages was examined. We found that smokers with COPD had elevated levels of YKL-40 in serum (p <= 0.027) and BAL (p <= 0.007), more YKL-40-positive cells in bronchial biopsies (p <= 0.03), and a greater proportion of alveolar macrophages expressing YKL-40 than smokers without COPD or never-smokers. YKL-40 levels in serum and BAL were associated with airflow obstruction (pre-beta(2) agonist forced expiratory volume in 1 s, r(s) = -0.3892,p = 0.0072 and r(s) = -0.5491, p < 0.0001, respectively) and impaired diffusion lung capacity (transfer factor of the lung for carbon monoxide, r(s) = -0.4667, p = 0.002 and r(s) = -0.3854, p = 0.0045, respectively). TNF-alpha stimulated YKL-40 synthesis in alveolar macrophages from smokers with COPD, and exposure of these cells to YKL-40 promoted the release of IL-8, MCP-1, MIP-1 alpha, and metalloproteinase-9. We conclude that YKL-40 is up-regulated in COPD, in which it may contribute to tissue inflammation and remodeling by sustaining the synthesis of proinflammatory and fibrogenic chemokines and of metalloproteinases by alveolar macrophages.	[Pretolani, Marina] INSERM, Unite 700, Fac Med Denis Diderot, F-75018 Paris, France; [Letuve, Severine; Arouche, Nassim; Grandsaigne, Martine; Aubier, Michel; Pretolani, Marina] Univ Paris 07, Fac Med Denis Diderot, Paris, France; [Kozhich, Alexander; Reed, Jennifer; Kiener, Peter A.; Coyle, Anthony J.] MedImmune, Dept Autoimmun Inflammat & Resp Dis, Gaithersburg, MD 20878 USA; [Dombret, Marie-Christine; Aubier, Michel] CHU Bichat Claude Bernard, Dept Pneumol A, Paris, France; [Dombret, Marie-Christine; Aubier, Michel; Pretolani, Marina] AP HP, Paris, France	Pretolani, M (reprint author), INSERM, Unite 700, Fac Med Denis Diderot, Site Bichat 16,Rue Henri Huchard, F-75018 Paris, France.	marina.pretolani@inserm.fr	Pretolani, Marina/G-6643-2017		Agence Nationale de la Recherche (Sante et Environnement-Sante Travail); MedImmune	This work was supported by the Fondation pour la Recherche Medicale (fellowship to S.L.) and by grants from the Agence Nationale de la Recherche (Sante et Environnement-Sante Travail) and from MedImmune.	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Immunol.	OCT 1	2008	181	7					5167	5173		10.4049/jimmunol.181.7.5167		7	Immunology	Immunology	356CG	WOS:000259755700081	18802121	
J	Halonen, JI; Lanki, T; Yli-Tuomi, T; Kulmala, M; Tiittanen, P; Pekkanen, J				Halonen, J. I.; Lanki, T.; Yli-Tuomi, T.; Kulmala, M.; Tiittanen, P.; Pekkanen, J.			Urban air pollution, and asthma and COPD hospital emergency room visits	THORAX			English	Article							ULTRAFINE PARTICLES; PARTICULATE MATTER; SHORT-TERM; NUMBER; HEALTH; ADMISSIONS; INFLAMMATION; POLLUTANTS; EXPOSURE; DISEASE	Background: There is little previous information of the effects of size fractioned particulate air pollution and source specific fine particles (PM(2.5); <2.5 mu m) on asthma and chronic obstructive pulmonary disease (COPD) among children, adults and the elderly. Objectives: To determine the effects of daily variation in levels of different particle size fractions and gaseous pollutants on asthma and COPD by age group. Methods: Levels of particulate air pollution, NO(2) and CO were measured from 1998 to 2004 at central outdoor monitoring sites in Helsinki, Finland. Associations between daily pollution levels and hospital emergency room visits were evaluated for asthma (ICD10: J45+J46) in children,15 years old, and for asthma and COPD (ICD10: J41+J44) in adults (15-64 years) and the elderly (>= 65 years). Results: Three to 5 day lagged increases in asthma visits were found among children in association with nucleation (<0.03 mu m), Aitken (0.03-0.1 mu m) and accumulation (0.1-0.29 mu m) mode particles, gaseous pollutants and traffic related PM(2.5) (7.8% (95% CI 3.5 to 12.3) for 1.1 mu g/m(3) increase in traffic related PM(2.5) at lag 4). Pooled asthma-COPD visits among the elderly were associated with lag 0 of PM(2.5), coarse particles, gaseous pollutants and long range transported and traffic related PM(2.5) (3.9% (95% CI 0.28 to 7.7) at lag 0). Only accumulation mode and coarse particles were associated with asthma and COPD among adults. Conclusions: Among children, traffic related PM(2.5) had delayed effects, whereas among the elderly, several types of particles had effects that were more immediate. These findings suggest that the mechanisms of the respiratory effects of air pollution, and responsible pollutants, differ by age group.	[Halonen, J. I.; Lanki, T.; Yli-Tuomi, T.; Tiittanen, P.; Pekkanen, J.] Natl Publ Hlth Inst KTL, Environm Epidemiol Unit, FIN-70701 Kuopio, Finland; [Lanki, T.] GSF, Helmholtz Zentrum Munchen, Inst Epidemiol, Munich, Germany; [Kulmala, M.] Univ Helsinki, Dept Phys Sci, FIN-00014 Helsinki, Finland; [Pekkanen, J.] Univ Kuopio, Sch Publ Hlth & Clin Nutr, FIN-70211 Kuopio, Finland	Halonen, JI (reprint author), Natl Publ Hlth Inst KTL, Environm Epidemiol Unit, POB 95, FIN-70701 Kuopio, Finland.	jaana.halonen@ktl.fi	Kulmala, Markku/I-7671-2016	Kulmala, Markku/0000-0003-3464-7825; Yli-Tuomi, Tarja/0000-0001-9332-2241			ANDERSEN ZJ, 2007, J EXPO SCI ENV EPID, V7, P625; Anderson HR, 1998, THORAX, V53, P842; ANDERSON PJ, 1990, CHEST, V97, P1115, DOI 10.1378/chest.97.5.1115; Atkinson RW, 2001, AM J RESP CRIT CARE, V164, P1860; Barnett AG, 2005, AM J RESP CRIT CARE, V171, P1272, DOI 10.1164/rccm.200411-1586OC; Buzorius G, 1999, ATMOS ENVIRON, V33, P553, DOI 10.1016/S1352-2310(98)00287-8; Casillas AM, 1999, ANN ALLERG ASTHMA IM, V83, P624, DOI 10.1016/S1081-1206(10)62884-0; de Kok TMCM, 2006, MUTAT RES-REV MUTAT, V613, P103, DOI 10.1016/j.mrrev.2006.07.001; Dominici F, 2006, JAMA-J AM MED ASSOC, V295, P1127, DOI 10.1001/jama.295.10.1127; Donaldson K, 2001, OCCUP ENVIRON MED, V58, P211, DOI 10.1136/oem.58.3.211; Eberly S.I., 2005, EPA PMF 1 1 USERS GU; Galan I, 2003, EUR RESPIR J, V22, P802, DOI 10.1183/09031936.03.00013003; Hoek G, 2008, ATMOS ENVIRON, V42, P156, DOI 10.1016/j.atmosenv.2007.09.026; Hussein T, 2004, ATMOS CHEM PHYS, V4, P391; JANSSEN NA, 2005, OCCUP ENVIRON MED, V12, P868; Kettunen J, 2007, STROKE, V38, P918, DOI 10.1161/01.STR.0000257999.49706.3b; Kraft M, 2005, INT J HYG ENVIR HEAL, V208, P305, DOI 10.1016/j.ijheh.2005.04.002; Kulmala M, 2004, J AEROSOL SCI, V35, P143, DOI 10.1016/j.jaerosci.2003.10.003; Li N, 2003, ENVIRON HEALTH PERSP, V111, P455, DOI 10.1289/ehp.6000; Peel JL, 2005, EPIDEMIOLOGY, V16, P164, DOI 10.1097/01.ede.0000152905.42113.db; Pekkanen J, 2004, SCAND J WORK ENV HEA, V30, P9; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Pietropaoli AP, 2004, INHAL TOXICOL, V16, P59, DOI 10.1080/08958370490443079; R_Development_Core_Team, 2005, R LANG ENV STAT COMP; Schulz H, 2000, PARTICLE LUNG INTERA, P229; Schwarze PE, 2006, HUM EXP TOXICOL, V25, P559, DOI 10.1177/096032706072520; Thurston GD, 2005, ENVIRON HEALTH PERSP, V113, P1768, DOI 10.1289/ehp.7989; WHO, 2005, AIR QUAL GUID GLOB U, P275; Wong GWK, 2004, CURR OPIN PULM MED, V10, P62, DOI 10.1097/00063198-200401000-00011; Wood SN, 2000, J ROY STAT SOC B, V62, P413, DOI 10.1111/1467-9868.00240; Yang QY, 2005, ENVIRON RES, V99, P99, DOI 10.1016/j.envres.2004.09.014; Zanobetti A, 2000, ENVIRON HEALTH PERSP, V108, P841, DOI 10.2307/3434991	32	112	116	6	30	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	JUL	2008	63	7					635	641		10.1136/thx.2007.091371		7	Respiratory System	Respiratory System	319LY	WOS:000257166300014	18267984	
J	Elliott, DE; Summers, RW; Weinstock, JV				Elliott, David E.; Summers, Robert W.; Weinstock, Joel V.			Helminths as governors of immune-mediated inflammation	INTERNATIONAL JOURNAL FOR PARASITOLOGY			English	Review						immune regulation; inflammation; inflammatory bowel disease; asthma; multiple sclerosis; autoimmune type 1 diabetes; immune-mediated inflammatory disease; Trichuris suis; whipworm; hookworm	EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; TRICHURIS-SUIS THERAPY; REGULATORY T-CELLS; BOWEL-DISEASE; NECATOR-AMERICANUS; INDUCED COLITIS; CROHNS-DISEASE; INTESTINAL PARASITES; MULTIPLE-SCLEROSIS; ULCERATIVE-COLITIS	Immune-mediated diseases (e.g. inflammatory bowel disease, asthma, multiple sclerosis and autoimmune diabetes) are increasing in prevalence and emerge as populations adopt meticulously hygienic lifestyles. This change in lifestyles precludes exposure to helminths (parasitic worms). Loss of natural helminth exposure removes a previously universal Th2 and regulatory immune biasing imparted by these organisms. Helminths protect animals from developing immune-mediated diseases (colitis, reactive airway disease, encephalitis and diabetes). Clinical trials show that exposure to helminths can reduce disease activity in patients with ulcerative colitis or Crohn's disease. This paper summarises work by multiple groups demonstrating that colonization with helminths alters immune reactivity and protects against disease from dysregulated inflammation. (c) 2007 Australian Society for Parasitology Inc. Published by Elsevier Ltd. All rights reserved.	Univ Iowa, Roy J & Lucille A Carver Coll Med, Dept Internal Med, Div Gastroenterol & Hepatol, Iowa City, IA 52242 USA; Tufts Univ New England Med Ctr, Dept Internal Med, Div Gastroenterol & Hepatol, Boston, MA USA	Elliott, DE (reprint author), Univ Iowa, Roy J & Lucille A Carver Coll Med, Dept Internal Med, Div Gastroenterol & Hepatol, 200 Hawkins Dr, Iowa City, IA 52242 USA.	david-elliott@uiowa.edu			NIAID NIH HHS [AI49382]; NIDDK NIH HHS [DK58755, DK02428, DK25295, DK38327]		Araujo ML, 2004, MEM I OSWALDO CRUZ, V99, P27, DOI 10.1590/S0074-02762004000900005; Asher MI, 2006, LANCET, V368, P733, DOI 10.1016/S0140-6736(06)69283-0; BEER RJS, 1976, RES VET SCI, V20, P47; Bethony J, 2006, LANCET, V367, P1521, DOI 10.1016/S0140-6736(06)68653-4; Braman SS, 2006, CHEST, V130, p4S, DOI 10.1378/chest.130.1_suppl.4S; Cabre P, 2005, BRAIN, V128, P2899, DOI 10.1093/brain/awh624; Carr I, 1999, AM J GASTROENTEROL, V94, P2918; Cernea S, 2006, NAT CLIN PRACT ENDOC, V2, P89, DOI 10.1038/ncpendmet0082; Cooke A, 1999, PARASITE IMMUNOL, V21, P169, DOI 10.1046/j.1365-3024.1999.00213.x; Croese J, 2006, GUT, V55, P136, DOI 10.1136/gut.2005.079129; Crompton DWT, 1999, J PARASITOL, V85, P397, DOI 10.2307/3285768; Delco F, 1998, AM J GASTROENTEROL, V93, P1457, DOI 10.1111/j.1572-0241.1998.463_i.x; Doetze A, 2000, INT IMMUNOL, V12, P623, DOI 10.1093/intimm/12.5.623; Doria A, 2005, RHEUM DIS CLIN N AM, V31, P355, DOI 10.1016/j.rdc.2005.01.006; EKBOM A, 1991, GASTROENTEROLOGY, V100, P350; Eldeirawi KM, 2006, J ASTHMA, V43, P279, DOI 10.1080/0277090060022869; Elliott DE, 2005, CURR OPIN GASTROEN, V21, P51; Elliott DE, 2004, EUR J IMMUNOL, V34, P2690, DOI 10.1002/eji.200324833; Elliott DE, 2003, AM J PHYSIOL-GASTR L, V284, pG385, DOI 10.1152/ajpgi.00049.2002; Elliott DE, 2000, FASEB J, V14, P1848, DOI 10.1096/fj.99-0885hyp; Falcone FH, 2005, TRENDS PARASITOL, V21, P157, DOI 10.1016/j.pt.2005.02.002; FLEMING JO, 2006, MULTIPLE SCLEROSIS H; Gale EAM, 2002, DIABETOLOGIA, V45, P588, DOI 10.1007/s00125-002-0801-1; Goncalves MLC, 2003, MEM I OSWALDO CRUZ, V98, P103, DOI 10.1590/S0074-02762003000900016; Hotez PJ, 2004, NEW ENGL J MED, V351, P799, DOI 10.1056/NEJMra032492; HUBBARD DW, 1974, PEDIATR RES, V8, P652, DOI 10.1203/00006450-197406000-00006; Hunter MM, 2005, J IMMUNOL, V174, P7368; Ince MN, 2006, J IMMUNOL, V176, P726; JAYANTHI V, 1992, Q J MED, V82, P125; Khan WI, 2002, INFECT IMMUN, V70, P5931, DOI 10.1128/IAI.70.11.5931-5937.2002; Kitagaki K, 2006, J IMMUNOL, V177, P1628; La Flamme AC, 2003, INFECT IMMUN, V71, P4996, DOI 10.1128/IAI.71.9.4996-5004.2003; Lakatos L, 2004, WORLD J GASTROENTERO, V10, P404; Loftus EV, 2004, GASTROENTEROLOGY, V126, P1504, DOI 10.1053/j.gastro.2004.01.063; Maizels RM, 2003, NAT REV IMMUNOL, V3, P733, DOI 10.1038/nri1183; Mangan NE, 2006, J IMMUNOL, V176, P138; Marrie RA, 2004, LANCET NEUROL, V3, P709, DOI 10.1016/S1474-4422(04)00933-0; MAXWELL C, 1987, AM J TROP MED HYG, V37, P126; Metwali A, 2006, AM J PHYSIOL-GASTR L, V291, pG253, DOI 10.1152/ajpgi.00409.2005; Moreels TG, 2004, GUT, V53, P99, DOI 10.1136/gut.53.1.99; Onkamo P, 1999, DIABETOLOGIA, V42, P1395, DOI 10.1007/s001250051309; Pritchard DI, 2001, TRENDS PARASITOL, V17, P169, DOI 10.1016/S1471-4922(01)01941-9; Scrivener S, 2001, LANCET, V358, P1493, DOI 10.1016/S0140-6736(01)06579-5; Sellon RK, 1998, INFECT IMMUN, V66, P5224; Sewell D, 2003, INT IMMUNOL, V15, P59, DOI 10.1093/intimm/dxg012; Shivananda S, 1996, GUT, V39, P690, DOI 10.1136/gut.39.5.690; SONNENBERG A, 1990, GUT, V31, P1037, DOI 10.1136/gut.31.9.1037; SONNENBERG A, 1991, GASTROENTEROLOGY, V100, P143; Summers RW, 2005, GASTROENTEROLOGY, V128, P825, DOI 10.1053/j.gastro.2005.01.005; Summers RW, 2005, GUT, V54, P87, DOI 10.1136/gut.2004.041749; Summers RW, 2003, AM J GASTROENTEROL, V98, P2034, DOI 10.1016/S0002-9270(03)00623-3; van den Biggelaar AHJ, 2004, J INFECT DIS, V189, P892, DOI 10.1086/381767; van den Biggelaar AHJ, 2000, LANCET, V356, P1723, DOI 10.1016/S0140-6736(00)03206-2; VERMUND SH, 1988, AM J DIS CHILD, V142, P566; Wilson MS, 2005, J EXP MED, V202, P1199, DOI 10.1084/jem.20042572; Zaccone P, 2006, PARASITE IMMUNOL, V28, P515, DOI 10.1111/j.1365-3024.2006.00879.x; Zaccone P, 2003, EUR J IMMUNOL, V33, P1439, DOI 10.1002/eji.200323910	57	112	119	1	31	PERGAMON-ELSEVIER SCIENCE LTD	OXFORD	THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND	0020-7519			INT J PARASITOL	Int. J. Parasit.	APR	2007	37	5					457	464		10.1016/j.ijpara.2006.12.009		8	Parasitology	Parasitology	158ET	WOS:000245774800001	17313951	
J	Price, DB; Tinkelman, DG; Halbert, RJ; Nordyke, RJ; Isonaka, S; Nonikov, D; Juniper, EF; Freeman, D; Hausen, T; Levy, ML; Ostrem, A; van der Molen, T; van Schayck, CP				Price, David B.; Tinkelman, David G.; Halbert, R. J.; Nordyke, Robert J.; Isonaka, Sharon; Nonikov, Dmitry; Juniper, Elizabeth F.; Freeman, Daryl; Hausen, Thomas; Levy, Mark L.; Ostrem, Anders; van der Molen, Thys; van Schayck, Constant P.			Symptom-based questionnaire for identifying COPD in smokers	RESPIRATION			English	Article						chronic obstructive pulmonary disease; diagnosis; primary care; questionnaires; spirometry; validation studies	OBSTRUCTIVE PULMONARY-DISEASE; AIR-FLOW OBSTRUCTION; GENERAL-PRACTICE; RISK; POPULATION; GUIDELINES; DIAGNOSIS; SMOKING; PROGRAM; ASTHMA	Background: Symptom-based questionnaires may enhance chronic obstructive pulmonary disease (COPD) screening in primary care. Objectives: We prospectively tested questions to help identify COPD among smokers without prior history of lung disease. Methods: Subjects were recruited via random mailing to primary care practices in Aberdeen, UK, and Denver, Colo., USA. Current and former smokers aged 40 or older with no prior respiratory diagnosis and no respiratory medications in the past year were enrolled. Participants answered questions covering demographics and symptoms and then underwent spirometry with reversibility testing. A study diagnosis of COPD was defined as fixed airway obstruction as measured by postbronchodilator FEV1/FVC <0.70. We examined the ability of individual questions in a multivariate framework to correctly discriminate between persons with and without COPD. Results: 818 subjects completed all investigations and proceeded to analysis. The list of 54 questions yielded 52 items for analysis, which was reduced to 17 items for entry into multivariate regression. Eight items had significant relationships with the study diagnosis of COPD, including age, pack-years, body mass index, weather-affected cough, phlegm without a cold, morning phlegm, wheeze frequency, and history of any allergies. Individual items yielded odds ratios ranging from 0.23 to 12. This questionnaire demonstrated a sensitivity of 80.4 and specificity of 72.0. Conclusions: A simple patient self-administered questionnaire can be used to identify patients with a high likelihood of having COPD, for whom spirometric testing is particularly important. Implementation of this questionnaire could enhance the efficiency and diagnostic accuracy of current screening efforts. Copyright (C) 2006 S. Karger AG, Basel.	Cerner Hlth Insights, Beverly Hills, CA 90212 USA; Univ Aberdeen, Aberdeen, Scotland; Natl Jewish Med & Res Ctr, Denver, CO USA; Univ Calif Los Angeles, Sch Publ Hlth, Los Angeles, CA USA; McMaster Univ, Hamilton, ON, Canada; Univ Groningen, Groningen, Netherlands; Univ Maastricht, Maastricht, Netherlands; Univ Edinburgh, Edinburgh, Midlothian, Scotland	Halbert, RJ (reprint author), Cerner Hlth Insights, 9100 Wilshire Blvd,Suite 655E, Beverly Hills, CA 90212 USA.	rhalbert@cerner.com		Price, David/0000-0002-9728-9992			American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Anthonisen N R, 2001, Can Respir J, V8, P421; Calverley PMA, 2003, LANCET, V362, P1053, DOI 10.1016/S0140-6736(03)14416-9; CALVERLEY PMA, 2005, J COPD, V2, P225; Celli BR, 2004, NEW ENGL J MED, V350, P1005, DOI 10.1056/NEJMoa021322; Chinn S, 2002, THORAX, V57, P1028, DOI 10.1136/thorax.57.12.1028; COX DR, 1975, BIOMETRIKA, V62, P441, DOI 10.1093/biomet/62.2.441; den Otter JJ, 1998, J ASTHMA, V35, P381, DOI 10.3109/02770909809075672; Fagerstrom KO, 2005, RESPIRATION, V72, P216, DOI 10.1159/000084057; Ferguson GT, 2000, CHEST, V117, P1146, DOI 10.1378/chest.117.4.1146; FLETCHER C, 1977, BRIT MED J, V1, P1645; Freeman D, 2005, RESP MED, V99, P1311, DOI 10.1016/j.rmed.2005.02.037; Godtfredsen NS, 2002, THORAX, V57, P967, DOI 10.1136/thorax.57.11.967; Hardie JA, 2002, EUR RESPIR J, V20, P1117, DOI 10.1183/09031936.02.00023202; Hurd Suzanne, 2000, Chest, V117, p1S, DOI 10.1378/chest.117.2_suppl.1S; Iqbal A, 2002, RESPIROLOGY, V7, P233, DOI 10.1046/j.1440-1843.2002.00399.x; Juniper EF, 1995, QUALITY LIFE PHARMAC, V2nd, P49; KIDA K, 2002, 12 ANN C EUR RESP SO; KIM JO, 1978, SAGE U PAPER SERIES, V714; Kornmann O, 2003, RESPIRATION, V70, P67, DOI 10.1159/000068417; Korsten AMMH, 2003, REV FR ALLERGOL, V43, P246, DOI 10.1016/S0335-7457(03)00111-4; LEBOWITZ MD, 1976, AM REV RESPIR DIS, V113, P627; LEVY M, 2003, 13 ANN C EUR RESP SO; Menard S., 2002, SAGE U PAPER SERIES, V07-106; Mullerova H, 2004, RESP MED, V98, P78, DOI 10.1016/j/rmed.2003.08.009; *NAT I CLIN EXC, 2004, THORAX S1, V59, P175; The National Lung Health Education Program Executive Committee, 1998, CHEST S, V113, p123S; *NIH NAT HEART LUN, 2001, GLOB IN CHRON OBSTR; Petty T L, 1998, Respir Care Clin N Am, V4, P345; StataCorp, 2001, STATA STAT SOFTW REL; Tirimanna PRS, 1996, BRIT J GEN PRACT, V46, P277; van den Boom G, 1998, EUR RESPIR J, V11, P67, DOI 10.1183/09031936.98.11010067; Van Schayck CP, 2005, RESPIROLOGY, V10, P323, DOI 10.1111/j.1440-1843.2005.00720.x; van Schayck CP, 2002, BRIT MED J, V324, P1370, DOI 10.1136/bmj.324.7350.1370; van Weel C, 2002, Monaldi Arch Chest Dis, V57, P65; *WHO NAT HEART LUN, 2002, NIH PUBL	36	112	115	2	14	KARGER	BASEL	ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND	0025-7931			RESPIRATION	Respiration		2006	73	3					285	295		10.1159/000090142		11	Respiratory System	Respiratory System	101XT	WOS:000241775300006	16330875	
J	Mehl, A; Wahn, U; Niggemann, B				Mehl, A; Wahn, U; Niggemann, B			Anaphylactic reactions in children - a questionnaire-based survey in Germany	ALLERGY			English	Article						anaphylaxis; children; food allergy; immunotherapy; infants; insect sting allergy	ALLERGIC DISEASES; FOOD ALLERGY; IMMUNOTHERAPY; EPIDEMIOLOGY; FATALITIES; FEATURES	Background: Severe anaphylactic reactions are medical emergencies requiring immediate recognition and treatment. Despite this, little is known on their clinical features, especially in infants and children. Objective: To evaluate trigger factors, patterns of clinical reaction, site of occurrence and treatment modalities of reported reaction in infants and children below 12 years of age in Germany. Methods: Paediatricians throughout Germany were asked by questionnaire to report accidental anaphylactic reactions over the previous 12 months. Severity of reported reactions was classified in grades I-IV according to reported symptoms. Results: Hundred and three cases of anaphylaxis were evaluated. Median age was 5 years, 58% were boys. Site of occurrence was the child's home in the majority of cases (58%). Foods were the most common causative allergen (57%), followed by insect stings (13%) and immunotherapy (SIT) (12%); in 8% anaphylactic agent was unknown. Among foods, peanuts and tree nuts were the most frequent allergens (20% of food allergens in each case). Severe reactions with cardiovascular involvement occurred in 24% of cases. No fatal reaction was observed. Recurrent episodes of anaphylaxis were reported in 27% of cases, half of these caused by the same allergen again. For treatment, 20% of children received adrenaline, in 8% of cases intravenously. Thirty-six per cent of patients with grade-IV reactions received adrenaline, 24% intravenously. In 17% of all children an adrenaline self-injector was prescribed after the episode. Conclusion: Our data: (i) shows an uncertainty of physicians in diagnosing anaphylaxis, (ii) reveals remarkable under-treatment of the majority of children with anaphylaxis, (iii) reflects the need for guidelines and training for physicians in managing children with anaphylaxis and (iv) should encourage the development of self-management programmes for patients and families.	Charite Univ Med Ctr Berlin, Dept Pediat Pneumol & Immunol, D-13353 Berlin, Germany	Niggemann, B (reprint author), Charite Univ Med Ctr Berlin, Dept Pediat Pneumol & Immunol, Augustenburger Pl 1, D-13353 Berlin, Germany.						AAAAI Board of Directors, 1998, J ALLERGY CLIN IMMUN, V102, P173; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Bock SA, 2001, J ALLERGY CLIN IMMUN, V107, P191, DOI 10.1067/mai.2001.112031; Bousquet J, 1998, J ALLERGY CLIN IMMUN, V102, P558, DOI 10.1016/S0091-6749(98)70271-4; Brazil E, 1998, J ACCID EMERG MED, V15, P252; BUSINCO L, 1995, PEDIATR ALLERGY IMMU, V6, P44, DOI 10.1111/j.1399-3038.1995.tb00257.x; Cianferoni A, 2004, ANN ALLERG ASTHMA IM, V92, P464; Cianferoni A, 2001, ANN ALLERG ASTHMA IM, V87, P27; Dibs S D, 1997, Pediatrics, V99, pE7, DOI 10.1542/peds.99.1.e7; JOHANSSON SGO, 2003, ALLERGY, V113, P832; Lee JM, 2000, PEDIATRICS, V106, P762, DOI 10.1542/peds.106.4.762; Macdougall CF, 2002, ARCH DIS CHILD, V86, P236, DOI 10.1136/adc.86.4.236; Moneret-Vautrin DA, 2005, ALLERGY, V60, P443, DOI 10.1111/j.1398-9995.2005.00785.x; Niggemann B, 2005, ALLERGY, V60, P104, DOI 10.1111/j.1398-9995.2004.00591.x; Niggemann B, 2004, ALLERGY, V59, P806, DOI 10.1111/j.1398-9995.2004.00495.x; Novembre E, 1998, PEDIATRICS, V101, DOI 10.1542/peds.101.4.e8; Pumphrey Richard, 2004, Curr Opin Allergy Clin Immunol, V4, P285, DOI 10.1097/01.all.0000136762.89313.0b; Pumphrey RSH, 2000, J CLIN PATHOL, V53, P273, DOI 10.1136/jcp.53.4.273; Pumphrey RSH, 2000, CLIN EXP ALLERGY, V30, P1144, DOI 10.1046/j.1365-2222.2000.00864.x; REID MJ, 1993, J ALLERGY CLIN IMMUN, V92, P6, DOI 10.1016/0091-6749(93)90030-J; Sampson HA, 2003, PEDIATRICS, V111, P1601; SAMPSON HA, 1992, NEW ENGL J MED, V327, P380, DOI 10.1056/NEJM199208063270603; Sheetz AH, 2004, J SCHOOL HEALTH, V74, P155; Simons FER, 2004, J ALLERGY CLIN IMMUN, V113, P837, DOI 10.1016/j.jaci.2004.01.079; SIMONS FER, 2004, ALL CLIN IMMUNOL  S1, V242; Yocum MW, 1999, J ALLERGY CLIN IMMUN, V104, P452, DOI 10.1016/S0091-6749(99)70392-1	26	112	117	1	1	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0105-4538			ALLERGY	Allergy	NOV	2005	60	11					1440	1445		10.1111/j.1398-9995.2005.00909.x		6	Allergy; Immunology	Allergy; Immunology	969NS	WOS:000232241600017	16197479	
J	Schnuch, A; Lessmann, H; Geier, J; Frosch, PJ; Uter, W				Schnuch, A; Lessmann, H; Geier, J; Frosch, PJ; Uter, W			Contact allergy to fragrances: frequencies of sensitization from 1996 to 2002. Results of the IVDK	CONTACT DERMATITIS			English	Article						contact allergy; fragrance mix; frequency of sensitization; multicentre study; Myroxylon pereirae resin; oil of turpentine	PATCH-TEST; INFORMATION NETWORK; STANDARD SERIES; DERMATOLOGY IVDK; SKIN-SENSITIZATION; CHEMICAL-ANALYSIS; ESSENTIAL OILS; DERMATITIS; MULTICENTER; PERFUMES	Increasing frequencies of sensitization to the fragrance mix (FM) have been acknowledged as a serious problem for many years. It is well known that the single compounds (SCs) of the FM contribute differently to the FM patch rest reactions. In this study, we were interested in the time trends of the FM, the SCs, Myroxylon pereirae resin (MP; balsam of Peru) and oil of turpentine (OT) as possible further indicators of perfume allergy and analysed the data collected by the Information Network of Departments of Dermatology multicentre project from 1996 to 2002. During the study period (1996-2002), the FM [8% petrolatum (pet.)], MP (25% pet.) and OT (1% pet.) were tested in 59 298, 59 334 and 59 478 patients, respectively. SCs were tested in a selected group of patients, ranging from n = 1083 to n = 1924 per year. A significant increase in the proportions of patients with positive reactions to FM, MP and OT between 1996 and 1998 is noted, and a significant decline from 1999 to 2002 (Cochrane Armitage trend test, P < 0.0001). The highest frequency of sensitization to the FM was 13.1% in 1999, and the lowest 7.8% in 2002. The number of concomitant reactions to OT, a surrogate marker for terpenes, in FM-positive patients was significantly increased between 1997 and 1999. Reactions to SCs in FM-positive patients were observed in 29.9% (oak moss absolute) to 5.9% (geraniol). There was no time trend in reactions to SCs, although the relative share was increased for isoeugenol, cinnamic aldehyde and geraniol in 1999. In summary, we report for the first time, a significant decline in sensitization to the FM, very probably due to a reduced exposure (less potent allergens used in fine fragrances, possibly less use of natural ingredient-based cosmetics and lowered use concentration of important fragrance allergens). The differences in ranking of SCs could stimulate (a) a redefinition of the FM and (b) a differentiated preventive and regulatory approach, with oak moss and isoeugenol being regulated strictly by prohibition, concentration limits further reconsidered and/or health warnings and clearly less noxious substances like geraniol treated less restrictively.	Univ Gottingen, IVDK Zent Inst, Informat Network Dept Dermatol IVDK, D-37075 Gottingen, Germany; Klinikum Dortmund, Dept Dermatol, Dortmund, Germany; Univ Witten Herdecke, Dortmund, Germany; Univ Erlangen Nurnberg, Dept Med Informat Biometry & Epidemiol, Erlangen, Germany	Schnuch, A (reprint author), Univ Gottingen, IVDK Zent Inst, Informat Network Dept Dermatol IVDK, Von Siebold Str 3, D-37075 Gottingen, Germany.	aschnuch@med.uni-goettingen.de		Uter, Wolfgang/0000-0002-4498-3710			Albert M R, 1999, Am J Contact Dermat, V10, P219, DOI 10.1016/S1046-199X(99)90072-6; Basketter DA, 2003, CLIN EXP DERMATOL, V28, P218, DOI 10.1046/j.1365-2230.2003.01247.x; Bertrand F, 1997, CHEM RES TOXICOL, V10, P335, DOI 10.1021/tx960087v; Bonnevie P, 1939, AETIOLOGIE PATHOGENE; BRASCH J, 1992, CONTACT DERMATITIS, V27, P203, DOI 10.1111/j.1600-0536.1992.tb05267.x; Brasch J, 2001, Am J Contact Dermat, V12, P197, DOI 10.1053/ajcd.2001.26669; Brites MM, 2000, CONTACT DERMATITIS, V43, P181; BRUN R, 1982, DERMATOLOGICA, V165, P24; Buckley DA, 2000, BRIT J DERMATOL, V142, P279, DOI 10.1046/j.1365-2133.2000.03298.x; CADBY PA, 2003, REGUL TOXICOL PHARM, V36, P246; Cheung C, 2003, J DERMATOL SCI, V31, P9, DOI 10.1016/S0923-1811(02)00139-1; CRONIN E, 1979, CONTACT DERMATITIS, V5, P308, DOI 10.1111/j.1600-0536.1979.tb04884.x; DAHLQUIST I, 1980, CONTACT DERMATITIS, V6, P111, DOI 10.1111/j.1600-0536.1980.tb03917.x; DAHLQUIST I, 1981, CONTACT DERMATITIS, V7, P168, DOI 10.1111/j.1600-0536.1981.tb04610.x; Dharmagunawardena B, 2002, CONTACT DERMATITIS, V47, P288, DOI 10.1034/j.1600-0536.2002.470506.x; FISHER AA, 1990, CUTIS, V45, P21; Fregert S, 1969, Trans St Johns Hosp Dermatol Soc, V55, P17; Frosch PJ, 2002, CONTACT DERMATITIS, V47, P279, DOI 10.1034/j.1600-0536.2002.470204.x; Frosch PJ, 2002, CONTACT DERMATITIS, V47, P78; FROSCH PJ, 1995, CONTACT DERMATITIS, V33, P333, DOI 10.1111/j.1600-0536.1995.tb02048.x; Frosch PJ, 1999, BRIT J DERMATOL, V141, P1076, DOI 10.1046/j.1365-2133.1999.03208.x; Frosch P. 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J	Mari, A; Schneider, P; Wally, V; Breitenbach, M; Simon-Nobbe, B				Mari, A; Schneider, P; Wally, V; Breitenbach, M; Simon-Nobbe, B			Sensitization to fungi: epidemiology, comparative skin tests, and IgE reactivity of fungal extracts	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergens; comparative study; epidemiology; fungal allergy diagnosis; fungal extract; IgE detection; immunoblotting; prevalence; skin tests	CANDIDA-ALBICANS; ALTERNARIA-ALTERNATA; IMMUNOLOGICAL CHARACTERIZATION; ASPERGILLUS-FUMIGATUS; CROSS-REACTIVITY; CLADOSPORIUM-HERBARUM; PENICILLIUM-CITRINUM; VAGINAL CANDIDIASIS; RESPIRATORY ALLERGY; DESERT ENVIRONMENT	Background Several fungal species are known to cause severe respiratory and cutaneous allergic diseases. Extracts from several allergenic fungi are used for in vivo and in vitro tests, as standard preparations are still not available. Objective The aims are to de. ne the pattern of in vivo and in vitro IgE reactivity to fungal species in an allergic population with respiratory symptoms; to determine the influence of different extract preparations on diagnostic results; and to evaluate whether there exists a relationship between the diagnostic pattern of reactivity and the pattern of specific IgE reactivity in immunoblots. Methods Skin prick tests were applied to a cohort of 4962 respiratory subjects, aged 3 - 80 years. Fungal extracts from Alternaria, Aspergillus, Candida, Cladosporium, Penicillium, Saccharomyces, and Trichophyton were used, along with extracts from pollens, mites, and animal dander. Demographical and diagnostic data were recorded. IgE detection was carried out with the same allergenic extracts plus Malassezia. Comparative skin tests and IgE detection were carried out using extracts from three commercial suppliers. IgE immunoblots were carried out with the same panel of commercial fungal extracts and were compared with in-house extracts. Data analysis was carried out by grouping the population on the basis of their reactivity to a single, to two or to more than two, mould species. Results Nineteen percent of the allergic population reacted to at least one fungal extract by means of the skin test. Alternaria and Candida accounted for the largest number of positive tests, and along with Trichophyton they were the main sensitizers in the subset of patients with an isolated sensitization. The prevalence of skin test reactivity increased for these three fungi in the subsets with two associated reactivities and, furthermore, in the subset showing reactivity to more than two mould species. In the latter group, a steady increase of the skin test reactivity was recorded for all the other fungal sources, suggesting a clustered reactivity. Comparative skin and IgE testing with different groups of subjects with a simple pattern of skin reactivity resulted in sensitivity differences between in vivo and in vitro tests, whereas discrepant results were recorded in the subsets of patients with multiple fungi sensitization. Although hampered by the limited reliability of fungal extracts, IgE immunoblots revealed differing patterns of reactivity when sera from the three subsets were used. This suggests a link between the diagnostic reactivity pattern and the IgE sensitization to extracts' components. Age and gender distribution differed among the Alternaria-, Candida-, and Trichophyton-sensitized subjects, but not in the subset with more than two fungi sensitizations. Conclusions The preliminary assessment of a new classification of the mould-sensitized population has been reached. The limiting quality of fungal extracts requires future studies using an allergenic molecule-based approach. The diagnostic process and the definition of the reactivity pattern would thus be easy, and it could lead to a novel specific immunotherapy approach.	Natl Hlth Serv, Allergy Unit, Rome, Italy; Salzburg Univ, Dept Genet & Gen Biol, A-5020 Salzburg, Austria	Mari, A (reprint author), Via Malipiero 28, I-04100 Latina, Italy.						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Exp. Allergy	OCT	2003	33	10					1429	1438		10.1046/j.1365-2222.2003.01783.x		10	Allergy; Immunology	Allergy; Immunology	727KN	WOS:000185657300017	14519151	
J	Vandenplas, O; Toren, K; Blanc, PD				Vandenplas, O; Toren, K; Blanc, PD			Health and socioeconomic impact of work-related asthma	EUROPEAN RESPIRATORY JOURNAL			English	Review						asthma; disability; occupational disease	AIRWAYS DYSFUNCTION SYNDROME; DIISOCYANATE-INDUCED ASTHMA; INDUCED OCCUPATIONAL ASTHMA; TOLUENE DIISOCYANATE; FOLLOW-UP; BRONCHIAL HYPERRESPONSIVENESS; PERSISTENT ASTHMA; REPEATED EXPOSURE; INHALATION CHALLENGE; CHLORINE INHALATION	There is accumulating evidence that the workplace environment contributes significantly to the general burden of asthma. The purpose of this review is to explore the respiratory health and socioeconomic consequences of work-related asthma by addressing a series of controversial issues: 1) what is the natural history of occupational asthma and in what ways does ongoing exposure to the causal agent impact clinical outcomes?; 2) how does the natural history of irritant-induced asthma differ in its health outcomes from immunologically-mediated occupational asthma?; 3) do working conditions have a significant impact on asthma regardless of the aetiology of the disease?; 4) what is the scope of work disability from work-related-asthma in social and economic terms?; 5) what is the clinician's role in reducing the respiratory health consequences of work-related asthma? 6) to what extent do existing compensation and other social insurance schemes successfully address occupational asthma and work-aggravated asthma?	Univ Catholique Louvain, Serv Pneumol, Clin Mont Godinne, B-5530 Yvoir, Belgium; Sahlgrens Univ Hosp, Dept Resp Med & Allergol, S-41345 Gothenburg, Sweden; Sahlgrens Univ Hosp, Dept Occupat & Environm Med, S-41345 Gothenburg, Sweden; Univ Calif San Francisco, Dept Med, Div Occupat & Environm Med, San Francisco, CA 94143 USA	Vandenplas, O (reprint author), Univ Catholique Louvain, Serv Pneumol, Clin Mont Godinne, B-5530 Yvoir, Belgium.						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Resp. J.	OCT	2003	22	4					689	697		10.1183/09031936.03.00053203		9	Respiratory System	Respiratory System	732WR	WOS:000185969000022	14582924	
J	Pitchford, SC; Yano, H; Lever, R; Riffo-Vasquez, Y; Ciferri, S; Rose, MJ; Giannini, S; Momi, S; Spina, D; O'Connor, B; Gresele, P; Page, CP				Pitchford, SC; Yano, H; Lever, R; Riffo-Vasquez, Y; Ciferri, S; Rose, MJ; Giannini, S; Momi, S; Spina, D; O'Connor, B; Gresele, P; Page, CP			Platelets are essential for leukocyte recruitment in allergic inflammation	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						platelet; leukocyte; platelet-leukocyte interaction; asthma; allergy; eosinophil; lymphocyte; vascular endothelium; CD11b	P-SELECTIN; FLOW-CYTOMETRY; WHOLE-BLOOD; ASTHMA; ADHESION; ACTIVATION; NEUTROPHILS; CELLS; PAF; AGGREGATION	Background: The role of platelets in inflammation is recognized but poorly characterized, and little is known of their interaction with leukocytes. However, platelet-leukocyte interactions have been demonstrated in cardiovascular disease, culminating in enhanced leukocyte recruitment. Objectives: This study was undertaken to assess the possibility and potential role of similar phenomena occurring in asthmatic patients, a murine model of allergic inflammation, and in vitro adhesion studies. Methods: Asthmatic patients had blood taken at various time points to document the degree of leukocyte activation and the presence of platelet-leukocyte aggregates through FACS analysis before and after allergen exposure. Similar studies were carried out in mice exposed to allergen after previous sensitization, with some groups being selectively depleted of platelets through both an immunologic (antiplatelet antiserum) and nonimmunologic (busulfan) method. Additionally, lavage fluid and airway tissue were analyzed to assess the degree of pulmonary leukocyte recruitment. The importance of platelets on leukocyte adhesion to the endothelium was then assessed with in vitro incubation of radiolabeled leukocytes in the presence of activated platelets on cultured human vascular endothelial cells. Results: We have observed circulating platelet-leukocyte aggregates in the blood of allergic asthmatic patients during the allergen-induced late asthmatic response and in sensitized mice after allergen exposure. In platelet-depleted mice infiltration of leukocytes into airways after allergen challenge was significantly reduced and could be restored by means of infusion of platelets from allergic animals, indicating an essential role for platelets in leukocyte recruitment. CD11b expression on leukocytes involved in aggregates with platelets, although not on free leukocytes, was upregulated. Furthermore, the presence of autologous platelets augmented the adhesion of human polymorphonuclear leukocytes to cultured vascular endothelial cells, an effect that was found to be endothelial cell dependent and to involve platelet activation. Conclusion: These results suggest that platelet participation in cell recruitment occurs at the level of the circulation and might involve the priming of leukocytes for subsequent adhesion and transmigration into tissues.	Kings Coll London, GKT Sch Biomed Sci, Sackler Inst Pulm Pharmacol, London SE1 1UL, England; Univ Perugia, Dept Internal Med, Sect Internal & Cardiovasc Med, I-06100 Perugia, Italy; Kings Coll Hosp London, Dept Resp Med & Allergy, London, England	Page, CP (reprint author), Kings Coll London, GKT Sch Biomed Sci, Sackler Inst Pulm Pharmacol, 5th Floor,Hodgkin Bldg,Guys Campus, London SE1 1UL, England.		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Allergy Clin. Immunol.	JUL	2003	112	1					109	118		10.1067/mai.2003.1514		10	Allergy; Immunology	Allergy; Immunology	698QQ	WOS:000184010600018	12847487	
J	Whitehead, GS; Walker, JKL; Berman, KG; Foster, WM; Schwartz, DA				Whitehead, GS; Walker, JKL; Berman, KG; Foster, WM; Schwartz, DA			Allergen-induced airway disease is mouse strain dependent	AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY			English	Editorial Material						asthma; airway hyperreactivity; eosinophils; cytokines	LATE ASTHMATIC REACTIONS; LUNG DAMAGE; MICE; HYPERRESPONSIVENESS; HYPERREACTIVITY; INTERLEUKIN-5; INFLAMMATION; RESPONSIVENESS; EOSINOPHILIA; NEUTROPHILS	We investigated the development of airway hyperreactivity ( AHR) and inflammation in the lungs of nine genetically diverse inbred strains of mice [129/SvIm, A/J, BALB/cJ, BTBR+(T)/tf/tf, CAST/Ei, C3H/HeJ, C57BL/6J, DBA/2J, and FVB/NJ] after sensitization and challenge with ovalbumin (OVA). At 24, 48, and 72 h post-OVA exposure, the severity of AHR and eosinophilic inflammation of the mouse strains ranged from relatively unresponsive to responsive. The severity of the airway eosinophilia of some strains did not clearly correlate with the development of AHR. The temporal presence of T helper type 2 cytokines in lung lavage fluid also varied markedly among the strains. The levels of IL-4 and IL-13 were generally increased in the strains with the highest airway eosinophilia at 24 and 72 h postexposure, respectively; the levels of IL-5 were significantly increased in most of the strains with airway inflammation over the 72-h time period. The differences of physiological and biological responses among the inbred mouse strains after OVA sensitization and challenge support the hypothesis that genetic factors contribute, in part, to the development of allergen-induced airway disease.	Duke Univ, Med Ctr, Dept Pulm & Crit Care Med, Durham, NC 27710 USA	Whitehead, GS (reprint author), Duke Univ, Med Ctr, Dept Pulm & Crit Care Med, Rm 275 MSRB,DUMC Box 2629, Durham, NC 27710 USA.				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J. Physiol.-Lung Cell. Mol. Physiol.	JUL	2003	285	1					L32	L42		10.1152/ajplung.00390.2002		11	Physiology; Respiratory System	Physiology; Respiratory System	686HB	WOS:000183314400005	12626335	
J	Coulson, FR; Fryer, AD				Coulson, FR; Fryer, AD			Muscarinic acetylcholine receptors and airway diseases	PHARMACOLOGY & THERAPEUTICS			English	Review						prejunctional receptors; postjunctional receptors; parasympathetic nerves; airway hyperreactivity; eosinophils; viruses	OBSTRUCTIVE PULMONARY-DISEASE; UPPER RESPIRATORY-TRACT; MAJOR BASIC-PROTEIN; GUINEA-PIG TRACHEA; INDUCED BRONCHIAL HYPERREACTIVITY; INHALED IPRATROPIUM BROMIDE; EXERCISE-INDUCED ASTHMA; VITAMIN-A-DEFICIENCY; SMOOTH-MUSCLE; INDUCED BRONCHOCONSTRICTION	Parasympathetic nerves provide the dominant autonomic innervation of the airways. Release of acetylcholine from parasympathetic nerves activates postjunctional muscarinic receptors present on airway smooth muscle, submucosal glands, and blood vessels to cause bronchoconstriction, mucus secretion, and vasodilatation, respectively. Acetylcholine also feeds back onto prejunctional muscarinic receptors to enhance or inhibit further acetylcholine release. In asthma and chronic obstructive pulmonary disease, bronchoconstriction and mucus secretion is increased and the airways are hyperresponsive to contractile agents. These changes are due to increased parasympathetic nerve activity. The number and function of postjunctional muscarinic receptors in the airways are unchanged in animal models of asthma. Rather, it is the supply of acetylcholine to the postjunctional cells (smooth muscle and submucosal gland) that is increased. The increase in acetylcholine release occurs because prejunctional, inhibitory M-2 muscarinic receptors on the parasympathetic nerves are dysfunctional. M-2 muscarinic receptor dysfunction and subsequent airway hyperreactivity have been demonstrated to occur in animals in response to a variety of triggers, including antigen challenge, virus infection, ozone exposure, and vitamin A deficiency. In humans, there is evidence that loss of M-2 muscarinic receptor function is related to asthma. The mechanisms by which neuronal M-2 muscarinic receptor function is lost and its relevance to human airway disease are discussed in this review. (C) 2003 Elsevier Science Inc. All rights reserved.	Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Div Physiol, Baltimore, MD 21205 USA	Fryer, AD (reprint author), Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Div Physiol, 615 N Wolfe St, Baltimore, MD 21205 USA.		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Ther.	APR	2003	98	1					59	69		10.1016/S0163-7258(03)00004-4		11	Pharmacology & Pharmacy	Pharmacology & Pharmacy	666XY	WOS:000182202800003	12667888	
J	Oddy, WH; Sly, PD; de Klerk, NH; Landau, LI; Kendall, GE; Holt, PG; Stanley, FJ				Oddy, WH; Sly, PD; de Klerk, NH; Landau, LI; Kendall, GE; Holt, PG; Stanley, FJ			Breast feeding and a birth cohort study respiratory morbidity in infancy: a birth cohort study	ARCHIVES OF DISEASE IN CHILDHOOD			English	Article							FORMULA-FED INFANTS; 1ST YEAR; TRACT ILLNESS; OTITIS-MEDIA; HUMAN-MILK; FOLLOW-UP; LIFE; INFECTIONS; CHILDHOOD; ASTHMA	Aim: To examine the relation between the duration of breast feeding and morbidity as a result of respiratory illness and infection in the first year of life. Methods: Prospective birth cohort study of 2602 live born children ascertained through antenatal clinics at the major tertiary obstetric hospital in Perth, Western Australia. Main outcome measures were hospital, doctor, or clinic visits, and hospital admissions for respiratory illness and infection in the first year of life. Main exposure measures were the duration of predominant breast feeding (defined as the age other milk was introduced) and partial (any) breast feeding (defined as the age breast feeding was stopped). Main confounders were gender, gestational age less than 37 weeks, smoking in pregnancy, older siblings, maternal education, and maternal age. Results: Hospital, doctor, or clinic visits for four or more upper respiratory tract infections were significantly greater if predominant breast feeding was stopped before 2 months or partial breast feeding was stopped before 6 months. Predominant breast feeding for less than six months was associated with an increased risk for two or more hospital, doctor, or clinic visits and hospital admission for wheezing, lower respiratory illness. Breast feeding for less than eight months was associated with a significantly increased risk for two or more hospital, doctor, or clinic visits or hospital admissions because of wheezing lower respiratory illnesses. Conclusions: Predominant breast feeding for at least six months and partial breast feeding for up to one year may reduce the prevalence and subsequent morbidity of respiratory illness and infection in infancy.	Univ Western Australia, Telethon Inst Child Hlth Res, Ctr Child Hlth Res, Perth, WA 6872, Australia; Curtin Univ Technol, Dept Nutr Dietet & Food Sci, Bentley, WA 6845, Australia; Univ Western Australia, Fac Med & Dent, Nedlands, WA 6872, Australia	Oddy, WH (reprint author), Univ Western Australia, Telethon Inst Child Hlth Res, Ctr Child Hlth Res, POB 855, Perth, WA 6872, Australia.		Sly, Peter/F-1486-2010; Holt, Patrick/H-1548-2011; Osborne, Nicholas/N-4915-2015; de Klerk, Nicholas/D-8388-2016	Sly, Peter/0000-0001-6305-2201; Holt, Patrick/0000-0003-1193-0935; Osborne, Nicholas/0000-0002-6700-2284; de Klerk, Nicholas/0000-0001-9223-0767			Armitage P, 1996, STAT METHODS MED RES; Ball TM, 1999, PEDIATRICS, V103, P870; BAUCHNER H, 1986, JAMA-J AM MED ASSOC, V256, P887, DOI 10.1001/jama.256.7.887; BEAUDRY M, 1995, J PEDIATR-US, V126, P191, DOI 10.1016/S0022-3476(95)70544-9; Betran AP, 2001, BRIT MED J, V323, P303, DOI 10.1136/bmj.323.7308.303; Cesar JA, 1999, BRIT MED J, V318, P1316; CHANDRA RK, 1979, ACTA PAEDIATR SCAND, V68, P691; Cushing AH, 1998, AM J EPIDEMIOL, V147, P863; DEWEY KG, 1995, J PEDIATR-US, V126, P696, DOI 10.1016/S0022-3476(95)70395-0; EIGER MS, 1984, CLIN PEDIATR, V23, P492, DOI 10.1177/000992288402300908; Elder DE, 1999, J PAEDIATR CHILD H, V35, P145, DOI 10.1046/j.1440-1754.1999.00308.x; FERGUSSON DM, 1981, AUST PAEDIATR J, V17, P191; Hamosh M, 2001, PEDIATR CLIN N AM, V48, P69, DOI 10.1016/S0031-3955(05)70286-8; Hanson LA, 1999, ACTA PAEDIATR, V88, P42, DOI 10.1080/080352599750029727; Hasselbalch H, 1999, EUR J PEDIATR, V158, P964, DOI 10.1007/s004310051258; HOLBERG CJ, 1991, AM J EPIDEMIOL, V133, P1135; HOWIE PW, 1990, BRIT MED J, V300, P11; Jones CA, 2000, CLIN EXP ALLERGY, V30, P599, DOI 10.1046/j.1365-2222.2000.00884.x; KOVAR MG, 1984, PEDIATRICS 2 S, V74, P659; MAGENIS C, 1995, BR J GEN PRACT, V45, P65; MARKS GB, 1993, J CLIN EPIDEMIOL, V46, P1103, DOI 10.1016/0895-4356(93)90109-E; MYERS MG, 1984, AM J DIS CHILD, V138, P629; NEWNHAM JP, 1993, LANCET, V342, P887; Oddy WH, 1999, BRIT MED J, V319, P815; Oddy WH, 2002, EUR RESPIR J, V19, P899, DOI 10.1183/09031936.02.00103602; PARADISE JL, 1994, PEDIATRICS, V94, P853; RUBIN DH, 1990, PEDIATRICS, V85, P464; SAARINEN UM, 1995, LANCET, V346, P1065, DOI 10.1016/S0140-6736(95)91742-X; SAARINEN UM, 1982, ACTA PAEDIATR SCAND, V71, P567, DOI 10.1111/j.1651-2227.1982.tb09476.x; SCARIATI PD, 1997, PEDIATRICS, V99, pE51; TAYLOR B, 1982, LANCET, V1, P1227; Victora CG, 2000, LANCET, V355, P451, DOI 10.1016/S0140-6736(00)82011-5; *WHO, 2001, NOTE PRESS, V7; *WHO, 1995, PONTIF ACAD SCI DOC, V20, P1; Wilson AC, 1998, BRIT MED J, V316, P21; WRIGHT AL, 1989, BRIT MED J, V299, P946; Wright AL, 1998, PEDIATRICS, V101, P837, DOI 10.1542/peds.101.5.837; WRIGHT AL, 1989, AM J EPIDEMIOL, V129, P1232; Wright AL, 2001, THORAX, V56, P192, DOI 10.1136/thorax.56.3.192	39	112	121	1	8	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0003-9888			ARCH DIS CHILD	Arch. Dis. Child.	MAR	2003	88	3					224	228		10.1136/adc.88.3.224		5	Pediatrics	Pediatrics	652ET	WOS:000181367400013	12598384	
J	von Mutius, E				von Mutius, E			Environmental factors influencing the development and progression of pediatric asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; atopy; environmental factors; risk factors; sensitization	ALLERGIC SENSITIZATION; HAY-FEVER; EARLY-CHILDHOOD; CHILDREN; EXPOSURE; COHORT; RISK; AGE; PREVALENCE; COMMUNITY	Recent data underscore the importance of environmental factors in the sensitization of children to certain allergens and the development of asthma. Maternal smoking and family (especially maternal) history of atopy appear to be risk factors for persistent sensitization and development of asthma. Indeed, exposure to tobacco smoke in utero significantly increases asthma risk and influences the timing of sensitization. It must be stated that any smoking at home has consequences for the development of asthma and other respiratory conditions. In addition, reports of possible protective effects of specific environmental conditions suggest that exposure to certain stimuli may reduce or block the development and progression of asthma. Attendance at a day care center early in life appears to offer protective effects against wheezing, as do early episodes of rhinitis, herpes, and measles. Children raised on a farm also have a decreased prevalence of atopic diseases. The protective effect of contact with livestock and poultry is consistent among several studies. Although the pathophysiologic mechanisms involved remain undefined, studies suggest that exposure to endotoxin and other components of bacteria may play an important role in protecting against childhood atopic diseases. Whether in utero exposure is beneficial remains to be determined.	Univ Munich, Childrens Hosp, D-80337 Munich, Germany	von Mutius, E (reprint author), Univ Munich, Childrens Hosp, Lindwurmstr 4, D-80337 Munich, Germany.			von Mutius, Erika/0000-0002-8893-4515			Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; CHARPIN D, 1991, AM REV RESPIR DIS, V143, P983; Cook DG, 1999, THORAX, V54, P357; Gereda JE, 2000, JAMA-J AM MED ASSOC, V284, P1652, DOI 10.1001/jama.284.13.1652; Illi S, 2001, BRIT MED J, V322, P390, DOI 10.1136/bmj.322.7283.390; Illi S, 2001, J ALLERGY CLIN IMMUN, V108, P709, DOI 10.1067/mai.2001.118786; Kramer U, 1999, LANCET, V353, P450, DOI 10.1016/S0140-6736(98)06329-6; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; MARTINEZ FD, 1992, PEDIATRICS, V89, P21; Nickel R, 1997, J ALLERGY CLIN IMMUN, V99, P613, DOI 10.1016/S0091-6749(97)70021-6; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; SPORIK R, 1995, AM J RESP CRIT CARE, V151, P1388; Strachan DP, 1996, BRIT MED J, V312, P1195; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; YUNGINGER JW, 1992, AM REV RESPIR DIS, V146, P888	19	112	116	0	8	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUN	2002	109	6		S			S525	S532		10.1067/mai.2002.124565		8	Allergy; Immunology	Allergy; Immunology	568JU	WOS:000176539300003	12063508	
J	Wolfe, AH; Patz, JA				Wolfe, AH; Patz, JA			Reactive nitrogen and human health: Acute and long-term implications	AMBIO			English	Article; Proceedings Paper	2nd International Nitrogen Conference	OCT, 2001	POTOMAC, MARYLAND				OUTDOOR AIR-POLLUTION; PUBLIC-HEALTH; DRINKING-WATER; DIOXIDE; ASTHMA; OZONE; CONTAMINATION; ENVIRONMENT; ADMISSIONS; MANAGEMENT	Reactive-nitrogen (Nr) has a wide variety of beneficial and detrimental effects on human health. The most important of the beneficial effects are increasing global and regional food supplies and increased nutritional quality of available foods. However, lack of adequate dietary intake of amino acids and proteins is a serious cause of malnutrition when food supplies are inadequate because of poverty, drought, floods, wars, and displacements of people as refugees. There is sufficient, though limited, quantitative data indicating that increased circulation of Nr in the environment is responsible for significant human health effects via other exposure pathways. Nr can lead to harmful health effects from airborne occupational exposures and population-wide indoor and outdoor air pollution exposures to nitrogen dioxide and ozone. Nr can also affect health via water pollution problems, including methemoglobinemia from contaminated ground water, eutrophication causing fish kills and algal blooms that can be toxic to humans, and via global warming. The environmental pollutants stemming from reactive nitrogen are ubiquitous, making it difficult to identify the extent to which Nr exerts a specific health effect. As all populations are susceptible, continued interdisciplinary investigations are needed to determine the extent and nature of the beneficial and harmful effects on human health of nitrogen-related pollutants and their derivatives.	Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Program Hlth Effects Global Environm Change, Baltimore, MD 21205 USA	Wolfe, AH (reprint author), Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Program Hlth Effects Global Environm Change, 615 N Wolfe St, Baltimore, MD 21205 USA.						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J	Ziska, LH; Caulfield, FA				Ziska, LH; Caulfield, FA			Rising CO2 and pollen production of common ragweed (Ambrosia artemisiifolia), a known allergy-inducing species: implications for public health	AUSTRALIAN JOURNAL OF PLANT PHYSIOLOGY			English	Article						allergens; elevated carbon dioxide; photosynthesis; pollen; relative growth rate	CARBON-DIOXIDE; ELEVATED CO2; GROWTH-RESPONSE; ATMOSPHERIC CO2; UNITED-STATES; ENRICHMENT; PLANTS; PHOTOSYNTHESIS; WEEDS	Although environmental factors such as precipitation and temperature are recognized as influencing pollen production, the impact of rising atmospheric carbon dioxide concentration ([ CO2]) on the potential growth and pollen production of hay- fever- inducing plants is unknown. Here we present measurements of growth and pollen production of common ragweed (Ambrosia artemisiifolia L.) from pre- industrial [CO2] (280 mu mol mol(-1)) to current concentrations (370 mu mol mol(-1)) to a projected 21st century concentration (600 mu mol mol(-1)). We found that exposure to current and elevated [CO2] increased ragweed pollen production by 131 and 320%, respectively, compared to plants grown at pre- industrial [CO2]. The observed stimulations of pollen production from the pre- industrial [CO2] were due to an increase in the number (at 370 mu mol mol(-1)) and number and size (at 600 mu mol mol(-1)) of floral spikes. Overall, floral weight as a percentage of total plant weight decreased (from 21% to 13%), while investment in pollen increased (from 3.6 to 6%) between 280 and 600 mu mol mol(-1) CO2. Our results suggest that the continuing increase in atmospheric [CO2] could directly influence public health by stimulating the growth and pollen production of allergy- inducing species such as ragweed.	ARS, Climate Stress Lab, USDA, Beltsville Agr Res Ctr, Beltsville, MD 20705 USA	Ziska, LH (reprint author), ARS, Climate Stress Lab, USDA, Beltsville Agr Res Ctr, Bldg 046A,10300 Baltimore Ave, Beltsville, MD 20705 USA.						ACKERLY DD, 1995, GLOB CHANGE BIOL, V1, P199, DOI 10.1111/j.1365-2486.1995.tb00021.x; BIANCHI D. E., 1959, BOT GAZ, V120, P235, DOI 10.1086/336030; BUCK P, 1982, ANN ALLERGY, V49, P272; BUNCE JA, 1992, PLANT CELL ENVIRON, V15, P541, DOI 10.1111/j.1365-3040.1992.tb01487.x; CARLSON RW, 1982, OECOLOGIA, V54, P50, DOI 10.1007/BF00541106; Curtis PS, 1998, OECOLOGIA, V113, P299, DOI 10.1007/s004420050381; Deng X, 1998, ANN BOT-LONDON, V81, P67, DOI 10.1006/anbo.1997.0535; Durham OC, 1929, J ALLERGY, V1, P12, DOI 10.1016/S0021-8707(29)90080-0; EMBERLIN J, 1994, ALLERGY, V49, P15, DOI 10.1111/j.1398-9995.1994.tb04233.x; Frenz DA, 1999, ANN ALLERG ASTHMA IM, V82, P41, DOI 10.1016/S1081-1206(10)62658-0; Frenz DA, 1999, ANN ALLERG ASTHMA IM, V83, P341, DOI 10.1016/S1081-1206(10)62828-1; FRENZ DA, 1995, ANN ALLERG ASTHMA IM, V75, P417; GARBUTT K, 1984, NEW PHYTOL, V98, P443; GERGEN PJ, 1992, J ALLERGY CLIN IMMUN, V90, P579, DOI 10.1016/0091-6749(92)90130-T; Gregory P. H., 1973, MICROBIOLOGY ATMOSPH; Houghton J. T., 1996, IPCC CLIMATE CHANGE; IDSO KE, 1994, AGR FOREST METEOROL, V69, P153, DOI 10.1016/0168-1923(94)90025-6; Jablonski LM, 1997, CAN J BOT, V75, P533; KEELING CD, 1994, TRENDS 93 COMPENDIUM, P20; KIMBALL BA, 1993, VEGETATIO, V104, P65, DOI 10.1007/BF00048145; LAWLOR DW, 1991, PLANT CELL ENVIRON, V14, P807, DOI 10.1111/j.1365-3040.1991.tb01444.x; Meggs WJ, 1996, ARCH ENVIRON HEALTH, V51, P275; PlattsMills TAE, 1997, NEW ENGL J MED, V336, P1382, DOI 10.1056/NEJM199705083361909; POORTER H, 1993, VEGETATIO, V104, P77, DOI 10.1007/BF00048146; Reekie JYC, 1997, ANN BOT-LONDON, V80, P57, DOI 10.1006/anbo.1997.0407; ROBINSON JM, 1984, PLANT PHYSIOL, V75, P397, DOI 10.1104/pp.75.2.397; TREMMEL DC, 1993, CAN J PLANT SCI, V73, P1249; WOOLCOCK AJ, 1997, CIBA F SYMP, V206, P123; Ziska LH, 1999, WEED SCI, V47, P608; Ziska LH, 1997, PHOTOSYNTH RES, V54, P199, DOI 10.1023/A:1005947802161	30	112	121	2	21	C S I R O PUBLISHING	COLLINGWOOD	150 OXFORD ST, PO BOX 1139, COLLINGWOOD, VICTORIA 3066, AUSTRALIA	0310-7841			AUST J PLANT PHYSIOL	Aust. J. Plant Physiol.		2000	27	10					893	898				6	Plant Sciences	Plant Sciences	362QU	WOS:000089790400002		
J	Cayrol, C; Girard, JP				Cayrol, Corinne; Girard, Jean-Philippe			IL-33: an alarmin cytokine with crucial roles in innate immunity, inflammation and allergy	CURRENT OPINION IN IMMUNOLOGY			English	Review							T-CELL RESPONSES; LYMPHOID-CELLS; TYPE-2 IMMUNITY; LUNG INFLAMMATION; AIRWAY INFLAMMATION; ENDOGENOUS IL-33; IN-VIVO; ASTHMA; EXPRESSION; ASSOCIATION	IL-33 is a nuclear cytokine from the IL-1 family constitutively expressed in epithelial barrier tissues and lymphoid organs, which plays important roles in type-2 innate immunity and human asthma. Recent studies indicate that IL-33 induces production of large amounts of IL-5 and IL-13 by group 2 innate lymphoid cells (ILC2s), for initiation of allergic inflammation shortly after exposure to allergens or infection with parasites or viruses. IL-33 appears to function as an alarmin (alarm signal) rapidly released from producing cells upon cellular damage or cellular stress. In this review, we discuss the cellular sources, mode of action and regulation of IL-33, and we highlight its crucial roles in vivo with particular emphasis on results obtained using IL33-deficient mice.	[Cayrol, Corinne; Girard, Jean-Philippe] CNRS, IPBS, F-31077 Toulouse, France; [Cayrol, Corinne; Girard, Jean-Philippe] Univ Toulouse, UPS, IPBS, F-31077 Toulouse, France	Girard, JP (reprint author), CNRS, IPBS, 205 Route Narbonne, F-31077 Toulouse, France.	Jean-Philippe.Girard@ipbs.fr	CAYROL, Corinne/C-2106-2011; GIRARD, Jean-Philippe/F-5229-2010		Agence Nationale pour la Recherche [ANR-12-BSV3-0005-01]; Fondation ARC [SL220110603471]	We thank members of the Girard lab for fruitful discussions. Research in Girard lab is supported by grants from Agence Nationale pour la Recherche (ANR-12-BSV3-0005-01) and Fondation ARC (SL220110603471).	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Opin. Immunol.	DEC	2014	31						31	37		10.1016/j.coi.2014.09.004		7	Immunology	Immunology	AX8BS	WOS:000347136200007	25278425	
