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	Cho, YS; Choi, MG; Jeong, JJ; Chung, WC; Lee, IS; Kim, SW; Han, SW; Choi, KY; Chung, IS				Cho, YS; Choi, MG; Jeong, JJ; Chung, WC; Lee, IS; Kim, SW; Han, SW; Choi, KY; Chung, IS			Prevalence and clinical spectrum of gastroesophageal reflux: A population-based study in Asan-si, Korea	AMERICAN JOURNAL OF GASTROENTEROLOGY			English	Article							HELICOBACTER-PYLORI INFECTION; GASTRIC-ACID-SECRETION; DUODENAL-ULCER; DISEASE; SYMPTOMS; ESOPHAGITIS; QUESTIONNAIRE; VALIDATION; CHINESE	BACKGROUND AND AIMS: This study estimated the prevalence and clinical spectrum of gastroesophageal reflux disease (GERD) in Asan-si, Korea, as the prevalence is believed to be lower than in Western countries. METHODS: A cross-sectional survey, using a reliable and valid questionnaire, was performed on randomly selected 2,240 Asan-si residents aged between 18 and 69 yr. All respondents were interviewed at their homes or offices by a team of interviewers. RESULTS: Of the 1,902 eligible subjects, 1,417 (78.4%: male 762; female 655) were surveyed. The prevalence of heartburn occurring at least once a month, at least once a week, and at least twice a week was 4.71% (95% confidence interval (CI), 3.6-5.8), 2.0% (95% CI, 1.2-2.7), and 1.3% (95% CI, 0.7-1.9), respectively. The corresponding figures for acid regurgitation were 4.4% (95% CI, 3.3-5.5) and 2.0% (95% CI, 1.3-2.8), respectively. The prevalence of GERD, defined as heartburn and/or acid regurgitation experienced at least weekly, was 3.5% (95% CI, 2.6-4.5). No significant difference was detected between sexes. The prevalence of heartburn was associated with increasing age (p < 0.001). Nineteen percent of our population reported at least one of the atypical symptoms, for instance, chest pain, dysphagia, globus sensation, asthma, bronchitis, pneumonia, or hoarseness. The frequency of frequent GERD among subjects reporting any of the atypical symptoms was 12.6%, which was higher than that of the subjects without atypical symptoms. Patients with typical reflux symptoms were more common among those with atypical symptoms, compared to those without such symptoms (p < 0.001). Using a logistic regression model after adjusting for age and sex, typical reflux symptoms were associated with chest pain (odds ratio (OR), 9.3; 95% CI, 5.9-14.7), dysphagia (OR, 6.4; 95% CI, 2.8-14.7), globus sensation (OR, 3.9; 95% CI, 1.5-9.7), hoarseness (OR, 4.3; 95% CI, 1.4-13.1), asthma (OR, 2.6; 95% CI, 1.4-4.8), and bronchitis (OR, 1.2; 95% CI, 0.6-2.3). CONCLUSION: The prevalence of GERD was 3.5% in this Korean population. Heartburn and acid regurgitation were significantly associated with chest pain, dysphagia, globus sensation, hoarseness, and asthma.	Catholic Univ Korea, Coll Med, Dept Internal Med, Div Gastroenterol, Seoul, South Korea	Choi, MG (reprint author), Kangnam St Marys Hosp, Dept Internal Med, Div Gastroenterol, 505 Banpo Dong, Seoul 137040, South Korea.		Choi, Myung-Gyu/D-6079-2014	Choi, Myung-Gyu/0000-0003-4083-5187			Chang CS, 1997, AM J GASTROENTEROL, V92, P668; Choi H, 1999, KOREAN J GASTROENTER, V33, P741; Choo KY, 2000, KOREAN J GASTROINTES, V6, P31; Dent J, 1999, GUT, V44, pS1; DROSSMAN DA, 1993, DIGEST DIS SCI, V38, P1569, DOI 10.1007/BF01303162; El-Serag HB, 1998, GUT, V43, P327; FELDMAN M, 1988, GASTROENTEROLOGY, V95, P630; Gislason T, 2002, CHEST, V121, P158, DOI 10.1378/chest.121.1.158; Goh KL, 2000, J GASTROEN HEPATOL, V15, P230, DOI 10.1046/j.1440-1746.2000.02148.x; Ho KY, 1998, AM J GASTROENTEROL, V93, P1816; Hu WHC, 1997, GASTROENTEROLOGY, V112, pA153; Jeon SG, 2000, KOREAN J INTERN MED, V58, P145; JOCHEM VJ, 1992, GASTROENTEROLOGY, V102, P1400; Kinoshita Y, 1997, GUT, V41, P452; KLAUSER AG, 1990, LANCET, V335, P205, DOI 10.1016/0140-6736(90)90287-F; Labenz J, 1997, GASTROENTEROLOGY, V112, P1442, DOI 10.1016/S0016-5085(97)70024-6; Lagergren J, 2000, GUT, V47, P26, DOI 10.1136/gut.47.1.26; LAM SK, 1980, GUT, V21, P324, DOI 10.1136/gut.21.4.324; Lee JI, 2003, J GASTROENTEROL, V38, P23, DOI 10.1007/s005350300002; Lee SJ, 2001, J GASTROEN HEPATOL, V16, P373, DOI 10.1046/j.1440-1746.2001.02464.x; Locke GR, 1997, GASTROENTEROLOGY, V112, P1448, DOI 10.1016/S0016-5085(97)70025-8; LOCKE GR, 1994, MAYO CLIN PROC, V69, P539; Locke GR, 1999, AM J MED, V106, P642, DOI 10.1016/S0002-9343(99)00121-7; Lundell LR, 1999, GUT, V45, P172; Manterola C, 2002, J CLIN EPIDEMIOL, V55, P1041, DOI 10.1016/S0895-4356(02)00454-7; Moayyedi P, 2001, GASTROENTEROLOGY, V121, P1120, DOI 10.1053/gast.2001.29332; NEBEL OT, 1972, GASTROENTEROLOGY, V63, P778; Nebel OT, 1976, DIGEST DIS SCI, V21, P953; Park Hyo Jin, 1996, Yonsei Medical Journal, V37, P278; PARSONNET J, 1995, ALIMENT PHARM THERAP, V9, P45; Spechler SJ, 2002, ALIMENT PHARM THERAP, V16, P1795, DOI 10.1046/j.0269-2813.2002.01351.x; Wilson LJ, 1999, AM J GASTROENTEROL, V94, P2840, DOI 10.1016/S0002-9270(99)00482-7	32	105	110	1	1	NATURE PUBLISHING GROUP	NEW YORK	75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA	0002-9270			AM J GASTROENTEROL	Am. J. Gastroenterol.	APR	2005	100	4					747	753		10.1111/j.1572-0241.2005.41245.x		7	Gastroenterology & Hepatology	Gastroenterology & Hepatology	907LU	WOS:000227720400005	15784014	
J	Ariga, M; Neitzert, B; Nakae, S; Mottin, G; Bertrand, C; Pruniaux, MP; Jin, SLC; Conti, M				Ariga, M; Neitzert, B; Nakae, S; Mottin, G; Bertrand, C; Pruniaux, MP; Jin, SLC; Conti, M			Nonredundant function of phosphodiesterases 4D and 4B in neutrophil recruitment to the site of inflammation	JOURNAL OF IMMUNOLOGY			English	Article							CYCLIC ADENOSINE-MONOPHOSPHATE; NECROSIS-FACTOR-ALPHA; PROTEIN-KINASE-A; T-CELL-ACTIVATION; LEUKOCYTE ADHESION; INTRACELLULAR CAMP; PDE4 INHIBITORS; BETA-ARRESTINS; TNF-ALPHA; AMP	Neutrophils have been implicated in the pathogenesis of many inflammatory lung diseases, including chronic obstructive pulmonary disease and asthma. With this study, we investigated how disruption of cAMP signaling impacts the function of neutrophil recruitment to the lung. Four genes code for type 4 phosphodiesterases (PDE4s), enzymes critical for regulation of cAMP levels and cell signaling. Ablation of two of these genes, PDE4B and PDE4D, but not PDE4A, has profound effects on neutrophil function. In a paradigm of mouse lung injury induced by endotoxin inhalation, the number of neutrophils recovered in the bronchoalveolar lavage was markedly decreased in PDE4D(-/-) and PDE4B(-/-) mice 4 and 24 h after exposure to LPS. Acute PDE4 inhibition with rolipram had additional inhibitory effects on nentrophil migration in PDE4B(-/-) and, to a lesser extent, PDE4D(-/-) mice. This decreased neutrophil recruitment occurred without major changes in chemokine accumulation in bronchoalveolar lavage, suggesting a dysfunction intrinsic to neutrophils. This hypothesis was confirmed by investigating the expression of adhesion molecules on the surface of neutrophils and chemotaxis in vitro. CD18 expression was decreased after ablation of both PDE4B and PDE4D, whereas CD11 expression was not significantly affected. Chemotaxis in response to KC and macrophage inflammatory protein-2 was markedly reduced in PDE4B(-/-) and PDE4D(-/-) neutrophils. The effect of PDE4 ablation on chemotaxis was comparable, but not additive, to the effects of acute PDE4 inhibition with rolipram. These data demonstrate that PDE4B and PDE4D play complementary, but not redundant, roles in the control of neutrophil function.	Stanford Univ, Sch Med, Dept Obstet & Gynecol, Div Reprod Biol, Stanford, CA 94305 USA; Stanford Univ, Sch Med, Dept Pathol, Stanford, CA 94305 USA; Pfizer Global Res & Dev, Fresnes, France	Conti, M (reprint author), Stanford Univ, Sch Med, Dept Obstet & Gynecol, Div Reprod Biol, 300 Pasteur Dr, Stanford, CA 94305 USA.	marco.conti@stanford.edu			NCI NIH HHS [9R01CA72074-18]; NHLBI NIH HHS [1P01HL67674-02, HL67674]; NIAID NIH HHS [2R37AI23990-16, R01AI50209]		ACKERMAN V, 1994, CHEST, V105, P687, DOI 10.1378/chest.105.3.687; Au BT, 1998, BRIT J PHARMACOL, V123, P1260, DOI 10.1038/sj.bjp.0701723; Baillie GS, 2003, P NATL ACAD SCI USA, V100, P940, DOI 10.1073/pnas.262787199; Barlic J, 2000, NAT IMMUNOL, V1, P227, DOI 10.1038/79767; Barnette MS, 1996, BIOCHEM PHARMACOL, V51, P949; Barnette MS, 1998, J PHARMACOL EXP THER, V284, P420; BESSLER H, 1986, J LEUKOCYTE BIOL, V40, P747; Campbell JJ, 1997, EUR J IMMUNOL, V27, P2571, DOI 10.1002/eji.1830271016; Conti M, 1999, Prog Nucleic Acid Res Mol Biol, V63, P1; Corbel M, 2002, J PHARMACOL EXP THER, V301, P258, DOI 10.1124/jpet.301.1.258; Dasi FJ, 2000, INFLAMM RES, V49, P600, DOI 10.1007/s000110050637; de Moraes VLG, 1998, BRIT J PHARMACOL, V123, P631; DERIAN CK, 1995, J IMMUNOL, V154, P308; DEVI S, 1995, J IMMUNOL, V154, P5376; DUBRAVEC DB, 1990, P NATL ACAD SCI USA, V87, P6758, DOI 10.1073/pnas.87.17.6758; ENGELS P, 1994, FEBS LETT, V350, P291, DOI 10.1016/0014-5793(94)00788-8; Fine JS, 2001, INFLAMMATION, V25, P61, DOI 10.1023/A:1007152903135; Fong AM, 2002, P NATL ACAD SCI USA, V99, P7478, DOI 10.1073/pnas.112198299; FREVERT CW, 1995, J IMMUNOL, V154, P335; Gantner F, 1997, J ALLERGY CLIN IMMUN, V100, P527; Giembycz MA, 2000, DRUGS, V59, P193, DOI 10.2165/00003495-200059020-00004; Glavas NA, 2001, P NATL ACAD SCI USA, V98, P6319, DOI 10.1073/pnas.101131098; Haddad E, 2001, BRIT J PHARMACOL, V132, P1715, DOI 10.1038/sj.bjp.0704022; Haddad JJ, 2002, J PHARMACOL EXP THER, V300, P559, DOI 10.1124/jpet.300.2.559; Hansen G, 2000, P NATL ACAD SCI USA, V97, P6751, DOI 10.1073/pnas.97.12.6751; HARVATH L, 1991, J IMMUNOL, V146, P224; Houslay MD, 1998, ADV PHARMACOL, V44, P225, DOI 10.1016/S1054-3589(08)60128-3; HOWELL RE, 1990, LIFE SCI, V46, P563, DOI 10.1016/0024-3205(90)90123-9; Jin SLC, 1999, P NATL ACAD SCI USA, V96, P11998, DOI 10.1073/pnas.96.21.11998; Jin SLC, 2002, P NATL ACAD SCI USA, V99, P7628, DOI 10.1073/pnas.122041599; Jones SL, 2002, J LEUKOCYTE BIOL, V71, P1042; KAMMER GM, 1988, IMMUNOL TODAY, V9, P222, DOI 10.1016/0167-5699(88)91220-0; Laudanna C, 1997, J BIOL CHEM, V272, P24141, DOI 10.1074/jbc.272.39.24141; Li LS, 1999, SCIENCE, V283, P848, DOI 10.1126/science.283.5403.848; Luttrell LM, 2002, J CELL SCI, V115, P455; Mizgerd JP, 1997, J EXP MED, V186, P1357, DOI 10.1084/jem.186.8.1357; NIELSON CP, 1990, J ALLERGY CLIN IMMUN, V86, P801, DOI 10.1016/S0091-6749(05)80186-1; PARHAMI F, 1993, J CLIN INVEST, V92, P471, DOI 10.1172/JCI116590; Perry SJ, 2002, SCIENCE, V298, P834, DOI 10.1126/science.1074683; Profita M, 2003, THORAX, V58, P573, DOI 10.1136/thorax.58.7.573; RIVKIN I, 1976, INT ARCH ALLER A IMM, V50, P95; Robinson CH, 2002, RADIOACTIV ENVIRONM, V2, P1; Seldon PM, 2001, BRIT J PHARMACOL, V134, P58, DOI 10.1038/sj.bjp.0704238; Servant G, 2000, SCIENCE, V287, P1037, DOI 10.1126/science.287.5455.1037; Seybold J, 1998, J BIOL CHEM, V273, P20575, DOI 10.1074/jbc.273.32.20575; SKALHEGG BS, 1992, J BIOL CHEM, V267, P15707; Souness JE, 2000, IMMUNOPHARMACOLOGY, V47, P127, DOI 10.1016/S0162-3109(00)00185-5; TANNENBAUM CS, 1989, J IMMUNOL, V142, P1274; Tasken K, 2004, PHYSIOL REV, V84, P137, DOI 10.1152/physrev.00021.2003; Tasken KA, 2001, J BIOL CHEM, V276, P21999, DOI 10.1074/jbc.C000911200; Teixeira MM, 1997, TRENDS PHARMACOL SCI, V18, P164, DOI 10.1016/S0165-6147(97)01049-3; TENOR H, 1995, J INVEST DERMATOL, V105, P70, DOI 10.1111/1523-1747.ep12313330; THOMPSON WJ, 1971, BIOCHEMISTRY-US, V10, P311; Torphy TJ, 1998, AM J RESP CRIT CARE, V157, P351; TORPHY TJ, 1994, TRENDS PHARMACOL SCI, V15, P370, DOI 10.1016/0165-6147(94)90157-0; Trifilieff A, 2002, J PHARMACOL EXP THER, V301, P241, DOI 10.1124/jpet.301.1.241; VanUffelen BE, 1998, BIOCHEM PHARMACOL, V56, P1061, DOI 10.1016/S0006-2952(98)00147-6; Wang SH, 1999, SCI TECHNOL WELD JOI, V4, P170, DOI 10.1179/136217199101537716	58	105	112	0	4	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	DEC 15	2004	173	12					7531	7538				8	Immunology	Immunology	878RT	WOS:000225665100052	15585880	
J	Hollingsworth, JW; Cook, DN; Brass, DM; Walker, JKL; Morgan, DL; Foster, WM; Schwartz, DA				Hollingsworth, JW; Cook, DN; Brass, DM; Walker, JKL; Morgan, DL; Foster, WM; Schwartz, DA			The role of toll-like receptor 4 in environmental airway injury in mice	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						toll-like receptor; innate immunity; endotoxin; ozone; residual oil fly ash	OIL FLY-ASH; INDUCED LUNG INFLAMMATION; 18-20 H POSTEXPOSURE; GRAIN DUST; ALVEOLAR MACROPHAGES; POLLUTION PARTICLES; CYTOKINE PRODUCTION; EPITHELIAL-CELLS; OZONE EXPOSURE; CUTTING EDGE	Inhalation of toxins commonly found in air pollution contributes to the development and progression of asthma and environmental airway injury. In this study, we investigated the requirement of toll-like receptor 4 (TLR4) in mice for pulmonary responses to three environmental toxins: aerosolized lipopolysaccharide, particulate matter (residual oil fly ash), and ozone. The physiologic and biologic responses to these toxins were evaluated by the extent of airway responsiveness, neutrophil recruitment to the lower respiratory tract, changes in inflammatory cytokines, and the concentration of protein in the lavage fluid. Genetically engineered, TLR4-deficient mice (C57BL/6(TLR4-/-)) were unresponsive to inhaled lipopolysaccharide, except for minimal increases in some inflammatory cytokines. In contrast, C57BL/6(TLR4-/-) mice did not differ from wild-type mice in their airway response to instilled residual oil fly ash or acute ozone exposure; however, we found that, despite a robust inflammatory response, C57BL/6(TLR4-/-) mice are protected against the development of airway hyperresponsiveness after subchronic ozone exposure. These data demonstrate in the mouse that the requirement of TLR4 for pulmonary inflammation depends on the nature of the toxin and appears specific to toxin and exposure conditions.	Duke Univ, Med Ctr, Div Pulm & Crit Care Med, Durham, NC 27710 USA; NIEHS, Res Triangle Pk, NC 27709 USA	Hollingsworth, JW (reprint author), Duke Univ, Med Ctr, Div Pulm & Crit Care Med, Durham, NC 27710 USA.	holli017@mc.duke.edu			NHLBI NIH HHS [HL074518, HL07538, HL62641, HL66604, HL66611]; NIEHS NIH HHS [ES012496, ES00703, ES012717, ES07498, ES11375, ES7031]		Arbour NC, 2000, NAT GENET, V25, P187; Balmes JR, 1996, AM J RESP CRIT CARE, V153, P904; Becker S, 2002, AM J RESP CELL MOL, V27, P611, DOI 10.1165/rcmb.4868; Becker S, 1996, TOXICOL APPL PHARM, V141, P637, DOI 10.1006/taap.1996.0330; Brass DM, 2003, AM J PHYSIOL-LUNG C, V285, pL755, DOI 10.1152/ajplung.00001.2003; Carter JD, 1997, TOXICOL APPL PHARM, V146, P180, DOI 10.1006/taap.1997.8254; COOK DN, IN PRESS GENETICS; Delfino RJ, 1997, AM J RESP CRIT CARE, V155, P568; Devlin RB, 1994, AM J PHYSIOL, V266, P612; Dockery D.W., 1993, NEW ENGL J MED, V329, P1754; Dong WM, 1996, EXP LUNG RES, V22, P577, DOI 10.3109/01902149609046043; Drazen JM, 1999, ANNU REV PHYSIOL, V61, P593, DOI 10.1146/annurev.physiol.61.1.593; Dreher KL, 1997, J TOXICOL ENV HEALTH, V50, P285, DOI 10.1080/009841097160492; Foster WM, 1996, J APPL PHYSIOL, V81, P1143; Foster WM, 2000, J APPL PHYSIOL, V89, P1804; Gavett SH, 1999, AM J RESP CRIT CARE, V160, P1897; Gavett SH, 1997, ENVIRON RES, V72, P162, DOI 10.1006/enrs.1997.3732; Ghio AJ, 2002, ENVIRON HEALTH PERSP, V110, P89; Ghio AJ, 2001, AM J RESP CRIT CARE, V164, P704; HAGLIND P, 1987, J OCCUP ENVIRON MED, V29, P904; Hamelmann E, 1997, AM J RESP CRIT CARE, V156, P766; Hirschfeld M, 2000, J IMMUNOL, V165, P618; Hoebe K, 2003, NATURE, V424, P743, DOI 10.1038/nature01889; HOLLINGSWORTH JW, 2002, AM J RESP CELL MOL B, V165, pA417; Hoshino K, 1999, J IMMUNOL, V162, P3749; Jagielo PJ, 1996, AM J PHYSIOL-LUNG C, V270, pL1052; Jagielo PJ, 1996, CHEST, V110, P263, DOI 10.1378/chest.110.1.263; KEHRL HR, 1987, AM REV RESPIR DIS, V135, P1124; Kleeberger SR, 1997, NAT GENET, V17, P475, DOI 10.1038/ng1297-475; Kleeberger SR, 2000, AM J RESP CELL MOL, V22, P620; Kleeberger SR, 2001, AM J PHYSIOL-LUNG C, V280, pL326; Kline JN, 1999, AM J RESP CRIT CARE, V160, P297; Kodavanti UP, 1997, AM J PHYSIOL-LUNG C, V272, pL521; KOREN HS, 1989, AM REV RESPIR DIS, V139, P407; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; MOTUSKY H, 1995, INTUITIVE BIOSTATIST; O'Grady NP, 2001, AM J RESP CRIT CARE, V163, P1591; Okamura Y, 2001, J BIOL CHEM, V276, P10229, DOI 10.1074/jbc.M100099200; Poltorak A, 1998, SCIENCE, V282, P2085, DOI 10.1126/science.282.5396.2085; Quay JL, 1998, AM J RESP CELL MOL, V19, P98; Rizzo MC, 1997, PEDIATR ALLERGY IMMU, V8, P121; Samet JM, 2000, NEW ENGL J MED, V343, P1742, DOI 10.1056/NEJM200012143432401; SCHWARTZ DA, 1994, AM J PHYSIOL-LUNG C, V267, pL609; Schwartz DA, 1996, CHEST, V109, pS57, DOI 10.1378/chest.109.3_Supplement.57S; Schwarze J., 1996, Journal of Allergy and Clinical Immunology, V97, P293, DOI 10.1016/S0091-6749(96)80662-2; Soukup JM, 2001, TOXICOL APPL PHARM, V171, P20, DOI 10.1006/taap.2000.9096; van Eeden SF, 2001, AM J RESP CRIT CARE, V164, P826; Visscher PM, 1999, GENET RES, V74, P81, DOI 10.1017/S0016672399003857; WEINMANN GG, 1995, AM J RESP CRIT CARE, V151, P33; Whitehead GS, 2003, AM J PHYSIOL-LUNG C, V285, pL32, DOI 10.1152/ajplung.00390.2002; Yazawa N, 2003, BLOOD, V102, P1374, DOI 10.1182/blood-2002-11-3573	51	105	107	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.	JUL 15	2004	170	2					126	132		10.1164/rccm.200311-1499OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	837NU	WOS:000222643000007	15020293	
J	Powe, DG; Jagger, C; Kleinjan, A; Carney, AS; Jenkins, D; Jones, NS				Powe, DG; Jagger, C; Kleinjan, A; Carney, AS; Jenkins, D; Jones, NS			'Entopy': localized mucosal allergic disease in the absence of systemic responses for atopy	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						atopy; idiopathic; IgE; inflammation; mast cells; nasal mucosa; rhinitis	IDIOPATHIC RHINITIS; NASAL-MUCOSA; SERUM IGE; B-CELLS; SKIN; PROVOCATION; EXPRESSION; ANTIBODIES	Background The Th2 immune response in the nasal mucosa of subjects with allergic rhinitis is mediated by allergen-specific IgE. Moreover, these subjects show positive responses for markers of systemic atopy, including allergen-specific skin sensitivity and raised serum IgE titres. In contrast, idiopathic rhinitis (IR) subjects with similar histological nasal mucosal features differ in being defined as non-allergic because they have negative atopic responses. Objective We hypothesized that it is possible to have an allergic Th2 disease pathway localized in the nasal mucosa of 'non-allergic' rhinitis subjects despite an absence of atopic responses. Methods The presence of house dust mite and grass pollen-specific IgE antibodies was investigated in non-atopic ( n=10) and atopic ( n=11) subjects with persistent rhinitis and compared to normal ( n=12) control subjects. Biotin-labelled allergen was used to localize specific allergen-binding antibodies in situ in sections of nasal mucosa. Results Grass pollen allergen binding was detected in the nasal mucosa of 3/10 non-atopic IR subjects but, in contrast, dust mite-specific antibodies were not detected. Specific antibodies were present in a total of 8/11 mucosal samples from the allergic group, but none was detected in normal control tissues. Conclusion These findings support the concept of localized nasal allergy in 'non-atopic' rhinitis subjects. We propose the term 'entopy' to define this phenomenon and believe that this concept has a wider implication for localized allergic responses in other mucosal sites.	Erasmus Univ, Dept Clin Lab Sci, Rotterdam, Netherlands; Erasmus Univ, Dept Otorhinolaryngol, Rotterdam, Netherlands; Flinders Med Ctr, Dept Otolaryngol, Bedford Pk, SA 5042, Australia; Med & Surg Sci Univ Hosp, Queens Med Ctr, Nottingham, England	Powe, DG (reprint author), Univ Nottingham Hosp, Queens Med Ctr, Dept Clin Lab Sci, Div Pathol, Nottingham NG7 2UH, England.						ARSHAD SH, 2001, PEDIATRICS, V108, pU82; BLOM HM, 1995, EUR ARCH OTO-RHINO-L, V1, pS33; BOBROW MN, 1989, J IMMUNOL METHODS, V125, P279, DOI 10.1016/0022-1759(89)90104-X; Burney P, 1997, J ALLERGY CLIN IMMUN, V99, P314, DOI 10.1016/S0091-6749(97)70048-4; CALDERON MA, 1994, J ALLERGY CLIN IMMUN, V93, P635, DOI 10.1016/S0091-6749(94)70075-3; Carney AS, 2002, CLIN EXP ALLERGY, V32, P1436, DOI 10.1046/j.1365-2745.2002.01465.x; Carney AS, 1996, CLIN OTOLARYNGOL, V21, P198, DOI 10.1111/j.1365-2273.1996.tb01724.x; Durham SR, 1997, INT ARCH ALLERGY IMM, V113, P128; DURHAM SR, 1992, J IMMUNOL, V148, P2390; Fahlbusch B, 2001, ALLERGY, V56, P1081, DOI 10.1034/j.1398-9995.2001.00106.x; FROESE A, 1980, J IMMUNOL, V139, P600; GAUCHAT JF, 1990, J EXP MED, V172, P463, DOI 10.1084/jem.172.2.463; HUGGINS KG, 1975, LANCET, V2, P148; Johansson SGO, 2001, ALLERGY, V56, P813, DOI 10.1034/j.1398-9995.2001.t01-1-00001.x; KAUR B, 1998, INT STUDY ASTHMA ALL; KleinJan A, 2000, EUR RESPIR J, V15, P491, DOI 10.1034/j.1399-3003.2000.15.11.x; KleinJan A, 1997, J ALLERGY CLIN IMMUN, V99, P515, DOI 10.1016/S0091-6749(97)70079-4; LEECH S, 2001, BRIT SOC ALL CLIN IM; LUND VJ, 1994, ALLERGY S, V91, P1; Mari A, 1999, J ALLERGY CLIN IMMUN, V103, P1005, DOI 10.1016/S0091-6749(99)70171-5; Naclerio RM, 1997, J ALLERGY CLIN IMMUN, V100, P505; NACLERIO RM, 1983, AM REV RESPIR DIS, V128, P597; Ng MLS, 2000, CLIN EXP ALLERGY, V30, P1417, DOI 10.1046/j.1365-2222.2000.00913.x; ORYSZCZYN MP, 1995, AM J RESP CRIT CARE, V151, P663; Panzani RC, 2001, ALLERGY, V56, P1, DOI 10.1111/j.1398-9995.2001.tb04419.x; Powe DG, 2001, CLIN EXP ALLERGY, V31, P864, DOI 10.1046/j.1365-2222.2001.01106.x; POWE DG, 2001, J ALLERGY CLIN IMMUN, V107, P784; Salzano FA, 1997, ALLERGY, V52, P32; SIBBALD B, 1991, THORAX, V46, P895, DOI 10.1136/thx.46.12.895; Simola M, 1999, ANN ALLERG ASTHMA IM, V82, P152, DOI 10.1016/S1081-1206(10)62589-6; SOLLEY GO, 1976, J CLIN INVEST, V58, P408, DOI 10.1172/JCI108485; VARNEY VA, 1992, AM REV RESPIR DIS, V146, P170; WANG AC, 1970, P NATL ACAD SCI USA, V66, P337, DOI 10.1073/pnas.66.2.337	33	105	113	0	2	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	OCT	2003	33	10					1374	1379		10.1046/j.1365-2222.2003.01737.x		6	Allergy; Immunology	Allergy; Immunology	727KN	WOS:000185657300009	14519143	
J	Werner, M; Topp, R; Wimmer, K; Richter, K; Bischof, W; Wjst, M; Heinrich, J				Werner, M; Topp, R; Wimmer, K; Richter, K; Bischof, W; Wjst, M; Heinrich, J			TLR4 gene variants modify endotoxin effects on asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						endotoxin; TLR4; gene polymorphism; asthma; ECRHS	HOUSE-DUST ENDOTOXIN; TOLL-LIKE RECEPTOR-4; INNATE IMMUNITY; INHALED LIPOPOLYSACCHARIDE; RESPIRATORY SYMPTOMS; EUROPEAN-COMMUNITY; EXPOSURE; CHILDREN; CD14; HYPERRESPONSIVENESS	Background: Environmental exposure to endotoxin might have a crucial role in immune maturation and development of asthma. Objective: The aim of this study was to investigate whether the effect of endotoxin concentration in settled house dust on asthma is modified by the presence of variation in the TLR4 gene. Methods: We performed a cross-sectional study within the German follow-up of the European Community Respiratory Health Survey. Multivariate logistic regression analysis and nonparametric effect estimates (S-Plus) were applied to examine the association between endotoxin exposure and diagnosed asthma, related clinical symptoms, and bronchial hyperreactivity (BHR) stratified for noncarriers and carriers of G299/1399 polymorphism in the TLR4 gene. Results: In the noncarrier group (n = 279), the prevalence of asthma was significantly increased with elevated endotoxin levels in house dust with adjusted odds ratio 6.24 (95% CI, 1.33-29.17) in the second tertile, and 4.54 (95% CI, 0.94-21.96) in the third tertile compared with the lowest endotoxin fertile. The carriers of the polymorphisms (n = 55) showed a nonsignificant trend to have a lower risk of asthma (crude odds ratio, 0.67; 95% CI, 0.06-8.06 for the second tertile and 1.33; 95% CI, 0.17-10.58 for the third tertile). We found a similar association for wheeze and endotoxin exposure that was also attenuated in subjects with G299/1399 polymorphisms. Conclusions: The G299/1399 polymorphisms were associated with a modified response to endotoxin, but the functional relationship still needs clarification.	GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, D-85764 Neuherberg, Germany; Grosshansdorf Hosp, Pulm Res Inst, Ctr Pneumol & Thorac Surg, Grosshansdorf, Germany; Univ Jena, Inst Occupat Social & Environm Med, Erfurt, Germany	Heinrich, J (reprint author), GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, Ingolstaedter Landstr 1, D-85764 Neuherberg, Germany.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Arbour NC, 2000, NAT GENET, V25, P187; Bischof W, 2002, INDOOR AIR, V12, P2, DOI 10.1034/j.1600-0668.2002.120102.x; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; Chinn S, 2002, THORAX, V57, P393, DOI 10.1136/thorax.57.5.393; Dabbagh K, 2002, J IMMUNOL, V168, P4524; Douwes J, 2002, THORAX, V57, P86, DOI 10.1136/thorax.57.1.86; Douwes J, 2002, THORAX, V57, P643, DOI 10.1136/thorax.57.7.643; Douwes J, 1997, INT J OCCUP ENV HL S, V3, pS26; Dubin W, 1996, AM J PHYSIOL-LUNG C, V270, pL736; 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; Gehring U, 2001, EUR RESPIR J, V18, P555, DOI 10.1183/09031936.01.00096801; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Heinrich J, 2001, CLIN EXP ALLERGY, V31, P1839, DOI 10.1046/j.1365-2222.2001.01220.x; Heinrich J, 2002, EUR RESPIR J, V20, P617, DOI 10.1183/09031936.02.02322001; Jansen DF, 1999, AM J RESP CRIT CARE, V159, P924; Kiechl S, 2002, NEW ENGL J MED, V347, P185, DOI 10.1056/NEJMoa012673; Kline JN, 1999, AM J RESP CRIT CARE, V160, P297; Kopp EB, 1999, CURR OPIN IMMUNOL, V11, P13, DOI 10.1016/S0952-7915(99)80003-X; Kurt-Jones EA, 2000, NAT IMMUNOL, V1, P398, DOI 10.1038/80833; Lauener RP, 2002, LANCET, V360, P465, DOI 10.1016/S0140-6736(02)09641-1; Martinez FD, 1999, LANCET S2, V354, pSII12; Medzhitov R, 2001, NAT REV IMMUNOL, V1, P135, DOI 10.1038/35100529; Medzhitov R, 1997, NATURE, V388, P394; MICHEL O, 1992, AM REV RESPIR DIS, V146, P352; 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, 2001, J ALLERGY CLIN IMMUN, V107, P797, DOI 10.1067/mai.2001.114249; Michel O, 1997, AM J RESP CRIT CARE, V156, P1157; Nowak D, 1996, EUR RESPIR J, V9, P2541, DOI 10.1183/09031936.96.09122541; O'Neill LAJ, 2002, TRENDS IMMUNOL, V23, P296, DOI 10.1016/S1471-4906(02)02222-6; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Park JH, 2000, ENVIRON HEALTH PERSP, V108, P1023, DOI 10.2307/3434953; QUANJER PH, 1993, EUR RESPIR J, V6, P5; Reed CE, 2001, J ALLERGY CLIN IMMUN, V108, P157, DOI 10.1067/mai.2001.116862; SANDSTROM T, 1992, EUR RESPIR J, V5, P992	37	105	113	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.	AUG	2003	112	2					323	330		10.1067/mai.2003.1648		8	Allergy; Immunology	Allergy; Immunology	709WY	WOS:000184650600016	12897738	
J	Guendelman, S; Meade, K; Benson, M; Chen, YQ; Samuels, S				Guendelman, S; Meade, K; Benson, M; Chen, YQ; Samuels, S			Improving asthma outcomes and self-management behaviors of inner-city children - A Randomized trial of the health buddy interactive device and an asthma diary	ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE			English	Article							QUALITY-OF-LIFE; INTERVENTION; EDUCATION; EMERGENCY; COMPUTER; PROGRAM; IMPACT; CARE; FLOW	Background: Asthma is an important cause of morbidity, absence from school, and use of health services among children. Computer-based educational programs can be designed to enhance children's self-management skills and to reduce adverse outcomes. Objective: To assess the effectiveness of an interactive device programmed for the management of pediatric asthma. Design: A randomized controlled trial (66 participants were in the intervention group and 68 were in the control group). Setting: Interventions conducted at home and in an outpatient hospital clinic. Participants: Inner-city children aged 8 to 16 years diagnosed as having asthma by a physician. Intervention: An asthma self-management and education program, the Health Buddy, designed to enable children to assess and monitor their asthma symptoms and quality of life and to transmit this information to health care providers (physicians, nurses, or other case managers) through a secure Web site. Control group participants used an asthma diary. Main Outcome Measures: Any limitation in activity was the primary outcome. Secondary outcomes included perceived asthma symptoms, absence from school, any peak flow reading in the yellow or red zone, and use of health services. Results: After adjusting for covariates, the odds of having any limitation in activity during the 90-day trial were significantly (P = .03) lower for children randomized to the Health Buddy. The intervention group also was significantly (P = .01) less likely to report peak flow readings in the yellow or red zone or to make urgent calls to the hospital (P = .05). Self-care behaviors, which were important correlates of asthma outcomes, also improved far more for the intervention group. Conclusion: Compared with the asthma diary, monitoring asthma symptoms and functional status with the Health Buddy increases self-management skills and improves asthma outcomes.	Univ Calif Berkeley, Div Hlth Sci Policy & Management, Sch Publ Hlth, Berkeley, CA 94720 USA; Univ Calif Berkeley, Maternal & Child Hlth Program, Sch Publ Hlth, Berkeley, CA 94720 USA; Univ Calif Berkeley, Sch Publ Hlth, Div Biostat, Berkeley, CA 94720 USA; Childrens Hosp Oakland, Ambulatory Serv, Oakland, CA USA	Guendelman, S (reprint author), Univ Calif Berkeley, Div Hlth Sci Policy & Management, Sch Publ Hlth, 404 Earl Warren Hall,7360, Berkeley, CA 94720 USA.		eshaghian, azam/Q-8826-2016	eshaghian, azam/0000-0001-7918-2895			Bandura A., 1977, SOCIAL LEARNING THEO; BILLINGS J, 1996, HLTH AFF, V15, P245; Recommendations to prevent and control iron deficiency in the United States, 1998, MMWR-MORBID MORTAL W, V47, P1; Centers for Disease C Prevention, 1996, MMWR-MORBID MORTAL W, V45, P350; Gergen PJ, 1999, J ALLERGY CLIN IMMUN, V103, P501, DOI 10.1016/S0091-6749(99)70477-X; Gustafson DH, 1999, AM J PREV MED, V16, P1, DOI 10.1016/S0749-3797(98)00108-1; Homer C, 2000, PEDIATRICS, V106, P210; HOWLAND J, 1988, CHEST, V94, P964, DOI 10.1378/chest.94.5.964; Juniper EF, 1996, QUAL LIFE RES, V5, P35, DOI 10.1007/BF00435967; Lieu TA, 1997, PEDIATRICS, V100, P334, DOI 10.1542/peds.100.3.334; Mansour ME, 2000, PEDIATRICS, V106, P512, DOI 10.1542/peds.106.3.512; MELTZER AA, 1989, CHEST, V96, P329, DOI 10.1378/chest.96.2.329; Mitchell H, 1997, PEDIATR PULM, V24, P237; Murphy S J, 1996, Pediatr Rev, V17, P227, DOI 10.1542/pir.17-7-227; MURRAY AB, 1983, PEDIATRICS, V71, P418; National Asthma Education and Prevention Program, 1997, 2 US DEP HLTH HUM SE; National Asthma Education Program, 1991, GUID DIAGN MAN ASTHM; Redline S, 1996, PEDIATR PULM, V21, P203; RUBIN DB, 1976, BIOMETRIKA, V63, P581, DOI 10.1093/biomet/63.3.581; RUBIN DH, 1986, PEDIATRICS, V77, P1; SHIELDS MC, 1990, AM J PUBLIC HEALTH, V80, P36; Vollmer WM, 1999, AM J RESP CRIT CARE, V160, P1647; WICKMAN M, 1994, ALLERGY, V49, P114, DOI 10.1111/j.1398-9995.1994.tb00810.x; WIGAL J K, 1990, Pediatric Asthma Allergy and Immunology, V4, P17, DOI 10.1089/pai.1990.4.17; ZEGER SL, 1988, BIOMETRICS, V44, P1049, DOI 10.2307/2531734	25	105	113	0	9	AMER MEDICAL ASSOC	CHICAGO	515 N STATE ST, CHICAGO, IL 60610 USA	1072-4710			ARCH PEDIAT ADOL MED	Arch. Pediatr. Adolesc. Med.	FEB	2002	156	2					114	120				7	Pediatrics	Pediatrics	518WN	WOS:000173691000004	11814370	
J	Furlong, TJ; DeSimone, J; Sicherer, SH				Furlong, TJ; DeSimone, J; Sicherer, SH			Peanut and tree nut allergic reactions in restaurants and other food establishments	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						peanut; tree nut; allergy; restaurant		Background: The clinical features of food-allergic reactions in restaurants and other food establishments have not been studied. Of the registrants in the United States Peanut and Tree Nut Allergy Registry (PAR), 13.7% have reported reactions associated with such establishments. Objective: The purpose of this study was to determine the features of allergic reactions to peanut and tree nut in restaurant foods and foods purchased at other private establishments (eg, ice cream shops and bakeries). Methods: Telephone interviews were conducted through use of a structured questionnaire. Subjects/parental surrogates were randomly selected from among the 706 PAR registrants who reported a reaction in a restaurant or other food establishment. Results: Details were obtained for 156 episodes (29 first-time reactions) from 129 subjects/parental surrogates. Most reactions were caused by peanut (67%) or tree nut (24%); for some reactions (9%), the cause was a combination of peanut and another nut or was unknown. Symptoms began at a median of 5 minutes after exposure and were severe in 27% of reactions. Overall, 86% of reactions were treated (antihistamines, 86%; epinephrine, 40%). Establishments commonly cited were Asian food restaurants (19%), ice cream shops (14%), and bakeries/doughnut shops (13%). Among meal courses, desserts were a common cause (43%). Of 106 registrants with previously diagnosed allergy who ordered food specifically for ingestion by the allergic individual, only 45% gave prior notification about the allergy to the establishment. For 83 (78%) of these 106 reactions, someone in the establishment knew that the food contained peanut or tree nut as an ingredient; in 50% of these incidents, the food item was "hidden" (in sauces, dressings, egg rolls, etc), visual identification being prevented. In 23 (22%) of the 106 cases, exposures were reported from contamination caused primarily by shared cooking/serving supplies. In the remaining 21 subjects with previously diagnosed allergy, reactions resulted from ingestion of food not intended for them, ingestion of food selected from buffet/food bars, or skin contact/inhalation (residual food on tables, 2; peanut shells covering floors, 2; being within 2 feet of the cooking of the food, 1). Conclusions: Restaurants and other food establishments pose a number of dangers for peanut- and tree nut-allergic individuals, particularly with respect to cross-contamination and unexpected ingredients in desserts and Asian food. Failure to establish a clear line of communication between patron and establishment is a frequent cause of errors.	Mt Sinai Sch Med, Dept Pediat, Div Allergy & Immunol, Jaffe Food Allergy Inst, New York, NY USA; Food Allergy & Anaphylaxis Network, Fairfax, VA USA	Sicherer, SH (reprint author), Mt Sinai Hosp, Div Allergy Immunol, Box 1198,1 Gustave L Levy Pl, New York, NY 10029 USA.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	NIAID NIH HHS [K23 AI01709-01]; NICHD NIH HHS [HD28822-08]		Bock SA, 2001, J ALLERGY CLIN IMMUN, V107, P191, DOI 10.1067/mai.2001.112031; BOCK SA, 1989, J ALLERGY CLIN IMMUN, V83, P900, DOI 10.1016/0091-6749(89)90103-6; Hourihane JO, 1998, BRIT MED J, V316, P1271; SAMPSON HA, 1992, NEW ENGL J MED, V327, P380, DOI 10.1056/NEJM199208063270603; Sicherer SH, 2001, J ALLERGY CLIN IMMUN, V108, P128, DOI 10.1067/mai.2001.115755; Sicherer SH, 1999, J ALLERGY CLIN IMMUN, V103, P559, DOI 10.1016/S0091-6749(99)70224-1; SICHERER SH, 1999, J ALLERGY CLIN IMMUN, V103, P186; Sicherer S.H., 1998, PEDIATRICS, V102, P6; Skolnick HS, 2001, J ALLERGY CLIN IMMUN, V107, P367, DOI 10.1067/mai.2001.112129; YUNGINGER JW, 1988, JAMA-J AM MED ASSOC, V260, P1450, DOI 10.1001/jama.260.10.1450	10	105	107	0	13	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					867	870				4	Allergy; Immunology	Allergy; Immunology	498RG	WOS:000172523800032	11692117	
J	Bahceciler, NN; Isik, U; Barlan, IB; Basaran, MM				Bahceciler, NN; Isik, U; Barlan, IB; Basaran, MM			Efficacy of sublingual immunotherapy in children with asthma and rhinitis: A double-blind, placebo-controlled study	PEDIATRIC PULMONOLOGY			English	Article						sublingual immunotherapy; asthma; rhinitis; house dust mite; children	HOUSE-DUST-MITE; DERMATOPHAGOIDES-PTERONYSSINUS; POLLEN EXTRACT; TRIAL; SLIT	To evaluate the efficacy of specific sublingual immunotherapy (SLIT), we enrolled 15 children with asthma and rhinitis (7 girls, 8 boys, mean +/- SD age of 11.7 +/- 3.3) allergic to house dust mite (HDM) into a double-blind, placebo-controlled study. After a run-in period, patients were randomized to receive either placebo (n = 7) or SLIT (n = 8) with a standardized Dermatophagoides pteronyssinus (D. pteronyssinus) + Dermatophagoides farinea (D. farinea) 50/50 extract. They received increasing doses up to 100 index units of reactivity (IR) every day for 4 weeks, then 100 IR/day for another 4 weeks, followed by maintenance therapy consisting of 20 drops 2 times a week for 4 months. Efficacy was assessed at the end of 6 months of therapy according to symptom and medication scores, serum total IgE levels, results of lung function tests, methacholine provocation tests, and skin prick tests. Daily means for the asthma score and use of inhaled beta-2-mimetics decreased significantly in the SLIT group (P = 0.05, P = 0.028, respectively), whereas no such difference was observed in the placebo group. At the end of follow-up, mean daily doses of intranasal steroids needed for control of rhinitis symptoms decreased significantly in the SLIT group (P = 0.04). Baseline skin sensitivity to D. pteronyssinus and D. farinea was not significantly different between in the two groups, whereas end-point wheal diameter obtained with D.pteronyssinus extract was significantly less in the SLIT vs. the placebo group (p = 0.026). At the end of 6 months, peak expiratory flow (PEF) values in the placebo group was significantly lower than in the SLIT group (P = 0.049). Throughout the treatment period, the SLIT group was found to have less asthma exacerbations than the placebo group (p = 0.007). The provocation concentration causing a 20% drop in forced expired volume in 1 sec did not change throughout the treatment period in either groups. None of the patients reported local or systemic side effects from SLIT. Results of this study suggests that SLIT may be a useful alternative or additional therapy in the treatment of children with asthma/rhinitis due to HDM. (C) 2001 Wiley-Liss, Inc.	Marmara Univ Hosp, Dept Pediat, Div Allergy & Immunol, Istanbul, Turkey	Bahceciler, NN (reprint author), Vefa Bey Sok 2-B Yesil Apt D 39, TR-80680 Istanbul, Turkey.						BOUSQUET J, 1987, J ALLERGY CLIN IMMUN, V80, P591, DOI 10.1016/0091-6749(87)90013-3; Bousquet J, 1999, ALLERGY, V54, P249, DOI 10.1034/j.1398-9995.1999.00916.x; CASANOVAS M, 1994, J INVEST ALLERG CLIN, V4, P305; Committee on the safety of medicines, 1986, BRIT MED J, V293, P948, DOI 10.1136/bmj.293.6552.948; Feliziani V, 1995, Allergol Immunopathol (Madr), V23, P224; Guez S, 2000, ALLERGY, V55, P369, DOI 10.1034/j.1398-9995.2000.00413.x; HEDLIN G, 1990, CLIN EXP ALLERGY, V20, P491, DOI 10.1111/j.1365-2222.1990.tb03141.x; Hirsch T, 1997, PEDIATR ALLERGY IMMU, V8, P21, DOI 10.1111/j.1399-3038.1997.tb00138.x; HOLT PG, 1994, IMMUNOL TODAY, V15, P484, DOI 10.1016/0167-5699(94)90194-5; HOLT PG, 1988, CLIN ALLERGY, V18, P229, DOI 10.1111/j.1365-2222.1988.tb02864.x; MACHIELS JJ, 1990, J CLIN INVEST, V85, P1024, DOI 10.1172/JCI114532; *NAT HEART LUNG BL, 1992, PUBL NAT HEART LUNG; Polgar P, 1971, PULMONARY TESTING CH, P100; REID MJ, 1993, J ALLERGY CLIN IMMUN, V92, P6, DOI 10.1016/0091-6749(93)90030-J; SHEFFER AL, 1992, CLIN EXP ALLERGY   S, P22; STERK PJ, 1993, EUR RESPIR J, V6, P53, DOI 10.1183/09041950.053s1693; TARI MG, 1990, ALLERGOL IMMUNOPATH, V18, P277; TROISE C, 1995, J INVEST ALLERG CLIN, V5, P25; VANWILSEM EJG, 1994, IMMUNOLOGY, V83, P128; Vourdas D, 1998, ALLERGY, V53, P662, DOI 10.1111/j.1398-9995.1998.tb03952.x; WARNER JO, 1978, LANCET, V2, P912	21	105	111	1	11	WILEY-LISS	NEW YORK	DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA	8755-6863			PEDIATR PULM	Pediatr. Pulmonol.	JUL	2001	32	1					49	55		10.1002/ppul.1088		7	Pediatrics; Respiratory System	Pediatrics; Respiratory System	448LW	WOS:000169629200008	11416876	
J	Chapman, JT; Otterbein, LE; Elias, JA; Choi, AMK				Chapman, JT; Otterbein, LE; Elias, JA; Choi, AMK			Carbon monoxide attenuates aero allergen-induced inflammation in mice	AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY			English	Article						heme oxygenase; asthma; eosinophils; ovalbumin; cytokines	HYPEROXIC LUNG INJURY; CYTOKINE MESSENGER-RNA; MURINE MODEL; AIRWAY HYPERRESPONSIVENESS; BRONCHOALVEOLAR LAVAGE; BRONCHIAL HYPERRESPONSIVENESS; EOSINOPHILIC INFLAMMATION; PULMONARY INFLAMMATION; HEME OXYGENASE-1; OXIDATIVE STRESS	Carbon monoxide (CO) generated by catalysis of heme by heme oxygenase is increased in the exhaled air of asthmatic patients. Based on recent studies demonstrating that asthma is an inflammatory disease associated with increased oxidants and that CO confers cytoprotection in oxidant-induced lung injury and inflammation, we sought to better understand the functional role of CO in asthma by using an aeroallergen model. Mice were sensitized to ovalbumin, challenged with aerosolized ovalbumin, and maintained in either CO (250 parts/million) or room air for 48 h. The differential effects of CO on bronchoalveolar lavage (BAL) fluid cell types were observed, with a marked attenuation of BAL fluid eosinophils in the CO-treated animals at 24 and 48 h. A marked reduction of the proinflammatory cytokine interleukin-5 was observed in the CO-treated mice, with no significant changes for other proinflammatory cytokines. These differential Effects of CO were also observed with leukotrienes (LTs) and prostaglandins in that CO significantly decreased BAL fluid PGE(2), and LTB4 but exerted negligible effect on thromboxane B-2 or LTC4/D-4/E-4. Our data suggest a putative immunoregulatory role for CO in aeroallergen-induced inflammation in mice.	Univ Pittsburgh, Sch Med, Div Pulm Allergy & Crit Care Med, Pittsburgh, PA 15213 USA; Yale Univ, Sch Med, Pulm & Crit Care Med Sect, New Haven, CT 06520 USA; Connecticutt Vet Affairs Healthcare Syst, W Haven, CT 06516 USA; Cleveland Clin Fdn, Dept Pulm & Crit Care Med, Cleveland, OH 44195 USA	Choi, AMK (reprint author), Univ Pittsburgh, Sch Med, Div Pulm Allergy & Crit Care Med, MUH 628 NW, Pittsburgh, PA 15213 USA.				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J. Physiol.-Lung Cell. Mol. Physiol.	JUL	2001	281	1					L209	L216				8	Physiology; Respiratory System	Physiology; Respiratory System	447AR	WOS:000169546800027	11404264	
J	Kurup, VP; Banerjee, B; Hemmann, S; Greenberger, PA; Blaser, K; Crameri, R				Kurup, VP; Banerjee, B; Hemmann, S; Greenberger, PA; Blaser, K; Crameri, R			Selected recombinant Aspergillus fumigatus allergens bind specifically to IgE in ABPA	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergic asthma; allergic bronchopulmonary aspergillosis; ELISA; recombinant Aspergillus allergens; specific IgE	SKIN-TEST REACTIVITY; BRONCHOPULMONARY ASPERGILLOSIS; MAJOR ALLERGEN; CYSTIC-FIBROSIS; EXPRESSION; CLONING; SYSTEM; I/A; PURIFICATION; DIAGNOSIS	Background Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity lung disease resulting from exposure to Aspergillus fumigatus allergens. Patients with ABPA show elevated Aspergillus-specific serum IgE, a major criterion used in the diagnosis of the disease. Crude culture filtrate and mycelial antigens have been used widely to demonstrate IgE antibody to Aspergillus in the sera of patients. While these antigens have been useful in the diagnosis of ABPA, occasionally they present inconsistency in their reactivity and lack of specificity. Although in recent years, a number of purified A. fumigatus allergens have been produced by molecular cloning, no attempt was made to evaluate them systematically. Objective To evaluate the recombinant proteins from A. fumigatus for their IgE antibody binding, we studied sera from ABPA patients and controls by antigen specific enzyme linked immunosorbent assay (ELISA). Methods Recombinant Aspergillus allergens Asp f 1, f 2, f 3, f 4, and f 6 were studied for their specific binding to IgE in the sera of ABPA patients, A. fumigatus skin prick test positive asthmatics, and normal controls from the USA and Switzerland. The sera were blinded and studied by ELISA in two different laboratories. Results All the recombinant allergens showed IgE antibody binding with sera from patients with ABPA, whereas only fewer asthmatics and normal sera showed significant binding. The three selected recombinant allergens together reacted with all the ABPA patients studied. Conclusions The results demonstrate that Asp f 2, f 4, and f 6 can be used in the serodiagnosis of ABPA, while IgE antibody binding to Asp f 1 and f 3 was not specific.	Vet Affairs Med Ctr, Res Serv 151I, Milwaukee, WI 53295 USA; Med Coll Wisconsin, Dept Med, Div Allergy Immunol, Milwaukee, WI 53226 USA; Swiss Inst Allergy & Asthma Res, CH-7270 Davos, Switzerland; Northwestern Univ, Sch Med, Div Allergy Immunol, Chicago, IL 60611 USA	Kurup, VP (reprint author), Vet Affairs Med Ctr, Res Serv 151I, 5000 W Natl Ave, Milwaukee, WI 53295 USA.				NIAID NIH HHS [AI42349]		ARRUDA LK, 1992, J IMMUNOL, V149, P3354; Banerjee B, 1998, INFECT IMMUN, V66, P5175; Banerjee B, 1996, J LAB CLIN MED, V127, P253, DOI 10.1016/S0022-2143(96)90093-1; Banerjee B, 1997, J ALLERGY CLIN IMMUN, V99, P821, DOI 10.1016/S0091-6749(97)80017-6; Crameri R, 1998, INT IMMUNOL, V10, P1211, DOI 10.1093/intimm/10.8.1211; Crameri R, 1996, INT ARCH ALLERGY IMM, V110, P41; Crameri R, 1996, CLIN EXP ALLERGY, V26, P1411, DOI 10.1046/j.1365-2222.1996.d01-296.x; CRAMERI R, 1994, EUR J BIOCHEM, V226, P53, DOI 10.1111/j.1432-1033.1994.tb20025.x; Crameri R, 1998, INT ARCH ALLERGY IMM, V115, P99, DOI 10.1159/000023889; Crameri R, 1996, J EXP MED, V184, P265, DOI 10.1084/jem.184.1.265; GREENBERGER PA, 1988, ALLERGY PRINCIPLE PR, P1219; 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, 1997, AM J RESP CRIT CARE, V156, P1956; Hemmann S, 1998, CLIN EXP ALLERGY, V28, P860; HOCHULI E, 1988, BIO-TECHNOL, V6, P1321, DOI 10.1038/nbt1188-1321; KUMAR A, 1993, J ALLERGY CLIN IMMUN, V91, P1024, DOI 10.1016/0091-6749(93)90215-2; KURUP VP, 1991, CLIN MICROBIOL REV, V4, P439; KURUP VP, 1994, J LAB CLIN MED, V123, P749; KURUP VP, 1998, ALLERGIC BRONCHOPULM, P13; MOSER M, 1992, J IMMUNOL, V149, P454; MOSER M, 1994, J ALLERGY CLIN IMMUN, V93, P1, DOI 10.1016/0091-6749(94)90227-5; Nikolaizik WH, 1996, INT ARCH ALLERGY IMM, V111, P403; PATTERSON R, 1982, ANN INTERN MED, V96, P286; ROSENBERG M, 1977, ANN INTERN MED, V86, P405; SLAVIN RG, 1993, J LAB CLIN MED, V121, P380	25	105	118	0	3	BLACKWELL SCIENCE LTD	OXFORD	P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	JUL	2000	30	7					988	993				6	Allergy; Immunology	Allergy; Immunology	334CP	WOS:000088167800012	10848921	
J	Lee, SH; Heng, D; Ng, WK; Chan, HK; Tan, RBH				Lee, Sie Huey; Heng, Desmond; Ng, Wai Kiong; Chan, Hak-Kim; Tan, Reginald B. H.			Nano spray drying: A novel method for preparing protein nanoparticles for protein therapy	INTERNATIONAL JOURNAL OF PHARMACEUTICS			English	Article						Nano spray dryer; Protein therapy; Nanoparticles; Bovine serum albumin; Spray drying	FORMULATION APPROACH; AEROSOL PERFORMANCE; DRUG-DELIVERY; POWDERS; PARTICLES; STABILITY; TAGUCHI; CRYSTALLIZATION; MICROPARTICLES; OPTIMIZATION	There has been an increasing interest in the development of protein nanotherapeutics for diseases such as cancer, diabetes and asthma. Spray drying with prior micro mixing is commonly used to obtain these powders. However, the separation and collection of protein nanoparticles with conventional spray dryer setups has been known to be extremely challenging due to its typical low collection efficiency for fine particles less than 2 mu m. To date, there has been no feasible approach to produce these protein nanoparticles in a single step and with high yield (>70%). In this study, we explored the feasibility of the novel Nano Spray Dryer B-90 (equipped with a vibrating mesh spray technology and an electrostatic particle collector) for the production of bovine serum albumin (BSA) nanoparticles. A statistical experimental design method (Taguchi method based on three levels, five variables L-18 orthogonal array robust design) was implemented to study the effect of and optimize the experimental conditions of: (1) spray mesh size, (2) BSA solution concentration, (3) surfactant concentration, (4) drying air flow rate and (5) inlet temperature on: (1) size and (2) morphology (axial ratio). Particle size and morphology were predominantly influenced by the spray mesh size and surfactant concentration, respectively. The drying air flow rate and inlet temperature had minimal impact. Optimized production of smooth spherical nanoparticles (median size: 460 +/- 10 nm, axial ratio: 1.03 +/- 0.00, span 1.03 +/- 0.03, yield: 72 +/- 4%) was achieved using the 4 mu m spray mesh at BSA concentration of 0.1% (w/v), surfactant concentration of 0.05% (w/v), drying flow rate of 150 L/min and inlet temperature of 120 degrees C. The Nano Spray Dryer B-90 thus offers a new, simple and alternative approach for the production of protein nanoparticles suited for a variety of drug delivery applications. (C) 2010 Elsevier B.V. All rights reserved.	[Lee, Sie Huey; Heng, Desmond; Ng, Wai Kiong; Tan, Reginald B. H.] ASTAR, Inst Chem & Engn Sci, Singapore 627833, Singapore; [Chan, Hak-Kim] Univ Sydney, Fac Pharm, Adv Drug Delivery Grp, Sydney, NSW 2006, Australia; [Tan, Reginald B. H.] Natl Univ Singapore, Dept Chem & Biomol Engn, Singapore 117576, Singapore	Heng, D (reprint author), ASTAR, Inst Chem & Engn Sci, 1 Pesek Rd, Singapore 627833, Singapore.	desmond_heng@ices.a-star.edu.sg; reginald_tan@ices.a-star.edu.sg			Science and Engineering Research Council of A*STAR (Agency for Science, Technology and Research), Singapore [ICES/09-122A02]	This work was supported by the Science and Engineering Research Council of A*STAR (Agency for Science, Technology and Research), Singapore (grant no. ICES/09-122A02). We are grateful to Miss Tan Li Teng, Mr. Ng Jun Wei and Miss Shirley Yap for their assistance in the experiments. We also thank Dr. Cordin Arpagaus (BUCHI Labortechnik AG) for the fruitful discussion and Dr. Philip Kwok (The University of Sydney) for the helpful advice.	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J	Corren, J; Casale, TB; Lanier, B; Buhl, R; Holgate, S; Jimenez, P				Corren, J.; Casale, T. B.; Lanier, B.; Buhl, R.; Holgate, S.; Jimenez, P.			Safety and tolerability of omalizumab	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						anti-IgE; omalizumab; safety; tolerability	SEVERE ALLERGIC-ASTHMA; ANTI-IGE ANTIBODY; ANTIIMMUNOGLOBULIN-E THERAPY; CHURG-STRAUSS-SYNDROME; SEVERE PERSISTENT ASTHMA; LONG-TERM CONTROL; QUALITY-OF-LIFE; MONOCLONAL-ANTIBODY; CANCER INCIDENCE; CROHNS-DISEASE	Omalizumab (Xolair((R))) is a recombinant humanized monoclonal anti-IgE antibody with proven efficacy in patients with moderate-to-severe and severe persistent allergic (IgE-mediated) asthma. To review clinical study data to assess the safety profile of omalizumab. We analysed the safety of omalizumab using data from completed clinical studies (up to 1 year) involving more than 7500 patients with asthma, rhinitis or related conditions and up to 4 years in one study of patients with severe allergic asthma, as well as post-marketing safety data. Analysis focuses on the risk of immune-system effects, hypersensitivity reactions, malignant neoplasia, parasitic infections and thrombocytopenia. Omalizumab exhibited a good safety and tolerability profile that was maintained up to 4 years in one study. The incidence of anaphylaxis was 0.14% in omalizumab-treated patients and 0.07% in control patients. No omalizumab-treated patient developed measurable anti-omalizumab antibodies. Post-marketing, based on estimated exposure of 57 300 patients (June 2003-December 2006), the frequency of anaphylaxis attributed to omalizumab use was estimated to be at least 0.2% of patients. Current clinical trial data do not support an increased risk of malignant neoplasia or thrombocytopenia with omalizumab. Data indicate that the proven efficacy of add-on omalizumab in patients with moderate-to-severe or severe allergic asthma is accompanied by a favourable safety and tolerability profile.	[Casale, T. B.] Allergy Res Fdn, Los Angeles, CA 90025 USA; [Lanier, B.] Lanier Educ & Res Network, Ft Worth, TX USA; [Buhl, R.] Mainz Univ Hosp, Dept Pulm, Mainz, Germany; [Jimenez, P.] Novartis Pharmaceut, E Hanover, NJ USA; [Holgate, S.] Southampton Gen Hosp, Southampton SO9 4XY, Hants, England	Corren, J (reprint author), Allergy Res Fdn, 11620 Wilshire Blvd,Suite 200, Los Angeles, CA 90025 USA.	jcorren@ucla.edu	Casale, Thomas/K-4334-2013	Casale, Thomas/0000-0002-3149-7377	Novartis and Genentech	P. J. is an employee of Novartis Pharmaceuticals.	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Exp. Allergy	JUN	2009	39	6					788	797		10.1111/j.1365-2222.2009.03214.x		10	Allergy; Immunology	Allergy; Immunology	444XW	WOS:000266015200004	19302249	
J	Jartti, T; Lee, WM; Pappas, T; Evans, M; Lemanske, RF; Gern, JE				Jartti, T.; Lee, W-M.; Pappas, T.; Evans, M.; Lemanske, R. F., Jr.; Gern, J. E.			Serial viral infections in infants with recurrent respiratory illnesses	EUROPEAN RESPIRATORY JOURNAL			English	Article						infant; respiratory virus; rhinovirus; virus persistence; virus strain; wheezing	RHINOVIRUS INFECTION; ACUTE BRONCHIOLITIS; CHILDHOOD ASTHMA; CHILDREN; LIFE; ASSOCIATION; PERSISTENCE; 1ST-YEAR; SYMPTOMS; VIRUSES	To better understand the viral aetiology of recurrent and prolonged illnesses, nasal secretions were prospectively collected from 285 infants at increased risk of developing asthma. Of these, 27 infants had recurrent (at least five) moderate-to-severe respiratory illnesses (MSIs). The viral aetiology of the 150 MSIs and 86 scheduled visits was analysed by molecular diagnostics. The demographic and clinical data were compared with infants who had 0-4 MSIs. Frequently ill infants had higher exposure to other children and more wheezing illnesses than less symptomatic children. Viruses were detected in 136 (91 %) out of 150 MSIs, 14 (67%) out of 21 mild illnesses and 29 (45%) out of 65 asymptomatic visits. Human rhinovirus was the most common aetiological agent (61, 43 and 35% in MSIs, mild illnesses and asymptomatic visits, respectively). Mixed viral infections were generally associated with more severe illnesses (27, 0 and 5%, respectively). Among the 27 frequently ill infants, only eight (5.3%) out of 150 MSIs were prolonged (>= 2 weeks duration). Considering all samples, detection of the same virus strain >= 2 weeks apart was unusual (5.3% of all 244 positive findings). Human rhinovirus infections occur early, pervasively and repetitively in these high-risk infants. Infants with prolonged or recurrent respiratory illnesses most often have a series of infections rather than persistent infection with one virus strain.	[Jartti, T.; Lee, W-M.; Pappas, T.; Gern, J. E.] Univ Wisconsin, Dept Paediat, Madison, WI USA; [Evans, M.] Univ Wisconsin, Dept Biostat & Med Informat, Madison, WI USA; [Lemanske, R. F., Jr.] Univ Wisconsin, Dept Med, Madison, WI USA	Jartti, T (reprint author), Turku Univ Hosp, Dept Paediat, POB 52, FIN-20520 Turku, Finland.	tuomas.jartti@tyks.fi			NCRR NIH HHS [1UL1RR025011, UL1 RR025011, UL1 RR025011-01]; NHLBI NIH HHS [P01 HL070831, P01 HL070831-01, P01 HL70831, R01 HL061879, R01 HL061879-02, R01 HL61879]		Allander T, 2007, CLIN INFECT DIS, V44, P904, DOI 10.1086/512196; Brooks GD, 2003, AM J RESP CRIT CARE, V168, P1091, DOI 10.1164/rccm.200306-737OC; Contoli M, 2006, NAT MED, V12, P1023, DOI 10.1038/nm1462; Copenhaver CC, 2004, AM J RESP CRIT CARE, V170, P175, DOI 10.1164/rccm.200312-1647OC; Gern JE, 2006, J ALLERGY CLIN IMMUN, V117, P72, DOI 10.1016/j.jaci.2005.10.002; Gern JE, 2005, J ALLERGY CLIN IMMUN, V115, P668, DOI 10.1016/j.jaci.2005.01.057; HAMPARIAN VV, 1987, VIROLOGY, V159, P191; Heymann PW, 2004, J ALLERGY CLIN IMMUN, V114, P239, DOI 10.1016/j.jaci.2004.04.006; Hogg JC, 2001, AM J RESP CRIT CARE, V164, pS71; Jacques J, 2006, J CLIN VIROL, V35, P463, DOI 10.1016/j.jcv.2005.11.009; Jartti T, 2004, J MED VIROL, V72, P695, DOI 10.1002/jmv.20027; JOHNSTON SL, 1993, J CLIN MICROBIOL, V31, P111; Kaiser L, 2006, AM J RESP CRIT CARE, V174, P1392, DOI 10.1164/rccm.200604-489OC; Kling S, 2005, CLIN EXP ALLERGY, V35, P672, DOI 10.1111/j.1365-2222.2005.02244.x; Kotaniemi-Syrjanen A, 2003, J ALLERGY CLIN IMMUN, V111, P66, DOI 10.1067/mai.2003.33; Kusel MMH, 2007, J ALLERGY CLIN IMMUN, V119, P1105, DOI 10.1016/j.jaci.2006.12.669; Lee WM, 2007, PLOS ONE, V2, DOI 10.1371/journal.pone.0000966; Lee WM, 2007, J CLIN MICROBIOL, V45, P2626, DOI 10.1128/JCM.02501-06; Lehtinen P, 2007, J ALLERGY CLIN IMMUN, V119, P570, DOI 10.1016/j.jaci.2006.11.003; Lemanske RF, 2002, PEDIATR ALLERGY IMMU, V13, P38, DOI 10.1034/j.1399-3038.13.s.15.8.x; Lemanske RF, 2005, J ALLERGY CLIN IMMUN, V116, P571, DOI 10.1016/j.jaci.2005.06.024; Malmstrom K, 2006, J ALLERGY CLIN IMMUN, V118, P591, DOI 10.1016/j.jaci.2006.04.032; Mosser AG, 2005, AM J RESP CRIT CARE, V171, P645, DOI 10.1164/rccm.200407-970OC; Neaville WA, 2003, J ALLERGY CLIN IMMUN, V112, P740, DOI 10.1067/mai.2003.1716; Nokso-Koivisto J, 2002, CLIN INFECT DIS, V35, P540; Papadopoulos NG, 2002, AM J RESP CRIT CARE, V165, P1285, DOI 10.1164/rccm.200112-1188C; Rakes Gary P., 1999, American Journal of Respiratory and Critical Care Medicine, V159, P785; Smyth RL, 2006, LANCET, V368, P312, DOI 10.1016/S0140-6736(06)69077-6; Wark PAB, 2005, J EXP MED, V201, P937, DOI 10.1084/jem.20041901; Winther B, 2006, J MED VIROL, V78, P644, DOI 10.1002/jmv.20588	30	104	106	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.	AUG	2008	32	2					314	320		10.1183/09031936.00161907		7	Respiratory System	Respiratory System	337DZ	WOS:000258417000011	18448489	
J	Waser, M; Michels, KB; Bieli, C; Floistrup, H; Pershagen, G; von Mutius, E; Ege, M; Riedler, J; Schram-Bijkerk, D; Brunekreef, B; van Hage, M; Lauener, R; Braun-Fahrlander, C				Waser, M.; Michels, K. B.; Bieli, C.; Floistrup, H.; Pershagen, G.; von Mutius, E.; Ege, M.; Riedler, J.; Schram-Bijkerk, D.; Brunekreef, B.; van Hage, M.; Lauener, R.; Braun-Fahrlaender, C.		PARSIFAL Study Grp	Inverse association of farm milk consumption with asthma and allergy in rural and suburban populations across Europe	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergy; anthroposophy; asthma; children; diet; farming; gastrointestinal microflora; self-production; sensitization	ANTHROPOSOPHIC LIFE-STYLE; HAY-FEVER; FUNGAL MICROBIOTA; LOW-PREVALENCE; BIRTH COHORT; CHILDREN; ATOPY; CHILDHOOD; DISEASES; RISK	Background Dietary interventions as a means for atopy prevention attract great interest. Some studies in rural environments claimed an inverse association between consumption of farm-produced dairy products and the prevalence of allergic diseases, but current evidence is controversial. Objective To investigate whether consumption of farm-produced products is associated with a lower prevalence of asthma and allergy when compared with shop-purchased products. Methods Cross sectional multi-centre study (PARSIFAL) including 14 893 children aged 5-13 years from five European countries (2823 from farm families and 4606 attending Steiner Schools as well as 5440 farm reference and 2024 Steiner reference children). A detailed questionnaire including a dietary component was completed and allergen-specific IgE was measured in serum. Results Farm milk consumption ever in life showed a statistically significant inverse association with asthma: covariate adjusted odds ratio (aOR) 0.74 [95% confidence interval (CI) 0.61-0.88], rhinoconjunctivitis: aOR 0.56 (0.43-0.73) and sensitization to pollen and the food mix fx5 (cut-off level of >= 3.5 kU/L): aOR 0.67 (0.47-0.96) and aOR 0.42 (0.19-0.92), respectively, and sensitization to horse dander: aOR 0.50 (95% CI 0.28-0.87). The associations were observed in all four subpopulations and independent of farm-related co-exposures. Other farm-produced products were not independently related to any allergy-related health outcome. Conclusion Our results indicate that consumption of farm milk may offer protection against asthma and allergy. A deepened understanding of the relevant protective components of farm milk and a better insight into the biological mechanisms underlying this association are warranted as a basis for the development of a safe product for prevention.	Univ Basel, Inst Social & Prevent Med, CH-4051 Basel, Switzerland; Brigham & Womens Hosp, Obstet & Gynecol Epidemiol Ctr, Boston, MA 02115 USA; Harvard Univ, Sch Med, Boston, MA 02115 USA; Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; Univ Munich, Dr Hauner Childrens Hosp, D-80539 Munich, Germany; Childrens Hosp, Schwarzach, Austria; Univ Utrecht, Inst Risk Assessment Sci, Utrecht, Netherlands; Univ Utrecht, Julius Ctr Hlth Sci & Primary Care, Med Ctr, Utrecht, Netherlands; Karolinska Inst, Dept Med, Allergy & Clin Immunol Unit, Stockholm, Sweden; Univ Hosp, Stockholm, Sweden; Univ Zurich, Childrens Hosp, Zurich, Switzerland	Waser, M (reprint author), Univ Basel, Inst Social & Prevent Med, Steinengraben 49, CH-4051 Basel, Switzerland.	Marco.Waser@unibas.ch	Lauener, Roger/O-8612-2016; van Hage, Marianne/A-9678-2017	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; Douwes, Jeroen/0000-0003-3599-4036; Ege, Markus/0000-0001-6643-3923			Alfven T, 2006, ALLERGY, V61, P414, DOI 10.1111/j.1398-9995.2005.00939.x; Allerberger Franz, 2003, International Journal of Infectious Diseases, V7, P42, DOI 10.1016/S1201-9712(03)90041-5; Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; 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; Black PN, 1997, EUR RESPIR J, V10, P6, DOI 10.1183/09031936.97.10010006; Bolte G, 2001, AM J RESP CRIT CARE, V163, P277; Devereux G, 2005, J ALLERGY CLIN IMMUN, V115, P1109, DOI 10.1016/j.jaci.2004.12.11.39; Devereux G, 2005, J ALLERGY CLIN IMMUN, V115, P1118; Downs SH, 2001, CLIN EXP ALLERGY, V31, P570, DOI 10.1046/j.1365-2222.2001.01070.x; Dunder T, 2001, ALLERGY, V56, P425, DOI 10.1034/j.1398-9995.2001.056005425.x; Filipiak B, 2001, CLIN EXP ALLERGY, V31, P1829, DOI 10.1046/j.1365-2222.2001.01246.x; Gassner-Bachmann M, 2000, DEUT MED WOCHENSCHR, V125, P924, DOI 10.1055/s-2000-6778; Hauswirth CB, 2004, CIRCULATION, V109, P103, DOI 10.1161/01.CIR.0000105989.74749.DD; HEBEISEN DF, 1993, INT J VITAM NUTR RES, V63, P229; Hooper LV, 2001, SCIENCE, V292, P1115, DOI 10.1126/science.1058709; Isolauri E, 2000, HOSP MED, V61, P6; Kalliomaki M, 2001, LANCET, V357, P1076, DOI 10.1016/S0140-6736(00)04259-8; Klintberg B, 2001, EUR RESPIR J, V17, P1151, DOI 10.1183/09031936.01.00027301; Mazmanian SK, 2005, CELL, V122, P107, DOI 10.1016/j.cell.2005.05.007; McKeever TM, 2004, AM J RESP CRIT CARE, V170, P725, DOI 10.1164/rccm.200405-611PP; Noverr MC, 2005, INFECT IMMUN, V73, P30, DOI 10.1128/IAI.73.1.30-38.2005; Noverr MC, 2004, INFECT IMMUN, V72, P4996, DOI 10.1128/IAI.72.9.4996-5003.2004; Perkin MR, 2006, J ALLERGY CLIN IMMUN, V117, P1374, DOI 10.1016/j.jaci.2006.03.008; Portengen L, 2002, CLIN EXP ALLERGY, V32, P247, DOI 10.1046/j.1365-2222.2002.01310.x; Radon K, 2004, CLIN EXP ALLERGY, V34, P1178, DOI 10.1111/j.1365-2222.2004.02005.x; Remes ST, 2003, CLIN EXP ALLERGY, V33, P427, DOI 10.1046/j.1365-2222.2003.01566.x; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; SEATON A, 1994, THORAX, V49, P171, DOI 10.1136/thx.49.2.171; SHARP SJ, 1998, STATA TECHNICAL B, P16; Ublagger E, 2005, CLIN EXP ALLERGY, V35, P1033, DOI 10.1111/j.1365-2222.2005.02308.x; von Mutius E, 1998, LANCET, V351, P862, DOI 10.1016/S0140-6736(97)10100-3; Wickens K, 2002, ALLERGY, V57, P1171, DOI 10.1034/j.1398-9995.2002.t01-1-23644.x; Wijga AH, 2003, THORAX, V58, P567, DOI 10.1136/thorax.58.7.567; Woods RK, 2003, AM J CLIN NUTR, V78, P414	36	104	105	3	24	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	MAY	2007	37	5					661	670		10.1111/j.1365-2222.2006.02640.x		10	Allergy; Immunology	Allergy; Immunology	160KP	WOS:000245939700005	17456213	
J	Miller, GE; Chen, E				Miller, GE; Chen, E			Life stress and diminished expression of genes encoding glucocorticoid receptor and beta(2)-adrenergic receptor in children with asthma	PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA			English	Article							CYTOKINE PROFILES; CHILDHOOD ASTHMA; MESSENGER-RNA; BIRTH-COHORT; GENERATION; INFLAMMATION; DEPRESSION; RESISTANCE; CHALLENGE; EXPOSURE	Despite evidence that stressful experience can exacerbate the symptoms of asthma, little is known about the biological mechanisms through which this occurs. This study examined whether life stress reduces expression of the genes coding for the glucocorticoid receptor and the beta(2)-adrenergic receptor. A total of 77 children were enrolled in the study (59% male; mean age, 13.5 years). Thirty-nine of them were physician-diagnosed with asthma, and 38 were healthy. After an in-depth interview regarding stressful experiences, leukocytes were collected through antecubital venipuncture, and real-time RT-PCR was used to quantify mRNA. Chronic stress was associated with reduced expression of mRNA for the beta(2)-adrenergic receptor among children with asthma. In the sample of healthy children, however, the direction of this effect was reversed. The occurrence of a major life event in the 6 months before the study was not sufficient to influence patterns of gene expression. When such events occurred in the context of a chronic stressor, however, their association with patterns of gene expression was accentuated. Children with asthma who simultaneously experienced acute and chronic stress exhibited a 5.5-fold reduction in glucocorticoid receptor mRNA and a 9.5-fold reduction in beta(2)-adrenergic receptor mRNA relative to children with asthma without comparable stressor exposure. These findings suggest that stressful experience diminishes expression of the glucocorticoid and beta(2)-adrenergic receptor genes in children with asthma. To the extent that it diminishes sensitivity to the antiinflammatory properties of glucocorticoids or the bronchodilatory properties of beta-agonists, this process could explain the increased asthma morbidity associated with stress.	Univ British Columbia, Dept Psychol, Vancouver, BC V6T 1Z4, Canada	Miller, GE (reprint author), Univ British Columbia, Dept Psychol, 2136 W Mall, Vancouver, BC V6T 1Z4, Canada.	gemiller@psych.ubc.ca; echen@psych.ubc.ca					ADRIAN C, 1993, J CONSULT CLIN PSYCH, V61, P354, DOI 10.1037/0022-006X.61.2.354; Aiken L. S., 1991, MULTIPLE REGRESSION; BAI TR, 1993, AM J RESP CELL MOL, V8, P325; BLALOCK JE, 1994, IMMUNOL TODAY, V15, P504, DOI 10.1016/0167-5699(94)90205-4; Bloomberg GR, 2005, IMMUNOL ALLERGY CLIN, V25, P83, DOI 10.1016/j.iac.2004.09.001; Busse WW, 2001, NEW ENGL J MED, V344, P350; BUSSE WW, 1995, AM J RESP CRIT CARE, V151, P249; Cherniack R, 1999, CONTROL CLIN TRIALS, V20, P91; COHEN S, 2001, ASTHMA RESP INFECT, P193; Gagliardo R, 2000, AM J RESP CRIT CARE, V162, P7; Gao HP, 2001, CHINESE MED J-PEKING, V114, P1317; HAMMEN C, 1991, J ABNORM PSYCHOL, V100, P555, DOI 10.1037/0021-843X.100.4.555; HAMMEN C, 1988, BRIT J CLIN PSYCHOL, V27, P37; Heijink IH, 2004, CLIN EXP ALLERGY, V34, P1356, DOI 10.1111/j.1365-2222.2004.02037.x; Johnson Malcolm, 2002, Journal of Allergy and Clinical Immunology, V110, pS282, DOI 10.1067/mai.2002.129430; Kang DH, 1997, J INTERF CYTOK RES, V17, P481, DOI 10.1089/jir.1997.17.481; KLINNERT MD, 1994, PSYCHIATRY, V57, P51; Klinnert M. D., 2001, PEDIATRICS, V108, P69; Liu LY, 2002, AM J RESP CRIT CARE, V165, P1062, DOI 10.1164/rccm.2109065; McEwen BS, 1998, NEW ENGL J MED, V338, P171; Meduri GU, 2004, ANN NY ACAD SCI, V1024, P24, DOI 10.1196/annals.1321.004; Miller GE, 2002, HEALTH PSYCHOL, V21, P531, DOI 10.1037//0278-6133.21.6.531; Mills PJ, 2004, AM J GERIAT PSYCHIAT, V12, P281, DOI 10.1176/appi.ajgp.12.3.281; Mrazek DA, 1999, PEDIATR PULM, V27, P85, DOI 10.1002/(SICI)1099-0496(199902)27:2<85::AID-PPUL4>3.0.CO;2-B; NEWNHAM DM, 1993, EUR J CLIN PHARMACOL, V45, P535, DOI 10.1007/BF00315310; Rudolph KD, 1999, CHILD DEV, V70, P660, DOI 10.1111/1467-8624.00048; Sandberg S, 2004, THORAX, V59, P1046, DOI 10.1136/thx.2004.024604; Sandberg S, 2000, LANCET, V356, P982, DOI 10.1016/S0140-6736(00)02715-X; Umland SP, 2002, PULM PHARMACOL THER, V15, P35, DOI 10.1006/pupt.2001.0312; Vachier I, 1996, CLIN EXP IMMUNOL, V103, P311, DOI 10.1046/j.1365-2249.1996.d01-628.x; 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, 2004, AM J PUBLIC HEALTH, V94, P625, DOI 10.2105/AJPH.94.4.625; Wright RJ, 2002, AM J RESP CRIT CARE, V165, P358	34	104	107	4	12	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.	APR 4	2006	103	14					5496	5501		10.1073/pnas.0506312103		6	Multidisciplinary Sciences	Science & Technology - Other Topics	030LP	WOS:000236636400047	16567656	
J	Martinez, FD				Martinez, FD			Safety of long-acting beta agonists - An urgent need to clear the air	NEW ENGLAND JOURNAL OF MEDICINE			English	Editorial Material							BRONCHODILATOR TREATMENT; ASTHMA; SALMETEROL		Univ Arizona, Coll Med, Arizona Resp Ctr, Tucson, AZ 85721 USA	Martinez, FD (reprint author), Univ Arizona, Coll Med, Arizona Resp Ctr, Tucson, AZ 85721 USA.						Anderson HR, 2005, BRIT MED J, V330, P117, DOI 10.1136/bmj.38316.729907.8F; CASTLE W, 1993, BRIT MED J, V306, P1034; Getahun D, 2005, J ASTHMA, V42, P373, DOI 10.1081/JAS-200062995; GREENING AP, 1994, LANCET, V344, P219, DOI 10.1016/S0140-6736(94)92996-3	4	104	106	0	0	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.	DEC 22	2005	353	25					2637	2639		10.1056/NEJMp058299		3	Medicine, General & Internal	General & Internal Medicine	995IQ	WOS:000234094400003	16371628	
J	Hausermann, P; Harr, T; Bircher, AJ				Hausermann, P; Harr, T; Bircher, AJ			Baboon syndrome resulting from systemic drugs: is there strife between SDRIFE and allergic contact dermatitis syndrome?	CONTACT DERMATITIS			English	Article						allergic contact dermatitis syndrome; baboon syndrome; systemic contact dermatitis	ERUPTION; PSEUDOEPHEDRINE; EXANTHEM; HYPERSENSITIVITY; ETHYLENEDIAMINE; AMINOPHYLLINE; MANIFESTATION; AMOXICILLIN; CINCHOCAINE; MERCURY	The term 'baboon syndrome' (BS) was introduced 20 years ago to classify patients in whom a specific skin eruption resembling the red gluteal area of baboons occurred after systemic exposure to contact allergens. Thereafter, similar eruptions have been reported after systemic exposure to beta-lactam antibiotics and other drugs. In addition to the presentation of 2 of our own cases, we have reviewed and characterized the main clinical and histological aspects of published reports of drug-related baboon syndrome (DRBS) and compared the primary clinical signs from such cases to those found in other distinct drug eruptions. Of approximately 100 published baboon syndrome cases, 50 were identified as drug-induced. Of these, 8 were representatives of systemically induced contact dermatitis (SCD), and 42 were examples of drug eruptions elicited by systemic administration of either oral or intravenous drugs. The main clinical findings included a sharply defined symmetrical erythema of the gluteal area and in the flexural or intertriginous folds without any systemic symptoms and signs. 14 of 42 cases were elicited by amoxicillin, 30 of the 42 patients were male, and latency periods were between a few hours and a few days after exposure. DRBS is a rare, prognostically benign and often underdiagnosed drug eruption with distinct clinical features. The term baboon syndrome, however, does not reflect the complete range of symptoms and signs and is ethically and culturally problematic. Moreover, baboon syndrome is historically often equated with a mercury-induced exanthem in patients with previous contact sensitization. Symmetrical drug-related intertriginous and flexural exanthema, or SDRIFE, specifically refers to the distinctive clinical pattern of this drug eruption, and the following diagnostic criteria are proposed: 1) exposure to a systemically administered drug either at the first or repeated dose (excluding contact allergens); 2) sharply demarcated erythema of the gluteal/perianal area and/or V-shaped erythema of the inguinal/perigenital area; 3) involvement of at least one other intertriginous/flexural localization; 4) symmetry of affected areas; and 5) absence of systemic symptoms and signs.	Univ Basel Hosp, Dept Dermatol, Allergy Unit, CH-4031 Basel, Switzerland	Bircher, AJ (reprint author), Univ Basel Hosp, Dept Dermatol, Allergy Unit, Petersgraben 4, CH-4031 Basel, Switzerland.	andreas.bircher@unibas.ch					Amichai B, 2002, CLIN EXP DERMATOL, V27, P523; ANDERSEN KE, 1984, CONTACT DERMATITIS, V10, P97, DOI 10.1111/j.1600-0536.1984.tb00343.x; Barbaud A, 1999, DERMATOLOGY, V199, P258, DOI 10.1159/000018259; 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; Chowdhury MMU, 1999, CLIN EXP DERMATOL, V24, P336; DEGROOT AC, 1991, CONTACT DERMATITIS, V24, P201; DUVE S, 1994, ACTA DERM-VENEREOL, V74, P480; Erdmann SM, 2001, CONTACT DERMATITIS, V44, P260; Gallo R, 2002, CONTACT DERMATITIS, V46, P110, DOI 10.1034/j.1600-0536.2002.460211.x; Garcia-Bravo B, 2000, CONTACT DERMATITIS, V43, P359; Goossens C, 1997, DERMATOLOGY, V194, P421; Gordon Ellen, 2002, J Drugs Dermatol, V1, P66; Guin JD, 1999, CONTACT DERMATITIS, V40, P170, DOI 10.1111/j.1600-0536.1999.tb06026.x; HAPPLE R, 1994, HAUTARZT, V45, P1, DOI 10.1007/PL00013249; Helmbold P, 1998, DERMATOLOGY, V197, P402, DOI 10.1159/000018047; HERFS H, 1993, HAUTARZT, V44, P466; Isaksson M, 2003, ACTA DERM-VENEREOL, V83, P69, DOI 10.1080/00015550310002837; Kick G, 2000, CONTACT DERMATITIS, V43, P366; Kohler LD, 1996, INT J DERMATOL, V35, P502, DOI 10.1111/j.1365-4362.1996.tb01667.x; LACHAPELLE JM, 2003, PATCH TESTING PRICK, V189, P7; LECHNER T, 1987, MYCOSES, V30, P143; Lerch M, 2004, CONTACT DERMATITIS, V50, P349, DOI 10.1111/j.0105-1873.2004.00366.x; LOZE I, 2001, NOUV DERMATOL, V20, P624; Marques C, 1995, CONTACT DERMATITIS, V33, P443, DOI 10.1111/j.1600-0536.1995.tb02095.x; MENNE T, 1984, HAUTARZT, V35, P319; Menne T, 1994, AM J CONTACT DERMATI, V5, P1; MONTAG G, 1996, AKTUEL DERMATOL, V22, P311; NAKAYAMA H, 1983, CONTACT DERMATITIS, V9, P411, DOI 10.1111/j.1600-0536.1983.tb04439.x; Panhans-Gross A, 1999, CONTACT DERMATITIS, V41, P352, DOI 10.1111/j.1600-0536.1999.tb06195.x; Pfeiff B, 1991, DTSCH DERMATOLOGE, V39, P559; Proske S., 2003, DMW Deutsche Medizinische Wochenschrift, V128, P545, DOI 10.1055/s-2003-37850; RASMUSSEN LP, 1995, UGESKRIFT LAEGER, V147, P1341; RATNER JH, 1974, ARCH DERMATOL, V110, P921, DOI 10.1001/archderm.110.6.921; ROUJEAU JC, 1991, ARCH DERMATOL, V127, P8; Sanchez TS, 2000, CONTACT DERMATITIS, V42, P312; Sanchez-Morillas L, 2003, CONTACT DERMATITIS, V48, P234, DOI 10.1034/j.1600-0536.2003.00088.x; SCHULTZ ES, 1996, DERMATOSEN, V44, P266; SHELLEY WB, 1987, J AM ACAD DERMATOL, V17, P403, DOI 10.1016/S0190-9622(87)70220-5; STRUB C, 2002, SCHWEIZ RUNDSCH MED, V91, P232; STUBB S, 1989, BRIT J DERMATOL, V120, P583, DOI 10.1111/j.1365-2133.1989.tb01337.x; Wakelin SH, 1999, CLIN EXP DERMATOL, V24, P71; Weiss JM, 2001, HAUTARZT, V52, P1104, DOI 10.1007/s001050170022; WOLF R, 1992, ACTA DERM-VENEREOL, V72, P441; WOLF R, 1993, INT J DERMATOL, V32, P515, DOI 10.1111/j.1365-4362.1993.tb02837.x; WOLF R, 1995, INT J DERMATOL, V34, P341, DOI 10.1111/j.1365-4362.1995.tb03616.x; Wolf Ronni, 2003, Dermatol Online J, V9, P2	47	104	108	0	1	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-1873			CONTACT DERMATITIS	Contact Dermatitis	NOV	2004	51	5-6					297	310		10.1111/j.0105-1873.2004.00445.x		14	Allergy; Dermatology	Allergy; Dermatology	878ER	WOS:000225629900014	15606657	
J	Bottcher, MF; Hmani-Aifa, M; Lindstrom, A; Jenmalm, MC; Mai, XM; Nilsson, L; Zdolsek, HA; Bjorksten, B; Soderkvist, P; Vaarala, O				Bottcher, MF; Hmani-Aifa, M; Lindstrom, A; Jenmalm, MC; Mai, XM; Nilsson, L; Zdolsek, HA; Bjorksten, B; Soderkvist, P; Vaarala, O			A TLR4 polymorphism is associated with asthma and reduced lipopolysaccharide-induced interleukin-12(p70) responses in Swedish children	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; TLR4; lipopolysaccharide; IL-12; IL-10	TOLL-LIKE RECEPTOR-4; T-CELL; ENDOTOXIN EXPOSURE; INTERFERON-GAMMA; ALLERGIC DISEASE; IGE PRODUCTION; HOUSE-DUST; CD14 GENE; ATOPY; CHALLENGE	Background: Bacterial signals play an important role in the maturation of the immune system. Polymorphisms in genes coding for receptors to bacterial components can alter the immune responsiveness of the host to microbial agents and may indicate the development of aberrant immune responses that are associated with immune-mediated diseases such as atopic diseases. Objective: The study's objective was to investigate the relationship between TLR4 and CD14 gene polymorphisms, the LPS responsiveness of PBMCs, and the presence of asthma and allergic rhinoconjunctivitis in children. Methods: The TLR4 (Asp299Gly) and CD14/-159 polymorphisms were determined in 115 Swedish children aged 8 and 14 years. LPS-induced IL-12(p70), IL-10, and IFN-gamma responses of PBMCs from 69 of the children were analyzed by means of ELISA. The levels of soluble CD14 in serum samples were analyzed by means of ELISA, and the total IgE levels were analyzed by means of UniCAP Total IgE (Pharmacia Diagnostics, Uppsala, Sweden). Results: Decreased LPS-induced IL-12(p70) and IL-10 responses were associated with the TLR4 (Asp299Gly) polymorphism and independently with asthma, especially atopic asthma. The TLR4 (Asp299Gly) polymorphism was associated with a 4-fold higher prevalence of asthma in school-aged children (adjusted odds ratio 4.5, 95% CI 1.1-17.4) but not to allergic rhinoconjunctivitis. Conclusion: A TLR4 polymorphism modifies innate immune responses in children and may be an important determinant for the development of asthma. This may influence the outcome of intervention studies that use microbial stimuli as immune modulators.	Linkoping Univ, Dept Mol & Clin Med, Div Pediat, Linkoping, Sweden; Linkoping Univ, Fac Hlth Sci, Clin Res Ctr, Linkoping, Sweden; Linkoping Univ, Fac Hlth Sci, Dept Biomed & Surg, Div Cell Biol, Linkoping, Sweden; Karolinska Inst, Ctr Allergy Res, Stockholm, Sweden; Karolinska Inst, Inst Environm Med, Stockholm, Sweden; Natl Publ Hlth Inst, Dept Mol Med, Helsinki, Finland	Bottcher, MF (reprint author), Linkoping Univ Hosp, Div Paediat, KFC, S-58185 Linkoping, Sweden.	MalFa@imk.liu.se	Jenmalm, Maria/C-9679-2009	Jenmalm, Maria/0000-0002-2117-5366			Akashi S, 2000, BIOCHEM BIOPH RES CO, V268, P172, DOI 10.1006/bbrc.2000.2089; Akdis CA, 1999, FASEB J, V13, P603; Arbour NC, 2000, NAT GENET, V25, P187; Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Borish L, 1996, J ALLERGY CLIN IMMUN, V97, P1288, DOI 10.1016/S0091-6749(96)70197-5; Bottcher MF, 2003, CLIN EXP ALLERGY, V33, P295, DOI 10.1046/j.1365-2222.2003.01562.x; Bottcher MF, 2002, CLIN EXP ALLERGY, V32, P1690, DOI 10.1046/j.1365-2222.2002.01463.x; Chow JC, 1999, J BIOL CHEM, V274, P10689, DOI 10.1074/jbc.274.16.10689; Cleveland MG, 1996, INFECT IMMUN, V64, P1906; Corinti S, 2001, J IMMUNOL, V166, P4312; Egan RW, 1996, ALLERGY, V51, P71, DOI 10.1111/j.1398-9995.1996.tb04561.x; FREY EA, 1992, J EXP MED, V176, P1665, DOI 10.1084/jem.176.6.1665; 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; Gross E, 1999, HUM GENET, V105, P72, DOI 10.1007/s004390051066; Hattevig G, 1993, Pediatr Allergy Immunol, V4, P182, DOI 10.1111/j.1399-3038.1993.tb00089.x; Holt PG, 1997, PEDIATR ALLERGY IMMU, V8, P53, DOI 10.1111/j.1399-3038.1997.tb00145.x; Koppelman GH, 2001, AM J RESP CRIT CARE, V163, P965; Liu AH, 2002, J ALLERGY CLIN IMMUN, V109, P379, DOI 10.1067/mai.2002.122157; 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; MACATONIA SE, 1995, J IMMUNOL, V154, P5071; Mai XM, 2002, PEDIATR ALLERGY IMMU, V13, P361, DOI 10.1034/j.1399-3038.2002.01011.x; MANETTI R, 1994, J EXP MED, V179, P1273, DOI 10.1084/jem.179.4.1273; PENE J, 1988, P NATL ACAD SCI USA, V85, P6880, DOI 10.1073/pnas.85.18.6880; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; PUNNONEN J, 1993, J IMMUNOL, V151, P1280; Raby BA, 2002, AM J RESP CRIT CARE, V166, P1449, DOI 10.1164/rrcm.200207-634OC; Sudo N, 1997, J IMMUNOL, V159, P1739; Tulic MK, 2000, AM J RESP CELL MOL, V22, P604; ULEVITCH RJ, 1995, ANNU REV IMMUNOL, V13, P437, DOI 10.1146/annurev.iy.13.040195.002253; Yazdanbakhsh M, 2001, TRENDS IMMUNOL, V22, P372, DOI 10.1016/S1471-4906(01)01958-5	32	104	110	0	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.	SEP	2004	114	3					561	567		10.1016/j.jaci.2004.04.050		7	Allergy; Immunology	Allergy; Immunology	853AX	WOS:000223799600014	15356557	
J	Benn, CS; Melbye, M; Wohlfahrt, J; Bjorksten, B; Aaby, P				Benn, CS; Melbye, M; Wohlfahrt, J; Bjorksten, B; Aaby, P			Cohort study of sibling effect, infectious diseases, and risk of atopic dermatitis during first 18 months of life	BRITISH MEDICAL JOURNAL			English	Article							FAMILY-SIZE; HAY-FEVER; RESPIRATORY-INFECTIONS; BIRTH COHORT; CHILDREN; ASTHMA; PREVALENCE; ALLERGY; DETERMINANTS; ANTIBODIES	Objectives To determine whether early infectious diseases could explain the association between number of siblings and other markers of microbial exposure and the development of atopic dermatitis before the age of 18 months. Design Cohort study. Information on atopic dermatitis, infectious diseases occurring before 6 months of age, number of siblings, early day care, pet keeping, farm residence, and background factors was collected in telephone interviews. Setting Danish national birth cohort. Participants 24341 mother-child pairs. Main outcome measures Incidence rate ratios of atopic dermatitis. Results 13070 children (54%) had at least one clinically apparent infectious disease before 6 months of age. At age 18 months, 2638 (10.8%) of the children had had atopic dermatitis. The risk of atopic dermatitis increased with each infectious disease before 6 months of age (incidence rate ratio 1.08,95% confidence interval 1.04 to 1.13). The risk of atopic dermatitis decreased with each additional exposure to three or more siblings, day care, pet ownership, and farm residence (0.86, 0.81 to 0.93). Conclusions Early infections do not seem to protect against allergic diseases. The protective effect of number of siblings, day care, pet ownership, and farm residence remained after adjustment for clinically apparent infectious diseases, suggesting that the effect is established independently early in life.	Statens Serum Inst, Danish Epidemiol Sci Ctr, Dept Epidemiol Res, Copenhagen, Denmark; Projecto Saude Bandim, Bissau, Guinea Bissau; Karolinska Inst, Ctr Allergy Res, Stockholm, Sweden; Karolinska Inst, Inst Environm Med, Stockholm, Sweden	Benn, CS (reprint author), Statens Serum Inst, Danish Epidemiol Sci Ctr, Dept Epidemiol Res, Copenhagen, Denmark.	C.Benn.cb@ssi.dk					Benn CS, 2003, ACTA DERM-VENEREOL, V83, P347; Bjorksten B, 1999, J ALLERGY CLIN IMMUN, V104, P1119; Bodner C, 1998, THORAX, V53, P28; Bohme M, 2002, ACTA DERM-VENEREOL, V82, P98, DOI 10.1080/00015550252948112; Devereux G, 2002, CLIN EXP ALLERGY, V32, P43, DOI 10.1046/j.0022-0477.2001.01267.x; Forastiere F, 1997, EPIDEMIOLOGY, V8, P566, DOI 10.1097/00001648-199709000-00015; Harris JM, 2001, BRIT J DERMATOL, V144, P795, DOI 10.1046/j.1365-2133.2001.04135.x; Kalliomaki Marko, 2003, Curr Opin Allergy Clin Immunol, V3, P15, DOI 10.1097/00130832-200302000-00003; Karmaus W, 2002, J EPIDEMIOL COMMUN H, V56, P209, DOI 10.1136/jech.56.3.209; Karmaus W, 2001, AM J EPIDEMIOL, V154, P909, DOI 10.1093/aje/154.10.909; Linneberg A, 2003, J ALLERGY CLIN IMMUN, V111, P847, DOI 10.1067/mai.2003.1335; Matricardi P M, 2001, Curr Opin Allergy Clin Immunol, V1, P413, DOI 10.1097/01.all.0000011054.18314.67; Matricardi PM, 1997, BRIT MED J, V314, P999; McKeever TM, 2002, J ALLERGY CLIN IMMUN, V109, P43, DOI 10.1067/mai.2002.121016; Nafstad P, 2000, PEDIATRICS, V106, DOI 10.1542/peds.106.3.e38; Olsen J, 2001, SCAND J PUBLIC HEALT, V29, P300, DOI 10.1177/14034948010290040201; Ponsonby AL, 1999, THORAX, V54, P664; RYSTEDT I, 1986, BRIT J DERMATOL, V114, P575, DOI 10.1111/j.1365-2133.1986.tb04064.x; Strachan David P., 2000, Thorax, V55, pS2, DOI 10.1136/thorax.55.suppl_1.S2; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Strachan DP, 1996, ARCH DIS CHILD, V74, P422; Strannegard O, 2001, ALLERGY, V56, P91, DOI 10.1034/j.1398-9995.2001.056002091.x; Wickens KL, 1999, EPIDEMIOLOGY, V10, P699, DOI 10.1097/00001648-199911000-00009	23	104	104	1	3	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0959-535X			BRIT MED J	Br. Med. J.	MAY 22	2004	328	7450					1223	1226		10.1136/bmj.38069.512245.FE		6	Medicine, General & Internal	General & Internal Medicine	824HL	WOS:000221677200015	15121716	
J	Salam, MT; Li, YF; Langholz, B; Gilliland, FD				Salam, MT; Li, YF; Langholz, B; Gilliland, FD			Early-life environmental risk factors for asthma: Findings from the children's health study	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; breast-feeding; cockroach; day care; farm environment; herbicide; pesticide; sibship size; wood smoke	SOUTHERN CALIFORNIA COMMUNITIES; INNER-CITY CHILDREN; DAY-CARE ATTENDANCE; PULMONARY-FUNCTION; CHILDHOOD ASTHMA; 1ST YEAR; COCKROACH ALLERGEN; DIFFERING LEVELS; EARLY EXPOSURE; AIR-POLLUTION	Early-life experiences and environmental exposures have. been associated with childhood asthma. To investigate further whether the timing of such experiences and exposures is associated with the occurrence of asthma by 5 years of age, we conducted a prevalence case-control study nested within the Children's Health Study, a population-based study of > 4,000 school-aged children in 12 southern California communities. Cases were defined as physician-diagnosed asthma by age 5, and controls were asthma-free at study entry, frequency- matched on age, sex, and community of residence and countermatched on in utero exposure to maternal smoking. Telephone interviews were conducted with mothers to collect additional exposure and asthma histories. Conditional logistic regression models were fitted to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Asthma diagnosis before 5 years of age was associated with exposures in the first year of life to wood or oil smoke, soot, or exhaust (OR = 1.74; 95% CI, 1.02-2.96), cockroaches (OR = 2.03; 95% CI, 1.03-4.02), herbicides (OR = 4.58; 95% CI, 1.36-15.43), pesticides (OR = 2.39; 95% CI, 1.17-4.89), and farm crops, farm dust, or farm animals (OR = 1.88; 95% CI, 1.07-3.28). The ORs for herbicide, pesticide, farm animal, and crops were largest among children with early-onset persistent asthma. The risk of asthma decreased with an increasing number of siblings (P-trend 0.01). Day care attendance within the first 4 months of life was positively associated with early-onset transient wheezing (OR = 2.42; 95% CI, 1.28-4.59). In conclusion, environmental exposures during the first year of life are associated with childhood asthma risk.	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,CHP 236, Los Angeles, CA 90033 USA.	gillilan@use.edu	LI, YU-FEN/F-4770-2010		NHLBI NIH HHS [1R01HL61768]; NIEHS NIH HHS [5P30 ES07048, 1P01 ES09581]		Alp H, 2001, ANN ALLERG ASTHMA IM, V86, P51; Antony AB, 2002, J ALLERGY CLIN IMMUN, V110, P589, DOI 10.1067/mai.2002.127798; Apelberg BJ, 2001, J ALLERGY CLIN IMMUN, V107, P455, DOI 10.1067/mai.2001.113240; Belanger K, 2003, AM J EPIDEMIOL, V158, P195, DOI 10.1093/aje/kwg148; Bener A, 1999, Allerg Immunol (Paris), V31, P52; Bener A, 2002, Allerg Immunol (Paris), V34, P281; Braun-Fahrlander C, 2001, CLIN EXP ALLERGY, V31, P1799, DOI 10.1046/j.1365-2222.2001.01269.x; BURR ML, 1992, CLIN EXP ALLERGY, V22, P509, DOI 10.1111/j.1365-2222.1992.tb00158.x; Castro-Rodriguez JA, 1999, AM J RESP CRIT CARE, V159, P1891; Celedon JC, 1999, PEDIATRICS, V104, P495, DOI 10.1542/peds.104.3.495; Chen Ping, 2002, Zhonghua Jiehe He Huxi Zazhi, V25, P603; Devereux G, 2002, CLIN EXP ALLERGY, V32, P43, DOI 10.1046/j.0022-0477.2001.01267.x; Ernst P, 2002, AM J RESP CRIT CARE, V165, P563, DOI 10.1164/rccm.2201002; Faustman EM, 2000, ENVIRON HEALTH PERSP, V108, P13, DOI 10.2307/3454629; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Hoppin JA, 2002, AM J RESP CRIT CARE, V165, P683, DOI 10.1164/rccm.2106074; Infante-Rivard C, 2001, AM J EPIDEMIOL, V153, P653, DOI 10.1093/aje/153.7.653; Johnson CC, 2002, EPIDEMIOL REV, V24, P154, DOI 10.1093/epirev/mxf013; Karmaus W, 2001, ARCH ENVIRON HEALTH, V56, P485; Karmaus W, 2001, AM J EPIDEMIOL, V154, P909, DOI 10.1093/aje/154.10.909; KOENIG JQ, 1993, ENVIRON RES, V63, P26, DOI 10.1006/enrs.1993.1123; Landrigan PJ, 1999, ENVIRON HEALTH PERSP, V107, P431; Langholz B., 2001, BIOSTATISTICS, V2, P63, DOI 10.1093/biostatistics/2.1.63; LARSON TV, 1994, ANNU REV PUBL HEALTH, V15, P133; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; Litonjua AA, 2001, J ALLERGY CLIN IMMUN, V107, P41, DOI 10.1067/mai.2001.111143; Mannino DM, 1998, MMWR-MORBID MORTAL W, V47, P1; McConnell R, 2002, EPIDEMIOLOGY, V13, P288, DOI 10.1097/00001648-200205000-00009; Melen E, 2001, ALLERGY, V56, P646, DOI 10.1034/j.1398-9995.2001.00387.x; Nafstad P, 1999, PEDIATRICS, V103, P753, DOI 10.1542/peds.103.4.753; Nafstad P, 2001, ALLERGY, V56, P307, DOI 10.1034/j.1398-9995.2001.00881.x; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; Peters JM, 1999, AM J RESP CRIT CARE, V159, P768; Remes ST, 2001, J ALLERGY CLIN IMMUN, V108, P509, DOI 10.1067/mai.2001.117797; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Ronmark E, 2002, RESP MED, V96, P1006, DOI 10.1053/rmed.2002.1391; Sarpong SB, 1996, J ALLERGY CLIN IMMUN, V97, P1393, DOI 10.1016/S0091-6749(96)70209-9; Schwartz DA, 2001, AM J RESP CRIT CARE, V163, P305; Stevenson LA, 2001, J ALLERGY CLIN IMMUN, V108, P747, DOI 10.1067/mai.2001.119410; Strachan DP, 2000, THORAX S1, V55, pS2; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; Weiss KB, 2001, J ALLERGY CLIN IMMUN, V107, P3, DOI 10.1067/mai.2001.112262; Wickens KL, 1999, EPIDEMIOLOGY, V10, P699, DOI 10.1097/00001648-199911000-00009; Zheng TZ, 2002, AM J EPIDEMIOL, V156, P977, DOI 10.1093/aje/kwf127	45	104	106	0	10	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.	MAY	2004	112	6					760	765		10.1289/ehp.6662		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	822DD	WOS:000221514400044	15121522	
J	Ebo, DG; Hagendorens, MM; Bridts, CH; Schuerwegh, AJ; De Clerck, LS; Stevens, WJ				Ebo, DG; Hagendorens, MM; Bridts, CH; Schuerwegh, AJ; De Clerck, LS; Stevens, WJ			In vitro allergy diagnosis: should we follow the flow?	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review							BASOPHIL HISTAMINE-RELEASE; GRASS-POLLEN ALLERGENS; RUBBER LATEX ALLERGY; HUMAN MAST-CELLS; HYMENOPTERA-VENOM; RECOMBINANT ALLERGENS; CD63 EXPRESSION; ACTIVATION TEST; IGE ANTIBODIES; CDNA CLONING	During the last 5 years, an increasing number of studies have demonstrated that flow cytometric quantification of in vitro basophil activation can be a quite performant and reliable tool to measure IgE-dependent allergen-specific responses in allergic patients. So far, most assays have used CD63 as a basophil activation marker and native allergen extracts for stimulation. However, other basophil markers and recombinant allergens have recently been introduced. The technique has been applied for the diagnosis of allergy to pollen, house dust mite, food, natural rubber latex, hymenoptera venom and drugs. In addition, the technique has proven to be useful in non-IgE-mediated reactions such as hypersensitivity to drugs as well as detection of auto-antibodies in chronic urticaria. This review will focus on some specific issues: (1) principles of flow cytometric analysis of in vitro-activated basophils, (2) general technical aspects of the technique (including passive sensitization), (3) clinical applications and (4) recommendations for further development and evaluation of the technique.	Univ Antwerp, Dept Immunol Allergol Rheumatol, B-2020 Antwerp, Belgium	Stevens, WJ (reprint author), Immunol Lab, Univ Pl 1, B-2610 Antwerp, Belgium.	Immuno@uia.ua.ac.be	BRIDTS, Chris/M-7933-2016; EBO, Didier/H-4894-2016	BRIDTS, Chris/0000-0002-3324-7320; EBO, Didier/0000-0003-0672-7529			Aalberse RC, 2001, ALLERGY, V56, P478, DOI 10.1034/j.1398-9995.2001.056006478.x; ABRAHAMSEN O, 2001, CLIN EXP ALLERGY, P368; Abuaf N, 1999, J ALLERGY CLIN IMMUN, V104, P411, DOI 10.1016/S0091-6749(99)70386-6; Andersson K, 2003, INT ARCH ALLERGY IMM, V130, P87, DOI 10.1159/000069013; Asero R, 1999, ALLERGY, V54, P87, DOI 10.1034/j.1398-9995.1999.00922.x; Binder M, 2002, INT ARCH ALLERGY IMM, V129, P160, DOI 10.1159/000065875; BIRCHER AJ, 1994, CLIN EXP ALLERGY, V24, P367, DOI 10.1111/j.1365-2222.1994.tb00248.x; Bochner BS, 1997, METHODS, V13, P61, DOI 10.1006/meth.1997.0497; Bochner BS, 2000, J ALLERGY CLIN IMMUN, V106, P292; Boumiza R, 2003, CLIN EXP ALLERGY, V33, P259, DOI 10.1046/j.1365-2222.2003.01594.x; BUCKLEY MF, 1990, J BIOL CHEM, V265, P17506; Budde IK, 2001, INT ARCH ALLERGY IMM, V126, P277; Buhring HJ, 2001, BLOOD, V97, P3303, DOI 10.1182/blood.V97.10.3303; Buhring HJ, 1999, BLOOD, V94, P2343; Chapman MD, 1997, ALLERGY, V52, P374, DOI 10.1111/j.1398-9995.1997.tb01014.x; Cozon G, 1999, Allergol Immunopathol (Madr), V27, P182; Crockard AD, 2001, CLIN EXP ALLERGY, V31, P345, DOI 10.1046/j.1365-2222.2001.01043.x; de Weck AL, 2003, CLIN EXP ALLERGY, V33, P849; Decco ML, 1999, ANN ALLERG ASTHMA IM, V82, P29, DOI 10.1016/S1081-1206(10)62656-7; DEISSLER H, 1995, J BIOL CHEM, V270, P9849; Deissler H, 1999, FASEB J, V13, P657; Demoly P, 2003, ALLERGY, V58, P553, DOI 10.1034/j.1398-9995.2003.00253.x; DeWeck AL, 1997, ALLERGOLOGIE, V20, P487; De Weck AL, 2002, ACI INT, V14, P204, DOI 10.1027/0838-1925.14.5.204; De Weck A., 1993, ALLERGY CLIN IMMUNOL, V5, P9; Ebo D. 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Exp. Allergy	MAR	2004	34	3					332	339		10.1111/j.1365-2222.2004.01891.x		8	Allergy; Immunology	Allergy; Immunology	801LY	WOS:000220098600003	15005724	
J	Downs, SH; Marks, GB; Mitakakis, TZ; Leuppi, JD; Car, NG; Peat, JK				Downs, SH; Marks, GB; Mitakakis, TZ; Leuppi, JD; Car, NG; Peat, JK			Having lived on a farm and protection against allergic diseases in Australia	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						atopy; farming; children; allergic diseases	HAY-FEVER; ASTHMA; CHILDHOOD; CHILDREN; SENSITIZATION; EXPOSURE; PREVALENCE; HISTORY	Background Farmers' children in northern Europe have a lower prevalence of atopy, hay fever and asthma than other children. Farms in Australia differ in scale and operation from those in Europe and the prevalence of allergic diseases in children is higher. Objective To investigate whether having lived on a farm as a child in Australia is associated with a lower risk of allergic diseases. Methods Cross-sectional study of children (n = 1500) aged 7-12 years from two rural towns: Wagga Wagga in a mixed farming region, and Moree in a crop farming region. Parents answered a questionnaire and children had a skin prick test for atopy. Results Twenty percent of children had lived on a farm for at least 1 year. The effect of having lived on a farm differed between the towns (P < 0.001). It was associated with a lower risk of atopy in Wagga (adjusted odds ratio (aOR) 0.47, 95% confidence interval (CI) 0.32-0.72) but not in Moree (aOR 0.97, 95% CI 0.62-1.53). Children from Wagga were more likely to have lived on a livestock farm than children from Moree (26.1% vs. 9.1%, 95% CI for the difference 8.9-25.4). Conclusion Having lived on a farm in Australia can confer protection against atopy in children. Further studies are needed to identify possible protective mechanisms associated with farm animals or to establish whether the protective effect is explained by other related exposures.	Univ Sydney, Inst Resp Med, Sydney, NSW 2006, Australia; New Childrens Hosp, Westmead, NSW, Australia; Charles Sturt Univ, Sch Biomed Sci, Bathurst, NSW 2795, Australia	Downs, SH (reprint author), Inst Resp Med, POB M77,Missenden Rd PO, Camperdown, NSW 2050, Australia.		Downs, Sara/D-8478-2011	Downs, Sara/0000-0003-1044-3182			ABDELHAFEZ SII, 1990, J BASIC MICROB, V30, P467, DOI 10.1002/jobm.3620300702; American Thoracic Society, 1998, AM J RESP CRIT CARE, V158, pS1; *AUSTR BUR STAT, 1998, 71131 AUSTR BUR STAT; Beard M, 1996, APPL OCCUP ENV HYG, V11, P1409; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; *DEP TECHN SERV, 1998, WAGG WAGG DRAFT NAT; *GWYD CATCHM TASKF, 1997, GWYD COMM CATCHM PLA; HENSLEY MJ, 1988, THORAX, V43, P103, DOI 10.1136/thx.43.2.103; Holt PG, 1997, THORAX, V52, P1; Holt PG, 1997, PEDIATR ALLERGY IMMU, V8, P53, DOI 10.1111/j.1399-3038.1997.tb00145.x; JAMES AL, 1990, BRIT J IND MED, V47, P466; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; 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; Knoblauch A, 1996, OCCUP ENVIRON MED, V53, P577; LEON DA, 1993, LANCET, V342, P479, DOI 10.1016/0140-6736(93)91599-H; Lewis SA, 2000, CLIN EXP ALLERGY, V30, P153; MacDonald IAR, 1996, EPIDEMIOL INFECT, V116, P279; Matricardi PM, 2000, BRIT MED J, V320, P412, DOI 10.1136/bmj.320.7232.412; Parvaneh S, 1999, ALLERGY, V54, P229, DOI 10.1034/j.1398-9995.1999.00855.x; PEAT JK, 1995, MED J AUSTRALIA, V163, P22; PEAT JK, 1992, CHEST, V102, P153, DOI 10.1378/chest.102.1.153; Pepys J., 1975, BRIT J HOSP MED, V14, P412; Poppe C, 1998, CAN VET J, V39, P559; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; SALOME CM, 1987, CLIN ALLERGY, V17, P271, DOI 10.1111/j.1365-2222.1987.tb02015.x; *SCHWEIZ BAUERNV, 1998, STAT ERH SCHATZ LAND; SREERAMULU T, 1970, Journal of Palynology, V6, P31; Trevena WB, 1996, LANCET, V347, P60, DOI 10.1016/S0140-6736(96)91593-7; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; 1993, 71201 AUSTR BUR STAT	30	104	107	0	6	BLACKWELL SCIENCE LTD	OXFORD	P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	APR	2001	31	4					570	575		10.1046/j.1365-2222.2001.01070.x		6	Allergy; Immunology	Allergy; Immunology	431YN	WOS:000168659500010	11359424	
J	Blyth, DI; Wharton, TF; Pedrick, MS; Savage, TJ; Sanjar, S				Blyth, DI; Wharton, TF; Pedrick, MS; Savage, TJ; Sanjar, S			Airway subepithelial fibrosis in a murine model of atopic asthma - Suppression by dexamethasone or anti-interleukin-5 antibody	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article							BRONCHIAL-ASTHMA; BASEMENT-MEMBRANE; CELL HYPERPLASIA; INFLAMMATION; EXPRESSION; COLLAGEN; WALL; HYPERREACTIVITY; RESPONSIVENESS; METHACHOLINE	Fibrosis in the reticular layer beneath the epithelial basement membrane Is a feature of airway remodeling in human asthma, We previously reported the presence of subepithelial fibrosis (SEF) in a disease model of atopic asthma in which mice were sensitized and intratracheally challenged with ovalbumin (OVA) (Blyth and colleagues, Am. J. Respir. Cell Mol. Biol, 1996;14:425-438), Here, we describe further studies to quantify the degree of SEF after its induction by repeated exposure of the airways to allergen. The amount of subepithelial reticulin in the airways of animals challenged three times with 80 mu g OVA was typically increased 1.4-fold. The increased amount of reticulin showed no reduction after a 50-d period after the third allergen challenge. A reduction in SEF was achieved by daily treatment with dexamethasone (DEX) for 8 d during the allergen challenge period, or by treatment with anti-interleukin-5 antibody (TRFK5) at the time of allergen challenge, Postchallenge treatment with DEX for 15 d resulted in significant resolution of previously established SEF, Severe nonallergic inflammation during repeated exposure of airways to lipopolysaccharide did not induce SEF. The results indicate that development of SEF is associated with eosinophil infiltration into airways, and may occur only when the inflammatory stimulus is allergic in nature.	Glaxo Wellcome Res & Dev Ltd, Med Res Ctr, Resp Dis Unit, Stevenage SG1 2NY, Herts, England; Glaxo Wellcome Res & Dev Ltd, Mol Pathol Unit, Stevenage SG1 2NY, Herts, England	Blyth, DI (reprint author), Glaxo Wellcome Res & Dev Ltd, Med Res Ctr, Resp Dis Unit, Gunnels Wood Rd, Stevenage SG1 2NY, Herts, England.						Awadh N, 1998, THORAX, V53, P248; BEASLEY R, 1993, J ALLERGY CLIN IMMUN, V92, P148, DOI 10.1016/0091-6749(93)90097-Y; Blyth D. I., 1998, Journal of Pharmacy and Pharmacology, V50, P70; Blyth DI, 1998, AM J RESP CELL MOL, V19, P38; Blyth DI, 1996, AM J RESP CELL MOL, V14, P425; Boulet LP, 1997, CHEST, V112, P45, DOI 10.1378/chest.112.1.45; BREWSTER CEP, 1990, AM J RESP CELL MOL, V3, P507; Chakir J, 1996, LAB INVEST, V75, P735; Chetta A, 1997, CHEST, V111, P852, DOI 10.1378/chest.111.4.852; Chu HW, 1998, AM J RESP CRIT CARE, V158, P1936; DJUKANOVIC R, 1992, EUR RESPIR J, V5, P538; DUNNILL MS, 1960, J CLIN PATHOL, V13, P27, DOI 10.1136/jcp.13.1.27; Foster PS, 1996, J EXP MED, V183, P195, DOI 10.1084/jem.183.1.195; Garlisi CG, 1999, AM J RESP CELL MOL, V20, P248; Gizycki MJ, 1997, AM J RESP CELL MOL, V16, P664; Gordon H, 1936, AM J PATHOL, V12, P545; Hoshino M, 1998, THORAX, V53, P21; Hoshino M, 1998, CLIN EXP ALLERGY, V28, P568; Hoshino M, 1998, J ALLERGY CLIN IMMUN, V102, P783, DOI 10.1016/S0091-6749(98)70018-1; HOWARD CV, 1998, UNBIASED STEREOLOGY, P198; JAMES AL, 1989, AM REV RESPIR DIS, V139, P242; JEFFERY PK, 1989, AM REV RESPIR DIS, V140, P1745; JEFFERY PK, 1992, RESPIRATION, V59, P13; LAURENT GJ, 1991, CHEST, V99, pS67, DOI 10.1378/chest.99.3_Supplement.67S; LEE JV, 1985, SOC APPLIED BACTERIO, V21, P13; Olivieri D, 1997, AM J RESP CRIT CARE, V155, P1864; Orsida BE, 1999, THORAX, V54, P289; Pohunek P., 1997, European Respiratory Journal Supplement, V10, p160S; ROCHE WR, 1989, LANCET, V1, P520; ROGERS DF, 1992, BRIT MED BULL, V48, P120; SAETTA M, 1995, AM J RESP CRIT CARE, V151, P489; 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; TRIGG CJ, 1994, AM J RESP CRIT CARE, V150, P17; UNSWORTH DJ, 1982, BRIT J EXP PATHOL, V63, P154; Warner JO, 1998, CLIN EXP ALLERGY, V28, P71; Warner JO, 1998, PEDIATR ALLERGY IMMU, V9, P53, DOI 10.1111/j.1399-3038.1998.tb00302.x; WEIBEL ER, 1966, J CELL BIOL, V30, P23, DOI 10.1083/jcb.30.1.23; Wiggs BR, 1997, J APPL PHYSIOL, V83, P1814; Wilson JW, 1997, CLIN EXP ALLERGY, V27, P363; Zhu Zhou, 1999, Journal of Clinical Investigation, V103, P779, DOI 10.1172/JCI5909	42	104	108	0	5	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					241	246				6	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	344FW	WOS:000088749400019	10919992	
J	Kubo, A; Nagao, K; Amagai, M				Kubo, Akiharu; Nagao, Keisuke; Amagai, Masayuki			Epidermal barrier dysfunction and cutaneous sensitization in atopic diseases	JOURNAL OF CLINICAL INVESTIGATION			English	Review							THYMIC STROMAL LYMPHOPOIETIN; EPITHELIAL TIGHT JUNCTIONS; PROTEASE BLEOMYCIN HYDROLASE; DOWN-REGULATES FILAGGRIN; OF-FUNCTION MUTATIONS; STRATUM-CORNEUM; LANGERHANS CELLS; DENDRITIC CELLS; NETHERTON-SYNDROME; SKIN-BARRIER	Classic atopic dermatitis is complicated by asthma, allergic rhinitis, and food allergies, cumulatively referred to as atopic diseases. Recent discoveries of mutations in the filaggrin gene as predisposing factors for atopic diseases have refocused investigators' attention on epidermal barrier dysfunction as a causative mechanism. The skin's barrier function has three elements: the stratum corneum (air-liquid barrier), tight junctions (liquid-liquid barrier), and the Langerhans cell network (immunological barrier). Clarification of the molecular events underpinning epidermal barrier function and dysfunction should lead to a better understanding of the pathophysiological mechanisms of atopic diseases.	[Amagai, Masayuki] Keio Univ, Sch Med, Dept Dermatol, Shinjuku Ku, Tokyo 1608582, Japan; [Kubo, Akiharu] Keio Univ, Sch Med, Ctr Integrated Med Res, Tokyo 1608582, Japan	Amagai, M (reprint author), Keio Univ, Sch Med, Dept Dermatol, Shinjuku Ku, Shinanomachi 35, Tokyo 1608582, Japan.	amagai@a7.keio.jp	Nagao, Keisuke/J-5116-2013; Amagai, Masayuki/K-5325-2013; Kubo, Akiharu/I-2711-2014	Nagao, Keisuke/0000-0002-7005-3138; Amagai, Masayuki/0000-0003-3314-7052; Kubo, Akiharu/0000-0003-0902-3586	Ministry of Education, Culture, Sports, Science and Technology of Japan; Ministry of Health, Labour, and Welfare of Japan	This work was supported by Grants-in-Aid for Scientific Research and the "Promotion of Environmental Improvement for Independence of Young Researchers" program funding from the Ministry of Education, Culture, Sports, Science and Technology of Japan, and by Health Labour Sciences Research Grants for Research on Allergic Diseases and Immunology from the Ministry of Health, Labour, and Welfare of Japan.	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J	Martino, D; Prescott, S				Martino, David; Prescott, Susan			Epigenetics and Prenatal Influences on Asthma and Allergic Airways Disease	CHEST			English	Article							OBSTRUCTIVE PULMONARY-DISEASE; TOBACCO-SMOKE EXPOSURE; REGULATORY T-CELLS; IFN-GAMMA PROMOTER; MATERNAL SMOKING; CHILDHOOD ASTHMA; SUBSEQUENT DEVELOPMENT; DEVELOPMENTAL ORIGINS; POSTNATAL-DEVELOPMENT; CYTOKINE RESPONSES	Uterine life is arguably the most critical time in developmental programming, when environmental exposures may have the greatest potential to influence evolving fetal structure and function. There has been substantial progress in understanding the epigenetic mechanisms through which environmental exposures can permanently alter the expression of fetal genes and contribute to the increasing propensity for many complex diseases. These concepts of "developmental origins" of disease are being applied across virtually all fields of medicine, and emerging epigenetic paradigms are the likely mechanism behind the environment-driven epidemic of asthma and allergic disease. Here, we examine the epigenetic regulation of immune development and the early immune profiles that contribute to allergic risk. In particular we review new evidence that key environmental exposures, such as microbial exposure, dietary changes, tobacco smoke, and pollutants, can induce epigenetic changes in gene expression and alter disease risk. Although most of these factors have already been clearly implicated in epidemiologic studies of asthma and allergic disease, new studies investigating the mechanisms of these effects may provide new avenues for using these pathways for disease prevention. CHEST 2011; 139(3):640-647	[Martino, David; Prescott, Susan] Univ Western Australia, Sch Paediat & Child Hlth Res, Perth, WA 6840, Australia	Prescott, S (reprint author), Univ Western Australia, Princess Margaret Hosp Children, Sch Paediat & Child Hlth Res, GPO Box D 184, Perth, WA 6840, Australia.	sprescott@meddent.uwa.edu.au	Prescott, Susan/H-5665-2014	Martino, David/0000-0001-6823-4696	National Health and Medical Research Fellowship	Dr Prescott is funded by a National Health and Medical Research Fellowship.	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J	Jurewicz, J; Hanke, W				Jurewicz, Joanna; Hanke, Wojciech			EXPOSURE TO PHTHALATES: REPRODUCTIVE OUTCOME AND CHILDREN HEALTH. A REVIEW OF EPIDEMIOLOGICAL STUDIES	INTERNATIONAL JOURNAL OF OCCUPATIONAL MEDICINE AND ENVIRONMENTAL HEALTH			English	Review						Exposure to phthalates; Children health; Reproductive outcome	IN-UTERO EXPOSURE; SCHOOL-AGE-CHILDREN; N-BUTYL PHTHALATE; ANOGENITAL DISTANCE; SEMEN QUALITY; DI(2-ETHYLHEXYL) PHTHALATE; URINARY CONCENTRATIONS; ENDOCRINE DISRUPTORS; BIS(2-ETHYLHEXYL) PHTHALATE; ENVIRONMENTAL CHEMICALS	Phthalates are a family of industrial chemicals that have been used for a variety of purposes. As the potential consequences of human exposure to phthalates have raised concerns in the general population, they have been studied in susceptible subjects such as pregnant women, infants and children. This article aims at evaluating the impact of exposure to phthalates on reproductive outcomes and children health by reviewing most recent published literature. Epidemiological studies focusing on exposure to phthalates and pregnancy outcome, genital development, semen quality, precocious puberty, thyroid function, respiratory symptoms and neurodevelopment in children for the last ten years were identified by a search of the PubMed, Medline, Ebsco, Agricola and Toxnet literature bases. The results from the presented studies suggest that there are strong and rather consistent indications that phthalates increase the risk of allergy and asthma and have an adverse impact on children's neurodevelopment reflected by quality of alertness among girls, decreased (less masculine) composite score in boys and attention deficit hyperactivity disorder. Results of few studies demonstrate negative associations between phthalate levels commonly experienced by the public and impaired sperm quality (concentration, morphology, motility). Phthalates negatively impact also on gestational age and head circumference; however, the results of the studies were not consistent. In all the reviewed studies, exposure to phthalates adversely affected the level of reproductive hormones (luteinizing hormone, free testosterone, sex hormone-binding globulin), anogenital distance and thyroid function. The urinary levels of phthalates were significantly higher in the pubertal gynecomastia group, in serum in girls with premature thelarche and in girls with precocious puberty. Epidemiological studies, in spite of their limitations, suggest that phthalates may affect reproductive outcome and children health. Considering the suggested health effects, more epidemiologic data is urgently needed and, in the meantime, precautionary policies must be implemented.	[Jurewicz, Joanna; Hanke, Wojciech] Nofer Inst Occupat Med, Dept Environm Epidemiol, PL-91348 Lodz, Poland	Jurewicz, J (reprint author), Nofer Inst Occupat Med, Dept Environm Epidemiol, Sw Teresy 8, PL-91348 Lodz, Poland.	joannaj@imp.lodz.pl	Jurewicz, Joanna/F-7598-2010; Hanke, Wojciech/F-7604-2010	Hanke, Wojciech/0000-0001-7162-2569	Norwegian Financial Mechanism within the Polish-Norwegian Research Fund, Norway [PNRF-218-AI-1/07]	This study was performed under the project "Prenatal and postnatal exposure to tobacco smoke, PAHs and heavy metals and the risk of respiratory diseases, allergy and poor mental and physical development" supported by the grant PNRF-218-AI-1/07 from Norway through the Norwegian Financial Mechanism within the Polish-Norwegian Research Fund.	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Health		2011	24	2					115	141		10.2478/s13382-011-0022-2		27	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	808LN	WOS:000293979300001	21594692	
J	Lopata, AL; O'Hehir, RE; Lehrer, SB				Lopata, A. L.; O'Hehir, R. E.; Lehrer, S. B.			Shellfish allergy	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review							HOUSE-DUST-MITE; MAJOR SHRIMP ALLERGEN; INVERTEBRATE PAN-ALLERGEN; CROSS-REACTIVE ALLERGEN; CALCIUM-BINDING PROTEIN; FISH PROCESSING WORKERS; PEN A-1 TROPOMYOSIN; SEAFOOD ALLERGY; FOOD ALLERGY; ANISAKIS-SIMPLEX	Seafood plays an important role in human nutrition and health. The growing international trade in seafood species and products has added to the popularity and frequency of consumption of a variety of seafood products across many countries. This increased production and consumption of seafood has been accompanied by more frequent reports of adverse health problems among consumers as well as processors of seafood. Adverse reactions to seafood are often generated by contaminants but can also be mediated by the immune system and cause allergies. These reactions can result from exposure to the seafood itself or various non-seafood components in the product. Non-immunological reactions to seafood can be triggered by contaminants such as parasites, bacteria, viruses, marine toxins and biogenic amines. Ingredients added during processing and canning of seafood can also cause adverse reactions. Importantly all these substances are able to trigger symptoms which are similar to true allergic reactions, which are mediated by antibodies produced by the immune system against specific allergens. Allergic reactions to 'shellfish', which comprises the groups of crustaceans and molluscs, can generate clinical symptoms ranging from mild urticaria and oral allergy syndrome to life-threatening anaphylactic reactions. The prevalence of crustacean allergy seems to vary largely between geographical locations, most probably as a result of the availability of seafood. The major shellfish allergen is tropomyosin, although other allergens may play an important part in allergenicity such as arginine kinase and myosin light chain. Current observations regard tropomyosin to be the major allergen responsible for molecular and clinical cross-reactivity between crustaceans and molluscs, but also to other inhaled invertebrates such as house dust mites and insects. Future research on the molecular structure of tropomyosins with a focus on the immunological and particularly clinical cross-reactivity will improve diagnosis and management of this potentially life-threatening allergy and is essential for future immunotherapy.	[Lopata, A. L.] RMIT Univ, Allergy Res Grp, Melbourne, Vic 3083, Australia; [O'Hehir, R. E.] Alfred Hosp, Dept Allergy Immunol & Resp Med, Melbourne, Vic, Australia; [O'Hehir, R. E.] Monash Univ, Melbourne, Vic 3004, Australia; [Lehrer, S. B.] Tulane Univ, Dept Med, Sect Allergy Rheumatol & Clin Immunol, New Orleans, LA 70118 USA	Lopata, AL (reprint author), RMIT Univ, Allergy Res Grp, Bundoora W Campus, Melbourne, Vic 3083, Australia.	andreas.lopata@rmit.edu.au	Lopata, Andreas/C-3831-2012; O'Hehir, Robyn/H-3627-2011; Osborne, Nicholas/N-4915-2015	Lopata, Andreas/0000-0002-2940-9235; O'Hehir, Robyn/0000-0002-3489-7595; Osborne, Nicholas/0000-0002-6700-2284			Aalberse RC, 2001, ALLERGY, V56, P478, DOI 10.1034/j.1398-9995.2001.056006478.x; Arlian LG, 2003, ALLERGY, V58, P1299, DOI 10.1046/j.1398-9995.2003.00344.x; Asero R, 2005, INT ARCH ALLERGY IMM, V137, P62, DOI 10.1159/000085105; Asturias JA, 2000, MOL BIOCHEM PARASIT, V108, P263, DOI 10.1016/S0166-6851(00)00218-8; Audicana MT, 2008, CLIN MICROBIOL REV, V21, P360, DOI 10.1128/CMR.00012-07; Auerswald L, 2006, FOOD CHEM, V98, P231, DOI 10.1016/j.foodchem.2005.05.071; *AUSTR BUR AGR RES, 2006, AUSTR FISH STAT 2006; Ayuso R, 2002, INT ARCH ALLERGY IMM, V127, P27, DOI 10.1159/000048166; Ayuso R, 2002, INT ARCH ALLERGY IMM, V129, P38, DOI 10.1159/000065172; Ayuso R, 2002, J ALLERGY CLIN IMMUN, V109, pS94, DOI 10.1016/S0091-6749(02)81383-5; Ayuso R, 2008, J ALLERGY CLIN IMMUN, V122, P795, DOI 10.1016/j.jaci.2008.07.023; Ayuso R, 2009, J ALLERGY CLIN IMMUN, V124, P114, DOI 10.1016/j.jaci.2009.04.016; BANZET ML, 1992, REV FR ALLERGOL, V32, P198, DOI 10.1016/S0335-7457(05)80359-4; Barraclough RM, 2006, OCCUP MED-OXFORD, V56, P63, DOI 10.1093/occmed/kqi175; BERNSTEIN M, 1982, J ALLERGY CLIN IMMUN, V70, P205, DOI 10.1016/0091-6749(82)90043-4; Binder M, 2001, J IMMUNOL, V167, P5470; Blotzer IC, 2004, ALLERGOLOGIE, V27, P191; Chiang WC, 2007, CLIN EXP ALLERGY, V37, P1055, DOI 10.1111/j.1365-2222.2007.02752.x; CRESPO JF, 1995, PEDIATR ALLERGY IMMU, V6, P39, DOI 10.1111/j.1399-3038.1995.tb00256.x; CRESPO JF, 1995, ALLERGY, V50, P918, DOI 10.1111/j.1398-9995.1995.tb02499.x; DAUL CB, 1994, INT ARCH ALLERGY IMM, V105, P49; DAUL CB, 1988, J ALLERGY CLIN IMMUN, V81, P1180, DOI 10.1016/0091-6749(88)90888-3; DESJARDINS A, 1995, J ALLERGY CLIN IMMUN, V96, P608, DOI 10.1016/S0091-6749(95)70259-8; DOHI M, 1991, J ALLERGY CLIN IMMUN, V87, P34, DOI 10.1016/0091-6749(91)90210-F; Fernandes J, 2003, CLIN EXP ALLERGY, V33, P956, DOI 10.1046/j.1365-2222.2003.01722.x; Garcia-Orozco KD, 2007, INT ARCH ALLERGY IMM, V144, P23, DOI 10.1159/000102610; Gill BV, 2009, J ALLERGY CLIN IMMUN, V124, P1055, DOI 10.1016/j.jaci.2009.06.030; Goetz DW, 2000, ANN ALLERG ASTHMA IM, V85, P461; Goh DLM, 1999, ALLERGY, V54, P84, DOI 10.1034/j.1398-9995.1999.00925.x; Guarneri F, 2007, INT J DERMATOL, V46, P146; HEFLE SL, 1995, J ALLERGY CLIN IMMUN, V95, P332; Hill DJ, 1999, ANN MED, V31, P272, DOI 10.3109/07853899908995890; Hill DJ, 1997, ENVIRON TOXICOL PHAR, V4, P101, DOI 10.1016/S1382-6689(97)10049-7; HOFFMAN DR, 1981, ANN ALLERGY, V47, P17; Howse D, 2006, ENVIRON RES, V101, P163, DOI 10.1016/j.envres.2005.06.008; Ishikawa M, 1998, FISHERIES SCI, V64, P854; Jeebhay MF, 2007, INT ARCH ALLERGY IMM, V144, P143, DOI 10.1159/000103226; Jeebhay MF, 2005, ANN OCCUP HYG, V49, P423, DOI [10.1093/annhyg/meh113, 10.1093/annhyg/mch113]; Jeebhay MF, 2001, OCCUP ENVIRON MED, V58, P553, DOI 10.1136/oem.58.9.553; Jeebhay MF, 2008, AM J IND MED, V51, P899, DOI 10.1002/ajim.20635; Jenkins JA, 2007, J ALLERGY CLIN IMMUN, V120, P1399, DOI 10.1016/j.jaci.2007.08.019; Jeong KY, 2006, PROTEIN PEPTIDE LETT, V13, P835; Johansson E, 2001, ALLERGY, V56, P660, DOI 10.1034/j.1398-9995.2001.00798.x; LEHRER SB, 1987, J ALLERGY CLIN IMMUN, V80, P133, DOI 10.1016/0091-6749(87)90121-7; Lehrer SB, 2003, MAR BIOTECHNOL, V5, P339, DOI 10.1007/s10126-002-0082-1; LEHRER SB, 1988, J ALLERGY CLIN IMMUN, V81, P189, DOI 10.1016/0091-6749(88)90319-3; LEHRER SB, 1987, SOUTHERN MED J, V80, P2; Lehrer SB, 1998, REV FR ALLERGOL, V38, P846, DOI 10.1016/S0335-7457(98)80154-8; Leung PSC, 1996, J ALLERGY CLIN IMMUN, V98, P954, DOI 10.1016/S0091-6749(96)80012-1; LEUNG PSC, 1994, J ALLERGY CLIN IMMUN, V94, P882, DOI 10.1016/0091-6749(94)90156-2; Lopata AL, 1997, J ALLERGY CLIN IMMUN, V100, P642, DOI 10.1016/S0091-6749(97)70168-4; Lopata AL, 2005, ALLERGY, V60, P200, DOI 10.1111/j.1398-9995.2005.00661.x; Lopata A. 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J	Nagel, G; Weinmayr, G; Kleiner, A; Garcia-Marcos, L; Strachan, DP				Nagel, Gabriele; Weinmayr, Gudrun; Kleiner, Andrea; Garcia-Marcos, Luis; Strachan, David P.		ISAAC Phase Two Study Grp	Effect of diet on asthma and allergic sensitisation in the International Study on Allergies and Asthma in Childhood (ISAAC) Phase Two	THORAX			English	Article							MEDITERRANEAN DIET; FATTY-ACIDS; VITAMIN-C; ANTIOXIDANT VITAMIN; SYMPTOM PREVALENCE; PULMONARY-FUNCTION; SCHOOL-CHILDREN; LUNG-FUNCTION; SERUM LEVELS; RISK-FACTOR	Background The increasing prevalence of asthma and allergy might be related to diet, particularly in Western countries. A study was undertaken to assess the association between dietary factors, asthma and allergy in a large international study including objective measurements of atopy. Methods Between 1995 and 2005, cross-sectional studies were performed in 29 centres in 20 countries. Parental questionnaires were used to collect information on allergic diseases and exposure factors and data from 50 004 randomly selected schoolchildren (8-12 years, 29 579 with skin prick testing) were analysed. Random effect models for meta-analysis were applied to calculate combined ORs. Results Fruit intake was associated with a low prevalence of current wheeze in affluent (OR(adj) 0.86, 95% CI 0.73 to 1.02) and non-affluent countries (OR(adj) 0.71, 95% CI 0.57 to 0.88). Consumption of fish in affluent countries (OR(adj) 0.85, 95% CI 0.74 to 0.97) and of cooked green vegetables in non-affluent countries (OR(adj) 0.78, 95% CI 0.65 to 0.95) was associated with a lower prevalence of current wheeze. Overall, more frequent consumption of fruit, vegetables and fish was associated with a lower lifetime prevalence of asthma, whereas high burger consumption was associated with higher lifetime asthma prevalence. None of the food items was associated with allergic sensitisation. Except for fruit juice and fruit consumption, no associations were found with atopic wheeze. Food selection according to the 'Mediterranean diet' was associated with a lower prevalence of current wheeze and asthma ever (p(trend)=0.03). Conclusion Diet is associated with wheeze and asthma but not with allergic sensitisation in children. These results provide further evidence that adherence to the 'Mediterranean diet' may provide some protection against wheeze and asthma in childhood.	[Nagel, Gabriele; Weinmayr, Gudrun; Kleiner, Andrea] Univ Ulm, Inst Epidemiol, D-89081 Ulm, Germany; [Garcia-Marcos, Luis] Univ Murcia, Arrixaca Univ Childrens Hosp, Pediat Resp Units, Murcia, Spain; [Garcia-Marcos, Luis] Univ Murcia, Arrixaca Univ Childrens Hosp, Allergy Unit, Murcia, Spain; [Garcia-Marcos, Luis] CIBER Epidemiol & Publ Hlth CIBERSP, Murcia, Spain; [Strachan, David P.] Univ London, St Georges Hosp, Div Community Hlth Sci, London, England	Nagel, G (reprint author), Univ Ulm, Inst Epidemiol, Helmholtzstr 22, D-89081 Ulm, Germany.	gabriele.nagel@uni-ulm.de	Nagel, Gabriele/C-3635-2012; Hatziagorou, Elpis/D-3247-2012; MARTINEZ-GIMENO, ANTONIO/A-9416-2010; Ellwood, Philippa/G-7555-2015; De sario, Manuela/K-1932-2016; Forastiere, Francesco/J-9067-2016; Jones, Marcus/A-3580-2011	Nagel, Gabriele/0000-0001-6185-8535; MARTINEZ-GIMENO, ANTONIO/0000-0003-4051-1860; Ellwood, Philippa/0000-0002-1994-4023; De sario, Manuela/0000-0002-1117-2735; Forastiere, Francesco/0000-0002-9162-5684; Jones, Marcus/0000-0002-8263-1265; Pearce, Neil/0000-0002-9938-7852; brunekreef, bert/0000-0001-9908-0060; Beasley, Richard/0000-0003-0337-406X	European Commission [QLK4-CT-1999-01288]	The coordination and central laboratory analyses of the European centres were funded by the Fifth Framework Programme of the European Commission (QLK4-CT-1999-01288). 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S	Valenta, R; Ferreira, F; Focke-Tejkl, M; Linhart, B; Niederberger, V; Swoboda, I; Vrtala, S		Paul, WE; Littman, DR; Yokoyama, WM		Valenta, Rudolf; Ferreira, Fatima; Focke-Tejkl, Margarete; Linhart, Birgit; Niederberger, Verena; Swoboda, Ines; Vrtala, Susanne			From Allergen Genes to Allergy Vaccines	ANNUAL REVIEW OF IMMUNOLOGY, VOL 28	Annual Review of Immunology		English	Review; Book Chapter						allergy; recombinant allergen; specific immunotherapy; IgE; T cell; peptide; diagnosis	BIRCH-POLLEN ALLERGEN; HOUSE-DUST MITE; BET V 1; T-CELL EPITOPE; LATE ASTHMATIC REACTIONS; SHORT RAGWEED ALLERGEN; FC-EPSILON-RI; PHL P 5; OVERLAPPING SYNTHETIC PEPTIDES; RANDOMIZED CONTROLLED-TRIAL	IgE-mediated allergy is a hypersensitivity disease affecting more than 25% of the population. The structures of the most common allergens have been revealed through molecular cloning technology in the past two decades. On the basis of this knowledge of the sequences and three-dimensional structures of culprit allergens, investigators can now analyze the immune recognition of allergens and the mechanisms of allergic inflammation in allergic patients. Allergy vaccines have been constructed that are able to selectively target the aberrant immune responses in allergic patients via different pathways of the immune system. Here we review various types of allergy vaccines that have been developed based on allergen structures, results from their clinical application in allergic patients, and future strategies for allergen-specific immunotherapy and allergy prophylaxis.	[Valenta, Rudolf; Focke-Tejkl, Margarete; Swoboda, Ines] Med Univ Vienna, Christian Doppler Lab Allergy Res, A-1090 Vienna, Austria; [Valenta, Rudolf; Focke-Tejkl, Margarete; Linhart, Birgit; Swoboda, Ines; Vrtala, Susanne] Med Univ Vienna, Ctr Physiol & Pathophysiol, Dept Pathophysiol, Div Immunopathol, A-1090 Vienna, Austria; [Niederberger, Verena] Med Univ Vienna, Dept Otorhinolaryngol, A-1090 Vienna, Austria; [Ferreira, Fatima] Salzburg Univ, Christian Doppler Lab Allergy Diag & Therapy, A-5020 Salzburg, Austria	Valenta, R (reprint author), Med Univ Vienna, Christian Doppler Lab Allergy Res, A-1090 Vienna, Austria.	rudolf.valenta@meduniwien.ac.at	Ferreira, Fatima/E-4889-2011	Ferreira, Fatima/0000-0003-0989-2335	Austrian Science Fund FWF [F 4613]		Aghayan-Ugurluoglu R, 2000, J ALLERGY CLIN IMMUN, V105, P803, DOI 10.1067/mai.2000.104782; Akdis M, 2004, J EXP MED, V199, P1567, DOI 10.1084/jem.20032058; Alderuccio F, 2003, TRENDS IMMUNOL, V24, P176, DOI 10.1016/S1471-4906(03)00066-8; Alexander C, 2005, ALLERGY, V60, P1269, DOI 10.1111/j.1398-9995.2005.00885.x; 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Rev. Immunol.		2010	28						211	241		10.1146/annurev-immunol-030409-101218		31	Immunology	Immunology	BOR04	WOS:000277363600009	20192803	
J	Lopez-Souza, N; Favoreto, S; Wong, H; Ward, T; Yagi, S; Schnurr, D; Finkbeiner, WE; Dolganov, GM; Widdicombe, JH; Boushey, HA; Avila, PC				Lopez-Souza, Nilceia; Favoreto, Silvio; Wong, Hofer; Ward, Theresa; Yagi, Shigeo; Schnurr, David; Finkbeiner, Walter E.; Dolganov, Gregory M.; Widdicombe, Jonathan H.; Boushey, Homer A.; Avila, Pedro C.			In vitro susceptibility to rhinovirus infection is greater for bronchial than for nasal airway epithelial cells in human subjects	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Human rhinovirus; nasal and bronchial airway epithelial cells; air-liquid interface	HUMAN TRACHEAL EPITHELIUM; BIOELECTRIC PROPERTIES; SITU HYBRIDIZATION; CULTURES; ASTHMA; EXACERBATIONS; EXPRESSION; DIFFERENTIATION; REPLICATION; DISEASE	Background: Human rhinoviruses (HRVs) characteristically cause upper respiratory tract infection, but they also infect the lower airways, causing acute bronchitis and exacerbating asthma. Objective: Our purpose was to study ex vivo the differences in the response to HRV infection of nasal and bronchial epithelial cultures from the same healthy and asthmatic individuals using conditions favoring development of fully differentiated, pseudostratified mucociliary epithelium. Methods: Cells from the inferior turbinates and bronchial tree of 5 healthy and 6 asthmatic individuals were cultured at an air-liquid interface. Cultures were infected with HRV-16, and after 48 hours, the degree of infection was measured. Results: Baseline median transepithelial resistance was lower in human bronchial epithelial (HBE) cell cultures than in human nasal epithelial (HNE) cell cultures (195 Omega.cm(2) [95% CI, 164-252] vs 366 Omega.cm(2) [95% CI, 234-408], respectively; P < .01). Virus replicated more easily in HBE cells than in HNE cells based on virus shedding in apical wash (log tissue culture infective dose of 50%/0.1 mL = 2.0 [95% CI, 1.0-2.5] vs 0.5 [95% CI, 0.5-1.5], P < .01) and on a 20- to 30-fold greater viral load and number of infected cells in HBE cell cultures than in FINE cell cultures. The increases in expression of RANTES and double-stranded RNA-dependent protein kinase were greater in HBE cell cultures than in HNE cell cultures, as were the concentrations of IL-8, IL-1 alpha, RANTES, and IP-10 in basolateral medium. However, no significant differences between asthmatic and healthy subjects (including IFN-beta 1 expression) were found. Conclusions: Differentiated nasal epithelial cells might have mechanisms of increased resistance to rhinovirus infection compared with bronchial epithelial cells. We could not confirm previous reports of increased susceptibility to HRV infection in epithelial cells from asthmatic subjects. (J Allergy Clin Immunol 2009;123:1384-90.)	[Favoreto, Silvio; Avila, Pedro C.] Northwestern Univ, Feinberg Sch Med, Dept Med, Chicago, IL 60611 USA; [Lopez-Souza, Nilceia; Wong, Hofer; Ward, Theresa; Boushey, Homer A.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA; [Finkbeiner, Walter E.] Univ Calif San Francisco, Dept Pathol, San Francisco, CA USA; [Boushey, Homer A.] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA; [Yagi, Shigeo; Schnurr, David] Calif Dept Publ Hlth, Viral & Rickettsial Dis Lab, Richmond, CA USA; [Dolganov, Gregory M.] Stanford Med Sch, Div Infect Dis & Geog Med, Stanford, CA USA; [Widdicombe, Jonathan H.] Univ Calif Davis, Dept Physiol & Membrane Biol, Davis, CA 95616 USA	Avila, PC (reprint author), Northwestern Univ, Feinberg Sch Med, Dept Med, 676 N St Clair St,Rm 14-018, Chicago, IL 60611 USA.	pa@northwestern.edu			National Institutes of Health [P01A1050496]; Northwestern University; Cystic Fibrosis Foundation; Cystic Fibrosis Research, Inc; GlaxoSmithKline; Genentech	W. E. Finkbeiner has received research support from the Cystic Fibrosis Foundation and the National Institutes of Health. G. M. Dolganov has provided legal consultation or expert witness testimony on the topic of gene expression assays. J. H. Widdicombe has received research support from Cystic Fibrosis Research, Inc. H. A. Boushey has received research support from GlaxoSmithKline and honoraria from Genentech and Novartis and has served as a member and chair of the Health Effect's Institute's review committee. P.C. Avila has received research support from Genentech. The rest of the authors have declared that they have no conflict of interest.	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Allergy Clin. Immunol.	JUN	2009	123	6					1384	1390		10.1016/j.jaci.2009.03.010		7	Allergy; Immunology	Allergy; Immunology	455WO	WOS:000266799100033	19428098	
J	Burgel, PR; Nadel, JA				Burgel, P-R.; Nadel, J. A.			Epidermal growth factor receptor-mediated innate immune responses and their roles in airway diseases	EUROPEAN RESPIRATORY JOURNAL			English	Review						asthma; chronic obstructive pulmonary disease; cystic fibrosis; interleukin-8; mucins; neutrophils	OBSTRUCTIVE PULMONARY-DISEASE; NECROSIS-FACTOR-ALPHA; MUCIN GENE-EXPRESSION; PROTEIN-COUPLED RECEPTORS; GOBLET CELL HYPERPLASIA; RESPIRATORY EPITHELIAL-CELLS; ACTIVATING-FACTOR RECEPTOR; GRAM-NEGATIVE BACTERIA; C-ERBB RECEPTORS; NF-KAPPA-B	Inhaled air is contaminated with pathogens and particulates that may deposit in the airways and damage the host. In response to these invaders, the airway epithelium has developed innate immune responses that provide a defence against the invaders and protect the airway structure and function. Thus, the epithelium of conducting airways becomes the "battleground" between the invaders and the host. Recent evidence suggests that airway epithelial surface signalling through the epidermal growth factor receptor (EGFR) is a convergent pathway producing innate immune responses to a variety of infectious and noninfectious noxious stimuli. In the present review, the EGFR signalling pathways leading to airway mucin production, neutrophil recruitment (via interleukin-8 production) and airway epithelial repair were examined. The importance of these findings in human airway diseases was also investigated. The current authors suggest that the exaggerated innate immune responses found in chronic inflammatory airway diseases (e.g. chronic obstructive pulmonary disease, cystic fibrosis and severe asthma) contribute to the pathogenesis or the aggravation of these diseases. Potential therapies include inhibition of the various elements of the described epidermal growth factor receptor cascade. In considering each therapeutic intervention, the potential benefits must be considered in relation to potential deleterious effects.	[Nadel, J. A.] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA; [Nadel, J. A.] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA; [Nadel, J. 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J	Van Ree, R; Chapman, MD; Ferreira, F; Vieths, S; Bryan, D; Cromwell, O; Villalba, M; Durham, SR; Becker, WM; Aalbers, M; Andre, C; Barber, D; Bahima, AC; Custovic, A; Didierlaurent, A; Dolman, C; Dorpema, JW; Di Felice, G; Eberhardt, F; Fernandez Caldas, E; Fernandez Rivas, M; Fiebig, H; Focke, M; Fotisch, K; Gadermaier, G; Das, RG; Gonzalez Mancebo, E; Himly, M; Kinaciyan, T; Knulst, AC; Kroon, AM; Lepp, U; Marco, FM; Mari, A; Moingeon, P; Monsalve, R; Neubauer, A; Notten, S; Heer, PO; Pauli, G; Pini, C; Purohit, A; Quiralte, J; Rak, S; Raulf-Heimsoth, M; SanMiguel Moncin, MM; Simpson, B; Tsay, A; Vailes, L; Wallner, M; Weber, B				Van Ree, R.; Chapman, M. D.; Ferreira, F.; Vieths, S.; Bryan, D.; Cromwell, O.; Villalba, M.; Durham, S. R.; Becker, W. M.; Aalbers, M.; Andre, C.; Barber, D.; Bahima, A. Cistero; Custovic, A.; Didierlaurent, A.; Dolman, C.; Dorpema, J. W.; Di Felice, G.; Eberhardt, F.; Fernandez Caldas, E.; Fernandez Rivas, M.; Fiebig, H.; Focke, M.; Foetisch, K.; Gadermaier, G.; Das, R. G.; Gonzalez Mancebo, E.; Himly, M.; Kinaciyan, T.; Knulst, A. C.; Kroon, A. M.; Lepp, U.; Marco, F. M.; Mari, A.; Moingeon, P.; Monsalve, R.; Neubauer, A.; Notten, S.; Heer, P. Ooievaarde; Pauli, G.; Pini, C.; Purohit, A.; Quiralte, J.; Rak, S.; Raulf-Heimsoth, M.; SanMiguel Moncin, M. M.; Simpson, B.; Tsay, A.; Vailes, L.; Wallner, M.; Weber, B.			The CREATE Project: development of certified reference materials for allergenic products and validation of methods for their quantification	ALLERGY			English	Article							1ST INTERNATIONAL STANDARD; SMALL-ANGLE SCATTERING; DUST MITE ALLERGEN; DERMATOPHAGOIDES-PTERONYSSINUS; IMMUNOLOGICAL RESPONSE; RECOMBINANT ALLERGENS; CIRCULAR-DICHROISM; MASS-SPECTROMETRY; INDOOR ALLERGENS; COMPUTER-PROGRAM	Allergen extracts have been used for diagnosis and treatment of allergy for around 100 years. During the second half of 20th century, the notion increasingly gained foothold that accurate standardization of such extracts is of great importance for improvement of their quality. As a consequence, manufacturers have implemented extensive protocols for standardization and quality control. These protocols have overall IgE-binding potencies as their focus. Unfortunately, each company is using their own in-house reference materials and their own unique units to express potencies. This does not facilitate comparison of different products. During the last decades, most major allergens of relevant allergen sources have been identified and it has been established that effective immunotherapy requires certain minimum quantities of these allergens to be present in the administered maintenance dose. Therefore, the idea developed to introduce major allergens measurements into standardization protocols. Such protocols based on mass units of major allergen, quantify the active ingredients of the treatment and will at the same time allow comparison of competitor products. In 2001, an EU funded project, the CREATE project, was started to support introduction of major allergen based standardization. The aim of the project was to evaluate the use of recombinant allergens as reference materials and of ELISA assays for major allergen measurements. This paper gives an overview of the achievements of the CREATE project.	Acad Med Ctr, Amsterdam, Netherlands; [Chapman, M. D.; Tsay, A.; Vailes, L.] Indoor Biotechnol, Charlottesville, VA USA; [Ferreira, F.; Gadermaier, G.; Himly, M.; Wallner, M.] Salzburg Univ, A-5020 Salzburg, Austria; [Vieths, S.; Foetisch, K.] Paul Ehrlich Inst, D-6070 Langen, Germany; [Bryan, D.; Dolman, C.; Das, R. G.] NIBSC, Potters Bar, Herts, England; [Cromwell, O.; Fiebig, H.; Weber, B.] Allergopharma, Reinbek, Germany; [Villalba, M.] Univ Complutense, E-28040 Madrid, Spain; [Durham, S. R.] Univ London Imperial Coll Sci & Technol, London, England; [Becker, W. M.; Lepp, U.] Res Ctr, Borstel, Germany; [Aalbers, M.; Notten, S.; Heer, P. Ooievaarde] Sanquin, Amsterdam, Netherlands; [Andre, C.; Didierlaurent, A.; Moingeon, P.] Stallergenes SA, Antony, France; [Barber, D.; Monsalve, R.] ALK Abello, Madrid, Spain; [Bahima, A. Cistero; SanMiguel Moncin, M. M.] Univ Inst Dexeus, Barcelona, Spain; [Custovic, A.; Simpson, B.] Univ Manchester, Manchester, Lancs, England; [Dorpema, J. W.] HAL Allergy BV, Haarlem, Netherlands; [Di Felice, G.; Pini, C.] Ist Super Sanita, I-00161 Rome, Italy; [Fernandez Caldas, E.] CBF Leti SA, Madrid, Spain; [Fernandez Rivas, M.] Hosp Clin San Carlos, Madrid, Spain; [Focke, M.; Kinaciyan, T.] Med Univ Vienna, Vienna, Austria; [Gonzalez Mancebo, E.] Hosp Ramon & Cajal, E-28034 Madrid, Spain; [Knulst, A. C.] Univ Med Ctr Utrecht, Utrecht, Netherlands; [Kroon, A. M.] European Allergen Manufacturers Grp, Haarlem, Netherlands; [Marco, F. M.] ASAC Pharmaceut Int SA, Alicante, Spain; [Mari, A.] IRCCS, IDI, CACeS, Rome, Italy; [Neubauer, A.] Biomay AG, Vienna, Austria; [Pauli, G.; Purohit, A.] Univ Hosp, Strasbourg, France; [Quiralte, J.] Complejo Hosp Jaen, Jaen, Spain; [Rak, S.] Sahlgrens Univ Hosp, Gothenburg, Sweden; [Raulf-Heimsoth, M.] Ruhr Univ Bochum, BGFA, D-4630 Bochum, Germany	Van Ree, R (reprint author), Acad Med Ctr, Amsterdam, Netherlands.		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J	Hertz-Picciotto, I; Park, HY; Dostal, M; Kocan, A; Trnovec, T; Sram, R				Hertz-Picciotto, Irva; Park, Hye-Youn; Dostal, Miroslav; Kocan, Anton; Trnovec, Tomas; Sram, Radim			Prenatal exposures to persistent and non-persistent organic compounds and effects on immune system development	BASIC & CLINICAL PHARMACOLOGY & TOXICOLOGY			English	Article; Proceedings Paper	International Conference on Foetal Programming and Development Toxicity	MAY 20-24, 2007	Torshavn, DENMARK				ENVIRONMENTAL TOBACCO-SMOKE; INTERFERON-GAMMA PRODUCTION; IN-VITRO EXPOSURE; POLYCHLORINATED-BIPHENYLS; CRITICAL WINDOWS; CORD-BLOOD; CHILDRENS HEALTH; ULTRAFINE PARTICLES; AUTOIMMUNE-DISEASE; CONGENITAL-RUBELLA	Immune system development, particularly in the prenatal period, has far-reaching consequences for health during early childhood, as well as throughout life. Environmental disturbance of the complex balances of Th1 and Th2 response mechanisms can alter that normal development. Dysregulation of this process or an aberrant trajectory or timing of events can result in atopy, asthma, a compromised ability to ward off infection, or other auto-immune disease. A wide range of chemical, physical and biological agents appear to be capable of disrupting immune development. This MiniReview briefly reviews developmental milestones of the immune system in the prenatal period and early life, and then presents examples of environmentally induced alterations in immune markers. The first example involves a birth cohort study linked to an extensive programme of air pollution monitoring; the analysis shows prenatal ambient polycyclic aromatic hydrocarbons (PAH) and fine particle (PM2.5) exposures to be associated with altered lymphocyte immunophenotypic distributions in cord blood and possible changes in cord serum immunoglobulin E levels. The second example is a study of prenatal-polychlorinated biphenyl (PCB) exposures and the foetal development of the thymus, the organ responsible for lymphocyte maturation. Mothers with higher serum concentrations of PCBs gave birth to neonates having smaller indices of thymus size. Finally, this report underscores the tight connection between development of the immune system and that of the central nervous system, and the plausibility that disruption of critical events in immune development may play a role in neurobehavioural disorders.	Univ Calif Davis, Dept Publ Hlth Sci, Davis, CA 95616 USA; [Park, Hye-Youn] Univ Calif Davis, Dept Publ Hlth Sci, Davis, CA 95616 USA; [Dostal, Miroslav; Sram, Radim] Acad Sci Czech Republic, Inst Expt Med, Prague, Czech Republic; [Kocan, Anton; Trnovec, Tomas] Slovak Med Univ, Bratislava, Slovakia	Hertz-Picciotto, I (reprint author), Univ Calif Davis, Dept Publ Hlth Sci, TB 168, Davis, CA 95616 USA.	ihp@ucdavis.edu	Dostal, Miroslav/H-2832-2014; Sram, Radim/H-2455-2014	Sram, Radim/0000-0003-4256-3816	NCI NIH HHS [R01-CA96525]; NIEHS NIH HHS [1P01-ES11269]		ALLEN JR, 1976, TOXICOLOGY, V6, P331, DOI 10.1016/0300-483X(76)90037-8; Ashwood P, 2004, AUTOIMMUN REV, V3, P557, DOI 10.1016/j.autrev.2004.07.036; Ashwood P, 2008, J AUTISM DEV DISORD, V38, P169, DOI 10.1007/s10803-006-0353-1; Becker KG, 2007, MED HYPOTHESES, V69, P731, DOI 10.1016/j.mehy.2007.02.019; BERGMANN RL, 1995, ALLERGY, V50, P65, DOI 10.1111/j.1398-9995.1995.tb02484.x; Betancur C, 2002, MOL PSYCHIATR, V7, P67, DOI 10.1038/sj/mp/4000923; Boulanger LM, 2004, NAT REV NEUROSCI, V5, P521, DOI 10.1038/nrn1428; BRAUNSCHWEIG D, 2007, AUTISM MATERNALLY DE; Brown AS, 2004, ARCH GEN PSYCHIAT, V61, P774, DOI 10.1001/archpsyc.61.8.774; Brown-Connolly NE, 2002, J TELEMED TELECARE, V8, P7, DOI 10.1258/135763302320301812; Bunn TL, 2001, TOXICOL SCI, V64, P57; CHESS S, 1978, J PEDIATR-US, V93, P699, DOI 10.1016/S0022-3476(78)80921-4; CHESS S, 1971, J AUTISM CHILD SCHIZ, V1, P33, DOI 10.1007/BF01537741; Cook Edwin H. 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Pharmacol. Toxicol.	FEB	2008	102	2					146	154		10.1111/j.1742-7843.2007.00190.x		9	Pharmacology & Pharmacy; Toxicology	Pharmacology & Pharmacy; Toxicology	254LU	WOS:000252588900013	18226068	
J	Noakes, PS; Hale, J; Thomas, R; Lane, C; Devadason, SG; Prescott, SL				Noakes, P. S.; Hale, J.; Thomas, R.; Lane, C.; Devadason, S. G.; Prescott, S. L.			Maternal smoking is associated with impaired neonatal toll-like-receptor-mediated immune responses	EUROPEAN RESPIRATORY JOURNAL			English	Article						cord blood; cotinine; cytokines; innate immunity; smoking; toll-like receptors	ENVIRONMENTAL TOBACCO-SMOKE; BRONCHIAL EPITHELIAL-CELLS; RESPIRATORY-INFECTIONS; INHALANT ALLERGEN; DENDRITIC CELLS; EARLY-CHILDHOOD; LIPOPOLYSACCHARIDE; EXPOSURE; EXPRESSION; RESPONSIVENESS	Infants of smokers have much higher rates of respiratory infection, asthma and airway disease. The current study assessed the effects of maternal smoking in pregnancy on neonatal toll-like-receptor (TLR)-mediated immune responses as a possible contributing factor to the elevated rates of respiratory illness. In a prospective birth cohort, the cord blood immune responses of neonates of smoking and nonsmoking mothers were compared. Maternal and cord serum cotinine were measured to confirm the level of cigarette smoke exposure. Neonatal cytokine responses were assessed to optimal doses of TILR2, TLR3, TLR4 and TLR9 ligands. Cotinine levels confirmed maternal reporting of cigarette smoking in pregnancy, with significantly higher cotinine levels in maternal and cord blood compared with the nonsmoking group. Infants of smoking mothers showed significantly attenuated innate TLR-mediated responses compared with infants of nonsmokers. The current findings indicate that in addition to effects on developing airways, maternal smoking also has significant immunological effects in pregnancy, which could contribute to the well recognised, subsequent increased risk of respiratory infections and asthma. These effects appear to be mediated through effects on toll-like receptor-mediated innate response pathways, which also promote regulatory pathways in the inhibition of allergic immune responses in the postnatal period, suggesting that other environmental interactions are highly relevant to the "hygiene hypothesis".	Univ Western Australia, Sch Paediat & Child Hlth Res, Perth, WA 6009, Australia	Prescott, SL (reprint author), Univ Western Australia, Princess Margaret Hosp, Sch Paediat & Child Hlth Res, POB D184, Perth, WA 6001, Australia.	susanp@ichr.uwa.edu.au	Prescott, Susan/H-5665-2014				Blumer N, 2005, CLIN EXP ALLERGY, V35, P397, DOI 10.1111/j.1365-2222.2005.02184.x; Caramalho I, 2003, J EXP MED, V197, P403, DOI 10.1084/jem.20021633; Ceppa F, 2000, J CHROMATOGR B, V746, P115, DOI 10.1016/S0378-4347(00)00306-6; Chan-Yeung M, 2003, RESPIROLOGY, V8, P131, DOI 10.1046/j.1440-1843.2003.00453.x; Devereux G, 2002, CLIN EXP ALLERGY, V32, P43, DOI 10.1046/j.0022-0477.2001.01267.x; DiFranza JR, 2004, PEDIATRICS, V113, P1007; Eisenbarth SC, 2002, J EXP MED, V196, P1645, DOI 10.1084/jem.20021340; Holt PG, 1999, ALLERGY, V54, P12, DOI 10.1111/j.1398-9995.1999.tb04382.x; Jedrychowski W, 1997, ENVIRON HEALTH PERSP, V105, P302, DOI 10.1289/ehp.97105302; Kim E, 2005, IMMUNOL LETT, V99, P24, DOI 10.1016/j.imlet.2004.11.025; Kim I, 2005, J CHROMATOGR B, V814, P233, DOI 10.1016/j.jchromb.2004.10.034; Laan M, 2004, J IMMUNOL, V173, P4164; Macaubas C, 1999, CLIN EXP ALLERGY, V29, P1223; MAGNUSSON CGM, 1986, J ALLERGY CLIN IMMUN, V78, P898, DOI 10.1016/0091-6749(86)90237-X; Martinez F D, 1999, Lancet, V354 Suppl 2, pSII12, DOI 10.1016/S0140-6736(99)90437-3; MARTINEZ FD, 1988, AM REV RESPIR DIS, V138, P518; Monteil MA, 2004, REV PANAM SALUD PUBL, V16, P193, DOI 10.1590/S1020-49892004000900006; Nafstad P, 2005, PEDIATRICS, V116, pE255, DOI 10.1542/peds.2004-2785; Nareika A, 2005, AM J PHYSIOL-ENDOC M, V289, pE534, DOI 10.1152/ajpendo.00462.2004; Noakes PS, 2003, ALLERGY, V58, P1053, DOI 10.1034/j.1398-9995.2003.00290.x; Nouri-Shirazi M, 2003, IMMUNOLOGY, V109, P365, DOI 10.1046/j.1365-2567.2003.01655.x; Pasare C, 2003, CURR OPIN IMMUNOL, V15, P677, DOI 10.1016/j.coi.2003.09.002; Pasare C, 2003, SCIENCE, V299, P1033, DOI 10.1126/science.1078231; Prescott SL, 2005, CLIN EXP ALLERGY, V35, P358, DOI 10.1111/j.1365-2222.2005.02187.x; Prescott SL, 2003, CLIN EXP ALLERGY, V33, P566, DOI 10.1046/j.1365-2222.2003.01659.x; Prescott SL, 1998, J IMMUNOL, V160, P4730; Sousa CRE, 1999, CURR OPIN IMMUNOL, V11, P392; Tulic MK, 2000, AM J RESP CELL MOL, V22, P604; UPHAM JW, 1995, CLIN EXP ALLERGY, V25, P634, DOI 10.1111/j.1365-2222.1995.tb01111.x; Upham JW, 2004, J ALLERGY CLIN IMMUN, V114, P1202, DOI 10.1016/j.jaci.2004.06.051; Upham JW, 2002, INFECT IMMUN, V70, P6583, DOI 10.1128/IAI.70.12.6583-6588.2002; Valacchi G, 2005, ANTIOXID REDOX SIGN, V7, P25, DOI 10.1089/ars.2005.7.25; WEISS ST, 1985, AM REV RESPIR DIS, V131, P573; Wills-Karp M, 2001, NAT REV IMMUNOL, V1, P69, DOI 10.1038/35095579; Zhou LM, 2003, AM J RESP CELL MOL, V28, P762, DOI 10.1165/rcmb.2002-0261OC	35	103	105	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.	OCT	2006	28	4					721	729		10.1183/09031936.06.00050206		9	Respiratory System	Respiratory System	095YU	WOS:000241345000010	16870663	
J	Alexis, NE; Lay, JC; Zeman, K; Bennett, WE; Peden, DB; Soukup, JM; Devlin, RB; Becker, S				Alexis, NE; Lay, JC; Zeman, K; Bennett, WE; Peden, DB; Soukup, JM; Devlin, RB; Becker, S			Biological material on inhaled coarse fraction particulate matter activates airway phagocytes in vivo in healthy volunteers	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						PM(2.5-1)0; airway macrophages; TNF-alpha; mCD14; eotaxin	ALVEOLAR MACROPHAGE RESPONSES; DIESEL EXHAUST PARTICLES; POLLUTION PARTICLES; INSOLUBLE COMPONENTS; ATOPIC ASTHMATICS; ENDOTOXIN; EXPOSURE; INFLAMMATION; DEPOSITION; ULTRAFINE	Background: In vitro, endotoxin on coarse fraction particulate matter (PM2.5-10) accounts for the majority of the ability of PM2.5-10 to induce cytokine responses from alveolar macrophages. Objective: We examined in vivo whether inhaled PM2.5-10 from local ambient air induce inflammatory and immune responses in the airways of healthy human beings and whether biologic material on PM2.5-10 accounts for these effects. Methods: On 3 separate visits, 9 healthy subjects inhaled nebulized saline (0.9%, control), PM2.5-10 collected from local ambient air that was heated to inactivate biological material (PM2.5-10-), or nonheated PM (PM2.5-10+)- PM2.5-10 deposition (similar to 0.65 mg/subject) targeted the bronchial airways (confirmed by using radiolabeled aerosol), and induced sputum was obtained 2 to 3 hours postinhalation for analysis of cellular and biochemical markers of inflammation and innate immune function. Results: Inhaled PM2.5-10+ induced elevated inflammation (% PMNs, macrophage mRNA TNF-alpha), increased eotaxin, upregulated immune surface phenotypes on macrophages (mCD14, CD11b, HLA-DR), and increased phagocytosis (monocytes) versus saline (P < .05). Biological inactivation of PM2.5-10 (PM2.5-10-) had no effect on neutrophilia but significantly (P < .05) attenuated mRNA TNF-alpha, eotaxin levels, cell surface marker responses, and phagocytosis. Conclusion: Biological components of PM2.5-10 are not necessary to induce neutrophil responses but are essential in mediating macrophage responses. The ability Of PM2.5-10 to activate monocytic cells and potentially skew the airways toward an allergic phenotype by enhancing eotaxin levels may enhance responses to allergens or bacteria in individuals with allergy. Clinical implications: PM2.5-10 might enhance the response of individuals with allergy to airborne bacteria.	Univ N Carolina, Ctr Environm Med Asthma & Lung Biol, Chapel Hill, NC 27599 USA	Alexis, NE (reprint author), Univ N Carolina, Ctr Environm Med Asthma & Lung Biol, Chapel Hill, NC 27599 USA.	Neil_Alexis@med.unc.edu	Lay, John/A-6380-2012		NHLBI NIH HHS [R01 HL066559, R01 HL 66559, R01 HL062624, R01 HL062624-06, R01 HL066559-04, R01HL-62624]		Albert I, 2005, INT J FOOD MICROBIOL, V100, P197, DOI 10.1016/j.ijfoodmicro.2004.10.016; Alexis N, 2000, CLIN IMMUNOL, V97, P21, DOI 10.1006/clim.2000.4911; Alexis N, 2002, CLIN IMMUNOL, V104, P217, DOI 10.1006/clim.2002.5236; Alexis NE, 2004, J ALLERGY CLIN IMMUN, V114, P1325, DOI 10.1016/j.jaci.2004.09.002; Alexis NE, 2001, AM J RESP CRIT CARE, V164, P1964; Becker S, 2005, ENVIRON HEALTH PERSP, V113, P1032, DOI 10.1289/ehp.7996; Becker S, 2003, J TOXICOL ENV HEAL A, V66, P847, DOI 10.1080/15287390390156227; Becker S, 2003, EXP LUNG RES, V29, P29, DOI 10.1080/01902140390116535; Becker S, 2002, AM J RESP CELL MOL, V27, P611, DOI 10.1165/rcmb.4868; Becker Susanne, 2005, Toxicol Appl Pharmacol, V207, P269, DOI 10.1016/j.taap.2005.01.023; Bennett WD, 2002, J AEROSOL MED, V15, P179, DOI 10.1089/089426802320282301; Boehlecke B, 2003, J ALLERGY CLIN IMMUN, V112, P1241, DOI 10.1016/j.jaci.2003.08.052; BOVALLIUS A, 1978, APPL ENVIRON MICROB, V35, P1231; Conroy DM, 1997, MEM I OSWALDO CRUZ, V92, P183, DOI 10.1590/S0074-02761997000800024; 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; Diaz-Sanchez D, 1999, J ALLERGY CLIN IMMUN, V104, P1183; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; Eldridge MW, 2000, J TOXICOL ENV HEAL A, V61, P27, DOI 10.1080/00984100050116762; HEYDER J, 1986, J AEROSOL SCI, V17, P811, DOI 10.1016/0021-8502(86)90035-2; Ichinose T, 1998, TOXICOL SCI, V44, P70, DOI 10.1093/toxsci/44.1.70; ILOWITE JS, 1989, ARCH ENVIRON HEALTH, V44, P267; Imrich A, 2000, TOXICOL APPL PHARM, V167, P140, DOI 10.1006/taap.2000.9002; Kim CS, 1996, J APPL PHYSIOL, V81, P2203; Kitchens RL, 2000, CHEM IMMUNOL, V74, P61; Landmann R, 2000, MICROBES INFECT, V2, P295, DOI 10.1016/S1286-4579(00)00298-7; Lovik M, 1997, TOXICOLOGY, V121, P165, DOI 10.1016/S0300-483X(97)00075-9; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; POPE CA, 1995, AM J RESP CRIT CARE, V151, P669; Pope CA, 1998, AIR POLLUTION HLTH, P673; Roos-Engstrand E, 2005, EUR RESPIR J, V25, P797, DOI 10.1183/09031936.05.0007804; Schwartz J, 1996, J AIR WASTE MANAGE, V46, P927, DOI 10.1080/10473289.1996.10467528; Soukup JM, 2001, TOXICOL APPL PHARM, V171, P20, DOI 10.1006/taap.2000.9096	32	103	105	1	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.	JUN	2006	117	6					1396	1403		10.1016/j.jaci.2006.02.030		8	Allergy; Immunology	Allergy; Immunology	053UX	WOS:000238332300029	16751003	
J	Eggleston, PA; Butz, A; Rand, C; Curtin-Brosnan, J; Kanchanaraksa, S; Swartz, L; Breysse, P; Buckley, T; Diette, G; Merriman, B; Krishnan, JA				Eggleston, PA; Butz, A; Rand, C; Curtin-Brosnan, J; Kanchanaraksa, S; Swartz, L; Breysse, P; Buckley, T; Diette, G; Merriman, B; Krishnan, JA			Home environmental intervention in inner-city asthma: a randomized controlled clinical trial	ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY			English	Article							COCKROACH ALLERGEN; AIR-POLLUTION; CHILDREN; EXPOSURE; PARTICLES; MORBIDITY; ABATEMENT; SMOKING; FILTER	Background: Airborne pollutants and indoor allergens increase asthma morbidity in inner-city children; therefore, reducing exposure, if feasible, should improve asthma morbidity. Objective: To conduct a randomized controlled trial of methods to reduce environmental pollutant and allergen exposure in the homes of asthmatic children living in the inner city. Methods: After the completion of questionnaires, spirometry and allergen skin tests, home inspection, and measurement of home air pollutant and allergen levels, 100 asthmatic children aged 6 to 12 years were randomized to the treatment group (home-based education, cockroach and rodent extermination, mattress and pillow encasings, and high-efficiency particulate air cleaner) or to the control group (treated at the end of the I-year trial). Outcomes were evaluated by home evaluations at 6 and 12 months, clinic evaluation at 12 months, and multiple telephone interviews. Results: In the treatment group, 84% received cockroach extermination and 75% used the air cleaner. Levels of particulate matter 10 Am or smaller declined by LIP to 39% in the treatment group but increased in the control group (P < .001). Cockroach allergen levels decreased by 51% in the treatment group. Daytime symptoms increased in the control group and decreased in the treatment group (P = .04). Other measures of morbidity, such as spirometry findings, nighttime symptoms, and emergency department use, were not significantly changed. Conclusions: A tailored, multifaceted environmental treatment reduced airborne particulate matter and indoor allergen levels in inner-city homes, which, in turn, had a modest effect on morbidity.	Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21218 USA; Johns Hopkins Univ, Sch Med, Dept Internal Med, Baltimore, MD 21218 USA; Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD 21218 USA; Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21218 USA	Eggleston, PA (reprint author), Johns Hopkins Univ Hosp, Dept Pediat, 600 N Wolfe St,CMSC 1102, Baltimore, MD 21287 USA.	pegglest@jhmi.edu			NHLBI NIH HHS [HL058942]; NIEHS NIH HHS [ES09606]		Arbes SJ, 2003, J ALLERGY CLIN IMMUN, V112, P339, DOI 10.1067/mai.2003.1597; Breysse PN, 2005, ENVIRON RES, V98, P167, DOI 10.1016/j.envres.2004.07.018; Carter MC, 2001, J ALLERGY CLIN IMMUN, V108, P732, DOI 10.1067/mai.2001.119155; CHAPMAN MD, 1988, J IMMUNOL, V140, P812; *CHILDH ASTHM MAN, 2000, NEW ENGLAND J MED, V0343; Custovic A, 1998, THORAX, V53, P63; DiazSanchez D, 1996, J ALLERGY CLIN IMMUN, V98, P114, DOI 10.1016/S0091-6749(96)70233-6; Evans R, 1999, J PEDIATR-US, V135, P332, DOI 10.1016/S0022-3476(99)70130-7; Francis H, 2003, CLIN EXP ALLERGY, V33, P101, DOI 10.1046/j.1365-2222.2003.01570.x; Gavett SH, 1999, AM J RESP CRIT CARE, V160, P1897; Juniper EF, 1996, QUAL LIFE RES, V5, P35, DOI 10.1007/BF00435967; KOUTRAKIS P, 1993, ANAL CHEM, V65, P209, DOI 10.1021/ac00051a004; LIANG KY, 1986, BIOMETRIKA, V73, P13, DOI 10.1093/biomet/73.1.13; Mitchell H, 1997, PEDIATR PULM, V24, P237; Morgan WJ, 2004, NEW ENGL J MED, V351, P1068, DOI 10.1056/NEJMoa032097; Mortimer KM, 2002, EUR RESPIR J, V19, P699, DOI 10.1183/09031936.02.00247102; OHMAN JL, 1994, J ALLERGY CLIN IMMUN, V94, P810, DOI 10.1016/0091-6749(94)90147-3; PALMES ED, 1976, AM IND HYG ASSOC J, V37, P570, DOI 10.1080/0002889768507522; Peden DB, 1998, J ALLERGY CLIN IMMUN, V102, P32, DOI 10.1016/S0091-6749(98)70052-1; PLATTSMILLS TAE, 1992, J ALLERGY CLIN IMMUN, V89, P1046, DOI 10.1016/0091-6749(92)90228-T; POLLART SM, 1991, J ALLERGY CLIN IMMUN, V87, P505, DOI 10.1016/0091-6749(91)90009-D; Radloff L.S., 1997, APPL PSYCH MEAS, V3, P385; REISMAN RE, 1990, J ALLERGY CLIN IMMUN, V85, P1050, DOI 10.1016/0091-6749(90)90050-E; Romieu I, 1996, AM J RESP CRIT CARE, V154, P300; Rosenstreich DL, 1997, NEW ENGL J MED, V336, P1356, DOI 10.1056/NEJM199705083361904; SCHWARTZ J, 1994, AM J RESP CRIT CARE, V150, P1234; Strachan DP, 1998, THORAX, V53, P204; Swartz LJ, 2004, ENVIRON RES, V95, P156, DOI 10.1016/j.envres.2003.08.003; *US DEP HHS, 2003, US HHS POV GUID; *US EPA, 1997, FED REGISTER, V62, P130; VANDERHEIDE S, 1997, J ALLERGY CLIN IMMNO, V132, P1217; Wallace L, 1996, J AIR WASTE MANAGE, V46, P98; Wallace LA, 2003, ENVIRON HEALTH PERSP, V111, P1265, DOI 10.1289/ehp.6135; Wood RA, 2001, ANN ALLERG ASTHMA IM, V87, P60; Wood RA, 1998, AM J RESP CRIT CARE, V158, P115	35	103	106	1	17	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.	DEC	2005	95	6					518	524				7	Allergy; Immunology	Allergy; Immunology	996KV	WOS:000234173700007	16400889	
J	Medina-Ramon, M; Zock, JP; Kogevinas, M; Sunyer, J; Torralba, Y; Borrell, A; Burgos, F; Anto, JM				Medina-Ramon, M; Zock, JP; Kogevinas, M; Sunyer, J; Torralba, Y; Borrell, A; Burgos, F; Anto, JM			Asthma, chronic bronchitis, and exposure to irritant agents in occupational domestic cleaning: a nested case-control study	OCCUPATIONAL AND ENVIRONMENTAL MEDICINE			English	Article							RESPIRATORY-HEALTH-SURVEY; AIRWAYS DYSFUNCTION SYNDROME; WORK-RELATED ASTHMA; PERSISTENT ASTHMA; SYMPTOMS; PRODUCTS; GAS; RESPONSIVENESS; EXPERIENCE; DISEASE	Background: Women employed in domestic cleaning are at increased risk for symptoms of obstructive lung disease, but the agents responsible are unknown. Aims: To investigate common tasks and products in occupational domestic cleaning in relation to respiratory morbidity. Methods: Case-control study in domestic cleaning women nested within a large population based survey of women aged 30-65 years; 160 domestic cleaning women with asthma symptoms, chronic bronchitis symptoms, or both and 386 without a history of respiratory symptoms were identified. Detailed exposures were evaluated for 40 cases who reported still having symptoms at the recruitment interview, and 155 controls who reported not having symptoms. All tasks performed and products used when cleaning houses were determined in a face-to-face interview. Lung function, methacholine challenge, and serum IgE testing were performed. Personal exposure measurements of airborne chlorine and ammonia were performed in a subsample. Associations between asthma, chronic bronchitis, and cleaning exposures were evaluated using multiple logistic regression analysis. Results: Airborne chlorine (median level 0-0.4 ppm) and ammonia (0.6-6.4 ppm) were detectable during occupational domestic cleaning activities. Cases used bleach more frequently than controls; adjusted odds ratio (OR) for intermediate exposure was 3.3 (95% CI 0.9 to 11) and for high exposure 4.9 (1.5 to 15). Other independent associations included accidental inhalation of vapours and gases from cleaning agents and washing dishes. These associations were more pronounced for cases with asthma symptoms than for those with symptoms of chronic bronchitis, but were not related to sensitisation to common allergens. Conclusions: Asthma symptoms in domestic cleaning women are associated with exposure to bleach and possibly other irritant agents. The public health impact of the use of irritant cleaning products could be widespread since the use of these products is common both in the workplace and at home.	Inst Municipal Invest Med, Resp & Environm Hlth Res Unit, E-08003 Barcelona, Spain; Univ Barcelona, Hosp Clin, Dept Med, Serv Pneumol & Allergia Resp, Barcelona, Spain	Anto, JM (reprint author), Inst Municipal Invest Med, Resp & Environm Hlth Res Unit, Dr Aiguader 80, E-08003 Barcelona, Spain.	jmanto@imim.es	Burgos, Felip/E-5734-2015; Kogevinas, Manolis/C-3918-2017; Anto, J/H-2676-2014; Sunyer, J/G-6909-2014	Burgos, Felip/0000-0002-4938-4581; Anto, J/0000-0002-4736-8529; Sunyer, J/0000-0002-2602-4110			Alberts WM, 1996, CHEST, V109, P1618, DOI 10.1378/chest.109.6.1618; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Arif AA, 2003, AM J IND MED, V44, P368, DOI 10.1002/ajim.10291; Balmes JR, 2002, CLIN CHEST MED, V23, P727, DOI 10.1016/S0272-5231(02)00031-X; Becklake M, 1999, ASTHMA WORKPLACE, P27; Brooks SM, 1998, CHEST, V113, P42, DOI 10.1378/chest.113.1.42; BROOKS SM, 1985, CHEST, V88, P376, DOI 10.1378/chest.88.3.376; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; CHANYEUNG M, 1994, AM J RESP CRIT CARE, V149, P1676; Chinn S, 2004, THORAX, V59, P646, DOI 10.1136/thx.2004.021642; Chinn S, 1997, EUR RESPIR J, V10, P2495, DOI 10.1183/09031936.97.10112495; [Anonymous], 1997, THORAX S5, V52, pS1; DAS R, 1993, TOXICOL IND HEALTH, V9, P439; GAULTRIN D, 1999, ASTHMA WORKPLACE, P565; HATTIS RP, 1991, JAMA-J AM MED ASSOC, V266, P2529; Hendrick DJ, 1996, THORAX, V51, P947, DOI 10.1136/thx.51.9.947; Jarvis D, 2002, EUR RESPIR J, V20, P1071, DOI 10.1183/09031936.02.00046802; Karjalainen A, 2001, AM J RESP CRIT CARE, V164, P565; Kennedy SM, 2000, OCCUP ENVIRON MED, V57, P635, DOI 10.1136/oem.57.9.635; KIPEN HM, 1994, J OCCUP ENVIRON MED, V36, P1133, DOI 10.1097/00043764-199410000-00017; Kogevinas M, 1999, LANCET, V353, P1750, DOI 10.1016/S0140-6736(98)07397-8; Kruger D, 1997, RISK ASSESSMENT PREV; Medina-Ramon M, 2003, THORAX, V58, P950, DOI 10.1136/thorax.58.11.950; NG TP, 1994, AM J IND MED, V25, P709, DOI 10.1002/ajim.4700250510; *NIOSH, 2001, NIOSH PUBL; Pascuzzi TA, 1998, MIL MED, V163, P102; Quirce S, 2000, J ASTHMA, V37, P267, DOI 10.3109/02770900009055449; RACIOPPI F, 1994, FOOD CHEM TOXICOL, V32, P845, DOI 10.1016/0278-6915(94)90162-7; REILLY MJ, 1995, ARCH ENVIRON HEALTH, V50, P26; Roca J, 1998, EUR RESPIR J, V11, P1354, DOI 10.1183/09031936.98.11061354; Rosenman KD, 2003, J OCCUP ENVIRON MED, V45, P556, DOI 10.1097/01.jom.0000058347.05741.f9; Strachan DP, 1996, BRIT MED J, V312, P1195; Sunyer J, 1996, AM J RESP CRIT CARE, V153, P1273; Thickett KM, 2002, EUR RESPIR J, V19, P827, DOI 10.1183/09031936.02.00232802; Zock JP, 2002, EUR RESPIR J, V20, P679, DOI 10.1183/09031936.02.00279702; Zock JP, 2001, SCAND J WORK ENV HEA, V27, P76	36	103	105	0	21	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	1351-0711			OCCUP ENVIRON MED	Occup. Environ. Med.	SEP	2005	62	9					598	606		10.1136/oem.2004.017640		9	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	956JO	WOS:000231296200004	16109815	
J	Bornehag, CG; Sundell, J; Hagerhed-Engman, L; Sigsggard, T; Janson, S; Aberg, N				Bornehag, CG; Sundell, J; Hagerhed-Engman, L; Sigsggard, T; Janson, S; Aberg, N		DBH Study Grp	'Dampness' at home and its association with airway, nose, and skin symptoms among 10,851 preschool children in Sweden: a cross-sectional study	INDOOR AIR			English	Article; Proceedings Paper	9th International Conference on Indoor Air Quality and Climate (Indoor Air 2002)	2002	Monterey, CA	Swedish Assoc Asthma & Allergy		dampness; asthma; rhinitis; eczema; children	CHILDHOOD ASTHMA; BRONCHIAL OBSTRUCTION; SUBTROPICAL AREA; YOUNG-CHILDREN; HEALTH; PREVALENCE; BUILDINGS; EXPOSURE; BAMSE	There is convincing epidemiological evidence that 'dampness' in buildings is associated with respiratory effects. In order to identify health-relevant exposures in buildings with 'dampness', the study 'Dampness in Buildings and Health' (DBH) was initiated. In the first step of the study, cross-sectional data on home characteristics including 'dampness' problems, and symptoms in airway, nose, and skin among 10,851 children (1-6 years), were collected by means of a questionnaire to the parents. The prevalence of wheezing during the last 12 months was 18.9% and doctor-diagnosed asthma 5.4%. Rhinitis during the last 12 months was reported for 11.1% of the children and eczema during the last 12 months 18.7%. Gender, allergic symptoms among parents, and age of the child were associated with symptoms. Water leakage was reported in 17.8% of the buildings, condensation on windows in 14.3%, and detached flooring materials in 8.3%. Visible mould or damp spots were reported in only 1.5% of the buildings. The four 'dampness' indices were associated to higher prevalence of symptoms in both crude and adjusted analysis. Furthermore, it was found that the combination of water leakage in the home and PVC as flooring material in the child's or parent's bedroom was associated to higher prevalence of symptoms among children. However, the interpretation of this finding is unclear. The combination of water leakage and PVC may be a proxy, for example, reconstruction because of water damages.	Karlstad Univ, S-65188 Karlstad, Sweden; Swedish Natl & Testing Res Inst, Boras, Sweden; Tech Univ Denmark, Int Ctr Indoor Environm & Energy, DK-2800 Lyngby, Denmark; Aarhus Univ, Inst Environm & Occupat Med, Aarhus, Denmark; Sahlgrenska Univ Hosp, Gothenburg, Sweden	Bornehag, CG (reprint author), Karlstad Univ, S-65188 Karlstad, Sweden.	carl-gustaf.bornehag@kau.se	Sundell, Jan/B-2857-2012				Bjorksten B, 1998, EUR RESPIR J, V12, P432, DOI 10.1183/09031936.98.12020432; Bornehag CG, 2001, INDOOR AIR, V11, P72; Bornehag CG, 2004, INDOOR AIR, V14, P243, DOI 10.1111/j.1600-0668.2004.00240.x; Emenius G, 2004, ACTA PAEDIATR, V93, P899, DOI 10.1080/08035250410025582; Emenius G, 2004, INDOOR AIR, V14, P34, DOI 10.1046/j.1600-0668.2003.00207.x; Haverinen U, 2001, INDOOR AIR, V11, P192, DOI 10.1034/j.1600-0668.2001.011003192.x; Jaakkola JJK, 1999, AM J PUBLIC HEALTH, V89, P188, DOI 10.2105/AJPH.89.2.188; JAAKKOLA JJK, 1993, J EXPO ANAL ENV EPID, V3, P129; Nafstad P, 1998, AM J RESP CRIT CARE, V157, P410; Nicolai T, 1998, THORAX, V53, P1035; PEARCE N, 1993, EUR RESPIR J, V6, P1455; Yang CY, 1998, CHEST, V114, P393, DOI 10.1378/chest.114.2.393; Yang CY, 1998, PEDIATR PULM, V26, P120, DOI 10.1002/(SICI)1099-0496(199808)26:2<120::AID-PPUL8>3.0.CO;2-Q	13	103	114	2	20	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0905-6947			INDOOR AIR	Indoor Air	AUG	2005	15			10			48	55		10.1111/j.1600-0668.2005.00306.x		8	Construction & Building Technology; Engineering, Environmental; Public, Environmental & Occupational Health	Construction & Building Technology; Engineering; Public, Environmental & Occupational Health	930BJ	WOS:000229390500007	15926944	
J	Skoet, R; Olsen, J; Mathiesen, B; Iversen, L; Johansen, JD; Agner, T				Skoet, R; Olsen, J; Mathiesen, B; Iversen, L; Johansen, JD; Agner, T			A survey of occupational hand eczema in Denmark	CONTACT DERMATITIS			English	Article						allergic contact dermatitis; atopic dermatitis; contact urticaria; irritant contact dermatitis; occupational hand eczema; prevention; socio-economic impact	SKIN-DISEASE; CONTACT-DERMATITIS; RISK-FACTORS; ALLERGY; POPULATION; PROGNOSIS; WORKERS; NICKEL; DERMATOSES; PREVALENCE	Occupational hand eczema (OHE) is the most frequently recognized work-related disease in Denmark and the annual cost to society is high. Understanding of the epidemiology of OHE is essential to be able to give appropriate recommendations for its prevention. The study comprised 758 persons, 490 females and 268 males with recognized OHE in the period October 2001 to November 2002. Data were obtained prospectively from the National Board of Industrial Industry Registry and from a self-administered questionnaire (response rate, 82%). The most frequently recognized diagnosis was irritant contact dermatitis (ICD), mainly caused by wet occupations. The proportion of occupational ICD was equal for males and females, 59.7% and 63.1%, respectively. The estimated rates of OHE were high for bakers, hairdressers and dental surgery assistants, and a high proportion of apprentices were found among hairdressers. The prevalence of atopic dermatitis was low (16.4%) compared to previous studies among hand eczema patients. The prevalence of occupational allergic contact dermatitis in the study population was substantially higher among males than females, and the most frequent causes among males were allergy to chromium (leather exposure), rubber additives (gloves) and nickel due to exposure from work tools and metalworking industry.	Univ Copenhagen, Gentofte Hosp, Dept Dermatol, Copenhagen, Denmark; Danish Epidemiol Sci Ctr, Copenhagen, Denmark; Danish Epidemiol Sci Ctr, Aarhus, Denmark; Natl Board Ind Injuries, Copenhagen, Denmark; Ribe Cty, Ribe, Denmark; Univ Copenhagen, Gentofte Hosp, Natl Allergy Res Ctr, Copenhagen, Denmark	Skoet, R (reprint author), Univ Copenhagen, Gentofte Hosp, Dept Dermatol, Niels Andersensvej 65, DK-2900 Hellerup, Denmark.	risk@dadlnet.dk					Adisesh A, 2002, CONTACT DERMATITIS, V46, P273, DOI 10.1034/j.1600-0536.2002.460505.x; Agner T, 2002, CONTACT DERMATITIS, V47, P253, DOI 10.1034/j.1600-0536.2002.470501.x; AVNSTORP C, 1992, ACTA DERM-VENER    S, P179; Bock M, 2003, BRIT J DERMATOL, V149, P1165, DOI 10.1111/j.1365-2133.2003.05748.x; Bryld LE, 2003, BRIT J DERMATOL, V149, P1214, DOI 10.1111/j.1365-2133.2003.05678.x; COENRAADS PJ, 1984, CLIN EXP DERMATOL, V9, P149, DOI 10.1111/j.1365-2230.1984.tb00776.x; *DAN WORK ENV SERV, 1983, 661 DAN WORK ENV SER; Dickel H, 2003, J INVEST DERMATOL, V121, P37, DOI 10.1046/j.1523-1747.2003.12323.x; Dickel H, 2002, CONTACT DERMATITIS, V46, P197, DOI 10.1034/j.1600-0536.2002.460403.x; Dickel H, 2002, INT ARCH OCC ENV HEA, V75, P423, DOI 10.1007/s00420-002-0328-2; Diepgen TL, 1999, INT ARCH OCC ENV HEA, V72, P496, DOI 10.1007/s004200050407; Douglas E, 1999, OCCUP MED-OXFORD, V49, P85, DOI 10.1093/occmed/49.2.85; Halkier-Sorensen L, 1996, Contact Dermatitis, V35, P1; Kalimo K, 1997, CONTACT DERMATITIS, V37, P121, DOI 10.1111/j.1600-0536.1997.tb00316.x; Liden C, 1998, CONTACT DERMATITIS, V39, P127, DOI 10.1111/j.1600-0536.1998.tb05861.x; Liden C., 2001, TXB CONTACT DERMATIT, P933; Meding B, 2000, CONTACT DERMATITIS, V43, P65, DOI 10.1034/j.1600-0536.2000.043002065.x; MEDING B, 1990, CONTACT DERMATITIS, V22, P13, DOI 10.1111/j.1600-0536.1990.tb01499.x; NETHERCOTT JR, 1994, J AM ACAD DERMATOL, V30, P569; Nielsen NH, 2002, CONTACT DERMATITIS, V47, P71, DOI 10.1034/j.1600-0536.2002.470203.x; NIELSEN NH, 1992, ACTA DERM-VENEREOL, V72, P456; Papa G, 2000, INT J IMMUNOPATH PH, V13, P43; ROSEN RH, 1993, CONTACT DERMATITIS, V29, P88, DOI 10.1111/j.1600-0536.1993.tb03489.x; TAYLOR JS, 1988, ARCH DERMATOL, V124, P1557, DOI 10.1001/archderm.124.10.1557; Uter W, 1998, INT ARCH OCC ENV HEA, V71, P487, DOI 10.1007/s004200050310; Uter W, 2003, CONTACT DERMATITIS, V48, P33, DOI 10.1034/j.1600-0536.46.s4.29_102.x; VANDERWALLE HB, 1994, CONTACT DERMATITIS, V30, P265; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P383, DOI 10.1111/j.1365-2133.1994.tb08530.x; Zachariae COC, 1996, CONTACT DERMATITIS, V35, P83, DOI 10.1111/j.1600-0536.1996.tb02295.x; 1995, PRACTICAL GUIDE THEI	30	103	109	2	6	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-1873			CONTACT DERMATITIS	Contact Dermatitis	OCT	2004	51	4					159	166		10.1111/j.0105-1873.2004.00423.x		8	Allergy; Dermatology	Allergy; Dermatology	864PJ	WOS:000224645100001	15500664	
J	Rundell, KW; Anderson, SD; Spiering, BA; Judelson, DA				Rundell, KW; Anderson, SD; Spiering, BA; Judelson, DA			Field exercise vs laboratory eucapnic voluntary hyperventilation to identify airway hyperresponsiveness in elite cold weather athletes	CHEST			English	Article						airway hyperresponsiveness; dry air; exercise; exercise-induced bronchoconstriction; eucapnic volontary hyperpnea	WORKING PARTY STANDARDIZATION; EUROPEAN RESPIRATORY SOCIETY; THERMALLY-INDUCED ASTHMA; REFRACTORY PERIOD; BRONCHIAL RESPONSIVENESS; INDUCED BRONCHOSPASM; OFFICIAL STATEMENT; HYPERTONIC SALINE; CHALLENGE; CHILDREN	Study objective: For the 2002 Winter Olympic Games, athletes were required to submit objective evidence of asthma or exercise-induced bronchoconstriction (EIB) for approval to inhale a beta(2)-agonist. Eucapnic voluntary hyperventilation (EVH) was recommended as a laboratory challenge that would identify airway hyperresponsiveness (AHR) consistent with EIB. The objective was to compare the change in FEV1 provoked by EVH with that provoked by exercise in cold weather athletes. Design: Spirometry was measured before and for 15 min after challenges. The two challenges were performed in random order at least 24 h apart. Setting: EVH was performed in the laboratory at 19degreesC, and exercise took place in the field in the cold (2degreesC, 45% relative humidity). Participants: Thirty-eight athletes (25 female subjects; median age, 16 years). Interventions: For the EVH, athletes inhaled dry air containing 5% carbon dioxide for 6 min at a target ventilation equivalent to 30 times baseline FEV1. Exercise was performed by cross-country skiing, ice skating, or running for 6 to 8 min. Measurements and results: AHR consistent with EIB was defined as greater than or equal to10% fall in FEV1 from baseline after challenge. Eleven athletes were exercise positive (EX+) [FEV1 fall, 20.5 +/- 7.3%], and 17 athletes were EVH positive (FEV1 fall, 14.5 +/- 4.5%) [mean +/- SD]. Of 19 subjects with AHR, 58% were identified by exercise and 89% were identified by EVH. EVH identified 9 of 11 subjects who were EX+ and a further 8 subjects with potential for EIB. The average ventilation during EVH was 28 times FEV1. Conclusion: Performing EVH for 6 min in the laboratory had a greater chance of identifying AHR in these athletes compared with 6 to 8 min of field exercise in the cold. The EVH test will be useful to evaluate elite summer sports athletes whose widely different forms of exercise provide an "equipment" challenge to any laboratory.	Marywood Univ, Human Performance Lab, Scranton, PA 18509 USA; US Olymp Comm, Lake Placid, NY USA; Royal Prince Alfred Hosp, Camperdown, NSW 2050, Australia	Rundell, KW (reprint author), Marywood Univ, Human Performance Lab, 2300 Adams Ave, Scranton, PA 18509 USA.	rundell@marywood.edu		Anderson, Sandra/0000-0002-6308-8770			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, BRIT J SPORT MED, V35, P344, DOI 10.1136/bjsm.35.5.344; Anderson SD, 1997, ALLERGIC RESP DIS SP, P87; Anderson SD, 1999, EXERCISE INDUCED AST, P77; Anderson S, 2003, J ALLERGY CLIN IMMUN, V111, P44; 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; BACKER V, 1991, J ALLERGY CLIN IMMUN, V88, P68, DOI 10.1016/0091-6749(91)90302-5; BARYISHAY E, 1983, AM REV RESPIR DIS, V127, P572; Brannan JD, 1998, AM J RESP CRIT CARE, V158, P1120; Crapo RO, 2000, AM J RESP CRIT CARE, V161, P309; CUSTOVIC A, 1994, CHEST, V105, P1127, DOI 10.1378/chest.105.4.1127; Folgering H, 1997, EUR RESP MON, V6, P51; Godfrey S, 1999, EUR RESPIR J, V14, P659, DOI 10.1034/j.1399-3003.1999.14c28.x; HABY MM, 1995, EUR RESPIR J, V8, P729; Holzer K, 2003, AM J RESP CRIT CARE, V167, P534, DOI 10.1164/rccm.200208-916OC; Holzer K, 2002, J ALLERGY CLIN IMMUN, V110, P374, DOI 10.1067/mai.2002.127784; HURWITZ KM, 1995, CHEST, V108, P1240, DOI 10.1378/chest.108.5.1240; 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; OBYRNE PM, 1982, AM REV RESPIR DIS, V125, P281; QUANJER PH, 1993, EUR RESPIR J, V6, P5; RIEDLER J, 1994, AM J RESP CRIT CARE, V150, P1632; ROSENTHAL RR, 1990, AM REV RESPIR DIS, V141, P368; Rundell KW, 2000, MED SCI SPORT EXER, V32, P309, DOI 10.1097/00005768-200002000-00010; Rundell KW, 2003, MED SCI SPORT EXER, V35, P18, DOI 10.1249/01.MSS.0000043285.21875.E4; Rundell KW, 2001, MED SCI SPORT EXER, V33, P208; SILVERMAN M, 1972, ARCH DIS CHILD, V47, P882; SMITH CM, 1990, EUR RESPIR J, V3, P144; Spiering B. A., 2002, Medicine & Science in Sports & Exercise, V34, pS52, DOI 10.1097/00005768-200205001-00288; STERK PJ, 1993, EUR RESPIR J, V6, P53, DOI 10.1183/09041950.053s1693; Weiler JM, 1998, J ALLERGY CLIN IMMUN, V102, P722, DOI 10.1016/S0091-6749(98)70010-7; Weiler JM, 2000, J ALLERGY CLIN IMMUN, V106, P267, DOI 10.1067/mai.2000.108605; Wilber RL, 2000, MED SCI SPORT EXER, V32, P732, DOI 10.1097/00005768-200004000-00003	36	103	104	0	6	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	MAR	2004	125	3					909	915		10.1378/chest.125.3.909		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	802GS	WOS:000220152600019	15006949	
J	Gelfand, EW				Gelfand, Erwin W.			Inflammatory mediators in allergic rhinitis	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Allergic rhinitis; inflammation; inflammatory mediators; asthma; chronotherapy; chronobiology; unified airway	ANTIGEN CHALLENGE; NASAL SECRETIONS; MAST-CELLS; ASTHMA; EXPOSURE; EXPRESSION; EOSINOPHILS; IMMUNOLOGY; HISTAMINE; AIRWAYS	Allergic rhinitis (AR) is part of a systemic disease complex. There is a close relationship between AR and asthma, which has led to the "one airway, one disease" concept. Both conditions share common immunopathology and pathophysiology. In patients with AR, allergen-triggered early and late responses are mediated by a series of inflammatory cells. Within minutes of contact with allergen, IgE-sensitized mast cells degranulate, releasing both preformed and newly synthesized mediators. Immunologic processes in both nasal and bronchial tissue involve T(H)2 lymphocytes and eosinophils. Eosinophils are the predominant cell in the chronic inflammatory process characteristic of the late-phase allergic response. Eosinophils release an array of proinflammatory mediators, including cysteinyl leukotrienes, cationic proteins, eosinophil peroxidase, and major basic protein, and might serve as a major source of IL-3, IL-5, GM-CSF, and IL-13. Neuropeptides also appear to contribute to the pathophysiology of AR symptoms. Both AR and asthma exhibit marked day-night variation in symptom severity. Acknowledging both the chronobiology of AR and circadian rhythm-dependent attributes of antiallergy medications might enhance the beneficial effects of allergy therapies. (J Allergy Clin Immunol 2004; 114: S135-8.)		Gelfand, EW (reprint author), Care of Sweetman L, Amer Acad Allergy Asthma & Immunol, 611 E Wells St, Milwaukee, WI 53202 USA.						ADAMS PF, 1999, CURRENT ESTIMATES NA, P1; BASCOM R, 1988, AM REV RESPIR DIS, V138, P406; BINDER E, 1982, ALLERGY, V37, P389, DOI 10.1111/j.1398-9995.1982.tb02317.x; BISGAARD H, 1986, CLIN ALLERGY, V16, P289, DOI 10.1111/j.1365-2222.1986.tb01960.x; Bjornsdottir US, 1999, ALLERGY, V54, P55, DOI 10.1111/j.1398-9995.1999.tb04389.x; Bousquet J, 2000, AM J RESP CRIT CARE, V161, P1720; Bousquet J, 2001, J ALLERGY CLIN IMMUN, V108, pS147, DOI 10.1067/mai.2001.118891; Busse WW, 2001, NEW ENGL J MED, V344, P350; Chakir J, 2000, J ALLERGY CLIN IMMUN, V106, P904, DOI 10.1067/mai.2000.110100; CRETICOS PS, 1984, NEW ENGL J MED, V310, P1626, DOI 10.1056/NEJM198406213102502; DURHAM SR, 1992, J IMMUNOL, V148, P2390; Fregonese L, 2002, CLIN EXP ALLERGY, V32, P745, DOI 10.1046/j.1365-2222.2002.01384.x; Gelfaned EW, 2002, AM J MED, V113, p2S; HARLIN SL, 1988, J ALLERGY CLIN IMMUN, V81, P867, DOI 10.1016/0091-6749(88)90944-X; Howarth PH, 1997, ALLERGY, V52, P12; JULIUSSON S, 1992, J ALLERGY CLIN IMMUN, V90, P898, DOI 10.1016/0091-6749(92)90462-B; Kay AB, 2001, NEW ENGL J MED, V344, P30; Larsen WJ, 2001, HUMAN EMBRYOLOGY, p[351, 465]; LEDFORD DK, 1998, J RESP DIS, V19, P576; MA X, 2000, AM J CRIT CARE MED, V161, P325; MARTIN RJ, 1993, NOCTURNAL ASTHMA MEC; MIADONNA A, 1987, AM REV RESPIR DIS, V136, P357; Nathan RA, 1997, J ALLERGY CLIN IMMUN, V99, pS808, DOI 10.1016/S0091-6749(97)80040-1; OKUDA M, 1988, ANN ALLERGY, V60, P537; PIPKORN U, 1988, J ALLERGY CLIN IMMUN, V82, P1046, DOI 10.1016/0091-6749(88)90143-1; REINBERG A, 1988, J ALLERGY CLIN IMMUN, V81, P51, DOI 10.1016/0091-6749(88)90220-5; Reinberg A, 1989, CHRONOPHARMACOLOGY C, P115; REINBERG A, 1985, ANN REV CHRONOPHARMA, V3, P441; Simons FER, 1999, J ALLERGY CLIN IMMUN, V104, P534, DOI 10.1016/S0091-6749(99)70320-9; SMOLENSKY MH, 1995, J ALLERGY CLIN IMMUN, V95, P1087; Spada CS, 1997, ADV EXP MED BIOL, V400, P699; Togias A, 2003, J ALLERGY CLIN IMMUN, V111, P1171, DOI 10.1067/mai.2003.1592; Togias A, 2000, J ALLERGY CLIN IMMUN, V105, pS599, DOI 10.1067/mai.2000.106885; Trousseau A, 1865, CLIN MED HOTEL DIEU, V2, P373; VIEGAS M, 1987, BRIT MED J, V294, P414; WANG DY, 1995, INT ARCH ALLERGY IMM, V106, P278; WANG DY, 1994, ACTA OTO-LARYNGOL, V114, P552, DOI 10.3109/00016489409126103; WHITE MV, 1992, J ALLERGY CLIN IMMUN, V90, P699, DOI 10.1016/0091-6749(92)90155-U; WRIGHT AL, 1994, PEDIATRICS, V94, P895	39	103	108	1	6	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.		2004	114	5		S			S135	S138		10.1016/j.jaci.2004.08.043		4	Allergy; Immunology	Allergy; Immunology	V17HV	WOS:000207929200002	15536444	
J	Silverman, RA; Boudreaux, ED; Woodruff, PG; Clark, S; Camargo, CA				Silverman, RA; Boudreaux, ED; Woodruff, PG; Clark, S; Camargo, CA		Multicenter Airway Res Collaborati	Cigarette smoking among asthmatic adults presenting to 64 emergency departments	CHEST			English	Article						acute disease; asthma; emergency medicine; smoking	LUNG-FUNCTION; ALLERGIC RHINITIS; PASSIVE SMOKING; BRONCHIAL HYPERRESPONSIVENESS; PULMONARY-FUNCTION; MATERNAL SMOKING; CHILDREN; SYMPTOMS; PREVALENCE; EXPOSURE	Study objectives: The emergency department (ED) is an important focal point for asthmatic individuals with uncontrolled illness. Anecdotally, many adults presenting to the ED with acute asthma are active cigarette smokers. The present study determined the prevalence of cigarette smoking among adults presenting to the ED with acute asthma and identified the factors associated with current smoking status. Design: A prospective cohort study conducted as part of the Multicenter Airway Research Collaboration. Patients: A structured interview was performed in 1,847 patients, ages 18 to 54 years, who presented to the ED with acute asthma. Setting: Sixty-four EDs in 21 US states and 4 Canadian provinces. Results: Thirty-five percent of the enrolled asthmatic patients were current smokers with a median of 10 pack-years (interduartile range, 4 to 20 pack-years), while 23% were former smokers, and 42% were never-smokers. Current smokers comprised 33% of asthmatic patients aged 18 to 29 years, 40% for ages 30 to 39 years, and 33% for ages 40 to 54 (p < 0.001). In a multivariate analysis, the factors independently associated with current smoking status (p < 0.05) were as follows: age 30 to 39 years; white race/ethnicity; non-high school graduate; lower household income; lack of private insurance; no recent inhaled steroid usage; and no history of systemic steroid usage. Although 50% of current smokers admitted that smoking worsens their asthma symptoms, only 4% stated that smoking was responsible for their current exacerbation. Conclusions: Although cigarette smoke is generally recognized as a respiratory irritant, cigarette smoking is common among adults presenting to the ED with acute asthma. The ED visit may provide an opportunity for patients to be targeted for smoking cessation efforts.	Long Isl Jewish Med Ctr, Dept Emergency Med, New Hyde Pk, NY 11040 USA; Earl K Long Med Ctr, Dept Emergency Med, Baton Rouge, LA USA; Univ Calif San Francisco, Dept Med, Div Pulm & Crit Care Med, San Francisco, CA USA; Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA USA	Silverman, RA (reprint author), Long Isl Jewish Med Ctr, Dept Emergency Med, 270-05 76th Ave, New Hyde Pk, NY 11040 USA.			Boudreaux, Edwin/0000-0002-3223-6371	NHLBI NIH HHS [HL-03533, HL-63253]		ABULHOSN RS, 1987, AM REV RESPIR DIS, V135, P567; ANDERSON DO, 1962, NEW ENGL J MED, V267, P787, DOI 10.1056/NEJM196210182671601; ASHLEY F, 1975, ANN INTERN MED, V82, P739; Barkley R., 1997, ADHD REPORT, V5, P1; BECK GJ, 1981, AM REV RESPIR DIS, V123, P149; Belousova EG, 1997, CHEST, V112, P1539, DOI 10.1378/chest.112.6.1539; BRODER I, 1974, J ALLERGY CLIN IMMUN, V54, P100, DOI 10.1016/0091-6749(74)90038-4; BURCHFIEL CM, 1995, AM J RESP CRIT CARE, V151, P1778; BURROWS B, 1977, AM REV RESPIR DIS, V115, P195; [Anonymous], 1997, SOURC ZIP COD DEM; Cassino C, 1999, AM J RESP CRIT CARE, V159, P1773; Centers for Disease C Prevention, 1996, MMWR-MORBID MORTAL W, V45, P962; Centers for Disease Control and Prevention, 1998, BEH RISK FACT SURV S; CHILMONCZYK BA, 1993, NEW ENGL J MED, V328, P1665, DOI 10.1056/NEJM199306103282303; DOCKERY DW, 1988, AM REV RESPIR DIS, V137, P286; DODGE RR, 1980, AM REV RESPIR DIS, V122, P567; Eisner MD, 2000, AM J PUBLIC HEALTH, V90, P1307, DOI 10.2105/AJPH.90.8.1307; EVANS D, 1987, AM REV RESPIR DIS, V135, P567; FLODIN U, 1995, EPIDEMIOLOGY, V6, P503, DOI 10.1097/00001648-199509000-00007; Giovino Gary A., 1994, Morbidity and Mortality Weekly Report, V43, P1; HAGY GW, 1976, J ALLERGY CLIN IMMUN, V58, P330, DOI 10.1016/0091-6749(76)90139-1; Hankinson JL, 1999, AM J RESP CRIT CARE, V159, P179; *HLTH CAN, 1996, FED CENS DAT STAT CA; LARSSON L, 1995, THORAX, V50, P260, DOI 10.1136/thx.50.3.260; LEUENBERGER P, 1994, AM J RESP CRIT CARE, V150, P1222; LOWENSTEIN SR, 1995, ACAD EMERG MED, V2, P165, DOI 10.1111/j.1553-2712.1995.tb03189.x; MARTINEZ FD, 1992, PEDIATRICS, V89, P21; McCammond JP, 2000, INT J ALGEBR COMPUT, V10, P1, DOI 10.1142/S0218196700000029; MCCREA KA, 1994, AM J RESP CRIT CARE, V150, P696; MCWHORTER WP, 1989, AM REV RESPIR DIS, V139, P721; *METR INS CO, 1992, STAT B METR INS CO, V73, P12; MURRAY AB, 1986, J ALLERGY CLIN IMMUN, V77, P575, DOI 10.1016/0091-6749(86)90348-9; Oryszczyn MP, 2000, AM J RESP CRIT CARE, V161, P1241; PETERS JM, 1967, AM REV RESPIR DIS, V95, P774; Plaschke P, 1999, J ALLERGY CLIN IMMUN, V104, P58, DOI 10.1016/S0091-6749(99)70114-4; Plaschke PP, 2000, AM J RESP CRIT CARE, V162, P920; PROCHASKA JO, 1992, AM PSYCHOL, V47, P1102, DOI 10.1037/0003-066X.47.9.1102; PROCHASKA JO, 1994, HEALTH PSYCHOL, V13, P39, DOI 10.1037/0278-6133.13.1.39; Rasmussen F, 2000, CHEST, V117, P1330, DOI 10.1378/chest.117.5.1330; Richman PB, 1999, ACAD EMERG MED, V6, P807, DOI 10.1111/j.1553-2712.1999.tb01211.x; SANDVIK L, 1995, BRIT MED J, V311, P715; SEELEY JE, 1971, SCIENCE, V172, P41; SHEPHARD RJ, 1979, ENVIRON RES, V20, P392, DOI 10.1016/0013-9351(79)90015-X; Siegel M, 2000, AM J PUBLIC HEALTH, V90, P372, DOI 10.2105/AJPH.90.3.372; Siroux V, 2000, EUR RESPIR J, V15, P470, DOI 10.1034/j.1399-3003.2000.15.08.x; SOYSETH V, 1995, CHEST, V107, P389, DOI 10.1378/chest.107.2.389; STANKUS RP, 1988, J ALLERGY CLIN IMMUN, V82, P331, DOI 10.1016/0091-6749(88)90003-6; Strachan DP, 1996, BRIT MED J, V312, P1195; Sunyer J., 1997, European Respiratory Journal, V10, P2490, DOI 10.1183/09031936.97.10112490; TAGER IB, 1976, AM REV RESPIR DIS, V113, P619; TROISI RJ, 1995, CHEST, V108, P1557, DOI 10.1378/chest.108.6.1557; U. S. Department of Health and Human Services, 1984, HLTH CONS SMOK CHRON; VESTERINEN E, 1988, THORAX, V43, P534, DOI 10.1136/thx.43.7.534; WAGENKNECHT LE, 1992, AM J PUBLIC HEALTH, V82, P33, DOI 10.2105/AJPH.82.1.33; Wei HG, 2000, ACAD EMERG MED, V7, P710, DOI 10.1111/j.1553-2712.2000.tb02052.x; Weiss KB, 1992, CHEST, V101, P362; WEITZMAN M, 1990, PEDIATRICS, V85, P505; XU X, 1994, EUR RESPIR J, V7, P477, DOI 10.1183/09031936.94.07030477; MULTICENTER AIRWAY R	59	103	111	2	3	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	MAY	2003	123	5					1472	1479		10.1378/chest.123.5.1472		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	676VJ	WOS:000182773000027	12740263	
J	Jaakkola, MS; Nordman, H; Piipari, R; Uitti, J; Laitinen, J; Karjalainen, A; Hahtola, P; Jaakkola, JJK				Jaakkola, MS; Nordman, H; Piipari, R; Uitti, J; Laitinen, J; Karjalainen, A; Hahtola, P; Jaakkola, JJK			Indoor dampness and molds and development of adult-onset asthma: A population-based incident case-control study	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; case-control study; molds; occupational exposure; population-based	DAY-CARE-CENTERS; RESPIRATORY SYMPTOMS; HOME DAMPNESS; HEALTH; CHILDREN; EXPOSURE; INFLAMMATION; ASSOCIATIONS; BUILDINGS; DISEASE	Previous cross-sectional and prevalent case-control studies have suggested increased risk of asthma in adults related to dampness problems and molds in homes. We conducted a population-based incident case-control study to assess the effects of indoor dampness problems and molds at work and at home on development of asthma in adults. We recruited systematically all new cases of asthma during a 2.5-year study period (1997-2000) and randomly selected controls from a source population consisting of adults 21-63 years old living in the Pirkanmaa Hospital district, South Finland. The clinically diagnosed case series consisted of 521 adults with newly diagnosed asthma and the control series of 932 controls, after we excluded 76 (7.5%) controls with a history of asthma. In logistic regression analysis adjusting for confounders, the risk of asthma was related to the presence of visible mold and/or mold odor in the workplace (odds ratio, 1.54; 95% confidence interval, 1.01-2.32) but not to water damage or damp stains alone. We estimated the fraction of asthma attributable to workplace mold exposure to be 35.1% (95% confidence interval, 1.0-56.9%) among the exposed. Present results provide new evidence of the relation between workplace exposure to indoor molds and adult-onset asthma.	Finnish Inst Occupat Hlth, FIN-00250 Helsinki, Finland; Finnish Inst Occupat Hlth, Tampere, Finland; Tampere Univ Hosp, Dept Clin Physiol, Tampere, Finland; Tampere Univ Hosp, Dept Pulm Med, Tampere, Finland; Univ Helsinki, Dept Publ Hlth, Environm Epidemiol Unit, Helsinki, Finland; Nordic Sch Publ Hlth, Environm Hlth Program, Gothenburg, Sweden	Jaakkola, JJK (reprint author), Finnish Inst Occupat Hlth, FIN-00250 Helsinki, Finland.		Jaakkola, Jouni/G-4314-2012				American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Bornehag CG, 2001, INDOOR AIR, V11, P72; BRUNEKREEF B, 1992, ALLERGY, V47, P498, DOI 10.1111/j.1398-9995.1992.tb00672.x; BRUNEKREEF B, 1992, SCI TOTAL ENVIRON, V127, P79, DOI 10.1016/0048-9697(92)90471-4; BRUNEKREEF B, 1989, AM REV RESPIR DIS, V140, P1363; *COMM NATL ASTHM P, 1994, 16 MIN SOC AFF HLTH; DALES RE, 1991, AM REV RESPIR DIS, V143, P505; DALES RE, 1991, AM J EPIDEMIOL, V134, P196; Greenland S., 1998, MODERN EPIDEMIOLOGY, P295; Hodgson MJ, 1998, J OCCUP ENVIRON MED, V40, P241, DOI 10.1097/00043764-199803000-00006; Hu FB, 1997, J ASTHMA, V34, P67, DOI 10.3109/02770909709071205; Husman T, 1996, SCAND J WORK ENV HEA, V22, P5; HYNDMAN SJ, 1990, SOC SCI MED, V30, P131, DOI 10.1016/0277-9536(90)90336-Q; JAAKKOLA JJK, 1995, AM J EPIDEMIOL, V141, P755; JAAKKOLA JJK, 1993, J EXPO ANAL ENV EPID, V3, P129; Jaakkola MS, 1999, AM J EPIDEMIOL, V150, P1223; Johanning E, 1999, ENVIRON HEALTH PERSP, V107, P489; Li CS, 1997, ARCH ENVIRON HEALTH, V52, P68; Maier WC, 1997, ENVIRON HEALTH PERSP, V105, P208, DOI 10.1289/ehp.97105208; MIETTINE.OS, 1974, AM J EPIDEMIOL, V99, P325; Nafstad P, 1998, AM J RESP CRIT CARE, V157, P410; [Anonymous], 1998, INDOOR AIR S; Norback D, 1999, INT J TUBERC LUNG D, V3, P368; PLATT SD, 1989, BRIT MED J, V298, P1673; RUOTSALAINEN R, 1995, INT ARCH OCC ENV HEA, V66, P369, DOI 10.1007/BF00383142; SPENGLER J, 1994, INDOOR AIR, V4, P72, DOI 10.1111/j.1600-0668.1994.t01-2-00002.x; Thorn J, 1998, AM J RESP CRIT CARE, V157, P1798; Thorn J, 2001, ALLERGY, V56, P287, DOI 10.1034/j.1398-9995.2001.00805.x; VILJANEN AA, 1982, SCAND J CLIN LAB INV, V42, P5; WAEGEMAEKERS M, 1989, ALLERGY, V44, P192, DOI 10.1111/j.1398-9995.1989.tb02261.x; Wan GH, 1999, ARCH ENVIRON HEALTH, V54, P58; Williamson IJ, 1997, THORAX, V52, P229	32	103	104	1	4	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.	MAY	2002	110	5					543	547				5	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	552NL	WOS:000175626400033	12003761	
J	Otterbein, LE				Otterbein, LE			Carbon monoxide: Innovative anti-inflammatory properties of an age-old gas molecule	ANTIOXIDANTS & REDOX SIGNALING			English	Review							TUMOR-NECROSIS-FACTOR; HEME OXYGENASE-1 SUPPRESSES; OXIDATIVE STRESS; LUNG INJURY; EXHALED AIR; PROVIDES PROTECTION; PHYSIOLOGICAL IMPORTANCE; IMMUNOLOGICAL RESPONSE; ACTIVATED MACROPHAGES; FACTOR BIOSYNTHESIS	Observations of the effects of carbon monoxide (CO) on mammalian systems have been known for thousands of years. To be sure, CO is deadly under certain conditions and concentrations, but perhaps as the data presented here will make clear, it also possesses other diverse functional and immunomodulatory properties. This review, together with the other reviews in this issue, will detail that over the past three decades, fundamental functional role(s) for this gas molecule are beginning to emerge. This review outlines that at low concentrations, exogenously administered CO is a molecule involved in the regulation of the inflammatory response in a variety of disease models. CO has been shown to modulate such cellular functions as cytokine production, cell proliferation and apoptosis, protecting the lungs and hearts of rodents from such stressors as endotoxin, ischemia/reperfusion injury, cardiac xenograft rejection, and asthma. Although the mechanism by which this simple diatomic gas provides this protection remains obscure, the conclusions are the same: CO at low concentrations, concentrations that are well below those that would otherwise create toxic effects, is proving beneficial in models of acute injury. CO, akin to nitric oxide, is proving to be an extraordinary signaling molecule generated by the cell that is vital in the regulation of cellular homeostasis.	Univ Pittsburgh, Montefiore Univ Hosp, Sch Med, Div Pulm & Crit Care Med, Pittsburgh, PA 15213 USA	Univ Pittsburgh, Montefiore Univ Hosp, Sch Med, Div Pulm & Crit Care Med, 3459 5th Ave,Room 628 NW, Pittsburgh, PA 15213 USA.	lotterbein@usa.net					Antuni JD, 2000, THORAX, V55, P138, DOI 10.1136/thorax.55.2.138; BALLA J, 1993, P NATL ACAD SCI USA, V90, P9285, DOI 10.1073/pnas.90.20.9285; BENIGNUS VA, 1996, CARBON MONOXIDE, P211; BERNARD C, 1858, CR HEBD ACAD SCI, V48, P393; Bernard C., 1857, LECONS EFFECTS SUBST; BEUTLER B, 1986, SCIENCE, V232, P977, DOI 10.1126/science.3754653; Brouard S, 2000, J EXP MED, V192, P1015, DOI 10.1084/jem.192.7.1015; Chapman JT, 2001, AM J PHYSIOL-LUNG C, V281, pL209; CHOI AMK, 1995, AM J RESP CELL MOL, V13, P74; Christian JL, 1999, BIOESSAYS, V21, P382, DOI 10.1002/(SICI)1521-1878(199905)21:5<382::AID-BIES5>3.0.CO;2-V; CLERCH LB, 1993, J CLIN INVEST, V91, P499, DOI 10.1172/JCI116228; COBURN RF, 1967, J CLIN INVEST, V46, P346, DOI 10.1172/JCI105536; COBURN RF, 1979, PREV MED, V8, P310, DOI 10.1016/0091-7435(79)90008-2; De Saint-Martin L., 1898, CR HEBD ACAD SCI, V126, P1036; Downard PJ, 1997, J SURG RES, V71, P7, DOI 10.1006/jsre.1997.5135; Drabkin D. 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Redox Signal.	APR	2002	4	2					309	319		10.1089/152308602753666361		11	Biochemistry & Molecular Biology; Endocrinology & Metabolism	Biochemistry & Molecular Biology; Endocrinology & Metabolism	547HN	WOS:000175327100010	12006182	
J	Luque, I; Leyva, L; Torres, MJ; Rosal, M; Mayorga, C; Segura, JM; Blanca, M; Juarez, C				Luque, I; Leyva, L; Torres, MJ; Rosal, M; Mayorga, C; Segura, JM; Blanca, M; Juarez, C			In vitro T-cell responses to beta-lactam drugs in immediate and nonimmediate allergic reactions	ALLERGY			English	Article						drug allergy; beta-lactams; lymphocyte transformation test; skin tests; T cells	LYMPHOCYTE-TRANSFORMATION TEST; PENICILLIN ALLERGY; CROSS-REACTIVITY; GOOD TOLERANCE; CUTANEOUS REACTIONS; IGE ANTIBODIES; MODIFIED SELF; ANTIBIOTICS; HYPERSENSITIVITY; AMOXICILLIN	Background: beta -Lactam drugs may induce both cellular and humoral allergic reactions, and there is evidence that T cells play an important role in the pathogenesis of these reactions. The aim of this work was to assess the sensitivity and specificity of the lymphocyte transformation test (LTT) as an in vitro diagnostic tool, in patients with either an immediate or a nonimmediate reaction to penicillin G and/or amoxicillin. Methods: Fifty patients with a well-documented history of allergic reactions to beta -lactams (31 immediate and 19 nonimmediate) were studied by means of skin tests (prick and intradermal), radioallergosorbent test (RAST), and, when necessary, controlled administration of the drug. Twenty-eight healthy subjects with good tolerance to penicillins served as controls. LTT was performed in all subjects. Results: Skin tests were positive in 77.4% of the patients with immediate reactions and in 36.8% of those with nonimmediate reactions. The overall sensitivity of LTT in the allergic patients was 62%, but, when analyzed separately, sensitivity was 64.5% for the immediate group and 57.9% for the nonimmediate group. The LTT specificity was 92.8%. Conclusions: The LTT should be considered a useful in vitro diagnostic tool to identify subjects allergic to penicillins, especially patients with nonimmediate reactions where the LTT has a better diagnostic value than skin tests. Interestingly, positive T-cell proliferative responses can be observed 10 or more years after the occurrence of the reaction without further exposure to the drug.	Carlos Haya Hosp, Res Unit Allerg Dis, Malaga, Spain; Univ Hosp La Paz, Allergy Serv, Madrid, Spain; Carlos Haya Hosp, Dept Internal Med, Malaga, Spain	Leyva, L (reprint author), Hosp Civil, Res Unit Allerg Dis, Pab 5 Sotano,Plaza Hosp Civil S-N, Malaga 29009, Spain.		Luque, Inmaculada/K-9464-2014	Luque, Inmaculada/0000-0003-1838-2636			ASSEM E S K, 1975, Clinical Allergy, V5, P43, DOI 10.1111/j.1365-2222.1975.tb01835.x; BARNA BP, 1980, AM J CLIN PATHOL, V73, P172; BELL SJD, 1989, ALLERGY, V44, P199, DOI 10.1111/j.1398-9995.1989.tb02262.x; BLANCA M, 1989, J ALLERGY CLIN IMMUN, V83, P381, DOI 10.1016/0091-6749(89)90122-X; BLANCA M, 1994, CLIN EXP ALLERGY, V24, P407, DOI 10.1111/j.1365-2222.1994.tb00928.x; BLANCA M, 1990, CLIN EXP ALLERGY, V20, P475, DOI 10.1111/j.1365-2222.1990.tb03139.x; BLANCA M, 1995, ALLERGY, V50, P777; BLANCA M, 1991, ALLERGY, V46, P632, DOI 10.1111/j.1398-9995.1991.tb00635.x; BLANCA M, 1988, ALLERGY, V43, P508, DOI 10.1111/j.1398-9995.1988.tb01628.x; BRANDER C, 1995, J IMMUNOL, V155, P2670; Brugnolo F, 1999, J IMMUNOL, V163, P1053; Cederbrant K, 1998, ALLERGY, V53, P1155, DOI 10.1111/j.1398-9995.1998.tb03835.x; Cederbrant K, 1997, INT ARCH ALLERGY IMM, V112, P212; DEHAAN P, 1986, ALLERGY, V41, P75; DEWDNEY JM, 1977, ANTIGENS, V5, P73; De Weck A. 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J	Siegel, JP				Siegel, JP			The mammalian safety of Bacillus thuringiensis-based insecticides	JOURNAL OF INVERTEBRATE PATHOLOGY			English	Review						Bacillus thuringiensis; mammalian safety; infection of animals and man; Bacillus cereus enterotoxins; persistence of spores; clearance of spores	CEREUS; STRAINS; MICE; ENTEROTOXIN; ISRAELENSIS; PESTICIDES; RESPONSES; INFECTION; TOXICITY	United States Environmental Protection Agency between the years 1961 and 1995 registered 177 products containing viable Bacillus thuringiensis (Bt), Numerous laboratory studies have demonstrated that Bt and Bt products are noninfectious and are toxic to mammals only at a dose greater than or equal to 10(8) colony forming units (cfu) per mouse (a human equivalent based on the weight of >10(11) cfu), In contrast, as few as three vegetative cells of Bacillus anthracis can kill mice (a human equivalent of >10(3) cfu), There are only two literature reports of Bt infection in man between the year 1997 and the present, and all infected individuals had experienced either extensive burns or a blast injury, which predisposed them to infection. Two epidemiology studies conducted during large-scale aerial Bt serovar kurstaki spray campaigns reported no increased incidence of illness, Some recent papers have expressed concern about the production of Bacillus cereus enterotoxins by Bt isolates, Laboratory studies found no evidence of illness in rats and sheep fed Bt products, nor have epidemiology studies found increased incidence of diarrhea during Bt aerial spray campaigns, Increases in human antibody levels following exposure to Bt products have been reported but there was no increased incidence in asthma or other illness, Based on laboratory studies and field experience, Bt insecticides have an excellent safety record.	ARS, USDA, Hort Crops Res Ctr, Fresno, CA 93727 USA	Siegel, JP (reprint author), ARS, USDA, Hort Crops Res Ctr, 2021 S Peach Ave, Fresno, CA 93727 USA.						ABDELHAMEED A, 1994, WORLD J MICROB BIOT, V10, P406, DOI 10.1007/BF00144461; ADLERSBERG L, 1969, J RETICULOENDOTH SOC, V6, P536; BAUMANN L, 1984, J INVERTEBR PATHOL, V44, P329, DOI 10.1016/0022-2011(84)90031-4; Bernstein IL, 1999, ENVIRON HEALTH PERSP, V107, P575, DOI 10.2307/3434400; Bishop AH, 1999, WORLD J MICROB BIOT, V15, P375, DOI 10.1023/A:1008983818692; Burges HD, 1981, MICROBIAL CONTROL PE, P738; CARLSON CR, 1994, APPL ENVIRON MICROB, V60, P1719; DAMGAARD PH, 1995, FEMS IMMUNOL MED MIC, V12, P245, DOI 10.1111/j.1574-695X.1995.tb00199.x; Damgaard PH, 1997, FEMS IMMUNOL MED MIC, V18, P47, DOI 10.1016/S0928-8244(97)00021-7; DROBNIEWSKI FA, 1993, CLIN MICROBIOL REV, V6, P324; ELLIOTT LJ, 1988, APPL OCCUP ENV HYG, V3, P119; Fares Nagui H., 1998, Natural Toxins, V6, P219, DOI 10.1002/(SICI)1522-7189(199811/12)6:6<219::AID-NT30>3.0.CO;2-K; FISHER R, 1959, AGR FOOD CHEM, V7, P686; Gaviria A, 2000, FEMS MICROBIOL LETT, V190, P151, DOI 10.1016/S0378-1097(00)00317-7; GORDON RE, 1977, US DHEW PUBL; GREEN M, 1990, AM J PUBLIC HEALTH, V80, P848, DOI 10.2105/AJPH.80.7.848; HADLEY WM, 1987, FUND APPL TOXICOL, V8, P236, DOI 10.1016/0272-0590(87)90122-9; HART K, 2000, PESTIC TOXIC CHEM NE, V28, P13; Helgason E, 2000, J CLIN MICROBIOL, V38, P1615; Hernandez E, 1999, FEMS IMMUNOL MED MIC, V24, P43, DOI 10.1016/S0928-8244(99)00005-X; Hernandez E, 1998, J CLIN MICROBIOL, V36, P2138; IGNOFFO CM, 1973, ANN NY ACAD SCI, V217, P141, DOI 10.1111/j.1749-6632.1973.tb32756.x; JACKSON SG, 1995, LETT APPL MICROBIOL, V21, P103, DOI 10.1111/j.1472-765X.1995.tb01017.x; KRAMER JM, 1988, FOODBORNE BACTERIAL, P22; Laferriere M, 1987, IMMUNOLOGIC STUDY CO; LAMANNA C, 1963, J BACTERIOL, V85, P532; MCCLINTOCK JT, 1995, PESTIC SCI, V45, P95, DOI 10.1002/ps.2780450202; MIKESELL P, 1985, MICROBIOLOGY, P52; Noble M. A., 1992, MICROBIOLOGICAL EPID; PETRAS SF, 1985, APPL ENVIRON MICROB, V50, P1496; Ripabelli G, 2000, LETT APPL MICROBIOL, V30, P358, DOI 10.1046/j.1472-765X.2000.00729.x; SALMITOU S, 2000, MICROBIOL, V146, P2825; SAMPLES JR, 1983, J INFECT DIS, V148, P614; Siegel J. P., 1990, Bacterial control of mosquitoes & black flies: biochemistry, genetics & applications of Bacillus thuringiensis israelensis and Bacillus sphaericus., P202; Siegel Joel P., 1997, P325, DOI 10.1016/B978-012432555-5/50017-8; SIEGEL JP, 1987, J ECON ENTOMOL, V80, P717; SIEGEL JP, 1990, J ECON ENTOMOL, V83, P347; Sneath P. H., 1986, BERGEYS MANUAL SYSTE, V2, P1104; SPIRA WM, 1972, APPL MICROBIOL, V24, P341; Tsai San-Fu, 1997, Journal of the Chinese Society of Veterinary Science, V23, P515; Vazquez-Padron RI, 1999, LIFE SCI, V64, P1897, DOI 10.1016/S0024-3205(99)00136-8; Warren R. E., 1984, Lancet, P678	42	103	118	1	21	ACADEMIC PRESS INC	SAN DIEGO	525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA	0022-2011			J INVERTEBR PATHOL	J. Invertebr. Pathol.	JAN	2001	77	1					13	21		10.1006/jipa.2000.5000		9	Zoology	Zoology	402RH	WOS:000167001600002	11161988	
J	Holloway, JA; Warner, JO; Vance, GHS; Diaper, ND; Warner, JA; Jones, CA				Holloway, JA; Warner, JO; Vance, GHS; Diaper, ND; Warner, JA; Jones, CA			Detection of house-dust-mite allergen in amniotic fluid and umbilical-cord blood	LANCET			English	Article							FETAL	Mononuclear cells In umbilical-cord blood display allergen-specific reactivity, but how allergen exposure occurs In utero is unknown. We Investigated the presence of a common inhalant allergen (Der p 1), to which mothers are exposed throughout pregnancy, by ELISA in matched maternal blood and amniotic fluid samples at 16-17 weeks of gestation, and in matched maternal and umbilical-cord blood at term (greater than or equal to 37 weeks of gestation). Der p 1 was detectable In 24 of 43 amniotic fluid samples where It was also present In maternal blood, and in 15 of 24 cord-plasma samples at significantly higher concentrations than in the maternal plasma (p=0.022). The detection of Der p 1 In the amniotic fluid and the fetal circulation provides direct evidence of transamniotic and transplacental allergen exposure.	Univ Southampton, Allergy & Inflammat Sci Div, Southampton, Hants, England	Warner, JO (reprint author), Southampton Gen Hosp, Child Hlth Mailpoint 803,Level G Ctr Block, Southampton SO16 6YD, Hants, England.		Holloway, Judith/A-1757-2010	Holloway, Judith/0000-0002-2268-3071	NHLBI NIH HHS [HL-61858]		DAHL GMK, 1984, COMP BIOCHEM PHYS A, V77, P199, DOI 10.1016/0300-9629(84)90046-X; Jenmalm MC, 2000, CLIN EXP ALLERGY, V30, P34, DOI 10.1046/j.1365-2222.2000.00771.x; Jones AC, 1996, PEDIATR ALLERGY IMMU, V7, P109, DOI 10.1111/j.1399-3038.1996.tb00117.x; SPENCER J, 1986, CLIN EXP IMMUNOL, V64, P536; Szepfalusi Z, 2000, PEDIATR RES, V48, P404	5	103	106	1	2	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	DEC 2	2000	356	9245					1900	1902		10.1016/S0140-6736(00)03265-7		3	Medicine, General & Internal	General & Internal Medicine	379WD	WOS:000165665400017	11130390	
J	Ewart, SL; Kuperman, D; Schadt, E; Tankersley, C; Grupe, A; Shubitowski, DM; Peltz, G; Wills-Karp, M				Ewart, SL; Kuperman, D; Schadt, E; Tankersley, C; Grupe, A; Shubitowski, DM; Peltz, G; Wills-Karp, M			Quantitative trait loci controlling allergen-induced airway hyperresponsiveness in inbred mice	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article							GENOME-WIDE SEARCH; TRANSCRIPTION FACTOR GATA-3; BRONCHIAL HYPERREACTIVITY; UNDERLYING ASTHMA; LINKAGE ANALYSIS; MURINE MODEL; MOUSE MODEL; T-CELLS; EXPRESSION; INFLAMMATION	Identification of the genetic loci underlying asthma in humans has been hampered by variability in clinical phenotype, uncontrolled environmental influences, and genetic heterogeneity. To circumvent these complications, the genetic regulation of asthma-associated phenotypes was studied in a murine model. We characterized the strain distribution patterns for the asthma-related phenotypes airway hyperresponsiveness (AHR), lung eosinophils, and ovalbumin (OVA)-specific serum immunoglobulin (Ig) E induced by allergen exposure protocols in A/J, AKR/J, BALB/cJ, C3H/HeJ, and C57BL/6J inbred strains and in (C3H/HeJ x A/J)F1 mice. Expression of AHR differed between strains and was sometimes discordant with lung eosinophils or serum IgE. Furthermore, we identified two distinct quantitative trait loci (QTL) for susceptibility to allergen-induced AHR, Abhr1 (allergen-induced bronchial hyperresponsiveness) (lod = 4.2) and Abhr2 (lod = 3.7), on chromosome 2 in backcross progeny from A/J and C3H/HeJ mice. In addition, a QTL on chromosome 7 was suggestive of linkage to this trait. These QTL differ from those we have previously found to control noninflammatory AHR in the same crosses. Elucidation of the genes underlying these QTL will facilitate the identification of biochemical pathways regulating AHR in animal models of asthma and may provide insights into the pathogenesis of human disease.	Michigan State Univ, Dept Large Anim Clin Sci, E Lansing, MI 48824 USA; Johns Hopkins Univ, Dept Environm Hlth Sci, Baltimore, MD 21205 USA; Univ Calif Los Angeles, Dept Biomath, Los Angeles, CA 90024 USA; Rosette Inpharmat, Dept Bioinformat, Kirkland, WA USA; Roche BioSci, Palo Alto, CA USA	Wills-Karp, M (reprint author), Childrens Hosp, Med Ctr, 3333 Brunet Ave, Cincinnati, OH 45229 USA.				NCRR NIH HHS [RR00097]; NHLBI NIH HHS [R01-HL58527]; NIEHS NIH HHS [ES-03819]		BASTEN CA, 1994, QTL CARTOGRAPHER RES; Basten C.J., 1997, QTL CARTOGRAPHER REF; Basten C. 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J. Respir. Cell Mol. Biol.	OCT	2000	23	4					537	545				9	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	364JB	WOS:000089888300017	11017920	
J	Burge, HA; Rogers, CA				Burge, HA; Rogers, CA			Outdoor allergens	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; exposure; fungal spores; outdoor allergens; pollen; predictive models	RAGWEED-POLLEN DETERMINANTS; EMERGENCY ROOM VISITS; AIR-POLLUTION; SOYBEAN-DUST; GRASS-POLLEN; ATMOSPHERIC AEROSOL; EPIDEMIC ASTHMA; EXPOSURE; PARTICLES; SYMPTOMS	Outdoor allergens are an important part of the exposures that lead to allergic disease. Understanding the role of outdoor allergens requires a knowledge of the nature of outdoor allergen-bearing particles, the distributions of their source, and the nature of the aerosols (particle types, sizes, dynamics of concentrations). Primary sources for outdoor allergens include vascular plants (pollen, fern spores, soy dust), and fungi (spores. hyphae). Nonvascular plants, algae, and arthropods contribute small numbers of allergen-bearing particles. Particles are released from sources into the air by wind, rain, mechanical disturbance, or active discharge mechanisms. Once airborne, they follow the physical laws that apply to all airborne particles. Although some outdoor allergens penetrate indoor spaces, exposure occurs mostly outdoors. Even short-term peak outdoor exposures can be important in eliciting acute symptoms. Monitoring of airborne biological particles is usually by particle impaction and microscopic examination. Centrally located monitoring stations give regional-scale measurements for aeroallergen levels. Evidence for the role of outdoor allergens in allergic rhinitis is strong and is rapidly increasing for a role in asthma. Pollen and fungal spore exposures have both been implicated in acute exacerbations of asthma, and sensitivity to some fungal spores predicts the existence of asthma. Synergism and/or antagonism probably occurs with other outdoor air particles and gases. Control involves avoidance of exposure (staying indoors, preventing entry of outdoor aerosols) as well as immunotherapy. which is effective for pollen but of limited effect for spores. Outdoor allergens have been the subject of only limited studies with respect to the epidemiology of asthma. Much remains to be studied with respect to prevalence patterns, exposure acid disease relationships, and control.	Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA	Burge, HA (reprint author), Harvard Univ, Sch Publ Hlth, 665 Huntington Ave, Boston, MA 02115 USA.		Rogers, Christine/A-2189-2008	Rogers, Christine/0000-0003-0887-9606			ACEVES M, 1991, J ALLERGY CLIN IMMUN, V88, P124, DOI 10.1016/0091-6749(91)90309-C; AGARWAL MK, 1983, J ALLERGY CLIN IMMUN, V72, P40, DOI 10.1016/0091-6749(83)90050-7; AGARWAL MK, 1984, J ALLERGY CLIN IMMUN, V74, P687, DOI 10.1016/0091-6749(84)90231-8; Anto JM, 1999, THORAX, V54, P670; ARIZMENDI CM, 1993, INT J BIOMETEOROL, V37, P139, DOI 10.1007/BF01212623; Arx J. 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P., 1959, POLLEN GRAINS; ZEJDA JE, 1993, TUBERCLE LUNG DIS, V74, P74, DOI 10.1016/0962-8479(93)90031-R; 1999, POLLEN SPORE REPORT	85	103	111	1	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.	AUG	2000	108			4			653	659		10.2307/3454401		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	350VH	WOS:000089121500008	10931783	
J	Farsalinos, KE; Romagna, G; Tsiapras, D; Kyrzopoulos, S; Voudris, V				Farsalinos, Konstantinos E.; Romagna, Giorgio; Tsiapras, Dimitris; Kyrzopoulos, Stamatis; Voudris, Vassilis			Characteristics, Perceived Side Effects and Benefits of Electronic Cigarette Use: A Worldwide Survey of More than 19,000 Consumers	INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH			English	Article						lectronic cigarette; smoking; tobacco; nicotine; harm reduction; public health	NICOTINE DELIVERY; SMOKING-CESSATION; INTERNET SURVEY; VAPOR EXTRACT; SAFETY	Background: Electronic cigarette (EC) use has grown exponentially over the past few years. The purpose of this survey was to assess the characteristics and experiences of a large sample of EC users and examine the differences between those who partially and completely substituted smoking with EC use. Methods: A questionnaire was prepared, translated into 10 different languages and uploaded in an online survey tool. EC users were asked to participate irrespective of their current smoking status. Participants were divided according to their smoking status at the time of participation in two subgroups: former smokers and current smokers. Results: In total, 19,414 participants were included in the analysis, with 88 of them (0.5%) reported not being smokers at the time of EC use initiation. Complete substitution of smoking was reported by 81.0% of participants (former smokers) while current smokers had reduced smoking consumption from 20 to 4 cigarettes per day. They were using ECs for a median of 10 months. They initiated EC use with a median of 18 mg/mL nicotine-concentration liquids; 21.5% used higher than 20 mg/mL. Only 3.5% of participants were using 0-nicotine liquids at the time of the survey. Former smokers were highly dependent (Fagerstrom Test for Cigarette Dependence = 7) and were heavier smokers (21 cigarettes per day when smoking) compared to current smokers. The most important reasons for initiating EC use for both subgroups was to reduce the harm associated with smoking and to reduce exposure of family members to second-hand smoking. Most considered ECs as less harmful than tobacco cigarettes, while 11.0% considered them absolutely harmless. Side effects were reported by more than half of the participants (59.8%), with the most common being sore/dry mouth and throat; side effects were mild and in most cases were subsequently resolved (partially or completely). Participants experienced significant benefits in physical status and improvements in pre-existing disease conditions (including respiratory disease such as asthma and chronic obstructive lung disease). Being former smoker was independently associated with positive effects in health and improvements in disease conditions. Conclusions: The results of this worldwide survey of dedicated users indicate that ECs are mostly used to avoid the harm associated with smoking. They can be effective even in highly-dependent smokers and are used as long-term substitutes for smoking. High levels of nicotine are used at initiation; subsequently, users try to reduce nicotine consumption, with only a small minority using non-nicotine liquids. Side effects are minor and health benefits are substantial, especially for those who completely substitute smoking with EC use. Further population and interventional studies are warranted.	[Farsalinos, Konstantinos E.; Tsiapras, Dimitris; Kyrzopoulos, Stamatis; Voudris, Vassilis] Onassis Cardiac Surg Ctr, Kallithea 17674, Greece; [Romagna, Giorgio] ABICH Srl, Biol & Chem Toxicol Res Inst, I-28924 Verbania, VB, Italy	Farsalinos, KE (reprint author), Onassis Cardiac Surg Ctr, Sygrou 356, Kallithea 17674, Greece.	kfarsalinos@gmail.com; giorgio.romagna@gmail.com; dtsiapras@hotmail.com; stkyrz@gmail.com; vvoudris@otenet.gr		Farsalinos, Konstantinos/0000-0001-6839-4710	funding campaign of E-Cigarette Research Advocates Group	The study was funded by a funding campaign of E-Cigarette Research Advocates Group, the owners of the website www.ecigarette-research.com. This is a non-profit group of electronic cigarette users with no relation to the electronic cigarette or other industry. The website does not promote or present any electronic cigarette product and do not accept any advertisements. The sole purpose of the group is to inform about research conducted on electronic cigarettes. Konstantinos E. Farsalinos has been allowed to present studies and post comments concerning electronic cigarette research on this website, without providing or receiving any form of payment. The study was investigator-initiated and investigator-driven. The sponsor had no involvement in the study design, data collection, analysis and interpretation, writing or approving the manuscript and decision to submit the manuscript for publication.	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J. Environ. Res. Public Health	APR	2014	11	4					4356	4373		10.3390/ijerph110404356		18	Environmental Sciences; Public, Environmental & Occupational Health	Environmental Sciences & Ecology; Public, Environmental & Occupational Health	AG9TM	WOS:000335762700044	24758891	
J	Kessler, R; Partridge, MR; Miravitlles, M; Cazzola, M; Vogelmeier, C; Leynaud, D; Ostinelli, J				Kessler, R.; Partridge, M. R.; Miravitlles, M.; Cazzola, M.; Vogelmeier, C.; Leynaud, D.; Ostinelli, J.			Symptom variability in patients with severe COPD: a pan-European cross-sectional study	EUROPEAN RESPIRATORY JOURNAL			English	Article						Breathlessness; chronic obstructive pulmonary disease; symptoms; symptom variability; treatment	OBSTRUCTIVE PULMONARY-DISEASE; QUALITY-OF-LIFE; AIR-FLOW OBSTRUCTION; CIRCADIAN VARIATION; EXACERBATIONS; ASTHMA; VALIDATION; TIOTROPIUM; IMPACT	In between exacerbations, chronic obstructive pulmonary disease (COPD) is usually regarded as a stable condition, but there is increasing recognition of variability in this state. This cross-sectional study assessed patients' perception of symptom variability. Participants were outpatients >45 yrs old with COPD, current or ex-smokers, forced expiratory volume in 1 s (FEV1) <50% predicted, FEV1/forced vital capacity <0.7 and no exacerbation leading to therapeutic intervention in the previous 3 months. Patients' perceptions of COPD symptoms and their impact on daily life activities were recorded. Alterations in therapy use in response to COPD worsening were also recorded. COPD symptoms were experienced by 2,258 (92.5%) out of 2,441 patients during the 7 days before interview. Breathlessness was the most common symptom (72.5%). Daily and/or weekly symptom variability was reported by 62.7% of symptomatic patients; the morning was the worst time of day. Factors associated with perception of variability of breathlessness included younger age, symptom severity and recruitment to the study by general practitioners. The perception of variability was significantly different between European countries or regions. Patient-perceived COPD symptoms vary over the day and the week, and impact on daily activities; morning being the worst time of day. The majority of patients appear not to adjust treatment when symptoms worsen.	[Kessler, R.] Nouvel Hop Civil, Dept Pneumol, F-67000 Strasbourg, France; [Leynaud, D.; Ostinelli, J.] AstraZeneca, Dept Med, Rueil Malmaison, France; [Partridge, M. R.] Univ London Imperial Coll Sci Technol & Med, NHLI Div, Charing Cross Hosp, London, England; [Miravitlles, M.] Hosp Clin Barcelona, CIBERES, IDIBAPS, Fundacio Clin, Barcelona, Spain; [Cazzola, M.] Univ Roma Tor Vergata, Dept Internal Med, Rome, Italy; [Cazzola, M.] San Raffaele Pisana Hosp, Pulm Rehabil Grp, Rome, Italy; [Vogelmeier, C.] Univ Marburg, Div Resp Dis, Marburg, Germany	Kessler, R (reprint author), Nouvel Hop Civil, Dept Pneumol, 1 Pl Hop, F-67000 Strasbourg, France.	Romain.Kessler@chru-strasbourg.fr	Cazzola, Mario/G-9397-2012	Miravitlles, Marc/0000-0002-9850-9520	AstraZeneca	This study was funded by AstraZeneca.	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J	Delfino, RJ; Brummel, S; Wu, J; Stern, H; Ostro, B; Lipsett, M; Winer, A; Street, DH; Zhang, L; Tjoa, T; Gillen, DL				Delfino, R. J.; Brummel, S.; Wu, J.; Stern, H.; Ostro, B.; Lipsett, M.; Winer, A.; Street, D. H.; Zhang, L.; Tjoa, T.; Gillen, D. L.			The relationship of respiratory and cardiovascular hospital admissions to the southern California wildfires of 2003	OCCUPATIONAL AND ENVIRONMENTAL MEDICINE			English	Article							AIR-POLLUTION; FOREST-FIRES; PARTICULATE MATTER; LONGITUDINAL DATA; ACUTE ASTHMA; EXPOSURE; SMOKE; MORTALITY; QUALITY; CONSEQUENCES	Objective: There is limited information on the public health impact of wildfires. The relationship of cardiorespiratory hospital admissions (n=40 856) to wildfire-related particulate matter (PM(2.5)) during catastrophic wildfires in southern California in October 2003 was evaluated. Methods: Zip code level PM(2.5) concentrations were estimated using spatial interpolations from measured PM(2.5), light extinction, meteorological conditions, and smoke information from MODIS satellite images at 250 m resolution. Generalised estimating equations for Poisson data were used to assess the relationship between daily admissions and PM(2.5), adjusted for weather, fungal spores (associated with asthma), weekend, zip code-level population and sociodemographics. Results: Associations of 2-day average PM(2.5) with respiratory admissions were stronger during than before or after the fires. Average increases of 70 mu g/m(3) PM(2.5) during heavy smoke conditions compared with PM(2.5) in the pre-wildfire period were associated with 34% increases in asthma admissions. The strongest wildfire-related PM(2.5) associations were for people ages 65 99 years (10.1% increase per 10 mu g/m(3) PM(2.5), 95% CI 3.0% to 17.8%) and ages 0-4 years (8.3%, 95% CI 2.2% to 14.9%) followed by ages 20-64 years (4.1%, 95% CI 20.5% to 9.0%). There were no PM(2.5)-asthma associations in children ages 5-18 years, although their admission rates significantly increased after the fires. Per 10 mg/m3 wildfire-related PM(2.5), acute bronchitis admissions across all ages increased by 9.6% (95% CI 1.8% to 17.9%), chronic obstructive pulmonary disease admissions for ages 20-64 years by 6.9% (95% CI 0.9% to 13.1%), and pneumonia admissions for ages 5-18 years by 6.4% (95% CI 21.0% to 14.2%). Acute bronchitis and pneumonia admissions also increased after the fires. There was limited evidence of a small impact of wildfire-related PM(2.5) on cardiovascular admissions. Conclusions: Wildfire-related PM(2.5) led to increased respiratory hospital admissions, especially asthma, suggesting that better preventive measures are required to reduce morbidity among vulnerable populations.	[Delfino, R. J.; Wu, J.; Tjoa, T.] Univ Calif Irvine, Sch Med, Dept Epidemiol, Irvine, CA 92617 USA; [Brummel, S.; Stern, H.; Gillen, D. L.] Univ Calif Irvine, Sch Informat & Comp Sci, Dept Stat, Irvine, CA 92617 USA; [Wu, J.] Univ Calif Irvine, Program Publ Hlth, Irvine, CA 92617 USA; [Ostro, B.] Calif Off Environm Hlth Hazard Assessment, Air Pollut Epidemiol Sect, Oakland, CA USA; [Lipsett, M.; Zhang, L.] Calif Dept Hlth Serv, Environm Hlth Investigat Branch, Exposure Assessment Sect, Oakland, CA USA; [Winer, A.] Univ Calif Los Angeles, Sch Publ Hlth, Dept Environm Hlth Sci, Los Angeles, CA 90024 USA; [Street, D. H.] Independent Consultant, Salem, OR USA	Delfino, RJ (reprint author), Univ Calif Irvine, Sch Med, Dept Epidemiol, 100 Theory Dr,Suite 100, Irvine, CA 92617 USA.	rdelfino@uci.edu			South Coast Air Quality Management District [04182]; National Institutes of Health, National Institute of Environmental Health Sciences [ES-11615]	This study was funded by the South Coast Air Quality Management District contract no. 04182, and the National Institutes of Health, National Institute of Environmental Health Sciences grant no. ES-11615.	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Environ. Med.	MAR	2009	66	3					189	197		10.1136/oem.2008.041376		9	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	410DM	WOS:000263557000009	19017694	
J	Bridevaux, PO; Gerbase, MW; Probst-Hensch, NM; Schindler, C; Gaspoz, JM; Rochat, T				Bridevaux, P-O; Gerbase, M. W.; Probst-Hensch, N. M.; Schindler, C.; Gaspoz, J-M; Rochat, T.			Long-term decline in lung function, utilisation of care and quality of life in modified GOLD stage 1 COPD	THORAX			English	Article							OBSTRUCTIVE PULMONARY-DISEASE; SF-36 HEALTH SURVEY; NUTRITION-EXAMINATION-SURVEY; NATIONAL-HEALTH; AIR-POLLUTION; UNITED-STATES; RISK-FACTORS; FOLLOW-UP; PREVALENCE; POPULATION	Background: Little is known about the long-term outcomes of individuals with mild chronic obstructive pulmonary disease ( COPD) as defined by the Global Initiative for Chronic Obstructive Lung Disease ( GOLD). Methods: A population cohort of 6671 randomly selected adults without asthma was stratified into categories of modified GOLD-defined COPD (prebronchodilator spirometry). Further stratification was based on the presence or absence of respiratory symptoms. After 11 years, associations between baseline categories of COPD and decline in forced expiratory volume in 1 s (FEV(1)), respiratory care utilisation and quality of life as measured by the SF-36 questionnaire were examined after controlling for age, sex, smoking and educational status. Results: At baseline, modified GOLD criteria were met by 610 (9.1%) participants, 519 (85.1%) of whom had stage 1 COPD. At follow-up, individuals with symptomatic stage 1 COPD (n=224) had a faster decline in FEV1 (-9 ml/year (95% CI -13 to -5)), increased respiratory care utilisation (OR 1.6 (95% CI 1.0 to 2.6)) and a lower quality of life than asymptomatic subjects with normal lung function (n=3627, reference group). In contrast, individuals with asymptomatic stage 1 COPD (n=295) had no significant differences in FEV1 decline (-3 ml/year (95% CI -7 to +1)), respiratory care utilisation (OR 1.05 (95% CI 0.63 to 1.73)) or quality of life scores compared with the reference group. Conclusions: In population-based studies, respiratory symptoms are of major importance for predicting long-term clinical outcomes in subjects with COPD with mild obstruction. Population studies based on spirometry only may misestimate the prevalence of clinically relevant COPD.	[Bridevaux, P-O; Gerbase, M. W.; Rochat, T.] Hop Cantonal Geneva, Div Pulm Med, CH-1211 Geneva, Switzerland; [Gaspoz, J-M] Univ Geneva, Univ Hosp Geneva, Div Community Med & Primary Care, CH-1211 Geneva 4, Switzerland; [Probst-Hensch, N. M.] Univ Zurich, Inst Social & Prevent Med, Mol Epidemiol Canc Registry, CH-8006 Zurich, Switzerland; [Probst-Hensch, N. M.] Univ Zurich, Inst Surg Pathol, Mol Epidemiol Canc Registry, CH-8006 Zurich, Switzerland; [Schindler, C.] Univ Basel, Inst Social & Prevent Med, Basel, Switzerland	Bridevaux, PO (reprint author), Hop Cantonal Geneva, Div Pulm Med, 24 Rue Micheli du Crest, CH-1211 Geneva, Switzerland.	Pierre-Olivier.Bridevaux@hcuge.ch	Schindler, Christian/D-3472-2015		Swiss National Science Foundation [4026-28099, 3347CO-108796, 3247BO-104283, 3247BO-104288, 3247BO-104284, 32-65896.01, 32-59302.99, 32-52720.97, 32-4253.94]	The Swiss National Science Foundation ( grants no 4026-28099, 3347CO-108796, 3247BO-104283, 3247BO-104288, 3247BO-104284, 32-65896.01, 32-59302.99, 32-52720.97, 32-4253.94), the Federal Office for Forest, Environment and Landscape, the Federal Office of Public Health, the Federal Office of Roads and Transport, the canton's government of Aargau, Basel-Stadt, Basel-Land, Geneva, Luzern, Ticino, Zurich, the Swiss Lung League, the canton's Lung League of Basel Stadt/Basel Landschaft, Geneva, Ticino and Zurich.	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J	Mudarri, D; Fisk, WJ				Mudarri, D.; Fisk, W. J.			Public health and economic impact of dampness and mold	INDOOR AIR			English	Article						public; health; economic; impact; dampness; mold	BUILDING-RELATED SYMPTOMS; ADOLESCENT SCHOOL-CHILDREN; RESPIRATORY SYMPTOMS; OFFICE WORKERS; RISK-FACTORS; FLOOR DUST; AIRWAY INFLAMMATION; ASTHMA PREVALENCE; SYSTEMIC SYMPTOMS; EXPOSURE	The public health risk and economic impact of dampness and mold exposures was assessed using current asthma as a health endpoint. Individual risk of current asthma from exposure to dampness and mold in homes from W.J. Fisk, Q. Lei-Gomez & M.J. Mendell [(2007) Indoor Air 17, 226-235], and asthma risks calculated from additional studies that reported the prevalence of dampness and mold in homes were used to estimate the proportion of US current asthma cases that are attributable to dampness and mold exposure at 21% (95% confidence internal 12-29%). An examination of the literature covering dampness and mold in schools, offices, and institutional buildings, which is summarized in the Appendix, suggests that risks from exposure in these buildings are similar to risks from exposures in homes. Of the 21.8 million people reported to have asthma in the USA, approximately 4.6 (2.7-6.3) million cases are estimated to be attributable to dampness and mold exposure in the home. Estimates of the national cost of asthma from two prior studies were updated to 2004 and used to estimate the economic impact of dampness and mold exposures. By applying the attributable fraction to the updated national annual cost of asthma, the national annual cost of asthma that is attributable to dampness and mold exposure in the home is estimated to be $3.5 billion ($2.1-4.8 billion). Analysis indicates that exposure to dampness and mold in buildings poses significant public health and economic risks in the USA. These findings are compatible with public policies and programs that help control moisture and mold in buildings.	Lawrence Berkeley Natl Lab, Indoor Environm Dept, Berkeley, CA 94720 USA; US EPA, Indoor Environm Div, Off Radiat & Indoor Air, Washington, DC 20460 USA	Fisk, WJ (reprint author), Lawrence Berkeley Natl Lab, Indoor Environm Dept, 1 Cyclotron Rd,90R3058, Berkeley, CA 94720 USA.	wjfisk@lbl.gov					Bornehag CG, 2001, INDOOR AIR, V11, P72; Bornehag CG, 2004, INDOOR AIR, V14, P243, DOI 10.1111/j.1600-0668.2004.00240.x; BRUNEKREEF B, 1989, AM REV RESPIR DIS, V140, P1363; *CDC, 2006, ENV HAZ HLTH EFF AST; *CDC, 2006, NCHS NHIS DATA ASTHM; *CDC, 2006, NAT CTR HLTH STAT HL; Chao HJ, 2003, ENVIRON HEALTH PERSP, V111, P1242, DOI 10.1289/ehp.5697; CHIAVERINI LC, 2003, HLTH NUMBERS, V5; Cox-Ganser JM, 2005, ENVIRON HEALTH PERSP, V113, P485, DOI 10.1289/ehp.7559; Dangman Kenneth H, 2005, Conn Med, V69, P9; Ebbehoj NE, 2005, INDOOR AIR, V15, P7, DOI 10.1111/j.1600-0668.2005.00352.x; FISK WJ, 2007, IN PRESS INDOOR AIR; Freeman NCG, 2003, J EXPO ANAL ENV EPID, V13, P169, DOI 10.1038/sj.jea.7500266; Hu FB, 1997, J ASTHMA, V34, P67, DOI 10.3109/02770909709071205; *IOM, 2004, BOARD HLTH PROM DIS; Lander F, 2001, INFLAMM RES, V50, P227, DOI 10.1007/s000110050748; LEVIN H, 2005, 58694 LBNL; Maier WC, 1997, ENVIRON HEALTH PERSP, V105, P208, DOI 10.1289/ehp.97105208; Mannino D. 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J	Roth, U; von Roepenack-Lahaye, E; Clemens, S				Roth, Udo; von Roepenack-Lahaye, Edda; Clemens, Stephan			Proteome changes in Arabidopsis thaliana roots upon exposure to Cd2+	JOURNAL OF EXPERIMENTAL BOTANY			English	Article						cadmium; heavy metal accumulation; heavy metal tolerance; MALDI-TOF-MS; phytochelatins; proteomics	GLUTATHIONE S-TRANSFERASES; POLYACRYLAMIDE-GELS; MEMBRANE PROTEOME; CADMIUM RESPONSE; PLANT-RESPONSES; FISSION YEAST; PROTEINS; STRESS; METALS; ACCUMULATION	Cadmium is a major environmental pollutant that enters human food via accumulation in crop plants. Responses of plants to cadmium exposure-which directly influence accumulation rates-are not well understood. In general, little is known about stress-elicited changes in plants at the proteome level. Alterations in the root proteome of hydroponically grown Arabidopsis thaliana plants treated with 10 mu M Cd2+ for 24 h are reported here. These conditions trigger the synthesis of phytochelatins (PCs), glutathione-derived metal-binding peptides, shown here as PC2 accumulation. Two-dimensional gel electrophoresis using different pH gradients in the first dimension detected on average similar to 1100 spots per gel type. Forty-one spots indicated significant changes in protein abundance upon Cd2+ treatment. Seventeen proteins found in 25 spots were identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Selected results were independently confirmed by western analysis and selective enrichment of a protein family (glutathione S-transferases) through affinity chromatography. Most of the identified proteins belong to four different classes: metabolic enzymes such as ATP sulphurylase, glycine hydroxymethyltransferase, and trehalose-6-phosphate phosphatase; glutathione S-transferases; latex allergen-like proteins; and unknown proteins. These results represent a basis for reverse genetics studies to better understand plant responses to toxic metal exposure and to the generation of internal sinks for reduced sulphur.	Leibniz Inst Plant Biochem, Halle, Germany	Clemens, S (reprint author), Leibniz Inst Plant Biochem, Halle, Germany.	sclemens@ipb-halle.de	Clemens, Stephan/A-5107-2009	Clemens, Stephan/0000-0003-0570-1060			Amme S, 2006, J EXP BOT, V57, P1537, DOI 10.1093/jxb/erj129; Baginsky S, 2006, J EXP BOT, V57, P1485, DOI 10.1093/jxb/erj130; Barbey R, 2005, EMBO J, V24, P521, DOI 10.1038/sj.emboj.7600556; BLUM H, 1987, ELECTROPHORESIS, V8, P93, DOI 10.1002/elps.1150080203; Carter C, 2004, PLANT CELL, V16, P3285, DOI 10.1105/tpc.104.027078; Castro AJ, 2005, J EXP BOT, V56, P2783, DOI 10.1093/jxb/eri271; Chen DR, 2003, MOL BIOL CELL, V14, P214, DOI 10.1091/mbc.E02-08-0499; Clemens S, 1998, P NATL ACAD SCI USA, V95, P12043, DOI 10.1073/pnas.95.20.12043; Clemens S, 1999, EMBO J, V18, P3325, DOI 10.1093/emboj/18.12.3325; Cobbett C, 2002, ANNU REV PLANT BIOL, V53, P159, DOI 10.1146/annurev.arplant.53.100301.135154; Connolly EL, 2002, PLANT CELL, V14, P1347, DOI 10.1105/tpc.001263; DEKNECHT JA, 1995, PLANT SCI, V106, P9, DOI 10.1016/0168-9452(95)04066-4; Dixon DP, 2002, GENOME BIOL, V3; Edwards R, 2000, TRENDS PLANT SCI, V5, P193, DOI 10.1016/S1360-1385(00)01601-0; FAIRBANKS G, 1971, BIOCHEMISTRY-US, V10, P2606, DOI 10.1021/bi00789a030; Fauchon M, 2002, MOL CELL, V9, P713, DOI 10.1016/S1097-2765(02)00500-2; Friso G, 2004, PLANT CELL, V16, P478, DOI 10.1105/tpc.017814; Garg AK, 2002, P NATL ACAD SCI USA, V99, P15898, DOI 10.1073/pnas.252637799; Gorg A, 2000, ELECTROPHORESIS, V21, P1037, DOI 10.1002/(SICI)1522-2683(20000401)21:6<1037::AID-ELPS1037>3.0.CO;2-V; GRUBBS FE, 1969, TECHNOMETRICS, V11, P1, DOI 10.2307/1266761; Harrison C, 2005, EMBO J, V24, P599, DOI 10.1038/sj.emboj.7600536; Heiss S, 1999, PLANT MOL BIOL, V39, P847, DOI 10.1023/A:1006169717355; Jarup L, 2003, BRIT MED BULL, V68, P167, DOI 10.1093/bmb/ldg032; Jones AME, 2004, PHYTOCHEMISTRY, V65, P1805, DOI 10.1016/j.phytochem.2004.04.005; Kaul S, 2000, NATURE, V408, P796; Kovalchuk I, 2005, MUTAT RES-FUND MOL M, V570, P149, DOI 10.1016/j.mrfmmm.2004.10.004; Lane TW, 2005, NATURE, V435, P42, DOI 10.1038/435042a; Markovic-Housley Z, 2003, J MOL BIOL, V325, P123, DOI 10.1016/S0022-2836(02)01197-X; Marmagne A, 2004, MOL CELL PROTEOMICS, V3, P675, DOI 10.1074/mcp.M400001-MCP200; NEUHOFF V, 1988, ELECTROPHORESIS, V9, P255, DOI 10.1002/elps.1150090603; NRIAGU JO, 1988, NATURE, V333, P134, DOI 10.1038/333134a0; Peck SC, 2001, PLANT CELL, V13, P1467, DOI 10.1105/tpc.13.6.1467; Peck SC, 2005, PLANT PHYSIOL, V138, P591, DOI 10.1104/pp.105.060285; Pinot F, 2000, Rev Environ Health, V15, P299; Saito K, 2004, PLANT PHYSIOL, V136, P2443, DOI 10.1104/pp.10.1104.046755; Sappl PG, 2004, PLANT MOL BIOL, V54, P205, DOI 10.1023/B:PLAN.0000028786.57439.b3; Sarry JE, 2006, PROTEOMICS, V6, P2180, DOI 10.1002/pmic.200500543; Sharma SS, 2006, J EXP BOT, V57, P711, DOI 10.1093/jxb/erj073; Shevchenko A, 1996, ANAL CHEM, V68, P850, DOI 10.1021/ac950914h; Smith AP, 2004, J BIOL CHEM, V279, P26098, DOI 10.1074/jbc.M402807200; Smith AP, 2003, PLANT J, V36, P433, DOI 10.1046/j.1365-313X.2003.01890.x; Suzuki N, 2001, PLANT CELL ENVIRON, V24, P1177, DOI 10.1046/j.1365-3040.2001.00773.x; Utriainen M, 1998, PLANT CELL ENVIRON, V21, P821, DOI 10.1046/j.1365-3040.1998.00326.x; Vatamaniuk OK, 2004, J BIOL CHEM, V279, P22449, DOI 10.1074/jbc.M313142200; Vido K, 2001, J BIOL CHEM, V276, P8469, DOI 10.1074/jbc.M008708200; von Roepenack-Lahaye E, 2004, PLANT PHYSIOL, V134, P548, DOI 10.1104/pp.103.032714; WAGNER GJ, 1993, ADV AGRON, V51, P173, DOI 10.1016/S0065-2113(08)60593-3; Weber M, 2006, PLANT CELL ENVIRON, V29, P950, DOI 10.1111/j.1365-3040.2005.01479.x; Xiang CB, 1998, PLANT CELL, V10, P1539, DOI 10.1105/tpc.10.9.1539; Zimmermann P, 2004, PLANT PHYSIOL, V136, P2621, DOI 10.1104/pp.104.046367	50	102	112	2	30	OXFORD UNIV PRESS	OXFORD	GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND	0022-0957			J EXP BOT	J. Exp. Bot.	DEC	2006	57	15					4003	4013		10.1093/jxb/erl170		11	Plant Sciences	Plant Sciences	115DX	WOS:000242716100004	17075075	
J	Derendorf, H; Nave, R; Drollmann, A; Cerasoli, F; Wurst, W				Derendorf, H.; Nave, R.; Drollmann, A.; Cerasoli, F.; Wurst, W.			Relevance of pharmacokinetics and pharmacodynamics of inhaled corticosteroids to asthma	EUROPEAN RESPIRATORY JOURNAL			English	Review						ciclesonide; clinical relevance; cortisol; lipid conjugation; on-site activation; side-effects	METERED-DOSE INHALER; ADRENAL AXIS FUNCTION; HIGH LUNG DEPOSITION; DRY POWDER INHALER; MOMETASONE FUROATE; FLUTICASONE PROPIONATE; PERSISTENT ASTHMA; BECLOMETHASONE DIPROPIONATE; INTRANASAL CORTICOSTEROIDS; OROPHARYNGEAL DEPOSITION	The pharmacokinetic and pharmacodynamic effects of inhaled corticosterolds (ICS) have shaped the efficacy and safety of these agents in the treatment of asthma. Important pharmacokinetic and pharmacodynamic characteristics that can enhance the efficacy of ICS include small particle size, high glucocorticoid-receptor-binding affinity, long pulmonary residence time and lipid conjugation. These characteristics can increase or prolong the anti-inflammatory effects of an ICS. Important pharmacokinetic characteristics that can enhance the safety of ICS include on-site activation in the lung, low oropharyngeal exposure, negligible oral bioavailability, high protein-binding and rapid systemic clearance. The degree of oropharyngeal exposure is relevant to local side-effects, such as oropharyngeal candidiasis, dysphonia and coughing. Pharmacokinetic properties that influence the degree of systemic exposure are relevant to the pharmacodynamic effect of ICS-induced hypothalamic-pituitary-adrenal axis suppression and cortisol suppression, an indicator of potential long-term systemic side-effects, such as reduced growth velocity and bone density, fractures, and skin bruising and thinning. Therefore, significant differences in the pharmacokinetic and pharmacodynamic characteristics of the currently available inhaled corticosteroids warrant careful consideration when used in clinical practice as they may result in differences in efficacy and local and systemic safety profiles.	Univ Florida, Dept Pharmaceut, Coll Pharm 100494, Gainesville, FL 32610 USA; ALTANA Pharm, Constance, Germany; ALTANA Pharm, Florham Pk, NJ USA	Derendorf, H (reprint author), Univ Florida, Dept Pharmaceut, Coll Pharm 100494, Gainesville, FL 32610 USA.	hartmut@cop.ufl.edu	Derendorf, Hartmut/B-4628-2012	Derendorf, Hartmut/0000-0003-4016-1370			Affrime MB, 2000, J CLIN PHARMACOL, V40, P1227; Agertoft L, 1999, J AEROSOL MED, V12, P161, DOI 10.1089/jam.1999.12.161; Balter MS, 2001, CHEST, V120, P1829, DOI 10.1378/chest.120.6.1829; Banov CH, 2004, J ASTHMA, V41, P5, DOI 10.1081/JAS-120026092; Barnes PJ, 2003, ANN INTERN MED, V139, P359; BARNES PJ, 1990, AM REV RESPIR DIS S, V141, P70; Bender B, 1997, ANN ALLERG ASTHMA IM, V79, P177; Berger WE, 2005, DRUGS, V65, P1973, DOI 10.2165/00003495-200565140-00005; Borgstrom L, 1999, J ALLERGY CLIN IMMUN, V104, pS246; BORGSTROM L, 1994, EUR RESPIR J, V7, P69, DOI 10.1183/09031936.94.07010069; Boulet LP, 2006, RESP MED, V100, P785, DOI 10.1016/j.rmed.2005.11.030; 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Resp. J.	NOV	2006	28	5					1042	1050		10.1183/09031936.00074905		9	Respiratory System	Respiratory System	104XP	WOS:000241994200026	17074919	
J	Brasche, S; Bischof, W				Brasche, S; Bischof, W			Daily time spent indoors in German homes - Baseline data for the assessment of indoor exposure of German occupants	INTERNATIONAL JOURNAL OF HYGIENE AND ENVIRONMENTAL HEALTH			English	Article						time patterns; time spent at home; German homes; exposure estimation	ACTIVITY-PATTERNS	Comprehensive time-activity studies, for use as a basis for estimates of personal exposure, are not readily available in Germany. This analysis of time spent indoors at home is based on data from "Dampness and mould in homes" (2000/ 2001) - a study of about 12,000 persons living in 5530 randomly selected apartments and houses in Germany. The results show the mean times per day people in Germany spend in their homes, classified by gender, age group, building location, city size, region, building type, owner-occupier status, number of people at home, smoking and ventilation habits, moisture emission and ill health factors such as asthma, allergy and number of acute respiratory infections per year. The overall mean time spent at home, 15.7 h per, is in accordance with results from US-American (15.6 h/day) and Canadian (15.8h/day) human activity surveys carried out in the nineties, as well as being consistent with the German Environmental Survey (1990/92) and a small German study in 1987. (c) 2005 Elsevier GmbH. All rights reserved.	Univ Jena, Inst Occupat Social & Environm Med, Dept Indoor Climatol, D-07740 Jena, Germany	Brasche, S (reprint author), Univ Jena, Inst Occupat Social & Environm Med, Dept Indoor Climatol, Bachstr 18, D-07740 Jena, Germany.	sabine.brasche@med.uni-jena.de					BRASCHE S, 2003, BUNDESGESUNDHIETSBL, V8, P683; Chapin F. S., 1974, HUMAN ACTIVITY PATTE; Dorre WH, 1997, J EXPO ANAL ENV EPID, V7, P471; EHLING M, 2003, BLEIBT ZEIT ZEITVERW; HARTMANN T, 2001, THESIS TU DRESDEN I; Krause C., 1998, UMWELTMED FORSCH PRA, V4, P249; Leech JA, 2002, J EXPO ANAL ENV EPID, V12, P427, DOI 10.1038/sj.jea.7500244; SCHMIDTHOPFNER SH, 1995, STANDARDS EXPOSITION, P41; Szalai A, 1972, USE TIME DAILY ACTIV	9	102	105	4	30	URBAN & FISCHER VERLAG	JENA	BRANCH OFFICE JENA, P O BOX 100537, D-07705 JENA, GERMANY	1438-4639			INT J HYG ENVIR HEAL	Int. J. Hyg. Environ. Health.		2005	208	4					247	253		10.1016/j.ijheh.2005.03.003		7	Public, Environmental & Occupational Health; Infectious Diseases	Public, Environmental & Occupational Health; Infectious Diseases	952OT	WOS:000231016100003	16078638	
J	Basagana, X; Sunyer, J; Kogevinas, M; Zock, JP; Duran-Tauleria, E; Jarvis, D; Burney, P; Anto, JM				Basagana, X; Sunyer, J; Kogevinas, M; Zock, JP; Duran-Tauleria, E; Jarvis, D; Burney, P; Anto, JM		European Community Respiratory Hlt	Socioeconomic status and asthma prevalence in young adults - The European Community Respiratory Health Survey	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						adult; asthma; education; prevalence; social class	DIAGNOSED ASTHMA; ADMISSION RATES; AIR-POLLUTION; RISK-FACTORS; SOCIAL-CLASS; SYMPTOMS; EPIDEMIOLOGY; CHILDREN; AREA; DEPRIVATION	The authors assessed the association between asthma prevalence and socioeconomic status at both the individual and center levels simultaneously .by using data from 32 centers in 15 countries. Included were 10,971 subjects aged 20-44 years selected from the general population and interviewed in 1991-1992. Socioeconomic status at both the individual and aggregated levels was measured on the basis of occupation and educational level. Associations were assessed by using multilevel models adjusted for age, sex, body mass index, parental asthma, childhood respiratory infections, presence of immunoglobulin E to common allergens, rhinitis, smoking, and occupational exposure to irritants. Asthma prevalence was higher in lower socioeconomic groups, whether defined by educational level (odds ratio for finishing full-time studies-<16 vs. >19 years = 1.28, 95% confidence interval: 1.00, 1.64) or social class (odds ratio for semiskilled and unskilled manual workers vs. professional/managerial = 1.51, 95% confidence interval: 1.20, 1.90), regardless of atopic status. The relation was consistent between centers. Irrespective of individual socioeconomic status, subjects living in areas in which educational levels were lower had a higher risk of asthma (p < 0.05). This center-level association partially explained geographic differences in asthma prevalence, but considerable heterogeneity still remained. The authors concluded that community influences of living in a low-educational area are associated with asthma, independently of subjects' own educational level and social class.	Inst Municipal Invest Med, Resp & Environm Hlth Res Unit, E-08003 Barcelona, Spain; Univ Pompeu Fabra, Dept Expt & Hlth Sci, Barcelona, Spain; Kings Coll London, Dept Publ Hlth Sci, London WC2R 2LS, England	Sunyer, J (reprint author), Inst Municipal Invest Med, Resp & Environm Hlth Res Unit, Doctor Aiguader 80, E-08003 Barcelona, Spain.	jsunyer@imim.es	Jarvis, Deborah/E-6494-2011; Basagana, Xavier/C-3901-2017; Kogevinas, Manolis/C-3918-2017; Anto, J/H-2676-2014; Sunyer, J/G-6909-2014	Basagana, Xavier/0000-0002-8457-1489; Anto, J/0000-0002-4736-8529; Sunyer, J/0000-0002-2602-4110			Bozicevic I, 2000, COLLEGIUM ANTROPOL, V24, P325; Brunekreef B, 2003, EUR RESPIR J, V21, P913, DOI 10.1183/09031936.03.00014903; BURNEY PGJ, 1989, EUR RESPIR J, V2, P940; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; Chan-Yeung M., 1999, ASTHMA WORKPLACE, P129; Chatkin JM, 1999, CHEST, V116, P1780, DOI 10.1378/chest.116.6.1780; Chen JT, 2002, ENVIRON HEALTH PERSP, V110, P211; CLARK NM, 1990, PATIENT EDUC COUNS, V15, P191, DOI 10.1016/0738-3991(90)90062-P; CONNOLLY CK, 1989, POSTGRAD MED J, V65, P282; Court CS, 2002, THORAX, V57, P951, DOI 10.1136/thorax.57.11.951; *CTR MULT MOD, 2001, MLWIN VERS 1 1 MULT; Diez-Roux AV, 2000, ANNU REV PUBL HEALTH, V21, P171, DOI 10.1146/annurev.publhealth.21.1.171; Douwes J, 2002, INT J EPIDEMIOL, V31, P1098, DOI 10.1093/ije/31.6.1098; Duran-Tauleria E, 1999, THORAX, V54, P476; ERNST P, 1995, AM J RESP CRIT CARE, V152, P570; Erzen D, 1997, AM J RESP CRIT CARE, V155, P1060; Goldstein H., 1995, MULTILEVEL STAT MODE; Hedeker D, 1996, COMPUT METH PROG BIO, V49, P157, DOI 10.1016/0169-2607(96)01720-8; HOX JJ, 1995, APPL MULTILEVELS ANA; ISOAHO R, 1994, J CLIN EPIDEMIOL, V47, P1109, DOI 10.1016/0895-4356(94)90097-3; Janson C, 1997, EUR RESPIR J, V10, P1795, DOI 10.1183/09031936.97.10081795; Janson C, 2001, EUR RESPIR J, V18, P598, DOI 10.1183/09031936.01.00205801; Kogevinas M, 1998, EUR RESPIR J, V11, P1363, DOI 10.1183/09031936.98.11061363; Kreft Ita G. 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J	Bjorksten, B				Bjorksten, B			Effects of intestinal microflora and the environment on the development of asthma and allergy	SPRINGER SEMINARS IN IMMUNOPATHOLOGY			English	Article						intestinal microflora; environment; asthma and allergy	PLACEBO-CONTROLLED TRIAL; NEONATAL GUT FLORA; ATOPIC DISEASE; PARENTAL SMOKING; EARLY-CHILDHOOD; INFECTIOUS-DISEASES; BCG VACCINATION; EARLY EXPOSURE; HOUSE-DUST; SCHOOL-AGE	The aim of previous research into the causes of allergic diseases, including asthma was mostly to identify potential risk factors in the environment. No major risk factors have been identified, however. Over the past 10 years, focus has, therefore, more been directed towards protective factors that could enhance the development of tolerance to allergens which were previously encountered early in life, but are now lost in modern affluent societies. In particular, the role of childhood infections has been discussed, but so far these studies have not been conclusive. Recent epidemiological studies and experimental research suggest that the microbial environment and exposure to microbial products in infancy modifies immune responses and enhances the development of tolerance to ubiquitous allergens. The intestinal microflora may play a particular role in this respect, as it is the major external driving force in the maturation of the immune system after birth, and animal experiments have shown it to be a prerequisite for normal development of oral tolerance. Recent studies have shown differences in the composition of the microflora between healthy and allergic infants in countries with a high and low prevalence of allergies and between healthy and allergic infants within such countries. These differences are apparent within the first week of life and thus precede clinical symptoms. The use of live microorganisms that might be beneficial to health has a long tradition and the safety is well documented. Very recently, several prospective intervention studies, modifying the gut flora from birth have yielded encouraging results and may suggest a new mode of primary prevention of allergy in the future.	Karolinska Inst, Ctr Allergy Res, S-17177 Stockholm, Sweden; Karolinska Inst, Dept Environm Med, S-17177 Stockholm, Sweden	Bjorksten, B (reprint author), Karolinska Inst, Ctr Allergy Res, S-17177 Stockholm, Sweden.	bengt.bjorksten@cfa.ki.se					Adlerberth I, 1998, EPIDEMIOL INFECT, V121, P587, DOI 10.1017/S0950268898001484; Alm JS, 1997, LANCET, V350, P400, DOI 10.1016/S0140-6736(97)02207-1; Anyo G, 2002, CLIN EXP ALLERGY, V32, P361, DOI 10.1046/j.1365-2222.2002.01254.x; Azizi B. H. 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Immunopathol.	FEB	2004	25	3-4					257	270		10.1007/s00281-003-0142-2		14	Immunology; Pathology	Immunology; Pathology	801IP	WOS:000220089900003	15007630	
J	Hashimoto, M; Kisseleva, L; Sawa, S; Furukawa, T; Komatsu, S; Koshiba, T				Hashimoto, M; Kisseleva, L; Sawa, S; Furukawa, T; Komatsu, S; Koshiba, T			A novel rice PR10 protein, RSOsPR10, specifically induced in roots by biotic and abiotic stresses, possibly via the jasmonic acid signaling pathway	PLANT AND CELL PHYSIOLOGY			English	Article						fungal infection; jasmonic acid; Oryza sativa; pathogenesis-related (PR) protein; root specific; stress response	PATHOGENESIS-RELATED PROTEINS; BIRCH POLLEN ALLERGEN; PISUM-SATIVUM L; DISEASE RESISTANCE; ABSCISIC-ACID; RIBONUCLEASE-ACTIVITY; SEQUENCE SIMILARITY; TRANSGENIC TOBACCO; GENE-EXPRESSION; CDNA CLONING	Plant roots have important roles not only in absorption of water and nutrients, but also in stress tolerance such as desiccation, salt, and low temperature. We have investigated stress-response proteins from rice roots using 2-dimensional polyacrylamide-gel electrophoresis and found a rice protein, RO-292, which was induced specifically in roots when 2-week-old rice seedlings were subjected to salt and drought stress. The full-length RO-292 cDNA was cloned, and was determined to encode a protein of 160 amino acid residues (16.9 kDa, pI 4.74). The deduced amino acid sequence showed high similarity to known rice PR10 proteins, OSPR10a/PBZ1 and OsPR10b. RO-292 mRNA accumulated rapidly upon drought, NaCl, jasmonic acid and probenazole, but not by exposure to low temperature or by abscisic acid and salicylic acid. The RO-292 gene was also up-regulated by infection with rice blast fungus. Interestingly, induction was observed almost exclusively in roots, thus we named the gene RSOsPR10 (root specific rice PR10). The present results indicate that RSOsPR10 is a novel rice PR10 protein, which is rapidly induced in roots by salt, drought stresses and blast fungus infection possibly through activation of the jasmonic acid signaling pathway, but not the abscisic acid and salicylic acid signaling pathway.	Tokyo Metropolitan Univ, Dept Biol Sci, Hachioji, Tokyo 1920397, Japan; Moscow MV Lomonosov State Univ, Ctr Biotechnol, Moscow 119992, Russia; Univ Tokyo, Grad Sch Sci, Dept Biol Sci, Bunkyo Ku, Tokyo 1130033, Japan; Tokyo Metropolitan Coll, Akishima, Tokyo 1968540, Japan; Natl Inst Agrobiol Sci, Dept Mol Genet, Tsukuba, Ibaraki 3058602, Japan	Koshiba, T (reprint author), Tokyo Metropolitan Univ, Dept Biol Sci, Minami Osawa, Hachioji, Tokyo 1920397, Japan.	koshiba-tomokazu@c.metro-u.ac.jp					Agrawal Ganesh Kumar, 2002, Proteomics, V2, P947, DOI 10.1002/1615-9861(200208)2:8<947::AID-PROT947>3.0.CO;2-J; Agrawal GK, 2002, PLANT PHYSIOL BIOCH, V40, P1061, DOI 10.1016/S0981-9428(02)01471-7; ALEXANDER D, 1993, P NATL ACAD SCI USA, V90, P7327, DOI 10.1073/pnas.90.15.7327; Bantignies B, 2000, PLANT MOL BIOL, V42, P871, DOI 10.1023/A:1006475303115; BARRATT DHP, 1991, PLANTA, V184, P14, DOI 10.1007/BF00208230; BREITENEDER H, 1995, EUR J BIOCHEM, V233, P484, DOI 10.1111/j.1432-1033.1995.484_2.x; BREITENEDER H, 1989, EMBO J, V8, P1935; Bufe A, 1996, PLANTA, V199, P413; Carpin S, 1998, PLANT MOL BIOL, V36, P791, DOI 10.1023/A:1005951208815; CLAES B, 1990, PLANT CELL, V2, P19, DOI 10.1105/tpc.2.1.19; CROWELL DN, 1992, PLANT MOL BIOL, V18, P459, DOI 10.1007/BF00040662; Ekramoddoullah AKM, 2000, PHYSIOL PLANTARUM, V110, P240, DOI 10.1034/j.1399-3054.2000.110214.x; FRISTENSKY B, 1988, PLANT MOL BIOL, V11, P713, DOI 10.1007/BF00017470; Fujimoto Y, 1998, EUR J BIOCHEM, V258, P794, DOI 10.1046/j.1432-1327.1998.2580794.x; Gajhede M, 1996, NAT STRUCT BIOL, V3, P1040, DOI 10.1038/nsb1296-1040; Gonneau M, 2001, PLANT MOL BIOL, V46, P539, DOI 10.1023/A:1010693213437; HoffmannSommergruber K, 1997, GENE, V197, P91, DOI 10.1016/S0378-1119(97)00246-1; Huang JC, 1997, PLANT MOL BIOL, V34, P681, DOI 10.1023/A:1005824306560; ITURRIAGA EA, 1994, PLANT MOL BIOL, V24, P235, DOI 10.1007/BF00040591; Jwa NS, 2001, BIOCHEM BIOPH RES CO, V286, P973, DOI 10.1006/bbrc.2001.5507; Lee MW, 2001, MOL PLANT MICROBE IN, V14, P527, DOI 10.1094/MPMI.2001.14.4.527; LINTHORST HJM, 1991, CRIT REV PLANT SCI, V10, P123, DOI 10.1080/07352689109382309; Lo SCC, 1999, MOL PLANT MICROBE IN, V12, P479, DOI 10.1094/MPMI.1999.12.6.479; MATTON DP, 1989, MOL PLANT MICROBE IN, V2, P325, DOI 10.1094/MPMI-2-325; McGee J. 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J	Valenta, R; Kraft, D				Valenta, R; Kraft, D			From allergen structure to new forms of allergen-specific immunotherapy	CURRENT OPINION IN IMMUNOLOGY			English	Review							BIRCH POLLEN ALLERGEN; DUST MITE ALLERGEN; T-CELL EPITOPE; CROSS-REACTIVE ALLERGEN; SKIN PRICK TEST; BET-V-I; ENGINEERED HYPOALLERGENIC DERIVATIVES; ASPERGILLUS-FUMIGATUS ALLERGENS; QUANTITATIVE IGE INHIBITION; SITE-DIRECTED MUTAGENESIS	During the past decade, genetic information for most of the common allergens has been obtained. Using these genetic blueprints it has become possible to reconstruct, by recombinant DNA technology, almost complete repertoires of the relevant allergens and their epitopes. Recombinant allergens with the allergenic features of naturally occurring allergens have promoted allergy research and form the basis of new multiallergen tests for refined allergy diagnosis. Allergen derivatives with reduced allergenic activity have also been produced by recombinant DNA technology to increase safety and specificity of allergen-specific immunotherapy. These derivatives can be engineered to contain relevant T cell epitopes and to maintain those sequence motifs which are required for inducing protective antibody responses and therefore hold great promise for improving allergen-specific immunotherapy.	Univ Vienna, Sch Med, Dept Pathophysiol, A-1090 Vienna, Austria	Valenta, R (reprint author), Univ Vienna, Sch Med, Dept Pathophysiol, Waehringer Guertel 18-20, A-1090 Vienna, Austria.	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Opin. Immunol.	DEC	2002	14	6					718	727		10.1016/S0952-7915(02)00402-8		10	Immunology	Immunology	607VZ	WOS:000178812600007	12413521	
J	Portengen, L; Sigsgaard, T; Omland, O; Hjort, C; Heederik, D; Doekes, G				Portengen, L; Sigsgaard, T; Omland, O; Hjort, C; Heederik, D; Doekes, G			Low prevalence of atopy in young Danish farmers and farming students born and raised on a farm	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						atopy; Denmark; farm childhood; farming; IgE; skin prick tests; young farmers	HAY-FEVER; ALLERGIC SENSITIZATION; RESPIRATORY SYMPTOMS; STORAGE MITES; ASTHMA; EXPOSURE; CHILDREN; DUST; RISK; POPULATION	Background Recent studies have shown that in several countries atopic sensitization to common allergens (common atopy) and atopic symptoms are markedly less prevalent in children living on a farm, compared with non-farm children living in the same rural areas. Living conditions on farms may, however, vary largely between different countries. It is also not yet known whether the 'protective' effect of a farm environment can also be found in adults. Materials and methods Common atopy and respiratory health were assessed by skin prick tests (SPT), questionnaire and measurement of bronchial hyper-responsiveness (BHR) in the Sund Stald (SUS) study, a cohort study on respiratory health in Danish farming students and conscripts from the same rural areas as controls. Results of SPT were confirmed by IgE serology in all SPT+ subjects and a subset of SPT- subjects. Prevalences of common atopy, respiratory symptoms and bronchial hyper- responsiveness were compared for farmers and controls, and for those who had or had not lived on a farm in early childhood. Results In multiple logistic regression analyses adjusting for ever smoking and a familial history of allergy, both being a farmer (ORs 0.62-0.75) and having had a farm childhood (ORs 0.55-0.75) appeared to contribute independently to a lower risk of sensitization to common allergens as assessed by SPT and IgE serology. A farm childhood was also inversely associated with high total IgE (OR 0.68), presence of respiratory symptoms (ORs 0.69-0.79) and BHR (OR 0.61) in these analyses. Direction and strength of the association between being a farmer and respiratory symptoms or BHR varied widely (ORs 0.69-1.28). Conclusions The 'anti-atopy' protective effect of a farm childhood could be confirmed in Danish farming students: prevalences of positive SPT, specific and total IgE, allergic symptoms and BHR were lower in those being born or raised on a farm. Past exposure to the farm environment in early childhood may therefore also contribute to a lower risk of atopic sensitization and disease at a later age.	Univ Utrecht, Inst Risk Assessment Sci, NL-3508 TD Utrecht, Netherlands; Univ Aarhus, Dept Environm & Occupat Med, DK-8000 Aarhus C, Denmark	Doekes, G (reprint author), Univ Utrecht, Inst Risk Assessment Sci, POB 80176, NL-3508 TD Utrecht, Netherlands.						Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; Bjorksten B, 1999, CLIN EXP ALLERGY, V29, P342; BLAINEY AD, 1988, THORAX, V43, P697, DOI 10.1136/thx.43.9.697; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; CROOK B, 1991, AM IND HYG ASSOC J, V52, P271, DOI 10.1202/0002-8894(1991)052<0271:ADAMAA>2.0.CO;2; Doekes G, 1996, OCCUP ENVIRON MED, V53, P63; DONHAM KJ, 1986, AM J IND MED, V10, P294, DOI 10.1002/ajim.4700100318; Ernst P, 2000, AM J RESP CRIT CARE, V161, P1563; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Holt PG, 1997, PEDIATR ALLERGY IMMU, V8, P53, DOI 10.1111/j.1399-3038.1997.tb00145.x; 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; IVERSEN M, 1990, CLIN EXP ALLERGY, V20, P211, DOI 10.1111/j.1365-2222.1990.tb02670.x; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Lewis SA, 2000, CLIN EXP ALLERGY, V30, P153; Martinez FD, 1999, J ALLERGY CLIN IMMUN, V103, P355, DOI 10.1016/S0091-6749(99)70456-2; Matricardi PM, 2000, BRIT MED J, V320, P412, DOI 10.1136/bmj.320.7232.412; MATSON SC, 1983, J ALLERGY CLIN IMMUN, V72, P299, DOI 10.1016/0091-6749(83)90035-0; Omland O, 1999, EUR RESPIR J, V13, P31, DOI 10.1183/09031936.99.13103199; Parvaneh S, 1999, ALLERGY, V54, P229, DOI 10.1034/j.1398-9995.1999.00855.x; Radon K, 2000, ALLERGY, V55, P219, DOI 10.1034/j.1398-9995.2000.00461.x; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Schenker MB, 1998, AM J RESP CRIT CARE, V158, pS1; Sigsgaard T., 1997, J AGROMED, V4, P63, DOI 10.1300/J096v04n01_09; VANHAGEHAMSTEN M, 1987, CLIN ALLERGY, V17, P417; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; von Mutius E, 2000, J ALLERGY CLIN IMMUN, V105, P9, DOI 10.1016/S0091-6749(00)90171-4	28	102	103	1	8	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	FEB	2002	32	2					247	253		10.1046/j.1365-2222.2002.01310.x		7	Allergy; Immunology	Allergy; Immunology	537PM	WOS:000174767800017	11929489	
J	Weber, RW				Weber, RW			Cross-reactivity of plant and animal allergens	CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY			English	Review							BIRCH-POLLEN ALLERGEN; SHORT RAGWEED POLLEN; TIMOTHY GRASS-POLLEN; GROUP-I ALLERGENS; T-CELL EPITOPES; COMPLEMENTARY-DNA CLONING; MAJOR APPLE ALLERGEN; DUST-MITE ALLERGENS; AMINO-ACID-SEQUENCE; SHARE IGE EPITOPES		Austin Allergy Associates, Austin, TX 78749 USA	Weber, RW (reprint author), Austin Allergy Associates, 6600 S Mopac Expressway,Suite 2180, Austin, TX 78749 USA.						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Rev. Allergy Immunol.	OCT	2001	21	2-3					153	202		10.1385/CRIAI:21:2-3:153		50	Allergy; Immunology	Allergy; Immunology	485LC	WOS:000171755000005	11725603	
J	D'Amato, G; Liccardi, G; D'Amato, M; Cazzola, M				D'Amato, G; Liccardi, G; D'Amato, M; Cazzola, M			The role of outdoor air pollution and climatic changes on the rising trends in respiratory allergy	RESPIRATORY MEDICINE			English	Article						air pollution; bronchial asthma; airway hyper-responsiveness; hay fever; pollinosis; respiratory allergy; urban pollution	DIESEL EXHAUST PARTICLES; POLLEN-RELATED ALLERGY; GRASS-POLLEN; ASTHMATIC-CHILDREN; PARTICULATE MATTER; OZONE EXPOSURE; HEALTH; INFLAMMATION; MORTALITY; AIRWAYS	Evidence suggests that allergic respiratory diseases such as hay fever and bronchial asthma have become more common world-wide in the last two decades, and the reasons for this increase are still largely unknown. A major responsible factor could be outdoor air pollution, derived from cars and other vehicles. Studies have demonstrated that urbanization and high levels of vehicle emissions and westernized lifestyle is correlated with the increasing frequency of pollen-induced respiratory allergy. People who live in urban areas tend to be more affected by pollen-induced respiratory allergy than those from of rural areas. Pollen allergy has been one of the most frequent models used to study the interrelationship between air pollution and respiratory allergic diseases. Pollen grains or plant-derived paucimicronic components carry allergens that can produce allergic symptoms. They may also interact with air pollution (particulate matter; ozone) in producing these effects. There is evidence that air pollutants may promote airway sensitization by modulating the allergenicity of airborne allergens. Furthermore, airway mucosal damage and impaired mucociliary clearance induced by air pollution may facilitate the access Of inhaled allergens to the cells of the immune system. In addition, vegetation reacts with air pollution and environmental conditions and influence the plant allergenicity. Several factors influence this interaction, including type of air pollutants, plant species, nutrient balance: climatic factors, degree of airway sensitization and hyperresponsiveness of exposed subjects.	Azienda Osped Alta Specialita A Cardarelli, Div Pneumol & Allergol, I-80121 Naples, Italy	D'Amato, G (reprint author), Azienda Osped Alta Specialita A Cardarelli, Div Pneumol & Allergol, Via Rione Sirignano,10, I-80121 Naples, Italy.		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J	Belamarich, PF; Luder, E; Kattan, M; Mitchell, H; Islam, S; Lynn, H; Crain, EF				Belamarich, PF; Luder, E; Kattan, M; Mitchell, H; Islam, S; Lynn, H; Crain, EF			Do obese inner-city children with asthma have more symptoms than nonobese children with asthma?	PEDIATRICS			English	Article; Proceedings Paper	37th Annual Meeting of the Ambulatory-Pediatric-Association	MAY 02-06, 1997	WASHINGTON, D.C.	Ambulatory Pediat Assoc		asthma; obesity; children; peak expiratory flow; inner-city	BODY-MASS INDEX; UNITED-STATES; ADOLESCENTS; OVERWEIGHT; ASSOCIATION; SAMPLE; GROWTH; BLACK	Objective. To test whether obesity is associated with decreased peak expiratory flow rates (PEFR), increased asthma symptoms, and increased health service use. Design/Methods. Secondary analysis of data from a cross-sectional convenience sample. Setting. Emergency departments (EDs) and primary care clinics in 8 inner-city areas in 7 cities. Participants. One thousand three hundred twenty-two children aged 4 to 9 years with asthma. Measures. Obesity was defined as a body mass index (BMI, weight/height(2)) >95th percentile. Nonobese children were those with a BMI between the 5th and 95th percentile. Underweight children with a BMI <5th percentile were eliminated from the study. Demographic and anthropometric data were obtained during a baseline interview with the primary caretaker and the child. Symptoms, health service use data and measurements of PEFR were obtained by parental report during the baseline interview and at 3-month intervals by telephone interview over the following 9-month period. Results. Obese (n = 249) and nonobese (n = 1073) children did not differ in terms of age, gender, family income, passive smoke exposure, caretaker's mental health, and skin test reactivity to indoor allergens. Obese children were more often Latino (28% vs 17%) and, in the 3 months before the baseline interview, were more likely to have used oral steroids (30% vs 24%). There were no differences between groups in terms of baseline PEFR scores. During the 9 months after baseline assessment, the obese group had a higher mean number of days of wheeze per 2-week period (4.0 vs 3.4), and a greater proportion of obese individuals had unscheduled ED visits (39% vs 31%). There were no differences between the groups in terms of frequency of hospitalization, or in nocturnal awakening. Conclusions. In our sample of inner-city children with asthma, obese children used more medicine, wheezed more, and a greater proportion had unscheduled ED visits than the nonobese children.	Childrens Hosp Montefiore, Albert Einstein Coll Med, Dept Pediat, Div Gen Pediat, Bronx, NY USA; Mt Sinai Sch Med, Dept Pediat, New York, NY USA; Rho Inc, Chapel Hill, NC USA; Michigan State Univ, Flint, MI USA; Albert Einstein Coll Med, Jacobi Med Ctr, Dept Pediat, Bronx, NY 10467 USA	Belamarich, PF (reprint author), Pediat Acad Associates, 1621 Eastchester Rd, Bronx, NY 10461 USA.		Islam, Shaheen/E-3288-2011		NIAID NIH HHS [AI-30752, AI-30756, UO1 AI-30751]		Camargo CA, 1999, ARCH INTERN MED, V159, P2582, DOI 10.1001/archinte.159.21.2582; Dietz WH, 1998, J PEDIATR-US, V132, P191; Dixon JB, 1999, OBES SURG, V9, P385, DOI 10.1381/096089299765552981; Eid N, 2000, PEDIATRICS, V105, P354, DOI 10.1542/peds.105.2.354; FUNG KP, 1990, ARCH DIS CHILD, V65, P512; Gennuso J, 1998, ARCH PEDIAT ADOL MED, V152, P1197; GORTMAKER SL, 1987, AM J DIS CHILD, V141, P535; HSU KHK, 1979, J PEDIATR-US, V95, P192; INSELMAN LS, 1993, PEDIATR PULM, V16, P130, DOI 10.1002/ppul.1950160209; KAPLAN TA, 1993, CLIN PEDIATR, V32, P220, DOI 10.1177/000992289303200407; Lazarus R, 1997, PEDIATR PULM, V24, P187; Luder E, 1998, J PEDIATR-US, V132, P699, DOI 10.1016/S0022-3476(98)70363-4; McCowan C, 1998, BRIT MED J, V316, P668; Mitchell H, 1997, PEDIATR PULM, V24, P237; Najjar MF, 1987, VITAL HLTH STATISTIC, P238; Pietrobelli A, 1998, J PEDIATR-US, V132, P204, DOI 10.1016/S0022-3476(98)70433-0; RAY CS, 1983, AM REV RESPIR DIS, V128, P501; ROCHE AF, 1981, AM J CLIN NUTR, V34, P2831; Rosner B, 1998, J PEDIATR-US, V132, P211, DOI 10.1016/S0022-3476(98)70434-2; SCHWARTZ J, 1990, AM REV RESPIR DIS, V142, P555; SHOHAT M, 1987, ARCH DIS CHILD, V62, P63; TROIANO RP, 1995, ARCH PEDIAT ADOL MED, V149, P1085; Wade S, 1997, PEDIATR PULM, V24, P263, DOI 10.1002/(SICI)1099-0496(199710)24:4<263::AID-PPUL5>3.0.CO;2-L; 1992, MMWR MORB MORTAL WKL, V41, P733	24	102	108	1	4	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	DEC	2000	106	6					1436	1441		10.1542/peds.106.6.1436		6	Pediatrics	Pediatrics	383ZP	WOS:000165914800034	11099600	
