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	Kagawa, J				Kagawa, J			Health effects of diesel exhaust emissions - a mixture of air pollutants of worldwide concern	TOXICOLOGY			English	Article; Proceedings Paper	9th International Congress of Toxicology (ICT IX)	JUL 08-12, 2001	QUEENSLAND, AUSTRALIA			health effects; diesel exhaust; diesel particles		Diesel exhaust is a mixture of particles and gases. It contains more than several hundred different organic and inorganic components, including many chemicals that have been designated as toxic air pollutants. Because mutagens and carcinogens are present in both the gaseous and particulate components, lung cancer has been the focus of attention as a health risk in animal and human research. Moreover, since the epidemiologic data suggest carcinogenicity in humans, and the diesel exhaust exposure data in evaluations in rats by NIOSH, IARC, WHO, and the California EPA, are said to demonstrate or support carcinogenicity, agencies have designated them as latent occupational carcinogens (NIOSH) or toxic air pollutants (California EPA). In regard to their non-carcinogenic effects, a contribution to airway inflammation and allergies, and in relation to disease, the possibility of contracting asthma and chronic bronchitis, have been investigated both experimentally and epidemiologically, and concern has increased about their health effects, particularly in children. (C) 2002 Published by Elsevier Science Ireland Ltd.	Tokyo Womens Med Univ, Sch Med, Dept Hyg & Publ Hlth, Shinjuku Ku, Tokyo 1628666, Japan	Kagawa, J (reprint author), Tokyo Womens Med Univ, Sch Med, Dept Hyg & Publ Hlth, Shinjuku Ku, 8-1 Kawada Cho, Tokyo 1628666, Japan.						*HEI, 1999, PROGR SUMM RES DIES; *HEI, 1995, DIES EXH CRIT AN EM; International Agency for Research on Cancer, 1989, MON EV CARC RISKS HU, V46; *JAP AUT RES I, 1994, REP AUT EM CHRON OBS; *JAP ENV AG DEP EN, 1999, STUD REP RES METH HL; *JAP ENV AG HLTH R, 2000, INT REP HLTH RISK AS; Kato A, 2000, INHAL TOXICOL, V12, P469, DOI 10.1080/089583700402879; Mauderly JL, 1996, INHAL TOXICOL S, V8, P1; McClellan R.O., 1996, INHAL TOXICOL S, V8, P193; National Institute for Occupational Safety and Health, 1988, NIOSH CURR INT B, V50; *OFF ENV HLTH HAZ, 1998, HLTH RISK ASS DIES E; *US EPA, 1999, EPA600890057D NAT CT; *WHO, 1996, ENV HLTH CRIT, V171	13	84	89	1	21	ELSEVIER SCI IRELAND LTD	CLARE	CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND	0300-483X			TOXICOLOGY	Toxicology	DEC 27	2002	181						349	353	PII S0300-483X(02)00461-4	10.1016/S0300-483X(02)00461-4		5	Pharmacology & Pharmacy; Toxicology	Pharmacology & Pharmacy; Toxicology	639TX	WOS:000180646400060	12505335	
J	Hermiz, O; Comino, E; Marks, G; Daffurn, K; Wilson, S; Harris, M				Hermiz, O; Comino, E; Marks, G; Daffurn, K; Wilson, S; Harris, M			Randomised controlled trial of home based care of patients with chronic obstructive pulmonary disease	BRITISH MEDICAL JOURNAL			English	Article							AIR-FLOW LIMITATION; RESPIRATORY QUESTIONNAIRE; COPD; EXACERBATIONS; PROGRAM; ASTHMA	Objectives To evaluate usefulness of limited community based care for patients with chronic obstructive pulmonary disease after discharge from hospital. Design Randomised controlled trial. Setting Liverpool Health Service and Macarthur Health Service in outer metropolitan Sydney between September 1999 and July 2000. Participants 177 patients randomised into an intervention group (84 patients) and a control group (93 patients) which received current usual care. Interventions Home visits by community nurse at one and four weeks after discharge and preventive general practitioner care. Main outcome measures Frequency of patients' presentation and admission to hospital; changes in patients' disease-specific quality of life, measured with St George's respiratory questionnaire, over three months after discharge; patients' knowledge of illness, self management, and satisfaction with care at discharge and three months later; frequency of general practitioner and nurse visits and their satisfaction with care. Results Intervention and control groups showed no differences in presentation or admission to hospital or in overall functional status. However, the intervention group improved their activity scores and the control group worsened their symptom scores. While intervention group patients received more visits from community nurses and were more satisfied with their care, involvement of general practitioners was much less (with only 31% (22) remembering receiving a care plan). Patients in the intervention group had higher knowledge scores and were more satisfied. There were no differences in general practitioner visits or management. Conclusions This brief intervention after acute care improved patients' knowledge and some aspects of quality of life. However, it failed to prevent presentation and readmission to hospital.	Univ New S Wales, Sch Community Med, Sydney, NSW 2052, Australia; Liverpool Hlth Serv, Div Crit Care, Sydney, NSW, Australia; SW Sydney Area Hlth Serv, Macarthur Hlth Serv, Sydney, NSW, Australia	Harris, M (reprint author), Univ New S Wales, Sch Community Med, Sydney, NSW 2052, Australia.						Blakeman T, 2001, Aust Fam Physician, V30, P75; Crockett AJ, 1996, QUAL LIFE RES, V5, P330, DOI 10.1007/BF00433917; Crockett AJ, 2000, INT J QUAL HEALTH C, V12, P41, DOI 10.1093/intqhc/12.1.41; Farrero E, 2001, CHEST, V119, P364, DOI 10.1378/chest.119.2.364; Fried TR, 1998, J GEN INTERN MED, V13, P522, DOI 10.1046/j.1525-1497.1998.00162.x; Gallefoss F, 1999, AM J RESP CRIT CARE, V159, P812; Gibson P G, 1998, J Qual Clin Pract, V18, P125; GIBSON PG, 1988, J QUAL CLIN PRACT, V18, P125; Gravil JH, 1998, LANCET, V351, P1853, DOI 10.1016/S0140-6736(97)11048-0; JONES PW, 1991, RESP MED, V85, P25, DOI 10.1016/S0954-6111(06)80166-6; Keenan SP, 2000, CRIT CARE MED, V28, P2094, DOI 10.1097/00003246-200006000-00072; Ketelaars CAJ, 1998, HEART LUNG, V27, P109, DOI 10.1016/S0147-9563(98)90018-8; Madison JM, 1998, LANCET, V352, P467, DOI 10.1016/S0140-6736(97)11081-9; Rutten-van Molken M, 1999, THORAX, V54, P995; *S W SYDN AR HLTH, 1998, EP UN REP COPD ASTHM; Skwarska E, 2000, THORAX, V55, P907, DOI 10.1136/thorax.55.11.907; SMITH B, 2000, COCHRANE DATABASE SY, DOI UNSP CD000994; Smith BJ, 1999, AUST NZ J MED, V29, P718, DOI 10.1111/j.1445-5994.1999.tb01621.x; Strijbos JH, 1996, CHEST, V109, P366, DOI 10.1378/chest.109.2.366; Tirimanna PRS, 1996, BRIT J GEN PRACT, V46, P277; TRAVER GA, 1988, HEART LUNG, V17, P689; [Anonymous], 1987, AM REV RESP DIS, V136, P225	22	84	85	0	6	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0959-535X			BRIT MED J	Br. Med. J.	OCT 26	2002	325	7370					938	940C		10.1136/bmj.325.7370.938		6	Medicine, General & Internal	General & Internal Medicine	610XB	WOS:000178986300017	12399344	
J	Hammad, H; Lambrecht, BN; Pochard, P; Gosset, P; Marquillies, P; Tonnel, AB; Pestel, J				Hammad, H; Lambrecht, BN; Pochard, P; Gosset, P; Marquillies, P; Tonnel, AB; Pestel, J			Monocyte-derived dendritic cells induce a house dust mite-specific Th2 allergic inflammation in the lung of humanized SCID mice: Involvement of CCR7	JOURNAL OF IMMUNOLOGY			English	Article							EOSINOPHILIC AIRWAY INFLAMMATION; LYMPH-NODES; INHALED ANTIGEN; INTRATRACHEAL INSTILLATION; LACKING EXPRESSION; RESPIRATORY-TRACT; RESPONSES; CHEMOKINE; ASTHMA; MODEL	In rodents, airway dendritic cells (DCs) capture inhaled Ag, undergo maturation, and migrate to the draining mediastinal lymph nodes (MLN) to initiate the Ag-specific T cell response. However, the role of human DCs in the pathogenesis of the Th2 cell-mediated disease asthma remains to be clarified. Here, by using SCID mice engrafted with T cells from either house dust mite (HDM)-allergic patients or healthy donors, we show that DCs pulsed with Der p 1, one of the major allergens or HDM, and injected intratracheally into naive animals migrated into the MLN. In the NILN, Der p I-pulsed DCs from allergic patients induced the proliferation of IL-4-producing CD4(+) T cells, whereas those from healthy donors induced IFN-gamma-secreting cells. In reconstituted human PBM C-reconstituted SCID mice primed with pulsed DCs from allergic patients, repeated exposure to aerosols of HDM induced 1) a strong pulmonary inflammatory reaction rich in T cells and eosinophils, 2) an increase in IL-4 and IL-5 production in the lung lavage fluid, and 3) increased IgE production compared with that in mice primed with unpulsed DCs. All these effects were reduced following in vivo neutralization of the CCR7 ligand secondary lymphoid tissue chemokine. These data in human PBMC-reconstituted SCID mice show that monocyte-derived DCs might play a key role in the pathogenesis of the pulmonary allergic response by inducing Th2 effector function following migration to the MLN.	Inst Pasteur, Inst Natl Sante & Rech Med, Unit 416, Lille, France; Erasmus Univ, Dept Pulm & Crit Care Med, Rotterdam, Netherlands; Ctr Hosp Reg Univ Lille, Hop Calmette, Clin Malad Respiratoires, Lille, France	Pestel, J (reprint author), Inst Pasteur, Inst Natl Sante & Rech Med, Unit 416, 1 Rue Prof Clamette,BP 24559019, Lille, France.		Hammad, Hamida/J-9391-2015; Lambrecht, Bart/K-2484-2014	Hammad, Hamida/0000-0003-3762-8603; Lambrecht, Bart/0000-0003-4376-6834			Banchereau J, 1998, NATURE, V392, P245, DOI 10.1038/32588; Bellinghausen I, 2000, J ALLERGY CLIN IMMUN, V105, P988, DOI 10.1067/mai.2000.105526; BOUSQUET J, 1990, NEW ENGL J MED, V323, P1033, DOI 10.1056/NEJM199010113231505; Cochand L, 1999, AM J RESP CELL MOL, V21, P547; Cyster JG, 1999, J EXP MED, V189, P447, DOI 10.1084/jem.189.3.447; De Wit D, 2000, J ALLERGY CLIN IMMUN, V105, P346, DOI 10.1016/S0091-6749(00)90086-1; Duez C, 1996, EUR J IMMUNOL, V26, P1088, DOI 10.1002/eji.1830260520; Duez C, 1998, SCAND J IMMUNOL, V47, P110; Engeman TM, 2000, J IMMUNOL, V164, P5207; Forster R, 1999, CELL, V99, P23, DOI 10.1016/S0092-8674(00)80059-8; Gunn MD, 1999, J EXP MED, V189, P451, DOI 10.1084/jem.189.3.451; Hammad H, 2001, BLOOD, V98, P1135, DOI 10.1182/blood.V98.4.1135; Hammad H, 2000, LAB INVEST, V80, P605; HAVENITH CEG, 1993, AM J RESP CELL MOL, V9, P484; HOLT PG, 1994, J IMMUNOL, V153, P256; Holt PG, 2000, J ALLERGY CLIN IMMUN, V105, P421, DOI 10.1067/mai.2000.105010; Humbert M, 1999, IMMUNOL TODAY, V20, P528, DOI 10.1016/S0167-5699(99)01535-2; Iezzi G, 1999, EUR J IMMUNOL, V29, P4092, DOI 10.1002/(SICI)1521-4141(199912)29:12<4092::AID-IMMU4092>3.3.CO;2-1; Kalinski P, 1999, IMMUNOL TODAY, V20, P561, DOI 10.1016/S0167-5699(99)01547-9; Kellermann SA, 1999, J IMMUNOL, V162, P3859; KUEZ C, 2000, AM J RESP CRIT CARE, V161, P200; Lambrecht B N, 2001, Curr Opin Allergy Clin Immunol, V1, P51, DOI 10.1097/00130832-200102000-00010; Lambrecht BN, 2000, J CLIN INVEST, V106, P551, DOI 10.1172/JCI8107; Lambrecht BN, 1998, J IMMUNOL, V160, P4090; Lambrecht BN, 2000, CLIN EXP ALLERGY, V30, P214; Lambrecht BN, 2000, J IMMUNOL, V164, P2937; LYONS AB, 1994, J IMMUNOL METHODS, V171, P131, DOI 10.1016/0022-1759(94)90236-4; MACKAY CR, 1990, J EXP MED, V171, P801, DOI 10.1084/jem.171.3.801; MANZ R, 1995, P NATL ACAD SCI USA, V92, P1921, DOI 10.1073/pnas.92.6.1921; Mori S, 2001, J EXP MED, V193, P207, DOI 10.1084/jem.193.2.207; PESTEL J, 1994, J IMMUNOL, V153, P3804; Robbiani DF, 2000, CELL, V103, P757, DOI 10.1016/S0092-8674(00)00179-3; ROBINSON DS, 1992, NEW ENGL J MED, V326, P298, DOI 10.1056/NEJM199201303260504; Saeki H, 1999, J IMMUNOL, V162, P2472; Sallusto F, 1998, EUR J IMMUNOL, V28, P2760, DOI 10.1002/(SICI)1521-4141(199809)28:09<2760::AID-IMMU2760>3.0.CO;2-N; Sallusto F, 1999, NATURE, V401, P708, DOI 10.1038/44385; Stumbles PA, 1998, J EXP MED, V188, P2019, DOI 10.1084/jem.188.11.2019; UPHAM JW, 1995, CLIN EXP ALLERGY, V25, P634, DOI 10.1111/j.1365-2222.1995.tb01111.x; Vermaelen KY, 2001, J EXP MED, V193, P51; XIA WJ, 1995, J EXP MED, V181, P1275, DOI 10.1084/jem.181.4.1275	40	84	86	0	3	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	AUG 1	2002	169	3					1524	1534				11	Immunology	Immunology	576UV	WOS:000177025100048	12133980	
J	Woessner, KM; Simon, RA; Stevenson, DD				Woessner, KM; Simon, RA; Stevenson, DD			The safety of celecoxib in patients with aspirin-sensitive asthma	ARTHRITIS AND RHEUMATISM			English	Article							CYCLOOXYGENASE-2 INHIBITOR; INTOLERANT PATIENTS; CROSS-SENSITIVITY; COX-2; PATHOGENESIS; EXPRESSION; DRUGS	Objective. To determine whether celecoxib, a selective cyclooxygenase 2 (COX-2) inhibitor, cross-reacts in patients with aspirin-exacerbated respiratory disease (AERD) with asthma. Methods. Sixty patients with asthma underwent double-blinded, placebo-controlled oral challenges with celecoxib (100 mg, 200 mg, and 2 placebos) over 48 hours in our General Clinical Research Center. The next day, sensitivity to acetylsalicylic acid (ASA) was proven in all patients with the use of single-blinded ASA challenges. Results. None of the 60 patients experienced any symptoms, changes in nasal examinations, or declines in forced expiratory volume in 1 second during the celecoxib challenges. All 60 patients experienced oculo-nasal and/or asthmatic reactions to ASA, with a mean provoking dose of 69 mg. The exact 1-sided confidence interval for the probability of celecoxib inducing cross-reactions in AERD patients was calculated to be between 0% and 5%. Conclusion. Cross-reactivity between ASA and celecoxib does not occur in patients with AERD. These results do not preclude the possibility of other types of immune reactions occurring with celecoxib after prior exposure. Our results add to the growing body of evidence that inhibition of COX-1 is a critical initiating event in the precipitation of respiratory reactions in AERD patients following ingestion of nonsteroidal anti-inflammatory drugs.	Scripps Clin, Div Allergy Asthma & Immunol, La Jolla, CA 92037 USA	Woessner, KM (reprint author), Scripps Clin, Div Allergy Asthma & Immunol, 10666 N Torrey Pines Rd,W-205, La Jolla, CA 92037 USA.	woessner@scripps.edu			NCRR NIH HHS [M01-RR-0883]		ANDRI L, 1994, ANN ALLERGY, V72, P29; Dahlen B, 2001, NEW ENGL J MED, V344, P142, DOI 10.1056/NEJM200101113440215; Demoly P, 1997, AM J RESP CRIT CARE, V155, P670; FISCHER AR, 1994, J ALLERGY CLIN IMMUN, V94, P1046, DOI 10.1016/0091-6749(94)90123-6; Funk CD, 2001, SCIENCE, V294, P1871, DOI 10.1126/science.294.5548.1871; HAMBERG M, 1974, P NATL ACAD SCI USA, V71, P3400, DOI 10.1073/pnas.71.9.3400; Hawkey CJ, 1999, LANCET, V353, P307, DOI 10.1016/S0140-6736(98)12154-2; Hedman J, 1999, INT J EPIDEMIOL, V28, P717, DOI 10.1093/ije/28.4.717; Kosnik M, 1998, ALLERGY, V53, P1231, DOI 10.1111/j.1398-9995.1998.tb03854.x; Lehman E. L., 1986, TESTING STAT HYPOTHE; Levy MB, 2001, ANN ALLERG ASTHMA IM, V87, P72; *MED EC, 2001, PHYSICIANS DESK REFE; NIZANKOWSKA E, 1989, ANN ALLERGY, V63, P159; Pauls JD, 2000, ANN ALLERG ASTHMA IM, V85, P40; Schellenberg RR, 2001, NEW ENGL J MED, V345, P1856, DOI 10.1056/NEJM200112203452518; SETTIPANE RA, 1989, J ALLERGY CLIN IMMUN, V84, P26, DOI 10.1016/0091-6749(89)90174-7; Sousa AR, 1997, THORAX, V52, P940; SPECTOR SL, 1979, J ALLERGY CLIN IMMUN, V64, P500, DOI 10.1016/0091-6749(79)90059-9; Stevenson DD, 2000, J ALLERGY CLIN IMMUN, V105, pS273, DOI 10.1016/S0091-6749(00)91234-X; Stevenson DD, 2000, ANN ALLERG ASTHMA IM, V85, P477; Stevenson DD, 2001, J ALLERGY CLIN IMMUN, V108, P47, DOI 10.1067/mai.2001.116290; STEVENSON DD, 1990, J ALLERGY CLIN IMMUN, V86, P749, DOI 10.1016/S0091-6749(05)80179-4; Stevenson DD, 1996, J ALLERGY CLIN IMMUN, V98, P751, DOI 10.1016/S0091-6749(96)70123-9; Stevenson DD, 2001, ANN ALLERG ASTHMA IM, V87, P177; Stevenson DD, 1998, ALLERGY PRINCIPLES P, P1225; SZCZEKLIK A, 1979, THORAX, V34, P654, DOI 10.1136/thx.34.5.654; Szczeklik A, 1999, J ALLERGY CLIN IMMUN, V104, P5, DOI 10.1016/S0091-6749(99)70106-5; SZCZEKLIK A, 1977, J ALLERGY CLIN IMMUN, V60, P276, DOI 10.1016/0091-6749(77)90106-3; SZCZEKLIK A, 1990, EUR RESPIR J, V3, P588; Szczeklik A, 2001, CLIN EXP ALLERGY, V31, P219, DOI 10.1046/j.1365-2222.2001.01075.x; XIE WL, 1991, P NATL ACAD SCI USA, V88, P2692, DOI 10.1073/pnas.88.7.2692; Yoshida S, 2000, J ALLERGY CLIN IMMUN, V106, P1201	32	84	85	0	0	WILEY-LISS	NEW YORK	DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA	0004-3591			ARTHRITIS RHEUM	Arthritis Rheum.	AUG	2002	46	8					2201	2206		10.1002/art.10426		6	Rheumatology	Rheumatology	583WB	WOS:000177432800029	12209526	
J	Hogman, M; Holmkvist, T; Wegener, T; Emtner, M; Andersson, M; Hedenstrom, H; Merilainen, P				Hogman, M; Holmkvist, T; Wegener, T; Emtner, M; Andersson, M; Hedenstrom, H; Merilainen, P			Extended NO analysis applied to patients with COPD, allergic asthma and allergic rhinitis	RESPIRATORY MEDICINE			English	Article						nitric oxide; asthma; allergic rhinitis; smoker; COPD; airway inflammation; method	EXHALED NITRIC-OXIDE; RESPONSIVENESS; DISEASE; AIRWAYS; AIR	The recommended method to measure exhaled nitric oxide (NO) cannot reveal the source of NO production. We applied a model based on the classical Fick's first law of diffusion to partition NO in the lungs. The aim was to develop a simple and robust solution algorithm with a data quality control feature, and apply it to patients with known alterations in exhaled NO. Subjects with allergic rhinitis, allergic asthma, chronic obstructive pulmonary disease (COPD) smokers and controls were investigated. NO was measured at three expiratory flow rates. An iteration method was developed to partition NO. The airway tissue content of NO was increased in asthma, 144 +/- 80 ppb (P = 0(.)04) and decreased in smokers, 56 +/- 36 ppb (P = 0(.)02). There was no difference between subjects with rhinitis, 98 +/- 40 ppb and controls, 98 +/- 44 ppb. The airway transfer rate was increased in allergic asthma and allergic rhinithis, 12 +/- 4 vs. 12 +/- 5 ml sec(-1), compared to controls, 8 +/- 2 ml sec(-1) (P < 0(.)001). The alveolar levels were no different from controls, 2 +/- 1 ppb. In COPD the alveolar levels were increased, 4 +/- 2 ppb (P < 0(.)001). Extended NO analysis reveals from where in the respiratory system NO is generated. Hence, this new test can be added to the tools the physician has for the diagnosis and treatment of patients with respiratory disorders. (C) 2001 Harcourt Publishers Ltd.	Univ Uppsala, Dept Med Sci, SE-75123 Uppsala, Sweden	Hogman, M (reprint author), Univ Uppsala, Dept Med Cell Biol, Sect Integrat Physiol, Box 571, SE-75123 Uppsala, Sweden.						ALVING K, 1993, EUR RESPIR J, V6, P1368; ASSREUY J, 1993, BRIT J PHARMACOL, V108, P833; BLAND JM, 1986, LANCET, V1, P307; Clini E, 1998, THORAX, V53, P881; Corradi M, 1999, THORAX, V54, P572; FICK A, 1856, MED PHYSIK; Gow AJ, 1999, P NATL ACAD SCI USA, V96, P9027, DOI 10.1073/pnas.96.16.9027; GUSTAFSSON LE, 1991, BIOCHEM BIOPH RES CO, V181, P852, DOI 10.1016/0006-291X(91)91268-H; Henriksen AH, 1999, EUR RESPIR J, V13, P301, DOI 10.1034/j.1399-3003.1999.13b14.x; Hogman M, 2000, RESP MED, V94, P985, DOI 10.1053/rmed.2000.0872; Hogman M, 1997, ACTA PHYSIOL SCAND, V159, P345, DOI 10.1046/j.1365-201X.1997.00101.x; Hogman M, 1999, AM J RESP CRIT CARE, V159, pA862; Jorres RA, 2000, EUR RESPIR J, V16, P555, DOI 10.1034/j.1399-3003.2000.016003555.x; Kharitonov S, 1997, EUR RESPIR J, V10, P1683, DOI 10.1183/09031936.97.10071683; Ludviksdottir D, 1999, RESP MED, V93, P552, DOI 10.1016/S0954-6111(99)90154-3; Silkoff PE, 2000, AM J RESP CRIT CARE, V161, P1218; Silkoff PE, 1997, AM J RESP CRIT CARE, V155, P260; Tsoukias NM, 1998, J APPL PHYSIOL, V85, P653	18	84	84	1	8	W B SAUNDERS CO LTD	LONDON	24-28 OVAL RD, LONDON NW1 7DX, ENGLAND	0954-6111			RESP MED	Respir. Med.	JAN	2002	96	1					24	30		10.1053/rmed.2001.1204		7	Cardiac & Cardiovascular Systems; Respiratory System	Cardiovascular System & Cardiology; Respiratory System	521YY	WOS:000173870000005	11863206	
J	Ma, JYC; Ma, JKH				Ma, JYC; Ma, JKH			The dual effect of the particulate and organic components of diesel exhaust particles on the alteration of pulmonary immune/inflammatory responses and metabolic enzymes	JOURNAL OF ENVIRONMENTAL SCIENCE AND HEALTH PART C-ENVIRONMENTAL CARCINOGENESIS & ECOTOXICOLOGY REVIEWS			English	Review						diesel exhaust particles (DEP); particulate; organic extract; reactive oxygen species (ROS); metabolic enzymes; th1 and th2 immune responses; cytokines; infection; allergy; lung tumors	TUMOR-NECROSIS-FACTOR; CYTOCHROME P450 REDUCTASE; RAT ALVEOLAR MACROPHAGES; CELL-MEDIATED-IMMUNITY; OXIDATIVE DNA-DAMAGE; CARBON-BLACK; NITRIC-OXIDE; LISTERIA-MONOCYTOGENES; HEME OXYGENASE-1; IN-VIVO	Exposure to diesel exhaust particles (DEP) is an environmental and occupational health concern. This review examines the cellular actions of the organic and the particulate components of DEP in the development of various lung diseases. Both the organic and the particulate components cause oxidant lung injury. The particulate component is known to induce alveolar epithelial damage, alter thiol levels in alveolar macrophages (AM) and lymphocytes, and activate AM in the production of reactive oxygen species (ROS) and pro-inflammatory cytokines. The organic component, on the other hand, is shown to generate intracellular ROS, leading to a variety of cellular responses including apoptosis. There are a number of differences between the biological actions exerted by these two components. The organic component is responsible-for DEP induction of cytochrome P450 family 1 enzymes that are critical to the polycyclic aromatic hydrocarbons (PAH) and nitro-PAH metabolism in the lung as well as in the liver. The particulate component, on the other hand, causes a sustained down-regulation of CYP2B1 in the rat lung. The significance of this effect on pulmonary metabolism of xenobiotics and endobiotics remains to be seen, but may prove to be an important factor governing the interplay of the pulmonary metabolic and inflammatory systems. Long-term exposures to various particles including DEP, carbon black (CB), TiO(2), and washed DEP devoid of the organic content, have been shown to produce similar tumorigenic responses in rodents. There is a lack of correlation between tumor development and DEP chemical-derived DNA adduct formation. But the organic component has been shown to generate ROS that produce 8-hydroxydeoxyguanosine (8-OHdG) in cell culture. The organic, but not the particulate, component of DEP suppresses the production of pro-inflammatory cytokines by AM and the development of Th1 cell-mediated immunity. The mechanism for this effect is not yet clear, but may involve the induction of heme oxygenase-1 (HO-1), a cellular genetic response to oxidative stress. Both the organic and the particulate components of DEP enhance respiratory allergic sensitization. Part of the DEP effects may be due to a depletion of glutathione in lymphocytes. The organic component, which is shown to induce IL-4 and IL-10 productions, may skew the immunity toward Th2 response, whereas the particulate component may stimulate both the Th1 and Th2 responses. In conclusion, the literature shows that the particulate and organic components of DEP exhibit different biological actions but both involve the induction of cellular oxidative stress. Together, these effects inhibit cell-mediated immunity toward infectious agents, exacerbate respiratory allergy, cause DNA damage, and under long-term exposure, induce the development of lung tumors.	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Environ. Sci. Health Pt. C-Environ. Carcinog. Ecotoxicol. Rev.		2002	20	2					117	147		10.1081/GNC-120016202		31	Oncology; Environmental Sciences; Toxicology	Oncology; Environmental Sciences & Ecology; Toxicology	621VY	WOS:000179612800002	12515672	
J	Wachholz, PA; Nouri-Aria, KT; Wilson, DR; Walker, SM; Verhoef, A; Till, SJ; Durham, SR				Wachholz, PA; Nouri-Aria, KT; Wilson, DR; Walker, SM; Verhoef, A; Till, SJ; Durham, SR			Grass pollen immunotherapy for hayfever is associated with increases in local nasal but not peripheral Th1 : Th2 cytokine ratios	IMMUNOLOGY			English	Article							MESSENGER-RNA EXPRESSION; SEASONAL ALLERGIC RHINITIS; CD4+ T-CELLS; IMMUNOLOGICAL CHANGES; INTERFERON-GAMMA; ANTIBODY-LEVELS; PRIMARY CULTURE; IL-4 PRODUCTION; LYMPHOCYTES-T; IN-VITRO	Grass pollen immunotherapy is the only treatment for hayfever that is both effective and confers long-term benefit. Immunotherapy may act by altering the local nasal mucosal T helper type 2 (Th2) to type 1 (Th1) cytokine balance either by down-regulation and/or immune deviation of T-lymphocyte responses. There is controversy as to whether these changes are detectable in peripheral blood. We therefore examined both local nasal and peripheral T-cell responses to allergen exposure in the same subjects before and after immunotherapy. In a double-blind trial of grass pollen immunotherapy, nasal biopsies were obtained at baseline and during the peak pollen season following 2 years of immunotherapy. Placebo-treated patients showed a seasonal increase in CD3(+) T cells (P=0.02) and in interleukin-5 (IL-5) mRNA(+) cells (P=0.03) and no change in interferon-gamma (IFN-gamma) mRNA(+) cells (P=0.2) in the nasal mucosa. In contrast, in the immunotherapy-treated group, there were no changes in the number of CD3(+) T cells (P=0.3) and IL-5 mRNA(+) cells (P=0.2) but a significant increase in the number of IFN-gamma mRNA(+) cells (P=0.03). Furthermore, clinical improvement in the immunotherapy-treated group was accompanied by a seasonal increase in the ratio of IFN-gamma to IL-5 mRNA(+) cells in the nasal mucosa (P=0.03). In contrast, there were no significant changes in peripheral T-cell proliferative responses or cytokine production for IFN-gamma or IL-5 in response to grass pollen either within or between the two treatment groups. We conclude that successful grass pollen immunotherapy was associated with an increase in the ratio of IFN-gamma to IL-5 mRNA(+) cells in the nasal mucosa, whereas these changes were not reflected by alterations in peripheral blood T-cell proliferative responses or cytokine production before/after treatment.	Univ London Imperial Coll Sci Technol & Med, Sch Med, Natl Heart & Lung Inst, London SW3 6LY, England	Durham, SR (reprint author), Univ London Imperial Coll Sci Technol & Med, Sch Med, Natl Heart & Lung Inst, Dovehouse St, London SW3 6LY, England.		Walker, Samantha/B-9740-2013	Walker, Samantha/0000-0001-5503-8258			Akdis CA, 1998, J CLIN INVEST, V102, P98, DOI 10.1172/JCI2250; Akdis CA, 1999, FASEB J, V13, P603; Akdis CA, 1996, J CLIN INVEST, V98, P1676, DOI 10.1172/JCI118963; Benjaponpitak S, 1999, J ALLERGY CLIN IMMUN, V103, P468, DOI 10.1016/S0091-6749(99)70473-2; Bousquet J., 1998, Allergy (Copenhagen), V53, P1; CRETICOS PS, 1985, J CLIN INVEST, V76, P2247, DOI 10.1172/JCI112233; DEL PG, 1988, J IMMUNOL, V140, P4193; DJURUP R, 1984, ALLERGY, V39, P433, DOI 10.1111/j.1398-9995.1984.tb01965.x; DURHAM SR, 1992, J IMMUNOL, V148, P2390; Durham SR, 1999, NEW ENGL J MED, V341, P468, DOI 10.1056/NEJM199908123410702; Durham SR, 1996, J ALLERGY CLIN IMMUN, V97, P1356, DOI 10.1016/S0091-6749(96)70205-1; DURHAM SR, 1995, INT ARCH ALLERGY IMM, V107, P282; Ebner C, 1997, CLIN EXP ALLERGY, V27, P1007, DOI 10.1111/j.1365-2222.1997.tb01252.x; FOKKENS W J, 1988, Rhinology (Utrecht), V26, P293; FREW AJ, 1988, J IMMUNOL, V141, P4158; FURIN MJ, 1991, J ALLERGY CLIN IMMUN, V88, P27, DOI 10.1016/0091-6749(91)90297-2; GAGA M, 1991, J IMMUNOL, V147, P816; Gehlhar K, 1999, CLIN EXP ALLERGY, V29, P497; Hamid QA, 1997, J ALLERGY CLIN IMMUN, V99, P254, DOI 10.1016/S0091-6749(97)70106-4; IMADA M, 1995, IMMUNOLOGY, V85, P373; Kay AB, 2001, NEW ENGL J MED, V344, P30; Kay AB, 2001, NEW ENGL J MED, V344, P109; Klimek L, 1999, CLIN EXP ALLERGY, V29, P1326; Lu FM, 1998, ANN ALLERG ASTHMA IM, V80, P419; Magnan A, 2000, ALLERGY, V55, P286, DOI 10.1034/j.1398-9995.2000.00425.x; Moverare R, 2000, IMMUNOL LETT, V73, P51, DOI 10.1016/S0165-2478(00)00199-1; Moverare R, 2000, SCAND J IMMUNOL, V52, P200; Ohashi Y, 1997, SCAND J IMMUNOL, V46, P67, DOI 10.1046/j.1365-3083.1997.d01-87.x; OTSUKA H, 1991, CLIN EXP ALLERGY, V21, P115, DOI 10.1111/j.1365-2222.1991.tb00812.x; ROBINSON D, 1993, J ALLERGY CLIN IMMUN, V92, P313, DOI 10.1016/0091-6749(93)90175-F; Till S, 1997, CLIN EXP IMMUNOL, V110, P114, DOI 10.1111/j.1365-2249.1997.494-ce1392.x; Till S, 1997, J ALLERGY CLIN IMMUN, V99, P563, DOI 10.1016/S0091-6749(97)70085-X; van Neerven RJJ, 1999, J IMMUNOL, V163, P2944; Varga EM, 2000, J IMMUNOL, V165, P2877; VARNEY VA, 1992, AM REV RESPIR DIS, V146, P170; VARNEY VA, 1991, BRIT MED J, V302, P265; VARNEY VA, 1993, J CLIN INVEST, V92, P644, DOI 10.1172/JCI116633; VOLLENWEIDER S, 1991, J ALLERGY CLIN IMMUN, V87, P1088, DOI 10.1016/0091-6749(91)92154-S; Walker SM, 2001, J ALLERGY CLIN IMMUN, V107, P87, DOI 10.1067/mai.2001.112027; WIERENGA EA, 1991, J IMMUNOL, V147, P2942; WIERENGA EA, 1990, J IMMUNOL, V144, P4651; Wilson DR, 2001, J ALLERGY CLIN IMMUN, V107, P971, DOI 10.1067/mai.2001.115483; WILSON DR, 2001, IN PRESS CLIN EXP AL; YING S, 1993, AM J RESP CELL MOL, V9, P356	44	84	90	0	2	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0019-2805			IMMUNOLOGY	Immunology	JAN	2002	105	1					56	62		10.1046/j.1365-2567.2002.01338.x		7	Immunology	Immunology	516FX	WOS:000173544200007	11849315	
J	Lester, LA; Rich, SS; Blumenthal, MN; Togias, A; Murphy, S; Malveaux, F; Miller, ME; Dunston, GM; Solway, J; Wolf, RL; Samet, JM; Marsh, DG; Meyers, DA; Ober, C; Bleecker, ER				Lester, LA; Rich, SS; Blumenthal, MN; Togias, A; Murphy, S; Malveaux, F; Miller, ME; Dunston, GM; Solway, J; Wolf, RL; Samet, JM; Marsh, DG; Meyers, DA; Ober, C; Bleecker, ER		Collaborative Study Genetics Asthm	Ethnic differences in asthma and associated phenotypes: Collaborative Study on the Genetics of Asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; bronchial hyperresponsiveness; atopy; ethnic differences	SKIN-TEST REACTIVITY; GENOME-WIDE SEARCH; SERUM IGE LEVELS; SOCIOECONOMIC-STATUS; COCKROACH ALLERGEN; CHILDHOOD ASTHMA; INDOOR ALLERGENS; CHILDREN; RACE; SEVERITY	Background: In the Collaborative Study on the Genetics of Asthma, 314 families with 2584 subjects were characterized for asthma and allergy. Objective: The purpose of this investigation was to examine clinical heterogeneity observed in asthma and allergic characteristics among 3 ethnic groups (African American, white, and Hispanic family members). Methods: pulmonary function parameters and asthma-associated phenotypes were compared among the ethnic groups. Results: In comparison with the other groups, African American sibling pairs had a significantly lower baseline FEV, percent of predicted (P = .0001) and a higher rate of skin test reactivity to cockroach allergen (P = .0001); Hispanic sibling pairs had significantly more skin reactivity overall (P = .001); and white sibling pairs had significantly lower total serum IgE (P < .05). In addition, there were significantly more relatives with asthma among the African American families than among the white and the Hispanic families (P = .001). Conclusion: Although different environmental backgrounds should be considered, these clinical differences could be due to differences in genetic susceptibility among the ethnic groups, such as those suggested by our previous genome screen.	Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genom, Winston Salem, NC 27157 USA; Univ Chicago, Chicago, IL 60637 USA; Univ Minnesota, Minneapolis, MN 55455 USA; Johns Hopkins Univ, Baltimore, MD 21218 USA; Univ New Mexico, Albuquerque, NM 87131 USA; Howard Univ, Washington, DC 20059 USA; Univ Maryland, College Pk, MD 20742 USA	Bleecker, ER (reprint author), Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genom, Med Ctr Blvd, Winston Salem, NC 27157 USA.		Solway, Julian/B-1116-2008	Solway, Julian/0000-0002-0898-8530	NCRR NIH HHS [M01-RR00400, MR1 RR00055]; NHLBI NIH HHS [UO1 HL/AI49596, HL/AI 49609, U01 HL/AI 49612, U01 HL/AI49602, UO1 HL 58977]		ARSHAD SH, 1992, J ALLERGY CLIN IMMUN, V90, P235, DOI 10.1016/0091-6749(92)90077-F; Barnes KC, 1996, GENOMICS, V37, P41, DOI 10.1006/geno.1996.0518; BLUMENTHAL M, 1992, J IMMUNOL, V148, P411; BURROWS B, 1989, NEW ENGL J MED, V320, P271, DOI 10.1056/NEJM198902023200502; COGSWELL JJ, 1987, ARCH DIS CHILD, V62, P338; Daniels SE, 1996, NATURE, V383, P247, DOI 10.1038/383247a0; Doull IJM, 1996, AM J RESP CRIT CARE, V153, P1280; GOLD DR, 1994, AM J RESP CRIT CARE, V149, P1198; HOLGATE ST, 1997, NAT GENET, V15, P389; KANG BC, 1993, J ALLERGY CLIN IMMUN, V92, P393; Liang K. Y., 1992, BIOMETRIKA, V73, P12; LIGGETT S, 1996, LUNG BIOL HLTH DIS; Litonjua AA, 1998, AM J RESP CRIT CARE, V158, P176; Marsh DG, 1997, NAT GENET, V15, P389; MARSH DG, 1994, SCIENCE, V264, P1152, DOI 10.1126/science.8178175; MEYERS DA, 1994, GENOMICS, V23, P464, DOI 10.1006/geno.1994.1524; Mrazek DA, 1999, PEDIATR PULM, V27, P85, DOI 10.1002/(SICI)1099-0496(199902)27:2<85::AID-PPUL4>3.0.CO;2-B; Ober C, 1998, HUM MOL GENET, V7, P1393, DOI 10.1093/hmg/7.9.1393; Persky VW, 1998, ANN ALLERG ASTHMA IM, V81, P266; PLATTSMILLS TAE, 1991, INT ARCH ALLER A IMM, V94, P339; RICH SS, 1992, CLIN EXP ALLERGY, V22, P1070, DOI 10.1111/j.1365-2222.1992.tb00132.x; Rosenstreich DL, 1997, NEW ENGL J MED, V336, P1356, DOI 10.1056/NEJM199705083361904; Sarpong SB, 1998, ANN ALLERG ASTHMA IM, V80, P303; Sarpong SB, 1996, J ALLERGY CLIN IMMUN, V97, P1393, DOI 10.1016/S0091-6749(96)70209-9; SCHWARTZ J, 1990, AM REV RESPIR DIS, V142, P555; SHERMAN CB, 1993, AM REV RESPIR DIS, V148, P98; SHIRAKAWA T, 1994, NAT GENET, V7, P125, DOI 10.1038/ng0694-125; TASKIN DP, 1992, AM REV RESPIR DIS, V145, P301; TAUSSIG LM, 1989, AM J EPIDEMIOL, V129, P1219; Togias A, 1997, INT ARCH ALLERGY IMM, V113, P87; TURKI J, 1995, J CLIN INVEST, V95, P1635, DOI 10.1172/JCI117838; WEITZMAN M, 1990, AM J DIS CHILD, V144, P1189; Winer BJ, 1971, STAT PRINCIPLES EXPT; Xu JF, 2001, AM J HUM GENET, V68, P1437, DOI 10.1086/320589; 1987, AM J RESP CRIT CARE, V136, P1285	35	84	85	2	3	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	SEP	2001	108	3					357	362		10.1067/mai.2001.117796		6	Allergy; Immunology	Allergy; Immunology	476FK	WOS:000171215400005	11544453	
J	Mihrshahi, S; Peat, JK; Webb, K; Tovey, ER; Marks, GB; Mellis, CM; Leeder, SR				Mihrshahi, S; Peat, JK; Webb, K; Tovey, ER; Marks, GB; Mellis, CM; Leeder, SR		CAPS Team	The Childhood Asthma Prevention Study (CAPS): Design and research protocol of a randomized trial for the primary prevention of asthma	CONTROLLED CLINICAL TRIALS			English	Article						Asthma; atopy; allergen avoidance; benzyl benzoate; fatty acid supplementation; house dust mite; primary prevention of asthma	FOOD-ALLERGEN AVOIDANCE; DUST MITE ALLERGENS; BRONCHIAL HYPERRESPONSIVENESS; RESPIRATORY SYMPTOMS; POPULATION-SAMPLE; FATTY-ACIDS; CHILDREN; INFANCY; ATOPY; RISK	The Childhood Asthma Prevention Study is a randomized controlled trial to measure whether the incidence of atopy and asthma can be reduced by house dust mite allergen reduction, a diet supplemented with omega-3 fatty acids, or a combination of both interventions. Six hundred and sixteen pregnant women whose unborn children were at high risk of developing asthma because of a family history were randomized prenatally. Study groups are as follows: Group A (placebo diet intervention, no house dust mite reduction), Group B (placebo diet intervention, active house dust mite reduction), Group C (active diet intervention, no house dust mite reduction), and Group D (active diet intervention, active house dust mite reduction). The house dust mite reduction intervention comprises use of physical and chemical methods to reduce allergen contact. The dietary intervention comprises use of a daily oil supplement from 6 months or at onset of bottle-feeding, and use of margarine and cooking oils based on sunflower or canola oils to increase omega-3 dietary intake. Data is collected quarterly until the infant is 1 year old and then half yearly until age 5 years. Questionnaires are used ti, collect respiratory illness history and information about diet and home environment. Dust is collected from the child's bed and bedroom and playroom floors. Blinded assessments are conducted at 18 months, 3 years, and 5 years. Skin prick tests to common allergens, blood tests, and detailed illness, medication use, and vaccination histories are collected. Primary outcomes will be the development of allergic sensitization and the presence and severity of asthma. This study is designed to measure the effectiveness of allergen reduction and dietary supplementation, both separately and in combination, for the primary prevention of atopy and asthma. The results of this study may have important implications for public health policies to reduce the incidence of childhood asthma. (C) Elsevier Science Inc. 2001.	Childrens Hosp, Clin Epidemiol Unit, Westmead, NSW 2145, Australia; Univ Sydney, Dept Paediat & Child Hlth, Sydney, NSW 2006, Australia; Univ Sydney, Dept Biochem, Fac Med, Sydney, NSW 2006, Australia; Univ Sydney, Dept Publ Hlth & Community Med, Sydney, NSW 2006, Australia; Univ Sydney, Inst Resp Med, Sydney, NSW 2006, Australia	Mihrshahi, S (reprint author), Childrens Hosp, Clin Epidemiol Unit, Locked Bag 4001, Westmead, NSW 2145, Australia.		Mihrshahi, Seema/A-9877-2009; Tovey, Euan/G-8604-2017	Mihrshahi, Seema/0000-0001-6567-9884; Tovey, Euan/0000-0002-1802-7266			American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P225, DOI DOI 10.1164/AJRCCM/136.1.225; ARM J P, 1988, Thorax, V43, P84, DOI 10.1136/thx.43.2.84; Asher MI, 1998, EUR RESPIR J, V12, P315; BITTINER SB, 1988, LANCET, V1, P3; Bjorksten B, 1996, CLIN EXP ALLERGY, V26, P775, DOI 10.1046/j.1365-2222.1996.d01-380.x; Black PN, 1997, EUR RESPIR J, V10, P6, DOI 10.1183/09031936.97.10010006; Custovic A, 1996, J ALLERGY CLIN IMMUN, V98, P64, DOI 10.1016/S0091-6749(96)70227-0; Custovic A, 2000, J ALLERGY CLIN IMMUN, V105, P252, DOI 10.1016/S0091-6749(00)90073-3; DRY J, 1991, INT ARCH ALLER A IMM, V95, P156; ENHERT B, 1992, J ALLERGY CLIN IMMUN, V90, P135; GRAY EJ, 1994, AUST NZ J MED, V24, P168, DOI 10.1111/j.1445-5994.1994.tb00553.x; HALKEN S, 1992, ALLERGY, V47, P545, DOI 10.1111/j.1398-9995.1992.tb00680.x; HAMMARQUIST C, 2000, COCHRANE DATABASE SY, V2; 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; Hodge L, 1996, MED J AUSTRALIA, V164, P137; Hodge L, 1998, EUR RESPIR J, V11, P361, DOI 10.1183/09031936.98.11020361; KREMER J, 1995, LANCET, P184; Kremer JM, 2000, AM J CLIN NUTR, V71, p349S; LANDS WEM, 1991, ANNU REV NUTR, V11, P41; LUCZYNSKA CM, 1989, J IMMUNOL METHODS, V118, P227, DOI 10.1016/0022-1759(89)90010-0; MAKRIDES M, 1995, LIPIDS, V30, P941, DOI 10.1007/BF02537486; MAKRIDES M, 1995, LANCET, V345, P1463, DOI 10.1016/S0140-6736(95)91035-2; MUNIR AKM, 1995, ALLERGY, V50, P55, DOI 10.1111/j.1398-9995.1995.tb02483.x; *NAT ASTHM CAMP, 1996, NAT ASTHM MAN HDB; Nishioka K, 1998, J ALLERGY CLIN IMMUN, V101, P28, DOI 10.1016/S0091-6749(98)70189-7; PEAT JK, 1992, EUR RESPIR J, V5, P921; PEAT JK, 1994, AUST NZ J MED, V24, P270, DOI 10.1111/j.1445-5994.1994.tb02171.x; PEAT JK, 1990, J ALLERGY CLIN IMMUN, V85, P65, DOI 10.1016/0091-6749(90)90223-Q; 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; PERONI DG, 1994, AM J RESP CRIT CARE, V149, P1442; PISTELLI R, 1993, EUR RESPIR J, V6, P517; SCHWARTZ J, 1990, AM J EPIDEMIOL, V132, P67; Soutar A, 1997, THORAX, V52, P166; SPORIK R, 1992, CLIN EXP ALLERGY, V22, P897, DOI 10.1111/j.1365-2222.1992.tb02062.x; THIEN FCK, 1993, AM REV RESPIR DIS, V147, P1138; von Mutius E, 2000, J ALLERGY CLIN IMMUN, V105, P9, DOI 10.1016/S0091-6749(00)90171-4; Warner J, 1990, PEDIATR ALLERGY IMMU, V1, P79, DOI 10.1111/j.1399-3038.1990.tb00015.x; WOODS RK, 2000, COCHRANE LIB; ZEIGER RS, 1995, J ALLERGY CLIN IMMUN, V95, P1179, DOI 10.1016/S0091-6749(95)70074-9; ZEIGER RS, 1989, J ALLERGY CLIN IMMUN, V84, P72, DOI 10.1016/0091-6749(89)90181-4	42	84	84	2	6	ELSEVIER SCIENCE INC	NEW YORK	655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA	0197-2456			CONTROL CLIN TRIALS	Controlled Clin. Trials	JUN	2001	22	3					333	354		10.1016/S0197-2456(01)00112-X		22	Medicine, Research & Experimental; Pharmacology & Pharmacy	Research & Experimental Medicine; Pharmacology & Pharmacy	435PW	WOS:000168890700010	11384793	
J	Tsang, KW; Ip, SK; Leung, R; Tipoe, GL; Chan, SL; Shum, IH; Ip, MS; Yan, C; Fung, PC; Chan-Yeung, M; Lam, W				Tsang, KW; Ip, SK; Leung, R; Tipoe, GL; Chan, SL; Shum, IH; Ip, MS; Yan, C; Fung, PC; Chan-Yeung, M; Lam, W			Exhaled nitric oxide: The effects of age, gender and body size	LUNG			English	Article						exhaled nitric oxide; aging; gender; body mass index; body surface area	OBSTRUCTIVE PULMONARY-DISEASE; CYSTIC-FIBROSIS; AIR; CHILDREN; BRONCHIECTASIS; MARKERS; ASTHMA; LUNGS; NASAL; NO	Since little is known of the effects of age, gender, and body size on exhaled nitric oxide (NO) production, we have conducted a prospective study to examine these factors in a healthy nonsmoking women (mean age +/- SD 47.7 +/- 15.8, range 20-79 years). Exhaled NO was measured by an automatic chemiluminescence analyzer (Sievers NO Analyser 280) at steady expiration. Men had significantly higher exhaled NO levels than women (p = 0.001). Although exhaled NO levels did not correlate with age (r = 0.12, p = 0.17), it correlated significantly with height (r = 0.23,p = 0.02), weight (r = 0.34,p < 0.001), body mass index (r = 0.25,p = 0.009), and body surface area (r = 0.42,p < 0.001) for the entire cohort. After making adjustment for age, height, weight, body mass index, and body surface area, exhaled NO levels were still significantly higher for men than for women (p = 0.004). Our data, therefore, could help explain the discrepancy in results of previous studies on exhaled NO production, which had not taken these parameters into account. Our findings should help researchers design future studies on evaluation of exhaled NO levels.	Univ Hong Kong, Queen Mary Hosp, Dept Med, Hong Kong, Hong Kong, Peoples R China; Univ Hong Kong, Queen Mary Hosp, Dept Anat, Hong Kong, Hong Kong, Peoples R China	Tsang, KW (reprint author), Univ Hong Kong, Queen Mary Hosp, Dept Med, Pokfulam Rd, Hong Kong, Hong Kong, Peoples R China.						BalfourLynn IM, 1996, ARCH DIS CHILD, V75, P319; Baraldi E, 1999, PEDIATR PULM, V27, P54, DOI 10.1002/(SICI)1099-0496(199901)27:1<54::AID-PPUL10>3.0.CO;2-V; Becklake MR, 1999, THORAX, V54, P1119; Chambers DC, 1998, THORAX, V53, P677; Corradi M, 1999, THORAX, V54, P572; CREMONA G, 1995, J APPL PHYSIOL, V78, P59; Delen FM, 2000, CHEST, V117, P695, DOI 10.1378/chest.117.3.695; Du Bois D, 1916, ARCH INTERN MED, V17, P863; GIAID A, 1995, NEW ENGL J MED, V333, P214, DOI 10.1056/NEJM199507273330403; Grasemann H, 1997, PEDIATR PULM, V24, P173, DOI 10.1002/(SICI)1099-0496(199709)24:3<173::AID-PPUL2>3.0.CO;2-O; Ho LP, 1998, EUR RESPIR J, V12, P1290, DOI 10.1183/09031936.98.12061290; JANGHORBANI M, 1993, INT J EPIDEMIOL, V22, P1056, DOI 10.1093/ije/22.6.1056; Jilma B, 1996, LIFE SCI, V58, P469, DOI 10.1016/0024-3205(95)02311-9; Karadag B, 1999, EUR RESPIR J, V13, P1402, DOI 10.1183/09031936.99.13614069; KEYS A, 1972, J CHRON DIS, V25, P329, DOI 10.1016/0021-9681(72)90027-6; 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, V151, P1889; Ludviksdottir D, 1999, EUR RESPIR J, V13, P739, DOI 10.1034/j.1399-3003.1999.13d07.x; MANCINELLI RL, 1983, APPL ENVIRON MICROB, V46, P198; Mattes J, 1999, EUR RESPIR J, V13, P1391, DOI 10.1183/09031936.99.13613969; Maziak W, 1998, AM J RESP CRIT CARE, V157, P998; MONCADA S, 1991, PHARMACOL REV, V43, P109; Murphy AW, 1998, CHEST, V114, P452, DOI 10.1378/chest.114.2.452; NATHAN CF, 1991, CURR OPIN IMMUNOL, V3, P65, DOI 10.1016/0952-7915(91)90079-G; Paredi P, 1999, CHEST, V115, P1352, DOI 10.1378/chest.115.5.1352; Piacentini GL, 2000, EUR RESPIR J, V15, P730, DOI 10.1034/j.1399-3003.2000.15d17.x; Rutgers SR, 1999, THORAX, V54, P576; Steerenberg PA, 1999, EUR RESPIR J, V13, P334, DOI 10.1034/j.1399-3003.1999.13b19.x	30	84	87	1	4	SPRINGER-VERLAG	NEW YORK	175 FIFTH AVE, NEW YORK, NY 10010 USA	0341-2040			LUNG	Lung	MAR-APR	2001	179	2					83	91		10.1007/s004080000050		9	Respiratory System	Respiratory System	489TL	WOS:000172007700002	11733851	
J	Trifilieff, A; Fujitani, Y; Mentz, F; Dugas, B; Fuentes, M; Bertrand, C				Trifilieff, A; Fujitani, Y; Mentz, F; Dugas, B; Fuentes, M; Bertrand, C			Inducible nitric oxide synthase inhibitors suppress airway inflammation in mice through down-regulation of chemokine expression	JOURNAL OF IMMUNOLOGY			English	Article							CELL-ADHESION MOLECULE-1; LUNG EPITHELIAL-CELLS; IN-VITRO; GENE-EXPRESSION; RAT LUNG; ASTHMATIC-PATIENTS; MURINE MODEL; EXHALED AIR; MODULATION; INDUCTION	Growing evidence demonstrates that inducible NO synthase (iNOS) is induced in the airways of asthmatic patients. However, the precise role of NO in the lung inflammation is unknown. This study investigated the effect of both selective and nonselective iNOS inhibitors in an allergen-driven murine lung inflammation model. OVA challenge resulted in an accumulation of eosinophils and neutrophils in the airways. Expression of iNOS immunostaining in lung sections together with an increase in calcium-independent NOS activity in lung homogenates was also observed after OVA challenge. Treatment with iNOS inhibitors from the day of challenge to the day of sacrifice resulted in an inhibition of the inflammatory cell influx together with a down-regulation of macrophage inflammatory protein-2 and monocyte chemoattractant protein-1 production. In contrast, eosinophilic and neutrophilic inhibition was not observed with treatment during the sensitization. Both treatments induced an increased production of Th2-type cytokines (IL-4 and IL-5) with a concomitant decrease in production of Thl-type cytokine (IFN-gamma). In vitro exposure of primary cultures of murine lung fibroblasts to a NO donor, hydroxylamine, induced a dose-dependent release of macrophage inflammatory protein-2 and monocyte chemoattractant protein-1. Our results suggest that lung inflammation after allergen challenge in mice is partially dependent on NO produced mainly by iNOS. NO appears to increase lung chemokine expression and, thereby, to facilitate influx of inflammatory cells into the airways.	Novartis Horsham Res Ctr, Horsham RH12 5AB, W Sussex, England; Hop La Pitie Salpetriere, Immunohematol Grp, Paris, France; Roche Biosci, Palo Alto, CA USA	Trifilieff, A (reprint author), Novartis Horsham Res Ctr, Wimblehurst Rd, Horsham RH12 5AB, W Sussex, England.						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Immunol.	AUG 1	2000	165	3					1526	1533				8	Immunology	Immunology	337CV	WOS:000088340600048	10903760	
J	Ledogar, RJ; Penchaszadeh, A; Garden, CCI; Acosta, LG				Ledogar, RJ; Penchaszadeh, A; Garden, CCI; Acosta, LG			Asthma and Latino cultures: Different prevalence reported among groups sharing the same environment	AMERICAN JOURNAL OF PUBLIC HEALTH			English	Article							PUERTO-RICAN CHILDREN; NEW-YORK-CITY; MEXICAN-AMERICAN; HEALTH; ALPHA-1-ANTITRYPSIN; VARIANTS; RISK	Objectives. This 1999 study measured asthma prevalence among Latinos of different cultural traditions who live on the same streets and in the same buildings. Methods. Health promoters from El Puente in North Brooklyn, New York City, surveyed 3015 people in 946 households, asking standard asthma prevalence questions. Results. Some 46%, of households identified themselves as Dominican, 42% as Puerto Rican, 6% as other Latino, and 6% as other. Reported asthma period prevalence was 5.3% (93 of 1749) among Dominicans and other Latinos, compared with 13.2% (147 of 1115)among Puerto Ricans (odds ratio = 0.37; 95% confidence interval = 0.28, 0.49), a difference not explained by location (cluster or building), household size, use of home remedies, educational attainment, or country where education was completed. Differences were least detectable among 13- to 24-year-olds of both sexes and sharpest among women aged 45 years and older and girls from birth to 12 years. Conclusions, Further research oil gene-environment interactions is needed among Puerto Ricans and Dominicans, but asthma's associations with low income and unhealthy environment, which more recent immigrants seem better able to withstand, should not be overlooked.	CIETintl, New York, NY 10011 USA; EI Puente, Brooklyn, NY USA	Ledogar, RJ (reprint author), CIETintl, 511 Ave Amer, Suite 132, New York, NY 10011 USA.						ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Beckett WS, 1996, AM J RESP CRIT CARE, V154, P894; BOURNIGAL EC, 1985, ARCH DOMINICANOS PED, V21, P9; CARTERPOKRAS OD, 1993, AM J PUBLIC HEALTH, V83, P580, DOI 10.2105/AJPH.83.4.580; Claudio L, 1999, J ASTHMA, V36, P343, DOI 10.3109/02770909909068227; COLP C, 1990, ARCH INTERN MED, V150, P2349, DOI 10.1001/archinte.150.11.2349; COLP C, 1993, CHEST, V103, P812, DOI 10.1378/chest.103.3.812; CRAIN EF, 1994, PEDIATRICS, V94, P356; Lara M, 1999, WESTERN J MED, V170, P75; Ledogar RJ, 1999, AM J PUBLIC HEALTH, V89, P1795, DOI 10.2105/AJPH.89.12.1795; Mendoza FS, 1999, WESTERN J MED, V170, P85; MENDOZA FS, 1991, JAMA-J AM MED ASSOC, V265, P227, DOI 10.1001/jama.265.2.227; MICHELE MA, 1996, J RESP CRIT CARE MED, V153, P1285; Miller RL, 1999, AM J PUBLIC HEALTH, V89, P819, DOI 10.2105/AJPH.89.6.819; Montealegre F, 1996, P R Health Sci J, V15, P113; *NY CIT DEP HLTH O, 1991, SUMM VIT STAT, V20; ORENGO JC, 1996, CAT WORKSH PUERT RIC; Pelkonen AS, 1997, AM J RESP CRIT CARE, V156, P1178; RIOS L, 1982, J LATIN COMMUNITY HL, V1, P25; SCHWARZ K, 1992, RIGHT BREATHE RIGHT	20	84	85	0	4	AMER PUBLIC HEALTH ASSOC INC	WASHINGTON	1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 USA	0090-0036			AM J PUBLIC HEALTH	Am. J. Public Health	JUN	2000	90	6					929	935		10.2105/AJPH.90.6.929		7	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	319HQ	WOS:000087335800019	10846511	
J	Soyka, MB; Wawrzyniak, P; Eiwegger, T; Holzmann, D; Treis, A; Wanke, K; Kast, JI; Akdis, CA				Soyka, Michael B.; Wawrzyniak, Paulina; Eiwegger, Thomas; Holzmann, David; Treis, Angela; Wanke, Kerstin; Kast, Jeannette I.; Akdis, Cezmi A.			Defective epithelial barrier in chronic rhinosinusitis: The regulation of tight junctions by IFN-gamma and IL-4	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Chronic rhinosinusitis; chronic sinusitis; tight junctions; occludin; claudin; zonula occludens; regulation; cytokines; leaky epithelium	HUMAN AIRWAY EPITHELIA; NASAL POLYPOSIS; CHRONIC SINUSITIS; CELLS; EXPRESSION; DISEASES; ASTHMA; DIFFERENTIATION; EPIDEMIOLOGY; INFLAMMATION	Background: Chronic rhinosinusitis (CRS) is a common disease with still unclear pathophysiologic mechanisms. Epithelial tight junctions (TJs) have been shown to be involved in different chronic disorders, including bronchial asthma, inflammatory bowel diseases, and skin disorders. The regulation of epithelial barrier function and TJ expression has not been extensively studied in patients with CRS and in the paranasal sinus epithelium thus far. Objective: We sought to elucidate the TJ expression pattern in the epithelium of the sinonasal mucosa and its regulation in patients with CRS. Methods: Trans-tissue resistance was measured in biopsy specimens from healthy control subjects and patients with CRS with and without nasal polyps. TJ protein expression was determined by using immunofluorescence, Western blotting, and real-time PCR. Primary epithelial cell cultures from patients with CRS and control subjects were used in air-liquid interface (ALI) cultures for the measurement of transepithelial resistance (TER) and TJ expression. The effect of IFN-gamma, IL-4, and IL-17 on ALI cultures was assessed. Results: A decreased trans-tissue resistance was found in biopsy specimens from patients with CRS with nasal polyps along with an irregular, patchy, and decreased expression of the TJ molecules occludin and zonula occludens 1. TER was reduced in ALI cultures from patients with CRS with nasal polyps. The cytokines IFN-gamma and IL-4 decreased TER, whereas IL-17 did not have any influence on epithelial integrity. Conclusion: A defective epithelial barrier was found in patients with CRS with nasal polyps along with a decreased expression of TJ proteins. The disruption of epithelial integrity by IFN-gamma and IL-4 in vitro indicates a possible role for these proinflammatory cytokines in the pathogenesis of patients with CRS. (J Allergy Clin Immunol 2012;130:1087-96.)	[Soyka, Michael B.; Wawrzyniak, Paulina; Eiwegger, Thomas; Treis, Angela; Wanke, Kerstin; Kast, Jeannette I.; Akdis, Cezmi A.] Univ Zurich, Swiss Inst Allergy & Asthma Res SIAF, CH-7270 Davos, Switzerland; [Soyka, Michael B.; Holzmann, David] Univ Zurich Hosp, Dept Otorhinolaryngol Head & Neck Surg, Zurich, Switzerland; [Eiwegger, Thomas] Med Univ Vienna, Dept Pediat, Vienna, Austria	Akdis, CA (reprint author), Univ Zurich, Swiss Inst Allergy & Asthma Res SIAF, Obere Str 22,7270 Davos Pl, CH-7270 Davos, Switzerland.	akdisac@siaf.uzh.ch	Kast, Jeannette/I-2397-2013		European Allergy and Asthma Center Davos (EACD); Swiss National Science Foundation [32-132899, 32-112306]; Christine Kuhne Center for Allergy Research and Education (CK-CARE); Muller-Gierok-Foundation; University Hospital Zurich; Muller-Gierok Foundation; European Allergy and Asthma Center Davos; Swiss National Foundation; CK-CARE; Novartis; PREDICTA; Swiss National Science Foundation; MeDALL; Global Allergy and Asthma European Network	The laboratory of C.A.A. is supported by the European Allergy and Asthma Center Davos (EACD), Swiss National Science Foundation grants 32-132899 and 32-112306, the Christine Kuhne Center for Allergy Research and Education (CK-CARE), the Muller-Gierok-Foundation, and University Hospital Zurich.; Disclosure of potential conflict of interest: M. B. Soyka has received research support from the Muller-Gierok Foundation, the European Allergy and Asthma Center Davos, the Swiss National Foundation, University Hospital Zurich, and CK-CARE and is employed by University Hospital Zurich. C. A. Akdis has received research support from Novartis, PREDICTA, the Swiss National Science Foundation, MeDALL, the Global Allergy and Asthma European Network, and CK-CARE; has provided legal consultation/expert witness testimony on the topics of Acellion T<INF>H</INF>2-specific receptors, Aventis T-cell Bell regulation, and allergen-specific immunotherapy (for Stallergenes and Allergopharma); is president of the European Academy of Allergy and Clinical Immunology, a GA <SUP>2</SUP>LEN ex-committee member, director of CK-CARE, and a fellow and interest group member for the American Academy of Allergy, Asthma & Immunology. The rest of the authors declare that they have no relevant conflicts of interest.	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Allergy Clin. Immunol.	NOV	2012	130	5					1087	+		10.1016/j.jaci.2012.05.052		20	Allergy; Immunology	Allergy; Immunology	030LE	WOS:000310571400009	22840853	