J	Sastre, J				Sastre, J.			Molecular diagnosis in allergy	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review							LIPID-TRANSFER PROTEIN; CONTROLLED FOOD CHALLENGE; NATURAL-RUBBER LATEX; COMPONENT-RESOLVED DIAGNOSIS; EXERCISE-INDUCED ANAPHYLAXIS; PARIETARIA-JUDAICA POLLEN; COWS MILK ALLERGY; HOUSE-DUST MITE; ASPERGILLUS-FUMIGATUS ALLERGENS; PLANTAGO-LANCEOLATA POLLEN	Development and progress made in the field of recombinant allergens have allowed for the development of a new concept in allergy diagnosis, molecular diagnosis (MD), which makes it possible to identify potential disease-eliciting molecules. Microarray-based testing performed with a small amount of serum sample enables clinicians to determine specific-IgE antibodies against multiple recombinants or purified natural allergen components. Performance characteristics of allergens so far tested are comparable with current diagnostic tests, but have to be confirmed in larger studies. The use of allergen components and the successful interpretation of test results in the clinic require some degree of knowledge about the basis of allergen components and their clinical implications. Allergen components can be classified by protein families based on their function and structure. This review provides a brief overview of basic information on allergen components, recombinants or purified, currently available or soon to become commercially available in ImmunoCAP or ISAC (R) systems, including names, protein family and function. Special consideration is given to primary or species-specific sensitization and possible cross-reactivity, because one of the most important clinical utility of MD is its ability to reveal whether the sensitization is genuine in nature (primary, species-specific) or if it is due to cross-reactivity to proteins with similar protein structures, which may help to evaluate the risk of reaction on exposure to different allergen sources. MD can be a support tool for choosing the right treatment for the right patient with the right timing. Such information will eventually give clinicians the possibility to individualize the actions taken, including an advice on targeted allergen exposure reduction, selection of suitable allergens for specific immunotherapy, or the need to perform food challenges. Nevertheless, all in vitro tests should be evaluated together with the clinical history, because allergen sensitization does not necessarily imply clinical responsiveness.	[Sastre, J.] Fdn Jimenez Diaz, Dept Allergy, E-28040 Madrid, Spain; [Sastre, J.] Univ Autonoma Madrid, Inst Salud Carlos III, CIBER Enfermedades Resp CIBERES, Dept Med,Minist Sci & Innovat, Madrid, Spain	Sastre, J (reprint author), Fdn Jimenez Diaz, Dept Allergy, Av Reyes Catolicos 2, E-28040 Madrid, Spain.	jsastre@fjd.es			Novartis; GSK; Stallergenes; UCB; Phadia; ALK-Abello	Joaquin Sastre reports having served as a consultant to Phadia, Schering-Plough and GSK, having been paid lecture fees by Novartis, GSK, Stallergenes, UCB and having received grant support from Phadia, GSK and ALK-Abello.	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Exp. Allergy	OCT	2010	40	10					1442	1460		10.1111/j.1365-2222.2010.03585.x		19	Allergy; Immunology	Allergy; Immunology	647RJ	WOS:000281636000003	20682003	
J	Fitzpatrick, AM; Gaston, BM; Erzurum, SC; Teague, WG				Fitzpatrick, Anne M.; Gaston, Benjamin M.; Erzurum, Serpil C.; Teague, W. Gerald		Natl Inst Hlth; Natl Heart Lung Blood Inst Severe	Features of severe asthma in school-age children: Atopy and increased exhaled nitric oxide	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						children; asthma; atopy; nitric oxide; pulmonary function testing	TO-TREAT ASTHMA; CHILDHOOD ASTHMA; DIFFICULT ASTHMA; EOSINOPHILIC INFLAMMATION; INHALED CORTICOSTEROIDS; AIRWAY INFLAMMATION; ALLERGEN EXPOSURE; RISK-FACTORS; DISPARITIES; POPULATION	Background: Children with severe asthma have persistent symptoms despite treatment with inhaled corticosteroids (ICSs). The differentiating features of severe asthma in children are poorly defined. Objective: To identify features of severe versus mild-to-moderate asthma in school-age children using noninvasive assessments of lung function, atopy, and airway inflammation. Methods: A total of 75 children (median age, 10 years) with asthma underwent baseline characterization including spirometry and lung volume testing, methacholine bronchoprovocation, allergy evaluation, and offline measurement of exhaled nitric oxide (F-ENO). Twenty-eight were followed longitudinally over 6 months. Participants were assigned to the severe asthma subgroup if they required high-dose ICS plus 2 or more minor criteria. Results: Children with severe versus mild-to-moderate asthma had more symptoms, greater airway obstruction, more gas trapping, and increased bronchial responsiveness to methacholine. Subjects with severe asthma also had higher concentrations of F-ENO and significantly greater sensitization to aeroallergens. With long-term study, both the reduction in FEVI and increase in F-ENO persisted in the severe versus mild-to-moderate group. Furthermore, despite adjustments in ICS doses, the frequency of exacerbations was significantly higher in subjects with severe (83%) versus mild-to-moderate asthma (43%). Conclusion: Severe asthma in childhood is characterized by poor symptom control despite high-dose ICS treatment and can be differentiated from mild-to-moderate asthma by measurement of lung function and F-ENO. Clinical implications: Clinicians should suspect severe asthma in children with poor response to ICS, airway obstruction, and high F-ENO.	Emory Univ, Sch Med, Dept Pediat, Atlanta, GA 30322 USA; Univ Virginia, Dept Pediat, Charlottesville, VA 22903 USA	Fitzpatrick, AM (reprint author), Emory Univ, Sch Med, Dept Pediat, 2015 Uppergate Dr, Atlanta, GA 30322 USA.	anne.fitzpatrick@emory.edu			NHLBI NIH HHS [R01 HL069170-06, R01 HL069170, R01 HL69170]		Abraham B, 2003, EUR RESPIR J, V22, P470, DOI 10.1183/09031936.03.00261903; American Thoracic Society, 1991, AM REV RESPIR DIS, V144, P1202, DOI 10.1164/ajrccm/144.5.1202; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; American Thoracic Society, 2000, AM J RESP CRIT CARE, V162, P2341, DOI DOI 10.1164/AJRCCM.162.6.ATS9-00; *AM THOR SOC EUR R, 2005, AM H RESP CRIT CARE, V181, P912; Berkman N, 2005, THORAX, V60, P383, DOI 10.1136/thx.2004.031104; Borish L, 2005, ANN ALLERG ASTHMA IM, V95, P247; Brussee JE, 2005, EUR RESPIR J, V25, P455, DOI 10.1183/09031936.05.00079604; Cieslewicz G, 1999, J CLIN INVEST, V104, P301, DOI 10.1172/JCI7010; Crapo RO, 2000, AM J RESP CRIT CARE, V161, P309; CRAPO RO, 1981, AM REV RESPIR DIS, V123, P659; Crater SE, 1999, AM J RESP CRIT CARE, V159, P806; de Blic J, 2004, J ALLERGY CLIN IMMUN, V113, P94, DOI 10.1016/j.jaci.2003.10.045; de Kluijver J, 2002, AM J RESP CRIT CARE, V166, P294, DOI 10.1164/rccm.2112097; Frank TL, 1998, AM J RESP CRIT CARE, V158, P1032; Gruchalla RS, 2005, J ALLERGY CLIN IMMUN, V115, P478, DOI 10.1016/j.jaci.2004.12.006; Hankinson JL, 1999, AM J RESP CRIT CARE, V159, P179; Higgins PS, 2005, CHEST, V128, P3846, DOI 10.1378/chest.128.6.3846; Jones SL, 2001, AM J RESP CRIT CARE, V164, P738; JONES SL, 2002, EUR RESPIR J, V60, P601; McDaniel M, 2006, PEDIATRICS, V117, pE868, DOI 10.1542/peds.2005-1721; Miranda C, 2004, J ALLERGY CLIN IMMUN, V113, P101, DOI 10.1016/j.jaci.2003.10.041; *NAT ASTHM ED PREV, 2003, 025075 NAT HEART LUN; Nelson BV, 1997, J PEDIATR-US, V130, P423, DOI 10.1016/S0022-3476(97)70204-X; Payne DNR, 2003, AM J RESP CRIT CARE, V167, P78, DOI 10.1164/rccm.200205-414OC; Payne DNR, 2001, AM J RESP CRIT CARE, V164, P1376; Payne DNR, 2001, THORAX, V56, P345, DOI 10.1136/thorax.56.5.345; Pearlman DN, 2006, J NATL MED ASSOC, V98, P239; Pijnenburg MW, 2005, THORAX, V60, P215, DOI 10.1136/thx.2004.023374; Rasmussen F, 2002, J ALLERGY CLIN IMMUN, V110, P220, DOI 10.1067/mai.2002.125295; Roberts G, 2004, THORAX, V59, P752, DOI 10.1136/thx.2003.008722; Robinson DS, 2003, EUR RESPIR J, V22, P478, DOI 10.1183/09031936.03.00017003; Stirling RG, 1998, THORAX, V53, P1030; Szefler SJ, 2002, J ALLERGY CLIN IMMUN, V109, P410, DOI 10.1067/mai.2002.122635; Warke TJ, 2002, THORAX, V57, P383, DOI 10.1136/thorax.57.5.383; Woodhead M, 2002, EUR RESPIR J, V20, P1, DOI 10.1183/09031936.02.01042002; Wraight JM, 2002, RESPIROLOGY, V7, P133, DOI 10.1046/j.1440-1843.2002.00374.x	37	111	112	0	0	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	DEC	2006	118	6					1218	1225		10.1016/j.jaci.2006.08.019		8	Allergy; Immunology	Allergy; Immunology	117NP	WOS:000242880300003	17157650	
J	Sakaguchi, H; Ashikaga, T; Miyazawa, M; Yoshida, Y; Ito, Y; Yoneyama, K; Hirota, M; Itagaki, H; Toyoda, H; Suzuki, H				Sakaguchi, H; Ashikaga, T; Miyazawa, M; Yoshida, Y; Ito, Y; Yoneyama, K; Hirota, M; Itagaki, H; Toyoda, H; Suzuki, H			Development of an in vitro skin sensitization test using human cell lines; human Cell Line Activation Test (h-CLAT) II. An inter-laboratory study of the h-CLAT	TOXICOLOGY IN VITRO			English	Article						THP-1; U-937; CD86; CD54; inter laboratory; validation; cell line; in vitro skin sensitization	EPIDERMAL LANGERHANS CELLS; DENDRITIC CELLS; CONTACT ALLERGENS; T-CELLS; COSTIMULATORY MOLECULES; EXPRESSION; IRRITANTS; CHEMICALS; EXPOSURE; HAPTENS	Recent regulatory changes have placed a major emphasis on in vitro, safety testing and alternative models. In regard to skin sensitization tests, dendritic cells (DCs) derived from human peripheral blood have been considered in the development of new in vitro alternatives. Human cell lines have been also reported recently. In our previous study, we suggested that measuring CD86 and/or CD54 expression on THP-1 cells (human monocytic leukemia cell line) could be used as an in vitro skin sensitization method. An inter-laboratory study among two laboratories was undertaken in Japan in order to further develop an in vitro skin sensitization model. In the present study, we used two human cell lines: THP-1 and U-937 (human histiocytic lymphoma cell line). First we optimized our test protocol (refer to the related paper entitled "optimization of the h-CLAT protocol" within this journal) and then we did an inter-laboratory validation with nine chemicals using the optimized protocol. We measured the expression of CD86 and CD54 on the above cells using flow cytometry after a 24 h and 48 h exposure to six known allergens (e.g., DNCB, pPD, NiSO4) and three non-allergens (e.g., SLS, tween 80). For the sample test concentration, four doses (0.1x, 0.5x, 1x, and 2x of the 50% inhibitory concentration (IC50)) were evaluated. IC50 was calculated using MTT assay. We found that allergens/non-allergens were better predicted using THP-1 cells compared to U-937 cells following a 24 h and a 48 h exposure. We also found that the 24 h treatment time tended to have a better accuracy than the 48 h treatment time for THP-1 cells. Expression of CD86 and CD54 were good predictive markers for THP-1 cells, but for U-937 cells, expression of CD86 was a better predictor than CD54, at the 24 h and the 48 h treatment time. The accuracy also improved when both markers (CD86 and CD54) were used as compared with a single marker for THP-1 cells. Both laboratories gave a good prediction of allergen/non-allergen, especially using THP-1 cells. These results suggest that our method, human Cell Line Activation Test (h-CLAT), using human cell lines THP-1 and U-937, but especially THP-1 cells at 24 h treatment, may be a useful in vitro skin sensitization model to predict various contact allergens. (c) 2005 Elsevier Ltd. All rights reserved.	Kao Corp, Safety & Microbial Control Res Ctr, Haga, Tochigi 3213497, Japan; Shiseido Co Ltd, Safety & Analyt Res Ctr, Kanazawa Ku, Yokohama, Kanagawa 2368643, Japan	Sakaguchi, H (reprint author), Kao Corp, Safety & Microbial Control Res Ctr, 2606 Akabane, Haga, Tochigi 3213497, Japan.	sakaguchi.hitoshi@kao.co.jp		Itagaki, Hiroshi/0000-0001-9756-0730			Aeby P, 2004, J INVEST DERMATOL, V122, P1154, DOI 10.1111/j.0022-202X.2004.22402.x; Aiba S, 1997, EUR J IMMUNOL, V27, P3031, DOI 10.1002/eji.1830271141; Ashikaga T, 2002, TOXICOL IN VITRO, V16, P711, DOI 10.1016/S0887-2333(02)00060-7; ASHIKAGA T, 2003, P 28 ANN M JAP COSM; BECKER D, 1994, J IMMUNOL METHODS, V169, P195, DOI 10.1016/0022-1759(94)90263-1; Boisleve F, 2004, J INVEST DERMATOL, V123, P494, DOI 10.1111/j.0022-202X.2004.23229.x; Champagne B, 1998, J IMMUNOL, V161, P6398; Coutant KD, 1999, TOXICOL SCI, V52, P189, DOI 10.1093/toxsci/52.2.189; De Smedt ACA, 2002, ARCH DERMATOL RES, V294, P109, DOI 10.1007/s00403-002-0296-0; Hulette BC, 2002, TOXICOL APPL PHARM, V182, P226, DOI 10.1006/taap.2002.9447; Hulette BC, 2001, ARCH DERMATOL RES, V293, P147, DOI 10.1007/s004030000201; IWAMOTO S, 1999, DENDRITIC CELLS, V9, P41; Krasteva M, 1996, CLIN EXP ALLERGY, V26, P563, DOI 10.1046/j.1365-2222.1996.d01-342.x; Mossmann T, 1983, J IMMUNOL METHODS, V6, P55; MOULON C, 1993, IMMUNOLOGY, V80, P373; PYTHON F, 2004, P 10 INT C TOX; Rizova H, 1999, BRIT J DERMATOL, V140, P200, DOI 10.1111/j.1365-2133.1999.02650.x; Rougier N, 2000, TOXICOLOGY, V145, P73, DOI 10.1016/S0300-483X(99)00222-X; ROUSSET F, 2002, CONTACT DERMATITIS, V46, P6; Rustemeyer T, 2003, EXP DERMATOL, V12, P682, DOI 10.1034/j.1600-0625.2003.00077.x; Ryan CA, 2004, TOXICOL LETT, V150, P301, DOI 10.1016/j.toxlet.2004.02.002; Ryan CA, 2001, TOXICOL IN VITRO, V15, P43, DOI 10.1016/S0887-2333(00)00059-X; SAKAGUCHI H, 2003, P 17 ANN M JAP SOC A; Staquet MJ, 2004, TOXICOL IN VITRO, V18, P493, DOI 10.1016/j.tiv.2003.12.005; Verrier AC, 1999, INT ARCH ALLERGY IMM, V120, P56, DOI 10.1159/000024220; Yoshida Y, 2003, TOXICOL IN VITRO, V17, P221, DOI 10.1016/S0887-2333(03)00006-7	26	111	115	0	4	PERGAMON-ELSEVIER SCIENCE LTD	OXFORD	THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND	0887-2333			TOXICOL IN VITRO	Toxicol. Vitro	AUG	2006	20	5					774	784		10.1016/j.tiv.2005.10.014		11	Toxicology	Toxicology	058YP	WOS:000238700800029	16337770	
J	Lannero, E; Wickman, M; Pershagen, G; Nordvall, L				Lannero, E; Wickman, M; Pershagen, G; Nordvall, L			Maternal smoking during pregnancy increases the risk of recurrent wheezing during the first years of life (BAMSE)	RESPIRATORY RESEARCH			English	Article							ENVIRONMENTAL TOBACCO-SMOKE; CHILDHOOD LUNG-FUNCTION; RESPIRATORY-FUNCTION; IN-UTERO; PARENTAL SMOKING; PASSIVE SMOKING; ASTHMA; EXPOSURE; CHILDREN; BRONCHITIS	Background: Exposure to cigarette smoking during foetal and early postnatal life may have implications for lung health. The aim of this study was to assess the possible effects of such exposure in utero on lower respiratory disease in children up to two years of age. Methods: A birth cohort of 4089 newborn infants was followed for two years using parental questionnaires. When the infant was two months old the parents completed a questionnaire on various lifestyle factors, including maternal smoking during pregnancy and after birth. At one and two years of age information was obtained by questionnaire on symptoms of allergic and respiratory diseases as well as on environmental exposures, particularly exposure to environmental tobacco smoke (ETS). Adjustments were made for potential confounders. Results: When the mother had smoked during pregnancy but not after that, there was an increased risk of recurrent wheezing up to two years' age, ORadj = 2.2, (95% CI 1.3-3.6). The corresponding OR was 1.6, ( 95% CI 1.2-2.3) for reported exposure to ETS with or without maternal smoking in utero. Maternal smoking during pregnancy but no exposure to ETS also increased the risk of doctor's diagnosed asthma up to two years of age, ORadj = 2.1, ( 95% CI 1.2-3.7). Conclusion: Exposure to maternal cigarette smoking in utero is a risk factor for recurrent wheezing, as well as doctor's diagnosed asthma in children up to two years of age.	Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; Karolinska Univ Hosp, Dept Paediat, Huddinge, Sweden; Stockholm Cty Council, Dept Environm & Occupat Hlth, Stockholm, Sweden; Karolinska Inst, Ctr Allergy Res, Stockholm, Sweden; Uppsala Univ, Dept Womens & Childrens Hlth, Uppsala, Sweden	Lannero, E (reprint author), Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden.	eva.lannero@kbh.ki.se; magnus.wickman@sll.se; goran.pershagen@ki.se; lennart.nordvall@kbh.uu.se					Asher MI, 1998, CLIN EXP ALLERGY, V28, P52; Cunningham J, 1996, AM J RESP CRIT CARE, V153, P218; Elliot J, 1998, AM J RESP CRIT CARE, V158, P802; Elliot JG, 2003, AM J RESP CRIT CARE, V167, P45, DOI 10.1164/rccm.2110005; Foundas M, 1997, AUST NZ J OBSTET GYN, V37, P383, DOI 10.1111/j.1479-828X.1997.tb02443.x; Gilliland FD, 2000, THORAX, V55, P271, DOI 10.1136/thorax.55.4.271; Gilliland FD, 2003, AM J RESP CRIT CARE, V167, P917, DOI 10.1164/rccm.200206-616OC; Gilliland FD, 2001, AM J RESP CRIT CARE, V163, P429; Hoo AF, 1998, AM J RESP CRIT CARE, V158, P700; Horta BL, 1997, PAEDIATR PERINAT EP, V11, P140, DOI 10.1046/j.1365-3016.1997.d01-17.x; Kull I, 2002, ARCH DIS CHILD, V87, P478, DOI 10.1136/adc.87.6.478; LANNERO E, 2002, PAEDIAT ALLERGY IMMU, V13, P1; Li YF, 2000, AM J RESP CRIT CARE, V162, P2097; LINDFORS A, 1995, ARCH DIS CHILD, V73, P408; Lodrup Carlsen K C, 1997, Eur Respir J, V10, P1774, DOI 10.1183/09031936.97.10081774; Lux AL, 2000, ARCH DIS CHILD, V83, P307, DOI 10.1136/adc.83.4.307; Nafstad P, 1997, EPIDEMIOLOGY, V8, P293, DOI 10.1097/00001648-199705000-00011; RYLANDER E, 1993, EUR J EPIDEMIOL, V9, P517; Statistics Sweden, 1989, OCC POP HOUS CENS 19; Stick SM, 1996, LANCET, V348, P1060, DOI 10.1016/S0140-6736(96)04446-7; Strachan DP, 1997, THORAX, V52, P905; von Mutius E, 2002, J ALLERGY CLIN IMMUN, V109, pS525, DOI 10.1067/mai.2002.124565; Wennergren G, 1997, ACTA PAEDIATR, V86, P351, DOI 10.1111/j.1651-2227.1997.tb09021.x; Wickman M, 2002, PEDIATR ALLERGY IMMU, V13, P11, DOI 10.1034/j.1399-3038.13.s.15.10.x; WICKMAN M, 1992, PEDIATRIC ALLERGY IM, V3, P128, DOI 10.1111/j.1399-3038.1992.tb00036.x; Young S, 2000, PEDIATR PULM, V29, P331, DOI 10.1002/(SICI)1099-0496(200005)29:5<331::AID-PPUL1>3.0.CO;2-A	26	111	119	0	5	BIOMED CENTRAL LTD	LONDON	MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND	1465-9921			RESP RES	Respir. Res.	JAN 5	2006	7								3	10.1186/1465-9921-7-3		6	Respiratory System	Respiratory System	008ZD	WOS:000235080000001	16396689	
J	Brannan, JD; Anderson, SD; Perry, CP; Freed-Martens, R; Lassig, AR; Charlton, B				Brannan, JD; Anderson, SD; Perry, CP; Freed-Martens, R; Lassig, AR; Charlton, B		Aridol Study Grp	The safety and efficacy of inhaled dry powder mannitol as a bronchial provocation test for airway hyperresponsiveness: a phase 3 comparison study with hypertonic (4.5%) saline	RESPIRATORY RESEARCH			English	Article							ASTHMATIC SUBJECTS; INDUCED BRONCHOCONSTRICTION; EPIDEMIOLOGIC SURVEY; CHALLENGE; RESPONSIVENESS; EXERCISE; CHILDREN; METHACHOLINE; SENSITIVITY; HYPERVENTILATION	Background: Inhaled mannitol is a new bronchial provocation test (BPT) developed to improve portability and standardisation of osmotic challenge testing. Osmotic challenge tests have an advantage over the traditional methods of measuring airway hyperresponsiveness using methacholine as they demonstrate higher specificity to identify asthma and thus the need for treatment with inhaled corticosteroids (ICS). The safety and the efficacy of mannitol (M) as a BPT to measure airway hyperresponsiveness were compared to hypertonic (4.5%) saline (HS) in people both with and without signs and symptoms of asthma. Methods: A phase III, multi-centre, open label, operator-blinded, crossover design, randomised trial, with follow-up. Asthmatics and non-asthmatics (6-83 yr) were recruited and 592 subjects completed the study. Mannitol was delivered using a low resistance dry powder inhaler and HS was delivered using an ultrasonic nebuliser. The FEV1 was measured 60 seconds after each dose of mannitol (5,10,20,40,80,160,160,160 mg) and after each exposure to HS (0.5,1.0,2.0,4.0,8.0 minutes). A 15% fall in FEV1 defined a positive test. Adverse events were monitored and diaries kept for 7 days following the tests. Results: Mean pre-test FEV1 (mean +/- SD) was 95.5 +/- 14% predicted. 296 were positive to mannitol (M+) and 322 positive to HS (HS+). A post study physician conducted clinical assessment identified 82.3% asthmatic (44% classified mild) and 17.7% non-asthmatic. Of those M+, 70.1% were taking ICS and of those mannitol negative (M-), 81.1% were taking ICS. The % fall in FEV1 for mannitol in asthmatics was 21.0% +/- 5.7 and for the non-asthmatics, 5.5% +/- 4.8. The median PD15 M was 148 mg and PD15 HS 6.2 ml. The sensitivity of M to identify HS+ was 80.7% and the specificity 86.7%. The sensitivity of M compared with the clinical assessment was 59.8% and specificity 95.2% and increased to 88.7% and 95.0% respectively when the M- subjects taking ICS were excluded. Cough was common during testing. There were no serious adverse events. The diarised events were similar for mannitol and HS, the most common being headache (17.2% M, 19% HS), pharyngolaryngeal pain (5.1% M, 3% HS), nausea (4.3% M, 3% HS), and cough (2.2% M, 2.4% HS). Conclusion: The efficacy and safety of mannitol was demonstrated in non-asthmatic and clinically diagnosed asthmatic adults and children.	Royal Prince Alfred Hosp, Dept Resp Med, Camperdown, NSW 2050, Australia; Pharmaxis Ltd, Frenchs Forest, NSW 2086, Australia	Anderson, SD (reprint author), Royal Prince Alfred Hosp, Dept Resp Med, 11 W,Missenden Rd, Camperdown, NSW 2050, Australia.	johnb@med.usyd.edu.au; sandya@med.usyd.edu.au; clarep@med.usyd.edu.au; ruthm@med.usyd.edu.au; Anna.Lassig@pharmaxis.com.au; brett.charlton@pharmaxis.com.au					American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Anderson SD, 1997, AM J RESP CRIT CARE, V156, P758; Anderson SD, 2001, MED SCI SPORT EXER, V33, P893, DOI 10.1097/00005768-200106000-00007; Anderson SD, 2003, CLIN REV ALLERG IMMU, V24, P63; ANDERSON SD, 2005, MONITORING ASTHMA, P275; Anderson SD, 1995, PROVOCATION CHALLENG, P249; Barben J, 2005, PROG R RES, V33, P125; Brannan JD, 1998, AM J RESP CRIT CARE, V158, P1120; Brannan JD, 2000, AM J RESP CRIT CARE, V161, P2096; Brannan JD, 2002, RESPIROLOGY, V7, P37, DOI 10.1046/j.1440-1843.2002.00357.x; Brannan JD, 2001, AM J RESP CRIT CARE, V163, P1420; Cockcroft DW, 2005, CHEST, V127, P839, DOI 10.1378/chest.127.3.839; Currie GP, 2003, BRIT J CLIN PHARMACO, V56, P11, DOI 10.1046/j.1365-2125.2003.01831.x; Currie GP, 2003, ALLERGY, V58, P762, DOI 10.1034/j.1398-9995.2003.00226.x; de Meer G, 2005, EUR RESPIR J, V25, P153, DOI 10.1183/09031936.04.00008004; Global Initiative for Asthma, 2002, GLOB STRAT ASTHM MAN; Hofstra WB, 2000, PEDIATR PULM, V29, P415, DOI 10.1002/(SICI)1099-0496(200006)29:6<415::AID-PPUL1>3.0.CO;2-7; Holzer K, 2003, AM J RESP CRIT CARE, V167, P534, DOI 10.1164/rccm.200208-916OC; Koskela HO, 2004, CHEST, V125, P1985, DOI 10.1378/chest.125.6.1985; Koskela HO, 2003, CHEST, V124, P1341, DOI 10.1378/chest.124.4.1341; Leuppi JD, 2002, SWISS MED WKLY, V132, P151; Leuppi JD, 2001, AM J RESP CRIT CARE, V163, P406; Lim S, 1999, AM J RESP CRIT CARE, V159, P22; National Asthma Council, 2002, ASTHM MAN HDB 2002; Rabone SJ, 1996, OCCUP MED-OXFORD, V46, P177; RIEDLER J, 1994, AM J RESP CRIT CARE, V150, P1632; Riedler J, 1998, EUR RESPIR J, V11, P355, DOI 10.1183/09031936.98.11020355; SMITH CM, 1990, EUR RESPIR J, V3, P144; SMITH CM, 1986, J ALLERGY CLIN IMMUN, V77, P729, DOI 10.1016/0091-6749(86)90419-7; SMITH CM, 1989, J ALLERGY CLIN IMMUN, V84, P781, DOI 10.1016/0091-6749(89)90309-6; Sont JK, 1999, AM J RESP CRIT CARE, V159, P1043; YAGER D, 1991, AM REV RESPIR DIS, V143, pS52	32	111	112	0	4	BIOMED CENTRAL LTD	LONDON	236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND	1465-993X	1465-9921		RESP RES	Respir. Res.	DEC 9	2005	6								144	10.1186/1465-9921-6-144		12	Respiratory System	Respiratory System	006IM	WOS:000234891200001	16336673	
J	Duan, W; Chan, JHP; Mckay, K; Crosby, JR; Choo, HH; Leung, BP; Karras, JG; Wong, WSF				Duan, W; Chan, JHP; Mckay, K; Crosby, JR; Choo, HH; Leung, BP; Karras, JG; Wong, WSF			Inhaled p38 alpha mitogen-activated protein kinase antisense oligonucleotide attenuates asthma in mice	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; bronchoalveolar lavage fluid; eosinophilia; mucus hypersecretion; ovalbumin	AIRWAY SMOOTH-MUSCLE; CYTOKINE PRODUCTION; SIGNALING PATHWAYS; T-CELLS; ANTIGEN-RECEPTOR; EPITHELIAL-CELLS; MAP KINASE; MAST-CELL; EXPRESSION; INHIBITOR	The p38 mitogen-activated protein kinase (MAPK) plays a critical role in the activation of inflammatory cells. Therefore, we investigated the antiinflammatory effects of a respirable p38 alpha MAPK antisense oligonucleotide (p38 alpha-ASO) in a mouse asthma model. A potent and selective p38 alpha-ASO was characterized in vitro. Inhalation of aerosolized p38 alpha-ASO using an aerosol chamber dosing system produced measurable lung deposition of ASO and significant reduction of ovalbumin (OVA-)-induced increases in total cells, eosinophils, and interleukin 4 (IL-4), IL-5, and IL-13 levels in bronchoalveolar lavage fluid, and dose-dependent inhibition of airway hyperresponsiveness in allergen-challenged mice. Furthermore, inhaled p38 alpha-ASO markedly inhibited OVA-induced lung tissue eosinophilia and airway mucus hypersecretion. Quantitative polymerase chain reaction analysis of bronchoalveolar lavage fluid cells and peribronchial lymph node cells showed that p38 alpha-ASO significantly reduced p38 alpha MAPK mRNA expression. Nose-only aerosol exposure of mice verified the p38 alpha-ASO-induced inhibition of OVA-induced pulmonary eosinophilia, mucus hypersecretion, and airway hyperresponsiveness. None of the effects of the p38 alpha-ASO were produced by a six-base mismatched control oligonucleotide. These findings demonstrate antisense pharmacodynamic activity in the airways after aerosol delivery and suggest that a p38 alpha MAPK ASO approach may have therapeutic potential for asthma and other inflammatory lung diseases.	Natl Univ Singapore, Fac Med, Dept Pharmacol, Singapore 117597, Singapore; Tan Tock Seng Hosp, Dept Rheumatol Allergy & Immunol, Singapore, Singapore; ISIS Pharmaceut, Dept Antisense Drug Discovery, Carlsbad, CA 92008 USA	Wong, WSF (reprint author), Natl Univ Singapore, Fac Med, Dept Pharmacol, MD2,18 Med Dr, Singapore 117597, Singapore.	phcwongf@nus.edu.sg	Leung, Bernard/O-2409-2013; Wong, W.S. Fred/D-8205-2013				Adachi T, 2000, J IMMUNOL, V165, P2198; Adachi T, 2003, J ALLERGY CLIN IMMUN, V111, P113, DOI 10.1067/mai.2003.27; Atherton HC, 2003, AM J PHYSIOL-LUNG C, V285, pL730, DOI 10.1152/ajplung.00089.2003; Busse WW, 2001, NEW ENGL J MED, V344, P350; CANDRA E, 2003, KOREAN J PHYSL PH S1, V7, P161; Cui CH, 2002, AM J RESP CELL MOL, V27, P329, DOI 10.1165/rcmb.4762; Dong C, 2002, ANNU REV IMMUNOL, V20, P55, DOI 10.1146/annurev.immunol.20.091301.131133; Duan W, 2004, J IMMUNOL, V172, P7053; Elias JA, 2003, J CLIN INVEST, V111, P291, DOI 10.1172/JCI200317748; Fernandes DJ, 2003, J APPL PHYSIOL, V95, P844, DOI 10.1152/japplphysiol.00192.2003; Fitzgerald SM, 2004, AM J RESP CELL MOL, V30, P585, DOI 10.1165/rcmb.2003-0282OC; Geary RS, 1997, DRUG METAB DISPOS, V25, P1272; Gleich GJ, 2000, J ALLERGY CLIN IMMUN, V105, P651, DOI 10.1067/mai.2000.105712; Herrick CA, 2003, NAT REV IMMUNOL, V3, P1; Hirst SJ, 2003, RESP PHYSIOL NEUROBI, V137, P309, DOI 10.1016/S1569-9048(03)00155-1; Hirst SJ, 2002, AM J RESP CRIT CARE, V165, P1161, DOI 10.1164/rccm.2107158; Justice JP, 2002, AM J PHYSIOL-LUNG C, V282, pL1066, DOI 10.1152/ajplung.00195.2001; Kalesnikoff J, 2001, IMMUNITY, V14, P801, DOI 10.1016/S1074-7613(01)00159-5; Kampen GT, 2000, BLOOD, V95, P1911; Kawakami T, 2002, NAT REV IMMUNOL, V2, P773, DOI 10.1038/nri914; Koo GC, 2003, AM J RESP CRIT CARE, V167, P1400, DOI 10.1164/rccm.200207-696OC; Koprak S, 1999, CELL IMMUNOL, V192, P87, DOI 10.1006/cimm.1998.1448; LARCHE M, 2002, J ALLERGY CLIN IMMUN, V111, P450; Leeds JM, 1996, ANAL BIOCHEM, V235, P36, DOI 10.1006/abio.1996.0088; Li L, 1999, J IMMUNOL, V162, P2477; Lu BF, 2004, NAT IMMUNOL, V5, P38, DOI 10.1038/ni1020; Lukacs NW, 2001, NAT REV IMMUNOL, V1, P108, DOI 10.1038/35100503; Lundblad LKA, 2002, J APPL PHYSIOL, V93, P1198, DOI 10.1152/japplphysiol.00080.2002; McKay RA, 1999, J BIOL CHEM, V274, P1715, DOI 10.1074/jbc.274.3.1715; Mori A, 1999, J IMMUNOL, V163, P4763; Nel AE, 2002, J ALLERGY CLIN IMMUN, V109, P758, DOI 10.1067/mai.2002.124259; Niiro H, 2002, NAT REV IMMUNOL, V2, P945, DOI 10.1038/nri955; Nyce JW, 1997, NATURE, V385, P721, DOI 10.1038/385721a0; Panettieri Reynold A. 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J. Respir. Crit. Care Med.	MAR 15	2005	171	6					571	578		10.1164/rccm.200408		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	905HV	WOS:000227560100006	15557129	
J	Bugiani, M; Carosso, A; Migliore, E; Piccioni, P; Corsico, A; Olivieri, M; Ferrari, M; Pirina, P; de Marco, R				Bugiani, M; Carosso, A; Migliore, E; Piccioni, P; Corsico, A; Olivieri, M; Ferrari, M; Pirina, P; de Marco, R		ISAYA ECRHS Italy Study Grp	Allergic rhinitis and asthma comorbidity in a survey of young adults in Italy	ALLERGY			English	Article						allergic rhinitis; asthma; comorbidity; epidemiology	RESPIRATORY HEALTH SURVEY; NATURAL-HISTORY; AIR-POLLUTION; RISK-FACTORS; PREVALENCE; COMMUNITY; SYMPTOMS; EPIDEMIOLOGY; LUNG; QUESTIONNAIRE	Background: Several studies have provided evidence of a strong association between asthma and allergic or nonallergic rhinitis, leading to the hypothesis that allergic rhinitis (AR) and asthma represent a continuum of the same disease. Aim: The aims of our study were: (i) to measure the comorbidity of AR and asthma and asthma-like symptoms and (ii) to assess whether asthma, AR, and their coexistence share a common pattern of individual risk factors. Methods: The subjects are participants from the Italian multicentre, cross-sectional survey on respiratory symptoms in the young adult general population (Italian Study of Asthma in Young Adults, ISAYA). The relationship between individual risk factors and asthma, AR and their coexistence, was studied by means of a multinomial logistic regression. Results: About 60% of asthmatics reported AR. On the other hand, subjects with AR presented an eightfold risk of having asthma compared to subjects without AR. Age was negatively associated with asthma [OR = 0.89, 95% confidence interval (CI): 0.82-0.96], AR (OR = 0.92, 95% CI: 0.86-0.98), and asthma associated with AR (OR = 0.83, 95% CI: 0.79-0.88). The risk of AR without asthma was significantly higher in the upper social classes (OR = 1.23, 95% CI: 1.08-1.39). Active current smoking exposure was positively associated with asthma alone (OR = 1.24, 95% CI: 1.09-1.41) and negatively associated with AR with (OR = 0.69, 95% CI: 0.54-0.88) or without (OR = 0.76, 95% CI: 0.69-0.84) asthma. Conclusions: Asthma and AR coexist in a substantial percentage of patients; bronchial asthma and AR, when associated, seem to share the same risk factors as AR alone while asthma without AR seems to be a different condition, at least with respect to some relevant risk factors.	NHS CPA ASL 4, Unit Pneumol, I-10100 Turin, Italy; Univ Pavia, IRCCS, Policlin San Matteo, Div Resp Dis, I-27100 Pavia, Italy; Univ Verona, Dept Med & Publ Hlth, Unit Occupat Med, I-37100 Verona, Italy; Univ Verona, Dept Biomed & Surg Sci, Unit Internal Med, I-37100 Verona, Italy; Univ Sassari, Dept Resp Dis, I-07100 Sassari, Italy; Univ Verona, Dept Med & Publ Hlth, Unit Epidemiol & Med Stat, I-37100 Verona, Italy	Bugiani, M (reprint author), NHS CPA ASL 4, Unit Pneumol, Lungo Dora Savona 26, I-10100 Turin, Italy.		; de Marco, Roberto/A-5470-2008; SESM, SESM/C-1440-2008; bucca, caterina/C-9886-2009; Dalmasso, Paola/F-8555-2013; Ciccone, Giovannino/K-3136-2016	/0000-0003-2517-6515; Montomoli, Cristina/0000-0002-8526-5846; bucca, caterina/0000-0002-9941-9236; Dalmasso, Paola/0000-0001-6081-6966; Ciccone, Giovannino/0000-0001-7644-9574; ROMANO, Canzio/0000-0001-5294-9793; Bono, Roberto/0000-0002-2471-6594; Fanfulla, Francesco/0000-0002-8601-423X; Corsico, Angelo Guido/0000-0002-8716-4694; Rolla, Giovanni/0000-0001-5997-7172			Asher MI, 1998, CLIN EXP ALLERGY, V28, P52; Asher MI, 1998, CLIN EXP ALLERGY, V28, P90; Biggeri A, 2001, Epidemiol Prev, V25, P83; Bousquet J., 2002, Allergy (Copenhagen), V57, P841, DOI 10.1034/j.1398-9995.2002.23625.x; BRAMAN SS, 1987, CHEST, V91, P671, DOI 10.1378/chest.91.5.671; BraunFahrlander C, 1997, PEDIATR ALLERGY IMMU, V8, P75, DOI 10.1111/j.1399-3038.1997.tb00147.x; BRODER I, 1974, J ALLERGY CLIN IMMUN, V54, P100, DOI 10.1016/0091-6749(74)90038-4; BUCCA C, 1995, LANCET, V346, P791, DOI 10.1016/S0140-6736(95)91617-2; Burney P, 1996, EUR RESPIR J, V9, P687; CORREN J, 1998, J ALLERGY CLIN IMMUN, V101, P352; D'Amato G, 2002, CLIN EXP ALLERGY, V32, P1391, DOI 10.1046/j.1365-2745.2002.01519.x; de Marco R, 1999, EUR RESPIR J, V14, P1044, DOI 10.1183/09031936.99.14510449; de Marco R, 2003, ALLERGY, V58, P221, DOI 10.1034/j.1398-9995.2003.00059.x; de Marco R, 2002, CLIN EXP ALLERGY, V32, P1405, DOI 10.1046/j.1365-2745.2002.01466.x; de Marco R, 2002, J ALLERGY CLIN IMMUN, V110, P228, DOI 10.1067/mai.2002.125600; DEMARCO R, 1994, EUR RESPIR J, V7, P2139, DOI 10.1183/09031936.94.07122139; Grossman J, 1997, CHEST, V111, pS11, DOI 10.1378/chest.111.2_Supplement.11S; Guerra S, 2002, J ALLERGY CLIN IMMUN, V109, P419, DOI 10.1067/mai.2002.121701; International Consensus Report on the diagnosis and management of rhinitis, 1994, ALLERGY S19, V49, P1; Janson C, 2001, LANCET, V358, P2103, DOI 10.1016/S0140-6736(01)07214-2; Janson C, 2001, EUR RESPIR J, V18, P598, DOI 10.1183/09031936.01.00205801; Jones NS, 1998, CLIN OTOLARYNGOL, V23, P547, DOI 10.1046/j.1365-2273.1998.2360547.x; Kapsali T, 1997, J ALLERGY CLIN IMMUN, V99, P138; Lack G, 2001, J ALLERGY CLIN IMMUN, V108, pS9, DOI 10.1067/mai.2001.115562; Leynaert B., 2000, J ALLERGY CLIN IMMUN, V106, P201; Oglesby L, 2000, AM J EPIDEMIOL, V152, P75, DOI 10.1093/aje/152.1.75; Olivieri M, 2002, ALLERGY, V57, P600, DOI 10.1034/j.1398-9995.2002.23537.x; Passalacqua G, 2000, THORAX, V55, P26; Rusconi F, 1999, AM J RESP CRIT CARE, V160, P1617; SETTIPANE RJ, 1994, ALLERGY PROC, V15, P21, DOI 10.2500/108854194778816634; SHIM C, 1986, AM J MED, V80, P18, DOI 10.1016/0002-9343(86)90043-4; Shusterman D, 2002, ENVIRON HEALTH PERSP, V110, P649; SIBBALD B, 1991, THORAX, V46, P895, DOI 10.1136/thx.46.12.895; Simons FER, 1999, J ALLERGY CLIN IMMUN, V104, P534, DOI 10.1016/S0091-6749(99)70320-9; Smith JM, 1983, ALLERGY PRINCIPLES P, V771-803; Spector SL, 1997, J ALLERGY CLIN IMMUN, V99, pS773, DOI 10.1016/S0091-6749(97)70126-X; StataCorp, 2003, STAT STAT SOFTW REL; Tobin MJ, 2002, AM J RESP CRIT CARE, V165, P598, DOI 10.1164/rccm.2201062; Togias A, 2001, AM J RESP CRIT CARE, V164, P726; Townley RG, 1998, ANN ALLERG ASTHMA IM, V80, P137; Vignola AM, 2001, CLIN EXP ALLERGY, V31, P674, DOI 10.1046/j.1365-2222.2001.01115.x; Warner JO, 1998, PEDIATR ALLERGY IMMU, V9, P116; Weiland Stephan K., 1994, Annals of Epidemiology, V4, P243; WRIGHT AL, 1994, PEDIATRICS, V94, P895; WUTHRICH B, 1995, INT ARCH ALLERGY IMM, V106, P149	45	111	114	0	6	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	FEB	2005	60	2					165	170		10.1111/j.1398-9995.2005.00659.x		6	Allergy; Immunology	Allergy; Immunology	887VF	WOS:000226332900006	15647036	
J	Pittner, G; Vrtala, S; Thomas, WR; Weghofer, M; Kundi, M; Horak, F; Kraft, D; Valenta, R				Pittner, G; Vrtala, S; Thomas, WR; Weghofer, M; Kundi, M; Horak, F; Kraft, D; Valenta, R			Component-resolved diagnosis of house-dust mite allergy with purified natural and recombinant mite allergens	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						cross-reactivity; diagnosis; house-dust mites; IgE reactivity profile; immunotherapy; natural and recombinant allergens	DERMATOPHAGOIDES-PTERONYSSINUS ALLERGEN; DER-P-I; STANDARDIZED EXTRACTS; CROSS-REACTIVITY; HUMAN IGE; IMMUNOTHERAPY; BINDING; ASTHMA; CHILDREN; POLLEN	Background Mites belong to the most frequent and potent allergen sources. Immunotherapy with mite allergen extracts is frequently performed if allergen avoidance is not possible or successful. However, highly controversial results have been reported for mite-specific immunotherapy. Objective The aim of this study was to develop diagnostic concepts that may contribute to an improved selection of patients for immunotherapy with Der p allergen extracts and that may be used for immunological monitoring of patients undergoing this treatment. Methods The IgE reactivity profiles to Der p extract were determined in a Middle European mite-allergic population by IgE immunoblotting and by using a panel of seven purified natural or recombinant Der p allergens (nDer p 1, nDer p 4, rDer p 2, rDer p 5, rDer p 7, rDer p 8, rDer p 10). Furthermore, we investigated the sensitization and cross-reactivity to house-dust- and storage-mite allergen extracts by CAP FEIA measurements and by IgE competition studies. Results More than 95% of the patients could be diagnosed with a combination of nDer p 1 and rDer p 2. With the methods used, we could discriminate mite-allergic patients who were mainly sensitized to the major Der p allergens (Der p 1, Der p 2) from patients with a broad sensitization profile, including highly cross-reactive allergens (e.g. Der p 10: tropomyosin) as well as reactivity to storage mites. Conclusions Diagnostic tests containing the major mite allergens (i.e. Der p 1, Der p 2) and highly cross-reactive mite allergens (e.g. Der p 10) may improve the diagnostic selection of patients for immunotherapy with Der p extracts. These tests may also be used for the immunological monitoring of patients undergoing immunotherapy.	Med Univ Vienna, Vienna Gen Hosp, Dept Pathophysiol, Div Immunopathol, A-1090 Vienna, Austria; Univ Western Australia, Telethon Inst Child Hlth Res, Ctr Child Hlth Res, Nedlands, WA 6009, Australia; Med Univ Vienna, Inst Environm Hlth, Dept Occupat & Social Hyg, A-1090 Vienna, Austria; Univ Vienna, Med Vienna Gen Hosp, Dept ENT, A-1010 Vienna, Austria	Vrtala, S (reprint author), Med Univ Vienna, Vienna Gen Hosp, Dept Pathophysiol, Div Immunopathol, Wahringer Gurtel 18-20, A-1090 Vienna, Austria.	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Exp. Allergy	APR	2004	34	4					597	603		10.1111/j.1365-2222.2004.1930.x		7	Allergy; Immunology	Allergy; Immunology	812RQ	WOS:000220857000016	15080813	
J	Arif, AA; Delclos, GL; Lee, ES; Tortolero, SR; Whitehead, LW				Arif, AA; Delclos, GL; Lee, ES; Tortolero, SR; Whitehead, LW			Prevalence and risk factors of asthma and wheezing among US adults: an analysis of the NHANES III data	EUROPEAN RESPIRATORY JOURNAL			English	Article						asthma; epidemiology; National Health and Nutrition Examination; Survey III	NUTRITION EXAMINATION SURVEY; RESPIRATORY HEALTH SURVEY; 2ND NATIONAL-HEALTH; BODY-MASS INDEX; YOUNG-ADULTS; SYMPTOMS QUESTIONNAIRE; SOCIOECONOMIC-STATUS; CHILDHOOD ASTHMA; REPORTED ASTHMA; PUERTO-RICAN	The prevalence of asthma has been on the increase in the USA and worldwide. To understand the worsening epidemiological trends of asthma, this study analysed the data from the third National Health and Nutrition Examination Survey (NHANES III) to determine the prevalence and risk factors for asthma and wheezing among US adults. This analysis used data from, 18,825 US adults aged greater than or equal to 20 yrs who had participated in the NHANES III project. After excluding subjects with physician-diagnosed emphysema, a total of 18,393 subjects were included in the final analysis. The prevalence of current asthma (asthma) was 4.5% and the prevalence of wheezing in the previous 12 months (wheezing) was 16.4%. Mexican-Americans exhibited the lowest prevalence of asthma when compared with other race/ethnic groups. Multiple logistic regression analysis showed that Mexican-Americans were less likely to report asthma when compared to non-Hispanic whites. Low education level, female sex, current and past smoking status, pet ownership, lifetime diagnosis of physician-diagnosed hay fever and obesity were all significantly associated with asthma and/or wheezing. No significant effect of indoor air pollutants, as derived from the use of household heating/cooking appliances, on asthma and wheezing was observed in this study. In conclusion, this study observed racial/ethnic differences in the prevalence of asthma and wheezing and identified several important risk factors that may contribute to development and/or exacerbation of asthma and wheezing. Contrary to earlier reports, the proxy measures of indoor air pollution used in this study were not found to be associated with increased risk of asthma and wheezing.	Texas Tech Univ, Hlth Sci Ctr, Dept Hlth Serv Res & Management, Lubbock, TX 79430 USA; Univ Texas, Sch Publ Hlth, Houston, TX USA	Arif, AA (reprint author), Texas Tech Univ, Hlth Sci Ctr, Dept Hlth Serv Res & Management, 3601 4th St,MS 8161, Lubbock, TX 79430 USA.			Arif, Ahmed A./0000-0002-0237-9937			ANDERSON HR, 1989, ARCH DIS CHILD, V64, P172; Basagana X, 2001, AM J RESP CRIT CARE, V164, P1133; BURNEY PGJ, 1989, INT J EPIDEMIOL, V18, P165, DOI 10.1093/ije/18.1.165; Burr ML, 1999, THORAX, V54, P27; Camargo CA, 1999, ARCH INTERN MED, V159, P2582, DOI 10.1001/archinte.159.21.2582; CARTERPOKRAS OD, 1993, AM J PUBLIC HEALTH, V83, P580, DOI 10.2105/AJPH.83.4.580; de Marco R, 2000, AM J RESP CRIT CARE, V162, P68; Duran-Tauleria E, 1999, THORAX, V54, P476; Field S K, 2000, Can Respir J, V7, P167; FLODIN U, 1995, EPIDEMIOLOGY, V6, P503, DOI 10.1097/00001648-199509000-00007; Floreani A A, 1999, Curr Opin Pulm Med, V5, P38, DOI 10.1097/00063198-199901000-00007; Gern JE, 1999, J CLIN INVEST, V104, P837, DOI 10.1172/JCI8272; HIGGINS MW, 1977, AM REV RESPIR DIS, V116, P403; Homa DM, 2000, AM J RESP CRIT CARE, V161, P504; Janson C, 2001, EUR RESPIR J, V18, P598, DOI 10.1183/09031936.01.00205801; Jarvis D, 1996, LANCET, V347, P426, DOI 10.1016/S0140-6736(96)90009-4; Kaplan BA, 1997, J ASTHMA, V34, P219, DOI 10.3109/02770909709068192; Leynaert B, 1996, LANCET, V347, P1052, DOI 10.1016/S0140-6736(96)90197-X; LIAO Y, 1998, AM J PUBLIC HEALTH, V80, P227; Mannino DM, 1998, MMWR-MORBID MORTAL W, V47, P1; MCWHORTER WP, 1989, AM REV RESPIR DIS, V139, P721; Mielck A, 1996, INT J EPIDEMIOL, V25, P388, DOI 10.1093/ije/25.2.388; National Center for Health Statistics, 1992, DHHS PUBL; *NHANES, 1988, DAT CD DAT OCT 1996; RAY CS, 1983, AM REV RESPIR DIS, V128, P501; SAMET JM, 1988, AM REV RESPIR DIS, V137, P815; SAMET JM, 1982, AM REV RESPIR DIS, V125, P152; SAMET JM, 1993, ENVIRON HEALTH PERSP, V101, P149, DOI 10.2307/3431671; SCHWARTZ J, 1990, AM J EPIDEMIOL, V132, P67; Shaheen SO, 1999, THORAX, V54, P396; Sunyer J., 1997, European Respiratory Journal, V10, P2490, DOI 10.1183/09031936.97.10112490; Sunyer J, 1997, THORAX, V52, P235; TAYLOR WR, 1992, PEDIATRICS, V90, P657; TURKELTAUB PC, 1991, ANN ALLERGY, V67, P147; VENABLES KM, 1993, THORAX, V48, P214, DOI 10.1136/thx.48.3.214	35	111	116	0	2	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	MAY	2003	21	5					827	833		10.1183/09031936.03.00054103		7	Respiratory System	Respiratory System	678WW	WOS:000182890500018	12765429	
J	Becker, S; Soukup, JM; Gallagher, JE				Becker, S; Soukup, JM; Gallagher, JE			Differential particulate air pollution induced oxidant stress in human granulocytes, monocytes and alveolar macrophages	TOXICOLOGY IN VITRO			English	Article						oxidant stress; human alveolar macrophages; monocytes; granulocytes; environmental pollution; particles; induced apoptosis; necrosis	OIL FLY-ASH; REACTIVE OXYGEN METABOLITES; HYDROGEN-PEROXIDE; RADICAL GENERATION; INDUCED ACTIVATION; INDUCED APOPTOSIS; MINERAL DUSTS; AMBIENT AIR; METAL-IONS; PARTICLES	It has been proposed that oxidant stress of cells in the lung is one of the underlying mechanisms of particulate pollution-induced exacerbation of lung disease. Individuals who are considered most sensitive to particulate pollution are those with pre-existing airways inflammation, such as chronic obstructive pulmonary disease (COPD), lung infection or asthma. These diseases are characterized by a presence of inflammatory cells in the airways including neutrophils (PMN), eosinophils and monocytes (Mo), and increased numbers of alveolar macrophages (AM). These cells have a high capacity for production of oxygen radicals, as compared to other cell types of the lung. To assess the oxidative response of these various cell types to pollution particles of various sources, luminol-dependent chemiluminescence was employed. Particles including transition metal-rich residual oil fly ashes (ROFAs), coal fly ashes, diesel, SiO2, TiO2 and fugitive dusts were co-cultured with AM, Mo and PMN in a dose range of 10-100 mug/2x 10(5) cells and chemiluminescence determined following a 20-min interaction. A strong oxidant response of AM was restricted to oil fly ashes, while the PMN were most reactive to the dusts containing aluminium silicate. In general, the Mo response was less vigorous, but overlapped both AM- and PMN-stimulating dusts. However, in response to SiO2, and volcanic ash the Mo chemiluminescence exceeded that of the other cell types. Oxygen radicals generated in response to ROFA by the AM were likely to be dependent on mitochondrial processes, while the response in PMN involved the membrane NADPH oxidase complex, as determined by targeting inhibitors. The response of AM to SiO2 of various sizes and TiO2 in the fine size range obtained from different commercial sources, was highly variable, implying that composition rather than size was responsible for the oxidant response. A strong chemiluminescence response was not consistently associated with cytotoxicity in the responsive cell. Taken together, these results suggest that oxidant activation by various sources of particulate matter is cell specific. Therefore, the inflamed lung is likely to be more susceptible to harm of ambient air particulates because of the oxidant stress posed by a broader range of particles. (C), 2002 Published by Elsevier Science Ltd.	US EPA, Off Res & Dev, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA	Becker, S (reprint author), US EPA, Human Studies Bldg,104 Mason Farm Rd, Chapel Hill, NC 27599 USA.						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Vitro	JUN	2002	16	3					209	218	PII S0887-2333(02)00015-2	10.1016/S0887-2333(02)00015-2		10	Toxicology	Toxicology	568JM	WOS:000176538700001	12020593	
J	Wahn, U; von Mutius, E				Wahn, U; von Mutius, E			Childhood risk factors for atopy and the importance of early intervention	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						atopy; prediction; prevention; epidemiology; atopic march; asthma	INTERFERON-GAMMA PRODUCTION; BLOOD MONONUCLEAR-CELLS; HOUSE-DUST MITE; ALLERGIC SENSITIZATION; INHALANT ALLERGENS; DOMESTIC EXPOSURE; MATERNAL SMOKING; PARENTAL SMOKING; FOOD ALLERGY; HAY-FEVER	The increasing prevalence of atopic diseases, particularly atopy-associated asthma, has become a major challenge for allergists and public health authorities in many countries. The understanding of the natural history of the atopic march, including the determinants that are modifiable and might become candidates for preventive intervention, is still very limited, Information provided by cross-sectional studies can only generate hypotheses, which need to be supported by prospective, longitudinal, cohort studies. Ultimately, it will depend on the results of well-controlled intervention studies to identify which nutritional, environmental, or lifestyle-related factors should be considered for early intervention and might be useful to reverse the epidemiologic trend.	Charite Humboldt Univ Berlin, Dept Pediat Pneumol & Immunol, D-13353 Berlin, Germany; Dr Von Haunersches Kinderspital, Munich, Germany	Wahn, U (reprint author), Charite Humboldt Univ Berlin, Dept Pediat Pneumol & Immunol, Augustenburger Pl 1, D-13353 Berlin, Germany.						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Allergy Clin. Immunol.	APR	2001	107	4					567	574		10.1067/mai.2001.112943		8	Allergy; Immunology	Allergy; Immunology	423RG	WOS:000168190100001	11295640	
J	Park, JH; Spiegelman, DL; Burge, HA; Gold, DR; Chew, GL; Milton, DK				Park, JH; Spiegelman, DL; Burge, HA; Gold, DR; Chew, GL; Milton, DK			Longitudinal study of dust and airborne endotoxin in the home	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						endotoxin; house dust; humidity; indoor air pollution; seasonal variability; temperature	RESPIRATORY-INFECTIONS; LIMULUS ASSAY; EXPOSURE; ASTHMA; CHILDREN; SYMPTOMS; DAMPNESS; SEVERITY; HEALTH; WORKER	To characterize the seasonal variability of endotoxin levels, we measured endotoxin in dust from the bed, bedroom floor, and kitchen floor in 20 homes, and in air from the bedroom in 15 of the homes. All homes were located in the greater Boston, Massachusetts, area and were sampled each month from April 1995 to June 1996. Outdoor air was collected at two locations. We found greater within-home than between-home variance for bedroom floor, kitchen floor, and airborne endotoxin. However, the reverse was true for bed dust endotoxin. Thus, studies using single measurements of dust endotoxin are most likely to reliably distinguish between homes if bed dust is sampled. Dust endotoxin levels were not significantly associated with airborne endotoxin. Airborne endotoxin was significantly (p = 0.04) and positively associated with absolute humidity in a mixed-effect model adjusting for a random home effect and fixed effect of sampling month and home characteristics. This finding implies that indoor humidity may be an important factor controlling endotoxin exposure. We found a significant (p < 0.05) seasonal effect in kitchen door dust (spring > fall) and bedroom airborne endotoxin (spring > winter), but not in the other indoor samples. We found significant seasonal pattern in outdoor airborne endotoxin (summer > winter).	Harvard Univ, Sch Publ Hlth, Occupat Hlth Program, Dept Environm Hlth, Boston, MA 02115 USA; Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA; Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA; Brigham & Womens Hosp, Channing Lab, Dept Med, Boston, MA 02115 USA; Harvard Med Sch, Boston, MA USA; Columbia Univ, JL Mailman Sch Publ Hlth, Div Environm Hlth Sci, New York, NY 10027 USA	Milton, DK (reprint author), Harvard Univ, Sch Publ Hlth, Occupat Hlth Program, Dept Environm Hlth, 665 Huntington Ave, Boston, MA 02115 USA.		Milton, Donald/G-3286-2010	Milton, Donald/0000-0002-0550-7834	NIEHS NIH HHS [2P30ES00002, R01 ES-07036]		ANDREWS JH, 1992, MICROBIAL ECOLOGY LE; Andriessen JW, 1998, CLIN EXP ALLERGY, V28, P1191; AYRES JG, 1993, BRIT J GEN PRACT, V43, P361; Carroll R. J., 1995, MEASUREMENT ERROR NO, V63; Chew GL, 1999, ALLERGY, V54, P1058, DOI 10.1034/j.1398-9995.1999.00003.x; Dales RE, 1996, EUR RESPIR J, V9, P72, DOI 10.1183/09031936.96.09010072; DELUCCA AJ, 1987, AM IND HYG ASSOC J, V48, P106, DOI 10.1080/15298668791384472; DOUWES J, 1998, RESP HLTH EFFECTS IN; DOUWES J, 1998, RESP HLTH EFFECTS IN, P109; Edmonds RL, 1979, AEROBIOLOGY ECOLOGIC; Hastie T, 1990, GEN ADDITIVE MODELS; HEEDERIK D, 1991, APPL OCCUP ENV HYG, V6, P458; Johnston SL, 1996, AM J RESP CRIT CARE, V154, P654; Kendrick B, 1992, 5 KINGDOM; Kleinbaum D.G., 1987, APPL REGRESSION ANAL; Lyles RH, 1997, ANN OCCUP HYG, V41, P63; MICHEL O, 1991, CLIN EXP ALLERGY, V21, P441, DOI 10.1111/j.1365-2222.1991.tb01684.x; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; Milton DK, 1997, AM IND HYG ASSOC J, V58, P861; Milton DK, 1996, AM IND HYG ASSOC J, V57, P889, DOI 10.1202/0002-8894(1996)057<0889:WETEPC>2.0.CO;2; MILTON DK, 1992, ENVIRON RES, V57, P212, DOI 10.1016/S0013-9351(05)80081-7; Nafstad P, 1998, AM J RESP CRIT CARE, V157, P410; RAPPAPORT SM, 1995, ANN OCCUP HYG, V39, P469, DOI 10.1016/0003-4878(95)00021-6; RAPPAPORT SM, 1991, ANN OCCUP HYG, V35, P61, DOI 10.1093/annhyg/35.1.61; Rizzo MC, 1997, PEDIATR ALLERGY IMMU, V8, P121; Rosner B., 1995, FUNDAMENTALS BIOSTAT; SHAPIRO SS, 1965, BIOMETRIKA, V52, P591, DOI 10.2307/2333709; SIMARD C, 1983, J HYG-CAMBRIDGE, V91, P277; SPENGLER J, 1994, INDOOR AIR, V4, P72, DOI 10.1111/j.1600-0668.1994.t01-2-00002.x; Symanski E, 1996, AM IND HYG ASSOC J, V57, P724; Williamson IJ, 1997, THORAX, V52, P229; Yang CY, 1997, ENVIRON RES, V75, P49, DOI 10.1006/enrs.1997.3774	32	111	114	2	7	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	NOV	2000	108	11					1023	1028		10.1289/ehp.001081023		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	373XP	WOS:000165315600021	11102291	
J	Finkelstein, J; Cabrera, MR; Hripcsak, G				Finkelstein, J; Cabrera, MR; Hripcsak, G			Internet-based home asthma telemonitoring - Can patients handle the technology?	CHEST			English	Article						asthma; peak expiratory flow; self-management; spirometry; telemonitoring	EXPIRATORY FLOW-VOLUME; QUALITY-CONTROL; ALPHA(1)-ANTITRYPSIN DEFICIENCY; PULMONARY-FUNCTION; CYSTIC-FIBROSIS; SPIROMETRY; VARIABILITY; OBSTRUCTION; CHILDREN	Study objectice: To evaluate the validity of spirometry self-testing during home telemonitoring and to assess the acceptance of an Internet-based home asthma telemonitoring system by asthma patients. Design: We studied an Internet-based telemonitoring system that collected spirometry. data and symptom reports from asthma patients' homes for review by physicians in the medical center's clinical information system. After a 40-min training session, patients completed an electronic diary and performed spirometry testing twice daily on their own from their homes for 3 weeks. A medical professional visited each patient by the end of the third neck of monitoring, 10 to 40 min after the patient had performed self-testing, and asked the patient to perform the spirometry test again under his supervision, We evaluated the validity of self-testing and surveyed the patients attitude toward the technology using a standardized questionnaire, Setting: Telemonitoring was conducted in patients' homes in a low-income inner city area, Patients: Thirty-one consecutive asthma patients without regard to computer experience. Measurement and results: Thirty-one asthma patients completed 3 weeks of monitoring, A paired t test showed no difference between unsupervised and supervised home spirometry self-testing, The variability of FVC (4.1%), FEV(1), (3.7%), peak expiratory flow (7.9%), and other spirometric indexes in our study was similar to the within-subject variability reported by other researchers. Despite the fact that the majority of the patients (71%) had no computer experience, they indicated that the self-testing was "not complicated at all" or only "slightly complicated." The majority of patients (87.1%) were strongly interested in using home asthma telemonitoring in the future. Conclusions: Spirometry self-testing by asthma patients during telemonitoring is valid and comparable to those tests collected under the supervision of a trained medical professional, Internet-based home asthma telemonitoring can be successfully implemented in a group of patients with no computer background.	Columbia Univ, Dept Med Informat, New York, NY USA; Columbia Presbyterian Med Ctr, Div Pulm Med, New York, NY 10032 USA	Finkelstein, J (reprint author), Doctors Off Bldg,Suite 102,720 Harrison Ave, Boston, MA 02118 USA.	finkelj@bu.edu					AFSCHRIFT M, 1969, AM REV RESPIR DIS, V100, P147; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; BEASLEY R, 1989, THORAX, V44, P200, DOI 10.1136/thx.44.3.200; BLAND JM, 1986, LANCET, V1, P307; BYE MR, 1992, AM J DIS CHILD, V146, P977; Chiang CH, 1997, J ASTHMA, V34, P15, DOI 10.3109/02770909709071199; COCHRANE GM, 1977, THORAX, V32, P171, DOI 10.1136/thx.32.2.171; CONNETT JE, 1990, CONTROL CLIN TRIALS, V11, P24, DOI 10.1016/0197-2456(90)90029-2; COOPER PJ, 1990, PEDIATR PULM, V8, P16, DOI 10.1002/ppul.1950080107; Cork RD, 1998, J AM MED INFORM ASSN, V5, P164; DAWSON A, 1966, AM REV RESPIR DIS, V93, P264; ENRIGHT P, 1992, AM REV RESPIR DIS, V146, P1367; ENRIGHT PL, 1991, AM REV RESPIR DIS, V143, P1215; FERGUSON AC, 1988, J ALLERGY CLIN IMMUN, V82, P19, DOI 10.1016/0091-6749(88)90045-0; FIELD MJ, 1996, TELEMEDICINE GUIDE A; Finkelstein J, 1998, ST HEAL T, V52, P272; FINKELSTEIN J, 1997, SPRING C AM MED INF; Friedman CP, 1997, EVALUATION METHODS M; IGNACIOGARCIA JM, 1995, AM J RESP CRIT CARE, V151, P353; INTVEEN JCC, 1998, AM J RESP CRIT CARE, V158, P1134; LEEDER SR, 1977, B EUR PHYSIOPATH RES, V13, P249; LESSLER JT, 1995, MED CARE, V33, pAS203; LI JTC, 1995, MAYO CLIN PROC, V70, P649; Madsen F, 1996, RESP MED, V90, P131, DOI 10.1016/S0954-6111(96)90154-7; MCCARTHY DS, 1975, AM REV RESPIR DIS, V112, P407; MCFADDEN ER, 1973, NEW ENGL J MED, V288, P221, DOI 10.1056/NEJM197302012880501; National Asthma Education and Prevention Program, 1997, NIH PUBL, V97-4051; NICKERSON BG, 1980, AM REV RESPIR DIS, V122, P859; Reddel HK, 1998, EUR RESPIR J, V12, P853, DOI 10.1183/09031936.98.12040853; Rietveld S, 1997, J ASTHMA, V34, P133, DOI 10.3109/02770909709075658; RUBINFELD AR, 1976, LANCET, V1, P882; Stoller JK, 1997, CHEST, V111, P899, DOI 10.1378/chest.111.4.899; Valetta EA, 1997, J ASTHMA, V34, P127	33	111	112	3	10	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	JAN	2000	117	1					148	155		10.1378/chest.117.1.148		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	274PN	WOS:000084774400028	10631213	
J	Nadeau, K; McDonald-Hyman, C; Noth, EM; Pratt, B; Hammond, SK; Balmes, J; Tager, I				Nadeau, Kari; McDonald-Hyman, Cameron; Noth, Elizabeth M.; Pratt, Boriana; Hammond, S. Katharine; Balmes, John; Tager, Ira			Ambient air pollution impairs regulatory T-cell function in asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Ambient air pollution; asthma; immune system; regulatory T cell; Treg; epigenetics	DIESEL EXHAUST PARTICLES; DNA METHYLATION; IN-VIVO; CYTOKINE PRODUCTION; FOXP3 EXPRESSION; ALLERGIC-ASTHMA; LUNG-FUNCTION; EXPOSURE; CHALLENGE; CHILDREN	Background: Asthma is the most frequent chronic disease in children, and children are at high risk for adverse health consequences associated with ambient air pollution (AAP) exposure. Regulatory T (Treg) cells are suppressors of immune responses involved in asthma pathogenesis. Treg-cell impairment is associated with increased DNA methylation of Forkhead box transcription factor 3 (Foxp3), a key transcription factor in Treg-cell activity. Because AAP exposure can induce epigenetic changes, we hypothesized that Treg-cell function would be impaired by AAP, allowing amplification of an inflammatory response. Objectives: To assess whether exposure to AAP led to hypermethylation of the Foxp3 gene, causing impaired Treg-cell suppression and worsened asthma symptom scores. Methods: Children with and without asthma from Fresno, Calif (high pollution, Fresno Asthma Group [FA], n = 71, and Fresno Non Asthmatic Group, n = 30, respectively), and from Stanford, Calif (low pollution, Stanford Asthma Group, n = 40, and Stanford Non Asthmatic Group, n 5 40), were enrolled in a cross-sectional study. Peripheral blood Treg cells were used in functional and epigenetic studies. Asthma outcomes were assessed by Global Initiative in Asthma score. Results: Fresno Asthma Group Treg-cell suppression was impaired and FA Treg-cell chemotaxis were reduced compared with other groups (P <= .05). Treg-cell dysfunction was associated with more pronounced decreases in asthma Global Initiative in Asthma score in FA versus the Stanford Asthma Group. Foxp3 was decreased in FA compared with the Fresno Non Asthmatic Group (P <= .05). FA also contained significantly higher levels of methylation at the Foxp3 locus (P <= .05). Conclusion: Increased exposure to AAP is associated with hypermethylation of the Foxp3 locus, impairing Treg-cell function and increasing asthma morbidity. AAP could play a role in mediating epigenetic changes in Treg cells, which may worsen asthma by an immune mechanism. (J Allergy Clin Immunol 2010;126:845-52.)	[Nadeau, Kari] Stanford Univ, Div Immunol & Allergy, Sch Med, Stanford, CA 94305 USA; [Noth, Elizabeth M.; Pratt, Boriana; Hammond, S. Katharine; Balmes, John; Tager, Ira] Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA	Nadeau, K (reprint author), Stanford Univ, Div Immunol & Allergy, Sch Med, 269 Campus Dr,CCSR Bldg,Room 2115, Stanford, CA 94305 USA.	knadeau@stanford.edu	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	McCormick Fund at Stanford; American Academy of Allergy, Asthma, and Immunology Junior Faculty Fund; Westly Foundation; Global Health Research Foundation; NIEHS [R01 HL081521]; CDC [5U19EH000097-04]; California Air Resources Board [99-322, 99-323, 01-346]; US EPA [2A-0540-NASX]; Austin Memorial Fund; Mickey Leland National Urban Air Toxics Research Center [RFA 2005-01]	Supported by the McCormick Fund at Stanford, the American Academy of Allergy, Asthma, and Immunology Junior Faculty Fund, the Westly Foundation, the Global Health Research Foundation, NIEHS (R01 HL081521), CDC cooperative agreement 5U19EH000097-04, the California Air Resources Board (contract nos. 99-322, 99-323, and 01-346), the US EPA (PO no. 2A-0540-NASX), the Austin Memorial Fund, and the Mickey Leland National Urban Air Toxics Research Center (RFA 2005-01).; Disclosure of potential conflict of interest: S. K. Hammond has received research support from the National Institutes of Health-National Heart, Lung, and Blood Institute and National Institute of Environmental Health Sciences, the National Institute for Occupational Safety and Health, the Flight Attendant Medical Research Institute, and the Environmental Protection Agency and has provided legal consultation or expert witness testimony on the topic of exposure to chemicals in semiconductor manufacturing. J. Balmes is a member of the California Air Resources Board and has received research support from the National Institutes of Health, Centers for Disease Control and Prevention, and the California Air Resource Board. The rest of the authors have declared that they have no conflict of interest.	Baccarelli A, 2009, AM J RESP CRIT CARE, V179, P572, DOI 10.1164/rccm.200807-1097OC; Balmes JR, 2009, J ALLERGY CLIN IMMUN, V123, P626, DOI 10.1016/j.jaci.2008.10.062; Bergstrom SE, 2008, RESP MED, V102, P1335, DOI 10.1016/j.rmed.2008.03.020; Bluestone JA, 2008, AM J TRANSPLANT, V8, P2086, DOI 10.1111/j.1600-6143.2008.02377.x; Bour-Jordan H, 2009, J IMMUNOL, V183, P4147, DOI 10.4049/jimmunol.0990078; Cohen AC, 2006, J IMMUNOL, V177, P2770; D'Amato G, 2002, ALLERGY, V57, P30, DOI 10.1034/j.1398-9995.57.s72.5.x; Diaz-Sanchez D, 2000, CLIN IMMUNOL, V97, P140, DOI 10.1006/clim.2000.4921; Diaz-Sanchez D, 2005, AM J PHYSIOL-LUNG C, V289, pL722, DOI 10.1152/ajplung.00217.2005; Diaz-Sanchez D, 2000, J ALLERGY CLIN IMMUN, V106, P1140, DOI 10.1067/mai.2000.111144; DiazSanchez D, 1996, J ALLERGY CLIN IMMUN, V98, P114, DOI 10.1016/S0091-6749(96)70233-6; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; Hartl D, 2007, J ALLERGY CLIN IMMUN, V119, P1258, DOI 10.1016/j.jaci.2007.02.023; Huehn J, 2009, NAT REV IMMUNOL, V9, P83, DOI 10.1038/nri2474; Islam T, 2007, THORAX, V62, P957, DOI 10.1136/thx.2007.078964; Janson PCJ, 2008, PLOS ONE, V3, DOI 10.1371/journal.pone.0001612; Jerrett M, 2008, ENVIRON HEALTH PERSP, V116, P1433, DOI 10.1289/ehp.10968; Kim HP, 2007, J EXP MED, V204, P1543, DOI 10.1084/jem.20070109; Kohlmeier JE, 2006, CURR OPIN IMMUNOL, V18, P357, DOI 10.1016/j.coi.2006.03.012; Lal G, 2009, BLOOD, V114, P3727, DOI 10.1182/blood-2009-05-219584; Lal G, 2009, J IMMUNOL, V182, P259; Liu J, 2008, TOXICOL SCI, V102, P76, DOI 10.1093/toxsci/kfm290; Margolis HG, 2009, INT J ENVIRON HEAL R, V19, P139, DOI 10.1080/09603120802415792; Marson A, 2007, NATURE, V445, P931, DOI 10.1038/nature05478; Mastrangelo G, 2003, INT J IMMUNOPATH PH, V16, P145; Miller RL, 2008, AM J RESP CRIT CARE, V177, P567, DOI 10.1164/rccm.200710-1511PP; NGUYEN KD, 2008, J IMMUNOL, V25, P5386; Nguyen KD, 2009, J ALLERGY CLIN IMMUN, V123, pe910; Nguyen KD, 2008, J IMMUNOL, V181, P5386; Nguyen KD, 2008, EUR J IMMUNOL, V38, P2034, DOI 10.1002/eji.200738082; Nguyen KD, 2009, J ALLERGY CLIN IMMUN, V123, P933, DOI 10.1016/j.jaci.2008.11.037; Perera F, 2009, PLOS ONE, V4, DOI 10.1371/journal.pone.0004488; Peters JH, 2008, PLOS ONE, V3, DOI 10.1371/journal.pone.0002233; Sakaguchi S, 2009, EUR J IMMUNOL, V39, P2331, DOI 10.1002/eji.200939688; Sekiya T, 2002, ALLERGY, V57, P173, DOI 10.1034/j.1398-9995.2002.5720256.x; Shea KM, 2008, J ALLERGY CLIN IMMUN, V122, P443, DOI 10.1016/j.jaci.2008.06.032; Shea K. M., 2008, J ALLERGY CLIN IMMUN, V122, P454; TAGER I, 2006, FINAL REPORT FACES, P1; Taylor A, 2005, MICROBES INFECT, V7, P1049, DOI 10.1016/j.micinf.2005.03.029; Truyen E, 2006, THORAX, V61, P202, DOI 10.1136/thx.2005.052399; Umetsu D. T., 2006, ARB P EHRLICH I BUND, V95, P211; Umetsu D. T., 2006, ARB P EHRLICH I BUND, V95, P215; Yu GP, 2009, CLIN IMMUNOL, V131, P240, DOI 10.1016/j.clim.2008.12.006	43	110	118	3	36	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	OCT	2010	126	4					845	U280		10.1016/j.jaci.2010.08.008		18	Allergy; Immunology	Allergy; Immunology	658SP	WOS:000282510000024	20920773	