J	Nielsen, KG; Bisgaard, H				Nielsen, KG; Bisgaard, H			The effect of inhaled budesonide on symptoms, lung function, and cold air and methacholine responsiveness in 2-to 5-year-old asthmatic children	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							YOUNG-CHILDREN; DRY AIR; BRONCHIAL RESPONSIVENESS; INHALATION SUSPENSION; NEBULIZED BUDESONIDE; PERSISTENT ASTHMA; CHALLENGE; HISTAMINE; INFANTS; HYPERVENTILATION	We hypothesized that measurement of lung function (LF) and bronchial hyperresponsiveness (BHR) could serve as supplemental tools in evaluating the efficacy of treatment with inhaled corticosteroids in asthmatic children aged 2 to 5 yr. We studied 38 children (mean age: 53 mo; range: 35 to 71 mo) with moderately severe asthma in a single-center, randomized, double-blind, parallel-group, placebo-controlled study involving 8 wk of treatment. Budesonide (BUD) 400 mu g twice daily was administered via a pressurized metered-dose inhaler and metal spacer device. Symptom scores (SSc) and use of short-acting beta(2)-agonist were monitored with diary cards. LF in awake children was measured as the specific airway resistance (sRaw), using whole-body plethysmography; as resistance by the interrupter technique (Rint); and as resistance and reactance at 5 Hz (Rrs5, Xrs5) by the impulse oscillation technique. Cold air challenge (CACh) and methacholine challenge (MCh) were used to assess BHR. Children in the BUD group experienced significantly fewer night- and daytime symptoms (p < 0.05) and more symptom-free days (p < 0.05), but not nights (p = 0.07), than children in the placebo group. Daytime (p < 0.05) but not nighttime (p = 0.09) use of rescue medication and asthma exacerbation rates (3.7 versus 9.3 exacerbations/yr) (p = 0.006) were both in favor of BUD. LF measured with the Rint technique, Rrs5, and Xrs5 were significantly improved by BUD. BHR as measured by CACh improved significantly with BUD, whereas no improvement was found on MCh. In conclusion, inhaled BUD at a total dose of 800 mu g daily significantly Improved SSc, asthma exacerbation rates, lung function, and BHR as assessed by CACh in asthmatic children aged 2 to 5 yr.	Univ Copenhagen Hosp, Rigshosp, Dept Pediat, DK-2100 Copenhagen, Denmark	Bisgaard, H (reprint author), Univ Copenhagen Hosp, Rigshosp, Dept Pediat, DK-2100 Copenhagen, Denmark.		Kronow, Joern/B-1054-2011	Bisgaard, Hans/0000-0003-4131-7592			Baker JW, 1999, PEDIATRICS, V103, P414, DOI 10.1542/peds.103.2.414; BISGAARD H, 1990, LANCET, V336, P649, DOI 10.1016/0140-6736(90)92147-A; Bisgaard H, 1999, AM J RESP CRIT CARE, V160, P126; Bisgaard H, 2000, AM J RESP CRIT CARE, V162, P187; Bisgaard H, 1995, EUR RESPIR J, V8, P2067, DOI 10.1183/09031936.95.08122067; Claussen M, 1993, Pneumologie, V47, P209; CONNETT GJ, 1993, ARCH DIS CHILD, V69, P351; DEAL EC, 1980, AM REV RESPIR DIS, V121, P621; DEBENEDICTIS FM, 1995, PEDIATR PULM, V19, P326, DOI 10.1002/ppul.1950190603; deBlic J, 1996, J ALLERGY CLIN IMMUN, V98, P14, DOI 10.1016/S0091-6749(96)70221-X; Fischer AR, 1997, THORAX, V52, P1074; ILANGOVAN P, 1993, ARCH DIS CHILD, V68, P356; KANENGISER S, 1994, PEDIATR PULM, V18, P144, DOI 10.1002/ppul.1950180305; Kemp JP, 1999, ANN ALLERG ASTHMA IM, V83, P231, DOI 10.1016/S1081-1206(10)62646-4; Klug B, 1997, PEDIATR PULM, V23, P278, DOI 10.1002/(SICI)1099-0496(199704)23:4<278::AID-PPUL5>3.0.CO;2-I; 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; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; MCLAUGHLIN FJ, 1983, PEDIATRICS, V72, P503; MODL M, 1995, EUR RESPIR J, V8, P1742, DOI 10.1183/09031936.95.08101742; Nielsen KG, 2000, AM J RESP CRIT CARE, V161, P1805; REISMAN J, 1987, PEDIATR PULM, V3, P251, DOI 10.1002/ppul.1950030410; SLY PD, 1990, J ASTHMA, V27, P137, DOI 10.3109/02770909009073314; Sont JK, 1999, AM J RESP CRIT CARE, V159, P1043; STICK SM, 1995, ARCH DIS CHILD, V73, P327; TAL A, 1984, J PEDIATR-US, V104, P516, DOI 10.1016/S0022-3476(84)80539-9; VATHENEN AS, 1991, THORAX, V46, P811, DOI 10.1136/thx.46.11.811; Warner JO, 1998, PEDIATR PULM, V25, P1; ZACH M, 1995, PEDIATR PULM, V19, P323, DOI 10.1002/ppul.1950190602; ZACH M, 1984, PEDIATR RES, V18, P469, DOI 10.1203/00006450-198405000-00016; ZACH MS, 1987, J ALLERGY CLIN IMMUN, V80, P9, DOI 10.1016/S0091-6749(87)80184-7	33	102	104	0	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	2000	162	4					1500	1506				7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	364RD	WOS:000089905900052	11029368	
J	Kelly, D; Coutts, AGP				Kelly, D; Coutts, AGP			Early nutrition and the development of immune function in the neonate	PROCEEDINGS OF THE NUTRITION SOCIETY			English	Article; Proceedings Paper	Summer Meeting of the Nutrition-Society	JUN 29-JUL 02, 1999	UNIV GLASGOW, GLASGOW, SCOTLAND	Nutr Soc	UNIV GLASGOW	intestine; immunity; neonate; colostrum	INTESTINAL EPITHELIAL-CELLS; FIMBRIATED ESCHERICHIA-COLI; BLOOD GROUP ANTIGENS; HUMAN-MILK; T-CELLS; IMMUNOHISTOCHEMICAL ANALYSIS; MUCOSAL SURFACES; SUCKLING PIGS; EXPRESSION; COLOSTRUM	The present review will concentrate on the development of the gut-associated lymphoid tissue and the role of early nutrition in promoting immune function. The intestine is the largest immune organ in the body, and as such is the location for the majority of lymphocytes and other immune effector cells. The intestine is exposed to vast quantities of dietary and microbial antigens, and is the most common portal of entry for pathogens, some of which are potentially lethal. The development of normal immune function of the intestine is therefore vital for survival, and is dependent on appropriate antigen exposure and processing, and also an intact intestinal barrier. In early life innate mechanisms of defence are probably more important than active or adaptive mechanisms in responding to an infectious challenge, since the healthy neonate is immunologically naive (has not seen antigen) and has not acquired immunological memory. During this period maternal colostrum and milk can significantly augment resistance to enteric infections. The mechanisms of enhancing disease resistance are thought to be passive, involving a direct supply of anti-microbial factors, and active, by promoting the development of specific immune function. A tolerance response to dietary and non-invasive antigens is generally induced in the gut. However, it must also be able to mount an adequate immune response to ensure clearance of foreign antigens. It is now recognized that regulation of tolerance and active immune responses is critical to health, and failure to regulate these responses can lead to recurrent infections, inflammatory diseases and allergies. The education of the immune system in early life is thought to be critical in minimizing the occurrence of these immune-based disorders. During this phase of development maternal milk provides signals to the immune system that generate appropriate response and memory. One factor that has been proposed to contribute to the increase in the incidence of immune-based disorders, e.g. atopic diseases in Western countries, is thought to be the increased prevalence of formula-feeding.	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J	Little, SA; Chalmers, GW; MacLeod, KJ; McSharry, C; Thomson, NC				Little, SA; Chalmers, GW; MacLeod, KJ; McSharry, C; Thomson, NC			Non-invasive markers of airway inflammation as predictors of oral steroid responsiveness in asthma	THORAX			English	Article						airway inflammation; nitric oxide; induced sputum eosinophilia; asthma; corticosteroids	NITRIC-OXIDE; EXHALED AIR; SPUTUM	Background-Sputum eosinophil counts and exhaled nitric oxide (NO) levels are increased in asthma and both measurements fall in response to corticosteroids. Methods-Exhaled NO levels and sputum eosinophil counts were assessed as noninvasive markers of the response to an oral steroid in 37 patients (19 women) with stable chronic asthma (mean (SD) age 48.6 (12.2) years, asthma duration 25.9 (17.3) years, and baseline forced expiratory volume in one second (FEV1) 76.3 (21.9)% predicted). Spirometric tests, with reversibility to a beta agonist (2.5 mg nebulised salbutamol), and induced sputum (using nebulised 3% saline) were performed at recruitment and following treatment with 30 mg prednisolone/day for 14 days. Results-Baseline NO levels correlated with the percentage improvement in FEV, from baseline to the post-steroid, postbronchodilator value (r(s) = 0.47, p = 0.003), with an NO level of >10 ppb at baseline having a positive predictive value of 83% for an improvement in FEV, of greater than or equal to 15% (sensitivity 59%, specificity 90%). Sputum eosinophilia (greater than or equal to 4%) had a positive predictive value of 68% (sensitivity 54%, specificity 76%) for an increase in FEV1 of greater than or equal to 15%. A combination of sputum eosinophilia and increased NO levels resulted in a positive predictive value of 72% and a negative predictive value of 79% (sensitivity 76%, specificity 75%). Conclusion-Exhaled NO levels and sputum eosinophilia may be useful in predicting the response to a trial of oral steroid in asthma.	Univ Glasgow, Western Infirm, Dept Resp Med, Glasgow G11 6NT, Lanark, Scotland; Univ Glasgow, Western Infirm, Dept Immunol, Glasgow G11 6NT, Lanark, Scotland	Little, SA (reprint author), Univ Glasgow, Western Infirm, Dept Resp Med, Glasgow G11 6NT, Lanark, Scotland.			Thomson, Neil/0000-0003-1632-6630			Fabbri LM, 1998, AM J RESP CRIT CARE, V157, pS195; HARGREAVE FE, 1981, J ALLERGY CLIN IMMUN, V68, P347, DOI 10.1016/0091-6749(81)90132-9; Kharitonov S, 1997, EUR RESPIR J, V10, P1683, DOI 10.1183/09031936.97.10071683; KHARITONOV SA, 1994, LANCET, V343, P133, DOI 10.1016/S0140-6736(94)90931-8; Kharitonov SA, 1996, AM J RESP CRIT CARE, V153, P454; Pavord ID, 1999, LANCET, V353, P2213, DOI 10.1016/S0140-6736(99)01813-9; PIN I, 1992, THORAX, V47, P25, DOI 10.1136/thx.47.1.25; POPOV T, 1994, CLIN EXP ALLERGY, V24, P778, DOI 10.1111/j.1365-2222.1994.tb00990.x; TURNER MO, 1995, THORAX, V50, P1057, DOI 10.1136/thx.50.10.1057; Vignola AM, 1998, AM J RESP CRIT CARE, V157, P403	10	102	107	0	0	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	MAR	2000	55	3					232	234		10.1136/thorax.55.3.232		3	Respiratory System	Respiratory System	289JE	WOS:000085616400011	10679543	
J	Locke, GR; Zinsmeister, AR; Talley, NJ; Fett, SL; Melton, LJ				Locke, GR; Zinsmeister, AR; Talley, NJ; Fett, SL; Melton, LJ			Risk factors for irritable bowel syndrome: Role of analgesics and food sensitivities	AMERICAN JOURNAL OF GASTROENTEROLOGY			English	Article							FUNCTIONAL GASTROINTESTINAL DISORDERS; EPIDEMIOLOGY; POPULATION; PREVALENCE; SYMPTOMS; DYSPEPSIA; HISTORY	OBJECTIVE: Symptoms of irritable bowel syndrome (IBS) are reported by 10% of the general population; however, evaluation of traditional risk factors has not provided any insight into the pathogenesis of this condition. The objective of this study was to identify additional risk factors for irritable bowel syndrome. METHODS: A valid self-report questionnaire that records the gastrointestinal (GI) symptoms required for a diagnosis of IBS, self-reported measures of potential risk factors, and a psychosomatic symptom checklist was mailed to an age- and gender-stratified random sample of Olmsted County, Minnesota residents aged 30-64 yr. A logistic regression model that adjusted for age, gender, and psychosomatic symptom score was used to identify factors significantly associated with IBS. RESULTS: A total of 643 (72%) of 892 eligible subjects returned the survey. IBS symptoms were reported by 12% of the respondents. IBS was significantly associated with use of analgesics (acetaminophen, aspirin, or nonaspirin nonsteroidal antiinflammatory drugs) for reasons other than IBS, reporting a food allergy or sensitivity, and ratings of somatic symptoms. No association was detected for age, gender, body mass index, smoking history, alcohol use, educational level, exposure to pets in the household, or water supply. Among subjects reporting the use of just one type of analgesic, IBS was associated with acetaminophen but not aspirin or nonaspirin nonsteroidal antiinflammatory drugs used alone. The odds of having IBS were higher among subjects reporting more reasons for taking analgesics and intolerance to a higher number of foods. CONCLUSIONS: IBS is significantly associated with analgesic use. However, this is confounded by other somatic pain complaints. IBS symptoms are associated with the reporting of many food allergies or sensitivities. The role of food-induced symptoms in IBS requires further investigation.	Mayo Clin & Mayo Fdn, Div Gastroenterol & Internal Med, Rochester, MN 55905 USA; Mayo Clin & Mayo Fdn, Dept Hlth Sci Res, Rochester, MN 55905 USA	Locke, GR (reprint author), Mayo Clin & Mayo Fdn, Div Gastroenterol & Internal Med, 200 1st St SW, Rochester, MN 55905 USA.		Talley, nicholas/D-5399-2013	Talley, nicholas/0000-0003-2537-3092	NIA NIH HHS [AG09440]; NIAMS NIH HHS [AR30582]		AGREUS L, 1995, GASTROENTEROLOGY, V109, P671, DOI 10.1016/0016-5085(95)90373-9; AGREUS L, 1994, SCAND J GASTROENTERO, V29, P102, DOI 10.3109/00365529409090447; ATTANASIO V, 1984, J BEHAV MED, V7, P247, DOI 10.1007/BF00845390; DROSSMAN DA, 1993, DIGEST DIS SCI, V38, P1569, DOI 10.1007/BF01303162; Drossman DA, 1997, GASTROENTEROLOGY, V112, P2120, DOI 10.1053/gast.1997.v112.agast972120; KAY L, 1994, J INTERN MED, V236, P23; KURLAND LT, 1981, SCI AM, V245, P54; Locke GR, 1997, GASTROENTEROLOGY, V112, P1448, DOI 10.1016/S0016-5085(97)70025-8; Locke GR, 1996, GASTROENTEROL CLIN N, V25, P1, DOI 10.1016/S0889-8553(05)70362-9; LONGSTRETH GF, 1993, DIGEST DIS SCI, V38, P1581, DOI 10.1007/BF01303163; Melton LJ, 1996, MAYO CLIN PROC, V71, P266; Niec AM, 1998, AM J GASTROENTEROL, V93, P2184; TALLEY NJ, 1995, AM J EPIDEMIOL, V142, P76; TALLEY NJ, 1992, AM J EPIDEMIOL, V136, P165; TALLEY NJ, 1991, EUR J GASTROEN HEPAT, V3, P71; TALLEY NJ, 1994, GASTROENTEROLOGY, V107, P1040; TALLEY NJ, 1989, ANN INTERN MED, V111, P671; TALLEY NJ, 1993, GASTROENTEROLOGY, V105, P781; TALLEY NJ, 1991, GASTROENTEROLOGY, V101, P927; Thompson WG, 1989, GASTROENTEROL INT, P92	20	102	104	0	5	ELSEVIER SCIENCE INC	NEW YORK	655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA	0002-9270			AM J GASTROENTEROL	Am. J. Gastroenterol.	JAN	2000	95	1					157	165				9	Gastroenterology & Hepatology	Gastroenterology & Hepatology	273CY	WOS:000084690800028	10638576	
J	Kanatani, KT; Ito, I; Al-Delaimy, WK; Adachi, Y; Mathews, WC; Ramsdell, JW				Kanatani, Kumiko T.; Ito, Isao; Al-Delaimy, Wael K.; Adachi, Yuichi; Mathews, William C.; Ramsdell, Joe W.		Toyama Asian Desert Dust Asthma St	Desert Dust Exposure Is Associated with Increased Risk of Asthma Hospitalization in Children	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						Asian dust; Kosa; mineral dust; African dust; quartz	ASIAN SAND DUST; BIDIRECTIONAL CASE-CROSSOVER; OPTICAL-PARTICLE COUNTER; PEAK EXPIRATORY FLOW; RESPIRATORY SYMPTOMS; PARTICULATE MATTER; LIDAR MEASUREMENTS; HUMAN HEALTH; TRADE WINDS; AEROSOL	Rationale: Desert dust particles, including quartz, which causes inflammatory responses in the airway in animal studies, are transported to widespread regions around the globe. Epidemiologically, areas impacted by desert dust storms, such as communities in the Middle East and the Caribbean, seem to have higher incidences of asthma than might be expected. Objectives: We investigated the magnitude of association between airborne mineral dust concentration and hospitalization of children for asthma exacerbation by using Light Detection And Ranging (LIDAR) with a polarization analyzer for an exposure measurement, which can distinguish mineral dust particles from other particles. Methods: A case-crossover design was used. The exposure measurement was LIDAR's nonspherical extinction coefficient. The outcome measurement was hospitalization of children aged 1 to 15 years for asthma exacerbation in eight principal hospitals in Toyama, a local area in japan bordering the Japan Sea, during February to April, 2005 to 2009. Measurements and Main Results: During the study period, there were 620 admissions for asthma exacerbation, and 6 days with a heavy dust event (daily mineral dust concentration > 0.1 mg/m(3)). Conditional logistic regression showed a statistically significant association between asthma hospitalization and a heavy dust event. The crude odds ratio (OR) of the heavy dust event for hospitalization on the day was 1.88 (95% confidence interval [Cl], 1.04-3.41; P = 0.037), and the OR of heavy dust event during the previous week was 1.83 (95% Cl, 1.31-2.56; P = 0.00043). The OR adjusted by other air pollutant levels, pollen, and meteorological factors was 1.71 (95% Cl, 1.18-2.48; P = 0.0050). Conclusions: Heavy dust events are associated with an increased risk of hospitalizations for asthma.	[Kanatani, Kumiko T.] Kyoto Univ, Grad Sch Med, Sakyo Ku, Kyoto 6068507, Japan; [Ito, Isao] Kyoto Univ, Dept Resp Med, Kyoto 6068507, Japan; [Kanatani, Kumiko T.] Univ Calif San Diego, Clin Res Course, San Diego, CA 92103 USA; [Al-Delaimy, Wael K.] Univ Calif San Diego, Dept Family & Prevent Med, San Diego, CA 92103 USA; [Mathews, William C.] Univ Calif San Diego, Dept Med, San Diego, CA 92103 USA; [Adachi, Yuichi] Toyama Univ, Dept Pediat, Fac Med, Toyama 930, Japan	Kanatani, KT (reprint author), Kyoto Univ, Grad Sch Med, Sakyo Ku, 54 Shogoin Kawahara Cho, Kyoto 6068507, Japan.	kumiko.kanatani@ax7.ecs.kyoto-u.ac.jp	Kanatani, Kumiko/C-8276-2011; MORENO-GRAU, STELLA/E-6540-2012; Mathews, William/E-4451-2010	Mathews, William/0000-0002-2352-0725	National Institutes of Health	K.T.K. was a full-time employee for 1 year and a part-time employee for 2 years of Bayer Yakuhin, Ltd and received up to $1,000 from Taiho Seiyaku for a lecture at a seminar. I.I. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. W.K.A-D. received 85,001 S10,000 for serving as an expert witness for the Hansen Food Company. Y.A. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. W.C.M. received more than $100,001 from the National Institutes of Health in sponsored grants. J.W.R. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript.	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J	Thomas, WR; Hales, BJ; Smith, WA				Thomas, Wayne R.; Hales, Belinda J.; Smith, Wendy-Anne			House dust mite allergens in asthma and allergy	TRENDS IN MOLECULAR MEDICINE			English	Review							BLOMIA-TROPICALIS ALLERGENS; IGE CROSS-REACTIVITY; DERMATOPHAGOIDES-PTERONYSSINUS; MAJOR ALLERGEN; CYSTEINE PROTEASES; STRUCTURAL BIOLOGY; CRYSTAL-STRUCTURE; ESCHERICHIA-COLI; P 2; RECOMBINANT	IgE antibodies in house dust mite (HDM) allergy follow a predictable pattern. Half are directed against two dominant allergens and the remainder largely against four midpotency allergens. This hierarchical pattern is not changed by the titre of the IgE response or severity of disease. The structures of these allergens are known and they can be produced as authentic recombinant allergens. There is also evidence that the allergenicity is augmented by the biological activity of the key allergens, validating them as targets for vaccination. Collectively, these developments should facilitate the development of new diagnostics, improve immunotherapy and allow vaccination with defined reagents. Highly purified recombinant polypeptides representing the important mite allergens are now available so that informative and reproducible experiments can be performed with mite allergens in place of poorly defined and variable extracts.	[Thomas, Wayne R.; Hales, Belinda J.; Smith, Wendy-Anne] Univ Western Australia, Ctr Child Hlth Res, Telethon Inst Child Hlth Res, Subiaco, WA 6008, Australia	Thomas, WR (reprint author), Univ Western Australia, Ctr Child Hlth Res, Telethon Inst Child Hlth Res, 100 Roberts Rd, Subiaco, WA 6008, Australia.	wayne@ichr.uwa.edu.au	Hales, Belinda/C-3858-2013	Hales, Belinda/0000-0003-2193-3996	National Health and Medical Research Council	The authors are supported by the National Health and Medical Research Council.	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Med	JUL	2010	16	7					321	328		10.1016/j.molmed.2010.04.008		8	Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental	Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine	632YY	WOS:000280467200004	20605742	
J	Halonen, JI; Lanki, T; Yli-Tuomi, T; Tiittanen, P; Kulmala, M; Pekkanen, J				Halonen, Jaana I.; Lanki, Timo; Yli-Tuomi, Tarja; Tiittanen, Pekka; Kulmala, Markku; Pekkanen, Juha			Particulate Air Pollution and Acute Cardiorespiratory Hospital Admissions and Mortality Among the Elderly	EPIDEMIOLOGY			English	Article							EMERGENCY-DEPARTMENT VISITS; SOURCE APPORTIONMENT; ULTRAFINE PARTICLES; EUROPEAN CITIES; FINE PARTICLES; AMBIENT PM2.5; URBAN AIR; ASSOCIATIONS; HEALTH; HELSINKI	Background: It is known that particulate air pollution affects cardiorespiratory health; however, it is unclear which particle size fractions and sources of particles are responsible for the health effects. Methods: Daily levels of nucleation (<0.03 mu m), Aitken (0.03-0.1 mu m), accumulation (0.1-0.29 mu m), and coarse mode (2.5-10 mu m) particles, particles with diameter <2.5 mu m (PM(2.5)), and gaseous pollutants were measured at central outdoor measurement sites in Helsinki, Finland between 1998 and 2004. We determined the associations of particles with daily cardiorespiratory mortality and acute hospital admissions among the elderly (>= 65 years). For the analyses we used Poisson generalized additive models and for the source apportionment of PM(2.5) we used the EPA positive matrix factorization method. Results: There was a suggestion of an association of hospital admissions for arrhythmia with Aitken mode particles and PM,., from traffic. Otherwise few associations were observed between various sizes and types of particles and either cardiovascular admissions or mortality. In contrast, most particle fractions had positive associations with admissions for pneumonia and asthma-chronic obstructive pulmonary disease (COPD). The strongest and most consistent associations were found for accumulation mode particles (3.1%; 95% confidence interval = 0.43-5.8 for pneumonia over the 5-day mean, and 3.8%; 1.3-6.3 for asthma-COPD at lag 0, for an interquartile increase in particles). We also found a positive association of respiratory mortality mainly with accumulation mode particles (5.1%; 1.2-9.0 at lag 0). Conclusions: All particle fractions including Aitken, accumulation, and coarse mode had especially adverse respiratory health effects among the elderly. Overall associations were stronger for respiratory than for cardiovascular outcomes.	[Halonen, Jaana I.; Lanki, Timo; Yli-Tuomi, Tarja; Tiittanen, Pekka; Pekkanen, Juha] Natl Publ Hlth Inst KTL, Environm Epidemiol Unit, FIN-70701 Kuopio, Finland; [Kulmala, Markku] Univ Helsinki, Dept Phys Sci, Helsinki, Finland; [Pekkanen, Juha] 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	Centre of Excellence Programme 2002-2007 of the Academy of Finland [53307]; TEKES [40715/01]; Ministry of Education (Graduate School in Environment Health SYTYKE)	Supported by the Centre of Excellence Programme 2002-2007 of the Academy of Finland (Contract 53307), the National Technology Fund (TEKES, Contract 40715/01), and the Ministry of Education (Graduate School in Environment Health SYTYKE).	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A., 2008, ENV HLTH PERSPECT, V116, P459; Schwarze PE, 2006, HUM EXP TOXICOL, V25, P559, DOI 10.1177/096032706072520; Vallius M, 2005, SCI TOTAL ENVIRON, V337, P147, DOI 10.1016/j.scitotenv.2004.06.018; Vallius M, 2003, ATMOS ENVIRON, V37, P615, DOI 10.1016/S1352-2310(02)00925-1; WHO, 2007, WHO WORKSH BONN GERM; Wood SN, 2000, J ROY STAT SOC B, V62, P413, DOI 10.1111/1467-9868.00240; Zanobetti A, 2006, J EPIDEMIOL COMMUN H, V60, P890, DOI 10.1136/jech.2005.039834	42	101	107	5	23	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	1044-3983			EPIDEMIOLOGY	Epidemiology	JAN	2009	20	1					143	153		10.1097/EDE.0b013e31818c7237		11	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	387DB	WOS:000261930800023	19234403	
J	Farfel, M; DiGrande, L; Brackbill, R; Prann, A; Cone, J; Friedman, S; Walker, DJ; Pezeshki, G; Thomas, P; Galea, S; Williamson, D; Frieden, TR; Thorpe, L				Farfel, Mark; DiGrande, Laura; Brackbill, Robert; Prann, Angela; Cone, James; Friedman, Stephen; Walker, Deborah J.; Pezeshki, Grant; Thomas, Pauline; Galea, Sandro; Williamson, David; Frieden, Thomas R.; Thorpe, Lorna			An Overview of 9/11 Experiences and Respiratory and Mental Health Conditions among World Trade Center Health Registry Enrollees	JOURNAL OF URBAN HEALTH-BULLETIN OF THE NEW YORK ACADEMY OF MEDICINE			English	Article						World Trade Center; Asthma; Respiratory symptoms; Posttraumatic stress disorder; Serious psychological distress; Population estimates of WTC disaster health outcomes; World Trade Center Health Registry (WTCHR); Environmental exposures; New York City; Children; Terrorism; WTC attacks; Epidemiology; Mental health	POSTTRAUMATIC-STRESS-DISORDER; NEW-YORK-CITY; SEPTEMBER-11 TERRORIST ATTACKS; NATIONAL COMORBIDITY SURVEY; CENTER DISASTER SITE; ST-HELENS ERUPTIONS; PTSD CHECKLIST; PULMONARY-FUNCTION; CIVILIAN VERSION; POLICE OFFICERS	To date, health effects of exposure to the September 11, 2001 disaster in New York City have been studied in specific groups, but no studies have estimated its impact across the different exposed populations. This report provides an overview of the World Trade Center Health Registry (WTCHR) enrollees, their exposures, and their respiratory and mental health outcomes 2-3 years post-9/11. Results are extrapolated to the estimated universe of people eligible to enroll in the WTCHR to determine magnitude of impact. Building occupants, persons on the street or in transit in lower Manhattan on 9/11, local residents, rescue and recovery workers/volunteers, and area school children and staff were interviewed and enrolled in the WTCHR between September 2003 and November 2004. A total of 71,437 people enrolled in the WTCHR, for 17.4% coverage of the estimated eligible exposed population (nearly 410,000); 30% were recruited from lists, and 70% were self-identified. Many reported being in the dust cloud from the collapsing WTC Towers (51%), witnessing traumatic events (70%), or sustaining an injury (13%). After 9/11, 67% of adult enrollees reported new or worsening respiratory symptoms, 3% reported newly diagnosed asthma, 16% screened positive for probable posttraumatic stress disorder (PTSD), and 8% for serious psychological distress (SPD). Newly diagnosed asthma was most common among rescue and recovery workers who worked on the debris pile (4.1%). PTSD was higher among those who reported Hispanic ethnicity (30%), household income <$25,000 (31%), or being injured (35%). Using previously published estimates of the total number of exposed people per WTCHR eligibility criteria, we estimate between 3,800 and 12,600 adults experienced newly diagnosed asthma and 34,600-70,200 adults experienced PTSD following the attacks, suggesting extensive adverse health impacts beyond the immediate deaths and injuries from the acute event.	[Farfel, Mark; DiGrande, Laura; Prann, Angela; Cone, James; Friedman, Stephen; Walker, Deborah J.; Pezeshki, Grant; Frieden, Thomas R.; Thorpe, Lorna] New York City Dept Hlth & Mental Hyg, New York, NY USA; [Brackbill, Robert; Williamson, David] Agcy Tox Subst & Dis Registry, Atlanta, GA USA; [Thomas, Pauline] Univ Med & Dent New Jersey, New Jersey Med Sch, Newark, NJ 07103 USA; [Galea, Sandro] Univ Michigan, Sch Publ Hlth, Ann Arbor, MI 48109 USA	Farfel, M (reprint author), New York City Dept Hlth & Mental Hyg, New York, NY USA.	mfarfel@health.nyc.gov			CDC's National Center for Environmental Health [U50/ATU272750]	This research was supported by Cooperative Agreement Number U50/ATU272750 from the Agency for Toxic Substances and Disease Registry with additional funding from the CDC's National Center for Environmental Health. The contents of this article are solely the responsibility of the authors and do not necessarily represent the official views of the ATSDR. The manuscript underwent ATSDR external peer review.	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Urban Health	NOV	2008	85	6					880	909		10.1007/s11524-008-9317-4		30	Public, Environmental & Occupational Health; Medicine, General & Internal	Public, Environmental & Occupational Health; General & Internal Medicine	376JU	WOS:000261180700009	18785012	
J	Friedman, DS; Hahn, SR; Gelb, L; Tan, J; Shah, SN; Kim, EE; Zimmerman, TJ; Quigley, HA				Friedman, David S.; Hahn, Steven R.; Gelb, Laurie; Tan, Jason; Shah, Sonali N.; Kim, Elizabeth E.; Zimmerman, Thom J.; Quigley, Harry A.			Doctor-patient communication, health-related beliefs, and adherence in glaucoma	OPHTHALMOLOGY			English	Article							BEHAVIORAL SKILLS MODEL; MANAGED CARE POPULATION; PHARMACY CLAIMS DATA; OPEN-ANGLE GLAUCOMA; QUALITY-OF-LIFE; ANTIRETROVIRAL THERAPY; FUTURE-DIRECTIONS; ASTHMA-TREATMENT; CHRONIC DISEASE; EMPIRICAL-TEST	Objective: To use multiple data sources to determine drivers of patient adherence to topical ocular hypotensive therapy. Design: Retrospective database and chart reviews in combination with prospective patient surveys. Diverse medical environments where insured patients in the research database seek care. Participants: Three hundred patients with a new claim diagnosis for open-angle glaucoma who initially were prescribed one of three prostaglandins and 103 physicians participating in the same medical plans. Methods: A structured interview addressing self-reported adherence, experiences with medication, communication with the physician, and health-related beliefs associated with adherence behavior was administered to surveyed patients. Phone interviews were conducted with participating ophthalmologists. Main Outcome Measure: Of adherence, medication possession ratio. Results: Eight variables were associated independently with a lower medication possession ratio: (1) hearing all of what you know about glaucoma from your doctor (compared with some or nothing); (2) not believing that reduced vision is a risk of not taking medication as recommended; (3) having a problem paying for medications; (4) difficulty while traveling or away from home; (5) not acknowledging stinging and burning; (6) being nonwhite; (7) receiving samples; and (8) not receiving a phone call visit reminder. The multivariate model explained 21% of the variance. Conclusions: These findings indicate that doctor-patient communications and health-related beliefs of patients contribute to patient adherence. Patient learning styles that are associated with less concern about the future effects of glaucoma and the risks of not taking medications are associated with lower adherence. Specifically, knowledge about potential vision loss from glaucoma is a critical element that tends to be missed by more passive doctor-dependent patients who tend to be poorly adherent. These findings suggest that educational efforts in the office may improve patient adherence to medical therapies.	[Friedman, David S.; Quigley, Harry A.] Wilmer Eye Inst, Baltimore, MD 21287 USA; [Friedman, David S.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Int Hlth, Baltimore, MD USA; [Hahn, Steven R.] Albert Einstein Coll Med, Dept Med, Bronx, NY 10467 USA; [Hahn, Steven R.] Albert Einstein Coll Med, Dept Psychiat, Bronx, NY 10467 USA; [Hahn, Steven R.] Medintel On Call, Pleasantville, NY USA; [Tan, Jason] HealthCore Inc, Wilmington, DE USA; [Shah, Sonali N.; Kim, Elizabeth E.] Pfizer Inc, New York, NY USA; [Zimmerman, Thom J.] Univ Louisville, Sch Med, Dept Ophthalmol & Visual Sci, Louisville, KY 40292 USA	Friedman, DS (reprint author), Johns Hopkins Univ Hosp, 600 N Wolfe St,Wilmer 120, Baltimore, MD 21287 USA.	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J	Skold, M; Borje, A; Harambasic, E; Karlberg, AT				Skold, M; Borje, A; Harambasic, E; Karlberg, AT			Contact allergens formed on air exposure of linalool. Identification and quantification of primary and secondary oxidation products and the effect on skin sensitization	CHEMICAL RESEARCH IN TOXICOLOGY			English	Article							LYMPH-NODE ASSAY; 15-HYDROPEROXYABIETIC ACID; D-LIMONENE; HYDROPEROXIDE; AUTOXIDATION; REARRANGEMENT; MONOTERPENES; MECHANISM; ALDEHYDES; RESPONSES	Linalool (3,7-dimethyl-1,6-octadien-3-ol) is an important fragrance chemical, frequently used in scented products because of its fresh, flowery odor. Linalool is an unsaturated hydrocarbon and is therefore susceptible to oxidation in the presence of air. The primary oxidation products, that is, hydroperoxides, formed in the autoxidation process, are reactive compounds that can be suspected to act as sensitizers. In the present investigation, we studied the autoxidation of linalool with emphasis on the formation of hydroperoxides. The oxidation products were isolated using flash chromatography and preparative HPLC and were identified with NMR and GC/ MS, using synthesized reference compounds. Two hydroperoxides and several different secondary oxidation products were identified, among which some contain structural features that make them potential allergens. The amounts of linalool and the major oxidation products were quantified over time, using GC and an HPLC-method, suitable for the analysis of thermolabile primary oxidation products. The hydroperoxide 7-hydroperoxy-3,7-dimethylocta-1,5-diene-3-ol was found to be present in 15% in an oxidized sample. The local lymph node assay (LLNA) was used to investigate the sensitizing potential of pure linalool, two samples of air-exposed linalool, and oxidation products of linalool (an alpha,beta-unsaturated aldehyde, a mixture of two hydroperoxides, and an alcohol). Pure linalool showed no sensitizing potential. The air-exposed samples of linalool produced clearly positive responses, and the hydroperoxides were the strongest allergens of the tested oxidation products. The study demonstrates the importance of autoxidation on the sensitizing potential of linalool. We also conclude that the sensitizing potential differs with the composition of the oxidation mixture and thus with the air exposure time.	Univ Gothenburg, Dept Chem Dermatochem & Skin Allergy, SE-41296 Gothenburg, Sweden; Natl Inst Working Life, SE-11391 Stockholm, Sweden	Karlberg, AT (reprint author), Univ Gothenburg, Dept Chem Dermatochem & Skin Allergy, SE-41296 Gothenburg, Sweden.	karlberg@chem.gu.se	Borje, Anna/A-7581-2010; Karlberg, Ann-Therese/A-7706-2010	Skold, Maria/0000-0002-4231-8864			BACKSTROM P, 1982, ACTA CHEM SCAND B, V36, P31, DOI 10.3891/acta.chem.scand.36b-0031; Basketter DA, 2002, CONTACT DERMATITIS, V47, P161, DOI 10.1034/j.1600-0536.2002.470307.x; Basketter DA, 2001, CONTACT DERMATITIS, V45, P89, DOI 10.1034/j.1600-0536.2001.045002089.x; Basketter DA, 1999, J APPL TOXICOL, V19, P261, DOI 10.1002/(SICI)1099-1263(199907/08)19:4<261::AID-JAT572>3.0.CO;2-5; Basketter DA, 1998, FOOD CHEM TOXICOL, V36, P327, DOI 10.1016/S0278-6915(97)00158-0; Beckwith A. L. 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DEC	2004	17	12					1697	1705		10.1021/tx049831z		9	Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology	Pharmacology & Pharmacy; Chemistry; Toxicology	881XK	WOS:000225902600019	15606147	
J	Neidell, MJ				Neidell, MJ			Air pollution, health, and socio-economic status: the effect of outdoor air quality on childhood asthma	JOURNAL OF HEALTH ECONOMICS			English	Article						pollution; health; asthma; socio-economic status; avoidance behavior; zip code fixed effect	ACUTE RESPIRATORY ILLNESS; EMERGENCY-ROOM VISITS; CHILDREN; DISEASE; CITIES; IMPACT	This paper estimates the effect of air pollution on child hospitalizations for asthma using naturally occurring seasonal variations in pollution within zip codes. Of the pollutants considered, carbon monoxide (CO) has a significant effect on asthma for children ages 1-18: if 1998 pollution levels were at their 1992 levels, there would be a 5-14% increase in asthma admissions. Also, households respond to information about pollution with avoidance behavior, suggesting it is important to account for these endogenous responses when measuring the effect of pollution on health. Finally, the effect of pollution is greater for children of lower socio-economic status (SES), indicating that pollution is one potential mechanism by which SES affects health. (C) 2004 Elsevier B.V. All rights reserved.	Univ Chicago, CISES, Chicago, IL 60637 USA	Neidell, MJ (reprint author), Univ Chicago, CISES, 5734 S Ellis Ave, Chicago, IL 60637 USA.	mneidell@uchicago.edu					*AIR RES BOARD, 1990, AIR RES BOARD SETS N; Alberini A, 1998, J URBAN ECON, V44, P68, DOI 10.1006/juec.1997.2057; *AM AC PED, 2000, GUID CHILDS ALL ASTH; Bjorksten B, 1999, ALLERGY, V54, P17, DOI 10.1111/j.1398-9995.1999.tb04383.x; Bresnahan BW, 1997, LAND ECON, V73, P340, DOI 10.2307/3147172; Case A, 2002, AM ECON REV, V92, P1308, DOI 10.1257/000282802762024520; CHAY K, 2003, IN PRESS Q J EC; Chay K., 2000, DOES AIR QUALITY MAT; *COMM MED EFF AIR, 2000, ASTHM OUTD AIR POLL; Currie J, 1999, AM ECON REV, V89, P245, DOI 10.1257/aer.89.2.245; Desqueyroux H, 1999, REV EPIDEMIOL SANTE, V47, P361; Duhme Heinrich, 1998, Toxicology Letters (Shannon), V102-103, P307, DOI 10.1016/S0378-4274(98)00322-1; Eggleston PA, 1999, ENVIRON HEALTH PERSP, V107, P439; Ernster VL, 1996, ANNU REV PUBL HEALTH, V17, P97; Fauroux B, 2000, PEDIATR PULM, V30, P41; Friedman MS, 2001, JAMA-J AM MED ASSOC, V285, P897, DOI 10.1001/jama.285.7.897; Garty BZ, 1998, ANN ALLERG ASTHMA IM, V81, P563, DOI 10.1016/S1081-1206(10)62707-X; Gouveia N, 2000, OCCUP ENVIRON MED, V57, P477, DOI 10.1136/oem.57.7.477; Greenstone M, 2002, J POLIT ECON, V110, P1175, DOI 10.1086/342808; HARRINGTON W, 1987, J URBAN ECON, V22, P101, DOI 10.1016/0094-1190(87)90052-0; KRUPNICK A, 1990, J ENVIRON ECON MANAG, V17, P1; LETOURNEAU M, 1992, PEDIAT EMERGENCY MED; *MAN RISK MED INS, AIM FACT BOOK 1998; *NAT I ENV HLTH ST, 2000, ASTHM ALL PREV; Norris G, 1999, ENVIRON HEALTH PERSP, V107, P489, DOI 10.2307/3434632; NYSTAD W, 2000, INT J SPORTS MED, V21, P98, DOI 10.1055/s-2000-8498; NYSTROM M, 2001, CALIFORNIA AIR QUALI; PORTNEY PR, 1990, REG SCI URBAN ECON, V20, P407, DOI 10.1016/0166-0462(90)90019-Y; PORTNEY PR, 1986, J URBAN ECON, V20, P21, DOI 10.1016/0094-1190(86)90013-6; RANSOM MR, 1995, CONTEMP ECON POLICY, V13, P86; SEATON A, 1995, LANCET, V345, P176, DOI 10.1016/S0140-6736(95)90173-6; SHONKOFF J, 1990, HDB EARLY CHILDHOOD; SPEIZER F, 2001, HIGH EFF I ANN C AIR; *US EPA, 2003, CRIT POLL; *US EPA, 1999, CONC STRAT AMB AIR M; US EPA, 2000, 600P99001F US EPA; *US EPA, 1999, 454R99010 US EPA; Vacek L, 1999, ALLERGY ASTHMA PROC, V20, P87, DOI 10.2500/108854199778612536; von Mutius E, 2000, J ALLERGY CLIN IMMUN, V105, P9, DOI 10.1016/S0091-6749(00)90171-4; von Mutius E, 2000, REV FR ALLERGOL, V40, P689, DOI 10.1016/S0335-7457(00)80073-8; Wilson R., 1996, PARTICLES OUR AIR CO; ZECKHAUSER R, 1976, 41D KENN SCH	42	101	106	2	22	ELSEVIER SCIENCE BV	AMSTERDAM	PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS	0167-6296			J HEALTH ECON	J. Health Econ.	NOV	2004	23	6					1209	1236		10.1016/j.jhealeco.2004.05.002		28	Economics; Health Care Sciences & Services; Health Policy & Services	Business & Economics; Health Care Sciences & Services	877WZ	WOS:000225607100007	15556243	
J	Martin, AJ; Pratt, N; Kennedy, JD; Ryan, P; Ruffin, RE; Miles, H; Marley, J				Martin, AJ; Pratt, N; Kennedy, JD; Ryan, P; Ruffin, RE; Miles, H; Marley, J			Natural history and familial relationships of infant spilling to 9 years of age	PEDIATRICS			English	Article						children; gastroesophageal reflux; natural history	PEDIATRIC GASTROESOPHAGEAL REFLUX; BARRETTS-ESOPHAGUS; CHILDREN; PREVALENCE; SYMPTOMS; ADENOCARCINOMA; DISEASE; ASTHMA; QUESTIONNAIRE; CHILDHOOD	Objectives. To determine the natural history of infant spilling (regurgitation/vomiting) during the first 2 years of life and to determine the relationship between infant spilling and gastroesophageal reflux (GER) symptoms at 9 years of age. Methods. A prospective birth cohort was followed with daily symptom diaries during the first 2 years of life and reviewed at 9 years of age (range: 8-11 years). The prevalence of infant spilling during the first 2 years of life, the prevalence of GER symptoms between 8 and 11 years of age (mean age: 9.7 years), relative risk of infant spilling predisposing to GER symptoms at 9 years of age, and prevalence of maternal GER symptoms and relationship with infant spilling and GER at 9 years of age were measured. Results. A total of 693 children who represented 83% of an original sample of 836 children and were followed for 2 years from birth with daily symptom diaries were contacted at 9 (8-11) years of age. Spilling of most feeds each day was common in infancy and reached a peak prevalence of 41% between 3 and 4 months of age and thereafter declined to <5% between 13 and 14 months of age. Infants with spilling on 90 days or more during the first 2 years of life (classified as frequent spilling) were more likely to have GER symptoms at 9 years of age. Children with frequent infant spilling, compared with those with no spilling, had a relative risk of 2.3 (95% confidence interval [CI]: 1.3-4.0) of 1 or more GER symptoms at 9 years of age, 4.6 (95% CI: 1.5-13.8) for heartburn, 2.7 (95% CI: 1.4-5.5) for vomiting, and 4.7 (95% CI: 1.6-14.0) for acid regurgitation. Gender, breastfeeding, and environmental tobacco smoke exposure were not significant factors related to infant spilling. Prepregnancy smoking and smoking in the same room as the child at the 9-month and 18-month follow-ups had a significant effect on GER symptoms at 9 years of age. Infant spilling and GER at 9 years of age were significantly related to maternal GER symptoms but not to paternal GER symptoms. Conclusions. Spilling in infancy is very common, but the majority of children settle by 13 to 14 months of age. However, those with frequent spilling (> 90 days) are more likely to have GER symptoms at 9 years of age. In addition, a maternal history of GER was significantly related both to infant spilling and to GER at 9 years, suggesting that a genetic component may be involved. Physicians should consider studying children with a history of frequent infant spilling to determine whether this group is at increased risk for GER disease.	Womens & Childrens Hosp, Dept Pulm Med, Adelaide, SA 5006, Australia; Univ Adelaide, Dept Publ Hlth, Adelaide, SA, Australia; Univ Adelaide, Dept Med, Adelaide, SA 5001, Australia; Univ Adelaide, Dept Gen Practice, Adelaide, SA, Australia	Martin, AJ (reprint author), Womens & Childrens Hosp, Dept Pulm Med, Kermode St, Adelaide, SA 5006, Australia.		Marley, John/F-1239-2010; Pratt, Nicole/A-1348-2011				ABRAMSON M, 1992, AUST NZ J MED, V22, P358, DOI 10.1111/j.1445-5994.1992.tb02148.x; Alaswad B, 1996, J Okla State Med Assoc, V89, P233; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; *AUSTR I HLTH WELF, 1994, AUSTR HLTH 1994; BUTS JP, 1986, EUR J PEDIATR, V145, P396, DOI 10.1007/BF00439246; CARRE IJ, 1959, ARCH DIS CHILD, V34, P344; CRABB DW, 1985, ANN INTERN MED, V103, P52; DOUGLAS RM, 1994, INT J EPIDEMIOL, V23, P818, DOI 10.1093/ije/23.4.818; ENG C, 1993, CANCER EPIDEM BIOMAR, V2, P397; Hart JJ, 1996, AM FAM PHYSICIAN, V54, P2463; HEACOCK HJ, 1992, J PEDIATR GASTR NUTR, V14, P41, DOI 10.1097/00005176-199201000-00009; Hu FZ, 2000, JAMA-J AM MED ASSOC, V284, P325, DOI 10.1001/jama.284.3.325; JOCHEM VJ, 1992, GASTROENTEROLOGY, V102, P1400; LOCKE GR, 1994, MAYO CLIN PROC, V69, P539; Locke GR, 1999, AM J MED, V106, P642, DOI 10.1016/S0002-9343(99)00121-7; MCGREADY SJ, 1999, GASTROESOPHAGEAL REF, P237; Nelson SP, 2000, ARCH PEDIAT ADOL MED, V154, P150; Nelson SP, 1997, ARCH PEDIAT ADOL MED, V151, P569; NELSON SP, 1998, PEDIATRICS, V102; Omari TI, 1998, J PEDIATR-US, V133, P650, DOI 10.1016/S0022-3476(98)70106-4; ORENSTEIN S, 1999, GASTROESOPHAGEAL REF, P269; Orenstein S R, 1999, Pediatr Rev, V20, P24, DOI 10.1542/pir.20-1-24; ORENSTEIN SR, 1988, J PEDIATR-US, V112, P847, DOI 10.1016/S0022-3476(88)80204-X; Orenstein SR, 1996, CLIN PEDIATR, V35, P607, DOI 10.1177/000992289603501201; PEETERS S, 1991, J PEDIATR GASTR NUTR, V13, P314, DOI 10.1097/00005176-199110000-00015; Ramos A G, 1994, Pediatr Rev, V15, P24, DOI 10.1542/pir.15-1-24; ROBERTSON CF, 1991, BRIT MED J, V302, P1116; Romero Y, 1997, GASTROENTEROLOGY, V113, P1449, DOI 10.1053/gast.1997.v113.pm9352846; Sacco O, 2000, PEDIATR PULM, V30, P313, DOI 10.1002/1099-0496(200010)30:4<313::AID-PPUL7>3.0.CO;2-H; SHABIB SM, 1995, J PEDIATR-US, V127, P435, DOI 10.1016/S0022-3476(95)70078-1; SHEPHERD RW, 1987, CLIN PEDIATR, V26, P55, DOI 10.1177/000992288702600201; STANCIU C, 1972, BRIT MED J, V3, P793; Tolaymat N, 1998, W V Med J, V94, P22; TREEM WR, 1991, CLIN PEDIATR, V30, P435, DOI 10.1177/000992289103000705; VANDENPLAS Y, 1993, EUR J PEDIATR, V152, P704, DOI 10.1007/BF01953980; WEINTRAUB M, 1989, HOSP FORMUL, V24, P7	36	101	102	0	4	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	JUN	2002	109	6					1061	1067		10.1542/peds.109.6.1061		7	Pediatrics	Pediatrics	557KE	WOS:000175907100024	12042543	
J	Cavezzi, A; Frullini, A; Ricci, S; Tessari, L				Cavezzi, A; Frullini, A; Ricci, S; Tessari, L			Treatment of varicose veins by foam sclerotherapy: Two clinical series	PHLEBOLOGY			English	Article						sclerosing foam; sclerotherapy; ultrasound imaging; varicose veins	ULTRASOUND-GUIDED SCLEROTHERAPY; SCLEROSING FOAM; DETERMINANTS	Objective: To assess the efficacy and safety of sclerotherapy of varicose veins (VV) with sclerosing foam (SF) made using Tessari's method (three-way tap and two plastic syringes). Design: Two multi-centre prospective clinical series were documented (CS1 and CS2). In CS1, which ran from March to December 2000, 177 patients (39 men, 138 women), mean age 56 years, were treated in three centres for VV related to incompetence of saphenous veins, recurrence, perforators or collaterals. Conventional or duplex-guided sclerotherapy was performed using SF made of purified sodium tetradecyl sulphate (PSTS) 0.2-3% (Fibro-vein, STD Pharmaceuticals, UK) and air. An average of 1.6 (SD 0.8) sessions per patient were performed and 2.9 (SD 1.0) ml of SF (i.e. 0.6 ml of PSTS) per session was employed. An elastic stocking providing 20-30 or 30-40 mmHg compression was worn by patients following treatment. All the patients were reviewed (clinical examination and colour duplex ultrasonography) at 1 month. Sixty-six patients had a further follow-up 45-370 days after treatment. The 17 patients in CS2, a multi-centre study, were treated in March and April 2001. An independent observer assessed patients with major VV (CEAP and VV type distribution similar to CS1) before and after the treatment, and also observed the treatment, which was carried out using the technique employed in CS1. Results: In CS1 at 1 month follow-up there was: (A) obliteration of the vessel or antegrade flow in 161 (91%) patients, (13) minimal retrograde flow in the treated vein without visible VV, in 15 (8.4%) cases and (C) persistence of vessel patency with retrograde flow and visible VV (failure) in 1 (0.6%) case. At 45-370 days (mean 138 days) follow-up results were: type A in 44 (67%) cases, type B in 17 (26%) cases and type C in 5 (8%) cases. The main complications were extension of sclerothrombus from superficial to deep veins (n = 2), allergy (n = 1), malaise (n = 1) and scotoma (n = 1). In CS2 at 30 days follow-up 100% of the treated venous segments had a type A outcome after an average of 1.4 sessions. No relevant complication occurred in this series. Conclusions: Sclerotherapy of major VV by means of SF prepared by Tessari's method is a safe and effective form of treatment. Low doses and a low concentration of drug may be successfully employed. Further studies are needed to establish the long-term results and overall safety of this form of foam sclerotherapy.		Cavezzi, A (reprint author), Via Miramare 7, I-63039 San Benedetto Tronto, AP, Italy.						BACCAGLINI U, 1996, PHLEBOLOGIE, V3, P309; Bhowmick A, 2001, PHLEBOLOGY, V16, P41; BRIZZIO E, 1986, 9 WORLD C PHLEB KYOT, P25; Cabrera J, 2000, PHLEBOLOGY, V15, P19, DOI 10.1007/s005230070032; Cavendish R, 1999, HIST TODAY, V49, P50; CAVEZZI A, 2000, MINERVA CARDIOANG S1, V48, P248; CAVEZZI A, 2000, AUST NZ J PHLEBOL, V4, P100; DISTEFANO R, 1999, VASOMED S, V1, P7; Frullini A, 2000, DERMATOL SURG, V26, P705, DOI 10.1046/j.1524-4725.2000.00071.x; Frullini A., 2000, Phlebologie, V53, P431; Frullini A, 2002, DERMATOL SURG, V28, P11, DOI 10.1046/j.1524-4725.2002.01182.x; Frullini A, 2000, ACTA PHLEBOLOGICA, V1, P43; Gachet G., 2001, PHLEBOLOGIE, V54, P63; Mingo Garcia J, 1999, REV ESP MED CIR COSM, V7, P29; Cabrera Garrido JR, 1997, PHLEBOLOGIE, V50, P181; Henriet J. P., 1997, Phlebologie, V50, P355; Kanter A, 1996, DERMATOL SURG, V22, P648; Kanter A, 1998, DERMATOL SURG, V24, P131; Kanter A, 1998, DERMATOL SURG, V24, P136; Monfreux A., 1997, Phlebologie, V50, P351; ORBACH E J, 1950, J Int Coll Surg, V13, P765; SADOUN S, 1998, 13 WORLD C PHLEB; SCHADECK M, 1985, COMM 19 C PATH VASC; Tessari L, 2001, DERMATOL SURG, V27, P58, DOI 10.1111/j.1524-4725.2001.00192.x; Tessari L, 2000, PHLEBOLOGIE, V53, P129; VARCOE P, 2000, AUST NZ J PHLEBOL, V4, P117	26	101	110	0	2	SPRINGER-VERLAG LONDON LTD	GODALMING	SWEETAPPLE HOUSE CATTESHALL ROAD, GODALMING GU7 3DJ, SURREY, ENGLAND	0268-3555			PHLEBOLOGY	Phlebology		2002	17	1					13	18		10.1007/BF02667958		6	Surgery; Peripheral Vascular Disease	Surgery; Cardiovascular System & Cardiology	614CU	WOS:000179171400004		
J	Jeffery, PK				Jeffery, PK			Comparison of the structural and inflammatory features of COPD and asthma	CHEST			English	Article; Proceedings Paper	Thomas L Petty 42nd Annual Aspen Lung conference - Mechanisms of COPD	JUN 02-05, 1999	ASPEN, COLORADO	Glaxo Wellcome Inc		airway asthma; biopsy; chronic bronchitis; COPD; emphysema; inflammation	OBSTRUCTIVE PULMONARY-DISEASE; AIR-FLOW OBSTRUCTION; CHRONIC MUCUS HYPERSECRETION; ACTIVATED LYMPHOCYTES-T; CHRONIC-BRONCHITIS; PERIPHERAL AIRWAYS; CIGARETTE SMOKERS; ATOPIC ASTHMA; EOSINOPHILIC BRONCHITIS; EMPHYSEMATOUS LUNGS	At least three conditions contribute to COPD, (1) Chronic bronchitis (mucous hypersecretion) is an inflammatory condition in which CD8+ T-lymphocytes, neutrophils, and CD68+ monocytes/macrophages predominate. The condition is defined clinically by the presence of chronic cough and recurrent increases in bronchial secretions sufficient to cause expectoration, There is enlargement of mucus-secreting glands and goblet cell hyperplasia, which can occur in the absence of airflow limitation. (2) Adult chronic bronchiolitis (small or peripheral airways disease) is an inflammatory condition of small bronchi and bronchioli in which there are predominantly CD8+ and pigmented macrophages, The functional defect is difficult to detect clinically but may be recognized by sophisticated tests of small airway function. There is mucous metaplasia, enlargement of the mass of bronchiolar smooth muscle, and loss of alveolar attachments. (3) Emphysema is an inflammatory condition of the alveoli in which T-lymphocytes, neutrophils, and pigmented alveolar macrophages are involved, associated with the release of excessive amounts of elastases. It is defined anatomically by permanent, destructive enlargement of airspaces distal to terminal bronchioli without obvious fibrosis. In contrast, asthma is a clinical syndrome characterized by allergic inflammation of bronchi and bronchioli in which CD4+ (helper) T-lymphocytes and eosinophils predominate. There is increased production and release of interleukin (IL)-4 and IL-5, which is referred to as a The-type response. There is usually increased tracheobronchial responsiveness to a variety of stimuli, and the condition is usually manifest as variable airflow obstruction. While differences between COPD and asthma have been highlighted, new data are emerging that indicate there may also be similarities.	Univ London Imperial Coll Sci Technol & Med, Royal Brompton Hosp, Sch Med, Lung Pathol Unit, London SW3 6NP, England	Jeffery, PK (reprint author), Univ London Imperial Coll Sci Technol & Med, Royal Brompton Hosp, Sch Med, Lung Pathol Unit, Sydney St, London SW3 6NP, England.						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C., 1996, European Respiratory Journal Supplement, V9, p14S; OLLERENSHAW SL, 1992, AM REV RESPIR DIS, V145, P922; OShaughnessy TC, 1997, AM J RESP CRIT CARE, V155, P852; O'Shaughnessy TC, 1996, AM J RESP CRIT CARE, V153, pA879; PETO R, 1983, AM REV RESPIR DIS, V128, P491; PRESCOTT E, 1995, EUR RESPIR J, V8, P1333, DOI 10.1183/09031936.95.08081333; REID LM, 1954, LANCET, V1, P275; REYNOLDS HY, 1987, AM REV RESPIR DIS, V135, P250; ROBINSON DS, 1992, NEW ENGL J MED, V326, P298, DOI 10.1056/NEJM199201303260504; Robinson DS, 1996, AM J RESP CELL MOL, V14, P113; SAETTA M, 1993, AM REV RESPIR DIS, V147, P301; Saetta M, 1996, CLIN EXP ALLERGY, V26, P766, DOI 10.1046/j.1365-2222.1996.d01-386.x; Saetta M, 1998, AM J RESP CRIT CARE, V157, P822; SAETTA M, 1994, AM J RESP CRIT CARE, V150, P1646; Saetta M, 1997, AM J RESP CRIT CARE, V156, P1633; SAETTA M, 1985, AM REV RESPIR DIS, V132, P894; Shapiro SD, 1995, P ASSOC AM PHYSICIAN, V107, P346; Shimura S, 1996, EUR RESPIR J, V9, P1395, DOI 10.1183/09031936.96.09071395; SIAFAKAS NM, 1995, EUR RESPIR J, V8, P1398, DOI 10.1183/09031936.95.08081398; SNIDER GL, 1986, AM REV RESPIR DIS, V133, P942; THOMPSON AB, 1989, AM REV RESPIR DIS, V140, P1527; THURLBECK WM, 1985, CHRONIC OBSTRUCTIVE, P129; VERBEKEN EK, 1992, J APPL PHYSIOL, V72, P2343; Vestbo J, 1996, AM J RESP CRIT CARE, V153, P1530; VIGNOLA AM, 1993, AM REV RESPIR DIS, V148, P689; WANNER A, 1977, AM REV RESPIR DIS, V116, P73; WRIGHT JL, 1988, LUNG, V166, P277, DOI 10.1007/BF02714058; WRIGHT RR, 1965, MED THORAC, V22, P210; Zhu J, 1999, AM J RESP CRIT CARE, V159, pA450	84	101	103	1	4	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	MAY	2000	117	5		1			251S	260S		10.1378/chest.117.5_suppl_1.251S		10	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	316PY	WOS:000087178200022	10843939	
J	Wan, H; Winton, HL; Soeller, C; Gruenert, DC; Thompson, PJ; Cannell, MB; Stewart, GA; Garrod, DR; Robinson, C				Wan, H; Winton, HL; Soeller, C; Gruenert, DC; Thompson, PJ; Cannell, MB; Stewart, GA; Garrod, DR; Robinson, C			Quantitative structural and biochemical analyses of tight junction dynamics following exposure of epithelial cells to house dust mite allergen Der p 1	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						house dust mite; allergen; Der p 1; tight junction; epithelium; asthma; cysteine peptidase	DERMATOPHAGOIDES-PTERONYSSINUS; MEMBRANE-PROTEIN; OCCLUDIN; PERMEABILITY; SEQUENCE; DER-P-1; FIBROBLASTS; DISRUPTION; COMPONENT; CLAUDIN-1	Background House dust mite allergen Der p 1 is a cysteine peptidase. Previously, we have suggested that the proteolytic activity of this allergen may contribute to asthma by damaging the barrier formed by the airways epithelium. Objective The present study applied novel techniques to compare changes in permeability with quantitative events in tight junctions (TJs) and desmosomes (DMs) of epithelial cells exposed to Der p 1. Methods Confluent monolayers of Madin-Darby canine kidney (MDCK) and 16HBE14o-human bronchial epithelial cells were used as experimental models. Permeability was estimated from mannitol clearance. Digital imaging with quantification of TJs and DMs was achieved by fluorescent antibody staining and 2-photon molecular excitation microscopy (2PMEM). Biochemical changes in TJs were studied by immunoblotting, radiolabelling and immunoprecipitation. Results Der p 1 caused a time-dependent breakage of TJs and reduction in their content of the protein ZO-1. Reduction in ZO-1 immunofluorescence at TJs occurred with a small increase in the amount of diffuse, cytoplasmic immunoreactive ZO-1 staining. Morpho-logical changes in TJs occurred in synchrony with increases in epithelial permeability. DM puncta increased both in size and intensity of staining. Immunoblotting demonstrated that the disruption of TJ morphology was associated with cleavage of ZO-1 and occludin. Cells recovered from allergen exposure by de novo synthesis of occludin. Conclusion Der p 1 could contribute to sensitization and allergic responses by degrading the function of the airway epithelial barrier.	St George Hosp, Sch Med, Dept Pharmacol & Clin Pharmacol, London SW17 0RE, England; Univ Calif San Francisco, Dept Lab Med, Inst Cardiovasc Res, Gene Therapy Core Ctr, San Francisco, CA 94143 USA; Univ Western Australia, Queen Elizabeth II Med Ctr, Dept Med, Nedlands, WA 6009, Australia; Univ Western Australia, Queen Elizabeth II Med Ctr, Dept Microbiol, Nedlands, WA 6009, Australia; Univ Manchester, Sch Biol Sci, Manchester, Lancs, England	Robinson, C (reprint author), St George Hosp, Sch Med, Dept Pharmacol & Clin Pharmacol, Cranmer Terrace, London SW17 0RE, England.		Soeller, Christian/G-5525-2011	Robinson, Clive/0000-0001-6253-7864			ANDERSON JM, 1988, J CELL BIOL, V106, P1141, DOI 10.1083/jcb.106.4.1141; Anderson JM, 1995, AM J PHYSIOL, V32, P467; AndoAkatsuka Y, 1996, J CELL BIOL, V133, P43, DOI 10.1083/jcb.133.1.43; BACALLAO R, 1994, J CELL SCI, V107, P3301; Balda MS, 1996, J CELL BIOL, V134, P1031, DOI 10.1083/jcb.134.4.1031; BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1006/abio.1976.9999; Chambers Louise, 1997, Biochemical Society Transactions, V25, p85S; CHUA KY, 1988, J EXP MED, V167, P175, DOI 10.1084/jem.167.1.175; Denker BM, 1998, AM J PHYSIOL-RENAL, V274, pF1; FARQUHAR MG, 1963, J CELL BIOL, V17, P375, DOI 10.1083/jcb.17.2.375; Furuse M, 1998, J CELL BIOL, V143, P391, DOI 10.1083/jcb.143.2.391; FURUSE M, 1993, J CELL BIOL, V123, P1777, DOI 10.1083/jcb.123.6.1777; Furuse M, 1998, J CELL BIOL, V141, P1539, DOI 10.1083/jcb.141.7.1539; FURUSE M, 1994, J CELL BIOL, V127, P1617, DOI 10.1083/jcb.127.6.1617; Garrod DR, 1993, CURR OPIN CELL BIOL, V5, P30, DOI 10.1016/S0955-0674(05)80005-5; GONZALEZMARISCAL L, 1985, J MEMBRANE BIOL, V86, P113, DOI 10.1007/BF01870778; HERBERT CA, 1990, LANCET, V336, P1132, DOI 10.1016/0140-6736(90)92611-K; HERBERT CA, 1995, AM J RESP CELL MOL, V12, P369; Hewitt CRA, 1997, CLIN EXP ALLERGY, V27, P201, DOI 10.1111/j.1365-2222.1997.tb00694.x; King C, 1998, J IMMUNOL, V161, P3645; McCarthy KM, 1996, J CELL SCI, V109, P2287; MORITA S, 1999, P NATL ACAD SCI USA, V96, P511; Muresan Z, 1998, MOL BIOL CELL, V9, p83A; PARRISH EP, 1987, J PATHOL, V153, P265, DOI 10.1002/path.1711530311; Robinson C, 1997, CLIN EXP ALLERGY, V27, P10, DOI 10.1046/j.1365-2222.1997.d01-415.x; ROBINSON C, 1995, IMMUNOPHARMACOLOGY R, P187, DOI 10.1016/B978-012352325-9/50012-5; Schneeberger EE, 1992, AM J PHYSIOL, V262, P647; Schulz O, 1998, J EXP MED, V187, P271, DOI 10.1084/jem.187.2.271; Soeller C, 1996, PFLUG ARCH EUR J PHY, V432, P555, DOI 10.1007/s004240050169; STEWART GA, 1991, INT ARCH ALLER A IMM, V95, P248; STEWART GA, 1992, EXP APPL ACAROL, V16, P165, DOI 10.1007/BF01201499; VanItallie CM, 1997, J CELL SCI, V110, P1113; VESTWEBER D, 1985, EMBO J, V4, P3393; Wan H, 1999, J CLIN INVEST, V104, P123, DOI 10.1172/JCI5844; WAN H, 1998, MICROSC MICROANAL, V4, P416; Winton HL, 1998, CLIN EXP ALLERGY, V28, P1273; Winton HL, 1998, BRIT J PHARMACOL, V124, P1048, DOI 10.1038/sj.bjp.0701905; Wong V, 1997, AM J PHYSIOL-CELL PH, V273, pC1859	38	101	106	1	4	BLACKWELL SCIENCE LTD	OXFORD	P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	MAY	2000	30	5					685	698				14	Allergy; Immunology	Allergy; Immunology	314CU	WOS:000087037700013	10792361	
J	Kitch, BT; Chew, G; Burge, HA; Muilenberg, ML; Weiss, ST; Platts-Mills, TAE; O'Connor, G; Gold, DR				Kitch, BT; Chew, G; Burge, HA; Muilenberg, ML; Weiss, ST; Platts-Mills, TAE; O'Connor, G; Gold, DR			Socioeconomic predictors of high allergen levels in homes in the greater Boston area	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; cat; cockroach; dog; dust mite; indoor allergens; inner city	INNER-CITY CHILDREN; HOUSE DUST MITES; RISK-FACTORS; AFFINITY PURIFICATION; COCKROACH ALLERGEN; INDOOR ALLERGENS; ASTHMA MORTALITY; UNITED-STATES; P-I; EXPOSURE	In the United States, childhood asthma morbidity and prevalence rates are the highest in less affluent urban minority communities. More than 80% of childhood asthmatics are allergic to one or more inhalant allergens. We evaluated whether socioeconomic status was associated with a differential in the levels and types of indoor home allergens. Dust samples for an ELISA allergen assay were collected from the homes of 499 families as part of a metropolitan Boston, Massachusetts, longitudinal birth cohort study of home allergens and asthma in children with a parental history of asthma or allergy. The proportion of homes with maximum home allergen levels in the highest category was 42% for dust mite allergen (greater than or equal to 10 mu g/g Der p 1 or Der f 1), 13% for cockroach allergen (greater than or equal to 2 U/g Bla g 1 or Bla g 2), 26% for cat allergen (greater than or equal to 8 mu g/g Fel d 1), and 20% for dog allergen (greater than or equal to 10 mu g/g Can f 1). Homes in the high-poverty area (> 20% of the population below the poverty level) were more likely to have high cockroach allergen levels than homes in the low-poverty area [51 vs. 3%; OR, 33; 95% confidence interval (CI), 12-90], but less likely co have high levels of dust mite allergen (16 vs. 53%; OR, 0.2; CI, 0.1-0.4). Lower family income, less maternal education, and race/ethnicity (black or Hispanic vs. white) were also associated with a lower risk of high dust mite levels and a greater risk of high cockroach allergen levels. Within a single U.S. metropolitan area we found marked between-community differences in the types of allergens present in the home, bur not necessarily in the overall burden of allergen exposure.	Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA; Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA; Harvard Univ, Beth Israel Hosp, Sch Med, Div Pulm, Boston, MA 02215 USA; Univ Virginia, Med Ctr, Dept Med, Div Allergy & Immunol, Charlottesville, VA USA; Boston Univ, Sch Med, Dept Med, Ctr Pulm, Boston, MA 02118 USA; Harvard Univ, Sch Med, Boston, MA USA	Kitch, BT (reprint author), Channing Lab, 181 Longwood Ave, Boston, MA 02115 USA.			O'Connor, George/0000-0002-6476-3926	NHLBI NIH HHS [HL07427]; NIAID NIH HHS [R01 AI/EHS-35789]		ARLIAN LG, 1992, J ALLERGY CLIN IMMUN, V90, P292, DOI 10.1016/S0091-6749(05)80006-5; ARLIAN LG, 1989, IMMUNOL ALLERGY CLIN, V9, P339; BRANDT RL, 1976, J MED ENTOMOL, V13, P327; CALL RS, 1992, J PEDIATR-US, V121, P862, DOI 10.1016/S0022-3476(05)80329-4; CHANYEUNG M, 1995, CLIN EXP ALLERGY, V25, P240, DOI 10.1111/j.1365-2222.1995.tb01035.x; CHAPMAN MD, 1988, J IMMUNOL, V140, P812; Chew GL, 1998, AM J RESP CRIT CARE, V157, P1536; DEGROOT H, 1991, J ALLERGY CLIN IMMUN, V87, P1056, DOI 10.1016/0091-6749(91)92150-Y; EVANS R, 1992, CHEST, V101, pS368; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; GERGEN PJ, 1988, PEDIATRICS, V81, P1; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; GOTTLIEB DJ, 1995, CHEST, V108, P28, DOI 10.1378/chest.108.1.28; HARVING H, 1993, ALLERGY, V48, P106, DOI 10.1111/j.1398-9995.1993.tb00694.x; INGRAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449, DOI 10.1016/S0091-6749(95)70286-5; KANG BC, 1993, J ALLERGY CLIN IMMUN, V92, P802, DOI 10.1016/0091-6749(93)90057-M; KOEHLER PG, 1987, J ECON ENTOMOL, V80, P446; LUCZYNSKA CM, 1989, J IMMUNOL METHODS, V118, P227, DOI 10.1016/0022-1759(89)90010-0; MARDER D, 1992, CHEST, V101, pS426, DOI 10.1378/chest.101.6_Supplement.426S; Munir A K, 1993, Pediatr Allergy Immunol, V4, P136, DOI 10.1111/j.1399-3038.1993.tb00082.x; PLATTSMILLS TAE, 1992, J ALLERGY CLIN IMMUN, V89, P1046, DOI 10.1016/0091-6749(92)90228-T; POLLART SM, 1991, J ALLERGY CLIN IMMUN, V87, P505, DOI 10.1016/0091-6749(91)90009-D; Rosenstreich DL, 1997, NEW ENGL J MED, V336, P1356, DOI 10.1056/NEJM199705083361904; Sarpong SB, 1996, J ALLERGY CLIN IMMUN, V97, P1393, DOI 10.1016/S0091-6749(96)70209-9; 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; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; Warner AM, 1996, PEDIATR ALLERGY IMMU, V7, P61, DOI 10.1111/j.1399-3038.1996.tb00108.x; WEISS KB, 1990, JAMA-J AM MED ASSOC, V264, P1683, DOI 10.1001/jama.264.13.1683; WICKMAN M, 1991, J ALLERGY CLIN IMMUN, V88, P89, DOI 10.1016/0091-6749(91)90305-8	30	101	104	0	1	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	2000	108	4					301	307		10.2307/3454347		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	306KT	WOS:000086596400025	10753087	
J	Mansbach, JM; Piedra, PA; Teach, SJ; Sullivan, AF; Forgey, T; Clark, S; Espinola, JA; Camargo, CA				Mansbach, Jonathan M.; Piedra, Pedro A.; Teach, Stephen J.; Sullivan, Ashley F.; Forgey, Tate; Clark, Sunday; Espinola, Janice A.; Camargo, Carlos A., Jr.		MARC-30 Investigators	Prospective Multicenter Study of Viral Etiology and Hospital Length of Stay in Children With Severe Bronchiolitis	ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE			English	Article							RESPIRATORY SYNCYTIAL VIRUS; REAL-TIME PCR; RHINOVIRUS INFECTION; HUMAN METAPNEUMOVIRUS; ASTHMA DEVELOPMENT; CLINICAL SYMPTOMS; DISEASE SEVERITY; RISK-FACTORS; INFANTS; EXPRESSION	Objective: To determine whether hospital length of stay (LOS) for acute bronchiolitis is influenced by the infecting pathogen. Design: A prospective observational cohort study was performed during 3 consecutive years. Setting: Sixteen US hospitals participated in the study. Participants: Children younger than 2 years hospitalized with bronchiolitis were included. Main Exposure: The results of nasopharyngeal aspirate polymerase chain reaction pathogen testing served as the main exposure. Main Outcome Measure: Hospital LOS was determined. Results: Of 2207 participants, 72.0% had respiratory syncytial virus (RSV) and 25.6% had human rhinovirus (HRV); the incidence of each of the other viruses and bacteria was 7.8% or less. Multiple pathogen infections were present in 29.8% of the children. There were 1866 children (84.5%) with RSV and/or HRV. Among these 1866 children, the median age was 4 months and 59.5% were male. The median LOS was 2 days (interquartile range, 1-4 days). Compared with children who had only RSV, an LOS of 3 or more days was less likely among children with HRV alone (adjusted odds ratio [AOR], 0.36; 95% CI, 0.20-0.63; P < .001) and those with HRV plus non-RSV pathogens (AOR, 0.39; 95% CI, 0.23-0.66; P < .001) but more likely among children with RSV plus HRV(AOR, 1.33; 95% CI, 1.02-1.73; P =. 04), controlling for 15 demographic and clinical factors. Conclusions: In this multicenter study of children hospitalized with bronchiolitis, RSV was the most common virus detected, but HRV was detected in one-quarter of the children. Since 1 in 3 children had multiple virus infections and HRV was associated with LOS, these data challenge the effectiveness of current RSV-based cohorting practices, the sporadic testing for HRV in bronchiolitis research, and current thinking that the infectious etiology of severe bronchiolitis does not affect short-term outcomes.	[Mansbach, Jonathan M.] Harvard Univ, Sch Med, Childrens Hosp Boston, Dept Med, Boston, MA 02115 USA; [Sullivan, Ashley F.; Forgey, Tate; Espinola, Janice A.; Camargo, Carlos A., Jr.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02115 USA; [Piedra, Pedro A.] Baylor Coll Med, Dept Mol Virol & Microbiol, Houston, TX 77030 USA; [Piedra, Pedro A.] Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA; [Teach, Stephen J.] Childrens Natl Med Ctr, Dept Pediat, Washington, DC 20010 USA; [Clark, Sunday] Univ Pittsburgh, Dept Med, Pittsburgh, PA USA	Mansbach, JM (reprint author), Harvard Univ, Sch Med, Childrens Hosp Boston, Dept Med, 300 Longwood Ave,Main Clin Bldg 9 S,Ste 9157, Boston, MA 02115 USA.	jonathan.mansbach@childrens.harvard.edu			National Institutes of Health [U01 AI-67693, K23 AI-77801, UL1 RR-031988]	This study was supported by grants U01 AI-67693, K23 AI-77801, and UL1 RR-031988 from the National Institutes of Health.	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Pediatr. Adolesc. Med.	AUG	2012	166	8					700	706		10.1001/archpediatrics.2011.1669		7	Pediatrics	Pediatrics	984KU	WOS:000307189300003	22473882	
J	Holt, PG; Sly, PD				Holt, Patrick G.; Sly, Peter D.			Viral infections and atopy in asthma pathogenesis: new rationales for asthma prevention and treatment	NATURE MEDICINE			English	Review							FC-EPSILON-RI; RESPIRATORY SYNCYTIAL VIRUS; PLASMACYTOID DENDRITIC CELLS; HOUSE-DUST-MITE; INNATE IMMUNE-RESPONSE; MEMORY T-CELLS; LUNG-FUNCTION; BONE-MARROW; CHILDHOOD ASTHMA; ALLERGIC SENSITIZATION	Prospective birth cohort studies tracking asthma initiation and consolidation in community cohorts have identified viral infections occurring against a background of allergic sensitization to aeroallergens as a uniquely potent risk factor for the expression of acute severe asthma-like symptoms and for the ensuing development of asthma that can persist through childhood and into adulthood. A combination of recent experimental and human studies have suggested that underlying this bipartite process are a series of interactions between antiviral and atopic inflammatory pathways that are mediated by local activation of myeloid cell populations in the airway mucosa and the parallel programming and recruitment of their replacements from bone marrow. Targeting key components of these pathways at the appropriate stages of asthma provides new opportunities for the treatment of established asthma but, more crucially, for primary and secondary prevention of asthma during childhood.	[Holt, Patrick G.] Univ Western Australia, Ctr Child Hlth Res, Telethon Inst Child Hlth Res, Perth, WA 6009, Australia; [Sly, Peter D.] Univ Queensland, Queensland Childrens Med Res Inst, Brisbane, Qld, Australia	Holt, PG (reprint author), Univ Western Australia, Ctr Child Hlth Res, Telethon Inst Child Hlth Res, Perth, WA 6009, Australia.	patrick@ichr.uwa.edu.au	Sly, Peter/F-1486-2010	Sly, Peter/0000-0001-6305-2201			Al-Garawi A, 2012, J IMMUNOL, V188, P832, DOI 10.4049/jimmunol.1102349; ALBLAS ABV, 1981, J EXP MED, V154, P235; Beyer M, 2004, J ALLERGY CLIN IMMUN, V113, P127, DOI 10.1016/j.jaci.2004.10.057; Bisgaard H, 2007, NEW ENGL J MED, V357, P1487, DOI 10.1056/NEJMoa052632; Bochkov YA, 2011, NAT MED, V17, P627, DOI 10.1038/nm.2358; Bosco A, 2010, MUCOSAL IMMUNOL, V3, P399, DOI 10.1038/mi.2010.13; Buhl R, 2002, EUR RESPIR J, V20, P73, DOI 10.1183/09031936.02.00278102; Busse WW, 2011, NEW ENGL J MED, V364, P1005, DOI 10.1056/NEJMoa1009705; Busse WW, 2001, NEW ENGL J MED, V344, P350; 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J	Kelly, FJ; Fussell, JC				Kelly, F. J.; Fussell, J. C.			Air pollution and airway disease	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review							OBSTRUCTIVE PULMONARY-DISEASE; GLUTATHIONE-S-TRANSFERASE; DIESEL EXHAUST PARTICLES; LONG-TERM EXPOSURE; POLYCYCLIC AROMATIC-HYDROCARBONS; RESPIRATORY SYNCYTIAL VIRUS; CASE-CROSSOVER ANALYSIS; EMERGENCY-ROOM VISITS; TUMOR-NECROSIS-FACTOR; LUNG-FUNCTION	Epidemiological and toxicological research continues to support a link between urban air pollution and an increased incidence and/or severity of airway disease. Detrimental effects of ozone (O(3)), nitrogen dioxide (NO(2)) and particulate matter (PM), as well as traffic-related pollution as a whole, on respiratory symptoms and function are well documented. Not only do we have strong epidemiological evidence of a relationship between air pollution and exacerbation of asthma and respiratory morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD), but recent studies, particularly in urban areas, have suggested a role for pollutants in the development of both asthma and COPD. Similarly, while prevalence and severity of atopic conditions appear to be more common in urban compared with rural communities, evidence is emerging that traffic-related pollutants may contribute to the development of allergy. Furthermore, numerous epidemiological and experimental studies suggest an association between exposure to NO(2), O(3), PM and combustion products of biomass fuels and an increased susceptibility to and morbidity from respiratory infection. Given the considerable contribution that traffic emissions make to urban air pollution researchers have sought to characterize the relative toxicity of traffic-related PM pollutants. Recent advances in mechanisms implicated in the association of air pollutants and airway disease include epigenetic alteration of genes by combustion-related pollutants and how polymorphisms in genes involved in antioxidant pathways and airway inflammation can modify responses to air pollution exposures. Other interesting epidemiological observations related to increased host susceptibility include a possible link between chronic PM exposure during childhood and vulnerability to COPD in adulthood, and that infants subjected to higher prenatal levels of air pollution may be at greater risk of developing respiratory conditions. While the characterization of pollutant components and sources promise to guide pollution control strategies, the identification of susceptible subpopulations will be necessary if targeted therapy/prevention of pollution-induced respiratory diseases is to be developed.	[Kelly, F. J.; Fussell, J. 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Exp. Allergy	AUG	2011	41	8					1059	1071		10.1111/j.1365-2222.2011.03776.x		13	Allergy; Immunology	Allergy; Immunology	791WS	WOS:000292700000004	21623970	
J	Maisonneuve, P; Lowenfels, AB				Maisonneuve, Patrick; Lowenfels, Albert B.			Epidemiology of Pancreatic Cancer: An Update	DIGESTIVE DISEASES			English	Article; Proceedings Paper	173rd Falk Symposium From Chronic Inflammation to Cancer	JUN 04-05, 2010	Brno, CZECH REPUBLIC			Pancreatic cancer; Epidemiology; Time trends; Etiology; Risk factors	BODY-MASS INDEX; ABO BLOOD-GROUP; OF-THE-LITERATURE; VITAMIN-D STATUS; PHYSICAL-ACTIVITY; COHORT-CONSORTIUM; POOLED-ANALYSIS; PERIODONTAL-DISEASE; DIABETES-MELLITUS; CIGARETTE-SMOKING	Pancreatic cancer, although infrequent, has a very poor prognosis, making it one of the 4 or 5 most common causes of cancer mortality in developed countries. Its incidence varies greatly across regions, which suggests that lifestyle factors such as diet, and environmental factors, such as vitamin D exposure, play a role. Because pancreatic cancer is strongly age-dependent, increasing population longevity and ageing will lead to an increase of the global burden of pancreatic cancer in the coming decades. Smoking is the most common known risk factor, causing 20-25% of all pancreatic tumors. Although a common cause of pancreatitis, heavy alcohol intake is associated only with a modest increased risk of pancreatic cancer. While viruses do not represent a major risk factor, people infected with Helicobacter pylori appeared to be at high risk of pancreatic cancer. Many factors associated with the metabolic syndrome, including overweight and obesity, impaired glucose tolerance, and long-standing diabetes also increase the risk disease, while atopic allergy and use of metformin as a treatment for diabetes have been associated with a reduced risk of pancreatic cancer. A family history of pancreatic cancer is associated with an increased risk of pancreatic cancer and it is estimated that 5-10% of patients with pancreatic cancer have an underlying germline disorder. Having a non-O blood group, another inherited characteristic, has also been steadily associated with an increased risk of pancreatic cancer. While many risk factors for pancreatic cancer are not modifiable, adopting a healthy lifestyle could substantially reduce pancreatic cancer risk. Copyright (C) 2010 S. Karger AG, Basel	[Maisonneuve, Patrick] European Inst Oncol, Div Epidemiol & Biostat, IT-20141 Milan, Italy; [Lowenfels, Albert B.] New York Med Coll, Dept Surg, Valhalla, NY 10595 USA	Maisonneuve, P (reprint author), European Inst Oncol, Div Epidemiol & Biostat, Via Ripamonti 435, IT-20141 Milan, Italy.	patrick.maisonneuve@ieo.it		Maisonneuve, Patrick/0000-0002-5309-4704	C.D. Smithers Foundation; Solvay Pharmaceuticals	A.B. Lowenfels was supported by grants from the C.D. Smithers Foundation and Solvay Pharmaceuticals. The authors declare that no conflict of interest exists in relation to the content of the article.	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Dis.		2010	28	4-5					645	656		10.1159/000320068		12	Gastroenterology & Hepatology	Gastroenterology & Hepatology	684LK	WOS:000284551200015	21088417	
J	O'Hehir, RE; Gardner, LM; de Leon, MP; Hales, BJ; Biondo, M; Douglass, JA; Rolland, JM; Sandrini, A				O'Hehir, Robyn E.; Gardner, Leanne M.; de Leon, Maria P.; Hales, Belinda J.; Biondo, Mark; Douglass, Jo A.; Rolland, Jennifer M.; Sandrini, Alessandra			House Dust Mite Sublingual Immunotherapy The Role for Transforming Growth Factor-beta and Functional Regulatory T Cells	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						allergen immunotherapy; sublingual administration; regulatory T cells; transforming growth factor-beta; T lymphocytes	GRASS-POLLEN IMMUNOTHERAPY; STANDARDIZED 5-GRASS-POLLEN EXTRACT; SYSTEMIC IMMUNOLOGICAL CHANGES; RANDOMIZED CONTROLLED-TRIAL; SEASONAL ALLERGIC RHINITIS; DOUBLE-BLIND; SWALLOW IMMUNOTHERAPY; TGF-BETA; IMMUNE-RESPONSES; CLINICAL-EFFICACY	Rationale: Sublingual allergen-specific immunotherapy is gaining popularity for treatment of allergic diseases, but underlying immunological mechanisms are unresolved. Objectives: To perform detailed immunological investigation of sublingual house dust mite (HDM) immunotherapy. Methods: A 12-month randomized double-blind placebo-controlled study of sublingual HDM immunotherapy in 30 HDM-allergic subjects was performed, with 1-year open extension in 9 patients on active treatment. HDM-stimulated blood mononuclear cells were analyzed for proliferation, cytokines, and regulatory T cells (Tregs) by flow cytometry and ELISA. Effects of blocking transforming growth factor (TGF)-beta and IL-10 on proliferation were determined. Treg suppressor function and allergen-specific antibody levels were measured. Clinical efficacy was assessed by symptom, medication, and juniper quality-of-life scores. Measurements and Main Results: Allergen-induced CD4(+) T-cell division and IL-5 production were significantly decreased after 6- and 12-months' active treatment but not placebo. sTGF-beta RII blocked immunotherapy-induced suppression of allergen-specific T-cell proliferation, maximal at 6 months. Decreased allergen-specific CD4(+) T-cell proliferation and increased IL-10 secretion and serum Der p 2-specific IgG(4) were maximal at 24 months' active treatment. Treg (CD4(+)CD25(+)CD127(lo)/Foxp3(+)) function was demonstrated by suppression of allergen-specific effector T-cell (CD4(+)CD25(-)CD127(hi)) proliferation and cytokine production. Clinical efficacy of immunotherapy was supported by significantly decreased rhinitis symptom score, total asthma score, and Juniper quality-of-life score. Conclusions: This study establishes the novel finding that TGF-beta mediates the immunological suppression seen early in clinically effective sublingual HDM immunotherapy in addition to an increase in Tregs with suppressor function. Clinical trial registered with www.clinicaltrials.gov (NCT00250263).	[O'Hehir, Robyn E.; Gardner, Leanne M.; de Leon, Maria P.; Biondo, Mark; Douglass, Jo A.; Sandrini, Alessandra] Alfred Hosp, Dept Allergy Immunol & Resp Med, Melbourne, Vic 3004, Australia; [O'Hehir, Robyn E.; Gardner, Leanne M.; de Leon, Maria P.; Biondo, Mark; Rolland, Jennifer M.; Sandrini, Alessandra] Monash Univ, Dept Immunol, Melbourne, Vic 3004, Australia; [Hales, Belinda J.] Telethon Inst Child Hlth Res, Perth, WA, Australia	O'Hehir, RE (reprint author), Alfred Hosp, Dept Allergy Immunol & Resp Med, Commercial Rd, Melbourne, Vic 3004, Australia.	robyn.ohehir@med.monash.edu.au	Rolland, Jennifer/E-7543-2011; O'Hehir, Robyn/H-3627-2011; Hales, Belinda/C-3858-2013	O'Hehir, Robyn/0000-0002-3489-7595; Hales, Belinda/0000-0003-2193-3996	National Health and Medical Research Council, Australia; Cooperative Research Centre for Asthma and Airways, Australia; Alfred Research Trusts	Supported by Program Grant funding from the National Health and Medical Research Council, Australia; the Cooperative Research Centre for Asthma and Airways, Australia; and the Alfred Research Trusts.	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J. Respir. Crit. Care Med.	NOV 15	2009	180	10					936	947		10.1164/rccm.200905-0686OC		12	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	519VR	WOS:000271797600008	19696440	
J	Spitzer, C; Barnow, S; Volzke, H; John, U; Freyberger, HJ; Grabe, HJ				Spitzer, Carsten; Barnow, Sven; Voelzke, Henry; John, Ulrich; Freyberger, Harald J.; Grabe, Hans Joergen			Trauma, Posttraumatic Stress Disorder, and Physical Illness: Findings from the General Population	PSYCHOSOMATIC MEDICINE			English	Article						trauma; posttraumatic stress disorder (PTSD); physical health; cardiovascular and pulmonary disease; general population	ADVERSE CHILDHOOD EXPERIENCES; HEART-DISEASE; PRIMARY-CARE; MYOCARDIAL-INFARCTION; PSYCHIATRIC-DISORDERS; VIETNAM VETERANS; HEALTH; SYMPTOMS; EXPOSURE; COMMUNITY	Objective: To determine in a general population sample the differential impact on physical health of exposure to traumatic experiences and posttraumatic stress disorder (PTSD). Trauma exposure and PTSD have been associated with physical illness in specific populations, such as veterans. Methods: Medical histories including cardiovascular, endocrine, pulmonary, and other chronic diseases were obtained from 3171 adults living in the community. They were administered the PTSD module of the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV), and were assigned to three groups: no trauma (n = 1440); trauma, but no PTSD (n = 1669) and trauma with subsequent PTSD (n = 62). Results: After adjustments for sociodemographic factors, smoking, body mass index, blood pressure, depression, and alcohol use disorders, subjects with trauma history had higher odds ratios (ORs) for angina pectoris and heart failure (OR = 1.2; 95% Confidence Interval [CI] 1.1-1.3), stroke (OR = 1.2; 95 CI = 1.0-1.5), bronchitis, asthma, renal disease, and polyarthritis (ORs between 1.1 and 1.3) compared with nontraumatized participants. The PTSD positive subsample had increased ORs for angina (OR = 2.4; 95% CI = 1.3-4.5), heart failure (OR = 3.4; 95% CI = 1.9-6.0), bronchitis, asthma, liver, and peripheral arterial disease (ORs, range = 2.5-3.1). Conclusions: Our findings suggest a strong association between PTSD and cardiovascular and pulmonary diseases. Particular diagnostic and treatment attention should be paid to physical illness in PTSD positive patients in primary care, medical, and mental health settings.	[Spitzer, Carsten] Univ Med Ctr Hamburg Eppendorf, Dept Psychosomat Med & Psychotherapy, D-20246 Hamburg, Germany; Schon Kliniken, Klinikum Eilbek, Hamburg, Germany; [Barnow, Sven] Univ Heidelberg, Inst Psychol, Heidelberg, Germany; [Voelzke, Henry] Ernst Moritz Arndt Univ Greifswald, Inst Community Med, Greifswald, Germany; [John, Ulrich] Ernst Moritz Arndt Univ Greifswald, Inst Epidemiol & Social Med, Greifswald, Germany; [Freyberger, Harald J.; Grabe, Hans Joergen] Ernst Moritz Arndt Univ Greifswald, Dept Psychiat & Psychotherapy, Greifswald, Germany	Spitzer, C (reprint author), Univ Med Ctr Hamburg Eppendorf, Dept Psychosomat Med & Psychotherapy, Martinistr 52, D-20246 Hamburg, Germany.	c.spitzer@uke.uni-hamburg.de		John, Ulrich/0000-0003-0587-5298	Federal Ministry of Education and Research [ZZ9603, 01ZZ0103, 01ZZ0403]; Ministry of Cultural Affairs as well as the Social Ministry, of the Federal State of Mecklenburg-West Pomerania	The work is part of the Community, Medicine Research net of the University of Greifswald, Germany, which is funded by, the Federal Ministry of Education and Research (Grants ZZ9603, 01ZZ0103, 01ZZ0403), the Ministry of Cultural Affairs as well as the Social Ministry, of the Federal State of Mecklenburg-West Pomerania. The Community Medicine Research encompasses several research projects, which are sharing data of the population-based Study of Health in Pomerania (SHIP) (http://ship.community-medicine.de).	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J	Eduard, W; Pearce, N; Douwes, J				Eduard, Wijnand; Pearce, Neil; Douwes, Jeroen			Chronic Bronchitis, COPD, and Lung Function in Farmers The Role of Biological Agents	CHEST			English	Article							OBSTRUCTIVE PULMONARY-DISEASE; DOSE-RESPONSE RELATIONSHIPS; RESPIRATORY SYMPTOMS; ANIMAL FARMERS; EXPOSURE; ENDOTOXIN; WORKERS; ASTHMA; DUST; ENVIRONMENT	Background: Farmers have an increased risk of respiratory morbidity and mortality. The causal agents have not been fully established. Methods: In a cross-sectional study of 4,735 Norwegian farmers, we assessed respiratory symptoms and lung function. Atopy was assessed in a subsample (n = 1,213). Personal exposures to dust, fungal spores, actinomycete spores, endotoxins, bacteria, storage mites, (1 -> 3)-beta-D-glucans, fungal antigens, organic dust, inorganic dust, silica, ammonia, and hydrogen sulfide were measured for 127 randomly selected farms. Results: Compared to crop farmers, livestock farmers were more likely to have chronic bronchitis (odds ratio [OR], 1.9; 95% confidence interval [CI], 1.4 to 2.6) and COPD (OR, 1.4; 95% CI, 1.1 to 1.7). FEV(1) (-41 mL; 95% CI, -75 to -7) was significantly reduced, but FVC (-15 mL; 95% CI, -54 to 24) was not. Exposure to most agents were predictors of respiratory morbidity, except FVC. Ammonia, hydrogen sulfide, and inorganic dust were most strongly associated in multiple regression models adjusted for coexposures, but the effects of specific biological agents could not be assessed in multiple regression models because they were too highly correlated. Farmers with atopy had a significantly lower FEV(1) (OR, -87 mL; 95% CI, -170 to -7), but atopy was not directly associated with chronic bronchitis, COPD, and FVC. However, the effects of farming and specific exposures on COPI) were substantially greater in farmers with atopy. Conclusions: Livestock farmers have an increased risk of chronic bronchitis, COPD, and reduced FEV(1). Ammonia, hydrogen sulfide, inorganic dust, and organic dust may be causally involved, but a role for specific biological agents cannot be excluded. Farmers with atopy appear more susceptible to develop farming-related COPI). (CHEST 2009; 136:716-725)	[Eduard, Wijnand] Natl Inst Occupat Hlth, Oslo, Norway; [Pearce, Neil; Douwes, Jeroen] Massey Univ, Ctr Publ Hlth Res, Wellington, New Zealand	Eduard, W (reprint author), Natl Inst Occupat Hlth, POB 8149, NO-0033 Dep Oslo, Norway.	wijnand.eduard@stami.no		Pearce, Neil/0000-0002-9938-7852; Douwes, Jeroen/0000-0003-3599-4036	Agricultural Besearch Council of Norway; Agricultural Agreement Research Fund; Agricultural Investment Fund; Norske Meierier (Norwegian Dairies); Gjensidige (insurance company); Forenede (insurance company); Health Research Council (HRC) of New Zealand	Support/Funding: This project was financially supported by the Agricultural Besearch Council of Norway, the Agricultural Agreement Research Fund, the Agricultural Investment Fund, Norske Meierier (Norwegian Dairies), Gjensidige (insurance company), and Forenede (insurance company). Pharmacia Diagnostics supplied the reagents for the Phadebas Phadiatop and specific IgE tests, and Nycomed Pharma performed the RAST analyses. The Centre for Public Health Research is supported by a Programme Grant from the Health Research Council (HRC) of New Zealand.	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J	Mills, ENC; Mackie, AR; Burney, P; Beyer, K; Frewer, L; Madsen, C; Botjes, E; Crevel, RWR; van Ree, R				Mills, E. N. C.; Mackie, A. R.; Burney, P.; Beyer, K.; Frewer, L.; Madsen, C.; Botjes, E.; Crevel, R. W. R.; van Ree, R.			The prevalence, cost and basis of food allergy across Europe	ALLERGY			English	Review						allergy; diagnosis; foods prevalence; socioeconomic	MULTICENTER	The development of effective management strategies to optimize the quality of life for allergic patients is currently hampered by a lack of good quality information. Estimates of how many individuals suffer from food allergy and the major foods involved vary widely and inadequacies of in vitro diagnostics make food challenges the only reliable means of diagnosis in many instances. The EuroPrevall project brings together a multidisciplinary partnership to address these issues. Cohorts spanning the main climatic regions of Europe are being developed in infants through a birth cohort, community surveys in school-age children and adults and an outpatient clinic study. Confirmatory double-blind placebo-controlled food challenge diagnosis is being undertaken using foods as they are eaten with titrated doses to allow no-effect and lowest-observable effect levels for allergenic foods to be determined. The cohorts will also facilitate validation of novel in vitro diagnostics through the development of the EuroPrevall Serum Bank. Complementary studies in Ghana, western Siberia, India and China will allow LIS to gain insights into how different dietary patterns and exposure to microorganisms affect food allergies. New instruments to assess the socioeconomic impact of food allergy are being developed in the project and their application in the clinical cohorts will allow, for the first time, an assessment to be made of the burden this disease places on allergy sufferers and their communities.	Inst Food Res, Norwich NR4 7UA, Norfolk, England; Univ London Imperial Coll Sci Technol & Med, London, England; Humboldt Univ, Univ Childrens Hosp Charite, Dept Paediat Pneumol & Immunol, Berlin, Germany; Univ Wageningen & Res Ctr, Dept Mkt & Consumer Behav, Wageningen, Netherlands; Tech Univ Denmark, Natl Food Inst, Soborg, Denmark; European Federat Allergy & Airways Dis Patients A, Brussels, Belgium; SEAC, Unilever Colworth, Sharnbrook, Beds, England; Univ Amsterdam, Acad Med Ctr, Dept Expt Immunol, NL-1105 AZ Amsterdam, Netherlands	Mills, ENC (reprint author), Inst Food Res, Norwich Res Pk, Norwich NR4 7UA, Norfolk, England.						ASERO R, 2006, MOL NUTR FOOD RES, V51, P135; Beyer K, 2005, CURR OPIN ALLERGY CL, V5, P261, DOI 10.1097/01.all.0000168792.27948.f9; Bindslev-Jensen C, 2002, ALLERGY, V57, P741, DOI 10.1034/j.1398-9995.2002.23797.x; Clark S, 2004, J ALLERGY CLIN IMMUN, V113, P347, DOI 10.1016/j.jaci.2003.10.053; Crevel RWR, 2007, FOOD CHEM TOXICOL, V45, P691, DOI 10.1016/j.fct.2006.09.005; de Blok BMJ, 2007, ALLERGY, V62, P733, DOI 10.1111/j.1398-9995.2006.01303.x; DunnGalvin A, 2006, ALLERGY, V61, P1336, DOI 10.1111/j.1398-9995.2006.01181.x; Eigenmann PA, 2002, ALLERGY, V57, P449, DOI 10.1034/j.1398-9995.2002.13494.x; Fernandez-Rivas M., 2004, PLANT FOOD ALLERGENS, P1; Hourihane JOB, 2001, ALLERGY, V56, P86; Knibb R.C., 2000, PSYCHOL HEALTH MED, V5, P419, DOI 10.1080/713690215; Miles S, 2005, ALLERGY, V60, P996, DOI 10.1111/j.1398-9995.2005.00868.x; Mills ENC, 2004, ALLERGY, V59, P1262, DOI 10.1111/j.1398-9995.2004.00720.x; Nickel R, 2002, PEDIATR ALLERGY IMMU, V13, P7, DOI 10.1034/j.1399-3038.13.s.15.4.x; Niggemann B, 2005, ALLERGY, V60, P865, DOI 10.1111/j.1398-9995.2005.00828.x; ONG LML, 1995, SOC SCI MED, V40, P903, DOI 10.1016/0277-9536(94)00155-M; Ortolani C, 1999, ALLERGY, V54, P27, DOI 10.1034/j.1398-9995.1999.00913.x; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Taylor SL, 2004, CLIN EXP ALLERGY, V34, P689, DOI 10.1111/j.1365-2222.2004.1886.x; Woods RK, 2001, EUR J CLIN NUTR, V55, P298, DOI 10.1038/sj.ejcn.1601159	20	100	106	0	13	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0105-4538			ALLERGY	Allergy	JUL	2007	62	7					717	722		10.1111/j.1398-9995.2007.01425.x		6	Allergy; Immunology	Allergy; Immunology	179VP	WOS:000247318500001	17573717	
J	Galassi, C; De Sario, M; Biggeri, A; Bisanti, L; Chellini, E; Ciccone, G; Petronio, MG; Piffer, S; Sestini, P; Rusconi, F; Viegi, G; Forastiere, F				Galassi, C; De Sario, M; Biggeri, A; Bisanti, L; Chellini, E; Ciccone, G; Petronio, MG; Piffer, S; Sestini, P; Rusconi, F; Viegi, G; Forastiere, F			Changes in prevalence of asthma and allergies among children and adolescents in Italy: 1994-2002	PEDIATRICS			English	Article						asthma; rhinitis; eczema; children; adolescents	INCREASING PREVALENCE; HAY-FEVER; SYMPTOMS; SCHOOLCHILDREN; RHINITIS; GERMANY; ECZEMA; TRENDS; ISAAC; SENSITIZATION	BACKGROUND. Several studies conducted during the 1990s indicated an increase in the prevalence of symptoms of asthma; more recent investigations suggest that the trend is stabilizing or may even be reversing. OBJECTIVE. We compared 2 cross-sectional surveys conducted in 1994 and 2002 in 8 areas in northern and central Italy, to evaluate prevalence changes for asthma, allergic rhinitis, and eczema. METHODS. The International Study of Asthma and Allergies in Childhood methods and questionnaires were used to investigate 6- to 7-year-old children (16 115 and 11 287 questionnaires completed by parents in 1994-1995 and 2002, respectively) and 13- to 14-year-old adolescents (19 723 and 10 267 questionnaires completed by adolescents in 1994-1995 and 2002, respectively). In each phase, the overall response rate was > 90%. Prevalence changes were calculated as the absolute difference between the prevalence recorded on the 2 occasions. RESULTS. The prevalence of wheeze (past 12 months) increased slightly among children (change: 0.8%; 95% confidence interval [CI]: 0.0% to 1.6%) and was rather stable among adolescents. Symptoms of allergic rhinitis (children: change: 5.2%; 95% CI: 4.0% to 6.4%; adolescents: change: 4.1%; 95% CI: 1.9% to 6.3%) and symptoms of atopic eczema ( children: change: 4.4%; 95% CI: 3.6% to 5.2%; adolescents: change: 2.1%; 95% CI: 1.2% to 3.0%) increased clearly in both age groups. There was some heterogeneity across the centers among adolescents, especially for allergic rhinitis, with larger increases seen in the 3 metropolitan areas. The changes observed paralleled profound family changes, ie, better parental education, higher rates of maternal employment, and lower rates of exposure to parental smoke. These factors, however, do not explain all of the observed changes in prevalence. CONCLUSIONS. The results indicate that the epidemiologic features of asthma and allergies in Italy are changing rapidly, although the causes are still uncertain.	Reg Hlth Agcy, Bologna, Italy; San Giovanni Battista Hosp, Ctr Canc Prevent, Canc Epidemiol Unit, Turin, Italy; Rome E Local Hlth Author, Dept Epidemiol, Rome, Italy; Univ Florence, Dept Stat, Florence, Italy; Local Hlth Author, Milan, Italy; Ctr Study & Prevent Canc, Florence, Italy; Empoli Local Hlth Author, Empoli, Italy; Provincial Hlth Author, Epidemiol Unit, Trento, Italy; Univ Siena, Inst Resp Dis, I-53100 Siena, Italy; Univ Milan, A Meyer Childrens Univ Hosp, Florence, Italy; CNR, Inst Clin Physiol, Pisa, Italy	Galassi, C (reprint author), AO San Giovanni Battista CPO Piemonte, Serv Epidemiol Tumori, Via Santena 7, I-10126 Turin, Italy.	claudia.galassi@cpo.it	Forastiere, Francesco/J-9067-2016; De sario, Manuela/K-1932-2016; Rusconi, Franca/K-2346-2016; Galassi, Claudia/K-3041-2016; Ciccone, Giovannino/K-3136-2016	Forastiere, Francesco/0000-0002-9162-5684; De sario, Manuela/0000-0002-1117-2735; Rusconi, Franca/0000-0002-9544-6472; Galassi, Claudia/0000-0003-1502-4390; Ciccone, Giovannino/0000-0001-7644-9574			Anderson HR, 2004, BRIT MED J, V328, P1052, DOI 10.1136/bmj.38057.583727.47; Anthracopoulos M, 2001, THORAX, V56, P569, DOI 10.1136/thorax.56.7.569; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Behrens T, 2004, PEDIATR ALLERGY IMMU, V15, P331, DOI 10.1111/j.1399-3038.2004.00157.x; Braun-Fahrlander C, 2004, EUR RESPIR J, V23, P407, DOI 10.1183/09031936.04.00074004; Chinn S, 2004, THORAX, V59, P646, DOI 10.1136/thx.2004.021642; Ciccone G, 1997, EUR RESPIR J, V10, P1780; Deeks J, 2001, SYSTEMATIC REV HLTH, P285, DOI 10.1002/9780470693926.ch15; Douwes J, 2002, INT J EPIDEMIOL, V31, P1098, DOI 10.1093/ije/31.6.1098; Douwes J, 2002, THORAX, V57, P643, DOI 10.1136/thorax.57.7.643; Downs SH, 2001, ARCH DIS CHILD, V84, P20, DOI 10.1136/adc.84.1.20; Esamai F, 2002, East Afr Med J, V79, P514; Greenland S., 1998, MODERN EPIDEMIOLOGY, P643; Heinrich J, 2002, EUR RESPIR J, V19, P1040, DOI 10.1183/09031936.02.00261802; International Study of Asthma and Allergy in Children (ISAAC), 2000, PHAS 3 MAN; *ISAAC, 1993, PHAS ON MAN; Kalyoncu AF, 1999, PEDIATR ALLERGY IMMU, V10, P261; Kwong GNM, 2001, THORAX, V56, P312, DOI 10.1136/thorax.56.4.312; Lee SL, 2004, PEDIATR ALLERGY IMMU, V15, P72, DOI 10.1046/j.0905-6157.2003.00109.x; Linneberg A, 2001, RESP MED, V95, P258, DOI 10.1053/rmed.2001.1031; Maziak W, 2003, ALLERGY, V58, P572, DOI 10.1034/j.1398-9995.2003.00161.x; Renzoni E, 1999, EUR RESPIR J, V14, P597, DOI 10.1034/j.1399-3003.1999.14c19.x; Ronchetti R, 2001, EUR RESPIR J, V17, P881, DOI 10.1183/09031936.01.17508810; Sunyer J, 2003, OCCUP ENVIRON MED, V60, DOI 10.1136/oem.60.8.e2; Toelle BG, 2004, BRIT MED J, V328, P386, DOI 10.1136/bmj.328.7436.386; Verlato G, 2003, J ALLERGY CLIN IMMUN, V111, P1232, DOI 10.1067/mai.2003.1484	26	100	105	0	2	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	JAN	2006	117	1					34	42		10.1542/peds.2004-2709		9	Pediatrics	Pediatrics	999QV	WOS:000234406100006	16396858	
J	Beggs, PJ; Bambrick, HJ				Beggs, PJ; Bambrick, HJ			Is the global rise of asthma an early impact of anthropogenic climate change?	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article							RAGWEED AMBROSIA-ARTEMISIIFOLIA; OUTDOOR AIR-POLLUTION; CHILDHOOD ASTHMA; ENVIRONMENTAL-FACTORS; PUBLIC-HEALTH; RESPIRATORY ALLERGY; COMMON RAGWEED; ATOPIC ECZEMA; PREVALENCE; POLLEN	The increase in asthma incidence, prevalence, and morbidity over recent decades presents a significant challenge to public health. Pollen is an important trigger of some types of asthma, and both pollen quantity and season depend on climatic and meteorologic variables. Over the same period as the global rise in asthma, there have been considerable increases in atmospheric carbon dioxide concentration and global average surface temperature. We hypothesize anthropogenic climate change as a plausible contributor to the rise in asthma. Greater concentrations of carbon dioxide and higher temperatures may increase pollen quantity and induce longer pollen seasons. Pollen allergenicity can also increase as a result of these changes in climate. Exposure in early life to a more allergenic environment may also provoke the development of other atopic conditions, such as eczema and allergic rhinitis. Although the etiology of asthma is complex, the recent global rise in asthma could be an early, health effect of anthropogenic climate change.	Macquarie Univ, Div Environm & Life Sci, Dept Phys Geog, Sydney, NSW 2109, Australia; Australian Natl Univ, Natl Ctr Epidemiol & Populat Hlth, Canberra, ACT, Australia	Beggs, PJ (reprint author), Macquarie Univ, Div Environm & Life Sci, Dept Phys Geog, Sydney, NSW 2109, Australia.	paul.beggs@mq.edu.au					Ahlholm JU, 1998, CLIN EXP ALLERGY, V28, P1384; ALBRITTON L, 2001, SCI BASIS CONTRIBUTI, P21; 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; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; Beasley R, 2002, J ALLERGY CLIN IMMUN, V109, pS482, DOI 10.1067/mai.2002.122716; Beasley R, 2000, J ALLERGY CLIN IMMUN, V105, pS466, DOI 10.1016/S0091-6749(00)90044-7; Beggs PJ, 2004, CLIN EXP ALLERGY, V34, P1507, DOI 10.1111/j.1365-2222.2004.02061.x; BJORKSTEN F, 1981, ACTA MED SCAND, V209, P299; Burge HA, 2000, ENVIRON HEALTH PERSP, V108, P653, DOI 10.2307/3454401; Carlsen KCL, 2002, PEDIATR ALLERGY IMMU, V13, P29; Charpin D, 1999, CLIN EXP ALLERGY, V29, P1474; Cohet C, 2004, J EPIDEMIOL COMMUN H, V58, P852, DOI 10.1136/jech.2003.019182; Corden JM, 2001, AEROBIOLOGIA, V17, P127, DOI 10.1023/A:1010876917512; CURSON P, 1993, CLIMATIC CHANGE, V25, P405, DOI 10.1007/BF01098384; D'Amato G, 2001, RESP MED, V95, P606, DOI 10.1053/rmed.2001.1112; D'Amato G, 2000, J INVEST ALLERG CLIN, V10, P123; Droste JHJ, 2000, CLIN EXP ALLERGY, V30, P1547; Eder Waltraud, 2004, Curr Opin Allergy Clin Immunol, V4, P113, DOI 10.1097/00130832-200404000-00008; Eduard W, 2004, THORAX, V59, P381, DOI 10.1136/thx.2004.013326; Ellwood P, 2001, EUR RESPIR J, V17, P436, DOI 10.1183/09031936.01.17304360; Emberlin J, 2002, INT J BIOMETEOROL, V46, P159, DOI 10.1007/s00484-002-0139-x; Fitter AH, 2002, SCIENCE, V296, P1689, DOI 10.1126/science.1071617; Fleming DM, 2000, THORAX, V55, P657, DOI 10.1136/thorax.55.8.657; Foliaki S, 2004, INT J EPIDEMIOL, V33, P558, DOI 10.1093/ije/dyh031; Gehring U, 2001, J ALLERGY CLIN IMMUN, V108, P847, DOI 10.1067/mai.2001.119026; Grossman J, 1997, CHEST, V111, pS11, DOI 10.1378/chest.111.2_Supplement.11S; Hijazi N, 2000, THORAX, V55, P775, DOI 10.1136/thorax.55.9.775; HJELMROOS M, 1995, INT ARCH ALLERGY IMM, V108, P368; HUYNEN M, 2003, HLTH GLOBAL ENV CH S, V1; IPCC-Intergovernmental Panel on Climate Change, 2001, CLIM CHANG 2001 IMP; Isolauri E, 2004, CLIN EXP ALLERGY, V34, P1007, DOI 10.1111/j.1365-2222.2004.01999.x; Kaiser HB, 2004, ALLERGY ASTHMA PROC, V25, P7; Kao CC, 2001, ASIAN PAC J ALLERGY, V19, P63; KEELING CD, 2003, ATMOSPHERIC CARBON D; Kerr RA, 2002, SCIENCE, V297, P497; LONGSTRETH J, 1991, ENVIRON HEALTH PERSP, V96, P139, DOI 10.2307/3431222; Menzel A, 1999, NATURE, V397, P659, DOI 10.1038/17709; Menzel A, 2000, INT J BIOMETEOROL, V44, P76, DOI 10.1007/s004840000054; Nolte H, 2001, ANN ALLERG ASTHMA IM, V87, P7; Patz JA, 2002, P NATL ACAD SCI USA, V99, P12506, DOI 10.1073/pnas.212467899; Pearce N, 2000, J Epidemiol Biostat, V5, P5; Portengen L, 2002, CLIN EXP ALLERGY, V32, P247, DOI 10.1046/j.1365-2222.2002.01310.x; Yool A., 2001, CLIMATE CHANGE 2001, P183; Rios JLM, 2004, ANN ALLERG ASTHMA IM, V92, P629; Robertson CF, 2004, MED J AUSTRALIA, V180, P273; Rodo X, 2002, P NATL ACAD SCI USA, V99, P12901, DOI 10.1073/pnas.182203999; Root TL, 2003, NATURE, V421, P57, DOI 10.1038/nature01333; Seaton A, 2000, PEDIATR ALLERGY IMMU, V11, P37, DOI 10.1034/j.1399-3038.2000.00509.x; SIGURS N, 1992, PEDIATRICS, V89, P735; SPIEKSMA FTM, 1995, GRANA, V34, P51; Strachan DP, 2000, BRIT MED BULL, V56, P865, DOI 10.1258/0007142001903562; Strachan DP, 2000, THORAX S1, V55, pS2; Sunyer J, 1999, EUR RESPIR J, V14, P885, DOI 10.1034/j.1399-3003.1999.14d26.x; Ulrik CS, 2000, ANN ALLERG ASTHMA IM, V85, P293; von Hertzen LC, 2004, ALLERGY, V59, P124, DOI 10.1046/j.1398-9995.2003.00433.x; von Mutius E, 1998, CLIN EXP ALLERGY, V28, P50; Walther GR, 2002, NATURE, V416, P389, DOI 10.1038/416389a; Wayne P, 2002, ANN ALLERG ASTHMA IM, V88, P279; Weinberg EG, 2000, J ALLERGY CLIN IMMUN, V105, P224, DOI 10.1016/S0091-6749(00)90069-1; World Health Organization, 2002, WORLD HLTH REP 2002; Wilkinson P., 2003, CLIMATE CHANGE HUMAN, P204; Woodward A, 2003, CLIMATE CHANGE HUMAN, P61; WULFF RD, 1985, OECOLOGIA, V66, P458, DOI 10.1007/BF00378315; 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	66	100	101	1	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.	AUG	2005	113	8					915	919		10.1289/ehp.7724		5	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	951OV	WOS:000230941100025	16079058	
J	Galan, I; Tobias, A; Banegas, JR; Aranguez, E				Galan, I; Tobias, A; Banegas, JR; Aranguez, E			Short-term effects of air pollution on daily asthma emergency room admissions	EUROPEAN RESPIRATORY JOURNAL			English	Article						air pollution; asthma; emergency room admissions; pollen; time-series	HOSPITAL ADMISSIONS; ENVIRONMENTAL-FACTORS; CHILDHOOD ASTHMA; SULFUR-DIOXIDE; APHEA PROJECT; MEXICO-CITY; VISITS; ASSOCIATION; POLLUTANTS; MORTALITY	Many time-series studies have shown positive associations between air pollutants and asthma morbidity. However, few studies have included pollen as a potential confounder when examining this relationship. This study analysed the short-term association between air pollutants (sulphur dioxide (SO2), particles measured with a median aerodynamic diameter of <10 mum (PM10), nitrogen dioxide (NO2) and ozone (O-3)) and asthma emergency room admissions in Madrid, Spain, in 1995-1998, adjusting for four types of pollen with allergenic potential (Olea europaea, Plantago sp., Poaceae and Urticaceae). Data were analysed using autoregressive Poisson regression and generalised additive models (GAM). The strongest associations were observed at 1 day lag for O-3, and 3 days lag for the remaining pollutants. Using Poisson regression, a single-pollutant model showed that a 10-mug-m(-3) rise in pollutant level led to relative risks of: 1.039 for PM10; 1.029 for SO2; 1.033 for NO2; and 1.045 for O-3. Adjustment for the different types of pollen led to no substantial variation in these associations. In the multipollutant models for cold-season pollutants (including PM10, SO2 and the four types of pollen) and photochemical pollutants (including NO2, O-3 and the four types of pollen) the associations for PM10, NO2 and O-3 held, but no relationship with SO2 was evident. GAM analysis yielded the same results, both in terms of lags and of quantification of the effect for all pollutants. In conclusion, the usual air pollution levels in Madrid were associated with an increase in asthma emergency room admissions, and this association remained controlling for the presence of ambient pollen.	Univ Carlos III Madrid, Dept Stat & Econometr, E-28903 Getafe, Spain; Inst Publ Hlth, Dept Epidemiol, Madrid, Spain; Univ Autonoma Madrid, Dept Prevent Med & Publ Hlth, Madrid, Spain	Tobias, A (reprint author), Univ Carlos III Madrid, Dept Stat & Econometr, C Madrid 126, E-28903 Getafe, Spain.		Galan, Ignacio/P-6451-2015; Osborne, Nicholas/N-4915-2015	Galan, Ignacio/0000-0003-0624-9993; Osborne, Nicholas/0000-0002-6700-2284			AKAIKE H, 1974, IEEE T AUTOMAT CONTR, VAC19, P716, DOI 10.1109/TAC.1974.1100705; Anderson HR, 1998, THORAX, V53, P842; Atkinson RW, 1999, EUR RESPIR J, V13, P257, DOI 10.1183/09031936.99.13225799; Atkinson RW, 2001, AM J RESP CRIT CARE, V164, P1860; Atkinson RW, 1999, ARCH ENVIRON HEALTH, V54, P398; Ballester Diez F, 1999, Rev Esp Salud Publica, V73, P165, DOI 10.1590/S1135-57271999000200006; BATES DV, 1990, ENVIRON RES, V51, P51, DOI 10.1016/S0013-9351(05)80182-3; Brunekreef B, 2000, LANCET, V355, P1517, DOI 10.1016/S0140-6736(00)02168-1; Brunekreef B, 2002, LANCET, V360, P1233, DOI 10.1016/S0140-6736(02)11274-8; Casillas AM, 1999, ANN ALLERG ASTHMA IM, V83, P624, DOI 10.1016/S1081-1206(10)62884-0; CASTELLSAGUE J, 1995, THORAX, V50, P1051, DOI 10.1136/thx.50.10.1051; Chen L, 2001, Rev Environ Health, V16, P133; CODY RP, 1992, ENVIRON RES, V58, P184, DOI 10.1016/S0013-9351(05)80214-2; DEVALIA JL, 1998, EUR RESPIR REV, V8, P175; *DIR GEN SAL PUBL, 2000, B EPIDEMIOLOGICO COM, V12, P33; Dominici F, 2002, AM J EPIDEMIOL, V156, P193, DOI 10.1093/aje/kwf062; Fauroux B, 2000, PEDIATR PULM, V30, P41; Garty BZ, 1998, ANN ALLERG ASTHMA IM, V81, P563, DOI 10.1016/S1081-1206(10)62707-X; Hagen JA, 2000, EPIDEMIOLOGY, V11, P136, DOI 10.1097/00001648-200003000-00009; Hastie T, 1990, GEN ADDITIVE MODELS; Higgins BG, 2000, EUR RESPIR J, V16, P61, DOI 10.1034/j.1399-3003.2000.16a11.x; ISHIZAKI T, 1987, ANN ALLERGY, V58, P265; Johnston SL, 1996, AM J RESP CRIT CARE, V154, P654; Jonasson G, 2000, ALLERGY, V55, P232, DOI 10.1034/j.1398-9995.2000.00387.x; Katsouyanni K, 2002, EPIDEMIOLOGY, V13, P742, DOI 10.1097/01.EDE.0000032424.22670.3E; Kelsall JE, 1997, AM J EPIDEMIOL, V146, P750; Koenig JQ, 1999, J ALLERGY CLIN IMMUN, V104, P717; Linneberg A, 2001, RESP MED, V95, P258, DOI 10.1053/rmed.2001.1031; Lipsett M, 1997, ENVIRON HEALTH PERSP, V105, P216, DOI 10.1289/ehp.97105216; MAGNUSSEN H, 1998, EUR RESPIR REV, V8, P141; Polosa R, 1999, Can Respir J, V6, P436; ROMIEU I, 1995, AM J EPIDEMIOL, V141, P546; Rosas I, 1998, ALLERGY, V53, P394, DOI 10.1111/j.1398-9995.1998.tb03911.x; ROSSI OVJ, 1993, THORAX, V48, P244, DOI 10.1136/thx.48.3.244; Samet JM, 2000, NEW ENGL J MED, V343, P1742, DOI 10.1056/NEJM200012143432401; Samoli E, 2001, ENVIRON HEALTH PERSP, V109, P349, DOI 10.2307/3454893; SANDSTROM T, 1998, EUR RESPIR REV, V8, P168; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; SCHWARTZ JB, 1996, PDA J PHARM SCI TECH, V50, P1; Stieb DM, 1996, ENVIRON HEALTH PERSP, V104, P1354, DOI 10.2307/3432974; Strachan DP, 2000, BRIT MED BULL, V56, P865, DOI 10.1258/0007142001903562; SUBIZA J, 1995, J ALLERGY CLIN IMMUN, V96, P15, DOI 10.1016/S0091-6749(95)70028-5; Sunyer J, 1997, THORAX, V52, P760; SUNYER J, 1998, EUR RESPIR REV, V8, P139; Svartengren M, 2000, EUR RESPIR J, V15, P716, DOI 10.1034/j.1399-3003.2000.15d15.x; Tenias JM, 1998, OCCUP ENVIRON MED, V55, P541; THIBAUT G, 1991, AUDIT DEVALUATION RE; Thompson AJ, 2001, ARCH ENVIRON HEALTH, V56, P234; Tunnicliffe WS, 2001, EUR RESPIR J, V17, P604, DOI 10.1183/09031936.01.17406040; WALTERS S, 1994, THORAX, V49, P133, DOI 10.1136/thx.49.2.133; WARDLAW AJ, 1993, CLIN EXP ALLERGY, V23, P81, DOI 10.1111/j.1365-2222.1993.tb00303.x; Yang W, 1997, INHAL TOXICOL, V9, P15, DOI 10.1080/089583797198385	52	100	102	2	9	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.	NOV	2003	22	5					802	808		10.1183/09031936.03.00013003		7	Respiratory System	Respiratory System	739UE	WOS:000186364200017	14621088	
J	Linneberg, A; Ostergaard, C; Tvede, M; Andersen, LP; Nielsen, NH; Madsen, F; Frolund, L; Dirksen, A; Jorgensen, T				Linneberg, A; Ostergaard, C; Tvede, M; Andersen, LP; Nielsen, NH; Madsen, F; Frolund, L; Dirksen, A; Jorgensen, T			IgG antibodies against microorganisms and atopic disease in Danish adults: The Copenhagen Allergy Study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergic rhinitis; atopy; Campylobacter jejuni; Clostridium difficile; Helicobacter pylori; hepatitis A virus; respiratory hypersensitivity; Toxoplasma gondii	HEPATITIS-A; INTESTINAL MICROFLORA; HELICOBACTER-PYLORI; HYGIENE HYPOTHESIS; HAY-FEVER; PREVALENCE; INFECTION; ASTHMA; POPULATION; INFANTS	Background: Seropositivity to food-borne and orofecal microorganisms (hepatitis A virus, Helicobacter pylori, and Toxoplasma gondii), which are considered to be markers of poor hygiene, has been reported to be associated with a lower prevalence of atopy. In contrast, colonization of the gut with Clostridium difficile, a potential intestinal bacterial pathogen, in early childhood may be associated with a higher prevalence of atopy. Objective: The objective of this study was to investigate the association between atopy and exposure to 2 groups of food-borne and orofecal microorganisms: (1) markers of a poor hygiene and (2) intestinal bacterial pathogens. Methods: A cross-sectional population-based study of 15- to 69-year-olds living in Copenhagen, Denmark, was carried out in 1990 to 1991. Atopy was defined as a positive test result for specific IgE to at least 1 of 6 inhalant allergens. Exposure to microorganisms was assessed as IgG seropositivity to microorganisms. Results: Seropositivity to 2 or 3 markers of poor hygiene (hepatitis A virus, H pylori, and T gondii) was associated with a lower prevalence of atopy (adjusted odds ratio, 0.5; 95% CI, 0.3 to 0.8). In contrast, seropositivity to 2 or 3 intestinal bacterial pathogens (C difficile, Campylobacter jejuni, and Yersinia enterocolitica) was associated with a higher prevalence of atopy (adjusted odds ratio, 1.7; 95% Cl, 1.2 to 2.6). Conclusion: Exposure to markers of poor hygiene was associated with a lower prevalence of atopy, whereas exposure to intestinal bacterial pathogens was associated with a higher prevalence of atopy. These findings raise the hypothesis that different groups of food-borne and orofecal microorganisms may have different effects on the risk of atopy.	Glostrup Univ Hosp, Ctr Prevent Med, DK-2600 Glostrup, Denmark; Statens Serum Inst, Dept Res & Dev, DK-2300 Copenhagen, Denmark; Natl Univ Hosp, Dept Clin Microbiol, Rigshosp, Copenhagen, Denmark; Gentofte Univ Hosp, Dept Dermatol, Copenhagen, Denmark; Frederiksberg Univ Hosp, Dept Internal Med B, DK-2000 Copenhagen, Denmark; Gentofte Univ Hosp, Dept Resp Med Y, Copenhagen, Denmark	Linneberg, A (reprint author), Glostrup Univ Hosp, Ctr Prevent Med, 57 Ndr Ringvej,Entrance 8,7th Floor, DK-2600 Glostrup, Denmark.			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Allergy Clin. Immunol.	APR	2003	111	4					847	853		10.1067/mai.2003.1335		7	Allergy; Immunology	Allergy; Immunology	667WW	WOS:000182258500028	12704368	
J	Burke, W; Fesinmeyer, M; Reed, K; Hampson, L; Carlsten, C				Burke, W; Fesinmeyer, M; Reed, K; Hampson, L; Carlsten, C			Family history as a predictor of asthma risk	AMERICAN JOURNAL OF PREVENTIVE MEDICINE			English	Article							PRIMARY-SCHOOL CHILDREN; CHILDHOOD ASTHMA; ALLERGIC DISEASES; AIRWAY HYPERRESPONSIVENESS; BRONCHIAL-ASTHMA; PARENTAL SMOKING; YOUNG-CHILDREN; PREVALENCE; SYMPTOMS; ATOPY	Background: Asthma, one of the most important chronic diseases of children, disproportionately affects minority and low-income children. Many environmental risk factors for asthma have been identified, including animal, mite, and other allergens; cigarette smoke; and air pollutants. Genetics also play an important causative role, as indicated by familial aggregation and the identification of candidate genes and chromosomal regions linked to asthma risk. Using a positive family history of asthma to identify children at increased risk could provide a basis for targeted prevention efforts, aimed at reducing exposure to environmental risk factors. Methods: To assess the predictive value of family history as an indicator of risk for childhood asthma, we reviewed population-based studies that evaluated family history of asthma and atopic disease in children with asthma. Results: Our search identified 33 studies from all geographic regions of the world for review. The studies varied in definitions of positive family history and asthma phenotype and used study populations with asthma prevalence ranging from 2% to 26%. Nevertheless, family history of asthma in one or more first-degree relatives was consistently identified as a risk factor for asthma. In ten studies, sensitivity and predictive value of a positive family history of asthma could be calculated: sensitivity ranged from 4% to 43%, positive predictive value from 11% to 37%, and negative predictive value from 86% to 97%. Conclusion: Although a positive family history predicts an increased risk of asthma, it identifies a minority of children at risk. Positive family history may have utility in targeting some individual prevention efforts, but the low positive predictive value limits its value as a means to direct environmental remediation efforts.	Univ Washington, Dept Med Hist & Eth, Seattle, WA 98195 USA; Univ Washington, Inst Publ Hlth Genet, Seattle, WA 98195 USA; Univ Washington, Dept Med, Seattle, WA 98195 USA	Burke, W (reprint author), Univ Washington, Dept Med Hist & Eth, Box 357120,1959 NE Pacific, Seattle, WA 98195 USA.			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J. Prev. Med.	FEB	2003	24	2					160	169		10.1016/S0749-3797(02)00589-5		10	Public, Environmental & Occupational Health; Medicine, General & Internal	Public, Environmental & Occupational Health; General & Internal Medicine	643BV	WOS:000180842800007	12568822	
J	Paredi, P; Kharitonov, SA; Barnes, PJ				Paredi, P; Kharitonov, SA; Barnes, PJ			Analysis of expired air for oxidation products	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article; Proceedings Paper	17th Transatlantic Airway Conference on Oxidants and Antioxdants	2002	LUZERN, SWITZERLAND	Boehringer Ingelheim Co		oxidative stress; noninvasive assessment	EXHALED CARBON-MONOXIDE; OBSTRUCTIVE PULMONARY-DISEASE; SMOOTH-MUSCLE CELLS; MESSENGER-RNA EXPRESSION; NITRIC-OXIDE; CYSTIC-FIBROSIS; LIPID-PEROXIDATION; ASTHMATIC-PATIENTS; HEME OXYGENASE-1; BREATH CONDENSATE	Chronic inflammation is a critical feature of chronic obstructive pulmonary disease, cystic fibrosis, and asthma. This inflammation is associated with the increased production of reactive oxygen species or oxidative stress in the lungs. Oxidative stress may have several adverse effects and may amplify the inflammatory process; however, monitoring oxidative stress is difficult and may not be reflected by changes in blood markers. We have therefore developed several noninvasive markers in the exhaled breath that may indicate oxidative stress in the lungs, and we studied these in relationship to the severity of chronic inflammatory lung diseases. We analyzed the exhaled breath for the content of nitric oxide as a marker of inflammation, carbon monoxide as a marker of oxidative stress, and ethane, which is one of the end products of lipid peroxidation. In addition, we measured the concentration of markers of oxidative stress such as isoprostanes in exhaled breath condensate. Our results confirm that there are increased inflammation, oxidative stress, and lipid peroxidation in lung disease, as shown by elevated levels of nitric oxide, carbon monoxide, and ethane, respectively. The finding of lower levels of these gases in patients on steroid treatment and of higher levels in those with more severe lung disease, as assessed by lung function tests and clinical symptoms, reinforces the hypothesis that the noninvasive measurement of exhaled gases maybe useful in monitoring the underlying pathologic pathways of lung disease. Longitudinal studies are required to assess the clinical usefulness of these measurements in the monitoring of chronic inflammatory lung disease.	Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Thorac Med, London SW3 6LY, England	Barnes, PJ (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Thorac Med, Dovehouse St, London SW3 6LY, England.						ALVING K, 1993, EUR RESPIR J, V6, P1368; Antczak A, 1997, EUR RESPIR J, V10, P1235, DOI 10.1183/09031936.97.10061235; Antuni JD, 2000, THORAX, V55, P138, DOI 10.1136/thorax.55.2.138; AULIK I. 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J. Respir. Crit. Care Med.	DEC 15	2002	166	12		S			S31	S37		10.1164/rccm.2206012		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	625DT	WOS:000179802200007	12471086	
J	Hoffjan, S; Ober, C				Hoffjan, S; Ober, C			Present status on the genetic studies of asthma	CURRENT OPINION IN IMMUNOLOGY			English	Review							RECEPTOR-ALPHA-CHAIN; QUANTITATIVE-TRAIT LOCI; SERUM IGE LEVELS; GENOME-WIDE SEARCH; INTERLEUKIN-4 RECEPTOR; ATOPIC ASTHMA; IL-4 RECEPTOR; CODING REGION; AIRWAY HYPERRESPONSIVENESS; PROMOTER POLYMORPHISMS	Asthma, one of the most common chronic diseases, is a complex and heterogeneous disorder. The results of genome screens for asthma-related traits in 11 different populations identified at least 18 regions of the genome that probably house asthma/atopy genes. The most consistently replicated regions are on chromosomes 2% 5q, 6p, 12q and 13q. Positional cloning projects are ongoing in laboratories around the world to identify the asthma susceptibility loci in these regions. In addition, many candidate genes have been associated with asthma phenotypes, such as the genes in the IL-4/IL-13 pathway.	Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA	Hoffjan, S (reprint author), Univ Chicago, Dept Human Genet, 920 E 58th St, Chicago, IL 60637 USA.						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Opin. Immunol.	DEC	2002	14	6					709	717		10.1016/S0952-7915(02)00393-X		9	Immunology	Immunology	607VZ	WOS:000178812600006	12413520	
J	Comhair, SAA; Bhathena, PR; Farver, C; Thunnissen, FBJM; Erzurum, SC				Comhair, SAA; Bhathena, PR; Farver, C; Thunnissen, FBJM; Erzurum, SC			Extracellular glutathione peroxidase induction in asthmatic lungs: evidence for redox regulation of expression in human airway epithelial cells	FASEB JOURNAL			English	Article						reactive oxygen species; asthma; lung; nitrotyrosine	NITRIC-OXIDE SYNTHASE; PLASMA GLUTATHIONE; SUPEROXIDE-DISMUTASE; EXHALED AIR; GENE; ANTIOXIDANT; OXIDATION; PEROXYNITRITE; INFLAMMATION; SEQUENCE	A critical first-line antioxidant defense on the airway epithelial surface against reactive oxygen and nitrogen species (ROS and RNS) is extracellular glutathione peroxidase (eGPx). Little is known about the regulation of eGPx or its role in ROS-mediated lung diseases such as asthma. Here we show that eGPx is increased in the asthmatic airway in comparison to healthy controls. Higher levels of eGPx mRNA in asthmatic airway epithelium verified bronchial epithelial cells as the source for the increased eGPx, The eGPx mRNA in bronchial epithelial cells in vitro increased eightfold after exposure to ROS and glutathione, an essential cofactor for eGPx activity. Alterations in intracellular and extracellular oxidized and reduced glutathione were temporally associated with eGPx induction, further supporting redox mechanisms in gene expression, Overexpression of superoxide dismutase, but not catalase, inhibited induction and identified superoxide as a key intermediary. The eGPx mRNA half-life was not affected by ROS, suggesting a transcriptional mechanism for eGPx regulation. Fusion genes of deletion fragments of the eGPx gene 5' flanking region driving a reporter gene conclusively identified the ROS-responsive region, which contained the consensus DNA binding site for the redox-regulated transcription factor, activator protein 1.	Cleveland Clin Fdn, Dept Pulm & Crit Care Med, Lerner Res Inst, Cleveland, OH 44195 USA; Cleveland Clin Fdn, Dept Canc Biol, Lerner Res Inst, Cleveland, OH 44195 USA; Cleveland Clin Fdn, Dept Pathol, Lerner Res Inst, Cleveland, OH 44195 USA; Canisius Wilhelmina Hosp, Dept Pathol, NL-6500 GS Nijmegen, Netherlands	Erzurum, SC (reprint author), Cleveland Clin Fdn, Dept Pulm & Crit Care Med, Lerner Res Inst, 9500 Euclid Ave,A90, Cleveland, OH 44195 USA.				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J	Gagliardo, R; Chanez, P; Vignola, AM; Bousquet, J; Vachier, I; Godard, P; Bonsignore, G; Demoly, P; Mathieu, M				Gagliardo, R; Chanez, P; Vignola, AM; Bousquet, J; Vachier, I; Godard, P; Bonsignore, G; Demoly, P; Mathieu, M			Glucocorticoid receptor alpha and beta in glucocorticoid dependent asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							COLONY-STIMULATING FACTOR; NF-KAPPA-B; BRONCHIAL-MUCOSA; TRANSCRIPTION FACTORS; HUMAN NEUTROPHILS; MESSENGER-RNA; EXPRESSION; GENE; INFLAMMATION; ISOFORM	Patients with glucocorticoid (CC)-dependent asthma present an ongoing inflammation of the airways despite chronic long-term treatment with oral GC. Interleukin (IL)-8 and granulocyte/macrophage colony-stimulating factor (GM-CSF) have been implicated in airway inflammation in severe asthma and their synthesis is normally repressed by GC. To further characterize the inflammatory process in GC-dependent asthma, we measured the release of IL-8 and CM-CSF by peripheral blood mononuclear cells (PBMC) of eight normal subjects, six untreated controlled asthmatics, six untreated uncontrolled asthmatics, and nine CC-dependent asthmatics. We show that PBMC from CC-dependent asthmatics released high amounts of these cytokines despite chronic in vivo exposure to CC (p < 0.001 versus normal subjects). In contrast, when untreated uncontrolled asthmatics were given a short course of oral CC, IL-8 and CM-CSF production was inhibited (p = 0.0078). Release of IL-8 and GM-CSF by PBMC of CC-dependent asthmatics was reduced after in vitro GC treatment (p < 0.002). We investigated whether the incapacity of CC to inhibit production of these cytokines in vivo was the result of a dysregulation of the glucocorticoid receptor (GR) in CC-dependent asthma. GR alpha and GR beta are, respectively, the functional receptor and a putative dominant negative form of the receptor. Western blot and polymerase chain reaction (PCR) analyses indicated that GR alpha was expressed at similar level in all groups and was largely predominant over GR beta. Thus, persistent release of IL-8 and CM-CSF in CC-dependent asthma is not associated with low expression of GR alpha or overexpression of GR beta.	CHU Montpellier, INSERM U454, F-34095 Montpellier 5, France; CHU Montpellier, Serv Malad Resp, F-34095 Montpellier, France; CNRS, Ist Fisiopatol Resp, Palermo, Italy	Mathieu, M (reprint author), CHU Montpellier, INSERM U454, F-34095 Montpellier 5, France.						American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P225, DOI DOI 10.1164/AJRCCM/136.1.225; Andersson O, 1999, J ALLERGY CLIN IMMUN, V103, P595, DOI 10.1016/S0091-6749(99)70230-7; Bamberger CM, 1997, MOL CELL ENDOCRINOL, V136, P23, DOI 10.1016/S0303-7207(97)00209-8; BAMBERGER CM, 1995, J CLIN INVEST, V95, P2435, DOI 10.1172/JCI117943; BOUSQUET J, 1990, NEW ENGL J MED, V323, P1033, DOI 10.1056/NEJM199010113231505; Brogan IJ, 1999, MOL CELL ENDOCRINOL, V157, P95, DOI 10.1016/S0303-7207(99)00156-2; CARMICHAEL J, 1981, BRIT MED J, V282, P1419; Castro M, 1996, MOL MED, V2, P597; Cato ACB, 1996, BIOESSAYS, V18, P371, DOI 10.1002/bies.950180507; CHANEZ P, 1996, AM J RESP CRIT CARE, V153, pA212; CLARK SC, 1987, SCIENCE, V236, P1229, DOI 10.1126/science.3296190; COX G, 1995, J IMMUNOL, V154, P4719; de Lange P, 1999, MOL CELL ENDOCRINOL, V153, P163, DOI 10.1016/S0303-7207(99)00072-6; DYKEWICZ MS, 1986, ARCH INTERN MED, V146, P2369, DOI 10.1001/archinte.146.12.2369; Hamid QA, 1999, AM J RESP CRIT CARE, V159, P1600; Hancox RJ, 1999, THORAX, V54, P488; Hecht K, 1997, J BIOL CHEM, V272, P26659, DOI 10.1074/jbc.272.42.26659; HOLLENBERG SM, 1985, NATURE, V318, P635, DOI 10.1038/318635a0; Jatakanon A, 1999, AM J RESP CRIT CARE, V160, P1532; Leung DYM, 1997, J EXP MED, V186, P1567, DOI 10.1084/jem.186.9.1567; Mathieu M, 1999, GENE THER, V6, P245, DOI 10.1038/sj.gt.3300814; MUKAIDA N, 1994, J BIOL CHEM, V269, P13289; Oakley RH, 1996, J BIOL CHEM, V271, P9550; Pizzichini MMM, 1999, EUR RESPIR J, V13, P15, DOI 10.1183/09031936.99.13101599; SCHRECK R, 1990, MOL CELL BIOL, V10, P1281; SHER ER, 1994, J CLIN INVEST, V93, P33, DOI 10.1172/JCI116963; Shute JK, 1997, AM J RESP CRIT CARE, V155, P1877; TOBLER A, 1992, BLOOD, V79, P45; Vachier I, 1996, CLIN EXP IMMUNOL, V103, P311, DOI 10.1046/j.1365-2249.1996.d01-628.x; Vachier I, 1998, AM J RESP CRIT CARE, V158, P963; Vrugt B, 1999, EUR RESPIR J, V13, P1245, DOI 10.1183/09031936.99.13612539; WALLAERT B, 1995, J EXP MED, V182, P1897, DOI 10.1084/jem.182.6.1897; WALZ A, 1991, J LEUKOCYTE BIOL, V50, P279; Wenzel SE, 1999, AM J RESP CRIT CARE, V160, P1001; Wenzel SE, 1997, AM J RESP CRIT CARE, V156, P737	35	100	109	1	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					7	13				7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	333JH	WOS:000088126800003	10903212	
J	Zhou, Y; Wu, Y; Yang, L; Fu, LX; He, KB; Wang, SX; Hao, JM; Chen, JC; Li, CY				Zhou, Yu; Wu, Ye; Yang, Liu; Fu, Lixin; He, Kebin; Wang, Shuxiao; Hao, Jiming; Chen, Jinchuan; Li, Chunyan			The impact of transportation control measures on emission reductions during the 2008 Olympic Games in Beijing, China	ATMOSPHERIC ENVIRONMENT			English	Article						Olympic Games; Transportation control measures; Emission inventory; Beijing	URBAN AIR-QUALITY; MOTOR-VEHICLE GROWTH; VEHICULAR EMISSIONS; CHILDHOOD ASTHMA; POLLUTION; AREA; ROAD; MODELS; BUSAN; KOREA	Traffic congestion and air pollution were two major challenges for the planners of the 2008 Olympic Games in Beijing. The Beijing municipal government implemented a package of temporary transportation control measures during the event. In this paper. we report the results of a recent research project that investigated the effects of these measures on urban motor vehicle emissions in Beijing. Bottom-up methodology has been used to develop grid-based emission inventories with micro-scale vehicle activities and speed-dependent emission factors. The urban traffic emissions of volatile organic compounds (VOC). carbon monoxide (CO), nitrogen oxides (NO(x)) and particulate matter with an aerodynamic diameter of 10 mu m or less (PM(10)) during the 2008 Olympics were reduced by 55.5%, 56.8%, 45.7% and 51.6%, respectively, as compared to the grid-based emission inventory before the Olympics. Emission intensity was derived from curbside air quality monitoring at the North 4th Ring Road site, located about 7 km from the National Stadium. Comparison between the emission intensity before and during the 2008 Olympics shows a reduction of 44.5% and 49.0% in daily CO and NO(x) emission from motor vehicles. The results suggest that reasonable traffic system improvement strategies along with vehicle technology improvements can contribute to controlling total motor vehicle emissions in Beijing after the Olympic Games. (C) 2009 Elsevier Ltd. All rights reserved.	[Zhou, Yu; Wu, Ye; Yang, Liu; Fu, Lixin; He, Kebin; Wang, Shuxiao; Hao, Jiming] Tsinghua Univ, Dept Environm Sci & Engn, Beijing 100084, Peoples R China; [Zhou, Yu; Wu, Ye; Yang, Liu; Fu, Lixin; He, Kebin; Wang, Shuxiao; Hao, Jiming] Tsinghua Univ, State Key Joint Lab Environm Simulat & Pollut Con, Beijing 100084, Peoples R China; [Chen, Jinchuan; Li, Chunyan] Beijing Transportat Res Ctr, Beijing 100055, Peoples R China	Hao, JM (reprint author), Tsinghua Univ, Dept Environm Sci & Engn, Beijing 100084, Peoples R China.	hjm-den@tsinghua.edu.cn	wang, shuxiao/H-5990-2011; Wu, Ye/O-9779-2015	wang, shuxiao/0000-0001-9727-1963; 	State Key Joint Laboratory of Environment Simulation and Pollution Control [08Y04ESPCT]; National Natural Science Foundation of China [50678092, 50908121]	This study is sponsored by the Special Fund of State Key Joint Laboratory of Environment Simulation and Pollution Control (08Y04ESPCT) and National Natural Science Foundation of China (Project No. 50678092 and Project No. 50908121). The authors thank Mr. Chuck Freed of US EPA and Mr. Jerry Davis of North Carolina State University for their helpful advice to improve this paper. The contents of this paper are solely the responsibility of the authors and do not necessarily represent official views of the sponsors.	BENSON PE, 1992, ATMOS ENVIRON B-URB, V26, P379, DOI 10.1016/0957-1272(92)90013-I; *BSB, 2008, BEIJ STAT YB 2008; Frantzeskakis JM, 2006, ITE J, V76, P26; Friedman MS, 2001, JAMA-J AM MED ASSOC, V285, P897, DOI 10.1001/jama.285.7.897; Fu L., 1999, CHINA ENV SCI, V19, P552; Fu L. 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Environ.	JAN	2010	44	3					285	293		10.1016/j.atmosenv.2009.10.040		9	Environmental Sciences; Meteorology & Atmospheric Sciences	Environmental Sciences & Ecology; Meteorology & Atmospheric Sciences	553GE	WOS:000274353500001		
J	Nathan, AT; Peterson, EA; Chakir, J; Wills-Karp, M				Nathan, Amy T.; Peterson, Elizabeth A.; Chakir, Jamila; Wills-Karp, Marsha			Innate immune responses of airway epithelium to house dust mite are mediated through beta-glucan-dependent pathways	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Asthma; allergy; house dust mite; epithelium; dendritic cell; chemokine; pattern recognition; innate immunity	T-CELL RESPONSES; DERMATOPHAGOIDES-PTERONYSSINUS; DENDRITIC CELLS; RECEPTOR CCR6; ATOPIC ASTHMA; MOUSE LUNG; ALLERGEN; INFLAMMATION; ENDOTOXIN; CCL20	Background: House dust mite (HDM) induces allergic asthma in sensitized individuals, although the mechanisms by which HDM is sensed and recognized by the airway mucosa, leading to dendritic cell (DC) recruitment, activation, and subsequent T(H)2-mediated responses, are unknown. Objective: We sought to define the pathways by which HDM activates respiratory epithelium to induce allergic airway responses. Methods: Using a human airway epithelial cell line (16HBE14o-), we studied secretion of the DC chemokine CCL20 after exposure to HDM or other allergens, investigated components of the HDM responsible for the induction of chemokine release, and examined activation of signaling pathways. Central findings were also confirmed in primary human bronchial cells. Results: We demonstrate that exposure of airway epithelium to HDM results in specific and rapid secretion of CCL20, a chemokine attractant for immature DCs. The induction of CCL20 secretion is dose and time dependent and quite specific to HDM because other allergens, such as ragweed pollen and cockroach antigen, fail to significantly induce CCL20 secretion. Induction of CCL20 secretion is not protease or Toll-like receptor 2/4 dependent but, interestingly, relies on beta-glucan moieties within the HDM extract, as evidenced by the ability of other beta-glucans to competitively inhibit its secretion and by the fact that disruption of these structures by treatment of HDM with beta-glucanase significantly reduces subsequent chemokine secretion. Conclusion: Taken together, our results describe a novel mechanism for specific pattern recognition of HDM-derived beta-glucan moieties, which initiates allergic airway inflammation and, through recruitment of DCs, might link innate pattern recognition at the airway surface with adaptive immune responses. (J Allergy Clin Immunol 2009;123:612-8.)	[Nathan, Amy T.; Peterson, Elizabeth A.] Cincinnati Childrens Hosp, Med Ctr, Dept Pediat, Div Neonatol, Cincinnati, OH 45229 USA; [Wills-Karp, Marsha] Cincinnati Childrens Hosp, Med Ctr, Dept Pediat, Div Immunobiol, Cincinnati, OH 45229 USA; [Chakir, Jamila] Laval Hosp, Res Ctr, Dept Med, Laval, PQ, Canada	Nathan, AT (reprint author), Cincinnati Childrens Hosp, Med Ctr, Dept Pediat, Div Neonatol, 3333 Burnet Ave,MLC 7038, Cincinnati, OH 45229 USA.	Amy.Nathan@cchmc.org			National Institutes of Health [P01 HL076383, R01 H667737]	M.W.-K. received grant support from the National Institutes of Health (P01 HL076383 and R01 H667737).	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Allergy Clin. Immunol.	MAR	2009	123	3					612	618		10.1016/j.jaci.2008.12.006		7	Allergy; Immunology	Allergy; Immunology	426TQ	WOS:000264731200019	19178937	
J	Jeon, SK; Kim, HJ; Youm, JK; Ahn, SK; Choi, EH; Sohn, MH; Kim, KE; Hong, JH; Shin, DM; Lee, SH				Jeon, Se Kyoo; Kim, Hyun Jeong; Youm, Jong-Kyung; Ahn, Sung Ku; Choi, Eung Ho; Sohn, Myung Hyun; Kim, Kyu-Earn; Hong, Jeong Hee; Shin, Dong Min; Lee, Seung Hun			Mite and cockroach allergens activate protease-activated receptor 2 and delay epidermal permeability barrier recovery	JOURNAL OF INVESTIGATIVE DERMATOLOGY			English	Article							HOUSE-DUST MITES; ATOPY PATCH TEST; EPITHELIAL-CELLS; STRATUM-CORNEUM; THROMBIN RECEPTOR; TIGHT JUNCTIONS; HAIRLESS MICE; DERMATITIS; SKIN; ASSOCIATION	Protease-activated receptor-2 (PAR-2) is known to be involved in epidermal permeability barrier function homeostasis. PAR-2 activation occurs after barrier disruption and further activation of PAR-2 by activating peptide significantly delays barrier recovery rate. Cockroach and house dust mite allergens, both known to be associated with the development of asthma, allergic rhinitis, and atopic dermatitis, have protease activity, which can activate PAR-2. In this study, we investigated the effects of both allergens on the epidermal barrier function as well as on the epidermal calcium gradient. Both allergens, when topically applied on the barrier-disrupted site, increased protease activities in the epidermis and delayed barrier recovery and lamellar body secretion in murine skin. The topical application of PAR-2-specific antagonist or protease inhibitors normalized the barrier recovery. Cockroach allergens induced intracellular calcium oscillations in cultured human keratinocytes through PAR-2-involved pathway, which was confirmed by desensitization protocol. Abnormal calcium ion distribution after barrier disruption was also observed in allergens-applied skin. These results suggest that allergens with protease activity can influence the epidermal permeability barrier homeostasis through PAR-2 activation and consequent modulation of the calcium ions in skin.	[Jeon, Se Kyoo; Youm, Jong-Kyung] Yonsei Univ, Coll Med, Brain Korea Project Med Sci 21, Seoul 132720, South Korea; [Kim, Hyun Jeong; Lee, Seung Hun] Yonsei Univ, Coll Med, Dept Dermatol, Seoul 132720, South Korea; [Ahn, Sung Ku; Choi, Eung Ho] Yonsei Univ, Wonju Coll Med, Dept Dermatol, Wonju, South Korea; [Sohn, Myung Hyun; Kim, Kyu-Earn] Yonsei Univ, Coll Med, Dept Pediat, Seoul 132720, South Korea; [Hong, Jeong Hee; Shin, Dong Min] Yonsei Univ, Coll Dent, Oral Sci Res Ctr, Dept Oral Biochem,Brain Korea Project 21, Seoul 132720, South Korea	Lee, SH (reprint author), Yonsei Univ, Yongdong Severance Hosp, Coll Med, Dept Dermatol, 146-92 Dogok Dong, Seoul 132720, South Korea.	ydshderm@yumc.yonsei.ac.kr					Ahn SK, 2001, ARCH DERMATOL RES, V293, P308, DOI 10.1007/s004030100226; Ashida Y, 2001, J INVEST DERMATOL, V116, P261, DOI 10.1046/j.1523-1747.2001.01238.x; Asokananthan N, 2002, J IMMUNOL, V169, P4572; Beltrani Vincent, 2002, Am J Contact Dermat, V13, P80, DOI 10.1053/ajcd.2002.32026; Beltrani VS, 2003, CLIN DERMATOL, V21, P177, DOI 10.1016/S0738-081X(02)00366-8; Cork MJ, 2006, J ALLERGY CLIN IMMUN, V118, P3, DOI 10.1016/j.jaci.2006.04.042; D'Andrea MR, 1998, J HISTOCHEM CYTOCHEM, V46, P157; Darsow U, 2004, ALLERGY, V59, P1318, DOI 10.1111/j.1398-9995.2004.00556.x; Denda M, 1997, J INVEST DERMATOL, V109, P84, DOI 10.1111/1523-1747.ep12276640; Denda M, 2004, J INVEST DERMATOL, V122, P140, DOI 10.1046/j.0022-202X.2003.22115.x; Egelrud T, 2005, BRIT J DERMATOL, V153, P1200, DOI 10.1111/j.1365-2133.2005.06834.x; Elias PM, 2005, J INVEST DERMATOL, V125, P183, DOI 10.1111/j.0022-202X.2005.23668.x; Folster-Holst R, 2005, BRIT J DERMATOL, V152, P1365, DOI 10.1111/j.1365-2133.2005.06602.x; Gfesser M, 1996, BRIT J DERMATOL, V135, P560, DOI 10.1111/j.1365-2133.1996.tb03831.x; Goon A, 2005, CLIN EXP DERMATOL, V30, P627, DOI 10.1111/j.1365-2230.2005.01916.x; Hachem JP, 2006, J INVEST DERMATOL, V126, P2074, DOI 10.1038/sj.jid.5700351; Hansson L, 2002, J INVEST DERMATOL, V118, P444, DOI 10.1046/j.0022-202x.2001.01684.x; Holzhausen M, 2005, MEM I OSWALDO CRUZ, V100, P177, DOI 10.1590/S0074-02762005000900030; Hong JH, 2004, J ALLERGY CLIN IMMUN, V113, P315, DOI 10.1016/j.jaci.2003.11.026; HOU SYE, 1991, J INVEST DERMATOL, V96, P215; Ingordo V, 2002, J EUR ACAD DERMATOL, V16, P450, DOI 10.1046/j.1468-3083.2002.00525.x; Jeong KY, 2004, CLIN DIAGN LAB IMMUN, V11, P680, DOI 10.1128/CDLI.11.4.680-685.2004; Kanke T, 2005, J PHARMACOL SCI, V97, P38, DOI 10.1254/jphs.FMJ04005X7; Kato A, 2003, BRIT J DERMATOL, V148, P665, DOI 10.1046/j.1365-2133.2003.05243.x; Kelso EB, 2006, J PHARMACOL EXP THER, V316, P1017, DOI 10.1124/jpet.105.093807; Komatsu N, 2005, BRIT J DERMATOL, V153, P274, DOI 10.1111/j.1365-2133.2005.06754.x; Kondo S, 2004, INFLAMM RES, V53, P489, DOI 10.1007/s00011-004-1287-8; Lee SH, 2006, YONSEI MED J, V47, P293; LEE SH, 1992, J CLIN INVEST, V89, P530, DOI 10.1172/JCI115617; Loffler H, 2003, ACTA DERM-VENEREOL, V83, P328, DOI 10.1080/00015550310006554; Nakamura T, 2006, J INVEST DERMATOL, V126, P2719, DOI 10.1038/sj.jid.5700584; Nystedt S, 1996, J BIOL CHEM, V271, P14910; Palmer CNA, 2006, NAT GENET, V38, P441, DOI 10.1038/ng1767; Rattenholl A, 2003, DRUG DEVELOP RES, V59, P408, DOI 10.1002/ddr.10311; SANTULLI RJ, 1995, P NATL ACAD SCI USA, V92, P9151, DOI 10.1073/pnas.92.20.9151; Seiberg M, 2000, J INVEST DERMATOL, V115, P162, DOI 10.1046/j.1523-1747.2000.00035.x; Sharlow ER, 2000, J CELL SCI, V113, P3093; Smith FJD, 2006, NAT GENET, V38, P337, DOI 10.1038/ng1743; Sun G, 2001, J IMMUNOL, V167, P1014; Vergnolle N, 2001, NAT MED, V7, P821, DOI 10.1038/89945; Wan H, 1999, J CLIN INVEST, V104, P123, DOI 10.1172/JCI5844; Wan H, 2001, CLIN EXP ALLERGY, V31, P279, DOI 10.1046/j.1365-2222.2001.00970.x; Weidinger S, 2006, J ALLERGY CLIN IMMUN, V118, P214, DOI 10.1016/j.jaci.2006.05.004	43	99	104	0	3	NATURE PUBLISHING GROUP	NEW YORK	75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA	0022-202X			J INVEST DERMATOL	J. Invest. Dermatol.	AUG	2008	128	8					1930	1939		10.1038/jid.2008.13		10	Dermatology	Dermatology	331SA	WOS:000258031700011	18305573	
J	Barraza-Villarreal, A; Sunyer, J; Hernandez-Cadena, L; Escamilla-Nunez, MC; Sienra-Monge, JJ; Ramirez-Aguilar, M; Cortez-Lugo, M; Holguin, F; Diaz-Sanchez, D; Olin, AC; Romieu, I				Barraza-Villarreal, Albino; Sunyer, Jordi; Hernandez-Cadena, Leticia; Consuelo Escamilla-Nunez, Maria; Jose Sienra-Monge, Juan; Ramirez-Aguilar, Matiana; Cortez-Lugo, Marlene; Holguin, Fernando; Diaz-Sanchez, David; Olin, Anna Carin; Romieu, Isabelle			Air pollution, airway inflammation, and lung function in a cohort study of Mexico City schoolchildren	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; airway inflammation; asthma; epidemiology; lung function; schoolchildren	EXHALED NITRIC-OXIDE; DIESEL EXHAUST PARTICLES; PEAK EXPIRATORY FLOW; ASTHMATIC-CHILDREN; PARTICULATE MATTER; ANTIOXIDANT SUPPLEMENTATION; RESPIRATORY HEALTH; BREATH CONDENSATE; PULMONARY-FUNCTION; CHILDHOOD ASTHMA	BACKGROUND: The biological mechanisms involved in inflammatory response to air pollution are not dearly understood. OBJECTIVE: In this study we assessed the association of short-term air pollutant exposure with inflammatory markers and lung function. METHODS: We studied a cohort of 158 asthmatic and 50 nonasthmatic school-age children, followed an average of 22 weeks. We conducted spirometric tests, measurements of fractional exhaled nitric oxide (Fe(NO)), interleukin-8 (IL-8) in nasal lavage, and pH of exhaled breath condensate every 15 days during follow-up. Data were analyzed using linear mixed-effects models. RESULTS: An increase of 17.5 mu g/m(3) in the 8-hr moving average of PM(2.5) levels (interquartile range) was associated with a 1.08-ppb increase in Fe(NO) [95% confidence interval (CI), 1.01-1.16] and a 1.07-pg/mL increase in IL-8 (95% CI 0.98-1.19) in asthmatic children and a 1.16 pg/ml increase in IL-8 (95% CI, 1.00-1.36) in nonasthmatic children. The 5-day accumulated average of exposure to particulate matter < 2.5 pm in aerodynamic diamter (PM(2.5)) was significantly inversely associated with forced expiratory volume in 1 see (FEV(1)) (p = 0.048) and forced vital capacity (FVC) (p = 0.012) in asthmatic children and with FVC (p = 0.021) in nonasthmatic children. FeNO and FEV(1) were inversely associated (p = 0.005) in asthmatic children. CONCLUSIONS: Exposure to PM(2.5) resulted in acute airway inflammation and decrease in lung function in both asthmatic and nonasthmatic children.	[Barraza-Villarreal, Albino; Hernandez-Cadena, Leticia; Consuelo Escamilla-Nunez, Maria; Cortez-Lugo, Marlene; Romieu, Isabelle] Ist Nacl Salud Publ, Cuernavaca 62508, Morelos, Mexico; [Sunyer, Jordi] IMIM, Environm Epidemiol Res Ctr, CREAL, Barcelona, Spain; [Jose Sienra-Monge, Juan] Hosp Infantil Mexico Dr Federico Gomez, Mexico City, DF, Mexico; [Ramirez-Aguilar, Matiana] COFEPRIS, Mexico City, DF, Mexico; [Holguin, Fernando] Emory Univ, Sch Med, Dept Pulm Allergy & Crit Care, Atlanta, GA USA; [Diaz-Sanchez, David] US EPA, Human Studies Div, Chapel Hill, NC USA; [Olin, Anna Carin] Sahlgrens Univ Hosp, Dept Occupat & Environm Med, S-41345 Gothenburg, Sweden	Romieu, I (reprint author), Ist Nacl Salud Publ, 655 Ave Univ,Col Santa Maria Ahuacatitlan, Cuernavaca 62508, Morelos, Mexico.	iromieu@correo.insp.mx	Sunyer, J/G-6909-2014	Sunyer, J/0000-0002-2602-4110	NCATS NIH HHS [UL1 TR000454]		ATS statement, 1994, AM J RESP CRIT CARE, V152, P1107; Barnes PJ, 1996, THORAX, V51, P218, DOI 10.1136/thx.51.2.218; Barnes PJ, 1998, MOL MED TODAY, V4, P452, DOI 10.1016/S1357-4310(98)01335-5; Behndig AF, 2006, EUR RESPIR J, V27, P359, DOI 10.1183/09031936.06.00136904; Brunetti L, 2006, PEDIATR ALLERGY IMMU, V17, P422, DOI 10.1111/j.1399-3038.2006.00426.x; Calderon-Garciduenas L, 2006, ENVIRON HEALTH PERSP, V114, P1432, DOI 10.1289/ehp.8377; CASTILLEJOS M, 1992, AM REV RESPIR DIS, V145, P276; CASTILLEJOS M, 1995, AM J RESP CRIT CARE, V152, P1501; Delfino RJ, 2006, ENVIRON HEALTH PERSP, V114, P1736, DOI 10.1289/ehp.9141; Delfino RJ, 2004, ENVIRON HEALTH PERSP, V112, P932, DOI 10.1289/ehp.6815; DIAZSANCHEZ D, 1994, J CLIN INVEST, V94, P1417, DOI 10.1172/JCI117478; Diaz-Sanchez D, 2005, AM J PHYSIOL-LUNG C, V289, P722; Dinakar C, 2004, CURR ALLERGY ASTHM R, V4, P454, DOI 10.1007/s11882-004-0011-7; Fischer PH, 2002, INT ARCH OCC ENV HEA, V75, P348, DOI 10.1007/s00420-002-0320-x; GASTON B, 1994, AM J RESP CRIT CARE, V149, P538; Gauderman WJ, 2007, LANCET, V369, P571, DOI 10.1016/S0140-6736(07)60037-3; *GINA, 2006, GLOB IN ASTHM GINA W; *GOB DISTR FED, 1999, VOL TRANS EST MAESTR; HAUSMAN JA, 1978, ECONOMETRICA, V46, P1251, DOI 10.2307/1913827; Holguin F, 2007, AM J RESP CRIT CARE, V176, P1236, DOI 10.1164/rccm.200611-1616OC; Horvath I, 2005, EUR RESPIR J, V26, P523, DOI 10.1183/09031936.05.00029705; Hunt J, 2002, J ALLERGY CLIN IMMUN, V110, P28, DOI 10.1067/mai.2002.124966; Hunt JF, 2000, AM J RESP CRIT CARE, V161, P694; Ichinose T, 1997, TOXICOLOGY, V122, P183, DOI 10.1016/S0300-483X(97)00096-6; Janssen NAH, 2001, ATMOS ENVIRON, V35, P3875, DOI 10.1016/S1352-2310(01)00144-3; Kodama Y, 2002, ENVIRON RES, V89, P236, DOI 10.1006/enrs.2002.4350; 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; Leonardi GS, 2000, INHAL TOXICOL, V12, P1; Levy JI, 1998, J AIR WASTE MANAGE, V48, P553, DOI 10.1080/10473289.1998.10463704; Mar TF, 2005, ENVIRON HEALTH PERSP, V113, P1791, DOI 10.1289/ehp.7883; Moshammer H, 2006, EUR RESPIR J, V27, P1138, DOI 10.1183/09031936.06.00089605; Narayanan PK, 1999, RADIAT RES, V152, P57, DOI 10.2307/3580049; Nel AE, 1998, J ALLERGY CLIN IMMUN, V102, P539, DOI 10.1016/S0091-6749(98)70269-6; Romieu I, 2008, EUR RESPIR J, V31, P179, DOI 10.1183/09031936.00128106; Romieu I, 1997, ARCH ENVIRON HEALTH, V52, P368; Romieu I, 1996, AM J RESP CRIT CARE, V154, P300; Romieu I, 1998, AM J RESP CRIT CARE, V158, P226; Romieu I, 2004, THORAX, V59, P8; Romieu I, 2002, AM J RESP CRIT CARE, V166, P703, DOI 10.1164/rccm.2112074; Romieu I, 2008, J ALLERGY CLIN IMMUN, V121, P903, DOI 10.1016/j.jaci.2007.12.004; Rosias PPR, 2004, PEDIATR PULM, V38, P107, DOI 10.1002/ppul.20056; Schildcrout JS, 2006, AM J EPIDEMIOL, V164, P505, DOI 10.1093/aje/kwj225; Silkoff PE, 2000, J ALLERGY CLIN IMMUN, V105, P438, DOI 10.1067/mai.2000.104938; Slutsky AS, 1999, AM J RESP CRIT CARE, V160, P2104; Stamler JS, 2001, CELL, V106, P675, DOI 10.1016/S0092-8674(01)00495-0; Steerenberg PA, 1999, EUR RESPIR J, V13, P334, DOI 10.1034/j.1399-3003.1999.13b19.x; Steerenberg PA, 2001, ARCH ENVIRON HEALTH, V56, P167; Stenfors N, 2004, EUR RESPIR J, V23, P82, DOI 10.1183/09031936.03.00004603; Svendsen ER, 2007, ANN ALLERG ASTHMA IM, V99, P244; Takizawa Hajime, 2004, Curr Opin Allergy Clin Immunol, V4, P355, DOI 10.1097/00130832-200410000-00005; Van Amsterdam JGC, 2000, ARCH ENVIRON HEALTH, V55, P418; Ward DJ, 2004, OCCUP ENVIRON MED, V61, DOI 10.1136/oem.2003.007088; WATSON JG, 1999, ELEMENTAL ANAL AIRBO, P67; Wu H, 2007, J ALLERGY CLIN IMMUN, V120, P322, DOI 10.1016/j.jaci.2007.04.022; Yeatts K, 2007, ENVIRON HEALTH PERSP, V115, P709, DOI 10.1289/ehp.9499	56	99	100	8	40	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	2008	116	6					832	838		10.1289/ehp.10926		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	306NC	WOS:000256254100039	18560490	
J	Fang, L; Adkins, B; Deyev, V; Podack, ER				Fang, Lei; Adkins, Becky; Deyev, Vadim; Podack, Eckhard R.			Essential role of TNF receptor superfamily 25 (TNFRSF25) in the development of allergic lung inflammation	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article							DOMAIN-CONTAINING RECEPTOR; CD4(+) T-CELLS; NF-KAPPA-B; INDUCE AIRWAY HYPERREACTIVITY; DEATH-DOMAIN; NKT CELLS; SIGNAL-TRANSDUCTION; HUMAN EOSINOPHILS; CUTTING EDGE; MURINE MODEL	We identify the tumor necrosis factor receptor superfamily 25 (TNFRSF25)/TNFSF15 pair as critical trigger for allergic lung inflammation, which is a cardinal feature of asthma. TNFRSF25 (TNFR25) signals are required to exert T helper cell 2 (Th2) effector function in Th2-polarized CD4 cells and co-stimulate interleukin (IL)-13 production by glycosphingo-lipid-activated NKT cells. In vivo, antibody blockade of TNFSF15 (TL1A), which is the ligand for TNFR25, inhibits lung inflammation and production of Th2 cytokines such as IL-13, even when administered days after airway antigen exposure. Similarly, blockade of TNFR25 by a dominant-negative (DN) transgene, DN TNFR25, confers resistance to lung inflammation in mice. Allergic lung inflammation-resistant, NKT-deficient mice become susceptible upon adoptive transfer of wild-type NKT cells, but not after transfer of DN TNFR25 transgenic NKT cells. The TNFR25/TL1A pair appears to provide an early signal for Th2 cytokine production in the lung, and therefore may be a drug target in attempts to attenuate lung inflammation in asthmatics.	[Fang, Lei; Adkins, Becky; Deyev, Vadim; Podack, Eckhard R.] Univ Miami, Leonard Miller Sch Med, Dept Microbiol & Immunol, Miami, FL 33136 USA	Podack, ER (reprint author), Univ Miami, Leonard Miller Sch Med, Dept Microbiol & Immunol, Miami, FL 33136 USA.	epodack@miami.edu			NCI NIH HHS [CA 39201, R01 CA039201]; NIAID NIH HHS [AI 061807, R01 AI061807]		Akbari O, 2003, NAT MED, V9, P582, DOI 10.1038/nm851; Au-Yeung BB, 2006, J IMMUNOL, V176, P3895; Bamias G, 2006, P NATL ACAD SCI USA, V103, P8441, DOI 10.1073/pnas.0510903103; Bamias G, 2003, J IMMUNOL, V171, P4868; BEAUVAIS F, 1995, J LEUKOCYTE BIOL, V57, P851; Bodmer JL, 1997, IMMUNITY, V6, P79, DOI 10.1016/S1074-7613(00)80244-7; BOLDIN MP, 1995, J BIOL CHEM, V270, P7795; Chiba A, 2004, ARTHRITIS RHEUM, V50, P305, DOI 10.1002/art.11489; Chinnaiyan AM, 1996, SCIENCE, V274, P990, DOI 10.1126/science.274.5289.990; CHINNAIYAN AM, 1995, CELL, V81, P512; Cui JQ, 1997, SCIENCE, V278, P1623, DOI 10.1126/science.278.5343.1623; Fowell DJ, 1999, IMMUNITY, V11, P399, DOI 10.1016/S1074-7613(00)80115-6; Godfrey DI, 2004, J CLIN INVEST, V114, P1379, DOI 10.1172/JCI200423594; Harhaj EW, 2005, VIROLOGY, V333, P145, DOI 10.1016/j.virol.2004.12.008; Hoshino A, 2003, EUR J IMMUNOL, V33, P861, DOI 10.1002/eji.200323455; Hsu HL, 1996, CELL, V84, P299, DOI 10.1016/S0092-8674(00)80984-8; Kitson J, 1996, NATURE, V384, P372, DOI 10.1038/384372a0; Lisbonne M, 2003, J IMMUNOL, V171, P1637; Marsters SA, 1996, CURR BIOL, V6, P1669, DOI 10.1016/S0960-9822(02)70791-4; Meyer EH, 2006, P NATL ACAD SCI USA, V103, P2782, DOI 10.1073/pnas.0510282103; Meyer EH, 2007, J IMMUNOL, V179, P4661; Micheau O, 2003, CELL, V114, P181, DOI 10.1016/S0092-8674(03)00521-X; Migone TS, 2002, IMMUNITY, V16, P479, DOI 10.1016/S1074-7613(02)00283-2; Papadakis KA, 2004, J IMMUNOL, V172, P7002; Roh GS, 2005, INT IMMUNOPHARMACOL, V5, P427, DOI 10.1016/j.intimp.2004.09.036; Salek-Ardakani S, 2003, J EXP MED, V198, P315, DOI 10.1084/jem.20021937; Schneider T, 1997, AM J RESP CELL MOL, V17, P702; Screaton GR, 1997, P NATL ACAD SCI USA, V94, P4615, DOI 10.1073/pnas.94.9.4615; Sen Yang, 2005, J Immunol, V175, P4914; Tan KB, 1997, GENE, V204, P35, DOI 10.1016/S0378-1119(97)00509-X; Terabe M, 2004, CANCER IMMUNOL IMMUN, V53, P79, DOI 10.1007/s00262-003-0445-0; Tournoy KG, 2000, CLIN EXP ALLERGY, V30, P775; Van Kaer L, 2004, IMMUNOL RES, V30, P139, DOI 10.1385/IR:30:2:139; Wang ECY, 2001, MOL CELL BIOL, V21, P3451, DOI 10.1128/MCB.21.10.3451-3461.2001; Wang ECY, 2001, IMMUNOGENETICS, V53, P59, DOI 10.1007/s002510000290; Warzocha K, 1998, BIOCHEM BIOPH RES CO, V242, P376, DOI 10.1006/bbrc.1997.7948; Wen L, 2003, J BIOL CHEM, V278, P39251, DOI 10.1074/jbc.M305833200; Wills-Karp M, 2004, CURR ALLERGY ASTHM R, V4, P123; YAMAGUCHI Y, 1991, BLOOD, V78, P2542; Yang CR, 2004, CANCER RES, V64, P1122, DOI 10.1158/0008-5472.CAN-03-0609; Zhu Zhou, 1999, Journal of Clinical Investigation, V103, P779, DOI 10.1172/JCI5909	41	99	102	0	4	ROCKEFELLER UNIV PRESS	NEW YORK	1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA	0022-1007			J EXP MED	J. Exp. Med.	MAY 12	2008	205	5					1037	1048		10.1084/jem.20072528		12	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	317EE	WOS:000257001800007	18411341	
S	Thai, P; Loukoianov, A; Wachi, S; Wu, R				Thai, Philip; Loukoianov, Artem; Wachi, Shinichiro; Wu, Reen			Regulation of airway mucin gene expression	ANNUAL REVIEW OF PHYSIOLOGY	Annual Review of Physiology		English	Review; Book Chapter						mucus; transcription; lung; epigenetics; differentiation	GROWTH-FACTOR RECEPTOR; NF-KAPPA-B; NECROSIS-FACTOR-ALPHA; BRONCHIAL EPITHELIAL-CELLS; OBSTRUCTIVE PULMONARY-DISEASE; HUMAN RESPIRATORY-TRACT; IN-VITRO; NEUTROPHIL ELASTASE; PSEUDOMONAS-AERUGINOSA; DNA METHYLATION	Mucins are important components that exert a variety of functions in cell-cell interaction, epidermal growth factor receptor signaling, and air-ways protection. In the conducting airways of the lungs, mucins are the major contributor to the viscoelastic property of mucous secretion, which is the major barrier to trapping inhaled microbial organism, particulates, and oxidative pollutants. The homeostasis of mucin production is an important feature in conducting air-ways for the maintenance of mucociliary function. Aberrant mucin secretion and accumulation in airway lumen are clinical hallmarks associated with various lung diseases, such as asthma, chronic obstructive pulmonary disease, cystic fibrosis, emphysema, and lung cancer. Among 20 known mucin genes identified, 11 of them have been verified at either the mRNA and/or protein level in airways. The regulation of mucin genes is complicated, as are the mediators and signaling pathways. This review summarizes the current view on the mediators, the signaling pathways, and the transcriptional units that are involved in the regulation of airway mucin gene expression. In addition, we also point out essential features of epigenetic mechanisms for the regulation of these genes.	[Thai, Philip] Univ Calif Davis, Ctr Comparat Resp Biol & Med, Div Pulm & Crit Care, Dept Internal Med, Davis, CA 95616 USA	Thai, P (reprint author), Univ Calif Davis, Ctr Comparat Resp Biol & Med, Div Pulm & Crit Care, Dept Internal Med, Davis, CA 95616 USA.	rwu@ucdavis.edu			NHLBI NIH HHS [R01 HL077315, R01 HL077902, T32 HL007013, T32 HL07013]		Aarbiou J, 2004, AM J RESP CELL MOL, V30, P193, DOI 10.1165/rcmb.2002-02670C; Allen A, 1998, INT J BIOCHEM CELL B, V30, P797, DOI 10.1016/S1357-2725(98)00028-4; AN G, 1994, AM J RESP CELL MOL, V10, P546; Atherton HC, 2003, AM J PHYSIOL-LUNG C, V285, pL730, DOI 10.1152/ajplung.00089.2003; Bergeron C, 2006, CHEST, V129, P1068, DOI 10.1378/chest.129.4.1068; Bernacki SH, 1999, AM J RESP CELL MOL, V20, P595; Bhattacharya SK, 1999, NATURE, V397, P579; Borchers MT, 1999, AM J PHYSIOL-LUNG C, V276, pL549; Brar SS, 2002, AM J PHYSIOL-LUNG C, V282, pL782, DOI 10.1152/ajplung.00206.2001; Buisine MP, 1998, BIOCHEM J, V332, P729; Buisine MP, 1999, AM J RESP CELL MOL, V20, P209; 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J	Wright, RJ; Subramanian, SV				Wright, Rosalind J.; Subramanian, S. V.			Advancing a multilevel framework for epidemiologic research on asthma disparities	CHEST			English	Article; Proceedings Paper	National Workshop to Reduce Asthma Disparities	JAN, 2005	Chicago, IL			air pollution; asthma disparities; environmental justice; housing; indoor allergens; stress; tobacco smoke; violence	INNER-CITY CHILDREN; DIESEL EXHAUST PARTICLES; AROMATIC-HYDROCARBON CONCENTRATIONS; AIR-POLLUTION; HAY-FEVER; CIGARETTE-SMOKING; RISK-FACTORS; ALLERGIC SENSITIZATION; ENVIRONMENTAL EXPOSURE; SOCIOECONOMIC-STATUS	Our understanding of asthma epidemiology is growing increasingly complex. Asthma outcomes are clearly socially patterned, with asthma ranking as a leading cause of health disparities among minority and low socioeconomic groups. Yet, the increasing prevalence and marked disparities in asthma remain largely. unexplained by known risk factors. In the United States, asthma disproportionately affects nonwhite children living in urban areas and children living in poverty. Low socioeconomic status (SES), ethnic minority group status, and residence in an inner-city environment are closely intertwined in the United States, making it a challenge to fully disentangle the independent effects of each of these characteristics on asthma morbidity. In addition, studies show geographic variation in asthma outcomes across large cities and neighborhoods within cities that cannot be explained by economic factors alone. Although more limited data are available, studies in rural areas also suggest the stratification of risk based on SES and the proportion of minorities. Among low-SES areas, those with predominantly minority, segregated populations seem especially burdened. Marginalized populations of lower socioeconomic position are disproportionately exposed to irritants (eg, tobacco smoke), pollutants (eg, diesel-related particles), and indoor allergens (eg, cockroach and mouse allergen). Moreover, these marginalized individuals may also live in communities that are increasingly socially toxic, which, in turn, may be related to the increased experience of psychosocial stress that may influence asthma morbidity. Epidemiologic trends suggest that asthma may provide an excellent paradigm for understanding the role of community-level contextual factors in disease. Specifically, a multilevel approach that includes an ecological perspective may help to explain heterogeneities in asthma expression across socioeconomic and geographic boundaries that, to date, remain largely unexplained. Traditionally, asthma epidemiology has focused on individual-level risk factors and family factors. Far less attention has been given to the broader social context in which individuals live. A multilevel approach that explicitly recognizes the embedding of asthma within its biological, psycho-socioeconomic, environmental, and community contexts, is likely to provide a better understanding of asthma disparities at different stages in the life course. Is it simply asthma disparities or is it social disparities in asthma?	Brigham & Womens Hosp, Harvard Med Sch, Dept Med, Channing Lab, Boston, MA 02115 USA; Harvard Sch Publ Hlth, Dept Soc Human Dev & Hlth, Boston, MA USA	Wright, RJ (reprint author), Brigham & Womens Hosp, Channing Lab, 181 Longwood Ave, Boston, MA 02115 USA.	rosalind.wright@channing.harvard.edu					Adler A, 2005, J ALLERGY CLIN IMMUN, V115, P67, DOI 10.1016/j.jaci.2004.10.008; American Lung Association, 2001, ENVIRON HEALTH PER S, V109, P357; ANDA RF, 1990, JAMA-J AM MED ASSOC, V264, P1541, DOI 10.1001/jama.264.12.1541; ATTAR BK, 1994, J CLIN CHILD PSYCHOL, V23, P391, DOI 10.1207/s15374424jccp2304_5; BACHEN EA, 1995, PSYCHOSOM MED, V57, P366; BAUER K, 2003, INT J APPL PHIL, V17, P2410; BECKHAM JC, 1995, J TRAUMA STRESS, V8, P461, DOI 10.1007/BF02102970; BOR W, 1993, SOC SCI MED, V9, P27; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Braveman P, 2000, B WORLD HEALTH ORGAN, V78, P232; BURKART KM, 2005, ASTHMA PREVENTION, P377; BURROWS B, 1989, NEW ENGL J MED, V320, P271, DOI 10.1056/NEJM198902023200502; CALL RS, 1992, J PEDIATR-US, V121, P862, DOI 10.1016/S0022-3476(05)80329-4; CARR W, 1992, AM J PUBLIC HEALTH, V82, P59, DOI 10.2105/AJPH.82.1.59; CASTRO FG, 1987, J HEALTH SOC BEHAV, V28, P273, DOI 10.2307/2136846; Clougherty JE, 2007, ENVIRON HEALTH PERSP, V115, P1140, DOI 10.1289/ehp.9863; COHEN S, 1990, HEALTH PSYCHOL, V9, P466, DOI 10.1037/0278-6133.9.4.466; COHEN S, 1991, NEW ENGL J MED, V325, P606, DOI 10.1056/NEJM199108293250903; Cookson W, 1999, NATURE SB, V402, P5, DOI 10.1038/35037002; Crain EF, 2002, ENVIRON HEALTH PERSP, V110, P939; CRAIN EF, 1994, PEDIATRICS, V94, P356; Cunningham J, 1996, AM J PUBLIC HEALTH, V86, P1406, DOI 10.2105/AJPH.86.10.1406; CURRY SJ, 1993, AM J PREV MED, V9, P78; DEMPSTER AP, 1981, J AM STAT ASSOC, V76, P341, DOI 10.2307/2287835; DIAZSANCHEZ D, 1994, J CLIN INVEST, V94, P1417, DOI 10.1172/JCI117478; DiezRoux AV, 1997, AM J EPIDEMIOL, V146, P48; Dunn JR, 2002, J EPIDEMIOL COMMUN H, V56, P671, DOI 10.1136/jech.56.9.671; Dunn JR, 1999, ANN NY ACAD SCI, V896, P399, DOI 10.1111/j.1749-6632.1999.tb08153.x; Dunn JR, 2000, SOC SCI MED, V51, P563, DOI 10.1016/S0277-9536(99)00496-7; Duster T, 2005, SCIENCE, V307, P1050, DOI 10.1126/science.1110303; Evans GW, 2004, AM J PUBLIC HEALTH, V94, P1942, DOI 10.2105/AJPH.94.11.1942; Evans GW, 2001, HANDBOOK OF HEALTH PSYCHOLOGY, P365; EVANS R, 1992, CHEST, V101, pS368; FEIGELMAN W, 1989, J PSYCHOACTIVE DRUGS, V21, P299; FINKELHOR D, 1995, AM J ORTHOPSYCHIAT, V65, P177, DOI 10.1037/h0079618; FISHER E, 2001, HLTH BEHAV HDB; Ganz ML, 2000, AM J PUBLIC HEALTH, V90, P367, DOI 10.2105/AJPH.90.3.367; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; Gold DR, 2005, ANNU REV PUBL HEALTH, V26, P89, DOI 10.1146/annurev.publhealth.26.021304.144528; GOLDIN C, 1998, 6439 MAT BUR EC RES; Goldstein H., 2003, MULTILEVEL STAT MODE; GROVES BM, 1993, JAMA-J AM MED ASSOC, V269, P262, DOI 10.1001/jama.269.2.262; Haan M. 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J	Hayashi, N; Tsukamoto, Y; Sallas, WM; Lowe, PJ				Hayashi, Naoto; Tsukamoto, Yuko; Sallas, William M.; Lowe, Philip J.			A mechanism-based binding model for the population pharmacokinetics and pharmacodynamics of omalizumab	BRITISH JOURNAL OF CLINICAL PHARMACOLOGY			English	Article						atopic asthma; binding model monoclonal antibody; IgE; NONMEM	ANTI-IGE ANTIBODIES; MONOCLONAL-ANTIBODY; GAMMAE-ANTIBODIES; IMMUNOGLOBULIN-G; THERAPY; METABOLISM; DISEASE; MYELOMA; RABBITS	Aim Omalizumab, a humanized IgG monoclonal antibody that binds to human immunoglobulin E (IgE), interrupts the allergic cascade in asthmatic patients. The aim was to compare simultaneously drug exposure and IgE biomarker responses in Japanese and White patient populations. Methods An instantaneous equilibrium drug-ligand binding and turnover population model was built from 202 Japanese patients. A posterior predictive evaluation for the steady-state distributions of omalizumab and IgE was then carried out against 531 White patients. Results The mean parameters estimated from the Japanese patients were as follows: omalizumab clearance 7.32 +/- 0.153 ml h(-1), IgE clearance 71.0 +/- 4.68 ml h(-1) and the difference between that for omalizumab and the complex 5.86 +/- 0.920 ml h(-1), the volume of distribution for omalizumab and IgE 5900 +/- 107 ml, and that for the complex 3630 +/- 223 ml, the rate of IgE production 30.3 +/- 2.04 mu g h(-1). Half-lives of IgG (23 days) and IgE (2.4 days) were close to previous reports. The dissociation constant for binding, 1.07 nM, was similar to in vitro values. Clearance and volume of distribution for omalizumab varied with bodyweight, whereas the clearance and rate of production of IgE were predicted accurately by baseline IgE. Overall, these covariates explained much of the interindividual variability. Conclusions The predictiveness of the Japanese model was confirmed by Monte-Carlo simulations for a White population, also providing evidence that the pharmacokinetics of omalizumab and IgE were similar in these two populations. Furthermore, the model enabled the estimation of not only omalizumab disposition parameters, but also the binding with and the rate of production, distribution and elimination of its target, IgE.	Novartis Pharma AG, Modelling & Simulat, CH-4056 Basel, Switzerland; Novartis Pharma AG, Drug Metab & Pharmacokinet, Basel, Switzerland; Novartis Pharma KK, Drug Metab & Pharmacokinet, Tokyo, Japan; Nova Pharmaceut Corp, Modeling & Simulat, E Hanover, NJ USA	Lowe, PJ (reprint author), Novartis Pharma AG, Modelling & Simulat, Lichtstr 35, CH-4056 Basel, Switzerland.	phil.lowe@novartis.com		Lowe, Philip/0000-0003-4074-8227			Adelroth E, 2000, J ALLERGY CLIN IMMUN, V106, P253, DOI 10.1067/mai.2000.108310; BILL A, 1977, ACTA PHYSIOL SCAND, V101, P28, DOI 10.1111/j.1748-1716.1977.tb05980.x; Boushey H. A., 1998, Research in Immunology, V149, P189, DOI 10.1016/S0923-2494(98)80024-2; Busse W, 2001, J ALLERGY CLIN IMMUN, V108, P184, DOI 10.1067/mai.2001.117880; Charles P, 1999, J IMMUNOL, V163, P1521; Fick R B, 1999, Pediatr Pulmonol Suppl, V18, P115; Frazer JK, 1999, FUNDAMENTAL IMMUNOLO, P37; *GEN INC, 2003, XOL OM SUBC US PACK; HEDGER MP, 1994, J ANDROL, V15, P583; Heusser C, 1997, CURR OPIN IMMUNOL, V9, P805, DOI 10.1016/S0952-7915(97)80182-3; Holgate ST, 1998, ALLERGY, V53, P83; ISHIZAKA K, 1967, J IMMUNOL, V99, P1187; ISHIZAKA K, 1970, CLIN EXP IMMUNOL, V6, P25; Jardieu P, 1996, FROM GENETICS TO QUALITY OF LIFE, P193; Jardieu P, 1995, CURR OPIN IMMUNOL, V7, P779, DOI 10.1016/0952-7915(95)80047-6; Jardieu PM, 1999, INT ARCH ALLERGY IMM, V118, P112, DOI 10.1159/000024043; JOHANSSON SG, 1967, IMMUNOLOGY, V13, P381; Junghans RP, 1997, IMMUNOL RES, V16, P29, DOI 10.1007/BF02786322; JUWEID M, 1992, EUR J NUCL MED, V19, P159; LIU J, 1995, BIOCHEMISTRY-US, V34, P10474, DOI 10.1021/bi00033a020; Lobo ED, 2004, J PHARM SCI-US, V93, P2645, DOI 10.1002/jps.20178; Meno-Tetang GML, 2005, BASIC CLIN PHARMACOL, V96, P182, DOI 10.1111/j.1742-7843.2005.pto960307.x; Patalano F, 1999, ALLERGY, V54, P103; PRESTA LG, 1993, J IMMUNOL, V151, P2623; SABOURAUD AE, 1992, J PHARMACOL EXP THER, V260, P1214; SCHERRMANN JM, 1989, J TOXICOL-CLIN TOXIC, V27, P1; Soler M, 2001, EUR RESPIR J, V18, P254, DOI 10.1183/09031936.01.00092101; Streeten D. H., 1998, J CHRONIC FATIGUE SY, V4, P3, DOI 10.1300/J092v04n01_02; Valentine JL, 1996, J PHARMACOL EXP THER, V278, P717; WALDMANN TA, 1969, PROG ALLERGY, V13, P1, DOI 10.1159/000287491; WALDMANN TA, 1976, J IMMUNOL, V117, P1139	31	99	101	1	7	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0306-5251			BRIT J CLIN PHARMACO	Br. J. Clin. Pharmacol.	MAY	2007	63	5					548	561		10.1111/j.1365-2125.2006.02803.x		14	Pharmacology & Pharmacy	Pharmacology & Pharmacy	158RO	WOS:000245811700006	17096680	
J	Python, F; Goebel, C; Aeby, P				Python, Francois; Goebel, Carsten; Aeby, Pierre			Assessment of the U937 cell line for the detection of contact allergens	TOXICOLOGY AND APPLIED PHARMACOLOGY			English	Article						CD86; IL-1 beta; IL-8; U937 cell line; In vitro sensitization test	LYMPH-NODE ASSAY; SURFACE-MARKER EXPRESSION; GENERATED DENDRITIC CELLS; IN-VITRO MODEL; COSTIMULATORY MOLECULES; SIGNALING PATHWAYS; CHEMICAL ALLERGEN; SKIN SENSITIZERS; MESSENGER-RNA; CYTOKINE	The human myeloid cell line U937 was evaluated as an in vitro test system to identify contact sensitizers in order to develop alternatives to animal tests for the cosmetic industry. Specific culture conditions (i.e., presence of interleukin-4, IL-4) were applied to obtain a dendritic cell-like phenotype. In the described test protocol, these cells were exposed to test chemicals and then analyzed by flow cytometry for CD86 expression and by quantitative real-time reverse transcriptase-polymerase chain reaction for IL-I beta and IL-8 gene expressions. Eight sensitizers, three non-sensitizers and five oxidative hair dye precursors were examined after 24-, 48- and 72-h exposure times. Test item-specific modulations of the chosen activation markers (CD86, IL-1 beta and IL-8) suggest that this U937 activation test could discriminate test items classified as contact sensitizers or non-sensitizers in the local lymph node assay in mice (LLNA). More specifically, a test item can be considered as a potential sensitizer when it significantly induced the upregulation of the expression of at least two markers. Using this approach, we could correctly evaluate the dendritic cell (DC) activation potential for 15 out of 16 tested chemicals. We conclude that the U937 activation test may represent an useful tool in a future in vitro test battery for predicting sensitizing properties of chemicals. (c) 2007 Elsevier Inc. All rights reserved.	Procter & Gamble Co, Wella Cosmital SA, Expt Prod Safety, Marly, Switzerland; Procter & Gamble Co, Wella Serv GmbH, Human Safety Assessment, Darmstadt, Germany	Python, F (reprint author), Rte Chesalles 21, CH-1723 Marly, Switzerland.	python.f@pg.com					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; Azam P, 2006, TOXICOL APPL PHARM, V212, P14, DOI 10.1016/j.taap.2005.06.018; Banchereau J, 1998, NATURE, V392, P245, DOI 10.1038/32588; Basketter DA, 2002, FOOD CHEM TOXICOL, V40, P593, DOI 10.1016/S0278-6915(01)00130-2; BASKETTER DA, 1994, FOOD CHEM TOXICOL, V32, P543, DOI 10.1016/0278-6915(94)90112-0; Boisleve F, 2004, J INVEST DERMATOL, V123, P494, DOI 10.1111/j.0022-202X.2004.23229.x; Casati S, 2005, ATLA-ALTERN LAB ANIM, V33, P47; Coquette A, 2003, TOXICOL IN VITRO, V17, P311, DOI 10.1016/S0887-2333(03)00019-5; Coutant KD, 1999, TOXICOL SCI, V52, P189, DOI 10.1093/toxsci/52.2.189; de Baey A, 2000, J EXP MED, V191, P743, DOI 10.1084/jem.191.4.743; Dearman RJ, 1999, J APPL TOXICOL, V19, P299, DOI 10.1002/(SICI)1099-1263(199909/10)19:5<299::AID-JAT591>3.0.CO;2-C; ENK AH, 1992, P NATL ACAD SCI USA, V89, P1398, DOI 10.1073/pnas.89.4.1398; Feghali Carol A., 1997, Frontiers in Bioscience (online), V2, pD12; Gallucci S, 2001, CURR OPIN IMMUNOL, V13, P114, DOI 10.1016/S0952-7915(00)00191-6; Gerberick GF, 2004, CONTACT DERMATITIS, V50, P274, DOI 10.1111/j.0105-1873.2004.00290.x; Heydorn S, 2003, CONTACT DERMATITIS, V48, P317, DOI 10.1034/j.1600-0536.2003.00133.x; Hu ZB, 1996, LEUKEMIA, V10, P1025; 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; Hulette BC, 2001, ARCH DERMATOL RES, V293, P147, DOI 10.1007/s004030000201; Jugde F, 2005, TOXICOLOGY, V212, P227, DOI 10.1016/j.tox.2005.04.019; 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; Koss A, 1996, LEUKEMIA LYMPHOMA, V22, P163, DOI 10.3109/10428199609051744; LEPOITTEVIN JP, 1998, ALLERGIC CONTACT DER; Luster AD, 2002, CURR OPIN IMMUNOL, V14, P129, DOI 10.1016/S0952-7915(01)00308-9; Masterson AJ, 2002, BLOOD, V100, P701, DOI 10.1182/blood.V100.2.701; Nagorsen D, 2004, CYTOKINE, V25, P31, DOI 10.1016/j.cyto.2003.08.012; Pichowski JS, 2000, TOXICOL IN VITRO, V14, P351, DOI 10.1016/S0887-2333(00)00030-8; Reutter K, 1997, TOXICOL IN VITRO, V11, P619, DOI 10.1016/S0887-2333(97)00048-9; Rollins BJ, 1997, BLOOD, V90, P909; Ross DT, 2000, NAT GENET, V24, P227, DOI 10.1038/73432; Ryan CA, 2005, TOXICOL SCI, V88, P4, DOI 10.1093/toxsci/kfi245; Ryan CA, 2004, TOXICOL LETT, V150, P301, DOI 10.1016/j.toxlet.2004.02.002; Ryan CA, 2002, FOOD CHEM TOXICOL, V40, P1719, DOI 10.1016/S0278-6915(02)00116-3; Sakaguchi H, 2006, TOXICOL IN VITRO, V20, P774, DOI 10.1016/j.tiv.2005.10.014; Sallusto F, 1999, EUR J IMMUNOL, V29, P1617, DOI 10.1002/(SICI)1521-4141(199905)29:05<1617::AID-IMMU1617>3.0.CO;2-3; Scapini P, 2000, IMMUNOL REV, V177, P195, DOI 10.1034/j.1600-065X.2000.17706.x; St Louis DC, 1999, J IMMUNOL, V162, P3237; Staquet MJ, 2004, TOXICOL IN VITRO, V18, P493, DOI 10.1016/j.tiv.2003.12.005; Straube F, 2005, ARCH TOXICOL, V79, P37, DOI 10.1007/s00204-004-0606-8; Toebak MJ, 2006, TOXICOL IN VITRO, V20, P117, DOI 10.1016/j.tiv.2005.06.039; Tuschl H, 2000, TOXICOL IN VITRO, V14, P541, DOI 10.1016/S0887-2333(00)00051-5; Tuschl H, 2001, TOXICOL IN VITRO, V15, P327, DOI 10.1016/S0887-2333(01)00030-3; VANDEBRIEL RJ, 2005, TOXICOL APPL PHARM, V207, pS142; Yoshida Y, 2003, TOXICOL IN VITRO, V17, P221, DOI 10.1016/S0887-2333(03)00006-7	48	99	103	0	3	ACADEMIC PRESS INC ELSEVIER SCIENCE	SAN DIEGO	525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA	0041-008X			TOXICOL APPL PHARM	Toxicol. Appl. Pharmacol.	APR 15	2007	220	2					113	124		10.1016/j.taap.2006.12.026		12	Pharmacology & Pharmacy; Toxicology	Pharmacology & Pharmacy; Toxicology	157GX	WOS:000245707900001	17306317	
J	Arshad, SH; Bateman, B; Sadeghnejad, A; Gant, C; Matthews, SM				Arshad, Syed Hasan; Bateman, Belinda; Sadeghnejad, Alireza; Gant, Carole; Matthews, Sharon M.			Prevention of allergic disease during childhood by allergen avoidance: The Isle of Wight prevention study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						atopy; allergy; asthma; rhinitis; atopic dermatitis; food allergy; prevention; diet; house dust mite; randomized controlled trial	HOUSE-DUST MITE; BIRTH-COHORT; ASTHMA; EXPOSURE; INFANCY; SENSITIZATION; RISK; AGE; OUTCOMES; ATOPY	Background: Early life allergen exposure may increase the risk of childhood allergy, but the protective effect of reduction in allergen exposure remains uncertain. Objective: To evaluate the effect of reduction in food and house dust mite (HDM) allergen exposure in infancy in preventing asthma and allergy. Methods: Infants, at higher risk because of family predisposition, were recruited prenatally and randomized to prophylactic (n = 58) and control (n = 62) groups. Prophylactic group infants were either breast-fed with mother on a low allergen diet or given an extensively hydrolyzed formula. Exposure to HDM was reduced by the use of an acaricide and mattress covers. The control group followed standard advice. Development of allergic diseases and sensitization to common allergens (atopy) was assessed blindly at ages 1, 2, 4, and 8 years in all 120 children. Results: Repeated measurement analysis, adjusted for all relevant confounding variables, confirmed a preventive effect on asthma: adjusted odds ratio (OR), 0.24; 95% CI, 0.09-0.66; P = .005; atopic dermatitis, OR, 0.23; Cl, 0.08-0.64; P = .005; rhinitis, OR, 0.42; CI, 0.19-0.92; P = .03; and atopy, OR, 0.13; Cl, 0.05-0.32; P < .001. The protective effect was primarily observed in the subgroup of children with persistent disease (symptoms at all visits) and in those with evidence of allergic sensitization. Conclusion: Allergic diseases can be reduced, for at least the first 8 years of life, by combined food and HDM allergen avoidance in infancy. Clinical implications: Strict food and HDM allergen avoidance should be considered for prevention of allergy in high-risk infants.	St Marys Hosp, David Hide Asthma & Allergy Res Ctr, Newport PO30 5TG, Wight, Wales; Wake Forest Univ, Sch Med, Ctr Human Genom, Winston Salem, NC 27109 USA	Arshad, SH (reprint author), St Marys Hosp, David Hide Asthma & Allergy Res Ctr, Newport PO30 5TG, Wight, Wales.	sha@soton.ac.uk	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Arshad SH, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.2.e33; ARSHAD SH, 1992, LANCET, V339, P1493, DOI 10.1016/0140-6736(92)91260-F; Arshad SH, 2005, J ALLERGY CLIN IMMUN, V116, P3, DOI 10.1016/j.jaci.2005.03.043; Arshad SH, 2003, THORAX, V58, P489, DOI 10.1136/thorax.58.6.489; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Braman SS, 2006, CHEST S1, V130, p4S, DOI DOI 10.1378/CHEST.130.1_; Chan-Yeung M, 2005, J ALLERGY CLIN IMMUN, V116, P49, DOI 10.1016/j.jaci.2005.03.029; Custovic A, 2001, LANCET, V358, P188, DOI 10.1016/S0140-6736(01)05406-X; DOLD S, 1992, ARCH DIS CHILD, V67, P1018; Friedman NJ, 2005, J ALLERGY CLIN IMMUN, V115, P1238, DOI 10.1016/j.jaci.2005.01.069; Hanifin JM, 1980, ACTA DERM-VENEREOL S, V92, P44; Hays T, 2005, ARCH PEDIAT ADOL MED, V159, P810, DOI 10.1001/archpedi.159.9.810; Hide D W, 1994, Pediatr Allergy Immunol, V5, P61, DOI 10.1111/j.1399-3038.1994.tb00351.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; Host A, 1994, PEDIATR ALLERGY IMMU, V5, P5, DOI 10.1111/j.1399-3038.1994.tb00352.x; Illi S, 2006, LANCET, V368, P763, DOI 10.1016/S0140-6736(06)69286-6; KRAMER MS, 2001, COCHRANE LIB, V1, DOI UNSP CD000133; KUEHR J, 1994, J ALLERGY CLIN IMMUN, V94, P44, DOI 10.1016/0091-6749(94)90070-1; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; Oddy WH, 2002, J ALLERGY CLIN IMMUN, V110, P65, DOI 10.1067/mai.2002.125296; Peat JK, 2004, J ALLERGY CLIN IMMUN, V114, P807, DOI 10.1016/j.jaci.2004.06.057; Spergel Jonathan M., 2003, Journal of Allergy and Clinical Immunology, V112, pS118, DOI 10.1016/j.jaci.2003.09.033; 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; Stokes ME, 2001, CATEGORICAL DATA ANA; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; ZEGER SL, 1986, BIOMETRICS, V42, P121, DOI 10.2307/2531248; ZEIGER RS, 1989, J ALLERGY CLIN IMMUN, V84, P72, DOI 10.1016/0091-6749(89)90181-4	30	99	104	1	8	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					307	313		10.1016/j.jaci.2006.12.621		7	Allergy; Immunology	Allergy; Immunology	137YB	WOS:000244327900006	17291851	
J	Zambelli-Weiner, A; Ehrlich, E; Stockton, ML; Grant, AV; Zhang, S; Levett, PN; Beaty, TH; Barnes, KC				Zambelli-Weiner, A; Ehrlich, E; Stockton, ML; Grant, AV; Zhang, S; Levett, PN; Beaty, TH; Barnes, KC			Evaluation of the CD14/-260 polymorphism and house dust endotoxin exposure in the Barbados Asthma Genetics Study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						CD14; endotoxin; LPS; asthma; allergy; atopy; asthma severity; IgE; genetics; gene-environment interaction	CIRCULATING SOLUBLE CD14; INFLAMMATORY RESPONSE; PULMONARY-FUNCTION; INNATE IMMUNITY; VITAL CAPACITY; NORMAL MEN; TESTS; ASSOCIATION; POPULATIONS; INHALATION	Background: Both a functional promoter polymorphism in the gene encoding CD14 (C-260T) and exposure to endotoxin are believed to play key roles in modulating the immune response and expression of atopic disease. Objective: We aimed to evaluate the role of the CD14 C-260T polymorphism in a population of African descent and to test for interaction between this genotype and house dust endotoxin (HDE) exposure on atopic phenotypes. Methods: Asthmatic probands and their families were recruited as part of the Barbados Asthma Genetics Study. The C-260T polymorphism and two additional CD14 promoter markers (G-1461T, C-1721T) were genotyped. Endotoxin was measured in house dust samples. Results: Using a Family-Based Association Test, the C-260T allele appeared to be protective against asthma (z = -2.444; P = .015) and asthma severity (z = -2.615; P = .009) under a recessive model. No significant associations were observed for the G-1461T and C-1721T markers both individually and in haplotypes. In a case-control analysis, the CD14 TT genotype was found to reduce risk of asthma compared with the CD 14 CC/CT genotypes (odds ratio [OR], 0.26; 95% CI, 0.14-0.49) and was associated with lower asthma severity scores (P < .002). The TT genotype might protect against asthma for individuals with low HDE (OR, 0.09; 95% CI, 0.03-0.24), but may be a risk factor for individuals with high HDE (OR, 11.66; 95% CI, 1.03-131.7), suggesting a gene-environment interaction. Conclusion: These data suggest that the CD14-260 polymorphism may play a role in controlling risk to atopic disease and underscore the importance of incorporating key environmental exposures into studies of genetic risk factors.	Johns Hopkins Sch Med, Dept Med, Div Clin Immunol & Allergy, Baltimore, MD USA; Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA; Univ W Indies, Fac Med, Sch Clin Med & Res, Bridgetown, Barbados	Barnes, KC (reprint author), Johns Hopkins Asthma & Allergy Ctr, 3A-62A,5501 Hopkins Bayview Circle, Baltimore, MD 21224 USA.	kbarnes@jhmi.edu			NIAID NIH HHS [AI 20059]; NIEHS NIH HHS [T32 ES 07141]		Akashi S, 2000, BIOCHEM BIOPH RES CO, V268, P172, DOI 10.1006/bbrc.2000.2089; Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Barnes KC, 1996, GENOMICS, V37, P41, DOI 10.1006/geno.1996.0518; Barnes KC, 1999, J ALLERGY CLIN IMMUN, V104, P791; Barnes KC, 1997, J MED ENTOMOL, V34, P212; Cella M, 1997, CURR OPIN IMMUNOL, V9, P10, DOI 10.1016/S0952-7915(97)80153-7; Chun DTW, 2002, ANN AGR ENV MED, V9, P49; GAENSLER EA, 1951, AM REV TUBERC PULM, V64, P256; Gao PS, 1999, CLIN GENET, V56, P164; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; GOLDMAN HI, 1959, AM REV TUBERC PULM, V79, P457; Heinzmann A, 2003, EUR J IMMUNOGENET, V30, P345, DOI 10.1046/j.1365-2370.2003.00414.x; HORVATH S, 2001, GENET EPIDEMIOL S, V21, P403; Koppelman GH, 2001, AM J RESP CRIT CARE, V163, P965; KORY RC, 1961, AM J MED, V30, P243, DOI 10.1016/0002-9343(61)90096-1; Lake SL, 2000, AM J HUM GENET, V67, P1515, DOI 10.1086/316895; LANDMANN R, 1995, J INFECT DIS, V171, P639; LEUALLEN EC, 1955, AM REV TUBERC PULM, V72, P783; LEWONTIN RC, 1988, GENETICS, V120, P849; MICHEL O, 1992, AM REV RESPIR DIS, V146, P352; MICHEL O, 1992, THORAX, V47, P288, DOI 10.1136/thx.47.4.288; Michel O, 2000, TOXICOLOGY, V152, P25, DOI 10.1016/S0300-483X(00)00288-2; MILLER WF, 1959, J APPL PHYSIOL, V14, P157; Nickel RG, 1999, HUM IMMUNOL, V60, P738, DOI 10.1016/S0198-8859(99)00039-7; Ober C, 2000, AM J HUM GENET, V67, P1154, DOI 10.1016/S0002-9297(07)62946-2; Peden DB, 1999, J ALLERGY CLIN IMMUN, V104, P388, DOI 10.1016/S0091-6749(99)70383-0; PEMBERTON J, 1956, J APPL PHYSIOL, V9, P291; Rabinowitz D, 2000, HUM HERED, V50, P211, DOI 10.1159/000022918; Reed CE, 2001, J ALLERGY CLIN IMMUN, V108, P157, DOI 10.1067/mai.2001.116862; RIZZO MC, 1999, ACI INT, V11, P153; RYLANDER R, 1989, AM REV RESPIR DIS, V140, P981; Rylander R., 1997, INT J OCCUP ENV HL S, V3, P32; Sengler C, 2003, CLIN EXP ALLERGY, V33, P166, DOI 10.1046/j.1365-2222.2003.01549.x; StataCorp, 2003, STAT STAT SOFTW REL; Togias A, 1997, INT ARCH ALLERGY IMM, V113, P87; Vercelli D, 2001, J ENDOTOXIN RES, V7, P45, DOI 10.1179/096805101101532521; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; Woo JG, 2003, J ALLERGY CLIN IMMUN, V112, P438, DOI 10.1067/mai.2003.1634; [Anonymous], 1995, AM J RESP CRIT CARE, V152, P1107	39	99	101	1	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.	JUN	2005	115	6					1203	1209		10.1016/j.jaci.2005.03.001		7	Allergy; Immunology	Allergy; Immunology	935WZ	WOS:000229815400015	15940135	
J	Gidaro, GB; Marcucci, F; Sensi, L; Incorvaia, C; Frati, F; Ciprandi, G				Gidaro, GB; Marcucci, F; Sensi, L; Incorvaia, C; Frati, F; Ciprandi, G			The safety of sublingual-swallow immunotherapy: an analysis of published studies	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						high allergen dose; low allergen dose; safety; sublingual immunotherapy	DOUBLE-BLIND PLACEBO; HOUSE-DUST-MITE; STANDARDIZED 5-GRASS-POLLEN EXTRACT; LOCAL ALLERGOID IMMUNOTHERAPY; RANDOMIZED CONTROLLED-TRIAL; PARIETARIA-JUDAICA EXTRACT; GRASS-POLLEN; SEASONAL RHINOCONJUNCTIVITIS; PEDIATRIC-PATIENTS; CHILDREN	Background As the main target of sublingual immunotherapy (SLIT) is to reduce at most the occurrence of adverse events (AE), safety represents a critical issue. This aspect deserves particular mention when a higher dose of allergen extract than traditional subcutaneous immunotherapy (SCIT) is required to be effective: that may be up to 500 times that employed for SCIT. Objective All published controlled studies concerning SLIT-swallow were analysed to evaluate AE rates. Methods Studies were subdivided in two groups: (i) studies using low allergen dose (LAD), i.e. ranging from 1 to 50 times the dose commonly administered with SCIT, and (ii) studies with high allergen dose (HAD), i.e. ranging from 50 to 500 times the dose administered with SCIT. Results Twenty-five studies were altogether analysed: 13 studies belonged to the low-dose group, 12 belonged to the high-dose group. We considered all patients with at least one AE. Local reactions were significantly more frequent in the LAD group than in the HAD group (P < 0.0001), while there was no difference in the rate of systemic reactions. Severe systemic reactions were never reported. Conclusion This study represents the first analysis of the safety of SLIT concerning the allergen dose employed in the treatment. There is evidence that AE occurrence is substantially not dose-dependent. This fact highlights two main clinical aspects: the elevated tolerability of SLIT in general and the safety of HAD regimen.	Stallergenes, Dept Sci, Milan, Italy; Univ Perugia, Dept Obstet Gynaecol & Pediat, I-06100 Perugia, Italy; ICP Hosp, Allergy Rheumatol Unit, Milan, Italy; San Martino Hosp, Head Neck Dept, Genoa, Italy	Ciprandi, G (reprint author), AO Osped San Martino, Padigl Special Piano Terzo, Dipartimento Reg Testa Collo, Allergol UO ORL, Largo R Benzi 10, I-16132 Genoa, Italy.	gio.cip@libero.it					Almagro E, 1995, Allergol Immunopathol (Madr), V23, P153; Andre C, 2000, INT ARCH ALLERGY IMM, V121, P229, DOI 10.1159/000024322; Andre C, 2003, INT ARCH ALLERGY IMM, V131, P111, DOI 10.1159/000070926; Ariano R, 2001, Allergol Immunopathol (Madr), V29, P238; Bahceciler NN, 2001, PEDIATR PULM, V32, P49, DOI 10.1002/ppul.1088; Bousquet J, 1999, ALLERGY, V54, P249, DOI 10.1034/j.1398-9995.1999.00916.x; Bousquet J., 1998, Allergy (Copenhagen), V53, P1; BOUSQUET J, 2001, J ALLERGY CLIN IMMUN, V108, P315; Bufe A, 2004, ALLERGY, V59, P498, DOI 10.1111/j.1398-9995.2004.00457.x; Caffarelli C, 2000, ALLERGY, V55, P1142, DOI 10.1034/j.1398-9995.2000.00655.x; Canonica GW, 2003, J ALLERGY CLIN IMMUN, V111, P437, DOI 10.1067/mai.2003.129; CASANOVAS M, 1994, J INVEST ALLERG CLIN, V4, P305; Clavel R, 1998, ALLERGY, V53, P493, DOI 10.1111/j.1398-9995.1998.tb04086.x; Di Rienzo V, 1999, ALLERGY, V54, P1110, DOI 10.1034/j.1398-9995.1999.00267.x; Feliziani V, 1995, Allergol Immunopathol (Madr), V23, P224; Frew Anthony J., 2003, Journal of Allergy and Clinical Immunology, V111, pS712; Grosclaude M, 2002, INT ARCH ALLERGY IMM, V129, P248, DOI 10.1159/000066779; Guez S, 2000, ALLERGY, V55, P369, DOI 10.1034/j.1398-9995.2000.00413.x; 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; Ippoliti F, 2003, PEDIATR ALLERGY IMMU, V14, P216, DOI 10.1034/j.1399-3038.2003.00025.x; La Rosa M, 1999, J ALLERGY CLIN IMMUN, V104, P425, DOI 10.1016/S0091-6749(99)70388-X; Lima MT, 2002, CLIN EXP ALLERGY, V32, P507, DOI 10.1046/j.0954-7894.2002.01327.x; Lombardi C, 2001, ALLERGY, V56, P889; Malling HJ, 1998, ALLERGY, V53, P933, DOI 10.1111/j.1398-9995.1998.tb03793.x; Moller C, 2002, J ALLERGY CLIN IMMUN, V109, P251, DOI 10.1067/mai.2002.121317; Moreno C, 2004, CLIN EXP ALLERGY, V34, P527, DOI 10.1111/j.1365-2222.2004.1819.x; Mortemousque B, 2003, CLIN EXP ALLERGY, V33, P464, DOI 10.1046/j.1365-2222.2003.01622.x; Pajno GB, 2000, ALLERGY, V55, P842, DOI 10.1034/j.1398-9995.2000.00495.x; Pajno GB, 2003, CLIN EXP ALLERGY, V33, P1641, DOI 10.1111/j.1365-2222.2003.01809.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; Passalacqua Giovanni, 2004, Curr Opin Allergy Clin Immunol, V4, P31, DOI 10.1097/00130832-200402000-00007; Pradalier A, 1999, ALLERGY, V54, P819, DOI 10.1034/j.1398-9995.1999.00077.x; Purello-D'Ambrosio F, 1999, ALLERGY, V54, P968, DOI 10.1034/j.1398-9995.1999.00203.x; SABBAH A, 1994, ALLERGY, V49, P309, DOI 10.1111/j.1398-9995.1994.tb02273.x; STEWART GE, 1992, J ALLERGY CLIN IMMUN, V90, P567, DOI 10.1016/0091-6749(92)90129-P; TARI MG, 1990, ALLERGOL IMMUNOPATH, V18, P277; Tonnel AB, 2004, ALLERGY, V59, P491, DOI 10.1111/j.1398-9995.2004.00456.x; TROISE C, 1995, J INVEST ALLERG CLIN, V5, P25; Voltolini S, 2001, Allergol Immunopathol (Madr), V29, P103; Vourdas D, 1998, ALLERGY, V53, P662, DOI 10.1111/j.1398-9995.1998.tb03952.x; Williams AP, 2004, CLIN EXP ALLERGY, V34, P513, DOI 10.1111/j.1365-2222.2004.1927.x; Wilson DR, 2003, COCHRANE DB SYST REV, DOI [10.1016/S1081-1206(10)60004-X, DOI 10.1002/14651858.CD002893]	45	99	117	0	2	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	MAY	2005	35	5					565	571		10.1111/j.1365-2222.2005.02240.x		7	Allergy; Immunology	Allergy; Immunology	927ES	WOS:000229175800005	15898976	
J	Kandavelu, V; Kastien, H; Thampi, KR				Kandavelu, V; Kastien, H; Thampi, KR			Photocatalytic degradation of isothiazolin-3-ones in water and emulsion paints containing nanocrystalline TiO2 and ZnO catalysts	APPLIED CATALYSIS B-ENVIRONMENTAL			English	Article						titanium dioxide; zinc oxide; photodegradation; isothiazolin-3-ones; heterogeneous photocatalysis; allergens	MICROBICIDAL 3-ISOTHIAZOLONE COMPOUNDS; ELECTRODES; FILMS; PHOTODEGRADATION; DISPERSIONS; SUSPENSIONS; TEMPERATURE; IRRADIATION; ENVIRONMENT; POLLUTANTS	The photocatalytic degradation of isothiazolin-3-ones has been studied using the catalytically active TiO2 and ZnO and the inactive paint grade TiO2, under various illumination and chemical conditions. The reaction follows a pseudo-first-order kinetics. Three types of lamps have been used. The photocatalytic degradation is faster under UV lamp, when it is compared to reaction under suntest and fluorescent lamps. In the presence of oxygen and H2O2, the reaction proceeds faster than in air atmosphere. ZnO exhibits comparable activity with TiO2 and in some cases it was found to be even better than TiO2. The reaction was studied in aqueous suspensions as well as on gas-solid interfaces. The degradation of isothiazolin-3-ones in paint formulations was also studied. (C) 2003 Elsevier B.V. All rights reserved.	EPFL, LPI, CH-1015 Lausanne, Switzerland; Swisslack AG, CH-8304 Wallisellen, Switzerland	Thampi, KR (reprint author), EPFL, LPI, CH-1015 Lausanne, Switzerland.	ravindranathan.thampi@epfl.ch					ALSAYYED G, 1991, J PHOTOCH PHOTOBIO A, V58, P99, DOI 10.1016/1010-6030(91)87101-Z; Barbe CJ, 1997, J AM CERAM SOC, V80, P3157; CROW WD, 1967, AUST J CHEM, V20, P2729; CROW WD, 1969, AUST J CHEM, V22, P765; CROW WD, 1965, J ORG CHEM, V30, P2660, DOI 10.1021/jo01019a037; Dhananjeyan MR, 2000, CHEM COMMUN, P1443, DOI 10.1039/b003108i; Dhananjeyan MR, 2001, J PHYS CHEM B, V105, P12046, DOI 10.1021/jp011339q; Fujishima A., 1999, TIO2 PHOTOCATALYSIS; GOOSSENS A, 1997, CONTACT DERMATITIS, V39, P133; HARBOUR JR, 1979, J PHYS CHEM-US, V83, P652, DOI 10.1021/j100469a003; HOFFMANN MR, 1995, CHEM REV, V95, P69, DOI 10.1021/cr00033a004; Honda H, 1998, J ILLUM ENG SOC, V27, P42; Jerschow E, 2001, FOOD CHEM TOXICOL, V39, P1095, DOI 10.1016/S0278-6915(01)00059-X; KAMAT PV, 1993, CHEM REV, V93, P267, DOI 10.1021/cr00017a013; Kikuchi Y, 1997, J PHOTOCH PHOTOBIO A, V106, P51, DOI 10.1016/S1010-6030(97)00038-5; KORMANN C, 1988, ENVIRON SCI TECHNOL, V22, P798, DOI 10.1021/es00172a009; KRZEMINSKI SF, 1975, J AGR FOOD CHEM, V23, P1068, DOI 10.1021/jf60202a054; KRZEMINSKI SF, 1975, J AGR FOOD CHEM, V23, P1060, DOI 10.1021/jf60202a053; LI Y, 1996, STUD SURF SCI CATAL, V103, P391; LINDUIST I, 1963, INORGANIC ADDUCT MOL; Malato S, 2002, CATAL TODAY, V76, P209, DOI 10.1016/S0920-5861(02)00220-1; MARKHAM MC, 1965, J CATAL, V4, P229, DOI 10.1016/0021-9517(65)90013-8; Ollis D.F., 1993, PHOTOCATALYTIC PURIF; Rajesh B, 2002, FUEL, V81, P2177, DOI 10.1016/S0016-2361(02)00162-X; Rastogi SC, 2000, CONTACT DERMATITIS, V43, P339, DOI 10.1034/j.1600-0536.2000.043006339.x; Reinhardi E, 2001, CONTACT DERMATITIS, V45, P257, DOI 10.1034/j.1600-0536.2001.450501.x; RICHARD C, 1992, J PHOTOCH PHOTOBIO A, V66, P225, DOI 10.1016/1010-6030(92)85216-H; SAKAI H, 1995, CHEM LETT, P185, DOI 10.1246/cl.1995.185; Sunada K, 1998, ENVIRON SCI TECHNOL, V32, P726, DOI 10.1021/es970860o; THAMPI KR, 1983, J INDIAN CHEM SOC, V60, P1156; THAMPI KR, 1987, NATURE, V327, P506, DOI 10.1038/327506a0; THAMPI KR, 1983, ELECTROCHIM ACTA, V28, P1869; THAMPI KR, 1990, J CATAL, V126, P572; Toren K, 1997, AM J IND MED, V31, P551, DOI 10.1002/(SICI)1097-0274(199705)31:5<551::AID-AJIM8>3.0.CO;2-W; *US EPA, 1982, PEST ASS GUID SUBD N; WILLIAMS TM, 1999, 303 NACE; Yeber MC, 1999, CHEMOSPHERE, V39, P1679, DOI 10.1016/S0045-6535(99)00068-5; Zhang FL, 1998, APPL CATAL B-ENVIRON, V15, P147, DOI 10.1016/S0926-3373(97)00043-X	38	99	105	2	28	ELSEVIER SCIENCE BV	AMSTERDAM	PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS	0926-3373			APPL CATAL B-ENVIRON	Appl. Catal. B-Environ.	MAR 18	2004	48	2					101	111		10.1016/j.apcatb.2003.09.022		11	Chemistry, Physical; Engineering, Environmental; Engineering, Chemical	Chemistry; Engineering	803ZV	WOS:000220269900003		
J	Yang, IA; Barton, SJ; Rorke, S; Cakebread, JA; Keith, TP; Clough, JB; Holgate, ST; Holloway, JW				Yang, IA; Barton, SJ; Rorke, S; Cakebread, JA; Keith, TP; Clough, JB; Holgate, ST; Holloway, JW			Toll-like receptor 4 polymorphism and severity of atopy in asthmatics	GENES AND IMMUNITY			English	Article						asthma; atopy; Toll-like receptor 4; polymorphism (genetics)	TOLL-LIKE RECEPTOR-4; HOUSE-DUST ENDOTOXIN; MUTATIONS; EXPOSURE; GENE; SENSITIZATION; ASSOCIATION; CHILDREN; HYGIENE; RISK	Endotoxin exposure may have a protective effect against asthma and atopy. An Asp299Gly polymorphism in the Toll-like receptor 4 (TLR4) gene reduces responsiveness to endotoxin. This study determined the effect of TLR4 polymorphism on the risk and severity of asthma and atopy. In all, 336 UK Caucasian families with greater than or equal to2 affected sibs (physician's diagnosis of asthma and current medication use) and 179 Caucasians without asthma or a family history of asthma were genotyped using ARMS-PCR. No association of the TLR4 polymorphism was found with the risk of developing asthma, either in parent-affected sibling trios, or in case-control analyses (P>0.05). In the first affected asthmatic siblings, the atopy severity score (based on size and number of positive skin-prick tests and specific IgE) was higher in those with the Asp/Gly or Gly/Gly genotypes (mean 1.8, s.d. 1.1, n=39) compared to those with the Asp/Asp genotype (mean 1.2, s.d. 1.0, n=279) (P=0.003, t-test). No associations were found with total <LF>IgE, FEV1 % predicted, slope of FEV1 response to methacholine or asthma severity score (P>0.05). This study confirms the previously observed lack of association of TLR4 polymorphisms with asthma. In contrast, the findings suggest that genetically determined hyporesponsiveness to endotoxin may increase atopy severity.	Univ Southampton, Asthma Genet Lab, Div Human Genet, Southampton, Hants, England; Univ Southampton, Div Infection Inflammat & Repair, Southampton, Hants, England; Genome Therapeut Corp, Waltham, MA USA	Yang, IA (reprint author), Southampton Gen Hosp, Div Human Genet, Mailpoint 808,Tremona Rd, Southampton SO16 6YD, Hants, England.	I.Yang@soton.ac.uk	Yang, Ian/B-9609-2008; Holloway, John/B-5424-2009	Yang, Ian/0000-0001-8338-1993; Holloway, John/0000-0001-9998-0464; Barton, Sheila/0000-0003-4963-4242			Agnese DM, 2002, J INFECT DIS, V186, P1522, DOI 10.1086/344893; Arbour NC, 2000, NAT GENET, V25, P187; Beutler B, 2003, ANNU REV PHARMACOL, V43, P609, DOI 10.1146/annurev.pharmtox.43.100901.135729; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Davies DE, 2003, J ALLERGY CLIN IMMUN, V111, P215, DOI 10.1067/mai.2003.128; 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; Holgate ST, 1999, NATURE, V402, P2, DOI 10.1038/35037000; HOLLOWAY JW, 2001, SEVERE ASTHMA PATHOG, P19; Kiechl S, 2002, NEW ENGL J MED, V347, P185, DOI 10.1056/NEJMoa012673; Liu AH, 2003, J ALLERGY CLIN IMMUN, V111, P471, DOI 10.1067/mai.2003.172; Liu AH, 2002, J ALLERGY CLIN IMMUN, V109, P379, DOI 10.1067/mai.2002.122157; Lorenz E, 2002, ARCH INTERN MED, V162, P1028, DOI 10.1001/archinte.162.9.1028; Pearce N, 1999, THORAX, V54, P268; Raby BA, 2002, AM J RESP CRIT CARE, V166, P1449, DOI 10.1164/rrcm.200207-634OC; Sayers I, 2003, THORAX, V58, P417, DOI 10.1136/thorax.58.5.417; Strachan David P., 2000, Thorax, V55, pS2, DOI 10.1136/thorax.55.suppl_1.S2; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Van Eerdewegh P, 2002, NATURE, V418, P426, DOI 10.1038/nature00878; von Mutius E, 2002, J ALLERGY CLIN IMMUN, V109, pS525, DOI 10.1067/mai.2002.124565; Werner M, 2003, J ALLERGY CLIN IMMUN, V112, P323, DOI 10.1067/mai.2003.1648; Ye S, 2001, NUCLEIC ACIDS RES, V29, part. no., DOI 10.1093/nar/29.17.e88	22	99	110	0	5	NATURE PUBLISHING GROUP	LONDON	MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND	1466-4879			GENES IMMUN	Genes Immun.	JAN	2004	5	1					41	45		10.1038/sj.gene.6364037		5	Genetics & Heredity; Immunology	Genetics & Heredity; Immunology	765VG	WOS:000188304600006	14735148	
J	Gilliland, FD; Berhane, KT; Li, YF; Gauderman, WJ; McConnell, R; Peters, J				Gilliland, FD; Berhane, KT; Li, YF; Gauderman, WJ; McConnell, R; Peters, J			Children's lung function and antioxidant vitamin, fruit, juice, and vegetable intake	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						antioxidants; ascorbic acid; child; diet; respiratory function tests; vitamin A; vitamin E	SOUTHERN CALIFORNIA COMMUNITIES; FOOD FREQUENCY QUESTIONNAIRE; PULMONARY-FUNCTION; GENERAL-POPULATION; AIR-POLLUTION; DIETARY ANTIOXIDANTS; DIFFERING LEVELS; ASTHMA; OBSTRUCTION; ASSOCIATION	The authors investigated the relation between children's pulmonary function and intake of fruits, vegetables, juices, and vitamins A, C, and E by examining cross-sectional data from 2,566 children in the Children's Health Study collected during 1997-1998. Low total vitamin C intake (less than or equal to10th percentile) was associated with deficits in forced vital capacity for both boys and girls and with deficits in flows that were larger in girls (forced expiratory volume in 1 second (FEV1), -3.3%, 95% confidence interval (CI): -6.0, -0.5; forced expiratory flow between 25% and 75% of forced vital capacity (FEF25-75), -5.5%, 95% CI: -10.5, -0.3) compared with boys (FEV1, -2.3%, 95% CI: -4.8, 0.3; FEF25-75, -2.4%, 95% CI: -7.4, 2.8). Low dietary vitamin E intake was associated with lower FEF25-75 (boys: FEF25-75 , -8.9%, 95% CI: -14.2, -3.3; girls: FEF25-75 , -2.5%, 95% CI: -8.3, 3.7). Deficits in FEF25-75 were associated with low dietary vitamin A intake in girls (FEF25-75, -7.9%, 95% CI: -12.7, -2.8) and with low total vitamin A intake in boys with asthma (FEF25-75, -15.6%, 95% CI: -27.6, -1.6). Low intakes of orange and other fruit juices, which were the largest source of vitamin C, were associated with deficits in forced vital capacity and FEV1 in boys. In summary, lung function levels were lower in children with inadequate dietary antioxidant vitamin intake.	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,CHP 236, Los Angeles, CA 90033 USA.		LI, YU-FEN/F-4770-2010		NHLBI NIH HHS [1 R01 HL61768]; NIEHS NIH HHS [1P01 ES09581, 5P30 ES07048]		Becker R. A., 1988, NEW S LANGUAGE; BRITTON JR, 1995, AM J RESP CRIT CARE, V151, P1383; Butland BK, 2000, THORAX, V55, P102, DOI 10.1136/thorax.55.2.102; Chen RL, 2001, AM J EPIDEMIOL, V153, P157, DOI 10.1093/aje/153.2.157; Cook DG, 1997, THORAX, V52, P628; Enright PL, 2000, CHEST, V118, P665, DOI 10.1378/chest.118.3.665; Fogarty A, 2000, Curr Opin Pulm Med, V6, P86, DOI 10.1097/00063198-200001000-00015; Gilliland FD, 1999, ENVIRON HEALTH PERSP, V107, P403; Gilliland FD, 2002, AM J EPIDEMIOL, V155, P125, DOI 10.1093/aje/155.2.125; GOLD DR, 1994, AM J RESP CRIT CARE, V149, P1198; Grievink L, 1998, THORAX, V53, P166; HASTIE T, 1993, J ROY STAT SOC B MET, V55, P757; Hastie T, 1990, GEN ADDITIVE MODELS; Hu GZ, 2000, AM J EPIDEMIOL, V151, P975; Hu GZ, 1998, AM J EPIDEMIOL, V148, P594; Institute of Medicine, 2000, DIET REF INT VIT C V; *I MED, 2001, DIET REF INT VIT A V; Kassaye T, 2001, INT J EPIDEMIOL, V30, P457, DOI 10.1093/ije/30.3.457; Mathew R, 1991, Magnes Trace Elem, V10, P220; McKeever TM, 2002, AM J RESP CRIT CARE, V165, P1299, DOI 10.1164/rccm.2109030; Ness AR, 1996, EUR J CLIN NUTR, V50, P573; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; Peters JM, 1999, AM J RESP CRIT CARE, V159, P768; Rockett HRH, 1997, PREV MED, V26, P808, DOI 10.1006/pmed.1997.0200; Rockett HRH, 1997, AM J CLIN NUTR, V65, P1116; Romieu I, 2002, AM J RESP CRIT CARE, V166, P703, DOI 10.1164/rccm.2112074; Romieu I, 2001, EPIDEMIOL REV, V23, P268; Schunemann HJ, 1997, AM J EPIDEMIOL, V146, P939; Schunemann HJ, 2001, EPIDEMIOL REV, V23, P248; Schunemann HJ, 2002, AM J EPIDEMIOL, V155, P463, DOI 10.1093/aje/155.5.463; Schunemann HJ, 2001, AM J RESP CRIT CARE, V163, P1246; Sempertegui F, 2001, INT J EPIDEMIOL, V30, P465, DOI 10.1093/ije/30.3.465; Soutar A, 1997, THORAX, V52, P166; Tabak C, 2001, CLIN EXP ALLERGY, V31, P747, DOI 10.1046/j.1365-2222.2001.01064.x; TROISI RJ, 1995, AM J RESP CRIT CARE, V151, P1401; WANG XB, 1994, AM J RESP CRIT CARE, V149, P1420; Weiss ST, 1997, CIBA F SYMP, V206, P244; WEISS ST, 1997, CIBA F SYMP, V206, P253; WILLETT WC, 1985, AM J EPIDEMIOL, V122, P51; Wypij D, 1996, AM J RESP CRIT CARE, V154, pS223; WYPIJ D, 1994, STAT SINICA, V3, P329	41	99	101	0	4	OXFORD UNIV PRESS INC	CARY	JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA	0002-9262			AM J EPIDEMIOL	Am. J. Epidemiol.	SEP 15	2003	158	6					576	584		10.1093/aje/kwg181		9	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	721HK	WOS:000185310800010	12965883	
J	Almqvist, C; Egmar, AC; Hedlin, G; Lundqvist, M; Nordvall, SL; Pershagen, G; Svartengren, M; van Hage-Hamsten, M; Wickman, M				Almqvist, C; Egmar, AC; Hedlin, G; Lundqvist, M; Nordvall, SL; Pershagen, G; Svartengren, M; van Hage-Hamsten, M; Wickman, M			Direct and indirect exposure to pets - risk of sensitization and asthma at 4 years in a birth cohort	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergens; allergy and immunology; animals; asthma; cats; child; dogs; domestic; endotoxins; prevention; primary	CAT ALLERGEN; CHILDREN; CHILDHOOD; OWNERSHIP; SCHOOL; HOMES; LIFE; SYMPTOMS; ENVIRONMENT; PREVALENCE	Introduction There are conflicting data on the association between early exposure to pets and allergic diseases. Bias related to retrospective information on pet ownership has been addressed as a reason for distorted study results. Objective To elucidate how early exposure to cat and dog relates to IgE-sensitization and asthma in children at 2 and 4 years of age, in a prospective birth-cohort study. Methods Four thousand and eighty-nine families with children born 1994-1996 in predefined areas of Stockholm answered questionnaires on environmental factors and symptoms of allergic disease at birth, one, two and four years of age. Dust samples collected from the mothers' beds at birth were analysed for Fel d 1 and Can f 1 in a subgroup of the cohort. Blood samples taken at four years from 2614 children were analysed for allergen-specific IgE to common airborne allergens. Risk associations were calculated with a multiple logistic regression model, with adjustment for potential confounders. Results A correlation was seen between allergen levels and reported exposure to cat and dog. Exposure to cat seemed to increase the risk of cat sensitization, OR (odds ratio) 1.44 (95% confidence interval 1.03-2.01), whereas dog exposure did not have any effect on dog sensitization, OR 1.16 (0.79-1.72). Dog ownership was related to a reduced risk of sensitization to other airborne allergens, OR 0.36 (0.15-0.83), and a similar tendency was seen for cat ownership OR 0.63 (0.37-1.07). Early dog ownership seemed to be associated with a lower risk of asthma, OR 0.50 (0.24-1.03), with no corresponding effect after cat ownership, OR 0.88 (0.56-1.38). Conclusion Early exposure to cat seems to increase the risk of sensitization to cat but not of asthma at 4 years of age. Dog ownership, on the other hand, appears to be associated with lowered risk of sensitization to airborne allergens and asthma. Both aetiological relationships and selection effects have to be considered in the interpretation of these findings.	Karolinska Hosp, S-17176 Stockholm, Sweden; Karolinska Inst, Astrid Lindgren Childrens Hosp, Dept Woman & Child Hlth, Stockholm, Sweden; Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; Uppsala Univ, Inst Woman & Child Hlth, Uppsala, Sweden; Karolinska Inst, Dept Publ Hlth Sci, Stockholm, Sweden; Karolinska Hosp & Inst, Dept Med, Allergy & Clin Immunol Unit, Stockholm, Sweden; Karolinska Inst, Inst Sodersjukhuset, Sachs Childrens Hosp, Stockholm, Sweden	Almqvist, C (reprint author), Karolinska Hosp, Norrbacka 3rd Floor, S-17176 Stockholm, Sweden.		van Hage, Marianne/A-9678-2017	van Hage, Marianne/0000-0003-3091-1596			Ahlbom A, 1998, INDOOR AIR, V8, P219, DOI 10.1111/j.1600-0668.1998.00003.x; Almqvist C, 1999, J ALLERGY CLIN IMMUN, V103, P1012, DOI 10.1016/S0091-6749(99)70172-7; Almqvist C, 2003, J ALLERGY CLIN IMMUN, V111, P800, DOI 10.1067/mai.2003.1334; Almqvist C, 2001, AM J RESP CRIT CARE, V163, P694; Anyo G, 2002, CLIN EXP ALLERGY, V32, P361, DOI 10.1046/j.1365-2222.2002.01254.x; Apelberg BJ, 2001, J ALLERGY CLIN IMMUN, V107, P455, DOI 10.1067/mai.2001.113240; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Bollinger ME, 1996, J ALLERGY CLIN IMMUN, V97, P907, DOI 10.1016/S0091-6749(96)80064-9; 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, 1998, THORAX, V53, P33; Custovic A, 2001, J ALLERGY CLIN IMMUN, V108, P537, DOI 10.1067/mai.2001.118599; Egmar AC, 1998, PEDIATR ALLERGY IMMU, V9, P31, DOI 10.1111/j.1399-3038.1998.tb00297.x; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Lannero E, 2002, PEDIATR ALLERGY IMMU, V13, P182, DOI 10.1034/j.1399-3038.2002.01055.x; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; MURRAY AB, 1983, J ALLERGY CLIN IMMUN, V72, P145, DOI 10.1016/0091-6749(83)90522-5; Ownby DR, 2002, JAMA-J AM MED ASSOC, V288, P963, DOI 10.1001/jama.288.8.963; Parvaneh S, 1999, ALLERGY, V54, P229, DOI 10.1034/j.1398-9995.1999.00855.x; Pearce N, 1999, THORAX, V54, P268; 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, 2002, CLIN EXP ALLERGY, V32, P335, DOI 10.1046/j.1365-2222.2002.01352.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; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; *SOC IND, 1989, OCC POP HOUS CENS 19; Svanes C, 1999, J ALLERGY CLIN IMMUN, V103, P415, DOI 10.1016/S0091-6749(99)70465-3; Svedmyr J, 1999, ACTA PAEDIATR, V88, P42; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; Wahn U, 1997, PEDIATR ALLERGY IMMU, V8, P16	33	99	99	2	8	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	SEP	2003	33	9					1190	1197		10.1046/j.1365-2222.2003.01764.x		8	Allergy; Immunology	Allergy; Immunology	727UC	WOS:000185678400005	12956738	
J	Basketter, DA; Angelini, G; Ingber, A; Kern, PS; Menne, T				Basketter, DA; Angelini, G; Ingber, A; Kern, PS; Menne, T			Nickel, chromium and cobalt in consumer products: revisiting safe levels in the new millennium	CONTACT DERMATITIS			English	Review						nickel; chromate; cobalt; thresholds; consumer products; elicitation	ALLERGIC CONTACT-DERMATITIS; LYMPH-NODE ASSAY; RISK ASSESSMENT; HAND ECZEMA; EXPOSURE; SKIN; SENSITIZATION; THRESHOLDS; REACTIVITY; MODELS	The transition metals nickel (Ni), chromium (Cr) and cobalt (Co) are common causes of allergic contact dermatitis (ACD). Given the high frequency with which these allergens can be associated with hand eczema in those responsible for domestic work, it has been suggested that contamination of household consumer products with these metals may be of relevance to the causation/chronicity of hand dermatitis. Dose-response studies using 48 h occlusive patch test conditions in sensitized individuals show that greater than or equal to90% of sensitized patients fail to react below 1 p.p.m., even on irritated skin. Assessment under more realistic exposure conditions has shown that in the presence of irritants and/or following repeated exposures, such individuals rarely react to levels below 10 p.p.m. On the basis of this information, it was recommended a decade ago that household (and other consumer) products should not contain more than 5 p.p.m. of each of Ni, Cr or Co and that, for an even greater degree of protection, the ultimate target level should be 1 p.p.m. The data generated since the original recommendations were made serve to reinforce the validity of these recommendations. Indeed, it is our view that typically the level of each of these transition metals should not normally exceed 1 p.p.m. Then, where consumer products meet this guideline fully, modern quantitative risk assessment shows clearly that elicitation of ACD is highly improbable, and the chance of the induction of sensitization is even lower.	Unilever Colworth, SEAC, Sharnbrook MK44 1LQ, Beds, England; Univ Bari, Dept Internal Med Immunol & Infect Dis, Unit Dermatol, I-70121 Bari, Italy; Haddassah Hosp, Dept Dermatol, Jerusalem, Israel; Procter & Gamble Co, European Tech Ctr, Strombeek Bever, Belgium; Gentofte Univ Hosp, Dept Dermatol, Hellerup, Denmark	Basketter, DA (reprint author), Unilever Colworth, SEAC, Sharnbrook MK44 1LQ, Beds, England.						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J	Host, A; Andrae, S; Charkin, S; Diaz-Vazquez, C; Dreborg, S; Eigenmann, PA; Friedrichs, F; Grinsted, P; Lack, G; Meylan, G; Miglioranzi, P; Muraro, A; Nieto, A; Niggemann, B; Pascual, C; Pouech, MG; Rance, F; Rietschel, E; Wickman, M				Host, A; Andrae, S; Charkin, S; Diaz-Vazquez, C; Dreborg, S; Eigenmann, PA; Friedrichs, F; Grinsted, P; Lack, G; Meylan, G; Miglioranzi, P; Muraro, A; Nieto, A; Niggemann, B; Pascual, C; Pouech, MG; Rance, F; Rietschel, E; Wickman, M			Allergy testing in children: why, who, when and how?	ALLERGY			English	Editorial Material							HOUSE-DUST-MITE; LATE ASTHMATIC RESPONSES; BLIND CONTROLLED TRIAL; COMMON FOOD PROTEINS; SKIN PRICK TEST; ATOPIC-DERMATITIS; IGE CONCENTRATIONS; COWS MILK; IN-VITRO; BRONCHIAL HYPERREACTIVITY			Host, A (reprint author), Odense Univ Hosp, Dept Pediat, DK-5000 Odense C, Denmark.		Osborne, Nicholas/N-4915-2015; Eigenmann, Philippe/A-6569-2017	Osborne, Nicholas/0000-0002-6700-2284; Eigenmann, Philippe/0000-0003-1738-1826			Abramson M, 1999, ALLERGY, V54, P1022, DOI 10.1034/j.1398-9995.1999.00102.x; Abramson MJ, 2000, COCHRANE DB SYST REV; Ahlstedt S, 2002, CLIN EXP ALLERGY, V32, P11, DOI 10.1046/j.0022-0477.2001.01289.x; Annus T, 2001, CLIN EXP ALLERGY, V31, P1846, DOI 10.1046/j.1365-2222.2001.01238.x; *BAND LIB, BIAS DIAGN TEST LEV; Berger W E, 2001, Curr Allergy Asthma Rep, V1, P498, DOI 10.1007/s11882-001-0058-7; Board of Directors, 1993, J ALLERGY CLIN IMMUN, V92, P636; Bohme M, 2001, ACTA DERM-VENEREOL, V81, P193, DOI 10.1080/000155501750376294; BONER AL, 1985, ANN ALLERGY, V54, P42; Boulet LP, 1997, CLIN EXP ALLERGY, V27, P52, DOI 10.1046/j.1365-2222.1997.d01-418.x; Bousquet J, 2001, J ALLERGY CLIN IMMUN, V108, P147, DOI DOI 10.1067/MAI.2001.118891; Boyano-Martinez T, 2002, J ALLERGY CLIN IMMUN, V110, P304, DOI 10.1067/mai.2002.126081; Brehler R, 2001, ARCH INTERN MED, V161, P1057, DOI 10.1001/archinte.161.8.1057; 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Nishioka K, 1998, J ALLERGY CLIN IMMUN, V101, P28, DOI 10.1016/S0091-6749(98)70189-7; NOLTE H, 1987, ALLERGY, V42, P366, DOI 10.1111/j.1398-9995.1987.tb02223.x; OBYRNE PM, 1987, AM REV RESPIR DIS, V136, P740; OSTERGAARD PA, 1990, ALLERGY, V45, P1; Oxford Centre for Evidence-Based Medicine, 2001, LEV EV GRAD REC; Pearce N, 1999, THORAX, V54, P268; Piacentini GL, 1998, CLIN EXP ALLERGY, V28, P561; PIACENTINI GL, 1993, J ALLERGY CLIN IMMUN, V92, P644, DOI 10.1016/0091-6749(93)90006-2; Piacentini GL, 1996, J ALLERGY CLIN IMMUN, V97, P1079, DOI 10.1016/S0091-6749(96)70261-0; Ponsonby AL, 2002, CHEST, V121, P135, DOI 10.1378/chest.121.1.135; Resano A, 1998, J INVEST ALLERG CLIN, V8, P271; Roehr CC, 2001, J ALLERGY CLIN IMMUN, V107, P548, DOI 10.1067/mai.2001.112849; Salkind AR, 2001, JAMA-J AM MED ASSOC, V285, P2498, DOI 10.1001/jama.285.19.2498; Sampson HA, 1999, J ALLERGY CLIN IMMUN, V103, P981, DOI 10.1016/S0091-6749(99)70167-3; Sampson HA, 1997, J ALLERGY CLIN IMMUN, V100, P444; Sampson HA, 2001, J ALLERGY CLIN IMMUN, V107, P891, DOI 10.1067/mai.2001.114708; 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Vanlaar CH, 2000, J ALLERGY CLIN IMMUN, V105, P1130, DOI 10.1067/mai.2000.106213; Vanto T, 1999, ALLERGY, V54, P837, DOI 10.1034/j.1398-9995.1999.00134.x; VARNEY VA, 1993, J CLIN INVEST, V92, P644, DOI 10.1172/JCI116633; Wahn U, 2000, ALLERGY, V55, P591, DOI 10.1034/j.1398-9995.2000.00111.x; Wahn U, 1998, PEDIATR ALLERGY IMMU, V9, P116; Warner JA, 2000, J ALLERGY CLIN IMMUN, V105, P75, DOI 10.1016/S0091-6749(00)90181-7; Weeks J, 1995, CLIN EXP ALLERGY, V25, P1179, DOI 10.1111/j.1365-2222.1995.tb03041.x; WICKMAN M, 1994, ALLERGY, V49, P114, DOI 10.1111/j.1398-9995.1994.tb00810.x; Wolkerstorfer A, 2002, CLIN EXP ALLERGY, V32, P70, DOI 10.1046/j.0022-0477.2001.01265.x; Yman L, 2001, ALLERGY, V56, P70, DOI 10.1034/j.1398-9995.2001.00921.x; Yunginger JW, 2000, J ALLERGY CLIN IMMUN, V105, P1077, DOI 10.1067/mai.2000.107041; ZETTERSTROM O, 1981, ALLERGY, V36, P537, DOI 10.1111/j.1398-9995.1981.tb01871.x	114	99	110	0	6	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	JUL	2003	58	7					559	569		10.1034/j.1398-9995.2003.00238.x		11	Allergy; Immunology	Allergy; Immunology	693QZ	WOS:000183731000003	12823111	
J	Jain, VV; Kitagaki, K; Businga, T; Hussain, I; George, C; O'Shaughnessy, P; Kline, JN				Jain, VV; Kitagaki, K; Businga, T; Hussain, I; George, C; O'Shaughnessy, P; Kline, JN			CpG-oligodeoxynucleotides inhibit airway remodeling in a murine model of chronic asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; murine; CpG oligodeoxynucleotides; airway remodeling; collagen; subepithelial fibrosis; transforming growth factor beta; regulatory T lymphocytes	SUBEPITHELIAL FIBROSIS; FLOW OBSTRUCTION; BRONCHIAL-ASTHMA; INFLAMMATION; RESPONSIVENESS; CELLS; METHACHOLINE; GENERATION; MODULATION; RESPONSES	Background: We have previously demonstrated that CpG oligodeoxymicleotides (CpG-ODNs) protect against eosinophilia and airway hyperresponsiveness in marine models of allergen-induced asthma. Acute inflammation is hypothesized to induce chronic airway responses, but no previous studies have evaluated the effects of CpG-ODNs on allergen-induced airway remodeling. Because remodeling is thought to be responsible for many of the long-term adverse effects on asthmatic patients, we evaluated whether CpG-ODNs might similarly prevent these changes using a murine model of recurrent allergen exposure. Objective: The purpose of this study was to evaluate the effect of CpG-ODNs on chronic inflammatory changes and airway remodeling by using a marine model of chronic allergen-induced asthma. Methods: C57BL/6 mice were sensitized to ovalbumin (OVA) and subsequently exposed to nebulized OVA by means of inhalation 3 times weekly for 6 weeks. Some mice received CpG-ODNs by means of intraperitoneal injection at the time of sensitization. At the end of the exposure period, mice were evaluated for the development of airway inflammation, airway hyperresponsiveness, and airway remodeling. Results: OVA-sensitized mice exposed to recurrent airway challenge with OVA have chronic inflammation, persistent airway hyperresponsiveness, and evidence of airway remodeling, including subepithelial collagen deposition and goblet cell hyperplasia-metaplasia. These changes are significantly reduced in mice treated with CpG-ODNs. Interestingly, mice treated with CpG-ODNs exhibit increased levels of bronchoalveolar lavage transforming growth factor P, suggesting that regulatory T cells might be responsible for some of these protective effects. Conclusion: CpG-ODNs are effective not only in preventing acute inflammation but also appear to reduce markers of airway remodeling that develop after chronic allergen exposure.	Univ Iowa, Roy J & Lucille A Carver Coll Med, Dept Med, Iowa City, IA 52242 USA; Univ Iowa, Roy J & Lucille A Carver Coll Med, Dept Pediat, Iowa City, IA 52242 USA; Univ Iowa, Coll Publ Hlth, Dept Occupat & Environm Med, Iowa City, IA USA	Kline, JN (reprint author), UIHC, 200 Newton Rd, Iowa City, IA 52242 USA.			Jain, Vipul/0000-0001-5575-7869	NHLBI NIH HHS [HL59324]; NIDDK NIH HHS [DK54759]; NIEHS NIH HHS [ES05605]		AIKAWA T, 1992, CHEST, V101, P916, DOI 10.1378/chest.101.4.916; Blyth DI, 1996, AM J RESP CELL MOL, V14, P425; BOLENDER RP, 1993, AM J PHYSIOL, V265, pL521; BOULET LP, 1995, AM J RESP CRIT CARE, V152, P865; Boulet LP, 1997, CHEST, V112, P45, DOI 10.1378/chest.112.1.45; BREWSTER CEP, 1990, AM J RESP CELL MOL, V3, P507; Broide D, 1998, J IMMUNOL, V161, P7054; BROWN PJ, 1984, THORAX, V39, P131, DOI 10.1136/thx.39.2.131; CARROLL N, 1993, AM REV RESPIR DIS, V147, P405; Chu HW, 1998, AM J RESP CRIT CARE, V158, P1936; DUNNILL MS, 1960, J CLIN PATHOL, V13, P27, DOI 10.1136/jcp.13.1.27; Fahy JV, 2001, AM J RESP CRIT CARE, V164, pS46; Haneda K, 1997, J IMMUNOL, V159, P4484; JAMES AL, 1989, AM REV RESPIR DIS, V139, P242; JEFFERY PK, 1992, AM REV RESPIR DIS, V145, P890; JEFFERY PK, 1991, AM REV RESPIR DIS, V143, P1152; Kline JN, 1999, J ALLERGY CLIN IMMUN, V104, P1258; Kline JN, 2002, AM J PHYSIOL-LUNG C, V283, pL170, DOI 10.1152/ajplung.00402.2001; Kline JN, 1998, J IMMUNOL, V160, P2555; Krieg Arthur M., 2002, Trends in Immunology, V23, P64, DOI 10.1016/S1471-4906(01)02150-0; Okazawa M, 1996, AM J RESP CRIT CARE, V154, P1557; ROCHE WR, 1989, LANCET, V1, P520; Russ JC, 2001, PRACTICAL STEREOLOGY; Santeliz JV, 2002, J ALLERGY CLIN IMMUN, V109, P455, DOI 10.1067/mai.2002.122156; Serebrisky D, 2000, J IMMUNOL, V165, P5906; Shimura S, 1996, EUR RESPIR J, V9, P1395, DOI 10.1183/09031936.96.09071395; Sur S, 1999, J IMMUNOL, V162, P6284; Temelkovski J, 1998, THORAX, V53, P849; Terui T, 2001, J IMMUNOL, V167, P3661; Warshamana GS, 1998, AM J PHYSIOL-LUNG C, V274, pL499; WILSON JW, 1993, AM REV RESPIR DIS, V148, P806; Zhang XM, 2001, J IMMUNOL, V167, P4245; ZuanyAmorim C, 1996, J IMMUNOL, V157, P377	33	99	113	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.	DEC	2002	110	6					867	872		10.1067/mai.2002.129371		6	Allergy; Immunology	Allergy; Immunology	624TL	WOS:000179777400008	12464952	
J	Wickens, K; Lane, JM; Fitzharris, P; Siebers, R; Riley, G; Douwes, J; Smith, T; Crane, J				Wickens, K; Lane, JM; Fitzharris, P; Siebers, R; Riley, G; Douwes, J; Smith, T; Crane, J			Farm residence and exposures and the risk of allergic diseases in New Zealand children	ALLERGY			English	Article						animals; allergic rhinitis; asthma; eczema; endotoxin; Der p 1; farming; hayfever; probiotics; skin prick test; wheeze	HAY-FEVER; ASTHMA PREVALENCE; EARLY-CHILDHOOD; SENSITIZATION; ENDOTOXIN; ATOPY; ENVIRONMENT; COMMUNITY; URBAN; SIZE	Background: Studies in Europe have reported a reduced prevalence of allergy in farmers children. We aimed to determine if there is a similar reduction in allergy among New Zealand farm children. Methods: Two hundred and ninety-three children participated (60%) aged 7-10 years, from selected schools in small towns and the surrounding rural area. Skin prick tests (SPT) to eight common allergens were performed. Parents completed questionnaires about allergic and infectious diseases, place of residence, exposure to animals, and diet, and they provided dust from the livingroom floor. Endotoxin was measured using an Limulus amoebocyte lysate (LAL) assay and Der p 1 using enzyme-linked immunoassay ( ELISA). Results: Current farm abode was found to increase the risk of having symptoms associated with allergy, but not SPT positivity. Independent inverse associations were found for early-life exposures: at least weekly consumption of yoghurt with hayfever (odds ratio (OR) = 0.3, 95% confidence intervals (CI) 0.1-0.7) and allergic rhinitis (OR = 0.3, 95% CI 0.2-0.7); any unpasteurized milk consumption with atopic eczema/dermatitis syndrome (AEDS) (OR = 0.2, 95% CI 0.1-0.8); cats inside or outside with hayfever (OR = 0.4, 95% CI 0.1-1. 0) and AEDS (OR = 0.4, 95% CI 0.2-0.8); dogs inside or outside with asthma (OR = 0.4, 95% CI 0.2-0.8); and pigs with SPT positivity (OR = 0.2, 95% CI 0.1-0.9). Conclusions: Despite finding a protective effect of early-life animal exposures, we found a greater prevalence of allergic disease on farms.	Univ Otago, Wellington Asthma Res Grp, Wellington, New Zealand; Univ Utrecht, Div Environm & Occupat Hlth, IRAS, Utrecht, Netherlands	Wickens, K (reprint author), Wellington Sch Med, Wellington Asthma Res Grp, POB 7343, Wellington, New Zealand.		Siebers, Robert/A-4102-2009	Douwes, Jeroen/0000-0003-3599-4036; Siebers, Robert/0000-0002-6359-3144			ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Attena F, 1999, EUR J EPIDEMIOL, V15, P569, DOI 10.1023/A:1007564323390; Barnes M, 2001, CLIN EXP ALLERGY, V31, P1822, DOI 10.1046/j.1365-2222.2001.01240.x; Black PN, 1997, EUR RESPIR J, V10, P6, DOI 10.1183/09031936.97.10010006; Blackley CH, 1873, EXPT RES CAUSES NATU; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Donham KJ, 2000, J OCCUP ENVIRON MED, V42, P260, DOI 10.1097/00043764-200003000-00006; Douwes J, 2002, THORAX, V57, P86, DOI 10.1136/thorax.57.1.86; DOUWES J, 1995, APPL ENVIRON MICROB, V61, P1763; 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; Farooqi IS, 1998, THORAX, V53, P927; Gassner-Bachmann M, 2000, DEUT MED WOCHENSCHR, V125, P924, DOI 10.1055/s-2000-6778; Hasan MMS, 2000, J ASTHMA, V37, P353, DOI 10.3109/02770900009055459; Johansson SGO, 2001, ALLERGY, V56, P813, DOI 10.1034/j.1398-9995.2001.t01-1-00001.x; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Klintberg B, 2001, EUR RESPIR J, V17, P1151, DOI 10.1183/09031936.01.00027301; LUCZYNSKA CM, 1989, J IMMUNOL METHODS, V118, P227, DOI 10.1016/0022-1759(89)90010-0; Matsuzaki T, 1998, J DAIRY SCI, V81, P48; Melsom T, 2001, THORAX, V56, P477, DOI 10.1136/thorax.56.6.477; Min YG, 1997, CLIN OTOLARYNGOL, V22, P139, DOI 10.1046/j.1365-2273.1997.00879.x; Odhiambo JA, 1998, EUR RESPIR J, V12, P1105, DOI 10.1183/09031936.98.12051105; PEAT JK, 1994, BRIT MED J, V308, P1591; PEAT JK, 1995, MED J AUSTRALIA, V163, P22; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; Portengen L, 2002, CLIN EXP ALLERGY, V32, P247, DOI 10.1046/j.1365-2222.2002.01310.x; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Rosenberg R, 1999, Fam Med, V31, P276; Selim SA, 1997, J AM VET MED ASSOC, V211, P1029; STRACHAN DP, 1989, BRIT MED J, V299, P1259; STRACHAN DP, 1995, CLIN EXP ALLERGY, V25, P296, DOI 10.1111/j.1365-2222.1995.tb01046.x; Sudo N, 1997, J IMMUNOL, V159, P1739; Ukai K, 1998, Arerugi, V47, P420; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; vonMutius E, 1996, BRIT MED J, V312, P1448; WAITE DA, 1980, CLIN ALLERGY, V10, P71, DOI 10.1111/j.1365-2222.1980.tb02082.x; Wickens K, 1999, CLIN EXP ALLERGY, V29, P766; Wickens KL, 1999, EPIDEMIOLOGY, V10, P699, DOI 10.1097/00001648-199911000-00009; WOODS RK, 2000, AUSTR RESPIROL, V5, P257; WUTHRICH B, 1991, ALLERGY CLIN IMMUNOL, V3, P41; Yemaneberhan H, 1997, LANCET, V350, P85, DOI 10.1016/S0140-6736(97)01151-3; ZEJDA JE, 1994, J OCCUP ENVIRON MED, V36, P49	44	99	100	1	10	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	DEC	2002	57	12					1171	1179		10.1034/j.1398-9995.2002.t01-1-23644.x		9	Allergy; Immunology	Allergy; Immunology	621VH	WOS:000179611400012	12464046	
J	Perera, FP; Illman, SM; Kinney, PL; Whyatt, RM; Kelvin, EA; Shepard, P; Evans, D; Fullilove, M; Ford, J; Miller, RL; Mayer, IH; Rauh, VA				Perera, FP; Illman, SM; Kinney, PL; Whyatt, RM; Kelvin, EA; Shepard, P; Evans, D; Fullilove, M; Ford, J; Miller, RL; Mayer, IH; Rauh, VA			The challenge of preventing environmentally related disease in young children: Community-based research in New York City	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; cancer; children; development; environmental health; prenatal; prevention; susceptibility	POLYCYCLIC AROMATIC-HYDROCARBONS; DIESEL EXHAUST PARTICLES; SERUM COTININE LEVELS; MOLECULAR EPIDEMIOLOGY; BIRTH-WEIGHT; CANCER PREVENTION; INDOOR ALLERGENS; PASSIVE SMOKING; TOBACCO-SMOKE; RISK-FACTORS	Rates of developmental and respiratory diseases are disproportionately high in underserved, minority populations such as those in New York City's Washington Heights, Harlem, and the South Bronx. Blacks and Latinos in these neighborhoods represent high risk groups for asthma, adverse birth outcomes, impaired development, and some types of cancer. The Columbia Center for Children's Environmental Health in Washington Heights uses molecular epidermiologic methods to study the health effects of urban indoor and outdoor air pollutants on children, prenatally and postnatally, in a cohort of over 500 African-American and Dominican (originally from the Dominican Republic) mothers and newborns. Extensive data are collected to determine exposures to particulate matter < 2.5 &mu;m in aerodynamic diameter (PM2.5), polycyclic aromatic hydrocarbons (PAHs), diesel exhaust particulate (DEP), nitrogen oxide, nonpersistent pesticides, home allergens (dust mite, mouse, cockroach), environmental tobacco smoke (ETS), and lead and other metals. Biomarkers, air sampling, and clinical assessments are used to study the effects of these exposures on children's increased risk for allergic sensitization, asthma and other respiratory disorders, impairment of neurocognitive and behavioral development, and potential cancer risk. The center conducts its research and community education in collaboration with 10 community-based health and environmental advocacy organizations. This unique academic-community partnership helps to guide the center's research so that it is most relevant to the context of the low-income, minority neighborhoods in which the cohort resides, and information is delivered back to these communities in meaningful ways. In turn, communities become better equipped to relay environmental health concerns to policy makers. In this paper we describe the center's research and its academic-community partnership and present some preliminary findings.	Columbia Univ, Joseph L Mailman Sch Publ Hlth, Columbia Ctr Childrens Environm Hlth, New York, NY 10032 USA; W Harlem Environm Act Inc, New York, NY USA	Perera, FP (reprint author), Columbia Univ, Joseph L Mailman Sch Publ Hlth, Div Environm Hlth Sci, 60 Haven Ave,B-116, New York, NY 10032 USA.				NCRR NIH HHS [RR 00645]; NIEHS NIH HHS [R01 ES 08977, P01 ES009600, P50 ES 09600, R01 ES 06722, R01 ES008977]		*AM CANC SOC, 1996, CANC FACTS FIG 1996; Beasley R, 2000, J ALLERGY CLIN IMMUN, V105, pS466, DOI 10.1016/S0091-6749(00)90044-7; BINKOVA B, 1995, CARCINOGENESIS, V16, P1037, DOI 10.1093/carcin/16.5.1037; BUI QQ, 1986, TOXICOLOGY, V42, P195, DOI 10.1016/0300-483X(86)90009-0; Calabrese EJ, 1986, AGE SUSCEPTIBILITY T; Campbell CG, 1997, BRAIN RES BULL, V43, P179, DOI 10.1016/S0361-9230(96)00436-4; CASSEL J, 1976, AM J EPIDEMIOL, V104, P107; Centers for Disease Control and Prevention [CDC], 1998, MMWR-MORBID MORTAL W, V47, P1; Chanda SM, 1996, PHARMACOL BIOCHEM BE, V53, P771, DOI 10.1016/0091-3057(95)02105-1; CHEN LH, 1995, AM J EPIDEMIOL, V142, P158; Claudio L, 1999, J ASTHMA, V36, P343, DOI 10.3109/02770909909068227; *COMM STUD NEW YOR, INFOSHARE; CRAIN EF, 1994, PEDIATRICS, V94, P356; CRAWFORD MA, 1989, J INTERN MED, V225, P159; David RJ, 1997, NEW ENGL J MED, V337, P1209, DOI 10.1056/NEJM199710233371706; DAY NE, 1980, J NATL CANCER I, V64, P977; *DHHS, 1986, REP SECR TASK FORC B; Duran-Tauleria E, 1999, THORAX, V54, P476; ENGLISH PB, 1994, AM J PUBLIC HEALTH, V84, P1439, DOI 10.2105/AJPH.84.9.1439; Faustman EM, 2000, ENVIRON HEALTH PERSP, V108, P13, DOI 10.2307/3454629; FULLILOVE MT, 1991, B NEW YORK ACAD MED, V67, P571; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; Goldstein I F, 1987, Experientia Suppl, V51, P133; *GREAT BOST PHYS S, 2000, HARMS WAY TOX THREAT; GREENE LS, 1995, J AM COLL NUTR, V14, P317; GROOPMAN JD, 1994, CANCER RES, V54, pS1907; HARRIS CC, 1991, CANCER RES, V51, pS5023; HATCH GE, 1995, AM J CLIN NUTR S, V61, pS325; HECHT SS, 1994, CANCER RES, V54, pS1912; HULKA BS, 1991, CANCER EPIDEM BIOMAR, V1, P13; HULKA BS, 1991, HLTH ENV DIGEST, V5, P1; Jacobson JL, 1996, NEW ENGL J MED, V335, P783, DOI 10.1056/NEJM199609123351104; Kinney PL, 2000, ENVIRON HEALTH PERSP, V108, P213, DOI 10.2307/3454436; KLIEGMAN RM, 1992, PEDIATRICS, V89, P710; Knight JM, 1996, CHEST, V109, P446, DOI 10.1378/chest.109.2.446; KRASNER M, 1994, NEW YORK CITY COMMUN; LAIB RJ, 1985, CARCINOGENESIS, V6, P65, DOI 10.1093/carcin/6.1.65; LU LJW, 1986, CANCER RES, V46, P3046; LU LJW, 1990, CARCINOGENESIS, V11, P1367, DOI 10.1093/carcin/11.8.1367; MAKRIDES M, 1995, LANCET, V345, P1463, DOI 10.1016/S0140-6736(95)91035-2; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; May M, 2000, ENV HLTH PERSPECT, V108, P262; MCCLELLAN RO, 1987, ANNU REV PHARMACOL, V27, P279; MEYER I, UNPUB; Miller RL, 2001, AM J RESP CRIT CARE, V164, P995; MILLER RL, IN PRESS AM J RESP C; Mott L., 1994, HANDLE CARE CHILDREN; National Research Council, 1993, PEST DIETS INF CHILD; NEEDLEMAN HL, 1979, NEW ENGL J MED, V301, P163; NEUBERT D, 1988, ARCH TOXICOL, V35, P2943; *NEW YORK CIT HLTH, 1998, NEW YORK CIT HLTH DE; *NYPIRG, 1999, DIRT POW RIS NEW YOR; OMENN GS, 1991, MUTAT RES, V247, P283, DOI 10.1016/0027-5107(91)90023-H; Peat JK, 1987, CLIN ALLERGY, V17, P297; PEQUES M, COMMUNICATION; Perera FP, 2000, J NATL CANCER I, V92, P602, DOI 10.1093/jnci/92.8.602; Perera FP, 1998, AM J EPIDEMIOL, V147, P309; PERERA FP, 1982, J CHRON DIS, V35, P581, DOI 10.1016/0021-9681(82)90078-9; Perera FP, 1996, JNCI-J NATL CANCER I, V88, P496, DOI 10.1093/jnci/88.8.496; PERERA FP, 1987, J NATL CANCER I, V78, P887; Pirkle JL, 1996, JAMA-J AM MED ASSOC, V275, P1233; PLATTSMILLS TAE, 1992, J ALLERGY CLIN IMMUN, V89, P1046, DOI 10.1016/0091-6749(92)90228-T; PLATTSMILLS TAE, 1994, ANN ALLERGY, V72, P381; Plopper CG, 2000, ENVIRON HEALTH PERSP, V108, pA252, DOI 10.1289/ehp.108-a252; Rauh VA, 2001, AM J PUBLIC HEALTH, V91, P1815, DOI 10.2105/AJPH.91.11.1815; SARPONG SB, 1996, J ALLERGY CLIN IMMUN, V97, P1394; Perera F, 1993, MOL EPIDEMIOLOGY PRI; SHIMIZU Y, 1991, J RADIAT RES, V32, P54, DOI 10.1269/jrr.32.SUPPLEMENT2_54; SPORIK R, 1991, ARCH DIS CHILD, V66, P1050; SPORIK R, 1990, NEW ENGL J MED, V323, P505; SRIVASTAVA VK, 1986, J TOXICOL ENV HEALTH, V18, P459; Susser M, 1996, AM J PUBLIC HEALTH, V86, P674, DOI 10.2105/AJPH.86.5.674; *TEX NAT RES CONS, 2002, NAT AMB AIR QUAL STA; *US DEP HHS, 1982, SUMM HIST FIG FED RE; U. 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Environmental Protection Agency National Ambient Air Quality Standards (NAAQS)], 2002, NAT AMB AIR QUAL STA; U.S. Environmental Protection Agency, 1996, ENV HLTH THREATS CHI; VERBECK D, 1997, KEEPING TRACK NEW YO; Voigt RG, 1996, PEDIATR RES, V39, P1915; WAGENKNECHT LE, 1992, AM J PUBLIC HEALTH, V82, P33, DOI 10.2105/AJPH.82.1.33; WAGENKNECHT LE, 1993, ENVIRON RES, V63, P39, DOI 10.1006/enrs.1993.1124; Wang XB, 1997, ENVIRON HEALTH PERSP, V105, P514, DOI 10.1289/ehp.97105514; Weiss B, 2000, ENVIRON HEALTH PERSP, V108, P373; WHITMORE RW, 1994, ARCH ENVIRON CON TOX, V26, P47, DOI 10.1007/BF00212793; WHO, 1986, ENV HLTH CRIT, V59; WHYATT RM, 1995, ENVIRON HEALTH PERSP, V103, P105, DOI 10.2307/3432357; Whyatt RM, 2001, CANCER EPIDEM BIOMAR, V10, P581; Whyatt RM, 2001, ENVIRON HEALTH PERSP, V109, P417, DOI 10.2307/3454902; WHYATT RM, IN PRESS ENV HLTH PE; WISE PH, 1993, AM J PREV MED, V31, P7; ZAPATA BC, 1992, AM J PUBLIC HEALTH, V82, P685, DOI 10.2105/AJPH.82.5.685	91	99	100	3	14	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.	FEB	2002	110	2					197	204				8	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	526KR	WOS:000174130100031	11836150	
J	Ayuso, R; Lehrer, SB; Reese, G				Ayuso, R; Lehrer, SB; Reese, G			Identification of continuous, allergenic regions of the major shrimp allergen Pen a 1 (tropomyosin)	INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY			English	Article						tropomyosin; Pen a 1; invertebrate allergens; IgE-binding sequences	IGE-BINDING EPITOPES; MUSCLE PROTEIN TROPOMYOSIN; CROSS-REACTIVE ALLERGEN; MOLECULAR CHARACTERIZATION; MUTATIONAL ANALYSIS; AMERICAN COCKROACH; NITROCELLULOSE; CLONING; MITE; IMMUNOTHERAPY	Background: Crustaceans and mollusks are a frequent cause of allergic reactions. The only major allergen identified in shrimp is the muscle protein tropomyosin; at least 80% of shrimp-allergic subjects react to tropomyosin. Furthermore, tropomyosin is an important allergen in other crustaceans such as lobsters, crabs and mollusks, as well as other arthropods such as house dust mites and cockroaches, and has been implied as the cause of clinical cross-sensitivity among invertebrates. In contrast, vertebrate tropomyosins are considered nonallergenic. Objective: The basis of the allergenicity of proteins has not yet been resolved. Thus, tropomyosin molecules provide an excellent opportunity to study the relationship between protein structure and allergenicity. The aim of the current study was to identify the IgE-binding regions of Pen a 1 and compare these regions with homologous sequences in other allergenic and nonallergenic tropomyosins. Methods: Forty-six overlapping peptides (length: 15 amino acids; offset: 6 amino acids) spanning the entire Pen a 1 molecule were synthesized and tested for IgE antibody reactivity with sera from 18 shrimp-allergic subjects to identify the IgE-binding regions of shrimp tropomyosin. Results: Based on the frequency and intensity of the IgE reactivities, five major IgE-binding regions were identified. All five major IgE-binding regions were 15-38 amino acids long. The major IgE-binding regions identified were: region 1: Pen a 1 (43-57); region 2: Pen a 1 (85-105); region 3: Pen a 1 (133148); region 4: Pen a 1 (187-202), and region 5: Pen a 1 (247-284). In addition, 22 peptides were categorized as minor IgE-binding regions, and 12 peptides did not bind any IgE antibodies. No substantial differences in amino acid group composition in the five IgE-binding regions compared to the whole molecule were detected. Sequence identities and similarities of the Pen a 1 IgE-binding regions with homologous regions of allergenic arthropod tropomyosins were as high as 100%, whereas identities and similarities with homologous vertebrate sequences ranged from 36 to 76% and 53 to 85%, respectively. Conclusion: Five major IgE-binding regions of the allergenic shrimp tropomyosin, Pen a 1, were identified which are positioned at regular intervals of approximately 42 amino acids (7 heptads), suggesting a relationship with the repetitive coiled-coil structure of the tropomyosin molecule. The high degree of similarity between Pen a 1 IgE-binding regions and homologous sequences in invertebrate tropomyosins and the lower percentage of similarity with homologous regions of vertebrate tropomyosins supports a structural basis for cross-reactivity of allergenic tropomyosins. Copyright (C) 2002 S. Karger AG, Basel.	Tulane Univ, Sch Med SL57, New Orleans, LA 70112 USA	Lehrer, SB (reprint author), Tulane Univ, Sch Med SL57, 1700 Perdido St, New Orleans, LA 70112 USA.						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Arch. Allergy Immunol.	JAN	2002	127	1					27	37		10.1159/000048166		11	Allergy; Immunology	Allergy; Immunology	530LJ	WOS:000174358900006	11893851	
J	Wong, CM; Atkinson, RW; Anderson, HR; Hedley, AJ; Ma, S; Chau, PYK; Lam, TH				Wong, CM; Atkinson, RW; Anderson, HR; Hedley, AJ; Ma, S; Chau, PYK; Lam, TH			A tale of two cities: Effects of air pollution on hospital admissions in Hong Kong and London compared	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; cardiac and respiratory hospital admissions; daily time-series; Hong Kong; London	SHORT-TERM ASSOCIATIONS; MORTALITY; DISEASES; PHILADELPHIA; ASTHMA	The causal interpretation of reported associations between daily air pollution and daily admissions requires consideration of residual confounding, correlation between pollutants, and effect modification. If results obtained in Hong Kong and London-which differ in climate, lifestyle, and many other respects-were similar, a causal association would be supported. We used identical statistical methods for the analysis in each city. Associations between daily admissions and pollutant levels were estimated using Poisson regression. Nonparametric smoothing methods were used to model seasonality and the nonlinear dependence of admissions on temperature, humidity, and influenza admissions. For respiratory, admissions (greater than or equal to 65 years of age), significant positive associations were observed with particulate matter < 10 mum in aerodynamic diameter (PM10), nitrogen dioxide, sulfur dioxide, and ozone in both cities. These associations tended to be stronger at shorter lags in Hong Kong and at longer lap in London. Associations were stronger in the cool season in Hong Kong and in the warm season in London, periods during which levels of humidity are at their lowest in each city. For cardiac admissions (all ages) in both cities, significant positive associations were observed for PM10, NO2, and SO2 with similar lag patterns. Associations tended to be stronger in the cool season. The associations with NO2 and SO2 were the most robust in two-pollutant models. Patterns of association for pollutants with ischemic heart disease were similar in the two cities. The associations between O-3 and cardiac admissions were negative in London but positive in Hong Kong. We conclude that air pollution has remarkably similar associations with daily cardiorespiratory admissions in both cities, in spite of considerable differences between cities in social, lifestyle, and environmental factors. The results strengthen the argument that air pollution causes detrimental short-term health effects.	Univ Hong Kong, Dept Community Med, Hong Kong, Hong Kong, Peoples R China; Univ London St Georges Hosp, Sch Med, Dept Publ Hlth Sci, London SW17 0RE, England	Hedley, AJ (reprint author), Univ Hong Kong, Dept Community Med, Patrick Manson Bldg S Wing,7 Sassoon Rd, Hong Kong, Hong Kong, Peoples R China.		Hedley, Anthony/C-4305-2009; Wong, Chit Ming/C-4438-2009; Lam, Tai Hing/C-4317-2009; Hedley, Anthony/A-9113-2013				Akaike H, 1973, 2 INT S INF THEOR, P267, DOI DOI 10.1007/978-1-4612-1694-0_; Anderson HR, 1998, THORAX, V53, P842; Asher MI, 1998, EUR RESPIR J, V12, P315; Atkinson RW, 1999, ARCH ENVIRON HEALTH, V54, P398; Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; Bremner SA, 1999, OCCUP ENVIRON MED, V56, P237; Buckingham C., 1997, LONDON ATMOSPHERIC E; *CENS STAT DEP, 1998, HONG KONG ANN DIG ST; *CENS STAT DEP, 1998, 20 CENS STAT DEP; Cleveland RC, 1990, J OFF STAT, V6, P3; deLeon AP, 1996, J EPIDEMIOL COMMUN H, V50, pS63; *DEP HLTH, 1998, STAT SMOK ENGL 1976; *DEP HLTH, 1998, DEP HLTH ANN REP 199; *ENV PROT DEP, 1997, AIR QUAL HONG KONG 1; *ENV PROT DEP, 1996, AIR QUAL HONG KONG 1; *ENV PROT DEP, 1998, AIR QUAL HONG KONG 1; Hastie T, 1990, GEN ADDITIVE MODELS; JANUS ED, 1996, HONG KONG CARDIOVASC; Katsouyanni K, 1996, J EPIDEMIOL COMMUN H, V50, pS12, DOI 10.1136/jech.50.Suppl_1.S12; KATSOUYANNI K, COMMUNICATION; Kelsall JE, 1997, AM J EPIDEMIOL, V146, P750; LEUNG R, 1994, THORAX, V49, P1205, DOI 10.1136/thx.49.12.1205; Levy JI, 2000, ENVIRON HEALTH PERSP, V108, P109, DOI 10.2307/3454508; *OFF NAT STAT, 1996, MORT STAT ENGL WAL; *OFF NAT STAT, 1998, LIV BRIT RES 1996 GE; *OFF POP CENS SURV, 1992, SER DH5 OFF POP CENS, V19; *PLANN ENV LANDS B, CLEAN AIR HONG KONG; Pope III CAD, 1999, AIR POLLUTION HLTH, P673; Samet J, 1998, ENVIRON RES, V77, P9, DOI 10.1006/enrs.1997.3821; Samet J., 2000, 94 HLTH EFF I; SCHWARTZ JB, 1996, PDA J PHARM SCI TECH, V50, P1; Segi M., 1960, CANC MORTALITY SELEC; Spix C, 1998, ARCH ENVIRON HEALTH, V53, P54; STEDMAN JR, 2000, ATMOS ENVIRON, V35, P297; Thurston GD, 1999, AIR POLLUTION HLTH, P485, DOI 10.1016/B978-012352335-8/50097-1; World Health Organization, 1975, MAN INT STAT CLASS D; Wong CA, 1999, J EPIDEMIOL COMMUN H, V53, P580; Wong CM, 2001, ENVIRON HEALTH PERSP, V109, P335, DOI 10.2307/3454891; Wong TW, 1999, OCCUP ENVIRON MED, V56, P679; Wu Chengping, COMMUNICATION	40	99	111	5	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.	JAN	2002	110	1					67	77				11	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	521WH	WOS:000173864000028	11781167	
J	Maestrelli, P; Saetta, M; Mapp, CE; Fabbri, LM				Maestrelli, P; Saetta, M; Mapp, CE; Fabbri, LM			Remodeling in response to infection and injury - Airway inflammation and hypersecretion of mucus in smoking subjects with chronic obstructive pulmonary disease	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article; Proceedings Paper	16th Annual Transatlantic Airway Conference (TAC)	JAN, 2001	SAN FRANCISCO, CALIFORNIA			histology; sputum cytology; glands; goblet cells; biopsies	NEUTROPHIL CHEMOTACTIC FACTOR; T-CELL CLONES; CHRONIC-BRONCHITIS; PERIPHERAL AIRWAYS; FLOW LIMITATION; INDUCED SPUTUM; LYMPHOCYTES-T; UP-REGULATION; SMOKERS; ASTHMA	Airway epithelium represents the first line of defense against toxic inhalants. In some subjects, cigarette smoking causes airway inflammation, hypersecretion of mucus, and poorly reversible airflow limitation through mechanisms that are still largely unknown. Likewise, it is unclear why only some smokers develop chronic obstructive pulmonary disease (COPD). Two cell types consistently result in relation to chronic airflow limitation in COPD: neutrophils and CD8(+) cells. Neutrophils are compartmentalized in the mucosal surface of the airways and air spaces, that is, the epithelium and lumen, whereas CD8(+) cells exhibit a more extensive distribution along the subepithelial zone of the airways and lung parenchyma, including alveolar walls and arteries. This pattern of inflammatory cell distribution is observed in mild or moderate COPD, and in patients who have developed COPD, it is not modified by smoking cessation. The number of neutrophils further increases in the submucosa of patients with severe COPD, suggesting a role for these cells in the progression of the disease. Hypersecretion of mucus is a major manifestation in COPD. Mucus is produced by bronchial glands and goblet cells lining the airway epithelium. Unlike mucous gland enlargement, greater mucosal inflammation is associated with sputum production. Whereas neutrophil infiltration of submucosal glands occurs only in smokers with COPD, goblet cell hyperplasia in peripheral airways occurs both in smokers with or without COPD, suggesting that the major determinant of goblet cell hyperplasia is cigarette smoke itself.	Univ Padua, Resp Pathophysiol Unit, Dept Environm Med & Publ Hlth, I-35136 Padua, Italy; Univ Ferrara, I-44100 Ferrara, Italy; Univ Modena & Reggio Emilia, Modena, Italy	Maestrelli, P (reprint author), Univ Padua, Resp Pathophysiol Unit, Dept Environm Med & Publ Hlth, Via Giustiniani 2, I-35136 Padua, Italy.		Fabbri, Leonardo/I-4055-2012	Fabbri, Leonardo/0000-0001-8894-1689			AMADORI A, 1995, NAT MED, V1, P1279, DOI 10.1038/nm1295-1279; Balzano G, 1999, AM J RESP CRIT CARE, V160, P1486; BARNES PJ, 1991, AM REV RESPIR DIS, V144, P1187; CANNON MJ, 1988, J EXP MED, V168, P1163, DOI 10.1084/jem.168.3.1163; Chanez P, 1997, AM J RESP CRIT CARE, V155, P1529; COSIO M, 1978, NEW ENGL J MED, V298, P1277, DOI 10.1056/NEJM197806082982303; COYLE AJ, 1995, J EXP MED, V181, P1229, DOI 10.1084/jem.181.3.1229; DELPRETE GF, 1993, EUR J IMMUNOL, V23, P1445, DOI 10.1002/eji.1830230707; Di Stefano A, 1998, AM J RESP CRIT CARE, V158, P1277; DISTEFANO A, 1994, AM J RESP CRIT CARE, V149, P803; DiStefano A, 1996, AM J RESP CRIT CARE, V153, P629; Gibson PG, 1998, CLIN EXP ALLERGY, V28, P1081; HALE KA, 1984, AM REV RESPIR DIS, V130, P718; Keatings VM, 1997, AM J RESP CRIT CARE, V155, P449; Keatings VM, 1996, AM J RESP CRIT CARE, V153, P530; Lams BEA, 2000, EUR RESPIR J, V15, P512, DOI 10.1034/j.1399-3003.2000.15.14.x; Lucchini RE, 1997, AM J RESP CRIT CARE, V156, P1963; LUMSDEN AB, 1984, THORAX, V39, P844, DOI 10.1136/thx.39.11.844; Macklem PT, 1998, AM J RESP CRIT CARE, V157, pS181; MacNee W, 2000, CHEST, V117, p303S, DOI 10.1378/chest.117.5_suppl_1.303S-a; MAESTRELLI P, 1994, SCAND J WORK ENV HEA, V20, P376; MAESTRELLI P, 1988, IMMUNOLOGY, V64, P219; MAESTRELLI P, 1988, IMMUNOLOGY, V65, P605; Maestrelli P, 1996, AM J RESP CRIT CARE, V154, P1296; MAPP CE, 2000, AM J RESP CRIT CARE, V161, pA571; MULLEN JBM, 1985, BRIT MED J, V291, P1235; Nadel JA, 2000, CHEST, V117, p386S, DOI 10.1378/chest.117.5_suppl_2.386S; NAGAI A, 1985, AM REV RESPIR DIS, V132, P946; NIEWOEHNER DE, 1974, NEW ENGL J MED, V291, P755, DOI 10.1056/NEJM197410102911503; OShaughnessy TC, 1997, AM J RESP CRIT CARE, V155, P852; PETO R, 1983, AM REV RESPIR DIS, V128, P491; REID LM, 1954, LANCET, V1, P275; Rutgers SR, 2000, THORAX, V55, P12, DOI 10.1136/thorax.55.1.12; Saeta M, 1999, AM J RESP CRIT CARE, V160, P711; SAETTA M, 1993, AM REV RESPIR DIS, V147, P301; Saetta M, 1998, AM J RESP CRIT CARE, V157, P822; SAETTA M, 1994, AM J RESP CRIT CARE, V150, P1646; Saetta M, 1997, AM J RESP CRIT CARE, V156, P1633; Saetta M, 2000, AM J RESP CRIT CARE, V161, P1016; SALGAME P, 1991, SCIENCE, V254, P279, DOI 10.1126/science.1681588; Shim JJ, 2001, AM J PHYSIOL-LUNG C, V280, pL134; Stanescu D, 1996, THORAX, V51, P267, DOI 10.1136/thx.51.3.267; Takanashi S, 1999, EUR RESPIR J, V14, P309, DOI 10.1034/j.1399-3003.1999.14b12.x; Takeyama K, 2000, J IMMUNOL, V164, P1546; Takeyama K, 2001, AM J PHYSIOL-LUNG C, V280, pL165; THOMPSON AB, 1989, AM REV RESPIR DIS, V140, P1527; TURATO G, 1995, AM J RESP CRIT CARE, V152, P1262; Vestbo J, 1996, AM J RESP CRIT CARE, V153, P1530; Zheng T, 2000, J CLIN INVEST, V106, P1081, DOI 10.1172/JCI10458; Zhu J, 2001, AM J RESP CRIT CARE, V164, P109	50	99	101	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.	NOV 15	2001	164	10		S			S76	S80				5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	504AH	WOS:000172833700011	11734472	
J	Redington, AE; Meng, QH; Springall, DR; Evans, TJ; Creminon, C; Maclouf, J; Holgate, ST; Howarth, PH; Polak, JM				Redington, AE; Meng, QH; Springall, DR; Evans, TJ; Creminon, C; Maclouf, J; Holgate, ST; Howarth, PH; Polak, JM			Increased expression of inducible nitric oxide synthase and cyclo-oxygenase-2 in the airway epithelium of asthmatic subjects and regulation by corticosteroid treatment	THORAX			English	Article						asthma; corticosteroids; immunohistochemistry; in situ hybridisation; nitric oxide synthase; cyclo-oxygenase (COX)	HUMAN ENDOTHELIAL-CELLS; EXHALED AIR; HUMAN TISSUES; CYCLOOXYGENASE; CDNA; PROSTAGLANDIN-D2; LOCALIZATION; INHALATION; INDUCTION; CLONING	Background-Nitric oxide (NO) and prostanoids are mediators of vascular and bronchial tone that are postulated to be involved in asthma. increased levels of both are found in asthmatic subjects and are synthesised by enzymes that have cytokine inducible forms: inducible NO synthase (iNOS) and cyclo-oxygenase-2 (COX-2), respectively. We hypothesised that the in vivo expression of iNOS and COX-2 in the airways would be increased in asthma, and that these cytokine inducible enzymes may represent targets for regulation by corticosteroid treatment. Methods-Bronchial biopsy specimens were obtained from three groups of subjects: atopic asthmatics treated with p, agonists alone (n=7), atopic asthmatics additionally receiving regular treatment with corticosteroids (n=8), and nonasthmatic control subjects (n=10). Expression of iNOS and COX-2 mRNA and immunoreactive protein was studied using in situ hybridisation and quantitative immunohistochemistry. Results-Immunoreactivity and the hybridisation signal for iNOS and COX-2 were mainly localised in the airway epithelium. The proportion of epithelium immunostained was significantly greater in the non-steroid treated asthmatic subjects (iNOS 8.6 (1.8)%; COX-2 26.3 (4.6)%) than either the steroid treated asthmatics (iNOS 3.4 (1.0)%, p=0.009; COX-2 13.0 (0.6)%, p=0.0015) or the non-asthmatic controls (iNOS 4.2 (0.9)%, p=0.018; COX-2 11.6 (0.6)%, p=0.0003). Similarly, the hybridisation signal was stronger in the non-steroid treated group of asthmatic subjects than in the other two groups. Conclusions-These findings highlight the potential role of the airway epithelium both as a contributor to the inflammatory process in asthma and as a target for inhaled corticosteroid treatment in this disease.	Univ Southampton, Med Gen Hosp, Southampton SO16 6YD, Hants, England; Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Sch Med, Dept Histochem, London W12 0NN, England; Univ London Imperial Coll Sci Technol & Med, Sch Med, Dept Infect Dis, London SW7 2AZ, England; CEA Saclay, DRM, SPI, F-91191 Gif Sur Yvette, France; Hop Lariboisiere, INSERM U348, F-75475 Paris 10, France	Redington, AE (reprint author), Castle Hill Hosp, Acad Dept Med, Castle Rd, Cottingham HU16 5JQ, E Yorkshire, England.						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E., 1993, Regional Immunology, V5, P174; Redington AE, 1997, EUR RESPIR J, V10, P1026, DOI 10.1183/09031936.97.10051026; Redington AE, 1997, J ALLERGY CLIN IMMUN, V100, P544; Ricciardolo FLM, 1996, LANCET, V348, P374, DOI 10.1016/S0140-6736(96)04450-9; ROBBINS RA, 1994, BIOCHEM BIOPH RES CO, V203, P209, DOI 10.1006/bbrc.1994.2169; Saleh D, 1997, AM J RESP CRIT CARE, V155, P1763; SARIH M, 1993, BIOCHEM BIOPH RES CO, V191, P503, DOI 10.1006/bbrc.1993.1246; SHERMAN PA, 1993, BIOCHEMISTRY-US, V32, P11600, DOI 10.1021/bi00094a017; Sousa AR, 1997, THORAX, V52, P940; SPRINGALL DR, 1992, HISTOCHEMISTRY, V98, P259, DOI 10.1007/BF00271040; Taha R, 2000, AM J RESP CRIT CARE, V161, P636; Walenga RW, 1996, PROSTAGLANDINS, V52, P341, DOI 10.1016/S0090-6980(96)00101-3; Watkins DN, 1999, EUR RESPIR J, V13, P999, DOI 10.1034/j.1399-3003.1999.13e12.x; YATES DH, 1995, AM J RESP CRIT CARE, V152, P892; YOKOYAMA C, 1989, BIOCHEM BIOPH RES CO, V165, P888, DOI 10.1016/S0006-291X(89)80049-X	43	99	106	0	4	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	MAY	2001	56	5					351	357		10.1136/thorax.56.5.351		7	Respiratory System	Respiratory System	427LN	WOS:000168405800007	11312402	
J	Jacobs, EA; Joffe, A; Knight, JR; Kulig, J; Rogers, PD				Jacobs, EA; Joffe, A; Knight, JR; Kulig, J; Rogers, PD		Comm Substance Abuse	Tobacco's toll: Implications for the pediatrician	PEDIATRICS			English	Article							CIGARETTE-SMOKING; ADOLESCENTS; PREVENTION; DEPRESSION; ALCOHOL; YOUTH; RISK	The disease of tobacco addiction, which is pervasive in the United States, begins in childhood and adolescence. Twenty-five percent of the population regularly uses tobacco, despite evidence that such use is the leading preventable cause of death in the United States. Tobacco use reportedly kills 2.5 times as many people each year as alcohol and drug abuse combined. According to 1998 data from the World Health Organization, there were 1.1 billion smokers worldwide and 10 000 tobacco-related deaths per day. Furthermore, in the United States, 43% of children aged 2 to 11 years are exposed to environmental tobacco smoke, which has been implicated in sudden infant death syndrome, low birth weight, asthma, middle ear disease, pneumonia, cough, and upper respiratory infection. Pediatricians play a crucial role in reducing both tobacco use (by children, adolescents, and their parents) and exposure to tobacco smoke and should rank this among their highest health prevention priorities.	Amer Acad Pediat, Comm Subst Abuse, Elk Grove Village, IL 60007 USA	Jacobs, EA (reprint author), Amer Acad Pediat, Comm Subst Abuse, Elk Grove Village, IL 60007 USA.						American Psychiatric Association, 1994, DIAGN STAT MAN MENT; AMMERMAN SD, 1998, CONT PEDIAT, V15, P64; Belcher HME, 1998, ARCH PEDIAT ADOL MED, V152, P952; Bobo JK, 1998, ADDICTION, V93, P877, DOI 10.1046/j.1360-0443.1998.9368779.x; Brown RA, 1996, J AM ACAD CHILD PSY, V35, P1602, DOI 10.1097/00004583-199612000-00011; Recommendations to prevent and control iron deficiency in the United States, 1998, MMWR-MORBID MORTAL W, V47, P1; Centers for Disease Control and Prevention, 1998, MMWR-MORBID MORTAL W, V47, P229; Centers for Disease Control and Prevention, 1994, MMWR-MORBID MORTAL W, V43, P1; Cronk CE, 1997, AM J PUBLIC HEALTH, V87, P760, DOI 10.2105/AJPH.87.5.760; ELDERS MJ, 1994, AM J PUBLIC HEALTH, V84, P543, DOI 10.2105/AJPH.84.4.543; EPPS RP, 1993, NIH PUBL; Fiore MC, 2000, JAMA-J AM MED ASSOC, V283, P3244; FIORE MC, 2000, AHRQ PUBL; GIOVINO GA, 1995, EPIDEMIOL REV, V17, P48; Gold DR, 1996, NEW ENGL J MED, V335, P931, DOI 10.1056/NEJM199609263351304; HEYMAN R, 1997, ADOLESCENT HLTH UPDA, V9, P1; Heyman RB, 1998, PEDIATRICS, V101, P125; Hughes JR, 1999, JAMA-J AM MED ASSOC, V281, P72, DOI 10.1001/jama.281.1.72; Jackson C, 1997, AM J PUBLIC HEALTH, V87, P359, DOI 10.2105/AJPH.87.3.359; Jessor R., 1978, LONGITUDINAL RES DRU, P41; JOHNSTON LD, 2000, NIH PUBL; KINNEY H, 1998, J NEUROPATHOL EXP NE, V57, P1018; Klein JD, 1995, PEDIATR ANN, V24, P646; LYNCH BS, 1994, GROWING UP TOBACCO F, P71; Lynch B. S., 1994, GROWING UP TOBACCO F, P29; MILLBERGER S, 1997, J AM ACAD CHILD ADOL, V36, P37; Moskowitz WB, 1999, ARCH PEDIAT ADOL MED, V153, P446; MYERS MG, 1994, PEDIATRICS, V93, P561; National Institute on Drug Abuse, 1998, NIH PUBL; Patton GC, 1998, AM J PUBLIC HEALTH, V88, P1518, DOI 10.2105/AJPH.88.10.1518; Pomerleau O F, 1995, J Subst Abuse, V7, P373, DOI 10.1016/0899-3289(95)90030-6; PROCHASKA JO, 1983, J CONSULT CLIN PSYCH, V51, P390, DOI 10.1037/0022-006X.51.3.390; Rubes J, 1998, FERTIL STERIL, V70, P715, DOI 10.1016/S0015-0282(98)00261-1; SANDLER DP, 1985, AM J PUBLIC HEALTH, V75, P487, DOI 10.2105/AJPH.75.5.487; Smith TA, 1996, PEDIATRICS, V98, P659; *TOB CONTR SEC CA, 1997, CIG US CAL 1990 1996; Tomar SL, 1998, AM J PUBLIC HEALTH, V88, P20, DOI 10.2105/AJPH.88.1.20; *US DEPT HHS, 1998, TOB US AM US RAC ETH	38	99	99	1	3	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	APR	2001	107	4					794	798				5	Pediatrics	Pediatrics	422KC	WOS:000168116200053		
J	Dales, RE; Cakmak, S; Burnett, RT; Judek, S; Coates, F; Brook, JR				Dales, RE; Cakmak, S; Burnett, RT; Judek, S; Coates, F; Brook, JR			Influence of ambient fungal spores on emergency visits for asthma to a regional children's hospital	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							AIR-POLLUTION; RESPIRATORY-DISEASES; CANADIAN CITIES; ROOM VISITS; PARTICULATE; ASSOCIATION; ALTERNARIA; POLLEN; OZONE	The impact of ambient aeroallergens on morbidity from childhood asthma is largely unknown. To address this issue, we studied the association between daily emergency department visits for asthma to a childrens' hospital, and daily concentrations of both pollen grains and fungal spores during a 5-yr period between 1993 and 1997. Air pollution and meteorological data accounted for in the analyses included ozone, nitrogen dioxide, sulfur dioxide, sulfates, temperature, barometric pressure, and relative humidity. The daily number of asthma visits ranged from 0 to 36 per day with an average of 7.5. Fungal spores, but not pollen grains, were associated with visits (p < 0.05). The percentage increase associated with each group, independent of the others, was 1.9% (SE 0.9) for deuteromycetes, 4.1% (1.6) for basidiomycetes, 2.8% (1.0) for ascomycetes, and 8.8% for these spores combined. In summary, fungal spores account for a significant proportion of the asthma exacerbations in children that prompt an emergency department visit.	Univ Ottawa, Ottawa, ON K1H 8L6, Canada; Ottawa Gen Hosp, Ottawa, ON K1H 8L6, Canada; Hlth Canada, Ottawa, ON K1A 0L2, Canada; Aerobiol Res Labs, Ottawa, ON, Canada; Environm Canada, Atomospher Environm Serv, Toronto, ON M3H 5T4, Canada	Dales, RE (reprint author), Univ Ottawa, Gen Campus,501 Smyth Rd, Ottawa, ON K1H 8L6, Canada.			Cakmak, Sabit/0000-0001-9921-2107			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; CLEVELAND WS, 1979, J AM STAT ASSOC, V74, P829, DOI 10.2307/2286407; CLEVELAND WS, 1988, J AM STAT ASSOC, V83, P596, DOI 10.2307/2289282; Delfino RJ, 1996, AM J RESP CRIT CARE, V154, P633; Delfino RJ, 1997, AM J RESP CRIT CARE, V155, P568; Epton MJ, 1997, THORAX, V52, P528; Halonen M, 1997, AM J RESP CRIT CARE, V155, P1356; Hastie T, 1990, GEN ADDITIVE MODELS; JOHNSTON SL, 1995, BRIT MED J, V310, P1225; LI DW, 1995, MYCOLOGIA, V87, P190, DOI 10.2307/3760904; LICORISH K, 1985, J ALLERGY CLIN IMMUN, V76, P819, DOI 10.1016/0091-6749(85)90755-9; LOPEZ M, 1989, J ALLERGY CLIN IMMUN, V84, P246; Neas LM, 1996, AM J EPIDEMIOL, V143, P797; Perzanowski MS, 1998, J ALLERGY CLIN IMMUN, V101, P626; PLATTSMILLS T, 1999, ASTHMA LINK ENV IMMU; REED CE, 1985, J ALLERGY CLIN IMMUN, V76, P773, DOI 10.1016/0091-6749(85)90746-8; SALVAGGIO J, 1971, J ALLERGY CLIN IMMUN, V48, P96, DOI 10.1016/0091-6749(71)90091-1; SALVAGGIO J, 1981, J ALLERGY CLIN IMMUN, V68, P327, DOI 10.1016/0091-6749(81)90131-7; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; *STAT SCI INC, 1993, S PLUS US MAN; TARGONSKI PV, 1995, J ALLERGY CLIN IMMUN, V95, P955, DOI 10.1016/S0091-6749(95)70095-1; von Mutius E, 2000, J ALLERGY CLIN IMMUN, V105, P9, DOI 10.1016/S0091-6749(00)90171-4	25	99	102	1	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.	DEC	2000	162	6					2087	2090				4	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	381ZV	WOS:000165794700021	11112119	
J	Langdeau, JB; Turcotte, H; Bowie, DM; Jobin, J; Desgagne, P; Boulet, LP				Langdeau, JB; Turcotte, H; Bowie, DM; Jobin, J; Desgagne, P; Boulet, LP			Airway hyperresponsiveness in elite athletes	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							INDOOR SWIMMING POOLS; EXERCISE-INDUCED BRONCHOSPASM; CROSS-COUNTRY SKIERS; ICE HOCKEY PLAYERS; BRONCHIAL RESPONSIVENESS; HIGH PREVALENCE; FIGURE SKATERS; INDUCED ASTHMA; EXPOSURE; RISK	It has been suggested that high-level training could contribute to the development of airway hyperresponsiveness (AHR), but the comparative effects of different sports on airway function remains to be determined. We evaluated 150 nonsmoking volunteers 18 to 55 yr of age; 100 athletes divided into four subgroups of 25 subjects each according to the predominant estimated hydrocaloric characteristic of ambient air inhaled during training: dry air (DA), cold air (CA), humid air (HA) and a mixture of dry and humid air (MA), and 50 sedentary subjects. Each subject had a respiratory questionnaire, a methacholine challenge, allergy skin-prick tests, and heart rate variability recording for evaluation of parasympathetic tone. The athletes had a 49% prevalence of AHR (PC20 < 16 mg/ml), with a mean PC20 of 16.9 mg/ml, compared with 28% (PC20: 35.4) in sedentary subjects (p = 0.009). The prevalence (%) of AHR and mean PC,, (mg/ml) varied as followed in the four subgroups of athletes: DA: 32% and 30.9; CA: 52% and 15.8; HA: 76% and 7.3; and MA: 32% and 21.5 (p = 0.002). The estimated parasympathetic tone was higher in athletes (p < 0.001), but this parameter showed only a weak correlation with PC20 (r = -0.17, p = 0.04). This study has shown a significantly higher prevalence of AHR in athletes than in the control group because of the higher prevalence in the CA and HA groups. Parasympathetic activity may act as modulator of airway responsiveness, but the increased prevalence of AHR in our athlete population may be related to the type and possibly the content of inhaled air during training.	Univ Laval, Ctr Rech, Hop Laval, Inst Cardiol & Pneumol, St Foy, PQ G1V 4G5, Canada	Boulet, LP (reprint author), Univ Laval, Ctr Rech, Hop Laval, Inst Cardiol & Pneumol, 2725 Chemin St Foy, St Foy, PQ G1V 4G5, Canada.						Aggazzotti G, 1998, SCI TOTAL ENVIRON, V217, P155, DOI 10.1016/S0048-9697(98)00174-0; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; BARNES PJ, 1982, CLIN SCI, V62, P349; BRUDNO DS, 1994, ANN ALLERGY, V73, P227; Camm AJ, 1996, CIRCULATION, V93, P1043; CAMUS G, 1994, INTENS CARE MED, V20, P602, DOI 10.1007/BF01705731; DEMEERSMAN RE, 1992, EUR J APPL PHYSIOL O, V64, P434; GOLDSMITH RL, 1992, J AM COLL CARDIOL, V20, P552; HEDBERG K, 1989, JAMA-J AM MED ASSOC, V262, P3014; Helenius IJ, 1998, J ALLERGY CLIN IMMUN, V101, P646; Helenius IJ, 1997, THORAX, V52, P157; HERY M, 1995, ANN OCCUP HYG, V39, P427, DOI 10.1016/0003-4878(95)00013-5; Juniper EF, 1991, HISTAMINE METHACHOLI; KALLENBACH JM, 1985, CHEST, V87, P644, DOI 10.1378/chest.87.5.644; LARSSON K, 1993, BRIT MED J, V307, P1326; Leuppi JD, 1998, EUR RESPIR J, V12, P13, DOI 10.1183/09031936.98.12010013; LEVESQUE B, 1994, ENVIRON HEALTH PERSP, V102, P1082, DOI 10.2307/3431996; MALO JL, 1983, AM REV RESPIR DIS, V128, P8; MANFREDA J, 1996, AM J RESP CRIT CARE, V153, pA432; Mannix ET, 1996, CHEST, V109, P312, DOI 10.1378/chest.109.2.312; Massin N, 1998, OCCUP ENVIRON MED, V55, P258; NIEMAN DC, 1995, THORAX, V50, P1229, DOI 10.1136/thx.50.12.1229; Pennanen AS, 1997, J AIR WASTE MANAGE, V47, P1079, DOI 10.1080/10473289.1997.10464405; POMERANZ B, 1985, AM J PHYSIOL, V248, pH151; Potts J, 1996, SPORTS MED, V21, P256, DOI 10.2165/00007256-199621040-00002; Pribyl CR, 1996, CLIN J SPORT MED, V6, P232, DOI 10.1097/00042752-199610000-00005; ProvostCraig MA, 1996, J ASTHMA, V33, P67, DOI 10.3109/02770909609077764; RUPP NT, 1993, ANN ALLERGY, V70, P339; Sandsund M, 1997, ANN NY ACAD SCI, V813, P751, DOI 10.1111/j.1749-6632.1997.tb51778.x; SHEPHARD RJ, 1994, SPORTS MED, V18, P340, DOI 10.2165/00007256-199418050-00006; Shi X, 1995, MED SCI SPORTS EXERC, V10, P1406; SMITH ML, 1989, MED SCI SPORTS EXERC, V21, P4; STAND V, 1997, AM J RESP CRIT CARE, V155, P881; Sue-Chu M, 1998, AM J RESP CRIT CARE, V158, P597; ZWICK H, 1990, LUNG, V168, P111	35	99	102	0	6	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.	MAY	2000	161	5					1479	1484				6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	312LU	WOS:000086945400016	10806142	
J	Christodoulopoulos, P; Cameron, L; Durham, S; Hamid, Q				Christodoulopoulos, P; Cameron, L; Durham, S; Hamid, Q			Molecular pathology of allergic disease - II: Upper airway disease	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						allergic rhinitis; chronic sinusitis; inflammation; cytokines; chemokines	COLONY-STIMULATING FACTOR; MESSENGER-RNA EXPRESSION; MAJOR BASIC-PROTEIN; ENDOTHELIAL ADHESION MOLECULES; CHRONIC HYPERPLASTIC SINUSITIS; GRASS-POLLEN IMMUNOTHERAPY; NITRIC-OXIDE SYNTHASE; PHASE NASAL RESPONSES; NECROSIS-FACTOR-ALPHA; FC-EPSILON-RI	Allergic upper airway diseases such as allergic rhinitis and chronic sinusitis are an increasing problem. Although the pathogenesis remains elusive, an individual's genetic predisposition as well as exposure to the allergen are currently considered factors in their development. Clinical symptoms of sneezing, rhinorrhea, and congestion are primarily a consequence of granulocyte release of chemical mediators such as histamine, prostanoids, and leukotrienes as well as the infiltration of inflammatory cells, Observations subsequent to allergen provocation are comparable to natural exposure and as such much of our understanding of allergic responses is derived from this model, A prominence of CD4(+) T cells and eosinophils, synthesis and release of T(H)2 cytokines, and the coordinate expression of chemokines and adhesion molecules are all characteristic of the allergic response observed in rhinitis and sinusitis. Corticosteroids and immunotherapy target these inflammatory processes and have been observed to successfully reduce and shift the predominantly T(H)2 environment toward T(H)1 cytokine expression. As our understanding of the pathophysiologic features of allergic upper airway disease improves, as well as the relationship between their development and that of lower airway disease, new strategies of diagnosis and treatment will allow for more effective modulation of the allergic process and associated morbidity.	McGill Univ, Meakins Christie Labs, Montreal, PQ H2X 2P2, Canada; Royal Brompton Hosp, Natl Heart & Lung Inst, London SW3 6LY, England	Hamid, Q (reprint author), McGill Univ, Meakins Christie Labs, 3626 St Urbain St, Montreal, PQ H2X 2P2, Canada.						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Allergy Clin. Immunol.	FEB	2000	105	2	1				211	223		10.1016/S0091-6749(00)90068-X		13	Allergy; Immunology	Allergy; Immunology	285RQ	WOS:000085402200003	10669839	
J	Cortessis, VK; Thomas, DC; Levine, AJ; Breton, CV; Mack, TM; Siegmund, KD; Haile, RW; Laird, PW				Cortessis, Victoria K.; Thomas, Duncan C.; Levine, A. Joan; Breton, Carrie V.; Mack, Thomas M.; Siegmund, Kimberly D.; Haile, Robert W.; Laird, Peter W.			Environmental epigenetics: prospects for studying epigenetic mediation of exposure-response relationships	HUMAN GENETICS			English	Review							MONOZYGOTIC TWINS DISCORDANT; DNA METHYLATION PATTERNS; DIETHYLSTILBESTROL IN-UTERO; DIETARY-PROTEIN RESTRICTION; EPIGENOME-WIDE ASSOCIATION; GENE-EXPRESSION PROFILES; SQUAMOUS-CELL CARCINOMA; COLORECTAL-CANCER RISK; CPG ISLAND METHYLATION; IFN-GAMMA PROMOTER	Changes in epigenetic marks such as DNA methylation and histone acetylation are associated with a broad range of disease traits, including cancer, asthma, metabolic disorders, and various reproductive conditions. It seems plausible that changes in epigenetic state may be induced by environmental exposures such as malnutrition, tobacco smoke, air pollutants, metals, organic chemicals, other sources of oxidative stress, and the microbiome, particularly if the exposure occurs during key periods of development. Thus, epigenetic changes could represent an important pathway by which environmental factors influence disease risks, both within individuals and across generations. We discuss some of the challenges in studying epigenetic mediation of pathogenesis and describe some unique opportunities for exploring these phenomena.	[Cortessis, Victoria K.; Thomas, Duncan C.; Levine, A. Joan; Mack, Thomas M.; Haile, Robert W.] Univ So Calif, Dept Prevent Med, Keck Sch Med, USC Norris Comprehens Canc Ctr, Los Angeles, CA 90089 USA; [Laird, Peter W.] Univ So Calif, Dept Surg, Keck Sch Med, USC Norris Comprehens Canc Ctr,Epigenome Ctr, Los Angeles, CA 90089 USA; [Laird, Peter W.] Univ So Calif, Dept Biochem & Mol Biol, Keck Sch Med, USC Norris Comprehens Canc Ctr,Epigenome Ctr, Los Angeles, CA 90089 USA	Thomas, DC (reprint author), Univ So Calif, Dept Prevent Med, Keck Sch Med, USC Norris Comprehens Canc Ctr, 2001 N Soto St,SSB 202F, Los Angeles, CA 90089 USA.	dthomas@usc.edu	Laird, Peter/G-8683-2012		NIH [R21 ES020794, P30 ES 07048, P30 CA014089]; Whittier Foundation	Supported in part by NIH grants R21 ES020794, P30 ES 07048, P30 CA014089 and a Whittier Foundation grant to the Norris Comprehensive Cancer Center.	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Genet.	OCT	2012	131	10			SI		1565	1589		10.1007/s00439-012-1189-8		25	Genetics & Heredity	Genetics & Heredity	998OH	WOS:000308249300005	22740325	