J	Peiser, M; Tralau, T; Heidler, J; Api, AM; Arts, JHE; Basketter, DA; English, J; Diepgen, TL; Fuhlbrigge, RC; Gaspari, AA; Johansen, JD; Karlberg, AT; Kimber, I; Lepoittevin, JP; Liebsch, M; Maibach, HI; Martin, SF; Merk, HF; Platzek, T; Rustemeyer, T; Schnuch, A; Vandebriel, RJ; White, IR; Luch, A				Peiser, M.; Tralau, T.; Heidler, J.; Api, A. M.; Arts, J. H. E.; Basketter, D. A.; English, J.; Diepgen, T. L.; Fuhlbrigge, R. C.; Gaspari, A. A.; Johansen, J. D.; Karlberg, A. T.; Kimber, I.; Lepoittevin, J. P.; Liebsch, M.; Maibach, H. I.; Martin, S. F.; Merk, H. F.; Platzek, T.; Rustemeyer, T.; Schnuch, A.; Vandebriel, R. J.; White, I. R.; Luch, A.			Allergic contact dermatitis: epidemiology, molecular mechanisms, in vitro methods and regulatory aspects Current knowledge assembled at an international workshop at BfR, Germany	CELLULAR AND MOLECULAR LIFE SCIENCES			English	Review						Contact allergy; Dermatitis; Epidemiology; Molecular mechanisms; Regulatory aspects	LYMPH-NODE ASSAY; OCCUPATIONAL SKIN-DISEASE; HUMAN DENDRITIC CELLS; RECEPTOR ACCESSORY PROTEIN; PIG MAXIMIZATION TEST; NECROSIS-FACTOR-ALPHA; N-ACETYLTRANSFERASE 1; TOLL-LIKE RECEPTOR; EFFECTOR T-CELLS; TEST H-CLAT	Contact allergies are complex diseases, and one of the important challenges for public health and immunology. The German 'Federal Institute for Risk Assessment' hosted an 'International Workshop on Contact Dermatitis'. The scope of the workshop was to discuss new discoveries and developments in the field of contact dermatitis. This included the epidemiology and molecular biology of contact allergy, as well as the development of new in vitro methods. Furthermore, it considered regulatory aspects aiming to reduce exposure to contact sensitisers. An estimated 15-20% of the general population suffers from contact allergy. Workplace exposure, age, sex, use of consumer products and genetic predispositions were identified as the most important risk factors. Research highlights included: advances in understanding of immune responses to contact sensitisers, the importance of autoxidation or enzyme-mediated oxidation for the activation of chemicals, the mechanisms through which hapten-protein conjugates are formed and the development of novel in vitro strategies for the identification of skin-sensitising chemicals. Dendritic cell cultures and structure-activity relationships are being developed to identify potential contact allergens. However, the local lymph node assay (LLNA) presently remains the validated method of choice for hazard identification and characterisation. At the workshop the use of the LLNA for regulatory purposes and for quantitative risk assessment was also discussed.	[Peiser, M.; Tralau, T.; Heidler, J.; Platzek, T.; Luch, A.] German Fed Inst Risk Assessment BfR, Dept Prod Safety, D-14195 Berlin, Germany; [Api, A. M.] Res Inst Fragrance Mat, Hackensack, NJ USA; [Arts, J. H. E.] AkzoNobel NV, Arnhem, Netherlands; [Basketter, D. A.] DABMEB Consultancy Ltd, Sharnbrook, Beds, England; [English, J.] Univ Nottingham Hosp, Nottingham NG7 2UH, England; [Diepgen, T. L.] Univ Heidelberg, Dept Social Med Occupat & Environm Dermatol, Heidelberg, Germany; [Fuhlbrigge, R. C.] Harvard Skin Dis Res Ctr, Boston, MA USA; [Gaspari, A. A.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA; [Johansen, J. D.] Univ Copenhagen, Dept Dermaallergol, Gentofte Hosp, Copenhagen, Denmark; [Karlberg, A. T.] Univ Gothenburg, Dept Chem Dermatochem & Skin Allergy, Gothenburg, Sweden; [Kimber, I.] Univ Manchester, Fac Life Sci, Manchester, Lancs, England; [Lepoittevin, J. P.] Univ Strasbourg, Strasbourg, France; [Liebsch, M.; Luch, A.] German Fed Inst Risk Assessment BfR, Dept Expt Toxicol, D-14195 Berlin, Germany; [Liebsch, M.; Luch, A.] German Fed Inst Risk Assessment BfR, ZEBET, Ctr Alternat Anim Testing, D-14195 Berlin, Germany; [Maibach, H. I.] Univ Calif San Francisco, Dept Dermatol, San Francisco, CA 94143 USA; [Martin, S. F.] Univ Med Ctr Freiburg, Allergy Res Grp, Dept Dermatol, Freiburg, Germany; [Merk, H. F.] Univ Hosp Aachen, Dept Dermatol & Allergol, Aachen, Germany; [Rustemeyer, T.] Vrije Univ Amsterdam, Med Ctr, Amsterdam, Netherlands; [Schnuch, A.] Univ Gottingen, Dept Dermatol, Gottingen, Germany; [Vandebriel, R. J.] Natl Inst Publ Hlth & Environm, NL-3720 BA Bilthoven, Netherlands; [White, I. R.] St Thomas Hosp, St Johns Inst Dermatol, London, England	Tralau, T (reprint author), German Fed Inst Risk Assessment BfR, Dept Prod Safety, Thielallee 88-92, D-14195 Berlin, Germany.	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J	Chung, KF				Chung, Kian Fan			p38 Mitogen-Activated Protein Kinase Pathways in Asthma and COPD	CHEST			English	Article							AIRWAY SMOOTH-MUSCLE; NF-KAPPA-B; RELATIVE CORTICOSTEROID INSENSITIVITY; OBSTRUCTIVE PULMONARY-DISEASE; HUMAN ALVEOLAR MACROPHAGES; HEAT-SHOCK-PROTEIN; MAP-KINASE; GLUCOCORTICOID-RECEPTOR; CELL-MIGRATION; CYTOKINE RELEASE	The mitogen-activated protein kinase (MAPK) family includes the p38 kinases, which consist of highly conserved proline-directed serine-threonine protein kinases that are activated in response to inflammatory signals. Of the four isoforms, p38 alpha is the most abundant in inflammatory cells and has been the most studied through mainly the availability of small molecule inhibitors. The p38 substrates include transcription factors; other protein kinases, which in turn phosphorylate transcription factors; cytoskeletal proteins and translational components; and other enzymes. Both asthma and COPD are characterized by chronic airflow obstruction, airway and lung remodeling, and chronic inflammation. p38 is involved in the inflammatory responses induced by cigarette smoke exposure, endotoxin, and oxidative stress through activation and release of proinflammatory cytokines/chemokines, posttranslational regulation of these genes, and activation of inflammatory cell migration. Inhibition of p38 MAPK prevented allergen-induced pulmonary eosinophilia, mucus hypersecretion, and airway hyperresponsiveness, effects that may partly result from p38 activation on eosinophil apoptosis and on airway smooth muscle cell production of cytokines/chemokines. In addition, p38 regulates the augmented contractile response induced by oxidative stress. The activation of p38 observed in epithelial cells and macrophages also may underlie corticosteroid insensitivity of severe asthma and COPD. Therefore, p38 inhibitors present a potential attractive treatment of these conditions. Second-generation p38 inhibitors have been disappointing in the treatment of rheumatoid arthritis. In two 6-week studies in patients with COPD, the results were encouraging. Side effects such as liver toxicity remain a possibility, and whether the beneficial effects of p38 inhibitors are clinically significant and sustained need to be determined. CHEST 2011; 139(6):1470-1479	[Chung, Kian Fan] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW3 6LY, England; [Chung, Kian Fan] Royal Brompton Hosp, Biomed Res Unit, London SW3 6LY, England	Chung, KF (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dovehouse St, London SW3 6LY, England.	f.chung@imperial.ac.uk		Chung, Kian Fan/0000-0001-7101-1426	Wellcome Trust; Asthma UK; Medical Research Council; Biomedical Research Unit of Royal Brompton Hospital; National Heart and Lung Institute, Imperial College	Dr Chung is supported by grants from the Wellcome Trust, Asthma UK, and Medical Research Council and by the Biomedical Research Unit of Royal Brompton Hospital and National Heart and Lung Institute, Imperial College.	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J	Morello-Frosch, R; Zuk, M; Jerrett, M; Shamasunder, B; Kyle, AD				Morello-Frosch, Rachel; Zuk, Miriam; Jerrett, Michael; Shamasunder, Bhavna; Kyle, Amy D.			Understanding The Cumulative Impacts Of Inequalities In Environmental Health: Implications For Policy	HEALTH AFFAIRS			English	Article							SELF-RATED HEALTH; ADVERSE BIRTH OUTCOMES; AMBIENT AIR-POLLUTION; UNITED-STATES; CARDIOVASCULAR-DISEASE; CHILDHOOD ASTHMA; HAZARDOUS-WASTE; RISK-ASSESSMENT; OLDER-ADULTS; DISPARITIES	Racial or ethnic minority groups and low-income communities have poorer health outcomes than others. They are more frequently exposed to multiple environmental hazards and social stressors, including poverty, poor housing quality, and social inequality. Researchers are grappling with how best to characterize the cumulative effects of these hazards and stressors in order to help regulators and decision makers craft more-effective policies to address health and environmental disparities. In this article we synthesize the existing scientific evidence regarding the cumulative health implications of higher rates of exposure to environmental hazards, along with individual biological susceptibility and social vulnerability. We conclude that current environmental policy, which is focused narrowly on pollutants and their sources, should be broadened to take into account the cumulative impact of exposures and vulnerabilities encountered by people who live in neighborhoods consisting largely of racial or ethnic minorities or people of low socioeconomic status.	[Morello-Frosch, Rachel; Shamasunder, Bhavna] Univ Calif Berkeley, Dept Environm Sci Policy & Management, Berkeley, CA 94720 USA; [Jerrett, Michael; Kyle, Amy D.] Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA	Morello-Frosch, R (reprint author), Univ Calif Berkeley, Dept Environm Sci Policy & Management, Berkeley, CA 94720 USA.	rmf@berkeley.edu		Morello-Frosch, Rachel/0000-0003-1153-7287	California Environmental Protection Agency, Office of Environmental Health Hazard Assessment [07-E0009]; National Institute of Environmental Health Sciences	This work was funded in part by the California Environmental Protection Agency, Office of Environmental Health Hazard Assessment (07-E0009, Understanding and Acting on Cumulative Impacts on California Communities) and the Superfund Research Program of the National Institute of Environmental Health Sciences. The authors thank Valerie Tran for assistance with preparing this manuscript.	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MAY	2011	30	5					879	887		10.1377/hlthaff.2011.0153		9	Health Care Sciences & Services; Health Policy & Services	Health Care Sciences & Services	761WD	WOS:000290430800011	21555471	
J	McPherson, EG; Simpson, JR; Xiao, QF; Wu, CX				McPherson, E. Gregory; Simpson, James R.; Xiao, Qingfu; Wu, Chunxia			Million trees Los Angeles canopy cover and benefit assessment	LANDSCAPE AND URBAN PLANNING			English	Article						Ecosystem services; Urban forestry; Tree canopy cover; Tree benefits	URBAN FOREST; CALIFORNIA; VEGETATION; HEALTH; ASTHMA; COSTS; AREAS	The Million Trees LA initiative intends to improve Los Angeles's environment through planting and stewardship of 1 million trees. The purpose of this study was to measure Los Angeles's existing tree canopy cover (TCC), determine if space exists for 1 million additional trees, and estimate future benefits from the planting. High-resolution QuickBird remote sensing data, aerial photographs, and geographic information systems were used to classify land cover types, measure TCC, and identify potential tree planting sites. Benefits were forecast for planting of 1 million trees between 2006 and 2010, and their growth and mortality were projected until 2040. Two scenarios reflected low (17%) and high (56%) mortality rates. Numerical models were used with geographic data and tree size information for coastal and inland climate zones to calculate annual benefits and their monetary value. Los Angeles's existing TCC was 21%, and ranged from 7 to 37% by council district. There was potential to add 2.5 million additional trees to the existing population of approximately 10.8 million, but only 1.3 million of the potential tree sites are deemed realistic to plant. Benefits for the 1-million-tree planting for the 35-year period were $1.33 billion and $1.95 billion for the high- and low-mortality scenarios, respectively. Average annual benefits were $38 and $56 per tree planted. Eighty-one percent of total benefits were aesthetic/other, 8% were stormwater runoff reduction, 6% energy savings, 4% air quality improvement, and less than 1% atmospheric carbon reduction. Published by Elsevier B.V.	[McPherson, E. Gregory; Simpson, James R.] US Forest Serv, USDA, Pacific SW Res Stn, Ctr Urban Forest Res, Davis, CA 95618 USA; [Xiao, Qingfu; Wu, Chunxia] Univ Calif Davis, Dept Land Air & Water Resources, Davis, CA 95616 USA	McPherson, EG (reprint author), US Forest Serv, USDA, Pacific SW Res Stn, Ctr Urban Forest Res, 1731 Res Pk Dr, Davis, CA 95618 USA.	gmcpherson@fs.fed.us; jrsimpson@fs.fed.us; qxiao@ucdavis.edu; chelseawu2@gmail.com			City of Los Angeles, California	This research was supported by funds provided by the city of Los Angeles, California, and we thank Paula Daniels, George Gonzalez, Lisa Sarno, and Lillian Kawasaki for their support. We wish to acknowledge Patrice Gin, Randy Price. and Kirk Bishop (Public Works/Bureau of Engineering/Mapping Division, city of Los Angeles) for sharing their GIS data and aerial imagery with us. Rebecca Drayse, Edith Ben-Horin, and David O'Donnell of TreePeople led the survey of field plots. Thanks to Dan Knapp, Los Angeles Conservation Corp, who assisted with development of the planting scenarios. Kelaine Vargas and Paula Peper at the U.S. Forest Service Center for Urban Forest Research provided technical and editorial assistance throughout the course of the study.	*AM FOR, 2002, PROJ BEN COMM TREE P; *AM FOR, 2002, URB EC AN WASH DC ME; Anderson L. 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J	Chang, C				Chang, Christopher			The immune effects of naturally occurring and synthetic nanoparticles	JOURNAL OF AUTOIMMUNITY			English	Article; Proceedings Paper	7th International Congress on Autoimmunity	MAY 05-09, 2010	Ljubljana, SLOVENIA			Ultrafine particles; Nanoparticles; Nanotechnology; Air pollution; Climate change; Diesel exhaust particles; Asthma; Anthropogenic; Environmental tobacco smoke; Particulate matter; PM(2.5); PM(10); Oxidative stress; Adjuvants; Reactive oxygen species; Carbon nanotubes; Autoimmunity	DIESEL EXHAUST PARTICLES; INHALED ULTRAFINE PARTICLES; COLLAGEN-INDUCED ARTHRITIS; BLOOD MONONUCLEAR-CELLS; OXIDATIVE STRESS; AIR-POLLUTION; PARTICULATE MATTER; TITANIUM-DIOXIDE; IN-VIVO; EPITHELIAL-CELLS	Ultrafine particles and engineered nanoparticles have unique aerodynamic and biochemical properties that affect the immune system and human health in ways that are different from or exceed those seen with gases or larger particulates. These effects result from a unique set of physical characteristics and surface moieties, which generate an ability of UFPs to enter tissues and cells, interact with proteins and DNA at a molecular level and directly and indirectly modulate the immune system by novel mechanisms. In recent years, a new field known as nanotechnology has impacted multiple industries by taking advantage of the special qualities of these small "atomic-sized" particles. Nanomedicine has already opened up a new avenue of research in cancer therapy, drug delivery and immune regulation. While the benefits of this new science to human civilization are seemingly immeasurable, it is also important to appreciate that these particles can also lead to harmful effects on human health. In vitro and animal studies are showing that nanoparticles and UFPs are capable of activating proinflammatory cytokines, chemokines and adhesion molecules, with recruitment of inflammatory cells including basophils, macrophages, dendritic cells, T cells, neutrophils and eosinophils. These changes may have an impact on immune defense, but also on the Th1/Th2 balance, and even on non-immunologic function. Resulting immune system derangement can lead to increases in incidence of autoimmune, allergic and even neoplastic diseases. Cardiorespiratory effects have been observed to occur in humans. Much further research is needed to establish safe exposure levels for this important new class of particulates. (C) 2009 Elsevier Ltd. All rights reserved.	Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA	Chang, C (reprint author), Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, 451 Hlth Sci Dr,Suite 6510, Davis, CA 95616 USA.	c3chang@yahoo.com					Allen TM, 2004, SCIENCE, V303, P1818, DOI 10.1126/science.1095833; Araujo JA, 2008, CIRC RES, V102, P589, DOI 10.1161/CIRCRESAHA.107.164970; Asgharian B, 2007, INHAL TOXICOL, V19, P1045, DOI 10.1080/08958370701626501; Augustin MA, 2009, ADV FOOD NUTR RES, V58, P183, DOI 10.1016/S1043-4526(09)58005-9; BAINTON DF, 1989, AM J PATHOL, V134, P15; Bartra J, 2007, J INVEST ALLERG CLIN, V17, P3; Becker S, 2003, J TOXICOL ENV HEAL A, V66, P847, DOI 10.1080/15287390390156227; Bernstein JA, 2004, J ALLERGY CLIN IMMUN, V114, P1116, DOI 10.1016/j.jaci.2004.08.030; Bhattacharya K, 2008, J TOXICOL ENV HEAL A, V71, P976, DOI 10.1080/15287390801989218; Bleck B, 2006, J IMMUNOL, V176, P7431; Borchers AT, 2006, CLIN REV ALLERG IMMU, V31, P1, DOI 10.1385/CRIAI:31:1:1; Brauner EV, 2007, ENVIRON HEALTH PERSP, V115, P1177, DOI 10.1289/ehp.9984; 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J	Pergola, C; Werz, O				Pergola, Carlo; Werz, Oliver			5-Lipoxygenase inhibitors: a review of recent developments and patents	EXPERT OPINION ON THERAPEUTIC PATENTS			English	Review						arachidonic acid; asthma; inflammation; inhibitors; leukotriene; 5-lipoxygenase	PROSTAGLANDIN E-2 SYNTHASE-1; CYTOSOLIC PHOSPHOLIPASE A(2); PHARMACOPHORE BIOLOGICAL EVALUATION; HUMAN POLYMORPHONUCLEAR LEUKOCYTES; COACTOSIN-LIKE PROTEIN; DUAL INHIBITORS; LEUKOTRIENE B-4; ANTIINFLAMMATORY ACTIVITY; ARACHIDONATE 5-LIPOXYGENASE; PHARMACOLOGICAL PROFILE	Importance to the field: Leukotrienes (LTs) are pivotal lipid mediators of inflammation and allergy and results from recent studies also suggest roles of LTs in cardiovascular diseases, cancer and osteoporosis. 5-Lipoxygenase (5-LO) catalyzes the first step in the biosynthesis of LTs from arachidonic acid, and based on the multiple potent pathophysiological actions of LTs, the pharmacological intervention with 5-LO is a challenge in the development of therapeutics. Areas covered in this review: We first summarize the biochemical regulation of 5-LO and the general pharmacological concepts in 5-LO inhibition by currently available compounds, and subsequently we report recent developments deduced from recent scientific publications and patents. What the reader will gain: A comprehensive overview about the different molecular pharmacological strategies to inhibit 5-LO and the most successful previous 5-LO inhibitors. The review also gives insights into novel concepts, for example, dual prostaglandin/LT synthesis inhibition and reveals novel compounds patented or developed within the past 5 years. Take home message: Despite the increasing therapeutic indications of anti-LT therapy, the progress in the development of novel 5-LO inhibitors is moderate. However, novel molecular concepts in the intervention with LT biosynthesis seem promising.	[Pergola, Carlo; Werz, Oliver] Univ Tubingen, Inst Pharmaceut, Dept Pharmaceut Analyt, D-72076 Tubingen, Germany	Werz, O (reprint author), Univ Tubingen, Inst Pharmaceut, Dept Pharmaceut Analyt, Morgenstelle 8, D-72076 Tubingen, Germany.	oliver.werz@uni-tuebingen.de					Albert D, 2002, BIOCHEM PHARMACOL, V64, P1767, DOI 10.1016/S0006-2952(02)01387-4; Araico A, 2007, LIFE SCI, V80, P2108, DOI 10.1016/j.lfs.2007.03.017; Araico A, 2006, LIFE SCI, V78, P2911, DOI 10.1016/j.lfs.2005.11.017; Austen KF, 2007, PROSTAG OTH LIPID M, V83, P182, DOI 10.1016/j.prostaglandins.2007.01.004; Back M, 2005, P NATL ACAD SCI USA, V102, P17501, DOI 10.1073/pnas.0505845102; Back M, 2007, PROSTAG OTH LIPID M, V83, P209, DOI 10.1016/j.prostaglandins.2007.01.008; Back M, 2007, CIRC RES, V100, P946, DOI 10.1161/01.RES.0000264498.60702.0d; Back M, 2009, CURR PHARM DESIGN, V15, P3116; Bannenberg GL, 2009, CURR OPIN DRUG DISC, V12, P644; Bellido-Reyes YA, 2006, TRANSPLANTATION, V81, P1700, DOI 10.1097/01.tp.0000226065.82066.21; 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J	Martino, DJ; Prescott, SL				Martino, D. J.; Prescott, S. L.			Silent mysteries: epigenetic paradigms could hold the key to conquering the epidemic of allergy and immune disease	ALLERGY			English	Review						acetylation; allergic disease; epigenetics; methylation; susceptibility	IFN-GAMMA PROMOTER; DNA METHYLATION CHANGES; T-CELL DIFFERENTIATION; FOXP3 GENE-EXPRESSION; AIRWAY INFLAMMATION; IN-UTERO; HISTONE DEACETYLASES; TH2 DIFFERENTIATION; LINEAGE COMMITMENT; CYTOKINE RESPONSES	P>Epigenetic mechanisms provide new insights into how environmental changes may mediate the increasing propensity for complex immune diseases such as allergic disease. There is now strong evidence that early environmental exposures play a key role in activating or silencing genes by altering DNA and histone methylation, histone acetylation and chromatin structure. These modifications determine the degree of DNA compaction and accessibility for gene transcription, altering gene expression, phenotype and disease susceptibility. While there is already evidence that a number of early environmental exposures are associated with an increased risk of allergic disease, several new studies indicate in utero microbial and dietary exposures can modify gene expression and allergic disease propensity through epigenetic modification. This review explores the evidence that immune development is under clear epigenetic regulation, including the pattern of T helper (Th)1 and Th2 cell differentiation, regulatory T cell differentiation, and more recently, Th17 development. It also considers the mechanisms of epigenetic regulation and early immune defects in allergy prone neonates. The inherent plasticity conferred by epigenetic mechanisms clearly also provides opportunities for environmental strategies that can re-programme gene expression for disease prevention. Identifying genes that are differentially silenced or activated in relation to subsequent disease will not only assist in identifying causal pathways, but may also help identify the contributing environmental factors.	[Martino, D. J.; Prescott, S. L.] Univ Western Australia, Sch Pediat & Child Hlth Res, Perth, WA 6001, Australia	Martino, DJ (reprint author), Univ Western Australia, Sch Pediat & Child Hlth Res, Perth, WA 6001, Australia.		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J	Aguilera-Aguirre, L; Bacsi, A; Saavedra-Molina, A; Kurosky, A; Sur, S; Boldogh, I				Aguilera-Aguirre, Leopoldo; Bacsi, Attila; Saavedra-Molina, Alfredo; Kurosky, Alexander; Sur, Sanjiv; Boldogh, Istvan			Mitochondrial Dysfunction Increases Allergic Airway Inflammation	JOURNAL OF IMMUNOLOGY			English	Article							ELECTRON-TRANSPORT CHAIN; OXIDATIVELY DAMAGED PROTEINS; CYTOCHROME BC(1) COMPLEX; GEL-ELECTROPHORESIS; CORE PROTEINS; ASTHMA; STRESS; POLLEN; CELLS; IDENTIFICATION	The prevalence of allergies and asthma among the world's population has been steadily increasing due to environmental factors. It has been described that exposure to ozone, diesel exhaust particles, or tobacco smoke exacerbates allergic inflammation in the lungs. These environmental oxidants increase the levels of cellular reactive oxygen species (ROS) and induce mitochondrial dysfunction in the airway epithelium. In this study, we investigated the involvement of preexisting mitochondrial dysfunction in the exacerbation of allergic airway inflammation. After cellular oxidative insult induced by ragweed pollen extract (RWE) exposure, we have identified nine oxidatively damaged mitochondrial respiratory chain-complex and associated proteins. Out of these, the ubiquinol-cytochrome c reductase core II protein (UQCRC2) was found to be implicated in mitochondrial ROS generation from respiratory complex III. Mitochondrial dysfunction induced by deficiency of UQCRC2 in airway epithelium of sensitized BALB/c mice prior the RWE challenge increased the Ag-induced accumulation of eosinophils, mucin levels in the airways, and bronchial hyperresponsiveness. Deficiency of UQCRC1, another oxidative damage-sensitive complex III protein, did not significantly alter cellular ROS levels or the intensity of RWE-induced airway inflammation. These observations suggest that preexisting mitochondrial dysfunction induced by oxidant environmental pollutants is responsible for the severe symptoms in allergic airway inflammation. These data also imply that mitochondrial defects could be risk factors and may be responsible for severe allergic disorders in atopic individuals. The Journal of Immunology, 2009, 183: 5379-5387.	[Aguilera-Aguirre, Leopoldo; Bacsi, Attila; Boldogh, Istvan] Univ Texas Galveston, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA; [Kurosky, Alexander] Univ Texas Galveston, Med Branch, Dept Biochem & Mol Biol, Galveston, TX 77555 USA; [Sur, Sanjiv] Univ Texas Galveston, Med Branch, Dept Internal Med, Galveston, TX 77555 USA; [Aguilera-Aguirre, Leopoldo; Saavedra-Molina, Alfredo] Univ Michoacana, Inst Invest Quim Biol, Morelia, Michoacan, Mexico; [Bacsi, Attila] Univ Debrecen, Fac Med, Med & Hlth Sci Ctr, Inst Immunol, H-4012 Debrecen, Hungary	Boldogh, I (reprint author), Univ Texas Galveston, Med Branch, Dept Microbiol & Immunol, 301 Univ Blvd, Galveston, TX 77555 USA.	sboldogh@utmb.edu		Aguilera-Aguirre, Leopoldo/0000-0001-7964-7402	National Institute of Allergy and Infectious Diseases [P01 A1062885-01]; National Institutes of Health [HL071163, NO1HV-28184]; National Institute on Environmental Health Sciences Center [EOS 006677]; Hungarian Scientific Research Fund [73347]	This work was supported by National Institute of Allergy and Infectious Diseases Grant P01 A1062885-01 (to I.B. and S.S.), National Institutes of Health Grant HL071163 (to S.S. and I.B.), National Institutes of Health, National Heart. Lung, and Blood Institute Proteornics Initiative NO1HV-28184 (to A.K.), National Institute on Environmental Health Sciences Center Grant EOS 006677 (to I.B. and A.K.), and the Hungarian Scientific Research Fund 73347 (to A.B.).	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Immunol.	OCT 15	2009	183	8					5379	5387				9	Immunology	Immunology	507DC	WOS:000270830300065	19786549	
J	Douwes, J; Cheng, S; Travier, N; Cohet, C; Niesink, A; McKenzie, J; Cunningham, C; Le Gros, G; von Mutius, E; Pearce, N				Douwes, J.; Cheng, S.; Travier, N.; Cohet, C.; Niesink, A.; McKenzie, J.; Cunningham, C.; Le Gros, G.; von Mutius, E.; Pearce, N.			Farm exposure in utero may protect against asthma, hay fever and eczema	EUROPEAN RESPIRATORY JOURNAL			English	Article						asthma; farming; hygiene hypothesis; prenatal; timing	ALLERGY	The aim of the present study was to assess which factors contribute to the lower prevalence of allergic diseases in farmers' children, and the importance of timing of exposure. In a cross-sectional questionnaire survey, asthma symptoms, hay fever and eczema were assessed, as well as current, early and prenatal farm-related exposures in 1,333 farmers' children and 566 reference children aged 5-17 yrs. Farmers' children had a lower incidence of asthma symptoms and eczema. Current and maternal exposure during pregnancy to animals and/or grain and hay reduced the risk of asthma symptoms, hay fever and eczema. The exposure-response association for maternal exposure was nonlinear for most outcomes. After mutual adjustment, the effects of prenatal exposure remained unchanged whereas current exposure remained protective only for asthma medication, asthma ever and hay fever. Exposure during the first 2 yrs was not associated with symptoms, after controlling for prenatal exposure. A combination of prenatal and current exposure was most strongly associated with wheeze (odds ratio (OR) 0.48, 95% confidence interval (CI) 0.28-0.80), asthma medication (OR 0.50, 95% Cl 0.30-0.82), asthma ever (OR 0.50, 95% Cl 0.33-0.76), hay fever (OR 0.47, 95% Cl 0.30-0.73) and eczema (OR 0.46, 95% Cl 0.30-0.70). Prenatal exposure may contribute to the low prevalence of asthma, hay fever and eczema in farmers' children, but continued exposure may be required to maintain optimal protection.	[Douwes, J.; Cheng, S.; Travier, N.; Cohet, C.; Niesink, A.; Pearce, N.] Massey Univ, Res Sch Publ Hlth, Res Ctr Maori Hlth & Dev, Palmerston North, New Zealand; [Cunningham, C.] Massey Univ, Res Sch Publ Hlth, Res Ctr Maori Hlth & Dev, Palmerston North, New Zealand; [Le Gros, G.] Victoria Univ, Malaghan Inst Med Res, Wellington, New Zealand; [McKenzie, J.] Massey Univ, Inst Vet Anim & Biomed Sci, Epictr, Palmerston North, New Zealand; [von Mutius, E.] Univ Munich, Dr Von Hauner Childrens Hosp, Munich, Germany	Douwes, J (reprint author), Private Box 756, Wellington, New Zealand.	j.douwes@massey.ac.nz	Le Gros, Graham/C-6725-2011	Pearce, Neil/0000-0002-9938-7852; Douwes, Jeroen/0000-0003-3599-4036	Centre for Public Health Research; Sir Charles Hercus Research; Health Research Council of New Zealand	The Centre for Public Health Research is supported by a Programme Grant that includes funding for the current study and J. Douwes is supported by a Sir Charles Hercus Research Fellowship, both from the Health Research Council of New Zealand.	Douwes J, 2006, J ALLERGY CLIN IMMUN, V117, P1067, DOI 10.1016/j.jaci.2006.02.002; Perkin MR, 2006, J ALLERGY CLIN IMMUN, V117, P1374, DOI 10.1016/j.jaci.2006.03.008	2	83	86	1	13	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	SEP	2008	32	3					603	611		10.1183/09031936.00033707		9	Respiratory System	Respiratory System	351OG	WOS:000259433100012	18448493	
J	Purohit, A; Niederberger, V; Kronqvist, M; Horak, F; Gronneberg, R; Suck, R; Weber, B; Fiebig, H; van Hage, M; Pauli, G; Valenta, R; Cromwell, O				Purohit, A.; Niederberger, V.; Kronqvist, M.; Horak, F.; Gronneberg, R.; Suck, R.; Weber, B.; Fiebig, H.; van Hage, M.; Pauli, G.; Valenta, R.; Cromwell, O.			Clinical effects of immunotherapy with genetically modified recombinant birch pollen Bet v 1 derivatives	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergen variants; allergic rhinitis; allergy; Bet v 1; birch pollen; immunotherapy; recombinant allergens	BET V 1; ALLERGEN-SPECIFIC IMMUNOTHERAPY; QUANTITATIVE IGE INHIBITION; LATE ASTHMATIC REACTIONS; WILD-TYPE; VACCINATION; SENSITIVITY; TRANSITION; POPULATION; CANDIDATES	Background Birch pollen and pollen from related trees of the Fagales order are a major cause of allergic rhinitis, conjunctivitis, and asthma through the spring season in northern and central Europe. Objective To investigate the clinical effects of injection immunotherapy with genetically modified derivatives of major birch pollen allergen Bet v 1 on pollen-induced allergic symptoms. Methods A three-arm double-blind placebo-controlled immunotherapy study was conducted with one pre-seasonal course of treatment using two derivatives of Bet v 1, namely a recombinant Bet v 1 trimer and an equimolar mixture of two recombinant Bet v 1 fragments together representing the whole protein sequence. Analysis of local and systemic adverse events was performed for 124 patients who had received at least one dose of medication. Clinical efficacy was monitored by symptom medication scores and interval scoring in the per protocol-treated population (n=84). In addition, skin and nasal provocation responses and allergen-specific antibodies were assessed. Results There were trends towards improvement in the subjects' well-being and clinical symptoms (nasal scores), although comparisons with a placebo group did not show statistical significance in the main end-point, the combined symptom medication score. Reductions in skin and nasal sensitivity were observed for some subjects with a trend for the Bet v 1 trimer to be more effective than the fragments. Treatment induced strong IgG1 and IgG4 allergen-specific antibody responses. Local injection-site reactions were most frequent in the trimer group affecting 59.5% of patients as opposed to 37.8% and 30.6% in the fragment and placebo groups, respectively. Systemic reactions were elicited more frequently by fragments. A large proportion of adverse side-effects appeared hours following injections, and might be attributable to concurrent exposure to related pollens. Conclusion Single courses of injection immunotherapy with Bet v 1 allergen derivatives showed trends towards improved well-being and reduced reactivity to specific allergen provocation, but did not yield significant improvement in the combined symptom medication score in this study.	[Purohit, A.; Pauli, G.] Hop Univ Strasbourg, Serv Pneumol, Strasbourg, France; [Niederberger, V.; Kronqvist, M.; Horak, F.] Med Univ Vienna, Dept Otorhinolaryngol, Vienna, Austria; [Kronqvist, M.; van Hage, M.] Karolinska Inst, Dept Med, Allergy & Clin Immunol Unit, Stockholm, Sweden; [Kronqvist, M.; Gronneberg, R.; van Hage, M.] Univ Hosp, Stockholm, Sweden; [Gronneberg, R.] Karolinska Inst, Dept Med, Resp Med Unit, Stockholm, Sweden; [Suck, R.; Weber, B.; Fiebig, H.; Cromwell, O.] Allergopharma Joachim Ganzer KG, Reinbek, Germany; [Valenta, R.] Med Univ Vienna, Dept Pathophysiol, Div Immunopathol, Christian Doppler Lab Allergy Res, Vienna, Austria	Valenta, R (reprint author), Univ Vienna, Ctr Physiol & Pathophysiol, Dept Pathophysiol, Lab Allergy Res, Vienna, Austria.	rudolf.valenta@meduniwien.ac.at	van Hage, Marianne/A-9678-2017	van Hage, Marianne/0000-0003-3091-1596	Swedish Research Council; Swedish Foundation for Health Care Sciences and Allergy Research; Swedish Asthma and Allergy Association's Research Foundation; Swedish Cancer- and Allergy Foundation; Hesselman Foundation; King Gustaf V 80th Birthday Foundation; Swedish Heart-Lung Foundation [F1815, F01818, L214-B13]; Christian Doppler Research Association	Supported by the Swedish Research Council, the Swedish Foundation for Health Care Sciences and Allergy Research, the Swedish Asthma and Allergy Association's Research Foundation, the Swedish Cancer- and Allergy Foundation, the Hesselman Foundation, King Gustaf V 80th Birthday Foundation, the Swedish Heart-Lung Foundation, grants TRP, F1815, F01818 and L214-B13 of the Austrian Science Fund and by the Christian Doppler Research Association.	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Exp. Allergy	SEP	2008	38	9					1514	1525		10.1111/j.1365-2222.2008.03042.x		12	Allergy; Immunology	Allergy; Immunology	341PS	WOS:000258727400014	18564326	
J	Gotzsche, PC; Johansen, HK				Gotzsche, P. C.; Johansen, H. K.			House dust mite control measures for asthma: systematic review	ALLERGY			English	Review						asthma; house dust mites; systematic review	RANDOMIZED CONTROLLED-TRIAL; IMPERMEABLE BED COVERS; SENSITIVE ADULT ASTHMA; DOUBLE-BLIND TRIAL; ALLERGEN-AVOIDANCE; BENZYL-BENZOATE; HIGH-EFFICIENCY; MATTRESS ENCASINGS; CHILDHOOD ASTHMA; BRONCHIAL HYPERREACTIVITY	The major allergen in house dust comes from mites. We performed a systematic review of the randomized trials that had assessed the effects of reducing exposure to house dust mite antigens in the homes of people with mite-sensitive asthma, and had compared active interventions with placebo or no treatment. Fifty-four trials (3002 patients) were included. Thirty-six trials assessed physical methods (26 mattress covers), 10 chemical methods and eight a combination of chemical and physical methods. Despite the fact that many trials were of poor quality and would be expected to exaggerate the reported effect, we did not find an effect of the interventions. For the most frequently reported outcome, peak flow in the morning (1565 patients), the standardized mean difference was 0.00 (95% confidence interval (CI) -0.10 to 0.10). There were no statistically significant differences in number of patients improved (relative risk 1.01, 95% CI 0.80-1.27), asthma symptom scores (standardized mean difference -0.04, 95% CI -0.15 to 0.07) or in medication usage (standardized mean difference -0.06, 95% CI -0.18 to 0.07). Chemical and physical methods aimed at reducing exposure to house dust mite allergens cannot be recommended.	[Gotzsche, P. C.; Johansen, H. K.] Rigshosp, Nordic Cochrane Ctr, DK-2100 Copenhagen, Denmark	Gotzsche, PC (reprint author), Rigshosp, Nordic Cochrane Ctr, Dept 3343 Blegdamsvej 9, DK-2100 Copenhagen, Denmark.						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Immunology	Allergy; Immunology	292SB	WOS:000255285300003	18445182	
J	Chu, HW; Thaikoottathil, J; Rino, JG; Zhang, G; Wu, Q; Moss, T; Refaeli, Y; Bowler, R; Wenzel, SE; Chen, Z; Zdunek, J; Breed, R; Young, R; Allaire, E; Martin, RJ				Chu, Hong Wei; Thaikoottathil, Jyoti; Rino, John G.; Zhang, Gongyi; Wu, Qun; Moss, Taylor; Refaeli, Yosef; Bowler, Russell; Wenzel, Sally E.; Chen, Zhongzhou; Zdunek, Jeffrey; Breed, Rachel; Young, Ryan; Allaire, Erin; Martin, Richard J.			Function and regulation of SPLUNC1 protein in mycoplasma infection and allergic inflammation	JOURNAL OF IMMUNOLOGY			English	Article							NASAL LAVAGE FLUID; CHLAMYDIA-PNEUMONIAE; BRONCHIAL HYPERRESPONSIVENESS; COLLAGEN DEPOSITION; AIRWAY INFLAMMATION; MUCIN EXPRESSION; MURINE MODEL; LUNG; ASTHMA; PLUNC	Respiratory infections, including Mycoplasma pneumoniae (Mp), contribute to asthma pathobiology. To date, the mechanisms underlying the increased susceptibility of asthmatics to airway Mp infection remain unclear. Short palate, lung, and nasal epithelium clone 1 (SPLUNC1) protein is a recently described large airway epithelial cell-derived molecule that was predicted to exert host defense activities. However, SPLUNC1 function and regulation in an infectious or allergic milieu are still unknown. We determined host defense and anti-inflammatory functions of SPLUNC1 protein in Mp infection and the regulation of SPLUNC1 by Mp and allergic inflammation (e.g., IL-13). SPLUNC1 function was examined in Mp or human airway epithelial cell cultures by using SPLUNC1 recombinant protein, overexpression and RNA interference. Human and mouse bronchial epithelial SPLUNC1 was examined using immunostaining, Western blotting, ELISA, laser capture microdissection, and real-time PCR. Mouse models of Mp infection and allergic inflammation and air-liquid interface cultures of normal human primary bronchial epithelial cells were used to study SPLUNC1 regulation by Mp and IL-13. We found that: 1) SPLUNC1 protein decreased Mp levels and inhibited epithelial IL-8 production induced by Mp-derived lipoproteins; 2) normal human and mouse large airway epithelial cells expressed high levels of SPLUNC1; and 3) although Mp infection increased SPLUNC1, IL-13 significantly decreased SPLUNC1 expression and Mp clearance. Our results suggest that SPLUNC1 serves as a novel host defense protein against Mp and that an allergic setting markedly reduces SPLUNC1 expression, which may in part contribute to the persistent nature of bacterial infections in allergic airways.	Natl Jewish Med & Res Ctr, Dept Med, Denver, CO 80206 USA; Natl Jewish Med & Res Ctr, Dept Immunol, Denver, CO 80206 USA; Natl Jewish Med & Res Ctr, Dept Pediat, Denver, CO 80206 USA; Univ Colorado, Hlth Sci Ctr, Denver, CO 80206 USA; Univ Pittsburgh, Pittsburgh, PA 15260 USA	Chu, HW (reprint author), Natl Jewish Med & Res Ctr, Dept Med, 1400 Jackson St,Room A639, Denver, CO 80206 USA.	chuhw@njc.org	chen, zhong/E-3900-2015	chen, zhong/0000-0003-1319-9664	NHLBI NIH HHS [P01 HL073907]		Bals R, 2004, EUR RESPIR J, V23, P327, DOI 10.1183/09031936.03.00098803; Bingle CD, 2002, HUM MOL GENET, V11, P937, DOI 10.1093/hmg/11.8.937; Blasi F, 2002, THORAX, V57, P672, DOI 10.1136/thorax.57.8.672; Campos MA, 2004, AM J RESP CELL MOL, V30, P184, DOI 10.1165/rcmb.2003-01420C; Cartner SC, 1996, INFECT IMMUN, V64, P5326; Chen WE, 2005, WIREL NETW MOB COMP, V1, P3; Chen ZZ, 2006, CELL, V125, P691, DOI 10.1016/j.cell.2006.04.024; Chu H. 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Immunol.	SEP 15	2007	179	6					3995	4002				8	Immunology	Immunology	210ON	WOS:000249465600071	17785838	
J	Thyssen, JP; Johansen, JD; Menne, T				Thyssen, Jacob Pontoppidan; Johansen, Jeanne Duus; Menne, Torkil			Contact allergy epidemics and their controls	CONTACT DERMATITIS			English	Review						chromium; contact allergy; contact dermatitis; epidemic; formaldehyde; isothiazolinone; methyldibromo glutaronitrile; nickel; para-phenylenediamine; risk assessment	RINSE-OFF PRODUCTS; PATCH TEST; KATHON-CG; NICKEL-EXPOSURE; RISK-ASSESSMENT; METHYLDIBROMO GLUTARONITRILE; FERROUS SULFATE; GUINEA-PIG; HAIR-DYES; DERMATITIS	Contact dermatitis can be severe and lead to sick leave as well as significant healthcare expenses. The aim of this review is to present the published knowledge on 6 historical epidemics of contact allergy to apply this knowledge on the prevention and control of future contact allergy epidemics. A historical review is performed on nickel, chromium, methylchloroisothiazolinone/methylisothiazolinone, methyldibromo glutaronitrile, formaldehyde, and para-phenylenediamine. The first cases of contact dermatitis are mostly occupational, whereas consumer cases appear later. There is often a latency period from the first cases are observed until an epidemic occurs, and the problem is recognized. Finally, no one seems to take responsibility of dealing with the situation, and there are no attempts of regulation until an epidemic is consolidated among consumers for many years. Steps should be taken to prevent contact allergy epidemics. It is essential that dermatologist, scientists, administrators, and consumers organize and structure known methods to accelerate the control of emerging contact allergens.	Gentofte Univ Hosp, Dept Dermatovenerol, Natl Allery Res Ctr, DK-2820 Gentofte, Denmark	Thyssen, JP (reprint author), Gentofte Univ Hosp, Dept Dermatovenerol, Natl Allery Res Ctr, Ledreborg Alle 40,1, DK-2820 Gentofte, Denmark.	jacpth01@gentoftehosp.kbhamt.dk					AGNER T, 2006, CONTACT DERMATITIS, P127, DOI 10.1007/3-540-31301-X_9; Armstrong DKB, 1999, CONTACT DERMATITIS, V41, P348, DOI 10.1111/j.1600-0536.1999.tb06191.x; AVNSTORP C, 1989, CONTACT DERMATITIS, V20, P365, DOI 10.1111/j.1600-0536.1989.tb03174.x; AZUA J, 1910, ACTAS DERMO SIF, V2, P220; BELSITO DV, 2006, 8 C EUR SOC CONT DER; BJORKNER B, 1986, CONTACT DERMATITIS, V14, P85, DOI 10.1111/j.1600-0536.1986.tb01166.x; BLASCHKO A, 1989, DEUT MED WOCHENSCHR, V15, P925; BONNEVIE P, 1936, ACTA DERM-VENEREOL, V17, P376; BOSS A, 1982, CONTACT DERMATITIS, V8, P211, DOI 10.1111/j.1600-0536.1982.tb04191.x; BRANDRUP F, 1979, CONTACT DERMATITIS, V5, P148, DOI 10.1111/j.1600-0536.1979.tb04827.x; BRUZE M, 1988, CONTACT DERMATITIS, V18, P37, DOI 10.1111/j.1600-0536.1988.tb05487.x; Bryld LE, 2004, J INVEST DERMATOL, V123, P1025, DOI 10.1111/j.0022-202X.2004.23452.x; Bulmer FM, 1926, J IND HYG, V8, P517; Cathelineau H., 1898, B SOC FRANC SYPH, V9, P28; *CDC, 2006, GLOSS TERMS; CHAN PK, 1983, J INVEST DERMATOL, V81, P409, DOI 10.1111/1523-1747.ep12522544; Conde-Salazar L, 1995, AM J CONTACT DERMATI, V6, P19, DOI 10.1016/1046-199X(95)90064-0; Cosmetic Ingredient Review Expert panel of The Cosmetics Toiletry and Fragrance Association, 1992, J AM COLL TOXICOL, V11, P75; *CRAIN COMM INC, 2006, ADV CENT; deGroot AC, 1996, CONTACT DERMATITIS, V34, P118; DEGROOT AC, 1985, CONTACT DERMATITIS, V12, P76; Dillarstone A, 1997, CONTACT DERMATITIS, V37, P190, DOI 10.1111/j.1600-0536.1997.tb00205.x; DUBOIS C, 1931, SCHWEIZ MED WOCHENSC, V12, P278; Englehardt W E, 1931, ARCH GEWERBEPATH HYG, V2, P140; *EUR COMM, 2003, OFFICIAL J EUROPEAN, P28; European Commission, 2004, OFFICIAL J EUROPEAN; European Communities, 1994, OFFICIAL J EUR COMMU, V37, P1; Felter SP, 2003, REGUL TOXICOL PHARM, V37, P1, DOI 10.1016/S0273-2300(02)00021-1; Fewings J, 1999, CONTACT DERMATITIS, V41, P1, DOI 10.1111/j.1600-0536.1999.tb06200.x; Fischer LA, 2005, CONTACT DERMATITIS, V52, P57, DOI 10.1111/j.0105-1873.2005.00523.x; Flint GN, 1998, CONTACT DERMATITIS, V39, P213, DOI 10.1111/j.1600-0536.1998.tb05912.x; Flyvholm MA, 2005, CONTACT DERMATITIS, V53, P27, DOI 10.1111/j.0105-1873.2005.00629.x; Flyvholm MA, 1997, CONTACT DERMATITIS, V36, P26, DOI 10.1111/j.1600-0536.1997.tb00918.x; FORSCH P, 2006, CONTACT DERMATITIS; FOUSSEREAU J, 1990, CONTACT DERMATITIS, V22, P68, DOI 10.1111/j.1600-0536.1990.tb01519.x; Fransway A. 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Dermatology	Allergy; Dermatology	141WF	WOS:000244609000001	17343617	
J	Pincus-Knackstedt, MK; Joachim, RA; Blois, SM; Douglas, AJ; Orsal, AS; Klapp, BF; Wahn, U; Hamelmann, E; Arck, PC				Pincus-Knackstedt, Maike K.; Joachim, Ricarda A.; Blois, Sandra M.; Douglas, Alison J.; Orsal, Arif S.; Klapp, Burghard F.; Wahn, Ulrich; Hamelmann, Eckard; Arck, Petra C.			Prenatal stress enhances susceptibility of murine adult offspring toward airway inflammation	JOURNAL OF IMMUNOLOGY			English	Article							PULMONARY EOSINOPHILIA; ASTHMA; CELLS; RAT; HYPERRESPONSIVENESS; PREGNANCY; CYTOKINES; ENDOTOXIN; EXPOSURE; CORTISOL	Allergic asthma is one of the most prevalent and continuously increasing diseases in developed countries. Its clinical features include airway hyperresponsiveness and inflammation upon allergen contact. Furthermore, an emerging area of research subsumed as fetal programming evaluates the impact of environmental insults in utero on the incidence of diseases in later life. The aim of this study was to identify whether prenatal exposure to stress, which constitutes a severe environmental insult, perpetuates airway inflammation in later life. Our experiments were performed in mice and revealed that prenatally stressed adult offspring indeed show an increased vulnerability toward airway hyperresponsiveness and inflammation. Furthermore, we provide persuasive insights on dysregulated pathways of the cellular and humoral immune response upon Ag challenge in prenatally stressed adult offspring, reflected by a Th2 greater Th1 adaptive immune response and increased CCR3 and IgE levels in vivo. Additionally, APCs derived from prenatally stressed offspring trigger clonal expansion of Th2 cells in vitro. We also deliver experimental evidence for a reduced corticotrophin-releasing hormone expression in the paraventricular nucleus of adult offspring in response to prenatal stress. Furthermore, behavioral analyses indicate an increase in anxiety in these mice. In conclusion, our data will facilitate future research aiming to identify the individual impact, hierarchy, and redundancy of multiple key protagonists in airway inflammation in an interdisciplinary context. This will foster the substantiation of disease-prevention strategies, such as asthma, during the prenatal period.	Univ Med Berlin, Charite, Dept Internal Med Psychosomat, Div Psychoneuroimmunol, Berlin, Germany; Univ Med Berlin, Charite, Dept Pediat, Div Pneumol & Immunol, Berlin, Germany; Univ Med Berlin, Charite, Neurosci Program, Berlin, Germany; Univ Edinburgh, Ctr Integrat Physiol, Edinburgh EH8 9YL, Midlothian, Scotland	Arck, PC (reprint author), Univ Med Berlin, Charite, Dept Internal Med Psychosomat, Div Psychoneuroimmunol, Berlin, Germany.	petra.arck@charite.de	Arck, Petra/D-7094-2013				ABBAS AK, 2004, CELLULAR MOL IMMUNOL, P449; ARCK PC, 1995, BIOL REPROD, V53, P814, DOI 10.1095/biolreprod53.4.814; BARKER DJP, 1995, MOL MED TODAY, V1, P418, DOI 10.1016/S1357-4310(95)90793-9; Blois S, 2005, J IMMUNOL, V174, P1820; Blumer N, 2005, CLIN EXP ALLERGY, V35, P397, DOI 10.1111/j.1365-2222.2005.02184.x; Bousquet J, 2000, ALLERGY, V55, P1194, DOI 10.1034/j.1398-9995.2000.00923.x; BOUSQUET J, 2004, ALLERGY, V59, P38; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; BURNEY P, 2002, THORAX, V57, P1136; Coe CL, 2002, J CLIN ENDOCR METAB, V87, P675, DOI 10.1210/jc.87.2.675; COYLE AJ, 1995, AM J RESP CELL MOL, V13, P54; Douglas AJ, 2003, ENDOCRINOLOGY, V144, P5268, DOI 10.1210/en.2003-0461; Franklin KBJ, 1997, MOUSE BRAIN STEREOTA; GAVETT SH, 1994, AM J RESP CELL MOL, V10, P587; Hales CN, 2001, BRIT MED BULL, V60, P5, DOI 10.1093/bmb/60.1.5; Hamelmann E, 1999, INT ARCH ALLERGY IMM, V118, P90, DOI 10.1159/000024037; Hamelmann E, 1997, AM J RESP CRIT CARE, V156, P766; JINGAMI H, 1985, FEBS LETT, V191, P63, DOI 10.1016/0014-5793(85)80994-7; Joachim RA, 2003, PSYCHOSOM MED, V65, P811, DOI 10.1097/01.PSY.0000088582.50468.A3; Karrow NA, 2006, BRAIN BEHAV IMMUN, V20, P144, DOI 10.1016/j.bbi.2005.05.003; Kovacs KJ, 2004, ANN NY ACAD SCI, V1018, P466, DOI 10.1196/annals.1296.057; LANNERO E, 2006, RESP RES, V5, P7; Lesage J, 2004, J ENDOCRINOL, V181, P291, DOI 10.1677/joe.0.1810291; Lin YC, 2004, CLIN EXP ALLERGY, V34, P548, DOI 10.1111/j.1365-2222.2004.1928.x; Ma W, 2002, J CLIN INVEST, V109, P621, DOI 10.1172/JCI200214097; Matricardi PM, 2001, ANN ALLERG ASTHMA IM, V87, P24; Mitchell B, 2005, EMBRYOLOGY, P25; MURPHY BEP, 1974, AM J OBSTET GYNECOL, V118, P538; Nepomnaschy PA, 2006, P NATL ACAD SCI USA, V103, P3938, DOI 10.1073/pnas.0511183103; PELLOW S, 1985, J NEUROSCI METH, V14, P149, DOI 10.1016/0165-0270(85)90031-7; Pope SM, 2005, J IMMUNOL, V175, P5341; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; ROMAGNANI S, 1994, CURR OPIN IMMUNOL, V6, P838, DOI 10.1016/0952-7915(94)90002-7; Snijders A, 1998, INT IMMUNOL, V10, P1593, DOI 10.1093/intimm/10.11.1593; van Rijt LS, 2003, J IMMUNOL, V171, P3372; von Mutius E, 2000, J ALLERGY CLIN IMMUN, V105, P9, DOI 10.1016/S0091-6749(00)90171-4; Warburton D, 2000, MECH DEVELOP, V92, P55, DOI 10.1016/S0925-4773(99)00325-1; Wright RJ, 2005, J ALLERGY CLIN IMMUN, V116, P1301, DOI 10.1016/j.jaci.2005.09.050; Wright RJ, 2004, J ALLERGY CLIN IMMUN, V113, P1051, DOI 10.1016/j.jaci.2004.03.032	39	83	86	0	3	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	DEC 15	2006	177	12					8484	8492				9	Immunology	Immunology	125BP	WOS:000243416800025	17142746	