J	Compalati, E; Passalacqua, G; Bonini, M; Canonica, GW				Compalati, E.; Passalacqua, G.; Bonini, M.; Canonica, G. W.			The efficacy of sublingual immunotherapy for house dust mites respiratory allergy: results of a GA(2);LEN meta-analysis	ALLERGY			English	Review						efficacy; house dust mites; meta-analysis; specific immunotherapy	RANDOMIZED-CLINICAL-TRIALS; DOUBLE-BLIND; PEDIATRIC-PATIENTS; RHINITIS; ASTHMA; CHILDREN; COLLABORATION; ORGANIZATION; REVIEWS; QUALITY	Recent meta-analyses documented the efficacy and safety of sublingual immunotherapy (SLIT) in patients with allergic rhinitis (AR) and asthma (AA). Although SLIT appeared globally effective, the sub-analyses for single allergens provided uncertain results. This study is aimed to investigate the efficacy of SLIT with house dust mite (HDM) extracts in AR and AA through an updated reassessment of randomized controlled trials. Electronic databases were searched up to March 31, 2008, for randomized DBPC trials, assessing the efficacy of SLIT in AR and AA due to HDM sensitization. Outcomes were symptom scores and rescue medications use. For AR, eight studies fulfilled the selection criteria. A significant reduction in symptoms of AR (SMD -0.95; CI 95%-1.77 to -0.14 P = 0.02) was found in 194 patients (adults and children) receiving SLIT compared to 188 receiving placebo. For AA, with nine studies, similar results were found for symptoms (SMD -0.95; CI 95%-1.74 to -0.15 P = 0.02) in 243 patients (adults and children) receiving SLIT compared to 209 receiving placebo. A reduction in rescue medication use was found for AR (SMD -1.88; CI 95%-3.65 to -0.12 P = 0.04) in 89 patients, and AA (SMD -1.48; CI 95%-2.70 to -0.26 P = 0.02) in 202 patients. A relevant inter-study heterogeneity was detected. Promising evidence of efficacy for SLIT, using mite extract in allergic patients suffering from AR and AA, are herein shown. These findings suggest that more data are needed, derived from large-population-based high quality studies, and corroborated by objective outcomes, mainly for AA.	[Compalati, E.; Passalacqua, G.; Bonini, M.; Canonica, G. W.] Univ Genoa, Dept Internal Med, Allergy & Resp Dis Clin, I-16132 Genoa, Italy	Canonica, GW (reprint author), Univ Genoa, Dept Internal Med, Allergy & Resp Dis Clin, Lgo R Benzi 10, I-16132 Genoa, Italy.			BONINI, Matteo/0000-0002-3042-0765	GA<SUP>2</SUP>LEN; ARMIA	This study has been partially supported by GA<SUP>2</SUP>LEN (Global Allergy and Asthma European Network) and ARMIA (Associazione Ricerca Malattie Immunologiche e Allergiche).	Alderson P, 2004, COCHRANE LIB; ALDERSON P, 2002, GREEN S COCHRANE COL; Bahceciler NN, 2001, PEDIATR PULM, V32, P49, DOI 10.1002/ppul.1088; Bousquet J, 2008, ALLERGY, V63, P8, DOI 10.1111/j.1398-9995.2007.01620.x; Bousquet J, 1999, ALLERGY, V54, P249, DOI 10.1034/j.1398-9995.1999.00916.x; Calamita Z, 2006, ALLERGY, V61, P1162, DOI 10.1111/j.1395-9995.2006.01205.x; Canonica GW, 2007, ALLERGY, V62, P317, DOI 10.1111/j.1398-9995.2006.01312.x; Dawson BD, 2004, BASIC CLIN BIOSTATIS, P118; Deeks J, 2001, SYSTEMATIC REV HLTH, P285, DOI 10.1002/9780470693926.ch15; DICKERSIN K, 1994, BRIT MED J, V309, P1286; Guez S, 2000, ALLERGY, V55, P369, DOI 10.1034/j.1398-9995.2000.00413.x; Higgins JPT, 2003, BRIT MED J, V327, P557, DOI 10.1136/bmj.327.7414.557; Hirsch T, 1997, PEDIATR ALLERGY IMMU, V8, P21, DOI 10.1111/j.1399-3038.1997.tb00138.x; Ippoliti F, 2003, PEDIATR ALLERGY IMMU, V14, P216, DOI 10.1034/j.1399-3038.2003.00025.x; Jadad AR, 1996, CONTROL CLIN TRIALS, V17, P1, DOI 10.1016/0197-2456(95)00134-4; Jorgensen AW, 2006, BRIT MED J, V333, P782, DOI 10.1136/bmj.38973.444699.0B; Lue KH, 2006, PEDIATR ALLERGY IMMU, V17, P408, DOI 10.1111/j.1399-3038.2006.00443.x; MOHER D, 1995, CONTROL CLIN TRIALS, V16, P62, DOI 10.1016/0197-2456(94)00031-W; MOHER D, 2007, COCHRANE DB SYST REV, DOI DOI 10.1002/14651858.MR000025; Moher D, 1999, HEALTH TECHNOL ASSES, V3, P12; Niu CK, 2006, RESP MED, V100, P1374, DOI 10.1016/j.rmed.2005.11.016; Olaguibel JM, 2005, J INVEST ALLERG CLIN, V15, P9; Pajno GB, 2000, ALLERGY, V55, P842, DOI 10.1034/j.1398-9995.2000.00495.x; Passalacqua G, 2006, ALLERGY, V61, P849, DOI 10.1111/j.1395-9995.2006.01098.x; Passalacqua G, 1998, LANCET, V351, P629, DOI 10.1016/S0140-6736(97)07055-4; Penagos M, 2008, CHEST, V133, P599, DOI 10.1378/chest.06-1425; Penagos M, 2006, ANN ALLERG ASTHMA IM, V97, P141; Pham-Thi N, 2007, PEDIATR ALLERGY IMMU, V18, P47, DOI 10.1111/j.1399-3038.2006.00475.x; Shekelle PG, 1999, BRIT MED J, V318, P593; TARI MG, 1990, ALLERGOL IMMUNOPATH, V18, P277; Tonnel AB, 2004, ALLERGY, V59, P491, DOI 10.1111/j.1398-9995.2004.00456.x; Wilson DR, 2005, ALLERGY, V60, P4, DOI 10.1111/j.1398-9995.2005.00699.x; 2004, REVMAN 4 2 7 PROGRAM	33	110	117	0	1	WILEY-BLACKWELL	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0105-4538			ALLERGY	Allergy	NOV	2009	64	11					1570	1579		10.1111/j.1398-9995.2009.02129.x		10	Allergy; Immunology	Allergy; Immunology	504SR	WOS:000270638400002	19796205	
J	Jaakkola, JJK; Knight, TL				Jaakkola, Jouni J. K.; Knight, Trudy L.			The role of exposure to phthalates from polyvinyl chloride products in the development of asthma and allergies: A systematic review and meta-analysis	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Review						allergy; asthma; phthalates; polyvinyl chloride	MEAT-WRAPPERS ASTHMA; SUBCUTANEOUS INJECTION MODEL; INTERIOR SURFACE MATERIALS; BALB/C MICE; DI-(2-ETHYLHEXYL) PHTHALATE; MONO-2-ETHYLHEXYL PHTHALATE; OCCUPATIONAL ASTHMA; PULMONARY-FUNCTION; RESPIRATORY-TRACT; YOUNG-CHILDREN	BACKGROUND: Phthalates from polyvinyl chloride (PVC) plastics may have adverse effects on airways and immunologic systems, but the evidence has not been reviewed systematically. OBJECTIVE: We reviewed the evidence for the role of exposure to phthalates from PVC products in the development of asthma and allergies. Methods: We conducted a Medline database search (1950 through May 2007) for relevant studies on the respiratory and allergic effects of exposure to phthalates from PVC products. RESULTS: We based this review on 27 human and 14 laboratory toxicology studies. Two mouse inhalation experiments indicated that mono-2-ethylhexyl phthalate (MEHP) has the ability to modulate the immune response to exposure to a coallergen. The data suggested a no observed effect level of 30 mu g MEHp/m(3), calculated to be below the estimated level of human exposure in common environments. Case reports and series (n = 9) identified and verified cases of asthma that were very likely caused by fumes emitted from PVC film. Epidemiologic studies in adults (n = 10), mostly small studies in occupational settings, showed associations between heated PVC fumes and asthma and respiratory symptoms; studies in children (n = 5) showed an association between PVC surface materials in the home and the risk of asthma [fixed-effects model: summary odds ratio (OR), 1.55; 95% confidence interval (CI), 1.18-2-05; four studies] and allergies (OR, 1.32; 95% CI, 1.09-1.60; three studies). CONCLUSIONS: High levels of phthalates from PVC products can modulate the murine immune response to a coallergen. Heated PVC fumes possibly contribute to development of asthma in adults. Epidemiologic studies in children show associations between indicators of phthalate exposure in the home and risk of asthma and allergies. The lack of objective exposure information limits the epidemiologic data.	[Jaakkola, Jouni J. K.; Knight, Trudy L.] Univ Birmingham, Inst Occupat & Environm Med, Birmingham B15 2TT, W Midlands, England	Jaakkola, JJK (reprint author), Univ Birmingham, Inst Occupat & Environm Med, Birmingham B15 2TT, W Midlands, England.	j.jaakkola@bham.ac.uk	Jaakkola, Jouni/G-4314-2012				Adibi JJ, 2003, ENVIRON HEALTH PERSP, V111, P1719, DOI 10.1289/ehp.6235; ANDRASCH R H, 1976, Journal of the American Medical Association, V235, P937, DOI 10.1001/jama.235.9.937; ANDRASCH RH, 1976, J ALLERGY CLIN IMMUN, V58, P291, DOI 10.1016/0091-6749(76)90134-2; BALLY MB, 1980, TOXICOLOGY, V18, P49, DOI 10.1016/0300-483X(80)90037-2; Bornehag CG, 2005, INDOOR AIR, V15, P48, DOI 10.1111/j.1600-0668.2005.00306.x; Bornehag CG, 2004, ENVIRON HEALTH PERSP, V112, P1393, DOI 10.1289/ehp.7187; Bornehag CG, 2004, INDOOR AIR, V14, P59, DOI 10.1111/j.1600-0668.2004.00274.x; BROOKS SM, 1977, J OCCUP ENVIRON MED, V19, P192; Brunetti G, 1984, Med Lav, V75, P120; Butala JH, 2004, TOXICOLOGY, V201, P77, DOI 10.1016/j.tox.2004.04.004; Butler J, 1981, Chest, V80, P71; Cipolla C, 1999, Med Lav, V90, P513; Clark K, 2003, HANDB ENVIRON CHEM, V3, P125; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; DOELMAN CJA, 1990, LANCET, V335, P725, DOI 10.1016/0140-6736(90)90839-W; EISEN EA, 1985, SCAND J WORK ENV HEA, V11, P21; *EUR CHEM BUR, 2006, R0420402ENVHH46 EUR; FALK H, 1976, JAMA-J AM MED ASSOC, V235, P915, DOI 10.1001/jama.235.9.915; Frederiksen H, 2007, MOL NUTR FOOD RES, V51, P899, DOI 10.1002/mnfr.20060243; Glue C, 2005, BASIC CLIN PHARMACOL, V96, P140, DOI 10.1111/j.1742-7843.2005.pto960208.x; Glue C, 2002, TOXICOL IN VITRO, V16, P657, DOI 10.1016/S0887-2333(02)00082-6; Hansen JS, 2007, TOXICOLOGY, V232, P79, DOI 10.1016/j.tox.2006.12.011; Hauser R, 2005, Occup Environ Med, V62, P806, DOI 10.1136/oem.2004.017590; Hoppin JA, 2004, ENVIRON HEALTH PERSP, V112, P571; Jaakkola JJK, 1999, AM J PUBLIC HEALTH, V89, P188, DOI 10.2105/AJPH.89.2.188; Jaakkola JJK, 2000, AM J PUBLIC HEALTH, V90, P797, DOI 10.2105/AJPH.90.5.797; Jaakkola JJK, 2004, AM J PUBLIC HEALTH, V94, P560, DOI 10.2105/AJPH.94.4.560; Jaakkola JJK, 2006, AM J EPIDEMIOL, V164, P742, DOI 10.1093/aje/kwj249; Jepsen KF, 2004, TOXICOL IN VITRO, V18, P265, DOI 10.1016/j.tiv.2003.09.008; KLIMISCH HJ, 1992, FOOD CHEM TOXICOL, V30, P915, DOI 10.1016/0278-6915(92)90175-K; Kolarik B, 2008, ENVIRON HEALTH PERSP, V116, P98, DOI 10.1289/ehp.10498; Larsen ST, 2007, TOXICOLOGY, V235, P119, DOI 10.1016/j.tox.2007.03.010; Larsen ST, 2004, HUM EXP TOXICOL, V23, P537, DOI 10.1191/0960327104ht486oa; Larsen ST, 2003, FOOD CHEM TOXICOL, V41, P439, DOI 10.1016/S0278-6915(02)00248-X; Larsen ST, 2002, PHARMACOL TOXICOL, V91, P264, DOI 10.1034/j.1600-0773.2002.910508.x; Larsen ST, 2001, TOXICOL LETT, V125, P11; Larsen ST, 2001, TOXICOLOGY, V169, P37, DOI 10.1016/S0300-483X(01)00484-X; LEE HS, 1989, BRIT J IND MED, V46, P820; MANTEL N, 1959, J NATL CANCER I, V22, P719; MARKOWITZ JS, 1989, ARCH ENVIRON HEALTH, V44, P30; MEEK ME, 1994, ENVIRON CARCIN ECO R, V12, P179; MOISAN TC, 1991, J OCCUP ENVIRON MED, V33, P458; Munoz X, 2003, ARCH BRONCONEUMOL, V39, P324; Nakamura R, 2002, IMMUNOL LETT, V80, P119, DOI 10.1016/S0165-2478(01)00318-2; NIELSEN J, 1989, INT ARCH OCC ENV HEA, V61, P427, DOI 10.1007/BF00386474; Norback D, 2000, INT J TUBERC LUNG D, V4, P1016; Oie L, 1997, ENVIRON HEALTH PERSP, V105, P972; OIO L, 1999, EPIDEMIOLOGY, V110, P294; PAULI G, 1980, CLIN ALLERGY, V10, P263, DOI 10.1111/j.1365-2222.1980.tb02106.x; Petersen JH, 2000, FOOD ADDIT CONTAM, V17, P133, DOI 10.1080/026520300283487; *PLAST INF CTR, 2007, WHAT AR PLAST; POLAKOFF PL, 1975, ARCH ENVIRON HEALTH, V30, P269; Rudel RA, 2003, ENVIRON SCI TECHNOL, V37, P4543, DOI 10.1021/es0264596; SOKOL WN, 1973, JAMA-J AM MED ASSOC, V226, P639, DOI 10.1001/jama.226.6.639; Sterne J, 2001, SYSTEMATIC REV HLTH, P347, DOI DOI 10.1002/9780470693926; Tuomainen A, 2006, ENVIRON HEALTH PERSP, V114, P1409, DOI 10.1289/ehp.8965; Tuomainen Anneli, 2004, Int Arch Occup Environ Health, V77, P222, DOI 10.1007/s00420-003-0481-2; Wormuth M, 2006, RISK ANAL, V26, P803, DOI 10.1111/j.1539-6924.2006.00770.x	58	110	117	7	48	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765	1552-9924		ENVIRON HEALTH PERSP	Environ. Health Perspect.	JUL	2008	116	7					845	853		10.1289/ehp.10846		9	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	319ST	WOS:000257185000025	18629304	
J	Rogers, DF				Rogers, Duncan F.			Physiology of airway mucus secretion and pathophysiology of hypersecretion	RESPIRATORY CARE			English	Article; Proceedings Paper	39th Conference of the Respiratory-Care-Journal	2007	Orlando, FL	Respiratory Care Journal		mucin; mucus; asthma; chronic obstructive pulmonary disease; cystic fibrosis	GOBLET CELL HYPERPLASIA; OBSTRUCTIVE PULMONARY-DISEASE; HUMAN MUCIN GENES; RESPIRATORY-TRACT; MUCOCILIARY CLEARANCE; CYSTIC-FIBROSIS; PERIPHERAL AIRWAYS; SURFACE EPITHELIUM; CHRONIC-BRONCHITIS; STATUS-ASTHMATICUS	Mucus secretion is the first-line defense against the barrage of irritants that inhalation of approximately 500 L of air an hour brings into the lungs. The inhaled soot, dust, microbes, and gases can all damage the airway epithelium. Consequently, mucus secretion is extremely rapid, occurring in tens of milliseconds. In addition, mucus is held in cytoplasmic granules in a highly condensed state in which high concentrations of Ca2+ nullify the repulsive forces of the highly polyanionic mucin molecules. Upon initiation of secretion and dilution of the Ca2+, the repulsion forces of the mucin molecules cause many-hundred-fold swelling of the secreted mucus, to cover and protect the epithelium. Secretion is a highly regulated process, with coordination by several molecules, including soluble N-ethyl-maleimide-sensitive factor attachment protein receptor (SNARE) proteins, myristoylated alanine-rich C kinase substrate (MARCKS), and Munc proteins, to dock the mucin granules to the secretory cell membrane prior to exocytosis. Because mucus secretion appears to be such a fundamental airway homeostatic process, virtually all regulatory and inflammatory mediators and interventions that have been investigated increase secretion acutely. When given longer-term, many of these same mediators also increase mucin gene expression and mucin synthesis, and induce goblet cell hyperplasia. These responses induce (in contrast to the protective effects of acute secretion) long-term, chronic hypersecretion of airway mucus, which contributes to respiratory disease. In this case the homeostatic, protective function of airway mucus secretion is lost, and, instead, mucus hypersecretion contributes to pathophysiology of a number of severe respiratory conditions, including asthma, chronic obstructive pulmonary disease, and cystic fibrosis.	Univ London Imperial Coll Sci & Technol, Natl Heart & Lung Inst, London, England	Rogers, DF (reprint author), Univ London Imperial Coll Sci & Technol, Natl Heart & Lung Inst, London, England.	duncan.rogers@imperial.ac.uk					AIKAWA T, 1992, CHEST, V101, P916, DOI 10.1378/chest.101.4.916; AIKAWA T, 1989, AM REV RESPIR DIS, V140, P477; Aitken M L, 1989, Symp Soc Exp Biol, V43, P73; American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P225, DOI DOI 10.1164/AJRCCM/136.1.225; AUDIE JP, 1993, J HISTOCHEM CYTOCHEM, V41, P1479; AYERS MM, 1988, EUR RESPIR J, V1, P58; BASBAUM CB, 1990, ANNU REV PHYSIOL, V52, P97; BHASKAR KR, 1988, PEDIATR PULM, V5, P176, DOI 10.1002/ppul.1950050308; British Thoracic Society, 1997, THORAX S1, V52, pS1, DOI DOI 10.1136/THX.52.2008.S1]; BUIST AS, 2003, EXECUTIVE SUMMARY GL; Burgel PR, 2004, THORAX, V59, P992, DOI 10.1136/thx.2003.018879; Davies JR, 2002, NOVART FDN SYMP, V248, P76; Del Donno M, 2000, CHEST, V118, P1142, DOI 10.1378/chest.118.4.1142; Dell A, 2001, SCIENCE, V291, P2351, DOI 10.1126/science.1058890; Donnelly LE, 2003, EXPERT OPIN THER PAT, V13, P1345, DOI 10.1517/13543776.13.9.1345; DUNNILL MS, 1960, J CLIN PATHOL, V13, P27, DOI 10.1136/jcp.13.1.27; DUNNILL MS, 1975, P INT C ASTH 1974 AS, P213; Eapen SS, 2002, CL ALLER IM, V16, P325; FICK RB, 1987, J APPL PHYSIOL, V63, P1147; Finkbeiner WE, 1999, RESP PHYSIOL, V118, P77, DOI 10.1016/S0034-5687(99)00080-8; Foster KA, 2005, DRUG DISCOV TODAY, V10, P563, DOI 10.1016/S1359-6446(05)03389-1; Guyonnet Duperat Veronique, 1995, Biochemical Journal, V305, P211; Hanisch FA, 2001, BIOL CHEM, V382, P143, DOI 10.1515/BC.2001.022; Henke MO, 2007, AM J RESP CRIT CARE, V175, P816, DOI 10.1164/rccm.200607-1011OC; Henke MO, 2004, AM J RESP CELL MOL, V31, P86, DOI 10.1165/rcmb.2003-0345OC; Hewson CA, 2004, J MOL BIOL, V344, P683, DOI 10.1016/j.jmb.2004.09.059; Hollander W, 1986, Arch Toxicol Suppl, V9, P74; HOUSTON JC, 1953, THORAX, V8, P207, DOI 10.1136/thx.8.3.207; Houtmeyers E, 1999, EUR RESPIR J, V13, P1177, DOI 10.1034/j.1399-3003.1999.13e39.x; Hovenberg HW, 1996, BIOCHEM J, V318, P319; Hovenberg HW, 1996, GLYCOCONJUGATE J, V13, P839, DOI 10.1007/BF00702348; Kirkham S, 2002, BIOCHEM J, V361, P537, DOI 10.1042/0264-6021:3610537; Knowles MR, 2002, J CLIN INVEST, V109, P571, DOI 10.1172/JCI200215217; Koch H, 2000, BIOCHEM J, V349, P247, DOI 10.1042/0264-6021:3490247; Li YH, 2001, J BIOL CHEM, V276, P40982, DOI 10.1074/jbc.M105614200; LIPPMANN M, 1980, BRIT J IND MED, V37, P337; LIST SJ, 1978, BIOCHEM J, V175, P565; Maestrelli P, 2001, AM J RESP CRIT CARE, V164, pS76; MARRIOTT C, 1982, ADV EXP MED BIOL, V144, P89; METZGER WJ, 1987, AM REV RESPIR DIS, V135, P433; Moniaux N, 2001, FRONT BIOSCI, V6, pD1192, DOI 10.2741/Moniaux; MORGENROTH K, 1985, RESPIRATION, V47, P225; MULLEN JBM, 1987, THORAX, V42, P843, DOI 10.1136/thx.42.11.843; Nadel Jay A., 2001, Current Opinion in Pharmacology, V1, P254, DOI 10.1016/S1471-4892(01)00045-5; Newman TM, 1996, AM J RESP CELL MOL, V15, P529; Ordonez CL, 2001, AM J RESP CRIT CARE, V163, P517; Reid CJ, 1997, AM J RESP CELL MOL, V17, P592; REID L, 1956, Proc R Soc Med, V49, P771; REID LYNNE, 1960, THORAX, V15, P132, DOI 10.1136/thx.15.2.132; RESTREPO G, 1963, J PATHOL BACTERIOL, V85, P305, DOI 10.1002/path.1700850207; RESTREPO G. 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Care	SEP	2007	52	9					1134	1149				16	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	209OM	WOS:000249397900002	17716382	
J	Akei, HS; Mishra, A; Blanchard, C; Rothenberg, ME				Akei, HS; Mishra, A; Blanchard, C; Rothenberg, ME			Epicutaneous antigen exposure primes for experimental eosinophilic esophagitis in mice	GASTROENTEROLOGY			English	Article							STAT6-DEFICIENT MICE; ATOPIC-DERMATITIS; AIRWAY HYPERRESPONSIVENESS; GASTROINTESTINAL DISORDERS; ALLERGIC DERMATITIS; MURINE MODEL; T-CELLS; ASTHMA; CHILDREN; IL-5	Background & Aims: Eosinophilic esophagitis (EE) is frequently associated with atopic disease, including dermatitis and asthma. Data are emerging that atopic skin may provide an early entry point for antigen sensitization. We aimed to test the hypothesis that epicutaneous exposure to antigen primes for subsequent respiratory antigen-induced EE. Methods: Wild-type and genetically engineered mice were subjected to epicutaneous antigen sensitization and the development of experimental EE, and immune responses were examined. Results: We show that exposure to antigen via the epicutaneous route primes for marked eosinophilic inflammation in the esophagus triggered by a single airway antigen challenge. The development of experimental EE is associated with significant skin eosinophilia, accelerated bone marrow eosinophilopoiesis, blood eosinophilia, and large increases in serum antigen-specific immunoglobulin G1/immunoglobulin E using ovalbumin or Aspergillus fumigatus as the epicutaneous antigen. Mechanistic analysis with gene-targeted mice showed that interleukin-5 was required for esophageal eosinophilia and that interleukin-4, interleukin-13, and STAT6 contributed to a lesser extent. Conclusions: These findings provide the first evidence that epicutaneous exposure to allergens potently primes for EE via a Th2-dependent mechanism.	Univ Cincinnati, Childrens Hosp, Ctr Med, Div Allergy & Immunol,Dept Pediat, Cincinnati, OH 45229 USA; Univ Cincinnati, Coll Med, Cincinnati, OH 45221 USA	Rothenberg, ME (reprint author), Univ Cincinnati, Childrens Hosp, Ctr Med, Div Allergy & Immunol,Dept Pediat, 3333 Burnet Ave, Cincinnati, OH 45229 USA.	rothenberg@cchmc.org			NIAID NIH HHS [AI42242, AI45898]		Akimoto T, 1998, J EXP MED, V187, P1537, DOI 10.1084/jem.187.9.1537; Blease K, 2002, AM J PATHOL, V160, P481, DOI 10.1016/S0002-9440(10)64867-5; Bochner BS, 2001, IMMUNOL REV, V179, P5, DOI 10.1034/j.1600-065X.2001.790101.x; Brandt EB, 2001, J ALLERGY CLIN IMMUN, V108, P142, DOI 10.1067/mai.2001.116121; BUSSE WW, 2000, ANIMAL MODELS ASTHMA, V2, P1205; CELLO JP, 1979, AM J MED, V67, P1097, DOI 10.1016/0002-9343(79)90652-1; Corry David B, 2002, Am J Respir Med, V1, P185; Eichenfield LF, 2003, PEDIATRICS, V111, P608, DOI 10.1542/peds.111.3.608; Fox VL, 2002, GASTROINTEST ENDOSC, V56, P260, DOI 10.1067/mge.2002.126390; FURUTA GT, 1995, CURR OPIN GASTROEN, V11, P541, DOI 10.1097/00001574-199511000-00013; Garrett JK, 2004, J ALLERGY CLIN IMMUN, V113, P115, DOI 10.1016/j.jaci.2003.10.049; Guajardo JR, 2002, J PEDIATR-US, V141, P576, DOI 10.1067/mpd.2002.127663; Hamelmann E, 2001, IMMUNOL REV, V179, P182, DOI 10.1034/j.1600-065X.2001.790118.x; Herrick CA, 2000, J CLIN INVEST, V105, P765, DOI 10.1172/JCI8624; Hogan SP, 2000, P NATL ACAD SCI USA, V97, P6681, DOI 10.1073/pnas.97.12.6681; Justinich CJ, 1997, J PEDIATR GASTR NUTR, V25, P194, DOI 10.1097/00005176-199708000-00011; Kumar RK, 2002, AM J RESP CELL MOL, V27, P267, DOI 10.1165/rcmb.F248; Lai SY, 1996, EMBO J, V15, P4506; Lee NA, 2001, J ALLERGY CLIN IMMUN, V107, P945, DOI 10.1067/mai.2001.116002; Lee NA, 1997, J IMMUNOL, V158, P1332; Leung DYM, 2004, J CLIN INVEST, V113, P651, DOI 10.1172/JCI200421060; LEUNG DYM, 1995, J ALLERGY CLIN IMMUN, V96, P302, DOI 10.1016/S0091-6749(95)70049-8; Liacouras CA, 2003, J PEDIATR GASTR NUTR, V37, pS23, DOI 10.1097/00005176-200311001-00006; Ma W, 2002, J CLIN INVEST, V109, P621, DOI 10.1172/JCI200214097; Mishra A, 2003, GASTROENTEROLOGY, V125, P1419, DOI 10.1053/S0016-5085(03)01352-0; Mishra A, 2001, J CLIN INVEST, V107, P83, DOI 10.1172/JCI10224; Mishra A, 2002, J IMMUNOL, V168, P2464; Mishra A, 1999, J CLIN INVEST, V103, P1719, DOI 10.1172/JCI6560; Murata T, 1996, J IMMUNOL, V156, P2972; Nicholson AG, 1997, J PATHOL, V183, P233, DOI 10.1002/(SICI)1096-9896(199710)183:2<233::AID-PATH936>3.0.CO;2-Z; Noel RJ, 2004, CLIN GASTROENTEROL H, V2, P568, DOI 10.1053/S1542-3565(04)00240-X; Noel RJ, 2004, NEW ENGL J MED, V351, P940, DOI 10.1056/NEJM200408263510924; Orenstein SR, 2000, AM J GASTROENTEROL, V95, P1422; Pope SM, 2001, J ALLERGY CLIN IMMUN, V108, P594; Rothenberg ME, 2004, J ALLERGY CLIN IMMUN, V113, P11, DOI 10.1016/j.jaci.2003.10.047; Ruchelli E, 1999, PEDIATR DEVEL PATHOL, V2, P15, DOI 10.1007/s100249900084; Saito H, 2002, J IMMUNOL, V168, P3017; SALOGA J, 1994, AM J RESP CRIT CARE, V149, P65; Sampson HA, 1999, J ALLERGY CLIN IMMUN, V103, P717, DOI 10.1016/S0091-6749(99)70411-2; Spergel JM, 2002, J ALLERGY CLIN IMMUN, V109, P363, DOI 10.1067/mai.2002.121458; Spergel JM, 1998, J CLIN INVEST, V101, P1614, DOI 10.1172/JCI1647; Spergel JM, 1999, J CLIN INVEST, V103, P1103, DOI 10.1172/JCI5669; Spergel Jonathan M., 2003, Journal of Allergy and Clinical Immunology, V112, pS118, DOI 10.1016/j.jaci.2003.09.033; Straumann A, 2001, J ALLERGY CLIN IMMUN, V108, P954, DOI 10.1067/mai.2001.119917; Straumann A, 2003, GASTROENTEROLOGY, V125, P1660, DOI 10.1053/S0016-5085(03)01515-4; Takeda K, 1996, J IMMUNOL, V157, P3220; Takeda K, 1996, NATURE, V380, P627, DOI 10.1038/380627a0; Teitelbaum JE, 2002, GASTROENTEROLOGY, V122, P1216, DOI 10.1053/gast.2002.32998; Trifilieff A, 2000, BRIT J PHARMACOL, V130, P1581, DOI 10.1038/sj.bjp.0703501; van Neste D, 1985, Acta Derm Venereol Suppl (Stockh), V114, P67; Walsh SV, 1999, AM J SURG PATHOL, V23, P390, DOI 10.1097/00000478-199904000-00003; Wang L F, 1996, J Immunol, V156, P4077; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; Zimmermann N, 2004, J IMMUNOL, V172, P1815; ZURAWSKI G, 1994, STEM CELLS, V12, P169	55	110	113	0	1	W B SAUNDERS CO	PHILADELPHIA	INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA	0016-5085			GASTROENTEROLOGY	Gastroenterology	SEP	2005	129	3					985	994		10.1053/j.gastro.2005.06.027		10	Gastroenterology & Hepatology	Gastroenterology & Hepatology	963PO	WOS:000231816500024	16143136	
J	Jaakkola, JJK; Hwang, BF; Jaakkola, N				Jaakkola, JJK; Hwang, BF; Jaakkola, N			Home dampness and molds, parental atopy, and asthma in childhood: A six-year population-based cohort study	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; damp housing; effect modification; interaction; molds	ENVIRONMENTAL-FACTORS; RESPIRATORY SYMPTOMS; CHILDREN; HEALTH; INFLAMMATION; SIGNS	Previous studies of how parental atopy and exposure to dampness and molds contribute to the risk of asthma have been mainly cross-sectional or prevalent case-control studies, where selection and information bias and temporality constitute problems. We assessed longitudinally the independent and joint effects of parental atopy and exposure to molds in dwellings on the development of asthma in childhood. We conducted a population-based, 6-year prospective cohort study of 1,984 children 1-7 years of age at the baseline in 1991 (follow-up rate, 77%). The study population included 1,916 children without asthma at baseline and complete outcome information. The data collection included a baseline and follow-up survey. The outcome of interest was development of asthma during the study period. The studied determinants were parental allergic diseases and four indicators of exposure at baseline: histories of water damage, presence of moisture and visible molds, and perceived mold odor in the home. A total of 138 (7.2%) children developed asthma during the study period, resulting in an incidence rate of 125 cases per 10,000 person-years [95% confidence interval (CI), 104-146]. In Poisson regression adjusting for confounding, parental atopy [adjusted incidence rate ratio (IRR) 1.52; 95% Cl, 1.08-2.13] and the presence of mold odor in the home reported at baseline (adjusted IRR 2.44; 95% Cl, 1.07-5.60) were independent determinants of asthma incidence, but no apparent interaction was observed. The results of this cohort study with assessment of exposure before the onset of asthma strengthen the evidence on the independent effects of parental atopy and exposure to molds on the development of asthma.	Univ Birmingham, Inst Occupat & Environm Med, Birmingham B15 2TT, W Midlands, England; Univ Helsinki, Dept Publ Hlth, Environm Epidemiol Unit, FIN-00014 Helsinki, Finland; Diwan Coll Management, Dept Hlth Care Adm, Tainan, Taiwan	Jaakkola, JJK (reprint author), Univ Birmingham, Inst Occupat & Environm Med, Birmingham B15 2TT, W Midlands, England.	j.jaakkola@bham.ac.uk	Jaakkola, Jouni/G-4314-2012; Hwang, Bing-Fang /O-2709-2015	Hwang, Bing-Fang /0000-0002-5951-9662			ANDRAE S, 1988, ARCH DIS CHILD, V63, P473; BELANGER K, AM J EPIDEMIOL, V158, P195; BOMEHAG CG, INDOOR AIR, V11, P72; BRUNEKREEF B, 1989, AM REV RESPIR DIS, V140, P1363; BRUNEKREEF B, 1992, SCI TOTAL ENVIRON, V15, P79; DALES RE, 1991, AM J EPIDEMIOL, V134, P196; FERRIS BG, 1978, AM REV RESPIR DIS, V118, P1; Husman T, 1996, SCAND J WORK ENV HEA, V22, P5; JAAKKOLA JJK, 1993, J EXPO ANAL ENV EPID, V3, P129; Jaakkola JJK, 2001, ENVIRON HEALTH PERSP, V109, P579, DOI 10.2307/3455031; Johanning E, 1999, ENVIRON HEALTH PERSP, V107, P489; Laitinen T, 1998, AM J RESP CRIT CARE, V157, P1073; Mutitts E, 1994, AM J RESP CRIT CARE, V149, P358; Nafstad P, 1998, AM J RESP CRIT CARE, V157, P410; Norback D, 1999, INT J TUBERC LUNG D, V3, P368; Rothman KJ, 1985, MODERN EPIDEMIOLOGY, P311; SPENGLER J, 1994, INDOOR AIR, V4, P72, DOI 10.1111/j.1600-0668.1994.t01-2-00002.x; STRACHAN DP, 1989, J EPIDEMIOL COMMUN H, V43, P7, DOI 10.1136/jech.43.1.7; Thorn J, 1998, AM J RESP CRIT CARE, V157, P1798; Wickman M, 2003, ALLERGY, V58, P742, DOI 10.1034/j.1398-9995.2003.00078.x; Yang CY, 1997, ENVIRON RES, V75, P49, DOI 10.1006/enrs.1997.3774	21	110	114	2	15	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	MAR	2005	113	3					357	361		10.1289/ehp.7242		5	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	903MM	WOS:000227430100048	15743728	
J	Goodwin, RD; Fergusson, DM; Horwood, LJ				Goodwin, RD; Fergusson, DM; Horwood, LJ			Asthma and depressive and anxiety disorders among young persons in the community	PSYCHOLOGICAL MEDICINE			English	Article							POSTTRAUMATIC-STRESS-DISORDER; PSYCHIATRIC-DISORDERS; FUNCTIONAL STATUS; PANIC DISORDER; CHILDREN; PREVALENCE; CHILDHOOD; MORBIDITY; OUTCOMES; OUTPATIENTS	Background. The objectives of the study were to examine linkages between asthma and depressive and anxiety disorders in a birth cohort of over 1000 young persons studied to the age of 21 years. Specifically, the study aimed to ascertain the extent to which associations between asthma and depressive and anxiety disorders could be explained by non-observed fixed confounding factors. Method. Asthma and depressive and anxiety disorders were measured prospectively over the course of a 21-year longitudinal study. Fixed effects logistic regression models were used to determine the relationship between asthma and depressive and anxiety disorders, adjusting for potentially confounding factors. Results. Asthma in adolescence and young adulthood was associated with increased likelihood of major depression (OR 1(.)7, 95 % CI 1(.)3-2(.)3), panic attacks (OR 1(.)9, 95 % CI 1(.)3-2(.)8), and any anxiety disorder (OR 1(.)6, 95% CI 1(.)2-2(.)2). Associations between asthma and depressive and anxiety disorders were adjusted for confounding factors using a fixed effects regression model which showed that, after control for fixed confounding factors, asthma was no longer significantly related to major depression (OR 1(.)1), panic attacks (OR 1(.)1),or any anxiety disorder (OR 1(.)2). Additional post hoe analyses suggested that exposure to childhood adversity or unexamined familial factors may account for some of the co-morbidity of asthma and depressive and anxiety disorders. Conclusions. These results confirm and extend previous findings by documenting elevated rates of depressive and anxiety disorders among young adults with asthma, compared with their counterparts without asthma, in the community. The weight of the evidence from this study suggests that associations between asthma and depressive and anxiety symptoms may reflect effects of common factors associated with both asthma and depressive and anxiety disorders, rather than a direct causal link. Future research is needed to identify the specific factors underlying these associations.	Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, Unit 43, New York, NY 10032 USA; Christchurch Sch Med & Hlth Sci, Dept Psychol Med, Christchurch Hlth & Dev Study, Christchurch, New Zealand	Goodwin, RD (reprint author), Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, Unit 43, 1051 Riverside Dr, New York, NY 10032 USA.	rdg66@columbia.edu		Fergusson, David/0000-0002-8117-017X; Horwood, L./0000-0003-4881-1956	NIMH NIH HHS [MH64736]		Afari N, 2001, J CLIN PSYCHOL MED S, V8, P245, DOI 10.1023/A:1011912712262; American Psychiatric Association ( APA), 1994, DIAGN STAT MAN MENT; ASHER MI, 2000, NZ MED J, V23, P114; Brown ES, 2000, INT J PSYCHIAT MED, V30, P319; Bussing R, 1996, PSYCHOSOMATICS, V37, P108; Carlin JB, 1999, STAT MED, V18, P2655, DOI 10.1002/(SICI)1097-0258(19991015)18:19<2655::AID-SIM202>3.3.CO;2-R; Carr RE, 1998, J PSYCHOSOM RES, V44, P43, DOI 10.1016/S0022-3999(97)00137-2; Cunningham J, 1996, AM J PUBLIC HEALTH, V86, P1406, DOI 10.2105/AJPH.86.10.1406; ELLEY WB, 1976, NEW ZEAL J EDUC STUD, V11, P25; Fergusson DM, 1996, J AM ACAD CHILD PSY, V35, P1355, DOI 10.1097/00004583-199610000-00023; Fergusson DM, 1997, CHILD ABUSE NEGLECT, V21, P617, DOI 10.1016/S0145-2134(97)00021-5; Fergusson D. M., 2003, RESILIENCE VULNERABI, P130, DOI DOI 10.1017/CBO9780511615788.008; Goethe JW, 2001, ANN ALLERG ASTHMA IM, V87, P205; Goodwin RD, 2003, PSYCHOL MED, V33, P879, DOI 10.1017/S0033291703007633; Greaves CJ, 2002, THORAX, V57, P217, DOI 10.1136/thorax.57.3.217; Hamerle A, 1995, HDB STAT MODELING SO, P401; HOLT S, 2000, NZ MED J, V11, P39; Koltek M, 1998, CAN J PSYCHIAT, V43, P64; Mannino D. M., 2002, MMWR-MORBID MORTAL W, V51, P1; McQuaid EL, 2001, J DEV BEHAV PEDIATR, V22, P430; Nascimento I, 2002, PSYCHIAT RES, V110, P73, DOI 10.1016/S0165-1781(02)00029-X; Ortega AN, 2002, J NERV MENT DIS, V190, P275, DOI 10.1097/01.NMD.0000016250.84828.0D; Ortega AN, 2003, SOC PSYCH PSYCH EPID, V38, P220, DOI 10.1007/s00127-003-0623-6; Perna G, 1997, BIOL PSYCHIAT, V42, P625, DOI 10.1016/S0006-3223(96)00436-2; Rothman KJ, 1998, MODERN EPIDEMIOLOGY; Slattery MJ, 2002, J AM ACAD CHILD PSY, V41, P947, DOI 10.1097/00004583-200208000-00013; *STAT, 1999, STAT STAT SOFTW; Sterk PJ, 1999, EUR RESPIR J, V14, P1435, DOI 10.1183/09031936.99.14614359; STRAUS MA, 1979, J MARRIAGE FAM, V41, P75, DOI 10.2307/351733; Swadi H, 2001, J TROP PEDIATRICS, V47, P106, DOI 10.1093/tropej/47.2.106; Vila G, 2000, J AFFECT DISORDERS, V58, P223, DOI 10.1016/S0165-0327(99)00110-X; Weil CM, 1999, PEDIATRICS, V104, P1274, DOI 10.1542/peds.104.6.1274; Weisberg RB, 2002, PSYCHIATR SERV, V53, P848, DOI 10.1176/appi.ps.53.7.848; WEISS KB, 2000, ASTHMAS IMPACT SOC; World Health Organization, 1993, COMP INT DIAGN INT C; YELLOWLEES PM, 1987, MED J AUSTRALIA, V146, P305; ZEGER SL, 1986, BIOMETRICS, V42, P121, DOI 10.2307/2531248	37	110	115	1	11	CAMBRIDGE UNIV PRESS	NEW YORK	32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA	0033-2917			PSYCHOL MED	Psychol. Med.	NOV	2004	34	8					1465	1474		10.1017/S0033291704002739		10	Psychology, Clinical; Psychiatry; Psychology	Psychology; Psychiatry	878XM	WOS:000225680700009	15724877	
J	Marogna, M; Spadolini, I; Massolo, A; Canonica, GW; Passalacqua, G				Marogna, M; Spadolini, I; Massolo, A; Canonica, GW; Passalacqua, G			Randomized controlled open study of sublingual immunotherapy for respiratory allergy in real-life: clinical efficacy and more	ALLERGY			English	Article						adherence; bronchial hyperreactivity; preventive effect; respiratory allergy; sublingual immunotherapy	HOUSE-DUST MITE; CONTROLLED-TRIAL; SEASONAL RHINOCONJUNCTIVITIS; DOUBLE-BLIND; ASTHMA; CHILDREN; SENSITIZATIONS; STANDARDIZATION; RESPONSIVENESS; PREVENTION	Background: Some aspects of sublingual immunotherapy (SLIT) still need to be addressed: magnitude of the clinical efficacy, effect on the bronchial hyperreactivity adherence to treatment, preventive effect. We attempted to clarify these points in a randomized open, controlled, two parallel group study in a real-life setting. Methods: Five hundred and eleven patients with allergic rhinitis with or without intermittent asthma were randomized to drugs only or drugs + SLIT (rate 2 : 3) for 3 years. The clinical score (symptoms + drug intake) was measured each year during the allergen exposure. Pulmonary function test, methacholine challenge and skin tests were performed at the beginning and at the end of the study. Adherence to treatment was assessed by measuring the consumed extract. Results: Three hundred and nineteen patients received SLIT and 192 drugs only. Dropouts were 15% in the SLIT group and 12% in the controls. There was a significant improvement of clinical scores in the SLIT group: baseline 147 +/- 3.3, first year 72.9 +/- 1.3, second year 68.3 +/- 1.8, third year 54.7 +/- 2.8 (P < 0.0001 vs baseline). Control group: baseline 138 +/- 2.3, first year 124.1 +/- 3.7, second year 111 +/- 3.3, third year 121 +/- 3.8 (P = NS). Only four patients reported systemic itching. Adherence was >80% in 72% and >60% in 18% of patients. The number of patients with a positive MCh challenge decreased significantly after 3 years only in the SLIT group. New skin sensitizations appeared in 38% of the controls and in 5.9% of the SLIT patients (P = 0.01). Conclusion: Sublingual immunotherapy approximately halved the clinical scores and significantly reduced the bronchial hyperreactivity. Similarly to subcutaneous immunotherapy, SLIT displayed a preventive effect on the onset of new skin sensitizations. The adherence rate was quantitatively satisfactory.	Univ Genoa, Dept Internal Med, I-16132 Genoa, Italy; Macchi Hosp Fdn, Pneumol Unit, Varese, Italy; Anallergo SpA, Dept Med, Florence, Italy; Univ Siena, Sect Behav Ecol Ethol & Wildlife Management, Dept Environm Sci, I-53100 Siena, Italy	Passalacqua, G (reprint author), Univ Genoa, Dept Internal Med, Padiglione Maragliano Lgo R Benzi 10, I-16132 Genoa, Italy.		Massolo, Alessandro/I-3437-2012				Abramson M, 1999, ALLERGY, V54, P1022, DOI 10.1034/j.1398-9995.1999.00102.x; ALESSANDRO F, 1994, ANN ALLERGY, V73, P135; Andre C, 2000, INT ARCH ALLERGY IMM, V121, P229, DOI 10.1159/000024322; BOUSQUET J, 1998, ALLERGY S, V53, P20; BOUSQUET J, 2001, J ALLERGY CLIN IMM S, V107, P240; Canonica GW, 2003, J ALLERGY CLIN IMMUN, V111, P437, DOI 10.1067/mai.2003.129; Ciprandi G, 1998, INT ARCH ALLERGY IMM, V115, P157, DOI 10.1159/000023896; DesRoches A, 1997, J ALLERGY CLIN IMMUN, V99, P450, DOI 10.1016/S0091-6749(97)70069-1; Di Rienzo V, 1999, ALLERGY, V54, P1110, DOI 10.1034/j.1398-9995.1999.00267.x; Di Rienzo V, 2003, CLIN EXP ALLERGY, V33, P206, DOI 10.1046/j.1365-2222.2003.01587.x; DREBORG S, 1993, ALLERGY, V48, P49, DOI 10.1111/j.1398-9995.1993.tb04756.x; Frew AJ, 2001, J ALLERGY CLIN IMMUN, V107, P441, DOI 10.1067/mai.2001.113525; GOOD P, 2002, PERMUTATION TESTS PR; Grembiale RD, 2000, AM J RESP CRIT CARE, V162, P2048; HARGREAVE FE, 1981, J ALLERGY CLIN IMMUN, V68, P347, DOI 10.1016/0091-6749(81)90132-9; Kagi MK, 2002, ALLERGY, V57, P379, DOI 10.1034/j.1398-9995.2002.01153.x; KLEIJNEN J, 1994, LANCET, V344, P1347, DOI 10.1016/S0140-6736(94)90699-8; Lee SY, 2002, J ASTHMA, V39, P537, DOI 10.1081/JAS-120004924; Lima MT, 2002, CLIN EXP ALLERGY, V32, P507, DOI 10.1046/j.0954-7894.2002.01327.x; Lockey RF, 2001, ANN ALLERG ASTHMA IM, V87, P47; Lombardi C, 2001, J INVEST ALLERG CLIN, V11, P41; Lombardi C, 2001, ALLERGY, V56, P889; Malling H J, 2001, Curr Opin Allergy Clin Immunol, V1, P43, DOI 10.1097/00130832-200102000-00008; Moller C, 2002, J ALLERGY CLIN IMMUN, V109, P251, DOI 10.1067/mai.2002.121317; National Institutes of Health, 1997, NIH PUBL; Pajno GB, 2001, CLIN EXP ALLERGY, V31, P1392, DOI 10.1046/j.1365-2222.2001.01161.x; Passalacqua G, 1999, J ALLERGY CLIN IMMUN, V104, P964, DOI 10.1016/S0091-6749(99)70076-X; Passalacqua G, 1998, LANCET, V351, P629, DOI 10.1016/S0140-6736(97)07055-4; Purello-D'Ambrosio F, 2001, CLIN EXP ALLERGY, V31, P1295, DOI 10.1046/j.1365-2222.2001.01027.x; Siegel S., 1998, NONPARAMETRIC STAT B; Sokal RR, 1995, BIOMETRY PRINCIPLES; *SPSS INC, 1999, SPSS ADV MOD 9 0, P497; STERK PJ, 1993, EUR RESPIR J, V6, P53, DOI 10.1183/09041950.053s1693; Wilson DR, 2003, COCHRANE DB SYST REV, V2	34	110	121	0	2	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	NOV	2004	59	11					1205	1210		10.1111/j.1398-9995.2004.00508.x		6	Allergy; Immunology	Allergy; Immunology	859WI	WOS:000224298200011	15461603	
J	Mattos, W; Lim, S; Russell, R; Jatakanon, A; Chung, F; Barnes, PJ				Mattos, W; Lim, S; Russell, R; Jatakanon, A; Chung, F; Barnes, PJ			Matrix metalloproteinase-9 expression in asthma - Effect of asthma severity, allergen challenge, and inhaled corticosteroids	CHEST			English	Article						allergen challenge; asthma; corticosteroid; matrix metalloproteinase; matrix metalloproteinase-9; tisstue inhibitors of matrix metalloproteinase	BRONCHOALVEOLAR LAVAGE FLUID; MATRIX METALLOPROTEINASES; BASEMENT-MEMBRANE; TISSUE INHIBITOR; 92-KDA GELATINASE; IV COLLAGENASE; TNF-ALPHA; ALVEOLAR MACROPHAGES; AIRWAY INFLAMMATION; TIMP-1 PRODUCTION	Background: Asthma is associated with remodeling of the extracellular matrix (ECM) and increased airway obstruction, and the mechanisms of this process are unknown. Matrix metalloproteinases (MMPs) are a group of enzymes capable of degrading the ECM. They are released along with their inhibitors, tissue inhibitor of MMP (TIMP). Study objectives: To determine whether severe, persistent asthma is associated with increased levels of MMP-9 in the airway compared with mild asthma, and to assess the effect of both allergen exposure and steroid treatment on MMP-9 and TIMP-1 levels. Design: Prospective analysis of levels and activity of MMP-9 and TIMP-1 in BAL fluid (BALF) and induced sputum obtained from asthmatics of differing disease severity. In patients with mild asthma, MMP-9 and TIMP-1 levels were studied in induced sputum following allergen challenge and in BALF after inhaled steroid therapy. Patients: Eighteen patients with mild asthma, 10 patients with severe asthma, and 10 nonsmoking, atopic subjects had their sputum studied. Fourteen of the patients with mild asthma underwent allergen challenge. BAL was collected from 16 patients with mild asthma before and after 4 weeks treatment with inhaled budesonide, 800 mug bid, or placebo. Results: Patients with severe asthma had increased levels and activity of sputum MMP-9 in their sputum compared with patients with mild asthma and normal subjects. Allergen challenge increased the MMP-9/TIMP-1 ratio and MMP-9 activity. Inhaled budesonide had no effect on MMP-9 or TIMP-1 in patients with mild asthma. Conclusions: MMP-9 may play a role in chronic airway inflammation and remodeling in asthma, as concentrations are increased in severe, persistent asthma and following allergen challenge. Inhaled steroids may not affect MMP-9 and TIMP in patients with mild asthma, and additional studies in patients with more severe asthma are needed.	Univ London Imperial Coll Sci Technol & Med, Fac Med, Natl Heart & Lung Inst, Dept Thorac Med, London WS3 6LY, England	Barnes, PJ (reprint author), Univ London Imperial Coll Sci Technol & Med, Fac Med, Natl Heart & Lung Inst, Dept Thorac Med, Dovehouse St, London WS3 6LY, England.	p.j.barnes@ic.ac.uk		Chung, Kian Fan/0000-0001-7101-1426			American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P225, DOI DOI 10.1164/AJRCCM/136.1.225; Bosse M, 1999, AM J RESP CRIT CARE, V159, P596; CORCORAN ML, 1992, J BIOL CHEM, V267, P515; Dahlen B, 1999, THORAX, V54, P590; Delclaux C, 1996, AM J RESP CELL MOL, V14, P288; Di Girolamo N, 1998, EUR J IMMUNOL, V28, P1773, DOI 10.1002/(SICI)1521-4141(199806)28:06<1773::AID-IMMU1773>3.0.CO;2-B; GEARING AJH, 1994, NATURE, V370, P555, DOI 10.1038/370555a0; Hoshino M, 1999, J ALLERGY CLIN IMMUN, V104, P356, DOI 10.1016/S0091-6749(99)70379-9; JEFFERY PK, 1989, AM REV RESPIR DIS, V140, P1745; JEFFERY PK, 1992, AM REV RESPIR DIS, V145, P890; John M, 1998, AM J RESP CRIT CARE, V157, P256; Johnatty RN, 1997, J IMMUNOL, V158, P2327; KAYAGAKI N, 1995, J EXP MED, V182, P1777, DOI 10.1084/jem.182.6.1777; Keatings VM, 1997, AM J RESP CRIT CARE, V155, P542; LAITINEN LA, 1985, AM REV RESPIR DIS, V131, P599; Lemjabbar H, 1999, AM J RESP CRIT CARE, V159, P1298; LEPPERT D, 1995, J IMMUNOL, V154, P4379; Massova I, 1998, FASEB J, V12, P1075; Mautino G, 1999, AM J RESP CRIT CARE, V160, P324; Mautino G, 1997, AM J RESP CELL MOL, V17, P583; MERTZ PM, 1994, J BIOL CHEM, V269, P21322; MURPHY G, 1994, J BIOL CHEM, V269, P6632; MURPHY G, 1992, AM J RESP CELL MOL, V7, P120; OCONNOR CM, 1994, THORAX, V49, P602, DOI 10.1136/thx.49.6.602; Ohno I, 1997, AM J RESP CELL MOL, V16, P212; Okada S, 1997, AM J RESP CELL MOL, V17, P519; OKADA Y, 1992, J BIOL CHEM, V267, P21712; Redigton AE, 1998, ASTHMA ALLERGIC DIS, P443; Roberts CR, 1997, ASTHMA, P925; ROCHE WR, 1989, LANCET, V1, P520; Saren P, 1996, J IMMUNOL, V157, P4159; Sont JK, 1999, AM J RESP CRIT CARE, V159, P1043; TRIGG CJ, 1994, AM J RESP CRIT CARE, V150, P17; Vignola AM, 1998, AM J RESP CRIT CARE, V158, P1945; Warner JA, 1997, INT ARCH ALLERGY IMM, V113, P318; Xia MH, 1996, J IMMUNOL, V156, P160; Yao PM, 1997, AM J PHYSIOL-LUNG C, V273, pL866; Zhang YH, 1998, J IMMUNOL, V161, P3071	38	110	118	0	5	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	NOV	2002	122	5					1543	1552		10.1378/chest.122.5.1543		10	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	617TH	WOS:000179376600013	12426251	
J	Lin, M; Chen, Y; Burnett, RT; Villeneuve, PJ; Krewski, D				Lin, M; Chen, Y; Burnett, RT; Villeneuve, PJ; Krewski, D			The influence of ambient coarse particulate matter on asthma hospitalization in children: Case-crossover and time-series analyses	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma hospitalization; case-crossover analysis; coarse particulate matter; risk assessment; time-series analysis	CARBON-MONOXIDE LEVELS; EMERGENCY ROOM VISITS; AIR-POLLUTION; DAILY MORTALITY; FINE PARTICLES; PHILADELPHIA; ASSOCIATION; ADMISSIONS; SEATTLE; CALIFORNIA	In this study, we used both case-crossover and time-series analyses to assess the associations between size-fractionated particulate matter and asthma hospitalization among children 6-12 years old living in Toronto between 1981 and 1993. Specifically, we used exposures averaged over periods varying from 1 to 7 days to assess the effects of particulate matter on asthma hospitalization. We calculated estimates of the relative risk of asthma hospitalization adjusted for daily weather conditions (maximum and minimum temperatures, and average relative humidity) for an incremental exposure corresponding to the interquartile range in particulate matter. Both bidirectional case-crossover and time-series analyses revealed that coarse particulate matter (PM10-2.5) averaged over 5-6 days was significantly associated with asthma hospitalization in both males and females. The magnitude of this effect appeared to increase with increasing number of days of exposure averaging for most models, with the relative risk estimates stabilizing at about 6 days. Using a bidirectional case-crossover analysis, the estimated relative risks were 1.14 [95% confidence interval (CI), 1.02, 1.28] for males and 1.18 (95% CI, 1.02, 1.36) for females, for an increment of 8.4 mug/m(3) in 6-day averages of PM10-2.5. The corresponding relative risk estimates were 1.10 and 1.18, respectively, when we used time-series analysis. The effect Of PM10-2.5 remained positive after adjustment for the effects of the gaseous pollutants carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and ozone (O-3). We did not find significant effects of fine particulate matter (PM2.5) or of thoracic particulate matter (PM10) on asthma hospitalizations using either of these two analytic approaches. For the most part, relative risk estimates from the unidirectional case-crossover analysis were more pronounced compared with both bidirectional case-crossover and time-series analyses.	Univ Ottawa, Dept Epidemiol & Community Med, Fac Med, Ottawa, ON K1H 8M5, Canada; Univ Ottawa, McLaughlin Ctr Populat Hlth Risk Assessment, Ottawa, ON, Canada; Hlth Canada, Environm Hlth Directorate, Ottawa, ON, Canada	Chen, Y (reprint author), Univ Ottawa, Dept Epidemiol & Community Med, Fac Med, 451 Smyth Rd, Ottawa, ON K1H 8M5, Canada.						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B., 1981, SPECTRAL ANAL TIME S; Scarlett JF, 1996, THORAX, V51, P1109, DOI 10.1136/thx.51.11.1109; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; Schwartz J, 2000, EPIDEMIOLOGY, V11, P6, DOI 10.1097/00001648-200001000-00004; SCHWARTZ T, 1961, ANTHROPOL LINGUIST, V3, P1; Sheppard L, 1999, EPIDEMIOLOGY, V10, P23, DOI 10.1097/00001648-199901000-00006; Sunyer J, 2000, AM J EPIDEMIOL, V151, P50; THOMSON NC, 1990, HDB CLIN ALLERGY; *US EPA, 1995, AIR QUAL CRIT PART M; *US EPA OFF AIR QU, 2000, NAT AMB AIR QUAL STA; World Health Organization, 1975, MAN INT STAT CLASS D; Wordley J, 1997, OCCUP ENVIRON MED, V54, P108	38	110	113	1	11	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	JUN	2002	110	6					575	581				7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	561HV	WOS:000176134900021	12055048	
J	Hunt, JF; Erwin, E; Palmer, L; Vaughan, J; Malhotra, N; Platts-Mills, TAE; Gaston, B				Hunt, JF; Erwin, E; Palmer, L; Vaughan, J; Malhotra, N; Platts-Mills, TAE; Gaston, B			Expression and activity of pH-regulatory glutaminase in the human airway epithelium	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; glutaminase; ammonia; lung; breath condensate	MYCOBACTERIUM-TUBERCULOSIS; RESPIRATORY MUCUS; BUFFER CAPACITY; SURFACE LIQUID; TRACHEAL; MACROPHAGES; AMMONIA; ASTHMA; EOSINOPHILS; METABOLISM	Fluid condensed from the breath of patients with acute asthma is acidic. Several features of asthma pathophysiology can be initiated by exposure of the airway to acid. In renal tubular epithelium, glutaminase produces ammonia to buffer urinary acid excretion. We hypothesized that human airway epithelium could also express glutaminase. Here, we demonstrate that human airway epithelial cells in vitro have biochemical evidence for glutaminase activity and express mRNA for two glutaminase isoforms (KGA and GAC). Glutaminase activity increased in response to acidic stress (media PH 5.8) and was associated with both increased culture medium pH and improved cell survival. In contrast, activity was inhibited by interferon-gamma and tumor necrosis factor-a. Glutaminase protein was expressed in the human airway in vivo. Further, ammonia levels in the breath condensate of subjects with acute asthma were low (30 muM [range: 0-233], n = 18, age 23 +/- 2.5 yr) compared with control subjects (327 muM [14-1,220], n 24, age 24 +/- 2.4 yr, p < 0.001), and correlated with condensate pH (r = 0.58, p < 0.001). These data demonstrate that glutaminase is expressed and active in the human airway epithelium and may be relevant both to the regulation of airway pH and to the pathophysiology of acute asthmatic airway inflammation.	Univ Virginia, Hlth Syst, Dept Pediat, Div Pediat Resp Med, Charlottesville, VA 22908 USA; Univ Virginia, Hlth Syst, Div Allergy Asthma & Immunol, Charlottesville, VA 22908 USA	Gaston, B (reprint author), Univ Virginia, Hlth Syst, Dept Pediat, Div Pediat Resp Med, Box 386, Charlottesville, VA 22908 USA.				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J. Respir. Crit. Care Med.	JAN 1	2002	165	1					101	107				7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	509VY	WOS:000173171500019	11779738	
J	Rundell, KW; Jenkinson, DM				Rundell, KW; Jenkinson, DM			Exercise-induced bronchospasm in the elite athlete	SPORTS MEDICINE			English	Review							CROSS-COUNTRY SKIERS; ICE SKATING RINKS; HYPERTONIC SALINE CHALLENGE; NITROGEN-DIOXIDE EXPOSURES; VOCAL CORD DYSFUNCTION; INDUCED ASTHMA; INDUCED BRONCHOCONSTRICTION; FLUTICASONE PROPIONATE; RECEPTOR ANTAGONIST; WATER-LOSS	The term exercise-induced bronchospasm (EIB) describes the acute transient airway narrowing that occurs during and most often after exercise in 10 to 50% of elite athletes, depending upon the sport examined. Although multiple factors are unquestionably involved in the EIB response, airway drying caused by a high exercise-ventilation rate is primary in most cases. The severity of this reaction reflects the allergic predisposition of the athlete, the water content of the inspired air, the type and concentration of air pollutants inspired, and the intensity (or ventilation rate) of the exercise. The highest prevalence of EIB is seen in winter-sport populations, where athletes are chronically exposed to cold dry air and/or environmental pollutants found in indoor ice arenas. When airway surface liquid lost during the natural warming and humidification process of respiration is not replenished at a rate equal to the loss, the ensuing osmolarity change stimulates the release of inflammatory mediators and results in bronchospasm; this cascade of events is exacerbated by airway inflammation and airway remodelling. The acute EIB response is characterised by airway smooth muscle contraction, membrane swelling, and/or mucus plug formation. Evidence suggests that histamine, leukotrienes and prostanoids are likely mediators for this response. Although the presence of symptoms and a basic physical examination are marginally effective, objective measures of lung function should be used for accurate and reliable diagnosis of EIB. Diagnosis should include baseline spirometry, followed by an appropriate bronchial provocation test. To date, the best test to confirm EIB may simply be standard pulmonary function testing before and after high-intensity dry air exercise. A 10% post-challenge fall in forced expiratory volume in 1 second is used as diagnostic criteria. The goal of medical intervention is to limit EIB exacerbation and allow the athlete to train and compete symptom free. This is attempted through daily controller medications such as inhaled corticosteroids or by the prophylactic use of medications before exercise. In many cases, EIB is difficult to control. These and other data suggest that EIB in the elite athlete is in contrast with classic asthma.	Marywood Univ, Human Performance Lab, Scranton, PA 18509 USA; Univ Pittsburgh, Med Ctr, Ctr Sports Med, Pittsburgh, PA USA	Rundell, KW (reprint author), Marywood Univ, Human Performance Lab, Scranton, PA 18509 USA.						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J	Yu, OC; Sheppard, L; Lumley, T; Koenig, JQ; Shapiro, GG				Yu, OC; Sheppard, L; Lumley, T; Koenig, JQ; Shapiro, GG			Effects of ambient air pollution on symptoms of asthma in Seattle-area children enrolled in the CAMP study	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						ambient air pollution; asthma; carbon monoxide; children; panel study; particulate matter; sulfur dioxide; symptoms; within-subject effects	RESPIRATORY HEALTH; PARTICULATE MATTER; LONGITUDINAL DATA; LOS-ANGELES; PARTICLES; EMERGENCY; EXPOSURE; VISITS; TIME	We observed a panel of 133 children (5-13 years of age) with asthma residing in the greater Seattle, Washington, area for an average of 58 days (range 28-112 days) during screening for enrollment in the Childhood Asthma Management Program (CAMP) study. Daily self-reports of asthma symp toms were obtained from study diaries and compared with ambient air pollution levels in marginal repeated measures logistic regression models. We defined days with asthma symptoms as any day a child reported at least one mild asthma episode. All analyses were controlled for subject-specific variables [age, race, sex, baseline height, and FEV1 PC20 concentration (methacholine provocative concentration required to produce a 20% decrease in forced expiratory volume in 1 sec)] and potential rime-dependent confounders (day of week, season, and temperature). Because of variable observation periods for participants, we estimated both between- and within-subject air pollutant effects. Our primary interest was in the within-subject effects: the effect of air pollutant excursions from typical levels in each child's observation period on the odds of asthma symptoms. In single-pollutant models, the population average estimates indicated a 30% [95% confidence interval (CI), 11-52%] increase for a 1-ppm increment in carbon monoxide lagged I day, an 18% (95% CI, 5-33%) increase for a 10-mug/m(3) increment in same-day particulate matter < 1.0 <mu>m (PM1.0), and an 11% (95% CI, 3-20%) increase for a 10-mug/m(3) increment in particulate matter < 10 <mu>m (PM10) lagged 1 day. Conditional on the previous day's asthma symptoms, we estimated 25% (95% CI, 10-42%), 14% (95% CI, 4-26%), and 10% (95% CI, 3-16%) increases in the odds of asthma symptoms associated with increases in CO, PM1.0, and PM10, respectively. We did not find any association between sulfur dioxide (SO2) and the odds of asthma symptoms. In multipollutant models, the separate pollutant effects were smaller. The overall effect of an increase in both CO and PM1.0 was a 31% (95% CI, 11-55%) increase in the odds of symptoms of asthma. We conclude that there is an association between change in shea-term air pollution levels, as indexed by PM and CO, and the occurrence of asthma symptoms among children in Seattle. Although PM effects on asthma have been found in other studies, it is likely that CO is a marker for vehicle exhaust and other combustion by-products that aggravate asthma.	Univ Washington, Dept Biostat, Seattle, WA 98195 USA; Univ Washington, Dept Environm Hlth, Seattle, WA 98195 USA; Univ Washington, Dept Pediat, Seattle, WA 98195 USA	Sheppard, L (reprint author), Univ Washington, Dept Biostat, Box 357232, Seattle, WA 98195 USA.				NHLBI NIH HHS [N01 HR 16050]		Anuszewski J, 1998, J EXPO ANAL ENV EPID, V8, P483; Cherniack R, 1999, CONTROL CLIN TRIALS, V20, P91; Ciccone G, 1998, OCCUP ENVIRON MED, V55, P771; Delfino RJ, 1998, ENVIRON HEALTH PERSP, V106, P751, DOI 10.1289/ehp.98106751; Diggle P. 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Health Perspect.	DEC	2000	108	12					1209	1214		10.2307/3434835		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	385LJ	WOS:000166005700034	11133403	
J	Anderson, SD; Holzer, K				Anderson, SD; Holzer, K			Exercise-induced asthma: Is it the right diagnosis in elite athletes?	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						exercise-induced asthma; athletes; dehydration; airway injury; osmolarity	LEUKOTRIENE-RECEPTOR ANTAGONIST; NEUTROPHIL CHEMOTACTIC FACTOR; 4.5-PERCENT SODIUM-CHLORIDE; CROSS-COUNTRY SKIERS; INDUCED BRONCHOCONSTRICTION; BRONCHIAL HYPERRESPONSIVENESS; INDUCED BRONCHOSPASM; HYPERTONIC SALINE; MAST-CELLS; COLD-AIR	Exercise-induced asthma, as recognized in asthmatic subjects, is an exaggerated airway response to airway dehydration in the presence of inflammatory cells and their mediators. The airway narrowing is primarily caused by contraction of bronchial smooth muscle. The milder airway narrowing documented in response to exercise in elite athletes and otherwise healthy subjects may simply be the result of the physiologic responses and pathologic changes in airway cells arising from dehydration injury. These changes, which include excessive mucus production and airway edema, would serve both to cause cough and to amplify the narrowing effects of normal bronchial smooth muscle contraction, resulting in symptoms. These changes are more likely to occur in healthy subjects who exercise intensely for long periods of time breathing cold air, dry air, or both. Under these conditions, the ability to humidify inspired air may be overwhelmed, causing significant dehydration of the airway mucosa and an increase in osmolarity, even in small airways. In addition to dehydration injury, airway narrowing to pharmacologic and physical agents may occur as a result of injury caused by large volumes of air containing irritant gases, particulate matter, or allergens being inspired during exercise. As a result, the airways may become inflamed, and the airway smooth muscle may become more sensitive. These events could result in the same exaggerated airway response to dehydration, as documented in asthmatic subjects.	Royal Prince Alfred Hosp, Dept Resp Med, Camperdown, NSW 2050, Australia; Alfred Hosp, Dept Allergy Asthma & Clin Immunol, Prahan, Australia	Anderson, SD (reprint author), Royal Prince Alfred Hosp, Dept Resp Med, Level 9 Page Chest Pavil,Missenden Rd, Camperdown, NSW 2050, Australia.			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Allergy Clin. Immunol.	SEP	2000	106	3					419	428		10.1067/mai.2000.108914		10	Allergy; Immunology	Allergy; Immunology	356YN	WOS:000089471900002	10984359	