J	Roy, S; Byrne, J; Pickering, C				Roy, Sudipto; Byrne, Jason; Pickering, Catherine			A systematic quantitative review of urban tree benefits, costs, and assessment methods across cities in different climatic zones	URBAN FORESTRY & URBAN GREENING			English	Review						Cities; Ecosystem services; Ecosystem disservices; Land use policy; Trees	VALUING ECOSYSTEM SERVICES; STREET TREE; CARBON STORAGE; FOREST STRUCTURE; SHADE TREES; DECISION-MAKING; GREEN SPACE; AIR-QUALITY; POLLUTION MITIGATION; UNITED-STATES	Urban trees can potentially mitigate environmental degradation accompanying rapid urbanisation via a range of tree benefits and services. But uncertainty exists about the extent of tree benefits and services because urban trees also impose costs (e.g. asthma) and may create hazards (e.g. windthrow). Few researchers have systematically assessed how urban tree benefits and costs vary across different cities, geographic scales and climates. This paper provides a quantitative review of 115 original urban tree studies, examining: (i) research locations, (ii) research methods, and (iii) assessment techniques for tree services and disservices. Researchers published findings in 33 journals from diverse disciplines including: forestry, land use planning, ecology, and economics. Research has been geographically concentrated (64% of studies were conducted in North America). Nearly all studies (91.3%) used quantitative research, and most studies (60%) employed natural science methods. Demonstrated tree benefits include: economic, social, health, visual and aesthetic benefits; identified ecosystem services include: carbon sequestration, air quality improvement, storm water attenuation, and energy conservation. Disservices include: maintenance costs, light attenuation, infrastructure damage and health problems, among others. Additional research is required to better inform public policy, including comparative assessment of tree services and disservices, and assessment of urban residents and land managers' understanding of tree benefits and costs. (c) 2012 Elsevier GmbH. All rights reserved.	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Urban Green.		2012	11	4					351	363		10.1016/j.ufug.2012.06.006		13	Plant Sciences; Environmental Studies; Forestry; Urban Studies	Plant Sciences; Environmental Sciences & Ecology; Forestry; Urban Studies	062LY	WOS:000312922500001		
J	Mealing, NM; Banks, E; Jorm, LR; Steel, DG; Clements, MS; Rogers, KD				Mealing, Nicole M.; Banks, Emily; Jorm, Louisa R.; Steel, David G.; Clements, Mark S.; Rogers, Kris D.			Investigation of relative risk estimates from studies of the same population with contrasting response rates and designs	BMC MEDICAL RESEARCH METHODOLOGY			English	Article							SURVEY NONRESPONSE; PSYCHOLOGICAL DISTRESS; COHORT PROFILE; FOLLOW-UP; BIAS; HEALTH; SCORES	Background: There is little empirical evidence regarding the generalisability of relative risk estimates from studies which have relatively low response rates or are of limited representativeness. The aim of this study was to investigate variation in exposure-outcome relationships in studies of the same population with different response rates and designs by comparing estimates from the 45 and Up Study, a population-based cohort study (self-administered postal questionnaire, response rate 18%), and the New South Wales Population Health Survey (PHS) (computer-assisted telephone interview, response rate similar to 60%). Methods: Logistic regression analysis of questionnaire data from 45 and Up Study participants (n = 101,812) and 2006/2007 PHS participants (n = 14,796) was used to calculate prevalence estimates and odds ratios (ORs) for comparable variables, adjusting for age, sex and remoteness. ORs were compared using Wald tests modelling each study separately, with and without sampling weights. Results: Prevalence of some outcomes (smoking, private health insurance, diabetes, hypertension, asthma) varied between the two studies. For highly comparable questionnaire items, exposure-outcome relationship patterns were almost identical between the studies and ORs for eight of the ten relationships examined did not differ significantly. For questionnaire items that were only moderately comparable, the nature of the observed relationships did not differ materially between the two studies, although many ORs differed significantly. Conclusions: These findings show that for a broad range of risk factors, two studies of the same population with varying response rate, sampling frame and mode of questionnaire administration yielded consistent estimates of exposure-outcome relationships. However, ORs varied between the studies where they did not use identical questionnaire items.	[Mealing, Nicole M.; Banks, Emily; Jorm, Louisa R.; Rogers, Kris D.] Sax Inst, Broadway, NSW 2007, Australia; [Mealing, Nicole M.; Jorm, Louisa R.; Clements, Mark S.] Univ Western Sydney, Sch Med, Penrith, NSW 1797, Australia; [Banks, Emily] Australian Natl Univ, Natl Ctr Epidemiol & Populat Hlth, Canberra, ACT 0200, Australia; [Steel, David G.] Univ Wollongong, Ctr Stat & Survey Methodol, N Wollongong, NSW 2522, Australia	Mealing, NM (reprint author), Sax Inst, POB 123, Broadway, NSW 2007, Australia.	Nicole.Mealing@saxinstitute.org.au		Steel, David/0000-0002-3137-9952	National Health and Medical Research Council [402810]	The authors are grateful to Ms Margo Barr and Mrs Sandra Carlson for their expert assistance and advice on the NSW Population Health Survey and use of the NSW Population Health Survey data. We thank the men and women participating in the 45 and Up Study, and the NSW Department of Health for permitting use of the 2006 and 2007 NSW Population Health Survey Datasets. The 45 and Up Study is run by The Sax Institute in collaboration with the Cancer Council of New South Wales; the New South Wales Division of the National Heart Foundation of Australia; the New South Wales Department of Health; beyondblue: the national depression initiative and the New South Wales Department of Ageing, Disability and Home Care. This work was also supported by the National Health and Medical Research Council [402810]. NM was employed by the NSW Department of Health on the NSW Biostatistical Officer Training Program at the time this work was conducted.	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J	Horak, F; Zieglmayer, P; Zieglmayer, R; Lemell, P; Devillier, P; Montagut, A; Melac, M; Galvain, S; Jean-Alphonse, S; Van Overtvelt, L; Moingeon, P; Le Gall, M				Horak, Friedrich; Zieglmayer, Petra; Zieglmayer, Rene; Lemell, Patrick; Devillier, Philippe; Montagut, Armelle; Melac, Michel; Galvain, Sylvie; Jean-Alphonse, Stephanie; Van Overtvelt, Laurence; Moingeon, Philippe; Le Gall, Martine			Early onset of action of a 5-grass-pollen 300-IR sublingual immunotherapy tablet evaluated in an allergen challenge chamber	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Grass pollen; tablets; sublingual immunotherapy; allergen challenge chamber; Vienna Challenge Chamber	GRASS-POLLEN; RHINITIS; EXPOSURE; EFFICACY; PLACEBO; SYMPTOMS; RHINOCONJUNCTIVITIS; SAFETY; FLOW	Background: The efficacy and safety of a 5-grass-pollen sublingual immunotherapy (SLIT) tablet (Stallergenes SA, Antony, France) have been evaluated in clinical studies during the pollen season. The allergen challenge chamber (ACC) has been developed as a pharmacodynamic assessment tool to control the environmental allergens and to avoid all problems associated with unpredictable pollen seasons. Objective: We sought to evaluate the onset of action and efficacy of 300-IR (index of reactivity) SLIT tablets by using an ACC. Methods: Patients with grass pollen-induced rhinoconjunctivitis were randomized into the active or placebo groups. A standardized allergen challenge with grass pollen and symptom evaluation every 15 minutes was performed at baseline, 1 week, and 1, 2, and 4 months of treatment. The primary end point was the average rhinoconjunctivitis total symptom score (ARTSS). Allergen-specific basophil activation, T-cell proliferation, and plasmatic IgE and IgG responses were assessed before and after treatment. Results: In the intention-to-treat population (n = 89) a significant treatment effect was achieved after the first month (P = .0042) and second month (P = .0203) and was maintained through to the fourth month (P = .0007). In the active group the ARTSS (means +/- SDs) decreased at each challenge: week 1, 7.40 +/- 2.682; month 1, 5.89 +/- 2.431; month 2, 5.09 +/- 2.088; and month 4, 4.85 +/- 1.999. An improvement (vs placebo) of 29.3% for the mean ARTSS ( median, 33.3%) was observed at end point. Furthermore, the induction of grass pollen allergen specific IgGs was associated with clinical response. The most frequent adverse reactions were local: oral pruritus, ear pruritus, and throat irritation. Conclusions: In this ACC study the 300-IR 5-grass-pollen SLIT tablets had a significant effect on rhinoconjunctivitis symptoms (vs placebo) from the first month of treatment onward. (J Allergy Clin Immunol 2009;124:471-7.)	[Horak, Friedrich] Med Univ Vienna, ENT Dept, Vienna, Austria; [Zieglmayer, Petra; Zieglmayer, Rene; Lemell, Patrick] Allergy Ctr Vienna W, Dept Vienna Challenge Chamber, Vienna, Austria; [Devillier, Philippe] Univ Versailles St Quentin, Foch Hosp, UPRES EA 220, Suresnes, France; [Montagut, Armelle] Delta Consultants, Meylan, France; [Melac, Michel; Galvain, Sylvie; Jean-Alphonse, Stephanie; Van Overtvelt, Laurence; Moingeon, Philippe; Le Gall, Martine] Stallergenes SA, Antony, France	Horak, F (reprint author), AKH, Univ Klin, Wahringer Gurtel 18-20, A-1090 Vienna, Austria.	friedrich.horak@vienna.at			GlaxoSmithKline; Oxagen; Allergy Therapeutics; Altana-Nycomed; Boehringer-Ingelheim; Schering-Plough; Pierre Fabre; Servier; Novartis	F. Horak has received honoraria for lectures from Allergy Therapeutics, UCB, Schering-Plough, and Stallergenes and has received research support from GlaxoSmithKline, Oxagen, and Allergy Therapeutics. P. Devillier has received consulting fees from Stallergenes and has received research grants from Altana-Nycomed, Boehringer-Ingelheim, Schering-Plough, Pierre Fabre, Servier, and Novartis. The rest of the authors have declared that they have no conflict of interest.	ALVAREZCUESTA E, 2006, ALLERGY S82, V61, pS1; Dahl R, 2006, J ALLERGY CLIN IMMUN, V118, P434, DOI 10.1016/j.jaci.2006.05.003; Day J. H., 2006, Clinical and Experimental Allergy Reviews, V6, P31, DOI 10.1111/j.1365-2222.2005.00099.x; Didier A, 2009, ALLERGY, V64, P166, DOI 10.1111/j.1398-9995.2008.01767.x; Didier A, 2007, J ALLERGY CLIN IMMUN, V120, P1338, DOI 10.1016/j.jaci.2007.07.046; Donovan JP, 1996, ANN ALLERG ASTHMA IM, V77, P74; DOYLE WJ, 1995, ANN ALLERG ASTHMA IM, V74, P171; Durham SR, 2006, J ALLERGY CLIN IMMUN, V117, P802, DOI 10.1016/j.jaci.2005.12.1358; European Medicines Agency. 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Allergy Clin. Immunol.	SEP	2009	124	3					471	U126		10.1016/j.jaci.2009.06.006		8	Allergy; Immunology	Allergy; Immunology	552TG	WOS:000274315900011	19647862	
J	Kim, JL; Elfman, L; Mi, Y; Wieslander, G; Smedje, G; Norback, D				Kim, J. L.; Elfman, L.; Mi, Y.; Wieslander, G.; Smedje, G.; Norback, D.			Indoor molds, bacteria, microbial volatile organic compounds and plasticizers in schools - associations with asthma and respiratory symptoms in pupils	INDOOR AIR			English	Article						asthma; microbial volatile organic compounds (MVOCs); plasticizer; pupil; respiratory symptoms; school	BUILDING-DAMPNESS; AIR-QUALITY; YOUNG-CHILDREN; RISK-FACTORS; EXPOSURE; ENVIRONMENT; SCHOOLCHILDREN; HEALTH; FORMALDEHYDE; METABOLITES	We investigated asthma and atopy in relation to microbial and plasticizer exposure. Pupils in eight primary schools in Uppsala (Sweden) answered a questionnaire, 1014 (68%) participated. Totally, 7.7% reported doctor-diagnosed asthma, 5.9% current asthma, and 12.2% allergy to pollen/pets. Wheeze was reported by 7.8%, 4.5% reported daytime breathlessness, and 2.0% nocturnal breathlessness. Measurements were performed in 23 classrooms (May-June), 74% had < 1000 ppm CO2 indoors. None had visible mold growth or dampness. Mean total microbial volatile organic compound (MVOC) concentration was 423 ng/m(3) indoors and 123 ng/m(3) outdoors. Indoor concentration of TMPD-MIB (2,2,4-trimethyl-1,3-pentanediol monoisobutyrate, Texanol) and TMPD-DIB (2,2,4-trimethyl-1,3-pentanediol diisobutyrate, TXIB), two common plasticizers, were 0.89 and 1.64 mu g/m(3), respectively. MVOC and plasticizer concentration were correlated (r = 0.5; P < 0.01). Mold concentration was 360 cfu/m(3) indoors and 980 cfu/m(3) outdoors. At higher indoor concentrations of total MVOC, nocturnal breathlessness (P < 0.01) and doctor-diagnosed asthma (P < 0.05) were more common. Moreover, there were positive associations between nocturnal breathlessness and 3-methylfuran (P < 0.01), 3-methyl-1-butanol (P < 0.05), dimethyldisulfide (P < 0.01), 2-heptanone (P < 0.01), 1-octen-3-ol (P < 0.05), 3-octanone (P < 0.05), TMPD-MIB (P < 0.05), and TMPD-DIB (P < 0.01). TMPD-DIB was positively associated with wheeze (P < 0.05), daytime breathlessness (P < 0.05), doctor-diagnosed asthma (P < 0.05), and current asthma (P < 0.05). In conclusion, exposure to MVOC and plasticizers at school may be a risk factor for asthmatic symptoms in children.	Uppsala Univ, Dept Med Sci Occupat & Environm Med, Uppsala, Sweden; Univ Hosp, Uppsala, Sweden	Kim, JL (reprint author), Uppsala Univ, Dept Med Sci Occupat & Environm Med, Uppsala, Sweden.	jeong-lim.kim@medsci.uu.se		Norback, Dan/0000-0002-5174-6668			ANDERSSON K, 1981, SCAND J WORK ENV HEA, V7, P282; Anundi H, 1992, P 41 NORD M WORK ENV, P227; 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; Braun-Fahrlander Charlotte, 2003, Curr Opin Allergy Clin Immunol, V3, P325, DOI 10.1097/00130832-200310000-00001; Cain WS, 2005, INDOOR AIR, V15, P445, DOI 10.1111/j.1600-0668.2005.00390.x; Claeson AS, 2002, J ENVIRON MONITOR, V4, P667, DOI 10.1039/b202571j; Daisey JM, 2003, INDOOR AIR, V13, P53, DOI 10.1034/j.1600-0668.2003.00153.x; DOUWES J, 2004, J ALLERGY CLIN IMMUN, V115, P1325; Dsikowitzky L, 2004, CHEMOSPHERE, V57, P1289, DOI 10.1016/j.chemosphere.2004.08.053; Elke K, 1999, J ENVIRON MONITOR, V1, P445, DOI 10.1039/a903034d; Fischer G, 2003, ARCH MICROBIOL, V179, P75, DOI 10.1007/s00203-002-0495-2; Forsberg B, 1997, INT J EPIDEMIOL, V26, P610, DOI 10.1093/ije/26.3.610; Fox A, 2003, J ENVIRON MONITOR, V5, P246, DOI 10.1039/b212341j; Garrett MH, 1998, CLIN EXP ALLERGY, V28, P459; Holt PG, 1999, ALLERGY, V54, P12, DOI 10.1111/j.1398-9995.1999.tb04382.x; Jaakkola JJK, 2000, AM J PUBLIC HEALTH, V90, P797, DOI 10.2105/AJPH.90.5.797; Kamijima M, 2002, J OCCUP HEALTH, V44, P186, DOI 10.1539/joh.44.186; Kim JL, 2005, INDOOR AIR, V15, P170, DOI 10.1111/j.1600-0668.2005.00334.x; Korpi A, 1999, ARCH ENVIRON HEALTH, V54, P347; KOSTIAINEN R, 1995, ATMOS ENVIRON, V29, P693, DOI 10.1016/1352-2310(94)00309-9; Lee SC, 2000, CHEMOSPHERE, V41, P109, DOI 10.1016/S0045-6535(99)00396-3; Martinez FD, 1999, LANCET S2, V354, pSII12; Meklin T, 2005, INDOOR AIR, V15, P40, DOI 10.1111/j.1600-0668.2005.00357.x; Meyer HW, 2004, INDOOR AIR, V14, P65, DOI 10.1046/j.1600-0668.2003.00213.x; Mommers M, 2005, INT J HYG ENVIR HEAL, V208, P373, DOI 10.1016/j.ijheh.2005.04.007; MORGAN WJ, 1992, PEDIATR CLIN N AM, V39, P1185; Muniz G. 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J	Wichmann, HE				Wichmann, H.-E.			Diesel exhaust particles	INHALATION TOXICOLOGY			English	Article; Proceedings Paper	10th International Inhalation Symposium	MAY 31-JUN 03, 2006	Hannover, GERMANY	German Soc Toxicol, Fraunhofer Inst Toxicol & Expt Med, Natl Hlth & Environm Effects Res Lab, US EPA			LUNG-CANCER; AIR-POLLUTION; EXPOSURE	Diesel motor emission is a complex mixture of hundreds of constituents in either gas or particle form. Diesel particulate matter (DPM) is composed of a center core of elemental carbon and adsorbed organic compounds including PAHs and nitro-PAHs, and small amounts of sulfate, nitrate, metals, and other trace elements. DPM consists of fine particles including a high number of ultrafine particles. These particles are highly respirable and have a large surface area where organics can adsorb easily. Exposure to DPM can cause acute irritation and neurophysiological, respiratory, and asthma-like symptoms and can exacerbate allergenic responses to known allergens. Consistently, lung cancer risk is elevated among workers in occupations where diesel engines have been used. However, quantification of the cancer risk with respect to DPM concentrations is not possible. Furthermore, ambient fine and ultrafine particles, of which DPM is an important component, contribute to cardiopulmonary morbidity and mortality and lung cancer. In conclusion, diesel exhaust poses a cancer risk greater than that of any other air pollutant, as well as causing other short- and long-term health problems. One effective way to effectively reduce emission of DPM is the use of particle traps.	GSF, Inst Epidemiol, D-85764 Neuherberg, Germany	Wichmann, HE (reprint author), GSF, Inst Epidemiol, Ingolstaedter Landstr 1, D-85764 Neuherberg, Germany.	wichmann@gsf.de					*AM LUNG ASS, 2003, CLOS DIES DIV PROT P; Bhatia R, 1998, EPIDEMIOLOGY, V9, P84, DOI 10.1097/00001648-199801000-00017; Bruske-Hohlfeld I, 1999, AM J IND MED, V36, P405, DOI 10.1002/(SICI)1097-0274(199910)36:4<405::AID-AJIM1>3.0.CO;2-W; Cohen AJ, 2000, ENVIRON HEALTH PERSP, V108, P743, DOI 10.2307/3454411; Garshick E, 2004, ENVIRON HEALTH PERSP, V112, P1539; HEI, 1999, DIES EM LUNG CANC EP; Heinrich Joachim, 2004, Curr Opin Allergy Clin Immunol, V4, P341, DOI 10.1097/00130832-200410000-00003; Lipsett M, 1999, AM J PUBLIC HEALTH, V89, P1009, DOI 10.2105/AJPH.89.7.1009; Pope CA, 2002, JAMA-J AM MED ASSOC, V287, P1132, DOI 10.1001/jama.287.9.1132; Riedl M, 2005, J ALLERGY CLIN IMMUN, V115, P221, DOI 10.1016/j.jaci.2004.11.047; Wichmann H-E, 2004, UMWELTMED FORSCH PRA, V9, P85	11	98	105	0	19	TAYLOR & FRANCIS INC	PHILADELPHIA	325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA	0895-8378			INHAL TOXICOL	Inhal. Toxicol.		2007	19			1			241	244		10.1080/08958370701498075		4	Toxicology	Toxicology	210CM	WOS:000249434300031	17886072	
J	Flinterman, AE; Knulst, AC; Meijer, Y; Bruijnzeel-Koomen, CAFM; Pasmans, SGMA				Flinterman, AE; Knulst, AC; Meijer, Y; Bruijnzeel-Koomen, CAFM; Pasmans, SGMA			Acute allergic reactions in children with AEDS after prolonged cow's milk elimination diets	ALLERGY			English	Article						allergic reactions; atopic dermatitis; cow's milk; elimination; tolerance	ATOPIC-DERMATITIS; FOOD ALLERGY; DOUBLE-BLIND; ANAPHYLACTIC SHOCK; HYPERSENSITIVITY; CHALLENGES; IGE; DESENSITIZATION; INFANTS	Background: Food allergy is not always correctly diagnosed in children with atopic eczema dermatitis syndrome (AEDS) and treatment with an avoidance diet is not without danger. Methods: After admission to our clinic, 11 children with a prolonged cow's milk (CM) elimination diet because of AEDS and sensitization underwent double-blind placebo-controlled food challenge (DBPCFC). Retrospectively, the exposure to CM, sensitization and reactions to accidental ingestion were carefully documented. The DBPCFC was used to evaluate the childrens' current status. Results: Before the elimination period (median 2.3 years; started before the admission) all 11 children with AEDS were sensitized and had ingested CM (four bottle-fed; seven breast-fed without CM diet of the mother) without the development of acute reactions. The diagnosis of CM allergy was not confirmed by DBPCFC previously. After elimination the AEDS had not improved, but nevertheless the diet was continued. During the elimination period, eight of 11 children developed severe acute allergic reactions to CM after accidental ingestion. In evaluation, in our clinic all 11 children experienced acute allergic reactions to CM during DBPCFC. Conclusion: There is a considerable chance of developing acute allergic reactions to CM after elimination in children with AEDS without previous problems after CM intake.	Univ Med Ctr Utrecht, Dept Dermatol Allergol, NL-3508 GA Utrecht, Netherlands; Univ Med Ctr Utrecht, Dept Pediat, NL-3508 GA Utrecht, Netherlands	Pasmans, SGMA (reprint author), Univ Med Ctr Utrecht, Dept Dermatol Allergol, G-02-124,POB 85500, NL-3508 GA Utrecht, Netherlands.						Bahna SL, 2002, ANN ALLERG ASTHMA IM, V89, P56; Barbi E, 2004, ALLERGY, V59, P668, DOI 10.1111/j.1398-9995.2004.00398.x; Bauer A, 1999, ALLERGY, V54, P894, DOI 10.1034/j.1398-9995.1999.00228.x; Bindslev-Jensen C, 2004, ALLERGY, V59, P690, DOI 10.1111/j.1398-9995.2004.00466.x; BJORKSTEN B, 1983, ALLERGY, V38, P119, DOI 10.1111/j.1398-9995.1983.tb01595.x; BRUIJNZEELKOOMEN C, 1995, ALLERGY, V50, P623, DOI 10.1111/j.1398-9995.1995.tb02579.x; Burks AW, 1998, J PEDIATR-US, V132, P132, DOI 10.1016/S0022-3476(98)70498-6; Christie L, 2002, J AM DIET ASSOC, V102, P1648, DOI 10.1016/S0002-8223(02)90351-2; DAVID TJ, 1984, ARCH DIS CHILD, V59, P983; Eigenmann PA, 1998, PEDIATRICS, V101, DOI 10.1542/peds.101.3.e8; HANIFIN JM, 1984, J ALLERGY CLIN IMMUN, V73, P211, DOI 10.1016/S0091-6749(84)80008-1; Heine RG, 2002, CURR OPIN ALLERGY CL, V2, P217, DOI 10.1097/00130832-200206000-00011; Jarvinen KM, 2001, CLIN EXP ALLERGY, V31, P978, DOI 10.1046/j.1365-2222.2001.01151.x; LARRAMENDI CH, 1992, ALLERGY, V47, P490, DOI 10.1111/j.1398-9995.1992.tb00670.x; LIFSCHITZ CH, 1988, J PEDIATR GASTR NUTR, V7, P141, DOI 10.1097/00005176-198801000-00026; MARTIN EM, 1988, ALLERG IMMUNOL PARIS, V20, P55; Meglio P, 2004, ALLERGY, V59, P980, DOI 10.1111/j.1398-9995.2004.00542.x; MORISSET M, 2004, 9 INT S IMM CHEM CLI; Novembre E, 2001, ALLERGY, V56, P105, DOI 10.1034/j.1398-9995.2001.00931.x; Osterballe M, 2003, J ALLERGY CLIN IMMUN, V112, P196, DOI 10.1067/mai.2003.1603; Patriarca G, 2003, ALIMENT PHARM THERAP, V17, P459, DOI 10.1046/j.0269-2813.2003.01468.x; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; Rolinck-Werninghaus C, 2005, ALLERGY, V60, P1320, DOI 10.1111/j.1398-9995.2005.00882.x; Sampson HA, 2003, CLIN DERMATOL, V21, P183, DOI 10.1016/S0738-081X(02)00363-2; SAMPSON HA, 1984, J ALLERGY CLIN IMMUN, V74, P26, DOI 10.1016/0091-6749(84)90083-6; Schade R P, 2002, Ned Tijdschr Geneeskd, V146, P1739; Seidenari S, 2003, ALLERGY, V58, P495, DOI 10.1034/j.1398-9995.2003.00153.x; Sicherer SH, 2002, CURR OPIN ALLERGY CL, V2, P207, DOI 10.1097/00130832-200206000-00009; Sicherer SH, 2000, J ALLERGY CLIN IMMUN, V105, P582, DOI 10.1067/mai.2000.104941	29	98	101	1	2	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0105-4538			ALLERGY	Allergy	MAR	2006	61	3					370	374		10.1111/j.1398-9995.2006.01018.x		5	Allergy; Immunology	Allergy; Immunology	005VX	WOS:000234853900016	16436148	
J	Clark, S; Long, AA; Gaeta, TJ; Camargo, CA				Clark, S; Long, AA; Gaeta, TJ; Camargo, CA			Multicenter study of emergency department visits for insect sting allergies	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						insect sting allergy; emergency department; epinephrine; referral to allergist	UNITED-STATES; ANAPHYLAXIS; EPIDEMIOLOGY; HYPERSENSITIVITY; HYMENOPTERA; MANAGEMENT; SENSITIVITY; POPULATION; SEVERITY; DISEASE	Background: An earlier study of food-related anaphylaxis in the emergency department (ED) suggested low concordance with national guidelines for anaphylaxis management. Objective: To extend these findings, we performed a chart review study to describe current ED management of insect sting allergy. Methods: The Multicenter Airway Research Collaboration performed a chart review study in 15 North American EDs. Investigators reviewed 617 charts of patients with insect sting allergy. Patients were identified by using International Classification of Diseases, 9th Revision, codes 989.5 (toxic effect of venom), 995.0 (other anaphylactic shock), and 995.3 (allergy, unspecified). Results: The cohort was 42% female and 61% white, with a mean age of 36 +/- 19 years. In this cohort, 58% had local reactions, 11% had mild systemic reactions, and 31% had anaphylactic reactions, as defined by multisystem organ involvement or hypotension. Among patients with systemic reactions (mild or anaphylaxis), most (75%) were stung within 6 hours of ED arrival. While in the ED, 69% of systemic reaction patients received antihistamines, 50% systemic corticosteroids, and 12% epinephrine. Almost all systemic reaction patients (95%) were discharged to home. At ED discharge, 27% (95% CI, 22% to 33%) of systemic reaction patients received a prescription for self-injectable epinephrine. Only 20% (95% CI, 15% to 26%) had documentation of referral to an allergist. Conclusions: Although guidelines suggest specific approaches for the emergency management of insect sting allergy, concordance with these guidelines appears low in patients with a severe insect sting reaction.	Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA; Massachusetts Gen Hosp, Dept Rheumatol Allergy & Immunol, Boston, MA 02114 USA; New York Methodist Hosp, Dept Emergency Med, Brooklyn, NY USA; Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02138 USA	Clark, S (reprint author), Massachusetts Gen Hosp, Dept Emergency Med, 326 Cambridge St,Suite 410, Boston, MA 02114 USA.	sclark3@partners.org			NIAID NIH HHS [AI52338]; NIEHS NIH HHS [T32 ES07069]		Bohlke K, 2004, J ALLERGY CLIN IMMUN, V113, P536, DOI 10.1016/j.jaci.2003.11.033; Brown AFT, 2001, J ALLERGY CLIN IMMUN, V108, P861, DOI 10.1067/mai.2001.119028; BROWN H, 1970, ARCH INTERN MED, V125, P665, DOI 10.1001/archinte.125.4.665; Brown SGA, 2004, J ALLERGY CLIN IMMUN, V114, P371, DOI 10.1016/j.jaci.2004.04.029; *CACI, 2000, SOURC ZIP COD DEM; Clark S, 2004, J ALLERGY CLIN IMMUN, V113, P347, DOI 10.1016/j.jaci.2003.10.053; GAETA TJ, 2001, ACAD EMERG MED, V8, P449; Golden DBK, 2003, J ALLERGY CLIN IMMUN, V112, P495, DOI 10.1067/mai.2003.1606; GOLDEN DBK, 1989, JAMA-J AM MED ASSOC, V262, P240, DOI 10.1001/jama.262.2.240; HERBERT FA, 1982, ANN ALLERGY, V48, P12; *HLTH CAN, 1996, FED CAUS DAT STAT CA; Hosmer DW, 1989, APPL LOGISTIC REGRES; Jerrard DA, 1996, AM J EMERG MED, V14, P429, DOI 10.1016/S0735-6757(96)90067-4; KLEIN JS, 1995, J ALLERGY CLIN IMMUN, V95, P637, DOI 10.1016/S0091-6749(95)70329-2; Lieberman P, 2005, J ALLERGY CLIN IMMUN, V115, pS483, DOI 10.1016/j.jaci.2005.01.010; Matasar MJ, 2003, CURR ALLERGY ASTHM R, V3, P30, DOI 10.1007/s11882-003-0007-8; McDougle Leon, 1995, Journal of Emergency Medicine, V13, P9, DOI 10.1016/0736-4679(94)00105-7; Moffitt JE, 2004, J ALLERGY CLIN IMMUN, V114, P869, DOI 10.1016/j.jaci.2004.07.046; Neugut AI, 2001, ARCH INTERN MED, V161, P15, DOI 10.1001/archinte.161.1.15; O'Brien J, 2000, EMERG MED PRACT, V2, P1; Peng MM, 2004, ARCH INTERN MED, V164, P317, DOI 10.1001/archinte.164.3.317; Sampson HA, 2005, J ALLERGY CLIN IMMUN, V115, P584, DOI [10.1016/j.jaci.2005.01.008, 10.1016/j.jaci.2005.01.009]; SCHWARTZ HJ, 1995, ALLERGY PROC, V16, P247, DOI 10.2500/108854195778702639; SETTIPANE GA, 1970, ACTA ALLERGOL, V25, P286, DOI 10.1111/j.1398-9995.1970.tb01264.x; SETTIPANE GA, 1972, J ALLERGY CLIN IMMUN, V50, P146, DOI 10.1016/0091-6749(72)90045-0; Sicherer SH, 2004, J ALLERGY CLIN IMMUN, V114, P118, DOI 10.1016/j.jaci.2004.03.056; *STATA, 1985, STATA REF MAN; Stewart AG, 1996, QJM-MON J ASSOC PHYS, V89, P859; Valentine M D, 1992, JAMA, V268, P2830; YOCUM MW, 1996, MED PRACTICING PHYS	30	98	100	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.	SEP	2005	116	3					643	649		10.1016/j.jaci.2005.06.026		7	Allergy; Immunology	Allergy; Immunology	017IE	WOS:000235686500027	16159637	
J	Gueders, MM; Balbin, M; Rocks, N; Foidart, JM; Gosset, P; Louis, R; Shapiro, S; Lopez-Otin, C; Noel, W; Cataldo, DD				Gueders, MM; Balbin, M; Rocks, N; Foidart, JM; Gosset, P; Louis, R; Shapiro, S; Lopez-Otin, C; Noel, W; Cataldo, DD			Matrix metalloproteinase-8 deficiency promotes granulocytic allergen-induced airway inflammation	JOURNAL OF IMMUNOLOGY			English	Article							HUMAN NEUTROPHIL COLLAGENASE; BRONCHOALVEOLAR LAVAGE FLUID; ASTHMATIC-PATIENTS; MMP-8 EXPRESSION; TISSUE INHIBITOR; EPITHELIAL-CELLS; MATRIX-METALLOPROTEINASE-9; DISEASE; CANCER; HYPERRESPONSIVENESS	Matrix metalloproteinases (MMPs) are involved in inflammatory reaction, including asthma-related airway inflammation. MMP-8, mainly produced by neutrophils, has recently been reported to be increased in the bronchoalveolar lavage fluid (BALF) from asthmatic patients. To evaluate the role of MMP-8 in asthma, we measured MMP-8 expression in lung tissue in an OVAsensitized mouse model of asthma and addressed the effect of MMP-8 deletion on allergen-induced bronchial inflammation. MMP-8 production was increased in lungs from C57BL/6 mice exposed to allergens. After allergen exposure, MMP-8-1-mice developed an airway inflammation characterized by an increased neutrophilic inflammation in BALF and an increased neutrophilic and eosinophilic infiltration in the airway walls. MMP-8 deficiency was associated with increased levels of IL-4 and antiOVA IgE and IgG1 in BALF and serum, respectively. Although allergen exposure induced an enhancement of LPS-induced CXC chemokine, KC, and MIP-2 levels in BALF and lung parenchyma, no difference was observed between the two genotypes. Inflammatory cell apoptosis was reduced in the lungs from MMP-8(-/-) mice. For the first time, our study evidences an important role of MMP-8 in the control of neutrophilic and eosinophilic infiltration during allergen-induced lung inflammation, and demonstrates that the anti-inflammatory effect of MMP-8 is partly due to a regulation of inflammatory cell apoptosis.	Univ Liege, Dept Pneumol, B-4000 Liege, Belgium; Univ Liege, Dept Biol Tumors & Dev, Ctr Biomed Integrat Genoprot, B-4000 Liege, Belgium; Univ Oviedo, Inst Univ Oncol, Dept Bioquim & Biol Mol, Oviedo, Spain; INSERM, Unite 416, Inst Pasteur, F-59045 Lille, France; Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Pulm Med, Boston, MA 02115 USA	Univ Liege, Dept Pneumol, Tower Pathol B23, B-4000 Liege, Belgium.	Didier.Cataldo@ulg.ac.be	Balbin, Milagros/I-4206-2015; Lopez-Otin, Carlos/C-6657-2013	Lopez-Otin, Carlos/0000-0001-6964-1904; Noel, Agnes/0000-0002-7670-6179; Cataldo, Didier/0000-0002-3079-7941			Abraham B, 2003, EUR RESPIR J, V22, P470, DOI 10.1183/09031936.03.00261903; Anticevich SZ, 1996, CLIN EXP ALLERGY, V26, P549, DOI 10.1046/j.1365-2222.1996.d01-341.x; Balbin M, 2003, NAT GENET, V35, P252, DOI 10.1038/ng1249; Betsuyaku T, 1999, AM J RESP CRIT CARE, V159, P1985; BOUSQUET J, 1992, ALLERGY, V47, P3, DOI 10.1111/j.1398-9995.1992.tb02242.x; Brinckerhoff CE, 2002, NAT REV MOL CELL BIO, V3, P207, DOI 10.1038/nrm763; Cataldo D, 2001, ALLERGY, V56, P145, DOI 10.1034/j.1398-9995.2001.056002145.x; Cataldo D, 2000, INT ARCH ALLERGY IMM, V123, P259, DOI 10.1159/000024452; Cataldo DD, 2004, LAB INVEST, V84, P418, DOI 10.1038/labinvest.3700063; Cataldo DD, 2002, AM J PATHOL, V161, P491, DOI 10.1016/S0002-9440(10)64205-8; Cataldo DD, 2002, CHEST, V122, P1553, DOI 10.1378/chest.122.5.1553; Corry DB, 2002, NAT IMMUNOL, V3, P347, DOI 10.1038/ni773; Ding Y, 1996, J DENT RES, V75, P1986; Egeblad M, 2002, NAT REV CANCER, V2, P161, DOI 10.1038/nrc745; Fukuda T, 1996, AM J RESP CELL MOL, V14, P84; Girard D, 1997, BIOCHEM J, V325, P147; Gounni AS, 2001, FASEB J, V15, P940, DOI 10.1096/fj.00-0378com; HASTY KA, 1987, J BIOL CHEM, V262, P10048; HASTY KA, 1986, J BIOL CHEM, V261, P5645; Henderson WR, 2002, AM J RESP CRIT CARE, V165, P108; Holmbeck K, 1999, CELL, V99, P81, DOI 10.1016/S0092-8674(00)80064-1; Johnson S, 1999, AM J PHYSIOL-LUNG C, V277, pL1109; Lamblin C, 1998, AM J RESP CRIT CARE, V157, P394; Mautino G, 1997, AM J RESP CELL MOL, V17, P583; McMillan SJ, 2004, J IMMUNOL, V172, P2586; Meyer-Hoffert U, 2003, INT ARCH ALLERGY IMM, V131, P264, DOI 10.1159/000072138; MICHAELIS J, 1990, BIOCHEM J, V270, P809; Montel V, 2004, CANCER RES, V64, P1687, DOI 10.1158/0008-5472.CAN-03-2047; MURPHY G, 1977, BIOCHEM J, V162, P195; [Anonymous], 2000, J CELL BIOL; Overall CM, 2002, NAT REV CANCER, V2, P657, DOI 10.1038/nrc884; Owen CA, 2004, J IMMUNOL, V172, P7791; PAGGIARO PL, 1993, J INVEST ALLERG CLIN, V3, P237; Prikk K, 2002, LAB INVEST, V82, P1535, DOI 10.1097/01.LAB.0000035023.53893.B6; Prikk K, 2001, J PATHOL, V194, P232, DOI 10.1002/path.849; ROCHE WR, 1989, LANCET, V1, P520; SEPPER R, 1995, CHEST, V107, P1641, DOI 10.1378/chest.107.6.1641; Van den Steen PE, 2003, EUR J BIOCHEM, V270, P3739, DOI 10.1046/j.1432-1033.2003.03760.x; WEISS SJ, 1989, NEW ENGL J MED, V320, P365; [Anonymous], 2004, MATRIX METALLOPROTEI; Zucker S, 2003, CURR TOP DEV BIOL, V54, P1, DOI 10.1016/S0070-2153(03)54004-2	41	98	99	0	2	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767	1550-6606		J IMMUNOL	J. Immunol.	AUG 15	2005	175	4					2589	2597				9	Immunology	Immunology	966HJ	WOS:000232010400070	16081833	
J	Currie, J; Neidell, M				Currie, J; Neidell, M			Air pollution and infant health: What can we learn from California's recent experience?	QUARTERLY JOURNAL OF ECONOMICS			English	Article							LOW-BIRTH-WEIGHT; UTAH VALLEY; SOUTHERN CALIFORNIA; CHILDHOOD ASTHMA; PM(10) POLLUTION; CHILDREN BORN; MORTALITY; AMBIENT; EXPOSURE; QUALITY	We examine the impact of air pollution on infant death in California over the 1990s. Our work offers several innovations: first, most previous studies examine populations subject to far greater levels of pollution. Second, many studies examine a single pollutant in isolation. We examine three "criteria" pollutants in a common framework. Third, we use rich individual-level data and pollution measured at the weekly level. Our most novel finding is a significant effect of CO on infant mortality: we find that reductions in carbon monoxide over the 1990s saved approximately 1000 infant lives in California.	Univ Calif Los Angeles, Los Angeles, CA 90024 USA; Natl Bur Econ Res, Cambridge, MA 02138 USA; Columbia Univ, New York, NY 10027 USA	Currie, J (reprint author), Univ Calif Los Angeles, Los Angeles, CA 90024 USA.						ALLISON PD, 1982, SOCIOL METHODOL, V12, P61; ALMOND D, 2002, COST LOW BIRTH WEIGH; Chay K., 2003, 10053 NBER; Chay KY, 2003, Q J ECON, V118, P1121, DOI 10.1162/00335530360698513; COFFEY B, 2003, REEXAMINATION AIR PO; Currie J, 1996, J POLIT ECON, V104, P1263, DOI 10.1086/262059; CURRIE J, 2004, 10251 NBER; *ENV DEF, 1993, 400F92005 EPA OFF MO; *ENV DEF, 2003, PRES CLEAR SKIES IN; *ENV DEF, 2003, 2 PROSP AN PLAN MAY; *ENV DEF, 2002, NAT AMB AIR QUAL STA; *ENV DEF, 2003, CRIT POLL; Friedman MS, 2001, JAMA-J AM MED ASSOC, V285, P897, DOI 10.1001/jama.285.7.897; Greenstone M, 2002, J POLIT ECON, V110, P1175, DOI 10.1086/342808; HUEL G, 1993, J EXPO ANAL ENV EPID, V3, P187; IMBENS G, 1992, ECONOMETRICA, V150, P1187; LOGAN W P D, 1953, Lancet, V1, P336; LUBIN J, 1984, BIOMETRICS, V90, P63; LUI SL, 2003, ENVIRON HEALTH PERSP, V111, P1773; Maisonet M, 2001, ENVIRON HEALTH PERSP, V109, P351, DOI 10.2307/3434782; MANSKI CF, 1977, ECONOMETRICA, V45, P1977, DOI 10.2307/1914121; MANTEL N, 1973, BIOMETRICS, V29, P479, DOI 10.2307/2529171; NEIDELL M, 2005, 25 CISES; NEIDELL M, 2005, 24 CICES; Neidell MJ, 2004, J HEALTH ECON, V23, P1209, DOI 10.1016/j.jhealeco.2004.05.002; POPE CA, 1992, ARCH ENVIRON HEALTH, V47, P211; POPE CA, 1989, AM J PUBLIC HEALTH, V79, P623, DOI 10.2105/AJPH.79.5.623; PRENTICE RL, 1978, BIOMETRIKA, V65, P153, DOI 10.2307/2335290; RANSOM MR, 1992, ENVIRON RES, V58, P204, DOI 10.1016/S0013-9351(05)80216-6; Ritz B, 2000, EPIDEMIOLOGY, V11, P502, DOI 10.1097/00001648-200009000-00004; Ritz B, 1999, ENVIRON HEALTH PERSP, V107, P17, DOI 10.2307/3434285; SAMET J, 1997, ENV RES A, V127, P9; Schwartz J, 2000, AM J EPIDEMIOL, V151, P440; SEATON A, 1995, LANCET, V345, P176, DOI 10.1016/S0140-6736(95)90173-6; SEIGER H, 2000, 7744 NBER; Spengler JD, 2000, INDOOR AIR QUALITY H; STAFFORD RT, 2001, UPHILL DRIVE; VISCUSI WK, 1993, J ECON LIT, V31, P1912; Wilson WE, 2000, J AIR WASTE MANAGE, V50, P1167	39	98	99	4	23	M I T PRESS	CAMBRIDGE	238 MAIN STREET, STE 500, CAMBRIDGE, MA 02142-1046 USA	0033-5533			Q J ECON	Q. J. Econ.	AUG	2005	120	3					1003	1030		10.1093/qje/120.3.1003		28	Economics	Business & Economics	969HF	WOS:000232224500006		
J	Rook, GAW; Adams, V; Hunt, J; Palmer, R; Martinelli, R; Brunet, LR				Rook, GAW; Adams, V; Hunt, J; Palmer, R; Martinelli, R; Brunet, LR			Mycobacteria and other environmental organisms as immunomodulators for immunoregulatory disorders	SPRINGER SEMINARS IN IMMUNOPATHOLOGY			English	Review						regulatory T cell; allergies; regulatory antigen-presenting cell; innate immunity; autoimmunity	REGULATORY T-CELLS; MONOCLONAL-ANTIBODY TREATMENT; INFLAMMATORY-BOWEL-DISEASE; TOLL-LIKE RECEPTORS; IN-VIVO; MULTIPLE-SCLEROSIS; INTERFERON-GAMMA; ALLERGIC-ASTHMA; DENDRITIC CELLS; AIRWAY HYPERREACTIVITY	In the rich, developed parts of the world there has been a steady and simultaneous increase in at least three groups of disease: (1) allergies, (2) inflammatory bowel diseases (IBD; e.g. Crohn's disease and ulcerative colitis) and (3) autoimmunity (e.g. type 1 diabetes and multiple sclerosis). Because the medical world is so compartmentalised it was some time before the connection between these increases was noticed and understood. There is now evidence that the simultaneous increase in these diseases of immunodysregulation is at least partly attributable to malfunction of regulatory T cells (Treg). This paper provides an overview of relevant work in each of these fields of medicine (though with emphasis on the allergic disorders), and concludes that the increasing failure of Treg is a consequence of diminished exposure to certain micro-organisms that are "old friends", because of their continuous presence throughout mammalian evolution. These organisms, which include saprophytic mycobacteria, helminths and lactobacilli, are recognised by the innate immune system as harmless, and as adjuvants for Treg induction. Polymorphisms of components of the innate immune system such as TLR2 and NOD2 appear to define subsets of the population that will develop immunoregulatory disorders when living in the modern environment. A further role of the "old friends" and of the Treg that they induce might be to maintain the levels of regulatory IL-10 secreting macrophages and antigen-presenting cells, which are depleted in asthma and Crohn's disease. These concepts are leading to novel therapies based on harmless organisms or their components. Phase I/II clinical trials have yielded some statistically significant results, and phase II trials are in progress.	UCL Royal Free & Univ Coll, Windeyer Inst Med Sci, Sch Med, Dept Med Microbiol, London W1P 6DB, England	Rook, GAW (reprint author), UCL Royal Free & Univ Coll, Windeyer Inst Med Sci, Sch Med, Dept Med Microbiol, 46 Cleveland St, London W1P 6DB, England.	g.rook@ucl.ac.uk		Martinelli, Roberta/0000-0003-0784-5973; Rook, Graham/0000-0002-8041-8110			Akdis CA, 2001, INT ARCH ALLERGY IMM, V124, P180, DOI 10.1159/000053704; Alm JS, 2002, GENES IMMUN, V3, P71, DOI 10.1038/sj/gene/6363834; Ancuta P, 2000, EUR J IMMUNOL, V30, P1872, DOI 10.1002/1521-4141(200007)30:7<1872::AID-IMMU1872>3.0.CO;2-2; Arbour NC, 2000, NAT GENET, V25, P187; Arkwright PD, 2001, J ALLERGY CLIN IMMUN, V107, P531, DOI 10.1067/mai.20001.113081; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; Barclay AN, 2002, TRENDS IMMUNOL, V23, P285, DOI 10.1016/S1471-4906(02)02223-8; Bashir MEH, 2002, J IMMUNOL, V169, P3284; BAXTER AG, 1994, IMMUNOLOGY, V83, P227; Belkaid Y, 2002, NATURE, V420, P502, DOI 10.1038/nature01152; 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Immunopathol.	FEB	2004	25	3-4					237	255		10.1007/s00281-003-0148-9		19	Immunology; Pathology	Immunology; Pathology	801IP	WOS:000220089900002	15007629	
J	Epstein, MM				Epstein, MM			Do mouse models of allergic asthma mimic clinical disease?	INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY			English	Review						allergic asthma, pathophysiology; allergic asthma, pathology; allergic asthmam, therapy; immunoglobulin E; eosinophilic lung inflammation; immunological memory; Th2 cells; airway resistance; allergens, administration and dosage; mice, congenic	INDUCED AIRWAY HYPERREACTIVITY; CELL-DEFICIENT MICE; HOUSE-DUST MITE; TRACT DENDRITIC CELLS; REGULATORY T-CELLS; MURINE STRAIN DIFFERENCES; DIESEL EXHAUST PARTICLES; RECEPTOR TRANSGENIC MICE; BIRCH POLLEN ALLERGEN; TOLL-LIKE RECEPTOR-4	Experimental mouse models of allergic asthma established almost 10 years ago offered new opportunities to study disease pathogenesis and to develop new therapeutics. These models focused on the factors governing the allergic immune response, on modeling clinical behavior of allergic asthma, and led to insights into pulmonary pathophysiology. Although mouse models rarely completely reproduce all the features of human disease, after sensitization and respiratory tract challenges with antigen, wild-type mice develop a clinical syndrome that closely resembles allergic asthma, characterized by eosinophilic lung inflammation, airway hyperresponsiveness (AHR), increased IgE, mucus hypersecretion, and eventually, airway remodeling. There are, however, differences between mouse and human physiology that threaten to limit the value of mouse models. Three examples of such differences relate to both clinical manifestations of disease and underlying pathogenesis. First, in contrast to patients who have increased methacholine-induced AHR even when they are symptom-free, mice exhibit only transient methacholine-induced AHR following allergen exposure. Second, chronic allergen exposure in patients leads to chronic allergic asthma, whereas repeated exposures in sensitized mice causes suppression of disease. Third, IgE and mast cells, in humans, mediate early- and late-phase allergic responses, though both are unnecessary for the generation of allergic asthma in mice. Taken together, these observations suggest that mouse models of allergic asthma are not exact replicas of human disease and thus, question the validity of these models. However, observations from mouse models of allergic asthma support many existing paradigms, although some novel discoveries in mice have yet to be verified in patients. This review presents an overview of the clinical aspects of disease in mouse models of allergic asthma emphasizing ( 1) the factors influencing the pathophysiological responses during the initiation and perpetuation of disease, ( 2) the utility of mouse models for studying clinical manifestations of disease, and ( 3) the applicability of mouse models for testing new treatments for allergic asthma. Copyright (C) 2004 S. Karger AG, Basel.	Univ Vienna, Dept Dermatol, Div Immunol Allergy & Infect Dis, AT-1235 Vienna, Austria	Epstein, MM (reprint author), Univ Vienna, Dept Dermatol DIAID, VIRCC, Brunner Str 59, AT-1235 Vienna, Austria.	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Arch. Allergy Immunol.		2004	133	1					84	100		10.1159/000076131		17	Allergy; Immunology	Allergy; Immunology	800KZ	WOS:000220028500010	14726635	
J	Ichiura, H; Kitaoka, T; Tanaka, H				Ichiura, H; Kitaoka, T; Tanaka, H			Removal of indoor pollutants under UV irradiation by a composite TiO2-zeolite sheet prepared using a papermaking technique	CHEMOSPHERE			English	Article						photocatalyst; adsorbent; composite TiO2-zeolite sheet; papermaking technique; indoor pollution	VOLATILE ORGANIC-COMPOUNDS; PHOTOCATALYTIC OXIDATION; INCREMENTAL REACTIVITIES; FILM PHOTOCATALYST; AIR-QUALITY; TIO2; ZEOLITE; ILLUMINATION; ACETALDEHYDE; DEGRADATION	Toluene and formaldehyde are malodorous and cause indoor pollution. These materials have received much attention as hazardous and malodorous substances. It is well known that long-term exposure to even fairly low levels of toluene and formaldehyde brings about the risk of asthma, and eczema. In this study, a composite TiO2-zeolite (ZE) sheet prepared using a papermaking technique was applied to remove toluene and formaldehyde under UV irradiation. The optimum composition of the TiO2 (Ti)-ZE sheet was studied in detail with regard to the effective removal of various indoor pollutants. Gaseous toluene and formaldehyde were removed by a composite TiO2-ZE sheet with different efficiencies depending upon the ratio of Ti/ZE in the composite sheet. The composite sheets could decompose formaldehyde and toluene repeatedly after being recharged. It was shown that the sheets are potentially applicable as highly functional materials to be placed on walls and ceilings of houses for the removal of various indoor pollutants. (C) 2002 Elsevier Science Ltd. All rights reserved.	Kyushu Univ, Dept Forest & Forest Prod Sci, Fukuoka 8128581, Japan	Ichiura, H (reprint author), Kyushu Univ, Dept Forest & Forest Prod Sci, Fukuoka 8128581, Japan.		U-ID, Kyushu/C-5291-2016				Augugliaro V, 1999, APPL CATAL B-ENVIRON, V20, P15, DOI 10.1016/S0926-3373(98)00088-5; Chang TY, 1999, ATMOS ENVIRON, V33, P4695, DOI 10.1016/S1352-2310(99)00232-0; Ichiura H, 2002, J MATER SCI, V37, P2937, DOI 10.1023/A:1016060729376; Ichiura H, 2001, J MATER SCI, V36, P4921, DOI 10.1023/A:1011840405043; Ichiura H, 2001, J MATER SCI, V36, P913, DOI 10.1023/A:1004851101749; ICHIURA H, 2000, P INT S ENV FRIENDL, P42; Jones AP, 1998, SOC SCI MED, V47, P755, DOI 10.1016/S0277-9536(98)00151-8; Kelly NA, 1999, ATMOS ENVIRON, V33, P2101, DOI 10.1016/S1352-2310(98)00273-8; Lee SC, 2000, CHEMOSPHERE, V41, P109, DOI 10.1016/S0045-6535(99)00396-3; LINSEBIGLER AL, 1995, CHEM REV, V95, P735, DOI 10.1021/cr00035a013; MATSUBARA H, 1995, CHEM LETT, P767, DOI 10.1246/cl.1995.767; Mendez-Roman R, 1998, CATAL TODAY, V40, P353, DOI 10.1016/S0920-5861(98)00064-9; Ohko Y, 1997, J PHYS CHEM A, V101, P8057, DOI 10.1021/jp972002k; Rak ZS, 1997, REACT KINET CATAL L, V60, P303, DOI 10.1007/BF02475693; Rappengluck B, 1999, ATMOS ENVIRON, V33, P3843, DOI 10.1016/S1352-2310(98)00394-X; Sopyan I, 1996, J PHOTOCH PHOTOBIO A, V98, P79, DOI 10.1016/1010-6030(96)04328-6; SOPYAN J, 1994, CHEM LETT, P723; TABATA T, 1995, B CHEM SOC JPN, V68, P1905, DOI 10.1246/bcsj.68.1905; Takeda H, 1996, B CHEM SOC JPN, V69, P2735, DOI 10.1246/bcsj.69.2735; TANAKA H, 1993, J POLYM SCI POL CHEM, V31, P2687, DOI 10.1002/pola.1993.080311103; TANAKA H, 1994, LANGMUIR, V10, P3466, DOI 10.1021/la00022a018; Wolkoff P, 1998, SCI TOTAL ENVIRON, V215, P135, DOI 10.1016/S0048-9697(98)00110-7; Yu C, 1998, BUILD ENVIRON, V33, P357, DOI 10.1016/S0360-1323(97)00055-3	23	98	105	4	33	PERGAMON-ELSEVIER SCIENCE LTD	OXFORD	THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND	0045-6535			CHEMOSPHERE	Chemosphere	JAN	2003	50	1					79	83	PII S0045-6535(02)00604-5	10.1016/S0045-6535(02)00604-5		5	Environmental Sciences	Environmental Sciences & Ecology	629XH	WOS:000180077300011	12656232	
J	van Rijt, LS; Prins, JB; Leenen, PJM; Thielemans, K; de Vries, VC; Hoogsteden, HC; Lambrecht, BN				van Rijt, LS; Prins, JB; Leenen, PJM; Thielemans, K; de Vries, VC; Hoogsteden, HC; Lambrecht, BN			Allergen-induced accumulation of airway dendritic cells is supported by an increase in CD31(hi)Ly6C(neg) bone marrow precursors in a mouse model of asthma	BLOOD			English	Article							COLONY-STIMULATING FACTOR; LUNG INFLAMMATION; INHALED ANTIGEN; MURINE MODEL; LYMPH-NODES; ER-MP12; MICE; EOSINOPHILIA; RESPONSES; CHALLENGE	Airway dendritic cells (DCs) are held responsible for inducing sensitization to Inhaled antigen, leading to eosinophilic airway inflammation, typical of asthma. However, less information is available about the role of these cells in ongoing inflammation. In a mouse model of asthma, sensitization to ovalbumin (OVA) was induced by intratracheal injection of myeloid OVA-pulsed DCs. Upon OVA aerosol challenge and induction of eosinophilic airway inflammation in sensitized mice, there was a time-dependent and almost 100-fold increase In the number of MHCII+ CD11b(+) CD11c(+) endogenous air-way DCs as well as CD11b(+) blood DCs. The mechanism of this increase was studied. Adoptive transfer experiments demonstrated that accumulation of airway DCs was not due to reduced migration to the mediastinal lymph nodes. Rather, the massive increase in airway and lymph node DCs was supported by an almost 3-fold expansion of myeloid CD31(hi)Ly-6C(neg) hematopoietic precursor cells in the bone marrow (BM). There was no change in any of the other 5 populations revealed by CD31/Ly-6C staining. When these CD31(hi)Ly-6C(neg) BM precursors were sorted and grown in granulocyte macro-phage-colony-stimulating factor, they differentiated into MHCII+ CD11c(+) DCs. The same CD31(hi)Ly-6C(neg) precursors also expressed the eotaxin receptor CCR3 and differentiated into eosinophils when grown in interleukin 5. Serum levels of eotaxin were doubled in mice with inflammation. These findings in an animal model of asthma suggest that the BM increases its output of myeloid precursors to meet the enhanced demand for DCs and eosinophils in inflamed airways. (C) 2002 by The American Society of Hematology.	Erasmus Univ, Med Ctr, Dept Pulm & Crit Care Med, Rotterdam, Netherlands; Erasmus Univ, Med Ctr, Dept Immunol, Rotterdam, Netherlands; Free Univ Brussels, Dept Physiol, B-1050 Brussels, Belgium	van Rijt, LS (reprint author), Erasmus Univ, Dept Pulm Med, Room Ee2263,Dr Molewaterpl 50, NL-3015 GE Rotterdam, Netherlands.		Lambrecht, Bart/K-2484-2014; Leenen, Pieter/I-5839-2013	Lambrecht, Bart/0000-0003-4376-6834; Leenen, Pieter/0000-0001-9860-2920			Asselin-Paturel C, 2001, NAT IMMUNOL, V2, P1144, DOI 10.1038/ni736; Banchereau J, 1998, NATURE, V392, P245, DOI 10.1038/32588; Brasel K, 2000, BLOOD, V96, P3029; Bruno L, 2001, EUR J IMMUNOL, V31, P3403, DOI 10.1002/1521-4141(200111)31:11<3403::AID-IMMU3403>3.0.CO;2-T; de Bruijn MFTR, 1998, J IMMUNOL METHODS, V217, P27, DOI 10.1016/S0022-1759(98)00080-5; deBruijn MFTR, 1996, EUR J IMMUNOL, V26, P2850, DOI 10.1002/eji.1830261208; DEBRUIJN MFTR, 1994, EUR J IMMUNOL, V24, P2279, DOI 10.1002/eji.1830241003; Elsas MICG, 1997, AM J RESP CELL MOL, V17, P404; Ford JG, 2001, J IMMUNOL, V167, P1769; Ganzalo J A, 1996, Immunity, V4, P1; Grimaldi JC, 1999, J LEUKOCYTE BIOL, V65, P846; Harris NL, 2002, J EXP MED, V195, P317, DOI 10.1084/jem.20011558; HOLT PG, 1994, J IMMUNOL, V153, P256; Holt PG, 2000, J ALLERGY CLIN IMMUN, V105, P421, DOI 10.1067/mai.2000.105010; Iezzi G, 2001, J EXP MED, V193, P987, DOI 10.1084/jem.193.8.987; INABA K, 1992, J EXP MED, V176, P1693, DOI 10.1084/jem.176.6.1693; Inman MD, 1999, AM J RESP CELL MOL, V21, P473; Jahnsen FL, 2001, THORAX, V56, P823, DOI 10.1136/thorax.56.11.823; Lambrecht BN, 2000, J CLIN INVEST, V106, P551, DOI 10.1172/JCI8107; Lambrecht BN, 1998, J IMMUNOL, V160, P4090; Lambrecht BN, 2001, CLIN EXP ALLERGY, V31, P206, DOI 10.1046/j.1365-2222.2001.01061.x; Lambrecht BN, 2000, J IMMUNOL, V164, P2937; Ling V, 1997, EUR J IMMUNOL, V27, P509, DOI 10.1002/eji.1830270223; Lutz MB, 1999, J IMMUNOL METHODS, V223, P77, DOI 10.1016/S0022-1759(98)00204-X; Manz MG, 2001, BLOOD, V97, P3333, DOI 10.1182/blood.V97.11.3333; Nakano H, 2001, J EXP MED, V194, P1171, DOI 10.1084/jem.194.8.1171; Ohkawara Y, 1997, AM J RESP CELL MOL, V16, P510; Peled A, 1998, BLOOD, V91, P1909; Randolph GJ, 1998, SCIENCE, V282, P480, DOI 10.1126/science.282.5388.480; Saito H, 2001, IMMUNOLOGY, V104, P226, DOI 10.1046/j.1365-2567.2001.01253.x; Schlueter AJ, 2001, CYTOMETRY, V43, P297, DOI 10.1002/1097-0320(20010401)43:4<297::AID-CYTO1062>3.0.CO;2-9; SLIEKER WAT, 1993, INT IMMUNOL, V5, P1099, DOI 10.1093/intimm/5.9.1099; Sung SSJ, 2001, J IMMUNOL, V166, P1261; Throsby M, 2000, J IMMUNOL, V165, P1965; Tomaki M, 2000, J IMMUNOL, V165, P4040; VANDERLOO JCM, 1995, BLOOD, V85, P952; Vermaelen KY, 2001, J EXP MED, V193, P51; XIA WJ, 1995, J EXP MED, V181, P1275, DOI 10.1084/jem.181.4.1275	38	98	99	1	1	AMER SOC HEMATOLOGY	WASHINGTON	1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA	0006-4971			BLOOD	Blood	NOV 15	2002	100	10					3663	3671		10.1182/blood-2002-03-0673		9	Hematology	Hematology	613YE	WOS:000179158500031	12393720	
J	Burch, M; Levetin, E				Burch, M; Levetin, E			Effects of meteorological conditions on spore plumes	INTERNATIONAL JOURNAL OF BIOMETEOROLOGY			English	Article						spore plumes; fungal spores; asthma; hay fever; meteorological conditions	ALTERNARIA-ALTERNATA; RISK FACTOR; ASTHMA; WEATHER	Fungal spores are an ever-present component of the atmosphere, and have long been known to trigger asthma and hay fever symptoms in sensitive individuals. The atmosphere around Tulsa has been monitored for airborne spores and pollen with Burkard spore traps at several sampling stations. This study involved the examination of the hourly spore concentrations on days that had average daily concentrations near 50,000 spores/m(3) or greater. Hourly concentrations of Cladosporium, Alternaria, Epicoccum, Curvularia, Pithomyces, Drechslera, smut spores, ascospores, basidiospores, other, and total spores were determined on 4 days at three sites and then correlated with hourly meteorological data including temperature, rainfall, wind speed, dew point, air pressure, and wind direction. On each of these days there was a spore plume, a phenomenon in which spore concentrations increased dramatically over a very short period of time. Spore plumes generally occurred near midday, and concentrations were seen to increase from lows around 20,000 total spores/m(3) to highs over 170,000 total spores/m(3) in 2 h. Multiple regression analysis of the data indicated that increases in temperature, dew point, and air pressure correlated with the increase in spore concentrations, but no single weather variable predicted the appearance of a spore plume. The proper combination of changes in these meteorological parameters that result in a spore plume may be due to the changing weather conditions associated with thunderstorms, as on 3 of the 4 days when spore plumes occurred there were thunderstorms later that evening. The occurrence of spore plumes may have clinical significance, because other studies have shown that sensitization to certain spore types can occur during exposure to high spore concentrations.	Univ Tulsa, Fac Biol Sci, Tulsa, OK 74104 USA	Levetin, E (reprint author), Univ Tulsa, Fac Biol Sci, 600 S Coll Ave, Tulsa, OK 74104 USA.						AHRENS CD, 1998, METEOROLOGY; Allitt U, 2000, AEROBIOLOGIA, V16, P397, DOI 10.1023/A:1026503500730; AYLOR DE, 1990, ANNU REV PHYTOPATHOL, V28, P73, DOI 10.1146/annurev.py.28.090190.000445; Black PN, 2000, ALLERGY, V55, P501, DOI 10.1034/j.1398-9995.2000.00293.x; Dales RE, 2000, AM J RESP CRIT CARE, V162, P2087; Dixit A, 2000, GRANA, V39, P209, DOI 10.1080/00173130051084368; HASNAIN SM, 1993, GRANA, V32, P184; HIRST J. M., 1953, TRANS BRIT MYCOL SOC, V36, P375; HJELMROOS M, 1993, GRANA, V32, P40; Ingold C. T., 1971, FUNGAL SPORES THEIR; LEVETIN E, 1991, GRANA, V30, P123; Neukirch C, 1999, J ALLERGY CLIN IMMUN, V103, P709, DOI 10.1016/S0091-6749(99)70247-2; Ostro B, 2001, EPIDEMIOLOGY, V12, P200, DOI 10.1097/00001648-200103000-00012; Rosas I, 1998, ALLERGY, V53, P394, DOI 10.1111/j.1398-9995.1998.tb03911.x; Sterling M., 1999, Aerobiologia, V15, P9, DOI 10.1023/A:1007561201541; Timmer LW, 1998, PHYTOPATHOLOGY, V88, P1218, DOI 10.1094/PHYTO.1998.88.11.1218	16	98	100	1	12	SPRINGER-VERLAG	NEW YORK	175 FIFTH AVE, NEW YORK, NY 10010 USA	0020-7128			INT J BIOMETEOROL	Int. J. Biometeorol.	AUG	2002	46	3					107	117		10.1007/s00484-002-0127-1		11	Biophysics; Environmental Sciences; Meteorology & Atmospheric Sciences; Physiology	Biophysics; Environmental Sciences & Ecology; Meteorology & Atmospheric Sciences; Physiology	591TH	WOS:000177896000001	12194003	
J	D'Ambrosio, D; Mariani, M; Panina-Bordignon, P; Sinigaglia, F				D'Ambrosio, D; Mariani, M; Panina-Bordignon, P; Sinigaglia, F			Chemokines and their receptors guiding T lymphocyte recruitment in lung inflammation	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Review						lymphocyte homing; T cell; chemokines; asthma; COPD	MONOCYTE CHEMOATTRACTANT PROTEIN; OBSTRUCTIVE PULMONARY-DISEASE; ALLERGIC INFLAMMATION; AIRWAY HYPERRESPONSIVENESS; DENDRITIC CELLS; ATOPIC ASTHMA; L-SELECTIN; TH2 CELLS; BRONCHOALVEOLAR LAVAGE; NEUTROPHIL EMIGRATION		Roche Milano Ric, I-20132 Milan, Italy	Sinigaglia, F (reprint author), Roche Milano Ric, Via Olgettina 58, I-20132 Milan, Italy.						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J. Respir. Crit. Care Med.	OCT 1	2001	164	7					1266	1275				10	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	489VM	WOS:000172013200036	11673221	
J	Arlian, LG; Platts-Mills, TAE				Arlian, LG; Platts-Mills, TAE			The biology of dust mites and the remediation of mite allergens in allergic disease	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						house dust mite abatement; allergen remediation; mite allergy; dust mite biology	DERMATOPHAGOIDES-PTERONYSSINUS ACARI; SOLIDIFIED BENZYL BENZOATE; HOUSE-DUST; FARINAE ACARI; BRONCHIAL HYPERREACTIVITY; RELATIVE HUMIDITIES; EUROGLYPHUS-MAYNEI; ASTHMATIC-CHILDREN; BEDDING ENCASEMENT; SEASONAL-VARIATION	In most temperate humid areas of the world, house dust mites are a major source of multiple allergens in house dust Mite allergens sensitize and induce perennial rhinitis, asthma, or atopic dermatitis in a large portion of patients with allergic disease. There is convincing evidence that avoidance of mite allergen can effectively reduce allergic symptoms, Patients can be moved to a mite allergen-free environment, or mite and mite allergen abatement can be performed to reduce exposure in existing residences. Some knowledge of the biology of house dust mites is essential to understand the basis of the recommendations for reducing mites and mite allergens in homes and to appreciate the difficulty of eliminating house dust mites and mite allergens from homes. This article reviews key aspects of the biology of dust mites, the properties of mite allergens, recommendations for reducing mite and mite allergen concentrations in homes, and practical recommendations for treatment.	Wright State Univ, Dept Biol Sci, Dayton, OH 45435 USA; Univ Virginia, Asthma & Allerg Dis Ctr, Charlottesville, VA USA	Arlian, LG (reprint author), Wright State Univ, Dept Biol Sci, 235 Biol Sci Bldg, Dayton, OH 45435 USA.						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Allergy Clin. Immunol.	MAR	2001	107	3		S			S406	S413		10.1067/mai.2001.113670		8	Allergy; Immunology	Allergy; Immunology	418KR	WOS:000167891800002	11242601	
J	Koziel, JA; Odziemkowski, M; Pawliszyn, J				Koziel, JA; Odziemkowski, M; Pawliszyn, J			Sampling and analysis of airborne particulate matter and aerosols using in-needle trap and SPME fiber devices	ANALYTICAL CHEMISTRY			English	Article							SOLID-PHASE MICROEXTRACTION; PERFORMANCE LIQUID-CHROMATOGRAPHY; POLYCYCLIC AROMATIC-HYDROCARBONS; CAPILLARY-ELECTROPHORESIS; GAS-CHROMATOGRAPHY; AIR; SPECTROSCOPY; SEPARATION	A needle trap device (NTD) and commercial poly(dimethylsiloxane) (PDMS) 7-mum film thickness solid-phase microextraction (SPME) fibers were used for the sampling and analysis of aerosols and airborne particulate matter (PM) from an inhaler-administered drag, spray insect repellant, and tailpipe diesel exhaust. The NTD consisted of a 0.53-mm o.d. stainless steel needle having 5 mm of quartz wool packing section near the needle tip. Samples were collected by drawing air across the NTD with a Luer-tip syringe or via direct exposure of the SPME fiber. The mass loading of PM was varied by adjusting the volume of air pulled through the NTD or by varying the sampling time for the SPME fiber. The air volumes ranged from 0.1 to 50 mt, and sampling times varied from 10 s to 16 min; Particulates were either trapped on the needle packing or sorbed onto the SPME fiber, The devices were introduced to a chromatograph/mass spectrometer (GC/MS) injector for 5 min desorption, In the case of the NTD, 10 muL of clean air was delivered by a gas-tight syringe to aid the introduction of desorbed analytes. The compounds sorbed onto particles extracted by the SPME fiber or trapped in the needle device were desorbed in the injector and no carry-over was observed, Both devices performed well in extracting airborne polycyclic aromatic hydrocarbons: (PAHs) in diesel exhaust, triamcinolone acetonide in a dose of asthma drug and BEET in a dose of insect repellant spray, Results suggest that the NTDs and PDMS 7-mum fibers can be used for airborne particulate sampling and analysis, providing a simple, fast, reusable, and cost-effective screening tool, The advantage of the SPME fiber is the open-bed geometry allowing spectroscopic investigations of particulates; for example, with Raman microspectroscopy.	Univ Waterloo, Dept Chem, Waterloo, ON N2L 3G1, Canada; Univ Waterloo, Dept Earth Sci, Waterloo, ON N2L 3G1, Canada	Pawliszyn, J (reprint author), Univ Waterloo, Dept Chem, Waterloo, ON N2L 3G1, Canada.		Koziel, Jacek/B-5483-2014	Koziel, Jacek/0000-0002-2387-0354			Bernal JL, 1998, J CHROMATOGR A, V823, P423, DOI 10.1016/S0021-9673(98)00451-8; CHAI M, 1995, ENVIRON SCI TECHNOL, V29, P693, DOI 10.1021/es00003a017; Doppenschmitt SA, 1996, J CHROMATOGR B, V682, P79, DOI 10.1016/0378-4347(96)00060-6; HARRISON RM, 1986, HDB AIR POLLUTION AN; Kleeman MJ, 2000, ENVIRON SCI TECHNOL, V34, P1132, DOI 10.1021/es981276y; KNIGHT DS, 1989, J MATER RES, V4, P385, DOI 10.1557/JMR.1989.0385; Koziel J, 1999, ANAL CHIM ACTA, V400, P153, DOI 10.1016/S0003-2670(99)00614-5; KOZIEL J, IN PRESS J AIR WASTE; LESPADE P, 1982, CARBON, V20, P427, DOI 10.1016/0008-6223(82)90043-4; Lodge J. P., 1989, METHODS AIR SAMPLING; Martos PA, 1997, ANAL CHEM, V69, P402, DOI 10.1021/ac960633p; Martos PA, 1998, ANAL CHEM, V70, P2311, DOI 10.1021/ac9711394; Martos PA, 1999, ANAL CHEM, V71, P1513, DOI 10.1021/ac981028k; Martos PA, 1997, ANAL CHEM, V69, P206, DOI 10.1021/ac960415w; Mastral AM, 2000, ENVIRON SCI TECHNOL, V34, P3051, DOI 10.1021/es001028d; Nguyen AL, 1997, ANAL CHEM, V69, P1726, DOI 10.1021/ac960986o; ODZIEMKOWSKI M, UNPUB J ANAL CHEM; Offenberg JH, 1999, ENVIRON SCI TECHNOL, V33, P3324, DOI 10.1021/es990089c; Pawliszyn J., 1999, APPL SOLID PHASE MIC; Pawliszyn J., 1997, SOLID PHASE MICROEXT; RASCHDORF F, 1978, CHIMIA, V32, P478; SANTOSMONTES A, 1993, J CHROMATOGR-BIOMED, V620, P15, DOI 10.1016/0378-4347(93)80046-7; Seinfeld J. H., 1986, ATMOSPHERIC CHEM PHY; SHACKLETON CHL, 1986, J CHROMATOGR, V379, P91, DOI 10.1016/S0378-4347(00)80683-0; Shi JP, 2000, ENVIRON SCI TECHNOL, V34, P748, DOI 10.1021/es990530z; Shurmer B, 2000, ANAL CHEM, V72, P3660, DOI 10.1021/ac991395b; *US DEP HHS, 1994, NIOSH MAN AN METH; *US EPA, 1996, COMP METH DET TOX OR; YOUNG RJ, 1989, BRIT POLYM J, V21, P17, DOI 10.1002/pi.4980210104	29	98	101	1	61	AMER CHEMICAL SOC	WASHINGTON	1155 16TH ST, NW, WASHINGTON, DC 20036 USA	0003-2700			ANAL CHEM	Anal. Chem.	JAN 1	2001	73	1					47	54		10.1021/ac000835s		8	Chemistry, Analytical	Chemistry	389WW	WOS:000166262500017	11195511	
J	Gollwitzer, ES; Saglani, S; Trompette, A; Yadava, K; Sherburn, R; McCoy, KD; Nicod, LP; Lloyd, CM; Marsland, BJ				Gollwitzer, Eva S.; Saglani, Sejal; Trompette, Aurelien; Yadava, Koshika; Sherburn, Rebekah; McCoy, Kathy D.; Nicod, Laurent P.; Lloyd, Clare M.; Marsland, Benjamin J.			Lung microbiota promotes tolerance to allergens in neonates via PD-L1	NATURE MEDICINE			English	Article							REGULATORY T-CELLS; IMMUNE-SYSTEM; EARLY-LIFE; CHILDHOOD ASTHMA; COLONIZATION; FARM; INFLAMMATION; PREGNANCY; BACTERIUM; EXPOSURE	Epidemiological data point toward a critical period in early life during which environmental cues can set an individual on a trajectory toward respiratory health or disease(1-8). The neonatal immune system matures during this period(9), although little is known about the signals that lead to its maturation. Here we report that the formation of the lung microbiota is a key parameter in this process. Immediately following birth, neonatal mice were prone to develop exaggerated airway eosinophilia, release type 2 helper T cell cytokines and exhibit airway hyper-responsiveness following exposure to house dust mite allergens, even though their lungs harbored high numbers of natural CD4(+)Foxp3(+)CD25(+)Helios(+) regulatory T (T-reg cells. During the first 2 weeks after birth, the bacterial load in the lungs increased, and representation of the bacterial phyla shifts from a predominance of Gammaproteobacteria and Firmicutes towards Bacteroidetes. The changes in the microbiota were associated with decreased aeroallergen responsiveness and the emergence of a Helios(-) T-reg cell subset that required interaction with programmed death ligand 1 (PD-L1) for development. Absence of microbial colonization(10) or blockade of PD-L1 during the first 2 weeks postpartum maintained exaggerated responsiveness to allergens through to adulthood. Adoptive transfer of Treg cells from adult mice to neonates before aeroallergen exposure ameliorated disease. Thus, formation of the airway microbiota induces regulatory cells early in life, which, when dysregulated, can lead to sustained susceptibility to allergic airway inflammation in adulthood.	[Gollwitzer, Eva S.; Trompette, Aurelien; Yadava, Koshika; Nicod, Laurent P.; Marsland, Benjamin J.] Univ Lausanne, Fac Biol & Med, Ctr Hosp Univ Vaudois CHUV BH19206, Serv Pneumol, Lausanne, Switzerland; [Saglani, Sejal; Sherburn, Rebekah; Lloyd, Clare M.] Univ London Imperial Coll Sci Technol & Med, Fac Med, Natl Heart & Lung Inst, London, England; [McCoy, Kathy D.] Univ Bern, Univ Clin Visceral Surg & Med, Maurice Muller Labs, Bern, Switzerland	Marsland, BJ (reprint author), Univ Lausanne, Fac Biol & Med, Ctr Hosp Univ Vaudois CHUV BH19206, Serv Pneumol, Lausanne, Switzerland.	benjamin.marsland@chuv.ch		Lloyd, Clare/0000-0001-8977-6726; Saglani, Sejal/0000-0001-5192-6418	Leenaards Foundation in Lausanne; Swiss National Science Foundation [310030_146983]; Wellcome Trust [087618/Z/08/Z, 083586/Z/07/Z]	This work is supported by the Leenaards Foundation in Lausanne and the Swiss National Science Foundation grant 310030_146983, awarded to B.J.M. B.J.M. is a Cloetta Medical Research Fellow and, by holding this title, receives financial support. B.J.M. and C.M.L. are part of the European Cooperation in Science and Technology Action BM1201, Developmental Origins of Chronic Lung Disease. S.S. and C.M.L. are supported by the Wellcome Trust grants 087618/Z/08/Z and 083586/Z/07/Z. C.M.L. is a Wellcome Senior Fellow in Basic Biomedical Science and, by holding this title, receives financial support. We thank D. Pinschewer and S. Kallert for valuable discussions and critical feedback.	Burke H, 2012, PEDIATRICS, V129, P735, DOI 10.1542/peds.2011-2196; Cahenzli J, 2013, CELL HOST MICROBE, V14, P559, DOI 10.1016/j.chom.2013.10.004; de Lafaille MAC, 2009, IMMUNITY, V30, P626, DOI 10.1016/j.immuni.2009.05.002; Curotto de Lafaille M. 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Med.	JUN	2014	20	6					642	647		10.1038/nm.3568		6	Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental	Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine	AI7LB	WOS:000337071000026	24813249	
J	Savinko, T; Matikainen, S; Saarialho-Kere, U; Lehto, M; Wang, GY; Lehtimaki, S; Karisola, P; Reunala, T; Wolff, H; Lauerma, A; Alenius, H				Savinko, Terhi; Matikainen, Sampsa; Saarialho-Kere, Ulpu; Lehto, Maili; Wang, Guoying; Lehtimaki, Sari; Karisola, Piia; Reunala, Timo; Wolff, Henrik; Lauerma, Antti; Alenius, Harri			IL-33 and ST2 in Atopic Dermatitis: Expression Profiles and Modulation by Triggering Factors	JOURNAL OF INVESTIGATIVE DERMATOLOGY			English	Article							T-CELLS; MAST-CELLS; HUMAN MACROPHAGES; FAMILY CYTOKINE; MURINE MODEL; FLAKY TAIL; FILAGGRIN; DISEASE; RNA; SENSITIZATION	In the acute phase of atopic dermatitis (AD), T-helper type 2 (Th2) cytokines characterize the inflammatory response in the skin. IL-33 is a new tissue-derived cytokine, which is mainly expressed by cells of barrier tissues, and is known to activate Th2 lymphocytes, mast cells, and eosinophils. IL-33 signals through a receptor complex consisting of IL-33-specific receptor ST2 and a co-receptor IL-1RAcP. As IL-33 is known to promote Th2-type immunity, we examined expression profiles of IL-33 and its receptor components in human AD skin, in the murine model of AD, and in various cell models. We found increased expression of IL-33 and ST2 in AD skin after allergen or staphylococcal enterotoxin B (SEB) exposure, as well as in the skin of 22-week-old filaggrin-deficient mice. In addition, skin fibroblasts, HaCaT keratinocytes, primary macrophages, and HUVEC endothelial cells efficiently produced IL-33 in response to the combined stimulation of tumor necrosis factor-alpha and IFN-gamma, which was further enhanced by a mimetic of double-stranded RNA. Finally, the increased expression of IL-33 and ST2 caused by irritant, allergen, or SEB challenge was suppressed by topical tacrolimus treatment. These results suggest an important role for IL-33-ST2 interaction in AD and highlight the fact that bacterial and viral infections may increase the production of IL-33.	[Savinko, Terhi; Matikainen, Sampsa; Lehto, Maili; Lehtimaki, Sari; Karisola, Piia; Alenius, Harri] Finnish Inst Occupat Hlth, Unit Immunotoxicol, FIN-00250 Helsinki, Finland; [Saarialho-Kere, Ulpu; Lauerma, Antti] Univ Helsinki, Dept Dermatol Allergol & Venereol, Helsinki, Finland; [Wang, Guoying] Qingdao Univ, Dept Immunol, Coll Med, Qingdao 266071, Peoples R China; [Reunala, Timo; Lauerma, Antti] Univ Tampere, Dept Dermatol & Venereol, FIN-33101 Tampere, Finland	Alenius, H (reprint author), Finnish Inst Occupat Hlth, Unit Immunotoxicol, Topeliuksenkatu 41 AA, FIN-00250 Helsinki, Finland.	harri.alenius@ttl.fi	Lauerma, Antti/J-8180-2016		Academy of Finland; European Union [HEALTH-F2-2011-261366]	We kindly thank Sauli Savukoski for his expertise in immunohistological work. We also thank Paivi Alander and Santtu Hirvikorpi for their excellent technical assistance. This research was funded by the Academy of Finland and the European Union's FP7, grant agreement number HEALTH-F2-2011-261366.	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Invest. Dermatol.	MAY	2012	132	5					1392	1400		10.1038/jid.2011.446		9	Dermatology	Dermatology	926UA	WOS:000302856200015	22277940	
J	Clayton, EMR; Todd, M; Dowd, JB; Aiello, AE				Clayton, Erin M. Rees; Todd, Megan; Dowd, Jennifer Beam; Aiello, Allison E.			The Impact of Bisphenol A and Triclosan on Immune Parameters in the U.S. Population, NHANES 2003-2006	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						allergies; bisphenol A; cytomegalovirus; endocrine-disrupting compounds; NHANES; triclosan	NUTRITION EXAMINATION SURVEY; HUMAN CYTOMEGALOVIRUS; ENDOCRINE DISRUPTERS; NATIONAL-HEALTH; US POPULATION; ANTIBODIES; EXPOSURE; URINARY; SYSTEM; CELLS	BACKGROUND: Exposure to environmental toxicants is associated with numerous disease outcomes, many of which involve underlying immune and inflammatory dysfunction. OBJECTIVES: To address the gap between environmental exposures and immune dysfunction, we investigated the association of two endocrine-disrupting compounds (EDCs) with markers of immune function. METHODS: Using data from the 2003-2006 National Health and Nutrition Examination Survey, we compared urinary bisphenol A (BPA) and triclosan levels with serum cytomegalovirus (CMV) antibody levels and diagnosis of allergies or hay fever in U. S. adults and children >= 6 years of age. We used multivariate ordinary least squares linear regression models to examine the association of BPA and triclosan with CMV antibody titers, and multivariate logistic regression models to investigate the association of these chemicals with allergy or hay fever diagnosis. Statistical models were stratified by age (< 18 years and >= 18 years). RESULTS: In analyses adjusted for age, sex, race, body mass index, creatinine levels, family income, and educational attainment, in the >= 18-year age group, higher urinary BPA levels were associated with higher CMV antibody titers (p < 0.001). In the < 18-year age group, lower levels of BPA were associated with higher CMV antibody titers (p < 0.05). However, triclosan, but not BPA, showed a positive association with allergy or hay fever diagnosis. In the < 18-year age group, higher levels of triclosan were associated with greater odds of having been diagnosed with allergies or hay fever (p < 0.01). CONCLUSIONS: EDCs such as BPA and triclosan may negatively affect human immune function as measured by CMV antibody levels and allergy or hay fever diagnosis, respectively, with differential consequences based on age. Additional studies should be done to investigate these findings.	[Clayton, Erin M. Rees; Aiello, Allison E.] Univ Michigan, Sch Publ Hlth, Ctr Social Epidemiol & Populat Hlth, Ann Arbor, MI 48109 USA; [Clayton, Erin M. Rees; Aiello, Allison E.] Univ Michigan, Dept Epidemiol, Ann Arbor, MI 48109 USA; [Todd, Megan; Dowd, Jennifer Beam] CUNY, Inst Demog Res, New York, NY 10021 USA; [Todd, Megan] Princeton Univ, Woodrow Wilson Sch Publ & Int Affairs, Princeton, NJ 08544 USA; [Todd, Megan] Princeton Univ, Off Populat Res, Princeton, NJ 08544 USA; [Dowd, Jennifer Beam] CUNY, Hunter Coll, Sch Publ Hlth, New York, NY 10021 USA	Aiello, AE (reprint author), Univ Michigan, Sch Publ Hlth, Ctr Social Epidemiol & Populat Hlth, 1415 Washington Hts,Room 3663, Ann Arbor, MI 48109 USA.	aielloa@umich.edu	Dowd, Jennifer/C-1127-2012; Osborne, Nicholas/N-4915-2015	Dowd, Jennifer/0000-0003-2006-5656; Osborne, Nicholas/0000-0002-6700-2284	National Institutes of Health [1R21NR011181-01]; University of Michigan	This project was supported by an grant from the National Institutes of Health (1R21NR011181-01. E. M. R. C. acknowledges funding from the University of Michigan Robert Wood Johnson Health and Society Scholars Program during the writing of the manuscript.	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Health Perspect.	MAR	2011	119	3					390	396		10.1289/ehp.1002883		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	729CU	WOS:000287926700030	21062687	
J	Lee, RU; Stevenson, DD				Lee, Rachel U.; Stevenson, Donald D.			Aspirin-Exacerbated Respiratory Disease: Evaluation and Management	ALLERGY ASTHMA & IMMUNOLOGY RESEARCH			English	Review						Aspirin-exacerbated respiratory disease; aspirin desensitization; aspirin sensitivity; chronic sinusitis; asthma; nasal polyps; Samter's triad	LEUKOTRIENE-MODIFIER DRUGS; LONG-TERM TREATMENT; INDUCED ASTHMA; DESENSITIZATION-TREATMENT; SENSITIVE ASTHMATICS; INTOLERANT ASTHMA; CONTROLLED-TRIAL; NATURAL-HISTORY; LYSINE-ASPIRIN; CHALLENGE	The clinical syndrome of aspirin-exacerbated respiratory disease (AERD) is a condition where inhibition of cyclooxygenase-1 (COX-1) induces attacks of upper and lower airway reactions, including rhinorrhea and varying degrees of bronchospasm and laryngospasm. Although the reaction is not IgE-mediated, patients can also present with anaphylactic hypersensitivity reactions, including hypotension, after exposure to COX-1 inhibiting drugs. All patients with AERD have underlying nasal polyps and intractable sinus disease which may be difficult to treat with standard medical and surgical interventions. This review article focuses on the management of AERD patients with a particular emphasis on aspirin desensitization and continuous treatment with aspirin.	[Stevenson, Donald D.] Scripps Clin, Div Allergy Asthma & Immunol, San Diego, CA 92130 USA; [Lee, Rachel U.] Naval Med Ctr Portsmouth, Div Allergy Asthma & Immunol, Portsmouth, VA USA	Stevenson, DD (reprint author), Scripps Clin, Div Allergy Asthma & Immunol, 3811 Valley Ctr Dr,S99, San Diego, CA 92130 USA.	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Res.	JAN	2011	3	1					3	10		10.4168/aair.2011.3.1.3		8	Allergy; Immunology	Allergy; Immunology	776ZU	WOS:000291581600002	21217919	
J	Gurjar, BR; Jain, A; Sharma, A; Agarwal, A; Gupta, P; Nagpure, AS; Lelieveld, J				Gurjar, B. R.; Jain, A.; Sharma, A.; Agarwal, A.; Gupta, P.; Nagpure, A. S.; Lelieveld, J.			Human health risks in megacities due to air pollution	ATMOSPHERIC ENVIRONMENT			English	Article						Criteria pollutants; Mortality; Morbidity; Relative risk; Cardiovascular; Respiratory; Hospital admissions	UNITED-STATES; HOSPITAL ADMISSIONS; APHEA PROJECT; POLLUTANTS; MORTALITY; EXPOSURE; EMISSIONS; CITIES; ASTHMA	This study evaluates the health risks in megacities in terms of mortality and morbidity due to air pollution. A new spreadsheet model, Risk of Mortality/Morbidity due to Air Pollution (Ri-MAP), is used to estimate the excess numbers of deaths and illnesses. By adopting the World Health Organization (WHO) guideline concentrations for the air pollutants SO(2), NO(2) and total suspended particles (TSP), concentration-response relationships and a population attributable-risk proportion concept are employed. Results suggest that some megacities like Los Angeles, New York, Osaka Kobe, Sao Paulo and Tokyo have very low excess cases in total mortality from these pollutants. In contrast, the approximate numbers of cases is highest in Karachi (15,000/yr) characterized by a very high concentration of total TSP (similar to 670 mu g m(-3)). Dhaka (7000/yr), Beijing (5500/yr), Karachi (5200/yr), Cairo (5000/yr) and Delhi (3500/yr) rank highest with cardiovascular mortality. The morbidity (hospital admissions) due to Chronic Obstructive Pulmonary Disease (COPD) follows the tendency of cardiovascular mortality. Dhaka and Karachi lead the rankings, having about 2100/yr excess cases, while Osaka-Kobe (similar to 20/yr) and Sao Paulo (similar to 50/yr) are at the low end of all megacities considered. Since air pollution is increasing in many megacities, and our database of measured pollutants is limited to the period up to 2000 and does not include all relevant components (e.g. O(3)), these numbers should be interpreted as lower limits. South Asian megacities most urgently need improvement of air quality to prevent excess mortality and morbidity due to exceptionally high levels of air pollution. The risk estimates obtained from Ri-MAP present a realistic baseline evaluation for the consequences of ambient air pollution in comparison to simple air quality indices, and can be expanded and improved in parallel with the development of air pollution monitoring networks. (C) 2010 Elsevier Ltd. All rights reserved.	[Gurjar, B. R.; Jain, A.; Sharma, A.; Agarwal, A.; Gupta, P.] Indian Inst Technol, Dept Civil Engn, Roorkee 247667, Uttar Pradesh, India; [Nagpure, A. S.] Indian Inst Technol, Ctr Transportat Syst, Roorkee 247667, Uttar Pradesh, India; [Gurjar, B. R.; Lelieveld, J.] Max Planck Inst Chem, Div Atmospher Chem, D-55128 Mainz, Germany; [Lelieveld, J.] Cyprus Inst, Energy Environm & Water Res Ctr, CY-1645 Nicosia, Cyprus	Gurjar, BR (reprint author), Indian Inst Technol, Dept Civil Engn, Roorkee 247667, Uttar Pradesh, India.	brgurjar@gmail.com	Lelieveld, Johannes/A-1986-2013; Gurjar, Bhola Ram/L-1357-2013	Gurjar, Bhola Ram/0000-0002-7224-1802	Max Planck Society, Munich; Max Planck Institute for Chemistry, Mainz, Germany; Cyprus Institute	The Max Planck Society, Munich, and the Max Planck Institute for Chemistry, Mainz, Germany, have supported this study through the Max Planck Partner Group for Megacities and Global Change established at Indian Institute of Technology Roorkee, India. We thank the anonymous reviewers whose constructive suggestions have helped improve the manuscript. Support received from The Cyprus Institute during revision of the manuscript is gratefully acknowledged (ERC grant for the C8 project).	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J	Simons, FER				Simons, F. Estelle R.			Anaphylaxis: Recent advances in assessment and treatment	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						Anaphylaxis; systemic allergic reaction; food allergy; medication allergy; insect venom allergy; epinephrine; adrenaline	INDOLENT SYSTEMIC MASTOCYTOSIS; EPINEPHRINE AUTO-INJECTORS; ORAL TOLERANCE INDUCTION; LONG-TERM MANAGEMENT; INSECT STING ALLERGY; OF-THE-LITERATURE; FOOD ALLERGY; HYPERSENSITIVITY REACTIONS; EMERGENCY-DEPARTMENT; VENOM IMMUNOTHERAPY	The incidence rate of anaphylaxis is increasing, particularly during the first 2 decades of life. Common triggers include foods, medications, and insect stings. Clinical diagnosis is based on a meticulous history of an exposure or event preceding characteristic symptoms and signs, sometimes but not always supported by a laboratory test such as an elevated serum total tryptase level. Physician-initiated investigation of patients with anaphylaxis whose symptoms and signs are atypical sometimes leads to important insights into previously unrecognized triggers and mechanisms. In idiopathic anaphylaxis, in which no trigger can be confirmed by means of skin testing or measurement of specific IgE, the possibility of mastocytosis or a clonal mast cell disorder must be considered in addition to the possibility of a previously unrecognized trigger. Long-term risk reduction in patients with anaphylaxis focuses on optimal management of relevant comorbidities such as asthma and other respiratory diseases, cardiovascular disease, and mastocytosis or a clonal mast cell disorder; avoidance of the relevant confirmed allergen trigger; and relevant immunomodulation such as medication desensitization, venom immunotherapy, and possibly in the future, immunotherapy with food. Emergency preparedness for recurrence of anaphylaxis in community settings includes having epinephrine (adrenaline) autoinjectors available, knowing when and how to use them, and having a written, personalized anaphylaxis emergency action plan and up-to-date medical identification. Randomized controlled trials of the pharmacologic interventions used in an acute anaphylaxis episode are needed. (J Allergy Clin Immunol 2009;124:625-36.)	[Simons, F. Estelle R.] Univ Manitoba, Fac Med, Dept Pediat & Child Hlth, Winnipeg, MB R3T 2N2, Canada; [Simons, F. Estelle R.] Univ Manitoba, Fac Med, Dept Immunol, Winnipeg, MB R3T 2N2, Canada	Simons, FER (reprint author), FAAAAI,Room FE125,820 Sherbrook St, Winnipeg, MB R3A 1R9, Canada.	lmcniven@hsc.mb.ca			Canadian Institutes of Health Research	Dr. Simons has received research support from the Canadian Institutes of Health Research, and is a member of advisory boards for the Food Allergy and Anaphylaxis Network, Dey, Intelliject, ALK-Abello, and Sciele.	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Allergy Clin. Immunol.	OCT	2009	124	4					625	636		10.1016/j.jaci.2009.08.025		12	Allergy; Immunology	Allergy; Immunology	506UV	WOS:000270802800001	19815109	
J	Stieb, DM; Szyszkowicz, M; Rowe, BH; Leech, JA				Stieb, David M.; Szyszkowicz, Mieczyslaw; Rowe, Brian H.; Leech, Judith A.			Air pollution and emergency department visits for cardiac and respiratory conditions: a multi-city time-series analysis	ENVIRONMENTAL HEALTH			English	Article							HEART-RATE-VARIABILITY; ROOM VISITS; HOSPITAL ADMISSIONS; ASTHMA EMERGENCY; PARTICULATE MATTER; PULMONARY-DISEASE; CHILDHOOD ASTHMA; DAILY MORTALITY; SAINT-JOHN; ASSOCIATION	Background: Relatively few studies have been conducted of the association between air pollution and emergency department (ED) visits, and most of these have been based on a small number of visits, for a limited number of health conditions and pollutants, and only daily measures of exposure and response. Methods: A time-series analysis was conducted on nearly 400,000 ED visits to 14 hospitals in seven Canadian cities during the 1990s and early 2000s. Associations were examined between carbon monoxide (CO), nitrogen dioxide (NO(2)), ozone (O(3)), sulfur dioxide (SO(2)), and particulate matter (PM(10) and PM(2.5)), and visits for angina/myocardial infarction, heart failure, dysrhythmia/conduction disturbance, asthma, chronic obstructive pulmonary disease (COPD), and respiratory infections. Daily and 3-hourly visit counts were modeled as quasi-Poisson and analyses controlled for effects of temporal cycles, weather, day of week and holidays. Results: 24-hour average concentrations of CO and NO(2) lag 0 days exhibited the most consistent associations with cardiac conditions (2.1% (95% CI, 0.0-4.2%) and 2.6% (95% CI, 0.2-5.0%) increase in visits for myocardial infarction/angina per 0.7 ppm CO and 18.4 ppb NO(2) respectively; 3.8% (95% CI, 0.7-6.9%) and 4.7% (95% CI, 1.2-8.4%) increase in visits for heart failure). Ozone (lag 2 days) was most consistently associated with respiratory visits (3.2% (95% CI, 0.3-6.2%), and 3.7% (95% CI,-0.5-7.9%) increases in asthma and COPD visits respectively per 18.4 ppb). Associations tended to be of greater magnitude during the warm season (April-September). In particular, the associations of PM(10) and PM(2.5) with asthma visits were respectively nearly three-and over fourfold larger vs. all year analyses (14.4% increase in visits, 95% CI, 0.2-30.7, per 20.6 mu g/m(3) PM(10) and 7.6% increase in visits, 95% CI, 5.1-10.1, per 8.2 mu g/m(3) PM(2.5)). No consistent associations were observed between three hour average pollutant concentrations and same-day three hour averages of ED visits. Conclusion: In this large multicenter analysis, daily average concentrations of CO and NO(2) exhibited the most consistent associations with ED visits for cardiac conditions, while ozone exhibited the most consistent associations with visits for respiratory conditions. PM(10) and PM(2.5) were strongly associated with asthma visits during the warm season.	[Stieb, David M.; Szyszkowicz, Mieczyslaw; Leech, Judith A.] Hlth Canada, Healthy Environm & Consumer Safety Branch, Populat Studies Div, Ottawa, ON K1A 0K9, Canada; [Stieb, David M.] Univ Ottawa, Dept Epidemiol & Community Hlth, Ottawa, ON K1H 8M5, Canada; [Rowe, Brian H.] Univ Alberta, Dept Emergency Med, Univ Alberta Hosp, Edmonton, AB T6G 2B7, Canada; [Leech, Judith A.] Univ Ottawa, Ottawa Hosp, Dept Med, Ottawa, ON K1Y 4E9, Canada	Stieb, DM (reprint author), Hlth Canada, Healthy Environm & Consumer Safety Branch, Populat Studies Div, Postal Locator 4903C,269 Laurier Ave W, Ottawa, ON K1A 0K9, Canada.	dave_stieb@hc-sc.gc.ca; mietek_szyszkowicz@hc-sc.gc.ca; brian.rowe@ualberta.ca; jleech@ottawahospital.on.ca	Wang, Linden/M-6617-2014		Health Canada and Environment Canada	Drs. Robert Beveridge, Eric Grafstein, Simon Kingsley, Michael Schull, Douglas Sinclair and Bernard Unger provided emergency department visit data. Serge Beaulieu of Atlantic Health Sciences Corporation, Stacey Ackroyd of Dalhousie University, Chris Houston from Information Services, Capital Health and Virginia Willis, from the Emergency Medicine Research Group (EMeRG), assisted with data access. Anne Smith-Doiron assisted with the air pollution data. The study was funded by Health Canada and Environment Canada.	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Health	JUN 10	2009	8								25	10.1186/1476-069X-8-25		13	Environmental Sciences; Public, Environmental & Occupational Health	Environmental Sciences & Ecology; Public, Environmental & Occupational Health	472XE	WOS:000268165500001	19515235	
J	Schildcrout, JS; Sheppard, L; Lumley, T; Slaughter, JC; Koenig, JQ; Shapiro, GG				Schildcrout, Jonathan S.; Sheppard, Lianne; Lumley, Thomas; Slaughter, James C.; Koenig, Jane Q.; Shapiro, Gail G.			Ambient air pollution and asthma exacerbations in children: An eight-city analysis	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						air pollution; asthma; carbon monoxide; nitrogen dioxide; ozone; pediatrics; sulfur dioxide	LONGITUDINAL DATA-ANALYSIS; AFRICAN-AMERICAN CHILDREN; PARTICULATE MATTER; RESPIRATORY HEALTH; INHALED ALLERGEN; SYMPTOM SEVERITY; NITROGEN-DIOXIDE; OZONE EXPOSURE; MEDICATION USE; MEXICO-CITY	The authors investigated the relation between ambient concentrations of five of the Environmental Protection Agency's criteria pollutants and asthma exacerbations (daily symptoms and use of rescue inhalers) among 990 children in eight North American cities during the 22-month prerandomization phase (November 1993-September 1995) of the Childhood Asthma Management Program. Short-term effects of carbon monoxide, nitrogen dioxide, particulate matter less than 10 mu m in aerodynamic diameter (PM10), sulfur dioxide, and warm-season ozone were examined in both one-pollutant and two-pollutant models, using lags of up to 2 days. Lags in carbon monoxide and nitrogen dioxide were positively associated with both measures of asthma exacerbation, and the 3-day moving sum of sulfur dioxide levels was marginally related to asthma symptoms. PM10 and ozone were unrelated to exacerbations. The strongest effects tended to be seen with 2-day lags, where a 1-parts-per-million change in carbon monoxide and a 20-parts-per-billion change in nitrogen dioxide were associated with symptom odds ratios of 1.08 (95% confidence interval (CI): 1.02, 1.15) and 1.09 (95% CI: 1.03, 1.15), respectively, and with rate ratios for rescue inhaler use of 1.06 (95% CI: 1.01, 1.10) and 1.05 (95% CI: 1.01, 1.09), respectively. The authors believe that the observed carbon monoxide and nitrogen dioxide associations can probably be attributed to mobile-source emissions, though more research is required.	Vanderbilt Univ, Sch Med, Dept Biostat, Nashville, TN 37232 USA; Univ Washington, Sch Publ Hlth, Dept Biostat, Seattle, WA 98195 USA; Univ Washington, Environm Protect Agcy, NW Res Ctr Particulate Air Pollut & Hlth, Seattle, WA 98195 USA; Univ Washington, Sch Publ Hlth, Dept Environm Hlth, Seattle, WA 98195 USA; Univ N Carolina, Sch Publ Hlth, Dept Biostat, Chapel Hill, NC USA; Univ N Carolina, Sch Med, Dept Pediat, Chapel Hill, NC USA	Schildcrout, JS (reprint author), Vanderbilt Univ, Sch Med, Dept Biostat, S-2323 Med Ctr N, Nashville, TN 37232 USA.	jonathan.schildcrout@vanderbilt.edu		Slaughter, James/0000-0002-8770-980X	NHLBI NIH HHS [N01-HR-16047, N01-HR-16044, N01-HR-16045, N01-HR-16046, N01-HR-16048, N01-HR-16049, N01-HR-16050, N01-HR-16051, N01-HR-16052]		Akinbami LJ, 2002, PEDIATRICS, V110, P315, DOI 10.1542/peds.110.2.315; Asher MI, 1998, EUR RESPIR J, V12, P315; Beasley R, 2002, J ALLERGY CLIN IMMUN, V109, pS482, DOI 10.1067/mai.2002.122716; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Bernstein JA, 2004, J ALLERGY CLIN IMMUN, V114, P1116, DOI 10.1016/j.jaci.2004.08.030; Delfino RJ, 1998, ENVIRON HEALTH PERSP, V106, P751, DOI 10.1289/ehp.98106751; Delfino RJ, 1996, AM J RESP CRIT CARE, V154, P633; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; Dey Achintya N., 2005, VITAL HLTH STAT, V10, P1; LIANG KY, 1986, BIOMETRIKA, V73, P13, DOI 10.1093/biomet/73.1.13; LUMLEY T, 2005, RMETA META ANAL R PA; LUMLEY T, 2004, MITOOLS TOOLS MULTIP; Mortimer KM, 2002, EUR RESPIR J, V19, P699, DOI 10.1183/09031936.02.00247102; Neuhaus JM, 1998, BIOMETRICS, V54, P638, DOI 10.2307/3109770; Norris G, 2000, THORAX, V55, P466, DOI 10.1136/thorax.55.6.466; Ostro B, 2001, EPIDEMIOLOGY, V12, P200, DOI 10.1097/00001648-200103000-00012; OSTRO BD, 1995, INHAL TOXICOL, V7, P711, DOI 10.3109/08958379509014475; PEPE MS, 1994, COMMUN STAT SIMULAT, V23, P939, DOI 10.1080/03610919408813210; Peters A, 1996, AM J EPIDEMIOL, V144, P570; R Development Core Team, 2006, R LANG ENV STAT COMP; Romieu I, 1997, ARCH ENVIRON HEALTH, V52, P368; Romieu I, 1996, AM J RESP CRIT CARE, V154, P300; Rubin DB, 1987, MULTIPLE IMPUTATION; Sarnat JA, 2005, EPIDEMIOLOGY, V16, P385, DOI 10.1097/01.ede.0000155505.04775.33; SAS Institute Inc, 2001, SAS STAT US GUID REL; Schildcrout JS, 2005, BIOSTATISTICS, V6, P633, DOI 10.1093/biostatistics/kxi033; Sheppard L, 2003, BIOSTATISTICS, V4, P265, DOI 10.1093/biostatistics/4.2.265; Slaughter JC, 2005, J EXPO ANAL ENV EPID, V15, P153, DOI 10.1038/sj.jea.7500382; Slaughter JC, 2003, ANN ALLERG ASTHMA IM, V91, P346; Strand V, 1997, AM J RESP CRIT CARE, V155, P881; Szefler S, 2000, NEW ENGL J MED, V343, P1054; Thurston GD, 1997, AM J RESP CRIT CARE, V155, P654; Timonen KL, 1997, AM J RESP CRIT CARE, V156, P546; TUNNICLIFFE WS, 1994, LANCET, V344, P1733, DOI 10.1016/S0140-6736(94)92886-X; Vedal S, 1998, AM J RESP CRIT CARE, V157, P1034; Wang Li Yan, 2005, Prev Chronic Dis, V2, pA11; Ward DJ, 2004, OCCUP ENVIRON MED, V61, DOI 10.1136/oem.2003.007088; Weiss KB, 2001, J ALLERGY CLIN IMMUN, V107, P3, DOI 10.1067/mai.2001.112262; Yan J, 2004, STAT MED, V23, P859, DOI 10.1002/sim.1650; Yu OC, 2000, ENVIRON HEALTH PERSP, V108, P1209, DOI 10.2307/3434835; ZEGER SL, 1986, BIOMETRICS, V42, P121, DOI 10.2307/2531248	41	97	100	0	10	OXFORD UNIV PRESS INC	CARY	JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA	0002-9262			AM J EPIDEMIOL	Am. J. Epidemiol.	SEP 15	2006	164	6					505	517		10.1093/aje/kwj225		13	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	085FG	WOS:000240588300001	16798793	
J	Zock, JP; Heinrich, J; Jarvis, D; Verlato, G; Norback, D; Plana, E; Sunyer, J; Chinn, S; Olivieri, M; Soon, A; Villani, S; Ponzio, M; Dahlman-Hoglund, A; Svanes, C; Luczynska, C				Zock, Jan-Paul; Heinrich, Joachim; Jarvis, Deborah; Verlato, Giuseppe; Norback, Dan; Plana, Estel; Sunyer, Jordi; Chinn, Susan; Olivieri, Mario; Soon, Argo; Villani, Simona; Ponzio, Michela; Dahlman-Hoglund, Anna; Svanes, Cecilie; Luczynska, Christina		Indoor Working Grp European Comm	Distribution and determinants of house dust mite allergens in Europe: the European Community Respiratory Health Survey II	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						house dust mites; allergens; housing; risk factors; geographic; ECRHS	ASTHMA; PREVALENCE; DER-P-1; HOMES; MATTRESSES; SYMPTOMS; HUMIDITY; EXPOSURE	Background: Several studies in European homes have described allergen levels from the house dust mite species Dermatophagoides pteronyssinus and to a lesser extent Dermatophagoides farinae, but geographic comparisons of exposure levels and risk factors have been hampered by a lack of standardized methods. Objective: To study the distribution and determinants of the major house dust mite allergens Der p 1 and Der f 1 in 10 European countries using a common protocol. Methods: During home visits with 3580 participants of the European Community Respiratory Health Survey II from 22 study centers, mattress dust was sampled and analyzed for Der p 1, Der f 1, and Der 2 allergen. Information on housing characteristics was obtained by both observations and interview. Results: Der 1 and Der 2 allergens were detectable (>= 0.1 mu g/g) in 68% and 53% of the samples, respectively. Large differences in allergen levels between study centers were observed, and geographic patterns for Der p 1 and Der f 1 were different. Low winter temperatures reduced Der p 1 rather than Der f 1. Important risk factors for high allergen levels included an older mattress, a lower floor level of the bedroom, limited ventilation of the bedroom, and dampness for Der p 1 but not for Der f 1. Conclusion: There are large qualitative and quantitative differences of house dust mite allergen levels in Europe, which can partly be explained by geographic and housing characteristics. Clinical implications: Mite allergen exposure may be reduced by replacing the mattress regularly and increasing ventilation of the bedroom, particularly in winter.	Municipal Inst Med Res, Ctr Res Environm Epidemiol, Barcelona, Spain; Inst Epidemiol, Natl Res Ctr Environm & Hlth, Neuherberg, Germany; Univ London Imperial Coll Sci & Technol, Resp Epidemiol & Publ Hlth Grp, Natl Heart & Lung Inst, London, England; Univ Verona, Dept Med & Publ Hlth, I-37100 Verona, Italy; Uppsala Univ, Dept Med Sci Occupat & Environm Med, Uppsala, Sweden; Kings Coll London, Dept Publ Hlth Sci, London WC2R 2LS, England; Univ Verona, Unit Occupat Med, I-37100 Verona, Italy; Univ Tartu, Dept Publ Hlth, EE-50090 Tartu, Estonia; Univ Pavia, Dept Hlth Sci, Sect Epidemiol & Med Stat, I-27100 Pavia, Italy; Sahlgrens Univ Hosp, Dept Occupat & Environm Med, Gothenburg, Sweden; Univ Bergen, Dept Thorac Med, Inst Med, Bergen, Norway	Zock, JP (reprint author), IMIM, Dr Aiguader 80, E-08003 Barcelona, Spain.	jpzock@imim.es	; SESM, SESM/C-1440-2008; Jarvis, Deborah/E-6494-2011; Hervas, Daniel/H-4854-2011; Sanchez-Ramos, Jose Luis/G-1259-2011; Ciccone, Giovannino/K-3136-2016; Burgos, Felip/E-5734-2015; Sunyer, J/G-6909-2014	Rolla, Giovanni/0000-0001-5997-7172; Norback, Dan/0000-0002-5174-6668; /0000-0003-2517-6515; Sanchez-Ramos, Jose Luis/0000-0001-7187-9989; Ciccone, Giovannino/0000-0001-7644-9574; Burgos, Felip/0000-0002-4938-4581; Sunyer, J/0000-0002-2602-4110; ROMANO, Canzio/0000-0001-5294-9793; Bono, Roberto/0000-0002-2471-6594; Basagana, Xavier/0000-0002-8457-1489; Corsico, Angelo Guido/0000-0002-8716-4694	NHLBI NIH HHS [R01 HL62633-01]; NIEHS NIH HHS [5P30 ES07048]		Arbes SJ, 2003, J ALLERGY CLIN IMMUN, V111, P408, DOI 10.1067/mai.2003.16; Arlian LG, 2003, IMMUNOL ALLERGY CLIN, V23, P443, DOI 10.1016/S0889-8561(03)00005-5; Brunekreef B, 2005, ALLERGY, V60, P1083, DOI 10.1111/j.1398-9995.2005.00881.x; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; Dharmage S, 1999, CLIN EXP ALLERGY, V29, P461; El Sharif N, 2004, ALLERGY, V59, P623, DOI 10.1111/j.1398-9995.2004.00441.x; Gehring U, 2005, ALLERGY, V60, P1079, DOI 10.1111/j.1398-9995.2005.00872.x; Gross I, 2000, CLIN EXP ALLERGY, V30, P376, DOI 10.1046/j.1365-2222.2000.00780.x; Bleda Hernandez M.J., 2002, GAC SANIT, V16, P188; Jarvis D, 2002, EUR RESPIR J, V20, P1071, DOI 10.1183/09031936.02.00046802; LINTNER TJ, 1993, J ALLERGY CLIN IMMUN, V91, P862, DOI 10.1016/0091-6749(93)90343-E; Lubin JH, 2004, ENVIRON HEALTH PERSP, V112, P1691, DOI 10.1289/ehp.7199; Luczynska C, 1998, CLIN EXP ALLERGY, V28, P1201; Macan J, 2003, ALLERGY, V58, P780, DOI 10.1034/j.1398-9995.2003.00210.x; Melki IS, 2004, J EPIDEMIOL COMMUN H, V58, P476, DOI 10.1136/jech.2003.012690; Mihrshahi S, 2002, ALLERGY, V57, P137, DOI 10.1034/j.1398-9995.2002.5720999.x; Moscato G, 2000, ALLERGY, V55, P873, DOI 10.1034/j.1398-9995.2000.00584.x; Nelson HS, 2000, J ALLERGY CLIN IMMUN, V105, pS628; O'Connor GT, 2005, J ALLERGY CLIN IMMUN, V116, P26, DOI 10.1016/j.jaci.2005.02.013; Recer GM, 2004, CLIN EXP ALLERGY, V34, P268, DOI 10.1111/j.1365-2222.2004.01863.x; Schei MA, 2002, ALLERGY, V57, P538, DOI 10.1034/j.1398-9995.2002.23433.x; Sidenius KE, 2002, ANN AGR ENV MED, V9, P33; Simpson A, 2001, CLIN EXP ALLERGY, V31, P803, DOI 10.1046/j.1365-2222.2001.01110.x; van Strien RT, 2004, ALLERGY, V59, P645, DOI 10.1111/j.1398-9995.2004.00470.x; van Strien RT, 2003, CLIN EXP ALLERGY, V33, P490, DOI 10.1046/j.1365-2222.2003.01626.x; VANSTRIEN RT, 1994, CLIN EXP ALLERGY, V24, P843; Warner A, 1998, ALLERGY, V53, P698, DOI 10.1111/j.1398-9995.1998.tb03956.x; Wickens K, 2004, PEDIATR ALLERGY IMMU, V15, P55, DOI 10.1046/j.0905-6157.2003.00100.x; Zock JP, 2002, J ALLERGY CLIN IMMUN, V110, P285, DOI 10.1067/mai.2002.126383	29	97	105	0	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.	SEP	2006	118	3					682	690		10.1016/j.jaci.2006.04.060		9	Allergy; Immunology	Allergy; Immunology	086BV	WOS:000240649000022	16950288	
J	Nigo, YI; Yamashita, M; Hirahara, K; Shinnakasu, R; Inami, M; Kimura, M; Hasegawa, A; Kohno, Y; Nakayama, T				Nigo, YI; Yamashita, M; Hirahara, K; Shinnakasu, R; Inami, M; Kimura, M; Hasegawa, A; Kohno, Y; Nakayama, T			Regulation of allergic airway inflammation through Toll-like receptor 4-mediated modification of mast cell function	PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA			English	Article						cytokine; GATA1; mast cell; lipopolysaccharide; bone-marrow-derived mast cells	ENDOTOXIN EXPOSURE; GENE LOCUS; HISTONE HYPERACETYLATION; INNATE IMMUNITY; CUTTING EDGE; TNF-ALPHA; T-CELLS; ASTHMA; DIFFERENTIATION; LIPOPOLYSACCHARIDE	In a mouse experimental asthma model, the administration of bacterial lipopolysaccharide (LIPS), particularly at low doses, enhances the levels of ovalbumin (OVA)-induced eosinophilic airway inflammation. In an effort to clarify the cellular and molecular basis for the LPS effect, we demonstrate that the OVA-induced eosinophilic inflammation in the lung is dramatically increased by the administration of LPS in wild-type mice, whereas such increase was not observed in mast-cell-deficient mice or Toll-like receptor (TLR)4-deficient mice. Adoptive transfer of bone-marrow-derived mast cells (BMMCs) from wild-type, but not from TLR4-deficient, mice restored the increased eosinophilic inflammation in mast-cell-deficient mice. Wild-type BMMCs pretreated with LPS in vitro also reconstituted the eosinophilic inflammation. Moreover, in vitro analysis revealed that the treatment of BMMCs with LPS resulted in NF-kappa B activation, sustained up-regulation of GATA1 and -2 expression, and increased the capability to produce IL-5 and -13. Dramatic increases in the expression of IL-5 and -13 and Eotaxin 2 were detected in LIPS-treated BMMCs after costimulation with LIPS and IgE/Ag. Overexpression of GATA1, but not GATA2, in MC9 mast cells resulted in increased transcriptional activity of IL-4, -5, and -13. Furthermore, the levels of transcription of Th2 cytokines in BMMCs were decreased by the introduction of small interfering RNA for GATA1. Thus, mast cells appear to control allergic airway inflammation after their activation and modulation through TLR4-mediated induction of GATA1 and subsequent increase in Th2 cytokine production.	Chiba Univ, Grad Sch Med, Dept Immunol, Chuo Ku, Chiba 2608670, Japan; Chiba Univ, Grad Sch Med, Dept Pediat, Chuo Ku, Chiba 2608670, Japan	Nakayama, T (reprint author), Chiba Univ, Grad Sch Med, Dept Immunol, Chuo Ku, H3,1-8-1 Inohana, Chiba 2608670, Japan.	tnakayama@faculty.chiba-u.jp	Nakayama, Toshinori/E-1067-2017; Hirahara, Kiyoshi/E-2460-2017	Nakayama, Toshinori/0000-0002-1434-2007; Hirahara, Kiyoshi/0000-0002-9128-9449			Akira S, 2001, NAT IMMUNOL, V2, P675, DOI 10.1038/90609; Banchereau J, 1998, NATURE, V392, P245, DOI 10.1038/32588; Boyce JA, 2003, PROSTAG LEUKOTR ESS, V69, P195, DOI 10.1016/S0952-3278(03)00081-4; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Brightling CE, 2003, CLIN EXP ALLERGY, V33, P550, DOI 10.1046/j.1365-2222.2003.01636.x; Das J, 2001, NAT IMMUNOL, V2, P45, DOI 10.1038/83158; Drazen JM, 1996, J EXP MED, V183, P1, DOI 10.1084/jem.183.1.1; Echtenacher B, 1996, NATURE, V381, P75, DOI 10.1038/381075a0; Eisenbarth SC, 2002, J EXP MED, V196, P1645, DOI 10.1084/jem.20021340; Foster PS, 1996, J EXP MED, V183, P195, DOI 10.1084/jem.183.1.195; GALLI SJ, 1993, NEW ENGL J MED, V328, P257; Gern JE, 2000, J ALLERGY CLIN IMMUN, V105, pS497; Hamelmann E, 2001, IMMUNOL REV, V179, P182, DOI 10.1034/j.1600-065X.2001.790118.x; Harigae H, 1998, GENES CELLS, V3, P39, DOI 10.1046/j.1365-2443.1998.00166.x; Herrick CA, 2003, NAT REV IMMUNOL, V3, P405, DOI 10.1038/nri1084; Hoshino K, 1999, J IMMUNOL, V162, P3749; Inami M, 2004, J BIOL CHEM, V279, P23123, DOI 10.1074/jbc.M401248200; Iwasaki A, 2004, NAT IMMUNOL, V5, P987, DOI 10.1038/ni1112; Janeway CA, 2002, ANNU REV IMMUNOL, V20, P197, DOI 10.1146/annurev.immunol.20.083001.084359; Kamata T, 2003, J CLIN INVEST, V111, P109, DOI 10.1172/JCI200315719; Kimura M, 2001, IMMUNITY, V15, P275, DOI 10.1016/S1074-7613(01)00182-0; Kimura MY, 2005, J EXP MED, V201, P397, DOI 10.1084/jem.20040733; KITAMURA Y, 1978, BLOOD, V52, P447; Lee HJ, 1998, J IMMUNOL, V160, P2343; Lefort J, 1998, J IMMUNOL, V161, P474; Liu AH, 2002, J ALLERGY CLIN IMMUN, V109, P379, DOI 10.1067/mai.2002.122157; Malaviya R, 1996, NATURE, V381, P77, DOI 10.1038/381077a0; Masuda A, 2002, J IMMUNOL, V169, P3801; McCurdy JD, 2001, J LEUKOCYTE BIOL, V70, P977; McLachlan JB, 2003, NAT IMMUNOL, V4, P1199, DOI 10.1038/ni1005; Medzhitov R, 2001, NAT REV IMMUNOL, V1, P135, DOI 10.1038/35100529; METCALFE DD, 1981, CRC CR REV IMMUNOL, V3, P23; MICHEL O, 1991, CLIN EXP ALLERGY, V21, P441, DOI 10.1111/j.1365-2222.1991.tb01684.x; Migliaccio AR, 2003, J EXP MED, V197, P281, DOI 10.1084/jem.20021149; Okumura S, 2003, BLOOD, V102, P2547, DOI 10.1182/blood-2002-12-3929; Omori M, 2003, IMMUNITY, V19, P281, DOI 10.1016/S1074-7613(03)00210-3; Rizzo MC, 1997, PEDIATR ALLERGY IMMU, V8, P121; Schnare M, 2001, NAT IMMUNOL, V2, P947, DOI 10.1038/ni712; Schwartz DA, 2001, AM J RESP CRIT CARE, V163, P305; SCHWARTZ LB, 1984, PROG ALLERGY, V34, P271; Schwenger GTF, 2001, J BIOL CHEM, V276, P48502, DOI 10.1074/jbc.M107836200; Shibata Y, 2002, J IMMUNOL, V169, P2134; Supajatura V, 2002, J CLIN INVEST, V109, P1351, DOI 10.1172/JCI200214704; Supajatura V, 2001, J IMMUNOL, V167, P2250; Takeda K, 1996, NATURE, V380, P627, DOI 10.1038/380627a0; Takeda K, 2003, ANNU REV IMMUNOL, V21, P335, DOI 10.1146/annurev.immunol.21.120601.141126; Tulic MK, 2000, AM J RESP CELL MOL, V22, P604; Weiss DL, 2001, IMMUNOL REV, V179, P35, DOI 10.1034/j.1600-065X.2001.790104.x; Yamasaki S, 2004, BLOOD, V103, P3093, DOI 10.1182/blood-2003-08-2944; Yamashita M, 2005, J BIOL CHEM, V280, P29409, DOI 10.1074/jbc.M502333200; Yamashita M, 2002, J BIOL CHEM, V277, P42399, DOI 10.1074/jbc.M205876200; Zhang DH, 1998, J IMMUNOL, V161, P3817	52	97	110	1	5	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.	FEB 14	2006	103	7					2286	2291		10.1073/pnas.0510685103		6	Multidisciplinary Sciences	Science & Technology - Other Topics	013LU	WOS:000235411600052	16461458	
J	Prussin, C; Metcalfe, DD				Prussin, C; Metcalfe, DD			IgE, mast cells, basophils, and eosinophils	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						IgE; IgE receptor; mast cell; basophil; eosinophil	FC-EPSILON-RI; HOST-DEFENSE; HYPEREOSINOPHILIC SYNDROME; ASTHMA; RECEPTOR; ACTIVATION; EXPRESSION; DEFICIENT; SECRETION; ROLES	IgE, mast cells, basophils, and eosinophils constitute essential elements in allergic inflammation. Allergen-specific IgE, synthesized in response to allergens in the environment, becomes fixed to Fc epsilon RI on the membranes of mast cells and basophils. Aggregation of receptor-bound IgE molecules on re-exposure to specific allergen results in the production of mediators that produce the allergic response. Principal among the cells drawn to sites of mediator release is the eosinophil.	NIAID, LAD, NIH, Bethesda, MD 20892 USA	Metcalfe, DD (reprint author), NIAID, LAD, NIH, Bldg 10,Room 11C205,10 Ctr Dr,MSC 1881, Bethesda, MD 20892 USA.	dmetcalfe@niaid.nih.gov		Prussin, Calman/0000-0002-3917-3326			Adamko D, 2003, CURR OPIN PHARMACOL, V3, P227, DOI 10.1016/S1471-4892(03)00040-7; Akin C, 2004, ANNU REV MED, V55, P419, DOI 10.1146/annurev.med.55.091902.103822; Bieneman AP, 2005, J ALLERGY CLIN IMMUN, V115, P295, DOI 10.1016/j.jaci.2004.10.018; Bochner BS, 2001, IMMUNOL REV, V179, P5, DOI 10.1034/j.1600-065X.2001.790101.x; Bochner BS, 2000, J ALLERGY CLIN IMMUN, V106, P292; CAMERON L, 2003, MIDDLETONS ALLERGY P, P87; Devouassoux G, 1999, J ALLERGY CLIN IMMUN, V104, P811; Galli SJ, 2002, INT J HEMATOL, V75, P363, DOI 10.1007/BF02982125; GALLI SJ, 2001, WILLIAMS HEMATOLOGY, P801; Garman SC, 1999, ANNU REV IMMUNOL, V17, P973, DOI 10.1146/annurev.immunol.17.1.973; Gotlib J, 2004, BLOOD, V103, P2879, DOI 10.1182/blood-2003-06-1824; Gould HJ, 2003, ANNU REV IMMUNOL, V21, P579, DOI 10.1146/annurev.immunol.21.120601.141103; HAMILTON RG, 2001, CLIN IMMUNOLOGY, DOI UNSP 124.1-124.14; Humbles AA, 2004, SCIENCE, V305, P1776, DOI 10.1126/science.1100283; Kay AB, 2004, IMMUNOL ALLERGY CLIN, V24, P645, DOI 10.1016/j.iac.2004.06.007; Kepley CL, 2000, J IMMUNOL, V165, P5913; Kinet JP, 1999, ANNU REV IMMUNOL, V17, P931, DOI 10.1146/annurev.immunol.17.1.931; KITA H, 2001, CLIN IMMUNOLOGY PRIN; Klion AD, 2004, J ALLERGY CLIN IMMUN, V113, P30, DOI 10.1016/j.jaci.2003.10.050; Kulka M, 2004, J ALLERGY CLIN IMMUN, V114, P174, DOI 10.1016/j.jaci.2004.03.049; Lee JJ, 2004, SCIENCE, V305, P1773, DOI 10.1126/science.1099472; Marone G, 2005, TRENDS IMMUNOL, V26, P25, DOI 10.1016/j.it.2004.10.010; Mattes Joerg, 2003, Current Drug Targets - Inflammation and Allergy, V2, P169, DOI 10.2174/1568010033484214; Mitre E, 2004, J IMMUNOL, V172, P2439; Odemuyiwa SO, 2004, J IMMUNOL, V173, P5909; Oettgen HC, 2001, J ALLERGY CLIN IMMUN, V107, P429, DOI 10.1067/mai.2001.113759; Phillips C, 2003, J LEUKOCYTE BIOL, V73, P165, DOI 10.1189/jlb.0702356; Rosenberg HF, 2001, J LEUKOCYTE BIOL, V70, P691; Saini SS, 2000, J ALLERGY CLIN IMMUN, V106, P514, DOI 10.1067/mai.2000.108431; Saini SS, 2002, CURR OPIN IMMUNOL, V14, P694, DOI 10.1016/S0952-7915(02)00404-1; Schroeder JT, 2001, ADV IMMUNOL, V77, P93, DOI 10.1016/S0065-2776(01)77015-0; Schwartz LB, 2002, CL ALLER IM, V16, P3; Shi HZ, 2004, J LEUKOCYTE BIOL, V76, P520, DOI 10.1189/jlb.0404228; Tkaczyk C, 2002, MOL IMMUNOL, V38, P1289, DOI 10.1016/S0161-5890(02)00077-9	34	97	107	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.	FEB	2006	117	2		1			S450	S456		10.1016/j.jaci.2005.11.016		7	Allergy; Immunology	Allergy; Immunology	019VS	WOS:000235865400006	16455345	
J	Schram-Bijkerk, D; Doekes, G; Douwes, J; Boeve, M; Riedler, J; Ublagger, E; Mutius, E; Benz, MR; Pershagen, G; Hage, M; Scheynius, A; Braun-Fahrlander, C; Waser, M; Brunekreef, B				Schram-Bijkerk, D; Doekes, G; Douwes, J; Boeve, M; Riedler, J; Ublagger, E; Mutius, E; Benz, MR; Pershagen, G; Hage, M; Scheynius, A; Braun-Fahrlander, C; Waser, M; Brunekreef, B		PARSIFAL Study Grp	Bacterial and fungal agents in house dust and wheeze in children: the PARSIFAL study	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						asthma; beta(1,3)-glucans; endotoxin; farm; fungal extracellular polysaccharides	EXTRACELLULAR POLYSACCHARIDES; ALLERGIC SENSITIZATION; CULTURABLE FUNGI; HAY-FEVER; ASTHMA; FARM; ENDOTOXIN; EXPOSURE; ATOPY; (1->3)-BETA-D-GLUCAN	Background Growing up on a farm and an anthroposophic lifestyle are associated with a lower prevalence of allergic diseases in childhood. This might be related to increased inhalatory exposure to microbial agents. Objective To assess the association between microbial agents in house dust and atopic wheeze in farm children, Steiner school children and reference children. Methods Levels of bacterial endotoxin, fungal beta(1,3)-glucans and fungal extracellular polysaccharides (EPS) in mattress and living room floor dust were measured in a population of 270 atopic (=Phadiatop-positive) children with self-reported wheezing, including 168 current atopic wheezers, and 441 non-atopic, non-symptomatic controls. These children were selected from a cross-sectional study in five European countries. Results In the study population as a whole, average levels of mattress dust endotoxin, EPS and glucans were slightly (1.1-1.2-fold; P < 0.10) higher in control children than in atopic wheezers. Atopic wheeze was related to mattress levels of endotoxin, EPS and glucans in farm and farm-reference children. However, when adjusting for group (farm vs. farm-reference children), the associations became non-significant whereas the group effect remained. No associations between atopic wheeze and microbial agents were observed in Steiner and Steiner-reference children. For current atopic wheeze, the farm effect became non-significant after adjustment for microbial agent levels. Conclusion Not only bacterial endotoxin but also mould components might offer some protection against atopic wheeze in children. However, the protective effect of being raised on a farm was largely unexplained by the mattress microbial agent levels measured in this study.	Univ Utrecht, Inst Risk Assessment Sci, NL-3508 TD Utrecht, Netherlands; Massey Univ, Ctr Publ Hlth Res, Wellington, New Zealand; Childrens Hosp, Salzburg, Austria; Univ Munich, Childrens Hosp, D-8000 Munich, Germany; Karolinska Inst, Ctr Allergy Res, Inst Environm Med, Div Environm Epidemiol, Stockholm, Sweden; Karolinska Inst, Dept Med, Clin Immunol & Allergy Unit, Stockholm, Sweden; St Gorans Univ Hosp, S-11281 Stockholm, Sweden; Karolinska Inst, Dept Med, Clin Allergy Res Unit, Stockholm, Sweden; Univ Basel, Inst Social & Prevent Med, Basel, Switzerland	Schram-Bijkerk, D (reprint author), Univ Utrecht, Inst Risk Assessment Sci, POB 80176, NL-3508 TD Utrecht, Netherlands.	d.schram@iras.uu.nl	; van Hage, Marianne/A-9678-2017	brunekreef, bert/0000-0001-9908-0060; Douwes, Jeroen/0000-0003-3599-4036; van Hage, Marianne/0000-0003-3091-1596			ADACHI Y, 1994, BIOL PHARM BULL, V17, P1554; ALFVEN T, IN PRESS ALLERGY; Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; Arbes SJ, 2005, ENVIRON HEALTH PERSP, V113, P665, DOI 10.1289/ehp.7648; Beasley R, 2000, J ALLERGY CLIN IMMUN, V105, pS466, DOI 10.1016/S0091-6749(00)90044-7; Braback L, 2004, CLIN EXP ALLERGY, V34, P38, DOI 10.1111/j.1365-2222.2004.01841.x; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Chew GL, 2001, INDOOR AIR, V11, P171, DOI 10.1034/j.1600-0668.2001.011003171.x; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; Douwes J, 2003, AM J EPIDEMIOL, V158, P203, DOI 10.1093/aje/kwg149; 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; Downs SH, 2001, CLIN EXP ALLERGY, V31, P570, DOI 10.1046/j.1365-2222.2001.01070.x; Eduard W, 2004, THORAX, V59, P381, DOI 10.1136/thx.2004.013326; Ernst P, 2000, AM J RESP CRIT CARE, V161, P1563; 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; GOTO H, 1994, AM J IND MED, V25, P81, DOI 10.1002/ajim.4700250121; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Leynaert B, 2001, AM J RESP CRIT CARE, V164, P1829; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; SAKURAI T, 1994, BIOL PHARM BULL, V17, P617; Schram D, 2005, ALLERGY, V60, P611, DOI 10.1111/j.1398-9995.2005.00748.x; STONE BA, 1992, CHEM BIOL 1 3BETAGLU; SUZUKI T, 1992, J PHARMACOBIO-DYNAM, V15, P277; van Strien RT, 2002, ENVIRON HEALTH PERSP, V110, pA693; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; ZHANG K, 1994, J CELL BIOCHEM, V56, P225, DOI 10.1002/jcb.240560217	31	97	99	1	12	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	OCT	2005	35	10					1272	1278		10.1111/j.1365-2222.2005.02339.x		7	Allergy; Immunology	Allergy; Immunology	976ZK	WOS:000232772000004	16238785	
J	Ersu, R; Arman, AR; Save, D; Karadag, B; Karakoc, F; Berkem, M; Dagli, E				Ersu, R; Arman, AR; Save, D; Karadag, B; Karakoc, F; Berkem, M; Dagli, E			Prevalence of snoring and symptoms of sleep-disordered breathing in primary school children in Istanbul	CHEST			English	Article						children; hyperactivity; passive smoke exposure; prevalence; snoring	APNEA SYNDROME; NOCTURNAL HYPOXEMIA; PRESCHOOL-CHILDREN; PERFORMANCE; DISTURBANCE; ASSOCIATION; BEHAVIOR; SMOKING	Study objectives: Snoring during sleep is an important manifestation of obstructive sleep apnea syndrome (OSAS). Although clinical history is not sufficiently sensitive and specific to distinguish primary snoring from OSAS, snoring is indicative of upper airway obstruction and may be associated with the presence of diurnal symptoms. Our study aims were to determine the prevalence of snoring in primary school children in Istanbul, and to evaluate the diurnal symptoms and conditions that may be associated with sleep problems. Design, setting, and subjects: A parental questionnaire was used to assess the sleep and wake behavioral patterns in children. Eight representative schools in each of 9 school districts randomly selected from the 32 school districts in Istanbul were visited. Results: The response rate was 78.1%; 2,147 of 2,746 questionnaires were fully completed, returned, and analyzed. The prevalence of habitual snoring was 7.0%. Habitual snorers had significantly more nighttime symptoms, such as observed apneas (odds ratio [OR], 16.9; 95% confidence interval [CI], 10.0 to 28.8; p < 0.0001), difficulty breathing (OR, 17.8; CI, 10.9 to 29.2; p < 0.0001), restless sleep, parasomnias, and nocturnal enuresis, compared to occasional and nonsnorers. There were also increased prevalence of daytime symptoms, such as falling asleep while watching television (OR, 1.8; CI, 0.9 to 3.7; p = 0.01) and in public places (OR, 2.1; CI, 1.2 to 3.8; p = 0.03), and hyperactivity (OR, 2.7; CI, 1.8 to 3.9; p < 0.0001). Exposure to cigarette smoke and the presence of asthma and hay fever increased the likelihood of habitual snoring. Children with a higher risk for OSAS (habitual snoring, apnea, and difficulty breathing during sleep) were also compared to nonsnorers. Although nighttime symptoms were more likely in the high-risk group, the risk of daytime symptoms increased as well. Conclusions: Habitual snoring is a significant problem for children and may be associated with diurnal symptoms. Exposure to cigarette smoke at home and the presence of asthma and hay fever increase the likelihood of habitual snoring.	Marmara Univ, Atkatlar Istanbul, Turkey	Ersu, R (reprint author), Selcuklar Sokak,Elvan Apartmani 26-12, Atkatlar Istanbul, Turkey.	rersu@yahoo.com					ALI NJ, 1993, ARCH DIS CHILD, V68, P360; BILIR N, 1997, SMOKING BEHAV ATTITU, P17; Blunden S, 2000, J CLIN EXP NEUROPSYC, V22, P554, DOI 10.1076/1380-3395(200010)22:5;1-9;FT554; Brooks LJ, 2003, J PEDIATR-US, V142, P515, DOI 10.1067/mpd.2003.158; BROUILETTE R, 1984, J PEDIATR-US, V105, P10, DOI 10.1016/S0022-3476(84)80348-0; BROUILLETTE RT, 1982, J PEDIATR-US, V100, P31, DOI 10.1016/S0022-3476(82)80231-X; Brunetti L, 2001, CHEST, V120, P1930, DOI 10.1378/chest.120.6.1930; CARROLL JL, 1995, CHEST, V108, P610, DOI 10.1378/chest.108.3.610; Castronovo V, 2003, J PEDIATR-US, V142, P377, DOI 10.1067/mpd.2003.118; CORBO GM, 1989, BRIT MED J, V299, P1491; DELASNERIELAUPRETRE N, 1993, J SLEEP RES, V2, P138; Ferreira AM, 2000, PEDIATRICS, V106, DOI 10.1542/peds.106.5.e64; GISLASON T, 1995, CHEST, V107, P963, DOI 10.1378/chest.107.4.963; Goh DYT, 2000, AM J RESP CRIT CARE, V162, P682; Gozal D, 1998, PEDIATRICS, V102, P616, DOI 10.1542/peds.102.3.616; GUILLEMINAULT C, 1990, Pediatrician, V17, P46; HULTCRANTZ E, 1995, INT J PEDIATR OTORHI, V32, pS63, DOI 10.1016/0165-5876(94)01144-M; Larsson LG, 2003, CHEST, V124, P204, DOI 10.1378/chest.124.1.204; Lu LR, 2003, CHEST, V124, P587, DOI 10.1378/chest.124.2.587; Marcus CL, 2002, PEDIATRICS, V109, P704; MILLER AJ, 1982, AM J ORTHOD DENTOFAC, V81, P99, DOI 10.1016/0002-9416(82)90033-1; OWEN GO, 1995, CLIN OTOLARYNGOL, V20, P402, DOI 10.1111/j.1365-2273.1995.tb00070.x; Redline S, 1999, AM J RESP CRIT CARE, V159, P1527; Rosen CL, 1999, PEDIATR PULM, V27, P403, DOI 10.1002/(SICI)1099-0496(199906)27:6<403::AID-PPUL7>3.0.CO;2-8; STRADLING JR, 1990, LANCET, V335, P249, DOI 10.1016/0140-6736(90)90068-G; Strohl KP, 1996, AM J RESP CRIT CARE, V154, P279; TECULESCU DB, 1992, PEDIATR PULM, V13, P239, DOI 10.1002/ppul.1950130412; Urschitz MS, 2003, AM J RESP CRIT CARE, V168, P464, DOI 10.1164/rccm.200212-1397OC	28	97	100	1	14	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	JUL	2004	126	1					19	24		10.1378/chest.126.1.19		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	841XP	WOS:000222965900007	15249437	
J	Smith, KR; Mehta, S				Smith, KR; Mehta, S			The burden of disease from indoor air pollution in developing countries: comparison of estimates	INTERNATIONAL JOURNAL OF HYGIENE AND ENVIRONMENTAL HEALTH			English	Article						indoor air pollution; developing countries; household solid fuel use; risk assessment; global burden of disease	RESPIRATORY-INFECTIONS; DAILY MORTALITY; EXPOSURE; CHILDREN; HEALTH	Four different methods have been applied to estimate the burden of disease due to indoor air pollution from household solid fuel use in developing countries (LDCs). The largest number of estimates involves applying exposure-response information from urban ambient air pollution studies to estimate indoor exposure concentrations of particulate air pollution. Another approach is to construct child survival curves using the results of large-scale household surveys, as has been done for India. A third approach involves cross-national analyses of child survival and household fuel use. The fourth method, referred to as the 'fuel-based' approach, which is explored in more depth here, involves applying relative risk estimates from epidemiological studies that use exposure surrogates, such as fuel type, to estimates of household solid fuel use to determine population attributable fractions by disease and age group. With this method and conservative assumptions about relative risks, 4-5 percent of the global LDC totals for both deaths and DALYs (disability adjusted life years) from acute respiratory infections, chronic obstructive pulmonary disease, tuberculosis, asthma, lung cancer, ischaemic heart disease, and blindness can be attributed to solid fuel use in developing countries. Acute respiratory infections in children under five years of age are the largest single category of deaths (64%) and DALYs (81%) from indoor air pollution, apparently being responsible globally for about 1.2 million premature deaths annually in the early 1990s.	Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA	Smith, KR (reprint author), Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA.	krksmith@uclink.berkeley.edu					Bennett DH, 2002, ENVIRON SCI TECHNOL, V36, p206A, DOI 10.1021/es0222770; BLOOM D, 2000, INT C ENV OCC RESP D; Bloom D., 2002, QUALITY LIFE RURAL A; BRANDON C, 1995, C SUST FUT GLOB SYST; Bruce N, 2000, B WORLD HEALTH ORGAN, V78, P1078; COHEN AJ, 2003, IN PRESS COMP QUANTI; FLORIG HK, 1997, ENVIRON SCI TECHNOL, V31, pA276; Hong CJ, 1995, GLOBAL BURDEN DIS AI; HUGHES G, 2000, WHY BABIES YOUNG CHI; KUMAR P, 1997, DOWN EARTH, V6, P29; McMichael AJ, 1998, INT J EPIDEMIOL, V27, P450, DOI 10.1093/ije/27.3.450; Murray CJL, 1996, GLOBAL BURDEN DIS IN; Romieu I, 2002, J OCCUP ENVIRON MED, V44, P640, DOI 10.1097/01.jom.0000023383.41727.32; SAKSENA S, 1997, ENERGY ENV MONITOR, V13, P93; SCHWARTZ J, 1994, ENVIRON RES, V64, P36, DOI 10.1006/enrs.1994.1005; Schwela D, 1996, TOXICOL LETT, V86, P131, DOI 10.1016/0378-4274(96)03684-3; SINTON J, 1996, WHOEHG958; Smith KR, 2000, P NATL ACAD SCI USA, V97, P13286, DOI 10.1073/pnas.97.24.13286; Smith KR, 2000, THORAX, V55, P518, DOI 10.1136/thorax.55.6.518; SMITH KR, 1993, ANNU REV ENERG ENV, V18, P529, DOI 10.1146/annurev.energy.18.1.529; Smith K.R., 1988, ENVIRONMENT, V30, P10; Smith K.R., 2003, COMP QUANTIFICATION; SMITH KR, 1994, WORKSH EN ENV NEX IN; Smith K. R., 1987, BIOFUELS AIR POLLUTI; World Health Organization, 2002, WORLD HLTH REP RED R; *WHO, 1997, HTLH ENV SUST DEV; *WHO, 1979, ENV HLTH CRIT, V8; WHO, 1999, GLOB AIR QUAL GUID; World Health Organization, 2001, WORLD HLTH REP; *WORLD BANK, 1997, CLEAR WAT BLUE SKIES, P114	30	97	105	3	24	ELSEVIER GMBH, URBAN & FISCHER VERLAG	JENA	OFFICE JENA, P O BOX 100537, 07705 JENA, GERMANY	1438-4639			INT J HYG ENVIR HEAL	Int. J. Hyg. Environ. Health.	AUG	2003	206	4-5					279	289		10.1078/1438-4639-00224		11	Public, Environmental & Occupational Health; Infectious Diseases	Public, Environmental & Occupational Health; Infectious Diseases	716JD	WOS:000185024300004	12971683	
J	Delfino, RJ; Zeiger, RS; Seltzer, JM; Street, DH; McLaren, CE				Delfino, RJ; Zeiger, RS; Seltzer, JM; Street, DH; McLaren, CE			Association of asthma symptoms with peak particulate air pollution and effect modification by anti-inflammatory medication use	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; epidemiology; longitudinal data analysis; ozone; panel study; particulate air pollution	NITROGEN-DIOXIDE; INHALED ALLERGEN; SOUTHERN-CALIFORNIA; OZONE EXPOSURE; HOSPITAL ADMISSIONS; CHILDREN; RESPONSES; POLLUTANTS; EMERGENCY; MORTALITY	Maxima of hourly data from outdoor monitors may capture adverse effects of outdoor particulate matter (PM) exposures in asthmatic children better than do 24-hr PM averages, which form the basis of current regulations in the United States. Also, asthmatic children on anti-inflammatory medications may be protected against the proinflammatory effects of air pollutants and aeroallergens. We examined strengths of pollutant associations with asthma symptoms between subgroups of asthmatic children who were on versus not on regularly scheduled anti-inflammatory medications, and tested associations for different particle averaging times. This is a daily panel study of 22 asthmatic children (9-19 years of age) followed March through April 1996 (1,248 person-days). They lived in nonsmoking households in a semirural area of Southern California within the air inversion mixing zone (range, 1,200-2,100 feet) with transported air pollution from urban areas of Southern California. The dependent variable derived from diary ordinal scores is episodes of asthma symptoms that interfered with daily activities. Minimum to 90th-percentile levels of exposures at the outdoor monitoring site were 12-63 mug/m(3) for 1-hr PM < 10 mum in aerodynamic diameter (PM10); 8-46 mug/m(3) for 8-hr PM10; 7-32 mug/m(3) for 24-hr PM10; 45-88 ppb for 1-hr O-3; 6-26 ppb for 8-hr NO2; 70-4,714 particles/m(3) for 12-hr daytime fungi; and 12-744 particles/m(3) for 24-hr pollen. Data were analyzed with generalized estimating equations controlling for autocorrelation. There was no confounding by weather, day of week, or linear time trend. Associations were notably stronger in 12 asthmatic children who were not taking anti-inflammatory medications versus 10 subjects who were. Odds ratios (95% confidence intervals) for asthma episodes in relation to lag 0 minimum to 90th-percentile pollutant changes were, respectively, 1-hr maximum PM10, 1.92 (1.22-3.02) versus 0.96 (0.25-3.69); 8-hr maximum PM10, 1.68 (0.91-3.09) versus 0.75 (0.18-3.04); 24-hr average PM10, 1.35 (0.82-2.22) versus 0.80 (0.24-2.69); 1-hr maximum O-3, 1.28 (0.75-2.17) versus 0.76 (0.24-2.44); 8-hr maximum NO2, 1.91 (1.07-3.39) versus 1.08 (0.30-3.93); 12-hr fungi, 1.89 (1.24-2.89) versus 0.90 (0.35-2.30); 24-hr pollen, 1.90 (0.99-3.67) versus 0.85 (0.18-3.91). Pollutant associations were stronger during respiratory infections in subjects not on anti-inflammatory medications. Although lag 0 1-hr maximum PM10 showed the strongest association, the most robust associations were for lag 0 and 3-day moving averages (lags 0-2) of 8-hr maximum and 24-hr mean PM10 in sensitivity analyses testing for thresholds. Most pollutant effects were largely driven by concentrations in the upper quintile. The divergence of exposure-response relationships by anti-inflammatory medication use is consistent with experimental data on inflammatory mechanisms of airborne pollutants and allergens.	Univ Calif Irvine, Div Epidemiol, Dept Med, Coll Med, Irvine, CA 92697 USA; Univ Calif San Diego, Dept Pediat, Sch Med, La Jolla, CA 92093 USA; So Calif Permanente Med Grp, Dept Allergy, San Diego, CA 92120 USA; Indoor Hyg Technol Corp, Rancho Santa Fe, CA USA; Hollistier Stier Labs LLC, Allergy Prod, Independence, OR USA	Delfino, RJ (reprint author), Univ Calif Irvine, Div Epidemiol, Dept Med, Coll Med, 224 Irvine Hall, Irvine, CA 92697 USA.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	NIEHS NIH HHS [ES06214]		Allen G, 1997, J AIR WASTE MANAGE, V47, P682; Anderson HR, 1998, THORAX, V53, P842; Balmes J. 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Health Perspect.	OCT	2002	110	10					A607	A617				11	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	600VE	WOS:000178411800042	12361942	
J	Ghaemmaghami, AM; Gough, L; Sewell, HF; Shakib, F				Ghaemmaghami, AM; Gough, L; Sewell, HF; Shakib, F			The proteolytic activity of the major dust mite allergen Der p 1 conditions dendritic cells to produce less interleukin-12: allergen-induced Th2 bias determined at the dendritic cell level	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergen; dendritic cells; Der p 1; Th1/Th2	CYSTEINE PROTEASE ACTIVITY; T-HELPER CELL; FLOW-CYTOMETRY; ANTIGEN; DER-P-1; IL-12; LYMPHOCYTES; CAPACITY; CYTOKINE; REQUIRES	Background The proteolytic activity of the house dust mite allergen Der p 1 has recently been shown to bias Th cell subset development in favour of Th2. Apart from its direct effect on T cells, it is conceivable that the proteolytic activity of Der p 1 may induce the generation of dendritic cells (DCs) that favour a Th2 response. Objective To study the effect of the proteolytic activity of Der p 1 on DC functions; namely cell surface phenotype, IL-12 production and ability to favour a Th2 response. Methods We have generated immature DCs from peripheral blood monocytes, matured them with LPS in the presence of either proteolytically active or inactive Der p 1 and compared their functions using flow cytometric analysis. Results Here we demonstrate for the first time that DCs that have been matured in the presence of proteolytically active Der p 1 produce significantly less IL-12, compared to DCs that have been matured in the presence of proteolytically inactive Der p 1. The suppression of IL-12 production was due to the cleavage of CD40 by the proteolytic activity of Der p 1, hence rendering the DCs less responsive to stimulation through the CD40L-CD40 pathway. Furthermore, we demonstrate that DCs that have been matured in the presence of proteolytically active Der p 1 induce the production of significantly less IFN-gamma and more IL-4 by CD4 T cells, compared to DCs that have been matured in the presence of proteolytically inactive Der p 1. Conclusions Collectively, our data provide compelling evidence for the role of the proteolytic activity of Der p 1 in directing DCs to induce Th2 subset development.	Univ Nottingham, Queens Med Ctr, Fac Med & Hlth Sci, Div Mol & Clin Immunol, Nottingham NG7 2UH, England	Shakib, F (reprint author), Univ Nottingham, Queens Med Ctr, Fac Med & Hlth Sci, Div Mol & Clin Immunol, Nottingham NG7 2UH, England.			Fairclough, Lucy/0000-0003-4581-9741			Abbas AK, 1996, NATURE, V383, P787, DOI 10.1038/383787a0; Bell D, 1999, ADV IMMUNOL, V72, P255, DOI 10.1016/S0065-2776(08)60023-1; Cella M, 1996, J EXP MED, V184, P747, DOI 10.1084/jem.184.2.747; Gately MK, 1998, ANNU REV IMMUNOL, V16, P495, DOI 10.1146/annurev.immunol.16.1.495; Ghaemmaghami AM, 2001, EUR J IMMUNOL, V31, P1211, DOI 10.1002/1521-4141(200104)31:4<1211::AID-IMMU1211>3.0.CO;2-R; Gough L, 1999, J EXP MED, V190, P1897, DOI 10.1084/jem.190.12.1897; Grunvald E, 1996, INFECT IMMUN, V64, P2010; Kalinski P, 1999, IMMUNOL TODAY, V20, P561, DOI 10.1016/S0167-5699(99)01547-9; Kalinski P, 1998, J IMMUNOL, V161, P2804; Mascher B, 1999, J IMMUNOL METHODS, V223, P115, DOI 10.1016/S0022-1759(98)00200-2; O'Garra A, 1998, IMMUNITY, V8, P275, DOI 10.1016/S1074-7613(00)80533-6; Ohshima Y, 1997, J IMMUNOL, V158, P629; PORCELLI S, 1992, NATURE, V360, P593, DOI 10.1038/360593a0; Prussin C, 1995, J IMMUNOL METHODS, V188, P117, DOI 10.1016/0022-1759(95)00209-X; Reis E Sousa Caetano, 1997, Journal of Experimental Medicine, V186, P1819; Rissoan MC, 1999, SCIENCE, V283, P1183, DOI 10.1126/science.283.5405.1183; SALLUSTO F, 1994, J EXP MED, V179, P1109, DOI 10.1084/jem.179.4.1109; Schulz O, 2000, IMMUNITY, V13, P453, DOI 10.1016/S1074-7613(00)00045-5; Schulz O, 1998, J EXP MED, V187, P271, DOI 10.1084/jem.187.2.271; Schulz O, 1998, J CLIN PATHOL-MOL PA, V51, P222; SUTTON BJ, 1993, NATURE, V366, P421, DOI 10.1038/366421a0; TOVEY ER, 1981, NATURE, V289, P592, DOI 10.1038/289592a0; Trinchieri G, 1998, ADV IMMUNOL, V70, P83, DOI 10.1016/S0065-2776(08)60387-9; Vieira PL, 2000, J IMMUNOL, V164, P4507	24	97	99	0	3	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	OCT	2002	32	10					1468	1475		10.1046/j.1365-2745.2002.01504.x		8	Allergy; Immunology	Allergy; Immunology	601ZJ	WOS:000178479300014	12372127	
J	Jakob, T; Ring, J; Udey, MC				Jakob, T; Ring, J; Udey, MC			Multistep navigation of Langerhans/dendritic cells in and out of the skin	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Langerhans cells; dendritic cells; migration-trafficking; adhesion; chemokines; skin; allergy; immune regulation	HUMAN PERIPHERAL-BLOOD; CPG-CONTAINING OLIGODEOXYNUCLEOTIDES; INFLAMMATORY PROTEIN 3-ALPHA; CADHERIN-MEDIATED ADHESION; CUTANEOUS DENDRITIC CELLS; NECROSIS-FACTOR-ALPHA; DRAINING LYMPH-NODES; CONTACT HYPERSENSITIVITY; CHEMOKINE RECEPTORS; TH1 RESPONSES	Langerhans cells (LCs) are specialized antigen-presenting cells that reside in the epidermis as sentinels of the immune system. LCs constantly monitor the epidermal microenvironment by taking up antigen and processing it into fragments that can be recognized by cells of the adaptive immune response. Because of their unique migratory ability, LCs can transport antigen from the epidermis to regional lymph nodes, where they can initiate systemic immune responses. The mechanisms of LC trafficking thus seem to be of particular relevance for the induction and maintenance of cutaneous immunity. LCs or their putative precursors express surface molecules that allow them to home to skin and localize in the epidermis for prolonged periods of time. Tissue injury, microbial infection, and other perturbants of epidermal homeostasis (eg, contact allergens) provide danger signals, leading to a local production of proinflammatory cytokines that induce LC mobilization to the lymphoid tissue. At the same time, signals are generated that recruit LC precursors into the skin to maintain the epidermal LC population. Distinct pairs of chemokines and their receptors control the migration from blood to epidermis and from there to the regional lymphatics. In addition, trafficking is controlled at the level of cell adhesion, where LCs downregulate some adhesion molecules to exit the epidermis and upregulate others to migrate across the extracellular matrix and home to T-cell areas of regional lymphoid tissue. The improved understanding of mechanisms that regulate LC trafficking might offer new opportunities for therapeutic interventions to suppress, stimulate, or deviate cutaneous immune responses.	Tech Univ Munich, Dept Dermatol & Allergy Biederstein, Div Environm Dermatol & Allergy GSF TUM, D-80802 Munich, Germany; GSF, Natl Res Ctr Environm & Hlth, Div Environm Dermatol & Allergy GSF TUM, Neuherberg, Germany; NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA	Jakob, T (reprint author), Tech Univ Munich, Dept Dermatol & Allergy Biederstein, Div Environm Dermatol & Allergy GSF TUM, Biedersteiner Str 29, D-80802 Munich, Germany.		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Allergy Clin. Immunol.	NOV	2001	108	5					688	696				9	Allergy; Immunology	Allergy; Immunology	498RG	WOS:000172523800005	11692090	
J	Rahman, I; Mulier, B; Gilmour, PS; Watchorn, T; Donaldson, K; Jeffery, PK; MacNee, W				Rahman, I; Mulier, B; Gilmour, PS; Watchorn, T; Donaldson, K; Jeffery, PK; MacNee, W			Oxidant-mediated lung epithelial cell tolerance: the role of intracellular glutathione and nuclear factor-kappaB	BIOCHEMICAL PHARMACOLOGY			English	Article						GSH; NF-kappa B; hyperoxia; tolerance; 16HBE; A549	NECROSIS-FACTOR-ALPHA; TRANSCRIPTION FACTOR; SIGNAL-TRANSDUCTION; INDUCED APOPTOSIS; OXIDATIVE STRESS; B ACTIVATION; INFLAMMATION; ASTHMA; INTERLEUKIN-8; DEXAMETHASONE	The airway epithelium is injured by oxidants inhaled as atmospheric pollutants or produced during inflammatory responses. We studied the effect of modulating the antioxidant intracellular glutathione, both using thiol compounds and by the adaptive effect of hyperoxia, on oxidant-induced injury and activation of the nuclear factor-kappaB (NF-kappaB) in two cell lines: the human bronchial (16HBE) and type II alveolar epithelial cells (A549). The thiol antioxidants glutathione (GSH) and glutathione monoethyl ester (GSH-MEE) [2 mM] increased GSH levels (nmol/mg protein) in A549 cells (GSH 383 +/- 26 and GSH-MEE 336 +/- 23 vs control 171 +/- 13, P < 0.001) and in 16HBE cells (GSH 405 +/- 33, GSH-MEE 362 +/- 37 vs control 198 +/- 12, P < 0.001, N = 3). Treatment of hyperoxia (95% oxygen) also increased GSH levels between 4 and 24 hr exposure compared with control (P < 0.01). Hydrogen peroxide (H2O2) (0.01 mM) induced NF-kappaB activation, whereas hyperoxia exposure did not affect NF-kappaB activation in either cell line. Pretreatment with DL-buthionine (SR)sulfoximine, which decreased intracellular glutathione, increased NF-kappaB binding induced by H2O2 and increased lactate dehydrogenase (LDH) release (P < 0.001). Pretreatment with the thiol compounds and hyperoxia totally inhibited H2O2-induced NF-kappaB binding and cell injury as measured by LDH release. These data indicate the importance of intracellular glutathione and inhibition of NF-kappaB in both protection/tolerance against oxidant-induced epithelial cell injury, and NF-kappaB activation in response to oxidative stress which may be important in lung inflammation. Thus, increasing intracellular glutathione may be of therapeutic relevance if able to modulate NF-kappaB activation and hence attenuate inflammation. (C) 2001 Elsevier Science Inc. All rights reserved.	Univ Edinburgh, Sch Med, Resp Med Unit, ELEGI & Colt Res Lab, Edinburgh EH8 9AG, Midlothian, Scotland; Univ London, Natl Lung & Heart Inst, Lung Pathol Unit, London, England; Napier Univ, Dept Biol Sci, Edinburgh EH14 1DJ, Midlothian, Scotland	Rahman, I (reprint author), Univ Edinburgh, Sch Med, Resp Med Unit, ELEGI & Colt Res Lab, Wilkie Bldg,Teviot Pl, Edinburgh EH8 9AG, Midlothian, Scotland.						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Pharmacol.	SEP 15	2001	62	6					787	794		10.1016/S0006-2952(01)00702-X		8	Pharmacology & Pharmacy	Pharmacology & Pharmacy	463HB	WOS:000170470100016	11551525	
J	Kamps, AWA; Roorda, RJ; Brand, PLP				Kamps, AWA; Roorda, RJ; Brand, PLP			Peak flow diaries in childhood asthma are unreliable	THORAX			English	Article						asthma; children; home monitoring; peak expiratory flow; compliance	HOME MANAGEMENT; INNER-CITY; CHILDREN	Background-A study was undertaken to investigate the compliance with and accuracy of peak flow diaries in childhood asthma. Methods-Forty asthmatic children (5-16 years) were asked to perform peak flow measurements twice daily for 4 weeks by means of an electronic peak flow meter and to record values in a written diary. Patients and parents were unaware that the device stored the peak flow values on a microchip. In random order, half of the patients were only told that the device allowed for more accurate assessment of peak flow while the other half were told that accurate recording of peak flow was important because the results would be used in guiding adjustments to treatment. Data in the written diary (reported data) were compared with those from the electronic diary tactual data). Results-In the entire study population the mean (SD) actual compliance (77.1 (20.5)%) was much lower than the mean reported compliance (95.7 (9.1)%) (95% CI for difference 12.7% to 24.4%) The percentage of correct peak flow entries decreased from 56% to <50% from the first to the last study week (p<0.04), mainly as a result of an increase in self-invented peak flow entries. Results were comparable for both groups. For incorrect peak flow entries the mean difference between written and electronically recorded entries ranged from -72 to 34 l/min per patient. Conclusions-Peak how diaries kept by asthmatic children are unreliable. Electronic peak flow meters should be used if peak how monitoring is required in children with asthma.	Weezenlanden Hosp, Isala Klinieken, Dept Paediat, Div Pulm, NL-8000 GM Zwolle, Netherlands	Brand, PLP (reprint author), Weezenlanden Hosp, Isala Klinieken, Dept Paediat, Div Pulm, POB 10500, NL-8000 GM Zwolle, Netherlands.						British Thoracic Society, 1997, THORAX S1, V52, pS1, DOI DOI 10.1136/THX.52.2008.S1]; CHARLTON I, 1994, ARCH DIS CHILD, V70, P313; Cote J, 1998, CHEST, V113, P968, DOI 10.1378/chest.113.4.968; Eggleston PA, 1998, PEDIATRICS, V101, P349, DOI 10.1542/peds.101.3.349; HYLAND ME, 1993, BRIT MED J, V306, P487; Madge P, 1997, THORAX, V52, P223; MALO JL, 1995, J ALLERGY CLIN IMMUN, V96, P601, DOI 10.1016/S0091-6749(95)70258-X; Redline S, 1996, PEDIATR PULM, V21, P203; SHEFFER AL, 1992, EUR RESPIR J, V5, P601; Verschelden P, 1996, EUR RESPIR J, V9, P880, DOI 10.1183/09031936.96.09050880	10	97	98	1	4	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	MAR	2001	56	3					180	182		10.1136/thorax.56.3.180		3	Respiratory System	Respiratory System	406WL	WOS:000167239100006	11182008	
J	Linneberg, A; Nielsen, NH; Madsen, F; Frolund, L; Dirksen, A; Jorgensen, T				Linneberg, A; Nielsen, NH; Madsen, F; Frolund, L; Dirksen, A; Jorgensen, T			Increasing prevalence of specific IgE to aeroallergens in an adult population: Two cross-sectional surveys 8 years apart - The Copenhagen Allergy Study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						adult; epidemiology; prevalence; respiratory hypersensitivity; specific IgE positivity; specific IgE stability	SKIN-TEST REACTIVITY; CHANGING PREVALENCE; DANISH POPULATION; HAY-FEVER; RHINITIS; ASTHMA; CHILDREN; ANTIBODIES; DIAGNOSIS; SYMPTOMS	Background: There is evidence that the prevalence of respiratory allergy has increased in children in many countries. However, this evidence is largely based on questionnaire data, and little is known about similar trends in adults. Objective: We investigated whether the prevalence of specific IgE to aeroallergens had increased in an adult general population over an 8-year period. Methods: Two cross-sectional surveys were carried out in 1990 and 1998, A mailed screening questionnaire on respiratory symptoms sent to random samples of 15- to 41-year-old subjects living in Copenhagen (Denmark) preceded both surveys. Random samples of responders were invited to a health examination, including assessment of specific IgE to 6 common aeroallergens. Totals of 312 (74.6% of the invited subjects) and 482 (53.4% of the invited subjects) subjects were examined in 1990 and 1998, respectively, Analyses of serum samples from both surveys were performed in 1999, Results: The prevalence of specific IgE to at least one allergen increased significantly from 1990 to 1998 (26.5% vs 33.9%; odds ratio adjusted for sex, age, and season of examination, 1.63; 95% confidence interval, 1.15-2.32; P = .006), This increase remained unexplained after adjustment for changes in questionnaire variables on lifestyle and home environment, The clinical significance of this increase was underlined by a corresponding increase in the prevalence of allergic rhinitis symptoms associated with specific IgE positivity, Conclusion: We found that the prevalence of specific IgE positivity to aeroallergens increased in an adult Danish general population from 1990 and 1998.	Glostrup Hosp, Ctr Prevent Med, Dept Internal Med M, DK-2600 Glostrup, Denmark; Gentofte Hosp, Dept Dermatol, Gentofte, Denmark; Frederiksberg Hosp, Dept Internal Med B, Frederiksberg, Denmark; Bispebjerg Hosp, Clin Unit Prevent Med & Hlth Promot, Bispebjerg, Denmark; Univ Copenhagen, Rigshosp, Dept Resp Med, DK-2100 Copenhagen, Denmark	Linneberg, A (reprint author), Glostrup Hosp, Ctr Prevent Med, Dept Internal Med M, 57 Ndr Ringvej,Entrance 8,7th Floor, DK-2600 Glostrup, Denmark.			Jorgensen, Torben/0000-0001-9453-2830; Linneberg, Allan/0000-0002-0994-0184			Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; BLAND JM, 1986, LANCET, V1, P307; 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; Butland BK, 1997, BRIT MED J, V315, P717; Crobach MJJS, 1998, SCAND J PRIM HEALTH, V16, P30; Droste JHJ, 1996, J ALLERGY CLIN IMMUN, V97, P922, DOI 10.1016/S0091-6749(96)80066-2; Henderson CE, 1998, J IMMUNOL METHODS, V213, P99, DOI 10.1016/S0022-1759(98)00014-3; Johansen N., 1998, Allergy (Copenhagen), V53, P193; Linneberg A, 1999, ALLERGY, V54, P1194, DOI 10.1034/j.1398-9995.1999.00180.x; Magnus P, 1997, BRIT MED J, V314, P1795; Mygind N, 1996, PEDIATR ALLERGY IMMU, V7, P57, DOI 10.1111/j.1399-3038.1996.tb00397.x; NAKAGOMI T, 1994, LANCET, V343, P121, DOI 10.1016/S0140-6736(94)90854-0; NIELSEN NH, 1994, ALLERGY, V49, P86, DOI 10.1111/j.1398-9995.1994.tb00805.x; 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, 1994, BRIT MED J, V308, P1591; Sly RM, 1999, ANN ALLERG ASTHMA IM, V82, P233, DOI 10.1016/S1081-1206(10)62603-8; von Mutius E, 1998, LANCET, V351, P862, DOI 10.1016/S0140-6736(97)10100-3; Von Mutius E, 1998, CLIN EXP ALLERGY, V28, P45	20	97	98	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.	AUG	2000	106	2					247	252		10.1067/mai.2000.108312		6	Allergy; Immunology	Allergy; Immunology	343NH	WOS:000088708100005	10932066	
J	Rodrigo, CJ; Rodrigo, C				Rodrigo, CJ; Rodrigo, C			First-line therapy for adult patients with acute asthma receiving a multiple-bose protocol of ipratropium bromide plus albuterol in the emergency department	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							AIR-FLOW OBSTRUCTION; NEBULIZED IPRATROPIUM; SALBUTAMOL; CHILDREN; METAANALYSIS; MANAGEMENT; EFFICACY; BRONCHODILATOR; CHILDHOOD; AGONISTS	We designed a larger, double-blind, randomized, prospective trial to test our hypothesis that patients with acute asthma given combination high dose therapy with ipratropium bromide (IB) and beta(2)-agonists will have greater improvement in pulmonary function and fewer hospital admissions than those given beta(2)-agonists alone. One hundred eighty patients (mean age +/- SD, 34.3 +/- 10.5 yr) who presented to an emergency department (ED) for treatment of an exacerbation of asthma (baseline FEV1 < 50% of predicted) were assigned in a randomized, double-blind fashion to receive albuterol and placebo (n = 92) or albuterol and IB (n = 88). Both drugs were administered through a metered-dose inhaler and spacer at 10-min intervals for 3 h (24 puffs or 2,880 mu g of albuterol and 504 mu g of IB each hour). Primary outcome measures were improvement in pulmonary function (FEV1 or peak expiratory flow [PEF]), and hospital admission rates. In both groups, pulmonary function improved significantly over baseline values (p < 0.01). Subjects who received IB had an overall 20.5% (95% CI: 2.6 to 38.4%) (p = 0.02) greater improvement in PEF and a 48.1% (95% CI: 19.8 to 76.4%) (p = 0.001) greater improvement in FEV1 from the control group. At the end of protocol (3 h), 39% (n = 36) of patients in the control group and 20% (n = 18) in the IB group were admitted (p = 0.01). The use of high doses of is reduced the risk of hospital admission 49% (relative risk = 0.51, 95% CI: 0.31 to 0.83). Five (95% CI: 3 to 17) patients would need to be treated with high doses of IB to prevent a single admission. Kaplan-Meier-estimated curves of the proportion of patients who reached the discharge threshold during the 3 h of treatment, showed a significant difference in favor of the IB group (log-rank test = 0.005). A subgroup analysis showed that patients most likely to benefit from the addition of high doses of IB were those with more severe obstruction (FEV1 less than or equal to 30% of predicted) and long duration of symptoms before the ED presentation (greater than or equal to 24 h). On the contrary, previous use of inhaled beta(2)-agonists did not modify the admission rate and the pulmonary function response to IB. In conclusion, our data support a substantial therapeutic benefit from the addition of IB to albuterol administered in high doses through MDI plus spacer, particularly in patients with FEV1 less than 30%, and with long duration of symptoms before the ED presentation (greater than or equal to 24 h).	Hosp Cent FF AA, Dept Emergencia, Montevideo 11600, Uruguay; Asociac Espanola 1 Socorros Mutuos, Unidad Cuidado Intens, Montevideo, Uruguay	Rodrigo, CJ (reprint author), Hosp Cent FF AA, Dept Emergencia, Av 8 Octubre 3020, Montevideo 11600, Uruguay.						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J. Respir. Crit. Care Med.	JUN	2000	161	6					1862	1868				7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	325KV	WOS:000087675500021		
S	Broeckaert, F; Clippe, A; Knoops, B; Hermans, C; Bernard, A		Mukherjee, AB; Chilton, BS		Broeckaert, F; Clippe, A; Knoops, B; Hermans, C; Bernard, A			Clara cell secretory protein (CC16): Features as a peripheral lung biomarker	UTEROGLOBIN/CLARA CELL PROTEIN FAMILY	ANNALS OF THE NEW YORK ACADEMY OF SCIENCES		English	Article; Proceedings Paper	Conference on Uteroglobin/Calra Cell Protein Family	APR 14-16, 2000	BETHESDA, MARYLAND	NICHHD, NHLBI, New York Acad Sci			BRONCHOALVEOLAR LAVAGE; BIOLOGICAL-FLUIDS; 10-KDA PROTEIN; SERUM LEVELS; ASTHMA; EPITHELIUM; PERMEABILITY; POLYMORPHISM; UTEROGLOBIN; MARKER	Clara cell protein (CC16 or CC10) is a 15.8-kDa protein secreted all along the tracheobronchial tree and especially in the terminal bronchioles where Clara cells are localized. Even though the exact in vivo function of CC16 remains to be clarified, evidence is accumulating that CC16 plays an important protective role in the respiratory tract against oxidative stress and inflammatory response. CC16, however, presents also a major interest as a peripheral lung marker for assessing the cellular integrity or the permeability of the lung epithelium. The serum concentrations of CC16 are decreased in subjects with chronic lung damage caused by tobacco smoke and other air pollutants as a consequence of the destruction of Clara cells. By contrast, serum CC16 in. creases in acute or chronic lung disorders characterized by an increased airways permeability. The sensitivity of serum CC16 to an increased leakiness of the lung allows for the detection of defects of the epithelial barrier at ozone levels below current air-quality guidelines. Although the clinical significance of these early epithelial changes detected by serum CC16 remains to be determined, these results clearly show that the assay in serum of lung secretory proteins such as CC16 represents a new noninvasive approach to evaluate the integrity of the respiratory tract.	Univ Catholique Louvain, Sch Publ Hlth, Fac Med, Ind Toxicol & Occupat Med Unit, B-1200 Brussels, Belgium	Bernard, A (reprint author), Univ Catholique Louvain, Sch Publ Hlth, Fac Med, Ind Toxicol & Occupat Med Unit, 30-54 Clos Chapelle Champs, B-1200 Brussels, Belgium.		BERNARD, Alfred/A-6511-2010	BERNARD, Alfred/0000-0003-3171-3743			Arsalane K, 2000, AM J RESP CRIT CARE, V161, P1624; Arsalane K, 1999, TOXICOL APPL PHARM, V159, P169, DOI 10.1006/taap.1999.8738; BERNARD A, 1994, PEDIATR RES, V36, P771, DOI 10.1203/00006450-199412000-00015; BERNARD A, 1992, EUR RESPIR J, V5, P1231; BERNARD A, 1993, CLIN CHIM ACTA, V223, P189, DOI 10.1016/0009-8981(93)90077-H; Bernard A, 1997, OCCUP ENVIRON MED, V54, P63; BERNARD A, 1998, BIOMARKERS MED WORKP, P273; Buchet JP, 1993, ENVIRON RES, V66, P96; Bernard A M, 1994, Kidney Int Suppl, V47, pS34; BERNARD AM, 1994, EUR RESPIR J, V7, P1932; Broeckaert F, 2000, ENVIRON HEALTH PERSP, V108, P533, DOI 10.2307/3454615; Broeckaert F, 2000, CLIN EXP ALLERGY, V30, P469; DODGE DE, 1993, J HISTOCHEM CYTOCHEM, V41, P1171; FLOPPER CG, 1997, LUNG, P517; Halatek T, 1998, EUR RESPIR J, V11, P726; Hermans C, 1999, AM J RESP CRIT CARE, V159, P646; Hermans C, 1998, EUR RESPIR J, V11, P801, DOI 10.1183/09031936.98.11040801; Hermans C, 1999, EUR RESPIR J, V13, P1014, DOI 10.1034/j.1399-3003.1999.13e14.x; JACKSON PJ, 1988, J CHROMATOGR, V452, P359, DOI 10.1016/S0021-9673(01)81460-6; JENSEN SM, 1994, INT J CANCER, V58, P629, DOI 10.1002/ijc.2910580503; KABANDA A, 1995, KIDNEY INT, V48, P1946, DOI 10.1038/ki.1995.495; Laing IA, 1998, J MED GENET, V35, P463, DOI 10.1136/jmg.35.6.463; Laing IA, 2000, AM J RESP CRIT CARE, V161, P124; NIETO A, 1982, COMP BIOCHEM PHYS B, V71, P511, DOI 10.1016/0305-0491(82)90417-5; Shijubo N, 1997, EUR RESPIR J, V10, P1108, DOI 10.1183/09031936.97.10051108; Shijubo N, 1999, LUNG, V177, P45, DOI 10.1007/PL00007626; SINGH G, 1988, J HISTOCHEM CYTOCHEM, V36, P73; Stripp BR, 1995, AM J PHYSIOL-LUNG C, V269, pL791; VANVYVE T, 1995, J ALLERGY CLIN IMMUN, V95, P60, DOI 10.1016/S0091-6749(95)70153-2	29	97	101	0	6	NEW YORK ACAD SCIENCES	NEW YORK	2 EAST 63RD ST, NEW YORK, NY 10021 USA	0077-8923		1-57331-293-2	ANN NY ACAD SCI	Ann.NY Acad.Sci.		2000	923						68	77				10	Biochemistry & Molecular Biology; Multidisciplinary Sciences	Biochemistry & Molecular Biology; Science & Technology - Other Topics	BT10P	WOS:000171966400006	11193780	
J	Lange, P; Celli, B; Agusti, A; Jensen, GB; Divo, M; Faner, R; Guerra, S; Marott, JL; Martinez, FD; Martinez-Camblor, P; Meek, P; Owen, CA; Petersen, H; Pinto-Plata, V; Schnohr, P; Sood, A; Soriano, JB; Tesfaigzi, Y; Vestbo, J				Lange, Peter; Celli, Bartolome; Agusti, Alvar; Jensen, Gorm Boje; Divo, Miguel; Faner, Rosa; Guerra, Stefano; Marott, Jacob Louis; Martinez, Fernando D.; Martinez-Camblor, Pablo; Meek, Paula; Owen, Caroline A.; Petersen, Hans; Pinto-Plata, Victor; Schnohr, Peter; Sood, Akshay; Soriano, Joan B.; Tesfaigzi, Yohannes; Vestbo, Jorgen			Lung-Function Trajectories Leading to Chronic Obstructive Pulmonary Disease	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							AIR-FLOW OBSTRUCTION; FORCED EXPIRATORY VOLUME; FUNCTION DECLINE; NATURAL-HISTORY; INHALED BUDESONIDE; CHILDHOOD ASTHMA; CONTROLLED-TRIAL; COHORT; COPD; SMOKING	BACKGROUND Chronic obstructive pulmonary disease (COPD) is thought to result from an accelerated decline in forced expiratory volume in 1 second (FEV1) over time. Yet it is possible that a normal decline in FEV1 could also lead to COPD in persons whose maximally attained FEV1 is less than population norms. METHODS We stratified participants in three independent cohorts (the Framingham Offspring Cohort, the Copenhagen City Heart Study, and the Lovelace Smokers Cohort) according to lung function (FEV1 >= 80% or <80% of the predicted value) at cohort inception (mean age of patients, approximately 40 years) and the presence or absence of COPD at the last study visit. We then determined the rate of decline in FEV1 over time among the participants according to their FEV1 at cohort inception and COPD status at study end. RESULTS Among 657 persons who had an FEV1 of less than 80% of the predicted value before 40 years of age, 174 (26%) had COPD after 22 years of observation, whereas among 2207 persons who had a baseline FEV1 of at least 80% of the predicted value before 40 years of age, 158 (7%) had COPD after 22 years of observation (P<0.001). Approximately half the 332 persons with COPD at the end of the observation period had had a normal FEV1 before 40 years of age and had a rapid decline in FEV1 thereafter, with a mean (+/- SD) decline of 53 +/- 21 ml per year. The remaining half had had a low FEV1 in early adulthood and a subsequent mean decline in FEV1 of 27 +/- 18 ml per year (P<0.001), despite similar smoking exposure. CONCLUSIONS Our study suggests that low FEV1 in early adulthood is important in the genesis of COPD and that accelerated decline in FEV1 is not an obligate feature of COPD. (Funded by an unrestricted grant from GlaxoSmithKline and others.)	[Lange, Peter] Univ Copenhagen, Inst Publ Hlth, Sect Social Med, DK-1014 Copenhagen K, Denmark; [Lange, Peter] Univ Copenhagen, Resp Sect, Hvidovre Hosp, DK-1014 Copenhagen K, Denmark; [Lange, Peter; Jensen, Gorm Boje; Marott, Jacob Louis; Schnohr, Peter] Univ Copenhagen, Copenhagen City Heart Study, Frederiksberg Hosp, DK-1014 Copenhagen K, Denmark; [Vestbo, Jorgen] Univ Copenhagen, Dept Resp Med, Gentofte Hosp, DK-1014 Copenhagen K, Denmark; [Jensen, Gorm Boje] Univ Southern Denmark, Odense, Denmark; [Celli, Bartolome; Divo, Miguel; Owen, Caroline A.; Pinto-Plata, Victor] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA; [Agusti, Alvar] Univ Barcelona, Inst Invest Biomed August Pi & Sunyer, Hosp Clin, Serv Pneumol,Thorax Inst, Barcelona, Spain; [Faner, Rosa] Fundacio Clin Recerca Biomed, Barcelona, Spain; [Agusti, Alvar; Faner, Rosa] Ctr Invest Biomed Red Enfermedades Resp, Madrid, Spain; [Soriano, Joan B.] Univ Autonoma Madrid, Catedra UAM Linde, Inst Invest Hosp Univ Princesa, Madrid, Spain; [Guerra, Stefano; Martinez, Fernando D.] Univ Arizona, Arizona Resp Ctr, Tucson, AZ USA; [Martinez-Camblor, Pablo] Univ Autonoma Chile, Santiago, Chile; [Meek, Paula] Univ Colorado, Denver, CO 80202 USA; [Petersen, Hans; Tesfaigzi, Yohannes] Lovelace Resp Res Inst, Albuquerque, NM USA; [Sood, Akshay] Univ New Mexico, Albuquerque, NM 87131 USA; [Vestbo, Jorgen] Univ Manchester, Manchester Acad Hlth Sci Ctr, Resp & Allergy Res Grp, Manchester, Lancs, England	Lange, P (reprint author), Univ Copenhagen, Inst Publ Hlth, Sect Social Med, POB 2099,Oster Farimagsgade 5, DK-1014 Copenhagen K, Denmark.	peter.lange@sund.ku.dk	Martinez-Camblor, Pablo/Q-1715-2015; SMIRE+CODIRE, Research Group /E-7657-2017	SMIRE+CODIRE, Research Group /0000-0002-8871-4942; Faner, Rosa/0000-0002-8159-0115	GlaxoSmithKline	Funded by an unrestricted grant from GlaxoSmithKline and others.	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Engl. J. Med.	JUL 9	2015	373	2					111	122		10.1056/NEJMoa1411532		12	Medicine, General & Internal	General & Internal Medicine	CM3QP	WOS:000357598600004	26154786	
J	Agache, I; Ciobanu, C; Agache, C; Anghel, M				Agache, Ioana; Ciobanu, Cristina; Agache, Costel; Anghel, Mariana			Increased serum IL-17 is an independent risk factor for severe asthma	RESPIRATORY MEDICINE			English	Article						IL-17; Severe asthma; Risk factors	C-REACTIVE PROTEIN; AIR-FLOW LIMITATION; CELLS; TH17; INFLAMMATION; SPUTUM	Background: IL-17 expression was found to be associated with many inflammatory diseases in humans, such as rheumatoid arthritis, asthma, systemic lupus erythematosus and allograft rejection and many in vitro studies have indicated a proinflammatory function for IL-17. Objective: Prognostic value of increased serum IL-17 in asthma patients. Methods: Serum IL-17 (ELISA) was measured in 85 asthma patients (pts), mean age 46.99 +/- 14.1 years, 61% females, 23 mild persistent, 26 moderate persistent and 36 severe persistent asthma. Using multiple regression analysis (STATISTICA 7), increased serum IL-17 (>20 pg/ml) was tested as risk factor for severe asthma in comparison with "traditional" risk factors: smoke, NSAID intolerance, obesity, chronic rhinosinusitis, blood eosinophilia, FEV(1) at baseline < 50% predicted (low FEV(1)). Results: Medium serum IL-17 values were 14.21 pg/ml in mild asthma, 12.22 pg/ml in moderate asthma and 24.72 pg/ml in severe asthma. IL-17 values > 20 pg/ml were encountered in 3(13%) mild asthma pts (p < 0.001 vs. severe asthma), 2(8%) moderate asthma pts. (p < 0.001 vs. severe asthma), and in 11(31%) severe asthma pts. For severe asthma multiple regression analysis revealed as independent risk factors IL-17 (p = 0.000290), NSAID intolerance (p = 0.000585) and low FEV(1) (p = 0.000059). Conclusions: IL-17 is increased in severe asthma compared to mild/moderate forms of the disease and values above 20 pg/ml are an independent risk factor for severe asthma. (C) 2010 Elsevier Ltd. All rights reserved.	[Agache, Ioana] Transylvania Univ, Fac Med, Dept Allergy & Clin Immunol, Brasov 500036, Romania; [Ciobanu, Cristina; Agache, Costel] Theramed Med Ctr, Dept Allergy & Clin Immunol, Brasov 500112, Romania; [Anghel, Mariana] Brasov Cty Hosp, Immunol Lab, Brasov 500326, Romania	Agache, I (reprint author), Spatarul Luca Arbore 16, Brasov 500112, Romania.	ibrumaru@unitbv.ro					Barczyk A, 2003, RESP MED, V97, P726, DOI 10.1053/rmed.2003.1507; Bullens DMA, 2006, RESP RES, V7, DOI 10.1186/1465-9921-7-135; Kaminska M, 2009, J ALLERGY CLIN IMMUN, V124, P45, DOI 10.1016/j.jaci.2009.03.049; Kasayama S, 2009, CLIN CHIM ACTA, V399, P79, DOI 10.1016/j.cca.2008.09.013; Laan M, 2001, BRIT J PHARMACOL, V133, P200, DOI 10.1038/sj.bjp.0704063; Lee JH, 2007, CHEST, V132, P1882, DOI 10.1378/chest.07-0713; Molet S, 2001, J ALLERGY CLIN IMMUN, V108, P430, DOI 10.1067/mai.2001.117929; Pene J, 2008, J IMMUNOL, V180, P7423; Qian FH, 2008, RESPIROLOGY, V13, P664, DOI 10.1111/j.1440-1843.2008.01314.x; Saito H, 2009, INT ARCH ALLERGY IMM, V149, P61, DOI 10.1159/000210656; Tato CM, 2006, NATURE, V441, P166, DOI 10.1038/441166a; ten Brinke A, 2001, AM J RESP CRIT CARE, V164, P744; Wakashin H, 2008, AM J RESP CRIT CARE, V178, P1023, DOI 10.1164/rccm.200801-086OC; Wong CK, 2001, CLIN EXP IMMUNOL, V125, P177, DOI 10.1046/j.1365-2249.2001.01602.x; Zietkowski Z, 2009, RESP MED, V103, P379, DOI 10.1016/j.rmed.2008.10.003	15	96	103	0	16	W B SAUNDERS CO LTD	LONDON	32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND	0954-6111			RESP MED	Respir. Med.	AUG	2010	104	8					1131	1137		10.1016/j.rmed.2010.02.018		7	Cardiac & Cardiovascular Systems; Respiratory System	Cardiovascular System & Cardiology; Respiratory System	629EX	WOS:000280178900006	20338742	
J	Olivry, T; DeBoer, DJ; Favrot, C; Jackson, HA; Mueller, RS; Nuttall, T; Prelaud, P				Olivry, Thierry; DeBoer, Douglas J.; Favrot, Claude; Jackson, Hilary A.; Mueller, Ralf S.; Nuttall, Tim; Prelaud, Pascal		Int Task Force Canine Atopic Derma	Treatment of canine atopic dermatitis: 2010 clinical practice guidelines from the International Task Force on Canine Atopic Dermatitis	VETERINARY DERMATOLOGY			English	Article							ALLERGEN-SPECIFIC IMMUNOTHERAPY; HOUSE-DUST MITES; TYPE-1 HYPERSENSITIVITY REACTIONS; ADVERSE FOOD REACTIONS; DOUBLE-BLIND; TACROLIMUS OINTMENT; HEALTHY DOGS; CONTROLLED-TRIAL; MALASSEZIA-PACHYDERMATIS; FLUTICASONE PROPIONATE	Atopic dermatitis (AD) is a common chronic relapsing pruritic skin disease of dogs for which treatment has varied over time and geographical location. Recent high quality randomized controlled trials and systematic reviews have established which drugs are likely to offer consistent benefit. The International Task Force for Canine AD currently recommends a multifaceted approach to treat dogs with AD. Acute flares should be treated with a combination of nonirritating baths and topical glucocorticoids, once an attempt has been made to identify and remove the suspected causes of the flare. Oral glucocorticoids and antimicrobial therapy must be added when needed. In dogs with chronic AD, a combination of interventions should be considered. Again, factors that trigger flares of AD must be identified and, if possible, avoided. Currently recognized flare factors include food, flea and environmental allergens, Staphylococcus bacteria and Malassezia yeast. Skin and coat hygiene and care must be improved by bathing with nonirritating shampoos and dietary supplementation with essential fatty acids. The severity of pruritus and skin lesions can be reduced with a combination of anti-inflammatory drugs. Currently, medications with good evidence of high efficacy include topical and oral glucocorticoids, and calcineurin inhibitors such as oral ciclosporin and topical tacrolimus. The dose and frequency of administration of these drugs should be tailored to each patient considering each drug's efficacy, adverse effects and cost. Allergen-specific immunotherapy should be offered, whenever feasible, in an attempt to prevent recurrence of clinical signs upon further exposure to environmental allergens to which the patient is hypersensitive.	[Olivry, Thierry] N Carolina State Univ, Coll Vet Med, Dept Clin Sci, Raleigh, NC 27606 USA; [Olivry, Thierry; Int Task Force Canine Atopic Derma] N Carolina State Univ, Coll Vet Med, Ctr Comparat Med & Translat Res, Raleigh, NC 27606 USA; [DeBoer, Douglas J.] Univ Wisconsin, Sch Vet Med, Dept Med Sci, Madison, WI 53706 USA; [Favrot, Claude] Univ Zurich, Vetsuisse Fac, Dept Dermatol, Clin Small Anim Internal Med, Zurich, Switzerland; [Jackson, Hilary A.] Dermatol Referral Serv, Glasgow, Lanark, Scotland; [Mueller, Ralf S.] Univ Munich, Med Klin, Munich, Germany; [Nuttall, Tim] Univ Liverpool, Sch Vet Sci, Small Anim Teaching Hosp, Neston, England; [Prelaud, Pascal] Clin Advetia, Paris, France	Olivry, T (reprint author), N Carolina State Univ, Coll Vet Med, Dept Clin Sci, Res Bldg,4700 Hillsborough St, Raleigh, NC 27606 USA.	thierry_olivry@ncsu.edu	Olivry, Thierry/E-3289-2013	Mueller, Ralf/0000-0001-5835-5910			Arlian LG, 2001, J ALLERGY CLIN IMMUN, V107, pS406, DOI 10.1067/mai.2001.113670; 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Dermatol.	JUN	2010	21	3					233	248		10.1111/j.1365-3164.2010.00889.x		16	Dermatology; Veterinary Sciences	Dermatology; Veterinary Sciences	596WF	WOS:000277715500001	20456716	
J	Bornehag, CG; Nanberg, E				Bornehag, C. G.; Nanberg, E.			Phthalate exposure and asthma in children	INTERNATIONAL JOURNAL OF ANDROLOGY			English	Article; Proceedings Paper	5th Copenhagen Workshop on Endocrine Disruptgers - Ubiquitous Endocrine Disrupters and Possible Human Health Effects	MAY 20-22, 2009	Copenhagen, DENMARK			asthma; endocrine disrupters; environmental factors; epidemiology; immunology	SUBCUTANEOUS INJECTION MODEL; ENDOCRINE-DISRUPTING CHEMICALS; IN-HOUSE DUST; DI-N-BUTYL; DI-(2-ETHYLHEXYL) PHTHALATE; BALB/C MICE; DI(2-ETHYLHEXYL) PHTHALATE; AIRWAY INFLAMMATION; YOUNG-CHILDREN; MONO-2-ETHYLHEXYL PHTHALATE	P>During the last decades more than 100 000 new chemicals have been introduced to the environment. Many of these new chemicals and many common consumer products that include these have been shown to be toxic in animal studies and an increasing body of evidence suggests that they are also impacting human health. Among the suspect chemicals, the endocrine disrupting chemicals (EDCs) are of particular concern. One such chemical group is the phthalates, used in soft poly vinyl chloride (PVC) material and in a huge number of consumer products. During the same period of time that the prevalence of these modern chemicals has increased, there has been a remarkable increase in several chronic illnesses, including asthma and allergy in children. In this article we outline the scientific knowledge on phthalate exposure for asthma and airway diseases in children by examining epidemiological and experimental peer review data for potential explanatory mechanisms. Epidemiological data point to a possible correlation between phthalate exposure and asthma and airway diseases in children. Experimental studies present support for an adjuvant effect on basic mechanisms in allergic sensitization by several phthalates. Despite variations in the experimental design and reported result in the individual studies, a majority of published reports have identified adjuvant effects on Th2 differentiation, production of Th2 cytokines and enhanced levels of Th2 promoted immunoglobulins (mainly IgG1 but also IgE) in mice. A limited amount of data do also suggest phthalate-induced enhancement of mast cell degranulation and eosinophilic infiltration which are important parts in the early inflammation phase. Thus, some of the early key mechanisms in the pathology of allergic asthma could possibly be targeted by phthalate exposure. But the important questions of clinical relevance of real life exposure and identification of molecular targets that can explain interactions largely remain to be answered.	[Bornehag, C. G.; Nanberg, E.] Karlstad Univ, Dept Chem & Biomed Sci, SE-65188 Karlstad, Sweden	Bornehag, CG (reprint author), Karlstad Univ, Dept Chem & Biomed Sci, SE-65188 Karlstad, Sweden.	carl-gustaf.bornehag@kau.se					Adibi JJ, 2008, ENVIRON HEALTH PERSP, V116, P467, DOI 10.1289/ehp.10749; Adibi JJ, 2003, ENVIRON HEALTH PERSP, V111, P1719, DOI 10.1289/ehp.6235; Almqvist C, 2008, ALLERGY, V63, P47, DOI 10.1111/j.1398-9995.2007.01524.x; 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, 2005, ENVIRON HEALTH PERSP, V113, P1399, DOI 10.1289/ehp.7809; Bornehag CG, 2004, ENVIRON HEALTH PERSP, V112, P1393, DOI 10.1289/ehp.7187; Butala JH, 2004, TOXICOLOGY, V201, P77, DOI 10.1016/j.tox.2004.04.004; Calafat AM, 2006, TOXICOLOGY, V217, P22, DOI 10.1016/j.tox.2005.08.013; Calafat AM, 2005, ENVIRON HEALTH PERSP, V113, P391; Calafat AM, 2007, ENVIRON HEALTH PERSP, V115, P1596, DOI 10.1289/ehp.10598; Chalubinski M, 2006, ALLERGY, V61, P1326, DOI 10.1111/j.1398-9995.2006.01135.x; Clement LT, 2008, AM J MED SCI, V335, P260, DOI 10.1097/MAJ.0b013e318169031c; COFFMAN RL, 1993, ADV IMMUNOL, V54, P229, DOI 10.1016/S0065-2776(08)60536-2; Dearman RJ, 2008, TOXICOLOGY, V244, P231, DOI 10.1016/j.tox.2007.11.017; Dearman RJ, 2009, J APPL TOXICOL, V29, P118, DOI 10.1002/jat.1388; Deutschle T, 2008, ENVIRON HEALTH PERSP, V116, P1487, DOI 10.1289/ehp.11474; Engel SM, 2006, REPROD TOXICOL, V21, P110, DOI 10.1016/j.reprotox.2005.07.007; Epstein MM, 2004, INT ARCH ALLERGY IMM, V133, P84, DOI 10.1159/000076131; Fischer FP, 1998, PERITON DIALYSIS INT, V18, P620; Galli SJ, 2008, NATURE, V454, P445, DOI 10.1038/nature07204; 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; Gourlay T, 2003, ARTIF ORGANS, V27, P256, DOI 10.1046/j.1525-1594.2003.07107.x; Hansen JS, 2007, TOXICOLOGY, V232, P79, DOI 10.1016/j.tox.2006.12.011; Heudorf U, 2007, INT J HYG ENVIR HEAL, V210, P623, DOI 10.1016/j.ijheh.2007.07.011; Hogberg J, 2008, ENVIRON HEALTH PERSP, V116, P334, DOI 10.1289/ehp.10788; Hong CC, 2004, BIOL PHARM BULL, V27, P1136, DOI 10.1248/bpb.27.1136; Huang PC, 2009, ENVIRON INT, V35, P14, DOI 10.1016/j.envint.2008.05.012; 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; Jepsen KF, 2004, TOXICOL IN VITRO, V18, P265, DOI 10.1016/j.tiv.2003.09.008; Kato T, 2006, EUR J IMMUNOL, V36, P1199, DOI 10.1002/eji.200535140; Koike E, 2009, TOXICOLOGY, V259, P54, DOI 10.1016/j.tox.2009.02.002; Kolarik B, 2008, ENVIRON HEALTH PERSP, V116, P98, DOI 10.1289/ehp.10498; Krug N, 2008, CURR DRUG TARGETS, V9, P438, DOI 10.2174/138945008784533598; Kumar RK, 2008, CURR DRUG TARGETS, V9, P485, DOI 10.2174/138945008784533561; Larsen ST, 2007, TOXICOL LETT, V170, P223, DOI 10.1016/j.toxlet.2007.03.009; 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; LARSSON M, 2009, PVC FLOORING I UNPUB; Lee MH, 2004, INT ARCH ALLERGY IMM, V134, P213, DOI 10.1159/000078768; Manning P J, 2007, Ir Med J, V100, P614; McLeish S, 2007, ARCH DIS CHILD, V92, P1032, DOI 10.1136/adc.2006.112185; Miller RL, 2008, AM J RESP CRIT CARE, V177, P567, DOI 10.1164/rccm.200710-1511PP; Nakamura R, 2002, IMMUNOL LETT, V80, P119, DOI 10.1016/S0165-2478(01)00318-2; Oh PS, 2009, N-S ARCH PHARMACOL, V380, P115, DOI 10.1007/s00210-009-0423-y; Oie L, 1999, EPIDEMIOLOGY, V10, P294, DOI 10.1097/00001648-199905000-00018; Pearce N, 2007, THORAX, V62, P758, DOI 10.1136/thx.2006.070169; Sakai K, 2001, INT ARCH ALLERGY IMM, V126, P126, DOI 10.1159/000049503; Schettler T, 2006, INT J ANDROL, V29, P134, DOI 10.1111/j.1365-2605.2005.00567.x; SHERTZER HG, 1985, ARCH ENVIRON CON TOX, V14, P605; SNAPPER CM, 1988, IMMUNOL REV, V102, P51, DOI 10.1111/j.1600-065X.1988.tb00741.x; STEVENS TL, 1988, NATURE, V334, P255, DOI 10.1038/334255a0; Taube C, 2004, INT ARCH ALLERGY IMM, V135, P173, DOI 10.1159/000080899; Tsutsumi O, 2005, J STEROID BIOCHEM, V93, P325, DOI 10.1016/j.jsbmb.2004.12.008; Vandenberg LN, 2007, REPROD TOXICOL, V24, P139, DOI 10.1016/j.reprotox.2007.07.010; Wormuth M, 2006, RISK ANAL, V26, P803, DOI 10.1111/j.1539-6924.2006.00770.x; Yang GT, 2008, FOOD AGR IMMUNOL, V19, P351, DOI 10.1080/09540100802545869	64	96	102	6	52	WILEY-BLACKWELL PUBLISHING, INC	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0105-6263			INT J ANDROL	Int. J. Androl.	APR	2010	33	2					333	345		10.1111/j.1365-2605.2009.01023.x		13	Andrology	Endocrinology & Metabolism	569XO	WOS:000275636400017	20059582	
J	Marra, F; Marra, CA; Richardson, K; Lynd, LD; Kozyrskyj, A; Patrick, DM; Bowie, WR; FitzGerald, JM				Marra, Fawziah; Marra, Carlo A.; Richardson, Kathryn; Lynd, Larry D.; Kozyrskyj, Anita; Patrick, David M.; Bowie, William R.; FitzGerald, J. Mark			Antibiotic Use in Children Is Associated With Increased Risk of Asthma	PEDIATRICS			English	Article						asthma; antibiotics; epidemiology; children; pediatrics	EARLY-CHILDHOOD; ALLERGIC DISEASE; BIRTH COHORT; 1ST YEAR; LIFE; INFECTIONS; CAUSATION; COMMITTEE; RHINITIS; EXPOSURE	BACKGROUND. Antibiotic exposure in early childhood is a possible contributor to the increasing asthma prevalence in industrialized countries. Although a number of published studies have tested this hypothesis, the results have been conflicting. OBJECTIVE. To explore the association between antibiotic exposure before 1 year of age and development of childhood asthma. METHODS. Using administrative data, birth cohorts from 1997 to 2003 were evaluated (N = 251 817). Antibiotic exposure was determined for the first year of life. After the first 24 months of life, the incidence of asthma was determined in both those exposed and not exposed to antibiotics in the first 12 months of life. Cox proportional hazards models were used to adjust for potential confounders and determine the hazard ratios associated with antibiotic exposure for the development of asthma. RESULTS. Antibiotic exposure in the first year of life was associated with a small risk of developing asthma in early childhood after adjusting for gender, socioeconomic status at birth, urban or rural address at birth, birth weight, gestational age, delivery method, frequency of physician visits, hospital visit involving surgery, visits to an allergist, respirologist, or immunologist, congenital anomalies, and presence of otitis media, acute, or chronic bronchitis, and upper and lower respiratory tract infections during the first year of life. As the number of courses of antibiotics increased, this was associated with increased asthma risk, with the highest risk being in children who received > 4 courses. All antibiotics were associated with an increased risk of developing asthma, with the exception of sulfonamides. CONCLUSIONS. This study provides evidence that the use of antibiotics in the first year of life is associated with a small risk of developing asthma, and this risk increases with the number of courses of antibiotics prescribed. Pediatrics 2009;123:1003-1010	[Marra, Fawziah; Marra, Carlo A.; Richardson, Kathryn; Lynd, Larry D.; Patrick, David M.; Bowie, William R.; FitzGerald, J. Mark] Univ British Columbia, Fac Pharmaceut Sci, Vancouver, BC V6Z 1Y6, Canada; [Marra, Fawziah; Patrick, David M.] BC Ctr Dis Control, Dept Vaccine & Pharm, Vancouver, BC, Canada; [Kozyrskyj, Anita] Univ Manitoba, Dept Pharm, Winnipeg, MB, Canada; [FitzGerald, J. Mark] Vancouver Coastal Hlth Res Inst, Ctr Clin Epidemiol & Evaluat, Vancouver, BC, Canada	Marra, CA (reprint author), Univ British Columbia, Fac Pharmaceut Sci, Ctr Hlth Evaluat & Outcomes Sci, St Pauls Hosp, 620-1081 Burrard St, Vancouver, BC V6Z 1Y6, Canada.	carlo.marra@ubc.ca			BC Lung Association (British Columbia, Canada)	We thank data analysts at the Centre for Health Services and Policy Research, Data Access Services in the BC Ministry of Health, and the BC College of Pharmacists for providing these data.	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J	Ostro, B; Roth, L; Malig, B; Marty, M				Ostro, Bart; Roth, Lindsey; Malig, Brian; Marty, Melanie			The Effects of Fine Particle Components on Respiratory Hospital Admissions in Children	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						children; EC; hospital admissions; OC; PM(2.5); respiratory; species	PARTICULATE AIR-POLLUTION; DIESEL EXHAUST PARTICLES; 9 CALIFORNIA COUNTIES; AMBIENT AIR; SOURCE-APPORTIONMENT; DAILY MORTALITY; RISK-ASSESSMENT; CASE-CROSSOVER; UTAH VALLEY; GAS-PHASE	BACKGROUND: Epidemiologic studies have demonstrated an association between acute exposure to ambient fine particles and both mortality and morbidity. Less is known about the relative impacts of the specific chemical constituents of particulate matter < 2.5 mu m in aerodynamic diameter (PM(2.5)) on hospital admissions. OBJECTIVE: This study was designed to estimate the risks of exposure to PM(2.5) and several species on hospital admissions for respiratory diseases among children. DATA AND METHODS: We obtained data on daily counts of hospitalizations for children < 19 and < 5 years of age for total respiratory diseases and several subcategories including pneumonia, acute bronchitis, and asthma for six California counties from 2000 through 2003, as well as ambient concentrations Of PM2.5 and its constituents, including elemental carbon (EC), organic carbon (OC), and nitrates (NO(3)). We used Poisson regression to estimate risks while controlling for important covariates. RESULTS: We observed associations between several components of PM(2.5) and hospitalization for all of the respiratory outcomes examined. For example, for total respiratory admissions for children < 19 years of age, the interquartile range for a 3-day lag of PM(2.5), EC, OC, NO(3), and sulfates was associated with an excess risk of 4.1% [95% confidence interval (CI), 1.8-6.4], 5.4% (95% CI, 0.8-10-3), 3.4% (95% CI, 1.1-5-7), 3.3% (95% CI, 1.1-5.5), and 3.0% (95% CI, 0.4-5-7), respectively. We also observed associations for several metals. Additional associations with several of the species, including potassium, were observed in the cool season. CONCLUSION: Components of PM(2.5) were associated with hospitalization for several childhood respiratory diseases including pneumonia, bronchitis, and asthma. Because exposure to components (e.g., EC, OC, NO(3), and K) and their related sources, including diesel and gasoline exhaust, wood smoke, and other combustion sources, are ubiquitous in the urban environment, it likely represents an identifiable and preventable risk factor for hospitalization for children.	[Ostro, Bart; Roth, Lindsey; Malig, Brian; Marty, Melanie] Calif EPA, OEHHA, Oakland, CA 94612 USA	Ostro, B (reprint author), Calif EPA, OEHHA, 1515 Clay St,16th Floor, Oakland, CA 94612 USA.	bostro@oehha.ca.gov					Andersen ZJ, 2007, J EXPO SCI ENV EPID, V17, P625, DOI 10.1038/sj.jes.7500546; Barnett AG, 2005, AM J RESP CRIT CARE, V171, P1272, DOI 10.1164/rccm.200411-1586OC; Basu R, 2008, EPIDEMIOLOGY, V19, P138, DOI 10.1097/EDE.0b013e31815c1da7; Bell ML, 2007, ENVIRON HEALTH PERSP, V115, P989, DOI 10.1289/ehp.9621; Braga ALF, 2001, J OCCUP ENVIRON MED, V43, P927; BURNETT RT, 1995, AM J EPIDEMIOL, V142, P15; Burnett RT, 2000, INHAL TOXICOL, V12, P15, DOI 10.1080/089583700750019495; *CA AIR RES BOARD, 2007, 2007 ALM DAT OX SULF; CHALUPA D, 2000, ENV HLTH PERSPECT, V112, P879; Delfino RJ, 2006, ENVIRON HEALTH PERSP, V114, P1736, DOI 10.1289/ehp.9141; Delfino RJ, 2003, ENVIRON HEALTH PERSP, V111, P647, DOI 10.1289/ehp.5992; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; Diaz-Sanchez D, 2000, J ALLERGY CLIN IMMUN, V106, P1140, DOI 10.1067/mai.2000.111144; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; Dietert RR, 2000, ENVIRON HEALTH PERSP, V108, P483, DOI 10.2307/3454540; Dominici F, 2006, JAMA-J AM MED ASSOC, V295, P1127, DOI 10.1001/jama.295.10.1127; Franklin M, 2008, EPIDEMIOLOGY, V19, P680, DOI 10.1097/EDE.0b013e3181812bb7; Gauderman WJ, 2004, NEW ENGL J MED, V351, P1057, DOI 10.1056/NEJMoa040610; Ghio AJ, 2004, J AEROSOL MED, V17, P157, DOI 10.1089/0894268041457200; Ginsberg GL, 2005, J TOXICOL ENV HEAL A, V68, P573, DOI 10.1080/15287390590921793; Gottipolu RR, 2008, INHAL TOXICOL, V20, P473, DOI 10.1080/08958370701858427 ; Hertz-Picciotto I, 2007, ENVIRON HEALTH PERSP, V115, P1510, DOI 10.1289/ehp.9617; Hirshon JM, 2008, ENVIRON HEALTH PERSP, V116, P826, DOI 10.1289/ehp.10759; Hiura TS, 2000, J IMMUNOL, V165, P2703; Kaewamatawong T, 2006, TOXICOL PATHOL, V34, P958, DOI 10.1080/01926230601094552; Khalil MAK, 2003, ATMOS ENVIRON, V37, P1211, DOI 10.1016/S1352-2310(02)01014-2; Kodavanti UP, 2002, TOXICOL SCI, V70, P73, DOI 10.1093/toxsci/70.1.73; Laden F, 2000, ENVIRON HEALTH PERSP, V108, P941, DOI 10.2307/3435052; Li N, 2003, ENVIRON HEALTH PERSP, V111, P455, DOI 10.1289/ehp.6000; Lin M, 2002, ENVIRON HEALTH PERSP, V110, P575; Mar TF, 2004, INHAL TOXICOL, V16, P809, DOI 10.1080/08958370490506646; Mar TF, 2000, ENVIRON HEALTH PERSP, V108, P347, DOI 10.2307/3454354; Marcazzan GM, 2001, ATMOS ENVIRON, V35, P4639, DOI 10.1016/S1352-2310(01)00124-8; McConnell R, 2003, AM J RESP CRIT CARE, V168, P790, DOI 10.1164/rccm.200304-466OC; Miller MD, 2002, INT J TOXICOL, V21, P403, DOI 10.1080/10915810290096630; Naeher LP, 2007, INHAL TOXICOL, V19, P67, DOI 10.1080/08958370600985875; Nel A E, 2001, Curr Opin Pulm Med, V7, P20, DOI 10.1097/00063198-200101000-00004; Nel AE, 1998, J ALLERGY CLIN IMMUN, V102, P539, DOI 10.1016/S0091-6749(98)70269-6; Ostro B, 2006, ENVIRON HEALTH PERSP, V114, P29, DOI 10.1289/ehp.8335; Ostro B, 2007, ENVIRON HEALTH PERSP, V115, P13, DOI 10.1289/ehp.9281; Peel JL, 2005, EPIDEMIOLOGY, V16, P164, DOI 10.1097/01.ede.0000152905.42113.db; POPE CA, 1989, AM J PUBLIC HEALTH, V79, P623, DOI 10.2105/AJPH.79.5.623; Pritchard RJ, 1996, INHAL TOXICOL, V8, P457, DOI 10.3109/08958379609005440; R Development Core Team, 2006, LANG ENV STAT COMP; RUBIN JI, 2006, STI906201063103FR; Salvi S, 1999, AM J RESP CRIT CARE, V159, P702; Sarnat JA, 2008, ENVIRON HEALTH PERSP, V116, P459, DOI 10.1289/ehp.10873; SCHAUER J, 2006, RES REPORT CHARACTER; Schauer JJ, 2000, ENVIRON SCI TECHNOL, V34, P1821, DOI 10.1021/es981312t; Schlesinger RB, 2006, INHAL TOXICOL, V18, P95, DOI 10.1080/08958370500306016; Schwartz J, 1996, J AIR WASTE MANAGE, V46, P927, DOI 10.1080/10473289.1996.10467528; Schwartz J, 2004, PEDIATRICS, V113, P1037; Sinclair AH, 2004, J AIR WASTE MANAGE, V54, P1212; Tolbert PE, 2000, AM J EPIDEMIOL, V151, P798; van der Zee SC, 1999, OCCUP ENVIRON MED, V56, P802; World Health Organization, 1975, INT CLASS DIS 9 REV; Zanobetti A, 2000, ENVIRON HEALTH PERSP, V108, P841, DOI 10.2307/3434991; Zeka A, 2005, OCCUP ENVIRON MED, V62, P718, DOI 10.1136/oem.2004.017012; Zelikoff JT, 2002, ENVIRON HEALTH PERSP, V110, P871	59	96	104	5	36	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	2009	117	3					475	480		10.1289/ehp.11848		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	415KV	WOS:000263933600038	19337525	
J	Williams, DR; Sternthal, M; Wright, RJ				Williams, David R.; Sternthal, Michelle; Wright, Rosalind J.			Social Determinants: Taking the Social Context of Asthma Seriously	PEDIATRICS			English	Article; Proceedings Paper	Conference on the State of Childhood Asthma and Future Directions	DEC, 2006	Washington, DC	Merck Childhood Asthma Network		childhood asthma prevalence; low-income population; poverty; race; risk factors	RACIAL RESIDENTIAL SEGREGATION; AIR-POLLUTION; COLLECTIVE EFFICACY; LUNG-FUNCTION; URBAN ASTHMA; ATHEROSCLEROSIS RISK; SOCIOECONOMIC-STATUS; CHILDHOOD ASTHMA; SPATIAL DYNAMICS; CHILDRENS HEALTH	Although asthma has emerged as a major contributor to disease and disability among US children, the burden of this disease is unevenly distributed within the population. This article provides a brief overview of social-status variables that predict variations in asthma risks and social exposures, such as stress and violence, that are emerging as important risk factors. The central focus of the article is on the distal social variables that have given rise to unhealthy residential environments in which the risk factors for asthma and other diseases are clustered. Effective initiatives for the prevention and treatment of childhood asthma need to address these nonmedical determinants of the prevalence of asthma. Pediatrics 2009; 123:S174-S184	[Williams, David R.] Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Cambridge, MA 02138 USA; [Williams, David R.] Harvard Univ, Dept African & African Amer Studies, Cambridge, MA 02138 USA; [Williams, David R.] Harvard Univ, Dept Sociol, Cambridge, MA 02138 USA; [Sternthal, Michelle; Wright, Rosalind J.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA; [Wright, Rosalind J.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA; [Wright, Rosalind J.] Harvard Univ, Sch Med, Boston, MA 02115 USA	Williams, DR (reprint author), Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, 677 Huntington Ave,6th Floor, Boston, MA 02115 USA.	dwilliam@hsph.harvard.edu			NHLBI NIH HHS [R01 HL080674, R01HL080674]; NIEHS NIH HHS [R01 ES10932, R01 ES010932]; NIMH NIH HHS [5 T32 MH16806, R01 MH 59575, R01 MH059575, T32 MH016806]		Adler NE, 2003, CURR DIR PSYCHOL SCI, V12, P119, DOI 10.1111/1467-8721.01245; Austin JB, 2005, ARCH DIS CHILD, V90, P253, DOI 10.1136/adc.2004.049346; Bach PB, 2004, NEW ENGL J MED, V351, P575, DOI 10.1056/NEJMsa040609; Baicker K, 2004, HLTH AFF MILLWOOD S, pVAR33; BARBARIN OA, 1981, I RACISM COMMUNITY C; Bauman K. 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J, 1987, TRULY DISADVANTAGED; Wright AL, 1999, J ALLERGY CLIN IMMUN, V104, P589, DOI 10.1016/S0091-6749(99)70328-3; Wright RJ, 2005, CURR OPIN ALLERGY CL, V5, P23, DOI 10.1097/00130832-200502000-00006; Wright RJ, 2004, AM J PUBLIC HEALTH, V94, P625, DOI 10.2105/AJPH.94.4.625; Wright RJ, 2003, NEIGHBORHOODS HLTH, P233; Wright RJ, 2007, PAEDIATR PERINAT EP, V21, P8, DOI 10.1111/j.1365-3016.2007.00879.x; Wright RJ, 2006, CLIN CHEST MED, V27, P413, DOI 10.1016/j.ccm.2006.04.003; Zenk SN, 2005, AM J PUBLIC HEALTH, V95, P660, DOI 10.2105/AJPH.2004.042150; Zuckerman B, 2004, PEDIATRICS, V114, P224, DOI 10.1542/peds.114.1.224	94	96	96	4	10	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	MAR	2009	123						S174	S184		10.1542/peds.2008-2233H		11	Pediatrics	Pediatrics	413XL	WOS:000263826000007	19221161	
J	Liebers, V; Raulf-Heimsoth, M; Bruning, T				Liebers, V.; Raulf-Heimsoth, M.; Bruening, T.			Health effects due to endotoxin inhalation (review)	ARCHIVES OF TOXICOLOGY			English	Review						endotoxin; health effects; LAL-test; whole blood assay-allergy	DOSE-RESPONSE RELATIONSHIPS; ORGANIC DUST; LUNG-FUNCTION; FOLLOW-UP; OCCUPATIONAL-EXPOSURE; AIRBORNE ENDOTOXIN; CYTOKINE RESPONSES; LPS INHALATION; COTTON DUST; IN-VIVO	Endotoxins are ubiquitous in the environment and represent important components of bioaerosols. High exposure occurs in rural environment and at several workplaces (e.g. waste collecting, textile industry etc.). Adverse effects on human health induced by inhalation of endotoxin are described in several studies. Up to now the endotoxin levels are mainly measured using the Limulus amoebocyte-lysate (LAL) assay. This assay is well established, but for a suitable characterization of bioaerosols more parameters are necessary. Additional information, e.g. concerning the pyrogenic activity of organic dust samples may be delivered by whole blood assay. Whereas on the one hand protection measures at workplaces are demanded to avoid lung function impairment due to endotoxin exposure, on the other hand a protective effect of exposure to microbial agents like endotoxins with regard to allergy development has been observed. On the cellular level toll-like receptor 4 (TLR4) and IL-1 receptor as well as surface molecules like CD14 have been shown to play a pivotal role in the endotoxin activation cascade. In this review we summarize the mechanism of endotoxin recognition and its manifold effects on human health.	[Liebers, V.; Raulf-Heimsoth, M.; Bruening, T.] Ruhr Univ Bochum, Res Inst Occupat Med, German Social Accident Insurance, BGFA, D-44793 Bochum, Germany	Liebers, V (reprint author), Ruhr Univ Bochum, Res Inst Occupat Med, German Social Accident Insurance, BGFA, Allergol Immunol,Burkle Camp Pl 1, D-44793 Bochum, Germany.	liebers@bgfa.de	Bruning, Thomas/G-8120-2015	Bruning, Thomas/0000-0001-9560-5464			Acevedo F, 2005, INFLAMMATION, V29, P39, DOI 10.1007/s10753-006-8968-0; Alexis N, 2001, J ALLERGY CLIN IMMUN, V107, P31, DOI 10.1067/mai.2001.111594; Alexis NE, 2005, J ALLERGY CLIN IMMUN, V115, P345, DOI 10.1016/j.jaci.2004.11.040; Alexis NE, 2004, J ALLERGY CLIN IMMUN, V114, P1325, DOI 10.1016/j.jaci.2004.09.002; Aulock Sonja Von, 2006, J Interferon Cytokine Res, V26, P887, DOI 10.1089/jir.2006.26.887; Bakirci N, 2007, J OCCUP ENVIRON MED, V49, P853, DOI 10.1097/JOM.0b013e3180dca598; Beutler B, 2003, NAT REV IMMUNOL, V3, P169, DOI 10.1038/nri1004; Binding N, 2004, J ENVIRON MONITOR, V6, P65, DOI 10.1039/b309237b; 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Toxicol.	APR	2008	82	4					203	210		10.1007/s00204-008-0290-1		8	Toxicology	Toxicology	280BW	WOS:000254400900001	18322674	
J	Wheeler, AJ; Smith-Doiron, M; Xu, X; Gilbert, NL; Brook, JR				Wheeler, Amanda J.; Smith-Doiron, Marc; Xu, Xiaohong; Gilbert, Nicolas L.; Brook, Jeffrey R.			Intra-urban variability of air pollution in Windsor, Ontario - Measurement and modeling for human exposure assessment	ENVIRONMENTAL RESEARCH			English	Article						air pollution; land-use regression (LUR); geographic information systems (GIS); road traffic; exposure assessment	AMBIENT NITROGEN-DIOXIDE; CHILDHOOD ASTHMA; SPATIAL VARIABILITY; MORTALITY; ASSOCIATION; CHILDREN; INDICATORS; SYMPTOMS; CITIES; SULFUR	There are acknowledged difficulties in epidemiological studies to accurately assign exposure to air pollution for large populations, and large, long-term cohort studies have typically relied upon data from central monitoring stations. This approach has generally been adequate when populations span large areas or diverse cities. However, when the effects of intra-urban differences in exposure are being studied, the use of these existing central sites are likely to be inadequate for representing spatial variability that exists within an urban area. As part of the Border Air Quality Strategy (BAQS), an international agreement between the governments of Canada and the United States, a number of air health effects studies are being undertaken by Health Canada and the US EPA. Health Canada's research largely focuses on the chronic exposure of elementary school children to air pollution. The exposure characterization for this population to a variety of air pollutants has been assessed using land-use regression (LUR) models. This approach has been applied in several cities to nitrogen dioxide (NO2), as an assumed traffic exposure marker. However, the models have largely been developed from limited periods of saturation monitoring data and often only represent one or two seasons. Two key questions from these previous efforts, which are examined in this paper, are: If NO2 is a traffic marker, what other pollutants, potentially traffic related, might it actually represent? How well is the within city spatial variability of NO2, and other traffic-related pollutants, characterized by a single saturation monitoring campaign. Input data for the models developed in this paper were obtained across a network of 54 monitoring sites situated across Windsor, Ontario. The pollutants studied were NO2, sulfur dioxide (SO2) and volatile organic compounds, which were measured in all four seasons by deploying passive samplers for 2-week periods. Correlations among these pollutants were calculated to assess what other pollutants NO2 might represent, and correlations across seasons for a given pollutant were determined to assess how much the within-city spatial pattern varies with time. LUR models were then developed for NO2, SO2, benzene, and toluene. A multiple regression model including proximity to the Ambassador Bridge (the main Canada-US border crossing point), and proximity to highways and major roads, predicted NO2 concentrations with an R-2 = 0.77. The SO2 model predictors included distance to the Ambassador Bridge, dwelling density within 1500 in, and Detroit-based SO2 emitters within 3000 in resulting in a model with an R-2 = 0.69. Benzene and toluene LUR models included traffic predictors as well as point source emitters resulting in R-2 = 0.73 and 0.46, respectively. Between season pollutant correlations were all significant although actual concentrations for each site varied by season. This suggests that if one season were to be selected to represent the annual concentrations for a specific site this may lead to a potential under or overestimation in exposure, which could be significant for health research. All pollutants had strong inter-pollutant correlations suggesting that NO2 could represent SO2, benzene, and toluene. Crown Copyright (c) 2007 Published by Elsevier Inc. All rights reserved.	[Wheeler, Amanda J.; Smith-Doiron, Marc; Gilbert, Nicolas L.] Hlth Canada, Air Hlth Effects Div, Ottawa, ON K1A 0K9, Canada; [Xu, Xiaohong] Univ Windsor, Windsor, ON N9B 3P4, Canada; [Brook, Jeffrey R.] Environm Canada, Air Qual Res Branch, Toronto, ON M3H 5T4, Canada	Wheeler, AJ (reprint author), Hlth Canada, Air Hlth Effects Div, 3rd Floor,269 Laurier Ave W,PL 4903C, Ottawa, ON K1A 0K9, Canada.	Amanda_Wheeler@hc-sc.gc.ca	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Gilbert, Nicolas/0000-0001-6985-8046; Wheeler, Amanda/0000-0001-9288-8163			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; 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; BROOK JR, 2007, IN PRESS J EXPO SCI; 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; Gilbert NL, 2005, J AIR WASTE MANAGE, V55, P1059; Hoek G, 2001, J EXPO ANAL ENV EPID, V11, P459, DOI 10.1038/sj.jea.7500189; 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; Jerrett M, 2005, J EXPO ANAL ENV EPID, V15, P185, DOI 10.1038/sj.jea.7500388; Kanaroglou PS, 2005, ATMOS ENVIRON, V39, P2399, DOI 10.1016/j.atmosenv.2004.06.049; Kuenzli Nino, 2005, Environmental Health Perspectives, V113, P201; Laden F, 2000, ENVIRON HEALTH PERSP, V108, P941, DOI 10.2307/3435052; Lin S, 2002, ENVIRON RES, V88, P73, DOI 10.1006/enrs.2001.4303; Luginaah Isaac, 2006, International Journal of Environmental Studies, V63, P487, DOI 10.1080/00207230600802122; Pikhart H, 2000, EPIDEMIOLOGY, V11, P153, DOI 10.1097/00001648-200003000-00012; POPE CA, 1995, AM J RESP CRIT CARE, V151, P669; Pope CA, 2002, JAMA-J AM MED ASSOC, V287, P1132, DOI 10.1001/jama.287.9.1132; SCHAUG J, 1993, ATMOS ENVIRON A-GEN, V27, P831, DOI 10.1016/0960-1686(93)90005-J; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; Zmirou D, 2004, J EPIDEMIOL COMMUN H, V58, P18, DOI 10.1136/jech.58.1.18	23	96	96	3	48	ACADEMIC PRESS INC ELSEVIER SCIENCE	SAN DIEGO	525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA	0013-9351			ENVIRON RES	Environ. Res.	JAN	2008	106	1					7	16		10.1016/j.envres.2007.09.004		10	Environmental Sciences; Public, Environmental & Occupational Health	Environmental Sciences & Ecology; Public, Environmental & Occupational Health	257PP	WOS:000252811300002	17961539	
J	Hammer, KA; Carson, CF; Riley, TV; Nielsen, JB				Hammer, KA; Carson, CF; Riley, TV; Nielsen, JB			A review of the toxicity of Melaleuca alternifolia (tea tree) oil	FOOD AND CHEMICAL TOXICOLOGY			English	Review						essential oil; terpene; allergy; ecotoxicity	PLANT ESSENTIAL OILS; ALLERGIC CONTACT-DERMATITIS; BETA-MYRCENE; IN-VITRO; INSECTICIDAL ACTIVITY; RAINBOW-TROUT; SALMONELLA/MICROSOME ASSAY; FUMIGANT TOXICITY; ALPHA-TERPINENE; HUMAN MONOCYTES	The essential oil of Melaleuca alternifolia, also known as tea tree or melaleuca oil, is widely available and has been investigated as an alternative antimicrobial, anti-inflammatory and anti-cancer agent. While these properties are increasingly well characterised, relatively limited data are available on the safety and toxicity of the oil. Anecdotal evidence from almost 80 years of use suggests that the topical use of the oil is relatively safe, and that adverse events are minor, self-limiting and occasional. Published data indicate that TTO is toxic if ingested in higher doses and can also cause skin irritation at higher concentrations. Allergic reactions to TTO occur in predisposed individuals and may be due to the various oxidation products that are formed by exposure of the oil to light and/or air. Adverse reactions may be minimised by avoiding ingestion, applying only diluted oil topically and using oil that has been stored correctly. Data from individual components suggest that TTO has the potential to be developmentally toxic if ingested at higher doses, however, TTO and its components are not genotoxic. The limited ecotoxicity data available indicate that TTO is toxic to some insect species but more studies are required. (c) 2005 Elsevier Ltd. All rights reserved.	Univ Western Australia, Sch Biomed & Chem Sci, Nedlands, WA 6009, Australia; Queen Elizabeth II Med Ctr, Western Australian Ctr Pathol & Med Res, Nedlands, WA 6009, Australia; Univ So Denmark, DK-5000 Odense, Denmark	Hammer, KA (reprint author), Univ Western Australia, Sch Biomed & Chem Sci, M502,35 Stirling Hwy, Nedlands, WA 6009, Australia.	khammer@cyllene.uwa.edu.au	Hammer, Katherine/B-7023-2012; Carson, Christine/F-1521-2013	Hammer, Katherine/0000-0001-7878-4851; Carson, Christine/0000-0003-3669-1651			Apted J H, 1991, Australas J Dermatol, V32, P177; Araujo IB, 1996, FOOD CHEM TOXICOL, V34, P477, DOI 10.1016/0278-6915(96)87358-3; Aspres N., 2003, Exogenous Dermatology, V2, P258, DOI 10.1159/000078694; Aydin S, 2005, MUTAT RES-GEN TOX EN, V581, P43, DOI 10.1016/j.mrgetnox.2004.10.017; Belaiche P., 1985, PHYTOTHERAPY, V15, P13; Bhushan M, 1997, CONTACT DERMATITIS, V36, P117, DOI 10.1111/j.1600-0536.1997.tb00435.x; Bischoff K, 1998, J VET DIAGN INVEST, V10, P208; BLACKWELL R, 1991, BR J PHYTOTHER, V2, P26; Boon PI, 1997, ARCH HYDROBIOL, V138, P433; Brand C, 2001, INFLAMM RES, V50, P213, DOI 10.1007/s000110050746; Brenan J A, 1996, Australas J Dermatol, V37, P40, DOI 10.1111/j.1440-0960.1996.tb00993.x; BROPHY JJ, 1989, J AGR FOOD CHEM, V37, P1330, DOI 10.1021/jf00089a027; Cal K, 2003, J CONTROL RELEASE, V93, P369, DOI 10.1016/j.jconrel.2003.09.002; Campbell RE, 2001, AQUAC RES, V32, P223, DOI 10.1046/j.1365-2109.2001.00551.x; Choi WI, 2003, J ECON ENTOMOL, V96, P1479, DOI 10.1603/0022-0493-96.5.1479; COATS JR, 1991, ACS SYM SER, V449, P305; CONNOR TH, 1985, TOXICOL LETT, V25, P33, DOI 10.1016/0378-4274(85)90097-9; COUTTS I, 2002, BR J DERMATOL S62, V147, P70; DEGROOT AC, 1992, CONTACT DERMATITIS, V27, P279; DeGroot AC, 1996, CONTACT DERMATITIS, V35, P304; DELBECCARO MA, 1995, VET HUM TOXICOL, V37, P557; DELGADO IF, 1993, FOOD CHEM TOXICOL, V31, P623, DOI 10.1016/0278-6915(93)90044-Y; Draize J. 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A., 1997, Journal of Essential Oil Research, V9, P47; Stroh J, 1998, B ENVIRON CONTAM TOX, V60, P923; van der Valk P G, 1994, Ned Tijdschr Geneeskd, V138, P823; Veien NK, 2004, CONTACT DERMATITIS, V50, P378, DOI 10.1111/j.0105-1873.2004.0350f.x; VILLAR D, 1994, VET HUM TOXICOL, V36, P139; Vokou D, 2003, J CHEM ECOL, V29, P2281, DOI 10.1023/A:1026274430898; WATABE T, 1981, XENOBIOTICA, V11, P333; Watson WA, 2004, AM J EMERG MED, V22, P335, DOI 10.1016/j.ajem.2004.06.001; WEBB M, 1976, WATER RES, V10, P303, DOI 10.1016/0043-1354(76)90171-8; Yang YC, 2004, J MED ENTOMOL, V41, P699, DOI 10.1603/0022-2585-41.4.699; YOO Y S, 1985, Journal of the Osaka City Medical Center, V34, P267; ZAMITH HPS, 1993, BRAZ J MED BIOL RES, V26, P93; Zhang SY, 2000, AUDIOL NEURO-OTOL, V5, P64, DOI 10.1159/000013869	88	96	106	6	46	PERGAMON-ELSEVIER SCIENCE LTD	OXFORD	THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND	0278-6915			FOOD CHEM TOXICOL	Food Chem. Toxicol.	MAY	2006	44	5					616	625		10.1016/j.fct.2005.09.001		10	Food Science & Technology; Toxicology	Food Science & Technology; Toxicology	048FD	WOS:000237932100002	16243420	
J	Ray, P; Birolleau, S; Lefort, Y; Becquemin, MH; Beigelman, C; Isnard, R; Teixeira, A; Arthaud, M; Riou, B; Boddaert, J				Ray, Patrick; Birolleau, Sophie; Lefort, Yannick; Becquemin, Marie-Helene; Beigelman, Catherine; Isnard, Richard; Teixeira, Antonio; Arthaud, Martine; Riou, Bruno; Boddaert, Jacques			Acute respiratory failure in the elderly: etiology, emergency diagnosis and prognosis	CRITICAL CARE			English	Article; Proceedings Paper	Annual Congress Urgences	MAY   18, 2005	Paris, FRANCE				CONGESTIVE-HEART-FAILURE; COMMUNITY-ACQUIRED PNEUMONIA; CARDIOGENIC PULMONARY-EDEMA; QUALITY-OF-CARE; NATRIURETIC PEPTIDE; SURVEY PROGRAM; ACUTE DYSPNEA; MANAGEMENT; PATIENT; GUIDELINES	Introduction Our objectives were to determine the causes of acute respiratory failure (ARF) in elderly patients and to assess the accuracy of the initial diagnosis by the emergency physician, and that of the prognosis. Method In this prospective observational study, patients were included if they were admitted to our emergency department, aged 65 years or more with dyspnea, and fulfilled at least one of the following criteria of ARF: respiratory rate at least 25 minute(-1); arterial partial pressure of oxygen (PaO2) 70 mmHg or less, or peripheral oxygen saturation 92% or less in breathing room air; arterial partial pressure of CO2 (PaCO2) >= 45 mmHg, with pH <= 7.35. The final diagnoses were determined by an expert panel from the completed medical chart. Results A total of 514 patients ( aged ( mean +/- standard deviation) 80 +/- 9 years) were included. The main causes of ARF were cardiogenic pulmonary edema (43%), community-acquired pneumonia (35%), acute exacerbation of chronic respiratory disease (32%), pulmonary embolism (18%), and acute asthma (3%); 47% had more than two diagnoses. Inhospital mortality was 16%. A missed diagnosis in the emergency department was noted in 101 (20%) patients. The accuracy of the diagnosis of the emergency physician ranged from 0.76 for cardiogenic pulmonary edema to 0.96 for asthma. An inappropriate treatment occurred in 162 (32%) patients, and lead to a higher mortality (25% versus 11%; p < 0.001). In a multivariate analysis, inappropriate initial treatment ( odds ratio 2.83, p < 0.002), hypercapnia > 45 mmHg ( odds ratio 2.79, p < 0.004), clearance of creatinine < 50 ml minute(-1) ( odds ratio 2.37, p < 0.013), elevated NT-pro-B-type natriuretic peptide or B-type natriuretic peptide ( odds ratio 2.06, p < 0.046), and clinical signs of acute ventilatory failure ( odds ratio 1.98, p < 0.047) were predictive of death. Conclusion Inappropriate initial treatment in the emergency room was associated with increased mortality in elderly patients with ARF.	Univ Paris 06, CHU Pitie Salpetriere, Assistance Publ Hop Paris, Dept Emergency Med & Surg, F-75651 Paris 13, France; Univ Paris 06, CHU Pitie Salpetriere, Assistance Publ Hop Paris, Dept Pneumol, F-75651 Paris, France; Univ Paris 06, CHU Pitie Salpetriere, Assistance Publ Hop Paris, Resp Intens Care Unit, F-75651 Paris 13, France; Univ Paris 06, CHU Pitie Salpetriere, Assistance Publ Hop Paris, Lab Pulm Funct Test, F-75651 Paris 13, France; Univ Paris 06, CHU Pitie Salpetriere, Assistance Publ Hop Paris, UPRES 2397, F-75651 Paris 13, France; Univ Paris 06, CHU Pitie Salpetriere, Assistance Publ Hop Paris, Dept Radiol, F-75651 Paris 13, France; Univ Paris 06, CHU Pitie Salpetriere, Assistance Publ Hop Paris, Dept Cardiol, F-75651 Paris 13, France; Univ Paris 06, CHU Pitie Salpetriere, Assistance Publ Hop Paris, Dept Internal Med, F-75651 Paris 13, France; Univ Paris 06, CHU Pitie Salpetriere, Assistance Publ Hop Paris, Lab Emergency Biol, F-75651 Paris 13, France; Univ Paris 06, CHU Pitie Salpetriere, Assistance Publ Hop Paris, Dept Geriatry, F-75651 Paris 13, France	Ray, P (reprint author), Univ Paris 06, CHU Pitie Salpetriere, Assistance Publ Hop Paris, Dept Emergency Med & Surg, F-75651 Paris 13, France.	patrick.ray@psl.ap-hop-paris.fr	Beigelman-Aubry, Catherine/F-4305-2017	Beigelman-Aubry, Catherine/0000-0001-7092-6448			American thoracic society, 1995, AM J RESP CRIT CARE, V152, pS77; BARR RG, 2003, AM J RESP CRIT CARE, V167, pA84; Boumendil A, 2004, INTENS CARE MED, V30, P647, DOI 10.1007/s00134-003-2150-z; CHAKKO S, 1991, AM J MED, V90, P353, DOI 10.1016/0002-9343(91)90576-J; Chin MH, 1999, ANN EMERG MED, V34, P595, DOI 10.1016/S0196-0644(99)70161-7; Cleland JGF, 2003, EUR HEART J, V24, P442, DOI 10.1016/S0195-668X(02)00823-0; ERIKSSON H, 1987, EUR HEART J, V8, P1007; Gottdiener JS, 2000, J AM COLL CARDIOL, V35, P1628, DOI 10.1016/S0735-1097(00)00582-9; GROSS JS, 1988, ARCH INTERN MED, V148, P173, DOI 10.1001/archinte.148.1.173; HANLEY JA, 1982, RADIOLOGY, V143, P29; HO KKL, 1993, J AM COLL CARDIOL, V22, pA6; Hood S, 2000, BRIT J GEN PRACT, V50, P559; Hunt SA, 2001, J AM COLL CARDIOL, V38, P2101, DOI 10.1016/S0735-1097(01)01683-7; KATZ S, 1970, GERONTOLOGIST, V10, P20; Komajda M, 2003, EUR HEART J, V24, P464, DOI 10.1016/S0195-668X(02)00700-5; L'Her E, 2004, INTENS CARE MED, V30, P882, DOI 10.1007/s00134-004-2183-y; LANDAHL S, 1980, ACTA MED SCAND, V207, P225; Le Manach Y, 2005, ANESTHESIOLOGY, V102, P885, DOI 10.1097/00000542-200505000-00004; LEMESHOW S, 1982, AM J EPIDEMIOL, V115, P92; Lien CTC, 2002, EUR J HEART FAIL, V4, P91, DOI 10.1016/S1388-9842(01)00200-8; Marrie TJ, 2000, CLIN INFECT DIS, V31, P1066, DOI 10.1086/318124; McCullough PA, 2002, CIRCULATION, V106, P416, DOI 10.1161/01.CIR.0000025242.79963.4C; Metlay JP, 1997, ARCH INTERN MED, V157, P1453, DOI 10.1001/archinte.157.13.1453; Mueller C, 2005, J INTERN MED, V258, P77, DOI 10.1111/j.1365-2796.2005.01503.x; Mueller C, 2004, NEW ENGL J MED, V350, P647, DOI 10.1056/NEJMoa031681; MULROW CD, 1993, J GEN INTERN MED, V8, P383, DOI 10.1007/BF02600079; MUSTCHIN CP, 1982, LANCET, V1, P907; PEARSON SB, 1981, POSTGRAD MED J, V57, P419; PRATTER MR, 1989, ARCH INTERN MED, V149, P2277, DOI 10.1001/archinte.149.10.2277; Ray P, 2005, J AM GERIATR SOC, V53, P643, DOI 10.1111/j.1532-5415.2005.53213.x; Rich MW, 2001, J GERONTOL A-BIOL, V56, pM88; SCHMITT BP, 1986, J GEN INTERN MED, V1, P386, DOI 10.1007/BF02596424; Torbicki A, 2000, EUR HEART J, V21, P1301; WUERZ RC, 1992, ANN EMERG MED, V21, P669, DOI 10.1016/S0196-0644(05)82777-5	34	96	100	1	2	BIOMED CENTRAL LTD	LONDON	MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND	1466-609X			CRIT CARE	Crit. Care		2006	10	3							R82	10.1186/cc4926		12	Critical Care Medicine	General & Internal Medicine	083DQ	WOS:000240436500013	16723034	
J	Bai, TR; Knight, DA				Bai, TR; Knight, DA			Structural changes in the airways in asthma: observations and consequences	CLINICAL SCIENCE			English	Review						airway smooth muscle; asthma; corticosteroid; fibrosis; lung function; matrix; remodelling	OBSTRUCTIVE PULMONARY-DISEASE; AIR-FLOW LIMITATION; RETICULAR BASEMENT-MEMBRANE; SMOOTH-MUSCLE-CELLS; LONG-TERM TREATMENT; 30-YEAR FOLLOW-UP; LUNG-FUNCTION; FATAL ASTHMA; RISK-FACTORS; BRONCHIAL-ASTHMA	Structural changes reported in the airways of asthmatics include epithelial fragility, goblet cell hyperplasia, enlarged submucosal mucus glands, angiogenesis, increased matrix deposition in the airway wall, increased airway smooth muscle mass, wall thickening and abnormalities in elastin. Genetic influences, as well as fetal and early life exposures, may contribute to structural changes such as subepithelial fibrosis from an early age. Other structural alterations are related to duration of disease and/or long-term uncontrolled inflammation. The increase in smooth muscle mass in both large and small airways probably occurs via multiple mechanisms, and there are probably changes in the phenotype of smooth muscle cells, some showing enhanced synthetic capacity, others enhanced proliferation or contractility. Fixed airflow limitation is probably due to remodelling, whereas the importance of structural changes to the phenomenon of airways hyperresponsiveness may be dependent on the specific clinical phenotype of asthma evaluated. Reduced compliance of the airway wall secondary to enhanced matrix deposition may protect against airway narrowing. Conversely, in severe asthma, disruption of alveolar attachments and adventitial thickening may augment airway narrowing. The encroachment upon luminal area by submucosal thickening may be disadvantageous by increasing the risk of airway closure in the presence of the intraluminal cellular and mucus exudate associated with asthma exacerbations. Structural changes may increase airway narrowing by alteration of smooth muscle dynamics through limitation of the ability of the smooth muscle to periodically lengthen.	Univ British Columbia, St Pauls Hosp, James Hogg iCAPTURE Ctr Cardiovasc & Pulm Res, Vancouver, BC V6Z 1Y6, Canada	Bai, TR (reprint author), Univ British Columbia, St Pauls Hosp, James Hogg iCAPTURE Ctr Cardiovasc & Pulm Res, 1081 Burrard St, Vancouver, BC V6Z 1Y6, Canada.	tbai@mrl.ubc.ca					Abraham B, 2003, EUR RESPIR J, V22, P470, DOI 10.1183/09031936.03.00261903; AGERTOFT L, 1994, RESP MED, V88, P373, DOI 10.1016/0954-6111(94)90044-2; Altraja A, 1996, AM J RESP CELL MOL, V15, P482; Amin K, 2000, AM J RESP CRIT CARE, V162, P2295; Apostol GG, 2002, AM J RESP CRIT CARE, V166, P166, DOI 10.1164/rccm.2007035; AZZAWI M, 1992, AM REV RESPIR DIS, V145, P1477; Bai TR, 2000, AM J RESP CRIT CARE, V162, P663; BAI TR, 1990, AM REV RESPIR DIS, V141, P552; Bai TR, 2004, J APPL PHYSIOL, V97, P2029, DOI 10.1152/japplphysiol.00884.2004; Baluk P, 2004, AM J PATHOL, V165, P1071, DOI 10.1016/S0002-9440(10)63369-X; Balzar S, 2002, EUR RESPIR J, V20, P254, DOI 10.1183/09031936.020.0261102; BALZAR S, 2004, AM J RESP CRIT CARE; Barbato A, 2003, AM J RESP CRIT CARE, V168, P798, DOI 10.1164/rccm.200305-650OC; BEASLEY R, 1989, AM REV RESPIR DIS, V139, P806; Benayoun L, 2003, AM J RESP CRIT CARE, V167, P1360, DOI 10.1164/rccm.200209-1030OC; Boulet LP, 2000, AM J RESP CRIT CARE, V162, P1308; Boulet LP, 2003, AM J RESP CRIT CARE, V167, P371, DOI 10.1164/rccm.200111-184PP; Bousquet J, 2000, AM J RESP CRIT CARE, V161, P1720; Bousquet J, 1996, AM J RESP CRIT CARE, V153, P1648; Brackel HJL, 2000, AM J RESP CRIT CARE, V162, P896; Brightling CE, 2002, NEW ENGL J MED, V346, P1699, DOI 10.1056/NEJMoa012705; Brown RH, 1997, J APPL PHYSIOL, V83, P366; Brusasco V, 2003, J APPL PHYSIOL, V95, P1305, DOI 10.1152/japplphysiol.00001.2003; Bumbacea D, 2004, EUR RESPIR J, V24, P122, DOI 10.1183/09031936.04.00077803; Carroll N, 1997, EUR RESPIR J, V10, P292, DOI 10.1183/09031936.97.10020292; CARROLL N, 1993, AM REV RESPIR DIS, V147, P405; Carroll NG, 2002, THORAX, V57, P677, DOI 10.1136/thorax.57.8.677; Carroll NG, 2000, AM J RESP CRIT CARE, V161, P244; Carroll NG, 1997, AM J RESP CRIT CARE, V155, P689; Chetta A, 1997, CHEST, V111, P852, DOI 10.1378/chest.111.4.852; Chetta A, 2003, AM J RESP CRIT CARE, V167, P751, DOI 10.1164/rccm.200207.710OC; Choe MM, 2003, AM J PHYSIOL-LUNG C, V285, pL427, DOI 10.1152/ajplung.00005.2003; COLEBATCH HJ, 1973, J APPL PHYSIOL, V34, P143; Covar RA, 2004, AM J RESP CRIT CARE, V170, P234, DOI 10.1164/rccm.200308-11740C; DEMOLY P, 1994, AM J RESP CRIT CARE, V150, P214; 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; EBINA M, 1993, AM REV RESPIR DIS, V148, P720; Evans MJ, 1999, AM J RESP CELL MOL, V21, P655; Faul JL, 1997, EUR RESPIR J, V10, P301, DOI 10.1183/09031936.97.10020301; FREW AJ, 1995, AM J RESP CRIT CARE, V151, P340; Gelb AF, 2004, CHEST, V126, P1138, DOI 10.1378/chest.126.4.1138; Gilliland FD, 2003, AM J RESP CRIT CARE, V167, P917, DOI 10.1164/rccm.200206-616OC; Gillis HL, 1999, J APPL PHYSIOL, V86, P2001; Green RH, 2002, THORAX, V57, P875, DOI 10.1136/thorax.57.10.875; Grol MH, 1999, AM J RESP CRIT CARE, V160, P1830; Groneberg DA, 2002, HISTOPATHOLOGY, V40, P367, DOI 10.1046/j.1365-2559.2002.01378.x; Gronke L, 2002, CLIN EXP ALLERGY, V32, P57, DOI 10.1046/j.0022-0477.2001.01297.x; HAAHTELA T, 1994, NEW ENGL J MED, V331, P700, DOI 10.1056/NEJM199409153311103; HAITCHI HH, 2004, AM J RESP CRIT CARE, V169, pA546; Halayko AJ, 2004, AM J RESP CELL MOL, V31, P266, DOI 10.1165/rcmb.2003-02720C; Haley KJ, 1998, AM J RESP CRIT CARE, V158, P565; Hamid Q, 1997, J ALLERGY CLIN IMMUN, V100, P44; Hansen EF, 1999, AM J RESP CRIT CARE, V159, P1267; Haraguchi M, 1999, AM J RESP CRIT CARE, V159, P1005; Hirst Stuart J, 2004, J Allergy Clin Immunol, V114, pS2, DOI 10.1016/j.jaci.2004.04.039; Hogg JC, 2004, NEW ENGL J MED, V350, P2645, DOI 10.1056/NEJMoa032158; Hoshino M, 1998, THORAX, V53, P21; Huang J, 1999, AM J RESP CRIT CARE, V160, P725; Huber HL, 1922, ARCH INTERN MED, V30, P689; in 't Veen Johannes C. 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Sci.	JUN	2005	108	6					463	477				15	Medicine, Research & Experimental	Research & Experimental Medicine	936OX	WOS:000229866400001	15896192	
J	Almqvist, C; Pershagen, G; Wickman, M				Almqvist, C; Pershagen, G; Wickman, M			Low socioeconomic status as a risk factor for asthma, rhinitis and sensitization at 4 years in a birth cohort	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergy and immunology; asthma; child; primary prevention; rhinitis; socioeconomy	CHILDHOOD ASTHMA; ALLERGIC SENSITIZATION; BRONCHIAL-ASTHMA; CHILDREN; BAMSE; SEVERITY; STRESS; ADULTS; ATOPY	Background The relation between socioeconomic status and allergic diseases in childhood is controversial. Some studies have proposed childhood asthma to be more common in families with low socioeconomic status, while sensitization to airborne allergens seems to be more frequent in individuals with higher socioeconomic status in childhood. Objective To assess the relation between socioeconomic status and asthma, rhinitis and sensitization in an unselected prospective birth cohort. Methods Four thousand and eighty-nine families with children born 1994-1996 in predefined areas of Stockholm answered questionnaires on environmental factors, socioeconomic status (parental occupation), and symptoms of allergic disease at birth, 1, 2 and 4 years of age. Blood samples taken at 4 years from 2614 children were analysed for specific IgE to common airborne and food allergens. Odds ratios (OR) and 95% confidence intervals (CI) for various outcomes in relation to socioeconomic status were estimated with a multiple logistic regression model, adjusting for potential confounders such as heredity for allergic diseases, maternal smoking, short duration of breastfeeding and house construction. Results There was a decreasing risk of asthma and rhinitis with increasing socioeconomic status. The OR for asthma was 0.33 (95% CI 0.17-0.66) and for rhinitis 0.50 (0.32-0.79) comparing the highest and the lowest socioeconomic groups, with a tendency to stronger effects in those with heredity for allergic disease. The risk of sensitization to food allergens also decreased with increasing socioeconomic status; OR 0.65 (0.41-1.02) in the highest socioeconomic group (P-trend=0.03), which was not clearly seen for airborne allergens. Conclusion Asthma, rhinitis and sensitization is more common in lower than in higher socioeconomic groups after adjustment for traditional risk factors. This may be related to additional uncontrolled differences in life style and environmental exposures between the groups, and calls for further studies.	Karolinska Hosp, Dept Environm & Occupat Hlth, S-17176 Stockholm, Sweden; Astrid Lindgren Childrens Hosp, Karolinska Inst, Dept Woman & Child Hlth, Stockholm, Sweden; Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; Karolinska Inst, Ctr Allergy Res, Stockholm, Sweden	Almqvist, C (reprint author), Karolinska Hosp, Dept Environm & Occupat Hlth, Norrbacka 3rd Floor, S-17176 Stockholm, Sweden.	catarina.almqvist@kbh.ki.se	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Pershagen, Goran/0000-0002-9701-1130			Almqvist C, 2003, CLIN EXP ALLERGY, V33, P1190, DOI 10.1046/j.1365-2222.2003.01764.x; Amre DK, 2002, J ASTHMA, V39, P625, DOI 10.1081/JAS-120014927; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Bergmann RL, 2000, CLIN EXP ALLERGY, V30, P1740, DOI 10.1046/j.1365-2222.2000.00927.x; Boudreaux ED, 2003, PEDIATRICS, V111, P615; Cesaroni G, 2003, EUR RESPIR J, V22, P619, DOI 10.1183/09031936.03.00091202; Emenius G, 2004, ACTA PAEDIATR, V93, P899, DOI 10.1080/08035250410025582; Forastiere F, 1997, EPIDEMIOLOGY, V8, P566, DOI 10.1097/00001648-199709000-00015; Gilliland FD, 2003, AM J EPIDEMIOL, V158, P576, DOI 10.1093/aje/kwg181; Koopman LP, 2002, ARCH DIS CHILD, V87, P482, DOI 10.1136/adc.87.6.482; Kozyrskyj AL, 2003, PEDIATR PULM, V36, P241, DOI 10.1002/ppul.10335; Lannero E, 2002, PEDIATR ALLERGY IMMU, V13, P182, DOI 10.1034/j.1399-3038.2002.01055.x; Lindbaek M, 2003, EUR RESPIR J, V21, P105, DOI 10.1183/09031936.02.00241802; Mielck A, 1996, INT J EPIDEMIOL, V25, P388, DOI 10.1093/ije/25.2.388; Mihrshahi S, 2003, J ALLERGY CLIN IMMUN, V111, P162, DOI 10.1067/mai.2003.36; Nagakura T, 2000, EUR RESPIR J, V16, P861, DOI 10.1183/09031936.00.16586100; Poyser MA, 2002, EUR RESPIR J, V19, P892, DOI 10.1183/09031936.02.00238402; Rona RJ, 1999, J EPIDEMIOL COMMUN H, V53, P15; Schaffer T, 2001, ALLERGY, V56, P1206, DOI 10.1034/j.1398-9995.2001.00208.x; Strachan DP, 1997, J ALLERGY CLIN IMMUN, V99, P6, DOI 10.1016/S0091-6749(97)81038-X; von Hertzen LC, 2002, J ALLERGY CLIN IMMUN, V109, P923, DOI 10.1067/mai.2002.124776; Wickman M, 2002, PEDIATR ALLERGY IMMU, V13, P11, DOI 10.1034/j.1399-3038.13.s.15.10.x; Wright RJ, 2002, AM J RESP CRIT CARE, V165, P358	23	96	96	1	12	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	MAY	2005	35	5					612	618		10.1111/j.1365-2222.2005.02243.x		7	Allergy; Immunology	Allergy; Immunology	927ES	WOS:000229175800012	15898983	
J	Berkman, N; Avital, A; Breuer, R; Bardach, E; Springer, C; Godfrey, S				Berkman, N; Avital, A; Breuer, R; Bardach, E; Springer, C; Godfrey, S			Exhaled nitric oxide in the diagnosis of asthma: comparison with bronchial provocation tests	THORAX			English	Article							OBSTRUCTIVE PULMONARY-DISEASE; EXERCISE; CHILDREN; METHACHOLINE; AIR; CHALLENGES; RECOMMENDATIONS; RESPONSIVENESS; EOSINOPHILS; ADENOSINE	Background: Bronchial provocation tests such as exercise, methacholine (MCH), and adenosine-5'-monophosphate ( AMP) challenges are used extensively in the diagnosis of asthma. A study was undertaken to determine whether exhaled nitric oxide (eNO) can be used to diagnose asthma in patients with non-specific respiratory symptoms and to compare this test with conventional provocation tests. Methods: Patients with non-specific respiratory symptoms and normal spirometric parameters were included in the study. eNO was measured and exercise, MCH and AMP challenges performed in all subjects. Patients were defined as asthmatic based on clinical follow up 24 months after testing. Results: Forty patients were considered asthmatic and 45 were not. The area under receiver operating characteristic curves gave values of 0.896 for eNO, 0.781 for exercise, 0.924 for MCH, and 0.939 for AMP (p = 0.033, 0.575 and 0.085 for eNO v exercise, MCH and AMP respectively). From our data, a cut off value of NO>7 ppb at a flow rate of 250 ml/s best differentiates between asthmatics and nonasthmatics (sensitivity 82.5%, specificity 88.9%). Optimal cut off values for other tests were exercise: Delta FEV1 >= 10% (sensitivity 57.9%, specificity 100%); PC20-MCH: <= 3 mg/ml (sensitivity 87.5%, specificity 86.7%); and PC20-AMP: <= 150 mg/ml (sensitivity 89.5%, specificity 95.6%). Conclusions: Measurement of eNO can be used as a safe, simple and rapid test for the diagnosis of asthma and is as good as bronchial provocation tests.	Hadassah Hebrew Univ Med Ctr, Inst Pulmonol, Jerusalem, Israel	Berkman, N (reprint author), Hadassah Univ Hosp, Inst Pulmonol, POB 12000, IL-91120 Jerusalem, Israel.	neville@hadassah.org.il					Al-Ali MK, 1998, RESP MED, V92, P701, DOI 10.1016/S0954-6111(98)90000-2; Al-Ali MK, 1998, RESP MED, V92, P908, DOI 10.1016/S0954-6111(98)90189-5; ALVING K, 1993, EUR RESPIR J, V6, P1368; American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P225, DOI DOI 10.1164/AJRCCM/136.1.225; AVITAL A, 1995, THORAX, V50, P511, DOI 10.1136/thx.50.5.511; Avital A, 2000, PEDIATR PULM, V30, P207, DOI 10.1002/1099-0496(200009)30:3<207::AID-PPUL5>3.0.CO;2-Z; BENTLEY AM, 1992, AM REV RESPIR DIS, V146, P500; Byrnes CA, 1997, THORAX, V52, P697; Chatkin JM, 1999, AM J RESP CRIT CARE, V159, P1810; Crapo RO, 2000, AM J RESP CRIT CARE, V161, P309; Deykin A, 1998, AM J RESP CRIT CARE, V157, P769; DEYKIN A, 2003, AM J RESP CRIT CARE, V165, P1597; Dotsch J, 1996, EUR RESPIR J, V9, P2537, DOI 10.1183/09031936.96.09122537; Dupont LJ, 2003, CHEST, V123, P751, DOI 10.1378/chest.123.3.751; Godfrey S, 1999, EUR RESPIR J, V14, P659, DOI 10.1034/j.1399-3003.1999.14c28.x; GUSTAFSSON LE, 1991, BIOCHEM BIOPH RES CO, V181, P852, DOI 10.1016/0006-291X(91)91268-H; HANLEY JA, 1983, RADIOLOGY, V148, P839; Jatakanon A, 1998, THORAX, V53, P91; Kharitonov S, 1997, EUR RESPIR J, V10, P1683, DOI 10.1183/09031936.97.10071683; KHARITONOV SA, 1995, EUR RESPIR J, V8, P295, DOI 10.1183/09031936.95.08020295; KHARITONOV SA, 1994, LANCET, V343, P133, DOI 10.1016/S0140-6736(94)90931-8; KHARITONOV SA, 1995, AM J RESP CRIT CARE, V152, P609; Lim S, 2000, THORAX, V55, P184, DOI 10.1136/thorax.55.3.184; Maziak W, 1998, AM J RESP CRIT CARE, V157, P998; NIH National Asthma Education and Prevention Program, 1997, GUID DIAGN MAN ASTHM; PERSSON MG, 1993, AM REV RESPIR DIS, V148, P1210; Silkoff PE, 1998, AM J RESP CRIT CARE, V157, P1822; Slutsky AS, 1999, AM J RESP CRIT CARE, V160, P2104; Smith AD, 2004, AM J RESP CRIT CARE, V169, P473, DOI 10.1164/rccm.200310-1376OC; VAN RE, 1999, THORAX, V54, P403; ZWEIG MH, 1993, CLIN CHEM, V39, P561	31	96	108	0	4	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	MAY	2005	60	5					383	388		10.1136/thx.2004.031104		6	Respiratory System	Respiratory System	920YH	WOS:000228730900009	15860713	
J	Bahceciler, NN; Arikan, C; Taylor, A; Akdis, M; Blaser, K; Barlan, IB; Akdis, CA				Bahceciler, NN; Arikan, C; Taylor, A; Akdis, M; Blaser, K; Barlan, IB; Akdis, CA			Impact of sublingual immunotherapy on specific antibody levels in asthmatic children allergic to house dust mites	INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY			English	Article						asthma; house dust mites; specific IgA; sublingual immunotherapy	PLACEBO-CONTROLLED EVALUATION; DOUBLE-BLIND; SWALLOW IMMUNOTHERAPY; INDUCED RHINITIS; ORAL TOLERANCE; POLLEN EXTRACT; EFFICACY; RHINOCONJUNCTIVITIS; TRIAL; SLIT	Objective: To evaluate the clinical outcome and changes in allergen-specific antibodies during sublingual immunotherapy ( SLIT) in house dust mite (HDM)-allergic asthma patients and to compare levels of allergen-specific antibodies in HDM-allergic patients before and after treatment with that of healthy controls. Method: Thirty-one asthma patients allergic to HDM were studied. Patients in groups I ( n = 17) and II ( n = 14) received SLIT with a standardized Dermatophagoides pteronyssinus plus Dermatophagoides farinae 50/50 extract for 6 and 12 months, respectively. A group of healthy children ( n = 8) were enrolled as controls. Patients in both groups were evaluated at the start and at the end of treatment according to daily symptom and medication scores, lung function and skin prick tests, PC20, blood eosinophil count, and Der-p-1-specific IgE, IgA, IgG1 and IgG4 levels. Results: Drug consumption decreased significantly in both groups. Furthermore, PC20 and forced expiratory flow between 25 and 75% of vital capacity of patients in group II improved significantly. Although specific IgA, IgG1 and IgG4 levels did not change throughout the treatment period, total eosinophil count and specific IgE decreased significantly in both groups. According to baseline measurements, specific IgA levels of patients in groups I and II were significantly lower than that of controls. This difference disappeared at the end of the treatment period in both groups. Conclusion: SLIT seems to be effective in ameliorating clinical symptoms, drug consumption and bronchial hyperreactivity, and results in downregulation of Der-p-1-specific IgE production. Furthermore, at the end of SLIT, specific IgA levels, which were decreased compared to healthy controls initially, did no longer differ between patients and controls. Copyright (C) 2005 S. Karger AG, Basel.	Marmara Univ Hosp, Div Pediat Allergy & Immunol, TR-34335 Istanbul, Turkey; Swiss Inst Allergy & Asthma Res, CH-7270 Davos, Switzerland	Bahceciler, NN (reprint author), Marmara Univ Hosp, Div Pediat Allergy & Immunol, Nilufer Sokak 5,Gazeteciler Sitesi C-5 Blok D42, TR-34335 Istanbul, Turkey.	aonder@attglobal.net					Akdis CA, 1996, J CLIN INVEST, V98, P1676, DOI 10.1172/JCI118963; Arikan C, 2004, CLIN EXP ALLERGY, V34, P398, DOI 10.1111/j.1365-2222.2004.01869.x; BAHCECILER NN, 2001, PEDIAT PULMONOL, V22, P618; BOUSQUET J, 1987, J ALLERGY CLIN IMMUN, V80, P591, DOI 10.1016/0091-6749(87)90013-3; Bousquet J, 1999, ALLERGY, V54, P249, DOI 10.1034/j.1398-9995.1999.00916.x; Bousquet J., 1998, Allergy (Copenhagen), V53, P1; CASANOVAS M, 1994, J INVEST ALLERG CLIN, V4, P305; CHEN YH, 1994, SCIENCE, V265, P1237, DOI 10.1126/science.7520605; COCKROFT DW, 1998, J ALLERGY CLIN IMMUN, V81, P111; Groux H, 1997, NATURE, V389, P737; Guez S, 2000, ALLERGY, V55, P369, DOI 10.1034/j.1398-9995.2000.00413.x; HEDLIN G, 1990, CLIN EXP ALLERGY, V20, P491, DOI 10.1111/j.1365-2222.1990.tb03141.x; HOLT PG, 1994, IMMUNOL TODAY, V15, P484, DOI 10.1016/0167-5699(94)90194-5; HOWARD LW, 2001, IMMUNOL REV, V182, P207; La Rosa M, 1999, J ALLERGY CLIN IMMUN, V104, P425, DOI 10.1016/S0091-6749(99)70388-X; Ledford DK, 2000, IMMUNOL ALLERGY CLIN, V20, P503, DOI 10.1016/S0889-8561(05)70163-6; MACHIELS JJ, 1986, BRIT MED J, V293, P948; Mohapatra SS, 2000, IMMUNOL ALLERGY CLIN, V20, P625, DOI 10.1016/S0889-8561(05)70170-3; Mungan D, 1999, ANN ALLERG ASTHMA IM, V82, P485, DOI 10.1016/S1081-1206(10)62726-3; *NAT HEART LUNG BL, 1992, PUBL US DEP HLTH HUM; Pajno GB, 2000, ALLERGY, V55, P842, DOI 10.1034/j.1398-9995.2000.00495.x; Passalacqua G, 1998, ALLERGY, V53, P477, DOI 10.1111/j.1398-9995.1998.tb04084.x; Polgar P, 1971, PULMONARY TESTING CH, P100; Quirino T, 1996, CLIN EXP ALLERGY, V26, P1253, DOI 10.1046/j.1365-2222.1996.d01-280.x; REID MJ, 1993, J ALLERGY CLIN IMMUN, V92, P6, DOI 10.1016/0091-6749(93)90030-J; Sterk PJ, 1993, EUR RESPIR J S, V16, P53; STROBEL S, 1998, IMMUNOL TODAY, V12, P156; TARI MG, 1990, ALLERGOL IMMUNOPATH, V18, P277; TROISE C, 1995, J INVEST ALLERG CLIN, V5, P25; VANWILSEM EJG, 1994, IMMUNOLOGY, V83, P128; Vourdas D, 1998, ALLERGY, V53, P662, DOI 10.1111/j.1398-9995.1998.tb03952.x; WARNER JO, 1978, LANCET, V2, P912; WIEDERMANN U, 2002, RES TRENDS, P17; WILLIAMS PV, 1998, IMMUNOL ALLERGY CLIN, V18, P133	34	96	106	0	3	KARGER	BASEL	ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND	1018-2438			INT ARCH ALLERGY IMM	Int. Arch. Allergy Immunol.		2005	136	3					287	294		10.1159/000083956		8	Allergy; Immunology	Allergy; Immunology	907CY	WOS:000227694100010	15722639	
J	Bornehag, CG; Sundell, J; Sigsgaard, T				Bornehag, CG; Sundell, J; Sigsgaard, T			Dampness in buildings and health (DBH): Report from an ongoing epidemiological investigation on the association between indoor environmental factors and health effects among children in Sweden	INDOOR AIR			English	Article						asthma; allergy; home; dampness; ventilation; pets; plasticisers	SCIENTIFIC EVIDENCE; ASTHMA; EXPOSURE; PREVALENCE	With the aim of identifying health-relevant exposures in buildings, an epidemiological study "Dampness in Buildings and Health" (DBH) started in the year 2000 in Sweden. The health focus of the study is on asthma and allergic symptoms among small children and their parents. The first step in the study was an epidemiological cross-sectional questionnaire on housing and health involving 14,077 preschool children in the county of Varmland in Sweden (March-April 2000). Self-reported moisture-related problems in the building were strongly associated with asthma, allergic symptoms, and airway infections among children and adults. Other factors associated with symptoms among the children were allergic heredity, smoking in the family, male sex, urban living, short breast feeding, pet keeping, daycare attendance, non-farming life and some food habits. The second step in the study was a nested case-control study including 198 children with symptoms and 202 healthy controls. A detailed clinical examination by physicians in parallel with extensive inspections and measurements in the subjects' homes were conducted from October 2001 to April 2002. The influence of selection bias in case-control studies has been studied, and questionnaires on self-reported symptoms and building characteristics have been validated. Identified risk factors for allergic symptoms are, e.g., inspector-observed dampness, a low ventilation rate, endotoxin, Penicillium and phthalates in dust. In the third phase, a 5-year follow-up study will be carried out during 2005. The same questionnaire as used in DBH-phase 1 will be distributed to the 10,852 children/parents who responded to the first questionnaire in 2000. Finally, in a fourth phase, controlled experimental studies in climate chambers and in vitro tests regarding findings from DBH-Phase 2 are planned to be conducted during 2004-08.	Tech Univ Denmark, Int Ctr Indoor Environm & Energy, DK-2800 Lyngby, Denmark; Karlstad Univ, Div Publ Hlth Sci, Karlstad, Sweden; Karlstad Univ, Swedish Natl Testing & Res Inst, Karlstad, Sweden; Aarhus Univ, Inst Environm & Occupat Med, DK-8000 Aarhus C, 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; Beasley R, 2003, PEDIATR CLIN N AM, V50, P539, DOI 10.1016/S0031-3955(03)00050-6; BERNER A, 2004, P ANN M AM AC ALL AS; Bornehag CG, 2001, INDOOR AIR, V11, P72; Bornehag CG, 2004, ALLERGY, V59, P554, DOI 10.1111/j.1398-9995.2004.00496.x; Bornehag CG, 2003, ALLERGY, V58, P939, DOI 10.1034/j.1398-9995.2003.00050.x; BORNEHAG CG, 2004, IN PRESS EPIDEMIOLOG; BORNEHAG CG, 2003, P 7 INT C HLTH BUILD; BORNEHAG CG, 2003, P COLD CLIM HVAC 200; BORNEHAG CG, 2004, IN PRESS INDOOR AIR; BORNEHAG CG, 2004, IN PRESS ENV HLTH PE; BORNEHAG CG, 2002, P 9 INT C IND AIR QU, V3; BORNEHAG CG, 2004, UNPUB PHTHALATES IND; BORNEHAG CG, 2002, P 9 INT C IND AIR QU, V3, P431; BORNHEAG CG, 2004, IN PRESS INDOOR AIR; ENGSTROM M, 2001, DIFFERENCES POSSIBLE; Etzel RA, 2003, PEDIATRICS, V112, P233; FORSMAN G, 2001, DIFFERENCES PREVALEN; Hagerhed L., 2002, P 9 INT C IND AIR QU, VV, P7; Hederos CA, 2002, ACTA PAEDIATR, V91, P1246, DOI 10.1080/080352502320777504; JANSSON A, 2004, USE ELECT EQUIPMENT; LAZZARI P, 2002, FOOD HABITS FAMILIES; LUNDGREN B, 2002, P 9 INT C IND AIR QU, V4, P153; NILSSON A, 2004, IN PRESS ATMOSPHERIC; Schneider T, 2003, INDOOR AIR, V13, P38, DOI 10.1034/j.1600-0668.2003.02025.x; Strachan DP, 2000, BRIT MED BULL, V56, P865, DOI 10.1258/0007142001903562; van Odijk J, 2003, ALLERGY, V58, P833, DOI 10.1034/j.1398-9995.2003.00264.x; Wargocki P, 2002, INDOOR AIR, V12, P113, DOI 10.1034/j.1600-0668.2002.01145.x	29	96	105	6	29	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0905-6947			INDOOR AIR	Indoor Air	AUG	2004	14			7			59	66		10.1111/j.1600-0668.2004.00274.x		8	Construction & Building Technology; Engineering, Environmental; Public, Environmental & Occupational Health	Construction & Building Technology; Engineering; Public, Environmental & Occupational Health	850DF	WOS:000223590700008	15330773	
J	Reefer, AJ; Carneiro, RM; Custis, NJ; Platts-Mills, TAE; Sung, SSJ; Hammer, J; Woodfolk, JA				Reefer, AJ; Carneiro, RM; Custis, NJ; Platts-Mills, TAE; Sung, SSJ; Hammer, J; Woodfolk, JA			A role for IL-10-mediated HLA-DR7-restricted T cell-dependent events in development of the modified Th2 response to cat allergen	JOURNAL OF IMMUNOLOGY			English	Article							DELAYED-TYPE HYPERSENSITIVITY; LATE ASTHMATIC REACTIONS; FEL-D-I; MONOCLONAL-ANTIBODIES; POSITIVE ASSOCIATION; SEQUENCE-ANALYSIS; DENDRITIC CELLS; IGG4 ANTIBODIES; MAJOR ALLERGEN; DOMESTIC CAT	Although high dose exposure to inhaled cat allergen (Fel d 1) can cause a form of tolerance (modified Th2 response), the T cell mechanism for this phenomenon has not been studied. T cell responses to Fel d 1 were characterized in both allergic (IgE(pos)) and modified Th2 (IgE(neg)IgG(pos)) responders as well as serum Ab-negative controls (IgE(neg)IgG(neg)). Fel d 1 stimulated high levels of IL-10 in PBMC cultures from all individuals, with evidence of Th2 and Th1 cytokine skewing in allergic and control subjects, respectively. Using overlapping peptides, epitopes at the N terminus of Fel d 1 chain 2 were shown to stimulate strong T cell proliferation and to preferentially induce IL-10 (peptide 2:1 (P2:1)) or IFN-gamma (P2:2) regardless of the allergic status of the donor. Injection of cat extract during conventional immunotherapy stimulated expansion of IL-10- and IFN-gamma-producing chain 2 epitope-specific T cells along with increased Fel d 1-specific serum IgG and IgG4 Ab. Six of 12 modified responders expressed the major HLA-DRB1 allele, *0701, and both P2:1 and P2:2 were predicted ligands for this allele. Cultures from DR7-positive modified responders produced the highest levels of IL-10 to P2:1 in addition to other major and minor epitopes within chains 1 and 2. In the presence of anti-IL-10 mAb, both T cell proliferation and IFN-gamma production were enhanced in a Fel d 1- and epitope-specific manner. We conclude that IL-10-producing T cells specific for chain 2 epitopes are relevant to tolerance induction, and that DR7-restricted recognition of these epitopes favors a modified Th2 response.	Univ Virginia, Dept Internal Med, Asthma & Allerg Dis Ctr, Charlottesville, VA 22908 USA; Univ Virginia, Dept Rheumatol, Charlottesville, VA 22908 USA; Hoffmann La Roche Inc, Dept Genome & Informat Sci, Nutley, NJ 07110 USA	Woodfolk, JA (reprint author), Univ Hlth Syst, Asthma & Allerg Dis Ctr, POB 801355, Charlottesville, VA 22908 USA.	jaw4m@virginia.edu			NIAID NIH HHS [AI50989, AI20565]		AALBERSE RC, 1983, J IMMUNOL, V130, P722; Akbari O, 2001, NAT IMMUNOL, V2, P725, DOI 10.1038/90667; Akdis CA, 1998, J CLIN INVEST, V102, P98, DOI 10.1172/JCI2250; Alexius B, 2002, INT J LAW PSYCHIAT, V25, P109, DOI 10.1016/S0160-2527(01)00114-5; Bellinghausen I, 1997, EUR J IMMUNOL, V27, P1131, DOI 10.1002/eji.1830270513; Blumenthal MN, 2002, ANN ALLERG ASTHMA IM, V88, P147; Brossart P, 2000, BLOOD, V96, P3102; CAMEIRO R, IN PRESS J INVEST DE; Cardaba B, 1996, CLIN EXP ALLERGY, V26, P316; CHAPMAN MD, 1988, J IMMUNOL, V140, P812; Cho SH, 2000, CLIN EXP ALLERGY, V30, P1568, DOI 10.1046/j.1365-2222.2000.00915.x; Counsell CM, 1996, J ALLERGY CLIN IMMUN, V98, P884, DOI 10.1016/S0091-6749(96)80004-2; DEGROOT H, 1988, J ALLERGY CLIN IMMUN, V82, P778, DOI 10.1016/0091-6749(88)90079-6; Disis ML, 1999, CLIN CANCER RES, V5, P1289; DJURUP R, 1984, ALLERGY, V39, P433, DOI 10.1111/j.1398-9995.1984.tb01965.x; DURHAM SR, 1995, INT ARCH ALLERGY IMM, V107, P282; Ebner C, 1997, CLIN EXP ALLERGY, V27, P1007, DOI 10.1111/j.1365-2222.1997.tb01252.x; Erwin E. 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Immunol.	MAR 1	2004	172	5					2763	2772				10	Immunology	Immunology	777PD	WOS:000189186000010	14978075	
J	Neaville, WA; Tisler, C; Bhattacharya, A; Anklam, K; Gilbertson-White, S; Hamilton, R; Adler, K; DaSilva, DF; Roberg, KA; Carlson-Dakes, KT; Anderson, E; Yoshihara, D; Gangnon, R; Mikus, LD; Rosenthal, LA; Gern, JE; Lemanske, RF				Neaville, WA; Tisler, C; Bhattacharya, A; Anklam, K; Gilbertson-White, S; Hamilton, R; Adler, K; DaSilva, DF; Roberg, KA; Carlson-Dakes, KT; Anderson, E; Yoshihara, D; Gangnon, R; Mikus, LD; Rosenthal, LA; Gern, JE; Lemanske, RF			Developmental cytokine response profiles and the clinical and immunologic expression of atopy during the first year of life	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						cytokines; T(H)2; immune development; allergy; IgE	INTERFERON-GAMMA PRODUCTION; COMMON FOOD PROTEINS; SUBSEQUENT DEVELOPMENT; IGE RESPONSES; T-CELLS; CHILDREN; ALLERGEN; ASTHMA; BLOOD; SYMPTOMS	Background: Allergic diseases have been linked to abnormal patterns of immune development, and this has stimulated efforts to define the precise patterns of cytokine dysregulation that are associated with specific atopic phenotypes. Objective: Cytokine-response profiles were prospectively analyzed over the first year of life and compared with the clinical and immunologic expressions of atopy. Methods: Umbilical cord and 1-year PBMCs were obtained from 285 subjects from allergic families. PHA-stimulated cytokine-response profiles (IL-5, IL-10, IL-13, and IFN-gamma) were compared with blood eosinophil counts and total and specific IgE levels (dust mites, cat, egg, Alternaria species, peanut, milk, and dog) at age 1 year and at the development of atopic dermatitis and food allergy. Results: For the cohort as a whole, cytokine responses did not evolve according to a strict T(H)1 or T(H)2 polarization pattern. PHA-stimulated cord blood cells secreted low levels of IL-5 (2.1 pg/mL), moderate levels of IFN-gamma (57.4 pg/mL), and greater amounts of IL-13 (281.8 pg/mL). From birth to 1 year, IL-5 responses dramatically increased, whereas IL-13 and IFN-gamma responses significantly decreased. Reduced cord blood secretion of IL-10 and IFN-gamma was associated with subsequent sensitization to egg. In addition, there was evidence of T(H)2 polarization (increased IL-5 and IL-13 levels) associated with blood eosinophilia and increased total IgE levels by age 1 year. Conclusion: These findings demonstrate that cytokine responses change markedly during the first year of life and provide further evidence of a close relationship between T(H)2 skewing of immune responses and the incidence of atopic manifestations in children.	Univ Wisconsin, Dept Pediat, Madison, WI USA; Univ Wisconsin, Dept Med, Madison, WI USA; Univ Wisconsin, Dept Biostat & Med Informat, Madison, WI USA; Univ Wisconsin, Gen Clin Res Ctr, Madison, WI USA	Neaville, WA (reprint author), Univ Wisconsin Hosp, K4-916,600 Highland Ave, Madison, WI 53792 USA.		Rosenthal, Louis/A-8868-2008		NCRR NIH HHS [2 M01 RR03186-16]; NHLBI NIH HHS [1P01HL70831-01, 1R01HL61879-01]		Akbari O, 2001, NAT IMMUNOL, V2, P725, DOI 10.1038/90667; Akbari O, 2002, NAT MED, V8, P1024, DOI 10.1038/nm745; BOCHNER BS, 1995, J IMMUNOL, V154, P799; Gern JE, 1999, J CLIN INVEST, V104, P837, DOI 10.1172/JCI8272; Halonen M, 1997, CLIN EXP ALLERGY, V27, P1234; HATTEVIG G, 1987, CLIN ALLERGY, V17, P571, DOI 10.1111/j.1365-2222.1987.tb02053.x; HATTEVIG G, 1984, CLIN ALLERGY, V14, P551, DOI 10.1111/j.1365-2222.1984.tb02243.x; Hoekstra MO, 1997, CLIN EXP ALLERGY, V27, P1254; Jeannin P, 1998, J IMMUNOL, V160, P3555; MARTINEZ FD, 1995, J ALLERGY CLIN IMMUN, V96, P652, DOI 10.1016/S0091-6749(95)70264-4; Matsui E, 2000, CLIN EXP ALLERGY, V30, P1250, DOI 10.1046/j.1365-2222.2000.00931.x; MCKENZIE ANJ, 1993, P NATL ACAD SCI USA, V90, P3735, DOI 10.1073/pnas.90.8.3735; NAKAGOMI T, 1994, LANCET, V343, P121, DOI 10.1016/S0140-6736(94)90854-0; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; Prescott SL, 1998, CLIN EXP ALLERGY, V28, P39; Prescott SL, 1998, J IMMUNOL, V160, P4730; Prescott SL, 1998, CLIN EXP ALLERGY, V28, P1313; Sampson H.A., 1998, ALLERGY PRINCIPLES P, P1162; SHAW RA, 1990, ARCH DIS CHILD, V65, P1319; SIGURS N, 1994, J ALLERGY CLIN IMMUN, V94, P757, DOI 10.1016/0091-6749(94)90184-8; TANG MLK, 1994, LANCET, V344, P983, DOI 10.1016/S0140-6736(94)91641-1; von Mutius E, 1998, LANCET, V351, P862, DOI 10.1016/S0140-6736(97)10100-3; WARNER JA, 1994, CLIN EXP ALLERGY, V24, P423, DOI 10.1111/j.1365-2222.1994.tb00930.x; Williams TJ, 2000, J ALLERGY CLIN IMMUN, V105, P951, DOI 10.1067/mai.2000.106211; ZEIGER RS, 1995, J ALLERGY CLIN IMMUN, V95, P1179, DOI 10.1016/S0091-6749(95)70074-9; ZURAWSKI G, 1994, IMMUNOL TODAY, V15, P19, DOI 10.1016/0167-5699(94)90021-3	27	96	98	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	2003	112	4					740	746		10.1067/mai.2003.1716		7	Allergy; Immunology	Allergy; Immunology	730LA	WOS:000185831200014	14564354	
J	Langley, SJ; Goldthorpe, S; Craven, M; Morris, J; Woodcock, A; Custovic, A				Langley, SJ; Goldthorpe, S; Craven, M; Morris, J; Woodcock, A; Custovic, A			Exposure and sensitization to indoor allergens: Association with lung function, bronchial reactivity, and exhaled nitric oxide measures in asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma severity and control; allergen exposure-sensitization; bronchial reactivity; lung function	DUST-MITE ANTIBODIES; CHILDHOOD ASTHMA; RISK-FACTORS; F-I; ADULTS; CHILDREN; COMMUNITY; DECLINE; HYPERRESPONSIVENESS; RESPONSIVENESS	Background: Exposure to high levels of allergens in sensitized asthmatic patients causes worsening of pulmonary function in experimental studies. Chronic exposure to lower, naturally occurring levels of allergens might increase the severity of asthma. Objective: We sought to study the associations between sensitization and exposure to common indoor allergens (dust mite, cat; and dog) in the home on pulmonary function, exhaled nitric oxide (eNO), and airway reactivity in asthmatic patients. Methods: Dust samples were collected from the living room carpet and mattress of 311 subject's homes, and Der p 1, Fel d 1, and Can f 1 concentrations were measured by using ELISAs. Spirometry, nonspecific bronchial reactivity, and eNO were measured. Results: Subjects both sensitized and exposed to high levels of sensitizing allergen had significantly lower FEV1 percent predicted values (mean, 83.7% vs 89.3%; mean difference, 5.6%; 95% CI, 0.6% -10.6%; P = .03), higher eNO values (geometric mean [GM], 12.8 vs 8.7 ppb; GM ratio, 0.7; 95% CI, 0.5-0.8; P = .001), and more severe airways reactivity (PD20 GM, 0.25 vs 0.73 mg; GM ratio, 2.9; 95% CI, 1.6-5.0; P < .001) compared with subjects not sensitized and exposed. No significant effect of the interaction between sensitization and exposure was found for FEV1 percent predicted and eNO values. However, there was a significant effect of the interaction between sensitization and exposure to any allergen (P = .05) and between sensitization and exposure to cat allergen (P = .04) for nonspecific bronchial reactivity. Conclusion: Asthmatic subjects who are exposed in their homes to allergens to which they are sensitized have a more severe form of the disease.	Wythenshawe Hosp, NW Lung Ctr, Med Evaluat Unit, Manchester M23 9LT, Lancs, England; Wythenshawe Hosp, Dept Stat, Manchester M23 9LT, Lancs, England	Langley, SJ (reprint author), Wythenshawe Hosp, NW Lung Ctr, Med Evaluat Unit, Manchester M23 9LT, Lancs, England.		Custovic, Adnan/A-2435-2012	Custovic, Adnan/0000-0001-5218-7071; Woodcock, Ashley/0000-0002-5428-8578			CHAPMAN MD, 1988, J IMMUNOL, V140, P812; COCKCROFT DW, 1977, CLIN ALLERGY, V7, P503, DOI 10.1111/j.1365-2222.1977.tb01481.x; Custovic A, 1998, THORAX, V53, P63; Custovic A, 2001, Curr Opin Allergy Clin Immunol, V1, P133; Custovic A, 1996, J ALLERGY CLIN IMMUN, V98, P64, DOI 10.1016/S0091-6749(96)70227-0; DJUKANOVIC R, 1990, AM REV RESPIR DIS, V142, P434; Frank TL, 1998, AM J RESP CRIT CARE, V158, P1032; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; Gottlieb DJ, 1996, AM J RESP CRIT CARE, V153, P561; HAMID Q, 1993, LANCET, V342, P1510, DOI 10.1016/S0140-6736(05)80083-2; Henriksen AH, 2000, EUR RESPIR J, V15, P849, DOI 10.1034/j.1399-3003.2000.15e07.x; INGRAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449, DOI 10.1016/S0091-6749(95)70286-5; JUNIPER EF, 1978, THORAX, V33, P705, DOI 10.1136/thx.33.6.705; Kharitonov S, 1997, EUR RESPIR J, V10, P1683, DOI 10.1183/09031936.97.10071683; KHARITONOV SA, 1995, AM J RESP CRIT CARE, V151, P1894; LUCZYNSKA CM, 1989, J IMMUNOL METHODS, V118, P227, DOI 10.1016/0022-1759(89)90010-0; Nelson HS, 1999, J ALLERGY CLIN IMMUN, V104, P775; Nelson RP, 1996, J ALLERGY CLIN IMMUN, V98, P258, DOI 10.1016/S0091-6749(96)70148-3; Omenaas E, 1996, EUR RESPIR J, V9, P919, DOI 10.1183/09031936.96.09050919; OMENAAS E, 1995, AM J RESP CRIT CARE, V152, P1158; Palmans E, 2000, AM J RESP CRIT CARE, V161, P627; PEAT JK, 1987, EUR J RESPIR DIS, V70, P171; Piacentini GL, 1999, J ALLERGY CLIN IMMUN, V104, P1323; POLLART SM, 1989, J ALLERGY CLIN IMMUN, V83, P875, DOI 10.1016/0091-6749(89)90100-0; QUANJER PH, 1993, EUR RESPIR J, V6, P5; Rosenstreich DL, 1997, NEW ENGL J MED, V336, P1356, DOI 10.1056/NEJM199705083361904; Salmon M, 1999, EUR RESPIR J, V14, P633, DOI 10.1034/j.1399-3003.1999.14c25.x; SALOME CM, 1980, CLIN ALLERGY, V10, P541, DOI 10.1111/j.1365-2222.1980.tb02135.x; SCHOU C, 1991, J ALLERGY CLIN IMMUN, V88, P847, DOI 10.1016/0091-6749(91)90240-O; Simpson A, 1999, AM J RESP CRIT CARE, V160, P45; Sunyer J, 2000, INT J EPIDEMIOL, V29, P125, DOI 10.1093/ije/29.1.125; Tracey M, 1995, Am J Respir Crit Care Med, V151, P656; Tunnicliffe WS, 1999, EUR RESPIR J, V13, P654, DOI 10.1183/09031936.99.13365499; ULRIK CS, 1992, THORAX, V47, P14, DOI 10.1136/thx.47.1.14; WOODFOLK JA, 1992, ANN ALLERGY, V69, P273; YAN K, 1983, THORAX, V38, P760, DOI 10.1136/thx.38.10.760	36	96	96	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.	AUG	2003	112	2					362	368		10.1067/mai.2003.1654		7	Allergy; Immunology	Allergy; Immunology	709WY	WOS:000184650600021	12897743	
J	Svanes, C; Heinrich, J; Jarvis, D; Chinn, S; Omenaas, E; Gulsvik, A; Kunzli, N; Burney, P				Svanes, C; Heinrich, J; Jarvis, D; Chinn, S; Omenaas, E; Gulsvik, A; Kunzli, N; Burney, P			Pet-keeping in childhood and adult asthma and hay fever: European Community Respiratory Health Survey	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						cats; dogs; birds; asthma; hay fever; sensitization; tolerance; hygiene hypothesis; ECRHS	HOUSE-DUST ENDOTOXIN; ALLERGEN EXPOSURE; CAT ALLERGENS; SENSITIZATION; CHILDREN; SYMPTOMS; LIFE; ATOPY; RISK; ENVIRONMENT	Background: Whether pet-keeping early in life protects against or promotes allergy remains unclear. Objective: Our aim was to examine the effects of childhood pet-keeping on adult allergic disease in a large international population-based study, including information on sensitization, adult pet-keeping, and pet prevalence in the populations. Methods: We used information from structured interviews (n = 18,530) and specific IgE to common aeroallergens in blood samples (n = 13,932) from participants in the European Community Respiratory Health Survey (ECRHS) to analyze the associations between keeping pets and adult asthma and hay fever. Results: Keeping cats in childhood was associated with asthma only among atopic subjects, an association that varied between centers (P = .002) and was stronger where cats where less common (< 40% cats: odds ratio(wheeze) [ORwheeze] = 1.84, 95% CI = 1.31-2.57; 40%-60% cats: ORwheeze = 1.33, 95% CI = 1.10-1.61; greater than or equal to60% cats: ORwheeze = 0.98, 95% CI = 0.73-1.33). Dogs owned in childhood or adulthood were associated with asthma among nonatopic subjects (childhood: ORwheeze = 1.28, 95% CI = 1.13-1.46; adulthood: ORwheeze = 1.31, 95% CI = 1.14-1.51; both: ORwheeze = 1.69, 95% CI = 1.40-2.04). In atopic subjects, those who had owned dogs in childhood had less hay fever (OR = 0.85; 95% CI = 0.73-0.98) and no increased risk of asthma (ORwheeze = 1.01, 95 % CI = 0.87-1.17). Respiratory symptoms were more common in subjects who had owned birds during childhood (ORwheeze = 1.12; 95 % CI = 1.02-1.23) independent of sensitization. Conclusions: The effects of pet-keeping in childhood varied according to the type of pet, the allergic sensitization of the individual, and the wider environmental exposure to allergen. Cats owned in childhood were associated with more asthma in sensitized adults who grew up in areas with a low community prevalence of cats. Dogs owned in childhood seemed to protect against adult allergic disease but promote nonallergic asthma.	Haraldsplass Hosp, Dept Med, N-5009 Bergen, Norway; Univ Bergen, Inst Med, Sect Resp Med, N-5009 Bergen, Norway; GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, Neuherberg, Germany; Univ London Kings Coll, Dept Publ Hlth Sci, London WC2R 2LS, England; Univ So Calif, Los Angeles, CA USA; Univ Basel, Basel, Switzerland	Svanes, C (reprint author), Haraldsplass Hosp, Dept Med, N-5009 Bergen, Norway.		Jarvis, Deborah/E-6494-2011; Kunzli, Nino/F-7195-2014	Kunzli, Nino/0000-0001-8360-080X	NCRR NIH HHS [2 S07 RR05521-28]		Anyo G, 2002, CLIN EXP ALLERGY, V32, P361, DOI 10.1046/j.1365-2222.2002.01254.x; Apelberg BJ, 2001, J ALLERGY CLIN IMMUN, V107, P455, DOI 10.1067/mai.2001.113240; *AVMA COMM HUM AN, 1995, J AM VET MED ASSOC, V206, P961; Baldini M, 2002, ALLERGY, V57, P188, DOI 10.1034/j.1398-9995.2002.1r152.x; 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; Braun-Fahrlander C, 2001, CLIN EXP ALLERGY, V31, P1799, DOI 10.1046/j.1365-2222.2001.01269.x; BUIJS J, 1995, AM J RESP CRIT CARE, V151, P873; 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; Celedon JC, 2002, LANCET, V360, P781, DOI 10.1016/S0140-6736(02)09906-3; Chan PWK, 2001, PEDIATR INT, V43, P350, DOI 10.1046/j.1442-200X.2001.01421.x; COPPERMAN SM, 1982, NEW YORK STATE J MED, V82, P1685; Custovic A, 2001, J ALLERGY CLIN IMMUN, V108, P537, DOI 10.1067/mai.2001.118599; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; Douwes J, 2002, THORAX, V57, P86, DOI 10.1136/thorax.57.1.86; Gehring U, 2002, AM J RESP CRIT CARE, V166, P939, DOI 10.1164/rccm.200203-256OC; Gehring U, 2001, EUR RESPIR J, V18, P555, DOI 10.1183/09031936.01.00096801; Heinrich J, 2001, CLIN EXP ALLERGY, V31, P1839, DOI 10.1046/j.1365-2222.2001.01220.x; Henriksen AH, 2001, RESP MED, V95, P122, DOI 10.1053/rmed.2000.1004; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Hesselmar B, 2001, PEDIATR ALLERGY IMMU, V12, P208, DOI 10.1034/j.1399-3038.2001.012004208.x; HOLSCHER B, 2002, PEDIAT ALLERGY IMMUN, V13; Holt PG, 1999, ALLERGY, V54, P12, DOI 10.1111/j.1398-9995.1999.tb04382.x; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; Litonjua AA, 2002, J ALLERGY CLIN IMMUN, V110, P736, DOI 10.1067/mai.2002.128948; Martinez FD, 1999, LANCET S2, V354, pSII12; Matricardi PM, 2000, BRIT MED J, V320, P412, DOI 10.1136/bmj.320.7232.412; Melsom T, 2001, THORAX, V56, P477, DOI 10.1136/thorax.56.6.477; Nafstad P, 2001, ALLERGY, V56, P307, DOI 10.1034/j.1398-9995.2001.00881.x; Noertjojo K, 1999, J ALLERGY CLIN IMMUN, V103, P60, DOI 10.1016/S0091-6749(99)70526-9; 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; 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; Prescott SL, 2001, CLIN EXP ALLERGY, V31, P1653, DOI 10.1046/j.1365-2222.2001.01258.x; Radon K, 2001, EUR RESPIR J, V17, P747, DOI 10.1183/09031936.01.17407470; Rees D, 1998, S AFR MED J, V88, P1110; Remes ST, 2001, J ALLERGY CLIN IMMUN, V108, P509, DOI 10.1067/mai.2001.117797; Ronmark E, 2001, PEDIATRICS, V107, DOI 10.1542/peds.107.3.e37; Roost HP, 1999, J ALLERGY CLIN IMMUN, V104, P941, DOI 10.1016/S0091-6749(99)70072-2; Sporik R, 2001, THORAX, V56, P58; Stata Corp, STAT STAT SOFTW REL; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Sunyer J., 1997, European Respiratory Journal, V10, P2490, DOI 10.1183/09031936.97.10112490; Svanes C, 1999, J ALLERGY CLIN IMMUN, V103, P415, DOI 10.1016/S0091-6749(99)70465-3; Tan JS, 1997, ARCH INTERN MED, V157, P1933, DOI 10.1001/archinte.157.17.1933; Tariq SM, 1998, J ALLERGY CLIN IMMUN, V101, P587; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; Withers NJ, 1998, AM J RESP CRIT CARE, V158, P352; 1980, CLASS OCC LOND OFF P	51	96	99	0	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.	AUG	2003	112	2					289	300		10.1067/mai.2003.1596		12	Allergy; Immunology	Allergy; Immunology	709WY	WOS:000184650600012	12897734	
J	Staples, JA; Ponsonby, AL; Lim, LLY; McMichael, AJ				Staples, JA; Ponsonby, AL; Lim, LLY; McMichael, AJ			Ecologic analysis of some immune-related disorders, including type 1 diabetes, in Australia: Latitude, regional ultraviolet radiation, and disease prevalence	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; Australia; autoimmune disease; ecologic analysis; eczema/dermatitis; immune disorders; latitude; rheumatoid arthritis; type 1 diabetes; ultraviolet radiation	VITAMIN-D DEFICIENCY; MULTIPLE-SCLEROSIS; RHEUMATOID-ARTHRITIS; AUTOIMMUNE-DISEASE; MOLECULAR MIMICRY; BIRTH-COHORT; EXPOSURE; MECHANISMS; RESPONSES; ASTHMA	The apparent immune-suppressive effect of ultraviolet radiation (UVR) has suggested that this environmental exposure may influence the development of immune-related disorders. Self-reported prevalence rates of type 1 diabetes mellitus, rheumatoid arthritis (RA), eczema/dermatitis, and asthma, from the 1995 Australian National Health Survey, were therefore examined by latitude and ambient level of UVR. A positive association of type I diabetes mellitus prevalence was found with both increasing southern latitude of residence (r = 0.77; P = 0.026) and decreasing regional annual ambient UVR (r = -0.80; p = 0.018); a 3-fold increase in prevalence from the northernmost region to the southernmost region was evident. In contrast, asthma correlated negatively with latitude (r = -0.72; p = 0.046), although the change in asthma prevalence from the north to the south of Australia was only 0.7-fold. For both RA and eczema/dermatitis, there were no statistically significant associations between latitude/UVR and disease prevalence. These ecologic data provide some support for a previously proposed beneficial effect of UVR on T-helper 1-mediated autoimmune disorders such as type 1 diabetes. The inverse association of type 1 diabetes prevalence with UVR is consistent with that previously reported for another autoimmune disease, multiple sclerosis, in Australia, and also with type I diabetes latitudinal gradients in the Northern Hemisphere. The finding also accords with photoimmunologic evidence of UVR-induced immunosuppression and may suggest a beneficial effect of UVR in reducing the incidence of such autoimmune conditions. In light of this study, analytic epidemiologic studies investigating risk of immune disorders in relation to personal UVR exposure in humans are required.	Australian Natl Univ, Natl Ctr Epidemiol & Populat Hlth, Canberra, ACT, Australia	Staples, JA (reprint author), Australian Natl Univ, Natl Ctr Epidemiol & Populat Hlth, Canberra, ACT, Australia.						*ABS, 1995, 43680 ABS; *ABS, 1995, 43630001 ABS; *ABS, 1995, 43630 ABS; Albert LJ, 1999, NEW ENGL J MED, V341, P2068, DOI 10.1056/NEJM199912303412707; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; Blasi F, 2001, Monaldi Arch Chest Dis, V56, P276; Cantorna MT, 2000, P SOC EXP BIOL MED, V223, P230, DOI 10.1046/j.1525-1373.2000.22333.x; Clydesdale GJ, 2001, IMMUNOL CELL BIOL, V79, P547, DOI 10.1046/j.1440-1711.2001.01047.x; Couper D, 1998, CLIN EXP ALLERGY, V28, P715; Dahlquist G, 1999, DIABETOLOGIA, V42, P51; Dahlquist G, 1998, Acta Paediatr Suppl, V425, P5; Damian DL, 1998, J INVEST DERMATOL, V110, P824, DOI 10.1046/j.1523-1747.1998.00176.x; Davidson A, 2001, NEW ENGL J MED, V345, P340; Duthie MS, 1999, BRIT J DERMATOL, V140, P995; Ebringer A, 2000, J MED MICROBIOL, V49, P305; EURODIAB, 2000, DIABETOLOGIA, V43, P47, DOI DOI 10.1007/S001250050006; Garssen J, 1999, IMMUNOLOGY, V97, P506; GIES HP, 1999, TRENDS SUN PROTECTIO, P1; Grover SR, 2001, MED J AUSTRALIA, V175, P251; Hammond SR, 2000, BRAIN, V123, P968, DOI 10.1093/brain/123.5.968; Haverkos HW, 1997, DIABETOLOGIA, V40, P1235, DOI 10.1007/s001250050813; Hayes CE, 1997, P SOC EXP BIOL MED, V216, P21; HERSEY P, 1983, J IMMUNOL, V131, P1471; Hypponen E, 2001, LANCET, V358, P1500, DOI 10.1016/S0140-6736(01)06580-1; Kamradt T, 2001, NEW ENGL J MED, V344, P655; KARGES WJP, 1995, MOL ASPECTS MED, V16, P79, DOI 10.1016/0098-2997(95)00001-W; KARVONEN M, 1993, DIABETOLOGIA, V36, P883, DOI 10.1007/BF02374468; Kelly DA, 1998, J PHOTOCH PHOTOBIO B, V44, P130, DOI 10.1016/S1011-1344(98)00136-5; Kero J, 2001, J ALLERGY CLIN IMMUN, V108, P781, DOI 10.1067/mai.2001.119557; Lemus-Deschamps L, 1999, METEOROL APPL, V6, P241, DOI 10.1017/S1350482799001188; Mackay IR, 2000, BRIT MED J, V321, P93, DOI 10.1136/bmj.321.7253.93; Mason RS, 2001, MED J AUSTRALIA, V175, P236; McGrath JJ, 2001, MED J AUSTRALIA, V174, P150; MCLEOD JG, 1994, MED J AUSTRALIA, V160, P117; McMichael AJ, 1997, EPIDEMIOLOGY, V8, P642, DOI 10.1097/00001648-199710000-00005; McMichael AJ, 2001, NEUROEPIDEMIOLOGY, V20, P165, DOI 10.1159/000054782; McNally NJ, 2000, BRIT J DERMATOL, V142, P712, DOI 10.1046/j.1365-2133.2000.03416.x; MILLER DH, 1990, J NEUROL NEUROSUR PS, V53, P903, DOI 10.1136/jnnp.53.10.903; Nghiem DX, 2001, J INVEST DERMATOL, V117, P1193, DOI 10.1046/j.0022-202x.2001.01503.x; Norris JM, 2001, LANCET, V358, P1476, DOI 10.1016/S0140-6736(01)06570-9; Notkins AL, 2001, J CLIN INVEST, V108, P1247, DOI 10.1172/JCI14257; Pasco JA, 2001, MED J AUSTRALIA, V175, P401; Pearce N, 1999, THORAX, V54, P268; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; Platts-Mills Thomas A E, 2002, Curr Allergy Asthma Rep, V2, P175, DOI 10.1007/s11882-002-0013-2; Ponsoby AL, 2002, TOXICOLOGY, V181, P71, DOI 10.1016/S0300-483X(02)00257-3; REWERS M, 1988, DIABETES, V37, P1113; Reynolds NJ, 2001, LANCET, V357, P2012, DOI 10.1016/S0140-6736(00)05114-X; Selgrade MJK, 1997, ENVIRON HEALTH PERSP, V105, P332, DOI 10.1289/ehp.97105332; Sleijffers A, 2001, J INVEST DERMATOL, V117, P1144, DOI 10.1046/j.0022-202x.2001.01542.x; Stene LC, 2000, DIABETOLOGIA, V43, P1093, DOI 10.1007/s001250051499; van der Mei IAF, 2001, NEUROEPIDEMIOLOGY, V20, P168, DOI 10.1159/000054783; Weinshenker BG, 1996, NEUROL CLIN, V14, P291, DOI 10.1016/S0733-8619(05)70257-7; Wilson C, 2000, MICROBES INFECT, V2, P1489, DOI 10.1016/S1286-4579(00)01303-4; Yang Z, 1998, DIABETES CARE, V21, P525, DOI 10.2337/diacare.21.4.525	55	96	103	0	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.	APR	2003	111	4					518	523		10.1289/ehp.5941		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	665WM	WOS:000182144300041	12676609	
J	Mendell, MJ; Fisk, WJ; Kreiss, K; Levin, H; Alexander, D; Cain, WS; Girman, JR; Hines, CJ; Jensen, PA; Milton, DK; Rexroat, LP; Wallingford, KM				Mendell, MJ; Fisk, WJ; Kreiss, K; Levin, H; Alexander, D; Cain, WS; Girman, JR; Hines, CJ; Jensen, PA; Milton, DK; Rexroat, LP; Wallingford, KM			Improving the health of workers in indoor environments: Priority research needs for a national occupational research agenda	AMERICAN JOURNAL OF PUBLIC HEALTH			English	Article							SICK-BUILDING-SYNDROME; AIR EXCHANGE-RATE; OFFICE BUILDINGS; RESPIRATORY-DISEASES; RHINOVIRUS COLDS; VENTILATION; RISK; TRANSMISSION; ASTHMA; INFECTIONS	Indoor nonindustrial work environments were designated a priority research area through the nationwide stakeholder process that created the National Occupational Research Agenda. A multidisciplinary research team used member consensus and quantitative estimates, with extensive external review, to develop a specific research agenda. The team outlined the following priority research topics: building-influenced communicable respiratory infections, building-related asthma/allergic diseases, and nonspecific building-related symptoms; indoor environmental science; and methods for increasing implementation of healthful building practices. Available data suggest that improving building environments may result in health benefits for more than 15 million of the 89 million US indoor workers, with estimated economic benefits of $5 to $75 billion annually. Research on these topics, requiring new collaborations and resources, offers enormous potential health and economic returns.	Lawrence Berkeley Natl Lab, Berkeley, CA 94720 USA; NIOSH, Div Surveillance Hazard Evaluat & Field Studies, Cincinnati, OH USA; NIOSH, Div Resp Dis Studies, Cincinnati, OH USA; Bldg Ecol Res Grp, San Diego, CA USA; Amer Federat Teachers, Washington, DC USA; Univ Calif San Diego, Dept Surg, Sch Med, San Diego, CA 92103 USA; US Environm Protect Agcy, Indoor Environm Div, Washington, DC USA; Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA; US Gen Serv Adm, Publ Bldg Serv, Ft Worth, TX USA	Mendell, MJ (reprint author), Lawrence Berkeley Natl Lab, 1 Cyclotron Rd,MS 90-3058, Berkeley, CA 94720 USA.		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J. Public Health	SEP	2002	92	9					1430	1440		10.2105/AJPH.92.9.1430		11	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	587UM	WOS:000177661900016	12197969	
J	Sagi, HC; Beutler, W; Carroll, E; Connolly, PJ				Sagi, HC; Beutler, W; Carroll, E; Connolly, PJ			Airway complications associated with surgery on the anterior cervical spine	SPINE			English	Article						airway; respiratory; complications; anterior cervical surgery	VOCAL CORD PARALYSIS; CASPAR INSTRUMENTATION; PLATE FIXATION; FUSION; OBSTRUCTION; INJURY; STABILIZATION; DISKECTOMY; CORPECTOMY; DYSPHAGIA	Study Design. Retrospective chart review of 311 anterior cervical procedures. Objectives. To assess the incidence and variables that predispose to an airway complication in a large series of anterior cervical surgical procedures. Summary of Background Data. A rare but potentially lethal complication after anterior cervical spine surgery is respiratory compromise and airway obstruction, Some risk factors are thought to include two-level corpectomy in myelopathic patients with a history of heavy smoking and asthma. No previous study in the literature has been directed at examining the factors specifically related to airway complications after anterior cervical spine surgery, Methods. Each chart was examined for patient characteristics and pathology, anesthetic parameters and problems, operative procedure, and postoperative course and management. Statistical analysis was performed. Results. Nineteen patients (6.1%) had an airway complication and six (1.9%) required reintubation. One patient died. Symptoms developed on average 36 hours postoperatively. All complications except for two were attributable to pharyngeal edema. Variables that were found to be statistically associated with an airway complication (P < 0.05) were exposing more than three vertebral bodies, a blood loss >300 mL, exposures involving C2, C3, or C4, and an operative time >5 hours. A history of myelopathy, spinal cord injury, pulmonary problems, smoking, anesthetic risk factors, and the absence of a drain did not correlate with an airway complication, Conclusions. Patients with prolonged procedures (i.e., >5 hours) exposing more than three vertebral levels that include C2, C3, or C4 with more than 300-mL blood loss should be watched carefully for respiratory insufficiency.	Univ Calif San Francisco, Fresno Med Educ Program, Fresno, CA USA; SUNY Upstate Med Univ, Syracuse, NY USA	Sagi, HC (reprint author), Calif State Univ Fresno, Dept Orthopaed, Ctr Med, 445 S Cedar Ave, Fresno, CA 93702 USA.	eversosaggy@cs.com					ANDERSON PA, 1992, J BONE JOINT SURG AM, V74A, P683; ANDREWS ET, 1971, CLIN ORTHOP RELAT R, P15; BERTALANFFY H, 1989, ACTA NEUROCHIR, V99, P41, DOI 10.1007/BF01407775; Bookvar JA, 2001, J NEUROSURG, V94, P12; Bose B, 1998, SURG NEUROL, V49, P25, DOI 10.1016/S0090-3019(97)00306-6; BROWN JA, 1988, SPINE, V13, P236, DOI 10.1097/00007632-198803000-00003; Daniels SK, 1998, ENT-EAR NOSE THROAT, V77, P473; Drompp B W, 1964, Clin Orthop Relat Res, V34, P42; EMERY SE, 1991, J BONE JOINT SURG AM, V73A, P544; Henry AD, 1999, J BONE JOINT SURG BR, V81B, P472, DOI 10.1302/0301-620X.81B3.9109; Jellish WS, 1999, J NEUROSURG, V91, P170, DOI 10.3171/spi.1999.91.2.0170; Jonsson B, 1994, Eur Spine J, V3, P76, DOI 10.1007/BF02221444; Kirshblum S, 1999, ARCH PHYS MED REHAB, V80, P1101, DOI 10.1016/S0003-9993(99)90068-0; Krnacik MJ, 1997, SPINE, V22, P2188, DOI 10.1097/00007632-199709150-00019; Malca SA, 1996, SPINE, V21, P685, DOI 10.1097/00007632-199603150-00004; Manski TJ, 1998, J NEUROSURG, V89, P839, DOI 10.3171/jns.1998.89.5.0839; Morpeth JF, 2000, LARYNGOSCOPE, V110, P43, DOI 10.1097/00005537-200001000-00009; Muzumdar DP, 2000, SURG NEUROL, V53, P586, DOI 10.1016/S0090-3019(00)00245-7; Penberthy A, 1998, ANAESTH INTENS CARE, V26, P305; RIEW DK, 1999, J BONE JOINT SURG AM, V81, P950; Riew KD, 1999, SPINE, V24, P2404, DOI 10.1097/00007632-199911150-00019; ROBINSON RA, 1955, B JOHNS HOPKINS HOSP, V96, P223; STONE JL, 1989, J NEUROSURG, V70, P879, DOI 10.3171/jns.1989.70.6.0879; SUH PB, 1990, SPINE, V15, P1079, DOI 10.1097/00007632-199015100-00018; Swank M L, 1997, Eur Spine J, V6, P138, DOI 10.1007/BF01358747; Swank ML, 1997, SPINE, V22, P274, DOI 10.1097/00007632-199702010-00009; Tew J M Jr, 1976, Clin Neurosurg, V23, P424; TIPPETS RH, 1988, NEUROSURGERY, V22, P1008; Winslow CP, 1999, AM J OTOLARYNG, V20, P16, DOI 10.1016/S0196-0709(99)90046-7; Winslow CP, 2001, ARCH OTOLARYNGOL, V127, P51; Zeidman SM, 1997, J SPINAL DISORD, V10, P523	31	96	103	0	3	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	0362-2436			SPINE	SPINE	MAY 1	2002	27	9					949	953		10.1097/00007632-200205010-00013		5	Clinical Neurology; Orthopedics	Neurosciences & Neurology; Orthopedics	548ZL	WOS:000175420000012	11979168	