J	Mi, YH; Norback, D; Tao, J; Mi, YL; Ferm, M				Mi, Y-H.; Norback, D.; Tao, J.; Mi, Y-L.; Ferm, M.			Current asthma and respiratory symptoms among pupils in Shanghai, China: influence of building ventilation, nitrogen dioxide, ozone, and formaldehyde in classrooms	INDOOR AIR			English	Article							INDOOR AIR-QUALITY; SCHOOL ENVIRONMENT; DIFFUSION TUBES; HEALTH-SURVEY; HONG-KONG; EXPOSURE; POLLUTION; SCHOOLCHILDREN; PREVALENCE; CHILDREN	We investigated 10 naturally ventilated schools in Shanghai, in winter. Pupils (13-14 years) in 30 classes received a questionnaire, 1414 participated (99%). Classroom temperatures were 13-21 degrees C (mean 17 degrees C), relative air humidity was 36-82% (mean 56%). The air exchange rate was 2.9-29.4 ac/h (mean 9.1), because of window opening. Mean CO(2) exceeded 1000 ppm in 45% of the classrooms. NO(2) levels were 33-85 mu g/m(3) indoors, and 45-80 mu g/m(3) outdoors. Ozone were 1-9 mu g/m(3) indoors and 17-28 mu g/m(3) outdoors. In total, 8.9% had doctors' diagnosed asthma, 3.1% wheeze, 23.0% daytime breathlessness, 2.4% current asthma, and 2.3% asthma medication. Multiple logistic regression was applied. Observed indoor molds was associated with asthma attacks [odds ratio (OR) = 2.40: P < 0.05]. Indoor temperature was associated with daytime breathlessness (OR = 1.26 for 1 C; P < 0.001), and indoor CO(2) with current asthma (OR = 1.18 for 100 ppm; P < 0.01) and asthma medication (OR = 1.15 for 100 ppm; P < 0.05). Indoor NO(2) was associated with current asthma (OR = 1.51 for 10 mu g/m(3); P < 0.01) and asthma medication (OR = 1.45 for 10 mu g/m(3); P < 0.01). Outdoor NO(2) was associated with current asthma (OR = 1.44 for 10 mu g/m(3); P < 0.05). Indoor and outdoor ozone was negatively associated with daytime breathlessness. In conclusion, asthma symptoms among pupils in Shanghai can be influenced by lack of ventilation and outdoor air pollution from traffic.	Uppsala Univ, Dept Med Sci, SE-75185 Uppsala, Sweden; Univ Uppsala Hosp, SE-75185 Uppsala, Sweden; Jiao Tong Univ, Shanghai 200030, Peoples R China; Shanghai Teachers Univ, Shanghai, Peoples R China; IVL Swedish Environm Res Inst, Gothenburg, Sweden	Norback, D (reprint author), Uppsala Univ, Dept Med Sci, SE-75185 Uppsala, Sweden.	dan.norback@medsci.uu.se		Norback, Dan/0000-0002-5174-6668			Almqvist C, 2001, AM J RESP CRIT CARE, V163, P694; ANDERSSON K, 1981, SCAND J WORK ENV HEA, V7, P282; Baker M, 2000, SCIENCE, V288, P1317; Belsley DA, 1991, CONDITIONING DIAGNOS; Bornehag CG, 2001, INDOOR AIR, V11, P72; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; CALDER IC, 1993, B ENVIRON CONTAM TOX, V51, P185; CAMPBELL GW, 1994, ATMOS ENVIRON, V28, P477, DOI 10.1016/1352-2310(94)90125-2; Carmichael GR, 2003, ATMOS ENVIRON, V37, P1293, DOI 10.1016/S1352-2310(02)01009-9; Chen Yu-zhi, 2004, Zhonghua Jiehe He Huxi Zazhi, V27, P112; Chen Y Z, 1998, CHINESE J PEDIAT, V36, P353; Cooley JD, 1998, OCCUP ENVIRON MED, V55, P579; Daisey JM, 2003, INDOOR AIR, V13, P53, DOI 10.1034/j.1600-0668.2003.00153.x; ELLIOT L, 1991, APPL OCCUP ENV HYG, V6, P836; Ferm M, 1997, J ATMOS CHEM, V27, P17, DOI 10.1023/A:1005816621522; Ferm M, 1998, ATMOS ENVIRON, V32, P1377, DOI 10.1016/S1352-2310(97)00170-2; FERM M, 2001, P INT C MEAS AIR POL, P31; FERM M, 2001, P INT C MEAS AIR POL, P298; GEBSKI V, 1992, SPIDA USERS MANUAL V; Gilliland FD, 2001, EPIDEMIOLOGY, V12, P43, DOI 10.1097/00001648-200101000-00009; Godish T, 1996, INDOOR AIR, V6, P135, DOI 10.1111/j.1600-0668.1996.00010.x; HASSELBLAD V, 1992, J AIR WASTE MANAGE, V42, P662; Heal MR, 1999, ATMOS ENVIRON, V33, P513, DOI 10.1016/S1352-2310(98)00290-8; HEYMAN E, 1880, NORD MED ARK, V12, P1; Immonen J, 2001, PEDIATR ALLERGY IMMU, V12, P87, DOI 10.1034/j.1399-3038.2001.012002087.x; Janson C, 2001, EUR RESPIR J, V18, P598, DOI 10.1183/09031936.01.00205801; Kan HD, 2003, ARCH ENVIRON HEALTH, V58, P360; Lee SC, 2000, CHEMOSPHERE, V41, P109, DOI 10.1016/S0045-6535(99)00396-3; Mendell MJ, 2005, INDOOR AIR, V15, P27, DOI 10.1111/j.1600-0668.2004.00320.x; Norback D, 1999, INT J TUBERC LUNG D, V3, P368; NORBACK D, 1990, BRIT J IND MED, V47, P733; Norback Dan, 1992, INDOOR AIR, V2, P58, DOI 10.1111/j.1600-0668.1992.07-21.x; PALMES ED, 1976, AM IND HYG ASSOC J, V37, P570, DOI 10.1080/0002889768507522; Peat JK, 1998, ALLERGY, V53, P120, DOI 10.1111/j.1398-9995.1998.tb03859.x; Perzanowski MS, 1999, J ALLERGY CLIN IMMUN, V103, P1018, DOI 10.1016/S0091-6749(99)70173-9; Plaschke PP, 2000, AM J RESP CRIT CARE, V162, P920; Qian ZM, 2000, ARCH ENVIRON HEALTH, V55, P126; Ramadour M, 2000, ALLERGY, V55, P1163, DOI 10.1034/j.1398-9995.2000.00637.x; Salo PM, 2004, ANN EPIDEMIOL, V14, P543, DOI 10.1016/j.annepidem.2003.09.015; SESLINE D, 1994, ARCH ENVIRON HEALTH, V49, P439; SJOBERG K, 2001, P INT C MEAS AIR POL, P116; Smedje G, 1997, INDOOR AIR, V7, P143, DOI 10.1111/j.1600-0668.1997.00009.x; Smedje G, 1997, CLIN EXP ALLERGY, V27, P1270, DOI 10.1111/j.1365-2222.1997.tb01171.x; Smedje G, 2000, ARCH ENVIRON HEALTH, V55, P18; Smedje G, 2001, INT J TUBERC LUNG D, V5, P1059; Su HJJ, 2001, ARCH ENVIRON HEALTH, V56, P144; Sundell J, 1996, SCAND J WORK ENV HEA, V22, P5; Taskinen TM, 2002, ALLERGY, V57, P9, DOI 10.1034/j.1398-9995.2002.13154.x; THORNE PS, 1993, VET HUM TOXICOL, V35, P141; Wainman T, 2000, ENVIRON HEALTH PERSP, V108, P1139, DOI 10.2307/3434825; World Health Organization (WHO), 1987, EUR SER WHO, V23; WHO, 2005, WHO AIR QUAL GUID GL; Wieslander G, 1997, J OCCUP HEALTH, V39, P331, DOI 10.1539/joh.39.331; Wilkins CK, 2001, ENVIRON HEALTH PERSP, V109, P937, DOI 10.2307/3454995; Wong CM, 1998, J EPIDEMIOL COMMUN H, V52, P571; ZHAO R, 1991, ZHONGHUA YU FANG YI, V56, P149; 1993, VENTILATION QUALITY, P5	57	83	86	8	41	WILEY-BLACKWELL PUBLISHING, INC	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0905-6947			INDOOR AIR	Indoor Air	DEC	2006	16	6					454	464		10.1111/j.1600-0668.2006.00439.x		11	Construction & Building Technology; Engineering, Environmental; Public, Environmental & Occupational Health	Construction & Building Technology; Engineering; Public, Environmental & Occupational Health	102SC	WOS:000241832600006	17100666	
J	Bousquet, J; Flahault, A; Vandenplas, O; Ameille, J; Duron, JJ; Pecquet, C; Chevrie, K; Annesi-Maesano, I				Bousquet, Jean; Flahault, Antoine; Vandenplas, Olivier; Ameille, Jacques; Duron, Jean-Jacques; Pecquet, Corine; Chevrie, Karine; Annesi-Maesano, Isabella			Natural rubber latex allergy among health care workers: A systematic review of the evidence	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						latex allergy; health care workers; IgE; skin test; exposure-response relationship; meta-analysis	APPRENTICES STARTING EXPOSURE; OPERATING-ROOM NURSES; IN-HOSPITAL PERSONNEL; POWDER-FREE GLOVES; IGE ANTIBODIES; DENTAL STUDENTS; BLOOD-DONORS; OCCUPATIONAL EPIDEMIOLOGY; RESPIRATORY SYMPTOMS; NURSING STAFF	Background: Natural rubber latex is a recognized allergen, but a recent meta-analysis failed to find any association between latex exposure and allergy in health care workers (HCWs). Objectives: A meta-analysis was carried out under the auspices of the French National Regulatory Authority to assess the allergic risk induced by latex gloves in HCWs. Methods: The risk of work-related exposure to latex for the development of latex allergy was assessed. Prevalence and incidence rates of latex sensitization or allergy were compared in HCWs and in the general population. Exposure-response relationships were assessed in HCWs. Results: Latex allergy was found in 4.32% (range, 4.01% to 4.63%) of HCWs and in 1.37% (range, 0.43% to 2.31%) of the general population. Latex-positive skin prick test responses ranged from 2.1% to 3.7% in the general population and from 6.9% to 7.8% for the HCWs. HCWs exposed to latex showed an increased risk of hand dermatitis (odds ratio [OR], 2.46; 95% CI, 2.11-2.86), asthma or wheezing (OR, 1.55; 95% CI, 1.15-2.08), rhinoconjunctivitis (OR, 2.73; 95% CI, 1.97-3.81), and at least one generic symptom (OR, 1.27; 95% CI, 1.09-1.47). Sensitization to latex was significantly associated with asthma and rhinoconjunctivitis. By contrast, exposure to latex was not associated with a significantly increased risk of positive skin prick test responses to latex (OR, 1.47; 95% CI, 0.94-2.30). Conclusion: HCWs have an increased risk of sensitization and allergic symptoms to latex. Clinical implications: Prevention of latex allergy in HCWs is needed.	Univ Hosp, Clin Malad Resp, INSERM, U454,Hop Arnaud Villeneuve, F-34295 Montpellier 5, France; Univ Paris 06, INSERM, U707, Med Sch St Antoine, Paris, France; Clin Univ UCL Montgodinne, Serv Pneumol, Yvoir, France; Hop Raymond Poincare, Assistance Publ Hop Paris, Unit Occupat Hlth, Paris, France; CHU Pitie Salpetriere, Serv Chirurg Digest & Gen, Paris, France; Hop Tenon, Ctr Allergol, F-75970 Paris, France	Bousquet, J (reprint author), Univ Hosp, Clin Malad Resp, INSERM, U454,Hop Arnaud Villeneuve, F-34295 Montpellier 5, France.	jean.bousquet@wanadoo.fr	Annesi-Maesano, Isabella/D-9173-2016				Ahmed DDF, 2003, IMMUNOL ALLERGY CLIN, V23, P205, DOI 10.1016/S0889-8561(02)00079-6; Aichane A, 1997, REV MAL RESPIR, V14, P451; AKASAWA A, 1993, INT ARCH ALLERGY IMM, V101, P177; Allmers H, 1998, J ALLERGY CLIN IMMUN, V102, P841, DOI 10.1016/S0091-6749(98)70026-0; Allmers H, 2002, J ALLERGY CLIN IMMUN, V110, P318, DOI 10.1067/mai.2002.126461; Amin A, 1998, INT DENT J, V48, P77; Archambault S, 2001, J ALLERGY CLIN IMMUN, V107, P921; 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Allergy Clin. Immunol.	AUG	2006	118	2					447	454		10.1016/j.jaci.2006.03.048		8	Allergy; Immunology	Allergy; Immunology	075IH	WOS:000239877700022	16890771	
J	Cates, CJ; Crilly, JA; Rowe, BH				Cates, CJ; Crilly, JA; Rowe, BH			Holding chambers (spacers) versus nebulisers for beta-agonist treatment of acute asthma	COCHRANE DATABASE OF SYSTEMATIC REVIEWS			English	Review							METERED-DOSE INHALER; RANDOMIZED CONTROLLED-TRIAL; AIR-FLOW OBSTRUCTION; BRONCHODILATOR DELIVERY METHODS; HAND-HELD NEBULIZER; PEAR-SHAPED SPACER; YOUNG-CHILDREN; JET NEBULIZER; WET NEBULIZER; HOSPITALIZED-PATIENTS	Background In acute asthma inhaled beta 2-agonists are often administered to relieve bronchospasm by wet nebulisation, but some have argued that metered-dose inhalers with a holding chamber (spacer) can be equally effective. Nebulisers require a power source and need regular maintenance, and are more expensive in the community setting. Objectives To assess the effects of holding chambers (spacers) compared to nebulisers for the delivery of beta 2-agonists for acute asthma. Search strategy We last searched the Cochrane Airways Group trials register in January 2006 and the Cochrane Central Register of Controlled Trials (The Cochrane Library, Issue 4, 2005). Selection criteria Randomised trials in adults and children (from two years of age) with asthma, where spacer beta 2-agonist delivery was compared with wet nebulisation. Data collection and analysis Two reviewers independently applied study inclusion criteria (one reviewer for the first version of the review), extracted the data and assessed trial quality. Missing data were obtained from the authors or estimated. Results are reported with 95% confidence intervals (CI). Main results This review has been updated in January 2006 and four new trials have been added. 2066 children and 614 adults are now included in 25 trials from emergency room and community settings. In addition, six trials on in-patients with acute asthma (213 children and 28 adults) have been reviewed. Method of delivery of beta 2-agonist did not appear to affect hospital admission rates. In adults, the relative risk of admission for spacer versus nebuliser was 0.97 (95% CI 0.63 to 1.49). The relative risk for children was 0.65 (95% CI: 0.4 to 1.06). In children, length of stay in the emergency department was significantly shorter when the spacer was used, with a mean difference of -0.47 hours (95% CI: -0.58 to -0.37). Length of stay in the emergency department for adults was similar for the two delivery methods. Peak flow and forced expiratory volume were also similar for the two delivery methods. Pulse rate was lower for spacer in children, mean difference -7.6% baseline (95% CI: -9.9 to -5.3% baseline). Authors' conclusions Metered-dose inhalers with spacer produced outcomes that were at least equivalent to nebuliser delivery. Spacers may have some advantages compared to nebulisers for children with acute asthma.	Bushey Hlth Ctr, Watford WD23 2NN, Herts, England	Cates, CJ (reprint author), Bushey Hlth Ctr, London Rd, Watford WD23 2NN, Herts, England.	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J	Osborn, DA; Sinn, J				Osborn, D. A.; Sinn, J.			Formulas containing hydrolysed protein for prevention of allergy and food intolerance in infants	COCHRANE DATABASE OF SYSTEMATIC REVIEWS			English	Review							COWS MILK ALLERGY; HIGH-RISK INFANTS; AMINO-ACID-CONCENTRATIONS; LOW-BIRTH-WEIGHT; AUSTRALIAN ABORIGINAL CHILDREN; DIETARY INTERVENTION PROGRAM; DIFFERENT FEEDING REGIMENS; PARTIAL WHEY HYDROLYSATE; BRIEF NEONATAL EXPOSURE; PROSPECTIVE FOLLOW-UP	Background Allergies and food reactions are common and may be associated with foods including adapted cow's milk formula. Formulas containing hydrolysed proteins have been used to treat infants with allergy or food intolerance. However, it is unclear whether hydrolysed formula can be advocated for prevention of allergy and food intolerance in infants without evidence of allergy or food intolerance. Objectives To determine the effect of feeding hydrolysed formulas on allergy and food intolerance in infants and children compared to adapted cow's milk or human breast milk. If hydrolysed formulas are effective, to determine what type of hydrolysed formula is most effective including extensively and partially hydrolysed formulas. To determine which infants benefit, including infants at low or high risk of allergy and infants receiving early, short term or prolonged formula feeding. Search strategy The standard search strategy of the Cochrane Neonatal Review Group was used. The review was updated with searches of the Cochrane Central Register of Controlled Trials (CENTRAL, The Cochrane Library, Issue 1, 2006), MEDLINE (1966 - March 2006), EMBASE (1980 - March 2006) and CINAHL (1982 - March 2006) and previous reviews including cross references. Selection criteria Randomised and quasi-randomised trials that compare the use of a hydrolysed infant formula to human milk or cow's milk formula. Trials with > 80% follow up of participants were eligible for inclusion. Data collection and analysis Eligibility of studies for inclusion, methodological quality and data extraction were assessed independently by each review author. Primary outcomes included clinical allergy, specific allergies and food intolerance. Meta-analysis was conducted using a fixed effects model. Main results Two trials compared early, short termhydrolysed formula to human milk feeding. No significant difference in infant allergy or childhood cow's milk allergy (CMA) were reported. No eligible trial compared prolonged hydrolysed formula to human milk feeding. Two trials compared early, short term hydrolysed formula to cow's milk formula feeding. No significant benefits were reported. One large quasi-random study reported a reduction in infant CMA of borderline significance in low risk infants (RR 0.62, 95% CI 0.38, 1.00). Ten eligible studies compared prolonged feeding with hydrolysed formula versus cow's milk formula in high risk infants. Meta-analysis found a significant reduction in infant allergy (seven studies, 2514 infants; typical RR 0.79, 95% CI 0.66, 0.94), but not in the incidence of childhood allergy (two studies, 950 infants; typical RR 0.85, 95% CI 0.69, 1.05). There was no significant difference in infant eczema (eight studies, 2558 infants, typical RR 0.84, 95% CI 0.68, 1.04), childhood eczema incidence (two studies, 950 infants, typical RR 0.83, 95% CI 0.63, 1.10), childhood eczema prevalence (one study, 872 infants; RR 0.66, 95% CI 0.43, 1.02), or infant or childhood asthma, rhinitis and food allergy. One study reported a significant reduction in infants with CMA with confirmed atopy (RR 0.36, 95% CI 0.15, 0.89). Subgroup analysis of trials blinded to formula found no significant difference in infant allergy (four studies, 2156 infants; typical RR 0.87, 95% CI 0.69, 1.08) or childhood allergy incidence (one study, 872 infants; RR 0.91, 95% CI 0.73, 1.14). No eligible trial examined the effect of prolonged hydrolysed formula feeding on allergy beyond early childhood. There is evidence that preterm or low birthweight infants fed a hydrolysed preterm formula have significantly reduced weight gain, but not in other growth parameters (head circumference or length). Studies in term infants report no adverse effects on growth. Subgroup analysis of trials of partially hydrolysed versus cow's milk formula found a significant reduction in infant allergy (six studies, 1391 infants; typical RR 0.79, 95% CI 0.65, 0.97) but not childhood allergy, or infant or childhood asthma, eczema or rhinitis. Methodological concerns were the same as for the overall analysis. Analysis of trials of extensively hydrolysed formula versus cow's milk formula found no significant differences in allergy or food intolerance. Infants fed extensively hydrolysed formula compared with partially hydrolysed formula had a significant reduction in food allergy (two studies, 341 infants; typical RR 0.43, 95% CI 0.19, 0.99), but there was no significant difference in all allergy or any other specific allergy incidence. Comparing extensively hydrolysed casein containing formula with cow's milk formula, one study (431 infants) reported a significant reduction in childhood allergy incidence (RR 0.72, 95% CI 0.53, 0.97). Meta- analysis found a significant reduction in infant eczema (three studies, 1237 infants; typical RR 0.71, 95% CI 0.51, 0.97). One study reported a significant reduction in childhood eczema incidence (RR 0.66, 95% CI 0.44, 0.98) and prevalence (RR 0.50, 95% CI 0.27, 0.92). Authors' conclusions There is no evidence to support feeding with a hydrolysed formula for the prevention of allergy compared to exclusive breast feeding. In high risk infants who are unable to be completely breast fed, there is limited evidence that prolonged feeding with a hydrolysed formula compared to a cow's milk formula reduces infant and childhood allergy and infant CMA. In view of methodological concerns and inconsistency of findings, further large, well designed trials comparing formulas containing partially hydrolysed whey, or extensively hydrolysed casein to cow's milk formulas are needed.	Westmead Hosp, Neonatal Unit, Westmead, NSW 2145, Australia	Sinn, J (reprint author), Westmead Hosp, Neonatal Unit, Hawkesbury Rd, Westmead, NSW 2145, Australia.	johnsinn@westgate.wh.usyd.edu.au					Agosti M., 2003, Acta Paediatrica, V91, P34; Akimoto K, 1997, Arerugi, V46, P1044; 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, 1992, J ALLERGY CLIN IMMUN, V90, P235, DOI 10.1016/0091-6749(92)90077-F; Arshad SH, 2003, THORAX, V58, P489, DOI 10.1136/thorax.58.6.489; ARSHAD SH, 1993, CLIN EXP ALLERGY, V23, P504, DOI 10.1111/j.1365-2222.1993.tb03238.x; ATHERTON DJ, 1978, LANCET, V1, P401; Austin JB, 1999, ARCH DIS CHILD, V81, P225; Baker SS, 2000, PEDIATRICS, V106, P346; Barbee RA, 1998, J ALLERGY CLIN IMMUN, V102, pS65, DOI 10.1016/S0091-6749(98)70006-5; BARBERI I, 1993, 2 WORLD C PER MED; Becker A, 2004, J ALLERGY CLIN IMMUN, V113, P650, DOI 10.1016/j.jaci.2004.01.754; Bellioni-Businco B, 1999, J ALLERGY CLIN IMMUN, V103, P1191, DOI 10.1016/S0091-6749(99)70198-3; 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J	Nelson, DI; Concha-Barrientos, M; Driscoll, T; Steenland, K; Fingerhut, M; Punnett, L; Pruss-Ustun, A; Leigh, J; Corvalan, C				Nelson, DI; Concha-Barrientos, M; Driscoll, T; Steenland, K; Fingerhut, M; Punnett, L; Pruss-Ustun, A; Leigh, J; Corvalan, C			The global burden of selected occupational diseases and injury risks: Methodology and summary	AMERICAN JOURNAL OF INDUSTRIAL MEDICINE			English	Article						burden of disease; occupational health; DALYs; comparative risk assessment; health impact assessment	OBSTRUCTIVE PULMONARY-DISEASE; DUST EXPOSURE; UNITED-STATES; ASTHMA; DISABILITY; POPULATION; MORTALITY; HEALTH; CARCINOGENS; PREVALENCE	Background A round the globe, work has a heavy impact on health. To better advise policy makers, we assessed the global burden of disease and injury due to selected occupational hazards. This article presents an overview, and describes the methodology employed in the companion studies. Methods Using the World Health Organization (WHO) Comparative Risk Assessment methodology, we applied relative risk measures to the proportions of the population exposed to selected occupational hazards to estimate attributable fractions, deaths, and disability-adjusted life years (DALYs). Numerous occupational risk factors had to be excluded due to inadequate global data. Results In 2000, the selected risk factors were responsible worldwide for 37% of back pain, 16% of hearing loss, 13% of chronic obstructive. pulmonary disease (COPD), 11% of asthma, 8% of injuries, 9% of lung cancer, and 2% of leukemia. These risks at work caused 850, 000 deaths worldwide and resulted in the loss of about 24 million years of healthy life. Needlesticks accounted for about 40% of Hepatitis B and Hepatitis C infections and 4.4% of HIV infections in health care workers. Conclusions Exposure to occupational hazards accounts for a significant proportion of the global burden of disease and injury, which could be substantially reduced through application of proven risk prevention strategies. Am. J. Ind. Med. 48:400-418, 2005. (c) 2005 Wiley-Liss, Inc.	Geol Soc Amer, Boulder, CO 80301 USA; WHO, CH-1211 Geneva, Switzerland; Asociac Chilena Seguridad, Santiago, Chile; ELMATOM Pty Ltd, Sydney, NSW, Australia; Emory Univ, Atlanta, GA 30322 USA; NIOSH, Washington, DC USA; Univ Massachusetts, Lowell, MA USA; Univ Sydney, Sch Publ Hlth, Ctr Environm & Occupat Hlth, Sydney, NSW 2006, Australia	Nelson, DI (reprint author), Geol Soc Amer, PO 9140, Boulder, CO 80301 USA.	dnelson@geosociety.org					BADLEY EM, 1994, J RHEUMATOL, V21, P505; Balmes J, 2003, AM J RESP CRIT CARE, V167, P787, DOI 10.1164/rccm.167.5.787; BECKLAKE MR, 1989, AM REV RESPIR DIS, V140, pS85; BEIR V, 1990, HLTH EFF EXP LOW LEV; BUTLER S, 1979, SOCIOL ABSTR, V27; CHANYEUNG M, 1994, EUR RESPIR J, V7, P346, DOI 10.1183/09031936.94.07020346; Concha-Barrientos M, 2005, AM J IND MED, V48, P470, DOI 10.1002/ajim.20226; DAVIS AC, 1989, INT J EPIDEMIOL, V18, P911, DOI 10.1093/ije/18.4.911; Desai MA, 2004, WHO ENV BURDEN DIS S, V4; Dosemeci M, 1995, SCAND J WORK ENV HEA, V21, P39; Driscoll T, 2005, AM J IND MED, V48, P419, DOI 10.1002/ajim.20209; Driscoll T, 2005, AM J IND MED, V48, P432, DOI 10.1002/ajim.20210; Driscoll T, 2005, AM J IND MED, V48, P491, DOI 10.1002/aijm.20194; *EIU, 1995, BUS OP REP IND 4 Q; *EIU, 1996, CHIN HAND, pCH13; *EIU, 2001, COUNTR FOR AFR; Ezzati M, 2004, COMP QUANTIFICATION; *FINN I OCC HLTH, 1999, CAR DAT; Hendrick DJ, 1996, THORAX, V51, P947, DOI 10.1136/thx.51.9.947; Hewett P, 1996, OCCUP MED, V11, P561; IARC, 1994, SOM IND CHEM; *INT LAB ORG, 1995, ILO YB LAB STAT 1995; *INT LAB ORG, 2001, LAB LAB STAT DAT; International Labour Organisation, 2002, INT LAB C; *INT LAB ORG, 1995, SECT ACT PROGR REC D; *INT LAB ORG, 2001, ILO YB LAB STAT; *INT LAB ORG, 2002, EC ACT POP 1950 2010; JOHNSON AG, 1977, IND LABOR RELATIONS, V11, P18; JUENGPRASERT W, 1997, ASIAN PACIFIC REGION, V4; Karjalainen A, 2002, SCAND J WORK ENV HEA, V28, P49; Karjalainen A, 2001, AM J RESP CRIT CARE, V164, P565; Kauppinen T, 2000, OCCUP ENVIRON MED, V57, P10, DOI 10.1136/oem.57.1.10; KOCH JL, 1981, J VOCAT BEHAV, V18, P145, DOI 10.1016/0001-8791(81)90003-8; Kogevinas M, 1999, LANCET, V353, P1750, DOI 10.1016/S0140-6736(98)07397-8; KORN RJ, 1987, AM REV RESPIR DIS, V136, P298; Leigh J, 1999, EPIDEMIOLOGY, V10, P626, DOI 10.1097/00001648-199909000-00032; Leigh JP, 2003, SCAND J WORK ENV HEA, V29, P304; Leigh JP, 1997, ARCH INTERN MED, V157, P1557, DOI 10.1001/archinte.157.14.1557; LEIGH JP, 1989, BRIT J IND MED, V46, P651; Loewenson R, 1999, EPIDEMIOLOGY, V10, P632, DOI 10.1097/00001648-199909000-00033; Lucifora C, 1998, INT J IND ORGAN, V16, P353, DOI 10.1016/S0167-7187(96)01055-7; Lynge E, 1997, CANCER CAUSE CONTROL, V8, P406, DOI 10.1023/A:1018461406120; Mathers C, 2002, 50 WHO; MOFFETT M, 2002, NEW MEXICO LABOR MAR; Murray CJL, 1997, J HEALTH ECON, V16, P703, DOI 10.1016/S0167-6296(97)00004-0; MURRAY CJL, 1994, B WORLD HEALTH ORGAN, V72, P429; Murray CJL, 1997, LANCET, V349, P1436, DOI 10.1016/S0140-6736(96)07495-8; Murray C., 1996, GLOBAL BURDEN DIS CO, P1; MYERS JE, 1989, SCAND J WORK ENV HEA, V15, P180; *NAT I ENV HLTH SC, 1999, ENV HLTH PERSPECTIVE, V107; *NAT I OCC SAF HLT, 1995, SUMM CRIT REC STAND; *NAT I OCC SAF HLT, 1999, WORK REL LUNG DIS SU; National Institute for Occupational Safety and Health, 1998, CRIT REC STAND OCC N; National Institute of Occupational Safety and Health, 2000, INJ ILLN HAZ EXP MIN; Nelson DI, 2005, AM J IND MED, V48, P446, DOI 10.1002/aijm.20223; Nurminen M, 2001, SCAND J WORK ENV HEA, V27, P161; OLEINICK A, 1993, AM J IND MED, V23, P231, DOI 10.1002/ajim.4700230202; Partanen T, 1995, SCAND J WORK ENV HEA, V21, P84; Pearce N, 1994, IARC SCI PUBLICATION, V129; Pope MH, 1991, OCCUPATIONAL LOW BAC; Prince MM, 1997, J ACOUST SOC AM, V101, P950, DOI 10.1121/1.418053; Pruss-Ustun A, 2003, ENV BURDEN DIS SERIE, V1; Punnett L, 2005, AM J IND MED, V48, P459, DOI 10.1002/ajim.20232; QUINLAN M, 2002, GLOBAL OCCUPATIONAL; REES D, 1992, BRIT J IND MED, V49, P459; Riihimaki Hilkka, 1995, P207; ROACH S, 1992, HLTH RISKS HAZARDOUS; SON PH, 1999, USE GEOGRAPHICAL INF; Steenland K, 1996, AM J IND MED, V29, P474, DOI 10.1002/(SICI)1097-0274(199605)29:5<474::AID-AJIM6>3.0.CO;2-M; Steenland K, 2003, AM J IND MED, V43, P461, DOI 10.1002/ajim.10216; Takala J, 1999, EPIDEMIOLOGY, V10, P640, DOI 10.1097/00001648-199909000-00034; THI N, 2001, COMMUNICATION   0831; UN (United Nations), 2000, INT STAND IND CLASS; *USDHHS, 2001, NATL VITAL STAT SYST, V49; Venables KM, 1997, LANCET, V349, P1465, DOI 10.1016/S0140-6736(96)07219-4; World Health Organization, 2004, GLOB BURD DIS EST; World Health Organization, 2002, WORLD HLTH REP RED R; World Bank, 2001, WORLD DEV IND 2001; YIN SN, 1987, BRIT J IND MED, V44, P192; ZOU CQ, 1997, MINERAL DUSTS PREVEN, V4	80	83	90	1	11	WILEY-LISS	HOBOKEN	DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA	0271-3586			AM J IND MED	Am. J. Ind. Med.	DEC	2005	48	6					400	418		10.1002/ajim.20211		19	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	991KA	WOS:000233811700002	16299700	
J	Bailey, M; Haverson, K; Inman, C; Harris, C; Jones, P; Corfield, G; Miller, B; Stokes, C				Bailey, M; Haverson, K; Inman, C; Harris, C; Jones, P; Corfield, G; Miller, B; Stokes, C			The development of the mucosal immune system pre- and post-weaning: balancing regulatory and effector function	PROCEEDINGS OF THE NUTRITION SOCIETY			English	Article						oral tolerance; immune development; weaning; pig; allergy	GROWTH-FACTOR-BETA; INFLAMMATORY-BOWEL-DISEASE; RESIDENT INTESTINAL FLORA; ORAL TOLERANCE; T-CELL; LAMINA PROPRIA; PEYERS-PATCHES; SPLEEN-CELLS; BREAST-MILK; B-CELL	The mucosal immune system fulfils the primary function of defence against potential pathogens that may enter across vulnerable surface epithelia. However, a secondary function of the intestinal immune system is to discriminate between pathogen-associated and 'harmless' antigens, expressing active responses against the former and tolerance to the latter. Control of immune responses appears to be an active process, involving local generation of IgA and of regulatory and/or regulated T lymphocytes. Two important periods of maximum exposure to novel antigens occur in the young animal, immediately after birth and at weaning. In both cases the antigenic composition of the intestinal contents can shift suddenly, as a result of a novel diet and of colonisation by novel strains and species of bacteria. Changes in lifestyles of man, and husbandry of animals, have resulted in weaning becoming much more abrupt than previously in evolution, increasing the number of antigens that must be simultaneously evaluated by neonates. Thus, birth and weaning are likely to represent hazard and critical control points in the development of appropriate responses to pathogens and harmless dietary and commensal antigens. Neonates are born with relatively undeveloped mucosal immune systems. At birth this factor may prevent both expression of active immune responses and development of tolerance. However, colonisation by intestinal flora expands the mucosal immune system in antigen-specific and non-specific ways. At weaning antibody to fed proteins can be detected, indicating active immune responses to fed proteins. It is proposed that under normal conditions the ability of the mucosal immune system to mount active responses to foreign antigens develops simultaneously with the ability to control and regulate such responses. Problems arise when one or other arm of the immune system develops inappropriately, resulting in inappropriate effector responses to harmless food proteins (allergy) or inadequate responses to pathogens (disease susceptibility).	Univ Bristol, Sch Clin Vet Sci, Bristol BS4 5SU, Avon, England	Bailey, M (reprint author), Univ Bristol, Sch Clin Vet Sci, Langford House, Bristol BS4 5SU, Avon, England.	mick.bailey@bristol.ac.uk	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Inman, Charlotte/0000-0002-0801-4779			Adkins B, 2004, EUR J IMMUNOL, V34, P1901, DOI 10.1002/eji.200324271; Bailey M, 2004, CLIN DIAGN LAB IMMUN, V11, P337, DOI 10.1128/CDLI.11.2.337-343.2004; BAILEY M, 1993, INT ARCH ALLERGY IMM, V101, P266; BAILEY M., 2001, P NUTR SOC, V60, P1; BAILEY M, 2005, IN PRESS VET IMMUNOL; Beutler B, 2002, CURR TOP MICROBIOL, V270, P1; BIANCHI ATJ, 1992, VET IMMUNOL IMMUNOP, V33, P201, DOI 10.1016/0165-2427(92)90182-P; Borsutzky S, 2004, J IMMUNOL, V173, P3305; Brandtzaeg P, 2004, TRENDS IMMUNOL, V25, P570, DOI 10.1016/j.it.2004.09.005; BROWN TA, 1984, J IMMUNOL, V132, P780; Bu P, 2001, J IMMUNOL, V166, P6399; Butcher EC, 1999, ADV IMMUNOL, V72, P209, DOI 10.1016/S0065-2776(08)60022-X; Butler JE, 2000, IMMUNOLOGY, V100, P119, DOI 10.1046/j.1365-2567.2000.00013.x; CHALLACOMBE SJ, 1980, J EXP MED, V152, P1459, DOI 10.1084/jem.152.6.1459; Chun SK, 2004, J MICROBIOL BIOTECHN, V14, P1267; Duchmann R, 1995, CLIN EXP IMMUNOL, V102, P448; Duchmann R, 1996, EUR J IMMUNOL, V26, P934, DOI 10.1002/eji.1830260432; Flajnik Martin F., 2004, Trends in Immunology, V25, P640, DOI 10.1016/j.it.2004.10.001; Fujihashi K, 2001, P NATL ACAD SCI USA, V98, P3310, DOI 10.1073/pnas.061412598; Helm RM, 2000, CURR OPIN IMMUNOL, V12, P647, DOI 10.1016/S0952-7915(00)00157-6; Holt PG, 1997, PEDIATR ALLERGY IMMU, V8, P53, DOI 10.1111/j.1399-3038.1997.tb00145.x; Johansen FE, 2001, J IMMUNOL, V167, P5185; Kalliomaki M, 1999, J ALLERGY CLIN IMMUN, V104, P1251, DOI 10.1016/S0091-6749(99)70021-7; Kunkel EJ, 2002, IMMUNITY, V16, P1, DOI 10.1016/S1074-7613(01)00261-8; Levine AD, 2001, SEMIN IMMUNOL, V13, P195, DOI 10.1006/smim.2001.0309; Litman GF, 1999, ANNU REV IMMUNOL, V17, P109, DOI 10.1146/annurev.immunol.17.1.109; Luo CH, 2000, IMMUNOGENETICS, V51, P92, DOI 10.1007/s002510050017; MacPherson AJ, 2004, ANN NY ACAD SCI, V1029, P36, DOI 10.1196/annals.1309.005; Macpherson AJ, 2004, SCIENCE, V303, P1662, DOI 10.1126/science.1091334; Manzano M, 2002, J NUTR, V132, P2757; MCDERMOTT MR, 1979, J IMMUNOL, V122, P1892; MILLER BG, 1994, BRIT J NUTR, V71, P615, DOI 10.1079/BJN19940167; Mowat AM, 2004, ANN NY ACAD SCI, V1029, P1, DOI 10.1196/annals.1309.001; Ogawa J, 2004, EARLY HUM DEV, V77, P67, DOI 10.1016/j.earlhumdev.2004.01.005; Oz HS, 2004, J AM COLL NUTR, V23, P220; PENG HJ, 1989, PEDIATR RES, V26, P486, DOI 10.1203/00006450-198911000-00025; Peng YF, 2004, P NATL ACAD SCI USA, V101, P4572, DOI 10.1073/pnas.0400810101; PHILLIPSQUAGLIA.JM, 2002, FOOD ALLERGY INTOLER, pCH4; Prioult G, 2003, CLIN DIAGN LAB IMMUN, V10, P787, DOI 10.1128/CDLI.10.5.787-792.2003; ROTHKOTTER HJ, 1991, PEDIATR RES, V29, P237, DOI 10.1203/00006450-199103000-00004; Sait L, 2003, APPL ENVIRON MICROB, V69, P2100, DOI 10.1128/AEM.69.4.2100-2109.2003; Samsom JN, 2004, CRIT REV IMMUNOL, V24, P157, DOI 10.1615/CritRevImmunol.v24.i3.10; Schroder HC, 2003, J BIOL CHEM, V278, P32810, DOI 10.1074/jbc.M304116200; Spahn TW, 2001, EUR J IMMUNOL, V31, P1278, DOI 10.1002/1521-4141(200104)31:4<1278::AID-IMMU1278>3.0.CO;2-A; Stagg AJ, 2002, EUR J IMMUNOL, V32, P1445, DOI 10.1002/1521-4141(200205)32:5<1445::AID-IMMU1445>3.0.CO;2-E; STOKES CR, 1983, CLIN EXP IMMUNOL, V52, P678; STOKES CR, 1983, CLIN EXP IMMUNOL, V52, P399; Talham GL, 1999, INFECT IMMUN, V67, P1992; Teillet F, 2005, J IMMUNOL, V174, P2870; van den Biggelaar AHJ, 2000, LANCET, V356, P1723, DOI 10.1016/S0140-6736(00)03206-2; VEGALOPEZ MA, 1993, VET IMMUNOL IMMUNOP, V37, P49, DOI 10.1016/0165-2427(93)90015-V; VEGALOPEZ MA, 1995, VET IMMUNOL IMMUNOP, V44, P319, DOI 10.1016/0165-2427(94)05309-G; Wilson AD, 1996, IMMUNOLOGY, V88, P98, DOI 10.1046/j.1365-2567.1996.d01-640.x; Xu RJ, 1999, BIOL NEONATE, V75, P59, DOI 10.1159/000014078; Zapata A. G., 1990, IMMUNE SYSTEM COMP H	55	83	84	3	17	CABI PUBLISHING	WALLINGFORD	C/O PUBLISHING DIVISION, NOSWORTHY WAY, WALLINGFORD OX10 8DE, OXON, ENGLAND	0029-6651			P NUTR SOC	Proc. Nutr. Soc.	NOV	2005	64	4					451	457		10.1079/PNS2005452		7	Nutrition & Dietetics	Nutrition & Dietetics	987YM	WOS:000233553700005	16313686	
J	von Leupoldt, A; Dahme, B				von Leupoldt, A; Dahme, B			Cortical substrates for the perception of dyspnea	CHEST			English	Review						asthma; brain; breathlessness; COPD; dyspnea; emission-CT; MRI; pain; perception	POSITRON-EMISSION-TOMOGRAPHY; CEREBRAL BLOOD-FLOW; INSULAR CORTEX; AIR HUNGER; RESPIRATORY SENSATIONS; LUNG-VOLUME; CHEMORECEPTOR AFFERENTS; VOLITIONAL INSPIRATION; SOMATOSENSORY CORTEX; SYMPTOM PERCEPTION	Dyspnea is a common, unpleasant, and impairing symptom in various respiratory diseases and other diseases. Despite growing understanding of the multiple peripheral mechanisms giving rise to dyspnea, little is known about the cortical mechanisms underlying its perception. The results of neuroiniaging studies have shown that distinct brain areas process the dyspneic sensation, among which the anterior insular seems to be the most important. Based on the findings of the first relevant neuroimaging studies, this review describes the cortical structures associated with the perception of dyspnea. Moreover, similarities to the perception of pain are discussed, and implications for future research are provided.	Univ Hamburg, Psychol Inst 3, D-20146 Hamburg, Germany	von Leupoldt, A (reprint author), Univ Hamburg, Psychol Inst 3, Von Melle Pk 5, D-20146 Hamburg, Germany.	andreas.vonleupoldt@uni-hamburg.de	Frank, David/E-8213-2012				Augustine JR, 1996, BRAIN RES REV, V22, P229, DOI 10.1016/S0165-0173(96)00011-2; BANZETT RB, 1990, RESP PHYSIOL, V81, P1, DOI 10.1016/0034-5687(90)90065-7; Banzett RB, 2000, NEUROREPORT, V11, P2117, DOI 10.1097/00001756-200007140-00012; Banzett RB, 2000, AM J RESP CRIT CARE, V162, P1178; BANZETT RB, 1996, LUNG BIOL HEALTH DIS, V90, P155; Banzett RB, 2001, APS B, V11, P1; BARNES PJ, 1994, NEW ENGL J MED, V330, P1383, DOI 10.1056/NEJM199405123301910; Bauldoff GS, 2002, CHEST, V122, P948, DOI 10.1378/chest.122.3.948; BINDER JR, 1994, LOCALIZATION NEUROIM, V1, P185; Birbaumer N, 2003, BIOL PSYCHOL, P328; Bornhovd K, 2002, BRAIN, V125, P1326, DOI 10.1093/brain/awf137; Brannan S, 2001, P NATL ACAD SCI USA, V98, P2029, DOI 10.1073/pnas.98.4.2029; BUSHNELL MC, 2002, CAN J ANAESTH, V49, pR1; 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J	Di Lorenzo, G; Pacor, ML; Pellitteri, ME; Morici, G; Di Gregoli, A; Lo Bianco, C; Ditta, V; Martinelli, N; Candore, G; Mansueto, P; Rini, GB; Corrocher, R; Caruso, C				Di Lorenzo, G; Pacor, ML; Pellitteri, ME; Morici, G; Di Gregoli, A; Lo Bianco, C; Ditta, V; Martinelli, N; Candore, G; Mansueto, P; Rini, GB; Corrocher, R; Caruso, C			Randomized placebo-controlled trial comparing fluticasone aqueous nasal spray in mono-therapy, fluticasone plus cetirizine, fluticasone plus montelukast and cetirizine plus montelukast for seasonal allergic rhinitis	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						cetirizine; eosinophil cationic protein; eosinophils; fluticasone propionate; montelukast; nasal lavage; Parietaria; pollen season	LEUKOTRIENE RECEPTOR ANTAGONISTS; POLLEN SEASON; GRASS-POLLEN; DOUBLE-BLIND; PROPIONATE; CORTICOSTEROIDS; ASTHMA; ANTILEUKOTRIENE; LEVOCABASTINE; EOSINOPHILS	Background Corticosteroids are considered to be particularly effective in reducing nasal congestion and are therefore recommended as first-line treatment in allergic rhinitis patients with moderate to severe and/or persistent symptoms. Objective We compared the clinical efficacy of fluticasone propionate aqueous nasal spray (FPANS) 200 mug given once daily, administered in mono-therapy or combined therapy with a H-1 receptor antagonist (cetirizine, CTZ) or with a leukotriene antagonist (montelukast, MSK), and the combined therapy of CTZ plus MSK in the treatment of patients affected by allergic rhinitis to Parietaria during natural pollen exposure. In addition, we examined the effect of the treatment on eosinophil counts and eosinophil cationic protein (ECP) in nasal lavage performed at beginning of season, during season and at the end of the season. Methods One hundred patients aged 12-50 years (mean+/-SD 31.8+/-9.6) with a history of moderate to severe Parietaria pollen-induced seasonal allergic rhinitis were selected. A randomized, double-blind, double dummy, placebo (PLA)-controlled, parallel-group study design was used. Patients were treated FPANS 200 mug once daily (n=20) or with FPANS 200 mug once daily, plus CTZ (10 mg) in the morning (n=20), or with FPANS 200 mug once daily, plus MSK (10 mg) in the evening (n=20) or with CTZ (10 mg) in the morning plus MSK in the evening (n=20) or matched PLA (n=20). Assessment of efficacy was based on scores of daily nasal symptoms and on eosinophil counts and ECP in nasal lavage. Results All treatments showed significant differences (P<0.001) compared with PLA in terms of total symptom, rhinorrhea, sneezing and nasal itching scores. Concerning nasal congestion on waking and daily only the groups treated with FPANS in mono-therapy or in combined therapy showed significant differences compared with PLA. Comparing the group treated with FPANS alone and the groups treated with FPANS plus CTZ, we found significant differences for total symptom score (P=0.04) and for nasal itching (P=0.003). The comparison between FPANS plus CTZ and FPANS plus MSK showed significant difference for nasal itching (P=0.003). Finally, there were significant differences between the group treated with FPANS and the group treated with CTZ plus MSK for total symptom score (P=0.009), for nasal congestion on waking (P<0.001) and nasal congestion daily (P<0.001). Also the comparisons between the group treated with FPANS plus CTZ and the group treated with CTZ plus MSK demonstrated significant differences (P<0.001) for total symptom, for nasal congestion on waking and for nasal congestion on daily, for rhinorrhea (P=0.04) and for nasal itching (P=0.003) scores. Concerning the comparison between the group treated with FPANS plus MSK and the group treated with CTZ plus MSK we found significant differences for total symptom score (P=0.005), for nasal congestion on waking (P<0.001) and for nasal congestion on daily (P<0.001). No other differences were observed between the groups. Concerning blood eosinophil counts, significant differences were found between the treatments with FPANS in mono-therapy or in combined therapy with PLA group during and at the end of the season (P=0.0003 and P<0.0001, respectively). Concerning eosinophils and ECP in nasal lavage, all treatments showed significant differences (P<0.001) compared with PLA. Besides, there were significant differences (P<0.001) between the groups treated with FPANS alone or in combined therapy and the group treated with CTZ plus MSK. Conclusion The results of this comparative study demonstrate that FPANS is highly effective for treating patients affected by allergic rhinitis, with efficacy exceeding that of CTZ plus MSK in combined therapy. In addition, the regular combined therapy of FPANS plus CTZ or plus MSK would not seem to offer substantial advantage with respect to FPANS in mono-therapy in patients affected by seasonal allergic rhinitis.	Univ Palermo, Dipartimento Med Clin & Patol Emergenti, I-90127 Palermo, Italy; Univ Verona, Dipartimento Med Clin & Med Sperimentale, I-37100 Verona, Italy; Univ Palermo, Dipartimento Biopatol & Metodol Biomed, I-90133 Palermo, Italy	Di Lorenzo, G (reprint author), Univ Palermo, Dipartimento Med Clin & Patol Emergenti, Via Vespro 141, I-90127 Palermo, Italy.	dilo601@unipa.it	Martinelli, Nicola/J-5622-2016; Mansueto, Pasquale/K-3458-2016	Martinelli, Nicola/0000-0001-6465-5119; Mansueto, Pasquale/0000-0002-0406-0583; Di Lorenzo, Gabriele/0000-0002-0197-5665			Barnes PJ, 2001, ALLERGY, V56, P928, DOI 10.1034/j.1398-9995.2001.00001.x; Barnes PJ, 1998, AM J RESP CRIT CARE, V157, P1; BISGAARD H, 1986, CLIN ALLERGY, V16, P289, DOI 10.1111/j.1365-2222.1986.tb01960.x; Bousquet J, 2001, J ALLERGY CLIN IMMUN, V108, pS147, DOI 10.1067/mai.2001.118891; D'Ambrosio F P, 1998, Allergol Immunopathol (Madr), V26, P277; DACIE JV, 1984, PRACTICAL HAEMATOLOG, P42; DARNELL R, 1994, CLIN EXP ALLERGY, V24, P1144; Di Lorenzo G, 1997, J ALLERGY CLIN IMMUN, V100, P832, DOI 10.1016/S0091-6749(97)70281-1; Di Lorenzo G, 2002, MEDIAT INFLAMM, V11, P187, DOI 10.1080/09622935020138226; Di Lorenzo G, 1999, CLIN EXP ALLERGY, V29, P1367; Diamant Z, 1999, CLIN EXP ALLERGY, V29, P42; DiLorenzo G, 1997, CLIN EXP ALLERGY, V27, P1052; DILORENZO G, 2001, INT ARCH ALLERGY IMM, V25, P164; Ducharme FM, 2000, COCHRANE DB SYST REV, V3; DUJUKANOVIC R, 1996, CLIN EXP ALLERGY  S3, V26, P44; Erdfelder E, 1996, BEHAV RES METH INSTR, V28, P1, DOI 10.3758/BF03203630; GODTHELP T, 1995, ALLERGY, V50, P21, DOI 10.1111/j.1398-9995.1995.tb02737.x; Grossman J., 1997, Journal of Allergy and Clinical Immunology, V99, pS443; HOWARTH PH, 1995, ALLERGY, V50, P6, DOI 10.1111/j.1398-9995.1995.tb02734.x; Jordana G, 1996, J ALLERGY CLIN IMMUN, V97, P588, DOI 10.1016/S0091-6749(96)70303-2; Meltzer EO, 2000, J ALLERGY CLIN IMMUN, V105, P917, DOI 10.1067/mai.2000.106040; MIADONNA A, 1987, AM REV RESPIR DIS, V136, P357; Mygind N, 1996, CLIN EXP ALLERGY, V26, P2, DOI 10.1111/j.1365-2222.1996.tb00652.x; Nielsen LP, 2001, DRUGS, V61, P1563, DOI 10.2165/00003495-200161110-00004; OKUDA M, 1988, ANN ALLERGY, V60, P537; Ortolani C, 1999, ALLERGY, V54, P1173, DOI 10.1034/j.1398-9995.1999.00200.x; Palczynski C, 1996, Allergol Immunopathol (Madr), V24, P237; Pullerits T, 1999, AM J RESP CRIT CARE, V159, P1814; Pullerits T, 2002, J ALLERGY CLIN IMMUN, V109, P949, DOI 10.1067/mai.2002.124467; Smith LJ, 2001, BIODRUGS, V15, P239, DOI 10.2165/00063030-200115040-00004; Sorkness CA, 2001, PHARMACOTHERAPY, V21, p34S, DOI 10.1592/phco.21.4.34S.34262; van Cauwenberge P, 2000, ALLERGY, V55, P116, DOI 10.1034/j.1398-9995.2000.00526.x; Weiner JM, 1998, BRIT MED J, V317, P1624; Wilson AM, 2001, ANN ALLERG ASTHMA IM, V87, P344; Wilson AM, 2001, CLIN EXP ALLERGY, V31, P61, DOI 10.1046/j.1365-2222.2001.00964.x	35	83	89	0	2	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	FEB	2004	34	2					259	267		10.1111/j.1365-2222.2004.01877.x		9	Allergy; Immunology	Allergy; Immunology	779KL	WOS:000189293900016	14987306	
J	Taube, C; Dakhama, A; Gelfand, EW				Taube, C; Dakhama, A; Gelfand, EW			Insights into the pathogenesis of asthma utilizing murine models	INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY			English	Review						asthma; mouse model; airway hyperresponsiveness	DELTA-T-CELLS; ALLERGIC AIRWAY DISEASE; RESPIRATORY SYNCYTIAL VIRUS; ACTIVATED MAST-CELLS; NF-KAPPA-B; MOUSE MODEL; PULMONARY EOSINOPHILIA; MUCUS PRODUCTION; BRONCHIAL HYPERREACTIVITY; ANTIGEN EXPOSURE	Asthma is a common syndrome in children and adults. Despite the increasing prevalence and socioeconomic burden, the underlying pathophysiology remains poorly defined in a large percentage of asthmatics. Animal models and, in particular, murine models of allergic airway disease have helped to reveal some of the potential underlying mechanisms and have played an important role in identifying the importance of T cells and T(H)2 cytokines in development of allergen-induced inflammation and airway hyperresponsiveness. In addition, other cell types including mast cells and eosinophils have been implicated in the development of some aspects of the disease. To further understand this complex syndrome, the development of animal models which mimic elements of this chronic airway disease is essential. Copyright (C) 2004 S. Karger AG, Basel.	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Arch. Allergy Immunol.		2004	135	2					173	186		10.1159/000080899		14	Allergy; Immunology	Allergy; Immunology	861HB	WOS:000224405600012	15375327	
J	Mishra, V				Mishra, V			Indoor air pollution from biomass combustion and acute respiratory illness in preschool age children in Zimbabwe	INTERNATIONAL JOURNAL OF EPIDEMIOLOGY			English	Article						indoor air pollution; biomass; smoke; respiratory tract infections; child; Zimbabwe	ENVIRONMENTAL TOBACCO-SMOKE; DEVELOPING-COUNTRIES; CHRONIC-BRONCHITIS; IMMUNE-RESPONSE; LUNG IMMUNITY; BONE-MARROW; EXPOSURE; DISEASE; WOMEN; ASTHMA	Background Reliance on biomass for cooking and heating exposes many women and young children in developing countries to high levels of air pollution indoors. This study investigated the association between household use of biomass fuels for cooking and acute respiratory infections (ARI) in preschool age children (<5 years) in Zimbabwe. Methods Analysis is based on 3559 children age 0-59 months included in the 1999 Zimbabwe Demographic and Health Survey (ZDHS). Children who suffered from cough accompanied by short, rapid breathing during the 2 weeks preceding the survey were defined as having suffered from ARI. Logistic regression was used to estimate the odds of suffering from ARI among children from households using biomass fuels (wood, dung, or straw) relative to children from households using cleaner fuels (liquid petroleum gas [LPG]/natural gas, or electricity), after controlling for potentially confounding factors. Results About two-thirds (66%) of children lived in households using biomass fuels and 16% suffered from ARI during the 2 weeks preceding the survey interview. After adjusting for child's age, sex, birth order, nutritional status, mother's age at childbirth, education, religion, household living standard, and region of residence, children in households using wood, dung, or straw for cooking were more than twice as likely to have suffered from ARI as children from households using LPG/natural gas or electricity (OR = 2.20; 95% CI: 1.16, 4.19). Conclusions Household use of high pollution biomass fuels is associated with ARI in children in Zimbabwe. The relationship needs to be further investigated using more direct measures of smoke exposure and clinical measures of ARI.	East West Ctr, Honolulu, HI 96848 USA	Mishra, V (reprint author), East West Ctr, 1601 East West Rd, Honolulu, HI 96848 USA.						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J. Epidemiol.	OCT	2003	32	5					847	853		10.1093/ije/dyg240		7	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	735ZY	WOS:000186146300036	14559763	
J	Fernandes, J; Reshef, A; Patton, L; Ayuso, R; Reese, G; Lehrer, SB				Fernandes, J; Reshef, A; Patton, L; Ayuso, R; Reese, G; Lehrer, SB			Immunoglobulin E antibody reactivity to the major shrimp allergen, tropomyosin, in unexposed Orthodox Jews	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergen cross-reactivity; cockroaches; dust mites; Orthodox Jews; shrimp reactivity; tropomyosin	HOUSE-DUST MITE; CROSS-REACTIVITY; DERMATOPHAGOIDES-PTERONYSSINUS; IDENTIFICATION; NITROCELLULOSE; HYPERSENSITIVITY; PROTEINS; BINDING; SNAILS	Background Assessment of allergic (IgE antibody-mediated) reactions to foods may become complicated by cross-reactivity that can occur among certain food families and between foods and seemingly unrelated allergens. Objective The allergenic properties of tropomyosin (muscle-derived protein) have been recently demonstrated in invertebrates such as cockroaches, dust mites, and shrimp. In view of a possible cross-reactivity between food allergens and related allergens from animal sources, we designed a study to assess IgE antibody reactivity to the major shrimp allergen, Pen a 1, in an unexposed population of Orthodox Jews, who observe Kosher dietary laws that prohibit eating shellfish. Methods Nine subjects, who reacted positively by skin tests to shrimp (Penaeus setiferous ), were selected for the study. Subjects (two females, seven males) ranged in age from 14 to 32 years (mean 20.4). All subjects were strictly observant of Jewish tradition and had no prior exposure to seafood (regarded as a non-Kosher food). Serum was obtained from all the subjects and tested for IgE antibody reactivity to shrimp and dust mite. Results All subjects reported symptoms of perennial allergic rhinitis, five had history of asthma, atopic dermatitis, and/or sinusitis. All had positive skin prick tests to shrimp and house dust mite (HDM) (Dermatophagoides farinae, D. pteronyssinus , or both); 2/7 subjects were positive to cockroach mix (Blattella germanica and Periplaneta americana ). Sera of 4/9 subjects demonstrated specific IgE antibodies by RAST to shrimp (7.0-20.0%), 3/9 to Pen a 1 (6.3-24.1%), and 3/9 to shrimp or Pen a 1 by immunoblot. IgE binding to Pen a 1 was inhibited with either mite or cockroach extracts as demonstrated by RAST and/or immunoblot inhibition analysis. Conclusions These studies indicate that IgE antibody reactivity to a major food allergen, shrimp, can occur in an unexposed population of individuals; some subjects allergic to HDM and/or cockroach show substantial IgE antibody reactivity to the major shrimp allergen Pen a 1 (tropomyosin). Based on inhibition with cockroach and/or dust mite extracts, this reactivity appears to be due to cross-reacting tropomyosins.	Tulane Univ, Hlth Sci Ctr, New Orleans, LA 70112 USA; Chaim Sheba Med Ctr, IL-52621 Tel Hashomer, Israel	Lehrer, SB (reprint author), Tulane Univ, Hlth Sci Ctr, 1700 Perdido St SL-57, New Orleans, LA 70112 USA.						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Exp. Allergy	JUL	2003	33	7					956	961		10.1046/j.1365-2222.2003.01722.x		6	Allergy; Immunology	Allergy; Immunology	702AM	WOS:000184202400016	12859453	