J	Barnes, PJ				Barnes, PJ			Inhaled corticosteroids are not beneficial in chronic obstructive pulmonary disease	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Editorial Material							AIR-FLOW OBSTRUCTION; ASTHMA; COPD; GLUCOCORTICOIDS		Imperial Coll, Natl Heart & Lung Inst, London, England	Barnes, PJ (reprint author), Imperial Coll, Natl Heart & Lung Inst, London, England.						Barnes PJ, 1998, THORAX, V53, P137; Barnes PJ, 1998, AM J RESP CRIT CARE, V157, pS1; Burge PS, 1999, THORAX, V54, P287; Confalonieri M, 1998, THORAX, V53, P583; COX G, 1995, J IMMUNOL, V154, P4719; Culpitt SV, 1999, AM J RESP CRIT CARE, V160, P1635; DOMPELING E, 1992, EUR RESPIR J, V5, P945; Hattotuwa K, 1999, AM J RESP CRIT CARE, V159, pA523; Jeffery PK, 1998, THORAX, V53, P129; Keatings VM, 1997, AM J RESP CRIT CARE, V155, P542; Keatings VM, 1996, AM J RESP CRIT CARE, V153, P530; Kertjens HA, 1992, NEW ENGL J MED, V327, P1413; Meagher LC, 1996, J IMMUNOL, V156, P4422; NIGHTINGALE JA, 1999, IN PRESS AM J RESP C; Paggiaro PL, 1998, LANCET, V351, P773, DOI 10.1016/S0140-6736(97)03471-5; Pauwels RA, 1999, NEW ENGL J MED, V340, P1948, DOI 10.1056/NEJM199906243402503; Vestbo J, 1999, LANCET, V353, P1819, DOI 10.1016/S0140-6736(98)10019-3; WATSON A, 1992, CHEST, V101, P350, DOI 10.1378/chest.101.2.350; WEIR DC, 1993, THORAX, V48, P309, DOI 10.1136/thx.48.4.309	19	110	116	0	2	AMER LUNG ASSOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	FEB	2000	161	2					342	344				3	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	285ED	WOS:000085376000002	10673166	
J	Masuoka, M; Shiraishi, H; Ohta, S; Suzuki, S; Arima, K; Aoki, S; Toda, S; Inagaki, N; Kurihara, Y; Hayashida, S; Takeuchi, S; Koike, K; Ono, J; Noshiro, H; Furue, M; Conway, SJ; Narisawa, Y; Izuhara, K				Masuoka, Miho; Shiraishi, Hiroshi; Ohta, Shoichiro; Suzuki, Shoichi; Arima, Kazuhiko; Aoki, Shigehisa; Toda, Shuji; Inagaki, Naoki; Kurihara, Yuichi; Hayashida, Sayaka; Takeuchi, Satoshi; Koike, Kenta; Ono, Junya; Noshiro, Hirokazu; Furue, Masutaka; Conway, Simon J.; Narisawa, Yutaka; Izuhara, Kenji			Periostin promotes chronic allergic inflammation in response to Th2 cytokines	JOURNAL OF CLINICAL INVESTIGATION			English	Article							THYMIC STROMAL LYMPHOPOIETIN; NF-KAPPA-B; ATOPIC-DERMATITIS; BRONCHIAL-ASTHMA; DENDRITIC CELLS; EXTRACELLULAR-MATRIX; CANCER DEVELOPMENT; EPITHELIAL-CELLS; MITE ALLERGEN; TENASCIN-C	Allergic inflammation triggered by exposure of an allergen frequently leads to the onset of chronic inflammatory diseases such as atopic dermatitis (AD) and bronchial asthma. The mechanisms underlying chronicity in allergic inflammation remain unresolved. Periostin, a recently characterized matricellular protein, interacts with several cell surface integrin molecules, providing signals for tissue development and remodeling. Here we show that periostin is a critical mediator for the amplification and persistence of allergic inflammation using a mouse model of skin inflammation. Th2 cytokines IL-4 and IL-13 stimulated fibroblasts to produce periostin, which interacted with alpha(v) integrin, a functional periostin receptor on keratinocytes, inducing production of proinflammatory cytokines, which consequently accelerated Th2-type immune responses. Accordingly, inhibition of periostin or alpha(v) integrin prevented the development or progression of allergen-induced skin inflammation. Thus, periostin sets up a vicious circle that links Th2-type immune responses to keratinocyte activation and plays a critical role in the amplification and chronicity of allergic skin inflammation.	[Masuoka, Miho; Shiraishi, Hiroshi; Suzuki, Shoichi; Arima, Kazuhiko; Izuhara, Kenji] Saga Med Sch, Dept Biomol Sci, Div Med Biochem, Saga 8498501, Japan; [Ohta, Shoichiro; Izuhara, Kenji] Saga Med Sch, Dept Lab Med, Saga 8498501, Japan; [Aoki, Shigehisa; Toda, Shuji] Saga Med Sch, Dept Pathol & Biodef, Saga 8498501, Japan; [Inagaki, Naoki] Gifu Pharmaceut Univ, Dept Pharmacol, Gifu, Japan; [Kurihara, Yuichi; Hayashida, Sayaka; Takeuchi, Satoshi; Furue, Masutaka] Kyushu Univ, Dept Dermatol, Fukuoka 812, Japan; [Koike, Kenta; Noshiro, Hirokazu] Saga Med Sch, Dept Surg, Saga 8498501, Japan; [Ono, Junya] Shino Test Corp, Sagamihara, Kanagawa, Japan; [Conway, Simon J.] Indiana Univ Sch Med, Dev Biol & Neonatal Med Program, HB Wells Ctr Pediat Res, Indianapolis, IN USA; [Narisawa, Yutaka] Saga Med Sch, Dept Internal Med, Div Dermatol, Saga 8498501, Japan	Izuhara, K (reprint author), Saga Med Sch, Dept Biomol Sci, Div Med Biochem, 5-1-1 Nabeshima, Saga 8498501, Japan.	kizuhara@cc.saga-u.ac.jp	Arima, Kazuhiko/I-8962-2014	Arima, Kazuhiko/0000-0002-0607-8787	Japan Society for the Promotion of Science	We thank Koichi Akashi, Doyle R. Wylie, Hiroyuki Ideguchi, and Yumiko Ohishi for critical review of this manuscript and technical assistance. This work was supported in part by Grants-in-Aid for Scientific Research from the Japan Society for the Promotion of Science.	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Clin. Invest.	JUL	2012	122	7					2590	2600		10.1172/JCI58978		11	Medicine, Research & Experimental	Research & Experimental Medicine	969GV	WOS:000306044600030	22684102	
J	D'Amato, G; Cecchi, L				D'Amato, G.; Cecchi, L.			Effects of climate change on environmental factors in respiratory allergic diseases	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review							RAGWEED AMBROSIA-ARTEMISIIFOLIA; PARTICULATE AIR-POLLUTION; PLACEBO-CONTROLLED TRIAL; GRASS-POLLEN; DIESEL EXHAUST; HAY-FEVER; CHILDHOOD ASTHMA; OZONE EXPOSURE; COMMON RAGWEED; PUBLIC-HEALTH	A body of evidence suggests that major changes involving the atmosphere and the climate, including global warming induced by human activity, have an impact on the biosphere and the human environment. Studies on the effects of climate change on respiratory allergy are still lacking and current knowledge is provided by epidemiological and experimental studies on the relationship between asthma and environmental factors, such as meteorological variables, airborne allergens and air pollution. However, there is also considerable evidence that subjects affected by asthma are at an increased risk of developing obstructive airway exacerbations with exposure to gaseous and particulate components of air pollution. It is not easy to evaluate the impact of climate change and air pollution on the prevalence of asthma in general and on the timing of asthma exacerbations. However, the global rise in asthma prevalence and severity suggests that air pollution and climate changes could be contributing. Pollen allergy is frequently used to study the interrelationship between air pollution, rhinitis and bronchial asthma. Epidemiological studies have demonstrated that urbanization, high levels of vehicle emissions and westernized lifestyle are correlated to an increase in the frequency of pollen-induced respiratory allergy, prevalent in people who live in urban areas compared with those who live in rural areas. Meteorological factors (temperature, wind speed, humidity, etc.) along with their climatological regimes (warm or cold anomalies and dry or wet periods, etc.), can affect both biological and chemical components of this interaction. In addition, by inducing airway inflammation, air pollution overcomes the mucosal barrier priming allergen-induced responses. In conclusion, climate change might induce negative effects on respiratory allergic diseases. In particular, the increased length and severity of the pollen season, the higher occurrence of heavy precipitation events and the increasing frequency of urban air pollution episodes suggest that environmental risk factors will have a stronger effect in the following decades.	[D'Amato, G.] High Special Hosp A Cardarelli, Dept Chest Dis, Div Resp & Allerg Dis, Naples, Italy; [Cecchi, L.] Univ Florence, Interdepartmental Ctr Bioclimatol, Florence, Italy; [Cecchi, L.] Allergy Clin, Florence, Italy	D'Amato, G (reprint author), High Special Hosp A Cardarelli, Dept Chest Dis, Div Resp & Allerg Dis, Naples, Italy.	gdamato@qubisoft.it	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Ahas R, 2002, INT J CLIMATOL, V22, P1727, DOI 10.1002/joc.818; Ahlholm JU, 1998, CLIN EXP ALLERGY, V28, P1384; Allam MF, 2004, COCHRANE DB SYST REV, DOI DOI 10.1002/14651858.CD003538.pub2; Annesi-Maesano I, 2007, EUR RESPIR J, V29, P428, DOI 10.1183/09031936.00129506; Annesi-Maesano I, 2007, RESP MED, V101, P1721, DOI 10.1016/j.rmed.2007.02.022; Asher MI, 2006, LANCET, V368, P733, DOI 10.1016/S0140-6736(06)69283-0; Atkinson RW, 2004, THORAX, V59, P277, DOI 10.1136/thx.2003.019133; BALMES JR, 1993, ENVIRON HEALTH PERSP, V101, P219, DOI 10.2307/3431683; Bayram H, 2001, J ALLERGY CLIN IMMUN, V107, P287, DOI 10.1067/mai.2001.111141; 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Exp. Allergy	AUG	2008	38	8					1264	1274		10.1111/j.1365-2222.2008.03033.x		11	Allergy; Immunology	Allergy; Immunology	328DQ	WOS:000257778300005	18537982	
J	Riedl, MA; Nel, AE				Riedl, Marc A.; Nel, Andre E.			Importance of oxidative stress in the pathogenesis and treatment of asthma	CURRENT OPINION IN ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						air pollution; antioxidants; asthma; genetic polymorphisms; oxidative stress	DIESEL EXHAUST PARTICLES; PLACEBO-CONTROLLED TRIAL; AIRWAY EPITHELIAL-CELLS; GENE POLYMORPHISMS; ALLERGIC RESPONSES; RESPIRATORY HEALTH; N-ACETYLCYSTEINE; NASAL CHALLENGE; RISK-FACTORS; VITAMIN-C	Purpose of review The purpose of the current review is to summarize recent evidence demonstrating the important role of oxidative stress in asthma pathogenesis. The therapeutic implications of these findings will be presented. Recent findings Mechanistically, the effect of oxidative stress on dendritic cells has been demonstrated to have a potent effect on Th1/Th2 skewing of the immune response. Investigations of gene-environment interactions have identified genetic polymorphisms associated with individual susceptibility to poll utant-ind uced respiratory oxidative stress. The effects of current asthma therapy on oxidative stress are currently unclear, but previous trials using conventional antioxidant therapy in asthma have been largely ineffective. Recent investigations have identified two promising broad-based therapeutic approaches: Nrf2 pathway activation and the use of thiol precursors. Preliminary data suggest that fullerene nanomaterials and dietary interventions may also have potential benefits in asthma. Summary Our current understanding of the role of oxidative stress in asthma suggests that antioxidant therapy may be important in optimizing asthma treatment and prevention. The future success of antioxidant asthma therapy will require strategies with broad effects on airway redox equilibrium and the selection of appropriate target populations.	[Riedl, Marc A.] Univ Calif Los Angeles, David Geffen Sch Med, Allergy & Clin Immunol Sect, Div Pulm & Crit Care Med, Los Angeles, CA 90095 USA; [Nel, Andre E.] Univ Calif Los Angeles, David Geffen Sch Med, Div Nanomed, Asthma & Allergy Dis Clin Res Ctr, Los Angeles, CA 90095 USA	Riedl, MA (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Allergy & Clin Immunol Sect, Div Pulm & Crit Care Med, 10833 Le Conte Ave 37-131 CHS, Los Angeles, CA 90095 USA.	mriedl@mednet.ucla.edu	Nel, Andre/J-2808-2012		NIAID NIH HHS [U19 AI070453-01]; PHS HHS [K12 R011 7611]		Allam MF, 2004, COCHRANE DB SYST REV, V2004; Alzoghaibi MA, 2007, RESPIROLOGY, V12, P439, DOI 10.1111/j.1440-1843.2007.01034.x; Blesa S, 2003, EUR RESPIR J, V21, P394, DOI 10.1183/09031936.03.00039602; Bowler RP, 2002, J ALLERGY CLIN IMMUN, V110, P349, DOI 10.1067/mai.2002.126780; Burns JS, 2007, CHEST, V132, P238, DOI 10.1378/chest.07-0038; Chan RCF, 2006, J ALLERGY CLIN IMMUN, V118, P455, DOI 10.1016/j.jaci.2006.06.006; Comhair SAA, 2001, FASEB J, V15, P70, DOI 10.1096/fj.00-0085com; Diaz-Sanchez D, 1999, CLIN IMMUNOL, V90, P313, DOI 10.1006/clim.1998.4676; Diaz-Sanchez D, 1999, J ALLERGY CLIN IMMUN, V104, P1183; Fogarty A, 2006, RESP MED, V100, P174, DOI 10.1016/j.rmed.2005.03.038; Fogarty A, 2003, CLIN EXP ALLERGY, V33, P1355, DOI 10.1046/j.1365-2222.2003.01777.x; Fryer AA, 2000, AM J RESP CRIT CARE, V161, P1437; Fujieda S, 1998, AM J RESP CELL MOL, V19, P507; Garcia V, 2005, EUR RESPIR J, V26, P449, DOI 10.1183/09031936.05.00142104; Garte S, 2001, CANCER EPIDEM BIOMAR, V10, P1239; Gilliland FD, 2004, LANCET, V363, P119, DOI 10.1016/S0140-6736(03)15262-2; Gilliland FD, 2006, AM J RESP CRIT CARE, V174, P1335, DOI 10.1164/rccm.200509-1424OC; Gilmour M, 2006, ENVIRON HEALTH PERSP, V114, P627, DOI 10.1289/ehp.8380; Haque R, 2007, TOXICOL APPL PHARM, V220, P72, DOI 10.1016/j.taap.2006.12.017; He FJ, 2006, LANCET, V367, P320, DOI 10.1016/S0140-6736(06)68069-0; Hiura TS, 1999, J IMMUNOL, V163, P5582; Horwitz LD, 2003, CARDIOVASC DRUG REV, V21, P77; Ivaschenko TE, 2002, J MOL MED-JMM, V80, P39, DOI 10.1007/s001090100274; Johnson IT, 2007, P NUTR SOC, V66, P207, DOI 10.1017/S0029665107005459; Kamada F, 2007, INT ARCH ALLERGY IMM, V144, P275, DOI 10.1159/000106316; Kim HJ, 2007, J ALLERGY CLIN IMMUN, V119, P1225, DOI 10.1016/j.jaci.2007.01.016; Kobayashi T, 2000, AM J RESP CRIT CARE, V162, P352; Li N, 2006, ANTIOXID REDOX SIGN, V8, P88, DOI 10.1089/ars.2006.8.88; Li N, 2003, CLIN IMMUNOL, V109, P250, DOI 10.1016/j.clim.2003.08.006; London Stephanie J, 2007, Proc Am Thorac Soc, V4, P217, DOI 10.1513/pats.200701-031AW; Martinez-Losa M, 2007, CLIN EXP ALLERGY, V37, P714, DOI 10.1111/j.1365-2222.2007.02694.x; Marwick JA, 2004, AM J RESP CELL MOL, V31, P633, DOI 10.1165/rcmb.2004-0006OC; Muijsers RBR, 2001, BRIT J PHARMACOL, V134, P434, DOI 10.1038/sj.bjp.0704235; Nel A, 2005, SCIENCE, V308, P804, DOI 10.1126/science.1108752; Nel A, 2006, SCIENCE, V311, P622, DOI 10.1126/science.1114397; Ochs-Balcom HM, 2006, EUR J CLIN NUTR, V60, P991, DOI 10.1038/sj.ejcn.1602410; Pearson PJK, 2004, THORAX, V59, P652, DOI 10.1136/thx.2004.022616; Pereira B, 1995, BIOCHEM PHARMACOL, V50, P2093, DOI 10.1016/0006-2952(95)02116-7; Persinger RL, 2002, MOL CELL BIOCHEM, V234, P71, DOI 10.1023/A:1015973530559; Peterson JD, 1998, P NATL ACAD SCI USA, V95, P3071, DOI 10.1073/pnas.95.6.3071; Ram FS, 2004, COCHRANE DB SYST REV; Rangasamy T, 2005, J EXP MED, V202, P47, DOI 10.1084/jem.20050538; Reynaert NL, 2007, J IMMUNOL, V178, P3814; Riedl M, 2005, J ALLERGY CLIN IMMUN, V115, P221, DOI 10.1016/j.jaci.2004.11.047; Ritz SA, 2007, AM J PHYSIOL-LUNG C, V292, pL33, DOI 10.1152/ajplung.00170.2006; Romieu I, 2006, EUR RESPIR J, V28, P953, DOI 10.1183/09031936.06.00114905; Ryan JJ, 2007, J IMMUNOL, V179, P665; Sadowska AM, 2007, STEROIDS, V72, P1, DOI 10.1016/j.steroids.2006.10.007; Sekiguchi Naoya, 2006, Mod Rheumatol, V16, P85; Shaheen SO, 2007, THORAX, V62, P483, DOI 10.1136/thx.2006.071563; Steerenberg PA, 1999, INHAL TOXICOL, V11, P1109; Tamer L, 2004, RESPIROLOGY, V9, P493, DOI 10.1111/j.1440-1843.2004.00657.x; Voutilainen S, 2006, AM J CLIN NUTR, V83, P1265; Wan JX, 2006, J IMMUNOL, V177, P3477; Wang JR, 2006, FREE RADICAL BIO MED, V40, P1914, DOI 10.1016/j.freeradbiomed.2006.01.017; Wells SM, 2007, AM J RESP CELL MOL, V36, P520, DOI 10.1165/rcmb.2006-0302SM; Whitekus MJ, 2002, J IMMUNOL, V168, P2560; WIELANDT AM, 2006, BIOCHEM PHARMACOL, V14, P455; Willett WC, 2006, PUBLIC HEALTH NUTR, V9, P105, DOI 10.1079/PHN2005931	59	109	114	1	12	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	1528-4050			CURR OPIN ALLERGY CL	Curr. Opin. Allergy Clin. Immunol.	FEB	2008	8	1					49	56				8	Allergy; Immunology	Allergy; Immunology	254JN	WOS:000252583000009	18188018	
J	Huurre, A; Kalliomaki, M; Rautava, S; Rinne, M; Salminen, S; Isolauri, E				Huurre, Anu; Kalliomaki, Marko; Rautava, Samuli; Rinne, Minna; Salminen, Seppo; Isolauri, Erika			Mode of delivery - Effects on gut microbiota and humoral immunity	NEONATOLOGY			English	Article						caesarean section; vaginal delivery; gut microbiota; humoral immunity	IN-SITU HYBRIDIZATION; ATOPIC-DERMATITIS; BLOOD-LYMPHOCYTES; CHILDREN; INFANTS; BACTERIA; ALLERGY; PROBES; IDENTIFICATION; MICROFLORA	Background: The rate of caesarean deliveries has increased 10-fold worldwide during the past decades. Objective: To evaluate differences in the establishment of gut microbiota in infants born by vaginal or caesarean delivery and its impact on mucosal immunity. Methods: Altogether, 165 consecutive children, prospectively followed from birth at our clinic in Turku, Finland, were gathered; 141 (85%) were born by vaginal delivery and 24 (15%) by caesarean section. Blood was drawn at physician visits for indirect evaluation of mucosal immunity by ELISPOT assay. Faecal samples were obtained for determination of the gut microbiota by fluorescence in situ hybridization of bacterial cells. Results: Infants delivered by caesarean section harboured fewer bifidobacteria at an early age and were shown to mount a stronger humoral immune response. At 1 month of age, the total gut bacterial cell counts per 1 g faeces were higher in vaginally delivered infants (9.9 x 10(9), 95% CI 7.9 x 10(9)-1.2 x 10(10)) as compared to caesarean section delivered (3.1 x 10(9), 95% CI 1.1 x 10(9)-8.6 x 10(9)) (p = 0.001). This distinction was mainly due to the greater number of bifidobacteria in vaginally delivered infants (1.9 x 10(9), 95% CI 6.3 x 10(8)-5.6 x 10(9) vs. 1.5 x 10(6), 95% CI 4.1 x 10(2)-5.7 x 10(9), respectively) (p = 0.001). During the first year of life, the total number of IgA-, IgG- and IgM-secreting cells was lower (p = 0.03, p = 0.02, p = 0.11, respectively) in infants born by vaginal delivery than in those born by caesarean section, possibly reflecting excessive antigen exposure across the vulnerable gut barrier. Conclusions: Our findings demonstrate that the mode of delivery may have, possibly via gut microbiota development, significant effects on immunological functions in the infant (http://www.clinicaltrials.gov/ct/gui/show/NCT00167700). Copyright (C) 2007 S. Karger AG, Basel.	[Huurre, Anu; Kalliomaki, Marko; Rautava, Samuli; Rinne, Minna; Isolauri, Erika] Univ Turku, Dept Pediat, Turku Univ Cent Hosp, FI-20520 Turku, Finland; [Salminen, Seppo] Univ Turku, Funct Foods Forum, FI-20520 Turku, Finland	Huurre, A (reprint author), Univ Turku, Dept Pediat, Turku Univ Cent Hosp, Kiinanmyllynkatu 4-8, FI-20520 Turku, Finland.	anu.huurre@utu.fi					Edwards CA, 2002, BRIT J NUTR, V88, pS11, DOI [10.1079/BJNBJN2002580, 10.1079/BJN2002625]; Favier CF, 2002, APPL ENVIRON MICROB, V68, P219, DOI 10.1128/AEM.68.1.219-226.2002; FORREST BD, 1988, LANCET, V1, P81; Guarner F, 2003, LANCET, V361, P512, DOI 10.1016/S0140-6736(03)12489-0; HANIFIN JM, 1991, PEDIATR CLIN N AM, V38, P763; Harmsen Hermie J.M., 1999, Microbial Ecology in Health and Disease, V11, P3, DOI 10.1080/089106099435862; Harmsen HJM, 2000, FEMS MICROBIOL LETT, V183, P125, DOI 10.1016/S0378-1097(99)00649-7; Hart AL, 2004, GUT, V53, P1602, DOI 10.1136/gut.2003.037325; Isolauri E, 2005, GASTROENTEROL CLIN N, V34, P437, DOI 10.1016/j.gtc.2005.05.010; ISOLAURI E, 1990, PEDIATR RES, V28, P582, DOI 10.1203/00006450-199012000-00006; Isolauri E, 1996, J ALLERGY CLIN IMMUN, V97, P9, DOI 10.1016/S0091-6749(96)70277-4; Isolauri E, 2002, CURR OPIN ALLERGY CL, V2, P263, DOI 10.1097/00130832-200206000-00018; Johansson SGO, 2004, J ALLERGY CLIN IMMUN, V113, P832, DOI 10.1016/j.jaci.2003.12.591; Kirjavainen PV, 2002, GUT, V51, P51, DOI 10.1136/gut.51.1.51; Kraehenbuhl JP, 2004, SCIENCE, V303, P1624, DOI 10.1126/science.1096222; LANGENDIJK PS, 1995, APPL ENVIRON MICROB, V61, P3069; Li Y, 2005, J DENT RES, V84, P806; Manz W, 1996, MICROBIOL-UK, V142, P1097; Rakoff-Nahoum S, 2004, CELL, V118, P229, DOI 10.1016/j.cell.2004.07.002; Rigby RJ, 2005, CLIN EXP IMMUNOL, V139, P245, DOI 10.1111/j.1365-2249.2004.02674.x; Salminen S, 2004, GUT, V53, P1388, DOI 10.1136/gut.2004.041640; Tulic MK, 2004, LANCET, V363, P1689, DOI 10.1016/S0140-6736(04)16253-3	22	109	119	5	35	KARGER	BASEL	ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND	1661-7800			NEONATOLOGY	Neonatology		2008	93	4					236	240		10.1159/000111102		5	Pediatrics	Pediatrics	311AS	WOS:000256572900005	18025796	
J	Kim, YK; Oh, SY; Jeon, SG; Park, HW; Lee, SY; Chun, EY; Bang, B; Lee, HS; Oh, MH; Kim, YS; Kim, JH; Gho, YS; Cho, SH; Min, KU; Kim, YY; Zhu, Z				Kim, Yoon-Keun; Oh, Sun-Young; Jeon, Seong Gyu; Park, Heung-Woo; Lee, Soo-Yeon; Chun, Eun-Young; Bang, Boram; Lee, Hyun-Seung; Oh, Min-Hee; Kim, You-Sun; Kim, Jong-Hoon; Gho, Yong Song; Cho, Sang-Heon; Min, Kyung-Up; Kim, You-Young; Zhu, Zhou			Airway exposure levels of lipopolysaccharide determine type 1 versus type 2 experimental asthma	JOURNAL OF IMMUNOLOGY			English	Article							HOUSE-DUST ENDOTOXIN; T-CELL DEVELOPMENT; INTERFERON-GAMMA; DENDRITIC CELLS; ALLERGIC-ASTHMA; RESPONSES; MICE; HYPERRESPONSIVENESS; INFLAMMATION; ANTIGEN	Allergic asthma is characterized by airway inflammation initiated by adaptive immune responses to aeroallergens. Recent data suggest that severe asthma may be a different form of asthma rather than an increase in asthma symptoms and that innate immune responses to LPS can modulate adaptive immune responses to allergens. In this study, we evaluated the hypothesis that airway exposure to different doses of LPS induces different form of asthma. Our study showed that neutrophilic inflammation and IFN-gamma expression were higher in induced sputum from severe asthma patients than from mild to moderate asthmatics. Animal experiments indicated that allergen sensitization with low-dose LPS (0.1 mu g) induced type 2 asthma phenotypes, i.e., airway hyper-responsiveness, eosinophilic inflammation, and allergen-specific IgE up-regulation. In contrast, allergen sensitization with high-dose LPS (10 mu g) induced asthma phenotypes, i.e., airway hyperresponsiveness and noneosinophilic inflammation that were not developed in IFN-gamma-deficient mice, but unaffected in the absence of IL-4. During the allergen sensitization period, TNF-alpha expression was found to be enhanced by both low- and high-dose LPS, whereas IL-12 expression was only enhanced by high-dose LPS. Interestingly, the asthma phenotypes induced by low-dose LPS, but not by high-dose LPS, were completely inhibited in TNF-a receptor-deficient mice, whereas the asthma phenotypes induced by high-dose LPS were abolished in the homozygous null mutation of the STAT4 gene. These findings suggest that airway exposure levels of LPS induces different forms of asthma that are type 1 and type 2 asthma phenotypes by high and low LPS levels, respectively.	Johns Hopkins Univ, Div Clin Immunol & Allergy, Asthma & Allergy Ctr, Baltimore, MD 21224 USA; Pohang Univ Sci & Technol, Postech Biotech Ctr, Dept Life Sci, Pohang, South Korea; Seoul Natl Univ, Coll Med, Dept Internal Med, Inst Allergy & Clin Immunol, Seoul 151, South Korea; Korea Univ, Coll Life Sci & Biotechnol, Div Biotechnol, Seoul 136701, South Korea	Zhu, Z (reprint author), Johns Hopkins Univ, Div Clin Immunol & Allergy, Asthma & Allergy Ctr, 5501 Hopkins Bayview Circle-1A-2, Baltimore, MD 21224 USA.	juinea@postech.ac.kr; zzhu@jhmi.edu	Min, Kyung-Up/J-5468-2012; Cho, Sang Heon/J-2793-2012; Kim, Jong-Hoon/F-2504-2013; Kim, Jong-Hoon/H-1476-2015		NHLBI NIH HHS [R01 HL079349]		Akbari O, 2002, NAT MED, V8, P1024, DOI 10.1038/nm745; Ashwell JD, 2000, ANNU REV IMMUNOL, V18, P309, DOI 10.1146/annurev.immunol.18.1.309; BOCHNER BS, 1994, ANNU REV IMMUNOL, V12, P295; Bousquet J, 2000, CLIN EXP ALLERGY, V30, P2; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Bryan SA, 2000, LANCET, V356, P2149, DOI 10.1016/S0140-6736(00)03497-8; Cho SH, 2005, AM J RESP CRIT CARE, V171, P224, DOI 10.1164/rccm.200310-1416OC; CORRIGAN CJ, 1991, INT ARCH ALLER A IMM, V94, P270; CUTZ E, 1978, HISTOPATHOLOGY, V2, P407, DOI 10.1111/j.1365-2559.1978.tb01735.x; Dahl ME, 2004, NAT IMMUNOL, V5, P337, DOI 10.1038/ni1041; DENT LA, 1990, J EXP MED, V172, P1425, DOI 10.1084/jem.172.5.1425; Eisenbarth SC, 2002, J EXP MED, V196, P1645, DOI 10.1084/jem.20021340; GAVETT SH, 1995, J EXP MED, V182, P1527, DOI 10.1084/jem.182.5.1527; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Gern JE, 2004, PEDIATR INFECT DIS J, V23, pS78, DOI 10.1097/01.inf.0000108196.46134.a6; Grunig G, 1998, SCIENCE, V282, P2261, DOI 10.1126/science.282.5397.2261; Hessel EM, 1997, AM J RESP CELL MOL, V16, P325; HOGG JC, 1999, AM J RESP CRIT CARE, V160, P26; IWAMOTO I, 1993, J EXP MED, V177, P573, DOI 10.1084/jem.177.2.573; Kim YK, 1999, J ALLERGY CLIN IMMUN, V104, P311, DOI 10.1016/S0091-6749(99)70372-6; Kuipers H, 2003, J IMMUNOL, V171, P3645; Lack G, 1996, J IMMUNOL, V157, P1432; Leckie MJ, 2000, LANCET, V356, P2144, DOI 10.1016/S0140-6736(00)03496-6; Lee CG, 2004, NAT MED, V10, P1095, DOI 10.1038/nm1105; Lee CG, 2001, J EXP MED, V194, P809, DOI 10.1084/jem.194.6.809; Louis R, 2000, AM J RESP CRIT CARE, V161, P9; Magnan AO, 2000, AM J RESP CRIT CARE, V161, P1790; Magram J, 1996, IMMUNITY, V4, P471, DOI 10.1016/S1074-7613(00)80413-6; MICHEL O, 1991, CLIN EXP ALLERGY, V21, P441, DOI 10.1111/j.1365-2222.1991.tb01684.x; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; MOSMANN TR, 1986, J IMMUNOL, V136, P2348; MOSMANN TR, 1989, ANNU REV IMMUNOL, V7, P145, DOI 10.1146/annurev.immunol.7.1.145; Neurath MF, 2002, NAT MED, V8, P567, DOI 10.1038/nm0602-567; Olenchock S A, 1987, Prog Clin Biol Res, V231, P475; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Rankin JA, 1996, P NATL ACAD SCI USA, V93, P7821, DOI 10.1073/pnas.93.15.7821; SAVELKOUL HFJ, 1991, J IMMUNOL, V146, P1801; SIRAGANIAN RP, 1979, J ALLERGY CLIN IMMUN, V64, P526, DOI 10.1016/0091-6749(79)90063-0; Szabo SJ, 2003, ANNU REV IMMUNOL, V21, P713, DOI 10.1146/annurev.immunol.21.120601.140942; Vrugt B, 1999, EUR RESPIR J, V13, P1245, DOI 10.1183/09031936.99.13612539; Wang ZD, 2000, J EXP MED, V192, P1587, DOI 10.1084/jem.192.11.1587; Wenzel SE, 1999, AM J RESP CRIT CARE, V160, P1001; Wills-Karp M, 1999, ANNU REV IMMUNOL, V17, P255, DOI 10.1146/annurev.immunol.17.1.255; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; Zhu Zhou, 1999, Journal of Clinical Investigation, V103, P779, DOI 10.1172/JCI5909	45	109	121	0	10	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	APR 15	2007	178	8					5375	5382				8	Immunology	Immunology	155VA	WOS:000245605300083	17404323	
J	Pattenden, S; Antova, T; Neuberger, M; Nikiforov, B; De Sario, M; Grize, L; Heinrich, J; Hruba, F; Janssen, N; Luttmann-Gibson, H; Privalova, L; Rudnai, P; Splichalova, A; Zlotkowska, R; Fletcher, T				Pattenden, Sam; Antova, Temenuga; Neuberger, Manfred; Nikiforov, Bojidar; De Sario, Manuela; Grize, Leticia; Heinrich, Joachim; Hruba, Frantiska; Janssen, Nicole; Luttmann-Gibson, Heike; Privalova, Larissa; Rudnai, Peter; Splichalova, Anna; Zlotkowska, Renata; Fletcher, Tony			Parental smoking and children's respiratory health: independent effects of prenatal and postnatal exposure	TOBACCO CONTROL			English	Article							ENVIRONMENTAL TOBACCO-SMOKE; MATERNAL SMOKING; LUNG-FUNCTION; CHILDHOOD ASTHMA; PASSIVE SMOKING; AIR-POLLUTION; BIRTH-WEIGHT; IN-UTERO; SYMPTOMS; PREGNANCY	Objectives: Adverse effects have been reported of prenatal and/or postnatal passive exposure to smoking on children's health. Uncertainties remain about the relative importance of smoking at different periods in the child's life. We investigate this in a pooled analysis, on 53 879 children from 12 cross-sectional studies-components of the PATY study (Pollution And The Young). Methods: Effects were estimated, within each study, of three exposures: mother smoked during pregnancy, parental smoking in the first two years, current parental smoking. Outcomes were: wheeze, asthma, "woken by wheeze'', bronchitis, nocturnal cough, morning cough, "sensitivity to inhaled allergens'' and hay fever. Logistic regressions were used, controlling for individual risk factors and study area. Heterogeneity between study-specific results, and mean effects (allowing for heterogeneity) were estimated using meta-analytical tools. Results: There was strong evidence linking parental smoking to wheeze, asthma, bronchitis and nocturnal cough, with mean odds ratios all around 1.15, with independent effects of prenatal and postnatal exposures for most associations. Conclusions: Adverse effects of both pre- and postnatal parental smoking on children's respiratory health were confirmed. Asthma was most strongly associated with maternal smoking during pregnancy, but postnatal exposure showed independent associations with a range of other respiratory symptoms. All tobacco smoke exposure has serious consequences for children's respiratory health and needs to be reduced urgently.	Univ Vienna, Inst Environm Hlth, Ctr Publ Hlth, A-1095 Vienna, Austria; London Sch Hyg & Trop Med, London WC1, England; Hlth Author Rome, Dept Epidemiol, Rome, Italy; Univ Basel, Inst Social & Prevent Med, Basel, Switzerland; Natl Res Ctr Environm & Hlth, Inst Epidemiol, Neuherberg, Germany; Inst Publ Hlth, Dept Hlth Informat & Stat, Banska Bystrica, Slovakia; Univ Utrecht, Inst Risk Assessment Sci, Utrecht, Netherlands; Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA; Natl Publ Hlth Ctr, Natl Inst Environm Hlth, Budapest, Hungary; Inst Publ Hlth Ostrava, Ctr Occupat Med, Ostrava, Czech Republic; Inst Occupat Med & Environm Hlth, Dept Epidemiol, Sosnowiec, Poland	Neuberger, M (reprint author), Univ Vienna, Inst Environm Hlth, Ctr Publ Hlth, Kinderspitalgasse 15, A-1095 Vienna, Austria.	manfred.neuberger@meduniwien.ac.at	De sario, Manuela/K-1932-2016	De sario, Manuela/0000-0002-1117-2735; Neuberger, Manfred/0000-0002-8994-378X			Agabiti N, 1999, EPIDEMIOLOGY, V10, P692, DOI 10.1097/00001648-199911000-00008; Alati R, 2006, EPIDEMIOLOGY, V17, P138, DOI 10.1097/01.ede.0000198148.02347.33; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Butland BK, 1997, BRIT MED J, V315, P717; *CAL ENV PROG AG, 2004, PROP ID ENV TOB SMOK; Cook DG, 1999, THORAX, V54, P357; Cunningham J, 1996, AM J RESP CRIT CARE, V153, P218; Dales RE, 1997, EUR J EPIDEMIOL, V13, P541, DOI 10.1023/A:1007311912777; DELLORCO V, 1995, AM J EPIDEMIOL, V142, P419; Dempsey DA, 2001, DRUG SAFETY, V24, P277, DOI 10.2165/00002018-200124040-00005; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; Dockery DW, 1996, ENVIRON HEALTH PERSP, V104, P500, DOI 10.2307/3432990; Ehrlich RI, 1996, AM J RESP CRIT CARE, V154, P681; Gehring U, 2006, EUR RESPIR J, V27, P95, DOI 10.1183/09031936.06.00017205; Gilliland FD, 2001, AM J RESP CRIT CARE, V163, P429; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; Hajnal BL, 1999, SCHWEIZ MED WSCHR, V129, P723; Heinrich J, 1999, ENVIRON HEALTH PERSP, V107, P53, DOI 10.2307/3434289; Hu FB, 1997, ANN ALLERG ASTHMA IM, V79, P80; *INT AG RES CANC, 2002, TOB SMOK INV SMOK SU, V83; Jaakkola JJK, 2006, RESP RES, V7, DOI 10.1186/1465-9921-7-48; Janssen NAH, 2003, ENVIRON HEALTH PERSP, V111, P1512, DOI 10.1289/ehp.6243; Jedrychowski W, 1997, ENVIRON HEALTH PERSP, V105, P302, DOI 10.1289/ehp.97105302; Kharrazi M, 2004, EPIDEMIOLOGY, V15, P660, DOI 10.1097/01.ede.0000142137.39619.60; Lam TH, 1998, INT J EPIDEMIOL, V27, P41, DOI 10.1093/ije/27.1.41; Leonardi GS, 2002, EUR RESPIR J, V20, P890, DOI 10.1183/09031936.02.00260802; Misra DP, 1999, ENVIRON HEALTH PERSP, V107, P897, DOI 10.2307/3434572; Moshammer H, 2006, AM J RESP CRIT CARE, V173, P1255, DOI 10.1164/rccm.200510-1552OC; Neuberger M, 2002, ATMOS ENVIRON, V36, P1733, DOI 10.1016/S1352-2310(02)00179-6; NORMAN E, 1994, ALLERGY, V49, P808; Olesen AB, 1997, BRIT MED J, V314, P1003; Ronmark E, 1998, RESP MED, V92, P316, DOI 10.1016/S0954-6111(98)90115-9; Rudnai P., 2004, Egeszsegtudomany, V48, P173; Selcuk ZT, 1997, CLIN EXP ALLERGY, V27, P262, DOI 10.1111/j.1365-2222.1997.tb00704.x; SIERSTED HC, 2000, EUR RES REV, V10, P411; Skorge TD, 2005, AM J RESP CRIT CARE, V172, P61, DOI 10.1164/rccm.200409-1158OC; Spengler JD, 2004, AM J PUBLIC HEALTH, V94, P657, DOI 10.2105/AJPH.94.4.657; Stocks J, 2003, RESPIROLOGY, V8, P266, DOI 10.1046/j.1440-1843.2003.00478.x; Strachan DP, 1998, THORAX, V53, P204; U. S. Environmental Protection Agency, 1992, RESP HLTH EFF PASS S	40	109	116	0	5	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0964-4563			TOB CONTROL	Tob. Control	AUG	2006	15	4							294	10.1136/tc.2005.015065		8	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	069PA	WOS:000239459500012	16885578	
J	Blumer, N; Herz, U; Wegmann, M; Renz, H				Blumer, N; Herz, U; Wegmann, M; Renz, H			Prenatal lipopolysaccharide-exposure prevents allergic sensitization and airway inflammation, but not airway responsiveness in a murine model of experimental asthma	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						airway inflammation; allergy; immune response; lipopolysaccharide; materno-fetal interaction; mice; Th1/Th-2	HAY-FEVER; ATOPIC DISEASE; HOUSE-DUST; T-CELLS; ENDOTOXIN; CHILDREN; HYPERRESPONSIVENESS; HYPERREACTIVITY; PREVALENCE; ANTIBODIES	Background Epidemiological evidence underlines the impact of prenatal environmental factors on the development of postnatal allergies. In this regard an inverse correlation between lipopolysaccharide (LPS) exposure and development of childhood allergy has been found. Objective To assess the impact of prenatal LPS exposure on the development of postnatal respiratory allergies in a mouse model of experimental asthma. Methods Female BALB/c mice were exposed to LPS before conception and during pregnancy. Several weeks after birth offspring were sensitized to ovalbumin (OVA) followed by aerosol allergen challenges. Results Prenatal, maternal LPS-exposure enhanced neonatal IFN-gamma, but not IL-4 and IL-2 production. OVA sensitization of prenatally LPS-exposed mice was accompanied by a marked suppression in anti-OVA IgG1 and IgE as well as unchanged IgG2a antibody responses, paralleled by a significant reduction in IL-5 and IL-13 levels following mitogenic stimulation of splenic leucocytes. Assessment of bronchoalveolar lavage fluids following allergen challenges revealed a marked reduction in eosinophils and macrophages in these mice. Surprisingly, development of airway hyper-responsiveness, a hallmark of bronchial asthma, was not affected. Conclusion This study provides first experimental evidence that LPS may already operate in prenatal life in order to modulate the development of allergies in the offspring.	Hosp Philipps Univ Marburg, Dept Clin Chem & Mol Diagnost, Marburg, Germany	Renz, H (reprint author), Univ Marburg, Dept Clin Chem & Mol Diagnost, Baldinger Str, D-35033 Marburg, Germany.	renzh@med.uni-marburg.de					Alves-Rosa F, 2002, CLIN EXP IMMUNOL, V128, P221, DOI 10.1046/j.1365-2249.2002.01828.x; Bottcher MF, 2003, CLIN EXP ALLERGY, V33, P295, DOI 10.1046/j.1365-2222.2003.01562.x; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; BURD RS, 1993, ANN SURG, V218, P250, DOI 10.1097/00000658-199309000-00004; Eisenbarth SC, 2002, J EXP MED, V196, P1645, DOI 10.1084/jem.20021340; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Gereda JE, 2000, JAMA-J AM MED ASSOC, V284, P1652, DOI 10.1001/jama.284.13.1652; Gerhold K, 2002, J ALLERGY CLIN IMMUN, V110, P110, DOI 10.1067/mai.2002.125831; Glaab T, 2001, AM J PHYSIOL-LUNG C, V280, pL565; Hamada K, 2003, J IMMUNOL, V170, P1683; Herz U, 2000, EUR J IMMUNOL, V30, P714, DOI 10.1002/1521-4141(200002)30:2<714::AID-IMMU714>3.0.CO;2-P; Herz U, 1998, CLIN EXP ALLERGY, V28, P625; Herz U, 2001, INT ARCH ALLERGY IMM, V124, P193, DOI 10.1159/000053708; Holmlund U, 2002, IMMUNOLOGY, V107, P145, DOI 10.1046/j.1365-2567.2002.01491.x; Kalliomaki M, 2001, LANCET, V357, P1076, DOI 10.1016/S0140-6736(00)04259-8; Kerzel S, 2003, AM J RESP CELL MOL, V28, P170, DOI 10.1165/rcmb.4811; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Kopp MV, 2001, CLIN EXP ALLERGY, V31, P1536, DOI 10.1046/j.1365-2222.2001.01198.x; Lehmann I, 2002, ENVIRON TOXICOL, V17, P203, DOI 10.1002/tox.10055; Neuhaus-Steinmetz U, 2000, INT ARCH ALLERGY IMM, V121, P57, DOI 10.1159/000024298; Piccinni MP, 1996, EUR J IMMUNOL, V26, P2293, DOI 10.1002/eji.1830261004; RENZ H, 1992, CLIN IMMUNOL IMMUNOP, V64, P233, DOI 10.1016/0090-1229(92)90205-3; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Rinas U, 1993, Pediatr Allergy Immunol, V4, P60, DOI 10.1111/j.1399-3038.1993.tb00068.x; SCOTT BB, 1987, VOX SANG, V52, P272; Sugimoto T, 2004, J EXP MED, V199, P535, DOI 10.1084/jem.20031368; Tulic MK, 2000, AM J RESP CELL MOL, V22, P604; Uthoff H, 2003, J IMMUNOL, V171, P3485; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187	31	109	113	0	5	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	MAR	2005	35	3					397	402		10.1111/j.1365-2222.2005.02184.x		6	Allergy; Immunology	Allergy; Immunology	909CS	WOS:000227837300024	15784121	
J	Noguchi, E; Nishimura, F; Fukai, H; Kim, J; Ichikawa, K; Shibasaki, M; Arinami, T				Noguchi, E; Nishimura, F; Fukai, H; Kim, J; Ichikawa, K; Shibasaki, M; Arinami, T			An association study of asthma and total serum immunoglobin E levels for Toll-like receptor polymorphisms in a Japanese population	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						asthma; IgE; polymorphism; TDT; Toll-like receptor	PATTERN-RECOGNITION; TRANSCRIPTIONAL REGULATION; LINKAGE DISEQUILIBRIUM; ACTIVATION; GENE; PREVALENCE; HAPLOTYPES; MUTATIONS; ENDOTOXIN; SYMPTOMS	Background The prevalence of atopic diseases has been increasing in developed countries. This could be explained by the hygiene hypothesis, which states that exposure to specific infections or endotoxins during infancy drives the maturing immune system towards a Th1 phenotype and away from the Th2 phenotype, which is associated with allergic diseases. Toll-like receptors (TLRs) play important roles in the signalling of many pathogen-related molecules and endogenous proteins associated with immune activation. Objective The aim of the present study was to investigate whether polymorphisms in genes encoding TLRs are associated with asthma or total serum IgE levels. Methods We screened the 5' flanking and coding regions of the TLR2,TLR3, TLR4, and TLR9 genes for polymorphisms by direct sequencing of DNA from 32 asthmatics, and analysed the effect of the polymorphisms on the development of atopic asthma and on total serum IgE levels. Results We identified 16 variants in TLRs. The transmission disequilibrium test of the families revealed that none of the alleles or haplotypes were associated with asthma or total IgE levels (P>0.05). However, we found an insertion/deletion polymorphism in the 5' untranslated region of TLR2, and an expression construct containing the deletion allele showed lower luciferase activity than the wild-type alleles, suggesting that the deletion allele has reduced transcriptional activity. Conclusion Our results indicate that polymorphisms in TLRs are not likely to be associated with the development of atopy-related phenotypes in a Japanese population.	Univ Tsukuba, Inst Basic Med Sci, Dept Med Genet, Tsukuba, Ibaraki 3058575, Japan; Univ Tsukuba, Inst Clin Med, Dept Paediat, Tsukuba, Ibaraki 3058575, Japan; Tsukuba Coll Technol, Dept Paediat, Tsukuba, Ibaraki, Japan	Noguchi, E (reprint author), Univ Tsukuba, Inst Basic Med Sci, Dept Med Genet, Tsukuba, Ibaraki 3058575, Japan.	mo00f210@md.tsukuba.ac.jp					Abecasis GR, 2000, AM J HUM GENET, V66, P279, DOI 10.1086/302698; Abecasis GR, 2000, BIOINFORMATICS, V16, P182, DOI 10.1093/bioinformatics/16.2.182; Agnese DM, 2002, J INFECT DIS, V186, P1522, DOI 10.1086/344893; Alexopoulou L, 2001, NATURE, V413, P732, DOI 10.1038/35099560; Arbour NC, 2000, NAT GENET, V25, P187; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Clayton D, 1999, AM J HUM GENET, V65, P1161, DOI 10.1086/302566; Echchannaoui H, 2002, J INFECT DIS, V186, P798, DOI 10.1086/342845; GERGEN PJ, 1992, AM REV RESPIR DIS, V146, P823; Haehnel V, 2002, J IMMUNOL, V168, P5629; Hartmann G, 1999, P NATL ACAD SCI USA, V96, P9305, DOI 10.1073/pnas.96.16.9305; Hemmi H, 2000, NATURE, V408, P740; Kiechl S, 2002, NEW ENGL J MED, V347, P185, DOI 10.1056/NEJMoa012673; Kurt-Jones EA, 2000, NAT IMMUNOL, V1, P398, DOI 10.1038/80833; Lazarus R, 2003, GENOMICS, V81, P85, DOI 10.1016/S0888-7543(02)00022-8; Lemaitre B, 1996, CELL, V86, P973, DOI 10.1016/S0092-8674(00)80172-5; Lien E, 1999, J BIOL CHEM, V274, P33419, DOI 10.1074/jbc.274.47.33419; Lorenz E, 2002, PEDIATR RES, V52, P373, DOI 10.1203/01.PDR.0000025342.83436.53; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; NIH National Asthma Education and Prevention Program, 1997, GUID DIAGN MAN ASTHM; Ozinsky A, 2000, P NATL ACAD SCI USA, V97, P13766, DOI 10.1073/pnas.250476497; Raby BA, 2002, AM J RESP CRIT CARE, V166, P1449, DOI 10.1164/rrcm.200207-634OC; Risch N, 1996, SCIENCE, V273, P1516, DOI 10.1126/science.273.5281.1516; Risch N, 1999, AM J HUM GENET, V65, P493, DOI 10.1086/302497; Risma KA, 2002, J IMMUNOL, V169, P1604; Sabroe I, 2002, CLIN EXP ALLERGY, V32, P984, DOI 10.1046/j.1365-2745.2002.01451.x; Schauer U, 2002, EUR RESPIR J, V20, P1277, DOI 10.1183/09031936.02.00019902; Takeda K, 2001, GENES CELLS, V6, P733, DOI 10.1046/j.1365-2443.2001.00458.x; Takeuchi O, 2000, J IMMUNOL, V165, P5392; Takeuchi O, 2000, J IMMUNOL, V164, P554; van der Stoep N, 2002, J IMMUNOL, V169, P5061; van der Velden AW, 1999, INT J BIOCHEM CELL B, V31, P87, DOI 10.1016/S1357-2725(98)00134-4; Warner JO, 1999, THORAX, V54, pS46; Yokouchi Y, 2000, GENOMICS, V66, P152, DOI 10.1006/geno.2000.6201	35	109	120	0	9	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	FEB	2004	34	2					177	183		10.1111/j.1365-2222.2004.01839.x		7	Allergy; Immunology	Allergy; Immunology	779KL	WOS:000189293900004	14987294	
J	Zmirou, D; Gauvin, S; Pin, I; Momas, I; Sahraoui, F; Just, J; Le Moullec, Y; Bremont, F; Cassadou, S; Reungoat, P; Albertini, M; Lauvergne, N; Chiron, M; Labbe, A				Zmirou, D; Gauvin, S; Pin, I; Momas, I; Sahraoui, F; Just, J; Le Moullec, Y; Bremont, F; Cassadou, S; Reungoat, P; Albertini, M; Lauvergne, N; Chiron, M; Labbe, A		Vesta Investigators	Traffic related air pollution and incidence of childhood asthma: results of the Vesta case-control study	JOURNAL OF EPIDEMIOLOGY AND COMMUNITY HEALTH			English	Article							DIESEL EXHAUST; RESPIRATORY HEALTH; EAST-GERMANY; IN-VIVO; CHILDREN; EXPOSURE; ASSOCIATION; PREVALENCE; IMMUNOLOGY; RESIDENCE	Study objective: The Vesta project aims to assess the role of traffic related air pollution in the occurrence of childhood asthma. Design and setting: Case- control study conducted in five French metropolitan areas between 1998 and 2000. A set of 217 pairs of matched 4 to 14 years old cases and controls were investigated. An index of lifelong exposure to traffic exhausts was constructed, using retrospective information on traffic density close to all home and school addresses since birth; this index was also calculated for the 0 - 3 years age period to investigate the effect of early exposures. Main results: Adjusted on environmental tobacco smoke, personal and parental allergy, and several confounders, lifelong exposure was not associated with asthma. In contrast, associations before age of 3 were significant: odds ratios for tertiles 2 and 3 of the exposure index, relative to tertile 1, exhibited a positive trend ( 1.48 ( 95% CI = 0.7 to 3.0) and 2.28 ( 1.1 to 4.6)), with greater odds ratios among subjects with positive skin prick tests. Conclusions: These results suggest that traffic related pollutants might have contributed to the asthma epidemic that has taken place during the past decades among children.	Nancy Univ, Sch Med, Publ Hlth Lab, Nancy, France; Ctr Sci & Tech Batiment, Paris, France; Grenoble Univ Hosp, Dept Paediat, Grenoble, France; Univ Paris 05, Sch Pharm, Publ Hlth & Hyg Lab, Paris, France; Paris Univ Hosp Trousseau, Dept Paediat, Paris, France; City Paris, Hyg Lab, Paris, France; Toulouse Univ Hosp, Dept Paediat, Toulouse, France; Reg Hlth Observ Midi Pyrenees, Toulouse, France; Nice Univ Hosp, Dept Paediat, Nice, France; French Natl Inst Transport & Safety Res, INRETS, Lyon, France; Clermont Ferrand Univ Hosp, Dept Paediat, Clermont Ferrand, France	Zmirou, D (reprint author), Fac Med, INSERM, 9 Av Foret Haye,BP 164, F-54505 Vandoeuvre Les Nancy, France.		PIN, Isabelle/N-3020-2013; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Anderson HR, 1997, CIBA F SYMP, V206, P190; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; Busse WW, 2001, NEW ENGL J MED, V344, P350; Ciccone G, 1998, OCCUP ENVIRON MED, V55, P771; Clark NM, 1999, ENVIRON HEALTH PERSP, V107, P421; *COMM MED EFF AIR, 1995, ASTHM OUTD POLL; DIAZSANCHEZ D, 1994, J CLIN INVEST, V94, P1417, DOI 10.1172/JCI117478; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; Duhme H, 1996, EPIDEMIOLOGY, V7, P578, DOI 10.1097/00001648-199611000-00003; Ebelt S, 2001, ENVIRON HEALTH PERSP, V109, P325, DOI 10.2307/3454890; EDWARDS J, 1994, ARCH ENVIRON HEALTH, V49, P223; Gold DR, 2000, ENVIRON HEALTH PERSP, V108, P643, DOI 10.2307/3454400; *HLTH EFF I, 1995, DIES EXH CRIT AN EM; Holgate ST, 1997, CIBA F SYMP, V206, P1; Jantunen MJ, 1998, J EXPO ANAL ENV EPID, V8, P495; Jarvis D, 1998, BRIT MED J, V316, P607; Kay AB, 2001, NEW ENGL J MED, V344, P30; Koistinen KJ, 1999, J AIR WASTE MANAGE, V49, P1212, DOI 10.1080/10473289.1999.10463916; Kramer U, 2000, EPIDEMIOLOGY, V11, P64, DOI 10.1097/00001648-200001000-00014; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; LEIKAUF GD, 1995, ENVIRON HEALTH PERSP, V103, P253, DOI 10.2307/3432382; Martinez FD, 1999, J ALLERGY CLIN IMMUN, V103, P355, DOI 10.1016/S0091-6749(99)70456-2; Mattes J, 1999, CLIN EXP ALLERGY, V29, P729; NITTA H, 1993, ARCH ENVIRON HEALTH, V48, P53; Nyberg F, 2000, EPIDEMIOLOGY, V11, P487, DOI 10.1097/00001648-200009000-00002; Oglesby L, 2000, J EXPO ANAL ENV EPID, V10, P251, DOI 10.1038/sj.jea.7500088; PALTTSMILLS T, 1999, ASTHMA CAUSES MECH I, P2; Pandya RJ, 2002, ENVIRON HEALTH PERSP, V110, P103; Pearson RL, 2000, J AIR WASTE MANAGE, V50, P175; Peden DB, 2000, ENVIRON HEALTH PERSP, V108, P475, DOI 10.2307/3454539; PEDEN DB, 1999, ASTHMA CAUSES MECH I, P173; Pitz M, 2001, ATMOS ENVIRON, V35, P4357, DOI 10.1016/S1352-2310(01)00229-1; Platts-Mills TAE, 2000, ENVIRON HEALTH PERSP, V108, P725, DOI 10.2307/3454409; Raaschou-Nielsen O, 2001, AM J EPIDEMIOL, V153, P433, DOI 10.1093/aje/153.5.433; Takano H, 1997, AM J RESP CRIT CARE, V156, P36; VANMUTIUS E, 1998, LANCET, V351, P862; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; Venn A, 2000, OCCUP ENVIRON MED, V57, P152, DOI 10.1136/oem.57.3.152; Wilkinson P, 1999, THORAX, V54, P1070; WJST M, 1993, BRIT MED J, V307, P596; Woolcock AJ, 1997, CIBA F SYMP, V206, P122; Wyler C, 2000, EPIDEMIOLOGY, V11, P450, DOI 10.1097/00001648-200007000-00015; Zmirou D, 2002, J EXPO ANAL ENV EPID, V12, P186, DOI 10.1038/sj/jea/7500217	43	109	116	1	12	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0143-005X			J EPIDEMIOL COMMUN H	J. Epidemiol. Community Health	JAN	2004	58	1					18	23		10.1136/jech.58.1.18		6	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	755KK	WOS:000187401900005	14684722	
J	Kabesch, M; Peters, W; Carr, D; Leupold, W; Weiland, SK; von Mutius, E				Kabesch, M; Peters, W; Carr, D; Leupold, W; Weiland, SK; von Mutius, E			Association between polymorphisms in caspase recruitment domain containing protein 15 and allergy in two German populations	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; atopic dermatitis; allergic rhinitis; atopy; childhood; IgE; CARD15; NOD2; polymorphism; SNP	CROHNS-DISEASE; KAPPA-B; NOD2; SUSCEPTIBILITY; MONOCYTES; MUTATION; GENE	Background: Early exposure to microbial matter such as LPS may influence the development of asthma and allergies by activation of innate immunity pathways as indicated by studies in farming environments. Recently, polymorphisms in caspase recruitment domain containing protein 15 (CARD15), an intracellular LPS receptor protein, have been associated with Crohn's disease. Because these polymorphisms lead to changes in LPS recognition, they may affect the development of asthma and allergies. Objective: We genotyped a large population of German schoolchildren (N = 1872) from East and West Germany for 3 functional relevant CARD15 polymorphisms for their role in the development of asthma and allergy. Methods: By use of parental questionnaires, skin prick testing, pulmonary function tests, bronchial challenge tests, and measurements of serum IgE levels, children were phenotyped for the presence of atopic diseases. Genotyping was performed with PCR-based restriction enzyme assays. To assess associations between atopic phenotypes and genotypes standard statistical procedures were applied. Results: Children with the polymorphic allele C2722 had a more than 3-fold risk to develop allergic rhinitis (P < .001) and an almost 2-fold risk for atopic dermatitis (P < .05). Furthermore, the T2104 allele was associated with an almost 2-fold risk for allergic rhinitis (P < .05). When a C insertion at position 3020 was present, the risk of atopy increased by 50% (P < .05) and serum IgE levels were elevated (P < .01). Conclusion: The shared genetic background between Crohn's disease and atopy may indicate that an impaired recognition of microbial exposures results in an insufficient downregulation of excessive immune responses, giving rise to either T(H)2 dominated allergies or T(H)1 related Crohn's disease.	Univ Munich, Childrens Univ Hosp, D-80337 Munich, Germany; Univ Childrens Hosp, Dresden, Germany; Univ Ulm, Dept Epidemiol, Ulm, Germany	Kabesch, M (reprint author), Univ Munich, Childrens Univ Hosp, Lindwurmstr 4, D-80337 Munich, Germany.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; von Mutius, Erika/0000-0002-8893-4515			Arbour NC, 2000, NAT GENET, V25, P187; Baldini M, 1999, AM J RESP CELL MOL, V20, P976; BERBIG B, 1991, ALLERGOLOGIE, V14, P51; DEVLIN B, 1995, GENOMICS, V29, P311; Gale EAM, 2002, DIABETOLOGIA, V45, P588, DOI 10.1007/s00125-002-0801-1; Hampe J, 2001, LANCET, V357, P1925, DOI 10.1016/S0140-6736(00)05063-7; Hugot JP, 2001, NATURE, V411, P599, DOI 10.1038/35079107; Inohara N, 2001, J BIOL CHEM, V276, P2551, DOI 10.1074/jbc.M009728200; Kobayashi K, 2002, NATURE, V416, P194, DOI 10.1038/416194a; Koppelman GH, 2001, AM J RESP CRIT CARE, V163, P965; Ogura Y, 2001, NATURE, V411, P603, DOI 10.1038/35079114; Ogura Y, 2001, J BIOL CHEM, V276, P4812, DOI 10.1074/jbc.M008072200; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Simpson CR, 2002, CLIN EXP ALLERGY, V32, P37, DOI 10.1046/j.0022-0477.2001.01250.x; Ten RM, 1999, J ALLERGY CLIN IMMUN, V104, P376, DOI 10.1016/S0091-6749(99)70382-9; Weiland SK, 1999, EUR RESPIR J, V14, P862, DOI 10.1034/j.1399-3003.1999.14d23.x	16	109	110	0	3	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	APR	2003	111	4					813	817		10.1067/mai.2003.1336		5	Allergy; Immunology	Allergy; Immunology	667WW	WOS:000182258500023	12704363	
J	Hoffmann-Sommergruber, K				Hoffmann-Sommergruber, K			Pathogenesis-related (PR)-proteins identified as allergens	BIOCHEMICAL SOCIETY TRANSACTIONS			English	Article; Proceedings Paper	Colloquium on Plant Food Allergens	JUL 16-18, 2002	CARDIFF UNIV, CARDIFF, WALES		CARDIFF UNIV	chitinase; IgE; latex; lipid transfer protein; pathogenesis-related protein; plant allergens	LIPID TRANSFER PROTEIN; PEACH PRUNUS-PERSICA; AMINO-ACID-SEQUENCE; CLASS-I CHITINASES; MAJOR ALLERGEN; MOLECULAR CHARACTERIZATION; POLLEN ALLERGENS; ROSACEAE FRUITS; PR PROTEINS; EXPRESSION	Type I allergies are recognized as an important disease affecting around 25 % of the population of industrialized countries of the Northern hemisphere. Allergic patients produce specific IgE antibodies after frequent exposure to either inhaled or nutritive allergens. Of the plant allergens listed in the Official Allergen Database of the International Union of Immunological Societies, approx. 25 % belong to the group of pathogenesis-related proteins (PR-proteins). PR-proteins are defined as proteins that are induced upon stress, pathogen attack and abiotic stimuli. This inhomogeneous group of proteins has been classified into 14 PR-protein families. So far, plant-derived allergens have been identified with sequence similarities to PR-protein families 2, 3, 4, 5, 8, 10 and 14. In general, both protein groups, i.e. PR-proteins and allergens, comprise rather small proteins, which are stable at low pH and resistant to proteolysis. These features, and their level of expression, make PR-proteins good candidates for evoking an immune response in predisposed humans, when coming into contact with mucosal surfaces. The identification of PR-proteins with allergenic potential and their homologues is of importance for the allergic patient and the management of this disease. Firstly, plant foods derived from genetically modified plants could represent new allergen sources, and therefore should be evaluated carefully for their potential allergenicity. Secondly, complex plant-derived foods should be analysed for hidden allergens and labelled accordingly.	Univ Vienna, Dept Pathophysiol, A-1090 Vienna, Austria	Hoffmann-Sommergruber, K (reprint author), Univ Vienna, Dept Pathophysiol, AKH-EBO 3Q,Waehringer Guertel 18-20, A-1090 Vienna, Austria.						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Soc. Trans.	NOV	2002	30		6				930	935		10.1042/BST0300930		6	Biochemistry & Molecular Biology	Biochemistry & Molecular Biology	625KX	WOS:000179816600023	12440949	
J	Omland, O				Omland, O			Exposure and respiratory health in farming in temperate zones - A review of the literature	ANNALS OF AGRICULTURAL AND ENVIRONMENTAL MEDICINE			English	Review						farming; agriculture; temperate zones; confinement buildings; measurements; exposure; sensitisation; asthma; chronic bronchitis; bronchial responsiveness; lung function	SWINE-CONFINEMENT BUILDINGS; DOSE-RESPONSE RELATIONSHIPS; CROSS-SECTIONAL SURVEY; LUNG-FUNCTION DECLINE; NEW-ZEALAND FARMERS; CHRONIC-BRONCHITIS; DAIRY FARMERS; PIG FARMERS; STORAGE MITES; RISK-FACTORS	To review studies in farming populations from temperate zones focusing on: (1) exposure to dust, bacteria, moulds, endotoxin, and ammonia, (2) sensitisation to common airborne allergens, (3) prevalence, incidence and risk factors of chronic bronchitis, asthma and bronchial hyperresponsiveness, and (4) measurements of lung function. Working in animal housings can be associated with exposure to organic dust, bacteria, moulds, endotoxin, and ammonia in concentrations that can induce cellular and immunological responses and result in respiratory diseases. Working in poultry housing might be associated with higher exposures to dust, bacteria, and ammonia than in swine and cow housings, and endotoxin exposure seems to be higher in North America than in Europe. Working exposure might influence the domestic area on farms, and there might be a protective effect of being raised on a farm regarding sensitisation and allergic diseases. Sensitisation to mites seems to be the most prevalent of the common inhalant allergens. Chronic bronchitis is frequent and data suggests that it is work related in farmers. Findings concerning asthma are less uniform, and data regarding bronchial hyperresponsiveness are too sparse and inconsistent to evaluate the effect on farming. Several risk factors have been described, and age is shared for all three clinical manifestations, while male gender, atopy, smoking, pig farming, and animal production are common risk factors for chronic bronchitis and asthma. FEV1, and FEV1/FVC seems to be reduced in farmers, and longitudinal studies indicate an increased annual loss in FEV1 in farmers, especially in pig farmers. The increased annual decline has been associated with lung function, bronchial hyperresponsiveness, smoking, automatic dry feeding systems, and endotoxin. Despite studies with methodological weaknesses, heterogenity in sampling times, measurement techniques, equipment, and diagnostic criteria, the review has revealed that the exposure to organic dust in farming can be substantial and might lead to respiratory diseases and increased annual loss in lung function. Working exposure seems to influence the domestic area in farms, and being raised on a farm might have a protective effect regarding sensitisation and allergic diseases.	Aarhus Univ, Inst Environm & Occupat Med, DK-8000 Aarhus C, Denmark	Omland, O (reprint author), Aarhus Univ, Inst Environm & Occupat Med, Univ Pk,Bldg 260,Vennelyst Blvd 6, DK-8000 Aarhus C, Denmark.						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Agr. Env. Med.		2002	9	2					119	136				18	Environmental Sciences; Public, Environmental & Occupational Health	Environmental Sciences & Ecology; Public, Environmental & Occupational Health	627WU	WOS:000179959900001	12498578	
J	Carter, MC; Perzanowski, MS; Raymond, A; Platts-Mills, TAE				Carter, MC; Perzanowski, MS; Raymond, A; Platts-Mills, TAE			Home intervention in the treatment of asthma among inner-city children	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; allergen avoidance; dust mite; children; inner city	HOUSE-DUST MITE; COCKROACH ALLERGEN; BRONCHIAL HYPERREACTIVITY; RISK-FACTORS; P-I; EXPOSURE; AVOIDANCE; SENSITIZATION; ENVIRONMENT; ANTIBODIES	Background: In Atlanta, as in other major urban areas of the United States, asthma is a leading cause of school absenteeism, emergency department use, and hospitalization. Recent guidelines for asthma management recommend reducing exposure to relevant allergens, but neither the feasibility nor the efficacy of this form of treatment has been established for children living in poverty. Objective: We sought to investigate allergen avoidance as a treatment for asthma among inner-city children. Methods: One hundred four children with asthma living in the city of Atlanta were enrolled into a controlled trial of avoidance without being skin tested. The children were randomized to an active avoidance group, a placebo avoidance group, and a second control group for which no house visits occurred until the end of the first year. Avoidance included bed and pillow covers, hot washing of bedding, and cockroach bait. Eighty-five children completed the study, and the outcome was measured as unscheduled clinic visits, emergency department visits, and hospitalization for asthma, as well as changes in mite and cockroach allergen levels. Results: There was a significant decrease in acute visits for asthma among children whose homes were visited (P <.001). However, there was no significant difference between the active and placebo homes either in the effect on asthma visits or in allergen concentrations. When the children with mite allergy were considered separately, there was a significant correlation between decreased mite allergen and change in acute visits (P <.01). The avoidance measures for cockroach allergen appeared to be ineffective, and the changes observed did not correlate with changes in visits. Conclusions: Applying allergen avoidance as a treatment for asthma among children living in poverty is difficult because of multiple sensitivities and problems applying the protocols in this environment. The current results demonstrate that home visiting positively influences the management of asthma among families living in poverty. Furthermore, the results for children with mite allergy strongly suggest that decreasing relevant allergen exposure should be an objective of treatment in this population.	Emory Univ, Dept Family Med, Atlanta, GA 30322 USA; Univ Virginia, Asthma & Allerg Dis Ctr, Charlottesville, VA USA	Platts-Mills, TAE (reprint author), Univ Virginia Hlth Syst, Asthma & Allerg Dis Ctr, POB 801355, Charlottesville, VA 22908 USA.				NIAID NIH HHS [1P01 AI50989, AI-20565]		Almqvist C, 1999, J ALLERGY CLIN IMMUN, V103, P1012, DOI 10.1016/S0091-6749(99)70172-7; BUIST AS, 1990, JAMA-J AM MED ASSOC, V264, P1719, DOI 10.1001/jama.264.13.1719; CALL RS, 1992, J PEDIATR-US, V121, P862, DOI 10.1016/S0022-3476(05)80329-4; Celano M, 1998, J PEDIATR PSYCHOL, V23, P345, DOI 10.1093/jpepsy/23.6.345; CHAPMAN MD, 1988, J IMMUNOL, V140, P812; Eggleston PA, 1999, J ALLERGY CLIN IMMUN, V104, P842; EHNERT B, 1992, J ALLERGY CLIN IMMUN, V90, P135, DOI 10.1016/S0091-6749(06)80024-2; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; Gergen PJ, 1999, J ALLERGY CLIN IMMUN, V103, P501, DOI 10.1016/S0091-6749(99)70477-X; GOETZSCHE PC, 1998, BRIT MED J, V317, P1105; Hayden ML, 1997, ANN ALLERG ASTHMA IM, V79, P437; Hill DJ, 1997, J ALLERGY CLIN IMMUN, V99, P323, DOI 10.1016/S0091-6749(97)70049-6; Htut T, 2001, J ALLERGY CLIN IMMUN, V107, P55, DOI 10.1067/mai.2001.111240; LUCZYNSKA CM, 1989, J IMMUNOL METHODS, V118, P227, DOI 10.1016/0022-1759(89)90010-0; Mollet JA, 1997, J MED ENTOMOL, V34, P307; National Institutes of Health, 1997, NIH PUBL; PARSONS HM, 1974, SCIENCE, V183, P922, DOI 10.1126/science.183.4128.922; Peat JK, 1996, AM J RESP CRIT CARE, V153, P141; Perzanowski MS, 1999, J ALLERGY CLIN IMMUN, V103, P1018, DOI 10.1016/S0091-6749(99)70173-9; Perzanowski MS, 1998, J ALLERGY CLIN IMMUN, V101, P626; Phipatanakul W, 2000, J ALLERGY CLIN IMMUN, V106, P1075; Piacentini GL, 1996, J ALLERGY CLIN IMMUN, V97, P1079, DOI 10.1016/S0091-6749(96)70261-0; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; Platts-Mills TAE, 2000, J ALLERGY CLIN IMMUN, V106, P787, DOI 10.1067/mai.2000.110548; Platts-Mills Thomas A. 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NOV	2001	108	5					732	737		10.1067/mai.2001.119155		6	Allergy; Immunology	Allergy; Immunology	498RG	WOS:000172523800012	11692097	