J	Hoppin, JA; Umbach, DM; London, SJ; Alavanja, MCR; Sandler, DP				Hoppin, JA; Umbach, DM; London, SJ; Alavanja, MCR; Sandler, DP			Chemical predictors of wheeze among farmer pesticide applicators in the agricultural health study	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						wheeze; pesticides; organophosphates; paraquat; agricultural exposure	RESPIRATORY SYMPTOMS; OCCUPATIONAL ASTHMA; PARAQUAT; WORKERS; INSECTICIDE; POPULATION; PREVALENCE; SELECTION; EXPOSURE; INDUSTRY	Pesticides may contribute to respiratory symptoms among farmers. Using the Agricultural Health Study, a large cohort of certified pesticide applicators in Iowa and North Carolina, we explored the association between wheeze and pesticide use in the past year. Self-administered questionnaires contained items on 40 currently used pesticides and pesticide application practices. A total of 20,468 applicators, ranging in age from 16 to 88 years, provided complete information; 19% reported wheezing in the past year. Logistic regression models controlling for age, state, smoking, and history of asthma or atopy were used to evaluate associations between individual pesticides and wheeze. Among pesticides suspected to contribute to wheeze, paraquat, three organophosphates (parathion, malathion, and chlorpyrifos), and one thiocarbamate (S-ethyl-dipropylthiocarbamate [EPTC]) had elevated odds ratios (OR). Parathion had the highest OR (1.5, 95% confidence interval [CI] 1.0, 2.2). Chlorpyrifos, EPTC, paraquat, and parathion demonstrated significant dose-response trends. The herbicides, atrazine and alachlor, but not 2,4-D, were associated with wheeze. Atrazine had a significant dose-response trend with participants applying atrazine more than 20 days/year having an OR of 1.5 (95% CI 1.2, 1.9). Inclusion of crops and animals into these models did not significantly alter the observed OR. These associations, though small, suggest an independent role for specific pesticides in respiratory symptoms of farmers.	NIEHS, Epidemiol Branch, NIH, Res Triangle Pk, NC 27709 USA; NIEHS, Biostat Branch, NIH, Res Triangle Pk, NC 27709 USA; NCI, Occupat Epidemiol Branch, NIH, Rockville, MD USA	Hoppin, JA (reprint author), NIEHS, Epidemiol Branch, NIH, MD A3-05,POB 12233, Res Triangle Pk, NC 27709 USA.			Sandler, Dale/0000-0002-6776-0018; London, Stephanie/0000-0003-4911-5290			Alavanja MCR, 1996, ENVIRON HEALTH PERSP, V104, P362, DOI 10.2307/3432672; BLAIR A, 1993, EPIDEMIOLOGY, V4, P55, DOI 10.1097/00001648-199301000-00011; BRYANT DH, 1985, AUST NZ J MED, V15, P66, DOI 10.1111/j.1445-5994.1985.tb02740.x; Castro-Gutierrez N, 1997, SCAND J WORK ENV HEA, V23, P421; *CHEM PHARM PRESS, 1995, CROP PROT REF; CONE JE, 1994, CHEST, V106, P500, DOI 10.1378/chest.106.2.500; Dalvie MA, 1999, OCCUP ENVIRON MED, V56, P391; DESCHAMPS D, 1994, LANCET, V344, P1712, DOI 10.1016/S0140-6736(94)90498-7; DOSMAN JA, 1987, J OCCUP ENVIRON MED, V29, P38; Fishwick D, 1997, OCCUP ENVIRON MED, V54, P301; HONDA I, 1992, THORAX, V47, P760, DOI 10.1136/thx.47.9.760; HONORE P, 1994, ACTA CLIN BELG, V49, P220; 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; 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; Masley M L, 2000, J Agric Saf Health, V6, P103; Melbostad E, 1998, SCAND J WORK ENV HEA, V24, P262; Nathell L, 2000, SCAND J WORK ENV HEA, V26, P382; Ohayo-Mitoko GJA, 2000, OCCUP ENVIRON MED, V57, P195, DOI 10.1136/oem.57.3.195; POPENDORF W, 1985, AM IND HYG ASSOC J, V46, P154, DOI 10.1202/0002-8894(1985)046<0154:ASOARH>2.3.CO;2; Post W, 1998, OCCUP ENVIRON MED, V55, P349; ROYCE S, 1993, CHEST, V103, P295, DOI 10.1378/chest.103.1.295; SCHENKER M, 1991, OCCUP MED, V6, P415; Schenker MB, 1998, AM J RESP CRIT CARE, V158, pS1; Schwartz DA, 1999, ENVIRON HEALTH PERSP, V107, P393; SENTHILSELVAN A, 1992, AM REV RESPIR DIS, V146, P884; Sprince NL, 2000, AM J IND MED, V38, P455; Tarone RE, 1997, AM J IND MED, V31, P233; Tupi K, 1987, Eur J Respir Dis Suppl, V152, P206; Vogelzang PFJ, 1999, EUR RESPIR J, V13, P187, DOI 10.1034/j.1399-3003.1999.13a34.x; WEINER A, 1961, ANN ALLERGY, V19, P397; Wilkins JR, 1999, AM J IND MED, V35, P150, DOI 10.1002/(SICI)1097-0274(199902)35:2<150::AID-AJIM7>3.0.CO;2-5; Yemaneberhan H, 1997, LANCET, V350, P85, DOI 10.1016/S0140-6736(97)01151-3	32	96	97	1	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.	MAR 1	2002	165	5					683	689		10.1164/rccm.2106074		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	526LD	WOS:000174131200013	11874814	
J	Danahay, H; Atherton, H; Jones, G; Bridges, RJ; Poll, CT				Danahay, H; Atherton, H; Jones, G; Bridges, RJ; Poll, CT			Interleukin-13 induces a hypersecretory ion transport phenotype in human bronchial epithelial cells	AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY			English	Article						calcium-activated chloride channel; hypersecretion; asthma; interleukin-4	TRANSMEMBRANE CONDUCTANCE REGULATOR; AIRWAY EPITHELIUM; WILD-TYPE; EXPRESSION; ASTHMA; CHANNEL; DIFFERENTIATION; MODULATION; MEDIATORS; IL-13	Interleukin (IL)-13 has been associated with asthma, allergic rhinitis, and chronic sinusitis, all conditions where an imbalance in epithelial fluid secretion and absorption could impact upon the disease. We have investigated the effects of IL-13 on the ion transport characteristics of human bronchial epithelial cells cultured at an apical-air interface. Ussing chamber studies indicated that 48 h pretreatment with IL-13 or IL-4 significantly reduced the basal short-circuit current (I-sc) and inhibited the amiloride-sensitive current by >98%. Furthermore, the I-sc responses were increased by more than six- and twofold over control values when stimulated with UTP or forskolin, respectively, after cytokine treatment. The IL-13-enhanced response to UTP/ionomycin was sensitive to bumetanide and DIDS and was reduced in a low-chloride, bicarbonate-free solution. Membrane permeablization studies indicated that IL-13 induced the functional expression of an apical Ca2+-activated anion conductance and that changes in apical or basolateral K+ conductances could not account for the increased I-sc responses to UTP or ionomycin. The results indicate that IL-13 converts the human bronchial epithelium from an absorptive to a secretory phenotype that is the result of loss of amiloride-sensitive current and an increase in a DIDS-sensitive apical anion conductance.	Novartis Resp Res Ctr, Horsham RH12 5AB, W Sussex, England; Univ Pittsburgh, Dept Cell Biol & Physiol, Pittsburgh, PA 15261 USA	Danahay, H (reprint author), Novartis Resp Res Ctr, Wimblehurst Rd, Horsham RH12 5AB, W Sussex, England.						Alpert SE, 1995, AM J PHYSIOL-LUNG C, V269, pL734; BESANCON F, 1994, AM J PHYSIOL-CELL PH, V267, pC1398; Borok Z, 1998, AM J PHYSIOL-LUNG C, V274, pL149; BOUCHER RC, 1994, AM J RESP CRIT CARE, V150, P271; Brouillard F, 2001, J BIOL CHEM, V276, P9486, DOI 10.1074/jbc.M006636200; Cafferata EGA, 2001, J BIOL CHEM, V276, P15441, DOI 10.1074/jbc.M010061200; Chang MMJ, 1998, AM J PHYSIOL-LUNG C, V275, pL524; CHRISTOFFERSEN GRJ, 1975, COMP BIOCHEM PHYS A, V52, P317, DOI 10.1016/S0300-9629(75)80094-6; Devor DC, 2000, AM J PHYSIOL-CELL PH, V279, pC461; Devor DC, 1999, AM J PHYSIOL-CELL PH, V276, pC827; Fukuda N, 2001, AM J PHYSIOL-LUNG C, V280, pL1258; Fuller CM, 2000, CLIN EXP PHARMACOL P, V27, P906, DOI 10.1046/j.1440-1681.2000.03359.x; Galietta LJV, 2000, AM J PHYSIOL-LUNG C, V278, pL1186; Ghanshani S, 2000, J BIOL CHEM, V275, P37137, DOI 10.1074/jbc.M003941200; Gray TE, 1996, AM J RESP CELL MOL, V14, P104; HAMILOS DL, 1996, AM J RESP CELL MOL B, V15, P433; Holgate ST, 2000, AM J RESP CRIT CARE, V162, pS113; HUANG SK, 1995, J IMMUNOL, V155, P2688; Humbert M, 1997, J ALLERGY CLIN IMMUN, V99, P657, DOI 10.1016/S0091-6749(97)70028-9; Iwase N, 1997, J CLIN INVEST, V99, P1651, DOI 10.1172/JCI119328; Kerem E, 1999, NEW ENGL J MED, V341, P156, DOI 10.1056/NEJM199907153410304; Kotsimbos TC, 1996, P ASSOC AM PHYSICIAN, V108, P368; Kunzelmann K, 2000, PFLUG ARCH EUR J PHY, V440, P193, DOI 10.1007/s004240000255; Kunzelmann K, 2000, P NATL ACAD SCI USA, V97, P10282, DOI 10.1073/pnas.160041997; Martin LD, 1997, EUR RESPIR J, V10, P2139, DOI 10.1183/09031936.97.10092139; Martin LD, 2000, CHEST, V117, p267S, DOI 10.1378/chest.117.5_suppl_1.267S; NAKAMURA H, 1992, FEBS LETT, V314, P366, DOI 10.1016/0014-5793(92)81507-I; Nakanishi A, 2001, P NATL ACAD SCI USA, V98, P5175, DOI 10.1073/pnas.081510898; Nettesheim P, 1996, TOXICOL LETT, V88, P35, DOI 10.1016/0378-4274(96)03715-0; Paradiso AM, 2001, J GEN PHYSIOL, V117, P53; PAWANKAR RU, 1995, AM J RESP CRIT CARE, V152, P2059; Pilewski Joseph M., 1999, Physiological Reviews, V79, pS215; Schultz B. D., 1999, Physiological Reviews, V79, pS109; Temann UA, 1997, AM J RESP CELL MOL, V16, P471; Van den Berg JG, 2000, J AM SOC NEPHROL, V11, P413; Wang YB, 1999, J APPL PHYSIOL, V87, P1852; ZegarraMoran O, 1997, J MEMBRANE BIOL, V156, P297, DOI 10.1007/s002329900209; Zhu Zhou, 1999, Journal of Clinical Investigation, V103, P779, DOI 10.1172/JCI5909; Zund G, 1996, J BIOL CHEM, V271, P7460	39	96	101	0	1	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.	FEB	2002	282	2					L226	L236				11	Physiology; Respiratory System	Physiology; Respiratory System	511YA	WOS:000173292100009	11792627	
J	Li, YF; Gilliland, FD; Berhane, K; McConnell, R; Gauderman, WJ; Rappaport, EB; Peters, JM				Li, YF; Gilliland, FD; Berhane, K; McConnell, R; Gauderman, WJ; Rappaport, EB; Peters, JM			Effects of in utero and environmental tobacco smoke exposure on lung function in boys and girls with and without asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							SOUTHERN CALIFORNIA COMMUNITIES; MATERNAL SMOKING; PULMONARY-FUNCTION; CIGARETTE-SMOKING; PARENTAL SMOKING; PASSIVE SMOKING; RESPIRATORY ILLNESS; DIFFERING LEVELS; AIR-POLLUTION; CHILDREN	To investigate whether the effects of in utero exposure to maternal smoking and environmental tobacco smoke (ETS) exposure on lung function vary by sex or asthma status, we examined medical history and tobacco smoke exposure data for 5,263 participants in the Children's Health Study. At study enrollment, parents or guardians of each subject completed a questionnaire, and lung function was measured spirometrically with maximum forced expiratory flow-volume maneuvers. To assess the in utero effects of maternal smoking and ETS exposure on lung function, we used regression splines that accounted for the nonlinear relationship between pulmonary function, height, and age. In utero exposure to maternal smoking was independently associated with deficits in lung function that were larger for children with asthma. Boys and girls with a history of in utero exposure to maternal smoking showed deficits in maximum midexpiratory flow (MMEF) and a decrease in the FEV1/FVC ratio. As compared with children without asthma, boys with asthma had significantly larger deficits from in utero exposure in FVC, MMEF, and FEV1/FVC, and girls with asthma had larger decreases in FEV1/FVC. The effect of ETS exposure varied by children's gender and asthma status. Deficits in flows associated with current ETS exposure were present in children with and without asthma but were significant only among children without asthma. Past ETS exposure was associated with reduced FEV1, MMEF, and FEV1/FVC among boys with asthma. In contrast, past ETS exposure was associated with decreased flow rates in girls without asthma. In summary, both in utero exposure to maternal smoking and ETS exposure were associated with persistent deficits in lung function. The effects of in utero exposure were greatest among children with 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,CHP 236, Los Angeles, CA 90033 USA.		LI, YU-FEN/F-4770-2010		NHLBI NIH HHS [1 R01 HL61768-01]; NIEHS NIH HHS [5P30 ES07048-02, 1P01 ES09581-05]		Becker R. A., 1988, NEW S LANGUAGE; 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 EFFECTS EXPOSUR; 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; DIJKSTRA L, 1990, AM REV RESPIR DIS, V142, P1172; DODGE RR, 1980, AM REV RESPIR DIS, V122, P567; Gilliland FD, 2000, THORAX, V55, P271, DOI 10.1136/thorax.55.4.271; GOLD DR, 1993, AM REV RESPIR DIS, V148, P10; HABY MM, 1994, PEDIATR PULM, V18, P323, DOI 10.1002/ppul.1950180510; 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; Jedrychowski W, 1996, Przegl Epidemiol, V50, P457; Joad JP, 1999, TOXICOL APPL PHARM, V155, P253, DOI 10.1006/taap.1998.8612; KNIGHT A, 1985, MED J AUSTRALIA, V142, P194; MURRAY AB, 1988, CHEST, V94, P701, DOI 10.1378/chest.94.4.701; 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, 1992, AM REV RESPIR DIS, V145, P1136; 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; Ulrik CS, 1999, EUR RESPIR J, V13, P904, DOI 10.1034/j.1399-3003.1999.13d35.x; *US DEP HHS, 1986, PHS PUBL; U. S. Environmental Protection Agency, 1992, RESP HLTH EFF PASS S; WANG XB, 1994, AM J RESP CRIT CARE, V149, P1420; WEITZMAN M, 1990, PEDIATRICS, V85, P505; WYPIJ D, 1993, STAT SINICA, V3, P329	42	96	102	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.	DEC	2000	162	6					2097	2104				8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	381ZV	WOS:000165794700023	11112121	
J	Shima, M; Adachi, M				Shima, M; Adachi, M			Effect of outdoor and indoor nitrogen dioxide on respiratory symptoms in schoolchildren	INTERNATIONAL JOURNAL OF EPIDEMIOLOGY			English	Article						nitrogen dioxide; air pollution; indoor environment; wheeze; asthma; cohort study	AIR-POLLUTION; CHILDHOOD ASTHMA; INHALED ALLERGEN; LUNG-FUNCTION; EAST-GERMANY; CHILDREN; EXPOSURE; HEALTH; ASSOCIATION; PREVALENCE	Background Nitrogen dioxide (NO2), an oxidant gas that contaminates both outdoor and indoor air, is considered to be a potential risk factor for asthma. We investigated concurrently the effects of outdoor and indoor NO2 on the prevalence and incidence of respiratory symptoms among children. Methods A cohort study was carried out over 3 years on 842 schoolchildren living in seven different communities in Japan. Indoor NO2. concentrations over 24 hours were measured in both winter and summer in. the homes of the subjects, and a 3-year average of the outdoor NO2 concentration was determined for each community. Respiratory symptoms were evaluated every year from responses to questionnaires. Results The prevalence of bronchitis, wheeze, and asthma significantly increased with increases of indoor NO2 concentrations among girls, but not among boys. In neither boys nor girls were there significant differences in the prevalence of respiratory symptoms among urban, suburban, and rural districts. The incidence of asthma increased among children living in areas with high concentrations of outdoor NO2 Multiple logistic regression analysis showed that a 10 parts per billion (ppb) increase of outdoor NO2 concentration was associated with an increased incidence of wheeze and asthma (odds ratios [OR] = 1.76, 95% CI : 1.04-3.23 and OR = 2.10, 95% CI: 1.10-4.75, respectively), but that no such associations were found with indoor NO2 concentration (OR = 0.73, 95% CI:0.45-1.14 and OR = 0.87, 95% CI:0.51-1.43,respectively). Conclusions These findings suggest that outdoor NO2 air pollution may be particularly important for the development of wheeze and asthma among children. Indoor NO2 concentrations were associated with the prevalence of respiratory symptoms only among girls. Girls may be more susceptible to indoor air pollution than boys.	Chiba Univ, Sch Med, Dept Publ Hlth, Chuo Ku, Chiba 2608670, Japan	Shima, M (reprint author), Chiba Univ, Sch Med, Dept Publ Hlth, Chuo Ku, 1-8-1 Inohana, Chiba 2608670, Japan.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			ANTO JM, 1995, LANCET, V345, P402, DOI 10.1016/S0140-6736(95)90395-X; ARMITAGE P, 1994, STAT METHODS MED RES, P402; Bascom R, 1996, AM J RESP CRIT CARE, V153, P477; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; BraunFahrlander C, 1997, AM J RESP CRIT CARE, V155, P1042; BRAUNFAHRLANDER C, 1992, AM REV RESPIR DIS, V145, P42; CHINN S, 1991, J EPIDEMIOL COMMUN H, V45, P188, DOI 10.1136/jech.45.3.188; Ciccone G, 1998, OCCUP ENVIRON MED, V55, P771; DEKKER C, 1991, CHEST, V100, P922, DOI 10.1378/chest.100.4.922; Dockery DW, 1996, ENVIRON HEALTH PERSP, V104, P500, DOI 10.2307/3432990; Ferris B., 1978, AM REV RESPIR DIS, V118, P7; Forastiere F, 1996, AM J RESP CRIT CARE, V153, P1098; Garrett MH, 1998, AM J RESP CRIT CARE, V158, P891; HOEK G, 1984, INT ARCH OCC ENV HEA, V55, P79, DOI 10.1007/BF00378070; INFANTERIVARD C, 1993, AM J EPIDEMIOL, V137, P834; *JAP ENV AG, 1992, ANN REP QUAL ENV JAP, P2; Jarvis D, 1996, LANCET, V347, P426, DOI 10.1016/S0140-6736(96)90009-4; KOREN HS, 1995, ENVIRON HEALTH PERSP, V103, P235, DOI 10.2307/3432379; Kramer U, 1999, INT J EPIDEMIOL, V28, P865, DOI 10.1093/ije/28.5.865; Krishna MT, 1996, J ROY COLL PHYS LOND, V30, P61; Magnus P, 1998, INT J EPIDEMIOL, V27, P995, DOI 10.1093/ije/27.6.995; MELIA RJW, 1977, BRIT MED J, V2, P149; NEAS LM, 1991, AM J EPIDEMIOL, V134, P204; Nowak D, 1996, EUR RESPIR J, V9, P2541, DOI 10.1183/09031936.96.09122541; Oosterlee A, 1996, OCCUP ENVIRON MED, V53, P241; Pershagen G, 1995, INT J EPIDEMIOL, V24, P1147, DOI 10.1093/ije/24.6.1147; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; Pilotto LS, 1997, INT J EPIDEMIOL, V26, P788, DOI 10.1093/ije/26.4.788; SAMET JM, 1993, AM REV RESPIR DIS, V148, P1258; SAMET JM, 1987, AM REV RESPIR DIS, V136, P1486; SAMET JM, 1978, AM J EPIDEMIOL, V108, P435; Sears MR, 1997, LANCET, V350, P1015, DOI 10.1016/S0140-6736(97)01468-2; Shima M, 1998, OCCUP ENVIRON MED, V55, P428; SHIMA M, 1994, J EPIDEMIOL, V4, P137; Strachan DP, 1996, BRIT MED J, V312, P1195; Strand V, 1997, AM J RESP CRIT CARE, V155, P881; Studnicka M, 1997, EUR RESPIR J, V10, P2275, DOI 10.1183/09031936.97.10102275; TUNNICLIFFE WS, 1994, LANCET, V344, P1733, DOI 10.1016/S0140-6736(94)92886-X; VONMUTIUS E, 1994, AM J RESP CRIT CARE, V149, P358; Weiland Stephan K., 1994, Annals of Epidemiology, V4, P243; Wilson AC, 1998, BRIT MED J, V316, P21	41	96	98	0	11	OXFORD UNIV PRESS	OXFORD	GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND	0300-5771			INT J EPIDEMIOL	Int. J. Epidemiol.	OCT	2000	29	5					862	870		10.1093/ije/29.5.862		9	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	376DX	WOS:000165443900014	11034970	
J	Szepfalusi, Z; Loibichler, C; Pichler, J; Reisenberger, K; Ebner, C; Urbanek, R				Szepfalusi, Z; Loibichler, C; Pichler, J; Reisenberger, K; Ebner, C; Urbanek, R			Direct evidence for transplacental allergen transfer	PEDIATRIC RESEARCH			English	Article							CELL PROLIFERATIVE RESPONSES; PERFUSED HUMAN PLACENTA; ENVIRONMENTAL ALLERGENS; BABIES BORN; RESPONSIVENESS; CHILDHOOD; PROTEINS; NEWBORNS; ANTIGENS; PATTERNS	Allergies are increasing, and despite deeper insights into the immunologic basis of these diseases, preventive measures are not yet efficient. As the induction of allergic diseases is often triggered in early childhood, perinatal or prenatal preventive strategies would be beneficial. We investigated the transfer of inhalant and nutritive allergens across the human placenta. For this purpose, the maternal side of a placental cotyledon was perfused in vitro with an allergen-containing medium, and a specific ELISA was used to detect the allergens on the fetal side. Both allergens evaluated, birch pollen major allergen Bet vl and the milk allergen beta-lactoglobulin, could be shown to cross the placenta. The nutritive allergen beta-lactoglobulin was not only transferred across the placenta in all eight experiments, but was also detectable within the first minutes of perfusion. The peak allergen concentration on the fetal side could be increased by addition of human immunoglobulin. Far the inhalant allergen Bet v1, transfer was observed in two of 10 placental experiments, and only if human immunoglobulin was added. a pulsatility wave with a frequency of 30-35 min suggested tin active transfer mechanism We conclude that allergens are actively and selectively transferred across the placenta. Therefore, controlled maternal allergen exposure might offer new ways to induce tolerance to specific allergens in the fetus.	Univ Vienna, AKH, Dept Pediat, A-1090 Vienna, Austria; Univ Vienna, Dept Gynecol & Obstet, A-1090 Vienna, Austria; Univ Vienna, Inst Gen & Expt Pathol, A-1090 Vienna, Austria	Szepfalusi, Z (reprint author), Univ Vienna, AKH, Dept Pediat, Wahringer Gurtel 18-20, A-1090 Vienna, Austria.						ABERG N, 1995, CLIN EXP ALLERGY, V25, P815, DOI 10.1111/j.1365-2222.1995.tb00023.x; BJORKSTEN F, 1980, CLIN ALLERGY, V10, P585, DOI 10.1111/j.1365-2222.1980.tb02140.x; BROWNBILL P, 1995, J CLIN INVEST, V96, P2220, DOI 10.1172/JCI118277; DAHL GMK, 1984, COMP BIOCHEM PHYS A, V77, P199, DOI 10.1016/0300-9629(84)90046-X; FORTUNATO SJ, 1992, AM J OBSTET GYNECOL, V167, P1595; HAHNZORIC M, 1992, PEDIATR RES, V32, P150, DOI 10.1203/00006450-199208000-00005; Holt PG, 1998, ENVIRON HEALTH PERSP, V106, P795, DOI 10.2307/3434191; Jones AC, 1996, PEDIATR ALLERGY IMMU, V7, P109, DOI 10.1111/j.1399-3038.1996.tb00117.x; Jones CA, 1998, LANCET, V351, P1859, DOI 10.1016/S0140-6736(05)78805-X; KONDO N, 1992, ARCH DIS CHILD, V67, P1003; Miles EA, 1996, CLIN EXP ALLERGY, V26, P780, DOI 10.1046/j.1365-2222.1996.d01-383.x; MILES EA, 1995, J ALLERGY CLIN IMMUN, V95, P381; PIASTRA M, 1994, INT ARCH ALLERGY IMM, V104, P358; PICINNI MP, 1993, INT ARCH ALLERGY IMM, V102, P301; Prescott SL, 1997, INT ARCH ALLERGY IMM, V113, P75; Prescott SL, 1998, J IMMUNOL, V160, P4730; Reisenberger K, 1996, AM J OBSTET GYNECOL, V174, P1450, DOI 10.1016/S0002-9378(96)70587-2; SCHNEIDE.H, 1972, AM J OBSTET GYNECOL, V114, P822; Schneider H, 1985, Contrib Gynecol Obstet, V13, P40; SHAHEEN SO, 1995, CLIN EXP ALLERGY, V25, P1034; Szepfalusi Z, 1997, CLIN EXP ALLERGY, V27, P28, DOI 10.1046/j.1365-2222.1997.d01-417.x; Van Duren-Schmidt K, 1997, PEDIATR RES, V41, P1; WARNER JA, 1994, CLIN EXP ALLERGY, V24, P423, DOI 10.1111/j.1365-2222.1994.tb00930.x; WICHMANN HE, 1996, CLIN EXP ALLERGY, V25, P1034; Yabuhara A, 1997, CLIN EXP ALLERGY, V27, P1261	25	96	101	0	1	INT PEDIATRIC RESEARCH FOUNDATION, INC	BALTIMORE	351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA	0031-3998			PEDIATR RES	Pediatr. Res.	SEP	2000	48	3					404	407				4	Pediatrics	Pediatrics	345ZQ	WOS:000088845900025	10960510	
J	Lopuhaa, CE; Roseboom, TJ; Osmond, C; Barker, DJP; Ravelli, ACJ; Bleker, OP; van der Zee, JS; van der Meulen, JHP				Lopuhaa, CE; Roseboom, TJ; Osmond, C; Barker, DJP; Ravelli, ACJ; Bleker, OP; van der Zee, JS; van der Meulen, JHP			Atopy, lung function, and obstructive airways disease after prenatal exposure to famine	THORAX			English	Article						fetal origins of disease; atopy; obstructive airways disease; famine	BIRTH-WEIGHT; RISK-FACTORS; FETAL GROWTH; ADULT-RATS; ASTHMA; CHILDHOOD; IGE; ADOLESCENCE; PREVALENCE; ALLERGENS	Background-Associations have been found between a large head size at birth and atopy, and between low birth weight and obstructive airways disease. A study was undertaken of people born around the time of the Dutch famine in 1944-5 to determine the effects of maternal malnutrition during specific periods of gestation on the prevalence of obstructive airways disease and atopy. Methods-Nine hundred and twelve people aged about 50, born at term between November 1943 and February 1947 in Amsterdam, were asked about their medical history. Lung function was measured in 733 and serum concentrations of total IgE and specific IgE against mite, pollen and cat were measured in 726. Those exposed in late, mid, and early gestation (exposed participants) were compared with those born before or conceived after the famine (non-exposed participants). Results-Exposure to famine during gestation affected neither the concentrations of total or specific IgE nor lung function values. The prevalence of obstructive airways disease was increased in people exposed to famine in mid gestation (odds ratio adjusted for sex 1.7, 95% confidence interval (CI) 1.1 to 2.6) and tended to be higher in those exposed in early gestation (odds ratio 1.5, 95% CI: 0.9 to 2.6). Conclusions The observed increase in the prevalence of obstructive airways disease in people exposed to famine in mid and early gestation was not parallelled by effects on IgE concentrations or lung function. The link between exposure to famine in mid and early gestation and obstructive airways disease in adulthood suggests that fetal lungs can be permanently affected by nutritional challenges during periods of rapid growth.	Univ Amsterdam, Acad Med Ctr, Dept Pulmonol, NL-1105 AZ Amsterdam, Netherlands; Univ Southampton, Dept Biostat & Epidemiol, Southampton SO9 5NH, Hants, England; Univ Southampton, Dept Obstet & Gynaecol, Southampton SO9 5NH, Hants, England; Univ Southampton, MRC, Environm Epidemiol Unit, Southampton SO9 5NH, Hants, England	van der Meulen, JHP (reprint author), Univ London London Sch Hyg & Trop Med, Dept Publ Hlth & Policy, Hlth Serv Res Unit, Keppel St, London WC1E 7HT, England.		van der Zee, jaring/M-8462-2013				AALBERSE RC, 1992, CLIN EXP ALLERGY, V22, P1003, DOI 10.1111/j.1365-2222.1992.tb03028.x; American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P1285, DOI 10.1164/ajrccm/136.5.1285; ARSHAD SH, 1993, CLIN EXP ALLERGY, V23, P504, DOI 10.1111/j.1365-2222.1993.tb03238.x; Bakker B., 1997, SOCIALE WETENSCHAPPE, V40, P1; BARKER DJP, 1991, BRIT MED J, V303, P671; Barker DJP, 1998, MOTHERS BABIES HLTH; Bloomfield F., 1998, FETAL MAT MED REV, V10, P91, DOI 10.1017/S0965539597000235; Burger GCE, 1948, MALNUTRITION STARVAT; Fergusson DM, 1997, CLIN EXP ALLERGY, V27, P1394, DOI 10.1046/j.1365-2222.1997.1430947.x; GODFREY KM, 1994, CLIN EXP ALLERGY, V24, P641, DOI 10.1111/j.1365-2222.1994.tb00968.x; Gregory A, 1999, CLIN EXP ALLERGY, V29, P330; HARDING J, 1992, EARLY HUM DEV, V29, P193, DOI 10.1016/0378-3782(92)90149-B; Holt PG, 1997, THORAX, V52, P1; KELLY YJ, 1995, THORAX, V50, P525, DOI 10.1136/thx.50.5.525; LANGLEY SC, 1994, J NUTR, V124, P1588; LangleyEvans SC, 1997, J NUTR, V127, P202; MATTHES JWA, 1995, ARCH DIS CHILD, V73, P231; MCCANCE RA, 1974, PROC R SOC SER B-BIO, V185, P1, DOI 10.1098/rspb.1974.0001; Medical Research Council, 1986, QUEST RESP SYMPT; MULAY S, 1980, FED PROC, V39, P261; Oliveti JF, 1996, AM J EPIDEMIOL, V143, P570; Oryszczyn MP, 1999, CLIN EXP ALLERGY, V29, P334; Ravelli ACJ, 1998, LANCET, V351, P173, DOI 10.1016/S0140-6736(97)07244-9; ROMAGNANI S, 1992, INT ARCH ALLERGY IMM, V98, P279; RONA RJ, 1993, BRIT MED J, V306, P817; Schaubel D, 1996, J ASTHMA, V33, P255, DOI 10.3109/02770909609055366; Schuurman J, 1997, J ALLERGY CLIN IMMUN, V99, P545, DOI 10.1016/S0091-6749(97)70083-6; Sears MR, 1996, ARCH DIS CHILD, V75, P392; SEIDMAN DS, 1991, ARCH DIS CHILD, V66, P584; SHAHEEN S, 1994, THORAX, V49, P533, DOI 10.1136/thx.49.6.533; Shaheen SO, 1998, THORAX, V53, P549; Shaheen SO, 1999, THORAX, V54, P396; Slezak JA, 1998, J ASTHMA, V35, P203, DOI 10.3109/02770909809068208; Stein CE, 1997, THORAX, V52, P895; Stein Z. A., 1975, FAMINE HUMAN DEV DUT; Witteman AM, 1996, J ALLERGY CLIN IMMUN, V97, P16, DOI 10.1016/S0091-6749(96)70278-6	36	96	100	1	5	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	JUL	2000	55	7					555	561		10.1136/thorax.55.7.555		7	Respiratory System	Respiratory System	328EF	WOS:000087835400006	10856314	
J	Fujimura, KE; Demoor, T; Rauch, M; Faruqi, AA; Jang, S; Johnson, CC; Boushey, HA; Zoratti, E; Ownby, D; Lukacs, NW; Lynch, SV				Fujimura, Kei E.; Demoor, Tine; Rauch, Marcus; Faruqi, Ali A.; Jang, Sihyug; Johnson, Christine C.; Boushey, Homer A.; Zoratti, Edward; Ownby, Dennis; Lukacs, Nicholas W.; Lynch, Susan V.			House dust exposure mediates gut microbiome Lactobacillus enrichment and airway immune defense against allergens and virus infection	PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA			English	Article						house environment; airway adaptive immunity; gastrointestinal bacterial community; Lactobacilliaceae	T-CELLS; CHILDHOOD; RISK; MICE; SUPPRESSES; METABOLISM; BACTERIA; INFANCY	Exposure to dogs in early infancy has been shown to reduce the risk of childhood allergic disease development, and dog ownership is associated with a distinct house dust microbial exposure. Here, we demonstrate, using murine models, that exposure of mice to dog-associated house dust protects against ovalbumin or cockroach allergen-mediated airway pathology. Protected animals exhibited significant reduction in the total number of airway T cells, down-regulation of Th2-related airway responses, as well as mucin secretion. Following dog-associated dust exposure, the cecal microbiome of protected animals was extensively restructured with significant enrichment of, amongst others, Lactobacillus johnsonii. Supplementation of wild-type animals with L. johnsonii protected them against both airway allergen challenge or infection with respiratory syncytial virus. L. johnsonii-mediated protection was associated with significant reductions in the total number and proportion of activated CD11c(+)/CD11b(+) and CD11c(+)/CD8(+) cells, as well as significantly reduced airway Th2 cytokine expression. Our results reveal that exposure to dog-associated household dust results in protection against airway allergen challenge and a distinct gastrointestinal microbiome composition. Moreover, the study identifies L. johnsonii as a pivotal species within the gastrointestinal tract capable of influencing adaptive immunity at remote mucosal surfaces in a manner that is protective against a variety of respiratory insults.	[Fujimura, Kei E.; Rauch, Marcus; Faruqi, Ali A.; Lynch, Susan V.] Univ Calif San Francisco, Div Gastroenterol, San Francisco, CA 94143 USA; [Boushey, Homer A.] Univ Calif San Francisco, Div Pulm & Crit Care Med, San Francisco, CA 94143 USA; [Demoor, Tine; Jang, Sihyug; Lukacs, Nicholas W.] Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA; [Johnson, Christine C.] Henry Ford Hlth Syst, Dept Publ Hlth Sci, Detroit, MI 48202 USA; [Zoratti, Edward] Henry Ford Hlth Syst, Div Allergy & Clin Immunol, Detroit, MI 48202 USA; [Ownby, Dennis] Med Coll Georgia, Dept Pediat, Augusta, GA 30912 USA	Lukacs, NW (reprint author), Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA.	nlukacs@umich.edu; susan.lynch@ucsf.edu			National Institutes of Health, National Institute of Allergy and Infectious Diseases [P01AI089473-01A1]	This study was supported by the National Institutes of Health, National Institute of Allergy and Infectious Diseases P01AI089473-01A1.	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Natl. Acad. Sci. U. S. A.	JAN 14	2014	111	2					805	810		10.1073/pnas.1310750111		6	Multidisciplinary Sciences	Science & Technology - Other Topics	288LW	WOS:000329614500057	24344318	
J	Bisgaard, H; Jensen, SM; Bonnelykke, K				Bisgaard, Hans; Jensen, Signe M.; Bonnelykke, Klaus			Interaction between Asthma and Lung Function Growth in Early Life	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; lung function; young child; infant; neonate	1ST 6 YEARS; AIRWAY RESPONSIVENESS; PRESCHOOL-CHILDREN; CHILDHOOD ASTHMA; BIRTH COHORT; HIGH-RISK; BRONCHIAL RESPONSIVENESS; INHALED CORTICOSTEROIDS; YOUNG INFANTS; LONG-TERM	Rationale: The causal direction between asthma and lung function deficit is unknown, but important for the focus of preventive measures and research into the origins of asthma. Objectives: To analyze the interaction between lung function development and asthma from birth to 7 years of age. Methods: The Copenhagen Prospective Studies on Asthma in Childhood is a prospective clinical study of a birth cohort of 411 at-risk children. Spirometry was completed in 403 (98%) neonates and again by age 7 in 317 children (77%). Measurements and Main Results: Neonatal spirometry and bronchial responsiveness to methacholine was measured during sedation by forced flow-volume measurements. Asthma was diagnosed prospectively from daily diary cards and clinic visits every 6 months. Children with asthma by age 7(14%) already had a significant airflow deficit as neonates (forced expiratory flow at 50% of vital capacity second in neonates reduced by 0.34 z score by 1 mo; P = 0.03). This deficit progressed significantly during early childhood (forced expiratory flow at 0.5 seconds in neonates at age 7 reduced by 0.82 z score by age 7; P < 0.0001), suggesting that approximately 40% of the airflow deficit associated with asthma is present at birth, whereas 60% develops with clinical disease. Environmental tobacco exposure, but not allergic sensitization, also hampered airflow growth. Bronchial responsiveness to methacholine in the neonates was associated with the development of asthma (P = 0.01). Conclusions: Children developing asthma by age 7 had a lung function deficit and increased bronchial responsiveness as neonates. This lung function deficit progressed to age 7. Therefore, research into the origins and prevention of asthma should consider early life before and after birth.	[Bisgaard, Hans; Jensen, Signe M.; Bonnelykke, Klaus] Univ Copenhagen, Danish Pediat Asthma Ctr, Copenhagen, Denmark; [Bisgaard, Hans; Jensen, Signe M.; Bonnelykke, Klaus] Copenhagen Univ Hosp, Copenhagen, Denmark	Bisgaard, H (reprint author), Univ Copenhagen, Danish Pediat Asthma Ctr, Copenhagen, Denmark.	bisgaard@copsac.com	Kronow, Joern/B-1054-2011; Jensen, Signe/G-1026-2016; Bisgaard, Hans/N-4761-2016	Jensen, Signe/0000-0002-7738-5231; Bisgaard, Hans/0000-0003-4131-7592			Bisgaard H, 2004, ANN ALLERG ASTHMA IM, V93, P381; Bisgaard H, 2006, NEW ENGL J MED, V354, P1998, DOI 10.1056/NEJMoa054692; Bisgaard H, 2008, PLOS MED, V5, DOI 10.1371/journal.pmed.0050131; Bisgaard H, 2007, NEW ENGL J MED, V357, P1487, DOI 10.1056/NEJMoa052632; Bisgaard H, 2011, J ALLERGY CLIN IMMUN, V127, P1155, DOI 10.1016/j.jaci.2011.02.007; Bisgaard H, 2010, J ALLERGY CLIN IMMUN, V126, P187, DOI 10.1016/j.jaci.2010.07.011; Bisgaard H, 2009, J ALLERGY CLIN IMMUN, V123, P1355, DOI 10.1016/j.jaci.2009.03.046; Bisgaard H, 2009, J ALLERGY CLIN IMMUN, V123, P651, DOI 10.1016/j.jaci.2008.11.036; Brand PLP, 2008, EUR RESPIR J, V32, P1096, DOI 10.1183/09031936.00002108; Buchvald F, 2005, J ALLERGY CLIN IMMUN, V115, P1130, DOI 10.1016/j.jaci.2005.03.020; Chawes BLK, 2010, J ALLERGY CLIN IMMUN, V126, P567, DOI 10.1016/j.jaci.2010.06.026; CLARKE JR, 1995, AM J RESP CRIT CARE, V151, P1434; Giwercman C, 2010, J ALLERGY CLIN IMMUN, V125, P866, DOI 10.1016/j.jaci.2010.01.026; Guilbert TW, 2006, NEW ENGL J MED, V354, P1985, DOI 10.1056/NEJMoa051378; Haland G, 2006, NEW ENGL J MED, V355, P1682, DOI 10.1056/NEJMoa052885; Halkjaer LB, 2006, ARCH DERMATOL, V142, P561, DOI 10.1001/archderm.142.5.561; Henderson J, 2008, THORAX, V63, P974, DOI 10.1136/thx.2007.093187; Illi S, 2006, LANCET, V368, P763, DOI 10.1016/S0140-6736(06)69286-6; Loland L, 2006, CHEST, V129, P669, DOI 10.1378/chest.129.3.669; Loland L, 2008, CHEST, V133, P115, DOI 10.1378/chest.07-1328; Lowe L, 2002, LANCET, V359, P1904, DOI 10.1016/S0140-6736(02)08781-0; Lowe LA, 2005, AM J RESP CRIT CARE, V171, P231, DOI 10.1164/rccm.200406-695OC; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Morgan WJ, 2005, AM J RESP CRIT CARE, V172, P1253, DOI 10.1164/rccm.200504-525OC; Murray CS, 2006, LANCET, V368, P754, DOI 10.1016/S0140-6736(06)69285-4; Paganelli R, 1998, ALLERGY, V53, P763; 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; S. American Thoracic and S. European Respiratory, 2005, AM J RESP CRIT CARE, V171, P912; Sears MR, 2003, NEW ENGL J MED, V349, P1414, DOI 10.1056/NEJMoa022363; Sorensen M, 2007, BIOMARKERS, V12, P38, DOI 10.1080/13547500600943148; Turner SW, 2004, AM J RESP CRIT CARE, V169, P921, DOI 10.1164/rccm.200307-891OC; Wilson NM, 2004, PEDIATR PULM, V38, P75, DOI 10.1002/ppul.20049	33	95	95	0	6	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.	JUN 1	2012	185	11					1183	1189		10.1164/rccm.201110-1922OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	946VC	WOS:000304384600011	22461370	
J	Zeiger, RS; Mauger, D; Bacharier, LB; Guilbert, TW; Martinez, FD; Lemanske, RF; Strunk, RC; Covar, R; Szefler, SJ; Boehmer, S; Jackson, DJ; Sorkness, CA; Gern, JE; Kelly, HW; Friedman, NJ; Mellon, MH; Schatz, M; Morgan, WJ; Chinchilli, VM; Raissy, HH; Bade, E; Malka-Rais, J; Beigelman, A; Taussig, LM				Zeiger, Robert S.; Mauger, David; Bacharier, Leonard B.; Guilbert, Theresa W.; Martinez, Fernando D.; Lemanske, Robert F., Jr.; Strunk, Robert C.; Covar, Ronina; Szefler, Stanley J.; Boehmer, Susan; Jackson, Daniel J.; Sorkness, Christine A.; Gern, James E.; Kelly, H. William; Friedman, Noah J.; Mellon, Michael H.; Schatz, Michael; Morgan, Wayne J.; Chinchilli, Vernon M.; Raissy, Hengameh H.; Bade, Elizabeth; Malka-Rais, Jonathan; Beigelman, Avraham; Taussig, Lynn M.		CARE Network Natl Heart Lung	Daily or Intermittent Budesonide in Preschool Children with Recurrent Wheezing	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							INHALED FLUTICASONE PROPIONATE; RANDOMIZED CONTROLLED-TRIAL; 2 YEARS OLD; YOUNG-CHILDREN; INHALATION SUSPENSION; PERSISTENT ASTHMA; ORAL PREDNISOLONE; DOUBLE-BLIND; INFANTS; CORTICOSTEROIDS	BACKGROUND Daily inhaled glucocorticoids are recommended for young children at risk for asthma exacerbations, as indicated by a positive value on the modified asthma predictive index (API) and an exacerbation in the preceding year, but concern remains about daily adherence and effects on growth. We compared daily therapy with intermittent therapy. METHODS We studied 278 children between the ages of 12 and 53 months who had positive values on the modified API, recurrent wheezing episodes, and at least one exacerbation in the previous year but a low degree of impairment. Children were randomly assigned to receive a budesonide inhalation suspension for 1 year as either an intermittent high-dose regimen (1 mg twice daily for 7 days, starting early during a predefined respiratory tract illness) or a daily low-dose regimen (0.5 mg nightly) with corresponding placebos. The primary outcome was the frequency of exacerbations requiring oral glucocorticoid therapy. RESULTS The daily regimen of budesonide did not differ significantly from the intermittent regimen with respect to the frequency of exacerbations, with a rate per patient-year for the daily regimen of 0.97 (95% confidence interval [CI], 0.76 to 1.22) versus a rate of 0.95 (95% CI, 0.75 to 1.20) for the intermittent regimen (relative rate in the intermittent-regimen group, 0.99; 95% CI, 0.71 to 1.35; P = 0.60). There were also no significant between-group differences in several other measures of asthma severity, including the time to the first exacerbation, or adverse events. The mean exposure to budesonide was 104 mg less with the intermittent regimen than with the daily regimen. CONCLUSIONS A daily low-dose regimen of budesonide was not superior to an intermittent high-dose regimen in reducing asthma exacerbations. Daily administration led to greater exposure to the drug at 1 year. (Funded by the National Heart, Lung, and Blood Institute and others; MIST ClinicalTrials.gov number, NCT00675584.)	[Zeiger, Robert S.; Friedman, Noah J.; Mellon, Michael H.; Schatz, Michael] Kaiser Permanente So Calif, Dept Allergy, San Diego, CA USA; [Zeiger, Robert S.; Schatz, Michael] Univ Calif San Diego, Dept Pediat, San Diego, CA 92103 USA; [Mauger, David; Boehmer, Susan; Chinchilli, Vernon M.] Penn State Univ, Dept Publ Hlth Sci, Hershey, PA USA; [Bacharier, Leonard B.; Strunk, Robert C.; Beigelman, Avraham] Washington Univ, Dept Pediat, St Louis, MO 63130 USA; [Bacharier, Leonard B.; Strunk, Robert C.; Beigelman, Avraham] St Louis Childrens Hosp, St Louis, MO USA; [Guilbert, Theresa W.; Lemanske, Robert F., Jr.; Jackson, Daniel J.; Sorkness, Christine A.; Gern, James E.] Univ Wisconsin Madison, Sch Med & Publ Hlth, Dept Med, Madison, WI USA; [Guilbert, Theresa W.; Lemanske, Robert F., Jr.; Jackson, Daniel J.; Sorkness, Christine A.; Gern, James E.] Univ Wisconsin Madison, Sch Med & Publ Hlth, Dept Pediat, Madison, WI USA; [Guilbert, Theresa W.; Lemanske, Robert F., Jr.; Jackson, Daniel J.; Sorkness, Christine A.; Gern, James E.] Univ Wisconsin Madison, Sch Pharm, Madison, WI USA; [Martinez, Fernando D.; Morgan, Wayne J.] Univ Arizona, Arizona Resp Ctr, Tucson, AZ USA; [Covar, Ronina; Szefler, Stanley J.; Malka-Rais, Jonathan; Taussig, Lynn M.] Natl Jewish Hlth, Dept Pediat, Div Pediat Clin Pharmacol, Denver, CO USA; [Covar, Ronina; Szefler, Stanley J.; Malka-Rais, Jonathan; Taussig, Lynn M.] Natl Jewish Hlth, Dept Pediat, Div Allergy & Immunol, Denver, CO USA; [Covar, Ronina; Szefler, Stanley J.; Malka-Rais, Jonathan; Taussig, Lynn M.] Univ Colorado, Sch Med, Denver, CO USA; [Kelly, H. William; Raissy, Hengameh H.] Univ New Mexico, Sch Med, Dept Pediat, Albuquerque, NM 87131 USA; [Bade, Elizabeth] Univ Wisconsin Milwaukee, Sch Med & Publ Hlth, Dept Family Med, Milwaukee, WI USA	Zeiger, RS (reprint author), Kaiser Permanente, Dept Allergy, 7060 Clairemont Mesa Blvd, San Diego, CA 92111 USA.	robert.s.zeiger@kp.org		Guilbert, Theresa/0000-0002-6932-712X	National Heart, Lung, and Blood Institute [5U10HL064287, 5U10HL064288, 5U10HL064295, 5U10HL064307, 5U10HL064305, 5U10HL064313]; Washington University School of Medicine [5UL1RR02499204]; Madison CTSA [1UL1RR025011]; National Center for Research Resources, National Institutes of Health [UL1RR025780];  [M01 RR00036];  [M01 RR00051];  [5M01 RR00997]	Supported by grants (5U10HL064287, 5U10HL064288, 5U10HL064295, 5U10HL064307, 5U10HL064305, and 5U10HL064313) from the National Heart, Lung, and Blood Institute; a grant (5UL1RR02499204) from the Washington University School of Medicine Clinical and Translational Science Awards (CTSA) Infrastructure for Pediatric Research; a grant (1UL1RR025011) from the Madison CTSA; a grant (UL1RR025780) to the Colorado CTSA from the National Center for Research Resources, National Institutes of Health; and grants to the General Clinical Research Centers at Washington University School of Medicine (M01 RR00036), National Jewish Health (M01 RR00051), and the University of New Mexico (5M01 RR00997).	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J	Islam, SA; Chang, DS; Colvin, RA; Byrne, MH; McCully, ML; Moser, B; Lira, SA; Charo, IF; Luster, AD				Islam, Sabina A.; Chang, Daniel S.; Colvin, Richard A.; Byrne, Mike H.; McCully, Michelle L.; Moser, Bernhard; Lira, Sergio A.; Charo, Israel F.; Luster, Andrew D.			Mouse CCL8, a CCR8 agonist, promotes atopic dermatitis by recruiting IL-5(+) T(H)2 cells	NATURE IMMUNOLOGY			English	Article							CHEMOKINE RECEPTOR CCR8; T-CELLS; DENDRITIC CELLS; AIRWAY INFLAMMATION; IMMUNE-RESPONSES; CUTTING EDGE; TH1 CELLS; IN-VIVO; EXPRESSION; DIFFERENTIATION	Mouse CCL8 is a CC chemokine of the monocyte chemoattractant protein (MCP) family whose biological activity and receptor usage have remained elusive. Here we show that CCL8 is highly expressed in the skin, where it serves as an agonist for the chemokine receptor CCR8 but not for CCR2. This distinguishes CCL8 from all other MCP chemokines. CCL8 responsiveness defined a population of highly differentiated, CCR8-expressing inflammatory T helper type 2 (T(H)2) cells enriched for interleukin (IL)-5. Ccr8- and Ccl8-deficient mice had markedly less eosinophilic inflammation than wild-type or Ccr4-deficient mice in a model of chronic atopic dermatitis. Adoptive transfer studies established CCR8 as a key regulator of T(H)2 cell recruitment into allergen-inflamed skin. In humans, CCR8 expression also defined an IL-5-enriched T(H)2 cell subset. The CCL8-CCR8 chemokine axis is therefore a crucial regulator of T(H)2 cell homing that drives IL-5-mediated chronic allergic inflammation.	[Islam, Sabina A.; Chang, Daniel S.; Colvin, Richard A.; Byrne, Mike H.; Luster, Andrew D.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Rheumatol Allergy & Immunol,Ctr Immunol & Inf, Boston, MA 02163 USA; [McCully, Michelle L.; Moser, Bernhard] Cardiff Univ, Dept Infect Immun & Biochem, Cardiff, S Glam, Wales; [Lira, Sergio A.] Mt Sinai Sch Med, Inst Immunol, New York, NY USA; [Charo, Israel F.] Univ Calif San Francisco, Gladstone Inst Cardiovasc Dis, San Francisco, CA 94143 USA	Luster, AD (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Rheumatol Allergy & Immunol,Ctr Immunol & Inf, Boston, MA 02163 USA.	aluster@mgh.harvard.edu	McCully, Michelle/A-7705-2013	McCully, Michelle/0000-0003-1543-3629	US National Institutes of Health (Harvard Skin Disease Research Center Pilot & Feasibility Study) [K08-AI556663, P30AR042689, R37-AI040618]; Infectious Diseases Society of America	This work is funded by US National Institutes of Health grants K08-AI556663 and P30AR042689 (Harvard Skin Disease Research Center Pilot & Feasibility Study) to S. A. I. and R37-AI040618 to A. D. L., and the Infectious Diseases Society of America Young Investigator Award to S. A. I. The authors thank P. Murphy (National Institutes of Health) for 4DE4 cells, J. Pease (Imperial College London) for human CCR8 receptor transfectants, P. Shrikant (Roswell Park Cancer Institute) for transgenic Thy1.1 OTII mice, L. Lefrancois (University of Connecticut School of Medicine) for transgenic Thy1.2 OTII mice, C. Sanderson (National Institute for Medical Research, London) for Il5-transgenic mice, S. Thomas for assistance with calcium flux studies and T. Means for assistance with design and validation of QPCR primers.	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J	Ho, SM				Ho, Shuk-Mei			Environmental epigenetics of asthma: An update	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Pulmonary disorder; traffic-related pollutants; polycyclic aromatic hydrocarbons; microbial and viral infection; lipopoly-saccharide; endotoxin; oxidant early-life programming; nutrition; maternal exposure; T-H cells; dendritic cells; macrophages; lung epithelial cells; phenotype plasticity; developmental basis of disease; gene-environment interaction; DNA methylation; histone modification; microRNA; chromatin remodeling; allergen; inflammatory response	ADULT LUNG-FUNCTION; REGULATORY T-CELLS; MAMMALIAN DNA METHYLTRANSFERASES; DIESEL EXHAUST PARTICLES; TOBACCO-SMOKE EXPOSURE; EARLY-CHILDHOOD ASTHMA; BREAST-CANCER CELLS; IFN-GAMMA GENE; AIR-POLLUTION; DENDRITIC CELLS	Asthma, a chronic inflammatory disorder of the airway, is influenced by interplay between genetic and environmental factors now known to be mediated by epigenetics. Aberrant DNA methylation, altered histone modifications, specific microRNA expression, and other chromatin alterations orchestrate a complex early-life reprogramming of immune T-cell response, dendritic cell function, macrophage activation, and a breach of airway epithelial barrier that dictates asthma risk and severity in later life. Adult-onset asthma is under analogous regulation. The sharp increase in asthma prevalence over the past 2 or 3 decades and the large variations among populations of similar racial/ethnic background but different environmental exposures favors a strong contribution of environmental factors. This review addresses the fundamental question of whether environmental influences on asthma risk, severity, and steroid resistance are partly due to differential epigenetic modulations. Current knowledge on the epigenetic effects of tobacco smoke, microbial allergens, oxidants, airborne particulate matter, diesel exhaust particles, polycyclic aromatic hydrocarbons, dietary methyl donors and other nutritional factors, and dust mites is discussed. Exciting findings have been generated by rapid technological advances and well-designed experimental and population studies. The discovery and validation of epigenetic biomarkers linked to exposure, asthma, or both might lead to better epigenotyping of risk, prognosis, treatment prediction, and development of novel therapies. (J Allergy Clin Immunol 2010;126:453-65.)	[Ho, Shuk-Mei] Univ Cincinnati, Coll Med, Dept Environm Hlth, Ctr Environm Genet, Cincinnati, OH 45267 USA	Ho, SM (reprint author), 3223 Eden Ave,Kettering Complex,Suite 130, Cincinnati, OH 45267 USA.	shuk-mei.ho@uc.edu			National Institutes of Health [P30ES006096, R01ES015584, RC2ES018758, RC2ES018789, P50ES015905]	Supported by National Institutes of Health grants P30ES006096, R01ES015584, RC2ES018758, RC2ES018789, and P50ES015905.	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Allergy Clin. Immunol.	SEP	2010	126	3					453	465		10.1016/j.jaci.2010.07.030		13	Allergy; Immunology	Allergy; Immunology	646CF	WOS:000281512500007	20816181	
J	Gearry, RB; Richardson, AK; Frampton, CM; Dodgshun, AJ; Barclay, ML				Gearry, Richard B.; Richardson, Ann K.; Frampton, Christopher M.; Dodgshun, Andrew J.; Barclay, Murray L.			Population-based cases control study of inflammatory bowel disease risk factors	JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY			English	Article						Crohn's disease; epidemiology; inflammatory bowel diseases; risk factors; ulcerative colitis	ONSET CROHNS-DISEASE; ULCERATIVE-COLITIS; INTESTINAL MICROFLORA; CHILDHOOD EXPOSURE; HYGIENE HYPOTHESIS; CHINESE POPULATION; PASSIVE SMOKING; TOBACCO-SMOKE; NEW-ZEALAND; SUSCEPTIBILITY	Background and Aim: The rapid increase in inflammatory bowel disease (IBD) incidence confirms the importance of environment in its etiology. We aimed to assess the role of childhood and other environmental risk factors in IBD. Methods: A population-based case-control study was carried out in Canterbury, New Zealand. Participants comprised 638 prevalent Crohn's disease (CD) cases, 653 prevalent ulcerative colitis (UC) cases and 600 randomly-selected sex and age matched controls. Exposure rates to environmental risk factors were compared. Unadjusted and adjusted odds ratios (OR) with 95% confidence intervals (CI) are presented. Results: A family history of IBD (CD OR 3.06 [2.18-4.30], UC OR 2.52 [1.90-3.54]), cigarette smoking at diagnosis (CD OR 1.99 [1.48-2.68], UC OR 0.67 [0.48-0.94]), high social class at birth (CD and UC trend, P < 0.001) and Caucasian ethnicity (CD OR 2.04 [1.05-4.38], UC OR 1.47 [1.01-2.14]) were significantly associated with IBD. City living was associated with CD (P < 0.01). Being a migrant was associated with UC (UC OR 1.40 [1.14-2.01]). Having a childhood vegetable garden was protective against IBD (CD OR 0.52 [0.36-0.76], UC OR 0.65 [0.45-0.94]) as was having been breast-fed (CD OR 0.55 [0.41-0.74], UC OR 0.71 [0.52-0.96]) with a duration-response effect. Appendicectomy, tonsillectomy, infectious monomucleosis and asthma were more common in CD patients than controls (P < 0.01). Conclusions: The importance of childhood factors in the development of IBD is confirmed. The duration-response protective association between breast-feeding and subsequent development of IBD requires further evaluation, as does the protective effect associated with a childhood vegetable garden.	[Gearry, Richard B.; Frampton, Christopher M.; Dodgshun, Andrew J.; Barclay, Murray L.] Univ Otago, Dept Med, Christchurch 8140, New Zealand; [Gearry, Richard B.; Barclay, Murray L.] Christchurch Hosp, Dept Gastroenterol, Christchurch, New Zealand; [Richardson, Ann K.] Canterbury Dist Hlth Board, Christchurch, New Zealand	Gearry, RB (reprint author), Univ Otago, Dept Med, POB 4345, Christchurch 8140, New Zealand.	Richard.gearry@cdhb.govt.nz		Gearry, Richard/0000-0002-2298-5141	Canterbury Medical Research Foundation; Bowel and Liver Trust, Canterbury; Canterbury Gastroenterology Research Trust	This research was funded by the Canterbury Medical Research Foundation, Bowel and Liver Trust, Canterbury and the Canterbury Gastroenterology Research Trust. The researchers wish to thank people in Canterbury with and without inflammatory bowel disease who acted as cases and controls for this study.	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Gastroenterol. Hepatol.	FEB	2010	25	2					325	333		10.1111/j.1440-1746.2009.06140.x		9	Gastroenterology & Hepatology	Gastroenterology & Hepatology	551CX	WOS:000274184500019	20074146	
J	Knol, AB; de Hartog, JJ; Boogaard, H; Slottje, P; van der Sluijs, JP; Lebret, E; Cassee, FR; Wardekker, A; Ayres, JG; Borm, PJ; Brunekreef, B; Donaldson, K; Forastiere, F; Holgate, ST; Kreyling, WG; Nemery, B; Pekkanen, J; Stone, V; Wichmann, HE; Hoek, G				Knol, Anne B.; de Hartog, Jeroen J.; Boogaard, Hanna; Slottje, Pauline; van der Sluijs, Jeroen P.; Lebret, Erik; Cassee, Flemming R.; Wardekker, Arjan; Ayres, Jon G.; Borm, Paul J.; Brunekreef, Bert; Donaldson, Kenneth; Forastiere, Francesco; Holgate, Stephen T.; Kreyling, Wolfgang G.; Nemery, Benoit; Pekkanen, Juha; Stone, Vicky; Wichmann, H-Erich; Hoek, Gerard			Expert elicitation on ultrafine particles: likelihood of health effects and causal pathways	PARTICLE AND FIBRE TOXICOLOGY			English	Article							PARTICULATE AIR-POLLUTION; CORONARY-HEART-DISEASE; DIESEL-EXHAUST INHALATION; LONG-TERM EXPOSURE; URBAN AIR; CARDIOPULMONARY MORTALITY; AMBIENT FINE; NANOPARTICLES; ASSOCIATION; ASTHMA	Background: Exposure to fine ambient particulate matter (PM) has consistently been associated with increased morbidity and mortality. The relationship between exposure to ultrafine particles (UFP) and health effects is less firmly established. If UFP cause health effects independently from coarser fractions, this could affect health impact assessment of air pollution, which would possibly lead to alternative policy options to be considered to reduce the disease burden of PM. Therefore, we organized an expert elicitation workshop to assess the evidence for a causal relationship between exposure to UFP and health endpoints. Methods: An expert elicitation on the health effects of ambient ultrafine particle exposure was carried out, focusing on: 1) the likelihood of causal relationships with key health endpoints, and 2) the likelihood of potential causal pathways for cardiac events. Based on a systematic peernomination procedure, fourteen European experts (epidemiologists, toxicologists and clinicians) were selected, of whom twelve attended. They were provided with a briefing book containing key literature. After a group discussion, individual expert judgments in the form of ratings of the likelihood of causal relationships and pathways were obtained using a confidence scheme adapted from the one used by the Intergovernmental Panel on Climate Change. Results: The likelihood of an independent causal relationship between increased short-term UFP exposure and increased all-cause mortality, hospital admissions for cardiovascular and respiratory diseases, aggravation of asthma symptoms and lung function decrements was rated medium to high by most experts. The likelihood for long-term UFP exposure to be causally related to all cause mortality, cardiovascular and respiratory morbidity and lung cancer was rated slightly lower, mostly medium. The experts rated the likelihood of each of the six identified possible causal pathways separately. Out of these six, the highest likelihood was rated for the pathway involving respiratory inflammation and subsequent thrombotic effects. Conclusion: The overall medium to high likelihood rating of causality of health effects of UFP exposure and the high likelihood rating of at least one of the proposed causal mechanisms explaining associations between UFP and cardiac events, stresses the importance of considering UFP in future health impact assessments of (transport-related) air pollution, and the need for further research on UFP exposure and health effects.	[Knol, Anne B.; de Hartog, Jeroen J.; Slottje, Pauline; Lebret, Erik; Cassee, Flemming R.] Dutch Natl Inst Publ Hlth & Environm RIVM, Bilthoven, Netherlands; [de Hartog, Jeroen J.; Boogaard, Hanna; van der Sluijs, Jeroen P.; Lebret, Erik; Brunekreef, Bert; Hoek, Gerard] Univ Utrecht, Inst Risk Assessment Sci, Utrecht, Netherlands; [van der Sluijs, Jeroen P.; Wardekker, Arjan] Univ Utrecht, Copernicus Inst, Utrecht, Netherlands; [Ayres, Jon G.] Univ Birmingham, Inst Occupat & Environm Med, Birmingham, W Midlands, England; [Borm, Paul J.] Hogesch Zuyd, Ctr Expertise Life Sci, Heerlen, Netherlands; [Brunekreef, Bert] Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands; [Donaldson, Kenneth] Univ Edinburgh, Ctr Inflammat Res, Edinburgh, Midlothian, Scotland; [Forastiere, Francesco] Hlth Author Rome, Dept Epidemiol, Rome, Italy; [Holgate, Stephen T.] Univ Southampton, Sch Med, Southampton SO9 5NH, Hants, England; [Kreyling, Wolfgang G.; Wichmann, H-Erich] Helmholtz Ctr Munich, Inst Lung Biol & Focus Network Nanoparticles & Hl, Neuherberg, Germany; [Nemery, Benoit] Katholieke Univ Leuven, Lung Toxicol Res Unit, Leuven, Belgium; [Pekkanen, Juha] Natl Publ Hlth Inst, Environm Epidemiol Unit, Kuopio, Finland; [Stone, Vicky] Napier Univ, Sch Life Sci, Edinburgh EH14 1DJ, Midlothian, Scotland	Knol, AB (reprint author), Dutch Natl Inst Publ Hlth & Environm RIVM, Bilthoven, Netherlands.	anne.knol@rivm.nl; J.J.deHartog@uu.nl; J.M.C.Boogaard@uu.nl; Pauline.Slottje@uu.nl; J.P.vanderSluijs@uu.nl; Erik.Lebret@rivm.nl; Flemming.cassee@rivm.nl; J.A.Wardekker@uu.nl; j.g.ayres@bham.ac.uk; p.borm@hszuyd.nl; B.Brunekreef@uu.nl; ken.donaldson@ed.ac.uk; forastiere@asplazio.it; S.Holgate@soton.ac.uk; Kreyling@gsf.de; Ben.Nemery@med.kuleuven.be; Juha.Pekkanen@thl.fi; V.Stone@napier.ac.uk; wichmann@gsf.de; G.Hoek@uu.nl	van der Sluijs, Jeroen/B-6302-2008; Nemery, Benoit/D-1224-2013; Forastiere, Francesco/J-9067-2016	van der Sluijs, Jeroen/0000-0002-1346-5953; Forastiere, Francesco/0000-0002-9162-5684; brunekreef, bert/0000-0001-9908-0060; Kreyling, Wolfgang/0000-0002-0702-6567	EU 6th Framework research project INTARESE; Dutch National Institute for Public Health and the Environment (RIVM)	Anthony Seaton, as valuable member of the expert panel who chose ( from the onset) not be co-author of the paper. The study was performed within the framework of EU 6th Framework research project INTARESE and the strategic research project IQARUS of the Dutch National Institute for Public Health and the Environment (RIVM).	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J	Fedulov, AV; Leme, A; Yang, Z; Dahl, M; Lim, R; Mariani, TJ; Kobzik, L				Fedulov, Alexey V.; Leme, Adriana; Yang, Zhiping; Dahl, Morten; Lim, Robert; Mariani, Thomas J.; Kobzik, Lester			Pulmonary exposure to particles during pregnancy causes increased neonatal asthma susceptibility	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article						maternal asthma; environmental particles; titanuim dioxide; diesel exhaust particles; susceptibility	STEROID SEX-HORMONES; ALLERGIC AIRWAY INFLAMMATION; DIESEL EXHAUST; MATERNAL TRANSMISSION; ALVEOLAR MACROPHAGES; LANGERHANS CELLS; DENDRITIC CELLS; MURINE MODEL; MICE; RISK	Maternal immune responses can promote allergy development in offspring, as shown in a model of increased susceptibility to asthma in babies of ovalbumin (OVA)-sensitized and -challenged mother mice. We investigated whether inflammatory responses to air pollution particles (diesel exhaust particles, DEP) or control "Inert" titanium dioxide (TiO2) particles are enhanced during pregnancy and whether exposure to particles can cause increased neonatal susceptibility to asthma. Pregnant BALB/c mice (or nonpregnant controls) received particle suspensions intranasally at Day 14 of pregnancy. Lung inflammatory responses were evaluated 48 hours after exposure. Offspring of particle- or buffer-treated mothers were sensitized and aerosolized with OVA, followed by assays of airway hyperresponsiveness (AHR) and allergic inflammation (AI). Nonpregnant females had the expected minimal response to "inert" TiO2. In contrast, pregnant mice showed robust and persistent acute inflammation after both TiO2 and DEP. Genomic profiling identified genes differentially expressed in pregnant lungs exposed to TiO2 center dot Neonates of mothers exposed to TiO2 (and DEP, but not PBS) developed AHR and All, indicating that pregnancy exposure to both "inert" TiO2 and DEP caused increased asthma susceptibility in offspring. We conclude that (1) pregnancy enhances lung inflammatory responses to otherwise relatively innocuous inert particles; and (2) exposures of nonallergic pregnant females to inert or toxic environmental air particles can cause increased allergic susceptibility in offspring.	[Fedulov, Alexey V.; Leme, Adriana; Yang, Zhiping; Dahl, Morten; Lim, Robert; Kobzik, Lester] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Mol & Integrat Physiol Sci Program, Boston, MA 02115 USA; [Mariani, Thomas J.] Harvard Univ, Sch Med, Lung Biol Ctr, Boston, MA USA	Fedulov, AV (reprint author), Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Mol & Integrat Physiol Sci Program, 665 Huntington Ave,HSP 12,Room 1313, Boston, MA 02115 USA.	afedulov@hsph.harvard.edu	Dahl, Morten/F-4219-2014	Dahl, Morten/0000-0002-6686-312X	NHLBI NIH HHS [HL69760]		Adler A, 2004, J APPL PHYSIOL, V97, P286, DOI 10.1152/japplphysiol.00821.2003; Ahn MH, 2005, RESP RES, V6, DOI 10.1186/1465-9921-6-34; Albrecht ED, 2000, AM J OBSTET GYNECOL, V182, P432, DOI 10.1016/S0002-9378(00)70235-3; Arredondo F, 2006, SEMIN REPROD MED, V24, P33, DOI 10.1055/s-2006-931799; Baron RM, 2004, FASEB J, V18, P1276, DOI 10.1096/fj.04-1518fje; Bommel H, 2000, J ALLERGY CLIN IMMUN, V105, P796, DOI 10.1067/mai.2000.105124; Cahill M., 1995, HDB DIAGNOSTIC TESTS; Chao TC, 1996, AM J REPROD IMMUNOL, V35, P106; CHAO TC, 1995, CELL IMMUNOL, V160, P43, DOI 10.1016/0008-8749(95)80007-6; CHAO TC, 1994, AM J REPROD IMMUNOL, V32, P43; Chao TC, 2000, AM J REPROD IMMUNOL, V44, P310, DOI 10.1111/j.8755-8920.2000.440511.x; Cohn L, 2001, J IMMUNOL, V166, P2760; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; Dohi M, 1999, LAB INVEST, V79, P1559; Drumm K, 1999, LUNG, V177, P9, DOI 10.1007/PL00007628; Fedulov A, 2005, J IMMUNOL, V175, P4292; Fujimaki H, 1997, TOXICOLOGY, V116, P227, DOI 10.1016/S0300-483X(96)03539-1; Goldsmith Carroll-Ann W., 1999, Reviews on Environmental Health, V14, P121; Gomes RFM, 2000, J APPL PHYSIOL, V89, P908; GUNNISON AF, 1992, FUND APPL TOXICOL, V19, P607, DOI 10.1016/0272-0590(92)90100-V; Hamada K, 2003, J IMMUNOL, V170, P1683; HAMADA K, 2006, IN PRESS J TOXICOL E; Hamelmann E, 1997, AM J RESP CRIT CARE, V156, P766; HANTOS Z, 1992, J APPL PHYSIOL, V72, P168; Hubeau C, 2006, AM J PATHOL, V168, P1931, DOI 10.2353/ajpati.7.2006.051231; Huffman LJ, 2004, J TOXICOL ENV HEAL A, V67, P125, DOI 10.1080/15287390490264776; Ivanova E, 2005, AM J REPROD IMMUNOL, V53, P199, DOI 10.1111/j.1600-0897.2005.00266.x; Kang CM, 2005, AM J RESP CELL MOL, V33, P290, DOI 10.1165/rcmb.2005-0003OC; Leme AS, 2006, J IMMUNOL, V176, P762; LIN H, 1993, J IMMUNOL, V151, P4562; Lomax R, 2001, STAT CONCEPTS 2 COUR; LUTCHEN KR, 1993, J APPL PHYSIOL, V75, P478; Mao A, 2005, J IMMUNOL, V175, P5146; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Miyabara Y, 1998, AM J RESP CRIT CARE, V157, P1138; Miyake Yoshihiro, 2002, J Epidemiol, V12, P418; Pauwels RA, 1998, CLIN EXP ALLERGY, V28, P1; Piccinni MP, 2000, J NEUROIMMUNOL, V109, P30, DOI 10.1016/S0165-5728(00)00299-X; Prescott SL, 2006, CURR ALLERGY ASTHM R, V6, P75, DOI 10.1007/s11882-006-0014-7; Renwick LC, 2004, OCCUP ENVIRON MED, V61, P442, DOI 10.1136/oem.2003.008227; Southam DS, 2002, AM J PHYSIOL-LUNG C, V282, pL833, DOI 10.1152/ajplung.00173.2001; Suzuki Takahito, 1993, Japanese Journal of Allergology, V42, P963; Takano H, 1998, IMMUNOPHARM IMMUNOT, V20, P329, DOI 10.3109/08923979809038548; van Zijverden M, 2000, TOXICOL APPL PHARM, V168, P131, DOI 10.1006/taap.2000.9013; Venn AJ, 2001, AM J RESP CRIT CARE, V164, P2177, DOI 10.1164/rccm2106126; von Mutius E, 2006, ALLERGY, V61, P407, DOI 10.1111/j.1398-9995.2006.01009.x; VONMUTIUS E, 1994, AM J RESP CRIT CARE, V149, P358; Von Mutius E, 2000, ARCH DIS CHILD S, V2, P112; Warheit DB, 2005, TOXICOL SCI, V88, P514, DOI 10.1093/toxsci/kfi331; WEGMANN TG, 1993, IMMUNOL TODAY, V14, P353, DOI 10.1016/0167-5699(93)90235-D; Weiss ST, 2001, ANN ALLERG ASTHMA IM, V87, P5; Wieser F, 2001, FERTIL STERIL, V75, P1234, DOI 10.1016/S0015-0282(01)01796-4; Wills-Karp M, 2000, IMMUNOPHARMACOLOGY, V48, P263, DOI 10.1016/S0162-3109(00)00223-X	53	95	98	1	6	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.	JAN	2008	38	1					57	67		10.1165/rcmb.2007-0124OC		11	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	244DC	WOS:000251845200008	17656681	
J	Lundblad, LKA; Thompson-Figueroa, J; Allen, GB; Rinaldi, L; Norton, RJ; Irvin, CG; Bates, JHT				Lundblad, Lennart K. A.; Thompson-Figueroa, John; Allen, Gilman B.; Rinaldi, Lisa; Norton, Ryan J.; Irvin, Charles G.; Bates, Jason H. T.			Airway hyperresponsiveness in allergically inflamed mice - The role of airway closure	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; micro-computed tomography; input impedance; lung derecruitment; lung volume	SMOOTH-MUSCLE CONTRACTION; TEMPORAL DYNAMICS; ASTHMA; LUNG; DOGS; HYPEROXIA; RAT; BRONCHOCONSTRICTION; VENTILATION; CHALLENGE	Rationale: Allergically inflamed mice exhibit airway hyper-responsiveness to inhaled methacholine, which computer simulations of lung impedance suggest is due to enhanced lung derecruitment and which we sought to verify in the present study. Methods: BALB/c mice were sensitized and challenged with ovalbumin to induce allergic inflammation; the control mice were sensitized but received no challenge. The mice were then challenged with inhaled methacholine and respiratory system impedance tracked for the following 10 minutes. Respiratory elastance (H) was estimated from each impedance measurement. One group of mice was ventilated with 100% O-2 during this procedure and another group was ventilated with air. After the procedure, the mice were killed and ventilated with pure N-2, after which the trachea was tied off and the lungs were imaged with micro-computed tomography (micro-CT). Results: H was significantly higher in allergic mice than in control animals after methacholine challenge. The ratio of H at the end of the measurement period between allergic and nonallergic mice ventilated with O-2 was 1.36, indicating substantial derecruitment in the allergic animals. The ratio between lung volumes determined by micro-CT in the control and the allergic mice was also 1.36, indicative of a corresponding volume loss due to absorption atelectasis. Micro-CT images and histograms of Hounsfield units from the lungs also showed increased volume loss in the allergic mice compared with control animals after methacholine challenge. Conclusions: These results support the conclusion that airway closure is a major component of hyperresponsiveness in allergically inflamed mice.	Univ Vermont, Coll Med, Vermont Lung Ctr, Burlington, VT 05405 USA	Lundblad, LKA (reprint author), Univ Vermont, Coll Med, Vermont Lung Ctr, HSRF 230,149 Beaumont Ave, Burlington, VT 05405 USA.	lennart.lundblad@uvm.edu			NCRR NIH HHS [P20 RR15557]; NHLBI NIH HHS [R01 HL67273]		BATES JHT, 1994, J APPL PHYSIOL, V76, P616; Bates JHT, 1997, J APPL PHYSIOL, V82, P55; BECKETT WS, 1988, J APPL PHYSIOL, V64, P1683; Belik J, 2003, J APPL PHYSIOL, V94, P2303, DOI 10.1152/japplphysiol.00820.2002; Brusasco V, 2003, J APPL PHYSIOL, V95, P1305, DOI 10.1152/japplphysiol.00001.2003; DOMINO KB, 1989, J APPL PHYSIOL, V67, P730; Fredberg JJ, 2004, RESP RES, V5, DOI 10.1186/1465-9921-5-2; HANTOS Z, 1992, J APPL PHYSIOL, V72, P168; Harris RS, 2006, AM J RESP CRIT CARE, V174, P245, DOI 10.1164/rccm.200510-1634OC; Hohlfeld JM, 1999, AM J RESP CRIT CARE, V159, P1803; King GG, 1998, AM J RESP CRIT CARE, V158, P1900; Lakshminrusimha S, 2006, J APPL PHYSIOL, V101, P135, DOI 10.1152/japplphysiol.01382.2005; Laurent F, 2000, EUR RADIOL, V10, P1404, DOI 10.1007/s003300000504; Lauzon AM, 2000, J APPL PHYSIOL, V89, P2023; Lundblad LKA, 2004, ANN BIOMED ENG, V32, P1420, DOI 10.1114/B:ABME.0000042229.41098.6a; Lundblad LKA, 2005, AM J RESP CRIT CARE, V171, P1363, DOI 10.1164/rccm.200410-1349OC; LUNDBLAD LKA, 2006, P AM THORAC SOC, V3, pA789; Mann CM, 1998, J APPL PHYSIOL, V84, P2010; MITZNER W, 1992, J APPL PHYSIOL, V72, P158; MORGAN JJ, 1984, RESP PHYSIOL, V55, P309, DOI 10.1016/0034-5687(84)90053-7; Niimi A, 2003, AM J RESP CRIT CARE, V168, P983, DOI 10.1164/rccm.200211.1268OC; Pare PD, 2003, AM J RESP CRIT CARE, V168, P913, DOI 10.1164/rccm.2307005; Petak F, 2001, J APPL PHYSIOL, V90, P2221; Ricciardolo FLM, 2003, THORAX, V58, P175, DOI 10.1136/thorax.58.2.175; Venegas JG, 2005, NATURE, V434, P777, DOI 10.1038/nature03490; Wagers S, 2004, J APPL PHYSIOL, V96, P2019, DOI 10.1152/japplphysiol.00924.2003; Wagers S, 2002, J APPL PHYSIOL, V92, P1802, DOI 10.1152/japplphysiol.00883.2001; Wagers SS, 2004, J CLIN INVEST, V114, P104, DOI 10.1172/JC1200419569; WOLLNER A, 1991, ALLERGY, V46, P35, DOI 10.1111/j.1398-9995.1991.tb00540.x	29	95	98	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.	APR 15	2007	175	8					768	774		10.1164/rccm.200610-1410OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	157MR	WOS:000245724700007	17255559	
J	Adam, E; Hansen, KK; Astudillo, OF; Coulon, L; Bex, F; Duhant, X; Jaumotte, E; Hollenberg, MD; Jacquet, A				Adam, E; Hansen, KK; Astudillo, OF; Coulon, L; Bex, F; Duhant, X; Jaumotte, E; Hollenberg, MD; Jacquet, A			The house dust mite allergen Der p 1, unlike Der p 3, stimulates the expression of interleukin-8 in human airway epithelial cells via a proteinase-activated receptor-2-independent mechanism	JOURNAL OF BIOLOGICAL CHEMISTRY			English	Article							NF-KAPPA-B; TUMOR-NECROSIS-FACTOR; CYSTEINE PROTEASE ACTIVITY; INDUCE CYTOKINE RELEASE; TRANSCRIPTION FACTORS; GENE-EXPRESSION; INFLAMMATORY CYTOKINES; TIGHT JUNCTIONS; GM-CSF; RECEPTOR-2	We investigated and compared the mechanisms by which two dust mite proteolytic allergens, Der p 1 and Der p 3, and a peptide agonist of proteinase-activated receptor 2 (PAR(2)AP) trigger interleukin (IL)-8 release from human pulmonary epithelial cells (A549). Although all three stimuli tested induced the up-regulation of IL-8 ( mRNA and protein), the Der p 1-mediated signaling events did not exactly match those induced by PAR(2)AP and Der p 3. First, Der p 1 was less effective in stimulating IL-8 gene transcriptional activity than PAR(2)AP and Der p 3. Second, Der p 1-mediated IL-8 expression was mainly dependent on NF-kappa B, whereas Der p 3 and PAR(2)AP regulated IL-8 expression through the activation of both NF-kappa B and AP-1. Third, although all three MAP kinases, ERK1/2, p38, and JNK, were activated, Der p 1 induced IL-8 release exclusively via the ERK1/2 signaling pathway, whereas PAR(2)AP and Der p 3 also involved the other kinases. Fourth, in HeLa cells, Der p 1 was able to up-regulate IL-8 secretion independent of PAR(2) expression, and in contrast with PAR(2)AP and Der p 3, Der p 1 was unable to affect calcium signaling via PAR(2) in PAR(2)-expressing KNRK cells. Finally, cleavage by Der p 1 of a synthetic peptide representing the N-terminal activation-cleavage site of PAR(2) did not release a high potency activator of PAR(2) as does Der p 3. We conclude that Der p 1 ( but not Der p 3)-induced IL-8 production in A549 epithelial cells is independent of PAR(2) activation.	Univ Libre Bruxelles, Inst Biol & Med Mol, Dept Appl Genet, B-6041 Gosselies, Belgium; Univ Calgary, Dept Pharmacol & Therapeut, Canadian Inst Hlth Res Prot & Inflammat Network, Calgary, AB T2N 4N1, Canada; Univ Calgary, Dept Med, Canadian Inst Hlth Res Prot & Inflammat Network, Calgary, AB T2N 4N1, Canada; Univ Libre Bruxelles, Inst CERIA, Microbiol Lab, B-1060 Brussels, Belgium; Univ Libre Bruxelles, Erasme Hosp, Dept Immunol, Sch Med,Inst Interdisciplinary Res, B-1060 Brussels, Belgium	Jacquet, A (reprint author), Univ Libre Bruxelles, Inst Biol & Med Mol, Dept Appl Genet, B-6041 Gosselies, Belgium.	alain.jacquet@ulb.ac.be					Adam E, 2003, MOL CELL BIOL, V23, P6200, DOI 10.1128/MCB.23.17.6200-6209.2003; Al-Ani B, 2003, J PHARMACOL EXP THER, V304, P1120, DOI 10.1124/jpet.102.043844; Al-Ani B, 1999, J PHARMACOL EXP THER, V290, P753; ANGEL P, 1987, CELL, V49, P729, DOI 10.1016/0092-8674(87)90611-8; Ashburner BP, 2001, MOL CELL BIOL, V21, P7065, DOI 10.1128/MCB.21.20.7065-7077.2001; Asokananthan N, 2002, J IMMUNOL, V169, P4572; 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Biol. Chem.	MAR 17	2006	281	11					6910	6923		10.1074/jbc.M507140200		14	Biochemistry & Molecular Biology	Biochemistry & Molecular Biology	022BY	WOS:000236030900003	16293628	
J	Lucas, SR; Platts-Mills, TAE				Lucas, SR; Platts-Mills, TAE			Physical activity and exercise in asthma: Relevance to etiology and treatment	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma exercise; conditioning; etiology; pathophysiology; sedentary lifestyle; activity; therapy; incidence; severity	AIRWAY SMOOTH-MUSCLE; DEEP INSPIRATION; CHILDREN; PROGRAM; OBESITY; HYPERRESPONSIVENESS; OVERWEIGHT; INTENSITY; RISK	There is little doubt that the cause of the increased prevalence and severity of asthma is multifactorial. Although the factors of allergen exposure and hygiene are almost certainly necessary for its development, there is a growing body of literature that implicates lifestyle change, specifically decreased physical activity, as a contributor to the increase in asthma prevalence and severity. Several literature reviews of exercise conditioning in patients with asthma have been published. These reviews and recent controlled trials emphasize that although many of the studies of exercise conditioning in asthmatic patients involved different methods and outcome measures, the overwhelming majority of studies demonstrated the capacity for asthmatic subjects to exercise safely and significantly improve their cardiovascular fitness and quality of life. There are several proposed pathophysiologic mechanisms responsible for the effects of decreased activity on the lung function of patients with asthma. A prescription for exercise has been endorsed for all asthmatic subjects by the American College of Sports Medicine and the American Thoracic Society. The allergy community has placed emphasis on medical therapy and allergen avoidance; in addition, exercise avoidance has not been formally incorporated into the National Asthma Education and Prevention Program guidelines. It is our belief that an exercise prescription should be part of the treatment for all cases of asthma. The real question is whether prolonged physical activity and, in particular, outdoor play of children plays a role in prophylaxis against persistent wheezing. If so, the decrease in physical activity might have played a major role in recent increases in asthma prevalence and severity.	Univ Virginia, Asthma & Allerg Dis Ctr, Charlottesville, VA 22908 USA	Platts-Mills, TAE (reprint author), Univ Virginia, Asthma & Allerg Dis Ctr, POB 801355, Charlottesville, VA 22908 USA.	tap2z@virginia.edu			NIAID NIH HHS [P01-AI-50989, AI-20565]		American College of Sports Medicine, 2000, ACSMS GUID EX TEST P; American Thoracic Society, 1999, AM J RESP CRIT CARE, V159, P1666; Biring MS, 1999, AM J MED SCI, V318, P293, DOI 10.1097/00000441-199911000-00002; BUTTON B, 2004, PEDIATR PULM, V27, P213; Camargo CA, 1999, ARCH INTERN MED, V159, P2582, DOI 10.1001/archinte.159.21.2582; Cambach W, 1997, EUR RESPIR J, V10, P104, DOI 10.1183/09031936.97.10010104; Clark C. 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Allergy Clin. Immunol.	MAY	2005	115	5					928	934		10.1016/j.jaci.2005.01.033		7	Allergy; Immunology	Allergy; Immunology	925LR	WOS:000229055100005	15867847	
J	Pichavant, M; Charbonnier, AS; Taront, S; Brichet, AB; Wallaert, B; Pestel, J; Tonnel, AB; Gosset, P				Pichavant, M; Charbonnier, AS; Taront, S; Brichet, AB; Wallaert, B; Pestel, J; Tonnel, AB; Gosset, P			Asthmatic bronchial epithelium activated by the proteolytic allergen Der p 1 increases selective dendritic cell recruitment	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						epithelial cells; dendritic cells; chemokines; allergy; lung	INFLAMMATORY PROTEIN 3-ALPHA; BRONCHOALVEOLAR LAVAGE FLUID; NECROSIS-FACTOR-ALPHA; ATOPIC ASTHMA; PROINFLAMMATORY CYTOKINES; INTESTINAL EPITHELIUM; RESPIRATORY-TRACT; AIRWAY EPITHELIUM; ANATOMIC SITES; UP-REGULATION	Background: Airway dendritic cells (DCs) are crucial for allergen-induced sensitization and inflammation in allergic asthma. After allergen challenge, an increased number of DCs is observed in airway epithelium from patients with allergy. Objective: Because Der p 1, a cysteine protease allergen from Dermatophagoides pteronyssinus, induces chemokine production by bronchial epithelial cells (BECs), the purpose of this investigation was to evaluate the capacity of BEC exposed to Der p 1 to recruit DCs. Methods: Chemotactic activity of BEAS-2B, a bronchial epithelial cell line, and BECs from nonatopic controls and patients with allergic asthma was evaluated on the migration of precursors, immature and mature monocyte-derived DCs (MDDCs), and CD34(+)-derived Langerhans cells (LCs). Results: C-C chemokine ligand (CCL)-2, CCL5, and C-X-C chemokine ligand 10 production by BEAS-2B and BEC was increased after Der p 1 exposure, whereas the proenzyme proDer p 1 devoid of enzymatic activity had no effect. Der p I stimulation of BEAS-2B and BEC from both groups increased significantly the recruitment of MDDC precursors, depending on CCL2, CCL5, and C-X-C chemokine ligand 10 production. In a reconstituted polarized epithelium, apical application of Der p I enhanced MDDC precursor migration into the epithelial layer. Moreover, Der p 1 stimulation of BEC from patients with asthma but not from controls increased the migration of LC precursors, mainly dependent on CCL20 secretion. No migration of immature and mature DCs was observed. Conclusion: These data confirmed that BECs participate in the homeostasis of the DC network present within the bronchial epithelium through the secretion of chemokines. In allergic asthma, upregulation of CCL20 production induced LC recruitment, the role of which remains to be determined.	Inst Pasteur, INSERM, U416, IFR 17, F-59019 Lille, France	Gosset, P (reprint author), Inst Pasteur, INSERM, U416, IFR 17, 1 Rue Prof Calmette,BP 245, F-59019 Lille, France.	Philippe.Gosset@pasteur-lille.fr					Alam R, 1996, AM J RESP CRIT CARE, V153, P1398; Allam JP, 2003, J ALLERGY CLIN IMMUN, V112, P141, DOI 10.1067/mai.2003.1607; Asokananthan N, 2002, J IMMUNOL, V169, P4572; BELLINI A, 1993, CHEST, V103, P997, DOI 10.1378/chest.103.4.997; Bousquet J, 2000, AM J RESP CRIT CARE, V161, P1720; Caux C, 2000, SPRINGER SEMIN IMMUN, V22, P345, DOI 10.1007/s002810000053; Caux C, 1997, BLOOD, V90, P1458; Charbonnier AS, 1999, J EXP MED, V190, P1755, DOI 10.1084/jem.190.12.1755; Dieu MC, 1998, J EXP MED, V188, P373, DOI 10.1084/jem.188.2.373; Dieu-Nosjean MC, 2000, J EXP MED, V192, P705, DOI 10.1084/jem.192.5.705; Eisenbarth SC, 2002, J EXP MED, V196, P1645, DOI 10.1084/jem.20021340; GOSSET P, 1991, J ALLERGY CLIN IMMUN, V88, P561, DOI 10.1016/0091-6749(91)90149-I; Gosset P, 1999, J ALLERGY CLIN IMMUN, V103, P289, DOI 10.1016/S0091-6749(99)70504-X; Grassi F, 1998, J LEUKOCYTE BIOL, V64, P484; Hammad H, 2002, J IMMUNOL, V169, P1524; Hammad H, 2000, LAB INVEST, V80, P605; HERBERT CA, 1995, AM J RESP CELL MOL, V12, P369; Holgate ST, 2000, AM J RESP CRIT CARE, V162, pS113; HOLT PG, 1989, CLIN EXP ALLERGY, V19, P255, DOI 10.1111/j.1365-2222.1989.tb02380.x; Holt PG, 2000, J AEROSOL MED, V13, P361, DOI 10.1089/jam.2000.13.361; Holt PG, 2000, J ALLERGY CLIN IMMUN, V105, P421, DOI 10.1067/mai.2000.105010; Homey B, 2000, J IMMUNOL, V164, P6621; Izadpanah A, 2001, AM J PHYSIOL-GASTR L, V280, pG710; Jahnsen FL, 2001, THORAX, V56, P823, DOI 10.1136/thorax.56.11.823; Kheradmand F, 2002, J IMMUNOL, V169, P5904; King C, 1998, J IMMUNOL, V161, P3645; Knight DA, 2001, J ALLERGY CLIN IMMUN, V108, P797; Lambrecht BN, 2003, NAT REV IMMUNOL, V3, P994, DOI 10.1038/nri1249; Lanzavecchia A, 2001, CELL, V106, P263, DOI 10.1016/S0092-8674(01)00455-X; Lukacs NW, 2001, J EXP MED, V194, P551, DOI 10.1084/jem.194.4.551; Moller GM, 1996, CLIN EXP ALLERGY, V26, P517, DOI 10.1046/j.1365-2222.1996.d01-337.x; Novak N, 2004, ALLERGY, V59, P5, DOI 10.1046/j.1398-9995.2003.00337.x; Pichavant M, 2003, J IMMUNOL, V171, P6697; Reibman J, 2003, AM J RESP CELL MOL, V28, P648, DOI 10.1165/rcmb.2002-00950C; Rozyk KJ, 1997, IMMUNOL LETT, V58, P47; SCHONHEGRAD MA, 1991, J EXP MED, V173, P1345, DOI 10.1084/jem.173.6.1345; Stumbles PA, 2001, J IMMUNOL, V167, P228; Tanaka Y, 1999, EUR J IMMUNOL, V29, P633, DOI 10.1002/(SICI)1521-4141(199902)29:02<633::AID-IMMU633>3.0.CO;2-I; Tillie-Leblond I, 1999, AM J RESP CRIT CARE, V159, P487; Vanbervliet Beatrice, 2002, European Journal of Immunology, V32, P231, DOI 10.1002/1521-4141(200201)32:1<231::AID-IMMU231>3.0.CO;2-8; Vermaelen KY, 2001, J EXP MED, V193, P51; Wan H, 1999, J CLIN INVEST, V104, P123, DOI 10.1172/JCI5844	42	95	97	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.	APR	2005	115	4					771	778		10.1016/j.jaci.2004.11.043		8	Allergy; Immunology	Allergy; Immunology	916GM	WOS:000228373400016	15805997	
J	Cullinan, P; MacNeill, SJ; Harris, JM; Moffat, S; White, C; Mills, P; Taylor, AJN				Cullinan, P; MacNeill, SJ; Harris, JM; Moffat, S; White, C; Mills, P; Taylor, AJN			Early allergen exposure, skin prick responses, and atopic wheeze at age 5 in English children: a cohort study	THORAX			English	Article							HOUSE-DUST MITE; ASTHMA; SENSITIZATION; CHILDHOOD; ENVIRONMENT; RISK	Background: For many years it has been assumed that the risk of childhood respiratory allergies is related to allergen exposures in early life. There are, however, few prospective data in support. We aimed to examine this relationship in a representative cohort of children born in Ashford, Kent (UK). Methods: 625 children (94% of those eligible) were followed from birth to the age of 5.5 years at which time 552 underwent skin prick testing to extracts of house dust mite and cat fur allergens. Maternal reports of wheeze in the last year were collected by interview. These outcomes were related to individual domestic concentrations of Der p 1 and Fel d I allergens estimated from dust collection at the age of 8 weeks. Results: 10% of children were sensitised to house dust mite or cat at age 5.5 years; 7% had atopic wheeze. No significant relationships between allergen exposure and either sensitisation or wheeze were found but, on examination, the exposure-response relationships for both allergens and for each outcome rose steeply at low levels of exposure and were attenuated at high levels of exposure. These patterns were modified by paternal atopy and by birth order. Conclusions: There are no linear relationships between early allergen exposure and the induction of childhood respiratory allergy; rather, the risks of IgE sensitisation and asthma rise at very low levels of exposure and are attenuated thereafter. These patterns are influenced by parental atopy and birth order. These findings suggest important gene-environment interactions in the development of atopy and asthma and imply that reductions in domestic allergen exposure alone are unlikely to have a major impact in decreasing the incidence of these diseases in childhood.	Natl Heart & Lung Inst, Imperial Coll Sch Med, Dept Occupat & Environm Med, London SW3 6LR, England	Cullinan, P (reprint author), Natl Heart & Lung Inst, Imperial Coll Sch Med, Dept Occupat & Environm Med, Manresa Rd, London SW3 6LR, England.	p.cullinan@ic.ac.uk					Atkinson W, 1999, EUR RESPIR J, V13, P583, DOI 10.1183/09031936.99.13358599; CHECKOWAY H, 1989, RES METHODS OCCUPATI, P244; Cullinan P, 1999, EUR RESPIR J, V13, P1139, DOI 10.1034/j.1399-3003.1999.13e33.x; Heinrich J, 2003, J EXPO ANAL ENV EPID, V13, P152, DOI 10.1038/sj.jea.7500267; KALRA S, 1992, THORAX, V47, P928, DOI 10.1136/thx.47.11.928; KUEHR J, 1994, CLIN EXP ALLERGY, V24, P229, DOI 10.1111/j.1365-2222.1994.tb00224.x; KUEHR J, 1994, J ALLERGY CLIN IMMUN, V94, P44, DOI 10.1016/0091-6749(94)90070-1; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; Pearce N, 2000, THORAX, V55, P424, DOI 10.1136/thorax.55.5.424; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; Stayner L, 2003, SCAND J WORK ENV HEA, V29, P317; Sunyer J, 2001, CLIN EXP ALLERGY, V31, P1352, DOI 10.1046/j.1365-2222.2001.01187.x; Svanes C, 1999, J ALLERGY CLIN IMMUN, V103, P415, DOI 10.1016/S0091-6749(99)70465-3; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7	15	95	100	0	4	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	OCT	2004	59	10					855	861		10.1136/thx.2003.019877		7	Respiratory System	Respiratory System	858FC	WOS:000224175200009	15454651	
J	Gruber, A; Mancek, M; Wagner, H; Kirschning, CJ; Jerala, R				Gruber, A; Mancek, M; Wagner, H; Kirschning, CJ; Jerala, R			Structural model of MD-2 and functional role of its basic amino acid clusters involved in cellular lipopolysaccharide recognition	JOURNAL OF BIOLOGICAL CHEMISTRY			English	Article							TOLL-LIKE RECEPTOR-4; DUST-MITE ALLERGEN; SIGNAL-TRANSDUCTION; CRYSTAL-STRUCTURE; GM2-ACTIVATOR PROTEIN; TERTIARY STRUCTURE; INNATE IMMUNITY; DISULFIDE BONDS; RESPONSIVENESS; COMPLEX	The receptor complex resulting from association of MD-2 and the ectodomain of Toll-like receptor 4 (TLR4) mediates lipopolysaccharide (LPS) signal transduction across the cell membrane. We prepared a tertiary structure model of MD-2, based on the known structures of homologous lipid-binding proteins. Analysis of circular dichroic spectra of purified bacterially expressed MD-2 indicates high content of beta-type secondary structure, in agreement with the structural model. Bacterially expressed MD-2 was able to confer LPS responsiveness to cells expressing TLR4 despite lacking glycosylation. We identified several clusters of basic residues on the surface of MD-2. Mutation of each of two clusters encompassing the residues Lys(89)-Arg(90)-Lys(91) and Lys(125)-Lys(125) significantly decreased the signal transduction of the respective MD-2 mutants either upon co-expression with TLR4 or upon addition as soluble protein into the supernatant of cells overexpressing TLR4. These basic clusters lie at the edge of the beta-sheet sandwich, which in cholesterol-binding protein connected to Niemann-Pick disease C2 (NPC2), dust mite allergen Der p2, and ganglioside GM2-activator protein form a hydrophobic pocket. In contrast, mutation of another basic cluster composed of Arg(69)-Lys(72), which according to the model lies further apart from the hydrophobic pocket only weakly decreased MD-2 activity. Furthermore, addition of the peptide, comprising the surface loop between Cys(95) and Cys(105), predicted by model, particularly in oxidized form, decreased LPS-induced production of tumor necrosis factor alpha and interleukin-8 upon application to monocytic cells and fibroblasts, respectively, supporting its involvement in LPS signaling. Our structural model of MD-2 is corroborated by biochemical analysis and contributes to the unraveling of molecular interactions in LPS recognition.	Natl Inst Chem, Biotechnol Lab, Ljubljana 1000, Slovenia; Tech Univ Munich, Inst Med Microbiol Immunol & Hyg, D-81675 Munich, Germany	Jerala, R (reprint author), Natl Inst Chem, Biotechnol Lab, Ljubljana 1000, Slovenia.	roman.jerala@ki.si		Jerala, Roman/0000-0002-6337-5251			Akashi S, 2003, J EXP MED, V198, P1035, DOI 10.1084/jem.20031076; Alexander C, 2001, J ENDOTOXIN RES, V7, P167, DOI 10.1179/096805101101532675; Altschul SF, 1997, NUCLEIC ACIDS RES, V25, P3389, DOI 10.1093/nar/25.17.3389; Andreeva A, 2004, NUCLEIC ACIDS RES, V32, pD226, DOI 10.1093/nar/gkh039; da Silva CJ, 2002, J BIOL CHEM, V277, P1845, DOI DOI 10.1074/JBC.M109910200; Derewenda U, 2002, J MOL BIOL, V318, P189, DOI 10.0000/S0022-2836(02)00027-X; Ferguson AD, 1998, SCIENCE, V282, P2215, DOI 10.1126/science.282.5397.2215; Ferguson AD, 2000, STRUCT FOLD DES, V8, P585; Fiser A, 2003, BIOINFORMATICS, V19, P2500, DOI 10.1093/bioinformatics/btg362; Frecer V, 2000, EUR J BIOCHEM, V267, P837, DOI 10.1046/j.1432-1327.2000.01069.x; Friedland N, 2003, P NATL ACAD SCI USA, V100, P2512, DOI 10.1073/pnas.0437840100; Ginalski K, 2003, PROTEINS, V53, P410, DOI 10.1002/prot.10548; Gioannini TL, 2004, P NATL ACAD SCI USA, V101, P4186, DOI 10.1073/pnas.0306906101; Guyard-Dangremont V, 1999, PROTEIN SCI, V8, P2392; Inohara N, 2002, TRENDS BIOCHEM SCI, V27, P219, DOI 10.1016/S0968-0004(02)02084-4; Kawasaki K, 2003, J IMMUNOL, V170, P413; Kawasaki K, 2000, J BIOL CHEM, V275, P2251, DOI 10.1074/jbc.275.4.2251; LASKOWSKI RA, 1993, J APPL CRYSTALLOGR, V26, P283, DOI 10.1107/S0021889892009944; Latz E, 2002, J BIOL CHEM, V277, P47834, DOI 10.1074/jbc.M207873200; Lee HK, 2004, J BIOL CHEM, V279, P10564, DOI 10.1074/jbc.M311564200; Mancek M, 2002, BIOCHEM BIOPH RES CO, V292, P880, DOI 10.1006/bbrc.2002.6748; Medzhitov R, 2000, TRENDS MICROBIOL, V8, P452, DOI 10.1016/S0966-842X(00)01845-X; Meng GX, 2003, J BIOL CHEM, V278, P39822, DOI 10.1074/jbc.M304766200; Mueller GA, 1998, BIOCHEMISTRY-US, V37, P12707, DOI 10.1021/bi980578+; Mullen GED, 2003, P NATL ACAD SCI USA, V100, P3919, DOI 10.1073/pnas.0630495100; Nagai Y, 2002, NAT IMMUNOL, V3, P667, DOI 10.1038/ni809; Ohnishi T, 2003, CLIN DIAGN LAB IMMUN, V10, P405, DOI 10.1128/CDLI.10.3.405-410.2003; Ohnishi T, 2001, J IMMUNOL, V167, P3354; Poltorak A, 2000, P NATL ACAD SCI USA, V97, P2163, DOI 10.1073/pnas.040565397; Poltorak A, 1998, SCIENCE, V282, P2085, DOI 10.1126/science.282.5396.2085; Pristovsek P, 1999, J MED CHEM, V42, P4604, DOI 10.1021/jm991031b; Re F, 2003, J IMMUNOL, V171, P5272; Re F, 2002, J BIOL CHEM, V277, P23427, DOI 10.1074/jbc.M202554200; Rost B, 2003, NUCLEIC ACIDS RES, V31, P3300, DOI 10.1093/nar/gkg508; SALI A, 1995, PROTEINS, V23, P318, DOI 10.1002/prot.340230306; Schromm AB, 2001, J EXP MED, V194, P79, DOI 10.1084/jem.194.1.79; Schubert WD, 2001, J MOL BIOL, V312, P783, DOI 10.1006/jmbi.2001.4989; Shi JY, 2001, J MOL BIOL, V310, P243, DOI 10.1006/jmbi.2001.4762; Shimazu R, 1999, J EXP MED, V189, P1777, DOI 10.1084/jem.189.11.1777; STUDIER FW, 1986, J MOL BIOL, V189, P113, DOI 10.1016/0022-2836(86)90385-2; THANNHAUSER TW, 1984, ANAL BIOCHEM, V138, P181, DOI 10.1016/0003-2697(84)90786-3; Viriyakosol S, 2001, J BIOL CHEM, V276, P38044; Visintin A, 2003, J BIOL CHEM, V278, P48313, DOI 10.1074/jbc.M306802200; Visintin A, 2001, P NATL ACAD SCI USA, V98, P12156, DOI 10.1073/pnas.211445098; Wright CS, 2003, J MOL BIOL, V331, P951, DOI 10.1016/S0022-2836(03)00794-0; Wright CS, 2000, J MOL BIOL, V304, P411, DOI 10.1006/jmbi.2000.4225; ZHANG KYJ, 1994, PROTEIN SCI, V3, P687	47	95	99	0	4	AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA	0021-9258			J BIOL CHEM	J. Biol. Chem.	JUL 2	2004	279	27					28475	28482		10.1074/jbc.M400993200		8	Biochemistry & Molecular Biology	Biochemistry & Molecular Biology	832KC	WOS:000222265400082	15111623	
J	Jaakkola, JJK; Parise, H; Kislitsin, V; Lebedeva, NI; Spengler, JD				Jaakkola, JJK; Parise, H; Kislitsin, V; Lebedeva, NI; Spengler, JD			Asthma, wheezing, and allergies in Russian schoolchildren in relation to new surface materials in the home	AMERICAN JOURNAL OF PUBLIC HEALTH			English	Article							YOUNG-CHILDREN; SYMPTOMS; HEALTH	In a cross-sectional study of 5951 Russian 8-12-year-old schoolchildren, risks of current asthma, wheezing, and allergy were related to recent renovation and the installation of materials with potential chemical emissions. New linoleum flooring, synthetic carpeting, particleboard, wall coverings, and furniture and recent painting were determinants of 1 or several of these 3 health outcomes. These findings warrant further attention to the type of materials used in interior design.	Univ Birmingham, Inst Occupat Hlth, Birmingham B15 2TT, W Midlands, England; Univ Helsinki, Dept Publ Hlth, Helsinki, Finland; Boston Univ, Dept Math & Stat, Boston, MA 02215 USA; Ctr Preparat & Implementat Int Tech Assistance Pr, Moscow, Russia; Harvard Univ, Sch Publ Hlth, Environm Sci & Engn Program, Boston, MA 02115 USA	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				FERRIS BG, 1978, AM REV RESPIR DIS, V118, P1; Jaakkola JJK, 1999, AM J PUBLIC HEALTH, V89, P188, DOI 10.2105/AJPH.89.2.188; JAAKKOLA JJK, 1993, J EXPO ANAL ENV EPID, V3, P129; Jaakkola JJK, 2000, AM J PUBLIC HEALTH, V90, P797, DOI 10.2105/AJPH.90.5.797; Jaakkola JJK, 2000, ENVIRON HEALTH PERSP, V108, P589, DOI 10.2307/3434876; Mastrangelo G, 1995, Med Lav, V86, P503; Spengler JD, 2004, AM J PUBLIC HEALTH, V94, P657, DOI 10.2105/AJPH.94.4.657; Ucgun I, 1998, ALLERGY, V53, P1096, DOI 10.1111/j.1398-9995.1998.tb03822.x; WIESLANDER G, 1994, INT ARCH OCC ENV HEA, V66, P261, DOI 10.1007/BF00454365	9	95	101	0	9	AMER PUBLIC HEALTH ASSOC INC	WASHINGTON	1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 USA	0090-0036			AM J PUBLIC HEALTH	Am. J. Public Health	APR	2004	94	4					560	562		10.2105/AJPH.94.4.560		3	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	807IC	WOS:000220494200016	15054004	
J	Mueller-Anneling, L; Avol, E; Peters, JM; Thorne, PS				Mueller-Anneling, L; Avol, E; Peters, JM; Thorne, PS			Ambient endotoxin concentrations in PM10 from Southern California	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; bioaerosol; endotoxin; lipopolysaccharide; particulate matter	PARTICULATE AIR-POLLUTION; LUNG-FUNCTION GROWTH; ALVEOLAR MACROPHAGE RESPONSES; IN-HOUSE DUST; AIRBORNE ENDOTOXIN; DAILY MORTALITY; INSOLUBLE COMPONENTS; EXPOSURE-RESPONSE; INHALED ENDOTOXIN; COARSE PARTICLES	Concentrations of endotoxin in urban air pollution have not previously been extensively characterized. We measured 24-hr levels of PM10 (particulate matter < 10 mum in aerodynamic diameter) and the associated endotoxin component once every 6 weeks for 1 year in 13 communities in Southern California. All the samples collected had detectable PM10 and endotoxin levels. The geometric mean PM10 was 34.6 mug/m(3) [geometric SD (GSD), 2.1; range, 3.0-135]. By volume, the endotoxin geometric mean was 0.44 endotoxin units (EU)/m(3) (GSD, 3.1; range, 0.03-5.44). Per unit material collected, the geometric mean of endotoxin collected was 13.6 EU/mg (GSD, 3.2; range, 0.7-96.8). No correlation was found between endotoxin concentrations and other ambient pollutants concurrently measured [ozone, nitrogen dioxide, total acids, or PM2.5 (particulate matter < 2.5 put in aerodynamic diameter]. PM10 and endotoxin concentrations were significantly correlated, most strongly in summer. Samples collected in more rural and agricultural areas had lower PM10 and mid-range endotoxin levels. The high desert and mountain communities had lower PM10 levels but endotoxin levels comparable with or higher than the rural agricultural sites. By volume, endotoxin levels were highest at sites downwind of Los Angeles, California, which were also the locations of highest PM10. Endotoxin concentrations measured in this study were all < 5.5 EU/m(3), which is lower than recognized thresholds for acute adverse health effects for occupational exposures but in the same range as indoor household concentrations. This study provides the first extensive characterization of endotoxin concentration across a large metropolitan area in relation to PM10 and other pollutant monitoring, and supports the need for studies of the role of endotoxin in childhood asthma in urban settings.	Univ Iowa, Coll Publ Hlth, Dept Occupat & Environm Hlth, Iowa City, IA 52242 USA; Univ So Calif, Dept Prevent Med, Los Angeles, CA USA	Thorne, PS (reprint author), Univ Iowa, Coll Publ Hlth, Dept Occupat & Environm Hlth, 100 Oakdale Campus,IREH, Iowa City, IA 52242 USA.	peter-thorne@uiowa.edu			NIEHS NIH HHS [P30 ES 007048, P30 ES 05605]		Bonner JC, 1998, AM J RESP CELL MOL, V19, P672; CASTELLAN RM, 1987, NEW ENGL J MED, V317, P605, DOI 10.1056/NEJM198709033171005; CLAPP WD, 1994, AM J RESP CRIT CARE, V150, P611; Dockery DW, 2001, ENVIRON HEALTH PERSP, V109, P483, DOI 10.2307/3454657; Donaldson K, 2001, INT J HYG ENVIR HEAL, V203, P411, DOI 10.1078/1438-4639-00059; DONHAM K, 1989, BRIT J IND MED, V46, P31; 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, 2002, THORAX, V57, P86, DOI 10.1136/thorax.57.1.86; DOUWES J, 1995, APPL ENVIRON MICROB, V61, P1763; Douwes J, 1997, INT J OCCUP ENV HL S, V3, pS26; DOUWES J, 2003, MODERN IND HYGIENE, V2, P219; Fairley D, 1999, ENVIRON HEALTH PERSP, V107, P637, DOI 10.2307/3434455; 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; HEEDERIK D, 2003, MODERN IND HYGIENE, V2, P293; Heinrich J, 2001, CLIN EXP ALLERGY, V31, P1839, DOI 10.1046/j.1365-2222.2001.01220.x; Imrich A, 1999, TOXICOL APPL PHARM, V159, P117, DOI 10.1006/taap.1999.8731; Imrich A, 2000, TOXICOL APPL PHARM, V167, P140, DOI 10.1006/taap.2000.9002; Jagielo PJ, 1996, AM J PHYSIOL-LUNG C, V270, pL1052; Jedrychowski W, 1999, ENVIRON HEALTH PERSP, V107, P669, DOI 10.2307/3434460; Kline JN, 1999, AM J RESP CRIT CARE, V160, P297; Li XY, 1997, ENVIRON HEALTH PERSP, V105, P1279, DOI 10.2307/3433547; Lippmann M, 2000, ANNU REV PUBL HEALTH, V21, P309, DOI 10.1146/annurev.publhealth.21.1.309; McConnell R, 1999, ENVIRON HEALTH PERSP, V107, P757, DOI 10.2307/3434662; Menetrez MY, 2001, J AIR WASTE MANAGE, V51, P1436, DOI 10.1080/10473289.2001.10464365; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; MICHEL O, 1989, J APPL PHYSIOL, V66, P1059; Milton DK, 1996, AM J IND MED, V29, P3, DOI 10.1002/(SICI)1097-0274(199601)29:1<3::AID-AJIM2>3.0.CO;2-V; Monn C, 1999, TOXICOL APPL PHARM, V155, P245, DOI 10.1006/taap.1998.8591; Ning YY, 2000, J TOXICOL ENV HEAL A, V59, P165, DOI 10.1080/009841000156952; Ostro BD, 1999, ENVIRON RES, V81, P231, DOI 10.1006/enrs.1999.3978; Ostro BD, 2000, J EXPO ANAL ENV EPID, V10, P412, DOI 10.1038/sj.jea.7500094; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Park JH, 2000, ENVIRON HEALTH PERSP, V108, P1023, DOI 10.2307/3434953; Park JH, 2001, ENVIRON HEALTH PERSP, V109, P859, DOI 10.2307/3454831; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; Peters JM, 1999, AM J RESP CRIT CARE, V159, P768; Plopper CG, 2000, ENVIRON HEALTH PERSP, V108, pA252, DOI 10.1289/ehp.108-a252; Pope CA, 2000, ENVIRON HEALTH PERSP, V108, P713, DOI 10.2307/3454408; Pope CA, 1999, ENVIRON HEALTH PERSP, V107, P613, DOI 10.2307/3434450; POPE CA, 1995, ENVIRON HEALTH PERSP, V103, P472, DOI 10.2307/3432586; Rizzo MC, 1997, PEDIATR ALLERGY IMMU, V8, P121; Rylander R., 1997, INT J OCCUP ENV HL S, V3, P32; Samet J M, 2000, Res Rep Health Eff Inst, V94, P5; Samet JM, 2000, NEW ENGL J MED, V343, P1742, DOI 10.1056/NEJM200012143432401; SCHWARTZ DA, 1995, AM J RESP CRIT CARE, V152, P603; Soukup JM, 2001, TOXICOL APPL PHARM, V171, P20, DOI 10.1006/taap.2000.9096; Thorne PS, 2000, TOXICOLOGY, V152, P13, DOI 10.1016/S0300-483X(00)00287-0; THORNE PS, 2003, AM J RESP CRIT CARE, V167, pA470; THORNE PS, 2001, AM J RESP CRIT CARE, V163, pA844; THORNE PS, 2003, AM J RESP CRIT CARE, V167, pA972; Wouters IM, 2000, APPL ENVIRON MICROB, V66, P627, DOI 10.1128/AEM.66.2.627-631.2000; Zock JP, 1998, AM J IND MED, V33, P384, DOI 10.1002/(SICI)1097-0274(199804)33:4<384::AID-AJIM9>3.0.CO;2-U	54	95	96	3	21	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	2004	112	5					583	588		10.1289/ehp.6552		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	811KI	WOS:000220770400046	15064165	
J	Green, BJ; Mitakakis, TZ; Tovey, ER				Green, BJ; Mitakakis, TZ; Tovey, ER			Allergen detection from 11 fungal species before and after germination	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergen; fungi; germination; halogen; immunoassay	ASP-F-I; ASPERGILLUS-FUMIGATUS; ALTERNARIA-ALTERNATA; BINDING PROTEIN; DIFFERENT MEDIA; MAJOR ALLERGEN; IGE ANTIBODIES; RISK FACTOR; EXPRESSION; ASTHMA	Background: Allergens dispersed by airborne fungal spores play an important but poorly understood role in the underlying cause and exacerbation of asthma. Previous studies suggest that spores of Alternaria and Aspergillus release greater quantities of allergen after germination than before germination. It is unknown whether this is true of other allergenic fungi. Objective: Our purpose was to investigate the release of allergen from a range of individual fungal-spores before and after germination. Methods: Allergen expression from spores of Alternaria alternata, Cladosporium herbarum, Aspergillius fumigatus, Botrytis cinerea, Epicoccum nigrum, Exserohilum rostralum, Penicillium chrysogenum, Stemphylium botryosum, Curvularia lunata, Trichoderma viride, and Bipolaris spicifera was examined by halogen immunoassays through the use of pooled serum IgE from patients allergic to fungus. Spores were deposited onto proteinbinding membranes direct, from culture. To germinate spores, samples were incubated in high humidity at room temperature for 48 hours. Ungerminated and germinated samples were then laminated with an adhesive film and immunostained by the halogen assay. The samples were examined by light microscopy, and positive counts (haloed particles) were expressed as percentages of total spores. Results: For 9 of 11 species, between 5.7% and 92% of spores released allergen before germination. Spores of Penicillium and Trichodemia did not release detectable allergen. After germination, all spores that germinated had allergen elution from their hyphae. Eight of I I species showed a significant increase (P <.05) in the percentage of spores eluting detectable allergen. Localization of allergen along the hyphae varied with species, such that some eluted allergen mainly from hyphal tips and septal junctions whereas others eluted allergen along the entire length. Conclusions: Increased elution of allergen after germination might be a common feature of many species of allergenic fungi. Although allergens from both spores and hyphae were recognized by human IgE, the extent to which human exposure occurs to allergens eluted from inhaled spores or from hyphae that germinate after deposition in the respiratory tract remains to be explored. The patterns of allergen expression might affect the clinical response to such exposure. (J Allergy Clin Immunol 2003;111:285-9.).	Univ Sydney, Fac Med, Woolcock Allergen Unit, Sydney, NSW 2006, Australia; Royal Prince Alfred Hosp, Woolcock Inst Med Res, Sydney, NSW, Australia	Green, BJ (reprint author), Univ Sydney, Fac Med, Woolcock Allergen Unit, Room 461,Blackburn Bldg D06, Sydney, NSW 2006, Australia.		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Allergy Clin. Immunol.	FEB	2003	111	2					285	289		10.1067/mai.2003.57		5	Allergy; Immunology	Allergy; Immunology	644WF	WOS:000180942700010	12589346	
J	Allmers, H; Schmengler, J; Skudlik, C				Allmers, H; Schmengler, J; Skudlik, C			Primary prevention of natural rubber latex allergy in the German health care system through education and intervention	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						occupational asthma; natural rubber latex allergy; powder free latex gloves; latex allergens; primary prevention	IGE ANTIBODIES; GLOVES; SENSITIZATION; PREVALENCE; WORKERS; NURSES	Background: The development of occupational asthma and allergic skin reactions caused by natural rubber latex (NRL) allergy are risks for health care workers. There are few published studies to suggest that intervention programs to reduce exposure will lead to primary prevention of sensitization. Objective: This study assesses the effects of intervention to reduce the incidence of NRL allergy in personnel working in health care facilities insured by the German statutory accident insurance company for health care workers, Berufsgenossenschaft fur Gesundheitsdienst und Wohlfahrtspflege, with approximately 3 million insured employees, by switching to powder-free NRL gloves. Methods: The timing of introduction of intervention strategies, such as education of both physicians and administrators, together with regulations demanding that health care facilities only purchase low-protein, powder-free NRL gloves are reported. We reviewed the annual numbers of reported suspected cases of NRL-caused occupational allergies and the amount and type of gloves used in German acute-care hospitals since 1986. Results: The purchase of powder-free NRL examination gloves exceeded that of powdered gloves for the first time in 1998. This only became true for powder-free NRL sterile gloves 2 years later in 2000. The incidence of suspected occupational NRL allergy cases rose until 1998 and has declined steadily since. There was a 2-year lag between the beginning of the decline in the purchase of powdered NRL examination gloves and the beginning of a decline in suspected NRL-caused occupational asthma cases. Conclusions: Despite the effect of increased recognition of NRL allergies, education about NRL allergies in health care facilities combined with the introduction of powder-free gloves with reduced protein levels has been associated with a decline in the number of suspected cases of occupational allergies caused by NRL in Germany on a nationwide scale. These results clearly indicate that primary prevention of occupational NRL allergies can be achieved if these straightforward and practical interventions are properly carried out and maintained.	Univ Osnabruck, Dept Dermatol Environm Med & Hlth Sci, D-49090 Osnabruck, Germany; Harvard Sch Publ Hlth, Boston, MA USA; Berufsgenossenschaft & Gesundheitsdienst & Wohlfa, Delmenhorst, Germany	Allmers, H (reprint author), Univ Osnabruck, Dept Dermatol Environm Med & Hlth Sci, Sedanstr 115, D-49090 Osnabruck, Germany.						Allmers H, 1997, DEUT MED WOCHENSCHR, V122, P1308, DOI 10.1055/s-2008-1047764; Allmers H, 1998, J ALLERGY CLIN IMMUN, V102, P841, DOI 10.1016/S0091-6749(98)70026-0; Allmers H, 1996, DEUT MED WOCHENSCHR, V121, P823, DOI 10.1055/s-2008-1043073; ARELLANO R, 1992, ANESTHESIOLOGY, V77, P905, DOI 10.1097/00000542-199211000-00011; Baur X, 1998, J ALLERGY CLIN IMMUN, V101, P24, DOI 10.1016/S0091-6749(98)70188-5; Baur X, 1996, ANAESTHESIST, V45, P653, DOI 10.1007/s001010050299; Grzybowski M, 1996, J ALLERGY CLIN IMMUN, V98, P535, DOI 10.1016/S0091-6749(96)70087-8; HAAMANN F, 2001, ERFOLGREICHE PRAVENT; KELLY KJ, 1993, J ALLERGY CLIN IMMUN, V91, P1140, DOI 10.1016/0091-6749(93)90316-8; LAGIER F, 1992, J ALLERGY CLIN IMMUN, V90, P319, DOI 10.1016/S0091-6749(05)80009-0; Levy DA, 1999, JAMA-J AM MED ASSOC, V281, P988, DOI 10.1001/jama.281.11.988; Liss GM, 2001, AM J IND MED, V40, P347, DOI 10.1002/ajim.1108; Liss GM, 1997, OCCUP ENVIRON MED, V54, P335; Roy A, 1997, J Can Dent Assoc, V63, P297; SAARY J, 2001, AM J RESP CRIT CARE, V163, pA809; Shoup A J, 1997, AORN J, V66, P729, DOI 10.1016/S0001-2092(06)62931-1; Shoup AJ, 1997, AORN J, V66, P729; Sussman GL, 1998, J ALLERGY CLIN IMMUN, V102, P333; TARLO SM, 1994, J ALLERGY CLIN IMMUN, V93, P985, DOI 10.1016/S0091-6749(94)70045-1; Tarlo SM, 2001, J ALLERGY CLIN IMMUN, V108, P628; TUJANMAA K, 2000, J ALLERGY CLIN IMMUN, V104; TURJANMAA K, 1987, CONTACT DERMATITIS, V17, P270, DOI 10.1111/j.1600-0536.1987.tb01476.x; WITT S, 1999, TECHNICAL INFORMATIO; YASSIN MS, 1994, ANN ALLERGY, V85, P626	24	95	98	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.	AUG	2002	110	2					318	323	UNSP 1/87/126461	10.1067/mai.2002.126461		6	Allergy; Immunology	Allergy; Immunology	585DY	WOS:000177509800019	12170275	
J	Koopman, LP; van Strien, RT; Kerkhof, M; Wijga, A; Smit, HA; de Jongste, JC; Gerritsen, J; Aalberse, RC; Brunekreef, B; Neijens, HJ				Koopman, LP; van Strien, RT; Kerkhof, M; Wijga, A; Smit, HA; de Jongste, JC; Gerritsen, J; Aalberse, RC; Brunekreef, B; Neijens, HJ		Prevention Incidence Asthma Mite	Placebo-controlled trial of house dust mite-impermeable mattress covers - Effect on symptoms in early childhood	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						mite control; wheezing; asthma; atopy; allergens	DER-P-I; RESPIRATORY SYMPTOMS; ALLERGEN EXPOSURE; EARLY-LIFE; HIGH-RISK; ASTHMA; INFANTS; IGE; SENSITIZATION; SENSITIVITY	We investigated the effect of house dust mite (HDM)-allergen avoidance on the development of respiratory Symptoms, atopic dermatitis, and atopic sensitization by performing a double blind, placebo-controlled trial. In total, 1,282 allergic pregnant women were selected (416 received HDM allergen-impermeable mattress covers for the parents' and child's mattress in the third trimester of pregnancy [active], 394 received placebo covers, 472 received no intervention). Data on allergen exposure, clinical symptoms, and immunoglobulin E were collected prospectively. The prevalence of night cough without a cold in the second year of life was lower in the group with active covers compared with the group with placebo covers (adjusted odds ratio 0.65; 95% confidence interval 0.4-1.0). No effect of the intervention was seen on other respiratory symptoms, atopic dermatitis, and total and specific immunoglobulin E. It can be concluded that application of HDM-impermeable mattress covers on the child's and parents' beds reduced night cough, but not other respiratory symptoms, atopic dermatitis, and atopic sensitization in the first 2 years of life. Follow-up will determine the long-term effect of the intervention on the development of atopic disease.	Erasmus Univ, Sophia Childrens Hosp, Med Ctr, Dept Pediat, NL-3000 CB Rotterdam, Netherlands; Univ Utrecht, Inst Risk Assessment, Dept Environm & Occupat Hlth, Utrecht, Netherlands; Univ Groningen, Dept Epidemiol & Stat, Groningen, Netherlands; Natl Inst Publ Hlth & Environm, Dept Chron Dis Epidemiol, Groningen, Netherlands; Univ Groningen, Beatrix Childrens Hosp, Dept Pediat Pulmonol, Groningen, Netherlands; Blood Transfus Serv, Cent Lab, Amsterdam, Netherlands	Neijens, HJ (reprint author), Erasmus Univ, Sophia Childrens Hosp, Med Ctr, Dept Pediat, POB 2060, NL-3000 CB Rotterdam, Netherlands.		Kerkhof, Marjan/A-8846-2008	brunekreef, bert/0000-0001-9908-0060			ARSHAD SH, 1992, LANCET, V339, P1493, DOI 10.1016/0140-6736(92)91260-F; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Bergmann R L, 1994, Pediatr Allergy Immunol, V5, P19, DOI 10.1111/j.1399-3038.1994.tb00343.x; BURR ML, 1989, J EPIDEMIOL COMMUN H, V43, P125, DOI 10.1136/jech.43.2.125; 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; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; HIDE DW, 1994, J ALLERGY CLIN IMMUN, V93, P842, DOI 10.1016/0091-6749(94)90375-1; Koopman LP, 2001, PEDIATR ALLERGY IMMU, V12, P118, DOI 10.1034/j.1399-3038.2001.012003118.x; Lakwijk N, 1998, CLIN EXP ALLERGY, V28, P454; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Moher D, 2001, BMC Med Res Methodol, V1, P2, DOI 10.1186/1471-2288-1-2; Nishioka K, 1998, J ALLERGY CLIN IMMUN, V101, P28, DOI 10.1016/S0091-6749(98)70189-7; Pearce N, 2000, THORAX, V55, P424, DOI 10.1136/thorax.55.5.424; PEAT JK, 1994, AUST NZ J MED, V24, P270, DOI 10.1111/j.1445-5994.1994.tb02171.x; PEAT JK, 1991, CLIN EXP ALLERGY, V21, P573, DOI 10.1111/j.1365-2222.1991.tb00849.x; PLATTSMILLS TAE, 1995, J ALLERGY CLIN IMMUN, V96, P435, DOI 10.1016/S0091-6749(95)70284-9; Schuurman J, 1997, J ALLERGY CLIN IMMUN, V99, P545, DOI 10.1016/S0091-6749(97)70083-6; SEARS MR, 1989, CLIN EXP ALLERGY, V19, P419, DOI 10.1111/j.1365-2222.1989.tb02408.x; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; STALLMAN PJ, 1977, INT ARCH ALLER A IMM, V54, P443; vanStrien RT, 1995, CLIN EXP ALLERGY, V25, P1184; vanStrien RT, 1996, EUR RESPIR J, V9, P926, DOI 10.1183/09031936.96.09050926; VANSTRIEN RT, 1994, CLIN EXP ALLERGY, V24, P853; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; Williams HC, 1995, BRIT J DERMATOL, V133, P941, DOI 10.1111/j.1365-2133.1995.tb06930.x	28	95	97	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					307	313		10.1164/rccm.2106026		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	580QV	WOS:000177246000012	12153962	
J	Giguere, S; Viel, L; Lee, E; MacKay, EJ; Hernandez, J; Franchini, M				Giguere, S; Viel, L; Lee, E; MacKay, EJ; Hernandez, J; Franchini, M			Cytokine induction in pulmonary airways of horses with heaves and effect of therapy with inhaled fluticasone propionate	VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY			English	Article						cytokine; chemokine; heaves; COPD; horse; fluticasone	BRONCHOALVEOLAR LAVAGE FLUID; NF-KAPPA-B; OBSTRUCTION HEAVES; BRONCHIAL HYPERRESPONSIVENESS; PHENOTYPIC ANALYSIS; STRAW CHALLENGES; PERIPHERAL-BLOOD; ATOPIC ASTHMA; ANIMAL-MODEL; NATURAL HAY	Work in humans and laboratory animals has identified a central role for cytokines and chemokines in development and persistence of lower airway inflammation. The objectives of this study were to determine interleukin (IL)-1beta, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha induction in bronchoalveolar lavage (BAL) of control horses and horses with heaves both during remission and exacerbation of the disease, and to determine the effect of therapy with inhaled fluticasone propionate on the cytokine profile of horses with heaves. IL-1beta and TNF-alpha mRNA expression was significantly higher in horses with heaves after exposure to moldy hay compared to either values obtained during clinical remission or to healthy controls. IL-8 mRNA expression and protein concentrations were significantly higher in horses with heaves than in controls. Both IL-4 and IFN-gamma mRNA expression was increased at various times in heaves-susceptible horses compared to controls. IL-2, IL-5 and IL-10 mRNA expression was not detected in BAL cells of either group. Therapy with inhaled fluticasone propionate after induction of a severe heaves exacerbation resulted in complete resolution of clinical signs, normalization of pulmonary function tests, and significant decrease in BAL neutrophilia. This was associated with a significant decrease in IL-4 mRNA expression and increase in IFN-gamma/IL-4 ratio in horses with heaves. These results demonstrate the clinical efficacy of inhaled fluticasone propionate for the treatment of heaves and suggest a role for cytokines in the development of lower airway inflammation in heaves-susceptible horses. (C) 2002 Elsevier Science B.V. All rights reserved.	Univ Florida, Coll Vet Med, Dept Large Anim Clin Sci, Gainesville, FL 32610 USA; Univ Guelph, Ontario Vet Coll, Dept Clin Studies, Guelph, ON N1G 2W1, Canada; Univ Zurich, Inst Virol, Fac Vet, CH-8057 Zurich, Switzerland	Giguere, S (reprint author), Univ Florida, Coll Vet Med, Dept Large Anim Clin Sci, POB 100136, Gainesville, FL 32610 USA.						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Immunol. Immunopathol.	MAR	2002	85	3-4					147	158	PII S0165-2427(01)00420-2	10.1016/S0165-2427(01)00420-2		12	Immunology; Veterinary Sciences	Immunology; Veterinary Sciences	551HW	WOS:000175555500004	11943316	
J	Douwes, J; Pearce, N; Heederik, D				Douwes, J; Pearce, N; Heederik, D			Does environmental endotoxin exposure prevent asthma?	THORAX			English	Review							ANIMAL FEED-INDUSTRY; LUNG-FUNCTION CHANGES; IN-HOUSE DUST; INFLAMMATORY RESPONSE; HAY-FEVER; AIRBORNE ENDOTOXIN; INHALED ENDOTOXIN; ALLERGIC SENSITIZATION; RESPIRATORY SYMPTOMS; BRONCHIAL REACTIVITY	The evidence as to whether exposure to environmental airborne endotoxin plays a protective or an inducing role in the development of asthma is reviewed. Studies of endotoxin and atopy, endotoxin and asthma, and farming and asthma are considered and, in each instance, a distinction is made between evidence of primary causation and evidence of secondary causation. It is concluded that, although it is plausible that bacterial endotoxin may protect against the development of asthma, there is considerable reason for caution regarding this hypothesis.	Univ Utrecht, Inst Risk Assessment Sci, Div Environm & Occupat Hlth, NL-3508 TD Utrecht, Netherlands; Massey Univ, Ctr Publ Hlth Res, Wellington, New Zealand	Douwes, J (reprint author), Univ Utrecht, Inst Risk Assessment Sci, Div Environm & Occupat Hlth, POB 80176, NL-3508 TD Utrecht, Netherlands.			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J	Litonjua, AA; Carey, VJ; Burge, HA; Weiss, ST; Gold, DR				Litonjua, AA; Carey, VJ; Burge, HA; Weiss, ST; Gold, DR			Exposure to cockroach allergen in the home is associated with incident doctor-diagnosed asthma and recurrent wheezing	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article; Proceedings Paper	Annual Meeting of the American-Thoracic-Society	APR 24-29, 1998	CHICAGO, ILLINOIS	Amer Thorac Soc		cockroach; indoor allergens; asthma; wheeze	INNER-CITY CHILDREN; CHILDHOOD ASTHMA; RESPIRATORY ILLNESS; UNITED-STATES; RISK FACTOR; SENSITIZATION; SMOKING; RACE; RESPONSIVENESS; PREVALENCE	Background: Indoor inhaled allergens have been repeatedly demonstrated to worsen asthma In sensitized individual, but their role in incident asthma is more controversial, Objective: We investigated the relationship between exposure to allergens (dust mite, cat, and cockroach) measured in the home and incident doctor-diagnosed asthma and recurrent wheezing in children born to parents with asthma, allergies, or both. Methods: From an ongoing longitudinal family and birth cohort study, rye identified 222 siblings (median age, 2.87 years) of the index children. Allergen levels in the home were measured from dust samples obtained at the beginning of the study. Incident doctor-diagnosed asthma and recurrent wheezing were determined from questionnaires administered at 14 months and 22 months after the initial questionnaire, Results: Thirteen (5.9%) children were reported to have Incident asthma, twenty (9.0%) children had recurrent asthmatic wheezing, and 18 (8.1%) had recurrent wheezing without asthma, Compared with children living in homes with Bla g 1 or 2 levels of less than 0.05 U/g, children exposed to Bra g 1 or 2 levels of 0.05 to less than 2 U/g had a relative risk for incident asthma of 8.27 (95% confidence interval, 1.04-66.04), whereas children exposed to Bla g 1 or 2 levels of 2 U/g or greater bad a relative risk for incident asthma of 35.87 (95% confidence Interval, 4.49-286.62). Cockroach allergen exposure was likewise a significant predictor for recurrent asthmatic wheezing. Neither dust mite nor cat allergen levels were significantly associated with either outcome. These findings remained after control for several covariates, Conclusion: Exposure to cockroach allergen early in life may contribute to the development of asthma in susceptible children.	Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA	Litonjua, AA (reprint author), Brigham & Womens Hosp, Dept Med, Channing Lab, 181 Longwood Ave, Boston, MA 02115 USA.				NHLBI NIH HHS [HL07427]; NIAID NIH HHS [AI35786]		BJORKSTEN B, 1987, CLIN REV ALLERG, V5, P339; Chew GL, 1998, AM J RESP CRIT CARE, V157, P1536; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; GOLD DR, 1993, AM REV RESPIR DIS, V148, P10; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; INFANTERIVARD C, 1995, EPIDEMIOLOGY, V6, P178, DOI 10.1097/00001648-199503000-00016; INGRAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449, DOI 10.1016/S0091-6749(95)70286-5; KANG B, 1976, J ALLERGY CLIN IMMUN, V58, P357, DOI 10.1016/0091-6749(76)90115-9; Kattan M, 1997, PEDIATR PULM, V24, P253, DOI 10.1002/(SICI)1099-0496(199710)24:4<253::AID-PPUL4>3.0.CO;2-L; KUEHR J, 1994, J ALLERGY CLIN IMMUN, V94, P44, DOI 10.1016/0091-6749(94)90070-1; 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; 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; Martinez FD, 1998, EUR RESPIR J, V12, p3S; OPENSHAW PJM, 1994, THORAX, V49, P101, DOI 10.1136/thx.49.2.101; Peat JK, 1996, AM J RESP CRIT CARE, V153, P141; Platts-Mills Thomas A. E., 1997, Journal of Allergy and Clinical Immunology, V100, pS1; 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; SCHWARTZ J, 1990, AM REV RESPIR DIS, V142, P555; SHERMAN CB, 1993, AM REV RESPIR DIS, V148, P98; SPORIK R, 1995, AM J RESP CRIT CARE, V151, P1388; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; TAGER IB, 1993, AM REV RESPIR DIS, V147, P811; TOLLERUD DJ, 1995, J CLIN LAB ANAL, V9, P37, DOI 10.1002/jcla.1860090107; WEISS KB, 1992, CHEST, V101, pS362, DOI 10.1378/chest.101.6_Supplement.362S; ZEGER SL, 1986, BIOMETRICS, V42, P121, DOI 10.2307/2531248	29	95	95	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	2001	107	1					41	47		10.1067/mai.2001.111143		7	Allergy; Immunology	Allergy; Immunology	394PW	WOS:000166533300008	11149989	
J	KleinJan, A; Vinke, JG; Severijnen, LWFM; Fokkens, WJ				KleinJan, A; Vinke, JG; Severijnen, LWFM; Fokkens, WJ			Local production and detection of (specific) IgE in nasal B-cells and plasma cells of allergic rhinitis patients	EUROPEAN RESPIRATORY JOURNAL			English	Article						allergic rhinitis; B-cells; biotinylated allergen; nasal mucosa; plasma cells; specific IgE	MESSENGER-RNA; MAST-CELLS; MUCOSA; EXPRESSION; IL-4; ANTIBODIES; CHALLENGE; INDUCTION; POLYPS; LUNG	Allergic diseases are characterized by allergic complaints in the shock organ and specific immunoglobulin (Ig)E in serum. Literature data indicate that the nasal mucosa itself could produce at least a large part of the specific IgE in allergic rhinitis patients. In order to investigate this hypothesis, nasal mucosal biopsies from the inferior turbinate were taken from symptomatic grass pollen allergic rhinitis patients, symptomatic house dust mite allergic rhinitis patients and nonallergic healthy controls, confirmed by radioallergosorbent test and skin-prick test, Immunohistochemical double-staining was performed for B-cells (CD19) with IgE, plasma cells (CD138) with IgE and plasma cells with biotinylated allergens. Significantly more IgE-positive B-cells and IgE-positive plasma cells were found in biotinylated a the nasal mucosa of allergic patients than in that of nonallergic controls. Double staining with biotinylated allergens and plasma cells showed allergen-positive plasma cells in the nasal mucosa of allergic patients and no allergen-positive plasma cells in the nasal mucosa of nonallergic patients. Blocking experiments using polyclonal antibodies directed against IgE showed a significant reduction in the number of allergen-positive cells in contrast to experiments using polyclonal antibodies directed against IgG, IgA or IgM. This study describes new evidence that specific immunoglobulin E is produced locally in the nasal mucosa in patients with seasonal allergic rhinitis and perennial allergic rhinitis, but not in nonallergic controls.	Erasmus Univ, Dept Otorhinolaryngol, Med Ctr, NL-3015 GD Rotterdam, Netherlands	KleinJan, A (reprint author), Erasmus Univ, Dept Otorhinolaryngol, Med Ctr, Room Ee1655,Dr Molewaterpl 50, NL-3015 GD Rotterdam, Netherlands.						Abbas AK, 1997, CELLULAR MOL IMMUNOL; ALI M, 1979, ARCH PATHOL LAB MED, V103, P274; BOUWHUIJSEN ECA, 1996, ALLERGOLOGIE, V19, P56; BRADDING P, 1993, J IMMUNOL, V151, P3853; Brandtzaeg P, 1996, ACTA OTO-LARYNGOL, V116, P149, DOI 10.3109/00016489609137812; Chvatchko Y, 1996, J EXP MED, V184, P2353, DOI 10.1084/jem.184.6.2353; COCKS BG, 1993, INT IMMUNOL, V5, P657, DOI 10.1093/intimm/5.6.657; CORRIS PA, 1993, LANCET, V341, P1369, DOI 10.1016/0140-6736(93)90941-9; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; DRAKELEE AB, 1984, J LARYNGOL OTOL, V98, P795, DOI 10.1017/S0022215100147474; Durham SR, 1997, INT ARCH ALLERGY IMM, V113, P128; Durham SR, 1997, EUR J IMMUNOL, V27, P2899, DOI 10.1002/eji.1830271123; DURHAM SR, 1992, J IMMUNOL, V148, P2390; ELSHAMI AS, 1989, ALLERGY MOL BIOL, P191; FOKKENS W J, 1988, Rhinology (Utrecht), V26, P293; FOKKENS WJ, 1990, INT ARCH ALLER A IMM, V93, P66; GANZER U, 1988, ORL J OTO-RHINO-LARY, V50, P257; GAUCHAT JF, 1993, NATURE, V365, P340, DOI 10.1038/365340a0; Ghaffar O, 1997, AM J RESP CELL MOL, V17, P17; GILLON J, 1981, IMMUNOL TODAY, V2, P80, DOI 10.1016/0167-5699(81)90035-9; HUGGINS KG, 1975, LANCET, V2, P148; KleinJan A, 1997, J ALLERGY CLIN IMMUN, V99, P515, DOI 10.1016/S0091-6749(97)70079-4; KleinJan A, 1999, J ALLERGY CLIN IMMUN, V103, P441, DOI 10.1016/S0091-6749(99)70469-0; LeGros G, 1996, EUR J IMMUNOL, V26, P3042, DOI 10.1002/eji.1830261233; MCMENAMIN C, 1992, IMMUNOLOGY, V77, P592; MERRETT TG, 1976, CLIN ALLERGY, V6, P69, DOI 10.1111/j.1365-2222.1976.tb01413.x; MYGIND N, 1975, LANCET, V2, P502; Pawankar R, 1997, J CLIN INVEST, V99, P1492, DOI 10.1172/JCI119311; PLATTSMILLS TAE, 1979, J IMMUNOL, V122, P2218; Savelkoul H F, 1996, Eur Respir J Suppl, V22, p67s; Vinke JG, 1999, INT J PEDIATR OTORHI, V51, P73, DOI 10.1016/S0165-5876(99)00244-X; Yanagihara Y, 1997, CLIN EXP IMMUNOL, V108, P295, DOI 10.1046/j.1365-2249.1997.d01-1001.x; ZOLA H, 1987, IMMUNOL TODAY, V8, P308, DOI 10.1016/0167-5699(87)90018-1; Zurcher AW, 1996, INT ARCH ALLERGY IMM, V111, P77	34	95	97	0	7	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0903-1936			EUR RESPIR J	Eur. Resp. J.	MAR	2000	15	3					491	497		10.1034/j.1399-3003.2000.15.11.x		7	Respiratory System	Respiratory System	295JG	WOS:000085962500011	10759442	
J	Kabashima, K				Kabashima, Kenji			New concept of the pathogenesis of atopic dermatitis: Interplay among the barrier, allergy, and pruritus as a trinity	JOURNAL OF DERMATOLOGICAL SCIENCE			English	Review						Atopic dermatitis; Skin barrier; Filaggrin; Langerhans cells; Pruritus; Hapten-atopy hypothesis	REGULATORY T-CELLS; LANGERIN(+) DENDRITIC CELLS; STROMAL LYMPHOPOIETIN EXPRESSION; OF-FUNCTION VARIANTS; LANGERHANS CELLS; IMMUNE-RESPONSES; NC/NGA MICE; CONTACT-DERMATITIS; SKIN INFLAMMATION; TH17 CELLS	Atopic dermatitis (AD) is a common skin condition, characterized by a complex, heterogeneous pathogenesis, including skin barrier dysfunctions, allergy/immunology, and pruritus. When the skin barrier is disrupted by, for example, the filaggrin gene mutation and/or environmental factors, the skin is predisposed to being penetrated by external stimuli. Foreign antigens can be subdivided into two subsets by size: haptens (including metals) and protein antigens. It is known that a single hapten challenge provokes Th1 initially, but that repeated elicitation with haptens results in a shift toward Th2-dominated responses. On the other hand, exposure to protein antigens directly induces Th2-dominant conditions via the thymic stromal lymphopoietin (TSLP) receptor on Langerhans cells. Recently, it has been revealed that Th2 cells produce IL-31, which provokes pruritus, and that Th2 cytokines decrease filaggrin expressions by keratinocytes. These findings suggest that Th2 conditions lead to pruritus and barrier dysfunctions. In this review, we will examine the highly complex interplay among skin barrier abnormality, allergy/immunology, and pruritus as a trinity in the development of AD. (C) 2013 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.	Kyoto Univ, Grad Sch Med, Dept Dermatol, Sakyo Ku, Kyoto 6068507, Japan	Kabashima, K (reprint author), Kyoto Univ, Grad Sch Med, Dept Dermatol, Sakyo Ku, 54 Shogoin Kawara, Kyoto 6068507, Japan.	kaba@kuhp.kyoto-u.ac.jp	Kabashima, Kenji/G-2521-2014	Kabashima, Kenji/0000-0002-0773-0554	Ministries of Education, Culture, Sports, Science and Technology	This work was supported in part by Grants-in-Aid for Scientific Research from the Ministries of Education, Culture, Sports, Science and Technology.	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Dermatol. Sci.	APR	2013	70	1					3	11		10.1016/j.jdermsci.2013.02.001		9	Dermatology	Dermatology	136RF	WOS:000318380400001	23473856	
J	Kawasaki, H; Nagao, K; Kubo, A; Hata, T; Shimizu, A; Mizuno, H; Yamada, T; Amagai, M				Kawasaki, Hiroshi; Nagao, Keisuke; Kubo, Akiharu; Hata, Tsuyoshi; Shimizu, Atsushi; Mizuno, Hideaki; Yamada, Taketo; Amagai, Masayuki			Altered stratum corneum barrier and enhanced percutaneous immune responses in filaggrin-null mice	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Filaggrin; filaggrin-null mice; atopic dermatitis; ichthyosis vulgaris; barrier function; flaky tail mice; stratum corneum; percutaneous immune response	OF-FUNCTION MUTATIONS; ICHTHYOSIS-VULGARIS; ATOPIC-DERMATITIS; SKIN-BARRIER; HOUSE-MOUSE; FLAKY TAIL; CLINICAL SEVERITY; KERATIN FILAMENTS; LANGERHANS CELLS; DISEASE	Background: Loss-of-function mutations in filaggrin are major predisposing factors for atopic dermatitis. Although various reports suggest a critical role for filaggrin in stratum corneum (SC) barrier formation, the lack of filaggrin-null (Flg(-/-)) mice has hampered detailed in vivo analysis of filaggrin's functions. Objective: We sought to generate Flg(-/-) mice and to assess the effect of filaggrin loss on SC barrier function and percutaneous immune responses. Methods: We generated Flg(-/-) mice using gene targeting and assessed the morphology, hydration, mechanical strength, and antigen permeability of their SC. Percutaneous immune responses were evaluated through irritant-and hapten-induced contact hypersensitivity studies and by measuring humoral responses to epicutaneous sensitization with protein antigen. Results: Newborn Flg(-/-) mice exhibited dry scaly skin. Despite marked decreases in natural moisturizing factor levels, which are filaggrin degradation products, SC hydration and transepidermal water loss were normal. Microscopic analyses suggested premature shedding of SC layers, and indeed, increased desquamation under mechanical stress was demonstrated. Loss of keratin patterns, which are critical for corneocyte stabilization, is likely attributable to fragility in the Flg(-/-) SC. Antigens penetrated the Flg(-/-) SC more efficiently, leading to enhanced responses in hapten-induced contact hypersensitivity and higher serum levels of anti-ovalbumin IgG(1) and IgE. Conclusion: Complete filaggrin deficiency led to altered barrier integrity and enhanced sensitization, which are important factors in early-phase atopic dermatitis. Flg(-/-) mice should provide a valuable tool to further explore additional factors the dysfunction of which leads to uncontrolled inflammation in patients with atopic diseases. (J Allergy Clin Immunol 2012;129:1538-46.)	[Amagai, Masayuki] Keio Univ, Sch Med, Dept Dermatol, Shinjyuku Ku, Tokyo, Japan; [Kubo, Akiharu] Keio Univ, Sch Med, Ctr Integrated Med Res, Tokyo, Japan; [Yamada, Taketo] Keio Univ, Sch Med, Dept Pathol, Tokyo 160, Japan; [Hata, Tsuyoshi] KOSE Corp, Fundamental Res Labs, Tokyo, Japan; [Mizuno, Hideaki] RIKEN, Brain Sci Inst, Wako, Saitama, Japan	Amagai, M (reprint author), Keio Univ, Sch Med, Dept Dermatol, Shinjyuku Ku, 35 Shinanomachi, Tokyo, Japan.	amagai@a7.keio.jp	Nagao, Keisuke/J-5116-2013; Amagai, Masayuki/K-5325-2013; Kubo, Akiharu/I-2711-2014	Nagao, Keisuke/0000-0002-7005-3138; Amagai, Masayuki/0000-0003-3314-7052; Kubo, Akiharu/0000-0003-0902-3586	Ministry of Health, Labour and Welfare of Japan; Ministry of Education, Culture, Sports, Science and Technology of Japan; Keio University	Supported by a Health Labour Sciences Research Grant for Research on Allergic Diseases and Immunology from the Ministry of Health, Labour and Welfare of Japan; Grants-in-Aid for Scientific Research; the "Promotion of Environmental Improvement for Independence of Young Researchers" program and a Matching Fund Subsidy for Private Universities from the Ministry of Education, Culture, Sports, Science and Technology of Japan; Research Grants for Life Sciences and Medicine from Keio University Medical Science Fund; and a Keio University Grant-in-Aid for Encouragement of Young Medical Scientists.	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Allergy Clin. Immunol.	JUN	2012	129	6					1538	+		10.1016/j.jaci.2012.01.068		15	Allergy; Immunology	Allergy; Immunology	952BL	WOS:000304764600014	22409988	
J	Oschatz, C; Maas, C; Lecher, B; Jansen, T; Bjorkqvist, J; Tradler, T; Sedlmeier, R; Burfeind, P; Cichon, S; Hammerschmidt, S; Muller-Esterl, W; Wuillemin, WA; Nilsson, G; Renne, T				Oschatz, Chris; Maas, Coen; Lecher, Bernd; Jansen, Thomas; Bjorkqvist, Jenny; Tradler, Thomas; Sedlmeier, Reinhard; Burfeind, Peter; Cichon, Sven; Hammerschmidt, Sven; Mueller-Esterl, Werner; Wuillemin, Walter A.; Nilsson, Gunnar; Renne, Thomas			Mast Cells Increase Vascular Permeability by Heparin-Initiated Bradykinin Formation In Vivo	IMMUNITY			English	Article							COAGULATION-FACTOR-XII; ADVERSE CLINICAL EVENTS; CHONDROITIN SULFATE-E; HEREDITARY ANGIOEDEMA; CONTACT SYSTEM; ALLERGIC REACTIONS; ACTIVATION; MECHANISMS; RECEPTOR; ENZYME	Activated mast cells trigger edema in allergic and inflammatory disease. We report a paracrine mechanism by which mast cell-released heparin increases vascular permeability in vivo. Heparin activated the protease factor XII, which initiates bradykinin formation in plasma. Targeting factor XII or kinin B2 receptors abolished heparin-triggered leukocyte-endothelium adhesion and interfered with a mast cell-driven drop in blood pressure in rodents. Intravital laser scanning microscopy and tracer measurements showed heparin-driven fluid extravasation in mouse skin microvessels. Ablation of factor XII or kinin B2 receptors abolished heparin-induced skin edema and protected mice from allergen-activated mast cell-driven leakage. In contrast, heparin and activated mast cells induced excessive edema in mice deficient in the major inhibitor of factor XII, Cl esterase inhibitor. Allergen exposure triggered edema attacks in hereditary angioedema patients, lacking Cl esterase inhibitor. The data indicate that heparin-initiated bradykinin formation plays a fundamental role in mast cell-mediated diseases.	[Oschatz, Chris; Maas, Coen; Jansen, Thomas; Bjorkqvist, Jenny; Renne, Thomas] Karolinska Inst, Dept Mol Med & Surg, S-17176 Stockholm, Sweden; [Oschatz, Chris; Maas, Coen; Jansen, Thomas; Bjorkqvist, Jenny; Renne, Thomas] Karolinska Inst, Ctr Mol Med, S-17176 Stockholm, Sweden; [Nilsson, Gunnar] Karolinska Inst, Dept Med, Allergy & Clin Immunol Unit, S-17176 Stockholm, Sweden; [Lecher, Bernd] Mfd Diagnost GmbH, D-55234 Wendelsheim, Germany; [Jansen, Thomas] Univ Med Ctr Mainz, Dept Med 2, D-55131 Mainz, Germany; [Tradler, Thomas] Scil Prot GmbH, D-06120 Halle, Germany; [Sedlmeier, Reinhard] Ingenium Pharmaceut GmbH, D-82152 Martinsried, Germany; [Burfeind, Peter] Univ Gottingen, Inst Human Genet, D-37073 Gottingen, Germany; [Cichon, Sven] Univ Bonn, Life & Brain Ctr, Dept Genom, D-53105 Bonn, Germany; [Cichon, Sven] Univ Bonn, Inst Human Genet, D-53105 Bonn, Germany; [Cichon, Sven] Res Ctr Julich, Inst Neurosci & Med, D-52425 Julich, Germany; [Hammerschmidt, Sven] Ernst Moritz Arndt Univ Greifswald, Interfac Inst Genet & Funct Genom, Dept Genet Microorganisms, D-17487 Greifswald, Germany; [Mueller-Esterl, Werner] Goethe Univ Frankfurt, Inst Biochem 2, D-60590 Frankfurt, Germany; [Wuillemin, Walter A.] Luzerner Kantonsspital, Div Hematol, CH-6000 Luzern, Switzerland; [Wuillemin, Walter A.] Luzerner Kantonsspital, Cent Hematol Lab, CH-6000 Luzern, Switzerland; [Wuillemin, Walter A.] Univ Bern, CH-3010 Bern, Switzerland	Renne, T (reprint author), Karolinska Inst, Dept Mol Med & Surg, S-17176 Stockholm, Sweden.	thomas@renne.net	Cichon, Sven/H-8803-2013; Cichon, Sven/B-9618-2014	Cichon, Sven/0000-0002-9475-086X; Cichon, Sven/0000-0002-9475-086X; Nilsson, Gunnar/0000-0001-6795-5512; Maas, Coen/0000-0003-4593-0976	Vetenskapsradet [K2010-64X-21462-01-3]; Hjart Lungfonden [20090642]; Stockholms lans landsting (ALF) [20090540]; Stiftung fur Pathobiochemie und Molekulare Diagnostik of the DGKL,; Cancerfonden [100615]; Federal Ministry of Education and Research (BMBF); Rubicon fellowship [825-10-012]; Netherlands Organisation for Scientific Research (NWO); Margarete Waitz-foundation, Mainz	This work was supported in part by grants from Vetenskapsradet (K2010-64X-21462-01-3), Hjart Lungfonden (20090642), Stockholms lans landsting (ALF, 20090540), Stiftung fur Pathobiochemie und Molekulare Diagnostik of the DGKL, Cancerfonden (100615), and the Federal Ministry of Education and Research (BMBF)-funded ERARE program to T.R. C.M. is supported by a Rubicon fellowship (825-10-012), provided by the Netherlands Organisation for Scientific Research (NWO). T.J. holds a scholarship of the Margarete Waitz-foundation, Mainz. Part of the work of T.T. was performed at Jerini AG, Berlin. We thank L. Kjellen (Uppsala University, Uppsala, Sweden) for providing Ndst2<SUP>-/-</SUP> mice.	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J	Wright, RJ; Visness, CM; Calatroni, A; Grayson, MH; Gold, DR; Sandel, MT; Lee-Parritz, A; Wood, RA; Kattan, M; Bloomberg, GR; Burger, M; Togias, A; Witter, FR; Sperling, RS; Sadovsky, Y; Gern, JE				Wright, Rosalind J.; Visness, Cynthia M.; Calatroni, Agustin; Grayson, Mitchell H.; Gold, Diane R.; Sandel, Megan T.; Lee-Parritz, Aviva; Wood, Robert A.; Kattan, Meyer; Bloomberg, Gordon R.; Burger, Melissa; Togias, Alkis; Witter, Frank R.; Sperling, Rhoda S.; Sadovsky, Yoel; Gern, James E.			Prenatal Maternal Stress and Cord Blood Innate and Adaptive Cytokine Responses in an Inner-City Cohort	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						psychological stress; cord blood; cytokines; innate; adaptive	RESPIRATORY SYNCYTIAL VIRUS; T-REGULATORY CELLS; IMMUNE-RESPONSES; AIRWAY INFLAMMATION; DENDRITIC CELLS; ASTHMA; MATURATION; PREGNANCY; ALLERGENS; CHILDREN	Rationale: Stress-elicited disruption of immunity begins in utero. Objectives: Associations among prenatal maternal stress and cord blood mononuclear cell (CBMC) cytokine responses were prospectively examined in the Urban Environment and Childhood Asthma Study (n = 557 families). Methods: Prenatal maternal stress included financial hardship, difficult life circumstances, community violence, and neighborhood/block and housing conditions. Factor analysis produced latent variables representing three contexts: individual stressors and ecological-level strains (housing problems and neighborhood problems), which were combined to create a composite cumulative stress indicator. CBMCs were incubated with innate (lipopolysaccharide, polyinosinic-polycytidylic acid, cytosine-phosphate-guanine dinucleotides, peptidoglycan) and adaptive (tetanus, dust mite, cockroach) stimuli, respiratory syncytial virus, phytohemagglutinin, or medium alone. Cytokines were measured using multiplex ELISAs. Using linear regression, associations among increasing cumulative stress and cytokine responses were examined, adjusting for sociodemographic factors, parity, season of birth, maternal asthma and steroid use, and potential pathway variables (prenatal smoking, birth weight for gestational age). Measurements and Main Results Mothers were primarily minorities (Black [71%], Latino [19%]) with an income less than $15,000 (69%). Mothers with the highest cumulative stress were older and more likely to have asthma and deliver lower birth weight infants. Higher prenatal stress was related to increased IL-8 production after microbial (CpG, PIC, peptidoglycan) stimuli and increased tumor necrosis factor-a to microbial stimuli (CpG, PIC). In the adaptive panel, higher stress was associated with increased IL-13 after dust mite stimulation and reduced phytohemagglutinin-induced Conclusions Prenatal stress was associated with altered innate and adaptive immune responses in CBMCs. Stress-induced perinatal immunomodulation may impact the expression of allergic disease in these children.	[Wright, Rosalind J.; Gold, Diane R.] Harvard Univ, Brigham & Womens Hosp, Channing Lab, Dept Med,Med Sch, Boston, MA 02115 USA; [Wright, Rosalind J.; Gold, Diane R.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA; [Visness, Cynthia M.; Calatroni, Agustin] Rho Inc, Chapel Hill, NC USA; [Sandel, Megan T.; Lee-Parritz, Aviva] Boston Univ, Sch Med, Boston, MA 02118 USA; [Grayson, Mitchell H.] Med Coll Wisconsin, Milwaukee, WI 53226 USA; [Kattan, Meyer] Columbia Univ, Med Ctr, New York, NY USA; [Wood, Robert A.; Witter, Frank R.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA; [Burger, Melissa; Gern, James E.] Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI USA; [Bloomberg, Gordon R.] Washington Univ, St Louis Sch Med, St Louis, MO USA; [Sperling, Rhoda S.] Mt Sinai Sch Med, New York, NY USA; [Sadovsky, Yoel] Magee Womens Res Inst, Pittsburgh, PA USA; [Togias, Alkis] NIAID, Bethesda, MD 20892 USA	Wright, RJ (reprint author), Harvard Univ, Sch Med, Channing Lab, 181 Longwood Ave, Boston, MA 02115 USA.	rerjw@channing.harvard.edu		Lee-Parritz, Aviva/0000-0003-4655-7720	National Institute of Allergy and Infectious Diseases, National Institutes of Health [NO1-AI-25496, NO1-AI-25482]; National Center for Research Resources, National Institutes of Health [RR00052, M01RR00533, M01RR00071, 5 UL1RR024992-02]; National Institutes of Health [R01 HL080674]; Genentech	Supported by the National Institute of Allergy and Infectious Diseases, National Institutes of Health, under contracts NO1-AI-25496 and NO1-AI-25482, and by the National Center for Research Resources, National Institutes of Health grants RR00052, M01RR00533, M01RR00071, and 5 UL1RR024992-02. During preparation of this manuscript R.J.W. was also supported by National Institutes of Health grant R01 HL080674.; R.J.W. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. C.M.V. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. A.C. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. M.H.G. received 550,001-$100,000 from Genentech as an investigator-initiated research grant. D.R.G. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. M.T.S. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. At-P. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. R.A.W. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. M.K. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. G.R.B. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. M.B. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. AT. is an employee of the National Institutes of Health. F.R.W. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. R.S.S. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. Y.S. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. J.E.G. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript.	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J	Cho, HY; Kleeberger, SR				Cho, Hye-Youn; Kleeberger, Steven R.			Nrf2 protects against airway disorders	TOXICOLOGY AND APPLIED PHARMACOLOGY			English	Article						ARE; Keap1; Lung; Knockout mice; Oxidant; Polymorphism; Mutation	RESPIRATORY SYNCYTIAL VIRUS; ANTIOXIDANT RESPONSE ELEMENT; TRANSCRIPTION FACTOR NRF2; INDUCED LUNG INJURY; GLUTATHIONE-S-TRANSFERASE; EXTRACELLULAR-SUPEROXIDE DISMUTASE; IDIOPATHIC PULMONARY-FIBROSIS; TRANSPEPTIDASE-DEFICIENT MICE; INDUCED INFLAMMATORY RESPONSE; ADENOVIRUS-MEDIATED TRANSFER	Nuclear factor-erythroid 2 related factor 2 (Nrf2) is a ubiquitous master transcription factor that regulates antioxidant response elements (AREs)-mediated expression of antioxidant enzyme and cytoprotective proteins. In the unstressed condition, Kelch-like ECH-associated protein 1 (Keap1) suppresses cellular Nrf2 in cytoplasm and drives its proteasomal degradation. Nrf2 can be activated by diverse stimuli including oxidants, pro-oxidants, antioxidants, and chemopreventive agents. Nrf2 induces cellular rescue pathways against oxidative injury, abnormal inflammatory and immune responses, apoptosis, and carcinogenesis. Application of Nrf2 germ-line mutant mice has identified an extensive range of protective roles for Nrf2 in experimental models of human disorders in the liver, gastrointestinal tract, air-way, kidney, brain, circulation, and immune or nerve system. In the lung, lack of Nrf2 exacerbated toxicity caused by multiple oxidative insults including supplemental respiratory therapy (e.g., hyperoxia, mechanical ventilation), cigarette smoke, allergen, virus, bacterial endotoxin and other inflammatory agents (e.g., carrageenin), environmental pollution (e.g., particles), and a fibrotic agent bleomycin. Microarray analyses and bioinformatic studies elucidated functional AREs and Nrf2-directed genes that are critical components of signaling mechanisms in pulmonary protection by Nrf2. Association of loss of function with promoter polymorphisms in NRF2 or somatic and epigenetic mutations in KEAP1 and NRF2 has been found in cohorts of patients with acute lung injury/acute respiratory distress syndrome Or lung cancer, which further supports the role for NRF2 in these lung diseases. In the Current review, we address the role of Nrf2 in airways based on emerging evidence from experimental oxidative disease models and human studies. Published by Elsevier Inc.	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Appl. Pharmacol.	APR 1	2010	244	1			SI		43	56		10.1016/j.taap.2009.07.024		14	Pharmacology & Pharmacy; Toxicology	Pharmacology & Pharmacy; Toxicology	573DU	WOS:000275889400007	19646463	
J	Prescott, SL; Clifton, V				Prescott, Susan L.; Clifton, Vicki			Asthma and pregnancy: emerging evidence of epigenetic interactions in utero	CURRENT OPINION IN ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						allergic disease; asthma; cord blood; cytokines; epigenetics; fetus; folate; maternal diet; pregnancy	REGULATORY T-CELLS; POPULATION-BASED REGISTER; TOBACCO-SMOKE EXPOSURE; MATERNAL ASTHMA; CORD BLOOD; CHILDHOOD ASTHMA; CESAREAN-SECTION; FETAL SEX; ALLERGIC SENSITIZATION; GENE-EXPRESSION	Purpose of review Pregnancy is arguably the most critical period of developmental programming. Here, we particularly focus on the emerging paradigm that disease propensity is epigenetically determined by maternal exposures that have the capacity to activate or silence fetal genes through alterations in DNA and histone methylation, histone acetylation, and chromatin structure. Recent findings The most notable recent candidate to emerge in this role has been dietary folate, a methyl donor clearly associated with changes in gene expression and disease susceptibility through gene hypermethylation. Animal studies also provide the first evidence that the allergy protective effects of microbial exposure in pregnancy may be mediated by changes in methylation of Th1 genes of the offspring. There is also emerging evidence that perinatal differences in immune function of allergy-prone newborns extend beyond previously recognized differences in effector T cell (Th1/Th2) function, to also include differences in neonatal regulatory T cell (Treg) and Th17 function, and moreover, that these pathways are also epigenetically regulated. Summary New studies reinforce the importance of in-utero exposures (including dietary nutrients, microbial products, cigarette smoking, and certain maternal mediations) in fetal immune development and in programming the susceptibility to asthma and allergic disease.	[Prescott, Susan L.] Univ Western Australia, Sch Paediat & Child Hlth Res, Perth, WA 6001, Australia; [Clifton, Vicki] Univ Adelaide, Robinson Inst, 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	Prescott, Susan/H-5665-2014; Clifton, Vicki/A-1445-2012	Clifton, Vicki/0000-0002-4892-6748			Agostoni C, 2008, J PEDIATR GASTR NUTR, V46, P99; Bager P, 2008, CLIN EXP ALLERGY, V38, P634, DOI 10.1111/j.1365-2222.2008.02939.x; Bakhireva LN, 2008, ANN ALLERG ASTHMA IM, V101, P137, DOI 10.1016/S1081-1206(10)60201-3; Bakhireva LN, 2008, J ASTHMA, V45, P403, DOI 10.1080/02770900801971826; Bernsen RM, 2008, J ALLERGY CLIN IMMUN, V122, P841, DOI 10.1016/j.jaci.2008.07.046; Bhavsar P, 2008, J ALLERGY CLIN IMMUN, V121, P580, DOI 10.1016/j.jaci.2007.12.1156; Bisgaard H, 2009, J ALLERGY CLIN IMMUN, V123, P651, DOI 10.1016/j.jaci.2008.11.036; Blumer N, 2007, CLIN EXP ALLERGY, V37, P348, DOI 10.1111/j.1365-2222.2007.02671.x; 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Opin. Allergy Clin. Immunol.	OCT	2009	9	5					417	426		10.1097/ACI.0b013e328330634f		10	Allergy; Immunology	Allergy; Immunology	490OT	WOS:000269511100005	19652594	
J	Riedl, MA; Saxon, A; Diaz-Sanchez, D				Riedl, Marc A.; Saxon, Andrew; Diaz-Sanchez, David			Oral sulforaphane increases Phase II antioxidant enzymes in the human upper airway	CLINICAL IMMUNOLOGY			English	Article						Oxidative stress; Antioxidants; Asthma; Allergic inflammation; Sulforaphane; Phase II enzymes; Air pollution	DIESEL EXHAUST PARTICLES; OXIDATIVE STRESS; BROCCOLI SPROUTS; QUANTITATIVE-DETERMINATION; CRUCIFEROUS VEGETABLES; NASAL CHALLENGE; IGE PRODUCTION; IN-VIVO; ISOTHIOCYANATES; ASTHMA	Background: Cellular oxidative stress is an important factor in asthma and is thought to be the principle mechanism by which oxidant pollutants such as ozone and particulates mediate their pro-inflammatory effects. Endogenous Phase II enzymes abrogate oxidative stress through the scavenging of reactive oxygen species and metabolism of reactive chemicals. Objective: We conducted a placebo-controlled dose escalation trial to investigate the in vivo effects of sulforaphane, a naturally occurring potent inducer of Phase II enzymes, on the expression of glutathione-s-transferase M1 (GSTM1), glutathione-s-transferase P1 (GSTP1), NADPH quinone oxidoreductase (NQO1), and hemoxygenase-1 (HO-1) in the upper airway of human subjects. Methods: Study subjects consumed oral sulforaphane doses contained in a standardized broccoli sprout homogenate (BSH). RNA expression for selected Phase II enzymes was measured in nasal lavage cells by RT-PCR before and after sulforaphane dosing. Results: All subjects tolerated oral sulforaphane dosing without significant adverse events. Increased Phase II enzyme expression in nasal lavage cells occurred in a dose-dependent manner with maximal enzyme induction observed at the highest dose of 200 g broccoli sprouts prepared as BSH. Significant increases were seen in all sentinel Phase II enzymes RNA expression compared to baseline. Phase II enzyme induction was not seen with ingestion of non-sulforaphane containing alfalfa sprouts.	[Riedl, Marc A.; Saxon, Andrew] Univ Calif Los Angeles, David Geffen Sch Med, Hart & Louis Lab, Dept Med, Los Angeles, CA 90095 USA; [Diaz-Sanchez, David] US EPA, Human Studies Div, Chapel Hill, NC 27599 USA	Riedl, MA (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Div Pulm & Crit Care Med, Ctr Hlth Sci 37 131, 10833 Conte Ave, Los Angeles, CA 90095 USA.	mriedl@mednet.ucla.edu			NCRR NIH HHS [K12 RR017611, K12 RR017611-05]; NIAID NIH HHS [P01 AI050495, P01 AI050495-05]; NIEHS NIH HHS [5P01ES09581-10, P01 ES009581]; PHS HHS [K12 R011 7611]		BAUTIG A, 2003, LUNG CELL MOL PHYSL, V285, pL671; Boldogh I, 2005, J CLIN INVEST, V115, P2169, DOI 10.1172/JCI24422; Bowler RP, 2002, J ALLERGY CLIN IMMUN, V110, P349, DOI 10.1067/mai.2002.126780; Cho HY, 2006, ANTIOXID REDOX SIGN, V8, P76, DOI 10.1089/ars.2006.8.76; Cho HY, 2002, AM J RESP CELL MOL, V26, P175; Cornblatt BS, 2007, CARCINOGENESIS, V28, P1485, DOI 10.1093/carcin/bgm049; Davies RJ, 1997, ALLERGY, V52, P59; Dhakshinamoorthy S, 2000, CURR TOP CELL REGUL, V36, P201; Diaz-Sanchez D, 1999, CLIN IMMUNOL, V90, P313, DOI 10.1006/clim.1998.4676; Diaz-Sanchez D, 1999, J ALLERGY CLIN IMMUN, V104, P1183; Diaz-Sanchez D, 2006, J ALLERGY CLIN IMMUN, V118, P441, DOI 10.1016/j.jaci.2006.04.047; DIAZSANCHEZ D, 1994, J CLIN INVEST, V94, P1417, DOI 10.1172/JCI117478; Fahey JW, 1997, P NATL ACAD SCI USA, V94, P10367, DOI 10.1073/pnas.94.19.10367; Fahey JW, 2001, PHYTOCHEMISTRY, V56, P5, DOI 10.1016/S0031-9422(00)00316-2; Fahey JW, 1999, FOOD CHEM TOXICOL, V37, P973, DOI 10.1016/S0278-6915(99)00082-4; Fujieda S, 1998, AM J RESP CELL MOL, V19, P507; Gilliland FD, 2006, AM J RESP CRIT CARE, V174, P1335, DOI 10.1164/rccm.200509-1424OC; Gurgueira SA, 2002, ENVIRON HEALTH PERSP, V110, P749; Kensler TW, 2005, CANCER EPIDEM BIOMAR, V14, P2605, DOI 10.1158/1055-9965.EPI-05-0368; Kobayashi T, 2000, AM J RESP CRIT CARE, V162, P352; Lee JS, 2005, CANCER LETT, V224, P171, DOI 10.1016/j.canlet.2004.09.042; Li N, 2006, ANTIOXID REDOX SIGN, V8, P88, DOI 10.1089/ars.2006.8.88; Li N, 2004, J IMMUNOL, V173, P3467; Li N, 2003, CLIN IMMUNOL, V109, P250, DOI 10.1016/j.clim.2003.08.006; Li N, 2000, J IMMUNOL, V165, P3393; Lim HB, 1998, FREE RADICAL BIO MED, V25, P635, DOI 10.1016/S0891-5849(98)00073-2; London Stephanie J, 2007, Proc Am Thorac Soc, V4, P217, DOI 10.1513/pats.200701-031AW; Marwick JA, 2004, AM J RESP CELL MOL, V31, P633, DOI 10.1165/rcmb.2004-0006OC; Morimitsu Y, 2002, J BIOL CHEM, V277, P3456, DOI 10.1074/jbc.M110244200; Munday R, 2008, CANCER RES, V68, P1593, DOI 10.1158/0008-5472.CAN-07-5009; Pereira B, 1995, BIOCHEM PHARMACOL, V50, P2093, DOI 10.1016/0006-2952(95)02116-7; Riedl M, 2005, J ALLERGY CLIN IMMUN, V115, P221, DOI 10.1016/j.jaci.2004.11.047; Riedl MA, 2008, CURR OPIN ALLERGY CL, V8, P49, DOI 10.1097/ACI.0b013e3282f3d913; RITZ SA, 2007, LUNG CELLULAR MOL PH, V292, pL33; Romieu I, 2004, THORAX, V59, P8; Sadowska AM, 2007, STEROIDS, V72, P1, DOI 10.1016/j.steroids.2006.10.007; SANDERS SP, 1995, AM J RESP CRIT CARE, V151, P1725; Scandalios JG, 2005, BRAZ J MED BIOL RES, V38, P995, DOI 10.1590/S0100-879X2005000700003; Shapiro TA, 2001, CANCER EPIDEM BIOMAR, V10, P501; Shapiro TA, 1998, CANCER EPIDEM BIOMAR, V7, P1091; Shapiro TA, 2006, NUTR CANCER, V55, P53, DOI 10.1207/s15327914nc5501_7; Talalay P, 2007, P NATL ACAD SCI USA, V104, P17500, DOI 10.1073/pnas.0708710104; Thimmulappa RK, 2002, CANCER RES, V62, P5196; Troyer JK, 2001, J CHROMATOGR A, V919, P299, DOI 10.1016/S0021-9673(01)00842-1; Wan JX, 2007, INHAL TOXICOL, V19, P177, DOI 10.1080/08958370701496145; Wan JX, 2006, J IMMUNOL, V177, P3477; Ye LX, 2002, CLIN CHIM ACTA, V316, P43, DOI 10.1016/S0009-8981(01)00727-6; Zhang YS, 1996, ANAL BIOCHEM, V239, P160, DOI 10.1006/abio.1996.0311	48	94	99	0	8	ACADEMIC PRESS INC ELSEVIER SCIENCE	SAN DIEGO	525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA	1521-6616			CLIN IMMUNOL	Clin. Immunol.	MAR	2009	130	3					244	251		10.1016/j.clim.2008.10.007		8	Immunology	Immunology	409UD	WOS:000263530400002	19028145	
J	Julvez, J; Ribas-Fito, N; Torrent, M; Forns, M; Garcia-Esteban, R; Sunyer, J				Julvez, Jordi; Ribas-Fito, Nuria; Torrent, Maties; Forns, Maria; Garcia-Esteban, Raquel; Sunyer, Jordi			Maternal smoking habits and cognitive development of children at age 4 years in a population-based birth cohort	INTERNATIONAL JOURNAL OF EPIDEMIOLOGY			English	Article						maternal smoking habits; smoking during pregnancy; paternal smoking habits; cognitive development; neurocognitive functions; pre-school children; populatin based study; birth cohort	FOLLOW-UP; PREGNANT-WOMEN; IN-UTERO; EXPOSURE; ALCOHOL; TOBACCO; CIGARETTES; MARIJUANA; RISK; NEURODEVELOPMENT	Background Active maternal smoking during pregnancy has been associated with a higher risk of behavioural disorders in children, but a few cohort studies measuring smoking data prospectively have studied its specific effects on the cognitive abilities of pre-schoolers. Method A birth cohort was set up in Menorca Island in 1997 within the Asthma Multicenter Infants Cohort Study. A total of 420 (87% of those eligible) children had complete data for final analyses at age 4 years. Interviewer-administered questionnaires were completed by mothers during the third trimester of pregnancy and then every year up to age 4 years of their child. A standardized version of the McCarthy Scales of Children's Abilities (MCSA) was used to evaluate the child's motor and cognitive capabilities. Multivariable regressions were used with MCSA`s assessed outcomes adjusting for: home location, maternal alcohol consumption, mother's social class and level of education during pregnancy, parity, marital status, father's education level, child's gender, birth weight and height, breastfeeding duration, passive smoking, school season, age during test administration and evaluator (psychologist). Results A high global consistency in maternal smoking habits was found (total agreement= 88.7%). Maternal social class and education level were inversely associated with maternal smoking behaviour. Maternal smoking during pregnancy (in cig./day) was associated with a decrease (in points) of children's global cognitive score [beta=-0.60, (95% CI: -1.10; -0.09)]; as wen as global cognitive sub-areas like verbal score [beta = -0.59, (95% CI: -1.11; -0.07)]; quantitative score [beta=-0.57, (95% CI: -1.08; -0.06)]; executive function score [beta = -0.71, (95% CI: -1.23; -0.20)]; and working memory score [beta=-0.46, (95% CI: -0.92; -0.01)]. Conclusion Our findings suggest an association with maternal smoking during pregnancy and lowered cognitive development in children at age 4 years.	Ctr Res Environm Epidemiol, Inst Municipal Invest Med, E-08003 Barcelona, Spain; Menorca Hlth Area, Menorca, Spain; Univ Barcelona, Dept Personality Evaluat & Psychol Treatment, E-08007 Barcelona, Spain; Univ Pompeu Fabra, Dept Expt Hlth Sci, Barcelona, Spain	Julvez, J (reprint author), Ctr Res Environm Epidemiol, Inst Municipal Invest Med, C Dr Aiguader,88, E-08003 Barcelona, Spain.	jjulvez@imim.es	Forns, Maria/F-9549-2010; Sunyer, J/G-6909-2014	Sunyer, J/0000-0002-2602-4110			Barkley RA, 2001, NEUROPSYCHOL REV, V11, P1, DOI 10.1023/A:1009085417776; Baron SI, 2004, NEUROPSYCHOLOGICAL E; Batstra L, 2003, EARLY HUM DEV, V75, P21, DOI 10.1016/j.earlhumdev.2003.09.001; Batty GD, 2006, PEDIATRICS, V118, P943, DOI 10.1542/peds.2006-0168; Breslau N, 2005, INT J EPIDEMIOL, V34, P1047, DOI 10.1093/ije/dyi163; Buka SL, 2003, AM J PSYCHIAT, V160, P1978, DOI 10.1176/appi.ajp.160.11.1978; Cornelius MD, 2001, J DEV BEHAV PEDIATR, V22, P217; Cornelius MD, 2000, ALCOHOL RES HEALTH, V24, P242; ESKENAZI B, 1995, AM J EPIDEMIOL, V142, pS19; Espy K A, 2001, J Pediatr Psychol, V26, P1, DOI 10.1093/jpepsy/26.1.1; Fergusson DM, 1998, ARCH GEN PSYCHIAT, V55, P721, DOI 10.1001/archpsyc.55.8.721; Fried PA, 2001, NEUROTOXICOL TERATOL, V23, P1, DOI 10.1016/S0892-0362(00)00119-7; FRIED PA, 1992, J DEV BEHAV PEDIATR, V13, P383; FRIED PA, 1988, NEUROTOXICOL TERATOL, V10, P305, DOI 10.1016/0892-0362(88)90032-3; FRIED PA, 1992, NEUROTOXICOL TERATOL, V14, P299, DOI 10.1016/0892-0362(92)90036-A; Fried PA, 1998, NEUROTOXICOL TERATOL, V20, P293, DOI 10.1016/S0892-0362(97)00091-3; Haynes G, 2003, NEUROTOXICOL TERATOL, V25, P659, DOI 10.1016/j.ntt.2003.07.003; HELLSTROMLINDAH.E, 1998, BRAIN RES DEV BRAIN, V108, P147; Huizink AC, 2006, NEUROSCI BIOBEHAV R, V30, P24, DOI 10.1016/j.neubiorev.2005.04.005; JACOBSEN SW, 1992, LONGITUDINAL STUDIE; Jacobson JL, 2005, NEUROTOXICOL TERATOL, V27, P395, DOI 10.1016/j.ntt.2005.01.009; JULVEZ J, 2007, IN PRESS ACTA PAEDIA; Kolb B, 1996, FUNDAMENTALS HUMAN N; Lawlor DA, 2007, AM J EPIDEMIOL, V165, P418, DOI 10.1093/aje/kwk030; Levin ED, 1998, HANDBOOK OF DEVELOPMENTAL NEUROTOXICOLOGY, P587; LEZAK MD, 2004, NEUROPSYCHOLOGICAL A; Li Y, 2004, PHARMACOL RES, V49, P467, DOI 10.1016/j.phrs.2003.11.002; Linnet KM, 2003, AM J PSYCHIAT, V160, P1028, DOI 10.1176/appi.ajp.160.6.1028; Lynch ME, 2003, J STUD ALCOHOL, V64, P678; McCarthy D., 1996, MANUAL MCCARTHY SCAL; Mortensen EL, 2002, JAMA-J AM MED ASSOC, V287, P2365, DOI 10.1001/jama.287.18.2365; OLDS D, 1997, MENTAL RETARDATION D, V3, P357; Paule MG, 2000, NEUROTOXICOL TERATOL, V22, P631, DOI 10.1016/S0892-0362(00)00095-7; Perera FP, 2006, ENVIRON HEALTH PERSP, V114, P1287, DOI 10.1289/ehp.9084; Ramsay MC, 2000, NEUROPSYCHOL REV, V10, P1, DOI 10.1023/A:1009065713389; Roy TS, 2002, J PHARMACOL EXP THER, V300, P124, DOI 10.1124/jpet.300.1.124; SUZUKI K, 1980, AM J OBSTET GYNECOL, V136, P1009; Trasti N, 1999, EARLY HUM DEV, V55, P137, DOI 10.1016/S0378-3782(99)00017-1; Walker A, 1999, CHILD ADOL PSYCH CL, V8, P845; Watson R, 1998, BRIT MED J, V316, P9; Weissman MM, 1999, J AM ACAD CHILD PSY, V38, P892, DOI 10.1097/00004583-199907000-00020; Weitzman M, 2002, NEUROTOXICOL TERATOL, V24, P397, DOI 10.1016/S0892-0362(02)00201-5; Wisborg K, 1999, PEDIATRICS, V104, part. no., DOI 10.1542/peds.104.4.e46; Yuan KH, 1998, BRIT J MATH STAT PSY, V51, P289	44	94	95	3	18	OXFORD UNIV PRESS	OXFORD	GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND	0300-5771			INT J EPIDEMIOL	Int. J. Epidemiol.	AUG	2007	36	4					825	832		10.1093/ije/dym107		8	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	218XW	WOS:000250050300024	17550944	
J	Blumer, N; Sel, S; Virna, S; Patrascan, CC; Zimmermann, S; Herz, U; Renz, H; Garn, H				Blumer, N.; Sel, S.; Virna, S.; Patrascan, C. C.; Zimmermann, S.; Herz, U.; Renz, H.; Garn, H.			Perinatal maternal application of Lactobacillus rhamnosus GG suppresses allergic airway inflammation in mouse offspring	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						airway inflammation; allergy; materno-fetal interaction; mice; probiotics	PLACEBO-CONTROLLED TRIAL; DENDRITIC CELL-FUNCTION; CD4(+) T-CELLS; MURINE MODEL; PROBIOTIC BACTERIA; ATOPIC DISEASE; EXPERIMENTAL ASTHMA; HYGIENE HYPOTHESIS; IMMUNE-SYSTEM; FOOD ALLERGY	Clinical studies indicate that maternal exposure to probiotic bacteria may protect from the development of allergic disease later in life. The purpose of this study was to analyse the effects of a perinatal Lactobacillus rhamnosus GG (LGG) supplementation on the development of allergic disorders in offspring. Female BALB/c mice received intragastric LGG every other day before conception, during pregnancy and lactation (perinatal supplementation group) or before conception and during pregnancy only (prenatal supplementation group). Cytokine expression of placental tissues was examined. Offspring of LGG-supplemented and sham-exposed mothers were sensitized to Ovalbumin (OVA), followed by aerosol allergen challenges. Development of experimental asthma was assessed by bronchoalveolar lavage analysis, lung histology and lung function measurement. Cytokine production of splenic mononuclear cells was analysed following in vitro stimulation. Intestinal colonization with LGG was observed in mother mice only, but not in the offspring. However, a reduced expression of TNF-alpha, IFN-gamma, IL-5 as well as IL-10 was observed in mice derived from perinatally LGG-supplemented mothers, whereas IL-13 and IL-4 expression remained unchanged. Moreover, in offspring of prenatally or perinatally LGG-supplemented mothers allergic airway and peribronchial inflammation as well as goblet cell hyperplasia were significantly reduced as compared with mice derived from non-supplemented mothers. In contrast, airway hyperresponsiveness to methacholine was not affected. Exposure to LGG during pregnancy only shifted the placental cytokine expression pattern with a markedly increased TNF-alpha level. Our data suggest that LGG may exert beneficial effects on the development of experimental allergic asthma, when applied in a very early phase of life. Immunological effects are, at least in parts, mediated via the placenta, probably by induction of pro-inflammatory cell signals.	Hosp Philipps Univ Marburg, Dept Clin Chem & Mol Diagnost, Berlin, Germany; Hosp Philipps Univ Marburg, Dept Med Microbiol, Berlin, Germany; Bristol Myers Squibb Co, Mead Johnson Nutrit, Evanston, IL USA	Blumer, N (reprint author), Hosp Philipps Univ Marburg, Dept Clin Chem & Mol Diagnost, Berlin, Germany.	bluemer@mailer.uni-marburg.de					Atasoy U, 2003, J IMMUNOL, V171, P4369; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Bjorksten B, 2001, J ALLERGY CLIN IMMUN, V108, P516; Blumer N, 2005, CLIN EXP ALLERGY, V35, P397, DOI 10.1111/j.1365-2222.2005.02184.x; Braat H, 2004, AM J CLIN NUTR, V80, P1618; Bunder R, 2004, J ALLERGY CLIN IMMUN, V114, P422, DOI 10.1016/j.jaci.2004.05.029; de Vrese M, 2002, BRIT J NUTR, V88, pS59, DOI 10.1079/BJN2002630; Erickson KL, 2000, J NUTR, V130, P403; Foster PS, 2000, LAB INVEST, V80, P655; Foster PS, 1996, J EXP MED, V183, P195, DOI 10.1084/jem.183.1.195; FULLER R, 1989, J APPL BACTERIOL, V66, P365; Geha RS, 2003, NAT REV IMMUNOL, V3, P721, DOI 10.1038/nri1181; Helin T, 2002, ALLERGY, V57, P243, DOI 10.1034/j.1398-9995.2002.1s3299.x; Hessle C, 1999, CLIN EXP IMMUNOL, V116, P276; Ishida Y, 2003, BIOSCI BIOTECH BIOCH, V67, P951, DOI 10.1271/bbb.67.951; Isolauri E, 2000, CLIN EXP ALLERGY, V30, P1604, DOI 10.1046/j.1365-2222.2000.00943.x; 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; Kalliomaki Marko, 2003, Curr Opin Allergy Clin Immunol, V3, P15, DOI 10.1097/00130832-200302000-00003; Kerzel S, 2003, AM J RESP CELL MOL, V28, P170, DOI 10.1165/rcmb.4811; Kirjavainen PV, 2003, J PEDIATR GASTR NUTR, V36, P223, DOI 10.1097/00005176-200302000-00012; Kirjavainen PV, 1999, ALLERGY, V54, P909, DOI 10.1034/j.1398-9995.1999.00103.x; Macpherson AJ, 2004, NAT REV IMMUNOL, V4, P478, DOI 10.1038/nri1373; Majamaa H, 1997, J ALLERGY CLIN IMMUN, V99, P179, DOI 10.1016/S0091-6749(97)70093-9; Matricardi PM, 2002, ALLERGY, V57, P185, DOI 10.1034/j.1398-9995.2002.1a3299.x; Matricardi PM, 2000, CLIN EXP ALLERGY, V30, P1506, DOI 10.1046/j.1365-2222.2000.00994.x; Mohamadzadeh M, 2005, P NATL ACAD SCI USA, V102, P2880, DOI 10.1073/pnas.0500098102; Noverr MC, 2004, TRENDS MICROBIOL, V12, P562, DOI 10.1016/j.tim.2004.10.008; Ohno H, 2005, BIOL PHARM BULL, V28, P1462, DOI 10.1248/bpb.28.1462; PERDIGON G, 1995, J DAIRY SCI, V78, P1597; RENZ H, 1992, J ALLERGY CLIN IMMUN, V89, P1127, DOI 10.1016/0091-6749(92)90296-E; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Rosenfeldt V, 2003, J ALLERGY CLIN IMMUN, V111, P389, DOI 10.1067/mai.2003.389; Schrezenmeir J., 2001, AM J CLIN NUTR, V73, P361; Smits HH, 2005, J ALLERGY CLIN IMMUN, V115, P1260, DOI 10.1016/j.jaci.2005.03.036; Solomon A, 2005, CLIN EXP ALLERGY, V35, P941, DOI 10.1111/j.1365-2222.2005.02285.x; Strachan David P., 2000, Thorax, V55, pS2, DOI 10.1136/thorax.55.suppl_1.S2; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Vaarala O, 2003, CLIN EXP ALLERGY, V33, P1634, DOI 10.1111/j.1365-2222.2003.01835.x; Viljanen M, 2005, J ALLERGY CLIN IMMUN, V115, P1254, DOI 10.1016/j.jaci.2005.03.047; Viljanen M, 2005, ALLERGY, V60, P494, DOI 10.1111/j.1398-9995.2004.00514.x; von der Weid T, 2001, CLIN DIAGN LAB IMMUN, V8, P695, DOI 10.1128/CDLI.8.4.695-701.2001; Wills-Karp M, 2001, NAT REV IMMUNOL, V1, P69, DOI 10.1038/35095579	43	94	100	0	9	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	MAR	2007	37	3					348	357		10.1111/j.1365-2222.2007.02671.x		10	Allergy; Immunology	Allergy; Immunology	144DO	WOS:000244776000007	17359385	
J	Bernard, A; Carbonnelle, S; de Burbure, C; Michel, O; Nickmilder, M				Bernard, Alfred; Carbonnelle, Sylviane; de Burbure, Claire; Michel, Olivier; Nickmilder, Marc			Chlorinated pool attendance, atopy, and the risk of asthma during childhood	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						aeroallergens; atopy; childhood asthma; chlorine; exercise-induced asthma; exhaled nitric oxide; nitrogen trichloride; swimming pool; total IgE; trichloramine	SERUM IMMUNOGLOBULIN-E; NITROGEN TRICHLORIDE; HYGIENE HYPOTHESIS; SWIMMING POOLS; SODIUM-HYPOCHLORITE; TIGHT JUNCTIONS; NITRIC-OXIDE; LUNG; SCHOOLCHILDREN; CHLORAMINES	The pool chlorine hypothesis postulates that the rise in childhood asthma in the developed world could result at least partly from the increasing exposure of children to toxic gases and aerosols contaminating the air of indoor chlorinated pools. To further assess this hypothesis, we explored the relationships between childhood asthma, atopy, and cumulated pool attendance (CPA). We studied 341 schoolchildren 10-13 years of age who attended at a variable rate the same public pool in Brussels (trichloramine in air, 0.3-0.5 mg/m(3)). Examination of the children included a questionnaire, an exercise-induced bronchoconstriction (EIB) test, and the measurement of exhaled nitric oxide (eNO) and total and aeroallergen-specific serum IgE. CPA by children (range, 0-1,818 hr) emerged among the most consistent predictors of asthma (doctor diagnosed or screened with the EIB test) and of elevated eNO, ranking immediately after atopy and family history of asthma or hay fever. Although the risk of elevated eNO increased with CPA [odds ratio (OR) = 1.30; 95% confidence interval (CI), 1.10-1.43] independently of total or specific serum IgE, the probability of developing asthma increased with CPA only in children with serum IgE > 100 kIU/L (OR for each 100-hr increase in CPA = 1.79; 95% CI, 1.07-2.72). All these effects were dose related and most strongly linked to pool attendance before 6-7 years of age. Use of indoor chlorinated pools especially by young children interacts with atopic status to promote the development of childhood asthma. These findings further support the hypothesis implicating pool chlorine in the rise of childhood asthma in industrialized countries. Key words: aeroallergens, atopy, childhood asthma, chlorine, exercise-induced asthma, exhaled nitric oxide, nitrogen trichloride, swimming pool, total IgE, trichloramine.	Univ Catholique Louvain, Toxicol Unit, Dept Publ Hlth, B-1200 Brussels, Belgium; Free Univ Brussels, Clin Allergol, Brussels, Belgium; Free Univ Brussels, Clin Resp Dis, Brussels, Belgium	Bernard, A (reprint author), Univ Catholique Louvain, Toxicol Unit, Dept Publ Hlth, 30-54 Clos Chapelle aux Champs, B-1200 Brussels, Belgium.	bernard@toxi.ucl.ac.be	Nickmilder, Marc/A-9060-2010; BERNARD, Alfred/A-6511-2010	BERNARD, Alfred/0000-0003-3171-3743; michel, olivier/0000-0002-1528-1277			Allison PD, 1999, LOGISTIC REGRESSION; *AM LUNG ASS, 2004, TRENDS ASTHM MORB MO; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Beeh KM, 2000, EUR RESPIR J, V16, P609, DOI 10.1034/j.1399-3003.2000.16d07.x; Bernard A, 2003, OCCUP ENVIRON MED, V60, P385, DOI 10.1136/oem.60.6.385; Carbonnelle S, 2002, BIOMARKERS, V7, P464, DOI 10.1080/13547500210166612; Chen P, 2001, CLIN EXP ALLERGY, V31, P1086, DOI 10.1046/j.1365-2222.2001.01127.x; EXON JH, 1987, TOXICOLOGY, V44, P257, DOI 10.1016/0300-483X(87)90028-X; Finkelstein JN, 2004, PEDIATRICS, V113, P1092; GAGNAIRE F, 1994, J APPL TOXICOL, V14, P405, DOI 10.1002/jat.2550140604; Gilmour I. 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D., 2001, PEDIATRICS, V108, P69; Kramer MS, 2004, CLIN EXP ALLERGY, V34, P753, DOI 10.1111/j.1365-2222.2004.01940.x; Lagerkvist BJ, 2004, ENVIRON HEALTH PERSP, V112, P1768, DOI 10.1289/ehp.7027; Liu AH, 2003, J ALLERGY CLIN IMMUN, V111, P471, DOI 10.1067/mai.2003.172; Massin N, 1998, OCCUP ENVIRON MED, V55, P258; MCFADDEN ER, 1994, NEW ENGL J MED, V330, P1362, DOI 10.1056/NEJM199405123301907; MCGEADY SJ, 2004, PEDIATRICS, V112, P1107; Michel O, 1999, AM J RESP CRIT CARE, V159, pA145; Schuetze G, 1999, PEDIATR ALLERGY IMMU, V10, P138, DOI 10.1034/j.1399-3038.1999.00025.x; Sheikh A, 2003, J ALLERGY CLIN IMMUN, V111, P131, DOI 10.1067/mai.2003.8; Silkoff PE, 2004, J ALLERGY CLIN IMMUN, V114, P1241, DOI 10.1016/j.jaci.2004.08.042; Skoner DP, 2002, PEDIATRICS, V109, P393; Slutsky AS, 1999, AM J RESP CRIT CARE, V160, P2104; Strachan David P., 2000, Thorax, V55, pS2, DOI 10.1136/thorax.55.suppl_1.S2; STRACHAN DP, 1989, BRIT MED J, V299, P1259; TATSUMI T, 1994, AM J PHYSIOL-HEART C, V267, pH1597; Thickett KM, 2002, EUR RESPIR J, V19, P827, DOI 10.1183/09031936.02.00232802; Tulic MK, 2003, CHEST, V123, p348S, DOI 10.1378/chest.123.3_suppl.348S; Umetsu DT, 2004, NAT MED, V10, P232, DOI 10.1038/nm0304-232; von Mutius E, 2001, CLIN EXP ALLERGY, V31, P1651, DOI 10.1046/j.1365-2222.2001.01272.x; Wan H, 1999, J CLIN INVEST, V104, P123, DOI 10.1172/JCI5844; Wan H, 2001, CLIN EXP ALLERGY, V31, P279, DOI 10.1046/j.1365-2222.2001.00970.x; WHO, 2000, EUR SER WHO, V91	35	94	95	0	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.	OCT	2006	114	10					1567	1573		10.1289/ehp.8461		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	090RW	WOS:000240969700035	17035144	
J	Cruse, G; Duffy, SM; Brightling, CE; Bradding, P				Cruse, G.; Duffy, S. M.; Brightling, C. E.; Bradding, P.			Functional K(Ca)3.1 K+ channels are required for human lung mast cell migration	THORAX			English	Article							ACTIVATED POTASSIUM CHANNEL; AIRWAY SMOOTH-MUSCLE; SELECTIVE INHIBITOR; EPITHELIAL-CELLS; ION CHANNELS; BONE-MARROW; EXPRESSION; PROLIFERATION; IMMUNOMODULATION; INFILTRATION	Background: Mast cell recruitment and activation are critical for the initiation and progression of inflammation and fibrosis. Mast cells infiltrate specific structures in many diseased tissues such as the airway smooth muscle (ASM) in asthma. This microlocalisation of mast cells is likely to be key to disease pathogenesis. Human lung mast cells (HLMC) express the Ca2+ activated K+ channel K(Ca)3.1 which modulates mediator release, and is proposed to facilitate the retraction of the cell body during migration of several cell types. A study was undertaken to test the hypothesis that blockade of K(Ca)3.1 would attenuate HLMC proliferation and migration. Methods: HLMC were isolated and purified from lung material resected for bronchial carcinoma. HLMC proliferation was assessed by cell counts at various time points following drug exposure. HLMC chemotaxis was assayed using standard Transwell chambers (8 mm pore size). Ion currents were measured using the single cell patch clamp technique. Results: K(Ca)3.1 blockade with triarylmethane-34 (TRAM-34) did not inhibit HLMC proliferation and clotrimazole had cytotoxic effects. In contrast, HLMC migration towards the chemokine CXCL10, the chemoattractant stem cell factor, and the supernatants from tumour necrosis factor a stimulated asthmatic ASM was markedly inhibited with both the non-selective K(Ca)3.1 blocker charybdotoxin and the highly specific K(Ca)3.1 blocker TRAM-34 in a dose dependent manner. Although K(Ca)3.1 blockade inhibits HLMC migration, K(Ca)3.1 is not opened by the chemotactic stimulus, suggesting that it must be involved downstream of the initial receptor-ligand interactions. Conclusions: Since modulation of K(Ca)3.1 can inhibit HLMC chemotaxis to diverse chemoattractants, the use of K(Ca)3.1 blockers such as TRAM-34 could provide new therapeutic strategies for mast cell mediated diseases such as asthma.	Univ Leicester, Dept Resp Med, Glenfield Gen Hosp, Inst Lung Hlth,Dept Infect Immun & Inflammat,Sch, Leicester LE3 9QP, Leics, England	Cruse, G (reprint author), Univ Leicester, Dept Resp Med, Glenfield Gen Hosp, Inst Lung Hlth,Dept Infect Immun & Inflammat,Sch, Groby Rd, Leicester LE3 9QP, Leics, England.	glenncruse@hotmail.com	Cruse, Glenn/B-4597-2012	Bradding, Peter/0000-0001-8403-0319	Wellcome Trust [, 076264]		Aktas H, 1998, P NATL ACAD SCI USA, V95, P8280, DOI 10.1073/pnas.95.14.8280; Berger P, 2003, FASEB J, V17, P2139, DOI 10.1096/fj.03-0041fje; Bradding P, 2005, CHEM IMMUNOL ALLERGY, V87, P163; Bradding P, 1999, CRIT REV ONCOL HEMAT, V31, P119, DOI 10.1016/S1040-8428(99)00010-4; Bradding P, 2003, J LEUKOCYTE BIOL, V73, P614, DOI 10.1189/jlb.1202602; Brightling CE, 2005, AM J RESP CRIT CARE, V171, P1103, DOI 10.1164/rccm.200409-1220OC; Brightling CE, 2005, J LEUKOCYTE BIOL, V77, P759, DOI 10.1189/jlb.0904511; Brightling CE, 2002, NEW ENGL J MED, V346, P1699, DOI 10.1056/NEJMoa012705; Chandy KG, 2004, TRENDS PHARMACOL SCI, V25, P280, DOI 10.1016/j.tips.2004.03.010; Duffy SM, 2005, FASEB J, V19, P1006, DOI 10.1096/fj.04-3439fie; Duffy SM, 2004, J ALLERGY CLIN IMMUN, V114, P66, DOI 10.1016/j.jaci.2004.04.005; Duffy SM, 2003, J ALLERGY CLIN IMMUN, V112, P965, DOI 10.1067/mai.2003.1779; Duffy SM, 2001, J IMMUNOL, V167, P4261; Ghanshani S, 2000, J BIOL CHEM, V275, P37137, DOI 10.1074/jbc.M003941200; GIMENEZGALLEGO G, 1988, P NATL ACAD SCI USA, V85, P3329, DOI 10.1073/pnas.85.10.3329; Grgic I, 2005, ARTERIOSCL THROM VAS, V25, P704, DOI 10.1161/01.ATV.0000156399.12787.5c; HOTH M, 1992, NATURE, V355, P353, DOI 10.1038/355353a0; Jensen BS, 1999, P NATL ACAD SCI USA, V96, P10917, DOI 10.1073/pnas.96.19.10917; Jones SE, 2003, KIDNEY INT, V64, P906, DOI 10.1046/j.1523-1755.2003.00183.x; Kassel O, 1999, EUR RESPIR J, V13, P951, DOI 10.1034/j.1399-3003.1999.13e04.x; Kaur D, 2005, CLIN EXP ALLERGY, V35, P226, DOI 10.1111/j.1365-2222.2005.02161.x; Kohler R, 2003, CIRCULATION, V108, P1119, DOI 10.1161/01.CIR.0000086464.04719.DD; Logsdon NJ, 1997, J BIOL CHEM, V272, P32723, DOI 10.1074/jbc.272.52.32723; PENSO J, 2002, EUR J PHARMACOL, V45, P227; Schilling T, 2004, EUR J NEUROSCI, V19, P1469, DOI 10.1111/j.1460-9568.2004.03265.x; Schneider SW, 2000, PFLUG ARCH EUR J PHY, V439, P297, DOI 10.1007/s004240050943; Schwab A, 2006, J CELL PHYSIOL, V206, P86, DOI 10.1002/jcp.20434; Schwab A, 1999, PFLUG ARCH EUR J PHY, V438, P330, DOI 10.1007/s004240050917; TETLOW LC, 1995, ANN RHEUM DIS, V54, P549, DOI 10.1136/ard.54.7.549; URBAHNS K, 2005, BIOORG MED CHEM LETT, V13, P2637; WOJTULEWSKI JA, 1980, ANN RHEUM DIS, V39, P469, DOI 10.1136/ard.39.5.469; Wulff H, 2000, P NATL ACAD SCI USA, V97, P8151, DOI 10.1073/pnas.97.14.8151; Wulff H, 2001, J BIOL CHEM, V276, P32040, DOI 10.1074/jbc.M105231200; Wulff H, 2004, J IMMUNOL, V173, P776; Zhang WJ, 2002, DRUG METAB DISPOS, V30, P314, DOI 10.1124/dmd.30.3.314	35	94	96	0	7	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	OCT	2006	61	10					880	885		10.1136/thx.2006.060319		6	Respiratory System	Respiratory System	088YO	WOS:000240847200012	16809411	
J	Johnston, NW; Sears, MR				Johnston, N. W.; Sears, M. R.			Asthma exacerbations center dot 1: Epidemiology	THORAX			English	Review							INHALED CORTICOSTEROIDS; RESPIRATORY-INFECTIONS; INDUSTRIAL POPULATION; RHINOVIRUS INFECTIONS; HOSPITAL ADMISSIONS; AIR-POLLUTION; UNITED-STATES; CHILDREN; SYMPTOMS; ILLNESS	Asthma exacerbations may be triggered by a number of atmospheric and domiciliary environmental factors as well as by those encountered in schools and workplaces. The majority of exacerbations, particularly in children, coincide with respiratory viral infections, most commonly rhinovirus. As most respiratory viruses and many aeroallergens appear in seasonal patterns, asthma exacerbations, particularly those requiring emergency treatment, show analogous seasonal cycles which differ in form in children and adults. While similar in form between the sexes, they differ in amplitude, with boys having higher risks of exacerbation in childhood and women in adult life. Simultaneous exposure of asthmatics with respiratory viral infections to allergens or air pollutants may significantly increase the risks of exacerbation. Access to and compliance with inhaled corticosteroid treatment is an important predictor of the likelihood of asthma exacerbations occurring, including those that occur during respiratory viral infections. Epidemiologically, the degree of asthma control achieved by asthmatics is an important predictor of the likelihood of disease exacerbation including respiratory failure, death, and health service consumption.	St Josephs Healthcare, Firestone Inst Resp Hlth, Hamilton, ON L8N 4A6, Canada	Johnston, NW (reprint author), St Josephs Healthcare, Firestone Inst Resp Hlth, 50 Charlton Ave E, Hamilton, ON L8N 4A6, Canada.	njohnsto@sympatico.ca					ANDERSSON F, 2003, J ASTHMA, V5, P615; ANTO JM, 1989, NEW ENGL J MED, V320, P1097, DOI 10.1056/NEJM198904273201701; ATKINSON RW, 2004, THORAX, V569, P277; Brenner BE, 2005, THORAX, V60, P806, DOI 10.1136/thx.2004.033928; Campbell MJ, 1997, BRIT MED J, V315, P1012; Cerveri I, 1999, EUR RESPIR J, V14, P288, DOI 10.1034/j.1399-3003.1999.14b09.x; Chauhan AJ, 2003, BRIT MED BULL, V68, P95, DOI 10.1093/bmb/ldg022; Dales RE, 2004, J ALLERGY CLIN IMMUN, V113, P303, DOI 10.1016/j.jaci.2003.11.016; Dales RE, 1996, EUR RESPIR J, V9, P72, DOI 10.1183/09031936.96.09010072; Dales RE, 2003, CHEST, V123, P745, DOI 10.1378/chest.123.3.745; Doull IJM, 1997, BRIT MED J, V315, P858; FLOYER JA, TREATISE ASTHMA, P1717; Friedlander SL, 2005, J ALLERGY CLIN IMMUN, V116, P267, DOI 10.1016/j.jaci.2005.06.003; Gern JE, 2002, AM J MED, V112, p19S; Getahun D, 2005, J ASTHMA, V42, P373, DOI 10.1081/JAS-200062995; Grunberg K, 2001, AM J RESP CRIT CARE, V164, P1816; GWALTNEY JM, 1966, NEW ENGL J MED, V275, P1261, DOI 10.1056/NEJM196612082752301; Hales S, 1998, ENVIRON HEALTH PERSP, V106, P607, DOI 10.1289/ehp.98106607; HENDLEY JO, 1969, AM J EPIDEMIOL, V89, P184; Hersoug LG, 2005, INDOOR AIR, V15, P363, DOI 10.1111/j.1600-0668.2005.00382.x; Higham J, 1997, J EPIDEMIOL COMMUN H, V51, P233, DOI 10.1136/jech.51.3.233; HYNDMAN SJ, 1994, BRIT MED J, V308, P1596; Ivey Marsha A., 2001, Allergology International, V50, P29, DOI 10.1046/j.1440-1592.2001.00198.x; Jamason PF, 1997, AM J RESP CRIT CARE, V156, P1781; Johnston NW, 2006, J ALLERGY CLIN IMMUN, V117, P557, DOI 10.1016/j.jaci.2005.11.034; JOHNSTON NW, 2006, IN PRESS EXACERBATIO; JOHNSTON NW, 2005, J ALLERGY CLIN IMMUN, V112, P132; Johnston Sebastian L, 2005, Proc Am Thorac Soc, V2, P150, DOI 10.1513/pats.200502-018AW; Johnston SL, 1996, AM J RESP CRIT CARE, V154, P654; Jones C, 2003, J ASTHMA, V40, P93, DOI 10.1081/JAS-120017212; Kimbell-Dunn M, 2000, Respirology, V5, P241, DOI 10.1046/j.1440-1843.2000.00255.x; Lane S, 2006, RESP MED, V100, P434, DOI 10.1016/j.rmed.2005.06.012; LISTER S, 2001, AUST NZ J PUBL HEAL, V255, P14; Maimonides Moses, 1963, TREATISE ASTHMA, P1; Manfreda J, 2001, CAN MED ASSOC J, V164, P995; Marks GB, 2001, THORAX, V56, P468, DOI 10.1136/thorax.56.6.468; McKean M, 2000, COCHRANE DB SYST REV, V1; Murray Clare S, 2004, Proc Am Thorac Soc, V1, P99, DOI 10.1513/pats.2306027; MURRAY CS, 2005, THORAX, V61, P376; OHOLLAREN MT, 1991, NEW ENGL J MED, V324, P359, DOI 10.1056/NEJM199102073240602; Panickar JR, 2005, THORAX, V60, P1035, DOI 10.1136/thx.2005.044750; Parameswaran K, 2003, J ASTHMA, V40, P107, DOI 10.1081/JAS-120017980; Pauwels RA, 1997, NEW ENGL J MED, V337, P1405, DOI 10.1056/NEJM199711133372001; Peden DB, 2005, J ALLERGY CLIN IMMUN, V115, P213, DOI 10.1016/j.jaci.2004.12.003; 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; Rennard Stephen I, 2004, Proc Am Thorac Soc, V1, P88, DOI 10.1513/pats.2306026; Riedl M, 2005, J ALLERGY CLIN IMMUN, V115, P221, DOI 10.1016/j.jaci.2004.11.047; Salter HH, 1860, ASTHMA ITS PATHOLOGY; SKOBELOFF EM, 1992, JAMA-J AM MED ASSOC, V268, P3437, DOI 10.1001/jama.268.24.3437; Skrepnek GH, 2004, AM J MANAG CARE, V10, pS129; Suissa S, 2001, J ALLERGY CLIN IMMUN, V107, P937, DOI 10.1067/mai.2001.115653; TAN WC, 2004, CURR OPIN PULM MED, V11, P21; TARGONSKI PV, 1995, J ALLERGY CLIN IMMUN, V95, P955, DOI 10.1016/S0091-6749(95)70095-1; Tattersfield AE, 1999, AM J RESP CRIT CARE, V160, P594; THOMAS KE, 1991, BRIT J IND MED, V48, P314; UNGER L, 1974, ANN ALLERGY, V32, P214; Vermeire PA, 2002, RESP MED, V96, P142, DOI 10.1053/rmed.2001.1241; Weiland SK, 2004, OCCUP ENVIRON MED, V61, P609, DOI 10.1136/oem.2002.006809; Weinberger M, 2003, J PEDIATR-US, V142, pS34, DOI 10.1067/mpd.2003.24; WEISS KB, 1990, JAMA-J AM MED ASSOC, V263, P2323	61	94	97	1	5	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	AUG	2006	61	8					722	728		10.1136/thx.2005.045161		7	Respiratory System	Respiratory System	068JL	WOS:000239369700017	16877691	
J	Purvis, DJ; Thompson, JMD; Clark, PM; Robinson, E; Black, PN; Wild, CJ; Mitchell, EA				Purvis, DJ; Thompson, JMD; Clark, PM; Robinson, E; Black, PN; Wild, CJ; Mitchell, EA			Risk factors for atopic dermatitis in New Zealand children at 3.5 years of age	BRITISH JOURNAL OF DERMATOLOGY			English	Article						allergic diseases; atopic dermatitis; atopy; breastfeeding; eczema; hygiene hypothesis	ALLERGIC DISEASE; HAY-FEVER; CHILDHOOD ECZEMA; BIRTH COHORT; EARLY-LIFE; ASTHMA; EXPOSURE; SYMPTOMS; INFANTS; HYGIENE	Background The prevalence of atopic dermatitis (AD) is increasing in Western societies. The hygiene hypothesis proposes that this is due to reduced exposure to environmental allergens and infections during early life. Objectives To examine factors associated with a diagnosis of AD at 3.5 years of age, especially those factors implicated by the hygiene hypothesis. Methods The Auckland Birthweight Collaborative study is a case-control study of risk factors for small for gestational age babies. Cases were born at term with birthweight <= 10th centile; controls were appropriate for gestational age, with birthweight > 10th centile. The infants were assessed at birth, 1 year and 3.5 years of age. Data were collected by parental interview and examination of the child. AD was defined as the presence of an itchy rash in the past 12 months with three or more of the following: history of flexural involvement; history of generally dry skin; history of atopic disease in parents or siblings; and visible flexural dermatitis as per photographic protocol. Statistical analyses took into account the disproportionate sampling of the study population. Results Analysis was restricted to European subjects. Eight hundred and seventy-one children were enrolled at birth, 744 (85.4%) participated at 1 year, and 550 (63.2%) at 3.5 years. AD was diagnosed in 87 (15.8%) children seen at 3.5 years. The prevalence of AD did not differ by birthweight. AD at 3.5 years was associated with raised serum IgE > 200 kU L-1, and wheezing, asthma, rash or eczema at 1 year. In multivariate analysis, adjusted for parental atopy and breastfeeding, AD at 3.5 years was associated with atopic disease in the parents: maternal atopy only, adjusted odds ratio (OR) 3.83, 95% confidence interval (CI) 1.20-12.23; paternal atopy only, adjusted OR 3.59, 95% CI 1.09-11.75; both parents atopic, adjusted OR 6.12, 95% CI 2.02-18.50. There was a higher risk of AD with longer duration of breastfeeding: < 6 months, adjusted OR 6.13, 95% CI 1.45-25.86; >= 6 months, adjusted OR 9.70, 95% CI 2.47-38.15 compared with never breastfed. These findings remained significant after adjusting for environmental factors and a personal history of atopy. AD at 3.5 years was associated with owning a cat at 3.5 years (adjusted OR 0.45, 95% CI 0.21-0.97) but not with owning a dog at 3.5 years, pets at 1 year, nor with older siblings. Furthermore, AD at 3.5 years was not associated with gender, socioeconomic status, maternal smoking, parity, damp, mould, immunizations, body mass index or antibiotic use in first year of life. Conclusions A personal and a parental history of atopic disease are risk factors for AD at 3.5 years. Duration of breastfeeding was associated with an increased risk of AD. No association was found with those factors implicated by the hygiene hypothesis. This study suggests that breastfeeding should not be recommended for the prevention of AD.	Univ Auckland, Dept Paediat, Auckland, New Zealand; Univ Auckland, Sch Populat Hlth, Auckland 1, New Zealand; Univ Auckland, Dept Med, Auckland, New Zealand; Univ Auckland, Dept Stat, Auckland 1, New Zealand	Mitchell, EA (reprint author), Univ Auckland, Dept Paediat, Private Bag 92019, Auckland, New Zealand.	e.mitchell@auckland.ac.nz	Wild, Christopher/A-1449-2012	Wild, Christopher/0000-0003-0115-6448			Asher MI, 2001, NEW ZEAL MED J, V114, P114; Bergmann RL, 2002, CLIN EXP ALLERGY, V32, P205, DOI 10.1046/j.1365-2222.2002.01274.x; Bottcher MF, 2002, CLIN EXP ALLERGY, V32, P159, DOI 10.1046/j.1365-2222.2002.01343.x; Braback L, 2001, PEDIATR ALLERGY IMMU, V12, P4, DOI 10.1034/j.1399-3038.2001.012001004.x; BRAUNFAHRLANDER C, 2002, CURR OPIN ALLERGY CL, V3, P325; Butland BK, 1997, BRIT MED J, V315, P717; Farooqi IS, 1998, THORAX, V53, P927; FERGUSSON DM, 1990, PEDIATRICS, V86, P541; FERGUSSON DM, 1981, CLIN ALLERGY, V11, P325; FERGUSSON DM, 1982, J EPIDEMIOL COMMUN H, V36, P118, DOI 10.1136/jech.36.2.118; Gdalevich M, 2001, J AM ACAD DERMATOL, V45, P520, DOI 10.1067/mjd.2001.114741; HARPER J, 2000, TXB PEDIAT DERMATOLO, V1, P161; Harris JM, 2001, BRIT J DERMATOL, V144, P795, DOI 10.1046/j.1365-2133.2001.04135.x; Holscher B, 2002, PEDIATR ALLERGY IMMU, V13, P334, DOI 10.1034/j.1399-3038.2002.02063.x; Isolauri E, 1999, J PEDIATR-US, V134, P27, DOI 10.1016/S0022-3476(99)70368-9; Kramer MS, 2001, JAMA-J AM MED ASSOC, V285, P413, DOI 10.1001/jama.285.4.413; Kull I, 2002, ARCH DIS CHILD, V87, P478, DOI 10.1136/adc.87.6.478; Leadbitter P, 1999, THORAX, V54, P905; Lewis SA, 1998, RESP MED, V92, P1237, DOI 10.1016/S0954-6111(98)90427-9; McKeever TM, 2002, J ALLERGY CLIN IMMUN, V109, P43, DOI 10.1067/mai.2002.121016; McKeever TM, 2001, THORAX, V56, P758, DOI 10.1136/thorax.56.10.758; Nafstad P, 2001, ALLERGY, V56, P307, DOI 10.1034/j.1398-9995.2001.00881.x; Olesen AB, 1997, BRIT MED J, V314, P1003; Oranje AP, 2002, CURR OPIN PEDIATR, V14, P410, DOI 10.1097/01.MOP.0000021894.75794.BE; OWNBY DR, 2004, CURR OPIN ALLERGY CL, V3, P517; Ponsonby AL, 1998, ARCH DIS CHILD, V79, P328; Sears MR, 2002, LANCET, V360, P901, DOI 10.1016/S0140-6736(02)11025-7; Sherriff A, 2002, ARCH DIS CHILD, V87, P26, DOI 10.1136/adc.87.1.26; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Thompson JMD, 2001, J PAEDIATR CHILD H, V37, P369, DOI 10.1046/j.1440-1754.2001.00684.x; Williams H, 1999, J ALLERGY CLIN IMMUN, V103, P125, DOI 10.1016/S0091-6749(99)70536-1; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P406, DOI 10.1111/j.1365-2133.1994.tb08532.x; Williams HC, 2000, CLIN EXP DERMATOL, V25, P522, DOI 10.1046/j.1365-2230.2000.00698.x; WILLIAMS HC, DO I MAKE DIAGNOSIS	34	94	96	1	7	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0007-0963			BRIT J DERMATOL	Br. J. Dermatol.	APR	2005	152	4					742	749		10.1111/j.1365-2133.2005.06540.x		8	Dermatology	Dermatology	915NC	WOS:000228309900020	15840107	
J	Lehrer, PM; Vaschillo, E; Vaschillo, B; Lu, SE; Scardella, A; Siddique, M; Habib, RH				Lehrer, PM; Vaschillo, E; Vaschillo, B; Lu, SE; Scardella, A; Siddique, M; Habib, RH			Biofeedback treatment for asthma	CHEST			English	Article						airway resistance; alternative and complementary medicine; disease severity; heart rate variability; oscillation mechanics; psychology; self-regulation	HEART-RATE-VARIABILITY; RESPIRATORY SINUS ARRHYTHMIA; BONE-MINERAL DENSITY; INHALED CORTICOSTEROIDS; CONTROLLED TRIAL; IMPEDANCE; THERAPY; COMPLEMENTARY; RELAXATION; AGONISTS	Study objectives: We evaluated the effectiveness of heart rate variability (HRV) biofeedback as a complementary treatment for asthma. Patients: Ninety-four adult outpatient paid volunteers with asthma. Setting: The psychophysiology laboratory at The University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, and the private outpatient offices of participating asthma physicians. Interventions: The interventions were as follows: (1) a full protocol (ie, HRV biofeedback and abdominal breathing through pursed lips and prolonged exhalation); (2) HRV biofeedback alone; (3) placebo EEG biofeedback; and (4) a waiting list control. Design: Subjects were first prestabilized using controller medication and then were randomly assigned to experimental groups. Medication was titrated biweekly by blinded asthma specialists according to a protocol based on National Heart, Lung, and Blood Institute guidelines, according to symptoms, spirometry, and home peak flows. Measurements: Subjects recorded daily asthma symptoms and twice-daily peak expiratory flows. Spirometry was performed before and after each weekly treatment session under the HRV and placebo biofeedback conditions, and at triweekly assessment sessions under the waiting list condition. Oscillation resistance was measured approximately triweekly. Results: Compared with the two control groups, subjects in both of the two HRV biofeedback groups were prescribed less medication, with minimal differences between the two active treatments. Improvements averaged one full level of asthma severity. Measures from forced oscillation pneumography similarly showed improvement in pulmonary function. A placebo effect influenced an improvement in asthma symptoms, but not in pulmonary function. Groups did not differ in the occurrence of severe asthma flares. Conclusions: The results suggest that HRV biofeedback may prove to be a useful adjunct to asthma treatment and may help to reduce dependence on steroid medications. Further evaluation of this method is warranted.	Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Psychiat, Piscataway, NJ 08854 USA; Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Neurosci, Piscataway, NJ 08854 USA; Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Div Biometr, Piscataway, NJ 08854 USA; Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Div Biometr, Piscataway, NJ 08854 USA; Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Sch Publ Hlth, Piscataway, NJ 08854 USA; Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Med, Piscataway, NJ 08854 USA; Childrens Mercy Hosp, Toledo, OH USA	Lehrer, PM (reprint author), Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Psychiat, 671 Hoes Ln, Piscataway, NJ 08854 USA.	lehrer@umdnj.edu			NHLBI NIH HHS [R01 HL058805-03, R01 HL58805]		AKAIKE H, 1974, IEEE T AUTOMAT CONTR, VAC19, P716, DOI 10.1109/TAC.1974.1100705; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Baldwin CM, 2002, ARCH INTERN MED, V162, P1697, DOI 10.1001/archinte.162.15.1697; Barnes PJ, 2001, RESP PHYSIOL, V125, P145, DOI 10.1016/S0034-5687(00)00210-3; Birrell MA, 2002, BRIT J PHARMACOL, V136, P620, DOI 10.1038/sj.bjp.0704758; BORKOVEC TD, 1972, J BEHAV THER EXP PSY, V3, P257, DOI 10.1016/0005-7916(72)90045-6; Camm AJ, 1996, CIRCULATION, V93, P1043; Chan PWK, 2000, PEDIATR INT, V42, P547, DOI 10.1046/j.1442-200x.2000.01278.x; CRAPO RO, 1981, AM REV RESPIR DIS, V123, P659; HABIB RH, 1993, J APPL PHYSIOL, V74, P1045; Hand CH, 1996, J ASTHMA, V33, P331, DOI 10.3109/02770909609055374; Kazuma N, 1997, CHRONOBIOL INT, V14, P597, DOI 10.3109/07420529709001450; KELLOWAY JS, 1994, ARCH INTERN MED, V154, P1349; Lee E. T., 1992, STAT METHODS SURVIVA; Lehrer P, 1997, APPL PSYCHOPHYS BIOF, V22, P95, DOI 10.1023/A:1026224211993; Lehrer P, 2000, APPL PSYCHOPHYS BIOF, V25, P193, DOI 10.1023/A:1009506909815; LEHRER PM, 1994, J BEHAV MED, V17, P1, DOI 10.1007/BF01856879; Lehrer PM, 2003, PSYCHOSOM MED, V65, P796, DOI 10.1097/01.PSY.0000089200.81962.19; LEHRER PM, 1986, J PSYCHOSOM RES, V30, P13, DOI 10.1016/0022-3999(86)90061-9; Lehrer PM, 2000, APPL PSYCHOPHYS BIOF, V25, P177, DOI 10.1023/A:1009554825745; Lemanske RF, 2001, JAMA-J AM MED ASSOC, V285, P2594, DOI 10.1001/jama.285.20.2594; Lofdahl CG, 1999, BRIT MED J, V319, P87; LUTCHEN KR, 1990, J APPL PHYSIOL, V68, P2139; LUTCHEN KR, 1987, J APPL PHYSIOL, V62, P403; Martin RM, 1998, THORAX, V53, P558; Matsumoto H, 2001, CHEST, V120, P1468, DOI 10.1378/chest.120.5.1468; NAGELS J, 1980, J APPL PHYSIOL, V49, P408; National Asthma Education and Prevention Program, 2002, EXP PAN REP GUID DIA; RUBIN DB, 1976, BIOMETRIKA, V63, P581, DOI 10.1093/biomet/63.3.581; Simon RA, 1999, ALLERGY ASTHMA PROC, V20, P161, DOI 10.2500/108854199778552993; Singh V, 2002, RESP MED, V96, P835, DOI 10.1053/rmed.2002.1368; Sivri A, 2001, Respirology, V6, P131, DOI 10.1046/j.1440-1843.2001.00323.x; Tsugeno H, 2002, OSTEOPOROSIS INT, V13, P650, DOI 10.1007/s001980200088; VANDENELSHOUT FJJ, 1990, CHEST, V98, P358, DOI 10.1378/chest.98.2.358; Wong CA, 2000, LANCET, V355, P1399, DOI 10.1016/S0140-6736(00)02138-3	35	94	109	1	15	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	AUG	2004	126	2					352	361		10.1378/chest.126.2.352		10	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	846CZ	WOS:000223293900011	15302717	
J	Deveci, SE; Deveci, F; Acik, Y; Ozan, AT				Deveci, SE; Deveci, F; Acik, Y; Ozan, AT			The measurement of exhaled carbon monoxide in healthy smokers and non-smokers	RESPIRATORY MEDICINE			English	Article						exhaled carbon monoxide; smoking; passive smoking	EXPIRED-AIR; SMOKING CESSATION; PASSIVE SMOKING; CYSTIC-FIBROSIS; BREATH; EXPOSURE; ADOLESCENTS; ASTHMA; TRIAL	The measurement of exhaled carbon monoxide (CO) level may provide an immediate, non-invasive method of assessing smoking status. The aims of this study were to use a portable CO monitor to compare the exhaled CO levels in established smokers and non-smokers. The exhaled CO levels were measured in 322 subjects (243 healthy smokers, 55 healthy non-smokers, 24 passive smokers) who applied to healthy stand during the spring student activity of Firat University in Elazig. Exhaled CO concentration was measured using the EC50 Smokerlyser. The mean exhaled CO level was 17.13 +/- 8.50 parts per million (ppm) for healthy smokers and 3.61 +/- 2.15 ppm for healthy non-smokers, and 5.20 +/- 3.38 ppm for passive smokers. There were significant positive correlation between CO levels and daily cigarette consumption, and CO levels and duration of smoking in healthy smokers (r = +0.550, P<0.001, r = +0.265, P<0.001, respectively. Spearman's test). When smokers and non-smokers were looked at as a whole, a cutoff of 6.5 ppm had a sensitivity of 90% and specificity of 83%. In conclusion, exhaled CO level provides an easy, an immediate way of assessing a subject's smoking status. (C) (C) 2004 Elsevier Ltd. All rights reserved.	Firat Univ, Fac Med, Dept Publ Hlth, TR-23119 Elazig, Turkey; Firat Univ, Fac Med, Dept Chest Dis, TR-23119 Elazig, Turkey	Deveci, F (reprint author), Firat Univ, Fac Med, Dept Publ Hlth, TR-23119 Elazig, Turkey.	drfigen@hotmail.com					Antuni JD, 2000, THORAX, V55, P138, DOI 10.1136/thorax.55.2.138; Bonita R, 1999, TOB CONTROL, V8, P156; CROWLEY TJ, 1989, ADDICT BEHAV, V14, P493, DOI 10.1016/0306-4603(89)90069-5; Cunnington AJ, 2002, POSTGRAD MED J, V78, P233, DOI 10.1136/pmj.78.918.233; Ece A, 2000, Allergol Immunopathol (Madr), V28, P255; Gourgoulianis KI, 2002, ACTA PAEDIATR, V91, P712, DOI 10.1080/080352502760069160; Hewat VN, 1998, NEW ZEAL MED J, V111, P343; Horvath I, 1999, CLIN EXP ALLERGY, V29, P1276; IRVING JM, 1988, PREV MED, V17, P109, DOI 10.1016/0091-7435(88)90076-X; JAMROZIK K, 1984, BRIT MED J, V288, P1499; JARVIS M, 1984, J EPIDEMIOL COMMUN H, V38, P335, DOI 10.1136/jech.38.4.335; JARVIS MJ, 1987, AM J PUBLIC HEALTH, V77, P1435, DOI 10.2105/AJPH.77.11.1435; JARVIS MJ, 1986, THORAX, V41, P886, DOI 10.1136/thx.41.11.886; JARVIS MJ, 1980, BRIT MED J, V281, P484; Jimenez-Ruiz CA, 2001, CHEST, V119, P1365, DOI 10.1378/chest.119.5.1365; JONES RH, 1958, J LAB CLIN MED, V51, P553; JORENBY DE, 1995, JAMA-J AM MED ASSOC, V274, P1347, DOI 10.1001/jama.274.17.1347; LARENJEIRA R, 2000, SAO PAULO MED J, V118, P89; LeSon S, 1995, Allergol Immunopathol (Madr), V23, P235; Mastora I, 2001, RADIOLOGY, V218, P695; Middleton ET, 2000, CHEST, V117, P758, DOI 10.1378/chest.117.3.758; Montuschi P, 2001, CHEST, V120, P496, DOI 10.1378/chest.120.2.496; Nakayama T, 1998, J Epidemiol, V8, P140; REA JN, 1973, BRIT J PREV SOC MED, V27, P114; RINGOLD A, 1962, ARCH ENVIRON HEALTH, V5, P308; Ruiz JMG, 1998, REV CLIN ESP, V198, P440; TONNESEN P, 1993, JAMA-J AM MED ASSOC, V269, P1268, DOI 10.1001/jama.269.10.1268; VOGT TM, 1977, AM J PUBLIC HEALTH, V67, P545, DOI 10.2105/AJPH.67.6.545; WALD NJ, 1981, THORAX, V36, P366, DOI 10.1136/thx.36.5.366; Yamaya M, 1998, AM J RESP CRIT CARE, V158, P311; Yamaya M, 2001, CLIN EXP ALLERGY, V31, P417, DOI 10.1046/j.1365-2222.2001.01013.x; Zayasu K, 1997, AM J RESP CRIT CARE, V156, P1140; Zetterquist W, 2002, EUR RESPIR J, V20, P92, DOI 10.1183/09031936.02.00245302	33	94	97	2	17	W B SAUNDERS CO LTD	LONDON	32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND	0954-6111			RESP MED	Respir. Med.	JUN	2004	98	6					551	556		10.1016/j.rmed.2003.11.018		6	Cardiac & Cardiovascular Systems; Respiratory System	Cardiovascular System & Cardiology; Respiratory System	825HH	WOS:000221746400011	15191041	
J	Braback, L; Hjern, A; Rasmussen, F				Braback, L; Hjern, A; Rasmussen, F			Trends in asthma, allergic rhinitis and eczema among Swedish conscripts from farming and non-farming environments. A nationwide study over three decades	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergic rhinitis; asthma; conscripts; eczema; epidemiology; farm environment; rural; time trend; urban	HAY-FEVER; RESPIRATORY SYMPTOMS; ATOPIC-DERMATITIS; YOUNG MEN; PREVALENCE; CHILDREN; SENSITIZATION; ADULTS; DISEASES; EXPOSURE	Background Asthma and allergies are less common in children who have been raised in farming environments. Objectives To assess whether children who grow up in a farming environment have been protected against the general increase in atopic disorders in Sweden and whether other rural environments could also be protective. Method Linkage at an individual level of three national registers in Sweden: The Swedish Military Service Conscription Register (MSCR), the Register of the Total Population (RTP) and the Population and Housing Censuses (PHC). Asthma, allergic rhinitis and eczema at conscription were analysed in relation to area of residence, parental occupation, maternal age, family size and being the first born for 1 309 652 male conscripts in three successive cohorts born between 1952 and 1981. Results Allergic rhinitis and eczema displayed a continuous increase throughout the study period, whereas the rise in asthma mainly occurred in conscripts born after 1961. Farming environments and rural living already provided protection from allergic rhinitis in conscripts born during the 1950s, but the protective effect was greater in later cohorts. An inverse association was observed between farm living and asthma, but mainly in conscripts born after 1970. The adjusted risk ratios for asthma in conscripts from farming vs. non-farming families were 1.00 (95% CI 0.93-1.07), 0.94 (95% CI 0.88-1.01) and 0.85 (95% CI 0.79-0.91) in conscripts born in 1952-1961, 1962-1971 and 1972-1981, respectively. Rural living per se had no effect on the occurrence of asthma. Eczema was less common in rural areas, but the time trend was similar in urban and rural areas. Conclusions Our findings suggest that environmental changes affecting the whole of society have promoted an increase in asthma, allergic rhinitis and eczema in both farming and non-farming environments. A lower risk of allergic rhinitis in conscripts whose parents were involved in farming was observed in all birth cohorts, whereas the protective effect of growing up on a farm on the risk of asthma appears to be a fairly recent phenomenon.	Karolinska Inst, Dept Publ Hlth Sci, Epidemiol Res Grp, Epidemiol Res Unit, SE-17176 Stockholm, Sweden; Sundsvall Hosp, Mid Sweden Res & Dev Ctr, Sundsvall, Sweden; Uppsala Univ, Dept Womens & Childrens Hlth, Unit Paediat, Uppsala, Sweden; Swedish Natl Board Hlth & Welf, Ctr Epidemiol, Stockholm, Sweden	Rasmussen, F (reprint author), Karolinska Inst, Dept Publ Hlth Sci, Epidemiol Res Grp, Epidemiol Res Unit, SE-17176 Stockholm, Sweden.	finn.rasmussen@phs.ki.se					ABERG N, 1989, CLIN EXP ALLERGY, V19, P59, DOI 10.1111/j.1365-2222.1989.tb02345.x; Braback L, 1998, CLIN EXP ALLERGY, V28, P936; Braback L, 1991, PEDIATR ALLERGY IMMU, V2, P14, DOI 10.1111/j.1399-3038.1991.tb00174.x; 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; Downs SH, 2001, CLIN EXP ALLERGY, V31, P570, DOI 10.1046/j.1365-2222.2001.01070.x; Heinrich J, 1998, ALLERGY, V53, P89, DOI 10.1111/j.1398-9995.1998.tb03779.x; Herd RM, 1996, BRIT J DERMATOL, V135, P18; Hjern A, 1999, PEDIATR ALLERGY IMMU, V10, P101, DOI 10.1034/j.1399-3038.1999.00023.x; Horak F, 2002, CLIN EXP ALLERGY, V32, P1155, DOI 10.1046/j.1365-2745.2002.01448.x; Jogi R, 1996, ALLERGY, V51, P331, DOI 10.1111/j.1398-9995.1996.tb00094.x; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Krause TG, 2002, LANCET, V360, P691, DOI 10.1016/S0140-6736(02)09841-0; Leynaert B, 2001, AM J RESP CRIT CARE, V164, P1829; Magnus P, 1997, BRIT MED J, V314, P1795; Matricardi PM, 1998, J ALLERGY CLIN IMMUN, V101, P439, DOI 10.1016/S0091-6749(98)70350-1; Mortz CG, 2001, BRIT J DERMATOL, V144, P523, DOI 10.1046/j.1365-2133.2001.04078.x; Pearce N, 2000, EUR RESPIR J, V16, P420, DOI 10.1183/9031936.00.16337700; Pearce N, 1999, THORAX, V54, P268; Radon K, 2001, EUR RESPIR J, V17, P747, DOI 10.1183/09031936.01.17407470; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; ROTHMAN KJ, 1998, MODERN EPIDEMIOLOGY, P270; Strachan DP, 1997, J ALLERGY CLIN IMMUN, V99, P6, DOI 10.1016/S0091-6749(97)81038-X; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; von Mutius E, 1998, LANCET, V351, P862, DOI 10.1016/S0140-6736(97)10100-3; Von Mutius E, 1998, CLIN EXP ALLERGY, V28, P45; Weiland SK, 1999, EUR RESPIR J, V14, P862, DOI 10.1034/j.1399-3003.1999.14d23.x; Weiss ST, 2002, NEW ENGL J MED, V347, P930, DOI 10.1056/NEJMe020092; WUTHRICH B, 1995, INT ARCH ALLERGY IMM, V106, P149	32	94	95	1	8	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	JAN	2004	34	1					38	43		10.1111/j.1365-2222.2004.01841.x		6	Allergy; Immunology	Allergy; Immunology	763LF	WOS:000188086500007	14720260	
J	Zhang, JF; Hu, W; Wei, FS; Wu, GP; Korn, LR; Chapman, RS				Zhang, JF; Hu, W; Wei, FS; Wu, GP; Korn, LR; Chapman, RS			Children's respiratory morbidity prevalence in relation to air pollution in four Chinese cities	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; children; China; particulate matter; respiratory health	LONG-TERM EXPOSURE; PARTICULATE MATTER; PASSIVE SMOKING; HEALTH; COMMUNITIES; CALIFORNIA; PARTICLES; SYMPTOMS; PM10	We examined respiratory health effects of long-term exposure to ambient air pollution in 7,621 schoolchildren residing in eight districts of four Chinese cities. The four cities exhibited wide between-city and within-city gradients in ambient levels of four size fractions of particulate matter [less than or equal to 2.5 pro in aerodynamic diameter (PM2.5), between 2.5 and 10 mum (PM10-2.5), less than or equal to 10 mum (PM10), and total suspended particulates (TSP)] and two gaseous pollutants (SO2 and NOx). Informed consent and written responses to questionnaires about children's personal, residential, and family information, as well as their health histories and status, were obtained with the help of the parents and the school personnel. We used a two-stage regression approach in data analyses. In the first-stage logistic regressions, we obtained logits of district-specific prevalence of wheeze, asthma, bronchitis, hospitalization for respiratory diseases, persistent cough, and persistent phlegm, adjusted for covariates representing personal, household, and family parameters. Some of these covariates were found to be risk factors of children's respiratory health, including being younger in the study group, being male, having been breast-fed, sharing bedrooms, sharing beds, room being smoky during cooking, eye irritation during cooking, parental smoking, and a history of parental asthma. In several of the second-stage variance-weighted linear regressions, we examined associations between district-specific adjusted prevalence rates and district-specific ambient levels of each pollutant. We found positive associations between morbidity prevalence and outdoor levels of PM of all size fractions, but the association appeared to be stronger for coarse particles (PM10-2.5). The results also present some evidence that ambient levels of NOx and SO2 were positively associated with children's respiratory symptoms, but the evidence for these two gaseous pollutants appeared to be weaker than that for the PM.	EOHSI, Piscataway, NJ 08854 USA; Rutgers State Univ, Piscataway, NJ USA; China Natl Environm Monitoring Ctr, Beijing, Peoples R China; US EPA, Natl Ctr Environm Assessment, Res Triangle Pk, NC 27711 USA; Univ Med & Dent New Jersey, Piscataway, NJ 08854 USA	Zhang, JF (reprint author), EOHSI, Room 358,170 Frelinghuysen Rd, Piscataway, NJ 08854 USA.		Hu, Wei/M-3524-2013				Bascom R, 1996, AM J RESP CRIT CARE, V153, P477; Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; BraunFahrlander C, 1997, AM J RESP CRIT CARE, V155, P1042; Cunningham J, 1996, AM J RESP CRIT CARE, V153, P218; DOCKERY DW, 1989, AM REV RESPIR DIS, V139, P587; Dockery DW, 1996, ENVIRON HEALTH PERSP, V104, P500, DOI 10.2307/3432990; FERRIS BG, 1978, AM REV RESPIR DIS, V118, P1; FORASTIERE F, 1992, INT J EPIDEMIOL, V21, P66, DOI 10.1093/ije/21.1.66; GOLD DR, 1993, AM REV RESPIR DIS, V148, P10; Health Effects Institute, 2001, AIRB PART HLTH HEI E; Hruba F, 2001, J EXPO ANAL ENV EPID, V11, P33, DOI 10.1038/sj.jea.7500141; NEAS LM, 1994, AM J EPIDEMIOL, V139, P1088; Ostro BD, 1999, ENVIRON RES, V81, P231, DOI 10.1006/enrs.1999.3978; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; Pikhart H, 2000, EPIDEMIOLOGY, V11, P153, DOI 10.1097/00001648-200003000-00012; Pope CA, 2000, AEROSOL SCI TECH, V32, P4, DOI 10.1080/027868200303885; Qian ZM, 2001, J EXPO ANAL ENV EPID, V11, P341, DOI 10.1038/sj.jea.7500170; Qian ZM, 2000, ARCH ENVIRON HEALTH, V55, P126; *SEPA, 1992, STAND ENV MON AN MET; Shen S, 1992, Biomed Environ Sci, V5, P136; WARE JH, 1986, AM REV RESPIR DIS, V133, P834; WARE JH, 1984, AM REV RESPIR DIS, V129, P366; Wei F, 1999, ENVIRON SCI TECHNOL, V33, P4188, DOI 10.1021/es9904944; Wilson R., 1996, PARTICLES OUR AIR CO; Zhang JFJ, 1999, ARCH ENVIRON HEALTH, V54, P373	25	94	110	3	30	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					961	967				7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	591RJ	WOS:000177893800040	12204833	
J	Gerhold, K; Blumchen, K; Bock, A; Seib, C; Stock, P; Kallinich, T; Lohning, M; Wahn, U; Hamelmann, E				Gerhold, K; Blumchen, K; Bock, A; Seib, C; Stock, P; Kallinich, T; Lohning, M; Wahn, U; Hamelmann, E			Endotoxins prevent murine IgE production,T(H)2 immune responses, and development of airway eosinophilia but not airway hyperreactivity	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						mice; eosinophils; T(H)1/T(H)2 cells; cytokines; lipopolysaccharides	TOLL-LIKE RECEPTOR-4; DENDRITIC CELLS; BACTERIAL LIPOPOLYSACCHARIDE; INFLAMMATORY RESPONSE; ALLERGEN CHALLENGE; SENSITIZED MICE; TNF-ALPHA; TH2 CELLS; ASTHMA; MACROPHAGES	Background: Contact with immunomodulatory factors, such as LPS, in early infancy is associated with decreased allergen sensitization. Objective: We sought to study the effects of systemic or airway exposure with LPS on the development of allergen sensitization, eosinophilic airway inflammation, and increased in vivo airway reactivity (AR) in a mouse model. Methods: BALB/c mice were systemically sensitized with ovalbumin (OVA) plus adjuvant on days 1 and W and challenged through the airways with allergen on days 34 to 36. We performed measurement of OVA-specific IgE serum levels, in vitro T(H)2 cytokine production, differential cell counts in bronchoalveolar lavage fluids, and assessment of in vivo AR to inhaled methacholine by means of barometric whole-body plethysmography. Results: Systemic LPS administration before OVA sensitization reduced OVA-specific IgE serum levels (426 76 is 880 104 U/mL, P <.01), T(H)2 cytokine production by splenic mononuclear cells (IL-4: 0.08 +/- 0.01 vs 0.17 +/- 0.01 ng/mL; IL-5: 1.98 +/- 0.52 vs 4.11 +/- 0.54 ng/mL; P <.01), and extent of airway eosinophilia (total cell counts: 93 vs 376 x 10(3)/mL, eosinophils: 23% vs 51%; P <.01) compared with that in OVA-sensitized mice. Local LPS administration to sensitized mice before airway allergen challenges particularly induced IFN-gamma production by peribronchial lymph node cells in vitro (1718 +/- 315 vs 483 +/- 103 ng/mL, P <.01) associated with reduced airway eosinophilia compared with that seen in OVA-sensitized mice. Development of increased AR was not affected by systemic or local LPS exposure. Inhibitory effects of LPS on allergen sensitization and eosinophilic airway inflammation were inhibited bY administration of anti-IL-12 antibodies before LPS exposure. Conclusion: These data indicate that local and systemic application of LPS modulates systemic and local T(H)1/T(H)2 immune responses in a distinct but similarly IL-12-dependent mode.	Univ Hosp Charite, Dept Pediat Pneumol & Immunol, D-13353 Berlin, Germany; Deutsch Rheuma Forschungszentrum, Berlin, Germany	Hamelmann, E (reprint author), Univ Hosp Charite, Dept Pediat Pneumol & Immunol, Augustenburger Pl 1, D-13353 Berlin, Germany.						Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; Blunck R, 2001, J IMMUNOL, V166, P1009; BORCHERS MT, 2001, AM J PHYSIOL, V281, P1653; Desmedt M, 1998, J IMMUNOL, V160, P5300; 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; Gereda JE, 2001, J ALLERGY CLIN IMMUN, V107, P790, DOI 10.1067/mai.2001.115245; Hamelmann E, 2000, AM J RESP CELL MOL, V23, P327; Hamelmann E, 1997, AM J RESP CRIT CARE, V156, P766; Hamelmann E, 1997, AM J RESP CRIT CARE, V155, P819; Hansen G, 1999, J CLIN INVEST, V103, P175, DOI 10.1172/JCI5155; Henderson WR, 2000, J IMMUNOL, V164, P1086; Hilkens CMU, 1997, BLOOD, V90, P1920; HOLT PG, 1981, INT ARCH ALLER A IMM, V65, P42; Lambrecht BN, 1998, J IMMUNOL, V160, P4090; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; Levitt RC, 1999, J ALLERGY CLIN IMMUN, V103, pS485, DOI 10.1016/S0091-6749(99)70165-X; LeyvaCobian F, 1997, CLIN IMMUNOL IMMUNOP, V85, P1, DOI 10.1006/clin.1997.4426; Liu AH, 2002, J ALLERGY CLIN IMMUN, V109, P379, DOI 10.1067/mai.2002.122157; MARTINEZ FD, 1995, AM J RESP CRIT CARE, V151, P1644; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; Moreland JG, 2001, AM J PHYSIOL-LUNG C, V280, pL173; Nomura F, 2000, J IMMUNOL, V164, P3476; Ogata H, 2000, J EXP MED, V192, P23, DOI 10.1084/jem.192.1.23; Ohmori Y, 2001, J LEUKOCYTE BIOL, V69, P598; Randolph DA, 1999, J CLIN INVEST, V104, P1021, DOI 10.1172/JCI7631; 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; Schwarze J, 1998, J ALLERGY CLIN IMMUN, V102, P86, DOI 10.1016/S0091-6749(98)70058-2; Snijders A, 1998, INT IMMUNOL, V10, P1593, DOI 10.1093/intimm/10.11.1593; Stumbles PA, 1998, J EXP MED, V188, P2019, DOI 10.1084/jem.188.11.2019; Szabo SJ, 1997, J EXP MED, V185, P817, DOI 10.1084/jem.185.5.817; Tang CB, 2001, J IMMUNOL, V166, P1471; Tournoy KG, 2001, J ALLERGY CLIN IMMUN, V107, P483, DOI 10.1067/mai.2001.112693; Tsan MF, 2001, AM J PHYSIOL-CELL PH, V280, pC1422; Tulic MK, 2000, AM J RESP CELL MOL, V22, P604; Verhasselt V, 1997, J IMMUNOL, V158, P2919; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; Yang M, 2001, AM J RESP CELL MOL, V25, P522	40	94	98	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	2002	110	1					110	116		10.1067/mai.2002.125831		7	Allergy; Immunology	Allergy; Immunology	574CF	WOS:000176870300021	12110829	
J	Smart, JM; Kemp, AS				Smart, JM; Kemp, AS			Increased Th1 and Th2 allergen-induced cytokine responses in children with atopic disease	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergens; atopy; childhood; cytokines; house dust mite; interferon-gamma; interleukins-4/-5/-13; rye grass pollen; superantigens	BLOOD MONONUCLEAR-CELLS; INTERFERON-GAMMA PRODUCTION; MESSENGER-RNA EXPRESSION; PERIPHERAL-BLOOD; IFN-GAMMA; NONATOPIC CHILDREN; INTERLEUKIN-4 PRODUCTION; MITE ALLERGEN; T-CELLS; ASTHMA	Background Polyclonal cytokine responses following stimulation of T cells with mitogens or superantigens provides information on cytokine production from a wide range of T cells. Alternatively allergen-induced T cell responses can provide information on cytokine production by allergen-reactive T cells. While there is evidence of increased Th2 and reduced Th1 cytokine production following T cell stimulation with non-specific mitogens and superantigens, the evidence that Th1 cytokine production to allergens is decreased in line with a postulated imbalance in Th1/Th2 responses is unclear, with studies finding decreased, no difference or increased IFN-gamma responses to allergens in atopic subjects. Objecgive To examine childhood polyclonal and allergen-induced cytokine responses in parallel to evaluate cytokine imbalances in childhood atopic disease. Methods PBMC cytokine responses were examined in response to a polyclonal stimulus, staphylococcal superantigen (SEB), in parallel with two inhalant allergens, house dust mite (HDM) and rye grass pollen (RYE), and an ingested allergen, ovalbumin (OVA), in (a) 35 healthy children (non-atopic) and (b) 36 children with atopic disease (asthma, eczema and/or rhinitis) (atopic). Results Atopic children had significantly reduced IFN-gamma and increased IL-4 and IL-5 but not IL13 production to SEB superantigen stimulation when compared with non-atopic children. HDM and RYE allergens stimulated significantly increased IFN-gamma, IL-5 and IL-13, while OVA stimulated significantly increased IFN-gamma production in atopic children. Conclusion We show that a polyclonal stimulus induces a reduced Th1 (IFN-gamma) and increased Th2 (IL-4 and IL-5) cytokine pattern. In contrast, the allergen-induced cytokine responses in atopic children were associated with both increased Th1 (INF-gamma) and Th2 (IL-5 and IL-13) cytokine production. The increased Th1 response to allergen is likely to reflect prior sensitization and indicates that increases in both Th1 and Th2 cytokine production to allergens exists concomitantly with a decreased Th1 response to a polyclonal stimulus in atopic children.	Royal Childrens Hosp, Dept Immunol, Murdoch Childrens Res Inst, Parkville, Vic 3052, Australia	Kemp, AS (reprint author), Royal Childrens Hosp, Dept Immunol, Murdoch Childrens Res Inst, Flemington Rd, Parkville, Vic 3052, Australia.						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Exp. Allergy	MAY	2002	32	5					796	802		10.1046/j.1365-2222.2002.01391.x		7	Allergy; Immunology	Allergy; Immunology	549GP	WOS:000175436400024	11994108	
J	Burnett, RT; Smith-Doiron, M; Stieb, D; Raizenne, ME; Brook, JR; Dales, RE; Leech, JA; Cakmak, S; Krewski, D				Burnett, RT; Smith-Doiron, M; Stieb, D; Raizenne, ME; Brook, JR; Dales, RE; Leech, JA; Cakmak, S; Krewski, D			Association between ozone and hospitalization for acute respiratory diseases in children less than 2 years of age	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						air pollution; child; hospitalization; ozone; respiratory tract diseases	AIR-POLLUTION; DAILY MORTALITY; UPPER AIRWAYS; ADMISSIONS; ASTHMA; PARTICULATE; TORONTO; EMERGENCY; ILLNESSES; MONTREAL	To clarify the health effects of ozone exposure in young children, the authors studied the association between air pollution and hospital admissions for acute respiratory problems in children less than 2 years of age during the 15-year period from 1980 to 1994 in Toronto, Canada. The daily time series of admissions was adjusted for the influences of day of the week, season, and weather. A 35% (95% confidence interval: 19%, 52%) increase in the daily hospitalization rate for respiratory problems was associated with a 5-day moving average of the daily 1-hour maximum ozone concentration of 45 parts per billion, the May-August average value. The ozone effect persisted after adjustment for other ambient air pollutants or weather variables. Ozone was not associated with hospital admissions during the September-April period. Ambient ozone levels in the summertime should be considered a risk factor for respiratory problems in children less than 2 years of age.	Hlth Canada, Environm Hlth Directorate, Ottawa, ON K1A 0L2, Canada; Environm Canada, Meteorol Serv Canada, Downsview, ON, Canada; Univ Ottawa, Fac Med, Dept Epidemiol & Community Med, Ottawa, ON, Canada	Burnett, RT (reprint author), Hlth Canada, Environm Hlth Directorate, 200 Environm Hlth Ctr, Ottawa, ON K1A 0L2, Canada.			Cakmak, Sabit/0000-0001-9921-2107			Anderson HR, 1998, THORAX, V53, P842; Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; BorjaAburto VH, 1997, AM J EPIDEMIOL, V145, P258; Burnett RT, 1999, ARCH ENVIRON HEALTH, V54, P130; 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; BURNETT RT, 1994, ENVIRON RES, V65, P172, DOI 10.1006/enrs.1994.1030; Burnett RT, 1998, J AIR WASTE MANAGE, V48, P689; CAMPBELL ME, 1995, CAN J PUBLIC HEALTH, V86, P351; CHITANO P, 1995, EUR RESPIR J, V8, P1357, DOI 10.1183/09031936.95.08081357; CLEVELAND WS, 1979, J AM STAT ASSOC, V74, P829, DOI 10.2307/2286407; Dab W, 1996, J EPIDEMIOL COMMU S1, V50, ps42; DELEON P, 1996, J EPIDEMIOL COMMU S1, V50, pS63; DELFINO RJ, 1994, ENVIRON RES, V67, P1, DOI 10.1006/enrs.1994.1061; Delfino RJ, 1997, AM J RESP CRIT CARE, V155, P568; FRISCHER TM, 1993, AM REV RESPIR DIS, V148, P961; GERRITY TR, 1988, J APPL PHYSIOL, V65, P393; HARKEMA JR, 1987, AM J PATHOL, V128, P129; Hastie T, 1990, GEN ADDITIVE MODELS; KNOBEL HH, 1995, PEDIATRICS, V96, P1106; Leech J A, 1996, Chronic Dis Can, V17, P118; MCBRIDE DE, 1994, AM J RESP CRIT CARE, V149, P1192; Ponka A, 1996, J EPIDEMIOL COMMUN H, V50, pS59, DOI 10.1136/jech.50.Suppl_1.s59; PONKA A, 1991, ARCH ENVIRON HEALTH, V46, P262; POPE CA, 1991, ARCH ENVIRON HEALTH, V46, P90; PRIESTLEY MB, 1981, SPECTRAL ANAN TIME S; SALDIVA PHN, 1994, ENVIRON RES, V65, P218, DOI 10.1006/enrs.1994.1033; Schouten JP, 1996, J EPIDEMIOL COMMUN H, V50, pS22, DOI 10.1136/jech.50.Suppl_1.s22; SCHWARTZ J, 1991, ENVIRON RES, V56, P1, DOI 10.1016/S0013-9351(05)80104-5; SCHWARTZ J, 1994, ARCH ENVIRON HEALTH, V49, P366; Schwartz J, 1996, EPIDEMIOLOGY, V7, P20, DOI 10.1097/00001648-199601000-00005; SCHWARTZ J, 1995, THORAX, V50, P531, DOI 10.1136/thx.50.5.531; SCHWARTZ J, 1995, AM J EPIDEMIOL, V142, P23; 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; SPREM N, 1993, INT J PEDIATR OTORHI, V26, P245, DOI 10.1016/0165-5876(93)90094-J; *STAT SCI INC, 1993, S PLUS MAN; Steib DM, 2000, CAN J PUBLIC HEALTH, V91, P107; TAKAHASHI N, 1995, J APPL PHYSIOL, V79, P1753; THURSTON GD, 1992, J EXPO ANAL ENV EPID, V2, P429; THURSTON GD, 1994, ENVIRON RES, V65, P271, DOI 10.1006/enrs.1994.1037; TSENG RYM, 1992, ANN ALLERGY, V68, P425; Vigotti MA, 1996, J EPIDEMIOL COMMUN H, V50, pS71, DOI 10.1136/jech.50.Suppl_1.s71; WYZGA RE, 1995, PARTICULATE MATTER H, P3	46	94	98	1	9	OXFORD UNIV PRESS INC	CARY	JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA	0002-9262			AM J EPIDEMIOL	Am. J. Epidemiol.	MAR 1	2001	153	5					444	452		10.1093/aje/153.5.444		9	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	405YZ	WOS:000167189300006	11226976	
J	Simpson, BM; Custovic, A; Simpson, A; Hallam, CL; Walsh, D; Marolia, H; Campbell, J; Woodcock, A				Simpson, BM; Custovic, A; Simpson, A; Hallam, CL; Walsh, D; Marolia, H; Campbell, J; Woodcock, A			NAC Manchester Asthma and Allergy Study ((NAC)MAAS): risk factors for asthma and allergic disorders in adults	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						asthma; eczema; hay fever; allergens; skin prick tests	HOUSE-DUST MITE; RESPIRATORY HEALTH SURVEY; CHILDHOOD ASTHMA; EXPOSURE; SENSITIZATION; CHILDREN; POPULATION; CAT; SENSITIVITY; ENVIRONMENT	Background Asthma and atopic disorders are the most common chronic diseases in the developed countries. Knowledge of the risk factors for these disorders may facilitate the development of preventive strategies aimed at reducing prevalence rates. Objectives To investigate the risk factors for asthma and allergic diseases in a large number of adults who are the parents of children in the National Asthma Campaign Manchester Asthma and Allergy Study. Methods All pregnant women and their partners attending 'Booking' antenatal clinics were invited to take part in the study. Questionnaire data were collected including the history of asthma and other atopic diseases, pet ownership and smoking habits, and skin prick tests were performed. The prevalence of atopy and the risk factors for asthma and allergic disorders were investigated in all subjects who completed the questionnaire and underwent skin testing. Statistical analysis was carried out using logistic regression. Initially, risk factors were assessed by univariate analysis to see how each potential explanatory variable affected the probability of having allergic disease. Variables were then tested in a forward stepwise multivariate analysis. Results In 5687 adult subjects there was a very high (48.2%) prevalence of atopy, and 9.7% of subjects had a diagnosis of asthma. In a multivariate regression analysis sensitization to dust mite, cat, dog and mixed grasses were all independently associated with asthma. The odds ratios for current asthma increased with the increasing number of positive skin tests (any two allergens - OR 4.3, 95% CI 3.3-5.5; any three allergens - OR 7.0 95% CI 5.3-9.3; all four allergens - OR 10.4, 95% CI 7.7-14; P < 0.00001). Dog ownership (OR 1.31, 95% CI 1.10-1.57; P = 0.003) and current smoking (OR 1.36, 95% CI 1.15-1.62; P = 0.0004) were significantly and directly associated with 'asthma ever'. Thirteen per cent of participants reported a history of eczema. In the multivariate analysis the strongest independent associate of eczema was sensitization to dog (OR 1.37, 95% CI 1.14-1.63, P < 0.0001). Apart from dog, the strength of the association between sensitization to common allergens and eczema appeared to be much lower than in the case of asthma. The prevalence of hay fever was high (20.6%), and in the multivariate analysis the association between sensitization to pollen and hay fever was extremely strong (OR 13.6, 95% CI 11.3-16.3; P < 0.0001). Conclusions The results of the current study emphasize the importance of sensitization to indoor allergens in asthma. However, evidence of a possible direct role of allergen exposure in asthma causation remains unclear.	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			ARRUDA LK, 1991, CLIN EXP ALLERGY, V21, P433, DOI 10.1111/j.1365-2222.1991.tb01683.x; BECKLAKE MR, 1990, RESPIRATION, V57, P137; Bodner CH, 1998, AM J RESP CRIT CARE, V157, P35; Brown MA, 1997, CLIN EXP ALLERGY, V27, P4, DOI 10.1046/j.1365-2222.1997.d01-430.x; Burr ML, 1997, CLIN EXP ALLERGY, V27, P1247; BURROWS B, 1995, J ALLERGY CLIN IMMUN, V95, P548, DOI 10.1016/S0091-6749(95)70317-9; CHARPIN D, 1988, CHEST, V93, P758, DOI 10.1378/chest.93.4.758; CHARPIN D, 1991, AM REV RESPIR DIS, V143, P983; CHAVARRIA JF, 1992, INT ARCH ALLERGY IMM, V99, P466; Custovic A, 1998, THORAX, V53, P63; Eisner MD, 1998, AM J RESP CRIT CARE, V158, P170; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Hopkin JM, 1999, CLIN EXP ALLERGY, V29, P733; Jarvis D, 1999, J ALLERGY CLIN IMMUN, V104, P934, DOI 10.1016/S0091-6749(99)70071-0; Leung R, 1997, J ALLERGY CLIN IMMUN, V99, P594, DOI 10.1016/S0091-6749(97)70018-6; MILLS TAE, 1997, J ALLERGY CLIN IMMUN, V100, pS1; 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; PEAT JK, 1994, AUST NZ J MED, V24, P473; PLATTSMILLS TAE, 1989, J ALLERGY CLIN IMMUN, V83, P416, DOI 10.1016/0091-6749(89)90128-0; Roost HP, 1999, J ALLERGY CLIN IMMUN, V104, P941, DOI 10.1016/S0091-6749(99)70072-2; SEARS MR, 1989, CLIN EXP ALLERGY, V19, P419, DOI 10.1111/j.1365-2222.1989.tb02408.x; SEATON A, 1994, THORAX, V49, P171, DOI 10.1136/thx.49.2.171; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; Squillace SP, 1997, AM J RESP CRIT CARE, V156, P1760; Strachan DP, 1997, CLIN EXP ALLERGY, V27, P235; Svanes C, 1999, J ALLERGY CLIN IMMUN, V103, P415, DOI 10.1016/S0091-6749(99)70465-3; Tan JS, 1997, ARCH INTERN MED, V157, P1933, DOI 10.1001/archinte.157.17.1933; Tunnicliffe WS, 1999, EUR RESPIR J, V13, P654, DOI 10.1183/09031936.99.13365499; WARNER JA, 1991, PEDIATR ALLERGY IMMU, V1, P79	30	94	97	0	3	BLACKWELL SCIENCE LTD	OXFORD	P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	MAR	2001	31	3					391	399		10.1046/j.1365-2222.2001.01050.x		9	Allergy; Immunology	Allergy; Immunology	417UB	WOS:000167851600009	11260150	
J	Martinez, FD				Martinez, FD			The coming-of-age of the hygiene hypothesis	RESPIRATORY RESEARCH			English	Editorial Material						atopy; CD14; endotoxin; genetics; hygiene	HAY-FEVER; ALLERGIC SENSITIZATION; EARLY-LIFE; ASTHMA; ATOPY; CHILDREN; EXPOSURE; ASSOCIATION; ENDOTOXIN; RISK	The hygiene hypothesis, as originally proposed, postulated an inverse relation between the incidence of infectious diseases in early life and the subsequent development of allergies and asthma. New evidence from epidemiological, biological and genetic studies has significantly enlarged the scope of the hypothesis. It now appears probable that environmental 'danger' signals regulate the pattern of immune responses in early life. Microbial burden in general, and not any single acute infectious illness, is the main source of these signals. The latter interact with a sensitive and complex receptor system, and genetic variations in this receptor system may be an important determinant of inherited susceptibility to asthma and allergies.	Univ Arizona, Resp Sci Ctr, Tucson, AZ USA	Martinez, FD (reprint author), 1501 N Campbell Ave,Suite 2349, Tucson, AZ 85725 USA.				NHLBI NIH HHS [HL 66800, HL 56177, HL 61892, HL 64307, HL 66447, R01 HL056177, R01 HL066447, U10 HL064307]		AMELUNG PJ, 2000, AM J RESP CRIT CARE, V161, pA927; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; CELEDON JC, 2000, AM J RESP CRIT CARE, V161, pA927; Ernst P, 2000, AM J RESP CRIT CARE, V161, P1563; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Holt PG, 2000, ALLERGY, V55, P688, DOI 10.1034/j.1398-9995.2000.00118.x; Hubacek JA, 1999, CIRCULATION, V99, P3218; JOOS L, 2000, AM J RESP CRIT CARE, V161, pA928; MARTINEZ FD, 1995, J ALLERGY CLIN IMMUN, V96, P652, DOI 10.1016/S0091-6749(95)70264-4; MARTINEZ FD, 1995, THORAX, V50, P1067, DOI 10.1136/thx.50.10.1067; MARTINEZ FD, 1999, LANCET S2, V354; Matricardi PM, 2000, BRIT MED J, V320, P412, DOI 10.1136/bmj.320.7232.412; MATZINGER P, 1994, ANNU REV IMMUNOL, V12, P991, DOI 10.1146/annurev.immunol.12.1.991; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; ODONNELL AR, 2000, AM J RESP CRIT CARE, V161, pA928; Paunio M, 2000, JAMA-J AM MED ASSOC, V283, P343, DOI 10.1001/jama.283.3.343; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; PUGIN J, 1994, IMMUNITY, V1, P509, DOI 10.1016/1074-7613(94)90093-0; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; ROMAGNANI S, 1992, IMMUNOL TODAY, V13, P379, DOI 10.1016/0167-5699(92)90083-J; Shaheen SO, 1996, LANCET, V347, P1792, DOI 10.1016/S0140-6736(96)91617-7; Sherrill D, 1999, CLIN EXP ALLERGY, V29, P905; Shirakawa T, 1997, SCIENCE, V275, P77, DOI 10.1126/science.275.5296.77; Strachan David P., 2000, Thorax, V55, pS2, DOI 10.1136/thorax.55.suppl_1.S2; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Tulic MK, 2000, AM J RESP CELL MOL, V22, P604; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; Woolcock AJ, 1997, CIBA F SYMP, V206, P122	29	94	96	0	6	BIOMED CENTRAL LTD	LONDON	MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND	1465-993X			RESPIR RES	Respir. Res.		2001	2	3					129	132		10.1186/rr48		4	Respiratory System	Respiratory System	443VC	WOS:000169361500002	11686875	
J	Gautrin, D; Ghezzo, H; Infante-Rivard, C; Malo, JL				Gautrin, D; Ghezzo, H; Infante-Rivard, C; Malo, JL			Incidence and determinants of IgE-mediated sensitization in apprentices - A prospective study	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							EXPOSURE-RESPONSE RELATIONSHIPS; LABORATORY-ANIMAL WORKERS; OCCUPATIONAL ASTHMA; GENERAL-POPULATION; LATEX; ALLERGY; SYMPTOMS; ATOPY; RATS; FLOUR	We investigated prospectively the incidence and determinants of work-related specific skin sensitization in a cohort of 769 apprentices, including 417 in animal health technology, 230 in pastry-making, and 122 in dental-hygiene technology. Subjects were recruited when starting exposure to laboratory animals, flour, or latex. A questionnaire and skin-prick tests with common and work-related allergens were administered on entry and at follow-up visits from 8 to 44 mo; information on number of hours of exposure to specific allergens was obtained. Among 769 apprentices, 698 attended greater than or equal to 1 follow-up visit. A total of 111 subjects developed specific sensitization over the study period. The incidence of work-related sensitization (per person-year) was 8.9% (95% CI 7.3 to 11.0%) in the animal-health program, 4.2% (95% CI 1.8 to 8.2%) in the pastry-making program, and 2.5% (95% CI = 0.7 to 4.3%) in the dental-hygiene program. In the animal health group, Cox regression analyses showed that atopy, nasal, and respiratory symptoms in the pollen season, and exposure assessed by the school attended or by duration of exposure to rodents were the most significant predictors of sensitization. In the dental-hygiene program, atopy and asthma were significant determinants. This study shows that: (1) an apprenticeship in animal-health technology carries a greater risk of developing specific sensitization than do apprenticeships in pastry-making and dental-hygiene; (2) atopy, respiratory symptoms in the pollen season, and number of hours in contact with rodents determine the risk of sensitization in apprentices in the animal health program.	Hop Sacre Coeur, Dept Chest Med, Montreal, PQ H4J 1C5, Canada; McGill Univ, Joint Dept Epidemiol & Biostat, Montreal, PQ, Canada; McGill Univ, Joint Dept Occupat Hlth, Montreal, PQ, Canada	Gautrin, D (reprint author), Hop Sacre Coeur, Dept Chest Med, 5400 Gouin Blvd W, Montreal, PQ H4J 1C5, Canada.						AOYAMA K, 1992, BRIT J IND MED, V49, P41; BALDO BA, 1982, PROG ALLERGY, V30, P1; BARBEE RA, 1976, ANN INTERN MED, V84, P129; BRITTON J, 1994, EUR RESPIR J, V7, P881; BURNEY PGJ, 1989, EUR RESPIR J, V2, P940; Chan-Yeung M., 1999, ASTHMA WORKPLACE, P129; COCKCROFT A, 1981, LANCET, V1, P827; Cockcroft DW, 1984, ANN ALLERGY, V53, P26; COOKSON WOCM, 1986, CLIN ALLERGY, V16, P425, DOI 10.1111/j.1365-2222.1986.tb01977.x; CULLINAN P, 1994, OCCUP ENVIRON MED, V51, P589; CULLINAN P, 1994, OCCUP ENVIRON MED, V51, P579; DUFRESNE A, 1997, ANN OCCUP HYG, V41, P621; Gautrin D, 1997, AM J RESP CRIT CARE, V155, P1841; Gordon S, 1997, J ALLERGY CLIN IMMUN, V99, P716, DOI 10.1016/S0091-6749(97)70036-8; Heederik D, 1999, J ALLERGY CLIN IMMUN, V103, P678, DOI 10.1016/S0091-6749(99)70242-3; HEEDERIK D, 1999, ASTHMA WORKPLACE, P377; HERXHEIMER H, 1967, LANCET, V1, P83; Hollander A, 1997, AM J RESP CRIT CARE, V155, P562; MCDONALD JC, 1995, EPIDEMIOLOGY WORK RE, P325; MUSK AW, 1989, BRIT J IND MED, V46, P636; Newman-Taylor Anthony, 1995, P117; NEWMANTAYLOR AJ, 1999, ASTHMA WORKPLACE, P399; PEPYS J, 1973, CLIN ALLERGY, V3, P491, DOI 10.1111/j.1365-2222.1973.tb03057.x; PLATTSMILLS TAE, 1987, J ALLERGY CLIN IMMUN, V79, P505, DOI 10.1016/0091-6749(87)90369-1; Sussman GL, 1998, J ALLERGY CLIN IMMUN, V101, P171; Tarlo SM, 1997, J ALLERGY CLIN IMMUN, V99, P396, DOI 10.1016/S0091-6749(97)70058-7; TARLO SM, 1990, J ALLERGY CLIN IMMUN, V85, P626, DOI 10.1016/0091-6749(90)90103-B; THIEL H, 1983, P INV S 11 INT C ALL, P429; VANDENPLAS O, 1995, AM J RESP CRIT CARE, V151, P54; VANDENPLAS O, 1995, EUR RESPIR J, V8, P1957, DOI 10.1183/09031936.95.08111957; VENABLES KM, 1988, BRIT J IND MED, V45, P660	31	94	96	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.	OCT	2000	162	4					1222	1228				7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	364RD	WOS:000089905900005	11029321	
J	Blease, K; Mehrad, B; Standiford, TJ; Lukacs, NW; Kunkel, SL; Chensue, SW; Lu, B; Gerard, CJ; Hogaboam, CM				Blease, K; Mehrad, B; Standiford, TJ; Lukacs, NW; Kunkel, SL; Chensue, SW; Lu, B; Gerard, CJ; Hogaboam, CM			Airway remodeling is absent in CCR1(-/-) mice during chronic fungal allergic airway disease	JOURNAL OF IMMUNOLOGY			English	Article							HUMAN LUNG FIBROBLASTS; BRONCHOPULMONARY ASPERGILLOSIS; SUBEPITHELIAL FIBROSIS; CHEMOKINE RECEPTORS; TH1 RESPONSES; MURINE MODEL; HOST-DEFENSE; INFLAMMATION; ASTHMA; HYPERREACTIVITY	Asthmatic-like reactions characterized by elevated IgE, Th2 cytokines, C-C chemokines, eosinophilic inflammation, and persistent airway hyperresponsiveness follow pulmonary exposure to the spores or conidia from Aspergillus fumigatus fungus in sensitized individuals. In addition to these features, subepithelial fibrosis and goblet cell hyperplasia characterizes fungal-induced allergic airway disease in mice. Because lung concentrations of macrophage inflammatory protein-1 alpha and RANTES were significantly elevated after A. fumigatus-sensitized mice received an intrapulmonary challenge with A. fumigatus spores or conidia, the present study addressed the role of their receptor, C-C chemokine receptor 1 (CCR1), in this model. A. fumigatus-sensitized CCR1 wild-type (+/+) and CCR1 knockout (-/-) mice exhibited similar increases in serum IgE and polymorphonuclear leukocyte numbers in the bronchoalveolar lavage, Airway hyperresponsiveness was prominent in both groups of mice at 30 days after an intrapulmonary challenge with A. fumigatus spores or conidia, However, whole lung levels of IFN-gamma were significantly higher whereas IL-4, IL-13, and Th2-inducible chemokines such as C10, eotaxin, and macrophage-derived chemokine were significantly lower in whole lung samples from CCR1(-/-) mice compared with CCR1(+/+) mice at 30 days after the conidia challenge. Likewise, significantly fewer goblet cells and less subepithelial fibrosis were observed around large airways in CCR1-/- mice at the same time after the conidia challenge. Thus, these findings demonstrate that CCR1 is a major contributor to the airway remodeling responses that arise from A. fumigatus-induced allergic airway disease.	Univ Michigan, Sch Med, Dept Pathol, Ann Arbor, MI 48109 USA; Univ Michigan, Sch Med, Dept Internal Med, Div Pulm & Crit Care, Ann Arbor, MI 48109 USA; Vet Affairs Med Ctr, Dept Pathol, Ann Arbor, MI 48105 USA; Childrens Hosp, Dept Med, Boston, MA 02115 USA; Harvard Univ, Sch Med, Boston, MA 02115 USA	Hogaboam, CM (reprint author), Univ Michigan, Sch Med, Dept Pathol, 1301 Catherine Rd, Ann Arbor, MI 48109 USA.		Mehrad, Borna/D-9363-2015	Mehrad, Borna/0000-0001-5198-065X	NHLBI NIH HHS [1P50-HL60289, HL35276, P01-HL31963]		Alam R, 1996, AM J RESP CRIT CARE, V153, P1398; Barnes PJ, 1996, BRIT J CLIN PHARMACO, V42, P3, DOI 10.1046/j.1365-2125.1996.03721.x; Boulet L P, 1998, Can Respir J, V5, P16; Campbell EM, 1998, J IMMUNOL, V161, P7047; Chu HW, 1998, AM J RESP CRIT CARE, V158, P1936; Cockrill BA, 1999, ANNU REV MED, V50, P303; Cohn L, 1999, J EXP MED, V190, P1309, DOI 10.1084/jem.190.9.1309; Corry DB, 1998, MOL MED, V4, P344; Doucet C, 1998, INT IMMUNOL, V10, P1421, DOI 10.1093/intimm/10.10.1421; Doucet C, 1998, J CLIN INVEST, V101, P2129, DOI 10.1172/JCI741; Douwes J, 1999, J ALLERGY CLIN IMMUN, V103, P494, DOI 10.1016/S0091-6749(99)70476-8; Drazen JM, 1999, CLIN EXP ALLERGY, V29, P37; EVANOFF HL, 1992, IMMUNOL INVEST, V21, P39, DOI 10.3109/08820139209069361; Gao JL, 1997, J EXP MED, V185, P1959, DOI 10.1084/jem.185.11.1959; Garlisi CG, 1997, AM J RESP CELL MOL, V17, P642; Gerard C, 1997, J CLIN INVEST, V100, P2022, DOI 10.1172/JCI119734; Gonzalo JA, 1999, J IMMUNOL, V163, P403; Gonzalo JA, 1998, J EXP MED, V188, P157, DOI 10.1084/jem.188.1.157; Hofstra CL, 1998, J IMMUNOL, V161, P5054; Hogaboam CM, 1999, J IMMUNOL, V162, P6071; Hogaboam CM, 2000, AM J PATHOL, V156, P723, DOI 10.1016/S0002-9440(10)64775-X; Holgate ST, 1997, AM J RESP CRIT CARE, V156, P1377; Holgate ST, 1997, CIBA F SYMP, V206, P5; Holt PG, 1999, NATURE, V402, pB12; Hoshino M, 1998, J ALLERGY CLIN IMMUN, V102, P783, DOI 10.1016/S0091-6749(98)70018-1; JEFFERY PK, 1991, AM REV RESPIR DIS, V143, P1152; JEFFERY PK, 1992, RESPIRATION S1, V5, P13; Katz Y, 1999, CLIN EXP ALLERGY, V29, P186; Keane MP, 1999, J IMMUNOL, V162, P5511; KRISHNASWAMY G, 1999, VETERANS HLTH SYSTEM, V4, P44; Li L, 1998, J IMMUNOL, V161, P3128; Lukacs NW, 1999, J CLIN INVEST, V104, P995, DOI 10.1172/JCI8125; Lukacs NW, 1996, J LEUKOCYTE BIOL, V60, P573; Lukacs NW, 1997, J IMMUNOL, V158, P4478; MALO JL, 1979, CLIN ALLERGY, V9, P377, DOI 10.1111/j.1365-2222.1979.tb02496.x; Mehrad B, 1999, J IMMUNOL, V162, P1633; Proudfoot AEI, 1999, BIOCHEM PHARMACOL, V57, P451; Reed CE, 1999, J ALLERGY CLIN IMMUN, V103, P539, DOI 10.1016/S0091-6749(99)70221-6; ROCHE WR, 1989, LANCET, V1, P520; SCHAFFNER A, 1982, J CLIN INVEST, V69, P617, DOI 10.1172/JCI110489; SMITH RE, 1995, J LEUKOCYTE BIOL, V57, P782; Smith RE, 1996, BIOL SIGNAL, V5, P223; Stafford S, 1997, J IMMUNOL, V158, P4953; Taramelli D, 1996, J MED VET MYCOL, V34, P49; Topham PS, 1999, J CLIN INVEST, V104, P1549, DOI 10.1172/JCI7707; Wells TNC, 1996, J LEUKOCYTE BIOL, V59, P53; Zhu Zhou, 1999, Journal of Clinical Investigation, V103, P779, DOI 10.1172/JCI5909	47	94	101	0	3	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	AUG 1	2000	165	3					1564	1572				9	Immunology	Immunology	337CV	WOS:000088340600053	10903765	
J	Zollner, TM; Wichelhaus, TA; Hartung, A; Von Mallinckrodt, C; Wagner, TOF; Brade, V; Kaufmann, R				Zollner, TM; Wichelhaus, TA; Hartung, A; Von Mallinckrodt, C; Wagner, TOF; Brade, V; Kaufmann, R			Colonization with superantigen-producing Staphylococcus aureus is associated with increased severity of atopic dermatitis	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						atopic dermatitis; cutaneous lymphocyte-associated antigen; Staphylococcus aureus; SCORAD; specific IgE against SEA/SEB; staphylococcal enterotoxins; superantigen; T cell skin homing	SHOCK SYNDROME TOXIN-1; LYMPHOCYTE-ASSOCIATED ANTIGEN; BLOOD MONONUCLEAR-CELLS; HUMAN T-LYMPHOCYTES; BACTERIAL SUPERANTIGENS; IGE ANTIBODIES; UP-REGULATION; SKIN; ENTEROTOXINS; EXPRESSION	Background Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with colonization of the skin with Staphylococcus aureus known to produce toxins with superantigen (SAg) activity. Besides T-cell activation these toxins induce T-cell skin homing in vitro. This may contribute to the observed induction or enhancement of skin inflammation. Objective The aim of this study was to determine whether colonization with SAg-producing S. aureus isolates modulates the intensity of AD. If so, it was of interest whether this may be primarily due to the toxins' effects as SAgs or as allergens. Methods In AD patients, healthy controls, and atopic controls SAg production by S. aureus isolated from skin or mucous membranes was investigated and correlated to the severity of the disease. Total IgE, SAg-specific IgE, and T-cell activation and recirculation markers were analysed and correlated with SAg production. Results Fifty-seven percent of S. aureus strains isolated from AD patients produced SAgs. This frequency was higher compared to healthy controls (33%). SAg production by S. aureus was correlated with a significantly higher scoring of AD (SCORAD index, 58 +/- 19 in SAg-producing vs 41 +/- 7 in non-SAg-producing germs; P < 0.05). However, the severity of the disease was not associated with sensitization against the SAgs staphylococcal enterotoxin A (SEA) and staphylococcal enterotoxin B (SEB). Furthermore, SAg production by S. aureus was inversely correlated with total IgE concentration (P < 0.05) and positively correlated with T-cell activation (as measured by HLA-DR and CD69 expression) and the expression of the T-cell skin homing phenotype cutaneous lymphocyte-associated antigen. Conclusion SAg production by S. aureus is suggested to be associated with an increased severity of atopic dermatitis. Since SAg production was found neither exclusively in AD patients nor in all patients, other pathogenic factors may be additionally effective.	Univ Frankfurt, Sch Med, Dept Dermatol, D-60590 Frankfurt, Germany; Univ Frankfurt, Sch Med, Dept Med Microbiol, D-60590 Frankfurt, Germany; Univ Frankfurt, Sch Med, Dept Pulmonol, D-60590 Frankfurt, Germany	Zollner, TM (reprint author), Univ Frankfurt, Sch Med, Dept Dermatol, Theodor Stern Kai 7, D-60590 Frankfurt, Germany.						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Michael, 1995, P19; NEUBER K, 1995, INT ARCH ALLERGY IMM, V107, P179; Nissen D, 1997, ANN ALLERG ASTHMA IM, V79, P403; Piletta PA, 1996, ARCH DERMATOL, V132, P1171, DOI 10.1001/archderm.132.10.1171; PODDA M, 1999, ARCH DERMATOL RES, V291, pA108; Reekers R, 1999, J ALLERGY CLIN IMMUN, V104, P466, DOI 10.1016/S0091-6749(99)70395-7; SALOGA J, 1996, J INVEST DERMATOL, V107, P603; SCHMIDT A, 1996, MUNCH MED WSCHR, V138, P432; STALDER JF, 1993, DERMATOLOGY, V186, P23; Strange P, 1996, ARCH DERMATOL, V132, P27, DOI 10.1001/archderm.132.1.27; Strickland I, 1999, J INVEST DERMATOL, V112, P249, DOI 10.1046/j.1523-1747.1999.00502.x; Tada J, 1996, EUR J DERMATOL, V6, P552; Torres MJ, 1998, CLIN EXP ALLERGY, V28, P1264; Zollner TM, 1996, IMMUNOL LETT, V49, P111, DOI 10.1016/0165-2478(95)02491-3; Zollner TM, 1999, J INVEST DERMATOL, V112, P118; Zollner TM, 1997, EXP DERMATOL, V6, P161, DOI 10.1111/j.1600-0625.1997.tb00200.x	39	94	101	0	3	BLACKWELL SCIENCE LTD	OXFORD	P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	JUL	2000	30	7					994	1000				7	Allergy; Immunology	Allergy; Immunology	334CP	WOS:000088167800013	10848922	
J	Muraro, A; Halken, S; Arshad, SH; Beyer, K; Dubois, AEJ; Du Toit, G; Eigenmann, PA; Grimshaw, KEC; Hoest, A; Lack, G; O'Mahony, L; Papadopoulos, NG; Panesar, S; Prescott, S; Roberts, G; de Silva, D; Venter, C; Verhasselt, V; Akdis, AC; Sheikh, A				Muraro, A.; Halken, S.; Arshad, S. H.; Beyer, K.; Dubois, A. E. J.; Du Toit, G.; Eigenmann, P. A.; Grimshaw, K. E. C.; Hoest, A.; Lack, G.; O'Mahony, L.; Papadopoulos, N. G.; Panesar, S.; Prescott, S.; Roberts, G.; de Silva, D.; Venter, C.; Verhasselt, V.; Akdis, A. C.; Sheikh, A.		EAACI Food Allergy Anaphylaxis	EAACI Food Allergy and Anaphylaxis Guidelines. Primary prevention of food allergy	ALLERGY			English	Article						primary prevention; food allergy; children; EAACI; guidelines	RANDOMIZED CONTROLLED-TRIAL; HYDROLYZED INFANT FORMULAS; FISH-OIL SUPPLEMENTATION; PLACEBO-CONTROLLED TRIAL; BRIEF NEONATAL EXPOSURE; HIGH-RISK CHILDREN; COWS MILK ALLERGY; ATOPIC DISEASE; FOLLOW-UP; BIRTH COHORT	Food allergy can have significant effects on morbidity and quality of life and can be costly in terms of medical visits and treatments. There is therefore considerable interest in generating efficient approaches that may reduce the risk of developing food allergy. This guideline has been prepared by the European Academy of Allergy and Clinical Immunology's (EAACI) Taskforce on Prevention and is part of the EAACI Guidelines for Food Allergy and Anaphylaxis. It aims to provide evidence-based recommendations for primary prevention of food allergy. A wide range of antenatal, perinatal, neonatal, and childhood strategies were identified and their effectiveness assessed and synthesized in a systematic review. Based on this evidence, families can be provided with evidence-based advice about preventing food allergy, particularly for infants at high risk for development of allergic disease. The advice for all mothers includes a normal diet without restrictions during pregnancy and lactation. For all infants, exclusive breastfeeding is recommended for at least first 4-6months of life. If breastfeeding is insufficient or not possible, infants at high-risk can be recommended a hypoallergenic formula with a documented preventive effect for the first 4months. There is no need to avoid introducing complementary foods beyond 4months, and currently, the evidence does not justify recommendations about either withholding or encouraging exposure to potentially allergenic foods after 4months once weaning has commenced, irrespective of atopic heredity. There is no evidence to support the use of prebiotics or probiotics for food allergy prevention.	[Muraro, A.] Univ Padua, Dept Mother & Child Hlth, Referral Ctr Food Allergy Diag & Treatment, I-35128 Padua, Italy; [Halken, S.; Hoest, A.] Odense Univ Hosp, Hans Christian Andersen Childrens Hosp, DK-5000 Odense, Denmark; [Arshad, S. H.; Grimshaw, K. E. C.; Roberts, G.] Univ Southampton, Fac Med, Clin & Expt Sci Acad Unit, Southampton SO9 5NH, Hants, England; [Arshad, S. H.; Roberts, G.; Venter, C.] St Marys Hosp, David Hide Asthma & Allergy Res Ctr, Newport, Wight, England; [Arshad, S. H.; Roberts, G.] Univ Hosp Southampton NHS Fdn Trust, NIHR Resp Biomed Res Unit, Southampton, Hants, England; [Beyer, K.] Charite, Clin Pediat Pneumol & Immunol, D-13353 Berlin, Germany; [Dubois, A. E. J.] Univ Groningen, Univ Med Ctr Groningen, GRIAC Res Inst, Dept Pediat Pulmonol & Paediat Allergy, Groningen, Netherlands; [Du Toit, G.; Lack, G.] Kings Coll London, Guys & St Thomas NHS Fdn Trust, Dept Paediat Allergy, MRC,Div Asthma Allergy & Lung Biol, London WC2R 2LS, England; [Du Toit, G.; Lack, G.] Kings Coll London, Guys & St Thomas NHS Fdn Trust, Asthma UK Ctr Allerg Mechanisms Asthma, London WC2R 2LS, England; [Eigenmann, P. A.] Univ Hosp Geneva, Dept Child & Adolescent, Allergy Unit, Geneva, Switzerland; [O'Mahony, L.] Univ Zurich, Swiss Inst Allergy & Asthma Res, Zurich, Switzerland; [Papadopoulos, N. G.] Univ Manchester, Inst Human Dev, Manchester, Lancs, England; [Papadopoulos, N. G.] Univ Athens, Dept Allergy, Pediat Clin 2, Athens, Greece; [Panesar, S.; de Silva, D.] Evidence Based Hlth Care Ltd, Edinburgh, Midlothian, Scotland; [Prescott, S.] Univ Western Australia, Sch Paediat & Child Hlth Res, Perth, WA 6009, Australia; [Venter, C.] Univ Portsmouth, Sch Hlth Sci & Social Work, Portsmouth, Hants, England; [Verhasselt, V.] Univ Nice Sophia Antipolis, Hop Archet, EA Tolerance Immunitaire 6302, F-06189 Nice, France; [Akdis, A. C.] Univ Zurich, Swiss Inst Allergy & Asthma Res SIAF, Davos, Switzerland; [Sheikh, A.] Univ Edinburgh, Ctr Populat Hlth Sci, Allergy & Resp Res Grp, Edinburgh EH8 9YL, Midlothian, Scotland; [Sheikh, A.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Gen Internal Med & Primary Care, Boston, MA 02115 USA	Muraro, A (reprint author), Univ Padua, Dept Mother & Child Hlth, Referral Ctr Food Allergy Diag & Treatment, Via Giustiniani 3, I-35128 Padua, Italy.	muraro@centroallergiealimentari.eu	Sheikh, Aziz /D-2818-2009; Prescott, Susan/H-5665-2014; Eigenmann, Philippe/A-6569-2017	Sheikh, Aziz /0000-0001-7022-3056; Eigenmann, Philippe/0000-0003-1738-1826; Grimshaw, Kate/0000-0003-3649-7963	Medical Research Council [G1000758]		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; BARDARE M, 1993, ANN ALLERGY, V71, P366; Brouwers MC, 2010, PREV MED, V51, P421, DOI 10.1016/j.ypmed.2010.08.005; 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Immunology	AE2QB	WOS:000333816900006	24697491	
J	Soroosh, P; Doherty, TA; Duan, W; Mehta, AK; Choi, H; Adams, YF; Mikulski, Z; Khorram, N; Rosenthal, P; Broide, DH; Croft, M				Soroosh, Pejman; Doherty, Taylor A.; Duan, Wei; Mehta, Amit Kumar; Choi, Heonsik; Adams, Yan Fei; Mikulski, Zbigniew; Khorram, Naseem; Rosenthal, Peter; Broide, David H.; Croft, Michael			Lung-resident tissue macrophages generate Foxp3(+) regulatory T cells and promote airway tolerance	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article							HOUSE-DUST MITE; ALVEOLAR MACROPHAGES; DENDRITIC CELLS; RETINOIC-ACID; ALLERGIC INFLAMMATION; INHALED ANTIGEN; TGF-BETA; ASPERGILLUS-FUMIGATUS; IMMUNE-RESPONSE; FLOW-CYTOMETRY	Airway tolerance is the usual outcome of inhalation of harmless antigens. Although T cell deletion and anergy are likely components of tolerogenic mechanisms in the lung, increasing evidence indicates that antigen-specific regulatory T cells (inducible T-reg cells [iT(reg) cells]) that express Foxp3 are also critical. Several lung antigen-presenting cells have been suggested to contribute to tolerance, including alveolar macrophages (Mempty sets), classical dendritic cells (DCs), and plasmacytoid DCs, but whether these possess the attributes required to directly promote the development of Foxp3(+) iT(reg) cells is unclear. Here, we show that lung-resident tissue Mempty sets coexpress TGF-beta and retinal dehydrogenases (RALDH1 and RALDH 2) under steady-state conditions and that their sampling of harmless airborne antigen and presentation to antigen-specific CD4 T cells resulted in the generation of Foxp3(+) T-reg cells. T-reg cell induction in this model depended on both TGF-beta and retinoic acid. Transfer of the antigen-pulsed tissue Mempty sets into the airways correspondingly prevented the development of asthmatic lung inflammation upon subsequent challenge with antigen. Moreover, exposure of lung tissue Mempty sets to allergens suppressed their ability to generate iT(reg) cells coincident with blocking airway tolerance. Suppression of T-reg cell generation required proteases and TLR-mediated signals. Therefore, lung-resident tissue Mempty sets have regulatory functions, and strategies to target these cells might hold promise for prevention or treatment of allergic asthma.	[Soroosh, Pejman; Duan, Wei; Mehta, Amit Kumar; Choi, Heonsik; Adams, Yan Fei; Croft, Michael] La Jolla Inst Allergy & Immunol, Div Immune Regulat, La Jolla, CA 92037 USA; [Mikulski, Zbigniew] La Jolla Inst Allergy & Immunol, Div Inflammat Biol, La Jolla, CA 92037 USA; [Doherty, Taylor A.; Khorram, Naseem; Rosenthal, Peter; Broide, David H.] Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA	Croft, M (reprint author), La Jolla Inst Allergy & Immunol, Div Immune Regulat, La Jolla, CA 92037 USA.	mick@liai.org	Mehta, Amit Kumar/D-7585-2016	Mikulski, Zbigniew/0000-0002-1918-9216	National Institutes of Health [CA91837, AI70535]	This work was supported by National Institutes of Health grants CA91837 and AI70535 to M. Croft. This is manuscript number # 1534 from the La Jolla Institute for Allergy and Immunology.	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Exp. Med.	APR 8	2013	210	4					775	788		10.1084/jem.20121849		14	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	121ZP	WOS:000317284900012	23547101	
J	Ramasamy, A; Curjuric, I; Coin, LJ; Kumar, A; McArdle, WL; Imboden, M; Leynaert, B; Kogevinas, M; Schmid-Grendelmeier, P; Pekkanen, J; Wjst, M; Bircher, AJ; Sovio, U; Rochat, T; Hartikainen, AL; Balding, DJ; Jarvelin, MR; Probst-Hensch, N; Strachan, DP; Jarvis, DL				Ramasamy, Adaikalavan; Curjuric, Ivan; Coin, Lachlan J.; Kumar, Ashish; McArdle, Wendy L.; Imboden, Medea; Leynaert, Benedicte; Kogevinas, Manolis; Schmid-Grendelmeier, Peter; Pekkanen, Juha; Wjst, Matthias; Bircher, Andreas J.; Sovio, Ulla; Rochat, Thierry; Hartikainen, Anna-Liisa; Balding, David J.; Jarvelin, Marjo-Riitta; Probst-Hensch, Nicole; Strachan, David P.; Jarvis, Deborah L.			A genome-wide meta-analysis of genetic variants associated with allergic rhinitis and grass sensitization and their interaction with birth order	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Hay fever; IgE sensitization to grass; hygiene hypothesis; older siblings; gene-environment interaction; genome-wide association study; European Community Respiratory Health Survey; British 1958 Birth Cohort; Northern Finland Birth Cohort of 1966; Swiss Study on Air Pollution and Lung Disease in Adults	RESPIRATORY-HEALTH-SURVEY; HAY-FEVER; ENVIRONMENT INTERACTION; FILAGGRIN MUTATIONS; CHILDHOOD ECZEMA; CHROMOSOME 11Q13; ASTHMA; COHORT; EXPOSURE; DISEASES	Background: Hay fever or seasonal allergic rhinitis (AR) is a chronic disorder associated with IgE sensitization to grass. The underlying genetic variants have not been studied comprehensively. There is overwhelming evidence that those who have older siblings have less AR, although the mechanism for this remains unclear. Objective: We sought to identify common genetic variant associations with prevalent AR and grass sensitization using existing genome-wide association study (GWAS) data and to determine whether genetic variants modify the protective effect of older siblings. Method: Approximately 2.2 million genotyped or imputed single nucleotide polymorphisms were investigated in 4 large European adult cohorts for AR (3,933 self-reported cases vs 8,965 control subjects) and grass sensitization (2,315 cases vs 10,032 control subjects). Results: Three loci reached genome-wide significance for either phenotype. The HLAvariant rs7775228, which cis-regulates HLA-DRB4, was strongly associated with grass sensitization and weakly with AR (P-grass = 1.6 x 10(-9); P-AR = 8.0 x 10(-3)). Variants in a locus near chromosome 11 open reading frame 30 (C11orf30) and leucine-rich repeat containing 32 (LRRC32), which was previously associated with atopic dermatitis and eczema, were also strongly associated with both phenotypes (rs2155219; P-grass = 9.4 x 10(-9); P-AR = 3.8 x 10(-8))(.) The third genome-wide significant variant was rs17513503 (P-grass = 1.2 x 10(-8); PAR = 7.4 x 10(-7)) which was located near transmembrane protein 232 (TMEM232) and solute carrier family 25, member 46 (SLC25A46). Twelve further loci with suggestive associations were also identified. Using a candidate gene approach, where we considered variants within 164 genes previously thought to be important, we found variants in 3 further genes that may be of interest: thymic stromal lymphopoietin (TSLP), Toll-like receptor 6 (TLR6) and nucleotide-binding oligomerization domain containing 1 (NOD1/CARD4). We found no evidence for variants that modified the effect of birth order on either phenotype. Conclusions: This relatively large meta-analysis of GWASs identified few loci associated with AR and grass sensitization. No birth order interaction was identified in the current analyses. (J Allergy Clin Immunol 2011;128:996-1005.)	[Ramasamy, Adaikalavan] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW3 6LR, England; [Curjuric, Ivan; Kumar, Ashish; Imboden, Medea; Probst-Hensch, Nicole] Swiss Trop & Publ Hlth Inst, Basel, Switzerland; [Curjuric, Ivan; Imboden, Medea; Bircher, Andreas J.; Probst-Hensch, Nicole] Univ Basel, CH-4003 Basel, Switzerland; [Coin, Lachlan J.; Sovio, Ulla; Jarvelin, Marjo-Riitta] Univ London Imperial Coll Sci Technol & Med, Dept Epidemiol & Biostat, London SW3 6LR, England; [Kumar, Ashish] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX1 2JD, England; [Kumar, Ashish] Univ Oxford, Oxford Ctr Diabet Endocrinol & Metab, Oxford OX1 2JD, England; [McArdle, Wendy L.] Univ Bristol, Dept Social & Community Med, Avon Longitudinal Study Parents & Children ALSPAC, Bristol BS8 1TH, Avon, England; [Leynaert, Benedicte] INSERM, U700, Paris, France; [Kogevinas, Manolis] Ctr Res Environm Epidemiol, Barcelona, Spain; [Kogevinas, Manolis] IMIM Hosp del Mar, Municipal Inst Med Res, Barcelona, Spain; [Kogevinas, Manolis] CIBER Epidemiol & Salud Publ, Barcelona, Spain; [Kogevinas, Manolis] Univ Crete, Sch Med, Dept Social Med, Iraklion, Greece; [Schmid-Grendelmeier, Peter] Univ Zurich Hosp, Dept Dermatol, Allergy Unit, Zurich, Switzerland; [Pekkanen, Juha] Natl Inst Hlth & Welf THL, Dept Environm Hlth, Helsinki, Finland; [Pekkanen, Juha] Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland; [Wjst, Matthias] Helmholtz Zentrum Munchen German Res Ctr Environm, Munich, Germany; [Bircher, Andreas J.] Univ Basel Hosp, Dept Dermatol, Allergy Unit, Basel, Switzerland; [Sovio, Ulla] London Sch Hyg & Trop Med, Dept Med Stat, London, England; [Rochat, Thierry] Univ Hosp Geneva, Div Pulm Med, Geneva, Switzerland; [Hartikainen, Anna-Liisa] Univ Oulu, Inst Clin Med, Dept Clin Sci Obstet & Gynecol, Oulu, Finland; [Balding, David J.] UCL, Inst Genet, London WC1E 6BT, England; [Jarvelin, Marjo-Riitta; Jarvis, Deborah L.] Univ London Imperial Coll Sci Technol & Med, MRC HPA Ctr Environm & Hlth, London SW3 6LR, England; [Strachan, David P.] Univ London, Div Community Hlth Sci, London WC1E 7HU, England	Jarvis, DL (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Emmanuel Kaye Bldg,Manressa Rd, London SW3 6LR, England.	d.jarvis@imperial.ac.uk	Balding, David/G-9898-2011; Ramasamy, Adaikalavan/G-2632-2010; Coin, Lachlan/A-9001-2014; Kogevinas, Manolis/C-3918-2017	Balding, David/0000-0002-1480-6115; Ramasamy, Adaikalavan/0000-0002-7598-2892; Coin, Lachlan/0000-0002-4300-455X; Kumar, Ashish/0000-0002-7075-5930; Jarvelin, Marjo-Riitta/0000-0002-2149-0630	European Commission [018996]; Department of Health, United Kingdom; Medical Research Council [G0500539]; Helmholtz Center; EU Project European; Swiss National Foundation for Scientific Research	Details of the many charities, governmental bodies, and scientific funding organizations that supported the epidemiologic study, including phenotyping, DNA collection, and genotyping for the British 1958 Birth Cohort (B58C), the European Community Respiratory Health Survey (ECRHS2), the Northern Finland Birth Cohort of 1966 (NFBC1966), and the Swiss Study on Air Pollution and Lung Disease in Adults (SAPALDIA), can be found in this article's Online Repository at www.jacionline.org. A. R. has received research support from the European Commission (through project GABRIEL, contract no. 018996 under the Integrated Program LSH-2004-1.2.5-1) and the Department of Health, United Kingdom. U.S. was supported by Medical Research Council studentship grant G0500539.; Disclosure of potential conflict of interest: M. Wjst receives research support from the Helmholtz Center and EU Project European. T. Rochat receives research support from the Swiss National Foundation for Scientific Research. 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					996	1005		10.1016/j.jaci.2011.08.030		10	Allergy; Immunology	Allergy; Immunology	842FJ	WOS:000296578200012	22036096	
J	Apeagyei, E; Bank, MS; Spengler, JD				Apeagyei, Eric; Bank, Michael S.; Spengler, John D.			Distribution of heavy metals in road dust along an urban-rural gradient in Massachusetts	ATMOSPHERIC ENVIRONMENT			English	Article						Heavy metal; Road dust; Tire wear; Brake wear; Traffic-related emissions	PARTICULATE MATTER; HONG-KONG; PARTICLE RESUSPENSION; SOURCE PROFILES; AIR-POLLUTION; STREET DUSTS; CONTAMINATION; ASTHMA; SOILS; EMISSIONS	Human exposures to particulate matter emitted from on-road motor vehicles include complex mixtures of metals from tires, brakes, parts wear and resuspended road dust. The aim of this study was to assess road dust for metals associated with motor vehicle traffic, particularly those metals coming from brake and tire wears. We hypothesized that the road dust would show significant difference in both composition and concentration by traffic type, road class and by location. X-ray fluorescence (XRF) analyses of 115 parked car tires showed Zn and Ca were likely associated with tire wear dust. XRF results of three used brake pads indicated high concentrations of Fe, Ti, Cu, Ba, Mo and Zr. To assess heavy metal exposures associated with tires and brake wear adjacent to roads of varying traffic and functional classes, 85 samples of road dust were collected from road surfaces adjacent to the curb and analyzed by XRF. Median concentrations for Fe. Ca and K were greater than Ti (1619 ppm), with concentration ratios of Fe: Ca: K: Ti [16:5:3:1]. Cumulative frequency distribution graphs showed distribution of Fe, Ba, Cu, and Mo were similar regardless of road traffic rating. However, Zn, Ti, and Zr varied significantly (p < 0.05) with traffic ratings of roadways (heavy > moderate > low traffic). Fe, Ba, Cu, and Mo also had similar distributions regardless of road class while composition of Zn, Ti, and Zr varied significantly across road class (p < 0.05) (Major roads > Minor roads > highway). In comparing urban road dust to rural road dust, we observed Fe, Ca, K, and Ti were significantly greater in urban road dust (p < 0.05). In urban road dust the Fe: Ca: K: Ti relationship with median Ti of 2216 ppm was 12: 6: 3.5: 1. These results indicate that roadway dust may be important sources of metals for runoff water and localized resuspended particulate matter. (C) 2010 Elsevier Ltd. All rights reserved.	[Spengler, John D.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Landmark Ctr W, Boston, MA 02215 USA	Spengler, JD (reprint author), Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Landmark Ctr W, Room 406,401 Pk Dr, Boston, MA 02215 USA.	spengler@hsph.harvard.edu			Harvard NIEHS Center for Environmental Health [ES00002]	The authors gratefully acknowledge Dr. James Shine, Yongmei Shen, Jose Vallerino and Steve Melly of the Harvard School of Public Health for their help with XRF analyses, sample preparation, and traffic classification of roads, respectively. We wish to thank David Moscaritolo and Derick Brain for their road dust sampling work at the early stage of the project. This research was supported by the Harvard NIEHS Center for Environmental Health grant (ES00002).	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Environ.	APR	2011	45	13					2310	2323		10.1016/j.atmosenv.2010.11.015		14	Environmental Sciences; Meteorology & Atmospheric Sciences	Environmental Sciences & Ecology; Meteorology & Atmospheric Sciences	753ZG	WOS:000289819200016		
J	Heinrich, J				Heinrich, Joachim			Influence of indoor factors in dwellings on the development of childhood asthma	INTERNATIONAL JOURNAL OF HYGIENE AND ENVIRONMENTAL HEALTH			English	Review						Asthma; Children; Incidence; Indoor factor; Epidemiology	POLYCYCLIC AROMATIC-HYDROCARBONS; VOLATILE ORGANIC-COMPOUNDS; HOUSE-DUST MITE; ENVIRONMENTAL TOBACCO-SMOKE; NITROGEN-DIOXIDE EXPOSURE; CHILDRENS RESPIRATORY HEALTH; OUTDOOR AIR-POLLUTION; SCHOOL-AGE-CHILDREN; 1ST 5 YEARS; YOUNG-CHILDREN	Asthma has become the most common, childhood chronic disease in the industrialized world, and it is also increasing in developing regions. There are huge differences in the prevalence of childhood asthma across countries and continents, and there is no doubt that the prevalence of asthma was strongly increasing during the past decades worldwide. Asthma, as a complex disease, has a broad spectrum of potential determinants ranging from genetics to life style and environmental factors. Environmental factors are likely to be important in explaining the regional differences and the overall increasing trend towards asthma's prevalence. Among the environmental conditions, indoor factors are of particular interest because people spend more than 80% of their time indoors globally. Increasing prices for oil, gas and other sources of primary energy will further lead to better insulation of homes, and ultimately to reduced energy costs. This will decrease air exchange rates and will lower the dilution of indoor air mass with ambient air. Indoor air quality and potential health effects will therefore be an area for future research and for gaining a better understanding of asthma epidemics. This strategic review will summarize the current knowledge of the effects of a broad spectrum of indoor factors on the development of asthma in childhood in Western countries based on epidemiological studies. In conclusion, several epidemiological studies point out, that indoor factors might cause asthma in childhood. Stronger and more consistent findings are seen when exposure to these indoor factors is assessed by surrogates for the source of the actual toxicants. Measurement-based exposure assessments for several indoor factors are less common than using surrogates of the exposure. These studies, however, mainly showed heterogeneous results. The most consistent finding for an induction of asthma in childhood is related to exposure to environmental tobacco smoke, to living in homes close to busy roads, and in damp homes where are visible moulds at home. The causing agents of the increased risk of living in damp homes remained uncertain and needs clarification. Exposure to pet-derived allergens and house dust mites are very commonly investigated and thought to be related to asthma onset. The epidemiological evidence is not sufficient to recommend avoidance measures against pet and dust mites as preventive activities against allergies. More research is also needed to clarify the potential risk for exposure to volatile and semi-volatile organic compounds due to renovation activities, phthalates and chlorine chemicals due to cleaning. (C) 2010 Elsevier GmbH. All rights reserved.	[Heinrich, Joachim] Helmholtz Zentrum Munchen, Natl Res Ctr Environm Hlth, Inst Epidemiol, Munich, Germany	Heinrich, J (reprint author), Helmholtz Zentrum Munchen, Inst Epidemiol, Ingolstadter Landstr 1, D-85764 Neuherberg, Germany.	joachim.heinrich@helmholtz-muenchen.de			European Centre for Ecotoxicology and Toxicology of Chemicals (ECETOC)	This literature review was supported by a contract from the European Centre for Ecotoxicology and Toxicology of Chemicals (ECETOC). The views expressed and conclusions drawn are those of the author.	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J. Hyg. Environ. Health.	JAN	2011	214	1					3	27		10.1016/j.ijheh.2010.08.009		25	Public, Environmental & Occupational Health; Infectious Diseases	Public, Environmental & Occupational Health; Infectious Diseases	739BL	WOS:000288687200001	20851050	