J	Eichenfield, LF; Hanifin, JM; Beck, LA; Lemanske, RF; Sampson, HA; Weiss, ST; Leung, DYM				Eichenfield, LF; Hanifin, JM; Beck, LA; Lemanske, RF; Sampson, HA; Weiss, ST; Leung, DYM			Atopic dermatitis and asthma: Parallels in the evolution of treatment	PEDIATRICS			English	Article						allergy; asthma; atopic dermatitis; treatment guidelines	DENDRITIC CELLS; EARLY-LIFE; CHILDHOOD; PREVALENCE; ALLERGY; EPIDEMIOLOGY; POPULATION; EXPOSURE; LINKAGE; INTERVENTION	Objectives. To review epidemiologic correlations between asthma and atopic dermatitis (AD), identify common features in disease pathophysiology, and review steps involved in the development of asthma therapy guidelines to assess the appropriateness of a similar process and approach for AD. Methods. A 7-member panel representing specialists in dermatology, allergy, asthma, immunology, and pediatrics from around the United States convened to review the current literature and evolving data on AD. Participants presented reviews to the panel on the epidemiology of asthma and AD, the genetic predisposition to allergic disease, the current understanding of the immunopathophysiology of AD, interrelationships between the pathologic pathways of asthma and AD, evolving treatment concepts and options in AD, and the applicability of the asthma treatment model and how it may be adapted for guideline development for AD. Commentary and criticism were recorded for use in document preparation. Results. There are clear epidemiologic parallels in asthma and AD. Importantly, AD frequently is the first manifestation of an atopic diathesis, which occurs in genetically predisposed individuals and also includes asthma and allergic rhinitis. Up to 80% of children with AD will eventually develop allergic rhinitis or asthma later in childhood. This classic "atopic triad" has numerous pathophysiologic elements in common, including cyclic nucleotide regulatory abnormalities, immune cell alterations, and inflammatory mediators and allergic triggers. New therapeutic options that target underlying immune mechanisms are available, and their place among treatments for AD is becoming established. Guidelines of care have been developed for asthma. The panel noted that the National Institutes of Health/National Heart, Lung, and Blood Institute guidelines for diagnosis and management of asthma, first issued in 1991, had a tremendous positive impact on many aspects of asthma treatment. It not only created a heightened awareness that asthma is a disease of chronic inflammation, but it also provided unified approaches for therapy and opened new areas of basic science and clinical research. In addition, the guidelines spurred interactions among physicians of various specialties and stimulated a great quantity of research in asthma therapy. It is anticipated that AD therapy guidelines would have similar positive outcomes. Conclusions. The panel concluded that, on the basis of current information and evolving therapeutic options, a clear rationale exists to support AD guideline development. The many parallels between AD and asthma suggest that processes and approaches used for the asthma therapy guidelines would be appropriate for AD.	Childrens Hosp, San Diego, CA 92123 USA; Univ Calif San Diego, Sch Med, San Diego, CA 92103 USA; Oregon Hlth Sci Univ, Dermatol Clin, Portland, OR 97201 USA; Johns Hopkins Asthma & Allergy Ctr, Baltimore, MD USA; Univ Wisconsin, Sch Med, Madison, WI USA; CUNY Mt Sinai Sch Med, New York, NY 10029 USA; Brigham & Womens Hosp, Boston, MA 02115 USA; Natl Jewish Med & Res Ctr, Denver, CO USA	Eichenfield, LF (reprint author), Childrens Hosp, 8010 Frost St,Ste 602, San Diego, CA 92123 USA.		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J	Martin, RJ				Martin, RJ			Therapeutic significance of distal airway inflammation in asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; distal airway inflammation; nocturnal asthma; inhaled corticosteroids; chlorofluorocarbon-based preparations; hydrofluoroalkane propellants	INHALED BECLOMETHASONE DIPROPIONATE; OBSTRUCTIVE PULMONARY-DISEASE; METERED-DOSE INHALER; LONG-TERM TREATMENT; NOCTURNAL ASTHMA; PSEUDOPHYSIOLOGIC EMPHYSEMA; EOSINOPHILIC INFLAMMATION; TRIAMCINOLONE ACETONIDE; FLUTICASONE PROPIONATE; PERIPHERAL AIRWAYS	Inflammation In asthma is not merely confined to the large central airways but also extends to the small peripheral airways. Distal lung inflammation can be observed even In patients with asthma with mild disease and normal spirometric readings. Subjects with asymptomatic asthma can exhibit significant Increases In peripheral airway resistance, likely the result of distal lung inflammation. As determined from measurements of eosinophilic and other cellular infiltrates, the inflammatory response in the distal lung can exceed that in the large airways. Nocturnal asthma, a natural model of cyclic asthma worsening, is associated with an increase in nighttime distal lung inflammation, as evidenced by the accumulation of alveolar tissue eosinophils. Distal lung disease appears to Increase the risk of recurrent asthma exacerbation, whereas disease-related anatomic changes in the small airways of the distal lung are prominent in fatal asthma. The clinical significance of distal lung disease makes this region an important therapeutic target. Chlorofluorocarbon (CFC)-based preparations of inhaled corticosteroids used to treat airway inflammation produce aerosols of relatively large particle size (similar to4 mum); such aerosols have poor access to the distal lung. New formulations of Inhaled corticosteroids that use hydrofluoroalkane (HFA) propellants can have smaller particle sizes (similar to1 mum). Extrafine HFA aerosols have better access to the distal lung, with less oropharyngeal deposition. Imaging studies suggest that anti-inflammatory medication delivered as an extrafine aerosol produces beneficial changes in distal lung function. In one study, an HFA formulation of an inhaled corticosteroid reduced air trapping to a greater degree than a CFC formulation of the same corticosteroid. By extending the delivery of anti-inflammatory medication to the distal lung, the new HFA-based corticosteroids have the potential to treat asthma more effectively and at reduced steroid doses.	Natl Jewish Med & Res Ctr, Dept Med, Div Pulm, Denver, CO 80206 USA	Martin, RJ (reprint author), Natl Jewish Med & Res Ctr, Dept Med, Div Pulm, 1400 Jackson St, Denver, CO 80206 USA.						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Allergy Clin. Immunol.	FEB	2002	109	2		S			S447	S460		10.1067/mai.2002.121409		14	Allergy; Immunology	Allergy; Immunology	529VQ	WOS:000174322000001	11842317	
J	Tanaka, H; Masuda, T; Tokuoka, S; Komai, M; Nagao, K; Takahashi, Y; Nagai, H				Tanaka, H; Masuda, T; Tokuoka, S; Komai, M; Nagao, K; Takahashi, Y; Nagai, H			The effect of allergen-induced airway inflammation on airway remodeling in a murine model of allergic asthma	INFLAMMATION RESEARCH			English	Article						airway inflammation; bronchial hyperresponsiveness; goblet cells; subepithelial fibrosis; TGF-beta 1	GROWTH-FACTOR-BETA; BRONCHIAL HYPERRESPONSIVENESS; PULMONARY FIBROSIS; CELL HYPERPLASIA; EXPRESSION; MICE; COLLAGEN; EXPOSURE; RESPONSIVENESS; METHACHOLINE	Objective and design: We examined the effect of airway inflammation on airway remodeling and bronchial responsiveness in a mouse model of allergic asthma. Materials and methods: BALB/c mice were sensitized to ovalbumin (OA), and exposed to aerosolized OA (0.01, 0.1 and 1%). Twenty-four hours after the final antigen challenge, bronchial responsiveness was measured, and bronchoalveolar lavage (BAL) and histological examinations were carried out. Results: Repeated antigen exposure induced airway inflammation, IgE/IgG1 responses, epithelial changes, collagen deposition in the lungs, subepithelial fibrosis associated with increases in the amount of transforming growth factor (TGF)-beta1 in BAL fluid (BALF), and bronchial hyperresponsiveness to acetylcholine. The number of eosinophils in BALF was significantly correlated with TGF-beta1 production in BALF and the amount of hydroxyproline. Furthermore, significant correlations were found between these fibrogenic parameters and the bronchial responsiveness. Conclusion: These findings demonstrated that in this murine model airway eosinophilic inflammation is responsible for the development of airway remodeling as well as bronchial hyperresponsiveness in allergic bronchial asthma.	Gifu Pharmaceut Univ, Dept Pharmacol, Gifu 5028585, Japan	Nagai, H (reprint author), Gifu Pharmaceut Univ, Dept Pharmacol, 5-6-1 Mitahora Higashi, Gifu 5028585, Japan.						AIKAWA T, 1992, CHEST, V101, P916, DOI 10.1378/chest.101.4.916; Blobe GC, 2000, NEW ENGL J MED, V342, P1350, DOI 10.1056/NEJM200005043421807; Blyth DI, 1996, AM J RESP CELL MOL, V14, P425; BORDER WA, 1994, NEW ENGL J MED, V331, P1286; Busse W, 1999, AM J RESP CRIT CARE, V160, P1035; Chetta A, 1996, AM J RESP CRIT CARE, V153, P910; Chu HW, 1998, AM J RESP CRIT CARE, V158, P1936; Cui ZH, 1999, ALLERGY, V54, P1074, DOI 10.1034/j.1398-9995.1999.00133.x; DJUKANOVIC R, 1990, AM REV RESPIR DIS, V142, P434; EBINA M, 1973, AM REV RESPIR DIS, V48, P720; Elias JA, 1999, J CLIN INVEST, V104, P1001, DOI 10.1172/JCI8124; Fahy J V, 2000, Curr Opin Pulm Med, V6, P15, DOI 10.1097/00063198-200001000-00004; GAULDIE J, 1993, THORAX, V48, P931, DOI 10.1136/thx.48.9.931; Haneda K, 1999, AM J RESP CELL MOL, V21, P268; HEARD BE, 1973, J PATHOL, V110, P319, DOI 10.1002/path.1711100406; Hoshino M, 1998, THORAX, V53, P21; JEFFERY PK, 1992, AM REV RESPIR DIS, V145, P890; KIVIRIKKO KI, 1967, ANAL BIOCHEM, V19, P249, DOI 10.1016/0003-2697(67)90160-1; LAIHO M, 1989, CANCER RES, V49, P2533; Lee JJ, 1997, J EXP MED, V185, P2143, DOI 10.1084/jem.185.12.2143; MAGNAN A, 1994, THORAX, V49, P789, DOI 10.1136/thx.49.8.789; Matsuoka T, 2000, SCIENCE, V287, P2013, DOI 10.1126/science.287.5460.2013; Minshall EM, 1997, AM J RESP CELL MOL, V17, P326; MORI H, 1995, JPN J PHARMACOL, V67, P279, DOI 10.1254/jjp.67.279; Nagai H, 1997, CLIN EXP ALLERGY, V27, P218; Nagai Hiroichi, 1993, Life Sciences, V53, P243; OHNO I, 1992, J CLIN INVEST, V89, P1662, DOI 10.1172/JCI115764; PADRID P, 1995, AM J RESP CRIT CARE, V151, P184; Palmans E, 2000, AM J RESP CRIT CARE, V161, P627; ROCHE WR, 1989, LANCET, V1, P520; Tanaka H, 1998, LIFE SCI, V62, P169; Temann UA, 1998, J EXP MED, V188, P1307, DOI 10.1084/jem.188.7.1307; Temelkovski J, 1998, THORAX, V53, P849; VARGA J, 1987, BIOCHEM J, V247, P597; YAMAGUCHI S, 1994, LIFE SCI, V54, P471; Zhu Zhou, 1999, Journal of Clinical Investigation, V103, P779, DOI 10.1172/JCI5909	36	83	86	0	2	BIRKHAUSER VERLAG AG	BASEL	VIADUKSTRASSE 40-44, PO BOX 133, CH-4010 BASEL, SWITZERLAND	1023-3830			INFLAMM RES	Inflamm. Res.	DEC	2001	50	12					616	624		10.1007/PL00000243		9	Cell Biology; Immunology	Cell Biology; Immunology	508WB	WOS:000173111800007	11822788	
J	Walters, DM; Breysse, PN; Wills-Karp, M				Walters, DM; Breysse, PN; Wills-Karp, M			Ambient urban Baltimore particulate-induced airway hyperresponsiveness and inflammation in mice	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						air pollution; allergy; asthma; inflammation	DIESEL EXHAUST PARTICLES; RESPIRATORY-DISEASE; LUNG INJURY; POLLUTION; METALS; HYPERREACTIVITY; EXPRESSION	Airborne particulate matter (PM) is hypothesized. to play a role in increases in asthma prevalence, although a causal relationship has yet to be established. To investigate the effects of real-world PM exposure on airway reactivity (AHR) and bronchoalveolar lavage (BAL) cellularity, we exposed naive mice to a single dose (0.5 mg/ mouse) of ambient PM, coal fly ash, or diesel PM. We found that ambient PM exposure induced increases in AHR and BAL cellularity, whereas diesel PM induced significant increases in BAL cellularity, but not AHR. On the other hand, coal fly ash exposure did not elicit significant changes in either of these parameters. We further examined ambient PM-induced temporal changes in AHR, BAL cells, and lung cytakine levels over a 2-wk period. Ambient PM-induced AHR was sustained over 7 d. The increase in AHR was preceded by dramatic increases in BAL eosinophils, whereas a decline in AHR was associated with increases. in macrophages. A Th2 cytokine pattern (IL-5, IL-13, eotaxin) was observed early on with a shift toward a Th1 pattern (IFN-gamma). In additional studies, we found that the active component(s) of ambient PM are not water-soluble and that ambient PM-induced AHR and inflammation are dose-dependent. We conclude that ambient PM can induce asthmalike parameters in naive mice, suggesting that PM exposure may be an important factor in increases in asthma prevalence.	Childrens Hosp, Med Ctr, Div Immunobiol, Cincinnati, OH 45229 USA; Johns Hopkins Sch Hyg & Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD USA	Wills-Karp, M (reprint author), Childrens Hosp, Med Ctr, Div Immunobiol, 3333 Burnet Ave, Cincinnati, OH 45229 USA.			Walters, Dianne/0000-0003-3888-2646	NIEHS NIH HHS [P01 ES-09606, P30 ES-03819]		ABBEY DE, 1993, ARCH ENVIRON HEALTH, V48, P33; AUST S D, 1985, Journal of Free Radicals in Biology and Medicine, V1, P3, DOI 10.1016/0748-5514(85)90025-X; Costa DL, 1997, ENVIRON HEALTH PERSP, V105, P1053, DOI 10.2307/3433509; DiazSanchez D, 1996, J ALLERGY CLIN IMMUN, V98, P114, DOI 10.1016/S0091-6749(96)70233-6; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; DOCKERY DW, 1994, ANNU REV PUBL HEALTH, V15, P107, DOI 10.1146/annurev.pu.15.050194.000543; DREHER KL, 1997, TOXICOL ENV HLTH, V50, P285; Evans R, 1987, CHEST S, V91, P65; Foster WM, 2001, J APPL PHYSIOL, V90, P1111; Gavett SH, 1997, ENVIRON RES, V72, P162, DOI 10.1006/enrs.1997.3732; Ghio AJ, 1999, INHAL TOXICOL, V11, P37, DOI 10.1080/089583799197258; HINDS WC, 1982, AEROSOL TECHNOLOGY P, P83; LEVITT RC, 1988, FASEB J, V2, P2605; MOORE ME, 1993, ENVIRON SCI TECHNOL, V27, P1842, DOI 10.1021/es00046a012; Nel AE, 1998, J ALLERGY CLIN IMMUN, V102, P539, DOI 10.1016/S0091-6749(98)70269-6; OBERDORSTER G, 1992, EXP LUNG RES, V18, P87, DOI 10.3109/01902149209020653; Ohta K, 1999, J ALLERGY CLIN IMMUN, V104, P1024; Peterson B, 1996, ANN ALLERG ASTHMA IM, V77, P263; Pritchard RJ, 1996, INHAL TOXICOL, V8, P457, DOI 10.3109/08958379609005440; SCHWARTZ J, 1993, ENVIRON RES, V62, P7, DOI 10.1006/enrs.1993.1083; Sly RM, 1999, ANN ALLERG ASTHMA IM, V82, P233, DOI 10.1016/S1081-1206(10)62603-8; Takano H, 1998, TOXICOL APPL PHARM, V150, P328, DOI 10.1006/taap.1998.8437; Takano H, 1997, AM J RESP CRIT CARE, V156, P36; WILLSKARP MA, 1909, IN VIVO MODELS INFLA, P137	24	83	83	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.	OCT 15	2001	164	8					1438	1443				6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	494WW	WOS:000172309700022	11704592	
J	Malo, JL; Chan-Yeung, M				Malo, JL; Chan-Yeung, M			Occupational asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						asthma; occupational asthma; irritant-induced asthma; reactive airways dysfunction syndrome	WESTERN RED CEDAR; AIRWAYS DYSFUNCTION SYNDROME; ISOCYANATE-INDUCED ASTHMA; TOLUENE DIISOCYANATE TDI; MOLECULAR-WEIGHT AGENTS; EXHALED NITRIC-OXIDE; HLA CLASS-II; BRONCHIAL-MUCOSA; IGE ANTIBODIES; ADULT ASTHMA	The workplace can be responsible for approximately one in 10 cases of adult-onset asthma. Two types of occupational asthma (OA) are distinguished by whether they arise after a latency period that is necessary for acquiring sensitization or as a result of acute exposure to irritant materials (irritant-induced asthma). The pathophysiology of OA with a latency period is similar to that of nonoccupational asthma, whereas the mechanism of irritant-induced asthma is still uncertain. HLA haplotypes and other genetic polymorphisms have been found to be associated with OA. According to various sources of data, the overall frequency of OA has remained stable in the last 10 years, although the frequency of causal agents vary. Registers of causal occupations and agents have been issued on Web sites (eg, www.asmanet.com). Improved sampling methods have shown that the degree of exposure plays a key role in the onset of the disease, whereas prospective data collected in high-risk workplaces have also identified personal risk factors (eg, atopy, smoking, and rhinoconjunctivitis). A diagnosis of OA should no longer be based on a compatible history only but should be confirmed by means of objective testing. Once the diagnosis is confirmed, the worker should be removed from exposure, and satisfactory compensation programs should be offered, the most important being retraining programs with financial compensations because affected workers are generally young. The cost-effectiveness of prevention programs in high-risk workforces should be assessed.	Hop Sacre Coeur, Dept Resp Med, Montreal, PQ H4J 1C5, Canada; Univ British Columbia, Vancouver Gen Hosp, Dept Med, Vancouver, BC V5Z 1M9, Canada	Malo, JL (reprint author), Hop Sacre Coeur, Dept Resp Med, 5400 W Gouin Blvd, Montreal, PQ H4J 1C5, Canada.						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Allergy Clin. Immunol.	SEP	2001	108	3					317	328		10.1067/mai.2001.116432		12	Allergy; Immunology	Allergy; Immunology	476FK	WOS:000171215400001	11544449	
J	Troutt, C; Levetin, E				Troutt, C; Levetin, E			Correlation of spring spore concentrations and meteorological conditions in Tulsa, Oklahoma	INTERNATIONAL JOURNAL OF BIOMETEOROLOGY			English	Article						aerobiology; Cladosporium; basidiospores; ascospores; multiple regression	ENVIRONMENTAL-FACTORS; AIRBORNE; POPULATIONS; ALTERNARIA; RELEASE; ASTHMA	Different spore types are abundant in the atmosphere depending on the weather conditions. Ascospores generally follow precipitation, while spore types such as Atternaria and Cladosporium are abundant in dry conditions. This project attempted to correlate fungal spore concentrations with meteorological data from Tulsa, Oklahoma during May 1998 and May 1999, Air samples were collected and analyzed by the 12-traverse method. The spore types included were Cladosporium, Alternaria, Epicoccum, Curvularia, Pithomyces, Drechslera. smut spores, ascospores, basidiospores, and other spores. Weather variables included precipitation levels, temperature, dew point, air pressure. wind speed, wind direction and wind gusts. There were over 242.57 mm of rainfall in May 1999 and only 64.01 mm in May 1998. The most abundant spore types during May 1998 and May 1999 were Cladosporium, ascospores, and basidiospores. Results showed that there were significant differences in the dry-air spora between May 1998 and May 1999. There were twice as many Cladosporium in May 1998 as in May 1999; both ascospores and basidiospores showed little change. Multiple regression analysis was used to determine which meteorological variables influenced spore concentrations. Results showed that there was no single model for all spore types. Different combinations of factors were predictors of concentration for the various fungi examined: however. temperature and dew point seemed to be the most important meteorological factors.	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.						BURGE HA, 1986, GRANA, V25, P143; Bush R K, 1989, J Allergy Clin Immunol, V84, P1120, DOI 10.1016/0091-6749(89)90167-X; Crotzer V., 1996, Aerobiologia, V12, P177, DOI 10.1007/BF02248147; CUTTEN AEC, 1988, NEW ZEAL MED J, V101, P361; Epton MJ, 1997, THORAX, V52, P528; Gadoury DM, 1998, PHYTOPATHOLOGY, V88, P902, DOI 10.1094/PHYTO.1998.88.9.902; Gottwald TR, 1997, PHYTOPATHOLOGY, V87, P1078, DOI 10.1094/PHYTO.1997.87.10.1078; HASNAIN SM, 1993, GRANA, V32, P184; HJELMROOS M, 1993, GRANA, V32, P40; HORNER WE, 1992, CLIN REV ALLERG, V10, P191; Katial RK, 1997, INT J BIOMETEOROL, V41, P17, DOI 10.1007/s004840050048; LEVETIN E, 1991, GRANA, V30, P123; LEVETIN E, 1998, 13 C BIOM AER AM MET, P335; Levestin E., 1995, BIOAEROSOLS, P87; LI DW, 1994, GRANA, V33, P166; Richardson MJ, 1996, MYCOL RES, V100, P213; TARLO SM, 1979, J ALLERGY CLIN IMMUN, V64, P43, DOI 10.1016/0091-6749(79)90082-4; Timmer LW, 1998, PHYTOPATHOLOGY, V88, P1218, DOI 10.1094/PHYTO.1998.88.11.1218; Venables KM, 1997, CLIN EXP ALLERGY, V27, P725, DOI 10.1046/j.1365-2222.1997.790893.x	19	83	89	0	7	SPRINGER-VERLAG	NEW YORK	175 FIFTH AVE, NEW YORK, NY 10010 USA	0020-7128			INT J BIOMETEOROL	Int. J. Biometeorol.	JUL	2001	45	2					64	74		10.1007/s004840100087		11	Biophysics; Environmental Sciences; Meteorology & Atmospheric Sciences; Physiology	Biophysics; Environmental Sciences & Ecology; Meteorology & Atmospheric Sciences; Physiology	457DX	WOS:000170122800003	11513049	
J	Cullinan, P; Cook, A; Nieuwenhuijsen, MJ; Sandiford, C; Tee, RD; Venables, KM; McDonald, JC; Taylor, AJN				Cullinan, P; Cook, A; Nieuwenhuijsen, MJ; Sandiford, C; Tee, RD; Venables, KM; McDonald, JC; Taylor, AJN			Allergen and dust exposure as determinants of work-related symptoms and sensitization in a cohort of flour-exposed workers; a case-control analysis	ANNALS OF OCCUPATIONAL HYGIENE			English	Article						sensitization; asthma; flour; alpha-amylase; bakers' asthma	BAKERS ASTHMA; MILLS	Objectives: To estimate the incidence of specific IgE sensitization and allergic respiratory symptoms among UK bakery and flour mill workers; and to examine the roles of flour aeroallergen and total dust exposures in determining these outcomes. Methods: A cohort of 300 new employees, without previous occupational exposure to flour, were followed prospectively for a median (range) of 40 (1-91) months. Cases-defined as those developing work-related symptoms or a positive skin prick test to hour or alpha -amylase during follow up-were compared with controls, matched for duration of employment. Exposures to hour aeroallergen and total inhalable dust were estimated using a questionnaire and personal sampling techniques. Results: Incidence rates for work-related eye/nose and chest symptoms were 11.8 and 4.1 cases per 100 person years (py), respectively. Few er employees developed positive skin prick tests to hour (2.2 cases per 100 py) or alpha -amylase (2.5 cases per 100 py), Positive skin tests to occupational allergens were more common among those with new work-related symptoms. There were clear relationships between the risks of developing work-related symptoms or a positive skin prick test and three categories of estimated exposure to total dust or hour aeroallergen. Atopic employees were more likely to develop a positive skin prick test-but not work-related symptoms, These findings were unaffected by age, sex or cigarette smoking. Conclusions: In this population, many work-related symptoms which develop after first employment in modern UK bakeries or hour mills were not accompanied by evidence of IgE sensitization to flour or alpha -amylase, Although average dust exposures were within current occupational standards, the risks of development of upper and lower respiratory symptoms and of specific sensitization were clearly related to total dust and/or flour aeroallergen exposure. The incidence of work-related chest symptoms in the presence of a positive skin test to flour or alpha -amylase in this setting was approximately 1 case per 100 py, (C) 2001 British Occupational Hygiene Society. Published by Elsevier Science Ltd, All rights reserved.	Univ London Imperial Coll Sci Technol & Med, NHLI, Dept Occupat & Environm Med, London SW3 6LR, England	Cullinan, P (reprint author), Univ London Imperial Coll Sci Technol & Med, NHLI, Dept Occupat & Environm Med, London SW3 6LR, England.		Nieuwenhuijsen, Mark/C-3914-2017	Nieuwenhuijsen, Mark/0000-0001-9461-7981			CULLINAN P, 1994, OCCUP ENVIRON MED, V51, P579; Gordon SB, 1997, OCCUP MED-OXFORD, V47, P361, DOI 10.1093/occmed/47.6.361; HERXHEIMER H, 1973, ACTA ALLERGOL, V28, P42, DOI 10.1111/j.1398-9995.1973.tb02564.x; Houba R, 1996, AM J RESP CRIT CARE, V154, P130; HOUBA R, 1996, THESIS LANDBOUWUNIVE; MCDONALD JC, 2000, UNPUB OCCUPATIONAL E; NIEUWENHUIJSEN MJ, 1994, OCCUP ENVIRON MED, V51, P584; NIEUWENHUIJSEN MJ, 1995, ANN OCCUP HYG, V39, P291, DOI 10.1016/0003-4878(94)00127-M; Nieuwenhuijsen MJ, 1999, OCCUP ENVIRON MED, V56, P197; QUIRCE S, 1992, J ALLERGY CLIN IMMUN, V90, P970, DOI 10.1016/0091-6749(92)90470-M; Ross DJ, 1997, OCCUP MED-OXFORD, V47, P377, DOI 10.1093/occmed/47.6.377	11	83	84	0	2	PERGAMON-ELSEVIER SCIENCE LTD	OXFORD	THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND	0003-4878			ANN OCCUP HYG	Ann. Occup. Hyg.	MAR	2001	45	2					97	103		10.1016/S0003-4878(00)00028-4		7	Public, Environmental & Occupational Health; Toxicology	Public, Environmental & Occupational Health; Toxicology	409HU	WOS:000167378900003	11182423	
J	Huang, TJ; MacAry, PA; Eynott, P; Moussavi, A; Daniel, KC; Askenase, PW; Kemeny, DM; Chung, KF				Huang, TJ; MacAry, PA; Eynott, P; Moussavi, A; Daniel, KC; Askenase, PW; Kemeny, DM; Chung, KF			Allergen-specific Th1 cells counteract efferent Th2 cell-dependent bronchial hyperresponsiveness and eosinophilic inflammation partly via IFN-gamma	JOURNAL OF IMMUNOLOGY			English	Article							BROWN-NORWAY RATS; INDUCED AIRWAY HYPERRESPONSIVENESS; CD4+ T-CELLS; INTERFERON-GAMMA; IGE PRODUCTION; ATOPIC ASTHMA; SMOOTH-MUSCLE; MESSENGER-RNA; CUTTING EDGE; MURINE MODEL	Th2 T cell immune-driven inflammation plays an important role in allergic asthma, We studied the effect of counterbalancing Th1 T cells in an asthma model in Brown Norway rats that favors Th2 responses. Rats received i.v. transfers of syngeneic allergen-specific Th1 or Th2 cells, 24 h before aerosol exposure to allergen, and were studied 18-24 h later. Adoptive transfer of OVA-specific Th2 cells, but not Th1 cells, and OVA, but not BSA exposure, induced bronchial hyperresponsiveness (BHR) to acetylcholine and eosinophilia in a cell number-dependent manner. Importantly, cotransfer of OVA-specific Th1 cells dose-dependently reversed BHR and bronchoalveolar lavage (BAL) eosinophilia, but not mucosal eosinophilia, OVA-specific Th1 cells transferred alone induced mucosal eosinophilia, but neither BHR nor BAL eosinophilia. Th1 suppression of BHR and BAL eosinophilia was allergen specific, since cotransfer of BSA-specific Th1 cells with the OVA-specific Th2 cells was not inhibitory when OVA aerosol alone was used, but was suppressive with OVA and BSA challenge, Furthermore, recipients of Th1 cells alone had increased gene expression for IFN-gamma in the Lungs, while those receiving Th2 cells alone showed increased IL-4 mRNA, Importantly, induction of these Th2 cytokines was inhibited in recipients of combined Th1 and Th2 tells. Anti-IFN-gamma treatment attenuated the down-regulatory effect of Th1 cells. Allergen-specific Th1 cells down-regulate efferent Th2 cytokine-dependent BHR and BAL eosinophilia in an asthma model via mechanisms that depend on IFN-gamma, Therapy designed to control the efferent phase of established asthma by augmenting down-regulatory Th1 counterbalancing mechanisms should be effective.	Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW3 6LY, England; Chang Gung Mem Hosp, Keelung, Taiwan; Univ London Kings Coll, Sch Med & Dent, Dept Immunol, London, England	Chung, KF (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dovehouse St, London SW3 6LY, England.						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Immunol.	JAN 1	2001	166	1					207	217				11	Immunology	Immunology	385PG	WOS:000166012400027	11123294	
J	Cullinan, P; Harris, JM; Taylor, AJN; Hole, AM; Jones, M; Barnes, F; Jolliffe, G				Cullinan, P; Harris, JM; Taylor, AJN; Hole, AM; Jones, M; Barnes, F; Jolliffe, G			An outbreak of asthma in a modern detergent factory	LANCET			English	Article							ENZYMES	The striking decrease in the occurrence of protease-induced occupational asthma in the detergent industry has been attributed to enzyme encapsulation. We report an outbreak of asthma, at least equal in sire to those reported in the 1960s, in a modern European factory which has exclusively used encapsulated enzymes. A survey revealed that enzyme sensitisation and work-related respiratory symptoms were positively correlated with airborne enzyme exposure. We suggest that encapsulation alone is insufficient to prevent enzyme-induced allergy and asthma.	Imperial Coll Sch Med, Dept Occupat & Environm Med, London SW3 6LR, England	Cullinan, P (reprint author), Imperial Coll Sch Med, Dept Occupat & Environm Med, London SW3 6LR, England.						BELIN L, 1970, LANCET, V2, P1153; FLINDT MLH, 1969, LANCET, V1, P1177; JUNIPER CP, 1977, J SOC OCCUP MED, V27, P3; PERDU D, 1992, REV MAL RESPIR, V9, P443; Sarlo K, 1997, J ALLERGY CLIN IMMUN, V100, P480	5	83	83	0	4	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	DEC 2	2000	356	9245					1899	1900		10.1016/S0140-6736(00)03264-5		2	Medicine, General & Internal	General & Internal Medicine	379WD	WOS:000165665400016	11130389	
J	Platts-Mills, TAE; Vaughan, JW; Carter, MC; Woodfolk, JA				Platts-Mills, TAE; Vaughan, JW; Carter, MC; Woodfolk, JA			The role of intervention in established allergy: Avoidance of indoor allergens in the treatment of chronic allergic disease	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						allergy; indoor allergens; intervention	HOUSE-DUST MITE; FEL-D-I; PARTICLE-SIZE DISTRIBUTION; PLACEBO-CONTROLLED TRIAL; AIRBORNE CAT ALLERGEN; INNER-CITY CHILDREN; ASTHMATIC-CHILDREN; COCKROACH ALLERGEN; VACUUM CLEANERS; REDUCE ALLERGEN	Avoidance of exposure to indoor allergens is an important element in the treatment of allergic disease. The results of several studies provide strong evidence in support of a role for allergen avoidance; however, strategies that optimize allergen reduction in houses have not been determined. Complex issues regarding the efficacy of physical and chemical measures that target house dust mite, pet, and cockroach allergens in the home are discussed. The greatest challenge is to educate allergic patients so that they can play an important role in controlling their own disease.	Univ Virginia, Dept Med, Div Asthma Allergy & Immunol, Charlottesville, VA 22908 USA	Platts-Mills, TAE (reprint author), Univ Virginia, Dept Med, Div Asthma Allergy & Immunol, POB 801355, Charlottesville, VA 22908 USA.						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Allergy Clin. Immunol.	NOV	2000	106	5					787	804		10.1067/mai.2000.110548		18	Allergy; Immunology	Allergy; Immunology	417ZK	WOS:000167865200001	11080699	
J	Nordenhall, C; Pourazar, J; Blomberg, A; Levin, JO; Sandstrom, T; Adelroth, E				Nordenhall, C; Pourazar, J; Blomberg, A; Levin, JO; Sandstrom, T; Adelroth, E			Airway inflammation following exposure to diesel exhaust: a study of time kinetics using induced sputum	EUROPEAN RESPIRATORY JOURNAL			English	Article						airway inflammation; diesel exhaust; induced sputum; neutrophils	EPITHELIAL-CELLS; HEALTHY-SUBJECTS; DAILY MORTALITY; POLLUTION; PARTICLES; INDUCTION; COUNTS; ASTHMA; INTERLEUKIN-6; ASSOCIATION	The adverse health effects of particulate matter pollution are of increasing concern. In a recent bronchoscopic study in healthy volunteers, pronounced airway inflammation was detected following exposure to diesel exhaust (DE), The present study was conducted in order to evaluate the time kinetics of the inflammatory response following exposure to DE using induced sputum from healthy volunteers. Fifteen healthy nonsmoking volunteers were exposed to DE particles,vith a 50% cut-off aerodynamic diameter of 10 mu m 300 mu g.m(-3) and air for 1 h on two separate occasions. Sputum induction with hypertonic saline was performed 6 and 24 h after each exposure. Analyses of sputum differential cell counts and soluble protein concentrations were performed. Six hours after exposure to DE, a significant increase was found in the percentage of sputum neutrophils (37.7 versus 26.2% p=0.002) together with increases in the concentrations of interleukin-6 (12.0 versus 6.3 pg.mL(-1), p=0.006) and methylhistamine (0.11 versus 0.12 mu g.L-1, p=0.024). Irrespective of exposure, a significant increase was found in the percentage of sputum neutrophils at 24 as compared to 6 h. indicating that the procedure of sputum induction itself may change the composition of sputum. This study demonstrates that exposure to diesel exhaust induces inflammatory response in healthy human airways, represented by an early increase in interleukin-6 and methylhistamine concentration and the percentage of neutrophils. Induced sputum provides a safe tool for the investigation of the inflammatory effects of diesel exhaust, but care must be taken when interpreting results from repeated sputum inductions.	Umea Univ Hosp, Dept Resp Med & Allergy, S-90185 Umea, Sweden; Inst Working Life, Dept Occupat Chem, Umea, Sweden	Adelroth, E (reprint author), Umea Univ Hosp, Dept Resp Med & Allergy, S-90185 Umea, Sweden.						BARRY CC, 1994, ENVIRONMENT, V36, P5; Carter JD, 1997, TOXICOL APPL PHARM, V146, P180, DOI 10.1006/taap.1997.8254; CLENCHAAS J, 1996, QUANTIFICATION HLTH; DiazSanchez D, 1997, ALLERGY, V52, P52; DIAZSANCHEZ D, 1994, J CLIN INVEST, V94, P1417, DOI 10.1172/JCI117478; DOCKERY DW, 1993, NEW ENGL J MED, V329, P1753, DOI 10.1056/NEJM199312093292401; FAHY JV, 1995, AM J RESP CRIT CARE, V152, P53; FAHY JV, 1994, J ALLERGY CLIN IMMUN, V93, P1031, DOI 10.1016/S0091-6749(94)70052-4; Fahy JV, 1995, ENVIRON RES, V70, P77, DOI 10.1006/enrs.1995.1051; FAHY JV, 1993, AM REV RESPIR DIS, V147, P1126; FLOREANI AA, 1995, AM J RESP CRIT CARE, V151, pA704; GAMBLE J, 1987, ENVIRON RES, V42, P201, DOI 10.1016/S0013-9351(87)80022-1; Grootendorst DC, 1997, CLIN EXP ALLERGY, V27, P769, DOI 10.1046/j.1365-2222.1997.890900.x; Holz O, 1998, THORAX, V53, P83; KISHIMOTO T, 1992, SCIENCE, V258, P593, DOI 10.1126/science.1411569; Nightingale JA, 1998, THORAX, V53, P87; OSTRO B, 1993, ARCH ENVIRON HEALTH, V48, P336; Pavord ID, 1997, THORAX, V52, P498; PIN I, 1992, THORAX, V47, P25, DOI 10.1136/thx.47.1.25; Pizzichini E, 1996, AM J RESP CRIT CARE, V154, P308; Pizzichini MMM, 1996, AM J RESP CRIT CARE, V154, P866; POPE CA, 1995, ENVIRON HEALTH PERSP, V103, P472, DOI 10.2307/3432586; *QUAL URB AIR REV, 1996, SOURC EM PRIM PART M, P37; Quay JL, 1998, AM J RESP CELL MOL, V19, P98; REGER R, 1982, ANN OCCUP HYG, V26, P799, DOI 10.1093/annhyg/26.8.799; RUDELL B, 1994, INT ARCH OCC ENV HEA, V66, P77, DOI 10.1007/BF00383361; Rudell B, 1999, OCCUP ENVIRON MED, V56, P527; Rudell B, 1996, OCCUP ENVIRON MED, V53, P658; Rudell B, 1990, J AEROSOL SCI     S1, V21, P411; Salvi S, 1999, AM J RESP CRIT CARE, V159, P702; SCHWARTZ J, 1992, AM J EPIDEMIOL, V135, P12; SCHWARTZ J, 1993, AM J EPIDEMIOL, V137, P1136; Steerenberg PA, 1998, EXP LUNG RES, V24, P85; ULFVARSON U, 1991, AM J IND MED, V19, P283, DOI 10.1002/ajim.4700190303; Vagaggini B, 1996, EUR RESPIR J, V9, P1852, DOI 10.1183/09031936.96.09091852; VISTAL JJ, 1980, B NY ACAD MED, V56, P914	36	83	88	1	6	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0903-1936			EUR RESPIR J	Eur. Resp. J.	JUN	2000	15	6					1046	1051		10.1034/j.1399-3003.2000.01512.x		6	Respiratory System	Respiratory System	327KA	WOS:000087792000012	10885423	
J	D'Amato, G				D'Amato, G			Urban air pollution and plant-derived respiratory allergy	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review							DIESEL EXHAUST PARTICLES; POLLEN-RELATED ALLERGY; GRASS-POLLEN; EPITHELIAL-CELLS; OZONE EXPOSURE; IN-VITRO; MEDITERRANEAN AREA; PARIETARIA-JUDAICA; ASTHMA EPIDEMICS; NITROGEN-DIOXIDE		Azienda Osped Alta Special, Dept Chest Dis, Div Pneumol & Allergol, Naples, Italy	D'Amato, G (reprint author), Hosp A Cardarelli, Div Pneumol & Allergol, Via Rione Sirignano 10, I-80121 Naples, Italy.						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N., 1995, European Respiratory Journal, V8, p500S; White MC, 1997, AM J EPIDEMIOL, V145, P432; Wichmann HE, 1996, CLIN EXP ALLERGY, V26, P621, DOI 10.1111/j.1365-2222.1996.tb00587.x; Woolcock AJ, 1997, CIBA F SYMP, V206, P122	84	83	85	0	12	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					628	636				9	Allergy; Immunology	Allergy; Immunology	314CU	WOS:000087037700005	10792353	
J	Eberlein-Konig, B; Schafer, T; Huss-Marp, J; Darsow, U; Mohrenschlager, M; Herbert, O; Abeck, D; Kramer, U; Behrendt, H; Ring, J				Eberlein-Konig, B; Schafer, T; Huss-Marp, J; Darsow, U; Mohrenschlager, M; Herbert, O; Abeck, D; Kramer, U; Behrendt, H; Ring, J			Skin surface pH, stratum corneum hydration, trans-epidermal water loss and skin roughness related to atopic eczema and skin dryness in a population of primary school children	ACTA DERMATO-VENEREOLOGICA			English	Article						skin morphology; epidemiological study; MIRIAM (Multicentre International Study for Risk Assessment of Indoor and Outdoor-Air Pollution on Allergy and Eczema Morbidity); non-invasive technologies; cutaneous properties	CLINICALLY UNINVOLVED SKIN; LOSS TEWL; DRY SKIN; DERMATITIS; PROFILOMETRY; CAPACITANCE; PARAMETERS	Non-invasive investigations of skin morphology and function are standard tools to study the pathophysiology of several cutaneous disorders, yet they have not been used in population-based epidemiological studies. Here we examined skin surface pH, stratum corneum hydration, trans-epidermal water loss (TEWL) and skin roughness by profilometry in a study population comprising 377 primary school children (8-9 years old) as part of a multicentre survey on risk factors for allergic diseases in school children. Skin surface pH showed significant higher values (p=0.029) in the group with atopic eczema (n=45) compared with the group without atopic eczema; all other parameters did not differ significantly between children,vith and without atopic eczema. With increasing skin dryness there was a significant increase in pH values (p = 0.004). Stratum corneum hydration showed a significant decrease with increasing dryness (p<0.001). Measurement of skin roughness also revealed a significant linear relationship with skin dryness (p = 0.02). It is concluded that measurement of skin surface pH, corneometry and profilometry are useful non-invasive techniques to objectively assess skin dryness in epidemiological studies regarding atopic skin disease.	Tech Univ Munich, Klin & Poliklin Dermatol & Allergol Biederstein, Dept Dermatol & Allergy Biederstein, D-80802 Munich, Germany; GSF, TUM, Div Environm Dermatol & Allergol, Neuherberg, Germany	Eberlein-Konig, B (reprint author), Tech Univ Munich, Klin & Poliklin Dermatol & Allergol Biederstein, Dept Dermatol & Allergy Biederstein, Biedersteiner Str 29, D-80802 Munich, Germany.						ABE T, 1978, Journal of Dermatology (Tokyo), V5, P223; ABECK D, 1997, NEW TRENDS ALLERGY, V4, P213; BERARDESCA E, 1990, ACTA DERM-VENEREOL, V70, P400; BRAUNFALCO O, 1986, HAUTARZT, V37, P126; COOK TH, 1985, J SOC COSMET CHEM, V36, P143; Dikstein S, 1994, Acta Derm Venereol Suppl (Stockh), V185, P18; Eberlein-Konig B, 1998, J ALLERGY CLIN IMMUN, V101, P141, DOI 10.1016/S0091-6749(98)70212-X; EberleinKonig B, 1996, ACTA DERM-VENEREOL, V76, P447; Gfatter R, 1997, DERMATOLOGY, V195, P258; GLOOR M, 1985, J SOC COSMET CHEM, V36, P153; GOLLHAUSEN R, 1991, HDB ATOPIC ECZEMA, P306; Hanifin JM, 1980, ACTA DERM-VENEREOL S, V92, P44; HUSSMARP J, 1999, ALLERGO J, V8, P356; Leveque JL, 1987, J SOC COSMET CHEM, V82, P171; Linde Y W, 1992, Acta Derm Venereol Suppl (Stockh), V177, P9; LINDE YW, 1989, ACTA DERM-VENEREOL, V69, P315; LODEN M, 1992, BRIT J DERMATOL, V126, P137, DOI 10.1111/j.1365-2133.1992.tb07810.x; Marchionini A, 1938, KLIN WOCHENSCHR, V17, P663, DOI 10.1007/BF01778645; OHMAN H, 1994, ACTA DERM-VENEREOL, V74, P375; PINNAGODA J, 1990, CONTACT DERMATITIS, V22, P164, DOI 10.1111/j.1600-0536.1990.tb01553.x; PRZYBILLA B, 1991, ACTA DERM-VENEREOL, V71, P407; Ring J, 1998, ALLERGY AND ALLERGIC DISEASES, P481; RING J, 1992, ALLERGY, V47, P265, DOI 10.1111/j.1398-9995.1992.tb02051.x; Schafer T, 1997, BRIT J DERMATOL, V137, P558, DOI 10.1111/j.1365-2133.1997.tb03786.x; SCHIAVI ME, 1992, G INT DERM PED, V3, P119; Seidenari S, 1995, ACTA DERM-VENEREOL, V75, P429; TUPKER RA, 1990, BRIT J DERMATOL, V123, P199, DOI 10.1111/j.1365-2133.1990.tb01847.x; WERNER Y, 1986, ACTA DERM-VENEREOL, V66, P281; WERNER Y, 1985, ACTA DERM-VENEREOL, V65, P102; YAMAMOTO A, 1991, ARCH DERMATOL RES, V283, P219, DOI 10.1007/BF01106105	30	83	94	0	12	TAYLOR & FRANCIS AS	OSLO	CORT ADELERSGT 17, PO BOX 2562, SOLLI, 0202 OSLO, NORWAY	0001-5555			ACTA DERM-VENEREOL	Acta Derm.-Venereol.	MAY	2000	80	3					188	191				4	Dermatology	Dermatology	338BW	WOS:000088399100008	10954209	
J	Bailey, LC; Forrest, CB; Zhang, PX; Richards, TM; Livshits, A; DeRusso, PA				Bailey, L. Charles; Forrest, Christopher B.; Zhang, Peixin; Richards, Thomas M.; Livshits, Alice; DeRusso, Patricia A.			Association of Antibiotics in Infancy With Early Childhood Obesity	JAMA PEDIATRICS			English	Article							INFECTIOUS-DISEASES SOCIETY; GUT MICROBIOME; OTITIS-MEDIA; BODY-MASS; MANAGEMENT; CHILDREN; DIAGNOSIS; AMERICA	IMPORTANCE Obesity in children and adults is associated with significant health burdens, making prevention a public health imperative. Infancy may be a critical period when environmental factors exert a lasting effect on the risk for obesity; identifying modifiable factors may help to reduce this risk. OBJECTIVE To assess the impact of antibiotics prescribed in infancy (ages 0-23 months) on obesity in early childhood (ages 24-59 months). DESIGN, SETTING, AND PARTICIPANTS We conducted a cohort study spanning 2001-2013 using electronic health records. Cox proportional hazard models were used to adjust for demographic, practice, and clinical covariates. The study spanned a network of primary care practices affiliated with the Children's Hospital of Philadelphia including both teaching clinics and private practices in urban Philadelphia, Pennsylvania, and the surrounding region. All children with annual visits at ages 0 to 23 months, as well 1 or more visits at ages 24 to 59 months, were enrolled. The cohort comprised 64 580 children. EXPOSURES Treatment episodes for prescribed antibiotics were ascertained up to 23 months of age. MAIN OUTCOMES AND MEASURES Obesity outcomes were determined directly from anthropometric measurements using National Health and Nutrition Examination Survey 2000 body mass index norms. RESULTS Sixty-nine percent of children were exposed to antibiotics before age 24 months, with a mean (SD) of 2.3 (1.5) episodes per child. Cumulative exposure to antibiotics was associated with later obesity (rate ratio [RR], 1.11; 95% CI, 1.02-1.21 for >= 4 episodes); this effect was stronger for broad-spectrum antibiotics (RR, 1.16; 95% CI, 1.06-1.29). Early exposure to broad-spectrum antibiotics was also associated with obesity (RR, 1.11; 95% CI, 1.03-1.19 at 0-5 months of age and RR, 1.09; 95% CI, 1.04-1.14 at 6-11 months of age) but narrow-spectrum drugs were not at any age or frequency. Steroid use, male sex, urban practice, public insurance, Hispanic ethnicity, and diagnosed asthma or wheezing were also predictors of obesity; common infectious diagnoses and antireflux medications were not. CONCLUSIONS AND RELEVANCE Repeated exposure to broad-spectrum antibiotics at ages 0 to 23 months is associated with early childhood obesity. Because common childhood infections were the most frequent diagnoses co-occurring with broad-spectrum antibiotic prescription, narrowing antibiotic selection is potentially a modifiable risk factor for childhood obesity.	[Bailey, L. Charles; Forrest, Christopher B.; Zhang, Peixin; Richards, Thomas M.; Livshits, Alice; DeRusso, Patricia A.] Childrens Hosp Philadelphia, Dept Pediat, Philadelphia, PA 19104 USA; [Bailey, L. Charles; Forrest, Christopher B.; DeRusso, Patricia A.] Univ Penn, Dept Pediat, Perelman Sch Med, Philadelphia, PA 19104 USA; [Richards, Thomas M.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA	Bailey, LC (reprint author), Childrens Hosp Philadelphia, Div Oncol, CTRB 10407, 34th St & Civ Ctr Blvd, Philadelphia, PA 19104 USA.	baileyc@email.chop.edu			American Beverage Foundation	Funding was provided by an unrestricted donation from the American Beverage Foundation for a Healthy America to the Children's Hospital of Philadelphia to support the Healthy Weight Program.	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J	Hinds, DA; McMahon, G; Kiefer, AK; Do, CB; Eriksson, N; Evans, DM; St Pourcain, B; Ring, SM; Mountain, JL; Francke, U; Davey-Smith, G; Timpson, NJ; Tung, JY				Hinds, David A.; McMahon, George; Kiefer, Amy K.; Do, Chuong B.; Eriksson, Nicholas; Evans, David M.; St Pourcain, Beate; Ring, Susan M.; Mountain, Joanna L.; Francke, Uta; Davey-Smith, George; Timpson, Nicholas J.; Tung, Joyce Y.			A genome-wide association meta-analysis of self-reported allergy identifies shared and allergy-specific susceptibility loci	NATURE GENETICS			English	Article							DISEASE SUSCEPTIBILITY; ATOPIC-DERMATITIS; GENOTYPE DATA; RISK LOCI; T-CELLS; ASTHMA; POPULATION; VARIANTS; GENE; DIFFERENTIATION	Allergic disease is very common and carries substantial public-health burdens. We conducted a meta-analysis of genome-wide associations with self-reported cat, dust-mite and pollen allergies in 53,862 individuals. We used generalized estimating equations to model shared and allergy-specific genetic effects. We identified 16 shared susceptibility loci with association P < 5 x 10(-8), including 8 loci previously associated with asthma, as well as 4p14 near TLR1, TLR6 and TLR10 (rs2101521, P = 5.3 x 10(-21)); 6p21.33 near HLA-C and MICA (rs9266772, P = 3.2 x 10(-12)); 5p13.1 near PTGER4 (rs7720838, P = 8.2 x 10(-11)); 2q33.1 in PLCL1 (rs10497813, P = 6.1 x 10(-10)), 3q28 in LPP (rs9860547, P = 1.2 x 10(-9)); 20q13.2 in NFATC2 (rs6021270, P = 6.9 x 10(-9)), 4q27 in ADAD1 (rs17388568, P = 3.9 x 10(-8)); and 14q21.1 near FOXA1 and TTC6 (rs1998359, P = 4.8 x 10(-8)). We identified one locus with substantial evidence of differences in effects across allergies at 6p21.32 in the class II human leukocyte antigen (HLA) region (rs17533090, P = 1.7 x 10(-12)), which was strongly associated with cat allergy. Our study sheds new light on the shared etiology of immune and autoimmune disease.	[Hinds, David A.; Kiefer, Amy K.; Do, Chuong B.; Eriksson, Nicholas; Mountain, Joanna L.; Francke, Uta; Tung, Joyce Y.] 23andMe Inc, Mountain View, CA USA; [McMahon, George; Evans, David M.; Davey-Smith, George; Timpson, Nicholas J.] Univ Bristol, MRC, Ctr Causal Anal Translat Epidemiol, Sch Social & Community Med, Bristol, Avon, England; [St Pourcain, Beate; Ring, Susan M.] Univ Bristol, Sch Social & Community Med, Bristol, Avon, England	Hinds, DA (reprint author), 23andMe Inc, Mountain View, CA USA.	dhinds@23andMe.com	Fox, Laura /C-6249-2016; Osborne, Nicholas/N-4915-2015; Davey Smith, George/A-7407-2013	Osborne, Nicholas/0000-0002-6700-2284; Davey Smith, George/0000-0002-1407-8314; St Pourcain, Beate/0000-0002-4680-3517; Timpson, Nicholas/0000-0002-7141-9189; Evans, David/0000-0003-0663-4621	National Heart, Lung, and Blood Institute of the US National Institutes of Health [1R43HL115873-01]; UK MRC [74882]; Wellcome Trust [092731]	We thank the customers of 23andMe who answered surveys, as well as the employees of 23andMe, who together made this research possible. We also thank K. Nadeau for assistance in survey development and S. Nelson and R. Altman for reviewing surveys. This work was supported in part by the National Heart, Lung, and Blood Institute of the US National Institutes of Health under grant 1R43HL115873-01.; We are extremely grateful to all the families who took part in ALSPAC, to the midwives for their help in recruiting them and to the whole ALSPAC team, which includes interviewers, computer and laboratory technicians, clerical workers, research scientists, volunteers, managers, receptionists and nurses. The UK MRC (grant 74882), the Wellcome Trust (grant 092731) and the University of Bristol provide core support for ALSPAC.	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J	Rondon, C; Campo, P; Togias, A; Fokkens, WJ; Durham, SR; Powe, DG; Mullol, J; Blanca, M				Rondon, Carmen; Campo, Paloma; Togias, Alkis; Fokkens, Wytske J.; Durham, Stephen R.; Powe, Desmond G.; Mullol, Joaquim; Blanca, Miguel			Local allergic rhinitis: Concept, pathophysiology, and management	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Allergic rhinitis; eosinophil cationic protein; entopy; local allergic rhinitis; local specific IgE; nasal polyps; nonallergic rhinitis; nasal allergen provocation test; tryptase	PERSISTENT NONALLERGIC RHINITIS; IDIOPATHIC RHINITIS; PROVOCATION TEST; NASAL POLYPOSIS; IGE ANTIBODIES; MESSENGER-RNA; MAST-CELLS; ABSENCE; ASTHMA; ATOPY	Local allergic rhinitis (LAR) is a localized nasal allergic response in the absence of systemic atopy characterized by local production of specific IgE (sIgE) antibodies, a T(H)2 pattern of mucosal cell infiltration during natural exposure to aeroallergens, and a positive nasal allergen provocation test response with release of inflammatory mediators (tryptase and eosinophil cationic protein). Although the prevalence remains to be established, a number of patients previously given a diagnosis of nonallergic rhinitis or idiopathic rhinitis are now being classified as having LAR. Culprit allergens responsible include house dust mite, grass and olive pollens, and many others. For the diagnosis of LAR, neither skin prick testing nor determination of the presence of serum sIgE antibodies is useful, and a nasal allergen provocation test is needed to identify the culprit allergen or allergens. In a certain proportion of cases, local sIgE can be detected, and conjunctivitis, asthma, or both can be associated. Whether patients with LAR will have systemic atopy in the future is a matter of debate. Further studies are needed for examine the prevalence of this phenomenon in different areas, to improve the diagnostic methods to better identify these patients, and to develop therapeutic approaches, including the use of immunotherapy. (J Allergy Clin Immunol 2012;129:1460-7.)	[Rondon, Carmen; Campo, Paloma; Blanca, Miguel] Carlos Haya Hosp, Allergy Serv, Malaga, Spain; [Togias, Alkis] NIAID, Asthma Allergy & Inflammat Branch, Div Allergy Immunol & Transplantat, NIH, Bethesda, MD 20892 USA; [Fokkens, Wytske J.] Univ Amsterdam, Acad Med Ctr, Dept Otorhinolaryngol, NL-1105 AZ Amsterdam, Netherlands; [Durham, Stephen R.] Imperial Coll Sch Med, Natl Heart & Lung Inst, London, England; [Powe, Desmond G.] Nottingham Trent Univ, John Van Geest Canc Res Ctr, Nottingham, England; [Powe, Desmond G.] Nottingham Trent Univ, Nottingham Univ Hosp NHS Trust, Queens Med Ctr, Dept Cellular Pathol, Nottingham, England; [Mullol, Joaquim] CIBERES, Hosp Clin IDIBAPS, ENT Dept, Rhinol Unit, Barcelona, Spain; [Mullol, Joaquim] CIBERES, Hosp Clin IDIBAPS, ENT Dept, Smell Clin, Barcelona, Spain	Rondon, C (reprint author), Hosp Civil, Lab Invest, Pabellon 5,Plaza Hosp Civil, Malaga 29009, Spain.	carmenrs61@gmail.com			GlaxoSmithKline; Medtronic	W. J. Fokkens has received research support from GlaxoSmithKline and Medtronic and has served as an advisor to GlaxoSmith Kline, MSD, and Stallergenes. The rest of the authors declare that they have no relevant conflicts of interest.	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Allergy Clin. Immunol.	JUN	2012	129	6					1460	1467		10.1016/j.jaci.2012.02.032		8	Allergy; Immunology	Allergy; Immunology	952BL	WOS:000304764600004	22516477	
J	Royer, PJ; Emara, M; Yang, CX; Al-Ghouleh, A; Tighe, P; Jones, N; Sewell, HF; Shakib, F; Martinez-Pomares, L; Ghaemmaghami, AM				Royer, Pierre-Joseph; Emara, Mohamed; Yang, Chaoxing; Al-Ghouleh, Abeer; Tighe, Paddy; Jones, Nick; Sewell, Herb F.; Shakib, Farouk; Martinez-Pomares, Luisa; Ghaemmaghami, Amir M.			The Mannose Receptor Mediates the Uptake of Diverse Native Allergens by Dendritic Cells and Determines Allergen-Induced T Cell Polarization through Modulation of IDO Activity	JOURNAL OF IMMUNOLOGY			English	Article							INDOLEAMINE 2,3-DIOXYGENASE IDO; TRYPTOPHAN-METABOLITES; ANTIGEN PRESENTATION; EXPERIMENTAL ASTHMA; TH2 POLARIZATION; IL-4 PRODUCTION; RESPONSES; SUPPRESSION; INHIBITION; MATURATION	The mannose receptor (MR) is a C-type lectin expressed by dendritic cells (DCs). We have investigated the ability of MR to recognize glycosylated allergens. Using a gene silencing strategy, we have specifically inhibited the expression of MR on human monocyte-derived DCs. We show that MR mediates internalization of diverse allergens from mite (Der p 1 and Der p 2), dog (Can f 1), cockroach (Bla g 2), and peanut (Ara h 1) through their carbohydrate moieties. All of these allergens bind to the C-type lectin-like carbohydrate recognition domains 4-7 of MR. We have also assessed the contribution of MR to T cell polarization after allergen exposure. We show that silencing MR expression on monocyte-derived DCs reverses the Th2 cell polarization bias, driven by Der p 1 allergen exposure, through upregulation of IDO activity. In conclusion, our work demonstrates a major role for MR in glycoallergen recognition and in the development of Th2 responses. The Journal of Immunology, 2010, 185: 1522-1531.	[Royer, Pierre-Joseph; Emara, Mohamed; Yang, Chaoxing; Al-Ghouleh, Abeer; Tighe, Paddy; Sewell, Herb F.; Shakib, Farouk; Martinez-Pomares, Luisa; Ghaemmaghami, Amir M.] Univ Nottingham, Queens Med Ctr, Sch Mol Med Sci, Nottingham NG7 2UH, England; [Jones, Nick] Univ Nottingham, Queens Med Ctr, Div Otorhinolaryngol, Sch Clin Sci, Nottingham NG7 2UH, England; [Shakib, Farouk; Martinez-Pomares, Luisa; Ghaemmaghami, Amir M.] Univ Nottingham, Queens Med Ctr, Resp Biomed Res Unit, Nottingham NG7 2UH, England	Ghaemmaghami, AM (reprint author), Univ Nottingham, Queens Med Ctr, Sch Mol Med Sci, A Floor,West Block, Nottingham NG7 2UH, England.	luisa.m@nottingham.ac.uk; amg@nottingham.ac.uk	Emara, Mohamed/C-8220-2013; Royer, Pierre-Joseph/D-4768-2015	Royer, Pierre-Joseph/0000-0001-5534-7982; Emara, Mohamed/0000-0001-7708-9435; Martinez-Pomares, Luisa/0000-0002-2331-127X	Asthma U.K. [06/001]; Faculty of Pharmacy, Helwan University, Egypt	This work was supported by an Asthma U.K. Research Grant (06/001). M.E. is a recipient of a Ph.D. scholarship from the Faculty of Pharmacy, Helwan University, Egypt.	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Immunol.	AUG 1	2010	185	3					1522	1531		10.4049/jimmunol.1000774		10	Immunology	Immunology	629EI	WOS:000280177400028	20610655	