J	Park, JH; Spiegelman, DL; Gold, DR; Burge, HA; Milton, DK				Park, JH; Spiegelman, DL; Gold, DR; Burge, HA; Milton, DK			Predictors of airborne endotoxin in the home	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						airborne endotoxin; dust endotoxin; predictive model; seasonal variability	LUNG-FUNCTION; HOUSE-DUST; RESPIRATORY SYMPTOMS; LIMULUS ASSAY; COTTON DUST; EXPOSURE; CHILDREN; ASTHMA; FARMERS; SEVERITY	We identified home characteristics associated with the level of airborne endotoxin in 111 Boston-area homes enrolled in a cohort study of home exposures and childhood asthma, and we developed a predictive model to estimate airborne endotoxin. We measured endotoxin in family-room air and in dust from the baby's bed, family room, bedroom, and kitchen floor. Level of airborne endotoxin was weakly correlated (r < 0.3) with level of endotoxin in each of the four types of dust samples and was significantly correlated with endotoxin in family-room dust (p < 0.05). Endotoxin in family-room dust accounted for < 6% of the variability of airborne endotoxin. In a multivariate model, certain home characteristics were positively (p < 0.05) associated with airborne endotoxin. These included current presence of dog (difference in level, dog vs. no dog = 72%, partial R-2 = 12.8%), past presence of dog (partial R-2 = 5.5%), and endotoxin level in family-room dust (partial R-2 = 5.3%). Use of a dehumidifier (partial R-2 = 6.4%) was negatively associated (p = 0.02; difference = -31%) with airborne endotoxin. Other home characteristics were identified as important determinants of increased airborne endotoxin in this model, but individual coefficients were not statistically significant (alpha = 0.05): total amount of fine dust collected in the home (partial R-2 = 3.8%), concrete floor in family room (3.7%), water damage (3.6%), and use of cool-mist humidifier in past year (2.7%). This multivariate model explained 42% of the variability of airborne endotoxin levels, a substantial improvement over that with dust endotoxin alone. Airborne endotoxin in Boston-area homes appears to be determined by the presence of dogs, moisture sources, and increased a-mounts of settled dust.	Harvard Univ, Sch Publ Hlth, Occupat Hlth Program, Dept Environm Hlth, Boston, MA 02115 USA; Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA; Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA; Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA; Harvard Univ, Sch Med, Boston, MA USA	Milton, DK (reprint author), Harvard Univ, Sch Publ Hlth, Occupat Hlth Program, Dept Environm Hlth, 665 Huntington Ave, Boston, MA 02115 USA.		Milton, Donald/G-3286-2010	Milton, Donald/0000-0002-0550-7834	NIAID NIH HHS [R01 AI/EHS-35786]; NIEHS NIH HHS [2P30ES00002, R01 ES-07036]		ALLEN DM, 1971, TECHNOMETRICS, V13, P469, DOI 10.2307/1267161; BRUNEKREEF B, 1989, AM REV RESPIR DIS, V140, P1363; Carroll R. 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Health Perspect.	AUG	2001	109	8					859	864		10.2307/3454831		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	470BZ	WOS:000170851700032	11564624	
J	Phipps, S; Lam, CE; Kaiko, GE; Foo, SY; Collison, A; Mattes, J; Barry, J; Davidson, S; Oreo, K; Smith, L; Mansell, A; Matthaei, KI; Foster, PS				Phipps, Simon; Lam, Chuan En; Kaiko, Gerard E.; Foo, Shen Yun; Collison, Adam; Mattes, Joerg; Barry, Jessica; Davidson, Sophia; Oreo, Kevin; Smith, Lauren; Mansell, Ashley; Matthaei, Klaus I.; Foster, Paul S.			Toll/IL-1 Signaling Is Critical for House Dust Mite-specific Th1 and Th2 Responses	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; innate immunity; eosinophil; neutrophil	ALLERGIC AIRWAY INFLAMMATION; ACTIVATED PROTEIN-KINASE; ANTIGEN-PRESENTING CELLS; TOLL-LIKE RECEPTORS; DENDRITIC CELLS; IMMUNE-RESPONSES; ASTHMATIC-PATIENTS; INHALED ANTIGEN; CUTTING EDGE; OX40 LIGAND	Rationale: One of the immunopathological features of allergic inflammation is the infiltrationof helper T type 2 (Th2) cells to the site of disease. Activation of innate pattern recognition receptors such as Toll-like receptors (TLRs) plays a critical role in helper T type I cell differentiation, yet their contribution to the generation of Th2 responses to clinically relevant aeroallergens remains poorly defined. Objectives: To determine the requirement for TLR2, TLR4, and the Toll/IL-1 receptor domain adaptor protein MyD88 in a murine model of allergic asthma. Methods: Wild-type and factor-deficient ((-/-)) mice were sensitized intranasally to the common allergen house dust mite (HDM) and challenged 2 weeks later on four consecutive days. Measurements of allergic airway inflammation, T-cell cytokine production, and airway hyperreactivity, were performed 24 hours later. Measurements and Main Results: Mice deficient in MyD88 were protected from the cardinal features of allergic asthma, including granulocytic inflammation, Th2 cytokine production and airway hyperreactivity. Although HDM activated NF-kappa B in TLR2- or TLR4-expressing HEK cells, only in TLR4(-/-) mice was the magnitude of allergic airway inflammation and hyperreactivity attenuated. The diminished Th2 response present in MyD88(-/-) and TLR4(-/-) mice was associated with fewer OX40 ligand-expressing myeloid dendritic cells in the draining lymph nodes during allergic sensitization. Finally, HDM-specific IL-17 production and airway neutrophilia were attenuated in MyD88(-/-) but not TLR4(-/-) mice. Conclusions: Together, these data suggest that Th2- and Th17-mediated inflammation generated on inhalational HDM exposure is differentially regulated by the presence of microbial products and the activation of distinct MyD88-dependent pattern recognition receptors.	[Phipps, Simon; Lam, Chuan En; Kaiko, Gerard E.; Foo, Shen Yun; Collison, Adam; Mattes, Joerg; Barry, Jessica; Davidson, Sophia; Oreo, Kevin; Smith, Lauren; Foster, Paul S.] Univ Newcastle, Ctr Asthma & Resp Dis, Sch Biomed Sci, Newcastle, NSW 2300, Australia; [Mansell, Ashley] Monash Univ, Monash Inst Med Res, Clayton, Vic, Australia; [Matthaei, Klaus I.] Australian Natl Univ, John Curtin Sch Med Res, Gene Targeting Grp, Canberra, ACT 2601, Australia; [Matthaei, Klaus I.] King Saud Univ, Coll Med, Dept Anat, Stem Cell Unit, Riyadh 11461, Saudi Arabia; [Matthaei, Klaus I.] King Saud Univ, King Khalid Univ Hosp, Riyadh 11461, Saudi Arabia	Foster, PS (reprint author), Univ Newcastle, Ctr Asthma & Resp Dis, Sch Biomed Sci, David Maddison Clin Sci Bldg,Watt St, Newcastle, NSW 2300, Australia.	simon.phipps@newcastle.edu.au; paul.foster@newcastle.edu.au	Mansell, Ashley/B-9553-2008; Klaus, Matthaei/D-8691-2011; Phipps, Simon/F-9170-2010; Foster, Paul/G-5057-2013	Mansell, Ashley/0000-0002-6540-1281; Phipps, Simon/0000-0002-7388-3612; 	National Health and Medical Research (NHMRC) [224207]; Australian Lung Foundation/Boehringer Ingelheim Chronic Airflow Limitation Research	Supported by a National Health and Medical Research (NHMRC) program grant (224207). S.P. is a recipient of an Australian Lung Foundation/Boehringer Ingelheim Chronic Airflow Limitation Research Fellowship.	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J. Respir. Crit. Care Med.	MAY 15	2009	179	10					883	893		10.1164/rccm.200806-974OC		11	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	444AG	WOS:000265951500006	19246719	
J	McGrath, JA; Uitto, J				McGrath, John A.; Uitto, Jouni			The filaggrin story: novel insights into skin-barrier function and disease	TRENDS IN MOLECULAR MEDICINE			English	Review							OF-FUNCTION MUTATIONS; EPIDERMAL DIFFERENTIATION COMPLEX; CAUSE ICHTHYOSIS VULGARIS; ATOPIC-DERMATITIS; FUNCTION VARIANTS; GRANULAR LAYER; GENE; PREDISPOSE; EXPRESSION; PSORIASIS	Recent reports have uncovered the key role of the protein filaggrin in maintaining an effective skin barrier against the external environment. Loss-of-function mutations in the profilaggrin gene (FLG) are common and are present in up to 10% of the population. These mutations are the cause of the semi-dominant skin-scaling disorder ichthyosis vulgaris and are a major risk factor for the development of atopic dermatitis. The discovery of these mutations also provides new data concerning the genetics of atopic asthma as well as intriguing insight into disease mechanisms of systemic allergies involving antigen exposure in skin with defective barrier function. Collectively, these novel findings have significant implications for the classification and future clinical management of patients with atopic and allergic diseases.	[Uitto, Jouni] Thomas Jefferson Univ, Jefferson Med Coll, Dept Dermatol & Cutaneous Biol, Philadelphia, PA 19107 USA; [Uitto, Jouni] Thomas Jefferson Univ, Jefferson Inst Mol Med, Philadelphia, PA 19107 USA; [McGrath, John A.] Guys Kings Coll, St Johns Inst Dermatol, Genet Skin Dis Grp, Div Genet & Mol Med, London, England; [McGrath, John A.] St Thomas Sch Med, London, England	Uitto, J (reprint author), Thomas Jefferson Univ, Jefferson Med Coll, Dept Dermatol & Cutaneous Biol, Philadelphia, PA 19107 USA.	Jouni.Uitto@jefferson.edu	McGrath, John/D-6824-2012	McGrath, John/0000-0002-3708-9964			Barker JNWN, 2007, J INVEST DERMATOL, V127, P564, DOI 10.1038/sj.jid.5700587; Betz RC, 2007, J INVEST DERMATOL, V127, P2539, DOI 10.1038/sj.jid.5700915; Bouwstra JA, 2006, BBA-BIOMEMBRANES, V1758, P2080, DOI 10.1016/j.bbamem.2006.06.021; Callard RE, 2007, TRENDS IMMUNOL, V28, P294, DOI 10.1016/j.it.2007.05.003; Candi E, 2005, NAT REV MOL CELL BIO, V6, P328, DOI 10.1038/nrm1619; Compton JG, 2002, EXP DERMATOL, V11, P518, DOI 10.1034/j.1600-0625.2002.110604.x; Denecker G, 2007, NAT CELL BIOL, V9, P666, DOI 10.1038/ncb1597; ELELUND E, 2006, AM J HUM GENET, V78, P1060; Enomoto Hisako, 2007, BMC Dermatol, V7, P5, DOI 10.1186/1471-5945-7-5; Fleckman P, 2002, EXP DERMATOL, V11, P327, DOI 10.1034/j.1600-0625.2002.110406.x; GAN SQ, 1990, BIOCHEMISTRY-US, V29, P9432, DOI 10.1021/bi00492a018; Ginger RS, 2005, ARCH DERMATOL RES, V297, P235, DOI 10.1007/s00403-005-0590-8; Gruber R, 2007, EUR J HUM GENET, V15, P179, DOI 10.1038/sj.ejhg.5201742; HAMADA T, 2007, J INVEST DERMATOL; Howell MD, 2007, J ALLERGY CLIN IMMUN, V120, P150, DOI 10.1016/j.jaci.2007.04.031; Huffmeier U, 2007, J INVEST DERMATOL, V127, P1367, DOI 10.1038/sj.jid.5700720; Irvine AD, 2007, J INVEST DERMATOL, V127, P504, DOI 10.1038/sj.jid.5700695; Irvine AD, 2006, J INVEST DERMATOL, V126, P1200, DOI 10.1038/sj.jid.5700365; Judge MR, 2004, ROOKS TXB DERMATOLOG; KANG K, DERMATOLOGY, P199; Liao HH, 2007, J INVEST DERMATOL, V127, P2795, DOI 10.1038/sj.jid.5700971; Macaluso F, 2007, EXP DERMATOL, V16, P692, DOI 10.1111/j.1600-0625.2007.00589.x; Marenholz I, 2006, J ALLERGY CLIN IMMUN, V118, P866, DOI 10.1016/j.jaci.2006.07.026; McGrath JA, 2006, CLIN EXP DERMATOL, V31, P826, DOI 10.1111/j.1365-2230.2006.02287.x; McLean WHI, 2007, J INVEST DERMATOL, V127, P8, DOI 10.1038/sj.jid.5700609; Morar N, 2007, J INVEST DERMATOL, V127, P1667, DOI 10.1038/sj.jid.5700739; Nicotera P, 2007, NAT CELL BIOL, V9, P621, DOI 10.1036/ncb0607-619; NOMURA T, IN PRESS J INVEST DE; Nomura T, 2007, J ALLERGY CLIN IMMUN, V119, P434, DOI 10.1016/j.jaci.2006.12.646; Palmer CNA, 2006, NAT GENET, V38, P441, DOI 10.1038/ng1767; Palmer CNA, 2007, J ALLERGY CLIN IMMUN, V120, P64, DOI 10.1016/j.jaci.2007.04.001; Pulkkinen L, 2002, J AM ACAD DERMATOL, V47, P91, DOI 10.1067/mjd.2002.120601; Rawlings A V, 2004, Dermatol Ther, V17 Suppl 1, P43, DOI 10.1111/j.1396-0296.2004.04S1005.x; SANDILANDS A, 2007, NAT GENET, V39, P250; Sandilands A, 2007, J INVEST DERMATOL, V127, P1282, DOI 10.1038/sj.jid.5700876; Sandilands A, 2006, J INVEST DERMATOL, V126, P1770, DOI 10.1038/sj.jid.5700459; Seguchi T, 1996, ARCH DERMATOL RES, V288, P442, DOI 10.1007/BF02505232; Shwayder Tor, 2005, Dermatol Ther, V18, P87, DOI 10.1111/j.1529-8019.2005.05011.x; Smith FJD, 2006, NAT GENET, V38, P337, DOI 10.1038/ng1743; Soderhall C, 2007, PLOS BIOL, V5, P1952, DOI 10.1371/journal.pbio.0050242; Sohn MH, 2007, J PEDIATR-US, V150, P106, DOI 10.1016/j.jpeds.2006.08.065; South AP, 1999, J INVEST DERMATOL, V112, P910, DOI 10.1046/j.1523-1747.1999.00613.x; Tsai KY, 2007, J AM ACAD DERMATOL, V56, P719, DOI 10.1016/j.jaad.2006.10.985; Uitto J, 2007, EXP CELL RES, V313, P1995, DOI 10.1016/j.yexcr.2007.03.029; Weichenthal M, 2007, J INVEST DERMATOL, V127, P1535, DOI 10.1038/sj.jid.5700771; Weidinger S, 2006, J ALLERGY CLIN IMMUN, V118, P214, DOI 10.1016/j.jaci.2006.05.004; Ying S, 2006, J ALLERGY CLIN IMMUN, V118, P1386, DOI 10.1016/j.jaci.2006.08.030; Zhao Y, 2007, J INVEST DERMATOL, V127, P1878, DOI 10.1038/sj.jid.5700817; Zhong W, 2003, J HUM GENET, V48, P390, DOI 10.1007/s10038-003-0043-1	49	108	117	0	12	ELSEVIER SCI LTD	OXFORD	THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND	1471-4914			TRENDS MOL MED	Trends Mol. Med	JAN	2008	14	1					20	27		10.1016/j.molmed.2007.10.006		8	Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental	Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine	260HY	WOS:000253002600004	18068483	
J	Kercsmar, CM; Dearborn, DG; Schluchter, M; Xue, L; Kirchner, HL; Sobolewski, J; Greenberg, SJ; Vesper, SJ; Allan, T				Kercsmar, Carolyn M.; Dearborn, Dorr G.; Schluchter, Mark; Xue, Lintong; Kirchner, H. Lester; Sobolewski, John; Greenberg, Stuart J.; Vesper, Stephen J.; Allan, Terry			Reduction in asthma morbidity in children as a result of home remediation aimed at moisture sources	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; children; damp housing; home remediation; indoor mold	INNER-CITY ASTHMA; RESPIRATORY HEALTH SURVEY; ENVIRONMENTAL INTERVENTION; COCKROACH ALLERGEN; SYMPTOMS; EXPOSURE; DAMPNESS; SENSITIZATION; MOLDS; DUST	OBJECTIVES: Home dampness and the presence of mold and allergens have been associated with asthma morbidity. We examined changes in asthma morbidity in children as a result of home remediation aimed at moisture sources. DESIGN: In this prospective, randomized controlled trial, symptomatic, asthmatic children (n = 62), 2-17 years of age, living in a home with indoor mold, received an asthma intervention including an action plan, education, and individualized problem solving. The remediation group also received household repairs, including reduction of water infiltration, removal of water-damaged building materials, and heating/ventilation/air-conditioning alterations. The control group received only home cleaning information. We measured children's total and allergen-specific serum immunoglobulin E, peripheral blood eosinophil counts, and urinary cotinine. Environmental dust samples were analyzed for dust mite, cockroach, rodent urinary protein, endotoxin, and fungi. The follow-up period was 1 year. RESULTS: Children in both groups showed improvement in asthma symptomatic days during the preremediation portion of the study. The remediation group had a significant decrease in symptom days (p = 0.003, as randomized; p = 0.004, intent to treat) after remodeling, whereas these parameters in the control group did not significantly change. In the postremediation period, the remediation group had a lower rate of exacerbations compared with control asthmatics (as treated: 1 of 29 vs. 11 of 33, respectively, p = 0.003; intent to treat: 28.1% and 10.0%, respectively, p = 0.11). CONCLUSION: Construction remediation aimed at the root cause of moisture sources and combined with a medical/behavioral intervention significantly reduces symptom days and health care use for asthmatic children who live in homes with a documented mold problem.	Case Western Reserve Univ, Dept Pediat, Rainbow Babies & Childrens Hosp, Cleveland, OH 44106 USA; Cuyahoga Cty Board Hlth, Parma, OH USA; Environm Hlth Watch, Cleveland, OH USA; US EPA, Natl Environm Res Lab, Cincinnati, OH 45268 USA	Kercsmar, CM (reprint author), Case Sch Med, Dept Pediat, 11100 Euclid Ave, Cleveland, OH 44106 USA.	carolyn.kercsmar@uhhs.com			NCRR NIH HHS [M01 RR000080, M01 RR00080]		Asmussen L, 1999, PEDIATRICS, V104, part. no., DOI 10.1542/peds.104.6.e71; Belanger K, 2003, AM J EPIDEMIOL, V158, P195, DOI 10.1093/aje/kwg148; Crain EF, 2002, ENVIRON HEALTH PERSP, V110, P939; Daisey JM, 2003, INDOOR AIR, V13, P53, DOI 10.1034/j.1600-0668.2003.00153.x; Dales RE, 1999, ENVIRON HEALTH PERSP, V107, P481; Eggleston PA, 1999, J ALLERGY CLIN IMMUN, V104, P842; Engvall K, 2001, INT J TUBERC LUNG D, V5, P468; *ENV HLTH WATCH, 2005, CONTR ASTHM TRIGG HO; Evans R, 1999, J PEDIATR-US, V135, P332, DOI 10.1016/S0022-3476(99)70130-7; Gergen PJ, 1999, J ALLERGY CLIN IMMUN, V103, P501, DOI 10.1016/S0091-6749(99)70477-X; Institute of Medicine of the National Academies, 2004, DAMP IND SPAC HLTH; Jaakkola JJK, 2005, ENVIRON HEALTH PERSP, V113, P357, DOI 10.1289/ehp.7242; Kattan M, 1997, PEDIATR PULM, V24, P253, DOI 10.1002/(SICI)1099-0496(199710)24:4<253::AID-PPUL4>3.0.CO;2-L; Mannino D. 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Health Perspect.	OCT	2006	114	10					1574	1580		10.1289/ehp.8742		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	090RW	WOS:000240969700036	17035145	
J	Salo, PM; Arbes, SJ; Sever, M; Jaramillo, R; Cohn, RD; London, SJ; Zeldin, DC				Salo, Paivi M.; Arbes, Samuel J., Jr.; Sever, Michelle; Jaramillo, Renee; Cohn, Richard D.; London, Stephanie J.; Zeldin, Darryl C.			Exposure to Alternaria alternata in US homes is associated with asthma symptoms	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						alternaria alternata; fungal allergen; antigen; indoor; exposure; asthma; allergy	NUTRITION EXAMINATION SURVEY; FUNGAL ALLERGENS; INDOOR ALLERGENS; NATIONAL-HEALTH; AIRBORNE FUNGI; RISK-FACTOR; CHILDREN; OUTDOOR; SPORES; RHINITIS	Background: Exposure to the fungus Alternaria alternata is a risk factor for asthma. Few studies have examined Alternaria exposures in indoor environments. Objective: We examined whether exposure to A alternata in US homes was associated with asthma-related outcomes. Methods: The data for this study were collected as part of the National Survey of Lead and Allergens in Housing. This cross-sectional study surveyed a nationally representative sample of 831 housing units inhabited by 2456 individuals in 75 different locations throughout the United States. An interviewer-administered questionnaire obtained information on demographics, household characteristics, and occupants' health status. Exposure to A alternata was assessed by measuring concentrations of A alternata antigens in vacuumed dust samples using a polyclonal anti-A alternata antibody assay. Dust samples were collected from a bed, a sofa, or a chair, and from bedroom, living room, and kitchen floors. Results: Lifetime prevalence of doctor-diagnosed asthma was 11.2%, and 6.9% of the study subjects reported active asthma symptoms in the past 12 months. The prevalence of current symptomatic asthma increased with increasing Alternaria concentrations in US homes; higher levels of A alternata antigens increased the odds of having asthma symptoms in the past year (relative to the lowest tertile, adjusted odds ratio was 1.52, 95% CI, 0.90-2.55 for the 2nd tertile; and 1.84, 95% Cl, 1.18-2.85 for the 3rd tertile). Conclusion: Exposure to A alternata in US homes is associated with active asthma symptoms. Clinical implications: Measures that reduce indoor exposure to A alternata may help control asthma exacerbations.	NIH, NIEHS, Res Triangle Pk, NC 27709 USA; Constella Grp LLC, Durham, NC USA	Zeldin, DC (reprint author), NIH, NIEHS, 111 Alexander Dr,Mail Drop D2-01, Res Triangle Pk, NC 27709 USA.	zeldin@niehs.nih.gov		Sever, Michelle/0000-0002-2435-1214; London, Stephanie/0000-0003-4911-5290	Intramural NIH HHS [Z01 ES025041-10]		Andersson M, 2003, PEDIATR ALLERGY IMMU, V14, P100, DOI 10.1034/j.1399-3038.2003.00031.x; Arbes SJ, 2005, J ALLERGY CLIN IMMUN, V116, P133, DOI 10.1016/j.jaci.2005.04.022; Arbes SJ, 2005, J ALLERGY CLIN IMMUN, V116, P377, DOI 10.1016/j.jaci.2005.05.017; Barnes C, 2001, ANN ALLERG ASTHMA IM, V86, P517; Barnes C, 2000, ANN ALLERG ASTHMA IM, V84, P47, DOI 10.1016/S1081-1206(10)62740-8; Berger WE, 2003, ANN ALLERG ASTHMA IM, V90, P7; Black PN, 2000, ALLERGY, V55, P501, DOI 10.1034/j.1398-9995.2000.00293.x; Britton J, 1998, CLIN EXP ALLERGY, V28, P2; Burge HA, 2000, ENVIRON HEALTH PERSP, V108, P653, DOI 10.2307/3454401; Bush RK, 2004, J ALLERGY CLIN IMMUN, V113, P227, DOI 10.1016/j.jaci.2003.11.023; Bush R., 2001, J ALLERGY CLIN IMMUN, V107, P430, DOI 10.1067/mai.2001.113669; *CDCP, 2005, ASTHM NAT HLTH INT S; Chapman MD, 2000, CLIN REV ALLERG IMMU, V18, P285, DOI 10.1385/CRIAI:18:3:285; *COMM ASS ASTHM IN, 2000, CLEAR AIR ASTHM IND, P105; Corden JM, 2001, AEROBIOLOGIA, V17, P127, DOI 10.1023/A:1010876917512; Delfino RJ, 1997, ENVIRON HEALTH PERSP, V105, P622; Dharmage S, 1999, CLIN EXP ALLERGY, V29, P1481, DOI 10.1046/j.1365-2222.1999.00640.x; Downs SH, 2001, AM J RESP CRIT CARE, V164, P455; Eggleston PA, 1998, J ALLERGY CLIN IMMUN, V102, P563, DOI 10.1016/S0091-6749(98)70272-6; Garrett MH, 1998, CLIN EXP ALLERGY, V28, P459; GERGEN PJ, 1992, J ALLERGY CLIN IMMUN, V90, P579, DOI 10.1016/0091-6749(92)90130-T; Green BJ, 2005, J ALLERGY CLIN IMMUN, V115, P1043, DOI 10.1016/j.jaci.2005.02.009; Green BJ, 2003, J ALLERGY CLIN IMMUN, V111, P285, DOI 10.1067/mai.2003.57; Greisner WA, 1998, ALLERGY ASTHMA PROC, V19, P271, DOI 10.2500/108854198778557728; Halonen M, 1997, AM J RESP CRIT CARE, V155, P1356; HORNER WE, 1995, CLIN MICROBIOL REV, V8, P161; Instanes C, 2004, CLIN EXP ALLERGY, V34, P1634, DOI 10.1111/j.1365-2222.2004.02076.x; Kauffman HF, 2000, J ALLERGY CLIN IMMUN, V105, P1185, DOI 10.1067/mai.2000.106210; Leech JA, 2002, J EXPO ANAL ENV EPID, V12, P427, DOI 10.1038/sj.jea.7500244; LICORISH K, 1985, J ALLERGY CLIN IMMUN, V76, P819, DOI 10.1016/0091-6749(85)90755-9; Mitakakis TZ, 2000, CLIN EXP ALLERGY, V30, P1733, DOI 10.1046/j.1365-2222.2000.00966.x; Neukirch C, 1999, J ALLERGY CLIN IMMUN, V103, P709, DOI 10.1016/S0091-6749(99)70247-2; O'Connor GT, 2004, J ALLERGY CLIN IMMUN, V114, P599, DOI 10.1016/j.jaci.2004.05.064; OHOLLAREN MT, 1991, NEW ENGL J MED, V324, P359, DOI 10.1056/NEJM199102073240602; Perzanowski MS, 1998, J ALLERGY CLIN IMMUN, V101, P626; Platts-Mills TAE, 2004, J ALLERGY CLIN IMMUN, V113, P388, DOI 10.1016/j.jaci.2003.12.027; PORTNOY J, 1993, J ALLERGY CLIN IMMUN, V91, P773, DOI 10.1016/0091-6749(93)90197-N; Portnoy JM, 2005, ANN ALLERG ASTHMA IM, V94, P313; Portnoy JM, 2004, J ALLERGY CLIN IMMUN, V113, P189, DOI 10.1016/j.jaci.2003.11.021; Ren P, 1999, J EXPO ANAL ENV EPID, V9, P560, DOI 10.1038/sj.jea.7500061; Salo PM, 2005, J ALLERGY CLIN IMMUN, V116, P623, DOI 10.1016/j.jaci.2005.05.030; Schmechel D, 2005, INDOOR AIR, V15, P11, DOI 10.1111/j.1600-0668.2005.00340.x; Shelton BG, 2002, APPL ENVIRON MICROB, V68, P1743, DOI 10.1128/AEM.68.4.1743-1753.2002; Stark PC, 2005, ENVIRON HEALTH PERSP, V113, P1405, DOI 10.1289/ehp.7844; Sterling DA, 1998, ANN ALLERG ASTHMA IM, V80, P279; Vailes L, 2001, J ALLERGY CLIN IMMUN, V107, P641, DOI 10.1067/mai.2001.114118; Vojta PJ, 2002, ENVIRON HEALTH PERSP, V110, P527	47	108	111	0	11	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	OCT	2006	118	4					892	898		10.1016/j.jaci.2006.07.037		7	Allergy; Immunology	Allergy; Immunology	097GD	WOS:000241434200017	17030243	
J	Mondoulet, L; Paty, E; Drumare, MF; Ah-Leung, S; Scheinmann, P; Willemot, RM; Wal, JM; Bernard, H				Mondoulet, L; Paty, E; Drumare, MF; Ah-Leung, S; Scheinmann, P; Willemot, RM; Wal, JM; Bernard, H			Influence of thermal processing on the allergenicity of peanut proteins	JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY			English	Article						thermal processing; peanut allergens; allergenicity	CONTROLLED FOOD CHALLENGE; ATOPIC-DERMATITIS; DOUBLE-BLIND; IGE-BINDING; ALLERGY; IDENTIFICATION; COOKING; UPDATE	Peanuts are one of the most common and severe food allergens. Nevertheless, the occurrence of peanut allergy varies between countries and depends on both the exposure and the way peanuts are consumed. Processing is known to influence the allergenicity of peanut proteins. The aim of this study was to assess the effect of thermal processing on the IgE-binding capacity of whole peanut protein extracts and of the major peanut allergens Ara h 1 and Ara h 2. Whole proteins, Ara h 1, and Ara h 2 were extracted and purified from raw, roasted and boiled peanuts using selective precipitation and multiple chromatographic steps, and were then characterized by electrophoresis and mass spectrometry. The immunoreactivity of whole peanut extracts and purified proteins was analyzed by the enzyme allergosorbent test (EAST) and EAST inhibition using the sera of 37 peanut-allergic patients. The composition of the whole protein extracts was modified after heat processing, especially after boiling. The electrophoretic pattern showed protein bands of low molecular weight that were less marked in boiled than in raw and roasted peanuts. The same low-molecular-weight proteins were found in the cooking water of peanuts. Whole peanut protein extracts obtained after the different processes were all recognized by the IgE of the 37 patients. The IgE-binding capacity of the whole peanut protein extracts prepared from boiled peanuts was 2-fold lower than that of the extracts prepared from raw and roasted peanuts. No significant difference was observed between protein extracts from raw and roasted peanuts. It is noteworthy that the proteins present in the cooking water were also recognized by the IgE of peanut-allergic patients. IgE immunoreactivity of purified Ara h 1 and Ara h 2 prepared from roasted peanuts was higher than that of their counterparts prepared from raw and boiled peanuts. The IgE-binding capacity of purified Ara h 1 and Ara h 2 was altered by heat treatment and in particular was increased by roasting. However, no significant difference in IgE immunoreactivity was observed between whole protein extracts from raw and roasted peanuts. The decrease in allergenicity of boiled peanuts results mainly from a transfer of low-molecular-weight allergens into the water during cooking.	CEA Saclay, SPI, INRA, Lab Immunoallergie Alimentaire, F-91191 Gif Sur Yvette, France; Grp Hop Necker, Serv Pneumol & Allergol Pediat, F-75743 Paris, France; INRA, CNRS, UMR 5504, Dept Genie Biochim & Alimentaire,Ctr Bioingn Gilb, F-31077 Toulouse, France	Mondoulet, L (reprint author), CEA Saclay, SPI, INRA, Lab Immunoallergie Alimentaire, F-91191 Gif Sur Yvette, France.	mondoulet@cea.fr	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Bannon G. A., 2000, INTERNET S FOOD ALLE, V2, P87; Bernard H, 2003, ALLERGY, V58, P1285, DOI 10.1046/j.1398-9995.2003.00300.x; Beyer KB, 2001, J ALLERGY CLIN IMMUN, V107, P1077, DOI 10.1067/mai.2001.115480; BURKS AW, 1992, J ALLERGY CLIN IMMUN, V90, P962, DOI 10.1016/0091-6749(92)90469-I; BURKS AW, 1991, J ALLERGY CLIN IMMUN, V88, P172, DOI 10.1016/0091-6749(91)90325-I; CARUELLE D, 1988, ANAL BIOCHEM, V173, P328, DOI 10.1016/0003-2697(88)90197-2; Chung SY, 2003, J AGR FOOD CHEM, V51, P4273, DOI 10.1021/jf02121d; Davis PJ, 1998, ALLERGY, V53, P102; Dean TP, 1996, PEDIATR ALLERGY IMMU, V7, P171, DOI 10.1111/j.1399-3038.1996.tb00128.x; GRASSI J, 1986, J ALLERGY CLIN IMMUN, V77, P808, DOI 10.1016/0091-6749(86)90378-7; Hansen KS, 2003, ALLERGY, V58, P132, DOI 10.1034/j.1398-9995.2003.23959.x; LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0; Maleki S. J., 2004, Journal of Allergy and Clinical Immunology, V113, pS154, DOI 10.1016/j.jaci.2003.12.561; Maleki SJ, 2000, J ALLERGY CLIN IMMUN, V106, P763, DOI 10.1067/mai.2000.109620; Maleki SJ, 2003, J ALLERGY CLIN IMMUN, V112, P190, DOI 10.1067/mai.2003.1551; Pastorello E., 2004, EFSA J, V34, P76; Pastorello EA, 2003, J ALLERGY CLIN IMMUN, V112, P775, DOI 10.1067/mai.2003.1748; Sampson HA, 1999, J ALLERGY CLIN IMMUN, V103, P717, DOI 10.1016/S0091-6749(99)70411-2; Sampson HA, 2004, J ALLERGY CLIN IMMUN, V113, P805, DOI 10.1016/j.jaci.2004.03.014; Schocker F, 2000, EUR J NUTR, V39, P172, DOI 10.1007/s003940070021; SELLERS CL, 2000, J ALLERGY CLIN IMMUN, V105, P140; Sicherer SH, 2002, ANN ALLERG ASTHMA IM, V88, P350; Sicherer SH, 1999, J ALLERGY CLIN IMMUN, V103, P559, DOI 10.1016/S0091-6749(99)70224-1; Tariq SM, 1996, BRIT MED J, V313, P514; Wal JM, 2003, ALLERGY, V58, P727, DOI 10.1034/j.1398-9995.2003.00225.x; Wal JM, 1995, FOOD AGRIC IMMUNOL, V7, P175, DOI 10.1080/09540109509354876; Wigotzki M, 2001, J CHROMATOGR B, V756, P239, DOI 10.1016/S0378-4347(01)00084-6	27	108	119	4	28	AMER CHEMICAL SOC	WASHINGTON	1155 16TH ST, NW, WASHINGTON, DC 20036 USA	0021-8561			J AGR FOOD CHEM	J. Agric. Food Chem.	JUN 1	2005	53	11					4547	4553		10.1021/jf050091p		7	Agriculture, Multidisciplinary; Chemistry, Applied; Food Science & Technology	Agriculture; Chemistry; Food Science & Technology	930GX	WOS:000229405000036	15913323	
J	Zutavern, A; von Mutius, E; Harris, J; Mills, P; Moffatt, S; White, C; Cullinan, P				Zutavern, A; von Mutius, E; Harris, J; Mills, P; Moffatt, S; White, C; Cullinan, P			The introduction of solids in relation to asthma and eczema	ARCHIVES OF DISEASE IN CHILDHOOD			English	Article							FOLLOW-UP; INFANT DIET; CHILDREN; ATOPY; LIFE; SENSITIZATION; COHORT; RISK; FOOD; AGE	Background: Despite scarce scientific evidence, current feeding guidelines recommend delayed introduction of solids for the prevention of asthma and allergy. Aims: To explore whether late introduction of solids is protective against the development of asthma, eczema, and atopy. Methods: A total of 642 children were recruited before birth and followed to the age of 5 1/2 years. Main outcome measures were: doctor's diagnosis of eczema ever, atopy according to skin prick test results against inhalant allergens, preschool wheezing, transient wheezing, all defined at age 5 - 5 1/2 years. Introduction of solids as main exposure measure was assessed retrospectively at age 1 year. Results: There was no evidence for a protective effect of late introduction of solids for the development of preschool wheezing, transient wheezing, atopy, or eczema. On the contrary, there was a statistically significant increased risk of eczema in relation to late introduction of egg (aOR 1.6, 95% CI 1.1 to 2.4) and milk (aOR 1.7, 95% CI 1.1 to 2.5). Late introduction of egg was furthermore associated with a nonsignificant increased risk of preschool wheezing (aOR 1.5, 95% CI 0.92 to 2.4). There was no statistical evidence of feeding practices playing a different role in the development of asthma and eczema after stratification for parental asthma and atopy status. Conclusions: Results do not support the recommendations given by present feeding guidelines stating that a delayed introduction of solids is protective against the development of asthma and allergy.	Univ Childrens Hosp, Dr Von Haunerschen Kinderspital, D-80337 Munich, Germany; Natl Heart & Lung Inst, Imperial Coll Sci & Technol, Dept Occupat & Environm Med, London SW3 6LR, England	Zutavern, A (reprint author), Univ Munich, Dr Von Haunerschen Kinderspital, Lindwurmstr 4, D-80337 Munich, Germany.	anne.zutavern@kk-i.med.uni-muenchen.de					*DGKJ, 2002, LEITL KIND JUG MED, pD11; FERGUSSON DM, 1990, PEDIATRICS, V86, P541; FERGUSSON DM, 1983, ARCH DIS CHILD, V58, P48; FORSYTH JS, 1993, BRIT MED J, V306, P1572; Harris JM, 2001, BRIT J DERMATOL, V144, P795, DOI 10.1046/j.1365-2133.2001.04135.x; Illi S, 2001, J ALLERGY CLIN IMMUN, V108, P709, DOI 10.1067/mai.2001.118786; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Martinez FD, 2002, PEDIATRICS, V109, P362; Nickel R, 1997, J ALLERGY CLIN IMMUN, V99, P613, DOI 10.1016/S0091-6749(97)70021-6; Office for National Statistics, 1990, STAND OCC CLASS; PEAT JK, 1990, J ALLERGY CLIN IMMUN, V85, P65, DOI 10.1016/0091-6749(90)90223-Q; Rhodes HL, 2002, AM J RESP CRIT CARE, V165, P176; *SCHWEIZ GES PAED, 1998, EMPF SAEUGL, V79, P1143; Sears MR, 2002, LANCET, V360, P901, DOI 10.1016/S0140-6736(02)11025-7; *STAT JOINT WORK G, 1998, DIET CAN HLTH CAN NU; von Berg A, 2003, J ALLERGY CLIN IMMUN, V111, P533, DOI 10.1067/mai.2003.101; Wilson AC, 1998, BRIT MED J, V316, P21; ZEIGER RS, 1995, J ALLERGY CLIN IMMUN, V95, P1179, DOI 10.1016/S0091-6749(95)70074-9; 2001, BMJ, V322, P1266	19	108	119	0	4	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0003-9888			ARCH DIS CHILD	Arch. Dis. Child.	APR 1	2004	89	4					303	308		10.1136/adc.2002.025353		6	Pediatrics	Pediatrics	805AX	WOS:000220340300006	15033835	
J	Taylor, PE; Flagan, RC; Valenta, R; Glovsky, MM				Taylor, PE; Flagan, RC; Valenta, R; Glovsky, MM			Release of allergens as respirable aerosols: A link between grass pollen and asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						grass; pollen; allergen; aerosol; asthma; air pollution	RYE-GRASS; ENVIRONMENTAL-FACTORS; DIESEL EXHAUST; AIR-POLLUTION; CITY; PARTICLES; MELBOURNE; WEATHER; RISK	Background: Asthma incidence has long been linked to pollen, even though pollen grains are too large to penetrate into the airways where asthmatic responses originate. Pollen allergens found in small, respirable particles have been implicated in a number of asthma epidemics, particularly ones following rainfall or thunderstorms. Objective: The aim of this study was to determine how pollen allergens form the respirable aerosols necessary for triggering asthma. Methods: Flowering grasses were humidified and then dried in a controlled-environment chamber connected to a cascade impactor and an aerosol particle counter. Particles shed from the flowers were analyzed with high-resolution microscopy and immunolabeled with rabbit anti-Phl p 1 antibody, which is specific for group 1 pollen allergens. Results: Contrary to what has been reported in other published accounts, most of the pollen in this investigation remained on the open anthers of wind pollinated plants unless disturbed-eg, by wind. Increasing humidity caused anthers to close. After a cycle of wetting and drying followed by wind disturbance, grasses flowering within a chamber produced an aerosol of particles that were collected in a cascade impactor. These particles consisted of fragmented pollen cytoplasm in the size range 0.12 to 4.67 mum; they were loaded with group I allergens. Conclusion: Here we provide the first direct observations of the release of grass pollen allergens as respirable aerosols. They can emanate directly from the flower after a moisture-drying cycle. This could explain asthmatic responses associated with grass pollination, particularly after moist weather conditions.	CALTECH, Div Chem & Chem Engn, Pasadena, CA 91125 USA; Huntington Mem Hosp, Huntington Med Res Inst, Ctr Asthma & Allergy, Pasadena, CA USA; Univ Vienna, Dept Pathophysiol, A-1010 Vienna, Austria	Flagan, RC (reprint author), CALTECH, Div Chem & Chem Engn, 210-41, Pasadena, CA 91125 USA.						ARBER A., 1934, GRAMINEAE; Bates D V, 1966, Health Phys, V12, P173; Bayram H, 1998, J ALLERGY CLIN IMMUN, V102, P771, DOI 10.1016/S0091-6749(98)70017-X; BELLOMO R, 1992, MED J AUSTRALIA, V156, P834; Blackley CH, 1873, EXPT RES CAUSES NATU; Crane P. R., 1986, POLLEN SPORES FORM F, P179; D'Amato G, 2000, J INVEST ALLERG CLIN, V10, P123; Davies RJ, 1998, CLIN EXP ALLERGY, V28, P8; Diaz-Sanchez D, 2000, J ALLERGY CLIN IMMUN, V106, P1140, DOI 10.1067/mai.2000.111144; Downs SH, 2001, ARCH DIS CHILD, V84, P20, DOI 10.1136/adc.84.1.20; EDWARDS J, 1992, AM J BOT, V79, P144, DOI 10.2307/2445101; Foster AS, 1974, COMP MORPHOLOGY VASC; Girgis ST, 2000, EUR RESPIR J, V16, P3, DOI 10.1034/j.1399-3003.2000.16a02.x; Grote M, 2000, J ALLERGY CLIN IMMUN, V105, P1140, DOI 10.1067/mai.2000.107044; Haberlandt G, 1914, PHYSL PLANT ANATOMY; HILL DJ, 1979, MED J AUSTRALIA, V1, P426; KNOX RB, 1981, P 6 AUSTR WEEDS C 19, V2, P125; Knox R. B., 1979, STUDIES BIOL, V107; Lindon JC, 1996, PROG NUCL MAG RES SP, V29, P1, DOI 10.1016/0079-6565(95)01027-0; Marks GB, 2001, THORAX, V56, P468, DOI 10.1136/thorax.56.6.468; Miyabara Y, 1998, J ALLERGY CLIN IMMUN, V102, P805, DOI 10.1016/S0091-6749(98)70021-1; Nel AE, 1998, J ALLERGY CLIN IMMUN, V102, P539, DOI 10.1016/S0091-6749(98)70269-6; Newson R, 1997, THORAX, V52, P680; ONG EK, 1994, THESIS U MELBOURNE; PACINI E, 1992, ANN BOT-LONDON, V70, P179; PACINI E, 1982, CARYOLOGIA, V35, P205; Rosas I, 1998, ALLERGY, V53, P394, DOI 10.1111/j.1398-9995.1998.tb03911.x; Schappi GF, 1999, CLIN EXP ALLERGY, V29, P633; Schauer JJ, 1996, ATMOS ENVIRON, V30, P3837, DOI 10.1016/1352-2310(96)00085-4; SMART IJ, 1979, AUST J BOT, V27, P333, DOI 10.1071/BT9790333; SPIEKSMA FTM, 1995, CLIN EXP ALLERGY, V25, P234, DOI 10.1111/j.1365-2222.1995.tb01034.x; SPIEKSMA FTM, 1990, CLIN EXP ALLERGY, V20, P273, DOI 10.1111/j.1365-2222.1990.tb02683.x; STEWART GA, 1985, MED J AUSTRALIA, V143, P426; SUPHIOGLU C, 1992, LANCET, V339, P569, DOI 10.1016/0140-6736(92)90864-Y; TAYLOR PE, 1994, HISTOCHEM J, V26, P392, DOI 10.1007/BF00160051; Venables KM, 1997, CLIN EXP ALLERGY, V27, P725, DOI 10.1046/j.1365-2222.1997.790893.x; WILSON AF, 1973, NEW ENGL J MED, V288, P1056, DOI 10.1056/NEJM197305172882006; WUTHRICH B, 1991, ALLERGY CLIN IMMUNOL, V3, P41	38	108	108	10	30	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JAN	2002	109	1					51	56		10.1067/mai.2002.120759		6	Allergy; Immunology	Allergy; Immunology	519RM	WOS:000173739300008	11799365	
J	Yunginger, JW; Ahlstedt, S; Eggleston, PA; Homburger, HA; Nelson, HS; Ownby, DR; Platts-Mills, TAE; Sampson, HA; Sicherer, SH; Weinstein, AM; Williams, PB; Wood, RA; Zeiger, RS				Yunginger, JW; Ahlstedt, S; Eggleston, PA; Homburger, HA; Nelson, HS; Ownby, DR; Platts-Mills, TAE; Sampson, HA; Sicherer, SH; Weinstein, AM; Williams, PB; Wood, RA; Zeiger, RS			Quantitative IgE antibody assays in allergic diseases	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						IgE antibody; quantitative immunoassay; allergic disease	SKIN-TEST REACTIVITY; HIGH-RISK CHILDREN; ATOPIC-DERMATITIS; PERFORMANCE-CHARACTERISTICS; FOOD ALLERGENS; EGG ALLERGY; FOLLOW-UP; SENSITIZATION; DIAGNOSIS; ASTHMA	During the past several years, immunoassays for specific IgE antibodies have been refined to permit reporting results in mass units. Thus quantitative immunoassays for IgE antibodies may be an adjunct to skin tests. In cases of food allergy among children with atopic dermatitis, cutoff values for IgE antibody concentrations to egg, milk, peanut, and fish have been derived to provide 95% positive and 90% negative predictive values. Food-specific IgE antibody determinations can also be used to predict which food allergies are resolving spontaneously. Elevated egg-specific IgE antibody levels in infancy are associated with significantly increased risk for development of inhalant allergies later in childhood. In cases of inhalant allergy, specific IgE antibody levels correlate closely with results of inhalation challenge studies in cat-sensitive persons. Also, mite-specific IgE antibody levels correlate significantly with the mite allergen contents of reservoir dust in the homes of mite-sensitive persons. Immunoassays for quantitation of specific IgE antibodies may be used to document allergen sensitization over time and to evaluate the risk of reaction on allergen exposure. However, immunoassays and skin tests are not entirely interchangeable, and neither will replace the other in appropriate circumstances.	Mayo Clin & Mayo Fdn, Allerg Dis Res Lab, Rochester, MN 55905 USA; Mayo Clin & Mayo Fdn, Dept Lab Med & Pathol, Rochester, MN 55905 USA; Univ Gothenburg, Dept Clin Immunol, Gothenburg, Sweden; Pharmacia & Upjohn Diagnost, Kalamazoo, MI USA; Johns Hopkins Univ, Dept Pediat, Baltimore, MD 21218 USA; Natl Jewish Med & Res Ctr, Denver, CO USA; Med Coll Georgia, Sect Allergy Immunol, Augusta, GA 30912 USA; Univ Virginia, Hlth Sci Ctr, Dept Med, Div Asthma Allergy & Immunol, Charlottesville, VA USA; Mt Sinai Sch Med, Jaffe Food Allergy Inst, New York, NY USA; Georgetown Univ, Sch Med, Washington, DC USA; Univ Missouri Kansas City, Sch Med, IBT Reference Lab, Lenexa, KS USA; So Calif Permanente Med Grp, Dept Allergy, San Diego, CA 92120 USA	Yunginger, JW (reprint author), Mayo Clin & Mayo Fdn, Allerg Dis Res Lab, 406 Guggenheim Bldg,200 1st St SW, Rochester, MN 55905 USA.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			ADINOFF AD, 1990, J ALLERGY CLIN IMMUN, V86, P766, DOI 10.1016/S0091-6749(05)80181-2; AGATA H, 1993, J ALLERGY CLIN IMMUN, V91, P668, DOI 10.1016/0091-6749(93)90273-I; Bernardini R, 1999, CLIN EXP ALLERGY, V29, P681; BERNHISELBROADBENT J, 1994, J ALLERGY CLIN IMMUN, V93, P1047, DOI 10.1016/S0091-6749(94)70054-0; BONER AL, 1993, CLIN EXP ALLERGY, V23, P1021, DOI 10.1111/j.1365-2222.1993.tb00294.x; BROWN WG, 1979, J ALLERGY CLIN IMMUN, V63, P328, DOI 10.1016/0091-6749(79)90127-1; Brunnee T, 1996, CLIN EXP ALLERGY, V26, P1420; Burr ML, 1997, CLIN EXP ALLERGY, V27, P1247; COSTONGS GMPJ, 1995, EUR J CLIN CHEM CLIN, V33, P295; CRESPO JF, 1994, ALLERGY PROC, V15, P73, DOI 10.2500/108854194778703099; Croner S, 1990, PEDIATR ALLERGY IMMU, V1, P14, DOI 10.1111/j.1399-3038.1990.tb00003.x; DANTZLER BS, 1980, ANN ALLERGY, V45, P213; DELOVINFOSSE S, 1994, ALLERGY, V49, P64; Des Roches A., 1996, Allergy (Copenhagen), V51, P430; Halonen M, 1997, AM J RESP CRIT CARE, V155, P1356; Hamilton RG, 1999, J ALLERGY CLIN IMMUN, V103, pS52; HATTEVIG G, 1987, CLIN ALLERGY, V17, P571, DOI 10.1111/j.1365-2222.1987.tb02053.x; Hide DW, 1996, ALLERGY, V51, P89, DOI 10.1111/j.1398-9995.1996.tb04563.x; JAMES JM, 1992, J PEDIATR-US, V121, P371, DOI 10.1016/S0022-3476(05)81788-3; KELSO JM, 1991, ANN ALLERGY, V67, P511; Kulig M, 1998, PEDIAT ALLERG IMM-UK, V9, P61, DOI 10.1111/j.1399-3038.1998.tb00305.x; Kulig M, 1998, CLIN EXP ALLERGY, V28, P1397, DOI 10.1046/j.1365-2222.1998.00439.x; LEIMGRUBER A, 1993, ALLERGY, V48, P415, DOI 10.1111/j.1398-9995.1993.tb00739.x; LIAPPIS N, 1996, CLIN LAB, V42, P707; LILJA G, 1991, PEDIATR ALLERGY IMMU, V2, P6, DOI 10.1111/j.1399-3038.1991.tb00173.x; LINDQVIST A, 1995, P 16 EUR C ALL CLIN, P195; Nelson HS, 1998, J ALLERGY CLIN IMMUN, V101, P153; Nelson HS, 1996, J ALLERGY CLIN IMMUN, V97, P1193, DOI 10.1016/S0091-6749(96)70184-7; Nickel R, 1997, J ALLERGY CLIN IMMUN, V99, P613, DOI 10.1016/S0091-6749(97)70021-6; Nishioka K, 1998, J ALLERGY CLIN IMMUN, V101, P28, DOI 10.1016/S0091-6749(98)70189-7; NORMAN PS, 1981, J ALLERGY CLIN IMMUN, V68, P460, DOI 10.1016/0091-6749(81)90200-1; OHOLLAREN MT, 1991, NEW ENGL J MED, V324, P359, DOI 10.1056/NEJM199102073240602; Paganelli R, 1998, ALLERGY, V53, P763; PASTORELLO EA, 1995, J ALLERGY CLIN IMMUN, V96, P580, DOI 10.1016/S0091-6749(95)70255-5; Peat JK, 1999, J ALLERGY CLIN IMMUN, V103, P1, DOI 10.1016/S0091-6749(99)70517-8; Perzanowski MS, 1998, J ALLERGY CLIN IMMUN, V101, P626; Peterman J. H., 1991, IMMUNOCHEMISTRY SOLI, P47; *PHS, REV CRIT ASS ALL SPE, P1; SAMPSON HA, 1989, J PEDIATR-US, V115, P23, DOI 10.1016/S0022-3476(89)80323-3; Sampson HA, 1997, J ALLERGY CLIN IMMUN, V100, P444; Sanz ML, 1996, J INVEST ALLERG CLIN, V6, P89; SENSI LG, 1994, CLIN EXP ALLERGY, V24, P377, DOI 10.1111/j.1365-2222.1994.tb00250.x; Sicherer SH, 1999, CLIN EXP ALLERGY, V29, P507; SICHERER SH, 1998, PEDIATRICS, V102, P131; STRUCKEY MS, 1985, J ALLERGY CLIN IMMUN, V75, P373; Williams PB, 2000, J ALLERGY CLIN IMMUN, V105, P1221, DOI 10.1067/mai.2000.105219; Wood RA, 1999, J ALLERGY CLIN IMMUN, V103, P773, DOI 10.1016/S0091-6749(99)70419-7; ZEIGER RS, 1995, J ALLERGY CLIN IMMUN, V95, P1179, DOI 10.1016/S0091-6749(95)70074-9; 1992, FED REG 405, V57, P7002	49	108	114	0	7	MOSBY-YEAR BOOK INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUN	2000	105	6	1				1077	1084		10.1067/mai.2000.107041		8	Allergy; Immunology	Allergy; Immunology	327EX	WOS:000087781800006	10856139	
J	Andre, C; Vatrinet, C; Galvain, S; Carat, F; Sicard, H				Andre, C; Vatrinet, C; Galvain, S; Carat, F; Sicard, H			Safety of sublingual-swallow immunotherapy in children and adults	INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY			English	Article						immunotherapy, sublingual-swallow; asthma; rhinoconjunctivitis; mites; pollen	PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND PLACEBO; HOUSE-DUST MITE; POLLEN EXTRACT; RHINITIS; RHINOCONJUNCTIVITIS; EFFICACY; ASTHMA	Background: Immunotherapy is an established treatment of allergic diseases. The safety of this treatment, particularly when administered without direct medical surveillance, as in the case of the sublingual-swallow route needs to be established. The aim of this paper is to review the safety of the sublingual-swallow immunotherapy as reported in eight double-blind, placebo-controlled trials carried out in France, Italy and Greece. Methods: Six hundred and ninety subjects, 472 adults and 218 children, took part in trials of specific immunotherapy (SIT) for the treatment of rhinoconjunctivitis and/or asthma. Three hundred and forty-seven patients received SIT and 343 patients received placebo. Treatment with specific immunotherapy with allergen extracts or placebo was administered using the sublingual-swallow technique. The allergens administered were grass, ambrosia, parietaria and olive pollens, and mites. The daily dose taken during maintenance therapy ranged from 100 to 300 IR (index of reactivity) and cumulative doses ranged from 4,500 to 104,000 IR. Treatment duration ranged from 4 months to 2 years. Adverse events reported either spontaneously by the patient or on direct questioning by the investigator were analysed. Results: One hundred and forty-five unusual events were reported in the subjects receiving active SIT and 79 in those receiving placebo (p < 0.001). Of these 85 were children aged 15 years or less (50 received active SIT, 35 placebo) and 139 were adults (95 received SIT, 44 placebo). Unusual events involving the buccal cavity (61 SIT, 13 placebo) and the gastro-intestinal tract (47 SIT, 15 placebo) were significantly more frequent in the SIT-treated patients (p < 0.001). Wheezing (9 SIT, 21 placebo) was more frequent in the placebo-treated patients (p < 0.05). There were no differences in the frequency of unusual events between adults and children and in the frequency of events involving other body systems. No event was reported as serious. Two events reported as laryngeal oedema were not considered to be accurate descriptions. Conclusions: No serious adverse event was reported in the studies monitored, confirming the good safety profile of the sublingual-swallow method both in children and adults with rhinitis or moderate asthma. (C) 2000 S. Karger AG, Basel.	Stallergenes SA, Sci & Med Dept, F-92183 Antony, France	Andre, C (reprint author), Stallergenes SA, Sci & Med Dept, 6 Rue Alexis de Tocqueville, F-92183 Antony, France.						Andre C., 1998, Allergy (Copenhagen), V53, P116; ANDRE C, UNPUB RAGWEED SUBLIN; Bousquet J, 1999, ALLERGY, V54, P249, DOI 10.1034/j.1398-9995.1999.00916.x; Bousquet J., 1998, Allergy (Copenhagen), V53, P1; Clavel R, 1998, ALLERGY, V53, P493, DOI 10.1111/j.1398-9995.1998.tb04086.x; Committee on the safety of medicines, 1986, BRIT MED J, V293, P948, DOI 10.1136/bmj.293.6552.948; Di Rienzo V, 1999, ALLERGY, V54, P1110, DOI 10.1034/j.1398-9995.1999.00267.x; Edwards A. M., 1998, Allergy (Copenhagen), V53, P169; Feliziani V, 1995, Allergol Immunopathol (Madr), V23, P224; GUEZ S, IN PRESS ALLERGY; Hirsch T, 1997, PEDIATR ALLERGY IMMU, V8, P21, DOI 10.1111/j.1399-3038.1997.tb00138.x; Horak F, 1998, J INVEST ALLERG CLIN, V8, P165; Hordijk G J, 1998, Allergol Immunopathol (Madr), V26, P234; La Rosa M, 1999, J ALLERGY CLIN IMMUN, V104, P425, DOI 10.1016/S0091-6749(99)70388-X; Malling HJ, 1998, ALLERGY, V53, P461; Malling HJ, 1993, ALLERGY, V14, P9; Passalacqua G, 1998, LANCET, V351, P629, DOI 10.1016/S0140-6736(97)07055-4; Pradalier A, 1999, ALLERGY, V54, P819, DOI 10.1034/j.1398-9995.1999.00077.x; SABBAH A, 1994, ALLERGY, V49, P309, DOI 10.1111/j.1398-9995.1994.tb02273.x; TARI MG, 1990, ALLERGOL IMMUNOPATH, V18, P277; TROISE C, 1995, J INVEST ALLERG CLIN, V5, P25; Vourdas D, 1998, ALLERGY, V53, P662, DOI 10.1111/j.1398-9995.1998.tb03952.x; White P, 1998, CLIN EXP ALLERGY, V28, P266	23	108	112	0	0	KARGER	BASEL	ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND	1018-2438			INT ARCH ALLERGY IMM	Int. Arch. Allergy Immunol.	MAR	2000	121	3					229	234		10.1159/000024322		6	Allergy; Immunology	Allergy; Immunology	298BW	WOS:000086120300008	10729782	
J	Schneider, L; Tilles, S; Lio, P; Boguniewicz, M; Beck, L; LeBovidge, J; Novak, N				Schneider, Lynda; Tilles, Stephen; Lio, Peter; Boguniewicz, Mark; Beck, Lisa; LeBovidge, Jennifer; Novak, Natalija			Atopic dermatitis: A practice parameter update 2012	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Atopic dermatitis/atopic eczema; pathogenesis; genetics; diagnosis; management; therapy; triggers; Staphylococcus; quality of life; sleep; cyclosporine; immunomodulating agents; phototherapy; allergen immunotherapy	PIMECROLIMUS CREAM 1-PERCENT; RANDOMIZED CONTROLLED-TRIAL; LONG-TERM TREATMENT; QUALITY-OF-LIFE; STAPHYLOCOCCUS-AUREUS COLONIZATION; PLACEBO-CONTROLLED TRIAL; ORAL FOOD CHALLENGES; WET-WRAP DRESSINGS; HOUSE-DUST MITE; THIOPURINE METHYLTRANSFERASE ACTIVITY	This parameter was developed by the Joint Task Force on Practice Parameters, representing the American Academy of Allergy, Asthma & Immunology (AAAAI); the American College of Allergy, Asthma & Immunology (ACAAI); and the Joint Council of Allergy, Asthma and Immunology. The AAAAI and the ACAAI have jointly accepted responsibility for establishing "Atopic dermatitis: a practice parameter update 2012.'' This is a complete and comprehensive document at the current time. The medical environment is a changing environment, and not all recommendations will be appropriate for all patients. Because this document incorporated the efforts of many participants, no single individual, including those who served on the Joint Task Force, is authorized to provide an official AAAAI or ACAAI interpretation of these practice parameters. Any request for information about or an interpretation of these practice parameters by the AAAAI or ACAAI should be directed to the Executive Offices of the AAAAI, the ACAAI, and the Joint Council of Allergy, Asthma & Immunology. These parameters are not designed for use by pharmaceutical companies in drug promotion. Published practice parameters of the Joint Task Force on Practice Parameters for Allergy & Immunology are available online at http://www.jcaai.org. (J Allergy Clin Immunol 2013;131:295-9.)	[Schneider, Lynda] Harvard Univ, Sch Med, Boston Childrens Hosp, Dept Pediat, Boston, MA USA; [Lio, Peter] Northwestern Univ, Feinberg Sch Med, Dept Clin Dermatol, Chicago, IL 60611 USA; [Lio, Peter] Northwestern Univ, Feinberg Sch Med, Dept Pediat, Chicago, IL 60611 USA; [Boguniewicz, Mark] Natl Jewish Hlth, Dept Pediat, Denver, CO USA; [Boguniewicz, Mark] Univ Colorado Denver, Sch Med, Denver, CO USA; [Beck, Lisa] Univ Rochester, Med Ctr, Dept Dermatol, Rochester, NY 14642 USA; [LeBovidge, Jennifer] Harvard Univ, Sch Med, Boston Childrens Hosp, Dept Psychol, Boston, MA USA; [Novak, Natalija] Univ Bonn, Dept Dermatol, Bonn, Germany; [Novak, Natalija] Univ Bonn, Dept Allergy, Bonn, Germany; [Tilles, Stephen] Univ Washington, Sch Med, Dept Med, Redmond, WA USA	Schneider, L (reprint author), Joint Task Force Practice Parameters, 59 N Brockway St,304, Palatine, IL 60067 USA.	info@jcaai.org			National Institutes of Health (NIH)/National Institute of Allergy and Infectious Disease (NIAID) Atopic Dermatitis Research Network; Astellas; Amphastar; Medimmune; Genentech; Merck; TEVA; Sunovion; Boehringer Ingelheim; Nutricia; Array; Rigel; AstraZeneca; Atopic Dermatitis Foundation; NIH; NIAID; National Institute of Arthritis and Musculoskeletal and Skin Diseases; German Research Council; Regeneron	L. Schneider has received research support from the National Institutes of Health (NIH)/National Institute of Allergy and Infectious Disease (NIAID) Atopic Dermatitis Research Network and Astellas, is on the Research Advisory Board for the Food Allergy Initiative, and is on the Scientific Advisory Board for the National Eczema Association. S. Tilles has consultant arrangements with SRXA, Sunovion, and Hyrox; has received grants from Astellas, Amphastar, Medimmune, Genentech, Merck, TEVA, Sunovion, Boehringer Ingelheim, Nutricia, Array, Rigel, and AstraZeneca; is Associate Editor for AllergyWatch and the Annals of Allergy; is Assistant Editor for the Joint Task Force for Practice Parameters; and is on the Executive Committee for the Seattle Food Allergy Consortium. P. Lio is a speaker and consultant for Johnson & Johnson's Neosporin line, has received grants from the Atopic Dermatitis Foundation, and is an Advisory Board Member for the National Eczema Association. M. Boguniewicz has received grants from the NIH. L. Beck has received remuneration from Regeneron and Genentech and has received grants from the NIH, the NIAID, and the National Institute of Arthritis and Musculoskeletal and Skin Diseases; is a board member for the Society for Investigative Dermatology; and is a Scientific Advisory Board member for the National Eczema Association. J. LeBovidge is a consultant/writer for Anaphylaxis Canada. N. Novak has received grants from the German Research Council and has consultant arrangements with ALK-Abello, Bencard Allergy Therapeutics, Astellas, GlaxoSmithKline, LETI Pharma, and HAL Allergy.	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Allergy Clin. Immunol.	FEB	2013	131	2					295	+		10.1016/j.jaci.2012.12.672		32	Allergy; Immunology	Allergy; Immunology	086CT	WOS:000314661500004	23374261	
J	Volk, HE; Hertz-Picciotto, I; Delwiche, L; Lurmann, F; McConnell, R				Volk, Heather E.; Hertz-Picciotto, Irva; Delwiche, Lora; Lurmann, Fred; McConnell, Rob			Residential Proximity to Freeways and Autism in the CHARGE Study	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						autism; epidemiology; gene-environment interaction; roadway proximity; traffic emissions	POLYCYCLIC AROMATIC-HYDROCARBONS; HAZARDOUS AIR-POLLUTANTS; SPECTRUM DISORDERS; PRENATAL EXPOSURE; CHILDHOOD ASTHMA; OXIDATIVE STRESS; MULTIETHNIC POPULATION; ULTRAFINE PARTICLES; NITROGEN-DIOXIDE; GENE-EXPRESSION	BACKGROUND: Little is known about environmental causes and contributing factors for autism. Basic science and epidemiologic research suggest that oxidative stress and inflammation may play a role in disease development. Traffic-related air pollution, a common exposure with established effects on these pathways, contains substances found to have adverse prenatal effects. OBJECTIVES: We examined the association between autism and proximity of residence to freeways and major roadways during pregnancy and near the time of delivery, as a surrogate for air pollution exposure. METHODS: Data were from 304 autism cases and 259 typically developing controls enrolled in the Childhood Autism Risks from Genetics and the Environment (CHARGE) study. The mother's address recorded on the birth certificate and trimester-specific addresses derived from a residential history obtained by questionnaire were geocoded, and measures of distance to freeways and major roads were calculated using ArcGIS software. Logistic regression models compared residential proximity to freeways and major roads for autism cases and typically developing controls. RESULTS: Adjusting for sociodemographic factors and maternal smoking, maternal residence at the time of delivery was more likely be near a freeway (<= 309 m) for cases than for controls [odds ratio (OR) = 1.86; 95% confidence interval (CI), 1.04-3.45]. Autism was also associated with residential proximity to a freeway during the third trimester (OR = 2.22; CI, 1.16-4.42). After adjustment for socioeconomic and sociodemographic characteristics, these associations were unchanged. Living near other major roads at birth was not associated with autism. CONCLUSIONS: Living near a freeway was associated with autism. Examination of associations with measured air pollutants is needed.	[Volk, Heather E.; McConnell, Rob] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA; [Volk, Heather E.] Univ So Calif, Keck Sch Med, Childrens Hosp Los Angeles, Dept Prevent Med,Zilkha Neurogenet Inst, Los Angeles, CA 90033 USA; [Volk, Heather E.] Univ So Calif, Keck Sch Med, Childrens Hosp Los Angeles, Dept Pediat,Zilkha Neurogenet Inst, Los Angeles, CA 90033 USA; [Hertz-Picciotto, Irva; Delwiche, Lora] Univ Calif Davis, Dept Publ Hlth Sci, Davis, CA 95616 USA; [Lurmann, Fred] Sonoma Technol Inc, Petaluma, CA USA	Volk, HE (reprint author), Univ So Calif, Keck Sch Med, Dept Prevent Med, 1540 Alcazar St,CHP 209G, Los Angeles, CA 90033 USA.	hvolk@usc.edu			National Institute of Environmental Health Sciences [ES019002, ES009581, ES013578, ES007048, ES11269, ES015359, RD831861]; U.S. Environmental Protection Agency [R-823392, R-833292]; MIND Institute; Autism Speaks	This work was supported by National Institute of Environmental Health Sciences grants ES019002, ES009581, ES013578, ES007048, ES11269, ES015359, and RD831861; U.S. Environmental Protection Agency Science to Achieve Results (STAR) grants R-823392 and R-833292; the MIND Institute matching funds and pilot grant program; and Autism Speaks.	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Health Perspect.	JUN	2011	119	6					873	877		10.1289/ehp.1002835		5	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	771JC	WOS:000291152000034	21156395	
J	Richardson, SD; DeMarini, DM; Kogevinas, M; Fernandez, P; Marco, E; Lourencetti, C; Balleste, C; Heederik, D; Meliefste, K; McKague, AB; Marcos, R; Font-Ribera, L; Grimalt, JO; Villanueva, CM				Richardson, Susan D.; DeMarini, David M.; Kogevinas, Manolis; Fernandez, Pilar; Marco, Esther; Lourencetti, Carolina; Balleste, Clara; Heederik, Dick; Meliefste, Kees; McKague, A. Bruce; Marcos, Ricard; Font-Ribera, Laia; Grimalt, Joan O.; Villanueva, Cristina M.			What's in the Pool? A Comprehensive Identification of Disinfection By-products and Assessment of Mutagenicity of Chlorinated and Brominated Swimming Pool Water	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						bromination; bromine; chlorination; chlorine; DBPs; disinfection by-products; mutagenicity; swimming pools; Salmonella; water	GLUTATHIONE-S-TRANSFERASE; DRINKING-WATER; TRIHALOMETHANE CONCENTRATIONS; SALMONELLA MUTAGENICITY; EXPOSURE; GENOTOXICITY; BROMODICHLOROMETHANE; CHLORAMINES; CHLOROFORM; EXPRESSION	BACKGROUND: Swimming pool disinfectants and disinfection by-products (DBPs) have been linked to human health effects, including asthma and bladder cancer, but no studies have provided a comprehensive identification of DBPs in the water and related that to mutagenicity. OBJECTIVES: We performed a comprehensive identification of DBPs and disinfectant species in waters from public swimming pools in Barcelona, Catalonia, Spain, that disinfect with either chlorine or bromine and we determined the mutagenicity of the waters to compare with the analytical results. METHODS: We used gas chromatography/mass spectrometry (GC/MS) to measure trihalomethanes in water, GC with electron capture detection for air, low- and high-resolution GC/MS to comprehensively identify DBPs, photometry to measure disinfectant species (free chlorine, monochloroamine, dichloramine, and trichloramine) in the waters, and an ion chromatography method to measure trichloramine in air. We assessed mutagenicity with the Salmonella mutagenicity assay. RESULTS: We identified > 100 DBPs, including many nitrogen-containing DBPs that were likely formed from nitrogen-containing precursors from human inputs, such as urine, sweat, and skin cells. Many DBPs were new and have not been reported previously in either swimming pool or drinking waters. Bromoform levels were greater in brominated than in chlorinated pool waters, but we also identified many brominated DBPs in the chlorinated waters. The pool waters were mutagenic at levels similar to that of drinking water (similar to 1,200 revertants/L-equivalents in strain TA100-S9 mix). CONCLUSIONS: This study identified many new DBPs not identified previously in swimming pool or drinking water and found that swimming pool waters are as mutagenic as typical drinking waters.	[Richardson, Susan D.] US EPA, Natl Exposure Res Lab, Athens, GA 30605 USA; [DeMarini, David M.] US EPA, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA; [Kogevinas, Manolis; Font-Ribera, Laia; Villanueva, Cristina M.] Ctr Res Environm Epidemiol, Barcelona, Spain; [Kogevinas, Manolis; Font-Ribera, Laia; Villanueva, Cristina M.] Hosp del Mar, Municipal Inst Med Res, Barcelona, Spain; [Kogevinas, Manolis; Villanueva, Cristina M.] CIBER Epidemiol & Salud Publ, Barcelona, Spain; [Kogevinas, Manolis] Univ Athens, Sch Med, GR-10679 Athens, Greece; [Fernandez, Pilar; Marco, Esther; Lourencetti, Carolina; Balleste, Clara; Grimalt, Joan O.] Inst Environm Assessment & Water Res, Dept Environm Chem, Barcelona, Spain; [Heederik, Dick; Meliefste, Kees] Univ Utrecht, Inst Risk Assessment Sci, Div Environm Epidemiol, Utrecht, Netherlands; [McKague, A. Bruce] CanSyn Chem Corp, Toronto, ON, Canada; [Marcos, Ricard] Univ Autonoma Barcelona, Dept Genet & Microbiol, Grp Mutagenesi, Bellaterra, Cerdanyola Vall, Spain	Richardson, SD (reprint author), US EPA, Natl Exposure Res Lab, 960 Coll Stn Rd, Athens, GA 30605 USA.	richardson.susan@epa.gov	Grimalt, Joan/E-2073-2011; Fernandez, Pilar/E-6182-2010; Villanueva, Cristina/N-1942-2014; Kogevinas, Manolis/C-3918-2017	Grimalt, Joan/0000-0002-7391-5768; Fernandez, Pilar/0000-0002-4535-5214; Villanueva, Cristina/0000-0002-0783-1259; Font-Ribera, Laia/0000-0001-8447-4905; Marcos, Ricard/0000-0001-7891-357X	U.S. Environmental Protection Agency (EPA); Plan Nacional [SAF2005-07643-C03-01]; Fondo de Investigacion Sanitaria [CP06/00341]; Instituto de Salud Carlos III [CP06/00341, FI06/00651]; Santander-Central Hispano; Consejo Superior de Investigaciones Cientificas	This research was supported by the U.S. Environmental Protection Agency (EPA) intramural research program and Spanish grants SAF2005-07643-C03-01 (Plan Nacional) and CP06/00341 (Fondo de Investigacion Sanitaria). C.M.V. and L.F.-R. have, respectively, a contract and a predoctoral fellowship by the Instituto de Salud Carlos III (CP06/00341, FI06/00651). C. L. acknowledges a grant from the Agreement between Santander-Central Hispano and Consejo Superior de Investigaciones Cientificas.	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Health Perspect.	NOV	2010	118	11					1523	1530		10.1289/ehp.1001965		8	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	674CR	WOS:000283711800021	20833605	