J	Zuberbier, T; Bachert, C; Bousquet, PJ; Passalacqua, G; Canonica, GW; Merk, H; Worm, M; Wahn, U; Bousquet, J				Zuberbier, T.; Bachert, C.; Bousquet, P. J.; Passalacqua, G.; Canonica, G. Walter; Merk, H.; Worm, M.; Wahn, U.; Bousquet, J.			GA(2)LEN/EAACI pocket guide for allergen-specific immunotherapy for allergic rhinitis and asthma	ALLERGY			English	Article						allergen; European Academy of Allergy and Immunology (EAACI); Global Allergy and Asthma European Network (GA(2)LEN); immunotherapy; subcutaneous; sublingual	HOUSE-DUST MITE; DERMATOPHAGOIDES-PTERONYSSINUS EXTRACT; CONSORT STATEMENT; GRASS-POLLEN; FOLLOW-UP; SUBLINGUAL IMMUNOTHERAPY; RANDOMIZED-TRIALS; CLINICAL-EFFICACY; DOUBLE-BLIND; 2008 UPDATE	This pocket guide is the result of a consensus reached during several GA(2)LEN and EAACI meetings. The aim of the current pocket guide is to offer a comprehensive set of recommendations on the use of immunotherapy in allergic rhinoconjunctivitis and asthma in daily practice. This pocket guide is meant to give simple answers to the most frequent questions of practitioners in Europe, including 'practising allergists', general practitioners and any other physicians with special interest in allergen-specific immunotherapy (SIT). It is not a long or detailed scientific review of the topic. However, the recommendations in this pocket guide were compiled following an in-depth review of existing guidelines and publications, including the 1998 EAACI position paper, the 1998 WHO Position Paper on SIT and the 2001 Allergic Rhinitis and its Impact on Asthma (ARIA). It is also based on the ARIA update 2008 (prepared in collaboration with GA(2)LEN), the 'Sub-lingual Immunotherapy: WAO Position Paper 2009' (from the World Allergy Organisation) and the Methodology paper of ARIA. The recommendations cover patient selection, allergen extract to be used, route of administration of SIT (in particular, sublingual and subcutaneous immunotherapy), and necessary precautions to be followed in using SIT.	[Zuberbier, T.; Worm, M.; Wahn, U.] Charite, Dept Dermatol & Allergy, D-13353 Berlin, Germany; [Bachert, C.] Ghent Univ Hosp, Dept Otorhinolaryngol, B-9000 Ghent, Belgium; [Bousquet, P. J.; Bousquet, J.] CHU Montpellier, Montpellier, France; [Passalacqua, G.; Canonica, G. Walter] Univ Genoa, Dept Internal Med, I-16126 Genoa, Italy; [Merk, H.] Rhein Westfal TH Aachen, Univ Clin, Dept Dermatol & Allergol, Aachen, Germany; [Bousquet, J.] INSERM, CSEP, F-1018 Villejuif, France	Zuberbier, T (reprint author), Charite, Dept Dermatol & Allergy, D-13353 Berlin, Germany.	torsten.zuberbier@charite.de					Alvarez-Cuesta E, 2006, ALLERGY, V61, P1, DOI 10.1111/j.1398-9995.2006.01219_1.x; Begg C, 1996, JAMA-J AM MED ASSOC, V276, P637, DOI 10.1001/jama.276.8.637; Bousquet J, 2008, ALLERGY, V63, P8, DOI 10.1111/j.1398-9995.2007.01620.x; BOUSQUET J, 1988, J ALLERGY CLIN IMMUN, V82, P971, DOI 10.1016/0091-6749(88)90133-9; Bousquet J., 1998, Allergy (Copenhagen), V53, P1; Bousquet J, 2001, J ALLERGY CLIN IMMUN, V108, pS147, DOI 10.1067/mai.2001.118891; Bousquet J, 2009, J ALLERGY CLIN IMMUN, V124, P428, DOI 10.1016/j.jaci.2009.06.027; Bousquet PJ, 2009, ALLERGY, V64, P1737, DOI 10.1111/j.1398-9995.2009.02232.x; Boutron I, 2008, ANN INTERN MED, V148, P295; Brozek JL, 2008, ALLERGY, V63, P38, DOI 10.1111/j.1398-9995.2007.01560.x; Canonica GW, 2009, ALLERGY, V64, P1, DOI 10.1111/j.1398-9995.2009.02309.x; Casanovas M, 2005, CLIN EXP ALLERGY, V35, P1377, DOI 10.1111/j.1365-2222.2005.02343.x; Cools M, 2000, ALLERGY, V55, P69, DOI 10.1034/j.1398-9995.2000.00191.x; DesRoches A, 1997, J ALLERGY CLIN IMMUN, V99, P450, DOI 10.1016/S0091-6749(97)70069-1; Didier A, 2007, J ALLERGY CLIN IMMUN, V120, P1338, DOI 10.1016/j.jaci.2007.07.046; DURHAM SR, 1999, NEW ENGL J MED, V12, P341; Durham SR, 2010, J ALLERGY CLIN IMMUN, V125, P131, DOI 10.1016/j.jaci.2009.10.035; Eng PA, 2006, ALLERGY, V61, P198, DOI 10.1111/j.1398-9995.2006.01011.x; *EUR MED AG, 2008, HMPEWP85042006 EUR M; Inal A, 2007, J INVEST ALLERG CLIN, V17, P85; Jacobsen L, 2007, ALLERGY, V62, P943, DOI 10.1111/j.1398-9995.2007.01451.x; Khinchi MS, 2004, ALLERGY, V59, P45, DOI 10.1046/j.1398-9995.2003.00387.x; Malling HJ, 1998, ALLERGY, V53, P933, DOI 10.1111/j.1398-9995.1998.tb03793.x; Marogna M, 2007, ANN ALLERG ASTHMA IM, V98, P274; Moher D, 2001, LANCET, V357, P1191, DOI 10.1016/S0140-6736(00)04337-3; Pajno GB, 2001, CLIN EXP ALLERGY, V31, P1392, DOI 10.1046/j.1365-2222.2001.01161.x; Purello-D'Ambrosio F, 2001, CLIN EXP ALLERGY, V31, P1295, DOI 10.1046/j.1365-2222.2001.01027.x	27	93	111	0	5	WILEY-BLACKWELL	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0105-4538			ALLERGY	Allergy	DEC	2010	65	12					1525	1530		10.1111/j.1398-9995.2010.02474.x		6	Allergy; Immunology	Allergy; Immunology	673UG	WOS:000283688400003	21039596	
J	Holgate, ST; Arshad, HS; Roberts, GC; Howarth, PH; Thurner, P; Davies, DE				Holgate, Stephen T.; Arshad, Hasan S.; Roberts, Graham C.; Howarth, Peter H.; Thurner, Philipp; Davies, Donna E.			A new look at the pathogenesis of asthma	CLINICAL SCIENCE			English	Review						allergen; asthma; inflammation; remodelling; T-cell; virus infection	AIRWAY EPITHELIAL-CELLS; RESOLUTION COMPUTED-TOMOGRAPHY; THYMIC STROMAL LYMPHOPOIETIN; SMOOTH-MUSCLE; CHILDHOOD ASTHMA; BRONCHIAL HYPERRESPONSIVENESS; BARRIER FUNCTION; LUNG-FUNCTION; PERSISTENT ASTHMA; ATOPIC ASTHMA	Asthma is an inflammatory disorder of the conducting airways that has strong association with allergic sensitization. The disease is characterized by a polarized Th-2 (T-helper-2)-type T-cell response, but in general targeting this component of the disease with selective therapies has been disappointing and most therapy still relies on bronchodilators and corticosteroids rather than treating underlying disease mechanisms. With the disappointing outcomes of targeting individual Th-2 cytokines or manipulating T-cells, the time has come to re-evaluate the direction of research in this disease. A case is made that asthma has its origins in the airways themselves involving defective structural and functional behaviour of the epithelium in relation to environmental insults. Specifically, a defect in barrier function and an impaired innate immune response to viral infection may provide the substrate upon which allergic sensitization takes place. Once sensitized, the repeated allergen exposure will lead to disease persistence. These mechanisms could also be used to explain airway wall remodelling and the susceptibility of the asthmatic lung to exacerbations provoked by respiratory viruses, air pollution episodes and exposure to biologically active allergens. Variable activation of this epithelial mesenchymal trophic unit could also lead to the emergence of different asthma phenotypes and a more targeted approach to the treatment of these. It also raises the possibility of developing treatments that increase the lung's resistance to the inhaled environment rather than concentrating all efforts on trying to suppress inflammation once it has become established.	[Holgate, Stephen T.; Arshad, Hasan S.; Roberts, Graham C.; Howarth, Peter H.; Davies, Donna E.] Univ Southampton, Div Infect Inflammat & Immun, Southampton Gen Hosp, Southampton S016 6YD, Hants, England; [Thurner, Philipp] Univ Southampton, Bioengn Sci Res Grp, Southampton S017 1BJ, Hants, England	Holgate, ST (reprint author), Univ Southampton, Div Infect Inflammat & Immun, Southampton Gen Hosp, Southampton S016 6YD, Hants, England.	sth@soton.ac.uk	Thurner, Philipp/A-3887-2012; Davies, Donna/H-2993-2012	Thurner, Philipp/0000-0001-7588-9041	Medical Research Council (MRC), Asthma UK, Asthma; Allergy Inflammation and Repair (AAIR); British Lung Foundation	We wish to acknowledge the Medical Research Council (MRC), Asthma UK, Asthma, Allergy Inflammation and Repair (AAIR), and the British Lung Foundation for supporting research that underpins this review. S.T.H. is an MRC Clinical Professor.	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J	Holloway, JW; Yang, IA; Holgate, ST				Holloway, John W.; Yang, Ian A.; Holgate, Stephen T.			Genetics of allergic disease	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Heritability; genetics; genetic testing; pharmacogenetics; epigenetics	GENOME-WIDE ASSOCIATION; DIISOCYANATE-INDUCED ASTHMA; SEVERE PERSISTENT ASTHMA; IMPROVED LUNG-FUNCTION; OF-FUNCTION MUTATIONS; DUST-MITE EXPOSURE; HYPER-IGE SYNDROME; CHILDHOOD ASTHMA; FILAGGRIN MUTATIONS; ATOPIC-DERMATITIS	Allergic diseases are complex genetic diseases resulting from the effect of multiple genetic and interacting environmental factors on their pathophysiology. Recent years have seen considerable progress in unraveling the contribution of these factors to an individual subject's susceptibility to, subsequent development of, and severity of disease. This has resulted in increasing insight into novel areas of allergic disease pathophysiology, for example the significant role played by locally acting tissue susceptibility factors like epithelial/epidermal barrier function and remodeling, such as filaggrin, ADAM33, and GSDML/ORMDL3, in patients with atopic dermatitis and asthma. Furthermore, studies of gene-environment interactions and Mendelian randomization approaches have led to increased insight into the importance of environmental triggers for allergic disease. Studies of the timing of action of genetic variants in determining disease susceptibility have highlighted the importance of in utero development and early life in determining susceptibility to allergic disease. In the future, genetic discoveries in allergic disease will potentially lead to better endophenotyping, prognostication, prediction of treatment response, and insights into molecular pathways to develop more targeted therapy for these conditions. (J Allergy Clin Immunol 2010;125:S81-94.)	[Holloway, John W.; Holgate, Stephen T.] Southampton Gen Hosp, Sch Med, Div Infect Inflammat & Immun, Southampton SO16 6YD, Hants, England; [Holloway, John W.] Southampton Gen Hosp, Sch Med, Div Human Genet, Southampton SO16 6YD, Hants, England; [Yang, Ian A.] Univ Queensland, Dept Thorac Med, Prince Charles Hosp, Brisbane, Qld, Australia; [Yang, Ian A.] Univ Queensland, Sch Med, Brisbane, Qld, Australia	Holloway, JW (reprint author), Southampton Gen Hosp, Sch Med, Div MP810 3, Southampton SO16 6YD, Hants, England.	J.W.Holloway@southampton.ac.uk	Holloway, John/B-5424-2009; Yang, Ian/B-9609-2008	Holloway, John/0000-0001-9998-0464; Yang, Ian/0000-0001-8338-1993	Medical Research Council [G19/34, G0400473, G0800766]		Allen M, 2003, NAT GENET, V35, P258, DOI 10.1038/ng1256; Altshuler D, 2005, NATURE, V437, P1299, DOI 10.1038/nature04226; Altshuler D, 2008, SCIENCE, V322, P881, DOI 10.1126/science.1156409; Anderson GP, 2008, LANCET, V372, P1107, DOI 10.1016/S0140-6736(08)61452-X; Baccarelli A, 2009, AM J RESP CRIT CARE, V179, P572, DOI 10.1164/rccm.200807-1097OC; Balaci L, 2007, AM J HUM GENET, V80, P1103, DOI 10.1016/518259; Barton SJ, 2009, J ALLERGY CLIN IMMUN, V123, P1391, DOI 10.1016/j.jaci.2009.03.014; Barton SJ, 2009, J ALLERGY CLIN IMMUN, V123, pe17; Baurecht H, 2007, J ALLERGY CLIN IMMUN, V120, P1406, DOI 10.1016/j.jaci.2007.08.067; Benn CS, 2001, CLIN EXP ALLERGY, V31, P1862, DOI 10.1046/j.1365-2222.2001.01128.x; Bieli C, 2007, J ALLERGY CLIN IMMUN, V120, P1308, DOI 10.1016/j.jaci.2007.07.034; 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Allergy Clin. Immunol.	FEB	2010	125	2		2			S81	S94		10.1016/j.jaci.2009.10.071		14	Allergy; Immunology	Allergy; Immunology	629CC	WOS:000280170600008	20176270	
J	Pettipher, R				Pettipher, R.			The roles of the prostaglandin D-2 receptors DP1 and CRTH2 in promoting allergic responses	BRITISH JOURNAL OF PHARMACOLOGY			English	Article; Proceedings Paper	Joint Life Science Meeting of the British-Pharmacological-Society/Physiological-Society/Biochemical-Society	JUL, 2007	Glasgow, SCOTLAND	British Pharmacol Soc, Physiol Soc, Biochem Soc		prostaglandin D-2; DP1; CRTH2; mast cells; Th2 lymphocytes; eosinophils; PI3K; allergic rhinitis; asthma	EOSINOPHILIC AIRWAY INFLAMMATION; D-PROSTANOID RECEPTOR-1; HUMAN DENDRITIC CELLS; HELPER TYPE-2 CELLS; CHEMOATTRACTANT RECEPTOR; TH2 CELLS; IN-VIVO; MAST-CELLS; ANTAGONIST BAY-U-3405; CYTOKINE PRODUCTION	Prostaglandin D-2 (PGD(2)) is produced by mast cells, Th2 lymphocytes and dendritic cells and has been detected in high concentrations at sites of allergic inflammation. PGD2 exerts its inflammatory effects through high affinity interactions with the G protein coupled receptors DP1 and chemoattractant-homologous receptor expressed on Th2 cells (CRTH2, also known as DP2). DP1 and CRTH2 act in concert to promote a number of biological effects associated with the development and maintenance of the allergic response. During the process of allergen sensitization, DP1 activation may enhance polarization of Th0 cells to Th2 cells by inhibiting production of interleukin 12 by dendritic cells. Upon exposure to allergen in sensitized individuals, activation of DP1 may contribute to the long lasting blood flow changes in the target organ. CRTH2 is expressed by Th2 lymphocytes, eosinophils and basophils and may mediate the recruitment of these cell types during the late phase allergic response. The role played by CRTH2 in promoting the production of Th2 cytokines and IgE make antagonism of this receptor a particularly attractive approach to the treatment of chronic allergic disease.	Oxagen Ltd, Abingdon OX14 4RY, Oxon, England	Pettipher, R (reprint author), Oxagen Ltd, 91 Milton Pk, Abingdon OX14 4RY, Oxon, England.	r.pettipher@oxagen.co.uk					Ajuebor MN, 2000, AM J PHYSIOL-GASTR L, V279, pG238; Almishri W, 2005, J PHARMACOL EXP THER, V313, P64, DOI 10.1124/jpet.104.079079; ALSINAWI LAH, 1985, PROSTAGLANDINS, V29, P99; ALVING K, 1991, BRIT J PHARMACOL, V104, P452; Angeli W, 2004, J IMMUNOL, V172, P3822; Arimura A, 2001, J PHARMACOL EXP THER, V298, P411; Armer RE, 2005, J MED CHEM, V48, P6174, DOI 10.1021/jm050519b; Barnes PJ, 2004, NAT REV DRUG DISCOV, V3, P831, DOI 10.1038/nrd1524; Bochenek G, 2003, J ALLERGY CLIN IMMUN, V111, P743, DOI 10.1067/mai.2003.1387; Bohm E, 2004, J BIOL CHEM, V279, P7663, DOI 10.1074/jbc.M310270200; Busse W, 2001, J ALLERGY CLIN IMMUN, V107, P461, DOI 10.1067/mai.2001.114657; Caron G, 2001, J IMMUNOL, V167, P3682; CHARLESWORTH EN, 1991, J IMMUNOL, V146, P671; Cheng K, 2006, P NATL ACAD SCI USA, V103, P6682, DOI 10.1073/pnas.0601574103; 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J. Pharmacol.	MAR	2008	153			1			S191	S199		10.1038/sj.bjp.0707488		9	Pharmacology & Pharmacy	Pharmacology & Pharmacy	268OA	WOS:000253587900023	17965752	
J	Kessler, R; Stahl, E; Vogelmeier, C; Haughney, J; Trudeau, E; Lofdahl, CG				Kessler, Romain; Stahl, Elisabeth; Vogelmeier, Claus; Haughney, John; Trudeau, Elyse; Lofdahl, Claes-Goran			Patient understanding, detection, and experience of COPD exacerbations - An observational, interview-based study	CHEST			English	Article						burden; COPD; exacerbation; patient's perspective	OBSTRUCTIVE PULMONARY-DISEASE; QUALITY-OF-LIFE; CHRONIC-BRONCHITIS; HEALTH-STATUS; LUNG-FUNCTION; TIME-COURSE; ASTHMA; IMPACT; HOSPITALIZATION; SALMETEROL	Study objectives: This study was conducted to gain insight into patients' comprehension, recognition, and experience of exacerbations of COPD, and to explore the patient burden associated with these events. Design: A qualitative, multinational, cross-sectional, interview-based study. Setting: Patients' homes. Patients: Patients (n = 125) with predominantly moderate-to-very severe COPD (age >= 50 years; with two or more exacerbations during the previous year). Interventions: Patients underwent a 1-h face-to-face interview with a trained interviewer. Measurements and results: During the preceding year, patients experienced a mean +/- SD of 4.6 +/- 5.4 exacerbations, after which 19.2% (n = 24) believed they had not fully recovered. Although commonly used by physicians, only 1.6% (n = 2) of patients understood the term exacerbation, preferring to use simpler terms, such as chest infection (16.0%; n = 20) or crisis (16.0%; n = 20) instead. Approximately two thirds of patients stated that they were aware of when an exacerbation was imminent and, in most cases, patients recounted that symptoms were consistent from one exacerbation to another. Some patients (32.8%; n = 41), however, reported no recognizable warning signs. At the onset of an exacerbation, 32.8% of patients (n = 41) stated that they reacted by self-administering their medication. Some patients spontaneously mentioned a fear of dying (12.0%; n = 15) or suffocating (9.6%; n = 12) during exacerbations, and effects on activities, mood, and personal/family relationships were frequently reported. Physicians tended to underestimate the psychological impact of exacerbations compared with patient reports. Conclusions: This study shows that patients with frequent exacerbations have a poor understanding of the term exacerbation. Patient recollections suggest that exacerbation profiles vary enormously between patients but that symptoms/warning signs are fairly consistent within individuals, and are generally recognizable. Exacerbations appear to have a significant impact on patient well-being, including psychological well-being, and this may be underestimated by physicians.	Hop Univ Strasbourg, Hop Hautpierre, Dept Pulmonol, Strasbourg, France; Univ Aberdeen, Aberdeen, Scotland; Marburg Univ Hosp, Marburg, Germany; Mapi Values, Lyon, France; Univ Lund Hosp, S-22185 Lund, Sweden; Univ London Imperial Coll Sci & Technol, London, England	Kessler, R (reprint author), Hop Univ Strasbourg, Hop Hautpierre, Dept Pulmonol, Strasbourg, France.	romain.kessler@chru-strasbourg.fr		kessler, romain/0000-0002-5798-5715			Andersson F, 2003, J ASTHMA, V40, P615, DOI 10.1081/JAS-120019032; Andersson F, 2002, RESP MED, V96, P700, DOI 10.1053/rmed.2002.1334; Breslin E, 1998, CHEST, V114, P958, DOI 10.1378/chest.114.4.958; Burge S, 2003, Eur Respir J Suppl, V41, p46s; Calverley P, 2003, LANCET, V361, P449, DOI 10.1016/S0140-6736(03)12459-2; Calverley PM, 2003, EUR RESPIR J, V22, P912, DOI 10.1183/09031936.03.00027003; Casaburi R, 2002, EUR RESPIR J, V19, P217, DOI 10.1183/09031936.02.00269802; Connors AF, 1996, AM J RESP CRIT CARE, V154, P959; Doll H, 2005, PHARMACOECONOMICS, V23, P345, DOI 10.2165/00019053-200523040-00005; Doll H, 2002, RESP MED, V96, P39, DOI 10.1053/rmed.2001.1208; Donaldson GC, 2002, THORAX, V57, P847, DOI 10.1136/thorax.57.10.847; Donohue JF, 2002, CHEST, V122, P47, DOI 10.1378/chest.122.1.47; Engstrom CP, 2001, EUR RESPIR J, V18, P69, DOI 10.1183/09031936.01.00044901; Eriksen Nanna, 2003, Ugeskr Laeger, V165, P3499; Garcia-Aymerich J, 2001, AM J RESP CRIT CARE, V164, P1002; Groenewegen KH, 2003, CHEST, V124, P459, DOI 10.1378/chest.124.2.459; Miravitlles M, 2004, THORAX, V59, P387, DOI 10.1136/thx.2003.008730; Nguyen BP, 1996, ANN ALLERG ASTHMA IM, V77, P209; Nicolson P, 2000, J ANTIMICROB CHEMOTH, V45, P25, DOI 10.1093/jac/45.suppl_2.25; Oliver SM, 2001, FAM PRACT, V18, P430, DOI 10.1093/fampra/18.4.430; Partridge MR, 2000, EUR RESPIR J, V16, P333, DOI 10.1183/09031936.00.16233400; Patil SP, 2003, ARCH INTERN MED, V163, P1180, DOI 10.1001/archinte.163.10.1180; Pauwels R, 2004, RESP MED, V98, P99, DOI 10.1016/j.med.2003.09.001; PEACH H, 1981, THORAX, V36, P585, DOI 10.1136/thx.36.8.585; Perfetto EM, 2001, CLIN THER, V23, P1747, DOI 10.1016/S0149-2918(01)80142-9; Rabe KF, 2004, J ALLERGY CLIN IMMUN, V114, P40, DOI 10.1016/j.jaci.2004.04.042; Rennard S, 2002, EUR RESPIR J, V20, P799, DOI 10.1183/09031936.02.03242002; Seemungal TAR, 1998, AM J RESP CRIT CARE, V157, P1418; Seemungal TAR, 2000, AM J RESP CRIT CARE, V161, P1608; Spencer S, 2004, EUR RESPIR J, V23, P698, DOI 10.1183/09031936.04.00121404; Spencer S, 2003, THORAX, V58, P589, DOI 10.1136/thorax.58.7.589; Szafranski W, 2003, EUR RESPIR J, V21, P74, DOI 10.1183/09031936.03.00031402; *US DEP HHS, NIH PUBL, V2701; Vestbo J, 2004, EUR RESPIR REV, V13, P6; Wilkinson TMA, 2004, AM J RESP CRIT CARE, V169, P1298, DOI 10.1164/rccm.200310-1443OC; Wouters EFM, 2003, RESP MED, V97, pS3, DOI 10.1016/S0954-6111(03)80020-3	36	93	102	1	6	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	JUL	2006	130	1					133	142		10.1378/chest.130.1.133		10	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	066HC	WOS:000239219300023	16840393	
J	Perzanowski, MS; Miller, RL; Thorne, PS; Barr, RG; Divjan, A; Sheares, BJ; Garfinkel, RS; Perera, FP; Goldstein, IF; Chew, GL				Perzanowski, MS; Miller, RL; Thorne, PS; Barr, RG; Divjan, A; Sheares, BJ; Garfinkel, RS; Perera, FP; Goldstein, IF; Chew, GL			Endotoxin in inner-city homes: Associations with wheeze and eczema in early childhood	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						endotoxin; asthma; allergy; hygiene hypothesis; wheeze; inner-city; eczema	HOUSE-DUST ENDOTOXIN; HYGIENE HYPOTHESIS; ALLERGIC DISEASES; INDOOR ALLERGENS; NATIONAL-SURVEY; BIRTH COHORT; HIGH-RISK; EXPOSURE; ASTHMA; CHILDREN	Background: An inverse association between domestic exposure to endotoxin and atopy in childhood has been observed. The relevance of this aspect of the hygiene hypothesis to US inner-city communities that have disproportionately high asthma prevalence has not been determined. Objectives: To measure endotoxin in the dust from inner-city homes, evaluate associations between endotoxin and housing/lifestyle characteristics, and determine whether endotoxin exposure predicted wheeze, allergic rhinitis, and eczema over the first 3 years of life. Methods: As part of an ongoing prospective birth cohort study, children of Dominican and African-American mothers living in New York City underwent repeated questionnaire measures. Dust samples collected from bedroom floors at age 12 or 36 months were assayed for endotoxin. Results: Among the samples collected from 301 participants' homes, the geometric mean endotoxin concentration (95% CI) was 75.9 EU/mg (66-87), and load was 3892 EU/m(2) (3351-4522). Lower endotoxin concentrations were associated with wet mop cleaning and certain neighborhoods. Endotoxin concentration correlated weakly with cockroach (Bla g 2: r = 0.22, P < .001) and mouse (mouse urinary protein: r = 0.28; P < .001) allergens in the dust. Children in homes with higher endotoxin concentration were less likely to have eczema at age 1 year (odds ratio, 0.70 [0.53-0.93]) and more likely to wheeze at age 2 years (odds ratio, 1.34 [1.01-1.78]). These associations were stronger among children with a maternal history of asthma. Conclusion: Endotoxin levels in this inner-city community are similar to those in nonfarm homes elsewhere. In this community, domestic endotoxin exposure was inversely associated with eczema at age 1 year, but positively associated with wheeze at age 2 years. Clinical implications: Endotoxin exposure in the inner-city community may be related to wheeze in the early life; however, given the inverse association seen with eczema, the long-term development of allergic disease is still in question.	Columbia Univ, Mailman Sch Publ Hlth, Columbias Ctr Childrens Environm Hlth, New York, NY 10032 USA; Columbia Univ, Mailman Sch Publ Hlth, Dept Environm Hlth Sci, New York, NY 10032 USA; Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY 10032 USA; Columbia Univ, Mailman Sch Publ Hlth, Data Coordinating Ctr, New York, NY 10032 USA; Columbia Univ, Coll Phys & Surg, Div Pulm Allergy & Crit Care Med, New York, NY USA; Columbia Univ, Coll Phys & Surg, Div Gen Med, Dept Med, New York, NY USA; Columbia Univ, Coll Phys & Surg, Dept Pediat, New York, NY USA; Univ Iowa, Dept Environm & Occupat Hlth, Iowa City, IA USA	Chew, GL (reprint author), Columbia Univ, Mailman Sch Publ Hlth, Columbias Ctr Childrens Environm Hlth, 60 Haven Ave,B-1, New York, NY 10032 USA.	cg2gg@columbia.edu			NCRR NIH HHS [M01 RR000645, RR00645]; NIEHS NIH HHS [P30 ES009089-09, 5 P30 ES009089, 5 R01 ES08977, P01 ES009600, P01 ES009600-09, P30 ES005605, P30 ES005605-17, P30 ES009089, P30 ES05605, P50 ES009600, P50 ES09600, R01 ES008977, R01 ES008977-10, R01 ES011158, R01 ES011158-03, R01 ES012468, R01 ES012468-03, R01ES111158]		Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Bischof W, 2002, INDOOR AIR, V12, P2, DOI 10.1034/j.1600-0668.2002.120102.x; 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; Chew GL, 2003, ENVIRON HEALTH PERSP, V111, P1348, DOI 10.1289/ehp.6124; Chrischilles E, 2004, J ALLERGY CLIN IMMUN, V113, P66, DOI 10.1016/j.jaci.2003.09.037; *CIT NEW YORK DEP, 2003, ASTHM FACTS; 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, 1995, APPL ENVIRON MICROB, V61, P1763; Eisenbarth SC, 2002, J EXP MED, V196, P1645, DOI 10.1084/jem.20021340; 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; INGRAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449, DOI 10.1016/S0091-6749(95)70286-5; Litonjua AA, 2002, J ALLERGY CLIN IMMUN, V110, P736, DOI 10.1067/mai.2002.128948; Liu AH, 2002, J ALLERGY CLIN IMMUN, V109, P379, DOI 10.1067/mai.2002.122157; LUCZYNSKA CM, 1989, J IMMUNOL METHODS, V118, P227, DOI 10.1016/0022-1759(89)90010-0; Martinez FD, 2001, RESPIR RES, V2, P129, DOI 10.1186/rr48; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Meyer IH, 2003, J ASTHMA, V40, P545, DOI 10.1081/JAS-120018789; Miller RL, 2004, CHEST, V126, P1071, DOI 10.1378/chest.126.4.1071; Miller RL, 2001, AM J RESP CRIT CARE, V164, P995; Mueller-Anneling L, 2004, ENVIRON HEALTH PERSP, V112, P583, DOI 10.1289/ehp.6552; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Phipatanakul W, 2004, PEDIATRICS, V114, P13, DOI 10.1542/peds.114.1.13; PLATTSMILLS TAE, 1992, J ALLERGY CLIN IMMUN, V89, P1046, DOI 10.1016/0091-6749(92)90228-T; POLLART SM, 1991, J ALLERGY CLIN IMMUN, V87, P511, DOI 10.1016/0091-6749(91)90010-L; Rauh VA, 2002, ENVIRON HEALTH PERSP, V110, P323; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Strachan DP, 2000, THORAX S1, V55, pS2; Thorne PS, 2005, AM J RESP CRIT CARE, V172, P1371, DOI 10.1164/rccm.200505-758OC; Thorne PS, 2000, TOXICOLOGY, V152, P13, DOI 10.1016/S0300-483X(00)00287-0; Vojta PJ, 2002, ENVIRON HEALTH PERSP, V110, P527; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; Weiss ST, 2002, NEW ENGL J MED, V347, P930, DOI 10.1056/NEJMe020092; Wickens K, 2004, INDOOR AIR, V14, P217, DOI 10.1111/j.1600-0668.2004.00253.x; Wickens K, 2002, ALLERGY, V57, P1171, DOI 10.1034/j.1398-9995.2002.t01-1-23644.x; Yazdanbakhsh M, 2002, SCIENCE, V296, P490, DOI 10.1126/science.296.5567.490	39	93	95	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	2006	117	5					1082	1089		10.1016/j.jaci.2005.12.1348		8	Allergy; Immunology	Allergy; Immunology	041EM	WOS:000237436300016	16675336	
J	Fischer, G; Braun, S; Thissen, R; Dott, W				Fischer, G; Braun, S; Thissen, R; Dott, W			FT-IR spectroscopy as a tool for rapid identification and intra-species characterization of airborne filamentous fungi	JOURNAL OF MICROBIOLOGICAL METHODS			English	Article						FT-IR; fungi; identification; Penicillium; Aspergillus; Conidia; chemotaxonomy	TRANSFORM-INFRARED-SPECTROSCOPY; PERFORMANCE LIQUID-CHROMATOGRAPHY; PYROLYSIS MASS-SPECTROMETRY; SECONDARY METABOLITES; VOLATILE METABOLITES; TYPING METHODS; MYCOTOXINS; STRAINS; DIFFERENTIATION; CLASSIFICATION	Identification of microfungi is time-consuming due to cultivation and microscopic examination and can be influenced by the interpretation of the macro- and micro-morphological characters observed. Fungal conidia contain mycotoxins that may be present in bioaerosols and thus the capacity for production of mycotoxins (and allergens) needs to be investigated to create a basis for reliable risk assessment in environmental and occupational hygiene. The present investigation aimed to create a simple but sophisticated method for the preparation of samples and the identification of airborne fungi by FT-IR spectroscopy. The method was suited to reproducibly differentiate Aspergillus and Penicillium species on the generic, the species.. and the strain level. There are strong indications that strains of one taxon differing in metabolite production can be reliably distinguished by FT-IR spectroscopy (e.g. Aspergillus parasiticus). On the other hand, species from different taxa being similar in secondary metabolite production showed comparably higher similarities. The results obtained here can serve as a basis for the development of a database for species identification and strain characterization of microfungi. The method presented here will improve and facilitate the risk assessment in case of bioaerosol exposure, as strains with different physiological properties (e.g. toxic, non-toxic) could be differentiated. Moreover, it has the potential to significantly improve the identification of microfungi in various fields of applied microbiological research, e.g. high throughput screening in view of specific physiological properties, biodiversity studies, inventories in environmental microbiology, and quality control measures. (c) 2005 Elsevier B.V. All rights reserved.	Univ Hosp RWTH Aachen, Inst Hyg & Environm Med, D-52057 Aachen, Germany	Fischer, G (reprint author), Univ Hosp RWTH Aachen, Inst Hyg & Environm Med, Pauwelsstr 30, D-52057 Aachen, Germany.	Guido.Fischer@post.rwth-aachen.de					Bondy GS, 2000, J TOXICOL ENV HEAL B, V3, P109, DOI 10.1080/109374000281113; Fischer G, 1999, CHEMOSPHERE, V38, P1745, DOI 10.1016/S0045-6535(98)00391-9; Fischer G, 1999, CHEMOSPHERE, V39, P795; Fischer G, 2000, INT J HYG ENVIR HEAL, V203, P97, DOI 10.1078/S1438-4639(04)70014-0; Fischer G, 2003, ARCH MICROBIOL, V179, P75, DOI 10.1007/s00203-002-0495-2; Fischer G, 2002, INT J HYG ENVIR HEAL, V205, P433, DOI 10.1078/1438-4639-00190; Fischer G, 2000, INT J HYG ENVIR HEAL, V203, P105, DOI 10.1078/S1438-4639(04)70015-2; FRISVAD JC, 1987, J CHROMATOGR, V404, P195, DOI 10.1016/S0021-9673(01)86850-3; FRISVAD JC, 1998, THESIS TU DENMARK; Frisvad JC, 1990, MODERN CONCEPTS PENI, P159; FRISVAD JC, 1993, J CHROMATOGR LIBR, V54, P253; Goodacre R, 1998, MICROBIOL-UK, V144, P1157; Haag H, 1996, J MICROBIOL METH, V27, P157, DOI 10.1016/S0167-7012(96)00943-8; HELM D, 1991, J GEN MICROBIOL, V137, P69; HENDRY KM, 1993, J TOXICOL ENV HEALTH, V38, P183; Kirschner C, 2001, J CLIN MICROBIOL, V39, P1763, DOI 10.1128/JCM.39.5.1763-1770.2001; Klich M.A., 2002, IDENTIFICATION COMMO; Kummerle M, 1998, APPL ENVIRON MICROB, V64, P2207; LACEY J, 1994, J AEROSOL SCI, V25, P1371, DOI 10.1016/0021-8502(94)90215-1; LARSEN TO, 1995, MYCOL RES, V99, P1153; LARSEN TO, 1995, MYCOL RES, V99, P1167; Miller J. D., 1994, ORGANIC DUSTS EXPOSU, P87; Mitchell Julian I., 1995, Mycologist, V9, P67; Mohacek-Grosev V, 2001, SPECTROCHIM ACTA A, V57, P2815, DOI 10.1016/S1386-1425(01)00584-4; NAUMANN D, 1991, NATURE, V351, P81, DOI 10.1038/351081a0; Naumann D., 1990, BUNDESGESUNDHEITSBLA, V33, P387; NICHOLS PD, 1985, J MICROBIOL METH, V4, P79, DOI 10.1016/0167-7012(85)90023-5; Orsini F, 2000, J MICROBIOL METH, V42, P17, DOI 10.1016/S0167-7012(00)00168-8; Pitt JI, 1979, GENUS PENICILLIUM; Pitt JI, 1985, FUNGI FOOD SPOILAGE; Pitt JL, 1988, LAB GUIDE COMMON PEN; Raper K B, 1977, GENUS ASPERGILLUS; Riedel A, 1996, PHARM IND, V58, P853; Robbins C A, 2000, Appl Occup Environ Hyg, V15, P773; Rozynek P, 2004, INT J HYG ENVIR HEAL, V207, P297, DOI 10.1078/1438-4639-00289; Samson RA, 2000, INTRO FOOD AIRBORNE; Sandt C, 2003, J CLIN MICROBIOL, V41, P954, DOI 10.1128/JCM.41.3.954-959.2003; Schmalreck AF, 2000, MYCOSES, V43, P61; Schmitt J, 1998, INT BIODETER BIODEGR, V41, P1, DOI 10.1016/S0964-8305(98)80002-4; SELTMANN G, 1995, ZBL BAKT-INT J MED M, V282, P372; SELTMANN G, 1994, EPIDEMIOL INFECT, V113, P411; SOCKALINGUM GW, 1997, BIOCHEM BIOPH RES CO, V23, P240; Sugiyama Junta, 1998, Mycoscience, V39, P487, DOI 10.1007/BF02460912; SVENDSEN A, 1994, MYCOL RES, V98, P1317; Timmins EM, 1998, J CLIN MICROBIOL, V36, P367; Timmins EM, 1998, YEAST, V14, P885, DOI 10.1002/(SICI)1097-0061(199807)14:10<885::AID-YEA286>3.0.CO;2-G; Tintelnot K, 2000, J CLIN MICROBIOL, V38, P1599; Wenning M, 2002, APPL ENVIRON MICROB, V68, P4717, DOI 10.1128/AEM.68.10.4717-4721.2002	48	93	97	2	21	ELSEVIER SCIENCE BV	AMSTERDAM	PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS	0167-7012			J MICROBIOL METH	J. Microbiol. Methods	JAN	2006	64	1					63	77		10.1016/j.mimet.2005.04.005		15	Biochemical Research Methods; Microbiology	Biochemistry & Molecular Biology; Microbiology	003PU	WOS:000234694900006	16229914	
J	Matura, M; Skold, M; Borje, A; Andersen, KE; Bruze, M; Frosch, P; Goossens, A; Johansen, JD; Svedman, C; White, IR; Karlberg, AT				Matura, M; Skold, M; Borje, A; Andersen, KE; Bruze, M; Frosch, P; Goossens, A; Johansen, JD; Svedman, C; White, IR; Karlberg, AT			Selected oxidized fragrance terpenes are common contact allergens	CONTACT DERMATITIS			English	Article						allergic contact dermatitis; autoxidation; caryophyllene; fragrance allergy; fragrance mix; hydroperoxides; linalool; myrcene; oxidation products; patch testing	AIRBORNE COMPOSITAE DERMATITIS; D-LIMONENE; HAND ECZEMA; COLOPHONY; OIL; SENSITIZATION; LINALOOL; HYDROPEROXIDE; MONOTERPENES; TURPENTINE	Terpenes are widely used fragrance compounds in fine fragrances, but also in domestic and occupational products. Terpenes oxidize easily due to autoxidation on air exposure. Previous studies have shown that limonene, linalool and caryophyllene are not allergenic themselves but readily form allergenic products on air-exposure. This study aimed to determine the frequency and characteristics of allergic reactions to selected oxidized fragrance terpenes other than limonene. In total 1511 consecutive dermatitis patients in 6 European dermatology centres were patch tested with oxidized fragrance terpenes and some oxidation fractions and compounds. Oxidized linalool and its hydroperoxide fraction were found to be common contact allergens. Of the patients tested, 1.3% showed a positive reaction to oxidized linalool and 1.1% to the hydroperoxide fraction. About 0.5% of the patients reacted to oxidized caryophyllene whereas 1 patient reacted to oxidized myrcene. Of the patients reacting to the oxidized terpenes, 58% had fragrance-related contact allergy and/or a positive history for adverse reaction to fragrances. Autoxidation of fragrance terpenes contributes greatly to fragrance allergy, which emphasizes the need of testing with compounds that patients are actually exposed to and not only with the ingredients originally applied in commercial formulations.	Gothenburg Univ, Dept Chem, SE-41296 Gothenburg, Sweden; Sahlgrenska Univ Hosp, Dept Dermatol, Gothenburg, Sweden; Univ So Denmark, Odense Univ Hosp, Dept Dermatol, Odense, Denmark; Univ Hosp, Dept Occupat & Environm Dermatol, Malmo, Sweden; Dept Dermatol, Dortmund, Germany; Univ Witten Herdecke, Dortmund, Germany; Catholic Univ Leuven, Univ Hosp, Dept Dermatol, Louvain, Belgium; Univ Copenhagen, Gentofte Hosp, Dept Dermatol, Natl Allergy Res Ctr, Copenhagen, Denmark; St Thomas Hosp, St Johns Inst Dermatol, London, England	Matura, M (reprint author), Gothenburg Univ, Dept Chem, SE-41296 Gothenburg, Sweden.	mihaly.matura@chem.gu.se	Borje, Anna/A-7581-2010; Karlberg, Ann-Therese/A-7706-2010; andersen, klaus/H-2117-2011				Al-Malaika S., 1993, ATMOSPHERIC OXIDATIO, VI, P45, DOI 10.1016/B978-0-444-89615-5.50006-8; Andersen KE, 1998, CONTACT DERMATITIS, V38, P222, DOI 10.1111/j.1600-0536.1998.tb05718.x; BRUZE M, 1986, CONTACT DERMATITIS, V14, P119, DOI 10.1111/j.1600-0536.1986.tb01178.x; Christensen LP, 1999, ARCH DERMATOL RES, V291, P425, DOI 10.1007/s004030050433; CRONIN E, 1979, CONTACT DERMATITIS, V5, P308, DOI 10.1111/j.1600-0536.1979.tb04884.x; DeGroot AC, 1997, CONTACT DERMATITIS, V36, P57; DEGROOT AC, 1983, CONTACT DERMATITIS, V9, P230; DOOMSGOOSSENS A, 1977, CONTACT DERMATITIS, V3, P304, DOI 10.1111/j.1600-0536.1977.tb03692.x; Farm G, 1996, CONTACT DERMATITIS, V34, P93, DOI 10.1111/j.1600-0536.1996.tb02137.x; Fregert S, 1969, CONTACT DERMATITIS N, V5, P85; Frosch PJ, 2005, CONTACT DERMATITIS, V52, P207, DOI 10.1111/j.0105-1873.2005.00565.x; Frosch PJ, 1999, BRIT J DERMATOL, V141, P1076, DOI 10.1046/j.1365-2133.1999.03208.x; GROOT A, 1994, UNWANTED EFFECTS COS; HELLERSTROM S, 1955, J INVEST DERMATOL, V24, P217; Heydorn S, 2003, CONTACT DERMATITIS, V48, P317, DOI 10.1034/j.1600-0536.2003.00133.x; Heydorn S, 2003, CONTACT DERMATITIS, V48, P59, DOI 10.1034/j.1600-0536.2003.480201.x; Johansen JD, 2001, CONTACT DERMATITIS, V44, P304, DOI 10.1034/j.1600-0536.2001.440510.x; Johansen JD, 2000, BRIT J DERMATOL, V142, P490, DOI 10.1046/j.1365-2133.2000.03362.x; Johansen Jeanne Duus, 2002, Contact Dermatitis, V46, P1; KARLBERG AT, 1994, ARCH DERMATOL RES, V286, P97, DOI 10.1007/BF00370734; KARLBERG AT, 1992, CONTACT DERMATITIS, V26, P332, DOI 10.1111/j.1600-0536.1992.tb00129.x; KARLBERG AT, 1985, BRIT J DERMATOL, V113, P475, DOI 10.1111/j.1365-2133.1985.tb02363.x; Karlberg AT, 1996, CONTACT DERMATITIS, V35, P201, DOI 10.1111/j.1600-0536.1996.tb02358.x; Karlberg AT, 1997, CONTACT DERMATITIS, V36, P201, DOI 10.1111/j.1600-0536.1997.tb00270.x; Matura M, 2002, J AM ACAD DERMATOL, V47, P709, DOI 10.1067/mjd.2002.124817; Matura M, 2003, CONTACT DERMATITIS, V49, P15, DOI 10.1111/j.0105-1873.2003.00135.x; Nielsen NH, 2001, ACTA DERM-VENEREOL, V81, P31, DOI 10.1080/000155501750208155; OPDYKE DLJ, 1976, FOOD COSMET TOXICOL, V14, P615, DOI 10.1016/S0015-6264(76)80022-3; PAULSEN E, 1993, CONTACT DERMATITIS, V29, P138, DOI 10.1111/j.1600-0536.1993.tb03511.x; Paulsen E, 2002, CONTACT DERMATITIS, V47, P14, DOI 10.1034/j.1600-0536.2002.470103.x; 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, 2001, CONTACT DERMATITIS, V45, P221, DOI 10.1034/j.1600-0536.2001.450406.x; RYCROFT RJG, 1980, CONTACT DERMATITIS, V6, P325, DOI 10.1111/j.1600-0536.1980.tb04957.x; SCHALLER M, 1995, CLIN EXP DERMATOL, V20, P143; Schnuch A, 2004, CONTACT DERMATITIS, V50, P117, DOI 10.1111/j.0105-1873.2004.0313.x; Skold M, 2004, CHEM RES TOXICOL, V17, P1697, DOI 10.1021/tx049831z; Skold M, 2002, CONTACT DERMATITIS, V46, P267, DOI 10.1034/j.1600-0536.2002.460504.x; SKOLD M, 2005, UNPUB FRAGRANCE CHEM; Sugiura M, 2000, CONTACT DERMATITIS, V43, P157, DOI 10.1034/j.1600-0536.2000.043003157.x; Verghese J., 1994, PAFAI J, V16, P21; VESTEY JP, 1986, CONTACT DERMATITIS, V15, P119, DOI 10.1111/j.1600-0536.1986.tb01310.x; Wahlberg J, 1995, TXB CONTACT DERMATIT, P241; Wakelin SH, 1998, CONTACT DERMATITIS, V38, P164, DOI 10.1111/j.1600-0536.1998.tb05686.x; Wohrl S, 2001, BRIT J DERMATOL, V145, P268, DOI 10.1046/j.1365-2133.2001.04345.x	45	93	96	3	28	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0105-1873			CONTACT DERMATITIS	Contact Dermatitis	JUN	2005	52	6					320	328		10.1111/j.0105-1873.2005.00605.x		9	Allergy; Dermatology	Allergy; Dermatology	931OS	WOS:000229495200007	15932583	
J	Brussee, JE; Smit, HA; van Strien, RT; Corver, K; Kerkhof, M; Wijga, AH; Aalberse, RC; Postma, D; Gerritsen, J; Grobbee, DE; de Jongste, JC; Brunekreef, B				Brussee, JE; Smit, HA; van Strien, RT; Corver, K; Kerkhof, M; Wijga, AH; Aalberse, RC; Postma, D; Gerritsen, J; Grobbee, DE; de Jongste, JC; Brunekreef, B			Allergen exposure in infancy and the development of sensitization, wheeze, and asthma at 4 years	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						cohort studies; child; preschool; allergens; house dust mites; cats; dogs; sensitization; wheezing; asthma	HOUSE-DUST MITE; BIRTH COHORT; MATERNAL HISTORY; INDOOR ALLERGENS; RISK-FACTOR; 1ST YEAR; LIFE; CHILDHOOD; ATOPY; PET	Background: The relationship between mite and pet allergen exposure in infancy and the subsequent development of sensitization and asthma is complex. Objective: We prospectively investigated the effect of allergen exposure at 3 months of age on the development of sensitization, wheeze, and physician-diagnosed asthma in the first 4 years of life in a birth cohort of children with and without an atopic mother. Methods: Children participated in the Prevention and Incidence of Asthma and Mite Allergy study. Allergen exposure at 3 months of age was determined from mattress dust samples. Specific IgE to inhalant allergens was measured at 4 years of age, and information about wheeze and physician-diagnosed asthma was collected with yearly questionnaires. Results: Mite and cat allergen exposure in infancy were associated with an increased risk of specific sensitization to house dust mite and cat, respectively, at 4 years of age. There were borderline significant associations between cat allergen exposure and persistent wheeze in the total study population and between dog allergen exposure and persistent wheeze in children with a nonatopic mother. In children with an atopic mother, there was some indication of a positive association between mite allergen exposure and physician-diagnosed asthma. Conclusion: Early house dust mite and cat allergen exposure might lead to sensitization and, in case of cat allergen exposure, to persistent wheeze. Early mite and dog allergen exposure might lead to asthma and persistent wheeze, respectively, but only in subgroups defined by maternal atopy.	Natl Inst Publ Hlth & Environm, Ctr Prevent & Hlth Serv Res, NL-3720 BA Bilthoven, Netherlands; Univ Utrecht, Med Ctr, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands; Univ Munich, Inst Occupat & Environm Med, Munich, Germany; Erasmus MC, Dept Pediat, Div Resp Med, Rotterdam, Netherlands; Univ Groningen, Dept Epidemiol & Stat, Groningen, Netherlands; Sanquin Res CLB, Dept Immunopathol, Amsterdam, Netherlands; Univ Groningen Hosp, Dept Pulmonol, Groningen, Netherlands; Univ Groningen Hosp, Dept Paediat Resp Med, Groningen, Netherlands; Univ Utrecht, Inst Risk Assessment Sci, Utrecht, Netherlands	Smit, HA (reprint author), Natl Inst Publ Hlth & Environm, Ctr Prevent & Hlth Serv Res, POB 1, NL-3720 BA Bilthoven, Netherlands.	jet.smit@rivm.nl	Kerkhof, Marjan/A-8846-2008; Grobbee, Diederick/C-7651-2014	Grobbee, Diederick/0000-0003-4472-4468; brunekreef, bert/0000-0001-9908-0060			Almqvist C, 2003, CLIN EXP ALLERGY, V33, P1190, DOI 10.1046/j.1365-2222.2003.01764.x; Almqvist C, 2003, J ALLERGY CLIN IMMUN, V111, P800, DOI 10.1067/mai.2003.1334; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Belanger K, 2003, AM J EPIDEMIOL, V158, P195, DOI 10.1093/aje/kwg148; Brunekreef B, 2002, PEDIAT ALLERG IMM-UK, V13, P55, DOI 10.1034/j.1399-3038.13.s.15.1.x; Brussee JE, 2004, AM J RESP CRIT CARE, V169, P209, DOI 10.1164/rccm.200306-800OC; Carter PM, 2003, ANN ALLERG ASTHMA IM, V90, P41; Celedon JC, 2002, LANCET, V360, P781, DOI 10.1016/S0140-6736(02)09906-3; COLLOFF MJ, 1992, CLIN EXP ALLERGY, V22, P1, DOI 10.1111/j.1365-2222.1992.tb01763.x; Crestani E, 2004, J ALLERGY CLIN IMMUN, V113, P284, DOI 10.1016/j.jaci.2003.11.009; Cullinan P, 2004, THORAX, V59, P855, DOI 10.1136/thx.2003.019877; Gehring U, 2004, ENVIRON HEALTH PERSP, V112, P834, DOI 10.1289/ehp.6685; Johnson CC, 2004, J ALLERGY CLIN IMMUN, V114, P105, DOI 10.1016/j.jaci.2004.04.007; Lakwijk N, 1998, CLIN EXP ALLERGY, V28, P454; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Munir AKM, 1997, J ALLERGY CLIN IMMUN, V100, P177, DOI 10.1016/S0091-6749(97)70221-5; Murray C S, 2001, Curr Opin Allergy Clin Immunol, V1, P407, DOI 10.1097/00130832-200110000-00005; Nafstad P, 2001, ALLERGY, V56, P307, DOI 10.1034/j.1398-9995.2001.00881.x; 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; Platts-Mills TA, 2000, J ALLERGY CLIN IMMUN, V105, P503; Polk S, 2004, AM J RESP CRIT CARE, V170, P273, DOI 10.1164/rccm.200310-1348OC; Remes ST, 2001, J ALLERGY CLIN IMMUN, V108, P509, DOI 10.1067/mai.2001.117797; Sandin A, 2004, PEDIATR ALLERGY IMMU, V15, P316, DOI 10.1111/j.1399-3038.2004.00166.x; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; van Strien RT, 2003, CLIN EXP ALLERGY, V33, P490, DOI 10.1046/j.1365-2222.2003.01626.x; van Strien RT, 2002, ENVIRON HEALTH PERSP, V110, pA693; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7	29	93	97	0	7	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					946	952		10.1016/j.jaci.2005.02.035		7	Allergy; Immunology	Allergy; Immunology	925LR	WOS:000229055100008	15867850	
J	Velasco, G; Campo, M; Manrique, OJ; Bellou, A; He, HZ; Arestides, RSS; Schaub, B; Perkins, DL; Finn, PW				Velasco, G; Campo, M; Manrique, OJ; Bellou, A; He, HZ; Arestides, RSS; Schaub, B; Perkins, DL; Finn, PW			Toll-like receptor 4 or 2 agonists decrease allergic inflammation	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article						innate; immunity; asthma; Toll-like receptor 4; Toll-like receptor 2; allergy	AIRWAY HYPERRESPONSIVENESS; PULMONARY INFLAMMATION; IMMUNE-RESPONSES; MURINE MODEL; BACTERIAL LIPOPOLYSACCHARIDE; DENDRITIC CELLS; TH2 RESPONSES; T-CELLS; ASTHMA; ENDOTOXIN	Toll-like receptors (TLRs) recognize highly conserved microbial molecular patterns, such as found in endotoxin. This study tested whether TLR4 and TLR2 stimulation in vivo would modulate subsequent adaptive (allergic) immune responses. We analyzed the effects of pulmonary administration of a TLR4 agonist, lipid A (LpA), and two TLR2 agonists, peptidoglycan (Ppg) and PamCys, in a murine model of allergic inflammation. The TLR agonists were administered during allergen sensitization or challenge. Both TLR agonists decreased the allergen-induced pulmonary recruitment of eosinophils when administered at sensitization or challenge. When given before sensitization, the TLR4 and TLR2 agonists decreased additional allergen-induced parameters of inflammation (pulmonary eosinophilia, bronchoalveolar lavage IL-13, total serum IgE, and airway hyperresponsiveness). Interestingly, TLR4 and TLR2 agonists decreased the number of CD4+ cells in the lung. Also, at the site of local allergen stimulation, the draining thoracic lymph nodes, allergen-induced lymphocyte proliferation, and IL-13 secretion were decreased by administration of LpA and Ppg. These data provide a distinct example of the modulation of adaptive (allergic) responses by non-antigen-dependent stimuli. Our findings also demonstrate that both TLR4 and TLR2 agonists decrease allergic responses, supporting the concept that exposure to bacterial components under defined conditions may protect against allergic disease.	Brigham & Womens Hosp, Div Resp & Crit Care, Boston, MA 02115 USA; Brigham & Womens Hosp, Dept Med, Lab Immunogenet & Transplant, Boston, MA 02115 USA	Finn, PW (reprint author), Brigham & Womens Hosp, Div Resp & Crit Care, 75 Francis St, Boston, MA 02115 USA.	pwfinn@rics.bwh.harvard.edu			NHLBI NIH HHS [HL 56723, HL 67684]		Adler A, 2004, J APPL PHYSIOL, V97, P286, DOI 10.1152/japplphysiol.00821.2003; Akdis CA, 2003, EUR J IMMUNOL, V33, P2717, DOI 10.1002/eji.200323329; Arestides RSS, 2002, EUR J IMMUNOL, V32, P2874, DOI 10.1002/1521-4141(2002010)32:10<2874::AID-IMMU2874>3.0.CO;2-4; Banchereau J, 1998, NATURE, V392, P245, DOI 10.1038/32588; Banerjee B, 2004, INFECT IMMUN, V72, P6087, DOI 10.1128/IAI.72.10.6087-6094.2004; Bellou Abdelouahab, 2003, Curr Opin Allergy Clin Immunol, V3, P487, DOI 10.1097/00130832-200312000-00011; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Broide DH, 2001, J CLIN IMMUNOL, V21, P175, DOI 10.1023/A:1011078930363; Caramalho I, 2003, J EXP MED, V197, P403, DOI 10.1084/jem.20021633; Chisholm D, 2004, J ALLERGY CLIN IMMUN, V113, P448, DOI 10.1016/j.jaci.2003.12.011; Dabbagh K, 2003, CURR OPIN INFECT DIS, V16, P199, DOI 10.1097/01.qco.0000073767.11390.47; Dodge IL, 2003, J IMMUNOL, V170, P4457; Donovan CE, 1999, J IMMUNOL, V163, P6827; Eder W, 2004, J ALLERGY CLIN IMMUN, V113, P482, DOI 10.1016/j.jaci.2003.12.374; Eisenbarth SC, 2002, J EXP MED, V196, P1645, DOI 10.1084/jem.20021340; Gelman AE, 2004, J IMMUNOL, V172, P6065; Gerhold K, 2003, J ALLERGY CLIN IMMUN, V112, P389, DOI 10.1067/mai.2003.1646; Gerhold K, 2002, J ALLERGY CLIN IMMUN, V110, P110, DOI 10.1067/mai.2002.125831; Hamelmann E, 1997, AM J RESP CRIT CARE, V156, P766; Iwasaki A, 2004, NAT IMMUNOL, V5, P987, DOI 10.1038/ni1112; JANEWAY CA, 1989, COLD SPRING HARB SYM, V54, P1; Janeway CA, 2002, ANNU REV IMMUNOL, V20, P197, DOI 10.1146/annurev.immunol.20.083001.084359; Krinzman SJ, 1996, AM J PHYSIOL-LUNG C, V271, pL476; Krinzman SJ, 1996, J CLIN INVEST, V98, P2693, DOI 10.1172/JCI119093; Lauener RP, 2002, LANCET, V360, P465, DOI 10.1016/S0140-6736(02)09641-1; LIO J, 2000, INT ARCH ALLERGY IMM, V127, P217; Mark DA, 2000, AM J RESP CELL MOL, V22, P265; Mark DA, 1998, INT IMMUNOL, V10, P1647, DOI 10.1093/intimm/10.11.1647; Redecke V, 2004, J IMMUNOL, V172, P2739; Rincon M, 1997, J EXP MED, V185, P461, DOI 10.1084/jem.185.3.461; Rodriguez D, 2003, J IMMUNOL, V171, P1001; Schwartz DA, 2001, AM J RESP CRIT CARE, V163, P305; Schwartz DA, 1994, AM J PHYSIOL, V267, P609; Takeda K, 2003, ANNU REV IMMUNOL, V21, P335, DOI 10.1146/annurev.immunol.21.120601.141126; Tulic MK, 2000, AM J RESP CELL MOL, V22, P604; Wan GH, 2000, CLIN EXP ALLERGY, V30, P426; Watanabe J, 2003, J BIOL CHEM, V278, P42361, DOI 10.1074/jbc.M307752200; Werner M, 2003, J ALLERGY CLIN IMMUN, V112, P323, DOI 10.1067/mai.2003.1648	38	93	99	1	13	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.	MAR	2005	32	3					218	224		10.1165/rcmb.2003-0435OC		7	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	900DS	WOS:000227196200007	15576672	
J	Arbes, SJ; Cohn, RD; Yin, M; Muilenberg, ML; Friedman, W; Zeldin, DC				Arbes, SJ; Cohn, RD; Yin, M; Muilenberg, ML; Friedman, W; Zeldin, DC			Dog allergen (Can f 1) and cat allergen (Fel d 1) in US homes: Results from the National Survey of Lead and Allergens in Housing	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergens; asthma; cat allergen; Can f 1; dog allergen; epidemiology; Fel d 1; survey	DUST MITE; D-I; COCKROACH ALLERGENS; DOMESTIC ALLERGENS; PUBLIC PLACES; PARTICLE-SIZE; RISK-FACTORS; LOS-ALAMOS; NEW-MEXICO; F I	Background: Exposures to dog and cat allergens are believed to play important roles in the etiology of asthma; however, the levels of these allergens have never been assessed in a representative sample of US homes. Objective: The objective of this study was to estimate and characterize exposures to Can f 1 (dog allergen) and Fell d 1 (cat allergen) in US homes. Methods: Data were obtained from the National Survey of Lead and Allergens in Housing, a nationally representative survey of 831 US homes. Vacuumed-collected dust samples from the bed, bedroom floor, living room floor, and living room sofa were analyzed for concentrations of Can f 1 and Fel d 1 (micrograms of allergen per gram of dust). Results: Although a dog or cat had lived in only 49.1% of homes in the previous 6 months, Can f 1 and Fel d 1 were detected in 100% and 99.9% of homes, respectively. Averaged over the sampled sites, geometric mean concentrations (mug/g) were 4.69 for Can f 1 and 4.73 for Fel d 1. Among homes with an indoor dog and cat, respectively, geometric mean concentrations were 69 for Can f 1 and 200 for Fel d 1. Among homes without the indoor pet, geometric mean concentrations were above 1.0. The independent predictors of elevated concentrations in homes without pets were all demographic variables that were also linked to a higher prevalence of pet ownership. Conclusions: Can f 1 and Fel d 1 are universally present in US homes. Levels that have been associated with an increased risk of allergic sensitization were found even in homes without pets. Because of the transportability of these allergens on clothing, elevated levels in homes without pets, particularly among demographic groups in which pet ownership is more prevalent, implicate the community as an important source of these pet allergens.	NIEHS, NIH, Res Triangle Pk, NC 27709 USA; Constella Grp Inc, Durham, NC USA; Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA; US Dept Housing & Urban Dev, Off Healthy Homes & Lead Hazard Control, Washington, DC USA	Zeldin, DC (reprint author), NIEHS, NIH, POB 12233,Mail Drop D2-01, Res Triangle Pk, NC 27709 USA.						Almqvist C, 1999, J ALLERGY CLIN IMMUN, V103, P1012, DOI 10.1016/S0091-6749(99)70172-7; Arbes SJ, 2003, J ALLERGY CLIN IMMUN, V111, P408, DOI 10.1067/mai.2003.16; Arshad SH, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.2.e33; Berge M, 1998, PEDIATR ALLERGY IMMU, V9, P25, DOI 10.1111/j.1399-3038.1998.tb00296.x; Bollinger ME, 1996, J ALLERGY CLIN IMMUN, V97, P907, DOI 10.1016/S0091-6749(96)80064-9; CALL RS, 1992, J PEDIATR-US, V121, P862, DOI 10.1016/S0022-3476(05)80329-4; Cohn RD, 2004, J ALLERGY CLIN IMMUN, V113, P1167, DOI 10.1016/j.jaci.2003.12.592; Custovic A, 1998, CLIN EXP ALLERGY, V28, P53; Custovic A, 1996, CLIN EXP ALLERGY, V26, P1246, DOI 10.1046/j.1365-2222.1996.d01-278.x; Custovic A, 1997, AM J RESP CRIT CARE, V155, P94; DEBLAY F, 1991, AM REV RESPIR DIS, V143, P1334; EGGLESTON PA, 1992, ALLERGY PROC, V13, P289, DOI 10.2500/108854192778816942; ENBERG RN, 1993, ANN ALLERGY, V70, P471; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; GERGEN PJ, 1992, J ALLERGY CLIN IMMUN, V90, P579, DOI 10.1016/0091-6749(92)90130-T; INGRAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449, DOI 10.1016/S0091-6749(95)70286-5; Jacobs DE, 2002, ENVIRON HEALTH PERSP, V110, pA599; LUCZYNSKA CM, 1990, AM REV RESPIR DIS, V141, P361; MUNIR AKM, 1993, J ALLERGY CLIN IMMUN, V91, P1067, DOI 10.1016/0091-6749(93)90221-Z; Nelson RP, 1996, J ALLERGY CLIN IMMUN, V98, P258, DOI 10.1016/S0091-6749(96)70148-3; Partti-Pellinen K, 2000, ALLERGY, V55, P65, DOI 10.1034/j.1398-9995.2000.00226.x; Patchett K, 1997, J ALLERGY CLIN IMMUN, V100, P755, DOI 10.1016/S0091-6749(97)70269-0; Plaschke P, 1999, ALLERGY, V54, P843, DOI 10.1034/j.1398-9995.1999.00162.x; Platts-Mills TA, 1997, J ALLERGY CLIN IMM S, V100, P2; PLATTSMILLS TAE, 1995, INT ARCH ALLERGY IMM, V107, P301; Pope A. M., 1993, INDOOR ALLERGENS ASS; Roost HP, 1999, J ALLERGY CLIN IMMUN, V104, P941, DOI 10.1016/S0091-6749(99)70072-2; SCHOU C, 1991, J ALLERGY CLIN IMMUN, V88, P847, DOI 10.1016/0091-6749(91)90240-O; SEARS MR, 1989, CLIN EXP ALLERGY, V19, P419, DOI 10.1111/j.1365-2222.1989.tb02408.x; Squillace SP, 1997, AM J RESP CRIT CARE, V156, P1760; Vojta PJ, 2002, ENVIRON HEALTH PERSP, V110, P527; WOOD RA, 1992, J ALLERGY CLIN IMMUN, V89, P126, DOI 10.1016/S0091-6749(05)80049-1	32	93	97	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.	JUL	2004	114	1					111	117		10.1016/j.jaci.2004.04.036		7	Allergy; Immunology	Allergy; Immunology	836DA	WOS:000222534300016	15241352	
J	Svanes, C; Omenaas, E; Jarvis, D; Chinn, S; Gulsvik, A; Burney, P				Svanes, C; Omenaas, E; Jarvis, D; Chinn, S; Gulsvik, A; Burney, P			Parental smoking in childhood and adult obstructive lung disease: results from the European Community Respiratory Health Survey	THORAX			English	Article							MATERNAL SMOKING; TOBACCO-SMOKE; CIGARETTE-SMOKING; YOUNG-ADULTS; ASTHMA; EXPOSURE; LIFE; PREVALENCE; PREGNANCY; POPULATION	Background: Early exposure to parental smoking appears to influence the development of the airways and predispose to respiratory symptoms. A study was undertaken to determine whether the consequences of parental smoking could be traced in adulthood. Methods: Information from interviewer-led questionnaires was available for 18922 subjects aged 20-44 years from random population samples in 37 areas participating in the European Community Respiratory Health Survey. Lung function data were available for 15-901 subjects. Results: In men, father's smoking in childhood was associated with more respiratory symptoms (ORwheeze 1.13 (95% CI 1.00 to 1.28); never smokers: ORwheeze 1.21 (95% CI 0.96 to 1.50)) and there was a dose-dependent association between number of parents smoking and wheeze (one: OR 1.08 (95% CI 0.94 to 1.24); both: OR 1.24 (95% CI 1.05 to 1.47); p(trend)=0.010). A reduced ratio of forced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC) was related to father's smoking (-0.3% (95% CI -0.6 to 0)) and number of parents smoking (p(trend)<0.001) among men. In women, mother's smoking was associated with more respiratory symptoms and poorer lung function (ORwheeze 1.15 (95% CI 1.01 to 1.31), never smokers: ORwheeze 1.21 (95% CI 0.98-1.51); FEV1-24 ml (95% CI -45 to -3); FEV1/FVC ratio -0.6% (95% CI -0.9 to -0.3)). These effects were possibly accounted for by maternal smoking in pregnancy (ORwheeze 1.39 (95% CI 1.17 to 1.65); FEV1-23 ml (95% CI -52 to 7); FEV1/FVC ratio -0.9% (95% CI -1.3 to -0.4)) as there was no association with paternal smoking among women (interaction by sex, p<0.05). These results were homogeneous across centres. Conclusion: Both intrauterine and environmental exposure to parental tobacco smoking was related to more respiratory symptoms and poorer lung function in adulthood in this multicultural study. The age window of particular vulnerability appeared to differ by sex, postnatal exposure being important only in men and a role for prenatal exposure being more evident in women.	Haraldsplass Hosp, Dept Med, N-5009 Bergen, Norway; Haukeland Univ Hosp, Dept Thorac Med, N-5021 Bergen, Norway; Univ London Kings Coll, Dept Publ Hlth Sci, London SE1 3QD, England	Svanes, C (reprint author), Haraldsplass Hosp, Dept Med, N-5009 Bergen, Norway.	cecilie.svanes@med.uib.no	Jarvis, Deborah/E-6494-2011		NCRR NIH HHS [S07 RR05521-28]		Becklake MR, 1999, THORAX, V54, P1119; 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; Carlsen KCL, 1997, EUR RESPIR J, V10, P1774; Chinn S, 1997, EUR RESPIR J, V10, P2495, DOI 10.1183/09031936.97.10112495; COLLINS MH, 1985, PEDIATR RES, V19, P408; Cook DG, 1997, THORAX, V52, P1081; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; ESCOLAR JD, 1995, EXP LUNG RES, V21, P255, DOI 10.3109/01902149509068831; *EUR COMM RESP HLT, 1994, MED HLTH EC DIR GEN, V13; Gold DR, 1996, NEW ENGL J MED, V335, P931, DOI 10.1056/NEJM199609263351304; HANRAHAN JP, 1992, AM REV RESPIR DIS, V145, P1129; Hu FB, 1997, J ASTHMA, V34, P67, DOI 10.3109/02770909709071205; JENKINS MA, 1994, BRIT MED J, V309, P90; Larsson ML, 2001, CHEST, V120, P711, DOI 10.1378/chest.120.3.711; Leynaert B, 1997, AM J RESP CRIT CARE, V156, P1413; MASI MA, 1988, AM REV RESPIR DIS, V138, P296; Morgan WJ, 1998, AM J RESP CRIT CARE, V158, P689; Office of Population Censuses and Surveys, 1980, CLASS OCC; POLGAR G, 1979, AM REV RESPIR DIS, V120, P625; Prescott E, 1997, EUR RESPIR J, V10, P822; Roca J, 1998, EUR RESPIR J, V11, P1354, DOI 10.1183/09031936.98.11061354; RONA RJ, 1993, THORAX, V48, P21, DOI 10.1136/thx.48.1.21; Stein RT, 1999, AM J EPIDEMIOL, V149, P1030; Stick SM, 1996, LANCET, V348, P1060, DOI 10.1016/S0140-6736(96)04446-7; Strachan DP, 1996, BRIT MED J, V312, P1195; Strachan DP, 1998, THORAX, V53, P204; TAGER IB, 1995, AM J RESP CRIT CARE, V152, P977; Upton MN, 1998, LANCET, V352, P453, DOI 10.1016/S0140-6736(05)79187-X; Wasowicz Marcin, 1994, Polish Journal of Pathology, V45, P155	30	93	95	0	2	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	APR 1	2004	59	4					295	302		10.1136/thx.2003.009746		8	Respiratory System	Respiratory System	807CT	WOS:000220480300007	15047948	
J	Dales, RE; Cakmak, S; Judek, S; Dann, T; Coates, F; Brook, JR; Burnett, RT				Dales, RE; Cakmak, S; Judek, S; Dann, T; Coates, F; Brook, JR; Burnett, RT			Influence of outdoor aeroallergens on hospitalization for asthma in Canada	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; fungus; pollen; air pollution; epidemiology	INHALED ALLERGEN; AIRWAY RESPONSE; OZONE EXPOSURE; POLLEN	Background: The risk of hospitalization for asthma caused by outdoor aeroallergens is largely unknown. Objective: The objective of this study was to determine the association between changes in outdoor aeroallergens and hospitalizations for asthma from the Pacific coast to the Atlantic coast of Canada. Methods: A daily time series analysis was done to test the association between daily changes in aeroallergens and daily changes in hospitalizations for asthma during a 7-year period between 1993 and 2000 in 10 of the largest cities in Canada. Results were adjusted for long-term trends, day of the week, climate, and air pollution. Results: A daily increase, equivalent to the mean value of each allergen, was associated with the following percentage increase in asthma hospitalizations: 3.3% (95% CI, 2.3 to 4.1) for basidiomycetes, 3.1 % (95 % CI, 2.8 to 5.7) for ascomycetes, 3.2% (95% CI, 1.6 to 4.8) for deuteromycetes, 3.0% (95% CI, 1.1 to 4.9) for weeds, 2.9 % (95 % CI, 0.9 to 5.0) for trees, and 2.0% (95% CI, 1.1 to 2.8) for grasses. After accounting for the independent effects of trees and ozone, the combination of the 2 was associated with an additional 0.22% increase in admissions averaged across cities (P < .05). Conclusion: These findings provide evidence for the hypothesis that aeroallergens are an important cause of severe asthma morbidity across Canada,, and in some situations there might be a modest synergistic adverse effect of ozone and aeroallergens combined.	Univ Ottawa, Ottawa, ON K1N 6N5, Canada; Ottawa Hlth Res Inst, Ottawa, ON, Canada; Hlth Canada, Ottawa, ON, Canada	Dales, RE (reprint author), Ottawa Gen Hosp, Gen Campus,501 Smyth Rd,Box 211, Ottawa, ON K1H 8L6, Canada.			Cakmak, Sabit/0000-0001-9921-2107			AKAIKE H, 1974, IEEE T AUTOMAT CONTR, VAC19, P716, DOI 10.1109/TAC.1974.1100705; Burnett RT, 2001, AM J EPIDEMIOL, V153, P444, DOI 10.1093/aje/153.5.444; Hoog GSde, 2000, ATLAS CLIN FUNGI, P1; Delfino RJ, 1996, AM J RESP CRIT CARE, V154, P633; Delfino RJ, 1997, AM J RESP CRIT CARE, V155, P568; Epton MJ, 1997, THORAX, V52, P528; HASTIE T, 1990, GEN ADDICTIVE MODELS; Hoek G, 1997, ARCH ENVIRON HEALTH, V52, P455; Jenkins HS, 1999, AM J RESP CRIT CARE, V160, P33; LEHRER SB, 1994, ALLERGY, V49, P460, DOI 10.1111/j.1398-9995.1994.tb00840.x; Lewis SA, 2000, CLIN EXP ALLERGY, V30, P1724, DOI 10.1046/j.1365-2222.2000.00947.x; Lierl MB, 2003, ANN ALLERG ASTHMA IM, V90, P28; LOPEZ M, 1989, J ALLERGY CLIN IMMUN, V84, P246; McCallagh P, 1989, GEN LINEAR MODELS; MOLFINO NA, 1991, LANCET, V338, P199, DOI 10.1016/0140-6736(91)90346-Q; OHOLLAREN MT, 1991, NEW ENGL J MED, V324, P359, DOI 10.1056/NEJM199102073240602; PLATTSMILLS T, 1999, ASTHAM LINK ENV IMMU; SALVAGGIO J, 1971, J ALLERGY CLIN IMMUN, V48, P96, DOI 10.1016/0091-6749(71)90091-1; Schappi GF, 1999, CLIN EXP ALLERGY, V29, P633; Schappi GF, 1999, ALLERGY, V54, P478, DOI 10.1034/j.1398-9995.1999.00838.x; TARGONSKI PV, 1995, J ALLERGY CLIN IMMUN, V95, P955, DOI 10.1016/S0091-6749(95)70095-1; Vagaggini B, 2002, AM J RESP CRIT CARE, V166, P1073, DOI 10.1164/rccm.2201013; von Mutius E, 2000, J ALLERGY CLIN IMMUN, V105, P9, DOI 10.1016/S0091-6749(00)90171-4	23	93	93	4	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					303	306		10.1016/j.jaci.2003.11.016		4	Allergy; Immunology	Allergy; Immunology	773EX	WOS:000188885700019	14767446	
J	Buentke, E; Heffler, LC; Wilson, JL; Wallin, RPA; Lofman, C; Chambers, BJ; Ljunggren, HG; Scheynius, A				Buentke, E; Heffler, LC; Wilson, JL; Wallin, RPA; Lofman, C; Chambers, BJ; Ljunggren, HG; Scheynius, A			Natural killer and dendritic cell contact in lesional atopic dermatitis skin - Malassezia-influenced cell interaction	JOURNAL OF INVESTIGATIVE DERMATOLOGY			English	Article						cell communication; cell death; eczema	NK CELLS; PITYROSPORUM ORBICULARE; MEDIATED LYSIS; HUMAN BLOOD; IN-VIVO; EXPRESSION; RECEPTORS; SUBSETS; FURFUR; MATURATION	The regulation of dendritic cells is far from fully understood. Interestingly, several recent reports have suggested a role for natural killer cells in affecting dendritic cell maturation and function upon direct contact between the cells. It is not known if this interaction takes place also in vivo, or if a potential interaction of natural killer cells and dendritic cells would be affected by allergen exposure of the dendritic cells. The yeast Malassezia can act as an allergen in atopic eczema/dermatitis syndrome, and induce maturation of dendritic cells. Our aims were to study the distribution of natural killer cells in the skin from atopic eczema/dermatitis syndrome patients with the emphasis on possible natural killer cell-dendritic cell interaction, and to assess whether the interaction of Malassezia with dendritic cells would affect subsequent interaction between dendritic cells and natural killer cells. A few scattered natural killer (CD56(+)/CD3(-)) cells were found in the dermis of healthy individuals and in nonlesional skin from atopic eczema/dermatitis syndrome patients. In lesional skin and in biopsies from Malassezia atopy-patch-test-positive skin, however, natural killer cells were differentially distributed and for the first time we could show close contact between natural killer cells and CD1a(+) dendritic cells. Dendritic cells preincubated with Malassezia became less susceptible to natural-killer-cell-induced cell death, suggesting a direct effect imposed by Malassezia upon interaction of dendritic cells with natural killer cells. These findings indicate that natural killer cells and dendritic cells can interact in the skin and that Malassezia affects the interaction between natural killer cells and dendritic cells. Our data suggest that natural killer cells may play a role in regulating dendritic cells in atopic eczema/dermatitis syndrome.	Karolinska Hosp, Karolinska Inst, Dept Med, Unit Clin Allergy Res, S-17176 Stockholm, Sweden; Karolinska Inst, Ctr Microbiol & Tumor Biol, Stockholm, Sweden; Uppsala Univ, Dept Anim Dev & Genet, Uppsala, Sweden	Buentke, E (reprint author), Karolinska Hosp, Karolinska Inst, Dept Med, Unit Clin Allergy Res, L2-04, S-17176 Stockholm, Sweden.			Chambers, Benedict/0000-0003-0437-8441			Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; Banchereau J, 2000, ANNU REV IMMUNOL, V18, P767, DOI 10.1146/annurev.immunol.18.1.767; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Bouloc A, 2000, J INVEST DERMATOL, V115, P1160, DOI 10.1046/j.1523-1747.2000.0202a-4.x; Buentke E, 2000, CLIN EXP ALLERGY, V30, P1759, DOI 10.1046/j.1365-2222.2000.00937.x; Buentke E, 2001, CLIN EXP ALLERGY, V31, P1583, DOI 10.1046/j.1365-2222.2001.01199.x; Carbone E, 1999, EUR J IMMUNOL, V29, P4022, DOI 10.1002/(SICI)1521-4141(199912)29:12<4022::AID-IMMU4022>3.0.CO;2-O; Chambers BJ, 1996, IMMUNITY, V5, P311, DOI 10.1016/S1074-7613(00)80257-5; CHIARELLI F, 1987, BRIT J DERMATOL, V116, P651, DOI 10.1111/j.1365-2133.1987.tb05898.x; COOPER KD, 1994, J INVEST DERMATOL, V102, P128, DOI 10.1111/1523-1747.ep12371746; Eriksson M, 1999, J EXP MED, V190, P1005, DOI 10.1084/jem.190.7.1005; Faergemann J, 1999, ALLERGY, V54, P413, DOI 10.1034/j.1398-9995.1999.00089.x; Ferlazzo G, 2002, J EXP MED, V195, P343, DOI 10.1084/jem.20011149; Ferlazzo G, 2001, IMMUNOL LETT, V76, P37, DOI 10.1016/S0165-2478(00)00323-0; Fernandez NC, 1999, NAT MED, V5, P405; Geldhof AB, 1998, BLOOD, V91, P196; Gerosa F, 2002, J EXP MED, V195, P327, DOI 10.1084/jem.20010938; Goodier MR, 2000, J IMMUNOL, V165, P139; Granucci F, 2001, NAT IMMUNOL, V2, P882, DOI 10.1038/ni0901-882; Grufman P, 2000, EUR J IMMUNOL, V30, P1088, DOI 10.1002/(SICI)1521-4141(200004)30:4<1088::AID-IMMU1088>3.0.CO;2-O; Hashiro M, 1998, J DERMATOL SCI, V16, P231, DOI 10.1016/S0923-1811(97)00074-1; Johansson C, 2002, J INVEST DERMATOL, V118, P1044, DOI 10.1046/j.1523-1747.2002.01758.x; Johansson SGO, 2001, ALLERGY, V56, P813, DOI 10.1034/j.1398-9995.2001.t01-1-00001.x; JOHNSON GD, 1982, J IMMUNOL METHODS, V55, P231, DOI 10.1016/0022-1759(82)90035-7; Kaburagi Y, 2001, ARCH DERMATOL RES, V293, P350, DOI 10.1007/s004030100230; Korsgren M, 1999, J EXP MED, V189, P553, DOI 10.1084/jem.189.3.553; LESKO MJ, 1989, CLIN EXP ALLERGY, V19, P633, DOI 10.1111/j.1365-2222.1989.tb02759.x; Leung DYM, 2000, J ALLERGY CLIN IMMUN, V105, P860, DOI 10.1067/mai.2000.106484; Linder MT, 2000, CLIN EXP ALLERGY, V30, P122, DOI 10.1046/j.1365-2222.2000.00702.x; Mayser P, 2000, ACTA DERM-VENEREOL, V80, P357, DOI 10.1080/000155500459303; Minter RM, 2001, P NATL ACAD SCI USA, V98, P277, DOI 10.1073/pnas.250489297; Moretta A, 2001, ANNU REV IMMUNOL, V19, P197, DOI 10.1146/annurev.immunol.19.1.197; NAKAMURA S, 1995, AM J SURG PATHOL, V19, P284, DOI 10.1097/00000478-199503000-00006; Piccioli D, 2002, J EXP MED, V195, P335, DOI 10.1084/jem.20010934; ROMANI N, 1994, J EXP MED, V180, P83, DOI 10.1084/jem.180.1.83; Romani N, 1996, J IMMUNOL METHODS, V196, P137, DOI 10.1016/0022-1759(96)00078-6; SALLUSTO F, 1994, J EXP MED, V179, P1109, DOI 10.1084/jem.179.4.1109; Scheynius A, 2002, INT ARCH ALLERGY IMM, V127, P161, DOI 10.1159/000053860; Spaggiari GM, 2001, EUR J IMMUNOL, V31, P1656, DOI 10.1002/1521-4141(200106)31:6<1656::AID-IMMU1656>3.0.CO;2-V; STRANNEGAARD IL, 1980, ACTA DERM-VENER    S, V92, P48; Vulcano M, 2001, EUR J IMMUNOL, V31, P812, DOI 10.1002/1521-4141(200103)31:3<812::AID-IMMU812>3.0.CO;2-L; WEHRMANN W, 1990, INT ARCH ALLER A IMM, V92, P318; Werfel T, 1998, ALLERGY, V53, P731; Wilson JL, 1999, J IMMUNOL, V163, P6365; ZACHARY CB, 1985, BRIT J DERMATOL, V112, P149, DOI 10.1111/j.1365-2133.1985.tb00078.x; Zhou LJ, 1996, P NATL ACAD SCI USA, V93, P2588, DOI 10.1073/pnas.93.6.2588	46	93	101	0	2	BLACKWELL PUBLISHING INC	MALDEN	350 MAIN ST, MALDEN, MA 02148 USA	0022-202X			J INVEST DERMATOL	J. Invest. Dermatol.	OCT	2002	119	4					850	857		10.1046/j.1523-1747.2002.00132.x		8	Dermatology	Dermatology	612KC	WOS:000179072800013	12406330	
J	Jarvis, D; Chinn, S; Potts, J; Burney, P				Jarvis, D; Chinn, S; Potts, J; Burney, P		European Community Resp Hlth Surve	Association of body mass index with respiratory symptoms and atopy: results from the European Community Respiratory Health Survey	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article							YOUNG-ADULTS; ASTHMA; OBESITY; WEIGHT; OVERWEIGHT; CHILDREN; WHEEZE; LEPTIN; RISK	Background There are several reports showing that obese adults report more respiratory symptoms suggestive of asthma than those who are not obese. Objective To determine the association of body mass index with respiratory symptoms and atopy in young adults Method Information collected from 15 454 participants in the European Community Respiratory Health Survey, a multicentre cross-sectional survey of young adults, was analysed to determine the association of body mass index with respiratory symptoms and atopy. Results Men and women with a body mass index of greater than 30 were at an increased risk of wheeze with shortness of breath compared with those with a body mass of 20-24.99 (OR in men 1.85, 95% confidence interval 1.41-2.42; OR in women 2.03, 95% confidence interval 1.59-2.58). Similar associations were observed for other symptoms suggestive or asthma, Body mass index was not associated with 'hayfever or nasal allergies', specific IgE to house dust mite. grass or cat or with total IgE in men or women. Conclusion Reported associations of body mass index with symptoms suggestive of asthma are unlikely to be explained by a higher risk of atopy in the obese. Alternative explanations must be sought.	Dept Publ Hlth Sci, London SE1 3QD, England	Jarvis, D (reprint author), Dept Publ Hlth Sci, Capital House,42 Weston St, London SE1 3QD, England.		Jarvis, Deborah/E-6494-2011				Bodner C, 1999, EUR RESPIR J, V13, P22, DOI 10.1183/09031936.99.13102299; BURNEY PGJ, 1989, INT J EPIDEMIOL, V18, P165, DOI 10.1093/ije/18.1.165; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; Camargo CA, 1999, ARCH INTERN MED, V159, P2582, DOI 10.1001/archinte.159.21.2582; Chen Y, 1999, AM J EPIDEMIOL, V150, P255; Chinn S, 2001, THORAX, V56, P845, DOI 10.1136/thorax.56.11.845; Clement K, 1999, DIABETES, V48, P398, DOI 10.2337/diabetes.48.2.398; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; Grievink L, 1999, EUR J CLIN NUTR, V53, P813, DOI 10.1038/sj.ejcn.1600854; Hu GZ, 2000, AM J EPIDEMIOL, V151, P975; Huang SL, 1999, CLIN EXP ALLERGY, V29, P323; Isidori AM, 1999, J CLIN ENDOCR METAB, V84, P3673, DOI 10.1210/jc.84.10.3673; JANSON C, 1995, J INTERN MED, V237, P277; Janson C, 1997, EUR RESPIR J, V10, P1795, DOI 10.1183/09031936.97.10081795; Luder E, 1998, J PEDIATR-US, V132, P699, DOI 10.1016/S0022-3476(98)70363-4; Patterson P E, 1999, Curr Opin Pulm Med, V5, P63, DOI 10.1097/00063198-199901000-00011; Schachter LM, 2001, THORAX, V56, P4, DOI 10.1136/thorax.56.1.4; SEIDELL JC, 1986, AM J PUBLIC HEALTH, V76, P264, DOI 10.2105/AJPH.76.3.264; Shaheen SO, 1999, THORAX, V54, P396; SOMERVILLE SM, 1984, ARCH DIS CHILD, V59, P940; Spicer LJ, 1997, ENDOCRINOLOGY, V138, P3374, DOI 10.1210/en.138.8.3374; Stenius-Aarniala B, 2000, BRIT MED J, V320, P827, DOI 10.1136/bmj.320.7238.827; Tantisira K, 2001, THORAX S2, V56; VALDIVIA GS, 1999, EUR RESPIR J, V14, P143; WHEELDON NM, 1994, BRIT J CLIN PHARMACO, V37, P583; Xu BZ, 2000, J ALLERGY CLIN IMMUN, V105, P393, DOI 10.1016/S0091-6749(00)90095-2	26	93	94	0	2	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	JUN	2002	32	6					831	837		10.1046/j.1365-2222.2002.01380.x		7	Allergy; Immunology	Allergy; Immunology	568NL	WOS:000176548400006	12047427	
J	Rauh, VA; Chew, GL; Garfinkel, RS				Rauh, VA; Chew, GL; Garfinkel, RS			Deteriorated housing contributes to high cockroach allergen levels in inner-city households	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						childhood asthma; cockroach allergens; housing problems; inner-city minority populations	INDOOR ALLERGENS; SOCIOECONOMIC-STATUS; RISK-FACTORS; BLACK-WOMEN; ASTHMA; EXPOSURE; CHILDREN; CHILDHOOD; HEALTH; SENSITIZATION	The high prevalence of childhood asthma in low-income, inner-city populations is not fully understood but has been at least partly attributed to the disproportionate exposures associated with socioeconomic disadvantage. The contribution of indoor allergens to asthma is well documented, but links between socioeconomic disadvantage and indoor allergen levels are not clear. We investigated levels of cockroach allergens (Bla g 2) in a sample of 132 Dominican or African American low-income households with young children in northern Manhattan in New York City (40% were receiving public assistance) to determine whether the distribution of allergens is a function of housing deterioration. Deterioration was measured by the presence and number of physical housing problems (holes in the ceilings and walls, water damage, etc.). More than 50% of the sample had two or more types of housing dilapidation, and 67% of the sample reported cockroach sightings in their homes. Samples of dust were collected from kitchen and bedroom surfaces. We hypothesized that the greater the dilapidation, the higher the allergen levels, independent of income, sociocultural factors, and pest-control methods. In addition, we hypothesized that the homes of families characterized by frequent moves (23.5%) would have higher allergen levels than more stable families. Results showed significant positive associations between housing deterioration and allergen levels in kitchens, after adjusting for income and ethnicity, with independent effects of residential stability (p < 0.05). Bedroom allergen levels were associated with housing instability (p < 0.01) and etlinicity (p < 0.01). Findings demonstrated that indoor household allergen levels are related to degree of household disrepair, after adjusting for individual family attributes, suggesting that social-structural aspects of housing may be appropriate targets for public health interventions designed to reduce allergen exposure.	Columbia Univ, Mailman Sch Publ Hlth, Heilbrunn Ctr Populat & Family Hlth, New York, NY 10032 USA; Columbia Univ, Mailman Sch Publ Hlth, Dept Environm Hlth, New York, NY 10032 USA; Columbia Univ Coll Phys & Surg, Dept Psychiat, New York, NY 10032 USA	Rauh, VA (reprint author), Columbia Univ, Mailman Sch Publ Hlth, Heilbrunn Ctr Populat & Family Hlth, 60 Haven Ave,B-2, New York, NY 10032 USA.				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Health Perspect.	APR	2002	110			2			323	327				5	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	542WE	WOS:000175066600026	11929744	
J	Fahy, JV				Fahy, JV			Remodeling of the airway epithelium in asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article; Proceedings Paper	16th Annual Transatlantic Airway Conference (TAC)	JAN, 2001	SAN FRANCISCO, CALIFORNIA			asthma; desquamation; epithelium; goblet cell; mucin	GOBLET CELL METAPLASIA; BRONCHOALVEOLAR LAVAGE FLUID; GLAND SEROUS CELLS; MILD ASTHMA; BRONCHIAL EPITHELIUM; MUCUS PRODUCTION; INDUCED SPUTUM; PLASMA EXUDATION; MURINE MODEL; INFLAMMATION	Several pathologic changes occur in the airway epithelium in asthma, but the relationship between these changes and the initiation and progression of asthma remains poorly understood. One possibility is that changes in the structure and function of the epithelium induced by environmental exposure in genetically susceptible subjects represent primary pivotal events that occur early in the pathogenesis of asthma. Alternatively, these epithelial changes may occur simply as a consequence of pivotal early events in other systems, such as immune deviation in childhood to a helper T cell type 2 (Th2) subtype of CD4* cells. Epithelial desquamation in asthma represents a pathologic change that is frequently cited as important for the mechanisms of airway remodeling and airway hyperresponsiveness. Desquamation of the epithelium may not represent true pathology, however, but may instead be an artifact of tissue sampling and handling. Evidence is more firm for other pathologic changes in the epithelium. For example, goblet cell numbers are increased in asthma, leading to increases in stored mucins in the epithelium and in secreted mucins in sputum. The functional consequences of these changes include sputum production and airway narrowing, which lead to asthma exacerbations. Currently available data suggest that an important mechanism for goblet cell hyperplasia in asthma is the action of Th2 cytokines. Improved understanding of epithelial goblet cell abnormalities in asthma will hopefully lead to novel therapies for mucin hypersecretion, which is an important cause of morbidity and mortality.	Univ Calif San Francisco, Dept Med, Div Pulm & Crit Care, San Francisco, CA 94143 USA; Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA	Fahy, JV (reprint author), Univ Calif San Francisco, Dept Med, Div Pulm & Crit Care, Box 0111,505 Parnassus Ave, San Francisco, CA 94143 USA.				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J. Respir. Crit. Care Med.	NOV 15	2001	164	10		S			S46	S51				6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	504AH	WOS:000172833700005	11734466	
J	ten Brinke, A; van Dissel, JT; Sterk, PJ; Zwinderman, AH; Rabe, KF; Bel, EH				ten Brinke, A; van Dissel, JT; Sterk, PJ; Zwinderman, AH; Rabe, KF; Bel, EH			Persistent airflow limitation in adult-onset nonatopic asthma is associated with serologic evidence of Chlamydia pneumoniae infection	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; severity of illness index; airway obstruction; prognosis; chronic disease; phenotype; Chlamydia pneumoniae; infection; immunology; human	AIR-FLOW OBSTRUCTION; BRONCHOALVEOLAR LAVAGE; LUNG-FUNCTION; PULMONARY-DISEASE; INTRINSIC ASTHMA; PERIPHERAL-BLOOD; BRONCHIAL-ASTHMA; FOLLOW-UP; ANTIBODIES; IMMUNOPATHOLOGY	Background: Persistent airflow limitation may develop in patients with asthma, particularly in adults with nonatopic (intrinsic) disease. Although the underlying mechanisms are still unknown, respiratory infections might be involved. Objective: We investigated the annual loss of lung function in relation to seropositivity to Chlamydia pneumoniae in different subgroups of patients with severe asthma according to age at onset of asthma and atopic status. Methods: One hundred one nonsmoking outpatients with a pulmonologist's diagnosis of severe asthma (32 men and 69 women; mean age, 46.0 years; range, 18-75 years) were included in a cross-sectional study. C pneumoniae-specific serum IgG and IgA were measured by means of ELISA. The estimated decline in lung function was calculated from the relationship between postbronchodilator FEV1/vital capacity (percent predicted) and the duration of asthma and expressed as the slope of the regression line. Results: Patients with adult-onset nonatopic asthma and positive IgG antibodies to C pneumoniae had a significantly steeper slope of the regression line compared with the other subgroups of asthmatic patients (P = .001), being indicative of a 4-fold greater estimated decline in postbronchodilator FEV1/vital capacity (2.3% vs 0.5% predicted per year of asthma duration). Conclusion: These results suggest that C pneumoniae infection might promote the development of persistent airflow limitation in patients with nonatopic adult-onset asthma. It remains to be established whether viable pathogens that are accessible for therapeutic intervention are still present in the lower airways.	Leiden Univ, Med Ctr, Dept Pulm Dis, NL-2300 RC Leiden, Netherlands; Leiden Univ, Med Ctr, Dept Infect Dis, NL-2300 RC Leiden, Netherlands; Leiden Univ, Med Ctr, Dept Med Stat, NL-2300 RC Leiden, Netherlands	ten Brinke, A (reprint author), Leiden Univ, Med Ctr, Dept Pulm Dis, C3-P,POB 9600, NL-2300 RC Leiden, Netherlands.						Barnes PJ, 1998, EUR RESPIR J, V12, P1209, DOI 10.1183/09031936.98.12051209; Black PN, 2000, EUR RESPIR J, V15, P254, DOI 10.1034/j.1399-3003.2000.15b06.x; BROWN PJ, 1984, THORAX, V39, P131, DOI 10.1136/thx.39.2.131; Cook PJ, 1998, THORAX, V53, P254; Cunningham AF, 1998, EUR RESPIR J, V11, P345, DOI 10.1183/09031936.98.11020345; Hahn DL, 1996, EPIDEMIOL INFECT, V117, P513; HAHN DL, 1991, JAMA-J AM MED ASSOC, V266, P225, DOI 10.1001/jama.266.2.225; Hansen EF, 1999, AM J RESP CRIT CARE, V159, P1267; Humbert M, 1999, IMMUNOL TODAY, V20, P528, DOI 10.1016/S0167-5699(99)01535-2; Humbert M, 1996, AM J RESP CRIT CARE, V154, P1497; Kroegel C, 1997, EUR RESPIR J, V10, P513; Lange P, 1998, NEW ENGL J MED, V339, P1194, DOI 10.1056/NEJM199810223391703; MABEY DCW, 1987, LANCET, V2, P1491; MACEK V, 1994, AM J RESP CRIT CARE, V150, P7; MCINTOSH JC, 1992, INFECT IMMUN, V60, P2936; Miyashita N, 1998, ANN ALLERG ASTHMA IM, V80, P405; MOORE DE, 1982, LANCET, V2, P574; Quanjer PH, 1993, EUR RESPIR J, V6, P16; RACKEMANN FM, 1947, AM J MED, V3, P601, DOI 10.1016/0002-9343(47)90204-0; Reed CE, 1999, J ALLERGY CLIN IMMUN, V103, P539, DOI 10.1016/S0091-6749(99)70221-6; Tang C, 1997, EUR RESPIR J, V10, P624; Tang WL, 1996, J CLIN INVEST, V98, P2845, DOI 10.1172/JCI119113; Ulrik CS, 1999, EUR RESPIR J, V14, P892, DOI 10.1034/j.1399-3003.1999.14d27.x; Ulrik CS, 1999, EUR RESPIR J, V13, P904, DOI 10.1034/j.1399-3003.1999.13d35.x; ULRIK CS, 1994, AM J RESP CRIT CARE, V150, P629; ULRIK CS, 1992, THORAX, V47, P14, DOI 10.1136/thx.47.1.14; Virchow JC, 1996, J ALLERGY CLIN IMMUN, V98, pS27; von Hertzen L, 1999, CLIN EXP ALLERGY, V29, P522; WALKER C, 1992, AM REV RESPIR DIS, V146, P109; Ward ME, 1995, APMIS, V103, P769; Wong YK, 1999, HEART, V81, P232; Wu L, 2000, AM J RESP CRIT CARE, V162, P1148; YAMADA K, 2000, AM J RESP CRIT CARE, V161, pA606	33	93	96	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.	MAR	2001	107	3					449	454		10.1067/mai.2001.113047		6	Allergy; Immunology	Allergy; Immunology	416RE	WOS:000167793300005	11240944	
J	Su, HJ; Wu, PC; Chen, HL; Lee, FC; Lin, LL				Su, HJ; Wu, PC; Chen, HL; Lee, FC; Lin, LL			Exposure assessment of indoor allergens, endotoxin, and airborne fungi for homes in southern Taiwan	ENVIRONMENTAL RESEARCH			English	Article						airborne fungi; allergen; endotoxin; Der p 1; Der p 2	DUST MITE ALLERGENS; RESIDENTIAL CHARACTERISTICS; CONTROL CHILDREN; RISK-FACTORS; ENVIRONMENTAL EXPOSURE; DOMESTIC INTERIORS; CHILDHOOD ASTHMA; YOUNG-ADULTS; SENSITIZATION; PREVALENCE	This study was undertaken to examine the seasonal variations of domestic Der p 1, Der p 2, and endotoxin on mattress and airborne fungal concentrations in homes of asthmatic and nonasthmatic children in southern Taiwan, where temperature and relative humidity are usually high throughout the year. A group of asthmatic children (10-12 years old) were selected randomly based on a citywide questionnaire survey. The nonasthmatic children were chosen to be in the comparison group by matching in age, gender, and proximity of residence. Environmental sampling of domestic microbes was conducted once a month for a year, Twelve calendar months were grouped into spring, summer, fall, and winter according to weather data (mainly average temperature and humidity) from the Central Weather Bureau. Dust samples from a child's mattress and airborne samples fi om a child's bedroom were collected and analyzed for allergens of Der p 1 and Der p 2, endotoxin, and fungi respectively. Results show that about 65% of children's mattresses in our region have Der p 1 levels greater than 2 mug/g. It is also apparent that most airborne fungal concentrations found in homes of either asthmatic or nonasthmatic children are higher than the recommended levels of concern. The predominant genera are Cladosporium, Aspergillus, Penicillium, Alternaria, and yeast, In addition, seasonal effects seem to be a critical factor for the concentrations and distributions of domestic endotoxin in these study homes. The implication of long-term exposure to these high levels of environmental microbes and how their effects vary with seasons remain to be further characterized. (C) 2001 Academic Press.	Natl Cheng Kung Univ, Coll Med, Dept Environm & Occupat Hlth, Tainan 70428, Taiwan	Wu, PC (reprint author), Natl Cheng Kung Univ, Coll Med, Dept Environm & Occupat Hlth, 138 Sheng Li Rd, Tainan 70428, Taiwan.			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Res.	FEB	2001	85	2					135	144		10.1006/enrs.2000.4113		10	Environmental Sciences; Public, Environmental & Occupational Health	Environmental Sciences & Ecology; Public, Environmental & Occupational Health	403DT	WOS:000167027900009	11161663	
J	Buckley, DA; Wakelin, SH; Seed, PT; Holloway, D; Rycroft, RJG; White, IR; McFadden, JP				Buckley, DA; Wakelin, SH; Seed, PT; Holloway, D; Rycroft, RJG; White, IR; McFadden, JP			The frequency of fragrance allergy in a patch-test population over a 17-year period	BRITISH JOURNAL OF DERMATOLOGY			English	Article						allergic contact dermatitis; cosmetic allergy; fragrances; patch testing; perfumes	CONTACT-DERMATITIS; CONSTITUENTS; MIX; PERFUMES	Fragrances are widely encountered in our daily environment and are known to be a common cause of allergic contact dermatitis. We have reviewed our patch test data from 1980 to 1996 to establish whether the pattern of fragrance allergy has changed with time. During this period, 25,545 patients (10,450 male, 15,005 female) were patch tested with the European standard series, The mean annual frequency of positive reactions to the fragrance mix was 8.5% in females (range 6.1-10.9) and 6.7% in males (range 5.1-12.9). Females were 1.3 times more Likely to be allergic to fragrance (P < 0.001, 95% confidence interval, CI 1.17-1.41). Males with fragrance allergy were older than females by 5.6 years (mean age 48.2 vs. 42.6 years; P ( 0.001, 95% CI 3.9-7.3). The incidence of a concomitant positive patch test to balsam of Peru in fragrance-sensitive patients showed wide variation. suggesting that it is not a reliable marker of fragrance allergy, There was a positive correlation between the isomers isoeugenol and eugenol, Oak moss remained the most common overall allergen throughout the study, positive in 38.3% of females and 35.6% of males who were tested to the constituents of the fragrance mix. During the period of the study the incidence of positive tests to oak moss increased by 5% yearly (P = 0.001, 95% CI 3.2-8.7). The frequency of allergic reactions to eugenol and geraniol remained relatively constant. Isoeugenol and alpha-amyl cinnamic aldehyde sensitivity increased and hydroxycitronellal showed a slow decline. There was a striking reduction in the frequency of sensitivity to cinnamic aldehyde (by 18% yearly; P < 0.001, 95% CI 14.3-21.0) and cinnamic alcohol. (by 9% yearly; P < 0.001, 95% CI 5.2-12.9): these are now uncommon fragrance allergens. These data show temporal trends which may reflect the frequency of population exposure to individual fragrances.	St Thomas Hosp, Inst Dermatol, London SE1 7EH, England; Kings Coll London, Guys Kings & St Thomas Sch Med, Dept Publ Hlth Med, London SE1 3QD, England	St Thomas Hosp, Inst Dermatol, London SE1 7EH, England.	j.mcfadden@umds.ac.uk	Seed, Paul/C-4435-2008	Seed, Paul/0000-0001-7904-7933			BASKETTER DA, 1991, CONTACT DERMATITIS, V25, P160, DOI 10.1111/j.1600-0536.1991.tb01822.x; BECKER K, 1994, CONTACT DERMATITIS, V30, P185, DOI 10.1111/j.1600-0536.1994.tb00713.x; CALNAN CD, 1980, CONTACT DERMATITIS, V6, P500, DOI 10.1111/j.1600-0536.1980.tb05581.x; DEGROOT AC, 1993, CONTACT DERMATITIS, V28, P139, DOI 10.1111/j.1600-0536.1993.tb03373.x; DeGroot AC, 1997, CONTACT DERMATITIS, V36, P57; EDMAN B, 1994, CONTACT DERMATITIS, V31, P291, DOI 10.1111/j.1600-0536.1994.tb02021.x; EDMAN B, 1985, CONTACT DERMATITIS, V13, P129, DOI 10.1111/j.1600-0536.1985.tb02524.x; ENDERS F, 1989, CONTACT DERMATITIS, V20, P237; FROSCH PJ, 1995, CONTACT DERMATITIS, V33, P333, DOI 10.1111/j.1600-0536.1995.tb02048.x; Huber P. J., 1967, P 5 BERK S MATH STAT, P221; JOHANSEN JD, 1995, CONTACT DERMATITIS, V32, P18, DOI 10.1111/j.1600-0536.1995.tb00834.x; Johansen JD, 1996, BRIT J DERMATOL, V135, P419, DOI 10.1111/j.1365-2133.1996.tb01506.x; Larsen W G, 1987, Acta Derm Venereol Suppl (Stockh), V134, P83; LARSEN WG, 1985, J AM ACAD DERMATOL, V12, P1, DOI 10.1016/S0190-9622(85)70001-1; LARSEN WG, 1977, ARCH DERMATOL, V113, P623, DOI 10.1001/archderm.113.5.623; LEYDEN JJ, 1977, CONTACT DERMATITIS, V3, P333, DOI 10.1111/j.1600-0536.1977.tb03698.x; NIELSEN NH, 1992, ACTA DERM-VENEREOL, V72, P456; Scheinman P L, 1996, Am J Contact Dermat, V7, P65, DOI 10.1016/S1046-199X(96)90077-9; SCHNUCH A, 1993, DERMATOS BER UMWELT, V41, P60; SHEHADE S A, 1991, Contact Dermatitis, V24, P119, DOI 10.1111/j.1600-0536.1991.tb01663.x; VESTEY JP, 1986, CONTACT DERMATITIS, V15, P119, DOI 10.1111/j.1600-0536.1986.tb01310.x	21	93	94	1	5	WILEY	HOBOKEN	111 RIVER ST, HOBOKEN 07030-5774, NJ USA	0007-0963	1365-2133		BRIT J DERMATOL	Br. J. Dermatol.	FEB	2000	142	2					279	283		10.1046/j.1365-2133.2000.03298.x		5	Dermatology	Dermatology	291LX	WOS:000085737300014	10730761	
J	Montuschi, P; Santonico, M; Mondino, C; Pennazza, G; Mantini, G; Martinelli, E; Capuano, R; Ciabattoni, G; Paolesse, R; Di Natale, C; Barnes, PJ; D'Amico, A				Montuschi, Paolo; Santonico, Marco; Mondino, Chiara; Pennazza, Giorgio; Mantini, Giulia; Martinelli, Eugenio; Capuano, Rosamaria; Ciabattoni, Giovanni; Paolesse, Roberto; Di Natale, Corrado; Barnes, Peter J.; D'Amico, Arnaldo			Diagnostic Performance of an Electronic Nose, Fractional Exhaled Nitric Oxide, and Lung Function Testing in Asthma	CHEST			English	Article							VOLATILE ORGANIC-COMPOUNDS; SENSOR ARRAY; BREATH; IDENTIFICATION; CANCER; METALLOPORPHYRINS; DISCRIMINATION; CHILDREN	Background: Analysis of exhaled breath by biosensors discriminates between patients with asthma and healthy subjects. An electronic nose consists of a chemical sensor array for the detection of volatile organic compounds (VOCs) and an algorithm for pattern recognition. We compared the diagnostic performance of a prototype of an electronic nose with lung function tests and fractional exhaled nitric oxide (FENO) in patients with atopic asthma. Methods: A cross-sectional study was undertaken in 27 patients with intermittent and persistent mild asthma and in 24 healthy subjects. Two procedures for collecting exhaled breath were followed to study the differences between total and alveolar air. Seven patients with asthma and seven healthy subjects participated in a study with mass spectrometry (MS) fingerprinting as an independent technique for assessing between group discrimination. Classification was based on principal component analysis and a feed-forward neural network. Results: The best results were obtained when the electronic nose analysis was performed on alveolar air. Diagnostic performance for electronic nose, FENO, and lung function testing was 87.5%, 79.2%, and 70.8%, respectively. The combination of electronic nose and FENO had the highest diagnostic performance for asthma (95.8%). MS fingerprints of VOCs could discriminate between patients with asthma and healthy subjects. Conclusions: The electronic nose has a high diagnostic performance that can be increased when combined with FENO. Large studies are now required to definitively establish the diagnostic performance of the electronic nose. Whether this integrated noninvasive approach will translate into an early diagnosis of asthma has to be clarified. Trial registration: EUDRACT https://eudralink.emea.europa.eu; Identifier: 2007-000890-51; and clinicaltrials.gov; Identifier: NCT00819676. CHEST 2010; 137(4):790-796	[Montuschi, Paolo] Univ Cattolica Sacro Cuore, Fac Med, Dept Pharmacol, I-00168 Rome, Italy; [Santonico, Marco; Mantini, Giulia; Martinelli, Eugenio; Capuano, Rosamaria; Paolesse, Roberto; Di Natale, Corrado; D'Amico, Arnaldo] Univ Roma Tor Vergata, Dept Elect Engn, I-00173 Rome, Italy; [Pennazza, Giorgio] Univ Campus Biomed, Fac Engn, Rome, Italy; [Mondino, Chiara] IDI, Dept Immunodermatol, Rome, Italy; [Ciabattoni, Giovanni] Univ G dAnnunzio, Fac Pharm, Dept Drug Sci, Chieti, Italy; [Barnes, Peter J.] Univ London Imperial Coll Sci Technol & Med, Sch Med, Airway Dis Sect, Natl Heart & Lung Inst, London, England	Montuschi, P (reprint author), Univ Cattolica Sacro Cuore, Fac Med, Dept Pharmacol, Largo F Vito 1, I-00168 Rome, Italy.	pmontuschi@rm.unicatt.it	Paolesse, Roberto/B-8966-2013; Santonico, Marco/K-4465-2016; Capuano, Rosamaria/K-9258-2016	Paolesse, Roberto/0000-0002-2380-1404; Santonico, Marco/0000-0002-3755-6198; MONTUSCHI, Paolo/0000-0001-5589-1750; Di Natale, Corrado/0000-0002-0543-4348; Pennazza, Giorgio/0000-0003-4843-9445	Merck; Sharp; Dohme; Catholic University of the Sacred Heart [2008-2009]	Supported by Merck, Sharp, and Dohme, and Catholic University of the Sacred Heart academic grant 2008-2009.	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A., 1992, APPL MULTIVARIATE ST; Kusch P, 2004, J POLYM ENVIRON, V12, P83, DOI 10.1023/B:JOOE.0000010053.20382.d7; Machado RF, 2005, AM J RESP CRIT CARE, V171, P1286, DOI 10.1164/rccm.200409-1184OC; Malerba M, 2008, CHEST, V134, P733, DOI 10.1378/chest.08-0763; Montuschi P, 2006, J ALLERGY CLIN IMMUN, V118, P347, DOI 10.1016/j.jaci.2006.04.010; National Asthma Education and Prevention Program, 2007, NIH PUBL; Paredi P, 2000, AM J RESP CRIT CARE, V162, P1450; Pavon JLP, 2006, TRAC-TREND ANAL CHEM, V25, P257, DOI 10.1016/j.trac.2005.09.003; Petsky HL, 2007, COCHRANE DB SYST REV, DOI 10.1002/14651858.CD005603.pub2; Phillips M, 1999, J CHROMATOGR B, V729, P75, DOI 10.1016/S0378-4347(99)00127-9; Phillips M, 1997, ANAL BIOCHEM, V247, P272, DOI 10.1006/abio.1997.2069; Rock F, 2008, CHEM REV, V108, P705, DOI 10.1021/cr068121q; Sivan Y, 2009, J PEDIATR-US, V155, P211, DOI 10.1016/j.jpeds.2009.02.034; Turner APF, 2004, NAT REV MICROBIOL, V2, P161, DOI 10.1038/nrmicro823; van den Velde S, 2007, ANAL CHEM, V79, P3425, DOI 10.1021/ac062009a; [Anonymous], 1999, AM J RESP CRIT CARE, V160, P2104	25	92	95	1	20	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	APR	2010	137	4					790	796		10.1378/chest.09-1836		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	582XA	WOS:000276632400009	20081096	
J	Abramson, MJ; Puy, RM; Weiner, JM				Abramson, Michael J.; Puy, Robert M.; Weiner, John M.			Injection allergen immunotherapy for asthma	COCHRANE DATABASE OF SYSTEMATIC REVIEWS			English	Review						*Desensitization, Immunologic; Allergens [administration & dosage; immunology]; Asthma [immunology; *therapy]; Injections, Subcutaneous; Randomized Controlled Trials as Topic; Humans	HOUSE-DUST-MITE; PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND PLACEBO; DERMATOPHAGOIDES-PTERONYSSINUS EXTRACT; SUBLINGUAL-SWALLOW IMMUNOTHERAPY; GRASS-POLLEN IMMUNOTHERAPY; 3-YEAR DOUBLE-BLIND; STANDARDIZED 5-GRASS-POLLEN EXTRACT; ENZYME-POTENTIATED DESENSITIZATION; RANDOMIZED CONTROLLED-TRIAL	Background Allergen specific immunotherapy has long been a controversial treatment for asthma. Although beneficial effects upon clinically relevant outcomes have been demonstrated in randomised controlled trials, there remains a risk of severe and sometimes fatal anaphylaxis. The recommendations of professional bodies have ranged from cautious acceptance to outright dismissal. With increasing interest in new allergen preparations and methods of delivery, we updated the systematic review of allergen specific immunotherapy for asthma. Objectives The objective of this review was to assess the effects of allergen specific immunotherapy for asthma. Search strategy We searched the Cochrane Airways Group Trials Register up to 2005, Dissertation Abstracts and Current Contents. Selection criteria Randomised controlled trials using various forms of allergen specific immunotherapy to treat asthma and reporting at least one clinical outcome. Data collection and analysis Three authors independently assessed eligibility of studies for inclusion. Two authors independently performed quality assessment of studies. Main results Eighty-eight trials were included (13 new trials). There were 42 trials of immunotherapy for house mite allergy; 27 pollen allergy trials; 10 animal dander allergy trials; two Cladosporium mould allergy, two latex and six trials looking at multiple allergens. Concealment of allocation was assessed as clearly adequate in only 16 of these trials. Significant heterogeneity was present in a number of comparisons. Overall, there was a significant reduction in asthma symptoms and medication, and improvement in bronchial hyper-reactivity following immunotherapy. There was a significant improvement in asthma symptom scores (standardised mean difference -0.59, 95% confidence interval -0.83 to -0.35) and it would have been necessary to treat three patients (95% CI 3 to 5) with immunotherapy to avoid one deterioration in asthma symptoms. Overall it would have been necessary to treat four patients (95% CI 3 to 6) with immunotherapy to avoid one requiring increased medication. Allergen immunotherapy significantly reduced allergen specific bronchial hyper-reactivity, with some reduction in non-specific bronchial hyper-reactivity as well. There was no consistent effect on lung function. If 16 patients were treated with immunotherapy, one would be expected to develop a local adverse reaction. If nine patients were treated with immunotherapy, one would be expected to develop a systemic reaction (of any severity). Authors' conclusions Immunotherapy reduces asthma symptoms and use of asthma medications and improves bronchial hyper-reactivity. One trial found that the size of the benefit is possibly comparable to inhaled steroids. The possibility of local or systemic adverse effects (such as anaphylaxis) must be considered.	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J	Annesi-Maesano, I; Moreau, D; Caillaud, D; Lavaud, F; Le Moullec, Y; Taytard, A; Pauli, G; Charpin, D				Annesi-Maesano, Isabella; Moreau, David; Caillaud, Denis; Lavaud, Francois; Le Moullec, Yvon; Taytard, Andre; Pauli, Gabrielle; Charpin, Denis			Residential proximity fine particles related to allergic sensitisation and asthma in primary school children	RESPIRATORY MEDICINE			English	Article						air pollution; asthma; allergic rhinitis; traffic; NO2; PM2.5	DIESEL EXHAUST PARTICLES; AIR-POLLUTION; RESPIRATORY HEALTH; EXPOSURE; POLLUTANTS; ATOPY; IGE; SCHOOLCHILDREN; INFLAMMATION; PARTICULATE	Background: Fine particulate matter has been linked to allergies by experimental and epidemiological data having used aggregated data or concentrations provided by fixed-site monitoring stations, which may have led to misclassification of individual exposure to air pollution. Methods: A semi-individual design was employed to relate individual data on asthma and allergy of 5338 school children (10.4 +/- 0.7 years) attending 108 randomly chosen schools in 6 French cities to the concentrations of PM2.5 (fine particles with aerodynamic diameter <= 2.5 mu m) assessed in proximity of their homes. Children underwent a medical visit including skin prick test (SPT) to common allergens, exercise-induced bronchial (EIB) reactivity and skin examination for flexural dermatitis. Their parents fitted in a standardised health questionnaire. Results: After adjustment for confounders and NO2 as a potential modifier, the odds of suffering from EIB and flexural dermatitis at the period of the survey, past year atopic asthma and SPT positivity to indoor allergens were significantly increased in residential settings with PM2.5 concentrations exceeding 10 mu g/m(3) (WHO air quality limit values). The relationships were strengthened in long-term residents (current address for at least 8 years). Conclusions: Findings support the hypothesis that changes in allergy prevalence observed in recent decades might be partly related to interactions between traffic-related air pollution and allergens. Further longitudinal investigations are needed to corroborate such results. (c) 2007 Elsevier Ltd. All rights reserved.	Univ Paris 06, INSERM, UMR S 707, EPAR,Med Sch St Antoine, F-75571 Paris, France; Hop Maison Blanche, Reims, France; Lab Hyg Paris, Paris, France; Hop Haut Leveque Bordeaux, Bordeaux, France; Hop Civils, Strasbourg, France; Hop Nord Marseille, Marseille, France	Annesi-Maesano, I (reprint author), Univ Paris 06, INSERM, UMR S 707, EPAR,Med Sch St Antoine, 27 Rue Chaligny, F-75571 Paris, France.	annesi@u707.jussieu.fr	Wang, Linden/M-6617-2014; Annesi-Maesano, Isabella/D-9173-2016; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Annesi-Maesano I, 2007, EUR RESPIR J, V29, P428, DOI 10.1183/09031936.00129506; Annesi-Maesano I, 2004, CLIN EXP ALLERGY, V34, P1017, DOI 10.1111/j.1365-2222.2004.02002.x; ANNESIMAESANO I, 2001, WORLD CLEAN AIR ENV, P1; Behrendt H, 1997, INT ARCH ALLERGY IMM, V113, P69; BROOK JR, 1995, AIR WASTE MANAGE ASS, V45, P709; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; D'Amato G, 2000, J INVEST ALLERG CLIN, V10, P123; 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; EDWARDS J, 1994, ARCH ENVIRON HEALTH, V49, P223; Festy B, 1997, B ACAD NAT MED PARIS, V181, P461; Gilliland FD, 2004, LANCET, V363, P119, DOI 10.1016/S0140-6736(03)15262-2; Gilmour MI, 1995, TOXICOLOGY, V105, P335, DOI 10.1016/0300-483X(95)03230-D; 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; Knox RB, 1997, CLIN EXP ALLERGY, V27, P246; Kobayashi T, 2000, AM J RESP CRIT CARE, V162, P352; Kramer U, 2000, EPIDEMIOLOGY, V11, P64, DOI 10.1097/00001648-200001000-00014; Kunzli N, 2000, LANCET, V356, P795, DOI 10.1016/S0140-6736(00)02653-2; Lee E., 1980, STAT METHODS SURVIVA; LIANG KY, 1986, BIOMETRIKA, V73, P13, DOI 10.1093/biomet/73.1.13; Mastrangelo G, 2003, INT ARCH OCC ENV HEA, V76, P63, DOI 10.1007/s00420-002-0373-x; McConnell R, 2002, LANCET, V359, P386, DOI 10.1016/S0140-6736(02)07597-9; Miyake Yoshihiro, 2002, J Epidemiol, V12, P418; 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; Penard-Morand C, 2005, CLIN EXP ALLERGY, V35, P1279, DOI 10.1111/j.1365-2222.2005.02336.x; POPP W, 1989, ALLERGY, V44, P572, DOI 10.1111/j.1398-9995.1989.tb04202.x; Priftanji A, 2001, LANCET, V358, P1426, DOI 10.1016/S0140-6736(01)06521-7; Steerenberg PA, 2003, J TOXICOL ENV HEAL A, V66, P1421, DOI 10.1080/15287390390202054; 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; Wan H, 2001, CLIN EXP ALLERGY, V31, P279, DOI 10.1046/j.1365-2222.2001.00970.x; 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	38	92	93	1	21	W B SAUNDERS CO LTD	LONDON	32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND	0954-6111			RESP MED	Respir. Med.	AUG	2007	101	8					1721	1729		10.1016/j.rmed.2007.02.022		9	Cardiac & Cardiovascular Systems; Respiratory System	Cardiovascular System & Cardiology; Respiratory System	195IW	WOS:000248406900016	17442561	
J	Luebke, RW; Chen, DH; Dietert, R; Yang, Y; King, M; Luster, MI				Luebke, RW; Chen, DH; Dietert, R; Yang, Y; King, M; Luster, MI			The comparative immunotoxicity of five selected compounds following developmental or adult exposure	JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART B-CRITICAL REVIEWS			English	Review							DELAYED-TYPE HYPERSENSITIVITY; DEVELOPING IMMUNE-SYSTEM; TETRACHLORODIBENZO-P-DIOXIN; PRENATAL DIAZEPAM EXPOSURE; NATURAL-KILLER-CELLS; HUMORAL IMMUNITY; 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN TCDD; PERINATAL EXPOSURE; HOST-RESISTANCE; LEAD-EXPOSURE	It is well established that human diseases associated with abnormal immune function, including some common infectious diseases and asthma, are considerably more prevalent at younger ages. Although not established absolutely, it is generally believed that development constitutes a period of increased immune system susceptibility to xenobiotics, since adverse effects may occur at lower doses and/or immunomodulation may be more persistent, thus increasing the relative risk of xenobiotic exposure to the immunologically immature organism. To address this issue, a brief overview of immune maturation in humans is provided to demonstrate that functional immaturity alone predisposes the young to infection. Age-dependent differences in the immunotoxic effects of five diverse compounds, diethylstilbestrol (DES), diazepam (DZP), lead (Pb), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and tributyltin oxide (TBTO), which have undergone adult and developmental immunotoxicity testing in rodents, are then reviewed, as are human data when available. For all five chemicals, the developing immune system was found to be at greater risk than that of the adult, either because lower doses produced immunotoxicity, adverse effects were more persistent, or both.	US EPA, Immunotoxicol Branch, Expt Toxicol Div, Natl Hlth & Environm Effects Res Lab,Off Res & De, Res Triangle Pk, NC 27711 USA; US EPA, Off Childrens Hlth Protect, Washington, DC 20460 USA; Cornell Univ, Dept Microbiol & Immunol, Ithaca, NY USA; Cornell Univ, Inst Comparat & Environm Toxicol, Ithaca, NY 14853 USA; US EPA, Off Pesticides Program, Washington, DC 20460 USA; US EPA, Off Pollut Prevent & Tox, Washington, DC 20460 USA; NIOSH, Toxicol & Mol Biol Branch, Hlth Effects Lab Div, Ctr Dis Control & Prevent, Morgantown, WV USA	Luebke, RW (reprint author), US EPA, Immunotoxicol Branch, Expt Toxicol Div, Natl Hlth & Environm Effects Res Lab,Off Res & De, Res Triangle Pk, NC 27711 USA.	luebke.robert@epi.gov					AMBRUSO DR, 1984, PEDIATR RES, V18, P1148, DOI 10.1203/00006450-198411000-00019; Anetor J I, 1998, Afr J Med Med Sci, V27, P169; Baccarelli A, 2002, ENVIRON HEALTH PERSP, V110, P1169; Baird DD, 1996, J CLIN EPIDEMIOL, V49, P263, DOI 10.1016/0895-4356(95)00521-8; BALEY JE, 1985, J IMMUNOL, V134, P3042; 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Toxicol. Env. Health-Pt b-Crit. Rev.	JAN-FEB	2006	9	1					1	26		10.1080/15287390500194326		26	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	998AO	WOS:000234290500001	16393867	
J	Liao, SC; Cheng, YC; Wang, YC; Wang, CW; Yang, SM; Yu, CK; Shieh, CC; Cheng, KC; Lee, MF; Chiang, SR; Shieh, JM; Chang, MS				Liao, SC; Cheng, YC; Wang, YC; Wang, CW; Yang, SM; Yu, CK; Shieh, CC; Cheng, KC; Lee, MF; Chiang, SR; Shieh, JM; Chang, MS			IL-19 induced Th2 cytokines and was up-regulated in asthma patients	JOURNAL OF IMMUNOLOGY			English	Article							HUMAN INTERLEUKIN-10; STIMULATORY FACTOR; TRANSGENIC MICE; MURINE MODEL; T-CELLS; INFLAMMATION; RESPONSES; DETERMINES; INDUCTION; EFFECTORS	IL-19 belongs to the IL-10 family, which includes IL-10, IL-19, IL-20, IL-22, melanoma differentiation-associated gene-7 (IL-24), and AK155 (IL-26). IL-10 has been shown to inhibit allergen-induced airway hyperreactivity and inflammation. To determine whether IL-19 was also associated with asthma, we used ELISA to analyze the serum level of IL-19 in patients with asthma and found that their serum IL-19 levels were twice those of healthy controls. Patients with a high level of IL-19 also had high levels of IL-4 and IL-13. In a dust mite-induced murine model of asthma, we found that IL-19 level in asthmatic BALB/cJ mice was also twice that of healthy control mice. IL-19 transcript was also induced in the lungs of asthmatic mice. Electroporation i.m. of the IL-19 gene into healthy mice up-regulated IL-4 and IL-5, but not IL-13. However, IL-19 up-regulated IL-13 in asthmatic mice. In vitro, IL-19 induced IL-4, IL-5, IL-10, and IL-13 production by activated T cells. Activation of T cells was required for induction of IL-13 because IL-19 did not induce IL-13 production on nonstimulated T cells. Taken together, these results demonstrated that IL-19 up-regulates Th2 cytokines on activated T cells and might play an important role in the pathogenesis of asthma.	Natl Cheng Kung Univ, Coll Med, Grant Inst Biochem, Tainan 701, Taiwan; Natl Cheng Kung Univ, Coll Med, Grad Inst Microbiol & Immunol, Tainan 701, Taiwan; Chi Mei Med Ctr, Tainan, Taiwan	Chang, MS (reprint author), Natl Cheng Kung Univ, Coll Med, Grant Inst Biochem, 1 Dahsueh Rd, Tainan 701, Taiwan.	mschang@mail.ncku.edu.tw					Aihara H, 1998, NAT BIOTECHNOL, V16, P867, DOI 10.1038/nbt0998-867; CLUTTERBUCK EJ, 1989, BLOOD, V73, P1504; DEWAAL MR, 1998, CYTOKINE, P151; de Waal Malefyt R., 1991, J EXP MED, V174, P1209, DOI DOI 10.1084/JEM.174.5.1209; Ding YZ, 2000, J EXP MED, V191, P213, DOI 10.1084/jem.191.2.213; Emson CL, 1998, J EXP MED, V188, P399, DOI 10.1084/jem.188.2.399; FINKELMAN FD, 1988, J IMMUNOL, V141, P2335; Gallagher G, 2004, INT IMMUNOPHARMACOL, V4, P615, DOI 10.1016/j.intimp.2004.01.005; Gallagher G, 2000, GENES IMMUN, V1, P442, DOI 10.1038/sj.gene.6363714; Gesser B, 1997, P NATL ACAD SCI USA, V94, P14620, DOI 10.1073/pnas.94.26.14620; GO NF, 1990, J EXP MED, V172, P1625, DOI 10.1084/jem.172.6.1625; Grunig G, 1998, SCIENCE, V282, P2261, DOI 10.1126/science.282.5397.2261; Grunig G, 1997, J EXP MED, V185, P1089, DOI 10.1084/jem.185.6.1089; KOPF M, 1993, NATURE, V362, P245, DOI 10.1038/362245a0; KUNG TT, 1995, AM J RESP CELL MOL, V13, P360; Liao YC, 2002, J IMMUNOL, V169, P4288; McKenzie GJ, 1998, IMMUNITY, V9, P423, DOI 10.1016/S1074-7613(00)80625-1; Parronchi P, 1999, J IMMUNOL, V163, P5946; ROUSSET F, 1992, P NATL ACAD SCI USA, V89, P1890, DOI 10.1073/pnas.89.5.1890; SEDER RA, 1992, J EXP MED, V176, P1091, DOI 10.1084/jem.176.4.1091; SWAIN SL, 1990, J IMMUNOL, V145, P3796; THOMPSONSNIPES LA, 1991, J EXP MED, V173, P507, DOI 10.1084/jem.173.2.507; VANOOSTERHOUT AJM, 1995, J ALLERGY CLIN IMMUN, V96, P104, DOI 10.1016/S0091-6749(95)70039-0; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; Yu CK, 1999, J ALLERGY CLIN IMMUN, V104, P228, DOI 10.1016/S0091-6749(99)70140-5	25	92	101	0	4	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	DEC 1	2004	173	11					6712	6718				7	Immunology	Immunology	873UV	WOS:000225307500027	15557163	
J	Chan, HK; Chew, NYK				Chan, HK; Chew, NYK			Novel alternative methods for the delivery of drugs for the treatment of asthma	ADVANCED DRUG DELIVERY REVIEWS			English	Review						dry powder aerosol formulation; powder production process; spray drying; solvent precipitation; milling; powder properties; carrier blend; dry powder inhaler	SALBUTAMOL SULFATE; POROUS PARTICLES; INHALATION; FORMULATIONS; POWDERS; CARRIER; LACTOSE	Successful delivery of dry powder aerosols to the lung requires careful consideration of the powder production process, formulation and inhaler device. Newer production methods are emerging to prepare powders with desirable characteristics for inhalational administration. The conventional formulation approach of adding coarse lactose carriers to the drug to form binary powder systems to enhance powder flow and dispersion properties has been expanded to using finer carrier particles and hydrophobic materials, as well as ternary systems. Particle morphology and surface properties have also been explored to enhance powder performance. For the inhaler device, the new generation inhalers are designed to reduce or completely decouple the influence of air flow on the aerosol generation. Each of these determinants for powder aerosol delivery is reviewed with a strong focus on the patent literature that contains enormous information about the latest development in this field. (C) 2003 Elsevier Science B.V. All rights reserved.	Univ Sydney, Fac Pharm, Sydney, NSW 2006, Australia	Chan, HK (reprint author), Univ Sydney, Fac Pharm, A15, Sydney, NSW 2006, Australia.						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J	Clarisse, B; Laurent, AM; Seta, N; Le Moullec, Y; El Hasnaoui, A; Momas, I				Clarisse, B; Laurent, AM; Seta, N; Le Moullec, Y; El Hasnaoui, A; Momas, I			Indoor aldehydes: measurement of contamination levels and identification of their determinants in Paris dwellings	ENVIRONMENTAL RESEARCH			English	Article						aldehyde; indoor air quality; determinants; passive sampling; ventilation	FORMALDEHYDE CONCENTRATIONS; EXPOSURE; AIR; ENVIRONMENTS; TOBACCO; HEALTH	The recent increased prevalence of childhood asthma and atopy has brought into question the impact of outdoor pollutants and indoor air quality. The contributory role of aldehydes to this problem and the fact that they are mainly derived from the domestic environment make them of particular interest. This study therefore measures six different aldehyde levels in Paris dwellings from potentially different sources and identifies their indoor determinants. The study was carried out in the three principal rooms of 61 flats with no previous history of complaint for olfactory nuisance or specific symptoms, two-thirds of the flats having been recently refurbished. Aldehydes were sampled in these rooms using passive samplers, and a questionnaire on potential aldehyde sources was filled out at the same time. A multiple linear regression model was used to investigate indoor aldehyde determinants. Our study revealed that propionaldehyde and benzaldehyde were of minor importance compared to formaldehyde, acetaldehyde, pentanal, and hexanal. We found that levels of these last four compounds depended on the age of wall or floor coverings (renovations less than I year old), smoking, and ambient parameters (carbon dioxide levels, temperature). These results could help in the assessment of ndoor aldehyde emissions. (C) 2003 Elsevier Science (USA). All rights reserved.	Univ Paris 05, Lab Hyg & Sante Publ, Fac Sci Pharmaceut & Biol, F-75270 Paris 6, France; Hyge Lab Ville Paris, Paris, France; Epidemiol Unit, Lab GlaxoSmithKline, Marly Le Roi, France; Direct Act Sociale Enfance & Sante Mairie Paris, Paris, France	Momas, I (reprint author), Univ Paris 05, Lab Hyg & Sante Publ, Fac Sci Pharmaceut & Biol, 4 Ave Observ, F-75270 Paris 6, France.						Andreini BP, 2000, MICROCHEM J, V67, P11, DOI 10.1016/S0026-265X(00)00087-4; Baumann MGD, 2000, FOREST PROD J, V50, P75; BROWN V, 1996, 299 BRE BUILD RES ES; *CAL EPA, 1997, 979 CAL EPA; *COMM COST CONC CO, 1990, 13219 EUR COMM EUR C; DALLY KA, 1981, ARCH ENVIRON HEALTH, V36, P277; Garrett MH, 1998, CLIN EXP ALLERGY, V28, P459; GODISH T, 1989, AM J PUBLIC HEALTH, V79, P1044, DOI 10.2105/AJPH.79.8.1044; Gonzalez-Flesca N, 1999, ENVIRON SCI POLLUT R, V6, P95, DOI 10.1007/BF02987560; GOUPIL G, 2001, QUALITE AIR PARIS 20, P1; IARC Monographs on the evaluation of the carcinogenic risk of chemicals to humans, 1998, IARC MON, V1-29; *ITS, 1996, RES IND AIR QUAL GUI; Koeck M, 1997, Cent Eur J Public Health, V5, P127; Krieger P, 1998, REV MAL RESPIR, V15, P11; KUSKE M, POLLUTIONS AIR INTER, P1; *NAT RES COUNC COM, 1980, FORM ASS ITS HLTH DI; NORBACK D, 1995, OCCUP ENVIRON MED, V52, P388; *OFF SMOK HLTH, 1979, DHEW PHS PUBLLL, P14; SAMET JM, 1988, AM REV RESPIR DIS, V137, P221; Schleibinger H, 2001, GEFAHRST REINHALT L, V61, P26; SEXTON K, 1986, JAPCA J AIR WASTE MA, V36, P698; SEXTON K, 1989, ENVIRON SCI TECHNOL, V23, P985, DOI 10.1021/es00066a009; VANNETTEN C, 1983, CAN J PUBLIC HEALTH, V74, P55; WHO, 2000, GUID AIR QUAL; Wiglusz R, 1990, Bull Inst Marit Trop Med Gdynia, V41, P73; Wiglusz R, 1990, Bull Inst Marit Trop Med Gdynia, V41, P79	26	92	94	1	17	ACADEMIC PRESS INC ELSEVIER SCIENCE	SAN DIEGO	525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA	0013-9351			ENVIRON RES	Environ. Res.	JUL	2003	92	3					245	253		10.1016/S0013-9351(03)00039-2		9	Environmental Sciences; Public, Environmental & Occupational Health	Environmental Sciences & Ecology; Public, Environmental & Occupational Health	693WG	WOS:000183740900009	12804521	
J	Yeatts, K; Davis, KJ; Sotir, M; Herget, C; Shy, C				Yeatts, K; Davis, KJ; Sotir, M; Herget, C; Shy, C			Who gets diagnosed with asthma? Frequent wheeze among adolescents with and without a diagnosis of asthma	PEDIATRICS			English	Article						asthma; adolescents; wheezing; diagnosis; demographics; allergies	CHILDHOOD ASTHMA; VIDEO QUESTIONNAIRE; PERSISTENT WHEEZE; AFRICAN-AMERICAN; HEALTH-SERVICES; UNITED-STATES; GREAT-BRITAIN; RISK-FACTORS; CHILDREN; PREVALENCE	Objective. 1) To describe the factors associated with not receiving an asthma diagnosis among children with frequent wheezing symptoms and 2) to determine risk factors for frequent wheezing in the population. Methods. The North Carolina School Asthma Survey provided self-reported questionnaire data on respiratory health from 122 829 children ages 12 to 18 years enrolled in 499 public middle schools in North Carolina during the 1999 - 2000 school year. Questions from the International Survey of Allergies and Asthma in Childhood were used to estimate the prevalence of asthma and wheezing-related illness and associated factors. Results. Factors independently associated with undiagnosed frequent wheezing versus asymptomatic children included female gender ( odds ratio [ OR]: 1.45; 95% confidence interval [CI]: 1.35-1.54), current smoking ( OR: 2.60; 95% CI: 2.43-2.79), exposure to household smoke ( OR: 1.59; 95% CI: 1.50-1.70), low socioeconomic status ( OR: 1.52; 95% CI: 1.42-1.63), and African American ( OR: 1.25; 95% CI: 1.15-1.34), Native American ( OR: 1.35; 95% CI: 1.11-1.62), and Mexican American ( OR: 1.32; 95% CI: 1.17-1.48) race/ethnicity. Urban residence showed a weak negative association ( OR: 0.91; 95% CI: 0.85-0.96). A similar pattern of results was observed for analyses comparing odds of undiagnosed frequent wheeze versus diagnosed asthmatics. Report of allergies was less likely in frequent wheezers (70%) compared with diagnosed asthmatics (86%), but much higher than in asymptomatic children (36%). Thirty-three percent of children with undiagnosed frequent wheezing reported 1 or more physician visits in the last year for wheezing or breathing problems compared with 71% of children with diagnosed asthma, and 4% in asymptomatic children. The prevalence of any inhaler use in the past 12 months was 12% for undiagnosed frequent wheezers versus 78% for diagnosed asthmatics. The proportion of undiagnosed frequent wheezers with fair or poor self-rated health (23%) was slightly higher than diagnosed asthmatics (20%) and much higher than asymptomatic children ( 4%). Conclusions. In one of the largest adolescent asthma surveys ever reported in the United States, undiagnosed frequent wheezing was independently associated with female gender, current smoking, exposure to household smoke, low socioeconomic status, allergies, and African American, Native American, and Mexican American race/ ethnicity. Children with undiagnosed frequent wheezing were not receiving adequate health care for their asthma-like illness. Clinicians who treat adolescents should consider asking adolescents specifically about wheezing. This information may assist primary care physicians in identifying children with undiagnosed asthma in need of treatment.	Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27599 USA; GlaxoSmithKline, Worldwide Epidemiol, Res Triangle Pk, NC USA; N Carolina Dept Hlth & Human Serv, Div Publ Hlth, Raleigh, NC USA	Yeatts, K (reprint author), Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Campus Box 7435,McGavran Greenberg Hall, Chapel Hill, NC 27599 USA.						Adams P. 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J	Jones, CA; Holloway, JA; Popplewell, EJ; Diaper, ND; Holloway, JW; Vance, GHS; Warner, JA; Warner, JO				Jones, CA; Holloway, JA; Popplewell, EJ; Diaper, ND; Holloway, JW; Vance, GHS; Warner, JA; Warner, JO			Reduced soluble CD14 levels in amniotic fluid and breast milk are associated with the subsequent development of atopy, eczema, or both	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						soluble CD14; amniotic fluid; breast milk; eczema	EARLY-CHILDHOOD; IGE PRODUCTION; IMMUNE-SYSTEM; CUTTING EDGE; HAY-FEVER; LIPOPOLYSACCHARIDE; CHILDREN; ASTHMA; RECOGNITION; MICROFLORA	Background: Exposure to various microbial products in early life reduces the risk of atopy. Such exposure induces down-regulation of T(H)2 allergy-biased responses by means of pattern recognition molecules, such as CD14, an LPS receptor. Objective: We sought to determine whether infant and maternal levels of soluble CD14 (sCD14) are associated with the atopic outcomes of infants. Methods: Levels of sCD14 in plasma, amniotic fluid, and breast milk were measured with a specific ELISA in different cohorts. Expression of toll-like receptors in the fetal gut was examined by using RT-PCR. Results: Soluble CD14 levels increased during fetal development and postnatally, attaining adult levels by around 4 months of age, with an overshoot of adult levels from 6 months of age. There was no difference in plasma sCD14 levels at birth of children with a high compared with those with a low risk of development of atopy. Amniotic fluid sCD14 levels at midgestation (16-17 weeks) were significantly lower when the child was subsequently atopic (P < .05). Soluble CD14 levels in breast milk collected 3 months postpartum were significantly lower in children with eczema at 6 months of age, irrespective of whether they were atopic (P = .003). Transcripts for toll-like receptor 4, which would enable transmembrane signaling for LPS/sCD14 complexes, were expressed within fetal gut and skin. Conclusion: Exposure to reduced levels of sCD14 in the fetal and neonatal gastrointestinal tract is associated with the development of atopy, eczema, or both. Thus the exogenous supply of sCD14 might influence immunologic reactivity both locally and systemically in early life and thereby influence disease outcome.	Southampton Gen Hosp, Sch Med, Div Infect Inflammat & Repair, Southampton SO16 6YD, Hants, England; Southampton Gen Hosp, Sch Med, Div Human Genet, Southampton SO16 6YD, Hants, England	Jones, CA (reprint author), Southampton Gen Hosp, Sch Med, Div Infect Inflammat & Repair, Level G Mailpoint 803, Southampton SO16 6YD, Hants, England.		Holloway, Judith/A-1757-2010; Holloway, John/B-5424-2009	Holloway, Judith/0000-0002-2268-3071; Holloway, John/0000-0001-9998-0464	NHLBI NIH HHS [HL61858]		Arias MA, 2000, J IMMUNOL, V164, P3480; Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Beutler B, 2000, CURR OPIN IMMUNOL, V12, P20, DOI 10.1016/S0952-7915(99)00046-1; Bjorksten B, 1999, CLIN EXP ALLERGY, V29, P342; Bottcher MF, 2000, CLIN EXP ALLERGY, V30, P1590; ETAC Study Group, 1998, ALLERGY IMMUNOL, V9, P116; Farooqi IS, 1998, THORAX, V53, P927; FREY EA, 1992, J EXP MED, V176, P1665, DOI 10.1084/jem.176.6.1665; HAZIOT A, 1988, J IMMUNOL, V141, P547; Holt PG, 1997, PEDIATR ALLERGY IMMU, V8, P53, DOI 10.1111/j.1399-3038.1997.tb00145.x; Horrobin DF, 2000, AM J CLIN NUTR, V71, p367S; JANEWAY CA, 1992, IMMUNOL TODAY, V13, P11, DOI 10.1016/0167-5699(92)90198-G; Jiang QQ, 2000, J IMMUNOL, V165, P3541; Jones A C, 1994, Pediatr Allergy Immunol, V5, P230, DOI 10.1111/j.1399-3038.1994.tb00245.x; Jones CA, 2001, J ALLERGY CLIN IMMUN, V108, P235, DOI 10.1067/mai.2001.117178; Kalliomaki M, 2001, LANCET, V357, P1076, DOI 10.1016/S0140-6736(00)04259-8; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Koppelman GH, 2001, AM J RESP CRIT CARE, V163, P965; Labeta MO, 2000, J EXP MED, V191, P1807, DOI 10.1084/jem.191.10.1807; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; Lien E, 2000, J CLIN INVEST, V105, P497, DOI 10.1172/JCI8541; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; Prescott SL, 1998, J IMMUNOL, V160, P4730; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Roos T, 1997, AM J OBSTET GYNECOL, V177, P1230, DOI 10.1016/S0002-9378(97)70044-9; SPENCER J, 1986, CLIN EXP IMMUNOL, V64, P536; Strachan David P., 2000, Thorax, V55, pS2, DOI 10.1136/thorax.55.suppl_1.S2; Sudo N, 1997, J IMMUNOL, V159, P1739; Sugiyama T, 2001, J IMMUNOL, V166, P826; TALEUCHI O, 1999, IMMUNITY, V11, P443; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; Wickens K, 1999, CLIN EXP ALLERGY, V29, P766	32	92	103	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.	MAY	2002	109	5					858	866		10.1067/mai.2002.123535		9	Allergy; Immunology	Allergy; Immunology	553QW	WOS:000175687800018	11994712	
J	Anyo, G; Brunekreef, B; de Meer, G; Aarts, F; Janssen, NAH; van Vliet, P				Anyo, G; Brunekreef, B; de Meer, G; Aarts, F; Janssen, NAH; van Vliet, P			Early, current and past pet ownership: associations with sensitization, bronchial responsiveness and allergic symptoms in school children	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						pets; cats; dogs; sensitization; bronchial responsiveness; asthma	HAY-FEVER; EARLY EXPOSURE; RISK FACTOR; ASTHMA; ATOPY; FARM; LIFE; CAT; ENVIRONMENT; INFECTIONS	Background Studies have suggested that early contact with pets may prevent the development of allergy and asthma. Objective To study the association between early, current and past pet ownership and sensitization, bronchial responsiveness and allergic symptoms in school children. Methods A population of almost 3000 primary school children was investigated using protocols of the International Study on Asthma and Allergies in Childhood (ISAAC). Allergic symptoms were measured using the parent-completed ISAAC questionnaire. Sensitization to common allergens was measured using skin prick tests (SPT)s and/or serum immunoglobulin (Ig)E determinations. Bronchial responsiveness was tested using a hypertonic saline challenge. Pet ownership was investigated by questionnaire. Current, past and early exposure to pets was documented separately for cats, dogs, rodents and birds. The data on current, past and early pet exposure were then related to allergic symptoms, sensitization and bronchial responsiveness. Results Among children currently exposed to pets, there was significantly less sensitization to cat (odds ratio (OR) = 0.69) and dog (OR = 0.63) allergens, indoor allergens in general (OR = 0.64), and outdoor allergens (OR = 0.60) compared to children who never had pets in the home. There was also less hayfever (OR=0.66) and rhinitis (OR=0.76). In contrast, wheeze, asthma and bronchial responsiveness were not associated with current pet ownership. Odds ratios associated with past pet ownership were generally above unity, and significant for asthma in the adjusted analysis (OR= 1.85), suggesting selective avoidance in families with sensitized and/or symptomatic children. Pet ownership in the first two years of life only showed an inverse association with sensitization to pollen: OR = 0.71 for having had furry or feathery pets in general in the first two years of life, and OR = 0.73 for having had cats and/or dogs in the first two years of life, compared to not having had pets in the first two years of life. Conclusion These results suggest that the inverse association between current pet ownership and sensitization and hayfever symptoms was partly due to the removal of pets in families with sensitized and/or symptomatic children. Pet ownership in the first two years of life only seemed to offer some protection against sensitization to pollen.	IRAS, Div Environm & Occupat Hlth, NL-3508 TD Utrecht, Netherlands	Brunekreef, B (reprint author), IRAS, Div Environm & Occupat Hlth, POB 80176, NL-3508 TD Utrecht, Netherlands.			brunekreef, bert/0000-0001-9908-0060			Ahlbom A, 1998, INDOOR AIR, V8, P219, DOI 10.1111/j.1600-0668.1998.00003.x; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; BRUNEKREEF B, 1992, INT J EPIDEMIOL, V21, P338, DOI 10.1093/ije/21.2.338; DUC J, 1988, ALLERGY, V43, P332, DOI 10.1111/j.1398-9995.1988.tb00426.x; Ernst P, 2000, AM J RESP CRIT CARE, V161, P1563; Subcommitte on Skin Tests of the European Academy of Allergology and Clinical Immunology, 1989, ALLERGY S10, V44, P1; Forastiere F, 1997, EPIDEMIOLOGY, V8, P566, DOI 10.1097/00001648-199709000-00015; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; *ISAAC STEER COMM, 1998, PHAS 2 MOD INT STUD, P1; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Kulig M, 2000, J ALLERGY CLIN IMMUN, V105, P274, DOI 10.1016/S0091-6749(00)90076-9; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; 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; Nystad W, 1998, ALLERGY, V53, P1189, DOI 10.1111/j.1398-9995.1998.tb03840.x; RIEDLER J, 1994, AM J RESP CRIT CARE, V150, P1632; 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, 1997, J ALLERGY CLIN IMMUN, V99, P6, DOI 10.1016/S0091-6749(97)81038-X; 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; 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; Wijga A, 2001, CLIN EXP ALLERGY, V31, P576, DOI 10.1046/j.1365-2222.2001.01072.x	26	92	94	0	7	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	MAR	2002	32	3					361	366		10.1046/j.1365-2222.2002.01254.x		6	Allergy; Immunology	Allergy; Immunology	541QB	WOS:000174994300008	11940064	
J	Sicherer, SH; Furlong, TJ; DeSimone, J; Sampson, HA				Sicherer, SH; Furlong, TJ; DeSimone, J; Sampson, HA			The US Peanut and Tree Nut Allergy Registry: Characteristics of reactions in schools and day care	JOURNAL OF PEDIATRICS			English	Article							DOUBLE-BLIND; FOOD; CHILDREN; ANAPHYLAXIS; LIFE	Objective: Severe food-allergic reactions occur in schools, but. the features have not been described. Study design: Participants in the US Peanut and Tree Nut Allergy Registry (PAR) who indicated that their child experienced an allergic reaction in school or day care were randomly selected for a telephone interview conducted with a structured questionnaire. Results: Of 4586 participants in the PAR, 750 (16%) indicated a reaction in school or day care, and 100 subjects or parental surrogates described 124 reactions to peanut (115) or tree nuts (9); 64% of the reactions occurred in day care or preschool, and the remainder in elementary school or higher grades. Reactions were reported from ingestion (60%), skin contact/possible ingestion (24%), and inhalation/possible skin contact or ingestion (16%). In the majority of reactions caused by inhalation, concomitant ingestion/skin contact could not be ruled out. Various foods caused by ingestion, but peanut butter crab projects were commonly responsible for the skin contact (44%) or inhalation (41%) reactions. For 90% of reactions, medications were given (86% antihistamines, 28% epinephrine). Epinephrine was given in school by teachers in 4 cases, nurses in 7, and parents or others in the remainder. Treatment delays were attributed to delayed recognition of reactions, calling parents, not following emergency plans, and an unsuccessful attempt to administer epinephrine. Conclusions: School personnel must be educated to recognize and treat food-allergic reactions. Awareness must be increased to avoid accidental exposures, including exposure from peanut butter craft projects.	CUNY Mt Sinai Sch Med, Elliot & Roslyn Jaffe Food Allergy Inst, Dept Pediat, Div Pediat Allergy Immunol, New York, NY 10029 USA; Food Allergy Network, Fairfax, VA USA	Sicherer, SH (reprint author), CUNY Mt Sinai Sch Med, Elliot & Roslyn Jaffe Food Allergy Inst, Dept Pediat, Div Pediat Allergy Immunol, Box 1198,1 Gustave L Levy Pl, New York, NY 10029 USA.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	NICHD NIH HHS [5 P30 HD28822]		AAAAI Board of Directors, 1998, J ALLERGY CLIN IMMUN, V102, P173; BOCK SA, 1987, PEDIATRICS, V79, P683; CRESPO JF, 1995, ALLERGY, V50, P257, DOI 10.1111/j.1398-9995.1995.tb01143.x; Frazier C A, 1993, Pediatrics, V91, P516; Furlong TJ, 1998, J ALLERGY CLIN IMMUN, V101, pS104; GERN JE, 1991, NEW ENGL J MED, V324, P976, DOI 10.1056/NEJM199104043241407; HAY GH, 1994, J SCHOOL HEALTH, V64, P119; Hourihane JO, 1998, BRIT MED J, V316, P1271; Hourihane JO, 1997, J ALLERGY CLIN IMMUN, V100, P596, DOI 10.1016/S0091-6749(97)70161-1; IGEA JM, 1994, J ALLERGY CLIN IMMUN, V94, P33, DOI 10.1016/0091-6749(94)90068-X; Kalogeromitros D, 1996, ANN ALLERG ASTHMA IM, V77, P480; Mudd K E, 1995, J Sch Nurs, V11, P30; Novembre E, 1998, PEDIATRICS, V101, DOI 10.1542/peds.101.4.e8; Polasani R, 1997, ANN ALLERG ASTHMA IM, V78, P35; SAMPSON HA, 1992, NEW ENGL J MED, V327, P380, DOI 10.1056/NEJM199208063270603; Sicherer SH, 2000, J ALLERGY CLIN IMMUN, V105, P582, DOI 10.1067/mai.2000.104941; Sicherer SH, 2000, PEDIATRICS, V105, P359, DOI 10.1542/peds.105.2.359; 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; SICHERER SH, 1999, J ALLERGY CLIN IMMUN, V103, P186; Simons FER, 1998, J ALLERGY CLIN IMMUN, V101, P33, DOI 10.1016/S0091-6749(98)70190-3; YUNGINGER JW, 1988, JAMA-J AM MED ASSOC, V260, P1450, DOI 10.1001/jama.260.10.1450	22	92	93	0	14	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0022-3476	1097-6833		J PEDIATR-US	J. Pediatr.	APR	2001	138	4					560	565		10.1067/mpd.2001.111821		6	Pediatrics	Pediatrics	423KL	WOS:000168175400025	11295721	
J	Kulig, M; Klettke, U; Wahn, V; Forster, J; Bauer, CP; Wahn, U				Kulig, M; Klettke, U; Wahn, V; Forster, J; Bauer, CP; Wahn, U		MAS Study Grp	Development of seasonal allergic rhinitis during the first 7 years of life	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						seasonal allergic rhinitis; allergic sensitization; atopic family history; children	SCHOOL-CHILDREN; EAST-GERMANY; LATE-ONSET; PREVALENCE; ASTHMA; SENSITIZATION; ATOPY; RISK; ISAAC; ADOLESCENTS	Background: Against the background of the controversial discussion about an increase in allergic rhinitis in recent years, intraindividual longitudinal data is lacking for IgE-mediated seasonal allergic rhinitis (SAR), Little is known about the development of SAR in terms of prevalence and incidence rates from birth to school age. Objective: In a prospective birth cohort, we investigated the development of sensitization and symptoms of SAR. SAR should be defined with high specificity, and associated risk factors should be determined. Methods: Annual longitudinal data about seasonal allergic symptoms and sensitization was available for 587 children from birth to their seventh birthday The definition of SAR was based on a combination of exposure-related symptoms and sensitization. Results: Up to 7 years of age, SAR developed in 15% of the children. Incidence and prevalence of symptoms and sensitization were low during early childhood (<2%) and increased steadily with age. Children in which SAR had already developed in the second year all were born in spring or early summer, resulting in at least two seasons of pollen exposure before manifestation of SAR. Risk factors assessed by multiple logistic regression analysis were male sex (odds ratio [OR] = 2.4), atopic mothers (OR = 2.6) and fathers (OR = 3.6) having allergic rhinitis themselves, first-born child (OR = 2.0), early sensitization to food (OR = 3.3), and atopic dermatitis (OR = 2.5), whereas early wheezing was not associated with SAR. Conclusion: The development of SAR is characterized by a marked increase in prevalence and incidence after the second year of life. Our longitudinal data further indicate that in combination with the risk of allergic predisposition, at least 2 seasons of pollen allergen exposure are needed before allergic rhinitis becomes clinically manifest.	Tech Univ, Childrens Hosp, Munich, Germany; Univ Freiburg, Childrens Hosp, Freiburg, Germany; Humboldt Univ, Dept Pediat Pneumol & Immunol, Berlin, Germany; Humboldt Univ, Charite Hosp, Inst Social Med & Epidemiol, Berlin, Germany	Kulig, M (reprint author), Univ Klinikum Charite, Inst Arbeitsmed Sozialmed & Epidemiol, D-10098 Berlin, Germany.						ABERG N, 1995, CLIN EXP ALLERGY, V25, P815, DOI 10.1111/j.1365-2222.1995.tb00023.x; BENER A, 1994, EUR J EPIDEMIOL, V10, P271, DOI 10.1007/BF01719349; Bergmann R L, 1994, Pediatr Allergy Immunol, V5, P19, DOI 10.1111/j.1399-3038.1994.tb00343.x; Bergmann RL, 1997, CLIN EXP ALLERGY, V27, P752, DOI 10.1046/j.1365-2222.1997.310899.x; BraunFahrlander C, 1997, PEDIATR ALLERGY IMMU, V8, P75, DOI 10.1111/j.1399-3038.1997.tb00147.x; Duhme H, 1998, EUR RESPIR J, V11, P840, DOI 10.1183/09031936.98.11040840; Hosmer DW, 1989, APPL LOGISTIC REGRES; Jones NS, 1998, J LARYNGOL OTOL, V112, P1019; KUEHR J, 1995, J ALLERGY CLIN IMMUN, V95, P655, DOI 10.1016/S0091-6749(95)70168-0; LAU S, 1989, J ALLERGY CLIN IMMUN, V84, P718, DOI 10.1016/0091-6749(89)90300-X; LUCK W, 1985, J PEDIATR, V99, P763; Martinez F D, 1998, Eur Respir J Suppl, V27, p3s; MEINERT R, 1994, ALLERGY, V49, P526, DOI 10.1111/j.1398-9995.1994.tb01124.x; POYSA L, 1991, ALLERGY, V46, P161, DOI 10.1111/j.1398-9995.1991.tb00564.x; Remes ST, 1998, ALLERGY, V53, P682, DOI 10.1111/j.1398-9995.1998.tb03954.x; Rusconi F, 1999, AM J RESP CRIT CARE, V160, P1617; SCHAFER T, 1993, ALLERGY, V48, P291, DOI 10.1111/j.1398-9995.1993.tb00731.x; Sherrill DL, 1999, J ALLERGY CLIN IMMUN, V104, P28, DOI 10.1016/S0091-6749(99)70110-7; Strachan DP, 1997, PEDIATR ALLERGY IMMU, V8, P161, DOI 10.1111/j.1399-3038.1997.tb00156.x; VARONIER HS, 1984, HELV PAEDIATR ACTA, V39, P129; von Mutius E, 1998, LANCET, V351, P862, DOI 10.1016/S0140-6736(97)10100-3; VONMUTIUS E, 1992, BRIT MED J, V305, P1395; Weeke E R, 1992, Rhinol Suppl, V13, P5; Wright A L, 1998, Eur Respir J Suppl, V27, p17s; WRIGHT AL, 1994, PEDIATRICS, V94, P895; ZEIGER RS, 1995, J ALLERGY CLIN IMMUN, V95, P1179, DOI 10.1016/S0091-6749(95)70074-9	26	92	98	2	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.	NOV	2000	106	5					832	839		10.1067/mai.2000.110098		8	Allergy; Immunology	Allergy; Immunology	417ZK	WOS:000167865200005	11080703	
J	Jorres, RA; Holz, O; Zachgo, W; Timm, P; Koschyk, S; Muller, B; Grimminger, F; Seeger, W; Kelly, FJ; Dunster, C; Frischer, T; Lubec, G; Waschewski, M; Niendorf, A; Magnussen, H				Jorres, RA; Holz, O; Zachgo, W; Timm, P; Koschyk, S; Muller, B; Grimminger, F; Seeger, W; Kelly, FJ; Dunster, C; Frischer, T; Lubec, G; Waschewski, M; Niendorf, A; Magnussen, H			The effect of repeated ozone exposures on inflammatory markers in bronchoalveolar lavage fluid and mucosal biopsies	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							AIRWAY INFLAMMATION; NITROGEN-DIOXIDE; HUMANS; LUNG; RESPONSES; ALLERGEN; RESPONSIVENESS; ADAPTATION; POLLUTION; FIBROSIS	The aim of this study was to investigate the cellular and biochemical events associated with repeated exposures to ozone. Twenty-three healthy subjects underwent single exposures to 200 ppb ozone and to filtered air (FA), as well as repeated exposures to 200 ppb ozone on 4 consecutive days, each for 4 h of intermittent exercise. Bronchoalveolar lavage was performed and mucosal biopsies were taken 20 h after the single or the last of the repeated exposures. As compared with FA, the single exposure to ozone caused a decrease in FEV1, an increase in the percentages of neutrophils and lymphocytes, the concentrations of total protein, IL-6, IL-8, reduced glutathione, urate, and ortho-tyrosine in BAL fluid (BALF), but no changes in the cellular composition of biopsy. After the repeated exposure, the effect on lung function was abolished and differential cell counts in BALF were not significantly different from those after FA. However, the concentrations of total protein, IL-6, IL-8, reduced glutathione, and ortho-tyrosine were still increased. IL-10 could only be detected in BALF after repeated ozone exposures. Furthermore, macroscopic scores for bronchitis, erythema, and hypervulnerability of airway mucosa were increased, as well as numbers of neutrophils in bronchial mucosal biopsies. Our data demonstrate that airway inflammation persists after repeated ozone exposure, despite attenuation of some inflammatory markers in BALF and adaptation of lung function.	Krankenhaus Grosshansdorf, Zentrum Pneumol & Thoraxchirurg, D-22927 Grosshansdorf, Germany; Univ Marburg, Policlin Dept Internal Med, Lab Resp Cell Biol, D-3550 Marburg, Germany; Univ Giessen, Zentrum Innere Med, Giessen, Germany; Univ Hamburg, Krankenhaus Eppendorf, Inst Pathol, D-2000 Hamburg, Germany; St Thomas Hosp, Rayne Inst, London SE1 7EH, England; Univ Vienna, Childrens Hosp, Vienna, Austria	Jorres, RA (reprint author), Krankenhaus Grosshansdorf, Zentrum Pneumol & Thoraxchirurg, D-22927 Grosshansdorf, Germany.		Kelly, Frank/C-6125-2009	Kelly, Frank/0000-0003-2558-8392			ARIS RM, 1993, AM REV RESPIR DIS, V148, P1363; Balmes JR, 1996, AM J RESP CRIT CARE, V153, P904; Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; BLIGH EG, 1959, CAN J BIOCHEM PHYS, V37, P911; CHANG LY, 1992, TOXICOL APPL PHARM, V115, P241, DOI 10.1016/0041-008X(92)90329-Q; Christian DL, 1998, AM J RESP CRIT CARE, V158, P532; Devlin RB, 1997, INHAL TOXICOL, V9, P211; DEVRIES JE, 1995, ANN MED, V27, P537, DOI 10.3109/07853899509002465; FARRELL BP, 1979, AM REV RESPIR DIS, V119, P725; FOLINSBEE LJ, 1994, AM J RESP CRIT CARE, V149, P98; Holz O, 1999, AM J RESP CRIT CARE, V159, P776; Holz O, 1999, AM J RESP CRIT CARE, V159, pA493; HURD SZ, 1991, J ALLERGY CLIN IMMUN, V88, P808; Jorres R, 1996, AM J RESP CRIT CARE, V153, P56; JORRES R, 1995, EUR RESPIR J, V8, P416, DOI 10.1183/09031936.95.08030416; Kelly FJ, 1996, AM J RESP CRIT CARE, V154, P1700; LUBEC G, 1994, FASEB J, V8, P1166; MAGNUSSEN H, 1998, EUR RESPIR REV, V8, P141; MCDONNELL WF, 1991, ARCH ENVIRON HEALTH, V46, P145; MULLER B, 1994, LUNG, V172, P61; PEDEN DB, 1995, AM J RESP CRIT CARE, V151, P1336; Quanjer PH, 1993, EUR RESPIR J S, V16, P5, DOI 10.1183/09041950.005s1693; SCHELEGLE ES, 1991, AM REV RESPIR DIS, V143, P1353; Sun J, 1997, RESP MED, V91, P47, DOI 10.1016/S0954-6111(97)90136-0; Tellez-Rojo MM, 1997, SALUD PUBLICA MEXICO, V39, P513, DOI 10.1590/S0036-36341997000600004; TEPPER JS, 1989, AM REV RESPIR DIS, V140, P493; THOMPSON AB, 1989, AM REV RESPIR DIS, V140, P1527; Torres A, 1997, AM J RESP CRIT CARE, V156, P728; Ward PA, 1998, AM J RESP CRIT CARE, V157, pS123	29	92	93	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.	JUN	2000	161	6					1855	1861				7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	325KV	WOS:000087675500020	10852757	
J	Johnson, SB; Riley, AW; Granger, DA; Riis, J				Johnson, Sara B.; Riley, Anne W.; Granger, Douglas A.; Riis, Jenna			The Science of Early Life Toxic Stress for Pediatric Practice and Advocacy	PEDIATRICS			English	Article						toxic stress; health disparities; social determinants of health	CHILDHOOD SOCIOECONOMIC-STATUS; INNER-CITY COHORT; IMMUNE-SYSTEM; MATERNAL-CARE; EARLY EXPERIENCE; SOCIAL-ENVIRONMENT; METABOLIC SYNDROME; INDOOR ALLERGENS; CORTISOL-LEVELS; CHILDREN	Young children who experience toxic stress are at high risk for a number of health outcomes in adulthood, including cardiovascular disease, cancers, asthma, and depression. The American Academy of Pediatrics has recently called on pediatricians, informed by research from molecular biology, genomics, immunology, and neuroscience, to become leaders in science-based strategies to build strong foundations for children's life-long health. In this report, we provide an overview of the science of toxic stress. We summarize the development of the neuroendocrine-immune network, how its function is altered by early life adversity, and how these alterations then increase vulnerability to disease. The fact that early environments shape and calibrate the functioning of biological systems very early in life is both a cautionary tale about overlooking critical periods in development and reason for optimism about the promise of intervention. Even in the most extreme cases of adversity, well-timed changes to children's environments can improve outcomes. Pediatricians are in a unique position to contribute to the public discourse on health and social welfare by explaining how factors that seem distal to child health may be the key to some of the most intractable public health problems of our generation. We consider the challenges and opportunities for preventing toxic stress in the context of contemporary pediatric practice. Pediatrics 2013;131:319-327	[Johnson, Sara B.; Riley, Anne W.] Johns Hopkins Sch Med, Dept Pediat, Baltimore, MD USA; [Johnson, Sara B.; Granger, Douglas A.; Riis, Jenna] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Populat Family & Reprod Hlth, Baltimore, MD USA; [Granger, Douglas A.] Johns Hopkins Sch Nursing, Ctr Interdisciplinary Salivary Biosci Res, Dept Acute & Chron Care, Baltimore, MD USA	Johnson, SB (reprint author), 200 N Wolfe St,Room 2017, Baltimore, MD 21287 USA.	sjohnson@jhsph.edu			National Institute on Drug Abuse [K01DA027229]	Dr Johnson is supported by a Career Development Award sponsored by the National Institute on Drug Abuse (K01DA027229).	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J	Islam, SA; Luster, AD				Islam, Sabina A.; Luster, Andrew D.			T cell homing to epithelial barriers in allergic disease	NATURE MEDICINE			English	Review							CUTANEOUS LYMPHOCYTE ANTIGEN; CHEMOKINE RECEPTORS CCR4; ACTIVATION-REGULATED CHEMOKINE; SMOOTH-MUSCLE-CELLS; ATOPIC-DERMATITIS; DENDRITIC CELLS; RETINOIC-ACID; T(H)2 CELLS; MOUSE MODEL; TH2 CELLS	Allergic inflammation develops in tissues that have large epithelial surface areas that are exposed to the environment, such as the lung, skin and gut. In the steady state, antigen-experienced memory T cells patrol these peripheral tissues to facilitate swift immune responses against invading pathogens. In at least two allergy-prone organs, the skin and the gut, memory T cells are programmed during the initial antigen priming to express trafficking receptors that enable them to preferentially home to these organs. In this review we propose that tissue-specific memory and inflammation-specific T cell trafficking facilitates the development of allergic disease in these organs. We thus review recent advances in our understanding of tissue-specific T cell trafficking and how regulation of T cell trafficking by the chemokine system contributes to allergic inflammation in mouse models and in human allergic diseases of the skin, lung and gut. Inflammation-and tissue-specific T lymphocyte trafficking pathways are currently being targeted as new treatments for non-allergic inflammatory diseases and may yield effective new therapeutics for allergic diseases.	[Islam, Sabina A.; Luster, Andrew D.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Immunol & Inflammatory Dis,Div Rheumatol Alle, Boston, MA 02115 USA	Luster, AD (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Immunol & Inflammatory Dis,Div Rheumatol Alle, Boston, MA 02115 USA.	aluster@mgh.harvard.edu			US National Institutes of Health [R37AI040618, U19AI095261]	The authors were supported by US National Institutes of Health grants R37AI040618 and U19AI095261 to A.D.L.	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Med.	MAY	2012	18	5					705	715		10.1038/nm.2760		11	Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental	Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine	938WE	WOS:000303763500038	22561834	
J	Murk, W; Risnes, KR; Bracken, MB				Murk, William; Risnes, Kari R.; Bracken, Michael B.			Prenatal or Early-Life Exposure to Antibiotics and Risk of Childhood Asthma: A Systematic Review	PEDIATRICS			English	Review						antibiotics; asthma; meta-analysis; systematic review	BIRTH COHORT; ALLERGIC DISEASE; 1ST YEAR; RESPIRATORY ILLNESS; AIRWAY INFLAMMATION; SCHOOL-AGE; CHILDREN; ECZEMA; INFECTIONS; PREVALENCE	CONTEXT: The increasing prevalence of childhood asthma has been associated with low microbial exposure as described by the hygiene hypothesis. OBJECTIVE: We sought to evaluate the evidence of association between antibiotic exposure during pregnancy or in the first year of life and risk of childhood asthma. METHODS: PubMed was systematically searched for studies published between 1950 and July 1, 2010. Those that assessed associations between antibiotic exposure during pregnancy or in the first year of life and asthma at ages 0 to 18 years (for pregnancy exposures) or ages 3 to 18 years (for first-year-of-life exposures) were included. Validity was assessed according to study design, age at asthma diagnosis, adjustment for respiratory infections, and consultation rates. RESULTS: For exposure in the first year of life, the pooled odds ratio (OR) for all studies (N = 20) was 1.52 (95% confidence interval [CI]: 1.30-1.77). Retrospective studies had the highest pooled risk estimate for asthma (OR: 2.04 [95% CI: 1.83-2.27]; n = 8) compared with database and prospective studies (OR: 1.25 [95% CI: 1.08-1.45]; n = 12). Risk estimates for studies that adjusted for respiratory infections (pooled OR: 1.16 [95% CI: 1.08-1.25]; n = 5) or later asthma onset (pooled OR for asthma at or after 2 years: OR: 1.16 [95% CI: 1.06-1.25]; n = 3) were weaker but remained significant. For exposure during pregnancy (n = 3 studies), the pooled OR was 1.24 (95% CI: 1.02-1.50). CONCLUSIONS: Antibiotics seem to slightly increase the risk of childhood asthma. Reverse causality and protopathic bias seem to be possible confounders for this relationship. Pediatrics 2011;127:1125-1138	[Murk, William; Risnes, Kari R.; Bracken, Michael B.] Yale Univ, Sch Publ Hlth, Ctr Perinatal Pediat & Environm Epidemiol, New Haven, CT 06510 USA; [Risnes, Kari R.] Norwegian Univ Sci & Technol, Dept Publ Hlth, N-7034 Trondheim, Norway	Bracken, MB (reprint author), Yale Univ, Sch Publ Hlth, Ctr Perinatal Pediat & Environm Epidemiol, 1 Church St, New Haven, CT 06510 USA.	michael.bracken@yale.edu			Liaison Committee; Central Norway Regional Health Authority; Norwegian University of Science and Technology	Dr Risnes was financially supported by a grant from the Liaison Committee between the Central Norway Regional Health Authority and the Norwegian University of Science and Technology.	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J	Varshney, P; Steele, PH; Vickery, BP; Bird, JA; Thyagarajan, A; Scurlock, AM; Perry, TT; Jones, SM; Burks, AW				Varshney, Pooja; Steele, Pamela H.; Vickery, Brian P.; Bird, J. Andrew; Thyagarajan, Ananth; Scurlock, Amy M.; Perry, Tamara T.; Jones, Stacie M.; Burks, A. Wesley			Adverse reactions during peanut oral immunotherapy home dosing	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Letter							COWS MILK ALLERGY; CHILDREN		[Varshney, Pooja; Steele, Pamela H.; Vickery, Brian P.; Bird, J. Andrew; Thyagarajan, Ananth; Burks, A. Wesley] Duke Univ, Med Ctr, Dept Pediat, Durham, NC 27710 USA; [Scurlock, Amy M.; Perry, Tamara T.; Jones, Stacie M.] Univ Arkansas Med Sci, Arkansas Childrens Hosp, Dept Pediat, Little Rock, AR 72205 USA	Varshney, P (reprint author), Duke Univ, Med Ctr, Dept Pediat, Durham, NC 27710 USA.	wesley.burks@duke.edu		Bird, John/0000-0003-3772-6078	NIAID NIH HHS [R01 AI068074-02, R01 AI068074, R01 AI068074-01A1, R01 AI068074-03, T32 AI007062, T32 AI007062-28A2, T32 AI007062-29, T32 AI007062-30, T32 AI007062-31]		Cox L, 2007, J ALLERGY CLIN IMMUN, V120, pS25, DOI 10.1016/j.jaci.2007.06.019; Hofmann AM, 2009, J ALLERGY CLIN IMMUN, V124, P286, DOI 10.1016/j.jaci.2009.03.045; Jones SM, 2009, J ALLERGY CLIN IMMUN, V124, P292, DOI 10.1016/j.jaci.2009.05.022; Meglio P, 2004, ALLERGY, V59, P980, DOI 10.1111/j.1398-9995.2004.00542.x; Skripak JM, 2008, J ALLERGY CLIN IMMUN, V122, P1154, DOI 10.1016/j.jaci.2008.09.030; Staden U, 2007, ALLERGY, V62, P1261, DOI 10.1111/j.1398-9995.2007.01501.x	6	91	91	2	6	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	2009	124	6					1351	1352		10.1016/j.jaci.2009.09.042		2	Allergy; Immunology	Allergy; Immunology	536VH	WOS:000273071500030	19913285	
J	Cooper, PJ				Cooper, Philip J.			Interactions between helminth parasites and allergy	CURRENT OPINION IN ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						allergy; asthma; geohelminths; helminths	SKIN-TEST REACTIVITY; ASCARIS-IMMUNOGLOBULIN-E; SOUTH-AFRICAN CHILDREN; INDUCED INTERLEUKIN-10; RISK-FACTORS; RURAL AREA; GABONESE SCHOOLCHILDREN; GEOHELMINTH INFECTIONS; ANTHELMINTIC TREATMENT; ATOPIC SENSITIZATION	Purpose of review To review the findings of recent human studies of the association between helminth parasite infections and allergy and discuss their potential relevance to public health. Recent findings Different helminth parasites may have different effects on allergy that may depend on the timing or intensity of the exposure or host genetic factors. Infections with Trichuris trichiura in early life are associated with a reduced prevalence of allergen skin test reactivity later in life and infants of helminth-infected mothers have been reported to have a reduced prevalence of eczema. Hookworm infection has been associated with a reduced prevalence of asthma in Ethiopia. Several studies have reported that anti-Ascaris IgE is an important risk factor for asthma, but this could be explained by an enhanced ability of atopics to produce IgE. Toxocara infections may be associated with an increased risk of wheeze in some populations that may be caused by the host response to the parasite or by parasite-enhanced Th2 responses to aeroallergens. Summary Although helminth infections can modulate the host inflammatory response directed against the parasite, a causal association between helminths and atopic diseases remains uncertain.	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van Riet E, 2007, IMMUNOBIOLOGY, V212, P475, DOI 10.1016/j.imbio.2007.03.009; von Mutius Erika, 2007, Proc Am Thorac Soc, V4, P212, DOI 10.1513/pats.200701-028AW; Weinmayr G, 2007, AM J RESP CRIT CARE, V176, P565, DOI 10.1164/rccm.200607-994OC; Wilson MS, 2007, IMMUNOL CELL BIOL, V85, P148, DOI 10.1038/sj.icb.7100014; Wordemann M, 2008, TROP MED INT HEALTH, V13, P180, DOI 10.1111/j.1365-3156.2007.01988.x	70	91	105	4	17	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	1528-4050			CURR OPIN ALLERGY CL	Curr. Opin. Allergy Clin. Immunol.	FEB	2009	9	1					29	37		10.1097/ACI.0b013e32831f44a6		9	Allergy; Immunology	Allergy; Immunology	400SH	WOS:000262888400006	19106698	
J	Flohr, C; Quinnell, RJ; Britton, J				Flohr, C.; Quinnell, R. J.; Britton, J.			Do helminth parasites protect against atopy and allergic disease?	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review							SCHISTOSOMA-MANSONI INFECTION; NECATOR-AMERICANUS INFECTION; SKIN-TEST REACTIVITY; IGE ANTIBODY-LEVELS; HOUSE-DUST MITE; ASCARIS-LUMBRICOIDES; RURAL AREA; GABONESE SCHOOLCHILDREN; INDUCED INTERLEUKIN-10; INTESTINAL PARASITES	Allergic diseases are rare in areas with high helminth parasite exposure and common where helminth exposure is lacking or significantly reduced, such as urban areas of developing countries and industrialized nations. Studies suggest that helminths induce a systemic immuno-modulatory network, including regulatory T cells and anti-inflammatory IL-10, which might play a key role in the protection against the allergic phenotype. Here, we review the current cross-sectional, birth cohort, and intervention study evidence for a protective effect of helminth infection on allergy. There is increasing evidence for a causal relationship between helminth infection and reduced skin prick test responsiveness to allergens. Cross-sectional studies have shown a consistent negative relationship, and these results have been confirmed in several, although not all, intervention studies. The immunological basis for this protective effect is less clear. Recent studies do not support the mast-cell IgE saturation hypothesis, but suggest that protection is associated with IL-10 production. As for allergic disease, cross-sectional studies support a negative relationship between clinical asthma and infection with some helminth species, particularly hookworm, but more studies are required to draw conclusions for eczema and rhinitis. In addition, none of the few intervention studies to date have demonstrated an increase in clinical allergy after helminth treatment, and further studies are needed. Furthermore, we are only beginning to understand the host genetic factors that are potentially involved. A genetically predetermined T-helper type 2 cell-dominated cytokine milieu reduces parasite burden and may enhance host survival in an environment where helminth parasites are prevalent. Lack of parasite exposure in such hosts might lead to hypersensitivity to seemingly minor environmental allergen stimuli. Large birth cohort studies in helminth-endemic areas that use epidemiological, genetic, and immunological tools are required to further examine how helminth parasites affect the development of atopy and allergic disease. Intervention studies with hookworm in parasite-naive allergic individuals are currently ongoing in the United Kingdom to test the above hypotheses further.	[Flohr, C.] Univ Nottingham, Inst Clin Res, Nottingham NG7 2UH, England; [Quinnell, R. J.] Univ Leeds, Fac Biol Sci, Inst Integrat & Comparat Biol, Leeds, W Yorkshire, England; [Britton, J.] Univ Nottingham, Dept Epidemiol & Publ Hlth, Nottingham NG7 2RD, England; [Flohr, C.] Univ Nottingham, Ctr Evidence Based Dermatol, Nottingham NG7 2UH, England	Flohr, C (reprint author), Univ Nottingham, Inst Clin Res, Nottingham NG7 2UH, England.	carsten.flohr@nottingham.ac.uk					ALSHISHTAWY MM, 1991, INT ARCH ALLER A IMM, V96, P348; Araujo MI, 2000, INT ARCH ALLERGY IMM, V123, P145, DOI 10.1159/000024433; Araujo MIAS, 2004, J INFECT DIS, V190, P1797, DOI 10.1086/425017; Arruda LK, 2005, CURR OPIN ALLERGY CL, V5, P399, DOI 10.1097/01.all.0000182536.55650.d0; Babu S, 2006, J IMMUNOL, V176, P3248; Barnes KC, 2005, CURR OPIN ALLERGY CL, V5, P379, DOI 10.1097/01.all.0000182543.37724.7b; Bashir MEH, 2002, J IMMUNOL, V169, P3284; BAZARAL M, 1973, CLIN EXP IMMUNOL, V14, P117; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; BURRELMORRIS C, 2000, EPIDEMIOLOGY CAUSE P, P169; 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Exp. Allergy	JAN	2009	39	1					20	32		10.1111/j.1365-2222.2008.03134.x		13	Allergy; Immunology	Allergy; Immunology	392DE	WOS:000262282300006	19128351	
J	O'Connor, GT; Neas, L; Vaughn, B; Kattan, M; Mitchell, H; Crain, EF; Evans, R; Gruchalla, R; Morgan, W; Stout, J; Adams, GK; Lippmann, M				O'Connor, George T.; Neas, Lucas; Vaughn, Benjamin; Kattan, Meyer; Mitchell, Herman; Crain, Ellen F.; Evans, Richard, III; Gruchalla, Rebecca; Morgan, Wayne; Stout, James; Adams, G. Kenneth; Lippmann, Morton			Acute respiratory health effects of air pollution on children with asthma in US inner cities	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						nitrogen dioxide; ozone; sulfur dioxide; carbon monoxide; fine particle emissions; asthma in children	PEAK EXPIRATORY FLOW; FINE PARTICLES; DAILY MORTALITY; ENVIRONMENTAL INTERVENTION; HOSPITAL ADMISSIONS; CHILDHOOD ASTHMA; SYMPTOM SEVERITY; MEDICATION USE; MEXICO-CITY; URBAN AIR	Background: Children with asthma in inner-city communities may be particularly vulnerable to adverse effects of air pollution because of their airways disease and exposure to relatively high levels of motor vehicle emissions. Objective: To investigate the association between fluctuations in outdoor air pollution and asthma morbidity among inner-city children with asthma. Methods: We analyzed data from 861 children with persistent asthma in 7 US urban communities who performed 2-week periods of twice-daily pulmonary function testing every 6 months for 2 years. Asthma symptom data were collected every 2 months. Daily pollution measurements were obtained from the Aerometric Information Retrieval System. The relationship of lung function and symptoms to fluctuations in pollutant concentrations was examined by using mixed models. Results: Almost all pollutant concentrations measured were below the National Ambient Air Quality Standards. In single-pollutant models, higher 5-day average concentrations of NO(2), sulfur dioxide, and particles smaller than 2.5 mu m were associated with significantly lower pulmonary function. Higher pollutant levels were independently associated with reduced lung function in a 3-pollutant model. Higher concentrations of NO(2) and particles smaller than 2.5 mu m were associated with asthma-related missed school days, and higher NO(2) concentrations were associated with asthma symptoms. Conclusion: Among inner-city children with asthma, short-term increases in air pollutant concentrations below the National Ambient Air Quality Standards were associated with adverse respiratory health effects. The associations with NO(2) suggest that motor vehicle emissions may be causing excess morbidity in this population.	[O'Connor, George T.] Boston Univ, Sch Med, Ctr Pulm, Dept Med, Boston, MA 02118 USA; [Neas, Lucas; Mitchell, Herman] US EPA, Res Triangle Pk, NC 27711 USA; [Vaughn, Benjamin] Rho Fed Syst Div Inc, Chapel Hill, NC USA; [Kattan, Meyer] Mt Sinai Sch Med, Dept Pediat, New York, NY USA; [Crain, Ellen F.] Albert Einstein Coll Med, Dept Pediat Emergency Med, Jacobi Med Ctr, Bronx, NY 10467 USA; [Evans, Richard, III] Northwestern Univ, Sch Med, Dept Pediat & Med, Chicago, IL 60611 USA; [Gruchalla, Rebecca] Univ Texas SW Med Ctr Dallas, Dept Med, Dallas, TX 75390 USA; [Gruchalla, Rebecca] Univ Texas SW Med Ctr Dallas, Dept Pediat, Dallas, TX 75390 USA; [Morgan, Wayne] Univ Arizona, Coll Med, Resp Sci Ctr, Tucson, AZ 85721 USA; [Stout, James] Univ Washington, Sch Med, Dept Pediat, Seattle, WA 98195 USA; [Adams, G. Kenneth] Natl Inst Allergy & Infect Dis, Bethesda, MD USA; [Lippmann, Morton] NYU, Sch Med, Dept Environm Med, Tuxedo Pk, NY USA	O'Connor, GT (reprint author), Boston Univ, Sch Med, Ctr Pulm, Dept Med, 715 Albany St,Room 304, Boston, MA 02118 USA.	goconnor@bu.edu	Neas, Lucas/J-9378-2012; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; O'Connor, George/0000-0002-6476-3926	NCRR NIH HHS [M01RR00533]; NIAID NIH HHS [AI-39902, AI-39761, AI-39769, AI-39776, AI-39785, AI-39789, AI-39900, AI-39901]		Barnett AG, 2005, AM J RESP CRIT CARE, V171, P1272, DOI 10.1164/rccm.200411-1586OC; Belanger K, 2006, AM J RESP CRIT CARE, V173, P297, DOI 10.1164/rccm.200408-1123OC; Burnett RT, 2000, INHAL TOXICOL, V12, P15, DOI 10.1080/089583700750019495; Crain EF, 2002, ENVIRON HEALTH PERSP, V110, P939; 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; Friedman MS, 2001, JAMA-J AM MED ASSOC, V285, P897, DOI 10.1001/jama.285.7.897; Gauderman WJ, 2004, NEW ENGL J MED, V351, P1057, DOI 10.1056/NEJMoa040610; Gold DR, 1999, EPIDEMIOLOGY, V10, P8, DOI 10.1097/00001648-199901000-00004; Hoek G, 2002, LANCET, V360, P1203, DOI 10.1016/S0140-6736(02)11280-3; HSU KHK, 1979, J PEDIATR-US, V95, P14, DOI 10.1016/S0022-3476(79)80075-X; ITO K, 2005, J EXPO ANAL ENV EPID, V15, P173; Krewski D, 2007, J TOXICOL ENV HEAL A, V70, P275, DOI 10.1080/15287390600884859; Laden F, 2000, ENVIRON HEALTH PERSP, V108, P941, DOI 10.2307/3435052; McConnell R, 2003, AM J RESP CRIT CARE, V168, P790, DOI 10.1164/rccm.200304-466OC; Morgan WJ, 2004, NEW ENGL J MED, V351, P1068, DOI 10.1056/NEJMoa032097; Mortimer KM, 2002, EUR RESPIR J, V19, P699, DOI 10.1183/09031936.02.00247102; Neas LM, 1999, EPIDEMIOLOGY, V10, P550, DOI 10.1097/00001648-199909000-00015; NEAS LM, 1995, AM J EPIDEMIOL, V141, P111; Norris G, 1999, ENVIRON HEALTH PERSP, V107, P489, DOI 10.2307/3434632; Ostro B, 2001, EPIDEMIOLOGY, V12, P200, DOI 10.1097/00001648-200103000-00012; Pekkanen J, 1997, ENVIRON RES, V74, P24, DOI 10.1006/enrs.1997.3750; Peters A, 1997, EUR RESPIR J, V10, P872; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Phalen R., 2002, PARTICULATE AIR POLL; Pope CA, 2002, JAMA-J AM MED ASSOC, V287, P1132, DOI 10.1001/jama.287.9.1132; POPE CA, 1992, AM REV RESPIR DIS, V145, P1123; Romieu I, 1996, AM J RESP CRIT CARE, V154, P300; Sarnat JA, 2000, J AIR WASTE MANAGE, V50, P1184; Schwartz J, 1996, J AIR WASTE MANAGE, V46, P927, DOI 10.1080/10473289.1996.10467528; Schwartz J, 2000, EPIDEMIOLOGY, V11, P6, DOI 10.1097/00001648-200001000-00004; Sheppard L, 1999, EPIDEMIOLOGY, V10, P23, DOI 10.1097/00001648-199901000-00006; Sinclair AH, 2004, J AIR WASTE MANAGE, V54, P1212; Slaughter JC, 2003, ANN ALLERG ASTHMA IM, V91, P346; SPEKTOR DM, 1988, AM REV RESPIR DIS, V137, P313; Thurston GD, 1997, AM J RESP CRIT CARE, V155, P654; Tiittanen P, 1999, EUR RESPIR J, V13, P266, DOI 10.1034/j.1399-3003.1999.13b08.x; U. S. Environmental Protection Agency, 2004, EPA600P99002AF; [Anonymous], TECHN TRANSF NETW AI; Venn AJ, 2001, AM J RESP CRIT CARE, V164, P2177, DOI 10.1164/rccm2106126; Ward DJ, 2004, OCCUP ENVIRON MED, V61, DOI 10.1136/oem.2003.007088; Ward DJ, 2002, THORAX, V57, P489, DOI 10.1136/thorax.57.6.489; WHITE MC, 1994, ENVIRON RES, V65, P56, DOI 10.1006/enrs.1994.1021; Zanobetti A, 2000, ENVIRON HEALTH PERSP, V108, P1071, DOI 10.2307/3434961	44	91	99	3	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.	MAY	2008	121	5					1133	1139		10.1016/j.jaci.2008.02.020		7	Allergy; Immunology	Allergy; Immunology	302IJ	WOS:000255961700009	18405952	
J	Bello, D; Herrick, CA; Smith, TJ; Woskie, SR; Streicher, RP; Cullen, MR; Liu, YC; Redlich, CA				Bello, Dhimiter; Herrick, Christina A.; Smith, Thomas J.; Woskie, Susan R.; Streicher, Robert P.; Cullen, Mark R.; Liu, Youcheng; Redlich, Carrie A.			Skin exposure to isocyanates: Reasons for concern	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Review						asthma; dermal exposure; isocyanates; sensitization; skin	ALLERGIC CONTACT-DERMATITIS; METHYLENE DIPHENYL DIISOCYANATE; TOLUENE DIISOCYANATE; OCCUPATIONAL ASTHMA; POLYURETHANE FOAM; BODY REPAIR; IN-VIVO; 1,6-HEXAMETHYLENE DIISOCYANATE; TRIMELLITIC ANHYDRIDE; RESPIRATORY ALLERGY	OBJECTIVE: Isocyanates (di- and poly-), important chemicals used worldwide to produce polyurethane products, are a leading cause of occupational asthma. Respiratory exposures have been reduced through improved hygiene controls and the use of less-volatile isocyanates. Yet isocyanate asthma continues to occur, not uncommonly in settings with minimal inhalation exposure but opportunity for skin exposure. In this review we evaluate the potential role of skin exposure in the development of isocyanate asthma. DATA SOURCES: We reviewed the published animal and human literature on isocyanate skin-exposure methods, workplace skin exposure, skin absorption, and the role of skin exposure in isocyanate sensitization and asthma. DATA EXTRACTION: We selected relevant articles from computerized searches on Medline, U.S. Environmental Protection Agency, Occupational Safety and Health Administration, National Institute for Occupational Safety and Health, and Google databases using the keywords "isocyanate," "asthma," "skin," "sensitization," and other synonymous terms, and our own extensive collection of isocyanate publications. DATA SYNTHESIS: Isocyanate production and use continues to increase as the polyurethane industry expands. There is substantial opportunity for isocyanate skin exposure in many work settings, but such exposure is challenging to quantify and continues to be underappreciated. Isocyanate skin exposure can occur at work, even with the use of personal protective equipment, and may also occur with consumer use of certain isocyanate products. In animals, isocyanate skin exposure is an efficient route to induce sensitization, with subsequent inhalation challenge resulting in asthma-like responses. Several lines of evidence support a similar role for human isocyanate skin exposure, namely, that such exposure occurs and can contribute to the development of isocyanate asthma in certain settings, presumably by inducing systemic sensitization. CONCLUSIONS: Integrated animal and human research is needed to better understand the role of skin exposure in human isocyanate asthma and to improve diagnosis and prevention. In spite of substantial research needs, sufficient evidence already exists to justify greater emphasis on the potential risks of isocyanate skin exposure and the importance of preventing such exposures at work and during consumer use of certain isocyanate products.	Univ Massachusetts, Dept Work Environm, Lowell, MA 01854 USA; Harvard Univ, Sch Publ Hlth, Exposure Epidemiol & Risk Program, Boston, MA 02115 USA; Yale Univ, Sch Med, Dept Dermatol, New Haven, CT 06510 USA; NIOSH, Div Appl Res & Technol, Cincinnati, OH 45226 USA; Yale Univ, Sch Med, Occupat & Environm Med Program, New Haven, CT USA	Bello, D (reprint author), Univ Massachusetts, Dept Work Environm, KI 200,1 Univ Ave, Lowell, MA 01854 USA.	dhimiter_bello@uml.edu			NIEHS NIH HHS [K24 ES00355, K24 ES000355, T32 ES007069, T32 ES07069]; NIOSH CDC HHS [5 R01 OH004246, R01 OH004246, R01 OH3457]		ABBAS A. 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Health Perspect.	MAR	2007	115	3					328	335		10.1289/ehp.9557		8	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	142LN	WOS:000244651500022	17431479	
J	Maantay, J				Maantay, Juliana			Asthma and air pollution in the Bronx: Methodological and data considerations in using GIS for environmental justice and health research	HEALTH & PLACE			English	Article; Proceedings Paper	Workshop on New Approaches to Researching Environmental Justice	OCT, 2003	Univ British Columbia, Vancouver, CANADA		Univ British Columbia	asthma; air pollution; Geographic Information Systems (GIS); environmental justice; environmental health; proximity analysis	GEOGRAPHIC INFORMATION-SYSTEMS; DISPARITIES GEOCODING PROJECT; CHRONIC RESPIRATORY SYMPTOMS; PUBLIC-HEALTH; CHILDHOOD ASTHMA; CHILDREN; EQUITY; EPIDEMIOLOGY; ROAD; POLLUTANTS	This paper examines methods of environmental justice assessment with Geographic Information Systems, using research on the spatial correspondence between asthma and air pollution in the Bronx, New York City as a case study. Issues of spatial extent and resolution, the selection of environmental burdens to analyze, data and methodological limitations, and different approaches to delineating exposure are discussed in the context of the asthma study, which, through proximity analysis, found that people living near (within specified distance buffers) noxious land uses were up to 66 percent more likely to be hospitalized for asthma, and were 30 percent more likely to be poor and 13 percent more likely to be a minority than those outside the buffers. (c) 2005 Elsevier Ltd. All rights reserved.	CUNY Herbert H Lehman Coll, Dept Environm Geog & Geol Sci, Bronx, NY 10468 USA	Maantay, J (reprint author), CUNY Herbert H Lehman Coll, Dept Environm Geog & Geol Sci, 250 Bedford Pk Blvd W, Bronx, NY 10468 USA.	juliana.maantay@lehman.cuny.edu					ANDERTON DL, 1994, DEMOGRAPHY, V31, P229, DOI 10.2307/2061884; Becker KM, 1998, AM J EPIDEMIOL, V147, P709; Boer JT, 1997, SOC SCI QUART, V78, P793; Bowen WM, 1995, ANN ASSOC AM GEOGR, V85, P641, DOI 10.1111/j.1467-8306.1995.tb01818.x; BOWMAN JD, 2000, PUBLIC HLTH GIS NEWS, V32, P7; BRUNEKREEF B, 1995, ENVIRON HEALTH PERSP, V103, P3, DOI 10.2307/3432443; BRYANT B., 1995, ENV JUSTICE ISSUES P; Bullard R. 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J	Ciprandi, G; Fenoglio, D; Cirillo, I; Vizzaccaro, A; Ferrera, A; Tosca, MA; Puppo, F				Ciprandi, G; Fenoglio, D; Cirillo, I; Vizzaccaro, A; Ferrera, A; Tosca, MA; Puppo, F			Induction of interleukin 10 by sublingual immunotherapy for house dust mites: a preliminary report	ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY			English	Article							REGULATORY T-CELLS; GRASS-POLLEN IMMUNOTHERAPY; CLINICAL IMMUNOLOGY; AIRWAY INFLAMMATION; CYTOKINE PRODUCTION; ALLERGIC RHINITIS; ORAL TOLERANCE; IL-10; SUPPRESSION; DISEASE	Background: Subcutaneous specific immunotherapy has been demonstrated to be capable of inducing T-cell regulatory response. Interleukin 10 (IL-10) plays a crucial role in inducing allergen-specific tolerance; however, no previous studies have examined IL-10 production after sublingual immunotherapy (SLIT). Objective: To evaluate T-cell proliferation and IL-10 production in patients successfully treated with SLIT for house dust mites (HDMs). Methods: Peripheral blood mononuclear cells were isolated from patients after at least 3 years of successful HDM SLIT and from matched untreated allergic patients and healthy control subjects. After 3 and 6 days of in vitro stimulation with phytohemagglutinin (PHA), Candida albicans, and Dermatophagoides farinae, proliferation and production of IL-10 were measured. Results: Patients treated with SLIT showed a significant reduction of proliferation induced by C albicans compared with untreated atopic patients (P < .001), but a significant reduction was also demonstrated in healthy controls compared with untreated atopic patients (P < .001). Patients treated with SLIT also showed a significant increase of IL-10 production after Candida and PHA stimuli compared with patients with untreated rhinitis (P < .001 for both). Patients with untreated rhinitis did not produce IL-10. Conclusion: This preliminary study confirms reduced T-cell proliferation and preliminarily provides the first evidence, to our knowledge, of peripheral IL-10 production in allergic patients successfully treated with HDM SLIT.	Azienda Osped Univ San Marino, Genoa, Italy; Univ Genoa, DIMI, CEBR, I-16126 Genoa, Italy; Osped Marina Milit, La Spezia, Italy; Ist Giannina Gaslini, I-16148 Genoa, Italy	Ciprandi, G (reprint author), Osped San Martino Genova, Dipartimento Reg Testa Coll, Largo R Benzi 10, I-16132 Genoa, Italy.	gio.cip@libero.it					Akbari O, 2003, CURR OPIN IMMUNOL, V15, P627, DOI 10.1016/j.coi.2003.09.012; Arikan C, 2004, CLIN EXP ALLERGY, V34, P398, DOI 10.1111/j.1365-2222.2004.01869.x; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; Bachert C, 1999, INT ARCH ALLERGY IMM, V118, P375, DOI 10.1159/000024141; Blaser K, 2004, CLIN EXP ALLERGY, V34, P328, DOI 10.1111/j.1365-2222.2004.01909.x; Bousquet J, 1998, ALLERGY S, V53, P44; Bousquet J, 2001, J ALLERGY CLIN IMMUN, V108, P147, DOI DOI 10.1067/MAI.2001.118891; Bullens DMA, 2004, CLIN EXP ALLERGY, V34, P879, DOI 10.1111/j.1365-2222.2004.01955.x; Canonica GW, 2003, J ALLERGY CLIN IMMUN, V111, P437, DOI 10.1067/mai.2003.129; CHEN YH, 1994, SCIENCE, V265, P1237, DOI 10.1126/science.7520605; Fanta C, 1999, INT ARCH ALLERGY IMM, V120, P218, DOI 10.1159/000024270; Francis JN, 2003, J ALLERGY CLIN IMMUN, V111, P1255, DOI 10.1067/mai.2003.1570; Frew Anthony J., 2003, Journal of Allergy and Clinical Immunology, V111, pS712; Frieri M, 1999, ALLERGY ASTHMA PROC, V20, P281, DOI 10.2500/108854199778251988; Giannarini L, 1998, CLIN EXP ALLERGY, V28, P404; Groux H, 1996, J EXP MED, V184, P19, DOI 10.1084/jem.184.1.19; Hansen G, 1999, J CLIN INVEST, V103, P175, DOI 10.1172/JCI5155; Herrick CA, 2003, NAT REV IMMUNOL, V3, P1; HOLT PG, 1988, CLIN ALLERGY, V18, P229, DOI 10.1111/j.1365-2222.1988.tb02864.x; HSU CH, 2004, J AM COLL IMMUNOL, V115, P1084; HUSBY S, 1994, J IMMUNOL, V152, P4663; Ippoliti F, 2003, PEDIATR ALLERGY IMMU, V14, P216, DOI 10.1034/j.1399-3038.2003.00025.x; Jeannin P, 1998, J IMMUNOL, V160, P3555; Jutel M, 2003, EUR J IMMUNOL, V33, P1205, DOI 10.1002/eji.200322919; Kon OM, 1999, INT ARCH ALLERGY IMM, V118, P133, DOI 10.1159/000024049; Lima MT, 2002, CLIN EXP ALLERGY, V32, P507, DOI 10.1046/j.0954-7894.2002.01327.x; Ling EM, 2004, LANCET, V363, P608, DOI 10.1016/S0140-6736(04)15592-X; Malling HJ, 1998, ALLERGY, V53, P933, DOI 10.1111/j.1398-9995.1998.tb03793.x; Montagnoli C, 2002, J IMMUNOL, V169, P6298; MOWAT AM, 1987, IMMUNOL TODAY, V8, P93, DOI 10.1016/0167-5699(87)90853-X; Norman PS, 2004, J ALLERGY CLIN IMMUN, V113, P1013, DOI 10.1016/j.jaci.2004.03.020; Nouri-Aria KT, 2004, J IMMUNOL, V172, P3252; Passalacqua Giovanni, 2004, Curr Opin Allergy Clin Immunol, V4, P31, DOI 10.1097/00130832-200402000-00007; Royer B, 2001, CLIN EXP ALLERGY, V31, P694, DOI 10.1046/j.1365-2222.2001.01069.x; Savolainen J, 2004, CLIN EXP ALLERGY, V34, P413, DOI 10.1111/j.1365-2222.2004.01823.x; SCHANDENE L, 1994, J IMMUNOL, V152, P4368; Sheikh S, 1996, PEDIATR ASTHMA ALLER, V10, P161, DOI 10.1089/pai.1996.10.161; TAKANASKI S, 1994, J EXP MED, V180, P711, DOI 10.1084/jem.180.2.711; Tang CB, 2001, J IMMUNOL, V166, P1471; TePas EC, 2004, ANN ALLERG ASTHMA IM, V92, P25; TEPAS EC, 2004, ANN ALLERG ASTHMA IM, V92, P1; Till SJ, 2004, J ALLERGY CLIN IMMUN, V113, P1025, DOI 10.1016/j.jaci.2004.03.024; Umetsu DT, 2003, J ALLERGY CLIN IMMUN, V112, P480, DOI 10.1067/mai.2003.1717; WEINER L, 1997, IMMUNOL TODAY, V18, P335; Wilson DR, 2003, COCHRANE DB SYST REV, V2	45	91	98	0	1	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.	JUL	2005	95	1					38	44				7	Allergy; Immunology	Allergy; Immunology	949IO	WOS:000230778800008	16095140	
J	Voynow, JA; Fischer, BM; Malarkey, DE; Burch, LH; Wong, T; Longphre, M; Ho, SB; Foster, WM				Voynow, JA; Fischer, BM; Malarkey, DE; Burch, LH; Wong, T; Longphre, M; Ho, SB; Foster, WM			Neutrophil elastase induces mucus cell metaplasia in mouse lung	AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY			English	Article; Proceedings Paper	100th International Conference of the American-Thoracic-Society	MAY 21-26, 2004	Orlando, FL	Amer Thorac Soc		neutrophil elastase; goblet cell metaplasia; Muc5ac	AIRWAY EPITHELIAL-CELLS; FACTOR RECEPTOR ACTIVATION; INDUCED MUC5AC EXPRESSION; RAT BRONCHIAL EPITHELIUM; MUCIN GENE-EXPRESSION; GLAND SEROUS CELLS; NASAL EPITHELIUM; PROTEIN EXPRESSION; MESSENGER-RNA; ASTHMA	Goblet cell hyperplasia in the superficial airway epithelia is a signature pathological feature of chronic bronchitis and cystic fibrosis. In these chronic inflammatory airway diseases, neutrophil elastase (NE) is found in high concentrations in the epithelial lining fluid. NE has been reported to trigger mucin secretion and increase mucin gene expression in vitro. We hypothesized that chronic NE exposure to murine airways in vivo would induce goblet cell metaplasia. Human NE (50 mug) or PBS saline was aspirated intratracheally by male Balb/c (6 wk of age) mice on days 1, 4, and 7. On days 8, 11, and 14, lung tissues for histology and bronchoalveolar lavage (BAL) samples for cell counts and cytokine levels were obtained. NE induced Muc5ac mRNA and protein expression and goblet cell metaplasia on days 8, 11, and 14. These cellular changes were the result of proteolytic activity, since the addition of an elastase inhibitor, methoxysuccinyl Ala-Ala-Pro-Val chloromethylketone (AAPV-CMK), blocked NE-induced Muc5ac expression and goblet cell metaplasia. NE significantly increased keratinocyte-derived chemokine and IL-5 in BAL and increased lung tissue inflammation and BAL leukocyte counts. The addition of AAPV-CMK reduced these measures of inflammation to control levels. These experiments suggest that NE proteolytic activity initiates an inflammatory process leading to goblet cell metaplasia.	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J	Bisgaard, H				Bisgaard, H			The Copenhagen Prospective Study on Asthma in Childhood (COPSAC): design, rationale, and baseline data from a longitudinal birth cohort study	ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY			English	Article							RESPIRATORY SYNCYTIAL VIRUS; ATOPIC-DERMATITIS; INCREASING PREVALENCE; PERSONAL EXPOSURE; HEALTHY-CHILDREN; HAY-FEVER; 1ST YEAR; AGE; POPULATION; SYMPTOMS	Background: The atopic diseases asthma, atopic dermatitis, and allergic rhinitis are the most common chronic diseases in children, and their prevalence has increased recently in industrialized nations. Little is known about the genetic-environmental interaction factors driving such proliferation. Objective: To investigate the relationships among genetic, environmental, and lifestyle factors in the development of atopic diseases in high-risk children with the aim of developing evidence-based prevention strategies. Methods: The Copenhagen Prospective Study on Asthma in Childhood is a single-center, birth cohort study of children of asthmatic mothers. Objective assessments begin at birth, with scheduled visits every 6 months and when acute symptoms manifest. Clinical outcomes comprise preasthma, asthma, atopic dermatitis, allergic rhinitis, allergy, lung function, and bronchial responsiveness. Exposure assessments comprise respiratory, intestinal, and skin microbiology; the child's diet; indoor and outdoor air quality; allergens; and indicators of lifestyle. Genetic characteristics of probands and parents are evaluated. Quality assurance follows Good Clinical Practice guidelines. Results: Four hundred eleven infants of asthmatic mothers were enrolled at the age of I month. The children were born between August 2, 1998, and December 28, 2001. Compared with the Copenhagen population, mothers of the cohort population were less likely to have given natural childbirth. The households were slightly less affluent, with fewer children and fewer pets. Whites may be overrepresented. At age 2 years, 93% of the infants were still actively participating in the cohort. Conclusions: This longitudinal birth cohort study of high-risk Danish infants consists of objective phenotyping, detailed information on exposure, high data quality, and a high participant retention rate.	Copenhagen Univ Hosp, Dept Pediat, COPSAC Clin Res Unit L213, DK-2100 Copenhagen, Denmark	Bisgaard, H (reprint author), Copenhagen Univ Hosp, Dept Pediat, COPSAC Clin Res Unit L213, DK-2100 Copenhagen, Denmark.	Bisgaard@copsac.dk	Kronow, Joern/B-1054-2011; Bisgaard, Hans/N-4761-2016	Bisgaard, Hans/0000-0003-4131-7592			Al-Delaimy W. 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Allergy Asthma Immunol.	OCT	2004	93	4					381	389				9	Allergy; Immunology	Allergy; Immunology	864TL	WOS:000224655700013	15521375	
J	Susitaival, P; Flyvholm, MA; Meding, B; Kanerva, L; Lindberg, M; Svensson, A; Olafsson, JH				Susitaival, P; Flyvholm, MA; Meding, B; Kanerva, L; Lindberg, M; Svensson, A; Olafsson, JH			Nordic Occupational Skin Questionnaire (NOSQ-2002): a new tool for surveying occupational skin diseases and exposure	CONTACT DERMATITIS			English	Review						eczema; epidemiology; exposure; hand dermatitis; NOSQ-2002; occupational; questionnaire design; questionnaire methods; skin diseases	PARTY DIAGNOSTIC-CRITERIA; REPORTED HAND ECZEMA; ALLERGIC CONTACT SENSITIZATION; ATOPIC-DERMATITIS; DANISH POPULATION; GLOSTRUP ALLERGY; PREVALENCE; DERMATOSES; VALIDATION; NETHERLANDS	Occupational skin diseases are among the most frequent work-related diseases in industrialized countries. Good occupational skin disease statistics exist in few countries. Questionnaire studies are needed to get more data on the epidemiology of occupational skin diseases. The Nordic Occupational Skin Questionnaire Group has developed a new questionnaire tool - Nordic Occupational Skin Questionnaire (NOSQ-2002) - for surveys on work-related skin disease and exposures to environmental factors. The 2 NOSQ-2002 questionnaires have been compiled by using existing questionnaires and experience. NOSQ-2002/SHORT is a ready-to-use 4-page questionnaire for screening and monitoring occupational skin diseases, e.g. in a population or workplace. All the questions in the short questionnaire (NOSQ-2002/SHORT) are included in the long version, NOSQ-2002/LONG, which contains a pool of questions to be chosen according to research needs and tailored to specific populations. The NOSQ-2002 report includes, in addition to the questionnaires, a comprehensive manual for researchers on planning and conducting a questionnaire survey on hand eczema and relevant exposures. NOSQ-2002 questionnaires have been compiled in English and translated into Danish, Swedish, Finnish and Icelandic. The use of NOSQ-2002 will benefit research on occupational skin diseases by providing more standardized data, which can be compared between studies and countries.	Natl Inst Occupat Hlth, DK-2100 Copenhagen, Denmark; N Karelia Cent Hosp, Dept Dermatol, Joensuu, Finland; Natl Inst Working Life, Stockholm, Sweden; Finnish Inst Occupat Hlth, Helsinki, Finland; Stockholm Cty Council, Stockholm, Sweden; Univ Hosp, Dept Dermatol, Malmo, Sweden; Univ Hosp, Landspitali, Dept Dermatol, Reykjavik, Iceland	Flyvholm, MA (reprint author), Natl Inst Occupat Hlth, Lerso Parkalle 105, DK-2100 Copenhagen, Denmark.						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J	Buhl, R; Hanf, G; Soler, M; Bensch, G; Wolfe, J; Everhard, F; Champain, K; Fox, H; Thirlwell, J				Buhl, R; Hanf, G; Soler, M; Bensch, G; Wolfe, J; Everhard, F; Champain, K; Fox, H; Thirlwell, J			The anti-IgE antibody omalizumab improves asthma-related quality of life in patients with allergic asthma	EUROPEAN RESPIRATORY JOURNAL			English	Article						allergic asthma; anti-immunoglobulin E; omalizumab; quality of life	OF-LIFE; AIRWAY HYPERRESPONSIVENESS; CLINICAL-TRIALS; DISEASE; QUESTIONNAIRE; INFLAMMATION; INHIBITION; SEVERITY; THERAPY	The aim of the present study was to determine the effect of treatment with omalizumab, an anti-immunoglobulin E antibody, on asthma-related quality of life (AQoL) in patients with moderate-to-severe allergic asthma. A total of 546 patients with allergic asthma were randomised to double-blind subcutaneous treatment with either placebo or omalizumab for 52 weeks. A constant beclomethasone dipropionate dose was maintained during the first 16 weeks (steroid-stable phase). This was followed by a 12-week steroid-reduction phase. The core study was followed by a 24-week double-blind extension phase. AQoL was evaluated at baseline and at the end of the steroid-stable (week 16), steroid-reduction (week 28) and extension phases (week 52) using the Juniper Asthma Quality of Life Questionnaire (AQLQ). Baseline AQLQ scores were comparable for the two treatment groups. Relative to placebo, omalizumab-treated patients demonstrated statistically significant improvements from baseline across all four AQLQ domains, as well as overall AQoL score, at weeks 16 (except environmental exposure), 28 and 52. Patients on omalizumab were also more likely to achieve clinically significant improvements in AQoL during the course of the study. Overall, almost 70% of patients and investigators rated treatment with omalizumab as "excellent/good", compared with similar to40% of placebo recipients. Clinical studies show that omalizumab enhances disease control whilst reducing corticosteroid consumption in patients with allergic asthma. The results of the present study show that these changes are paralleled by improvements in asthma-related quality of life that are meaningful to such patients.	Univ Hosp, Div Pulm, D-55131 Mainz, Germany; Charite Berlin, Allergy & Asthma Clin, Berlin, Germany; Univ Basel Hosp, Div Pulm, CH-4031 Basel, Switzerland; Allergy Immunol & Asthma Med Grp, Stockton, CA USA; Allergy & Asthma Associates, San Jose, CA USA; Novartis Pharma AG, Basel, Switzerland; Novartis Horsham Res Ctr, Horsham, W Sussex, England	Buhl, R (reprint author), Univ Hosp, Div Pulm, Langenbeckstr 1, D-55131 Mainz, Germany.						Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Boulet LP, 1997, AM J RESP CRIT CARE, V155, P1835; Buhl R, 2002, EUR RESPIR J, V20, P73, DOI 10.1183/09031936.02.00278102; Coyle AJ, 1996, J EXP MED, V183, P1303, DOI 10.1084/jem.183.4.1303; Drazen JM, 1996, J EXP MED, V183, P1, DOI 10.1084/jem.183.1.1; Easthope S, 2001, DRUGS, V61, P253, DOI 10.2165/00003495-200161020-00008; Fahy JV, 1997, AM J RESP CRIT CARE, V155, P1828; Hamelmann E, 1999, ALLERGY, V54, P297, DOI 10.1034/j.1398-9995.1999.00085.x; Holt PG, 1999, NATURE, V402, pB12; Israel E, 2001, NEW ENGL J MED, V345, P941, DOI 10.1056/NEJMoa002304; Jardieu PM, 1999, INT ARCH ALLERGY IMM, V118, P112, DOI 10.1159/000024043; Joyce DP, 2000, J ASTHMA, V37, P303, DOI 10.3109/02770900009055454; Juniper E F, 1998, Can Respir J, V5 Suppl A, p77A; Juniper EF, 2000, AM J RESP CRIT CARE, V162, P1330; Juniper EF, 1997, ALLERGY, V52, P971, DOI 10.1111/j.1398-9995.1997.tb02416.x; JUNIPER EF, 1995, AM J RESP CRIT CARE, V151, P66; JUNIPER EF, 1994, J CLIN EPIDEMIOL, V47, P81, DOI 10.1016/0895-4356(94)90036-1; JUNIPER EF, 1992, THORAX, V47, P76, DOI 10.1136/thx.47.2.76; JUNIPER EF, 1993, AM REV RESPIR DIS, V147, P832; Milgrom H, 1999, NEW ENGL J MED, V341, P1966, DOI 10.1056/NEJM199912233412603; Moy ML, 2001, AM J RESP CRIT CARE, V163, P924; PRESTA LG, 1993, J IMMUNOL, V151, P2623; SHIELDS RL, 1995, INT ARCH ALLERGY IMM, V107, P412; Soler M, 2001, EUR RESPIR J, V18, P254, DOI 10.1183/09031936.01.00092101; Spector SL, 1999, ANN ALLERG ASTHMA IM, V83, P435, DOI 10.1016/S1081-1206(10)62848-7; Thompson WG, 2000, AM J GASTROENTEROL, V95, P1637; Wijnhoven HAH, 2001, CHEST, V119, P1034, DOI 10.1378/chest.119.4.1034; Williams CMM, 2000, J ALLERGY CLIN IMMUN, V105, P847, DOI 10.1067/mai.2000.106485; Wills-Karp M, 1999, ANNU REV IMMUNOL, V17, P255, DOI 10.1146/annurev.immunol.17.1.255	29	91	98	0	4	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.	NOV	2002	20	5					1088	1094		10.1183/09031936.02.00016502		7	Respiratory System	Respiratory System	614EZ	WOS:000179176500004	12449159	
J	Schneider, P; Gebefugi, I; Richter, K; Wolke, G; Schnelle, J; Wichmann, HE; Heinrich, J				Schneider, P; Gebefugi, I; Richter, K; Wolke, G; Schnelle, J; Wichmann, HE; Heinrich, J		INGA Study Grp	Indoor and outdoor BTX levels in German cities	SCIENCE OF THE TOTAL ENVIRONMENT			English	Article						volatile organic compounds; BTX; passive sampling; indoor air quality; homes	VOLATILE ORGANIC-COMPOUNDS; EASTERN GERMANY; AIR; HAMBURG; ERFURT; HOMES; EMISSIONS	On the basis of the ongoing study INGA (INdoor exposure and Genetics in Asthma), Germany's most detailed and standardized epidemiological study on indoor exposure to both allergens in house dust and volatile compounds in the air of the home environment has been performed. The purpose of this paper is to describe the spatial and seasonal variability of indoor and outdoor BTX (Benzene, toluene, ethyl benzene, ortho-xylene, meta- and para-xylene) concentrations for the study period from June 1995 to November 1996. Within this framework, air concentrations of volatile organic compounds (BTX) were measured in 204 households in Erfurt (Eastern Germany) and 201 households in Hamburg (Western Germany). BTX sampling was conducted over one week using OVM 3500 passive diffusion sampling devices in the indoor (living room and bedroom) and outdoor environment (outside the window of the living room). Indoor and outdoor median BTX concentrations in Erfurt were slightly, but significantly higher than those in Hamburg. This gap was most pronounced in the levels of indoor toluene (37.3 mug/m(3) for Erfurt and 20.5 mug/m(3) for Hamburg, P < 0.0001). In both cities, winter indoor and outdoor concentrations for the five compounds exceeded the summer values. Outdoor concentrations of ethyl benzene and ortho-xylene were very low (50% < L.D.). In general, the indoor BTX air concentrations were significantly higher than the outdoor concentrations, the lowest I/O ratios were found in the case of benzene. Living room and bedroom values for the five compounds were highly correlated (Spearman coefficient 0.5-0.9). Despite the better insulation of the homes in West Germany, no indication for the expected higher indoor concentrations of BTX in the West could be found. The strong and yet undiscovered indoor source for toluene in East Germany might lead to a further increase in the indoor air load in those homes in the East, which undergo renovations which will lead to improved insulation (C) 2001 Elsevier Science B.V. All rights reserved.	GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, Neuherberg, Germany; GSF, Natl Res Ctr Environm & Hlth, Inst Ecol Chem, Neuherberg, Germany; Grosshansdorf Hosp, Ctr Pneumol & Thorac Surg, Hamburg, Germany; Univ Munich, Inst Med Data Management Biometr & Epidemiol, Dept Epidemiol, Munich, Germany	Heinrich, J (reprint author), GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, D-85764 Oberschleissheim, Germany.		Schnelle-Kreis, Jurgen/M-9845-2014	Schnelle-Kreis, Jurgen/0000-0003-4846-2303			BEGEROW J, 1995, FRESEN J ANAL CHEM, V351, P549, DOI 10.1007/BF00322731; BISCHOF W, 2000, P HLTH BUILD, V1, P151; Cyrys J, 2000, SCI TOTAL ENVIRON, V250, P51, DOI 10.1016/S0048-9697(00)00361-2; DEBORTOLI M, 1986, ENVIRON INT, V12, P343, DOI 10.1016/0160-4120(86)90048-6; EIKMANN T, 1992, HDB UMWELTMEDIZIN; FAHLBUSCH B, 1999, ALLERGY 2000, V54, P1; 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, 1998, ALLERGY, V53, P89, DOI 10.1111/j.1398-9995.1998.tb03779.x; HERBARTH O, 1994, UMWELTMED FORSCH PRA, V5, P281; Koch A, 2000, ALLERGY, V55, P176, DOI 10.1034/j.1398-9995.2000.00233.x; KRAUSE C, 1991, UMWELT SURVEY WOHN C, V3; LEBRET E, 1986, Environment International, V12, P323, DOI 10.1016/0160-4120(86)90046-2; LEVSEN W, 1999, BELASTUNG MENSCHEN D; OTSON R, 1996, P 7 INT C IND AIR 1, V21, P565; PORSTMANN F, 1994, STAUB REINHALT LUFT, V54, P147; RANFT U, 1997, EPIDEMIOLOGISCHE UNT; Richter K, 1999, ALLERGOLOGIE, V22, P14; Rosner B, 1990, FUNDAMENTALS BIOSTAT; *SAS I, 1996, VERSION 6 12; SCHLIPKOTER HW, 1994, DESKRIPTION SCHULANF; Schneider P, 1998, GEFAHRST REINHALT L, V58, P191; SCHNEIDER P, 1995, ALLERGOLOGIE, V18, P518; Schneider P, 1999, J EXPO ANAL ENV EPID, V9, P282, DOI 10.1038/sj.jea.7500030; SEIFERT B, 1992, ECOMED VERLAG LANDSB; SOLLINGER S, 1993, ATMOS ENVIRON B-URB, V27, P183, DOI 10.1016/0957-1272(93)90004-P; Wallace L, 1991, J Expo Anal Environ Epidemiol, V1, P157; WALLACE LA, 1988, ATMOS ENVIRON, V22, P2141, DOI 10.1016/0004-6981(88)90125-4; WALLACE LA, 1987, ATMOS ENVIRON, V21, P385, DOI 10.1016/0004-6981(87)90017-5; WARE JH, 1993, AM J EPIDEMIOL, V137, P1287; WICHMANN HE, 1991, RISIKOGRUPPENBEZOGEN; YOCOM JE, 1982, JAPCA J AIR WASTE MA, V32, P500	32	91	95	2	16	ELSEVIER SCIENCE BV	AMSTERDAM	PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS	0048-9697			SCI TOTAL ENVIRON	Sci. Total Environ.	FEB 21	2001	267	1-3					41	51		10.1016/S0048-9697(00)00766-X		11	Environmental Sciences	Environmental Sciences & Ecology	412DC	WOS:000167537900004	11286215	
J	Gilliland, FD; Berhane, K; Rapaport, EB; Thomas, DC; Avol, E; Gauderman, WJ; London, SJ; Margolis, HG; McConnell, R; Islam, KT; Peters, JM				Gilliland, FD; Berhane, K; Rapaport, EB; Thomas, DC; Avol, E; Gauderman, WJ; London, SJ; Margolis, HG; McConnell, R; Islam, KT; Peters, JM			The effects of ambient air pollution on school absenteeism due to respiratory illnesses	EPIDEMIOLOGY			English	Article						air pollution; ozone; respiratory illnesses and children; school absenteeism	SOUTHERN CALIFORNIA COMMUNITIES; PULMONARY-FUNCTION; DIFFERING LEVELS; MEXICO-CITY; CHILDREN; ASTHMA; PARTICULATE; EXPOSURES; MORBIDITY; SYMPTOMS	We investigated the relations between ozone (O-3), nitrogen dioxide (NO2), and respirable particles less than 10 mum in diameter (PM10) and school absenteeism in a cohort of 4th-grade school children who resided in 12 southern California communities. An active surveillance system ascertained the numbers and types of absences during the first 6 months of 1996. Pollutants were measured hourly at central-site monitors in each of the 12 communities. To examine acute effects of air pollution on absence rates, we fitted a two-stage time series model to the absence count data that included distributed lag effects of exposure adjusted for long-term pollutant levels. Short-term change in O-3, but not NO2 or PM10, was associated with a substantial increase in school absences from both upper and lower respiratory illness. An increase of 20 ppb of O-3 was associated with an increase of 62.9% [95% confidence interval (95% CI) = 18.4-124.1%] for illness-related absence rates, 82.9% (95% CI = 3.9-222.0%) for respiratory illnesses, 45.1% (95% CI = 21.3-73.7%) for upper respiratory illnesses, and 173.9% (95% CI = 91.3-292.3%) for lower respiratory illnesses with wet cough. The short-term effects of a 20-ppb change of O-3 on illness-related absenteeism were larger in communities with lower long-term average PM10 [223.5% (95% CI = 90.4-449.7)] compared with communities with high average levels [38.1% (95% CI = 8.5-75.8)]. Increased school absenteeism from O-3 exposure in children is an important adverse effect of ambient air pollution worthy of public policy consideration.	Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA; NIEHS, Res Triangle Pk, NC 27709 USA; Calif Air Resources Board, Sacramento, CA USA	Gilliland, FD (reprint author), Univ So Calif, Keck Sch Med, Dept Prevent Med, 1540 Alcazar St,CHP 236, Los Angeles, CA 90033 USA.			London, Stephanie/0000-0003-4911-5290	NHLBI NIH HHS [1R01 HL61768]; NIEHS NIH HHS [5 P30 ES07048-02, 5ES09581-01]		AKAIKE H, 1970, ANN I STAT MATH, V22, P203, DOI 10.1007/BF02506337; ALMON S, 1965, ECONOMETRICA, V33, P178, DOI 10.2307/1911894; AVOL E, 1997, AM J RESP CRIT CARE, V155, pA747; Bascom R, 1996, AM J RESP CRIT CARE, V153, P477; Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; BATES DV, 1995, ENVIRON HEALTH PERSP, V103, P49, DOI 10.2307/3432345; Bateson TF, 1999, EPIDEMIOLOGY, V10, P539, DOI 10.1097/00001648-199909000-00013; BLOOM B, 1981, CURRENT ESTIMATES NA; CELANO MP, 1993, J LEARN DISABIL, V26, P23; Dominici F, 2000, J ROY STAT SOC A STA, V163, P263, DOI 10.1111/1467-985X.00170; FERRIS BG, 1970, AM REV RESPIR DIS, V102, P591; Gauderman J.W., 2000, AM J RESP CRIT CARE, V162, P1383; Gold DR, 1999, EPIDEMIOLOGY, V10, P8, DOI 10.1097/00001648-199901000-00004; Hastie T, 1990, GEN ADDITIVE MODELS; LINN WS, 1988, TOXICOL IND HEALTH, V4, P505; Linn WS, 1996, J EXPO ANAL ENV EPID, V6, P449; LIPPMANN M, 2000, ENV TOXICANTS HUMAN, P655; LUMLEY T, IN PRESS ENVIRONMETR; McConnell R, 1999, ENVIRON HEALTH PERSP, V107, P757, DOI 10.2307/3434662; McCullagh P., 1989, GEN LINEAR MODELS; Navidi W., 1999, RES REP HLTH EFF I, V86, P1; NEAS LM, 1991, AM J EPIDEMIOL, V134, P204; OSTRO B, 1993, ENVIRON RES, V50, P238; OSTRO BD, 1990, RISK ANAL, V10, P421, DOI 10.1111/j.1539-6924.1990.tb00525.x; OSTRO BD, 1984, SCI TOTAL ENVIRON, V39, P111, DOI 10.1016/0048-9697(84)90029-9; PARCEL GS, 1979, PEDIATRICS, V64, P878; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; Peters JM, 1999, AM J RESP CRIT CARE, V159, P768; PONKA A, 1990, ENVIRON RES, V52, P34, DOI 10.1016/S0013-9351(05)80149-5; Pope CA, 1996, AM J RESP CRIT CARE, V154, pS229; Raizenne M, 1998, CAN J PUBLIC HEALTH, V89, pS43; RANSOM MR, 1992, ENVIRON RES, V58, P204, DOI 10.1016/S0013-9351(05)80216-6; ROGERS KD, 1965, AM J DIS CHILD, V109, P9; ROMIEU I, 1992, AM J EPIDEMIOL, V136, P1524; ROZELLE RM, 1968, EDUC PSYCHOL MEAS, V28, P1151, DOI 10.1177/001316446802800415; SAMET JM, 1993, ENVIRON HEALTH PERSP, V101, P149, DOI 10.2307/3431671; Samet J. M., 1995, PARTICULATE AIR POLL; SCHIFFER CG, 1963, ILLNESS CHILDREN DAT; SCHLESINGER R, 2000, ENV TOXICANTS HUMAN, P595; Schwartz J, 2000, EPIDEMIOLOGY, V11, P320, DOI 10.1097/00001648-200005000-00016; SCHWARTZ J, 1993, AM J EPIDEMIOL, V137, P1136; *US EPA, 1996, AIR QUAL CRIT OZ REL, V3; WAYNE WS, 1969, ARCH ENVIRON HEALTH, V19, P315; WEITZMAN M, 1986, J CHRON DIS, V39, P799, DOI 10.1016/0021-9681(86)90082-2; Zeger SL, 2000, ENVIRON HEALTH PERSP, V108, P419, DOI 10.2307/3454382	45	91	98	3	22	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	1044-3983			EPIDEMIOLOGY	Epidemiology	JAN	2001	12	1					43	54		10.1097/00001648-200101000-00009		12	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	385LR	WOS:000166006400009	11138819	
J	Kanehiro, A; Ikemura, T; Makela, MJ; Lahn, M; Joetham, A; Dakhama, A; Gelfand, EW				Kanehiro, A; Ikemura, T; Makela, MJ; Lahn, M; Joetham, A; Dakhama, A; Gelfand, EW			Inhibition of phosphodiesterase 4 attenuates airway hyperresponsiveness and airway inflammation in a model of secondary allergen challenge	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							HUMAN NEUTROPHIL FUNCTIONS; MURINE MODEL; PDE INHIBITORS; ATOPIC ASTHMA; TYPE-4; LUNG; EOSINOPHILIA; RESPONSES; ROLIPRAM; CAMP	We compared for the first time the therapeutic potential of a specific phosphodiesterase 4 (PDE4) inhibitor, rolipram, with anti-VLA-4 and anti-IL-5 in a model of secondary allergen exposure of previously sensitized and challenged mice. To address these issues, mice were sensitized and challenged with ovalbumin (OVA) (primary challenge). Six weeks later, sensitized/challenged mice were reexposed to OVA (secondary challenge) and airway response (resistance [RL] and dynamic compliance [Cdyn]) to inhaled methacholine was monitored. After secondary OVA challenge, Rr significantly increased as did the number of lung inflammatory cells and IL-4 and IL-5 production in bronchoalveolar lavage fluid (BALF). Administration of rolipram, in a dose-dependent manner, significantly prevented both changes in Rr and Cdyn, as well as eosinophil, lymphocyte, and neutrophil accumulation in the BALF; IL-4 and IL-5 levels in BALF were also significantly reduced. In contrast, treatment with anti-VLA-4 and anti-IL-5 only prevented changes in RL and eosinophil numbers and IL-5 production in BALF. Further, goblet cell hyperplasia was suppressed only by treatment with rolipram. None of the treatments affected OVA-specific antibody levels. These studies confirm that IL-5 dependent eosinophilic inflammation plays an essential role in the development of certain aspects of airway function after rechallenge of sensitized mice and that lymphocytes and neutrophils are also important in the development of altered airway function. The use of agents that inhibit PDE4 may have an important role in the treatment of asthma in previously sensitized mice.	Natl Jewish Med & Res Ctr, Dept Pediat, Div Basic Sci, Denver, CO 80206 USA; Natl Jewish Med & Res Ctr, Dept Immunol, Denver, CO 80206 USA	Gelfand, EW (reprint author), Natl Jewish Med & Res Ctr, Dept Pediat, Div Basic Sci, 1400 Jackson St, Denver, CO 80206 USA.		KANEHIRO, Arihiko/B-1926-2011		NHLBI NIH HHS [HL-36577, HL-61005]		AZZAWI M, 1990, AM REV RESPIR DIS, V142, P1407; Blyth DI, 1998, AM J RESP CELL MOL, V19, P38; Danahay H, 1997, BRIT J PHARMACOL, V120, P289, DOI 10.1038/sj.bjp.0700901; DERIAN CK, 1995, J IMMUNOL, V154, P308; Essayan DM, 1997, BIOCHEM PHARMACOL, V53, P1055, DOI 10.1016/S0006-2952(97)00102-0; Foissier L, 1996, J PHARMACOL EXP THER, V278, P1484; Foster PS, 1996, J EXP MED, V183, P195, DOI 10.1084/jem.183.1.195; FRIGAS E, 1986, J ALLERGY CLIN IMMUN, V77, P527, DOI 10.1016/0091-6749(86)90341-6; Gozzard N, 1996, BRIT J PHARMACOL, V117, P1405; Hamelmann E, 1997, AM J RESP CRIT CARE, V155, P819; HATZELMANN A, 1995, BRIT J PHARMACOL, V114, P821; Howell RE, 1995, PULM PHARMACOL, V8, P83, DOI 10.1006/pulp.1995.1010; Kanehiro A, 2000, AM J RESP CRIT CARE, V162, P1132; KANEKO T, 1995, CELL SIGNAL, V7, P527, DOI 10.1016/0898-6568(95)00023-I; KLEMM P, 1995, EUR J PHARMACOL, V281, P69, DOI 10.1016/0014-2999(95)00232-A; LAGENTE V, 1994, EUR J PHARMACOL, V255, P253, DOI 10.1016/0014-2999(94)90107-4; LAVNIKOVA N, 1993, AM J RESP CELL MOL, V8, P384; MARTIN TR, 1988, J APPL PHYSIOL, V64, P2318; Miotla JM, 1998, AM J RESP CELL MOL, V18, P411; Moy ML, 1998, SEM RESP CRIT CARE M, V19, P349, DOI 10.1055/s-2007-1009412; OTTONELLO L, 1995, CLIN EXP IMMUNOL, V101, P502; POBER JS, 1993, J IMMUNOL, V150, P5114; Schudt C, 1999, PULM PHARMACOL THER, V12, P123, DOI 10.1006/pupt.1999.0182; SCHUDT C, 1991, N-S ARCH PHARMACOL, V344, P682; SPRINGER TA, 1994, CELL, V76, P301, DOI 10.1016/0092-8674(94)90337-9; Takeda K, 1997, J EXP MED, V186, P449, DOI 10.1084/jem.186.3.449; TEMANN U, 1997, AM J RESP CELL MOL B, V13, P54; Tomkinson A, 1999, AM J RESP CRIT CARE, V160, P1283; TORPHY TJ, 1993, J PHARMACOL EXP THER, V265, P1213; TURNER CR, 1994, AM J RESP CRIT CARE, V149, P1153; UNDERWOOD DC, 1993, J PHARMACOL EXP THER, V264, P609; WOOLCOCK AJ, 1969, J CLIN INVEST, V48, P1097, DOI 10.1172/JCI106066; WRIGHT CD, 1990, BIOCHEM PHARMACOL, V40, P699, DOI 10.1016/0006-2952(90)90304-4	33	91	93	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					173	184				12	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	394TV	WOS:000166540100033	11208644	
J	Diez, U; Kroessner, T; Rehwagen, M; Richter, M; Wetzig, H; Schulz, R; Borte, M; Metzner, G; Krumbiegel, P; Herbarth, O				Diez, U; Kroessner, T; Rehwagen, M; Richter, M; Wetzig, H; Schulz, R; Borte, M; Metzner, G; Krumbiegel, P; Herbarth, O			Effects of indoor painting and smoking on airway symptoms in atopy risk children in the first year of life - results of the LARS-study	INTERNATIONAL JOURNAL OF HYGIENE AND ENVIRONMENTAL HEALTH			English	Article; Proceedings Paper	7th Congress of the Society-of-Hygiene-and-Environmental-Medicine	1999	LEIPZIG, GERMANY	Soc Hygiene & Environm Med		atopy risk children; air pollution; VOC; restoration; smoking; pulmonary infections	VOLATILE ORGANIC-COMPOUNDS; ASTHMA	Introduction: The Leipzig Allergy High-Risk Children Study (LARS) is a prospective nested cohort control study about the influence of chemical indoor exposure in dwellings on the health outcome of atopy-risk children during the first years of life. Design and Methods: 475 premature children and children with allergic risk factors have been selected out of the 1995/1996 birth cohort in the city of Leipzig. Twenty-five volatile organic compounds (VOC) were measured in the infant's bedrooms using passive sampling systems for 4 weeks after birth. The babies underwent a medical examination at the age of sis weeks and 1 year. The parents answered a questionnaire. Results: Correlations between VOC exposures and infections were calculated by multiple logistic regression. Selected VOC show a direct association to actually painted dwellings (OR = 2.4; 95 % Cl 1.1-5.3). An increase of risk of pulmonary infections was observed in infants aged 6 weeks if restoration (painting OR 5.6; 95 % Cl 1.3-24.0) or flooring connected with painting had occurred during the pregnancy period. Higher concentration of styrene (>2.0 mu g/m(3), indicator for flooring) elevated the risk of pulmonary infections in six-week-old infants (OR = 2.1; 95 % Cl 1.1-4.2). Environmental benzene > 5.6 mu g/m(3) increased the risk of airway infections in six-week-old babies (OR = 2.4; 95 % Cl 1.28-4.48). Smoking in the dwelling (OR = 2.0; 95 % Cl 1.1-3.5) as well as restoration (OR = 1.9; 95 % Cl 1.1-3.5) are also risk factors of the development of wheezing in the one-year-old child. Conclusions: The data give indications in order to prevent allergies and chronic lung diseases in atopy risk children exposure to chemicals from indoor air should be minimised from birth on.	UFZ Helmholtz Ctr Environm Res, Dept Human Exposure Res & Epidemiol, D-04318 Leipzig, Germany; Univ Leipzig, Childrens Hosp, Fac Med, Leipzig, Germany; Univ Leipzig, Fac Med, Inst Clin Immunol & Transfus Med, Leipzig, Germany	Diez, U (reprint author), UFZ Helmholtz Ctr Environm Res, Dept Human Exposure Res & Epidemiol, Permoser Str 15, D-04318 Leipzig, Germany.	diez@expo.ufz.de					Bergmann R L, 1994, Pediatr Allergy Immunol, V5, P19, DOI 10.1111/j.1399-3038.1994.tb00343.x; Carswell F, 1995, CLIN EXP ALLERGY, V25, P52, DOI 10.1111/j.1365-2222.1995.tb00044.x; DIEZ U, 1996, PADIATR GRENZGEB, V34, P507; DIEZ U, 1998, PADIATR GRENZGEB, V36, P375; FERGUSSON DM, 1981, J EPIDEMIOL COMMUN H, V35, P180, DOI 10.1136/jech.35.3.180; HANRAHAN JP, 1998, AM REV RESPIR DIS, V141, pA282; Hempel-Jorgensen A, 1998, INT ARCH OCC ENV HEA, V71, P225, DOI 10.1007/s004200050274; Herbarth O, 1998, ADV AIR POLLUT SER, V6, P619; Jones AP, 1998, SOC SCI MED, V47, P755, DOI 10.1016/S0277-9536(98)00151-8; Karaman O, 1999, PEDIATR INT, V41, P147; MERRETT TG, 1988, ANN ALLERGY, V61, P13; MOLHAVE L, 1986, Environment International, V12, P167, DOI 10.1016/0160-4120(86)90027-9; MUTIUS E, 1994, KINDERARZT UMWELT JA, P90; REINHARDT D, 1997, THERAPIE KRANKHEITEN; SEIFERT B, 1986, BUNDESGESUNDHBL, V29, P417; TAGER IB, 1993, AM REV RESPIR DIS, V147, P811; WALLACE L, 1987, ARCH ENVIRON HEALTH, V42, P272; Wieslander G, 1997, INT ARCH OCC ENV HEA, V69, P115; 1998, BUNDESGESUNDHBL, V9, P392	19	91	93	1	12	ELSEVIER GMBH, URBAN & FISCHER VERLAG	JENA	OFFICE JENA, P O BOX 100537, 07705 JENA, GERMANY	1438-4639			INT J HYG ENVIR HEAL	Int. J. Hyg. Environ. Health.	MAR	2000	203	1					23	28		10.1078/S1438-4639(04)70004-8		6	Public, Environmental & Occupational Health; Infectious Diseases	Public, Environmental & Occupational Health; Infectious Diseases	317HG	WOS:000087219500004	10956586	
J	Eyerich, K; Novak, N				Eyerich, K.; Novak, N.			Immunology of atopic eczema: overcoming the Th1/Th2 paradigm	ALLERGY			English	Review						dendritic cell; dermatitis; eczema; immunology; T cell	THYMIC STROMAL LYMPHOPOIETIN; FC-EPSILON-RI; ANTI-CD20 RITUXIMAB TREATMENT; IFN-GAMMA RESPONSE; ALLERGIC CONTACT; DENDRITIC CELLS; PATCH TEST; IN-SITU; T-CELLS; KERATINOCYTE DIFFERENTIATION	Atopic eczema (AE) is a challenge for modern medicine, because it is prevalent, severely affects quality of life of patients and their families, and causes high socioeconomic costs. The pathogenesis of AE is complex. While initial studies suggested a Th2 deviation as primary reason for the disease, numerous studies addressed a genetically predetermined impaired epidermal barrier as leading cause in a subgroup of patients. Recently, immune changes beyond the initial Th2 concept were defined in AE, with a role for specialized dendritic cells as well as newly identified T helper cell subsets such as Th17 and Th22 cells. Furthermore, trigger factors are expanded beyond classical Th2 allergens such as pollen or house dust mites to microbial products as well as self-antigens. This review pieces together our current understanding of immune as well as barrier abnormalities into the pathogenesis mosaic of AE.	[Eyerich, K.] Tech Univ Munich, Dept Dermatol & Allergy, D-80290 Munich, Germany; [Eyerich, K.] Helmholtz Ctr, ZAUM Ctr Allergy & Environm, Munich, Germany; [Eyerich, K.] Tech Univ Munich, D-80290 Munich, Germany; [Novak, N.] Univ Bonn, Med Ctr, Dept Dermatol & Allergy, Bonn, Germany	Eyerich, K (reprint author), Dept Dermatol & Allergy, Biedersteiner Str 29, D-80802 Munich, Germany.	kilian.eyerich@lrz.tum.de					Antoniu SA, 2010, CURR OPIN INVEST DR, V11, P1286; Barnes KC, 2010, J ALLERGY CLIN IMMUN, V125, P16, DOI 10.1016/j.jaci.2009.11.008; Baurecht H, 2007, J ALLERGY CLIN IMMUN, V120, P1406, DOI 10.1016/j.jaci.2007.08.067; Belloni B, 2007, J ALLERGY CLIN IMMUN, V120, P1223, DOI 10.1016/j.jaci.2007.08.060; Bieber T, 2012, ALLERGY, V67, P969, DOI 10.1111/j.1398-9995.2012.02845.x; Bieber T, 2012, ALLERGY, V67, P1475, DOI 10.1111/all.12049; Bieber T, 2008, NEW ENGL J MED, V358, P1483, DOI 10.1056/NEJMra074081; Bisgaard H, 2008, PLOS MED, V5, DOI 10.1371/journal.pmed.0050131; Brandt EB, 2011, J CLIN CELL IMMUNOL, V2; 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Strachan DR, 2001, J ALLERGY CLIN IMMUN, V108, P901, DOI 10.1067/mai.2001.119408; Suarez-Farinas M, 2011, J ALLERGY CLIN IMMUN, V127, P954, DOI 10.1016/j.jaci.2010.12.1124; Takiguchi R, 2007, J AM ACAD DERMATOL, V56, P222, DOI 10.1016/j.jaad.2006.08.031; Tintle S, 2011, J ALLERGY CLIN IMMUN, V128, P583, DOI 10.1016/j.jaci.2011.05.042; Traidl-Hoffmann C, 2005, J EXP MED, V201, P627, DOI 10.1084/jem.20041065; Traidl-Hoffmann C, 2002, J ALLERGY CLIN IMMUN, V109, P831, DOI 10.1067/mai.2002.124655; Trompette A, 2009, NATURE, V457, P585, DOI 10.1038/nature07548; Volf EM, 2012, J DRUGS DERMATOL, V11, P341; Vu AT, 2010, J ALLERGY CLIN IMMUN, V126, P985, DOI 10.1016/j.jaci.2010.09.002; Walley AJ, 2001, NAT GENET, V29, P175, DOI 10.1038/ng728; Zeller S, 2009, J ALLERGY CLIN IMMUN, V124, P278, DOI 10.1016/j.jaci.2009.05.015	102	90	96	1	29	WILEY-BLACKWELL	HOBOKEN	111 RIVER ST, HOBOKEN 07030-5774, NJ USA	0105-4538			ALLERGY	Allergy	AUG	2013	68	8					974	982		10.1111/all.12184		9	Allergy; Immunology	Allergy; Immunology	204SV	WOS:000323390500005	23889510	
J	Leuppi, JD; Schuetz, P; Bingisser, R; Bodmer, M; Briel, M; Drescher, T; Duerring, U; Henzen, C; Leibbrandt, Y; Maier, S; Miedinger, D; Muller, B; Scherr, A; Schindler, C; Stoeckli, R; Viatte, S; von Garnier, C; Tamm, M; Rutishauser, J				Leuppi, Joerg D.; Schuetz, Philipp; Bingisser, Roland; Bodmer, Michael; Briel, Matthias; Drescher, Tilman; Duerring, Ursula; Henzen, Christoph; Leibbrandt, Yolanda; Maier, Sabrina; Miedinger, David; Mueller, Beat; Scherr, Andreas; Schindler, Christian; Stoeckli, Rolf; Viatte, Sebastien; von Garnier, Christophe; Tamm, Michael; Rutishauser, Jonas			Short-term vs Conventional Glucocorticoid Therapy in Acute Exacerbations of Chronic Obstructive Pulmonary Disease The REDUCE Randomized Clinical Trial	JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION			English	Article							SYSTEMIC GLUCOCORTICOIDS; ORAL PREDNISONE; COPD; MORTALITY	Importance International guidelines advocate a 7- to 14-day course of systemic glucocorticoid therapy in acute exacerbations of chronic obstructive pulmonary disease (COPD). However, the optimal dose and duration are unknown. Objective To investigate whether a short-term (5 days) systemic glucocorticoid treatment in patients with COPD exacerbation is noninferior to conventional (14 days) treatment in clinical outcome and whether it decreases the exposure to steroids. Design, Setting, and Patients REDUCE (Reduction in the Use of Corticosteroids in Exacerbated COPD), a randomized, noninferiority multicenter trial in 5 Swiss teaching hospitals, enrolling 314 patients presenting to the emergency department with acute COPD exacerbation, past or present smokers (>= 20 pack-years) without a history of asthma, from March 2006 through February 2011. Interventions Treatment with 40 mg of prednisone daily for either 5 or 14 days in a placebo-controlled, double-blind fashion. The predefined noninferiority criterion was an absolute increase in exacerbations of at most 15%, translating to a critical hazard ratio of 1.515 for a reference event rate of 50%. Main Outcome and Measure Time to next exacerbation within 180 days. Results Of 314 randomized patients, 289 (92%) of whom were admitted to the hospital, 311 were included in the intention-to-treat analysis and 296 in the per-protocol analysis. Hazard ratios for the short-term vs conventional treatment group were 0.95 (90% CI, 0.70 to 1.29; P=.006 for noninferiority) in the intention-to-treat analysis and 0.93 (90% CI, 0.68 to 1.26; P=.005 for noninferiority) in the per-protocol analysis, meeting our noninferiority criterion. In the short-term group, 56 patients (35.9%) reached the primary end point; 57 (36.8%) in the conventional group. Estimates of reexacerbation rates within 180 days were 37.2% (95% CI, 29.5% to 44.9%) in the short-term; 38.4% (95% CI, 30.6% to 46.3%) in the conventional, with a difference of -1.2% (95% CI, -12.2% to 9.8%) between the short-term and the conventional. Among patients with a reexacerbation, the median time to event was 43.5 days (interquartile range [IQR], 13 to 118) in the short-term and 29 days (IQR, 16 to 85) in the conventional. There was no difference between groups in time to death, the combined end point of exacerbation, death, or both and recovery of lung function. In the conventional group, mean cumulative prednisone dose was significantly higher (793 mg [95% CI, 710 to 876 mg] vs 379 mg [95% CI, 311 to 446 mg], P<.001), but treatment-associated adverse reactions, including hyperglycemia and hypertension, did not occur more frequently. Conclusions and Relevance In patients presenting to the emergency department with acute exacerbations of COPD, 5-day treatment with systemic glucocorticoids was noninferior to 14-day treatment with regard to reexacerbation within 6 months of follow-up but significantly reduced glucocorticoid exposure. These findings support the use of a 5-day glucocorticoid treatment in acute exacerbations of COPD.	[Leuppi, Joerg D.; Drescher, Tilman; Maier, Sabrina; Miedinger, David; Scherr, Andreas] Univ Basel Hosp, Clin Internal Med, Basel, Switzerland; [Bingisser, Roland; Bodmer, Michael] Univ Basel Hosp, Interdisciplinary Emergency Dept, Basel, Switzerland; [Briel, Matthias] Univ Basel Hosp, Basel Inst Clin Epidemiol & Biostat, Basel, Switzerland; [Drescher, Tilman; Duerring, Ursula; Stoeckli, Rolf] Univ Basel Hosp, Clin Endocrinol Diabetol & Metab, Basel, Switzerland; [Scherr, Andreas; Tamm, Michael] Univ Basel Hosp, Clin Pneumol, Basel, Switzerland; [Schuetz, Philipp; Mueller, Beat] Kantonsspital, Med Univ Clin, Aarau, Switzerland; [Henzen, Christoph] Kantonsspital, Dept Internal Med, Luzern, Switzerland; [Rutishauser, Jonas] Univ Basel, Biozentrum, CH-4003 Basel, Switzerland; [Schindler, Christian] Univ Basel, Swiss Trop & Publ Hlth Inst, CH-4003 Basel, Switzerland; [Viatte, Sebastien] Univ Manchester, Arthrit Res UK Epidemiol Unit, Manchester Acad Hlth Sci Ctr, Manchester M13 9PL, Lancs, England; [von Garnier, Christophe] Inselspital Bern, Univ Hosp Bern, Resp Med Clin, Bern, Switzerland; [Leibbrandt, Yolanda; Viatte, Sebastien; Rutishauser, Jonas] Hosp Ctr Biel Bienne, Clin Internal Med, Dept Med, Biel, Switzerland	Rutishauser, J (reprint author), Ctr Hosp, Clin Internal Med, Dept Med, Vogelsang 84, CH-2501 Biel, Switzerland.	j.rutishauser@unibas.ch	Bodmer, Michael/K-1873-2013; Schindler, Christian/D-3472-2015	Bingisser, Roland/0000-0001-8223-9792; Briel, Matthias/0000-0002-2070-5230	Department of Medicine, University Hospital Basel; Clinic of Internal Medicine, Hospital Center of Biel-Bienne; Freie Akademische Gesellschaft; Fonds fur Lehre und Forschung; AstraZeneca; Viollier Laboratory; Gottfried und Julia Bangerter-Rhyner-Stiftung fur Medizinische Forschung	The REDUCE trial was an investigator-initiated study supported by the Department of Medicine, University Hospital Basel; the Clinic of Internal Medicine, Hospital Center of Biel-Bienne; Freie Akademische Gesellschaft; Fonds fur Lehre und Forschung; AstraZeneca; Viollier Laboratory; Gottfried und Julia Bangerter-Rhyner-Stiftung fur Medizinische Forschung.	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Am. Med. Assoc.	JUN 5	2013	309	21					2223	2231		10.1001/jama.2013.5023		9	Medicine, General & Internal	General & Internal Medicine	156YC	WOS:000319859200026	23695200	
J	Mugler, JP; Altes, TA; Ruset, IC; Dregely, IM; Mata, JF; Miller, GW; Ketel, S; Ketel, J; Hersman, FW; Ruppert, K				Mugler, John P., III; Altes, Talissa A.; Ruset, Iulian C.; Dregely, Isabel M.; Mata, Jaime F.; Miller, G. Wilson; Ketel, Stephen; Ketel, Jeffrey; Hersman, F. William; Ruppert, Kai			Simultaneous magnetic resonance imaging of ventilation distribution and gas uptake in the human lung using hyperpolarized xenon-129	PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA			English	Article						gas exchange; pulmonary function; pulmonary ventilation	AIR SPACES; HE-3 GAS; IN-VIVO; MRI; DYNAMICS; NMR	Despite a myriad of technical advances in medical imaging, as well as the growing need to address the global impact of pulmonary diseases, such as asthma and chronic obstructive pulmonary disease, on health and quality of life, it remains challenging to obtain in vivo regional depiction and quantification of the most basic physiological functions of the lung-gas delivery to the airspaces and gas uptake by the lung parenchyma and blood-in a manner suitable for routine application in humans. We report a method based on MRI of hyperpolarized xenon-129 that permits simultaneous observation of the 3D distributions of ventilation (gas delivery) and gas uptake, as well as quantification of regional gas uptake based on the associated ventilation. Subjects with lung disease showed variations in gas uptake that differed from those in ventilation in many regions, suggesting that gas uptake as measured by this technique reflects such features as underlying pathological alterations of lung tissue or of local blood flow. Furthermore, the ratio of the signal associated with gas uptake to that associated with ventilation was substantially altered in subjects with lung disease compared with healthy subjects. This MRI-based method provides a way to quantify relationships among gas delivery, exchange, and transport, and appears to have significant potential to provide more insight into lung disease.	[Mugler, John P., III; Altes, Talissa A.; Mata, Jaime F.; Miller, G. Wilson; Ruppert, Kai] Univ Virginia, Dept Radiol, Ctr Vivo Hyperpolarized Gas MR Imaging, Charlottesville, VA 22908 USA; [Ruset, Iulian C.; Ketel, Stephen; Ketel, Jeffrey; Hersman, F. William] Xemed LLC, Durham, NH 03824 USA; [Ruset, Iulian C.; Dregely, Isabel M.; Hersman, F. William] Univ New Hampshire, Dept Phys, Durham, NH 03824 USA	Mugler, JP (reprint author), Univ Virginia, Dept Radiol, Ctr Vivo Hyperpolarized Gas MR Imaging, Charlottesville, VA 22908 USA.	John.Mugler@virginia.edu	Mugler, John/B-9432-2013	Mugler, John/0000-0002-4140-308X; Dregely, Isabel/0000-0003-4146-7363	National Institutes of Health [R41 HL091578, R01 EB003202, R01 HL079077]; Siemens Medical Solutions	This work was supported by National Institutes of Health Grants R41 HL091578, R01 EB003202, and R01 HL079077 and by a research grant from Siemens Medical Solutions.	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Natl. Acad. Sci. U. S. A.	DEC 14	2010	107	50					21707	21712		10.1073/pnas.1011912107		6	Multidisciplinary Sciences	Science & Technology - Other Topics	697NY	WOS:000285521500087	21098267	
J	Wagner, E; Frank, MM				Wagner, Eric; Frank, Michael M.			Therapeutic potential of complement modulation	NATURE REVIEWS DRUG DISCOVERY			English	Review							HEMOLYTIC-UREMIC SYNDROME; MANNOSE-BINDING LECTIN; ELEVATION MYOCARDIAL-INFARCTION; ENTIRE C1QR(2)S(2) COMPLEX; TRAUMATIC BRAIN-INJURY; TH2 EFFECTOR FUNCTIONS; ALTERNATIVE PATHWAY; FACTOR-H; C1 INHIBITOR; FACTOR-B	The complement system is an essential component of innate immunity that has been more recently recognized as an unexpected player in various pathological states. These include age-related macular degeneration, atypical haemolytic uraemic syndrome, allergy, foetal loss, and axonal and myelin degradation after trauma. Its importance has also been recognized in physiological processes including haematopoietic stem cell homing to the bone marrow, liver regeneration and modulation of adaptive immune responses. Although the complement system has long been known to be involved in autoimmune and inflammatory diseases, few agents that target the complement system are currently approved for clinical use. However, renewed interest in modulating this system in various pathological conditions has emerged, and several agents are now in development.	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Rev. Drug Discov.	JAN	2010	9	1					43	56		10.1038/nrd3011		14	Biotechnology & Applied Microbiology; Pharmacology & Pharmacy	Biotechnology & Applied Microbiology; Pharmacology & Pharmacy	566GD	WOS:000275357200023	19960015	
J	Blanc, PD; Iribarren, C; Trupin, L; Earnest, G; Katz, PP; Balmes, J; Sidney, S; Eisner, MD				Blanc, P. D.; Iribarren, C.; Trupin, L.; Earnest, G.; Katz, P. P.; Balmes, J.; Sidney, S.; Eisner, M. D.			Occupational exposures and the risk of COPD: dusty trades revisited	THORAX			English	Article							OBSTRUCTIVE PULMONARY-DISEASE; WORK DISABILITY; HEALTH OUTCOMES; US POPULATION; LUNG-FUNCTION; ASTHMA; BURDEN; ASSOCIATION; PREVALENCE; LIMITATION	Background: The contribution of occupational exposures to chronic obstructive pulmonary disease (COPD) and, in particular, their potential interaction with cigarette smoking remains underappreciated. Methods: Data from the FLOW study of 1202 subjects with COPD (of which 742 had disease classified as stage II or above by Global Obstructive Lung Disease (GOLD) criteria) and 302 referent subjects matched by age, sex and race recruited from a large managed care organisation were analysed. Occupational exposures were assessed using two methods: self-reported exposure to vapours, gas, dust or fumes on the longest held job (VGDF) and a job exposure matrix (JEM) for probability of exposure based on occupation. Multivariate analysis was used to control for age, sex, race and smoking history. The odds ratio (OR) and adjusted population attributable fraction (PAF) associated with occupational exposure were calculated. Results: VGDF exposure was associated with an increased risk of COPD (OR 2.11; 95% CI 1.59 to 2.82) and a PAF of 31% (95% CI 22% to 39%). The risk associated with high probability of workplace exposure by JEM was similar (OR 2.27; 95% CI 1.46 to 3.52), although the PAF was lower (13%; 95% CI 8% to 18%). These estimates were not substantively different when the analysis was limited to COPD GOLD stage II or above. Joint exposure to both smoking and occupational factors markedly increased the risk of COPD (OR 14.1; 95% CI 9.33 to 21.2). Conclusions: Workplace exposures are strongly associated with an increased risk of COPD. On a population level, prevention of both smoking and occupational exposure, and especially both together, is needed to prevent the global burden of disease.	[Blanc, P. D.; Earnest, G.; Balmes, J.; Eisner, M. D.] Univ San Francisco, Div Occupat & Environm Med, San Francisco, CA 94117 USA; [Blanc, P. D.; Earnest, G.; Balmes, J.; Eisner, M. D.] Univ San Francisco, Dept Med, Div Pulm & Crit Care Med, San Francisco, CA 94117 USA; [Iribarren, C.; Sidney, S.; Eisner, M. D.] Kaiser Permanente, Div Res, Oakland, CA USA; [Trupin, L.; Katz, P. P.] Univ San Francisco, Dept Med, Inst Hlth Policy Studies, San Francisco, CA 94117 USA	Eisner, MD (reprint author), Univ San Francisco, Div Occupat & Environm Med, 350 Parnassus Ave,Ste 609, San Francisco, CA 94117 USA.	mark.eisner@ucsf.edu			NHLBI/NIH [R01HL077618]	NHLBI/NIH R01HL077618.	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M., 2002, MMWR-MORBID MORTAL W, V51, P1; Pauwels Romain A., 2001, American Journal of Respiratory and Critical Care Medicine, V163, P1256; Perez-Padilla R, 2006, RESPIR CARE, V51, P1167; Sidney S, 2005, CHEST, V128, P2068, DOI 10.1378/chest.128.4.2068; Trupin L, 2003, EUR RESPIR J, V22, P462, DOI 10.1183/09031936.03.00094203; *US BUR CENS, 2000, IND OCC CLASS SYST; Walters JAE, 2006, RESPIROLOGY, V11, P306, DOI 10.1111/j.1440-1843.2006.00842.x; Weinmann S, 2008, J OCCUP ENVIRON MED, V50, P561, DOI 10.1097/JOM.0b013e3181651556; Whitney E, 2008, AM J RESP CRIT CARE, V177, P1172; Zock JP, 2001, AM J RESP CRIT CARE, V163, P1572; 1999, MMWR MORBIDITY MORTA, V48, P993	39	90	94	1	7	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	JAN	2009	64	1					6	12		10.1136/thx.2008.099390		7	Respiratory System	Respiratory System	387CF	WOS:000261928600004	18678700	
J	Wang, CH; Huang, CD; Lin, HC; Lee, KY; Lin, SM; Liu, CY; Huang, KH; Ko, YS; Chung, KF; Kuo, HP				Wang, Chun-Hua; Huang, Chien-Da; Lin, Horng-Chyuan; Lee, Kang-Yun; Lin, Shu-Min; Liu, Chien-Ying; Huang, Kuo-Hsiung; Ko, Yu-Shien; Chung, Kian Fan; Kuo, Han-Pin			Increased circulating fibrocytes in asthma with chronic airflow obstruction	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; fibrocytes; myofibroblasts; transforming growth factor-beta; airway remodeling	PERIPHERAL-BLOOD FIBROCYTES; RETICULAR BASEMENT-MEMBRANE; TISSUE-REPAIR; CELLS; DIFFERENTIATION; EXPRESSION; FIBROSIS; GROWTH; ANGIOGENESIS; INFLAMMATION	Rationale A proportion of patients with asthma present with chronic airflow obstruction (CAO). We hypothesized that this effect may result from increased activity of circulating fibroblast-like progenitor cells (fibrocytes) that could home to the airway mucosal wall. Objectives: To compare the proportion, proliferation, and differentiation of circulating fibrocytes from patients with asthma with CAO or no airflow obstruction (NOA) and control subjects. Methods: We investigated circulating fibrocytes in 11 patients with asthma with CAO and a rapid decline in FEV(1), 9 patients with asthma with NOA, and 10 nonasthmatic control subjects. Blood nonadherent non-T (NANT) cells were incubated with fetal calf serum or each patient's own serum and fibrocytes expressing CD34, CD45, and collagen I with a-smooth muscle actin were identified by flow cytometry. Measurements and Main Results: A higher percentage of circulating fibrocytes in NANT cells was found in patients with CAO when compared with patients with NOA and control subjects. In CAO, the slope of the yearly decline in FEV(1) correlated with circulating fibrocytes (r = -0.756, n = 11, P < 0.01). When NANT cells from patients with CAO were cultured in the patients' own sera, more fibrocytes were detected than when cultured in sera from patients with NOA or from normal subjects. An anti-transforming growth factor (TGF)-beta(1)-neutralizing antibody inhibited a-smooth muscle actin-positive fibrocyte transformation from NANT cells of patients with CAO. Serum TGF-beta(1) levels were higher in patients with CAO than in patients with NOA or in normal subjects. Conclusions: Circulating fibrocytes are increased in patients with asthma with CAO and can be transformed by TGF-beta(1) to myofibroblasts. Fibrocytes may contribute to airway obstruction in asthma.	[Wang, Chun-Hua; Huang, Chien-Da; Lin, Horng-Chyuan; Lee, Kang-Yun; Lin, Shu-Min; Liu, Chien-Ying; Huang, Kuo-Hsiung; Kuo, Han-Pin] Chang Gung Mem Hosp, Dept Thorac Med, Taipei 10591, Taiwan; [Wang, Chun-Hua; Lin, Horng-Chyuan] Chang Gung Univ, Dept Chinese Med, Tao Yuan, Taiwan; [Huang, Chien-Da; Lee, Kang-Yun; Liu, Chien-Ying; Kuo, Han-Pin] Chang Gung Univ, Dept Med, Tao Yuan, Taiwan; [Ko, Yu-Shien] Chang Gung Mem Hosp, Cardiovasc Div 1, Taipei 10591, Taiwan; [Chung, Kian Fan] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London, England	Kuo, HP (reprint author), Chang Gung Mem Hosp, Dept Thorac Med, 199 Tung Hwa N Rd, Taipei 10591, Taiwan.	q8828@ms11.hinet.net		Wang, Chun-Hua/0000-0002-3514-9353			Abe R, 2001, J IMMUNOL, V166, P7556; American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P225, DOI DOI 10.1164/AJRCCM/136.1.225; Balzar S, 2005, J ALLERGY CLIN IMMUN, V115, P110, DOI 10.1016/j.jaci.2004.09.034; BLANC PD, 1993, CHEST, V104, P1371, DOI 10.1378/chest.104.5.1371; BOUSQUET J, 1992, ALLERGY, V47, P3, DOI 10.1111/j.1398-9995.1992.tb02242.x; Bousquet J, 2000, AM J RESP CRIT CARE, V161, P1720; BUCALA R, 1994, MOL MED, V1, P71; Chesney J, 1997, BIOCHEM SOC T, V25, P520; Davies DE, 2003, J ALLERGY CLIN IMMUN, V111, P215, DOI 10.1067/mai.2003.128; 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; Gizycki MJ, 1997, AM J RESP CELL MOL, V16, P664; Hartlapp I, 2001, FASEB J, V15, P2215, DOI 10.1096/fj.01-0049com; Hong KM, 2007, J BIOL CHEM, V282, P22910, DOI 10.1074/jbc.M703597200; Hoshino M, 2003, EUR RESPIR J, V21, P804, DOI 10.1183/09031936.03.00082002; Huang J, 1999, AM J RESP CRIT CARE, V160, P725; Ko YS, 2004, CIRCULATION, V109, P1172, DOI 10.1161/01.CIR.0000117233.57190.BD; Kuo HP, 2001, BRIT J PHARMACOL, V134, P1539, DOI 10.1038/sj.bjp.0704389; Marini M, 1996, BIOCHEM BIOPH RES CO, V220, P896, DOI 10.1006/bbrc.1996.0502; Metz CN, 2003, CELL MOL LIFE SCI, V60, P1342, DOI 10.1007/s00018-003-2328-0; Moore BB, 2005, AM J PATHOL, V166, P675, DOI 10.1016/S0002-9440(10)62289-4; Mori L, 2005, EXP CELL RES, V304, P81, DOI 10.1016/j.yexcr.2004.11.011; Murdoch C, 2000, IMMUNOL REV, V177, P175, DOI 10.1034/j.1600-065X.2000.17715.x; Nihlberg K, 2006, RESP RES, V7, DOI 10.1186/1465-9921-7-50; Pascual RM, 2005, J ALLERGY CLIN IMMUN, V116, P477, DOI 10.1016/j.jaci.2005.07.011; Payne DNR, 2003, AM J RESP CRIT CARE, V167, P78, DOI 10.1164/rccm.200205-414OC; Phillips RJ, 2004, J CLIN INVEST, V114, P438, DOI 10.1172/jci200420997; Quan TE, 2004, INT J BIOCHEM CELL B, V36, P598, DOI 10.1016/j.biocel.2003.10.005; Redington AE, 2000, CLIN EXP ALLERGY, V30, P42; Redington AE, 1997, THORAX, V52, P310; Schmidt M, 2003, J IMMUNOL, V171, P380; Torrego A, 2007, THORAX, V62, P307, DOI 10.1136/thx.2006.063487; Vignola AM, 2000, J ALLERGY CLIN IMMUN, V105, pS514, DOI 10.1016/S0091-6749(00)90053-8; Wang CH, 1999, J ALLERGY CLIN IMMUN, V104, P803; Wang JF, 2007, WOUND REPAIR REGEN, V15, P113, DOI 10.1111/j.1524-475X.2006.00192.x; WESTERGRENTHORSSON G, 1993, J CLIN INVEST, V92, P632, DOI 10.1172/JCI116631	36	90	91	0	1	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.	SEP 15	2008	178	6					583	591		10.1164/rccm.200710-1557OC		9	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	347RL	WOS:000259158600008	18583572	
J	Marschan, E; Kuitunen, M; Kukkonen, K; Poussa, T; Sarnesto, A; Haahtela, T; Korpela, R; Savilahti, E; Vaarala, O				Marschan, E.; Kuitunen, M.; Kukkonen, K.; Poussa, T.; Sarnesto, A.; Haahtela, T.; Korpela, R.; Savilahti, E.; Vaarala, O.			Probiotics in infancy induce protective immune profiles that are characteristic for chronic low-grade inflammation	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						atopic; CRP; IgA; IgE; IL-10; oral tolerance; probiotic; regulatory cells	PLACEBO-CONTROLLED TRIAL; ORAL TOLERANCE INDUCTION; COWS MILK ALLERGY; ATOPIC-DERMATITIS; DOUBLE-BLIND; ANTIBODY-RESPONSES; HYGIENE HYPOTHESIS; T-CELLS; CHILDREN; PREVENTION	Background Probiotics are widely studied both in the treatment and prevention of allergic diseases, but their mode of action is poorly known. Objective Our aim was to examine the effect of probiotic bacteria on in vivo cytokine, antibody, and inflammatory responses in allergy-prone infants. Methods In a randomized double-blind study, probiotic bacteria or placebo were given for 1 month before delivery to mothers and for 6 months to infants with a family history of allergy. Plasma samples were analysed for C-reactive protein (CRP), total IgA and IgE, food-specific IgA, IgG, and IgE, IL-2, IL-4, IL-6, IL-10, TNF-alpha, and IFN-gamma. We analysed the associations of immunological and inflammatory parameters at age 6 months with probiotic treatment and allergic phenotype at 2 years. Results Infants receiving probiotic bacteria had higher plasma levels of CRP (P=0.008), total IgA (P=0.016), total IgE (P=0.047), and IL-10 (P=0.002) than infants in the placebo group. Increased plasma CRP level at age 6 months was associated with a decreased risk of eczema [odds ratio (OR) 0.41 [95% confidence interval (CI) 0.17-0.99], P=0.046], and with a decreased risk of allergic disease [OR 0.38 (95% CI 0.16-0.87), P=0.023] at age 2 years, when adjusted with probiotic use. Conclusion The association of CRP with a decreased risk of eczema at 2 years of age in allergy-prone children supports the view that chronic, low-grade inflammation protects from eczema. Probiotic-induced low-grade inflammation was characterized by elevation of IgE, IgA, and IL-10, the changes typically observed in helminth infection-associated induction of regulatory mechanisms. The findings emphasize the role of chronic microbial exposure as an immune modulator protecting from allergy.	[Marschan, E.; Sarnesto, A.; Savilahti, E.] Univ Helsinki, Hosp Children & Adolescents, FIN-00029 Helsinki, Finland; [Kuitunen, M.; Kukkonen, K.; Haahtela, T.] Univ Helsinki, Skin & Allergy Hosp, FIN-00029 Helsinki, Finland; [Poussa, T.] STAT Consulting, Tampere, Finland; [Korpela, R.] Valio Res & Dev, Helsinki, Finland; [Korpela, R.] Univ Helsinki, Inst Biomed, FIN-00029 Helsinki, Finland; [Vaarala, O.] Natl Publ Hlth Inst, Dept Viral Dis & Immunol, Helsinki, Finland	Marschan, E (reprint author), Univ Helsinki, Hosp Children & Adolescents, Haartmaninkatu 8,POB 700, FIN-00029 Helsinki, Finland.	emma.marschan@hus.fi					BRUIJNZEELKOOMEN C, 1995, ALLERGY, V50, P623, DOI 10.1111/j.1398-9995.1995.tb02579.x; Dreborg S, 1989, ALLERGY S10, V44, P1; Fang H, 2000, FEMS IMMUNOL MED MIC, V29, P47, DOI 10.1016/S0928-8244(00)00187-5; Harris NL, 2006, J IMMUNOL, V177, P6256; HEUMANN D, 1994, INFECT IMMUN, V62, P2715; *INT RHIN MAN WORK, 1994, ALLERGY, V49, pS1; ISOLAURI E, 1995, VACCINE, V13, P310, DOI 10.1016/0264-410X(95)93319-5; Isolauri E, 2000, CLIN EXP ALLERGY, V30, P1604, DOI 10.1046/j.1365-2222.2000.00943.x; Johansson SGO, 2004, J ALLERGY CLIN IMMUN, V113, P832, DOI 10.1016/j.jaci.2003.12.591; 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; Kukkonen K, 2007, J ALLERGY CLIN IMMUN, V119, P192, DOI 10.1016/j.jaci.2006.09.009; Kukkonen K, 2006, PEDIATR ALLERGY IMMU, V17, P416, DOI 10.1111/j.1399-3038.2006.00420.x; LYNCH NR, 1987, CLIN ALLERGY, V17, P199, DOI 10.1111/j.1365-2222.1987.tb02004.x; Maeda Y, 2001, IMMUNOBIOLOGY, V204, P442, DOI 10.1078/0171-2985-00054; Maizels RM, 2005, CURR OPIN IMMUNOL, V17, P656, DOI 10.1016/j.coi.2005.09.001; Majamaa H, 1997, J ALLERGY CLIN IMMUN, V99, P179, DOI 10.1016/S0091-6749(97)70093-9; Miettinen M, 1998, INFECT IMMUN, V66, P6058; *NAT ASTHM ED PREV, 2002, J ALLERGY CLIN IMMUN, V110, pS147; Pohjavuori E, 2004, J ALLERGY CLIN IMMUN, V114, P131, DOI 10.1016/j.jaci.2004.03.036; Rodriguez OL, 2004, J TROP PEDIATRICS, V50, P68, DOI 10.1093/tropej/50.2.68; Rosenfeldt V, 2004, J PEDIATR-US, V145, P612, DOI 10.1016/j.jpeds.2004.06.068; Rosenfeldt V, 2003, J ALLERGY CLIN IMMUN, V111, P389, DOI 10.1067/mai.2003.389; Saarinen KM, 1999, J ALLERGY CLIN IMMUN, V104, P1093, DOI 10.1016/S0091-6749(99)70094-1; Sanders ME, 2003, NUTR REV, V61, P91, DOI 10.1301/nr.2003.marr.91-99; SAVILAHTI E, 1993, DIABETES CARE, V16, P984, DOI 10.2337/diacare.16.7.984; STALDER JF, 1993, DERMATOLOGY, V186, P23; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Sudo N, 1997, J IMMUNOL, V159, P1739; Umetsu DT, 2004, NAT MED, V10, P232, DOI 10.1038/nm0304-232; 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; Vartiainen E, 2002, J ALLERGY CLIN IMMUN, V109, P643, DOI 10.1067/mai.2002.123307; Viljanen M, 2005, J ALLERGY CLIN IMMUN, V115, P1254, DOI 10.1016/j.jaci.2005.03.047; Viljanen M, 2005, ALLERGY, V60, P494, DOI 10.1111/j.1398-9995.2004.00514.x; Voor T, 2005, CLIN EXP ALLERGY, V35, P153, DOI 10.1111/j.1365-2222.2005.02157.x; Weston S, 2005, ARCH DIS CHILD, V90, P892, DOI 10.1136/adc.2004.060673; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P406, DOI 10.1111/j.1365-2133.1994.tb08532.x; Wilson MS, 2005, J EXP MED, V202, P1199, DOI 10.1084/jem.20042572; Yazdanbakhsh M, 2002, SCIENCE, V296, P490, DOI 10.1126/science.296.5567.490	40	90	94	1	5	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	APR	2008	38	4					611	618		10.1111/j.1365-2222.2008.02942.x		8	Allergy; Immunology	Allergy; Immunology	275ET	WOS:000254055400009	18266878	
J	Michils, A; Baldassarre, S; Van Muylem, A				Michils, A.; Baldassarre, S.; Van Muylem, A.			Exhaled nitric oxide and asthma control: a longitudinal study in unselected patients	EUROPEAN RESPIRATORY JOURNAL			English	Article						asthma control; exhaled nitric oxide; lung function	RANDOMIZED CONTROLLED-TRIAL; GUIDE; QUESTIONNAIRE; EXACERBATIONS; MARKERS; AIR	Controlled studies have shown that monitoring of the exhaled nitric oxide fraction (FeNO) improves asthma management. However, the studies seldom consider the full range of patients seen in clinical practise. In the present study, the ability of FeNO to reflect asthma control over time is investigated in a regular clinical setting, and meaningful FeNO cut-off points and changes are identified. Answers to the Asthma Control Questionnaire and FeNO were recorded at least once in 341 unselected asthma patients. The whole population and subgroups were considered, i.e. both inhaled corticosteroid (ICS)-naive and low or high-to-medium (<= or >500 mu g beclomethasone dipropionate equivalents(.)day(-1)) ICS-dose groups. An FeNo decrease <40% or increase <30% precludes asthma control optimisation or deterioration, respectively (negative predictive value 79 and 82%, respectively). In the present study's low-dose group, a decrease >40% indicated asthma control optimisation (positive predictive value (PPV) 83%). In ICS-naive patients, FeNO >35 ppb predicted asthma control improvement in response to ICS (PPV 68%). In most cases, forced expiratory volume in one second assessments were not useful. In conclusion, in a given patient, exhaled nitric oxide fraction was found to be significantly related to asthma control over time. The overall ability of exhaled nitric oxide fraction to reflect asthma control was reduced in patients using high doses of inhaled corticosteroids. Forced expiratory volume in one second had little additional value in assessing asthma control.	[Michils, A.; Baldassarre, S.; Van Muylem, A.] Erasme Univ Hosp, Chest Dept, B-1070 Brussels, Belgium	Van Muylem, A (reprint author), CUB Erasme, Chest Dept, 808 Route de Lennik, B-1070 Brussels, Belgium.	avmuylem@ulb.ac.be					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; CRATER SE, 1999, AM RESP CRIT CARE ME, V158, P806; [Anonymous], 1993, EUR RESP J S16, V6, P5; Gelb AF, 2006, CHEST, V129, P1492, DOI 10.1378/chest.129.6.1492; *GLOB IN ASTHM, 2002, NHLBI PUBL; Green RH, 2002, LANCET, V360, P1715, DOI 10.1016/S0140-6736(02)11679-5; Jatakanon A, 1999, THORAX, V54, P108; Jatakanon A, 2000, AM J RESP CRIT CARE, V161, P64; Jones SL, 2001, AM J RESP CRIT CARE, V164, P738; Jones SL, 2002, EUR RESPIR J, V20, P601, DOI 10.1183/09031936.02.00285302; Juniper EF, 2005, RESP MED, V99, P553, DOI 10.1016/j.rmed.2004.10.008; Juniper EF, 1999, EUR RESPIR J, V14, P902, DOI 10.1034/j.1399-3003.1999.14d29.x; JUNIPER EF, 2006, RESP MED, V73, P296; Kharitonov SA, 1996, AM J RESP CRIT CARE, V153, P454; Leuppi JD, 2001, AM J RESP CRIT CARE, V163, P406; Lopes C, 2006, J ALLERGY CLIN IMMUN, V117, pS177, DOI 10.1016/j.jaci.2005.12.705; McSharry CP, 2005, J ALLERGY CLIN IMMUN, V116, P88, DOI 10.1016/j.jaci.2005.03.025; Senna G, 2007, ALLERGY, V62, P207, DOI 10.1111/j.1398-9995.2006.01250.x; Shaw DE, 2007, AM J RESP CRIT CARE, V176, P231, DOI 10.1164/rccm.200610-14270C; Silkoff PE, 2005, J ALLERGY CLIN IMMUN, V116, P1249, DOI 10.1016/j.jaci.2005.09.029; Smith AD, 2005, AM J RESP CRIT CARE, V172, P453, DOI 10.1164/rccm.200411-1498OC; Smith AD, 2005, NEW ENGL J MED, V352, P2163, DOI 10.1056/NEJMoa043596; Sont JK, 1999, AM J RESP CRIT CARE, V159, P1043; Szefler SJ, 2005, J ALLERGY CLIN IMMUN, V115, P233, DOI 10.1016/j.jaci.2004.11.014; TAYLOR RD, 2006, THORAX, V61, P817; Teeter JG, 1998, CHEST, V113, P272, DOI 10.1378/chest.113.2.272; Travers J, 2007, THORAX, V62, P219, DOI 10.1136/thx.2006.066837; Wenzel S, 2005, AM J RESP CRIT CARE, V172, P149, DOI 10.1164/rccm.200409-1181PP; YOUDEN WJ, 1950, CANCER, V3, P32, DOI 10.1002/1097-0142(1950)3:1<32::AID-CNCR2820030106>3.0.CO;2-3	30	90	97	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.	MAR	2008	31	3					539	546		10.1183/09031936.00020407		8	Respiratory System	Respiratory System	272RA	WOS:000253876000010	18057062	
J	Schulte, PA; Wagner, GR; Ostry, A; Blanciforti, LA; Icutlip, RG; Krajnak, KM; Luster, M; Munson, AE; O'Callaghan, JP; Parks, CG; Simeonova, PP; Miller, DB				Schulte, Paul A.; Wagner, Gregory R.; Ostry, Aleck; Blanciforti, Laura A.; Icutlip, Robert G.; Krajnak, Kristine M.; Luster, Michael; Munson, Albert E.; O'Callaghan, James P.; Parks, Christine G.; Simeonova, Petia P.; Miller, Diane B.			Work, obesity, and occupational safety and health	AMERICAN JOURNAL OF PUBLIC HEALTH			English	Review							BODY-MASS INDEX; CARDIOVASCULAR RISK-FACTORS; CARPAL-TUNNEL SYNDROME; DIET-INDUCED OBESITY; PHYSICAL-ACTIVITY; FAT DISTRIBUTION; UNITED-STATES; WEIGHT-GAIN; NUTRITION EXAMINATION; PARKINSONS-DISEASE	There is increasing evidence that obesity and overweight may be related, in part, to adverse work conditions. In particular, the risk of obesity may increase in high-demand, low-control work environments, and for those who work long hours. In addition, obesity may modify the risk for vibration-induced injury and certain occupational musculoskeletal disorders. We hypothesized that obesity may also be a co-risk factor for the development of occupational asthma and cardiovascular disease that and it may modify the worker's response to occupational stress, immune response to chemical exposures, and risk of disease from occupational neurotoxins. We developed 5 conceptual models of the interrelationship of work, obesity, and occupational safety and health and highlighted the ethical, legal, and social issues related to fuller consideration of obesity's role in occupational health and safety.	NIOSH, Educ & Informat Div, Ctr Dis Control & Prevent, Cincinnati, OH 45226 USA; Univ British Columbia, Vancouver, BC V5Z 1M9, Canada	Schulte, PA (reprint author), NIOSH, Educ & Informat Div, Ctr Dis Control & Prevent, 4676 Columbia Pkwy, Cincinnati, OH 45226 USA.	pas4@cdc.gov	O'Callaghan, James/O-2958-2013	Parks, Christine/0000-0002-5734-3456			Abbott RD, 2002, NEUROLOGY, V59, P1051; ALBANES D, 1987, Nutrition and Cancer, V9, P199; Aldana SG, 2001, J OCCUP ENVIRON MED, V43, P36, DOI 10.1097/00043764-200101000-00009; AYDIN N, 2003, TURKISH J SURG, V19, P133; Balmes J, 2003, AM J RESP CRIT CARE, V167, P787, DOI 10.1164/rccm.167.5.787; BARBEAU EM, 2004, PREV CHRONIC DIS JUL; Baur X, 1998, AM J IND MED, V33, P114; Bernard B.P., 1997, DHHS NIOSH PUBLICATI, V97B141; Bhatia J Y, 2003, Indian J Med Microbiol, V21, P246; Bhattacherjee A, 2003, J OCCUP HEALTH, V45, P382, DOI 10.1539/joh.45.382; Brisson C, 2000, J OCCUP ENVIRON MED, V42, P40, DOI 10.1097/00043764-200001000-00011; Brown Norman DePaul, 2003, AAOHN J, V51, P470; 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J	Maneechotesuwan, K; Xin, Y; Ito, K; Jazrawi, E; Lee, KY; Usmani, OS; Barnes, PJ; Adcock, IM				Maneechotesuwan, Kittipong; Xin, Yao; Ito, Kazuhiro; Jazrawi, Elen; Lee, Kang-Yun; Usmani, Omar S.; Barnes, Peter J.; Adcock, Ian M.			Regulation of Th2 cytokine genes by p38 MAPK-mediated phosphorylation of GATA-3	JOURNAL OF IMMUNOLOGY			English	Article							ACTIVATED PROTEIN-KINASE; NUCLEAR-LOCALIZATION SEQUENCE; CD4(+) T-CELLS; AIRWAY INFLAMMATION; SIGNAL INTEGRATION; IL-4 PRODUCTION; EXPRESSION; ASTHMA; LYMPHOCYTES; INHIBITION	GATA-3 plays a critical role in allergic diseases by regulating the release of cytokines from Th2 lymphocytes. However, the molecular mechanisms involved in the regulation of GATA-3 in human T lymphocytes are not yet understood. Using small interfering RNA to knock down GATA-3, we have demonstrated its critical role in regulating IL-4, IL-5, and IL-13 release from a human T cell line. Specific stimulation of T lymphocytes by costimulation of CD3 and CD28 to mimic activation by APCs induces translocation of GATA-3 from the cytoplasm to the nucleus, with binding to the promoter region of Th2 cytokine genes, as determined by chromatin immunoprecipitation. GATA-3 nuclear translocation is dependent on its phosphorylation on serine residues by p38 MAPK, which facilitates interaction with the nuclear transporter protein importin-a. This provides a means whereby allergen exposure leads to the expression of Th2 cytokines, and this novel mechanism may provide new approaches to treating allergic diseases.	Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Sect Airway Dis, London SW3 6LY, England	Barnes, PJ (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Sect Airway Dis, Dovehouse St, London SW3 6LY, England.	p.j.barnes@imperial.ac.uk		Adcock, Ian/0000-0003-2101-8843			Barnes PJ, 2006, PHARMACOL THERAPEUT, V109, P238, DOI 10.1016/j.pharmthera.2005.08.001; Barnes PJ, 2004, NAT REV DRUG DISCOV, V3, P831, DOI 10.1038/nrd1524; Caramori G, 2001, EUR RESPIR J, V18, P466, DOI 10.1183/09031936.01.00040701; Chen CH, 2000, J IMMUNOL, V165, P5597; Chialda L, 2005, RESP RES, V6, DOI 10.1186/1465-9921-6-36; Chook YM, 2001, CURR OPIN STRUC BIOL, V11, P703, DOI 10.1016/S0959-440X(01)00264-0; Conti E, 1998, CELL, V94, P193, DOI 10.1016/S0092-8674(00)81419-1; Duan W, 2005, AM J RESP CRIT CARE, V171, P571, DOI 10.1164/rccm.200408; England Karen, 2003, Methods Mol Biol, V233, P217; Finotto S, 2001, J EXP MED, V193, P1247, DOI 10.1084/jem.193.11.1247; Goldfarb DS, 2004, TRENDS CELL BIOL, V14, P505, DOI 10.1016/j.tcb.2004.07.016; GOOTENBERG JE, 1981, J EXP MED, V154, P1403, DOI 10.1084/jem.154.5.1403; Ito K, 2000, MOL CELL BIOL, V20, P6891, DOI 10.1128/MCB.20.18.6891-6903.2000; Ito K, 2001, J BIOL CHEM, V276, P30208, DOI 10.1074/jbc.M103604200; Ito K, 2001, FASEB J, V15, P1100; Koprak S, 1999, CELL IMMUNOL, V192, P87, DOI 10.1006/cimm.1998.1448; Lavenu-Bombled C, 2002, J BIOL CHEM, V277, P18313, DOI 10.1074/jbc.M110013200; Lee CY, 2001, J SCHED, V4, P3, DOI 10.1002/1099-1425(200101/02)4:1<3::AID-JOS57>3.0.CO;2-D; Li LS, 1999, SCIENCE, V283, P848, DOI 10.1126/science.283.5403.848; Matsuda S, 1998, J BIOL CHEM, V273, P12378, DOI 10.1074/jbc.273.20.12378; Mori A, 1999, J IMMUNOL, V163, P4763; Nakamura Yutaka, 2005, Current Drug Targets - Inflammation and Allergy, V4, P267, DOI 10.2174/1568010053586273; Nunes JA, 1996, MOL IMMUNOL, V33, P63, DOI 10.1016/0161-5890(95)00121-2; Ohno M, 1998, CELL, V92, P327, DOI 10.1016/S0092-8674(00)80926-5; Pahl A, 2002, BRIT J PHARMACOL, V135, P1915, DOI 10.1038/sj.bjp.0704656; Ray A, 1999, J CLIN INVEST, V104, P985, DOI 10.1172/JCI8204; Salmon RA, 1997, J IMMUNOL, V159, P5309; Schaeffer HJ, 1999, MOL CELL BIOL, V19, P2435; Schafer PH, 1999, J IMMUNOL, V162, P7110; Schwenger GTF, 2001, J BIOL CHEM, V276, P48502, DOI 10.1074/jbc.M107836200; Staples KJ, 2000, BIOCHEM BIOPH RES CO, V273, P811, DOI 10.1006/bbrc.2000.3023; STOCHAJ U, 1992, EUR J CELL BIOL, V59, P1; SU B, 1994, CELL, V77, P727, DOI 10.1016/0092-8674(94)90056-6; Takemoto N, 2002, J IMMUNOL, V169, P4103; Torgerson TR, 1998, J IMMUNOL, V161, P6084; Underwood DC, 2000, J PHARMACOL EXP THER, V293, P281; Xiao CY, 1997, J BIOL CHEM, V272, P22191, DOI 10.1074/jbc.272.35.22191; Yagi R, 2002, INT IMMUNOL, V14, P1, DOI 10.1093/intimm/14.1.1; Yamane H, 2005, J EXP MED, V202, P793, DOI 10.1084/jem.20051304; Yamashita M, 2004, J BIOL CHEM, V279, P26983, DOI 10.1074/jbc.M403688200; YANG ZY, 1994, MOL CELL BIOL, V14, P2201; Zhang DH, 1999, IMMUNITY, V11, P473, DOI 10.1016/S1074-7613(00)80122-3; Zhang J, 1999, J IMMUNOL, V162, P3819; Zhu JF, 2004, NAT IMMUNOL, V5, P1157, DOI 10.1038/ni1128	44	90	100	1	3	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	FEB 15	2007	178	4					2491	2498				8	Immunology	Immunology	133QF	WOS:000244026800059	17277157	
J	de Haar, C; Hassing, I; Bol, M; Bleumink, R; Pieters, R				de Haar, C.; Hassing, I.; Bol, M.; Bleumink, R.; Pieters, R.			Ultrafine but not fine particulate matter causes airway inflammation and allergic airway sensitization to co-administered antigen in mice	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						adjuvant; airway; allergic; inflammation; intranasal; mouse; particulate matter; sensitization; ultrafine particles	DIESEL EXHAUST PARTICLES; CARBON-BLACK PARTICLES; ADJUVANT ACTIVITY; POLLEN ALLERGENS; TRANSITION-METALS; AMBIENT PARTICLES; OXIDATIVE STRESS; DENDRITIC CELLS; IGE PRODUCTION; IN-VITRO	Background Airborne particulate matter (PM) is an important factor associated with the enhanced prevalence of respiratory allergy. The PM adjuvant activity on allergic sensitization is a possible mechanism of action involved, and the induction of airway inflammation is suggested to be of importance in PM-induced adjuvant activity. Objective Because differently sized PM have different toxic potentials, we studied the role of particle size in the induction of airway inflammation and allergic sensitization. This was done using fine (0.250 and 0.260 mu m) and ultrafine (0.029 and 0.014 mu m) titanium dioxide (TiO2) and carbon black particles (CBP) with known differences in airway toxicity. Methods Mice were intranasally exposed to ovalbumin (OVA) alone or in combination with one of the different particles. The induction of airway inflammation and the immune adjuvant activity were studied in the lungs and lung-draining peribronchial lymph nodes (PBLN) at day 8. OVA-specific antibodies were measured at day 21, and the development of allergic airway inflammation was studied after OVA challenges (day 28). Results When administered at the same total particle mass (200 mu g), exposure to ultrafine TiO2 and CBP-induced airway inflammation, and had immune adjuvant activity. The latter was shown by increasing both the PBLN cell numbers and the production of OVA-specific T-helper type 2 (Th2) cytokines (IL-4, IL-5, IL-10 and IL-13). Whereas OVA-specific IgE and IgG1 levels in serum were only increased in animals exposed to the ultrafine TiO2, allergic airway inflammation could be detected in both ultrafine TiO2- and CBP-treated groups after challenges with OVA. Conclusion Our data show that only the ultrafine particles, with a small diameter and a large total surface area/mass, cause airway inflammation and have immune adjuvant activity in the current model supporting the hypothesis that particle toxicity is site-dependent and related to adjuvant activity.	Univ Utrecht, Inst Risk Assessment Sci, Dept Immunotoxicol, NL-3508 TC Utrecht, Netherlands	de Haar, C (reprint author), Erasmus MC, Div Gastroenterol & Nutr, Pediat Lab, Ee 1571,Dr Molewaterpl 50, NL-3015 GE Rotterdam, Netherlands.	c.dehaar@erasmusmc.nl					AMATO GD, 1998, PULM PHARMACOL THER, V11, P369; AMATO GD, 2002, ALLERGY S7I, V57, P30; Behrendt H, 2001, CURR OPIN IMMUNOL, V13, P709, DOI 10.1016/S0952-7915(01)00283-7; Bevan D R, 1985, Toxicol Ind Health, V1, P57; Borm PJA, 2005, TOXICOL APPL PHARM, V205, P157, DOI 10.1016/j.taap.2004.10.020; Brown DM, 2004, AM J PHYSIOL-LUNG C, V286, pL344, DOI 10.1152/ajplung.00139.2003; Brown DM, 2001, TOXICOL APPL PHARM, V175, P191, DOI 10.1006/taap.2001.9240; Brown DM, 2000, OCCUP ENVIRON MED, V57, P685, DOI 10.1136/oem.57.10.685; Chvatchko Y, 1996, J EXP MED, V184, P2353, DOI 10.1084/jem.184.6.2353; Cox JC, 1997, VACCINE, V15, P248, DOI 10.1016/S0264-410X(96)00183-1; de Haar C, 2005, TOXICOL SCI, V87, P409, DOI 10.1093/toxsci/kfi255; Diaz-Sanchez D, 1999, J ALLERGY CLIN IMMUN, V104, P1183; DiazSanchez D, 1997, ALLERGY, V52, P52; Elder ACP, 2000, INHAL TOXICOL, V12, P227, DOI 10.1080/089583700750019585; Englert N, 2004, TOXICOL LETT, V149, P235, DOI 10.1016/j.toxlet.2003.12.035; Foged C, 2005, INT J PHARM, V298, P315, DOI 10.1016/j.ijpharm.2005.03.035; Ford JG, 2001, J IMMUNOL, V167, P1769; FUJIMAKI H, 1994, TOXICOLOGY, V92, P261, DOI 10.1016/0300-483X(94)90182-1; Gallucci S, 2001, CURR OPIN IMMUNOL, V13, P114, DOI 10.1016/S0952-7915(00)00191-6; Gilmour PS, 2004, TOXICOL APPL PHARM, V195, P35, DOI 10.1016/j.taap.2003.10.003; Granum B, 2002, TOXICOL SCI, V65, P7, DOI 10.1093/toxsci/65.1.7; Greenwell LL, 2002, FREE RADICAL BIO MED, V32, P898, DOI 10.1016/S0891-5849(02)00782-7; Gupta RK, 1998, ADV DRUG DELIVER REV, V32, P155, DOI 10.1016/S0169-409X(98)00008-8; Hamelmann E, 1999, AM J RESP CRIT CARE, V160, P934; Hamelmann E, 2000, AM J RESP CELL MOL, V23, P327; Hofstra CL, 1999, INFLAMM RES, V48, P602, DOI 10.1007/s000110050510; Johnson RL, 2004, CIRCULATION, V109, P5, DOI 10.1161/01.CIR.0000110643.19575.79; Korsgren M, 1997, J EXP MED, V185, P885, DOI 10.1084/jem.185.5.885; KUBO S, 2003, J IMMUNOL, V17, P775; Lambert AL, 1999, TOXICOL APPL PHARM, V158, P269, DOI 10.1006/taap.1999.8709; Lambert AL, 2000, TOXICOL APPL PHARM, V165, P84, DOI 10.1006/taap.2000.8932; Li N, 2003, CLIN IMMUNOL, V109, P250, DOI 10.1016/j.clim.2003.08.006; Maejima K, 1997, J TOXICOL ENV HEALTH, V52, P231, DOI 10.1080/009841097159674; Mortimer KM, 2002, EUR RESPIR J, V19, P699, DOI 10.1183/09031936.02.00247102; Nightingale JA, 2000, AM J RESP CRIT CARE, V162, P161; Nilsen A, 1997, TOXICOLOGY, V124, P225, DOI 10.1016/S0300-483X(97)00150-9; Peters A, 1997, EUR RESPIR J, V10, P872; Peterson B, 1996, ANN ALLERG ASTHMA IM, V77, P263; Pope CA, 2004, CIRCULATION, V109, P71, DOI 10.1161/01.CIR.0000108927.80044.7F; POPE CA, 1995, AM J RESP CRIT CARE, V151, P669; Renwick LC, 2004, OCCUP ENVIRON MED, V61, P442, DOI 10.1136/oem.2003.008227; Samet JM, 2000, NEW ENGL J MED, V343, P1742, DOI 10.1056/NEJM200012143432401; Schappi GF, 1999, CLIN EXP ALLERGY, V29, P633; Schaumann F, 2004, AM J RESP CRIT CARE, V170, P898, DOI 10.1164/rccm.200403-423OC; Steerenberg PA, 2003, J TOXICOL ENV HEAL A, V66, P1421, DOI 10.1080/15287390390202054; Tumas DB, 2001, J ALLERGY CLIN IMMUN, V107, P1025, DOI 10.1067/mai.2001.115625; Van Rijt LS, 2001, MICROSC RES TECHNIQ, V53, P256, DOI 10.1002/jemt.1092; Whitekus MJ, 2002, J IMMUNOL, V168, P2560; Wilson MR, 2002, TOXICOL APPL PHARM, V184, P172, DOI 10.1006/taap.2002.9501; Zielinski H, 1999, AM J PHYSIOL-LUNG C, V277, pL719	50	90	92	0	9	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	NOV	2006	36	11					1469	1479		10.1111/j.1365-2222.2006.02586.x		11	Allergy; Immunology	Allergy; Immunology	101IK	WOS:000241734300016	17083358	
J	Fritsch, M; Uxa, S; Horak, F; Putschoegl, B; Dehlink, E; Szepfalusi, Z; Frischer, T				Fritsch, Maria; Uxa, Sabine; Horak, Friedrich, Jr.; Putschoegl, Bettina; Dehlink, Eleonora; Szepfalusi, Zsoit; Frischer, Thomas			Exhaled nitric oxide in the management of childhood asthma: A prospective 6-months study	PEDIATRIC PULMONOLOGY			English	Article						airway inflammation; childhood asthma; fractional exhaled nitric oxide; exhaled air; exacerbations; inhaled corticosteroids	DOSE-RESPONSE RELATIONSHIP; CHILDREN; HEALTHY; REPRODUCIBILITY; RECOMMENDATIONS; REDUCTION; THERAPY; ADULTS; AIR	Fractional exhaled nitric oxide (FeNO) is elevated in asthma and reflects eosinophilic airway inflammation. The aim of this prospective, randomized, single-blind study was to examine whether the inclusion of repeated FeNO measurements into asthma monitoring leads to an improvement in asthma outcome. Forty-seven children with mild to moderate asthma were allocated to a FeNO group (n = 22) and to a control group (n = 25). In the FeNO group therapy was based on symptoms, beta-agonist use, lung function, and FeNO whereas in the control group therapy was based on symptoms, beta-agonist use and lung function only Patients performed five visits in 6 weeks intervals. Frequency of respiratory symptoms, beta-agonist use, FEV1% predicted and the frequency of exacerbations were similar between groups. Patients in the FeNO group received higher doses of inhaled corticosteroids (ICS) (control group: median (interquartile range): 241 mu g (26-607 mu g); FeNo group: 316 mu g (200-500 mu g) and had significantly higher MEF,50% predicted (control group: median (interquartile range): 68.5% (55.8-83.1%); FeNO group: 83.2% (62.9%-98.3%). At a cut-off point of 22.9 ppb FeNO the best predictive value for exacerbations with a sensitivity of 80% and specificity of 60% was found. Significant relationships were observed between FeNO and dose of ICS (beta = 8.77; P < 0.002), beta-agonist use 2 weeks prior to a visit (beta = 0.11; P < 0.05), asthma symptoms (beta = 0.02; P < 0.0001), and bronchial hyperresponsiveness (beta = 0.04; P = 0.02). In conclusion, FeNO was related to important markers of asthma control. A therapy regimen aimed at lowering FeNO in children with asthma improved parameters of small airway function, but was not able to improve clinical markers of asthma control.	Univ Vienna, Childrens Hosp, Dept Gen Paediat, A-1090 Vienna, Austria	Frischer, T (reprint author), Univ Vienna, Childrens Hosp, Dept Gen Paediat, Waehringer Guertel 18-20, A-1090 Vienna, Austria.	thomas.frischer@meduniwien.ac.at		Fritsch, Maria/0000-0001-5304-673X			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; Bratton DL, 1999, PEDIATR PULM, V28, P402, DOI 10.1002/(SICI)1099-0496(199912)28:6<402::AID-PPUL3>3.0.CO;2-V; Buchvald F, 2005, J ALLERGY CLIN IMMUN, V115, P1130, DOI 10.1016/j.jaci.2005.03.020; Covar RA, 2003, J PEDIATR-US, V142, P469, DOI 10.1067/mpd.2003.187; Franklin PJ, 1999, AM J RESP CRIT CARE, V159, P69; Frischer T, 1999, WIEN KLIN WOCHENSCHR, V111, P900; Horak F, 2002, EUR RESPIR J, V19, P838, DOI 10.1183/09031936.02.00512001; Jones SL, 2001, AM J RESP CRIT CARE, V164, P738; Jones SL, 2002, EUR RESPIR J, V20, P601, DOI 10.1183/09031936.02.00285302; 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, P454; Leuppi JD, 2001, AM J RESP CRIT CARE, V163, P406; Milgrom H, 1996, J ALLERGY CLIN IMMUN, V98, P1051, DOI 10.1016/S0091-6749(96)80190-4; Pijnenburg MW, 2005, THORAX, V60, P215, DOI 10.1136/thx.2004.023374; PIJNENBURG MW, 2005, AM J RESP CRIT CARE, V173, P831; Pijnenburg MWH, 2005, CLIN EXP ALLERGY, V35, P920, DOI 10.1111/j.1365-2222.2005.02279.x; RIEDLER J, 1994, AM J RESP CRIT CARE, V150, P1632; Silkoff PE, 2001, CHEST, V119, P1322, DOI 10.1378/chest.119.5.1322; Silvestri M, 2001, THORAX, V56, P857, DOI 10.1136/thorax.56.11.857; Slutsky AS, 1999, AM J RESP CRIT CARE, V160, P2104; Smith AD, 2005, NEW ENGL J MED, V352, P2163, DOI 10.1056/NEJMoa043596; Sont JK, 1996, THORAX, V51, P496, DOI 10.1136/thx.51.5.496; WALLS AF, 1992, CLIN EXP ALLERGY, V22, P1, DOI 10.1111/j.1365-2222.1992.tb00106.x; Zacharasiewicz A, 2005, AM J RESP CRIT CARE, V171, P1077, DOI 10.1164/rccm.200409-1242OC; ZAPLETAL A, 1987, LUNG FUNCTION CHILDR, P174	27	90	94	0	1	WILEY-LISS	HOBOKEN	DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA	8755-6863			PEDIATR PULM	Pediatr. Pulmonol.	SEP	2006	41	9					855	862		10.1002/ppul.20455		8	Pediatrics; Respiratory System	Pediatrics; Respiratory System	077NC	WOS:000240035300008	16850457	
J	Hales, BJ; Martin, AC; Pearce, LJ; Laing, IA; Hayden, CM; Goldblatt, J; Le Souef, PN; Thomas, WR				Hales, Belinda J.; Martin, Andrew C.; Pearce, Leigh J.; Laing, Ingrid A.; Hayden, Catherine M.; Goldblatt, Jack; Le Souef, Peter N.; Thomas, Wayne R.			IgE and IgG anti-house dust mite specificities in allergic disease	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						house dust mite allergens; IgE; IgG(4); IgG(1); asthma	MODIFIED TH2 RESPONSE; DERMATOPHAGOIDES-PTERONYSSINUS; CHILDREN; ASTHMA; ANTIBODIES; EXTRACT; DER-P-2; BINDING; POPULATION; CHILDHOOD	Background: There are few studies that quantitatively compare IgE and IgG antibody binding to the major and minor house dust mite allergens. Objective: To measure the IgE and IgG antibody specificities produced by adults and children, including children admitted to an emergency department for asthma. Methods: Antibodies were measured by solid-phase microliter assays. Results: Children recruited from the emergency department had similar titers and patterns of IgE antibody binding compared with children without acute disease. Der p 1 and 2 bound 50 % to 65 % of the IgE antibody, and most of the remaining binding was to Der p 4, 5, and 7. Der p 3, 8, 10, and 20 induced low titers. The pattern was similar across a wide range of antibouse.dust mite titers. IgG(1) and IgG(4) antibodies predominantly bound the major and midrange allergens and were mainly found in children with allergy. Children recruited in the emergency department had lower titers. Conclusion: The same IgE antibody-binding pattern and predominant contribution of Der p 1 and 2 was found across a wide range of total IgE antibody titers and for children admitted to an emergency department. IgG, and IgG(4) antibodies bound to the more allergenic specificities and were largely found in children with allergy. The IgG antibody titers were lower in sera from children admitted to the emergency department for asthma exacerbations. Clinical implications: Der p 1 and 2 and possibly Der p 4, 5, and 7 provide a formulation suitable for immunotherapy and diagnosis. Low IgG antibodies were a feature of acute disease.	Univ Western Australia, Ctr Child Hlth Res, Telethon Inst Child Hlth Res, Div Mol Biotechnol, Subiaco, WA 6008, Australia; Univ Western Australia, Sch Paediat & Child Hlth, Nedlands, WA 6009, Australia	Hales, BJ (reprint author), Univ Western Australia, Ctr Child Hlth Res, Telethon Inst Child Hlth Res, Div Mol Biotechnol, 100 Roberts Rd, Subiaco, WA 6008, Australia.	belinda@ichr.uwa.edu.au	Hales, Belinda/C-3858-2013; Laing, Ingrid/I-7092-2013	Hales, Belinda/0000-0003-2193-3996; Laing, Ingrid/0000-0002-1641-9899			Arbes SJ, 2005, J ALLERGY CLIN IMMUN, V116, P377, DOI 10.1016/j.jaci.2005.05.017; CHAPMAN MD, 1978, CLIN EXP IMMUNOL, V34, P126; Erwin EA, 2005, J ALLERGY CLIN IMMUN, V115, P1029, DOI 10.1016/j.jaci.2004.12.1131; Hales BJ, 2004, INT ARCH ALLERGY IMM, V135, P101, DOI 10.1159/000080652; Heaton T, 2005, LANCET, V365, P142, DOI 10.1016/S0140-6736(05)17704-6; HEYMANN PW, 1989, J ALLERGY CLIN IMMUN, V83, P1055, DOI 10.1016/0091-6749(89)90447-8; O'Brien RM, 2000, CLIN EXP ALLERGY, V30, P333; Ong YE, 2005, J ALLERGY CLIN IMMUN, V116, P558, DOI 10.1016/j.jaci.2005.05.035; Peat JK, 1996, AM J RESP CRIT CARE, V153, P141; Pittner G, 2004, CLIN EXP ALLERGY, V34, P597, DOI 10.1111/j.1365-2222.2004.1930.x; 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; Satinover SM, 2005, J ALLERGY CLIN IMMUN, V115, P803, DOI 10.1016/j.jaci.2005.01.018; Schuurman J, 1997, CLIN EXP ALLERGY, V27, P1095, DOI 10.1111/j.1365-2222.1997.tb01262.x; Smart JM, 2002, CLIN EXP ALLERGY, V32, P796, DOI 10.1046/j.1365-2222.2002.01391.x; Smith AM, 1998, CLIN IMMUNOL IMMUNOP, V86, P102, DOI 10.1006/clin.1997.4454; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; Sunyer J, 2004, J ALLERGY CLIN IMMUN, V114, P1033, DOI 10.1016/j.jaci.2004.05.072; Thomas WR, 2002, INT ARCH ALLERGY IMM, V129, P1, DOI 10.1159/000065179; Trombone APF, 2002, CLIN EXP ALLERGY, V32, P1323, DOI 10.1046/j.1365-2745.2002.01455.x; Van Der Veen MJ, 2001, CLIN EXP ALLERGY, V31, P705, DOI 10.1046/j.1365-2222.2001.01120.x; VANDERHEIJDEN FL, 1995, CLIN EXP IMMUNOL, V99, P289; Weghofer M, 2005, CLIN EXP ALLERGY, V35, P1384, DOI 10.1111/j.1365-2222.2005.02345.x	23	90	97	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.	AUG	2006	118	2					361	367		10.1016/j.jaci.2006.04.001		7	Allergy; Immunology	Allergy; Immunology	075IH	WOS:000239877700010	16890759	