J	Li, J; Sun, B; Huang, Y; Lin, X; Zhao, D; Tan, G; Wu, J; Zhao, H; Cao, L; Zhong, N				Li, J.; Sun, B.; Huang, Y.; Lin, X.; Zhao, D.; Tan, G.; Wu, J.; Zhao, H.; Cao, L.; Zhong, N.		CARRAD	A multicentre study assessing the prevalence of sensitizations in patients with asthma and/or rhinitis in China	ALLERGY			English	Article						aeroallergens; asthma; epidemiology; rhinitis; sensitization; skin prick test	DERMATOPHAGOIDES-PTERONYSSINUS; BLOMIA-TROPICALIS; ALLERGIC RHINITIS; INDOOR ALLERGENS; DUST MITES; EPITHELIAL-CELLS; RISK-FACTOR; CHILDREN; SEVERITY; EXPOSURE	The prevalence of sensitization in patients with asthma and rhinitis in mainland China remains unclear. Our aim was to estimate the prevalence of allergy in patients with respiratory allergic diseases such as asthma and/or rhinitis attending respiratory clinics within mainland China. The study also investigated regional and annual differences in the prevalence and pattern of sensitization among the patients in China. A cross-sectional survey was performed in 6304 patients suffering from asthma and/or rhinitis in 17 cities from 4 regions of China. Patients completed a standardized questionnaire asking for the presence of respiratory and allergic symptoms. They also underwent skin prick tests with 13 common aeroallergens. Among the 6304 patients, 4545 (72.1%) had at least one positive skin prick reaction. The overall prevalence of positive skin prick responses was 59.0% for Dermatophagoides farinae, 57.6% for Dermatophagoides pteronyssinus, 40.7% for Blomia tropicalis, 16.1% for American cockroach, 14.0% for dog, 11.5% for Blatella germanica, 11.3% for Artemisia vulgaris, 10.3% for cat, 6.5% for Ambrosia artemisifolia, 6.3% for mixed mould I, 4.4% for mixed mould IV, 3.5% for mixed grass pollen and 2.2% for mixed tree pollen. Sensitizations to common allergens varied widely between geographical areas and demonstrated unique pattern in patients by stratification with age groups, with asthma and/or rhinitis. Severity of rhinitis and asthma was significantly correlated with skin index of reactivity to Artemisia vulgaris, Ambrosia artemisifolia and to D. pteronyssinus, D. farinae and Blomia tropicalis respectively (P < 0.001). Positive reactivity to the tested allergens and concomitant reactivity to multiple allergens including to house dust mites and Blomia tropicalis was markedly increased in patients with both asthma and rhinitis. House dust mites were the most prevalent allergens in patients with asthma and/or rhinitis in China. There were significant differences in patterns of sensitizations in patients from different geographical areas, age groups as well as asthma and/or rhinitis.	[Li, J.; Sun, B.; Zhong, N.] Guangzhou Med Coll, Affiliated Hosp 1, State Key Lab Resp Dis, Guangzhou 510120, Guangdong, Peoples R China; [Huang, Y.] Chongqing Univ Med Sci, Childrens Hosp, Chongqing, Peoples R China; [Lin, X.] Gen Hosp Shenyang Mil Command, Shenyang, Liaoning, Peoples R China; [Zhao, D.] Nanjing Childrens Hosp, Nanjing, Jiangsu, Peoples R China; [Tan, G.] Xiangya Med Univ, Hosp 3, Changsha, Hunan, Peoples R China; [Wu, J.] First Hosp Xiamen, Xiamen, Fujian, Peoples R China; [Zhao, H.] Shanxi Med Univ, Hosp 2, Taiyuan, Shanxi, Peoples R China; [Cao, L.] Capital Inst Pediat, Beijing, Peoples R China	Zhong, N (reprint author), Guangzhou Med Coll, Affiliated Hosp 1, State Key Lab Resp Dis, Guangzhou 510120, Guangdong, Peoples R China.				ALK-Abello A/S [FC409(10441)-ALK]	This study was supported by ALK-Abello A/S (FC409(10441)-ALK).	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J	Bryant-Stephens, T				Bryant-Stephens, Tyra			Asthma disparities in urban environments	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						Asthma; disparities; children; community-based; asthma morbidity; asthma interventions	INNER-CITY CHILDREN; INSURANCE PROGRAM SCHIP; COCKROACH ALLERGEN; MANAGEMENT PROGRAM; HEALTH-CARE; AFRICAN-AMERICAN; CHILDHOOD ASTHMA; CONTROLLED-TRIAL; SELF-MANAGEMENT; UNITED-STATES	Asthma continues to disproportionately affect minority and low-income groups, with African American and Latino children who live in low-socioeconomic-status urban environments experiencing higher asthma morbidity and mortality than white children. This uneven burden in asthma morbidity has been ever increasing despite medical advancement. Many factors have contributed to these disparities in the areas of health care inequities, which result in inadequate treatment; poor housing, which leads to increased exposure to asthma allergens; and social and psychosocial stressors, which are often unappreciated. Interventions to reduce individual areas of disparities have had varying successes. Because asthma is a complex disease that affects millions of persons, multifaceted comprehensive interventions that combine all evidence-based successful strategies are essential to finally closing the gap in asthma morbidity. (J Allergy Clin Immunol 2009;123:1199-206.)	Univ Penn, Childrens Hosp Philadelphia, Community Asthma Prevent Program, Dept Gen Pediat,Sch Med, Philadelphia, PA 19104 USA	Bryant-Stephens, T (reprint author), Univ Penn, Childrens Hosp Philadelphia, Community Asthma Prevent Program, Dept Gen Pediat,Sch Med, 3535 Market St,Suite 1032, Philadelphia, PA 19104 USA.	stephenst@email.chop.edu					AKINBAMI LJ, 1980, STATE CHILDHOOD ASTH; Apter AJ, 1998, AM J RESP CRIT CARE, V157, P1810; Bartholomew LK, 2006, J SCHOOL HEALTH, V76, P283; Bloomberg GR, 2005, IMMUNOL ALLERGY CLIN, V25, P83, DOI 10.1016/j.iac.2004.09.001; Bryant-Stephens T, 2004, J NATL MED ASSOC, V96, P954; Bryant-Stephens T, 2008, J NATL MED ASSOC, V100, P306; Cabana MD, 2006, PEDIATRICS, V117, P2149, DOI 10.1542/peds.2005-1055; Canino G, 2008, J ALLERGY CLIN IMMUN, V121, P665, DOI 10.1016/j.jaci.2007.10.022; Chen E, 2007, AM J RESP CRIT CARE, V176, P644, DOI 10.1164/rccm.200610-1473OC; CHRISTIAANSE ME, 1989, J DEV BEHAV PEDIATR, V10, P75; Clark NM, 2000, EUR RESPIR J, V16, P15, DOI 10.1034/j.1399-3003.2000.16a04.x; 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Allergy Clin. Immunol.	JUN	2009	123	6					1199	1206		10.1016/j.jaci.2009.04.030		8	Allergy; Immunology	Allergy; Immunology	455WO	WOS:000266799100007	19501229	
J	Glasser, R; Navid, F; Schuller, W; Jantschitsch, C; Harder, J; Schroder, JM; Schwarz, A; Schwarz, T				Glaesser, Regine; Navid, Fatemeh; Schuller, Winfried; Jantschitsch, Christian; Harder, Juergen; Schroeder, Jens M.; Schwarz, Agatha; Schwarz, Thomas			UV-B radiation induces the expression of antimicrobial peptides in human keratinocytes in vitro and in vivo	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						UV radiation; immunosuppression; adaptive immune response; innate immune response; antimicrobial peptides; skin; keratinocytes	NORMAL HUMAN SKIN; ULTRAVIOLET-RADIATION; ATOPIC-DERMATITIS; PSORIASIN S100A7; GENE-EXPRESSION; MESSENGER-RNA; T-CELLS; INNATE; PHOTOTHERAPY; INFECTION	Background: Suppression of the adaptive immune system by UV radiation plays an important role in photocarcinogenesis. Exacerbation of skin infections has been proposed as a further consequence of UV-induced immunosuppression. Clinically bacterial infections are not a problem. For defense against bacteria, the innate immune response including the release of antimicrobial peptides is much more relevant than the adaptive immune response. Keratinocytes; have the capacity to release antimicrobial peptides. Objective: We asked whether UV radiation induces antimicrobial peptides in vitro and in vivo. Methods: Antimicrobial peptide expression by normal human keratinocytes was measured by real-time PCR and fluorescence-activated cell sorting analysis. Biopsies taken from human volunteers and skin explants were studied with immunohistochemistry. Results: Real-time PCR of normal human keratinocytes revealed a dose-dependent increase of human beta-defensin-2, -3, ribonuclease 7, and psoriasin (S100A7) after UV radiation. This was confirmed at the protein level by intracellular fluorescence-activated cell sorting and in vitro immunofluorescence analysis. Immunohistochemistry of biopsies taken from healthy volunteers exposed to different UV radiation doses revealed enhanced epidermal expression of antimicrobial peptides after UV exposure. This was also confirmed by exposing human skin explants to UV radiation. Conclusion: UV radiation exerts diverse effects on the immune system, suppressing the adaptive but inducing the innate immune response. This may explain why T-cell-mediated immune reactions are suppressed on UV exposure but not host defense reactions against bacterial attacks. (J Allergy Clin Immunol 2009;123:1117-23.)	[Glaesser, Regine; Navid, Fatemeh; Schuller, Winfried; Jantschitsch, Christian; Harder, Juergen; Schroeder, Jens M.; Schwarz, Agatha; Schwarz, Thomas] Univ Kiel, Dept Dermatol & Allergol, D-24105 Kiel, Germany	Schwarz, T (reprint author), Univ Kiel, Dept Dermatol & Allergol, Schittenhelmstr 7, D-24105 Kiel, Germany.	tschwarz@dermatology.uni-kiel.de	Harder, Juergen/B-3162-2010; Glaser, Regine/B-3168-2010; Schwarz, Thomas/A-9148-2010		German Research Foundation [SFB 617, A21]; Federal Ministry of Education and Research	Supported by grants front the German Research Foundation (SFB 617, A21) to T.S. and from the Federal Ministry of Education and Research (Bundesministerium fur Bildung und Forschung, SkinSlaph) to R.G.	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Allergy Clin. Immunol.	MAY	2009	123	5					1117	1123		10.1016/j.jaci.2009.01.043		7	Allergy; Immunology	Allergy; Immunology	449CW	WOS:000266309400021	19342087	
J	Maestrelli, P; Boschetto, P; Fabbri, LM; Mapp, CE				Maestrelli, Piero; Boschetto, Piera; Fabbri, Leonardo M.; Mapp, Cristina E.			Mechanisms of occupational asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Workplace exposure; asthma; airway hyperresponsiveness; antigen; chemical; genetics; mechanisms; inflammation	DIISOCYANATE-INDUCED ASTHMA; AIRWAYS DYSFUNCTION SYNDROME; ISOCYANATE-INDUCED ASTHMA; SERUM-ALBUMIN CONJUGATE; TUMOR-NECROSIS-FACTOR; GENE-ENVIRONMENT INTERACTIONS; LABORATORY-ANIMAL WORKERS; WESTERN RED CEDAR; HLA CLASS-II; TOLUENE DIISOCYANATE	Inhalation of agents in the workplace can induce asthma in a relatively small proportion of exposed workers. Like nonoccupational asthma, occupational asthma is probably the result of multiple genetic, environmental, and behavioral influences. It is important that occupational asthma be recognized clinically because it has serious medical and socioeconomic consequences. Environmental factors that can affect the initiation of occupational asthma include the intrinsic characteristics of causative agents as well as the influence of the level and route of exposure at the workplace. The identification of host factors, polymorphisms, and candidate genes associated with occupational asthma may improve our understanding of mechanisms involved in asthma. High-molecular-weight compounds from biological sources and low-molecular-weight chemicals cause occupational asthma after a latent period of exposure. Although the clinical, functional, and pathologic features of occupational asthma caused by low-molecular-weight agents resemble those of allergic asthma, the failure to detect specific IgE antibodies against most low-molecular-weight agents has resulted in a search for alternative or complementary physiopathologic mechanisms leading to airway sensitization. Recent advances have been made in the characterization of the immune response to low-molecular-weight agents. In contrast, the mechanism of the type of occupational asthma that occurs without latency after high-level exposure to irritants remains undetermined. (J Allergy Clin Immunol 2009;123:531-42.)	[Fabbri, Leonardo M.] Univ Modena & Reggio Emilia, Dept Oncol Hematol & Resp Dis, Policlin Modena, I-41100 Modena, Italy; [Maestrelli, Piero] Univ Padua, Dept Environm Med & Publ Hlth, I-35100 Padua, Italy; [Boschetto, Piera; Mapp, Cristina E.] Univ Ferrara, Dept Clin & Expt Med, Sect Hyg & Occupat Med, I-44100 Ferrara, Italy	Fabbri, LM (reprint author), Univ Modena & Reggio Emilia, Dept Oncol Hematol & Resp Dis, Policlin Modena, Largo Pozzo 71, I-41100 Modena, Italy.	leonardo.fabbri@unimore.it	Fabbri, Leonardo/I-4055-2012	Fabbri, Leonardo/0000-0001-8894-1689	Ministry of University and Scientific Research; University of Padova; University of Ferrara; Consorzio Ferrara Ricerche; Associazione per la Ricerca e Cara dell' Asma, Padova; Associazione per to Studio dei Tumori e delle Malattie Polmonari, Padova	Supported by the Ministry of University and Scientific Research: University of Padova; University of Ferrara; Consorzio Ferrara Ricerche; the Associazione per la Ricerca e Cara dell' Asma, Padova; and the Associazione per to Studio dei Tumori e delle Malattie Polmonari, Padova.	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Allergy Clin. Immunol.	MAR	2009	123	3					531	542		10.1016/j.jaci.2009.01.057		12	Allergy; Immunology	Allergy; Immunology	426TQ	WOS:000264731200008	19281901	
J	Weghofer, M; Thomas, WR; Kronqvist, M; Mari, A; Purohit, A; Pauli, G; Horak, F; Gronlund, H; Van Hage, M; Valenta, R; Vrtala, S				Weghofer, M.; Thomas, W. R.; Kronqvist, M.; Mari, A.; Purohit, A.; Pauli, G.; Horak, F.; Gronlund, H.; van Hage, M.; Valenta, R.; Vrtala, S.			Variability of IgE reactivity profiles among European mite allergic patients	EUROPEAN JOURNAL OF CLINICAL INVESTIGATION			English	Article						Diagnosis; HDM allergy; IgE prevalence; recombinant allergens; storage mite allergy	HOUSE-DUST MITE; DERMATOPHAGOIDES-PTERONYSSINUS; CROSS-REACTIVITY; LEPIDOGLYPHUS-DESTRUCTOR; TYROPHAGUS-PUTRESCENTIAE; RECOMBINANT ALLERGENS; SWEDISH FARMERS; STORAGE MITES; P 7; RESPONSES	House dust mites (HDM) Dermatophagoides pteronyssinus are a frequent indoor allergen source. Our aim was to determine the frequencies of IgE reactivity to purified HDM allergen molecules in mite allergic patients from different parts of Europe in order to establish an allergen panel for diagnosis of HDM allergy. Populations of D. pteronyssinus-allergic patients from Austria (n = 56), France (n = 55), Italy (n = 67) and Sweden (n = 65) and storage mite allergic patients from Sweden (n = 31) were analysed for IgE reactivity to eight purified natural (n) and recombinant (r) D. pteronyssinus allergens (nDer p 1, rDer p 2, nDer p 4, rDer p 5, rDer p 7, rDer p 8, rDer p 10 and rDer p 14) in RAST-based dot blot assays. Using a combination of Der p 1 and Der p 2, at least 97% of the D. pteronyssinus-allergic patients could be diagnosed in each of the HDM allergic populations. However, more than 50% of the patients also reacted with other allergens and significant variabilities regarding the frequencies of IgE reactivity to individual allergen molecules were found. Patients with a predominant storage mite allergy showed none or only very weak IgE reactivity to purified D. pteronyssinus allergens. Purified Der p 1 and Der p 2 are sufficient for the diagnosis of >= 97% of D. pteronyssinus allergic patients in Europe, but other allergens may also play an important role for the diagnosis and treatment of HDM allergy. Eur J Clin Invest 2008; 38 (12): 959-965.	[Vrtala, S.] Med Univ Vienna, Div Immunopathol, Dept Pathophysiol, Ctr Physiol & Pathophysiol, A-1090 Vienna, Austria; [Kronqvist, M.; Gronlund, H.; van Hage, M.] Karolinska Inst, Stockholm, Sweden; [Kronqvist, M.; Gronlund, H.; van Hage, M.] Univ Hosp, Stockholm, Sweden; [Mari, A.] IDI IRCCS, Rome, Italy; [Purohit, A.; Pauli, G.] Strasbourg Univ Hosp, Strasbourg, France	Vrtala, S (reprint author), Med Univ Vienna, Div Immunopathol, Dept Pathophysiol, Ctr Physiol & Pathophysiol, Wachringer Guertel 18-20, A-1090 Vienna, Austria.	susanne.vrtala@meduniwien.ac.at	van Hage, Marianne/A-9678-2017	van Hage, Marianne/0000-0003-3091-1596	Austrian Science Fund [F1803, F1815]; Christian Doppler Research Association, Biomay, Vienna, Austria; Swedish Asthma and Allergy Association's Research Foundation; Swedish Research Council	This work was supported by grants F1803 and F1815 of the Austrian Science Fund, the Christian Doppler Research Association, Biomay, Vienna, Austria, the Swedish Asthma and Allergy Association's Research Foundation and the Swedish Research Council.	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J. Clin. Invest.	DEC	2008	38	12					959	965		10.1111/j.1365-2362.2008.02048.x		7	Medicine, General & Internal; Medicine, Research & Experimental	General & Internal Medicine; Research & Experimental Medicine	375GT	WOS:000261102800012	19021722	
J	Ghadimi, D; Folster-Holst, R; de Vrese, M; Winkler, P; Heller, KJ; Schrezenmeir, J				Ghadimi, Darab; Foelster-Holst, Regina; de Vrese, Michael; Winkler, Petra; Heller, Knut J.; Schrezenmeir, Juergen			Effects of probiotic bacteria and their genomic DNA on T(H)1/T(H)2-cytokine production by peripheral blood mononuclear cells (PBMCs) of healthy and allergic subjects	IMMUNOBIOLOGY			English	Article						T(H)1/T(H)2-cytokines; Immune system; Allergy; Probiotics; Lactobacilli; Bifidobacteria	LACTIC-ACID BACTERIA; RANDOMIZED CONTROLLED-TRIAL; PLACEBO-CONTROLLED TRIAL; COMMON COLD EPISODES; IFN-GAMMA PRODUCTION; CPG OLIGODEOXYNUCLEOTIDES; LACTOBACILLUS-RHAMNOSUS; ATOPIC-DERMATITIS; AIRWAY INFLAMMATION; INTERFERON-GAMMA	Among the factors potentially involved in the increased prevalence of allergic diseases, modification of the intestinal flora or lack of microbial exposure during childhood has been proposed. TH2-cytokines increase the production of IgE and stimulate mast cells and eosinophils, whereas T(H)1-cytokines, Such Lis IFN-gamma, may suppress IgE synthesis and Stimulate the expression of the secretory piece of IgA. Thus, a dysregulation In the expression of T(H)1- and T(H)2-cytokines may contribute to the initiation and maintenance of allergic diseases. Lactobacilli belonging to the natural intestinal rnicroflora were reported to reduce the incidence of atopic dermatitis and the severity of allergic manifestations and to modulate T(H)1/T(H)2 responses. The mechanisms still remain to be elucidated. We Sought to assess the effect of different probiotics, Lactobacillus rhamnosus GG, Lactobacillus gasseri (PA 16/8) Bifidobacterium bifidum (MP20/5), and B Bifidobacterium longum (SP07/3), on the T(H)1 I and T(H)2 responses of peripheral blood mononuclear cells (PBMCs) from healthy subjects and from patients with allergy against house dust mite to Staphylococcus enterotoxin A (SEA) and Dermatophagoides pteronyssinus (Dpt). To elucidate the Molecular basis of these effects, the effects of bacterial genomic DNA were compared with the effects of viable bacteria. PBMCs from allergic patients and from healthy donors were incubated for 24 or 48h, respectively, With Or Without SEA and Dpt allergens. The effects of preincubation with live probiotic bacteria and the effect of their genomic DNA, Lidded Simultaneously to Cultures and incubated for 24h, were assessed by measuring T(H)1/T(H)2-cytokine production. The tested live Gram-positive probiotic bacteria and their genomic DNA inhibited SEA- and Dpt-stimulated secretion of T(H)2-cytokines (IL-4 and IL-5) and enhanced the Stimulation of IFN-gamma. This effect was dose-dependent with a dosage-optimum, which was identical for all lactic acid producing bacteria (LAB) tested (10 bacteria per (PBMC) and their DNA (75 ng/rnl). Based on the maximal effects achieved with LAB and their DNA, more than 50% of the effects seem to be contributed by DNA. No significant effect was induced by the control, Gram-negative Escherichia coli TGl. Lactobacilli and bifidobacteria reduced SEA-stimulated IL-4 and IL-5 production more effectively in PBMCs from healthy subjects than from allergic patients. In contrast to this, inhibition of Dpt-stimulated IL-4- and IL-5-secretion was more pronounced in cells from allergic subjects. Compared with living LAB, bacterial DNA inhibited IL-4- and IL-5-secretion in a similar manner. SEA- and even more so Dpt-stimulated IFN-gamma stimulation by living LAB was less pronounced in allergic than in healthy Subjects, whereas IFN-gamma Stimulation by their DNA was more Pronounced in allergic subjects. The tested probiotic bacteria as well as their genomic DNA modulated the T(H)1/T(H)2 response to some allergens dose-dependently. DNA seems to contribute to 50% of the effect exerted by living bacteria in this in vitro model. The magnitude of the probiotic effects differed between healthy and allergic subjects. Whether the modulation found for the tested strains might be useful for the prevention and treatment of allergic diseases has to be assessed In clinical trials. (C) 2008 Published by Elsevier GmbH.	[Ghadimi, Darab; de Vrese, Michael; Winkler, Petra; Schrezenmeir, Juergen] Fed Res Ctr Nutr & Food, Inst Physiol & Biochem Nutr, D-24103 Kiel, Germany; [Foelster-Holst, Regina] Univ Hosp Schleswig Holstein, Dermatol Clin, D-24105 Kiel, Germany; [Heller, Knut J.] Fed Res Ctr Nutr & Food, Inst Microbiol, D-24103 Kiel, Germany	Schrezenmeir, J (reprint author), Fed Res Ctr Nutr & Food, Inst Physiol & Biochem Nutr, Hermann Weigmann Str 1, D-24103 Kiel, Germany.	pbe.kiel@bfel.de	Folster-Holst, Regina/A-9560-2010; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Behera AK, 2002, HUM GENE THER, V13, P1697, DOI 10.1089/104303402760293547; Bjorksten B, 1997, CLIN REV ALLERG IMMU, V15, P125, DOI 10.1007/BF02826583; Bohle B, 1999, EUR J IMMUNOL, V29, P2344, DOI 10.1002/(SICI)1521-4141(199907)29:07<2344::AID-IMMU2344>3.0.CO;2-R; Broide DH, 2001, J ALLERGY CLIN IMMUN, V108, P759; CAYZER C, 2001, J GASTROEN HEPATOL, V16, P36, DOI 10.1111/j.1440-1746.2001.ca01-36.x; de Vrese M, 2005, EUR J NUTR, V44, P406, DOI 10.1007/s00394-004-0541-8; de Vrese M, 2005, CLIN NUTR, V24, P481, DOI 10.1016/j.clnu.2005.02.006; de Vrese M, 2006, VACCINE, V24, P6670, DOI 10.1016/j.vaccine.2006.05.048; Flinterman AE, 2007, INT ARCH ALLERGY IMM, V143, P237, DOI 10.1159/000099467; Folster-Holst R, 2006, BRIT J DERMATOL, V155, P1256, DOI 10.1111/j.1365-2133.2006.07558.x; Foligne B, 2007, WORLD J GASTROENTERO, V13, P236; Helin T, 2002, ALLERGY, V57, P243, DOI 10.1034/j.1398-9995.2002.1s3299.x; Helwig U, 2006, WORLD J GASTROENTERO, V12, P5978; Hessel EM, 2005, J EXP MED, V202, P1563, DOI 10.1084/jem.20050631; Hessle C, 2000, INFECT IMMUN, V68, P3581, DOI 10.1128/IAI.68.6.3581-3586.2000; Holt PG, 1997, PEDIATR ALLERGY IMMU, V8, P53, DOI 10.1111/j.1399-3038.1997.tb00145.x; Hussain I, 2002, LARYNGOSCOPE, V112, P1819, DOI 10.1097/00005537-200210000-00021; Iliev ID, 2005, CELL MICROBIOL, V7, P403, DOI 10.1111/j.1462-5822.2004.00470.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, LANCET, V357, P1076, DOI 10.1016/S0140-6736(00)04259-8; Kitagaki K, 2002, CLIN DIAGN LAB IMMUN, V9, P1260, DOI 10.1128/CDLI.9.6.1260-1269.2002; Kline JN, 1999, J ALLERGY CLIN IMMUN, V104, P1258; Kline JN, 1998, J IMMUNOL, V160, P2555; Klinman DM, 1996, P NATL ACAD SCI USA, V93, P2879, DOI 10.1073/pnas.93.7.2879; 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, 1999, LANCET, V354, pSII12; Matsuguchi T, 2003, CLIN DIAGN LAB IMMUN, V10, P259, DOI 10.1128/CDLI.10.2.259.266.2003; Matsuzaki T, 1998, J DAIRY SCI, V81, P48; Medina M, 2007, CLIN EXP IMMUNOL, V150, P531, DOI 10.1111/j.1365-2249.2007.03522.x; Meier R, 2005, CURR OPIN CRIT CARE, V11, P318, DOI 10.1097/01.ccx.0000166396.42894.60; Miettinen M, 1998, INFECT IMMUN, V66, P6058; MullerAlouf H, 1996, INFECT IMMUN, V64, P1450; O'Byrne PM, 2006, CHEST, V130, P244, DOI 10.1378/chest.130.1.244; O'Mahony L, 2006, AM J PHYSIOL-GASTR L, V290, pG839, DOI 10.1152/ajpgi.00112.2005; Pena JA, 2003, CELL MICROBIOL, V5, P277, DOI 10.1046/j.1462-5822.2003.t01-1-00275.x; Peng GC, 2005, PEDIATR ALLERGY IMMU, V16, P433, DOI 10.1111/j.1399-3038.2005.00284.x; Pochard P, 2005, J ALLERGY CLIN IMMUN, V116, P198, DOI 10.1016/j.jaci.2005.02.037; Pochard P, 2002, J ALLERGY CLIN IMMUN, V110, P617, DOI 10.1067/mai.2002.128528; Pohjavuori E, 2004, J ALLERGY CLIN IMMUN, V114, P131, DOI 10.1016/j.jaci.2004.03.036; Prescott SL, 2005, CLIN EXP ALLERGY, V35, P1557, DOI 10.1111/j.1365-2222.2005.02376.x; Rosenfeldt V, 2003, J ALLERGY CLIN IMMUN, V111, P389, DOI 10.1067/mai.2003.389; Sambrook J., 2001, MOL CLONING; Shida K, 1998, INT ARCH ALLERGY IMM, V115, P278, DOI 10.1159/000069458; Strachan David P., 2000, Thorax, V55, pS2, DOI 10.1136/thorax.55.suppl_1.S2; van der Velden VHJ, 2001, CLIN EXP ALLERGY, V31, P997, DOI 10.1046/j.1365-2222.2001.01176.x; Wang MF, 2004, PEDIATR ALLERGY IMMU, V15, P152, DOI 10.1111/j.1399-3038.2004.00156.x; Weston S, 2005, ARCH DIS CHILD, V90, P892, DOI 10.1136/adc.2004.060673; Winkler P, 2007, J NUTR, V137, p756S	50	82	90	2	14	ELSEVIER GMBH, URBAN & FISCHER VERLAG	JENA	OFFICE JENA, P O BOX 100537, 07705 JENA, GERMANY	0171-2985			IMMUNOBIOLOGY	Immunobiology		2008	213	8					677	692		10.1016/j.imbio.2008.02.001		16	Immunology	Immunology	359YY	WOS:000260025400008	18950596	
J	Salvi, S				Salvi, Sundeep			Health effects of ambient air pollution in children	PAEDIATRIC RESPIRATORY REVIEWS			English	Article						air pollution; particulate matter; nitrogen oxides; oxidative stress	DIESEL EXHAUST PARTICLES; LUNG-FUNCTION GROWTH; LOW-BIRTH-WEIGHT; RESPIRATORY SYMPTOMS; ANTIOXIDANT SUPPLEMENTATION; ALLERGIC SENSITIZATION; ASTHMATIC-CHILDREN; PARTICULATE MATTER; PULMONARY-FUNCTION; INFANT-MORTALITY	Children seem to be most vulnerable to the harmful effects of ambient air air pollution; pollutants because their defence mechanisms are still evolving and because they inhale a particulate matter; higher volume of air per body weight than adults. Air pollutants can also harm the foetus if nitrogen oxides; the mother is exposed to high levels of air pollution during pregnancy. An increase in oxidative stress respiratory neonatal mortality has been associated with ambient levels of air pollutants. Exposure to fine particles has been shown to increase allergen sensitisation, increase the risk of worsening asthma and decrease lung function. Lung growth, as measured by lung function, seems to be adversely affected in children exposed to various oxidant air pollutants. Oxidative stress is the main underlying mechanism responsible for the harmful effects of air pollutants and preliminary studies have indicated that antioxicant supplementation can offer some protection. (c) 2007 Elsevier Ltd. All rights reserved.	Chest Res Fdn, Pune 411014, Maharashtra, India	Salvi, S (reprint author), Chest Res Fdn, Marigold Complex, Pune 411014, Maharashtra, India.	ssalvi@crfindia.com					Annesi-Maesano I, 2007, RESP MED, V101, P1721, DOI 10.1016/j.rmed.2007.02.022; Avol EL, 2001, AM J RESP CRIT CARE, V164, P2067; Behrens T, 2004, PEDIATR ALLERGY IMMU, V15, P331, DOI 10.1111/j.1399-3038.2004.00157.x; Bennett WD, 2004, J APPL PHYSIOL, V97, P821, DOI 10.1152/japplphysiol.01403.2003; Bobak M, 1999, EPIDEMIOLOGY, V10, P666, DOI 10.1097/00001648-199911000-00004; BRABACK L, 1994, CLIN EXP ALLERGY, V24, P826, DOI 10.1111/j.1365-2222.1994.tb01805.x; Brauer M, 2007, EUR RESPIR J, V29, P879, DOI 10.1183/09031936.00083406; Brauer M, 2002, AM J RESP CRIT CARE, V166, P1092, DOI 10.1164/rccm.200108-007OC; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; Calderon-Garciduenas L, 2001, AM J RESP CELL MOL, V24, P132; CHATHAM MD, 1987, ANN NY ACAD SCI, V498, P269, DOI 10.1111/j.1749-6632.1987.tb23767.x; Ciccone G, 1998, OCCUP ENVIRON MED, V55, P771; Dales R, 2004, PEDIATRICS, V113, pE628, DOI 10.1542/peds.113.6.e628; Dales RE, 2006, ENVIRON HEALTH PERSP, V114, P1751, DOI 10.1289/ehp.9044; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; DOCKERY DW, 1982, JAPCA J AIR WASTE MA, V32, P937; EDWARDS J, 1994, ARCH ENVIRON HEALTH, V49, P223; Environmental Working Group, 2005, BOD BURD POLL NEWB B; Frew AJ, 1997, CLIN EXP ALLERGY, V27, P237; Frischer T, 1999, AM J RESP CRIT CARE, V160, P390; Fujieda S, 1998, AM J RESP CELL MOL, V19, P507; Gauderman WJ, 2004, NEW ENGL J MED, V351, P1057, DOI 10.1056/NEJMoa040610; Gauderman WJ, 2002, AM J RESP CRIT CARE, V166, P76, DOI 10.1164/rccm.2111021; Gilliland FD, 2004, LANCET, V363, P119, DOI 10.1016/S0140-6736(03)15262-2; Ha EH, 2001, EPIDEMIOLOGY, V12, P643, DOI 10.1097/00001648-200111000-00011; Holloway JA, 2000, LANCET, V356, P1900, DOI 10.1016/S0140-6736(00)03265-7; Horak F, 2002, EUR RESPIR J, V19, P838, DOI 10.1183/09031936.02.00512001; Janssen NAH, 2003, ENVIRON HEALTH PERSP, V111, P1512, DOI 10.1289/ehp.6243; Jedrychowski W, 1999, ENVIRON HEALTH PERSP, V107, P669, DOI 10.2307/3434460; Kelly FJ, 2003, OCCUP ENVIRON MED, V60, P612, DOI 10.1136/oem.60.8.612; Kim JJ, 2004, AM J RESP CRIT CARE, V170, P520, DOI 10.1164/rccm.200403-2810C; Knox RB, 1997, CLIN EXP ALLERGY, V27, P246; Kulkarni N, 2006, NEW ENGL J MED, V355, P21, DOI 10.1056/NEJMoa052972; Lacasana M, 2005, EUR J EPIDEMIOL, V20, P183, DOI 10.1007/s10654-004-3005-9; Lee SL, 2006, CLIN EXP ALLERGY, V36, P1138, DOI 10.1111/j.1365-2222.2006.02555.x; Lee YL, 2004, CLIN EXP ALLERGY, V34, P1707, DOI 10.1111/j.1365-2222.2004.02099.x; Lipfert FW, 2000, J AIR WASTE MANAGE, V50, P1350; Liu SL, 2003, ENVIRON HEALTH PERSP, V111, P1773, DOI 10.1289/ehp.6251; Miller RL, 2004, CHEST, V126, P1071, DOI 10.1378/chest.126.4.1071; Motta AC, 2006, INT ARCH ALLERGY IMM, V139, P294, DOI 10.1159/000091600; Moya J, 2004, PEDIATRICS, V113, P996; Nel AE, 1998, J ALLERGY CLIN IMMUN, V102, P539, DOI 10.1016/S0091-6749(98)70269-6; Ostro B, 2001, EPIDEMIOLOGY, V12, P200, DOI 10.1097/00001648-200103000-00012; Pino P, 2004, EPIDEMIOLOGY, V15, P702, DOI 10.1097/01.ede.0000142153.28496.d0; Rogers JF, 2000, AM J EPIDEMIOL, V151, P602; Romieu I, 1996, AM J RESP CRIT CARE, V154, P300; Romieu I, 2004, THORAX, V59, P8; Romieu I, 2002, AM J RESP CRIT CARE, V166, P703, DOI 10.1164/rccm.2112074; Salvi S, 2001, Curr Opin Allergy Clin Immunol, V1, P35; Samet JM, 2001, AM J RESP CRIT CARE, V164, P819; SCHWARTZ DA, 1994, AM J RESP CRIT CARE, V150, P1243; Schwartz J, 2004, PEDIATRICS, V113, P1037; STROM KA, 1990, J TOXICOL ENV HEALTH, V29, P377; TAGER IB, 1983, NEW ENGL J MED, V309, P699, DOI 10.1056/NEJM198309223091204; Tang CS, 2007, SCI TOTAL ENVIRON, V382, P43, DOI 10.1016/j.scitotenv.2007.04.016; Trasande L, 2005, J ALLERGY CLIN IMMUN, V115, P689, DOI 10.1016/j.jaci.2005.01.056; Trenga CA, 2001, ARCH ENVIRON HEALTH, V56, P242; van der Zee SC, 1999, OCCUP ENVIRON MED, V56, P802; WANG XB, 1994, AM J RESP CRIT CARE, V149, P1420; Wang XB, 1997, ENVIRON HEALTH PERSP, V105, P514, DOI 10.1289/ehp.97105514; Weiland Stephan K., 1994, Annals of Epidemiology, V4, P243; WJST M, 1993, BRIT MED J, V307, P596; Woodruff TJ, 1997, ENVIRON HEALTH PERSP, V105, P608; Wyler C, 2000, EPIDEMIOLOGY, V11, P450, DOI 10.1097/00001648-200007000-00015; Xu XP, 1995, ARCH ENVIRON HEALTH, V50, P407	65	82	87	3	19	ELSEVIER SCI LTD	OXFORD	THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND	1526-0542			PAEDIATR RESPIR REV	Paediatr. Respir. Rev.	DEC	2007	8	4					275	280		10.1016/j.prrv.2007.08.008		6	Pediatrics; Respiratory System	Pediatrics; Respiratory System	241XA	WOS:000251687900002	18005894	
J	Nielsen, GD; Larsen, ST; Olsen, O; Lovik, M; Poulsen, LK; Glue, C; Wolkoff, P				Nielsen, G. D.; Larsen, S. T.; Olsen, O.; Lovik, M.; Poulsen, L. K.; Glue, C.; Wolkoff, P.			Do indoor chemicals promote development of airway allergy?	INDOOR AIR			English	Review						volatile organic compounds; quaternary ammonium compounds; cleaning agents; surfactants; phthalates; adjuvant	VOLATILE ORGANIC-COMPOUNDS; SUSPENDED PARTICULATE MATTER; SUBTILISIN CARLSBERG ALCALASE; QUATERNARY AMMONIUM-COMPOUNDS; SUBCUTANEOUS INJECTION MODEL; OZONE OXIDATION-PRODUCTS; WORK-RELATED ASTHMA; IN-HOUSE DUST; YOUNG-CHILDREN; OCCUPATIONAL EXPOSURES	Allergic asthma has increased worldwide in the industrialized countries. This review evaluates whether the major groups of indoor chemical exposures possess allergy-promoting (adjuvant) effects; formaldehyde was excluded, because of the size of the literature. Volatile organic compounds (VOCs) are used as an example of gases and vapors. The precipitation of asthmatic symptoms by VOC exposures is probably because of VOC levels considerably above typical indoor levels, or VOCs may be a surrogate for exposure to allergens, combustion products or dampness. Indoor particles possessed adjuvant effects in animal studies and allergy-promoting effects in humans. Quaternary ammonium compounds may possess adjuvant effects in animal studies and promoted sensitization in humans in occupational settings. The use of cleaning agents, anionic and non-ionic surfactants are not considered to possess an important adjuvant effect in the general population. Regarding phthalate exposures, results from animal and epidemiological studies were found to be discordant. There is little evidence that the indoor chemicals evaluated possess important adjuvant effects. If buildings are kept clean, dry and free of combustion products, the important question may be would it be profitable to look for lifestyle factors and non-chemical indoor exposures in order to abate airway allergy?	Natl Inst Occupat Hlth Denmark, DK-2100 Copenhagen O, Denmark; Norwegian Inst Publ Hlth, Dept Environm Immunol, Div Environm Med, Oslo, Norway; Natl Univ Hosp, Allergy Clin, Copenhagen, Denmark	Nielsen, GD (reprint author), Natl Inst Occupat Hlth Denmark, Lerso Parkalle 105, DK-2100 Copenhagen O, Denmark.	gdn@ami.dk		Wolkoff, Peder/0000-0003-1933-7351			Ameille J, 2003, OCCUP ENVIRON MED, V60, P136, DOI 10.1136/oem.60.2.136; Arif AA, 2003, AM J IND MED, V44, P368, DOI 10.1002/ajim.10291; Becher R, 1996, TOXICOL LETT, V86, P155, DOI 10.1016/0378-4274(96)03685-5; Blanc PD, 2005, J OCCUP ENVIRON MED, V47, P362, DOI 10.1097/01.jom.0000158708.32491.9d; Bluyssen PM, 1996, INDOOR AIR, V6, P221, DOI 10.1111/j.1600-0668.1996.00002.x; Bornehag CG, 2005, ENVIRON HEALTH PERSP, V113, P1399, DOI 10.1289/ehp.7809; Bornehag CG, 2005, INDOOR AIR, V15, P275, DOI 10.1111/j.1600-0668.2005.00372.x; Bornehag CG, 2004, INDOOR AIR, V14, P243, DOI 10.1111/j.1600-0668.2004.00240.x; Bornehag CG, 2005, ENVIRON HEALTH PERSP, V113, pA152; 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J	Chan, DS; Callahan, CW; Hatch-Pigott, VB; Lawless, A; Proffitt, HL; Manning, NE; Schweikert, M; Malone, FJ				Chan, Debora S.; Callahan, Charles W.; Hatch-Pigott, Virginia B.; Lawless, Annette; Proffitt, H. Lorraine; Manning, Nola E.; Schweikert, Mary; Malone, Francis J.			Internet-based home monitoring and education of children with asthma is comparable to ideal office-based care: Results of a 1-year asthma in-home monitoring trial	PEDIATRICS			English	Article						telemedicine; home; telehealth; telemonitoring; store-and-forward; clinic; case management; pediatric	METERED-DOSE INHALER; MANAGEMENT; TELEMEDICINE; IMPROVEMENT; PREVENTION; DEPOSITION; QUALITY; THERAPY; PROGRAM	OBJECTIVE. The goal was to determine whether home asthma telemonitoring with store- and- forward technology improved outcomes, compared with in- person, office- based visits. METHODS. A total of 120 patients, 6 to 17 years of age, with persistent asthma were assigned randomly to the office- based or virtual group. The 2 groups followed the same ambulatory clinical pathway for 12 months. Office- based group patients received traditional in- person education and case management. Virtual group patients received computers, Internet connections, and in- home, Internet- based case management and received education through the study Web site. Disease control outcome measures included quality of life, utilization of services, and symptom control. RESULTS. A total of 120 volunteers ( 45 female) were enrolled. The groups were clinically comparable ( office- based: 22 female/ 38 male; mean age: 9.0 +/- 3.0 years; virtual: 23 female/ 37 male; mean age: 10.2 +/- 3.1 years). Virtual patients had higher metered- dose inhaler with valved holding chamber technique scores than did the office- based group at 52 weeks ( 94% vs 89%), had greater adherence to daily asthma symptom diary submission ( 35.4% vs 20.8%), had less participant time ( 636 vs 713 patient- months), and were older. Caregivers in both groups perceived an increase in quality of life and an increase in asthma knowledge scores from baseline. There were no other differences in therapeutic or disease control outcome measures. CONCLUSIONS. Virtual group patients achieved excellent asthma therapeutic and disease control outcomes. Compared with those who received standardized officebased care, they were more adherent to diary submission and had better inhaler scores at 52 weeks. Store- and- forward telemedicine technology and case management provide additional tools to assist in the management of children with persistent asthma.	Tripler Army Med Ctr, Dept Pediat, MCHK PE, Honolulu, HI 96859 USA	Chan, DS (reprint author), Tripler Army Med Ctr, Dept Pediat, MCHK PE, 1 Jarrett White Rd, Honolulu, HI 96859 USA.	debora.chan@haw.tamc.amedd.army.mil					Barry E, 1998, Telemed Virtual Real, V3, P61; Blais L, 1998, AM J RESP CRIT CARE, V158, P126; Bynum A, 2001, TELEMED J E-HEALTH, V7, P207, DOI 10.1089/153056201316970902; Callahan CW, 2000, CHEST, V117, P1226, DOI 10.1378/chest.117.5.1226; Chan DS, 2001, AM J HEALTH-SYST PH, V58, P1413; CHAN DS, 2003, AM J HEALTH-SYST PH, V60, P1; Cote J, 1998, CHEST, V113, P968, DOI 10.1378/chest.113.4.968; Eliasson AH, 1998, MIL MED, V163, P530; Finkelstein J, 1998, Proc AMIA Symp, P336; FINKELSTEIN J, 2000, CHEST, V117, P147; Greenberger PA, 1996, AM J MED, V100, P381, DOI 10.1016/S0002-9343(97)89511-3; Hartert TV, 1996, AM J MED, V100, P386, DOI 10.1016/S0002-9343(97)89513-7; Headrick L, 1996, AM J RESP CRIT CARE, V154, pS96; Institute of Medicine, 2001, CROSS QUAL CHASM NEW; Karp WB, 2000, PEDIATRICS, V105, P843, DOI 10.1542/peds.105.4.843; Kokubu F, 2000, Arerugi, V49, P19; Malone F, 2004, TELEMED J E-HEALTH, V10, P138, DOI 10.1089/1530562041641192; MCQUESTON JA, 1996, DOD ASTHMA OUTCOMES; National Heart Lung and Blood Institute National Asthma Education Program, 1997, NIH PUBL; Person D A, 2000, Pac Health Dialog, V7, P29; Reddel HK, 1998, EUR RESPIR J, V12, P853, DOI 10.1183/09031936.98.12040853; Romano MJ, 2001, TELEMED J E-HEALTH, V7, P281, DOI 10.1089/15305620152814683; Tal A, 1996, J PEDIATR-US, V128, P479, DOI 10.1016/S0022-3476(96)70357-8; *US DEP HHS NAT HE, 2002, GUID DIAGN MAN ASTHM; Wildhaber JH, 1999, J PEDIATR-US, V135, P28, DOI 10.1016/S0022-3476(99)70323-9; Wojtczak H, 1999, AM J RESP CRIT CARE, V159, pA756	26	82	85	2	19	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	MAR	2007	119	3					569	578		10.1542/peds.2006-1884		10	Pediatrics	Pediatrics	141LK	WOS:000244579800017	17332210	
J	Lienhardt, C; Fielding, K; Sillah, JS; Bah, B; Gustafson, P; Warndorff, D; Palayew, M; Lisse, I; Donkor, S; Diallo, S; Manneh, K; Adegbola, R; Aaby, P; Bah-Sow, O; Bennett, S; McAdam, K				Lienhardt, C; Fielding, K; Sillah, JS; Bah, B; Gustafson, P; Warndorff, D; Palayew, M; Lisse, I; Donkor, S; Diallo, S; Manneh, K; Adegbola, R; Aaby, P; Bah-Sow, O; Bennett, S; McAdam, K			Investigation of the risk factors for tuberculosis: a case-control study in three countries in West Africa	INTERNATIONAL JOURNAL OF EPIDEMIOLOGY			English	Article						tuberculosis; risk factors; epidemiology; developing countries	SUB-SAHARAN AFRICA; PULMONARY TUBERCULOSIS; SOCIOECONOMIC-STATUS; NORTHERN MALAWI; BCG SCARS; SUSCEPTIBILITY; SMOKING; HIV; EPIDEMIOLOGY; DEPRIVATION	Background Host-related and environment-related factors have been shown to play a role in the development of tuberculosis (TB), but few studies were carried out to identify their respective roles in resource-poor countries. Methods A multicentre case-control study was conducted in Guinee, Guinea Bissau, and The Gambia, from January 1999 to March 2001. Cases were newly detected smear positive TB patients. TWO controls were recruited for each case, one within the household of the case, and one in the community. Results Regarding host-related factors, univariate analysis by conditional logistic regression of 687 matched pairs of cases and household controls showed that TB was associated with male sex, family history of TB, absence of a BCG scar, smoking, alcohol, anaemia, HIV infection, and history and treatment of worm infection. In a multivariable model based on 601 matched pairs, male sex, family history of TB, smoking, and HIV infection were independent risk factors of TB. The investigation of environmental factors based on the comparison of 816 cases/community control pairs showed that the risk of TB was associated with single marital status, family history of TB, adult crowding, and renting the house. In a final model assessing the combined effect of host and environmental factors, TB was associated with male sex, HIV infection, smoking (with a dose-effect relationship), history of asthma, family history of TB, marital status, adult crowding, and renting the house. Conclusion TB is a multifactorial disorder, in which environment interacts with host-related factors. This study provided useful information for the assessment of host and environmental factors of TB for the improvement of TB control activities in developing countries.	Inst Rech Dev, Dakar, Senegal; MRC Labs, Fajara, Gambia; London Sch Hyg & Trop Med, London WC1, England; CHU Ignace Deen, Programme Natl Lutte AntiTuberculeuse, Serv Pneumol, Conakry, Guinea; Danish Epidemiol Sci Ctr, Projecto Saude Bandim, Bissau, Guinea Bissau; McGill Univ, Jewish Gen Hosp, Div Pulm Med, Montreal, PQ H3A 2T5, Canada	Lienhardt, C (reprint author), Inst Rech Dev, UR 36,BP 1386, Dakar, Senegal.	lienhardt@dakar.ird.sn					Alcaide J, 1996, TUBERCLE LUNG DIS, V77, P112, DOI 10.1016/S0962-8479(96)90024-6; ANDERSEN S, 1960, Bull World Health Organ, V22, P39; Aubry MC, 2000, CLIN CHEST MED, V21, P11, DOI 10.1016/S0272-5231(05)70005-8; Bellamy R, 2000, P NATL ACAD SCI USA, V97, P8005, DOI 10.1073/pnas.140201897; Bennett S, 2002, AM J EPIDEMIOL, V155, P1074, DOI 10.1093/aje/155.11.1074; BHATTI N, 1995, BRIT MED J, V310, P967; Bornman L, 2004, J INFECT DIS, V190, P1631, DOI 10.1086/424462; Brightbill HD, 1999, SCIENCE, V285, P732, DOI 10.1126/science.285.5428.732; BRUDNEY K, 1991, AM REV RESPIR DIS, V144, P7415; BUSKIN SE, 1994, AM J PUBLIC HEALTH, V84, P1750, DOI 10.2105/AJPH.84.11.1750; Cantwell MF, 1998, AM J RESP CRIT CARE, V157, P1016; COMSTOCK GW, 1982, AM REV RESPIR DIS, V125, P8; Corbett EL, 2003, ARCH INTERN MED, V163, P1009, DOI 10.1001/archinte.163.9.1009; DECOCK KM, 1994, TUBERCULOSIS BACK FU; Diwan VK, 1999, LANCET, V353, P1000, DOI 10.1016/S0140-6736(99)01318-5; DRUCKER E, 1994, LANCET, V343, P1482, DOI 10.1016/S0140-6736(94)92588-7; Dubos R, 1987, WHITE PLAGUE TUBERCU; FINE PEM, 1981, INT J LEPROSY, V49, P437; Fine PEM, 1996, LANCET, V348, P17; FINE PEM, 1989, B WORLD HEALTH ORGAN, V67, P35; Floyd S, 2000, INT J TUBERC LUNG D, V4, P1133; Frost WH, 1933, AM J PUBLIC HEALTH N, V23, P426, DOI 10.2105/AJPH.23.5.426; GAVETT SH, 1995, J EXP MED, V182, P1527, DOI 10.1084/jem.182.5.1527; Glynn JR, 2000, T ROY SOC TROP MED H, V94, P500, DOI 10.1016/S0035-9203(00)90065-8; Gustafson P, 2004, INT J EPIDEMIOL, V33, P163, DOI 10.1093/ije/dyh026; Harper M, 2003, T ROY SOC TROP MED H, V97, P506, DOI 10.1016/S0035-9203(03)80007-X; Holmes CB, 1998, INT J TUBERC LUNG D, V2, P96; Hudelson P, 1996, TUBERCLE LUNG DIS, V77, P391, DOI 10.1016/S0962-8479(96)90110-0; KASS EH, 1971, J INFECT DIS, V123, P110; Kolappan C, 2002, THORAX, V57, P964, DOI 10.1136/thorax.57.11.964; Lienhardt C, 2003, AM J RESP CRIT CARE, V168, P448, DOI 10.1164/rccm.200212-1483OC; Lienhardt C, 2002, EUR J IMMUNOL, V32, P1605, DOI 10.1002/1521-4141(200206)32:6<1605::AID-IMMU1605>3.0.CO;2-6; Lienhardt C, 2001, EPIDEMIOL REV, V23, P288; Lienhardt C, 2002, AM J EPIDEMIOL, V155, P1066, DOI 10.1093/aje/155.11.1066; MANGTANI P, 1995, BRIT MED J, V310, P963; Mukadi YD, 1997, AIDS, V11, P1151, DOI 10.1097/00002030-199709000-00011; Rieder HL, 1999, EPIDEMIOLOGICAL BASI; SCHOEMAN JH, 1991, INT J EPIDEMIOL, V20, P435, DOI 10.1093/ije/20.2.435; SHIRAKAWA T, 1997, SCIENCE, V275, P7; SPENCE DPS, 1993, BRIT MED J, V307, P759; Stein L, 1952, BR J SOC MED, V6, P1; Tocque K, 1998, INT J TUBERC LUNG D, V2, P213; Van Rie A, 1999, NEW ENGL J MED, V341, P1174, DOI 10.1056/NEJM199910143411602; von Mutius E, 2000, THORAX, V55, P449, DOI 10.1136/thorax.55.6.449; World Health Organization, 2001, WHOCDSTB2001287; World Health Organization, 2003, WHO FRAM CONV TOB CO	46	82	88	0	11	OXFORD UNIV PRESS	OXFORD	GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND	0300-5771			INT J EPIDEMIOL	Int. J. Epidemiol.	AUG	2005	34	4					914	923		10.1093/ije/dyi100		10	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	957HG	WOS:000231360300038	15914505	
J	Russo, C; Polosa, R				Russo, C; Polosa, R			TNF-alpha as a promising therapeutic target in chronic asthma: a lesson from rheumatoid arthritis	CLINICAL SCIENCE			English	Review						asthma; biological therapy; cytokine; inflammation; rheumatoid arthritis; TNF-alpha (turnout necrosis factor-alpha)	TUMOR-NECROSIS-FACTOR; ADHESION MOLECULE EXPRESSION; EPIDERMAL-GROWTH-FACTOR; LUNG MAST-CELLS; NF-KAPPA-B; ENDOTHELIAL-CELLS; EPITHELIAL-CELLS; MESSENGER-RNA; SMOOTH-MUSCLE; IN-VITRO	TNF-alpha (tumour necrosis factor-alpha) is known to play a critical role in the pathogenic mechanisms of a number of chronic inflammatory diseases, including RA (rheumatoid arthritis), Crohn's disease and psoriasis. The notion that TNF-alpha is released in allergic responses from both mast cells and macrophages via IgE-dependent mechanisms, the demonstration that elevated levels of TNF-a are frequently observed in bronchoalveolar fluid of asthmatic subjects undergoing allergen challenge and the results from exposure studies of TNF-alpha in vivo showing increases in airway responsiveness in both normal and asthmatic subjects emphasize the importance of TNF-alpha in the initiation of allergic asthmatic airway inflammation and the generation of airway hyper-responsiveness. Drugs targeting TNF-alpha have been developed to neutralize the deleterious effects of this inflammatory cytokine and have proved to be safe and effective in the treatment of patients with RA, Crohn's disease and psoriasis refractory to conventional treatments. Biological therapies blocking TNF-alpha are likely to constitute a considerable advance in the management of those difficult cases of asthma that are particularly resistant to typical treatment modalities. In this review article, we intend to address the potential role of TNF-alpha in asthma and to put forward the idea that drugs that have been developed to neutralize the deleterious effects of TNF-alpha may also be useful in the management of chronic severe asthma.	Catania Univ, Ascoli Tomaselli Hosp, Dipartimento Med Interna & Specialistica, I-95125 Catania, Italy	Polosa, R (reprint author), Catania Univ, Ascoli Tomaselli Hosp, Dipartimento Med Interna & Specialistica, Via Passo Gravina 187, I-95125 Catania, Italy.	rp5@soton.ac.uk					ABDELAZIZ MM, 1995, AM J RESP CELL MOL, V13, P728; Aggarwal BB, 2003, NAT REV IMMUNOL, V3, P745, DOI 10.1038/nri1184; Amrani Y, 2000, Respir Res, V1, P49, DOI 10.1186/rr12; Babu K., 2003, Journal of Allergy and Clinical Immunology, V111, pS277, DOI 10.1016/S0091-6749(03)80997-1; Barnes PJ, 1996, EUR RESPIR J, V9, P636, DOI 10.1183/09031936.96.09040636; Bazzoni F, 1996, NEW ENGL J MED, V334, P1717; BAZZONI F, 1996, NEW ENGL J MED, V334, pS1; Bodey KJ, 1999, ALLERGY, V54, P1083, DOI 10.1034/j.1398-9995.1999.00889.x; Brown SL, 2002, ARTHRITIS RHEUM, V46, P3151, DOI 10.1002/art.10679; Busse William W., 2000, Journal of Allergy and Clinical Immunology, V106, P1033; Busse WW, 2001, NEW ENGL J MED, V344, P350; CEMBRZYNSKANOWAK M, 1993, AM REV RESPIR DIS, V147, P291; Chagani T, 1999, AM J RESP CRIT CARE, V160, P278; Chung KF, 1999, EUR RESPIR J, V13, P1198; Coward WR, 2002, J IMMUNOL, V169, P5287; ECK MJ, 1989, J BIOL CHEM, V264, P17595; Elias JA, 1999, J CLIN INVEST, V104, P1001, DOI 10.1172/JCI8124; Ellerin T, 2003, ARTHRITIS RHEUM, V48, P3013, DOI 10.1002/art.11301; Fernandes DJ, 2003, J APPL PHYSIOL, V95, P844, DOI 10.1152/japplphysiol.00192.2003; FINOTTO S, 1994, J IMMUNOL, V153, P2278; GOSSET P, 1992, AM REV RESPIR DIS, V146, P768; GOSSET P, 1991, J ALLERGY CLIN IMMUN, V88, P561, DOI 10.1016/0091-6749(91)90149-I; Grant EN, 1999, J ALLERGY CLIN IMMUN, V104, pS1, DOI 10.1016/S0091-6749(99)70268-X; Hamilos DL, 1999, J ALLERGY CLIN IMMUN, V103, P79, DOI 10.1016/S0091-6749(99)70529-4; Idriss HT, 2000, MICROSC RES TECHNIQ, V50, P184, DOI 10.1002/1097-0029(20000801)50:3<184::AID-JEMT2>3.0.CO;2-H; Jobanputra P, 2002, Health Technol Assess, V6, P1; Keane J, 2001, NEW ENGL J MED, V345, P1098, DOI 10.1056/NEJMoa011110; KHALILSAADEH C, 2002, J ALLERGY CLIN IM S1, V109, pS243; KIPS JC, 1992, AM REV RESPIR DIS, V145, P332; Kobelt G, 2003, RHEUMATOLOGY, V42, P326, DOI 10.1093/rheumatology/keg107; LASSALLE P, 1993, CLIN EXP IMMUNOL, V94, P105; LEVINE SJ, 1995, AM J RESP CELL MOL, V12, P196; Li Kam Wa TC, 1999, CLIN EXP ALLERGY, V29, P1204, DOI 10.1046/j.1365-2222.1999.00638.x; Lorenz HM, 2002, ARTHRITIS RES THER, V4, pS17, DOI 10.1186/ar564; Louis R, 2000, EUR RESPIR J, V16, P604, DOI 10.1034/j.1399-3003.2000.16d06.x; Mariette X, 2002, BLOOD, V99, P3909, DOI 10.1182/blood.V99.11.3909; Matheson JM, 2002, AM J RESP CELL MOL, V27, P396, DOI 10.1165/rcmb.4614; MICHEL O, 1992, AM REV RESPIR DIS, V146, P352; Moffatt MF, 1999, THORAX, V54, P757; Mohan N, 2001, ARTHRITIS RHEUM, V44, P2862, DOI 10.1002/1529-0131(200112)44:12<2862::AID-ART474>3.0.CO;2-W; Moreland LW, 2001, J RHEUMATOL, V28, P1238; Nakamura Y, 2004, J IMMUNOL, V172, P1945; [Anonymous], 1997, NIH PUBL; OHKAWARA Y, 1992, AM J RESP CELL MOL, V7, P385; PALOMBELLA VJ, 1988, J CELL PHYSIOL, V135, P23, DOI 10.1002/jcp.1041350104; Panettieri Reynold A. 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Sci.	AUG	2005	109	2					135	142				8	Medicine, Research & Experimental	Research & Experimental Medicine	954FC	WOS:000231138500002	16033328	