J	Weinmayr, G; Romeo, E; De Sario, M; Weiland, SK; Forastiere, F				Weinmayr, Gudrun; Romeo, Elisa; De Sario, Manuela; Weiland, Stephan K.; Forastiere, Francesco			Short-Term Effects of PM10 and NO2 on Respiratory Health among Children with Asthma or Asthma-like Symptoms: A Systematic Review and Meta-Analysis	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Review						air pollution; asthma; children; NO2; PM; short-term effects	PARTICULATE AIR-POLLUTION; ANTIINFLAMMATORY MEDICATION USE; PEAK EXPIRATORY FLOW; NITROGEN-DIOXIDE; AUSTRALIAN CHILDREN; PUBLICATION BIAS; MEXICO-CITY; PARTICLES; EXPOSURE; PROJECT	OBJECTIVE: Our goal was to quantify the short-term effects of particulate matter with aerodynamic diameter <= 10 mu m (PM10) and nitrogen dioxide (NO2) on respiratory health of asthmatic children from published panel studies, and to investigate the influence of study and population characteristics as effect modifiers. DATA EXTRACTION: After a systematic literature review, we extracted quantitative estimates of the association of PM10 and/or NO2 with respiratory symptoms and peak expiratory flow (PEF). Combined effect estimates for an increase of 10 mu g/m(3) were calculated by random effects meta-analysis for all studies and for different strata defined by study characteristics. The effect of publication bias was investigated with Egger's and Begg's tests and "trim-and-fill" analyses. DATA SYNTHESIS: We identified 36 studies; 14 were part of the European Pollution Effects on Asthmatic Children in Europe (PEACE) study. Adverse associations of PM10 with asthma symptoms were statistically significant [odds ratio (OR) = 1.028; 95% confidence interval (CI), 1.006-1.051]. There were also associations, although not statistically significant, of PM10 with cough (OR = 1.012; 95% CI, 0.997-1.026) and on PEF (decrease of-0.082 L/min; 95% CI, -0.214 to 0.050). NO2 had statistically significant associations with asthma symptoms in the overall analysis considering all possible lags (OR = 1.031; 95% CI, 1.001-1.062), but not when we evaluated only the 0-1 lag. We found no publication bias, although it appeared when excluding the PEACE studies. When we applied the trim-and-fill method to the data set without the PEACE studies, the results were similar to the overall estimates from all studies. There was an indication for stronger PM10 associations for studies conducted in summer, outside of Europe, with longer lags, and in locations with higher NO2 concentrations. CONCLUSIONS: We found clear evidence of effects of PM10 on the occurrence of asthma symptom episodes, and to a lesser extent on cough and PEF. The results for NO2 are more difficult to interpret because they depend on the lag times examined. There was an indication of effect modification by several study conditions.	[Weinmayr, Gudrun; Weiland, Stephan K.] Univ Ulm, Inst Epidemiol, D-89081 Ulm, Germany; [Romeo, Elisa; De Sario, Manuela; Forastiere, Francesco] Local Hlth Author Rome E, Dept Epidemiol, Rome, Italy	Weinmayr, G (reprint author), Univ Ulm, Inst Epidemiol, Helmholtzstr 22, D-89081 Ulm, Germany.	gudrun.weinmayr@uni-ulm.de	De sario, Manuela/K-1932-2016; Forastiere, Francesco/J-9067-2016	De sario, Manuela/0000-0002-1117-2735; Forastiere, Francesco/0000-0002-9162-5684			Ackermann-Liebrich U., 1999, AIR POLLUTION HLTH, P559; Aekplakorn W, 2003, INT J EPIDEMIOL, V32, P854, DOI 10.1093/ije/dyg237; Anderson HR, 2004, METAANALYSIS TIME SE; Atkinson RW, 2001, AM J RESP CRIT CARE, V164, P1860; BALDINI G, 1998, EUR RESPIR REV, V8, P108; BEGG CB, 1994, BIOMETRICS, V50, P1088, DOI 10.2307/2533446; BEYER U, 1998, EUR RESPIR REV, V8, P61; CLENCHAAS J, 1998, EUR RESPIR REV, V8, P36; Delfino RJ, 1998, ENVIRON HEALTH PERSP, V106, P751, DOI 10.1289/ehp.98106751; Delfino RJ, 2003, ENVIRON HEALTH PERSP, V111, P647, DOI 10.1289/ehp.5992; Delfino RJ, 2002, ENVIRON HEALTH PERSP, V110, pA607; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; DEVALIA JL, 1993, AM J RESP CELL MOL, V9, P271; DOCKERY DW, 1994, ANNU REV PUBL HEALTH, V15, P107, DOI 10.1146/annurev.pu.15.050194.000543; Duval S, 2000, J AM STAT ASSOC, V95, P89, DOI 10.2307/2669529; Egger M, 1997, BRIT MED J, V315, P629; ENGLERT N, 1998, EUR RESPIR REV, V8, P53; FORSBERG B, 1998, EUR RESPIR REV, V8, P12; Gielen MH, 1997, AM J RESP CRIT CARE, V155, P2105; Halonen JI, 2008, THORAX, V63, P635, DOI 10.1136/thx.2007.091371; HALUSZKA J, 1998, EUR RESPIR REV, V8, P94; Higgins JPT, 2002, STAT MED, V21, P1539, DOI 10.1002/sim.1186; Jalaludin BB, 2000, INT J EPIDEMIOL, V29, P549, DOI 10.1093/ije/29.3.549; Jalaludin BB, 2004, ENVIRON RES, V95, P32, DOI 10.1016/S0013-9351(03)00038-0; Just J, 2002, EUR RESPIR J, V20, P899, DOI 10.1183/09031936.02.00236902; KALANDIDI A, 1998, EUR RESPIR REV, V8, P117; Katsouyanni K, 2001, EPIDEMIOLOGY, V12, P521, DOI 10.1097/00001648-200109000-00011; Kimber Ian, 1998, Toxicology Letters (Shannon), V102-103, P301, DOI 10.1016/S0378-4274(98)00320-8; KOTESOVEC F, 1998, EUR RESPIR REV, V8, P70; Levy JI, 2000, ENVIRON HEALTH PERSP, V108, P109, DOI 10.2307/3454508; McCreanor J, 2007, NEW ENGL J MED, V357, P2348, DOI 10.1056/NEJMoa071535; Mortimer KM, 2002, EUR RESPIR J, V19, P699, DOI 10.1183/09031936.02.00247102; *NAT LIB MED, 2008, PUBMED; NIELSEN J, 1998, EUR RESPIR REV, V8, P20; Niepsuj G., 1998, EUR RESPIR REV, V8, P86; Ostro B, 2001, EPIDEMIOLOGY, V12, P200, DOI 10.1097/00001648-200103000-00012; Peacock JL, 2003, OCCUP ENVIRON MED, V60, P82, DOI 10.1136/oem.60.2.82; Peters A, 1997, EUR RESPIR J, V10, P872; Petitti DB, 2001, STAT MED, V20, P3625, DOI 10.1002/sim.1091; POPE CA, 1992, AM REV RESPIR DIS, V145, P1123; ROEMER W, 1993, AM REV RESPIR DIS, V147, P118; Roemer W, 1998, EUR RESPIR J, V12, P1354, DOI 10.1183/09031936.98.12061354; Roemer W, 2000, CLIN EXP ALLERGY, V30, P1067; ROEMER W, 1998, EUR RESPIR REV, V8, P4; Romieu I, 1997, ARCH ENVIRON HEALTH, V52, P368; Romieu I, 1996, AM J RESP CRIT CARE, V154, P300; RUDNAI P, 1998, EUR RESPIR REV, V8, P101; Schildcrout JS, 2006, AM J EPIDEMIOL, V164, P505, DOI 10.1093/aje/kwj225; Seaton A, 2003, THORAX, V58, P1012, DOI 10.1136/thorax.58.12.1012; Segala C, 1998, EUR RESPIR J, V11, P677; Strand V, 1998, EUR RESPIR J, V12, P6, DOI 10.1183/09031936.98.12010006; Tiittanen P, 1999, EUR RESPIR J, V13, P266, DOI 10.1034/j.1399-3003.1999.13b08.x; TIMONEN KL, 1998, EUR RESPIR REV, V8, P27; TUNNICLIFFE WS, 1994, LANCET, V344, P1733, DOI 10.1016/S0140-6736(94)92886-X; *US EPA, 2008, 2008 INT SCI ASS ISA; U.S. Environmental Protection Agency (E.P.A.), 2005, REV NAT AMB AIR QUAL; The U.S. Environmental Protection Agency (U.S. EPA), 2008, RISK EXP ASS SUPP RE; van der Zee SC, 1999, OCCUP ENVIRON MED, V56, P802; VANDERZEE S, 1998, EUR RESPIR REV, V8, P44; Vedal S, 1998, AM J RESP CRIT CARE, V157, P1034; VONDRA V, 1998, EUR RESPIR REV, V8, P78; Ward DJ, 2004, OCCUP ENVIRON MED, V61, DOI 10.1136/oem.2003.007088; WHO Regional Office for Europe, 2006, AIR QUAL GUID GLOB U; *WHO REG OFF EUR, 2000, EUR SER WHO, V91; Williams M. L, 1999, AIR POLLUTION HLTH, P83, DOI 10.1016/B978-012352335-8/50081-8; Yu OC, 2000, ENVIRON HEALTH PERSP, V108, P1209, DOI 10.2307/3434835	66	107	114	1	44	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	APR	2010	118	4					449	457		10.1289/ehp.0900844		9	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	580NA	WOS:000276454800015	20064785	
J	Brandtzaeg, P				Brandtzaeg, Per			The Mucosal Immune System and Its Integration with the Mammary Glands	JOURNAL OF PEDIATRICS			English	Article; Proceedings Paper	Conference on Emerging Roles Functioning Proteins in Pediatric Nutrition	OCT 29-31, 2008	San Francisco, CA				CESAREAN-SECTION; EPITHELIAL-CELLS; DENDRITIC CELLS; FOOD ALLERGY; B-CELLS; J-CHAIN; TOLERANCE; TRANSPORT; RESPONSES; COMPONENT	Mucosal immunity reduces the need for elimination of penetrating exogenous antigens by proinflammatory systemic immunity. The adult gut mucosa contains some 80% of the body's activated B cells-differentiated to plasmablasts and plasma cells (PCs). Most mucosal PCs produce dimeric immunoglobulin A (IgA), which, along with pentameric immunoglobulin M (IgM), can be exported by secretory epithelia expressing the polymeric immunoglobulin receptor. Immune exclusion of antigens is performed mainly by secretory IgA in cooperation with innate defenses, but, in newborns and in IgA deficiency, secretory IgM is important. In the gut, induction and regulation of mucosal immunity occurs primarily in gut-associated lymphoid tissue-particularly the Peyer's patches-and also in mesenteric lymph nodes. Terminal differentiation to PCs is accomplished in the lamina propria to which the activated memory/effector T and B cells home. Lactating mammary glands are part of the secretory immune system, and IgA antibodies in breast milk reflect antigenic stimulation of gut-associated lymphoid tissue and nasopharynx-associated lymphoid tissue such as the tonsils. Breast-milk antibodies are thus highly targeted against infectious agents and other exogenous antigens in the mother's environment, which are those likely to be encountered by the infant. Therefore breast-feeding represents an ingenious immunologic integration of mother and child. (J Pediatr 2010;156:S8-15).	[Brandtzaeg, Per] Univ Oslo, Rikshosp, Div Pathol, LIIPAT, N-0027 Oslo, Norway; [Brandtzaeg, Per] Univ Oslo, Rikshosp, Ctr Immune Regulat, Inst Pathol, N-0027 Oslo, Norway	Brandtzaeg, P (reprint author), Univ Oslo, Rikshosp, Div Pathol, LIIPAT, N-0027 Oslo, Norway.	per.brandtzaeg@medisin.uio.no					Agency for Healthcare Research and Quality (AHRQ), 2007, AHRQ PUBL; BRANDTZAEG P, 1991, GASTROENTEROL CLIN N, V20, P397; Brandtzaeg P, 2005, IMMUNOL REV, V206, P32, DOI 10.1111/j.0105-2896.2005.00283.x; BRANDTZAEG P, 1983, ANN NY ACAD SCI, V409, P353, DOI 10.1111/j.1749-6632.1983.tb26883.x; Brandtzaeg P, 2004, TRENDS IMMUNOL, V25, P570, DOI 10.1016/j.it.2004.09.005; Brandtzaeg P, 2003, VACCINE, V21, P3382, DOI 10.1016/S0264-410X(03)00338-4; Brandtzaeg P, 2002, ANN NY ACAD SCI, V964, P13; BRANDTZAEG P, 1984, NATURE, V311, P71, DOI 10.1038/311071a0; Brandtzaeg P, 1998, NUTR REV, V56, pS5; Brandtzaeg P, 2002, FRONTIERS NUTR SCI, VI, P273; Brandtzaeg Per, 2007, P221, DOI 10.1007/978-0-387-72232-0_10; Dickinson EC, 1998, SURGERY, V124, P284, DOI 10.1016/S0039-6060(98)70132-1; Eggesbo M, 2003, J ALLERGY CLIN IMMUN, V112, P420, DOI 10.1067/mai.2003.1610; GOLDMAN AS, 1993, PEDIATR INFECT DIS J, V12, P664, DOI 10.1097/00006454-199308000-00008; Hanson LA, 2007, P NUTR SOC, V66, P384, DOI 10.1017/S0029665107005654; Helgeland Lars, 2000, Microbial Ecology in Health and Disease, V12, P110, DOI 10.1080/089106000750060378; Hooper LV, 2001, SCIENCE, V291, P881, DOI 10.1126/science.291.5505.881; Johansen FE, 2000, SCAND J IMMUNOL, V52, P240; Johansen FE, 2005, BLOOD, V106, P593, DOI 10.1182/blood-2004-12-4630; Johansen FE, 1999, J EXP MED, V190, P915, DOI 10.1084/jem.190.7.915; Kraus TA, 2004, GASTROENTEROLOGY, V126, P1771, DOI 10.1053/j.gastro.2004.03.076; Lotz M, 2006, J EXP MED, V203, P973, DOI 10.1084/jem.20050625; Massacand JC, 2008, PLOS ONE, V3, DOI 10.1371/journal.pone.0002588; MELLANDER L, 1985, J PEDIATR-US, V107, P430, DOI 10.1016/S0022-3476(85)80528-X; Mora JR, 2008, MUCOSAL IMMUNOL, V1, P96, DOI 10.1038/mi.2007.14; Neish AS, 2000, SCIENCE, V289, P1560, DOI 10.1126/science.289.5484.1560; Pistiner M, 2008, J ALLERGY CLIN IMMUN, V122, P274, DOI 10.1016/j.jaci.2008.05.007; Rimoldi M, 2005, NAT IMMUNOL, V6, P507, DOI 10.1038/ni1192; Sait LC, 2007, INT IMMUNOL, V19, P257, DOI 10.1093/intimm/dxl142; Tollanes MC, 2008, J PEDIATR-US, V153, P112, DOI 10.1016/j.jpeds.2008.01.029; Wilson E, 2004, J EXP MED, V200, P805, DOI 10.1084/jem.20041069; [Anonymous], 1994, LANCET, V344, P1239	32	107	110	0	8	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0022-3476			J PEDIATR-US	J. Pediatr.	FEB	2010	156	2		1			S8	S15		10.1016/j.jpeds.2009.11.014		8	Pediatrics	Pediatrics	549LV	WOS:000274051400003	20105666	
J	von Mutius, E				von Mutius, Erika			Gene-environment interactions in asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						Asthma; genes; environment; interactions	GLUTATHIONE-S-TRANSFERASE; CHILDHOOD ASTHMA; TOBACCO-SMOKE; AIR-POLLUTION; LUNG-FUNCTION; BRONCHIAL HYPERRESPONSIVENESS; RESPIRATORY HEALTH; ORMDL3 EXPRESSION; MATERNAL SMOKING; IMMUNOGLOBULIN-E	Asthma is a complex disease, and its incidence is determined by an intricate interplay of genetic and environmental factors. The Identification of novel genes for asthma suggests that many genes with small effect,; rather than few genes with strong effects contribute to the development of asthma. These genetic effects may in part differ with respect to a subject's environmental exposures, although some genes may also exert their effect independently of the environment. Whereas the geneticist uses highly advanced, rapid, comprehensive technologies to assess even subtle changes in the human genome, the researcher interested in environmental exposures is often confronted with crude information obtained from questionnaires or interviews. There is thus substantial need to develop better tools for individual exposure assessment in all relevant environmental fields. Despite these limitations, a number of important gene-environment interactions have been identified. These interactions point to the biology of environmental exposures as the involved genetic variation is suggestive of certain underlying mechanisms. Furthermore, the identification of subjects who are particularly susceptible to environmental hazards through genetic analyses helps to estimate better the strength of effect of environmental exposures. Finally, the analysis of gene-environment interactions may result in a reconciliation of seemingly contradictory findings from studies not taking environmental exposures into account. (J Allergy Clin Immunol 2009;123:3-11.)	Univ Childrens Hosp, D-80337 Munich, Germany	von Mutius, E (reprint author), Univ Childrens Hosp, Lindwurmstr 4, D-80337 Munich, Germany.	Erika.von.Mutius@med.uni-muenchen.de		von Mutius, Erika/0000-0002-8893-4515			Alexandrov K, 2002, CARCINOGENESIS, V23, P1969, DOI 10.1093/carcin/23.12.1969; Atkinson RW, 2001, AM J RESP CRIT CARE, V164, P1860; Atkinson RW, 2004, AM J RESP CRIT CARE, V169, P1257; Bergamaschi E, 2001, AM J RESP CRIT CARE, V163, P1426; Bieli C, 2007, J ALLERGY CLIN IMMUN, V120, P1308, DOI 10.1016/j.jaci.2007.07.034; Bottema RWB, 2008, EUR RESPIR J, V32, P593, DOI 10.1183/09031936.00162407; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; CALIGARI PDS, 1975, PROC R SOC SER B-BIO, V191, P387, DOI 10.1098/rspb.1975.0135; Cameron L, 2006, J IMMUNOL, V177, P8633; Choudhry S, 2005, AM J RESP CRIT CARE, V172, P173, DOI 10.1164/rccm.200409-1232OC; Christiani DC, 2008, OCCUP ENVIRON MED, V65, P430, DOI 10.1136/oem.2007.033977; [Anonymous], 2008, OCCUP ENVIRON MED; [Anonymous], 2008, OCCUP ENVIRON MED; Colilla S, 2003, J ALLERGY CLIN IMMUN, V111, P840, DOI 10.1067/mai.2003.170; David GL, 2003, AM J RESP CRIT CARE, V168, P1199, DOI 10.1164/rccm.200305-684OC; 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Taylor DR, 2007, EXPERT OPIN PHARMACO, V8, P3195, DOI 10.1517/14656566.8.18.3195; van Strien RT, 2004, J ALLERGY CLIN IMMUN, V113, P860, DOI 10.1016/j.jaci.2004.01.078; Vercelli D, 2008, NAT REV IMMUNOL, V8, P169, DOI 10.1038/nri2257; Wang ZX, 2001, AM J RESP CRIT CARE, V163, P1404; Weinmayr G, 2007, AM J RESP CRIT CARE, V176, P565, DOI 10.1164/rccm.200607-994OC; Wenzel SE, 2006, LANCET, V368, P804, DOI 10.1016/S0140-6736(06)69290-8; Werner M, 2003, J ALLERGY CLIN IMMUN, V112, P323, DOI 10.1067/mai.2003.1648; Wong GWK, 2008, PEDIATR PULM, V43, P107, DOI 10.1002/ppul.20755; Wu H, 2007, ENVIRON HEALTH PERSP, V115, P616, DOI 10.1289/ehp.9740; Yang IA, 2005, AM J RESP CRIT CARE, V171, P171, DOI 10.1164/rccm.200402-194OC; Yang IA, 2007, CURR OPIN ALLERGY CL, V7, P75, DOI 10.1097/ACI.0b013e328012ce39	80	107	108	1	11	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JAN	2009	123	1					3	11		10.1016/j.jaci.2008.10.046		9	Allergy; Immunology	Allergy; Immunology	399IP	WOS:000262793900002	19130922	
J	Christensen, LH; Holm, J; Lund, G; Riise, E; Lund, K				Christensen, Lars Harder; Holm, Jens; Lund, Gitte; Riise, Erik; Lund, Kaare			Several distinct properties of the IgE repertoire determine effector cell degranulation in response to allergen challenge	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergy; recombinant IgE; human IgE; chimeric IgE; antibody; affinity; epitope; allergen; Der p 2; effector cell degranulation; basophil activation test; basophils; diagnosis	HUMAN BASOPHIL ACTIVATION; HISTAMINE-RELEASE; CROSS-REACTIVITY; LEUKEMIA-CELLS; MITE ALLERGEN; ANTI-IGE; AFFINITY; IMMUNOASSAY; EXPRESSION; EPITOPES	Background: On cross-linking of receptor-bound IgE antibodies by allergens, effector cells (basophils and mast cells) involved in type I allergic reactions degranulate and release the potent chemical mediators stored inside their granules. Total and allergen-specific IgE concentrations, IgE affinity for allergen, and IgE clonality are all distinct properties of allergic patients' IgE repertoires. However, the inability to isolate individual IgE antibodies from allergic patients' sera presents a major barrier to understanding the importance of patient-specific IgE repertoires for the manifestation and severity of allergic symptoms. Objective: We sought to investigate how individual properties of an IgE repertoire affect effector cell degranulation. Methods: A panel of recombinant IgE (rIgE) antibodies specific for the major house dust mite allergen Der p 2 was developed and characterized in regard to Der p 2 affinity, as well as Der p 2 epitope specificity, by using surface plasmon resonance technology. Human basophils were sensitized with different combinations of rIgEs, and degranulation responses were measured by means of flow cytometry after challenge with Der p 2. Results: A total of 31 Der p 2-specific rIgEs were produced. They bound a total of 9 different Der p 2 epitopes in the affinity range (KD value) of 0.0358 to 291 nM. Factors increasing human basophil degranulation were increased total IgE concentrations, increased concentrations of allergen-specific IgE relative to non-allergen-specific IgE, more even concentration of individual allergen-specific IgE clones, increased IgE affinity for allergen, and increased number of allergen epitopes recognized by the IgE repertoire (increased IgE clonality). Conclusion: This study demonstrates how distinct properties of the IgE repertoire, such as total and allergen-specific IgE antibody concentration, IgE affinity, and IgE clonality, affect effector cell degranulation.	[Christensen, Lars Harder; Holm, Jens; Lund, Gitte; Lund, Kaare] ALK Abello AS, Dept Expt Immunol, DK-2970 Horsholm, Denmark; [Christensen, Lars Harder; Riise, Erik] Univ Copenhagen, Fac Pharmaceut Sci, Antibody Technol Grp, Copenhagen, Denmark	Christensen, LH (reprint author), ALK Abello AS, Dept Expt Immunol, Boge Alle 6-8, DK-2970 Horsholm, Denmark.	lars-harder@hotmail.com					Aalberse RC, 2001, ALLERGY, V56, P27, DOI 10.1034/j.1398-9995.2001.00909.x; Aalberse RC, 2001, ALLERGY, V56, P478, DOI 10.1034/j.1398-9995.2001.056006478.x; Beyer K, 2003, J ALLERGY CLIN IMMUN, V112, P202, DOI 10.1067/mai.2003.1621; CHUA KY, 1990, INT ARCH ALLER A IMM, V91, P118; COLLINS AM, 1995, INT ARCH ALLERGY IMM, V107, P547; Derewenda U, 2002, J MOL BIOL, V318, P189, DOI 10.0000/S0022-2836(02)00027-X; FEWTRELL C, 1980, J IMMUNOL, V125, P701; Gieras A, 2007, J ALLERGY CLIN IMMUN, V119, P384, DOI 10.1016/j.jaci.2006.09.034; Hahn EL, 2005, IMMUNOL ALLERGY CLIN, V25, P231, DOI 10.1016/j.iac.2005.02.004; HEALICON RM, 1986, IMMUNOLOGY, V57, P611; Jarvinen KM, 2002, J ALLERGY CLIN IMMUN, V110, P293, DOI 10.1067/mai.2002.126080; Johansson SGO, 2006, ALLERGY, V61, P1216, DOI 10.1111/j.1398-9995.2006.01172.x; KAGEYSOBOTKA A, 1981, J IMMUNOL, V127, P2285; Kleine-Tebbe J, 2006, INT ARCH ALLERGY IMM, V141, P79, DOI 10.1159/000094495; KNOL EF, 1991, J ALLERGY CLIN IMMUN, V88, P328, DOI 10.1016/0091-6749(91)90094-5; KOHLER G, 1975, NATURE, V256, P495, DOI 10.1038/256495a0; Marchand F, 2003, ALLERGY, V58, P1037, DOI 10.1034/j.1398-9995.2003.00251.x; Mita H, 2000, Clin Exp Allergy, V30, P1583, DOI 10.1046/j.1365-2222.2000.00921.x; Norderhaug L, 1997, J IMMUNOL METHODS, V204, P77, DOI 10.1016/S0022-1759(97)00034-3; Nott A, 2003, RNA, V9, P607, DOI 10.1261/rna.5250403; Persson H, 2007, MOL IMMUNOL, V44, P2729, DOI 10.1016/j.molimm.2006.11.024; Pierson-Mullany LK, 2002, CLIN EXP ALLERGY, V32, P107, DOI 10.1046/j.0022-0477.2001.01244.x; PRUZANSKY JJ, 1988, IMMUNOLOGY, V64, P307; Romano A, 2007, CURR OPIN ALLERGY CL, V7, P299; Sainte-Laudy J, 1998, INFLAMM RES, V47, P401, DOI 10.1007/s000110050351; Schroeder JT, 2001, ADV IMMUNOL, V77, P93, DOI 10.1016/S0065-2776(01)77015-0; Shreffler WG, 2004, J ALLERGY CLIN IMMUN, V113, P776, DOI 10.1016/j.jaci.2003.12.588; Turner H, 1999, NATURE, V402, pB24	28	107	108	0	10	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	AUG	2008	122	2					298	304		10.1016/j.jaci.2008.05.026		7	Allergy; Immunology	Allergy; Immunology	337HO	WOS:000258426300013	18572230	
J	Marogna, M; Tomassetti, D; Bernasconi, A; Colombo, F; Massolo, A; Businco, ADR; Canonica, GW; Passalacqua, G; Tripodi, S				Marogna, Maurizio; Tomassetti, Dante; Bernasconi, Antonella; Colombo, Fausto; Massolo, Alessandro; Businco, Andrea Di Rienzo; Canonica, Giorgio W.; Passalacqua, Giovanni; Tripodi, Salvatore			Preventive effects of sublingual immunotherapy in childhood: an open randomized controlled study	ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY			English	Article							HOUSE-DUST MITE; ALLERGIC RHINITIS; LONG-TERM; PEDIATRIC-PATIENTS; RESPIRATORY ALLERGY; REAL-LIFE; FOLLOW-UP; CHILDREN; ASTHMA; EFFICACY	Background: Sublingual immunotherapy (SLIT) has been proved to be effective in allergic rhinitis and asthma, but there are few data on its preventive effects, especially in children. Objective: To evaluate the clinical and preventive effects of SLIT in children by assessing onset of persistent asthma and new sensitizations, clinical symptoms, and bronchial hyperreactivity. Methods: A total of 216 children with allergic rhinitis, with or without intermittent asthma, were evaluated and then randomized to receive drugs alone or drugs plus SLIT openly for 3 years. The clinical score was assessed yearly during allergen exposure. Pulmonary function testing, methacholine challenge, and skin prick testing were performed at the beginning and end of the study. Results: One hundred forty-four children received SLIT and 72 received drugs only. Dropouts were 9.7% in the SLIT group and 8.3% in the controls. New sensitizations appeared in 34.8% of controls and in 3.1% of SLIT patients (odds ratio, 16.85; 95% confidence interval, 5.73-49.13). Mild persistent asthma was less frequent in SLIT patients (odds ratio, 0.04; 95% confidence interval, 0.01-0.17). There was a significant decrease in clinical scores in the SLIT group vs the control group since the first year. The number of children with a positive methacholine challenge result decreased significantly after 3 years only in the SLIT group. Adherence was 80% or higher in 73.8% of patients. Only 1 patient reported systemic itching. Conclusions: In everyday clinical practice, SLIT reduced the onset of new sensitizations and mild persistent asthma and decreased bronchial hyperreactivity in children with respiratory allergy.	[Canonica, Giorgio W.; Passalacqua, Giovanni] Univ Genoa, Dept Internal Med, I-16132 Genoa, Italy; [Marogna, Maurizio; Tomassetti, Dante; Bernasconi, Antonella; Colombo, Fausto] Macchi Hosp Fdn, Pneumol Unit, Varese, Italy; [Massolo, Alessandro] Univ Pavia, Dept Anim Biol, I-27100 Pavia, Italy; [Businco, Andrea Di Rienzo; Tripodi, Salvatore] S Pertini Hosp, Pediat Allergy Unit, Rome, Italy	Passalacqua, G (reprint author), Univ Genoa, Dept Internal Med, Padiglione Maragliano,Lgo R Benzi 10, I-16132 Genoa, Italy.	possalacqua@unige.it	Massolo, Alessandro/I-3437-2012				Agostinis F, 2005, ALLERGY, V60, P133, DOI 10.1111/j.1398-9995.2004.00616.x; Bousquet J, 2001, J ALLERGY CLIN IMMUN, V108, pS147, DOI 10.1067/mai.2001.118891; Ciprandi G, 1998, INT ARCH ALLERGY IMM, V115, P157, DOI 10.1159/000023896; Di Rienzo V, 2005, CLIN EXP ALLERGY, V35, P560, DOI 10.1111/j.1365-2222.2005.02219.x; Di Rienzo V, 1999, ALLERGY, V54, P1110, DOI 10.1034/j.1398-9995.1999.00267.x; Di Rienzo V, 2003, CLIN EXP ALLERGY, V33, P206, DOI 10.1046/j.1365-2222.2003.01587.x; Gillings D, 1991, DRUG INF J, V25, P411; Global Initiative for Asthma, 2006, GLOB STRAT ASTHM MAN; GOOD P, 2002, PERMUTATION TESTS PR; Jacobsen L, 2007, ALLERGY, V62, P943, DOI 10.1111/j.1398-9995.2007.01451.x; KLEIJNEN J, 1994, LANCET, V344, P1347, DOI 10.1016/S0140-6736(94)90699-8; Lombardi C, 2001, ALLERGY, V56, P889; Madonini E, 2003, INT J IMMUNOPATH PH, V16, P73; Marogna M, 2004, ALLERGY, V59, P1205, DOI 10.1111/j.1398-9995.2004.00508.x; Marogna M, 2007, INT ARCH ALLERGY IMM, V142, P70, DOI 10.1159/000096001; Moller C, 2002, J ALLERGY CLIN IMMUN, V109, P251, DOI 10.1067/mai.2002.121317; Novembre E, 2004, J ALLERGY CLIN IMMUN, V114, P851, DOI 10.1016/j.jaci.2004.07.012; Ozdemir C, 2007, PEDIATR ALLERGY IMMU, V18, P508, DOI 10.1111/j.1399-3038.2007.00549.x; Pajno GB, 2004, ALLERGY, V59, P883, DOI 10.1111/j.1398-9995.2004.00578.x; Pajno GB, 2001, CLIN EXP ALLERGY, V31, P1392, DOI 10.1046/j.1365-2222.2001.01161.x; Pajno Giovanni B, 2003, Paediatr Drugs, V5, P777, DOI 10.2165/00148581-200305110-00006; Passalacqua G, 2007, PEDIATR ALLERGY IMMU, V18, P58, DOI 10.1111/j.1399-3038.2006.00471.x; Penagos M, 2008, CHEST, V133, P599, DOI 10.1378/chest.06-1425; Penagos M, 2006, ANN ALLERG ASTHMA IM, V97, P141; Polosa R, 2005, RESP RES, V6, DOI 10.1186/1465-9921-6-153; Polosa R, 2004, ALLERGY, V59, P1224, DOI 10.1111/j.1398-9995.2004.00537.x; Purello-D'Ambrosio F, 2001, CLIN EXP ALLERGY, V31, P1295, DOI 10.1046/j.1365-2222.2001.01027.x; SCADDING GK, 2003, COCHRANE DB SYST REV, V2, DOI UNSP CD002893; Siegel S., 1998, NONPARAMETRIC STAT B; Sokal RR, 1995, BIOMETRY PRINCIPLES; Sopo SM, 2004, ARCH DIS CHILD, V89, P620, DOI 10.1136/adc.2003.030411; Sterk PJ, 1993, EUR RESPIR J S, V16, P53; Tripodi S, 2006, INT ARCH ALLERGY IMM, V139, P149, DOI 10.1159/000090391; Wilson DR, 2003, COCHRANE DB SYST REV, V2	34	107	117	0	2	AMER COLL ALLERGY ASTHMA IMMUNOLOGY	ARLINGTON HTS	85 WEST ALGONQUIN RD SUITE 550, ARLINGTON HTS, IL 60005 USA	1081-1206			ANN ALLERG ASTHMA IM	Ann. Allergy Asthma Immunol.	AUG	2008	101	2					206	211				6	Allergy; Immunology	Allergy; Immunology	336LU	WOS:000258366100015	18727478	
J	Zock, JP; Plana, E; Jarvis, D; Anto, JM; Kromhout, H; Kennedys, SM; Kuenzli, N; Villani, S; Olivieri, M; Toren, K; Radon, K; Sunyer, J; Dahlman-Hoglund, A; Norbaeck, D; Kogevinas, M				Zock, Jan-Paul; Plana, Estel; Jarvis, Deborah; Anto, Josep M.; Kromhout, Hans; Kennedys, Susan M.; Kuenzli, Nino; Villani, Simona; Olivieri, Mario; Toren, Kjell; Radon, Katja; Sunyer, Jordi; Dahlman-Hoglund, Anna; Norbaeck, Dan; Kogevinas, Manolis			The use of household cleaning sprays and adult asthma - An international longitudinal study	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						airway irritants; epidemiology; incidence; ECRHS	RESPIRATORY HEALTH SURVEY; HYDROCHLORIC-ACID; EXPOSURE; CLEANERS; PRODUCTS; RISK; SYMPTOMS; MIXTURE	Rationale Cleaning work and professional use of certain cleaning products have been associated with asthma, but respiratory effects of nonprofessional home cleaning have rarely been studied. Objectives: To investigate the risk of new-onset asthma in relation to the use of common household cleaners. Methods: Within the follow-up of the European Community Respiratory Health Survey in 10 countries, we identified 3,503 persons doing the cleaning in their homes and who were free of asthma at baseline. Frequency of use of 15 types of cleaning products was obtained in a face-to-face interview at follow-up. We studied the incidence of asthma defined as physician diagnosis and as symptoms or medication usage at follow-up. Associations between asthma and the use of cleaning products were evaluated using multivariable Cox proportional hazards or log-binomial regression analysis. Measurements and Main Results: The use of cleaning sprays at least weekly (42 70 of participants) was associated with the incidence of asthma symptoms or medication (relative risk [RR], 1.49; 95070 confidence interval [Cl], 1.12-1.99) and wheeze (RR, 1.39; 95 % Cl, 1.06-1.80). The incidence of physician-diagnosed asthma was higher among those using sprays at least 4 days per week (RR, 2.11; 95% Cl, 1.15-3.89). These associations were consistent for subgroups and not modified by atopy. Dose-response relationships (P < 0.05) were apparent for the frequency of use and the number of different sprays. Risks were predominantly found for the commonly used glass-cleaning, furniture, and air-refreshing sprays. Cleaning products not applied in spray form were not associated with asthma. Conclusions: Frequent use of common household cleaning sprays may be an important risk factor for adult asthma.	CREAL, IMIM, E-08003 Barcelona, Spain; Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Resp Epidemiol & Publ Hlth Grp, London, England; Pompeu Fabra Univ, Dept Expt & Hlth Sci, Barcelona, Spain; Univ Utrecht, Inst Risk Assessment Sci, Environm Epidemiol Div, Utrecht, Netherlands; Univ British Columbia, Sch Occupat & Environm Hyg, Vancouver, BC V5Z 1M9, Canada; ICREA, Barcelona, Spain; Univ Pavia, Dept Hlth Sci, Sect Epidemiol & Med Stat, I-27100 Pavia, Italy; Univ Verona, Dept Med & Publ Hlt, Unit Occupat Med, I-37100 Verona, Italy; Sahlgrens Univ Hosp, Dept Occupat & Environm Med, Gothenburg, Sweden; Univ Munich, Inst Occupat & Environm Med, Munich, Germany; Uppsala Univ, Dept med Sci Occupat & Environm Med, Uppsala, Sweden; Univ Crete, Sch Med, Dept Social Med, Iraklion, Crete, Greece	Zock, JP (reprint author), CREAL, IMIM, Dr Aiguader 88, E-08003 Barcelona, Spain.	jpzock@imim.es	Ciccone, Giovannino/K-3136-2016; Burgos, Felip/E-5734-2015; Kromhout, Hans/A-9159-2008; Kogevinas, Manolis/C-3918-2017; Sunyer, J/G-6909-2014; Jarvis, Deborah/E-6494-2011; bucca, caterina/C-9886-2009; Kunzli, Nino/F-7195-2014; Sanchez-Ramos, Jose Luis/G-1259-2011	Ciccone, Giovannino/0000-0001-7644-9574; Burgos, Felip/0000-0002-4938-4581; Sunyer, J/0000-0002-2602-4110; ROMANO, Canzio/0000-0001-5294-9793; bucca, caterina/0000-0002-9941-9236; Kunzli, Nino/0000-0001-8360-080X; Sanchez-Ramos, Jose Luis/0000-0001-7187-9989; Bono, Roberto/0000-0002-2471-6594; Basagana, Xavier/0000-0002-8457-1489; Corsico, Angelo Guido/0000-0002-8716-4694; Rolla, Giovanni/0000-0001-5997-7172; /0000-0003-2517-6515	NHLBI NIH HHS [1R01HL062633]		Baldwin CM, 1999, TOXICOL IND HEALTH, V15, P403, DOI 10.1177/074823379901500314; Balmes JR, 2002, CLIN CHEST MED, V23, P727, DOI 10.1016/S0272-5231(02)00031-X; Basagana X, 2004, AM J EPIDEMIOL, V160, P178, DOI 10.1093/aje/kwh186; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; DESCHAMPS D, 1994, CHEST, V105, P1895, DOI 10.1378/chest.105.6.1895; *EUR AER FED, 2006, EUR AER PROD 2005; Fedoruk MJ, 2005, J EXPO ANAL ENV EPID, V15, P534, DOI 10.1038/sj.jea.7500431; Gorguner M, 2004, INHAL TOXICOL, V16, P87, DOI 10.1080/08958370490265004; Jarvis D, 2002, EUR RESPIR J, V20, P1071, DOI 10.1183/09031936.02.00046802; Karjalainen A, 2002, EUR RESPIR J, V19, P90, DOI 10.1183/09031936.02.00201002; Kogevinas M, 1999, LANCET, V353, P1750, DOI 10.1016/S0140-6736(98)07397-8; Mapp CE, 2000, EUR RESPIR J, V16, P570, DOI 10.1034/j.1399-3003.2000.016003570.x; Medina M, 2000, EUR RESPIR J, V16, pS520; Medina-Ramon M, 2005, OCCUP ENVIRON MED, V62, P598, DOI 10.1136/oem.2004.017640; Medina-Ramon M, 2003, THORAX, V58, P950, DOI 10.1136/thorax.58.11.950; Nazaroff WW, 2004, ATMOS ENVIRON, V38, P2841, DOI 10.1016/j.atmosenv.2004.02.040; Nielsen J, 1999, OCCUP MED-OXFORD, V49, P291, DOI 10.1093/occmed/49.5.291; Pekkanen J, 2006, J CLIN EPIDEMIOL, V59, P281, DOI 10.1016/j.jclinepi.2005.07.013; Rosenman KD, 2003, J OCCUP ENVIRON MED, V45, P556, DOI 10.1097/01.jom.0000058347.05741.f9; Sherriff A, 2005, THORAX, V60, P45, DOI 10.1136/thx.2004.021154; Tanen DA, 1999, NEW ENGL J MED, V341, P848, DOI 10.1056/NEJM199909093411115; Wolkoff P, 1998, SCI TOTAL ENVIRON, V215, P135, DOI 10.1016/S0048-9697(98)00110-7; ZOCK J, 2005, EUR RESP J S49, V26, pS207; Zock JP, 2001, SCAND J WORK ENV HEA, V27, P76	24	107	108	0	28	AMER THORACIC SOC	NEW YORK	61 BROADWAY, FL 4, NEW YORK, NY 10006 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	OCT 15	2007	176	8					735	741		10.1164/rccm.200612-17930C		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	220DF	WOS:000250136400004	17585104	
J	Olin, AC; Bake, B; Toren, K				Olin, Anna-Carin; Bake, Bjorn; Toren, Kjell			Fraction of exhaled nitric oxide at 50 mL/s - Reference values for adult lifelong never-smokers	CHEST			English	Article						allergy; asthma; practice	AGE; AIR; SENSITIZATION; SYMPTOMS; CHILDREN; HEIGHT; ASTHMA; ATOPY	Background: The measurement of fractional exhaled nitric oxide (FENO) is used as a marker of airway inflammation. The aim of this study was to establish reference values of FENO for adults. Methods: FENO at a flow rate of 50 mL/s was analyzed in 3,376 adults using a chemiluminescence analyzer according to American Thoracic Society/European Respiratory Society guidelines. Blood samples were analyzed, and atopy was defined as the presence of specific IgE. All subjects responded to a respiratory questionnaire. Those who had never smoked (n = 1,803) were selected for this study. After the exclusion of subjects with physician-diagnosed asthma, asthma symptoms, ever wheezing, dry cough, or use of inhaled steroids, 1,131 healthy never-smokers remained, including 845 nonatopic and 286 atopic subjects. Results: Based on multiple regression modeling, we propose the following reference equation for healthy never-smoking adults: Ln(FENO) = 0.057 + 0.013 x height (in centimeters) + 0.0088 x age (in years). The residual SD was 0.51, and the explanatory value was 9%. In a model, based on nonatopic subjects alone, the reference equation obtained was slightly different, as follows: Ln(FENO) = -0.0026 + 0.013 x height (in centimeters) + 0.010 x age (in years). The residual SD for this equation was 0.48, and the explanatory value was 11%. Conclusions: Normal values of FENO for adults may be predicted on the basis of age and height. However, as the reference equations only account for about 9 to 11% of the variation, the most important information that could be extracted from the study is that the upper limits of FENO range from 24.0 to 54.0 parts per billion, depending on age and height.	Sahlgrens Univ Hosp, Dept Occupat & Environm Med, SE-40530 Gothenburg, Sweden; Sahlgrens Univ Hosp, Dept Resp Med & Allergol, SE-40530 Gothenburg, Sweden	Olin, AC (reprint author), Sahlgrens Univ Hosp, Dept Occupat & Environm Med, Box 414, SE-40530 Gothenburg, Sweden.	anna-carin.olin@amm.gu.se					ALVING K, 1993, EUR RESPIR J, V6, P1368; American Thoracic Society, 2005, AM J RESP CRIT CARE, V171, P912, DOI DOI 10.1164/RCCM.200406-710ST; Baranowska B, 2006, FRONT NEUROENDOCRIN, V27, P54, DOI 10.1016/j.yfrne.2006.03.110; Bousquet J, 2006, ALLERGY, V61, P671, DOI 10.1111/j.1398-9995.2006.01048.x; Buchvald F, 2005, J ALLERGY CLIN IMMUN, V115, P1130, DOI 10.1016/j.jaci.2005.03.020; Franklin PJ, 1999, AM J RESP CRIT CARE, V159, P69; Grasemann H, 2003, AM J RESP CRIT CARE, V167, P1113, DOI 10.1164/rccm.200211-1342OC; GUSTAFSSON LE, 1991, BIOCHEM BIOPH RES CO, V181, P852, DOI 10.1016/0006-291X(91)91268-H; Haight RR, 2006, LUNG, V184, P113, DOI 10.1007/s00408-005-2570-3; Langhammer A, 2001, EUR RESPIR J, V18, P770, DOI 10.1183/09031936.01.00255301; Malmberg LP, 2006, PEDIATR PULM, V41, P635, DOI 10.1002/ppul.20417; MATRICARDI PM, 1990, CLIN EXP ALLERGY, V20, P151, DOI 10.1111/j.1365-2222.1990.tb02660.x; Olin AC, 2004, CLIN EXP ALLERGY, V34, P221, DOI 10.1111/j.1365-2222.2004.01888.x; Olin AC, 2001, RESP MED, V95, P153, DOI 10.1053/rmed.2000.1010; Olin AC, 2006, CHEST, V130, P1319, DOI 10.1378/chest.130.5.1319; Olivieri M, 2006, RESP RES, V7, DOI 10.1186/1465-9921-7-94; Pearce N, 1999, THORAX, V54, P268; Taylor DR, 2006, THORAX, V61, P817, DOI 10.1136/thx.2005.056093; TOREN K, 1993, CHEST, V104, P600, DOI 10.1378/chest.104.2.600	19	107	119	0	3	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	JUN	2007	131	6					1852	1856		10.1378/chest.06-2928		5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	180CD	WOS:000247336600038	17565022	
J	Jahnsen, FL; Strickland, DH; Thomas, JA; Tobagus, IT; Napoli, S; Zosky, GR; Turner, DJ; Sly, PD; Stumbles, PA; Holt, PG				Jahnsen, Frode L.; Strickland, Deborah H.; Thomas, Jennifer A.; Tobagus, Iriani T.; Napoli, Sylvia; Zosky, Graeme R.; Turner, Debra J.; Sly, Peter D.; Stumbles, Philip A.; Holt, Patrick G.			Accelerated antigen sampling and transport by airway mucosal dendritic cells following inhalation of a bacterial stimulus	JOURNAL OF IMMUNOLOGY			English	Article							INHALED ANTIGEN; LYMPH-NODES; RESPONSES; EXPOSURE; INHIBITION; INDUCTION; TOLERANCE; ASTHMA; PHASE; MICE	An increase in the tempo of local dendritic cell (DC)-mediated immune surveillance is a recognized feature of the response to acute inflammation at airway mucosal surfaces, and transient up-regulation of the APC functions of these DC preceding their emigration to regional lymph nodes has recently been identified as an important trigger for T cell-mediated airway tissue damage in diseases such as asthma. In this study, using a rat model, we demonstrate that the kinetics of the airway mucosal DC (AMDC) response to challenge with heat-killed bacteria is considerably more rapid and as a consequence more effectively compartmentalized than that in recall responses to soluble Ag. Notably, Ag-bearing AMDC expressing full APC activity reach regional lymph nodes within 30 min of cessation of microbial exposure, and in contrast to recall responses to nonpathogenic Ags, there is no evidence of local expression of APC activity within the airway mucosa preceding DC emigration. We additionally demonstrate that, analogous to that reported in the gut, a subset of airway intraepithelial DC extend their processes into the airway lumen. This function is constitutively expressed within the AMDC population, providing a mechanism for continuous immune surveillance of the airway luminal surface in the absence of "danger", signals.	Univ Western Australia, Telethon Inst Child Hlth Res, Div Cell Biol, Perth, WA 6872, Australia; Univ Oslo, Inst Pathol, Lab Immunohistochem & Immunopathol, N-0316 Oslo, Norway; Rikshosp Radiumhosp Med Ctr, Pathol Clin, Oslo, Norway	Holt, PG (reprint author), Univ Western Australia, Telethon Inst Child Hlth Res, Div Cell Biol, POB 855, Perth, WA 6872, Australia.	patrick@ichr.uwa.edu.au	Sly, Peter/F-1486-2010; Holt, Patrick/H-1548-2011; Zosky, Graeme/B-2048-2014	Sly, Peter/0000-0001-6305-2201; Holt, Patrick/0000-0003-1193-0935; Zosky, Graeme/0000-0001-9039-0302			Akbari O, 2001, NAT IMMUNOL, V2, P725, DOI 10.1038/90667; CUMBERBATCH M, 1995, IMMUNOLOGY, V84, P31; Dhodapkar MV, 2001, J EXP MED, V193, P233, DOI 10.1084/jem.193.2.233; Eisenbarth SC, 2002, J EXP MED, V196, P1645, DOI 10.1084/jem.20021340; HOLT PG, 1981, IMMUNOLOGY, V42, P409; HOLT PG, 1994, J IMMUNOL, V153, P256; Huang Q, 2001, SCIENCE, V294, P870, DOI 10.1126/science.294.5543.870; Huh JC, 2003, J EXP MED, V198, P19, DOI 10.1084/jem.20021328; Kapsenberg ML, 2003, NAT REV IMMUNOL, V3, P984, DOI 10.1038/nri1246; Lambrecht BN, 1998, J IMMUNOL, V160, P4090; Legge KL, 2003, IMMUNITY, V18, P265, DOI 10.1016/S1074-7613(03)00023-2; Liu AH, 2002, J ALLERGY CLIN IMMUN, V109, P379, DOI 10.1067/mai.2002.122157; MCMENAMIN C, 1993, J EXP MED, V178, P889, DOI 10.1084/jem.178.3.889; MCWILLIAM AS, 1994, J EXP MED, V179, P1331, DOI 10.1084/jem.179.4.1331; Niess JH, 2005, SCIENCE, V307, P254, DOI 10.1126/science.1102901; Rescigno M, 2001, NAT IMMUNOL, V2, P361, DOI 10.1038/86373; Steinman RM, 2000, J EXP MED, V191, P411, DOI 10.1084/jem.191.3.411; Stumbles PA, 1998, J EXP MED, V188, P2019, DOI 10.1084/jem.188.11.2019; Vermaelen KY, 2001, J EXP MED, V193, P51	19	107	112	0	2	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	NOV 1	2006	177	9					5861	5867				7	Immunology	Immunology	097VN	WOS:000241477400014	17056510	
J	Kulkarni, N; Pierse, N; Rushton, L; Grigg, J				Kulkarni, Neeta; Pierse, Nevil; Rushton, Lesley; Grigg, Jonathan			Carbon in airway macrophages and lung function in children	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							FINE-PARTICLE DEPOSITION; INDUCED SPUTUM; ALVEOLAR MACROPHAGES; PHYSICAL-ACTIVITY; POLLUTION; ASTHMA; INHALATION; RETENTION; EXPOSURE; COTININE	Background Epidemiologic studies indirectly suggest that the inhalation of carbonaceous particulate matter impairs lung function in children. Using the carbon content of airway macrophages as a marker of individual exposure to particulate matter derived from fossil fuel, we sought direct evidence of this association. Methods Airway macrophages were obtained from healthy children through sputum induction, and the area of airway macrophages occupied by carbon was measured. Lung function was measured with the use of spirometry. We modeled the exposure to primary particulate matter ( PM) that is less than 10 mu m in aerodynamic diameter (PM10) at or near each child's home address. Linear regression was used to evaluate associations between carbon content of alveolar macrophages and variables that may affect individual exposure. To determine whether lung function that is reduced for other reasons is associated with an increase in the carbon content of airway macrophages, we also studied children with severe asthma. Results We were able to assess the carbon content of airway macrophages in 64 of 114 healthy children (56 percent). Each increase in primary PM10 of 1.0 mu g per cubic meter was associated with an increase of 0.10 mu m(2) (95 percent confidence interval, 0.01 to 0.18) in the carbon content of airway macrophages, and each increase of 1.0 mu m(2) in carbon content was associated with a reduction of 17 percent (95 percent confidence interval, 5.6 to 28.4 percent) in forced expiratory volume in one second, of 12.9 percent (95 percent confidence interval, 0.9 to 24.8 percent) in forced vital capacity, and of 34.7 percent ( 95 percent confidence interval, 11.3 to 58.1 percent) in the forced expiratory flow between 25 and 75 percent of the forced vital capacity. The carbon content of airway macrophages was lower in children with asthma than in healthy children. Conclusions There is a dose-dependent inverse association between the carbon content of airway macrophages and lung function in children. We found no evidence that reduced lung function itself causes an increase in carbon content.	Univ Leicester, Dept Infect Immun & Inflammat, Div Child Hlth, Leicester, Leics, England; Univ Leicester, Inst Environm & Hlth, Leicester, Leics, England	Grigg, J (reprint author), Barts & London Queen Marys Sch Med & Dent, Inst Cell & Mol Sci, London E1 2AT, England.	j.grigg@qmul.ac.uk					AARON DJ, 1993, MED SCI SPORT EXER, V25, P847, DOI 10.1249/00005768-199307000-00014; Alexis NE, 2001, AM J RESP CRIT CARE, V164, P1964; Alexis NE, 2001, AM J PHYSIOL-LUNG C, V280, pL369; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Artinano B, 2004, SCI TOTAL ENVIRON, V334, P111, DOI 10.1016/j.scitotenv.2004.04.032; Bennett WD, 2004, J APPL PHYSIOL, V97, P821, DOI 10.1152/japplphysiol.01403.2003; Bennett WD, 1996, AM J RESP CRIT CARE, V153, P1641; Brainard JS, 2002, ENVIRON PLANN A, V34, P695, DOI 10.1068/a34184; Brauer M, 2001, ENVIRON HEALTH PERSP, V109, P1039, DOI 10.2307/3454959; Brightling Christopher E., 2000, American Journal of Respiratory and Critical Care Medicine, V162, P878; Bunn HJ, 2001, THORAX, V56, P932, DOI 10.1136/thorax.56.12.932; Cataldo D, 2001, CHEST, V120, P1815, DOI 10.1378/chest.120.6.1815; Daigle CC, 2003, INHAL TOXICOL, V15, P539, DOI 10.1080/08958370390205065; FEYERABEND C, 1990, J PHARM PHARMACOL, V42, P450; Finch GL, 2002, INHAL TOXICOL, V14, P1017, DOI 10.1080/08958370290084764; Fireman E, 1999, CHEST, V115, P1720, DOI 10.1378/chest.115.6.1720; FIREMAN E, 1999, CHEST, V116, P588; Fireman EM, 2004, ENVIRON HEALTH PERSP, V112, P1564, DOI 10.1289/ehp.7233; Gauderman WJ, 2004, NEW ENGL J MED, V351, P1057, DOI 10.1056/NEJMoa040610; Edward Avol M. S., 2005, NEW ENGL J MED, V352, P1276; Gibson PG, 2003, THORAX, V58, P116, DOI 10.1136/thorax.58.2.116; HE QC, 1993, ARCH ENVIRON HEALTH, V48, P382; Horak F, 2002, EUR RESPIR J, V19, P838, DOI 10.1183/09031936.02.00512001; JARVIS MJ, 1992, AM J PUBLIC HEALTH, V82, P1225, DOI 10.2105/AJPH.82.9.1225; KNUDSON RJ, 1983, AM REV RESPIR DIS, V127, P725; KRISKA AM, 1990, DIABETES CARE, V13, P401, DOI 10.2337/diacare.13.4.401; Kulkarni NS, 2005, SCI TOTAL ENVIRON, V345, P23, DOI 10.1016/j.scitotenv.2004.10.016; Lay JC, 1998, AM J RESP CELL MOL, V18, P687; *LEIC CIT COUNC PO, 2000, REV ASS AIR QUAL LEI; MCNEILL AD, 1987, BRIT J ADDICT, V82, P1355; Pavord ID, 1997, THORAX, V52, P498; Pierse N, 2006, THORAX, V61, P216, DOI 10.1136/thx.2004.036418; PILLING M, 2005, PARTICULATE MATTER U, P29; PILLING M, 2005, PARTICULATE MATTER U, P6; POLGAR G, 1979, AM REV RESPIR DIS, V120, P625; Quanjer PH, 1993, EUR RESPIR J S, V16, P5, DOI 10.1183/09041950.005s1693; ROSENTHAL M, 1993, THORAX, V48, P794, DOI 10.1136/thx.48.8.794; STROM KA, 1990, J TOXICOL ENV HEALTH, V29, P377	38	107	113	0	15	MASSACHUSETTS MEDICAL SOC	WALTHAM	WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA	0028-4793			NEW ENGL J MED	N. Engl. J. Med.	JUL 6	2006	355	1					21	30		10.1056/NEJMoa052972		10	Medicine, General & Internal	General & Internal Medicine	060DT	WOS:000238783200004	16822993	
J	Novak, N; Allam, JP; Hagemann, T; Jenneck, C; Laffer, S; Valenta, R; Kochan, J; Bieber, T				Novak, N; Allam, JP; Hagemann, T; Jenneck, C; Laffer, S; Valenta, R; Kochan, J; Bieber, T			Characterization of Fc epsilon RI-bearing CD123(+) blood dendritic cell antigen-2(+) plasmacytoid dendritic cells in atopic dermatitis	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						plasmacytoid dendritic cells; IgE; Fc epsilon RI; atopic dermatitis; IFN-alpha/beta	EPIDERMAL LANGERHANS CELLS; HIGH-AFFINITY RECEPTOR; PERIPHERAL-BLOOD; ALLERGEN PRESENTATION; ADAPTIVE IMMUNITY; PRESENTING CELLS; IGE RECEPTORS; SERUM IGE; INTERFERON; EXPRESSION	Background: The high-affinity receptor for IgE (FcepsilonRI) on myeloid dendritic cells has been shown to play a major role in atopic dermatitis (AD). Plasmacytoid dendritic cells (pDCs), which are instrumental in the defense of viral infections, are present in reduced amounts in the skin of patients with AD, which is characterized by a high susceptibility to viral infections. Objective: We explored phenotypical and functional characteristics of pDC in the peripheral blood of patients with AD and healthy individuals. Methods: Blood dendritic cell antigen-2(+)CD123(+) pDCs were enriched from the peripheral blood of patients with AD and studied in functional assays. Results: Skin-homing molecules such as cutaneous lymphocyte antigen and L-selectin CD62L were expressed in lower levels on pDCs of patients with AD. pDCs expressed high amounts of IgE-occupied FcepsilonRI. Further, FcepsilonRI aggregation on pDCs impaired the surface expression of MHC I and II, induced the production of IL-10, and enhanced the apoptosis of pDCs. Importantly, FcepsilonRI preactivated pDC produced less IFN-alpha and IFN-beta after stimulation with CpG motifs and enhanced the outcome of immune responses of the T(H)2 type. Conclusion: From these data, we conclude that FcepsilonRI-bearing pDCs from patients with AD (1) are different from pDCs of healthy individuals, (2) might be important in the pathophysiology of AD, and (3) contribute to the enhanced susceptibility of patients with AD to viral infections.	Univ Bonn, Dept Dermatol, Immunol Lab, D-53105 Bonn, Germany; Med Univ Vienna, Dept Pathophysiol, Allgemeines Krankenhaus Wien, Vienna, Austria; Hoffmann La Roche Inc, Dept Metabol Dis, Nutley, NJ USA	Novak, N (reprint author), Univ Bonn, Dept Dermatol, Immunol Lab, Sigmund Freud Str 25, D-53105 Bonn, Germany.	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Allergy Clin. Immunol.	AUG	2004	114	2					364	370		10.1016/j.jaci.2004.05.038		7	Allergy; Immunology	Allergy; Immunology	847OU	WOS:000223405600024	15316517	
J	Rubin, RN; Navon, L; Cassano, PA				Rubin, RN; Navon, L; Cassano, PA			Relationship of serum antioxidants to asthma prevalence in youth	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						antioxidants; asthma; child; second-hand smoke	NUTRITION EXAMINATION SURVEY; 3RD NATIONAL-HEALTH; KAPPA-B ACTIVATION; CHILDHOOD ASTHMA; REDUCED SELENIUM; DIETARY FACTORS; UNITED-STATES; LUNG-FUNCTION; VITAMIN-C; CHILDREN	The relationship of serum vitamin E, beta-carotene, vitamin C, and selenium to asthma was investigated among 7,505 youth (4-16 years old) in the Third National Health and Nutrition Examination Survey. Logistic regression models adjusted for potentially confounding variables, which generally had no effect on the coefficients for the antioxidants. Serum vitamin E had little or no association with asthma. In separate models, a SD increase in beta-carotene (odds ratio [OR], 0.9; 95% confidence interval [CI], 0.7, 1.0), vitamin C (OR, 0.8; 95% Cl, 0.7,0.9), and selenium (OR, 0.9; 95% Cl, 0.7, 1.1) was associated with a 10-20% reduction in asthma prevalence. Serum cotinine was used to identify youth with no cigarette smoke exposure and passive exposure (7%): Active smokers were too few to be studied further. The selenium-asthma association was stronger in youth who were smoke exposed (p = 0.075). A SD increase in selenium was associated with a 50% reduction in asthma prevalence (OR, 0.5; 95% Cl, 0.2, 1.4) in youth with passive smoke exposure compared with a 10% reduction in youth with no smoke exposure. The findings support an association of antioxidants with prevalent asthma, which for some antioxidants is stronger among children exposed to cigarette smoke.	Cornell Univ, Div Nutr Sci, Ithaca, NY 14853 USA	Cassano, PA (reprint author), Cornell Univ, Div Nutr Sci, 209 Savage Hall, Ithaca, NY 14853 USA.	pac6@cornell.edu			NHLBI NIH HHS [R03-HL6659, R03 HL066539]		Baker JC, 2000, RESP MED, V94, P925, DOI 10.1053/rmed.2000.0873; BLACKWELL DL, 1999, VITAL HLTH STAT, V10; Bowie AG, 2000, J IMMUNOL, V165, P7180; Burney P, 1997, CIBA F SYMP, V206, P111; Cook DG, 1997, THORAX, V52, P628; Ellwood P, 2001, EUR RESPIR J, V17, P436, DOI 10.1183/09031936.01.17304360; FLATT A, 1990, THORAX, V45, P95, DOI 10.1136/thx.45.2.95; Fogarty A, 2000, CLIN EXP ALLERGY, V30, P615, DOI 10.1046/j.1365-2222.2000.00766.x; Forastiere F, 2000, THORAX, V55, P283, DOI 10.1136/thorax.55.4.283; Fuhlbrigge AL, 2002, AM J RESP CRIT CARE, V166, P1044, DOI 10.1164/rccm.2107057; Gilliland FD, 2003, AM J EPIDEMIOL, V158, P576, DOI 10.1093/aje/kwg181; Greene LS, 1999, NUTRITION, V15, P899, DOI 10.1016/S0899-9007(99)00209-9; Gunter EW, 1996, LAB PROCEDURES USED; Hatch GE, 1995, AM J CLIN NUTR S, V61, p625S; HEFFNER JE, 1989, AM REV RESPIR DIS, V140, P531; Hijazi N, 2000, THORAX, V55, P775, DOI 10.1136/thorax.55.9.775; Huang SL, 2001, CLIN EXP ALLERGY, V31, P259, DOI 10.1046/j.1365-2222.2001.00938.x; Jeffery P, 2001, Pediatr Pulmonol Suppl, V21, P3; Jeong DW, 2002, J BIOL CHEM, V277, P17871, DOI 10.1074/jbc.M200808200; Lanphear BP, 2001, PEDIATRICS, V107, P505, DOI 10.1542/peds.107.3.505; Mannino DM, 2002, CHEST, V122, P409, DOI 10.1378/chest.122.2.409; Mannino DM, 2001, ARCH PEDIAT ADOL MED, V155, P36; Misso NLA, 1996, CLIN EXP ALLERGY, V26, P838, DOI 10.1046/j.1365-2222.1996.d01-376.x; Picado C, 2001, ALLERGY, V56, P43, DOI 10.1034/j.1398-9995.2001.00793.x; POWELL CVE, 1994, PEDIATR PULM, V18, P34, DOI 10.1002/ppul.1950180109; Remes ST, 2002, THORAX, V57, P120, DOI 10.1136/thorax.57.2.120; Rodriguez MA, 2002, ARCH PEDIAT ADOL MED, V156, P269; Romieu I, 2002, AM J RESP CRIT CARE, V166, P703, DOI 10.1164/rccm.2112074; Romieu I, 2001, EPIDEMIOL REV, V23, P268; SCHWARTZ J, 1990, AM J EPIDEMIOL, V132, P67; Seear M, 1997, EUR RESPIR J, V10, P342, DOI 10.1183/09031936.97.10020342; Shaheen SO, 2001, AM J RESP CRIT CARE, V164, P1823; STONE J, 1989, CLIN SCI, V77, P495; SUNDE R, 2000, BIOCH PHYSL ASPECTS; TROISI RJ, 1995, AM J RESP CRIT CARE, V151, P1401; *US DEP HHS, 2002, NCHS CD ROM SER 11 A, V1; von Mutius E, 2001, THORAX, V56, P835, DOI 10.1136/thorax.56.11.835; Wijga AH, 2003, THORAX, V58, P567, DOI 10.1136/thorax.58.7.567; Willett W., 1998, NUTR EPIDEMIOLOGY; Woods RK, 2003, AM J CLIN NUTR, V78, P414; Woolcock AJ, 1997, CIBA F SYMP, V206, P122; YOUNGMAN L, 1998, BIOMARKERS MED WORKP, P257; 2002, TRENDS ASTHMA MORBID	43	107	116	0	4	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	FEB 1	2004	169	3					393	398		10.1164/rccm.200301-055OC		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	767BA	WOS:000188417800016	14630617	
J	Gur, C; Diav-Citrin, O; Shechtman, S; Arnon, J; Ornoy, A				Gur, C; Diav-Citrin, O; Shechtman, S; Arnon, J; Ornoy, A			Pregnancy outcome after first trimester exposure to corticosteroids: a prospective controlled study	REPRODUCTIVE TOXICOLOGY			English	Article						glucocorticosteroids; prednisone; pregnancy; congenital anomalies	SYSTEMIC-LUPUS-ERYTHEMATOSUS; CHILDREN BORN; WOMEN; PREDNISONE; THERAPY; HUMANS; COHORT; ASTHMA; GROWTH	Objective: To evaluate the safety of glucocorticosteroids (GCS) in pregnancy. Study design: The Israeli Teratogen Information Service (TIS) prospectively collected and followed 311 pregnancies counseled regarding systemic use of different GCS in the first trimester. The rate of major congenital anomalies was compared to that of 790 controls who were counseled for non-teratogenic exposure. Results: The rate of major anomalies did not significantly differ between the groups [12/262 = 4.6% (GCS), 19/728 = 2.6% (control), P = 0.116]. There was no case of oral cleft and no pattern of anomalies among the GCS exposed group. Higher rates of miscarriages (11.5% versus 7.0%, P = 0.013) and preterm births (22.7% versus 10.8%, P < 0.001) were observed among the GCS exposed group compared to the controls. GCS exposed infants had a lower median birth weight [3080g versus 3290g, P < 0.001] and were born at an earlier median gestational age [39 weeks versus 40, P < 0.001] compared to the control. Conclusions: The present study supports that GCS do not represent a major teratogenic risk in humans. The study was powered to find a 2.5-fold increase in the overall rate of major anomalies. (C) 2003 Elsevier Inc. All rights reserved.	Israeli Minist Hlth, Israeli Teratogen Informat Serv, Hadassah Med Sch, IL-91120 Jerusalem, Israel; Hebrew Univ Jerusalem, Israeli Minist Hlth, IL-91120 Jerusalem, Israel; Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Anat & Cell Biol, Lab Teratol, IL-91120 Jerusalem, Israel	Diav-Citrin, O (reprint author), Israeli Minist Hlth, Israeli Teratogen Informat Serv, Hadassah Med Sch, POB 12272, IL-91120 Jerusalem, Israel.	diavcit@netvision.net.il					BEHRMAN RE, 1987, NELSON TXB PEDIAT, P268; BRIGGS GG, 2002, DRUGS PREGNANCY LACT, P326; Carmichael SL, 1999, AM J MED GENET, V86, P242, DOI 10.1002/(SICI)1096-8628(19990917)86:3<242::AID-AJMG9>3.0.CO;2-U; CUNNINGHAM FG, 1997, WILLIAMS OBSTETRICS, P2579; Czeizel AE, 1997, TERATOLOGY, V56, P335, DOI 10.1002/(SICI)1096-9926(199711)56:5<335::AID-TERA7>3.0.CO;2-W; Diav-Citrin O, 2001, TERATOLOGY, V63, P186, DOI 10.1002/tera.1033; DOIG RK, 1956, LANCET, V2, P730; FINE LG, 1981, ANN INTERN MED, V94, P667; FITZSIMONS R, 1986, J ALLERGY CLIN IMMUN, V78, P349, DOI 10.1016/S0091-6749(86)80088-4; FRASER FC, 1995, TERATOLOGY, V51, P45, DOI 10.1002/tera.1420510107; HARPER PS, 1998, PRACTICAL GENETIC CO, P210; HARRIS JWS, 1956, LANCET, V1, P1045; Heinonen OP, 1977, BIRTH DEFECTS DRUGS, P389; Holmes LB, 1999, TERATOLOGY, V59, P1; Laskin CA, 1997, NEW ENGL J MED, V337, P148, DOI 10.1056/NEJM199707173370302; MINTZ G, 1986, J RHEUMATOL, V13, P732; MOGADAM M, 1981, GASTROENTEROLOGY, V80, P72; Mok CC, 2001, POSTGRAD MED J, V77, P157, DOI 10.1136/pmj.77.905.157; ORNOY A, 1972, TERATOLOGY, V6, P153, DOI 10.1002/tera.1420060206; PARFITT K, 1999, MARTINDALE COMPLETE, P1010; Park-Wyllie L, 2000, TERATOLOGY, V62, P385, DOI 10.1002/1096-9926(200012)62:6<385::AID-TERA5>3.0.CO;2-Z; PIRSON Y, 1985, NEW ENGL J MED, V313, P328; POLLARD JK, 1992, OBSTET GYNECOL, V80, P365; POPERT AJ, 1962, BMJ-BRIT MED J, P967; REINISCH JM, 1978, SCIENCE, V202, P436, DOI 10.1126/science.705336; Robert E, 1994, Int J Risk Saf Med, V6, P75, DOI 10.3233/JRS-1994-6201; Rodriguez-Pinilla E, 1998, TERATOLOGY, V58, P2, DOI 10.1002/(SICI)1096-9926(199807)58:1<2::AID-TERA2>3.0.CO;2-4; RUDOLPH AM, 1987, PEDIATRICS, P1291; SCHARDEIN JL, 1993, CHEM INDUCED BIRTH D, P1; SCHATZ M, 1975, JAMA-J AM MED ASSOC, V233, P804, DOI 10.1001/jama.233.7.804; Schatz M, 1997, J ALLERGY CLIN IMMUN, V100, P301, DOI 10.1016/S0091-6749(97)70241-0; WARRELL DW, 1968, LANCET, V1, P117	32	107	112	0	6	PERGAMON-ELSEVIER SCIENCE LTD	OXFORD	THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND	0890-6238			REPROD TOXICOL	Reprod. Toxicol.	JAN-FEB	2004	18	1					93	101		10.1016/j.reprotox.2003.10.007		9	Reproductive Biology; Toxicology	Reproductive Biology; Toxicology	775YP	WOS:000189088500009	15013068	