J	Bousquet, J; Anto, JM; Bachert, C; Bousquet, PJ; Colombo, P; Crameri, R; Daeron, M; Fokkens, W; Leynaert, B; Lahoz, C; Maurer, M; Passalacqua, G; Valenta, R; van Hage, M; van Ree, R				Bousquet, J; Anto, JM; Bachert, C; Bousquet, PJ; Colombo, P; Crameri, R; Daeron, M; Fokkens, W; Leynaert, B; Lahoz, C; Maurer, M; Passalacqua, G; Valenta, R; van Hage, M; van Ree, R			Factors responsible for differences between asymptomatic subjects and patients presenting an IgE sensitization to allergens. A GA(2)LEN project	ALLERGY			English	Review						allergy; asthma; basophil; IgE; IgG; rhinitis	FC-EPSILON-RI; REGULATORY T-CELLS; HOUSE-DUST MITE; GENERAL-POPULATION SAMPLE; STAPHYLOCOCCUS-AUREUS ENTEROTOXINS; HUMAN BASOPHIL RELEASABILITY; MOUNTAIN CEDAR POLLINOSIS; BIRCH POLLEN ALLERGEN; SKIN-TEST REACTIVITY; TOTAL SERUM IGE	The synthesis of allergen-specific IgE is required for the development of allergic diseases including allergic rhinitis and allergic asthma (patients), but many individuals with allergen-specific IgE do not develop symptoms (asymptomatic subjects). Differences may exist between asymptomatic subjects and patients. Whether the presence of allergen-specific IgE translates into clinical allergy most likely depends on a complex interplay of multiple factors. These include a family history of atopy, the levels of total serum IgE and, allergen-specific IgE or IgG, epitope-specificity of IgE and their degree of polyclonality (mono- vs polysensitized), as yet unidentified serum factors, the balance of T regulatory cells (Treg) and Th1/Th2 cells, the polymorphisms of the high affinity receptor for IgE (Fc epsilon RI) and other factors regulating the activation of Fc epsilon RI-bearing cells. Asymptomatic subjects may be more often monosensitized than patients who may be more often polysensitized. There are many unanswered important questions that need to be addressed in order to better understand how IgE sensitization translates into clinical allergy. The assessment of differences between the asymptomatic and symptomatic groups of subjects represent one of the scientific programs of Global Allergy and Asthma European Network funded by the European Union and the hypotheses underlying these differences are presented in this paper.	Univ Hosp Montpellier, INSERM, Serv Maladies Resp, U454, Montpellier, France; Inst Municipal Invest Med, Resp & Environm Hlth Res Unit, E-08003 Barcelona, Spain; State Univ Ghent Hosp, ENT Dept, B-9000 Ghent, Belgium; CNR, Ist Biomed & Immunol Mol, Palermo, Italy; Swiss Inst Allergy & Asthma Res, CH-7270 Davos, Switzerland; Inst Pasteur, Unite Allergol Mol & Cellulaire, Paris, France; Univ Amsterdam, Dept Otorhinolaryngol, Amsterdam, Netherlands; INSERM, U700, Paris, France; Univ Autonoma Madrid, Dept Immunol, Fdn Jimenez Diaz, E-28049 Madrid, Spain; Univ Med Berlin, Klin Dermatol Venerol & Allergol, Berlin, Germany; Dept Internal Med Padiglione Maragliano, Genoa, Italy; Med Univ Vienna, Ctr Physiol & Pathophysiol, Dept Pathophysiol, Div Immunopathol, Vienna, Austria; Karolinska Inst, Dept Med, Allergy & Clin Immunol Unit, Stockholm, Sweden; Karolinska Univ Hosp, Stockholm, Sweden; Univ Amsterdam, Acad Med Ctr, Dept Expt Immunol, NL-1105 AZ Amsterdam, Netherlands	Bousquet, J (reprint author), Univ Hosp Montpellier, INSERM, Serv Maladies Resp, U454, Montpellier, France.		Colombo, Paolo/G-2200-2013; van Hage, Marianne/A-9678-2017; Anto, J/H-2676-2014	van Hage, Marianne/0000-0003-3091-1596; Anto, J/0000-0002-4736-8529; Bousquet, Philippe Jean/0000-0002-0217-5483; Colombo, Paolo/0000-0002-0908-1359			Addo Yobo Emmanuel O. 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J	van der Deen, M; de Vries, EGE; Timens, W; Scheper, RJ; Timmer-Bosscha, H; Postma, DS				van der Deen, M; de Vries, EGE; Timens, W; Scheper, RJ; Timmer-Bosscha, H; Postma, DS			ATP-binding cassette (ABC) transporters in normal and pathological lung	RESPIRATORY RESEARCH			English	Review							MULTIDRUG-RESISTANCE PROTEIN; TRANSMEMBRANE CONDUCTANCE REGULATOR; P-GLYCOPROTEIN EXPRESSION; DENSITY-LIPOPROTEIN DEFICIENCY; BRONCHIAL EPITHELIAL-CELLS; ORGANIC ANION TRANSPORTER; CYSTIC-FIBROSIS PATIENTS; DEPENDENT EXPORT PUMP; NITRIC-OXIDE SYNTHASE; BLOOD-BRAIN-BARRIER	ATP-binding cassette ( ABC) transporters are a family of transmembrane proteins that can transport a wide variety of substrates across biological membranes in an energy-dependent manner. Many ABC transporters such as P-glycoprotein ( P-gp), multidrug resistance-associated protein 1 ( MRP1) and breast cancer resistance protein ( BCRP) are highly expressed in bronchial epithelium. This review aims to give new insights in the possible functions of ABC molecules in the lung in view of their expression in different cell types. Furthermore, their role in protection against noxious compounds, e. g. air pollutants and cigarette smoke components, will be discussed as well as the ( mal) function in normal and pathological lung. Several pulmonary drugs are substrates for ABC transporters and therefore, the delivery of these drugs to the site of action may be highly dependent on the presence and activity of many ABC transporters in several cell types. Three ABC transporters are known to play an important role in lung functioning. Mutations in the cystic fibrosis transmembrane conductance regulator ( CFTR) gene can cause cystic fibrosis, and mutations in ABCA1 and ABCA3 are responsible for respectively Tangier disease and fatal surfactant deficiency. The role of altered function of ABC transporters in highly prevalent pulmonary diseases such as asthma or chronic obstructive pulmonary disease ( COPD) have hardly been investigated so far. We especially focused on polymorphisms, knock-out mice models and in vitro results of pulmonary research. Insight in the function of ABC transporters in the lung may open new ways to facilitate treatment of lung diseases.	Dept Pulm Med, NL-9713 GZ Groningen, Netherlands; Univ Groningen, Univ Med Ctr Groningen, Dept Internal Med, NL-9713 GZ Groningen, Netherlands; Dept Pathol & Lab Med, NL-9713 GZ Groningen, Netherlands; Free Univ Amsterdam, Dept Pathol, NL-1081 HV Amsterdam, Netherlands	Postma, DS (reprint author), Dept Pulm Med, Hanzepl 1, NL-9713 GZ Groningen, Netherlands.	m.van.der.deen@int.umcg.nl; e.g.e.de.vries@int.umcg.nl; w.timens@path.umcg.nl; rj.scheper@vumc.nl; h.timmer-bosscha@int.umcg.nl; d.s.postma@int.umcg.nl	Timens, Wim/K-5570-2013	Timens, Wim/0000-0002-4146-6363			Agassandian M, 2004, AM J RESP CELL MOL, V31, P227, DOI 10.1165/rcmb.2004-0038OC; Bain LJ, 2003, XENOBIOTICA, V33, P1173, DOI 10.1080/00498250310001609138; Bandi N, 2002, EUR J PHARMACOL, V437, P9, DOI 10.1016/S0014-2999(02)01267-0; Baudouin-Legros M, 2003, AM J PHYSIOL-CELL PH, V284, pC620, DOI 10.1152/ajpcell.00457.2002; Bebok Z, 2002, J BIOL CHEM, V277, P43041, DOI 10.1074/jbc.M203154200; Beck K, 2003, J HISTOCHEM CYTOCHEM, V51, P887; 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Res.	JUN 20	2005	6								59	10.1186/1465-9921-6-59		16	Respiratory System	Respiratory System	960AW	WOS:000231563600001	15967026	
J	Halvorsen, T; Skadberg, BT; Eide, GE; Roksund, OD; Carlsen, KH; Bakke, P				Halvorsen, T; Skadberg, BT; Eide, GE; Roksund, OD; Carlsen, KH; Bakke, P			Pulmonary outcome in adolescents of extreme preterm birth: a regional cohort study	ACTA PAEDIATRICA			English	Article						infant; premature; bronchopulmonary dysplasia; lung diseases; obstructive; cohort studies	LUNG-FUNCTION; BRONCHOPULMONARY DYSPLASIA; RESPIRATORY HEALTH; WEIGHT; DISEASE; RESPONSIVENESS; SEQUELAE; CHILDREN; AGE; METHACHOLINE	Aims: The pulmonary outcome of extreme prematurity remains to be established in adults. We determined respiratory health and lung function status in a population-based, complete cohort of young preterms approaching adulthood. Methods. Forty-six preterms with gestational age less than or equal to28 wk or birthweight less than or equal to1000 g, born between 1982 and 1985, were compared to the temporally nearest term-born subject of equal gender. Spirometry, plethysmography, reversibility test to salbutamol and methacholine bronchial provocation test were performed. Neonatal data were obtained from hospital records and current symptoms from validated questionnaires. Results: When entering the study at a mean age of 17.7 (SD: 1.2) y, a doctor's diagnosis of asthma and use of asthma inhalers were significantly more prevalent among preterms than controls (one asthmatic control compared to nine preterms, all but one using asthma inhalers). Peak expiratory flow (PEF) and forced expiratory volume in 1 s (FEV1) were decreased and the discrepancies relative to controls increased parallel to increased severity of neonatal lung disease. Parameters of increased neonatal oxygen exposure significantly predicted FEV1. Adjusted for height, gender and age, FEV1 was reduced by a mean of 580 ml/s in subjects with a history of bronchopulmonary dysplasia. Fifty-six percent of preterms had a positive methacholine provocation test compared to 26% of controls. Conclusion: A substantially decreased FEV1, increased bronchial hyperresponsiveness and a number of established risk factors for steeper age-related decline in lung function were observed in preterms. A potential for early onset chronic obstructive pulmonary disease is present in subsets of this group.	Haukeland Univ Hosp, Dept Paediat, NO-5021 Bergen, Norway; Univ Bergen, Inst Clin & Mol Med, N-5020 Bergen, Norway; Haukeland Univ Hosp, Clin Res Ctr, NO-5021 Bergen, Norway; Univ Bergen, Dept Publ Hlth & Primary Hlth Care, Sect Epidemiol & Med Stat, N-5020 Bergen, Norway; Voksentoppen Natl Hosp, Oslo, Norway; Res Inst Asthma Allergy & Chron Lung Dis Children, Oslo, Norway; Haukeland Univ Hosp, Dept Thorac Med, NO-5021 Bergen, Norway; Univ Bergen, Inst Med, N-5020 Bergen, Norway	Halvorsen, T (reprint author), Haukeland Univ Hosp, Dept Paediat, NO-5021 Bergen, Norway.	thornas.halvorsen@helse-bergen.no	Halvorsen, Thomas/P-6741-2015	Halvorsen, Thomas/0000-0003-1471-0225			Anand D, 2003, ARCH DIS CHILD, V88, P135, DOI 10.1136/adc.88.2.135; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; CUNNINGHAM CK, 1991, PEDIATRICS, V88, P527; DEKLEINE MJK, 1990, THORAX, V45, P941, DOI 10.1136/thx.45.12.941; Doyle LW, 2001, ARCH DIS CHILD, V84, P40, DOI 10.1136/adc.84.1.40; Eber E, 2001, THORAX, V56, P317, DOI 10.1136/thorax.56.4.317; [Anonymous], 1993, ALLERGY, V48, P48; Godfrey S, 1999, EUR RESPIR J, V14, P659, DOI 10.1034/j.1399-3003.1999.14c28.x; Gross SJ, 1998, J PEDIATR-US, V133, P188, DOI 10.1016/S0022-3476(98)70219-7; Jacob SV, 1998, J PEDIATR-US, V133, P193, DOI 10.1016/S0022-3476(98)70220-3; Jobe Alan H., 2001, American Journal of Respiratory and Critical Care Medicine, V163, P1723; KNUDSON RJ, 1983, AM REV RESPIR DIS, V127, P725; McLeod A, 1996, ARCH DIS CHILD, V74, P188; *MED BIRTH REG, 1997, BIRTHS NORW 30 YEARS; NIEMINEN MM, 1988, THORAX, V43, P896, DOI 10.1136/thx.43.11.896; NORTHWAY WH, 1990, NEW ENGL J MED, V323, P1793, DOI 10.1056/NEJM199012273232603; NTP Technical Report, 2002, NIH PUBLICATION; OCONNOR G, 1987, AM REV RESPIR DIS, V136, P1412; Palta M, 2001, AM J EPIDEMIOL, V154, P521, DOI 10.1093/aje/154.6.521; PEAT JK, 1987, EUR J RESPIR DIS, V70, P171; Pelkonen AS, 1997, AM J RESP CRIT CARE, V156, P1178; Pelkonen AS, 2001, RESP MED, V95, P565, DOI 10.1053/rmed.2001.1104; Quanjer PH, 1993, EUR RESPIR J S, V16, P5, DOI 10.1183/09041950.005s1693; QUANJER PH, 1995, PEDIATR PULM, V19, P135, DOI 10.1002/ppul.1950190209; Rijcken B, 1996, AM J RESP CRIT CARE, V154, pS246; SHAHEEN SO, 1995, AM J RESP CRIT CARE, V151, P1649; Skjaerven R, 2000, ACTA OBSTET GYN SCAN, V79, P440, DOI 10.1034/j.1600-0412.2000.079006440.x; Stevenson DK, 1998, AM J OBSTET GYNECOL, V179, P1632, DOI 10.1016/S0002-9378(98)70037-7; STEWART AL, 1981, LANCET, V1, P1038; Weiss ST, 2000, AM J RESP CRIT CARE, V162, pS134; Weiss ST, 1996, AM J RESP CRIT CARE, V154, pS208; YAN K, 1983, THORAX, V38, P760, DOI 10.1136/thx.38.10.760; YUDKIN PL, 1987, EARLY HUM DEV, V15, P45, DOI 10.1016/0378-3782(87)90099-5; 2001, SPSS WINDOWS RELEASE, P136	34	90	94	0	5	TAYLOR & FRANCIS AS	OSLO	CORT ADELERSGT 17, PO BOX 2562, SOLLI, 0202 OSLO, NORWAY	0803-5253			ACTA PAEDIATR	Acta Paediatr.	OCT	2004	93	10					1294	1300		10.1080/08035250410028101		7	Pediatrics	Pediatrics	859GT	WOS:000224252100006	15499947	
J	Kramer, U; Lemmen, CH; Behrendt, H; Link, E; Schafer, T; Gostomzyk, J; Scherer, G; Ring, J				Kramer, U; Lemmen, CH; Behrendt, H; Link, E; Schafer, T; Gostomzyk, J; Scherer, G; Ring, J			The effect of environmental tobacco smoke on eczema and allergic sensitization in children	BRITISH JOURNAL OF DERMATOLOGY			English	Article						eczema; parental atopy; predisposition; respiratory allergies; sensitization; tobacco smoke	PARENTAL SMOKING; PASSIVE-SMOKING; EARLY-CHILDHOOD; RESPIRATORY HEALTH; ATOPIC-DERMATITIS; URINARY COTININE; RISK-FACTORS; EXPOSURE; ASSOCIATION; ASTHMA	Background The negative impact of environmental tobacco smoke (ETS) on airway diseases in children is well known. Whether there is an effect on atopic eczema is not clear. Objectives To determine the impact of ETS on atopic eczema, allergic sensitization and allergic airway diseases in 1669 school beginners. Methods The prevalence of atopy-related health outcomes was assessed by questionnaire, dermatological examination, skin prick testing and specific immunoglobulin E measurement. Exposure assessments were based on measurement of cotinine [expressed as cotinine to creatine ratio (CCR)] in spot urine samples (n = 1220) together with questionnaire and interview data on smoking behaviour of the parents. Results In the total study group, prevalence of atopic eczema diagnosed on examination was significantly associated with urinary CCR values. The odds ratio (OR) and 95% confidence interval (CI), calculated for an increase of 100 ng mg(-1) CCR was 1.97 (95% CI 1.23-3.16). The prevalence of skin manifestations according to questionnaire data as well as a history of asthma, wheezing, and hay fever were positively although not significantly associated with ETS exposure. When genetically predisposed children (defined by the presence of parental atopy) were compared with children whose parents had no atopy, the ORs of allergic outcome variables were generally higher in the first group. In the group of predisposed children, significant associations with urinary CCR were found for allergic sensitization against house dust mites as measured by skin prick test (OR 3.10, 95% CI 1.63-5.90). Conclusions Children are at a higher risk of developing an atopic eczema when exposed to ETS and genetically predisposed children are at higher risk of developing a sensitization against house dust mites.	Univ Dusseldorf, Inst Umweltmed Forsch, D-40225 Dusseldorf, Germany; Tech Univ Munich, Natl Res Ctr Environm & Hlth GSF, Div Environm Dermatol & Allergol, D-8000 Munich, Germany; Med Univ Lubeck, Dept Social Med, D-23538 Lubeck, Germany; Dept Publ Hlth, Augsburg, Germany; Analyt Biol Res Lab ABF, Munich, Germany; Tech Univ Munich, Clin Dermatol & Allergol, D-8000 Munich, Germany	Kramer, U (reprint author), Univ Dusseldorf, Inst Umweltmed Forsch, Hennekamp 50, D-40225 Dusseldorf, Germany.	kraemeru@uni-duesseldorf.de					Agabiti N, 1999, EPIDEMIOLOGY, V10, P692, DOI 10.1097/00001648-199911000-00008; ARSHAD SH, 1992, J ALLERGY CLIN IMMUN, V90, P235, DOI 10.1016/0091-6749(92)90077-F; BAKOULA CG, 1995, LANCET, V346, P280, DOI 10.1016/S0140-6736(95)92167-2; BRABACK L, 1995, ARCH DIS CHILD, V72, P487; CHILMONCZYK BA, 1993, NEW ENGL J MED, V328, P1665, DOI 10.1056/NEJM199306103282303; Cook DG, 1999, THORAX, V54, P357; DOMINO EF, 1995, CLIN PHARMACOL THER, V57, P479, DOI 10.1016/0009-9236(95)90219-8; HALEY NJ, 1983, AM J PUBLIC HEALTH, V73, P1204, DOI 10.2105/AJPH.73.10.1204; HALKEN S, 1995, ALLERGY, V50, P97; Jaakkola JJK, 2001, ENVIRON HEALTH PERSP, V109, P579, DOI 10.2307/3455031; JAAKKOLA N, 1994, SCAND J SOC MED, V22, P107; Jarvis D, 1999, J ALLERGY CLIN IMMUN, V104, P934, DOI 10.1016/S0091-6749(99)70071-0; Kabesch M., 2000, ACI INT, V12, P146, DOI 10.1027/0838-1925.12.4.146; Kulig M, 1999, HUM EXP TOXICOL, V18, P241, DOI 10.1191/096032799678839987; Li JS, 1999, PEDIATR PULM, V27, P5, DOI 10.1002/(SICI)1099-0496(199901)27:1<5::AID-PPUL3>3.0.CO;2-5; Lindfors A, 1999, J ALLERGY CLIN IMMUN, V104, P755; Nafstad P, 1997, EPIDEMIOLOGY, V8, P293, DOI 10.1097/00001648-199705000-00011; REESE AC, 1992, AM REV RESPIR DIS, V146, P66; RYLANDER E, 1995, EPIDEMIOLOGY, V6, P289, DOI 10.1097/00001648-199505000-00017; SAMET MJ, 2000, INDOOR AIR QUALITY H; Schafer T, 1997, J AM ACAD DERMATOL, V36, P550, DOI 10.1016/S0190-9622(97)70242-1; Scherer G, 1999, HUM EXP TOXICOL, V18, P297, DOI 10.1191/096032799678840075; SCHERER G, 1988, KLIN WOCHENSCHR, V66, P5; Seymour BWP, 1997, J IMMUNOL, V159, P6169; STALDER JF, 1993, DERMATOLOGY, V186, P23; Strachan DP, 1998, THORAX, V53, P117; Strachan DP, 1997, THORAX, V52, P905; Strachan DP, 1998, THORAX, V53, P204; U.S. Environmental Protection Agency, 1992, EPA600690006F; Wardlaw AJ, 1995, CLIN EXP ALLERGY, V25, P56, DOI 10.1111/j.1365-2222.1995.tb00045.x; Weaver VM, 1996, CANCER EPIDEM BIOMAR, V5, P135; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P383, DOI 10.1111/j.1365-2133.1994.tb08530.x; WJST M, 1994, ALLERGY, V49, P766, DOI 10.1111/j.1398-9995.1994.tb02100.x	33	90	92	0	2	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0007-0963			BRIT J DERMATOL	Br. J. Dermatol.	JAN	2004	150	1					111	118		10.1111/j.1365-2133.2004.05710.x		8	Dermatology	Dermatology	766YA	WOS:000188410300012	14746624	
J	Bryld, LE; Hindsberger, C; Kyvik, KO; Agner, T; Menne, T				Bryld, LE; Hindsberger, C; Kyvik, KO; Agner, T; Menne, T			Risk factors influencing the development of hand eczema in a population-based twin sample	BRITISH JOURNAL OF DERMATOLOGY			English	Article						atopy; contact allergy; hand eczema; twins; wet work	CONTACT-DERMATITIS; ATOPIC-DERMATITIS; NICKEL ALLERGY; SENSITIZATION; ASSOCIATION; OCCUPATION; WORKERS	Background A population-based twin study has recently shown that genetic factors are of significance for hand eczema. Objectives To characterize further a sample of this twin material with regard to contact allergy, atopic dermatitis and wet work. Methods In total, 1076 individual twins were examined clinically and patch tested. The diagnosis of atopic dermatitis was based on the U.K. Working Party criteria. The decision concerning wet work was based on the individual job description, taking into account the later introduced definition of at least 2 h of water exposure daily. The data were analysed by a newly developed statistical method which makes it possible to analyse the individual risk factor and at the same time discriminate between genetic and environmental factors. Results The statistical analysis confirmed atopic dermatitis as an important risk factor for hand eczema. Contact allergy was also confirmed as a significant risk factor for hand eczema, and the risk was related to strength (+ to + + +) of contact allergy. The results indicated that the high frequency of hand eczema in women in comparison with men was caused by environmental and not genetic factors. Aggregation of hand eczema within twin pairs was only to a minor degree explained by atopic dermatitis and nickel allergy (or other contact allergies). Conclusions We suggest that a hitherto unrecognized genetic risk factor for hand eczema independent of atopic dermatitis and contact allergy is probably of importance for the development of irritant contact dermatitis on the hands.	Copenhagen Univ Hosp, Dept Dermatol, DK-2900 Hellerup, Denmark; Univ Copenhagen, Dept Biostat, DK-1168 Copenhagen, Denmark; Univ So Denmark, Inst Publ Hlth, Danish Twin Registry, DK-5000 Odense, Denmark	Agner, T (reprint author), Copenhagen Univ Hosp, Dept Dermatol, DK-2900 Hellerup, Denmark.			Kyvik, Kirsten Ohm/0000-0003-2981-0245			Agner T, 1992, Acta Derm Venereol Suppl (Stockh), V173, P1; Andersen KE, 2001, TOXICOL APPL PHARM, V170, P166, DOI 10.1006/taap.2000.9095; Berndt U, 1999, BRIT J DERMATOL, V140, P922, DOI 10.1046/j.1365-2133.1999.02827.x; Betensky RA, 2001, GENET EPIDEMIOL, V20, P228; Bryld LE, 2000, BRIT J DERMATOL, V142, P298, DOI 10.1046/j.1365-2133.2000.03301.x; Buckley DA, 2000, CONTACT DERMATITIS, V43, P304; CHRISTENSEN OB, 1982, CONTACT DERMATITIS, V8, P7, DOI 10.1111/j.1600-0536.1982.tb04127.x; COENRAADS PJ, 1983, CLIN EXP DERMATOL, V8, P495, DOI 10.1111/j.1365-2230.1983.tb01816.x; Coenraads PJ, 1998, INT ARCH OCC ENV HEA, V71, P7, DOI 10.1007/s004200050243; Diepgen TL, 1999, INT ARCH OCC ENV HEA, V72, P496, DOI 10.1007/s004200050407; Hindsberger C, 2003, GENET EPIDEMIOL, V25, P225, DOI 10.1002/gepi.10253; LAMMINTAUSTA K, 1981, CONTACT DERMATITIS, V7, P301, DOI 10.1111/j.1600-0536.1981.tb04085.x; MEDING B, 1990, CONTACT DERMATITIS, V23, P154, DOI 10.1111/j.1600-0536.1990.tb04776.x; MEDLING B, 1990, CONTACT DERMATITIS, V23, P6; Menne T, 1979, Derm Beruf Umwelt, V27, P129; MENNE T, 1982, ACTA DERM-VENEREOL, V62, P35; MENNE T, 1997, CONTACT DERMATITIS, V24, P375; Mortz CG, 2002, ACTA DERM-VENEREOL, V82, P359, DOI 10.1080/000155502320624096; NIELSEN MH, 2002, CONTACT DERMATITIS, V46, P71; Nielsen NH, 2001, ACTA DERM-VENEREOL, V81, P31, DOI 10.1080/000155501750208155; NILSSON E, 1985, CONTACT DERMATITIS, V13, P216, DOI 10.1111/j.1600-0536.1985.tb02553.x; RYCROFT RJG, 1981, THESIS U CAMBRIDGE U; Rystedt I, 1985, Acta Derm Venereol Suppl (Stockh), V117, P1; Skytthe A, 2002, TWIN RES, V5, P352; Svensson A, 2002, BRIT J DERMATOL, V147, P281, DOI 10.1046/j.1365-2133.2002.04799.x; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P383, DOI 10.1111/j.1365-2133.1994.tb08530.x; Willis CM, 2002, CONTACT DERMATITIS, V47, P267, DOI 10.1034/j.1600-0536.2002.470503.x	27	90	91	0	4	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0007-0963			BRIT J DERMATOL	Br. J. Dermatol.	DEC	2003	149	6					1214	1220		10.1111/j.1365-2133.2003.05678.x		7	Dermatology	Dermatology	752HE	WOS:000187154400014	14674899	
J	Lane, SE; Watts, RA; Bentham, G; Innes, NJ; Scott, DGI				Lane, SE; Watts, RA; Bentham, G; Innes, NJ; Scott, DGI			Are environmental factors important in primary systemic vasculitis? A case-control study	ARTHRITIS AND RHEUMATISM			English	Article							CHURG-STRAUSS-SYNDROME; RHEUMATOLOGY 1990 CRITERIA; WEGENER GRANULOMATOSIS; OCCUPATIONAL EXPOSURE; HYDROCARBON EXPOSURE; SILICA EXPOSURE; UNITED-KINGDOM; DISEASE; GLOMERULONEPHRITIS; ANTIBODIES	Objective. To investigate the association between primary systemic vasculitis (PSV) and environmental risk factors. Methods. Seventy-five PSV cases and 273 controls (220 nonvasculitis, 19 secondary vasculitis and 34 asthma controls) were interviewed using a structured questionnaire. Factors investigated were social class, occupational and residential history, smoking, pets, allergies, vaccinations, medications, hepatitis, tuberculosis, and farm exposure in the year before symptom onset (index year). The Standard Occupational Classification 2000 and job-exposure matrices were used to assess occupational silica, solvent, and metal exposure. Stepwise multiple logistic regression was used to calculate the odds ratio (OR) and 95% confidence interval (95% CI) adjusted for potential confounders. Total PSV, subgroups (47 Wegener's granulomatosis [WG], 12 microscopic polyangiitis, 16 Churg-Strauss syndrome [CSS]), and antineutrophil cytoplasmic antibody (ANCA)-positive cases were compared with control groups. Results. Farming in the index year was significantly associated with PSV (OR 2.3 [95% CI 1.2-4.6]), with WG (2.7 [1.2-5.8]), with MPA (6.3 [1.9-21.6]), and with perinuclear ANCA (pANCA) (4.3 [1.5-12.7]). Farming during working lifetime was associated with PSV (2.2 [1.2-3.81) and with WG (2.7 [1.3-5.7]). Significant associations were found for high occupational silica exposure in the index year (with PSV 3.0 [1.0-8.4], with CSS 5.6 [1.3-23.5], and with ANCA 4.9 [1.3-18.6]), high occupational solvent exposure in the index year (with PSV 3.4 [0.9-12.5], with WG 4.8 [1.2-19.8], and with classic ANCA [cANCA] 3.9 [1.6-9.5]), high occupational solvent exposure during working lifetime (with PSV 2.7 [1.1-6.6], with WG 3.4 [1.3-8.9], and with cANCA 3.3 [1.0-10.8]), drug allergy (with PSV 3.6 [1.8-7.0], with WG 4.0 [1.8-8.7], and with cANCA 4.7 [1.9-11.7]), and allergy overall (with PSV 2.2 [1.2-3.9], with WG 2. 7 [1.4-5.7]). No other significant associations were found. Conclusion. A significant association between farming and PSV has been identified for the first time. Results also support previously reported associations with silica, solvents, and allergy.	Norfolk & Norwich Univ Hosp, Norwich, Norfolk, England; Ipswich Hosp, NHS Trust, Ipswich, Suffolk, England; Univ E Anglia, Norwich NR4 7TJ, Norfolk, England	Lane, SE (reprint author), Addenbrookes Hosp, Dept Rheumatol, Hills Rd,POB 204, Cambridge CB2 2QQ, England.						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A. F. J., 2000, Clinical and Experimental Immunology, V120, P60; VOZNESENSKII NK, 1995, GIG SANIT, V6, P20; Watts R. A., 1998, Clinical and Experimental Immunology, V112, P30; Watts RA, 2000, ARTHRITIS RHEUM, V43, P414, DOI 10.1002/1529-0131(200002)43:2<414::AID-ANR23>3.0.CO;2-0; Wichmann I, 1996, ANN RHEUM DIS, V55, P205, DOI 10.1136/ard.55.3.205; WITTE KW, 1982, PHARMACOTHERAPY, V2, P54; Yashiro M, 2000, AM J KIDNEY DIS, V35, P889, DOI 10.1016/S0272-6386(00)70260-5	40	90	94	1	2	WILEY-LISS	NEW YORK	DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA	0004-3591			ARTHRITIS RHEUM	Arthritis Rheum.	MAR	2003	48	3					814	823		10.1002/art.10830		10	Rheumatology	Rheumatology	653LY	WOS:000181438800031	12632437	
J	Liu, AH; Murphy, JR				Liu, AH; Murphy, JR			Hygiene hypothesis: Fact or fiction?	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						hygiene; allergy; atopy; asthma; autoimmunity; childhood; endotoxin; epidemiology type 1diabetes; celiac disease; inflammatory bowel disease; rheumatoid arthritis; microbiology	HOUSE-DUST ENDOTOXIN; DAY-CARE ATTENDANCE; ATOPIC DISEASE; CHILDHOOD ASTHMA; UNITED-STATES; SCHOOL-AGE; EARLY-LIFE; EXPOSURE; CHILDREN; RISK	The hygiene hypothesis of asthma and allergy has recently received a swell of popularity and published supporting evidence, and has been extended to autoimmune conditions of childhood. Broadly stated, naturally occurring infections and microbial exposures might essentially immunize against the development of asthma and allergic and autoimmune diseases. If true, then reductions in nature's immunotherapy over the past century might be a major factor in the global increase of these conditions (eg, the higher prevalence of asthma and allergies in urban metropolitan areas compared with rural and farm communities) and might lead to new therapies for these conditions. Although such a unifying hypothesis has great appeal, currently it is only speculation about what might be at the end of the investigative road. How close are the current studies to establishing a causal relationship between microbial exposures and a reduction in allergic, asthmatic, and autoimmune disease prevalence? A systematic epidemiologic appraisal of the current hygiene hypothesis evidence can provide a critical analysis of what is currently known and an investigative blueprint for future studies that can ultimately prove causation and improve recommendations, interventions, and therapies. (J Allergy Clin Immunol 2003;111:471-8.).	Natl Jewish Med & Res Ctr, Div Pediat Allergy & Immunol, Denver, CO 80206 USA; Univ Colorado, Ctr Hlth Sci, Dept Pediat, Boulder, CO 80309 USA; Natl Jewish Med & Res Ctr, Div Biostat, Denver, CO 80206 USA; Univ Colorado, Ctr Hlth Sci, Dept Prevent Med & Biometr, Boulder, CO 80309 USA	Liu, AH (reprint author), Natl Jewish Med & Res Ctr, Div Pediat Allergy & Immunol, 1400 Jackson St K1023, Denver, CO 80206 USA.				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Allergy Clin. Immunol.	MAR	2003	111	3					471	478		10.1067/mai.2003.172		8	Allergy; Immunology	Allergy; Immunology	656YW	WOS:000181639500005	12642824	
J	Sengler, C; Haider, A; Sommerfeld, C; Lau, S; Baldini, M; Martinez, F; Wahn, U; Nickel, R				Sengler, C; Haider, A; Sommerfeld, C; Lau, S; Baldini, M; Martinez, F; Wahn, U; Nickel, R		German Multicenter Allergy Study c	Evaluation of the CD14 C-159 T polymorphism in the German Multicenter Allergy Study cohort	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						atopy; CD14; genetics; IgE	ENDOTOXIN; EXPOSURE; ASTHMA; ATOPY; GENE	Background Multiple genetic studies have shown linkage of atopy-related phenotypes to chromosome 5q31. In this region several candidate genes for atopy are localized such as the Th2 cytokines IL-4, IL-5 and IL-13, but also CD14, a receptor for LPS. Recently, a functional CD14 promoter polymorphism was related to total and specific IgE responsiveness. Objective The aim of our study was to evaluate the role of this single nucleotide polymorphism (SNP) in a large German birth cohort. Methods Atopy-related phenotypes were longitudinally carefully evaluated in over 800 children from birth to the age of 10 years. Yearly visits included standardized interviews, physical examinations and determination of total and specific IgE antibodies. Pulmonary function tests and histamine provocations were performed at the age of seven. Eight-hundred and seventy-two children of the Multicenter Allergy Study (MAS) cohort were genotyped using melting curve and restriction digest analyses. Results CD14-159 allele frequencies were consistent with previous reports, however, no association of the SNP with asthma, atopic dermatitis, allergic rhinitis, total or specific IgE levels could be observed. Conclusion The CD14-159 SNP might not play a major role in the development of atopy in German children.	Humboldt Univ, Charite, Dept Pediat Pneumol & Immunol, D-13353 Berlin, Germany; Univ Arizona, Dept Pediat, Tucson, AZ 85721 USA	Nickel, R (reprint author), Humboldt Univ, Charite, Dept Pediat Pneumol & Immunol, Augustenburger Pl 1, D-13353 Berlin, Germany.						Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Bergmann RL, 1998, CLIN EXP ALLERGY, V28, P965; Illi S, 2001, BRIT MED J, V322, P390, DOI 10.1136/bmj.322.7283.390; Koppelman GH, 2001, AM J RESP CRIT CARE, V163, P965; Kulig M, 2000, J ALLERGY CLIN IMMUN, V106, P832, DOI 10.1067/mai.2000.110098; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; LeVan TD, 2001, J IMMUNOL, V167, P5838; Nickel R, 1997, GENOMICS, V46, P159, DOI 10.1006/geno.1997.5013; Sengler Claudia, 2002, Respir Res, V3, P7, DOI 10.1186/rr179; ULEVITCH RJ, 1995, ANNU REV IMMUNOL, V13, P437, DOI 10.1146/annurev.iy.13.040195.002253; Vercelli D, 2001, INT ARCH ALLERGY IMM, V124, P20, DOI 10.1159/000053658; Verhasselt V, 1997, J IMMUNOL, V158, P2919; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230	13	90	90	0	3	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	FEB	2003	33	2					166	169		10.1046/j.1365-2222.2003.01549.x		4	Allergy; Immunology	Allergy; Immunology	644PN	WOS:000180927400005	12580907	
J	Redd, SC				Redd, SC			Asthma in the United States: Burden and current theories	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; epidemiology; hygiene; incidence; indoor environment; obesity	BODY-MASS INDEX; FAMILY-SIZE; WEIGHT; CHILDHOOD; ADULTS; RISK	Asthma has emerged as a major public health problem in the United States over the past 20 years. Currently, nearly 15 million Americans have asthma, including almost 5 million children. The number of asthma cases has more than doubled since 1980. Approximately 5,500 persons die from asthma each year, and rates have increased over the past 20 years. Rates of death, hospitalization, and emergency department visits are 2-3 times higher among African Americans than among white Americans. The costs of asthma have also increased to $12.7 billion in 1998. Both lifestyle and environmental hypotheses have been invoked to explain the increase in asthma prevalence. Several studies have examined the relationship of obesity and asthma and found associations suggesting that obesity predisposes to the development of asthma. Some studies have found that day care attendance and having older siblings protect against the development of asthma. This observation has led investigators to hypothesize that increased exposure to microbial agents might protect against asthma (the hygiene hypothesis). Environmental exposures found to predispose to asthma include house dust mite allergen and environmental tobacco smoke. Although current knowledge does not permit definitive conclusions about the causes of asthma onset, better adherence to current recommendations for medical therapy and environmental management of asthma would reduce the burden of this disease.	Ctr Dis Control & Prevent, Natl Ctr Environm Hlth, Air Pollut & Resp Hlth Branch, Atlanta, GA 30341 USA	Redd, SC (reprint author), CDC, 6 Execut Pk Dr,Bldg 6,Room 1019, Atlanta, GA 30329 USA.						Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; Bernstein DI, 1997, JAMA-J AM MED ASSOC, V278, P1907, DOI 10.1001/jama.278.22.1907; Bodner C, 1998, THORAX, V53, P28; Busse WW, 2001, NEW ENGL J MED, V344, P350; Camargo CA, 1999, ARCH INTERN MED, V159, P2582, DOI 10.1001/archinte.159.21.2582; *CDCP, 2001, MMWR-MORBID MORTAL W, V50, P682; CHEN Y, 1993, THORAX, V48, P375, DOI 10.1136/thx.48.4.375; Custovic A, 2001, LANCET, V358, P188, DOI 10.1016/S0140-6736(01)05406-X; Hartert TV, 1996, AM J MED, V100, P386, DOI 10.1016/S0002-9343(97)89513-7; HIDE DW, 1994, J ALLERGY CLIN IMMUN, V93, P842, DOI 10.1016/0091-6749(94)90375-1; Homa DM, 2000, AM J RESP CRIT CARE, V161, P504; IOM (Committee on the Assessment of Asthma and Indoor Air of the Institute of Medicine), 2000, CLEAR AIR ASTHM IND; Jatulis DE, 1998, ANN ALLERG ASTHMA IM, V81, P82; Linn W S, 1999, Curr Opin Pulm Med, V5, P21, DOI 10.1097/00063198-199901000-00004; Mannino DM, 1998, MMWR-MORBID MORTAL W, V47, P1; McConnell R, 2002, LANCET, V359, P386, DOI 10.1016/S0140-6736(02)07597-9; Mokdad AH, 1999, JAMA-J AM MED ASSOC, V282, P1519, DOI 10.1001/jama.282.16.1519; National Asthma Education Prevention Program (NAEPP), 1997, NIH PUBL; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; PLATTSMILLS TA, 2001, AM J RESP CRIT CARE, V164, P1106; Rona RJ, 1997, J ALLERGY CLIN IMMUN, V99, P454, DOI 10.1016/S0091-6749(97)70070-8; Salvi SS, 2001, AM J RESP CRIT CARE, V164, P1343; Shaheen SO, 1999, THORAX, V54, P396; Tolbert PE, 2000, AM J EPIDEMIOL, V151, P798; *US EPA NAT AIR QU, 2001, 454R01004 EPA NAT AI; Weiss KB, 2000, J ALLERGY CLIN IMMUN, V106, P493; WEISS KB, 1992, NEW ENGL J MED, V326, P862, DOI 10.1056/NEJM199203263261304; YUNGINGER JW, 1992, AM REV RESPIR DIS, V146, P888	28	90	92	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.	AUG	2002	110			4			557	560				4	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	586ER	WOS:000177572100008	12194886	
J	De Meer, G; Heederik, D; Postma, DS				De Meer, G; Heederik, D; Postma, DS			Bronchial responsiveness to adenosine 5 '-monophosphate (AMP) and methacholine differ in their relationship with airway allergy and baseline FEV	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						adenosine; bronchial hyperresponsiveness; methacholine; airway allergy	NITRIC-OXIDE LEVELS; ASTHMA; HYPERRESPONSIVENESS; INFLAMMATION; RHINITIS; MARKERS; NONASTHMATICS; EOSINOPHILS; PREVALENCE; POPULATION	Bronchial hyperresponsiveness (BHR) and inflammation are central hallmarks of asthma. Studies in patients with asthma suggest that BHR to adenosine 5'-monophosphate (AMP) is a better marker of bronchial inflammation than BHR to methacholine. The association between markers of airway inflammation and BHR to methacholine and AMP in a population of young adults, with mild symptoms if any, was evaluated. A total of 230 subjects who participated in a follow-up study on occupational allergy were included. Before exposure to occupational allergens, subjects completed a questionnaire on respiratory symptoms and were tested for atopy, blood eosinophilia (greater than or equal to 275/mm(3)), and BHR to methacholine and AMP (greater than or equal to 15% fall in FEV1). Risk estimates were expressed as prevalence ratios (PR) and 95% confidence intervals (95% CI). Dose-response slopes (DRS) for methacholine and AMP were compared between healthy control subjects, self-reported allergic rhinitis, and allergic asthma. BHR to AMP was associated with allergic rhinitis (PR 2.51, 95% Cl: 1.22;5.17), allergic asthma (PR 4.38, 95% Cl: 1.98;9.66), with atopy (PR 3.87, 95% Cl: 1.76;8.52), and blood eosinophilia (PR 3.57, 95% Cl: 1.48;8.77), but not with baseline FEV1. BHR to methacholine was inversely related to prechallenge FEV1 (PR 0.97, 95% Cl: 0.96;0.99). For both methacholine and AMP the geometric mean DRS increased along the axis asymptomatic-allergic rhinitis-allergic asthma, but for AMP the increase was the strongest. In this population study among young adults, BHR to AMP refers to allergic background of airway lability and BHR to methacholine is related to a diminished airway caliber.	Univ Utrecht, Div Environm & Occupat Hlth, Inst Risk Assessment Sci, NL-3508 TD Utrecht, Netherlands; Univ Groningen Hosp, Dept Pulmonol, Groningen, Netherlands	De Meer, G (reprint author), Univ Utrecht, Div Environm & Occupat Hlth, Inst Risk Assessment Sci, POB 80176, NL-3508 TD Utrecht, Netherlands.						Alvarez MJ, 2000, ALLERGY, V55, P355, DOI 10.1034/j.1398-9995.2000.00312.x; BRADLEY BL, 1991, J ALLERGY CLIN IMMUN, V88, P661, DOI 10.1016/0091-6749(91)90160-P; Crimi E, 1998, AM J RESP CRIT CARE, V157, P4; De Meer G, 2001, THORAX, V56, P362, DOI 10.1136/thorax.56.5.362; DJUKANOVIC R, 1992, EUR RESPIR J, V5, P538; HOLGATE ST, 1986, ARCH INT PHARMACOD T, V280, P240; Ichinose M, 2000, EUR RESPIR J, V15, P248, DOI 10.1034/j.1399-3003.2000.15b05.x; IHRE E, 1993, CLIN EXP ALLERGY, V23, P298, DOI 10.1111/j.1365-2222.1993.tb00326.x; MENSINGA TT, 1990, J ALLERGY CLIN IMMUN, V86, P99, DOI 10.1016/S0091-6749(05)80129-0; OCONNOR G, 1987, AM REV RESPIR DIS, V136, P1412; OOSTERHOFF Y, 1993, AM REV RESPIR DIS, V147, P512; PEACHELL PT, 1988, AM REV RESPIR DIS, V138, P1143; PHILLIPS GD, 1990, AM REV RESPIR DIS, V141, P9; Polosa R, 2000, EUR RESPIR J, V15, P30, DOI 10.1183/09031936.00.15103000; POLOSA R, 1995, AM J RESP CRIT CARE, V151, P624; PRIETO L, 1993, CLIN EXP ALLERGY, V23, P172, DOI 10.1111/j.1365-2222.1993.tb00878.x; PRIETO L, 1994, ANN ALLERGY, V72, P534; Rutgers SR, 2000, CLIN EXP ALLERGY, V30, P657; SEPPALA OP, 1991, RESP MED, V85, P365, DOI 10.1016/S0954-6111(06)80179-4; Thompson ML, 1998, OCCUP ENVIRON MED, V55, P272; van den Toorn LM, 2000, AM J RESP CRIT CARE, V162, P953; Van dn Berge M, 2001, AM J RESP CRIT CARE, V163, P1546; van Rensen ELJ, 1999, THORAX, V54, P403; vanVelzen E, 1996, THORAX, V51, P582, DOI 10.1136/thx.51.6.582; Weersink EJM, 1997, AM J RESP CRIT CARE, V155, P1241	25	90	92	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.	FEB 1	2002	165	3					327	331				5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	517PA	WOS:000173618100005	11818315	
J	Taylor, SL; Hefle, SL				Taylor, SL; Hefle, SL			Will genetically modified foods be allergenic?	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						biotechnology; allergy; food; sequence homology; digestion; exposure; classification; heat stability	BREAST-FED INFANTS; COWS MILK ALLERGY; BETA-LACTOGLOBULIN; HYPERSENSITIVITY REACTIONS; BACILLUS-THURINGIENSIS; PEANUT PROTEIN; DOUBLE-BLIND; IN-VITRO; CHILDREN; IDENTIFICATION	Foods produced through agricultural biotechnology, including such staples as corn, soybeans, canola, and potatoes, are already reaching the consumer marketplace. Agricultural biotechnology offers the promise to produce crops with improved agronomic characteristics (eg, insect resistance, herbicide tolerance, disease resistance, and climatic tolerance) and enhanced consumer benefits (eg, better taste and texture, longer shelf life, and more nutritious). Certainly, the products of agricultural biotechnology should be subjected to a careful and complete safety assessment before commercialization. Because the genetic modification ultimately results in the introduction of new proteins into the food plant, the safety, including the potential allergenicity, of the newly introduced proteins must be assessed. Although most allergens are proteins, only a few of the many proteins found in foods are allergenic under the typical circumstances of exposure. The potential allergenicity of the introduced proteins call be evaluated by focusing on the source of the gene, the sequence homology of the newly introduced protein to known allergens, the expression level of the novel protein in the modified crop, the functional classification of the novel protein, the reactivity of the novel protein with IgE from the serum of individuals with known allergies to the source of the transferred genetic material, and various physicochemical properties of the newly introduced protein, such as heat stability and digestive stability. Few products of agricultural biotechnology (and none of the current products) will involve the transfer of genes from known allergenic sources, Applying such criteria provides reasonable assurance that the newly introduced protein has limited capability to become an allergen.	Univ Nebraska, Food Allergy Res & Resource Program, Lincoln, NE 68588 USA	Taylor, SL (reprint author), 143 Food Ind Complex, Lincoln, NE 68583 USA.						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Allergy Clin. Immunol.	MAY	2001	107	5					765	771				7	Allergy; Immunology	Allergy; Immunology	434JX	WOS:000168812300001	11344340	
J	Whigham, LD; Cook, EB; Stahl, JL; Saban, R; Bjorling, DE; Pariza, MW; Cook, ME				Whigham, LD; Cook, EB; Stahl, JL; Saban, R; Bjorling, DE; Pariza, MW; Cook, ME			CLA reduces antigen-induced histamine and PGE(2) release from sensitized guinea pig tracheae	AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY			English	Article						type I hypersensitivity; conjugated linoleic acid; immunity; allergies; asthma	CONJUGATED LINOLEIC-ACID; 3T3-L1 PREADIPOCYTES; BODY-COMPOSITION; FATTY-ACIDS; LYMPHOCYTE; MODULATION; GROWTH; RATS; MICE; PROLIFERATION	Conjugated linoleic acid (CLA) has been shown to enhance immune reactions such as lymphocyte blastogenesis and delayed-type hypersensitivity. We investigated the role of CLA in type I (immediate) hypersensitivity, using a guinea pig tracheal superfusion model for measuring antigen-induced airway smooth muscle contraction and inflammatory mediator release. Female Hartley guinea pigs were fed a diet supplemented with 0.25 g corn oil or linoleic acid/100 g of diet (control) or 0.25 g CLA/100 g of diet for at least 1 wk before and during active sensitization to ovalbumin antigen. Tracheae from sensitized guinea pigs were suspended in air-filled water-jacketed (37 degrees C) tissue chambers in a superfusion apparatus. Tracheae were superfused with buffer containing antigen, and tissue contraction was recorded. Superfusate was collected at 90-s intervals for evaluation of histamine and PGE(2) release. CLA did not affect antigen-induced tracheal contractions when expressed as gram contraction per gram tissue. CLA significantly reduced antigen-induced histamine and PGE(2) release. CLA appears to decrease release of some inflammatory mediators during type I hypersensitivity reactions.	Univ Wisconsin, Coll Agr & Life Sci, Dept Anim Sci, Madison, WI 53706 USA; Univ Wisconsin, Coll Agr & Life Sci, Dept Nutr Sci, Madison, WI 53706 USA; Univ Wisconsin, Sch Med, Dept Med, Madison, WI 53706 USA; Univ Wisconsin, Sch Vet Med, Dept Surg Sci, Madison, WI 53706 USA; Univ Wisconsin, Food Res Inst, Madison, WI 53706 USA; Univ Texas, Dept Internal Med, Galveston, TX 77555 USA	Cook, ME (reprint author), Univ Wisconsin, Coll Agr & Life Sci, Dept Anim Sci, 1675 Observ Dr, Madison, WI 53706 USA.						*AM AC ALL ASTHM I, 1998, EX SUMM; Banni S, 1996, J NUTR BIOCHEM, V7, P150, DOI 10.1016/0955-2863(95)00193-X; Black PN, 1997, EUR RESPIR J, V10, P6, DOI 10.1183/09031936.97.10010006; Black PN, 1999, J ALLERGY CLIN IMMUN, V103, P351, DOI 10.1016/S0091-6749(99)70513-0; Brodie AE, 1999, J NUTR, V129, P602; Chew BP, 1997, ANTICANCER RES, V17, P1099; Chin S. F., 1992, Journal of Food Composition and Analysis, V5, P185, DOI 10.1016/0889-1575(92)90037-K; CHIN SF, 1994, J NUTR, V124, P2344; CONSTANTINE JW, 1965, J PHARM PHARMACOL, V17, P384; COOK ME, 1993, POULTRY SCI, V72, P1301; FISHLEDER RI, 1984, J PHARMACOL EXP THER, V230, P534; GOLD KN, 1994, ARTHRITIS RHEUM, V37, P925, DOI 10.1002/art.1780370623; HA YL, 1987, CARCINOGENESIS, V8, P1881, DOI 10.1093/carcin/8.12.1881; KLEEBERGER SR, 1995, ASTHMA RHINITIS, P825; LEE KN, 1994, ATHEROSCLEROSIS, V108, P19, DOI 10.1016/0021-9150(94)90034-5; Lee KN, 1998, BIOCHEM BIOPH RES CO, V248, P817, DOI 10.1006/bbrc.1998.8994; Li Y, 1998, LIPIDS, V33, P417, DOI 10.1007/s11745-998-0223-9; Liu KL, 1997, LIPIDS, V32, P725, DOI 10.1007/s11745-997-0092-2; MILLER CC, 1994, BIOCHEM BIOPH RES CO, V198, P1107, DOI 10.1006/bbrc.1994.1157; NUGTEREN DH, 1970, BIOCHIM BIOPHYS ACTA, V210, P171, DOI 10.1016/0005-2760(70)90072-X; Park Y, 1997, LIPIDS, V32, P853, DOI 10.1007/s11745-997-0109-x; Park Y, 1999, LIPIDS, V34, P235, DOI 10.1007/s11745-999-0358-8; Park Y., 1996, THESIS U WISCONSIN M; ROPER RL, 1992, J IMMUNOL, V149, P2984; Satory DL, 1999, J NUTR, V129, P92; Sebedio JL, 1997, BBA-LIPID LIPID MET, V1345, P5, DOI 10.1016/S0005-2760(97)00015-5; Sugano M, 1997, J NUTR BIOCHEM, V8, P38, DOI 10.1016/S0955-2863(96)00150-7; Sugano M, 1998, LIPIDS, V33, P521, DOI 10.1007/s11745-998-0236-4; SUNSHINE C, 1994, BBA-BIOMEMBRANES, V1191, P59, DOI 10.1016/0005-2736(94)90233-X; UNDEM BJ, 1985, AM REV RESPIR DIS, V131, P260; WONG DTO, 1976, INT ARCH ALLER A IMM, V50, P155; Wong MW, 1997, ANTICANCER RES, V17, P987; WOODBAKER R, 1995, ASTHMA RHINITIS, P791	33	90	92	0	2	AMER PHYSIOLOGICAL SOC	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0363-6119			AM J PHYSIOL-REG I	Am. J. Physiol.-Regul. Integr. Comp. Physiol.	MAR	2001	280	3					R908	R912				5	Physiology	Physiology	401FQ	WOS:000166917900038	11171673	
J	Brenner, AV; Wang, ZY; Kleinerman, RA; Wang, LD; Zhang, SZ; Metayer, C; Chen, K; Lei, SW; Cui, HX; Lubin, JH				Brenner, AV; Wang, ZY; Kleinerman, RA; Wang, LD; Zhang, SZ; Metayer, C; Chen, K; Lei, SW; Cui, HX; Lubin, JH			Previous pulmonary diseases and risk of lung cancer in Gansu Province, China	INTERNATIONAL JOURNAL OF EPIDEMIOLOGY			English	Article						case-control studies; lung neoplasms; tuberculosis; pulmonary; bronchitis; pulmonary emphysema; asthma; pneumonia	NONSMOKING WOMEN; FAMILY HISTORY; TUBERCULOSIS PATIENTS; RESPIRATORY-DISEASE; MORTALITY; SMOKING; COHORT; EXPOSURE; ASTHMA; MINERS	Backgrounds Although active smoking is well established as the main cause of lung cancer, there is accumulating evidence that history of prior lung diseases may be an independent risk factor for lung cancer. Methods A population-based case-control study in Gansu Province, China identified 886 lung cancer cases (656 male, 230 female) diagnosed between January 1994 and April 1998. A standardized interview collected information on a variety of potential risk factors including a history of physician-diagnosed non-malignant lung diseases (pulmonary tuberculosis, chronic bronchitis/emphysema, asthma, pneumonia), age and year in which each condition was first diagnosed, and any therapy or hospitalization received. Results Pulmonary tuberculosis (odds ratio [OR] = 2.1, 95% CI:1.4-3.1) and chronic bronchitis/emphysema (OR = 1.4 95% CI : 1.1-1.8) were associated with increased risk of lung cancer, after adjustment for active smoking and socioeconomic status. The OR for asthma (OR = 1.4, 95% CI : 0.9-2.1) and pneumonia (OR = 1.5, 95% CI: 1.0-2.3) were also elevated. The risk of lung cancer remained significant for pulmonary tuberculosis and chronic bronchitis/emphysema when analysis was limited to the pathologically confirmed cases and self-responders. Conclusions This study provides additional evidence that previous pulmonary tuberculosis and chronic bronchitis/emphysema are causally related to lung cancer, although the precise mechanism is still unclear. The results for asthma and pneumonia, while suggestive of a positive association, did not reach the traditional level of statistical significance and should be interpreted with caution.	NCI, Div Canc Epidemiol & Genet, Radiat Epidemiol Branch, Bethesda, MD 20892 USA	Brenner, AV (reprint author), NCI, Div Canc Epidemiol & Genet, Radiat Epidemiol Branch, 6120 Execut Blvd,MSC 7362, Bethesda, MD 20892 USA.			Kleinerman, Ruth/0000-0001-7415-2478	NCI NIH HHS [N01-CP-50509]		ALAVANJA MCR, 1992, AM J EPIDEMIOL, V136, P623; BAKRIS GL, 1983, CANCER, V52, P493, DOI 10.1002/1097-0142(19830801)52:3<493::AID-CNCR2820520319>3.0.CO;2-Y; Blot WJ, 1996, CANC EPIDEMIOLOGY PR, P637; Breslow N. 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J. Epidemiol.	FEB	2001	30	1					118	124		10.1093/ije/30.1.118		7	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	413AG	WOS:000167587300032	11171871	
J	Bugajska-Schretter, A; Grote, M; Vangelista, L; Valent, P; Sperr, WR; Rumpold, H; Pastore, A; Reichelt, R; Valenta, R; Spitzauer, S				Bugajska-Schretter, A; Grote, M; Vangelista, L; Valent, P; Sperr, WR; Rumpold, H; Pastore, A; Reichelt, R; Valenta, R; Spitzauer, S			Purification, biochemical, and immunological characterisation of a major food allergen: different immunoglobulin E recognition of the apo- and calcium-bound forms of carp parvalbumin	GUT			English	Article						food allergy; parvalbumin; circular dichroism; epitopes; antibodies; immunochemistry	BINDING PROTEIN PARVALBUMIN; BIRCH POLLEN ALLERGEN; FISH HYPERSENSITIVITY; MUSCULAR PARVALBUMINS; ADVERSE REACTIONS; IGE-BINDING; MUSCLE; SITES; EXPRESSION; CHALLENGE	Background-Almost 4% of the population suffer from food allergy which is an adverse reaction to food with an underlying immunological mechanism. Aims-To characterise one of the most frequent IgE defined food allergens, fish parvalbumin. Methods-Tissue and subcellular distribution of carp parvalbumin was analysed by immunogold electron microscopy and cell fractionation. Parvalbumin was purified to homogeneity, analysed by mass spectrometry and circular dichroism (CD) spectroscopy, and its allergenic activity was analysed by IgE binding and basophil histamine release tests. Results-The isoelectric point (pI) 4.7 form of carp parvalbumin, a three EF-hand calcium-binding protein, was purified to homogeneity. CD analysis revealed a remarkable stability and refolding capacity of calcium-bound parvalbumin. This may explain why parvalbumin, despite cooking and exposure to the gastrointestinal tract, can sensitise patients. Purified parvalbumin reacted with IgE of more than 95% of individuals allergic to fish, induced dose-dependent basophil histamine release and contained, on average, 83% of the IgE epitopes present in other fish species. Calcium depletion reduced the IgE binding capacity of parvalbumin which, according to CD analysis, may be due to conformation-dependent IgE recognition. Conclusions-Purified carp parvalbumin represents an important cross reactive food allergen. It can be used for in vitro and in vivo diagnosis of fish-induced food allergy. Our finding that the ape-form of parvalbumin had a greatly reduced IgE binding capacity indicates that this form may be a candidate for safe immunotherapy of fish-related food allergy.	Univ Vienna, AKH, Inst Med & Chem Lab, A-1090 Vienna, Austria; Univ Munster, Inst Med Phys & Biophys, D-4400 Munster, Germany; European Mol Biol Lab, Heidelberg, Germany; Univ Vienna, AKH, Dept Internal Med 1, Div Haematol, A-1090 Vienna, Austria; Natl Inst Med Res, Mol Struct Div, London NW7 1AA, England; Univ Vienna, AKH, Dept Pathophysiol, A-1090 Vienna, Austria	Valenta, R (reprint author), Univ Vienna, Vienna Gen Hosp, Dept Pathophysiol, Immunopathol Grp, Wahringer Gurtel 18-20, A-1090 Vienna, Austria.				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J	Guez, S; Vatrinet, C; Fadel, R; Andre, C				Guez, S; Vatrinet, C; Fadel, R; Andre, C			House-dust-mite sublingual-swallow immunotherapy (SLIT) in perennial rhinitis: a double-blind, placebo-controlled study	ALLERGY			English	Article						house-dust mite; perennial rhinitis; sublingual immunotherapy	CONTROLLED TRIAL; ALLERGIC RHINITIS; POLLEN EXTRACT; ASTHMA; RHINOCONJUNCTIVITIS; EFFICACY; CHILDREN; EXPOSURE; IGE	Background: The safety and efficacy of sublingual-swallow immunotherapy (SLIT) in rhinitis caused by house-dust mite were evaluated in a double-blind, placebo-controlled study including 75 patients for 24 months. Methods: Patients received either placebo or SLIT with a standardized Dermatophagoides pteronyssinus (D.pt.) - D. farinae (D.f.) 50/50 extract. The mean cumulative dose was 90 000 IR, equivalent to 2.2 mg of Der p 1 and 1.7 mg of Der f I. Symptom and medication scores were assessed throughout the study. Exposure to house-dust mite, skin sensitivity, and serum specific IgE and IgG4 were assessed before starting treatment and after 12 and 24 months. Results: Seventy-two patients (36 active-36 placebo) were eligible for intent-to-treat analysis. Thirty-six patients dropped out of the study. The number of patients who dropped out due to lack of efficacy was eight out of 37 (21.6%) in the active treatment group compared to 15 out of 38 (39.5%) in the placebo group (chi-square = 2.81, P = 0.09). Total symptom and medication scores decreased significantly after 12 and 24 months (P < 0.05) of treatment in both groups, but no significant difference was observed between the active and placebo groups. After 24 months, the number of patients with high levels of indoor allergenic load decreased significantly in both groups compared to baseline data (P = 0.01). Specific IgE (D.pt. and D.f.) increased significantly in the active treatment group after 12 and 24 months, while no change was observed in the placebo group. Specific IgG4 levels were not significantly modified in either group. Two patients in each group reported mild adverse effects. No severe adverse effects were reported. Conclusions: We conclude that SLIT in rhinitis caused by house-dust mite was safe, but there was a lack of consistent clinical benefit compared to placebo, probably due to the impact of the allergen avoidance measures that lowered the allergen burden.	Stallergenes SA, Sci & Med Dept, F-92183 Antony, France; Assoc Promot Allergol Aquitaine, Bordeaux, France	Andre, C (reprint author), Stallergenes SA, Sci & Med Dept, 6 Rue Alexis Tocqueville, F-92183 Antony, France.						ABRAMSON MJ, 1995, AM J RESP CRIT CARE, V151, P969; Bousquet J, 1999, ALLERGY, V54, P249, DOI 10.1034/j.1398-9995.1999.00916.x; Bousquet J., 1998, Allergy (Copenhagen), V53, P1; BOUSQUET J, 1990, J ALLERGY CLIN IMMUN, V86, P292, DOI 10.1016/S0091-6749(05)80091-0; BOUSQUET J, 1992, ALLERGIC NONALLERGIC, P136; Clavel R, 1998, ALLERGY, V53, P493, DOI 10.1111/j.1398-9995.1998.tb04086.x; EWAN PW, 1988, CLIN ALLERGY, V18, P501, DOI 10.1111/j.1365-2222.1988.tb02900.x; Feliziani V, 1995, Allergol Immunopathol (Madr), V23, P224; Frederick JM, 1997, EUR RESPIR J, V10, P361, DOI 10.1183/09031936.97.10020361; Hirsch T, 1997, PEDIATR ALLERGY IMMU, V8, P21, DOI 10.1111/j.1399-3038.1997.tb00138.x; MALLING HJ, 1993, ALLERGY, V48, P9; Malling HJ, 1998, ALLERGY, V53, P461; MCHUGH SM, 1990, J ALLERGY CLIN IMMUN, V86, P521, DOI 10.1016/S0091-6749(05)80208-8; Passalacqua G, 1998, LANCET, V351, P629, DOI 10.1016/S0140-6736(97)07055-4; Platts-Mills Thomas A. E., 1997, Journal of Allergy and Clinical Immunology, V100, pS1; QUOIX E, 1993, ALLERGY, V48, P306, DOI 10.1111/j.1398-9995.1993.tb02397.x; REID MJ, 1993, J ALLERGY CLIN IMMUN, V92, P6, DOI 10.1016/0091-6749(93)90030-J; SABBAH A, 1994, ALLERGY, V49, P309, DOI 10.1111/j.1398-9995.1994.tb02273.x; SENSI LG, 1994, CLIN EXP ALLERGY, V24, P377, DOI 10.1111/j.1365-2222.1994.tb00250.x; SPORIK R, 1992, CLIN EXP ALLERGY, V22, P897, DOI 10.1111/j.1365-2222.1992.tb02062.x; TARI MG, 1990, ALLERGOL IMMUNOPATH, V18, P277; TROISE C, 1995, J INVEST ALLERG CLIN, V5, P25; VARNEY VA, 1991, BRIT MED J, V302, P265; Vourdas D, 1998, ALLERGY, V53, P662, DOI 10.1111/j.1398-9995.1998.tb03952.x; Weeks J, 1995, CLIN EXP ALLERGY, V25, P1179, DOI 10.1111/j.1365-2222.1995.tb03041.x	25	90	92	0	4	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	APR	2000	55	4					369	375		10.1034/j.1398-9995.2000.00413.x		7	Allergy; Immunology	Allergy; Immunology	300WT	WOS:000086277300008	10782522	
J	Jefferson, T; Jones, M; Doshi, P; Spencer, EA; Onakpoya, I; Heneghan, CJ				Jefferson, Tom; Jones, Mark; Doshi, Peter; Spencer, Elizabeth A.; Onakpoya, Igho; Heneghan, Carl J.			Oseltamivir for influenza in adults and children: systematic review of clinical study reports and summary of regulatory comments	BMJ-BRITISH MEDICAL JOURNAL			English	Article							NEUROPSYCHIATRIC ADVERSE EVENTS; PROPHYLAXIS	Objective To describe the potential benefits and harms of oseltamivir by reviewing all clinical study reports (or similar document when no clinical study report exists) of randomised placebo controlled trials and regulatory comments ("regulatory information"). Design Systematic review of regulatory information. Data sources Clinical study reports, trial registries, electronic databases, regulatory archives, and correspondence with manufacturers. Eligibility criteria for selecting studies Randomised placebo controlled trials on adults and children who had confirmed or suspected exposure to natural influenza. Main outcome measures Time to first alleviation of symptoms, influenza outcomes, complications, admissions to hospital, and adverse events in the intention to treat population. Results From the European Medicines Agency and Roche, we obtained clinical study reports for 83 trials. We included 23 trials in stage 1 (reliability and completeness screen) and 20 in stage 2 (formal analysis). In treatment trials on adults, oseltamivir reduced the time to first alleviation of symptoms by 16.8 hours (95% confidence interval 8.4 to 25.1 hours, P<0.001). There was no effect in children with asthma, but there was an effect in otherwise healthy children (mean difference 29 hours, 95% confidence interval 12 to 47 hours, P=0.001). In treatment trials there was no difference in admissions to hospital in adults (risk difference 0.15%, 95% confidence interval -0.91% to 0.78%, P=0.84) and sparse data in children and for prophylaxis. In adult treatment trials, oseltamivir reduced investigator mediated unverified pneumonia (risk difference 1.00%, 0.22% to 1.49%; number needed to treat to benefit (NNTB) 100, 95% confidence interval 67 to 451). The effect was not statistically significant in the five trials that used a more detailed diagnostic form for "pneumonia," and no clinical study reports reported laboratory or diagnostic confirmation of "pneumonia." The effect on unverified pneumonia in children and for prophylaxis was not significant. There was no significant reduction in risk of unverified bronchitis, otitis media, sinusitis, or any complication classified as serious or that led to study withdrawal. 14 of 20 trials prompted participants to self report all secondary illnesses to an investigator. Oseltamivir in the treatment of adults increased the risk of nausea (risk difference 3.66%, 0.90% to 7.39%; number needed to treat to harm (NNTH) 28, 95% confidence interval 14 to 112) and vomiting (4.56%, 2.39% to 7.58%; 22, 14 to 42). In treatment of children, oseltamivir induced vomiting (5.34%, 1.75% to 10.29%; 19, 10 to 57). In prophylaxis trials, oseltamivir reduced symptomatic influenza in participants by 55% (3.05%, 1.83% to 3.88%; NNTB 33, 26 to 55) and households (13.6%, 9.52% to 15.47%; NNTB 7, 6 to 11) based on one study, but there was no significant effect on asymptomatic influenza and no evidence of a reduction in transmission. In prophylaxis studies, oseltamivir increased the risk of psychiatric adverse events during the combined "on-treatment" and "off-treatment" periods (risk difference 1.06%, 0.07% to 2.76%; NNTH 94, 36 to 1538) and there was a dose-response effect on psychiatric events in two "pivotal" treatment trials of oseltamivir, at 75 mg (standard dose) and 150 mg (high dose) twice daily (P=0.038). In prophylaxis studies, oseltamivir increased the risk of headaches on-treatment (risk difference 3.15%, 0.88% to 5.78%; NNTH 32, 18 to 115), renal events with treatment (0.67%, -0.01% to 2.93%), and nausea while receiving treatment (4.15%, 0.86% to 9.51%; NNTH 25, 11 to 116). Conclusions In prophylactic studies oseltamivir reduces the proportion of symptomatic influenza. In treatment studies it also modestly reduces the time to first alleviation of symptoms, but it causes nausea and vomiting and increases the risk of headaches and renal and psychiatric syndromes. The evidence of clinically significant effects on complications and viral transmission is limited because of rarity of such events and problems with study design. The trade-off between benefits and harms should be borne in mind when making decisions to use oseltamivir for treatment, prophylaxis, or stockpiling.	[Jefferson, Tom] Cochrane Acute Resp Infect Grp, I-00187 Rome, Italy; [Jones, Mark] Univ Queensland, Sch Populat Hlth, Brisbane, Qld, Australia; [Doshi, Peter] Univ Maryland, Sch Pharm, Dept Pharmaceut Hlth Serv Res, Baltimore, MD 21201 USA; [Spencer, Elizabeth A.; Onakpoya, Igho; Heneghan, Carl J.] Univ Oxford, Nuffield Dept Primary Care Hlth Sci, Oxford, England	Jefferson, T (reprint author), Cochrane Acute Resp Infect Grp, Via Puglie 23, I-00187 Rome, Italy.	jefferson.tom@gmail.com		Spencer, Elizabeth/0000-0002-9079-8006	NIHR Health Technology Assessment programme	This project was funded by the NIHR Health Technology Assessment programme and will be published in full in the Health Technology Assessment journal series (more details are available at www.nets.nihr.ac.uk/projects/hta/108001). The views and opinions expressed therein are those of the authors and do not necessarily reflect those of the Department of Health. The study sponsor had no role in study design; the collection, analysis, and interpretation of data; the writing of the article; and the decision to submit the article for publication. All the authors have no ties to the manufacturer or the sponsor (apart from those disclosed) and had access to all parts of the deidentified clinical study reports from the oseltamivir trial programme.	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J	Ly, NP; Litonjua, A; Gold, DR; Celedon, JC				Ly, Ngoc P.; Litonjua, Augusto; Gold, Diane R.; Celedon, Juan C.			Gut microbiota, probiotics, and vitamin D: Interrelated exposures influencing allergy, asthma, and obesity?	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						Microbiota; asthma; obesity; allergic; eczema; vitamin D; probiotics; cytokines	PLACEBO-CONTROLLED TRIAL; DIET-INDUCED OBESITY; RANDOMIZED CONTROLLED-TRIAL; BODY-MASS INDEX; AGE 5 YEARS; ANTIBIOTIC USE; INTESTINAL MICROFLORA; EARLY-LIFE; 1ST YEAR; AIRWAY INFLAMMATION	Current evidence supports a role for gut colonization in promoting and maintaining a balanced immune response in early life. An altered or less diverse gut microbiota composition has been associated with atopic diseases, obesity, or both. Moreover, certain gut microbial strains have been shown to inhibit or attenuate immune responses associated with chronic inflammation in experimental models. However, there has been no fully adequate longitudinal study of the relation between the neonatal gut microbiota and the development of allergic diseases (eg, atopic asthma) and obesity. The emergence of promising experimental studies has led to several clinical trials of probiotics (live bacteria given orally that allow for intestinal colonization) in human subjects. Probiotic trials thus far have failed to show a consistent preventive or therapeutic effect on asthma or obesity. Previous trials of probiotics have been limited by small sample size, short duration of follow-up, or lack of state-of-the art analyses of the gut microbiota. Finally, there is emerging evidence that the vitamin D pathway might be important in gut homeostasis and in signaling between the microbiota and the host. Given the complexity of the gut micriobiota, additional research is needed before we can confidently establish whether its manipulation in early life can prevent or treat asthma, obesity, or both. (J Allergy Clin Immunol 2011;127:1087-94.)	[Ly, Ngoc P.] Univ Calif San Francisco, Dept Pediat, Div Pediat Pulm Med, San Francisco, CA 94143 USA; [Litonjua, Augusto; Gold, Diane R.] Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA; [Litonjua, Augusto; Gold, Diane R.] Harvard Univ, Sch Med, Boston, MA USA; [Celedon, Juan C.] Univ Pittsburgh, Childrens Hosp Pittsburgh, Sch Med, UPMC, Pittsburgh, PA USA	Ly, NP (reprint author), 521 Parnassus Ave,C344, San Francisco, CA 94143 USA.	lyn@peds.ucsf.edu	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Litonjua, Augusto/0000-0003-0422-5875	NIAID NIH HHS [R01 AI035786-17, R01 AI035786]		Adlerberth I, 2009, ACTA PAEDIATR, V98, P229, DOI 10.1111/j.1651-2227.2008.01060.x; Adlerberth I, 2007, J ALLERGY CLIN IMMUN, V120, P343, DOI 10.1016/j.jaci.2007.05.018; Adorini L, 2009, HUM IMMUNOL, V70, P345, DOI 10.1016/j.humimm.2009.01.016; Antonio MAD, 2005, J INFECT DIS, V192, P394, DOI 10.1086/430926; Asher MI, 2006, LANCET, V368, P733, DOI 10.1016/S0140-6736(06)69283-0; 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Allergy Clin. Immunol.	MAY	2011	127	5					1087	1094		10.1016/j.jaci.2011.02.015		8	Allergy; Immunology	Allergy; Immunology	756NG	WOS:000290018600001	21419479	
J	Rook, GAW				Rook, G. A. W.			99th Dahlem Conference on Infection, Inflammation and Chronic Inflammatory Disorders: Darwinian medicine and the 'hygiene' or 'old friends' hypothesis	CLINICAL AND EXPERIMENTAL IMMUNOLOGY			English	Article						Darwinian medicine; dendritic cells; 'hygiene hypothesis'; 'old friends' hypothesis; T(reg)	INNATE IMMUNITY; HAY-FEVER; DISEASE; ASTHMA; VIRUSES; PATHOGENESIS; ASSOCIATION; EVOLUTION; PARASITES; LESSONS	P>The current synthesis of the 'hygiene hypothesis' suggests that the recent increase in chronic inflammatory disorders is at least partly attributable to immunodysregulation resulting from lack of exposure to microorganisms that have evolved an essential role in the establishment of the immune system. This document provides a background for discussion of the following propositions. The essential role of these organisms is an example of 'evolved dependence'. The most relevant organisms are those that co-evolved with mammals, and already accompanied early hominids in the Paleolithic. More recently evolved 'childhood infections' are not likely to have evolved this role, and recent epidemiology supports this contention. This mechanism is interacting with other modern environmental changes that also lead to enhanced inflammatory responses [inappropriate diet, obesity, psychological stress, vitamin D deficiency, pollution (dioxins), etc.]. The range of chronic inflammatory disorders that is affected is potentially larger than usually assumed [allergies, autoimmunity, inflammatory bowel disease, but also vascular disease, some cancers, depression/anxiety (when accompanied by raised inflammatory cytokines), and perhaps neurodegenerative disorders and type 2 diabetes].	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Exp. Immunol.	APR	2010	160	1					70	79		10.1111/j.1365-2249.2010.04133.x		10	Immunology	Immunology	567JN	WOS:000275443000011	20415854	
J	Siebenhaar, F; Degener, F; Zuberbier, T; Martus, P; Maurer, M				Siebenhaar, Frank; Degener, Franziska; Zuberbier, Torsten; Martus, Peter; Maurer, Marcus			High-dose desloratadine decreases wheal volume and improves cold provocation thresholds compared with standard-dose treatment in patients with acquired cold urticaria: A randomized, placebo-controlled, crossover study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Urticaria; cold; chronic; objective; antihistamine; desloratadine	CHRONIC IDIOPATHIC URTICARIA; DOUBLE-BLIND; EAACI/GA(2)LEN/EDF GUIDELINE; MULTICENTER; DIAGNOSIS; EFFICACY; SAFETY; ADULTS; TRIAL	Background: Increased dosing of nonsedating antihistamines is recommended by the current European Academy of Allergology and Clinical Immunology/Global Allergy and Asthma European Network/European Dermatology Forum guidelines on patients with acquired cold urticaria (ACU) who do not respond satisfactorily to the standard dose. Prospective data supporting this recommendation are scant. Objective: We sought to assess the effects of 5 and 20 mg of desloratadine and placebo on cold-induced urticarial reactions in patients with ACU. Methods: In this prospective, randomized, double-blind, 3-way crossover trial, patients with ACU (n = 30) received placebo, 5 mg of desloratadine, and 20 mg of desloratadine every day each for 7 days separated by 14-day washout periods. At the end of each treatment, patients underwent cold provocation with the TempTest 2.0/2.1 system, and urticarial reactions were assessed by using digital 3-dimensional time-lapse photography and thermography; the critical temperature threshold (CTT) and critical stimulation time threshold (CSTT) were measured. Adverse events (AEs) reported during the study were assessed. Results: Compared with placebo, 7 days of desloratadine at 5 and 20 mg/d significantly reduced the volume of cold-induced wheals and areas of hyperthermic skin and improved CTT and CSTT results. Desloratadine at 20 mg/d significantly reduced cold-induced wheal volume and CTT and CSTT values versus desloratadine at 5 mg/d. Desloratadine was well tolerated, with no increased rate of somnolence or other AEs with 20 mg of desloratadine. Conclusions: Desloratadine at standard and high doses significantly improved objective signs of ACU provoked by cold exposure. Desloratadine at 4 times the standard dose significantly reduced ACU lesion severity versus 5 mg of desloratadine without an increase in AEs. This study supports current guidelines that increased desloratadine dosing might benefit patients with urticaria who do not respond to standard doses. (J Allergy Clin Immunol 2009;123:672-9.)	[Siebenhaar, Frank; Degener, Franziska; Zuberbier, Torsten; Maurer, Marcus] Charite Univ Med Berlin, Dept Dermatol & Allergy, Allergie Ctr Charite, D-10117 Berlin, Germany; [Martus, Peter] Charite Univ Med Berlin, Inst Biostat & Clin Epidemiol, D-10117 Berlin, Germany	Maurer, M (reprint author), Charite Univ Med Berlin, Dept Dermatol & Allergy, Allergie Ctr Charite, Charitepl 1, D-10117 Berlin, Germany.	marcus.maurer@charite.de			DFG; Schering-Plough; Novartis; Leti; Stallergenes; Bayer Schering; Ansell; Kryolan; UCB; MSD; Proctor Gamble	F Siebenhaar has received research support from DFG and Schering-Plough. T. Zuberbier has received research grants from Schering-Plough, Novartis, Leti, Stallergenes, Bayer Schering, Ansell, Kryolan, UCB, MSD, and Proctor & Gamble; has been affiliated with the Editorial Board of the Journal of Allergy, the Scientific Advisory Board of the German Society for Allergy and Clinical Immunology, and the Expert Commission "Novel Food" of the German Federal Ministry of Consumer Protection; has served as the Chairman of the European Academy of Allergology and Clinical Immunology Dermatology Section, the Head of the European Centre for Allergy Research Foundation, a committee member of the World Health Organization Initiative Allergic Rhinitis and its Impact on Asthma, a member of the World Allergy Organisation Communications Council, and Secretary General of the Global Allergy and Asthma European Network and has provided expert testimony for the US Food and Drug Administration. M. Maurer is or recently was an investigator, speaker, and/or advisor for Almirall Hermal, Bayer Schering Pharma, Biofrontera, Essex Pharma, Genentech, JADO Technologies, Jerini, Novartis, Schering-Plough, Symbiopharm, UCB, and Uriach. The rest of the authors have declared that they have no conflict of interest.	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J	Cazzola, M; Matera, MG				Cazzola, M.; Matera, M. G.			Novel long-acting bronchodilators for COPD and asthma	BRITISH JOURNAL OF PHARMACOLOGY			English	Review						aclidinium; asthma; bronchodilators; carmoterol; chronic obstructive pulmonary disease; combination therapy; indacaterol; long-acting antimuscarinic agents; NVA237; ultra-long-acting beta-agonists	OBSTRUCTIVE PULMONARY-DISEASE; AIR-FLOW OBSTRUCTION; BETA(2)-ADRENOCEPTOR AGONIST; GUINEA-PIGS; PHARMACOLOGICAL CHARACTERIZATION; ADRENOCEPTOR AGONIST; POSITIVE INTERACTION; GLOBAL STRATEGY; STABLE COPD; TIOTROPIUM	An important step in simplifying asthma and chronic obstructive pulmonary disease (COPD) management and improving adherence with prescribed therapy is to reduce the dose frequency to the minimum necessary to maintain disease control. Therefore, the incorporation of once-daily dose administration is an important strategy to improve adherence and is a regimen preferred by most patients, which may also lead to enhancement of compliance, and may have advantages leading to improved overall clinical outcomes. Once-daily beta(2)-agonists or ultra long-acting beta(2)-agonists (LABAs) such as carmoterol, indacaterol, GSK-159797, GSK-597901, GSK-159802, GSK-642444 and GSK-678007 are under development for the treatment of asthma and COPD. Also some new long-acting antimuscarinic agents (LAMAs) such as aclidinium, LAS-35201, GSK656398, GSK233705, NVA-237 (glycopyrrolate) and OrM3 are under development. In any case, the current opinion is that it will be advantageous to develop inhalers containing combination of several classes of long-acting bronchodilator drugs in an attempt to simplify treatment regimens as much as possible. Consequently, several options for once-daily dual-action ultra LABA+LAMA combination products are currently being evaluated. A different approach is to have a dimer molecule in which both pharmacologies are present (these molecules are known as M(3) antagonist-beta(2) agonist (MABA) bronchodilators). The advent of a successful MABA product will revolutionize the field and open the door for a new range of combination products.	[Matera, M. G.] Univ Naples 2, Dept Expt Med, Pharmacol Unit, Naples, Italy; [Cazzola, M.] Univ Roma Tor Vergata, Dipartimento Med Interna, Unit Resp Dis, I-00133 Rome, Italy	Cazzola, M (reprint author), Univ Roma Tor Vergata, Dipartimento Med Interna, Unit Resp Dis, Via Montpellier 1, I-00133 Rome, Italy.	mario.cazzola@uniroma2.it	Cazzola, Mario/G-9397-2012		AstraZeneca; Boehringer Ingelheim; Chiesi Farmaceutici; Dey; GSK; Menarini Farmaceutici; Novartis; Nycomed; Pfizer; Sanovel	Mario Cazzola has received honoraria for speaking and consulting and/or financial support for attending meetings from AstraZeneca, Boehringer Ingelheim, Chiesi Farmaceutici, Dey, GSK, Menarini Farmaceutici, Novartis, Nycomed (former Altana), Pfizer and Sanovel. Maria Gabriella Matera has received honoraria for consulting and/or financial support for attending meetings from Altana, AstraZeneca, Boehringer Ingelheim, GSK, Novartis and Pfizer. No funding has been provided for this article.	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J	Snijders, BEP; Thijs, C; van Ree, R; van den Brandt, PA				Snijders, Bianca E. P.; Thijs, Carel; van Ree, Ronald; van den Brandt, Piet A.			Age at first introduction of cow milk products and other food products in relation to infant atopic manifestations in the first 2 years of life: The KOALA birth cohort study	PEDIATRICS			English	Article						cow milk; solids; atopy; reverse causation; oral tolerance; infant	BRIEF NEONATAL EXPOSURE; ASTHMA; ALLERGY; CHILDREN; SENSITIZATION; PREVENTION; ECZEMA; RISK; ASSOCIATION; DERMATITIS	OBJECTIVES. Scientific evidence is scarce about timing of solid-food introduction and its association with the development of atopy. We aimed to evaluate any associations between the introduction of cow milk products/other solid food products and infant atopic manifestations in the second year of life, taking into account reverse causation. METHODS. Data from 2558 infants in an ongoing prospective birth cohort study in the Netherlands were analyzed. Data on the main determinants (introduction of cow milk products and other food products), outcomes (eczema; atopic dermatitis [United Kingdom Working Party criteria]; recurrent wheeze; any sensitization; sensitization against cow milk, hen egg, peanut, and at least 1 inhalant allergen), and confounders were collected by repeated questionnaires at 34 weeks of gestation and 3, 7, 12, and 24 months postpartum. Information on sensitization was gathered by venous blood collections performed during home visits at age 2. Analyses were performed by multiple logistic regression analyses. RESULTS. More delay in introduction of cow milk products was associated with a higher risk for eczema. In addition, a delayed introduction of other food products was associated with an increased risk for atopy development at the age of 2 years. Exclusion of infants with early symptoms of eczema and recurrent wheeze (to avoid reverse causation) did not essentially change our results. DISCUSSION. Delaying the introduction of cow milk or other food products may not be favorable in preventing the development of atopy.	[Snijders, Bianca E. P.; Thijs, Carel; van den Brandt, Piet A.] Maastricht Univ, Dept Epidemiol, Care & Publ Hlth Res Inst, NL-6200 MD Maastricht, Netherlands; [Thijs, Carel; van den Brandt, Piet A.] Maastricht Univ, Dept Epidemiol, Nutr & Toxicol Res Inst, NL-6200 MD Maastricht, Netherlands; [van Ree, Ronald] Univ Amsterdam, Acad Med Ctr, Dept Expt Immunol, NL-1105 AZ Amsterdam, Netherlands	Snijders, BEP (reprint author), Maastricht Univ, Dept Epidemiol, Care & Publ Hlth Res Inst, POB 616, NL-6200 MD Maastricht, Netherlands.	bep.snijders@epid.unimaas.nl					AALBERSE RC, 1981, J ALLERGY CLIN IMMUN, V68, P356, DOI 10.1016/0091-6749(81)90133-0; Andreasyan K, 2007, PEDIATR ALLERGY IMMU, V18, P250, DOI 10.1111/j.1399-3038.2006.00509.x; Arshad SH, 2005, J ALLERGY CLIN IMMUN, V116, P3, DOI 10.1016/j.jaci.2005.03.043; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; de Jong MH, 1998, ARCH DIS CHILD, V79, P126; de Jong MH, 2002, ARCH DIS CHILD, V86, P365, DOI 10.1136/adc.86.5.365; Illi S, 2001, J ALLERGY CLIN IMMUN, V108, P709, DOI 10.1067/mai.2001.118786; Ivarsson A, 2002, AM J CLIN NUTR, V75, P914; Khakoo GA, 2004, ARCH DIS CHILD, V89, P295, DOI 10.1136/adc.2003.039016; Kummeling I, 2005, PEDIATR ALLERGY IMMU, V16, P679, DOI 10.1111/j.1399-3038.2005.00333.x; Liem JJ, 2007, J ALLERGY CLIN IMMUN, V119, P1203, DOI 10.1016/j.jaci.2006.12.671; Magnus P, 1997, BRIT MED J, V314, P1795; Mihrshahi S, 2007, CLIN EXP ALLERGY, V37, P671, DOI 10.1111/j.1365-2222.2007.02696.x; Morgan J, 2004, ARCH DIS CHILD, V89, P309, DOI 10.1136/adc.2002.020065; Oddy WH, 1999, BRIT MED J, V319, P815; Poole JA, 2006, PEDIATRICS, V117, P2175, DOI 10.1542/peds.2005-1803; Siltanen M, 2001, J ALLERGY CLIN IMMUN, V107, P229, DOI 10.1067/mai.2001.112128; SNIJDERS BE, 2007, PEDIATRICS, V119; Snijders BFP, 2007, J PEDIATR-US, V151, P347, DOI 10.1016/j.jpeds.200703.022; Tarini BA, 2006, ARCH PEDIAT ADOL MED, V160, P502, DOI 10.1001/archpedi.160.5.502; van Wijk F, 2007, BIOMED PHARMACOTHER, V61, P8, DOI 10.1016/j.biopha.2006.11.003; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P383, DOI 10.1111/j.1365-2133.1994.tb08530.x; Wood RA, 2006, ARCH PEDIAT ADOL MED, V160, P552, DOI 10.1001/archpedi.160.5.552; Zeiger RS, 2003, PEDIATRICS, V111, P1662; 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	26	89	92	0	5	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	JUL	2008	122	1					E115	E122		10.1542/peds.2007-1651		8	Pediatrics	Pediatrics	320YN	WOS:000257271200075	18595956	
J	Salam, MT; Islam, T; Gilliland, FD				Salam, Muhammad T.; Islam, Talat; Gilliland, Frank D.			Recent evidence for adverse effects of residential proximity to traffic sources on asthma	CURRENT OPINION IN PULMONARY MEDICINE			English	Article						air pollution; asthma; freeway; traffic; wheeze	VOLATILE ORGANIC-COMPOUNDS; 3 EUROPEAN AREAS; AIR-POLLUTION; RESPIRATORY SYMPTOMS; NITROGEN-DIOXIDE; ADULT ASTHMA; EXPOSURE; CHILDREN; ASSOCIATION; COHORT	There is consistent evidence that living near traffic sources is associated with asthma occurrence and exacerbations. Future studies have the opportunity to improve exposure estimates by measuring traffic-related pollutants near homes and schools and including time/activity patterns in prediction models. Further research is also warranted to investigate the differential impact of traffic by genetic and other susceptibility factors and to identify specific pollutants that underlie the adverse effect of traffic on asthma.	[Salam, Muhammad T.; Islam, Talat; Gilliland, Frank D.] 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.	gillilan@usc.edu		Salam, Muhammad/0000-0002-3565-8916			ANDERSEN ZJ, 2007, J EXPO SCI ENV  0509; Annesi-Maesano I, 2007, RESP MED, V101, P1721, DOI 10.1016/j.rmed.2007.02.022; Arif AA, 2007, INT ARCH OCC ENV HEA, V80, P711, DOI 10.1007/s00420-007-0183-2; Bayer-Oglesby L, 2006, AM J EPIDEMIOL, V164, P1190, DOI 10.1093/aje/kwj338; Beck JP, 2007, SCI TOTAL ENVIRON, V372, P440, DOI 10.1016/j.scitotenv.2006.10.009; Benhamou S, 1998, CANCER RES, V58, P5291; 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; Brugge D, 2007, ENVIRON HEALTH-UK, V6, DOI 10.1186/1476-069X-6-13; Chardon B, 2007, OCCUP ENVIRON MED, V64, P320, DOI 10.1136/oem.2005.026187; Chen CH, 2006, J ASTHMA, V43, P287, DOI 10.1080/02770900600622935; Gauderman WJ, 2007, LANCET, V369, P571, DOI 10.1016/S0140-6736(07)60037-3; Gordian ME, 2006, J EXPO SCI ENV EPID, V16, P49, DOI 10.1038/sj.jea.7500436; Ho WC, 2007, ENVIRON RES, V104, P402, DOI 10.1016/j.envres.2007.01.007; Hoek G, 2002, ATMOS ENVIRON, V36, P4077, DOI 10.1016/S1352-2310(02)00297-2; HOLGUIN F, 2007, AM J RESP CRIT  0719; Kan HD, 2007, THORAX, V62, P873, DOI 10.1136/thx.2006.073015; Kim Sun-Young, 2006, J Prev Med Public Health, V39, P309; Kim SY, 2007, INT ARCH OCC ENV HEA, V80, P701, DOI 10.1007/s00420-007-0182-3; Kuehni CE, 2006, INT J EPIDEMIOL, V35, P779, DOI 10.1093/ije/dyl022; Lee SL, 2006, CLIN EXP ALLERGY, V36, P1138, DOI 10.1111/j.1365-2222.2006.02555.x; Lewne M, 2004, SCI TOTAL ENVIRON, V332, P217, DOI 10.1016/j.scitotenv.2004.04.014; McConnell R, 2006, ENVIRON HEALTH PERSP, V114, P766, DOI 10.1289/ehp.8594; Meng YY, 2007, ANN ALLERG ASTHMA IM, V98, P455; MENG YY, 2006, LIVING NEAR HEAVY TR, P1; Mi YH, 2006, INDOOR AIR, V16, P454, DOI 10.1111/j.1600-0668.2006.00439.x; Modig L, 2006, EUR RESPIR J, V28, P75, DOI 10.1183/09031936.06.00071505; Morgenstern V, 2007, OCCUP ENVIRON MED, V64, P8, DOI 10.1136/oem.2006.028241; Nitschke M, 2006, J OCCUP ENVIRON MED, V48, P462, DOI 10.1097/01.jom.0000215802.43229.62; Pattenden S, 2006, OCCUP ENVIRON MED, V63, P828, DOI 10.1136/oem.2006.025213; Ramos RG, 2006, J ENVIRON HEALTH, V68, P26; Ryan PH, 2007, ENVIRON HEALTH PERSP, V115, P278, DOI 10.1289/ehp.9480; Ryan PH, 2005, J ALLERGY CLIN IMMUN, V116, P279, DOI 10.1016/j.jaci.2005.014; SALAM MT, 2007, THORAX          0821; SALAM MT, 2007, AM J RESP CRIT  0802; Sole D, 2007, J INVEST ALLERG CLIN, V17, P6; Tavernier G, 2006, J ALLERGY CLIN IMMUN, V117, P656, DOI 10.1016/j.jaci.2005.12.1311; Yang CY, 2007, J TOXICOL ENV HEAL A, V70, P111, DOI 10.1080/15287390600755059; Yen IH, 2006, AM J PUBLIC HEALTH, V96, P873, DOI 10.2105/AJPH.2004.059253	39	89	94	1	8	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	1070-5287			CURR OPIN PULM MED	Curr. Opin. Pulm. Med.	JAN	2008	14	1					3	8		10.1097/MCP.0b013e3282f1987a		6	Respiratory System	Respiratory System	242AU	WOS:000251697700002	18043269	
J	Wang, HB; Ghiran, I; Matthaei, K; Weller, PF				Wang, Hai-Bin; Ghiran, Ionita; Matthaei, Klaus; Weller, Peter F.			Airway eosinophils: Allergic inflammation recruited professional antigen-presenting cells	JOURNAL OF IMMUNOLOGY			English	Article							CD4 T-CELLS; DENDRITIC CELLS; IN-VIVO; HLA-DR; RESPIRATORY-TRACT; LYMPH-NODES; HUMAN LUNG; ASTHMA; EXPRESSION; CHALLENGE	The capacity of airway eosinophils, potentially pertinent to allergic diseases of the upper and lower airways, to function as professional APCs, those specifically able to elicit responses from unprimed, Ag-naive CD4(+) T cells has been uncertain. We investigated whether airway eosinophils are capable of initiating naive T cell responses in vivo. Eosinophils, isolated free of other APCs from the spleens of IL-5 transgenic mice, following culture with GM-CSF expressed MHC class 11 and the costimulatory proteins, CD40, CD80, and CD86. Eosinophils, incubated with OVA Ag in vitro, were instilled intratracheally into wild-type recipient mice that adoptively received i.v. infusions of OVA Ag-specific CD4(+) T cells from OVA TCR transgenic mice. OVA-exposed eosinophils elicited activation (CD69 expression), proliferation (BrdU incorporation), and IL-4, but not IFN-gamma, cytokine production by OVA-specific CD4(+) T cells in paratracheal lymph nodes (LN). Exposure of eosinophils to lysosomotropic NH4Cl which inhibits Ag processing, blocked each of these eosinophil-mediated activation responses of CD4(+) T cells. By three-color fluorescence microscopy, OVA Ag-loaded eosinophil APCs were physically interacting with naive OVA-specific CD4(+) T cells in paratracheal LN after eosinophil airway instillation. Thus, recruited luminal airway eosinophils are distinct allergic "inflammatory" professional APCs able to activate primary CD4(+) T cell responses in regional LNs.	Harvard Med Sch, Beth Israel Deaconess Med Ctr, Dept Med, Div Allergy, Boston, MA 02115 USA; Harvard Med Sch, Beth Israel Deaconess Med Ctr, Dept Med, Div Inflammat & Infect Dis, Boston, MA 02115 USA; Australian Natl Univ, John Curtin Sch Med Res, Div Mol Biosci, Gene Targeting Lab, Canberra, ACT 2601, Australia	Weller, PF (reprint author), Beth Israel Deaconess Med Ctr, Dept Med, DA-617,330 Brookline Ave, Boston, MA 02215 USA.	pweller@bidmc.harvard.edu	Klaus, Matthaei/D-8691-2011		NHLBI NIH HHS [HL70270, R01 HL070270, R01 HL070270-03, R01 HL070270-04]; NIAID NIH HHS [R01 AI020241, AI051645, AI20241, R01 AI020241-21A1, R01 AI020241-22, R01 AI020241-23, R01 AI051645, R01 AI051645-03, R01 AI051645-04, R01 AI051645-05, R01 AI051645-06A1, R37 AI020241, U19 AI041995, U19 AI041995-040003]		Burg J, 2002, AM J PHYSIOL-LUNG C, V283, pL460, DOI 10.1152/ajplung.00249.2001; Busse WW, 2001, NEW ENGL J MED, V344, P350; Byersdorfer CA, 2001, J IMMUNOL, V167, P6756; 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; Freeman GL, 1995, J PARASITOL, V81, P1010, DOI 10.2307/3284059; Fulkerson PC, 2006, P NATL ACAD SCI USA, V103, P16418, DOI 10.1073/pnas.0607863103; Geissmann F, 2007, NAT IMMUNOL, V8, P558, DOI 10.1038/nio607-558; Grayson MH, 1998, J EXP MED, V188, P2187, DOI 10.1084/jem.188.11.2187; GREGSON N, 2003, EUROPEAN URBAN REGIO, V3, P5; GUIDA L, 1994, BLOOD, V84, P2733; HANSEL TT, 1991, CLIN EXP IMMUNOL, V86, P271; Hmama Z, 1998, J IMMUNOL, V161, P4882; Ingulli E, 2002, J IMMUNOL, V169, P2247; Itano AA, 2003, NAT IMMUNOL, V4, P733, DOI 10.1038/ni957; Jacobsen EA, 2007, J ALLERGY CLIN IMMUN, V119, P1313, DOI 10.1016/j.jaci.2007.03.043; Jenkins MK, 2001, ANNU REV IMMUNOL, V19, P23, DOI 10.1146/annurev.immunol.19.1.23; Kato M, 1998, ANAT REC, V252, P418, DOI 10.1002/(SICI)1097-0185(199811)252:3<418::AID-AR10>3.0.CO;2-1; Klion AD, 2004, J ALLERGY CLIN IMMUN, V113, P30, DOI 10.1016/j.jaci.2003.10.050; Kuipers H, 2004, CURR OPIN IMMUNOL, V16, P702, DOI 10.1016/j.coi.2004.09.010; Lee JJ, 2004, SCIENCE, V305, P1773, DOI 10.1126/science.1099472; Liu LY, 2002, J IMMUNOL, V169, P6452; LOSS GE, 1993, J IMMUNOL, V150, P3187; LUCEY DR, 1989, P NATL ACAD SCI USA, V86, P1348, DOI 10.1073/pnas.86.4.1348; MacKenzie JR, 2001, J IMMUNOL, V167, P3146; Masten BJ, 2006, J IMMUNOL, V177, P7784; Mattes J, 2002, J EXP MED, V195, P1433, DOI 10.1084/jem.20020009; MENGELERS HJ, 1994, AM J RESP CRIT CARE, V149, P345; Mishra A, 1999, J CLIN INVEST, V103, P1719, DOI 10.1172/JCI6560; Moqbel R., 2006, SCI STKE, V2006, ppe26; Padigel UM, 2006, INFECT IMMUN, V74, P3232, DOI 10.1128/IAI.02067-05; Rothenberg ME, 2006, ANNU REV IMMUNOL, V24, P147, DOI 10.1146/annurev.immunol.24.021605.090720; SEDGWICK JB, 1992, J IMMUNOL, V149, P3710; Shi HZ, 2000, J CLIN INVEST, V105, P945, DOI 10.1172/JCI8945; Throsby M, 2000, J IMMUNOL, V165, P1965; Trombetta ES, 2005, ANNU REV IMMUNOL, V23, P975, DOI 10.1146/annurev.immunol.22.012703.104538; Umetsu DT, 2002, NAT IMMUNOL, V3, P715, DOI 10.1038/ni0802-715; van Rijt LS, 2005, J EXP MED, V201, P981, DOI 10.1084/jem.20042311; van Rijt LS, 2004, J IMMUNOL METHODS, V288, P111, DOI 10.1016/j.jim.2004.03.004; van Rijt LS, 2003, J IMMUNOL, V171, P3372; Varol C, 2007, J EXP MED, V204, P171, DOI 10.1084/jem.20061011; Voehringer D, 2004, IMMUNITY, V20, P267, DOI 10.1016/S1074-7613(04)00026-3; Voehringer D, 2007, J LEUKOCYTE BIOL, V81, P1434, DOI 10.1189/jlb.1106686; von Garnier C, 2005, J IMMUNOL, V175, P1609; WELLER PF, 1993, J IMMUNOL, V150, P2554; Wikstrom ME, 2007, IMMUNOL CELL BIOL, V85, P182, DOI 10.1038/sj.icb.7100039; Yamamoto H, 2000, AM J RESP CELL MOL, V23, P379; ZIEGLER HK, 1982, P NATL ACAD SCI-BIOL, V79, P175, DOI 10.1073/pnas.79.1.175	48	89	92	2	7	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	DEC 1	2007	179	11					7585	7592				8	Immunology	Immunology	237MK	WOS:000251378300047	18025204	
J	Rees, VW; Connolly, GN				Rees, Vaughan W.; Connolly, Gregory N.			Measuring air quality to protect children from secondhand smoke in cars	AMERICAN JOURNAL OF PREVENTIVE MEDICINE			English	Article							ENVIRONMENTAL TOBACCO-SMOKE; NUTRITION EXAMINATION SURVEY; INFANT-DEATH-SYNDROME; 3RD NATIONAL-HEALTH; PASSIVE SMOKING; EXPOSURE; ASTHMA; HOME; HOUSEHOLDS; CHILDHOOD	Background: Secondhand tobacco smoke (SHS) is a major, preventable contributor to acute and chronic adverse health outcomes that affect children disproportionately. The predominant source of SHS among children is domestic exposure, and while up to two thirds of U.S. households have car smoking bans, an unacceptable number of children remain vulnerable. To help promote more effective protection through legislation, health communication strategies, or behavioral interventions, data demonstrating the adverse effect of SHS on air quality in cars are needed. Methods: Secondhand tobacco smoke in a motor vehicle under actual driving conditions was monitored by measuring respirable suspended particles (RSPs) of less than 2.5 microns in diameter, and carbon monoxide. Forty-five driving trials were conducted, using teams of volunteer drivers and smokers recruited from the general community. Three smoking conditions (nonsmoking baseline, active smoking, and immediate post-smoking period, each 5 minutes) were crossed with two ventilation conditions (windows open, closed) in a 3 x 2 within-sessions factorial design. Results: The highest mean observed RSP level was 271 mu g/m(3), which is unsafe, particularly for children. Peak RSP levels were considerably higher. RSPs and carbon monoxide increased significantly from baseline after smoking, and these increases were greatest during the closed ventilation condition, compared with open ventilation. Conclusions: Private passenger cars are a domestic environment with the potential to yield unsafe levels of SHS contaminants. These data may assist policymakers and health advocates to promote protective strategies to ensure smoke-free domestic environments for children.	Harvard Univ, Sch Publ Hlth, Div Publ Hlth Practice, Boston, MA 02115 USA	Rees, VW (reprint author), Harvard Univ, Sch Publ Hlth, Div Publ Hlth Practice, Landmark Bldg,Level 3 E,677 Huntington Ave, Boston, MA 02115 USA.	vrees@hsph.harvard.cdu					Adair-Bischoff CE, 1998, ARCH PEDIAT ADOL MED, V152, P127; *AM LEG FDN, 2006, DONT PASS GAS; BAUMAN A, 1995, BRIT MED J, V311, P1164; *CAL ENV PROG AG, 1997, HLTH EFF EXP ENV TOB; Connolly GN, 2005, EVALUATION MASSACHUS; CROCKER P J, 1985, Journal of Emergency Medicine, V3, P443, DOI 10.1016/0736-4679(85)90002-2; EMMONS KM, 1994, HEALTH PSYCHOL, V13, P516, DOI 10.1037//0278-6133.13.6.516; EMMONS KM, 1992, AM J PUBLIC HEALTH, V82, P24, DOI 10.2105/AJPH.82.1.24; Emmons KM, 2001, PEDIATRICS, V108, P18, DOI 10.1542/peds.108.1.18; Gehrman CA, 2003, NICOTINE TOB RES, V5, P289, DOI 10.1080/1462220031000094231; Gergen P.J, 1998, PEDIATRICS, P101; Gilpin E A, 1999, Nicotine Tob Res, V1, P153, DOI 10.1080/14622299050011261; Gurkan F, 2000, EUR J EPIDEMIOL, V16, P465, DOI 10.1023/A:1007658411953; Halterman JS, 2006, AMBUL PEDIATR, V6, P115, DOI 10.1016/j.ambp.2005.10.004; Jaakkola JJK, 2001, ENVIRON HEALTH PERSP, V109, P579, DOI 10.2307/3455031; Jedrychowski W, 1997, ENVIRON HEALTH PERSP, V105, P302, DOI 10.1289/ehp.97105302; Keppel G., 1991, DESIGN ANAL RES HDB; KLONOFFCOHEN HS, 1995, JAMA-J AM MED ASSOC, V273, P795, DOI 10.1001/jama.273.10.795; Mannino DM, 2002, CHEST, V122, P409, DOI 10.1378/chest.122.2.409; Matt GE, 2000, HEALTH PSYCHOL, V19, P232, DOI 10.1037//0278-6133.19.3.232; Matt GE, 2004, TOB CONTROL, V13, P29, DOI 10.1136/tc.2003.003889; MITCHELL EA, 1993, PEDIATRICS, V91, P893; Nardini S, 2004, Monaldi Arch Chest Dis, V61, P183; *NEW YORK STAT DEP, 2005, NEW YORK STAT DEP HL; Norman GJ, 1999, PREV MED, V29, P581, DOI 10.1006/pmed.1999.0574; Ott W, 1992, J EXPO ANAL ENV EPID, V2, P175; Park JH, 1998, J EXPO ANAL ENV EPID, V8, P65; Pirkle JL, 1996, JAMA-J AM MED ASSOC, V275, P1233; REPACE JL, 1980, SCIENCE, V208, P464, DOI 10.1126/science.7367873; Roberts LM, 1996, MED J AUSTRALIA, V165, P350; SCHUSTER MA, 2002, ARCH PEDIAT ADOLESC, V156, P1095; Strachan DP, 1997, THORAX, V52, P905; Thaqi A, 2005, INDOOR AIR, V15, P302, DOI 10.1111/j.1600-0668.2005.00361.x; Travers M. J., 2004, Morbidity and Mortality Weekly Report, V53, P1040; U.S. DHHS, 2000, RED TOB US REP SURG; *US EPA, 1993, RESP HLTH EFF PASS S, V4; *US EPA, AIR QUAL GUID PART P; *US EPA, 2005, AIR QUAL CRIT PART M; Wakefield M, 2000, AM J PREV MED, V19, P188, DOI 10.1016/S0749-3797(00)00197-5; YIOW L, 2005, CAR HOME SMOKE FREE; Zhou RQ, 2000, MUTAT RES-GEN TOX EN, V465, P191, DOI 10.1016/S1383-5718(99)00229-6	41	89	89	0	10	ELSEVIER SCIENCE INC	NEW YORK	360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA	0749-3797			AM J PREV MED	Am. J. Prev. Med.	NOV	2006	31	5					363	368		10.1016/j.ampere.2006.07.021		6	Public, Environmental & Occupational Health; Medicine, General & Internal	Public, Environmental & Occupational Health; General & Internal Medicine	098RX	WOS:000241541600002	17046406	
J	Ribas-Fito, N; Ramon, R; Ballester, F; Grimalt, J; Marco, A; Olea, N; Posada, M; Rebagliato, M; Tardon, A; Torrent, M; Sunyer, J				Ribas-Fito, Nuria; Ramon, Rosa; Ballester, Ferran; Grimalt, Joan; Marco, Alfredo; Olea, Nicolas; Posada, Manuel; Rebagliato, Marisa; Tardon, Adonina; Torrent, Maties; Sunyer, Jordi		INMA Study Grp	Child health and the environment: The INMA spanish study	PAEDIATRIC AND PERINATAL EPIDEMIOLOGY			English	Article						longitudinal cohort study; prenatal exposures; pollution; diet; genetics; study design; biological samples; childhood growth; child development; endocrine disruptors	OXIDATIVE STRESS; POLYCHLORINATED-BIPHENYLS; PRENATAL EXPOSURE; ARACHIDONIC-ACID; AIR-POLLUTANTS; BIRTH-WEIGHT; ASTHMA; PREECLAMPSIA; SUPPLEMENTATION; PREGNANCY	The INMA (INfancia y Medio Ambiente [Environment and Childhood]) is a population-based cohort study in different Spanish cities, that focuses on prenatal environmental exposures and growth, development and health from early fetal life until childhood. The study focuses on five primary areas of research: (1) growth and physical development; (2) behavioural and cognitive development; (3) asthma and allergies; (4) sexual and reproductive development; and (5) environmental exposure pathways. The general aims of the project are: (1) to describe the degree of individual prenatal exposure to environmental pollutants, and the internal dose of chemicals during pregnancy, at birth and during childhood in Spain; (2) to evaluate the impact of the exposure to different contaminants on fetal and infant growth, health and development; (3) to evaluate the role of diet on fetal and infant growth, health and development; and (4) to evaluate the interaction between persistent pollutants, nutrients and genetic determinants on fetal and infant growth, health and development. Extensive assessments will be carried out on 3100 pregnant women and children. Data will be collected by physical examinations, questionnaires, interviews, ultrasound and biological samples. Pregnant women are being assessed at 12, 20 and 32 weeks of gestation to collect information about environmental exposures and fetal growth. The children will be followed until the age of 4 years.	Inst Municipal Invest Med, Resp & Environm Hlth Res Unit, E-08003 Barcelona, Spain; Inst Invest Quim & Ambientals, Barcelona, Spain; Univ Pompeu Fabra, Barcelona, Spain; Univ Alicante, Dept Salud Publ, E-03080 Alicante, Spain; Escola Valenciana Estudis Salut CS GV, Valencia, Spain; Hosp Univ La Fe, CS GV, Valencia, Spain; Hosp Univ San Cecilio SAS UGR, Granada, Spain; Inst Invest Enfermedades Raras ISCIII, Madrid, Spain; Univ Oviedo, Oviedo, Spain; Area Salut Menorca IB Salut, Mao, Spain	Ribas-Fito, N (reprint author), Inst Municipal Invest Med, Resp & Environm Hlth Res Unit, C Dr Aiguader,80, E-08003 Barcelona, Spain.	nribas@imim.es	Grimalt, Joan/E-2073-2011; Olea, Nicolas/H-3198-2014; Sunyer, J/G-6909-2014	Grimalt, Joan/0000-0002-7391-5768; Olea, Nicolas/0000-0002-8938-3743; Sunyer, J/0000-0002-2602-4110; Posada, Manuel/0000-0002-8372-4180			Birch EE, 1998, PEDIATR RES, V44, P201, DOI 10.1203/00006450-199808000-00011; Chappell LC, 2002, AM J OBSTET GYNECOL, V187, P777, DOI 10.1067/mob.2002.125735; Counter SA, 2004, TOXICOL APPL PHARM, V198, P209, DOI 10.1016/j.taap.2003.11.032; Daniels JL, 2004, EPIDEMIOLOGY, V15, P394, DOI 10.1097/01.ede.0000129514.46451.ce; Grandjean P, 2003, AM J CLIN NUTR, V77, P715; Helland I. B., 2003, PEDIATRICS, V111, P39; Hornstra G., 2000, AM J CLIN NUTR, V71, P1262; Hubbard R, 2004, THORAX, V59, P3; Hubel CA, 1999, P SOC EXP BIOL MED, V222, P222, DOI 10.1046/j.1525-1373.1999.d01-139.x; Jacobson JL, 2003, J PEDIATR-US, V143, P780, DOI 10.1067/S0022-3476(03)00577-8; Lacasana M, 2005, EUR J EPIDEMIOL, V20, P183, DOI 10.1007/s10654-004-3005-9; Lin M, 2004, AM J EPIDEMIOL, V159, P294, DOI 10.1093/aje/kwh043; Nieuwenhuijsen MJ, 2002, EPIDEMIOLOGY, V13, P725, DOI 10.1097/01.EDE.0000030722.16351.91; Ribas-Fito N, 2003, PEDIATRICS, V111, pE580, DOI 10.1542/peds.111.5.e580; Roberts JM, 1999, LANCET, V354, P788; Romieu I, 2002, AM J RESP CRIT CARE, V166, P703, DOI 10.1164/rccm.2112074; Rumchev K, 2004, THORAX, V59, P746, DOI 10.1136/thx.2003.013680; Vreugdenhil HJI, 2004, DEV MED CHILD NEUROL, V46, P398, DOI 10.1017/S0012162204000647; Weiss B, 2000, ENVIRON HEALTH PERSP, V108, P375, DOI 10.2307/3454523; WEISSKOPF MG, 2005, ENVIRON RES, V97, P148; Williams C, 2001, AM J CLIN NUTR, V73, P316; Wright JM, 2004, ENVIRON HEALTH PERSP, V112, P920, DOI 10.1289/ehp.6779	22	89	89	2	14	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0269-5022			PAEDIATR PERINAT EP	Paediatr. Perinat. Epidemiol.	SEP	2006	20	5					403	410		10.1111/j.1365-3016.2006.00745.x		8	Public, Environmental & Occupational Health; Obstetrics & Gynecology; Pediatrics	Public, Environmental & Occupational Health; Obstetrics & Gynecology; Pediatrics	073YA	WOS:000239777400005	16911019	
J	Yu, JW; Kagan, R; Verreault, N; Nicolas, N; Joseph, L; Pierre, YS; Clarke, A				Yu, Joyce W.; Kagan, Rhoda; Verreault, Nina; Nicolas, Nathalie; Joseph, Lawrence; Pierre, Yvan St.; Clarke, Ann			Accidental ingestions in children with peanut allergy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						peanut allergy; accidental ingestion; treatment; peanut safe policies	TREE-NUT-ALLERGY; SKIN PRICK TESTS; NATURAL-HISTORY; FOOD ALLERGY; HYPERSENSITIVITY REACTIONS; ANAPHYLACTIC REACTIONS; IGE CONCENTRATIONS; PREVALENCE; ADOLESCENTS; RESOLUTION	Background: Accidental exposure to peanut has been reported to occur frequently. Total avoidance of peanut is difficult because of its widespread use, manufacturing and labeling errors, utensil contamination, and label misinterpretation. Objective: Given the apparent increased awareness of peanut allergy by both consumers and food manufacturers, we aimed to determine the current frequency of accidental exposures occurring in peanut allergic children in Quebec and to identify factors associated with exposure. Methods: The parents of children with peanut allergy diagnosed at the Montreal Children's Hospital completed questionnaires about accidental exposure to peanut occurring over the period of the preceding year. Logistic regression was used to identify associated factors. Results: Of 252 children, 62% were boys, with a mean age of 8.1 years (SD, 2.9). The mean age at diagnosis was 2.0 years (SD, 2.1). Thirty-five accidental exposures occurred in 29 children over a period of 244 patient-years, yielding an annual incidence rate of 14.3% (95% CI, 10.0% to 19.9%). Fifteen reactions were mild, 16 moderate, and 4 severe. Of 20 reactions that were moderate to severe, only 4 received epinephrine. Eighty percent of children attended schools prohibiting peanut, and only 1 accidental exposure occurred at school. No associated factors were identified. Conclusion: Accidental exposure to peanut occurs at a lower frequency than previously reported, but most reactions are managed inappropriately. Clinical implications: Enhanced awareness, access to safer environments, and good food manufacturing practices may have contributed to a lower incidence of inadvertent peanut exposure, but a further reduction and better education on allergy management are desirable.	McGill Univ, Div Clin Immunol & Allergy, Ctr Hlth, Montreal, PQ H3G 1A4, Canada; McGill Univ, Div Pediat Allergy & Clin Immunol, Ctr Hlth, Montreal, PQ H3G 1A4, Canada; McGill Univ, Div Clin Epidemiol, Ctr Hlth, Montreal, PQ H3G 1A4, Canada; McGill Univ, Dept Epidemiol & Biostat, Montreal, PQ H3G 1A4, Canada	Clarke, A (reprint author), McGill Univ, Div Clin Immunol & Allergy, Ctr Hlth, 1650 Cedar Ave,L10-413, Montreal, PQ H3G 1A4, Canada.	ann.clarke@mcgill.ca					Al-Muhsen S, 2003, CAN MED ASSOC J, V168, P1279; Avery NJ, 2003, PEDIATR ALLERGY IMMU, V14, P378, DOI 10.1034/j.1399-3038.2003.00072.x; Banerjee D. 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Allergy Clin. Immunol.	AUG	2006	118	2					466	472		10.1016/j.jaci.2006.04.024		7	Allergy; Immunology	Allergy; Immunology	075IH	WOS:000239877700024	16890773	
J	Bleck, B; Tse, DB; Jaspers, I; de Lafaille, MAC; Reibman, J				Bleck, B; Tse, DB; Jaspers, I; de Lafaille, MAC; Reibman, J			Diesel exhaust particle-exposed human bronchial epithelial cells induce dendritic cell maturation	JOURNAL OF IMMUNOLOGY			English	Article							COLONY-STIMULATING FACTOR; AMBIENT PARTICULATE MATTER; REGULATORY T-CELLS; GM-CSF; INFLAMMATORY RESPONSE; TRANSGENE EXPRESSION; ASTHMA; ANTIGEN; SENSITIZATION; TOLERANCE	Increased exposure to air pollutants such as diesel exhaust particles (DEP) has been proposed as one mechanism to explain the rise in allergic disorders. However, the immunologic mechanisms by which DEP enhance allergic sensitization and asthma remain unclear. We hypothesized that DEP act as an adjuvant for immature dendritic cell (DC) maturation via its effect on airway epithelial cell-derived microenvironment for DC. Immature monocyte-derived DC (iMDDC) failed to undergo phenotypic (CD80, CD83, CD86) or functional (T cell activation) maturation in response to exposure to DEP (0.001-100 mu g/ml). In contrast, primary cultures of human bronchial epithelial cells (HBEC) treated with DEP induced iMDDC phenotypic maturation (2.6 +/- 0.1-fold increase in CD83 expression, n = 4, p < 0.05) and functional maturation (2.6 +/- 0.2-fold increase in T cell activation, n = 4, p < 0.05). Functional maturation of iMDDC was induced by conditioned medium derived from DEP-treated HBEC, and was inhibited in cultures with DEP-treated HBEC and blocking Abs against GM-CSF, or GM-CSF-targeted small interfering RNA. These data suggest that DEP induce Ag-independent DC maturation via epithelial cell-DC interactions mediated by HBEC-derived GM-CSF. Although additional signals may be required for polarization of DC, these data suggest a novel mechanism by which environmental pollutants alter airway immune responses.	NYU, Sch Med, Dept Med, New York, NY 10016 USA; NYU, Sch Med, Div Pulm & Crit Care Med, New York, NY 10016 USA; NYU, Sch Med, Div Infect Dis, New York, NY 10016 USA; NYU, Sch Med, Dept Environm Med, New York, NY 10016 USA; NYU, Sch Med, Dept Pathol, New York, NY 10016 USA; NYU, Sch Med, Skirball Inst Biomol Med, Mol Pathogenesis Program, New York, NY 10016 USA; Univ N Carolina, Ctr Environm Med Asthma & Lung Biol, Chapel Hill, NC 27599 USA	Reibman, J (reprint author), NYU, Sch Med, Dept Med, 550 1st Ave,Room NB7N24, New York, NY 10016 USA.	reibmj01@gcrc.med.nyu.edu			NCRR NIH HHS [M01RR00096]; NIAID NIH HHS [AI27742-129007, AI44729]; NIEHS NIH HHS [ES013611]		Akbari O, 2002, NAT MED, V8, P1024, DOI 10.1038/nm745; Beasley R, 2000, J ALLERGY CLIN IMMUN, V105, pS466, DOI 10.1016/S0091-6749(00)90044-7; Becker S, 2005, TOXICOL APPL PHARM, V203, P45, DOI 10.1016/j.taap.2004.07.007; Beckwith CI, 2002, BRILLS TIBET STU LIB, V2, P27; Boisleve F, 2005, TOXICOLOGY, V206, P233, DOI 10.1016/j.tox.2004.08.015; Boland S., 1999, AM J PHYSIOL, V276, P604; Bonvallot V, 2002, BIOFACTORS, V16, P15; Byrd RS, 2006, CURR OPIN PULM MED, V12, P68, DOI 10.1097/01.mcp.0000199001.68908.45; Cates EC, 2003, J ALLERGY CLIN IMMUN, V111, P1076, DOI 10.1067/mai.2003.1460; Cohn L, 2004, ANNU REV IMMUNOL, V22, P789, DOI 10.1146/annurev.immunol.22.012703.104716; COZENS AL, 1994, AM J RESP CELL MOL, V10, P38; de Jong EC, 2005, SPRINGER SEMIN IMMUN, V26, P289, DOI 10.1007/s00281-004-0167-1; de Lafaille MAC, 2001, J EXP MED, V194, P1349, DOI 10.1084/jem.194.9.1349; DeMarini DM, 2004, ENVIRON HEALTH PERSP, V112, P814; Dhodapkar MV, 2001, J EXP MED, V193, P233, DOI 10.1084/jem.193.2.233; Diaz-Sanchez D, 2005, AM J PHYSIOL-LUNG C, V289, pL722, DOI 10.1152/ajplung.00217.2005; Diaz-Sanchez D, 1999, J ALLERGY CLIN IMMUN, V104, P1183; Gruchalla RS, 2005, J ALLERGY CLIN IMMUN, V115, P478, DOI 10.1016/j.jaci.2004.12.006; Hauben E, 2005, MICROBES INFECT, V7, P1023, DOI 10.1016/j.micinf.2005.03.027; HOLT PG, 1990, INT ARCH ALLER A IMM, V91, P155; Holt PG, 2000, J AEROSOL MED, V13, P361, DOI 10.1089/jam.2000.13.361; Kalia R, 1999, COMPUT SCI ENG, V1, P2; Kapsenberg ML, 2003, NAT REV IMMUNOL, V3, P984, DOI 10.1038/nri1246; Langenkamp A, 2000, NAT IMMUNOL, V1, P311, DOI 10.1038/79758; Lei XF, 1998, CLIN EXP IMMUNOL, V113, P157; Li N, 2003, CLIN IMMUNOL, V109, P250, DOI 10.1016/j.clim.2003.08.006; MCWILLIAM AS, 1994, J EXP MED, V179, P1331, DOI 10.1084/jem.179.4.1331; Mellman I, 2001, CELL, V106, P255, DOI 10.1016/S0092-8674(01)00449-4; Ohtoshi T, 1998, J ALLERGY CLIN IMMUN, V101, P778, DOI 10.1016/S0091-6749(98)70307-0; Pasare C, 2005, ADV EXP MED BIOL, V560, P11; Pourazar J, 2005, AM J PHYSIOL-LUNG C, V289, pL724, DOI 10.1152/ajplung.00055.2005; Reddy A, 1997, BLOOD, V90, P3640; Reibman J, 2000, J IMMUNOL, V165, P1618; Reibman J, 2003, AM J RESP CELL MOL, V28, P648, DOI 10.1165/rcmb.2002-00950C; Reibman J, 2002, AM J RESP CELL MOL, V27, P455, DOI 10.1165/rcmb.2001-0005OC; Rescigno M, 2001, NAT IMMUNOL, V2, P361, DOI 10.1038/86373; Riedl M, 2005, J ALLERGY CLIN IMMUN, V115, P221, DOI 10.1016/j.jaci.2004.11.047; Sakaguchi S, 2000, CELL, V101, P455, DOI 10.1016/S0092-8674(00)80856-9; Singh P, 2004, ENVIRON HEALTH PERSP, V112, P820, DOI 10.1289/ehp.6579; Stampfli MR, 1998, J CLIN INVEST, V102, P1704, DOI 10.1172/JCI4160; Steinman RM, 2003, PATHOL BIOL, V51, P59, DOI 10.1016/S0369-8114(03)00096-8; Steinman RM, 2002, P NATL ACAD SCI USA, V99, P351, DOI 10.1073/pnas.231606698; Swirski FK, 2002, J IMMUNOL, V169, P3499; Takizawa Hajime, 2004, Curr Opin Allergy Clin Immunol, V4, P355, DOI 10.1097/00130832-200410000-00005; Upham JW, 2005, CURR OPIN ALLERGY CL, V5, P167, DOI 10.1097/01.all.0000162310.79555.ed; Van Rijt LS, 2005, CLIN EXP ALLERGY, V35, P1125, DOI 10.1111/j.1365-2222.2005.02321.x; von Boehmer H, 2005, NAT IMMUNOL, V6, P338, DOI 10.1038/ni1180	47	89	93	1	4	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	JUN 15	2006	176	12					7431	7437				7	Immunology	Immunology	050QA	WOS:000238101800034	16751388	
J	Spurzem, JR; Rennard, SI				Spurzem, JR; Rennard, SI			Pathogenesis of COPD	SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE			English	Review						bronchitis; emphysema; peribronchiolar fibrosis; cigarette smoking; protease; antioxidant; repair	OBSTRUCTIVE-PULMONARY-DISEASE; NECROSIS-FACTOR-ALPHA; GROWTH-FACTOR-BETA; BRONCHOALVEOLAR LAVAGE FLUID; BRONCHIAL EPITHELIAL-CELLS; COLLAGEN GEL CONTRACTION; FIBROBLAST-MEDIATED CONTRACTION; HUMAN NEUTROPHIL ELASTASE; LOWER RESPIRATORY-TRACT; HUMAN LUNG FIBROBLASTS	Chronic obstructive pulmonary disease (COPD) is characterized and defined by limitation of expiratory airflow. This can result from several types of anatomical lesions, including loss of lung elastic recoil and fibrosis and narrowing of small airways. Inflammation, edema, and secretions also contribute variably to airflow limitation. Smoking can cause COPD through several mechanisms. First, smoke is a powerful inducer of an inflammatory response. Inflammatory mediators, including oxidants and proteases, are believed to play a major role in causing lung damage. Smoke can also alter lung repair responses in several ways. Inhibition of repair may lead to tissue destruction that characterizes emphysema, whereas abnormal repair can lead to the peribronchiolar fibrosis that causes airflow limitation in small airways. Genetic factors likely play a major role and probably account for much of the heterogeneity susceptibility to smoke and other factors. Many factors may play a role, but to date, only alpha-1 protease inhibitor deficiency has been unambiguously identified. Exposures other than cigarette smoke can contribute to the development of COPD. Inflammation of the lower respiratory tract that results from asthma or other chronic disorders may also contribute to the development of fixed airway obstruction. COPD is not only a disease of the lungs but is also a systemic inflammatory disorder. Muscular weakness, increased risk for atherosclerotic vascular disease, depression, osteoporosis, and abnormalities in fluids and electrolyte balance may all be consequences of COPD. Advances in understanding the pathogenesis of COPD have the potential for identifying new therapeutic targets that could alter the natural history of this devastating disorder.	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Respir. Crit. Care Med.	APR	2005	26	2					142	153		10.1055/s-2005-869535		12	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	922UU	WOS:000228866200003	16088433	
J	Smith, LA; Hatcher-Ross, JL; Wertheimer, R; Kahn, RS				Smith, LA; Hatcher-Ross, JL; Wertheimer, R; Kahn, RS			Rethinking race/ethnicity, income, and childhood asthma: Racial/ethnic disparities concentrated among the very poor	PUBLIC HEALTH REPORTS			English	Article							INNER-CITY CHILDREN; SOCIOECONOMIC-STATUS; PEDIATRIC ASTHMA; INDOOR ALLERGENS; MEDICATION-USE; RISK-FACTORS; MANAGEMENT-PRACTICES; COCKROACH ALLERGEN; ETHNIC-DIFFERENCES; HEALTH-SERVICES	Objective. Past studies of the prevalence of childhood asthma have yielded conflicting findings as to whether racial/ethnic disparities remain after other factors such as, income, are taken into account. The objective of this study was to examine the association of race/ethnicity and family income with the prevalence of childhood asthma and to assess whether racial/ethnic disparities vary by income strata. Methods. Cross-sectional data on 14,244 children aged < 18 years old in the 1997 National Health Interview Survey were examined. The authors used logistic regression to analyze the independent and joint effects of race/ethnicity and income-to-federal poverty level (FPL) ratio, adjusting for demographic covariates. The main outcome measure was parental report of the child having ever been diagnosed with asthma. Results. Bivariate analyses, based on weighted percentages, revealed that asthma was more prevalent among non-Hispanic black children (13.6%) than among non-Hispanic white children (11.2%; p < 0.01), but the prevalence of asthma did not differ significantly between Hispanic children (10.1%) and non-Hispanic white children (11.2%; p = 0.13). Overall, non-Hispanic black children were at higher risk for asthma than non-Hispanic white children (adjusted odds ratio [OR]= 1.20; 95% confidence interval [CI] 1.03, 1.40), after adjustment for sociodemographic variables, including the ratio of annual family income to the FPL. Asthma prevalence did not differ between Hispanic children and non-Hispanic white children in adjusted analyses (adjusted OR = 0.85; 95% CI 0.71, 1.02). Analyses stratified by income revealed that only among children from families with incomes less than half the FPL did non-Hispanic black children have a higher risk of asthma than non-Hispanic white children (adjusted OR = 1.99; 95% CI 1.09, 3.64). No black vs. white differences existed at other income levels. Subsequent analyses of these very poor children that took into account additional potentially explanatory variables did not attenuate the higher asthma risk for very poor non-Hispanic black children relative to very poor non-Hispanic white children. Conclusions. Non-Hispanic black children were at substantially higher risk of asthma than non-Hispanic white children only among the very poor. The concentration of racial/ethnic differences only among the very poor suggests that patterns of social and environmental exposures must overshadow any hypothetical genetic risk.	Boston Univ, Med Ctr, Div Gen Pediat, Dept Pediat, Boston, MA 02118 USA; Boston Univ, Sch Med, Boston, MA 02118 USA; Univ Minnesota, Dept Educ Psychol, Counseling & Student Personnel Psychol Program, Minneapolis, MN 55455 USA; Child Trends Inc, Washington, DC USA; Childrens Hosp, Med Ctr, Div Gen & Community Pediat, Cincinnati, OH 45229 USA	Smith, LA (reprint author), Boston Univ, Med Ctr, Div Gen Pediat, Dept Pediat, Matern Bldg,4th Floor,91 E Concord St, Boston, MA 02118 USA.	lauren.smith@bmc.org			NICHD NIH HHS [K23 HD40362-01]		Akinbami LJ, 2002, AMBUL PEDIATR, V2, P382, DOI 10.1367/1539-4409(2002)002<0382:RAIDIC>2.0.CO;2; Aligne CA, 2000, AM J RESP CRIT CARE, V162, P873; Braveman P, 2001, PUBLIC HEALTH REP, V116, P449, DOI 10.1016/S0033-3549(04)50073-0; Butz AM, 2000, ARCH PEDIAT ADOL MED, V154, P984; 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; Cooper RS, 2003, NEW ENGL J MED, V348, P1166, DOI 10.1056/NEJMsb022863; 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MAR-APR	2005	120	2					109	116				8	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	915JW	WOS:000228301500003	15842111	
J	Marotta, A; Klinnert, MD; Price, MR; Larsen, GL; Liu, AH				Marotta, A; Klinnert, MD; Price, MR; Larsen, GL; Liu, AH			Impulse oscillometry provides an effective measure of lung dysfunction in 4-year-old children at risk for persistent asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; atopy; children; early intervention; lung function; bronchodilator response; impulse oscillometry; spirometry	FORCED OSCILLATION TECHNIQUE; CHILDHOOD ASTHMA; AIRWAY-OBSTRUCTION; METHACHOLINE RESPONSIVENESS; INTERRUPTER TECHNIQUE; RESPIRATORY SYMPTOMS; PRESCHOOL-CHILDREN; YOUNG-CHILDREN; PEAK FLOW; COLD-AIR	Background: Objective lung function measurements are routinely used to diagnose and manage asthma, but their utility for young children has not been defined. Objective: Bronchodilator responses were measured by means of impulse oscillometry (IOS) and compared with conventional spirometry to determine the value of lung function measures in 4-year-old asthma-prone children. Methods: The study participants were in the Childhood Asthma Prevention Study (National Institute of Health/National Institute of Allergy and Infectious Diseases) and at risk for asthma. At age 4 years, concurrent asthma was determined by using a previously validated modified American Thoracic Society questionnaire. Children performed IOS and spirometry before and after albuterol administration and underwent skin prick testing to 13 common allergens to assess atopy. IOS measures were as follows: airways resistance at 5 Hz and 10 Hz, airways reactance at 5 Hz and 10 Hz, and resonant frequency. Results: Asthmatic patients versus nonasthmatic patients significantly differed in their IOS-assessed bronchodilator responses through Delta resistance at 5 Hz (medians, 27% vs 17%; P = .02) and Delta resistance at 10 Hz (24% vs 16%; P = .03). Because atopic children who have frequent wheezing are at risk for persistent asthma, the data were analyzed in regard to atopic patients with or without asthma. IOS strongly distinguished atopic asthmatic children through A resistance at 5 Hz (36% vs 13 %, P = .007), Delta resistance at 10 Hz (25% vs 11%, P = .02), and Delta reactance at 10 Hz (47 % vs 12 %, P = .03). Conventional spirometry did not establish similar statistically significant findings. Conclusion: IOS bronchodilator responses are remarkably abnormal in 4-year-old children, who are most likely to have persistent asthma. IOS is a useful diagnostic tool in early asthma development and might be a helpful objective outcome measure of early interventions.	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Allergy Clin. Immunol.	AUG	2003	112	2					317	322		10.1067/mai.2003.1627		6	Allergy; Immunology	Allergy; Immunology	709WY	WOS:000184650600015	12897737	
J	Perez-Machado, MA; Ashwood, P; Thomson, MA; Latcham, F; Sim, R; Walker-Smith, JA; Murch, SH				Perez-Machado, MA; Ashwood, P; Thomson, MA; Latcham, F; Sim, R; Walker-Smith, JA; Murch, SH			Reduced transforming growth factor-beta 1-producing T cells in the duodenal mucosa of children with food allergy	EUROPEAN JOURNAL OF IMMUNOLOGY			English	Article						food allergy; lymphocytes; TGF-beta; celiac disease	INFLAMMATORY-BOWEL-DISEASE; ATOPIC DISEASE; EXPRESSION; BETA; PROBIOTICS; INDUCTION; IMMUNITY; INFANTS; ANTIGEN; PROTEIN	Infant food allergies are increasing, and many breast-fed infants now sensitize to maternally-ingested antigens. As low-dose oral tolerance requires generation of suppressor lymphocytes producing TGF-beta1 (Th3 cells), we studied these cells in duodenal biopsies after diagnostic endoscopy. Spontaneous production of Th1, Th2 and Th3 cytokines by duodenal lymphocytes was studied using flow cytometry in 20 children with no eventual clinicopathological diagnosis (controls), 30 children with multiple food allergy, nine with celiac disease and six with inflammatory enteropathies. Immunohistochemistry and in situ hybridization were used to localize TGF-beta1 protein and mRNA in matched biopsies. We found no significant Th1/Th2 skewing amongst mucosal lymphocytes in allergic children compared to controls, although celiac and inflammatory enteropathy patients showed increased Th1 responses. By contrast, the allergic children showed reduction of TGF-beta1(+) lymphocytes in both epithelial and lamina propria compartments. Reduction of TGF-beta1 expression was also seen in mononuclear cells and epithelium in food allergy by immunohistochemistry and in situ hybridization. The dominant mucosal abnormality in food allergic children was, thus, not Th2 deviation but impaired generation of Th3 cells. As generation of these cells requires innate immune response to enteric bacteria, we suggest that changing infectious exposures may inhibit primary establishment of basic oral tolerance mechanisms.	UCL Royal Free & Univ Coll, Sch Med, Ctr Paediat Gastroenterol, London NW3 2PF, England; UCL Royal Free & Univ Coll, Sch Med, Dept Histopathol, London, England	Murch, SH (reprint author), UCL Royal Free & Univ Coll, Sch Med, Ctr Paediat Gastroenterol, Royal Free Campus,Rowland Hill St, London NW3 2PF, England.	s.murch@rfc.ucl.ac.uk					Beyer K, 2002, J ALLERGY CLIN IMMUN, V109, P707, DOI 10.1067/mai.2002.122503; Bonen DK, 2003, GASTROENTEROLOGY, V124, P140, DOI 10.1053/gast.2003.50019; CAMPBELL DI, 2003, IN PRESS PEDIAT RES; Chung HL, 2002, J ALLERGY CLIN IMMUN, V109, P150, DOI 10.1067/mai.2002.120562; Forsthuber T, 1996, SCIENCE, V271, P1728, DOI 10.1126/science.271.5256.1728; Garba ML, 2001, J IMMUNOL METHODS, V258, P193, DOI 10.1016/S0022-1759(01)00491-4; Groux H, 1999, IMMUNOL TODAY, V20, P442, DOI 10.1016/S0167-5699(99)01510-8; Hansen G, 2000, J CLIN INVEST, V105, P61, DOI 10.1172/JCI7589; Hill DJ, 1999, ANN MED, V31, P272, DOI 10.3109/07853899908995890; Hooper LV, 2001, SCIENCE, V292, P1115, DOI 10.1126/science.1058709; Isolauri E, 1999, J PEDIATR-US, V134, P27, DOI 10.1016/S0022-3476(99)70368-9; JUNG T, 1993, J IMMUNOL METHODS, V159, P197, DOI 10.1016/0022-1759(93)90158-4; Kalliomaki M, 2001, LANCET, V357, P1076, DOI 10.1016/S0140-6736(00)04259-8; LATCHAM F, 2003, IN PRESS J PEDIAT; LINDFORS A, 1988, ALLERGY, V43, P11, DOI 10.1111/j.1398-9995.1988.tb02038.x; Lionetti P, 1999, J PEDIATR GASTR NUTR, V29, P308, DOI 10.1097/00005176-199909000-00013; Matricardi PM, 2000, BRIT MED J, V320, P412, DOI 10.1136/bmj.320.7232.412; Mayer L, 2000, J PEDIATR GASTR NUTR, V30, pS4, DOI 10.1097/00005176-200001001-00002; MILLER A, 1994, EUR J IMMUNOL, V24, P1026, DOI 10.1002/eji.1830240503; Murch S, 1996, LANCET, V348, P1656, DOI 10.1016/S0140-6736(05)65716-9; Murch SH, 2000, CURR OPIN GASTROEN, V16, P552, DOI 10.1097/00001574-200011000-00016; Murch SH, 2001, LANCET, V357, P1057, DOI 10.1016/S0140-6736(00)04305-1; Newberry RD, 1999, NAT MED, V5, P900; Poltorak A, 1998, SCIENCE, V282, P2085, DOI 10.1126/science.282.5396.2085; Ridge JP, 1996, SCIENCE, V271, P1723, DOI 10.1126/science.271.5256.1723; Strober W, 1998, GASTROENTEROLOGY, V114, P214, DOI 10.1016/S0016-5085(98)70649-3; Sudo N, 1997, J IMMUNOL, V159, P1739; Taams LS, 2001, EUR J IMMUNOL, V31, P1122, DOI 10.1002/1521-4141(200104)31:4<1122::AID-IMMU1122>3.0.CO;2-P; von Mutius E, 1998, LANCET, V351, P862, DOI 10.1016/S0140-6736(97)10100-3; WALKERSMITH JA, 1999, DIS SMALL INTESTINE, P205; Weiner HL, 1997, IMMUNOL TODAY, V18, P335, DOI 10.1016/S0167-5699(97)01053-0; Xian CJ, 1999, SCAND J GASTROENTERO, V34, P591; Yazdanbakhsh M, 2002, SCIENCE, V296, P490, DOI 10.1126/science.296.5567.490	33	89	93	0	3	WILEY-BLACKWELL	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0014-2980			EUR J IMMUNOL	Eur. J. Immunol.	AUG	2003	33	8					2307	2315		10.1002/eji.200323308		9	Immunology	Immunology	709WC	WOS:000184648700028	12884306	
J	Stark, PC; Burge, HA; Ryan, LM; Milton, DK; Gold, DR				Stark, PC; Burge, HA; Ryan, LM; Milton, DK; Gold, DR			Fungal levels in the home and lower respiratory tract illnesses in the first year of life	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						fungi; respiratory tract infections; infants; public health	INDOOR ALLERGEN LEVELS; CHILDHOOD ASTHMA; CHILDREN; DAMPNESS; HEALTH; SPORES; ASSOCIATIONS; PREDICTORS; ACTIVATION; DISEASES	The association between home dampness and lower respiratory symptoms in children has been well documented. Whether fungal exposures contribute to this association is uncertain. In a prospective birth cohort of 499 children of parents with asthma/allergies, we examined in-home fungal concentrations as predictors of lower respiratory illnesses (LRI) (croup, pneumonia, bronchitis, and bronchiolitis) in the first year. In multivariate analyses, we found a significant increased relative risk (RR) between LRI and high levels (more than the 90th percentile) of airborne Penicillium (RR = 1.73, 95% confidence interval [CI], 1.23, 2.43), dust-borne Clodosporium (RR = 1.52; Cl, 1.02, 2.25), Zygornycetes (RR = 1.96; CI, 1.35, 2.83), and Alternaria (RR = 1.51; CI, 1.00, 2.28), after controlling for sex, presence of water damage or visible mold/mildew, born in winter, breastfeeding, and being exposed to other children through siblings. In a multivariate analysis, the RR of LRI was elevated in households with any fungal level at more than the 90th percentile (RR = 1.86; CI, 1.21, 2.88). Exposure to high fungal levels increased the risk of LRI in infancy, even for infants with nonwheezing LRI. Actual mechanisms remain unknown, but fungi and their components (glucans, mycotoxins, and proteins) may increase the risk of LRI by acting as irritants or through increasing susceptibility to infection.	Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Cambridge, MA 02138 USA; Tufts New England Med Ctr, Dept Med, Div Clin Care Res, Biostat Res Ctr, Boston, MA USA; Harvard Univ, Sch Publ Hlth, Dept Biostat, Cambridge, MA 02138 USA; Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Channing Lab, Boston, MA 02115 USA	Gold, DR (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	NIAID NIH HHS [AI/EHS35786]		ANDERSEN AA, 1958, J BACTERIOL, V76, P471; BRUNEKREEF B, 1989, AM REV RESPIR DIS, V140, P1363; Chew GL, 1999, ALLERGY, V54, P1058, DOI 10.1034/j.1398-9995.1999.00003.x; Chew GL, 1998, AM J RESP CRIT CARE, V157, P1536; Clark NM, 1999, ENVIRON HEALTH PERSP, V107, P421; Dales RE, 1999, ENVIRON HEALTH PERSP, V107, P481; Dharmage S, 2001, AM J RESP CRIT CARE, V164, P65; Garrett MH, 1998, CLIN EXP ALLERGY, V28, P459; GERBERICK GF, 1984, ENVIRON RES, V33, P246, DOI 10.1016/0013-9351(84)90021-5; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; Gold DR, 2000, ENVIRON HEALTH PERSP, V108, P643, DOI 10.2307/3454400; Halonen M, 1997, AM J RESP CRIT CARE, V155, P1356; Hegele RG, 2001, J PEDIATR-US, V138, P831, DOI 10.1067/mpd.2001.114479; Illi S, 2001, BRIT MED J, V322, P390, DOI 10.1136/bmj.322.7283.390; JAAKKOLA JJK, 1993, J EXPO ANAL ENV EPID, V3, P129; Johnston R, 2000, CLEARING AIR ASTHMA; Kauffman HF, 2000, J ALLERGY CLIN IMMUN, V105, P1185, DOI 10.1067/mai.2000.106210; Kilpelainen M, 2001, THORAX, V56, P462, DOI 10.1136/thorax.56.6.462; Koskinen OM, 1999, INT J ENVIRON HEAL R, V9, P143; MACHER J, 2000, BIOAEROSOLS ASSESSME; Nikulin M, 1997, FUND APPL TOXICOL, V35, P182, DOI 10.1006/faat.1996.2274; Oie L, 1999, EPIDEMIOLOGY, V10, P294, DOI 10.1097/00001648-199905000-00018; Park JH, 2001, ENVIRON HEALTH PERSP, V109, P859, DOI 10.2307/3454831; POPE AM, 1993, INDOOR ALLERGENS; ROBINSON D, 1993, J ALLERGY CLIN IMMUN, V92, P313, DOI 10.1016/0091-6749(93)90175-F; Rylander R, 1998, AM J RESP CRIT CARE, V158, P1685; Sorenson WG, 1999, ENVIRON HEALTH PERSP, V107, P469; SU HJ, 1992, APPL ENVIRON MICROB, V58, P181; Tibshirani R, 1997, STAT MED, V16, P385, DOI 10.1002/(SICI)1097-0258(19970228)16:4<385::AID-SIM380>3.0.CO;2-3; WEEMS JJ, 1987, J CLIN MICROBIOL, V25, P1459; WELLIVER RC, 1993, PEDIATR PULM, V15, P19, DOI 10.1002/ppul.1950150104	31	89	93	2	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.	JUL 15	2003	168	2					232	237		10.1164/rccm.200207-730OC		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	699XL	WOS:000184082000018	12724122	
J	Medeiros, M; Figueiredo, JP; Almeida, MC; Matos, MA; Araujo, MI; Cruz, AA; Atta, AM; Rego, MAV; de Jesus, AR; Taketomi, EA; Carvalho, EM				Medeiros, M; Figueiredo, JP; Almeida, MC; Matos, MA; Araujo, MI; Cruz, AA; Atta, AM; Rego, MAV; de Jesus, AR; Taketomi, EA; Carvalho, EM			Schistosoma mansoni infection is associated with a reduced course of asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; skin prick test; dust mites; helminths; Schistosoma mansoni; IL-10; IgE	INVERSE ASSOCIATION; ATOPY; REACTIVITY; EXPOSURE; ACTIVATION; ALLERGENS; CHILDREN; IL-10	Background: Helminthic infections decrease skin reactivity to indoor allergens, but data on whether they influence asthma severity are lacking. Objective: This study evaluated the course of asthma in patients with and without Schistosoma mansoni infection. Methods: Asthmatic subjects were enrolled from 3 low-socioeconomic areas: a rural area endemic for schistosomiasis (group 1) in addition to a rural area (group 2) and a slum area (group 3), both of which were not endemic for schistosomiasis. A questionnaire on the basis of the International Study of Asthma and Allergies in Childhood study was applied in these 3 areas, and from each area, 21 age- and sex-matched asthmatic subjects were selected for a prospective 1-year study. Pulmonary function tests, skin prick tests with indoor allergens, stool examinations, and serum evaluations were performed in these subjects. Every 3 months, the subjects were evaluated for asthma exacerbation through physical examination, and a questionnaire regarding asthma symptoms and use of antiasthma medicine was administered. Results: The prevalence of S mansoni infection was greater in group I compared with in groups 2 and 3 (P < .0001), whereas the frequency of other helminth and protozoa infections was similar among the 3 groups. The frequency of positive skin test responses to indoor allergens was less (19.0%) in group I subjects relative to those in group 2 (76.2%) and group 3 (57.1%; P < .001). The frequencies of symptoms, use of antiasthma drugs, and pulmonary abnormal findings at physical examination were less in group 1 subjects than in group 2 and 3 subjects (P = .0001). Conclusion: Our results suggest that S mansoni infection is associated with a milder course of asthma.	Hosp Univ Prof Edgar Santos, Serv Imunol, BR-40110160 Salvador, BA, Brazil; Inst Saude Coletiva, Salvador, BA, Brazil; Univ Fed Bahia, Dept Anal Clin & Toxicol, Salvador, BA, Brazil; Escola Baiana Med & Saude Publ, Salvador, BA, Brazil; Univ Fed Uberlandia, Dept Microbiol Immunol & Parasitol, BR-38400 Uberlandia, MG, Brazil	Medeiros, M (reprint author), Hosp Univ Prof Edgar Santos, Serv Imunol, Rua Joao Botas S-N,5 Andar, BR-40110160 Salvador, BA, Brazil.		Cruz, Alvaro/I-1676-2012	Cruz, Alvaro/0000-0002-7403-3871			Araujo MI, 2000, INT ARCH ALLERGY IMM, V123, P145, DOI 10.1159/000024433; Araujo MI, 1996, EUR J IMMUNOL, V26, P1399, DOI 10.1002/eji.1830260633; 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; BURROWS B, 1989, NEW ENGL J MED, V320, P271, DOI 10.1056/NEJM198902023200502; Catapani WR, 1997, J ALLERGY CLIN IMMUN, V100, P142; Cookson WOCM, 1997, SCIENCE, V275, P41, DOI 10.1126/science.275.5296.41; Cooper PJ, 2002, CLIN EXP IMMUNOL, V128, P398, DOI 10.1046/j.1365-2249.2002.01908.x; Howard TD, 2000, J ALLERGY CLIN IMMUN, V105, pS477, DOI 10.1016/S0091-6749(00)90046-0; HUSSAIN R, 1992, J IMMUNOL, V148, P2731; Kalliomaki M, 2001, J ALLERGY CLIN IMMUN, V107, P129, DOI 10.1067/mai.2001.111237; KATZ N, 1968, Revista do Instituto de Medicina Tropical de Sao Paulo, V10, P295; KATZ N, 1970, J PARASITOL, V56, P1032, DOI 10.2307/3277532; King CL, 1996, J IMMUNOL, V156, P4715; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; LINCH NR, 1998, J ALLERGY CLIN IMMUN, V101, P217; Liu AH, 2002, J ALLERGY CLIN IMMUN, V109, P379, DOI 10.1067/mai.2002.122157; LYNCH NR, 1993, J ALLERGY CLIN IMMUN, V92, P401; Matricardi PM, 2000, BRIT MED J, V320, P412, DOI 10.1136/bmj.320.7232.412; Medeiros M, 2002, J ALLERGY CLIN IMMUN, V109, pS139, DOI 10.1016/S0091-6749(02)81542-1; MOREL AM, 1988, J ALLERGY CLIN IMMUN, V82, P646, DOI 10.1016/0091-6749(88)90978-5; Royer B, 2001, CLIN EXP ALLERGY, V31, P694, DOI 10.1046/j.1365-2222.2001.01069.x; 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; van den Biggelaar AHJ, 2000, LANCET, V356, P1723, DOI 10.1016/S0140-6736(00)03206-2; Velupillai P, 2000, HUM IMMUNOL, V61, P225, DOI 10.1016/S0198-8859(99)00136-6; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; Weiss ST, 2000, J ALLERGY CLIN IMMUN, V105, P205, DOI 10.1016/S0091-6749(00)90067-8	28	89	97	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.	MAY	2003	111	5					947	951		10.1067/mai.2003.1381		5	Allergy; Immunology	Allergy; Immunology	679DA	WOS:000182904500006	12743556	
J	Morafo, V; Srivastava, K; Huang, CK; Kleiner, G; Lee, SY; Sampson, HA; Li, XM				Morafo, V; Srivastava, K; Huang, CK; Kleiner, G; Lee, SY; Sampson, HA; Li, XM			Genetic susceptibility to food allergy is linked to differential T(H)2-T(H)1 responses in C3H/HeJ and BALB/c mice	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						marine strains; food allergy susceptibility; T(H)2-T(H)1 cytokines	MAJOR PEANUT ALLERGEN; HOUSE-DUST ENDOTOXIN; T-CELL; IFN-GAMMA; MURINE MODEL; ATOPIC-DERMATITIS; IMMUNE-RESPONSES; INTERFERON-GAMMA; ORAL TOLERANCE; IL-10	Background: Although food allergy is a serious health problem in westernized countries, factors influencing the development of food allergy are largely unknown. Appropriate marine models of food allergy would be useful in understanding the mechanisms underlying food allergy in human subjects. Objective: We sought to determine the susceptibility of different strains of mice to food hypersensitivity. Methods: C3H/HeJ and BALB/c mice were sensitized to cow's milk (CM) or peanut by means of intragastric administration, with cholera toxin as a mucosal adjuvant. Mice were then challenged with CM or peanut Antigen-specific IgE levels, anaphylactic symptoms, plasma histamine levels, and splenocyte cytokine profiles of these 2 strains were compared. Results: CM-specific IgE levels were significantly increased only in the C3HMeJ strain, 87% of which exhibited systemic anaphylactic reactions accompanied by significantly increased plasma histamine levels in response to challenge. BALB/c mice exhibited no significant CM-specific IgE response, increased plasma histamine levels, or anaphylactic symptoms. After peanut challenge, 100% of peanut-sensitized C3H/HeJ mice exhibited high levels of peanut-specific IgE and anaphylactic symptoms. In contrast, no hypersensitivity reactions were detected in BALB/c mice, despite the presence of significant serum peanut-specific IgE levels. Splenocytes from CM- and peanut-sensitized C3H/HeJ mice exhibited significantly increased IL-4 and IL-10 secretion, whereas splenocytes from BALB/c mice exhibited significantly increased IFN-gamma secretion. Conclusion: induction of food-induced hypersensitivity reactions in mice is strain dependent, with C3H/HeJ mice being susceptible and BALB/c mice being resistant. This strain-dependent susceptibility to food allergy is associated with differential T(H)2-T(H)1 responses after intragastric food allergen sensitization.	CUNY Mt Sinai Sch Med, Dept Pediat, New York, NY 10029 USA	Morafo, V (reprint author), CUNY Mt Sinai Sch Med, Dept Pediat, 1 Gustave L Levy Pl, New York, NY 10029 USA.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	NIAID NIH HHS [P01-AI44236-01]		Atherton KT, 2002, ANN NY ACAD SCI, V964, P163; Barnes PJ, 2001, CLIN EXP ALLERGY, V31, P667, DOI 10.1046/j.1365-2222.2001.01118.x; Bashir MEH, 2002, J IMMUNOL, V169, P3284; BISSONNETTE EY, 1990, J IMMUNOL, V145, P3385; Bjorksten B, 2001, Curr Opin Allergy Clin Immunol, V1, P225, DOI 10.1097/01.all.0000011018.32315.1d; BURKS AW, 1992, J ALLERGY CLIN IMMUN, V90, P962, DOI 10.1016/0091-6749(92)90469-I; Dabbagh K, 2002, J IMMUNOL, V168, P4524; Daser A, 1998, INT ARCH ALLERGY IMM, V117, P239, DOI 10.1159/000024017; De Jong EC, 1998, CLIN EXP ALLERGY, V28, P743; DONON BJ, 1994, J ALLERGY CLIN IMMUN, V93, P93; FIORENTINO DF, 1989, J EXP MED, V170, P2081, DOI 10.1084/jem.170.6.2081; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; HEINZEL FP, 1994, INFECT IMMUN, V62, P4244; Helm RM, 2002, ANN NY ACAD SCI, V964, P139; Hourihane JO, 1997, CLIN EXP ALLERGY, V27, P634, DOI 10.1046/j.1365-2222.1997.d01-559.x; HSU DH, 1992, INT IMMUNOL, V4, P563, DOI 10.1093/intimm/4.5.563; *I LAB AN RES COMM, 1996, GUID CAR US LAB AN; JOHANSSON SGO, 1984, ANN ALLERGY, V53, P665; Lee HO, 2000, GASTROENTEROLOGY, V119, P129, DOI 10.1053/gast.2000.8542; Lee SY, 2001, CLIN IMMUNOL, V101, P220, DOI 10.1006/clim.2001.5122; Lewkowich IP, 2002, EUR J IMMUNOL, V32, P3536, DOI 10.1002/1521-4141(200212)32:12<3536::AID-IMMU3536>3.0.CO;2-U; Li XM, 1999, J ALLERGY CLIN IMMUN, V103, P206, DOI 10.1016/S0091-6749(99)70492-6; Li XM, 2000, J ALLERGY CLIN IMMUN, V106, P150, DOI 10.1067/mai.2000.107395; Li XM, 1999, J IMMUNOL, V162, P3045; Lin CC, 2000, IMMUNOL LETT, V73, P57, DOI 10.1016/S0165-2478(00)00200-5; MacDonald TT, 2000, INFLAMM BOWEL DIS, V6, P116; Maitland AL, 2001, J ALLERGY CLIN IMMUN, V107, pS140; Morafo V, 2002, J ALLERGY CLIN IMMUN, V109, pS287, DOI 10.1016/S0091-6749(02)82014-0; MOSMANN TR, 1986, J IMMUNOL, V136, P2348; MOWAT AM, 1986, IMMUNOLOGY, V58, P677; Nilsen EM, 1998, GASTROENTEROLOGY, V115, P551, DOI 10.1016/S0016-5085(98)70134-9; Oh JW, 2002, J ALLERGY CLIN IMMUN, V110, P460, DOI 10.1067/mai.2002.127512; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Pierkes M, 1999, J ALLERGY CLIN IMMUN, V103, P326, DOI 10.1016/S0091-6749(99)70509-9; Poltorak A, 1998, SCIENCE, V282, P2085, DOI 10.1126/science.282.5396.2085; Romagnani S, 2000, J ALLERGY CLIN IMMUN, V105, P399, DOI 10.1067/mai.2000.104575; ROMAGNANI S, 1991, IMMUNOL TODAY, V12, P256, DOI 10.1016/0167-5699(91)90120-I; Ruffilli A, 1997, ALLERGY, V52, P256, DOI 10.1111/j.1398-9995.1997.tb00990.x; Sampson HA, 1997, J ALLERGY CLIN IMMUN, V100, P444; Sampson HA, 2002, NEW ENGL J MED, V346, P1294, DOI 10.1056/NEJMcp012667; Sampson HA, 1999, J ALLERGY CLIN IMMUN, V103, P717, DOI 10.1016/S0091-6749(99)70411-2; Schade RP, 2000, J ALLERGY CLIN IMMUN, V106, P1155, DOI 10.1067/mai.2000.110802; Sicherer SH, 2002, ANN ALLERG ASTHMA IM, V88, P350; Strobel S, 2002, ANN NY ACAD SCI, V958, P47; VANNIER E, 1991, J CLIN INVEST, V87, P1936, DOI 10.1172/JCI115219; VOGEL SN, 1994, INFECT IMMUN, V62, P4454; Wong CK, 2001, CLIN EXP IMMUNOL, V125, P177, DOI 10.1046/j.1365-2249.2001.01602.x	47	89	94	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.	MAY	2003	111	5					1122	1128		10.1067/mai.2003.1463		7	Allergy; Immunology	Allergy; Immunology	679DA	WOS:000182904500030	12743580	
J	Phillips, C; Coward, WR; Pritchard, DI; Hewitt, CRA				Phillips, C; Coward, WR; Pritchard, DI; Hewitt, CRA			Basophils express a type 2 cytokine profile on exposure to proteases from helminths and house dust mites	JOURNAL OF LEUKOCYTE BIOLOGY			English	Article						hookworm; allergy; Dermatophagoides pteronyssinus	PERIPHERAL-BLOOD BASOPHILS; DER-P-I; ACTIVATED RECEPTORS; ENZYMATIC-ACTIVITY; TIGHT JUNCTIONS; IL-4 PRODUCTION; ALLERGEN; INTERLEUKIN-4; RELEASE; IGE	The proteolytic activities frequently associated with sources of allergens and parasite secretions have been suggested as important immunomodulators. We have investigated whether the protease activity of the house dust mite allergen Der p1. and the secreted proteases of the hookworm Necator americanus are able to directly induce type 2 cytokine production by basophils. Der p1 and the secretions of N. americanus induced interleukin (IL)-4, IL-5, and IL-13 but not interferon-gamma mRNA in KU812 basophils. Enzyme-linked immunosorbent assay confirmed that IL-4 and IL-13 were secreted. A nonproteolytic antigen failed to induce cytokine expression, and preincubation of Der p1. or N. americanus secretions with protease inhibitors inhibited cytokine expression. Data were confirmed using basophils purified from human peripheral blood. We speculate that this innate mechanism may contribute to the development of a cytokine milieu that could promote immunoglobulin E synthesis, eosinophil recruitment, and the development of type 2 T cells.	Univ Leicester, Dept Microbiol & Immunol, Inst Lung Hlth, Leicester LE1 9HN, Leics, England; Univ Nottingham, Sch Pharm, Sch Pharmaceut Sci, Nottingham, England	Hewitt, CRA (reprint author), Univ Leicester, Dept Microbiol & Immunol, Inst Lung Hlth, POB 138,Univ Rd, Leicester LE1 9HN, Leics, England.						Agis H, 1996, IMMUNOLOGY, V87, P535, DOI 10.1046/j.1365-2567.1996.493578.x; BROWN A, 1995, PARASITOLOGY, V110, P555; BRUNNER T, 1993, J EXP MED, V177, P605, DOI 10.1084/jem.177.3.605; Coughlin SR, 2000, NATURE, V407, P258, DOI 10.1038/35025229; Culley FJ, 2000, J IMMUNOL, V165, P6447; Dahinden CA, 1997, INT ARCH ALLERGY IMM, V113, P134; DEMEURE CE, 1994, J IMMUNOL, V152, P4775; Falcone FH, 1996, EUR J IMMUNOL, V26, P1147, DOI 10.1002/eji.1830260528; Gibbs BF, 1996, EUR J IMMUNOL, V26, P2493, DOI 10.1002/eji.1830261033; Haas H, 1999, INT ARCH ALLERGY IMM, V119, P86, DOI 10.1159/000024182; Haas H, 1999, EUR J IMMUNOL, V29, P918, DOI 10.1002/(SICI)1521-4141(199903)29:03<918::AID-IMMU918>3.3.CO;2-K; Hara T, 1998, BIOCHEM BIOPH RES CO, V247, P542, DOI 10.1006/bbrc.1998.8816; Hewitt CRA, 1997, CLIN EXP ALLERGY, V27, P201, DOI 10.1111/j.1365-2222.1997.tb00694.x; Hewitt CRA, 1998, ALLERGY, V53, P60; HEWITT CRA, 1995, J EXP MED, V182, P1537, DOI 10.1084/jem.182.5.1537; Kasaian MT, 1996, INT IMMUNOL, V8, P1287, DOI 10.1093/intimm/8.8.1287; KISHI K, 1985, LEUKEMIA RES, V9, P381, DOI 10.1016/0145-2126(85)90060-8; Li HM, 1996, J IMMUNOL, V156, P4833; Macfarlane SR, 2001, PHARMACOL REV, V53, P245; MACGLASHAN D, 1994, J IMMUNOL, V152, P3006; Machado DC, 1996, EUR J IMMUNOL, V26, P2972, DOI 10.1002/eji.1830261224; MAGGI E, 1992, J IMMUNOL, V148, P2142; MUELLER R, 1994, EUR J IMMUNOL, V24, P2935, DOI 10.1002/eji.1830241203; Ochensberger B, 1996, BLOOD, V88, P3028; PRITCHARD DI, 1997, PULMONARY DEFENCES, P305; Redrup AC, 1998, J IMMUNOL, V160, P1957; Robinson C, 1997, CLIN EXP ALLERGY, V27, P10, DOI 10.1046/j.1365-2222.1997.d01-415.x; SCHULZ O, 1995, EUR J IMMUNOL, V25, P3191, DOI 10.1002/eji.1830251131; Schulz O, 1998, J EXP MED, V187, P271, DOI 10.1084/jem.187.2.271; SEN HG, 1967, NATURE, V214, P609, DOI 10.1038/214609b0; Stewart GA, 1996, CLIN EXP ALLERGY, V26, P1020, DOI 10.1046/j.1365-2222.1996.d01-405.x; van Oort E, 2002, EUR J BIOCHEM, V269, P671, DOI 10.1046/j.0014-2956.2001.02700.x; Wan H, 2000, CLIN EXP ALLERGY, V30, P685, DOI 10.1046/j.1365-2222.2000.00820.x; Wan H, 1999, J CLIN INVEST, V104, P123, DOI 10.1172/JCI5844; Wan H, 2001, CLIN EXP ALLERGY, V31, P279, DOI 10.1046/j.1365-2222.2001.00970.x; Wang M, 1999, CLIN IMMUNOL, V90, P47, DOI 10.1006/clim.1998.4628; Yamashita M, 1996, J IMMUNOL, V157, P714	37	89	96	0	4	FEDERATION AMER SOC EXP BIOL	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA	0741-5400			J LEUKOCYTE BIOL	J. Leukoc. Biol.	JAN	2003	73	1					165	171		10.1189/jlb.0702356		7	Cell Biology; Hematology; Immunology	Cell Biology; Hematology; Immunology	636MY	WOS:000180460900017	12525574	
J	Carbonnelle, S; Francaux, M; Doyle, I; Dumont, X; De Burbure, C; Morel, G; Michel, O; Bernard, A				Carbonnelle, S; Francaux, M; Doyle, I; Dumont, X; De Burbure, C; Morel, G; Michel, O; Bernard, A			Changes in serum pneumoproteins caused by short-term exposures to nitrogen trichloride in indoor chlorinated swimming pools	BIOMARKERS			English	Article						nitrogen trichloride; exercise; pneumoproteins; swimming; lung epithelium; Clara cell protein; surfactant-associated proteins; chlorine-based disinfectants; chlorine	CLARA CELL PROTEIN; BRONCHIAL RESPONSIVENESS; RESPIRATORY SYMPTOMS; FAILURE; BARRIER; ASTHMA; INJURY; OZONE; GAS	Nitrogen trichloride (NCl3) is an irritant gas released in the air of indoor pools sanitized with chlorine-based disinfectants. In the present study we investigated the effects of NCl3 on the pulmonary epithelium of pool attendees by measuring the leakage into serum of three lung-specific proteins (pneumoproteins): the alveolar surfactant-associated proteins A and B (SP-A and SP-B) and the bronchiolar 16 kDa Clara cell protein (CC16). These pneumoproteins were measured in the serum of 29 recreational swimmers (16 children and 13 adults) before and after attending a chlorinated pool with a mean NCl3 concentration of 490 mug m(-3). Pneumoprotein changes in serum were also studied in 14 trained swimmers performing an intensive 45 min standardized swimming session in a chlorinated pool (mean NCl3 concentration of 355 mug m(-1)) and for the purposes of comparison in a non-chlorinated pool sanitized by the copper silver method. Serum CC16 was not increased in recreational swimmers, but in trained swimmers serum levels of this protein peaked immediately after strenuous exercise, both in the copper/silver pool and in the chlorinated pool. This acute increase in airway permeability is probably the consequence of the mechanical stress on the epithelial barrier caused by overinflation and, or hyperventilation during intense exercise. Serum levels of SP-A and SP-B were unaffected by strenuous exercise in the copper silver pool. The two proteins were, however, significantly increased in a time-dependent manner in recreational and trained swimmers attending the chlorinated pool. The intravascular leakage of SP-A and SP-B was already statistically significant after only 1 h of exposure to pool air without exercising and remained elevated for 12 h after. These changes were knot associated with decrements in lung function. The ability of NCl3 to acutely disrupt the lung epithelium barrier was confirmed in mice using serum CC16 and plasma proteins in bronchoalveolar lavage fluid as permeability markers. The significance of these permeability changes induced by NCl3 in the deep lung is presently unknown. In view of the increasing and widespread human exposure to this gas not only in indoor pools but also in a variety of other situations, these findings warrant further study.	Catholic Univ Louvain, Ind Toxicol Unit, B-1200 Brussels, Belgium; Catholic Univ Louvain, Fac Med, Unit Phys Educ, B-1200 Brussels, Belgium; Flinders Univ S Australia, Sch Med, Dept Human Physiol & Crit Care Med, Adelaide, SA 5001, Australia; Inst Natl Rech & Secur, F-54501 Vandoeuvre Les Nancy, France; Free Univ Brussels, St Pierre Univ Hosp, Clin Allergol & Resp Dis, B-1000 Brussels, Belgium	Bernard, A (reprint author), Catholic Univ Louvain, Toxicol Unit, 30-54 Clos Chapelle Aux Champs, B-1200 Brussels, Belgium.		Francaux, Marc/C-5594-2008; BERNARD, Alfred/A-6511-2010	BERNARD, Alfred/0000-0003-3171-3743; michel, olivier/0000-0002-1528-1277; Francaux, Marc/0000-0001-8182-1588			Agabiti N, 2001, OCCUP ENVIRON MED, V58, P399, DOI 10.1136/oem.58.6.399; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Arsalane K, 1999, TOXICOL APPL PHARM, V159, P169, DOI 10.1006/taap.1999.8738; BARBEE SJ, 1983, AM IND HYG ASSOC J, V44, P145, DOI 10.1202/0002-8894(1983)044<0145:AITONT>2.3.CO;2; BERNARD A, 1992, EUR RESPIR J, V5, P1231; Bernard A, 1996, CLIN CHEM, V42, P1120; BERNARD AM, 1994, ENVIRON RES, V66, P96, DOI 10.1006/enrs.1994.1047; BERNARD AM, 1994, EUR RESPIR J, V7, P1932; Broeckaert F, 2000, ENVIRON HEALTH PERSP, V108, P533, DOI 10.2307/3454615; DOYLE IR, 1995, AM J RESP CRIT CARE, V152, P307; Doyle IR, 1997, AM J RESP CRIT CARE, V156, P1217; GAGNAIRE F, 1994, J APPL TOXICOL, V14, P405, DOI 10.1002/jat.2550140604; Halatek T, 1998, EUR RESPIR J, V11, P726; Helenius IJ, 1998, ALLERGY, V53, P346, DOI 10.1111/j.1398-9995.1998.tb03904.x; Helenius IJ, 1998, J ALLERGY CLIN IMMUN, V101, P646; 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; HERMANS C, 1996, BIOMARKERS, V1, P1; HERY M, 1995, ANN OCCUP HYG, V39, P437; Hopkins SR, 1997, AM J RESP CRIT CARE, V155, P1090; JENSEN HJ, 1988, ZEITUNG GESAMTE HYGI, V34, P248; Karnak I, 1996, CLIN PEDIATR, V35, P471, DOI 10.1177/000992289603500908; Massin N, 1998, OCCUP ENVIRON MED, V55, P258; Musch MW, 1999, GASTROENTEROLOGY, V117, P115, DOI 10.1016/S0016-5085(99)70557-3; NAKAMURA TY, 1995, J CELL BIOL, V131, P509, DOI 10.1083/jcb.131.2.509; Nanson CJ, 2001, RESP PHYSIOL, V127, P259, DOI 10.1016/S0034-5687(01)00251-1; Newman D J, 1994, Kidney Int Suppl, V47, pS20; ROBIN M, 2002, IN PRESS EUROPEAN RE; Shijubo N, 1997, EUR RESPIR J, V10, P1108, DOI 10.1183/09031936.97.10051108; Tanen DA, 1999, NEW ENGL J MED, V341, P848, DOI 10.1056/NEJM199909093411115; TATSUMI T, 1994, AM J PHYSIOL-HEART C, V267, pH1597; Weiler JM, 1998, J ALLERGY CLIN IMMUN, V102, P722, DOI 10.1016/S0091-6749(98)70010-7; WEST JB, 1991, J APPL PHYSIOL, V70, P1731; WHO, 2000, GUID SAF RECR WAT EN, V2	35	89	89	0	7	TAYLOR & FRANCIS LTD	ABINGDON	4 PARK SQUARE, MILTON PARK,, ABINGDON OX14 4RN, OXON, ENGLAND	1354-750X			BIOMARKERS	Biomarkers	NOV-DEC	2002	7	6					464	478		10.1080/13547500210166612		15	Biotechnology & Applied Microbiology; Toxicology	Biotechnology & Applied Microbiology; Toxicology	630QV	WOS:000180120600003	12581482	
J	Grenier, PA; Beigelman-Aubry, C; Fetita, C; Preteux, F; Brauner, MW; Lenoir, S				Grenier, PA; Beigelman-Aubry, C; Fetita, C; Preteux, F; Brauner, MW; Lenoir, S			New frontiers in CT imaging of airway disease	EUROPEAN RADIOLOGY			English	Review						chronic obstructive pulmonary disease; airways; helical CT; 3D images	THIN-SECTION CT; RESOLUTION COMPUTED-TOMOGRAPHY; PULMONARY-FUNCTION TESTS; DIFFUSE ASPIRATION BRONCHIOLITIS; EXPIRATORY CT; SPIRAL CT; TRACHEOBRONCHIAL TREE; LUNG TRANSPLANTATION; VIRTUAL BRONCHOSCOPY; HELICAL CT	Combining helical volumetric CT acquisition and thin-slice thickness during breath hold provides an accurate assessment of both focal and diffuse airway diseases. With multiple detector rows, compared with single-slice helical CT, multislice CT can cover a greater volume, during a simple breath hold, and with better longitudinal and in-plane spatial resolution and improved temporal resolution. The result in data set allows the generation of superior multiplanar and 3D images of the airways, including those obtained from techniques developed specifically for airway imaging, such as virtual bronchography and virtual bronchoscopy. Complementary CT evaluation at suspended or continuous full expiration is mandatory to detect air trapping that is a key finding for depicting an obstruction on the small airways. Indications for CT evaluation of the airways include: (a) detection of endobronchial lesions in patients with an unexplained hemoptysis; (b) evaluation of extent of tracheobronchial stenosis for planning treatment and follow-up; (c) detection of congenital airway anomalies revealed by hemoptysis or recurrent infection; (d) detection of postinfectious or postoperative airway fistula or dehiscence, and (e) diagnosis and assessment of extent of bronchiectasis and small airway disease. Improvement in image analysis technique and the use of spirometrically control Of lung Volume acquisition have made possible accurate and reproducible quantitative assessment of airway wall and lumen areas and lung density. This contributes to better insights in physiopathology of obstructive lung disease, particularly in chronic obstructive pulmonary disease and asthma.	Univ Paris 06, Pitie Salpetriere Hosp, Dept Radiol, Assistance Publ Hop Paris, F-75651 Paris, France; Inst Natl Telecommun, Dept ARTEMIS, F-91011 Evry, France; UFR SMBH Paris XIII, Avicenne Hosp, Bobigny, France; Inst Mutualiste Montsouris, Paris, France	Grenier, PA (reprint author), Univ Paris 06, Pitie Salpetriere Hosp, Dept Radiol, Assistance Publ Hop Paris, 47-83 Blvd Hop, F-75651 Paris, France.		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Radiol.	MAY	2002	12	5					1022	1044		10.1007/s00330-002-1342-1		23	Radiology, Nuclear Medicine & Medical Imaging	Radiology, Nuclear Medicine & Medical Imaging	552HJ	WOS:000175613700006	11976844	
J	van den Biggelaar, AHJ; Lopuhaa, C; van Ree, R; van der Zee, JS; Jans, J; Hoek, A; Migombet, B; Borrmann, S; Luckner, D; Kremsner, PG; Yazdanbakhsh, M				van den Biggelaar, AHJ; Lopuhaa, C; van Ree, R; van der Zee, JS; Jans, J; Hoek, A; Migombet, B; Borrmann, S; Luckner, D; Kremsner, PG; Yazdanbakhsh, M			The prevalence of parasite infestation and house dust mite sensitization in Gabonese schoolchildren	INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY			English	Article						atopy; skin test reactivity; malaria; helminth; schistosomiasis; filariasis; IgE; Africa	HUMAN LYMPHATIC FILARIASIS; SCHISTOSOMA-HAEMATOBIUM; ALLERGIC REACTIVITY; INTERFERON-GAMMA; ATOPY; IGE; INFECTION; MALARIA; ASTHMA; CHILDREN	Background: Allergic diseases seem less prevalent in communities in less developed parts of the world, where parasite infections are highly prevalent. Altogether not much is known about the association between chronic infections with tissue and blood-dwelling parasites and atopy. Methods: In an area in Gabon endemic for blood and tissue parasites, 520 schoolchildren were parasitologically examined and skin prick-tested for a set of common environmental aeroallergens. Levels of allergen-specific IgE and polyclonal IgE were measured. Results: In schoolchildren schistosome and filarial infections increased with age, whereas malaria was more prevalent in younger children. In contrast to allergen sensitization that increased with age, skin test reactivity tended to decline. The number of children with mite-specific IgE antibodies (47%) by far exceeded the number responding to skin prick testing (11%). Mite sensitization was found to be the highest in children infected with schistosomes and/or filariae whereas skin test reactivity was lowest. The multiple logistic regression showed that the risk of a positive skin test was 8-fold higher with increasing levels of mite-specific IgE but was reduced by 72% when infected with blood stage helminths. Conclusions: Chronic blood and tissue parasite infections that are often capable of modulating immune responses in the host are negatively associated with skin test reactivity in a sensitized population. Copyright (C) 2001 S. Karger AG, Basel.	Leiden Univ, Med Ctr P4, Dept Parasitol, NL-2300 RC Leiden, Netherlands; Univ Amsterdam, Acad Med Ctr, Dept Pulmonol, NL-1105 AZ Amsterdam, Netherlands; Cent Lab Blood Transfus, Dept Allergy, Amsterdam, Netherlands; Albert Schweitzer Hosp, Res Unit, Lambarene, Gabon; Univ Tubingen, Inst Trop Med, Dept Parasitol, D-72074 Tubingen, Germany	Yazdanbakhsh, M (reprint author), Leiden Univ, Med Ctr P4, Dept Parasitol, POB 9605, NL-2300 RC Leiden, Netherlands.		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Arch. Allergy Immunol.	NOV	2001	126	3					231	238		10.1159/000049519		8	Allergy; Immunology	Allergy; Immunology	508WD	WOS:000173112000009	11752881	
J	Giembycz, MA				Giembycz, MA			Cilomilast: a second generation phosphodiesterase 4 inhibitor for asthma and chronic obstructive pulmonary disease	EXPERT OPINION ON INVESTIGATIONAL DRUGS			English	Review						airways inflammation; asthma; Ariflo; cilomilast; chronic obstructive pulmonary disease; cyclic AMP; phosphodiesterase 4; SB-207439	HUMAN-LIVER-MICROSOMES; AFFINITY ROLIPRAM BINDING; SELECTIVE PDE4 INHIBITOR; THEOPHYLLINE METABOLISM; ARIFLO(TM) SB-207499; INHALED CORTICOSTEROIDS; CATALYTIC ACTIVITY; CIGARETTE-SMOKING; SE-207499 ARIFLO; HUMAN MONOCYTES	Cilomilast (Ariflo(TM), SE-207499) is an orally-active, second generation phosphodiesterase (PDE) inhibitor that may be effective in the treatment of asthma and chronic obstructive pulmonary disease (COPD). It has high selectivity for the cyclic AMP-specific, or PDE4, isoenzyme that predominates in pro-inflammatory and immune cells and is ten-fold more selective for PDE4D than for PDE4A, B and C. In vitro, cilomilast suppresses the activity of many pro-inflammatory and immune cells that have been implicated in the pathogenesis of asthma and COPD and is highly active in animal models of these diseases. Cilomilast demonstrates a markedly improved side effect profile over the archetypal PDE4 inhibitor, rolipram, which has been attributed to its inability to discriminate between the high affinity rolipram binding site and the catalytic domain of the enzyme, and the fact that it is negatively charged which at physiological pH should limit its penetration in to the CNS. In humans cilomilast is rapidly absorbed after oral administration, providing dose-proportional systemic exposure up to 4 mg, completely bioavailable, has a half-life of similar to 7 h and is subject to negligible first pass hepatic metabolism. Cilomilast is extensively metabolised with decyclopentylation, acyl glucuronidation and 3-hydroxylation of the cyclopentyl ring representing the principal routes. Most of the drug is excreted in the urine (similar to 90%) and faeces (6-7%) with unchanged cilomilast accounting for less than 1% of the administered dose. Cilomilast has been evaluated in Phase I, Phase II and Phase III trials and dose-response experiments have demonstrated a clinically significant increase in lung function and a perceived improvement in quality of life in patients with COPD. Trials of cilomilast in asthma have been less impressive although a trend towards improved lung function has been reported. Cilomilast is safe and well-tolerated at doses up to 15 mg in both short- and long-term dosing trials with a low incidence of adverse effects. No evidence for drug-drug interactions with commonly prescribed medications for COPD and asthma such as digoxin, corticosteroids, salbutamol, theophylline or warfarin has been found. Moreover, the pharmacokinetics of cilomilast are essentially the same in smokers and non-smokers, indicating that no dose adjustments of cilomilast will be required in patients with COPD. Thus, cilomilast displays a promising clinical profile in the treatment of inflammatory airway diseases, in particular COPD and the results of further Phase III trials are awaited with interest.	Imperial Coll, Sch Med, Natl Heart & Lung Inst, London SW3 6LY, England	Giembycz, MA (reprint author), Imperial Coll, Sch Med, Natl Heart & Lung Inst, Dovehouse St, London SW3 6LY, England.						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Investig. Drugs	JUL	2001	10	7					1361	1379		10.1517/13543784.10.7.1361		19	Pharmacology & Pharmacy	Pharmacology & Pharmacy	450YL	WOS:000169772400014	11772257	
J	Kimber, I; Basketter, DA; Berthold, K; Butler, M; Garrigue, JL; Lea, L; Newsome, C; Roggeband, R; Steiling, W; Stropp, G; Waterman, S; Wiemann, C				Kimber, I; Basketter, DA; Berthold, K; Butler, M; Garrigue, JL; Lea, L; Newsome, C; Roggeband, R; Steiling, W; Stropp, G; Waterman, S; Wiemann, C			Skin sensitization testing in potency and risk assessment	TOXICOLOGICAL SCIENCES			English	Article						skin sensitization; sensitization potency; risk assessment; guinea pig tests; local lymph node assay; human sensitization	LYMPH-NODE ASSAY; PIG MAXIMIZATION TEST; ALLERGIC CONTACT SENSITIZATION; FALSE-POSITIVE RESPONSES; PREDICTIVE TEST METHODS; GUINEA-PIG; CELL; PRODUCTS; AGENTS; SENSITIVITY	The purpose of this article is to review, and make recommendations for, the use of relevant skin sensitization test methods, for the purposes of determination of relative potency and the threshold dose necessary for the induction of skin sensitization, and for risk assessment, In addressing the first area, the utility of three guinea pig tests (the guinea pig maximization test, the occluded patch test, and the open epicutaneous test) of the local lymph node assay (LLNA) and of human volunteer testing for the assessment of relative potency and identification of thresholds for sensitization were considered. The following conclusions were drawn. (1) Although attempts have been made to modify the guinea pig maximization test for the purposes of deriving dose-response relationships, this method is usually unsuitable for determination of relative sensitizing potency. (2) Guinea pig methods that do not require the use of adjuvant and which employ a relevant route of exposure (the occluded patch test and the open epicutaneous test) are more appropriate for the assessment of relative skin-sensitizing potency. (3) The LLNA is suitable for the determination of relative skin sensitizing potency, and the adaptation of this method for derivation of comparative criteria such as EC3 values (the estimated concentration of test chemical required to induce a stimulation index of 3 in the LLNA) provides an effective and quantitative basis for such measurements, (4) For all the methods identified above, potency is assessed relative to other chemical allergens of known skin sensitizing potential. The estimation of likely threshold concentrations is dependent upon the availability of suitable benchmark chemicals of known potency for human sensitization. (5) Human testing (and specifically, the Human Repeat Insult Patch Test) can provide information of value in confirming the absence of skin sensitizing activity of formulations and products under specific conditions of use and exposure. Based on the above, the following recommendations are made. (1) If results are already available from suitable guinea pig tests, then judicious interpretation of the data may provide information of value in assessing relative skin sensitizing potency. This option should be explored before other analyses are conducted. (2) The LLNA is the recommended method for new assessments of relative potency, and/or for the investigation of the influence of vehicle or formulation on skin sensitizing potency. (3) Whenever available, human skin sensitization data should be incorporated into an assessment of relative potency. With respect to risk assessment, the conclusion drawn is that all the available data on skin-sensitizing activity in animals and man should be integrated into the risk-assessment process. Appropriate interpretation of existing data from suitable guinea pig studies can provide valuable information with respect to potency, as the first step in the development of a risk assessment. However, for de novo investigations, the LLNA is the method favored for providing quantitative estimations of skin-sensitizing potency that are best suited to the risk assessment process. Finally, human testing is of value in the risk assessment process, but is performed only for the purposes of confirming product safety.	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Sci.	FEB	2001	59	2					198	208		10.1093/toxsci/59.2.198		11	Toxicology	Toxicology	396LR	WOS:000166638300003	11158712	
J	Ross, MA; Curtis, L; Scheff, PA; Hryhorczuk, DO; Ramakrishnan, V; Wadden, RA; Persky, VW				Ross, MA; Curtis, L; Scheff, PA; Hryhorczuk, DO; Ramakrishnan, V; Wadden, RA; Persky, VW			Association of asthma symptoms and severity with indoor bioaerosols	ALLERGY			English	Article						allergens; asthma; bacteria; dampness; dust mites; flooding; mold spores	DUST-MITE-ALLERGEN; ENDOTOXIN EXPOSURE; RESPIRATORY HEALTH; CONTROL CHILDREN; RISK FACTOR; HOUSE; HOME; CHILDHOOD; FUNGI	Background: In this study, repeated measurements were made of levels of mold spores, bacteria, and dust-mite allergens over a 7-month period in the homes of asthmatics, and relationships with measures of asthma severity were evaluated. Methods: A sample of 57 asthmatic individuals, living in 44 homes in East Moline, Illinois, and nearby communities, participated in a panel study. The homes were visited up to nine times during the study to collect air and dust samples. Asthma severity indicators were derived from questionnaire data and from the daily health records from the panel study. Associations between indoor levels of mold spores, bacteria, and dust-mite allergens were tested with several asthma severity indicators. Results: There was evidence of associations between all asthma severity measures and levels of total and Gram-negative bacteria, but mold-spore abundance was associated only with emergency room (ER) visits for asthma. No significant associations were found with house-dust-mite allergen and any of the asthma severity indicators, but the levels of dust-mite allergen were low, with median concentrations of 0.18 mu g/g dust Der f 1 and 0.19 mu g/g dust Der p 1. Conclusions: Some evidence was found for associations of increased concentrations of Gram-negative bacteria and mold spores with asthma severity, particularly with ER visits. No association was found between house-dust-mite allergen and asthma severity indicators; however, the mite-allergen levels in the study homes were generally well below the proposed threshold level of 2 mu g/g dust.	US EPA, Off Air Qual Planning & Stand, Hlth & Ecosyst Effects Grp, Res Triangle Pk, NC 27711 USA; Univ Illinois, Sch Publ Hlth, Chicago, IL USA	Ross, MA (reprint author), US EPA, Off Air Qual Planning & Stand, Hlth & Ecosyst Effects Grp, Mail Code 15, Res Triangle Pk, NC 27711 USA.				NIOSH CDC HHS [2T15OH07104]; PHS HHS [94IA0025]		BJORNSSON E, 1995, CLIN EXP ALLERGY, V25, P423, DOI 10.1111/j.1365-2222.1995.tb01073.x; Curtis L, 1997, ALLERGY, V52, P642, DOI 10.1111/j.1398-9995.1997.tb01043.x; CURTIS L, 2000, IN PRESS INDOOR BUIL; Custovic A, 1996, J ALLERGY CLIN IMMUN, V98, P64, DOI 10.1016/S0091-6749(96)70227-0; DEKOSTER JA, 1995, AM IND HYG ASSOC J, V56, P573, DOI 10.1202/0002-8894(1995)056<0573:BCINCA>2.0.CO;2; LI CS, 1995, ARCH ENVIRON HEALTH, V50, P38; Li CS, 1997, ARCH ENVIRON HEALTH, V52, P72; 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; Peat JK, 1996, AM J RESP CRIT CARE, V153, P141; Peat JK, 1998, ALLERGY, V53, P120, DOI 10.1111/j.1398-9995.1998.tb03859.x; RIZZO M, 1997, P 90 ANN M EXH AIR W; Rizzo MC, 1997, PEDIATR ALLERGY IMMU, V8, P121; SAS Institute Inc, 1990, SAS STAT US GUID VER; Smedje G, 1997, CLIN EXP ALLERGY, V27, P1270, DOI 10.1111/j.1365-2222.1997.tb01171.x; 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; SU HJ, 1992, APPL ENVIRON MICROB, V58, P181; vanStrien RT, 1996, EUR RESPIR J, V9, P926, DOI 10.1183/09031936.96.09050926; Verhoeff AP, 1997, ANN ALLERG ASTHMA IM, V78, P544; ZOCK JP, 1994, EUR RESPIR J, V7, P1254, DOI 10.1183/09031936.94.07071254	23	89	98	0	6	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	AUG	2000	55	8					705	711		10.1034/j.1398-9995.2000.00551.x		7	Allergy; Immunology	Allergy; Immunology	341JE	WOS:000088586600004	10955695	
J	Collison, A; Mattes, J; Plank, M; Foster, PS				Collison, Adam; Mattes, Joerg; Plank, Maximilian; Foster, Paul S.			Inhibition of house dust mite-induced allergic airways disease by antagonism of microRNA-145 is comparable to glucocorticoid treatment	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						miRNA; asthma; allergy; inflammation; dexamethasone; glucocorticoid; HDM; antagomir	EXPERIMENTAL ASTHMA; EOSINOPHIL RECRUITMENT; IMMUNE-SYSTEM; T(H)2 CELLS; IN-VIVO; EXPRESSION; MODULATION; INFLAMMATION; MECHANISMS; MODEL	Background: Glucocorticoids are used as mainstay therapy for asthma, but some patients remain resistant to therapy. MicroRNAs (miRNAs) are important regulators of the immune system by promoting the catabolism of their target transcripts as well as attenuating their translation. The role of miRNA in regulating allergic inflammation remains largely unknown. Blocking miRNA function may provide a new nonsteroidal anti-inflammatory approach to treatment. Objectives: To (1) determine the role of specific miRNAs in the regulation of hallmark features of allergic airways inflammation and (2) compare the efficacy of antagonizing miRNA function with that of steroid treatment. Methods: Mice were sensitized and then aeroallergen-challenged with house dust mite to induce allergic airways disease, and alterations in the expression of miRNAs were characterized. Next mice were treated with antagomirs that inhibited the function of specific miRNAs in the lung or treated with dexamethasone and inflammatory lesions, and airway hyperresponsiveness was measured. Results: miR-145, miR-21, and let-7b have been implicated in airway smooth muscle function, inflammation, and airways epithelial cell function, respectively. Inhibition of miR-145, but not miR-21 or lethal-7b, inhibited eosinophilic inflammation, mucus hypersecretion, T(H)2 cytokine production, and airway hyperresponsiveness. The anti-inflammatory effects of miR-145 antagonism were comparable to steroid treatment. Conclusion: Our study highlights the importance of understanding the contribution of miRNAs to pathogenesis of human allergic disease and their potential as novel anti-inflammatory targets. (J Allergy Clin Immunol 2011; 128: 160-7.)	[Collison, Adam; Plank, Maximilian; Foster, Paul S.] Univ Newcastle, Cooperat Res Ctr Asthma & Airways, Ctr Asthma & Resp Dis, Sch Biomed Sci & Pharm,Fac Hlth, Newcastle, NSW 2300, Australia; [Collison, Adam; Mattes, Joerg] Univ Newcastle, Cooperat Res Ctr Asthma & Airways, Expt & Translat Resp Grp, Sch Biomed Sci & Pharm,Fac Hlth, Newcastle, NSW 2300, Australia	Foster, PS (reprint author), Univ Newcastle, Cooperat Res Ctr Asthma & Airways, Ctr Asthma & Resp Dis, Sch Biomed Sci & Pharm,Fac Hlth, 5th Floor David Maddison Clin Sci Bldg, Newcastle, NSW 2300, Australia.	joerg.mattes@newcastle.edu.au; paul.foster@newcastle.edu.au	Foster, Paul/G-5057-2013		National Health and Medical Research Council; Cooperative Research Centre for Asthma and Airways	Supported by a National Health and Medical Research Council project grant (to J.M. and P.S.F.), a National Health and Medical Research Council Health Professional Research Fellowship (to J.M.), and the Cooperative Research Centre for Asthma and Airways (to J.M. and P.S.F.).	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Allergy Clin. Immunol.	JUL	2011	128	1					160	U251		10.1016/j.jaci.2011.04.005		12	Allergy; Immunology	Allergy; Immunology	785RE	WOS:000292245600021	21571357	
J	Barrett, NA; Rahman, OM; Fernandez, JM; Parsons, MW; Xing, W; Austen, KF; Kanaoka, Y				Barrett, Nora A.; Rahman, Opu M.; Fernandez, James M.; Parsons, Matthew W.; Xing, Wei; Austen, K. Frank; Kanaoka, Yoshihide			Dectin-2 mediates Th2 immunity through the generation of cysteinyl leukotrienes	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article							HUMAN POLYMORPHONUCLEAR LEUKOCYTES; PATTERN-RECOGNITION RECEPTOR; MANSONI EGG ANTIGENS; DUST MITE ALLERGEN; DENDRITIC CELLS; INHALED ANTIGEN; VASCULAR-PERMEABILITY; AIRWAY INFLAMMATION; SCHISTOSOMA-MANSONI; MICE LACKING	The innate signaling pathways for Th2 immunity activated by inhaled antigens are not well defined. We previously identified Dectin-2 as a receptor for glycans in allergen extracts from the house dust mite Dermatophagoides farinae (Df) that mediates cysteinyl leukotriene (cys-LT) generation from pulmonary CD11c(+) cells and from GM-CSF-cultured bone marrow cells (BMCsGM-CSF) Using lentiviral knockdown of Dectin-2 in BMCsGM-CSF and adoptive transfer of Df-pulsed BMCsGm-csF to sensitize naive mice, we now report that Dectin-2 is critical for the development of Df-elicited eosinophilic and neutrophilic pulmonary inflammation and Th2 cytokine generation in the lungs and restimulated lymph nodes. Sensitization with Df-pulsed BMCsGM-CSF from LTC4 synthase(LTC,S)-deficient mice or type 1 cys-LT receptor (CysLT,R)-deficient mice demonstrated that both proteins were required for Df-elicited eosinophilic pulmonary inflammation and Th2 cytokine generation in the lungs and restimulated lymph nodes. Direct sensitization and challenge of Ltc4s(-/-) and Cysitr1(-/-) mice confirmed that cys-LTs mediate these parameters of Df-elicited Th2 pulmonary inflammation. Thus, the Dectin-2-cys-LT pathway is critical for the induction of Th2 immunity to a major allergen, in part through CysLT(1)R. These findings identify a previously unrecognized link between a myeloid C-type lectin receptor and Th2 immunity.	[Barrett, Nora A.; Rahman, Opu M.; Fernandez, James M.; Parsons, Matthew W.; Xing, Wei; Austen, K. Frank; Kanaoka, Yoshihide] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA; [Barrett, Nora A.; Rahman, Opu M.; Fernandez, James M.; Parsons, Matthew W.; Xing, Wei; Austen, K. Frank; Kanaoka, Yoshihide] Brigham & Womens Hosp, Div Rheumatol Immunol & Allergy, Boston, MA 02115 USA	Kanaoka, Y (reprint author), Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.	ykanaoka@rics.bwh.harvard.edu			National Institutes of Health [101HL36110, R01HL090630, K08A1080948]; Joycelyn C. Austen Fund for the Career Development of Women Physician Scientists	This work is supported by National Institutes of Health grants 101HL36110, RO1HL090630 (to Y. Kanaoka), and K08A1080948 (to. NA. Barrett). N.A. Barrett is supported by the Joycelyn C. Austen Fund for the Career Development of Women Physician Scientists.	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Exp. Med.	MAR 14	2011	208	3					593	604		10.1084/jem.20100793		12	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	735ZW	WOS:000288460300015	21357742	
J	Andersen, ZJ; Hvidberg, M; Jensen, SS; Ketzel, M; Loft, S; Sorensen, M; Tjonneland, A; Overvad, K; Raaschou-Nielsen, O				Andersen, Zorana J.; Hvidberg, Martin; Jensen, Steen S.; Ketzel, Matthias; Loft, Steffen; Sorensen, Mette; Tjonneland, Anne; Overvad, Kim; Raaschou-Nielsen, Ole			Chronic Obstructive Pulmonary Disease and Long-Term Exposure to Traffic-related Air Pollution A Cohort Study	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						COPD; air pollution; hospital admission; asthma; diabetes	LUNG-FUNCTION; RESPIRATORY SYMPTOMS; NITROGEN-DIOXIDE; HEALTH; RISK; COPD; CANCER; ATHEROSCLEROSIS; INFLAMMATION; POPULATION	Rationale: Short-term exposure to air pollution has been associated with exacerbation of chronic obstructive pulmonary disease (COPD), whereas the role of long-term exposures on the development of COPD is not yet fully understood. Objectives: We assessed the effect of exposure to traffic-related air pollution over 35 years on the incidence of COPD in a prospective cohort study. Methods: We followed 57,053 participants in the Danish Diet, Cancer, and Health cohort in the Hospital Discharge Register for their first hospital admission for COPD between 1993 and 2006. We estimated the annual mean levels of nitrogen dioxide (NO(2)) and nitrogen oxides (NO(x)) at all residential addresses of the cohort participants since 1971 to an event or 2006 and used indicators of traffic near the residential address at recruitment. We assessed the association between exposure to air pollution and COPD incidence by Cox regression analyses for the full cohort, and for participants with and without comorbid conditions, including asthma, diabetes, or cardiovascular disease. Measurements and Main Results: A first hospital admission for COPD was recorded for 1,786 (3.4%) of 52,799 eligible subjects between recruitment (1993-1997) and 2006. COPD incidence was associated with the 35-year mean NO(2) level (hazard ratio, 1.08; 95% confidence interval, 1.02-1.14, per interquartile range of 5.8 mu g/m(3)), with stronger associations in subjects with diabetes (1.29; 1.05-1.50) and asthma (1.19; 1.03-1.38). Conclusions: Long-term exposure to traffic-related air pollution may contribute to the development of COPD with possibly enhanced susceptibility in people with diabetes and asthma.	[Andersen, Zorana J.; Sorensen, Mette; Tjonneland, Anne; Raaschou-Nielsen, Ole] Danish Canc Soc, Inst Canc Epidemiol, DK-2100 Copenhagen O, Denmark; [Hvidberg, Martin; Jensen, Steen S.; Ketzel, Matthias] Aarhus Univ, Natl Environm Res Inst, Roskilde, Denmark; [Loft, Steffen] Univ Copenhagen, Dept Environm Hlth, Copenhagen, Denmark; [Overvad, Kim] Aarhus Univ, Sch Publ Hlth, Aarhus, Denmark; [Overvad, Kim] Aarhus Univ Hosp, Aalborg Hosp, Ctr Cardiovasc Res, Aalborg, Denmark	Andersen, ZJ (reprint author), Danish Canc Soc, Inst Canc Epidemiol, Strandboulevarden 49, DK-2100 Copenhagen O, Denmark.	zorana@cancer.dk	Andersen, Zorana /P-4983-2014; Ketzel, Matthias/K-4246-2015	Andersen, Zorana /0000-0003-4138-9828; Ketzel, Matthias/0000-0001-9519-1935; Hvidberg, Martin/0000-0003-3991-2667; Sorensen, Mette/0000-0002-7302-4789; Loft, Steffen/0000-0001-9552-8518	Danish Research Council	Supported by The Danish Research Council.	Berkowicz R, 2008, ENVIRON MODELL SOFTW, V23, P296, DOI 10.1016/j.envsoft.2007.04.007; Downs SH, 2007, NEW ENGL J MED, V357, P2338, DOI 10.1056/NEJMoa073625; Eriksen Nanna, 2003, Ugeskr Laeger, V165, P3499; Gotschi T, 2008, INT J EPIDEMIOL, V37, P1349, DOI 10.1093/ije/dyn136; Hart JE, 2010, AM J RESP CRIT CARE, V183, P73; Hesterberg TW, 2009, CRIT REV TOXICOL, V39, P195, DOI 10.1080/10408440802220603; Hoek G, 2002, LANCET, V360, P1203, DOI 10.1016/S0140-6736(02)11280-3; Hogg JC, 2009, RESPIROLOGY, V14, P336, DOI 10.1111/j.1440-1843.2009.01497.x; Ingebrigtsen T, 2010, RESP MED, V104, P1890, DOI 10.1016/j.rmed.2010.05.004; Jensen SS, 2001, TRANSPORT RES D-TR E, V6, P229, DOI 10.1016/S1361-9209(00)00026-2; Jensen SS, 2009, ATMOS ENVIRON, V43, P4544, DOI 10.1016/j.atmosenv.2009.06.042; Kan HD, 2007, THORAX, V62, P873, DOI 10.1136/thx.2006.073015; Karakatsani A, 2003, EUR J EPIDEMIOL, V18, P45; Kunzli N, 2009, THORAX, V64, P664, DOI 10.1136/thx.2008.110031; Kurmi OP, 2010, THORAX, V65, P221, DOI 10.1136/thx.2009.124644; Lindgren A, 2009, INT J HEALTH GEOGR, V8, DOI 10.1186/1476-072X-8-2; Ling Sean H, 2009, Int J Chron Obstruct Pulmon Dis, V4, P233; Lokke A, 2006, THORAX, V61, P935, DOI 10.1136/thx.2006.062802; Naess O, 2007, AM J EPIDEMIOL, V165, P435, DOI 10.1093/aje/kwk016; Probst-Hensch NM, 2010, THORAX, V65, P150, DOI 10.1136/thx.2009.115063; Pujades-Rodriguez Mar, 2009, BMC Pulm Med, V9, P42, DOI 10.1186/1471-2466-9-42; Raaschou-Nielsen O, 2001, AM J EPIDEMIOL, V153, P433, DOI 10.1093/aje/153.5.433; Raaschou-Nielsen O, 2000, J EXPO ANAL ENV EPID, V10, P4, DOI 10.1038/sj.jea.7500070; Raaschou-Nielsen O, 2010, CANCER EPIDEM BIOMAR, V19, P1284, DOI 10.1158/1055-9965.EPI-10-0036; Salvi SS, 2009, LANCET, V374, P733, DOI 10.1016/S0140-6736(09)61303-9; Schikowski T, 2005, RESP RES, V6, DOI 10.1186/1465-9921-6-152; Schindler C, 2009, AM J RESP CRIT CARE, V179, P579, DOI 10.1164/rccm.200803-388OC; Silva GE, 2004, CHEST, V126, P59, DOI 10.1378/chest.126.1.59; Sint T, 2008, INHAL TOXICOL, V20, P25, DOI 10.1080/08958370701758759 ; Sun QH, 2009, CIRCULATION, V119, P538, DOI 10.1161/CIRCULATIONAHA.108.799015; Sunyer J, 2009, THORAX, V64, P645, DOI 10.1136/thx.2009.115071; Tjonneland A, 2007, SCAND J PUBLIC HEALT, V35, P432, DOI 10.1080/14034940601047986; VESTBO J, 1989, EUR RESPIR J, V2, P710; Viegi G, 2006, RESPIROLOGY, V11, P523, DOI 10.1111/j.1400-1843.2006.00886.x; Wegmann M, 2005, EXP TOXICOL PATHOL, V56, P341, DOI 10.1016/j.etp.2004.12.004	35	88	91	2	29	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.	FEB 15	2011	183	4					455	461		10.1164/rccm.201006-0937OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	724IE	WOS:000287568500009	20870755	
J	Norval, M; Lucas, RM; Cullen, AP; de Gruijl, FR; Longstreth, J; Takizawa, Y; van der Leun, JC				Norval, M.; Lucas, R. M.; Cullen, A. P.; de Gruijl, F. R.; Longstreth, J.; Takizawa, Y.; van der Leun, J. C.			The human health effects of ozone depletion and interactions with climate change	PHOTOCHEMICAL & PHOTOBIOLOGICAL SCIENCES			English	Review							NONMELANOMA SKIN-CANCER; BASAL-CELL CARCINOMA; VITAMIN-D STATUS; TYPE-1 DIABETES-MELLITUS; CUTANEOUS MALIGNANT-MELANOMA; POLYMORPHIC LIGHT ERUPTION; HEPATITIS-B VACCINATION; REGULATORY-T-CELLS; CIRCULATING 25-HYDROXYVITAMIN-D LEVELS; RADIATION-INDUCED IMMUNOSUPPRESSION	Depletion of the stratospheric ozone layer has led to increased solar UV-B radiation (280-315 nm) at the surface of the Earth. This change is likely to have had an impact on human exposure to UV-B radiation with consequential detrimental and beneficial effects on health, although behavioural changes in society over the past 60 years or so with regard to sun exposure are of considerable importance. The present report concentrates on information published since our previous report in 2007. The adverse effects of UV radiation are primarily on the eye and the skin. While solar UV radiation is a recognised risk factor for some types of cataract and for pterygium, the evidence is less strong, although increasing, for ocular melanoma, and is equivocal at present for age-related macular degeneration. For the skin, the most common harmful outcome is skin cancer, including melanoma and the non-melanoma skin cancers, basal cell carcinoma and squamous cell carcinoma. The incidence of all three of these tumours has risen significantly over the past five decades, particularly in people with fair skin, and is projected to continue to increase, thus posing a significant world-wide health burden. Overexposure to the sun is the major identified environmental risk factor in skin cancer, in association with various genetic risk factors and immune effects. Suppression of some aspects of immunity follows exposure to UV radiation and the consequences of this modulation for the immune control of infectious diseases, for vaccination and for tumours, are additional concerns. In a common sun allergy (polymorphic light eruption), there is an imbalance in the immune response to UV radiation, resulting in a sun-evoked rash. The major health benefit of exposure to solar UV-B radiation is the production of vitamin D. Vitamin D plays a crucial role in bone metabolism and is also implicated in protection against a wide range of diseases. Although there is some evidence supporting protective effects for a range of internal cancers, this is not yet conclusive, but strongest for colorectal cancer, at present. A role for vitamin D in protection against several autoimmune diseases has been studied, with the most convincing results to date for multiple sclerosis. Vitamin D is starting to be assessed for its protective properties against several infectious and coronary diseases. Current methods for protecting the eye and the skin from the adverse effects of solar UV radiation are evaluated, including seeking shade, wearing protective clothing and sunglasses, and using sunscreens. Newer possibilities are considered such as creams that repair UV-induced DNA damage, and substances applied topically to the skin or eaten in the diet that protect against some of the detrimental effects of sun exposure. It is difficult to provide easily understandable public health messages regarding "safe" sun exposure, so that the positive effects of vitamin D production are balanced against the negative effects of excessive exposure. The international response to ozone depletion has included the development and deployment of replacement technologies and chemicals. To date, limited evidence suggests that substitutes for the ozone-depleting substances do not have significant effects on human health. In addition to stratospheric ozone depletion, climate change is predicted to affect human health, and potential interactions between these two parameters are considered. These include altering the risk of developing skin tumours, infectious diseases and various skin diseases, in addition to altering th efficiency by which pathogenic microorganisms are inactivated in the environment.	[Norval, M.] Univ Edinburgh, Sch Med, Edinburgh EH8 9AG, Midlothian, Scotland; [Lucas, R. M.] Australian Natl Univ, Natl Ctr Epidemiol & Populat Hlth, Canberra, ACT 0200, Australia; [Cullen, A. P.] Univ Waterloo, Sch Optometry, Waterloo, ON N2L 5T6, Canada; [de Gruijl, F. R.] Leiden Univ, Med Ctr, Dept Dermatol, NL-2300 RC Leiden, Netherlands; [Longstreth, J.] Inst Global Risk Res, Bethesda, MD 20817 USA; [Takizawa, Y.] Natl Inst Minamata Dis, Minamata, Kumamoto 8670008, Japan; [van der Leun, J. C.] Ecofys, NL-3526 KL Utrecht, Netherlands	Norval, M (reprint author), Univ Edinburgh, Sch Med, Edinburgh EH8 9AG, Midlothian, Scotland.	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Photobiol. Sci.		2011	10	2					199	225		10.1039/c0pp90044c		27	Biochemistry & Molecular Biology; Biophysics; Chemistry, Physical	Biochemistry & Molecular Biology; Biophysics; Chemistry	714UV	WOS:000286835400002	21253670	
J	Penard-Morand, C; Raherison, C; Charpin, D; Kopferschmitt, C; Lavaud, F; Caillaud, D; Annesi-Maesano, I				Penard-Morand, C.; Raherison, C.; Charpin, D.; Kopferschmitt, C.; Lavaud, F.; Caillaud, D.; Annesi-Maesano, I.			Long-term exposure to close-proximity air pollution and asthma and allergies in urban children	EUROPEAN RESPIRATORY JOURNAL			English	Article						Air pollution; allergic rhinitis; allergic sensitisation; asthma; eczema; exposure assessment	RESPIRATORY HEALTH; CHILDHOOD ASTHMA; NITROGEN-DIOXIDE; DIESEL EXHAUST; PARTICLES; SCHOOLCHILDREN; SYMPTOMS; OUTDOOR; COHORT; ISAAC	The aim of this study was to evaluate the impact of urban air pollution, assessed through reliable indicators of exposure, on asthma and allergies in schoolchildren. A validated dispersion model combining data on traffic conditions, topography, meteorology and background pollution was used to relate 3-yrs averaged concentrations of major urban pollutants at the sites of schools to skin prick tests, exercise-induced asthma and reported asthma and allergies in 6,683 children (9-11 yrs) attending 108 schools randomly selected in six French communities. For the 4,907 children who had resided at their current address for the past 3 yrs, asthma (exercise induced, past year and lifetime) was significantly positively associated with benzene, SO(2), particles with a 50% cut-off aerodynamic diameter of 10 mm (PM(10)), nitrogen oxides (NO(x)) and CO. In the same children, eczema (lifetime and past year) was significantly positively associated with benzene, PM(10), NO(2), NO x and CO, lifetime allergic rhinitis with PM(10) and sensitisation to pollens with benzene and PM(10). Among the 2,213 children residing at their current address since birth, the associations persisted for lifetime asthma with benzene (adjusted OR per interquartile range (95% CI) 1.3 (1.0-1.9)) and PM10 (1.4 (1.0-2.0)), and for sensitisation to pollens with volatile organic compounds (1.3 (1.0-1.9)) and PM10 (1.2 (1.0-1.9)). Accurately modelled urban air pollution was associated with some measures of childhood asthma and allergies.	[Penard-Morand, C.; Annesi-Maesano, I.] INSERM, UMR S 707, F-75654 Paris 13, France; [Penard-Morand, C.; Annesi-Maesano, I.] Univ Paris 06, UMR S 707, F-75252 Paris 05, France; [Penard-Morand, C.] AgroParisTech, Inst Sci & Ind Vivant & Environm, ENGREF, Paris, France; [Raherison, C.] Hop Haut Leveque, Ctr Francois Magendie, Pessac, France; [Raherison, C.] Univ Bordeaux 2, Inst Publ Hlth, EA 3672, F-33076 Bordeaux, France; [Charpin, D.] Hop Nord Marseille, Serv Pneumol, Marseille, France; [Kopferschmitt, C.] Nouvel Hop Civil, Serv Pneumol, Strasbourg, France; [Lavaud, F.] CHU Reims, Hop Maison Blanche, Serv Pneumol, Reims, France; [Caillaud, D.] CHU Clermont Ferrand, Hop Gabriel Montpied, Serv Pneumol, Clermont Ferrand, France	Penard-Morand, C (reprint author), INSERM UPMC Paris 6, Med Sch St Antoine, UMR S 707, 27 Rue Chaligny, F-75571 Paris 12, France.	celine.morand@polytechnique.org	Annesi-Maesano, Isabella/D-9173-2016; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			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; 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; Carr D, 2002, ENVIRON RES, V90, P111, DOI 10.1006/enrs.2002.4393; Chen TM, 2007, AM J MED SCI, V333, P249, DOI 10.1097/MAJ.0b013e31803b900f; CORBO GM, 1993, J ALLERGY CLIN IMMUN, V92, P616, DOI 10.1016/0091-6749(93)90086-U; Diaz-Sanchez D, 2000, J ALLERGY CLIN IMMUN, V106, P1140, DOI 10.1067/mai.2000.111144; DOCKERY DW, 1989, AM REV RESPIR DIS, V139, P587; Fenger J, 1999, ATMOS ENVIRON, V33, P4877, DOI 10.1016/S1352-2310(99)00290-3; Fischer PH, 2000, ATMOS ENVIRON, V34, P3713, DOI 10.1016/S1352-2310(00)00067-4; Gauderman WJ, 2005, EPIDEMIOLOGY, V16, P737, DOI 10.1097/01.ede.00001813087.51440.75; Heinrich Joachim, 2004, Curr Opin Allergy Clin Immunol, V4, P341, DOI 10.1097/00130832-200410000-00003; 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; Jerrett M, 2008, ENVIRON HEALTH PERSP, V116, P1433, DOI 10.1289/ehp.10968; Kim JJ, 2004, AM J RESP CRIT CARE, V170, P520, DOI 10.1164/rccm.200403-2810C; Kramer U, 2000, EPIDEMIOLOGY, V11, P64, DOI 10.1097/00001648-200001000-00014; Morgenstern V, 2007, OCCUP ENVIRON MED, V64, P8, DOI 10.1136/oem.2006.028241; Nel A, 2005, SCIENCE, V308, P804, DOI 10.1126/science.1108752; Nicolai T, 2003, EUR RESPIR J, V21, P956, DOI 10.1183/09031936.03.00041103; Penard-Morand C, 2008, REV MAL RESPIR, V25, P1013, DOI 10.1019/200820019; Penard-Morand C, 2005, CLIN EXP ALLERGY, V35, P1279, DOI 10.1111/j.1365-2222.2005.02336.x; Penard-Morand C, 2006, ATMOS ENVIRON, V40, P2274, DOI 10.1016/j.atmosenv.2005.11.057; Reungoat P, 2005, J EXPO ANAL ENV EPID, V15, P524, DOI 10.1038/sj.jea.7500430; Salvi S, 1999, AM J RESP CRIT CARE, V159, P702; Sunyer J, 1997, THORAX, V52, P760; Weiland SK, 2004, EUR RESPIR J, V24, P406, DOI 10.1183/09031936.04.00090303; Wilkinson P, 1999, THORAX, V54, P1070; WJST M, 1993, BRIT MED J, V307, P596; Zmirou D, 2004, J EPIDEMIOL COMMUN H, V58, P18, DOI 10.1136/jech.58.1.18; 1998, LANCET, V351, P1225	32	88	92	2	22	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	442 GLOSSOP RD, SHEFFIELD S10 2PX, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	JUL	2010	36	1					33	40		10.1183/09031936.00116109		8	Respiratory System	Respiratory System	618YY	WOS:000279394100009	20075054	
J	Senti, G; Johansen, P; Haug, S; Bull, C; Gottschaller, C; Muller, P; Pfister, T; Maurer, P; Bachmann, MF; Graf, N; Kundig, TM				Senti, G.; Johansen, P.; Haug, S.; Bull, C.; Gottschaller, C.; Muller, P.; Pfister, T.; Maurer, P.; Bachmann, M. F.; Graf, N.; Kundig, T. M.			Use of A-type CpG oligodeoxynucleotides as an adjuvant in allergen-specific immunotherapy in humans: a phase I/IIa clinical trial	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergy; house dust mite; specific immunotherapy; Type A CpG; virus-like particles	HOUSE-DUST-MITE; MONOPHOSPHORYL-LIPID-A; DERMATOPHAGOIDES-PTERONYSSINUS; BRONCHIAL HYPERREACTIVITY; IMMUNOSTIMULATORY DNA; POLLEN IMMUNOTHERAPY; ASTHMATIC-CHILDREN; DENDRITIC CELLS; RAGWEED ALLERGY; BACTERIAL-DNA	B-type CpG oligodeoxynucleotides (ODN) is currently used in clinical trials because of its prolonged half-life, which is due to its phosphorothioate backbone. A-type CpG ODN is a stronger inducer of IFN but has an unstable phosphodiester backbone that has so far prohibited its clinical use. However, upon association with virus-like particles (VLP) consisting of the bacteriophage Q beta coat protein, A-type CpG ODN can be stabilized and can become an efficient adjuvant in mice. Therefore, the phase I/IIa study presented represents the first test of A-type CpGs in humans. To test the safety, tolerability and clinical efficacy of QbG10 as an adjuvant for subcutaneous immunotherapy with a house dust mite (HDM) allergen extract in allergic patients. A single centre, open-label phase I/IIa study evaluated the safety, tolerability and clinical efficacy of QbG10 as an adjuvant to immunotherapy with a subcutaneous HMD allergen extract in 20 patients suffering from HDM allergy. Twenty-one patients were enrolled between March and July 2005. Individual immunotherapy lasted 10 weeks. Clinical end-points included questionnaires, conjunctival provocation, skin prick tests and the measurement of allergen-specific IgG and IgE. QbG10 was well tolerated. Almost complete tolerance to the allergen was observed in conjunctival provocation testing after treatment with QbG10, and symptoms of rhinitis and allergic asthma were significantly reduced. Within 10 weeks of therapy, patients were nearly symptom-free and this amelioration lasted for at least 38 weeks post-treatment. Following injections of QbG10 and HDM allergen extract, allergen-specific IgG increased, while there was a transient increase in allergen-specific IgE titres. Skin reactivity to HDM was reduced. The subcutaneous application of HDM allergen, together with A-type CpG ODN packaged into VLP, was safe. All patients achieved practically complete alleviation of allergy symptoms after 10 weeks of immunotherapy. This promising clinical outcome calls for larger placebo-controlled phase II studies. G. Senti, P. Johansen, S. Haug, C. Bull, C. Gottschaller, P. Muller, T. Pfister, P. Maurer, M. F. Bachmann, N. Graf and T. M. Kundig, Clinical & Experimental Allergy, 2009 (39) 562-570.	[Senti, G.; Johansen, P.; Haug, S.; Bull, C.; Gottschaller, C.; Kundig, T. M.] Univ Zurich Hosp, Dept Dermatol, Unit Expt Immunotherapy, CH-8091 Zurich, Switzerland; [Senti, G.; Graf, N.] Univ Zurich Hosp, Clin Res Ctr, CH-8091 Zurich, Switzerland; [Muller, P.; Pfister, T.; Maurer, P.; Bachmann, M. F.] Cytos Biotechnol AG, Schlieren, Switzerland	Kundig, TM (reprint author), Univ Zurich Hosp, Dept Dermatol, Unit Expt Immunotherapy, Gloriastr 31, CH-8091 Zurich, Switzerland.	thomas.kuendig@usz.ch	Johansen, Pal/A-1403-2013				Arbes SJ, 2005, J ALLERGY CLIN IMMUN, V116, P377, DOI 10.1016/j.jaci.2005.05.017; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Bousquet J, 1998, J ALLERGY CLIN IMMUN, V102, P558, DOI 10.1016/S0091-6749(98)70271-4; CASTELAIN PY, 1988, CONTACT DERMATITIS, V19, P58, DOI 10.1111/j.1600-0536.1988.tb02869.x; Comoy EE, 1997, INT IMMUNOL, V9, P523, DOI 10.1093/intimm/9.4.523; Cox JC, 1997, VACCINE, V15, P248, DOI 10.1016/S0264-410X(96)00183-1; Creticos PS, 2006, NEW ENGL J MED, V355, P1445, DOI 10.1056/NEJMoa052916; Drachenberg KJ, 2001, ALLERGY, V56, P498, DOI 10.1034/j.1398-9995.2001.056006498.x; DREBORG S, 1993, ALLERGY, V48, P473, DOI 10.1111/j.1398-9995.1993.tb01102.x; Durham SR, 1999, NEW ENGL J MED, V341, P468, DOI 10.1056/NEJM199908123410702; Gauvreau GM, 2006, AM J RESP CRIT CARE, V174, P15, DOI 10.1164/rccm.200601-057OC; Guez S, 2000, ALLERGY, V55, P369, DOI 10.1034/j.1398-9995.2000.00413.x; Hartmann G, 1999, P NATL ACAD SCI USA, V96, P9305, DOI 10.1073/pnas.96.16.9305; HAUGAARD L, 1993, J ALLERGY CLIN IMMUN, V91, P709, DOI 10.1016/0091-6749(93)90190-Q; Kline Joel N, 2007, Proc Am Thorac Soc, V4, P283, DOI 10.1513/pats.200701-019AW; Klinman Dennis M, 2004, Nat Rev Immunol, V4, P249, DOI 10.1038/nri1329; Kohama Y, 1999, J ALLERGY CLIN IMMUN, V104, P1231; Krieg AM, 2002, ANNU REV IMMUNOL, V20, P709, DOI 10.1146/annurev.immunol.20.100301.064842; Larche M, 2006, NAT REV IMMUNOL, V6, P761, DOI 10.1038/nri1934; Manolova V, 2008, EUR J IMMUNOL, V38, P1404, DOI 10.1002/eji.200737984; Marshall JD, 2001, J ALLERGY CLIN IMMUN, V108, P191, DOI 10.1067/mai.2001.116984; Moller C, 2002, J ALLERGY CLIN IMMUN, V109, P251, DOI 10.1067/mai.2002.121317; Mothes N, 2003, CLIN EXP ALLERGY, V33, P1198, DOI 10.1046/j.1365-2222.2003.01699.x; Mutwiri GK, 2004, J CONTROL RELEASE, V97, P1, DOI 10.1016/j.jcornel.2004.02.022; Olsen OT, 1997, ALLERGY, V52, P853, DOI 10.1111/j.1398-9995.1997.tb02157.x; OSTERBALLE O, 1982, ALLERGY, V37, P553, DOI 10.1111/j.1398-9995.1982.tb02340.x; Pajno GB, 2001, CLIN EXP ALLERGY, V31, P1392, DOI 10.1046/j.1365-2222.2001.01161.x; Pajno GB, 2007, J ALLERGY CLIN IMMUN, V119, P796, DOI 10.1016/j.jaci.2007.01.009; Pichler CE, 1997, ALLERGY, V52, P274, DOI 10.1111/j.1398-9995.1997.tb00991.x; Pichler CE, 2001, ALLERGY, V56, P301, DOI 10.1034/j.1398-9995.2001.00834.x; Pierson-Mullany LK, 2000, ANN ALLERG ASTHMA IM, V84, P241, DOI 10.1016/S1081-1206(10)62761-5; Pifferi M, 2002, ALLERGY, V57, P785, DOI 10.1034/j.1398-9995.2002.23498.x; Rothenfusser S, 2002, HUM IMMUNOL, V63, P1111, DOI 10.1016/S0198-8859(02)00749-8; Rueff F, 2004, ALLERGY, V59, P589, DOI 10.1111/j.1398-9995.2004.00505.x; SANDS H, 1994, MOL PHARMACOL, V45, P932; Senti Gabriela, 2006, Inflammation & Allergy Drug Targets, V5, P243, DOI 10.2174/187152806779010963; Simons FER, 2004, J ALLERGY CLIN IMMUN, V113, P1144, DOI 10.1016/j.jaci.2004.03.003; Sledge RF, 1938, US NAVAL MED B, V36, P18; Sparwasser T, 1997, NATURE, V386, P336, DOI 10.1038/386336a0; Storni T, 2004, J IMMUNOL, V172, P1777; SUSSMAN GL, 1982, ANN ALLERGY, V48, P75; Terreehorst I, 2003, NEW ENGL J MED, V349, P237, DOI 10.1056/NEJMoa023171; Tighe H, 2000, J ALLERGY CLIN IMMUN, V106, P124, DOI 10.1067/mai.2000.107927; Till SJ, 2004, J ALLERGY CLIN IMMUN, V113, P1025, DOI 10.1016/j.jaci.2004.03.024; VARNEY VA, 1991, BRIT MED J, V302, P265; Verthelyi D, 2002, J IMMUNOL, V168, P1659; Verthelyi D, 2001, J IMMUNOL, V166, P2372; Vissers JLM, 2004, J ALLERGY CLIN IMMUN, V113, P1204, DOI 10.1016/j.jaci.2004.02.041; von Beust BR, 2005, EUR J IMMUNOL, V35, P1869, DOI 10.1002/eji.200526124; Wheeler AW, 2004, EXPERT OPIN BIOL TH, V4, P1473, DOI 10.1517/14712598.4.9.1473; Wilcock LK, 2004, CLIN EXP ALLERGY, V34, P1373, DOI 10.1111/j.1365-2222.2004.02052.x; Woodcock A, 2003, NEW ENGL J MED, V349, P225, DOI 10.1056/NEJMoa023175	52	88	93	1	10	WILEY-BLACKWELL PUBLISHING, INC	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	APR	2009	39	4					562	570		10.1111/j.1365-2222.2008.03191.x		9	Allergy; Immunology	Allergy; Immunology	418YA	WOS:000264184800015	19226280	
J	Matricardi, PM; Illi, S; Gruber, C; Keil, T; Nickel, R; Wahn, U; Lau, S				Matricardi, P. M.; Illi, S.; Grueber, C.; Keil, T.; Nickel, R.; Wahn, U.; Lau, S.			Wheezing in childhood: incidence, longitudinal patterns and factors predicting persistence	EUROPEAN RESPIRATORY JOURNAL			English	Article						asthma; atopic dermatitis; children; epidemiology; prediction of persistence; wheezing	BIRTH COHORT; INHALED CORTICOSTEROIDS; ASTHMA-TREATMENT; FOLLOW-UP; HIGH-RISK; CHILDREN; PREVENTION; LIFE; AGE; SENSITIZATION	Childhood asthma is frequently perceived as a disease with uniform clinical pathways. This perception might be an oversimplification. The aim of the present study was to investigate the incidence and natural course of wheeze over the first 13 yrs of life and analyse the risk factors predicting wheeze at 11-13 yrs of age. The Multicentre Allergy Study, a German birth cohort, recruited 1,314 children in 1990. Physical examinations, interviews on atopic diseases, immunoglobulin (Ig)E and lung function tests were performed up to 13 yrs of age. Complete data on the course of wheeze were available for 441 children. It was found that incidence of wheezing declined with age. The first wheezing episode was reported by 299 9 and 9% of participants at <= 3 (early wheezers), 3-6 (late wheezers), and >6 yrs (very late wheezers) of age, respectively. Wheezing at the age of 13 yrs was associated with parental atopy, and with IgE sensitisation to common allergens, elevated total IgE and exposure to high levels of indoor allergens in early life. All these associations were remarkably stronger among early wheezers than among early nonwheezers. In conclusion, the relevance of an early expression of atopy as a predictor of wheezing at age 13 yrs declines with increasing age of wheezing onset.	[Keil, T.] Charite Univ Med Ctr, Inst Social Med Epidemiol & Hlth Econ, Berlin, Germany; [Illi, S.] Univ Childrens Hosp, Munich, Germany; [Matricardi, P. M.; Grueber, C.; Nickel, R.; Wahn, U.; Lau, S.] Charite Univ Med Ctr, Dept Paediat Pneumol & Immunol, Berlin, Germany	Matricardi, PM (reprint author), Charite Univ Med Berlin, Dept Paediat Pneumol & Immunol, Augustenburger Pl 1, D-13353 Berlin, Germany.	paolo.matricardi@charite.de			German Ministry of Education and Research (BMBF) [O1EE9406]	The present study was supported by the German Ministry of Education and Research (BMBF), grant number O1EE9406.	Asher I, 2004, INT ARCH ALLERGY IMM, V135, P83, DOI 10.1159/000080524; Asher MI, 2006, LANCET, V368, P733, DOI 10.1016/S0140-6736(06)69283-0; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Balemans WAF, 2006, J CLIN EPIDEMIOL, V59, P1207, DOI 10.1016/j.jclinepi.2006.02.011; Bergmann R L, 1994, Pediatr Allergy Immunol, V5, P19, DOI 10.1111/j.1399-3038.1994.tb00343.x; Bisgaard H, 2006, NEW ENGL J MED, V354, P1998, DOI 10.1056/NEJMoa054692; Castro-Rodriguez JA, 2000, AM J RESP CRIT CARE, V162, P1403; Eid NS, 2004, CLIN PEDIATR, V43, P793, DOI 10.1177/000992280404300903; Eysink PED, 2005, BRIT J GEN PRACT, V55, P125; Guerra S, 2004, AM J RESP CRIT CARE, V170, P78, DOI 10.1164/rccm.200309-1224OC; Guilbert TW, 2006, NEW ENGL J MED, V354, P1985, DOI 10.1056/NEJMoa051378; Hyvarinen MK, 2005, PEDIATR PULM, V40, P316, DOI 10.1002/ppul.20273; Illi S, 2001, BRIT MED J, V322, P390, DOI 10.1136/bmj.322.7283.390; Illi S, 2004, J ALLERGY CLIN IMMUN, V113, P925, DOI 10.1016/j.jaci.2004.01.778; Illi S, 2006, LANCET, V368, P763, DOI 10.1016/S0140-6736(06)69286-6; KJELLMAN NIM, 1976, CLIN ALLERGY, V6, P51, DOI 10.1111/j.1365-2222.1976.tb01411.x; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; Lieu TA, 1998, AM J RESP CRIT CARE, V157, P1173; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Martinez FD, 2007, J ALLERGY CLIN IMMUN, V119, P30, DOI 10.1016/j.jaci.2006.10.020; Rhodes HL, 2002, AM J RESP CRIT CARE, V165, P176; Simpson A, 2005, CURR OPIN ALLERGY CL, V5, P223, DOI 10.1097/01.all.0000168785.51711.27; Toelle BG, 2004, EUR RESPIR J, V23, P66, DOI 10.1183/09031936.03.00046903; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; [Anonymous], 2006, LANCET, V368, P705	25	88	92	1	6	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	2008	32	3					585	592		10.1183/09031936.00066307		8	Respiratory System	Respiratory System	351OG	WOS:000259433100010	18480107	
J	Bousquet, J; Boulet, LP; Peters, MJ; Magnussen, H; Quiralte, J; Martinez-Aguilarf, NE; Carlsheimer, A				Bousquet, Jean; Boulet, Louis-Philippe; Peters, Matthew J.; Magnussen, Helgo; Quiralte, Joaquin; Martinez-Aguilarf, Nora E.; Carlsheimer, Asa			Budesonide/formoterol for maintenance and relief in uncontrolled asthma vs. high-dose salmeterol/fluticasone	RESPIRATORY MEDICINE			English	Article						asthma control; exacerbations; hospitatisations; combination therapy; maintenance plus as needed	RANDOMIZED CONTROLLED-TRIAL; INHALED BUDESONIDE; SINGLE INHALER; FORMOTEROL; EXACERBATIONS; COMBINATION; THERAPY; SALMETEROL; METAANALYSIS; MEDICATION	Background: Budesonide/formoterol maintenance and reliever therapy (Symbicort SMART (R)) improves asthma control compared with fixed-dose inhaled corticosteroid/ long-acting beta(2)-agonist (ICS/LABA) regimens, but its efficacy has not been assessed in comparison with sustained high-dose satmeterol/fluticasone (Seretide(TM)) plus a short-acting beta(2)-agonist (SABA). Methods: Patients (N = 2309) with symptomatic asthma (aged _> 12 years; forced expiratory volume in 1 s > 50% predicted), who had experienced an asthma exacerbation in the previous year, were randomised to receive budesonide/formoterol 160/4.5 mu g two inhalations twice daily and as needed, or one inhalation of salmeterot/fluticasone 50/500 mu g twice daily plus terbutaline as needed, for 6 months. Results: Time to first severe exacerbation, the pre-specified primary outcome, was not significantly prolonged (risk ratio 0.82; 95% confidence interval 0.63, 1.05). Budesonide/ formoterol maintenance and reliever therapy reduced total exacerbations from 31 to 25 events/100 patients/year (P=0.039), and exacerbations requiring hospitalisation/ emergency room (ER) treatment from 13 to 9 events/100 patients/year (P=0.046). The treatments showed no difference in measures of lung function or asthma symptoms. The mean dose of ICS received was lower using budesonide/formoterol maintenance and reliever therapy (792 mu g/day budesonide [1238 mu g/day beclomethasone dipropionate (BDP) equivalent] versus 1000 mu g/day fluticasone [2000 mu g/day BDP equivalent] with salmeterol/ fluticasone therapy; P<0.0001). Both treatments were well tolerated. Conclusion: In the treatment of uncontrolled asthma, budesonide/formoterol maintenance and reliever therapy reduces the incidence of severe asthma exacerbations and hospitalisation/ER treatment with similar daily symptom control compared with sustained high-dose salmeterol/fluticasone plus SABA. This benefit is achieved with substantially less ICS exposure. (C) 2007 Published by Elsevier Ltd.	Hop Arnaud Villeneuve, F-34000 Montpellier, France; Hop Laval, Inst Cardiol & Pneumol, Quebec City, PQ, Canada; Concord Hosp, Concord, Australia; Krankenhaus Grosshansdorf, Zentrum Pneumol & Thoraxchirurg, Lehrstuhl Innere Med Pneumol, Grosshansdorf, Germany; Complejo Hosp Jaen, Unidad Alergia, Jaen, Spain; AstraZeneca, Lund, Sweden	Bousquet, J (reprint author), Hop Arnaud Villeneuve, 371 Ave Doyen Gaston Giraud, F-34000 Montpellier, France.	jean.bousquet@orange.fr	IBIS, ALERGICAS/C-1733-2016				Anderson HR, 2005, BRIT MED J, V330, P117, DOI 10.1136/bmj.38316.729907.8F; Angus R, 2005, INT J CLIN PRACT, V59, P156, DOI 10.1111/j.1368-5031.2004.00455.x; Barnes PJ, 2007, EUR RESPIR J, V29, P587, DOI 10.1183/09031936.00080306; Bateman ED, 2004, AM J RESP CRIT CARE, V170, P836, DOI 10.1164/rccm.200401-033OC; Bousquet J, 2007, ALLERGY, V62, P102, DOI 10.1111/j.1398-9995.2006.01305.x; *BRIT5 THOR SOC SC, 2005, BRIT GUID MAN ASTHM; Duong M, 2007, J ALLERGY CLIN IMMUN, V119, P322, DOI 10.1016/j.jaci.2006.10.018; Edwards SJ, 2007, CURR MED RES OPIN, V23, P1809, DOI 10.1185/030079907X210697; FitzGerald JM, 2006, THORAX, V61, P992, DOI 10.1136/thx.2005.045195; FitzGerald JM, 2004, THORAX, V59, P550, DOI 10.1136/thx.2003.014936; Gibson PG, 2001, AM J RESP CRIT CARE, V163, P32; Global Initiative for Asthma, 2006, GLOB STRAT ASTHM MAN; Harrison TW, 2004, LANCET, V363, P271, DOI 10.1016/S0140-6736(03)15384-6; Humbert M, 2007, ALLERGY, V62, P95, DOI 10.1111/j.1398-9995.2006.01308.x; Juniper EF, 2005, RESP MED, V99, P553, DOI 10.1016/j.rmed.2004.10.008; Kuna P, 2007, INT J CLIN PRACT, V61, P725, DOI 10.1111/j.1742-1241.2007.01338.x; Lai CKW, 2003, J ALLERGY CLIN IMMUN, V111, P263, DOI 10.1067/mai.2003.30; Lanes SF, 2002, THORAX, V57, P683, DOI 10.1136/thorax.57.8.683; Mendes ES, 2003, EUR RESPIR J, V21, P989, DOI 10.1183/09031936.03.00072402; *NIH, 974051 NIH PUBL; O'Byrne PM, 2001, AM J RESP CRIT CARE, V164, P1392; O'Byrne PM, 2005, AM J RESP CRIT CARE, V171, P129, DOI 10.1164/rccm.200407-884OC; Palmqvist M, 1997, EUR RESPIR J, V10, P2484, DOI 10.1183/09031936.97.10112489; Palmqvist M, 1999, AM J RESP CRIT CARE, V160, P244; Paredi P, 2005, RESP RES, V6, DOI 10.1186/1465-9921-6-15; Partridge Martyn R, 2006, BMC Pulm Med, V6, P13, DOI 10.1186/1471-2466-6-13; Pauwels RA, 1997, NEW ENGL J MED, V337, P1405, DOI 10.1056/NEJM199711133372001; Pauwels RA, 2003, EUR RESPIR J, V22, P787, DOI 10.1183/09031936.03.00055803; Rabe KF, 2004, J ALLERGY CLIN IMMUN, V114, P40, DOI 10.1016/j.jaci.2004.04.042; Rabe KF, 2006, LANCET, V368, P744, DOI 10.1016/S0140-6736(06)69284-2; Sin DD, 2004, JAMA-J AM MED ASSOC, V292, P367, DOI 10.1001/jama.292.3.367; Tattersfield AE, 2001, LANCET, V357, P257, DOI 10.1016/S0140-6736(00)03611-4; Tintinger GR, 2000, INFLAMMATION, V24, P239, DOI 10.1023/A:1007013530072; van Veen A, 2003, PULM PHARMACOL THER, V16, P153, DOI 10.1016/S1094-5539(03)00003-8; Vogelmeier C, 2005, EUR RESPIR J, V26, P819, DOI 10.1183/09031936.05.00028305	35	88	91	1	12	W B SAUNDERS CO LTD	LONDON	32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND	0954-6111			RESP MED	Respir. Med.	DEC	2007	101	12					2437	2446		10.1016/j.rmed.2007.07.014		10	Cardiac & Cardiovascular Systems; Respiratory System	Cardiovascular System & Cardiology; Respiratory System	235DC	WOS:000251212700002	17905575	
J	Lee, JH; Haselkorn, T; Borish, L; Rasouliyan, L; Chipps, BE; Wenzel, SE				Lee, June H.; Haselkorn, Tmirah; Borish, Larry; Rasouliyan, Lawrence; Chipps, Bradley E.; Wenzel, Sally E.			Risk factors associated with persistent airflow limitation in severe or difficult-to-treat asthma	CHEST			English	Article						airway remodeling; difficult-to-treat asthma; irreversible airway obstruction; persistent airflow limitation; severe asthma	ETHNICALLY DIVERSE POPULATIONS; TREATMENT REGIMENS TENOR; LUNG-FUNCTION; BETA(2)-ADRENERGIC RECEPTOR; COMPUTED-TOMOGRAPHY; SUSCEPTIBILITY LOCI; CIGARETTE-SMOKING; NATURAL-HISTORY; WALL THICKNESS; MILD ASTHMA	Background: The Epidemiology and Natural History of Asthma: Outcomes and Treatment Regimens study is among the largest to assess persistent airflow limitation and the first to evaluate a wide range of potential risk factors in high-risk patients with severe or difficult-to-treat asthma. A better understanding is needed regarding factors associated with persistent airway obstruction; this study was performed to determine demographic and clinical characteristics associated with persistent airflow limitation. Methods: Data from adult patients (>= 18 years old) with severe or difficult-to-treat asthma were evaluated. Patients with COPD, obesity with a restrictive respiratory pattern, or a >= 30 pack-year history of smoking were excluded. Patients with persistent airflow limitation (postbronchodilator FEV1/FVC ratio <= 70% at two annual consecutive visits) and normal postbronchodilator FEV1/ FVC ratio (75 to 85%) were compared. Multivariate analysis identified factors independently associated with persistent airflow limitation. Results: Of 1,017 patients, 612 patients (60%) showed evidence of persistent airflow limitation. Risk factors were as follows: older age (odds ratio [OR] per 10 years, 1.4; 95 % confidence interval [CI], 1.3 to 1.6); male gender (OR, 4.5; 95% CI, 2.3 to 8.5); black ethnicity (OR, 2.2; 95% CI, 1.3 to 3.8); current or past smoking (OR, 3.9; 95% CI, 1.8 to 8.6; and OR, 1.6; 95% CI, 1.2 to 2.3, respectively); aspirin sensitivity (OR, 1.5; 95% CI, 1.0 to 2.4); and longer asthma duration (OR per 10 years, 1.6; 95% CI, 1.4 to 1.8). Protective factors were Hispanic ethnicity, higher education, family history of atopic dermatitis, pet(s) in the home, and dust sensitivity. Conclusions: Persistent airflow limitation is prevalent in patients with severe or difficult-to-treat asthma and is associated with identifiable clinical and demographic characteristics.	[Lee, June H.; Haselkorn, Tmirah] Genentech Inc, San Francisco, CA 94080 USA; [Borish, Larry] Univ Virginia Hlth Syst, Charlottesville, VA USA; [Rasouliyan, Lawrence] ICON Clin Res, San Francisco, CA USA; [Chipps, Bradley E.] Capital Allergy & Resp Dis Ctr, Sacramento, CA USA; [Wenzel, Sally E.] Univ Pittsburgh, Pittsburgh, PA USA	Lee, JH (reprint author), Genentech Inc, 1 DNA Way,MS 453B, San Francisco, CA 94080 USA.	lee.june@gene.com	panduru, mihaela/H-2411-2011; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Abraham B, 2003, EUR RESPIR J, V22, P470, DOI 10.1183/09031936.03.00261903; American Lung Association Epidemiology and Statistics Unit Research and Scientific Affairs, 2006, TRENDS ASTHM MORB MO; American Thoracic Society, 2000, AM J RESP CRIT CARE, V162, P2341, DOI DOI 10.1164/AJRCCM.162.6.ATS9-00; Bleecker Eugene R, 2004, Chest, V126, p93S, DOI 10.1378/chest.126.2_suppl_1.93S; Bumbacea D, 2004, EUR RESPIR J, V24, P122, DOI 10.1183/09031936.04.00077803; Chalmers GW, 2002, THORAX, V57, P226, DOI 10.1136/thorax.57.3.226; Covar RA, 2004, AM J RESP CRIT CARE, V170, P234, DOI 10.1164/rccm.200308-11740C; Dolan CM, 2004, ANN ALLERG ASTHMA IM, V92, P32; Federico MJ, 2005, CHEST, V127, P571, DOI 10.1378/chest.127.2.571; Fuhlbrigge AL, 2002, IMMUNOL ALLERGY CLIN, V22, P753, DOI 10.1016/S0889-8561(02)00022-X; Gono H, 2003, EUR RESPIR J, V22, P965, DOI 10.1183/09031936.03.00085302; Grol MH, 1999, AM J RESP CRIT CARE, V160, P1830; Hansen JE, 2007, CHEST, V131, P349, DOI 10.1378/chest.06-1349; Hunninghake GM, 2006, AM J RESP CRIT CARE, V173, P143, DOI 10.1164/rccm.200508-1232SO; Israel E, 2000, AM J RESP CRIT CARE, V162, P75; James AL, 2005, AM J RESP CRIT CARE, V171, P109, DOI 10.1164/rccm.200402-230OC; Lange P, 1998, NEW ENGL J MED, V339, P1194, DOI 10.1056/NEJM199810223391703; Lee JH, 2006, J ASTHMA, V43, P179, DOI 10.1080/02770900600566405; Marsh DG, 1997, NAT GENET, V15, P389; Mascia K, 2005, J ALLERGY CLIN IMMUN, V116, P970, DOI 10.1016/j.jaci.2005.08.035; Miranda C, 2004, J ALLERGY CLIN IMMUN, V113, P101, DOI 10.1016/j.jaci.2003.10.041; *NAT HEART LUNG BL, 1997, 974051 NIH; Niimi A, 2000, AM J RESP CRIT CARE, V162, P1518; Ober C, 2000, AM J HUM GENET, V66, P517, DOI 10.1086/302781; Orie NGM, 1961, BRONCHITIS, P43; Pepe C, 2005, J ALLERGY CLIN IMMUN, V116, P544, DOI 10.1016/j.jaci.2005.06.011; Rasmussen F, 2002, AM J RESP CRIT CARE, V165, P1480, DOI 10.1164/rccm.2108009; SIAFAKAS NM, 1995, EUR RESPIR J, V8, P1398, DOI 10.1183/09031936.95.08081398; Taylor DR, 2000, THORAX, V55, P762, DOI 10.1136/thorax.55.9.762; ten Brinke A, 2001, AM J RESP CRIT CARE, V164, P744; Tomlinson JEM, 2005, THORAX, V60, P282, DOI 10.1136/thx.2004.033688; Vignola AM, 2004, EUR RESPIR J, V24, P910, DOI 10.1183/09031936.04.00032603; Vignola AM, 1998, AM J RESP CRIT CARE, V158, P1945; Vignola A. M., 2003, CHEST, V123, P417; Weir TD, 1998, AM J RESP CRIT CARE, V158, P787; Wenzel S, 2005, AM J RESP CRIT CARE, V172, P149, DOI 10.1164/rccm.200409-1181PP; Wenzel SE, 1999, AM J RESP CRIT CARE, V160, P1001; Xu JF, 2001, AM J HUM GENET, V68, P1437, DOI 10.1086/320589	38	88	91	0	2	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	DEC	2007	132	6					1882	1889		10.1378/chest.07-0713		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	246HA	WOS:000251996900029	18079222	
J	Nieuwenhuizen, N; Lopata, AL; Jeebhay, MLF; Herbert, DR; Robins, TG; Brombacher, F				Nieuwenhuizen, N; Lopata, AL; Jeebhay, MLF; Herbert, DR; Robins, TG; Brombacher, F			Exposure to the fish parasite Anisakis causes allergic airway hyperreactivity and dermatitis	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						anisakis; nematode; parasitc; gene-deficient mice; food allergy; dermatitis; asthma; occupational allergy; IL4; IL-13	LEISHMANIA-MAJOR INFECTION; FOOD ALLERGY; GASTROALLERGIC ANISAKIASIS; LARVAL ANTIGENS; SEAFOOD ALLERGY; UNITED-STATES; T-CELLS; SIMPLEX; ASTHMA; RESPONSES	Background: Several case reports show allergy and anaphylactic reactions to the fish parasite Anisakis in the domestic and occupational setting. Further research is needed on the prevalence and mechanisms of disease. Objective: To determine the prevalence of Anisakis sensitization and related symptoms among workers in 2 fish-processing factories, and to use gene-deficient mice to determine the working mechanisms of Anisakis allergy. Methods: A modified version of the European Community Respiratory Health Survey was used to interview 578 South African fish-processing workers. Sensitization to Anisakis, seafood, and common aeroallergens was determined by skin prick test. Lung function was measured by spirometry and methacholine challenge. Serum eicosapentaenoic acid levels were used as an index of seafood consumption. Sensitized wildtype, IL-4, or IL-4 receptor alpha-deficient mice were challenged orally with Anisakis extract. Allergic reactions, lung pathology, antibodies, cytokines, mast cell proteases, and histamine were evaluated. Results: The prevalence of sensitization to Anisakis was higher than the prevalence of sensitization to fish (8% vs 6%). Anisakis-specific IgE reactivity was associated with bronchial hyperreactivity and dermatitis, and significantly increased with fish consumption. In mice, Anisakis infective larvae (1,3) induced a striking T(H)2/type 2 response. Food-allergic-type reactions induced by oral challenge with Anisakis extract were absent in IL-4 receptor a knockout mice. Conclusion: Anisakis sensitization in fish-processing workers is associated with allergic symptoms and correlates with high levels of fish consumption. Anisakis proteins induce allergic reactions in sensitized mice by IL-4/IL-13-mediated mechanisms. Clinical implications: Anisakis allergy should be considered in fish-processing workers with allergic symptoms.	Univ Cape Town, Observ, Div Immunol, IIDMM,Fac Hlth Sci,Natl Hlth Lab Serv, ZA-7925 Cape Town, South Africa; Univ Cape Town, Occupat & Environm Hlth Res Unit, Sch Publ Hlth & Family Med, ZA-7925 Cape Town, South Africa; Univ Michigan, Dept Environm Hlth Sci, Ann Arbor, MI 48109 USA	Brombacher, F (reprint author), Univ Cape Town, Observ, Div Immunol, IIDMM,Fac Hlth Sci,Natl Hlth Lab Serv, ZA-7925 Cape Town, South Africa.	fbrombac@mweb.co.za	Lopata, Andreas/C-8160-2009; Lopata, Andreas/C-3831-2012; Herbert, De'Broski/J-7357-2012	Lopata, Andreas/0000-0002-2940-9235; Herbert, De'Broski/0000-0002-2449-5365	PHS HHS [R01 F002304]		Alonso-Gomez A, 2004, PARASITOL RES, V93, P378, DOI 10.1007/s00436-004-1085-9; Araujo MIAS, 2004, J INFECT DIS, V190, P1797, DOI 10.1086/425017; Armentia A, 1998, J ALLERGY CLIN IMMUN, V102, P831, DOI 10.1016/S0091-6749(98)70024-7; Audicana MT, 2002, TRENDS PARASITOL, V18, P20, DOI 10.1016/S1471-4922(01)02152-3; AUDICANA MT, 1995, J ALLERGY CLIN IMMUN, V96, P558, DOI 10.1016/S0091-6749(95)70301-2; Bashir MEH, 2002, J IMMUNOL, V169, P3284; Brewer JM, 1999, J IMMUNOL, V163, P6448; Buhl R, 2005, CURR OPIN PULM MED, V11, P27; Caballero ML, 2004, PARASITOL RES, V93, P248, DOI 10.1007/s00436-004-1099-3; Cooper PJ, 2003, J ALLERGY CLIN IMMUN, V111, P995, DOI 10.1067/mai.2003.1348; Couture C, 2003, AM J SURG PATHOL, V27, P1167, DOI 10.1097/00000478-200308000-00017; Daschner A, 2002, PARASITE IMMUNOL, V24, P243, DOI 10.1046/j.1365-3024.2002.00458.x; Daschner A, 2000, J ALLERGY CLIN IMMUN, V105, P176, DOI 10.1016/S0091-6749(00)90194-5; Daschner A, 2001, ALLERGY, V56, P1003, DOI 10.1034/j.1398-9995.2001.00207.x; Davey G, 2005, CLIN EXP ALLERGY, V35, P301, DOI 10.1111/j.1365-2222.2005.02181.x; del Pozo V, 1999, J ALLERGY CLIN IMMUN, V104, P637, DOI 10.1016/S0091-6749(99)70336-2; Dominguez-Ortega J, 2001, INT ARCH ALLERGY IMM, V125, P86, DOI 10.1159/000053801; Falcao H, 2002, ALLERGY, V57, P44, DOI 10.1034/j.1398-9995.2002.13429.x; GarciaPalacios L, 1996, J HELMINTHOL, V70, P281; Grunig G, 1998, SCIENCE, V282, P2261, DOI 10.1126/science.282.5397.2261; Heinzmann A, 2000, HUM MOL GENET, V9, P549, DOI 10.1093/hmg/9.4.549; IGLESIAS R, 1993, PARASITE IMMUNOL, V15, P243, DOI 10.1111/j.1365-3024.1993.tb00607.x; James JM, 2003, PEDIATRICS, V111, P1625; Jeebhay MF, 2004, OCCUP ENVIRON MED, V61, P471, DOI 10.1136/oem.2002.001099; Jeebhay MF, 2001, OCCUP ENVIRON MED, V58, P553, DOI 10.1136/oem.58.9.553; Jung SK, 2000, J IMMUNOL, V165, P1491; KASUYA S, 1990, LANCET, V335, P665, DOI 10.1016/0140-6736(90)90455-E; Kimura S, 2001, Rinsho Byori, V49, P376; KLIKS MM, 1983, AM J TROP MED HYG, V32, P526; Kuperman DA, 2002, NAT MED, V8, P885, DOI 10.1038/nm734; Leung DYM, 2003, NEW ENGL J MED, V348, P986, DOI 10.1056/NEJMoa022613; Li XM, 2000, J ALLERGY CLIN IMMUN, V106, P150, DOI 10.1067/mai.2000.107395; Mohrs M, 2000, INFECT IMMUN, V68, P1773, DOI 10.1128/IAI.68.4.1773-1780.2000; Murase T, 1998, BLOOD, V92, P2182; NobenTrauth N, 1996, SCIENCE, V271, P987, DOI 10.1126/science.271.5251.987; OSHIMA T, 1987, PARASITOL TODAY, V3, P44, DOI 10.1016/0169-4758(87)90212-2; Palmer LJ, 2002, AM J RESP CRIT CARE, V165, P1489, DOI 10.1164/rccm.2107020; Perteguer MJ, 2001, PARASITOL RES, V87, P396, DOI 10.1007/s004360000362; Pichler WJ, 1999, CLIN EXP ALLERGY, V29, P1161, DOI 10.1046/j.1365-2222.1999.00646.x; Ring Johannes, 2004, Novartis Found Symp, V257, P6; SAKANARI JA, 1990, PARASITOL TODAY, V6, P323, DOI 10.1016/0169-4758(90)90176-5; Sampson HA, 2004, J ALLERGY CLIN IMMUN, V113, P805, DOI 10.1016/j.jaci.2004.03.014; Scala E, 2001, EUR J DERMATOL, V11, P249; Sicherer SH, 2004, J ALLERGY CLIN IMMUN, V114, P159, DOI 10.1016/j.jaci.2004.04.018; Sicherer SH, 2002, LANCET, V360, P701, DOI 10.1016/S0140-6736(02)09831-8; van den Biggelaar AHJ, 2004, J INFECT DIS, V189, P892, DOI 10.1086/381767; VANTHIEL PH, 1966, TROP GEOGR MED, V18, P310; Webb DC, 2000, J IMMUNOL, V165, P108; Wills-Karp M, 2004, IMMUNOL REV, V202, P175, DOI 10.1111/j.0105-2896.2004.00215.x; Wilson MS, 2005, J EXP MED, V202, P1199, DOI 10.1084/jem.20042572; Yazdanbakhsh M, 2005, CURR OPIN ALLERGY CL, V5, P386, DOI 10.1097/01.all.0000182541.52971.eb; ZURAWSKI G, 1994, IMMUNOL TODAY, V15, P19, DOI 10.1016/0167-5699(94)90021-3	52	88	91	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	2006	117	5					1098	1105		10.1016/j.jaci.2005.12.1357		8	Allergy; Immunology	Allergy; Immunology	041EM	WOS:000237436300018	16675338	
J	Walker, S; Monteil, M; Phelan, K; Lasserson, TJ; Walters, EH				Walker, S; Monteil, M; Phelan, K; Lasserson, TJ; Walters, EH			Anti-IgE for chronic asthma in adults and children	COCHRANE DATABASE OF SYSTEMATIC REVIEWS			English	Review						anti-asthmatic agents [therapeutic use]; antibodies, anti-idiotypic [*therapeutic use]; antibodies, monoclonal [*therapeutic use]; asthma [*drug therapy; immunology]; chronic disease; immunoglobulin E [blood; immunology]; randomized controlled trials	SEVERE ALLERGIC-ASTHMA; QUALITY-OF-LIFE; ANTIIMMUNOGLOBULIN-E ANTIBODY; HUMANIZED MONOCLONAL-ANTIBODY; COMPLEX-FORMATION; SERUM IGE; E THERAPY; OMALIZUMAB; EFFICACY; DISEASE	Background Omalizumab is a recombinant humanised monoclonal antibody directed against immunoglobulin E (anti-IgE) to inhibit the immune system's response to allergen exposure. Omalizumab is directed against the binding site of IgE for its high affinity Fc receptor. It prevents free serum IgE from attaching to mast cells and other effector cells and prevents IgE mediated inflammatory changes. Objectives To determine the efficacy of anti-IgE compared with placebo in patients with allergic asthma. Search strategy We searched the Cochrane Airways Group Asthma trials register for potentially relevant studies (February 2006). Selection criteria Randomised controlled trials examining anti-IgE administered in any manner for any duration. Trials with co-interventions were included as long as they were the same in each arm. Data collection and analysis Two reviewers independently assessed study quality and extracted and entered data. Three modes of administration were identified from the published literature (inhaled, intravenous and subcutaneous injection). Subgroup analysis was performed by asthma severity. Data were extracted from published and unpublished sources. Main results Fourteen trials (15 group comparisons) were included in the review, contributing a total of 3143 mild to severe allergic asthmatic participants with high levels of IgE. Treatment with intravenous and subcutaneous Omalizumab significantly reduced free IgE compared with placebo. Omalizumab led to a significant reduction in inhaled steroid (ICS) consumption compared with placebo (-119 mcg/day (95% CI -154 to -83, three trials)). There were significant increases in the number of participants who were able to reduce ICS by over 50% (odds ratio (OR) 2.50, 95% confidence interval (CI) 2.02 to 3.10 (four trials)); or completely withdraw their daily ICS intake (OR 2.50 (95% CI 2.00 to 3.13; four trials)). Participants treated with Omalizumab were less likely to suffer an asthma exacerbation with treatment as an adjunct to ICS (OR 0.52, 95% CI 0.41 to 0.65, five trials), or as an ICS tapering agent (OR 0.47, 95% CI 0.37 to 0.60, four trials). Authors' conclusions Omalizumab was significantly more effective than placebo at increasing the numbers of patients who were able to reduce or withdraw their inhaled steroids, but the clinical value of the reduction in steroid consumption has be considered in the light of the high cost of Omalizumab. The impressive placebo effects observed in control groups bring into question the true effect of Omalizumab. Omalizumab was effective in reducing asthma exacerbations as an adjunctive therapy to inhaled steroids, and during steroid tapering phases of clinical trials. Omalizumab was generally well tolerated, although there were more injection site reactions with Omalizumab. Patient and physician assessments of the drug were positive. Further assessment in paediatric populations is necessary, as is direct double-dummy comparison with ICS.	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J	Sathe, SK; Teuber, SS; Roux, KH				Sathe, SK; Teuber, SS; Roux, KH			Effects of food processing on the stability of food allergens	BIOTECHNOLOGY ADVANCES			English	Review						food allergy; processing; stability; epitope	DOUBLE-BLIND; PROTEINS; CHALLENGE; FISH; KIWI; NUT	The ubiquitous presence of allergens in the human food supply coupled with increased awareness of food allergies warrants undertaking appropriate preventive measures to protect sensitive consumers from unwanted exposure to offending food allergens. Attempts to reduce or eliminate food allergenicity through food processing have met with mixed results. The rationale for using food processing to reduce/eliminate allergenicity and limitations to using this approach are discussed. (C) 2005 Elsevier Inc. All rights reserved.	Florida State Univ, Coll Human Sci, Dept Nutr Food & Exercise Sci, Tallahassee, FL 32306 USA; Univ Calif Davis, Sch Med, Div Rheumatol Allergy & Clin Immunol, Genome & Biomed Sci Facil, Davis, CA 95616 USA; Florida State Univ, Dept Biol Sci, Tallahassee, FL 32306 USA	Sathe, SK (reprint author), Florida State Univ, Coll Human Sci, Dept Nutr Food & Exercise Sci, 402 Sandels Bldg, Tallahassee, FL 32306 USA.	ssathe@mailer.fsu.edu					Aleman A, 2004, J ALLERGY CLIN IMMUN, V113, P543, DOI 10.1016/j.jaci.2003.11.043; BERNHISELBROADBENT J, 1992, J ALLERGY CLIN IMMUN, V90, P622, DOI 10.1016/0091-6749(92)90135-O; Brenna O, 2000, J AGR FOOD CHEM, V48, P493, DOI 10.1021/jf9906681; DAUSSANT J, 1976, J AGR FOOD CHEM, V24, P103, DOI 10.1021/jf60203a029; Dube M, 2004, J AGR FOOD CHEM, V52, P3938, DOI 10.1021/jf030792r; EHN BM, 2004, J AGR FOOD CHEM, V52, P398; Fiocchi A, 2004, PEDIATR ALLERGY IMMU, V15, P454, DOI 10.1111/j.1399-3038.2004.00186.x; Gruber P, 2004, J AGR FOOD CHEM, V52, P4002, DOI 10.1021/jf035458+; Hansen KS, 2003, ALLERGY, V58, P132, DOI 10.1034/j.1398-9995.2003.23959.x; HEFLE SL, 2005, J ALLERGY CLIN IMMUN, V115, pS32, DOI 10.1016/j.jaci.2004.12.143; Leduc V, 2003, J ALLERGY CLIN IMMUN, V111, P897, DOI 10.1067/mai.2003.1345; Malanin K, 1995, ALLERGY, V50, P988, DOI 10.1111/j.1398-9995.1995.tb02513.x; Maleki SJ, 2000, J ALLERGY CLIN IMMUN, V106, P763, DOI 10.1067/mai.2000.109620; Sanchez C, 2003, REV FR ALLERGOL, V43, P13, DOI 10.1016/S0335-7457(02)00003-5; Sen M, 2002, J IMMUNOL, V169, P882; SPIES JR, 1974, J AGR FOOD CHEM, V22, P30, DOI 10.1021/jf60191a005; Su M, 2004, J SCI FOOD AGR, V84, P1119, DOI 10.1002/jsfa.1748; Taylor SL, 2004, J FOOD SCI, V69, pR175; Varjonen E, 1996, CLIN EXP ALLERGY, V26, P436, DOI 10.1046/j.1365-2222.1996.d01-328.x	19	88	98	2	28	PERGAMON-ELSEVIER SCIENCE LTD	OXFORD	THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND	0734-9750			BIOTECHNOL ADV	Biotechnol. Adv.	SEP	2005	23	6					423	429		10.1016/j.biotechadv.2005.05.008		7	Biotechnology & Applied Microbiology	Biotechnology & Applied Microbiology	954PS	WOS:000231167600005	15978770	
J	Meyers, DA; Postma, DS; Stine, OC; Koppelman, GH; Ampleford, EJ; Jongepier, H; Howard, TD; Bleecker, ER				Meyers, DA; Postma, DS; Stine, OC; Koppelman, GH; Ampleford, EJ; Jongepier, H; Howard, TD; Bleecker, ER			Genome screen for asthma and bronchial hyperresponsiveness: Interactions with passive smoke exposure	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						smoking; bronchial hyperresponsiveness; asthma; lung function; linkage; genome-wide sereen	ENVIRONMENTAL TOBACCO-SMOKE; WIDE SEARCH; RESPIRATORY SYMPTOMS; CHROMOSOME 5Q31-Q33; SUSCEPTIBILITY LOCI; FOUNDER POPULATION; LINKAGE ANALYSIS; LUNG-FUNCTION; SERUM IGE; GENE	Background: Asthma is a common respiratory disease caused by the interaction of genetic susceptibility and exposure to various environmental factors. Passive smoke exposure, characterized by parental smoking, has been shown to be a risk factor for the development of atopy and asthma. Objective: We sought to perform a genome-wide linkage screen for asthma and bronchial hyperresponsiveness (BHR) and to determine the influence of passive tobacco smoke exposure during childhood on the results of genetic linkage studies to investigate gene-environment interactions. Methods: A genome-wide linkage screen for asthma and BHR was performed in 200 families ascertained through a parent with asthma. Analyses were performed separately for the entire sample and for the smoking-exposed and nonexposed families. Results: For asthma and BHR, the strongest evidence for linkage was observed for chromosomes 3p and 5q. The families in which the children were exposed to passive smoking accounted for the evidence for linkage of BHR to 5q (P < .001), but evidence for linkage to 3p was found in both sets of families. Similar results were observed for asthma. However, there was no observed difference in the frequency of asthma or BHR in the offspring from the smoke-exposed compared with the nonexposed families. Conclusion: The results from this study demonstrate that the influence of susceptibility genes for a common disease such as asthma might not be apparent unless there is the appropriate exposure to environmental stimuli, such as passive exposure to cigarette smoke. This approach should be useful for identification of asthma susceptibility genes.	Wake Forest Univ, Sch Med, Ctr Human Genom, Dept Pediat, Winston Salem, NC 27157 USA; Wake Forest Univ, Sch Med, Dept Med, Winston Salem, NC USA; Wake Forest Univ, Sch Med, Dept Publ Hlth Sci, Winston Salem, NC USA; Univ Hosp, Dept Pulmonol, Groningen, Netherlands; Univ Maryland, Sch Med, Dept Epidemiol & Prevent Med, Baltimore, MD 21201 USA	Meyers, DA (reprint author), Wake Forest Univ, Sch Med, Ctr Human Genom, Dept Pediat, Med Ctr Blvd, Winston Salem, NC 27157 USA.	dmeyers@wfubmc.edu	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	NHLBI NIH HHS [R01 HL 48341, R01 HL 66393]		BURROWS B, 1992, J ALLERGY CLIN IMMUN, V90, P376, DOI 10.1016/S0091-6749(05)80018-1; Carey VJ, 1996, AM J RESP CRIT CARE, V153, P356; Colilla S, 2003, J ALLERGY CLIN IMMUN, V111, P840, DOI 10.1067/mai.2003.170; Daniels SE, 1996, NATURE, V383, P247, DOI 10.1038/383247a0; DEVRIES K, 1962, INT ARCH ALLERGY, V20, P63; Dizier MH, 2000, AM J RESP CRIT CARE, V162, P1812; Ehrlich F, 1906, BIOCHEM Z, V1, P8; Gilliland FD, 2003, AM J EPIDEMIOL, V157, P861, DOI 10.1093/aje/kwg037; Gilliland FD, 2001, AM J RESP CRIT CARE, V163, P429; Hakonarson H, 2002, AM J HUM GENET, V71, P483, DOI 10.1086/342205; HIRSCHHORN JN, 2005, J CLIN ENDOCR METAB, V87, P4438; Howard TD, 2002, J ALLERGY CLIN IMMUN, V110, P743, DOI 10.1067/mai.2002.128723; Howard TD, 2001, AM J RESP CELL MOL, V25, P377; Howard TD, 2002, AM J HUM GENET, V70, P230, DOI 10.1086/338242; Koppelman GH, 2001, AM J RESP CRIT CARE, V163, P965; Kruglyak L, 1996, AM J HUM GENET, V58, P1347; LAITINEN T, 2001, NAT GENET, V28, P89; Lanphear BP, 2001, PEDIATRICS, V107, P505, DOI 10.1542/peds.107.3.505; 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; MARSH DG, 1994, SCIENCE, V264, P1152, DOI 10.1126/science.8178175; 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; MORTON NE, 1956, AM J HUM GENET, V8, P80; 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, 1998, HUM MOL GENET, V7, P1393, DOI 10.1093/hmg/7.9.1393; Panhuysen CIM, 1998, AM J RESP CRIT CARE, V157, P1734; PEAT JK, 1993, EUR RESPIR J, V6, P662; POSTMA DS, 1995, NEW ENGL J MED, V333, P894, DOI 10.1056/NEJM199510053331402; VANDERLENDE R, 1972, SCAND J RESPIR DIS, V53, P218; Wjst M, 1999, GENOMICS, V58, P1, DOI 10.1006/geno.1999.5806; Wright AL, 2002, CLIN REV ALLERG IMMU, V22, P33, DOI 10.1385/CRIAI:22:1:033; XU J, 2001, AM J HUM GENET, V69, P1271; 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; Young S, 2000, PEDIATR PULM, V29, P331, DOI 10.1002/(SICI)1099-0496(200005)29:5<331::AID-PPUL1>3.0.CO;2-A	39	88	91	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.	JUN	2005	115	6					1169	1175		10.1016/j.jaci.2005.01.070		7	Allergy; Immunology	Allergy; Immunology	935WZ	WOS:000229815400010	15940130	
J	Sugimoto, T; Ishikawa, Y; Yoshimoto, T; Hayashi, N; Fujimoto, J; Nakanishi, K				Sugimoto, T; Ishikawa, Y; Yoshimoto, T; Hayashi, N; Fujimoto, J; Nakanishi, K			Interleukin 18 acts on memory T helper cells type 1 to induce airway inflammation and hyperresponsiveness in a naive host mouse	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article						IL-9; IL-13; IL-18; Th1; bronchial asthma	ALLERGEN-SPECIFIC TH1; IFN-GAMMA PRODUCTION; MAST-CELL; BRONCHIAL HYPERRESPONSIVENESS; MONOCLONAL-ANTIBODY; EPITHELIAL-CELLS; IL-18 RECEPTOR; MURINE MODEL; ASTHMA; EXPRESSION	Interleukin (IL)-18 was originally regarded to induce T helper cell (Th)1-related cytokines. In general, factors favoring interferon (IFN)-gamma production are believed to abolish allergic diseases. Thus, we tested the role of IL-18 in regulation of bronchial asthma. To avoid a background response of host-derived T cells, we administered memory type Th1 or Th2 cells into unsensitized mice and examined their role in induction of bronchial asthma. Administration of antigen (Ag) induced both air-way inflammation and airway hyperresponsiveness (AHR) in mice receiving memory Th2 cells. In contrast, the same treatment induced only airway inflammation but not AHR in mice receiving memory Th1 cells. However, these mice developed striking AHR when they were coadministered with IL-18. Furthermore, mice having received IFN-gamma-expressing Th1 cells sorted from polarized Th1 cells developed severe airway inflammation and AHR after intranasal administration of Ag and IL-18. Thus, Th1 cells become harmful when they are stimulated with Ag and IL-18. Newly polarized Th1 cells and IFN-gamma-expressing Th1 cells, both of which express IL-18 receptor alpha chain strongly, produce IFN-gamma, IL-9, IL-13, granulocyte/macrophage colony-stimulating factor, tumor necrosis factor alpha, regulated on activation, normal T cell expressed and secreted, and macrophage inflammatory protein 1alpha upon stimulation with Ag, IL-2, and IL-18 in vitro. Thus, Ag and IL-18 stimulate memory Th1 cells to induce severe airway inflammation and AHR in the naive host.	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J	Burge, PS				Burge, PS			Sick building syndrome	OCCUPATIONAL AND ENVIRONMENTAL MEDICINE			English	Article							INDOOR AIR-QUALITY; DIFFERENT VENTILATION SYSTEMS; 2 OFFICE BUILDINGS; OCCUPATIONAL ASTHMA; SYNDROME SBS; PERSONAL FACTORS; SKIN SYMPTOMS; CASE-REFERENT; RISK-FACTORS; WORKERS		Birmingham Heartlands Hosp, Occupat Lung Dis Unit, Birmingham B9 5SS, W Midlands, England	Burge, PS (reprint author), Birmingham Heartlands Hosp, Occupat Lung Dis Unit, Bordesley Green E, Birmingham B9 5SS, W Midlands, England.	sherwood.burge@heartsol.wmids.nhs.uk					ANDERSEN I, 1973, ARCH ENVIRON HEALTH, V26, P22; BERGLUND B, 2002, ARCH CTR SENSORY RES, V7, P83; BLASCO A, 1992, J INVEST ALLERG CLIN, V2, P167; Brasche S, 2001, INDOOR AIR, V11, P217, DOI 10.1034/j.1600-0668.2001.110402.x; Brasche S, 2001, INT J HYG ENVIR HEAL, V203, P311, DOI 10.1078/1438-4639-00042; BURGE PS, 1994, THORAX, V49, P842, DOI 10.1136/thx.49.8.842; BURGE PS, 1993, INDOOR AIR 93, P731; Burge PS, 1990, INDOOR AIR 90, V1, P479; 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Environ. Med.	FEB 1	2004	61	2					185	190		10.1136/oem.2003.008813		6	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	766DJ	WOS:000188329900018	14739390	
J	Fung, F; Clark, RF				Fung, F; Clark, RF			Health effects of mycotoxins: A toxicological overview	JOURNAL OF TOXICOLOGY-CLINICAL TOXICOLOGY			English	Review						mycotoxins; toxicological; gastrointestinal; fungi; mycotoxicosis; indoor; agricultural	VOLATILE ORGANIC MIXTURE; STACHYBOTRYS-CHARTARUM; PULMONARY HEMORRHAGE; OCHRATOXIN-A; T-2 TOXIN; TRICHOTHECENE MYCOTOXINS; ESOPHAGEAL CANCER; FUNGAL TOXINS; CELL-LINES; EXPOSURE	Diseases caused by fungi are spread by direct implantation or inhalation of spores. Fungi can cause adverse human health effects to many organ systems. In addition to infection and allergy, fungi can produce mycotoxins and organic chemicals that are responsible for various toxicologic effects. We reviewed the published literature on important mycotoxins and systemic effects of mycotoxins. Scientific literature revealed a linkage between ingesting mycotoxin contaminated food and illness, especially hepatic, gastrointestinal, and carcinogenic diseases. Issues related to mycotoxin exposure, specific diseases, and management are discussed. Although there is agreement that diet is the main source of mycotoxin exposure, specific health effects and risk assessment from indoor nonagricultural exposure are limited by the paucity of scientific evidence currently available. Further research on the health effects of inhaling mycotoxins in indoor settings is needed.	Univ Calif San Diego, Sharp Rees Stealy Med Grp, San Diego, CA 92101 USA; Univ Calif San Diego, Div Med Toxicol, San Diego, CA 92101 USA	Fung, F (reprint author), Univ Calif San Diego, Sharp Rees Stealy Med Grp, 2001 4th Ave, San Diego, CA 92101 USA.	fred.fung@sharp.com					Baldo Juliana V, 2002, Appl Neuropsychol, V9, P193, DOI 10.1207/S15324826AN0904_1; BAREL S, 1990, J PHARM SCI, V79, P548, DOI 10.1002/jps.2600790619; BEASLEY VR, 1986, TOXICON, V24, P13, DOI 10.1016/0041-0101(86)90161-3; BERGMANN F, 1988, TOXICON, V26, P923, DOI 10.1016/0041-0101(88)90257-7; Bhat RV, 1997, J TOXICOL-CLIN TOXIC, V35, P249; Bondy GS, 2000, J TOXICOL ENV HEAL B, V3, P109, DOI 10.1080/109374000281113; Breton P, 1998, TOXICON, V36, P645, DOI 10.1016/S0041-0101(97)00084-6; Broussard Crystal N., 2001, American Journal of Gastroenterology, V96, P3195, DOI 10.1016/S0002-9270(01)03845-X; CASTEGNARO M, 1991, IARC SCI PUBL, V113, P9; CHANG FC, 1977, FOOD COSMET TOXICOL, V15, P199, DOI 10.1016/S0015-6264(77)80390-8; CHAO TC, 1991, J PATHOL, V164, P225, DOI 10.1002/path.1711640307; Chapman JA, 2003, ALLERGY ASTHMA PROC, V24, P1; Chu F S, 1974, CRC Crit Rev Toxicol, V2, P499; CHU FS, 1994, APPL ENVIRON MICROB, V60, P847; CHU FS, 1992, J ANIM SCI, V70, P3950; CORRIER DE, 1991, VET IMMUNOL IMMUNOP, V30, P73, DOI 10.1016/0165-2427(91)90010-A; CREPPY EE, 1984, FOOD CHEM TOXICOL, V22, P883, DOI 10.1016/0278-6915(84)90170-4; CROFT WA, 1986, ATMOS ENVIRON, V20, P549, DOI 10.1016/0004-6981(86)90096-X; Dales R, 1998, ARCH ENVIRON HEALTH, V53, P190; Dalton P, 2003, TOXICOL LETT, V140, P239, DOI 10.1016/S0378-4274(02)00510-6; Dees C, 1997, ENVIRON HEALTH PERSP, V105, P633, DOI 10.2307/3433382; DENNING DW, 1987, ADVERSE DRUG REACT T, V6, P175; DIPAOLO N, 1993, NEPHRON, V64, P621, DOI 10.1159/000187411; Domijan Ana-Marija, 1999, Arhiv za Higijenu Rada i Toksikologiju, V50, P263; Drobotko V. 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Toxicol.-Clin. Toxicol.		2004	42	2					217	234		10.1081/CLT-120030947		18	Toxicology	Toxicology	828YM	WOS:000222009700014	15214629	
J	Woodruff, TJ; Parker, JD; Kyle, AD; Schoendorf, KC				Woodruff, TJ; Parker, JD; Kyle, AD; Schoendorf, KC			Disparities in exposure to air pollution during pregnancy	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; birth outcomes; criteria air pollutants; environmental justice	LOW-BIRTH-WEIGHT; EMERGENCY ROOM VISITS; NORTH-AMERICAN CHILDREN; UNITED-STATES; SOUTHERN CALIFORNIA; RESPIRATORY SYMPTOMS; INDUSTRIAL SOURCES; INFANT-MORTALITY; ACID AEROSOLS; ASTHMA	Previous research shows poorer birth outcomes for racial and ethnic minorities and for persons with low socioeconomic status (SES). We evaluated whether mothers in groups at higher risk for poor birth outcomes live in areas of higher air pollution and whether higher exposure to air pollution contributes to poor birth outcomes. An index representing long-term exposure to criteria air pollutants was matched with birth certificate data at the county level for the United States in 1998-1999. We used linear regression to estimate associations between the air pollution index and maternal race and educational attainment, a marker for SES of the mother, controlling for age, Parity, marital status, and region of the country. Then we used logistic regression models both to estimate likelihood of living in counties with the highest levels of air pollution for different racial groups and by educational attainment, adjusting for other maternal risk factors, and to estimate the effect of living in counties with higher levels of air pollution on preterm delivery and births small for gestational age (SGA). Hispanic, African-American, and Asian/Pacific Islander mothers experienced higher mean levels of air pollution and were more than twice as likely to live in the most polluted counties compared with white mothers after controlling for maternal risk factors, region, and educational status [Hispanic mothers: adjusted odds ratio (AOR) = 4.66; 95% confidence interval (95% CI), 1.92-11.32; African-American mothers: AOR = 2.58; 95% CI, 1.00-6.62; Asian/Pacific Islander mothers: AOR = 2.82; 95% CI, 1.07-7.39]. Educational attainment was not associated with living in counties with highest levels of the air pollution index (AOR = 0.95; 95% CI, 0.40-2.26) after adjusting for maternal risk factors, region of the country, and race/ethnicity. There was a small increase in the odds of preterm delivery (AOR = 1.05; 95% CI, 0.99-1.12) but not SGA (AOR = 0.96; 95% CI, 0.86-1-07) in a county with high air pollution. Additional risk of residing in areas with poor air, quality may exacerbate health problems of infants and children already at increased risk for poor health.	US EPA, Natl Ctr Environm Econ, San Francisco, CA 94105 USA; Ctr Dis Control & Prevent, Natl Ctr Hlth Stat, Infant & Child Hlth Studies Branch, Hyattsville, MD 20782 USA; Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA	Woodruff, TJ (reprint author), US EPA, Natl Ctr Environm Econ, 75 Hawthorne St,SPE-1, San Francisco, CA 94105 USA.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			ANDERTON DL, 1994, DEMOGRAPHY, V31, P229, DOI 10.2307/2061884; Avol EL, 2001, AM J RESP CRIT CARE, V164, P2067; BATES DV, 1995, ENVIRON HEALTH PERSP, V103, P49, DOI 10.2307/3432345; 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; Council of Economic Advisers for the President's Initiative on Race, 1998, CHANG AM IND SOC EC; Dejmek J, 1999, ENVIRON HEALTH PERSP, V107, P475, DOI 10.2307/3434630; DOCKERY DW, 1989, AM REV RESPIR DIS, V139, P587; Dockery DW, 1996, ENVIRON HEALTH PERSP, V104, P500, DOI 10.2307/3432990; DOCKERY DW, 1993, NEW ENGL J MED, V329, P1753, DOI 10.1056/NEJM199312093292401; *FED INT FOR CHILD, 2002, AM CHILDR KEY NAT IN; Ha EH, 2001, EPIDEMIOLOGY, V12, P643, DOI 10.1097/00001648-200111000-00011; Institute of Medicine, 1999, ENV JUST RES ED HLTH; Koenig JQ, 1999, J ALLERGY CLIN IMMUN, V104, P717; Kramer MS, 2000, PAEDIATR PERINAT EP, V14, P194, DOI 10.1046/j.1365-3016.2000.00266.x; Kyle AD, 2002, ENVIRON HEALTH PERSP, V110, P95; Lipsett M, 1997, ENVIRON HEALTH PERSP, V105, P216, DOI 10.1289/ehp.97105216; Loomis D, 1999, EPIDEMIOLOGY, V10, P118, DOI 10.1097/00001648-199903000-00006; Maisonet M, 2001, ENVIRON HEALTH PERSP, V109, P351, DOI 10.2307/3434782; 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; *NAT CTR HLTH STAT, 2003, NAT DAT PUBL US DAT; National Center for Health Statistics, 2001, HLTH US 2001 URB RUR; Norris G, 1999, ENVIRON HEALTH PERSP, V107, P489, DOI 10.2307/3434632; Pamuk E., 1998, SOCIOECONOMIC STATUS; Perlin SA, 1999, J EXPO ANAL ENV EPID, V9, P29, DOI 10.1038/sj.jea.7500024; Perlin SA, 2001, J AIR WASTE MANAGE, V51, P406; PICKLE L, 1999, STAT MED, V18, P3221; Raizenne M, 1996, ENVIRON HEALTH PERSP, V104, P506, DOI 10.2307/3432991; Ritz B, 2000, EPIDEMIOLOGY, V11, P502, DOI 10.1097/00001648-200009000-00004; Ritz B, 1999, ENVIRON HEALTH PERSP, V107, P17, DOI 10.2307/3434285; Rogers JF, 2000, AM J EPIDEMIOL, V151, P602; Samet JM, 2000, NEW ENGL J MED, V343, P1742, DOI 10.1056/NEJM200012143432401; Samet J.M., 2000, NATL MORBIDITY MORTA; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; SCHWARTZ J, 1994, AM J RESP CRIT CARE, V150, P1234; *STAT CORP, 1999, STAT STAT SOFTW; Studnicka M, 1997, EUR RESPIR J, V10, P2275, DOI 10.1183/09031936.97.10102275; Tolbert PE, 2000, AM J EPIDEMIOL, V151, P798; *US EPA, 2003, AM CHILD ENV MEAS CO; *US EPA, 2000, AER INF RETR SYST; Wang XB, 1997, ENVIRON HEALTH PERSP, V105, P514, DOI 10.1289/ehp.97105514; Woodruff TJ, 1997, ENVIRON HEALTH PERSP, V105, P608	44	88	88	0	10	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	2003	111	7					942	+		10.1289/ehp.5317		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	689ND	WOS:000183498900033	12782496	
J	Halken, S; Host, A; Niklassen, U; Hansen, LG; Nielsen, F; Pedersen, S; Osterballe, O; Veggerby, C; Poulsen, LK				Halken, S; Host, A; Niklassen, U; Hansen, LG; Nielsen, F; Pedersen, S; Osterballe, O; Veggerby, C; Poulsen, LK			Effect of mattress and pillow encasings on children with asthma and house dust mite allergy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						mattress encasing; house dust mite allergy; childhood asthma; inhaled steroids	CHILDHOOD ASTHMA; AIRBORNE ALLERGENS; AVOIDANCE MEASURES; EXPOSURE; SENSITIZATION; MANAGEMENT; ANTIGEN	Background: House dust mite (HDM) allergy is a frequent cause of allergic asthma in children. Reduction of exposure seems to be the most logical way to treat these patients. Objective: Our aim was to investigate whether mattress and pillow encasings resulted in an effective long-term control of HDM allergen levels, thereby reducing the need for asthma medication in children with asthma and HDM allergy. Methods: In a prospective, double-blind, placebo-controlled study 60 children (age range, 6-15 years) with asthma and HDM allergy were randomized to active (allergy control) or placebo mattress and pillow encasings. After a 2-week baseline period, follow-up was performed every 3 months for I year. During the entire study period, the dose of inhaled steroids was tapered off to the lowest effective dose according to well-defined criteria. Results: Fifty-two patients completed the trial, and 5 were excluded, leaving data from 47 children (26 in the active treatment group and 21 in the placebo group) for analysis. A significant perennial reduction in HDM allergen concentrations was seen only for the active treatment group. Also, a significant decrease in the dose of inhaled steroids (mean, 408 to 227 mug/d; P <.001) was found for the active treatment group only, with significant differences between groups after 9 and 12 months. After 1 year, the dose of inhaled steroids was reduced by at least 50% in significantly more children in the active treatment group than in the placebo group (73% vs 24%, P <.01). Conclusion: Encasing of mattresses and pillows resulted in a significant long-term reduction in HDM allergen concentrations in mattresses and in the need for inhaled steroids in children with asthma and HDM allergy.	Sonderborg Hosp, Dept Pediat, DK-6400 Sonderberg, Denmark; Lab Med Allergol, Copenhagen, Denmark; Viborg Hosp, Dept Pediat, Viborg, Denmark; Kolding Cty Hosp, Dept Pediat, Kolding, Denmark; Odense Univ Hosp, Dept Pediat, Odense, Denmark	Halken, S (reprint author), Sonderborg Hosp, Dept Pediat, DK-6400 Sonderberg, Denmark.						Arlian LG, 2001, J ALLERGY CLIN IMMUN, V107, pS406, DOI 10.1067/mai.2001.113670; Boulet LP, 1997, CLIN EXP ALLERGY, V27, P52, DOI 10.1046/j.1365-2222.1997.d01-418.x; Carswell F, 1999, CLIN EXP ALLERGY, V29, P193; Cloosterman SGM, 1999, CLIN EXP ALLERGY, V29, P1336, DOI 10.1046/j.1365-2222.1999.00627.x; Custovic A, 2000, CLIN REV ALLERG IMMU, V18, P397, DOI 10.1385/CRIAI:18:3:397; 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, 1998, BRIT MED J, V317, P1105; Host A, 2000, ALLERGY, V55, P600, DOI 10.1034/j.1398-9995.2000.00122.x; Huss K, 2001, J ALLERGY CLIN IMMUN, V107, P48, DOI 10.1067/mai.2001.111146; Jirapongsananuruk O, 2000, ANN ALLERG ASTHMA IM, V84, P305, DOI 10.1016/S1081-1206(10)62778-0; MATTHYS H, 1993, RESPIRATION, V60, P343; OWEN S, 1990, LANCET, V335, P396, DOI 10.1016/0140-6736(90)90219-U; Peat JK, 1996, AM J RESP CRIT CARE, V153, P141; Shapiro GG, 1999, J ALLERGY CLIN IMMUN, V103, P1069, DOI 10.1016/S0091-6749(99)70181-8; Silvestri M, 1996, ANN ALLERG ASTHMA IM, V76, P239; SPORIK R, 1993, CLIN EXP ALLERGY, V23, P740, DOI 10.1111/j.1365-2222.1993.tb00361.x; Tovey E, 1999, J ALLERGY CLIN IMMUN, V103, P179, DOI 10.1016/S0091-6749(99)70488-4; Vanlaar CH, 2000, J ALLERGY CLIN IMMUN, V105, P1130, DOI 10.1067/mai.2000.106213; VERVLOET D, 1991, ALLERGY, V46, P554, DOI 10.1111/j.1398-9995.1991.tb00620.x; Weeks J, 1995, CLIN EXP ALLERGY, V25, P1179, DOI 10.1111/j.1365-2222.1995.tb03041.x; WICKMAN M, 1991, J ALLERGY CLIN IMMUN, V88, P89, DOI 10.1016/0091-6749(91)90305-8	22	88	91	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.	JAN	2003	111	1					169	176		10.1067/mai.2003.5		8	Allergy; Immunology	Allergy; Immunology	636PR	WOS:000180465500026	12532114	
J	Apostol, GG; Jacobs, DR; Tsai, AW; Crow, RS; Williams, OD; Townsend, MC; Beckett, WS				Apostol, GG; Jacobs, DR; Tsai, AW; Crow, RS; Williams, OD; Townsend, MC; Beckett, WS			Early life factors contribute to the decrease in lung function between ages 18 and 40 - The coronary artery risk development in young adults study	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						lung development; family smoking; smoking; asthma	OBSTRUCTIVE PULMONARY-DISEASE; FORCED EXPIRATORY VOLUME; TOBACCO-SMOKE EXPOSURE; RESPIRATORY SYMPTOMS; CIGARETTE-SMOKING; REFERENCE VALUES; FUNCTION DECLINE; CHILDREN; ASTHMA; CARDIA	Early life factors may influence pulmonary function. We measured forced expiratory volume in 1 second (FEV1) in 1985-1986 and 2, 5, and 10 years later in approximately 4,000 black and white men and women initially aged 18-30 years. We estimated the age pattern of FEV1 according to family smoking status, early diagnosis of asthma, early smoking initiation, adult asthma, and cigarette smoking. FEV1 followed a quadratic pattern from age of peak through age 40. The pattern varied by race and sex. Early smoking initiation was associated with a faster decrease in FEV1. Smoking by family members was related to early life asthma and may have contributed to faster FEV1 decrease by encouraging behaviors such as heavier smoking or earlier smoking initiation. Prevalence of smoking was 28% when no family member smoked, compared with 59% when four or more members smoked. The FEV1 decline was 8.5% in never-smokers without asthma; 10.1% in nonsmoking individuals diagnosed with asthma; and 11.1% in baseline smokers who smoked 15 or more cigarettes per day. The combination of asthma and heavier smoking was synergistic (17.8% decline). This study delineates an increased rate of decline in those with asthma or in those who smoke cigarettes and implicates early life exposures as contributing to the faster rate of FEV1 decline.	Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55454 USA; Univ Oslo, Inst Nutr Res, Oslo, Norway; Ingenix Pharmaceut Serv, Eden Prairie, MN USA; Univ Alabama, Div Prevent Med, Birmingham, AL USA; MC Townsend Associates, Pittsburgh, PA USA; Univ Rochester, Dept Environm Med, Occupat Med Div, Rochester, NY USA	Jacobs, DR (reprint author), Univ Minnesota, Sch Publ Hlth, Div Epidemiol, 1300 S 2nd St,Suite 300, Minneapolis, MN 55454 USA.						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J. Respir. Crit. Care Med.	JUL 15	2002	166	2					166	172		10.1164/rccm.2007035		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	571XX	WOS:000176745400010	12119228	
J	Kero, J; Gissler, M; Gronlund, MM; Kero, P; Koskinen, O; Hemminki, E; Isolauri, E				Kero, J; Gissler, M; Gronlund, MM; Kero, P; Koskinen, O; Hemminki, E; Isolauri, E			Mode of delivery and asthma - Is there a connection?	PEDIATRIC RESEARCH			English	Article							FOLLOW-UP; BIRTH COHORT; CHILDREN; PREVALENCE; ATOPY; CHILDHOOD; INFANTS; LIFE; MICROFLORA; HEALTH	Genetic factors cannot explain the recent rapid increase in the incidence of atopic diseases. The phenomenon has been explained by environmental factors, and there are data for and against the hypothesis that a decline in the pressure of microbial stimulation early in life could be behind the allergy epidemic. Changes have also occurred in maternity care, among them a rise in the caesarean section rate, which could diminish initial microbial exposure and thereby alter T helper 1 cell/T helper-2 cell development and affect the risk of developing atopy. In this study, we sought to establish whether mode of delivery does influence the development of atopic asthma, Finnish 1987 Medical Birth Register (n = 59,927 Live births) information was linked between several national health registers to obtain information on asthma and mode of delivery in children registered. The data were adjusted for maternal age, previous deliveries, child's sex, and birth size. Atopy was evaluated in the second study (Turku Birth Cohort), which involved 219 children born by vaginal delivery (n = 106) or caesarean section (n = 113); history of atopic symptoms was established by questionnaire and a clinical examination was conducted, including skin prick testing and determination of total and allergen-specific I-E in serum, The register study showed the Cumulative incidence of asthma at the age of seven to be significantly higher in children born by caesarean section (4.2%) than in those vaginally delivered (3.3%), the adjusted odds ratio (OR) for confounding variables being 1.21 (1.08-1.36), p < 0.01, In the second study, significantly more positive allergy tests were reported in questionnaires in the caesarean (22%) than in the vaginal delivery group (I M, OR 2.22 (1.06-4.64), p < 0.01, and a trend toward more positive skin prick reactions was documented at clinical examination; 41% versits 29%, OR 1.31 (0.65-2.65), p = 0.11. In conclusion, these results suggest that caesarean section delivery may be associated with an increased prevalence of atopic asthma.	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Res.	JUL	2002	52	1					6	11		10.1023/01.PDR.0000017263.01840.F0		6	Pediatrics	Pediatrics	564ZT	WOS:000176344000002	12084840	
J	Derewenda, U; Li, J; Derewenda, Z; Dauter, Z; Mueller, GA; Rule, GS; Benjamin, DC				Derewenda, U; Li, J; Derewenda, Z; Dauter, Z; Mueller, GA; Rule, GS; Benjamin, DC			The crystal structure of a major dust mite allergen Der p 2, and its biological implications	JOURNAL OF MOLECULAR BIOLOGY			English	Article						allergen; asthma; X-ray structure; immunoglobulin fold; hydrophobic cavity	MACROMOLECULAR STRUCTURES; IMMUNOGLOBULIN FOLD; PROTEIN; DER-P-2; FAMILY; RHOGDI; BINDS; DERMATOPHAGOIDES; REFINEMENT; ASTHMA	The crystal structure of the common house mite (Dermatophagoides sp.) Der p 2 allergen was solved at 2.15 Angstrom resolution using the MAD phasing technique, and refined to an R-factor of 0.209. The refined atomic model, which reveals an immunoglobulin-like tertiary fold, differs in important ways from the previously described NMR structure, because the two beta-sheets are significantly further apart and create an internal cavity, which is occupied by a hydrophobic ligand. This interaction is structurally reminiscent of the binding of a prenyl group by a regulatory protein, the Rho guanine nucleotide exchange inhibitor. The crystal structure suggests that binding of non-polar molecules may be essential to the physiological function of the Der p 2 protein, (C) 2002 Elsevier Science Ltd. All rights reserved.	Univ Virginia, Dept Mol Physiol & Biol Phys, Charlottesville, VA 22908 USA; Brookhaven Natl Lab, Upton, NY 11973 USA; Beirne Carter Ctr Immunol Res, Charlottesville, VA 22908 USA; Univ Virginia, Asthma & Allerg Dis Ctr, Charlottesville, VA 22908 USA; Carnegie Mellon Univ, Dept Biol Sci, Pittsburgh, PA 15213 USA	Derewenda, U (reprint author), Univ Virginia, Dept Mol Physiol & Biol Phys, Charlottesville, VA 22908 USA.		Rule, Gordon/Q-2422-2015; Mueller, Geoffrey/I-2909-2017	Rule, Gordon/0000-0002-4396-3363; Mueller, Geoffrey/0000-0001-8361-5323	NIAID NIH HHS [AI-34607]		Asero R, 2001, ANN ALLERG ASTHMA IM, V87, P65; BORK P, 1994, J MOL BIOL, V242, P309, DOI 10.1016/S0022-2836(84)71582-8; BRUNGER AT, 1990, ACTA CRYSTALLOGR A, V46, P585, DOI 10.1107/S0108767390002355; Cruickshank DWJ, 1999, ACTA CRYSTALLOGR D, V55, P583, DOI 10.1107/S0907444998012645; Esnouf RM, 1997, J MOL GRAPH MODEL, V15, P132, DOI 10.1016/S1093-3263(97)00021-1; Halaby DM, 1999, PROTEIN ENG, V12, P563, DOI 10.1093/protein/12.7.563; HENDERSON IC, 1990, ANN ONCOL, V1, P9; HEYMANN PW, 1989, J ALLERGY CLIN IMMUN, V83, P1055, DOI 10.1016/0091-6749(89)90447-8; Hoffman GR, 2000, CELL, V100, P345, DOI 10.1016/S0092-8674(00)80670-4; JONES TA, 1991, ACTA CRYSTALLOGR A, V47, P110, DOI 10.1107/S0108767390010224; Keep NH, 1997, STRUCTURE, V5, P623, DOI 10.1016/S0969-2126(97)00218-9; KLEYWEGT GJ, 1994, ACTA CRYSTALLOGR D, V50, P178, DOI 10.1107/S0907444993011333; KLEYWEGT GJ, 1994, FIRST MAP FINAL MODE, P59; LASKOWSKI RA, 1993, J APPL CRYSTALLOGR, V26, P283, DOI 10.1107/S0021889892009944; LEMASTER DM, 1985, BIOCHEMISTRY-US, V24, P7263, DOI 10.1021/bi00346a036; Longenecker K, 1999, ACTA CRYSTALLOGR D, V55, P1503, DOI 10.1107/S090744499900801X; Mantyjarvi R, 2000, BBA-PROTEIN STRUCT M, V1482, P308, DOI 10.1016/S0167-4838(00)00139-4; Mueller GA, 1998, BIOCHEMISTRY-US, V37, P12707, DOI 10.1021/bi980578+; Mueller GA, 2001, J BIOL CHEM, V276, P9359, DOI 10.1074/jbc.M010812200; Mueller GA, 1997, J BIOL CHEM, V272, P26893, DOI 10.1074/jbc.272.43.26893; Murshudov GN, 1997, ACTA CRYSTALLOGR D, V53, P240, DOI 10.1107/S0907444996012255; NAURECKIENE S, 2000, SCIENCE, V290, P2227; NICHOLLS A, 1991, PROTEINS, V11, P281, DOI 10.1002/prot.340110407; Okamura N, 1999, BBA-MOL CELL BIOL L, V1438, P377, DOI 10.1016/S1388-1981(99)00070-0; Otwinowski Z., 1991, DARESBURY STUDY WEEK, P80; OVSYANNIKOVA IG, 1994, J ALLERGY CLIN IMMUN, V94, P537, DOI 10.1016/0091-6749(94)90211-9; Platts-Mills TAE, 1997, J ALLERGY CLIN IMMUN, V100, pS2, DOI 10.1016/S0091-6749(97)70292-6; POWTAN KD, 1993, ACTA CRYSTALLOGR D, V49, P148; SHAKIB F, 2001, J CLIN PATHOL, V54, P155; SHELDRICK G, 1991, DARESBURY STUDY WEEK, P23; SPORIK R, 1992, CLIN EXP ALLERGY, V22, P897, DOI 10.1111/j.1365-2222.1992.tb02062.x; 1994, ACTA CRSYSTALLOG D, V50, P760	32	88	93	0	3	ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD	LONDON	24-28 OVAL RD, LONDON NW1 7DX, ENGLAND	0022-2836			J MOL BIOL	J. Mol. Biol.	APR 19	2002	318	1					189	197		10.0000/S0022-2836(02)00027-X		9	Biochemistry & Molecular Biology	Biochemistry & Molecular Biology	548MY	WOS:000175392800016	12054778	
J	Arlian, LG				Arlian, LG			Arthropod allergens and human health	ANNUAL REVIEW OF ENTOMOLOGY			English	Review						allergic reactions to arthropods; allergic reactions to insects and mites	HOUSE-DUST-MITE; IMPORTED FIRE ANT; AMERICAN PERIPLANETA-AMERICANA; COCKROACH BLATTELLA-GERMANICA; ANTIGENIC CROSS-REACTIVITY; IGE ANTIBODY-RESPONSES; AMINO-ACID-SEQUENCES; INNER-CITY CHILDREN; DERMATOPHAGOIDES-PTERONYSSINUS ACARI; GLUTATHIONE-S-TRANSFERASE	Many species of arthropods are the sources of potent allergens that sensitize and induce IgE-mediated allergic reactions in humans. Most of these arthropod allergens are proteins, and the allergic response mechanism to these allergens is the same as it is for allergens from other sources such as plant pollens, molds, and foods. Aside from ingestion of crustaceans (shrimp, lobster), among arthropods, humans have the greatest contact with insects and mites, and as a result allergies to these two groups of arthropods have been the most frequently reported. Because of the large number of people affected by allergic reactions to stinging insects, cockroaches, and dust mites. Many allergens of these organisms have been extensively studied, purified, and characterized and for some recombinant allergens, produced. Cocktails of these recombinant allergens have the potential for use in diagnosis and immunotherapy. In this chapter, we review the insects and mites that induce allergic reactions. Where the information exists, the immunobiochemical characterization of the allergens and the frequency, of sensitivity or clinical reactivity in the human population are also reviewed. As background, the beginning of this review includes sections that define allergens, explain the allergic reaction mechanism, and describe the methods for naming allergens.	Wright State Univ, Dept Biol Sci, Dayton, OH 45435 USA	Arlian, LG (reprint author), Wright State Univ, Dept Biol Sci, Dayton, OH 45435 USA.						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Rev. Entomol.		2002	47						395	433		10.1146/annurev.ento.47.091201.145224		39	Entomology	Entomology	514DC	WOS:000173421900014	11729080	
J	Binder, M; Mahler, V; Hayek, B; Sperr, WR; Scholler, M; Prozell, S; Wiedermann, G; Valent, P; Valenta, R; Duchene, M				Binder, M; Mahler, V; Hayek, B; Sperr, WR; Scholler, M; Prozell, S; Wiedermann, G; Valent, P; Valenta, R; Duchene, M			Molecular and immunological characterization of arginine kinase from the indianmeal moth, Plodia interpunctella, a novel cross-reactive invertebrate pan-allergen	JOURNAL OF IMMUNOLOGY			English	Article							REAGINIC SENSITIVITY; COCKROACH ALLERGEN; BRONCHIAL-ASTHMA; IGE ANTIBODIES; SILKWORM MOTH; HOUSE-DUST; SEQUENCE; INSECTS; CLONING; SITES	IgE recognition of indoor allergens represents a major cause of allergic asthma in atopic individuals. We found that 52 of 102 patients suffering from allergic symptoms indoors contained IgE Abs against allergens from the Indianmeal moth (Plodia interpunctella), a ubiquitous food pest. Using serum IgE from a moth-sensitized patient we screened an expression cDNA library constructed from A interpunctella larvae. cDNAs coding for arginine kinase (EC 2.7.3.3), a 40-kDa enzyme commonly occurring in invertebrates that is involved in the storage of such high-energy phosphate bonds as phosphoarginine, were isolated. Recombinant moth arginine kinase, designated Plo i 1, was expressed in Escherichia coli as a histidine-tagged protein with enzymatic activity, and purified to homogeneity by nickel chelate affinity chromatography. Purified recombinant arginine kinase induced specific basophil histamine release and immediate as well as late-phase skin reactions. It reacted with serum IgE from 13 of the 52 (25%) moth-allergic patients and inhibited the binding of allergic patients' IgE to an immunologically related 40-kDa allergen present in house dust mite, cockroach, king prawn, lobster, and mussel. Our results indicate that arginine kinases represent a new class of cross-reactive invertebrate pan-allergens. Recombinant arginine kinase may be used to identify a group of polysensitized indoor allergic patients and for immunotherapy of these individuals.	Univ Vienna, Dept Pathophysiol, Div Specif Prophylaxis & Trop Med, AKH, A-1090 Vienna, Austria; Univ Vienna, Div Immunopathol, Dept Pathophysiol, A-1090 Vienna, Austria; Univ Vienna, Div Hematol & Hemostaseol, Dept Internal Med 1, A-1090 Vienna, Austria; Biol Res Ctr Agr & Forestry, Inst Stored Prod Protect, Berlin, Germany	Duchene, M (reprint author), Univ Vienna, Dept Pathophysiol, Div Specif Prophylaxis & Trop Med, AKH, Wahringer Gurtel 18-20, A-1090 Vienna, Austria.						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J	Marks, GB; Colquhoun, JR; Girgis, ST; Koski, MH; Treloar, ABA; Hansen, P; Downs, SH; Car, NG				Marks, GB; Colquhoun, JR; Girgis, ST; Koski, MH; Treloar, ABA; Hansen, P; Downs, SH; Car, NG			Thunderstorm outflows preceding epidemics of asthma during spring and summer	THORAX			English	Article						asthma; thunderstorms; season	GRASS-POLLEN; AIR-POLLUTION; AUSTRALIA; MORTALITY; ENGLAND; CITY	Background-A study was undertaken to assess the importance of thunderstorms as a cause of epidemics of asthma exacerbations and to investigate the underlying mechanism. Methods-A case control study was performed in six towns in south eastern Australia. Epidemic case days (n = 48) and a random sample of control days (n = 191) were identified by reference to the difference between the observed and expected number of emergency department attendances for asthma. The occurrence of thunderstorms, their associated outflows and cold fronts were ascertained, blind to case status, for each of these days. In addition, the relation of hourly pollen counts to automatic weather station data was examined in detail for the period around one severe epidemic of asthma exacerbations. The main outcome measure was the number of epidemics of asthma exacerbations. Results-Thunderstorm outflows were detected on 33% of epidemic days and only 3% of control days (odds ratio 15.0, 95% confidence interval 6.0 to 37.6). The association was strongest in late spring and summer. Detailed examination of one severe epidemic showed that its onset coincided with the arrival of the thunderstorm outflow and a 4-12 fold increase in the ambient concentration of grass pollen grains. Conclusions-These findings are consistent with the hypothesis that some epidemics of exacerbations of asthma are caused by high concentrations of allergenic particles produced by an outflow of colder air, associated with the downdraught from a thunderstorm, sweeping up pollen grains and particles and then concentrating them in a shallow band of air at ground level. This is a common cause of exacerbations of asthma during the pollen season.	Univ Sydney, Inst Resp Med, Sydney, NSW 2050, Australia; Bur Meteorol, NSW Reg Off, Sydney, NSW, Australia; Charles Sturt Univ, Sch Biomed Sci, Wagga Wagga, NSW, Australia	Marks, GB (reprint author), Univ Sydney, Inst Resp Med, Sydney, NSW 2050, Australia.		Downs, Sara/D-8478-2011; Osborne, Nicholas/N-4915-2015	Downs, Sara/0000-0003-1044-3182; Osborne, Nicholas/0000-0002-6700-2284			BELLOMO R, 1992, MED J AUSTRALIA, V156, P834; Celenza A, 1996, BRIT MED J, V312, P604; Davidson AC, 1996, BRIT MED J, V312, P601; Epton MJ, 1997, THORAX, V52, P528; Girgis ST, 2000, EUR RESPIR J, V16, P3, DOI 10.1034/j.1399-3003.2000.16a02.x; HIRST JM, 1952, ANN APPL BIOL, V39, P257, DOI 10.1111/j.1744-7348.1952.tb00904.x; Jamason PF, 1997, AM J RESP CRIT CARE, V156, P1781; KAPYLA M, 1981, Grana, V20, P131; Katsouyanni K, 1996, J EPIDEMIOL COMMUN H, V50, pS12, DOI 10.1136/jech.50.Suppl_1.S12; MACKENBACH JP, 1993, J EPIDEMIOL COMMUN H, V47, P121, DOI 10.1136/jech.47.2.121; Newson R, 1997, THORAX, V52, P680; Newson R, 1998, EUR RESPIR J, V11, P694; ODGEN E, 1974, MANUAL SAMPLING AIRB; PACKE GE, 1985, LANCET, V2, P199; ROSENBERG GL, 1983, J ALLERGY CLIN IMMUN, V71, P302, DOI 10.1016/0091-6749(83)90084-2; Simpson RW, 1997, ARCH ENVIRON HEALTH, V52, P442; SUPHIOGLU C, 1992, LANCET, V339, P569, DOI 10.1016/0140-6736(92)90864-Y; TOBIAS A, 1998, STATA TECH B, V46, P33; Venables KM, 1997, CLIN EXP ALLERGY, V27, P725, DOI 10.1046/j.1365-2222.1997.790893.x	19	88	89	2	4	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	JUN	2001	56	6					468	471		10.1136/thorax.56.6.468		4	Respiratory System	Respiratory System	438XL	WOS:000169079500011	11359963	