J	Bradley, JP; Bacharier, LB; Bonfiglio, J; Schechtman, KB; Strunk, R; Storch, G; Castro, M				Bradley, JP; Bacharier, LB; Bonfiglio, J; Schechtman, KB; Strunk, R; Storch, G; Castro, M			Severity of respiratory syncytial virus bronchiolitis is affected by cigarette smoke exposure and atopy	PEDIATRICS			English	Article						RSV; bronchiolitis; asthma	ENVIRONMENTAL TOBACCO-SMOKE; MATERNAL SMOKING; LUNG-FUNCTION; RISK-FACTORS; CHILDHOOD ASTHMA; MECHANICAL VENTILATION; ALLERGIC SENSITIZATION; CHILDREN; INFECTION; PREGNANCY	Objective. Respiratory syncytial virus (RSV) bronchiolitis is a common cause of hospitalizations in children and has been increasingly identified as a risk factor in the development of asthma. Little is known about what determines the severity of RSV bronchiolitis, which may be helpful in the initial assessment of these children. Design. We evaluated a variety of environmental and host factors that may contribute to the severity of RSV bronchiolitis in the RSV Bronchiolitis in Early Life prospective cohort study. Severity of bronchiolitis was based on the quantization of lowest O-2 saturation and the length of stay. These factors included the child's and family's demographics, presence of household allergens (dust mite, cat, dog, and cockroach), peripheral blood eosinophil count, immunoglobulin E level, infant feeding, prior illnesses, exposure to intrauterine and postnatal cigarette smoke, and family history of atopy. Patients. We prospectively enrolled 206 hospitalized infants, all under 12 months old (4.0 +/- 3.3 months old), with their first episode of severe RSV bronchiolitis (mean O-2 saturation: 91.6 +/- 7.3%; length of stay: 2.5 +/- 2.5 days; presence of radiographic opacities: 75%). Patients were excluded for a variety of reasons including previous wheezing, regular use of bronchodilator or antiinflammatory medications, any preexisting lung disease including asthma, chronic lung disease of prematurity/bronchopulmonary dysplasia, or cystic fibrosis; gastroesophageal reflux disease on medical therapy; or congenital anomalies of the chest or lung. Results. Age was found to be a significant factor in the severity of infection. The younger an infant was, the more severe the infection tended to be as measured by the lowest oxygen (O-2) saturation. We also found that infants exposed to postnatal cigarette smoke from the mother had a lower O-2 saturation than those not exposed. However, there was no significant difference in RSV bronchiolitis severity between infants exposed only to intrauterine smoke and those infants never exposed to cigarette smoke. Infants with a family history of atopy, especially a maternal history of asthma or hay fever, had a higher O-2 saturation. Although a history of maternal atopy seemed to be protective, there was no association between allergens and bronchiolitis severity, although 25% of households had elevated allergen levels. Black infants demonstrated less severe RSV bronchiolitis than their white counterparts. Multivariate analysis revealed age, race, maternal atopy, and smoking to be associated with severity of RSV bronchiolitis. Conclusion. The severity of RSV bronchiolitis early in life seems modified by postnatal maternal cigarette smoke exposure and atopy and age of the infant, not by levels of allergens in the home environment.	Washington Univ, Sch Med, Dept Internal Med, St Louis, MO 63110 USA; Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA; Washington Univ, Sch Med, Dept Biostat, St Louis, MO 63110 USA	Castro, M (reprint author), Washington Univ, Sch Med, Dept Internal Med, Campus Box 8052,660 S Euclid Ave, St Louis, MO 63110 USA.	castrom@wustl.edu		Bradley, Joseph/0000-0001-6408-9700	NHLBI NIH HHS [HL61895]		Aligne CA, 1997, ARCH PEDIAT ADOL MED, V151, P648; Castro M, 2001, J ASTHMA, V38, P625, DOI 10.1081/JAS-100107540; Corbo GM, 1996, AM J RESP CRIT CARE, V154, P695; COULTAS DB, 1993, AM J RESP CRIT CARE, V149, pS93; Dezateux C, 1999, AM J RESP CRIT CARE, V159, P403; Ehrlich RI, 1996, AM J RESP CRIT CARE, V154, P681; EVERARD ML, 1992, EUR J PEDIATR, V151, P638, DOI 10.1007/BF01957564; FRANKEL LR, 1986, PEDIATR PULM, V2, P307, DOI 10.1002/ppul.1950020511; Gilliland FD, 2002, AM J RESP CRIT CARE, V166, P457, DOI 10.1164/rccm.2112064; Gilliland FD, 2001, AM J RESP CRIT CARE, V163, P429; GREEN M, 1989, PEDIATR INFECT DIS J, V8, P601, DOI 10.1097/00006454-198909000-00007; Gurkan F, 2000, EUR J EPIDEMIOL, V16, P465, DOI 10.1023/A:1007658411953; Hamilton RG, 1997, METHODS, V13, P53, DOI 10.1006/meth.1997.0495; HANRAHAN JP, 1992, AM REV RESPIR DIS, V145, P1129; Hofhuis W, 2003, ARCH DIS CHILD, V88, P1086, DOI 10.1136/adc.88.12.1086; Infante-Rivard C, 1999, AM J EPIDEMIOL, V150, P528; Lanari M, 2002, PEDIATR PULM, V33, P458, DOI 10.1002/ppul.10052; Larsson ML, 2001, CHEST, V120, P711, DOI 10.1378/chest.120.3.711; LAVIA WV, 1993, CLIN PEDIATR, V32, P450, DOI 10.1177/000992289303200801; Li YF, 2000, AM J RESP CRIT CARE, V162, P2097; Martinez FD, 2001, J ALLERGY CLIN IMMUN, V107, pS449, DOI 10.1067/mai.2001.114993; Moler FW, 1999, AM J RESP CRIT CARE, V159, P1234; Robinson PJ, 1997, J ALLERGY CLIN IMMUN, V100, P492; Sigurs N, 2000, AM J RESP CRIT CARE, V161, P1501; Singh SP, 2003, AM J RESP CRIT CARE, V168, P342, DOI 10.1164/rccm.200211.1262OC; Stein R, 1999, LANCET, V354, P541, DOI 10.1016/S0140-6736(98)10321-5; Strannegard O, 1997, PEDIATR ALLERGY IMMU, V8, P1, DOI 10.1111/j.1399-3038.1997.tb00134.x; TAGER IB, 1995, AM J RESP CRIT CARE, V152, P977; TISSING WJE, 1993, EUR J PEDIATR, V152, P125, DOI 10.1007/BF02072488; Weiss ST, 2001, J ALLERGY CLIN IMMUN, V107, P634, DOI 10.1067/mai.2001.113869	30	82	84	1	3	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	JAN	2005	115	1					E7	E14		10.1542/peds.2004-0059		8	Pediatrics	Pediatrics	884KN	WOS:000226083700002	15629968	
J	Rolinck-Werninghaus, C; Wolf, H; Liebke, C; Baars, JC; Lange, J; Kopp, MV; Hammermann, J; Leupold, W; Bartels, P; Gruebl, A; Bauer, CP; Schnitker, J; Wahn, U; Niggemann, B				Rolinck-Werninghaus, C; Wolf, H; Liebke, C; Baars, JC; Lange, J; Kopp, MV; Hammermann, J; Leupold, W; Bartels, P; Gruebl, A; Bauer, CP; Schnitker, J; Wahn, U; Niggemann, B			A prospective, randomized, double-blind, placebo-controlled multi-centre study on the efficacy and safety of sublingual immunotherapy (SLIT) in children with seasonal allergic rhinoconjunctivitis to grass pollen	ALLERGY			English	Article						children; conjunctival provocation test; grass pollen; immunoglobulin E; immunoglobulin G(4); rye pollen; skin prick test; specific immunotherapy; sublingual immunotherapy	STANDARDIZED 5-GRASS-POLLEN EXTRACT; HOUSE-DUST MITE; CONTROLLED TRIAL; SWALLOW IMMUNOTHERAPY; CLINICAL-EFFICACY; HAY-FEVER; RHINITIS; ASTHMA; SENSITIZATIONS	Background: Especially in childhood, sublingual immunotherapy (SLIT) could offer advantages over subcutaneous therapy. However, limited data on its efficacy is available. Methods: In four German centres 97 children (age 3-14 years) with allergic rhinoconjunctivitis to grass pollen were enrolled in a prospective, double-blind trial comparing SLIT (Pangramin SLIT(R); ALK-SCHERAX, 0.5 mug major allergens, three times per week, 32 months) with placebo. Primary endpoint was a multiple symptom-medication score for changes in seasonal diary entries between the first and third year of the study (SLIT n = 39; placebo n = 38). Results: The multiple symptom-medication score was significantly reduced by SLIT to 77.3% of the placebo group (P = 0.0498). The subsequent analysis of the single endpoints did not reveal significant differences for symptom scores in favour of SLIT (85.1% of placebo group; P = 0.22). However, the medication score improved significantly (67.1% of placebo group; P = 0.0025). Furthermore, secondary endpoints assessing in vivo immune responses did not differ significantly between the groups. However, retrospective analysis showed some inhomogeneity for clinical and in vitro parameters at the beginning of the study. Allergic side effects with possible relation to the study drug were reported in both groups (SLIT 49%, placebo 27%, P = 0.026). Conclusion: Our study indicates that SLIT had a positive effect on the reduction of a multiple symptom-medication score, mainly by significantly reducing rescue medication use, but had no significant effect on symptoms alone in children with rhinoconjunctivitis to grass pollen compared with a placebo.	Humboldt Univ, Charite, Dept Pediat Pneumol & Immunol, D-13353 Berlin, Germany; ALK SCHERAX Arzneimittel GmbH, Clin Res, Hamburg, Germany; Univ Freiburg, Dept Pediat & Adolescent Med, Freiburg, Germany; Univ Childrens Hosp, Dresden, Germany; Tech Univ, Childrens Hosp, Munich, Germany; Inst Appl Stat Dr Joerg Schnitker GmbH, Bielefeld, Germany	Niggemann, B (reprint author), Humboldt Univ, Charite, Dept Pediat Pneumol & Immunol, Augustenburger Pl 1, D-13353 Berlin, Germany.						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J	Viegi, G; Simoni, M; Scognamiglio, A; Baldacci, S; Pistelli, F; Carrozzi, L; Annesi-Maesano, I				Viegi, G; Simoni, M; Scognamiglio, A; Baldacci, S; Pistelli, F; Carrozzi, L; Annesi-Maesano, I			Indoor air pollution and airway disease	INTERNATIONAL JOURNAL OF TUBERCULOSIS AND LUNG DISEASE			English	Review						indoor pollution; biomass; ETS; particles; nitrogen oxides; VOC; epidemiology; asthma; COPD; respiratory health; prevention	VOLATILE ORGANIC-COMPOUNDS; ENVIRONMENTAL TOBACCO-SMOKE; EXPOSURE ASSESSMENT SURVEY; RESPIRATORY HEALTH SURVEY; NONCANCER END-POINTS; DEVELOPING-COUNTRIES; BRONCHIAL RESPONSIVENESS; PARTICULATE MATTER; PULMONARY-FUNCTION; CHILDHOOD ASTHMA	Scientific interest in indoor pollution has been increasing since the second half of the 1980s. Growing scientific evidence has shown that because people generally spend the majority of their time indoors, indoor pollution plays a significant role in affecting health and is thus an important health issue. Indoor environments include dwellings, workplaces, schools and day care centres, bars, discotheques and vehicles. Common indoor pollutants are environmental tobacco smoke, particulate matter, nitrogen dioxide, carbon monoxide, volatile organic compounds and biological allergens. In developing countries, relevant sources of indoor pollution include biomass and coal burning for cooking and heating. Concentrations of these pollutants can be many times higher indoors than outdoors. Indoor air pollution may increase the risk of irritation phenomena, allergic sensitisation, acute and chronic respiratory disorders and lung function impairment. Recent conservative estimates have shown that 1.5-2 million deaths per year worldwide could be attributed to indoor air pollution. Approximately I million of these deaths occur in children aged tinder 5 years due to acute respiratory infections and significant proportions of deaths occur due to chronic obstructive pulmonary disease and lung cancer in women. Today, indoor air pollution ranks tenth among preventable risk factors contributing to the global burden of disease. Further research is necessary to better evaluate the respiratory health effects of indoor pollution and to implement protective programmes for public health.	CNR, Inst Clin Physiol, Pulm Environm Epidemiol Unit, I-56126 Pisa, Italy; INSERM, U472, Epidemiol Allerg & Resp Dis Dept, Villejuif, France; Univ Hosp Pisa, Cardiothorac Dept, Pisa, Italy	Viegi, G (reprint author), CNR, Inst Clin Physiol, Pulm Environm Epidemiol Unit, Via Trieste 41, I-56126 Pisa, Italy.	viegig@ifc.cnr.it	Annesi-Maesano, Isabella/D-9173-2016				ALBERTS WM, 1994, J ALLERGY CLIN IMMUN, V94, P289, DOI 10.1016/0091-6749(94)90088-4; Almqvist C, 2003, CLIN EXP ALLERGY, V33, P1167, DOI 10.1046/j.1365-2222.2003.t01-1-01759.x; *AM THOR SOC, 1997, J RESP CRIT CARE M 2, V156, pS33; Annesi-Maesano I, 2003, EUR RESPIR J, V21, p57S, DOI 10.1183/09031936.03.00402103; Anyo G, 2002, CLIN EXP ALLERGY, V32, P361, DOI 10.1046/j.1365-2222.2002.01254.x; BALDACCI S, 2001, EUR RESPIR J, V18, pS274; Bardana EJ, 2001, ANN ALLERG ASTHMA IM, V87, P33; Battistini A, 2000, Acta Biomed Ateneo Parmense, V71, P27; Billings C G, 1998, Monaldi Arch Chest Dis, V53, P43; BLANC PD, 2003, EUR RESP MON, V8, P118; 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J	Seppanen, OA; Fisk, WJ				Seppanen, OA; Fisk, WJ			Summary of human responses to ventilation	INDOOR AIR			English	Article						ventilation; ventilation rate; HVAC-system SBS symptoms; productivity; sick leave; CO2; air-conditioning; infectious disease; cleanliness	INDOOR AIR-QUALITY; SICK BUILDING SYNDROME; HOUSE-DUST MITES; MECHANICAL VENTILATION; OFFICE ENVIRONMENT; AEROSOL FRACTION; SBS SYMPTOMS; HEALTH; POLLEN; POLLUTION	It is known that ventilation is necessary to remove indoor-generated pollutants from indoor air or dilute their concentration to acceptable levels. But as the limit values of all pollutants are not known the exact determination of required ventilation rates based on pollutant concentrations is seldom possible. The selection of ventilation rates has to be based also on epidemiological research, laboratory and field experiments and experience. The existing literature indicates that ventilation has a significant impact on several important human outcomes including: (1) communicable respiratory illnesses; (2) sick building syndrome symptoms; (3) task performance and productivity, and (4) perceived air quality (PAQ) among occupants or sensory panels (5) respiratory allergies and asthma. In many studies, prevalence of sick building syndrome symptoms has also been associated with characteristics of HVAC-systems. Often the prevalence of SBS symptoms is higher in air-conditioned buildings than in naturally ventilated buildings. The evidence suggests that better hygiene, commissioning, operation and maintenance of air handling systems may be particularly important for reducing the negative effects of HVAC systems. Ventilation may also have harmful effects on indoor air quality and climate if not properly designed, installed, maintained and operated. Ventilation may bring indoors harmful substances or deteriorate indoor environment. Ventilation interacts also with the building envelope and may deteriorate the structures of the building. Ventilation changes the pressure differences across the structures of building and may cause or prevent infiltration of pollutants from structures or adjacent spaces. Ventilation is also in many cases used to control the thermal environment or humidity in buildings. The paper summarises the current knowledge on positive and negative effects of ventilation on health and other human responses. The focus is on office-type working environment and residential buildings.	Helsinki Univ Technol, FIN-02015 Espoo, Finland; Univ Calif Berkeley, Lawrence Berkeley Lab, Indoor Environm Dept, Berkeley, CA 94720 USA	Seppanen, OA (reprint author), Helsinki Univ Technol, POB 4100, FIN-02015 Espoo, Finland.	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J	Sutherland, ER; Martin, RJ				Sutherland, ER; Martin, RJ			Airway inflammation in chronic obstructive pulmonary disease: Comparisons with asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						inflammation; chronic obstructive pulmonary disease; small airway; asthma; lymphocyte	CHRONIC-BRONCHITIS; PERIPHERAL AIRWAYS; LUNG-FUNCTION; MACROPHAGE METALLOELASTASE; STRUCTURAL-CHANGES; CIGARETTE SMOKERS; FLOW OBSTRUCTION; ALVEOLAR TISSUE; T-LYMPHOCYTES; EMPHYSEMA	Chronic obstructive pulmonary disease (COPD) is a progressive syndrome of expiratory airflow limitation caused by chronic inflammation of the airways and lung parenchyma. The airway inflammatory response in COPD is initiated by smoking in the overwhelming majority of cases, and chronic exposure to cigarette smoke initiates a series of events that causes damage to central airways, peripheral airways, and terminal airspaces, leading to physiologic and clinical abnormalities. Although COPD shares some clinical features with asthma, another prevalent airway inflammatory disease, there are distinct differences in the phenotypic characteristics of airway inflammation between COPD and asthma. The eosinophil is the most prominent inflammatory cell in asthma, with mast cells, lymphocytes, and macrophages playing important but less prominent roles. In COPD the cellular composition of the airway inflammatory infiltrate differs, with neutrophils, macrophages, and lymphocytes assuming prominence and the eosinophil playing a minor role, except in the setting of exacerbations. The contrasting inflammatory phenotypes of asthma and COPD have important implications for clinical and physiologic manifestations of disease, as well as for therapy.	Natl Jewish Med & Res Ctr, Dept Med, Denver, CO USA; Univ Colorado, Hlth Sci Ctr, Boulder, CO 80309 USA	Martin, RJ (reprint author), 1400 Jackson St, Denver, CO 80206 USA.		Sutherland, Everett/B-7666-2008				American Thoracic Society, 1991, AM REV RESPIR DIS, V144, P1202, DOI 10.1164/ajrccm/144.5.1202; American thoracic society, 1995, AM J RESP CRIT CARE, V152, pS77; Amin K, 2003, THORAX, V58, P135, DOI 10.1136/thorax.58.2.135; Anthonisen NR, 2002, AM J RESP CRIT CARE, V166, P675, DOI 10.1164/rccm.2112096; ANTHONISEN NR, 1994, JAMA-J AM MED ASSOC, V272, P1497, DOI 10.1001/jama.272.19.1497; Arias Elizabeth, 2003, Natl Vital Stat Rep, V51, P1; BOSKEN CH, 1990, AM REV RESPIR DIS, V142, P563; Churg A, 2003, AM J RESP CRIT CARE, V167, P1083, DOI 10.1164/rccm.200212-1396OC; Churg A, 2002, AM J RESP CELL MOL, V27, P368, DOI 10.1165/rcmb.4791; COSIO M, 1978, NEW ENGL J MED, V298, P1277, DOI 10.1056/NEJM197806082982303; DJUKANOVIC R, 1990, AM REV RESPIR DIS, V142, P434; Fabbri LM, 2003, AM J RESP CRIT CARE, V167, P418, DOI 10.1164/rccm.200203-183OC; FINKELSTEIN R, 1995, AM J RESP CRIT CARE, V152, P1666; FLETCHER C, 1977, BRIT MED J, V1, P1645; Fujimoto K, 1999, CHEST, V115, P697, DOI 10.1378/chest.115.3.697; HOGG JC, 1968, NEW ENGL J MED, V278, P1355, DOI 10.1056/NEJM196806202782501; Hogg JC, 2002, THORAX, V57, P830, DOI 10.1136/thorax.57.9.830; HUNNINGHAKE GW, 1983, AM REV RESPIR DIS, V128, P833; Kraft M, 1999, AM J RESP CRIT CARE, V159, P228; Kraft M, 1996, AM J RESP CRIT CARE, V154, P1505; Lams BEA, 1998, AM J RESP CRIT CARE, V158, P1518; Lopez AD, 1998, NAT MED, V4, P1241, DOI 10.1038/3218; LUSUARDI M, 1994, THORAX, V49, P1211, DOI 10.1136/thx.49.12.1211; Majo J, 2001, EUR RESPIR J, V17, P946, DOI 10.1183/09031936.01.17509460; NIEWOEHNER DE, 1974, NEW ENGL J MED, V291, P755, DOI 10.1056/NEJM197410102911503; O'Donnell DE, 1999, AM J RESP CRIT CARE, V160, P542; O'Donnell DE, 2001, AM J RESP CRIT CARE, V164, P770; OShaughnessy TC, 1997, AM J RESP CRIT CARE, V155, P852; Pauwels Romain A., 2001, American Journal of Respiratory and Critical Care Medicine, V163, P1256; Pizzichini E, 1998, AM J RESP CRIT CARE, V158, P1511; Retamales I, 2001, AM J RESP CRIT CARE, V164, P469; Rutgers SR, 2000, THORAX, V55, P12, DOI 10.1136/thorax.55.1.12; 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; Shapiro SD, 1999, AM J RESP CRIT CARE, V160, pS29; Stanescu D, 1996, THORAX, V51, P267, DOI 10.1136/thx.51.3.267; Tashkin DP, 1996, AM J RESP CRIT CARE, V153, P1802; TASHKIN DP, 1992, AM REV RESPIR DIS, V145, P301; Turato G, 2002, AM J RESP CRIT CARE, V166, P105, DOI 10.1164/rccm.2111084; WAGNER EM, 1990, AM REV RESPIR DIS, V141, P584; WRIGHT JL, 1983, AM REV RESPIR DIS, V127, P474	42	82	86	0	6	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	NOV	2003	112	5					819	827		10.1067/mai.2003.1760		9	Allergy; Immunology	Allergy; Immunology	743BV	WOS:000186553300001	14610463	
J	Hamscher, G; Pawelzick, HT; Sczesny, S; Nau, H; Hartung, J				Hamscher, G; Pawelzick, HT; Sczesny, S; Nau, H; Hartung, J			Antibiotics in dust originating from a pig-fattening farm: A new source of health hazard for farmers?	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						antibiotics; dust; farmer; liquid chromatography; mass spectrometry; pig fattening; veterinary drugs	ALLERGIC CONTACT-DERMATITIS; LIVESTOCK BUILDINGS; LIQUID MANURE; ENVIRONMENT; PHARMACEUTICALS; CONTAMINANTS; SUBSTANCES; POLLUTANTS; EMISSIONS; RESIDUES	Pig-house dust originates from feed, bedding, feces, and the animals themselves. If the animals receive drugs such as antibiotics, residues of these substances may occur in manure, in the air, or on surfaces of the respective animal house. In a retrospective study, we investigated dust samples collected during two decades from the same piggery for the occurrence of various antibiotics. In 90% of these samples, we detected up to five different antibiotics, including tylosin, various tetra-cyclines, sulfamethazine, and chloramphenicol, in total amounts up to 12.5 mg/kg dust. High dust exposure in animal confinement buildings is believed to be a respiratory health hazard because of the high content of microorganisms, endotoxins, and allergens. Further risks may arise from the inhalation of dust contaminated with a cocktail of antibiotics. Apart from that, our data provide first evidence for a new route of entry for veterinary drugs in the environment.	Tierarztlichen Hsch Hannover, Dept Food Toxicol, Ctr Food Sci, D-30173 Hannover, Germany; Tierarztlichen Hsch Hannover, Inst Anim Hyg Anim Welf & Behav Farm Anim, D-30173 Hannover, Germany	Hamscher, G (reprint author), Tierarztlichen Hsch Hannover, Dept Food Toxicol, Ctr Food Sci, Bischofsholer Damm 15, D-30173 Hannover, Germany.		Hamscher, Gerd/B-2100-2012				BARBERA E, 1989, CONTACT DERMATITIS, V20, P308, DOI 10.1111/j.1600-0536.1989.tb03155.x; BERGER K, 1986, ARCH LEBENSMITTELHYG, V37, P99; CARAFFINI S, 1994, CONTACT DERMATITIS, V5, P327; Choquet-Kastylevsky Genevieve, 2002, Curr Allergy Asthma Rep, V2, P16, DOI 10.1007/s11882-002-0033-y; DANESE P, 1994, CONTACT DERMATITIS, V30, P122, DOI 10.1111/j.1600-0536.1994.tb00587.x; Daughton CG, 1999, ENVIRON HEALTH PERSP, V107, P907, DOI 10.2307/3434573; DONHAM KJ, 1993, SEMIN RESPIR MED, V14, P49, DOI 10.1055/s-2007-1006308; Halling-Sorensen B, 1998, CHEMOSPHERE, V36, P357, DOI 10.1016/S0045-6535(97)00354-8; Hamscher G, 2000, DEUT TIERARZTL WOCH, V107, P332; Hamscher G, 2002, ANAL CHEM, V74, P1509, DOI 10.1021/ac015588m; Hartung J, 1998, DEUT TIERARZTL WOCH, V105, P213; HARTUNG J, 1995, DEUT TIERARZTL WOCH, V102, P283; HARTUNG J, 1997, ZENTRALBL ARBEITSMED, V47, P65; Heberer T, 2002, TOXICOL LETT, V131, P5, DOI 10.1016/S0378-4274(02)00041-3; HJORTH N, 1980, CONTACT DERMATITIS, V6, P27, DOI 10.1111/j.1600-0536.1980.tb03885.x; HOLT D, 1993, ADVERSE DRUG REACT T, V12, P83; Iversen M, 2000, J Agric Saf Health, V6, P283; *JECFA, 1994, WHO FOOD ADD SER, V33; Kolpin DW, 2002, ENVIRON SCI TECHNOL, V36, P1202, DOI 10.1021/es011055j; Kummerer K, 2001, PHARM ENV SOURCES FA; LANGHAMMER IP, 1988, TIERARZTL UMSCHAU, V43, P375; Lindsey ME, 2001, ANAL CHEM, V73, P4640, DOI 10.1021/ac010514w; Nowak D, 1998, DEUT TIERARZTL WOCH, V105, P225; Nwosu VC, 2001, RES MICROBIOL, V152, P421, DOI 10.1016/S0923-2508(01)01215-3; Pedersen S, 2000, J Agric Saf Health, V6, P261; PLATZ S, 1995, ZBL HYG UMWELTMED, V196, P399; Radon K, 2002, ANN AGR ENV MED, V9, P41; SEEDORF J, 2002, DUST MICRO ORGANISMS; Takai H, 1998, J AGR ENG RES, V70, P59, DOI 10.1006/jaer.1997.0280; Winckler C., 2001, Journal of Soils and Sediments, V1, P66, DOI 10.1007/BF02987711; Witte W, 1998, SCIENCE, V279, P996, DOI 10.1126/science.279.5353.996; 2001, DEUT TIERARZTEBLATT, V8, P841	32	82	88	2	24	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	2003	111	13					1590	1594		10.1289/ehp.6288		5	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	732JU	WOS:000185940800023	14527837	
S	Hanson, LA; Korotkova, M; Lundin, S; Haversen, L; Silfverdal, SA; Mattsby-Baltzer, I; Strandvik, B; Telemo, E		Chiorazzi, N; Lahita, RG; Capra, JD; Ferrarini, M; Zabriskie, JB		Hanson, LA; Korotkova, M; Lundin, S; Haversen, L; Silfverdal, SA; Mattsby-Baltzer, I; Strandvik, B; Telemo, E			The transfer of immunity from mother to child	IMMUNE MECHANISMS AND DISEASE	ANNALS OF THE NEW YORK ACADEMY OF SCIENCES		English	Article; Proceedings Paper	Conference on Immune Mechanisms and Disease	APR 14-17, 2002	ST GEORGES, W IND ASSOC ST	Henry Kunkel Soc, NY Acad Sci		anti-idiotypic; secretory IgA; lactoferrin; Bramwell receptor; immune system; breastfeeding	BREAST-FED INFANTS; ANTIBODY-RESPONSE; HUMAN-MILK; IGG ANTIBODIES; MICE; PROTECTION; DIARRHEA; CELLS; COLONIZATION; IMMUNIZATION	The newborn's immune system grows fast from a small size at birth by exposure primarily to the intestinal microflora normally obtained from the mother at and after birth. While building up its immune system, the infant is supported by the transplacental IgG antibodies, which also contain anti-idiotypic antibodies, possibly also actively priming the offspring. The second mode of transfer of immunity occurs via the milk. Numerous major protective components, including secretory IgA (SIgA) antibodies and lactoferrin, are present. The breastfed infant is better protected against numerous common infections than the non-breastfed. Breastfeeding also seems to actively stimulate the infant's immune system by anti-idiotypes, uptake of milk lymphocytes, cytokines, etc. Therefore, the breastfed child continues to be better protected against various infections for some years. Vaccine responses are also often enhanced in breastfed infants. Long-lasting protection against certain immunological diseases such as allergies and celiac disease is also noted.	Univ Gothenburg, Dept Clin Immunol, SE-41346 Gothenburg, Sweden; Univ Gothenburg, Dept Med Microbiol & Immunol, SE-41346 Gothenburg, Sweden; Univ Gothenburg, Dept Clin Bacteriol, SE-41346 Gothenburg, Sweden; Univ Gothenburg, Dept Pediat, SE-41346 Gothenburg, Sweden; Orebro Med Ctr Hosp, Dept Pediat, S-70185 Orebro, Sweden	Hanson, LA (reprint author), Univ Gothenburg, Dept Clin Immunol, Guldheosgatan 10, SE-41346 Gothenburg, Sweden.						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J	Skold, M; Borje, A; Matura, M; Karlberg, AT				Skold, M; Borje, A; Matura, M; Karlberg, AT			Studies on the autoxidation and sensitizing capacity of the fragrance chemical linalool, identifying a linalool hydroperoxide	CONTACT DERMATITIS			English	Article						autoxidation; fragrance allergy; FCAT; gas chromatographic analysis; guinea pigs; hydroperoxide; linalool; NMR; sensitization studies; terpene	OXIDIZED D-LIMONENE; CONTACT ALLERGENS; 15-HYDROPEROXYABIETIC ACID; CITRUS SOLVENT; ESSENTIAL OILS; COLOPHONY; DERMATITIS	Fragrances are among the most common causes of allergic contact dermatitis. The two monoterpenes linalool and d -limonene are the most frequently incorporated fragrance chemicals in scented products. Previous studies on d -limonene show that this monoterpene oxidizes on air exposure (autoxidation) and that allergenic oxidation products are formed. Due to structural similarities, linalool might also form allergenic oxidation products on air exposure. The aim of the present study was to study the autoxidation of linalool and to investigate the sensitizing potential of linalool before and after air exposure. Linalool was oxidized for 10 weeks and gas chromatographic analyses showed that the content of linalool decreased to about 80%. The chromatograms revealed the formation of other compounds during oxidation. One of the major oxidation products was isolated and identified as 7-hydroperoxy-3,7-dimethyl-octa-1,5-diene-3-ol. This substance is, to the best of our knowledge, described for the first time. In sensitization studies in guinea pigs, linalool of high purity gave no reactions, while linalool that had been oxidized for 10 weeks sensitized the animals. It is concluded that autoxidation of linalool is essential for its sensitizing potential.	Univ Gothenburg, Dept Chem Med Chem Dermatochem & Skin Allergy, SE-41296 Gothenburg, Sweden; Natl Inst Working Life, Stockholm, Sweden	Karlberg, AT (reprint author), Univ Gothenburg, Dept Chem Med Chem Dermatochem & Skin Allergy, SE-41296 Gothenburg, Sweden.		Borje, Anna/A-7581-2010; Karlberg, Ann-Therese/A-7706-2010				Bezard M, 1997, CHEM RES TOXICOL, V10, P987, DOI 10.1021/tx970014r; BOMAN A, 1988, CONTACT DERMATITIS, V18, P25, DOI 10.1111/j.1600-0536.1988.tb05485.x; Casabianca H, 1998, HRC-J HIGH RES CHROM, V21, P107, DOI 10.1002/(SICI)1521-4168(19980201)21:2<107::AID-JHRC107>3.0.CO;2-A; DeGroot AC, 1997, CONTACT DERMATITIS, V36, P57; DEGROOT AC, 1983, CONTACT DERMATITIS, V9, P230; DEGROOT AC, 1994, UNWANTED EFFECTS COS, P579; Fielder S, 1998, TETRAHEDRON, V54, P12907, DOI 10.1016/S0040-4020(98)00782-0; Fregert S, 1969, CONTACT DERMATITIS N, V5, P85; GAFVERT E, 1994, CHEM RES TOXICOL, V7, P260, DOI 10.1021/tx00038a020; Greif N., 1967, AM PERFUM COSMET, V82, P54; KARLBERG AT, 1994, ARCH DERMATOL RES, V286, P97, DOI 10.1007/BF00370734; KARLBERG AT, 1994, ANN OCCUP HYG, V38, P199, DOI 10.1093/annhyg/38.2.199; KARLBERG AT, 1985, CONTACT DERMATITIS, V13, P209, DOI 10.1111/j.1600-0536.1985.tb02552.x; KARLBERG AT, 1988, J PHARM PHARMACOL, V40, P42; KARLBERG AT, 1992, CONTACT DERMATITIS, V26, P332, DOI 10.1111/j.1600-0536.1992.tb00129.x; KARLBERG AT, 1991, ANN OCCUP HYG, V35, P419, DOI 10.1093/annhyg/35.4.419; Karlberg AT, 1997, CONTACT DERMATITIS, V36, P201, DOI 10.1111/j.1600-0536.1997.tb00270.x; Andersen KE, 1985, CONTACT ALLERGY PRED, V14, P152; MATURA M, IN PRESS J AM DERMAT; Mutterer V, 2000, CHEM RES TOXICOL, V13, P1028, DOI 10.1021/tx9901433; Opdyke D. L., 1975, FOOD COSMET TOXICO S, V13, P827; PORTER NA, 1976, J AM CHEM SOC, V98, P6000, DOI 10.1021/ja00435a037; 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; Ryan CA, 2000, CONTACT DERMATITIS, V43, P95, DOI 10.1034/j.1600-0536.2000.043002095.x; SCHALLER M, 1995, CLIN EXP DERMATOL, V20, P143; WILKINS AL, 1993, J AGR FOOD CHEM, V41, P873, DOI 10.1021/jf00030a006	27	82	82	4	27	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-1873			CONTACT DERMATITIS	Contact Dermatitis	MAY	2002	46	5					267	272		10.1034/j.1600-0536.2002.460504.x		6	Allergy; Dermatology	Allergy; Dermatology	568AY	WOS:000176521300004	12084079	
J	Wilson, SR; Yamada, EG; Sudhakar, R; Roberto, L; Mannino, D; Mejia, C; Huss, N				Wilson, SR; Yamada, EG; Sudhakar, R; Roberto, L; Mannino, D; Mejia, C; Huss, N			A controlled trial of an environmental tobacco smoke reduction intervention in low-income children with asthma	CHEST			English	Article						asthma; behavior change; children; controlled trial; cotinine; education; environmental tobacco smoke; low-income	COTININE-ASSISTED INTERVENTION; PASSIVE SMOKING; RELAPSE PREVENTION; YOUNG-CHILDREN; BODY-FLUIDS; EXPOSURE; PREGNANCY; PROGRAM; PARENTS; POSTPARTUM	Study objectives: To determine the effectiveness of a cotinine-feedback, behaviorally based education intervention in reducing environmental tobacco smoke (ETS) exposure and health-care utilization of children with asthma. Design: Randomized controlled trial of educational intervention vs usual care. Setting: The pediatric pulmonary service of a regional pediatric hospital. Participants: ETS-exposed, Medicaid/Niedi-Cal-eligible, predominantly minority children who were 3 to 12 years old and who were seen for asthma in the hospital's emergency, inpatient, and outpatient services departments (n = 87). Intervention: Three nurse-led sessions employing behavior-changing strategies and basic asthma education and that incorporated repeated feedback on the child's urinary cotinine level. Measurements: The primary measurements were the urinary cotinine/creatinine ratio (CCR) and the number of acute asthma medical visits. The secondary measurements were number of hospitalizations, smoking restrictions in home, amount smoked, reported exposures of children, and asthma control. Results: The intervention was associated with a significantly lower odds ratio (OR) for more than one acute asthma medical visit in the follow-up year, after adjusting for baseline visits (total visits, 87; OR, 0.32; p = 0.03), and a comparably sized but nonsignificant OR for one or more hospitalization (OR, 0.34; p = 0.14). The follow-up CCR measurement and the determination of whether smoking was prohibited inside the home strongly favored the intervention group (n = 51) (mean difference in CCR adjusted for baseline, -0.38; p = 0.26; n = 51) (60; OR [for proportion of subjects prohibiting smoking], 0.24; p = 0.11; n = 60). Conclusions: This intervention significantly reduced asthma health-care utilization in ETS-exposed, low-income, minority children. Effects sizes for urine cotinine and proportion prohibiting smoking were moderate to large but not statistically significant, possibly the result of reduced precision due to the loss of patients to active follow-up. Improving ETS reduction interventions and understanding their mechanism of action on asthma outcomes requires further controlled trials that measure ETS exposure and behavioral and disease outcomes concurrently.	Palo Alto Med Fdn, Res Inst, Dept Hlth Serv Res, Palo Alto, CA 94301 USA; Calif Dept Hlth Serv, Chron Dis Control Branch, Sacramento, CA USA; Valley Childrens Hosp, Pediat Pulm Dept, Madera, CA USA; US Ctr Dis Control & Prevent, Atlanta, GA USA	Wilson, SR (reprint author), Palo Alto Med Fdn, Res Inst, Dept Hlth Serv Res, 795 El Camino Real,Ames Bldg, Palo Alto, CA 94301 USA.			Mannino, David/0000-0003-3646-7828	PHS HHS [U60/CCU912212]		*AM AC OT, 1995, 4763355 AM AC OT HEA; Benowitz NL, 1999, ENVIRON HEALTH PERSP, V107, P349, DOI 10.2307/3434427; BENOWITZ NL, 1994, CLIN PHARMACOL THER, V56, P483; BUTZ AM, 1992, J ASTHMA, V29, P265, DOI 10.3109/02770909209048941; California Environmental Protection Agency, 1997, HLTH EFF EXP ENV TOB; CARR W, 1992, AM J PUBLIC HEALTH, V82, P59, DOI 10.2105/AJPH.82.1.59; Centers for Disease Control and Prevention (CDC), 1998, MMWR-MORBID MORTAL W, V47, P1022; CHILMONCZYK BA, 1992, AM J DIS CHILD, V146, P357; Cook DG, 1999, THORAX, V54, P357; DOLANMULLEN P, 1994, AM J OBSTET GYNECOL, V171, P1328; Efron B., 1993, INTRO BOOTSTRAP; Eriksen W, 1996, ACTA PAEDIATR, V85, P209, DOI 10.1111/j.1651-2227.1996.tb13994.x; ERSHOFF DH, 1995, AM J PREV MED, V11, P178; FINGERHUT LA, 1990, AM J PUBLIC HEALTH, V80, P541, DOI 10.2105/AJPH.80.5.541; Fish L, 1996, AM J PUBLIC HEALTH, V86, P246, DOI 10.2105/AJPH.86.2.246; GERGEN PJ, 1990, JAMA-J AM MED ASSOC, V264, P1688, DOI 10.1001/jama.264.13.1688; GREENBERG RA, 1994, J BEHAV MED, V17, P273, DOI 10.1007/BF01857953; HADDOW JE, 1991, BRIT J OBSTET GYNAEC, V98, P859, DOI 10.1111/j.1471-0528.1991.tb13506.x; HOVELL MF, 1994, CHEST, V106, P440, DOI 10.1378/chest.106.2.440; Institute of Medicine, 2000, CLEAR AIR ASTHM IND; Irvine L, 1999, BRIT MED J, V318, P1456; JARVIS MJ, 1988, AM J PUBLIC HEALTH, V78, P696, DOI 10.2105/AJPH.78.6.696; JARVIS MJ, 1984, EUR J RESPIR DIS S, V133, P68; Mannino DM, 1998, MMWR-MORBID MORTAL W, V47, P1; MCBRIDE CM, 1992, HEALTH EDUC RES, V7, P381, DOI 10.1093/her/7.3.381; MCINTOSH NA, 1994, J ASTHMA, V31, P453, DOI 10.3109/02770909409089487; MULLEN PD, 1990, AM J PUBLIC HEALTH, V80, P992, DOI 10.2105/AJPH.80.8.992; National Asthma Education and Prevention Program, 1997, NIH PUBL, V97-4051; Ockene Judith K., 1993, Annals of Behavioral Medicine, V15, P135; Polgar G, 1971, PULMONARY FUNCTION T; Prochaska JO, 1997, AM J HEALTH PROMOT, V12, P38; *SCI COMM TOB HLTH, 1999, REP SCI COMM TOB HLT; Secker-Walker RH, 1998, AM J PREV MED, V15, P25, DOI 10.1016/S0749-3797(98)00029-4; *U CAL, 1998, CANC PREV CONTR PROG; U. S. Environmental Protection Agency, 1992, EPA600690006F OFF HL; VINEIS P, 1993, TUMORI, V79, P183; Wahlgren DR, 1997, CHEST, V111, P81, DOI 10.1378/chest.111.1.81; WALL MA, 1995, PEDIATRICS, V96, P622; WATTS RR, 1990, ENVIRON HEALTH PERSP, V84, P173, DOI 10.2307/3430719; World Health Organization, 1999, WHO LAB MAN EX HUM S, P11; Wilson SR, 1996, J ASTHMA, V33, P239, DOI 10.3109/02770909609055365; WOODWARD A, 1987, PEDIATR PULM, V3, P173, DOI 10.1002/ppul.1950030311	42	82	85	1	5	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	NOV	2001	120	5					1709	1722		10.1378/chest.120.5.1709		14	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	494GW	WOS:000172274300049	11713157	
J	Miller, RL; Chew, GL; Bell, CA; Biedermann, SA; Aggarwal, M; Kinney, PL; Tsai, WY; Whyatt, RM; Perera, FP; Ford, JG				Miller, RL; Chew, GL; Bell, CA; Biedermann, SA; Aggarwal, M; Kinney, PL; Tsai, WY; Whyatt, RM; Perera, FP; Ford, JG			Prenatal exposure, maternal sensitization,, and sensitization in utero to indoor allergens in an inner-city cohort	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						in utero sensitization; indoor antigens; lymphocyte proliferation	HOUSE-DUST MITE; T-CELL RESPONSES; DER-P-I; DERMATOPHAGOIDES-PTERONYSSINUS; ENVIRONMENTAL ALLERGENS; ASTHMA; CHILDREN; LIFE; COCKROACH; IGE	Primary sensitization to antigens may occur prenatally. We hypothesized that high prenatal exposure to indoor antigens increases the risk for sensitization in newborns in New York City populations with increased risk for asthma. We also investigated whether maternal sensitization is required for in utero sensitization to occur. One hundred sixty-seven pregnant African American or Dominican women residing in northern Manhattan were recruited and antigen was measured from home dust. After delivery, newborn cord and maternal blood were assayed for IgE and mononuclear cell proliferation and cytokine production in response to antigen. Cockroach, mouse, but not dust mite antigens, were commonly elevated in the kitchens and pregnant mothers' beds. Increased mononuclear cell proliferation occurred in 54% of newborns in response to cockroach, 25% in response to dust mite Dermatophagoides pteronyssinus, 40% in response to dust mite D. farinae, and 34% in response to mouse protein extracts. Antigen-induced mononuclear cell proliferation occurred in cord blood even in the absence of antigen-induced mononuclear cell proliferation in the mother. Proliferation in response to antigens did not correlate with IgE levels, but proliferation in response to dust mite extracts correlated with interluekin-5 (IL-5) production in cord blood. These results suggest that (1) high prenatal exposures to cockroach and mouse antigens are prevalent; (2) in utero sensitization to multiple indoor antigens is common, occurs to a different degree than maternal sensitization, and may involve IL-5 uprequlation.	Columbia Univ Coll Phys & Surg, Harlem Hosp Ctr, Dept Med, New York, NY 10032 USA; Columbia Univ Coll Phys & Surg, Div Environm Hlth Sci, New York, NY 10032 USA; Columbia Univ Coll Phys & Surg, Div Biostat, Columbia Ctr Childrens Environm Hlth, Joseph L Mailman Sch Publ Hlth, New York, NY 10032 USA	Miller, RL (reprint author), Columbia Univ Coll Phys & Surg, Div Pulm Allergy Crit Care, Dept Med, 630 W 168th St, New York, NY 10032 USA.	rim14@columbia.edu			NCRR NIH HHS [RR00645]; NIEHS NIH HHS [5 R01 ES08977, P50 ES09600]		Boyum A, 1968, Scand J Clin Lab Invest Suppl, V97, P77; CARR W, 1992, AM J PUBLIC HEALTH, V82, P58; Curriculum Development Council (CDC), 1998, SEX TRANSM DIS TREAT; Chan-Yeung M, 1999, J ALLERGY CLIN IMMUN, V104, P317, DOI 10.1016/S0091-6749(99)70373-8; Eggleston PA, 1998, J ALLERGY CLIN IMMUN, V102, P563, DOI 10.1016/S0091-6749(98)70272-6; ELOISANTOS SM, 1989, J CLIN INVEST, V84, P1028, DOI 10.1172/JCI114225; Finn PW, 2000, J ALLERGY CLIN IMMUN, V105, P933, DOI 10.1067/mai.2000.106546; Fleiss J. 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J. Respir. Crit. Care Med.	SEP 15	2001	164	6					995	1001				7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	480DD	WOS:000171446000018	11587985	
J	Juncadella, IJ; Kadl, A; Sharma, AK; Shim, YM; Hochreiter-Hufford, A; Borish, L; Ravichandran, KS				Juncadella, Ignacio J.; Kadl, Alexandra; Sharma, Ashish K.; Shim, Yun M.; Hochreiter-Hufford, Amelia; Borish, Larry; Ravichandran, Kodi S.			Apoptotic cell clearance by bronchial epithelial cells critically influences airway inflammation	NATURE			English	Article							DUST MITE ALLERGEN; ASTHMA; RESPONSES; FAMILY; ENGULFMENT; MECHANISM; MIMICRY; PROTEIN; INNATE; MOUSE	Lung epithelial cells can influence immune responses to airway allergens(1,2). Airway epithelial cells also undergo apoptosis after encountering environmental allergens(3); yet, relatively little is known about how these are cleared, and their effect on airway inflammation. Here we show that airway epithelial cells efficiently engulf apoptotic epithelial cells and secrete anti-inflammatory cytokines, dependent upon intracellular signalling by the small GTPase Rac1. Inducible deletion of Rac1 expression specifically in airway epithelial cells in a mouse model resulted in defective engulfment by epithelial cells and aberrant anti-inflammatory cytokine production. Intranasal priming and challenge of these mice with house dust mite extract or ovalbumin as allergens led to exacerbated inflammation, augmented Th2 cytokines and airway hyper-responsiveness, with decreased interleukin (IL)-10 in bronchial lavages. Rac1-deficient epithelial cells produced much higher IL-33 upon allergen or apoptotic cell encounter, with increased numbers of nuocyte-like cells(1,4,5). Administration of exogenous IL-10 'rescued' the airway inflammation phenotype in Rac1-deficient mice, with decreased IL-33. Collectively, these genetic and functional studies suggest a new role for Rac1-dependent engulfment by airway epithelial cells and in establishing the anti-inflammatory environment, and that defects in cell clearance in the airways could contribute to inflammatory responses towards common allergens.	[Juncadella, Ignacio J.; Hochreiter-Hufford, Amelia; Borish, Larry; Ravichandran, Kodi S.] Univ Virginia, Beirne Carter Ctr Immunol Res, Charlottesville, VA 22908 USA; [Juncadella, Ignacio J.; Hochreiter-Hufford, Amelia; Ravichandran, Kodi S.] Univ Virginia, Dept Microbiol, Charlottesville, VA 22908 USA; [Juncadella, Ignacio J.; Hochreiter-Hufford, Amelia; Ravichandran, Kodi S.] Univ Virginia, Ctr Cell Clearance, Charlottesville, VA 22908 USA; [Kadl, Alexandra; Shim, Yun M.; Borish, Larry] Univ Virginia, Dept Med, Charlottesville, VA 22908 USA; [Sharma, Ashish K.] Univ Virginia, Dept Surg, Charlottesville, VA 22908 USA; [Borish, Larry] Univ Virginia, Ctr Asthma & Allerg Dis, Charlottesville, VA 22908 USA	Ravichandran, KS (reprint author), Univ Virginia, Beirne Carter Ctr Immunol Res, Charlottesville, VA 22908 USA.	Ravi@virginia.edu			Immunology Training Grant; NHLBI; American Asthma Foundation; National Institutes of Health	We thank the members of the Ravichandran laboratory for their suggestions, especially J. Kinchen and P. Trampont. We thank J. Whitsett for the rtTA-CCSP/Cre mice, X. Liu for the TGF-beta responsive cell line PE25, and J. Steinke and J. Kennedy for providing human nasal epithelial cells. This work was supported by an Immunology Training Grant (I. J. J.), a F32 postdoctoral fellowship from the NHLBI (I. J. J.), and grants from the American Asthma Foundation and the National Institutes of Health (K. S. R.). K. S. R. has been a William Benter Senior Fellow of the American Asthma Foundation.	Barlow JL, 2012, J ALLERGY CLIN IMMUN, V129, P191, DOI 10.1016/j.jaci.2011.09.041; Borish L, 1996, J ALLERGY CLIN IMMUN, V97, P1288, DOI 10.1016/S0091-6749(96)70197-5; Cates EC, 2004, J IMMUNOL, V173, P6384; Daidoji T, 2008, J VIROL, V82, P11294, DOI 10.1128/JVI.01192-08; Eisenbarth SC, 2002, J EXP MED, V196, P1645, DOI 10.1084/jem.20021340; Elliott MR, 2010, ANN NY ACAD SCI, V1209, P30, DOI 10.1111/j.1749-6632.2010.05764.x; Fadok VA, 1998, J CLIN INVEST, V101, P890, DOI 10.1172/JCI1112; Fahy JV, 2011, AM J RESP CRIT CARE, V184, P390, DOI 10.1164/rccm.201107-1258ED; Glogauer M, 2003, J IMMUNOL, V170, P5652; Hammad H, 2009, NAT MED, V15, P410, DOI 10.1038/nm.1946; Jyonouchi H, 1999, APOPTOSIS, V4, P407, DOI 10.1023/A:1009607607603; Kirsch T, 2007, BLOOD, V109, P2854, DOI 10.1182/blood-2006-06-026187; Lambrecht BN, 2012, NAT MED, V18, P684, DOI 10.1038/nm.2737; Liew FY, 2010, NAT REV IMMUNOL, V10, P103, DOI 10.1038/nri2692; Lloyd CM, 2010, CURR OPIN IMMUNOL, V22, P800, DOI 10.1016/j.coi.2010.10.006; Locksley RM, 2010, CELL, V140, P777, DOI 10.1016/j.cell.2010.03.004; Monks J, 2005, CELL DEATH DIFFER, V12, P107, DOI 10.1038/sj.cdd.4401517; NAYLOR BERNARD, 1962, THORAX, V17, P69, DOI 10.1136/thx.17.1.69; Park D, 2011, NATURE, V477, P220, DOI 10.1038/nature10340; Park D, 2009, CURR BIOL, V19, P346, DOI 10.1016/j.cub.2009.01.042; Perl AKT, 2002, TRANSGENIC RES, V11, P21; Ravichandran KS, 2007, NAT REV IMMUNOL, V7, P964, DOI 10.1038/nri2214; Ravichandran KS, 2011, IMMUNITY, V35, P445, DOI 10.1016/j.immuni.2011.09.004; Shutes A, 2007, J BIOL CHEM, V282, P35666, DOI 10.1074/jbc.M703571200; Soumelis V, 2002, NAT IMMUNOL, V3, P673, DOI 10.1038/ni805; Thomas WR, 2010, TRENDS MOL MED, V16, P321, DOI 10.1016/j.molmed.2010.04.008; Thomas WR, 2009, EXPERT REV CLIN IMMU, V5, P233, DOI [10.1586/eci.09.5, 10.1586/ECI.09.5]; Trompette A, 2009, NATURE, V457, P585, DOI 10.1038/nature07548; White SR, 2011, J ALLERGY CAIRO, V2011, DOI DOI 10.1155/2011/948406; Yamada Y, 2004, PEDIATR ALLERGY IMMU, V15, P159, DOI 10.1111/j.1399-3038.2004.00155.x	30	81	83	6	45	NATURE PUBLISHING GROUP	LONDON	MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND	0028-0836			NATURE	Nature	JAN 24	2013	493	7433					547	+		10.1038/nature11714		7	Multidisciplinary Sciences	Science & Technology - Other Topics	075GF	WOS:000313871400041	23235830	
J	Chu, DK; Llop-Guevara, A; Walker, TD; Flader, K; Goncharova, S; Boudreau, JE; Moore, CL; In, TS; Waserman, S; Coyle, AJ; Kolbeck, R; Humbles, AA; Jordana, M				Chu, Derek K.; Llop-Guevara, Alba; Walker, Tina D.; Flader, Kristin; Goncharova, Susanna; Boudreau, Jeanette E.; Moore, Cheryl Lynn; In, Tracy Seunghyun; Waserman, Susan; Coyle, Anthony J.; Kolbeck, Roland; Humbles, Alison A.; Jordana, Manel			IL-33, but not thymic stromal lymphopoietin or IL-25, is central to mite and peanut allergic sensitization	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						T(H)2; allergy; asthma; house dust mite; peanut; thymic stromal lymphopoietin; IL-25; IL-33; OX40 ligand; innate lymphoid cells	AIRWAY INFLAMMATION; DENDRITIC CELLS; IMMUNE-RESPONSES; IN-VIVO; TH2 RESPONSES; OX40 LIGAND; TSLP; ASTHMA; RECEPTOR; INNATE	Background: Allergen exposure at lung and gut mucosae can lead to aberrant T(H)2 immunity and allergic disease. The epithelium-associated cytokines thymic stromal lymphopoietin (TSLP), IL-25, and IL-33 are suggested to be important for the initiation of these responses. Objective: We sought to investigate the contributions of TSLP, IL-25, and IL-33 in the development of allergic disease to the common allergens house dust mite (HDM) or peanut. Methods: Neutralizing antibodies or mice deficient in TSLP, IL-25, or IL-33 signaling were exposed to HDM intranasally or peanut intragastrically, and immune inflammatory and physiologic responses were evaluated. In vitro assays were performed to examine specific dendritic cell (DC) functions. Results: We showed that experimental HDM-induced allergic asthma and food allergy and anaphylaxis to peanut were associated with TSLP production but developed independently of TSLP, likely because these allergens functionally mimicked TSLP inhibition of IL-12 production and induction of OX40 ligand (OX40L) on DCs. Blockade of OX40L significantly lessened allergic responses to HDM or peanut. Although IL-25 and IL-33 induced OX40L on DCs in vitro, only IL-33 signaling was necessary for intact allergic immunity, likely because of its superior ability to induce DC OX40L and expand innate lymphoid cells in vivo. Conclusion: These data identify a nonredundant, IL-33-driven mechanism initiating T(H)2 responses to the clinically relevant allergens HDM and peanut. Our findings, along with those in infectious and transgenic/surrogate allergen systems, favor a paradigm whereby multiple molecular pathways can initiate T(H)2 immunity, which has implications for the conceptualization and manipulation of these responses in health and disease. (J Allergy Clin Immunol 2013;131:187-200.)	[Chu, Derek K.; Llop-Guevara, Alba; Walker, Tina D.; Flader, Kristin; Goncharova, Susanna; Boudreau, Jeanette E.; Moore, Cheryl Lynn; In, Tracy Seunghyun; Coyle, Anthony J.; Jordana, Manel] McMaster Univ, McMaster Immunol Res Ctr, Dept Pathol & Mol Med, Hamilton, ON L8N 3Z5, Canada; [Waserman, Susan] McMaster Univ, Dept Med, Hamilton, ON L8N 3Z5, Canada; [Coyle, Anthony J.] Pfizer, Cambridge, MA USA; [Kolbeck, Roland; Humbles, Alison A.] MedImmune LLC, Dept Resp Inflammat & Autoimmun, Gaithersburg, MD USA	Jordana, M (reprint author), McMaster Univ, McMaster Immunol Res Ctr, Dept Pathol & Mol Med, MDCL 4013,1200 Main St W, Hamilton, ON L8N 3Z5, Canada.	jordanam@mcmaster.ca			CIHR; Anaphylaxis Canada; MedImmune LLC; Fundacion Caja Madrid doctoral scholarship (Spain); NSERC Doctoral Canada Graduate Scholarship; Canadian Institutes of Health Research	Supported by CIHR, Anaphylaxis Canada, and grants from MedImmune LLC. D.K.C. is a CIHR Vanier Scholar. A.L.-G. is supported by a Fundacion Caja Madrid doctoral scholarship (Spain). J.E.B. holds an NSERC Doctoral Canada Graduate Scholarship. M.J. holds a Senior Canada Research Chair in Immunobiology of Respiratory Diseases and Allergy.; Disclosure of potential conflict of interest: S. Waserman has received research support from Anaphylaxis Canada and is employed by McMaster University. A. J. Coyle was an employee of MedImmune LLC and is now an employee of Pfizer. R. Kolbeck is employed by and has stock options in MedImmune LLC. A. A. Humbles is employed by MedImmune LLC and has stock options in MedImmune (AZ). M. Jordana has received research support from MedImmune LLC, Anaphylaxis Canada, and the Canadian Institutes of Health Research and is employed by McMaster University. The rest of the authors declare that they have no relevant conflicts of interest.	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Allergy Clin. Immunol.	JAN	2013	131	1					187	U283		10.1016/j.jaci.2012.08.002		22	Allergy; Immunology	Allergy; Immunology	062YR	WOS:000312961200024	23006545	
J	Wisnivesky, JP; Teitelbaum, SL; Todd, AC; Boffetta, P; Crane, M; Crowley, L; de la Hoz, RE; Dellenbaugh, C; Harrison, D; Herbert, R; Kim, H; Jeon, Y; Kaplan, J; Katz, C; Levin, S; Luft, B; Markowitz, S; Moline, JM; Ozbay, F; Pietrzak, RH; Shapiro, M; Sharma, V; Skloot, G; Southwick, S; Stevenson, LA; Udasin, I; Wallenstein, S; Landrigan, PJ				Wisnivesky, Juan P.; Teitelbaum, Susan L.; Todd, Andrew C.; Boffetta, Paolo; Crane, Michael; Crowley, Laura; de la Hoz, Rafael E.; Dellenbaugh, Cornelia; Harrison, Denise; Herbert, Robin; Kim, Hyun; Jeon, Yunho; Kaplan, Julia; Katz, Craig; Levin, Stephen; Luft, Ben; Markowitz, Steven; Moline, Jacqueline M.; Ozbay, Fatih; Pietrzak, Robert H.; Shapiro, Moshe; Sharma, Vansh; Skloot, Gwen; Southwick, Steven; Stevenson, Lori A.; Udasin, Iris; Wallenstein, Sylvan; Landrigan, Philip J.			Persistence of multiple illnesses in World Trade Center rescue and recovery workers: a cohort study	LANCET			English	Article							POSTTRAUMATIC STRESS SYMPTOMS; CENTER DISASTER; LUNG-FUNCTION; HEALTH; FIREFIGHTERS; ASTHMA; STRATEGIES; EXPOSURE; COLLAPSE; ATTACKS	Background More than 50000 people participated in the rescue and recovery work that followed the Sept 11, 2001 (9/11) attacks on the World Trade Center (WTC). Multiple health problems in these workers were reported in the early years after the disaster. We report incidence and prevalence rates of physical and mental health disorders during the 9 years since the attacks, examine their associations with occupational exposures, and quantify physical and mental health comorbidities. Methods In this longitudinal study of a large cohort of WTC rescue and recovery workers, we gathered data from 27 449 participants in the WTC Screening, Monitoring, and Treatment Program. The study population included police officers, firefighters, construction workers, and municipal workers. We used the Kaplan-Meier procedure to estimate cumulative and annual incidence of physical disorders (asthma, sinusitis, and gastro-oesophageal reflux disease), mental health disorders (depression, post-traumatic stress disorder [PTSD], and panic disorder), and spirometric abnormalities. Incidence rates were assessed also by level of exposure (days worked at the WTC site and exposure to the dust cloud). Findings 9-year cumulative incidence of asthma was 27.6% (number at risk: 7027), sinusitis 42.3% (5870), and gastro-oesophageal reflux disease 39.3% (5650). In police officers, cumulative incidence of depression was 7.0% (number at risk: 3648), PTSD 9.3% (3761), and panic disorder 8.4% (3780). In other rescue and recovery workers, cumulative incidence of depression was 27.5% (number at risk: 4200), PTSD 31.9% (4342), and panic disorder 21.2% (4953). 9-year cumulative incidence for spirometric abnormalities was 41.8% (number at risk: 5769); three-quarters of these abnormalities were low forced vital capacity. Incidence of most disorders was highest in workers with greatest WTC exposure. Extensive comorbidity was reported within and between physical and mental health disorders. Interpretation 9 years after the 9/11 WTC attacks, rescue and recovery workers continue to have a substantial burden of physical and mental health problems. These findings emphasise the need for continued monitoring and treatment of the WTC rescue and recovery population.	[Wisnivesky, Juan P.] Mt Sinai Sch Med, Dept Med, Div Gen Internal Med, New York, NY 10029 USA; [Wisnivesky, Juan P.; Skloot, Gwen] Mt Sinai Sch Med, Div Pulm & Crit Care Med, New York, NY 10029 USA; [Teitelbaum, Susan L.; Todd, Andrew C.; Crane, Michael; Crowley, Laura; de la Hoz, Rafael E.; Dellenbaugh, Cornelia; Herbert, Robin; Jeon, Yunho; Kaplan, Julia; Levin, Stephen; Shapiro, Moshe; Stevenson, Lori A.; Wallenstein, Sylvan; Landrigan, Philip J.] Mt Sinai Sch Med, Dept Prevent Med, New York, NY 10029 USA; [Boffetta, Paolo] Mt Sinai Sch Med, Inst Translat Epidemiol, New York, NY 10029 USA; [Katz, Craig; Ozbay, Fatih; Sharma, Vansh] Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA; [Harrison, Denise] NYU, Bellevue Hosp Ctr, Sch Med, Dept Med, New York, NY 10016 USA; [Kim, Hyun; Moline, Jacqueline M.] Hofstra N Shore LIJ Sch Med, Dept Populat Hlth, Great Neck, NY USA; [Luft, Ben] SUNY Stony Brook, Dept Med, Port Jefferson, NY USA; [Markowitz, Steven] CUNY Queens Coll, Flushing, NY 11367 USA; [Pietrzak, Robert H.; Southwick, Steven] Yale Univ, Sch Med, Dept Psychiat, West Haven, CT 06516 USA; [Pietrzak, Robert H.; Southwick, Steven] Vet Adm Connecticut Healthcare Syst, Natl Ctr Posttraumat Stress Disorder, West Haven, CT USA; [Udasin, Iris] Univ Med & Dent New Jersey, Piscataway, NJ 08854 USA	Wisnivesky, JP (reprint author), Mt Sinai Sch Med, Dept Med, Div Gen Internal Med, 1 Gustave L Pl,Box 1087, New York, NY 10029 USA.	juan.wisnivesky@mssm.edu		Luft, Benjamin/0000-0001-9008-7004; de la Hoz, Rafael E./0000-0002-8949-9279	Centers for Disease Control and Prevention; National Institute for Occupational Safety and Health [200-2002-0038, 5U1O 0H008232]; American Red Cross Liberty Fund; September 11th Recovery Program; Bear Stearns Charitable Foundation; September 11th Fund; Robin Hood Foundation	We thank the staff of the World Trade Center (WTC) Worker and Volunteer Medical Screening, Medical Monitoring, and Treatment programmes; the labour, community, and volunteer organisation stake-holders; and the WTC rescue and recovery workers, who gave of themselves so readily in response to the WTC attacks and to whom the WTC programmes are dedicated. This work was supported by the Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health (contract 200-2002-0038 and grant 5U1O 0H008232), the American Red Cross Liberty Fund, The September 11th Recovery Program, The Bear Stearns Charitable Foundation, The September 11th Fund, The Robin Hood Foundation Relief Fund, and many others. The contents of this report are solely the responsibility of the authors and do not necessarily represent the official views of Centers for Disease Control or the National Institute for Occupational Safety and Health.	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J	Ziegler, SF				Ziegler, Steven F.			The role of thymic stromal lymphopoietin (TSLP) in allergic disorders	CURRENT OPINION IN IMMUNOLOGY			English	Review							RESPIRATORY SYNCYTIAL VIRUS; AIRWAY EPITHELIAL-CELLS; IGM(+) B-CELLS; ATOPIC-DERMATITIS; EOSINOPHILIC ESOPHAGITIS; NETHERTON-SYNDROME; IN-VITRO; INFLAMMATION; EXPRESSION; RECEPTOR	The importance of the epithelium in initiating and controlling immune responses is becoming more appreciated. For example, allergen contact first occurs at mucosal sites exposed to the external environment, such as the skin, airways and gastrointestinal tract. This exposure leads to the production of a variety of cytokines and chemokines that are involved in driving allergic inflammatory responses. One such product is thymic stromal lymphopoietin (TSLP). Recent studies, in both humans and mouse models, have implicated TSLP in the development and progression of atopy and atopic diseases. This review will discuss this work and place TSLP in the inflammatory cascade that leads to allergic disease.	Benaroya Res Inst, Program Immunol, Seattle, WA 98101 USA	Ziegler, SF (reprint author), Benaroya Res Inst, Program Immunol, Seattle, WA 98101 USA.	sziegler@benaroyaresearch.org			NIAID NIH HHS [R01 AI068731-05, R01 AI044259, R01 AI044259-01A1, R01 AI044259-02, R01 AI044259-03, R01 AI044259-04, R01 AI044259-05A1, R01 AI068731, R01 AI068731-01, R01 AI068731-02, R01 AI068731-03, R01 AI068731-04]; NIAMS NIH HHS [R01 AR055695, R01 AR055695-01A2, R01 AR055695-02, R01 AR055695-03, R01 AR056113, R01 AR056113-01A1, R01 AR056113-02, R01 AR056113-03]		Al-Shami A, 2005, J EXP MED, V202, P829, DOI 10.1084/jem.20050199; Arima K, 2010, SCI SIGNAL, V3, DOI 10.1126/scisignal.2000567; Blazquez AB, 2010, GASTROENTEROLOGY; Boehme SA, 2009, INT IMMUNOL, V21, P81, DOI 10.1093/intimm/dxn127; Bogiatzi SI, 2007, J IMMUNOL, V178, P3373; Briot A, 2009, J EXP MED, V206, P1135, DOI 10.1084/jem.20082242; Chavanas S, 2000, NAT GENET, V25, P141; Corrigan CJ, 2009, ALLERGY, V64, P1014, DOI 10.1111/j.1398-9995.2009.01947.x; Demehri S, 2008, PLOS BIOL, V6, P992, DOI 10.1371/journal.pbio.0060123; Demehri S, 2009, PLOS BIOL, V7, DOI 10.1371/journal.pbio.1000067; Dumortier A, 2010, PLOS ONE, V5, DOI 10.1371/journal.pone.0009258; Fang CL, 2010, ARCH IMMUNOL THER EX, V58, P81, DOI 10.1007/s00005-010-0064-3; FRIEND SL, 1994, EXP HEMATOL, V22, P321; Gudbjartsson DF, 2009, NAT GENET, V41, P342, DOI 10.1038/ng.323; Hall CB, 2001, NEW ENGL J MED, V344, P1917, DOI 10.1056/NEJM200106213442507; Harada H, 2010, AM J RESP C IN PRESS; Harada M, 2009, AM J RESP CELL MOL, V40, P368, DOI 10.1165/rcmb.2008-0041OC; He R, 2008, P NATL ACAD SCI USA, V105, P11875, DOI 10.1073/pnas.0801532105; Headley MB, 2009, J IMMUNOL, V182, P1641; Holt PG, 2002, J EXP MED, V196, P1271, DOI 10.1084/jem.20021572; Hulse KE, 2010, J ALLERGY CLIN IMMUN, V125, P247, DOI 10.1016/j.jaci.2009.10.027; Hunninghake GM, 2008, AM J RESP CRIT CARE, V177, P830, DOI 10.1164/rccm.200711-1697OC; Hunninghake G. 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Opin. Immunol.	DEC	2010	22	6					795	799		10.1016/j.coi.2010.10.020		5	Immunology	Immunology	701HP	WOS:000285809300016	21109412	