J	Arshad, SH; Bateman, B; Matthews, SM				Arshad, SH; Bateman, B; Matthews, SM			Primary prevention of asthma and atopy during childhood by allergen avoidance in infancy: a randomised controlled study	THORAX			English	Article							HOUSE-DUST MITE; EXPOSURE; RISK; INTERVENTION; PREDICTION; PREVALENCE; RHINITIS; AGE	Background: Recent increases in the prevalence of asthma and atopy emphasise the need for devising effective methods for primary prevention in children at high risk of atopy. Method: A birth cohort of genetically at risk infants was recruited in 1990 to a randomised controlled study. Allergen avoidance measures were instituted from birth in the prophylactic group (n=58). Infants were either breast fed with mother on a low allergen diet or given an extensively hydrolysed formula. Exposure to house dust mite was reduced by the use of an acaricide and mattress covers. The control group (n=62) followed standard advice as normally given by the health visitors. At age 8, all 120 children completed a questionnaire and 110 (92%) had all assessments (skin prick test, spirometry, and bronchial challenges). Results: In the prophylactic group eight children (13.8%) had current wheeze compared with 17 (27.4%) in the control group (p=0.08). Respective figures were eight (13.8%) and 20 (32.3%) for nocturnal cough (p=0.02) and 11 of 55 (20.0%) and 29 of 62 (46.8%) for atopy (p=0.003). After adjusting for confounding variables, the prophylactic group was found to be at a significantly reduced risk for current wheeze (odds ratio (OR) 0.26 (95% confidence interval (CI) 0.07 to 0.96)), nocturnal cough (OR 0.22 (95% CI 0.06 to 0.83)), asthma as defined by wheeze and bronchial hyperresponsiveness (OR 0.11 (95% CI 0.01 to 1.02)), and atopy (OR 0.21 (95% CI 0.07 to 0.62)). Conclusion: Strict allergen avoidance in infancy in high risk children reduces the development of allergic sensitisation to house dust mite. Our results suggest that this may prevent some cases of childhood asthma.	St Marys Hosp, David Hide Asthma & Allergy Res Ctr, Newport PO30 5TG, Wight, England	Arshad, SH (reprint author), St Marys Hosp, David Hide Asthma & Allergy Res Ctr, Newport PO30 5TG, Wight, England.						ABERG N, 1995, CLIN EXP ALLERGY, V25, P815, DOI 10.1111/j.1365-2222.1995.tb00023.x; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; ARSHAD SH, 1992, LANCET, V339, P1493, DOI 10.1016/0140-6736(92)91260-F; ASHER MI, 1995, EUR RESPIR J, V8, P383; CHAI H, 1975, J ALLERGY CLIN IMMUN, V56, P323, DOI 10.1016/0091-6749(75)90107-4; Chan-Yeung M, 2000, ARCH PEDIAT ADOL MED, V154, P657; COOKSON W, 1999, NATURE S, V402, pB12; Custovic A, 2001, LANCET, V358, P188, DOI 10.1016/S0140-6736(01)05406-X; DOLD S, 1992, ARCH DIS CHILD, V67, P1018; Global Initiative for Asthma, 1995, PUBL NIH; HIDE DW, 1991, CLIN EXP ALLERGY, V21, P739, DOI 10.1111/j.1365-2222.1991.tb03204.x; HIDE DW, 1994, J ALLERGY CLIN IMMUN, V93, P842, DOI 10.1016/0091-6749(94)90375-1; Hide DW, 1996, ALLERGY, V51, P89, DOI 10.1111/j.1398-9995.1996.tb04563.x; HOST A, 1988, ACTA PAEDIATR SCAND, V77, P663, DOI 10.1111/j.1651-2227.1988.tb10727.x; Kjellman NLM, 1998, ALLERGY, V53, P67; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; OCONNOR G, 1987, AM REV RESPIR DIS, V136, P1412; Pearce N, 1999, THORAX, V54, P268; Peat JK, 1999, J ALLERGY CLIN IMMUN, V103, P1, DOI 10.1016/S0091-6749(99)70517-8; PEAT JK, 1995, MED J AUSTRALIA, V163, P22; RIDOUT S, 1993, BRIT J CLIN PRACT, V47, P141; SAARINEN UM, 1995, LANCET, V346, P1065, DOI 10.1016/S0140-6736(95)91742-X; SEARS MR, 1993, CLIN EXP ALLERGY, V23, P941, DOI 10.1111/j.1365-2222.1993.tb00279.x; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; SUONIEMI I, 1981, ALLERGY, V36, P236; Wahn U, 2001, J ALLERGY CLIN IMMUN, V107, P567, DOI 10.1067/mai.2001.112943; ZEIGER RS, 1989, J ALLERGY CLIN IMMUN, V84, P72, DOI 10.1016/0091-6749(89)90181-4	27	107	117	0	1	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	JUN	2003	58	6					489	493		10.1136/thorax.58.6.489		5	Respiratory System	Respiratory System	684HR	WOS:000183199800006	12775858	
J	Celedon, JC; Wright, RJ; Litonjua, AA; Sredl, D; Ryan, L; Weiss, ST; Gold, DR				Celedon, JC; Wright, RJ; Litonjua, AA; Sredl, D; Ryan, L; Weiss, ST; Gold, DR			Day care attendance in early life, maternal history of asthma, and asthma at the age of 6 years	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						day care; maternal history; asthma	LOWER RESPIRATORY ILLNESS; HOUSE-DUST ENDOTOXIN; EARLY-CHILDHOOD; SCHOOL-AGE; RISK; EXPOSURE; CHILDREN; WHEEZE; SENSITIZATION; COCKROACH	Among children not selected on the basis of a parental history of atopy, day care attendance in early life is inversely associated with asthma at school age. We examined the relation between day care in the first year of life and asthma, recurrent wheezing, and eczema at the age of 6 years and wheezing in the first 6 years of life among 453 children with parental history of atopy followed from birth. Among all study participants, day care in the first year of life was inversely associated with eczema (odds ratio [OR] = 0.3, 95% confidence interval [CI] = 0.1-0.8). Day care attendance in early life was associated with a decreased risk of asthma (OR = 0.3, 95% CI = 0.1-0.7) and recurrent wheezing (OR = 0.3, 95% CI = 0.1-0.9) at the age of 6 years and with a decreased risk of any wheezing after the age of 4 years only among children without maternal history of asthma. Among children with maternal history of asthma, day care in early life had no protective effect on asthma or recurrent wheezing at the age of 6 years but was instead associated with an increased risk of wheezing in the first 6 years of life. Our findings suggest that maternal history of asthma influences the relation between day care-related exposures and childhood asthma.	Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA; Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Pulm & Crit Care Med, Boston, MA 02115 USA; Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA; Dana Farber Canc Inst, Boston, MA 02115 USA	Celedon, JC (reprint author), Channing Labs, 181 Longwood Ave, Boston, MA 02115 USA.		Ryan, Louise/A-4562-2009	Ryan, Louise/0000-0001-5957-2490	NHLBI NIH HHS [KO1 HL04370-01A1]; NIAID NIH HHS [AIEHS35786]		Andersen P.K., 1982, ANN STAT, V10, P1110; Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; *CDC, 1995, MMWR-MORBID MORTAL W, V43, P952; Centers for Disease Control and Prevention [CDC], 1998, MMWR-MORBID MORTAL W, V47, P1; Celedon JC, 1999, PEDIATRICS, V104, P495, DOI 10.1542/peds.104.3.495; Celedon JC, 2002, LANCET, V360, P781, DOI 10.1016/S0140-6736(02)09906-3; Celedon JC, 2002, ARCH PEDIAT ADOL MED, V156, P241; Gehring U, 2002, AM J RESP CRIT CARE, V166, P939, DOI 10.1164/rccm.200203-256OC; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; Illi S, 2001, BRIT MED J, V322, P390, DOI 10.1136/bmj.322.7283.390; Kramer U, 1998, LANCET, V352, P450; Litonjua AA, 1998, AM J RESP CRIT CARE, V158, P176; Marbury MC, 1997, AM J RESP CRIT CARE, V155, P156; Martinez FD, 1999, J ALLERGY CLIN IMMUN, V103, P355, DOI 10.1016/S0091-6749(99)70456-2; Nafstad P, 1999, PEDIATRICS, V103, P753, DOI 10.1542/peds.103.4.753; Rullo VEV, 2002, J ALLERGY CLIN IMMUN, V110, P582, DOI 10.1067/mai.2002.127511; Rusconi F, 1999, AM J RESP CRIT CARE, V160, P1617; Stein R, 1999, LANCET, V354, P541, DOI 10.1016/S0140-6736(98)10321-5; STRACHAN DP, 1989, BRIT MED J, V299, P1259; THERNEAU TM, 2000, MODELING SURVIVAL DA, P185; WEST J, 1995, DHEW PUBLICATION; Wright AL, 2001, THORAX, V56, P192, DOI 10.1136/thorax.56.3.192	24	107	109	0	3	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	MAY 1	2003	167	9					1239	1243		10.1164/rccm.200209-1063OC		5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	675NC	WOS:000182700600015	12446273	
J	Hauswirth, AW; Natter, S; Ghannadan, M; Majlesi, Y; Schernthaner, GH; Sperr, WR; Buhring, HJ; Valenta, R; Valent, P				Hauswirth, AW; Natter, S; Ghannadan, M; Majlesi, Y; Schernthaner, GH; Sperr, WR; Buhring, HJ; Valenta, R; Valent, P			Recombinant allergens promote expression of CD203c on basophils in sensitized individuals	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						basophils; allergy; recombinant allergens; diagnostic test; E-NPP3; CD203c	FC-EPSILON-RI; HISTAMINE-RELEASE; POLLEN ALLERGENS; BLOOD BASOPHILS; ANTIBODY 97A6; ACTIVATION; GRASS; IGE; DIAGNOSIS; CYCLOSPORINE	Background: Traditionally, the diagnosis of type I allergies is based on clinical data, skin test results, and laboratory test results with allergen extracts. During the past few years, several attempts have been made to refine diagnostic assays in clinical allergy by introducing recombinant allergens and novel markers of IgE-dependent cell activation. Objectives: We have identified the ectoenzyme CD203c as a novel basophil antigen that is upregulated on IgE receptor cross-linkage. In this study A e applied CD203c and a panel of recombinant allergens to establish a novel basophil test that,allows for a reliable quantification of IgE-dependent responses at the effector cell level. Methods: Patients allergic to birch (Bet v, 1, n = 15; Bet v 2, n := 8) and grass (Phl p 1, n = 15; Phl p 2, n = 10; Phl p 5, n = 14) pollen allergens, as well as 10 nonallergic donors, were examined. Basophils were exposed to various concentrations of recombinant allergens for 15 minutes and then examined for expression of CD203c by means of flow cytometry. CD203c upregulation was correlated with the increase in CD63. Results: Exposure to recombinant allergens resulted in a dose-dependent increase in expression of CD203c on peripheral blood basophils in sensitized individuals, whereas no increase,was seen in healthy control subjects. The effects of the recombinant allergens on CD203c expression were also time dependent. There was a good correlation between allergen-induced upregulation of CD203c and upregulation of CD63 (R = 0.76). Conclusion: Flow cytometric quantitation of CD203c on blood basophils exposed to recombinant allergens is a useful approach to determine the allergic state in sensitized individuals and represents a basis for a sensitive novel allergy test.	Univ Vienna, Dept Internal Med 1, Div Hematol & Hemostaseol, A-1090 Vienna, Austria; Univ Vienna, Inst Pathophysiol, A-1090 Vienna, Austria; Univ Vienna, Dept Internal Med 2, Div Angiol, A-1090 Vienna, Austria; Univ Tubingen, Dept Internal Med 2, Div Hematol & Immunol, Tubingen, Germany	Valent, P (reprint author), Univ Vienna, Dept Internal Med 1, Div Hematol & Hemostaseol, Wahringer Gurtel 18-20, A-1090 Vienna, Austria.						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B., 1997, ALLERGY ALLERGIC DIS; KNOL EF, 1991, J ALLERGY CLIN IMMUN, V88, P328, DOI 10.1016/0091-6749(91)90094-5; MAURER D, 1994, J EXP MED, V179, P745, DOI 10.1084/jem.179.2.745; MODDERMAN PW, 1989, LEUKOCYTE TYPING, V4, P1042; Niederberger V, 2001, J INVEST DERMATOL, V117, P848, DOI 10.1046/j.0022-202x.2001.01470.x; Paris-Kohler A, 2000, J ALLERGY CLIN IMMUN, V105, P339, DOI 10.1016/S0091-6749(00)90085-X; PELIKAN Z, 1983, ANN ALLERGY, V51, P395; Platz IJ, 2001, INT ARCH ALLERGY IMM, V126, P335, DOI 10.1159/000049531; RASANEN L, 1994, ALLERGY, V49, P342, DOI 10.1111/j.1398-9995.1994.tb02279.x; Sainte-Laudy J, 1998, INFLAMM RES, V47, P401, DOI 10.1007/s000110050351; Sihra BS, 1997, J ALLERGY CLIN IMMUN, V99, P699, DOI 10.1016/S0091-6749(97)70033-2; SOBOTKA AK, 1979, J IMMUNOL, V122, P511; Sperr WR, 1997, INT ARCH ALLERGY IMM, V114, P68; SUSANI M, 1995, BIOCHEM BIOPH RES CO, V215, P250, DOI 10.1006/bbrc.1995.2460; VALENT P, 1989, P NATL ACAD SCI USA, V86, P5542, DOI 10.1073/pnas.86.14.5542; VALENTA R, 1993, J ALLERGY CLIN IMMUN, V91, P88, DOI 10.1016/0091-6749(93)90300-5; Valenta R, 1998, ALLERGY, V53, P552, DOI 10.1111/j.1398-9995.1998.tb03930.x; Valenta R, 1999, CLIN EXP ALLERGY, V29, P896; Valenta R, 2001, IMMUNOL REV, V179, P119, DOI 10.1034/j.1600-065X.2001.790112.x; VALENTI JAM, 1995, ENCYC ENVIR, V7, P1; VRTALA S, 1993, J IMMUNOL, V151, P4773; Vrtala S, 1996, J ALLERGY CLIN IMMUN, V97, P781, DOI 10.1016/S0091-6749(96)80156-4	33	107	112	0	4	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUL	2002	110	1					102	109		10.1067/mai.2002.125257		8	Allergy; Immunology	Allergy; Immunology	574CF	WOS:000176870300020	12110828	
J	Deykin, A; Massaro, AF; Drazen, JM; Israel, E				Deykin, A; Massaro, AF; Drazen, JM; Israel, E			Exhaled nitric oxide as a diagnostic test for asthma - Online versus offline techniques and effect of flow rate	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						nitric oxide; asthma; diagnosis	REPEATED SPIROMETRY; INHALATION; COLLECTION; AIR; NO	Measurement of the fraction of exhaled nitric oxide (FENO) has been proposed as a noninvasive assessment of asthmatic airway inflammation. The influence of the expiratory flow rate during the collection maneuver on the ability of FENO to discriminate healthy subjects from those with asthma is unknown. We compared online and offline measurement of FENO at different flow rates. FENO was collected with expiratory flows of 50-500 ml/second in 34 patients with asthma (PC20 of less than 8 mg/ml) and 28 healthy subjects (PC20 of more than 10 mg/ml) using offline collection techniques. In a subgroup of 18 individuals with asthma and 17 healthy subjects, we additionally measured FENO at multiple expiratory flow rates (47-250 ml/second) using online methods. FENO fell with an increasing expiratory flow rate; FENO was higher in subjects with asthma as compared with healthy subjects at each flow rate studied with both techniques (p < 0.001). Receiver operating characteristic (ROC) curves for the diagnosis of asthma indicated that FENO is a robust discriminator between individuals with asthma and healthy subjects (area under the ROC curves 0.79 +/- 0.06 to 0.86 +/- 0.06, p for significant discrimination < 0.0001). Neither expiratory flow rate nor collection technique (online versus offline) significantly altered this discriminatory capacity (area under the ROC curves = 0.84 +/- 0.07 with the slowest online method versus 0.80 +/- 0.07 with the fastest offline method, p = 0.46). These data indicate that the choice of expiratory flow rate and collection method can be based on practicality and patient comfort without compromising the utility of this test for asthma.	Brigham & Womens Hosp, Dept Med, Div Pulm & Crit Care, Boston, MA 02115 USA; Harvard Univ, Sch Med, Boston, MA USA	Deykin, A (reprint author), Brigham & Womens Hosp, Div Pulm, 75 Francis St, Boston, MA 02115 USA.		Drazen, Jeffrey/E-5841-2012		NHLBI NIH HHS [P50-HL-56383]		BARNES PJ, 1995, IMMUNOL TODAY, V16, P128, DOI 10.1016/0167-5699(95)80128-6; Bisgaard H, 1999, AM J RESP CRIT CARE, V160, P1227; Canady RG, 1999, AM J RESP CRIT CARE, V159, P311; Chatkin JM, 1999, AM J RESP CRIT CARE, V159, P1810; Crater SE, 1999, AM J RESP CRIT CARE, V159, P806; Delclaux C, 2002, AM J RESP CRIT CARE, V165, P332; Deykin A, 2000, AM J RESP CRIT CARE, V161, P1237; Deykin A, 1998, AM J RESP CRIT CARE, V157, P769; Deykin A, 2000, AM J RESP CRIT CARE, V162, P1685; Georges G, 1999, J ASTHMA, V36, P467, DOI 10.3109/02770909909087289; HANLEY JA, 1983, RADIOLOGY, V148, P839; Jones SL, 2001, AM J RESP CRIT CARE, V164, P738; Kharitonov S, 1997, EUR RESPIR J, V10, P1683, DOI 10.1183/09031936.97.10071683; Kharitonov SA, 1996, AM J RESP CRIT CARE, V153, P454; Kissoon N, 2000, AM J RESP CRIT CARE, V162, P539; Massaro AF, 1996, AM J RESP CRIT CARE, V153, P1510; MASSARO AF, 1995, AM J RESP CRIT CARE, V152, P800; MASSARO AF, 1998, AM J RESP CRIT CARE, V157, pA614; PULEO PR, 1994, NEW ENGL J MED, V331, P561, DOI 10.1056/NEJM199409013310901; Salome CM, 1999, AM J RESP CRIT CARE, V159, P911; Silkoff PE, 1999, CHEST, V116, P754, DOI 10.1378/chest.116.3.754; Silkoff PE, 2000, AM J RESP CRIT CARE, V161, P1218; Silkoff PE, 1999, AM J RESP CRIT CARE, V159, P940; Silkoff PE, 1997, AM J RESP CRIT CARE, V155, P260; Slutsky AS, 1999, AM J RESP CRIT CARE, V160, P2104; Tobin MJ, 2001, AM J RESP CRIT CARE, V164, P1559; YATES DH, 1995, AM J RESP CRIT CARE, V152, P892; [Anonymous], 1987, AM REV RESP DIS, V136, P225	28	107	110	0	5	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	JUN 15	2002	165	12					1597	1601		10.1164/rccm.2201081		5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	566AB	WOS:000176402200007	12070059	
J	Heinrich, J; Gehring, U; Douwes, J; Koch, A; Fahlbusch, B; Bischof, W; Wichmann, HE				Heinrich, J; Gehring, U; Douwes, J; Koch, A; Fahlbusch, B; Bischof, W; Wichmann, HE		INGA-Study Grp	Pets and vermin are associated with high endotoxin levels in house dust	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						pets; vermin; endotoxin; indoor factors; house dust	HAY-FEVER; ALLERGIC SENSITIZATION; EXPOSURE; ASTHMA; CHILDREN; FARMERS; ENVIRONMENT; COMMUNITY; SEVERITY; PROTECT	Background Previous studies have shown that the risk for allergic sensitization is lower in children who grew up on farms and in young adults who were exposed to dogs in early childhood. A higher microbial exposure in general and in particular to endotoxin in early childhood might contribute to this lower risk of atopy. Objective We examined whether the presence of pets or vermin in the home is associated with higher endotoxin concentrations in settled house dust. Methods House dust was sampled in a standardized manner on the living room floors of 454 homes of German children aged 5-10 years (participation rate 61%). Endotoxin was assessed with a quantitative kinetic chromogenic Limulus Amebocyte Lysate (LAL) method. Associations between endotoxin levels, pets and vermin are presented as ratios of the crude and confounder adjusted geometric means (means ratios) in the category of study vs. a reference category using multiple linear regression models. Results Endotoxin concentrations in living room floor dust sampled in homes without pets and vermin were lower (1246 ng per square meter, 1519 no, endotoxin/g dust, n = 157) than those sampled in homes with pets or vermin (2267 ng per square meter, 2200 ng endotoxin/g dust, n = 296). After adjustment for city of residence, season of dust sampling, age of the building and story of the dwelling, means ratios for endotoxin expressed per gram of dust were statistically significantly increased for dog (1.64, 95% Cl 1.09-2.46), for cat (1.50, 95% CI 1.03-2.18) and for cockroach (3.01, 95% CI 1.37-6.60), whereas no major statistically significant associations were found for other pets, ants and mice. Conclusion Keeping a dog or, a cat in the home is consistent with higher exposure to endotoxin and might therefore contribute to the lower risk of atopy in later life.	GSF, Inst Epidemiol, D-85758 Neuherberg, Germany; Univ Munich, Inst Med Data Management Biometr & Epidemiol, Munich, Germany; Univ Utrecht, Inst Risk Assessment Sci, Div Environm & Occupat Hlth, Utrecht, Netherlands; Univ Jena, Dept Indoor Climatol, D-6900 Jena, Germany; Inst Clin Immunol, Erfurt, Germany	Heinrich, J (reprint author), GSF, Inst Epidemiol, POB 1129, D-85758 Neuherberg, Germany.			Douwes, Jeroen/0000-0003-3599-4036; Gehring, Ulrike/0000-0003-3612-5780			Bischof W, 2000, P HLTH BUILDINGS, V1, P251; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Douwes J, 2000, AM J RESP CRIT CARE, V162, P1348; Douwes J, 1998, INDOOR AIR, V8, P255, DOI 10.1111/j.1600-0668.1998.00006.x; Douwes J, 1997, INT J OCCUP ENV HEAL, V3, pS26; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Gross I, 2000, CLIN EXP ALLERGY, V30, P376, DOI 10.1046/j.1365-2222.2000.00780.x; HEILEMANN KJ, 1999, GESUNDHEITS INGENIEU, V120, P239; Heinrich J, 1999, ENVIRON HEALTH PERSP, V107, P53, DOI 10.2307/3434289; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; HINES CJ, 1998, BIOAEROSOLS PAPERS A, P146; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Martinez FD, 1999, LANCET S2, V354, pSII12; MICHEL O, 1991, CLIN EXP ALLERGY, V21, P441, DOI 10.1111/j.1365-2222.1991.tb01684.x; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; Michel O., 1997, INT J OCCUP ENV HL S, V3, P18; Nowak D, 1998, ARBEITSMED SOZIALMED, V33, P233; PARK JH, 2000, AM J RESP CRIT CARE, V161, pA908; Pearce N, 2000, J Epidemiol Biostat, V5, P5; Richter K, 1999, ALLERGOLOGIE, V22, P14; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Rizzo MC, 1997, PEDIATR ALLERGY IMMU, V8, P121; Roost HP, 1999, J ALLERGY CLIN IMMUN, V104, P941, DOI 10.1016/S0091-6749(99)70072-2; Shaheen SO, 1996, BRIT MED J, V313, P969; SMID T, 1992, AM REV RESPIR DIS, V146, P1474; Svanes C, 1999, J ALLERGY CLIN IMMUN, V103, P415, DOI 10.1016/S0091-6749(99)70465-3; THORNE PS, 2000, AM J RESP CRIT CARE, V161, P1; Vogelzang PFJ, 1998, AM J RESP CRIT CARE, V157, P15; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230	30	107	107	0	2	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	DEC	2001	31	12					1839	1845		10.1046/j.1365-2222.2001.01220.x		7	Allergy; Immunology	Allergy; Immunology	503NP	WOS:000172804800008	11737034	
J	Marple, BF				Marple, BF			Allergic fungal rhinosinusitis: Current theories and management strategies	LARYNGOSCOPE			English	Review						fungus; allergy; rhinosinusitis	NEWLY RECOGNIZED FORM; ASPERGILLUS-SINUSITIS; SURGICAL-MANAGEMENT; IMMUNOTHERAPY; DIAGNOSIS; EXPERIENCE; ORGANISMS; THERAPY; DISEASE; CT	The combination of nasal polyposis, crust formation, and sinus cultures yielding Aspergillus was first noted in 1976 by Safirstein,(1) who observed the clinical similarity that this constellation of findings shared with allergic bronchopulmonary Aspergillosis (ABPA). Eventually this disease came to be known as allergic fungal rhinosinusitis (AFS), As clinical evidence of AFS accumulated, controversy regarding its etiology, pathogenesis, natural history, and appropriate treatment naturally emerged. Despite past and current efforts, many of these controversies remain incompletely resolved, but continuing clinical study has illuminated some aspects of the disease and has Zed to an improved understanding of AFS and its treatment. Fungi associated with the development of AFS are ubiquitous and predominantly of the dematiaceous family, The eosinophilic host response to the presence of these fungi within the nose and paranasal sinuses gives rise to those clinical manifestations of the disease (nasal polyps, expansile mucocele formation, allergic fungal mucin, etc.). Exposure alone to these fungi, however, appears to be insufficient to initiate the disease. At the present time it is likely that initiation of the inflammatory cascade leading to AFS is a multifactorial event, requiring the simultaneous occurrence of such things as IgE-mediated sensitivity (atopy), specific T-cell HLA receptor expression, exposure to specific fungi, and aberration of local mucosal defense mechanisms. A variety of treatment plans for AFS have emerged, but the potential for recidivism remains well recognized, ranging from 10% to nearly 100% suggesting the need for continued study of this disease and fueling present controversy. This article is intended to review current data and theories regarding the pathophysiology of AFS, as well as the role of various surgical and nonsurgical forms of therapy.	Parkland Mem Hosp, Dept Otolaryngol, Dallas, TX USA; Dallas Vet Adm Hosp, Dept Otolaryngol, Dallas, TX USA	Marple, BF (reprint author), Univ Texas, SW Med Ctr, Dept Otolaryngol Head & Neck Surg, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.						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J	Vadas, P; Wai, Y; Burks, W; Perelman, B				Vadas, P; Wai, Y; Burks, W; Perelman, B			Detection of peanut allergens in breast milk of lactating women	JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION			English	Article							BOVINE BETA-LACTOGLOBULIN; COWS MILK; MATERNAL DIET; NUT ALLERGY; FED INFANTS; FOOD; CHILDREN; MOTHERS; EGG; HYPERSENSITIVITY	Context Most individuals who react to peanuts do so on their first known exposure. A potential but unproven route of occult exposure resulting in sensitization to peanut is via breast milk during lactation. Objective To investigate the ability of maternal dietary peanut protein to pass into breast milk during lactation, Design and Setting Clinical investigation conducted at 2 North American hospitals from March 1999 to October 2000, Patients Twenty-three healthy, lactating women aged 21 to 35 years. Intervention Each woman consumed 50 g of dry roasted peanuts, after which breast milk samples were collected at hourly intervals. Main Outcome Measures Presence in breast milk of total peanut protein, analyzed by a sandwich enzyme-linked immunosorbent assay, and 2 major peanut allergens, Ara h 1 and Ara h 2, detected by immunoblot analysis. Results Peanut protein was detected in 11 of 23 subjects, It was detected in 10 subjects within 2 hours of ingestion and in 1 subject within 6 hours. The median peak peanut protein concentration in breast milk was 200 ng/mL (mean, 222 ng/mL; range, 120-430 ng/mL). Both major peanut allergens Ara h 1 and Ara h 2 were detected. Conclusions Peanut protein is secreted into breast milk of lactating women following maternal dietary ingestion, Exposure to peanut protein during breastfeeding is a route of occult exposure that may result in sensitization of at-risk infants.	Univ Toronto, St Michaels Hosp, Div Clin Immunol & Allergy, Toronto, ON M5B 1W8, Canada; Univ Arkansas Med Sci, Arkansas Childrens Hosp, Little Rock, AR 72205 USA	Vadas, P (reprint author), Univ Toronto, St Michaels Hosp, Div Clin Immunol & Allergy, Room 8-161,Victoria Wing,30 Bond St, Toronto, ON M5B 1W8, Canada.						ASSEM ESK, 1990, BRIT MED J, V300, P1377; AXELSSON I, 1986, ACTA PAEDIATR SCAND, V75, P702, DOI 10.1111/j.1651-2227.1986.tb10277.x; BOCK SA, 1989, J ALLERGY CLIN IMMUN, V83, P900, DOI 10.1016/0091-6749(89)90103-6; CANT A, 1985, BRIT MED J, V291, P932; Chirdo FG, 1998, SCAND J GASTROENTERO, V33, P1186; Duchen K, 1991, Adv Exp Med Biol, V310, P427; Ewan PW, 1996, BRIT MED J, V312, P1074; Frank L, 1999, PEDIATR ALLERGY IMMU, V10, P27, DOI 10.1034/j.1399-3038.1999.101010.x; Fukushima Y, 1997, AM J CLIN NUTR, V65, P30; GERRARD JW, 1986, ANN ALLERGY, V56, P351; HOST A, 1990, CLIN EXP ALLERGY, V20, P383, DOI 10.1111/j.1365-2222.1990.tb02798.x; Hourihane JO, 1996, BRIT MED J, V313, P518; Hourihane JO, 1997, CLIN EXP ALLERGY, V27, P1240, DOI 10.1046/j.1365-2222.1997.1520954.x; Hourihane JO, 1998, BRIT MED J, V316, P1271; KILSHAW PJ, 1984, INT ARCH ALLER A IMM, V75, P8; SAMPSON HA, 1992, NEW ENGL J MED, V327, P380, DOI 10.1056/NEJM199208063270603; Sicherer SH, 1998, PEDIATRICS, V102, part. no., DOI 10.1542/peds.102.1.e6; Sicherer SH, 1999, J ALLERGY CLIN IMMUN, V103, P559, DOI 10.1016/S0091-6749(99)70224-1; SORVA R, 1994, J ALLERGY CLIN IMMUN, V93, P787, DOI 10.1016/0091-6749(94)90259-3; Tariq SM, 1996, BRIT MED J, V313, P514; TRONCONE R, 1987, ACTA PAEDIATR SCAND, V76, P453, DOI 10.1111/j.1651-2227.1987.tb10498.x; VANASPEREN PP, 1983, ARCH DIS CHILD, V58, P253; WARNER JO, 1980, CLIN ALLERGY, V10, P133, DOI 10.1111/j.1365-2222.1980.tb02090.x	23	107	113	0	9	AMER MEDICAL ASSOC	CHICAGO	515 N STATE ST, CHICAGO, IL 60610 USA	0098-7484			JAMA-J AM MED ASSOC	JAMA-J. Am. Med. Assoc.	APR 4	2001	285	13					1746	1748		10.1001/jama.285.13.1746		3	Medicine, General & Internal	General & Internal Medicine	415FR	WOS:000167710600028	11277829	
J	Han, JY; Takeshita, K; Utsumi, H				Han, JY; Takeshita, K; Utsumi, H			Noninvasive detection of hydroxyl radical generation in lung by diesel exhaust particles	FREE RADICAL BIOLOGY AND MEDICINE			English	Article						l-band ESR; diesel exhaust particles; nitroxide radical; lung; free radicals; reactive oxygen species; superoxide dismutase	RESPIRATORY-DISTRESS-SYNDROME; REACTIVE OXYGEN METABOLITES; IN-VIVO ESR; OXIDATIVE STRESS; WHOLE MICE; INTRATRACHEAL INSTILLATION; RESONANCE SPECTROSCOPY; NITROXIDE RADICALS; PULSE-RADIOLYSIS; INSPIRED OXYGEN	Diesel exhaust particles (DEP) induce pulmonary tumors, asthma-like symptoms, and the like in experimental animals. The involvement of reactive oxygen species (ROS) is suggested in the injuries induced by DEP, though the generation of ROS has not been proven. The present study provided the first direct evidence of (OH)-O-. generation in the lungs of living mice after intratracheal instillation of DEP, using noninvasive L-band ESR spectroscopy and a membrane-impermeable nitroxyl probe. (OH)-O-. generation is confirmed with the enhancement of in vivo ESR signal decay rate of the probe. The decay rate at mid-thorax was significantly enhanced in DEP-treated mice compared to that in vehicle-treated mice. The enhancement was completely suppressed by the administration of either (OH)-O-. scavengers, catalase, or desferrioxamine, while the administration of SOD further increased the rate. The administration of Fenton's reagents into the lung also enhanced the decay rate of the probe at mid-thorax of mice. These results clearly provided evidence that the intratracheal exposure to DEP in mice produced (OH)-O-. in the lung through an iron-catalyzed reaction of superoxide/H2O2. This first direct evidence of (OH)-O-. generation in DEP-treated mice lung may be utilized to determine treatments for DEP-induced lung injury. (C) 2001 Elsevier Science Inc.	Kyushu Univ, Grad Sch Pharmaceut Sci, Dept Biophys, Fukuoka 8128582, Japan	Kyushu Univ, Grad Sch Pharmaceut Sci, Dept Biophys, Fukuoka 8128582, Japan.	utsumi@pch.phar.kyushu-u.ac.jp	U-ID, Kyushu/C-5291-2016				ASMUS KD, 1976, INT J RADIAT BIOL, V29, P211, DOI 10.1080/09553007614550241; BACIC G, 1989, MAGNET RESON MED, V10, P266, DOI 10.1002/mrm.1910100211; BERLINER LJ, 1989, MAGNET RESON MED, V9, P430, DOI 10.1002/mrm.1910090317; BUFFINTON GD, 1992, FREE RADICAL RES COM, V16, P99, DOI 10.3109/10715769209049163; CHENG YS, 1984, AM IND HYG ASSOC J, V45, P547, DOI 10.1202/0002-8894(1984)045<0547:CODEIA>2.3.CO;2; DiazSanchez D, 1996, J ALLERGY CLIN IMMUN, V98, P114, DOI 10.1016/S0091-6749(96)70233-6; DIAZSANCHEZ D, 1994, J CLIN INVEST, V94, P1417, DOI 10.1172/JCI117478; DRAPER WM, 1986, CHEMOSPHERE, V15, P437, DOI 10.1016/0045-6535(86)90537-0; Eaton GR, 1991, EPR IMAGING IN VIVO; FERRARI M, 1990, BIOCHEM BIOPH RES CO, V166, P168, DOI 10.1016/0006-291X(90)91926-J; FIELDEN EM, 1971, INT J RADIAT BIOL RE, V20, P355, DOI 10.1080/09553007114551241; FINKELSTEIN E, 1984, BIOCHIM BIOPHYS ACTA, V802, P90; Gonzalez PK, 1996, SHOCK, V6, pS23, DOI 10.1097/00024382-199610001-00006; GOODGLICK LA, 1986, CANCER RES, V46, P5558; HALLIWELL B, 1987, ANAL BIOCHEM, V165, P215, DOI 10.1016/0003-2697(87)90222-3; Halliwell B., 1985, FREE RADICALS BIOL M; HEINRICH U, 1986, J APPL TOXICOL, V6, P383, DOI 10.1002/jat.2550060602; HENDERSON RF, 1988, FUND APPL TOXICOL, V11, P546, DOI 10.1016/0272-0590(88)90119-4; HYDE DM, 1985, LAB INVEST, V52, P195; ICHINOSE T, 1995, TOXICOLOGY, V99, P153, DOI 10.1016/0300-483X(94)03013-R; Ichinose T, 1997, INT J ONCOL, V11, P571; ISHIDA S, 1989, PHYS MED BIOL, V34, P1317, DOI 10.1088/0031-9155/34/9/017; IWAI K, 1986, J JPN SOC AIR POLLUT, V21, P38; JARJOUR NN, 1994, J LAB CLIN MED, V123, P131; KAMP DW, 1992, FREE RADICAL BIO MED, V12, P293, DOI 10.1016/0891-5849(92)90117-Y; KRISHNA MC, 1992, P NATL ACAD SCI USA, V89, P5537, DOI 10.1073/pnas.89.12.5537; KVEDER M, 1988, MAGNET RESON MED, V8, P241, DOI 10.1002/mrm.1910080302; Liu KJ, 1999, FREE RADICAL BIO MED, V26, P714, DOI 10.1016/S0891-5849(98)00251-2; MASUDA S, 1992, INT CONGR SER, V998, P175; MATUSHITA H, 1986, CARCINOGENIC MUTAGEN, P103; MAUDERLY JL, 1987, FUND APPL TOXICOL, V9, P208, DOI 10.1016/0272-0590(87)90044-3; MCCLELLAN RO, 1987, ANNU REV PHARMACOL, V27, P279; MCCORD JM, 1994, ENVIRON HEALTH PERSP, V102, P57, DOI 10.2307/3432215; MIURA Y, 1995, FREE RADICAL RES, V22, P209, DOI 10.3109/10715769509147540; MIURA Y, 1992, BIOCHEM BIOPH RES CO, V182, P1108, DOI 10.1016/0006-291X(92)91846-I; NAGASHIMA M, 1995, CARCINOGENESIS, V16, P1441, DOI 10.1093/carcin/16.6.1441; NIGAM S, 1976, PHYS ORG CHEM, V85, P2324; Omar B A, 1992, Adv Pharmacol, V23, P109, DOI 10.1016/S1054-3589(08)60964-3; OZAWA T, 1991, J CHEM SOC CHEM COMM, P330, DOI 10.1039/c39910000330; Phumala N, 1999, FREE RADICAL BIO MED, V26, P1209, DOI 10.1016/S0891-5849(98)00314-1; Reymao MSF, 1997, ENVIRON RES, V74, P150, DOI 10.1006/enrs.1997.3740; SAGAI M, 1993, FREE RADICAL BIO MED, V14, P37, DOI 10.1016/0891-5849(93)90507-Q; Sagai M, 1996, FREE RADICAL BIO MED, V21, P199, DOI 10.1016/0891-5849(96)00032-9; Sano T, 1998, DIABETOLOGIA, V41, P1355, DOI 10.1007/s001250051076; SCHUETZLE D, 1986, ANAL CHEM, V58, P1060, DOI 10.1021/ac00124a001; SCHUETZLE D, 1983, ENVIRON HEALTH PERSP, V47, P65, DOI 10.2307/3429500; Schuetzle D, 1986, CARCINOGENIC MUTAGEN, P41; SUBCZYNSKI WK, 1986, MAGNET RESON MED, V3, P747, DOI 10.1002/mrm.1910030510; SUN JD, 1985, FUND APPL TOXICOL, V5, P913, DOI 10.1016/0272-0590(85)90173-3; SUZUKI T, 1990, J JPN SOC AIR POLLUT, V25, P192; SWARTZ HM, 1986, BIOCHIM BIOPHYS ACTA, V888, P82, DOI 10.1016/0167-4889(86)90073-X; TAKAFUJI S, 1987, J ALLERGY CLIN IMMUN, V79, P639, DOI 10.1016/S0091-6749(87)80161-6; Takeshita K, 1999, FREE RADICAL BIO MED, V26, P951, DOI 10.1016/S0891-5849(98)00278-0; TUOMALA MH, 1992, FEBS LETT, V296, P57, DOI 10.1016/0014-5793(92)80402-3; UTSUMI H, 1993, FREE RADICAL RES COM, V19, pS219; UTSUMI H, 1990, BIOCHEM BIOPH RES CO, V172, P1342, DOI 10.1016/0006-291X(90)91597-L; VALLYATHAN V, 1995, AM J RESP CRIT CARE, V152, P1003; VOGL G, 1989, TOXICOL LETT, V47, P17, DOI 10.1016/0378-4274(89)90082-9; White H, 1983, J Appl Toxicol, V3, P332, DOI 10.1002/jat.2550030612; WILLSON RL, 1972, INT J RADIAT BIOL RE, V21, P401, DOI 10.1080/09553007214550471	60	107	111	2	14	ELSEVIER SCIENCE INC	NEW YORK	360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA	0891-5849	1873-4596		FREE RADICAL BIO MED	Free Radic. 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J	Pritchard, JN				Pritchard, JN			The influence of lung deposition on clinical response	JOURNAL OF AEROSOL MEDICINE-DEPOSITION CLEARANCE AND EFFECTS IN THE LUNG			English	Article						asthma; chronic obstructive disease; lung deposition; efficacy; metered dose inhalers	BECLOMETHASONE DIPROPIONATE; BUDESONIDE; PHARMACOKINETICS; TURBUHALER(R); TERBUTALINE	Delivery of more drug to the lung may appear to be a desirable goal in the treatment of asthma and chronic obstructive pulmonary disease, since only 10 to 15% of a drug dose administered via a metered dose inhaler (MDI) reaches the lung. However, increasing the dose of most inhaled drugs may only lead to an increase in side effects, since maximal clinical benefit is usually obtained with the currently recommended dosages. Improving the regional deposition of inhaled drugs may be a more effective way of modifying clinical response. Particle size is the most significant determinant of the deposition pattern of inhaled drugs. Optimum drug delivery to the conducting airways occurs with particles ranging from 2.5 to 6 mum; particles <2.5 <mu>m are deposited mainly in the alveoli where they may exert no pharmacodynamic effect and are rapidly absorbed, increasing the risk of systemic adverse events. Delivery devices can be compared by estimating the lung and systemic exposures, taking into account the efficacy and safety dose-response relationships for the drug-device combination. Current devices have profoundly different lung deposition profiles that could affect clinical efficacy when switching devices. Devices that achieve a high lung to systemic ratio for the inhaled drug are preferable.	Glaxo Wellcome Plc, Uxbridge UB11 1BT, Middx, England	Pritchard, JN (reprint author), Glaxo Wellcome Plc, Stockley Pk W, Uxbridge UB11 1BT, Middx, England.						Arvidsson Peter, 1998, European Respiratory Journal, V12, p67S; Barnes NC, 1998, RESP MED, V92, P95, DOI 10.1016/S0954-6111(98)90039-7; Borgstrom L, 1998, J AEROSOL MED, V11, P55, DOI 10.1089/jam.1998.11.55; BORGSTROM L, 1994, EUR RESPIR J, V7, P69, DOI 10.1183/09031936.94.07010069; BUSSE W, 1998, AM J RESP CRIT CARE, V157, pA405; Derendorf H, 1998, J ALLERGY CLIN IMMUN, V101, pS440, DOI 10.1016/S0091-6749(98)70156-3; ENGEL T, 1992, BRIT J CLIN PHARMACO, V33, P439; Harrison L., 1997, European Respiratory Journal Supplement, V10, p349S; Harrison L., 1997, AM J RESP CRIT CAR S, V155, pA666; Jeffery PK, 1998, EUR RESPIR J, V11, P524; Kobrich R, 1994, ANN OCCUP HYG     S1, V38, P15; Lipworth BJ, 1997, EUR J CLIN PHARMACOL, V53, P47, DOI 10.1007/s002280050335; Mackie A. E., 1997, British Journal of Clinical Pharmacology, V43, p540P; MARTONEN TB, 1993, J AEROSOL MED, V6, P251, DOI 10.1089/jam.1993.6.251; PRITCHARD J, 1998, RESP DRUG DELIVERY, V6, P401; PRITCHARD JN, 1996, P 6 C DRUG DEL LUNGS, P101; Rott Z., 1998, European Respiratory Journal, V12, p324S; Seale JP, 1998, RESP MED, V92, P9, DOI 10.1016/S0954-6111(98)90212-8; THORSSON L, 1994, EUR RESPIR J, V7, P1839, DOI 10.1183/09031936.94.07101839	19	107	108	0	5	MARY ANN LIEBERT INC PUBL	LARCHMONT	2 MADISON AVENUE, LARCHMONT, NY 10538 USA	0894-2684			J AEROSOL MED	J. Aerosol Med.-Depos. Clear. Eff. Lung		2001	14			1			S19	S26				8	Public, Environmental & Occupational Health; Respiratory System	Public, Environmental & Occupational Health; Respiratory System	408NQ	WOS:000167332600004	11424889	
J	Wyler, C; Braun-Fahrlander, C; Kunzli, N; Schindler, C; Ackermann-Liebrich, U; Perruchoud, AP; Leuenberger, P; Wuthrich, B				Wyler, C; Braun-Fahrlander, C; Kunzli, N; Schindler, C; Ackermann-Liebrich, U; Perruchoud, AP; Leuenberger, P; Wuthrich, B		Swiss Study Air Pollution Lung Di	Exposure to motor vehicle traffic and allergic sensitization	EPIDEMIOLOGY			English	Article						air pollution; allergies; pollen; traffic density	CHRONIC RESPIRATORY SYMPTOMS; DIESEL EXHAUST PARTICLES; AIR-POLLUTANTS; ADJUVANT ACTIVITY; ASTHMA; POLLUTION; CHILDREN; MICE; POLLEN; ADULTS	We examined the association between the presence of an allergic sensitization and seasonal allergic diseases or symptoms and the exposure to road traffic in Basel, Switzerland. Traffic counts at the domiciles of subjects ranged from 24 to 32,504 cars per 24 hours, with a median of 1,624. To investigate the relation of road traffic and allergies, we matched the data of the traffic inventory of Basel with those of the 820 participants of the SAPALDIA study (Swiss Study on Air Pollution and Lung Diseases in Adults), ages 18-60 years, who had completed a detailed respiratory health questionnaire and had undergone allergy testing (skin prick tests and serologic examinations). We observed a positive association with a sensitization to pollen that was most pronounced among persons with a duration of residence of at least 10 years. The odds ratios (adjusted for educational level, smoking behavior, number of siblings, age, sex, and family history of atopy) for cars, contrasting four exposure categories with the lowest quartile as referent category, were 1.99 [95% confidence interval (CI) = 0.91-4.38], 2.47 (95% CI = 1.06-5.73), and 2.83 (95% CI = 1.26-6.31). These results suggest that living on busy roads is associated with a higher risk for a sensitization to pollen and could possibly he interpreted as an indication for interactions between pollen and air pollutants. We did not, however, find a similar relation between motor vehicle traffic and hay fever or seasonal allergic symptoms, and we saw no trend that increasing traffic exposure was associated with a rise in sensitization rates to indoor allergens.	Univ Basel, Inst Social & Prevent Med, CH-4051 Basel, Switzerland; Univ Basel Hosp, Dept Internal Med, CH-4031 Basel, Switzerland; Univ Lausanne Hosp, Dept Pneumol, Lausanne, Switzerland; Univ Zurich Hosp, Dept Dermatol, Allergy Unit, CH-8091 Zurich, Switzerland	Braun-Fahrlander, C (reprint author), Univ Basel, Inst Social & Prevent Med, Steinengraben 49, CH-4051 Basel, Switzerland.		Schindler, Christian/D-3472-2015; Kunzli, Nino/F-7195-2014	Kunzli, Nino/0000-0001-8360-080X			AckermannLiebrich U, 1997, AM J RESP CRIT CARE, V155, P122; *BAUD KANT BAS STA, 1994, GES REG BAS KURZB, P1; Behrendt H, 1997, INT ARCH ALLERGY IMM, V113, P69; BEHRENDT H, 1992, INT ARCH ALLERGY IMM, V99, P425; BRAUNFAHRLANDER C, 1996, NEW TRENDS ALLERGY 4; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; Chinn S, 1996, EUR J EPIDEMIOL, V12, P155, DOI 10.1007/BF00145501; Ciccone G, 1998, OCCUP ENVIRON MED, V55, P771; Devalia JL, 1997, ALLERGY, V52, P45; Duhme H, 1996, EPIDEMIOLOGY, V7, P578, DOI 10.1097/00001648-199611000-00003; Emberlin J, 1995, CLIN EXP ALLERGY, V25, P33, DOI 10.1111/j.1365-2222.1995.tb00040.x; HELSTAB J, 1998, NO2 IMMISIONEN KANTO; ISHIZAKI T, 1987, ANN ALLERGY, V58, P265; Jorres R, 1996, AM J RESP CRIT CARE, V153, P56; JUNKER M, IN PRESS ATMOSPH ENV; Knox RB, 1997, CLIN EXP ALLERGY, V27, P246; Dolgner R, 1991, EPIDEMIOLOGIE ALLERG, P165; LEUENBERGER P, 1994, AM J RESP CRIT CARE, V150, P1222; Martin BW, 1997, SOZ PRAVENTIV MED, V42, P67, DOI 10.1007/BF01318136; MATSUMUR.Y, 1970, AM REV RESPIR DIS, V102, P430; Miyabara Y, 1998, AM J RESP CRIT CARE, V157, P1138; MOLFINO NA, 1991, LANCET, V338, P199, DOI 10.1016/0140-6736(91)90346-Q; MURANAKA M, 1986, J ALLERGY CLIN IMMUN, V77, P616, DOI 10.1016/0091-6749(86)90355-6; Oosterlee A, 1996, OCCUP ENVIRON MED, V53, P241; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; RUFFIN J, 1986, CYTOBIOS, V46, P119; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Studnicka M, 1997, EUR RESPIR J, V10, P2275, DOI 10.1183/09031936.97.10102275; TAKAFUJI S, 1987, J ALLERGY CLIN IMMUN, V79, P639, DOI 10.1016/S0091-6749(87)80161-6; Takano H, 1997, AM J RESP CRIT CARE, V156, P36; USSETTI P, 1984, LANCET, V1, P156; VONMUTIUS E, 1994, BRIT MED J, V308, P692; Weiland Stephan K., 1994, Annals of Epidemiology, V4, P243; WJST M, 1993, BRIT MED J, V307, P596; WUTHRICH B, 1995, INT ARCH ALLERGY IMM, V106, P149	35	107	110	3	17	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	1044-3983			EPIDEMIOLOGY	Epidemiology	JUL	2000	11	4					450	456		10.1097/00001648-200007000-00015		7	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	326CD	WOS:000087713600015	10874554	
J	Papadopoulos, NG; Arakawa, H; Carlsen, KH; Custovic, A; Gern, J; Lemanske, R; Le Souef, P; Makela, M; Roberts, G; Wong, G; Zar, H; Akdis, CA; Bacharier, LB; Baraldi, E; van Bever, HP; de Blic, J; Boner, A; Burks, W; Casale, TB; Castro-Rodriguez, JA; Chen, YZ; El-Gamal, YM; Everard, ML; Frischer, T; Geller, M; Gereda, J; Goh, DY; Guilbert, TW; Hedlin, G; Heymann, PW; Hong, SJ; Hossny, EM; Huang, JL; Jackson, DJ; de Jongste, JC; Kalayci, O; Ait-Khaled, N; Kling, S; Kuna, P; Lau, S; Ledford, DK; Lee, SI; Liu, AH; Lockey, RF; Lodrup-Carlsen, K; Lotvall, J; Morikawa, A; Nieto, A; Paramesh, H; Pawankar, R; Pohunek, P; Pongracic, J; Price, D; Robertson, C; Rosario, N; Rossenwasser, LJ; Sly, PD; Stein, R; Stick, S; Szefler, S; Taussig, LM; Valovirta, E; Vichyanond, P; Wallace, D; Weinberg, E; Wennergren, G; Wildhaber, J; Zeiger, RS				Papadopoulos, N. G.; Arakawa, H.; Carlsen, K. -H.; Custovic, A.; Gern, J.; Lemanske, R.; Le Souef, P.; Makela, M.; Roberts, G.; Wong, G.; Zar, H.; Akdis, C. A.; Bacharier, L. B.; Baraldi, E.; van Bever, H. P.; de Blic, J.; Boner, A.; Burks, W.; Casale, T. B.; Castro-Rodriguez, J. A.; Chen, Y. Z.; El-Gamal, Y. M.; Everard, M. L.; Frischer, T.; Geller, M.; Gereda, J.; Goh, D. Y.; Guilbert, T. W.; Hedlin, G.; Heymann, P. W.; Hong, S. J.; Hossny, E. M.; Huang, J. L.; Jackson, D. J.; de Jongste, J. C.; Kalayci, O.; Ait-Khaled, N.; Kling, S.; Kuna, P.; Lau, S.; Ledford, D. K.; Lee, S. I.; Liu, A. H.; Lockey, R. F.; Lodrup-Carlsen, K.; Lotvall, J.; Morikawa, A.; Nieto, A.; Paramesh, H.; Pawankar, R.; Pohunek, P.; Pongracic, J.; Price, D.; Robertson, C.; Rosario, N.; Rossenwasser, L. J.; Sly, P. D.; Stein, R.; Stick, S.; Szefler, S.; Taussig, L. M.; Valovirta, E.; Vichyanond, P.; Wallace, D.; Weinberg, E.; Wennergren, G.; Wildhaber, J.; Zeiger, R. S.			International consensus on (ICON) pediatric asthma	ALLERGY			English	Review						asthma; children; consensus; guidelines; wheeze	INHALED FLUTICASONE PROPIONATE; RANDOMIZED CONTROLLED-TRIAL; GRASS-POLLEN IMMUNOTHERAPY; NITRIC-OXIDE MEASUREMENTS; ACTING BETA-AGONISTS; HOUSE-DUST MITE; LONG-TERM; CHILDHOOD ASTHMA; AIRWAY HYPERRESPONSIVENESS; PRESCHOOL-CHILDREN	Asthma is the most common chronic lower respiratory disease in childhood throughout the world. Several guidelines and/or consensus documents are available to support medical decisions on pediatric asthma. Although there is no doubt that the use of common systematic approaches for management can considerably improve outcomes, dissemination and implementation of these are still major challenges. Consequently, the International Collaboration in Asthma, Allergy and Immunology (iCAALL), recently formed by the EAACI, AAAAI, ACAAI, and WAO, has decided to propose an International Consensus on (ICON) Pediatric Asthma. The purpose of this document is to highlight the key messages that are common to many of the existing guidelines, while critically reviewing and commenting on any differences, thus providing a concise reference. The principles of pediatric asthma management are generally accepted. Overall, the treatment goal is disease control. To achieve this, patients and their parents should be educated to optimally manage the disease, in collaboration with healthcare professionals. Identification and avoidance of triggers is also of significant importance. Assessment and monitoring should be performed regularly to re-evaluate and fine-tune treatment. Pharmacotherapy is the cornerstone of treatment. The optimal use of medication can, in most cases, help patients control symptoms and reduce the risk for future morbidity. The management of exacerbations is a major consideration, independent of chronic treatment. There is a trend toward considering phenotype-specific treatment choices; however, this goal has not yet been achieved.	[Papadopoulos, N. G.] Univ Athens, Dept Allergy, Pediat Clin 2, Athens 11527, Greece; [Arakawa, H.] Gunma Univ, Grad Sch Med, Dept Pediat, Gunma, Japan; [Carlsen, K. -H.] Oslo Univ Hosp, Dept Pediat, Oslo, Norway; [Custovic, A.] Univ Hosp S Manchester NHS Fdn Trust, Resp Res Grp, Manchester, Lancs, England; [Gern, J.] Univ Wisconsin, Sch Med, Dept Pediat, Madison, WI USA; [Lemanske, R.] Univ Wisconsin, Sch Med & Publ Hlth, Div Pediat Allergy Immunol & Rheumatol, Madison, WI USA; [Le Souef, P.] Univ Western Australia, Princess Margaret Hosp, Sch Pediat & Child Hlth, Perth, WA 6009, Australia; [Makela, M.] Univ Helsinki, Cent Hosp, Pediat Unit, Helsinki, Finland; [Roberts, G.] Southampton Univ Hosp NHS Trust, Acad Unit Human Dev & Hlth, Southampton, Hants, England; [Wong, G.] Chinese Univ Hong Kong, Dept Pediat, Sha Tin, Hong Kong, Peoples R China; [Zar, H.] Univ Cape Town, Red Cross War Mem Childrens Hosp, Dept Pediat & Child Hlth, ZA-7925 Cape Town, South Africa; [Akdis, C. A.] Swiss Inst Allergy & Asthma Res SIAF, Davos, Switzerland; [Bacharier, L. B.] Washington Univ, Sch Med, Dept Pediat, Div Pediat Allergy Immunol & Pulm Med, St Louis, MO 63110 USA; [Baraldi, E.] Univ Padua, Dept Pediat, Unit Allergy & Resp Med, Padua, Italy; [Bacharier, L. B.] St Louis Childrens Hosp, St Louis, MO 63178 USA; [van Bever, H. P.] Natl Univ Hlth Syst, Natl Univ Hosp, Childrens Med Inst, Dept Paediat, Singapore, Singapore; [de Blic, J.] Univ Paris 05, AP HP, Serv Pneumol & Allergol Pediat, Paris, France; [Boner, A.] Univ Verona, Dept Paediat, I-37100 Verona, Italy; [Burks, W.] Duke Univ, Med Ctr, Dept Pediat, Div Allergy & Immunol, Durham, NC 27710 USA; [Casale, T. B.] Creighton Univ, Div Allergy & Immunol, Dept Med, Omaha, NE 68178 USA; [Castro-Rodriguez, J. A.] Pontificia Univ Catolica Chile, Sch Med, Santiago, Chile; [El-Gamal, Y. M.] Ain Shams Univ, Pediat Allergy & Immunol Unit, Cairo, Egypt; [Chen, Y. Z.] Capital Inst Pediat, Beijing, Peoples R China; [Everard, M. L.] Sheffield Childrens Hosp, Dept Resp Med, Sheffield, S Yorkshire, England; [Geller, M.] Geller Allergy & Immunol Clin, Rio De Janeiro, Brazil; [Frischer, T.] Univ Childrens Hosp Vienna, Vienna, Austria; [Gereda, J.] Clin Ricardo Palma, Dept Allergy & Immunol, Lima, Peru; [Goh, D. Y.] Natl Univ Singapore Hosp, Dept Paediat, Singapore 117548, Singapore; [Hedlin, G.] Karolinska Univ Hosp, Astrid Lindgren Childrens Hosp, Stockholm, Sweden; [Heymann, P. W.] Univ Virginia, Asthma & Allerg Dis Ctr, Charlottesville, VA USA; [Hong, S. J.] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Pediat,Childhood Asthma Atopy Ctr, Seoul, South Korea; [Hossny, E. M.] Ain Shams Univ, Childrens Hosp, Pediat Allergy & Immunol Unit, Cairo, Egypt; [Huang, J. L.] Chang Gung Childrens Hosp, Dept Pediat, Div Allergy Asthma & Rheumatol, Tao Yuan, Taiwan; [Jackson, D. J.] Univ Wisconsin, Dept Pediat, Sch Med & Publ Hlth, Madison, WI USA; [de Jongste, J. C.] Erasmus Univ, Sophia Childrens Hosp, Med Ctr, Dept Pediat, Rotterdam, Netherlands; [Kalayci, O.] Hacettepe Univ, Sch Med, Ihsan Dogramaci Childrens Hosp, Pediat Allergy & Asthma Unit, Ankara, Turkey; [Ait-Khaled, N.] Int Union TB & Lung Dis, Algiers, Algeria; [Kling, S.] Univ Stellenbosch, Tygerberg Childrens Hosp, Dept Paediat & Child Hlth, Cape Town, South Africa; [Kuna, P.] Med Univ Lodz, Barlicki Univ Hosp, Dept Med 2, Lodz, Poland; [Lau, S.] Charite, Dept Pediat Pneumol & Immunol, D-13353 Berlin, Germany; [Ledford, D. K.; Lockey, R. F.] Univ S Florida, Div Allergy Immunol, Tampa, FL USA; [Lee, S. I.] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pediat,Environm Hlth Ctr, Seoul, South Korea; [Liu, A. H.] Univ Colorado Denver, Sch Med, Denver, CO USA; [Szefler, S.] Natl Jewish Hlth, Dept Pediat, Denver, CO USA; [Lodrup-Carlsen, K.] Ullevaal Univ Hosp, Dept Paediat, Woman & Child Div, Oslo, Norway; [Morikawa, A.] Gunma Univ, Kita Kanto Allergy Inst, Gunma, Japan; [Lotvall, J.] Univ Gothenburg, Krefting Res Ctr, Gothenburg, Sweden; [Nieto, A.] Childrens Hosp La Fe, Pediat Allergy Unit, Valencia, Spain; [Paramesh, H.] Lakeside Med Ctr & Hosp, Bangalore, Karnataka, India; [Pawankar, R.] Nippon Med Sch, Dept Pediat, Div Allergy & Immunol, Tokyo 113, Japan; [Pohunek, P.] Charles Univ Prague, Dept Pediat, Univ Hosp Motol, Prague, Czech Republic; [Pongracic, J.] Childrens Mem Hosp, Div Allergy & Immunol, Chicago, IL 60614 USA; [Price, D.] Univ Aberdeen, Primary Care Resp Soc UK, Aberdeen, Scotland; [Robertson, C.] Royal Childrens Hosp, Melbourne, Vic, Australia; [Rosario, N.] Hosp Clin UFPR, Div Pediat Allergy, Curitiba, Parana, Brazil; [Rossenwasser, L. J.] Childrens Mercy Hosp, Kansas City, MO 64108 USA; [Sly, P. D.] Univ Queensland, Queensland Childrens Med Res Inst, Brisbane, Qld, Australia; [Stein, R.] Pontificia Univ Catolica RGS, Hosp Sao Lucas, Pediat Pulm Serv, Porto Alegre, RS, Brazil; [Stick, S.] Princess Margaret Hosp Children, Dept Resp Med, Perth, WA, Australia; [Taussig, L. M.] Univ Denver, Off Provost, Denver, CO USA; [Valovirta, E.] Univ Turku, Allergy Clin, Terveystalo Turku, Turku, Finland; [Vichyanond, P.] Siriraj Hosp, Fac Med, Int Affairs & Ctr Excellence, Bangkok, Thailand; [Weinberg, E.] Univ Cape Town, Red Cross Childrens Hosp, Allergy Unit, ZA-7925 Cape Town, South Africa; [Wallace, D.] Nova SE Univ, Ft Lauderdale, FL 33314 USA; [Wennergren, G.] Univ Gothenburg, Dept Pediat, Gothenburg, Sweden; [Wildhaber, J.] Univ Childrens Hosp, Dept Resp Med, Zurich, Switzerland; [Zeiger, R. S.] Kaiser Permanente So Calif, Dept Allergy, San Diego, CA USA	Papadopoulos, NG (reprint author), Univ Athens, Dept Allergy, Pediat Clin 2, 41 Fidippidou St, Athens 11527, Greece.	ngp@allergy.gr	Sly, Peter/F-1486-2010; Casale, Thomas/K-4334-2013; Stein, Renato/K-2568-2014; Stick, Stephen/O-5683-2014; Van Bever, Hugo PS/D-8473-2015; Goh, Daniel/D-8573-2015; Custovic, Adnan/A-2435-2012	Sly, Peter/0000-0001-6305-2201; Papadopoulos, Nikolaos/0000-0002-2508-3872; BARALDI, EUGENIO/0000-0002-1829-3652; Kling, Sharon/0000-0002-4498-1811; Casale, Thomas/0000-0002-3149-7377; Custovic, Adnan/0000-0001-5218-7071; Guilbert, Theresa/0000-0002-6932-712X; Lotvall, Jan/0000-0001-9195-9249; Price, David/0000-0002-9728-9992; Makela, Mika/0000-0002-2933-3111	Nestle; MSD; Deviblis (EBT); MRC Moulton Charitable Foundation; Merck Inc; Astra Zeneca; GlaxoSmithKline; AstraZeneca; Novartis Research; PREDICTA: European Commission [260895]; Swiss National Science Foundation Research; MeDALL: European Commission [261357]; Christine Kuhne-Center for Allergy Research and Education Research; Food Allergy and Anaphylaxis Network; Food Allergy Initiative; NIH; National Peanut Board; SHS; Wallace Research Foundation; Altus Pharmaceuticals; Inspire Pharmaceuticals; National Institutes of Health; NIH [U01]; AAAAI/GlaxoSmithKline; Pharmaxis; Grupo Uriach Pharma; Turkish National Science Foundation; Hacettepe University; GSK; Adamed; SymbioPharm; Airsonett; Forest Pharmaceuticals; Viro Pharma; Novartis; ALA, Pharmaceuticals; National and regional grants for research in our group; Novartis Pharma; MEDA Pharma; CBF LETI; Allergopharma; Inmunotek; UK National Health Service; Aerocrine; Boehringer Ingelheim; Merck; Mundipharma; Nycomed; Pfizer; Teva; Ross; Abbott; Merck Sharp Dohme; Genentech; MedImmune; Thermofisher	N. G. Papadopoulos has received payment for consultancy from Abbott and for lectures from MSD, and grants from Nestle, MSD, Deviblis (EBT). K.-H. Carlsen has served on an international consultatory paediatric board for GSK, and given presentations for GSK, MSD, PolarMed and Schering Plough. A. Custovic has received payment for consultancy and lectures from Novartis and for lectures from Glaxo-SmithKline, Thermo Fisher Scientific, Airsonet, MSD, and grants from MRC Moulton Charitable Foundation. J. Gern has received payment for board membership from 3V Bio-Sciences, for consultancy form GlaxoSmithKline, Biota, Centocor, Boehringer Ingelheim, MedImmune, Gilead, Theraclone, Synairgen, Pulmatrix, and grants from Merck Inc, Astra Zeneca, GlaxoSmithKline. R. Lemanske has received payment for consultancy from Merck, Sepracor, SA Boney and Associates Ltd, GlaxoSmithKline, American Institute of Research, Genentech, Inc., Double Helix Development, Inc., for lectures from Michigan Public Health Institute, Allegheny General Hospital, American Academy of Pediatrics, West Allegheny Health Systems, Inc., California Chapter 4, AAP, Colorado Allergy Society, Pennsylvania Allergy and Asthma Association, Harvard Pilgrim Health, California Society of Allergy, NYC Allergy Society, World Allergy Organization, American College of Chest Physicians, AAAAI, for Employment from University of Wisconsin School of Medicine and Public Health, for Royalties from Elsevier, and grants from National Heart Lung and Blood Institute, Pharmaxis. P. Le Souef has received a grant from AstraZeneca. G. Roberts is a member of the steering committee for the GAP trial, paid by ALK. C. A. Akdis has received payment for consultancy from Actellion, Aventis, Stallergenes, Allergopharma, Circacia, Swiss Institute of Allergy and Asthma Research, University of Zurich, Switzerland, and grants from Novartis Research on immunoregulation in asthma, PREDICTA: European Commission's Seventh Framework programme No. 260895 Research on virus induced exacerbations, Swiss National Science Foundation Research on T cell interaction with the epithelium, MeDALL: European Commission's Seventh Framework Programme No. 261357 Research on early initiation of asthma, Christine Kuhne-Center for Allergy Research and Education Research on severe allergies. L. B. Bacharier has received payment for consultancy from Aerocrine, GlaxoSmithKline, Genentech/Novartis, Merck, Schering, Cephalon and for lectures from Aerocrine, AstraZeneca, Genentech, GlaxoSmithKline, Merck, Schering. J. de Blic is member of the steering committee for the GAP trial, paid by ALK. He is also a member of the advisory board on asthma in children for GSK, MSD, CHIESI, and Stallergenes. W. Burks has consulted for Dannon Co. Probiotics, Exploramed Development LLC, Intelliject, McNeil Nutritionals, Merck & Co., Novartis, Nutricia, Pfizer, Portola Pharmaceuticals and Schering-Plough; has received grants from the Food Allergy and Anaphylaxis Network, the Food Allergy Initiative, the NIH, the National Peanut Board, SHS, and the Wallace Research Foundation; and owns stock or stock options in Allertein and Mast Cell, Inc. T. B. Casale has received payment from consultancy from MedImmune. J. A. Castro-Rodriguez has received payment for development of educational presentation from AZ, GSK, MSD, Novartis. T. Frischer has worked on a national advisory board for MSD. T. W.; Guilbert has received honoraria from GlaxoSmithKline, AstraZeneca, PeerPoint Medical Education Institute, Merck, and Antidote; has received research support from Altus Pharmaceuticals, Inspire Pharmaceuticals, and the National Institutes of Health; and is a member of the American Lung Association, the American Thoracic Society, and the American Academy of Pediatrics. P. W. Heymann has received payment for Employment from University of Virginia and grant from NIH/U01 grant. D. J. Jackson has received payment for consultancy from Gilead and grants from NIH, AAAAI/GlaxoSmithKline, Pharmaxis. O. Kalayci has received payment for consultancy from MERCK and received lecture fee from Grupo Uriach Pharma, and grants from Turkish National Science Foundation, Hacettepe University. S. Kling has received payment for Ethics lectures from MSD (Merck) and travel expenses from Cipla Medpro with Sponsorship to Allergy Society of South Africa (ALLSA) Congress 2010; money paid to ALLSA. P. Kuna has received payment for board membership and for lectures from AstraZeneca, Boehringer, MSD, and lecture fee from GSK, Adamed. S. Lau has received payment for consultancy from Merck, for lectures from Symbiopharm, Novartis, ALK, AstraZeneca, and grants from SymbioPharm, Airsonett. D. K. Ledford has received payment for consultancy from Genentech, for expert testimony from Shook Hardy & Bacon, and grants from Forest Pharmaceuticals, Viro Pharma. A. H. Liu has served on the speakers' bureau for Merck, Aerocrine, and Phadia; has served on the speakers' bureau and advisory board for GlaxoSmithKline and AstraZeneca; and has received a research grant from Novartis. R. F. Lockey has received payment for Board membership from the World Allergy Organization, for consultancy from Merck, ALK, for employment from the University of Florida, VA Hospital, for expert testimony from two law firms, and received grants from ALA, Pharmaceuticals. He has also received payment for lectures from Merck, AstraZeneca, royalties from Informa Publishing, for travel expenses to World Allergy Organization meetings, international congresses for presenting lectures; and owns stock or stock options in Roth IRA acct. K. Lodrup Carlsen has received payment for lectures from GlaxoSmithKline in the last year (once) and grants from National and regional grants for research in our group. J. Lotvall has consulted for Glaxo-SmithKline, Novartis, and Merck; has received grants from GlaxoSmithKline; and has received payment for lectures from AstraZeneca, Glaxo-SmithKline, Novartis, and Merck. A. Nieto has received payment for board membership, consultancy and lecture fee from Novartis Pharma, MEDA Pharma, CBF LETI, MSD, Allergopharma, and also for development of educational presentations from Schering-Plough and grants from Inmunotek. P. Pohunek has received lecture honoraria from AstraZeneca, GSK, MSD, UCB Pharma and travel support for scientific meetings by AstraZeneca, GSK, MSD and Chiesi. D. Price has consultant arrangements with Boehringer Ingelheim, GlaxoSmithKline, Merck, Mundipharma, Novartis and Teva; he or his research team have received grants and support for research in respiratory disease from the following organizations in the last 5 years: UK National Health Service, Aerocrine, AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Merck, Mundipharma, Novartis, Nycomed, Pfizer and Teva. He has spoken for Boehringer Ingelheim, Chiesi, GlaxoSmithKline, Merck, Mundipharma, Pfizer and Teva, he has shares in AKL Ltd.; , which produces phytopharmaceuticals, and he is the sole owner of Research n Real Life Ltd. N. Rosario has received payment for board membership from Sanofi Aventis, Takeda, MSD, for consultancy from MSD, Sanofi Aventis, GSK, for lectures from MSD, Sanofi Aventis, GSK, Takeda, Ache, Danone and for development of educational presentations from MSD, Sanofi Aventis, Danone. L. J. Rosenwasser has received payment for board membership from WAO and for consultancy from Genentech, Novartis, AZ, Regeneron, Sanofi. R. Stein has received payment for lectures from Abbott. S. Szefler has received payment for consultancy from Merck, Genentech, Schering, Boehringer-Ingehlheim, Novartis, GlaxoSmithKline, for lectures from Merck, manuscript preparation from Genentech, for patents from NHLBI CARE Network, and grants from GlaxoSmithKline, Ross, Abbott. G. Wennergren has received has received fees for lectures from Novartis, Merck Sharp & Dohme, AstraZeneca and GlaxoSmithKline. J. Wildhaber has served on national and international advisory boards of Nycomed and MSD and has received research grants from AstraZeneca, GSK and MSD. R. S. Zeiger has received payment for consultancy from Aerocrine, AstraZeneca, Genentech, GlaxoSmithKline, MedImmune, ScheringPlough, Sunovion, Novartis, NHLBI/Penn State and grants from Genentech, GlaxoSmithKline, Aerocrine, Merck, MedImmune, Thermofisher. H. Arakawa, M. Makela, G. Wong, H. Zar, E. Baraldi, H. P. van Bever, A. Boner, Y. Z. Chen, Y. M. El-Gamal, M. L. Everard, M. Geller, J. Gereda, D. Y. Goh, G. Hedlin, S. J. Hong, E. M. Hossny, J. L. Huang, J. C. de Jongste, N. Ait-Khaled, S. I. Lee, A. Morikawa, H. Paramesh, R. Pawankar, J. Pongracic, C. Robertson, D. Sly, S. Stick, L. M. Taussig, E. Valovirta, P. Vichyanond, D. Wallace, E. Weinberg, have no conflicts of interest to declare.	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J	Holz, O; Khalilieh, S; Ludwig-Sengpiel, A; Watz, H; Stryszak, P; Soni, P; Tsai, M; Sadeh, J; Magnussen, H				Holz, O.; Khalilieh, S.; Ludwig-Sengpiel, A.; Watz, H.; Stryszak, P.; Soni, P.; Tsai, M.; Sadeh, J.; Magnussen, H.			SCH527123, a novel CXCR2 antagonist, inhibits ozone-induced neutrophilia in healthy subjects	EUROPEAN RESPIRATORY JOURNAL			English	Article						Anti-inflammatory; chronic obstructive pulmonary disease; interleukin-8; myeloperoxidase; pharmacodynamics	OBSTRUCTIVE PULMONARY-DISEASE; AIRWAY INFLAMMATION; HISTONE DEACETYLASE; ACTIVATION MARKERS; INDUCED SPUTUM; BONE-MARROW; ASTHMA; COPD; RECRUITMENT; EXPOSURES	SCH527123 is a novel, selective CXC chemokine receptor 2 antagonist that inhibits neutrophil activation and modulates neutrophil trafficking in animal models, characteristics that may be beneficial in the treatment of conditions with unbalanced pulmonary neutrophilia, such as chronic obstructive pulmonary disease. The purpose of this proof-of-principle study was to determine whether SCH527123 inhibits ozone-induced neutrophil recruitment in healthy humans. In a randomised, double-blind, placebo-controlled, three-way crossover study, oral SCH527123 (50 mg once daily, 4 days), prednisolone (50 mg once), or placebo was alternated with 2-week washouts. 18 healthy ozone responders (>20% increase in sputum neutrophils) underwent ozone challenge tests (250 ppb, 3 h intermittent exercise) 1 h after the last treatment dose. Sputum was induced at 3 h post-challenge. After SCH527123 treatment, the ozone challenge resulted in significantly lower sputum neutrophil counts (0.13 x 10(6).mL(-1)) compared with prednisolone (0.84 x 10(6).mL(-1); p<0.001) or placebo (2.98 x 10(6).mL(-1); p<0.001). Comparable results were obtained for total cell count, percentage of sputum neutrophils, and for interleukin-8 and myeloperoxidase in sputum supernatant. Post-challenge, SCH527123 inhibited neutrophilia in peripheral blood but significantly less than in sputum. All treatments were safe and well tolerated. SCH527123 causes significant attenuation of ozone-induced airway neutrophilia in healthy subjects. Further evaluation in a large trial of patients with pulmonary disorders is warranted.	[Holz, O.; Ludwig-Sengpiel, A.; Watz, H.; Magnussen, H.] Hosp Grosshansdorf, Pulm Res Inst, D-22927 Grosshansdorf, Germany; [Khalilieh, S.; Stryszak, P.; Soni, P.; Tsai, M.; Sadeh, J.] Schering Plough Res Inst, Kenilworth, NJ USA	Magnussen, H (reprint author), Hosp Grosshansdorf, Pulm Res Inst, Woehrendamm 80, D-22927 Grosshansdorf, Germany.	magnussen@pulmoresearch.de			Schering-Plough Research Institute	This research was funded by Schering-Plough Research Institute.	Adams DH, 1997, LANCET, V349, P490, DOI 10.1016/S0140-6736(96)07524-1; Alexis NE, 2008, ENVIRON HEALTH PERSP, V116, P799, DOI 10.1289/ehp.10981; Balmes JR, 1996, AM J RESP CRIT CARE, V153, P904; Barnes PJ, 2006, CHEST, V129, P151, DOI 10.1378/chest.129.1.151; Chapman RW, 2007, J PHARMACOL EXP THER, V322, P486, DOI 10.1124/jpet.106.119040; EVANS E, 2007, EUR RESP J S51, V30, pS775; Holz O, 1998, CLIN EXP ALLERGY, V28, P284; Holz O, 1999, AM J RESP CRIT CARE, V159, P776; Holz O, 2005, J CLIN PHARMACOL, V45, P498, DOI 10.1177/0091270004273527; Holz O, 2002, CLIN EXP ALLERGY, V32, P681, DOI 10.1046/j.1365-2222.2002.01358.x; Ito K, 2005, NEW ENGL J MED, V352, P1967, DOI 10.1056/NEJMoa041892; Jorres RA, 1997, CHEST, V111, P866, DOI 10.1378/chest.111.4.866; Jorres RA, 2000, AM J RESP CRIT CARE, V161, P1855; Keatings VM, 1996, AM J RESP CRIT CARE, V153, P530; Khalilieh S, 2007, EUR RESP J S51, V30, p613s; KHALILIEH S, 2007, EUR RESP J S51, V30, pS612; Mann BS, 2006, RESP RES, V7, DOI 10.1186/1465-9921-7-59; Martin C, 2003, IMMUNITY, V19, P583, DOI 10.1016/S1074-7613(03)00263-2; Nathan C, 2006, NAT REV IMMUNOL, V6, P173, DOI 10.1038/nri1785; O'Donnell RA, 2004, THORAX, V59, P837, DOI 10.1136/thx.2003.019349; PIN I, 1992, THORAX, V47, P25, DOI 10.1136/thx.47.1.25; Rabe KF, 2007, AM J RESP CRIT CARE, V176, P532, DOI 10.1164/rccm.200703-456SO; Rutgers SR, 2000, THORAX, V55, P12, DOI 10.1136/thorax.55.1.12; Semerad CL, 2002, IMMUNITY, V17, P413, DOI 10.1016/S1074-7613(02)00424-7; Stanescu D, 1996, THORAX, V51, P267, DOI 10.1136/thx.51.3.267; Stockley RA, 1999, AM J RESP CRIT CARE, V160, pS49; Stockley RA, 2002, CHEST, V121, P151, DOI DOI 10.1378/CHEST.121.5_; Suratt BT, 2004, BLOOD, V104, P565, DOI 10.1182/blood-2003-10-3638; Thatcher TH, 2005, AM J PHYSIOL-LUNG C, V289, pL322, DOI 10.1152/ajplung.00039.2005; van Beurden WJC, 2003, RESP MED, V97, P401, DOI 10.1053/rmed.2002.1461	30	106	107	1	4	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	442 GLOSSOP RD, SHEFFIELD S10 2PX, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	MAR	2010	35	3					564	570		10.1183/09031936.00048509		7	Respiratory System	Respiratory System	564TA	WOS:000275239000016	19643947	