J	Yoshimura, S; Bondeson, J; Brennan, FM; Foxwell, BMJ; Feldmann, M				Yoshimura, S; Bondeson, J; Brennan, FM; Foxwell, BMJ; Feldmann, M			Role of NF kappa B in antigen presentation and development of regulatory T cells elucidated by treatment of dendritic cells with the proteasome inhibitor PSI	EUROPEAN JOURNAL OF IMMUNOLOGY			English	Article						antigen presentation; NF kappa B; tolerance	NECROSIS-FACTOR-ALPHA; PROINFLAMMATORY CYTOKINES; FUNCTIONAL-HETEROGENEITY; BLOOD MONOCYTES; ACTIVATION; TOLERANCE; INDUCTION; EXPRESSION; APOPTOSIS; UNRESPONSIVENESS	Dendritic cells (DC) are the most potent antigen-presenting cells for naive T cells, due to their high expression of MHC and costimulatory molecules, but relatively little is known about the biochemical pathways that regulate this function. We used the proteasome inhibitor N-benzyloxycarbonyl-IIe-Glu(O-tert-butyl)-Ala-leucinal (PSI) to demonstrate that DC antigen presentation is NF kappaB dependent. As PSI is not a specific inhibitor of NF kappaB, we reproduced this finding using a very specific approach, namely adenoviral gene transfer of I kappaB alpha, the naturally occurring inhibitor of NF kappaB. The mechanism for this inhibition of DC antigen presentation involves at least three aspects of antigen presenting function: down-regulation of HLA class II, down-regulation of CD86, and inhibition of the immunostimulatory cytokines IL-12 and TNF-alpha. In the light of the marked down-regulation of antigen-presentation cell function, it was of interest to investigate what effects exposure to PSI-treated DC might have on T cell function. It was found that immunological tolerance was induced, as challenge of T cells previously exposed to PSI-treated DC, with normal DG from the same donor did not restore their response, despite the presence of viable T cells. There were also changes in T cell surface markers, with down-regulation of CD3 and CD25 expression, and inhibition of the production of Th1 cytokines like IL-2 and IFN-gamma. These results demonstrates that NF kappaB is an effective target for blocking DC antigen presentation and inhibiting T cell-dependent immune responses, and this has implications for the development of therapeutic agents for use in multiple conditions, including transplantation, allergy and autoimmune diseases.	Imperial Coll Sch Med, Div Rheumatol, Kennedy Inst, London, England	Feldmann, M (reprint author), Imperial Coll Sch Med, Div Rheumatol, Kennedy Inst, 1 Aspenlea Rd, London, England.						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J. Immunol.	JUN	2001	31	6					1883	1893		10.1002/1521-4141(200106)31:6<1883::AID-IMMU1883>3.0.CO;2-V		11	Immunology	Immunology	442TY	WOS:000169302100027	11433385	
J	Wechsler, ME; Grasemann, H; Deykin, A; Silverman, EK; Yandava, CN; Israel, E; Wang, M; Drazen, JM				Wechsler, ME; Grasemann, H; Deykin, A; Silverman, EK; Yandava, CN; Israel, E; Wang, M; Drazen, JM			Exhaled nitric oxide in patients with asthma - Association with NOS1 genotype	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							SYNTHASE GENE NOS1; APOLIPOPROTEIN-E; POPULATION; POLYMORPHISMS; INFLAMMATION; MUTATIONS; DISORDERS; LINKAGE; MARKERS; LOCUS	An increased concentration of nitric oxide (NO) in exhaled air (FENO) is now recognized as a critical component of the asthmatic phenotype. When we identified patients with asthma on the basis of a standard case definition alone, we found that they were remarkably heterogeneous with respect to their FENO. However, when we included genotype at a prominent asthma candidate gene (i.e., NOS1) in the case definition, and determined the number of AAT repeats in intron 20, we identified a remarkably homogenous cohort of patients with respect to FENO. Both mean FENO (p = 0.00008) and variability around the mean (p = 0.000002) were significantly lower in asthmatic individuals with a high number (greater than or equal to 12) of AAT repeats at this locus than in those with fewer repeats. These data provide a biologically tenable link between genotype at a candidate gene in a region of linkage, NOS1, and an important component of the asthmatic phenotype, FENO. We show that addition of NOS1 genotype to the case definition of asthma allows the identification of a uniform cohort of patients, with respect to FENO, that would have been indistinguishable by other physiologic criteria. Our isolation of this homogenous cohort of patients ties together the well-established associations among asthma, increased concentrations of NO in the exhaled air of asthmatic individuals, and variations of trinucleotide repeat sequences as identified in several neurologic conditions.	Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA; Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA; Harvard Univ, Sch Publ Hlth, Dept Med, Boston, MA 02115 USA	Drazen, JM (reprint author), Brigham & Womens Hosp, Div Pulm & Crit Care Med, 75 Francis St,Tower 4B, Boston, MA 02115 USA.		Drazen, Jeffrey/E-5841-2012; Wechsler, Michael /B-3979-2013; Wand, Matt /F-9413-2012	Wechsler, Michael /0000-0003-3505-2946; Wand, Matt /0000-0003-2555-896X	NHLBI NIH HHS [P50-HL-56383]		American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P225, DOI DOI 10.1164/AJRCCM/136.1.225; Barnes KC, 1996, GENOMICS, V37, P41, DOI 10.1006/geno.1996.0518; BARNES PJ, 1995, CHEST, V107, pS119, DOI 10.1378/chest.107.3_Supplement.119S; BARNES PJ, 1993, EUR RESPIR J, V6, P163; Barnes PJ, 1996, THORAX, V51, P233, DOI 10.1136/thx.51.3.233; BOERWINKLE E, 1986, AM J HUM GENET, V39, P137; BOERWINKLE E, 1988, AM J HUM GENET, V42, P104; Chung E, 1996, AM J HUM GENET, V58, P363; De Sanctis GT, 1999, J EXP MED, V189, P1621, DOI 10.1084/jem.189.10.1621; DeSanctis GT, 1997, AM J PHYSIOL-LUNG C, V273, pL883; Deykin A, 1998, AM J RESP CRIT CARE, V157, P769; FERNANDES L, 1995, AM J RESP CRIT CARE, V151, P1689; Grasemann H, 1999, HUM HERED, V49, P139, DOI 10.1159/000022861; Grasemann H, 1999, CLIN EXP ALLERGY, V29, P39; HALL AV, 1994, J BIOL CHEM, V269, P33082; Hedenstierna G, 1998, EUR RESPIR J, V12, P1248, DOI 10.1183/09031936.98.12061248; HUANG PL, 1993, CELL, V75, P1273, DOI 10.1016/0092-8674(93)90615-W; In KH, 1997, J CLIN INVEST, V99, P1130, DOI 10.1172/JCI119241; Kharitonov S, 1997, EUR RESPIR J, V10, P1683, DOI 10.1183/09031936.97.10071683; KHARITONOV SA, 1994, LANCET, V343, P133, DOI 10.1016/S0140-6736(94)90931-8; KHARITONOV SA, 1995, CHEST, V107, pS156, DOI 10.1378/chest.107.3_Supplement.156S; Marsh DG, 1997, NAT GENET, V15, P389; Martin JB, 1999, NEW ENGL J MED, V340, P1970; Massaro AF, 1996, AM J RESP CRIT CARE, V153, P1510; MASSARO AF, 1995, AM J RESP CRIT CARE, V152, P800; Nickel R, 1997, GENOMICS, V46, P159, DOI 10.1006/geno.1997.5013; Ober C, 1998, HUM MOL GENET, V7, P1393, DOI 10.1093/hmg/7.9.1393; Pearson CE, 1998, CURR OPIN STRUC BIOL, V8, P321, DOI 10.1016/S0959-440X(98)80065-1; REILLY SL, 1991, AM J HUM GENET, V49, P1155; Ricciardolo FLM, 1998, LANCET, V351, P449, DOI 10.1016/S0140-6736(05)78400-2; Robbins RA, 1996, AM J RESP CRIT CARE, V153, P1631; Salome CM, 1999, AM J RESP CRIT CARE, V159, P911; Silkoff PE, 1999, CHEST, V116, P754, DOI 10.1378/chest.116.3.754; Slutsky AS, 1999, AM J RESP CRIT CARE, V160, P2104; Timchenko LT, 1999, CELL MOL LIFE SCI, V55, P1432, DOI 10.1007/s000180050383; Togashi H, 1997, P NATL ACAD SCI USA, V94, P2676, DOI 10.1073/pnas.94.6.2676; TWELLS R, 1995, AM J HUM GENET, V56, P336; Wang Y, 1999, CRIT REV NEUROBIOL, V13, P21; WEBER JL, 1989, AM J HUM GENET, V44, P388	39	88	93	0	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.	DEC	2000	162	6					2043	2047				5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	381ZV	WOS:000165794700013	11112111	
J	Gelb, AF; Zamel, N				Gelb, AF; Zamel, N			Unsuspected pseudophysiologic emphysema in chronic persistent asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							AIR-FLOW OBSTRUCTION; TOTAL LUNG CAPACITY; SMALL-AIRWAYS; FOLLOW-UP; DIAPHRAGM; DISEASE; HYPERINFLATION; MECHANISM; MUSCLE; ADULTS	The current literature emphasizes the role of airway remodeling in chronic persistent asthma and its putative effect on causing fixed expiratory airflow limitation. We studied 18 adults with chronic persistent asthma; 12 men, six women, age 59 +/- 15 yr (mean +/- SD) with fixed expiratory airflow obstruction. We measured lung elastic recoil and examined the mechanism of expiratory airflow limitation. Diaphragmatic strength was also measured in six asthmatics, using both sniff and partially occluded airway technique. All 18 asthmatics had markedly abnormal maximal expiratory flow-volume curves at both high and low lung volumes. Hyperinflation was present at residual volume (RV), FRC, and TLC in all subjects. Diffusing capacity was normal or elevated and lung computed tomography (CT) was normal in all 18 asthmatic subjects. There was a significant loss of lung elastic recoil in three of four asthmatics age 30 to 49, all five age 51 to 60 yr, and seven of nine age 61 to 82 yr. Maximal expiratory airflow limitation in only four elderly asthmatics and only at low lung volumes was due completely to loss of lung elastic recoil. In the others, we estimate the reduction in lung elastic recoil was responsible for 35% reduction in maximal expiratory airflow at 80% of TLC, and 55% at 70% of TLC. Despite hyperinflation, transdiaphragmatic pressures and strength were normal. The mechanisms responsible for loss of lung elastic recoil remain elusive. The high incidence of loss of lung elastic recoil in chronic persistent asthma was unexpected, and its contribution to abnormal lung function needs to be emphasized.	Univ Calif Los Angeles, Sch Med, Div Pulm, Dept Med, Los Angeles, CA USA; Univ Calif Los Angeles, Sch Med, Lakewood Reg Med Ctr, Los Angeles, CA USA; Univ Toronto, Fac Med, Toronto, ON, Canada	Gelb, AF (reprint author), 3650 E South St,Suite 308, Lakewood, CA 90712 USA.						BEALE HD, 1952, J ALLERGY, V23, P1, DOI 10.1016/0021-8707(52)90067-1; BECKMAN KS, 1997, CHEST, V112, P1234; Biernacki W, 1997, EUR RESPIR J, V10, P2455, DOI 10.1183/09031936.97.10112455; BLACK LF, 1969, AM REV RESPIR DIS, V99, P696; BLACKIE SP, 1990, AM REV RESPIR DIS, V142, P79; BOUSQUET J, 1992, ALLERGY, V47, P3, DOI 10.1111/j.1398-9995.1992.tb02242.x; BROWN PJ, 1984, THORAX, V39, P131, DOI 10.1136/thx.39.2.131; CADE JF, 1973, AUST NZ J MED, V3, P545, DOI 10.1111/j.1445-5994.1973.tb04293.x; Chetta A, 1997, CHEST, V111, P852, DOI 10.1378/chest.111.4.852; FINUCANE KE, 1969, J APPL PHYSIOL, V26, P330; GELB AF, 1975, CHEST, V68, P538, DOI 10.1378/chest.68.4.538; Gelb AF, 1998, AM J RESP CRIT CARE, V158, P815; Gelb AF, 1996, AM J RESP CRIT CARE, V154, P945; Gelb AF, 1996, CHEST, V109, P353, DOI 10.1378/chest.109.2.353; GOLD WM, 1967, J APPL PHYSIOL, V23, P433; KINSELLA M, 1988, CHEST, V94, P286, DOI 10.1378/chest.94.2.286; KNOX AJ, 1994, CLIN SCI, V86, P647; Laghi F, 1998, AM J RESP CRIT CARE, V157, P475; LAITINEN LA, 1993, AM REV RESPIR DIS, V147, P697; Lange P, 1998, NEW ENGL J MED, V339, P1194, DOI 10.1056/NEJM199810223391703; MANWELL A, 1974, J APPL PHYSIOL, V37, P297; MCCARTHY DS, 1980, THORAX, V35, P298, DOI 10.1136/thx.35.4.298; MILLER JM, 1985, CLIN SCI, V69, P91; MULLER N, 1980, J APPL PHYSIOL, V49, P869; MULLER N, 1981, J APPL PHYSIOL, V50, P279; PALMER KNV, 1975, BRIT MED J, V1, P485; Pellegrino R, 1996, J APPL PHYSIOL, V81, P964; PERESS L, 1976, AM J MED, V61, P165, DOI 10.1016/0002-9343(76)90165-0; PRIDE NB, 1967, J APPL PHYSIOL, V23, P646; Redington AE, 1997, THORAX, V52, P310; RODARTE JR, 1999, J APPL PHYSIOL, V81, P964; SIMILOWSKI T, 1991, NEW ENGL J MED, V325, P917, DOI 10.1056/NEJM199109263251304; Ulrik CS, 1999, EUR RESPIR J, V14, P892, DOI 10.1034/j.1399-3003.1999.14d27.x; ULRIK CS, 1992, THORAX, V47, P14, DOI 10.1136/thx.47.1.14; WOOLCOCK AJ, 1968, AM REV RESPIR DIS, V98, P788; WOOLCOCK AJ, 1971, AM REV RESPIR DIS, V104, P703; ZAMEL N, 1976, AM REV RESPIR DIS, V113, P337	37	88	88	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.	NOV	2000	162	5					1778	1782				5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	371WU	WOS:000165202900032	11069812	
J	Wakefield, M; Banham, D; Martin, J; Ruffin, R; McCaul, K; Badcock, N				Wakefield, M; Banham, D; Martin, J; Ruffin, R; McCaul, K; Badcock, N			Restrictions on smoking at home and urinary cotinine levels among children with asthma	AMERICAN JOURNAL OF PREVENTIVE MEDICINE			English	Article						asthma; child; cotinine; family relations; tobacco smoke pollution; smoking	ENVIRONMENTAL TOBACCO-SMOKE; PARENTAL SMOKING; PASSIVE SMOKING; EXPOSURE; HOUSEHOLD	Objectives: The purpose of this study was to determine the extent to which various levels of restrictions on smoking in the home may be associated with children's exposure to environmental tobacco smoke (ETS). Methods: The methodology consisted of a cross-sectional survey involving 249 children with asthma aged 1 to 11 attending hospital outpatient clinics, with at least one parent who smoked, linked to the child's urinary cotinine to creatinine rations (CCR). Results: After adjustment for child's age, mother's smoking status, and total parental daily cigarette consumption, a total ban was associated with significantly lower urinary CCR levels (7.6 nmol/mmol) than bans with exceptions or limited smoking in the home. Where exceptions to bans were made (14.9 nmol/mmol), children's urinary CCR levels were no different from homes in which smoking was allowed in rooms the child rarely frequented (14.1 nmol/mmol). These two intermediate levels of restriction were in turn associated with significantly lower CCR levels than unrestricted smoking in the home (26.0 nmol/mmol). Conclusions: Making exceptions to bans on smoking at home measurably undermines the protective effect of a ban. However, making some exceptions to a ban and limiting smoking to rooms where the child rarely goes may result in reduced exposure to ETS, compared with unrestricted smoking.	Univ Illinois, Hlth Res Ctr, Chicago, IL 60607 USA; Univ Illinois, Policy Ctr, Chicago, IL 60607 USA; Womens & Childrens Hosp, Dip Food Technol, Adelaide, SA, Australia; Queen Elizabeth Hosp, Adelaide, SA, Australia; S Australian Dept Human Serv, Adelaide, SA, Australia	Wakefield, M (reprint author), Univ Illinois, Hlth Res Ctr, 850 W jackson Blvd,Suite 400, Chicago, IL 60607 USA.		McCaul, Kieran/B-8751-2008				Abulhosn RS, 1997, ARCH PEDIAT ADOL MED, V151, P135; Ashley MJ, 1998, TOB CONTROL, V7, P61; Bakoula CG, 1997, CANCER CAUSE CONTROL, V8, P73, DOI 10.1023/A:1018487222533; Benowitz NL, 1999, ENVIRON HEALTH PERSP, V107, P349, DOI 10.2307/3434427; Benowitz NL, 1996, EPIDEMIOL REV, V18, P188; Cook DG, 1999, THORAX, V54, P357; COOK DG, 1994, BRIT MED J, V308, P384; COULTAS DB, 1990, AM REV RESPIR DIS, V142, P602; DELLORCO V, 1995, AM J EPIDEMIOL, V142, P419; EMERSON JA, 1994, ADDICT BEHAV, V19, P677, DOI 10.1016/0306-4603(94)90022-1; EVANS D, 1987, AM REV RESPIR DIS, V135, P567; Farkas AJ, 1999, TOB CONTROL, V8, P261; FRIED PA, 1995, CLIN BIOCHEM, V28, P415, DOI 10.1016/0009-9120(94)00092-A; GREENLAND S, 1989, AM J PUBLIC HEALTH, V79, P340, DOI 10.2105/AJPH.79.3.340; Henschen M, 1997, ENVIRON RES, V72, P65, DOI 10.1006/enrs.1996.3688; Irvine L, 1999, BRIT MED J, V318, P1456; Jaakkola MS, 1997, EUR RESPIR J, V10, P2384, DOI 10.1183/09031936.97.10102384; Lofroth G, 1993, TOB CONTROL, V2, P222, DOI 10.1136/tc.2.3.222; McBride SJ, 1999, J EXPO ANAL ENV EPID, V9, P602, DOI 10.1038/sj.jea.7500057; Oddoze C, 1999, CLIN CHEM, V45, P505; Ott WR, 1999, ENVIRON HEALTH PERSP, V107, P375, DOI 10.2307/3434430; RONCHETTI R, 1994, EUR RESPIR J, V7, P472, DOI 10.1183/09031936.94.07030472; ROSIER MJ, 1994, AM J RESP CRIT CARE, V149, P1431; STRECHER V J, 1989, Health Education Research, V4, P225, DOI 10.1093/her/4.2.225; Tabachnick B. G., 1996, USING MULTIVARIATE S; THOMPSON SG, 1990, CLIN CHIM ACTA, V187, P289, DOI 10.1016/0009-8981(90)90114-8; WAKEFIELD M, IN PRESS HLTH PROM J; Winkelstein ML, 1997, ANN ALLERG ASTHMA IM, V78, P419	28	88	89	2	2	ELSEVIER SCIENCE INC	NEW YORK	655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA	0749-3797			AM J PREV MED	Am. J. Prev. Med.	OCT	2000	19	3					188	192		10.1016/S0749-3797(00)00197-5		5	Public, Environmental & Occupational Health; Medicine, General & Internal	Public, Environmental & Occupational Health; General & Internal Medicine	361ME	WOS:000089726200008	11020596	
J	Bodner, C; Anderson, WJ; Reid, TS; Godden, DJ				Bodner, C; Anderson, WJ; Reid, TS; Godden, DJ		Aberdeen WHEASE Study Grp	Childhood exposure to infection and risk of adult onset wheeze and atopy	THORAX			English	Article						childhood infections; family size; adult onset wheeze; asthma; atopy	FAMILY-SIZE; HAY-FEVER; PREVALENCE; ASSOCIATION; SYMPTOMS; CHILDREN; ASTHMA	Background-The prevalence of asthma and allergic diseases in children and young adults is inversely associated with family size. It has been suggested that more frequent exposure to infections in a large family group, particularly those spread by the faecal-oral route, may protect against atopic diseases, although not all published data support this hypothesis. Whether similar considerations apply to adult onset wheeze is unknown. The relationship between adult onset wheezing and atopy measured in adulthood and childhood exposure to a range of infections was investigated. Methods-A nested case control study of participants in a 30 year follow up survey was conducted. Questionnaire data on childhood infections had been obtained in a 1964 survey. In 1995 a further questionnaire on respiratory symptoms and other risk factors for wheezing illness was administered, total IgE, skin and RAST tests were performed, and serum was stored. In 1999 serological tests for hepatitis A, Helicobacter pylori, and Toxoplasma gondii were performed on the stored samples. Information from the 1964 questionnaires was available for 97 cases and 208 controls and serological tests were obtained for 85 cases and 190 controls. The potential risk factors were examined for all cases, those who reported doctor diagnosed asthma, those who described persistent cough and phlegm with wheeze, and subjects stratified by atopic status. Results-The sibship structure was similar in cases and controls. In univariate analysis of all cases, childhood infections reported by parents as acquired either before or after the age of three years did not influence case:control or atopic status. Seropositivity was also similar for all cases and controls, but cases in the subgroup with chronic cough and phlegm were more likely to be seropositive for hepatitis A and H pylori. Seropositivity was unrelated to atopic status. In multivariate analyses both the effect of having two or more younger siblings (OR 0.1, 95% CI 0.03 to 0.8) and of acquiring measles up to the age of three (OR 0.2, CI 0.03 to 0.8) were significantly related to a lower risk of doctor diagnosed asthma. Conclusions-In these well characterised subjects, exposure to infections as measured by parental reports obtained at age 10-14 years and by serological tests obtained in adulthood did not influence the development of wheezing symptoms or atopic status in adulthood. However, early exposure to measles and family size may be associated with a lower risk of adult onset doctor diagnosed asthma.	Univ Aberdeen, Dept Environm & Occupat Med, Aberdeen AB25 2ZD, Scotland; Aberdeen Royal Infirm, Dept Thorac Med, Aberdeen AB25 2ZN, Scotland; Grampian Univ Hosp Trust, Dept Med Microbiol, Aberdeen AB25 2ZN, Scotland	Godden, DJ (reprint author), Univ Aberdeen, Dept Environm & Occupat Med, Aberdeen AB25 2ZD, Scotland.						Bodner C, 1998, THORAX, V53, P28; Bodner C, 1997, BRIT MED J, V314, P792; Bodner CH, 1998, AM J RESP CRIT CARE, V157, P35; DAWSON B, 1969, LANCET, V1, P827; GODDEN DJ, 1994, AM J RESP CRIT CARE, V149, P106; GOLDING J, 1986, STUDY HLTH BEHAV BRI, P171; Jarvis D, 1997, CLIN EXP ALLERGY, V27, P240; Matricardi PM, 1997, BRIT MED J, V314, P999; MATRICARDI PM, 1997, LANCET, V349, P67; Omran M, 1996, BRIT MED J, V312, P34; PEAT JK, 1994, BRIT MED J, V308, P1591; ROMAGNANI S, 1992, INT ARCH ALLERGY IMM, V98, P279; 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; Strachan DP, 1997, CLIN EXP ALLERGY, V27, P151; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Strachan DP, 1997, J ALLERGY CLIN IMMUN, V99, P6, DOI 10.1016/S0091-6749(97)81038-X; Strachan DP, 1996, ARCH DIS CHILD, V74, P422; von Mutius E, 1999, EUR RESPIR J, V14, P4, DOI 10.1034/j.1399-3003.1999.14a03.x; VONMUTIUS E, 1994, BRIT MED J, V308, P692	20	88	88	0	3	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	MAY	2000	55	5					383	387		10.1136/thorax.55.5.383		5	Respiratory System	Respiratory System	310GD	WOS:000086817400009	10770819	
J	Fleischer, DM; Perry, TT; Atkins, D; Wood, RA; Burks, AW; Jones, SM; Henning, AK; Stablein, D; Sampson, HA; Sicherer, SH				Fleischer, David M.; Perry, Tamara T.; Atkins, Dan; Wood, Robert A.; Burks, A. Wesley; Jones, Stacie M.; Henning, Alice K.; Stablein, Donald; Sampson, Hugh A.; Sicherer, Scott H.			Allergic Reactions to Foods in Preschool-Aged Children in a Prospective Observational Food Allergy Study	PEDIATRICS			English	Article						food allergy; IgE-mediated allergic reaction; epinephrine	TREE-NUT-ALLERGY; PEANUT ALLERGY; UNITED-STATES; EPINEPHRINE; IGE; ANAPHYLAXIS; CHALLENGES; PREVALENCE; FEATURES; REGISTRY	OBJECTIVE: To examine circumstances of allergic reactions to foods in a cohort of preschool-aged children. METHODS: We conducted a prospective, 5-site observational study of 512 infants aged 3 to 15 months with documented or likely allergy to milk or egg, and collected data prospectively examining allergic reactions. RESULTS: Over a median follow-up of 36 months (range: 0-48.4), the annualized reaction rate was 0.81 per year (367/512 subjects reporting 1171 reactions [95% confidence interval: 0.76-0.85]). Overall, 269/512 (52.5%) reported >1 reaction. The majority of reactions (71.2%) were triggered by milk (495 [42.3%]), egg (246 [21.0%]), and peanut (93 [7.9%]), with accidental exposures attributed to unintentional ingestion, label-reading errors, and cross-contact. Foods were provided by persons other than parents in 50.6% of reactions. Of 834 reactions to milk, egg, or peanut, 93 (11.2%) were attributed to purposeful exposures to these avoided foods. A higher number of food allergies (P < .0001) and higher food-specific immunoglobulin E (P < .0001) were associated with reactions. Of the 11.4% of reactions (n = 134) that were severe, 29.9% were treated with epinephrine. Factors resulting in undertreatment included lack of recognition of severity, epinephrine being unavailable, and fears about epinephrine administration. CONCLUSIONS: There was a high frequency of reactions caused by accidental and nonaccidental exposures. Undertreatment of severe reactions with epinephrine was a substantial problem. Areas for improved education include the need for constant vigilance, accurate label reading, avoidance of nonaccidental exposure, prevention of cross-contamination, appropriate epinephrine administration, and education of all caretakers. Pediatrics 2012;130:e25-e32	[Fleischer, David M.; Atkins, Dan] Natl Jewish Hlth, Denver, CO 80206 USA; [Perry, Tamara T.; Jones, Stacie M.] Univ Arkansas Med Sci, Little Rock, AR 72205 USA; [Wood, Robert A.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA; [Burks, A. Wesley] Duke Univ, Med Ctr, Durham, NC USA; [Henning, Alice K.; Stablein, Donald] EMMES Corp, Rockville, MD USA; [Burks, A. Wesley] Univ N Carolina, Chapel Hill, NC USA; [Sampson, Hugh A.; Sicherer, Scott H.] Mt Sinai Sch Med, Jaffe Food Allergy Inst, New York, NY USA	Fleischer, DM (reprint author), Natl Jewish Hlth, 1400 Jackson St,J321, Denver, CO 80206 USA.	fleischerd@njhealth.org			National Institutes of Health (NIH)-National Institute of Allergy and Infectious Diseases (NIAID) [U19AI066738, U01AI066560]; National Center for Research Resources, a component of the NIH [UL1 RR025780, UL1 RR029887, UL1 RR029884, UL1 RR024128, UL1 RR025005]; NIH-NIAID; NIH-National Heart, Lung, and Blood Institute; Marion B. Lyon Award; Food Allergy & Anaphylaxis Network; Wallace Research Foundation; National Peanut Board; Food Allergy Initiative; Dyax Corp.; National Institutes of Health (NIH)	Supported by the National Institutes of Health (NIH)-National Institute of Allergy and Infectious Diseases (NIAID) U19AI066738 and U01AI066560. The project was also supported by grants UL1 RR025780 (National Jewish Health), UL1 RR029887 (Mount Sinai School of Medicine), UL1 RR029884 (University of Arkansas for Medical Sciences), UL1 RR024128 (Duke University Medical Center), and UL1 RR025005 (Johns Hopkins University School of Medicine) from the National Center for Research Resources, a component of the NIH. Dr Fleischer received grant support from the NIH-NIAID. Dr Perry received research support from the NIH-National Heart, Lung, and Blood Institute and the Marion B. Lyon Award. Dr Atkins received grant support from the NIH. Dr Wood received grant support from the NIH. Dr Burks received grant support from the NIH, the Food Allergy & Anaphylaxis Network, and the Wallace Research Foundation. Dr Jones received research support from the National Peanut Board, the NIH-NIAID, the Food Allergy Initiative, and Dyax Corp. Dr Stablein received grant support from the NIH. Dr Sampson received research support from the NIH-NIAID and the Food Allergy Initiative. Dr Sicherer received research support from the NIH-NIAID and the Food Allergy Initiative. Funded by the National Institutes of Health (NIH).	American Academy of Pediatrics, 2000, PEDIATRICS 1, V106, P346; Bock SA, 2007, J ALLERGY CLIN IMMUN, V119, P1016, DOI 10.1016/j.jaci.2006.12.622; Boyano-Martinez T, 2009, J ALLERGY CLIN IMMUN, V123, P883, DOI 10.1016/j.jaci.2008.12.1125; Boyce J. A., 2010, Journal of Allergy and Clinical Immunology, V126, pS1; Branum AM, 2009, PEDIATRICS, V124, P1549, DOI 10.1542/peds.2009-1210; Eigenmann PA, 1998, PEDIATRICS, V101, DOI 10.1542/peds.101.3.e8; Eigenmann PA, 2002, ALLERGY, V57, P449, DOI 10.1034/j.1398-9995.2002.13494.x; Furlong TJ, 2001, J ALLERGY CLIN IMMUN, V108, P867, DOI 10.1067/mai.2001.119157; Greenhawt MJ, 2009, J ALLERGY CLIN IMMUN, V124, P598, DOI 10.1016/j.jaci.2009.06.039; Gupta RS, 2011, PEDIATRICS, V128, pE9, DOI 10.1542/peds.2011-0204; Hourihane JO, 1997, CLIN EXP ALLERGY, V27, P634, DOI 10.1046/j.1365-2222.1997.d01-559.x; Jarvinen KM, 2008, J ALLERGY CLIN IMMUN, V122, P133, DOI 10.1016/j.jaci.2008.04.031; Jarvinen KM, 2009, J ALLERGY CLIN IMMUN, V124, P1267, DOI 10.1016/j.jaci.2009.10.006; Kemp SF, 2008, ALLERGY, V63, P1061, DOI 10.1111/j.1398-9995.2008.01733.x; Monks H, 2010, CLIN EXP ALLERGY, V40, P1533, DOI 10.1111/j.1365-2222.2010.03586.x; Nowak-Wegrzyn A, 2001, ARCH PEDIAT ADOL MED, V155, P790; Perry TT, 2004, J ALLERGY CLIN IMMUN, V114, P1164, DOI 10.1016/j.jaci.2004.07.063; Perry TT, 2004, J ALLERGY CLIN IMMUN, V113, P973, DOI 10.1016/j.jaci.2004.02.035; Ross MP, 2008, J ALLERGY CLIN IMMUN, V121, P166, DOI 10.1016/j.jaci.2007.10.012; Rudders SA, 2010, PEDIATRICS, V125, pE711, DOI 10.1542/peds.2009-2832; Sampson HA, 2001, J ALLERGY CLIN IMMUN, V107, P891, DOI 10.1067/mai.2001.114708; Sampson MA, 2006, J ALLERGY CLIN IMMUN, V117, P1440, DOI 10.1016/j.jaci.2006.03.009; Sicherer SH, 2012, J PEDIATR-US, V160, P651, DOI 10.1016/j.jpeds.2011.09.056; Sicherer SH, 2010, J ALLERGY CLIN IMMUN, V126, P1191, DOI 10.1016/j.jaci.2010.08.036; Sicherer SH, 2010, J ALLERGY CLIN IMMUN, V125, P1077, DOI 10.1016/j.jaci.2010.02.038; Sicherer SH, 2001, J PEDIATR-US, V138, P560, DOI 10.1067/mpd.2001.111821; Sicherer SH, 1998, PEDIATRICS, V102, part. no., DOI 10.1542/peds.102.1.e6; Sicherer SH, 2001, J ALLERGY CLIN IMMUN, V108, P128, DOI 10.1067/mai.2001.115755; Simonte SJ, 2003, J ALLERGY CLIN IMMUN, V112, P180, DOI 10.1067/mai.2003.1486; Vander Leek TK, 2000, J PEDIATR-US, V137, P749, DOI 10.1067/mpd.2000.109376; Yu JW, 2006, J ALLERGY CLIN IMMUN, V118, P466, DOI 10.1016/j.jaci.2006.04.024	31	87	88	2	14	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	JUL	2012	130	1					E25	E32		10.1542/peds.2011-1762		8	Pediatrics	Pediatrics	967KH	WOS:000305905900004	22732173	
J	Bowers, RM; Sullivan, AP; Costello, EK; Collett, JL; Knight, R; Fierer, N				Bowers, Robert M.; Sullivan, Amy P.; Costello, Elizabeth K.; Collett, Jeff L., Jr.; Knight, Rob; Fierer, Noah			Sources of Bacteria in Outdoor Air across Cities in the Midwestern United States	APPLIED AND ENVIRONMENTAL MICROBIOLOGY			English	Article							RIBOSOMAL-RNA GENE; MICROBIAL COMMUNITIES; BIOLOGICAL PARTICLES; AIRBORNE BACTERIAL; DIVERSITY; SEQUENCES; ATMOSPHERE; ECOLOGY; BIODIVERSITY; VARIABILITY	Bacteria are abundant in the atmosphere, where they often represent a major portion of the organic aerosols. Potential pathogens of plants and livestock are commonly dispersed through the atmosphere, and airborne bacteria can have important effects on human health as pathogens or triggers of allergic asthma and seasonal allergies. Despite their importance, the diversity and biogeography of airborne microorganisms remain poorly understood. We used high-throughput pyrosequencing to analyze bacterial communities present in the aerosol fraction containing fine particulate matter of <= 2.5 mu m from 96 near-surface atmospheric samples collected from cities throughout the midwestern United States and found that the communities are surprisingly diverse and strongly affected by the season. We also directly compared the airborne communities to those found in hundreds of samples representing potential source environments. We show that, in addition to the more predictable sources (soils and leaf surfaces), fecal material, most likely dog feces, often represents an unexpected source of bacteria in the atmosphere at more urbanized locations during the winter. Airborne bacteria are clearly an important, but understudied, component of air quality that needs to be better integrated into efforts to measure and model pollutants in the atmosphere.	[Bowers, Robert M.; Fierer, Noah] Univ Colorado, Dept Ecol & Evolutionary Biol, Boulder, CO 80309 USA; [Sullivan, Amy P.; Collett, Jeff L., Jr.] Colorado State Univ, Dept Atmospher Sci, Ft Collins, CO 80523 USA; [Costello, Elizabeth K.] Stanford Univ, Sch Med, Dept Microbiol & Immunol, Stanford, CA 94305 USA; [Knight, Rob] Univ Colorado, Dept Chem & Biochem, Boulder, CO 80309 USA; [Knight, Rob] Howard Hughes Med Inst, Boulder, CO 80309 USA; [Fierer, Noah] Univ Colorado, Cooperat Inst Res Environm Sci, Boulder, CO 80309 USA	Fierer, N (reprint author), Univ Colorado, Dept Ecol & Evolutionary Biol, UCB 216, Boulder, CO 80309 USA.	noah.fierer@colorado.edu	Collett, Jeffrey/F-2862-2010; Knight, Rob/D-1299-2010	Collett, Jeffrey/0000-0001-9180-508X; 	CIRES IRP program; U.S. Environmental Protection Agency; National Science Foundation; Howard Hughes Medical Institute; National Institutes of Health	Support for this work was provided by grants from the CIRES IRP program (to N.F.), the U.S. Environmental Protection Agency (to N.F.), the National Science Foundation (to N.F.), the Howard Hughes Medical Institute, and the National Institutes of Health, and aerosol sample collection for this project was supported by the Lake Michigan Air Directors Consortium (LADCO).	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Environ. Microbiol.	SEP	2011	77	18					6350	6356		10.1128/AEM.05498-11		7	Biotechnology & Applied Microbiology; Microbiology	Biotechnology & Applied Microbiology; Microbiology	817RJ	WOS:000294691400005	21803902	
J	Andersen, B; Frisvad, JC; Sondergaard, I; Rasmussen, IS; Larsen, LS				Andersen, Birgitte; Frisvad, Jens C.; Sondergaard, Ib; Rasmussen, Ib S.; Larsen, Lisbeth S.			Associations between Fungal Species and Water-Damaged Building Materials	APPLIED AND ENVIRONMENTAL MICROBIOLOGY			English	Article							DANISH HOMES; RESIDENTIAL CHARACTERISTICS; STACHYBOTRYS-CHARTARUM; MOLDY HOMES; MICRO-FUNGI; HOUSE DUST; INDOOR AIR; AIRBORNE; MOISTURE; IDENTIFICATION	Fungal growth in damp or water-damaged buildings worldwide is an increasing problem, which has adverse effects on both the occupants and the buildings. Air sampling alone in moldy buildings does not reveal the full diversity of fungal species growing on building materials. One aim of this study was to estimate the qualitative and quantitative diversity of fungi growing on damp or water-damaged building materials. Another was to determine if associations exist between the most commonly found fungal species and different types of materials. More than 5,300 surface samples were taken by means of V8 contact plates from materials with visible fungal growth. Fungal identifications and information on building material components were analyzed using multivariate statistic methods to determine associations between fungi and material components. The results confirmed that Penicillium chrysogenum and Aspergillus versicolor are the most common fungal species in water-damaged buildings. The results also showed Chaetomium spp., Acremonium spp., and Ulocladium spp. to be very common on damp building materials. Analyses show that associated mycobiotas exist on different building materials. Associations were found between (i) Acremonium spp., Penicillium chrysogenum, Stachybotrys spp., Ulocladium spp., and gypsum and wallpaper, (ii) Arthrinium phaeospermum, Aureobasidium pullulans, Cladosporium herbarum, Trichoderma spp., yeasts, and different types of wood and plywood, and (iii) Aspergillus fumigatus, Aspergillus melleus, Aspergillus niger, Aspergillus ochraceus, Chaetomium spp., Mucor racemosus, Mucor spinosus, and concrete and other floor-related materials. These results can be used to develop new and resistant building materials and relevant allergen extracts and to help focus research on relevant mycotoxins, microbial volatile organic compounds (MVOCs), and microparticles released into the indoor environment.	[Andersen, Birgitte; Frisvad, Jens C.; Sondergaard, Ib] Tech Univ Denmark, CMB, DTU Syst Biol, DK-2800 Lyngby, Denmark; [Rasmussen, Ib S.; Larsen, Lisbeth S.] Danish Technol Inst, DK-2630 Taastrup, Denmark	Andersen, B (reprint author), Tech Univ Denmark, CMB, DTU Syst Biol, Bldg 221, DK-2800 Lyngby, Denmark.	ba@bio.dtu.dk	Andersen, Birgitte/F-3922-2012	Andersen, Birgitte/0000-0002-4544-9886	Villum Fonden	We thank Villum Fonden for financial support.	Andersen B, 2003, MYCOLOGIA, V95, P1227, DOI 10.2307/3761923; Andersen B, 2000, INT BIODETER BIODEGR, V46, P111, DOI 10.1016/S0964-8305(00)00092-5; Andersen B, 2008, INT J FOOD MICROBIOL, V126, P172, DOI 10.1016/j.ijfoodmicro.2008.05.036; Bellanger AP, 2009, LETT APPL MICROBIOL, V49, P260, DOI 10.1111/j.1472-765X.2009.02653.x; Chao HJ, 2002, ENVIRON HEALTH PERSP, V110, P777; de Hoog G. 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Environ. Microbiol.	JUN	2011	77	12					4180	4188		10.1128/AEM.02513-10		9	Biotechnology & Applied Microbiology; Microbiology	Biotechnology & Applied Microbiology; Microbiology	773WI	WOS:000291341800032	21531835	
J	Eden, T				Eden, Tim			Aetiology of childhood leukaemia	CANCER TREATMENT REVIEWS			English	Review						Aetiology; Childhood leukaemia	ACUTE LYMPHOBLASTIC-LEUKEMIA; CHILDRENS-CANCER-GROUP; NON-HODGKINS-LYMPHOMA; DAY-CARE ATTENDANCE; PARENTAL ALCOHOL-CONSUMPTION; ACUTE LYMPHOCYTIC-LEUKEMIA; ACUTE MYELOID-LEUKEMIA; VOLTAGE POWER-LINES; VITAMIN-K; IONIZING-RADIATION	The acute leukaemias account for about 30% of all malignancy seen in childhood across the Western world. A peak incidence of precursor B cell ALL has emerged as socio-economic conditions have improved in countries worldwide. From twin studies and the use of neonatal blood spots it has been possible to back track the first initiating genetic events within critical haemopoietic cells to foetal development in utero for most precursor B cell ALL and some cases of AML These events may occur as part of normal foetal development. Whether other factors (environmental or constitutional) are involved to increase the chance of these first genetic changes happening is unclear. For some leukaemias (e.g. infant MLL positive ALL) the first event appears adequate to create a malignant clone but for the majority of ALL and AML further 'genetic' changes are required, probably postnatal. Many environmental factors have been proposed as causative for leukaemia but only ionising irradiation and certain chemicals, e.g. benzene and cytotoxics (alkylators and topoisomerase II inhibitors) have been confirmed and then principally for acute myeloid leukaemia. It appears increasingly likely that delayed. dysregulated responses to 'common' infectious agents play a major part in the conversion of pre-leukaemic clones into overt precursor B cell ALL the most common form of childhood leukaemia. Constitutional polymorphic alleleic variants in immune response genes (especially the HLA Class II proteins) and cytokines may play a role in determining the type of immune response. High penetrance germ-line mutations are involved in only about 5% of childhood leukaemias (more in AML than ALL). There is little evidence to support any role of viral transformation in causation, unlike in animals. Other environmental factors for which some evidence exists include non-ionising electromagnetic radiation and electric fields, although their mode of action in leukaemogenesis remains unclear. There is no single cause for childhood leukaemia and for most individuals a combination of factors appears to be necessary; all involving gene-environment interactions. To date few clear preventative measures have emerged, except the complete avoidance of first trimester X-rays in pregnancy; a healthy diet with adequate oral folic acid intake both preconception and early in pregnancy; and the early exposure of children to other children outside the home to facilitate stimulation and maturation of the natural immune system. Here then are clear echoes of the "hygiene hypothesis" regarding the initiation of allergies, autoimmune disease and type I diabetes mellitus in children and young people. (C) 2010 Published by Elsevier Ltd.	Univ Manchester, Christie Hosp NHS Fdn Trust, Acad Unit Paediat & Adolescent Oncol, Teenage Canc Trust Young Oncol Unit, Manchester M20 4BX, Lancs, England	Eden, T (reprint author), Univ Manchester, Christie Hosp NHS Fdn Trust, Acad Unit Paediat & Adolescent Oncol, Teenage Canc Trust Young Oncol Unit, Wilmslow Rd, Manchester M20 4BX, Lancs, England.	Tim.eden@manchester.ac.uk			Teenage Cancer Trust	T.E. is funded by the Teenage Cancer Trust. The author would wish to acknowledge the long term collaboration and friendship of the team with who he has been involved over the last 30 years in epidemiological research especially Jill Birch, Mel Greaves, Richard McNally and Malcolm Taylor.	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Rev.	JUN	2010	36	4			SI		286	297		10.1016/j.ctrv.2010.02.004		12	Oncology	Oncology	614XZ	WOS:000279094400002	20223594	
J	Eifan, AO; Akkoc, T; Yildiz, A; Keles, S; Ozdemir, C; Bahceciler, NN; Barlan, IB				Eifan, A. O.; Akkoc, T.; Yildiz, A.; Keles, S.; Ozdemir, C.; Bahceciler, N. N.; Barlan, I. B.			Clinical efficacy and immunological mechanisms of sublingual and subcutaneous immunotherapy in asthmatic/rhinitis children sensitized to house dust mite: an open randomized controlled trial	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						asthma; cytokines; nasal provocation; rhinitis; sublingual-subcutaneous immunotherapy	GRASS-POLLEN IMMUNOTHERAPY; ALLERGEN-SPECIFIC IMMUNOTHERAPY; T-REGULATORY CELLS; DOUBLE-BLIND; PEDIATRIC-PATIENTS; DOUBLE-DUMMY; ASTHMA; RHINITIS; CHILDHOOD; METAANALYSIS	Background In children, the clinical efficacy and immunological mechanisms of sublingual immunotherapy (SLIT) compared with subcutaneous immunotherapy (SCIT) is still to be elucidated. Objectives To compare SLIT, SCIT and pharmacotherapy in relation to clinical efficacy and immunological mechanisms that govern its effect in asthmatic/rhinitis children who were sensitized to house dust mite (HDM). Methods In this single centre, prospective, randomized, controlled, open labelled, three parallel group trial, 48 patients mono-sensitized to HDM were randomized to receive either SLIT (n = 16), SCIT (n = 16) or pharmacotherapy alone (n = 16). Symptom, medication and visual analogue score (VAS) were collected and bronchial-nasal hyper-reactivity, skin prick tests, total-specific IgE were performed at baseline and 12 months after treatment. In addition, peripheral blood mononuclear cells were cultured with recombinant Der p 1 and Bet v 1 extracts and allergen-specific IL-4, IL-5, IL-13, IFN-gamma, IL-10, and TGF-beta secretions were measured. Results SLIT and SCIT demonstrated a significant reduction of total rhinitis and asthma symptom score, total medication score, VAS and skin reactivity to HDM (P<0.05) when compared with pharmacotherapy. A significant reduction of serum-specific HDM-IgE in SCIT and SLIT were observed. Moreover, titrated nasal provocative dose significantly increased in both immunotherapy groups when compared with the pharmacotherapy group. No adverse effects were reported in SLIT, while two patients demonstrated serious adverse events in SCIT. After 1 year of treatment, Der p 1-driven IL-10 significantly increased in SLIT compared with pharmacotherapy, whereas Bet v 1-driven TGF-beta (negative control) increased significantly in SLIT only. No changes were observed for Th1-Th2 cytokines. Conclusion Both SLIT and SCIT demonstrated clinical improvement compared with pharmacotherapy in asthma/rhinitis children sensitized to HDM.	[Eifan, A. O.; Akkoc, T.; Yildiz, A.; Keles, S.; Ozdemir, C.; Bahceciler, N. N.; Barlan, I. B.] Marmara Univ, Fac Med, Div Pediat Allergy & Immunol, Istanbul, Turkey; [Eifan, A. O.] Univ London Imperial Coll Sci Technol & Med, Fac Med, NHLI, Allergy & Clin Immunol Sect, London SW7 2AZ, England	Eifan, AO (reprint author), Marmara Univ, Fac Med, Div Pediat Allergy & Immunol, Istanbul, Turkey.	a.eifan@imperial.ac.uk		Eifan, Aarif/0000-0003-4098-4211	The Marmara University Scientific Research Committee [TIP/SAG-TUS-140607-0114]	We express our appreciation to Aysegul Izgi, M.Sc. and Ayzer Tevetoglu, M.Sc., for their contributions to the study. This work was supported by The Marmara University Scientific Research Committee (BAPKO no. TIP/SAG-TUS-140607-0114, 2007).	Abramson M. 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Exp. Allergy	JUN	2010	40	6					922	932		10.1111/j.1365-2222.2009.03448.x		11	Allergy; Immunology	Allergy; Immunology	592TE	WOS:000277402400013	20100188	
J	Juhn, YJ; Kita, H; Yawn, BP; Boyce, TG; Yoo, KH; McGree, ME; Weaver, AL; Wollan, P; Jacobson, RM				Juhn, Young J.; Kita, Hirohito; Yawn, Barbara P.; Boyce, Thomas G.; Yoo, Kwang H.; McGree, Michaela E.; Weaver, Amy L.; Wollan, Peter; Jacobson, Robert M.			Increased risk of serious pneumococcal disease in patients with asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; invasive pneumococcal disease; epidemiology; risk; microbial infection; pneumococcal pneumonia; adults; Rochester Epidemiology Project	IMMUNE-RESPONSE; VACCINE; EPIDEMIOLOGY; COMMUNITY; MICE; INFECTIONS; PNEUMONIAE; CHILDHOOD; CLEARANCE; SYMPTOMS	Background: Individuals with asthma have been reported to be at increased risk of invasive pneumococcal disease (IPD). These findings need to be confirmed in a different population-based study setting. Objective: We assessed whether serious pneumococcal disease (SPD), defined as an IPD, pneumococcal pneumonia, or both, was associated with asthma status. Methods: This is a retrospective case-control study using criteria-based methods for ascertaining SPD, as well as asthma. Subjects were residents of Rochester, Minnesota, who had SPD between 1964 and 1983 (the primarily pre-pneumococcal vaccine era) and their age-and sex-matched control subjects using 1:2 matching. Potential cases and control subjects were identified by using the Rochester Epidemiology project database and confirmed by medical record reviews. All cases and control subjects were merged with the database comprising the entire pool of Rochester residents with and without asthma between 1964 and 1983. Results: A total of 3941 records of potential patients with SPD were reviewed, and we identified 174 cases of SPD (51% male subjects and 94% white subjects). SPD was associated with a history of asthma among all ages (odds ratio, 2.4; 95% CI, 0.96.6; P = .09) and among adults (odds ratio, 6.7; 95% CI, 1.627.3; P = .01), controlling for high-risk conditions for IPD and smoking exposure. The population-attributable risk percentage was 17% in the adult population. Conclusion: Adults with asthma might be at increased risk of SPD.	[Juhn, Young J.] Mayo Clin, Dept Pediat & Adolescent Med, Div Community Pediat & Adolescent Med, Rochester, MN 55905 USA; [Yawn, Barbara P.; Wollan, Peter] Olmsted Med Ctr, Dept Res, Rochester, MN USA; [Yoo, Kwang H.] Konkuk Univ, Sch Med, Dept Internal Med, Seoul, South Korea; [McGree, Michaela E.; Weaver, Amy L.] Mayo Clin, Dept Hlth Sci Res, Rochester, MN 55905 USA	Juhn, YJ (reprint author), Mayo Clin, Dept Pediat & Adolescent Med, Div Community Pediat & Adolescent Med, 200 1st St SW, Rochester, MN 55905 USA.	juhn.young@mayo.edu		Jacobson, Robert/0000-0002-6355-8752	National Institutes of Health [R01 AI 56133]	Supported by a National Institutes of Health grant (R01 AI 56133) from the National Institute of Allergy and Infectious Diseases.	*AM AC PED, 2006, RED BOOK 2006; Arkwright PD, 2000, CLIN EXP IMMUNOL, V122, P16, DOI 10.1046/j.1365-2249.2000.01338.x; Asher MI, 2006, LANCET, V368, P733, DOI 10.1016/S0140-6736(06)69283-0; BEARD CM, 1992, J CLIN EPIDEMIOL, V45, P1013; BRODER I, 1974, J ALLERGY CLIN IMMUN, V54, P100, DOI 10.1016/0091-6749(74)90038-4; BUSSE WW, 1991, REV INFECT DIS, V13, pS477; *CDC, 1997, ACT BACT COR SURV RE; Chaplin DD, 2007, J ALLERGY CLIN IMMUN, V119, pS132, DOI 10.1016/j.jaci.2006.11.647; Chinn S, 2004, THORAX, V59, P646, DOI 10.1136/thx.2004.021642; Contoli M, 2006, NAT MED, V12, P1023, DOI 10.1038/nm1462; Fahy J V, 2000, Curr Opin Pulm Med, V6, P15, DOI 10.1097/00063198-200001000-00004; Fischer JE, 1997, J VIROL, V71, P8672; GREENLAND S, 1989, AM J PUBLIC HEALTH, V79, P340, DOI 10.2105/AJPH.79.3.340; GROVE DI, 1975, J ALLERGY CLIN IMMUN, V55, P152, DOI 10.1016/0091-6749(75)90011-1; Juhn YJ, 2006, ANN ALLERG ASTHMA IM, V97, P469; Katusic SK, 1998, MAYO CLIN PROC, V73, P1053; Kelsey JL, 1996, METHODS OBSERVATIONA; KincyCain T, 1996, INFECT IMMUN, V64, P1437; KURLAND LT, 1981, SCI AM, V245, P54; LAHOOD N, 1993, ANN ALLERGY, V70, P289; LEE HJ, 1995, VACCINE, V13, P1533; Lethbridge-Cejku M, 2005, VITAL HLTH STAT, V10, P1; Nuorti JP, 2000, NEW ENGL J MED, V342, P681, DOI 10.1056/NEJM200003093421002; Robinson KA, 2001, JAMA-J AM MED ASSOC, V285, P1729, DOI 10.1001/jama.285.13.1729; Talbot TR, 2005, NEW ENGL J MED, V352, P2082, DOI 10.1056/NEJMoa044113; TSIGRELIS C, 1999, 45 ANN INF DIS SOC A; *US BUR CENS, 1980, PHC802305 US BUR CEN; Wark PAB, 2005, J EXP MED, V201, P937, DOI 10.1084/jem.20041901; *WHO, 2005, N307 WHO; YUNGINGER JW, 1992, AM REV RESPIR DIS, V146, P888; [Anonymous], 1998, MMWR MORB MORTAL WKL, V47, P1022	31	87	88	0	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.	OCT	2008	122	4					719	723		10.1016/j.jaci.2008.07.029		5	Allergy; Immunology	Allergy; Immunology	359LU	WOS:000259989000014	18790525	
J	Bousquet, J; Fokkens, W; Burney, P; Durham, SR; Bachert, C; Akdis, CA; Canonica, GW; Dahlen, SE; Zuberbier, T; Bieber, T; Bonini, S; Bousquet, PJ; Brozek, JL; Cardell, LO; Crameri, R; Custovic, A; Demoly, P; van Wijk, RG; Gjomarkaj, M; Holland, C; Howarth, P; Humbert, M; Johnston, SL; Kauffmann, F; Kowalski, ML; Lambrecht, B; Lehmann, S; Leynaert, B; Lodrup-Carlsen, K; Mullol, J; Niggemann, B; Nizankowska-Mogilnicka, E; Papadopoulos, N; Passalacqua, G; Schunemann, HJ; Simon, HU; Todo-Bom, A; Toskala, E; Valenta, R; Wickman, M; Zock, JP				Bousquet, J.; Fokkens, W.; Burney, P.; Durham, S. R.; Bachert, C.; Akdis, C. A.; Canonica, G. W.; Dahlen, S. -E.; Zuberbier, T.; Bieber, T.; Bonini, S.; Bousquet, P. J.; Brozek, J. L.; Cardell, L. -O.; Crameri, R.; Custovic, A.; Demoly, P.; van Wijk, R. G.; Gjomarkaj, M.; Holland, C.; Howarth, P.; Humbert, M.; Johnston, S. L.; Kauffmann, F.; Kowalski, M. L.; Lambrecht, B.; Lehmann, S.; Leynaert, B.; Lodrup-Carlsen, K.; Mullol, J.; Niggemann, B.; Nizankowska-Mogilnicka, E.; Papadopoulos, N.; Passalacqua, G.; Schuenemann, H. J.; Simon, H. -U.; Todo-Bom, A.; Toskala, E.; Valenta, R.; Wickman, M.; Zock, J. P.			Important research questions in allergy and related diseases: nonallergic rhinitis: a GA(2)LEN paper	ALLERGY			English	Review						asthma; epidemiology; GA(2)LEN; inflammation; nonallergic; rhinitis	NONINFECTIOUS PERENNIAL RHINITIS; RESPIRATORY-HEALTH-SURVEY; QUALITY-OF-LIFE; INDEPENDENT RISK-FACTOR; EUROPEAN BIRTH COHORT; LOCAL IGE PRODUCTION; SKIN-TEST REACTIVITY; NASAL-MUCOSA; AIR-POLLUTION; EOSINOPHIL APOPTOSIS	Nonallergic rhinitis (NAR) can be defined as a chronic nasal inflammation which is not caused by systemic IgE-dependent mechanisms. It is common and probably affects far more than 200 million people worldwide. Both children and adults are affected. However, its exact prevalence is unknown and its phenotypes need to be evaluated using appropriate methods to better understand its pathophysiology, diagnosis and management. It is important to differentiate between infectious rhinitis, allergic/NAR and chronic rhinosinusitis, as management differs for each of these cases. Characterization of the phenotype, mechanisms and management of NAR represents one of the major unmet needs in allergic and nonallergic diseases. Studies on children and adults are required in order to appreciate the prevalence, phenotype, severity and co-morbidities of NAR. These studies should compare allergic and NAR and consider different age group populations including elderly subjects. Mechanistic studies should be carried out to better understand the disease(s) and risk factors and to guide towards an improved diagnosis and therapy. These studies need to take the heterogeneity of NAR into account. It is likely that neuronal mechanisms, T cells, innate immunity and possibly auto-immune responses all play a role in NAR and may also contribute to the symptoms of allergic rhinitis.	[Bousquet, J.; Bousquet, P. J.; Demoly, P.] Univ Hosp, Montpellier, France; [Bousquet, J.; Bousquet, P. J.; Demoly, P.] CNRS, INSERM, Montpellier, France; [Fokkens, W.; Holland, C.] Univ Amsterdam, Dept Otorhinolaryngol, NL-1012 WX Amsterdam, Netherlands; [Burney, P.; Durham, S. R.] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London, England; [Bachert, C.; Johnston, S. L.] Ghent Univ Hosp, URL, B-9000 Ghent, Belgium; [Akdis, C. A.; Crameri, R.] Swiss Inst Allergy & Asthma Res SIAF, Davos, Switzerland; [Canonica, G. 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J	Kormann, MSD; Depner, M; Harti, D; Klopp, N; Illig, T; Adamski, J; Vogelberg, C; Weiland, SK; von Mutius, E; Kabesch, M				Kormann, Michael S. D.; Depner, Martin; Harti, Dominik; Klopp, Norman; Illig, Thomas; Adamski, Jerzy; Vogelberg, Christian; Weiland, Stephan K.; von Mutius, Erika; Kabesch, Michael			Toll-like receptor heterodimer variants protect from childhood asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; atopic asthma; toll-like receptor; heterodimer; polymorphism	HAY-FEVER; CHILDREN; CELLS; ATOPY; POLYMORPHISMS; POPULATION; PREVALENCE; MECHANISMS; EXPRESSION; HAPLOTYPES	Background: Early exposure to microbes reduces the risk for asthma. Toll-like receptors (TLRs) represent a major group of receptors for the specific recognition of pathogen-associated molecular patterns of microbes capable of activating innate and adaptive immunity. Objective: Because TLRs can influence key events in the induction and perpetuation of asthma and atopy, we sought to determine whether genetic alterations in TLR genes affect asthma risk. Methods: We systematically evaluated putatively functional genetic variants in all 10 human TLR genes for their association with different asthma phenotypes in a case-control study (n = 1872) by using matrix-assisted laser desorption/ionization time-of-flight genotyping. For polymorphisms showing association with atopic asthma, effects on gene and protein expression were studied by means of RT-PCR and flow cytometry ex vivo. T-cell cytokine production was evaluated by means of ELISA after stimulation of the respective TLRs with specific ligands. Results: Protective effects on atopic asthma were identified for single nucleotide polymorphisms in TLR1 (odds ratio [OR], 0.54; 95% CI, 0.37-0.81; P =.002), TLR6 (OR, 0.54; 95% CI, 0.37-0.79; P =.003), and TLR10 (OR, 0.58; 95% CI, 0.39-0.86; P =.006), all capable of forming heterodimers with TLR2. Effects remained significant after correction for multiple comparisons. PBMCs of minor allele carriers showed increased levels of the respective TLR mRNA and proteins, augmented inflammatory responses, increased T(H)1 cytokine expression, and reduced T(H)2-associated IL-4 production after specific stimulation. Conclusion: These results suggest that functional relevant TLR1 and TLR6 variants are directly involved in asthma development.	[Kormann, Michael S. D.; Depner, Martin; Harti, Dominik; Klopp, Norman; Illig, Thomas; von Mutius, Erika; Kabesch, Michael] Univ Munich, Univ Childrens Hosp, D-80337 Munich, Germany; [Weiland, Stephan K.] Univ Ulm, Inst Epidemiol, D-89069 Ulm, Germany; [Vogelberg, Christian] Univ Childrens Hosp, Dresden, Germany; [Adamski, Jerzy] GSF Natl Res Ctr Environm & Hlth, Inst Expt Genet, Neuherberg, Germany; [Klopp, Norman; Illig, Thomas] GSF Natl Res Ctr Environm & Hlth, Inst Epidemiol, Neuherberg, Germany	Kabesch, M (reprint author), Univ Munich, Univ Childrens Hosp, Lindwurmstr 4, D-80337 Munich, Germany.	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Allergy Clin. Immunol.	JUL	2008	122	1					86	92		10.1016/j.jaci.2008.04.039		7	Allergy; Immunology	Allergy; Immunology	325RD	WOS:000257605100014	18547625	
J	Fiocchi, A; Assa'ad, A; Bahna, S				Fiocchi, Alessandro; Assa'ad, Amal; Bahna, Sami		Amer Coll Allergy Asthma Immunolog	Food allergy and the introduction of solid foods to infants: a consensus document	ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY			English	Review							BOVINE SERUM-ALBUMIN; BREAST-FED INFANTS; COWS MILK ALLERGY; HIGH-RISK INFANTS; PARTIAL WHEY HYDROLYSATE; HOUSE-DUST-MITE; PEANUT ALLERGY; NATURAL-HISTORY; ATOPIC DISEASE; CROSS-REACTIVITY	Objective: To make recommendations based on a critical review of the evidence for the timing of the introduction of solid foods and its possible role in the development of food allergy. Data Sources: MEDLINE searches using the following search algorithm: [weaning AND infant AND allergy]/[food allergy AND sensitization]/[dietary prevention AND food allergy OR allergens]/[Jan 1980-Feb 2006]. Study Selection: Using the authors' clinical experience and research expertise, 52 studies were retrieved that satisfied the following conditions: English language, journal impact factor above I or scientific society, expert, or institutional publication, and appraisable using the World Health Organization categories of evidence. Results: Available information suggests that early introduction can increase the risk of food allergy, that avoidance of solids can prevent the development of specific food allergies, that some foods are more allergenic than others, and that some food allergies are more persistent than others. Conclusions: Pediatricians and allergists should cautiously individualize the introduction of solids into the infants' diet. With assessed risk of allergy, the optimal age for the introduction of selected supplemental foods should be 6 months, dairy products 12 months, hen's egg 24 months, and peanut, tree nuts, fish, and seafood at least 36 months. For all infants, complementary feeding can be introduced from the sixth month, and egg, peanut, tree nuts, fish, and seafood introduction require caution. Foods should be introduced one at a time in small amounts. Mixed foods containing various food allergens should not be given unless tolerance to every ingredient has been assessed.	Univ Milan, Melloni Hosp, Sch Med, Amer Coll Allergy Asthma & Immunol Mellini Paedia, I-20129 Milan, Italy	Fiocchi, A (reprint author), Univ Milan, Melloni Hosp, Sch Med, Amer Coll Allergy Asthma & Immunol Mellini Paedia, Via Melloni 52, I-20129 Milan, Italy.	allerg@tin.it		Fiocchi, Alessandro/0000-0002-2549-0523			Anandan C, 2005, BRIT MED J, V331, P1155, DOI 10.1136/bmj.331.7526.1155; Garcia Ara M. 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Allergy Asthma Immunol.	JUL	2006	97	1					10	20				11	Allergy; Immunology	Allergy; Immunology	065TA	WOS:000239181000006	16892776	
J	Taramarcaz, P; Lambelet, C; Clot, B; Keimer, C; Hauser, C				Taramarcaz, P; Lambelet, C; Clot, B; Keimer, C; Hauser, C			Ragweed (Ambrosia) progression and its health risks: will Switzerland resist this invasion?	SWISS MEDICAL WEEKLY			English	Review						Ambrosia; allergy; health risk; allergic rhinits; asthma; Switzerland	ALLERGIC RHINITIS; POLLEN ALLERGY; HAY-FEVER; LATE SUMMER; IMMUNOTHERAPY; SENSITIZATION; EFFICACY; ASTHMA; OMALIZUMAB; EXPOSURE	The purpose of this article is to alert physicians for the environmental and health threats of Ambrosia artemisiifolia (common ragweed) in Switzerland. Switzerland borders several heavily ragweed colonised areas. Up to 12% of the population suffers from allergies (hay fever, asthma) to ragweed pollen in these areas. Switzerland is beginning to be invaded by this plant. Currently, the ragweed pollen counts are still low but can reach local peaks that induce symptoms in allergic individuals. Ragweed allergy, however, is still rare in Switzerland. Because the amount of ragweed pollen was increasing in the last few years, identification and surveillance of ragweed plant foci was started. Colonisation is currently systematically monitored in Geneva and southern Tessin. Major accumulation of ragweed foci have been detected in the canton of Geneva, the western shore of the lake of Geneva belonging to the canton of Vaud, and in the southern part of the canton of Tessin, aside from minor foci registered all over Switzerland. The routes of ragweed invasion are presented and discussed. Current measures of ragweed containment and needs for the future are presented. The urge for these measures at an early stage of ragweed spread is underlined by the impracticability of eradication in highly colonised areas. The costs of preventing ragweed spread in Switzerland are likely to be several magnitudes lower than the treatment of a significant percentage of the Swiss population for ragweed pollen allergy. Because areas can change from low to heavy ragweed colonisation within a few years, the current window of opportunity to prevent further colonisation by ragweed should not be missed.	Univ Hosp Geneva, Serv Allergol & Immunol, CH-1211 Geneva, Switzerland; Univ Geneva, Sch Med, CH-1211 Geneva, Switzerland; Conservatoire & Jardin Bot Ville Geneve, Geneva, Switzerland; MeteoSuisse, Biometeorol & Environm, Stn Aerol, Payerne, Switzerland; Serv Agr, Stn Phytosanit, Geneva, Switzerland; Geneva Ambrosia Grp, Geneva, Switzerland	Hauser, C (reprint author), Univ Hosp Geneva, Serv Allergol & Immunol, 24 Rue Micheli du Crest, CH-1211 Geneva, Switzerland.	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J	de Jong, PA; Muller, NL; Pare, PD; Coxson, HO				de Jong, PA; Muller, NL; Pare, PD; Coxson, HO			Computed tomographic imaging of the airways: relationship to structure and function	EUROPEAN RESPIRATORY JOURNAL			English	Review						airways; asthma; chronic obstructive pulmonary disease; computed tomography; cystic fibrosis; lung structure and function	THIN-SECTION CT; HIGH-RESOLUTION CT; OBSTRUCTIVE PULMONARY-DISEASE; CYSTIC-FIBROSIS LUNG; BRONCHIAL-WALL THICKNESS; PLACEBO-CONTROLLED TRIAL; ATOMIC-BOMB SURVIVORS; AIR-FLOW OBSTRUCTION; YOUNG-CHILDREN; ASYMPTOMATIC SUBJECTS	Alterations in the structure of the airways, collectively termed airway remodelling, contribute to airflow obstruction in a variety of chronic lung diseases. While histology has provided valuable insights into the structure of airway wall remodelling, this technique is invasive and does not allow the longitudinal analysis of airway wall dimensions. Technical advances in computed tomography allow the assessment of airway wall dimensions, and are ideally suited for the noninvasive investigation of the pathogenesis of airway wall remodelling and the evaluation of new therapeutic interventions. The aim of this article is to review the use of computed tomography in the investigation of airway structure and function in health and disease.	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Resp. J.	JUL	2005	26	1					140	152		10.1183/09031936.05.00007105		13	Respiratory System	Respiratory System	945JG	WOS:000230498200022	15994401	
J	Jarvis, J; Seed, MJ; Elton, RA; Sawyer, L; Agius, RM				Jarvis, J; Seed, MJ; Elton, RA; Sawyer, L; Agius, RM			Relationship between chemical structure and the occupational asthma hazard of low molecular weight organic compounds	OCCUPATIONAL AND ENVIRONMENTAL MEDICINE			English	Article							RESPIRATORY SENSITIZATION; SUBSTANCES; IDENTIFICATION; ALLERGENS; TOXICITY; EXPOSURE; DISEASE	Aims: To investigate quantitatively, relationships between chemical structure and reported occupational asthma hazard for low molecular weight (LMW) organic compounds; to develop and validate a model linking asthma hazard with chemical substructure; and to generate mechanistic hypotheses that might explain the relationships. Methods: A learning dataset used 78 LMW chemical asthmagens reported in the literature before 1995, and 301 control compounds with recognised occupational exposures and hazards other than respiratory sensitisation. The chemical structures of the asthmagens and control compounds were characterised by the presence of chemical substructure fragments. Odds ratios were calculated for these fragments to determine which were associated with a likelihood of being reported as an occupational asthmagen. Logistic regression modelling was used to identify the independent contribution of these substructures. A post-1995 set of 21 asthmagens and 77 controls were selected to externally validate the model. Results: Nitrogen or oxygen containing functional groups such as isocyanate, amine, acid anhydride, and carbonyl were associated with an occupational asthma hazard, particularly when the functional group was present twice or more in the same molecule. A logistic regression model using only statistically significant independent variables for occupational asthma hazard correctly assigned 90% of the model development set. The external validation showed a sensitivity of 86% and specificity of 99%. Conclusions: Although a wide variety of chemical structures are associated with occupational asthma, bifunctional reactivity is strongly associated with occupational asthma hazard across a range of chemical substructures. This suggests that chemical cross-linking is an important molecular mechanism leading to the development of occupational asthma. The logistic regression model is freely available on the internet and may offer a useful but inexpensive adjunct to the prediction of occupational asthma hazard.	Univ Manchester, Ctr Environm & Occupat Hlth, Manchester M13 9PL, Lancs, England; Univ Edinburgh, Univ Comp Serv, Edinburgh EH8 9YL, Midlothian, Scotland; Univ Edinburgh, Sch Biol Sci, Edinburgh EH8 9YL, Midlothian, Scotland	Agius, RM (reprint author), Univ Manchester, Ctr Environm & Occupat Hlth, Oxford Rd, Manchester M13 9PL, Lancs, England.	agius@manchester.ac.uk	Seed, Martin/A-2132-2013				AGIUS RM, 1994, OCCUP MED-OXFORD, V44, P34, DOI 10.1093/occmed/44.1.34; AGIUS RM, 1991, ANN OCCUP HYG, V35, P129, DOI 10.1093/annhyg/35.2.129; Agius RM, 2000, OCCUP MED, V15, P369; *AM C GOV IND HYG, 2002, THRESH LIM VAL BIOL; Armitage P, 1994, STAT METHODS MED RES, P443; Avashia B, 1996, J OCCUP ENVIRON MED, V38, P625, DOI 10.1097/00043764-199606000-00015; Barratt MD, 2001, CURR OPIN CHEM BIOL, V5, P383, DOI 10.1016/S1367-5931(00)00218-0; Bernstein DI, 2003, IMMUNOL ALLERGY CLIN, V23, P221, DOI 10.1016/S0889-8561(02)00084-X; DALBY A, 1992, J CHEM INF COMP SCI, V32, P244, DOI 10.1021/ci00007a012; Dearman RJ, 2003, J APPL TOXICOL, V23, P199, DOI 10.1002/jat.907; *ECETOC, 2003, 89 ECETOC QSARS; Fairhurst S, 2003, FOOD CHEM TOXICOL, V41, P1453, DOI 10.1016/S0278-6915(03)00193-5; Graham C, 1997, REGUL TOXICOL PHARM, V26, P296, DOI 10.1006/rtph.1997.1170; *HLTH SAF EX, 1994, EH4094 HLTH SAF EX; *HLTH SAF EX, 2002, EH402002 HLTH SAF EX; Karol MH, 2001, ANN ALLERG ASTHMA IM, V87, P28; Karol MH, 1996, TOXICOL LETT, V86, P187, DOI 10.1016/0378-4274(96)03689-2; Kimber I, 2001, TOXICOL IN VITRO, V15, P307, DOI 10.1016/S0887-2333(01)00027-3; MENARD S, 1995, APPL LOGISTIC REGRES, P54; Meyer JD, 1999, OCCUP MED-OXFORD, V49, P485, DOI 10.1093/occmed/49.8.485; Nasser SMS, 2001, CLIN EXP ALLERGY, V31, P1014, DOI 10.1046/j.1365-2222.2001.01090.x; Pearl Greg M., 2001, Current Topics in Medicinal Chemistry, V1, P247, DOI 10.2174/1568026013395074; Piipari R, 1998, CLIN EXP ALLERGY, V28, P358; SARLO K, 1997, TOXICOLOGY CHEM RESP, P107; SAVONIUS B, 1993, CLIN EXP ALLERGY, V23, P416, DOI 10.1111/j.1365-2222.1993.tb00348.x; TERPSTRA GK, 1981, EUR J PHARMACOL, V73, P107, DOI 10.1016/0014-2999(81)90154-0; van Kampen V, 2000, AM J IND MED, V38, P164, DOI 10.1002/1097-0274(200008)38:2<164::AID-AJIM7>3.0.CO;2-2; Vandenplas O, 2003, EUR RESPIR J, V21, P706, DOI 10.1183/09031936.03.00113303; VENABLES KM, 1989, BRIT J IND MED, V46, P222; Wild LG, 2003, IMMUNOL ALLERGY CLIN, V23, P235, DOI 10.1016/S088908561(02)00083-8; Zeiss C Raymond, 2002, Curr Opin Allergy Clin Immunol, V2, P89, DOI 10.1097/00130832-200204000-00001	31	87	88	2	10	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	1351-0711			OCCUP ENVIRON MED	Occup. Environ. Med.	APR	2005	62	4					243	250		10.1136/oem.2004.016402		8	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	907TC	WOS:000227739900008	15778257	
J	Graham-Bermann, SA; Seng, J				Graham-Bermann, SA; Seng, J			Violence exposure and traumatic stress symptoms as additional predictors of health problems in high-risk children	JOURNAL OF PEDIATRICS			English	Article							POSTTRAUMATIC-STRESS; COMMUNITY VIOLENCE; DOMESTIC VIOLENCE; ABUSE; WOMEN; DISORDER; PTSD; AGGRESSION; DEPRESSION; WITNESSES	Objective To test the hypotheses that both violence and traumatic stress symptoms are associated with negative health status among poor preschool children. Study design This cross-sectional analysis of a Head Start preschool age cohort (n = 160) studied health outcomes parallel to those assessed in the 2001 National Health Interview Survey of child health (asthma, allergy, attention deficit hyperactivity disorder, global appraisal) its well as two stress-related somatic complaints, gastrointestinal problems and headache. Risk factors include sociodemographics, mothers' health factors, extent of exposure to violence and maltreatment, and mother- and teacher-reported traumatic stress symptoms. Results Compared with poor children in the National Health Interview Survey and their Head Start peers, children exposed to violence and those with high levels of traumatic stress had significantly, worse outcomes, in a dose-response relation. Being abused, exposed to domestic violence, and having a mother using substances were associated with a higher number of health problems. The hierarchical model established the mother's own poor physical health and the child's level of traumatic stress as the strongest predictors of poor child health. Conclusions These two risk factors are amenable to intervention by health care providers who treat children.	Univ Michigan, Dept Psychol, Ann Arbor, MI 48109 USA; Univ Michigan, Sch Nursing, Ann Arbor, MI 48109 USA; Univ Michigan, Dept Obstet & Gynecol, Ann Arbor, MI 48109 USA	Graham-Bermann, SA (reprint author), Univ Michigan, Dept Psychol, 525 E Univ Ave, Ann Arbor, MI 48109 USA.			Graham-Bermann, Sandra A/0000-0002-3811-7330; Seng, Julia/0000-0002-7066-6348	PHS HHS [90-YD-0066]		Achenbach T. M., 1991, MANUAL TEACHERS REPO; American Psychiatric Association, 1994, DIAGN STAT MAN MENT; Applegate B, 1997, J AM ACAD CHILD PSY, V36, P1211, DOI 10.1097/00004583-199709000-00013; Bassuk E L, 2001, J Am Med Womens Assoc (1972), V56, P79; BECK AT, 1961, ARCH GEN PSYCHIAT, V4, P561; BECK AT, 1988, CLIN PSYCHOL REV, V8, P77, DOI 10.1016/0272-7358(88)90050-5; BLOOM B, 2004, SUMMARY HLTH STAT US; Felitti VJ, 1998, AM J PREV MED, V14, P245, DOI 10.1016/S0749-3797(98)00017-8; Friedman Matthew J., 1995, P507; Graham-Bermann SA, 1998, J INTERPERS VIOLENCE, V13, P111, DOI 10.1177/088626098013001007; GrahamBermann SA, 1996, J CLIN CHILD PSYCHOL, V25, P280, DOI 10.1207/s15374424jccp2503_4; GRAHAMBERMANN SA, IN PRESS VIOLENCE WO; Graham-Bermann S. A., 1994, J FAMILY PSYCHOL, V8, P224, DOI 10.1037//0893-3200.8.2.224; GRAHAMBERMANN SA, 2001, PRESCHOOL POSTTRAUMA; Holden GW, 2003, CLIN CHILD FAM PSYCH, V6, P151, DOI 10.1023/A:1024906315255; JOURILES EN, 1995, J FAM PSYCHOL, V9, P69, DOI 10.1037//0893-3200.9.1.69; Kilpatrick KL, 1998, CHILD ABUSE NEGLECT, V22, P319, DOI 10.1016/S0145-2134(97)00178-6; Kimerling R, 2000, J TRAUMA STRESS, V13, P115, DOI 10.1023/A:1007729116133; Kimerling R, 2002, GENDER PTSD, P271; Klinnert MD, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.4.e69; Litrownik AJ, 2003, J FAM VIOLENCE, V18, P59, DOI 10.1023/A:1021405515323; MARTINEZ P, 1993, PSYCHIATRY, V56, P22; O'Brien M, 1994, Violence Vict, V9, P45; OSOFSKY JD, 1993, PSYCHIATRY, V56, P36; RICHTERS JE, 1993, PSYCHIATRY, V56, P7; Richters J. E., 1990, SURVEY CHILDRENS EXP; Rossman BBR, 1997, J AM ACAD CHILD PSY, V36, P1089; Roth S, 1997, J TRAUMA STRESS, V10, P539, DOI 10.1002/jts.2490100403; Sadler AG, 2000, OBSTET GYNECOL, V96, P473, DOI 10.1016/S0029-7844(00)00919-4; Seng JS, 2002, J MIDWIFERY WOM HEAL, V47, P337, DOI 10.1016/S1526-9523(02)00275-1; STRAUS MA, 1979, J MARRIAGE FAM, V41, P75, DOI 10.2307/351733; Straus M. M. A., 1980, CLOSED DOORS VIOLENC; Vogel LCM, 2001, J TRAUMA STRESS, V14, P569, DOI 10.1023/A:1011116824613; WOLFE VV, 1989, BEHAV THER, V20, P215, DOI 10.1016/S0005-7894(89)80070-X; Wright RJ, 2004, J ALLERGY CLIN IMMUN, V113, P1051, DOI 10.1016/j.jaci.2004.03.032	35	87	87	2	22	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0022-3476	1097-6833		J PEDIATR-US	J. Pediatr.	MAR	2005	146	3					349	354		10.1016/j.jpeds.2004.10.065		6	Pediatrics	Pediatrics	906SI	WOS:000227662600015	15756218	
J	Ishida, Y; Nakamura, F; Kanzato, H; Sawada, D; Hirata, H; Nishimura, A; Kajimoto, O; Fujiwara, S				Ishida, Y; Nakamura, F; Kanzato, H; Sawada, D; Hirata, H; Nishimura, A; Kajimoto, O; Fujiwara, S			Clinical effects of Lactobacillus acidophilus strain L-92 on perennial allergic rhinitis: A double-blind, placebo-controlled study	JOURNAL OF DAIRY SCIENCE			English	Article						Lactobacillus acidophilus; perennial allergic rhinitis; double-blind placebo-controlled study	LACTIC-ACID BACTERIA; REGULATORY-CELLS; CONTROLLED TRIAL; DENDRITIC CELLS; ATOPIC DISEASE; T-CELLS; CHILDREN; ASTHMA; MICE; PREVENTION	Studies in animals have suggested that lactic acid bacteria alleviate allergic diseases, however, little information is available on their clinical effect on allergy in humans. Thus, we examined the efficacy of orally administered Lactobacillus acidophilus strain L-92 (L-92) on perennial allergic rhinitis. In a randomized, double-blind, placebo-controlled clinical trial, 49 patients with perennial allergic rhinitis were randomized to receive either 100 mL of heat-treated fermented milk containing L-92 (n = 25) or acidified milk without lactic acid bacteria (placebo; n = 24) for 8 wk. The severity of symptoms was evaluated based on the changes in the scores of clinical symptoms. Oral administration of milk fermented with L-92 resulted in a statistically significant improvement of nasal symptom-medication scores. Ocular symptom-medication scores of patients in the L-92 intervention group tended to improve compared with those in the placebo group. In addition, clear decreases of the scores of swelling and color of the nasal mucosa were observed in the L-92 intervention group at 6 and 8 wk after the start of ingestion of fermented milk. There were no significant differences in serum antihouse dust mite immunoglobulin E levels nor in T helper type 1/T helper type 2 ratio between the 2 groups. These results suggest that oral administration of L-92 can alleviate the symptoms of perennial allergic rhinitis, however, statistically significant changes were not shown in blood parameters.	Calpis Co Ltd, Ctr Res & Dev, Kanagawa, Japan; Okayama Univ, Sch Med, Dept Internal Med 3, Okayama 700, Japan; Soiken Inc, Osaka, Japan	Fujiwara, S (reprint author), Calpis Co Ltd, Ctr Res & Dev, Kanagawa, Japan.	shigeru.fujiwara@calpis.co.jp					Bjorksten B, 1999, CLIN EXP ALLERGY, V29, P342; CHEN YH, 1994, SCIENCE, V265, P1237, DOI 10.1126/science.7520605; Cross ML, 2001, INT IMMUNOPHARMACOL, V1, P891, DOI 10.1016/S1567-5769(01)00025-X; de Lafaille MAC, 2002, CURR OPIN IMMUNOL, V14, P771; Groux H, 1997, NATURE, V389, P737; Helin T, 2002, ALLERGY, V57, P243, DOI 10.1034/j.1398-9995.2002.1s3299.x; Herrick CA, 2003, NAT REV IMMUNOL, V3, P405, DOI 10.1038/nri1084; HOLT PG, 1995, PEDIAT ALLERG IMM-UK, V6, P59, DOI 10.1111/j.1399-3038.1995.tb00261.x; Ishida Y, 2003, BIOSCI BIOTECH BIOCH, V67, P951, DOI 10.1271/bbb.67.951; 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, 2001, J ALLERGY CLIN IMMUN, V108, P781, DOI 10.1067/mai.2001.119557; Levings MK, 2002, INT ARCH ALLERGY IMM, V129, P263, DOI 10.1159/000067596; Matsuzaki T, 1998, J DAIRY SCI, V81, P48; McGuirk P, 2002, J EXP MED, V195, P221, DOI 10.1084/jem.20011288; Miettinen M, 1998, INFECT IMMUN, V66, P6058; Murosaki S, 1998, J ALLERGY CLIN IMMUN, V102, P57, DOI 10.1016/S0091-6749(98)70055-7; OKUDA M, 2002, CLIN GUIDELINES ALLE, P24; Pessi T, 2000, CLIN EXP ALLERGY, V30, P1804, DOI 10.1046/j.1365-2222.2000.00948.x; ROMAGNANI S, 1994, CURR OPIN IMMUNOL, V6, P838, DOI 10.1016/0952-7915(94)90002-7; Rosenfeldt V, 2003, J ALLERGY CLIN IMMUN, V111, P389, DOI 10.1067/mai.2003.389; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Weiner HL, 2001, NAT IMMUNOL, V2, P671, DOI 10.1038/90604; Wheeler JG, 1997, ANN ALLERG ASTHMA IM, V79, P229	24	87	91	0	2	AMER DAIRY SCIENCE ASSOC	SAVOY	1111 N DUNLAP AVE, SAVOY, IL 61874 USA	0022-0302			J DAIRY SCI	J. Dairy Sci.	FEB	2005	88	2					527	533				7	Agriculture, Dairy & Animal Science; Food Science & Technology	Agriculture; Food Science & Technology	892QQ	WOS:000226665500010	15653517	
J	Meystre, S				Meystre, S			The current state of telemonitoring: A comment on the literature	TELEMEDICINE JOURNAL AND E-HEALTH			English	Editorial Material							MONITORING-SYSTEM; TELEMEDICINE; INTERNET; CARE; MANAGEMENT; TELEMETRY; PATIENT; EVEREST; TOP	Telemonitoring, is defined as the use of information technology to monitor patients at a distance. This literature review suggests that the most promising applications for telemonitoring is for chronic illnesses such as cardiopulmonary disease, asthma, and heart failure in the home. Fetal heart rate monitoring and infant cardiopulmonary functions have also been monitored at a distance, as well as coagulation, or the level of activity of elderly people, assessed by the intelligent home monitoring devices. Hospitals, clinics, and prisons all have used telemonitoring, as have ambulances equipped with systems connected to the receiving hospital. Telemonitoring allows reduction of chronic disease complications thanks to a better followup; provides health care services without using hospital beds; and reduces patient travel, time off from work, and overall costs. Several systems have proven to be cost effective. Telemonitoring is also a way of responding to the new needs of home care in an ageing population. Real- time monitoring of patients in ambulances reduces the time to initiate treatment and allows the emergency crew to be better prepared. The obstacles to telemonitoring development include the initial costs of systems, physician licensing, and reimbursement. In the future, virtual reality, immersive environments, haptic feedback and nanotechnology promise new ways in improving the capabilities of telemonitoring.	Univ Utah, Sch Med, Dept Med Informat, Salt Lake City, UT 84132 USA	Meystre, S (reprint author), Univ Utah, Sch Med, Dept Med Informat, 30 North 1900 East,Room AB 193, Salt Lake City, UT 84132 USA.	s.meystre@utah.edu					Anagnostaki A, 2001, MEDINFO, V10, P77; Anantharaman V, 2001, INT J MED INFORM, V61, P147, DOI 10.1016/S1386-5056(01)00137-X; Angood PB, 2000, TELEMED J E-HEALTH, V6, P315, DOI 10.1089/153056200750040174; Artinian NT, 2001, HEART LUNG, V30, P191, DOI 10.1067/mhl.2001.112684; *ASS TEL SERV PROV, 1999, 1999 REP US TEL ACT; Barbaro V, 1997, J Telemed Telecare, V3, P96, DOI 10.1258/1357633971930931; Barro S, 1999, IEEE ENG MED BIOL, V18, P80, DOI 10.1109/51.775492; Belmont J M, 1995, Telemed J, V1, P133, DOI 10.1089/tmj.1.1995.1.133; Cai J, 2000, Proc AMIA Symp, P116; CALAGAN J, 2001, TELEMED J E HLTH, V7, P174; *CEN WORK GROUP 4, 2000, PRENV1064 CEN WORK G; *CMS, 2002, MED TEL; *CMS, 2003, MED INT MAN 3; Cordisco ME, 1999, AM J CARDIOL, V84, P860, DOI 10.1016/S0002-9149(99)00452-X; CORDISCO ME, 1999, AM J CARDIOL, V84, pA8; de Lusignan S, 2000, J Telemed Telecare, V6 Suppl 1, pS119; Einthoven W., 1906, ARCH INT PHYSIOL, V4, P132; Field MJ, 2002, JAMA-J AM MED ASSOC, V288, P423, DOI 10.1001/jama.288.4.423; Finkelstein J, 2000, CHEST, V117, P148, DOI 10.1378/chest.117.1.148; FITZGERALD J, 1996, BUSINESS DATA COMMUN, V19, P562; Frim DM, 2000, J NEUROSURG, V92, P927, DOI 10.3171/jns.2000.92.6.0927; Gandsas A, 2000, AVIAT SPACE ENVIR MD, V71, P68; Gomez EJ, 2002, COMPUT METH PROG BIO, V69, P163, DOI 10.1016/S0169-2607(02)00039-1; Gray JE, 2000, PEDIATRICS, V106, P1318, DOI 10.1542/peds.106.6.1318; Guler Nihal Fatma, 2002, J Med Syst, V26, P199, DOI 10.1023/A:1015010316958; Guler Nihal Fatma, 2002, J Med Syst, V26, P159, DOI 10.1023/A:1014862027454; Harnett BM, 2001, AVIAT SPACE ENVIR MD, V72, P1125; HINES J, 1999, BIOTELEMETRY USING I; *I MED US COMM EV, 1996, TEL GUID ASS TEL HLT, V14, P271; Johnson P, 1996, J Telemed Telecare, V2, P107, DOI 10.1258/1357633961929871; JOHNSON P, 1998, J TELEMED TELECARE, V18, P86; Jovanov E, 2001, Biomed Sci Instrum, V37, P373; Karlsten R, 2000, J TELEMED TELECARE, V6, P1, DOI 10.1258/1357633001933835; LEITNER P, 1999, TELEMEDICINE WILL GR; Maree DM, 2001, RESPIRATION, V68, P400, DOI 10.1159/000050534; Morlion B, 2002, AM J RESP CRIT CARE, V165, P694, DOI 10.1164/rccm.2107059; Naef R W 3rd, 1998, J Perinatol, V18, P226; *NAT RES COUNC, 2000, NETW HLTH PRESCR INT, V18, P358; Nicogossian AE, 2001, TELEMED J E-HEALTH, V7, P1, DOI 10.1089/153056201300093813; Oohashi T, 2002, CLIN NEUROPHYSIOL, V113, P435, DOI 10.1016/S1388-2457(02)00002-0; Orlov OI, 2001, TELEMED J E-HEALTH, V7, P33, DOI 10.1089/153056201300093877; Quemere M P, 2000, J Gynecol Obstet Biol Reprod (Paris), V29, P571; Satava R, 2000, TELEMED J E-HEALTH, V6, P303, DOI 10.1089/153056200750040165; Sixsmith AJ, 2000, J TELEMED TELECARE, V6, P63, DOI 10.1258/1357633001935059; Tsang MW, 2001, J TELEMED TELECARE, V7, P47, DOI 10.1258/1357633011936138; Vincent JA, 1997, PEDIATR CARDIOL, V18, P86, DOI 10.1007/s002469900121; 2002, WPSM WARFIGHTER PHYS; 2002, HLTH LEVEL 7; 2001, VITALINK 1200	49	87	89	3	13	MARY ANN LIEBERT INC	NEW ROCHELLE	140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA	1530-5627			TELEMED J E-HEALTH	Telemed. J. e-Health	FEB	2005	11	1					63	69		10.1089/tmj.2005.11.63		7	Health Care Sciences & Services	Health Care Sciences & Services	912RK	WOS:000228096900023	15785222	
J	Ostojic, V; Cvoriscec, B; Ostojic, SB; Reznikoff, D; Stipic-Markovic, A; Tudjman, Z				Ostojic, V; Cvoriscec, B; Ostojic, SB; Reznikoff, D; Stipic-Markovic, A; Tudjman, Z			Improving asthma control through telemedicine: A study of short-message service	TELEMEDICINE JOURNAL AND E-HEALTH			English	Article							PEAK EXPIRATORY FLOW; SELF-MANAGEMENT; OBSTRUCTION; MEDICATION; EDUCATION; SYMPTOMS; PROGRAM; HEALTH; COSTS; DIARY	Home peak expiratory flow ( PEF) measurement is recommended by asthma guidelines. In a 16-week randomized controlled study on there exists 6 subjects with asthma ( 24.6 +/- 6.5 years old, asthma duration. 6 months), we examined Global System for Mobile Communications ( GSM) mobile telephone short- message service ( SMS) as a novel means of telemedicine in PEF monitoring. All subjects received asthma education, self- management plan, and standard treatment. All measured PEF three times daily and kept a symptom diary. In the study group, therapy was adjusted weekly by an asthma specialist according to PEF values received daily from the patients. There was no significant difference between the groups in absolute PEF, but PEF variability was significantly smaller in the study group ( 16.12 +/- 6.93% vs. 27.24 +/- 10.01%, p = 0.049). forced expiratory flow in 1 second ( FEV(1); % predicted) in the study group was slightly but significantly increased ( 81.25 +/- 17.31 vs. 77.63 +/- 14.80, p = 0.014) and in the control group, unchanged ( 78.25 +/- 21.09 vs. 78.88 +/- 22.02, p = 0.497). Mean FEV(1) was similar in the two groups both before and after the study. Controls had significantly higher scores for cough ( 1.85 +/- 0.43 vs. 1.42 +/- 0.28, p < 0.05) and night symptoms ( 1.22 +/- 0.23 vs. 0.85 +/- 0.32, p < 0.05). There was no significant difference between the groups in daily consumption of inhaled medicine, forced vital capacity, or compliance. Per patient, per week, the additional cost of follow- up by SMS was A E1.67 ( equivalent to approximately $ 1.30 per 1 Euro), and SMS transmission required 11.5 minutes. Although a study group of 40 patients is needed for the follow- up study to achieve the power of 80% within the 95% confidence interval, we conclude that SMS is a convenient, reliable, affordable, and secure means of telemedicine that may improve asthma control when added to a written action plan and standard follow- up.	Univ Zagreb, Gen Hosp Sveti Duh, Dept Internal Dis, Div Clin Immunol & Pulmonol, Zagreb, Croatia; Winthrop Univ Hosp, Dept Internal Med, Mineola, NY 11501 USA	Ostojic, V (reprint author), Univ Zagreb, Dept Internal Med, Div Clin Immunol & Pulmonol, HR-10000 Zagreb, Croatia.	vostojic@astma.hr					Anderson K, 2001, LANCET, V358, P1343, DOI 10.1016/S0140-6736(01)06451-0; ARCHER LNJ, 1985, ARCH DIS CHILD, V60, P473; BAGG LR, 1980, EUR J RESPIR DIS, V61, P298; BARNES PJ, 1986, AM REV RESPIR DIS, V134, P1289; Bousquet J, 2002, CLIN THER, V24, P1, DOI 10.1016/S0149-2918(02)85002-0; BREWIS RAL, 1991, RESP MED, V85, P457, DOI 10.1016/S0954-6111(06)80262-3; Bruderman I, 1997, Telemed J, V3, P127, DOI 10.1089/tmj.1.1997.3.127; Burney P, 1996, EUR RESPIR J, V9, P687; BURR M L, 1989, Archives of Disease in Childhood, V64, P1452; CHMELIK F, 1994, ANN ALLERGY, V73, P527; CHOWIENCZYK PJ, 1994, BRIT MED J, V309, P1618; COUTTS JAP, 1992, ARCH DIS CHILD, V67, P332; Cowie RL, 1997, CHEST, V112, P1534, DOI 10.1378/chest.112.6.1534; CROSS D, 1991, J ALLERGY CLIN IMMUN, V87, P120, DOI 10.1016/0091-6749(91)90223-B; ENRIGHT P, 1992, AM REV RESPIR DIS, V146, P1367; Enright PL, 1994, AM J RESP CRIT CAR S, V149, P9; Finkelstein J, 2000, CHEST, V117, P148, DOI 10.1378/chest.117.1.148; FINKELSTEIN J, 1998, MEDINFO 1, V9, P272; Finkelstein J, 2001, MEDINFO 1, V10, P810; HORN CR, 1984, LANCET, V1, P1143; IGNACIOGARCIA JM, 1995, AM J RESP CRIT CARE, V151, P353; JONES KP, 1995, THORAX, V50, P851, DOI 10.1136/thx.50.8.851; Juniper EF, 1996, QUAL LIFE RES, V5, P35, DOI 10.1007/BF00435967; LEBOWITZ MD, 1982, CHEST, V81, P566, DOI 10.1378/chest.81.5.566; MALO JL, 1993, J ALLERGY CLIN IMMUN, V91, P702, DOI 10.1016/0091-6749(93)90189-M; National Asthma Education and Prevention Program, 1997, PUBL NIH; National Institutes of Health, 2002, GLOB STRAT ASTHM MAN; Ostojic V, 2000, J TELEMED TELECARE, V6, P172, DOI 10.1258/1357633001935176; Rietveld S, 1997, J ASTHMA, V34, P133, DOI 10.3109/02770909709075658; RUBINFELD AR, 1976, LANCET, V1, P882; Serra-Batlles J, 1998, EUR RESPIR J, V12, P1322, DOI 10.1183/09031936.98.12061322; Smith DH, 1997, AM J RESP CRIT CARE, V156, P787; TAITEL MS, 1995, J ALLERGY CLIN IMMUN, V95, P672, DOI 10.1016/S0091-6749(95)70171-0; TURNERWARWICK M, 1977, BRIT J DIS CHEST, V71, P73, DOI 10.1016/0007-0971(77)90086-9	34	87	88	0	7	MARY ANN LIEBERT INC	NEW ROCHELLE	140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA	1530-5627			TELEMED J E-HEALTH	Telemed. J. e-Health	FEB	2005	11	1					28	35		10.1089/tmj.2005.11.28		8	Health Care Sciences & Services	Health Care Sciences & Services	912RK	WOS:000228096900019	15785218	
J	Olaguibel, JM; Puebla, MJA				Olaguibel, JM; Puebla, MJA			Efficacy of sublingual allergen vaccination for respiratory allergy in children. Conclusions from one meta-analysis	JOURNAL OF INVESTIGATIONAL ALLERGOLOGY AND CLINICAL IMMUNOLOGY			English	Article						sublingual allergen vaccination; immunotherapy; rhinitis; asthma; children; efficacy; meta-analysis	HOUSE-DUST MITE; PLACEBO-CONTROLLED EVALUATION; DOUBLE-BLIND; POSTMARKETING SURVEILLANCE; SWALLOW IMMUNOTHERAPY; PEDIATRIC-PATIENTS; GRASS-POLLEN; ASTHMA; SAFETY; EXTRACT	Background. Sunlingual route, that allows the safe administration of allergen vaccination at home and without injections, is highly attractive alternative to parential delivery, especially amongthe youngest population. However, it's efficiacy in children has been questioned. Objuctive. To evaluate the efficiacy (symptom and medication scores) of sublingual allergen vaccination compared to placebo in pediatric patients. Search strategy: MEDLINE, EMBASE, ISI and the Cochrane Central Register of Controlled trials were explored (completed in january/04) for potentially relevant studies. Selection Criteria: Randomized double blind placebo-controlled clinical trials involving children <= 14 years-old with either rhinitis or asthma of proved allergic aetiology. Data collection and analysis. Two reviewers analyzed independently the eligiblility of studies for inclusions. The combined standardized mean difference (SMD) method was used the random effect model to obtain SMD. However, we also present the SMD values from the fixed effect model. The main outcomes were clinical symptom (asthma, rhinitis and conjunctivitis) and drug requirement scores. Safely, immunological and clinical changes were also reviewed. Results. Seven double blind placebo-controlled trials, enrolling 256 children (129 treatment and 127 placebo recipients), wee analyzed. We observed decreases in symptom (SMD: -1.42 for asthma, -0.44 for rhinitis and -1.49 for conjunctivitis) and medication requirement (SMD - 1.01) scores. Only reductions in asthma (p = 0.01) and drug dosage (p = 0.06) scores reached statistical significance with the random effect model but changes in rhinitis fixed effect model were similar in magnitude (SMD: - 1.60 for asthma, SMD: -0.47 for rhinitis, SMD: -1.09 for conjunctivitis and SMD: 0.54 for drug intake). Safety was constant in all the studies, neither severe nor systemic reactions were observed and oral and gastrointestinal complaints complaints were the most common adverse effects. Conclusion: In children, sublingual delivery of allergen vaccination constitutes a safe and effective alternative to the sublingual route to reduce allergy respiratory symptoms and drug intake. Further studies in this group of age are required to establish the optimal conditions for sublingual allergen vaccination.	Hosp Virgen Del Camino, Secc Alergol, Pamplona, Spain	Olaguibel, JM (reprint author), Secc Alergol, Plaza de la Paz S-N, Pamplona 31003, Spain.	jmolaguibel@telefonica.net					Alderson P, 2003, COCHRANE LIB; Almagro E, 1995, Allergol Immunopathol (Madr), V23, P153; Andre C, 2000, INT ARCH ALLERGY IMM, V121, P229, DOI 10.1159/000024322; Bahceciler NN, 2001, PEDIATR PULM, V32, P49, DOI 10.1002/ppul.1088; Bernardis P, 1996, J INVEST ALLERG CLIN, V6, P55; Bousquet J, 1998, ALLERGY S, V53, P44; Canonica GW, 2003, J ALLERGY CLIN IMMUN, V111, P437, DOI 10.1067/mai.2003.129; Des Roches A., 1996, Allergy (Copenhagen), V51, P430; 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; Di Rienzo V, 1999, Allergol Immunopathol (Madr), V27, P145; Durham SR, 1996, J ALLERGY CLIN IMMUN, V97, P1356, DOI 10.1016/S0091-6749(96)70205-1; FREW AJ, 1993, BRIT MED J, V307, P919; Grosclaude M, 2002, INT ARCH ALLERGY IMM, V129, P248, DOI 10.1159/000066779; Hirsch T, 1997, PEDIATR ALLERGY IMMU, V8, P21, DOI 10.1111/j.1399-3038.1997.tb00138.x; La Rosa M, 1999, J ALLERGY CLIN IMMUN, V104, P425, DOI 10.1016/S0091-6749(99)70388-X; Lombardi C, 2001, ALLERGY, V56, P989, DOI 10.1034/j.1398-9995.2001.00181.x; LOPEZ S, 1994, CONTACT DERMATITIS, V31, P37, DOI 10.1111/j.1600-0536.1994.tb01903.x; Malling HJ, 2002, CURR OPIN ALLERGY CL, V2, P523, DOI 10.1097/01.all.0000044538.45448.80; Mastrandrea F, 2000, Allergol Immunopathol (Madr), V28, P54; Moller C, 2002, J ALLERGY CLIN IMMUN, V109, P251, DOI 10.1067/mai.2002.121317; Olaguibel JM, 1997, ALLERGY, V52, P168, DOI 10.1111/j.1398-9995.1997.tb00971.x; OLAGUIBEL JM, MISCLASIFICATION CLI; Pajno GB, 2000, ALLERGY, V55, P842, DOI 10.1034/j.1398-9995.2000.00495.x; Pajno GB, 2003, CLIN EXP ALLERGY, V33, P1641, DOI 10.1111/j.1365-2222.2003.01809.x; Passalacqua G, 1996, J INVEST ALLERG CLIN, V6, P81; TABAR AI, 1993, ALLERGY, V48, P450, DOI 10.1111/j.1398-9995.1993.tb00743.x; Tari M G, 1994, Allergol Immunopathol (Madr), V22, P209; TARI MG, 1990, ALLERGOL IMMUNOPATH, V18, P277; Vourdas D, 1998, ALLERGY, V53, P662, DOI 10.1111/j.1398-9995.1998.tb03952.x; Wilson DR, 2003, COCHRANE DB SYST REV, V2; Wuthrich B, 2003, J INVEST ALLERG CLIN, V13, P145; Yuksel H, 1999, J INVEST ALLERG CLIN, V9, P305	33	87	94	0	1	HOGREFE & HUBER PUBLISHERS	GOTTINGEN	ROHNSWEG 25, D-37085 GOTTINGEN, GERMANY	1018-9068			J INVEST ALLERG CLIN	J. Invest. Allergol. Clin. Immunol.		2005	15	1					9	16				8	Allergy; Immunology	Allergy; Immunology	919JA	WOS:000228613100002	15864877	
J	Platts-Mills, TAE; Erwin, E; Heymann, P; Woodfolk, J				Platts-Mills, TAE; Erwin, E; Heymann, P; Woodfolk, J			Is the hygiene hypothesis still a viable explanation for the increased prevalence of asthma?	ALLERGY			English	Article; Proceedings Paper	Conference on Addressing the Allergy Epidemic	MAY, 2004	Uppsala, SWEDEN			allergen exposure; asthma; hygiene; lifestyle; prevalence	MODIFIED TH2 RESPONSE; DOG OWNERSHIP; CAT ALLERGEN; CHILDREN; EXPOSURE; SENSITIZATION; RISK; ATOPY; AGE; MORBIDITY	The hygiene hypothesis states that a reduced exposure to allergens in early life is solely implicated in the growing propensity for allergy sensitization. Important elements of the hypothesis include helminth infection, exposure to endotoxins, exposure to pets and growing up on a farm. However, the hygiene hypothesis alone does not provide an adequate explanation for the observed increase in allergic disease. For example, in North American inner cities, asthma is increasing among children who live in very poor housing, which might be assumed to be somewhat dirty. In order to explain the increase in asthma, we need to take a broader view and also consider alterations related to the adoption of a western lifestyle. It has been suggested that lifestyle changes related to obesity (e.g. a change in diet) are associated with asthma. Other changes include a progressive decrease in physical activity. This lifestyle factor seems to correlate best with the recent increase in asthma. Clearly, the link between physical activity and asthma needs to be investigated in more detail.	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.						Bach JF, 2003, ANN NY ACAD SCI, V998, P161, DOI 10.1196/annals.1254.017; Beasley R, 2000, J ALLERGY CLIN IMMUN, V105, pS466, DOI 10.1016/S0091-6749(00)90044-7; Berkey CS, 2000, PEDIATRICS, V105, DOI 10.1542/peds.105.4.e56; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; BURROWS B, 1989, NEW ENGL J MED, V320, P271, DOI 10.1056/NEJM198902023200502; Crater DD, 2001, PEDIATRICS, V108, DOI 10.1542/peds.108.6.e97; Custis N., 2004, Journal of Allergy and Clinical Immunology, V113, pS259, DOI 10.1016/j.jaci.2004.01.400; Custis NJ, 2003, CLIN EXP ALLERGY, V33, P986, DOI 10.1046/j.1365-2222.2003.01706.x; Erwin EA, 2005, J ALLERGY CLIN IMMUN, V115, P74, DOI 10.1016/j.jaci.2004.10.030; FIRINCIELLI V, 2005, IN PRESS PEDIAT PULM; Fredberg JJ, 1999, AM J RESP CRIT CARE, V159, P959; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Gern JE, 2004, J ALLERGY CLIN IMMUN, V113, P307, DOI 10.1016/j.jaci.2003.11.017; Green RM, 2002, BRIT MED J, V324, P763, DOI 10.1136/bmj.324.7340.763; HAAHTELA T, 1990, BRIT MED J, V301, P266; HARK WT, 2004, IN PRESS ANN ALLERGY; Haselden BM, 1999, J EXP MED, V189, P1885, DOI 10.1084/jem.189.12.1885; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Heymann PW, 2004, J ALLERGY CLIN IMMUN, V114, P239, DOI 10.1016/j.jaci.2004.04.006; LUCAS S, 2005, IN PRESS J ALLERGY C; Luder E, 2004, RESP MED, V98, P29, DOI 10.1016/j.rmed.2003.08.004; Matricardi PM, 2003, CLIN EXP ALLERGY, V33, P717, DOI 10.1046/j.1365-2222.2003.01695.x; McLean DE, 2004, ARCH PEDIAT ADOL MED, V158, P244, DOI 10.1001/archpedi.158.3.244; Ownby DR, 2002, JAMA-J AM MED ASSOC, V288, P963, DOI 10.1001/jama.288.8.963; 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, 2002, CLIN EXP ALLERGY, V32, P335, DOI 10.1046/j.1365-2222.2002.01352.x; Platts-Mills TA, 1997, J ALLERGY CLIN IMM S, V100, P2; PlattsMills TAE, 1997, CIBA F SYMP, V206, P173; PLATTSMILLS TAE, 1982, CLIN ASPECTS IMMUNOL, P579; Reefer AJ, 2004, J IMMUNOL, V172, P2763; Rosenstreich DL, 1997, NEW ENGL J MED, V336, P1356, DOI 10.1056/NEJM199705083361904; SKLOOT G, 1995, J CLIN INVEST, V96, P393; SMITH JM, 1976, BRIT J DIS CHEST, V70, P73; 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; WALZER M, 1956, J ALLERGY, V27, P113, DOI 10.1016/0021-8707(56)90002-8; WEISS KB, 1993, ANNU REV PUBL HEALTH, V14, P491, DOI 10.1146/annurev.pu.14.050193.002423; Westerterp KR, 2001, NATURE, V410, P539, DOI 10.1038/35069142	39	87	88	1	23	WILEY-BLACKWELL	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0105-4538			ALLERGY	Allergy		2005	60			79			25	31		10.1111/j.1398-9995.2005.00854.x		7	Allergy; Immunology	Allergy; Immunology	915NX	WOS:000228312000006	15842230	
J	Phipps, S; Benyahia, F; Ou, TT; Barkans, J; Robinson, DS; Kay, AB				Phipps, S; Benyahia, F; Ou, TT; Barkans, J; Robinson, DS; Kay, AB			Acute allergen-induced airway remodeling in atopic asthma	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article							BASEMENT-MEMBRANE; TGF-BETA; BRONCHIAL BIOPSIES; EPITHELIAL-CELLS; GENE-EXPRESSION; MODERATE ASTHMA; INFLAMMATION; MILD; ACTIVATION; EOSINOPHILS	Studies in animals and in human atopic skin suggest that allergen challenge may activate acute tissue remodeling changes via transforming growth factor-beta pathways. We determined whether inhalational allergen challenge in subjects with mild asthma induces similar acute changes to the airway epithelial mesenchymal trophic unit (EMTU). Endobronchial mucosal biopsies obtained before and 24 h after challenge were examined by confocal microscopy for extracellular matrix deposition in the reticular basement membrane (RBM). Cells actively involved in extracellular matrix synthesis were identified as immunoreactive to heat shock protein 47, a chaperone of Collagen synthesis. Interleukin-4/13 and transforming growth factor-beta-activated cells were identified by specific antibodies to phosphorylated (phospho-) signal transducer and activator of transcription 6 and phospho-Smad2, respectively. After allergen challenge, there was a significant increase in the number of heat shock protein 47-positive airway fibroblasts (P = 0.003) and in the thickness of tenascin in the RBM (P = 0.031). There were also increases in the number of phospho-Smad2+ epithelial cells (P = 0.04) and nuclear phospho-Smad2+ fibroblasts (P = 0.03), as well as phospho-signal transducer and activator of transcription 6+ epithelial cells (P = 0.03), after allergen challenge. Thus, allergen challenge in patients with mild asthma induces activation of epithelial cells and fibroblasts in the EMTU as well as increased tenascin deposition within the RBM. Airway remodeling in asthma may, in part, result from repeated acute activation of the EMTU by allergen exposure.	Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Leukocyte Biol Sect, Div Biomed Sci,Fac Med, London SW3 6LY, England	Kay, AB (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Leukocyte Biol Sect, Div Biomed Sci,Fac Med, Guy Scadding Bldg,Dovehouse St, London SW3 6LY, England.	a.b.kay@imperial.ac.uk	Phipps, Simon/F-9170-2010	Phipps, Simon/0000-0002-7388-3612			Buckley CD, 2001, TRENDS IMMUNOL, V22, P199, DOI 10.1016/S1471-4906(01)01863-4; CHAI H, 1975, J ALLERGY CLIN IMMUN, V56, P323, DOI 10.1016/0091-6749(75)90107-4; Cho JY, 2004, J CLIN INVEST, V113, P551, DOI 10.1172/JCI200419133; Davies DE, 2002, INT J BIOCHEM CELL B, V34, P1520, DOI 10.1016/S1357-2725(02)00048-1; Evans MJ, 1999, AM J RESP CELL MOL, V21, P655; Flood-Page P, 2003, J CLIN INVEST, V112, P1029, DOI 10.1172/JCI200317974; Gizycki MJ, 1997, AM J RESP CELL MOL, V16, P664; Goumans MJ, 2002, EMBO J, V21, P1743, DOI 10.1093/emboj/21.7.1743; 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; Khan LN, 2000, AM J RESP CRIT CARE, V162, P1377; Kuperman DA, 2002, NAT MED, V8, P885, DOI 10.1038/nm734; Laitinen A, 1997, AM J RESP CRIT CARE, V156, P951; Lee CG, 2001, J EXP MED, V194, P809, DOI 10.1084/jem.194.6.809; Li X, 1997, AM J RESP CRIT CARE, V156, P229; Ordonez CL, 2001, AM J RESP CRIT CARE, V163, P517; Payne DNR, 2003, AM J RESP CRIT CARE, V167, P78, DOI 10.1164/rccm.200205-414OC; Phipps S, 2004, J INVEST DERMATOL, V122, P1406, DOI 10.1111/j.0022-202X.2004.22619.x; Phipps S, 2002, J IMMUNOL, V169, P4604; Redington AE, 1998, J PATHOL, V186, P410, DOI 10.1002/(SICI)1096-9896(199812)186:4<410::AID-PATH198>3.0.CO;2-9; Rosendahl A, 2002, AM J RESP CELL MOL, V27, P160; Rosendahl A, 2001, AM J RESP CELL MOL, V25, P60; Sagara H, 2002, J ALLERGY CLIN IMMUN, V110, P249, DOI 10.1067/mai.2002.126078; Sasaki H, 2002, J IMMUNOL, V168, P5178; Venkayya R, 2002, AM J RESP CELL MOL, V26, P202; Wenzel SE, 2002, J IMMUNOL, V169, P4613; WONG DTW, 1993, AM J PATHOL, V143, P130; Woodruff PG, 2004, AM J RESP CRIT CARE, V169, P1001, DOI 10.1164/rccm.200311-1529OC; Ying S, 1999, J IMMUNOL, V163, P6321	29	87	92	0	0	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.	DEC	2004	31	6					626	632		10.1165/rcmb.2004-0193OC		7	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	877BA	WOS:000225541600007	15333330	
J	Wilson, MS; Maizels, RM				Wilson, MS; Maizels, RM			Regulation of allergy and autoimmunity in helminth infection	CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY			English	Review						cytokines; asthma; immunoregulation; parasites	INDUCED AIRWAY HYPERREACTIVITY; KILLED MYCOBACTERIUM-VACCAE; T-CELL RESPONSES; DEPENDENT DIABETES-MELLITUS; MODIFIED TH2 RESPONSE; HOUSE-DUST MITE; SCHISTOSOMA-MANSONI; MAST-CELLS; IMMUNE-RESPONSES; EOSINOPHILIC INFLAMMATION	Parasitic infections are a major theme in the "hygiene hypothesis", as allergies and autoimmune diseases are less prevalent in countries with higher burdens of helminths and other parasitic organisms. Helminths"-the grouping of multicellular worm parasistes including nematodes, cestodes and trematodes-tend to establish long-lived, chronic infections indicating successful down-modulation of the host immune system. In this review, we describe the intricate immunology of host-helminth interactions and how parasites manipulate immune responses to enhance their survival. In so doing, they often minimise immunopathology and, it is suggested, reduce host susceptibility to, and severity of allergic and autoimmune diseases. Studies on helminth-infected communities and individuals support the hypothesis that an immuno-regulatory network promoted by parasites extends its influence to limiting allergies. Experimental models are now probing more deeply into the area of immune modulation by helminths, and we discuss the likely mechanisms by which helminths could be establishing a strongly regulatory environment. Understanding and harnessing the modulatory capacity of helminths may uncover novel therapeutic interventions, mimicking and exploiting their evolution for our benefit. Parasitic infections are a major theme in the-"hygiene hypothesis", as allergies and autoimmune diseases are less prevalent in countries with higher burdens of helminths and other parasitic organisms. Helminths"-the grouping of multicellular worm parasistes including nematodes, cestodes and trematodes-tend to establish long-lived, chronic infections indicating successful down-modulation of the host immune system. In this review, we describe the intricate immunology of host-helminth interactions and how parasites manipulate immune responses to enhance their survival. In so doing, they often minimise immunopathology and, it is suggested, reduce host susceptibility to, and severity of allergic and autoimmune diseases. Studies on helminth-infected communities and individuals support the hypothesis that an immuno-regulatory network promoted by parasites extends its influence to limiting allergies. Experimental models are now probing more deeply into the area of immune modulation by helminths, and we discuss the likely mechanisms by which helminths could be establishing a strongly regulatory environment. Understanding and harnessing the modulatory capacity of helminths may uncover novel therapeutic interventions, mimicking and exploiting their evolution for our benefit.	Univ Edinburgh, Inst Cell Anim & Populat Biol, Edinburgh, Midlothian, Scotland	Maizels, RM (reprint author), Univ Edinburgh, Inst Cell Anim & Populat Biol, W Mains Rd, Edinburgh, Midlothian, Scotland.	rick.maizels@ed.ac.uk					ACTOR JK, 1993, P NATL ACAD SCI USA, V90, P948, DOI 10.1073/pnas.90.3.948; Akbari O, 2003, INT ARCH ALLERGY IMM, V130, P108, DOI 10.1159/000069012; Akbari O, 2002, NAT MED, V8, P1024, DOI 10.1038/nm745; Al-Qaoud KM, 2000, INT IMMUNOL, V12, P899, DOI 10.1093/intimm/12.6.899; ALI NMH, 1984, PARASITOLOGY, V88, P153; Allen JE, 1997, IMMUNOL TODAY, V18, P387, DOI 10.1016/S0167-5699(97)01102-X; ANDERSEN E, 1981, ACTA NEUROL SCAND, V63, P131; Angeli W, 2001, EUR J IMMUNOL, V31, P2751; Apostolou I, 2002, NAT IMMUNOL, V3, P756, DOI 10.1038/ni816; Araujo MI, 2000, INT ARCH ALLERGY IMM, V123, P145, DOI 10.1159/000024433; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; Barthlott T, 2003, J EXP MED, V197, P451, DOI 10.1084/jem.20021387; Bashir MEH, 2002, J IMMUNOL, V169, P3284; 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Rev. Allergy Immunol.	FEB	2004	26	1					35	50		10.1385/CRIAI:26:1:35		16	Allergy; Immunology	Allergy; Immunology	778MF	WOS:000189244800005	14755074	
J	Pitchford, SC; Riffo-Vasquez, Y; Sousa, A; Momi, S; Gresele, P; Spina, D; Page, CP				Pitchford, SC; Riffo-Vasquez, Y; Sousa, A; Momi, S; Gresele, P; Spina, D; Page, CP			Platelets are necessary for airway wall remodeling in a murine model of chronic allergic inflammation	BLOOD			English	Article							SMOOTH-MUSCLE-CELLS; GROWTH-FACTOR; BRONCHIAL-ASTHMA; MUCOSAL BIOPSIES; MOUSE MODEL; MILD ASTHMA; IN-VIVO; PROLIFERATION; HYPERPLASIA; MICE	Asthma is associated with airway remodeling. Evidence of platelet recruitment to the lungs of asthmatics after allergen exposure suggests platelets participate in various aspects of asthma; although their importance is unknown in the context of airway remodeling, their involvement in atherosclerosis is established. Studies from our laboratory have shown a requirement for platelets in pulmonary leukocyte recruitment in a murine model of allergic lung inflammation. Presently, the effects of platelet depletion and corticosteroid administration on airway remodeling and lung function were examined. Ovalbumin (OVA)-sensitized mice, exposed to aerosolized OVA for 8 weeks, demonstrated epithelial and smooth muscle thickening, and subepithelial reticular fiber deposition in the distal airways. The depletion of platelets via an immunologic (antiplatelet antisera) or nonimmunologic (busulfan) method, markedly reduced airway remodeling. In contrast, dexamethasone administration did not affect epithelial thickening or subepithelial fibrosis, despite significantly inhibiting leukocyte recruitment. Thus, pathways leading to certain aspects of airway remodeling may not depend on leukocyte recruitment, whereas platelet activation is obligatory. OVA-sensitized mice exhibited airway hyperresponsiveness (AHR) compared with sham-sensitized mice following chronic OVA exposure. Neither platelet depletion nor dexamethasone administration inhibited chronic AHR; thus, mechanisms other than inflammation and airway remodeling may be involved in the pathogenesis of chronic AHR.	Kings Coll London, Sackler Inst Pulm Pharmacol, GKT Sch Biomed Sci, London SE1 1UL, England; Univ Perugia, Dept Internal Med, Sect Internal & Cardiovasc Med, I-06100 Perugia, Italy	Spina, D (reprint author), Kings Coll London, Sackler Inst Pulm Pharmacol, GKT Sch Biomed Sci, 5th Fl,Hodgkin Bldg,Guys Campus, London SE1 1UL, England.	domenico.spina@kci.ac.uk	Gresele, Paolo/F-6775-2013	Gresele, Paolo/0000-0001-5365-8445; Spina, Domenico/0000-0002-6815-1564			Anderson HV, 2001, CIRCULATION, V104, P2331, DOI 10.1161/hc4401.098434; BEASLEY R, 1989, AM REV RESPIR DIS, V139, P806; Bonacci JV, 2003, BRIT J PHARMACOL, V138, P1203, DOI 10.1038/sj.bjp.0705135; Bonner JC, 1998, AM J PHYSIOL-LUNG C, V274, pL72; BOULET LP, 1995, EUR RESPIR J, V8, P913; Boulet LP, 2000, AM J RESP CRIT CARE, V162, P1308; BRECHER G, 1950, J APPL PHYSIOL, V3, P365; Burger PC, 2003, BLOOD, V101, P2661, DOI 10.1182/blood-2002-07-2209; CARROLL N, 1993, AM REV RESPIR DIS, V147, P405; Ciferri S, 2000, THROMB HAEMOSTASIS, V83, P157; EBINA M, 1993, AM REV RESPIR DIS, V148, P720; FALCINELLI E, 2001, THROMB HAEMOST S, V86, pOC916; FINGERLE J, 1989, P NATL ACAD SCI USA, V86, P8412, DOI 10.1073/pnas.86.21.8412; Foster PS, 2000, LAB INVEST, V80, P655; Foster PS, 2002, LAB INVEST, V82, P455; Golino P, 1997, THROMB HAEMOSTASIS, V77, P783; Gresele P, 1987, Agents Actions Suppl, V21, P119; GRESELE P, 1993, J ALLERGY CLIN IMMUN, V91, P894, DOI 10.1016/0091-6749(93)90347-I; HIRST SJ, 1992, AM J RESP CELL MOL, V7, P574; HOGEVOLD HE, 1990, THROMB RES, V57, P21, DOI 10.1016/0049-3848(90)90192-F; Holgate ST, 2000, AM J RESP CRIT CARE, V162, pS113; Hoyle GW, 1999, AM J PATHOL, V154, P1763, DOI 10.1016/S0002-9440(10)65432-6; Ichii T, 2002, ARTERIOSCL THROM VAS, V22, P1286, DOI 10.1161/01.ATV.0000024684.67566.45; IHNATOWYCZ IO, 1981, ARTERY, V9, P316; IP JH, 1991, J AM COLL CARDIOL, V17, pB77; JEFFERY PK, 1989, AM REV RESPIR DIS, V140, P1745; Kawasaki T, 2000, BLOOD, V96, P153; KUWANO K, 1993, AM REV RESPIR DIS, V148, P1220; Leigh R, 2002, AM J RESP CELL MOL, V27, P526, DOI 10.1165/rcmb.2002-0048OC; LELLOUCHTUBIANA A, 1985, BRIT J EXP PATHOL, V66, P345; LUNDGREN R, 1988, EUR RESPIR J, V1, P883; MAKILA UM, 1984, PROSTA LEUKOTR MED, V16, P11, DOI 10.1016/0262-1746(84)90081-7; MARTIN JF, 1983, LANCET, V1, P793; Massberg S, 2002, J EXP MED, V196, P887, DOI 10.1084/jem.20012044; MEHRI Y, 1997, ARTERIOSCLER THROMB, V17, P1185; Metzger W J, 1987, Agents Actions Suppl, V21, P151; Minshall EM, 1997, AM J RESP CELL MOL, V17, P326; MORLEY J, 1984, LANCET, V2, P1142; MUSTARD JF, 1972, BRIT J HAEMATOL, V22, P193, DOI 10.1111/j.1365-2141.1972.tb08800.x; Okona-Mensah KB, 1998, BRIT J PHARMACOL, V125, P599, DOI 10.1038/sj.bjp.0702046; Pitchford SC, 2003, J ALLERGY CLIN IMMUN, V112, P109, DOI 10.1067/mai.2003.1514; Pitchford SC, 2002, PLATELETS THROMBOTIC, P852, DOI 10.1017/CBO9780511545283.057; PLATTSMILLS TAE, 1987, J ALLERGY CLIN IMMUN, V79, P781, DOI 10.1016/0091-6749(87)90211-9; Puddicombe SM, 2000, FASEB J, V14, P1362, DOI 10.1096/fj.14.10.1362; ROCHE WR, 1989, LANCET, V1, P520; Ross R, 1999, NEW ENGL J MED, V340, P115; Sakai K, 2001, INT ARCH ALLERGY IMM, V126, P126, DOI 10.1159/000049503; Sanner SM, 2002, STEROIDS, V67, P715; SHURE D, 1992, BIOCHEM BIOPH RES CO, V186, P1510, DOI 10.1016/S0006-291X(05)81577-3; Spina D, 2002, TRENDS PHARMACOL SCI, V23, P311, DOI 10.1016/S0165-6147(02)02022-9; Stewart AG, 1995, BRIT J PHARMACOL, V116, P3219; Tomioka S, 2002, J APPL PHYSIOL, V93, P263, DOI 10.1152/japplphysiol.01129.2001; Ulfman LH, 2003, AM J RESP CELL MOL, V28, P512, DOI 10.1165/rcmb.4806; Vanacker NJ, 2001, AM J RESP CRIT CARE, V163, P674; Vignola AM, 1997, AM J RESP CRIT CARE, V156, P591; Vignola AM, 2000, J ALLERGY CLIN IMMUN, V105, P1041, DOI 10.1067/mai.2000.107195; Ward C, 2002, THORAX, V57, P309, DOI 10.1136/thorax.57.4.309; Weber AA, 1999, BIOCHEM BIOPH RES CO, V259, P341, DOI 10.1006/bbrc.1999.0793; Yamashita N, 2001, J ALLERGY CLIN IMMUN, V107, P135, DOI 10.1067/mai.2001.111433; Yoshida A, 2002, BRIT J PHARMACOL, V137, P146, DOI 10.1038/sj.bjp.0704852	60	87	93	2	6	AMER SOC HEMATOLOGY	WASHINGTON	1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA	0006-4971			BLOOD	Blood	JAN 15	2004	103	2					639	647		10.1182/blood-2003-05-1707		9	Hematology	Hematology	762CY	WOS:000187954000050	14504080	
J	Gono, H; Fujimoto, K; Kawakami, S; Kubo, K				Gono, H; Fujimoto, K; Kawakami, S; Kubo, K			Evaluation of airway wall thickness and air trapping by HRCT in asymptomatic asthma	EUROPEAN RESPIRATORY JOURNAL			English	Article						air trapping; airflow obstruction; airway remodelling; airway wall; bronchial asthma; high-resolution computed tomography	RESOLUTION COMPUTED-TOMOGRAPHY; OBSTRUCTIVE PULMONARY-DISEASE; FLOW OBSTRUCTION; BRONCHIAL-ASTHMA; FUNCTION TESTS; FATAL ASTHMA; EMPHYSEMA; CT; HYPERRESPONSIVENESS; DIMENSIONS	The aim of this study was to examine the relationship between the structural changes in large and small airways in asymptomatic asthmatics quantified by high-resolution computed tomography (HRCT) and airflow obstruction. The bronchial wall thickness at the trunk of the apical bronchus (B1) of the right upper lobe was used for assessment of the large airways. Air trapping, evaluated by the ratio of the average. CT-determined values for the bilateral upper and lower lung segments at full expiration to that at full inspiration (E/I ratio), was used for assessment of the small airways. Measurements were obtained with a helical HRCT in 24 asymptomatic asthmatics followed by optimal treatment with inhaled and/or oral corticosteroids for >6 months. Prior (20-30 min) to the HRCT examination, all patients were given an inhaled bronchodilator. The ratio of airway wall thickness to outer diameter (T/D) and the percentage wall area (WA%) at the B1 bronchus and the E/I ratio were significantly greater for the 14 asthmatics with deficient reversible airflow obstruction (forced expiratory volume in one second (FEV1) <80% prediced or FEV1/forced vital capacity <70% after bronchodilator inhalation) than for the 10 asthmatics with normal spirometry and seven normal subjects. T/D, WA%, and E/I ratio showed significant negative correlations with FEV1 % pred after bronchodilator inhalation. The E/I ratio also showed significant positive correlations with T/D, WA%, and residual volume/total lung capacity. These findings suggest that, in spite of optimal treatment, structural changes in both large and small airways may simultaneously occur in asthmatics with deficient reversible airflow obstruction.	Shinshu Univ, Sch Med, Dept Internal Med 1, Matsumoto, Nagano 3908621, Japan; Shinshu Univ, Sch Med, Dept Radiol, Matsumoto, Nagano 3908621, Japan	Fujimoto, K (reprint author), Shinshu Univ, Sch Med, Dept Internal Med 1, 3-1-1 Asahi, Matsumoto, Nagano 3908621, Japan.						Arakawa H, 1998, AM J ROENTGENOL, V170, P1349; Awadh N, 1998, THORAX, V53, P248; BALDWIN ED, 1948, MEDICINE, V27, P243; BERGLUND E, 1963, ACTA MED SCAND, V173, P185; BOULET L, 1995, AM J RESP CRIT CARE, V153, P865; BOULET LP, 1994, CHEST, V105, P1024, DOI 10.1378/chest.105.4.1024; BOUSQUET J, 1992, ALLERGY, V47, P3, DOI 10.1111/j.1398-9995.1992.tb02242.x; BROWN PJ, 1984, THORAX, V39, P131, DOI 10.1136/thx.39.2.131; Carr DH, 1998, RESP MED, V92, P448, DOI 10.1016/S0954-6111(98)90290-6; CARROLL N, 1993, AM REV RESPIR DIS, V147, P405; Eda S, 1997, AM J RESP CRIT CARE, V155, P1290; FERGUSON AC, 1988, J ALLERGY CLIN IMMUN, V82, P19, DOI 10.1016/0091-6749(88)90045-0; Hudon C, 1997, ANN ALLERG ASTHMA IM, V78, P195; JAMES AL, 1989, AM REV RESPIR DIS, V139, P242; James AL, 1997, AIRWAY WALL REMODELI, P1; King GG, 1999, AM J RESP CRIT CARE, V159, P992; Kubo K, 1998, AM J RESP CRIT CARE, V158, P979; KUWANO K, 1993, AM REV RESPIR DIS, V148, P1220; Macklem PT, 1996, AM J RESP CRIT CARE, V153, P83; Mochizuki T, 1997, CHEST, V112, P1522, DOI 10.1378/chest.112.6.1522; Nakano Y, 2000, AM J RESP CRIT CARE, V162, P1102; NEWMAN KB, 1994, CHEST, V106, P105, DOI 10.1378/chest.106.1.105; Nishida O, 1976, JPN J CLIN PATHOL, V24, P941; Okazawa M, 1996, AM J RESP CRIT CARE, V154, P1557; Paganin F, 1996, AM J RESP CRIT CARE, V153, P110; Park JW, 1997, J INVEST ALLERG CLIN, V7, P186; Rennard SI, 1996, J ALLERGY CLIN IMMUN, V98, pS278, DOI 10.1016/S0091-6749(96)70076-3	27	87	89	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.	DEC	2003	22	6					965	971		10.1183/09031936.03.00085302		7	Respiratory System	Respiratory System	750RA	WOS:000187009900020	14680087	
J	Tschumperlin, DJ; Shively, JD; Kikuchi, T; Drazen, JM				Tschumperlin, DJ; Shively, JD; Kikuchi, T; Drazen, JM			Mechanical stress triggers selective release of fibrotic mediators from bronchial epithelium	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article							GROWTH-FACTOR-BETA; BRONCHOALVEOLAR LAVAGE FLUID; INDUCED CARDIOMYOCYTE HYPERTROPHY; ENDOTHELIN-1 GENE-EXPRESSION; AIR-FLOW OBSTRUCTION; PROTEIN-KINASE-C; LATENT TGF-BETA; EXTRACELLULAR-MATRIX; TRANSFORMING GROWTH-FACTOR-BETA-1; CELL-PROLIFERATION	Transforming growth factor-beta (TGF-beta) and endothelin (ET) are found in elevated amounts in the airways of individuals with asthma. The cellular source of these peptides and their role in mediating the airway fibrosis of chronic asthma are unknown. In response to mechanical stresses similar to those occurring in vivo during airway constriction, bronchial epithelial cells increase the steady-state level of mRNA for both ET-1 and ET-2, followed by increased release of ET protein. Mechanical stress also enhances release of TGF-beta2 from a preformed cell-associated pool. TGF-beta2 and ET act individually and, more importantly, synergistically to promote fibrotic protein synthesis in reporter fibroblasts. To confirm the role of these intermediates in stress-induced fibrosis, conditioned medium from mechanically stressed bronchial epithelial cells was shown to elicit fibrotic protein synthesis in reporter fibroblasts; this effect was significantly inhibited by combined treatment with ET receptor antagonists and a neutralizing antibody to TGF-beta2. These data are consistent with a primary pathogenic role for mechanical stress-induced release of both TGF-beta2 and ET in the subepithelial fibrosis that characterizes chronic asthma.	Harvard Univ, Pulm & Crit Care Div, Dept Med, Brigham & Womens Hosp,Sch Med, Boston, MA 02115 USA; Harvard Univ, Sch Publ Hlth, Phys Programs, Dept Environm Hlth, Boston, MA USA	Drazen, JM (reprint author), Harvard Univ, Pulm & Crit Care Div, Dept Med, Brigham & Womens Hosp,Sch Med, 75 Francis St, Boston, MA 02115 USA.	jdrazen@nejm.org	Drazen, Jeffrey/E-5841-2012		NHLBI NIH HHS [HL-33009]		Aoki S K, 1994, J Viral Hepat, V1, P73, DOI 10.1111/j.1365-2893.1994.tb00064.x; Bousquet J, 2000, AM J RESP CRIT CARE, V161, P1720; BROEKELMANN TJ, 1991, P NATL ACAD SCI USA, V88, P6642, DOI 10.1073/pnas.88.15.6642; CHEN J, 2001, J PHYSL CELL PHYSL, V280, pC1475; DALLAS SL, 1995, J CELL BIOL, V131, P539, DOI 10.1083/jcb.131.2.539; Eickelberg O, 1999, AM J PHYSIOL-LUNG C, V276, pL814; Elias JA, 1999, J CLIN INVEST, V104, P1001, DOI 10.1172/JCI8124; ENDO T, 1992, BIOCHEM BIOPH RES CO, V186, P1594, DOI 10.1016/S0006-291X(05)81590-6; FINE A, 1987, J BIOL CHEM, V262, P3897; Fish JE, 1999, J ALLERGY CLIN IMMUN, V104, P509, DOI 10.1016/S0091-6749(99)70315-5; Gandhi CR, 2000, EUR J PHARMACOL, V406, P311, DOI 10.1016/S0014-2999(00)00683-X; Gonzalez W, 2001, J CARDIOVASC PHARM, V37, P219, DOI 10.1097/00005344-200102000-00009; Huang M, 2002, J CLIN INVEST, V109, P931, DOI 10.1172/JCI14685; INOUE A, 1989, P NATL ACAD SCI USA, V86, P2863, DOI 10.1073/pnas.86.8.2863; Kakinuma Y, 1999, LIFE SCI, V65, P1671, DOI 10.1016/S0024-3205(99)00416-6; KAWANA M, 1995, MOL CELL BIOL, V15, P4225; Khalil MK, 1996, CAN J OPHTHALMOL, V31, P32; KURIHARA H, 1989, BIOCHEM BIOPH RES CO, V159, P1435, DOI 10.1016/0006-291X(89)92270-5; Lambert GL, 2000, J MOL ENDOCRINOL, V24, P273, DOI 10.1677/jme.0.0240273; Lauth M, 2000, J MOL MED-JMM, V78, P441, DOI 10.1007/s001090000129; Lee CG, 2001, J EXP MED, V194, P809, DOI 10.1084/jem.194.6.809; LEE ME, 1990, J BIOL CHEM, V265, P10446; LEE ME, 1991, J BIOL CHEM, V266, P19034; MAGNAN A, 1994, THORAX, V49, P789, DOI 10.1136/thx.49.8.789; MALEK AM, 1993, P NATL ACAD SCI USA, V90, P5999, DOI 10.1073/pnas.90.13.5999; MATTOLI S, 1991, J ALLERGY CLIN IMMUN, V88, P376, DOI 10.1016/0091-6749(91)90100-3; Munger JS, 1999, CELL, V96, P319, DOI 10.1016/S0092-8674(00)80545-0; O'Callaghan CJ, 2000, HYPERTENSION, V36, P319; OHNO M, 1995, J CLIN INVEST, V95, P1363, DOI 10.1172/JCI117787; PELTON RW, 1991, AM J RESP CELL MOL, V5, P522; RAGHOW R, 1989, J CLIN INVEST, V84, P1836; REDINGTON AE, 1995, AM J RESP CRIT CARE, V151, P1034; Redington AE, 1997, AM J RESP CRIT CARE, V156, P642; Ressler B, 2000, AM J PHYSIOL-LUNG C, V278, pL1264; Richter A, 2001, AM J RESP CELL MOL, V25, P385; Riser BL, 1996, AM J PATHOL, V148, P1915; Ruwhof C, 2000, MOL CELL BIOCHEM, V208, P89, DOI 10.1023/A:1007046105745; Sharma P, 1998, BIOCHEM BIOPH RES CO, V245, P709, DOI 10.1006/bbrc.1998.8507; Sime PJ, 1997, J CLIN INVEST, V100, P768, DOI 10.1172/JCI119590; SPRINGALL DR, 1991, LANCET, V337, P697, DOI 10.1016/0140-6736(91)90279-X; Swartz MA, 2001, P NATL ACAD SCI USA, V98, P6180, DOI 10.1073/pnas.111133298; TAIPALE J, 1995, J BIOL CHEM, V270, P4689; TAIPALE J, 1994, J CELL BIOL, V124, P171, DOI 10.1083/jcb.124.1.171; TAIPALE J, 1992, J BIOL CHEM, V267, P25378; Tschumperlin DJ, 2002, AM J PHYSIOL-LUNG C, V282, pL904, DOI 10.1152/ajplung.00270.2001; Ueba H, 1997, ARTERIOSCL THROM VAS, V17, P1512; van Wamel AJET, 2001, MOL CELL BIOCHEM, V218, P113, DOI 10.1023/A:1007279700705; Vignola AM, 1997, AM J RESP CRIT CARE, V156, P591; Vignola AM, 1996, CLIN EXP IMMUNOL, V106, P114, DOI 10.1046/j.1365-2249.1996.d01-811.x; VITTORI E, 1992, AM REV RESPIR DIS, V146, P1320; WANG DL, 1995, J CELL PHYSIOL, V163, P400, DOI 10.1002/jcp.1041630220; WANG DL, 1993, BIOCHEM BIOPH RES CO, V195, P1050, DOI 10.1006/bbrc.1993.2150; Wiggs BR, 1997, J APPL PHYSIOL, V83, P1814; Yamazaki T, 1996, J BIOL CHEM, V271, P3221; Yasuda T, 1996, J CLIN INVEST, V98, P1991, DOI 10.1172/JCI119003	55	87	89	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.	FEB	2003	28	2					142	149		10.1165/rcmb.2002-0121OC		8	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	643HG	WOS:000180855400005	12540481	
J	Mortz, CG; Lauritsen, JM; Bindslev-Jensen, C; Andersen, KE				Mortz, CG; Lauritsen, JM; Bindslev-Jensen, C; Andersen, KE			Nickel sensitization in adolescents and association with ear piercing, use of dental braces and hand eczema. The Odense Adolescence Cohort Study on Atopic Diseases and Dermatitis (TOACS)	ACTA DERMATO-VENEREOLOGICA			English	Article						schoolchildren; atopic dermatitis; inhalant allergy; hand eczema; multivariate graphical analysis	NORTH NORWEGIAN SCHOOLCHILDREN; ALLERGIC CONTACT-DERMATITIS; CHILDREN; SENSITIVITY; POPULATION; PREVALENCE; HISTORY; TESTS	The prevalence of nickel allergy (sensitization) and the associations with ear piercing, use of dental braces and hand eczema were assessed in a cohort of 1, 501 8th grade schoolchildren (aged 12-16 years) in Odense, Denmark. Nickel allergy was found in 8.6% and was clinically relevant in 69% of cases. Nickel allergy was found most frequently in girls and the association with ear piercing was confirmed. Application of dental braces (oral nickel exposure) prior to ear piercing (cutaneous nickel exposure) was associated with a significantly reduced prevalence of nickel allergy. In adolescents a significant association was found between hand eczema and nickel allergy. A follow-up study of this population is planned in order to assess the course and development of contact dermatitis, hand eczema and atopic diseases in adulthood and after choice of occupation.	Odense Univ Hosp, Dept Dermatol, DK-5000 Odense C, Denmark	Mortz, CG (reprint author), Odense Univ Hosp, Dept Dermatol, DK-5000 Odense C, Denmark.		andersen, klaus/H-2117-2011; Bindslev-Jensen, Carsten/H-1877-2011	Bindslev-Jensen, Carsten/0000-0002-8940-038X			Agresti A, 1984, ANAL ORDINAL CATEGOR; ANDERSEN KE, 1993, BRIT J DERMATOL, V129, P50, DOI 10.1111/j.1365-2133.1993.tb03311.x; AYALA F, 1992, CONTACT DERMATITIS, V26, P307; BALATO N, 1989, CONTACT DERMATITIS, V20, P305, DOI 10.1111/j.1600-0536.1989.tb03153.x; BARROS MA, 1991, CONTACT DERMATITIS, V25, P156; Brasch J, 1997, CONTACT DERMATITIS, V37, P286, DOI 10.1111/j.1600-0536.1997.tb02466.x; BRUNE D, 1986, BIOMATERIALS, V7, P163, DOI 10.1016/0142-9612(86)90097-9; Christensen O B, 1975, Contact Dermatitis, V1, P129, DOI 10.1111/j.1600-0536.1975.tb05353.x; DOTTERUD LK, 1994, CONTACT DERMATITIS, V31, P308, DOI 10.1111/j.1600-0536.1994.tb02025.x; DOTTERUD LK, 1995, ACTA PAEDIATR, V84, P402, DOI 10.1111/j.1651-2227.1995.tb13659.x; FISCHER TI, 1985, BRIT J DERMATOL, V112, P63, DOI 10.1111/j.1365-2133.1985.tb02292.x; GAWKRODGER DJ, 1986, CONTACT DERMATITIS, V14, P165, DOI 10.1111/j.1600-0536.1986.tb01198.x; GONCALO S, 1992, CONTACT DERMATITIS, V26, P112, DOI 10.1111/j.1600-0536.1992.tb00894.x; Johansen JD, 2000, BRIT J DERMATOL, V142, P490, DOI 10.1046/j.1365-2133.2000.03362.x; Katsarou A, 1996, CONTACT DERMATITIS, V34, P70, DOI 10.1111/j.1600-0536.1996.tb02125.x; Kerosuo H, 1996, AM J ORTHOD DENTOFAC, V109, P148, DOI 10.1016/S0889-5406(96)70175-0; KIEFFER M, 1979, CONTACT DERMATITIS, V5, P398, DOI 10.1111/j.1600-0536.1979.tb04913.x; KLEIN JP, 1995, STAT MED, V14, P1265, DOI 10.1002/sim.4780141202; 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; MEIJER C, 1995, CONTACT DERMATITIS, V32, P147, DOI 10.1111/j.1600-0536.1995.tb00804.x; Menne T, 1996, ANN CLIN LAB SCI, V26, P133; MENNE T, 1982, ACTA DERM-VENEREOL, V62, P35; MENNE T, 1983, CONTACT DERMATITIS, V9, P289, DOI 10.1111/j.1600-0536.1983.tb04393.x; MOLLER H, 1986, CONTACT DERMATITIS, V14, P57, DOI 10.1111/j.1600-0536.1986.tb01154.x; Mortz CG, 2002, ACTA DERM-VENEREOL, V82, P352, DOI 10.1080/000155502320624087; Mortz CG, 2001, BRIT J DERMATOL, V144, P523, DOI 10.1046/j.1365-2133.2001.04078.x; Mortz CG, 1999, CONTACT DERMATITIS, V41, P121, DOI 10.1111/j.1600-0536.1999.tb06102.x; NIELSEN NH, 1993, CONTACT DERMATITIS, V29, P16; PAMBOR M, 1992, CONTACT DERMATITIS, V27, P326, DOI 10.1111/j.1600-0536.1992.tb03292.x; PEVNY I, 1984, CONTACT DERMATITIS, V11, P201, DOI 10.1111/j.1600-0536.1984.tb00983.x; RADEMAKER M, 1989, CONTACT DERMATITIS, V20, P104, DOI 10.1111/j.1600-0536.1989.tb03116.x; ROMAGUERA C, 1985, CONTACT DERMATITIS, V12, P283, DOI 10.1111/j.1600-0536.1985.tb01140.x; Rudzki E, 1996, CONTACT DERMATITIS, V34, P66, DOI 10.1111/j.1600-0536.1996.tb02121.x; Rycroft RJG, 1995, TXB CONTACT DERMATIT; SEVILA A, 1994, CONTACT DERMATITIS, V30, P292, DOI 10.1111/j.1600-0536.1994.tb00601.x; Susitaival P, 1996, PEOPLE WORK, V10, P1; VANHOOGSTRATEN IMW, 1991, CLIN EXP IMMUNOL, V85, P441; VEIEN NK, 1993, J AM ACAD DERMATOL, V29, P1002; VEIEN NK, 1982, CONTACT DERMATITIS, V8, P373, DOI 10.1111/j.1600-0536.1982.tb04261.x; WAHLBERG JE, 1971, BRIT J DERMATOL, V85, P97, DOI 10.1111/j.1365-2133.1971.tb07192.x; WESTON WL, 1986, PEDIATRICS, V78, P1070	42	87	88	1	5	TAYLOR & FRANCIS AS	OSLO	CORT ADELERSGT 17, PO BOX 2562, SOLLI, 0202 OSLO, NORWAY	0001-5555			ACTA DERM-VENEREOL	Acta Derm.-Venereol.	SEP	2002	82	5					359	364		10.1080/000155502320624096		6	Dermatology	Dermatology	604UL	WOS:000178639400008	12430735	
J	Jacob, B; Ritz, B; Gehring, U; Koch, A; Bischof, W; Wichmann, HE; Heinrich, J				Jacob, B; Ritz, B; Gehring, U; Koch, A; Bischof, W; Wichmann, HE; Heinrich, J		INGA-Study Grp	Indoor exposure to molds and allergic sensitization	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						allergic sensitization; house dust; indoor allergen exposure; molds	IN-HOUSE DUST; REPORTED HOME DAMPNESS; RESPIRATORY SYMPTOMS; BRONCHIAL HYPERRESPONSIVENESS; RESIDENTIAL CHARACTERISTICS; CHILDHOOD ASTHMA; HEALTH; CHILDREN; FUNGI; PROPAGULES	Evidence that indoor dampness and mold growth are associated with respiratory health has been accumulating, but few studies have been able to examine health risks in relation to measured levels of indoor mold exposure. In particular, little is known about the contribution of indoor molds to the development of allergic sensitization. As a part of an ongoing study examining the effects of ambient air pollutants on respiratory health and atopic diseases in German school children, we examined the relation between viable mold levels indoors and allergic sensitization in 272 children. We examined whether allergic sensitization in children is associated with higher fungal spore count in settled house dust sampled from living room floors. Adjusting for age, sex, parental education, region of residency, and parental history of atopy, we found that mold spore counts for Cladosporium and Aspergillus were associated with an increased risk of allergic sensitization. Sensitized children exposed to high levels of mold spores (> 90th percentile) were more likely to suffer from symptoms of rhinoconjunctivitis. We conclude that elevated indoor concentrations of molds in wintertime might play a role in increasing the risk of developing atopic symptoms and allergic sensitization not only to molds but also to other common, inhaled allergens. These effects were strongest in the group of children who had lived in the same home since birth.	GSF, Inst Epidemiol, Munich, Germany; Univ Munich, Inst Med Data Management Biometr & Epidemiol, Munich, Germany; Univ Calif Los Angeles, Sch Publ Hlth, Ctr Environm & Occupat Hlth, Los Angeles, CA 90024 USA; Univ Jena, Dept Indoor Climatol, Erfurt, Germany	Jacob, B (reprint author), GSF, Inst Epidemiol, Ingolstadter Landstr 1, D-85758 Neuherberg, Germany.		Ritz, Beate/E-3043-2015	Gehring, Ulrike/0000-0003-3612-5780			BJORNSSON E, 1995, CLIN EXP ALLERGY, V25, P423, DOI 10.1111/j.1365-2222.1995.tb01073.x; BURR ML, 1988, J ROY SOC HEALTH, V108, P99, DOI 10.1177/146642408810800311; COREY JP, 1994, OTOLARYNG HEAD NECK, V111, P340; Dales RE, 1997, INT J EPIDEMIOL, V26, P120, DOI 10.1093/ije/26.1.120; DAMATO G, 1995, ALLERGY, V50, P870, DOI 10.1111/j.1398-9995.1995.tb02492.x; Douwes J, 1999, J ALLERGY CLIN IMMUN, V103, P494, DOI 10.1016/S0091-6749(99)70476-8; 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; GRAVESEN S, 1979, ALLERGY, V34, P135, DOI 10.1111/j.1398-9995.1979.tb01562.x; Gross I, 2000, CLIN EXP ALLERGY, V30, P376, DOI 10.1046/j.1365-2222.2000.00780.x; Heinrich J, 1999, ENVIRON HEALTH PERSP, V107, P53, DOI 10.2307/3434289; Katz Y, 1999, CLIN EXP ALLERGY, V29, P186; Koch A, 2000, ALLERGY, V55, P176, DOI 10.1034/j.1398-9995.2000.00233.x; KUEHR J, 1994, J ALLERGY CLIN IMMUN, V94, P44, DOI 10.1016/0091-6749(94)90070-1; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; LIAPPRIS N, 1993, ALLERGO J S3, V2, P133; MARTIN CJ, 1987, BRIT MED J, V294, P1125; Munir AKM, 1997, J ALLERGY CLIN IMMUN, V100, P177, DOI 10.1016/S0091-6749(97)70221-5; Nelson HS, 1999, J ALLERGY CLIN IMMUN, V104, P775; Nowak D, 1996, EUR RESPIR J, V9, P2541, DOI 10.1183/09031936.96.09122541; Peat JK, 1998, ALLERGY, V53, P120, DOI 10.1111/j.1398-9995.1998.tb03859.x; PLATT SD, 1989, BRIT MED J, V298, P1673; Richter K, 1999, ALLERGOLOGIE, V22, P14; Senkpiel K, 1996, ZBL HYG UMWELTMED, V198, P191; Sporik R, 1999, THORAX, V54, P675; STRACHAN DP, 1990, THORAX, V45, P382, DOI 10.1136/thx.45.5.382; SU HJ, 1992, APPL ENVIRON MICROB, V58, P181; Verhoeff AP, 1997, ANN ALLERG ASTHMA IM, V78, P544; VERHOEFF AP, 1994, ALLERGY, V49, P533, DOI 10.1111/j.1398-9995.1994.tb01125.x; VERHOEFF AP, 1994, ALLERGY, V49, P540, DOI 10.1111/j.1398-9995.1994.tb01126.x; VERHOEFF AP, 1992, ALLERGY, V47, P83; VERHOEFF AP, 1995, AM J EPIDEMIOL, V141, P103; WAEGEMAEKERS M, 1989, ALLERGY, V44, P192, DOI 10.1111/j.1398-9995.1989.tb02261.x; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; WARNER JA, 1991, PEDIATR ALLERGY IMMU, V1, P79; WICKMAN M, 1992, J ALLERGY CLIN IMMUN, V89, P752, DOI 10.1016/0091-6749(92)90384-E; WOOD RA, 1988, AM REV RESPIR DIS, V137, P358	37	87	94	0	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.	JUL	2002	110	7					647	653				7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	585VZ	WOS:000177546400024	12117641	
J	Wichmann, G; Herbarth, O; Lehmann, I				Wichmann, G; Herbarth, O; Lehmann, I			The mycotoxins citrinin, gliotoxin, and patulin affect interferon-gamma rather than interleukin-4 production in human blood cells	ENVIRONMENTAL TOXICOLOGY			English	Article; Proceedings Paper	10th International Symposium on Toxicity Assessment (ISTA 10)	AUG 26-31, 2001	QUEBEC CITY, CANADA			mycotoxins; citrinin; gliotoxin; patulin; Th1 cells; Th2 cells; IL-4; IFN-gamma; cytokine immunotoxicity	RESPIRATORY HEALTH; KAPPA-B; FUNGI; RISK; PROLIFERATION; CHILDREN; DAMP	Exposure to molds diminishes the numbers of T-helper type 1 (Th1) cells in the peripheral blood of children and is a risk factor for the development of allergic diseases (results of LARS: Leipzig Allergy Risk Children Study, Mueller et al. 2002). We hypothesized that mycotoxins are responsible for this effect and therefore investigated the influence of citrinin, gliotoxin, and patulin on human peripheral blood mononuclear cells (PBMC). CD3/CD28-stimulated PBMC of healthy donors were incubated for 24 h with the mycotoxins in serial dilutions and triplicates. Vitality and proliferation were tested using the MTT assay and T-cell function by the expression of cytokines (ELISA, intracellular cytokine staining, and real-time polymerase chain reaction (RT-PCR) for interferon-gamma (IFN-gamma) and interleukin-4 (IL-4). The cytokine secretion was inhibited at concentrations 2-130 times lower compared to vitality (ELISA versus MTT assay). The strongest inhibition of cytokine expression was found for IFN-gamma: 8.3 mug/mL citrinin, 34.2 ng/mL gliotoxin, and 64.8 ng/mL patulin caused a 50% inhibition of the IFN-gamma release (50% inhibitory dose, ID50). For IL-4 release the corresponding ID50 values were 21.6 mug/mL citrinin, 82.8 ng/mL gliotoxin, and 243.2 ng/mL patulin. Furthermore, 3 ng/mL patulin caused a significant increase of IL-4 but a significant suppression of IFN-gamma. On the mRNA level, after 24 h an unaltered or enhanced IL-4 was observed compared to a reduced IFN-gamma expression. Using a method of intracellular cytokine staining, we were able to show that the described effects are caused by a reduction of the number of IFN-gamma-producing T lymphocytes rather than by a reduced functional capacity of the single cell. We suggest that mycotoxins primarily cause stronger inhibition of IFN-gamma-producing Th1 cells, which may lead to T-cell polarization toward the Th2 phenotype and may raise the risk for the development of allergies. (C) 2002 Wiley Periodicals, Inc.	UFZ Helmholtz Ctr Environm Res, Ctr Environm Res Leipzig Halle, Dept Human Exposure Res & Epidemiol, D-04318 Leipzig, Germany; Univ Leipzig, Fac Med, Dept Environm Hyg, Leipzig, Germany	Wichmann, G (reprint author), UFZ Helmholtz Ctr Environm Res, Ctr Environm Res Leipzig Halle, Dept Human Exposure Res & Epidemiol, Permoser Str 15, D-04318 Leipzig, Germany.	guwich@expo.xfz.de					Charoenpornsook K, 1998, MYCOPATHOLOGIA, V143, P105, DOI 10.1023/A:1006971724678; Diez U, 2000, INT J HYG ENVIR HEAL, V203, P23, DOI 10.1078/S1438-4639(04)70004-8; Fischer G, 2000, INT J HYG ENVIR HEAL, V203, P105, DOI 10.1078/S1438-4639(04)70015-2; Flannigan B, 1991, Soc Appl Bacteriol Symp Ser, V20, p61S; Garrett MH, 1998, CLIN EXP ALLERGY, V28, P459; Gravesen S, 1999, ENVIRON HEALTH PERSP, V107, P505; Herbarth O., 2000, P HLTH BUILDINGS, V1, P281; Herfarth H, 2000, CLIN EXP IMMUNOL, V120, P59, DOI 10.1046/j.1365-2249.2000.01184.x; HORAK B, 1987, ALLERGOL IMMUNOPATH, V15, P161; Husman T, 1996, SCAND J WORK ENV HEA, V22, P5; Lehmann I., 2001, Allergy (Copenhagen), V56, P43; LEHMANN I, 2001, INT J HYG ENVIR HEAL, V204, P1; LICORISH K, 1985, J ALLERGY CLIN IMMUN, V76, P19; MOSMANN T, 1983, J IMMUNOL METHODS, V65, P55, DOI 10.1016/0022-1759(83)90303-4; MUELLER A, 2002, IN PRESS INT J HYG E; Pahl HL, 1996, J EXP MED, V183, P1829, DOI 10.1084/jem.183.4.1829; Peat JK, 1998, ALLERGY, V53, P120, DOI 10.1111/j.1398-9995.1998.tb03859.x; ROMAGNANI S, 1997, IGE REGULATION MOL M, P1; Rossano F, 1999, RES MICROBIOL, V150, P13, DOI 10.1016/S0923-2508(99)80042-4; Sutton P, 1995, BIOCHEM PHARMACOL, V50, P2009, DOI 10.1016/0006-2952(95)02101-9; SUTTON P, 1994, INFECT IMMUN, V62, P1192; TARGONSKI PV, 1995, J ALLERGY CLIN IMMUN, V95, P955, DOI 10.1016/S0091-6749(95)70095-1; TOBIN RS, 1987, CAN J PUBLIC HLTH S, V78, P1	23	87	92	0	10	WILEY-BLACKWELL	HOBOKEN	111 RIVER ST, HOBOKEN 07030-5774, NJ USA	1520-4081			ENVIRON TOXICOL	Environ. Toxicol.	JUN	2002	17	3			SI		211	218		10.1002/tox.10050		8	Environmental Sciences; Toxicology; Water Resources	Environmental Sciences & Ecology; Toxicology; Water Resources	571KW	WOS:000176717400008	12112629	
J	Hancox, RJ; Subbarao, P; Kamada, D; Watson, RM; Hargreave, FE; Inman, MD				Hancox, RJ; Subbarao, P; Kamada, D; Watson, RM; Hargreave, FE; Inman, MD			B-2-agonist tolerance and exercise-induced bronchospasm	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; exercise-induced; adrenergic beta-agonists; tolerance	REGULAR INHALED ALBUTEROL; INDUCED BRONCHOCONSTRICTION; ASTHMATIC SUBJECTS; BRONCHODILATOR; SALMETEROL; SUBSENSITIVITY; TERBUTALINE; BUDESONIDE; SALBUTAMOL; RESPONSES	The effect of regular inhaled beta-agonist on the treatment of exercise-induced bronchoconstriction was studied. Eight subjects with exercise-induced bronchoconstriction took 1 week each of salbutamol 200 mug qid or placebo in a random-order, double-blind, crossover study. They then withheld this treatment for 8 hours before performing a dry-air, sub-maximal exercise challenge at a work-rate previously shown to induce a 15% fall in forced expiratory volume in 1 second (FEV1). Five minutes after exercise, they inhaled salbutamol 100, 100, and 200 mug at 5-minute intervals. The mean pre-exercise FEV1 was similar on both study days. However, pretreatment for 1 week with salbutamol led to a significantly greater fall in FEV1 after exercise. The FEV1 remained lower than during the placebo arm despite the administration of salbutamol after exercise. This difference persisted 25 minutes after exercise. It is concluded that regular beta-agonist treatment leads to Increased exercise-induced bronchoconstriction and a suboptimal bronchodilator response to beta-agonist. The data suggest that previous regular beta-agonist treatment may lead to a failure to respond to emergency bronchodilator treatment during an acute asthma attack and support current opinion that regular short-acting beta-agonist therapy should not be used to treat asthma.	St Josephs Hosp, Firestone Inst Resp Hlth, Asthma Res Grp, Hamilton, ON L8N 4A6, Canada	Inman, MD (reprint author), St Josephs Hosp, Firestone Inst Resp Hlth, Asthma Res Grp, Hamilton, ON L8N 4A6, Canada.		Hancox, Robert/G-4746-2011				Aldridge RE, 2000, AM J RESP CRIT CARE, V161, P1459; Cockcroft DW, 1996, THORAX, V51, P1051, DOI 10.1136/thx.51.10.1051; Gauvreau GM, 1997, AM J RESP CRIT CARE, V156, P1738; GROVE A, 1995, LANCET, V346, P201, DOI 10.1016/S0140-6736(95)91265-7; Hancox RJ, 1999, EUR RESPIR J, V14, P283, DOI 10.1034/j.1399-3003.1999.14b08.x; Inman MD, 1996, AM J RESP CRIT CARE, V153, P65; Jones SL, 2001, EUR RESPIR J, V17, P368, DOI 10.1183/09031936.01.17303680; LARSSON K, 1992, CHEST, V101, P953, DOI 10.1378/chest.101.4.953; NEWNHAM DM, 1995, THORAX, V50, P497, DOI 10.1136/thx.50.5.497; Pauwels RA, 1997, NEW ENGL J MED, V337, P1405, DOI 10.1056/NEJM199711133372001; RAMAGE L, 1994, RESP MED, V88, P363, DOI 10.1016/0954-6111(94)90042-6; ROBERTSON CF, 1990, MED J AUSTRALIA, V152, P511; Taylor DR, 1998, THORAX, V53, P744; Wraight JM, 2001, RESPIROLOGY, V6, pA48	14	87	91	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.	APR 15	2002	165	8					1068	1070		10.1164/rccm.200111-091BC		3	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	542CX	WOS:000175026900009	11956046	
J	Gerberick, GF; Robinson, MK; Felter, SP; White, IR; Basketter, DA				Gerberick, GF; Robinson, MK; Felter, SP; White, IR; Basketter, DA			Understanding fragrance allergy using an exposure-based risk assessment approach	CONTACT DERMATITIS			English	Article						skin; allergic contact sensitization; fragrances; exposure; potency; risk assessment; margin of safety	LYMPH-NODE ASSAY; SODIUM LAURYL SULFATE; SKIN SENSITIZATION RISK; CONTACT SENSITIZATION; CINNAMIC-ALDEHYDE; GUINEA-PIG; ACTIVATION; DERMATITIS; RESPONSES; TESTS	Conducting a sound skin sensitization risk assessment prior to the introduction of new ingredients and products into the market place is essential. The process by which low-molecular-weight chemicals induce and elicit skin sensitization is dependent on many factors, including the ability of the chemical to penetrate the skin, react with protein, and trigger a cell-mediated immune response. Based on our chemical, cellular and molecular understanding of allergic contact dermatitis, it is possible to carry out a quantitative risk assessment. Specifically, by estimating the exposure to the allergen and its allergenic potency, it is feasible to assess quantitatively the sensitization risk of an ingredient in a particular product type. This paper focuses on applying exposure-based risk assessment tools to understanding fragrance allergy for 2 hypothetical products containing the fragrance allergen cinnamic aldehyde. The risk assessment process predicts that an eau de toilette leave-on product containing 1000 ppm or more cinnamic aldehyde would pose an unacceptable risk of induction of skin sensitization, while a shampoo, containing the same level of cinnamic aldehyde, would pose an acceptable risk of induction of skin sensitization, based on limited exposure to the ingredient from a rinse-off product application.	Procter & Gamble Co, Miami Valley Labs, Cincinnati, OH USA; St Thomas Hosp, St Johns Inst Dermatol, London SE1 7EH, England; Unilever, SEAC Toxicol Unit, Sharnbrook, Beds, England	Gerberick, GF (reprint author), Procter & Gamble Co, Miami Valley Labs, Cincinnati, OH USA.			Robinson, Michael/0000-0002-6914-8543			Andersen KE, 1995, ACTA DERM-VENEREOL, V75, P463; Andersen K. E., 1985, CURRENT PROBLEMS DER, V14, P59; Basketter D. A., 1998, International Journal of Cosmetic Science, V20, P141, DOI 10.1046/j.1467-2494.1998.171746.x; Basketter DA, 2000, CONTACT DERMATITIS, V42, P344, DOI 10.1034/j.1600-0536.2000.042006344.x; Basketter DA, 1999, CONTACT DERMATITIS, V40, P150, DOI 10.1111/j.1600-0536.1999.tb06013.x; Basketter DA, 1996, FOOD CHEM TOXICOL, V34, P985, DOI 10.1016/S0278-6915(96)00059-2; BASKETTER DA, 1999, COMMENTS TOXICOL, V7, P79; Robinson M., 1996, TOXICOLOGY CONTACT H, P152; BOTHAM PA, 1991, FOOD CHEM TOXICOL, V29, P275, DOI 10.1016/0278-6915(91)90025-3; Buckley DA, 2000, BRIT J DERMATOL, V142, P279, DOI 10.1046/j.1365-2133.2000.03298.x; CUMBERBATCH M, 1993, TOXICOLOGY, V77, P181, DOI 10.1016/0300-483X(93)90148-L; DANNEMAN PJ, 1983, FOOD CHEM TOXICOL, V21, P721, DOI 10.1016/0278-6915(83)90203-X; Dearman RJ, 1999, J APPL TOXICOL, V19, P299, DOI 10.1002/(SICI)1099-1263(199909/10)19:5<299::AID-JAT591>3.0.CO;2-C; DeGroot AC, 1997, CONTACT DERMATITIS, V36, P57; European Centre for Ecotoxicology and Toxicology of Chemicals (ECETOC), 1994, 58 ECETOC; Effendy I, 1996, BRIT J DERMATOL, V135, P428; Environmental Protection Agency (EPA), 1999, EXP FACT HDB; EPA, 1992, US EPA PUBL; *EPA, 1998, US EPA PUBL; FRIEDMANN PS, 1983, CLIN EXP IMMUNOL, V53, P709; FRIEDMANN PS, 1983, BRIT J DERMATOL, V109, P86; FUNK JO, 1994, CONTACT DERMATITIS, V31, P236, DOI 10.1111/j.1600-0536.1994.tb01995.x; Gerberick G F, 2000, Am J Contact Dermat, V11, P65, DOI 10.1053/AC.2000.3191; Gerberick G F, 2000, Am J Contact Dermat, V11, P3; GERBERICK GF, 1993, AM J CONTACT DERMATI, V4, P205; GERBERICK GF, IN PRESS AM J CONTAC; Heylings JR, 1996, TOXICOLOGY, V109, P57, DOI 10.1016/0300-483X(96)03304-5; Hilton J, 1998, Am J Contact Dermat, V9, P29, DOI 10.1016/S1046-199X(98)90142-7; Johansen JD, 1996, CONTACT DERMATITIS, V34, P165, DOI 10.1111/j.1600-0536.1996.tb02167.x; Johansen JD, 2000, BRIT J DERMATOL, V142, P490, DOI 10.1046/j.1365-2133.2000.03362.x; KIMBER I, 1992, FOOD CHEM TOXICOL, V30, P165, DOI 10.1016/0278-6915(92)90153-C; KIMBER I, 1989, ARCH TOXICOL, V63, P274, DOI 10.1007/BF00278640; Kimber I, 1997, HUM ECOL RISK ASSESS, V3, P385; KLIGMAN AM, 1966, J INVEST DERMATOL, V47, P393, DOI 10.1038/jid.1966.160; Larsen W, 1996, Am J Contact Dermat, V7, P77, DOI 10.1016/S1046-199X(96)90078-0; LARSEN W, 1977, ARCH DERMATOL, V12, P623; LARSEN WG, 1985, J AM ACAD DERMATOL, V12, P1, DOI 10.1016/S0190-9622(85)70001-1; Lunder T, 2000, CONTACT DERMATITIS, V43, P107, DOI 10.1034/j.1600-0536.2000.043002107.x; MALTEN KE, 1984, CONTACT DERMATITIS, V11, P1, DOI 10.1111/j.1600-0536.1984.tb00162.x; McFadden JP, 1998, CONTACT DERMATITIS, V39, P79, DOI 10.1111/j.1600-0536.1998.tb05837.x; REES JL, 1990, BRIT J DERMATOL, V122, P29, DOI 10.1111/j.1365-2133.1990.tb08236.x; *RES I FRAGR MAT F, UNPUB ASS DAT; Robinson MK, 1996, FOOD CHEM TOXICOL, V34, P495, DOI 10.1016/0278-6915(96)87361-3; Robinson MK, 2000, CONTACT DERMATITIS, V42, P251, DOI 10.1034/j.1600-0536.2000.042005251.x; ROBINSON MK, 1989, FOOD CHEM TOXICOL, V27, P479, DOI 10.1016/0278-6915(89)90036-7; ROBINSON MK, 1991, FUND APPL TOXICOL, V17, P103, DOI 10.1016/0272-0590(91)90243-W; *SCI COMM COSM PRO, 1999, SCCNFP011999; *SCI COMM COSM PRO, 1999, SCCNFP001798; Seidenari S, 1996, CONTACT DERMATITIS, V34, P88, DOI 10.1111/j.1600-0536.1996.tb02136.x; WHITE SI, 1986, BRIT J DERMATOL, V115, P663, DOI 10.1111/j.1365-2133.1986.tb06646.x	50	87	87	1	8	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-1873			CONTACT DERMATITIS	Contact Dermatitis	DEC	2001	45	6					333	340		10.1034/j.1600-0536.2001.450603.x		8	Allergy; Dermatology	Allergy; Dermatology	512WP	WOS:000173346800003	11846748	
J	Vanacker, NJ; Palmans, E; Kips, JC; Pauwels, RA				Vanacker, NJ; Palmans, E; Kips, JC; Pauwels, RA			Fluticasone inhibits but does not reverse allergen-induced structural airway changes	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							BROWN-NORWAY RATS; INHALED CORTICOSTEROIDS; SMOOTH-MUSCLE; MURINE MODEL; MILD ASTHMA; SUBEPITHELIAL FIBROSIS; BASEMENT-MEMBRANE; ANTIGEN CHALLENGE; BRONCHIAL-ASTHMA; TERM TREATMENT	Ethical and technical reasons limit the possibility of evaluating the effects of inhaled corticosteroids on structural changes in airways of humans with asthma. We therefore evaluated whether fluticasone propionate (FP) modifies airway remodeling, induced by repeated allergen exposure in rats. Sensitized EN-rats were exposed to aerosolized ovalbumin (OA) for 2 wk. To assess the effect of FP on the development of or on established airway remodeling, animals were treated with aerosolized FP or placebo during allergen exposure or for 2 wk afterward. Compared with animals exposed to phosphate-buffered saline (PBS), OA-challenged animals developed an increase in total airway wall area, enhanced fibronectin deposition, epithelial cell proliferation, goblet cell hyperplasia, and airway hyperresponsiveness. Concomitant treatment with FP decreased all allergen-induced structural changes without being able to reverse them to normal. Initiating FP treatment after the allergen exposure had no effect on any of the OA-induced structural airway changes. The increase in total airway wall area, enhanced fibronectin deposition, and epithelial cell proliferation persisted. The goblet cell hyperplasia disappeared spontaneously. In conclusion, concomitant treatment with FP partly inhibits structural airway changes as well as hyperresponsiveness induced by OA exposure. Post hoc treatment fails to reverse established airway remodeling.	State Univ Ghent Hosp, Dept Resp Dis, B-9000 Ghent, Belgium	Vanacker, NJ (reprint author), State Univ Ghent Hosp, Dept Resp Dis, De Pintelaan 185, B-9000 Ghent, Belgium.						AGERTOFT L, 1994, RESP MED, V88, P373, DOI 10.1016/0954-6111(94)90044-2; Anstead G M, 1998, Adv Wound Care, V11, P277; Blyth DI, 1998, AM J RESP CELL MOL, V19, P38; Bousquet J, 2000, AM J RESP CRIT CARE, V161, P1720; BREWSTER CEP, 1990, AM J RESP CELL MOL, V3, P507; Brieva JL, 2000, AM J RESP CRIT CARE, V161, P293; Chakir J, 1996, LAB INVEST, V75, P735; Cui ZH, 1999, ALLERGY, V54, P1074, DOI 10.1034/j.1398-9995.1999.00133.x; Druilhe A, 1998, AM J RESP CELL MOL, V19, P747; DUBAYBO BA, 1991, RES COMMUN CHEM PATH, V71, P365; HAAHTELA T, 1994, NEW ENGL J MED, V331, P700, DOI 10.1056/NEJM199409153311103; Herard AL, 1996, AM J PHYSIOL-LUNG C, V271, pL726; Hirst SJ, 1998, AM J RESP CRIT CARE, V158, pS201; Holgate ST, 2000, J ALLERGY CLIN IMMUN, V105, P193, DOI 10.1016/S0091-6749(00)90066-6; Hoshino M, 1999, J ALLERGY CLIN IMMUN, V104, P356, DOI 10.1016/S0091-6749(99)70379-9; Hoshino M, 1998, CLIN EXP ALLERGY, V28, P568; IGNOTZ RA, 1986, J BIOL CHEM, V261, P4337; Laitinen A, 1997, AM J RESP CRIT CARE, V156, P951; LUNDGREN R, 1988, EUR RESPIR J, V1, P883; Mathur M, 1999, AM J RESP CRIT CARE, V159, P580; Meerschaert J, 1999, AM J RESP CRIT CARE, V159, P619; Olivieri D, 1997, AM J RESP CRIT CARE, V155, P1864; Overbeek SE, 1996, CHEST, V110, P35, DOI 10.1378/chest.110.1.35; Palmans E, 2000, AM J RESP CRIT CARE, V161, P627; Pavlovic D, 1998, EUR RESPIR J, V11, P575; Pedersen S, 1997, Pediatr Pulmonol Suppl, V15, P22; ROCHE WR, 1989, LANCET, V1, P520; Salmon M, 1999, EUR RESPIR J, V14, P633, DOI 10.1034/j.1399-3003.1999.14c25.x; SAPIENZA S, 1991, AM REV RESPIR DIS, V144, P423; SELROOS O, 1995, CHEST, V108, P1228, DOI 10.1378/chest.108.5.1228; Shiels IA, 1999, INFLAMMATION, V23, P321; SOUSA AR, 1993, AM REV RESPIR DIS, V147, P1557; Stewart AG, 1995, BRIT J PHARMACOL, V116, P3219; Temelkovski J, 1998, THORAX, V53, P849; Tournoy KG, 2000, CLIN EXP ALLERGY, V30, P79; TRIGG CJ, 1994, AM J RESP CRIT CARE, V150, P17; Warshamana GS, 1998, AM J PHYSIOL-LUNG C, V274, pL499; WIGGS BR, 1992, AM REV RESPIR DIS, V145, P1251; YOUNG PG, 1995, EUR J PHARMACOL, V273, P137, DOI 10.1016/0014-2999(94)00679-2	39	87	104	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.	MAR	2001	163	3					674	679				6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	419HW	WOS:000167944100017	11254522	
J	Davis, PJ; Smales, CM; James, DC				Davis, PJ; Smales, CM; James, DC			How can thermal processing modify the antigenicity of proteins?	ALLERGY			English	Article; Proceedings Paper	Symposium on Immunological, Chemical and Clinical Problems of Food Allergy	MAR 11-13, 2001	VENICE, ITALY			antigenicity; thermal processing	HEATED PECAN NUT; MAILLARD REACTION; NEOALLERGENS; GLYCATION; N-EPSILON-(CARBOXYMETHYL)LYSINE; ANTIBODIES; PRODUCTS	This paper is a brief review of thermally induced covalent modifications to proteins in foods, focussing mainly on the advanced glycation end-products (AGE) of the Maillard reaction. Most foods are subjected to thermal processing, either in the home or during their production/manufacture. Thermal processing provides many beneficial effects, but also brings about major changes in allergenicity. Far from being a general way to decrease allergenic risk, thermal processing is as likely to increase allergenicity as to reduce it, through the introduction of neoantigens. These changes are highly complex and not easily predictable, but there are a number of major chemical pathways that lead to distinct patterns of modification. Perhaps the most important of these is through the reaction of protein amino groups with sugars, leading to an impressive cocktail of AGE-modified protein derivatives. These are antigenic and many of the important neoantigens found in cooked or stored foods are probably such Maillard reaction products. A deeper understanding of thermally induced chemical changes is essential for more advanced risk assessments, more effective QC protocols, production of more relevant diagnostic allergen extracts and the development of novel protein engineering and therapeutic approaches to minimise allergenic risk.	Unilever Res, Colworth Lab, Sharnbrook MK44 1LQ, Beds, England; Univ Kent, Res Sch Biosci, Canterbury, Kent, England	Davis, PJ (reprint author), Unilever Res, Colworth Lab, Sharnbrook MK44 1LQ, Beds, England.		James, David/N-3794-2015				BERENS L, 1974, CLIN EXP IMMUNOL, V17, P703; Berrens L, 1996, ALLERGY, V51, P277, DOI 10.1111/j.1398-9995.1996.tb00085.x; BLEUMINK E, 1966, NATURE, V212, P541, DOI 10.1038/212541a0; BUCALA R, 1996, DIAGN ENDOCRIN METAB, V14, P99; Codina R, 1998, INT ARCH ALLERGY IMM, V117, P120, DOI 10.1159/000023998; Davis PJ, 1998, ALLERGY, V53, P102; DOKE S, 1989, AGR BIOL CHEM TOKYO, V53, P1231; Ikeda K, 1998, J IMMUNOL METHODS, V215, P95, DOI 10.1016/S0022-1759(98)00064-7; Ikeda K, 1996, BIOCHEMISTRY-US, V35, P8075, DOI 10.1021/bi9530550; Kalluri R, 2000, J BIOL CHEM, V275, P20027, DOI 10.1074/jbc.M904549199; Kilara Arun, 1996, P71; Malanin K, 1995, ALLERGY, V50, P988, DOI 10.1111/j.1398-9995.1995.tb02513.x; Maleki SJ, 2000, J ALLERGY CLIN IMMUN, V106, P763, DOI 10.1067/mai.2000.109620; Prausnitz C, 1921, ZBL BAKT           1, V86, P160; Prowse CV, 1998, BLOOD REV, V12, P99, DOI 10.1016/S0268-960X(98)90021-2; REDDY S, 1995, BIOCHEMISTRY-US, V34, P10872, DOI 10.1021/bi00034a021; ROSEN JP, 1994, J ALLERGY CLIN IMMUN, V93, P1068, DOI 10.1016/S0091-6749(94)70056-7; Smales CM, 2000, BIOTECHNOL APPL BIOC, V32, P109, DOI 10.1042/BA20000032; SUAREZ G, 1989, J BIOL CHEM, V264, P3674; Urisu A, 1997, J ALLERGY CLIN IMMUN, V100, P171, DOI 10.1016/S0091-6749(97)70220-3	20	87	97	1	18	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy		2001	56			67			56	60		10.1034/j.1398-9995.2001.00918.x		5	Allergy; Immunology	Allergy; Immunology	448PA	WOS:000169634200015	11298011	
J	Mallol, J; Sole, D; Asher, I; Clayton, T; Stein, R; Soto-Quiroz, M				Mallol, J; Sole, D; Asher, I; Clayton, T; Stein, R; Soto-Quiroz, M		Latin Amer ISAAC Collaborators Grp	Prevalence of asthma symptoms in Latin America: The International Study of Asthma and Allergies in Childhood (ISAAC)	PEDIATRIC PULMONOLOGY			English	Article						asthma; children; epidemiology; Latin America; ISAAC; prevalence	CHILDREN; AUSTRALIA; GERMANY	The prevalence of respiratory symptoms indicative of asthma in children from Latin America has been largely ignored. As part of the International Study of Asthma and Allergies in Childhood (ISAAC), 17 centers in 9 different Latin American countries participated in the study, and data from 52,549 written questionnaires (WQ) in children aged 13-14 years and from 36,264 WQ in 6-7 year olds are described here. In children aged 13-14 years, the prevalence of asthma ever ranged from 5.5-28%, and the prevalence of wheezing in the last 12 months from 6.6-27%. In children aged 6-7 years, the prevalence of asthma ever ranged from 4.1-26.9%, and the prevalence of wheezing in the last 12 months ranged from 8.6-32.1%. The lower prevalence in centers with higher levels of atmospheric pollution suggests that chronic inhalation of polluted air in children does not contribute to asthma. Furthermore, the high figures for asthma in a region with a high level of gastrointestinal parasite infestation, and a high burden of acute respiratory infections occurring early in life, suggest that these factors, considered as protective in other regions, do not have the same effect in this region. The present study indicates that the prevalence of asthma and related symptoms in Latin America is as high and variable as described in industrialized or developed regions of the world. Pediatr Pulmonol. 2000; 30:439-444. (C) 2000 Wiley-Liss. Inc.	Univ Santiago Chile, Dept Pediat Resp Med, Santiago, Chile; Univ Fed Sao Paulo, Div Allergy, Sao Paulo, Brazil; Univ Auckland, Dept Paediat, Auckland 1, New Zealand; Catholic Univ, Pediat Pulm Unit, Porto Alegre, RS, Brazil	Mallol, J (reprint author), Univ Santiago Chile, Dept Pediat Resp Med, Clasificador 23,Correo 9, Santiago, Chile.		Clayton, Tadd/B-7914-2009; Sole, Dirceu/D-7789-2013; Stein, Renato/K-2568-2014; Jones, Marcus/A-3580-2011; Asher, Innes/O-2604-2016	Jones, Marcus/0000-0002-8263-1265; Asher, Innes/0000-0003-1768-3832			Asher MI, 1998, EUR RESPIR J, V12, P315; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; ASHER MI, 1988, AM REV RESPIR DIS, V138, P524; Burney P, 1996, EUR RESPIR J, V9, P687; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; BURR ML, 1994, INT J EPIDEMIOL, V23, P341, DOI 10.1093/ije/23.2.341; CARRASCO E, 1987, CHEST S, V91, P93; CARTERPOKRAS OD, 1993, AM J PUBLIC HEALTH, V83, P580, DOI 10.2105/AJPH.83.4.580; DENNY FW, 1995, AM J RESP CRIT CAR S, V152, P5; KEELEY DJ, 1991, THORAX, V46, P549, DOI 10.1136/thx.46.8.549; LEUNG R, 1994, THORAX, V49, P1205, DOI 10.1136/thx.49.12.1205; LOPEZANTUNANOF J, 1997, RESP INFECT CHILDREN, P3; Lynch NR, 1997, AM J RESP CRIT CARE, V156, P50; OYARZUN M, 1993, AM REV RESPIR DIS, V147, P826; PEARCE N, 1993, EUR RESPIR J, V6, P1455; ROBERTSON CF, 1991, BRIT MED J, V302, P1116; ROBERTSON CF, 1993, PEDIATR PULM, V16, P219, DOI 10.1002/ppul.1950160403; ROBERTSON CF, 1995, CLIN PAEDIAT ASTHMA, P253; SOTOQUIROS M, 1994, CLIN EXP ALLERGY, V24, P1130; VONMUTIUS E, 1992, BRIT MED J, V305, P1395	20	87	101	0	4	WILEY-LISS	NEW YORK	DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA	8755-6863			PEDIATR PULM	Pediatr. Pulmonol.	DEC	2000	30	6					439	444		10.1002/1099-0496(200012)30:6<439::AID-PPUL1>3.0.CO;2-E		6	Pediatrics; Respiratory System	Pediatrics; Respiratory System	380CN	WOS:000165680900001	11109054	
J	Thorne, PS				Thorne, PS			Inhalation toxicology models of endotoxin- and bioaerosol-induced inflammation	TOXICOLOGY			English	Article; Proceedings Paper	Symposium on Indoor Environmental Factors Enhancing Allergic Immune Response: Focus on Endotoxin and Particles	JUN   26, 1999	OSLO, NORWAY	EUROTOX, Immunotoxicol & Chem Allergy Special Sect		inhalation toxicology; exposure chambers; bioaerosols; endotoxin; glucans	PULMONARY HYPERSENSITIVITY RESPONSES; POLYMERASE CHAIN-REACTION; MURINE MODEL; GUINEA-PIGS; COTTON DUST; RAT NASAL; (1->3)-BETA-D-GLUCAN; BACTERIA; SYSTEM; HYBRIDIZATION	Inhalation toxicology studies in rodents have proven their usefulness for furthering our understanding of the causal agents, mechanisms, and pathology associated with exposures to environmental endotoxins and bioaerosols. Inhalation animal models are used to determine which components of a mixture are the most important toxicants for inducing the observed adverse outcome. They are used to obtain exposure-response relationships for allergens and pro-inflammatory agents to help elucidate disease mechanisms and contribute quantitative data to the risk assessment process. Inhalation models serve as important adjuncts to epidemiology studies and human exposure studies. They are also useful for establishing phenotype in studies of genetic polymorphisms and disease susceptibility and are widely applied for evaluation of safety and efficacy for potential therapeutic agents. In order to produce reliable data, rigorous exposure chamber design, aerosol generation systems, exposure quantitation and experimental protocols must be utilized. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.	Univ Iowa, Coll Publ Hlth, Dept Environm & Occupat Hlth, Iowa City, IA 52242 USA	Thorne, PS (reprint author), Univ Iowa, Coll Publ Hlth, Dept Environm & Occupat Hlth, Iowa City, IA 52242 USA.						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S., 1992, COMP BIOL NORMAL LUN, P37	47	87	89	0	6	ELSEVIER SCI IRELAND LTD	CLARE	CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND	0300-483X			TOXICOLOGY	Toxicology	NOV 2	2000	152	1-3					13	23		10.1016/S0300-483X(00)00287-0		11	Pharmacology & Pharmacy; Toxicology	Pharmacology & Pharmacy; Toxicology	379EC	WOS:000165627100003	11090935	
J	Farr, BM; Bartlett, CLR; Wadsworth, J; Miller, DL				Farr, BM; Bartlett, CLR; Wadsworth, J; Miller, DL		British Thoracic Soc Pneumonia Stu	Risk factors for community-acquired pneumonia diagnosed upon hospital admission	RESPIRATORY MEDICINE			English	Article						case-control study; chronic obstructive pulmonary disease; congestive heart failure; epidemiology; occupational; pneumonia; risk factors; smoking	BACTERIAL PNEUMONIA; ETIOLOGY; MORTALITY; EPIDEMIOLOGY; INFECTION; SMOKING	A case-control study of risk factors for community-acquired pneumonia in adults admitted to hospital is reported. Cases were surviving patients (n = 178) admitted to 14 hospitals in England. Controls were individuals (n = 385) randomly selected from the electoral registers of the areas served by the hospitals. The two groups were compared with regard to risk factors for pneumonia using a standardized postal questionnaire. Independent risk factors associated with cases in log-linear regression analysis were age, heart disease (as indicated by congestive heart Failure and/or digitalis treatment), lifetime smoking history, chronic airway disease (chronic bronchitis and/or asthma), occupational dust exposure, pneumonia as a child, single marital status and unemployment. Corticosteroid and bronchodilator therapy were also independent risk factors in the log-linear regression analysis, but may reflect the severity of underlying lung disease for which these drugs were prescribed. These data suggest that cigarette smoking is the major avoidable risk factor for acute pneumonia in adults.	Univ Virginia, Sch Med, Dept Internal Med, Charlottesville, VA 22908 USA; Univ London, St Marys Hosp, Sch Med, Dept Epidemiol & Publ Hlth, London, England; Publ Hlth Lab Serv, Ctr Communicable Dis Surveillance, London NW9 5EQ, England	Farr, BM (reprint author), Univ Virginia, Sch Med, Dept Internal Med, Box 800743, Charlottesville, VA 22908 USA.						Aguirre I, 1993, Aten Primaria, V12, P359; ANDREWS BE, 1987, Q J MED, V62, P195; AUSTRIAN R, 1964, ANN INTERN MED, V60, P759; BAKER RJ, 1978, OXFORD NUMERICAL ALG; BATES JH, 1992, CHEST, V101, P1005, DOI 10.1378/chest.101.4.1005; BATH JCJL, 1964, BRIT J DIS CHEST, V58, P1, DOI 10.1016/S0007-0971(64)80017-6; BERKSON J, 1946, BIOMETRICS BULL, V2, P47, DOI 10.2307/3002000; Broome C V, 1979, Epidemiol Rev, V1, P1; CAIAFFA WT, 1993, AM J EPIDEMIOL, V138, P909; Centers for disease control and prevention (CDC), 1988, MMWR-MORBID MORTAL W, V37, P593; CHARLTON JRH, 1983, LANCET, V1, P691; COLBY JRT, 1974, LANCET, V2, P1031; DOLL R, 1976, BRIT MED J, V2, P1525; FANG GD, 1990, MEDICINE, V69, P307; Farr BM, 2000, RESP MED, V94, P422, DOI 10.1053/rmed.1999.0743; FARR BM, 1991, ANN INTERN MED, V115, P428; Fekety F R Jr, 1971, Am Rev Respir Dis, V104, P499; FERGUSSON DM, 1981, J EPIDEMIOL COMMUN H, V35, P180, DOI 10.1136/jech.35.3.180; JAY SJ, 1975, NEW ENGL J MED, V293, P798, DOI 10.1056/NEJM197510162931604; JOKINEN C, 1993, AM J EPIDEMIOL, V137, P977; KLIMEK JJ, 1983, AM J INFECT CONTROL, V11, P79, DOI 10.1016/0196-6553(83)90117-7; KOIVULA I, 1994, AM J MED, V96, P313, DOI 10.1016/0002-9343(94)90060-4; LACROIX AZ, 1989, PUBLIC HEALTH REP, V104, P350; LANGE P, 1995, EUR RESPIR J, V8, P1695; LIM I, 1989, MED J AUSTRALIA, V151, P87; LIPSKY BA, 1986, ARCH INTERN MED, V146, P2179, DOI 10.1001/archinte.146.11.2179; MACFARLANE JT, 1982, LANCET, V2, P255; Marrie T J, 1990, Semin Respir Infect, V5, P260; MCNABB WR, 1984, J ROY SOC MED, V77, P550; MERCER J, 1985, POSTGRAD MED J, V61, P713; MOINE P, 1994, CHEST, V105, P1487, DOI 10.1378/chest.105.5.1487; MOORE MA, 1977, JOHNS HOPKINS MED J, V140, P9; MORRIS K, 1990, AM J DIS CHILD, V144, P105; MUFSON MA, 1967, AM J EPIDEMIOL, V86, P526; *OFF NAT STAT, 1998, STAT OFF DH2, V23; ORT S, 1983, JAMA-J AM MED ASSOC, V249, P214, DOI 10.1001/jama.249.2.214; PROUT S, 1983, S AFR MED J, V64, P443; SAS, 1985, SAS US GUID STAT; SULLIVAN RJ, 1972, ARCH INTERN MED, V129, P935, DOI 10.1001/archinte.129.6.935; TORRES A, 1991, AM REV RESPIR DIS, V144, P312; US Department of Health and Human Services, 1984, DHHS PUBL; WHITE RJ, 1981, THORAX, V36, P566, DOI 10.1136/thx.36.8.566; WOODHEAD MA, 1987, LANCET, V1, P671; 1988, MMWR, V37, P249; 1995, MMWR, V44, P535	45	87	93	0	3	W B SAUNDERS CO LTD	LONDON	24-28 OVAL RD, LONDON NW1 7DX, ENGLAND	0954-6111			RESP MED	Respir. Med.	OCT	2000	94	10					954	963		10.1053/rmed.2000.0865		10	Cardiac & Cardiovascular Systems; Respiratory System	Cardiovascular System & Cardiology; Respiratory System	366RE	WOS:000090017700005	11059948	
J	Palmer, LJ; Burton, PR; Faux, JA; James, AL; Musk, AW; Cookson, WOCM				Palmer, LJ; Burton, PR; Faux, JA; James, AL; Musk, AW; Cookson, WOCM			Independent inheritance of serum immunoglobulin E concentrations and airway responsiveness	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							SKIN-TEST REACTIVITY; COMMUNITY POPULATION-SAMPLE; BRONCHIAL RESPONSIVENESS; QUANTITATIVE TRAIT; GENERAL-POPULATION; ASTHMA; IGE; PREVALENCE; ATOPY; TWINS	Elevated serum Immunoglobulin E (IgE) levels and increased airway responsiveness (AR) are correlated traits that are characteristic of asthma. It is not known to what extent these traits arise from distinct or shared genetic determinants. We investigated the genetic and environmental components of variance of serum total and specific IgE levels and AR in an Australian population-based sample of 232 Caucasian nuclear families. The inter-relationships of the genetic determinants of these traits were also investigated. Log, total serum IgE levels had a narrow-sense heritability (h(N)(2)) of 47.3% (SE = 10.0%). Specific serum IgE levels against house dust mite and timothy grass, measured as a RAST Index, ad a h(N)(2) Of 33.8% (SE = 7.3%). AR, quantified by the log, dose-response slope to methacholine (DRS), had a h(N)(2) of 30.0% (SE = 12.3%). Extended modeling demonstrated an approximate 70% overlap in the genetic determinants of total and specific serum IgE levels. The genetic determinants of serum IgE levels and AR exhibited less than 30% sharing. These data are consistent with the existence of multiple genetic determinants of the pathophysiologic traits associated with asthma, and suggest that AR is genetically distinct from atopy. These results have implications for gene discovery programs.	Case Western Reserve Univ, Dept Epidemiol & Biostat, Cleveland, OH 44106 USA; Univ Leicester, Dept Epidemiol & Publ Hlth, Genet Epidemiol Unit, Leicester, Leics, England; John Radcliffe Hosp, Nuffield Dept Clin Med, Oxford OX3 9DU, England; Univ Perth, Dept Med, Dept Pulm Physiol, Perth, WA, Australia; Sir Charles Gairdiner Hosp, Dept Resp Med, Perth, WA, Australia; TVW Telethon Inst Child Hlth Res, Div Populat Sci, Genet Epidemiol Unit, Perth, WA, Australia	Palmer, LJ (reprint author), Harvard Univ, Sch Med, Channing Lab, 181 Longwood Ave, Boston, MA 02115 USA.		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J	Violari, A; Lindsey, JC; Hughes, MD; Mujuru, HA; Barlow-Mosha, L; Kamthunzi, P; Chi, BH; Cotton, MF; Moultrie, H; Khadse, S; Schimana, W; Bobat, R; Purdue, L; Eshleman, SH; Abrams, EJ; Millar, L; Petzold, E; Mofenson, LM; Jean-Philippe, P; Palumbo, P				Violari, Avy; Lindsey, Jane C.; Hughes, Michael D.; Mujuru, Hilda A.; Barlow-Mosha, Linda; Kamthunzi, Portia; Chi, Benjamin H.; Cotton, Mark F.; Moultrie, Harry; Khadse, Sandhya; Schimana, Werner; Bobat, Raziya; Purdue, Lynette; Eshleman, Susan H.; Abrams, Elaine J.; Millar, Linda; Petzold, Elizabeth; Mofenson, Lynne M.; Jean-Philippe, Patrick; Palumbo, Paul			Nevirapine versus Ritonavir-Boosted Lopinavir for HIV-Infected Children	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							SINGLE-DOSE NEVIRAPINE; RANDOMIZED CONTROLLED-TRIAL; ANTIRETROVIRAL THERAPY; PROTEASE INHIBITOR; DRUG-RESISTANCE; GROWTH; INITIATION; DYNAMICS; EXPOSURE; FAILURE	BACKGROUND Nevirapine-based antiretroviral therapy is the predominant (and often the only) regimen available for children in resource-limited settings. Nevirapine resistance after exposure to the drug for prevention of maternal-to-child human immunodeficiency virus (HIV) transmission is common, a problem that has led to the recommendation of ritonavir-boosted lopinavir in such settings. Regardless of whether there has been prior exposure to nevirapine, the performance of nevirapine versus ritonavir-boosted lopinavir in young children has not been rigorously established. METHODS In a randomized trial conducted in six African countries and India, we compared the initiation of HIV treatment with zidovudine, lamivudine, and either nevirapine or ritonavir-boosted lopinavir in HIV-infected children 2 to 36 months of age who had no prior exposure to nevirapine. The primary end point was virologic failure or discontinuation of treatment by study week 24. RESULTS A total of 288 children were enrolled; the median percentage of CD4+ T cells was 15%, and the median plasma HIV type 1 (HIV-1) RNA level was 5.7 log(10) copies per milliliter. The percentage of children who reached the primary end point was significantly higher in the nevirapine group than in the ritonavir-boosted lopinavir group (40.8% vs. 19.3%; P < 0.001). Among the nevirapine-treated children with virologic failure for whom data on resistance were available, more than half (19 of 32) had resistance at the time of virologic failure. In addition, the time to a protocol-defined toxicity end point was shorter in the nevirapine group (P=0.04), as was the time to death (P=0.06). CONCLUSIONS Outcomes were superior with ritonavir-boosted lopinavir among young children with no prior exposure to nevirapine. Factors that may have contributed to the suboptimal results with nevirapine include elevated viral load at baseline, selection for nevirapine resistance, background regimen of nucleoside reverse-transcriptase inhibitors, and the standard ramp-up dosing strategy. The results of this trial present policymakers with difficult choices. (Funded by the National Institute of Allergy and Infectious Diseases and others; P1060 ClinicalTrials.gov number, NCT00307151.)	[Violari, Avy] Univ Witwatersrand, Perinatal HIV Res Unit, ZA-2050 Johannesburg, South Africa; [Mujuru, Hilda A.] Univ Witwatersrand, Reprod Hlth & HIV Inst, Fac Hlth Sci, Johannesburg, South Africa; [Cotton, Mark F.] Univ Stellenbosch, Tygerberg Childrens Hosp, ZA-7505 Tygerberg, South Africa; [Bobat, Raziya] Univ KwaZulu Natal, Nelson R Mandela Sch Med, Durban, South Africa; [Lindsey, Jane C.; Hughes, Michael D.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA; [Mujuru, Hilda A.] Univ Zimbabwe, Coll Hlth Sci, Dept Paediat & Child Hlth, Harare, Zimbabwe; [Barlow-Mosha, Linda] Johns Hopkins Univ, Res Collaborat, Makerere Univ, Kampala, Uganda; [Kamthunzi, Portia] Univ N Carolina Project, Lilongwe, Malawi; [Chi, Benjamin H.] Ctr Infect Dis Res Zambia, Lusaka, Zambia; [Khadse, Sandhya] BJ Med Coll & Sassoon Gen Hosp, Dept Pediat, Pune, Maharashtra, India; [Schimana, Werner] Duke Univ, Kilimanjaro Christian Med Ctr Collaborat, Moshi, Tanzania; [Purdue, Lynette] NIAID, NIH, Div Aids, Pharmaceut Affairs Branch, Bethesda, MD 20892 USA; [Jean-Philippe, Patrick] NIAID, NIH, Div Aids, Henry Jackson Fdn, Bethesda, MD 20892 USA; [Petzold, Elizabeth] Social & Sci Syst, Silver Spring, MD USA; [Mofenson, Lynne M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pediat Adolescent & Maternal AIDS Branch, NIH, Rockville, MD USA; [Eshleman, Susan H.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA; [Abrams, Elaine J.] Columbia Univ, Sch Publ Hlth, Int Ctr AIDS Care Program, New York, NY USA; [Abrams, Elaine J.] Columbia Univ, Sch Publ Hlth, Treatment Program, New York, NY USA; [Abrams, Elaine J.] Columbia Univ Coll Phys & Surg, New York, NY 10032 USA; [Millar, Linda] Frontier Sci & Technol Res Fdn Inc, Amherst, NY USA; [Palumbo, Paul] Dartmouth Med Sch, Lebanon, NH USA	Palumbo, P (reprint author), Dartmouth Hitchcock Med Ctr, Int Pediat HIV Program, 1 Med Ctr Dr, Lebanon, NH 03756 USA.	paul.e.palumbo@dartmouth.edu		Mofenson, Lynne/0000-0002-2818-9808	National Institute of Allergy and Infectious Diseases (NIAID) [U01 AI068632]; Eunice Kennedy Shriver National Institute of Child Health and Human Development; National Institute of Mental Health [U01 AI068632, 5 U01 AI41110, 1 U01 AI068616]; NIAID [HHSN272200800014C]; Abbott; Tibotec; Boehringer Ingelheim; Pfizer; Medicines Development; GlaxoSmithKline; ViiV Healthcare	Supported by a grant [U01 AI068632] from the National Institute of Allergy and Infectious Diseases (NIAID), the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and the National Institute of Mental Health to the Pediatric AIDS Clinical Trials Group (PACTG) and the International Maternal Pediatric Adolescent AIDS Clinical Trials (IMPAACT) Group; the Statistical and Data Analysis Center at Harvard School of Public Health under NIAID cooperative agreements (5 U01 AI41110 with the PACTG and 1 U01 AI068616 and U01 AI068632 with the IMPAACT Group); and by a contract from the NIAID (HHSN272200800014C).; Dr. Avy Violari reports receiving lecture fees from Abbott, consulting fees from Tibotec, and trial drugs from GlaxoSmithKline; Dr. Hughes, consulting fees from Boehringer Ingelheim, Pfizer, Medicines Development, and Tibotec and support for a scientific workshop from Merck; Dr. Cotton, lecture fees from Abbott; and Dr. Moultrie, grants from GlaxoSmithKline, ViiV Healthcare, and Tibotec. No other potential conflict of interest relevant to this article was reported.	Aldrovandi GM, 2009, AIDS, V23, P661, DOI 10.1097/QAD.0b013e3283269dfb; Babiker A, 2011, LANCET INFECT DIS, V11, P273, DOI 10.1016/S1473-3099(10)70313-3; Boltz VF, 2011, P NATL ACAD SCI USA, V108, P9202, DOI 10.1073/pnas.1105688108; Buchacz K, 2001, PEDIATRICS, V108, DOI 10.1542/peds.108.4.e72; Coovadia A, 2010, JAMA-J AM MED ASSOC, V304, P1082, DOI 10.1001/jama.2010.1278; Dreimane D, 2001, PEDIATR INFECT DIS J, V20, P315, DOI 10.1097/00006454-200103000-00020; Hunt GM, 2011, AIDS, V25, P1461, DOI 10.1097/QAD.0b013e3283492180; Li JZ, 2011, JAMA-J AM MED ASSOC, V305, P1327, DOI 10.1001/jama.2011.375; Lockman S, 2010, NEW ENGL J MED, V363, P1499, DOI 10.1056/NEJMoa0906626; Luzuriaga K, 1999, J VIROL, V73, P362; Mulenga V, 2010, CLIN INFECT DIS, V51, P1081, DOI 10.1086/656628; Nachman SA, 2002, ARCH PEDIAT ADOL MED, V156, P497; Palumbo P, 2007, J INFECT DIS, V196, P23, DOI 10.1086/518508; Palumbo P, 2010, NEW ENGL J MED, V363, P1510, DOI 10.1056/NEJMoa1000931; Violari A, 2008, NEW ENGL J MED, V359, P2233, DOI 10.1056/NEJMoa0800971; [Anonymous], 2010, ANT THER HIV INF INF	16	86	88	0	6	MASSACHUSETTS MEDICAL SOC	WALTHAM	WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA	0028-4793			NEW ENGL J MED	N. 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J	Ko, TM; Chung, WH; Wei, CY; Shih, HY; Chen, JK; Lin, CH; Chen, YT; Hung, SI				Ko, Tai-Ming; Chung, Wen-Hung; Wei, Chun-Yu; Shih, Han-Yu; Chen, Jung-Kuei; Lin, Chia-Hsien; Chen, Yuan-Tsong; Hung, Shuen-Iu			Shared and restricted T-cell receptor use is crucial for carbamazepine-induced Stevens-Johnson syndrome	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Drug hypersensitivity; T-cell receptor; HLA; third complementarity-determining region; Stevens-Johnson syndrome; toxic epidermal necrolysis	TOXIC EPIDERMAL NECROLYSIS; HLA-B-ASTERISK-1502 ALLELE; DRUG HYPERSENSITIVITY; LIVER-INJURY; HAN CHINESE; OXCARBAZEPINE; RISK; ASSOCIATION; ACTIVATION; CLONES	Background: Stevens-Johnson syndrome (SJS) and its related disease, toxic epidermal necrolysis (TEN), are life-threatening drug hypersensitivities with robust immune responses to drugs. Despite the strong HLA predisposition to drug hypersensitivities, such as HLA-B*1502 to carbamazepine (CBZ)-induced SJS/TEN, it remains unknown whether particular T-cell receptors (TCRs) participate in recognition of small drug/peptide-HLA complexes. Objective: Using the strong HLA predisposition in patients with CBZ-induced SJS/TEN as a model, we aimed to study the use of TCR repertoire in patients with drug hypersensitivity. Method: We enrolled patients with CBZ-SJS/TEN, tolerant control subjects, and healthy subjects who had no history of CBZ exposure. We isolated PBMCs from the subjects, cultured CBZ-specific T cells, and globally investigated the expression level and third complementarity-determining region length distribution of the TCR profile. We further assessed the pathogenic role of the disease-specific clonotype using real-time PCR-based tests and functional analysis. Results: On drug stimulation, CBZ-specific CD8(+) T cells were expanded in vitro and activated to release granulysin. Notably, VB-11-ISGSY was identified as the most predominant clonotype and shared among different subjects. This clonotype was present in 16 (84%) of 19 patients with SJS/TEN, absent in all 17 tolerant patients, and present at a low frequency in healthy subjects (4/29 [14%]). CBZ-specific cytotoxicity could be primed in vitro in the PBMCs of healthy subjects who are carriers of HLA-B*1502 and VB-11-ISGSY; this cytotoxicity could be blocked by an anti-TCR-VB-11 antibody. Furthermore, a single T-cell clone expressing VA-22-FISGTY/VB-11-ISGSY showed significant cytotoxicity against HLA-B*1502-positive antigen-presenting cells and CBZ. Conclusion: This study establishes the key role of the TCR in the pathogenic mechanism of SJS/TEN, explains why some HLA-B*1502 carriers are tolerant to CBZ, and provides a biomarker profile for drug hypersensitivity. (J Allergy Clin Immunol 2011;128:1266-76.)	[Hung, Shuen-Iu] Natl Yang Ming Univ, Inst Pharmacol, Sch Med, Taipei 11221, Taiwan; [Ko, Tai-Ming; Shih, Han-Yu; Chen, Yuan-Tsong] Natl Taiwan Univ, Coll Med, Grad Inst Microbiol, Taipei 10764, Taiwan; [Ko, Tai-Ming; Wei, Chun-Yu; Shih, Han-Yu; Chen, Jung-Kuei; Lin, Chia-Hsien; Chen, Yuan-Tsong; Hung, Shuen-Iu] Acad Sinica, Inst Biomed Sci, Taipei 11529, Taiwan; [Chung, Wen-Hung] Chang Gung Mem Hosp, Dept Dermatol, Taipei 10591, Taiwan; [Hung, Shuen-Iu] Natl Yang Ming Univ, Infect & Immun Res Ctr, Taipei 11221, Taiwan	Hung, SI (reprint author), Natl Yang Ming Univ, Inst Pharmacol, Sch Med, 155 Linong St,Sect 2, Taipei 11221, Taiwan.	chen0010@ibms.sinica.edu.tw; sihung@ym.edu.tw			National Science Council, Taiwan [NSC95-2314-B-010-096, 95-2314-B-182A-048, 95-3112-B-001-010, 95-3112-B-001-011, 96-2320-B-010-021-MY2, 96-2628-B-182A-065-MY2, NSC 97-2745-B-010-001, 98-2320-B-010-002-MY3, 98-2314-B-182A-027-MY3]; Taiwanese Ministry of Education; Academia Sinica Thematic Research Program [AS 99 TP B12]; Chang-Gung Memorial Hospital	Supported by grants from the National Science Council, Taiwan (NSC95-2314-B-010-096, 95-2314-B-182A-048, 95-3112-B-001-010, 95-3112-B-001-011, 96-2320-B-010-021-MY2, 96-2628-B-182A-065-MY2, NSC 97-2745-B-010-001, 98-2320-B-010-002-MY3, 98-2314-B-182A-027-MY3); the Taiwanese Ministry of Education (Aim for the Top University Plan, National Yang-Ming University); the Academia Sinica Thematic Research Program (AS 99 TP B12); and Chang-Gung Memorial Hospital.	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Allergy Clin. Immunol.	DEC	2011	128	6					1266	U624		10.1016/j.jaci.2011.08.013		22	Allergy; Immunology	Allergy; Immunology	865WX	WOS:000298342700016	21924464	
J	Kremmyda, LS; Vlachava, M; Noakes, PS; Diaper, ND; Miles, EA; Calder, PC				Kremmyda, Lefkothea-Stella; Vlachava, Maria; Noakes, Paul S.; Diaper, Norma D.; Miles, Elizabeth A.; Calder, Philip C.			Atopy Risk in Infants and Children in Relation to Early Exposure to Fish, Oily Fish, or Long-Chain Omega-3 Fatty Acids: A Systematic Review	CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY			English	Review						Atopy; Allergy; Asthma; Eczema; Immune function; Inflammation; Eicosanoid; Cytokine; Fatty acid; Fish oil; Pregnancy	FATTY-ACID-COMPOSITION; RANDOMIZED CONTROLLED-TRIAL; CHILDHOOD ASTHMA PREVENTION; ALLERGIC RHINITIS; DIETARY FACTORS; CORD-BLOOD; EICOSAPENTAENOIC ACID; DOCOSAHEXAENOIC ACID; AIRWAY INFLAMMATION; CYTOKINE PRODUCTION	There are two main families of polyunsaturated fatty acids (PUFAs), the n-6 and the n-3 families. It has been suggested that there is a causal relationship between n-6 PUFA intake and allergic disease, and there are biologically plausible mechanisms, involving eicosanoid mediators of the n-6 PUFA arachidonic acid, that could explain this. Fish and fish oils are sources of long-chain n-3 PUFAs and these fatty acids act to oppose the actions of n-6 PUFAs. Thus, it is considered that n-3 PUFAs will protect against atopic sensitization and against the clinical manifestations of atopy. Evidence to examine this has been acquired from epidemiologic studies investigating associations between fish intake in pregnancy, lactation, infancy, and childhood, and atopic outcomes in infants and children and from intervention studies with fish oil supplements in pregnancy, lactation, infancy, and childhood, and atopic outcomes in infants and children. All five epidemiological studies investigating the effect of maternal fish intake during pregnancy on atopic or allergic outcomes in infants/children of those pregnancies concluded protective associations. One study investigating the effects of maternal fish intake during lactation did not observe any significant associations. The evidence from epidemiological studies investigating the effects of fish intake during infancy and childhood on atopic outcomes in those infants or children is inconsistent, although the majority of the studies (nine of 14) showed a protective effect of fish intake during infancy or childhood on atopic outcomes in those infants/children. Fish oil supplementation during pregnancy and lactation or during infancy or childhood results in a higher n-3 PUFA status in the infants or children. Fish oil provision to pregnant women is associated with immunologic changes in cord blood and such changes may persist. Studies performed to date indicate that provision of fish oil during pregnancy may reduce sensitization to common food allergens and reduce prevalence and severity of atopic dermatitis in the first year of life, with a possible persistence until adolescence with a reduction in eczema, hay fever, and asthma. Fish oil provision to infants or children may be associated with immunologic changes in the blood but it is not clear if these are of clinical significance and whether they persist. Fish oil supplementation in infancy may decrease the risk of developing some manifestations of allergic disease, but this benefit may not persist as other factors come into play. It is not clear whether fish oil can be used to treat children with asthma as the two studies conducted to date give divergent results. Further studies of increased long-chain n-3 PUFA provision in during pregnancy, lactation, and infancy are needed to more clearly identify the immunologic and clinical effects in infants and children and to identify protective and therapeutic effects and their persistence.	[Kremmyda, Lefkothea-Stella; Vlachava, Maria; Noakes, Paul S.; Diaper, Norma D.; Miles, Elizabeth A.; Calder, Philip C.] Univ Southampton, Southampton Gen Hosp MP887, Inst Human Nutr, Southampton SO16 6YD, Hants, England; [Kremmyda, Lefkothea-Stella; Vlachava, Maria; Noakes, Paul S.; Diaper, Norma D.; Miles, Elizabeth A.; Calder, Philip C.] Univ Southampton, Southampton Gen Hosp MP887, Sch Med, Inst Dev Sci, Southampton SO16 6YD, Hants, England	Miles, EA (reprint author), Univ Southampton, Southampton Gen Hosp MP887, Inst Human Nutr, IDS Bldg,Tremona Rd, Southampton SO16 6YD, Hants, England.	E.A.Miles@soton.ac.uk	Calder, Philip/E-9739-2013; Miles, Elizabeth/O-1861-2015	Calder, Philip/0000-0002-6038-710X; Miles, Elizabeth/0000-0002-8643-0655	European Commission [FOOD-CT-2006-16249]	L-SK, MV, PSN, NDD, and EAM are supported by funding from the European Commission under Framework 6 (FOOD-CT-2006-16249).	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Rev. Allergy Immunol.	AUG	2011	41	1					36	66		10.1007/s12016-009-8186-2		31	Allergy; Immunology	Allergy; Immunology	801UZ	WOS:000293467400004	19997989	
J	Forey, BA; Thornton, AJ; Lee, PN				Forey, Barbara A.; Thornton, Alison J.; Lee, Peter N.			Systematic review with meta-analysis of the epidemiological evidence relating smoking to COPD, chronic bronchitis and emphysema	BMC PULMONARY MEDICINE			English	Review								Background: Smoking is a known cause of the outcomes COPD, chronic bronchitis (CB) and emphysema, but no previous systematic review exists. We summarize evidence for various smoking indices. Methods: Based on MEDLINE searches and other sources we obtained papers published to 2006 describing epidemiological studies relating incidence or prevalence of these outcomes to smoking. Studies in children or adolescents, or in populations at high respiratory disease risk or with co-existing diseases were excluded. Study-specific data were extracted on design, exposures and outcomes considered, and confounder adjustment. For each outcome RRs/ORs and 95% CIs were extracted for ever, current and ex smoking and various dose response indices, and meta-analyses and meta-regressions conducted to determine how relationships were modified by various study and RR characteristics. Results: Of 218 studies identified, 133 provide data for COPD, 101 for CB and 28 for emphysema. RR estimates are markedly heterogeneous. Based on random-effects meta-analyses of most-adjusted RR/ORs, estimates are elevated for ever smoking (COPD 2.89, CI 2.63-3.17, n = 129 RRs; CB 2.69, 2.50-2.90, n = 114; emphysema 4.51, 3.38-6.02, n = 28), current smoking (COPD 3.51, 3.08-3.99; CB 3.41, 3.13-3.72; emphysema 4.87, 2.83-8.41) and ex smoking (COPD 2.35, 2.11-2.63; CB 1.63, 1.50-1.78; emphysema 3.52, 2.51-4.94). For COPD, RRs are higher for males, for studies conducted in North America, for cigarette smoking rather than any product smoking, and where the unexposed base is never smoking any product, and are markedly lower when asthma is included in the COPD definition. Variations by sex, continent, smoking product and unexposed group are in the same direction for CB, but less clearly demonstrated. For all outcomes RRs are higher when based on mortality, and for COPD are markedly lower when based on lung function. For all outcomes, risk increases with amount smoked and pack-years. Limited data show risk decreases with increasing starting age for COPD and CB and with increasing quitting duration for COPD. No clear relationship is seen with duration of smoking. Conclusions: The results confirm and quantify the causal relationships with smoking.	[Forey, Barbara A.; Lee, Peter N.] P N Lee Stat & Comp Ltd, Surrey, England	Forey, BA (reprint author), P N Lee Stat & Comp Ltd, Surrey, England.	BarbaraForey@pnlee.co.uk			Philip Morris International, Inc.	This research was funded by Philip Morris International, Inc. However the opinions and conclusions of the authors are their own, and do not necessarily reflect the position of Philip Morris International, Inc. We thank John Fry for assistance with the statistical analysis. We also thank Pauline Wassell, Diana Morris and Yvonne Cooper for assistance in typing the various drafts of the paper and obtaining the relevant literature.	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Med.		2011	11								36	10.1186/1471-2466-11-36		61	Respiratory System	Respiratory System	V27DB	WOS:000208592800036	21672193	
J	Fain, S; Schiebler, ML; McCormack, DG; Parraga, G				Fain, Sean; Schiebler, Mark L.; McCormack, David G.; Parraga, Grace			Imaging of Lung Function Using Hyperpolarized Helium-3 Magnetic Resonance Imaging: Review of Current and Emerging Translational Methods and Applications	JOURNAL OF MAGNETIC RESONANCE IMAGING			English	Review						pulmonary MRI; hyperpolarized noble gas; (3)He MRI; COPD; cystic fibrosis asthma	APPARENT DIFFUSION-COEFFICIENT; LONG-RANGE DIFFUSION; OXYGEN-SENSITIVE HE-3-MRI; AIR-FLOW OBSTRUCTION; QUANTITATIVE ASSESSMENT; PROJECTION ACQUISITION; VENTILATION DEFECTS; PULMONARY-FUNCTION; MULTIDETECTOR CT; COLLATERAL PATHS	During the past several years there has been extensive development and application of hyperpolarized helium-3 (HP (3)He) magnetic resonance imaging (MRI) in clinical respiratory indications such as asthma chronic obstructive pulmonary disease cystic fibrosis radiation-induced lung injury and transplantation This review focuses on the state-of-the-art of HP 3He MRI and its application to clinical pulmonary research This is not an overview of the physics of the method as this topic has been covered previously We focus here on the potential of this imaging method and its challenges in demonstrating new types of information that has the potential to influence clinical research and decision making in pulmonary medicine Particular attention is given to functional imaging approaches related to ventilation and diffusion-weighted imaging with applications in chronic obstructive pulmonary disease cystic fibrosis, asthma and radiation-induced lung injury The strengths and challenges of the application of 3He MRI in these indications are discussed along with a comparison to established and emerging imaging techniques	[McCormack, David G.; Parraga, Grace] Robarts Res Inst, Imaging Res Labs, London, ON N6A 5K8, Canada; [McCormack, David G.; Parraga, Grace] Univ Western Ontario, Dept Med Biophys, London, ON, Canada; [McCormack, David G.; Parraga, Grace] Univ Western Ontario, Dept Med Imaging, London, ON, Canada; [McCormack, David G.; Parraga, Grace] Univ Western Ontario, Dept Biomed Engn, London, ON, Canada; [Fain, Sean; Schiebler, Mark L.] Univ Wisconsin, Dept Med Phys, Madison, WI 53706 USA	Parraga, G (reprint author), Robarts Res Inst, Imaging Res Labs, 100 Perth Dr, London, ON N6A 5K8, Canada.		Parraga, Grace/K-6465-2013; Fain, Sean/K-4260-2016	Fain, Sean/0000-0001-5461-0646	Canadian Institutes of Health Research (CIHR) Canadian Lung Association (Ontario Thoracic Society); National Institutes of Health/National Heart Lung and Blood Institute (NHLBI); NHLBI; Hartwell Foundation; Academic Medical Organization of Southwestern Ontario; Canadian Institutes of Health Research Canadian Thoracic Society; Ontario Research Fund	Contract grant sponsors Canadian Institutes of Health Research (CIHR) Canadian Lung Association (Ontario Thoracic Society) National Institutes of Health/National Heart Lung and Blood Institute (NHLBI) SF is supported by the NHLBI the Hartwell Foundation and Sandler Program for Asthma Research GP, is supported by the Academic Medical Organization of Southwestern Ontario Canadian Institutes of Health Research Canadian Thoracic Society and Ontario Research Fund	Abdeen N, 2006, MAGN RESON MED, V56, P255, DOI 10.1002/mrm.20943; ALBERT MS, 1994, NATURE, V370, P199, DOI 10.1038/370199a0; 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Magn. Reson. Imaging	DEC	2010	32	6			SI		1398	1408		10.1002/jmri.22375		11	Radiology, Nuclear Medicine & Medical Imaging	Radiology, Nuclear Medicine & Medical Imaging	691LC	WOS:000285080300013	21105144	
J	Massanari, M; Nelson, H; Casale, T; Busse, W; Kianifard, F; Geba, GP; Zeldin, RK				Massanari, Marc; Nelson, Harold; Casale, Thomas; Busse, William; Kianifard, Farid; Geba, Gregory P.; Zeldin, Robert K.			Effect of pretreatment with omalizumab on the tolerability of specific immunotherapy in allergic asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Omalizumab; allergic asthma; immunotherapy; systemic allergic reactions; cluster immunotherapy; cat; dog; house dust mines	ANTI-IGE ANTIBODY; RI EXPRESSION; DOUBLE-BLIND; RHINITIS; CHILDREN	Background: Although specific immunotherapy is a valuable treatment option for patients with allergic asthma, the potential for systemic allergic reactions has limited its use, especially for patients with symptomatic disease. Objective: To evaluate omalizumab's effect on the tolerability of specific immunotherapy in patients with symptomatic persistent asthma not adequately controlled with inhaled corticosteroids. Methods: This multicenter, double-blind, parallel-group study randomized patients to treatment with omalizumab or placebo, after which they received specific immunotherapy to at least I of 3 perennial aeroallergens (cat, dog, and house dust mite) according to a 4-week, 18-injection cluster regimen, followed by 7 weeks of maintenance therapy. The primary efficacy variable, a systemic allergic reaction after immunotherapy, was analyzed by using the Cochrane-Mantel-Haenszel test. Results: A total of 248 randomized patients (126 omalizumab, 122 placebo) received at least I dose of immunotherapy and were evaluated for efficacy. Patients receiving omalizumab experienced significantly fewer systemic allergic reactions to immunotherapy than those receiving placebo (17/126 [13.5%] vs 32/122 [26.2%]; P = .017; 95% CI, 2.91% to 22.56%) and had fewer respiratory-related (grade 3) systemic allergic reactions (6 vs 24, respectively). Grade 4 reactions were reported in 2 patients in each group. More omalizumab patients were able to reach the target maintenance immunotherapy dose (110 [87.3%] vs 88 [72.1%], respectively; P = .004). Conclusion: Use of omalizumab in patients whose asthma was symptomatic despite use of inhaled corticosteroids was associated with fewer systemic allergic reactions to specific immunotherapy and enabled more patients to achieve the target immunotherapy maintenance dose. (J Allergy, Clin Immunol 2010; 125:383-9.)	[Massanari, Marc; Kianifard, Farid; Geba, Gregory P.; Zeldin, Robert K.] Novartis Pharmaceut, E Hanover, NJ 07936 USA; [Nelson, Harold] Natl Jewish Hlth, Denver, CO USA; [Casale, Thomas] Creighton Univ, Omaha, NE 68178 USA; [Busse, William] Univ Wisconsin, Madison, WI 53706 USA	Massanari, M (reprint author), Novartis Pharmaceut, 1 Hlth Plaza,Bldg 419-2326, E Hanover, NJ 07936 USA.	marc.massanari@novartis.com			Novartis Pharmaceuticals Corp; East Hanover, NJ; Genentech. Inc, South San Francisco, Calif; Schering-Plough; Genentech; Ception; AstraZeneca; Novartis; NIH-NIAID; NIH-NHLB1; Centocor; GlaxoSmithKline; MedImmuen	Supported by Novartis Pharmaceuticals Corp, East Hanover, NJ, and Genentech. Inc, South San Francisco, Calif.; Disclosure of potential conflict of interest: M. Massanari, F. Kianifard, and R. K. Zeldin are employed by Novartis. H. Nelson has consultant arrangements with Genentech/Novartis, Abbott Laboratories. MediciNova, AstraZeneca. Amgen, GlaxoSmithKline, Schering-Plough, Dyson, and Sepracor: receives research support from Schering-Plough, Genentech. Ception, and AstraZeneca; and is on the speakers' bureau for GlaxoSmithKline. T. Casale receives research support from Novartis and Genentech. W. Busse has consultant arrangements with Altair. GlaxoSmithKline, Merck. Wyeth, Pfizer, Centocor. Amgen, UCB. Johnson & Johnson, Novartis, AstraZeneca, Eisai. TEVA, CompleWare, KaloBios, Boehringer Ingelheim, and Sandoz and receives research support from the NIH-NIAID, NIH-NHLB1, Novartis, Centocor. GlaxoSmithKline, MedImmuen, and Ception. G. P. Geba is a former employee and current stockholder of Novartis.	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M., 2000, BIOSTATISTICAL METHO; Lockey RF, 2001, J ALLERGY CLIN IMMUN, V108, P497; MacGlashan DW, 1997, J IMMUNOL, V158, P1438; Muller HL, 1966, J ASTHMA RES, V3, P331; Nielsen L, 1996, J ALLERGY CLIN IMMUN, V97, P1207, DOI 10.1016/S0091-6749(96)70186-0; Prussin C, 2003, J ALLERGY CLIN IMMUN, V112, P1147, DOI 10.1016/j.jaci.2003.10.003; Rolinck-Werninghaus C, 2004, ALLERGY, V59, P973, DOI 10.1111/j.1398-9995.2004.00552.x; Soler M, 2001, EUR RESPIR J, V18, P254, DOI 10.1183/09031936.01.00092101; Stokes M. E., 2000, CATEGORICAL DATA ANA; Walker SM, 2001, J ALLERGY CLIN IMMUN, V107, P87, DOI 10.1067/mai.2001.112027	22	86	88	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.	FEB	2010	125	2					383	389		10.1016/j.jaci.2009.11.022		7	Allergy; Immunology	Allergy; Immunology	558RU	WOS:000274764000016	20159249	
J	Bracken, M; Fleming, L; Hall, P; Van Stiphout, N; Bossley, C; Biggart, E; Wilson, NM; Bush, A				Bracken, M.; Fleming, L.; Hall, P.; Van Stiphout, N.; Bossley, C.; Biggart, E.; Wilson, N. M.; Bush, A.			The importance of nurse-led home visits in the assessment of children with problematic asthma	ARCHIVES OF DISEASE IN CHILDHOOD			English	Article							QUALITY-OF-LIFE; DIFFICULT ASTHMA; RISK-FACTORS; INTERVENTION; SEVERITY; DOCTOR; COSTS	Objective: To evaluate and identify potentially modifiable factors in children with problematic asthma by a nurse-led assessment and home visit. Design: Observational cohort study. Setting: A tertiary paediatric respiratory centre. Patients: 71 children, aged 4.5-17.5 years, with problematic asthma currently under follow-up at a tertiary respiratory centre. Interventions: A nurse-led hospital visit followed by a home visit. Main outcome measures: Identification and attempted change of exacerbating factors so that further investigations and consideration of off-label, potentially toxic, asthma therapies were not necessary. Results: Potentially modifiable factors were identified in 56 (79%) children. Many children had multiple causes for poor control. The most important were ongoing allergen exposure, 22 children (31%); passive or active smoking, 18 children (25%); medication issues including adherence, 34 children (48%); psychosocial factors, 42 families (59%). The home visit contributed valuable information to this assessment. At the home visit house dust mite avoidance measures were found to be inadequate in 84% of those sensitised; medications were not easily available for inspection or were out of date in 23%; 74% of psychology referrals were made after the home visit. In 39 children (55%) the factors identified and the interventions recommended meant that further escalation of treatment was avoided. Conclusions: Nurse-led assessments including a home visit can help identify potentially modifiable factors for poorly controlled symptoms in children with problematic asthma.	[Bracken, M.; Hall, P.; Van Stiphout, N.; Bossley, C.; Biggart, E.; Wilson, N. M.; Bush, A.] Royal Brompton Hosp, Dept Paediat Respirol, London SW3 6NP, England; [Fleming, L.] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London, England	Bush, A (reprint author), Royal Brompton Hosp, Dept Paediat Respirol, Sydney St, London SW3 6NP, England.	a.bush@rbht.nhs.uk					American Thoracic Society, 2000, AM J RESP CRIT CARE, V162, P2341, DOI DOI 10.1164/AJRCCM.162.6.ATS9-00; Barry CA, 2001, SOC SCI MED, V53, P487, DOI 10.1016/S0277-9536(00)00351-8; Bender B, 1997, ANN ALLERG ASTHMA IM, V79, P177; British-Thoracic-Society/ Scottish-Intercollegiate-Guidelines-Network, 2008, THORAX S4, V63, piv1, DOI DOI 10.1136/THX.2008.097741; Bush A, 2008, LANCET, V372, P1019, DOI 10.1016/S0140-6736(08)61422-1; Carter MC, 2001, J ALLERGY CLIN IMMUN, V108, P732, DOI 10.1067/mai.2001.119155; Chung KF, 1999, EUR RESPIR J, V13, P1198; Gotzsche PC, 2008, ALLERGY, V63, P646, DOI 10.1111/j.1398-9995.2008.01690.x; Gotzsche PC, 2007, LANCET, V370, P2100, DOI 10.1016/S0140-6736(07)61899-6; Heaney LG, 2005, RESP MED, V99, P1152, DOI 10.1016/j.rmed.2005.02.013; Horner SD, 2006, J COMMUN HEALTH NURS, V23, P213, DOI 10.1207/s15327655jchn2304_2; Juniper EF, 1996, QUAL LIFE RES, V5, P35, DOI 10.1007/BF00435967; Juniper EF, 1996, QUAL LIFE RES, V5, P27, DOI 10.1007/BF00435966; Milgrom H, 1996, J ALLERGY CLIN IMMUN, V98, P1051, DOI 10.1016/S0091-6749(96)80190-4; Morgan WJ, 2004, NEW ENGL J MED, V351, P1068, DOI 10.1056/NEJMoa032097; Murray CS, 2006, THORAX, V61, P376, DOI 10.1136/thx.2005.042523; Ogden J, 2004, FAM PRACT, V21, P479, DOI 10.1093/fampra/cmh502; Orrell-Valente JK, 2008, PEDIATRICS, V122, pE1186, DOI 10.1542/peds.2008-0292; Pellegrino R, 2005, EUR RESPIR J, V26, P948, DOI 10.1183/09031936.05.00035205; Primomo J, 2006, PUBLIC HEALTH NURS, V23, P234, DOI 10.1111/j.1525-1446.2006.230306.x; Ranganathan SC, 2001, PEDIATR PULM, V31, P114, DOI 10.1002/1099-0496(200102)31:2<114::AID-PPUL1018>3.0.CO;2-O; Richardson LP, 2006, PEDIATRICS, V118, P1042, DOI 10.1542/peds.2006-0249; Serra-Batlles J, 1998, EUR RESPIR J, V12, P1322, DOI 10.1183/09031936.98.12061322; Smith DH, 1997, AM J RESP CRIT CARE, V156, P787; Smith JR, 2005, THORAX, V60, P1003, DOI 10.1136/thx.2005.043877	25	86	88	0	5	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0003-9888			ARCH DIS CHILD	Arch. Dis. Child.	OCT	2009	94	10					780	784		10.1136/adc.2008.152140		5	Pediatrics	Pediatrics	497BF	WOS:000270028100007	19546102	
J	Uter, W; Ramsch, C; Aberer, W; Ayala, F; Balato, A; Beliauskiene, A; Fortina, AB; Bircher, A; Brasch, J; Chowdhury, MMU; Coenraads, PJ; Schuttelaar, ML; Cooper, S; Corradin, MT; Elsner, P; English, JSC; Fartasch, M; Mahler, V; Frosch, PJ; Fuchs, T; Gawkrodger, DJ; Gimenez-Arnau, AM; Green, CM; Horne, HL; Jolanki, R; King, CM; Krecisz, B; Kiec-Swierczynska, M; Ormerod, AD; Orton, DI; Peserico, A; Rantanen, T; Rustemeyer, T; Sansom, JE; Simon, D; Statham, BN; Wilkinson, M; Schnuch, A				Uter, Wolfgang; Raemsch, Christiane; Aberer, Werner; Ayala, Fabio; Balato, Anna; Beliauskiene, Aiste; Fortina, Anna Belloni; Bircher, Andreas; Brasch, Jochen; Chowdhury, Mahbub M. U.; Coenraads, Pieter-Jan; Schuttelaar, Marie-Louise; Cooper, Sue; Corradin, Maria Teresa; Elsner, Peter; English, John S. C.; Fartasch, Manige; Mahler, Vera; Frosch, Peter J.; Fuchs, Thomas; Gawkrodger, David J.; Gimenez-Arnau, Ana-Maria; Green, Cathy M.; Horne, Helen L.; Jolanki, Riitta; King, Codagh M.; Krecisz, Beata; Kiec-Swierczynska, Marta; Ormerod, Anthony D.; Orton, David I.; Peserico, Andrea; Rantanen, Tapio; Rustemeyer, Thomas; Sansom, Jane E.; Simon, Dagmar; Statham, Barry N.; Wilkinson, Mark; Schnuch, Axel			The European baseline series in 10 European Countries, 2005/2006-Results of the European Surveillance System on Contact Allergies (ESSCA)	CONTACT DERMATITIS			English	Article						clinical epidemiology; contact allergy; patch testing	PATCH TEST SERIES; MULTIFACTORIAL ANALYSIS; METHYLDIBROMO GLUTARONITRILE; TIXOCORTOL PIVALATE; STANDARD SERIES; RECOMMENDATION; MULTICENTER; FREQUENCY; AGE	Background Continual surveillance based on patch test results has proved useful for the identification of contact allergy. Objectives To provide a current view on the spectrum of contact allergy to important sensitizers across Europe. Patients/Methods Clinical and patch test data of 19 793 patients patch tested in 2005/2006 in the 31 participating departments from 10 European countries (the European Surveillance System on Contact Allergies' (ESSCA) www.essca-dc.org) were descriptively analysed, aggregated to four European regions. Results Nickel sulfate remains the most common allergen with standardized prevalences ranging from 19.7% (central Europe) to 24.4% (southern Europe). While a number of allergens shows limited variation across the four regions, such as Myroxylon pereirae (5.3-6.8%), cobalt chloride (6.2-8.8%) or thiuram mix (1.7-2.4%), the differences observed with other allergens may hint on underlying differences in exposures, for example: dichromate 2.4% in the UK (west) versus 4.5-5.9% in the remaining EU regions, methylchloroisothiazolinone/methylisothiazolinone 4.1% in the South versus 2.1-2.7% in the remaining regions. Conclusions Notwithstanding residual methodological variation (affecting at least some 'difficult' allergens) tackled by ongoing efforts for standardization, a comparative analysis as presented provides (i) a broad overview on contact allergy frequencies and (ii) interesting starting points for further, in-depth investigation.	[Uter, Wolfgang; Raemsch, Christiane] Univ Erlangen Nurnberg, Dept Med Informat Biometry & Epidemiol, D-91054 Erlangen, Germany; [Aberer, Werner] Med Univ Graz, Dept Dermatol, Graz, Austria; [Ayala, Fabio; Balato, Anna] Univ Naples Federico 2, Dept Dermatol, Naples, Italy; [Beliauskiene, Aiste] Kaunas Univ Med, Dept Skin & Venereal Dis, Kaunas, Lithuania; [Fortina, Anna Belloni] Univ Padua, Dept Pediat, Dermatol Unit, I-35100 Padua, Italy; [Bircher, Andreas] Univ Basel Hosp, Allergy Unit, Dept Dermatol, Basel, Switzerland; [Brasch, Jochen] Univ Schleswig Holstein, Dept Dermatol, Lubeck, Germany; [Chowdhury, Mahbub M. U.] Univ Wales Hosp, Welsh Inst Dermatol, Cardiff CF4 4XW, S Glam, Wales; [Coenraads, Pieter-Jan; Schuttelaar, Marie-Louise] Univ Groningen, Univ Med Ctr Groningen, Dept Dermatol, Groningen, Netherlands; [Cooper, Sue] Slade Hosp, Oxford, England; [Corradin, Maria Teresa] S Maria delgi Angeli Hosp, Dermatol Unit, Pordenone, Italy; [Elsner, Peter] Univ Jena, Dept Dermatol & Allergol, Jena, Germany; [English, John S. C.] Queens Med Ctr, Dept Dermatol, Nottingham NG7 2UH, England; [Fartasch, Manige; Mahler, Vera] Univ Erlangen Nurnberg, Dept Dermatol, D-8520 Erlangen, Germany; [Frosch, Peter J.] Dept Dermatol, Dortmund, Germany; [Frosch, Peter J.] Univ Witten Herdecke, Witten, Germany; [Fuchs, Thomas] Univ Gottingen, Dept Dermatol, D-3400 Gottingen, Germany; [Gawkrodger, David J.] Royal Hallamshire Hosp, Dept Dermatol, Sheffield S10 2JF, S Yorkshire, England; [Gimenez-Arnau, Ana-Maria] Univ Autonoma Barcelona, IMAS, Hosp del Mar, Dept Dermatol, Barcelona, Spain; [Green, Cathy M.] Univ Dundee, Ninewells Hosp & Med Sch, Dept Dermatol, Dundee DD1 9SY, Scotland; [Horne, Helen L.] James Cook Univ Hosp, Middlesbrough, Cleveland, England; [Jolanki, Riitta] FIOH, Helsinki, Finland; [King, Codagh M.] Royal Liverpool Univ Hosp, Liverpool, Merseyside, England; [Krecisz, Beata; Kiec-Swierczynska, Marta] Nofer Inst, Dept Dermatol, Lodz, Poland; [Ormerod, Anthony D.] Aberdeen Royal Infirm, Dept Dermatol, Aberdeen, Scotland; [Peserico, Andrea] Univ Padua, Dept Dermatol, I-35100 Padua, Italy; [Rantanen, Tapio] Paijat Hame Cent Hosp, Dept Dermatol, Lahti, Finland; [Rustemeyer, Thomas] Free Univ Amsterdam, Dept Dermatol, NL-1081 HV Amsterdam, Netherlands; [Sansom, Jane E.] Royal Brisbane Hosp, Dept Dermatol, Brisbane, Qld, Australia; [Simon, Dagmar] Univ Hosp Bern, Dept Dermatol, Inselspital, CH-3010 Bern, Switzerland; [Statham, Barry N.] Abertawe Bromorgannwg Univ NHS Trust, Dept Dermatol, Swansea, W Glam, Wales; [Wilkinson, Mark] Gen Infirm, Dept Dermatol, Leeds LS1 3EX, W Yorkshire, England; [Schnuch, Axel] Univ Gottingen, Informat Network Dept Dermatol IVDK, D-3400 Gottingen, Germany	Uter, W (reprint author), Univ Erlangen Nurnberg, Dept Med Informat Biometry & Epidemiol, Waldstr 6, D-91054 Erlangen, Germany.	wolfgang.uter@imbe.med.uni-erlangen.de	Krecisz, Beata/G-4920-2010; Kiec-Swierczynska, Marta/G-4928-2010; Brasch, Jochen/A-9559-2010	Ayala, Fabio/0000-0002-2596-1268; Balato, Anna/0000-0001-5485-0172; Uter, Wolfgang/0000-0002-4498-3710			Bruze M, 2005, CONTACT DERMATITIS, V52, P24, DOI 10.1111/j.0105-1873.2005.00482.x; Bruze M, 1999, CONTACT DERMATITIS, V41, P241, DOI 10.1111/j.1600-0536.1999.tb06154.x; Bruze M, 2008, CONTACT DERMATITIS, V58, P129, DOI 10.1111/j.1600-0536.2007.01292.x; Buckley DA, 2003, BRIT J DERMATOL, V149, P986, DOI 10.1111/j.1365-2133.2003.05491.x; Hasan T, 2005, CONTACT DERMATITIS, V53, P40, DOI 10.1111/j.0105-1873.2005.00630.x; Hegewald J, 2008, J EUR ACAD DERMATOL, V22, P174; Isaksson M, 2000, CONTACT DERMATITIS, V43, P41; Johansen JD, 2008, CONTACT DERMATITIS, V59, P48, DOI 10.1111/j.1600-0536.2008.01364.x; Jong CT, 2007, CONTACT DERMATITIS, V57, P165, DOI 10.1111/j.1600-0536.2007.01181.x; Kalavala M, 2007, CONTACT DERMATITIS, V57, P44, DOI 10.1111/j.1600-0536.2007.01136.x; Menezes de Padua CA, 2005, PHARMACOEPIDEM DR S, V14, P725, DOI 10.1002/pds.1117; Schnuch A, 1996, CONTACT DERMATITIS, V34, P377, DOI 10.1111/j.1600-0536.1996.tb02236.x; Thyssen JP, 2007, CONTACT DERMATITIS, V56, P185, DOI 10.1111/j.1600-0536.2006.01058.x; Uter W, 2004, CONTACT DERMATITIS, V51, P47, DOI 10.1111/j.0105-1873.2004.00406.x; Uter W, 2005, CONTACT DERMATITIS, V53, P136, DOI 10.1111/j.0105-1873.2005.00673.x; Uter W, 2003, CONTACT DERMATITIS, V49, P270, DOI 10.1111/j.0105-1873.2003.0225n.x; Uter W, 2003, CONTACT DERMATITIS, V48, P33, DOI 10.1034/j.1600-0536.46.s4.29_102.x; Uter W, 2001, OCCUP ENVIRON MED, V58, P392, DOI 10.1136/oem.58.6.392; Uter W, 2008, CONTACT DERMATITIS, V59, P56, DOI 10.1111/j.1600-0536.2007.01313.x; Wahlberg JE, 2006, CONTACT DERMATITIS, P365, DOI 10.1007/3-540-31301-X_22	20	86	88	0	10	WILEY-BLACKWELL	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0105-1873			CONTACT DERMATITIS	Contact Dermatitis		2009	61	1					31	38				8	Allergy; Dermatology	Allergy; Dermatology	471IZ	WOS:000268052000004	19659962	
J	von Mutius, E; Radon, K				von Mutius, Erika; Radon, Katja			Living on a farm: Impact on asthma induction and clinical course	IMMUNOLOGY AND ALLERGY CLINICS OF NORTH AMERICA			English	Article							COMMUNITY RESPIRATORY HEALTH; YOUNG DANISH FARMERS; TOLL-LIKE RECEPTOR-2; SCHOOL-AGE-CHILDREN; ATOPIC SENSITIZATION; ALLERGIC DISEASES; INVERSE ASSOCIATION; HAY-FEVER; EUROPEAN FARMERS; NONATOPIC ASTHMA	Exposure to a farming environment protects individuals from respiratory allergy The timing and duration of exposure seem to play critical roles. The largest reduction in risk of developing respiratory allergies is seen among those who are exposed prenatally and continuously thereafter. Contact with farm animals, at least in childhood, likely confers protection; other factors have not been completely identified. Also, the consumption of milk directly from the farm during childhood has been shown to be beneficial with respect to childhood asthma and allergies. Increased levels of microbial substances may contribute to the protective effects. The mechanisms by which such environmental exposures confer protection from respiratory allergies are not well understood. A number of gene-by-environment interactions have been observed with polymorphisms in genes of innate immunity receptors and exposure to farming environments. Increased levels of microbial exposures recognized by innate immune responses may affect adaptive immune responses resulting in decreased levels of atopic sensitization and asthma.	[von Mutius, Erika] Univ Childrens Hosp, D-80337 Munich, Germany; [Radon, Katja] Univ Munich, Unit Occupat & Environm Epidemiol & Net Teaching, Inst & Outpatient Clin Occupat Social & Environm, Ctr Clin, D-80336 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			Alfven T, 2006, ALLERGY, V61, P414, DOI 10.1111/j.1398-9995.2005.00939.x; Asher MI, 1998, EUR RESPIR J, V12, P315; Braback L, 2004, CLIN EXP ALLERGY, V34, P38, DOI 10.1111/j.1365-2222.2004.01841.x; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Braun-Fahrlander C, 2002, ALLERGY, V57, P1094, DOI 10.1034/j.1398-9995.2002.23644.x; Brightbill HD, 2000, IMMUNOLOGY, V101, P1, DOI 10.1046/j.1365-2567.2000.00093.x; CHANYEUNG M, 2008, PEDIAT ALLERGY IMMUN; Dimich-Ward H, 2006, CLIN EXP ALLERGY, V36, P1122, DOI 10.1111/j.1365-2222.2006.02556.x; Dorevitch S, 2007, ANN ALLERG ASTHMA IM, V98, P440; 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VONMUTIUS E, 1994, AM J RESP CRIT CARE, V149, P358; vonMutius E, 1996, BRIT MED J, V312, P1448; Weinmayr G, 2007, AM J RESP CRIT CARE, V176, P565, DOI 10.1164/rccm.200607-994OC; Wickens K, 2002, ALLERGY, V57, P1171, DOI 10.1034/j.1398-9995.2002.t01-1-23644.x; Zhao TB, 2000, J PAEDIATR CHILD H, V36, P128, DOI 10.1046/j.1440-1754.2000.00457.x	73	86	87	3	20	W B SAUNDERS CO-ELSEVIER INC	PHILADELPHIA	1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA	0889-8561			IMMUNOL ALLERGY CLIN	Immunol. Allerg. Clin. North Am.	AUG	2008	28	3					631	+		10.1016/j.iac.2008.03.010		19	Allergy; Immunology	Allergy; Immunology	334IF	WOS:000258214800011	18572111	
J	Salo, PM; Arbes, SJ; Crockett, PW; Thorne, PS; Cohn, RD; Zeldin, DC				Salo, Paeivi M.; Arbes, Samuel J.; Crockett, Patrick W.; Thorne, Peter S.; Cohn, Richard D.; Zeldin, Darryl C.			Exposure to multiple indoor allergens in US homes and its relationship to asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergen; indoor exposure; asthma; allergy	HOUSE-DUST MITE; INNER-CITY CHILDREN; 1ST NATIONAL-SURVEY; ALTERNARIA-ALTERNATA; MOUSE ALLERGEN; ENVIRONMENTAL INTERVENTION; COCKROACH ALLERGEN; UNITED-STATES; DOG ALLERGEN; SENSITIZATION	Background: The National Survey of Lead and Allergens in Housing was the first population-based study to measure indoor allergen levels in US homes. Objective: We characterized the overall burden to multiple allergens and examined whether increased allergen levels were associated with occupants' asthma status. Methods: This cross-sectional study surveyed a nationally representative sample of 831 housing units in 75 different locations throughout the United States. Information was collected by means of questionnaire and environmental assessment. Allergen concentrations in dust samples were assessed by using immunoassays. The following cutoff points were used to define increased allergen levels: 10 mu g/g for Der p 1, Der f 1, and Can f 1; 8 mu g/g for Fel d 1; 8 U/g for Bla g 1; 1.6 mu g/g for mouse urinary protein; and 7 mu g/g for Alternaria alternata antigens. Allergen burden was considered high when 4 or more allergens exceeded increased levels in any of the sampling locations. Results: Exposure to multiple allergens was common in US homes. Of the surveyed homes, 51.5% had at least 6 detectable allergens and 45.8% had at least 3 allergens exceeding increased levels. Race, income, housing type, absence of children, and presence of smokers, pets, cockroaches, rodents, and mold/moisture-related problems were independent predictors of high allergen burden. Among atopic subjects, high allergen burden increased the odds of having asthma symptoms (odds ratio, 1.81; 95% CI, 1.04-3.15). Conclusion: Increased allergen levels in the home are associated with asthma symptoms in allergic individuals.	[Salo, Paeivi M.; Zeldin, Darryl C.] NIEHS, NIH, Res Triangle Pk, NC 27709 USA; [Arbes, Samuel J.] Rho Inc, Chapel Hill, NC USA; [Crockett, Patrick W.; Cohn, Richard D.] Constella Grp LLC, Durham, NC USA; [Thorne, Peter S.] Univ Iowa, Coll Publ Hlth, Iowa City, IA USA	Zeldin, DC (reprint author), NIEHS, NIH, 111 Alexander Dr,Mail Drop D2-01, Res Triangle Pk, NC 27709 USA.	zeldin@niehs.nih.gov			Intramural NIH HHS [Z01 ES025041-10]		Arbes SJ, 2004, J ALLERGY CLIN IMMUN, V114, P111, DOI 10.1016/j.jaci.2004.04.036; Arbes SJ, 2003, J ALLERGY CLIN IMMUN, V111, P408, DOI 10.1067/mai.2003.16; Barnes C, 2006, ANN ALLERG ASTHMA IM, V97, P350; Breysse PN, 2005, ENVIRON RES, V98, P167, DOI 10.1016/j.envres.2004.07.018; Chew GL, 1999, ALLERGY, V54, P1058, DOI 10.1034/j.1398-9995.1999.00003.x; Cho SH, 2006, SCI TOTAL ENVIRON, V371, P31, DOI 10.1016/j.scitotenv.2006.09.001; Cohn RD, 2006, ENVIRON HEALTH PERSP, V114, P522, DOI 10.1289/ehp.8561; Cohn RD, 2004, J ALLERGY CLIN IMMUN, V113, P1167, DOI 10.1016/j.jaci.2003.12.592; Committee on Damp Indoor Spaces and Health, 2004, DAMP IND SPAC HLTH; Crain EF, 2002, ENVIRON HEALTH PERSP, V110, P939; Custovic A, 1998, CLIN EXP ALLERGY, V28, P53; Elliott L, 2007, ENVIRON HEALTH PERSP, V115, P215, DOI 10.1289/ehp.9412; Gergen PJ, 2001, J ALLERGY CLIN IMMUN, V107, pS445, DOI 10.1067/mai.2001.114992; Gold DR, 2005, ANNU REV PUBL HEALTH, V26, P89, DOI 10.1146/annurev.publhealth.26.021304.144528; Gruchalla RS, 2005, J ALLERGY CLIN IMMUN, V115, P478, DOI 10.1016/j.jaci.2004.12.006; Huss K, 2001, J ALLERGY CLIN IMMUN, V107, P48, DOI 10.1067/mai.2001.111146; Institute of Medicine Committee on the Assessment of Asthma and Indoor Air, 2000, CLEAR AIR ASTHM IND; Illi S, 2006, LANCET, V368, P763, DOI 10.1016/S0140-6736(06)69286-6; 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; Langley SJ, 2003, J ALLERGY CLIN IMMUN, V112, P362, DOI 10.1067/mai.2003.1654; Leaderer BP, 2002, ENVIRON HEALTH PERSP, V110, P419; Leech JA, 2002, J EXPO ANAL ENV EPID, V12, P427, DOI 10.1038/sj.jea.7500244; Morgan WJ, 2004, NEW ENGL J MED, V351, P1068, DOI 10.1056/NEJMoa032097; Nelson HS, 2000, J ALLERGY CLIN IMMUN, V105, pS628; Perry TT, 2006, ANN ALLERG ASTHMA IM, V97, P628; Peters JL, 2007, J URBAN HEALTH, V84, P185, DOI 10.1007/s11524-006-9146-2; Phipatanakul W, 2000, J ALLERGY CLIN IMMUN, V106, P1070, DOI 10.1067/mai.2000.110796; Phipatanakul W, 2000, J ALLERGY CLIN IMMUN, V106, P1075; Platts-Mills TAE, 1997, J ALLERGY CLIN IMMUN, V100, pS2, DOI 10.1016/S0091-6749(97)70292-6; Rogers L, 2002, CHEST, V122, P1580, DOI 10.1378/chest.122.5.1580; Rosenstreich DL, 1997, NEW ENGL J MED, V336, P1356, DOI 10.1056/NEJM199705083361904; Salo PM, 2006, J ALLERGY CLIN IMMUN, V118, P892, DOI 10.1016/j.jaci.2006.07.037; Salo PM, 2005, J ALLERGY CLIN IMMUN, V116, P623, DOI 10.1016/j.jaci.2005.05.030; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; Thorne PS, 2005, AM J RESP CRIT CARE, V172, P1371, DOI 10.1164/rccm.200505-758OC; Vojta PJ, 2002, ENVIRON HEALTH PERSP, V110, P527; 2005, TOBACCO USE ADULTS U; 2000, SELF REPORTED ASTHMA	39	86	90	2	14	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	2008	121	3					678	684		10.1016/j.jaci.2007.12.1164		7	Allergy; Immunology	Allergy; Immunology	273GR	WOS:000253918900021	18255132	
J	Arbex, MA; Martins, LC; de Oliveira, RC; Pereira, LAA; Arbex, FF; Cancado, JED; Saldiva, PHN; Braga, ALF				Arbex, Marcos Abdo; Martins, Lourdes Conceicao; de Oliveira, Regiani Carvalho; Amador Pereira, Luiz Alberto; Arbex, Flavio Ferlin; Delfini Cancado, Jose Eduardo; Nascimento Saldiva, Paulo Hilario; Ferreira Braga, Alfesio Luis			Air pollution from biomass burning and asthma hospital admissions in a sugar cane plantation area in Brazil	JOURNAL OF EPIDEMIOLOGY AND COMMUNITY HEALTH			English	Article; Proceedings Paper	ALA/ATS International Conference	MAY, 2005	San Diego, CA	ALA, ATS			EMERGENCY-ROOM VISITS; CYTOKINE PRODUCTION; CHILDREN; POPULATION; CALIFORNIA; SYMPTOMS; EXPOSURE; SEATTLE; HAZE; UTAH	Objective: To evaluate the association between the total suspended particles (TSPs) generated from preharvest sugar cane burning and hospital admission due to asthma ( asthma hospital admissions) in the city of Araraquara. Design: An ecological time-series study. Total daily records of asthma hospital admissions (ICD 10th J15) were obtained from one of the main hospitals in Araraquara, Sao Paulo State, Brazil, from 23 March 2003 to 27 July 2004. The daily concentration of TSP (mu g/m(3)) was obtained using Handi-vol equipment (Energetica, Brazil) placed in downtown Araraquara. The local airport provided the daily mean figures of temperature and humidity. The daily number of asthma hospital admissions was considered as the dependent variable in Poisson's regression models and the daily concentration of TSP was considered the independent variable. The generalised linear model with natural cubic spline was adopted to control for long-time trend. Linear terms were used for weather variables. Results: TSP had an acute effect on asthma admissions, starting 1 day after TSP concentrations increased and remaining almost unchanged for the next four days. A 10 mu g/m(3) increase in the 5-day moving average (lag1-5) of TSP concentrations was associated with an increase of 11.6% (95% CI 5.4 to 17.7) in asthma hospital admissions. Conclusion: Increases in TSP concentrations were definitely associated with asthma hospital admissions in Araraquara and, despite using sugar cane alcohol to reduce air pollution from automotive sources in large Brazilian urban centres, the cities where sugar cane is harvested pay a high toll in terms of public health.	Univ Sao Paulo, Fac Med, Lab Poluicao Atmosfer Expt, Nucleo Estudos Epidemiol Ambiental, Sao Paulo, Brazil; Univ Fed Sao Paulo, Escola Paulista Med, Grp Fisiopatol Resp & Poluicao Ambiental, Sao Paulo, Brazil; Univ Catolica Santos, Programa Posgrad Saude Coletiva, Santos, SP, Brazil; Univ Santo Amaro, Fac Med, Programa Pediat Ambiental, Sao Paulo, Brazil; ABC, Fac Med, Dept Saude Coletividade, Santo Andre, SP, Brazil	Braga, ALF (reprint author), Rua Francisco Octavio Pacca 180,4 Andar, BR-04822030 Sao Paulo, SP, Brazil.	abraga@unisa.br	Carvalho Oliveira, Regiani/B-8471-2012; Saldiva, Paulo/D-7385-2012; Braga, Alfesio/G-6920-2012	Saldiva, Paulo/0000-0003-2005-8253; Braga, Alfesio/0000-0003-3254-3029			Akaike H, 1973, 2 INT S INF THEOR, P267, DOI DOI 10.1007/978-1-4612-1694-0_; Anderson HR, 1998, THORAX, V53, P842; Arbex MA, 2000, J AIR WASTE MANAGE, V50, P1745, DOI 10.1080/10473289.2000.10464211; Atkinson RW, 2001, AM J RESP CRIT CARE, V164, P1860; 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, 1996, TOXICOL APPL PHARM, V141, P637, DOI 10.1006/taap.1996.0330; Cancado JE, 2006, ENVIRON HEALTH PERSP, V114, P725, DOI 10.1289/ehp.8485; Carter JD, 1997, TOXICOL APPL PHARM, V146, P180, DOI 10.1006/taap.1997.8254; Centers for Disease Control and Prevention, 1998, CDC SURVEILL SUMM, V47, P1; CHEW FT, 1995, LANCET, V346, P1427, DOI 10.1016/S0140-6736(95)92443-4; DUCLOS P, 1990, ARCH ENVIRON HEALTH, V45, P53; Etzel RA, 2003, PEDIATRICS, V112, P233; Goldsmith Carroll-Ann W., 1999, Reviews on Environmental Health, V14, P121; GREEN PJ, 1994, NON PARAMETRIC REGRE; HOSIOKANGAS J, 1995, J AEROSOL SCI, V26, pS423, DOI 10.1016/0021-8502(95)97119-Y; JOHNSTON FH, 2002, MED J AUSTRALIA, V176, P536; Koenig JQ, 1999, J ALLERGY CLIN IMMUN, V104, P717; Lara LBLS, 2001, ATMOS ENVIRON, V35, P4937, DOI 10.1016/S1352-2310(01)00198-4; Lin CA, 2003, ENVIRON RES, V92, P57, DOI 10.1016/S0013-9351(02)00054-3; Lin M, 2002, ENVIRON HEALTH PERSP, V110, P575; Lipsett M, 1997, ENVIRON HEALTH PERSP, V105, P216, DOI 10.1289/ehp.97105216; Long WQ, 1998, CHEST, V113, P351, DOI 10.1378/chest.113.2.351; Magnus P, 1997, BRIT MED J, V314, P1795; Martins MCH, 2004, J EPIDEMIOL COMMUN H, V58, P41, DOI 10.1136/jech.58.1.41; MASSAD E, 1986, ENVIRON RES, V40, P479, DOI 10.1016/S0013-9351(86)80123-2; McCullagh P., 1989, GEN LINEAR MODELS; Migliaretti G, 2005, INT ARCH OCC ENV HEA, V78, P164, DOI 10.1007/s00420-004-0569-3; National Academy of Science, 2000, CLEAR AIR ASTHM IND; NORRIS G, 1999, ENV HLTH PERSPECT, V107, P389; PONKA A, 1991, ARCH ENVIRON HEALTH, V46, P262; POPE CA, 1991, ARCH ENVIRON HEALTH, V46, P90; POPE CA, 1989, AM J PUBLIC HEALTH, V79, P623, DOI 10.2105/AJPH.79.5.623; Samet J M, 2000, Res Rep Health Eff Inst, V94, P5; Schwartz J, 2000, EPIDEMIOLOGY, V11, P320, DOI 10.1097/00001648-200005000-00016; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; SCHWELA DH, 1909, HLTH GUIDELINES VEGE; Sheppard L, 1999, EPIDEMIOLOGY, V10, P23, DOI 10.1097/00001648-199901000-00006; Tan WC, 2000, AM J RESP CRIT CARE, V161, P1213; TSENG RYM, 1992, ANN ALLERGY, V68, P425; U.S. EPA, 2004, AIR QUAL CRIT PART M; VICENT R, 1997, AM J PATHOL, V151, P1563; WARD D, 1997, REC CONC C MISS; WARDLAW AJ, 1993, CLIN EXP ALLERGY, V23, P81, DOI 10.1111/j.1365-2222.1993.tb00303.x	45	86	95	2	23	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	MAY	2007	61	5					395	400		10.1136/jech.2005.044743		6	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	156YM	WOS:000245685800008	17435205	
J	Poulsen, LK; Hummelshoj, L				Poulsen, Lars K.; Hummelshoj, Lone			Triggers of IgE class switching and allergy development	ANNALS OF MEDICINE			English	Review						allergy; asthma; B lymphocytes; class switch recombination; IgE; OX40 ligand; Th2 lymphocytes; TSLP	HUMAN B-CELLS; SINGLE-STRANDED-DNA; ANTI-CD40 MONOCLONAL-ANTIBODIES; IMMUNOGLOBULIN-SECRETING CELLS; EPSILON GERMLINE TRANSCRIPTS; CYTIDINE DEAMINASE AID; REGULATORY T-CELLS; TOTAL SERUM IGE; PLASMA-CELL; IFN-GAMMA	The prevalence of immunoglobulin E (IgE)-mediated allergic diseases has been increasing for the last four decades. In this review determinants for an increased IgE synthesis are discussed on both an epidemiological and on an immunological level with special emphasis on the differentiation of the B cell to an IgE-producing plasma cell. Factors that favor an IgE immune response are low antigen doses and immunization via mucous membranes, but it is highly likely that other environmental factors besides exposure to the allergenic sources play a role. Important factors in the formation of the Thelper type 2 (Th2) T cell subset are the actions of thymic stromal lymphopoietin (TSLP) on dendritic cells and the OX40 ligand on CD4+ T cells. In order for a B lymphocyte to switch to IgE production it needs two signals provided by a Th2 cell in the form of the cytokines interleukin (IL-) 4/IL-13 and ligation of the CD40. In spite of a half-life of only a few days, there is evidence that the IgE response may last for years even without allergen stimulation. This is likely to be caused by long-lived IgE-producing plasma cells, and such cells may be difficult to target therapeutically thus emphasizing the need for more knowledge on preventable causes of IgE- and allergy development.	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Med.		2007	39	6					440	456		10.1080/07853890701449354		17	Medicine, General & Internal	General & Internal Medicine	222NR	WOS:000250304700004	17852040	
J	Wigle, DT; Arbuckle, TE; Walker, M; Wade, MG; Liu, SL; Krewski, D				Wigle, Donald T.; Arbuckle, Tye E.; Walker, Mark; Wade, Michael G.; Liu, Shiliang; Krewski, Daniel			Environmental hazards: Evidence for effects on child health	JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART B-CRITICAL REVIEWS			English	Review							BLOOD LEAD LEVELS; ACUTE LYMPHOBLASTIC-LEUKEMIA; NUTRITION EXAMINATION SURVEY; ADVERSE PREGNANCY OUTCOMES; PARTICULATE AIR-POLLUTION; DISINFECTION BY-PRODUCTS; WASTE LANDFILL SITES; BASAL-CELL CARCINOMA; INTRAUTERINE GROWTH-RETARDATION; PARENTAL OCCUPATIONAL EXPOSURES	The human fetus, child, and adult may experience adverse health outcomes from parental or childhood exposures to environmental toxicants. The fetus and infant are especially vulnerable to toxicants that disrupt developmental processes during relatively narrow time windows. This review summarizes knowledge of associations between child health and development outcomes and environmental exposures, including lead, methylmercury, polychlorinated biphenyls (PCBs), dioxins and related polyhalogenated aromatic hydrocarbons (PHAHs), certain pesticides, environmental tobacco smoke (ETS), aeroallergens, ambient air toxicants (especially particulate matter [PM] and ozone), chlorination disinfection by-products (DBPs), sunlight, power-frequency magnetic fields, radiofrequency (RF) radiation, residential proximity to hazardous waste disposal sites, and solvents. The adverse health effects linked to such exposures include fetal death, birth defects, being small for gestational age (SGA), preterm birth, clinically overt cognitive, neurologic, and behavioral abnormalities, subtle neuropsychologic deficits, childhood cancer, asthma, other respiratory diseases, and acute poisoning. Some environmental toxicants, notably lead, ionizing radiation, ETS, and certain ambient air toxicants, produce adverse health effects at relatively low exposure levels during fetal or child developmental time windows. For the many associations supported by limited or inadequate epidemiologic evidence, major sources of uncertainty include the limited number of studies conducted on specific exposure-outcome relationships and methodologic limitations. The latter include (1) crude exposure indices, (2) limited range of exposure levels, (3) small sample sizes, and (4) limited knowledge and control of potential confounders. Important knowledge gaps include the role of preconceptual paternal exposures, a topic much less studied than maternal or childhood exposures. Large longitudinal studies beginning before or during early pregnancy are urgently needed to accurately measure and assess the relative importance of parental and childhood exposures and evaluate relatively subtle health outcomes such as neuropsychologic and other functional deficits. Large case-control studies are also needed to assess the role of environmental exposures and their interactions with genetic factors in relatively uncommon outcomes such as specific types of birth defects and childhood cancers. There is also an urgent need to accelerate development and use of biomarkers of exposure and genetic susceptibility in epidemiologic studies. This review supports the priority assigned by international agencies to relationships between child health and air quality (indoor and outdoor), lead, pesticides, water contaminants, and ETS. To adequately address such priorities, governments and agencies must strengthen environmental health research capacities and adopt policies to reduce parental and childhood exposures to proven and emerging environmental threats.	Univ Ottawa, McLaughlin Ctr Populat Hlth Risk Assessment, Ottawa, ON K1N 6N5, Canada; Hlth Canada, Healthy Environm & Consumer Safety Branch, Ottawa, ON K1A 0L2, Canada; Univ Ottawa, Fac Med, Dept Obstet & Gynecol, Ottawa, ON K1N 6N5, Canada; Publ Hlth Agcy Canada, Ctr Hlth Human Dev, Ottawa, ON, Canada	Wigle, DT (reprint author), Univ Ottawa, McLaughlin Ctr Populat Hlth Risk Assessment, Room 318B,1 Stewart St, Ottawa, ON K1N 6N5, Canada.	don.wigle@sympatico.ca		Wade, Michael/0000-0002-7331-3839			Acquavella JF, 2006, EPIDEMIOLOGY, V17, P69, DOI 10.1097/01.ede.0000190603.52867.22; Adams PF, 1999, VITAL HLTH STAT, V10, P1; Agency for Toxic Substances and Disease Registry, 2005, TOX PROF LEAD DRAFT; Agency for Toxic Substances and Disease Registry, 1999, TOX PROF MERC UPD; Ahlbom A, 2000, BRIT J CANCER, V83, P692, DOI 10.1054/bjoc.2000.1376; Ahmad SA, 2001, ENVIRON HEALTH PERSP, V109, P629, DOI 10.2307/3455038; Alaluusua S, 1999, LANCET, V353, P206, DOI 10.1016/S0140-6736(05)77214-7; Aligne CA, 2003, JAMA-J AM MED ASSOC, V289, P1258, DOI 10.1001/jama.289.10.1258; 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Toxicol. Env. Health-Pt b-Crit. Rev.	JAN-MAR	2007	10	1-2					3	39		10.1080/10937400601034563		37	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	125GB	WOS:000243429300002	18074303	
J	Trenga, CA; Sullivan, JH; Schildcrout, JS; Shepherd, KP; Shapiro, GG; Liu, LJS; Kaufman, JD; Koenig, JQ				Trenga, CA; Sullivan, JH; Schildcrout, JS; Shepherd, KP; Shapiro, GG; Liu, LJS; Kaufman, JD; Koenig, JQ			Effect of particulate air, pollution on lung function in adult and pediatric subjects in a Seattle panel study	CHEST			English	Article						adults; asthma; children; COPD; lung function; particulate air pollution	ANTIINFLAMMATORY MEDICATION USE; EXHALED NITRIC-OXIDE; RESPIRATORY HEALTH; ASTHMATIC-CHILDREN; SYMPTOM SEVERITY; SMALL AIRWAYS; PARTICLES; EXPOSURE; MATTER; ASSOCIATION	Study objective: To determine whether increased exposure to particulate matter air pollution (PM), measured with personal, residential, or central site monitoring, was associated with pulmonary function decrements in either adults with COPD or children with asthma. Participants: We studied 57 adults with or without COPD and 17 children aged 6 to 13 years with physician-diagnosed asthma in Seattle during a 3-year panel study. Study design and measurements: Indoor and outdoor PM measurements were made at subjects' homes. The subjects wore personal exposure monitors for 10 consecutive 24-h periods, and PM was also measured at a central outdoor location. We assessed the within-subject effect of particulate exposure on FEV1 and peak expiratory flow (PEF) in adults, and maximal midexpiratory flow (MMEF), PEF, FEV1, and symptoms in children. Results: FEV1 decrements were associated with 1-day lagged central site PM <= 2.5 mu m in diameter (PM2.5) in adult subjects with COPD. In children not receiving antiinflammatory medication, same day indoor, outdoor, and central site exposures to PM2.5 were associated with decrements in MMEF, PEF, and FEV1. Associations with PM2.5 and lung function decrements were also observed for 1-day lagged indoor (MMEF, PEF, FEV1) and personal (PEF only) exposures. Antiinflammatory medication use in children significantly attenuated the PM effect on airflow rates and volumes. Conclusions: This study found consistent decrements in MMEF in children with asthma who were not receiving medications. It is notable that effects were observed even though PM exposures were low for an urban area. These findings suggest the need for future larger studies of PM effects in this susceptible population that repeatedly measure spirometry to include MMEF and potentially more sensitive markers of airway inflammation such as exhaled breath condensate and exhaled nitric oxide.	Univ Washington, Dept Environm Hlth, EPA NW Res Ctr Particulate Air Pollut & Hlth, Seattle, WA 98195 USA; Vanderbilt Univ, Dept Biostat, Nashville, TN USA; Univ Washington, Dept Pediat, Seattle, WA USA	Trenga, CA (reprint author), Univ Washington, Dept Environm Hlth, EPA NW Res Ctr Particulate Air Pollut & Hlth, Box 354695, Seattle, WA 98195 USA.	ctrenga@u.washington.edu	Kaufman, Joel/B-5761-2008	Kaufman, Joel/0000-0003-4174-9037	NIEHS NIH HHS [K24 ES013195, K24 ES013195-01A1, P30ES07033]		ALLEN R, 2003, ENVIRON SCI TECHNOL, V16, P3484; Blomberg A, 2000, CLIN EXP ALLERGY, V30, P310; Brauer M, 2001, J EXPO ANAL ENV EPID, V11, P490, DOI 10.1038/sj.jea.7500195; Delfino RJ, 1998, ENVIRON HEALTH PERSP, V106, P751, DOI 10.1289/ehp.98106751; Delfino RJ, 2004, ENVIRON HEALTH PERSP, V112, P932, DOI 10.1289/ehp.6815; Delfino RJ, 2002, ENVIRON HEALTH PERSP, V110, pA607; Fuhlbrigge AL, 2001, J ALLERGY CLIN IMMUN, V107, P61, DOI 10.1067/mai.2001.111590; Goswami E, 2002, J AIR WASTE MANAGE, V52, P324; Grievink L, 1999, EUR RESPIR J, V13, P1439, DOI 10.1183/09031936.99.13614479; Guyatt GH, 1997, PEDIATRICS, V99, P165, DOI 10.1542/peds.99.2.165; Hamid Q, 1997, J ALLERGY CLIN IMMUN, V100, P44; Jones SL, 2001, AM J RESP CRIT CARE, V164, P738; Koenig JQ, 2005, ENVIRON HEALTH PERSP, V113, P499, DOI 10.1289/ehp.7511; 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; Littell R., 1996, SAS SYSTEM MIXED MOD; Little RJA, 2002, STAT ANAL MISSING DA; 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; Macklem PT, 1998, AM J RESP CRIT CARE, V157, pS181; Penttinen P, 2001, ENVIRON HEALTH PERSP, V109, P319, DOI 10.2307/3454889; Peters A, 1997, ENVIRON HEALTH PERSP, V105, P430, DOI 10.1289/ehp.97105430; POPE CA, 1992, AM REV RESPIR DIS, V145, P1123; Romieu I, 1996, AM J RESP CRIT CARE, V154, P300; Sarnat JA, 2001, ENVIRON HEALTH PERSP, V109, P1053, DOI 10.2307/3454961; Schwartz J, 2004, ENVIRON HEALTH PERSP, V112, P557; Schwartz J, 2000, EPIDEMIOLOGY, V11, P6, DOI 10.1097/00001648-200001000-00004; Slaughter JC, 2003, ANN ALLERG ASTHMA IM, V91, P346; U.S. EPA, 2004, AIR QUAL CRIT PART M; van der Zee SC, 2000, EUR RESPIR J, V15, P700, DOI 10.1034/j.1399-3003.2000.15d13.x; Yu OC, 2000, ENVIRON HEALTH PERSP, V108, P1209, DOI 10.2307/3434835; [Anonymous], 1995, AM J RESP CRIT CARE, V152, P1107	32	86	95	2	33	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	JUN	2006	129	6					1614	1622		10.1378/chest.129.6.1614		9	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	054BA	WOS:000238349300036	16778283	
J	Casalino-Matsuda, SM; Monzon, ME; Forteza, RM				Casalino-Matsuda, SM; Monzon, ME; Forteza, RM			Epidermal growth factor receptor activation by epidermal growth factor mediates oxidant-induced goblet cell metaplasia in human airway epithelium	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article						EGFR; goblet cells; hyaluronan; NHBE cells; tissue kallikrein	MUCIN GENE-EXPRESSION; ALPHA-CONVERTING-ENZYME; TISSUE KALLIKREIN ACTIVITY; C-ERBB RECEPTORS; ASTHMATIC SUBJECTS; HYALURONIC-ACID; IN-VITRO; INCREASES MUC5AC; HOST-DEFENSE; MUCUS	Mucus overproduction in inflammatory and obstructive airway diseases is associated with goblet cell (GC) metaplasia in airways. Although the mechanisms involved in GC metaplasia and mucus hypersecretion are not completely understood, association with oxidative stress and epidermal growth factor receptor (EGFIR) signaling has been reported. To explore the mechanisms involved in oxidative stress-induced GC metaplasia, cultures of differentiated normal human bronchial epithelial cells grown at the air-liquid interface were exposed to reactive oxygen species (RIDS) generated by xanthine/xanthine oxidase. EGFIR activation and signaling was assessed by measuring EGF and transforming growth factor-alpha release and EGFIR and (44/42)MAPK phosphorylation. The GC population was evaluated by confocal microscopy. ROS-induced EGFIR activation resulted in GC proliferation and increased MUC5AC gene and protein expression. Signaling was due to pro-EGF processing by tissue kallikrein (TK), which was activated by ROS-induced hyaluronan breakdown. It was inhibited by catalase, a TK inhibitor, and EGF-blocking antibodies. Exposure to recombinant TK mimicked the ROS effects, increasing the expression of MUC5AC and lactoperoxidase. In addition, ROS induced the antiapoptotic factor Bcl-2 in a TK-dependent fashion. In conclusion, ROS-induced GC metaplasia in normal human bronchial epithelial cells is associated with HA depolymerization and EGF processing by TK followed by EGFR signaling, suggesting that increases in TK activity could contribute to GC metaplasia and mucus hypersecretion in diseases such as asthma and chronic bronchitis. The data also suggest that increases in GC population could be sustained by the associated upregulation of Bcl-2 in airway epithelial cells.	Univ Miami, Miller Sch Med, Div Pulm & Crit Care Med, Miami, FL 33136 USA	Forteza, RM (reprint author), Univ Miami, Miller Sch Med, Div Pulm & Crit Care Med, R-47,1600 NW 10th Ave,RMSB 7072A, Miami, FL 33136 USA.	rforteza@miami.edu		Casalino-Matsuda, S Marina/0000-0002-7566-4560	NHLBI NIH HHS [HL-073156, HL-68992]		Adler KB, 2001, AM J RESP CELL MOL, V25, P397; Agren UM, 1997, FREE RADICAL BIO MED, V23, P996, DOI 10.1016/S0891-5849(97)00098-1; AIKAWA T, 1992, CHEST, V101, P916, DOI 10.1378/chest.101.4.916; Asakura M, 2002, NAT MED, V8, P35, DOI 10.1038/nm0102-35; Atherton HC, 2003, AM J PHYSIOL-LUNG C, V285, pL730, DOI 10.1152/ajplung.00089.2003; BALAZS EA, 1967, ARTHRITIS RHEUM, V10, P357, DOI 10.1002/art.1780100407; Basbaum C, 2002, NOVART FDN SYMP, V248, P171; Bernacki SH, 1999, AM J RESP CELL MOL, V20, P595; Blanchet S, 2004, AM J RESP CELL MOL, V30, P421, DOI 10.1165/rcmb.2003-0281RC; Booth BW, 2001, AM J RESP CELL MOL, V25, P739; BRAY BA, 1994, EXP LUNG RES, V20, P317, DOI 10.3109/01902149409064390; 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Tesfaigzi Y, 2004, AM J PHYSIOL-LUNG C, V286, pL268, DOI 10.1152/ajplung.00172.2003; Vermeer PD, 2003, NATURE, V422, P322, DOI 10.1038/nature01440; Vignola AM, 2001, J ALLERGY CLIN IMMUN, V108, P738, DOI 10.1067/mai.2001.119160; Voynow JA, 2005, AM J RESP CRIT CARE, V172, P1013, DOI 10.1164/rccm.200410-1398OC; Voynow JA, 1999, AM J PHYSIOL-LUNG C, V276, pL835; WANNER A, 1990, CHEST S, V97, P11; Wijkstrom-Frei C, 2003, AM J RESP CELL MOL, V29, P206, DOI 10.1165/rcmb.2002-0152OC; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; Yoshisue H, 2004, BIOSCI BIOTECH BIOCH, V68, P2024, DOI 10.1271/bbb.68.2024; Zhang M, 1997, EUR RESPIR J, V10, P1747, DOI 10.1183/09031936.97.10081747	84	86	90	0	7	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.	MAY	2006	34	5					581	591		10.1165/rcmb.2005-0386OC		11	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	040JD	WOS:000237373900024	16424381	
J	Frampton, MW; Stewart, JC; Oberdorster, G; Morrow, PE; Chalupa, D; Pietropaoli, AP; Frasier, LM; Speers, DM; Cox, C; Huang, LS; Utell, MJ				Frampton, MW; Stewart, JC; Oberdorster, G; Morrow, PE; Chalupa, D; Pietropaoli, AP; Frasier, LM; Speers, DM; Cox, C; Huang, LS; Utell, MJ			Inhalation of ultrafine particles alters blood leukocyte expression of adhesion molecules in humans	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						blood leukocytes; human; monocytes; ultrafine particles	PARTICULATE AIR-POLLUTION; EMERGENCY-ROOM VISITS; BRONCHOALVEOLAR LAVAGE; PERIPHERAL-BLOOD; ATOPIC ASTHMA; ENVIRONMENTAL AEROSOLS; LYMPHOCYTE-ACTIVATION; OXIDATIVE STRESS; MENSTRUAL-CYCLE; CARBON-BLACK	Ultrafine particles (UFPs; aerodynamic diameter < 100 nm) may contribute to the respiratory and cardiovascular morbidity and mortality associated with particulate air pollution. We tested the hypothesis that inhalation of carbon UFPs has vascular effects in healthy and asthmatic subjects, detectable as alterations in blood leukocyte expression of adhesion molecules. Healthy subjects inhaled filtered air and freshly generated elemental carbon particles (count median diameter - 25 nm, geometric standard deviation similar to 1.6), for 2 hr, in three separate protocols: 10 mu g/m(3) at rest, 10 and 25 mu g/m(3) with exercise, and 50 mu g/m(3) with exercise. In a fourth protocol, subjects with asthma inhaled air and 10 mu g/m(3) UFPs with exercise. Peripheral venous blood was obtained before and at intervals after exposure, and leukocyte expression of surface markers was quantitated using multiparameter flow cytometry. In healthy subjects, particle exposure with exercise reduced expression of adhesion molecules CD54 and CD18 on monocytes and CD18 and CD49d on granulocytes. There were also concentration-related reductions in blood monocytes, basophils, and eosinophils and increased lymphocyte expression of the activation marker CD25. In subjects with asthma, exposure with exercise to 10 mu g/m(3) UFPs reduced expression of CD11b on monocytes and eosinophils and CD54 on granulocytes. Particle exposure also reduced the percentage of CD4(+) T cells, basophils, and eosinophils. Inhalation of elemental carbon UFPs alters peripheral blood leukocyte distribution and expression of adhesion molecules, in a pattern consistent with increased retention of leukocytes in the pulmonary vascular bed.	Univ Rochester, Med Ctr, Sch Med, Dept Med, Rochester, NY 14642 USA; Univ Rochester, Dept Environm Med, Sch Med, Rochester, NY 14642 USA; Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Biostat, Baltimore, MD USA; Univ Rochester, Dept Biostat, Sch Med, Rochester, NY 14642 USA	Frampton, MW (reprint author), Univ Rochester, Med Ctr, Sch Med, Dept Med, 601 Elmwood Ave,Box 692, Rochester, NY 14642 USA.	mark_frampton@urmc.rochester.edu			NCRR NIH HHS [M01 RR000044, RR00044]; NIEHS NIH HHS [R01 ES011853, ES01247, P30 ES001247]		Anderson GJ, 2001, J APPL PHYSIOL, V91, P1084; Atkinson RW, 2001, AM J RESP CRIT CARE, V164, P1860; Batalha JRF, 2002, ENVIRON HEALTH PERSP, V110, P1191; 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, P2451, DOI 10.1016/0960-1686(92)90375-U; Brook RD, 2002, CIRCULATION, V105, P1534, DOI 10.1161/01.CIR.0000013838.94747.64; Brown DM, 2001, TOXICOL APPL PHARM, V175, P191, DOI 10.1006/taap.2001.9240; Chalupa DC, 2004, ENVIRON HEALTH PERSP, V112, P879, DOI 10.1289/ehp.6851; Chalupa DC, 2002, CRUCIAL ISSUES INHAL, P241; CORRIGAN CJ, 1990, AM REV RESPIR DIS, V141, P970; CORRIGAN CJ, 1995, AM J RESP CELL MOL, V12, P567; Daigle CC, 2003, INHAL TOXICOL, V15, P539, DOI 10.1080/08958370390205065; De C. R., 1995, J CLIN INVEST, V96, P60; DOERSCHUK CM, 2003, THERAPEUTIC TARGETS, P249; FRAMPTON MW, 2004, AM J RESP CRIT CARE, V169, pA280; GAVRAS JB, 1994, INHAL TOXICOL, V6, P633, DOI 10.3109/08958379409003044; Ibald-Mulli A, 2001, AM J PUBLIC HEALTH, V91, P571, DOI 10.2105/AJPH.91.4.571; Jones B., 1989, DESIGN ANAL CROSS TR; Kim HJ, 2003, AM J RESP CELL MOL, V28, P111, DOI 10.1165/rcmb.4796; KITTELSON DB, 2001, 200112 MN DOT; Kunzli N, 2005, ENVIRON HEALTH PERSP, V113, P201, DOI 10.1289/ehp.7523; Lefer AM, 1997, CIRCULATION, V95, P553; LESLIE CA, 1994, PROSTAGLANDINS, V47, P41, DOI 10.1016/0090-6980(94)90073-6; Li N, 2003, ENVIRON HEALTH PERSP, V111, P455, DOI 10.1289/ehp.6000; Li XY, 1999, INHAL TOXICOL, V11, P709; Lipsett M, 1997, ENVIRON HEALTH PERSP, V105, P216, DOI 10.1289/ehp.97105216; Mukae H, 2001, AM J RESP CRIT CARE, V163, P201; Nemmar A, 2002, CIRCULATION, V105, P411, DOI 10.1161/hc0402.104118; National Institutes of Health, 1997, NIH PUBL; Oberdorster G, 2002, J TOXICOL ENV HEAL A, V65, P1531, DOI 10.1080/00984100290071658; OBERDORSTER G, 1995, INHAL TOXICOL, V7, P111, DOI 10.3109/08958379509014275; OHKAWARA Y, 1995, AM J RESP CELL MOL, V12, P4; Pekkanen J, 2002, CIRCULATION, V106, P933, DOI 10.1161/01.CIR.0000027561.41736.3C; Pekkanen J, 2000, OCCUP ENVIRON MED, V57, P818, DOI 10.1136/oem.57.12.818; Peters A, 2000, EPIDEMIOLOGY, V11, P11, DOI 10.1097/00001648-200001000-00005; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Peters A, 2001, EUR HEART J, V22, P1198, DOI 10.1053/euhj.2000.2483; Peters A, 2001, CIRCULATION, V103, P2810; Peters A, 1997, LANCET, V349, P1582, DOI 10.1016/S0140-6736(97)01211-7; Pietropaoli AP, 2004, INHAL TOXICOL, V16, P59, DOI 10.1080/08958370490443079; Pietropaoli A. P., 2004, EFFECTS AIR CONTAMIN, P181; PIETROPAOLI AP, 2004, AM J RESP CRIT CARE, V169, pA883; Pope CA, 2004, CIRCULATION, V109, P71, DOI 10.1161/01.CIR.0000108927.80044.7F; Schwartz J, 2001, ENVIRON HEALTH PERSP, V109, P405, DOI 10.2307/3434788; Schwarz E, 2000, CYTOKINE, V12, P413, DOI 10.1006/cyto.1999.0570; SEATON A, 1995, LANCET, V345, P176, DOI 10.1016/S0140-6736(95)90173-6; STEARNS RC, 1994, P INT C EL MICR PAR, P763; Tan WC, 2000, AM J RESP CRIT CARE, V161, P1213; Tolbert PE, 2000, AM J EPIDEMIOL, V151, P798; Utell MJ, 2002, INHAL TOXICOL, V14, P1231, DOI 10.1080/08958370290084881; Van Eeden SF, 1999, J APPL PHYSIOL, V86, P970; VIRCHOW JC, 1995, AM J RESP CRIT CARE, V151, P960; WALKER C, 1992, AM REV RESPIR DIS, V146, P109; WALLENSTEIN S, 1977, BIOMETRICS, V33, P261, DOI 10.2307/2529321; WICHMANN HE, 2000, HLTH EFF I RES REP, V98, P1; WILSON JW, 1994, AM J RESP CRIT CARE, V149, P86; WILSON JW, 1992, AM REV RESPIR DIS, V145, P958	57	86	91	0	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.	JAN	2006	114	1					51	58		10.1289/ehp.7962		8	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	999NR	WOS:000234396800038	16393658	
J	Prescott, SL; Dunstan, JA; Hale, J; Breckler, L; Lehmann, H; Weston, S; Richmond, P				Prescott, SL; Dunstan, JA; Hale, J; Breckler, L; Lehmann, H; Weston, S; Richmond, P			Clinical effects of probiotics are associated with increased interferon-gamma responses in very young children with atopic dermatitis	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergy; cytokines; food allergy; infantile atopic dermatitis; probiotics	PLACEBO-CONTROLLED TRIAL; EUROPEAN TASK-FORCE; INTESTINAL MICROFLORA; CONSENSUS REPORT; LYMPHOID-TISSUE; SCORAD INDEX; INFANTS; ALLERGY; GUT; BACTERIA	We recently demonstrated that administration of probiotics resulted in significant clinical improvement in very young children with moderate-to-severe atopic dermatitis (AD). The purpose of this study was to determine the underlying immunological effects that are associated with these apparent clinical benefits. Peripheral blood mononuclear cells (PBMC) were isolated from children (n=53) at baseline and at the end of an 8-week supplementation period during which they received a probiotic (Lactobacillus fermentum PCC (TM)) (n=26) or a placebo (n=27). A further sample was collected at 16 weeks (8 weeks after ceasing the supplement). Cytokine (IL-5, IL-6, IL-10, IL-13, IFN-gamma and TNF-alpha) responses to allergens (egg ovalbumin (OVA), beta lactoglobulin (BLG), house dust mite (HDM)), vaccines (tetanus toxoid (TT)), diphtheria toxoid (DT)), intestinal flora (heat-killed Lactobacillus (HKLB)), heat-killed Staphylococcus aureus (HKSA), Staphylococcus aureus enterotoxin B (SEB) and mitogen (phytohaemaglutinin (PHA)) were compared. The administration of probiotics was associated with a significant increase in T-helper type 1(Th1-type) cytokine IFN-gamma responses to PHA and SEB at the end of the supplementation period (week 8: P=0.004 and 0.046) as well as 8 weeks after ceasing supplementation (week 16: P=0.005 and 0.021) relative to baseline levels of response. No significant changes were seen in the placebo group. The increase in IFN-gamma responses to SEB was directly proportional to the decrease in the severity of AD (r=-0.445, P=0.026) over the intervention period. At the end of the supplementation period (week 8) children receiving probiotics showed significantly higher TNF-alpha responses to HKLB (P=0.018) and HKSA (P=0.011) but this was no longer evident when supplementation ceased (week 16). Although IL-13 responses to OVA were significantly reduced in children receiving probiotics after 8 weeks (P=0.008), there were no other effects on allergen-specific responses, and this effect was not sustained after ceasing supplementation (week 16). There were no effects on vaccine-specific responses, or on responses to any of the stimuli assessed. The improvement in AD severity with probiotic treatment was associated with significant increases in the capacity for Th1 IFN-gamma responses and altered responses to skin and enteric flora. This effect was still evident 2 months after the supplementation was ceased. The lack of consistent effects on allergen-specific responses suggests that the effects of probiotics may be mediated through other independent pathways, which need to be explored further.	UWA, Sch Paediat & Child Hlth, Princess Margaret Hosp, Perth, WA 6840, Australia	Prescott, SL (reprint author), UWA, Sch Paediat & Child Hlth, Princess Margaret Hosp, POB D184, Perth, WA 6840, Australia.	susanp@ichr.uwa.edu.au	Richmond, Peter/G-3379-2012; Prescott, Susan/H-5665-2014				Aderem A, 2000, NATURE, V406, P782, DOI 10.1038/35021228; Benyacoub J, 2003, J NUTR, V133, P1158; BIENENSTOCK J, 1982, ADV EXP MED BIOL, V149, P471; BIENENSTOCK J, 1984, AM J ANAT, V170, P437, DOI 10.1002/aja.1001700316; Bjorksten B, 2001, J ALLERGY CLIN IMMUN, V108, P516; Bjorksten B, 1999, CLIN EXP ALLERGY, V29, P342; Bottcher MF, 2000, CLIN EXP ALLERGY, V30, P1591, DOI 10.1046/j.1365-2222.2000.00982.x; Christensen HR, 2002, J IMMUNOL, V168, P171; Dunstan JA, 2005, CLIN EXP ALLERGY, V35, P1309, DOI 10.1111/j.1365-2222.2005.02348.x; Dunstan JA, 2003, J ALLERGY CLIN IMMUN, V112, P1178, DOI 10.1016/j.jaci.2003.09.009; GIACINTO CD, 2005, J IMMUNOL, V174, P3237; Haddeland U, 2005, PEDIATR ALLERGY IMMU, V16, P104, DOI 10.1111/j.1399-3038.2005.00250.x; Hanifin JM, 1980, ACTA DERM-VENEREOL S, V92, P44; Hart AL, 2004, GUT, V53, P1602, DOI 10.1136/gut.2003.037325; Holt PG, 1999, ALLERGY, V54, P12, DOI 10.1111/j.1398-9995.1999.tb04382.x; Isolauri E, 2000, CLIN EXP ALLERGY, V30, P1604, DOI 10.1046/j.1365-2222.2000.00943.x; 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; Kunz B, 1997, DERMATOLOGY, V195, P10; Lammers KM, 2003, FEMS IMMUNOL MED MIC, V38, P165, DOI 10.1016/S0928-8244(03)00144-5; Majamaa H, 1997, J ALLERGY CLIN IMMUN, V99, P179, DOI 10.1016/S0091-6749(97)70093-9; MARTINEZ FD, 1994, THORAX, V49, P1189, DOI 10.1136/thx.49.12.1189; Mastrandrea F., 2004, ALLERG IMMUNOL PARIS, V36, P118; Pohjavuori E, 2004, J ALLERGY CLIN IMMUN, V114, P131, DOI 10.1016/j.jaci.2004.03.036; Rehakova Z, 1998, PHYSIOL RES, V47, P357; Rowe J, 2001, J INFECT DIS, V184, P80, DOI 10.1086/320996; STALDER JF, 1993, DERMATOLOGY, V186, P23; Sudo N, 1997, J IMMUNOL, V159, P1739; UPHAM JW, 1995, CLIN EXP ALLERGY, V25, P634, DOI 10.1111/j.1365-2222.1995.tb01111.x; Viljanen M, 2005, ALLERGY, V60, P494, DOI 10.1111/j.1398-9995.2004.00514.x; WESTON S, 2005, ARCH DIS CHILD	31	86	89	0	7	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	DEC	2005	35	12					1557	1564		10.1111/j.1365-2222.2005.02376.x		8	Allergy; Immunology	Allergy; Immunology	990XT	WOS:000233777400007	16393321	
J	Moscato, G; Pignatti, P; Yacoub, MR; Romano, C; Spezia, S; Perfetti, L				Moscato, G; Pignatti, P; Yacoub, MR; Romano, C; Spezia, S; Perfetti, L			Occupational asthma and occupational rhinitis in hairdressers	CHEST			English	Article						hairdressers; occupational asthma; occupational rhinitis; persulfate	PERSULFATE SALTS; AIRWAY INFLAMMATION; INDUCED SPUTUM; TOLUENE DIISOCYANATE; AMMONIUM PERSULFATE; INHALATION; AGENTS; PREVALENCE; DIAGNOSIS; CELL	Background: Hairdressers are at risk for occupational respiratory diseases, but the risk factors, causal agents, and underlying mechanisms are not completely defined. Aim: To describe the features of a large group of hairdressers consecutively referred to our center for suspected occupational asthma (OA) over an 8-year period, the type of occupational respiratory diseases, the etiologic agents, and the diagnostic tests. Results: Forty-seven hairdressers (mean age, 25 years; range, 17 to 52 years) were studied. On the basis of the response to the specific inhalation challenge (SIC), 24 patients received a diagnosis of OA (51.1%), which was due to persulfate salts in 21 patients (87.5%), permanent hair dyes in 2 patients (8.3%), and latex in 1 patient (4.2%). Thirteen of these 24 patients (54.2%) also received a diagnosis of occupational rhinitis, which was due to persulfate salts in I I patients (84.6%) and to paraphenylenediamine in two patients (15.4%). Patients with persulfate asthma had a long period of exposure to bleaching agents, a long latent period between the start of exposure and the onset of symptoms, and a prevalent eosinophilic airway inflammation in induced sputum. The skin-prick test with ammonium persulfate performed in a subset of patients gave negative results Conclusions: In the present study, we confirmed that persulfate salts are the major agents involved in OA and occupational rhinitis in hairdressers. The positive response to the SIC in only a part of the population of symptomatic exposed workers, the period between the starting of exposure and the onset of symptoms, the type of response to the SIC, and the high frequency of association of asthma with other diseases such as dermatitis and rhinitis suggest an immunologic mechanism that remains to be elucidated.	Fdn Salvatore Maugeri, IRCCS, Serv Allergy & Immunol Clin,Sci Inst Pavia, Allergy & Immunol Unit,Inst Res & Care, I-27100 Pavia, Italy; Univ Turin, Allergy & Pneumol Unit, Dept Traumatol Orthopaed & Occupat Med, Turin, Italy; Fdn Salvatore Maugeri, IRCCS, Sci Inst Pavia, Lab Igiene Ambientale & Tossicol Ind, I-27100 Pavia, Italy	Moscato, G (reprint author), Fdn Salvatore Maugeri, IRCCS, Serv Allergy & Immunol Clin,Sci Inst Pavia, Allergy & Immunol Unit,Inst Res & Care, I-27100 Pavia, Italy.	gmoscato@fsm.it		ROMANO, Canzio/0000-0001-5294-9793			Akpinar-Elci M, 2002, J OCCUP ENVIRON MED, V44, P585, DOI 10.1097/00043764-200206000-00023; Ameille J, 2003, OCCUP ENVIRON MED, V60, P136, DOI 10.1136/oem.60.2.136; Anees W, 2002, THORAX, V57, P231, DOI 10.1136/thorax.57.3.231; BAUR X, 1979, RESPIRATION, V38, P144; BLAINEY AD, 1986, THORAX, V41, P42, DOI 10.1136/thx.41.1.42; Cortona G, 2001, G Ital Med Lav Ergon, V23, P64; Di Franco A, 1998, RESP MED, V92, P550; Djukanovic R, 2002, EUR RESPIR J, V20, p1S, DOI 10.1183/09031936.02.00000102; FABBRI LM, 1987, AM REV RESPIR DIS, V136, P36; FISHER AA, 1976, ARCH DERMATOL, V112, P1407, DOI 10.1001/archderm.112.10.1407; GAMBOA PM, 1989, ALLERGOL IMMUNOPATH, V17, P109; Koch P, 2001, Am J Clin Dermatol, V2, P353, DOI 10.2165/00128071-200102060-00002; Leino T, 1998, SCAND J WORK ENV HEA, V24, P398; Lemiere C, 2000, J ALLERGY CLIN IMMUN, V106, P1163; Lemiere Catherine, 2004, Curr Opin Allergy Clin Immunol, V4, P81, DOI 10.1097/00130832-200404000-00002; Macchioni P, 1999, Med Lav, V90, P776; Malo JL, 1997, EUR RESPIR J, V10, P1513, DOI 10.1183/09031936.97.10071513; MALO JL, 1991, AM REV RESPIR DIS, V143, P528; MALO JL, 1992, J ALLERGY CLIN IMMUN, V90, P937, DOI 10.1016/0091-6749(92)90466-F; Malo JL, 2001, J ALLERGY CLIN IMMUN, V108, P317, DOI 10.1067/mai.2001.116432; MEINDL K, 1969, ZBL ARBEITSMED, V3, P75; MEREDITH SK, 1991, BRIT J IND MED, V48, P292; MOSCATO G, 1991, J OCCUP ENVIRON MED, V33, P720, DOI 10.1097/00043764-199106000-00014; Moscato G, 2000, Monaldi Arch Chest Dis, V55, P66; Moscato G, 1999, CHEST, V115, P249, DOI 10.1378/chest.115.1.249; Moscato G, 2003, EUR RESPIR J, V21, P879, DOI 10.1183/09031936.03.00000403; Munoz X, 2004, OCCUP ENVIRON MED, V61, P861, DOI 10.1136/oem.2004.013177; Munoz X, 2003, CHEST, V123, P2124, DOI 10.1378/chest.123.6.2124; *NHLBI WHO, 1995, NHLBI WHO PUBL; Pankow W, 1989, Pneumologie, V43, P173; Parameswaran K, 2000, EUR RESPIR J, V15, P486, DOI 10.1034/j.1399-3003.2000.15.10.x; Park HS, 1999, CLIN EXP ALLERGY, V29, P1395; PARRA FM, 1992, ALLERGY, V47, P656, DOI 10.1111/j.1398-9995.1992.tb02391.x; PARSONS JF, 1979, FOOD COSMET TOXICOL, V17, P129, DOI 10.1016/0015-6264(79)90210-4; Pavord ID, 1997, THORAX, V52, P498; PEPYS J, 1975, AM REV RESPIR DIS, V112, P829; PEPYS J, 1976, CLIN ALLERGY, V6, P399, DOI 10.1111/j.1365-2222.1976.tb01922.x; Perfetti L, 2000, ALLERGY, V55, P94, DOI 10.1034/j.1398-9995.2000.00380.x; Pignatti P, 2002, J ALLERGY CLIN IMMUN, V110, P667, DOI 10.1067/mai.2002.128279; PISATI G, 1988, MED TOR, V10, P79; Pizzichini E, 1996, AM J RESP CRIT CARE, V154, P308; Quanjer PH, 1983, B EUR PHYSIOPATHO S5, V19, P45; Rietschel R. L, 2001, FISHERS CONTACT DERM; Schwaiblmair M, 1997, INT ARCH OCC ENV HEA, V70, P419, DOI 10.1007/s004200050239; SCHWARTZ HJ, 1990, J OCCUP ENVIRON MED, V32, P473, DOI 10.1097/00043764-199005000-00015; Siracusa A, 2000, CLIN EXP ALLERGY, V30, P1519, DOI 10.1046/j.1365-2222.2000.00946.x; Spanevello A, 2000, AM J RESP CRIT CARE, V162, P1172; Stern BJ, 2001, NEUROLOGIST, V7, P1; *SUBC SKIN TESTS E, 1989, ALLERGY S10, V44, P1; Vandenplas O, 1997, EUR RESPIR J, V10, P2612, DOI 10.1183/09031936.97.10112612; Vandenplas O, 2001, J ALLERGY CLIN IMMUN, V107, P542, DOI 10.1067/mai.2001.113519; WRBITZKY R, 1995, INT ARCH OCC ENV HEA, V67, P413, DOI 10.1007/BF00381054; Yawalkar N, 1999, ANN ALLERG ASTHMA IM, V82, P401	53	86	89	0	5	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	NOV	2005	128	5					3590	3598		10.1378/chest.128.5.3590		9	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	987HG	WOS:000233508400075	16304318	
J	Philip, G; Nayak, AS; Berger, WE; Leynadier, F; Vrijens, F; Dass, SB; Reiss, TF				Philip, G; Nayak, AS; Berger, WE; Leynadier, F; Vrijens, F; Dass, SB; Reiss, TF			The effect of montelukast on rhinitis symptoms in patients with asthma and seasonal allergic rhinitis	CURRENT MEDICAL RESEARCH AND OPINION			English	Article						allergic rhinitis; asthma; concomitant allergy and asthma; daily rhinitis symptoms; daytime nasal symptoms; montelukast; upper and lower airway disease	RANDOMIZED CONTROLLED-TRIAL; DOUBLE-BLIND; ORAL MONTELUKAST; PLACEBO; LEUKOTRIENES; INFLAMMATION; MULTICENTER; BUDESONIDE; LORATADINE; AIRWAYS	Objective:The objective of this study was to evaluate montelukast 10 mg daily as treatment for allergic rhinitis in patients with symptomatic allergic rhinitis and active asthma during the allergy season. Methods: This was a multicenter study of 831 patients (ages 15 years-85 years) with seasonal allergen sensitivity, active symptoms of seasonal allergic rhinitis, and active asthma. Following a single-blind, placebo run-in period of 3 days-5 days, patients were randomized to oral montelukast 10 mg (n = 415) or placebo (n = 416) daily during the 2-week, double-blind, active-treatment period. Main outcome measures: The primary endpoint was Daily Rhinitis Symptoms score, average of Daytime Nasal Symptoms and Nighttime Symptoms, as self-rated by patients on a 0-3 scale on daily diaries. Results: Montelukast reduced the Daily Rhinitis Symptoms score: difference between montelukast and placebo in mean change from baseline was -0.12 [95% CI -0.18, -0.06; p < 0.0011. Similar improvements were seen in Daytime Nasal Symptoms (-0.14 [-0.21, -0.07; p:less than or equal to 0.001]) and Nighttime Symptoms (-0.10 [-0.16,-0.04; p less than or equal to 0.001]). Improvements (p < 0.05) were seen in Daytime Eye Symptoms and in the secondary endpoints of Global Evaluations of AIR by Patient and by Physician, and Rhinoconjunctivitis Quality of Life. In exploratory analyses, improvement in rhinitis symptoms was numerically (though not statistically) larger in patients with greater levels of asthma at study start. Montelukast provided benefit in the Global Evaluations of Asthma by Patient and by Physician: mean differences were -0.24 [-0.41, -0.06; p = 0.008] and -0.17 [-0.33,-0.01; p = 0.037). Similarly, as-needed P-agonist use (puffs/day) was reduced with montelukast (p less than or equal to 0.005). Conclusion: Montelukast provides significant relief from symptoms of seasonal allergic rhinitis, while also conferring a benefit for asthma, in patients with both allergic rhinitis and asthma.	Merck Res Labs, Resp & Allergy Dept, Rahway, NJ 07065 USA; Univ Illinois, Peoria, IL 61656 USA; So Calif Res, Mission Viejo, CA USA; Univ Paris, F-75252 Paris, France	Philip, G (reprint author), Merck Res Labs, Resp & Allergy Dept, Mail Code RY34B-344,126 E Lincoln Ave, Rahway, NJ 07065 USA.						Baena-Cagnani CE, 2003, INT ARCH ALLERGY IMM, V130, P307, DOI 10.1159/000070218; Bjermer L, 2003, BRIT MED J, V327, P891, DOI 10.1136/bmj.327.7420.891; Borish L, 2003, J ALLERGY CLIN IMMUN, V112, P1021, DOI 10.1016/j.jaci.2003.90.015; Bousquet J., 2003, Clinical and Experimental Allergy Reviews, V3, P43, DOI 10.1046/j.1472-9725.2003.00063.x; Bousquet J, 2001, J ALLERGY CLIN IMMUN, V108, pS147, DOI 10.1067/mai.2001.118891; BOUSQUET J, 2004, 2004 ANN C EUR AC AL; Braunstahl GJ, 2000, AM J RESP CRIT CARE, V161, P2051; Braunstahl GJ, 2003, ALLERGY, V58, P1235, DOI 10.1046/j.0105-4538.2003.00354.x; Braunstahl GJ, 2001, J ALLERGY CLIN IMMUN, V107, P469, DOI 10.1067/mai.2001.113046; Canonica G. 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F., 2001, Clinical and Experimental Allergy Reviews, V1, P264, DOI 10.1046/j.1472-9725.2001.t01-1-00012.x; Reiss TF, 1998, ARCH INTERN MED, V158, P1213, DOI 10.1001/archinte.158.11.1213; Schramm B, 2003, EUR RESPIR J, V21, P116, DOI 10.1183/09031936.03.00019502; Simons FER, 1999, J ALLERGY CLIN IMMUN, V104, P534, DOI 10.1016/S0091-6749(99)70320-9; TOGIAS A, 2003, J ALLERGY CLIN IMMUN, V1111, P1171; van Adelsberg J, 2003, ALLERGY, V58, P1268, DOI 10.1046/j.1398-9995.2003.00261.x; van Adelsberg J, 2003, ANN ALLERG ASTHMA IM, V90, P214; Vignola A. M., 2003, Clinical and Experimental Allergy Reviews, V3, P63, DOI 10.1046/j.1472-9725.2003.00015.x; Von Mutius E, 1998, CLIN EXP ALLERGY, V28, P45; WENZEL SE, 2003, FATTY ACIDS, V69, P145; Wilson AM, 2001, CLIN EXP ALLERGY, V31, P616, DOI 10.1046/j.1365-2222.2001.01088.x	42	86	94	0	4	LIBRAPHARM	NEWBURY	C/O DR. PETER L CLARKE, 26-32 VENTURE WEST, NEW GREENHAM PARK, NEWBURY RG19 6HX, BERKSHIRE, ENGLAND	0300-7995			CURR MED RES OPIN	Curr. Med. Res. Opin.	OCT	2004	20	10					1549	1558		10.1185/030079904X3348		10	Medicine, General & Internal; Medicine, Research & Experimental	General & Internal Medicine; Research & Experimental Medicine	864MX	WOS:000224638700004	15462688	
J	Antonini, JM; Taylor, MD; Zimmer, AT; Roberts, JR				Antonini, JM; Taylor, MD; Zimmer, AT; Roberts, JR			Pulmonary responses to welding fumes: Role of metal constituents	JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES			English	Article; Proceedings Paper	42nd Annual Meeting of the Society-of-Toxicology	MAR   12, 2003	Lake city, UT	Soc Toxicol			OIL FLY-ASH; STAINLESS-STEEL WELDERS; MILD-STEEL; LUNG-CANCER; ARC WELDERS; SHIPYARD WORKERS; PARTICLES; HEALTH; MORTALITY; CHROMIUM	It is estimated that more than 1 million workers worldwide perform some type of welding as part of their work duties. Epidemiology studies have shown that a large number of welders experience some type of respiratory illness. Respiratory effects seen in full-time welders have included bronchitis, siderosis, asthma, and a possible increase in the incidence of lung cancer. Pulmonary infections are increased in terms of severity, duration, and frequency among welders. Inhalation exposure to welding fumes may vary due to differences in the materials used and methods employed. The chemical properties of welding fumes can be quite complex. Most welding materials are alloy mixtures of metals characterized by different steels that may contain iron, manganese, chromium, and nickel. Animal studies have indicated that the presence and combination of different metal constituents is an important determinant in the potential pneumotoxic responses associated with welding fumes. Animal models have demonstrated that stainless steel (SS) welding fumes, which contain significant levels of nickel and chromium, induce more lung injury and inflammation, and are retained in the longs longer than mild steel (MS) welding fumes, which contain mostly iron. In addition, SS fumes generated from welding processes using fluxes to protect the resulting weld contain elevated levels of soluble metals, which may affect respiratory health. Recent animal studies have indicated that the lung injury and inflammation induced by SS welding fumes that contain water-soluble metals are dependent on both the soluble and insoluble fractions of the fume. This article reviews the role that metals play in the pulmonary effects associated with welding fume exposure in workers and laboratory animals.	NIOSH, Hlth Effects Lab Div, Morgantown, WV 26505 USA; NIOSH, Div Appl Res & Technol, Cincinnati, OH 45226 USA	Antonini, JM (reprint author), NIOSH, Hlth Effects Lab Div, 1095 Willowdale Rd,M-S 2015, Morgantown, WV 26505 USA.	jga6@cdc.gov					ACGIH, 2001, DOC THRESH LIM VAL C, V3, P1726; AKBARKHANZADEH F, 1993, INT ARCH OCC ENV HEA, V64, P393, DOI 10.1007/BF00517944; AKBARKHANZADEH F, 1980, J OCCUP ENVIRON MED, V22, P337, DOI 10.1097/00043764-198005000-00007; Antonini JM, 2003, AM J IND MED, V43, P350, DOI 10.1002/ajim.10194; ANTONINI JM, 1994, ENVIRON HEALTH PERSP, V102, P37, DOI 10.2307/3432211; Antonini JM, 2003, CRIT REV TOXICOL, V33, P61, DOI 10.1080/713611032; Antonini JM, 1997, EXP LUNG RES, V23, P205, DOI 10.3109/01902149709087368; Antonini JM, 1996, TOXICOL APPL PHARM, V140, P188, DOI 10.1006/taap.1996.0212; Antonini JM, 1999, J TOXICOL ENV HEAL A, V58, P343, DOI 10.1080/009841099157205; ATTFIELD MD, 1978, BRIT J IND MED, V35, P117; Beach JR, 1996, AM J RESP CRIT CARE, V154, P1394; BECK BD, 1982, TOXICOL APPL PHARM, V66, P9, DOI 10.1016/0041-008X(82)90057-6; Becker N, 1999, J OCCUP ENVIRON MED, V41, P294, DOI 10.1097/00043764-199904000-00012; BOSHNAKOVA E, 1989, Journal of Hygiene Epidemiology Microbiology and Immunology (Prague), V33, P379; Buerke U, 2002, AM J IND MED, V41, P259, DOI 10.1002/ajim.10055; *BUR LAB STAT, 1999, OCC EMPL STAT 1999 N; CLAPP DE, 1977, WELD J, V56, pS380; COGGON D, 1994, LANCET, V344, P41, DOI 10.1016/S0140-6736(94)91056-1; COHEN MD, 1993, CRIT REV TOXICOL, V23, P255, DOI 10.3109/10408449309105012; DANIELSEN TE, 1993, BRIT J IND MED, V50, P1097; Danielsen TE, 2000, J OCCUP ENVIRON MED, V42, P101, DOI 10.1097/00043764-200001000-00023; DOIG A. 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G., 1995, European Respiratory Journal, V8, p194S; SJOGREN B, 1994, OCCUP ENVIRON MED, V51, P335; SJOGREN B, 1987, SCAND J WORK ENV HEA, V13, P247; Sobaszek A, 2000, J OCCUP ENVIRON MED, V42, P923, DOI 10.1097/00043764-200009000-00016; SREEKANTHAN P, 1997, THESIS MIT CAMBRIDGE; STEENLAND K, 1991, AM J EPIDEMIOL, V133, P220; STERN RM, 1983, ARCH ENVIRON HEALTH, V38, P148; STERN RM, 1981, ENVIRON HEALTH PERSP, V41, P235, DOI 10.2307/3429321; STERN RM, 1977, DANISH WELDING I PUB, V7705; Tuschl H, 1997, J APPL TOXICOL, V17, P377; Ulfarson U., 1981, SCAND J WORK ENV HEA, V2, P1; VILLAUME JE, 1979, EFFECTS WELDING HLTH, V1; Voitkevich V, 1995, WELDING FUMES FORMAT, P18; WANG ZP, 1994, AM J IND MED, V26, P741, DOI 10.1002/ajim.4700260603; Wergeland E, 2001, SCAND J WORK ENV HEA, V27, P353; Zimmer AT, 2001, J AEROSOL SCI, V32, P993, DOI 10.1016/S0021-8502(01)00035-0	60	86	92	2	9	TAYLOR & FRANCIS INC	PHILADELPHIA	325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA	1528-7394			J TOXICOL ENV HEAL A	J. Toxicol. Env. Health Part A	FEB 13	2004	67	3					233	249		10.1080/15287390490266909		17	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	802BG	WOS:000220138400005	14681078	