J	DeKruyff, RH; Bu, X; Ballesteros, A; Santiago, C; Chim, YLE; Lee, HH; Karisola, P; Pichavant, M; Kaplan, GG; Umetsu, DT; Freeman, GJ; Casasnovas, JM				DeKruyff, Rosemarie H.; Bu, Xia; Ballesteros, Angela; Santiago, Cesar; Chim, Yee-Ling E.; Lee, Hyun-Hee; Karisola, Piia; Pichavant, Muriel; Kaplan, Gerardo G.; Umetsu, Dale T.; Freeman, Gordon J.; Casasnovas, Jose M.			T Cell/Transmembrane, Ig, and Mucin-3 Allelic Variants Differentially Recognize Phosphatidylserine and Mediate Phagocytosis of Apoptotic Cells	JOURNAL OF IMMUNOLOGY			English	Article							TIM GENE FAMILY; IMMUNE-RESPONSES; IN-VIVO; PERIPHERAL TOLERANCE; AIRWAY INFLAMMATION; AUTOIMMUNE-DISEASE; ACTIVATION; RECEPTOR; MECHANISMS; EXPOSURE	T cell/transmembrane, Ig, and mucin (TIM) proteins, identified using a congenic mouse model of asthma, critically regulate innate and adaptive immunity. TIM-1 and TIM-4 are receptors for phosphatidylserine (PtdSer), exposed on the surfaces of apoptotic cells. Herein, we show with structural and biological studies that TIM-3 is also a receptor for PtdSer that binds in a pocket on the N-terminal IgV domain in coordination with a calcium ion. The TIM-3/PtdSer structure is similar to that of TIM-4/PtdSer, reflecting a conserved PtdSer binding mode by TIM family members. Fibroblastic cells expressing mouse or human TIM-3 bound and phagocytosed apoptotic cells, with the BALB/c allelic variant of mouse TIM-3 showing a higher capacity than the congenic C.D2 Es-Hba-allelic variant. These functional differences were due to structural differences in the BC loop of the IgV domain of the TIM-3 polymorphic variants. In contrast to fibroblastic cells, T or B cells expressing TIM-3 formed conjugates with but failed to engulf apoptotic cells. Together these findings indicate that TIM-3-expressing cells can respond to apoptotic cells, but the consequence of TIM-3 engagement of PtdSer depends on the polymorphic variants of and type of cell expressing TIM-3. These findings establish a new paradigm for TIM proteins as PtdSer receptors and unify the function of the TIM gene family, which has been associated with asthma and autoimmunity and shown to modulate peripheral tolerance. The Journal of Immunology, 2010,184: 1918-1930.	[Freeman, Gordon J.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA; [DeKruyff, Rosemarie H.; Chim, Yee-Ling E.; Lee, Hyun-Hee; Karisola, Piia; Pichavant, Muriel; Umetsu, Dale T.] Harvard Univ, Sch Med, Div Immunol, Childrens Hosp Boston, Cambridge, MA 02138 USA; [DeKruyff, Rosemarie H.; Chim, Yee-Ling E.; Lee, Hyun-Hee; Karisola, Piia; Pichavant, Muriel; Umetsu, Dale T.] Harvard Univ, Sch Med, Dept Pediat, Cambridge, MA 02138 USA; [Bu, Xia; Freeman, Gordon J.] Harvard Univ, Sch Med, Dept Med, Cambridge, MA 02138 USA; [Ballesteros, Angela; Santiago, Cesar; Casasnovas, Jose M.] Consejo Super Invest Cient, Ctr Nacl Biotecnol, Madrid, Spain; [Kaplan, Gerardo G.] US FDA, Ctr Biol Evaluat & Res, Bethesda, MD 20892 USA	Freeman, GJ (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA.	gordon_freeman@dfci.harvard.edu	Casasnovas, Jose/L-6299-2014; Santiago, Cesar/K-4240-2014	Casasnovas, Jose/0000-0002-2873-6410; Santiago, Cesar/0000-0002-5149-1722	National Institutes of Health [P01 AI054456, HL069507]; Ministerio de Ciencia e Innovacion [BFU2005-05972, BFU2008-00971]	This work was supported by National Institutes of Health Grants P01 AI054456 (to D.T.U., G.J.F., R.H.D., and G.G.K.) and HL069507 (to R.H.D.) and Ministerio de Ciencia e Innovacion Grants BFU2005-05972 and BFU2008-00971 (to J.M.C.).	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Immunol.	FEB 15	2010	184	4					1918	1930		10.4049/jimmunol.0903059		13	Immunology	Immunology	556IU	WOS:000274585100028	20083673	
J	Inoue, K; Koike, E; Yanagisaw, R; Hirano, S; Nishikawa, M; Takano, H				Inoue, Ken-ichiro; Koike, Eiko; Yanagisaw, Rie; Hirano, Seishiro; Nishikawa, Masataka; Takano, Hirohisa			Effects of multi-walled carbon nanotubes on a murine allergic airway inflammation model	TOXICOLOGY AND APPLIED PHARMACOLOGY			English	Article						Multi-walled carbon nanotubes; Allergic airway inflammation; Antigen-presenting cells; Dendritic cells; Th immunity	DIESEL EXHAUST PARTICLES; ANTIGEN-PRESENTING CELLS; MOUSE BONE-MARROW; DENDRITIC CELLS; LUNG INFLAMMATION; INTRATRACHEAL INSTILLATION; BACTERIAL-ENDOTOXIN; CYTOKINE EXPRESSION; PARTICULATE MATTER; PULMONARY TOXICITY	The development of nanotechnology has increased the risk of exposure to types of particles other than combustion-derived particles in the environment, namely, industrial nanomaterials. On the other hand, patients with bronchial asthma are sensitive to inhaled substances including particulate matters. This Study examined the effects of pulmonary exposure to a type of nano-sized carbon nanotube (multi-walled nanotubes: MWCNT) on allergic airway inflammation in vivo and their cellular mechanisms in vitro. In vivo, ICR mice were divided into 4 experimental groups. Vehicle, MWCNT (50 mu g/animal), ovalbumin (OVA), and OVA + MWCNT were repeatedly administered intratracheally. Bronchoalveolar lavage (BAL) cellularity, lung histology, levels of cytokines related to allergic inflammation in lung homogenates/BAL fluids (BALF's), and serum immunoglobulin levels were Studied. Also, we evaluated the impact of MWCNT (0.1-1 mu g/ml) on the phenotype and function of bone marrow-derived dendritic cells (DC) in vitro. MWCNT aggravated allergen-induced airway inflammation characterized by the infiltration of eosinophils, neutrophils, and mononuclear cells in the lung, and an increase in the number of goblet cells in the bronchial epithelium. MWCNT with allergen amplified lung protein levels of Th cytokines and chemokines compared with allergen alone. MWCNT exhibited adjuvant activity for allergen-specific IgG(1) and IgE. MWCNT significantly increased allergen (OVA)-specific syngeneic T-cell proliferation, particularly at a lower concentration in vitro. Taken together, MWCNT can exacerbate murine allergic airway inflammation, at least partly, via the promotion of a Th-dominant milieu. In addition, the exacerbation may be partly through the inappropriate activation of antigen-presenting cells including DC. (C) 2009 Elsevier Inc. All rights reserved.	[Inoue, Ken-ichiro; Koike, Eiko; Yanagisaw, Rie; Takano, Hirohisa] Natl Inst Environm Studies, Environm Hlth Sci Div, Tsukuba, Ibaraki 3058506, Japan; [Hirano, Seishiro] Natl Inst Environm Studies, Res Ctr Environm Risk, Tsukuba, Ibaraki 3058506, Japan; [Nishikawa, Masataka] Natl Inst Environm Studies, Div Environm Chem, Tsukuba, Ibaraki 3058506, Japan	Inoue, K (reprint author), Natl Inst Environm Studies, Environm Hlth Sci Div, 16-2 Onogawa, Tsukuba, Ibaraki 3058506, Japan.	inoue.kenichirou@nies.go.jp			Japan Society for the Promotion of Science [18390188, 19510037]	This study was supported by Grants-in-Aid for Scientific Research (B) 18390188 (to H. Takano) and (C) 19510037 (to K. Inoue) from the Japan Society for the Promotion of Science. The authors thank Naoko Ueki, Satomi Abe, and Rieko Shibahara for their assistance throughout the work.	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Appl. Pharmacol.	JUN 15	2009	237	3					306	316		10.1016/j.taap.2009.04.003		11	Pharmacology & Pharmacy; Toxicology	Pharmacology & Pharmacy; Toxicology	454NS	WOS:000266689800007	19371758	
J	Smit, LAM; Siroux, V; Bouzigon, E; Oryszczyn, MP; Lathrop, M; Demenais, F; Kauffmann, F				Smit, Lidwien A. M.; Siroux, Valerie; Bouzigon, Emmanuelle; Oryszczyn, Marie-Pierre; Lathrop, Mark; Demenais, Florence; Kauffmann, Francine		Epidemiological Study Genetics	CD14 and Toll-like Receptor Gene Polymorphisms, Country Living, and Asthma in Adults	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; atopy; epidemiology; gene-environment interaction; hygiene hypothesis	YOUNG DANISH FARMERS; BRONCHIAL HYPERRESPONSIVENESS; C-159T POLYMORPHISM; ENDOTOXIN EXPOSURE; IMMUNOGLOBULIN-E; ATOPY; ASSOCIATION; ENVIRONMENT; CHILDREN; EGEA	Rationale It has been shown that country living protects against asthma, which may be explained by microbial exposures. Objectives: To study whether single nucleotide polymorphisms (SNPs) in CD 14 and Toll-like receptor (TLR) 2, TLR4 and TLR9 genes are associated with asthma in adults, and whether these SNPs modify associations between country living and asthma. Methods: Twenty-five SNPs in CD14, TLR2, TLR4, and TLR9 genes were genotyped in adult subjects from the French Epidemiological study on the Genetics and Environment of Asthma, Bronchial Hyperresponsiveness, and Atopy (EGEA). We conducted a case-control analysis on unrelated subjects (239 with asthma and 596 without asthma), and a family-based association test (FBAT) in 192 families ascertained through probands with asthma. Measurements and Main Results: The TLR2/+596 C allele was associated with an increased risk for asthma in both case-control and family-based analyses (under a dominant model, odds ratio [OR] 1.91 and 95% confidence interval [CI] 1.34-2.72, P = 0.0003; Z statistics from FBAT = 2.48, P = 0.01). In skin prick test (SPT) positive subjects, the CD14/-260 C allele was negatively associated with asthma (additive model, OR 0.66; CI 0.48-0.91). Significant gene-environment interactions between variation in CD14 and TLR genes and country living during childhood were found for ten SNPs. In SPT positive subjects carrying CD14/-260 CC, country living protected against asthma (OR, 0.32; 95% CI, 0.12-0.85), whereas country living was not associated with asthma in subjects who were atopic and carrying CD14/-260 T (OR, 1.11; 95% CI, 0.65-1.90) (gene-environment interaction, P < 0.05). Conclusions: TLR2 and CD14 SNPs were associated with asthma and atopic asthma respectively. In addition, CD14, TLR2, TLR4, and TLR9 SNPs modified associations between country living and asthma.	[Smit, Lidwien A. M.; Oryszczyn, Marie-Pierre; Kauffmann, Francine] INSERM, U780, F-94807 Villejuif, France; [Smit, Lidwien A. M.] Inst Risk Assessment Sci, Div Environm Epidemiol, Utrecht, Netherlands; [Siroux, Valerie] Ctr Rech Albert Bonniot, INSERM, U823, La Tronche, France; [Siroux, Valerie] Univ Grenoble 1, Grenoble, France; [Bouzigon, Emmanuelle; Demenais, Florence] INSERM, U794, Paris, France; [Bouzigon, Emmanuelle; Demenais, Florence] Univ Evry, Evry, France; [Bouzigon, Emmanuelle; Demenais, Florence] Fdn Jean Dausset, CEPH, Paris, France; [Oryszczyn, Marie-Pierre; Kauffmann, Francine] Univ Paris 11, IFR69, Villejuif, France; [Lathrop, Mark] Ctr Natl Genotypage, Inst Genom, Commissariat Energie Atom, Evry, France	Kauffmann, F (reprint author), INSERM, U780, 16 Ave Paul Vaillant Couturier, F-94807 Villejuif, France.	francine.kauffmann@.inserm.fr	siroux, valerie/N-1865-2013; Demenais, Florence/G-3298-2013; LeMoual, Nicole/R-8976-2016	Demenais, Florence/0000-0001-8361-0936; LeMoual, Nicole/0000-0002-2723-5569; Smit, Lidwien AM/0000-0003-0292-0946	French Agency for Environmental and Occupational Health Safety [Afsset-APR-SE-2004]; French National Agency for Research [ANR 05-SEST-020-02/05-9-97]; European Academy of Allergology and Clinical Immunology-Global Allergy; Asthma European Network	Supported by the French Agency for Environmental and Occupational Health Safety (grant Afsset-APR-SE-2004), and the French National Agency for Research (grants ANR 05-SEST-020-02/05-9-97). Lidwien Smit is supported by a European Academy of Allergology and Clinical Immunology-Global Allergy and Asthma European Network (EAACI-GA<SUP>2</SUP>LEN) exchange fellowship award.	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J. Respir. Crit. Care Med.	MAR 1	2009	179	5					363	368		10.1164/rccm.200810-1533OC		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	413BG	WOS:000263767300005	19096003	
J	Willart, MAM; Lambrecht, BN				Willart, M. A. M.; Lambrecht, B. N.			The danger within: endogenous danger signals, atopy and asthma	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review							TOLL-LIKE RECEPTORS; REGULATORY T-CELLS; EOSINOPHILIC AIRWAY INFLAMMATION; NOD-LIKE RECEPTORS; DENDRITIC CELLS; INHALED ANTIGEN; NONATOPIC ASTHMA; TH2 RESPONSES; P2X RECEPTORS; MOUSE MODEL	In allergic asthmatics, airway inflammation is triggered by specific (inhalation of allergen such as house dust mite allergen and pollen spores) or non-specific triggers (such as air pollutants and viral infection). Most of these inhaled particles are immunologically inert. Dendritic cells (DCs) are essential for priming and T helper-2 differentiation of naive T cells towards aeroallergens. Contamination of antigens with pattern-associated molecular patterns (PAMPs), such as lipopolysaccharide (LPS), is required to activate DCs to mount an immune response. Damage-associated molecular patterns (DAMPs), such as uric acid and adenosine triphosphate (ATP), also contribute to the induction of inflammation by activation and recruitment of various inflammatory cells. Compelling evidence suggests that a tight collaboration between PAMPs and DAMPs is needed to start an immune response to allergens. Several studies have recently demonstrated an important role of endogenous danger signals at the inception and maintenance phase of allergic disease. Further research into this area should focus on the possible role of these factors in maintenance of chronic disease and induction of airway remodelling.	[Willart, M. A. M.; Lambrecht, B. N.] Univ Ghent, Dept Pulm Med, Lab Immunoregulat & Mucosal Immun, B-9000 Ghent, Belgium	Willart, MAM (reprint author), Univ Ghent, Dept Pulm Med, Lab Immunoregulat & Mucosal Immun, 0 Block B,Pintelaan 185, B-9000 Ghent, Belgium.	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Exp. Allergy	JAN	2009	39	1					12	19		10.1111/j.1365-2222.2008.03118.x		8	Allergy; Immunology	Allergy; Immunology	392DE	WOS:000262282300005	19016800	
J	Le Moual, N; Kauffmann, F; Eisen, EA; Kennedy, SM				Le Moual, Nicole; Kauffmann, Francine; Eisen, Ellen A.; Kennedy, Susan M.			The healthy worker effect in asthma - Work may cause asthma, but asthma may also influence work	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						epidemiology; asthma; occupational exposure; healthy worker effect	MARGINAL STRUCTURAL MODELS; BODY SHOP WORKERS; RESPIRATORY SYMPTOMS; OCCUPATIONAL EPIDEMIOLOGY; AIRWAY RESPONSIVENESS; METALWORKING FLUIDS; UNITED-STATES; FOLLOW-UP; SELECTION; POPULATION	Despite the increasing attention to the relationship between asthma and work exposures, occupational asthma remains underrecognized and its population burden underestimated. This may be due, in part, to the fact that traditional approaches to studying asthma in populations cannot adequately take into account the healthy worker effect (HWE). The HWE is the potential bias caused by the phenomenon that sicker individuals may choose work environments in which exposures are low, they may be excluded from being hired; or once hired, they may seek transfer to less exposed jobs or leave work. This article demonstrates that population- and workplace-based asthma studies are particularly subject to HWE bias, which leads to underestimates of relative risks. Our objective is to describe the HWE as it relates to asthma research, and to discuss the significance of taking HWE bias into account in designing and interpreting asthma studies. We also discuss the importance of understanding HWE bias for public health practitioners and for clinicians. Finally, we emphasize the timeliness of this review in light of the many longitudinal "child to young adult" asthma cohort studies currently underway. These prospective studies will soon provide an ideal opportunity to examine the impact of early workplace environments on asthma in young adults. We urge occupational and childhood asthma epidemiologists collaborate to ensure that this opportunity is not lost.	[Le Moual, Nicole; Kauffmann, Francine] INSERM U780, F-94807 Villejuif, France; [Le Moual, Nicole; Kauffmann, Francine] Univ Paris Sud, Fac Med, IFR69, Villejuif, France; [Eisen, Ellen A.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA; [Eisen, Ellen A.] Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA; [Kennedy, Susan M.] Univ British Columbia, Sch Occupat & Environm Hygiene, Vancouver, BC V5Z 1M9, Canada	Le Moual, N (reprint author), INSERM U780, 16 Ave Paul Vaillant Couturier, F-94807 Villejuif, France.	lemoual@vjf.inserm.fr	LeMoual, Nicole/R-8976-2016	LeMoual, Nicole/0000-0002-2723-5569			Arif AA, 2002, OCCUP ENVIRON MED, V59, P505, DOI 10.1136/oem.59.8.505; ARRIGHI HM, 1994, EPIDEMIOLOGY, V5, P189, DOI 10.1097/00001648-199403000-00009; Asher MI, 2006, LANCET, V368, P733, DOI 10.1016/S0140-6736(06)69283-0; Baillargeon J, 2001, OCCUP MED-STATE ART, V16, P359; Balmes J, 2003, AM J RESP CRIT CARE, V167, P787, DOI 10.1164/rccm.167.5.787; Beasley R, 2002, J ALLERGY CLIN IMMUN, V109, pS482, DOI 10.1067/mai.2002.122716; BECKLAKE MR, 1990, RESPIRATION, V57, P137; Blanc PD, 1999, CHEST, V115, P1259, DOI 10.1378/chest.115.5.1259; BLANC PD, 1993, CHEST, V104, P1371, DOI 10.1378/chest.104.5.1371; Blanc PD, 2001, J CLIN EPIDEMIOL, V54, P610, DOI 10.1016/S0895-4356(00)00349-8; Chan-Yeung Moira, 2003, Am J Respir Crit Care Med, V167, P450; Checkoway H, 1998, EPIDEMIOL REV, V20, P100; Chen R, 1996, OCCUP MED-OXFORD, V46, P345; Copilevitz C, 2003, IMMUNOL ALLERGY CLIN, V23, P155, DOI 10.1016/S0889-8561(03)00018-3; DAHL E, 1993, SOC SCI MED, V36, P1077, DOI 10.1016/0277-9536(93)90126-O; DOSMAN JA, 1991, J OCCUP ENVIRON MED, V33, P1007; Drexler H, 1999, OCCUP ENVIRON MED, V56, P202; Eisen E A, 1995, Med Lav, V86, P125; Eisen EA, 1997, AM J IND MED, V31, P671; ERNST P, 1989, THORAX, V44, P116, DOI 10.1136/thx.44.2.116; FOX AJ, 1976, BRIT J PREV SOC MED, V30, P225; Greaves IA, 1997, AM J IND MED, V32, P450, DOI 10.1002/(SICI)1097-0274(199711)32:5<450::AID-AJIM4>3.0.CO;2-W; Henneberger PK, 2003, ARCH ENVIRON HEALTH, V58, P781; Hernan MA, 2000, EPIDEMIOLOGY, V11, P561, DOI 10.1097/00001648-200009000-00012; Iwatsubo Y, 2003, OCCUP ENVIRON MED, V60, P831, DOI 10.1136/oem.60.11.831; Karjalainen A, 2001, AM J RESP CRIT CARE, V164, P565; KAUFFMANN F, 1982, BRIT J IND MED, V39, P221; Kennedy SM, 2000, OCCUP ENVIRON MED, V57, P635, DOI 10.1136/oem.57.9.635; Kennedy SM, 1999, AM J RESP CRIT CARE, V159, P87; KIVITY S, 1995, CHEST, V108, P24, DOI 10.1378/chest.108.1.24; Le Moual N, 2005, AM J RESP CRIT CARE, V172, P440, DOI 10.1164/rccm.200501-111OC; Le Moual N, 2004, AM J EPIDEMIOL, V160, P1108, DOI 10.1093/aje/kwh316; Lea CS, 1999, AM J EPIDEMIOL, V150, P1099; Li CY, 1999, OCCUP MED-OXFORD, V49, P225, DOI 10.1093/occmed/49.4.225; MARABINI A, 1993, CHEST, V104, P821, DOI 10.1378/chest.104.3.821; MCMICHAEL AJ, 1976, J OCCUP ENVIRON MED, V18, P165, DOI 10.1097/00043764-197603000-00009; Monso E, 2000, AM J RESP CRIT CARE, V161, P1508; MONSON RR, 1986, J OCCUP ENVIRON MED, V28, P425, DOI 10.1097/00043764-198606000-00009; OSTLIN P, 1989, SCAND J SOC MED, V17, P265; Pearce N, 2007, OCCUP ENVIRON MED, V64, P562, DOI 10.1136/oem.2006.026690; Radon K, 2006, EUR RESPIR J, V27, P774, DOI 10.1183/09031936.06.00093005; RAMAZZINI B, 1990, MALADIES TRAVAIL; Redlich CA, 2002, AM J IND MED, V42, P511, DOI 10.1002/ajim.10143; Redlich CA, 2001, AM J IND MED, V39, P587, DOI 10.1002/ajim.1058; Reijula K, 1996, CHEST, V110, P58, DOI 10.1378/chest.110.1.58; Robins JM, 2000, EPIDEMIOLOGY, V11, P550, DOI 10.1097/00001648-200009000-00011; Rosenman KD, 1997, J OCCUP ENVIRON MED, V39, P415, DOI 10.1097/00043764-199705000-00007; SIRACUSA A, 1995, AM J IND MED, V28, P411, DOI 10.1002/ajim.4700280310; STEENLAND K, 1991, EPIDEMIOLOGY, V2, P418, DOI 10.1097/00001648-199111000-00005; Toren K, 1999, EUR RESPIR J, V13, P496, DOI 10.1183/09031936.99.13349699; Turner S, 2005, OCCUP MED-OXFORD, V55, P287, DOI 10.1093/occmed/kqi055; Vogelzang PFJ, 1999, EUR RESPIR J, V13, P187, DOI 10.1034/j.1399-3003.1999.13a34.x; Zock JP, 1998, OCCUP ENVIRON MED, V55, P823	53	81	83	1	10	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 1	2008	177	1					4	10		10.1164/rccm.200703-415PP		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	246BN	WOS:000251982600003	17872490	
J	Singh, D; Richards, D; Knowles, RG; Schwartz, S; Woodcock, A; Langley, S; O'Connor, BJ				Singh, Dave; Richards, Duncan; Knowles, Richard G.; Schwartz, Sheila; Woodcock, Ashley; Langley, Steve; O'Connor, Brian J.			Selective inducible nitric oxide synthase inhibition has no effect on allergen challenge in asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						nitric oxide; bronchial hyperreactivity	REACTIVE NITROGEN; AIRWAY RESPONSIVENESS; EXHALED AIR; MILD ASTHMA; RESPIRATORY-TRACT; IN-VITRO; INFLAMMATION; GW274150; MONTELUKAST; POTENT	Rationale Exhaled breath nitric oxide (F-ENO) is increased in asthma. NO is produced predominantly by inducible nitric oxide synthase (NOS). Objectives: We evaluated the selective and potent NOS inhibitor GW274150 in asthma. Methods: Twenty-eight steroid-naive patients with asthma participated in a double-blind, randomized, double-dummy, placebo-controlled, three-period cross-over study. Subjects received GW274150 (90 mg), montelukast (10 mg), or placebo once daily for 14 days. FENO was assessed predose on Days 1, 7, 10, and 14. Adenosine 5 '-monophosphate (AMP) challenge was performed on Day 10, allergen challenge on Day 14 followed by methacholine challenge (MCh) 24 hours later, and then bronchoscopy. Measurements and Main Results: GW274150 reduced predose FENO by 73, 75, and 71% on Days 7, 10, and 14, respectively, compared with placebo. Montelukast did not reduce FENO. GW274150 did not inhibit AMP reactivity whereas for montelukast there was a trend toward inhibition: the mean doubling dose difference versus placebo was 0.64 (95% confidence interval [95% Cl], 0 to 1.28). GW274150 did not inhibit early (EAR) and late (LAR) asthmatic responses to allergen, or MCh reactivity, despite reduced FEND levels. Montelukast inhibited EAR and LAIR FEV1; the mean difference versus placebo for minimal FEV1 was 0.37 L (95% Cl, 0.19 to 0.55) and 0.18 L (95% Cl, 0.04 to 0.32), respectively. MCh reactivity was inhibited by montelukast (mean doubling dose difference vs. placebo, 0.51; 95% Cl, 0.02 to 1.01). GW271540 also had no effect on inflammatory cell numbers in bronchoalveolar lavage fluid after allergen challenge. Conclusions: Selective iNOS inhibition effectively reduces FENO but does not affect airway hyperreactivity or airway inflammatory cell numbers after allergen challenge in subjects with asthma.	Univ Manchester, S Manchester Univ Hosp Trust, Med Evaluat Unit, Manchester M23 9LT, Lancs, England; GlaxoSmithKline Inc, Stevenage, Herts, England; Kings Coll Hosp, Guys Kings & St Thomas Sch Med, Dept Asthma Allergy & Respirat Sci, London, England	Singh, D (reprint author), Univ Manchester, S Manchester Univ Hosp Trust, Med Evaluat Unit, Southmoor Rd, Manchester M23 9LT, Lancs, England.	dsingh@meu.org.uk		Woodcock, Ashley/0000-0002-5428-8578			Alderton WK, 2005, BRIT J PHARMACOL, V145, P301, DOI 10.1038/sj.bjp.0706168; Alderton WK, 2001, BIOCHEM J, V357, P593, DOI 10.1042/0264-6021:3570593; ALVING K, 1993, EUR RESPIR J, V6, P1368; Beckman JS, 1996, AM J PHYSIOL-CELL PH, V271, pC1424; Borrill Z, 2006, RESP MED, V100, P1392, DOI 10.1016/j.rmed.2005.11.018; Chatterjee PK, 2003, KIDNEY INT, V63, P853, DOI 10.1046/j.1523-1755.2003.00802.x; Cuzzocrea S, 2002, EUR J PHARMACOL, V453, P119, DOI 10.1016/S0014-2999(02)02338-5; De Alba J, 2006, PAIN, V120, P170, DOI 10.1016/j.pain.2005.10.028; Diamant Z, 1999, CLIN EXP ALLERGY, V29, P42; Dugo L, 2004, BRIT J PHARMACOL, V141, P979, DOI 10.1038/sj.bjp.0705683; Folkerts G, 2001, EUR J PHARMACOL, V429, P251, DOI 10.1016/S0014-2999(01)01324-3; Garvey EP, 1997, J BIOL CHEM, V272, P4959; Gaston B, 2006, AM J RESP CRIT CARE, V173, P1186, DOI 10.1164/rccm.200510-1584PP; HAMID Q, 1993, LANCET, V342, P1510, DOI 10.1016/S0140-6736(05)80083-2; Hansel TT, 2003, FASEB J, V17, P1298, DOI 10.1096/fj.02-0633fje; Holgate ST, 2000, J ALLERGY CLIN IMMUN, V105, P906, DOI 10.1067/mai.2000.105709; Ichinose M, 2000, AM J RESP CRIT CARE, V162, P701; Kanniess F, 2002, EUR RESPIR J, V20, P853, DOI 10.1183/09031936.02.00244602; Ketchell RI, 2002, J ALLERGY CLIN IMMUN, V110, P603, DOI 10.1067/mai.2002.128486; KHARITONOV SA, 1994, LANCET, V343, P133, DOI 10.1016/S0140-6736(94)90931-8; Kharitonov SA, 1996, AM J RESP CRIT CARE, V153, P454; Kidney JC, 1997, J ALLERGY CLIN IMMUN, V100, P65; Kim SF, 2005, SCIENCE, V310, P1966, DOI 10.1126/science.1119407; KNOWLES RG, 1994, BIOCHEM J, V298, P249; Knowles RG, 2007, P AM THOR SOC, V4, pA487; Koarai A, 2000, PULM PHARMACOL THER, V13, P267, DOI 10.1006/pupt.2000.0254; Koopmans JG, 2005, J ALLERGY CLIN IMMUN, V116, P1007, DOI 10.1016/j.jaci.2005.08.016; Laszlo F, 1997, EUR J PHARMACOL, V334, P99, DOI 10.1016/S0014-2999(97)01163-1; MONCADA S, 1995, FASEB J, V9, P1319; Muijsers RBR, 2001, BRIT J PHARMACOL, V134, P434, DOI 10.1038/sj.bjp.0704235; Palmqvist M, 2005, ALLERGY, V60, P65, DOI 10.1111/j.1398-9995.2005.00633.x; PERSSON MG, 1994, LANCET, V343, P146, DOI 10.1016/S0140-6736(94)90935-0; Prado CM, 2006, AM J RESP CELL MOL, V35, P457, DOI 10.1165/rcmb.2005-0391OC; Que LG, 2005, SCIENCE, V308, P1618, DOI 10.1126/science.1108228; Ricciardolo FLM, 2006, EUR J PHARMACOL, V533, P240, DOI 10.1016/j.cjphar.2005.12.057; Saleh D, 1998, FASEB J, V12, P929; Sandrini A, 2003, CHEST, V124, P1334, DOI 10.1378/chest.124.4.1334; SCHWARTZ S, 2007, P AM THOR SOC, V4, pA485; SINGH SD, 2007, P AM THOR SOC, V4, pA483; Smith AD, 2005, NEW ENGL J MED, V352, P2163, DOI 10.1056/NEJMoa043596; Taylor DA, 1998, AM J RESP CRIT CARE, V158, P99; Taylor DA, 1998, THORAX, V53, P483; van der Vliet A, 1999, AM J RESP CRIT CARE, V160, P1; Young RJ, 2000, BIOORG MED CHEM LETT, V10, P597, DOI 10.1016/S0960-894X(00)00055-X	44	81	81	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 15	2007	176	10					988	993		10.1164/rccm.200704-588OC		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	230PW	WOS:000250889400008	17717202	
J	Yang, PC; Xing, Z; Berin, CM; Soderholm, JD; Feng, BS; Wu, L; Yeh, C				Yang, Ping-Chang; Xing, Zhou; Berin, Cecilia M.; Soderholm, Johan D.; Feng, Bai-Sui; Wu, Linda; Yeh, Calvin			TIM-4 expressed by mucosal dendritic cells plays a critical role in food antigen-specific Th2 differentiation and intestinal allergy	GASTROENTEROLOGY			English	Article							MURINE MODEL; MOUSE MODEL; T-CELLS; TRANSPORT; PROTEINS; MICE; IGE; SENSITIZATION; ANTIBODIES; TOLERANCE	Background & Aims: Food allergy accounts for Significant morbidity. The etiology and immune mechanisms of food allergy, however, have remained poorly understood. In this study, we aimed to determine the role of T-cell immunoglobulin-domain and mucin-domain (TIM)-4, a recently identified member of cell surface molecules, in the pathogenesis of intestinal allergy in a murine model. Methods: We report that TIM-4 as well as costimulatory molecules were up-regulated in intestinal mucosal dendritic cells by in vitro or in vivo exposure to Staphylococcus enterotoxin B (SEB). SEB-conditioned intestinal dendritic cells loaded with a food macromolecule ovalbumin (OVA) induced potent OVA-specific T-helper (Th)2 lymphocyte responses in vitro and such Th2 responses were inhibited completely by TIM-4 blockade. Results: In vivo exposure to both SEB and OVA resulted in OVA-specific Th2 differentiation and intestinal allergic responses including increased serum immunoglobulin E and Th2 cytokine levels, activation of OVA-specific Th2 cells detected both ex vivo and in situ, and mast cell degranulation. Of importance, in vivo abrogation of TIM-4 or its cognate ligand TIM-1 by using a polyclonal antibody remarkably dampened Th2 differentiation and intestinal allergy. Conclusions: Our study thus identifies TIM-4 as a novel molecule critically required for the development of intestinal allergy.	McMaster Univ, Dept Pathol & Mol Med, Hamilton, ON, Canada; CUNY Mt Sinai Sch Med, Dept Med, Div Clin Immunol, New York, NY 10029 USA; Linkoping Univ Hosp, Dept Surg, Colorectal Surg Unit, S-58185 Linkoping, Sweden	Yang, PC (reprint author), St Josephs Hosp, Room T3330,50 Charlton Ave E, Hamilton, ON L8N 4A6, Canada.	yangp@mcmaster.ca					Becker Y, 2006, VIRUS GENES, V33, P235, DOI 10.1007/s11262-006-0064-x; Berin MC, 2006, ALLERGY, V61, P64, DOI 10.1111/j.1398-9995.2006.01012.x; BOSCHOFF SC, 2006, CURR GASTROENTEROL R, V8, P374; Chirdo FG, 2005, EUR J IMMUNOL, V35, P1831, DOI 10.1002/eji.200425882; Encinas JA, 2005, J ALLERGY CLIN IMMUN, V116, P1343, DOI 10.1016/j.jaci.2005.08.031; Fischer R, 2005, AM J PATHOL, V167, P1621, DOI 10.1016/S0002-9440(10)61246-1; Fukushima A, 2007, BIOCHEM BIOPH RES CO, V353, P211, DOI 10.1016/j.bbrc.2006.12.023; Gomez-Garcia L, 2006, PARASITOL RES, V99, P440, DOI 10.1007/s00436-006-0159-2; Kis Z, 2004, INFLAMM RES, V53, P413, DOI 10.1007/s00011-004-1274-0; LIU T, 2006, BMC GASTROENTEROL, V18, P6; Mandron M, 2006, J ALLERGY CLIN IMMUN, V117, P1141, DOI 10.1016/j.jaci.2005.12.1360; Mendoza L, 2006, BIOSYSTEMS, V84, P101, DOI 10.1016/j.biosystems.2005.10.004; Meyers JH, 2005, NAT IMMUNOL, V6, P455, DOI 10.1038/ni1185; Okano M, 2005, CLIN EXP ALLERGY, V35, P506, DOI 10.1111/j.1365-2222.2005.02195.x; Rey J, 2004, J IMMUNOL, V172, P3026; Savinko T, 2005, J IMMUNOL, V175, P8320; Sicherer SH, 2006, J ALLERGY CLIN IMMUN, V118, P170, DOI 10.1016/j.jaci.2006.04.018; Strobel S, 2006, CURR OPIN ALLERGY CL, V6, P207, DOI 10.1097/01.all.0000225162.98391.81; Umetsu SE, 2005, NAT IMMUNOL, V6, P447, DOI 10.1038/ni1186; Verdu EF, 2004, GASTROENTEROLOGY, V127, P826, DOI 10.1053/j.gastro.2004.06.007; Vesterlund S, 2006, MICROBIOL-SGM, V152, P1819, DOI 10.1099/mic.0.28522-0; Webb RA, 2007, PARASITE IMMUNOL, V29, P11, DOI 10.1111/j.1365-3024.2006.00908.x; Yang PC, 2000, J CLIN INVEST, V106, P879, DOI 10.1172/JCI9258; Yu LCH, 2001, GASTROENTEROLOGY, V121, P370, DOI 10.1053/gast.2001.26470	24	81	86	0	11	W B SAUNDERS CO-ELSEVIER INC	PHILADELPHIA	1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA	0016-5085			GASTROENTEROLOGY	Gastroenterology	NOV	2007	133	5					1522	1533		10.1053/j.gastro.2007.08.006		12	Gastroenterology & Hepatology	Gastroenterology & Hepatology	229QV	WOS:000250820100020	17915221	
J	Chapman, MD; Wunschmann, S; Pomes, A				Chapman, Martin D.; Wuenschmann, Sabina; Pomes, Anna			Proteases as Th2 adjuvants	CURRENT ALLERGY AND ASTHMA REPORTS			English	Review							HOUSE-DUST MITE; COCKROACH ALLERGEN BLA-G-2; DERMATOPHAGOIDES-PTERONYSSINUS; CRYSTAL-STRUCTURE; EPITHELIAL-CELLS; SERINE-PROTEASE; MOLECULAR CHARACTERIZATION; RECOMBINANT PRO-DER-P-1; PROTEOLYTIC ACTIVITY; ANTIBODY-RESPONSE	Several cysteine and serine protease allergens have been cloned from house dust mites, including Der p 1, Der p 3, Der p 6, and Der p 9. A significant body of evidence suggests that these allergens mimic helper T (Th) 2 cell adjuvants. Der p 1 cleaves CD23 from activated B cells and CD25 from T cells. Der p I proteolytically degrades tight junctions in lung epithelium and causes release of proinflammatory cytokines from bronchial epithelial cells, mast cells, and basophils. These synergistic effects of mite enzyme allergens may promote IgE synthesis and have direct inflammatory effects on lung epithelium, which could explain why mite allergens are associated with asthma. The crystal structures of the proenzyme and mature forms of Der p 1 have been determined, as have the structures of other indoor allergens that are not enzymes (eg, Der p 2, Fel d 1, and Bla g 2). Cockroach allergens are strongly associated with asthma in US inner cities, yet none of the cockroach allergens that have been cloned are proteolytic enzymes. Thus although mite proteases allergens may act as Th2 adjuvants, a paradoxical effect is that other allergens may elicit strong Th2 responses in the absence of enzyme activity.	INDOOR Biotechnol Inc, Charlottesville, VA 22903 USA	Chapman, MD (reprint author), INDOOR Biotechnol Inc, 1216 Harris St, Charlottesville, VA 22903 USA.	mdc@inbio.com					Allen GR, 2000, ETHOLOGY, V106, P409, DOI 10.1046/j.1439-0310.2000.00550.x; Asokananthan N, 2002, J IMMUNOL, V169, P4572; Bennett BJ, 1996, CLIN EXP ALLERGY, V26, P1150, DOI 10.1046/j.1365-2222.1996.d01-268.x; Best EA, 2000, PROTEIN EXPRES PURIF, V20, P462, DOI 10.1006/prep.2000.1327; Chapman MD, 2007, J ALLERGY CLIN IMMUN, V119, P414, DOI 10.1016/j.jaci.2006.11.001; Chapman MD, 2000, J ALLERGY CLIN IMMUN, V106, P409; CHUA KY, 1988, J EXP MED, V167, P175, DOI 10.1084/jem.167.1.175; de Halleux S, 2006, J ALLERGY CLIN IMMUN, V117, P571, DOI 10.1016/j.jaci.2005.11.032; Fan Y, 2005, INSECT MOL BIOL, V14, P45, DOI 10.1111/j.1365-2583.2004.00530.x; Flores I, 2003, INT ARCH ALLERGY IMM, V130, P12, DOI 10.1159/000068375; Gore JC, 2007, ANNU REV ENTOMOL, V52, P439, DOI 10.1146/annurev.ento.52.110405.091313; Gough L, 2001, CLIN EXP ALLERGY, V31, P1594, DOI 10.1046/j.1365-2222.2001.01207.x; Gough L, 1999, J EXP MED, V190, P1897, DOI 10.1084/jem.190.12.1897; Gruber A, 2004, J BIOL CHEM, V279, P28475, DOI 10.1074/jbc.M400993200; Gruchalla RS, 2005, J ALLERGY CLIN IMMUN, V115, P478, DOI 10.1016/j.jaci.2004.12.006; Gustchina A, 2005, J MOL BIOL, V348, P433, DOI 10.1016/j.jmb.2005.02.062; HEWITT CRA, 1995, J EXP MED, V182, P1537, DOI 10.1084/jem.182.5.1537; Kaiser L, 2003, J BIOL CHEM, V278, P37730, DOI 10.1074/jbc.M304740200; Kikuchi Y, 2006, J IMMUNOL, V177, P1609; King C, 1996, J ALLERGY CLIN IMMUN, V98, P739, DOI 10.1016/S0091-6749(96)70121-5; King C, 1998, J IMMUNOL, V161, P3645; Machado DC, 1996, EUR J IMMUNOL, V26, P2972, DOI 10.1002/eji.1830261224; Meno K, 2005, J IMMUNOL, V175, P3835; Morgan WJ, 2004, NEW ENGL J MED, V351, P1068, DOI 10.1056/NEJMoa032097; Nishiyama C, 1995, FEBS LETT, V377, P62, DOI 10.1016/0014-5793(95)01291-5; Pomes A, 2002, AM J RESP CRIT CARE, V165, P391; Robinson C, 1997, CLIN EXP ALLERGY, V27, P10, DOI 10.1046/j.1365-2222.1997.d01-415.x; Satinover SM, 2005, J ALLERGY CLIN IMMUN, V115, P803, DOI 10.1016/j.jaci.2005.01.018; 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; Sears MR, 2003, NEW ENGL J MED, V349, P1414, DOI 10.1056/NEJMoa022363; Shakib F, 1998, IMMUNOL TODAY, V19, P313, DOI 10.1016/S0167-5699(98)01284-5; Sharma S, 2003, CLIN EXP ALLERGY, V33, P163, DOI 10.1046/j.1365-2222.2003.01605.x; Sun G, 2001, J IMMUNOL, V167, P1014; Takai T, 2005, J ALLERGY CLIN IMMUN, V115, P555, DOI 10.1016/j.jaci.2004.11.024; Takai T, 2005, BIOCHEM BIOPH RES CO, V328, P944, DOI 10.1016/j.bbrc.2005.01.051; Tomee JFC, 1998, J ALLERGY CLIN IMMUN, V102, P75, DOI 10.1016/S0091-6749(98)70057-0; van Oort E, 2002, EUR J BIOCHEM, V269, P671, DOI 10.1046/j.0014-2956.2001.02700.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; Wunschmann S, 2005, J ALLERGY CLIN IMMUN, V116, P140, DOI 10.1016/j.jaci.2005.04.024	41	81	84	0	4	CURRENT SCIENCE INC	PHILADELPHIA	400 MARKET STREET, STE 700, PHILADELPHIA, PA 19106 USA	1529-7322			CURR ALLERGY ASTHM R	Curr. Allergy Asthma Rep.	SEP	2007	7	5					363	367		10.1007/s11882-007-0055-6		5	Allergy; Immunology	Allergy; Immunology	205LQ	WOS:000249115500011	17697645	
J	Rowe, J; Kusel, M; Holt, BJ; Suriyaarachchi, D; Serralha, M; Hollams, E; Yerkovich, ST; Subrata, LS; Ladyman, C; Sadowska, A; Gillett, J; Fisher, E; Loh, R; Soderstrom, L; Ahistedt, S; Sly, PD; Holt, PG				Rowe, Julie; Kusel, Merci; Holt, Barbara J.; Suriyaarachchi, Devinda; Serralha, Michael; Hollams, Elysia; Yerkovich, Stephanie T.; Subrata, Lily S.; Ladyman, Claire; Sadowska, Agata; Gillett, Jamie; Fisher, Elizabeth; Loh, Richard; Soderstrom, Lars; Ahistedt, Staffan; Sly, Peter D.; Holt, Patrick G.			Prenatal versus postnatal sensitization to environmental allergens in a high-risk birth cohort	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						atopy; cytokines; IgE; IgG(4); T-cell memory; T(H)2	HOUSE-DUST MITE; T-CELL RESPONSES; CORD-BLOOD; INHALANT ALLERGENS; INDOOR ALLERGENS; MATERNAL INTAKE; EARLY-CHILDHOOD; GRASS-POLLEN; DIETARY EGG; CHILDREN	Background: The timing of allergen sensitization is controversial, with conflicting evidence suggesting transplacental priming versus exclusively postnatal priming. Resolution of this question is important in relation to rational design of allergy prevention strategies, particularly the issue of allergen avoidance during pregnancy. Objective: To elucidate the kinetics of sensitization in high-risk children during their first 2 years of life. Methods: We prospectively studied house dust mite (HDM)specific IgE and IgG(4) antibody production and associated T-cell immunity in a cohort of 200 high-risk infants. Parallel antibody studies tracked responses against a broader panel of inhalant and dietary allergens including peanut. Results: HDM-induced T-H(2) responses in PBMC from 6 months onward, particularly IL-4 and IL-5, correlated increasingly strongly with sensitization outcomes at 2 years, and a I contrasting negative relationship was observed with IFN-T response capacity. HDM-induced T-cell responses in cord blood, although common, were unrelated to subsequent sensitization. Transient HDM-IgE (and IgG4) production frequently peaked at 6 or 12 months before returning to baseline, which suggests the onset of protective tolerance. This finding contrasted wi th progressively increasing HDM titers in children sensitized by 2 years of age. Comparably contrasting patterns were observed in peanut-specific responses in sensitized versus nonsensitized children. Conclusion: Priming of T-H(2) responses associated with persistent HDM-IgE production occurs entirely postnatally, as HDM reactivity in cord blood seems nonspecific and is unrelated to subsequent development of allergen-specific T-H(2) memory or TgE. Clinical implications: These findings question the scientific basis for existing recommendations for allergen avoidance by high-risk women during pregnancy.	Univ Western Australia, Telethon Inst Child Hlth Res, Div Cell Biol, Ctr Child Hlth Res, Perth, WA 6009, Australia; Princess Margaret Hosp Children, Subiaco, WA, Australia; Phadia AB, Uppsala, Sweden; Karolinska Inst, Stockholm, Sweden	Holt, PG (reprint author), Telethon Inst Child Hlth Res, POB 855, Perth, WA 6872, Australia.	patrick@ichr.uwa.edu.au	Sly, Peter/F-1486-2010; Holt, Patrick/H-1548-2011; Yerkovich, Stephanie/A-9004-2011; Osborne, Nicholas/N-4915-2015	Sly, Peter/0000-0001-6305-2201; Holt, Patrick/0000-0003-1193-0935; Osborne, Nicholas/0000-0002-6700-2284; Soderstrom, Lars/0000-0002-6474-6501; Hollams, Elysia/0000-0002-3481-6396			AALBERSE RC, 1992, CLIN EXP ALLERGY, V22, P1003, DOI 10.1111/j.1365-2222.1992.tb03028.x; Baker SS, 2000, PEDIATRICS, V106, P346; Ballardini N, 2006, ALLERGY, V61, P337, DOI 10.1111/j.1398-9995.2005.00936.x; Bjorksten B, 1996, CLIN EXP ALLERGY, V26, P775, DOI 10.1046/j.1365-2222.1996.d01-380.x; BJORKSTEN F, 1976, CLIN ALLERGY, V6, P165, DOI 10.1111/j.1365-2222.1976.tb01894.x; BUSINCO L, 1988, CLIN ALLERGY, V18, P269, DOI 10.1111/j.1365-2222.1988.tb02869.x; Cain TW, 2006, ALLERGY CLIN IMMUNOL, V18, P1; Casas R, 2004, CLIN EXP ALLERGY, V34, P591, DOI 10.1111/j.1365-2222.2004.1924.x; Committee on Toxicity of Chemicals in Food Consumer Products and the Environment, 1998, PEAN ALL; Cressy I, 2006, P 25 C EUR AC ALL CL, P296; Custovic A, 2001, LANCET, V358, P188, DOI 10.1016/S0140-6736(01)05406-X; Department of Health, 1998, PEAN ALL; Evans G, 2000, IMMUNOASSAY HDB; Gavin MA, 1995, IMMUNITY, V3, P793, DOI 10.1016/1074-7613(95)90068-3; GILL TJ, 1983, J CLIN INVEST, V72, P987, DOI 10.1172/JCI111071; Hagendorens MM, 2004, PEDIATR ALLERGY IMMU, V15, P308, DOI 10.1111/j.1399-3038.2004.00169.x; HANNAH ML, 2000, NZ MED MED DEVICES S, P22; Hattevig G, 1993, Pediatr Allergy Immunol, V4, P182, DOI 10.1111/j.1399-3038.1993.tb00089.x; Heaton T, 2005, LANCET, V365, P142, DOI 10.1016/S0140-6736(05)17704-6; Herrmann ME, 1996, EUR J PEDIATR, V155, P770, DOI 10.1007/BF02002904; HOLT PG, 1994, LANCET, V344, P456, DOI 10.1016/S0140-6736(94)91776-0; HOLT PG, 1995, PEDIATR ALLERGY IMMU, V6, P85, DOI 10.1111/j.1399-3038.1995.tb00264.x; HOLT PG, 1987, IMMUNOL TODAY, V8, P14, DOI 10.1016/0167-5699(87)90825-5; HOLT PG, 2006, PROPHYLAXIS ATOPY AS; Julge K, 2001, CLIN EXP ALLERGY, V31, P1854, DOI 10.1046/j.1365-2222.2001.01235.x; Kihlstrom A, 2003, ALLERGY, V58, P871, DOI 10.1034/j.1398-9995.2003.00232.x; KONDO N, 1992, ARCH DIS CHILD, V67, P1003; KORSGAARD J, 1983, CLIN ALLERGY, V13, P529, DOI 10.1111/j.1365-2222.1983.tb02634.x; Kulig M, 1999, J ALLERGY CLIN IMMUN, V103, P1173, DOI 10.1016/S0091-6749(99)70195-8; Kusel MMH, 2005, J ALLERGY CLIN IMMUN, V116, P1067, DOI 10.1016/j.jaci.2005.06.038; Malhotra I, 2006, J INFECT DIS, V193, P1005, DOI 10.1086/500472; Marchant A, 2003, J CLIN INVEST, V111, P1747, DOI 10.1172/JCI200317470; MCMENAMIN C, 1993, J EXP MED, V178, P889, DOI 10.1084/jem.178.3.889; Miller RL, 2001, AM J RESP CRIT CARE, V164, P995; Muraro A, 2004, PEDIATR ALLERGY IMMU, V15, P291, DOI 10.1111/j.1399-3038.2004.00127.x; PIASTRA M, 1994, INT ARCH ALLERGY IMM, V104, P358; Platts-Mills TAE, 2000, AM J RESP CRIT CARE, V162, pS128; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; Rowe J, 2004, VACCINE, V22, P3986, DOI 10.1016/j.vaccine.2004.03.052; Sasai K, 1996, J PEDIATR-US, V128, P834, DOI 10.1016/S0022-3476(96)70337-2; Strickland DH, 2006, J EXP MED, V203, P2649, DOI 10.1084/jem.20060155; Szepfalusi Z, 2000, PEDIATR RES, V48, P404; Thornton CA, 2004, J IMMUNOL, V173, P3084; Turke J, 2005, PEDIATR ALLERGY IMMU, V16, P512, DOI 10.1111/j.1399-3038.2005.00305.x; Vance GHS, 2005, CLIN EXP ALLERGY, V35, P1318, DOI 10.1111/j.1365-2222.2005.02346.x; Vance GHS, 2004, CLIN EXP ALLERGY, V34, P1855, DOI 10.1111/j.1365-2222.2004.02111.x; WOOD RA, 2007, IN PRESS ANN ALLERGY; YMAN L, 2000, IMMUNOASSAY HDB; ZEIGER R, 1995, J ALLERGY CLIN IMMUN, V96, P1179	49	81	83	2	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	2007	119	5					1164	1173		10.1016/j.jaci.2007.02.016		10	Allergy; Immunology	Allergy; Immunology	167CB	WOS:000246427200017	17412403	
J	Wenzel, S; Holgate, ST				Wenzel, Sally; Holgate, Stephen T.			The mouse trap - It still yields few answers in asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Editorial Material							FATAL ASTHMA; MURINE MODEL; UNRESTRAINED PLETHYSMOGRAPHY; AIRWAY HYPERRESPONSIVENESS; MONOCLONAL-ANTIBODY; ALLERGEN EXPOSURE; ATOPIC ASTHMA; SMOOTH-MUSCLE; TGF-BETA; MICE		Univ Pittsburgh, Med Ctr, Pittsburgh, PA 15260 USA; Univ Southampton, Southampton SO9 5NH, Hants, England	Wenzel, S (reprint author), Univ Pittsburgh, Med Ctr, Pittsburgh, PA 15260 USA.				Medical Research Council [G0800766]		Adler A, 2004, J APPL PHYSIOL, V97, P286, DOI 10.1152/japplphysiol.00821.2003; Balzar S, 2002, EUR RESPIR J, V20, P254, DOI 10.1183/09031936.020.0261102; Bates J, 2004, AM J RESP CELL MOL, V31, P373; BERKART JJB, 1889, ASTHMA ITS PATHOLOG; Berry MA, 2006, NEW ENGL J MED, V354, P697, DOI 10.1056/NEJMoa050580; Blyth DI, 2000, AM J RESP CELL MOL, V23, P241; Borish LC, 1999, AM J RESP CRIT CARE, V160, P1816; Boyce JA, 2005, J EXP MED, V201, P1869, DOI 10.1084/jem.20050584; Brightling CE, 2003, THORAX, V58, P528, DOI 10.1136/thorax.58.6.528; Brown V, 2003, THORAX, V58, P311, DOI 10.1136/thorax.58.4.311; Lodrup Carlsen K., 2001, CURR OPIN ALLERGY CL, V1, P139; CARROLL N, 1993, AM REV RESPIR DIS, V147, P405; Collins RA, 2003, RESP PHYSIOL NEUROBI, V139, P51, DOI 10.1016/j.resp.2003.09.003; Fulkerson PC, 2005, CLIN EXP ALLERGY, V35, P1251, DOI 10.1111/j.1365-2222.2005.02354.x; Gelb AF, 2004, CHEST, V126, P1138, DOI 10.1378/chest.126.4.1138; Greenough A, 2004, EUR RESPIR J, V24, P731, DOI 10.1183/09031936.04.00060304; Hamelmann E, 1999, ALLERGY, V54, P297, DOI 10.1034/j.1398-9995.1999.00085.x; Harris JR, 2003, J VIROL, V77, P4773, DOI 10.1128/JVI.77.8.4773-4780.2003; Hauber HP, 2003, THORAX, V58, P519, DOI 10.1136/thorax.58.6.519; Henderson WR, 2002, AM J RESP CRIT CARE, V165, P108; Howarth PH, 2005, THORAX, V60, P1012, DOI 10.1136/thx.2005.045260; Humbles AA, 2004, SCIENCE, V305, P1776, DOI 10.1126/science.1100283; James A, 2000, EUR RESPIR J, V15, P782, DOI 10.1034/j.1399-3003.2000.15d25.x; James AL, 2002, AM J RESP CRIT CARE, V166, P1590, DOI 10.1164/rccm.2108069; Kaviratne M, 2004, J IMMUNOL, V173, P4020; Kenyon NJ, 2000, ANN ALLERG ASTHMA IM, V85, P115; Kenyon NJ, 2003, TOXICOL APPL PHARM, V186, P90, DOI 10.1016/S0041-008X(02)00025-X; Kumar RK, 2002, AM J RESP CELL MOL, V27, P267, DOI 10.1165/rcmb.F248; LAITINEN LA, 1985, AM REV RESPIR DIS, V131, P599; Leckie MJ, 2000, LANCET, V356, P2144, DOI 10.1016/S0140-6736(00)03496-6; Lee JJ, 2004, SCIENCE, V305, P1773, DOI 10.1126/science.1099472; Lilly CM, 2005, AM J RESP CRIT CARE, V171, P579, DOI 10.1164/rccm.200404-532C; Lundblad LKA, 2002, J APPL PHYSIOL, V93, P1198, DOI 10.1152/japplphysiol.00080.2002; Mauad T, 2004, AM J RESP CRIT CARE, V170, P857, DOI 10.1164/rccm.200403-305OC; McMillan SJ, 2005, CLIN EXP ALLERGY, V35, P388, DOI 10.1111/j.1365-2222.2005.02193.x; Norris V, 2005, J ALLERGY CLIN IMMUN, V116, P761, DOI 10.1016/j.jaci.2005.04.045; Pauwels RA, 2003, LANCET, V361, P1071, DOI 10.1016/S0140-6736(03)12891-7; Pearce N, 2000, THORAX, V55, P424, DOI 10.1136/thorax.55.5.424; Pearce N, 1999, THORAX, V54, P268; Persson CGA, 1997, TRENDS PHARMACOL SCI, V18, P465; Shinagawa K, 2003, AM J RESP CRIT CARE, V168, P959, DOI 10.1164/rccm.200210-1188OC; Szefler S, 2000, NEW ENGL J MED, V343, P1054; Tormanen KR, 2005, AM J RESP CRIT CARE, V171, P19, DOI 10.1164/rccm.200406-498OC; Tumas DB, 2001, J ALLERGY CLIN IMMUN, V107, P1025, DOI 10.1067/mai.2001.115625; Wagers S, 2004, J APPL PHYSIOL, V96, P2019, DOI 10.1152/japplphysiol.00924.2003; Wenzel SE, 1999, AM J RESP CRIT CARE, V160, P1001; Wenzel SE, 2002, J IMMUNOL, V169, P4613; Xisto DG, 2005, AM J RESP CRIT CARE, V171, P829, DOI 10.1164/rccm.200408-997OC; Yang GY, 2005, J PHARMACOL EXP THER, V313, P8, DOI 10.1124/jpet.104.076133	49	81	82	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.	DEC 1	2006	174	11					1173	1176		10.1164/rccm.2609002		4	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	109BU	WOS:000242283700005	17110654	