J	Adenuga, D; Yao, H; March, TH; Seagrave, J; Rahman, I				Adenuga, David; Yao, Hongwei; March, Thomas H.; Seagrave, Jeanclare; Rahman, Irfan			Histone Deacetylase 2 Is Phosphorylated, Ubiquitinated, and Degraded by Cigarette Smoke	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article						COPD; HDAC2; cigarette smoke; lung; inflammation	PROINFLAMMATORY CYTOKINE RELEASE; PROTEIN-KINASE CK2; NF-KAPPA-B; OBSTRUCTIVE PULMONARY-DISEASE; ALVEOLAR EPITHELIAL-CELLS; INDUCED LUNG INFLAMMATION; OXIDATIVE STRESS; CHROMATIN MODIFICATION; REDOX REGULATION; DEGRADATION	Cigarette smoke (CS)-induced lung inflammation involves the reduction of histone deacetylase 2 (HDAC2) abundance, which is associated with steroid resistance in patients with chronic obstructive pulmonary disease and in individuals with severe asthma who smoke cigarettes. However, the molecular mechanism of CS-mediated reduction of HDAC2 is not clearly known. We hypothesized that HDAC2 is phosphorylated and subsequently degraded by the proteasome in vitro in macrophages (MonoMac6), human bronchial and primary small airway epithelial cells, and in vivo in mouse lungs in response to chronic CS exposure. Cigarette smoke extract (CSE) exposure in MonoMac6 and in bronchial and airway epithelial cells led to phosphorylation of HDAC2 on serine/threonine residues by a protein kinase CK2-mediated mechanism, decreased HDAC2 activity, and increased ubiquitin-proteasome-dependent HDAC2 degradation. CK2 and proteasome inhibitors reversed CSE-mediated HDAC2 degradation, whereas serine/threonine phosphatase inhibitor, okadaic acid, caused phosphorylation and subsequent ubiquitination of HDAC2. CS-induced HDAC2 phosphorylation was detected in mouse lungs from 2 weeks to 4 months of CS exposure, and mice showed significantly lower lung HDAC2 levels. Thus, CS-mediated down-regulation of HDAC2 in human macrophages and lung epithelial cells in vitro and in mouse lung in vivo involves the induction of serine/threonine phosphorylation and proteasomal degradation, which may have implications for steroid resistance and abnormal inflammation caused by cigarette smoke.	[Adenuga, David; Yao, Hongwei; Rahman, Irfan] Univ Rochester, Med Ctr, Dept Environm Med, Lung Biol & Dis Program, Rochester, NY 14642 USA; [Adenuga, David; Yao, Hongwei; Rahman, Irfan] Univ Rochester, Med Ctr, Dept Environm Med, Toxicol Training Program, Rochester, NY 14642 USA; [March, Thomas H.; Seagrave, Jeanclare] Lovelace Resp Res Inst, Albuquerque, NM USA	Rahman, I (reprint author), Univ Rochester, Med Ctr, Dept Environm Med, Lung Biol & Dis Program, 601 Elmwood Ave,Box 850, Rochester, NY 14642 USA.	Irfan_Rahman@urmc.rochester.edu	Yao, Hongwei/G-6444-2010		National Institutes of Health-NHLBI [R01-HL-085613]; NIEHS Toxicology [ES-07026]; NIEHS Environmental Health Sciences Center [ES-01247]	This work was supported by the National Institutes of Health-NHLBI Grant R01-HL-085613 (to I.R.), NIEHS Toxicology training grant ES-07026, and NIEHS Environmental Health Sciences Center Grant ES-01247.	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J	Byrne, M; Walsh, J; Murphy, AW				Byrne, M; Walsh, J; Murphy, AW			Secondary prevention of coronary heart disease: Patient beliefs and health-related behaviour	JOURNAL OF PSYCHOSOMATIC RESEARCH			English	Article						coronary heart disease; health-related behaviour; illness perceptions; primary care; secondary prevention; self-regulatory model	RANDOMIZED CONTROLLED-TRIAL; CHRONIC-FATIGUE-SYNDROME; ILLNESS PERCEPTION QUESTIONNAIRE; MYOCARDIAL-INFARCTION; PRIMARY-CARE; GENERAL-PRACTICE; PERSONAL MODELS; SELF-MANAGEMENT; CLINICAL-PRACTICE; INTERVENTION	Objective: Coronary heart disease (CHD) is a leading cause of illness and death in Western society. The present study was designed to evaluate the utility of illness perceptions and medication beliefs in predicting secondary preventive behaviour among patients with CHD. An extended version of Leventhal's self-regulatory model (SRM) was used as a theoretical framework for this study [Leventhal H, Nerenz DR, Steele DJ. Illness perceptions and coping with health threat. In: Baum A, Taylor SE, Singer JE, editors. Handbook of psychology and health, Volume IV: social psychological aspects of health. Hillsdale (NJ): Erlbaum,1984. pp. 21952; Home R, Weinman J. Self-regulation and self-management in asthma: exploring the role of illness perceptions and treatment beliefs in explaining non-adherence to preventer medication. Psychol Health 2002;17(l):17-32]. Method: Medical and demographic data were gathered from the medical charts of 1611 patients with established C14D from 35 randomly selected general practices. Self-report data about patients' lifestyles (diet, exercise, smoking, alcohol consumption and medication adherence) and information on illness and medication beliefs were provided from postal questionnaire (1084 patients responded; 69% response rate). The relationship between patients' beliefs and their secondary preventive behaviour was examined using regression analyses. Results: Illness perceptions appeared to be only weak predictors of smoking, exercise, diet, alcohol consumption and medication adherence, accounting for about 2% of the variance in these behaviours. Medication beliefs were moderately related to medication adherence, accounting for about 7% of the variance in scores. A strong belief in the necessity of one's medication and a lower level of concern about one's medication were associated with higher levels of adherence. Conclusions: An illness perception approach did not prove helpful in predicting secondary preventive behaviour among this group of patients. However, beliefs about medications appear to be reasonable predictive of medication adherence. (c) 2005 Elsevier Inc. All rights reserved.	Natl Univ Ireland Univ Coll Galway, Dept Psychol, Galway, Ireland; Natl Univ Ireland Univ Coll Galway, Dept Gen Practice, Galway, Ireland	Byrne, M (reprint author), Natl Univ Ireland Univ Coll Galway, Dept Psychol, Galway, Ireland.	molly.byrne@nuigalway.ie		Walsh, Jane/0000-0001-5476-1348			Campbell NC, 1998, BRIT MED J, V316, P1430; Campbell NC, 1998, HEART, V80, P447; Cooper A, 1999, HEART, V82, P234; CUPPLES ME, 1994, BRIT MED J, V309, P993; Department of Health, 2000, NAT SERV FRAM COR HE; Edwards R, 2001, J PSYCHOSOM RES, V50, P65, DOI 10.1016/S0022-3999(00)00204-X; Feder G, 1999, BRIT MED J, V318, P1522; Fortune DG, 2000, BRIT J HEALTH PSYCH, V5, P71, DOI 10.1348/135910700168775; FRIEL S, 1999, NATL HLTH LIFESTYLES; Glasgow RE, 1997, DIABETES CARE, V20, P556, DOI 10.2337/diacare.20.4.556; GODIN G, 1985, Canadian Journal of Applied Sport Sciences, V10, P141; Griva K, 2000, PSYCHOL HEALTH, V15, P733, DOI 10.1080/08870440008405578; Hagger MS, 2003, PSYCHOL HEALTH, V18, P141, DOI 10.1080/088704403100081321; Hampson S E, 1993, Arthritis Care Res, V6, P17, DOI 10.1002/art.1790060105; HAMPSON SE, 1990, HEALTH PSYCHOL, V9, P632, DOI 10.1037//0278-6133.9.5.632; Hampson SE, 2000, BRIT J HEALTH PSYCH, V5, P27, DOI 10.1348/135910700168748; HAMPSON SE, 1994, J BEHAV MED, V17, P143, DOI 10.1007/BF01858102; Haynes RB, 1996, LANCET, V348, P383; Horne R, 1999, J PSYCHOSOM RES, V47, P555, DOI 10.1016/S0022-3999(99)00057-4; Horne R, 2002, PSYCHOL HEALTH, V17, P17, DOI 10.1080/08870440290001502; Horne R, 2000, HEART, V83, P388, DOI 10.1136/heart.83.4.388; Horne R., 1997, PERCEPTIONS HLTH ILL, P155; HORNE R, IN PRESS MEDICATION; HORNE R, 1999, PSYCHOL HEALTH, V44, P1; JOHNSTON M, 1992, BRIT J CLIN PSYCHOL, V31, P89; Jolly K, 1999, BRIT MED J, V318, P706; Kahan T, 2001, J CARDIOVASC RISK, V8, P73, DOI 10.1097/00043798-200104000-00003; Ketterer MW, 2000, J PSYCHOSOM RES, V48, P357, DOI 10.1016/S0022-3999(00)00099-4; Leventhal H., 1984, HDB PSYCHOL HLTH, P219; Leventhal H, 1980, MED PSYCHOL, V2, P7; McAlister FA, 2001, BRIT MED J, V323, P957, DOI 10.1136/bmj.323.7319.957; Moss-Morris R, 2002, PSYCHOL HEALTH, V17, P1, DOI 10.1080/08870440290001494; MossMorris R, 1996, BRIT J HEALTH PSYCH, V1, P15; Murphy H, 1999, J PSYCHOSOM RES, V46, P155, DOI 10.1016/S0022-3999(98)00073-7; Ogden J, 1996, HLTH PSYCHOL TXB; PETRIE K, 1995, J PSYCHOSOM RES, V39, P31, DOI 10.1016/0022-3999(94)00071-C; Petrie KJ, 2002, PSYCHOSOM MED, V64, P580; Petrie KJ, 1996, BRIT MED J, V312, P1191; ROE L, 1994, FAM PRACT, V11, P375, DOI 10.1093/fampra/11.4.375; ROSENSTOCK IM, 1974, HEALTH EDUC QUART, V2, P354; Rudd P., 1993, DEV ASPECTS HLTH COM, P185; Scharloo M, 2000, J ASTHMA, V37, P17, DOI 10.3109/02770900009055425; Schauble R, 1998, DIAGNOSTICA, V44, P5; SCHIFFMAN S, 1998, HEALTH PSYCHOL, V17, P3; Skinner B. F., 1953, SCI HUMAN BEHAV; *SPSS INC, 1999, SPSS WIND VERS 10; Svilaas A, 2000, SCAND J PRIM HEALTH, V18, P232; Tabachnick B. G., 2001, USING MULTIVARIATE S; Weinman J, 2000, BRIT J HEALTH PSYCH, V5, P263, DOI 10.1348/135910700168900; Weinman J, 1996, PSYCHOL HEALTH, V11, P431, DOI 10.1080/08870449608400270; Wiles R, 1998, SOC SCI MED, V46, P1477, DOI 10.1016/S0277-9536(97)10140-X; Wood D, 1998, J HYPERTENS, V16, P1407, DOI 10.1097/00004872-199816100-00003; Wood D, 1998, EUR HEART J, V19, P1434; [Anonymous], 1988, J CLIN EPIDEMIOL, V41, P105	54	106	109	5	30	PERGAMON-ELSEVIER SCIENCE LTD	OXFORD	THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND	0022-3999			J PSYCHOSOM RES	J. Psychosomat. Res.	MAY	2005	58	5					403	415		10.1016/j.jpsychores.2004.11.010		13	Psychiatry	Psychiatry	955BV	WOS:000231200600003	16026655	
J	Colilla, S; Nicolae, D; Pluzhnikov, A; Blumenthal, MN; Beaty, TH; Bleecker, ER; Lange, EM; Rich, SS; Meyers, DA; Ober, C; Cox, NJ				Colilla, S; Nicolae, D; Pluzhnikov, A; Blumenthal, MN; Beaty, TH; Bleecker, ER; Lange, EM; Rich, SS; Meyers, DA; Ober, C; Cox, NJ		Collaborative Study Genetics Asthm	Evidence for gene-environment interactions in a linkage study of asthma and smoking exposure	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; genetics; linkage; smoking; gene-environment interaction; environmental tobacco smoke; genetic epidemiology	GENOME-WIDE SEARCH; TOBACCO-SMOKE; CHILDHOOD ASTHMA; HOUSEHOLD SMOKING; PAIR LINKAGE; RISK-FACTORS; CHILDREN; CHROMOSOME-5; POPULATION; MARKERS	Background: Asthma, a common and chronic disease of the airways, has a multifactorial cause involving both genetic and environmental factors. As a result, mapping genes that influence asthma susceptibility has been challenging. Objective: This study tests the hypothesis that inclusion of exposure to environmental tobacco smoke (ETS), a potential risk factor for asthma, would improve the ability to map genes for asthma. Methods: By using 144 white families from the Collaborative Study for the Genetics of Asthma, environmental information about exposure to ETS during infancy was incorporated into a genome-wide multipoint linkage analysis. Statistical significance of observed gene-environment interactions was assessed by means of simulation. Results: Three regions with nominal evidence for linkage when stratified on the basis of ETS exposure were identified (P < .01) and showed a significant increase from the baseline lod score (1p at 97 cM, D1S1669-D1S1665; 5q at 135 cM, D5S1505-D5S816; and 9q at 106 cM, D9S910; all P < .05). In addition, 2 other regions, although not meeting nominal significance after stratification on the basis of ETS exposure, showed a significant increase from baseline lod score when ETS was taken into account (1q at 240 cM, D1S549; 17p at 3 cM, D17S1308; all P < .01). Conclusion: These results illustrate how evidence for linkage of asthma can depend on exposure to an environmental factor, such as ETS. Future linkage analyses should include information on suspected environmental factors for asthma to help target new candidate susceptibility genes for asthma.	Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA; Univ Chicago, Dept Stat, Chicago, IL 60637 USA; Univ Minnesota, Dept Med, Minneapolis, MN 55455 USA; Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Epidemiol, Baltimore, MD USA; Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genom, Winston Salem, NC USA; Wake Forest Univ, Bowman Gray Sch Med, Dept Publ Hlth Sci, Winston Salem, NC 27103 USA	Cox, NJ (reprint author), Univ Chicago, Dept Human Genet, 920 E 58th St,Room 507, Chicago, IL 60637 USA.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	NCRR NIH HHS [RR 00055, RR 00400]; NHLBI NIH HHS [HL 49596, HL 49602, HL 49609, HL 49612, HL 58977]; NIDDK NIH HHS [DK 55889]		American Thoracic Society, 1991, AM REV RESPIR DIS, V144, P1202, DOI 10.1164/ajrccm/144.5.1202; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Barnes KC, 1999, CLIN EXP ALLERGY, V29, P47; Daniels SE, 1996, NATURE, V383, P247, DOI 10.1038/383247a0; Dizier MH, 2000, AM J RESP CRIT CARE, V162, P1812; Ehrlich R, 2001, J ASTHMA, V38, P239, DOI 10.1081/JAS-100000111; Ehrlich RI, 1996, AM J RESP CRIT CARE, V154, P681; Gauderman WJ, 2001, HUM HERED, V52, P34, DOI 10.1159/000053352; Gilliland FD, 2001, AM J RESP CRIT CARE, V163, P429; Goddard KAB, 2001, AM J HUM GENET, V68, P1197, DOI 10.1086/320103; Gold DR, 2000, ENVIRON HEALTH PERSP, V108, P643, DOI 10.2307/3454400; Greenwood CMT, 1997, GENET EPIDEMIOL, V14, P635; Greenwood CMT, 1999, AM J HUM GENET, V64, P871, DOI 10.1086/302288; Gudbjartsson DF, 2000, NAT GENET, V25, P12, DOI 10.1038/75514; Jaakkola JJK, 2001, ENVIRON HEALTH PERSP, V109, P579, DOI 10.2307/3455031; Jenkins MA, 1997, GENET EPIDEMIOL, V14, P317, DOI 10.1002/(SICI)1098-2272(1997)14:3<317::AID-GEPI9>3.0.CO;2-1; Jordaan ER, 1999, ARCH ENVIRON HEALTH, V54, P319; LANDER E, 1995, NAT GENET, V11, P241, DOI 10.1038/ng1195-241; Lanphear BP, 2001, PEDIATRICS, V107, P505, DOI 10.1542/peds.107.3.505; Larsson ML, 2001, CHEST, V120, P711, DOI 10.1378/chest.120.3.711; Lester LA, 2001, J ALLERGY CLIN IMMUN, V108, P357, DOI 10.1067/mai.2001.117796; Li YF, 2000, AM J RESP CRIT CARE, V162, P2097; Lux AL, 2000, ARCH DIS CHILD, V83, P307, DOI 10.1136/adc.83.4.307; Mannino DM, 2001, ARCH PEDIAT ADOL MED, V155, P36; Marsh DG, 1997, NAT GENET, V15, P389; MARSH DG, 1994, SCIENCE, V264, P1152, DOI 10.1126/science.8178175; Martin LJ, 2002, GENET EPIDEMIOL, V22, P105, DOI 10.1002/gepi.0135; Martinez FD, 1998, AM J RESP CRIT CARE, V158, P1739; MARTINEZ FD, 1992, PEDIATRICS, V89, P21; MEYERS DA, 1994, GENOMICS, V23, P464, DOI 10.1006/geno.1994.1524; Noguchi E, 1997, AM J RESP CRIT CARE, V156, P1390; Ober C, 2000, AM J HUM GENET, V67, P1154, DOI 10.1016/S0002-9297(07)62946-2; Ober C, 2000, CLIN CHEST MED, V21, P245, DOI 10.1016/S0272-5231(05)70264-1; Olson JM, 1999, AM J HUM GENET, V65, P1760, DOI 10.1086/302662; Palmer LJ, 2001, CLIN EXP ALLERGY, V31, P152; Ronmark E, 1999, ALLERGY, V54, P926, DOI 10.1034/j.1398-9995.1999.00044.x; Thorn J, 2001, ALLERGY, V56, P287, DOI 10.1034/j.1398-9995.2001.00805.x; von Mutius E, 2002, J ALLERGY CLIN IMMUN, V109, pS525, DOI 10.1067/mai.2002.124565; Walley AJ, 2001, GENOMICS, V72, P15, DOI 10.1006/geno.2000.6435; Wang ZX, 2001, AM J RESP CRIT CARE, V163, P1404; Wjst M, 1999, GENOMICS, V58, P1, DOI 10.1006/geno.1999.5806; Xu JF, 2001, AM J HUM GENET, V68, P1437, DOI 10.1086/320589	42	106	108	0	3	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	APR	2003	111	4					840	846		10.1067/mai.2003.170		7	Allergy; Immunology	Allergy; Immunology	667WW	WOS:000182258500027	12704367	
J	Gilliland, FD; Berhane, K; Li, YF; Rappaport, EB; Peters, JM				Gilliland, FD; Berhane, K; Li, YF; Rappaport, EB; Peters, JM			Effects of early onset asthma and in utero exposure to maternal smoking on childhood lung function	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; children; ETS; maternal smoking	ENVIRONMENTAL TOBACCO-SMOKE; SOUTHERN CALIFORNIA COMMUNITIES; PULMONARY-FUNCTION; CIGARETTE-SMOKING; PARENTAL SMOKING; RESPIRATORY ILLNESS; DIFFERING LEVELS; AIR-POLLUTION; IN-UTERO; CHILDREN	Both in utero exposures to maternal smoking and asthma are associated with chronic deficits in lung function. We hypothesized that in utero exposure affects lung function in children without asthma and synergistically affects children with early onset asthma. To investigate ate effects of in utero exposure and age at asthma diagnosis on lung function, we examined longitudinal medical history, tobacco smoke exposure, and lung function data from 5,933 participants in the Children's Health Study. We found that children exposed in utero, but without asthma, showed decreased FEV1/FVC, FEF25-75, and FEF25-75/FVC ratio. Among children without in utero exposure, early asthma diagnosis was associated. with larger decreases in FEV1, FEF25-75, and FEV1/FVC ratio compared with later diagnosed asthma. Children with in utero exposure alone and early onset asthma showed deficits in FEV1 (-13.6%; 95% confidence interval [CI], -18.9 to -8.2) and FEF25-75 (-29.7%; 95% Cl, -37.8 to -20.5) among boys; and FEF25-75 (-26.6%; 95% Cl, -36.4 to -15.1) and FEV1/FVC (-9.3%; 95% Cl, -12.9 to -5.4) among girls. The absolute differences in FEF25-75 associated with in utero exposure increased with age in children with early onset asthma. We found little evidence for effects from environmental tobacco smoke exposure alone. In summary, deficits in lung function were largest among children with in. utero exposure and early onset asthma.	Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA	Gilliland, FD (reprint author), Univ So Calif, Keck Sch Med, Dept Prevent Med, 1540 Alcazar St, Los Angeles, CA 90033 USA.		LI, YU-FEN/F-4770-2010		NHLBI NIH HHS [1 R01 HL61768-03]; NIEHS NIH HHS [1 P01 ES09581-04, 5 P30 ES07048-08]		Berhane K, 2000, AM J RESP CRIT CARE, V162, P1723; BURR ML, 1975, THORAX, V30, P663, DOI 10.1136/thx.30.6.663; BURROWS B, 1980, AM REV RESPIR DIS, V122, P813; *CA EPA, 1997, HLTH EFF EXP ENV TOB; Carlsen KCL, 1997, EUR RESPIR J, V10, P1774; Cook DG, 1998, THORAX, V53, P884; COULTAS DB, 1989, AM J EPIDEMIOL, V130, P338; COULTAS DB, 1990, AM REV RESPIR DIS, V142, P602; CUNNINGHAM J, 1995, AM J RESP CRIT CARE, V152, P565; CUNNINGHAM J, 1994, AM J EPIDEMIOL, V139, P1139; Cunningham J, 1996, AM J RESP CRIT CARE, V153, P218; Dezateux C, 1997, BRIT MED BULL, V53, P40; DODGE RR, 1980, AM REV RESPIR DIS, V122, P567; Gilliland FD, 2000, THORAX, V55, P271, DOI 10.1136/thorax.55.4.271; Gilliland FD, 2001, AM J RESP CRIT CARE, V163, P429; Hanrahan J P, 1998, Eur Respir J Suppl, V27, p46s; HANRAHAN JP, 1992, AM REV RESPIR DIS, V145, P1129; HASTIE T, 1993, J ROY STAT SOC B MET, V55, P757; Hastie T, 1990, GEN ADDITIVE MODELS; Joad JP, 1999, TOXICOL APPL PHARM, V155, P253, DOI 10.1006/taap.1998.8612; LI Y, 2001, AM J RESP CRIT CARE, V163, pA263; Li YF, 2000, AM J RESP CRIT CARE, V162, P2097; MARTINEZ FD, 1988, NEW ENGL J MED, V319, P1112, DOI 10.1056/NEJM198810273191702; Neas LM, 1998, AM J EPIDEMIOL, V147, P1011; ORYSZCZYN MP, 1991, J ALLERGY CLIN IMMUN, V87, P1169, DOI 10.1016/0091-6749(91)92163-U; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; Peters JM, 1999, AM J RESP CRIT CARE, V159, P768; RONCHETTI R, 1994, EUR RESPIR J, V7, P472, DOI 10.1183/09031936.94.07030472; SHERRILL DL, 1991, AM REV RESPIR DIS, V144, P17; Stick SM, 1996, LANCET, V348, P1060, DOI 10.1016/S0140-6736(96)04446-7; TAGER IB, 1988, AM REV RESPIR DIS, V138, P837; TAGER IB, 1995, AM J RESP CRIT CARE, V152, P977; TAGER IB, 1983, NEW ENGL J MED, V309, P699, DOI 10.1056/NEJM198309223091204; TAGER IB, 1993, AM REV RESPIR DIS, V147, P811; TAGER IB, 1987, AM REV RESPIR DIS, V136, P1366; WANG XB, 1993, PEDIATR PULM, V15, P75, DOI 10.1002/ppul.1950150204; WANG XB, 1994, AM J RESP CRIT CARE, V149, P1420; WEITZMAN M, 1990, PEDIATRICS, V85, P505; Wypij D, 1996, AM J RESP CRIT CARE, V154, pS223; WYPIJ D, 1994, STAT SINICA, V3, P329	40	106	115	0	6	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	MAR 15	2003	167	6					917	924		10.1164/rccm.200206-616OC		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	653MA	WOS:000181439100019	12480608	
J	Wiemels, JL; Wiencke, JK; Sison, JD; Miike, R; McMillan, A; Wrensch, M				Wiemels, JL; Wiencke, JK; Sison, JD; Miike, R; McMillan, A; Wrensch, M			History of allergies among adults with glioma and controls	INTERNATIONAL JOURNAL OF CANCER			English	Article						allergy; glioma; brain cancer; case-control study	BRAIN-TUMORS; MEDICAL HISTORY; RISK-FACTORS; ASSOCIATION; ASTHMA; INTERLEUKIN-4; INFECTION; CHILDREN; CANCERS; SAMPLE	The causes of most adult gliomas are essentially unknown. Previous studies have indicated associations between immune system factors and the incidence of adult glioma, specifically that those individuals with certain allergic conditions may have decreased risk of glioma. We obtained detailed allergy histories for 405 adults newly diagnosed with glioma in the San Francisco Bay Area from 1997-1999 and 402 age-gender-ethnicity frequency-matched population-based controls. Seventy-nine percent of eligible cases or their proxies and 74% of eligible controls completed in-person interviews about allergies, age at onset, frequency, duration and severity. Overall, cases were less likely than controls to report any allergy (72% vs. 85%; odds ratio [OR] = 0.5 [0.3-0.7]); for self-reported cases (n = 269), OR = 0.7 (0.4-0.97) and for proxy-reported cases, OR = 0.3 (0.2-0.5). Pollen, dairy and nut allergies were significantly less common in cases than controls and most other allergens had odds ratios of less than one. There were no apparent trends with numbers of symptoms, route of exposure of allergen or reported severity of allergy, but there was a significant dose-response with increasing numbers of allergens (p < 0.0001 for linear trend among all cases vs. controls and p = 0.02 among self-reported cases only vs. controls). Although our work displays strong and consistent associations, future efforts must attempt to establish whether an immune system typified by proclivity to allergies, or an immunologic consequence of the allergies themselves, might be capable of preventing nascent brain tumors. The dominance of humoral immunity in the central nervous system is consistent with either of these models. Alternatively, common genetic or environmental causes for allergies and gliomagenesis may mediate or confound these observed inverse risks for allergies and gliomas, or other explanations may exist. Future work might reveal an important role for immunologic factors in gliomagenesis and potential preventative and/or therapeutic modalities. (C) 2002 Wiley-Liss, Inc.	Univ Calif San Francisco, Sch Med, Dept Epidemiol & Biostat, San Francisco, CA 94102 USA; Univ Calif San Francisco, Ctr Comprehens Canc, San Francisco, CA 94102 USA	Wrensch, M (reprint author), Univ Calif San Francisco, Sch Med, Dept Epidemiol & Biostat, 44 Page St,Suite 503, San Francisco, CA 94102 USA.				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J. Cancer	APR 1	2002	98	4					609	615		10.1002/ijc.10239		7	Oncology	Oncology	527DT	WOS:000174171800018	11920623	
J	Custovic, A; Hallam, CL; Simpson, BM; Craven, M; Simpson, A; Woodcock, A				Custovic, A; Hallam, CL; Simpson, BM; Craven, M; Simpson, A; Woodcock, A		Natl Asthma Campaign Manchester As	Decreased prevalence of sensitization to cats with high exposure to cat allergen	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						sensitization; asthma; allergic disease; cat; dog; dust mite; allergens; exposure	ASTHMA; ENVIRONMENT; CHILDREN; RISK	We investigated the relationship between current exposure to cat allergen and sensitization to cats. A questionnaire was administered and skin prick testing and home visits for collection of dust samples (Fel d 1; ELISA) were performed in 2502 adults (mean age, 31.8 years; age range, 18-58 years; 1251 women). The results for Fel d 1 in relation to sensitization to cats were analyzed for 10 deciles of cat allergen exposure (cut points [mug/g]: 0.05, 0.34, 0.48, 0.72, 1.13, 1.92, 7.2, 44, 151). The prevalence of sensitization to cat was significantly decreased in the lowest and the highest exposure groups. In the multivariate regression analysis (age, sex, socioeconomic status, and current smoking being adjusted for), the risk of sensitization to cats was significantly increased with medium exposure to Fel d 1 (3rd centile, OR 2.3, 95% CI 1.2-4.4, P = .01; 4th centile, OR 2.1, 95% CI 1.1-4.0, P = .03; 5th centile, OR 2.2, 95% CI 1.2-4.3, P = .04, 6th centile, OR 2.5, 95% CI 1.3-4.9, P = .005). These results indicate that the prevalence of sensitization to cat is decreased in the lowest and highest cat allergen exposure groups.	Wythenshawe Hosp, NW Lung Ctr, Manchester M23 9LT, Lancs, England	Custovic, A (reprint author), Wythenshawe Hosp, NW Lung Ctr, Southmoor Rd, Manchester M23 9LT, Lancs, England.		Custovic, Adnan/A-2435-2012	Custovic, Adnan/0000-0001-5218-7071; Woodcock, Ashley/0000-0002-5428-8578; Simpson, Angela/0000-0003-2733-6666			Custovic A, 1998, THORAX, V53, P33; Custovic A, 2000, J ALLERGY CLIN IMMUN, V105, P252, DOI 10.1016/S0091-6749(00)90073-3; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; Lindfors A, 1999, J ALLERGY CLIN IMMUN, V104, P755; MILLS TAE, 2001, LANCET, V357, P752; Roost HP, 1999, J ALLERGY CLIN IMMUN, V104, P941, DOI 10.1016/S0091-6749(99)70072-2; Simpson BM, 2001, CLIN EXP ALLERGY, V31, P391, DOI 10.1046/j.1365-2222.2001.01050.x; WARNER JA, 1991, PEDIATR ALLERGY IMMU, V1, P79; Wickens K, 1999, PEDIATR ALLERGY IMMU, V10, P199, DOI 10.1034/j.1399-3038.1999.00033.x	10	106	107	0	1	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	OCT	2001	108	4					537	539				3	Allergy; Immunology	Allergy; Immunology	485NK	WOS:000171760300011	11590378	
J	Bousquet, J				Bousquet, J			Global Initiative for Asthma (GINA) and its objectives	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						asthma; guidelines; GINA; corticosteroids; leukotriene receptor antagonists; prevalence	CLINICAL GUIDELINES	Guidelines for the diagnosis and management of asthma have been available for the past 13 years and are updated regularly. However, asthma guidelines are rarely completely up-to-date because our knowledge about the pathophysiology and treatment of asthma is continually evolving. Guidelines are an increasingly familiar part of clinical practice and may have potential benefits and harms. The potential harms of guidelines can be minimized if they are rigorously developed using evidence-based medicine. Guidelines should identify key decisions and their consequences and should review the consequences of alternative decisions. In addition, guidelines should be simple, user-friendly and widely disseminated. Guidelines evolve over time and their recommendations should be supported by evidence from clinical trials. Evidence-based medicine is the new paradigm but the results and reaction to the recent meta-analysis on house-dust mite control measures highlights the need for care when incorporating such information into guidelines. Newer therapeutic agents such as the leukotriene receptor antagonists are included in the most recent revision of the GINA guidelines, but their position in asthma therapy is not yet fully established. In countries where asthma guidelines have been implemented, there appears to have been a reduction in the prevalence of moderate persistent asthma but no decrease in severe asthma. This indicates that there is still room for improvement.	Hop Arnaud de Villeneuve, Serv Malad Resp, F-34295 Montpellier 5, France	Bousquet, J (reprint author), Hop Arnaud de Villeneuve, Serv Malad Resp, F-34295 Montpellier 5, France.						Gotzsche PC, 1998, BRIT MED J, V317, P1105; GREENING AP, 1994, LANCET, V344, P219, DOI 10.1016/S0140-6736(94)92996-3; Guyatt GH, 1999, JAMA-J AM MED ASSOC, V281, P1836, DOI 10.1001/jama.281.19.1836; Jackson R, 1998, BRIT MED J, V317, P427; PEARCE N, 1995, LANCET, V345, P41, DOI 10.1016/S0140-6736(95)91159-6; Platts-Mills TAE, 1999, BRIT MED J, V318, P870; REDDEL H, 1999, LANCET, V553, P14; Strachan DP, 1998, BRIT MED J, V317, P1096; Vignola AM, 1998, AM J RESP CRIT CARE, V157, P403; WARNER JO, 1998, INT PEDIAT ASTHMA CO, V25, P1; *WHO NHLBI, 1995, NATL HEART LUNG BLOO; Woolf SH, 1999, BRIT MED J, V318, P527; [Anonymous], 1997, NIH PUBLICATION	13	106	114	1	3	BLACKWELL SCIENCE LTD	OXFORD	P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	JUN	2000	30			1			2	5				4	Allergy; Immunology	Allergy; Immunology	328RM	WOS:000087863900002	10849466	
J	Subbarao, P; Mandhane, PJ; Sears, MR				Subbarao, Padmaja; Mandhane, Piush J.; Sears, Malcolm R.			Asthma: epidemiology, etiology and risk factors	CANADIAN MEDICAL ASSOCIATION JOURNAL			English	Review							RESPIRATORY-SYNCYTIAL-VIRUS; HOUSE-DUST MITE; PROSPECTIVE BIRTH-COHORT; SKIN-TEST REACTIVITY; ADULT-ONSET ASTHMA; BODY-MASS INDEX; 1ST 2 YEARS; CHILDHOOD ASTHMA; LUNG-FUNCTION; PULMONARY-FUNCTION		[Subbarao, Padmaja] Univ Toronto, Hosp Sick Children, Dept Pediat Respirol, Toronto, ON M5G 1X8, Canada; [Mandhane, Piush J.] Univ Alberta, Dept Pediat Respirol, Edmonton, AB, Canada; [Sears, Malcolm R.] McMaster Univ, Dept Med, Hamilton, ON, Canada	Sears, MR (reprint author), Firestone Inst Resp Hlth, 50 Charlton Ave E, Hamilton, ON L8N 4A6, Canada.	searsm@mcmaster.ca			AstraZeneca Canada; GlaxoSmithKline Inc.; Merck Frosst Canada; Novartis Pharmaceuticals	The Canadian Thoracic Society has received funding to facilitate the knowledge translation activities of the CTS Asthma Committee from AstraZeneca Canada, GlaxoSmithKline Inc., Merck Frosst Canada and Novartis Pharmaceuticals. None of the sponsors played a role in the collection, review, analysis or interpretation of the scientific literature or in any decisions regarding the key messages presented in the case studies.	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Med. Assoc. J.	OCT 27	2009	181	9					E181	E190		10.1503/cmaj.080612		10	Medicine, General & Internal	General & Internal Medicine	507PI	WOS:000270866300023	19752106	
J	Marsh, SE; Travers, J; Weatherall, M; Williams, MV; Aldington, S; Shirtcliffe, PM; Hansell, AL; Nowitz, MR; McNaughton, AA; Soriano, JB; Beasley, RW				Marsh, S. E.; Travers, J.; Weatherall, M.; Williams, M. V.; Aldington, S.; Shirtcliffe, P. M.; Hansell, A. L.; Nowitz, M. R.; McNaughton, A. A.; Soriano, J. B.; Beasley, R. W.			Proportional classifications of COPD phenotypes	THORAX			English	Article							OBSTRUCTIVE PULMONARY-DISEASE; AIR-FLOW OBSTRUCTION; LUNG-FUNCTION; REFERENCE VALUES; VENN-DIAGRAM; RISK-FACTORS; MILD ASTHMA; FOLLOW-UP; POPULATION; PREVALENCE	Background: Chronic obstructive pulmonary disease (COPD) encompasses a group of disorders characterised by the presence of incompletely reversible airflow obstruction with overlapping subsets of different phenotypes including chronic bronchitis, emphysema or asthma. The aim of this study was to determine the proportion of adult subjects aged > 50 years within each phenotypic subgroup of COPD, defined as a post-bronchodilator ratio of forced expiratory volume in 1 s/forced vital capacity (FEV(1)/FVC) < 0.7, in accordance with current international guidelines. Methods: Adults aged > 50 years derived from a random population-based survey undertook detailed questionnaires, pulmonary function tests and chest CT scans. The proportion of subjects in each of 16 distinct phenotypes was determined based on combinations of chronic bronchitis, emphysema and asthma, with and without incompletely reversible airflow obstruction defined by a post-bronchodilator FEV(1)/FVC ratio of 0.7. Results: A total of 469 subjects completed the investigative modules, 96 of whom (20.5%) had COPD. Diagrams were constructed to demonstrate the relative proportions of the phenotypic subgroups in subjects with and without COPD. 18/96 subjects with COPD (19%) had the classical phenotypes of chronic bronchitis and/or emphysema but no asthma; asthma was the predominant COPD phenotype, being present in 53/96 (55%). When COPD was defined as a post-bronchodilator FEV(1)/FVC less than the lower limit of normal, there were one-third fewer subjects with COPD and a smaller proportion without a defined emphysema, chronic bronchitis or asthma phenotype. Conclusion: This study provides proportional classifications of the phenotypic subgroups of COPD which can be used as the basis for further research into the pathogenesis and treatment of this heterogeneous disorder.	[Marsh, S. E.; Travers, J.; Williams, M. V.; Aldington, S.; Shirtcliffe, P. M.; McNaughton, A. A.; Beasley, R. W.] Med Res Inst New Zealand, Wellington 6143, New Zealand; [Weatherall, M.; Nowitz, M. R.] Wellington Sch Med & Hlth Sci, Wellington, New Zealand; [Hansell, A. L.] Univ London Imperial Coll Sci Technol & Med, Dept Epidemiol & Publ Hlth, London, England; [Nowitz, M. R.] Pacific Radiol Ltd, Wellington, New Zealand; [Soriano, J. B.] Fundacao Caubet CIMERA Illes, Balears, Bunyola, Spain; [Beasley, R. W.] Univ Southampton, Southampton, Hants, England	Beasley, RW (reprint author), Med Res Inst New Zealand, POB 10055, Wellington 6143, New Zealand.	richard.beasley@mrinz.ac.nz		Travers, Justin/0000-0002-5992-7682; Beasley, Richard/0000-0003-0337-406X; Soriano, Joan B/0000-0001-9740-2994	GlaxoSmithKline; ALH [075883]	The study was funded by a research grant from GlaxoSmithKline. ALH is a Wellcome Trust Intermediate Clinical Fellow supported by Grant Number 075883.	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J	Jacobsen, EA; Taranova, AG; Lee, NA; Lee, JJ				Jacobsen, Elizabeth A.; Taranova, Anna G.; Lee, Nancy A.; Lee, James J.			Eosinophils: Singularly destructive effector cells or purveyors of immunoregulation?	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						eosinophil; immunoregulation; inflammation; innate; antigen presentation; granulocyte	SMOOTH-MUSCLE-CELLS; MAST-CELLS; CHEMOTACTIC ACTIVITIES; AIRWAY INFLAMMATION; LYMPH-NODES; T-CELLS; EXPRESSION; IL-4; ANTIGEN; ASTHMA	Eosinophils are granulocytes typically associated with immune responses to a limited number of specific insults, including helminth infection and exposure to various allergens. Moreover, the overwhelming consensus from the literature is that eosinophils evolved as uniquely destructive leukocytes with cytotoxic activities as an adaptation for host defense. However, recent studies now suggest that the parochial caricature of eosinophils as effector cells with nonspecific killing abilities that evolved as a host defense mechanism against large nonphagotizable parasites is incomplete. A new paradigm has emerged describing eosinophils as initial responders to cell death/tissue damage that are a part of remodeling/repair processes and, more importantly, significant contributors to localized innate and acquired immune responses as well as systemic adaptive immunity. Significantly, this new paradigm does not preclude roles for cosinophils in host defense leading to tissue damage but instead suggests the equal importance of eosinophil-associated regulatory mechanisms modulating local tissue immune responses. The goal of this review is to summarize the data in support of this new paradigm. In turn, we believe that this expanded role provides a probable explanation for the presence of eosinophils in diverse disease settings such as asthma, allergy, cancer, transplant rejection, gastrointestinal inflammation, and viral or helminth infection.	Mayo Clin, Coll Med, Div Pulm Med, Scottsdale, AZ 85259 USA; Mayo Clin, Coll Med, Div Hematol & Oncol, Dept Biochem & Mol Biol, Scottsdale, AZ 85259 USA	Lee, JJ (reprint author), Mayo Clin, Coll Med, Div Pulm Med, SC Johnson Med Res Bldg,13400 E Shea Blvd, Scottsdale, AZ 85259 USA.	jjlee@mayo.edu			NCI NIH HHS [CA112442]; NHLBI NIH HHS [F32HL085014, F32 HL083718, HL07897, HL58723, HL65228]		Chen LQ, 2004, J IMMUNOL, V172, P2059; Cormier SA, 2006, J LEUKOCYTE BIOL, V79, P1131, DOI 10.1189/jlb.0106027; DEBINSKI W, 1995, J BIOL CHEM, V270, P16775; DELPOZO V, 1992, EUR J IMMUNOL, V22, P1919; Duez C, 2004, J ALLERGY CLIN IMMUN, V114, P820, DOI 10.1016/j.jaci.2004.08.011; Fryer AD, 2006, J CLIN INVEST, V116, P228, DOI 10.1172/JCI25423; Fulkerson PC, 2006, P NATL ACAD SCI USA, V103, P16418, DOI 10.1073/pnas.0607863103; Fulkerson PC, 2005, CLIN EXP ALLERGY, V35, P1251, DOI 10.1111/j.1365-2222.2005.02354.x; Gessner A, 2005, J IMMUNOL, V174, P1063; Gharaee-Kermani M, 1998, INT J MOL MED, V1, P43; GLEICH GJ, 1984, ANNU REV IMMUNOL, V2, P429, DOI 10.1146/annurev.immunol.2.1.429; Gordon S, 1998, RES IMMUNOL, V149, P685, DOI 10.1016/S0923-2494(99)80039-X; Gutierrez-Ramos JC, 2000, IMMUNOL REV, V177, P31, DOI 10.1034/j.1600-065X.2000.17713.x; Joubert P, 2005, J IMMUNOL, V175, P2702; Justice JP, 2002, AM J PHYSIOL-LUNG C, V282, pL302; Lamkhioued B, 1996, ANN NY ACAD SCI, V796, P203, DOI 10.1111/j.1749-6632.1996.tb32582.x; Lampinen M, 2004, ALLERGY, V59, P793, DOI 10.1111/j.1398-9995.2004.00469.x; LEE I, 1995, PATHOL INT, V45, P655, DOI 10.1111/j.1440-1827.1995.tb03518.x; Lee JJ, 2004, SCIENCE, V305, P1773, DOI 10.1126/science.1099472; MacKenzie JR, 2001, J IMMUNOL, V167, P3146; Miyahara N, 2005, J IMMUNOL, V174, P4979; MULLER E, 1977, HISTOCHEMISTRY, V52, P273, DOI 10.1007/BF00495862; Nagase H, 2003, J IMMUNOL, V171, P3977; Odemuyiwa SO, 2004, J IMMUNOL, V173, P5909; Ohno I, 1996, AM J RESP CELL MOL, V15, P404; Padigel UM, 2006, INFECT IMMUN, V74, P3232, DOI 10.1128/IAI.02067-05; Pang LH, 2006, J IMMUNOL, V176, P3788; Prussin C, 2006, J ALLERGY CLIN IMMUN, V117, pS450, DOI 10.1016/j.jaci.2005.11.016; Puxeddu I, 2005, J ALLERGY CLIN IMMUN, V116, P531, DOI 10.1016/j.jaci.2005.06.007; Raines EW, 2005, J LIPID RES, V46, P1081, DOI 10.1194/jlr.R500004-JLR200; Rothenberg ME, 2006, ANNU REV IMMUNOL, V24, P147, DOI 10.1146/annurev.immunol.24.021605.090720; Sabin EA, 1996, J EXP MED, V184, P1871, DOI 10.1084/jem.184.5.1871; Schmid-Grendelmeier P, 2002, J IMMUNOL, V169, P1021; Shakoory B, 2004, J INTERF CYTOK RES, V24, P271, DOI 10.1089/107999004323065057; Shi HZ, 2004, ALLERGY, V59, P428, DOI 10.1046/j.1398-9995.2003.00405.x; Spina D, 2002, TRENDS PHARMACOL SCI, V23, P311, DOI 10.1016/S0165-6147(02)02022-9; Spoelstra FM, 2001, CLIN EXP ALLERGY, V31, P808, DOI 10.1046/j.1365-2222.2001.01111.x; Stellato C, 2000, CHEM IMMUNOL, V76, P156; Sur S, 1998, J LEUKOCYTE BIOL, V63, P715; Surquin M, 2002, J IMMUNOL, V169, P500; Swartz JM, 2006, BLOOD, V108, P2420, DOI 10.1182/blood-2006-04-015933; Tachimoto H, 2000, CHEM IMMUNOL, V76, P45; Throsby M, 2000, J IMMUNOL, V165, P1965; van Rijt LS, 2003, J IMMUNOL, V171, P3372; Voehringer D, 2006, J EXP MED, V203, P1435, DOI 10.1084/jem.20052448; Walsh GM, 2001, CLIN EXP ALLERGY, V31, P351, DOI 10.1046/j.1365-2222.2001.01032.x; Watt A. 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J	Landrigan, PJ; Trasande, L; Thorpe, LE; Gwynn, C; Lioy, PJ; D'Alton, ME; Lipkind, HS; Swanson, J; Wadhwa, PD; Clark, EB; Rauh, VA; Perera, FP; Susser, E				Landrigan, Philip J.; Trasande, Leonardo; Thorpe, Lorna E.; Gwynn, Charon; Lioy, Paul J.; D'Alton, Mary E.; Lipkind, Heather S.; Swanson, James; Wadhwa, Pathik D.; Clark, Edward B.; Rauh, Virginia A.; Perera, Frederica P.; Susser, Ezra			The National Children's Study: A 21-year prospective study of 100 000 American children	PEDIATRICS			English	Review						National Children's Study; epidemiology; asthma; attention-deficit/hyperactivity disorder; autism; schizophrenia; obesity	CORONARY HEART-DISEASE; TESTICULAR DYSGENESIS SYNDROME; IMPAIRED GLUCOSE-TOLERANCE; ABDOMINAL-WALL DEFECTS; ADULT-BLOOD PRESSURE; INNER-CITY HOMES; BONE LEAD LEVELS; PHYSICAL-ACTIVITY; ENVIRONMENTAL-HEALTH; RISK-FACTORS	Prospective, multiyear epidemiologic studies have proven to be highly effective in discovering preventable risk factors for chronic disease. Investigations such as the Framingham Heart Study have produced blueprints for disease prevention and saved millions of lives and billions of dollars. To discover preventable environmental risk factors for disease in children, the US Congress directed the National Institute of Child Health and Human Development, through the Children's Health Act of 2000, to conduct the National Children's Study. The National Children's Study is hypothesis-driven and will seek information on environmental risks and individual susceptibility factors for asthma, birth defects, dyslexia, attention-deficit/hyperactivity disorder, autism, schizophrenia, and obesity, as well as for adverse birth outcomes. It will be conducted in a nationally representative, prospective cohort of 100 000 US-born children. Children will be followed from conception to 21 years of age. Environmental exposures (chemical, physical, biological, and psychosocial) will be assessed repeatedly during pregnancy and throughout childhood in children's homes, schools, and communities. Chemical assays will be performed by the Centers for Disease Control and Prevention, and banks of biological and environmental samples will be established for future analyses. Genetic material will be collected on each mother and child and banked to permit study of gene-environment interactions. Recruitment is scheduled to begin in 2007 at 7 Vanguard Sites and will extend to 105 sites across the United States. The National Children's Study will generate multiple satellite studies that explore methodologic issues, etiologic questions, and potential interventions. It will provide training for the next generation of researchers and practitioners in environmental pediatrics and will link to planned and ongoing prospective birth cohort studies in other nations. Data from the National Children's Study will guide development of a comprehensive blueprint for disease prevention in children.	Ctr Childrens Hlth & Environm, Dept Community & Prevent Med, Mt Sinai Sch Med, New York, NY 10029 USA; Mt Sinai Sch Med, Dept Pediat, New York, NY USA; New York City Dept Hlth & Mental Hyg, Div Epidemiol, New York, NY USA; Univ Med & Dent New Jersey, Environm & Occupat Hlth & Safety Inst, Piscataway, NJ 08854 USA; Columbia Univ, Med Ctr, Div Maternal Fetal Med, New York, NY USA; Univ Calif Irvine, Dept Pediat, Irvine, CA 92717 USA; Univ Calif Irvine, Dept Psychiat & Human Behav, Irvine, CA 92717 USA; Univ Utah, Dept Pediat, Salt Lake City, UT USA; Mailman Sch Publ Hlth, Heilbrunn Dept Populat & Family Hlth, Dept Environm Hlth Sci, New York, NY USA; Mailman Sch Publ Hlth, Heilbrunn Dept Populat & Family Hlth, Dept Epidemiol, New York, NY USA	Landrigan, PJ (reprint author), Ctr Childrens Hlth & Environm, Dept Community & Prevent Med, Mt Sinai Sch Med, 1 Gustave L Levy Pl,POB 1057, New York, NY 10029 USA.	phil.landrigan@mssm.edu	Lioy, Paul/F-6148-2011	Trasande, Leonardo/0000-0002-1928-597X	NICHD NIH HHS [N01-HD-5-3411]		Ahlgren M, 2004, NEW ENGL J MED, V351, P1619, DOI 10.1056/NEJMoa040576; 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J	Perkin, MR; Strachan, DP				Perkin, MR; Strachan, DP			Which aspects of the farming lifestyle explain the inverse association with childhood allergy?	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						atopy; farm; unpasteurized milk; skin prick tests; children	FARMERS CHILDREN; HAY-FEVER; ASTHMA; PREVALENCE; ENDOTOXIN; LIMULUS; MILK; SENSITIZATION; EXPOSURE; DISEASES	Background: Farmers' children have a reduced prevalence of allergic disorders. The specific protective environmental factors responsible are not yet identified. Objective: We sought to determine whether farmers' children in the rural county of Shropshire, England, have a reduced risk of atopy and, if so, to identify the factors responsible. Methods: The Study of Asthma and Allergy in Shropshire was a 2-stage cross-sectional study. In stage 1 a questionnaire to elicit allergic status, diet, and farming exposure was completed by the parents of 4767 children. In stage 2 a stratified subsample of 879 children underwent skin prick testing and measurement of domestic endotoxin. Results: Compared with rural nonfarming children, farmers' children had significantly less current asthma symptoms. (adjusted odds ratio (OR), 0.67; 95% CI, 0.49-0.91; P =.01) and current seasonal allergic rhinitis (adjusted OR, 0.50; 95% CI, 0.33-0.77; P =.002) but not current eczema symptoms (adjusted OR, 0.91; 95% CI, 0.68-1.21; P =.53) or atopy (adjusted OR, 0.68; 95% CI, 0.40-1.16; P =.15). In contrast, current unpasteurized milk consumption was associated with significantly less current eczema symptoms (adjusted OR, 0.59; 95% CI, 0.40-0.87; P =.008) and a greater reduction in atopy (adjusted OR, 0.24; 95% CI, 0.10-0.53; P =.001). The effect was seen in all children, independent of farming status. Unpasteurized milk consumption was associated with a 59% reduction in total IgE levels (P <.001) and higher production of whole blood stimulated IFN-gamma (P = .02). Conclusion: Unpasteurized milk consumption was the exposure mediating the protective effect on skin prick test positivity. The effect was independent of farming status and present with consumption of infrequent amounts of unpasteurized milk. Clinical implications: Unpasteurized milk might be a modifiable influence on allergic sensitization in children.	Univ London, St Georges, Div Clin Dev Sci, London SW17 0RE, England; Univ London, St Georges, Div Community Hlth Sci, London SW17 0RE, England	Perkin, MR (reprint author), Univ London, St Georges, Div Clin Dev Sci, Cranmer Terrace, London SW17 0RE, England.	m.perkin@sgul.ac.uk			Wellcome Trust [056906/Z/99/Z]		Allerberger F, 2001, Euro Surveill, V6, P147; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; BRAUNFAHRLANDER C, 1996, EPIDEMIOLOGY, V7, pS47; Chrischilles E, 2004, J ALLERGY CLIN IMMUN, V113, P66, DOI 10.1016/j.jaci.2003.09.037; Cooper JF, 1997, PDA J PHARM SCI TECH, V51, P2; Downs SH, 2001, CLIN EXP ALLERGY, V31, P570, DOI 10.1046/j.1365-2222.2001.01070.x; Ernst P, 2000, AM J RESP CRIT CARE, V161, P1563; Harper Catherine M, 2002, Commun Dis Intell Q Rep, V26, P449; Isolauri E, 2000, CLIN EXP ALLERGY, V30, P1604, DOI 10.1046/j.1365-2222.2000.00943.x; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; KLEINETEBBE J, 1993, ALLERGY, V48, P49, DOI 10.1111/j.1398-9995.1993.tb02174.x; Klintberg B, 2001, EUR RESPIR J, V17, P1151, DOI 10.1183/09031936.01.00027301; LEVIN J, 1968, THROMB DIATH HAEMOST, V19, P186; MORGAN D, 1994, EUR J EPIDEMIOL, V10, P581, DOI 10.1007/BF01719576; Remes ST, 2003, CLIN EXP ALLERGY, V33, P427, DOI 10.1046/j.1365-2222.2003.01566.x; Remes ST, 2002, ACTA PAEDIATR, V91, P1163; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; StataCorp, 2003, STAT STAT SOFTW REL; SUHREN G, 1986, MILCHWISSENSCHAFT, V41, P156; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; Wickens K, 2002, ALLERGY, V57, P1171, DOI 10.1034/j.1398-9995.2002.t01-1-23644.x	24	105	108	5	17	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUN	2006	117	6					1374	1381		10.1016/j.jaci.2006.03.008		8	Allergy; Immunology	Allergy; Immunology	053UX	WOS:000238332300026	16751000	
J	Ross, Z; English, PB; Scalf, R; Gunier, R; Smorodinsky, S; Wall, S; Jerrett, M				Ross, Z; English, PB; Scalf, R; Gunier, R; Smorodinsky, S; Wall, S; Jerrett, M			Nitrogen dioxide prediction in Southern California using land use regression modeling: potential for environmental health analyses	JOURNAL OF EXPOSURE SCIENCE AND ENVIRONMENTAL EPIDEMIOLOGY			English	Article						nitrogen dioxide; traffic; land use regression; GIS	PARTICULATE AIR-POLLUTION; MORTALITY; INDICATORS; EXPOSURE; COHORT; ASTHMA	We modeled the intraurban distribution of nitrogen dioxide (NO2), a marker for traffic pollution, with land use regression, a promising new exposure classification technique. We deployed diffusion tubes to measure NO2 levels at 39 locations in the fall of 2003 in San Diego County, CA, USA. At each sample location, we constructed circular buffers in a geographic information system and captured information on roads, traffic flow, land use, population and housing. Using multiple linear regression, we were able to predict 79% of the variation in NO2 levels with four variables: traffic density within 40-300m of the sampling location, traffic density within 300-1000m, length of road within 40m and distance to the Paci. c coast. Applying this model to validation samples showed that the model predicted NO2 levels within, on average, 2.1 p.p.b for 12 training sites initially excluded from t he model. Our evaluation of this land use regression model showed that this method had excellent prediction and robustness in a North American context. These models may be useful tools in evaluating health effects of long-term exposure to traffic-related pollution.	Calif Dept Hlth Serv, Div Environm & Occupat Dis Control, Environm Hlth Invest Branch, Oakland, CA 94612 USA; ZevRoss Spatial Anal, Ithaca, NY 14850 USA; Impact Assessment Inc, Oakland, CA 94612 USA; Univ So Calif, Div Biostat, Dept Prevent Med, Los Angeles, CA 90089 USA; Univ So Calif, Div Biostat, Dept Geog, Los Angeles, CA 90089 USA	English, PB (reprint author), Calif Dept Hlth Serv, Div Environm & Occupat Dis Control, Environm Hlth Invest Branch, 1515 Clay St 1700, Oakland, CA 94612 USA.	PEnglish@dhs.ca.gov		Gunier, Robert/0000-0001-5485-9919	NCI NIH HHS [5-R21-CA094723-03]; NIEHS NIH HHS [5P01 ES09581, 1P01 ES11627, 5P30 ES05605-14, 5P30 ES07048]		Brauer M, 2003, EPIDEMIOLOGY, V14, P228, DOI 10.1097/00001648-200303000-00019; Briggs DJ, 1997, INT J GEOGR INF SCI, V11, P699, DOI 10.1080/136588197242158; Briggs DJ, 2000, SCI TOTAL ENVIRON, V253, P151, DOI 10.1016/S0048-9697(00)00429-0; Brunekreef B, 2002, LANCET, V360, P1233, DOI 10.1016/S0140-6736(02)11274-8; English P, 1999, ENVIRON HEALTH PERSP, V107, P761, DOI 10.2307/3434663; Finkelstein MM, 2003, CAN MED ASSOC J, V169, P397; Finkelstein MM, 2004, AM J EPIDEMIOL, V160, P173, DOI 10.1093/aje/kwh181; Hoek G, 2002, LANCET, V360, P1203, DOI 10.1016/S0140-6736(02)11280-3; Jerrett M, 2005, J EXPO ANAL ENV EPID, V15, P185, DOI 10.1038/sj.jea.7500388; JERRETT M, IN PRESS MODELLING I; Krewski D, 2000, REANALYSIS HARVARD 6; National Research Council, 2002, EST PUBL HLTH BEN PR; PALMES ED, 1976, AM IND HYG ASSOC J, V37, P570, DOI 10.1080/0002889768507522; Pope CA, 2002, JAMA-J AM MED ASSOC, V287, P1132, DOI 10.1001/jama.287.9.1132; Rijnders E, 2001, ENVIRON HEALTH PERSP, V109, P411, DOI 10.2307/3434789; *SANDAG, 2004, SANDAG GIS MET CURR; *USEPA, 2001, NAT SCAL AIR TOX ASS; Wilkinson P, 1999, THORAX, V54, P1070	18	105	106	5	31	NATURE PUBLISHING GROUP	NEW YORK	75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA	1559-0631			J EXPO SCI ENV EPID	J. Expo. Sci. Environ. Epidemiol.	MAR	2006	16	2					106	114		10.1038/sj.jea.7500442		9	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	020EG	WOS:000235890600001	16047040	
J	Penard-Morand, C; Charpin, D; Raherison, C; Kopferschmitt, C; Caillaud, D; Lavaud, F; Annesi-Maesano, I				Penard-Morand, C; Charpin, D; Raherison, C; Kopferschmitt, C; Caillaud, D; Lavaud, F; Annesi-Maesano, I			Long-term exposure to background air pollution related to respiratory and allergic health in schoolchildren	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						air pollution; allergic rhinitis; asthma; atopy; background monitoring stations; children; eczema; exercise-induced bronchial reactivity; skin prick test positivity	DIESEL EXHAUST PARTICLES; SPATIAL VARIABILITY; NITROGEN-DIOXIDE; CHILDHOOD ISAAC; SULFUR-DIOXIDE; CHILDREN; ASTHMA; SYMPTOMS; SENSITIZATION; OZONE	Background The impact of air pollution on asthma and allergies still remains a debate. Objective Our cross-sectional study was intended to analyse the associations between long-term exposure to background air pollution and atopic and respiratory outcomes in a large population-based sample of schoolchildren. Methods Six thousand six hundred and seventy-two children aged 9-11 years recruited from 108 randomly schools in six French cities underwent a clinical examination including a skin prick test (SPT) to common allergens, exercise-induced bronchial reactivity (EIB) and skin examination for flexural dermatitis. The prevalence of asthma, allergic rhinitis (AR) and atopic dermatitis was assessed by a standardized health questionnaire completed by the parents. Three-year-averaged concentrations of air pollutants (NO2, SO2, PM10 and O-3) were calculated at children' schools using measurements of background monitoring stations. Results After adjusting for confounders, EIB, lifetime asthma and lifetime AR were found to be positively related to an increase in the exposure to SO2, PM10 and O-3. The adjusted odds ratios (aOR) per increase of 5 mu g/m(3) of SO2 was 1.39 (95% confidence interval (CI)=1.15-1.66) for EIB and 1.19 (1.00-1.41) for lifetime asthma. The aOR for lifetime AR per increase of 10 mu g/m(3) of PM10 was 1.32 (CI=1.04-1.68). Moreover, SPT positivity was associated with O-3 (aOR=1.34; CI=1.24-1.46). Associations with past year symptoms were consistent, even if not always statistically significant. Results persisted in long-term resident (current address for at least 8 years) children. However, no consistent positive association was found with NO2. Conclusions A moderate increase in long-term exposure to background ambient air pollution was associated with an increased prevalence of respiratory and atopic indicators in children.	INSERM, EPAR, Epidemiol Allerg & Resp Dis Dept, U472, F-94807 Villejuif, France; Hop Nord Marseille, Marseille, France; ISPED Univ, Bordeaux, France; Hop Civils, Strasbourg, France; Hop Montpied, Clermont Ferrand, France; Hop Maison Blanche, Reims, France	Penard-Morand, C (reprint author), INSERM, EPAR, Epidemiol Allerg & Resp Dis Dept, U472, 16 Ave Paul Vaillant Couturier, F-94807 Villejuif, France.	celine.morand@polytechnique.org	Annesi-Maesano, Isabella/D-9173-2016				ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Baldi I, 1999, EUR RESPIR J, V14, P132, DOI 10.1034/j.1399-3003.1999.14a22.x; BALMES JR, 1987, AM REV RESPIR DIS, V136, P1117; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Blomberg A, 1997, AM J RESP CRIT CARE, V156, P418; Brauer M, 2002, AM J RESP CRIT CARE, V166, P1092, DOI 10.1164/rccm.200108-007OC; BraunFahrlander C, 1997, AM J RESP CRIT CARE, V155, P1042; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; Charpin D, 1999, CLIN EXP ALLERGY, V29, P1474; Chavance M, 1999, REV EPIDEMIOL SANTE, V47, P535; Ciccone G, 1998, OCCUP ENVIRON MED, V55, P771; Debrock C, 2002, REV EPIDEMIOL SANTE, V50, P519; DEVALIA JL, 1994, LANCET, V344, P1668, DOI 10.1016/S0140-6736(94)90458-8; DEVLIN RB, 1991, AM J RESP CELL MOL, V4, P72; Diaz-Sanchez D, 2000, J ALLERGY CLIN IMMUN, V106, P1140, DOI 10.1067/mai.2000.111144; DiazSanchez D, 1996, J ALLERGY CLIN IMMUN, V98, P114, DOI 10.1016/S0091-6749(96)70233-6; DOCKERY DW, 1989, AM REV RESPIR DIS, V139, P587; Duhme H, 1996, EPIDEMIOLOGY, V7, P578, DOI 10.1097/00001648-199611000-00003; EDWARDS J, 1994, ARCH ENVIRON HEALTH, V49, P223; Gauderman WJ, 2004, NEW ENGL J MED, V351, P1057, DOI 10.1056/NEJMoa040610; Hirsch T, 1999, EUR RESPIR J, V14, P669, DOI 10.1034/j.1399-3003.1999.14c29.x; Janssen NAH, 2003, ENVIRON HEALTH PERSP, V111, P1512, DOI 10.1289/ehp.6243; Jerrett M, 2005, J EXPO ANAL ENV EPID, V15, P185, DOI 10.1038/sj.jea.7500388; Kehrl HR, 1999, J ALLERGY CLIN IMMUN, V104, P1198; Kim JJ, 2004, AM J RESP CRIT CARE, V170, P520, DOI 10.1164/rccm.200403-2810C; Kobayashi T, 2000, AM J RESP CRIT CARE, V162, P352; Kramer U, 2000, EPIDEMIOLOGY, V11, P64, DOI 10.1097/00001648-200001000-00014; LIANG KY, 1986, BIOMETRIKA, V73, P13, DOI 10.1093/biomet/73.1.13; McDonnell WF, 1999, ENVIRON RES, V80, P110, DOI 10.1006/enrs.1998.3894; Monn C, 1997, ATMOS ENVIRON, V31, P2243, DOI 10.1016/S1352-2310(97)00030-7; MURANAKA M, 1986, J ALLERGY CLIN IMMUN, V77, P616, DOI 10.1016/0091-6749(86)90355-6; Nerriere E, 2005, ENVIRON RES, V97, P32, DOI 10.1016/j.envres.2004.07.009; Nicolai T, 2003, EUR RESPIR J, V21, P956, DOI 10.1183/09031936.03.00041103; Nordenhall C, 2000, EUR RESPIR J, V15, P1046, DOI 10.1034/j.1399-3003.2000.01512.x; OSEBOLD JW, 1988, P SOC EXP BIOL MED, V188, P259; Penard-Morand C, 2004, BREATHE, V1, P28; Priftanji A, 2001, LANCET, V358, P1426, DOI 10.1016/S0140-6736(01)06521-7; RIEDEL F, 1988, J ALLERGY CLIN IMMUN, V82, P527, DOI 10.1016/0091-6749(88)90961-X; SCHMITZBERGER R, 1993, PEDIATR PULM, V15, P68, DOI 10.1002/ppul.1950150203; Takano H, 1997, AM J RESP CRIT CARE, V156, P36; TAKENAKA H, 1995, J ALLERGY CLIN IMMUN, V95, P103, DOI 10.1016/S0091-6749(95)70158-3; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; Weiland SK, 2004, EUR RESPIR J, V24, P406, DOI 10.1183/09031936.04.00090303; Weiland Stephan K., 1994, Annals of Epidemiology, V4, P243; Williams HC, 1995, BRIT J DERMATOL, V133, P941, DOI 10.1111/j.1365-2133.1995.tb06930.x; WJST M, 1993, BRIT MED J, V307, P596; Wyler C, 2000, EPIDEMIOLOGY, V11, P450, DOI 10.1097/00001648-200007000-00015; Zmirou D, 2004, J EPIDEMIOL COMMUN H, V58, P18, DOI 10.1136/jech.58.1.18	48	105	111	5	19	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. 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