J	Ebo, DG; Hagendorens, MM; Bridts, CH; De Clerck, LS; Stevens, WJ				Ebo, DG; Hagendorens, MM; Bridts, CH; De Clerck, LS; Stevens, WJ			Sensitization to cross-reactive carbohydrate determinants and the ubiquitous protein profilin: mimickers of allergy	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						carbohydrate determinants; cross-reactivity; food; hymenoptera venom; IgE; latex; profilin	CORE ALPHA-1,3-LINKED FUCOSE; OLIVE TREE POLLEN; BIRCH POLLEN; IGE-BINDING; CLINICAL RELEVANCE; MAJOR ALLERGEN; GRASS-POLLEN; HEVEA-BRASILIENSIS; FOOD ALLERGENS; LATEX PROFILIN	Background During the last decade, evidence has been provided for profilins and cross-reactive carbohydrate determinants (CCDs) to be capable of inducing cross-reactive IgE antibodies with little clinical relevance. Objective To investigate the prevalence of sensitization to CCD and profilin in isolated allergies (birch, timothy grass, house dust mite, pets (cat and/or dog), natural rubber latex (NRL) and hymenoptera venom). To study the contribution of anti-CCD and anti-profilin IgE antibodies as a cause of clinically irrelevant IgE for NRL and apple. Methods For the first part of the study, 100 patients with inhalant allergy, 17 patients with NRL allergy and 40 patients with venom anaphylaxis were enrolled. Diagnosis was based on a questionnaire and a positive IgE determination and skin test for relevant allergen. Patients were identified as sensitized to CCD if they had a negative prick test and positive IgE for the glycoprotein bromelain. Sensitization to profilin was assessed by IgE for rBet v 2 (recombinant birch profilin). For the second part of the study, sera containing IgE against apple (n=82) or NRL (n=38) were classified as true-negative or false-positive according to the presence or absence of an oral allergy syndrome (OAS) or NRL-induced anaphylaxis. In these patients, sensitization to CCD and profilin was evaluated as described above. Results No sensitization to bromelain-type CCD and profilin was found in isolated birch pollen or NRL allergy. In contrast, sensitization to bromelain-type CCD was found in 4/17 patients with isolated grass pollinosis, 5/24 patients with combined pollinosis (birch, timothy, mugwort) and 7/33 patients with venom anaphylaxis. Sensitization to profilin was almost restricted to patients with combined pollen allergy (5/24). In pollen-allergic individuals with a false-positive IgE against NRL the prevalence of sensitization to bromelain-type CCD and profilin IgE was higher than in NRL-allergic patients (P<0.00001 and P=0.0006, respectively). In pollen-allergic individuals with a false-positive IgE to apple, the frequency of sensitization to bromelain-type CCD was higher than in OAS patients (P=0.004). Clinically irrelevant NRL and apple were also found in four and five out of the seven patients sensitized to venom CCD, respectively. In pollinosis, clinically irrelevant NRL and apple IgE antibodies were inhibited by bromelain and recombinant birch profilin, whereas in isolated venom anaphylaxis these antibodies were inhibited by bromelain. Conclusions Patients monoallergic to NRL or birch pollen showed no sensitization to bromelain-type CCD or profilin. Sensitization to profilin and/or bromelain-type CCD, caused by pollen (timothy grass, mugwort) or hymenoptera venom allergens, can elicit false-positive IgE antibodies against NRL and apple.	Univ Antwerp, Dept Immunol Allergol & Rheumatol, B-2610 Antwerp, Belgium	Stevens, WJ (reprint author), Univ Antwerp, Dept Immunol Allergol & Rheumatol, Univ Pl 1, B-2610 Antwerp, Belgium.	immuno@ua.ac.be	BRIDTS, Chris/M-7933-2016; EBO, Didier/H-4894-2016	BRIDTS, Chris/0000-0002-3324-7320; EBO, Didier/0000-0003-0672-7529			AALBERSE RC, 1981, J ALLERGY CLIN IMMUN, V68, P356, DOI 10.1016/0091-6749(81)90133-0; Aalberse RC, 2001, ALLERGY, V56, P478, DOI 10.1034/j.1398-9995.2001.056006478.x; Batanero E, 1999, J ALLERGY CLIN IMMUN, V103, P147, DOI 10.1016/S0091-6749(99)70538-5; BATANERO E, 1994, MOL IMMUNOL, V31, P31, DOI 10.1016/0161-5890(94)90135-X; BIRCHER AJ, 1994, CLIN EXP ALLERGY, V24, P367, DOI 10.1111/j.1365-2222.1994.tb00248.x; BREITENEDER H, 1989, EMBO J, V8, P1935; CANONICA GW, 1989, ALLERGY, V44, P1, DOI 10.1111/j.1398-9995.1989.tb00438.x; Daschner A, 1998, ALLERGY, V53, P614, DOI 10.1111/j.1398-9995.1998.tb03938.x; Diez-Gomez ML, 1999, ALLERGY, V54, P951, DOI 10.1034/j.1398-9995.1999.00145.x; EBNER C, 1995, J ALLERGY CLIN IMMUN, V95, P962, DOI 10.1016/S0091-6749(95)70096-X; Ebo DG, 2002, ALLERGY, V57, P706, DOI 10.1034/j.1398-9995.2002.23553.x; Elfman L, 1997, INT ARCH ALLERGY IMM, V113, P249; Fotisch K, 1999, INT ARCH ALLERGY IMM, V120, P30, DOI 10.1159/000024217; Fotisch K, 1998, ALLERGY, V53, P1043, DOI 10.1111/j.1398-9995.1998.tb03813.x; Fotisch K, 2001, GLYCOCONJUGATE J, V18, P373, DOI 10.1023/A:1014860030380; Fuchs T, 1997, J ALLERGY CLIN IMMUN, V100, P356, DOI 10.1016/S0091-6749(97)70249-5; GAILHOFER G, 1988, CLIN ALLERGY, V18, P445, DOI 10.1111/j.1365-2222.1988.tb02894.x; Ganglberger E, 2001, INT ARCH ALLERGY IMM, V125, P216, DOI 10.1159/000053819; Hemmer W, 2001, J ALLERGY CLIN IMMUN, V108, P1045, DOI 10.1067/mai.2001.120013; Hirschwehr R, 1998, J ALLERGY CLIN IMMUN, V101, P196; ISHIHARA H, 1979, J BIOL CHEM, V254, P715; KOCHUYT AM, 2000, THESIS U LEUVEN LEUV; Luttkopf D, 2000, J ALLERGY CLIN IMMUN, V106, P390, DOI 10.1067/mai.2000.108711; Mari A, 1999, J ALLERGY CLIN IMMUN, V103, P1005, DOI 10.1016/S0091-6749(99)70171-5; Mari A, 2001, INT ARCH ALLERGY IMM, V125, P57, DOI 10.1159/000053797; Nettis E, 2001, ALLERGY, V56, P257, DOI 10.1034/j.1398-9995.2001.056003257.x; Nieto A, 2000, CLIN EXP ALLERGY, V30, P264; Pauli G, 1996, J ALLERGY CLIN IMMUN, V97, P1100, DOI 10.1016/S0091-6749(96)70264-6; Petersen A, 1996, J ALLERGY CLIN IMMUN, V98, P805, DOI 10.1016/S0091-6749(96)70130-6; PETERSEN A, 1995, ELECTROPHORESIS, V16, P869, DOI 10.1002/elps.11501601144; Pike RN, 1997, INT ARCH ALLERGY IMM, V112, P412; Pridgeon C, 2000, CLIN EXP ALLERGY, V30, P1444, DOI 10.1046/j.1365-2222.2000.00908.x; Rihs HP, 2000, ALLERGY, V55, P712, DOI 10.1034/j.1398-9995.2000.00553.x; Rossi RE, 1996, ALLERGY, V51, P940; Schafer T, 1996, ALLERGY, V51, P372; TRETTER V, 1993, INT ARCH ALLERGY IMM, V102, P259; VALENTA R, 1992, J EXP MED, V175, P377, DOI 10.1084/jem.175.2.377; VALLIER P, 1995, CLIN EXP ALLERGY, V25, P332; van Ree R, 2002, INT ARCH ALLERGY IMM, V129, P189, DOI 10.1159/000066770; van Ree R, 2000, J BIOL CHEM, V275, P11451, DOI 10.1074/jbc.275.15.11451; vanderVeen MJ, 1997, J ALLERGY CLIN IMMUN, V100, P327, DOI 10.1016/S0091-6749(97)70245-8; VANREE R, 1993, J CLIN IMMUNOASSAY, V16, P124; van Ree R, 2000, ALLERGY CLIN IMMUNOL, V12, P7, DOI 10.1027/0838-1925.12.1.7; Vieths S, 2002, ANN NY ACAD SCI, V964, P47; Wensing M, 2002, J ALLERGY CLIN IMMUN, V110, P435, DOI 10.1067/mai.2002.126380; Wilson IBH, 2001, GLYCOBIOLOGY, V11, P261, DOI 10.1093/glycob/11.4.261; Wilson IBH, 1998, GLYCOCONJUGATE J, V15, P1055, DOI 10.1023/A:1006960401562; Yagami T, 2002, INT ARCH ALLERGY IMM, V129, P27, DOI 10.1159/000065180; Yagami T, 1998, J ALLERGY CLIN IMMUN, V101, P379; Yip L, 2000, INT ARCH ALLERGY IMM, V121, P292, DOI 10.1159/000024342	50	86	87	1	5	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	JAN	2004	34	1					137	144		10.1111/j.1365-2222.2004.01837.x		8	Allergy; Immunology	Allergy; Immunology	763LF	WOS:000188086500021	14720274	
J	Shepherd, GM				Shepherd, GM			Hypersensitivity reactions to chemotherapeutic drugs	CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY			English	Review						hypersensitivity; allergy; chemotherapy; desensitization; drug asparaginase; platinum compounds; epipodophyllotoxins; taxanes	ACUTE LYMPHOBLASTIC-LEUKEMIA; PEGYLATED LIPOSOMAL DOXORUBICIN; DESENSITIZATION PROTOCOL; ALLERGIC REACTIONS; CARBOPLATIN; PACLITAXEL; ASPARAGINASE; CANCER; CYCLOPHOSPHAMIDE; DOCETAXEL	There is an ever-increasing number of therapeutics used to treat cancer. A recent publication listed 86 currently available antineoplastic medications. Despite this large number, hypersensitivity reactions are not common except with platinum compounds (cisplatin, carboplatin), epipodophyllotoxins (teniposide, etoposide), asparaginase, taxanes (paclitaxel), and procarbazine. Doxorubicin and 6-mercaptopurine are occasionally associated with hypersensitivity reaction. Comparable reactions with other chemotherapeutic agents are. uncommon; many are only anecdotal reports. Reactions associated with individual drugs are discussed in detail. The mechanisms responsible for most of these reactions are not known, as they have generally not been evaluated. The term "hypersensitivity" is widely used in the chemotherapy literature without a common definition. Hypersensitivity is defined here as an unexpected reaction with signs and symptoms not consistent with known toxicity of the drug. Most reactions are coincident with or within hours of drug administration. Almost all are associated with parenteral administration. Symptoms include flushing, alterations in heart rate and blood pressure, dyspnea and bronchospasm, back pain, fever, pruritus, nausea and all types of rashes. Some cases may be due to non-immune mediated release of histamine or cytokines, as many patients can subsequently tolerate re-exposure after pretreatment with steroids and antihistamine, and slow readministration of the drug. This is more compatible with a graded challenge, than desensitization and is generally successful for taxanes, less so for platinum compounds. In most cases hypersensitivity reactions are associated with the specific chemotherapeutic drug. Reaction rates may vary with different forms of the drugs, e.g. pegylated. Occasionally excipients such as Cremaphor EL may induce hypersensitivity reactions.	Cornell Univ, Weill Med Coll, New York, NY 10021 USA	Shepherd, GM (reprint author), Cornell Univ, Weill Med Coll, New York, NY 10021 USA.						ABRAMOWICZ M, 2000, MED LETT, V42, P83; Alberts DS, 1997, DRUGS, V54, P30; Alkins SA, 1996, CANCER, V77, P2123, DOI 10.1002/(SICI)1097-0142(19960515)77:10<2123::AID-CNCR24>3.0.CO;2-W; BERNSTEIN BJ, 2000, ANN PHARMACOTHER, V11, P1332; Blanca M, 1997, ALLERGY, V52, P1009, DOI 10.1111/j.1398-9995.1997.tb02422.x; Chiara S, 1997, EUR J CANCER, V33, P967, DOI 10.1016/S0959-8049(96)00497-2; CORNWELL GG, 1979, CANCER TREAT REP, V63, P399; COYLE T, 1992, CANCER, V69, P2532, DOI 10.1002/1097-0142(19920515)69:10<2532::AID-CNCR2820691024>3.0.CO;2-I; Essayan DM, 1996, J ALLERGY CLIN IMMUN, V97, P42, DOI 10.1016/S0091-6749(96)70281-6; Fishman A, 1999, INT J GYNECOL CANCER, V9, P156, DOI 10.1046/j.1525-1438.1999.99014.x; FOSSELLA FV, 1994, J CLIN ONCOL, V12, P1238; Gabizon AA, 2001, CANCER INVEST, V19, P424, DOI 10.1081/CNV-100103136; GIGUERE JK, 1988, MED PEDIATR ONCOL, V16, P378, DOI 10.1002/mpo.2950160605; Goldberg A, 1996, J ALLERGY CLIN IMMUN, V98, P841, DOI 10.1016/S0091-6749(96)70134-3; GORAM AL, 2001, PHARMACOTHERAPY, V6, P751; GROSEN E, 2000, LANCET, V354, P288; Hoetelmans RWM, 1996, ANN PHARMACOTHER, V30, P367; HUDSON MM, 1993, J CLIN ONCOL, V11, P1080; KELLIE SJ, 1991, CANCER-AM CANCER SOC, V67, P1070, DOI 10.1002/1097-0142(19910215)67:4<1070::AID-CNCR2820670434>3.0.CO;2-X; Kintzel PE, 2001, ANN PHARMACOTHER, V35, P1114; Koppler H, 2001, ONKOLOGIE, V24, P283, DOI 10.1159/000055093; Korelitz BI, 1999, J CLIN GASTROENTEROL, V28, P341, DOI 10.1097/00004836-199906000-00011; Larson RA, 1998, LEUKEMIA, V12, P660, DOI 10.1038/sj.leu.2401007; Lehmann DF, 1997, CLIN PHARMACOL THER, V62, P225, DOI 10.1016/S0009-9236(97)90071-0; Markman M, 1999, J CLIN ONCOL, V17, P1141; Moon C, 2000, ANTI-CANCER DRUG, V11, P565, DOI 10.1097/00001813-200008000-00007; Mueller Hans-Joachim, 2001, British Journal of Haematology, V114, P794; Myers J S, 2000, Clin J Oncol Nurs, V4, P161; NOLTE H, 1988, AM J PEDIAT HEMATOL, V10, P308; Ozkan A, 2001, PEDIATR DERMATOL, V18, P38, DOI 10.1046/j.1525-1470.2001.018001038.x; PEEREBOOM DM, 1993, J CLIN ONCOL, V11, P885; Polyzos A, 2001, ONCOLOGY-BASEL, V61, P129, DOI 10.1159/000055363; Popescu MA, 1996, J ALLERGY CLIN IMMUN, V97, P26; RHEINHOLDKELLER E, 1992, CLIN INVESTIG, V70, P698; Robinson JB, 2001, GYNECOL ONCOL, V82, P550, DOI 10.1006/gyno.2001.6331; Sandhu H S, 2000, Can Respir J, V7, P491; Shukunami K, 1999, GYNECOL ONCOL, V72, P431, DOI 10.1006/gyno.1998.5273; Stone HD, 1998, J ALLERGY CLIN IMMUN, V101, P429; Szebeni J, 2001, INT IMMUNOPHARMACOL, V1, P721, DOI 10.1016/S1567-5769(01)00006-6; TORRICELLI R, 1995, SCHWEIZ MED WSCHR, V125, P1870; WEISS RB, 1992, SEMIN ONCOL, V19, P458; Woo MH, 2000, J CLIN ONCOL, V18, P1525; Zanotti KM, 2001, J CLIN ONCOL, V19, P3126; Zanotti KM, 2001, DRUG SAFETY, V24, P767, DOI 10.2165/00002018-200124100-00005; ZONZITS E, 1992, ARCH DERMATOL, V128, P80, DOI 10.1001/archderm.128.1.80; 2001, PHYSICIANS DESK REFE, P1925	46	86	93	0	7	HUMANA PRESS INC	TOTOWA	999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA	1080-0549			CLIN REV ALLERG IMMU	Clin. Rev. Allergy Immunol.	JUN	2003	24	3					253	262		10.1385/CRIAI:24:3:253		10	Allergy; Immunology	Allergy; Immunology	674JJ	WOS:000182633400006	12721396	
J	Fisk, WJ; Faulkner, D; Palonen, J; Seppanen, O				Fisk, WJ; Faulkner, D; Palonen, J; Seppanen, O			Performance and costs of particle air filtration technologies	INDOOR AIR			English	Article						allergen; building; concentration; filtration; particle; reduction	TOBACCO-SMOKE PARTICLES; AEROSOL FRACTION; MITE ALLERGEN; DEPOSITION; POLLEN; PENETRATION; EXPOSURE; OUTDOOR	This paper predicts the reductions in the indoor mass concentrations of particles attainable from use of filters in building supply airstreams and also from use of stand-alone fan-filter units. Filters with a wide efficiency range are considered. Predicted concentration reductions are provided for indoor-generated particles containing dust-mite and cat allergen, for environmental tobacco smoke (ETS) particles, and for outdoor air fine-mode particles. Additionally, this paper uses a simple model and available data to estimate the energy and total costs of the filtration options. Predicted reductions in cat and dust-mite allergen concentrations range from 20 to 80%. To obtain substantial, e.g. 50%, reductions in indoor concentrations of these allergens, the rate of airflow through the filter must be at least a few indoor volumes per hour. Increasing filter efficiencies above approximately ASHRAE Dust Spot 65% does not significantly reduce predicted indoor concentrations of these allergens. For ETS particles and outdoor fine-mode particles, calculations indicate that relatively large, e.g. 80%, decreases in indoor concentrations are attainable with practical filter efficiencies and flow rates. Increasing the filter efficiency above ASHRAE 85% results in only modest predicted incremental decreases in indoor concentration. Energy costs and total costs can be similar for filtration using filters with a wide range of efficiency ratings. Total estimated filtration costs of approximately $0.70 to $1.80 per person per month are insignificant relative to salaries, rent, or health insurance costs.	Univ Calif Berkeley, Lawrence Berkeley Lab, Indoor Environm Dept, Berkeley, CA 94720 USA; Helsinki Univ Technol, Lab Heating Ventilating & Air Condittioning, FIN-02150 Espoo, Finland	Fisk, WJ (reprint author), Univ Calif Berkeley, Lawrence Berkeley Lab, Indoor Environm Dept, MS 90-3058, Berkeley, CA 94720 USA.						Abt E, 2000, ENVIRON SCI TECHNOL, V34, P3579, DOI 10.1021/es990348y; *ASHRAE, 1992, 521 ANSIASHRAE; ASHRAE, 1999, 522 ASHRAE; *ASHRAE, 1996, ASHRAE HDB; *CA EPA, 1997, HLTH EFF EXP ENV TOB; Committee on the Assessment of Asthma and Indoor Air, 2000, CLEAR AIR ASTHM IND; COUCH RB, 1981, B NEW YORK ACAD MED, V57, P907; Custovic A, 1998, THORAX, V53, P33; DEBLAY F, 1991, J ALLERGY CLIN IMMUN, V88, P919, DOI 10.1016/0091-6749(91)90249-N; DICK EC, 1987, J INFECT DIS, V156, P442; *DOD, 1987, 8559 NAT TECHN INF S; *DOD, 1987, 4234 DOD TB; *EPA, 1996, EPA600AP95001C; *EPA, 1996, EPA600AP95001A; *EPA, 1992, EPA600690006F; Fogh CL, 1997, ATMOS ENVIRON, V31, P2193, DOI 10.1016/S1352-2310(97)00037-X; HANLEY JT, 1994, INDOOR AIR, V4, P169, DOI 10.1111/j.1600-0668.1994.t01-1-00005.x; Lai ACK, 2000, J AEROSOL SCI, V31, P463; LEWIS S, 1995, J HAZARD MATER, V43, P195, DOI 10.1016/0304-3894(95)00037-U; MEANS RS, 1999, FACILITIES MAINTENAN; Miller SL, 2001, ATMOS ENVIRON, V35, P2053, DOI 10.1016/S1352-2310(00)00506-9; Milton D.K., 1996, INDOOR AIR HUMAN HLT, P179; NAZAROFF WW, 1993, ASTM STANDARD TECHNI, V1205; Ozkaynak H, 1996, J EXPO ANAL ENV EPID, V6, P57; Pope A. M., 1993, INDOOR ALLERGENS ASS; RANTIOLEHTIMAKI A, 1994, CLIN EXP ALLERGY, V24, P23, DOI 10.1111/j.1365-2222.1994.tb00912.x; Schappi GF, 1997, J ALLERGY CLIN IMMUN, V100, P656, DOI 10.1016/S0091-6749(97)70170-2; SOOLE BW, 1971, AEROSOL SCI, V2, P1; SOOLE BW, 1971, AEROSOL SCIENCE, V2, P281; SPIEKSMA FTM, 1991, GRANA, V30, P98; SPIEKSMA FTM, 1990, CLIN EXP ALLERGY, V20, P273, DOI 10.1111/j.1365-2222.1990.tb02683.x; THATCHER TL, 1995, ATMOS ENVIRON, V29, P1487, DOI 10.1016/1352-2310(95)00016-R; TOVEY ER, 1981, AM REV RESPIR DIS, V124, P630; TSUBATA R, 1996, P IND AIR 96 SEEC IS, V3, P155; Vette AF, 2001, AEROSOL SCI TECH, V34, P118, DOI 10.1080/027868201300082120; WHITBY KT, 1978, ATMOS ENVIRON, V12, P135, DOI 10.1016/0004-6981(78)90196-8; XU MD, 1994, AEROSOL SCI TECH, V20, P194, DOI 10.1080/02786829408959676	37	86	89	2	36	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0905-6947			INDOOR AIR	Indoor Air	DEC	2002	12	4					223	234		10.1034/j.1600-0668.2002.01136.x		12	Construction & Building Technology; Engineering, Environmental; Public, Environmental & Occupational Health	Construction & Building Technology; Engineering; Public, Environmental & Occupational Health	625CD	WOS:000179798600004	12532754	
J	Burge, HA				Burge, HA			An update on pollen and fungal spore aerobiology	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						pollen; fungi; aerobiology; spores; allergen; immunodetection	IN-HOUSE DUST; THUNDERSTORM-ASSOCIATED ASTHMA; VOLATILE ORGANIC-COMPOUNDS; WATER-DAMAGED BUILDINGS; REPORTED HOME DAMPNESS; GRASS-POLLEN; STACHYBOTRYS-CHARTARUM; RESIDENTIAL CHARACTERISTICS; RESPIRATORY SYMPTOMS; INDOOR AIR	Changes in climate are altering pollen distribution. Predictive modeling can be used to forecast long- and short-term changes in pollen concentrations. Increasing evidence confirms the presence of pollen allergens on small, respirable particles in the air, explaining the occurrence of pollen-season increases in asthma. Like pollens, above ground indoor fungal aerosols primarily reflect outdoor concentrations. Basement spore concentrations might be higher and reflective of local sources. Fungal presence in the indoor or outdoor air can be monitored on an area basis or with personal monitors. The samples can be analyzed by means of microscopy, culture, DNA probes, HPLC, or immunodetection. Total fungal biomass can be estimated on the basis of measurements of ergosterol or glucan in environmental samples. Unfortunately, there are no generally accepted standards for interpretation of fungal levels in indoor or outdoor air. At present, the best approach to indoor fungal control is moisture control in the indoor environment. This will essentially prevent fungal growth, except from extraordinary events.	Harvard Univ, Sch Publ Hlth, Landmark Ctr, Boston, MA 02215 USA	Burge, HA (reprint author), Harvard Univ, Sch Publ Hlth, Landmark Ctr, Room 404M W,401 Pk Dr,POB 15677, Boston, MA 02215 USA.						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Zacharasiewicz A, 1999, WIEN KLIN WOCHENSCHR, V111, P882; Zhou G, 2000, MOL CELL PROBE, V14, P339, DOI 10.1006/mcpr.2000.0324; Zukowski K, 1998, Rocz Panstw Zakl Hig, V49, P67; Zukowski K, 1996, Rocz Panstw Zakl Hig, V47, P343	110	86	88	4	18	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					544	552		10.1067/mai.2002.128674		9	Allergy; Immunology	Allergy; Immunology	602JJ	WOS:000178501900001	12373259	
J	Wardlaw, AJ; Brightling, CE; Green, R; Woltmann, G; Bradding, P; Pavord, ID				Wardlaw, AJ; Brightling, CE; Green, R; Woltmann, G; Bradding, P; Pavord, ID			New insights into the relationship between airway inflammation and asthma	CLINICAL SCIENCE			English	Review						airway hyper-responsiveness; airway smooth muscle; asthma; eosinophils; inflammation	SMOOTH-MUSCLE CELLS; OBSTRUCTIVE PULMONARY-DISEASE; EXPIRATORY FLOW VARIABILITY; MAST-CELLS; BRONCHIAL HYPERREACTIVITY; EOSINOPHILIC BRONCHITIS; POPULATION-SAMPLE; NEDOCROMIL SODIUM; DEEP INSPIRATION; INDUCED SPUTUM	Asthma is a condition characterized by variable airflow obstruction, airway hyper-responsiveness (AHR) and airway inflammation which is usually, but not invariably, eosinophilic. Current thoughts on the pathogenesis of asthma are focused on the idea that it is caused by an inappropriate response of the specific immune system to harmless antigens, particularly allergens such as cat dander and house dust mite, that result in Th2-mediated chronic inflammation. However, the relationship between inflammation and asthma is complex, with no good correlation between the severity of inflammation, at least as measured by the number of eosinophils, and the severity of asthma. In addition, there are a number of conditions, such as eosinophilic bronchitis and allergic rhinitis, in which there is a Th2-mediated inflammatory response, but no asthma, as measured by variable airflow obstruction or AHR. Bronchoconstriction can also occur without obvious airway inflammation, and neutrophilic inflammation can in some cases be associated with asthma. When we compared the immunopathology of eosinophilic bronchitis and asthma, the only difference we observed was that, in asthma, the airway smooth muscle (ASM) was infiltrated by mast cells, suggesting that airway obstruction and AHR are due to an ASM mast cell myositis. This observation emphasizes that the features that characterize asthma, as opposed to bronchitis, are due to abnormalities in smooth muscle responsiveness, which could be intrinsic or acquired, and that inflammation is only relevant in that it leads to these abnormalities. It also emphasizes the importance of micro-localization as an organizing principle in physiological responses to airway inflammation. Thus, if inflammation is localized to the epithelium and lamina propria, then the symptoms of bronchitis (cough and mucus hypersecretion) result, and it is only if the ASM is involved -for reasons that remain to be established -that asthma occurs.	Glenfield Hosp, Leicester Warwick Med Sch, Inst Lung Hlth, Dept Resp Med, Leicester LE3 9QP, Leics, England	Wardlaw, AJ (reprint author), Glenfield Hosp, Leicester Warwick Med Sch, Inst Lung Hlth, Dept Resp Med, Groby Rd, Leicester LE3 9QP, Leics, England.						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Sci.	AUG	2002	103	2					201	211				11	Medicine, Research & Experimental	Research & Experimental Medicine	582PG	WOS:000177359900013	12149112	
J	Darvay, A; White, IR; Rycroft, RJG; Jones, AB; Hawk, JL; McFadden, JP				Darvay, A; White, IR; Rycroft, RJG; Jones, AB; Hawk, JL; McFadden, JP			Photoallergic contact dermatitis is uncommon	BRITISH JOURNAL OF DERMATOLOGY			English	Article						benzophenone-3; photoallergy; photodermatosis; photopatch test; sunscreens; ultraviolet filters	SCANDINAVIAN MULTICENTER PHOTOPATCH; PHOTOCONTACT SENSITIZATION; PHOTOSENSITIVITY; SENSITIVITY; EXPERIENCE; SUNSCREENS; 5-YEAR	Background Despite the enormous increase in sunscreen use, allergic contact (AC) and photoallergic (PA) reactions to ultraviolet (UV) filters are considered rare. Objectives To analyse the data from 2715 patients who underwent photopatch testing at St John's Institute of Dermatology during the period 1983-98. Methods A retrospective analysis of all positive photopatch test episodes was undertaken with the results retrieved from the environmental dermatology database and further verified with the original archived patch test documentation for each individual patient. Results In 111 patients with positive reactions (4.1%), there were 155 AC or PA reactions to allergens in the photopatch test series. Eighty PA reactions were observed in 62 (2.3%) patients (32 men and 30 women, age range 28-75 years), with UV filters accounting for 52 positive reactions (65%). drugs 16 (20%), musk ambrette 11 (14%) and the antiseptic trichlorocarbanilide one (1%). The most common UV filter photoallergen was benzophenone-3 with 14 positive results, followed by benzophenone-10 (n = 9), isopropyl dibenzoylmethane (n = 6), p-aminobenzoic acid (PABA) (n = 5), octyl dimethyl PABA (n = 5), butyl methoxydibenzoylmethane (n = 4), isoamyl methoxycinnamate (n = 2), ethyl methoxycinnamate (n = 2), octyl methoxycinnamate (n = 2). amyl dimethyl PABA (n = 2) and phenylbenzimidazole sulphonic acid (n = 1). A similar number of AC reactions to UV filters was detected in this study. Thus 49 patients (1.8%) had a total of 75 reactions: 51 due to UV filters and 24 as a result of exposure to fragrances and therapeutic agents. Benzophenone-10 accounted for 13 AC reactions and benzophenone-3 for eight reactions. Twenty-two patients had a PA reaction alone, whereas 19 patients had chronic actinic dermatitis and 15 patients polymorphic light eruption (PLE) in addition. Thus, 34 of the 62 patients (55%) had a preceding underlying photodermatosis. Conclusions These results show a low yield of positive photopatch tests. Thus, despite the large increase in the use of UV filters over the last decade, the development of PA reactions remains rare. Furthermore, most of the common UV filter photoallergens identified in this study, including PABA, amyl dimethyl PABA and benzophenone-10. are now rarely used in sunscreen manufacture, while isopropyl dibenzoylmethane was voluntarily removed from the market in 1993. Currently, benzophenone-3 is the commonest contact photoallergen still in widespread use. In contrast, the UVB filter octyl methoxycinnamate, used in a number of sunscreens, produced only two positive PA reactions in 12 years of testing. Nevertheless, although these reactions are extremely rare, patients with photodermatoses such as PIE and chronic actinic dermatitis do represent a group of patients at increased risk of developing photoallergy. Further photopatch test series should be regularly reviewed and updated, as the relevance of individual photoallergens changes over time. Currently, there is no evidence that PA reactions represent a common clinical problem.	St Thomas Hosp, St Johns Inst Dermatol, Dept Environm Dermatol, London SE1 7EH, England	Darvay, A (reprint author), St Thomas Hosp, St Johns Inst Dermatol, Dept Environm Dermatol, Lambeth Palace Rd, London SE1 7EH, England.						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J. Dermatol.	OCT	2001	145	4					597	601		10.1046/j.1365-2133.2001.04458.x		5	Dermatology	Dermatology	484MF	WOS:000171693600011	11703286	
J	Olesen, C; Sondergaard, C; Thrane, N; Nielsen, GL; de Jong-van den Berg, L; Olsen, J				Olesen, C; Sondergaard, C; Thrane, N; Nielsen, GL; de Jong-van den Berg, L; Olsen, J		EuroMAP Grp	Do pregnant women report use of dispensed medications?	EPIDEMIOLOGY			English	Article						compliance; exposure misclassification; pregnancy; prescription database; risk assessment; validation study	DRUG-USE; CONGENITAL-MALFORMATIONS; PATIENT COMPLIANCE; QUESTIONNAIRE DATA; RECALL BIAS; EXPOSURE; OUTCOMES; RECORDS; ASTHMA; POPULATION	Surveillance of drug safety in pregnancy often draws on administrative prescription registries. Noncompliance in the use of prescribed medication may be frequent among pregnant women owing to their fear of fetotoxic side effects. To estimate compliance in the use of prescription drugs dispensed during pregnancy, we compared prescription data from the North Jutland Prescription Database with information on drug use provided by pregnant women to the Danish National Birth Cohort (DNBC), which is a health inter-view survey. We used the North Jutland Prescription Database to identify all prescription drugs dispensed during pregnancy for the 2,041 women who were enrolled in the DNBC in the County of North Jutland, Denmark. Compliance was defined as the probability of reporting drug use in DNBC after purchasing a dispensed prescription drug. The overall compliance to drugs purchased within 120 days before the interview was 43% (95% confidence interval = 40-46). Drugs used for treating chronic diseases, for example, beta-blockers, insulin, thyroid hormones, and diuretic and antiepileptic drugs, were always reported to be used, but compliance was low for drugs used for local or short-term treatment such as antihistamines, antibiotics, antacids, nonsteroid anti-inflammatory drugs, and gynecologic drugs. Thus, for the latter drug groups the prescription database may provide an incomplete identification of exposure, Neither data source is unbiased regarding actual drug intake. Nevertheless, our results indicate that for some drug groups risk assessment studies based on prescription data may produce false negative results as a result of noncompliance.	Aarhus Univ, Danish Epidemiol Sci Ctr, Dept Epidemiol & Social Med, DK-8000 Aarhus C, Denmark; Med Res Unit, Ringkobing, Denmark; Aarhus Univ, Dept Clin Epidemiol, Aarhus, Denmark; Aalborg Hosp, Aalborg, Denmark; Univ Groningen, GUIDE, Dept Social Pharm & Pharmacoepidemiol, Groningen, Netherlands	Olesen, C (reprint author), Aarhus Univ, Danish Epidemiol Sci Ctr, Dept Epidemiol & Social Med, Vennelyst Blvd 6, DK-8000 Aarhus C, Denmark.						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J	Galan, C; Carinanos, P; Garcia-Mozo, H; Alcazar, P; Dominguez-Vilches, E				Galan, C; Carinanos, P; Garcia-Mozo, H; Alcazar, P; Dominguez-Vilches, E			Model for forecasting Olea europaea L. airborne pollen in South-West Andalusia, Spain	INTERNATIONAL JOURNAL OF BIOMETEOROLOGY			English	Article						aerobiology; forecasting; Olea europaea; pollen index; pollen production	ATMOSPHERE	Data on predicted average and maximum air-borne pollen concentrations and the dates on which these maximum values are expected are of undoubted value to allergists and allergy sufferers, as well as to agronomists. This paper reports on the development of predictive models for calculating total annual pollen output, on the basis of pollen and weather data compiled over the last 19 years (1982-2000) for Cordoba (Spain). Models were tested in order to predict the 2000 pollen season; in addition, and in view of the heavy rainfall recorded in spring 2000, the 1982-1998 data set was used to test the model for 1999. The results of the multiple regression analysis show that the variables exerting the greatest influence on the pollen index were rainfall in March and temperatures over the months prior to the flowering period. For prediction of maximum values and dates on which these values might be expected, the start of the pollen season was used as an additional independent variable. Temperature proved the best variable for this prediction. Results improved when the 5-day moving average was taken into account. Testing of the predictive model for 1999 and 2000 yielded fairly similar results. In both cases, the difference between expected and observed pollen data was no greater than 10%. However, significant differences were recorded between forecast and expected maximum and minimum values, owing to the influence of rainfall during the flowering period.	Univ Cordoba, Dept Bot, E-14071 Cordoba, Spain	Galan, C (reprint author), Univ Cordoba, Dept Bot, Colonia San Jose,Casa 4,Ctra Madrid Km 396, E-14071 Cordoba, Spain.		Carinanos, Paloma/K-5696-2014	Carinanos, Paloma/0000-0002-8955-2383			Alba F, 1998, AEROBIOLOGIA, V14, P191, DOI 10.1007/BF02694205; ARON R, 1983, AGR METEOROL, V28, P351, DOI 10.1016/0002-1571(83)90011-0; CANDAU P, 1981, BOT MACARONESICA, V8, P89; DAMATO G, 1994, CLIN EXP ALLERGY, V24, P210, DOI 10.1111/j.1365-2222.1994.tb00222.x; DELAGUARDIA CD, 1993, J INVEST ALLERG CLIN, V3, P251; DELAGUARDIA CD, 2000, POLEN, V10, P103; DOMINGUEZ E, 1992, MONOGRAFIAS REA EAN, V1; Dominguez Vilches Eugenio, 1993, Journal of Investigational Allergology and Clinical Immunology, V3, P121; *FAO, 1998, CROP EV TRANSP GUID; FLORIDO JF, 1999, INT ARCH ALLERGY IMM, V119, P199; Fornaciari M., 1997, Agricoltura Mediterranea, V127, P134; Fornaciari M, 1998, GRANA, V37, P110; Fornaciari M, 2000, PLANT BIOSYST, V134, P199, DOI 10.1080/11263500012331358474; Frenguelli G, 1989, AEROBIOLOGIA, V5, P64, DOI 10.1007/BF02446489; Galan C, 1998, INT J BIOMETEOROL, V41, P95, DOI 10.1007/s004840050059; Galan C, 2001, INT J BIOMETEOROL, V45, P8, DOI 10.1007/s004840000081; Galan C, 1988, AN ASOC PALINOL LENG, V4, P46; GALAN CD, 1993, J INVEST ALLERG CLIN, V3, P271; GARCIAMOZO H, 2001, IN PRESS GRANA; Gonzalez Minero F J, 1997, Ann Allergy Asthma Immunol, V78, P278; Gonzalez-Minero FJG, 1998, AGR ECOSYST ENVIRON, V69, P201, DOI 10.1016/S0167-8809(98)00105-4; Gonzalez-Minero F. J., 1996, AEROBIOLOGIA, V12, P91, DOI 10.1007/BF02446600; GUTIERREZBUSTIL.M, 2000, BOT MADR, V57, P357; HIRST JM, 1952, ANN APPL BIOL, V39, P257, DOI 10.1111/j.1744-7348.1952.tb00904.x; *I EST AND, 1999, AN EST AND; RALLO L, 1991, J AM SOC HORTIC SCI, V116, P1058; Recio M, 1996, GRANA, V35, P308; RUIZ L, 1998, STUDY SEASONAL DAILY	28	86	89	3	10	SPRINGER-VERLAG	NEW YORK	175 FIFTH AVE, NEW YORK, NY 10010 USA	0020-7128			INT J BIOMETEOROL	Int. J. Biometeorol.	JUL	2001	45	2					59	63		10.1007/s004840100089		5	Biophysics; Environmental Sciences; Meteorology & Atmospheric Sciences; Physiology	Biophysics; Environmental Sciences & Ecology; Meteorology & Atmospheric Sciences; Physiology	457DX	WOS:000170122800002	11513048	
J	Lynch, SV; Wood, RA; Boushey, H; Bacharier, LB; Bloomberg, GR; Kattan, M; O'Connor, GT; Sandel, MT; Calatroni, A; Matsui, E; Johnson, CC; Lynn, H; Visness, CM; Jaffee, KF; Gergen, PJ; Gold, DR; Wright, RJ; Fujimura, K; Rauch, M; Busse, WW; Gern, JE				Lynch, Susan V.; Wood, Robert A.; Boushey, Homer; Bacharier, Leonard B.; Bloomberg, Gordon R.; Kattan, Meyer; O'Connor, George T.; Sandel, Megan T.; Calatroni, Agustin; Matsui, Elizabeth; Johnson, Christine C.; Lynn, Henry; Visness, Cynthia M.; Jaffee, Katy F.; Gergen, Peter J.; Gold, Diane R.; Wright, Rosalind J.; Fujimura, Kei; Rauch, Marcus; Busse, William W.; Gern, James E.			Effects of early-life exposure to allergens and bacteria on recurrent wheeze and atopy in urban children	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Asthma; atopy; allergen exposure; microbial exposure; inner city	HOUSE-DUST MITE; CHILDHOOD ASTHMA; INNER-CITY; IMMUNE DEVELOPMENT; VIRUS-INFECTION; DOG OWNERSHIP; UNITED-STATES; LUNG-FUNCTION; BIRTH-COHORT; CAT ALLERGEN	Background: Wheezing illnesses cause major morbidity in infants and are frequent precursors to asthma. Objective: We sought to examine environmental factors associated with recurrent wheezing in inner-city environments. Methods: The Urban Environment and Childhood Asthma study examined a birth cohort at high risk for asthma (n = 560) in Baltimore, Boston, New York, and St Louis. Environmental assessments included allergen exposure and, in a nested case-control study of 104 children, the bacterial content of house dust collected in the first year of life. Associations were determined among environmental factors, aeroallergen sensitization, and recurrent wheezing at age 3 years. Results: Cumulative allergen exposure over the first 3 years was associated with allergic sensitization, and sensitization at age 3 years was related to recurrent wheeze. In contrast, first-year exposure to cockroach, mouse, and cat allergens was negatively associated with recurrent wheeze (odds ratio, 0.60, 0.65, and 0.75, respectively; P <= .01). Differences in house dust bacterial content in the first year, especially reduced exposure to specific Firmicutes and Bacteriodetes, was associated with atopy and atopic wheeze. Exposure to high levels of both allergens and this subset of bacteria in the first year of life was most common among children without atopy or wheeze. Conclusions: In inner-city environments children with the highest exposure to specific allergens and bacteria during their first year were least likely to have recurrent wheeze and allergic sensitization. These findings suggest that concomitant exposure to high levels of certain allergens and bacteria in early life might be beneficial and suggest new preventive strategies for wheezing and allergic diseases.	[Lynch, Susan V.; Boushey, Homer; Fujimura, Kei; Rauch, Marcus] Univ Calif San Francisco, Dept Med, San Francisco, CA USA; [Wood, Robert A.; Matsui, Elizabeth] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA; [Bacharier, Leonard B.; Bloomberg, Gordon R.] Washington Univ, St Louis Childrens Hosp, Sch Med, Dept Pediat, St Louis, MO 63110 USA; [Kattan, Meyer] Columbia Univ, Med Ctr, Div Pediat Allergy & Immunol, New York, NY USA; [O'Connor, George T.; Sandel, Megan T.] Boston Univ, Sch Med, Ctr Pulm, Chapel Hill, NC USA; [Calatroni, Agustin; Lynn, Henry; Visness, Cynthia M.; Jaffee, Katy F.] Rho Inc, Chapel Hill, NC USA; [Johnson, Christine C.] Div Allergy & Immunol Henry Ford Hlth Syst, Detroit, MI USA; [Gergen, Peter J.] Natl Inst Allergy & Infect Dis, Bethesda, MD USA; [Gold, Diane R.; Wright, Rosalind J.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Channing Lab, Boston, MA 02115 USA; [Busse, William W.; Gern, James E.] Univ Wisconsin, Sch Med & Publ Hlth, Dept Pediat, Madison, WI USA	Wood, RA (reprint author), Johns Hopkins Univ, Sch Med, 600 North Wolfe St,CMSC 1102, Baltimore, MD 21287 USA.	rwood@jhmi.edu			National Institute of Allergy and Infectious Diseases; National Institutes of Health [NO1-AI-25496, NO1-AI-25482, HHSN272200900052C, HHSN272201000052I]; National Center for Advancing Translational Sciences, National Institutes of Health [RR00052, M01RR00533, 1UL1RR025771, M01RR00071, 1UL1RR024156, 5UL1RR024992 02]	This project has been supported in whole or in part with federal funds from the National Institute of Allergy and Infectious Diseases, National Institutes of Health, under contract numbers NO1-AI-25496, NO1-AI-25482, HHSN272200900052C, and HHSN272201000052I. Additional support was provided by the National Center for Advancing Translational Sciences, National Institutes of Health, under grants RR00052, M01RR00533, 1UL1RR025771, M01RR00071, 1UL1RR024156, and 5UL1RR024992 02.	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Allergy Clin. Immunol.	SEP	2014	134	3					593	+		10.1016/j.jaci.2014.04.018		21	Allergy; Immunology	Allergy; Immunology	AO5GR	WOS:000341372400011	24908147	
J	Kumamoto, Y; Linehan, M; Weinstein, JS; Laidlaw, BJ; Craft, JE; Iwasaki, A				Kumamoto, Yosuke; Linehan, Melissa; Weinstein, Jason S.; Laidlaw, Brian J.; Craft, Joseph E.; Iwasaki, Akiko			CD301b(+) Dermal Dendritic Cells Drive T Helper 2 Cell-Mediated Immunity	IMMUNITY			English	Article							CD4(+) T-CELLS; TRANSCRIPTION FACTOR GATA-3; HELPER TYPE-2 RESPONSE; DUST MITE ALLERGEN; IN-VIVO; LANGERHANS CELLS; MUCOSAL IMMUNIZATION; AIRWAY INFLAMMATION; HELMINTH INFECTION; TH2 CELLS	Unlike other types of T helper (Th) responses, whether the development of Th2 cells requires instruction from particular subset of dendritic cells (DCs) remains unclear. By using an in vivo depletion approach, we have shown that DCs expressing CD301b were required for the generation of Th2 cells after subcutaneous immunization with ovalbumin (OVA) along with papain or alum. CD301b(+) DCs are distinct from epidermal or CD207(+) dermal DCs (DDCs) and were responsible for transporting antigen injected subcutaneously with Th2-type adjuvants. Transient depletion of CD301b(+) DCs resulted in less effective accumulation and decreased expression of CD69 by polyclonal CD4(+) T cells in the lymph node. Moreover, despite intact cell division and interferon-gamma production, CD301b(+) DC depletion led to blunted interleukin-4 production by OVA-specific OT-II transgenic CD4(+) T cells and significantly impaired Th2 cell development upon infection with Nippostrongylus brasiliensis. These results reveal CD301b(+) DDCs as the key mediators of Th2 immunity.	[Kumamoto, Yosuke; Linehan, Melissa; Weinstein, Jason S.; Laidlaw, Brian J.; Craft, Joseph E.; Iwasaki, Akiko] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT 06520 USA; [Craft, Joseph E.] Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06520 USA	Iwasaki, A (reprint author), Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT 06520 USA.	akiko.iwasaki@yale.edu		Kumamoto, Yosuke/0000-0001-9369-4934	National Institutes of Health (NIH) [AI054359, AI062428, AR40072, AR44076]; Yale Rheumatic Diseases Research Core Center, NIH (NIAMS) [P30 AR053495]	We thank D. Kaplan and R. Medzhitov for critical reading of the manuscript and H. Dong for technical support. This work is supported by National Institutes of Health (NIH) grants to A. I. (AI054359 and AI062428) and J.E.C. (AR40072 and AR44076). The study was partly funded by a pilot grant from the Yale Rheumatic Diseases Research Core Center, NIH (NIAMS) P30 AR053495. Y.K. was an Astellas Foundation for Research on Metabolic Disorders fellow.	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J	Hyson, DA				Hyson, Dianne A.			A Comprehensive Review of Apples and Apple Components and Their Relationship to Human Health	ADVANCES IN NUTRITION			English	Review								There has been an increasing appreciation and understanding of the link between dietary fruit and vegetable intake and improved health in humans. The widespread and growing intake of apples and apple juice/products and their rich phytochemical profile suggest their important potential to affect the health of the populations consuming them. This review summarizes current clinical, in vitro, and in vivo data and builds upon earlier published reports that apple may reduce the risk of chronic disease by various mechanisms, including antioxidant, antiproliferative, and cell signaling effects. Exposure to apples and apple products has been associated with beneficial effects on risk, markers, and etiology of cancer, cardiovascular disease, asthma, and Alzheimer's disease. Recent work suggests that these products may also be associated with improved outcomes related to cognitive decline of normal aging, diabetes, weight management, bone health, pulmonary function, and gastrointestinal protection. Adv. Nutr. 2: 408-420,2011.	Calif State Univ Sacramento, Dept Family & Consumer Sci Nutr & Food Dietet, Sacramento, CA 95819 USA	Hyson, DA (reprint author), Calif State Univ Sacramento, Dept Family & Consumer Sci Nutr & Food Dietet, Sacramento, CA 95819 USA.	dhyson@csus.edu			United States Apple Association; Apple Products Research and Education Council	Supported in part by the United States Apple Association and the Apple Products Research and Education Council.	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Nutr.	SEP	2011	2	5					408	420		10.3945/an.111.000513		13	Nutrition & Dietetics	Nutrition & Dietetics	V27BU	WOS:000208589500005	22332082	
J	Terzano, C; Di Stefano, F; Conti, V; Graziani, E; Petroianni, A				Terzano, C.; Di Stefano, F.; Conti, V.; Graziani, E.; Petroianni, A.			Air pollution ultrafine particles: toxicity beyond the lung	EUROPEAN REVIEW FOR MEDICAL AND PHARMACOLOGICAL SCIENCES			English	Article						Nanoparticles; Lung injury; Cardiovascular disease; Health effects	DIESEL EXHAUST PARTICLES; CORONARY-HEART-DISEASE; POLYCYCLIC AROMATIC-HYDROCARBONS; AIRBORNE PARTICULATE MATTER; LONG-TERM EXPOSURE; OXIDATIVE STRESS; FINE PARTICLES; CARBON-BLACK; IN-VIVO; HOSPITAL ADMISSIONS	Background: Ultrafine particles or nanoparticles (UFPs or PM0.1) are the fraction of ambient particulates with an aerodynamic diameter smaller than 0.1 mu m. Currently UFPs are emerging as the most abundant particulate pollutants in urban and industrial areas, as their exposures have increased dramatically because of anthropogenic sources such as internal combustion engines, power plants, incinerators and many other sources of thermo-degradation. Ultrafine particles have been less studied than PM2.5 and PM10 particulates, mass concentrations of particles smaller than 2.5 and 10 mu m, respectively. Objective, Evidence and Information Sources: We examined the current scientific literature about the health effects of ultrafine particles exposure. State of the Art: UFPs are able to inhibit phagocytosis, and to stimulate inflammatory responses, damaging epithelial cells and potentially gaining access to the interstitium. They could be responsible for consistent reductions in forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) in patients with asthma. Chronic exposure to UFPs can produce deleterious effects on the lung, also causing oxidative stress and enhancing pro-inflammatory effects in airways of COPD patients. Cardiovascular detrimental consequences due to UFPs exposure have observed in epidemiological studies, and could likely be explained by translocation of UFPs from the respiratory epithelium towards circulation and subsequent toxicity to vascular endothelium; alteration of blood coagulation; triggering of autonomic nervous system reflexes eventually altering the cardiac frequency and function. Once deposited deeply into the lung, UFPs - in contrast to larger-sized particles - appear to access to the blood circulation by different transfer routes and mechanisms, resulting in distribution throughout the body, including the brain, with potential neurotoxic consequences. Perspectives and Conclusions. UFPs represent an area of toxicology of emerging concern. A new concept of environmental medicine would help in understanding not only the environmental mechanisms of disease, but also in developing specific preventive or therapeutic strategies for minimizing the dangerous influence of pollution on health.	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WICHMANN HE, 2000, 98 HEI, P1; Zanobetti A, 2001, AM J RESP CRIT CARE, V164, P831; PARTICUALTE MATTER P, P63	119	85	91	5	69	VERDUCI PUBLISHER	ROME	VIA GREGORIO VII, ROME, 186-00165, ITALY	1128-3602			EUR REV MED PHARMACO	Eur. Rev. Med. Pharmacol. Sci.	OCT	2010	14	10					809	821				13	Pharmacology & Pharmacy	Pharmacology & Pharmacy	674MS	WOS:000283750900001	21222367	
J	Verma, D; Moghimi, B; LoDuca, PA; Singh, HD; Hoffman, BE; Herzog, RW; Daniell, H				Verma, Dheeraj; Moghimi, Babak; LoDuca, Paul A.; Singh, Harminder D.; Hoffman, Brad E.; Herzog, Roland W.; Daniell, Henry			Oral delivery of bioencapsulated coagulation factor IX prevents inhibitor formation and fatal anaphylaxis in hemophilia B mice	PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA			English	Article						allergy; chloroplast; genetic disorders; oral tolerance; plant-made therapeutics	HEAT-LABILE ENTEROTOXIN; CHOLERA-TOXIN; TRANSGENIC CHLOROPLASTS; FUNCTIONAL-EVALUATION; TOBACCO CHLOROPLASTS; ESCHERICHIA-COLI; VACCINE ANTIGENS; IMMUNE-RESPONSES; GENE-THERAPY; MOUSE MODEL	To address complications of pathogenic antibody or life-threatening anaphylactic reactions in protein replacement therapy for patients with hemophilia or other inherited protein deficiencies, we have developed a prophylactic protocol using a murine hemophilia B model. Oral delivery of coagulation factor IX fused with cholera toxin beta-subunit (with or without a furin cleavage site; CTB-FFIX or CTB-FIX), expressed in chloroplasts (up to 3.8% soluble protein or 0.4 mg/g leaf tissue), bioencapsulated in plant cells, effectively blocked formation of inhibitory antibodies (undetectable or up to 100-fold less than controls). Moreover, this treatment eliminated fatal anaphylactic reactions that occurred after four to six exposures to intravenous F. IX. Whereas only 20-25% of control animals survived after six to eight F. IX doses, 90-93% of F.IX-fed mice survived 12 injections without signs of allergy or anaphylaxis. Immunostaining confirmed delivery of F. IX to Peyer's patches in the ileum. Within 2-5 h, feeding of CTB-FFIX additionally resulted in systemic delivery of F. IX antigen. This high-responder strain of hemophilia B mice represents a new animal model to study anaphylactic reactions. The protocol was effective over a range of oral antigen doses (equivalent to 5-80 mu g recombinant F.IX/kg), and controlled inhibitor formation and anaphylaxis long-term, up to 7 months (similar to 40% life span of this mouse strain). Oral antigen administration caused a deviant immune response that suppressed formation of IgE and inhibitory antibodies. This cost-effective and efficient approach of antigen delivery to the gut should be applicable to several genetic diseases that are prone to pathogenic antibody responses during treatment.	[Verma, Dheeraj; Singh, Harminder D.; Daniell, Henry] Univ Cent Florida, Coll Med, Dept Mol Biol & Microbiol, Orlando, FL 32816 USA; [Moghimi, Babak; LoDuca, Paul A.; Hoffman, Brad E.; Herzog, Roland W.] Univ Florida, Coll Med, Dept Pediat, Gainesville, FL 32610 USA	Herzog, RW (reprint author), Univ Florida, Coll Med, Dept Pediat, Gainesville, FL 32610 USA.	rherzog@ufl.edu; daniell@mail.ucf.edu	Verma, Dheeraj/E-1654-2011; Hoffman, Brad/E-8363-2010	Hoffman, Brad/0000-0002-5560-9580; Daniell, Henry/0000-0003-4485-1176	NIH [R21 HL089813, R01 AI/HL51390, R01 GM 63879]	We thank Clive Wasserfall and David Markusic for their help. This work was supported by NIH Grant R21 HL089813 to R. W. H. and H. D., R01 AI/HL51390 to R. W. H., and R01 GM 63879 to H. D.	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J	Smith-Sivertsen, T; Diaz, E; Pope, D; Lie, RT; Diaz, A; McCracken, J; Bakke, P; Arana, B; Smith, KR; Bruce, N				Smith-Sivertsen, Tone; Diaz, Esperanza; Pope, Dan; Lie, Rolv T.; Diaz, Anaite; McCracken, John; Bakke, Per; Arana, Byron; Smith, Kirk R.; Bruce, Nigel			Effect of Reducing Indoor Air Pollution on Women's Respiratory Symptoms and Lung Function: The RESPIRE Randomized Trial, Guatemala	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						biomass; bronchitis; chronic; carbon monoxide; developing countries; pulmonary disease; chronic obstructive; smoke; spirometry; wood	OBSTRUCTIVE PULMONARY-DISEASE; WOOD SMOKE EXPOSURE; PARTICULATE MATTER; CARBON-MONOXIDE; HIGHLAND GUATEMALA; STOVE INTERVENTION; BIOMASS SMOKE; MEXICAN WOMEN; ASTHMA; RISK	Exposure to household wood smoke from cooking is a risk factor for chronic obstructive lung disease among women in developing countries. The Randomized Exposure Study of Pollution Indoors and Respiratory Effects (RESPIRE) is a randomized intervention trial evaluating the respiratory health effects of reducing indoor air pollution from open cooking fires. A total of 504 rural Mayan women in highland Guatemala aged 15-50 years, all using traditional indoor open fires, were randomized to either receive a chimney woodstove (plancha) or continue using the open fire. Assessments of chronic respiratory symptoms and lung function and individual measurements of carbon monoxide exposure were performed at baseline and every 6 months up to 18 months. Use of a plancha significantly reduced carbon monoxide exposure by 61.6%. For all respiratory symptoms, reductions in risk were observed in the plancha group during follow-up; the reduction was statistically significant for wheeze (relative risk = 0.42, 95% confidence interval: 0.25, 0.70). The number of respiratory symptoms reported by the women at each follow-up point was also significantly reduced by the plancha (odds ratio = 0.7, 95% confidence interval: 0.50, 0.97). However, no significant effects on lung function were found after 12-18 months. Reducing indoor air pollution from household biomass burning may relieve symptoms consistent with chronic respiratory tract irritation.	[Diaz, Esperanza] Univ Bergen, Sect Gen Practice, Dept Publ Hlth & Primary Hlth Care, Fac Med & Dent, N-5018 Bergen, Norway; [Pope, Dan; Bruce, Nigel] Univ Liverpool, Div Publ Hlth, Sch Populat Community & Behav Sci, Fac Med, Liverpool L69 3BX, Merseyside, England; [Diaz, Anaite; Arana, Byron] Univ Valle Guatemala, Ctr Hlth Studies, Guatemala City, Guatemala; [McCracken, John] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA; [McCracken, John] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA; [Bakke, Per] Haukeland Hosp, Dept Thorac Med, N-5021 Bergen, Norway; [Bakke, Per] Univ Bergen, Inst Med, Fac Med & Dent, N-5018 Bergen, Norway; [Smith, Kirk R.] Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA	Diaz, E (reprint author), Univ Bergen, Sect Gen Practice, Dept Publ Hlth & Primary Hlth Care, Fac Med & Dent, Kalfarveien 31, N-5018 Bergen, Norway.	esperanza.diaz@isf.uib.no	Pope, Daniel/C-3054-2014		Norwegian Research Council; US National Institute of Environmental Health Sciences	Funding was obtained from the Norwegian Research Council for this supplement to the main randomized trial (RESPIRE), which was funded by the US National Institute of Environmental Health Sciences.	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J	Yang, W; Omaye, ST				Yang, Wei; Omaye, Stanley T.			Air pollutants, oxidative stress and human health	MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS			English	Review						Air pollution; Oxidative stress; Free radicals; Human health; Antioxidants	OBSTRUCTIVE PULMONARY-DISEASE; INHALED NITROGEN-DIOXIDE; MICROSOMAL EPOXIDE HYDROLASE; EMERGENCY ROOM ADMISSIONS; CONGESTIVE-HEART-FAILURE; CARBON-MONOXIDE LEVELS; HOSPITAL ADMISSIONS; LUNG-CANCER; DAILY MORTALITY; AMBIENT AIR	Air pollutants have, and continue to be, major contributing factors to chronic diseases and mortality, subsequently impacting public health. Chronic diseases include: chronic obstructive pulmonary diseases (COPD), cardiovascular diseases (CVD), asthma, and cancer. Byproducts of oxidative stress found in air pollutants are common initiators or promoters of the damage produced in such chronic diseases. Such air pollutants include: ozone, sulfur oxides, carbon monoxide, nitrogen oxides, and particulate matter. Interaction between oxidative stress byproducts and certain genes within our population may modulate the expression of specific chronic diseases. in this brief review we attempt to provide some insight into what we currently know about the health problems associated with various air pollutants and their relationship in promoting chronic diseases through changes in oxidative stress and modulation of gene expression. Such insight eventually may direct the means for effective public health prevention and treatment of diseases associated with air pollution and treatment of diseases associated with air pollution. (C) 2008 Elsevier B.V. All rights reserved.	[Omaye, Stanley T.] Univ Nevada, Dept Nutr, Reno, NV 89557 USA; [Yang, Wei; Omaye, Stanley T.] Univ Nevada, Environm Sci Grad Program, Reno, NV 89557 USA; [Yang, Wei] Univ Nevada, Sch Community Hlth Sci, Reno, NV 89557 USA	Omaye, ST (reprint author), Univ Nevada, Dept Nutr, Reno, NV 89557 USA.	omaye@unr.edu					ADAMS KF, 1988, J AM COLL CARDIOL, V12, P900; ALTSHULLER AP, 1987, JAPCA J AIR WASTE MA, V37, P1409; AMDUR MO, 1980, CASARETT DOULLS TOXI, P608; Atkinson RW, 2001, AM J RESP CRIT CARE, V164, P1860; AVIADO DM, 1968, ARCH ENVIRON HEALTH, V16, P903; BARBONE F, 1995, AM J EPIDEMIOL, V141, P1161; Barnes PJ, 1999, THORAX, V54, P245; BARRY BE, 1988, EXP LUNG RES, V14, P225, DOI 10.3109/01902148809115126; Beelen R, 2008, ENVIRON HEALTH PERSP, V116, P196, DOI 10.1289/ehp.10767; Benhamou S, 1998, CANCER RES, V58, P5291; Bouchardy C, 1998, PHARMACOGENETICS, V8, P291, DOI 10.1097/00008571-199808000-00002; Bouchardy C, 2001, LUNG CANCER-J IASLC, V32, P109, DOI 10.1016/S0169-5002(00)00215-4; BOWLER PJ, 1993, ENV SCI PHILOS ANCIE, P137; Brimblecombe Peter, 1987, BIG SMOKE HIST AIR P; Brunekreef B, 2002, LANCET, V360, P1233, DOI 10.1016/S0140-6736(02)11274-8; Burnett RT, 1997, EPIDEMIOLOGY, V8, P162, DOI 10.1097/00001648-199703000-00007; Burnett RT, 1997, ENVIRON HEALTH PERSP, V105, P614, DOI 10.1289/ehp.97105614; CALVERT AF, 1987, AUST NZ J MED, V17, P472, DOI 10.1111/j.1445-5994.1987.tb00100.x; Capasso L, 2000, LANCET, V356, P1774, DOI 10.1016/S0140-6736(05)71971-1; Chen L, 2001, TOXICOL METHOD, V11, P233; CHEN L, 2000, J INHAL TOXICOL, V12, P281; DANIEL H, 2002, HR J NUTR, V87, pS305; Dockery DW, 2001, ENVIRON HEALTH PERSP, V109, P483, DOI 10.2307/3454657; Dominici F, 2006, JAMA-J AM MED ASSOC, V295, P1127, DOI 10.1001/jama.295.10.1127; DRISCOLL KE, 1986, FUND APPL TOXICOL, V7, P264, DOI 10.1016/0272-0590(86)90156-9; ELSOM D, 1992, ENV HLTH PERSPECT, V100, P47; Evelyn J., 1661, FUMIFUGIUM INCONVENI; FAIRLEY D, 1990, ENVIRON HEALTH PERSP, V89, P159, DOI 10.2307/3430912; Fakhrzadeh L, 2004, AM J PHYSIOL-LUNG C, V287, P279; FERIN J, 1977, INHALED PARTICLES, V4, P234; FRANK NR, 1962, J APPL PHYSIOL, V17, P252; Gent JF, 2003, JAMA-J AM MED ASSOC, V290, P1859, DOI 10.1001/jama.290.14.1859; Gilmour M, 2006, ENVIRON HEALTH PERSP, V114, P627, DOI 10.1289/ehp.8380; Goldsmith Carroll-Ann W., 1999, Reviews on Environmental Health, V14, P121; GOLDSTEIN E, 1977, AM REV RESPIR DIS, V115, P403; Halliwell B, 2002, FREE RADICAL BIO MED, V32, P968, DOI 10.1016/S0891-5849(02)00808-0; Hoek G, 2002, LANCET, V360, P1203, DOI 10.1016/S0140-6736(02)11280-3; Hong YC, 2002, STROKE, V33, P2165, DOI 10.1161/01.STR.0000026865.52610.5B; Hong YC, 2002, ENVIRON HEALTH PERSP, V110, P187; HORSTMAN DH, 1990, AM REV RESPIR DIS, V142, P1158; HORVATH SM, 1989, JAPCA J AIR WASTE MA, V39, P1323; HORVATH SM, 1988, J APPL PHYSIOL, V65, P2696; KINNEY PL, 1991, ENVIRON RES, V54, P99, DOI 10.1016/S0013-9351(05)80094-5; KOENIG JQ, 1987, AM REV RESPIR DIS, V136, P1152; Krishna M. 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Res. Genet. Toxicol. Environ. Mutagen.	MAR 31	2009	674	1-2					45	54		10.1016/j.mrgentox.2008.10.005		10	Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology	Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology	432KX	WOS:000265133000006	19013537	
J	Traidl-Hoffmann, C; Jakob, T; Behrendt, H				Traidl-Hoffmann, Claudia; Jakob, Thilo; Behrendt, Heidrun			Determinants of allergenicity	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Allergen; structure; intrinsic function; pollen-associated lipid mediators; adjuvant	HOUSE-DUST MITE; SERUM IGE LEVELS; ALLERGIC AIRWAY INFLAMMATION; CYSTEINE PROTEASE ACTIVITY; DIESEL EXHAUST PARTICLES; CD4(+)CD25(+) T-CELLS; AMINO-ACID-SEQUENCE; DER-P-I; DENDRITIC CELLS; PROTEOLYTIC ACTIVITY	The question "What makes an allergen an allergen?" has puzzled generations of researchers, and we still do not have a conclusive answer. Despite increasing knowledge about the molecular and functional characteristics of allergens that have been identified, we still do not fully understand why some proteins are clinically relevant allergens and most are not. Different approaches have been taken to identify the structural and functional features of allergens, aiming at developing methods to predict allergenicity and thus to identify allergens. However, none of these methods has allowed a reliable discrimination between allergenic and nonallergenic compounds on its own. This review sums up diverse determinants that contribute to the phenomenon of allergenicity and outlines that in addition to the structure and function of the allergen, factors derived from allergen carriers, the environment, and the susceptible individual are of importance. (J Allergy Clin Immunol 2009;123:558-66.)	[Traidl-Hoffmann, Claudia; Behrendt, Heidrun] Tech Univ Munich, Div Environm Dermatol & Allergy, Helmholtz Ctr Munich TUM, ZAUM Ctr Allergy & Environm,Dept Dermatol & Aller, D-80802 Munich, Germany; [Jakob, Thilo] Univ Med Ctr Freiburg, Allergy Res Grp, Dept Dermatol, Freiburg, Germany	Traidl-Hoffmann, C (reprint author), Tech Univ Munich, Div Environm Dermatol & Allergy, Helmholtz Ctr Munich TUM, ZAUM Ctr Allergy & Environm,Dept Dermatol & Aller, Biedersteinerstr 29, D-80802 Munich, Germany.	traidl-hoffmann@lrz.tum.de; thilo.jakob@uniklinik-freiburg.de	Jakob, Thilo/J-1621-2012; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Traidl-Hoffmann, Claudia/0000-0001-5085-5179	German Ministry of Research and Science; University of Freiburg Medical Faculty; Landesstifung Baden Wuettemberg	Disclosure of potential conflict of interest: T. Jakob receives grant support from the German Ministry of Research and Science, the University of Freiburg Medical Faculty, and the Landesstifung Baden Wuettemberg and is a member of the Executive Committee for the European Academy of Allergy and Clinical Immunology and a board member for the European Immunodermatology Society. The rest of the authors have declared that they have no conflict of interest.	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Allergy Clin. Immunol.	MAR	2009	123	3					558	566		10.1016/j.jaci.2008.12.003		9	Allergy; Immunology	Allergy; Immunology	426TQ	WOS:000264731200011	19152966	
J	Cox, L; Li, JT; Nelson, H; Lockey, R				Cox, Linda; Li, James T.; Nelson, Harold; Lockey, Richard			Allergen immunotherapy: A practice parameter second update	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review							GRASS-POLLEN IMMUNOTHERAPY; HOUSE-DUST-MITE; DERMATOPHAGOIDES-PTERONYSSINUS EXTRACT; PLACEBO-CONTROLLED TRIAL; SUBLINGUAL-SWALLOW IMMUNOTHERAPY; DOUBLE-BLIND PLACEBO; STANDARDIZED CAT EXTRACT; IMPORTED FIRE ANT; LOCAL NASAL IMMUNOTHERAPY; INSECT STING ALLERGY	These parameters were developed by the Joint Task Force on Practice Parameters, representing the American Academy of Allergy, Asthma and Immunology; the American College of Allergy, Asthma and Immunology; and the Joint Council of Allergy, Asthma and Immunology. The American Academy of Allergy, Asthma and Immunology (AAAAI) and the American College of Allergy, Asthma and Immunology (ACAAI) have jointly accepted responsibility for establishing the "Allergen immunotherapy: a practice parameter second update." 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 the ACAAI should be directed to the Executive Offices of the AAAAI, the ACAAI, and the Joint Council of Allergy, Asthma and Immunology. These parameters are not designed for use by pharmaceutical companies in drug promotion.	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Allergy Clin. Immunol.	SEP	2007	120	3		S			S25	S85		10.1016/j.jaci.2007.06.019		61	Allergy; Immunology	Allergy; Immunology	216OP	WOS:000249888200001		
J	Churg, A; Tai, H; Coulthard, T; Wang, R; Wright, JL				Churg, Andrew; Tai, Hsin; Coulthard, Tonya; Wang, Rona; Wright, Joanne L.			Cigarette smoke drives small airway remodeling by induction of growth factors in the airway wall	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						cigarette smoke; connective tissue growth factor; platelet-derived growth factor; small airway remodeling; transforming growth factor-beta	OBSTRUCTIVE PULMONARY-DISEASE; TRANSFORMING GROWTH-FACTOR-BETA-1; FACTOR BETA(1); FIBROSIS; LUNG; EXPRESSION; ASTHMA; MODEL; ACTIVATION; CELLS	Background: Small airway remodeling (SAR) is an important cause of airflow obstruction in cigarette smokers with chronic obstructive pulmonary disease, but the pathogenesis of SAR is not understood. Objective: To determine whether smoke causes production of profibrotic growth factors in the airway wall. Methods: We exposed C57BI/6 mice to cigarette smoke for up to 6 mo and examined growth factor/procollagen gene expression in laser-capture microdissected small airways by real-time reverse transcription-polymerase chain reaction. Results: With a single smoke exposure, increases in procollagen, connective tissue growth factor (CTGF), transforming growth factor (TGF)-beta(1), platelet-derived growth factor (PDGF)-A and -B expression were seen 2 h after the start of smoking and declined to baseline by 24 h. With repeated exposures and at killing of animals 24 h after the last exposure, increases in procollagen, CTGF, PDGF-B, and (minimally) PDGF-A expression persisted through 1 wk, 1 mo, and 6 mo. TGF-beta(1) gene expression declined over time; however, increased immunochemical staining for phopho-Smad 2 was present at all time points, indicating continuing TGF-beta downstream signaling. Morphometric analysis showed that the small airways in smoke-exposed mice had more Collagen at 6 mo. Conclusions: These findings suggest that smoke can induce growth factor and procollagen production in small airways in a time frame that initially is too short for a significant inflammatory response and that profibrotic growth factor and procollagen gene expression become self-sustaining with repeated smoke exposures. These results imply that the pathogenesis of and possible treatment approaches to emphysema and small airway remodeling might be quite different.	Univ British Columbia, Dept Pathol, Vancouver, BC V6T 2B5, Canada	Churg, A (reprint author), Univ British Columbia, Dept Pathol, 2211 Wesbrook Mail, Vancouver, BC V6T 2B5, Canada.	achurg@interchange.ubc.ca					Abdollahi A, 2005, J EXP MED, V201, P925, DOI 10.1084/jem.20041393; ANTONIADES HN, 1990, J CLIN INVEST, V86, P1055, DOI 10.1172/JCI114808; AUBERT JD, 1994, AM J PHYSIOL, V266, pL655; AUBERT JD, 1994, THORAX, V49, P225, DOI 10.1136/thx.49.3.225; Barnes PJ, 2003, EUR RESPIR J, V22, P672, DOI 10.1183/09031936.03.00040703; Bonner JC, 2004, CYTOKINE GROWTH F R, V15, P255, DOI 10.1016/j.cytogfr.2004.03.006; Bonniaud P, 2004, AM J RESP CELL MOL, V31, P510, DOI 10.1165/rcmb.2004-0158OC; Chambers RC, 2000, J BIOL CHEM, V275, P35584, DOI 10.1074/jbc.M003188200; Chapman HA, 2004, J CLIN INVEST, V113, P148, DOI 10.1172/JCI200420729; Chua F, 2005, AM J RESP CELL MOL, V33, P9, DOI 10.1165/rcmb.2005-0062TR; Chua Felix, 2006, Proc Am Thorac Soc, V3, P424, DOI 10.1513/pats.200603-078AW; CHURG A, 2006, P AM THORAC SOC, V3, pA546; COSIO M, 1978, NEW ENGL J MED, V298, P1277, DOI 10.1056/NEJM197806082982303; Cosio MG, 2002, CHEST, V121, p160S, DOI 10.1378/chest.121.5_suppl.160S; de Boer WI, 1998, AM J RESP CRIT CARE, V158, P1951; Dhami R, 2000, AM J RESP CELL MOL, V22, P244; Gauldie Jack, 2002, Respir Res, V3, P1, DOI 10.1186/rr158; HOGG JC, 1968, NEW ENGL J MED, V278, P1355, DOI 10.1056/NEJM196806202782501; Hogg JC, 2004, NEW ENGL J MED, V350, P2645, DOI 10.1056/NEJMoa032158; Ingram JL, 2004, FASEB J, V18, P1132, DOI 10.1096/fj.03-1492fje; Jeffery PK, 2001, AM J RESP CRIT CARE, V164, P28; Kelly MM, 2005, AM J RESP CELL MOL, V32, P99, DOI 10.1165/rcmb.2004-0190OC; Kenyon NJ, 2003, THORAX, V58, P772, DOI 10.1136/thorax.58.9.772; Kumar RK, 2004, CLIN EXP ALLERGY, V34, P567, DOI 10.1111/j.1365-2222.2004.1917.x; Lewis CC, 2005, J ALLERGY CLIN IMMUN, V115, P534, DOI 10.1016/j.jaci.2004.11.051; Liu JY, 1997, AM J RESP CELL MOL, V17, P129; MacNee W., 2000, CHEST, V117, P303; McCartney-Francis N, 1990, Growth Factors, V4, P27, DOI 10.3109/08977199009011007; NIEWOEHNER DE, 1974, J APPL PHYSIOL, V36, P412; Pare P D, 1997, Monaldi Arch Chest Dis, V52, P589; Saetta M, 1998, AM J RESP CRIT CARE, V157, P822; Selman M, 2001, ANN INTERN MED, V134, P136; Shapiro SD, 2005, AM J RESP CELL MOL, V32, P367, DOI 10.1165/rcmb.F296; Takizawa H, 2001, AM J RESP CRIT CARE, V163, P1476; THURLBECK WM, 1999, THURLBECKS CHRONIC A; Turato G, 2002, AM J RESP CRIT CARE, V166, P105, DOI 10.1164/rccm.2111084; Vignola AM, 1997, AM J RESP CRIT CARE, V156, P591; Wang RD, 2005, AM J RESP CELL MOL, V33, P387, DOI 10.1165/rcmb.2005-02030C; WIGGS BR, 1992, AM REV RESPIR DIS, V145, P1251; WRIGHT JL, 2004, AM J RESPIR CELL MOL, V3, P501; Yoshida K, 2005, AM J PATHOL, V166, P1029, DOI 10.1016/S0002-9440(10)62324-3; YOSHIDA M, 1995, P NATL ACAD SCI USA, V92, P9570, DOI 10.1073/pnas.92.21.9570; Yue JB, 2000, J BIOL CHEM, V275, P30765, DOI 10.1074/jbc.M000039200	43	85	90	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 15	2006	174	12					1327	1334		10.1164/rccm.200605-585OC		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	117RA	WOS:000242889400009	17008639	
J	Bussmann, C; Bockenhoff, A; Henke, H; Werfel, T; Novak, N				Bussmann, Caroline; Boeckenhoff, Anette; Henke, Henning; Werfel, Thomas; Novak, Natalija			Does allergen-specific immunotherapy represent a therapeutic option for patients with atopic dermatitis?	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						allergy; atopic dermatitis; house dust mite; allergen specific immunotherapy	HOUSE-DUST-MITE; BLIND CONTROLLED TRIAL; DERMATOPHAGOIDES-PTERONYSSINUS; SUBLINGUAL IMMUNOTHERAPY; ASTHMATIC-PATIENTS; HYPOSENSITIZATION; CHILDREN; RHINITIS; IMMUNOLOGY; AVOIDANCE	House dust mite (HDM) allergens are perennial indoor allergens, which may play a role as allergic trigger factors in atopic dermatitis (AD). Facilitated by their high enzymatic activity, HDM allergens are capable of penetrating the impaired epidermal skin barrier in patients with AD, gaining access to immune cells. In this way, HDM allergens induce both allergic reactions of the immediate type and allergic reactions of the delayed type, which contribute to impairment of AD. Because allergen reduction achieved by encasing strategies does not always lead to significant improvement of clinical symptoms, specific immunotherapy (SIT) might represent an attractive therapeutic option for long-time treatment of this subgroup of patients with AD. However, systematic studies on the effectiveness of SIT in patients with AD are rare. Furthermore, data on the immunologic changes induced by SIT in patients with AD are not well studied. In this review, we provide an overview of the pathogenic impact of HDM allergens as an example for aeroallergens on the course of AD. In addition, we discuss prophylactic and therapeutic options for the treatment of HDM allergy in patients with AD, including a summary of the current data available on SIT as a potential therapeutic option for patients with AD.	Univ Bonn, Dept Dermatol, D-53127 Bonn, Germany; Univ Dortmund, Dept Stat, D-44221 Dortmund, Germany; Hannover Med Sch, Dept Dermatol, D-3000 Hannover, Germany	Novak, N (reprint author), Univ Bonn, Dept Dermatol, Siegmund Freud Str 25, D-53127 Bonn, Germany.	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Allergy Clin. Immunol.	DEC	2006	118	6					1292	1298		10.1016/j.jaci.2006.07.054		7	Allergy; Immunology	Allergy; Immunology	117NP	WOS:000242880300013	17157659	
J	Grize, L; Gassner, M; Wuthrich, B; Bringolf-Isler, B; Takken-Sahli, K; Sennhauser, FH; Stricker, T; Eigenmann, PA; Braun-Fahrlander, C				Grize, L; Gassner, M; Wuthrich, B; Bringolf-Isler, B; Takken-Sahli, K; Sennhauser, FH; Stricker, T; Eigenmann, PA; Braun-Fahrlander, C		Swiss Surveillance Programme	Trends in prevalence of asthma, allergic rhinitis and atopic dermatitis in 5-7-year old Swiss children from 1992 to 2001	ALLERGY			English	Article						allergic rhinitis; asthma; atopic dermatitis; children; trend	ISAAC PHASE-I; INCREASING PREVALENCE; RESPIRATORY HEALTH; AIR-POLLUTION; HAY-FEVER; HONG-KONG; SCHOOLCHILDREN; ADOLESCENTS; CHILDHOOD; GERMANY	Background: Changing occurrence rates of asthma, allergic rhinitis and atopic dermatitis are of public health concern and require surveillance. Changes in prevalence rates of these atopic diseases were monitored during 10 years and their trend with time was determined taking into account the influence of personal and environmental risk factors. Methods: Four cross-sectional surveys in 5-7-year old children were performed in seven different communities in Switzerland between 1992 and 2001. Prevalence of respiratory and allergic symptoms and of affecting risk factors including parental environmental concern were assessed using a standardized parental questionnaire. Results: A total of 988 (74.1%), 1778 (79.0%), 1406 (82.6%) and 1274 (78.9%) children participated, respectively, in the 1992, 1995, 1998 and 2001 surveys. Prevalence rates of asthma and hay fever symptoms remained quite stable over time (wheeze/past year: 8.8%, 7.8%, 6.4% and 7.4%, sneezing attack during pollen season: 5.0%, 5.6%, 5.4% and 4.6%). Rates of reported atopic dermatitis symptoms (specific skin rash/past year: 4.6%, 6.5%,7.4% and 7.6%) showed an increase over time, but those of diagnosis of eczema did not show a clear pattern (18.4%, 15.7%, 14.0% and 15.2%). Stratified analysis by parental environmental concern and by parental atopy showed similar trends. Rates of atopic dermatitis symptoms showed significant increase in girls but stayed stable in boys. Conclusion: Results of these four consecutive surveys suggest that the increase in prevalence of asthma and hay fever in 5-7-year old children living in Switzerland may have ceased. However, symptoms of atopic dermatitis may still be on the rise, especially among girls.	Univ Basel, Inst Social & Prevent Med, CH-4051 Basel, Switzerland; Univ Hosp, Dept Dermatol, Zurich, Switzerland; Sch Hlth Serv, Zurich, Switzerland; Univ Childrens Hosp, Zurich, Switzerland; Paediat Univ Hosp, Allergy Clin, Geneva, Switzerland	Grize, L (reprint author), Univ Basel, Inst Social & Prevent Med, Steinengraben 49, CH-4051 Basel, Switzerland.		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J	Nicolaou, N; Siddique, N; Custovic, A				Nicolaou, N; Siddique, N; Custovic, A			Allergic disease in urban and rural populations: increasing prevalence with increasing urbanization	ALLERGY			English	Editorial Material							EXERCISE-INDUCED BRONCHOSPASM; CHILDHOOD ASTHMA; LIFE-STYLE; HAY-FEVER; CHILDREN; ATOPY; SENSITIZATION; RHINITIS; ADOLESCENTS; EXPOSURE		Univ Manchester, Wythenshawe Hosp, NW Lung Ctr, Acad Div Med & Surg Hlth, Manchester M23 9LT, Lancs, England; Royal Bournemouth Hosp, Dept Thorac Med, Bournemouth, Dorset, England	Nicolaou, N (reprint author), Univ Manchester, Wythenshawe Hosp, NW Lung Ctr, Acad Div Med & Surg Hlth, Manchester M23 9LT, Lancs, England.		Custovic, Adnan/A-2435-2012	Custovic, Adnan/0000-0001-5218-7071			Adler A, 2005, J ALLERGY CLIN IMMUN, V115, P67, DOI 10.1016/j.jaci.2004.10.008; Aligne CA, 2000, AM J RESP CRIT CARE, V162, P873; Braback L, 2004, CLIN EXP ALLERGY, V34, P38, DOI 10.1111/j.1365-2222.2004.01841.x; Braun-Fahrlander C, 2004, EUR RESPIR J, V23, P407, DOI 10.1183/09031936.04.00074004; Eder W, 2004, J ALLERGY CLIN IMMUN, V113, P482, DOI 10.1016/j.jaci.2003.12.374; Eduard W, 2004, THORAX, V59, P381, DOI 10.1136/thx.2004.013326; Filipiak B, 2001, CLIN EXP ALLERGY, V31, P1829, DOI 10.1046/j.1365-2222.2001.01246.x; Heinrich Joachim, 2004, Curr Opin Allergy Clin Immunol, V4, P341, DOI 10.1097/00130832-200410000-00003; Hijazi N, 2000, THORAX, V55, P775, DOI 10.1136/thorax.55.9.775; Kim YK, 2002, CLIN EXP ALLERGY, V32, P1305, DOI 10.1046/j.1365-2745.2002.01478.x; Linneberg A, 2005, ALLERGY, V60, P538, DOI 10.1111/j.1398-9995.2005.00721.x; Mercer MJ, 2004, PEDIATR ALLERGY IMMU, V15, P234, DOI 10.1111/j.1399-3038.2004.00125.x; Mistry R, 2004, EUR J PEDIATR, V163, P145, DOI 10.1007/s00431-003-1393-6; Miyamoto T, 1997, ALLERGY, V52, P30; Ng'ang'a LW, 1998, THORAX, V53, P919; Nicolai T, 2003, EUR RESPIR J, V21, P956, DOI 10.1183/09031936.03.00041103; Perzanowski MS, 2002, J PEDIATR-US, V140, P582, DOI 10.1067/mpd.2002.122937; Platts-Mills TAE, 2005, ALLERGY, V60, P25, DOI 10.1111/j.1398-9995.2005.00854.x; Platts-Mills TAE, 2005, PLOS MED, V2, P122, DOI 10.1371/journal.pmed.0020034; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Shapiro GG, 2002, PEDIATR PULM, V33, P47, DOI 10.1002/ppul.10029; Singh Meenu, 2005, Paediatr Respir Rev, V6, P14, DOI 10.1016/j.prrv.2004.11.003; Steinman HA, 2003, PEDIATR ALLERGY IMMU, V14, P383, DOI 10.1034/j.1399-3038.2003.00062.x; Sudhir P, 2003, J TROP PEDIATRICS, V49, P104, DOI 10.1093/tropej/49.2.104; VANNIEKERK CH, 1979, CLIN ALLERGY, V9, P319; Venn AJ, 2001, AM J RESP CRIT CARE, V164, P1660; Verlato G, 2003, J ALLERGY CLIN IMMUN, V111, P1232, DOI 10.1067/mai.2003.1484; Viinanen A, 2005, ALLERGY, V60, P1370, DOI 10.1111/j.1398-9995.2005.00877.x; Walraven GEL, 2001, CLIN EXP ALLERGY, V31, P1679, DOI 10.1046/j.1365-2222.2001.01094.x; Wong GWK, 2004, BRIT MED J, V329, P486, DOI 10.1136/bmj.329.7464.486; Yemaneberhan H, 1997, LANCET, V350, P85, DOI 10.1016/S0140-6736(97)01151-3; Yobo EODA, 1997, THORAX, V52, P161	32	85	88	3	9	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0105-4538			ALLERGY	Allergy	NOV	2005	60	11					1357	1360		10.1111/j.1398-9995.2005.00961.x		4	Allergy; Immunology	Allergy; Immunology	969NS	WOS:000232241600004	16197466	
J	Wheeler, BW; Ben-Shlomo, Y				Wheeler, BW; Ben-Shlomo, Y			Environmental equity, air quality, socioeconomic status, and respiratory health: a linkage analysis of routine data from the Health Survey for England	JOURNAL OF EPIDEMIOLOGY AND COMMUNITY HEALTH			English	Article							POLLUTION; JUSTICE; ASTHMA; ASSOCIATION; MORTALITY; EXPOSURE; COHORT	Study objective: To assess relations between socioeconomic status and local air quality, and combined effects on respiratory health, in the context of environmental and health inequality. Design: Data on people taking part in the Health Survey for England were attributed with a small area index of air pollution using annual mean concentrations of nitrogen dioxide, sulphur dioxide, benzene, and particulates (PM10). Regression models were used to measure associations between social class, air quality, forced expiratory volume in one second (FEV1), and self reported asthma. Participants: Participants aged 16 - 79 in the Health Survey for England 1995, 1996, and 1997. Main results: Urban lower social class households were more likely to be located in areas of poor air quality, but the association in rural areas was, if anything reversed. Low social class and poor air quality were independently associated with decreased lung function (FEV1), but not asthma prevalence, after adjustment for a number of potential confounders. Social class effects were not attenuated by adjustment for air quality. In men, a differential effect of air pollution on FEV1 was found, with its effect in social classes III to V about double that in social classes I and II ( p value for interaction = 0.04). This effect modification was not seen for women. Conclusions: Further evidence of environmental inequity in the UK is provided. The association between FEV1 and local air quality is of similar magnitude to that with social class, and the adverse effects of air pollution seem to be greater in men in lower social classes.	Univ Sheffield, Dept Geog, Sheffield S10 2TN, S Yorkshire, England; Univ Bristol, Dept Social Med, Bristol BS8 1TH, Avon, England	Wheeler, BW (reprint author), Univ Sheffield, Dept Geog, Winter St, Sheffield S10 2TN, S Yorkshire, England.	b.w.wheeler@sheffield.ac.uk	Wheeler, Benedict/G-1711-2012	Wheeler, Benedict/0000-0001-9404-5936			AckermannLiebrich U, 1997, AM J RESP CRIT CARE, V155, P122; Ben-Shlomo Y, 2002, INT J EPIDEMIOL, V31, P285, DOI 10.1093/ije/31.2.285; Bowen WM, 1995, ANN ASSOC AM GEOGR, V85, P641, DOI 10.1111/j.1467-8306.1995.tb01818.x; Brainard JS, 2002, ENVIRON PLANN A, V34, P695, DOI 10.1068/a34184; BROWN P, 1995, ENVIRON RES, V69, P15, DOI 10.1006/enrs.1995.1021; Brunekreef B, 2002, LANCET, V360, P1233, DOI 10.1016/S0140-6736(02)11274-8; Brunekreef B, 2003, EUR RESPIR J, V21, P913, DOI 10.1183/09031936.03.00014903; Bullard R. D., 1994, DUMPING DIXIE RACE C; CLINTON WJ, FEDERAL ACTIONS ADDR; Davis DL, 2002, ENVIRON HEALTH PERSP, V110, pA734, DOI 10.1289/ehp.110-a734; Department of Health, HLTH SURV ENGL; Ecob R, 1999, SOC SCI MED, V48, P693, DOI 10.1016/S0277-9536(98)00385-2; Elliott MR, 2004, J EPIDEMIOL COMMUN H, V58, P24, DOI 10.1136/jech.58.1.24; *ENV AG, POS STAT ADDR ENV IN; Hoek G, 2002, LANCET, V360, P1203, DOI 10.1016/S0140-6736(02)11280-3; Janssen NAH, 2000, J AIR WASTE MANAGE, V50, P1133; Jerrett M, 2004, J EPIDEMIOL COMMUN H, V58, P31, DOI 10.1136/jech.58.1.31; *JOINT HLTH SURV U, 2000, SN3979 JOINT HLTH SU; *JOINT HLTH SURV U, 2001, SN3796 JOINT HLTH SU; *JOINT HLTH SURV U, 2001, SN3886 JOINT HLTH SU; Martins MCH, 2004, J EPIDEMIOL COMMUN H, V58, P41, DOI 10.1136/jech.58.1.41; McConnell R, 2002, LANCET, V359, P386, DOI 10.1016/S0140-6736(02)07597-9; McLaren D., 1999, POLLUTION INJUSTICE; Mitchell G, 2003, ENVIRON PLANN A, V35, P909, DOI 10.1068/a35240; NOBLE M, 2004, ENGLISH INDICES DEPR, P180; O'Neill MS, 2003, ENVIRON HEALTH PERSP, V111, P1861, DOI 10.1289/ehp.6334; PYE S., 2001, FURTHER ANAL NO2 PM1; Rene AA, 2000, J NATL MED ASSOC, V92, P275; STRACHAN DP, 2004, LIFE COURSE APPROACH; Szasz A., 1997, CURR SOCIOL, V45, P99, DOI 10.1177/001139297045003006; TUDORHART J, 1971, LANCET, V1, P406; University of Essex, UK DAT ARCH; *USEPA, ENV JUST FREQ ASK QU; Walker G., 2000, CRITICAL URBAN STUDI; Wheeler BW, 2004, ENVIRON PLANN A, V36, P803, DOI 10.1068/a3691; Zemp E, 1999, AM J RESP CRIT CARE, V159, P1257; Zmirou D, 2004, J EPIDEMIOL COMMUN H, V58, P18, DOI 10.1136/jech.58.1.18	37	85	85	3	16	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	NOV	2005	59	11					948	954		10.1136/jech.2005.036418		7	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	975HO	WOS:000232651800009	16234422	
J	Franze, T; Weller, MG; Niessner, R; Poschl, U				Franze, T; Weller, MG; Niessner, R; Poschl, U			Protein nitration by polluted air	ENVIRONMENTAL SCIENCE & TECHNOLOGY			English	Article							POLYCYCLIC AROMATIC-HYDROCARBONS; BET V 1; LIQUID-CHROMATOGRAPHY; PARTICULATE MATTER; AQUEOUS-SOLUTION; FINE PARTICLES; GRASS-POLLEN; ALLERGENS; IGE; GAS	The effects of air pollution on allergic diseases are not yet well-understood. Here, we show that proteins, in particular birch pollen proteins including the allergen Bet v 1, are efficiently nitrated by polluted air. This posttranslational modification of proteins is likely to trigger immune reactions and provides a molecular rationale for the promotion of allergies by traffic-related air pollution. Enzyme immunoassays have been used to determine equivalent degrees of nitration (EDN) for protein samples exposed to urban outdoor air and synthetic gas mixtures. The observed rates of nitration were governed by the abundance of nitrogen oxides and ozone, and concentration levels typical for summer smog conditions led to substantial nitration within a few hours to days (EDN up to 20%). Moreover, nitrated proteins were detected in urban road dust, window dust, and fine air particulate matter (EDN up to 0.1%).	Tech Univ Munich, Inst Hydrochem, D-81377 Munich, Germany	Poschl, U (reprint author), Tech Univ Munich, Inst Hydrochem, Marchioninistr 17, D-81377 Munich, Germany.	ulrich.poeschl@ch.tum.de	Weller, Michael G./B-5015-2008; Poschl, Ulrich/A-6263-2010; Niessner, Reinhard/C-1414-2010; Niessner, Reinhard/D-1502-2010; Osborne, Nicholas/N-4915-2015	Weller, Michael G./0000-0003-2767-2029; Poschl, Ulrich/0000-0003-1412-3557; Osborne, Nicholas/0000-0002-6700-2284			Barzaghi P, 2002, PHYS CHEM CHEM PHYS, V4, P3669, DOI 10.1039/b201652d; BECKMAN JS, 1992, ARCH BIOCHEM BIOPHYS, V298, P438, DOI 10.1016/0003-9861(92)90432-V; Belloli R, 1999, J CHROMATOGR A, V846, P277, DOI 10.1016/S0021-9673(99)00030-8; Berrens L, 1997, INT ARCH ALLERGY IMM, V113, P236; Birnboim HC, 2003, J IMMUNOL, V171, P528; Bolzacchini E, 2001, ENVIRON SCI TECHNOL, V35, P1791, DOI 10.1021/es001290m; Brunekreef B, 2001, CLIN EXP ALLERGY, V31, P1170, DOI 10.1046/j.1365-2222.2001.01208.x; Brunekreef B, 2003, EUR RESPIR J, V21, P913, DOI 10.1183/09031936.03.00014903; Doyle HA, 2001, TRENDS IMMUNOL, V22, P443, DOI 10.1016/S1471-4906(01)01976-7; FALL BI, 2001, BIOS S TUB GERM; FinlaysonPitts BJ, 1997, SCIENCE, V276, P1045, DOI 10.1126/science.276.5315.1045; FINLAYSONPITTS BJ, 2000, CHEM LOWER ATMOSPHER; Franze T, 2004, ANALYST, V129, P589, DOI 10.1039/b402624a; Franze T, 2003, ANALYST, V128, P824, DOI 10.1039/b303132b; Franze T, 2003, J AEROSOL SCI, V34, pS777; GOSCHNICK J, 1996, J AEROSOL SCI, V27, P229; GRAHAM A, 1993, FEBS LETT, V330, P181, DOI 10.1016/0014-5793(93)80269-Z; Greenacre SAB, 2001, FREE RADICAL RES, V34, P541, DOI 10.1080/10715760100300471; HOLT PG, 1987, IMMUNOLOGY, V60, P97; Huby RDJ, 2000, TOXICOL SCI, V55, P235, DOI 10.1093/toxsci/55.2.235; James LC, 2003, SCIENCE, V299, P1362, DOI 10.1126/science.1079731; JAROLIM E, 1989, ALLERGY, V44, P385, DOI 10.1111/j.1398-9995.1989.tb04169.x; KNOX RB, 1993, CLIN EXP ALLERGY, V23, P354, DOI 10.1111/j.1365-2222.1993.tb00339.x; Kramer U, 1999, INT J EPIDEMIOL, V28, P865, DOI 10.1093/ije/28.5.865; Landsteiner K, 1935, J EXP MED, V61, P643, DOI 10.1084/jem.61.5.643; Lin JK, 2000, CHEM-BIOL INTERACT, V127, P219, DOI 10.1016/S0009-2797(00)00181-2; Miguel AG, 1999, ENVIRON SCI TECHNOL, V33, P4159, DOI 10.1021/es9904890; Mikhailov E, 2004, ATMOS CHEM PHYS, V4, P323; Neuhaus-Steinmetz U, 2000, AM J RESP CELL MOL, V23, P228; Petersen A, 1998, CLIN EXP ALLERGY, V28, P315; POSCHL U, 1982, J AEROSOL MED, V15, P203; Rehwagen M, 1999, ENVIRON TOXICOL, V14, P321, DOI 10.1002/(SICI)1522-7278(199907)14:3<321::AID-TOX5>3.0.CO;2-L; RIEDEL F, 1995, PEDR ALLERGY, V8, P65; Riediker M, 2001, ANN ALLERG ASTHMA IM, V87, P311; Ring J, 2001, ANN ALLERG ASTHMA IM, V87, P2; Ring J, 2001, CURR OPIN IMMUNOL, V13, P701, DOI 10.1016/S0952-7915(01)00282-5; Schappi GF, 1997, J ALLERGY CLIN IMMUN, V100, P656, DOI 10.1016/S0091-6749(97)70170-2; Schappi GF, 1997, SEX PLANT REPROD, V10, P315, DOI 10.1007/s004970050105; Schauer C, 2004, ANAL BIOANAL CHEM, V378, P725, DOI 10.1007/s00216-003-2449-1; SCHINKO HAE, 1994, ALLERGOLOGIE, V17, P514; Svartengren M, 2000, EUR RESPIR J, V15, P716, DOI 10.1034/j.1399-3003.2000.15d15.x; Umschlag T, 2002, PHYS CHEM CHEM PHYS, V4, P2975, DOI 10.1039/b110263j; Wahn U, 2000, ALLERGY, V55, P591, DOI 10.1034/j.1398-9995.2000.00111.x; Walcher W, 2003, J PROTEOME RES, V2, P534, DOI 10.1021/pr034034s; WUTHRICH B, 1995, INT ARCH ALLERGY IMM, V106, P149; Zhang Q, 2003, ATMOS ENVIRON, V37, P2247, DOI 10.1016/S1352-2310(03)00127-4	46	85	87	1	36	AMER CHEMICAL SOC	WASHINGTON	1155 16TH ST, NW, WASHINGTON, DC 20036 USA	0013-936X			ENVIRON SCI TECHNOL	Environ. Sci. Technol.	MAR 15	2005	39	6					1673	1678		10.1021/es0488737		6	Engineering, Environmental; Environmental Sciences	Engineering; Environmental Sciences & Ecology	906JF	WOS:000227636300044	15819224	
J	Pilette, C; Francis, JN; Till, SJ; Durham, SR				Pilette, C; Francis, JN; Till, SJ; Durham, SR			CCR4 ligands are up-regulated in the airways of atopic asthmatics after segmental allergen challenge	EUROPEAN RESPIRATORY JOURNAL			English	Article						allergen challenge; asthma; C-C chemokine receptor 4; chemokines; cytokines	BRONCHIAL EPITHELIAL-CELLS; CHEMOKINE RECEPTOR CXCR3; T-CELLS; IN-VIVO; TH2 CELLS; BRONCHOALVEOLAR LAVAGE; RESPIRATORY-DISEASE; EXPRESSION; LYMPHOCYTES; LUNG	T-helper (Th) 2 cytokines; are thought to mediate most features of allergic inflammation in atopic asthma. However, it remains unclear whether chemokine pathways direct selective recruitment of Th2 cells to the airways during human allergic responses. Bronchoalveolar lavage (BAL) was performed in 15 nonsmoking mild atopic asthmatics before and 24 h after a fibreoptic segmental allergen challenge, and chemokines related to T-cell recruitment were assayed by ELISA. The Th2-related C-C chemokine (CCR)4 ligands, macrophage-derived chemokine/C-C chemokine ligand (CCL)22 and thymus and activation-regulated chemokine/CCL17, were increased in BAL after challenge. These chemokines correlated significantly with lymphocyte numbers and with interleukin (IL)-5 and IL-13 in post-challenge B L. In contrast, two out of three putative Th1-related chemokines; did not change. There were no alterations in monokine induced by interferon (IFN)-gamma/CXC chemokine ligand (CXCL)9 or macrophage inflammatory protein-1alpha/CCL3; whereas a significant increase in IFN-induced protein-10kDa/CXCL 10 was observed, which did not correlate with the T-cell influx. In peripheral mononuclear cells from atopic donors, CCL22 and CCL17 were induced by IL-4 and IL-13, further supporting the relationship between CCL22/CCL17 and Th2 cytokines. Finally, CCL22 was able to trigger actin polymerisation in peripheral CD4+ T-cells expressing CCR4. Thus, C-C chemokine receptor 4 ligands are up-regulated in the airways of atopic asthmatics following allergen exposure, contribute to the T-cell influx to the airways and are closely related to the Th2-cytokine response.	Univ London Imperial Coll Sci & Technol, Natl Heart & Lung Inst, London SW3 6LY, England	Pilette, C (reprint author), Univ London Imperial Coll Sci & Technol, Natl Heart & Lung Inst, Dovehouse St, London SW3 6LY, England.	s.durham@imperial.ac.uk					Agostini C, 1998, J IMMUNOL, V161, P6413; Albanesi C, 2001, J LEUKOCYTE BIOL, V70, P617; Andrew DP, 2001, J IMMUNOL, V166, P103; Andrew DP, 1998, J IMMUNOL, V161, P5027; Annunziato F, 1999, J LEUKOCYTE BIOL, V65, P691; BENTLEY AM, 1993, AM J RESP CELL MOL, V8, P35; BRIGHTLING CE, 2003, EUR RESPIR J, pA187; Busse William W., 2003, Journal of Allergy and Clinical Immunology, V111, pS799, DOI 10.1067/mai.2003.158; CHO SH, 2002, CLIN EXP ALLERGY, V32, P1790; Ferrero E, 2003, IMMUNOLOGY, V108, P365, DOI 10.1046/j.1365-2567.2003.01600.x; Foussat A, 2000, EUR J IMMUNOL, V30, P87, DOI 10.1002/1521-4141(200001)30:1<87::AID-IMMU87>3.0.CO;2-7; Gallo SA, 2003, BBA-BIOMEMBRANES, V1614, P36, DOI 10.1016/S0005-2736(03)00161-5; Gonzalo JA, 1999, J IMMUNOL, V163, P403; Holt PG, 1998, IMMUNOL CELL BIOL, V76, P119; Kroegel C, 1996, EUR RESPIR J, V9, P899, DOI 10.1183/09031936.96.09050899; Kunkel EJ, 2002, AM J PATHOL, V160, P347, DOI 10.1016/S0002-9440(10)64378-7; Larche M, 2003, J ALLERGY CLIN IMMUN, V111, P450, DOI 10.1067/mai.2003.169; Lilly CM, 2001, AM J RESP CRIT CARE, V163, P1669; Lloyd CM, 2000, J EXP MED, V191, P265, DOI 10.1084/jem.191.2.265; Loetscher M, 1998, EUR J IMMUNOL, V28, P3696, DOI 10.1002/(SICI)1521-4141(199811)28:11<3696::AID-IMMU3696>3.0.CO;2-W; Magnan AO, 2000, AM J RESP CRIT CARE, V161, P1790; Medoff BD, 2002, J IMMUNOL, V168, P5278; Miotto D, 2001, J ALLERGY CLIN IMMUN, V107, P664, DOI 10.1067/mai.2001.113524; Nouri-Aria KT, 2002, EUR J IMMUNOL, V32, P1933, DOI 10.1002/1521-4141(200207)32:7<1933::AID-IMMU1933>3.0.CO;2-R; Panina-Bordignon P, 2001, J CLIN INVEST, V107, P1357, DOI 10.1172/JCI12655; PARRONCHI P, 1992, EUR J IMMUNOL, V22, P1615, DOI 10.1002/eji.1830220640; RENNARD SI, 1986, J APPL PHYSIOL, V60, P532; ROBINSON DS, 1993, J ALLERGY CLIN IMMUN, V92, P397, DOI 10.1016/0091-6749(93)90118-Y; Sabroe I, 2002, EUR RESPIR J, V19, P350, DOI 10.1183/09031936.02.00253602; Saetta M, 2002, AM J RESP CRIT CARE, V165, P1404, DOI 10.1164/rccm.2107139; Sallusto F, 1997, SCIENCE, V277, P2005, DOI 10.1126/science.277.5334.2005; Sauty A, 1999, J IMMUNOL, V162, P3549; Schipf A, 2003, EUR J IMMUNOL, V33, P1697, DOI 10.1002/eji.200323809; Schweitzer B, 2002, NAT BIOTECHNOL, V20, P359, DOI 10.1038/nbt0402-359; Sekiya T, 2000, J IMMUNOL, V165, P2205; Stephens R, 2002, J IMMUNOL, V169, P5458; Thomas MS, 2002, J IMMUNOL, V169, P7045; Till SJ, 1998, AM J RESP CRIT CARE, V158, P404	38	85	87	0	4	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	2004	23	6					876	884		10.1183/09031936.04.00102504		9	Respiratory System	Respiratory System	828TP	WOS:000221996500017	15219001	
J	Singh, P; DeMarini, DM; Dick, CAJ; Tabor, DG; Ryan, JV; Linak, WP; Kobayashi, T; Gilmour, MI				Singh, P; DeMarini, DM; Dick, CAJ; Tabor, DG; Ryan, JV; Linak, WP; Kobayashi, T; Gilmour, MI			Sample characterization of automobile and forklift diesel exhaust particles and comparative pulmonary toxicity in mice	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						automobile; diesel exhaust particles; forklift; mice; pulmonary toxicity; SRM 2975	AIRWAY INFLAMMATION; IGE PRODUCTION; EMISSIONS; PARTICULATE; EXPOSURE; HEALTH; HYPERRESPONSIVENESS; MUTAGENICITY; EXPRESSION; COMPONENTS	Two samples of diesel exhaust particles (DEPs) predominate in health effects research: an automobile-derived DEP (A-DEP) sample and the National Institute of Standards Technology standard reference material (SRM 2975) generated from a forklift engine. A-DEPs have been tested extensively for their effects on pulmonary inflammation and exacerbation of allergic asthma-like responses. In contrast, SRM 2975 has been tested thoroughly for its genotoxicity. In the present study, we combined physical and chemical analyses of both DEP samples with pulmonary toxicity testing in CD-I mice to compare the two materials and to make associations between their physicochemical properties and their biologic effects. A-DEPs had more than 10 times the amount of extractable organic material and less than one-sixth the amount of elemental carbon compared with SRM 2975. Aspiration of 100 mug of either DEP sample in saline produced mild acute lung injury; however, A-DEPs induced macrophage influx and activation, whereas SIRM 2975 enhanced polymorphonuclear cell inflammation. A-DEPs stimulated an increase in interleukin-6 (IL-6), tumor necrosis factor a, macrophage inhibitory protein-2, and the T(H)2 cytokine IL-5, whereas SRM 2975 only induced significant levels of IL-6. Fractionated organic extracts of the same quantity of DEPs (100 mug) did not have a discernable effect on lung responses and will require further study. The disparate results obtained highlight the need for chemical, physical, and source characterization of particle samples under investigation. Multidisciplinary toxicity testing of diesel emissions derived from a variety of generation and collection conditions is required to meaningfully assess the health hazards associated with exposures to DEPs.	US EPA, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA; Univ N Carolina, Ctr Environm Med & Lung Biol, Chapel Hill, NC USA; US EPA, Natl Risk Management Res Lab, Res Triangle Pk, NC 27711 USA; Natl Inst Environm Studies, Environm Hlth Sci Div, Tsukuba, Ibaraki, Japan	Singh, P (reprint author), US EPA, Natl Hlth & Environm Effects Res Lab, MD B143-01, Res Triangle Pk, NC 27711 USA.	singh.pramila@epa.gov					Boland S., 1999, AM J PHYSIOL, V276, P604; Claxton L, 1992, MUTAT RES, V276, P1; CLAXTON LD, 1983, ENVIRON MUTAGEN, V5, P609, DOI 10.1002/em.2860050410; DeMarini DM, 2004, ENVIRON HEALTH PERSP, V112, P814; DiazSanchez D, 1997, ALLERGY, V52, P52; Dick CAJ, 2003, INHAL TOXICOL, V15, P39, DOI 10.1080/08958370304454; Donaldson K, 1996, TOXICOL LETT, V88, P293, DOI 10.1016/0378-4274(96)03752-6; Driscoll KE, 2000, TOXICOL SCI, V55, P24, DOI 10.1093/toxsci/55.1.24; Foster WM, 2001, J APPL PHYSIOL, V90, P1111; Granum B, 2002, TOXICOL SCI, V65, P7, DOI 10.1093/toxsci/65.1.7; Heo Y, 2001, TOXICOLOGY, V159, P143, DOI 10.1016/S0300-483X(00)00418-2; Hughes TJ, 1997, MUTAT RES-GEN TOX EN, V391, P243, DOI 10.1016/S1383-5718(97)00075-2; Kawasaki S, 2001, AM J RESP CELL MOL, V24, P419; KOBAYASHI T, 1995, FUND APPL TOXICOL, V27, P195, DOI 10.1006/faat.1995.1124; Lewtas J., 1982, TOXICOLOGICAL EFFECT; Li N, 2003, ENVIRON HEALTH PERSP, V111, P455, DOI 10.1289/ehp.6000; Lovik M, 1997, TOXICOLOGY, V121, P165, DOI 10.1016/S0300-483X(97)00075-9; Madden MC, 2000, TOXICOL APPL PHARM, V168, P140, DOI 10.1006/taap.2000.9024; Mauderly JL, 2001, TOXICOL SCI, V62, P6, DOI 10.1093/toxsci/62.1.6; METZGER JM, 1988, IMMUNOPHARMACOLOGY, V15, P103, DOI 10.1016/0162-3109(88)90057-4; MILLER NJ, 1993, CLIN SCI, V84, P407; Miyabara Y, 1998, AM J RESP CRIT CARE, V157, P1138; Nel A E, 2001, Curr Opin Pulm Med, V7, P20, DOI 10.1097/00063198-200101000-00004; National Institute for Occupational Safety and Health (NIOSH), 1994, DHHS NIOSH PUBL; *NIST, 2000, CERT AN STAND REF MA; Pope CA, 2002, JAMA-J AM MED ASSOC, V287, P1132, DOI 10.1001/jama.287.9.1132; Rosenkranz HS, 1996, MUTAT RES-GENET TOX, V367, P65, DOI 10.1016/0165-1218(95)00066-6; SAGAI M, 1993, FREE RADICAL BIO MED, V14, P37, DOI 10.1016/0891-5849(93)90507-Q; Salvi SS, 2000, AM J RESP CRIT CARE, V161, P550; SCHUETZLE D, 1983, ENVIRON HEALTH PERSP, V47, P65, DOI 10.2307/3429500; Seagrave J, 2002, TOXICOL SCI, V70, P212, DOI 10.1093/toxsci/70.2.212; Sydbom A, 2001, EUR RESPIR J, V17, P733, DOI 10.1183/09031936.01.17407330; Takano H, 1997, AM J RESP CRIT CARE, V156, P36; Tsien A, 1997, TOXICOL APPL PHARM, V142, P256, DOI 10.1006/taap.1996.8063; Weir E, 2002, CAN MED ASSOC J, V167, P505; Wilhelm M, 2003, ENVIRON HEALTH PERSP, V111, P207, DOI 10.1289/ehp.5688	36	85	85	3	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.	JUN	2004	112	8					820	825		10.1289/ehp.6579		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	829BO	WOS:000222018200028	15175167	
J	Monninkhof, E; van der Valk, P; van der Palen, J; van Herwaarden, C; Zielhuis, G				Monninkhof, E; van der Valk, P; van der Palen, J; van Herwaarden, C; Zielhuis, G			Effects of a comprehensive self-management programme in patients with chronic obstructive pulmonary disease	EUROPEAN RESPIRATORY JOURNAL			English	Article						chronic obstructive lung disease; patient education; quality of life; randomised controlled trial; self-management	QUALITY-OF-LIFE; AIR-FLOW LIMITATION; 6-MINUTE WALK TEST; FLUTICASONE PROPIONATE; CONTROLLED TRIAL; HEALTH-STATUS; LUNG-DISEASE; EDUCATION; ASTHMA; COPD	The aim of this study was to assess the effects of a comprehensive self-management intervention on health-related quality of life (HRQoL), symptoms and walking distance in patients with stable moderately severe chronic obstructive pulmonary disease (COPD). This study was part of the overall COPD study of the Dept of Pulmonary Medicine, Enschede, which consisted of an inhaled corticosteroid (ICS) trial and a self-management trial. After the ICS trial, all patients were randomised again to a self-management and a control group. The self-management intervention consisted of a skill-oriented patient education programme and a near-home fitness programme, on top of usual care. The control group received usual care by the treating chest physician. HRQoL was measured by the St George's Respiratory Questionnaire (SGRQ) and walking distance by the 6-min walking test. Patients recorded their symptoms in diaries and graded their health status from 1-10 in a weekly report. Altogether, 248 COPD patients were randomly allocated to either an intervention (127) or control (121) group. No differences in the SGRQ scores within and between both groups were observed over I yr. Similarly, no differences in symptom scores and 6-min walking distance were found within and between groups. The intervention group reported more exacerbations than the control group. The majority (69%) of the exacerbations in the intervention group were self-treated at home. This study failed to show positive effects of a self-management programme among moderately severe chronic obstructive pulmonary disease patients.	Med Spectrum Twente, Dept Pulm Med, NL-7500 KA Enschede, Netherlands; Univ Nijmegen, Med Ctr, Dept Epidemiol & Biostat, Nijmegen, Netherlands; Univ Nijmegen, Med Ctr, Dept Pulm Med, Nijmegen, Netherlands	Monninkhof, E (reprint author), Med Spectrum Twente, Dept Pulm Med, POB 50000, NL-7500 KA Enschede, Netherlands.		Zielhuis, Gerhard/D-4229-2009; Zielhuis, Gerhard/H-8123-2014				American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P77; American Thoracic Society, 1999, AM J RESP CRIT CARE, V159, P1666; Barnes PJ, 2000, NEW ENGL J MED, V343, P269, DOI 10.1056/NEJM200007273430407; Bourbeau J, 2003, ARCH INTERN MED, V163, P585, DOI 10.1001/archinte.163.5.585; BRAND PLP, 1992, THORAX, V47, P429, DOI 10.1136/thx.47.6.429; Burge PS, 2000, BRIT MED J, V320, P1297, DOI 10.1136/bmj.320.7245.1297; BUTLAND RJA, 1982, BRIT MED J, V284, P1607; CASABURI R, 1991, AM REV RESPIR DIS, V143, P9; Crapo RO, 2002, AM J RESP CRIT CARE, V166, P111, DOI 10.1164/rccm.166/1/111; Gallefoss F, 1999, AM J RESP CRIT CARE, V160, P2000; Gallefoss F, 1999, AM J RESP CRIT CARE, V159, P812; GIBSON PG, 2000, COCHRANE DATABASE SY; Gosselink R, 1996, AM J RESP CRIT CARE, V153, P976; JONES PW, 1992, AM REV RESPIR DIS, V145, P1321; Jones PW, 1997, AM J RESP CRIT CARE, V155, P1283; Jones PW, 2002, EUR RESPIR J, V19, P398, DOI 10.1183/09031936.02.00063702; Klein JJ, 2001, EUR RESPIR J, V17, P386, DOI 10.1183/09031936.01.17303860; LITTLEJOHNS P, 1991, THORAX, V46, P559, DOI 10.1136/thx.46.8.559; LORIG KR, 1993, ARTHRITIS RHEUM, V36, P439, DOI 10.1002/art.1780360403; MONNINKHOF E, 2003, IN PRESS PATIENT ED; MONNINKHOF EM, 2003, COCHRANE DATABASE SY; Norris SL, 2001, DIABETES CARE, V24, P561, DOI 10.2337/diacare.24.3.561; Paggiaro PL, 1998, LANCET, V351, P773, DOI 10.1016/S0140-6736(97)03471-5; Pauwels Romain A., 2001, American Journal of Respiratory and Critical Care Medicine, V163, P1256; Redelmeier DA, 1997, AM J RESP CRIT CARE, V155, P1278; SCHOLS AMWJ, 1991, THORAX, V46, P695, DOI 10.1136/thx.46.10.695; Seemungal TAR, 1998, AM J RESP CRIT CARE, V157, P1418; SuperioCabuslay E, 1996, ARTHRIT CARE RES, V9, P292, DOI 10.1002/1529-0131(199608)9:4<292::AID-ANR1790090414>3.0.CO;2-4; van der Valk P, 2002, AM J RESP CRIT CARE, V166, P1358, DOI 10.1164/rccm.200206-512OC; Watson PB, 1997, EUR RESPIR J, V10, P1267, DOI 10.1183/09031936.97.10061267; Wouters EF, 2002, CHEST, V121, P127; WOUTERS EFM, 1999, EUR RESPIR REV, V9, P189	32	85	88	0	7	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.	NOV	2003	22	5					815	820		10.1183/09031936.03.00047003		6	Respiratory System	Respiratory System	739UE	WOS:000186364200019	14621090	
J	Gavett, SH; Haykal-Coates, N; Copeland, LB; Heinrich, J; Gilmour, MI				Gavett, SH; Haykal-Coates, N; Copeland, LB; Heinrich, J; Gilmour, MI			Metal composition of ambient PM2.5 influences severity of allergic airways disease in mice	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; airway hyperresponsiveness; allergic sensitization; asthma; epidemiology; inflammation; metals	OIL FLY-ASH; HOUSE-DUST MITE; AIR-POLLUTION; RESPIRATORY SYMPTOMS; PULMONARY TOXICITY; INTERFERON-GAMMA; UTAH VALLEY; LUNG INJURY; SENSITIZATION; ASTHMA	Children living in Hettstedt in eastern Germany have been reported to have a higher prevalence of sensitization to common aeroallergens than another cohort living in the neighboring city of Zerbst; these differences correlated with the presence of industrial air pollution. Samples of fine particulate matter (< 2.5 mum aerodynamic diameter; PM2.5) collected in Hettstedt in 1999 had several-fold higher levels of zinc, magnesium, lead, copper, and cadmium than samples from Zerbst. To determine if the results from epidemiologic studies could be repeated in an animal model, we administered PM2.5 from Hettstedt and Zerbst to ovalbumin-allergic mice. In Balb/c mice, PM2.5 from Hettstedt, but not PM2.5 from Zerbst or control filter extract, caused a significant increase in immediate responses to ovalbumin challenge when aspirated 2 hr before challenge, but not when aspirated immediately before sensitization 2 weeks earlier. Antigen-specific IgE was increased by Flettstedt PM2.5 whether administered before sensitization or challenge. Airway responsiveness to methacholine aerosol and lung inflammatory cell numbers were significantly increased only, in allergic mice exposed to Hettstedt PM2.5 before challenge. Both Hettstedt and Zerbst PM2.5 significantly increased lung injury parameters and proinflammatory cytokines. These results are consistent with epidemiologic findings and show that metal composition of ambient PM, 5 influences the severity of allergic respiratory disease.	US EPA, Div Environm Toxicol, Natl Hlth & Environm Effects Res Lab, Off Res & Dev, Res Triangle Pk, NC 27711 USA; GSF, Res Ctr Environm & Hlth, Inst Epidemiol, Neuherberg, Germany	Gavett, SH (reprint author), US EPA, Div Environm Toxicol, Natl Hlth & Environm Effects Res Lab, Off Res & Dev, B143-02, Res Triangle Pk, NC 27711 USA.						Biran R, 1996, INT J ENVIRON AN CH, V63, P315, DOI 10.1080/03067319608028327; Chew FT, 1999, ALLERGY, V54, P320, DOI 10.1034/j.1398-9995.1999.00012.x; Chung F, 2001, MEDIAT INFLAMM, V10, P51, DOI 10.1080/09629350120054518; Diaz-Sanchez D, 1999, J ALLERGY CLIN IMMUN, V104, P1183; Dye JA, 2001, ENVIRON HEALTH PERSP, V109, P395, DOI 10.2307/3434787; Dye JA, 1999, AM J PHYSIOL-LUNG C, V277, pL498; Foster WM, 2001, J APPL PHYSIOL, V90, P1111; Gavett SH, 1999, AM J RESP CRIT CARE, V160, P1897; Gavett SH, 1997, ENVIRON RES, V72, P162, DOI 10.1006/enrs.1997.3732; Ghio AJ, 2002, ENVIRON HEALTH PERSP, V110, P89; Ghio AJ, 2001, AM J RESP CRIT CARE, V164, P704; Hamelmann E, 1997, AM J RESP CRIT CARE, V156, P766; 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, 2002, EPIDEMIOLOGY, V13, P394, DOI 10.1097/01.EDE.00000016977.59359.B6; Heinrich J, 2000, AM J RESP CRIT CARE, V161, P1930; HENDERSON RF, 1985, FUND APPL TOXICOL, V5, P451, DOI 10.1016/0272-0590(85)90092-2; Hylkema MN, 2002, AM J RESP CELL MOL, V27, P244; Kobayashi T, 2000, AM J RESP CRIT CARE, V162, P352; Lambert AL, 2001, EXP LUNG RES, V27, P617, DOI 10.1080/019021401753181863; Lambert AL, 1999, TOXICOL APPL PHARM, V158, P269, DOI 10.1006/taap.1999.8709; Lambert AL, 2000, TOXICOL APPL PHARM, V165, P84, DOI 10.1006/taap.2000.8932; Medoff BD, 2002, J IMMUNOL, V168, P5278; Ostro B, 2001, EPIDEMIOLOGY, V12, P200, DOI 10.1097/00001648-200103000-00012; Patton L, 2002, ALLERGY ASTHMA PROC, V23, P9; Peden DB, 2001, ANN ALLERG ASTHMA IM, V87, P12; POPE CA, 1989, AM J PUBLIC HEALTH, V79, P623, DOI 10.2105/AJPH.79.5.623; Salvi S, 2001, Curr Opin Allergy Clin Immunol, V1, P35; Steerenberg PA, 1999, INHAL TOXICOL, V11, P1109; *US EPA, 2002, 6020A US EPA; *US EPA, 2002, EPA600491010; *US EPA, 2002, AIR TRENDS 6 PRINC P; Yoshida M, 2002, AM J RESP CRIT CARE, V166, P451, DOI 10.1164/rccm.200202-0950C	33	85	91	5	37	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	2003	111	12					1471	1477		10.1289/ehp.6300		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	733HZ	WOS:000185995500027	12948886	
J	Duits, LA; Nibbering, PH; van Strijen, E; Vos, JB; Mannesse-Lazeroms, SPG; van Sterkenburg, MAJA; Hiemstra, PS				Duits, LA; Nibbering, PH; van Strijen, E; Vos, JB; Mannesse-Lazeroms, SPG; van Sterkenburg, MAJA; Hiemstra, PS			Rhinovirus increases human beta-defensin-2 and -3 mRNA expression in cultured bronchial epithelial cells	FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY			English	Article						antimicrobial peptide; defensin; epithelium; rhinovirus; respiratory infection	DOUBLE-STRANDED-RNA; HUMAN AIRWAY EPITHELIA; NITRIC-OXIDE SYNTHASE; BETA-DEFENSINS; DENDRITIC CELLS; CYSTIC-FIBROSIS; INHIBITION; INTERFERON; GENE; REPLICATION	Human beta-defensins (hBDs) are antimicrobial peptides that play important roles in host defense against infection, inflammation and immunity. Previous studies showed that micro-organisms and proinflammatory mediators regulate the expression of these peptides in airway epithelial cells. The aim of the present study was to investigate the modulation of expression of hBDs in cultured primary bronchial epithelial cells (PBEC) by rhinovirus-16 (RV16), a respiratory virus responsible for the common cold and associated with asthma exacerbations. RV16 was found to induce expression of hBD-2 and -3 mRNA in PBEC, but did not affect hBD-1 mRNA. Viral replication appeared essential for rhinovirus-induced beta-defensin mRNA expression, since UV-inactivated rhinovirus did not increase expression of hBD-2 and hBD-3 mRNA. Exposure to synthetic double-stranded RNA (dsRNA) molecule polyinosinic:polycytidylic acid had a similar effect as RV16 on mRNA expression of these peptides in PBEC. In line with this, PBEC were found to express TLR3, a Toll-like receptor involved in recognition of dsRNA. This study shows that rhinovirus infection of PBEC leads to increased hBD-2 and hBD-3 mRNA expression, which may play a role in both the uncomplicated common cold and in virus-associated exacerbations of asthma. (C) 2003 Federation of European Microbiological Societies. Published by Elsevier Science B.V. All rights reserved.	Leiden Univ, Ctr Med, Dept Pulmonol, NL-2300 RC Leiden, Netherlands; Leiden Univ, Ctr Med, Dept Infect Dis, NL-2300 RC Leiden, Netherlands	Hiemstra, PS (reprint author), Leiden Univ, Ctr Med, Dept Pulmonol, POB 9600, NL-2300 RC Leiden, Netherlands.			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Med. Microbiol.	AUG 18	2003	38	1					59	64		10.1016/S0928-8244(03)00106-8		6	Immunology; Infectious Diseases; Microbiology	Immunology; Infectious Diseases; Microbiology	711GE	WOS:000184730600009	12900056	
J	Steerenberg, PA; Janssen, NAH; de Meer, G; Fischer, PH; Nierkens, S; van Loveren, H; Opperhuizen, A; Brunekreef, B; van Amsterdam, JGC				Steerenberg, PA; Janssen, NAH; de Meer, G; Fischer, PH; Nierkens, S; van Loveren, H; Opperhuizen, A; Brunekreef, B; van Amsterdam, JGC			Relationship between exhaled NO, respiratory symptoms, lung function, bronchial hyperresponsiveness, and blood eosinophilia in school children	THORAX			English	Article							NASAL NITRIC-OXIDE; ASTHMATIC-PATIENTS; ALLERGIC RHINITIS; AIR-POLLUTION; MILD ASTHMA; RESPONSIVENESS; INHIBITOR; SYNTHASE; SEASON; SAMPLE	Background: Exhaled nitric oxide (eNO) may serve as a non-invasive marker of airway inflammation but its relationship with other commonly used measures has not been evaluated. Methods: Levels of eNO in a sample of 450 children aged 7-12 years out of a total sample of 2504 school children living in different urban areas near motorways were determined. The aim of this cross-sectional study was to explore the relationship between eNO, impairment of lung function (PEF, FVC, FEV1 and MMEF), bronchial hyperresponsiveness (BHR), and blood eosinophilia in children with and without atopy as assessed by skin prick testing. Results: Regression analysis showed that wheezing and nasal discharge and conjunctivitis that had occurred during the previous 12 months were positively associated with eNO levels in atopic children (relative increase of 1.48 and 1.41, respectively; p<0.05) but not in non-atopic children. Similarly, BHR and the number of blood eosinophils per ml were positively associated with eNO levels in atopic children (relative increase of 1.55 and 2.29, respectively; p<0.05) but not in non-atopic children. The lung function indices PEF, FVC, FEV, and MMEF were not associated with eNO levels. Conclusions: In addition to conventional lung function tests and symptom questionnaires, eNO is a suitable measure of airway inflammation and its application may reinforce the power of epidemiological surveys on respiratory health.	Natl Inst Publ Hlth & Environm, RIVM, Lab Pathol & Immunobiol, NL-3720 BA Bilthoven, Netherlands; Natl Inst Publ Hlth & Environm, Dept Chron Dis & Environm Epidemiol, NL-3720 BA Bilthoven, Netherlands; Natl Inst Publ Hlth & Environm, Hlth Effects Res Lab, NL-3720 BA Bilthoven, Netherlands; Univ Utrecht, Inst Risk Assessment Sci, Environm & Occupat Hlth Div, Utrecht, Netherlands	Steerenberg, PA (reprint author), Natl Inst Publ Hlth & Environm, RIVM, Lab Pathol & Immunobiol, POB 1, NL-3720 BA Bilthoven, Netherlands.			brunekreef, bert/0000-0001-9908-0060			ABERG N, 1989, CLIN EXP ALLERGY, V19, P643, DOI 10.1111/j.1365-2222.1989.tb02761.x; ABERG N, 1989, ACTA PAEDIATR SCAND, V78, P246, DOI 10.1111/j.1651-2227.1989.tb11064.x; Adisesh LA, 1998, CLIN EXP ALLERGY, V28, P876; ALVING K, 1993, EUR RESPIR J, V6, P1368; Arnal JF, 1997, CLIN EXP ALLERGY, V27, P358; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Barnes PJ, 1996, THORAX, V51, P218, DOI 10.1136/thx.51.2.218; Berlyne G, 2000, LANCET, V355, P1029, DOI 10.1016/S0140-6736(00)02027-4; Boezen HM, 1996, AM J RESP CRIT CARE, V154, P30; BRUSASCO V, 1990, J APPL PHYSIOL, V69, P2209; DURHAM SR, 1985, CLIN ALLERGY, V15, P411, DOI 10.1111/j.1365-2222.1985.tb02290.x; Fischer PH, 2002, INT ARCH OCC ENV HEA, V75, P348, DOI 10.1007/s00420-002-0320-x; Frangova V, 1996, CHEST, V110, P1236, DOI 10.1378/chest.110.5.1236; Garnier P, 1996, EUR RESPIR J, V9, P1134, DOI 10.1183/09031936.96.09061134; Gratziou C, 2001, CLIN EXP ALLERGY, V31, P409, DOI 10.1046/j.1365-2222.2001.01001.x; GUSTAFSSON LE, 1998, EUR RESPIR J, V11, P49; Hoekstra MO, 1998, PEDIATR ALLERGY IMMU, V9, P143, DOI 10.1111/j.1399-3038.1998.tb00361.x; Jatakanon A, 1998, THORAX, V53, P91; Jobsis Q, 2001, THORAX, V56, P285, DOI 10.1136/thorax.56.4.285; KARTASAMITA CB, 1994, J ALLERGY CLIN IMMUN, V94, P981, DOI 10.1016/0091-6749(94)90116-3; Kharitonov S, 1997, EUR RESPIR J, V10, P1683, DOI 10.1183/09031936.97.10071683; KHARITONOV SA, 1994, LANCET, V343, P133, DOI 10.1016/S0140-6736(94)90931-8; Kharitonov SA, 1996, AM J RESP CRIT CARE, V153, P454; KUEHR J, 1994, EUR J PEDIATR, V153, P739, DOI 10.1007/BF01954491; MacPherson JC, 2001, J IMMUNOL, V166, P5763; Martin U, 1996, J ALLERGY CLIN IMMUN, V97, P768, DOI 10.1016/S0091-6749(96)80154-0; Quanjer PH, 1993, EUR RESPIR J S, V16, P5, DOI 10.1183/09041950.005s1693; Salome CM, 1999, AM J RESP CRIT CARE, V159, P911; Silvestri M, 1999, ANN ALLERG ASTHMA IM, V83, P335, DOI 10.1016/S1081-1206(10)62674-9; 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; Steerenberg PA, 2000, NITRIC OXIDE-BIOL CH, V4, P168, DOI 10.1006/niox.2000.0282; van Amsterdam JGC, 1999, NITRIC OXIDE-BIOL CH, V3, P492, DOI 10.1006/niox.1999.0258; van Amsterdam JGC, 1999, INT ARCH OCC ENV HEA, V72, P404, DOI 10.1007/s004200050392; VANAMSTERDAM JGC, 2003, IN PRESS CLIN EXP AL; YATES DH, 1995, AM J RESP CRIT CARE, V152, P892; Yates DH, 1996, AM J RESP CRIT CARE, V154, P247; [Anonymous], 1993, ALLERGY, V48, P48	38	85	90	0	4	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	MAR	2003	58	3					242	245		10.1136/thorax.58.3.242		4	Respiratory System	Respiratory System	654AV	WOS:000181470900013	12612304	
J	Schuster, MA; Franke, T; Pham, CB				Schuster, MA; Franke, T; Pham, CB			Smoking patterns of household members and visitors in homes with children in the United States	ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE			English	Article							ENVIRONMENTAL TOBACCO-SMOKE; NUTRITION EXAMINATION SURVEY; INFANT-DEATH-SYNDROME; PASSIVE SMOKING; PARENTAL SMOKING; MATERNAL SMOKING; CIGARETTE-SMOKING; CHILDHOOD ASTHMA; URINARY COTININE; NATIONAL-HEALTH	Background: Environmental tobacco smoke (ETS), also called passive smoking, has been shown to have adverse effects on the health of children. Objective: To determine the prevalence and pattern of ETS exposure in US homes with children younger than 18 years. Design: We analyzed data from the 1994 National Health Interview Survey and Year 2000 Objectives supplement. A multistage sample design was used to represent the civilian, noninstitutionalized population of the United States. Main Outcome Measures: Frequency of smoking by household residents and visitors in homes with children. Results: Thirty-five percent of children in the United States-21 million children-live in homes where residents or visitors smoke in the home on a regular basis (greater than or equal to I d/wk). From the household perspective, regular smoking by residents and visitors occurs in 36% of homes in which children reside. in 92% of homes with children where residents smoke at home, they do so every day of the week. Sixteen percent of nonsmoking respondents with children report that other residents or visitors smoke in the home. In 6% of the homes where no residents smoke, there is nevertheless regular smoking by visitors. In multivariate regression analysis, the prevalence of regular smoking in homes with children varies by age of youngest child, race/ethnicity, number of parents in the home, parental educational level, income, and region of the country. Conclusions: Many children live in homes with ETS. Most respondents who smoke report that smoking occurs in the home every day. Visitors are an additional source of ETS in homes, including some homes where residents do not smoke. Clinicians who take care of children can advise parents, whether or not they smoke, on how to limit their children's ETS exposure.	RAND Corp, Santa Monica, CA 90407 USA; Univ Calif Los Angeles, Sch Med, Los Angeles, CA 90024 USA; Univ Calif Los Angeles, Sch Social Welf, Los Angeles, CA 90024 USA; Univ Calif Los Angeles, Dept Pediat, Los Angeles, CA 90024 USA; Univ Calif Los Angeles, Dept Hlth Serv, Los Angeles, CA 90024 USA	Schuster, MA (reprint author), RAND Corp, 1700 Main St, Santa Monica, CA 90407 USA.				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J	Faergemann, J				Faergemann, J			Atopic dermatitis and fungi	CLINICAL MICROBIOLOGY REVIEWS			English	Review							IGE-MEDIATED HYPERSENSITIVITY; YEAST MALASSEZIA-FURFUR; CANDIDA-ALBICANS MANNAN; CROSS-REACTING IGE; PITYROSPORUM-OVALE; STAPHYLOCOCCUS-AUREUS; SEBORRHEIC DERMATITIS; PITYRIASIS-VERSICOLOR; HUMAN-SKIN; THERAPEUTIC IMPLICATIONS	Atopic dermatitis (AD) is a chronic, itching, inflammatory skin disease which is associated with asthma and/or hay fever and a familial occurrence of these conditions. Genetic factors are important in the development of AD, but the exact hereditary pathway is still unknown. Dry skin and the weakened barrier function in patients with AD is very important for the patient's reactions to irritants and other external trigger factors including microorganisms. The standard treatments are topical corticosteroids, topical immunomodulating agents, and emollients. If AD cannot be controlled by this type of treatment, systemic immunomodulating agents may be used. UVB, UVA, or psoralen-UVA may also be used for widespread severe lesions. However, some patients do not respond to these standard treatment, and then it is important to consider the role of microorganisms, house dust mites or food. The role of the Malassezia yeasts in AD, especially AD located to the head and neck region, is now documented in several papers. There are also several papers indicating the role of Candida as an aggravating factor in AD. Patients with AD also develop chronic dermatophyte infections more easily, and patients with AD and chronic dermatophyte infections may show improvement in their AD when treated with antifungal drugs.	Sahlgrens Univ Hosp, Dept Dermatol, S-41345 Gothenburg, Sweden	Faergemann, J (reprint author), Sahlgrens Univ Hosp, Dept Dermatol, S-41345 Gothenburg, Sweden.						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J	Oshikawa, K; Yanagisawa, K; Tominaga, S; Sugiyama, Y				Oshikawa, K; Yanagisawa, K; Tominaga, S; Sugiyama, Y			Expression and function of the ST2 gene in a murine model of allergic airway inflammation	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						asthma; allergy; gene therapy; type-2 helper T cell; T1/ST2	HELPER T-CELLS; INTERLEUKIN-1 RECEPTOR; EFFECTOR FUNCTION; RESPONSIVE GENE; PROMOTER USAGE; IL-1 RECEPTOR; MAST-CELLS; ASTHMA; PROTEIN; T1/ST2	Background We have recently reported that soluble ST2 protein levels are elevated in the sera of patients with asthma, and correlate well with the severity of asthma exacerbation. However, the role, function, and kinetics of soluble ST2 expression in asthma remain unclear. Objective The objective of the present study was to clarify the function and kinetics of soluble murine (m) ST2 expression in a murine asthma model. Methods We analyzed the kinetics of gene and protein expression of mST2 in sera or lung tissue after allergen (ovalbumin; OVA) challenge in a murine model of allergic airway inflammation, the effects of mST2 protein on OVA-induced Th2 cytokine production in vitro from splenocytes of sensitized mice, and the effects of soluble mST2 on Th2-dependent allergic airway inflammation by in vivo gene transfer of mST2. Results Serum mST2 protein levels increased to the maximal level 3 h after the allergen challenge, before serum IL-5 levels peaked. The mRNA expression of mST2 in lung tissue was induced after the allergen challenge, while that in the spleen was constitutively detected. Furthermore, pre-treatment with mST2 protein significantly inhibited the production of IL-4 and IL-5, but not IFN-gamma, from OVA-stimulated splenocytes in vitro, and intravenous mST2 gene transfer resulted in a drastic reduction in the number of eosinophils and in the levels of IL-4 and IL-5 in bronchoalveolar lavage fluid, compared with those in response to transfer of non-coding plasmid vector or of lipid alone. Conclusion These results suggest that increases in endogenous mST2 protein after allergen exposure may modulate Th2-mediated airway inflammation, and that in vivo gene transfer of mST2 can be applicable to use in a novel immunotherapy for allergic diseases.	Jichi Med Sch, Dept Med, Div Pulm Med, Minami Kawachi, Tochigi 3290498, Japan; Jichi Med Sch, Dept Biochem, Minami Kawachi, Tochigi, Japan	Oshikawa, K (reprint author), Jichi Med Sch, Dept Med, Div Pulm Med, 3311-1 Minamikawachi, Minami Kawachi, Tochigi 3290498, Japan.						BEAVEN MA, 1993, IMMUNOL TODAY, V14, P222, DOI 10.1016/0167-5699(93)90167-J; BERGERS G, 1994, EMBO J, V13, P1176; BOUSQUET J, 1990, NEW ENGL J MED, V323, P1033, DOI 10.1056/NEJM199010113231505; Corry DB, 1998, MOL MED, V4, P344; Coyle AJ, 1999, J EXP MED, V190, P895, DOI 10.1084/jem.190.7.895; Dow SW, 1999, HUM GENE THER, V10, P1905, DOI 10.1089/10430349950017266; Foster PS, 1996, J EXP MED, V183, P195, DOI 10.1084/jem.183.1.195; Freimark BD, 1998, J IMMUNOL, V160, P4580; Gajewska BU, 2001, AM J RESP CELL MOL, V25, P326; Grunig G, 1998, SCIENCE, V282, P2261, DOI 10.1126/science.282.5397.2261; Hoshino K, 1999, J EXP MED, V190, P1541, DOI 10.1084/jem.190.10.1541; Iwahana H, 1999, EUR J BIOCHEM, V264, P397, DOI 10.1046/j.1432-1327.1999.00615.x; Kuroiwa K, 2000, HYBRIDOMA, V19, P151, DOI 10.1089/02724570050031194; Lambrecht BN, 2000, J CLIN INVEST, V106, P551, DOI 10.1172/JCI8107; Lohning M, 1998, P NATL ACAD SCI USA, V95, P6930, DOI 10.1073/pnas.95.12.6930; MIZUSHIMA S, 1990, NUCLEIC ACIDS RES, V18, P5322, DOI 10.1093/nar/18.17.5322; Moritz DR, 1998, HYBRIDOMA, V17, P107, DOI 10.1089/hyb.1998.17.107; Moritz DR, 1998, J IMMUNOL, V161, P4866; Oshikawa K, 2001, AM J RESP CRIT CARE, V164, P277; ROBINSON DS, 1992, NEW ENGL J MED, V326, P298, DOI 10.1056/NEJM199201303260504; ROSSLER U, 1993, ONCOGENE, V8, P609; Sato Y, 1996, SCIENCE, V273, P352, DOI 10.1126/science.273.5273.352; TAKAGI T, 1993, BIOCHIM BIOPHYS ACTA, V1178, P194, DOI 10.1016/0167-4889(93)90009-E; TOMINAGA S, 1989, FEBS LETT, V258, P301, DOI 10.1016/0014-5793(89)81679-5; Tominaga S, 1996, HUM GENET, V97, P561; TOMINAGA S, 1991, BIOCHIM BIOPHYS ACTA, V1090, P1; Townsend MJ, 2000, J EXP MED, V191, P1069, DOI 10.1084/jem.191.6.1069; Umetsu DT, 1997, J ALLERGY CLIN IMMUN, V100, P1; WERENSKIOLD AK, 1989, MOL CELL BIOL, V9, P5207; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; Xu D, 1998, J EXP MED, V187, P787, DOI 10.1084/jem.187.5.787; YANAGISAWA K, 1993, FEBS LETT, V318, P83, DOI 10.1016/0014-5793(93)81333-U; Yanagisawa K, 1997, J BIOCHEM-TOKYO, V121, P95	33	85	91	0	1	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	OCT	2002	32	10					1520	1526		10.1046/j.1365-2745.2002.01494.x		7	Allergy; Immunology	Allergy; Immunology	601ZJ	WOS:000178479300022	12372135	
J	Gibson, PG; Fujimura, M; Niimi, A				Gibson, PG; Fujimura, M; Niimi, A			Eosinophilic bronchitis: clinical manifestations and implications for treatment	THORAX			English	Review							OBSTRUCTIVE PULMONARY-DISEASE; COUGH-VARIANT ASTHMA; CHRONIC NONPRODUCTIVE COUGH; AIR-FLOW OBSTRUCTION; SPUTUM EOSINOPHILIA; ALLERGIC RHINITIS; INFLAMMATION; HYPERRESPONSIVENESS; RESPONSIVENESS; CHILDREN	Airway inflammation with eosinophils is now reported to occur not only in asthma but in other airway diseases such as cough variant asthma, chronic cough, atopic cough, episodic symptoms without asthma, allergic rhinitis, and COPD. Although the prevalence of eosinophilic bronchitis (EB) is less than in asthma, the causes, mechanisms and treatment of EB in these conditions appears to be similar to asthma where allergen induced IL-5 secretion and symptoms are readily responsive to inhaled corticosteroids. The prognosis of EB without asthma is not known but it may be a precursor for asthma and, if so, recognition of this syndrome may permit effective treatment and reduction in the rising prevalence of asthma. Induced sputum analysis allows recognition of EB in clinical practice. The place of the asthma treatment paradigm with early and sustained corticosteroid treatment needs to be defined in EB without asthma. Airway wall remodelling can occur in rhinitis, COPD, and cough variant asthma with EB. The mechanisms and long term implications of this complication in EB without asthma need to be clarified.	Kanazawa Univ, Sch Med, Dept Internal Med 3, Kanazawa, Ishikawa 9208641, Japan; Kyoto Univ, Grad Sch Med, Dept Resp Med, Sakyo Ku, Kyoto 6068507, Japan							Alvarez MJ, 2000, ALLERGY, V55, P355, DOI 10.1034/j.1398-9995.2000.00312.x; Balzano G, 1999, AM J RESP CRIT CARE, V160, P1486; Belda J, 2000, AM J RESP CRIT CARE, V161, P475; Bhowmik A, 2000, THORAX, V55, P114, DOI 10.1136/thorax.55.2.114; BOULET LP, 1989, ANN ALLERGY, V63, P114; BRAMAN SS, 1985, PRIMARY CARE, V12, P217; Braunstahl GJ, 2001, J ALLERGY CLIN IMMUN, V107, P469, DOI 10.1067/mai.2001.113046; Brightling CE, 2000, LANCET, V356, P1480, DOI 10.1016/S0140-6736(00)02872-5; Brightling CE, 1999, EUR RESPIR J, V14, P1228, DOI 10.1183/09031936.99.14512289; Brightling CE, 2000, EUR RESPIR J, V15, P682, DOI 10.1034/j.1399-3003.2000.15d10.x; Brightling CE, 1999, AM J RESP CRIT CARE, V160, P406; Brightling CE, 1999, THORAX, V54, P563; Brightling Christopher E., 2000, American Journal of Respiratory and Critical Care Medicine, V162, P878; 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Lams BEA, 2000, EUR RESPIR J, V15, P512, DOI 10.1034/j.1399-3003.2000.15.14.x; Lams BEA, 1998, AM J RESP CRIT CARE, V158, P1518; Lemiere C, 1997, J ALLERGY CLIN IMMUN, V100, P852, DOI 10.1016/S0091-6749(97)70286-0; Leone C, 1997, J ALLERGY CLIN IMMUN, V100, P775, DOI 10.1016/S0091-6749(97)70273-2; Matsumoto H, 2001, CLIN EXP ALLERGY, V31, P637, DOI 10.1046/j.1365-2222.2001.01034.x; McGarvey L, 2000, AM J RESP CRIT CARE, V161, P1763; McGarvey LPA, 1999, EUR RESPIR J, V13, P59; Morikawa A., 1994, Acta Paediatrica Japonica, V36, P223; National Institutes of Health, 1997, NIH PUBL; Niimi A, 2000, LANCET, V356, P564, DOI 10.1016/S0140-6736(00)02584-8; Niimi A, 1998, EUR RESPIR J, V11, P1064, DOI 10.1183/09031936.98.11051064; NIIMI A, 1991, American Review of Respiratory Disease, V143, pA30; OGAWA H, 1995, RESP MED, V89, P219, DOI 10.1016/0954-6111(95)90251-1; Ogawa H, 1998, INT ARCH ALLERGY IMM, V116, P162, DOI 10.1159/000023940; Ohgou T, 1999, Arerugi, V48, P23; Papi A, 2000, AM J RESP CRIT CARE, V162, P1773; Pavord ID, 1997, THORAX, V52, P498; Pizzichini E, 1998, AM J RESP CRIT CARE, V158, P1511; Pizzichini M M, 1999, Can Respir J, V6, P323; Polosa R, 2000, EUR RESPIR J, V15, P30, DOI 10.1183/09031936.00.15103000; PUOLIJOKI H, 1987, EUR J RESPIR DIS, V71, P77; Remes ST, 1998, ACTA PAEDIATR, V87, P165, DOI 10.1080/08035259850157606; Rosi E, 2000, CLIN EXP ALLERGY, V30, P577; Rutgers SR, 2000, CLIN EXP ALLERGY, V30, P657; Rutgers SR, 2000, THORAX, V55, P12, DOI 10.1136/thorax.55.1.12; Rytila P, 2000, EUR RESPIR J, V16, P824, DOI 10.1183/09031936.00.16582400; SACHA RF, 1985, ANN ALLERGY, V54, P195; Saetta M, 1996, CLIN EXP ALLERGY, V26, P766, DOI 10.1046/j.1365-2222.1996.d01-386.x; Spanevello A, 2000, AM J RESP CRIT CARE, V162, P1172; SYED A, 1991, CLIN INVEST MED, V14, P28; ULRIK CS, 1995, CHEST, V108, P10, DOI 10.1378/chest.108.1.10; Wark P A, 2000, Respirology, V5, P51, DOI 10.1046/j.1440-1843.2000.00226.x; Wenzel SE, 1999, AM J RESP CRIT CARE, V160, P1001	82	85	109	0	3	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	FEB	2002	57	2					178	182		10.1136/thorax.57.2.178		5	Respiratory System	Respiratory System	520FF	WOS:000173769800018	11828051	
J	Custovic, A; Simpson, BM; Murray, CS; Lowe, L; Woodcock, A				Custovic, A; Simpson, BM; Murray, CS; Lowe, L; Woodcock, A		NAC Manchester Asthma Allergy Stu	The National Asthma Campaign Manchester Asthma and Allergy 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		allergens; asthma; atopy; prevention; sensitization	YOUNG-CHILDREN; EARLY-LIFE; PREGNANCY	The (NAC)Manchester Asthma and Allergy Study is a prospective study of the development of asthma and allergies in childhood. The subjects (995 children at age 3 years) were recruited in utero by screening parents in the antenatal clinic using skin prick testing and a questionnaire regarding allergic diseases. Children were assigned to risk groups according to parental atopic status (high risk, both parents atopic; medium risk, one parent atopic; low risk, neither parent atopic). A subgroup of those at high risk (with no pets in the home) was randomized to stringent environmental control (allergen impermeable covers for the parental and infant bed, hot washing of bedding weekly, HEPA vacuum cleaner, hard floor for the nursery), and the remainder followed a normal regime. The children have been followed prospectively. The environmental influences are very clearly defined. Measurements of environmental exposures include levels of house dust mite; cat and dog allergens during pregnancy and early life; pet ownership and exposure; childcare arrangements; number of siblings; vaccination uptake; thorough dietary questionnaire and endotoxin exposure. Further unique objective outcome in the cohort is the assessment of lung function in preschool children using specific airways resistance, which at age 3 years clearly reflects both genetic and environmental influences.	Wythenshawe Hosp, NW Lung Ctr, Manchester M23 9LT, Lancs, England	Custovic, A (reprint author), Wythenshawe Hosp, NW Lung Ctr, Manchester M23 9LT, Lancs, England.		Custovic, Adnan/A-2435-2012	Custovic, Adnan/0000-0001-5218-7071; Woodcock, Ashley/0000-0002-5428-8578			Bisgaard H, 1995, EUR RESPIR J, V8, P2067, DOI 10.1183/09031936.95.08122067; 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; Klug B, 1997, EUR RESPIR J, V10, P1599, DOI 10.1183/09031936.97.10071599; Lowe L, 2002, LANCET, V359, P1904, DOI 10.1016/S0140-6736(02)08781-0; Peat JK, 1999, J ALLERGY CLIN IMMUN, V103, P1, DOI 10.1016/S0091-6749(99)70517-8; Simpson BM, 2001, CLIN EXP ALLERGY, V31, P391, DOI 10.1046/j.1365-2222.2001.01050.x; SMILLIE FI, 2001, CLIN EXP ALLERGY, V311, P1194	8	85	87	1	3	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0905-6157			PEDIATR ALLERGY IMMU	Pediatr. Allergy Immunol.		2002	13			15			32	37		10.1034/j.1399-3038.13.s.15.3.x		6	Allergy; Immunology; Pediatrics	Allergy; Immunology; Pediatrics	638KW	WOS:000180571000008	12688622	
J	Sherriff, A; Peters, TJ; Henderson, J; Strachan, D				Sherriff, A; Peters, TJ; Henderson, J; Strachan, D		ALSPAC Study Team	Risk factor associations with wheezing patterns in children followed longitudinally from birth to 3 1/2 years	INTERNATIONAL JOURNAL OF EPIDEMIOLOGY			English	Article						ALSPAC; infant wheeze; risk factors	LOWER RESPIRATORY-TRACT; DAY-CARE ATTENDANCE; MATERNAL SMOKING; PARENTAL SMOKING; ASTHMA; ATOPY; LIFE; INFECTIONS; PERSISTENT; ILLNESSES	Background There is a paucity of detailed longitudinal data on wheeze in early childhood. Not. all children who wheeze in early infancy will continue to wheeze into childhood and beyond. This study aims to investigate possible risk factors for different patterns of wheeze in the pre-school years. Subjects and Study participants. were part of.the.Avon Longitudinal Study of.Parents.and Methods Children (ALSPAC). Maternal reports of child wheeze between birth and 6 months and again between 30 and 42 months were gathered prospectively. Children were categorized into early wheeze, persistent wheeze or late onset wheeze. A large number of risk factors were assessed for each wheezing phenotype using multivariable logistic regression models. Results Over 70% of children who wheezed in the first 6 months did not wheeze 3 years later. Wheezing between 0-6 months was independently associated with the presence of older siblings, male sex, delivery between April and December, bottle feeding, young maternal age, prenatal tobacco smoke exposure, atopy and parental history of asthma. From within this group of early wheezers, risk factors for wheeze that persisted beyond 6 months included pre-term delivery; young maternal age, living in rented local authority housing, atopy and a maternal (not paternal) history of asthma. Atopy and a family history of asthma emerged as the main predictors of wheeze that developed after 6 months of age. Conclusion It is clear that a number of wheezing syndromes exist by 3 1/2 years, albeit with some degree of overlap. Detailed follow-up of this cohort is underway to determine whether risk factor associations determined in the first 3 1/2 years have long-term significance for the clinical entity termed 'asthma'.	Univ Bristol, Unit Paediat & Perinatal Epidemiol, Inst Child Hlth, Bristol BS8 1TQ, Avon, England; Univ Bristol, Dept Social Med, Bristol BS8 1TQ, Avon, England; Univ Bristol, Royal Hosp Sick Children, Inst Child Hlth, Bristol BS8 1TQ, Avon, England; St George Hosp, Med Sch, Dept Publ Hlth Sci, London, England	Sherriff, A (reprint author), Univ Bristol, Unit Paediat & Perinatal Epidemiol, Inst Child Hlth, 24 Tyndall Ave, Bristol BS8 1TQ, Avon, England.			Peters, Tim/0000-0003-2881-4180			Burney P, 1997, AM J RESP CRIT CARE, V156, P1773; Celedon JC, 1999, PEDIATRICS, V104, P495, DOI 10.1542/peds.104.3.495; Cook DG, 1998, THORAX, V53, P884; Daniels SE, 1996, NATURE, V383, P247, DOI 10.1038/383247a0; Doull IJM, 1997, BRIT MED BULL, V53, P71; Doull IJM, 1996, CLIN EXP ALLERGY, V26, P613; Hernandez SF, 1999, ARCH MED RES, V30, P216, DOI 10.1016/S0188-0128(99)00008-1; HILL MR, 1995, BRIT MED J, V311, P776; HIZAWA N, 1995, J MED GENET, V32, P363, DOI 10.1136/jmg.32.5.363; Leach AJ, 1999, INT J PEDIATR OTORHI, V49, pS173; LIEBERMAN E, 1994, AM J PUBLIC HEALTH, V84, P1127, DOI 10.2105/AJPH.84.7.1127; LUX AL, IN PRESS ARCH DIS CH; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; MARTINEZ FD, 1992, AM J EPIDEMIOL, V136, P1258; Nystad W, 1999, INT J EPIDEMIOL, V28, P882, DOI 10.1093/ije/28.5.882; Oddy WH, 1999, BRIT MED J, V319, P815; Rahman M M, 1997, Bangladesh Med Res Counc Bull, V23, P47; Rusconi F, 1999, AM J RESP CRIT CARE, V160, P1617; SAARINEN UM, 1995, LANCET, V346, P1065, DOI 10.1016/S0140-6736(95)91742-X; SCHWARTZ J, 1990, AM REV RESPIR DIS, V142, P555; SHIRAKAWA T, 1994, NAT GENET, V7, P125, DOI 10.1038/ng0694-125; TAYLOR B, 1987, ARCH DIS CHILD, V62, P786; WILCOX AJ, 1993, AM J EPIDEMIOL, V137, P1098; YOUNG S, 1991, NEW ENGL J MED, V324, P1168, DOI 10.1056/NEJM199104253241704	24	85	89	2	9	OXFORD UNIV PRESS	OXFORD	GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND	0300-5771			INT J EPIDEMIOL	Int. J. Epidemiol.	DEC	2001	30	6					1473	1484		10.1093/ije/30.6.1473		12	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	520NC	WOS:000173787100055	11821366	
J	Kassel, O; De Blay, F; Duvernelle, C; Olgart, C; Israel-Biet, D; Krieger, P; Moreau, L; Muller, C; Pauli, G; Frossard, N				Kassel, O; De Blay, F; Duvernelle, C; Olgart, C; Israel-Biet, D; Krieger, P; Moreau, L; Muller, C; Pauli, G; Frossard, N			Local increase in the number of mast cells and expression of nerve growth factor in the bronchus of asthmatic patients after repeated inhalation of allergen at low-dose	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						neurotrophin; asthma; airway; mast cell; NGF; tryptase; allergy; bronchus; bronchoalveolar lavage; bronchial biopsy	AIRWAY MUCOSAL INFLAMMATION; SURVIVAL PROMOTION; PERIPHERAL-BLOOD; FUNCTIONAL TRKA; UP-REGULATION; MILD ASTHMA; PROGENITORS; EXPOSURE; RECEPTOR; MODEL	Background Repeated inhalation of allergen at low-dose induces an increase in bronchial hyper-responsiveness, without any associated symptom. The concomitant events in the bronchus have not been described. Objective We have studied the dynamic number of mast cells in the airways of patients with mild asthma before and after repeated inhalation of allergen at low-dose and the expression of nerve growth factor (NGF), which is reported to promote growth and survival of mast cells. Methods Twelve patients with mild asthma to cat allergen were enrolled at random in a blind placebo-controlled study, and submitted to repeated low-dose allergen exposure (1/5 of the provocative dose). Mast cells were immunolocalized using an antibody against mast cell tryptase. NGF and its high affinity receptor, TrkA, were immunolocalized using anti-NGF and anti-TrkA antibodies, respectively. NGF mRNA was quantified by competitive polymerase chain reaction (PCR) after reverse transcription of total RNA extracted from bronchial biopsy. NGF protein levels were measured by ELISA in bronchoalveolar lavage (BAL) fluid. Results Bronchial mast cell number was increased significantly after allergen exposure as compared with before. NGF expression in the bronchus was immunolocalized mainly to epithelial cells, but also to fibroblasts, blood vessels, and a few infiltrated cells. NGF mRNA levels in bronchial biopsies were increased significantly after allergen exposure. The high affinity receptor for NGF, TrkA, was immunolocalized to the infiltrated mast cell membrane. Conclusion Our study shows that the increase in the number of mast cells and in the expression of NGF induced by allergen exposure in the bronchus of asthmatic patients is occurring before the onset of symptoms. In addition, our finding of the presence of the TrkA receptor on the membrane of the infiltrated mast cell in situ brings evidence of the mast cell as a target cell for the growth factor activity of NGF in the airways in asthma.	Univ Strasbourg 1, Fac Pharm, INSERM, U425, F-67401 Illkirch Graffenstaden, France; Hop Univ Strasbourg, Serv Pneumol, Strasbourg, France; Hop Laennec, Immunol Pulm Lab, Paris, France; Fac Pharm, CNRS, UMR 7034, F-67401 Illkirch Graffenstaden, France	Frossard, N (reprint author), Univ Strasbourg 1, Fac Pharm, INSERM, U425, 74 Route Rhin,BP 24, F-67401 Illkirch Graffenstaden, France.		Kassel, Olivier/H-2117-2013; Frossard, Nelly/F-8301-2013	Kassel, Olivier/0000-0002-8616-3091; MULLER, Christian/0000-0002-3463-1025			ALOE L, 1977, BRAIN RES, V133, P358, DOI 10.1016/0006-8993(77)90772-7; ALOE L, 1994, NEUROREPORT, V5, P1030, DOI 10.1097/00001756-199405000-00003; Arshad SH, 1998, AM J RESP CRIT CARE, V157, P1900; BEASLEY R, 1989, AM REV RESPIR DIS, V139, P806; Bonini S, 1996, P NATL ACAD SCI USA, V93, P10955, DOI 10.1073/pnas.93.20.10955; BRADDING P, 1994, AM J RESP CELL MOL, V10, P471; Braun A, 1998, EUR J IMMUNOL, V28, P3240, DOI 10.1002/(SICI)1521-4141(199810)28:10<3240::AID-IMMU3240>3.0.CO;2-U; Bullock ED, 1996, J BIOL CHEM, V271, P27500; Campbell E, 1999, AM J PATHOL, V154, P1259, DOI 10.1016/S0002-9440(10)65377-1; CRIMI E, 1991, AM REV RESPIR DIS, V144, P1282; de Blay F, 1999, INT ARCH ALLERGY IMM, V120, P158, DOI 10.1159/000024234; de Vries A, 1999, AM J RESP CRIT CARE, V159, P1541; DENBURG JA, 1985, J ALLERGY CLIN IMMUN, V76, P466, DOI 10.1016/0091-6749(85)90728-6; FOX A, 1997, AM J RESP CRIT CARE, V155, pA157; Frew AJ, 1996, J ALLERGY CLIN IMMUN, V98, P133, DOI 10.1016/S0091-6749(96)70235-X; GALLI SJ, 1990, LAB INVEST, V62, P5; GIBSON PG, 1991, AM REV RESPIR DIS, V143, P331; HORIGOME K, 1994, J BIOL CHEM, V269, P2695; ISHIZAKA T, 1993, CURR OPIN IMMUNOL, V5, P937, DOI 10.1016/0952-7915(93)90109-6; KANNAN Y, 1993, INT ARCH ALLERGY IMM, V102, P362; Kassel O, 1999, EUR RESPIR J, V13, P951, DOI 10.1034/j.1399-3003.1999.13e04.x; Kassel O, 1998, MOL PHARMACOL, V54, P1073; KAWAMOTO K, 1995, BLOOD, V86, P4638; LAITINEN LA, 1993, AM REV RESPIR DIS, V147, P697; LEON A, 1994, P NATL ACAD SCI USA, V91, P3739, DOI 10.1073/pnas.91.9.3739; LEVIMONTALCINI R, 1987, SCIENCE, V237, P1154, DOI 10.1126/science.3306916; LOZEWICZ S, 1988, BRIT MED J, V297, P1515; MATSUDA H, 1991, J EXP MED, V174, P7, DOI 10.1084/jem.174.1.7; MONTEFORT S, 1994, J CLIN INVEST, V93, P1411, DOI 10.1172/JCI117118; Murakami M, 1997, J IMMUNOL, V159, P439; Nilsson G, 1997, EUR J IMMUNOL, V27, P2295, DOI 10.1002/eji.1830270925; OHNISHI M, 1988, J ALLERGY CLIN IMMUN, V81, P1149, DOI 10.1016/0091-6749(88)90883-4; Olgart C, 2001, EUR RESPIR J, V18, P115, DOI 10.1183/09031936.01.00069901; OLLERENSHAW SL, 1992, AM REV RESPIR DIS, V145, P922; Palmqvist M, 1998, RESP MED, V92, P1223, DOI 10.1016/S0954-6111(98)90425-5; PESCI A, 1993, AM REV RESPIR DIS, V147, P684; PURCELL WM, 1994, HUM EXP TOXICOL, V13, P429; Roquet A, 1998, APMIS, V106, P293; SAETTA M, 1992, AM REV RESPIR DIS, V145, P160; SANTAMBROGIO L, 1994, J IMMUNOL, V153, P4488; Sehmi R, 1996, AM J RESP CELL MOL, V15, P645; Solomon A, 1998, J ALLERGY CLIN IMMUN, V102, P454, DOI 10.1016/S0091-6749(98)70135-6; Tam SY, 1997, BLOOD, V90, P1807; Valent P, 1995, Exp Dermatol, V4, P255, DOI 10.1111/j.1600-0625.1995.tb00254.x; Virchow JC, 1998, AM J RESP CRIT CARE, V158, P2002; Welker P, 1998, IMMUNOLOGY, V94, P310; Wood Lorna J., 1998, American Journal of Respiratory and Critical Care Medicine, V157, P99	47	85	89	0	3	BLACKWELL SCIENCE LTD	OXFORD	P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	SEP	2001	31	9					1432	1440		10.1046/j.1365-2222.2001.01177.x		9	Allergy; Immunology	Allergy; Immunology	473CF	WOS:000171021400015	11591194	
J	Quirce, S; Maranon, F; Umpierrez, A; de las Heras, M; Fernandez-Caldas, E; Sastre, J				Quirce, S; Maranon, F; Umpierrez, A; de las Heras, M; Fernandez-Caldas, E; Sastre, J			Chicken serum albumin (Gal d 5*) is a partially heat-labile inhalant and food allergen implicated in the bird-egg syndrome	ALLERGY			English	Article						allergic asthma; bird-egg syndrome; chicken albumin; egg allergy; feathers	OCCUPATIONAL ASTHMA; CROSS-REACTIVITY; ALPHA-LIVETIN; PROTEINS; YOLK; IDENTIFICATION; DISEASE; WHITE; BEEF	Background: Chicken serum albumin (alpha -livetin) has been implicated as the causative allergen of the bird-egg syndrome. However, the clinical relevance of sensitization to this allergen has not been confirmed by specific challenge tests and environmental sampling. We investigated whether chicken albumin can be detected in air samples collected in a home with birds, and whether sensitization to this protein may cause respiratory and food allergy symptoms. The heat resistance of chicken albumin and the possible cross-reactivity with conalbumin were also investigated. Methods: We studied eight patients with food allergy to egg yolk who also suffered from respiratory symptoms (rhinitis and/or asthma) caused by exposure to birds. Sensitization to egg yolk and bird antigens was investigated by skin and serologic tests. Hypersensitivity to chicken albumin was confirmed by specific bronchial, conjunctival, and oral provocation tests. Results. All patients had positive skin tests and serum IgE against egg yolk, chicken serum, chicken meat, bird feathers, and chicken albumin. The presence of airborne chicken albumin in the domestic environment was confirmed. Specific bronchial challenge to chicken albumin elicited early asthmatic responses in six patients with asthma. An oral challenge with chicken albumin provoked digestive and systemic allergic symptoms in the two patients challenged. IgE reactivity to chicken albumin was reduced by 88% after heating at 90 degreesC for 30 min. ELISA inhibition demonstrated only partial cross-reactivity between chicken albumin and conalbumin. Conclusions: Chicken albumin (Gal d 5) is a partially heat-labile allergen that may cause both respiratory and food-allergy symptoms in patients with the bird-egg syndrome.	Fdn Jimenez Diaz, Serv Alergia, Dept Allergy, E-28040 Madrid, Spain; CBF LETI SA, Madrid, Spain	Quirce, S (reprint author), Fdn Jimenez Diaz, Serv Alergia, Dept Allergy, Av Reyes Catolicos 2, E-28040 Madrid, Spain.						AGARWAL MK, 1981, J ALLERGY CLIN IMMUN, V68, P194, DOI 10.1016/0091-6749(81)90183-4; ALKABELLO SAS, 1995, ALERGOLOGICA FACTORE, P281; BARR SE, 1961, J ALLERGY, V32, P17, DOI 10.1016/0021-8707(61)90034-X; BAUSELA BA, 1991, ALLERGY, V46, P614, DOI 10.1111/j.1398-9995.1991.tb00632.x; BERNSTEIN DI, 1987, J ALLERGY CLIN IMMUN, V80, P791, DOI 10.1016/S0091-6749(87)80267-1; BERNSTEIN JA, 1993, CHEST, V103, P532, DOI 10.1378/chest.103.2.532; BERRENS L, 1986, CLIN ALLERGY, V16, P355, DOI 10.1111/j.1365-2222.1986.tb01968.x; BERRENS L, 1987, CLIN ALLERGY, V17, P405, DOI 10.1111/j.1365-2222.1987.tb02033.x; Blanco Carmona J G, 1992, Allergy, V47, P190; Breiteneder H, 2000, J ALLERGY CLIN IMMUN, V106, P27, DOI 10.1067/mai.2000.106929; Calvert JE, 1999, CLIN EXP ALLERGY, V29, P166; COCKCROFT DW, 1977, CLIN ALLERGY, V7, P235, DOI 10.1111/j.1365-2222.1977.tb01448.x; CRAIG TJ, 1992, ANN ALLERGY, V69, P510; DEBLAY F, 1994, ALLERGY PROC, V15, P77, DOI 10.2500/108854194778703017; DEMAATBLEEKER F, 1985, ANN ALLERGY, V54, P245; Eigenmann PA, 2000, J ALLERGY CLIN IMMUN, V105, P587, DOI 10.1067/mai.2000.104255; FAUX J A, 1971, Clinical Allergy, V1, P159, DOI 10.1111/j.1365-2222.1971.tb03015.x; Fernandez-Caldas E, 1998, J ALLERGY CLIN IMMUN, V101, P554, DOI 10.1016/S0091-6749(98)70364-1; Fiocchi A, 1998, ALLERGY, V53, P798; HARGREAVE FE, 1972, J ALLERGY CLIN IMMUN, V50, P157, DOI 10.1016/0091-6749(72)90047-4; HOFFMAN DR, 1983, J ALLERGY CLIN IMMUN, V71, P481, DOI 10.1016/0091-6749(83)90465-7; HOFFMAN DR, 1988, J ALLERGY CLIN IMMUN, V81, P484, DOI 10.1016/0091-6749(88)90921-9; KING TP, 1994, INT ARCH ALLERGY IMM, V105, P224; LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0; MANDALLAZ M, 1991, ALLERGOLOGIE, V7, P275; MANDALLAZ MM, 1988, INT ARCH ALLER A IMM, V87, P143; MARKS MB, 1984, ANN ALLERGY, V52, P56; MOLLER C, 1984, ALLERGY, V39, P37, DOI 10.1111/j.1398-9995.1984.tb01931.x; OUCHTERLONY O, 1953, ACTA PATHOL MIC SC, V32, P231; Powrie W. D., 1985, FOOD CHEM, P829; Quirce S, 1998, CLIN EXP ALLERGY, V28, P478, DOI 10.1046/j.1365-2222.1998.00253.x; QUIRCE S, 1994, J ALLERGY CLIN IMMUN, V93, P44, DOI 10.1016/0091-6749(94)90231-3; Restani P, 1998, INT ARCH ALLERGY IMM, V117, P113, DOI 10.1159/000023997; SMITH AB, 1990, CHEST, V98, P398, DOI 10.1378/chest.98.2.398; SMITH AB, 1987, AM J IND MED, V12, P205, DOI 10.1002/ajim.4700120209; Spitzauer S, 1999, INT ARCH ALLERGY IMM, V120, P259, DOI 10.1159/000024278; Spitzauer S, 1995, J ALLERGY CLIN IMMUN, V96, P951, DOI 10.1016/S0091-6749(95)70233-4; SZEPFALUSI Z, 1994, J ALLERGY CLIN IMMUN, V93, P932, DOI 10.1016/0091-6749(94)90388-3; TAUERREICH I, 1994, ALLERGY, V49, P448, DOI 10.1111/j.1398-9995.1994.tb00838.x; TOWBIN H, 1979, P NATL ACAD SCI USA, V76, P4350, DOI 10.1073/pnas.76.9.4350; Werfel SJ, 1997, J ALLERGY CLIN IMMUN, V99, P293, DOI 10.1016/S0091-6749(97)70045-9; WILLIAMS J, 1962, BIOCHEM J, V83, P346; Zacharasiewicz A, 1999, WIEN KLIN WOCHENSCHR, V111, P882	43	85	87	0	3	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	AUG	2001	56	8					754	762		10.1034/j.1398-9995.2001.056008754.x		9	Allergy; Immunology	Allergy; Immunology	459CU	WOS:000170234200007	11488669	
J	Al Frayh, AR; Shakoor, Z; El Rab, MOG; Hasnain, SM				Al Frayh, AR; Shakoor, Z; El Rab, MOG; Hasnain, SM			Increased prevalence of asthma in saudi Arabia	ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY			English	Article							SWEDISH SCHOOL-CHILDREN; SKIN-TEST REACTIVITY; RESPIRATORY SYMPTOMS; CHANGING PREVALENCE; ALLERGIC DISEASES; BRONCHIAL-ASTHMA; SCHOOLCHILDREN; ATOPY; EPIDEMIOLOGY; ADOLESCENTS	Background: Branchial asthma is among the most common chronic illnesses of childhood. A number of reports in the recent past suggest that the prevalence of asthma is increasing globally. Objective: To investigate the changing prevalence of asthma in the Kingdom of Saudi Arabia. Subjects and Methods: Two populations of schoolchildren between the ages of 8 and 16 years were studied using an internationally designed protocol in 1986 and 1995. The questionnaire used in these studies was very similar to the one used in the International Study of Allergy and Asthma in Childhood. A total of 2,123 schoolchildren in 1986 (Jeddah and Riyadh) and 1,008 schoolchildren in 1995 (Hail and Gizan) were enrolled in the surveys. These cross-sectional studies of randomly selected schoolchildren were statistically analyzed using ANOVA and a Z test. Results: The comparison of data between Riyadh versus Hail (inland desert dry environment) and Jeddah versus Gizan (coastal humid environment) revealed that the prevalence of asthma in the similar populations increased significantly from 8% in 1986 to 23% in 1995 (P < .0001). Likewise, the prevalence of allergic rhinitis also increased from 20% to 25% (P < .003) since 1986. However, no significant change in the prevalence of eczema (from 12% to 13%) was noted between 1986 and 1995. Conclusions: The study indicates that there was a significant increase in the prevalence of bronchial asthma and, to a lesser extent, in the prevalence of allergic rhinitis in the Kingdom of Saudi Arabia during this 9-year period. The study also revealed increased exposure to environmental factors such as tobacco smoke and indoor animals in Saudi houses. It seems that the continuing changes in contemporary life may well have contributed to the increased prevalence of asthma in the country.	King Saud Univ, Coll Med, Dept Pediat, Riyadh 11461, Saudi Arabia; King Khalid Univ Hosp, Riyadh 11461, Saudi Arabia; King Saud Univ, Dept Pathol, Riyadh 11451, Saudi Arabia; King Faisal Specialist Hosp & Res Ctr, Dept Biol & Med Res, Riyadh 11211, Saudi Arabia	Al Frayh, AR (reprint author), King Saud Univ, Coll Med, Dept Pediat, Riyadh 11461, Saudi Arabia.						ABERG N, 1989, ACTA PAEDIATR SCAND, V78, P246, DOI 10.1111/j.1651-2227.1989.tb11064.x; al Frayh A R, 1989, Allerg Immunol (Paris), V21, P389; AL-NAHDI M, 1989, Allergie et Immunologie (Paris), V21, P278; ALFRAYH A, 1992, SAUDI MED J, V13, P521; ALFRAYH A, 1990, J ASTHMA, V27, P315, DOI 10.3109/02770909009073344; ALFRAYH AR, 1989, ALLERG IMMUNOL S, V89, P16; ALFRAYH AR, 1990, 9 INT C EG SOC ALL C, P3; BAUMAN A, 1992, MED J AUSTRALIA, V156, P827; BENER A, 1991, J ASTHMA, V28, P281, DOI 10.3109/02770909109073385; BESNIER E, 1892, ANN DERMATOL SYPHIL, V23, P634; BOUSQUET J, 1986, J ALLERGY CLIN IMMUN, V78, P1019, DOI 10.1016/0091-6749(86)90296-4; Brabin BJ, 1998, ANN TROP PAEDIATR, V18, pS33; BUIST AS, 1990, JAMA-J AM MED ASSOC, V264, P1719, DOI 10.1001/jama.264.13.1719; BURNEY PGJ, 1990, BRIT MED J, V300, P1306; GERGEN PJ, 1988, PEDIATRICS, V81, P1; GREGG I, 1983, ASTHMA, P242; HAAHTELA T, 1980, ALLERGY, V35, P433, DOI 10.1111/j.1398-9995.1980.tb01790.x; HATTEVIG G, 1987, ACTA PAEDIATR SCAND, V76, P349, DOI 10.1111/j.1651-2227.1987.tb10473.x; Hayashi T, 1995, ANN ALLERG ASTHMA IM, V75, P525; HOPPER JL, 1995, AUST J PUBLIC HEALTH, V19, P120; HURRY VM, 1988, AUST NZ J MED, V18, P745, DOI 10.1111/j.1445-5994.1988.tb00173.x; INGRAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449, DOI 10.1016/S0091-6749(95)70286-5; KJELLMAN NIM, 1977, ACTA PAEDIATR SCAND, V66, P465, DOI 10.1111/j.1651-2227.1977.tb07928.x; KORENYIBOTH AL, 1992, MIL MED, V157, P452; KORSGAARD J, 1982, AM REV RESPIR DIS, V125, P80; Lenney W, 1997, Pediatr Pulmonol Suppl, V15, P13; Lundback B, 1998, CLIN EXP ALLERGY, V28, P3; *NHLBI, 1995, NIH PUBL; NINAN TK, 1992, BRIT MED J, V304, P873; Nystad W, 1997, EUR RESPIR J, V10, P1046, DOI 10.1183/09031936.97.10051046; PEARCE N, 1995, EPIDEMIOLOGY, V6, P190, DOI 10.1097/00001648-199503000-00020; PEAT JK, 1994, EUR RESPIR J, V7, P1805, DOI 10.1183/09031936.94.07101805; PEAT JK, 1994, BRIT MED J, V308, P1591; ROBERTSON CF, 1991, BRIT MED J, V302, P1116; ROBIN ED, 1988, CHEST, V93, P614, DOI 10.1378/chest.93.3.614; SKARPAAS IJK, 1985, ALLERGY, V40, P295, DOI 10.1111/j.1398-9995.1985.tb00235.x; Sly RM, 1999, ANN ALLERG ASTHMA IM, V82, P233, DOI 10.1016/S1081-1206(10)62603-8; VARJONEN E, 1992, ALLERGY, V47, P243, DOI 10.1111/j.1398-9995.1992.tb00657.x; *WHO, 1975, B WORLD HEALTH ORGAN, V52, P251; Yemaneberhan H, 1997, LANCET, V350, P85, DOI 10.1016/S0140-6736(97)01151-3	40	85	91	0	1	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	2001	86	3					292	296				5	Allergy; Immunology	Allergy; Immunology	416GZ	WOS:000167773100009	11289327	
J	Lim, S; Groneberg, D; Fischer, A; Oates, T; Caramori, G; Mattos, W; Adcock, I; Barnes, PJ; Chung, KF				Lim, S; Groneberg, D; Fischer, A; Oates, T; Caramori, G; Mattos, W; Adcock, I; Barnes, PJ; Chung, KF			Expression of heme oxygenase isoenzymes 1 and 2 in normal and asthmatic airways - Effect of inhaled corticosteroids	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							PARTICULATE AIR-POLLUTION; HUMAN-SKIN FIBROBLASTS; NITRIC-OXIDE SYNTHASE; HYDROGEN-PEROXIDE; OXIDATIVE STRESS; MESSENGER-RNA; EPITHELIAL-CELLS; GENE-EXPRESSION; CARBON-MONOXIDE; IN-VITRO	Heme oxygenase (HO) is considered to be an antioxidant enzyme that catabolizes heme to produce carbon monoxide (CO) and biliverdin. We determined the expression and distribution of HO-1 and HO-2, two isoenzymes of HO, in the airways of patients with asthma, and determined the effect of inhaled corticosteroid therapy. Immunostaining for both enzymes was widely distributed in the airways' submucosa, particularly in airway epithelium and submucosal macrophages (CD68(+)) as determined by double immunostaining. There was no difference in intensity and extent of staining in biopsies from normal subjects (n = 10) and subjects with asthma (n = 10). Following 1 mo of treatment with inhaled corticosteroids (budesonide 1,600 mug/d), there was no significant change in the expression and distribution of either HO-1 or HO-2 in the airways' submucosa in eight subjects with mild asthma, despite a significant reduction in airway eosinophils and a reduction in bronchial responsiveness to methacholine. Levels of exhaled nitric oxide were significantly reduced, but exhaled CO levels remained unchanged by the treatment. Treatment with a placebo inhaler (n = 8) had no effects on these parameters. Thus, both HO-1 and HO-2 are extensively distributed equally in normal subjects and subjects with asthma, and are not modulated by inhaled corticosteroid therapy in subjects with asthma. HO may be an important endogenous antioxidant enzyme.	Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Thorac Med, London SW3 6LY, England; Univ Giessen, Inst Anat & Cell Biol, Giessen, Germany	Chung, KF (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Thorac Med, Dovehouse St, London SW3 6LY, England.			Adcock, Ian/0000-0003-2101-8843; Groneberg, David/0000-0001-8551-6556; Chung, Kian Fan/0000-0001-7101-1426			ADCOCK IM, 1994, BIOCHEM BIOPH RES CO, V199, P1518, DOI 10.1006/bbrc.1994.1403; Antczak A, 1997, EUR RESPIR J, V10, P1235, DOI 10.1183/09031936.97.10061235; Barnes PJ, 1998, PHARMACOL REV, V50, P515; BAUERLE PA, 1991, BIOCHIM BIOPHYS ACTA, V1072, P63; Berkman N, 1996, AM J RESP CRIT CARE, V154, P1804; CAMHI SL, 1995, AM J RESP CELL MOL, V13, P387; CANTONI L, 1991, BIOCHEM J, V279, P891; Datta PK, 1999, KIDNEY INT, V55, P1734, DOI 10.1046/j.1523-1755.1999.00429.x; Dennery PA, 1996, PEDIATR RES, V40, P815, DOI 10.1203/00006450-199612000-00007; Dennery PA, 1996, AM J PHYSIOL-LUNG C, V271, pL672; Foresti R, 1999, BIOCHEM J, V339, P729, DOI 10.1042/0264-6021:3390729; FREEMAN BA, 1981, J BIOL CHEM, V256, P986; HAMID Q, 1993, LANCET, V342, P1510, DOI 10.1016/S0140-6736(05)80083-2; Hart LA, 1998, AM J RESP CRIT CARE, V158, P1585; Horvath I, 1998, AM J RESP CRIT CARE, V158, P1042; Horvath I, 1998, THORAX, V53, P668; ISHIZAWA S, 1983, J BIOL CHEM, V258, P4220; JARJOUR NN, 1992, AM REV RESPIR DIS, V146, P905; KEYSE SM, 1990, MOL CELL BIOL, V10, P4967; KEYSE SM, 1989, P NATL ACAD SCI USA, V86, P99, DOI 10.1073/pnas.86.1.99; KINNULA VL, 1995, LAB INVEST, V73, P3; Lamkhioued B, 1997, J IMMUNOL, V159, P4593; Lavrovsky Y, 1996, BIOCHEM BIOPH RES CO, V218, P759, DOI 10.1006/bbrc.1996.0135; Lee PJ, 1996, P NATL ACAD SCI USA, V93, P10393, DOI 10.1073/pnas.93.19.10393; Lee PJ, 1996, AM J RESP CELL MOL, V14, P556; Li XY, 1996, THORAX, V51, P1216, DOI 10.1136/thx.51.12.1216; LUTTON JD, 1992, J CELL BIOCHEM, V49, P259, DOI 10.1002/jcb.240490308; MAINES MD, 1988, FASEB J, V2, P2557; Poss KD, 1997, P NATL ACAD SCI USA, V94, P10925, DOI 10.1073/pnas.94.20.10925; Raju VS, 1997, BBA-GENE STRUCT EXPR, V1351, P89, DOI 10.1016/S0167-4781(96)00183-2; Saleh D, 1998, FASEB J, V12, P929; SEATON A, 1995, LANCET, V345, P176, DOI 10.1016/S0140-6736(95)90173-6; SOUSA AR, 1993, AM REV RESPIR DIS, V147, P1557; VACHIER I, 1994, EUR RESPIR J, V7, P1585, DOI 10.1183/09031936.94.07091585; VILE GF, 1994, P NATL ACAD SCI USA, V91, P2607, DOI 10.1073/pnas.91.7.2607; Zayasu K, 1997, AM J RESP CRIT CARE, V156, P1140	36	85	87	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.	NOV	2000	162	5					1912	1918				7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	371WU	WOS:000165202900054	11069834	
J	Alvarez, MJ; Olaguibel, JM; Garcia, BE; Rodriguez, A; Tabar, AI; Urbiola, E				Alvarez, MJ; Olaguibel, JM; Garcia, BE; Rodriguez, A; Tabar, AI; Urbiola, E			Airway inflammation in asthma and perennial allergic rhinitis. Relationship with nonspecific bronchial responsiveness and maximal airway narrowing	ALLERGY			English	Article						airway inflammation; asthma; eosinophil cationic protein; eosinophils; induced sputum; maximal response plateau; nonspecific bronchial hyperresponsiveness; rhinitis; tryptase	INDUCED SPUTUM; MAST-CELLS; BRONCHOALVEOLAR LAVAGE; HEALTHY-SUBJECTS; EOSINOPHILS; BLOOD; HYPERRESPONSIVENESS; REPRODUCIBILITY; CHALLENGE; BIOPSIES	Background: Eosinophilic airway inflammation is the hallmark of asthma, but it has also been reported in other conditions such as allergic rhinitis. We have tested whether the analysis of cells and chemicals in sputum can distinguish between patients with mild allergic asthma, those with allergic rhinitis, and healthy controls. The relationship between inflammation markers in sputum and nonspecific bronchial hyperresponsiveness to methacholine (BHR) (PD20 and maximal response plateau [MRP] values) was also evaluated. Methods: We selected 31 mild asthmatics and 15 rhinitis patients sensitized to house-dust mite. As a control group, we studied 10 healthy subjects. Every subject underwent the methacholine bronchial provocation test (M-BPT) and sputum induction. Blood eosinophils and serum ECP levels were measured. Sputum cell differentials were assessed, and eosinophil cationic protein (ECP), tryptase, albumin, and interleukin (IL)-5 levels were measured in the entire sputum supernatant. Results: Blood eosinophils and serum ECP levels were higher in asthma patients and rhinitis than in healthy controls, but no difference: between asthma patients and rhinitis patients was found. Asthmatics had higher eosinophil counts and higher ECP and tryptase levels in sputum than rhinitis patients or control subjects. Sputum albumin levels were higher in asthmatics than in controls. Rhinitis patients exhibited higher sputum eosinophils than healthy controls. An association between sputum eosinophil numbers and MPR values (r = -0.57) was detected, and a trend toward correlation between sputum ECP levels and PD20 values (r = -0.47) was found in the rhinitis group, but not in asthmatics. No correlation between blood eosinophilic inflammation and lung functional indices was found. Conclusions: Induced sputum is an accurate method to study bronchial inflammation, allowing one to distinguish between rhinitis patients and mildly asthmatic patients. The fact that no relationship was detected between sputum inflammation and BHR suggests that other factors, such as airway remodeling, may be at least partly responsible for BHR in asthma.	Hosp Virgen Camino, Serv Alergol, Pamplona, Spain; Hosp Virgen Camino, Serv Patol, Pamplona, Spain	Olaguibel, JM (reprint author), Plaza La Paz SN, Pamplona 31002, Spain.						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J	Spiteri, MA; Bianco, A; Strange, RC; Fryer, AA				Spiteri, MA; Bianco, A; Strange, RC; Fryer, AA			Polymorphisms at the glutathione S-transferase, GSTP1 locus: a novel mechanism for susceptibility and development of atopic airway inflammation	ALLERGY			English	Article; Proceedings Paper	International Meeting on Experimental and Clinical-Therapeutic Features of Asthma	JUN 07-08, 1999	NAPLES, ITALY			airway inflammation; atopy; bronchial hyperresponsiveness; GSTP1 polymorphisms	POLYCYCLIC AROMATIC-HYDROCARBONS; HUMAN-LUNG; NITROGEN-DIOXIDE; DIOL EPOXIDES; EXPRESSION; EXPOSURE; ASTHMA; OZONE; PURIFICATION; ASSOCIATION	A common feature of environmental irritants is their ability to cause local inflammation which could alter airway function. The principal targets of such injury are the epithelial cells lining the airway passages and the lower respiratory gas-exchange areas. While host atopy is a recognized risk factor for airway inflammation, atopy alone cannot cause asthma. We hypothesize that susceptibility to persistent airway inflammation in atopic individuals is characterized by an inherited deficiency in the effectiveness of detoxification of inhaled irritants and products of oxidative stress such as reactive oxygen species (ROS). Our case-control studies show that polymorphisms at the glutathione S-transferase, GSTP1, locus on chromosome 11q13 may account for variation in host response to oxidative stress, a key component of airway inflammation. Frequency of the GSTP1 Val/Val genotype is reduced in atopic subjects compared with nonatopic subjects. Trend analysis also shows a significant decrease of GSTP1 Val/Val (with parallel increase of GSTP1 Ile/Ile) genotype frequency with increasing severity of airflow obstruction/bronchial hyperresponsiveness. The implication of specific polymorphisms at the GSTP1 locus in airway inflammation is entirely novel: however, GST are recognized as a supergene family of enzymes critical in 1) cell protection from the toxic products of ROS-mediated reactions, 2) modulation of eicosanoid synthesis.	Univ Keele, Dept Resp Med, Lung Injury & Inflammat Grp, Keele ST5 5BG, Staffs, England; Univ Keele, Ctr Cell & Mol Med, Clin Biochem Res Lab, Keele ST5 5BG, Staffs, England	Spiteri, MA (reprint author), N Staffordshire Hosp, Dept Resp Med, Lung Injury & Inflammat Grp, Stoke On Trent ST4 6QG, Staffs, England.						AliOsman F, 1997, J BIOL CHEM, V272, P10004; ANTTILA S, 1993, CANCER RES, V53, P5643; BARNES PJ, 1990, FREE RADICAL BIO MED, V9, P235, DOI 10.1016/0891-5849(90)90034-G; BECKETT GJ, 1990, BIOCHIM BIOPHYS ACTA, V1036, P176, DOI 10.1016/0304-4165(90)90031-Q; FRYER AA, 1986, BIOCHIM BIOPHYS ACTA, V883, P448, DOI 10.1016/0304-4165(86)90283-7; FRYER AA, 2000, IN PRESS AM J RESP C; GREENE LS, 1995, J AM COLL NUTR, V14, P317; 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; HAZUCHA MJ, 1987, J APPL PHYSIOL, V62, P1671; Hu X, 1997, BIOCHEM BIOPH RES CO, V238, P397, DOI 10.1006/bbrc.1997.7311; Kelly FJ, 1996, AM J RESP CRIT CARE, V154, P1700; KELLY FJ, 1995, RESP MED, V89, P647, DOI 10.1016/0954-6111(95)90131-0; KOSKELO K, 1981, SCAND J CLIN LAB INV, V41, P683, DOI 10.3109/00365518109090515; Krishna MT, 1996, J ROY COLL PHYS LOND, V30, P61; LIU DX, 1995, FREE RADICAL BIO MED, V18, P571, DOI 10.1016/0891-5849(94)00154-C; Martinez J, 1996, ARCH BIOCHEM BIOPHYS, V336, P191, DOI 10.1006/abbi.1996.0549; Mattey DL, 1999, ANN RHEUM DIS, V58, P164, DOI 10.1136/ard.58.3.164; NINAN TK, 1992, BRIT MED J, V304, P873; PARTRIDGE CA, 1984, LUNG, V162, P27, DOI 10.1007/BF02715625; REITJENS IMC, 1986, J TOXICOL ENV HLTH, V19, P555; SPITERI MA, 1994, EUR RESPIR J, V7, P1431, DOI 10.1183/09031936.94.07081431; STRANGE RC, 1990, GLUTATHIONE S-TRANSFERASES AND DRUG RESISTANCE, P262; Sundberg K, 1998, CARCINOGENESIS, V19, P433, DOI 10.1093/carcin/19.3.433; Thomas NS, 1997, AM J RESP CRIT CARE, V156, pS144; Watson MA, 1998, CARCINOGENESIS, V19, P275, DOI 10.1093/carcin/19.2.275; Willey JC, 1996, AM J RESP CELL MOL, V14, P262	27	85	90	0	2	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy		2000	55			61			15	20		10.1034/j.1398-9995.2000.00502.x		6	Allergy; Immunology	Allergy; Immunology	331NH	WOS:000088024800004	10919500	
J	Cao, C; Jiang, WJ; Wang, BY; Fang, JH; Lang, JD; Tian, G; Jiang, JK; Zhu, TF				Cao, Chen; Jiang, Wenjun; Wang, Buying; Fang, Jianhuo; Lang, Jidong; Tian, Geng; Jiang, Jingkun; Zhu, Ting F.			Inhalable Microorganisms in Beijing's PM2.5 and PM10 Pollutants during a Severe Smog Event	ENVIRONMENTAL SCIENCE & TECHNOLOGY			English	Article							AIRBORNE BACTERIAL COMMUNITIES; PARTICULATE MATTER; OXIDATIVE DAMAGE; AIR-POLLUTION; UNITED-STATES; CLEAN-AIR; HEALTH; CHINA; VARIABILITY; SIZE	Particulate matter (PM) air pollution poses a formidable public health threat to the city of Beijing. Among the various hazards of PM pollutants, microorganisms in PM2.5 and PM10 are thought to be responsible for various allergies and for the spread of respiratory diseases. While the physical and chemical properties of PM pollutants have been extensively studied, much less is known about the inhalable microorganisms. Most existing data on airborne microbial communities using 16S or 18S rRNA gene sequencing to categorize bacteria or fungi into the family or genus levels do not provide information on their allergenic and pathogenic potentials. Here we employed metagenomic methods to analyze the microbial composition of Beijing's PM pollutants during a severe January smog event. We show that with sufficient sequencing depth, airborne microbes including bacteria, archaea, fungi, and dsDNA viruses can be identified at the species level. Our results suggested that the majority of the inhalable microorganisms were soil-associated and nonpathogenic to human. Nevertheless, the sequences of several respiratory microbial allergens and pathogens were identified and their relative abundance appeared to have increased with increased concentrations of PM pollution. Our findings may serve as an important reference for environmental scientists, health workers, and city planners.	[Cao, Chen; Jiang, Wenjun; Zhu, Ting F.] Tsinghua Univ, Sch Life Sci,TNLIST, MOE Key Lab Bioinformat,Ctr Synth & Syst Biol, PTN Peking Univ Tsinghua Univ Natl Inst Biol Sci, Beijing 100084, Peoples R China; [Cao, Chen; Jiang, Wenjun; Zhu, Ting F.] Collaborat Innovat Ctr Diag & Treatment Infect Di, Hangzhou 310003, Zhejiang, Peoples R China; [Cao, Chen] Peking Univ, Grad Program Sch Life Sci, Beijing 100871, Peoples R China; [Wang, Buying; Jiang, Jingkun] Tsinghua Univ, Sch Environm, State Key Joint Lab Environm Simulat & Pollut Con, Beijing 100084, Peoples R China; [Jiang, Jingkun] State Environm Protect Key Lab Sources & Control, Beijing 100084, Peoples R China; [Fang, Jianhuo; Lang, Jidong; Tian, Geng] Tsinghua Univ, Sch Life Sci, Ctr Biomed Anal, Beijing 100084, Peoples R China	Zhu, TF (reprint author), Tsinghua Univ, Sch Life Sci,TNLIST, MOE Key Lab Bioinformat,Ctr Synth & Syst Biol, PTN Peking Univ Tsinghua Univ Natl Inst Biol Sci, Beijing 100084, Peoples R China.	tiangeng@biomed.tsinghua.edu.cn; jiangjk@tsinghua.edu.cn; tzhu@biomed.tsinghua.edu.cn	Jiang, Jingkun/A-1076-2010		Tsinghua University-Peking University Center for Life Sciences (CLS); Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases; Science and Technology Major Project of the Ministry of Science and Technology of China [2013ZX10003003]; National Natural Science Foundation of China [21190054, 21107060, 21221004]; Center for Marine Medicine and Rescue of Tsinghua University; Tsinghua Qian Ren Tuan Dui funding	We thank Gong Cheng, Lei Huang, Babak Javid, Masood Kayani, Yigong Shi, Melody Toosky, Hongwei Wang, Zhen Xie, Nieng Yan, Li Yu, Jingren Zhang, and Michael Q Zhang for helpful discussions and comments on the manuscript, and Qingran Bai, He Chen, Siyu Chen, Zhen Cheng, Hongliang Fu, Ru He, Long Hu, Dongfang Li, Junxiang Li, Cuihua Liu, Kaigui Luo, Peng Liang, Yu Liang, Yongbin Li, Zhixun Shen, Shuxiao Wang, Tingting Wang, Zhiying Xie, Siyin Zhang, and Wei Zhou for their assistance with the experiments. BGI-Shenzhen provided the sequencing platforms used in this study and assistance in preliminary sequence analysis. NSCC-TJ (D.L.) and Tsinghua University School of Information Science and Technology provided computational facilities and assistance with the data analysis. This work was supported in part by funding from the Tsinghua University-Peking University Center for Life Sciences (CLS), Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, the Science and Technology Major Project of the Ministry of Science and Technology of China (Grant No. 2013ZX10003003 to Z.Z.), National Natural Science Foundation of China (Grant No. 21190054, 21107060, and 21221004), Center for Marine Medicine and Rescue of Tsinghua University, and Tsinghua Qian Ren Tuan Dui funding (to M.Q.Z.).	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Sci. Technol.	FEB 4	2014	48	3					1499	1507		10.1021/es4048472		9	Engineering, Environmental; Environmental Sciences	Engineering; Environmental Sciences & Ecology	AA3TL	WOS:000331015100020	24456276	
J	Loss, G; Apprich, S; Waser, M; Kneifel, W; Genuneit, J; Buchele, G; Weber, J; Sozanska, B; Danielewicz, H; Horak, E; van Neerven, RJJ; Heederik, D; Lorenzen, PC; von Mutius, E; Braun-Fahrlander, C				Loss, Georg; Apprich, Silvia; Waser, Marco; Kneifel, Wolfgang; Genuneit, Jon; Buechele, Gisela; Weber, Juliane; Sozanska, Barbara; Danielewicz, Hanna; Horak, Elisabeth; van Neerven, R. J. Joost; Heederik, Dick; Lorenzen, Peter C.; von Mutius, Erika; Braun-Fahrlaender, Charlotte		GABRIELA Study Grp	The protective effect of farm milk consumption on childhood asthma and atopy: The GABRIELA study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Allergic diseases; asthma; atopy; children; farming; hay fever; microorganism; farm milk; risk; whey protein	SCHOOL-AGE-CHILDREN; INVERSE ASSOCIATION; INNATE IMMUNITY; EXPOSURE; ALLERGY; HEALTH; BETA; LIFE; PREVALENCE; EXPRESSION	Background: Farm milk consumption has been identified as an exposure that might contribute to the protective effect of farm life on childhood asthma and allergies. The mechanism of action and the role of particular constituents of farm milk, however, are not yet clear. Objective: We sought to investigate the farm milk effect and determine responsible milk constituents. Methods: In rural regions of Germany, Austria, and Switzerland, a comprehensive questionnaire about farm milk consumption and other farm-related exposures was completed by parents of 8334 school-aged children, and 7606 of them provided serum samples to assess specific IgE levels. In 800 cow's milk samples collected at the participants' homes, viable bacterial counts, whey protein levels, and total fat content were analyzed. Asthma, atopy, and hay fever were associated to reported milk consumption and for the first time to objectively measured milk constituents by using multiple regression analyses. Results: Reported raw milk consumption was inversely associated to asthma (adjusted odds ratio [aOR], 0.59; 95% CI, 0.46-0.74), atopy (aOR, 0.74; 95% CI, 0.61-0.90), and hay fever (aOR, 0.51; 95% CI, 0.37-0.69) independent of other farm exposures. Boiled farm milk did not show a protective effect. Total viable bacterial counts and total fat content of milk were not significantly related to asthma or atopy. Increased levels of the whey proteins BSA (aOR for highest vs lowest levels and asthma, 0.53; 95% CI, 0.30-0.97), alpha-lactalbumin (aOR for interquartile range and asthma, 0.71; 95% CI, 0.52-0.97), and beta-lactoglobulin (aOR for interquartile range and asthma, 0.62; 95% CI, 0.39-0.97), however, were inversely associated with asthma but not with atopy. Conclusions: The findings suggest that the protective effect of raw milk consumption on asthma might be associated with the whey protein fraction of milk. (J Allergy Clin Immunol 2011;128:766-73.)	[Loss, Georg; Waser, Marco; Braun-Fahrlaender, Charlotte] Swiss Trop & Publ Hlth Inst, CH-4002 Basel, Switzerland; [Loss, Georg; Waser, Marco; Braun-Fahrlaender, Charlotte] Univ Basel, CH-4003 Basel, Switzerland; [Apprich, Silvia; Kneifel, Wolfgang] Univ Nat Resources & Life Sci, BOKU Vienna, Dept Food Sci & Technol, Vienna, Austria; [Genuneit, Jon; Buechele, Gisela] Univ Ulm, Inst Epidemiol & Med Biometry, D-89069 Ulm, Germany; [Weber, Juliane; von Mutius, Erika] Ludwig Maximilians Univ Munchen, Univ Childrens Hosp, Munich, Germany; [Sozanska, Barbara; Danielewicz, Hanna] Wroclaw Med Univ, Dept Paediat Allergol & Cardiol 1, Wroclaw, Poland; [Horak, Elisabeth] Innsbruck Med Univ, Dept Pediat & Adolescents, Div Cardiol & Pulmonol, Innsbruck, Austria; [van Neerven, R. J. Joost] Friesland Campina Res, Deventer, Netherlands; [Heederik, Dick] Univ Utrecht, IRAS, Div Environm Epidemiol, NL-3508 TC Utrecht, Netherlands; [Lorenzen, Peter C.] Max Rubner Inst, Fed Res Inst Nutr & Food, Dept Safety & Qual Milk & Fish Prod, Kiel, Germany	Loss, G (reprint author), Swiss Trop & Publ Hlth Inst, Socinstr 57,POB, CH-4002 Basel, Switzerland.	georg.loss@unibas.ch	Loss, Georg/F-1557-2013; Genuneit, Jon/I-9323-2012; Lauener, Roger/O-8612-2016	Genuneit, Jon/0000-0001-5764-1528; Lauener, Roger/0000-0002-8412-606X; Ege, Markus/0000-0001-6643-3923; von Mutius, Erika/0000-0002-8893-4515	European Union [LSH-2004-1.2.5-1, 018996]; European Commission; InfectoPharm; Airsonett AB; Deutsche Forschungsgemeinschaft (DFG); BMBF	Supported by a European Union Research grant under the FP6-LifeSCIHEALTH Integrated Program LSH-2004-1.2.5-1 (contract no. 018996).; J. Weber, B. Sozanska, H. Danielewicz, A Boznanski, A. Debinska, M. Depner, A. Kosmeda, and C. Strunz-Lehner have received research support from the European Commission. D. Heederik and I. M. Wouters have received research support from the European Union. E. von Mutius is a consultant for Novartis, GlaxoSmithKline, ALK-Abello, and Protectimmun; has received a speaker's fee from InfectoPharm; has received research support from Airsonett AB; is a member of the Expert Panel for UK Research Excellence Framework; and is an Associate Editor for the Journal of Allergy and Clinical Immunology. M. Ege has received research support from the European Commission and the Deutsche Forschungsgemeinschaft (DFG). M. Kabesch has financial interests in Roxall, GlaxoSmithKline, Novartis, Sanofi-Aventis, Allergopharma, and AstraZeneca GmbH and has received research support from DFG, BMBF, and the European Union. The rest of the authors have declared that they have no conflict of interest.	Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Bieli C, 2007, J ALLERGY CLIN IMMUN, V120, P1308, DOI 10.1016/j.jaci.2007.07.034; Black PN, 1997, EUR RESPIR J, V10, P6, DOI 10.1183/09031936.97.10010006; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Conroy ME, 2009, CURR OPIN ALLERGY CL, V9, P197, DOI 10.1097/ACI.0b013e32832b3f1d; Desmasures N, 1997, J APPL MICROBIOL, V83, P53, DOI 10.1046/j.1365-2672.1997.00166.x; Eder W, 2006, NEW ENGL J MED, V355, P2226, DOI 10.1056/NEJMra054308; Ege MJ, 2011, NEW ENGL J MED, V364, P701, DOI 10.1056/NEJMoa1007302; Ege MJ, 2006, J ALLERGY CLIN IMMUN, V117, P817, DOI 10.1016/j.jaci.2005.12.1307; Genuneit J, 2011, PAEDIATR PERINAT EP, V25, P436, DOI 10.1111/j.1365-3016.2011.01223.x; International Dairy Federation, 1991, 100B IDF; Krissansen GW, 2007, J AM COLL NUTR, V26, p713S; Li MO, 2006, ANNU REV IMMUNOL, V24, P99, DOI 10.1146/annurev.immunol.24.021605.090737; Lorenzen PC, 2011, INT J DAIRY TECHNOL, V64, P166, DOI 10.1111/j.1471-0307.2010.00656.x; Mosconi E, 2010, MUCOSAL IMMUNOL, V3, P461, DOI 10.1038/mi.2010.23; Oddy WH, 2010, PEDIATR ALLERGY IMMU, V21, P47, DOI 10.1111/j.1399-3038.2009.00913.x; Perkin MR, 2007, CLIN EXP ALLERGY, V37, P627, DOI 10.1111/j.1365-2222.2007.02715.x; Perkin MR, 2006, J ALLERGY CLIN IMMUN, V117, P1374, DOI 10.1016/j.jaci.2006.03.008; Peroni DG, 2010, PEDIAT ALLERG IMM-UK, V21, P977, DOI 10.1111/j.1399-3038.2010.00995.x; Peroni DG, 2009, PEDIAT ALLERG IMM-UK, V20, P42, DOI 10.1111/j.1399-3038.2008.00737.x; Pfefferle PI, 2010, J ALLERGY CLIN IMMUN, V125, P108, DOI 10.1016/j.jaci.2009.09.019; Pfefferle PI, 2010, J ALLERGY CLIN IMMUN, V125, pe1; Puddu P, 2009, BIOCHIMIE, V91, P11, DOI 10.1016/j.biochi.2008.05.005; Remes ST, 2003, CLIN EXP ALLERGY, V33, P427, DOI 10.1046/j.1365-2222.2003.01566.x; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Rusu D, 2009, J NUTR, V139, P386, DOI 10.3945/jn.108.098459; Sly PD, 2008, LANCET, V372, P1100, DOI 10.1016/S0140-6736(08)61451-8; Thijs C, 2010, ALLERGY, V66, P58; von Mutius E, 2010, NAT REV IMMUNOL, V10, P861, DOI 10.1038/nri2871; Waser M, 2007, CLIN EXP ALLERGY, V37, P661, DOI 10.1111/j.1365-2222.2006.02640.x; Wijga AH, 2003, THORAX, V58, P567, DOI 10.1136/thorax.58.7.567; Yoshida T, 2005, J AGR FOOD CHEM, V53, P6851, DOI 10.1021/jf050772k	32	84	85	2	34	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	2011	128	4					766	U432		10.1016/j.jaci.2011.07.048		12	Allergy; Immunology	Allergy; Immunology	841UA	WOS:000296538100010	21875744	
J	Henneberger, PK; Redlich, CA; Callahan, DB; Harber, P; Lemiere, C; Martin, J; Tarlo, SM; Vandenplas, O; Toren, K				Henneberger, Paul K.; Redlich, Carrie A.; Callahan, David B.; Harber, Philip; Lemiere, Catherine; Martin, James; Tarlo, Susan M.; Vandenplas, Olivier; Toren, Kjell		ATS Ad Hoc Comm Work Exacerbated	An Official American Thoracic Society Statement: Work-Exacerbated Asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; occupational diseases; work-related asthma; exacerbation; work-exacerbated asthma	QUALITY-OF-LIFE; DIAGNOSING OCCUPATIONAL ASTHMA; WORKPLACE EXACERBATION; LUNG-FUNCTION; AIRWAY INFLAMMATION; CHRONIC-BRONCHITIS; RESPIRATORY-TRACT; SIGNALING CASCADE; SULFUR-DIOXIDE; INDUCED SPUTUM	Rationale: Occupational exposures can contribute to the exacerbation as well as the onset of asthma. However, work-exacerbated asthma (WEA) has received less attention than occupational asthma (OA) that is caused by work. Objectives: The purpose of this Statement is to summarize current knowledge about the descriptive epidemiology, clinical characteristics, and management and treatment of WEA; propose a case definition for WEA; and discuss needs for prevention and research. Methods: Information about WEA was identified primarily by systematic searches of the medical literature. Statements about prevention and research needs were reached by consensus. Measurements and Main Results: WEA is defined as the worsening of asthma due to conditions at work. WEA is common, with a median prevalence of 21.5% among adults with asthma. Different types of agents or conditions at work may exacerbate asthma. WEA cases with persistent work-related symptoms can have clinical characteristics (level of severity, medication needs) and adverse socioeconomic outcomes (unemployment, reduction in income) similar to those of OA cases. Compared with adults with asthma unrelated to work, WEA cases report more days with symptoms, seek more medical care, and have a lower quality of life. WEA should be considered in any patient with asthma that is getting worse or who has work-related symptoms. Management of WEA should focus on reducing work exposures and optimizing standard medical management, with a change in jobs only if these measures are not successful. Conclusions: WEA is a common and under recognized adverse outcome resulting from conditions at work. Additional research is needed to improve the understanding of the risk factors for, and mechanisms and outcomes of, WEA, and to inform and evaluate preventive interventions.						e Donaghue Research Foundation; American Conference Institute; BNSF Foundation; International Carbon Black Association; Kaiser Permanente; Astra Zeneca; Boehringer Ingelheim; Ception Therapeutics; MedImmune; Wyeth; Merck; Novartis; Allergen; British Columbia Workers Compensation Board; Manitoba Workers Compensation Board; Ontario Workplace Safety and Insurance Board	P.K.H., K.T., and O.V. reported that they received no payments or services from a third party for the work submitted, and had no relevant financial activities outside the submitted work. C. A. R. reported serving on an advisory board for Firmenich S. A. ($5,001-$10,000), receiving author royalties from Elsevier Medical Publishing ($1,000 or less), and a research grant from the Donaghue Research Foundation ($50,001-$100,000). She also reported review of medical records for law firms related to workers compensation, disability, or occupational issues ($1,001-$5,000). D. B. C. reported stock holdings in General Electric ($1,001-$5,000), 3M ($1,001-$5,000), Microsoft ($1,001-$5,000), and Proctor and Gamble ($5,001-$10,000). P. H. reported lecture fees from American Conference Institute ($1,000 or less), fees paid to his institution for medical evaluations and expert testimony regarding individuals with occupational issues ($50,001-$100,000), and research grants paid to his institution from BNSF Foundation ($50,001-$100,000), International Carbon Black Association ($50,001-$100,000), and Kaiser Permanente ($100,001 or more). C. L. reported consultancies for Glaxo Smith Kline ($5,001-$10,000) and Topigen ($1,001-$5,000), and advisory board service for Altana ($1,001-$5,000), Astra Zeneca (up to $1,000), Merck Frosst (up to $1,000), and Novartis (up to $1,000). She received lecture fees from Astra Zeneca ($1,001-$5,000) and Novartis (up to $1,000), and research grants from Astra Zeneca ($10,001-$50,000), Boehringer Ingelheim ($10,001-$50,000), Ception Therapeutics ($10,001-$50,000), MedImmune ($5001-$10,000), and Wyeth ($10,001-$50,000). J. M. received lecture fees from Merck ($1,001-$5,000) and Novartis ($1,001-$5,000), and a research grant from Merck ($50,001-$100,000). S. M. T. reported fees paid to her institution for patient medical assessments for workers compensation systems, their appeals tribunals, and insurance companies ($50,001-$100,000). She also reported research grants from Allergen ($100,001 or more), the British Columbia Workers Compensation Board ($10,001-$50,000), the Manitoba Workers Compensation Board ($100,001 or more), and the Ontario Workplace Safety and Insurance Board ($100,001 or more).	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J	Fujimura, KE; Johnson, CC; Ownby, DR; Cox, MJ; Brodie, EL; Havstad, SL; Zoratti, EM; Woodcroft, KJ; Bobbitt, KR; Wegienka, G; Boushey, HA; Lynch, SV				Fujimura, Kei E.; Johnson, Christine C.; Ownby, Dennis R.; Cox, Michael J.; Brodie, Eoin L.; Havstad, Suzanne L.; Zoratti, Edward M.; Woodcroft, Kimberley J.; Bobbitt, Kevin R.; Wegienka, Ganesa; Boushey, Homer A.; Lynch, Susan V.			Man's best friend? The effect of pet ownership on house dust microbial communities	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Letter							EXPOSURE; ALLERGY		[Fujimura, Kei E.; Cox, Michael J.; Lynch, Susan V.] Univ Calif San Francisco, Div Gastroenterol, Colitis & Crohns Dis Ctr, San Francisco, CA 94143 USA; [Boushey, Homer A.] Univ Calif San Francisco, Dept Med, Div Pulm & Crit Care, San Francisco, CA USA; [Johnson, Christine C.; Havstad, Suzanne L.; Woodcroft, Kimberley J.; Bobbitt, Kevin R.; Wegienka, Ganesa] Henry Ford Hosp, Dept Biostat & Res Epidemiol, Detroit, MI 48202 USA; [Zoratti, Edward M.] Henry Ford Hosp, Dept Internal Med, Div Allergy & Immunol, Detroit, MI 48202 USA; [Ownby, Dennis R.] Med Coll Georgia, Dept Pediat, Div Allergy Immunol, Augusta, GA 30912 USA; [Brodie, Eoin L.] Lawrence Berkeley Natl Lab, Ctr Environm Biotechnol, Berkeley, CA USA	Fujimura, KE (reprint author), Univ Calif San Francisco, Div Gastroenterol, Colitis & Crohns Dis Ctr, San Francisco, CA 94143 USA.	susan.lynch@ucsf.edu	Cox, Michael/A-6959-2010; Brodie, Eoin/A-7853-2008	Brodie, Eoin/0000-0002-8453-8435; Johnson, Christine Cole/0000-0002-6864-6604; Cox, Michael/0000-0002-4002-1506	NIAID NIH HHS [R01 AI059415-05, R01 AI050681, R01 AI050681-05, R01 AI059415]; PHS HHS [A150681, A159415]		Aichbhaumik N, 2008, CLIN EXP ALLERGY, V38, P1787, DOI 10.1111/j.1365-2222.2008.03079.x; Backhed F, 2005, SCIENCE, V307, P1915, DOI 10.1126/science.1104816; Bergmann RL, 1997, CLIN EXP ALLERGY, V27, P752, DOI 10.1046/j.1365-2222.1997.310899.x; Brodie EL, 2006, APPL ENVIRON MICROB, V72, P6288, DOI 10.1128/AEM.00246-06; Havaux X, 2005, CLIN EXP IMMUNOL, V139, P179, DOI 10.1111/j.1365-2249.2004.02679.x; Ownby DR, 2002, JAMA-J AM MED ASSOC, V288, P963, DOI 10.1001/jama.288.8.963; Penders J, 2006, CLIN EXP ALLERGY, V36, P1602, DOI 10.1111/j.1365-2222.2006.02599.x; Reese TA, 2007, NATURE, V447, P92, DOI 10.1038/nature05746; von Mutius E, 2008, IMMUNOL ALLERGY CLIN, V28, P631, DOI 10.1016/j.iac.2008.03.010	9	84	84	6	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.	AUG	2010	126	2								10.1016/j.jaci.2010.05.042		3	Allergy; Immunology	Allergy; Immunology	642IL	WOS:000281203800038	20633927	
J	Kull, I; Melen, E; Alm, J; Hallberg, J; Svartengren, M; van Hage, M; Pershagen, G; Wickman, M; Bergstrom, A				Kull, Inger; Melen, Erik; Alm, Johan; Hallberg, Jenny; Svartengren, Magnus; van Hage, Marianne; Pershagen, Goran; Wickman, Magnus; Bergstrom, Anna			Breast-feeding in relation to asthma, lung function, and sensitization in young schoolchildren	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Breast-feeding; asthma; sensitization; lung function; infant feeding; prevention; BAMSE	PROSPECTIVE BIRTH COHORT; ALLERGIC DISEASES; CHILDHOOD ASTHMA; ATOPIC DISEASE; RISK; CHILDREN; WHEEZE; LIFE; PREVENTION; PHENOTYPES	Background: The evidence from previous studies on beneficial effects of breast-feeding in relation to development of asthma is conflicting. Objective: To investigate the relation between breast-feeding and asthma and/or sensitization during the first 8 years of life. Method: In a birth cohort, children were followed up to 8 years by questionnaires at ages 2 months and 1, 2, 4, and 8 years to collect information on exposures and health effects. Determination of serum IgE antibodies to common inhalant and food allergens was performed at 4 and 8 years. Longitudinal analyses were applied by using general estimated equations. The study population consisted of 3825 children (93% of the original cohort), of whom 2370 gave blood and 2564 performed lung function measurements at 8 years. Results: Children exclusively breast-fed 4 months or more had a reduced risk of asthma during the first 8 years of life (adjusted odds ratio [OR], 0.63; 95% CI, 0.50-0.78) compared with children breast-fed less than 4 months. At 8 years, reduced risks of sensitization (adjusted OR, 0.79; 95% CI, 0.64-0.99) and asthma in combination with sensitization (adjusted OR, 0.59; 95% CI, 0.37-0.93) were seen among children exclusively breast-fed 4 months or more. This group also had a significantly better lung function measured with peak expiratory flow. Conclusion: Breast-feeding for 4 months or more seems to reduce the risk of asthma up to 8 years. At this age, a reduced risk was observed particularly for asthma combined with sensitization. Furthermore, breast-feeding seems to have a beneficial effect on lung function. (J Allergy Clin Immunol 2010;125:1013-9.)	[Kull, Inger; Melen, Erik; Pershagen, Goran; Wickman, Magnus; Bergstrom, Anna] Karolinska Inst, Inst Environm Med, SE-17176 Stockholm, Sweden; [Kull, Inger] Karolinska Inst, Ctr Allergy Res, SE-17176 Stockholm, Sweden; [Svartengren, Magnus] Karolinska Inst, Dept Publ Hlth Sci, SE-17176 Stockholm, Sweden; [Melen, Erik] Karolinska Univ Hosp, Astrid Lindgren Childrens Hosp, Stockholm, Sweden; [Alm, Johan; Hallberg, Jenny; Wickman, Magnus] Sachs Childrens Hosp, Dept Pediat, Stockholm, Sweden; [Alm, Johan] Soder Sjukhuset, Dept Clin Sci & Educ, Karolinska Inst, Stockholm, Sweden; [van Hage, Marianne] Karolinska Inst & Univ Hosp, Clin Immunol & Allergy Unit, Dept Med Solna, Stockholm, Sweden	Kull, I (reprint author), Karolinska Inst, Inst Environm Med, Norrbacka 3rd Level, SE-17176 Stockholm, Sweden.	inger.kull@ki.se	van Hage, Marianne/A-9678-2017	van Hage, Marianne/0000-0003-3091-1596; Alm, Johan/0000-0002-9062-4479; Pershagen, Goran/0000-0002-9701-1130; Kull, Inger/0000-0001-6096-3771	Swedish Asthma and Allergy Association's Research Foundation; Vardal Foundation for Health Care Sciences and Allergy Research; Swedish Heart and Lung Foundation, the Swedish Research Council; Stockholm County Council	Supported by the Swedish Asthma and Allergy Association's Research Foundation, the Vardal Foundation for Health Care Sciences and Allergy Research, the Swedish Heart and Lung Foundation, the Swedish Research Council, and the Stockholm County Council.	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Allergy Clin. Immunol.	MAY	2010	125	5					1013	1019		10.1016/j.jaci.2010.01.051		7	Allergy; Immunology	Allergy; Immunology	596LO	WOS:000277686700009	20392479	
J	Shankardass, K; McConnell, R; Jerrett, M; Milam, J; Richardson, J; Berhane, K				Shankardass, Ketan; McConnell, Rob; Jerrett, Michael; Milam, Joel; Richardson, Jean; Berhane, Kiros			Parental stress increases the effect of traffic-related air pollution on childhood asthma incidence	PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA			English	Article						socioeconomic status; tobacco smoke	ENVIRONMENTAL TOBACCO-SMOKE; DIESEL EXHAUST PARTICLES; MATERNAL SMOKING; SOCIOECONOMIC-STATUS; LUNG-FUNCTION; IN-VIVO; RESPIRATORY HEALTH; PROSPECTIVE COHORT; RISK-FACTORS; CHILDREN	Exposure to traffic-related pollution (TRP) and tobacco smoke have been associated with new onset asthma in children. Psychosocial stress-related susceptibility has been proposed to explain social disparities in asthma. We investigated whether low socioeconomic status (SES) or high parental stress modified the effect of TRP and in utero tobacco smoke exposure on new onset asthma. We identified 2,497 children aged 5-9 years with no history of asthma or wheeze at study entry (2002-2003) into the Children's Health Study, a prospective cohort study in southern California. The primary outcome was parental report of doctor-diagnosed new onset asthma during 3 years of follow-up. Residential exposure to TRP was assessed using a line source dispersion model. Information about maternal smoking during pregnancy, parental education (a proxy for SES), and parental stress were collected in the study baseline questionnaire. The risk of asthma attributable to TRP was significantly higher for subjects with high parental stress (HR 1.51 across the interquartile range for TRP; 95% CI 1.16-1.96) than for subjects with low parental stress (HR 1.05, 95% CI 0.74-1.49; interaction P value 0.05). Stress also was associated with larger effects of in utero tobacco smoke. A similar pattern of increased risk of asthma was observed among children from low SES families who also were exposed to either TRP or in utero tobacco smoke. These results suggest that children from stressful households are more susceptible to the effects of TRP and in utero tobacco smoke on the development of asthma.	[McConnell, Rob; Milam, Joel; Richardson, Jean; Berhane, Kiros] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90089 USA; [Shankardass, Ketan] St Michaels Hosp, Li Ka Shing Knowledge Inst, Ctr Res Inner City Hlth, Toronto, ON M5B 1W8, Canada; [Jerrett, Michael] Univ Calif Berkeley, Div Environm Hlth Sci, Sch Publ Hlth, Berkeley, CA 94720 USA	McConnell, R (reprint author), Univ So Calif, Keck Sch Med, Dept Prevent Med, 1540 Alcazar St,Suite 236, Los Angeles, CA 90089 USA.	rmcconne@usc.edu	Reis, Aline/G-9573-2012; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	National Institute of Environmental Health Sciences [5R03ES014046, 1R01ES016535, 5P01ES009581, 5P01ES011627, 5P30ES007048]	This work was supported by National Institute of Environmental Health Sciences Grants 5R03ES014046,1R01ES016535, 5P01ES009581, 5P01ES011627, and 5P30ES007048; U. S. 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Natl. Acad. Sci. U. S. A.	JUL 28	2009	106	30					12406	12411		10.1073/pnas.0812910106		6	Multidisciplinary Sciences	Science & Technology - Other Topics	476KV	WOS:000268440200038	19620729	
J	Nemoto-Hasebe, I; Akiyama, M; Nomura, T; Sandilands, A; McLean, WHI; Shimizu, H				Nemoto-Hasebe, Ikue; Akiyama, Masashi; Nomura, Toshifumi; Sandilands, Aileen; McLean, W. H. Irwin; Shimizu, Hiroshi			Clinical Severity Correlates with Impaired Barrier in Filaggrin-Related Eczema	JOURNAL OF INVESTIGATIVE DERMATOLOGY			English	Article							STRATUM-CORNEUM HYDRATION; CAUSE ICHTHYOSIS VULGARIS; ATOPIC-DERMATITIS; UNINVOLVED SKIN; GENE; MUTATIONS; PENETRATION; DISEASE	Mutations in the gene-encoding filaggrin (FLG), a key molecule involved in skin barrier function, have been shown to be a major predisposing factor for atopic dermatitis (AD; eczema). To elucidate the pathomechanisms underlying filaggrin-related AD, we investigated stratum corneum (SC) hydration and transepidermal water loss (TEWL) as parameters of barrier function in AD patients harboring FLG mutations compared to AD patients without any FLG mutation. In filaggrin-related AD, SC hydration was both significantly reduced ( P < 0.01-0.05) and thicker (P < 0.01-0.05) than that in healthy controls. TEWL was demonstrably increased in non-filaggrin AD compared to healthy controls ( P < 0.01-0.05). The objective score of atopic dermatitis (OSCORAD), a disease clinical severity index, significantly correlated with TEWL (r = 0.81, P < 0.005), SC hydration (r = -0.65, P < 0.05), and SC thickness (r = 0.59, P < 0.05) in filaggrin-related AD. On the contrary, there was no correlation between these parameters and the OSCORAD in non-filaggrin AD. Furthermore, a significant correlation was obtained between the OSCORAD and specific IgE for house dust (r = 0.66, P < 0.05), mite allergen (r = 0.53, P < 0.05), and cat dander (r = 0.64, P < 0.05) in filaggrin-related AD, but not in non-filaggrin AD. All these data suggest that experimentally demonstrable skin barrier defects due to FLG mutations may play a crucial role in the pathogenesis of AD.	[Nemoto-Hasebe, Ikue; Akiyama, Masashi; Nomura, Toshifumi; Shimizu, Hiroshi] Hokkaido Univ, Grad Sch Med, Dept Dermatol, Sapporo, Hokkaido 0608638, Japan; [Sandilands, Aileen; McLean, W. H. Irwin] Univ Dundee, Coll Life Sci & Med, Div Mol Med, Epithelial Genet Grp, Dundee, Scotland; [Sandilands, Aileen; McLean, W. H. Irwin] Univ Dundee, Coll Dent & Nursing, Div Mol Med, Epithelial Genet Grp, Dundee, Scotland	Akiyama, M (reprint author), Hokkaido Univ, Grad Sch Med, Dept Dermatol, North 15 West 7, Sapporo, Hokkaido 0608638, Japan.	akiyama@med.hokudai.ac.jp; shimizu@med.hokudai.ac.jp	McLean, William/C-6352-2009	McLean, William Henry Irwin/0000-0001-5539-5757	British Skin Foundation; National Eczema Society (UK); UK Medical Research Council [G0700314]; Ministry of Education, Science, Sports, and Culture of Japan [18390310, 20390304]	We thank Dr James R. McMillan for his critical reading of this paper. We thank Ms Akari Nagasaki, for her fine technical assistance on this project. Filaggrin/ichthyosis/eczema research in the McLean laboratory is supported by grants from the British Skin Foundation, National Eczema Society (UK), and the UK Medical Research Council ( reference number G0700314) and donations from anonymous families affected by eczema in the Tayside Region of Scotland. This work was supported in part by Grants-in-Aid from the Ministry of Education, Science, Sports, and Culture of Japan to M. Akiyama (Kiban B 18390310 and Kiban B 20390304).	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J	Gilman, SE; Gardener, H; Buka, SL				Gilman, Stephen E.; Gardener, Hannah; Buka, Stephen L.			Maternal smoking during pregnancy and children's cognitive and physical development: A causal risk factor?	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						child; child development; cognition; growth; intelligence; pregnancy; smoking	CIGARETTE-SMOKING; CHILDHOOD; EXPOSURE; OUTCOMES; AGE; PSYCHOPATHOLOGY; INTELLIGENCE; ASSOCIATION; PERFORMANCE; POPULATION	There remains considerable debate regarding the effects of maternal smoking during pregnancy on children's growth and development. Evidence that exposure to maternal smoking during pregnancy is associated with numerous adverse outcomes is contradicted by research suggesting that these associations are spurious. The authors investigated the relation between maternal smoking during pregnancy and 14 developmental outcomes of children from birth through age 7 years, using data from the Collaborative Perinatal Project (1959-1974; n = 52,919). In addition to adjusting for potential confounders measured contemporaneously with maternal smoking, the authors fitted conditional fixed-effects models among siblings that controlled for unmeasured confounders. Results from the conditional analyses indicated a birth weight difference of -85.63 g associated with smoking of >= 20 cigarettes daily during pregnancy (95% confidence interval: -131.91, -39.34) and 2.73 times' higher odds of being overweight at age 7 years (95% confidence interval: 1.30, 5.71). However, the associations between maternal smoking and 12 other outcomes studied (including Apgar score, intelligence, academic achievement, conduct problems, and asthma) were entirely eliminated after adjustment for measured and unmeasured confounders. The authors conclude that the hypothesized effects of maternal smoking during pregnancy on these outcomes either are not present or are not distinguishable from a broader range of familial factors associated with maternal smoking.	[Gilman, Stephen E.] Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Boston, MA 02115 USA; [Gilman, Stephen E.; Gardener, Hannah] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA; [Gardener, Hannah] Univ Miami, Miller Sch Med, Dept Neurol, Miami, FL 33136 USA; [Buka, Stephen L.] Brown Univ, Dept Community Hlth, Providence, RI 02912 USA	Gilman, SE (reprint author), Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, 677 Huntington Ave, Boston, MA 02115 USA.	sgilman@hsph.harvard.edu	Buka, Stephen/H-7335-2014; Gilman, Stephen/E-7632-2010	Buka, Stephen/0000-0002-8578-9308; Gilman, Stephen/0000-0002-8331-6419	National Research Service Award; Harvard Training Program in Psychiatric Epidemiology and Biostatistics [T32 MH17119]; Transdisciplinary Tobacco Use Research Center [P50 CA084719]; National Institutes of Health; Robert Wood Johnson Foundation	This research was supported in part by a National Research Service Award from the Harvard Training Program in Psychiatric Epidemiology and Biostatistics (grant T32 MH17119) and a Transdisciplinary Tobacco Use Research Center grant (grant P50 CA084719) from the National Institutes of Health, as well as by the Robert Wood Johnson Foundation. The authors appreciate the efforts and contributions of Dr. Andrea Roberts and Kathleen McGaffigan for data management, programming, and manuscript preparation.	Allison P. 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J. Epidemiol.	SEP 1	2008	168	5					522	531		10.1093/aje/kwn175		10	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	343MZ	WOS:000258859500008	18653646	
J	Anderson, SD; Kippelen, P				Anderson, Sandra D.; Kippelen, Pascale			Airway injury as a mechanism for exercise-induced bronchoconstriction in elite athletes	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						epithelial injury; airway smooth muscle; mast cells; microvascular permeability; eicosanoids; beta(2)-agonists	CROSS-COUNTRY SKIERS; CHLORINATED SWIMMING POOLS; FISH-OIL SUPPLEMENTATION; INDUCED PLASMA EXUDATION; MAST-CELL ACTIVATION; INDUCED ASTHMA; INDUCED BRONCHOSPASM; BRONCHIAL HYPERRESPONSIVENESS; SMOOTH-MUSCLE; PASSIVE SENSITIZATION	Exercise-induced bronchoconstriction (EIB) is a consequence of evaporative water loss in conditioning the inspired air. The water loss causes cooling and dehydration of the airway surface. One acute effect of dehydration is the release of mediators, such as prostaglandins, leukotrienes, and histamine, that can stimulate smooth muscle, causing contraction and a change in vascular permeability. Inspiring cold air increases dehydration of the surface area and causes changes in bronchial blood flow. This article proposes that the pathogenesis of EIB in elite athletes relates to the epithelial injury arising from breathing poorly conditioned air at high flows for long periods of time or high volumes of irritant particles or gases. The evidence to support this proposal comes from many markers of injury. The restorative process after injury involves plasma exudation and movement of cells into the airways, a process repeated many times during a season of training. This process has the potential to expose smooth muscle to a wide variety of plasma- and cell-derived substances. The exposure to these substances over time can lead to an alteration in the contractile properties of the smooth muscle, making it more sensitive to mediators of bronchoconstriction. It is proposed that cold-weather athletes have airway hyperresponsiveness (AHR) to pharmacollogic agents as a result of epithelial injury. In those who are allergic, AIIR can also be expressed as EIB. The role of beta(2)-receptor agonists in inhibiting and enhancing the development of AHR and EIB is discussed.	[Anderson, Sandra D.] Royal Prince Alfred Hosp, Dept Resp & Sleep Med, Camperdown, NSW 2050, Australia; Univ Aberdeen, Sch Med Sci, Aberdeen AB9 1FX, Scotland	Anderson, SD (reprint author), Royal Prince Alfred Hosp, Dept Resp & Sleep Med, 11 W,50 Missenden Rd, Camperdown, NSW 2050, Australia.	sandya@med.usyd.edu.au		Anderson, Sandra/0000-0002-6308-8770			AITKEN ML, 1985, AM REV RESPIR DIS, V131, P357; Ammit AJ, 1997, AM J RESP CRIT CARE, V155, P1123; Ammit AJ, 2000, AM J RESP CRIT CARE, V161, P257; Anderson GP, 2006, CLIN REV ALLERG IMMU, V31, P119, DOI 10.1385/CRIAI:31:2:119; Anderson SD, 2006, CLIN REV ALLERG IMMU, V31, P163, DOI 10.1385/CRIAI:31:2:163; Anderson Sandra D, 2004, Paediatr Drugs, V6, P161, DOI 10.2165/00148581-200406030-00003; ANDERSON SD, 1979, LANCET, V2, P629; Anderson SD, 2000, J ALLERGY CLIN IMMUN, V106, P419, DOI 10.1067/mai.2000.108914; ANDERSON SD, 1985, EUR J RESPIR DIS, V67, P20; Anderson SD, 2000, J ALLERGY CLIN IMMUN, V106, P453; Anderson SD, 2006, J ALLERGY CLIN IMMUN, V117, P767, DOI 10.1016/j.jaci.2005.12.1355; 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Allergy Clin. Immunol.	AUG	2008	122	2					225	235		10.1016/j.jaci.2008.05.001		11	Allergy; Immunology	Allergy; Immunology	337HO	WOS:000258426300001	18554705	
J	Ege, MJ; Herzum, I; Buchele, G; Krauss-Etschmann, S; Lauener, RP; Roponen, M; Hyvarinen, A; Vuitton, DA; Riedler, J; Brunekreef, B; Dalphin, JC; Braun-Fahrlander, C; Pekkanen, J; Renz, H; von Mutius, E				Ege, Markus Johannes; Herzum, Ileana; Buechele, Gisela; Krauss-Etschmann, Susanne; Lauener, Roger P.; Roponen, Marjut; Hyvaerinen, Anne; Vuitton, Dominique A.; Riedler, Josef; Brunekreef, Bert; Dalphin, Jean-Charles; Braun-Fahrlaender, Charlotte; Pekkanen, Juha; Renz, Harald; von Mutius, Erika		Protection Against Allergy Study	Prenatal exposure to a farm environment modifies atopic sensitization at birth	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						prenatal exposure; atopic sensitization; cord blood; farming; microbial components	HOUSE-DUST; ALLERGIC DISEASES; EARLY-LIFE; CHILDREN; ASTHMA; PARSIFAL; PROJECT	Background: Previous cross-sectional surveys have suggested that maternal exposure to animal sheds during pregnancy exerted a protective effect on atopic sensitization in children lasting until school age. Objective: We sought to evaluate the effects of maternal exposure to animal sheds and other farm-related exposures during pregnancy on cord blood IgE levels in a prospective birth cohort. Methods: Pregnant women living in rural areas in Austria, Finland, France, Germany, and Switzerland were recruited in the third trimester of pregnancy. Information on maternal farm-related exposures, nutrition, and health during pregnancy was obtained by means of interviews. Specific IgE levels for food and common inhalant allergens were assessed in cord blood of 922 children and peripheral blood samples of their mothers. Results: Different sensitization patterns in cord blood of farm and nonfarm children were observed. In multivariable analysis consumption of boiled, but not unboiled, farm milk during pregnancy was positively associated with specific IgE to cow's milk independently from maternal IgE. In contrast, there was an inverse relationship between maternal exposure to animal sheds and cord blood IgE levels against seasonal allergens (adjusted odds ratio, 0.38; 95% CI, 0.21-0.70). This association was not confounded by maternal IgE levels. Maternal contact with hay enhanced the protective effect of exposure to animal sheds on IgE levels to grass pollen in cord blood.	[Ege, Markus Johannes; Krauss-Etschmann, Susanne; von Mutius, Erika] Univ Childrens Hosp, Munich, Germany; [Herzum, Ileana; Renz, Harald] Univ Marburg, Dept Clin Chem & Mol Diagnost, Marburg, Germany; [Buechele, Gisela] Univ Ulm, Inst Epidemiol, Ulm, Germany; [Krauss-Etschmann, Susanne] HelmholtzZentrum Munchen German Res Ctr Environm, Munich, Germany; [Lauener, Roger P.] Univ Zurich, Childrens Hosp, Zurich, Switzerland; [Roponen, Marjut; Hyvaerinen, Anne; Pekkanen, Juha] Natl Publ Hlth Inst, Dept Environm Hlth, Kuopio, Finland; [Vuitton, Dominique A.] Univ Franche Comte, SERF Res Unit, F-25030 Besancon, France; [Riedler, Josef] Childrens Hosp, Schwarzach, Austria; [Brunekreef, Bert] Univ Med Ctr Utrecht, Inst Risk Assessment Sci, Utrecht, Netherlands; [Brunekreef, Bert] Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands; [Dalphin, Jean-Charles] Univ Hosp, Dept Resp Dis, Besancon, France; [Braun-Fahrlaender, Charlotte] Univ Basel, Inst Social & Prevent Med, Basel, Switzerland; [Pekkanen, Juha] Univ Kuopio, Sch Publ Hlth & Clin Nutr, FIN-70211 Kuopio, Finland	Ege, MJ (reprint author), Dr von Haunersche Kinderklin, Lindwurmstr 4, D-80337 Munich, Germany.	markus.ege@med.uni-muenchen.de	Huttunen, Kati/D-8755-2012; Genuneit, Jon/I-9323-2012; Lauener, Roger/O-8612-2016; Roponen, Marjut/C-2086-2017	Huttunen, Kati/0000-0002-4888-9203; Genuneit, Jon/0000-0001-5764-1528; Lauener, Roger/0000-0002-8412-606X; Roponen, Marjut/0000-0002-4442-9090; brunekreef, bert/0000-0001-9908-0060; Ege, Markus/0000-0001-6643-3923; Krauss-Etschmann, Susanne/0000-0001-5945-5702; von Mutius, Erika/0000-0002-8893-4515	European Union [QLK4-CT-2001-00250]	Supported by the European Union (research grant QLK4-CT-2001-00250).	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; Bonnelykke K, 2008, J ALLERGY CLIN IMMUN, V121, P646, DOI 10.1016/j.jaci.2007.12.1149; Boyle RJ, 2006, ALLERGY, V61, P1423, DOI 10.1111/j.1398-9995.2006.01113.x; 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; Ege MJ, 2007, J ALLERGY CLIN IMMUN, V119, P1140, DOI 10.1016/j.jaci.2007.01.037; Ege MJ, 2006, J ALLERGY CLIN IMMUN, V117, P817, DOI 10.1016/j.jaci.2005.12.1307; FERRIS BG, 1978, AM REV RESPIR DIS, V118, P1; Hagendorens MM, 2004, PEDIATR ALLERGY IMMU, V15, P308, DOI 10.1111/j.1399-3038.2004.00169.x; Herzum I, 2005, CLIN CHEM LAB MED, V43, P963, DOI 10.1515/CCLM.2005.165; Holt P, 2004, CHEM IMMUNOL, V84, P102; Korthals M, 2008, J MICROBIOL METH, V73, P49, DOI 10.1016/j.mimet.2008.01.010; Landau LI, 2006, PAEDIATR RESPIR REV, V7, pS251, DOI 10.1016/j.prrv.2006.04.186; Myatt L, 2006, J PHYSIOL-LONDON, V572, P25, DOI 10.1113/jphysiol.2006.104968; PFEFFERLE P, 2008, J ALLERGY C IN PRESS; Prescott SL, 2006, CURR ALLERGY ASTHM R, V6, P75, DOI 10.1007/s11882-006-0014-7; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Rothman K J, 1990, Epidemiology, V1, P43, DOI 10.1097/00001648-199001000-00010; Rowe J, 2007, J ALLERGY CLIN IMMUN, V119, P1164, DOI 10.1016/j.jaci.2007.02.016; Rytkonen J, 2002, PEDIATR ALLERGY IMMU, V13, P269, DOI 10.1034/j.1399-3038.2002.01028.x; Schram D, 2005, ALLERGY, V60, P611, DOI 10.1111/j.1398-9995.2005.00748.x; Stern DA, 2007, J ALLERGY CLIN IMMUN, V119, P351, DOI 10.1016/j.jaci.2006.10.013; Vance GHS, 2005, CLIN EXP ALLERGY, V35, P1318, DOI 10.1111/j.1365-2222.2005.02346.x; von Mutius E, 2006, ALLERGY, V61, P407, DOI 10.1111/j.1398-9995.2006.01009.x; Warner JO, 2004, ARCH DIS CHILD, V89, P97, DOI 10.1136/adc.2003.013029	27	84	85	2	17	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					407	412		10.1016/j.jaci.2008.06.011		6	Allergy; Immunology	Allergy; Immunology	337HO	WOS:000258426300030	18678343	
J	Schaub, B; Liu, J; Hoppler, S; Haug, S; Sattler, C; Lluis, A; Illi, S; von Mutius, E				Schaub, Bianca; Liu, Jing; Hoeppler, Sabine; Haug, Severine; Sattler, Christine; Lluis, Anna; Illi, Sabina; von Mutius, Erika			Impairment of T-regulatory cells in cord blood of atopic mothers	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						adaptive; cord blood; cytokines; innate; IL; regulatory T cells; T(H)17 cells; Toll-like receptor	NEONATAL IMMUNE-RESPONSES; SCHOOL-AGE-CHILDREN; EXPRESSION; STIMULATION; EXPOSURE; ASTHMA; INFLAMMATION; RECEPTOR-2; ALLERGY; FOXP3	Background: Maternal atopy is a strong predictor for the development of childhood allergic diseases. The underlying mechanisms are ill defined, yet regulatory T (Treg) and T(H)17 cells may play a key role potentially shaping the early immune system toward a proallergic or antiallergic immune regulation. Objective: We examined T(H)1/T(H)2, Treg, and T(H)17 cell responses to innate (lipid A/peptidoglycan) and mitogen/adaptive (phytohemagglutinin/Dermatophagoides pteronyssinus 1) immune stimulation in cord blood from offspring of atopic/nonatopic mothers. Methods: Cord blood mononuclear cells from 161 healthy neonates (59% nonatopic, 41% atopic mothers) were investigated regarding Treg and T(H)17 cells (mRNA/surface markers), suppressive function, and proliferation/cytokine secretion. Results: Cord blood from offspring of atopic mothers showed fewer innate-induced Treg cells (CD4(+)CD25(+) high), lower mRNA expression of associated markers (glucocorticoid-induced tumor necrosis factor receptor-related protein/lymphocyte activation gene 3; P < .05), and a trend toward lower Forkhead box transcription factor 3 (Foxp3) expression. Treg cell function was impaired in mitogen-induced suppression of T effector cells in cord blood of offspring from atopic mothers (P = .03). Furthermore, IL-10 and IFN-gamma secretion were decreased in innate-stimulated cord blood of offspring from atopic mothers (P = .04/.05). Innate-induced IL-17 was independent of maternal atopy and highly correlated with IL-13 secretion. Conclusion: In offspring of atopic mothers, Treg cell numbers, expression, and function were impaired at birth. T(H)17 cells were correlated with T(H)2 cells, independently of maternal atopy.	[Schaub, Bianca; Liu, Jing; Hoeppler, Sabine; Haug, Severine; Lluis, Anna; Illi, Sabina; von Mutius, Erika] Univ Children Hosp Munich, Dr Von Haunerschen Kinderspital, Dept Pulm & Allergy, D-80337 Munich, Germany; [Sattler, Christine] Univ Munich, Univ Hosp, Dept Gynecol, Munich, Germany; [Liu, Jing] Jilin Univ, Hosp 2, Dept Resp Med, Changchun 130023, Peoples R China	Schaub, B (reprint author), Univ Children Hosp Munich, Dr Von Haunerschen Kinderspital, Dept Pulm & Allergy, Lindwurmstr 4, D-80337 Munich, Germany.	Bianca.Schaub@med.uni-muenchen.de		von Mutius, Erika/0000-0002-8893-4515			Allakhverdi Z, 2006, J ALLERGY CLIN IMMUN, V118, P1342, DOI 10.1016/j.jaci.2006.07.034; Amoudruz P, 2005, J ALLERGY CLIN IMMUN, V115, P1304, DOI 10.1016/j.jaci.2005.02.036; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Ege MJ, 2006, J ALLERGY CLIN IMMUN, V117, P817, DOI 10.1016/j.jaci.2005.12.1307; Gavin MA, 2007, NATURE, V445, P771, DOI 10.1038/nature05543; Gold DR, 2006, J ALLERGY CLIN IMMUN, V117, P931, DOI 10.1016/j.jaci.2005.12.1322; Heid CA, 1996, GENOME RES, V6, P986, DOI 10.1101/gr.6.10.986; Heinrich J, 2002, Pneumologie, V56, P297, DOI 10.1055/s-2002-30699; Huang CT, 2004, IMMUNITY, V21, P503, DOI 10.1016/j.immuni.2004.08.010; Ivanov S, 2007, AM J RESP CELL MOL, V36, P442, DOI 10.1165/rcmb.2006-0020OC; Lauener RP, 2002, LANCET, V360, P465, DOI 10.1016/S0140-6736(02)09641-1; Liu WH, 2006, J EXP MED, V203, P1701, DOI 10.1084/jem.20060772; Patel M, 2005, EUR J IMMUNOL, V35, P3581, DOI 10.1002/eji.200535421; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; Prescott SL, 1998, J IMMUNOL, V160, P4730; Read S, 2000, J EXP MED, V192, P295, DOI 10.1084/jem.192.2.295; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Schaub B, 2006, RESP RES, V7, DOI 10.1186/1465-9921-7-40; Schaub B, 2005, J CLIN IMMUNOL, V25, P329, DOI 10.1007/s10875-005-4180-5; Schaub B, 2004, J INTERF CYTOK RES, V24, P543, DOI 10.1089/jir.2004.24.543; Shimizu J, 2002, NAT IMMUNOL, V3, P135, DOI 10.1038/ni759; Velasco G, 2005, AM J RESP CELL MOL, V32, P218, DOI 10.1165/rcmb.2003-0435OC; Weaver CT, 2006, IMMUNITY, V24, P677, DOI 10.1016/j.immuni.2006.06.002; Wright Anne L., 2004, Journal of Allergy and Clinical Immunology, V113, pS2, DOI 10.1016/j.jaci.2003.09.050	25	84	86	0	14	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					1491	1499		10.1016/j.jaci.2008.04.010		9	Allergy; Immunology	Allergy; Immunology	313WW	WOS:000256771700028	18539197	
J	Wolf, JM; Nicholls, E; Chen, E				Wolf, Jutta M.; Nicholls, Erin; Chen, Edith			Chronic stress, salivary cortisol, and alpha-amylase in children with asthma and healthy children	BIOLOGICAL PSYCHOLOGY			English	Article						salivary alpha-amylase; cortisol; childhood asthma; chronic stress; socioeconomic status	THREE-MILE-ISLAND; PSYCHOLOGICAL STRESS; SOCIOECONOMIC-STATUS; PSYCHOSOCIAL STRESS; ADRENERGIC ACTIVITY; BETA(2)-ADRENERGIC RECEPTOR; GLUCOCORTICOID-RECEPTOR; WHOLE SALIVA; RESPONSES; IMMUNE	The present study examined whether chronic stress is related to daily life levels of salivary a-amylase (sAA), a marker for sympathetic activity, and cortisol in healthy children versus children with asthma. Children's sAA and cortisol levels were measured repeatedly over 2 days. Chronic stress measures included interviews with children about chronic home life stress and interviews with parents about one marker of socioeconomic status, parental education. Among children with asthma, higher chronic stress was associated with lower daily sAA output, while among healthy children, higher chronic stress was associated with flatter cortisol slopes. In conclusion, chronically stressed children with asthma showed lower salivary a-amylase output, indicating lower sympathetic activity, and implying a possible mechanism for increased susceptibility to symptom exacerbations. In contrast, higher cortisol levels in healthy children with chronic stress may indicate, for example, an increased risk for infectious diseases. This dichotomy emphasizes the different biological effects of chronic stress depending on illness status. (c) 2007 Elsevier B.V. All tights reserved.	[Wolf, Jutta M.; Nicholls, Erin; Chen, Edith] Univ British Columbia, Dept Psychol, Vancouver, BC V6T 1Z4, Canada	Wolf, JM (reprint author), Univ British Columbia, Dept Psychol, 2136 W Mall, Vancouver, BC V6T 1Z4, Canada.	juttawolf@psych.ubc.ca					ARNETZ BB, 1987, PSYCHOSOM MED, V49, P3; Bacharier LB, 2004, AM J RESP CRIT CARE, V170, P426, DOI 10.1164/rccm.200308-1178OC; Bamberger CM, 1996, ENDOCR REV, V17, P245, DOI 10.1210/er.17.3.245; BAUM A, 1983, J CONSULT CLIN PSYCH, V51, P565, DOI 10.1037/0022-006X.51.4.565; BAUM BJ, 1993, ANN NY ACAD SCI, V694, P17; Bosch JA, 2003, PSYCHOSOM MED, V65, P245, DOI 10.1097/01.PSY.0000058376.50240.2D; Bosch JA, 1996, PSYCHOSOM MED, V58, P374; Buske-Kirschbaum A, 2003, PSYCHOSOM MED, V65, P806, DOI 10.1097/01.PSY.0000095916.25975.4F; Buske-Kirschbaum A, 1998, ANN NY ACAD SCI, V840, P747, DOI 10.1111/j.1749-6632.1998.tb09613.x; CAPLAN RD, 1979, J PSYCHOSOM RES, V23, P181, DOI 10.1016/0022-3999(79)90003-5; Chatterton RT, 1996, CLIN PHYSIOL, V16, P433, DOI 10.1111/j.1475-097X.1996.tb00731.x; Chen E, 2006, J ALLERGY CLIN IMMUN, V117, P1014, DOI 10.1016/j.jaci.2006.01.036; Chen E, 2006, HEALTH PSYCHOL, V25, P704, DOI 10.1037/0278-6133.25.6.704; CHIKANZA IC, 1992, ARTHRITIS RHEUM, V35, P1281; Chrousos G P, 1998, Adv Pharmacol, V42, P552; Chrousos GP, 1998, J CLIN ENDOCR METAB, V83, P1842, DOI 10.1210/jc.83.6.1842; Cohen S, 2006, PSYCHOSOM MED, V68, P41, DOI 10.1097/01.psy.0000195967.51768.ea; Cohen S, 2006, PSYCHOSOM MED, V68, P414, DOI 10.1097/01.psy.0000221236.37158.b9; DALLMAN MF, 1994, ANN NY ACAD SCI, V746, P22; De Kloet ER, 1998, ENDOCR REV, V19, P269, DOI 10.1210/er.19.3.269; Dickerson SS, 2004, PSYCHOL BULL, V130, P355, DOI 10.1037/0033-2909.130.3.355; Ehlert U, 2006, J CLIN ENDOCR METAB, V91, P5130, DOI 10.1210/jc.2006-0461; Elenkov IJ, 2000, PHARMACOL REV, V52, P595; GOLDSTEIN DS, 2000, ENCY STRESS, P558; Granger DA, 2006, J SOC PERS RELAT, V23, P267, DOI 10.1177/0265407506062479; GRANGER DA, 2007, HDB PHYSL RES METHOD; Granger DA, 2007, ANN NY ACAD SCI, V1098, P122, DOI 10.1196/annals.1384.008; HAMMEN C, 1991, J ABNORM PSYCHOL, V100, P555, DOI 10.1037/0021-843X.100.4.555; HAMMEN C, 1999, UCLA LIFE STRESS INT; Heim C, 2000, PSYCHONEUROENDOCRINO, V25, P1, DOI 10.1016/S0306-4530(99)00035-9; JENZANO JW, 1987, ARCH ORAL BIOL, V32, P757, DOI 10.1016/0003-9969(87)90123-3; KAHN JP, 1988, BIOL PSYCHIAT, V23, P335, DOI 10.1016/0006-3223(88)90284-3; KALLENBACH JM, 1985, CHEST, V87, P644, DOI 10.1378/chest.87.5.644; KIRSCHBAUM C, 1994, PSYCHONEUROENDOCRINO, V19, P313, DOI 10.1016/0306-4530(94)90013-2; Kirschbaum C., 2007, ENCY STRESS, P405; KOSTEN TR, 1984, J NERV MENT DIS, V172, P359, DOI 10.1097/00005053-198406000-00007; KVETNANSKY R, 2000, ENCY STRESS, P63; MacArthur Research Network on SES and Health, 2000, SAL CORT MEAS; Mannino DM, 1998, MMWR-MORBID MORTAL W, V47, P1; MENDEL CM, 1992, J ANDROL, V13, P107; 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; Nater UM, 2006, PSYCHONEUROENDOCRINO, V31, P49, DOI 10.1016/j.psyneuen.2005.05.010; Nater UM, 2005, INT J PSYCHOPHYSIOL, V55, P333, DOI 10.1016/j.ijpsycho.2004.09.009; Nater UM, 2007, PSYCHONEUROENDOCRINO, V32, P392, DOI 10.1016/j.psyneuen.2007.02.007; *NHLBI, 1997, PUBL NIH; *NHLBI, 2002, GUID DIAGN MAN ASTHM; Pearson-Murphy BE, 2000, GLUCOCORTICOIDS OVER, P244; Pruessner JC, 2003, PSYCHONEUROENDOCRINO, V28, P916, DOI 10.1016/S0306-4530(02)00108-7; Pruessner JC, 1999, PSYCHOSOM MED, V61, P197; Rantonen PJF, 2000, ACTA ODONTOL SCAND, V58, P160; Rohleder N, 2004, ANN NY ACAD SCI, V1032, P258, DOI 10.1196/annals.1314.033; Rohleder N, 2006, PSYCHOPHYSIOLOGY, V43, P645, DOI 10.1111/j.1469-8986.2006.00457.x; Sandberg S, 2000, LANCET, V356, P982, DOI 10.1016/S0140-6736(00)02715-X; Sanders VM, 1997, J IMMUNOL, V158, P4200; Sapolsky RM, 2000, ENDOCR REV, V21, P55, DOI 10.1210/er.21.1.55; SCHAEFFER MA, 1984, PSYCHOSOM MED, V46, P227; Sears MR, 1998, CLIN EXP ALLERGY, V28, P82; SEARS MR, 1998, CLIN EXP ALLERGY, V28, P90; SKOBELOFF EM, 1992, JAMA-J AM MED ASSOC, V268, P3437, DOI 10.1001/jama.268.24.3437; Skosnik PD, 2000, INT J PSYCHOPHYSIOL, V36, P59, DOI 10.1016/S0167-8760(99)00100-2; Smith P. M., 1996, SALIVA ORAL HLTH, P9; Tabachnick B. G., 2001, USING MULTIVARIATE S; van Stegeren A, 2006, PSYCHONEUROENDOCRINO, V31, P137, DOI 10.1016/j.psyneuen.2005.05.012; Van Cauter E, 1995, PRINCIPLES PRACTICE, P41; Vedhara K, 2002, J PSYCHOSOM RES, V53, P1153, DOI 10.1016/S0022-3999(02)00343-4; VINING RF, 1983, CLIN CHEM, V29, P1752; Yehuda R, 2000, J CLIN PSYCHIAT, V61, P14	69	84	86	6	20	ELSEVIER SCIENCE BV	AMSTERDAM	PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS	0301-0511			BIOL PSYCHOL	Biol. Psychol.	APR	2008	78	1					20	28		10.1016/j.biopsycho.2007.12.004		9	Psychology, Biological; Behavioral Sciences; Psychology; Psychology, Experimental	Psychology; Behavioral Sciences	297MR	WOS:000255621300003	18243483	
J	Runswick, S; Mitchell, T; Davies, P; Robinson, C; Garrod, DR				Runswick, Sarah; Mitchell, Thomas; Davies, Paul; Robinson, Clive; Garrod, David R.			Pollen proteolytic enzymes degrade tight junctions	RESPIROLOGY			English	Article						allergy; asthma; pollen; proteolytic enzyme; rhinitis; tight junction	DUST-MITE ALLERGEN; AMBROSIA-ARTEMISIIFOLIA POLLEN; EPITHELIAL-CELLS; ASTHMA; DER-P-1; PURIFICATION; ALPHA(1)-ANTITRYPSIN; PROTEINASES; PERMEABILITY; PEPTIDASE	Background and objective: Asthma and allergic rhinitis are significant, increasing causes of morbidity worldwide. Pollen, a major cause of seasonal rhinitis/conjunctivitis, carries proteolytic enzymes on its surface. We showed previously that peptidase allergens from house dust mites compromise epithelial barrier function by degrading the extracellular domains of the tight junction proteins, occludin and claudin, thus facilitating allergen delivery across epithelial layers. In this study, we aimed to determine whether peptidases from allergenic pollens should similarly be considered to have a role in disrupting tight junctions. Methods: Diffusates from stored pollen of Giant Ragweed, White Birch and Kentucky Blue Grass, and fresh pollen from Easter Lily were applied to confluent monolayers of Madin-Darby canine kidney (MDCK) and Calu-3 cells in serum-free medium. Immunofluorescence was performed for the tight junction proteins, occludin, claudin-1 and ZO-1. The effect of pollen diffusate on occludin was studied by Western blotting, and enzymatic activity in the diffusates was demonstrated by zymography. The ability of protease inhibitors to block the action of the diffusate on tight junctions was investigated. Results: Diffusates from all four allergenic pollens caused loss of immunofluorescence labelling for tight junction proteins on MDCK and Calu-3 cells. The effect was blocked by inhibitors of serine and cysteine proteases. Degradation of occludin was demonstrated by Western blotting and zymography indicated that diffusates contain proteolytic activity. Conclusion: Pollen peptidases directly or indirectly disrupt epithelial tight junctions, and this activity should be considered as a possible mechanism for facilitating allergen delivery across epithelia.	Univ Manchester, Fac Life Sci, Manchester M13 9PT, Lancs, England; St Georges Univ London, Ion Channels & Cell Signalling Ctr, Div Basic Med Sci, London, England; James Cook Univ N Queensland, Discipline Pharm, Townsville, Qld 4811, Australia	Garrod, DR (reprint author), Univ Manchester, Fac Life Sci, Michael Smith Bldg,Oxford Rd, Manchester M13 9PT, Lancs, England.	david.garrod@manchester.ac.uk		Robinson, Clive/0000-0001-6253-7864; Garrod, David/0000-0003-0300-3947	Medical Research Council [G0001362]; Wellcome Trust		Aijaz S, 2006, INT REV CYTOL, V248, P261, DOI 10.1016/S0074-7696(06)48005-0; AndoAkatsuka Y, 1996, J CELL BIOL, V133, P43, DOI 10.1083/jcb.133.1.43; Bagarozzi DA, 1996, J BIOL CHEM, V271, P26227; Bagarozzi DA, 1998, AM J RESP CELL MOL, V18, P363; Bagarozzi DA, 1998, PHYTOCHEMISTRY, V47, P593, DOI 10.1016/S0031-9422(97)00634-1; BROIDE DH, 1992, J ALLERGY CLIN IMMUN, V89, P958, DOI 10.1016/0091-6749(92)90218-Q; Cortes L, 2006, J ALLERGY CLIN IMMUN, V118, P878, DOI 10.1016/j.jaci.2006.05.029; D'Amato G, 2002, EUR RESPIR J, V20, P763, DOI 10.1183/09031936.02.00401402; Eden E, 2003, CHEST, V123, P765, DOI 10.1378/chest.123.3.765; FAHY JV, 1995, AM J RESP CRIT CARE, V152, P53; Ghaemmaghami AM, 2002, CLIN EXP ALLERGY, V32, P1468, DOI 10.1046/j.1365-2745.2002.01504.x; Gough L, 2003, CLIN EXP ALLERGY, V33, P1159, DOI 10.1046/j.1365-2222.2003.01716.x; Gough L, 2001, CLIN EXP ALLERGY, V31, P1594, DOI 10.1046/j.1365-2222.2001.01207.x; Grobe K, 1999, EUR J BIOCHEM, V263, P33, DOI 10.1046/j.1432-1327.1999.00462.x; Hassim Z, 1998, THORAX, V53, P368; Hou JH, 2006, J BIOL CHEM, V281, P36117, DOI 10.1074/jbc.M608853200; HYDE JS, 1979, ANN ALLERGY, V43, P8; Kalsheker NA, 1996, BIOCHEM BIOPH RES CO, V221, P59, DOI 10.1006/bbrc.1996.0544; Levenson T, 1997, ALLERGY ASTHMA PROC, V18, P213, DOI 10.2500/108854197778594016; Matheson NR, 1998, J BIOL CHEM, V273, P16771, DOI 10.1074/jbc.273.27.16771; Messent AJ, 2000, INVEST OPHTH VIS SCI, V41, P8; MURAGUCHI A, 1988, J EXP MED, V167, P332, DOI 10.1084/jem.167.2.332; Peat JK, 1996, AM J RESP CRIT CARE, V153, P141; Poppelmann M, 2002, ELECTROPHORESIS, V23, P993, DOI 10.1002/1522-2683(200204)23:7/8<993::AID-ELPS993>3.0.CO;2-V; Radlowski Marek, 2005, Journal of Applied Genetics, V46, P247; Raftery MJ, 2003, RESPIR RES, V4, DOI 10.1186/1465-9921-4-10; RUDOLPH R, 1978, ALLERGY, V33, P310, DOI 10.1111/j.1398-9995.1978.tb01556.x; Salib RJ, 2003, CLIN OTOLARYNGOL, V28, P291, DOI 10.1046/j.1365-2273.2003.00706.x; Sigsgaard T, 2000, EUR RESPIR J, V16, P50, DOI 10.1034/j.1399-3003.2000.16a09.x; STEWART GA, 2000, ASTHMA RHINITIS, V2, P1107; STEWART GA, 2003, MIDDLETONS ALLERGY P, P585; Stick SA, 2003, AM J RESP CELL MOL, V28, P641, DOI 10.1165/rcmb.F271; VERCELLI D, 1989, EUR J IMMUNOL, V19, P1419, DOI 10.1002/eji.1830190811; Wan H, 2000, CLIN EXP ALLERGY, V30, P685, DOI 10.1046/j.1365-2222.2000.00820.x; Wan H, 1999, J CLIN INVEST, V104, P123, DOI 10.1172/JCI5844; Wan H, 2001, CLIN EXP ALLERGY, V31, P279, DOI 10.1046/j.1365-2222.2001.00970.x; Widmer F, 2000, CLIN EXP ALLERGY, V30, P571, DOI 10.1046/j.1365-2222.2000.00784.x; Winton HL, 1998, CLIN EXP ALLERGY, V28, P1273; Winton HL, 1998, BRIT J PHARMACOL, V124, P1048, DOI 10.1038/sj.bjp.0701905	39	84	87	0	8	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	1323-7799			RESPIROLOGY	Respirology	NOV	2007	12	6					834	842		10.1111/j.1440-1843.2007.01175.x		9	Respiratory System	Respiratory System	226WI	WOS:000250618800008	17986111	
J	Narita, S; Goldblum, RM; Watson, CS; Brooks, EG; Estes, DM; Curran, EM; Midoro-Horiuti, T				Narita, Shin-ichiro; Goldblum, Randall M.; Watson, Cheryl S.; Brooks, Edward G.; Estes, D. Mark; Curran, Edward M.; Midoro-Horiuti, Terumi			Environmental estrogens induce mast cell degranulation and enhance IgE-mediated release of allergic mediators	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						allergy; asthma; beta-hexosaminidase; environmental estrogen; estradiol; estrogen receptor alpha; IgE; mast cells	PITUITARY-TUMOR CELLS; MEMBRANE ESTROGEN; POSTNATAL EXPOSURE; PROLACTIN-RELEASE; ASTHMA; ALPHA; XENOESTROGENS; STIMULATION; MECHANISMS; RECEPTORS	BACKGROUND: Prevalence and morbidity of allergic diseases have increased over the last decades. Based on the recently recognized differences in asthma prevalence between the sexes, we have examined the effect of endogenous estrogens on a key element of the allergic response. Some lipophilic pollutants have estrogen-like activities and are termed environmental estrogens. These pollutants tend to degrade slowly in the environment and to bioaccumulate and bioconcentrate in the no chain; they also have long biological half-lives. OBJECTIVES: Our goal in this study was to identify possible pathogenic roles for environmental estrogens in the development of allergic diseases. METHODS: We screened a number of environmental estrogens for their ability to modulate the release of allergic mediators from mast cells. We incubated a human mast cell line and primary mast cell cultures derived from bone marrow of wild type and estrogen receptor alpha (ER-alpha)-deficient mice with environmental estrogens with and without estradiol or IgE and allergens. We assessed degranulation of mast cells by quantifying the release of beta-hexosaminidase. RESULTS: All of the environmental estrogens tested caused rapid, dose-related release of beta-hexosaminidase from mast cells and enhanced IgE-mediated release. The combination of physiologic concentrations of 17 beta-estradiol and several concentrations of environmental estrogens had additive effects on mast cell degranulation. Comparison of bone marrow mast cells from ER-alpha-sufficient and ER-alpha-deficient mice indicated that much of the effect of environmental estrogens was mediated by ER-alpha. CONCLUSIONS: Our findings suggest that estrogenic environmental pollutants might promote allergic diseases by inducing and enhancing mast cell degranulation by physiologic estrogens and exposure to allergens.	Child Hlth Res Ctr, Dept Pediat, Galveston, TX USA; Univ Texas, Med Branch, Dept Biochem & Mol Biol, Galveston, TX 77550 USA	Midoro-Horiuti, T (reprint author), Univ Texas, Med Branch, Child Hlth Res Ctr, Childrens Hosp 2300, 301 Univ Blvd, Galveston, TX 77555 USA.	tmidoro@utmb.edu			NIAID NIH HHS [K08 AI055792, R01 AI052428]; NIEHS NIH HHS [R21 ES016428]		Aravindakshan J, 2004, TOXICOL SCI, V81, P179, DOI 10.1093/toxsci/kfh174; Ayotte P, 2003, ENVIRON HEALTH PERSP, V111, P1253, DOI 10.1289/ehp.6054; Bologa CG, 2006, NAT CHEM BIOL, V2, P207, DOI 10.1038/nchembio775; Bulayeva NN, 2005, AM J PHYSIOL-ENDOC M, V288, pE388, DOI 10.1152/ajpendo.00349.2004; Bulayeva NN, 2004, ENVIRON HEALTH PERSP, V112, P1481, DOI 10.1289/ehp.7175; Burr ML, 2006, THORAX, V61, P296, DOI 10.1136/thx.2005.045682; BUTTERFIELD JH, 1988, LEUKEMIA RES, V12, P345, DOI 10.1016/0145-2126(88)90050-1; Dastych J, 1999, J ALLERGY CLIN IMMUN, V103, P1108, DOI 10.1016/S0091-6749(99)70186-7; de Marco R, 2002, J ALLERGY CLIN IMMUN, V110, P228, DOI 10.1067/mai.2002.125600; DEWAILLY E, 1993, ENVIRON HEALTH PERSP, V101, P618, DOI 10.2307/3431646; Dijkstra A, 2006, J ALLERGY CLIN IMMUN, V117, P604, DOI 10.1016/j.jaci.2005.11.023; Falconer IR, 2006, ENVIRON TOXICOL, V21, P181, DOI 10.1002/tox.20172; Ibarluzea JM, 2004, CANCER CAUSE CONTROL, V15, P591, DOI 10.1023/B:CACO.0000036167.51236.86; Kos M, 2002, J MOL ENDOCRINOL, V29, P281, DOI 10.1677/jme.0.0290281; Lambert KC, 2005, J IMMUNOL, V175, P5716; Metcalfe CD, 2001, ENVIRON TOXICOL CHEM, V20, P297, DOI 10.1897/1551-5028(2001)020<0297:EPOCDI>2.0.CO;2; Newbold RR, 2006, ENDOCRINOLOGY, V147, pS11, DOI 10.1210/en.2005-1164; Odom S, 2004, J EXP MED, V199, P1491, DOI 10.1084/jem.20040382; Solomon GM, 2002, ENVIRON HEALTH PERSP, V110, pA339; Thomas P, 2005, ENDOCRINOLOGY, V146, P624, DOI 10.1210/en.2004-1064; Vartiainen T, 1997, CHEMOSPHERE, V34, P2571, DOI 10.1016/S0045-6535(97)00100-8; Wang SL, 2004, CHEMOSPHERE, V54, P1459, DOI 10.1016/j.chemosphere.2003.08.012; Watson CS, 1999, EXP PHYSIOL, V84, P1013, DOI 10.1111/j.1469-445X.1999.01903.x; Watson CS, 2001, INT IMMUNOPHARMACOL, V1, P1049, DOI 10.1016/S1567-5769(01)00036-4; Watson CS, 2003, EXP BIOL MED, V228, P1272; Welshons WV, 2003, ENVIRON HEALTH PERSP, V111, P994, DOI 10.1289/ehp.5494; Wozniak AL, 2005, ENVIRON HEALTH PERSP, V113, P431, DOI 10.1289/ehp.7505; YUNGINGER JW, 1992, AM REV RESPIR DIS, V146, P888; ZAITSU M, 2006, MOL IMMUNOL, DOI DOI 10.1016/J.MOLIMM.2006.09.030	29	84	89	0	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.	JAN	2007	115	1					48	52		10.1289/ehp.9378		5	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	123ME	WOS:000243299200031	17366818	
J	Matsui, EC; Eggleston, PA; Buckley, TJ; Krishnan, JA; Breysse, PN; Rand, CS; Diette, GB				Matsui, Elizabeth C.; Eggleston, Peyton A.; Buckley, Timothy J.; Krishnan, Jerry A.; Breysse, Patrick N.; Rand, Cynthia S.; Diette, Gregory B.			Household mouse allergen exposure and asthma morbidity in inner-city preschool children	ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY			English	Article							ENVIRONMENTAL TOBACCO-SMOKE; SKIN-TEST SENSITIVITY; COCKROACH ALLERGEN; HOMES; SENSITIZATION; DETERMINANTS; PREVALENCE; SYMPTOMS; SUBURBAN; RISK	Background: Inner-city children experience disproportionate asthma morbidity, and suspected reasons include indoor environmental exposures. Objective: To determine if mouse allergen exposure is a risk factor for asthma morbidity. Methods: Preschool children with asthma were recruited from inner-city Baltimore, MD. Skin testing was performed and blood was collected at the baseline visit for quantification of mouse allergen specific IgE. A questionnaire evaluated symptoms, medication, and health care use at baseline, 3 months, and 6 months. A trained technician collected dust samples from the child's home for analysis of Mus m 1 at baseline, 3 months, and 6 months. Outcomes were compared between mouse-sensitized, highly exposed children and all other children. Results: A total of 127 children had complete data for mouse sensitization status and bedroom settled dust mouse allergen levels at baseline. The mean age of the children was 4.4 years, 92% were African American, and 26% were sensitized to mouse. Mouse-sensitized children exposed to higher levels of Mus in 1 (> 0.5 mu g/g) had 50% more days of symptoms (incidence rate ratio [IRR], 1.5; 95% confidence interval [CI], 1.1-2.1) and 80% more days of beta-agonist use than other children (IRR, 1.8; 95% CI, 1.3-2.5). Children in the sensitized and highly exposed group were also more likely to have an unscheduled physician visit (odds ratio [OR], 3.1; 95% CI, 1.6-6.3), emergency department visit (OR, 2.1; 95% CI, 1.1-4.1), and hospitalization (OR, 36.6; 95% CI, 4.1-327.3) than other children. These associations between mouse allergen exposure and asthma symptoms and morbidity remained statistically significant after adjusting for potential confounders, including atopy and cockroach sensitization and exposure. Conclusions: In mouse-sensitized inner-city children, exposure to mouse allergen may be an important cause of asthma morbidity.	Johns Hopkins Univ, Dept Pediat, Baltimore, MD 21218 USA; Johns Hopkins Univ, Dept Environm Hlth Sci, Bloomberg Sch Publ Hlth, Baltimore, MD 21218 USA; Johns Hopkins Univ, Dept Med, Baltimore, MD 21218 USA	Matsui, EC (reprint author), Johns Hopkins Univ Hosp, 600 N Wolfe St,CMSC 1102, Baltimore, MD 21287 USA.	ematsui@jhmi.edu			NHLBI NIH HHS [HL04266, HL67850]; NIAID NIH HHS [AI060955, AI62974]; NIEHS NIH HHS [P30 ES 03819, ES09606]		Arshad SH, 2005, CHEST, V127, P502, DOI 10.1378/chest.127.2.502; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Asmussen L, 1999, PEDIATRICS, V104, part. no., DOI 10.1542/peds.104.6.e71; Chew GL, 2003, ENVIRON HEALTH PERSP, V111, P1348, DOI 10.1289/ehp.6124; Cohn RD, 2004, J ALLERGY CLIN IMMUN, V113, P1167, DOI 10.1016/j.jaci.2003.12.592; CULLINAN P, 1994, OCCUP ENVIRON MED, V51, P589; Eggleston PA, 1998, J ALLERGY CLIN IMMUN, V102, P563, DOI 10.1016/S0091-6749(98)70272-6; EGGLESTON PA, 1995, AM J RESP CRIT CARE, V151, P640; Gautrin D, 2001, AM J RESP CRIT CARE, V163, P899; Gilliland FD, 2001, AM J RESP CRIT CARE, V163, P429; Gruchalla RS, 2005, J ALLERGY CLIN IMMUN, V115, P478, DOI 10.1016/j.jaci.2004.12.006; Hollander A, 1998, SCAND J WORK ENV HEA, V24, P228; Lau Susanne, 2002, Paediatr Respir Rev, V3, P265, DOI 10.1016/S1526-0542(02)00189-6; Litonjua AA, 2001, J ALLERGY CLIN IMMUN, V107, P41, DOI 10.1067/mai.2001.111143; Matsui EC, 2005, J ALLERGY CLIN IMMUN, V115, P358, DOI 10.1016/j.jaci.2004.11.007; Matsui EC, 2004, J ALLERGY CLIN IMMUN, V113, P910, DOI 10.1016/j.jaci.2004.02.034; Mitchell H, 1997, PEDIATR PULM, V24, P237; Morkjaroenpong V, 2002, J ALLERGY CLIN IMMUN, V110, P147, DOI 10.1067/mai.2002.125832; OHMAN JL, 1994, J ALLERGY CLIN IMMUN, V94, P810, DOI 10.1016/0091-6749(94)90147-3; Perry T, 2003, J ALLERGY CLIN IMMUN, V112, P346, DOI 10.1067/mai.2003.1640; Phipatanakul W, 2005, ALLERGY, V60, P697, DOI 10.1111/j.1398-9995.2005.00825.x; Phipatanakul W, 2000, J ALLERGY CLIN IMMUN, V106, P1070, DOI 10.1067/mai.2000.110796; Phipatanakul W, 2000, J ALLERGY CLIN IMMUN, V106, P1075; Rosenstreich DL, 1997, NEW ENGL J MED, V336, P1356, DOI 10.1056/NEJM199705083361904; SCHUMACHER MJ, 1981, J ALLERGY CLIN IMMUN, V68, P310, DOI 10.1016/0091-6749(81)90157-3; Van Asperen P P, 1994, Pediatr Allergy Immunol, V5, P178; Wood RA, 2001, ANN ALLERG ASTHMA IM, V87, P60	27	84	84	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.	OCT	2006	97	4					514	520				7	Allergy; Immunology	Allergy; Immunology	097AW	WOS:000241419600017	17069107	
J	Card, JW; Carey, MA; Bradbury, JA; DeGraff, LM; Morgan, DL; Moorman, MP; Flake, GP; Zeldin, DC				Card, JW; Carey, MA; Bradbury, JA; DeGraff, LM; Morgan, DL; Moorman, MP; Flake, GP; Zeldin, DC			Gender differences in murine airway responsiveness and lipopolysaccharide-induced inflammation	JOURNAL OF IMMUNOLOGY			English	Article							SYNTHASE-DEFICIENT MICE; ACUTE LUNG INJURY; INHALED LIPOPOLYSACCHARIDE; TESTOSTERONE; ASTHMA; RATS; ESTRADIOL; RESPONSES; ESTROGEN; HORMONES	The roles of gender and sex hormones in lung function and disease are complex and not completely understood. The present study examined the influence. of gender on lung function and respiratory mechanics in naive mice and on acute airway inflammation and hyperresponsiveness induced by intratracheal LPS administration. Basal lung function characteristics did not differ between naive males and females, but males demonstrated significantly greater airway responsiveness than females following aerosolized methacholine challenge as evidenced by increased respiratory system resistance and elastance (p < 0.05). Following LPS administration, males developed more severe hypothermia and greater airway hyperresponsiveness than females (p < 0.05). Inflammatory indices including bronchoalveolar lavage fluid total cells, neutrophils, and TNF-alpha content were greater in males than in females 6 h following LPS administration (p < 0.05), whereas whole-lung TLR-4 protein levels did not differ among treatment groups, suggesting that differential expression of TLR-4 before or after LPS exposure did not underlie the observed inflammatory outcomes. Gonadectomy decreased airway inflammation in males but did not alter inflammation in females, whereas administration of exogenous testosterone to intact females increased their inflammatory responses to levels observed in intact males. LPS-induced airway hyperresponsiveness was also decreased in castrated males and was increased in females administered exogenous testosterone. Collectively, these data indicate that airway responsiveness in naive mice is influenced by gender, and that male mice have exaggerated airway inflammatory and functional responses to LPS compared with females. These gender differences are mediated, at least in part, by effects of androgens.	NIEHS, Div Intramural Res, NIH, Res Triangle Pk, NC 27709 USA	Zeldin, DC (reprint author), NIEHS, Div Intramural Res, NIH, 111 TW Alexander Dr,Bldg 101,Room D236, Res Triangle Pk, NC 27709 USA.	zeldin@niehs.nih.gov			Intramural NIH HHS [Z01 ES101885-03]		Ashcroft GS, 2002, J CLIN INVEST, V110, P615, DOI 10.1172/JCI200215704; Benten WPM, 1997, FEBS LETT, V407, P211, DOI 10.1016/S0014-5793(97)00346-3; Caracta CF, 2003, MT SINAI J MED, V70, P215; Cuzzocrea S, 2000, ENDOCRINOLOGY, V141, P1455, DOI 10.1210/endo.141.4.7404; de Oliveira APL, 2004, NEUROIMMUNOMODULAT, V11, P20, DOI 10.1159/000072965; Degano B, 2001, AM J RESP CRIT CARE, V164, P1849; Gavett SH, 1999, J CLIN INVEST, V104, P721, DOI 10.1172/JCI6890; Gharaee-Kermani M, 2005, AM J PATHOL, V166, P1593, DOI 10.1016/S0002-9440(10)62470-4; Guo ZY, 2002, J BIOL CHEM, V277, P29600, DOI 10.1074/jbc.M202997200; Haggerty CL, 2003, ANN ALLERG ASTHMA IM, V90, P284; Hollingsworth JW, 2004, AM J RESP CRIT CARE, V170, P126, DOI 10.1164/rccm.200311-1499OC; Kline JN, 1999, AM J RESP CRIT CARE, V160, P297; Lee JJ, 2004, SCIENCE, V305, P1773, DOI 10.1126/science.1099472; Lim CM, 2003, INTENS CARE MED, V29, P453, DOI 10.1007/s00134-002-1529-6; Ma J, 2004, MOL PHARMACOL, V65, P730, DOI 10.1124/mol.65.3.730; MASSARO GD, 1995, P NATL ACAD SCI USA, V92, P1105, DOI 10.1073/pnas.92.4.1105; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; Michel O, 2001, J ALLERGY CLIN IMMUN, V107, P797, DOI 10.1067/mai.2001.114249; Park KM, 2004, J BIOL CHEM, V279, P52282, DOI 10.1074/jbc.M407629200; Reinhard C, 2002, MAMM GENOME, V13, P429, DOI 10.1007/s00335-002-3005-6; SHIRAI M, 1995, EUR RESPIR J, V8, P272, DOI 10.1183/09031936.95.08020272; Speyer CL, 2005, AM J PHYSIOL-CELL PH, V288, pC881, DOI 10.1152/ajpcell.00467.2004; Tesfaigzi Y, 2001, J APPL PHYSIOL, V91, P2182; Wang GC, 2003, CHINESE J PHYSIOL, V46, P151; WONG CI, 1995, J BIOL CHEM, V270, P19998; Zeldin DC, 2001, AM J RESP CELL MOL, V25, P457	26	84	85	0	5	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	JUL 1	2006	177	1					621	630				10	Immunology	Immunology	055ST	WOS:000238471400073	16785560	
J	Inoue, Y; Matsuwaki, Y; Shin, SH; Ponikau, JU; Kita, H				Inoue, Y; Matsuwaki, Y; Shin, SH; Ponikau, JU; Kita, H			Nonpathogenic, environmental fungi induce activation and degranulation of human eosinophils	JOURNAL OF IMMUNOLOGY			English	Article							MAJOR BASIC-PROTEIN; BLOOD EOSINOPHILS; POTENT ACTIVATOR; MEDIATOR RELEASE; BRONCHIAL-ASTHMA; DE-GRANULATION; STIMULATION; CELLS; ALTERNARIA; RECEPTORS	Eosinophils and their products are probably important in the pathophysiology of allergic diseases, such as bronchial asthma, and in host immunity to certain organisms. An association between environmental fungal exposure and asthma has been long recognized clinically. Although products of microorganisms (e.g., lipopolysaccharides) directly activate certain inflammatory cells (e.g., macrophages), the mechanism(s) that triggers eosinophil degranulation is unknown. In this study we investigated whether human eosinophils have an innate immune response to certain fungal organisms. We incubated human eosinophils with extracts from seven environmental airborne fungi (Alternaria alternata, Aspergillus versicolor, Bipolaris sorokiniana, Candida albicans, Cladosporium herbarum, Curvularia spicifera, and Penicillium notatum). Alternaria and Penicillium induced calcium-dependent exocytosis (e.g., eosinophil-derived neurotoxin release) in eosinophils from normal individuals. Alternaria also strongly induced other activation events in eosinophils, including increases in intracellular calcium concentration, cell surface expression of CD63 and CD11b, and production of IL-8. Other fungi did not induce eosinophil degranulation, and Alternaria did not induce neutrophil activation, suggesting specificity for fungal species and cell type. The Alternaria-induced eosinophil degranulation was pertussis toxin sensitive and desensitized by preincubating cells with G protein-coupled receptor agonists, platelet-activating factor, or FMLP. The eosinophil-stimulating activity in Alternaria extract was highly heat labile and had an M-r of similar to 60 kDa. Thus, eosinophils, but not neutrophils, possess G protein-dependent cellular activation machinery that directly responds to an Alternaria protein product(s). This innate response by eosinophils to certain environmental fungi may be important in host defense and in the exacerbation of inflammation in asthma and allergic diseases.	Mayo Clin, Dept Immunol, Rochester, MN 55905 USA; Mayo Clin, Dept Med, Rochester, MN 55905 USA; Mayo Clin, Dept Otorhinolaryngol, Rochester, MN 55905 USA	Kita, H (reprint author), Mayo Clin, Dept Immunol, Rochester, MN 55905 USA.	kita.hirohito@mayo.edu			NIAID NIH HHS [AI49235]		AAS K, 1980, ALLERGY, V35, P443, DOI 10.1111/j.1398-9995.1980.tb01791.x; ABUGHAZALEH RI, 1989, J IMMUNOL, V142, P2393; Al-Ani B, 2002, J PHARMACOL EXP THER, V300, P702, DOI 10.1124/jpet.300.2.702; AYARS GH, 1985, J ALLERGY CLIN IMMUN, V76, P595, DOI 10.1016/0091-6749(85)90781-X; BACH MK, 1992, IMMUNOLOGY, V75, P680; Black PN, 2000, ALLERGY, V55, P501, DOI 10.1034/j.1398-9995.2000.00293.x; BRAUN RK, 1993, EUR J IMMUNOL, V23, P956, DOI 10.1002/eji.1830230429; BROFMAN JD, 1989, J APPL PHYSIOL, V66, P1867; Bush RK, 2004, J ALLERGY CLIN IMMUN, V113, P227, DOI 10.1016/j.jaci.2003.11.023; CHAM BP, 1994, AM J PATHOL, V144, P1369; D'Souza MP, 2000, JAMA-J AM MED ASSOC, V284, P215, DOI 10.1001/jama.284.2.215; Dill I, 1996, PEDIATR ALLERGY IMMU, V7, P151, DOI 10.1111/j.1399-3038.1996.tb00123.x; Elsner J, 1996, EUR J IMMUNOL, V26, P1919, DOI 10.1002/eji.1830260837; FILLEY WV, 1982, LANCET, V2, P11; GLEICH GJ, 1990, J ALLERGY CLIN IMMUN, V85, P422, DOI 10.1016/0091-6749(90)90151-S; GLEICH GJ, 1979, J IMMUNOL, V123, P2925; GLEICH GJ, 1986, ADV IMMUNOL, V39, P177, DOI 10.1016/S0065-2776(08)60351-X; Grady EF, 1997, AM J PHYSIOL-GASTR L, V273, pG586; GRYNKIEWICZ G, 1985, J BIOL CHEM, V260, P3440; GUNDEL RH, 1991, J CLIN INVEST, V87, P1470, DOI 10.1172/JCI115155; Halonen M, 1997, AM J RESP CRIT CARE, V155, P1356; HANSEL TT, 1991, J IMMUNOL METHODS, V145, P105, DOI 10.1016/0022-1759(91)90315-7; HORIE S, 1994, J IMMUNOL, V152, P5457; Kato M, 2002, J IMMUNOL, V169, P5252; KAUFFMAN HF, 1995, AM J RESP CRIT CARE, V151, P2109; Kauffman HF, 2000, J ALLERGY CLIN IMMUN, V105, P1185, DOI 10.1067/mai.2000.106210; KEMEN P, 1991, Journal of Clinical Investigation, V87, P2012; KHALIFE J, 1986, J IMMUNOL, V137, P1659; Kheradmand F, 2002, J IMMUNOL, V169, P5904; Kita H, 1999, J IMMUNOL, V162, P6901; Kita H, 2003, MIDDLETONS ALLERGY P, V1, P305; Kobayashi T, 1999, NAT CELL BIOL, V1, P113; KROEGEL C, 1994, J ALLERGY CLIN IMMUN, V93, P725, DOI 10.1016/0091-6749(94)90252-6; KROEGEL C, 1989, J IMMUNOL, V142, P3518; LEIFERMAN KM, 1985, NEW ENGL J MED, V313, P282, DOI 10.1056/NEJM198508013130502; Li CS, 1997, ARCH ENVIRON HEALTH, V52, P72; Logan MR, 2003, J ALLERGY CLIN IMMUN, V111, P923, DOI 10.1067/mai.2003.1573; Mahmudi-Azer S, 2002, BLOOD, V99, P4039, DOI 10.1182/blood.V99.11.4039; Matthews AN, 1998, P NATL ACAD SCI USA, V95, P6273, DOI 10.1073/pnas.95.11.6273; Miike S, 2001, J IMMUNOL, V167, P6615; Mitakakis TZ, 2001, J ALLERGY CLIN IMMUN, V107, P388, DOI 10.1067/mai.2001.112602; MOTOJIMA S, 1989, AM REV RESPIR DIS, V139, P801; Nagase H, 2003, J IMMUNOL, V171, P3977; OHOLLAREN MT, 1991, NEW ENGL J MED, V324, P359, DOI 10.1056/NEJM199102073240602; Ponikau JU, 2005, J ALLERGY CLIN IMMUN, V116, P362, DOI 10.1016/j.jaci.2005.03.049; RABINOVITCH PS, 1986, J IMMUNOL, V137, P952; Richardson RM, 1996, J BIOL CHEM, V271, P28717; Romani Luigina, 2004, Nat Rev Immunol, V4, P1; Seminario MC, 1999, J IMMUNOL, V162, P6893; SOLOMON WR, 1975, J ALLERGY CLIN IMMUN, V56, P235, DOI 10.1016/0091-6749(75)90095-0; Steinhoff M, 2005, ENDOCR REV, V26, P1, DOI 10.1210/er.2003-0025; THASTRUP O, 1990, P NATL ACAD SCI USA, V87, P2466, DOI 10.1073/pnas.87.7.2466; Tomee JFC, 2000, CLIN EXP ALLERGY, V30, P476, DOI 10.1046/j.1365-2222.2000.00796.x; van Burik JAH, 2001, ANNU REV MICROBIOL, V55, P743, DOI 10.1146/annurev.micro.55.1.743; WAGNER JM, 1993, PLACENTA, V14, P671, DOI 10.1016/S0143-4004(05)80384-4; Williams DL, 1997, MEDIAT INFLAMM, V6, P247, DOI 10.1080/09629359791550; Yoganathan K, 2003, J NAT PROD, V66, P1116, DOI 10.1021/np030146m; Zureik M, 2002, BRIT MED J, V325, P411, DOI 10.1136/bmj.325.7361.411	58	84	88	0	4	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	OCT 15	2005	175	8					5439	5447				9	Immunology	Immunology	972GY	WOS:000232443500070	16210651	
J	Behrendt, CE				Behrendt, CE			Mild and moderate-to-severe COPD in nonsmokers - Distinct demographic profiles	CHEST			English	Article						asthma; COPD; epidemiology; nonsmoker	OBSTRUCTIVE PULMONARY-DISEASE; NUTRITION EXAMINATION; NATIONAL-HEALTH; UNITED-STATES; LUNG-DISEASE; POPULATION; ASTHMA; MORTALITY; SAMPLE; NHANES	Study objective: To investigate the risk of COPD among nonsmokers. Design: Case-control study, logistic regression analysis. Setting: Third National Health and Nutrition Examination Survey, from 1988 to 1994. Participants: Community, residents 18 to 80 years of age, of white, black, or Mexican-American ethnicity. Nonsmokers included never-smokers and former smokers with a < 5 pack-year smoking history, who had never smoked cigars or pipes. Measurements: COPD (FEV1/FVC < 70%) was classified as mild (FEV1 >= 80% predicted) or moderate to severe (FEV1 23 to 79% predicted). Results: Among 13,995 examinees, 51.3 +/- 0.4% were female, mean age was 42.2 +/- 0.4 cars, 48.7 +/- 0.9% were nonsmokers, 8.8 +/- 0.3% had mild COPD, and 4.1 +/- 0.3% had moderate-to-severe COPD [+/- SE]. One fourth of mild and moderate-to-severe cases were nonsmokers. Among 7,526 nonsmokers, 4.7 +/- 0.3% had mild COPD (n = 403; age, 60.9 +/- 1.3 years) and were mostly, female (82.5%), while 1.9 +/- 0.3% had moderate-to-severe COPD (n = 92, age 39.3 +/- 1.3) and were mostly male (88.1%). Few nonsmokers with COPD (12.1 +/- 2.4%) had a previous diagnosis of chronic bronchitis or emphysema. Among nonsmokers, physician-diagnosed asthma increased the risk of mild and especially of moderate-to-severe COPD. Independently of asthma, risk of mild COPD in nonsmokers increased with age (doubling every, 12 years), before age 60 was lower among men than women, and was inversely associated with current exposure to tobacco smoke at home and at work. In contrast, the risk of moderate-to-severe COPD in nonsmokers was markedly associated with male gender, peaked in middle age, and was inversely associated with nonwhite ethnicity. COPD risks did not vary by minimal smoking history, longest-held occupation, urban residence, income, allergies, thyroid disease, or Helicobacter pylori antibody. Conclusions: Among nonsmokers, mild and moderate-to-severe COPD are associated with asthma but otherwise have distinct demographic profiles, suggesting that moderate-to-severe disease is not a mere progression of mild COPD.		Behrendt, CE (reprint author), 3413 Paseo Campo, Palos Verdes Estates, CA 90274 USA.	carolynbehrendt@yahoo.com					Bakke P S, 2003, Monaldi Arch Chest Dis, V59, P103; Birring SS, 2002, AM J RESP CRIT CARE, V166, P1078, DOI 10.1164/rccm.200203-245OC; Hankinson JL, 1999, AM J RESP CRIT CARE, V159, P179; Hollowell JG, 2002, J CLIN ENDOCR METAB, V87, P489, DOI 10.1210/jc.87.2.489; Hospers JJ, 1999, AM J RESP CRIT CARE, V160, P1869; Jaakkola MS, 2002, SCAND J WORK ENV HEA, V28, P52; Mannino David M, 2003, Respir Care, V48, P1185; Mannino DM, 2003, THORAX, V58, P388, DOI 10.1136/thorax.58.5.388; Mannino DM, 2003, AM J MED, V114, P758, DOI 10.1016/S0002-9343(03)00185-2; Molfino NA, 2004, CHEST, V125, P1929, DOI 10.1378/chest.125.5.1929; Montnemery P, 2000, EUR J EPIDEMIOL, V16, P1003, DOI 10.1023/A:1011004420173; Pauwels Romain A., 2001, American Journal of Respiratory and Critical Care Medicine, V163, P1256; Pena VS, 2000, CHEST, V118, P981, DOI 10.1378/chest.118.4.981; Sandford AJ, 2002, THORAX, V57, P736, DOI 10.1136/thorax.57.8.736; Shiotani A, 2002, J GASTROENTEROL, V37, P402, DOI 10.1007/s005350200058; Silva GE, 2004, CHEST, V126, P59, DOI 10.1378/chest.126.1.59; Snyder LD, 2004, CHEST, V125, P1719, DOI 10.1378/chest.125.5.1719; Sunyer J, 2001, EUR RESPIR J, V17, P1024, DOI 10.1183/09031936.01.17510240; *US DEP HHS NAT CT, 3 NAT HLTH NUTR EX S; *US DEP HHS NAT CT, 1994, PLAN OP 3 NAT HLTH N; WHITTEMORE AS, 1995, AM J PUBLIC HEALTH, V85, P702, DOI 10.2105/AJPH.85.5.702; 1998, 3 NATL HLTH NUTR EXA; [Anonymous], 1987, AM REV RESP DIS, V136, P1285	23	84	84	1	8	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	SEP	2005	128	3					1239	1244		10.1378/chest.128.3.1239		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	964YN	WOS:000231917000029	16162712	
J	Hoffjan, S; Nicolae, D; Ostrovnaya, I; Roberg, K; Evans, M; Mirel, DB; Steiner, L; Walker, K; Shult, P; Gangnon, RE; Gern, JE; Martinez, FD; Lemanske, RF; Ober, C				Hoffjan, S; Nicolae, D; Ostrovnaya, I; Roberg, K; Evans, M; Mirel, DB; Steiner, L; Walker, K; Shult, P; Gangnon, RE; Gern, JE; Martinez, FD; Lemanske, RF; Ober, C			Gene-environment interaction effects on the development of immune responses in the 1st year of life	AMERICAN JOURNAL OF HUMAN GENETICS			English	Article							INTERFERON-GAMMA PRODUCTION; DAY-CARE ATTENDANCE; BLOOD MONONUCLEAR-CELLS; ASTHMA SUSCEPTIBILITY GENE; HYGIENE HYPOTHESIS; HIGH-RISK; ALLERGIC DISEASES; ATOPIC DISEASE; AGE-CHILDREN; IFN-GAMMA	Asthma is a common disease that results from both genetic and environmental risk factors. Children attending day care in the 1st year of life have lower risks for developing asthma, although the mechanism for this "day care" effect is largely unknown. We investigated the interactions between day care exposure in the 1st 6 mo of life and genotypes for 72 polymorphisms at 45 candidate loci and their effects on cytokine response profiles and on the development of atopic phenotypes in the 1st year of life in the Childhood Onset of Asthma ( COAST) cohort of children. Six interactions ( at four polymorphisms in three loci) with "day care" that had an effect on early-life immune phenotypes were significant at P < .001. The estimated false-discovery rate was 33%, indicating that an estimated four P values correspond to true associations. Moreover, the " day care" effect at some loci was accounted for by the increased number of viral infections among COAST children attending day care, whereas interactions at other loci were independent of the number of viral infections, indicating the presence of additional risk factors associated with day care environment. This study identified significant gene-environment interactions influencing the early patterning of the immune system and the subsequent development of asthma and highlights the importance of considering environmental risk factors in genetic analyses.	Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA; Univ Chicago, Dept Stat, Chicago, IL 60637 USA; Univ Chicago, Dept Obstet & Gynecol, Chicago, IL 60637 USA; Univ Wisconsin, Dept Pediat, Madison, WI USA; Univ Wisconsin, Dept Med, Madison, WI USA; Univ Wisconsin, Dept Biostat & Med Bioinformat, Madison, WI USA; Univ Wisconsin, Wisconsin State Lab Hyg, Madison, WI 53706 USA; Roche Mol Syst, Alameda, CA USA; Univ Arizona, Tucson Resp Ctr, Tucson, AZ USA	Ober, C (reprint author), Univ Chicago, Dept Human Genet, 920 E 58th St,CLSC 507C, Chicago, IL 60637 USA.	c-ober@genetics.uchicago.edu			NCRR NIH HHS [M01 RR003186, M01 RR03186]; NHLBI NIH HHS [P01 HL070831, R01 HL61879, P01 HL70831]; NICHD NIH HHS [R01 HD061879]; NIDDK NIH HHS [R01 DK055889, R01 DK55889]; NIMH NIH HHS [R01 MH061879]		Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; Barr CS, 2004, ARCH GEN PSYCHIAT, V61, P1146, DOI 10.1001/archpsyc.61.11.1146; 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Martinez FD, 2001, RESPIR RES, V2, P129, DOI 10.1186/rr48; McIntire JJ, 2004, SPRINGER SEMIN IMMUN, V25, P335, DOI 10.1007/s00281-003-0141-3; Merikangas KR, 2003, SCIENCE, V302, P599, DOI 10.1126/science.1091468; Mirel DB, 2002, DIABETES, V51, P3336, DOI 10.2337/diabetes.51.11.3336; Neaville WA, 2003, J ALLERGY CLIN IMMUN, V112, P740, DOI 10.1067/mai.2003.1716; Nicolae D, 2005, AM J HUM GENET, V76, P349, DOI 10.1086/427763; Padyukov L, 2004, ARTHRITIS RHEUM, V50, P3085, DOI 10.1002/art.20553; Pohl D, 1997, ALLERGY, V52, P732, DOI 10.1111/j.1398-9995.1997.tb01230.x; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; Reifsnyder PC, 2000, GENOME RES, V10, P1568, DOI 10.1101/gr.147000; Rinas U, 1993, Pediatr Allergy Immunol, V4, P60, DOI 10.1111/j.1399-3038.1993.tb00068.x; Rowe J, 2004, J ALLERGY CLIN IMMUN, V113, P710, DOI 10.1016/j.jaci.2003.12.585; Sheikh A, 2003, J ALLERGY CLIN IMMUN, V111, P131, DOI 10.1067/mai.2003.8; Smart JM, 2002, CLIN EXP ALLERGY, V32, P796, DOI 10.1046/j.1365-2222.2002.01391.x; Storey JD, 2002, J ROY STAT SOC B, V64, P479, DOI 10.1111/1467-9868.00346; TANG M, 1993, CLIN EXP IMMUNOL, V92, P120; TANG MLK, 1994, LANCET, V344, P983, DOI 10.1016/S0140-6736(94)91641-1; Umetsu DT, 2003, J ALLERGY CLIN IMMUN, V112, P480, DOI 10.1067/mai.2003.1717; Ungerer MC, 2003, GENETICS, V165, P353; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; VONMUTIUS E, 1994, BRIT MED J, V308, P692; WARNER JA, 1994, CLIN EXP ALLERGY, V24, P423, DOI 10.1111/j.1365-2222.1994.tb00930.x; Weiss LA, 2005, AM J HUM GENET, V76, P33, DOI 10.1086/426697; Weiss ST, 2002, NEW ENGL J MED, V347, P930, DOI 10.1056/NEJMe020092; Werner M, 2003, J ALLERGY CLIN IMMUN, V112, P323, DOI 10.1067/mai.2003.1648; Wickens KL, 1999, EPIDEMIOLOGY, V10, P699, DOI 10.1097/00001648-199911000-00009	57	84	86	2	11	UNIV CHICAGO PRESS	CHICAGO	1427 E 60TH ST, CHICAGO, IL 60637-2954 USA	0002-9297			AM J HUM GENET	Am. J. Hum. Genet.	APR	2005	76	4					696	704		10.1086/429418		9	Genetics & Heredity	Genetics & Heredity	904RS	WOS:000227516000016	15726497	
J	Sakai, K; Norback, D; Mi, YH; Shibata, E; Kamijima, M; Yamada, T; Takeuchi, Y				Sakai, K; Norback, D; Mi, YH; Shibata, E; Kamijima, M; Yamada, T; Takeuchi, Y			A comparison of indoor air pollutants in Japan and Sweden: formaldehyde, nitrogen dioxide, and chlorinated volatile organic compounds	ENVIRONMENTAL RESEARCH			English	Article						formaldehyde; nitrogen dioxide; chlorinated VOC; indoor air pollution; international comparison	SICK BUILDING SYNDROME; EXPOSURE; PREVALENCE; SYMPTOMS; EMISSION; PRODUCTS; ASTHMA; AREAS; TEAM	Indoor and outdoor concentrations of formaldehyde (HCHO), nitrogen dioxide (NO2), and selected chlorinated volatile organic compounds (chlorinated VOC) were measured in 37 urban dwellings in Nagoya, Japan, and 27 urban dwellings in Uppsala, Sweden, using the same sampling procedures and analytical methods. Indoor as well as outdoor air concentrations of HCHO, NO2, and chlorinated VOC were significantly higher in Nagoya than in Uppsala (P<0.01), with the exception of tetrachlorocarbon in outdoor air. In Nagoya, HCHO and NO2 concentrations were significantly higher in modern concrete houses than in wooden houses and higher in newer (less than 10 years) than in older dwellings (P < 0.01), possibly due to less natural ventilation and more emission sources in modern buildings. Dwellings heated with unvented combustion sources had significantly higher indoor concentrations of NO2\ than those with clean heating (P<0.05). Moreover, dwellings with moth repellents containing p-dichlorobenzene had significantly higher indoor concentrations of p-dichlorobenzene (P < 0.01). In conclusion, there appear to be differences between Nagoya and Uppsala with respect to both indoor and outdoor pollution levels of the measured pollutants. More indoor pollution sources could be identified in Nagoya than in Uppsala, including construction and interior materials emitting VOC, use of unvented combustion space heaters, and moth repellents containing p-dichlorobenzene. (C) 2003 Elsevier Inc. All rights reserved.	Nagoya City Publ Hlth Res Inst, Mizuho Ku, Nagoya, Aichi 4678615, Japan; Univ Uppsala, Dept Med Sci Occupat & Environm Med, S-75185 Uppsala, Sweden; Nagoya Univ, Sch Hlth Sci, Dept Med Technol, Higashi Ku, Nagoya, Aichi 4618673, Japan; Nagoya Univ, Grad Sch Med, Dept Environm & Occupat Hlth, Showa Ku, Nagoya, Aichi 4668550, Japan; Natl Inst Radiol Sci, Res Ctr Radiat Emergency Med, Inage Ku, Chiba 2638555, Japan	Sakai, K (reprint author), Nagoya City Publ Hlth Res Inst, Mizuho Ku, 1-11 Hagiyama Cho, Nagoya, Aichi 4678615, Japan.			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Res.	JAN	2004	94	1					75	85		10.1016/S0013-9351(03)00140-3		11	Environmental Sciences; Public, Environmental & Occupational Health	Environmental Sciences & Ecology; Public, Environmental & Occupational Health	758DD	WOS:000187616500010	14643289	
J	Jaakkola, MS; Piipari, R; Jaakkola, N; Jaakkola, JJK				Jaakkola, MS; Piipari, R; Jaakkola, N; Jaakkola, JJK			Environmental tobacco smoke and adult-onset asthma: A population-based incident case-control study	AMERICAN JOURNAL OF PUBLIC HEALTH			English	Article							RESPIRATORY SYMPTOMS; PASSIVE SMOKING; EXPOSURE; NONSMOKING	Objectives. The authors assessed the effects of environmental tobacco smoke (ETS) on the development of asthma in adults. Methods. In the Pirkanmaa district of South Finland, all 21- to 63 year-old adults with new cases of asthma diagnosed during a 2.5-year period (n=521 case patients. out of 441000 inhabitants) and a random sample of control subjects from the source population (932 control subjects) participated in a population-based incident case-control study. Results. Risk of asthma was related to workplace ETS exposure (adjusted odds ratio [OR] = 2.16; 95% confidence interval [CI] = 1.26, 3.72) and home exposure (OR = 4.77; 95% CI = 1.29, 17.7) in the past year. Cumulative ETS exposure over a lifetime at work and at home increased the risk. Conclusions. This study indicates for the first time that both cumulative lifetime and recent ETS exposures increase the risk of adult-onset asthma.	Finnish Inst Occupat Hlth, Helsinki, Finland; Univ Helsinki, Dept Publ Hlth, Environm Epidemiol Unit, Helsinki, Finland	Jaakkola, MS (reprint author), Univ Birmingham, Inst Occupat Hlth, Birmingham B15 2TT, W Midlands, England.		Jaakkola, Jouni/G-4314-2012				American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; *COMM NAT ASTHM PR, 1994, ASTHM PROGR 1994 200, P16; FLODIN U, 1995, EPIDEMIOLOGY, V6, P503, DOI 10.1097/00001648-199509000-00007; Greenland S., 1998, MODERN EPIDEMIOLOGY; GREER JR, 1993, J OCCUP ENVIRON MED, V35, P909, DOI 10.1097/00043764-199309000-00014; Hoffmann D, 1997, J TOXICOL ENV HEALTH, V50, P307, DOI 10.1080/009841097160393; Hu FB, 1997, J ASTHMA, V34, P67, DOI 10.3109/02770909709071205; JAAKKOLA JJK, 1995, AM J EPIDEMIOL, V141, P755; Jaakkola MS, 1999, AM J EPIDEMIOL, V150, P1223; Jaakkola MS, 1997, EUR RESPIR J, V10, P2384, DOI 10.1183/09031936.97.10102384; Jaakkola MS, 2002, ENVIRON HEALTH PERSP, V110, P543; Jaakkola MS, 1999, ENVIRON HEALTH PERSP, V107, P829, DOI 10.2307/3434561; JAAKKOLA MS, 2002, SCAND J WORK ENV S2, V28, P54; Jaakkola MS, 2000, EUR RESP MONOGR, V15, P322; LEUENBERGER P, 1994, AM J RESP CRIT CARE, V150, P1222; MIETTINE.OS, 1974, AM J EPIDEMIOL, V99, P325; NG TP, 1993, J EPIDEMIOL COMMUN H, V47, P454, DOI 10.1136/jech.47.6.454; ROBBINS AS, 1993, INT J EPIDEMIOL, V22, P809, DOI 10.1093/ije/22.5.809; Strachan DP, 1998, THORAX, V53, P204; THORN J, 2001, ALLERGY, V56, P282; *US EPA OFF HLTH E, 1992, EPA PUBL; VILJANEN AA, 1982, SCAND J CLIN LAB INV, V42, P5	22	84	85	0	3	AMER PUBLIC HEALTH ASSOC INC	WASHINGTON	1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 USA	0090-0036			AM J PUBLIC HEALTH	Am. J. Public Health	DEC	2003	93	12					2055	2060		10.2105/AJPH.93.12.2055		6	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	748WH	WOS:000186848400024	14652334	
J	Jenkins, HA; Cherniack, R; Szefler, SJ; Covar, R; Gelfand, EW; Spahn, JD				Jenkins, HA; Cherniack, R; Szefler, SJ; Covar, R; Gelfand, EW; Spahn, JD			A comparison of the clinical characteristics of children and adults with severe asthma	CHEST			English	Article						adult-onset asthma; childbood-onset asthma; glucocorticoids; National Heart, Lung, and Blood Institute; guidelines; severe asthma	AIR-FLOW OBSTRUCTION; CHILDHOOD-ONSET; LUNG-FUNCTION; POPULATION; SAMPLE	Objectives: This study sought to better define the clinical characteristics of severe asthma in both children and adults, and to evaluate the effect of asthma duration on multiple parameters of disease severity. Design: Retrospective analysis of prospectively collected data on 275 patients (125 children) with severe asthma who were admitted to a tertiary asthma referral center. Methods: Demographics, lung function (ie, spirometry and body box plethysmography), glueocorticoid (GC) pharmacokinetic studies, and lymphocyte stimulation assays were performed on all patients. Results: Children were as likely to require therapy with high-dose inhaled GCs and long-term therapy with oral GCs, and to have had a prior intubation, yet they had significantly less airflow limitation (mean [+/-SEM] (.) FEV1, 74.0 +/- 2.1% predicted vs 57.1 +/- 1.8% predicted, respectively; p < 0.0001), less resistance to airflow (mean airway resistance, 140.3 +/- 8.5% predicted vs 311 +/- 18% predicted, respectively; p < 0.0001), and larger lung volumes (mean total lung capacity, 116.4 1.6% predicted vs 105.3 +/- 1.8% predicted, respectively; p < 0.0001) compared to adults. Children were more likely to be male and to display greater responsiveness to GCs in vitro. Lung function impairment was associated with asthma duration in children and in adults with onset of asthma in childhood, while there was no relationship between disease severity and asthma duration among those with adult-onset asthma. Despite significant differences in disease duration, patients with adult-onset asthma had equally compromised lung function compared to adults with long-standing asthma. Conclusions: Children with severe asthma tended to be male, to have less severe airflow obstruction, and to display greater responsiveness to GCs in vitro compared to adults. Symptoms and episodic acute declines in lung function may precede chronic airflow limitation in this group of children. As such, it may be more relevant to follow the deterioration in lung function over time in children. Finally, disease severity in children and adults whose onset of asthma occurred in childhood was related to disease duration, but not in patients with onset of asthma in adulthood.	Natl Jewish Med & Res Ctr, Div Clin Pharmacol, Denver, CO 80206 USA; Natl Jewish Med & Res Ctr, Div Allergy Clin Immunol, Denver, CO 80206 USA; Natl Jewish Med & Res Ctr, Ira J & Jacqueline Neimark Lab Clin Pharmacol Ped, Denver, CO 80206 USA; Natl Jewish Med & Res Ctr, Dept Med, Denver, CO 80206 USA; Univ Colorado, Hlth Sci Ctr, Denver, CO USA	Spahn, JD (reprint author), Natl Jewish Med & Res Ctr, Div Clin Pharmacol, 1400 Jackson St,K-926, Denver, CO 80206 USA.						Bacharier LB, 2002, J ALLERGY CLIN IMMUN, V109, pS266, DOI 10.1016/S0091-6749(02)81946-7; Bratton DL, 2001, PEDIATR PULM, V31, P177, DOI 10.1002/ppul.1027; BROWN PJ, 1984, THORAX, V39, P131, DOI 10.1136/thx.39.2.131; BURROWS B, 1991, J ALLERGY CLIN IMMUN, V88, P870, DOI 10.1016/0091-6749(91)90243-H; BUSSE W, 1995, AM J RESP CRIT CARE, V151, P1635; Busse William W., 2000, Journal of Allergy and Clinical Immunology, V106, P1033; Chan MTS, 1998, J ALLERGY CLIN IMMUN, V101, P594; Eid N, 2000, PEDIATRICS, V105, P354, DOI 10.1542/peds.105.2.354; Fuhlbrigge AL, 2001, J ALLERGY CLIN IMMUN, V107, P61, DOI 10.1067/mai.2001.111590; Gelb AF, 2002, CHEST, V121, P715, DOI 10.1378/chest.121.3.715; Hankinson JL, 1999, AM J RESP CRIT CARE, V159, P179; HILL MR, 1990, CLIN PHARMACOL THER, V48, P390; JENKINS MA, 1994, BRIT MED J, V309, P90; Lange P, 1998, NEW ENGL J MED, V339, P1194, DOI 10.1056/NEJM199810223391703; PEAT JK, 1987, EUR J RESPIR DIS, V70, P171; Segala C, 2000, ALLERGY, V55, P634, DOI 10.1034/j.1398-9995.2000.00488.x; Spahn JD, 1996, J ALLERGY CLIN IMMUN, V98, P1073, DOI 10.1016/S0091-6749(96)80194-1; YUNGINGER JW, 1992, AM REV RESPIR DIS, V146, P888	18	84	90	0	5	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	OCT	2003	124	4					1318	1324		10.1378/chest.124.4.1318		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	733LU	WOS:000186002500021	14555561	