J	Li, YF; Gauderman, WJ; Avol, E; Dubeau, L; Gilliland, FD				Li, YF; Gauderman, WJ; Avol, E; Dubeau, L; Gilliland, FD			Associations of tumor necrosis factor G-308A with childhood asthma and wheezing	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						child; genetic epidemiology; lung	GLUTATHIONE-S-TRANSFERASE; GENE-ENVIRONMENT INTERACTIONS; SOUTHERN CALIFORNIA COMMUNITIES; AIR-POLLUTION; FACTOR-ALPHA; TNF-ALPHA; ATOPIC ASTHMA; INDUCED INFLAMMATION; ALLERGIC RESPONSES; DIFFERING LEVELS	Rationale: Tumor necrosis factor (TNF) mediates a spectrum of airway inflammatory responses, including those to air pollutants, and is an asthma candidate gene. One TNF promoter variant (G-308A) affects expression of TNF and has been associated with inflammatory diseases; however, studies of asthma have been inconsistent. Because ozone produces oxidative stress, increased airway TNF, and inflammation, the associations of the -308 TNF polymorphism with asthma may vary by ozone exposure and variants of oxidant defense genes glutathione-S-transferase (GST) M1 and GSTP1. Objectives: To investigate the association of TNF G-308A with asthma and wheezing and to determine whether these associations vary with ozone exposure and GSTM1 and GSTP1 genotype. Methods: We studied associations of TNF-308 genotype with lifetime and current wheezing and asthma among 3,699 children in the Children's Health Study. We examined differences in associations with community ozone and by GSTM1 null and GSTP1 105 Ile/Val (A105G) genotype. Results: Children with TNF-308 GG had decreased risk of asthma (odds ratio, 0.8; 95% confidence interval, 0.7-0.9) and lifetime wheezing (odds ratio, 0.8; 95% confidence interval, 0.7-0.9). The protective effects of GG genotype on wheezing outcomes were of greater magnitude in lower compared with higher ozone communities. These findings were replicated in the two cohorts of fourth-grade children recruited in 1993 and 1996. The reduction of the protective effect from the -308 GG genotype with higher ozone exposure was most marked in the GSTM1 null and GSTP1 Ile/Ile groups. Conclusions: The TNF-308 GG genotype may have a protective role in asthma pathogenesis, depending on airway oxidative stress levels.	Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA; China Med Univ, Inst Environm Hlth, Taichung, Taiwan	Gilliland, FD (reprint author), Univ So Calif, Keck Sch Med, Dept Prevent Med, 1540 Alcazer St,CHP 236, Los Angeles, CA 90033 USA.	gillilan@usc.edu	LI, YU-FEN/F-4770-2010		NHLBI NIH HHS [5R01HL076647, 5R01HL61768]; NIEHS NIH HHS [5P01ES009581, 5P01ES011627, 5P30ES007048]		Albuquerque RV, 1998, CLIN EXP ALLERGY, V28, P578; Allcock RJN, 2004, HUM MUTAT, V24, P517, DOI 10.1002/humu.20100; Babu KS, 2004, IMMUNOL ALLERGY CLIN, V24, P583, DOI 10.1016/j.iac.2004.06.010; Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; Bilolikar H, 2005, EUR RESPIR J, V26, P637, DOI 10.1183/09031936.05.0007104; BRADDING P, 1994, AM J RESP CELL MOL, V10, P471; Buckova D, 2002, J INVEST ALLERG CLIN, V12, P192; BURR ML, 1992, CLIN EXP ALLERGY, V22, P509, DOI 10.1111/j.1365-2222.1992.tb00158.x; California Environmental Protection Agency, 1997, HLTH EFF EXP ENV TOB; CARROLL MC, 1987, P NATL ACAD SCI USA, V84, P8535, DOI 10.1073/pnas.84.23.8535; Chagani T, 1999, AM J RESP CRIT CARE, V160, P278; Choi IW, 2005, J ALLERGY CLIN IMMUN, V116, P537, DOI 10.1016/j.jaci.2005.05.034; Churg A, 2003, AM J RESP CRIT CARE, V167, P1083, DOI 10.1164/rccm.200212-1396OC; Colilla S, 2003, J ALLERGY CLIN IMMUN, V111, P840, DOI 10.1067/mai.2003.170; Committee on the Assessment of Asthma and Indoor Air, 2000, CLEAR AIR ASTHM IND; Di Somma C, 2003, HUM IMMUNOL, V64, P359, DOI 10.1016/S0198-8859(02)00819-4; FINOTTO S, 1994, J IMMUNOL, V153, P2278; Fryer AA, 2000, AM J RESP CRIT CARE, V161, P1437; Gauderman W J, 1999, J Natl Cancer Inst Monogr, P31; Gilliland FD, 1999, ENVIRON HEALTH PERSP, V107, P403; Gilliland FD, 2002, AM J RESP CRIT CARE, V166, P457, DOI 10.1164/rccm.2112064; Gilliland FD, 2004, LANCET, V363, P119, DOI 10.1016/S0140-6736(03)15262-2; GILLILAND FD, 2003, AM J RESP CRIT CARE, V167, pA580; Hayes JD, 1995, CRIT REV BIOCHEM MOL, V30, P445, DOI 10.3109/10409239509083491; Hiltermann JTN, 1999, FREE RADICAL BIO MED, V27, P1448, DOI 10.1016/S0891-5849(99)00191-4; Huang SL, 1997, AM J RESP CRIT CARE, V156, P1436; Kabesch M, 2004, THORAX, V59, P569, DOI 10.1136/thx.2003.016667; Kleeberger SR, 2005, ANNU REV MED, V56, P383, DOI 10.1146/annurev/med.56.062904.144908; Lee YL, 2004, CLIN EXP ALLERGY, V34, P1707, DOI 10.1111/j.1365-2222.2004.02099.x; Li Kam Wa TC, 1999, CLIN EXP ALLERGY, V29, P1204, DOI 10.1046/j.1365-2222.1999.00638.x; Liebhart J, 2002, J INVEST ALLERG CLIN, V12, P182; Lin YC, 2002, ALLERGY, V57, P831, DOI 10.1034/j.1398-9995.2002.23719.x; Louis R, 2000, EUR RESPIR J, V16, P604, DOI 10.1034/j.1399-3003.2000.16d06.x; McConnell R, 2002, LANCET, V359, P386, DOI 10.1016/S0140-6736(02)07597-9; McDonnell WF, 1999, ENVIRON RES, V80, P110, DOI 10.1006/enrs.1998.3894; Miller RL, 1999, AM J PUBLIC HEALTH, V89, P819, DOI 10.2105/AJPH.89.6.819; Millstein J, 2006, AM J HUM GENET, V78, P15, DOI 10.1086/498850; Mitsuta K, 2003, ALLERGY ASTHMA PROC, V24, P19; Moffatt MF, 1997, HUM MOL GENET, V6, P551, DOI 10.1093/hmg/6.4.551; Moffatt MF, 1999, THORAX, V54, P757; Noguchi E, 2002, AM J RESP CRIT CARE, V166, P43, DOI 10.1164/rccm.2110052; PAULESU L, 1991, LYMPHOKINE CYTOK RES, V10, P409; Peden DB, 2001, ANN ALLERG ASTHMA IM, V87, P12; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; Peters JM, 1999, AM J RESP CRIT CARE, V159, P768; Piirila P, 2001, PHARMACOGENETICS, V11, P437, DOI 10.1097/00008571-200107000-00007; Randolph AG, 2005, AM J RESP CRIT CARE, V172, P687, DOI 10.1164/rccm.200501.122OC; Romieu I, 2004, THORAX, V59, P8; Saxon A, 2005, NAT IMMUNOL, V6, P223, DOI 10.1038/ni0305-223; SHAH A, 1995, CLIN EXP ALLERGY, V25, P1038; Shore SA, 2001, AM J RESP CRIT CARE, V164, P602; Spiteri MA, 2000, ALLERGY, V55, P15, DOI 10.1034/j.1398-9995.2000.00502.x; Strange RC, 2000, TOXICOL LETT, V112, P357, DOI 10.1016/S0378-4274(99)00230-1; Talalay P, 1995, TOXICOL LETT, V82-3, P173, DOI 10.1016/0378-4274(95)03553-2; U. S. Environmental Protection Agency, 1992, RESP HLTH EFF PASS S; Wilson A. G., 1992, Human Molecular Genetics, V1, P353, DOI 10.1093/hmg/1.5.353; Winchester EC, 2000, HUM GENET, V107, P591, DOI 10.1007/s004390000410; Witte JS, 2002, EUR J HUM GENET, V10, P82, DOI 10.1038/sj/ejhg/5200746; Yang IA, 2005, AM J RESP CRIT CARE, V171, P171, DOI 10.1164/rccm.200402-194OC; Zhang J, 2002, EXP BIOL MED, V227, P823	60	81	83	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.	MAY 1	2006	173	9					970	976		10.1164/rccm.200508-1256OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	039UI	WOS:000237332400008	16456144	
J	Alessandrini, F; Schulz, H; Takenaka, S; Lentner, B; Karg, E; Behrendt, H; Jakob, T				Alessandrini, F; Schulz, H; Takenaka, S; Lentner, B; Karg, E; Behrendt, H; Jakob, T			Effects of ultrafine carbon particle inhalation on allergic inflammation of the lung	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						particulate matter; elemental carbon ultrafine particles; allergic inflammation	PARTICULATE AIR-POLLUTION; EMERGENCY-ROOM VISITS; DIESEL EXHAUST PARTICLES; FINE PARTICLES; IN-VIVO; RESPIRATORY HEALTH; ADJUVANT ACTIVITY; OXIDATIVE STRESS; ASTHMA; MICE	Background: Epidemiologic studies show that exposure to particulate air pollution is associated with asthma exacerbation. Ultrafine particles (diameter <100 nm) may contribute to these adverse effects. Objective: To investigate potential adjuvant activity of inhaled elemental carbon ultrafine particles (EC-UFPs) on allergic airway inflammation. Methods: The effects of ultrafine particle inhalation on allergic airway inflammation was analyzed in ovalbumin-sensitized mice and nonsensitized controls. Particle exposure (526 mu g/m(3), 24 hours) was performed 24, 96, or 168 hours before or 24 or 72 hours after ovalbumin aerosol challenge. Allergic inflammation was analyzed at different time points after allergen challenge by means of bronchoalveolar lavage cell count and cytokine/total protein assays, lung histology, and airway hyperresponsiveness. Results: In sensitized mice, inhalation of ultrafine particles 24 hours before allergen challenge caused a significant increase of bronchoalveolar lavage inflammatory cell infiltrate, protein, IL-4, IL-5, and IL-13 compared with relevant controls. These adjuvant effects were dose- and time-dependent and were still present when particle exposure was performed 4 days before allergen challenge. The adjuvant effect of ultrafine particles was also documented by increased mucus production, peribronchiolar and perivascular inflammation, and enhanced airway hyperresponsiveness. In contrast, particle exposure in sensitized mice after allergen challenge caused only moderate effects, such as a delay of inflammatory infiltrate and a reduction of cytokines in bronchoalveolar lavage fluid. Conclusion: Exposure to ultrafine carbon particles before allergen challenge exerts strong adjuvant effects on the manifestation of allergic airway inflammation. Allergen-sensitized individuals may therefore be more susceptible to detrimental health effects of ultrafine particles.	GSF, Div Environm Dermatol Allergy, Natl Res Ctr Environm Hlth, TUM,ZAUM Ctr Allergy Environm, D-85764 Neuherberg, Germany; GSF, Div Environm Dermatol Allergy, Natl Res Ctr Environm Hlth, TUM,ZAUM Ctr Allergy Environm, Munich, Germany; GSF, Natl Res Ctr Environm & Hlth, Focus Network Aerosols & Hlth, Neuherberg, Germany; Tech Univ Munich, Dept Dermatol & Allergy Biederstein, D-8000 Munich, Germany	Alessandrini, F (reprint author), GSF, Div Environm Dermatol Allergy, Natl Res Ctr Environm Hlth, TUM,ZAUM Ctr Allergy Environm, Bldg 34,Room 0340, D-85764 Neuherberg, Germany.	Franci@gsf.de	Jakob, Thilo/J-1621-2012; Karg, Erwin/E-1441-2013; Schulz, Holger/J-5643-2015	Schulz, Holger/0000-0002-1157-200X			Anjilvel S, 1999, MULTIPLE PATH PARTIC; Atkinson RW, 2001, AM J RESP CRIT CARE, V164, P1860; Barrett EG, 2003, INHAL TOXICOL, V15, P151, DOI 10.1080/08958370390168210; BIRCH ME, 1999, ELEMENTAL CARBON DIE; Bochner BS, 2005, J ALLERGY CLIN IMMUN, V115, P953, DOI 10.1016/j.jaci.2005.02.032; Brown DM, 2001, TOXICOL APPL PHARM, V175, P191, DOI 10.1006/taap.2001.9240; Cyrys J, 2003, SCI TOTAL ENVIRON, V305, P143, DOI 10.1016/S0048-9697(02)00494-1; de Haar C, 2005, TOXICOL SCI, V87, P409, DOI 10.1093/toxsci/kfi255; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; Dick CAJ, 2003, INHAL TOXICOL, V15, P39, DOI 10.1080/08958370304454; Dockery D. 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Allergy Clin. Immunol.	APR	2006	117	4					824	830		10.1016/j.jaci.2005.11.046		7	Allergy; Immunology	Allergy; Immunology	033QB	WOS:000236862800016	16630940	
J	Lee, SA; Adhikari, A; Grinshpun, SA; McKay, R; Shukla, R; Reponen, T				Lee, SA; Adhikari, A; Grinshpun, SA; McKay, R; Shukla, R; Reponen, T			Personal exposure to airborne dust and microorganisms in agricultural environments	JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL HYGIENE			English	Article						agricultural farms; bacteria; dust; fungi	N95 FILTERING FACEPIECE; ORGANIC DUST; URINARY ALLERGEN; AIR; FUNGI; BUILDINGS; PARTICLES; FARMS; BARNS; BIOAEROSOLS	Airborne dust and microorganisms are associated with respiratory diseases and increased mortality, and morbidity. Farmers are at high risk of exposure to both of these hazards. Very limited information, however is available on the combined exposures to both hazards on different types of farms. Moreover most of the previous studies have measured the mass concentration of particles ignoring the particle size. In this study, farmers' exposure to airborne dust and microorganisms was studied using our newly developed personal sampling system. Particle number concentration and size distribution were measured with an optical particle counter Simultaneously, particles were collected on a filter and analyzed for microorganisms. The field measurements were conducted in animal confinements (swine, poultry, and dairy) and during grain harvesting (corn and soybean). The ye concentrations on the results show the following avera workers' breathing zone.- 1. 7 x 10(6) to 2.9 x 10(7) particles/m(3) for total dust, 0.9 x 10(3) to 3.9 x 10(4) spores/m(3) for total fungal spores, 0.3 x 10(3) to 3.6 x 10(4) CFU/m(3) for culturable fungal spores, 0.3 x 10(4) to 3.3 x 10(8) CFU/m(3) for culturable bacteria, and limit of detection (LOD) to 2.8 x 103 CFU/m(3) for culturable actinomycetes in animal confinements. The respective concentrations were 4.4 x 10(6) to 5.8 x 10(7) particles/m(3), 3.4 x 10(4) to 6.1 x 10(6) spores/m(3), 8.2 x 10(4) to 7.4 x 10(6) CFU/m(3), 0.4 x 10(5) to 1.4 x 10(6) CFU/m(3), and LOD to 2.6 x 10(4) CFU/m(3) during grain harvesting. The highest contribution of large particles (3-10 mu m) in total particles was found during grain harvesting, whereas the size distribution was dominated by smaller particles (< 3 mu m) in animal confinements. High fraction (up to 37%) of particles between 2-10 mu m was found to be fungal spores. The results indicate that an increase in the concentration of large dust particles (2-10 mu m) during grain harvesting was partially, attributed to the increase in the concentration of the fungal spores. Overall, the combined exposure to airborne dust and microorganisms was found to be more severe during harvesting than in animal confinements.	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Occup. Environ. Hyg.	MAR	2006	3	3					118	130		10.1080/15459620500524607		13	Environmental Sciences; Public, Environmental & Occupational Health	Environmental Sciences & Ecology; Public, Environmental & Occupational Health	019YK	WOS:000235874400004	16484176	
J	Hunninghake, GM; Weiss, ST; Celedon, JC				Hunninghake, GM; Weiss, ST; Celedon, JC			Asthma in Hispanics	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Review						asthma; genetics; Hispanics; risk factors	BODY-MASS INDEX; GENOME-WIDE SEARCH; ETHNICALLY DIVERSE POPULATIONS; INNER-CITY CHILDREN; HOUSE-DUST MITE; BETA(2)-ADRENERGIC RECEPTOR POLYMORPHISMS; COMMUNITY RESPIRATORY HEALTH; REFERENCE SPIROMETRIC VALUES; IMMUNOGLOBULIN-E LEVELS; PUERTO-RICAN CHILDREN	Hispanic individuals trace their ancestry to countries that were previously under Spanish rule, including Mexico, large parts of Central and South America, and some Caribbean islands. Most-but not all-Hispanics have variable proportions of European, Amerindian, and African ancestry. Hispanics are diverse with regard to many factors, including racial ancestry, country of origin, area of residence, socioeconomic status, education, and access to health care. Recent findings suggest that there is marked variation in the prevalence, morbidity, and mortality of asthma in Hispanics in the United States and in Hispanic America. The reasons for differences in asthma and asthma morbidity among and within Hispanic subgroups are poorly understood but are likely due to the interaction between yet-unidentified genetic variants and other factors, including environmental tobacco smoke exposure, obesity, allergen exposure, and availability of health care. Barriers to optimal management of asthma in Hispanics in the United States and in Hispanic America include inadequate access to health care, suboptimal use of antiinflammatory medications, and lack of reference values for spirometric measures of lung function in many subgroups (e.g., Puerto Ricans). Future studies of asthma in Hispanics should include large samples of subgroups that are well characterized with regard to self-reported ethnicity, country of origin, place of birth, area of residence, and indicators of socioeconomic status. Because Hispanics are disproportionately represented among the poor in the United States, implementation of adequate access to health care and social reforms (e.g., improving housing conditions) would likely have a major impact on reducing asthma morbidity in this population.	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J	Kummeling, I; Thijs, C; Penders, J; Snijders, BEP; Stelma, F; Reimerink, J; Koopmans, M; Dagnelie, PC; Huber, M; Jansen, MCJF; de Bie, R; van den Brandt, PA				Kummeling, I; Thijs, C; Penders, J; Snijders, BEP; Stelma, F; Reimerink, J; Koopmans, M; Dagnelie, PC; Huber, M; Jansen, MCJF; de Bie, R; van den Brandt, PA			Etiology of atopy in infancy: The KOALA Birth Cohort Study	PEDIATRIC ALLERGY AND IMMUNOLOGY			English	Article						allergy; etiology; infant; risk factors; lifestyle; breast feeding; human milk; infections; gene-environment; diet; intestinal microbiota; cohort studies	PARTY DIAGNOSTIC-CRITERIA; ANTHROPOSOPHIC LIFE-STYLE; INTESTINAL MICROFLORA; FATTY-ACIDS; BREAST-MILK; ASTHMA; DERMATITIS; ENVIRONMENT; CHILDREN; ALLERGY	The aim of the KOALA Birth Cohort Study in the Netherlands is to identify factors that influence the clinical expression of atopic disease with a main focus on lifestyle (e.g., anthroposophy, vaccinations, antibiotics, dietary habits, breastfeeding and breast milk composition, intestinal microflora composition, infections during the first year of life, and gene-environment interaction). The recruitment of pregnant women started in October 2000. First, participants with 'conventional lifestyles' (n = 2343) were retrieved from an ongoing prospective cohort study (n = 7020) on pregnancy-related pelvic girdle pain. In addition, pregnant women (n = 491) with 'alternative lifestyles' with regard to child rearing practices, dietary habits (organic, vegetarian), vaccination schemes and/or use of antibiotics, were recruited through organic food shops, anthroposophic doctors and midwives, Steiner schools, and dedicated magazines. All participants were enrolled between 14 and 18 wk of gestation and completed an intake questionnaire on family history of atopy and infant care intentions. Documentation of other relevant variables started in the pregnant mother and covered the first and third trimester as well as early childhood by repeated questionnaires at 14-18, 30, and 34 wk of gestation and 3, 7, 12, and 24 months postpartum. A subgroup of participants, including both conventional and alternative lifestyles, was asked to consent to maternal blood sampling, breast milk and a faecal sample of the infant at I month post-partum, capillary blood at age 1 yr, venous blood and observation of manifestation of atopic dermatitis during home visits at the age of 2 yr (using the UK working party criteria and the severity scoring of atopic dermatitis index), and buccal swabs for DNA isolation from child-parent trios. From the start, ethical approval and informed consent procedures included gene-environment interaction studies. Follow-up at 3 and 7 months post-partum was completed with high response rates (respectively 90% and 88% in the conventional group, and 97% and 97% in the alternative group). The home visits at 2 yr of age will be completed in 2005. Preliminary results show that we have succeeded in recruiting a large population with various lifestyle choices with a fairly large contrast with regard to dietary habits (including organic foods, vegetarian diet), vaccination schemes and/or use of antibiotics. We have also been able to collect a large number of faecal samples (n = 1176) and capillary blood samples at age 1 yr (n = 956). Furthermore, a large proportion of the participants have consented with genetic studies. Mid 2006 we expect to report our first results on the relationship between the various exposures in early life and childhood atopy. An outline of the focus and design of the KOALA Birth Cohort Study is presented.	Maastricht Univ, Dept Epidemiol, Care & Publ Hlth Res Inst Caphri, NL-6200 MD Maastricht, Netherlands; TNO, Nutr & Food Res, NL-3700 AJ Zeist, Netherlands; Louis Bolk Inst, Driebergen, Netherlands; Natl Inst Publ Hlth & Environm, Diagnost Lab Infect Dis, NL-3720 BA Bilthoven, Netherlands; Univ Hosp Maastricht, Dept Med Microbiol, Maastricht, Netherlands; Maastricht Univ, Dept Epidemiol, Nutr & Toxicol Res Inst Maastricht, Maastricht, Netherlands	Kummeling, I (reprint author), Maastricht Univ, Dept Epidemiol, Care & Publ Hlth Res Inst Caphri, POB 616, NL-6200 MD Maastricht, Netherlands.	ischa.kummeling@epid.unimaas.nl	Penders, John/A-1280-2011				Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; Alm JS, 2002, PEDIATR ALLERGY IMMU, V13, P402, DOI 10.1034/j.1399-3038.2002.01062.x; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Bastiaanssen JM, 2005, BMC PUBLIC HEALTH, V5, DOI 10.1186/1471-2458-5-1; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Bjorksten B, 2004, SPRINGER SEMIN IMMUN, V25, P257, DOI 10.1007/s00281-003-0142-2; Bjorksten B, 2001, J ALLERGY CLIN IMMUN, V108, P516; Bjorksten B, 1999, CLIN EXP ALLERGY, V29, P342; Bleecker ER, 1997, CIBA F SYMP, V206, P90; Duffy DL, 1997, EPIDEMIOL REV, V19, P129; Hanson LA, 2002, PEDIATR INT, V44, P347, DOI 10.1046/j.1442-200X.2002.t01-1-01592.x; Kalliomaki M, 2001, J ALLERGY CLIN IMMUN, V107, P129, DOI 10.1067/mai.2001.111237; Kirjavainen PV, 2002, GUT, V51, P51, DOI 10.1136/gut.51.1.51; Kramer MS, 2003, COCHRANE DB SYST REV, V4; McNally NJ, 1998, SOC SCI MED, V46, P729, DOI 10.1016/S0277-9536(97)00174-3; Pershagen G, 2000, PEDIATR ALLERGY IMMU, V11, P26, DOI 10.1034/j.1399-3038.2000.00507.x; STALDER JF, 1993, DERMATOLOGY, V186, P23; Thijs C, 2000, EUR J CLIN NUTR, V54, P234, DOI 10.1038/sj.ejcn.1600926; van Gool CJAW, 2003, AM J CLIN NUTR, V77, P943; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P397, DOI 10.1111/j.1365-2133.1994.tb08531.x; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P406, DOI 10.1111/j.1365-2133.1994.tb08532.x; Williams Joan C., 1994, VA J SOC POLY L, V1, P383; Wright AL, 2000, ADV EXP MED BIOL, V478, P131; WRIGHT S, 1989, BRIT J NUTR, V62, P693, DOI 10.1079/BJN19890069	24	81	81	1	9	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0905-6157			PEDIATR ALLERGY IMMU	Pediatr. Allergy Immunol.	DEC	2005	16	8					679	684		10.1111/j.1399-3038.2005.00333.x		6	Allergy; Immunology; Pediatrics	Allergy; Immunology; Pediatrics	990MG	WOS:000233746800011	16343090	
J	Gyan, K; Henry, W; Lacaille, S; Laloo, A; Lamsee-Ebanks, C; McKay, S; Antoine, RM; Monteil, MA				Gyan, K; Henry, W; Lacaille, S; Laloo, A; Lamsee-Ebanks, C; McKay, S; Antoine, RM; Monteil, MA			African dust clouds are associated with increased paediatric asthma accident and emergency admissions on the Caribbean island of Trinidad	INTERNATIONAL JOURNAL OF BIOMETEOROLOGY			English	Article						Saharan dust; paediatric; asthma; accident and emergency; Caribbean	WEST-INDIES	A retrospective ecological study of paediatric asthma patients who attended the Accident and Emergency (A&E) department of the Paediatric Priority Care Facility at the Eric Williams Medical Sciences Complex in relation to Saharan dust visibility and other climatic variables for the period 23 May 2001 to 13 May 2002 was undertaken to determine if there is an association between paediatric A&E asthma visits and Saharan dust cloud cover. A Poisson regression model was used to determine the statistical relationship between acute paediatric asthma A&E visits and Saharan dust cover with and without other variables such as climatic parameters and month. During the study period, there were 2,655 A&E visits for acute asthma. There was an association between increased paediatric asthma admissions and increased Saharan dust cover. The best fitting model estimated that in one month, such as June, a deterioration of visibility due to increased Saharan dust cover from no dust (visibility =16 km) to very dusty (visibility =7 km) would increase a daily admission rate of 7.8 patients to 9.25 when climate variables such as barometric pressure and humidity were kept constant.	Univ W Indies, Fac Med Sci, Sch Basic Sci, St Augustine, Trinid & Tobago		mmonteil@tstt.net.tt					Blades E, 1998, W INDIAN MED J S2, V47, P34; DEPRADINE C, 1995, W INDIAN MED J S2, V44, P17; Howitt ME, 1997, AM J RESP CRIT CARE, V157, pA642; Ivey MA, 2003, CLIN EXP ALLERGY, V33, P1526, DOI 10.1046/j.1365-2222.2003.01801.x; Ivey Marsha A., 2001, Allergology International, V50, P29, DOI 10.1046/j.1440-1592.2001.00198.x; LENFANT C, 1993, NHLBI WHO WORKSH REP, P13; McCarthy M, 2001, LANCET, V358, P478, DOI 10.1016/S0140-6736(01)05677-X; Monteil MA, 2000, J ASTHMA, V37, P677, DOI 10.3109/02770900009087306; PEARSON R S B, 1973, Clinical Allergy, V3, P289, DOI 10.1111/j.1365-2222.1973.tb01336.x; Prospero JM, 1999, J GEOPHYS RES-ATMOS, V104, P15917, DOI 10.1029/1999JD900072; Rajkumar WS, 2000, ATMOS ENVIRON, V34, P1181, DOI 10.1016/S1352-2310(99)00381-7; SCHLATTER T, 1995, WEATHERWISE, V48, P38; Shinn EA, 2000, GEOPHYS RES LETT, V27, P3029, DOI 10.1029/2000GL011599; TAM HBT, 1998, W INDIAN MED J S2, V47, P22	14	81	85	3	10	SPRINGER	NEW YORK	233 SPRING STREET, NEW YORK, NY 10013 USA	0020-7128			INT J BIOMETEOROL	Int. J. Biometeorol.	JUL	2005	49	6					371	376		10.1007/s00484-005-0257-3		6	Biophysics; Environmental Sciences; Meteorology & Atmospheric Sciences; Physiology	Biophysics; Environmental Sciences & Ecology; Meteorology & Atmospheric Sciences; Physiology	946GE	WOS:000230559600003	15692817	
J	Kamradt, T; Goggel, R; Erb, KJ				Kamradt, T; Goggel, R; Erb, KJ			Induction, exacerbation and inhibition of allergic and autoimmune diseases by infection	TRENDS IN IMMUNOLOGY			English	Review							RESPIRATORY SYNCYTIAL VIRUS; INFLAMMATORY-BOWEL-DISEASE; CALMETTE-GUERIN VACCINATION; HELPER TYPE-1 RESPONSES; CENTRAL-NERVOUS-SYSTEM; BIRCH-POLLEN ALLERGY; REGULATORY T-CELLS; AIRWAY INFLAMMATION; DENDRITIC CELLS; MURINE MODEL	Epidemiological and experimental data suggest that infections or the exposure to non-pathogenic bacteria protect individuals from developing some autoimmune and atopic disorders. Generally, these findings support the 'hygiene hypothesis', which attributes the rise in autoimmune and atopic disorders to a lack of infections that normally keep the immune system balanced by inducing immunoregulation. The suspected key players for infection-mediated immune suppression of autoimmunity and atopy are T regulatory cells and dendritic cells, which produce immunosuppressive cytokines, such as interleukin-10 and transforming growth factor-beta. However, there is also solid evidence suggesting that infections can exacerbate or even directly cause autoimmune and allergic disorders. In this Review, we discuss which type of infections induce, exacerbate or inhibit allergic and autoimmune diseases and point at infection-induced immunological mechanisms influencing the development of autoimmunity and atopy.	Klinikum Univ Jena, Inst Immunol, D-07740 Jena, Germany; Boehringer Ingelheim Pharma GmbH & Co KG, Dept Pulm Res, D-88397 Biberach, Germany	Kamradt, T (reprint author), Klinikum Univ Jena, Inst Immunol, D-07740 Jena, Germany.	Immunologie@mti.uni-jena.de; Klaus.Erb@bc.boehringer-ingelheim.com		Kamradt, Thomas/0000-0001-8443-5893			Adams VC, 2004, EUR J IMMUNOL, V34, P631, DOI 10.1002/eji.200324659; Allen HF, 1999, DIABETES CARE, V22, P1703, DOI 10.2337/diacare.22.10.1703; Arkwright PD, 2003, BRIT J DERMATOL, V149, P1029, DOI 10.1111/j.1365-2133.2003.05557.x; Audicana MT, 2002, TRENDS PARASITOL, V18, P20, DOI 10.1016/S1471-4922(01)02152-3; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; Bashir MEH, 2002, J IMMUNOL, V169, P3284; Benoist C, 2001, NAT IMMUNOL, V2, P797, DOI 10.1038/ni0901-797; Blasi F, 2004, EUR RESPIR J, V24, P171, DOI 10.1183/09031936.04.00135703; Bouma G, 2003, NAT REV IMMUNOL, V3, P521, DOI 10.1038/nri1132; Brennan FM, 2002, ARTHRITIS RHEUM, V46, P31, DOI 10.1002/1529-0131(200201)46:1<31::AID-ART10029>3.0.CO;2-5; Camporota L, 2003, EUR RESPIR J, V21, P287, DOI 10.1183/09031936.03.00042103; Curiel TJ, 2004, NAT MED, V10, P942, DOI 10.1038/nm1093; Dahl ME, 2004, NAT IMMUNOL, V5, P337, DOI 10.1038/ni1041; 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Herz U, 2000, CURR OPIN IMMUNOL, V12, P632, DOI 10.1016/S0952-7915(00)00155-2; Hurst SD, 2001, J IMMUNOL, V166, P4922; Isolauri E, 2000, CLIN EXP ALLERGY, V30, P1604, DOI 10.1046/j.1365-2222.2000.00943.x; Iwasaki A, 2004, NAT IMMUNOL, V5, P987, DOI 10.1038/ni1112; John AE, 2003, EUR J IMMUNOL, V33, P1677, DOI 10.1002/eji.200323930; Kamradt T, 2002, ARTHRITIS RES, V4, P20, DOI 10.1186/ar379; Kamradt T, 2001, NEW ENGL J MED, V344, P655; Kamradt T, 2004, MOL DIVERS, V8, P271, DOI 10.1023/B:MODI.0000036236.11774.1b; Kondo Y, 2004, CLIN EXP ALLERGY, V34, P1307, DOI 10.1111/j.1365-2222.2004.02033.x; La Flamme AC, 2003, INFECT IMMUN, V71, P4996, DOI 10.1128/IAI.71.9.4996-5004.2003; Le Bon A, 2002, CURR OPIN IMMUNOL, V14, P432, DOI 10.1016/S0952-7915(02)00354-0; Lieberman D, 2003, AM J RESP CRIT CARE, V167, P406, DOI 10.1164/rccm.200209-996OC; Loftus EV, 2004, GASTROENTEROLOGY, V126, P1504, DOI 10.1053/j.gastro.2004.01.063; Lukacs NW, 2001, J IMMUNOL, V167, P1060; Madsen KL, 1999, GASTROENTEROLOGY, V116, P1107, DOI 10.1016/S0016-5085(99)70013-2; 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Sayers I, 2004, J ALLERGY CLIN IMMUN, V114, P302, DOI 10.1016/j.jaci.2004.03.057; Sewell D, 2003, INT IMMUNOL, V15, P59, DOI 10.1093/intimm/dxg012; Sewell DL, 2003, CLIN DIAGN LAB IMMUN, V10, P564, DOI 10.1128/CDLi.10.4.564-572.2003; Sharif S, 2001, NAT MED, V7, P1057, DOI 10.1038/nm0901-1057; Shirtcliffe PM, 2004, CLIN EXP ALLERGY, V34, P207, DOI 10.1111/j.1365-2222.2004.01861.x; Summers RW, 2005, GUT, V54, P87, DOI 10.1136/gut.2004.041749; Summers RW, 2003, AM J GASTROENTEROL, V98, P2034, DOI 10.1016/S0002-9270(03)00623-3; Trujillo C, 2003, INT J MED MICROBIOL, V293, P123, DOI 10.1078/1438-4221-00257; Umetsu DT, 2002, NAT IMMUNOL, V3, P715, DOI 10.1038/ni0802-715; van den Biggelaar AHJ, 2004, J INFECT DIS, V189, P892, DOI 10.1086/381767; Van der Kleij D, 2002, J INFECT DIS, V185, P531, DOI 10.1086/338574; Wakkach A, 2003, IMMUNITY, V18, P605, DOI 10.1016/S1074-7613(03)00113-4; Walzl G, 2000, J EXP MED, V192, P1317, DOI 10.1084/jem.192.9.1317; Wang CC, 2001, CLIN EXP ALLERGY, V31, P495, DOI 10.1046/j.1365-2222.2001.01044.x; Wark PAB, 2002, EUR RESPIR J, V19, P68, DOI 10.1183/09031936.02.00226302; Williams JV, 2004, NEW ENGL J MED, V350, P443, DOI 10.1056/NEJMoa025472; Wohlleben G, 2004, INT IMMUNOL, V16, P585, DOI 10.1093/intimm/dxh062; Wohlleben G, 2003, J IMMUNOL, V170, P4601; Yang JF, 2001, NAT IMMUNOL, V2, P157, DOI 10.1038/84264; Zaccone P, 2004, EUR J IMMUNOL, V34, P3246, DOI 10.1002/eji.200425285; Zaccone P, 2003, EUR J IMMUNOL, V33, P1439, DOI 10.1002/eji.200323910	78	81	87	1	6	ELSEVIER SCI LTD	OXFORD	THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND	1471-4906			TRENDS IMMUNOL	Trends Immunol.	MAY	2005	26	5					260	267		10.1016/j.it.2005.03.009		8	Immunology	Immunology	928CY	WOS:000229249900007	15866239	
J	Anderson, SD; Kippelen, P				Anderson, SD; Kippelen, P			Exercise-induced bronchoconstriction: Pathogenesis	CURRENT ALLERGY AND ASTHMA REPORTS			English	Review							CANINE PERIPHERAL AIRWAYS; THERMALLY-INDUCED ASTHMA; CROSS-COUNTRY SKIERS; MAST-CELL; BRONCHIAL HYPERRESPONSIVENESS; INDUCED BRONCHOSPASM; BETA(2)-ADRENOCEPTOR-MEDIATED RESPONSES; NONASTHMATIC SUBJECTS; ISOCAPNIC HYPERPNEA; ALLERGIC RHINITIS	There is still active debate on the acute mechanism of exercise-induced bronchoconstriction (EIB). Although it is unlikely that vasoconstriction and hyperemia of the bronchial vasculature are essential events for EIB, it is likely that this vasculature enhances the airway response to dehydration and contributes to the pathogenesis of EIB, particularly in elite athletes. Accumulating evidence suggests that airway smooth muscle (ASM) becomes more sensitive as a result of repeated exposure to bulk plasma in response to airway injury from dehydration. Recent evidence also demonstrates sufficient concentrations of mediators that could affect ASM. Paradoxically, mediator release from mast cells may be enhanced and their contractile effects greater when beta(2)-receptor agonists are taken daily. The effect of drugs that have the potential to reduce microvascular leak and reduce or inhibit release or action of these mediators needs to be investigated in elite athletes.	Royal Prince Alfred Hosp, Dept Resp Med, Camperdown, NSW 2050, Australia	Anderson, SD (reprint author), Royal Prince Alfred Hosp, Dept Resp Med, 11 West,Missenden Rd, Camperdown, NSW 2050, Australia.	sandya@mail.med.usyd.edu.au		Anderson, Sandra/0000-0002-6308-8770			Aldridge RE, 2000, AM J RESP CRIT CARE, V161, P1459; Anderson Sandra D, 2004, Paediatr Drugs, V6, P161, DOI 10.2165/00148581-200406030-00003; Anderson SD, 2000, J ALLERGY CLIN IMMUN, V106, P419, DOI 10.1067/mai.2000.108914; Anderson SD, 2000, J ALLERGY CLIN IMMUN, V106, P453; Anderson SD, 1997, AM J RESP CRIT CARE, V156, P758; ANDERSON SD, 1984, J ALLERGY CLIN IMMUN, V73, P660, DOI 10.1016/0091-6749(84)90301-4; Anderson SD, 2003, CLIN REV ALLERG IMMU, V24, P63; Anderson S, 2003, J ALLERGY CLIN IMMUN, V111, P44; Bonsignore MR, 2001, AM J PHYSIOL-LUNG C, V281, pL668; Brannan JD, 1998, AM J RESP CRIT CARE, V158, P1120; Brannan JD, 2003, EUR RESPIR J, V22, P491, DOI 10.1183/09031936.03.00113403; BRANNAN JD, 2004, J ALLERGY CLIN IMMUN, V113; Caillaud C, 2003, CAN J APPL PHYSIOL, V28, P793; Carroll NG, 2002, EUR RESPIR J, V19, P879, DOI 10.1183/09031936.02.00275802; Chong LK, 2003, BRIT J PHARMACOL, V138, P512, DOI 10.1038/sj.bjp.0705050; Crummy F, 2004, J ALLERGY CLIN IMMUN, V114, P34, DOI 10.1016/j.jaci.2004.03.006; Davis MS, 2003, J APPL PHYSIOL, V94, P2545, DOI 10.1152/japplphysiol.00018.2003; Davis MS, 2001, AM J RESP CRIT CARE, V164, P785; DAVISKAS E, 1995, EUR RESPIR J, V8, P742; Evans DW, 1997, THORAX, V52, P136; Freed AN, 1999, AM J RESP CRIT CARE, V159, P1101; HALLSTRAND TS, 2004, AM J RESP CRIT CARE, pA817; Hancox RJ, 2002, AM J RESP CRIT CARE, V165, P1068, DOI 10.1164/rccm.200111-091BC; Helenius IJ, 1998, BRIT J SPORT MED, V32, P125; Helenius IJ, 1998, J ALLERGY CLIN IMMUN, V101, P646; Holzer K, 2003, AM J RESP CRIT CARE, V167, P534, DOI 10.1164/rccm.200208-916OC; Johnson PRA, 2004, CURR ALLERGY ASTHM R, V4, P102, DOI 10.1007/s11882-004-0054-9; Kalra S, 1996, CHEST, V109, P953, DOI 10.1378/chest.109.4.953; Kanazawa H, 2002, CHEST, V122, P166, DOI 10.1378/chest.122.1.166; Kanazawa H, 2002, THORAX, V57, P885, DOI 10.1136/thorax.57.10.885; Karjalainen EM, 2000, AM J RESP CRIT CARE, V161, P2086; Koskela H, 2000, CLIN EXP ALLERGY, V30, P1627; Kotaru C, 2003, J APPL PHYSIOL, V94, P227, DOI 10.1152/japplphysiol.00551.2002; Langdeau JB, 2000, AM J RESP CRIT CARE, V161, P1479; Larsson K, 1998, EUR RESPIR J, V12, P825, DOI 10.1183/09031936.98.12040825; 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; Mickleborough TD, 2003, AM J RESP CRIT CARE, V168, P1181, DOI 10.1164/rccm.200303-373OC; OBASE Y, 2004, EUR RESP J S48, V24; OMORI C, 1995, J APPL PHYSIOL, V78, P2169; OMORI C, 1995, J APPL PHYSIOL, V78, P1043; Page S, 2001, AM J PHYSIOL-LUNG C, V281, pL1313; PERSSON CGA, 1997, LUNG, P2611; PLISS LB, 1990, AM REV RESPIR DIS, V142, P73; Polosa R, 2000, EUR RESPIR J, V15, P30, DOI 10.1183/09031936.00.15103000; Rundell KW, 2004, CHEST, V125, P909, DOI 10.1378/chest.125.3.909; Rundell KW, 2003, INHAL TOXICOL, V15, P237, DOI 10.1080/08958370390168256; Rundell KW, 2001, MED SCI SPORT EXER, V33, P208; Scola AM, 2004, BRIT J PHARMACOL, V141, P163, DOI 10.1038/sj.bjp.0705599; Sue-Chu M, 1999, EUR RESPIR J, V13, P626, DOI 10.1183/09031936.99.13362699; SueChu M, 1996, RESP MED, V90, P99, DOI 10.1016/S0954-6111(96)90206-1; SUECHU M, 2002, EUR RESP J; Swystun VA, 2000, J ALLERGY CLIN IMMUN, V106, P57	54	81	83	0	3	CURRENT SCIENCE INC	PHILADELPHIA	400 MARKET STREET, STE 700, PHILADELPHIA, PA 19106 USA	1529-7322			CURR ALLERGY ASTHM R	Curr. Allergy Asthma Rep.	MAR	2005	5	2					116	122		10.1007/s11882-005-0084-y		7	Allergy; Immunology	Allergy; Immunology	949SW	WOS:000230809400004	15683611	
J	Peden, DB				Peden, DB			The epidemiology and genetics of asthma risk associated with air pollution	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						air pollution; asthma; genetics; antioxidants	S-TRANSFERASE M1; ENVIRONMENTAL TOBACCO-SMOKE; DIESEL EXHAUST PARTICLES; INDOOR NITROGEN-DIOXIDE; CHILDHOOD ASTHMA; RESPIRATORY SYMPTOMS; ANTIOXIDANT SUPPLEMENTATION; MEXICO-CITY; OZONE EXPOSURE; LUNG-FUNCTION	The occurrence of asthma and allergic diseases has continued to increase in the United States and worldwide, despite general improvements in air quality over the past 40 years. This observation has led many to question whether air quality is truly a significant risk factor in the development and exacerbation of asthma and whether further improvement in air quality is likely to result in improved health outcomes. However, epidemiologic studies have shown that levels of pollutants of less than the current ambient air quality standards still result in exacerbations of asthma and are associated with other morbidities as well. Specific locations, such as living near a roadway, might pose a special exposure risk. Genetic factors almost certainly play a role in determining susceptibility to pollutants, such as including those involved with antioxidant defenses. The best studied of these in the context of air pollution risks are glutathione-S-transferase polymorphisms. Irrespective of whether pollutants contribute to the development of asthma or the well-documented increases in asthma results in more people having pollutant-induced disease, poor air quality in many places remains a significant problem for patients with asthma and allergic disease. A number of public health, pharmaceutical, and nutriceutical interventions might mitigate the effects of pollutant exposure and deserve further study.	Univ N Carolina, Sch Med, Ctr Environm Med Asthma & Lung Biol, Chapel Hill, NC 27599 USA; Univ N Carolina, Sch Med, Dept Pediat, Chapel Hill, NC 27599 USA; Univ N Carolina, Sch Med, Dept Med, Chapel Hill, NC 27599 USA	Peden, DB (reprint author), Univ N Carolina, Sch Med, Ctr Environm Med Asthma & Lung Biol, 104 Mason Farm Rd,CB 7310, Chapel Hill, NC 27599 USA.	peden@mcd.unc.edu					Alexis NE, 2001, J ALLERGY CLIN IMMUN, V108, P577; Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; Bastain TM, 2003, CLIN IMMUNOL, V109, P130, DOI 10.1016/S1521-6616(03)00168-2; Bernstein JA, 2004, J ALLERGY CLIN IMMUN, V114, P1116, DOI 10.1016/j.jaci.2004.08.030; BRUNEKREEF B, 1990, J AIR WASTE MANAGE, V40, P1252; Chauhan AJ, 2003, LANCET, V361, P1939, DOI 10.1016/S0140-6736(03)13582-9; Clancy L, 2002, LANCET, V360, P1210, DOI 10.1016/S0140-6736(02)11281-5; David GL, 2003, AM J RESP CRIT CARE, V168, P1199, DOI 10.1164/rccm.200305-684OC; Davies RJ, 1997, ALLERGY, V52, P59; Delfino RJ, 1996, AM J RESP CRIT CARE, V154, P633; Diaz-Sanchez D, 1999, CLIN IMMUNOL, V90, P313, DOI 10.1006/clim.1998.4676; DIJKSTRA L, 1990, AM REV RESPIR DIS, V142, P1172; EDWARDS J, 1994, ARCH ENVIRON HEALTH, V49, P223; Friedman MS, 2001, JAMA-J AM MED ASSOC, V285, P897, DOI 10.1001/jama.285.7.897; Garshick E, 2003, EPIDEMIOLOGY, V14, P728, DOI 10.1097/01.ede.0000082045.50073.66; Gauderman WJ, 2004, NEW ENGL J MED, V351, P1057, DOI 10.1056/NEJMoa040610; Gent JF, 2003, JAMA-J AM MED ASSOC, V290, P1859, DOI 10.1001/jama.290.14.1859; GERGEN PJ, 1992, AM REV RESPIR DIS, V146, P823; Gergen PJ, 2001, RESP PHYSIOL, V128, P39, DOI 10.1016/S0034-5687(01)00263-8; GERGEN PJ, 1998, PEDIATRICS, V101, P2; Gilliland FD, 2002, AM J RESP CRIT CARE, V166, P457, DOI 10.1164/rccm.2112064; Gilliland FD, 2002, AM J RESP CRIT CARE, V166, P710, DOI 10.1164/rccm.2112065; Gilliland FD, 2003, AM J EPIDEMIOL, V158, P576, DOI 10.1093/aje/kwg181; Gilliland FD, 2004, LANCET, V363, P119, DOI 10.1016/S0140-6736(03)15262-2; HATCH GE, 1995, AM J CLIN NUTR, V61, p625S; Kabesch M, 2004, THORAX, V59, P569, DOI 10.1136/thx.2003.016667; Kalayci O, 2000, TURKISH J PEDIATR, V42, P17; Kelly FK, 1999, LANCET, V354, P482, DOI 10.1016/S0140-6736(99)01812-7; Kongerud J, 2003, INHAL TOXICOL, V15, P101, DOI [10.1080/08958370390168184, 10.1080/08958370304477]; Lin S, 2002, ENVIRON RES, V88, P73, DOI 10.1006/enrs.2001.4303; McConnell R, 2002, LANCET, V359, P386, DOI 10.1016/S0140-6736(02)07597-9; McConnell R, 1999, ENVIRON HEALTH PERSP, V107, P757, DOI 10.2307/3434662; McConnell R, 2003, AM J RESP CRIT CARE, V168, P790, DOI 10.1164/rccm.200304-466OC; McDonnell WF, 1999, ENVIRON RES, V80, P110, DOI 10.1006/enrs.1998.3894; Mudway IS, 1999, EUR RESPIR J, V13, P1429, DOI 10.1183/09031936.99.13614399; NEAS LM, 1991, AM J EPIDEMIOL, V134, P204; Nicolai T, 2003, EUR RESPIR J, V21, P956, DOI 10.1183/09031936.03.00041103; Nightingale JA, 2000, AM J RESP CRIT CARE, V161, P479; Peden DB, 2003, MIDDLETONS ALLERGY P, P515; Peters A, 1996, AM J EPIDEMIOL, V144, P570; Peters A, 2004, NEW ENGL J MED, V351, P1721, DOI 10.1056/NEJMoa040203; Peters A, 1997, EUR RESPIR J, V10, P872; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Pope CA, 2000, ENVIRON HEALTH PERSP, V108, P713, DOI 10.2307/3454408; POPE CA, 1991, ARCH ENVIRON HEALTH, V46, P90; POPE CA, 1989, AM J PUBLIC HEALTH, V79, P623, DOI 10.2105/AJPH.79.5.623; Rahman I, 1996, AM J RESP CRIT CARE, V154, P1055; Romieu I, 1997, ARCH ENVIRON HEALTH, V52, P368; ROMIEU I, 1995, AM J EPIDEMIOL, V141, P546; 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, 2001, EPIDEMIOL REV, V23, P268; Samet JM, 2001, AM J RESP CRIT CARE, V164, P819; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; Trapp JF, 1998, CHEST, V113, P505, DOI 10.1378/chest.113.2.505; Trenga CA, 2001, ARCH ENVIRON HEALTH, V56, P242; Vagaggini B, 2001, AM J RESP CRIT CARE, V164, P2172, DOI 10.1164/rccm2009090; van Strien RT, 2004, EPIDEMIOLOGY, V15, P471, DOI 10.1097/01.ede.0000129511.61698.d8; WHITE MC, 1994, ENVIRON RES, V65, P56, DOI 10.1006/enrs.1994.1021; Whitekus MJ, 2002, J IMMUNOL, V168, P2560	62	81	83	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.	FEB	2005	115	2					213	219		10.1016/j.jaci.2004.12.003		7	Allergy; Immunology	Allergy; Immunology	897YU	WOS:000227043600001	15696070	
J	Singer, BD; Ziska, LH; Frenz, DA; Gebhard, DE; Straka, JG				Singer, BD; Ziska, LH; Frenz, DA; Gebhard, DE; Straka, JG			Increasing Amb a 1 content in common ragweed (Ambrosia artemisiifolia) pollen as a function of rising atmospheric CO2 concentration	FUNCTIONAL PLANT BIOLOGY			English	Article						allergenicity; climate change; public health	PUBLIC-HEALTH; CLIMATE-CHANGE; AEROALLERGENS; ALLERGY; PREVALENCE; MISSOURI; PROTEINS; ANTIGEN; ASTHMA	Although the impact of increasing atmospheric carbon dioxide concentration ([CO2]) on production of common ragweed ( Ambrosia artemisiifolia L.) pollen has been examined in both indoor and outdoor experiments, the relationship between allergen expression and [CO2] is not known. An enzyme-linked immunosorbent assay ( ELISA) was used to quantify Amb a 1, ragweed's major allergen, in protein extracted from pollen of A. artemisiifolia grown at different [CO2] values in a previous experiment. The concentrations used approximated atmospheric pre-industrial conditions (i.e. at the end of the 19th century), current conditions, and the CO2 concentration projected for the middle of the 21st century ( 280, 370 and 600 mu mol mol(-1) CO2, respectively). Although total pollen protein remained unchanged, significant increases in Amb a 1 allergen were observed between pre-industrial and projected future [CO2] and between current and projected future [CO2] (1.8 and 1.6 times, respectively). These data suggest that recent and projected increases in [CO2] could directly increase the allergenicity of ragweed pollen and consequently the prevalence and / or severity of seasonal allergic disease. However, genetic and abiotic factors governing allergen expression will need to be better established to fully understand these data and their implications for public health.	ARS, Crop Syst & Global Change Lab, USDA, Beltsville, MD 20705 USA; Macalester Coll, Dept Biol, St Paul, MN 55105 USA; Multidata LLC, St Louis Pk, MN 55416 USA	ARS, Crop Syst & Global Change Lab, USDA, 10 300 Baltimore Ave, Beltsville, MD 20705 USA.	lziska@asrr.arsusda.gov	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Singer, Benjamin/0000-0001-5775-8427			Ahlholm JU, 1998, CLIN EXP ALLERGY, V28, P1384; Beggs PJ, 1998, ATMOS ENVIRON, V32, P1777, DOI 10.1016/S1352-2310(97)00466-4; Beggs PJ, 2004, CLIN EXP ALLERGY, V34, P1507, DOI 10.1111/j.1365-2222.2004.02061.x; BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1006/abio.1976.9999; CHAPMAN JA, 1986, GRANA, V25, P235; Coca AF, 1922, J IMMUNOL, V7, P163; Engvall E, 1980, Methods Enzymol, V70, P419; Frenz DA, 2001, ANN ALLERG ASTHMA IM, V86, P150; GERGEN PJ, 1987, J ALLERGY CLIN IMMUN, V80, P669, DOI 10.1016/0091-6749(87)90286-7; GOLDFARB AR, 1967, J ALLERGY, V40, P237, DOI 10.1016/0021-8707(67)90086-X; HJELMROOS M, 1995, INT ARCH ALLERGY IMM, V108, P368; Kerim T, 2003, FUNCT PLANT BIOL, V30, P843, DOI 10.1071/FP03100; KNOX RB, 1971, CYTOBIOS, V4, P49; LEE YS, 1979, J ALLERGY CLIN IMMUN, V63, P336, DOI 10.1016/0091-6749(79)90128-3; LEWIS WH, 1975, ANN ALLERGY, V35, P180; MAASCH HJ, 1987, ANN ALLERGY, V58, P429; Sly RM, 1999, ANN ALLERG ASTHMA IM, V82, P233, DOI 10.1016/S1081-1206(10)62603-8; STRAKA JG, 1991, AM J HUM GENET, V48, P72; TSANG VCW, 1983, METHOD ENZYMOL, V92, P391; Wan SQ, 2002, AM J BOT, V89, P1843, DOI 10.3732/ajb.89.11.1843; Wayne P, 2002, ANN ALLERG ASTHMA IM, V88, P279; Wodehouse R, 1971, HAYFEVER PLANTS; 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	24	81	83	3	12	CSIRO PUBLISHING	CLAYTON	UNIPARK, BLDG 1, LEVEL 1, 195 WELLINGTON RD, LOCKED BAG 10, CLAYTON, VIC 3168, AUSTRALIA	1445-4408	1445-4416		FUNCT PLANT BIOL	Funct. Plant Biol.		2005	32	7					667	670		10.1071/FP05039		4	Plant Sciences	Plant Sciences	942TJ	WOS:000230305100009		
J	Sunyer, J; Jarvis, D; Pekkanen, J; Chinn, S; Janson, C; Leynaert, B; Luczynska, C; Garcia-Esteban, R; Burney, P; Anto, JM				Sunyer, J; Jarvis, D; Pekkanen, J; Chinn, S; Janson, C; Leynaert, B; Luczynska, C; Garcia-Esteban, R; Burney, P; Anto, JM		European Comm Resp Health	Geographic variations in the effect of atopy on asthma in the European Community Respiratory Health Study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						atopy; asthma; attributable fraction; house dust mite; allergens	HOUSE-DUST MITE; BRONCHIAL RESPONSIVENESS; INDIVIDUAL ALLERGENS; SERUM IGE; SENSITIZATION; EXPOSURE; RISK; ASSOCIATION; PREVALENCE; SYMPTOMS	Background: Atopy has long been related to asthma. The prevalences of both atopy and asthma have shown substantial variation. Objective: We sought to assess geographic variations in the fraction of asthma attributable to IgE sensitization to specific allergens in the European Community Respiratory Health Survey. Methods: A cross-sectional study was undertaken during the years 1991 and 1992 on 13,558 individuals in 36 centers in 16 countries. Asthma was defined in several ways, variously incorporating reported symptoms, bronchial responsiveness to methacholine, and physician diagnosis. Specific IgE against house dust mite (Dermatophagoides pteronyssinus), cat, timothy grass, Cladosporium herbarum, and a local allergen (birch, Parietaria judaica, or ragweed) were measured. Results: The overall attributable fraction (AF) of asthma symptoms caused by atopy was 30% but varied widely between centers, ranging from 4% to 61%. The overall AF increased to 43% when asthma was based on wheezing and bronchial responsiveness, to 45% with a physician diagnosis of asthma, and to 48% when the patient reported more than 12 attacks in the last year. Between centers, the AF for atopy was significantly correlated with the prevalence of atopy among the asthmatic patients (r = 0.91) and with the sensitization to house dust mite (r = 0.64), as well as with the prevalence of asthma among atopic individuals (r = 0.43) and the prevalence of asthma among nonatopic individuals (r = -0.51). Conclusion: The effect of atopy on the prevalence of asthma varies widely between centers, probably because of variations in factors related to the expression of asthma and to the prevalence of sensitization, particularly to house dust mite.	UPF, IMIM, Environm Resp Res Unit, Barcelona 08003, Spain; Kings Coll London, Dept Publ Hlth Sci, London, England; Nacl Publ Hlth Inst, Environm Epidemiol Unit, Kuopio, Finland; Uppsala Univ, Dept Med Sci Resp Med & Allergol, Uppsala, Sweden; INSERM, Paris, France	Sunyer, J (reprint author), UPF, IMIM, Environm Resp Res Unit, C Doctor Aiguader 80, Barcelona 08003, Spain.	jsunyer@imim.es	Jarvis, Deborah/E-6494-2011; Anto, J/H-2676-2014; Sunyer, J/G-6909-2014	Anto, J/0000-0002-4736-8529; Sunyer, J/0000-0002-2602-4110			Boezen HM, 1996, AM J RESP CRIT CARE, V154, P30; Braback L, 2004, CLIN EXP ALLERGY, V34, P38, DOI 10.1111/j.1365-2222.2004.01841.x; Burney P, 1997, J ALLERGY CLIN IMMUN, V99, P314, DOI 10.1016/S0091-6749(97)70048-4; BURNEY PGJ, 1989, EUR RESPIR J, V2, P940; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; Chinn S, 1999, EUR RESPIR J, V14, P876, DOI 10.1034/j.1399-3003.1999.14d25.x; Chinn S, 1998, THORAX, V53, P662; de Marco R, 2002, CLIN EXP ALLERGY, V32, P1405, DOI 10.1046/j.1365-2745.2002.01466.x; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; GREENLAND S, 1993, BIOMETRICS, V49, P865, DOI 10.2307/2532206; Janson C, 2001, EUR RESPIR J, V18, P598, DOI 10.1183/09031936.01.00205801; 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; Pearce N, 1999, THORAX, V54, P268; Pekkanen J, 1999, EUR RESPIR J, V14, P951, DOI 10.1034/j.1399-3003.1999.14d37.x; Plaschke P, 1999, J ALLERGY CLIN IMMUN, V104, P58, DOI 10.1016/S0091-6749(99)70114-4; Ponsonby AL, 2002, CHEST, V121, P135, DOI 10.1378/chest.121.1.135; Rockhill B, 1998, AM J PUBLIC HEALTH, V88, P15, DOI 10.2105/AJPH.88.1.15; Rothman KJ, 1998, MODERN EPIDEMIOLOGY, V2nd, P53; Soriano JB, 1999, INT J EPIDEMIOL, V28, P728, DOI 10.1093/ije/28.4.728; SPORIK R, 1995, AM J RESP CRIT CARE, V151, P1388; Sunyer J, 2000, AM J RESP CRIT CARE, V162, P930; WACHOLDER S, 1994, AM J EPIDEMIOL, V140, P303; Wieringa MH, 1997, EUR RESPIR J, V10, P1460, DOI 10.1183/09031936.97.10071460; Zocchetti C, 1997, INT J EPIDEMIOL, V26, P220, DOI 10.1093/ije/26.1.220; Zureik M, 2002, BRIT MED J, V325, P411, DOI 10.1136/bmj.325.7361.411	26	81	81	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.	NOV	2004	114	5					1033	1039		10.1016/j.jaci.2004.05.072		7	Allergy; Immunology	Allergy; Immunology	870HI	WOS:000225047800006	15536406	
J	Ainsworth, DM; Grunig, G; Matychak, MB; Young, J; Wagner, B; Erb, HN; Antczak, DF				Ainsworth, DM; Grunig, G; Matychak, MB; Young, J; Wagner, B; Erb, HN; Antczak, DF			Recurrent airway obstruction (RAO) in horses is characterized by IFN-gamma and IL-8 production in bronchoalveolar lavage cells	VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY			English	Article						cytokine horse; RAO; heaves; t-bet; IFN-gamma	PULMONARY-DISEASE COPD; INTERFERON-GAMMA; PHENOTYPIC ANALYSIS; ANTIBODY-RESPONSES; FLUID LYMPHOCYTES; PERIPHERAL-BLOOD; MESSENGER-RNA; HEAVES HORSES; T-BET; CHEMOKINES	In horses prone to developing recurrent airway obstruction (RAO), we tested the hypotheses that the cytokine profile in the bronchoalveolar lavage (BAL) cells of affected horses would reflect a polarized Th-2 response; that cytokine and chemokine alterations would occur within 24 h of allergen exposure; and that allergen exposure would induce alterations in the expression of the transcription factor t-bet (t-box-expressed in T-cells). The expression levels of interleukin-4 (IL-4), IL-13, Interferongamma (IFN-gamma). t-bet, IL-8 and granulocyte-macrophage colony stimulating factor (GM-CSF) were measured in BAL cells obtained from control and RAO-susceptible horses during an asymptomatic phase and at 24 It and 5 weeks post-stabling and hay exposure. At each sampling time, BAL neutrophil percentages in the RAO-group exceeded controls. In the RAO-group, only IL-13 expression was decreased 2-fold during the asymptomatic phase. No differences in cytokine or chemokine expression were detected during the acute exposure phase. During the chronic phase, IFN-gamma and IL-8 expression levels were 2.5- and 3-fold greater, respectively, in the RAO-group. No other differences in gene expression were detected. We conclude that the cytokine profile of the airway cells does not reflect a polarized Th-2 response; that increases in IFN-gamma result from a t-bet independent pathway and that chemokines from epithelial or interstitial cells may contribute to early neutrophil influx. (C) 2003 Elsevier B.V. All rights reserved.	Cornell Univ, Dept Clin Sci, Coll Vet Med, Ithaca, NY 14853 USA; Columbia Univ, Dept Pathol, New York, NY USA; Cornell Univ, James A Baker Inst Anim Hlth, Coll Vet Med, Ithaca, NY USA; Cornell Univ, Dept Populat Med & Diagnost Sci, Coll Vet Med, Ithaca, NY USA	Ainsworth, DM (reprint author), Cornell Univ, Dept Clin Sci, Coll Vet Med, Ithaca, NY 14853 USA.						Ainsworth DM, 2002, VET IMMUNOL IMMUNOP, V84, P169, DOI 10.1016/S0165-2427(01)00400-7; Ainsworth DM, 2003, VET IMMUNOL IMMUNOP, V91, P61, DOI 10.1016/S0165-2427(02)00274-X; COLOTTA F, 1992, BLOOD, V80, P2012; Davies D E, 2001, Curr Opin Allergy Clin Immunol, V1, P67, DOI 10.1097/00130832-200102000-00012; DERKSEN FJ, 1985, J APPL PHYSIOL, V58, P598; DERKSEN FJ, 1988, AM J VET RES, V49, P933; Eder C, 2000, VET IMMUNOL IMMUNOP, V73, P241, DOI 10.1016/S0165-2427(00)00154-9; Giguere S, 2002, VET IMMUNOL IMMUNOP, V85, P147, DOI 10.1016/S0165-2427(01)00420-2; Grogan JL, 2002, CURR OPIN IMMUNOL, V14, P366, DOI 10.1016/S0952-7915(02)00340-0; Gutierrez-Ramos JC, 2000, IMMUNOL REV, V177, P31, DOI 10.1034/j.1600-065X.2000.17713.x; HALLIWELL REW, 1993, VET IMMUNOL IMMUNOP, V38, P201, DOI 10.1016/0165-2427(93)90081-E; Joubert P, 2001, EQUINE VET J, V33, P730, DOI 10.2746/042516401776249246; Kleiber C, 1999, J VET MED A, V46, P177, DOI 10.1046/j.1439-0442.1999.00210.x; Lavoie JP, 2001, AM J RESP CRIT CARE, V164, P1410; Lukacs NW, 2000, IMMUNOL REV, V177, P21, DOI 10.1034/j.1600-065X.2000.17707.x; MCGORUM BC, 1993, EQUINE VET J, V25, P261; MCGORUM BC, 1993, VET IMMUNOL IMMUNOP, V36, P207, DOI 10.1016/0165-2427(93)90020-5; MCPHERSON EA, 1979, EQUINE VET J, V11, P159; Nelson KM, 1998, VACCINE, V16, P1306, DOI 10.1016/S0264-410X(98)00009-7; Olson TS, 2002, AM J PHYSIOL-REG I, V283, pR7, DOI 10.1152/ajpregu.00738.2001; Pirie RS, 2002, EQUINE VET J, V34, P337, DOI 10.2746/042516402776249074; Pirie RS, 2001, EQUINE VET J, V33, P311, DOI 10.2746/042516401776249732; Robinson DS, 2002, IMMUNITY, V16, P755, DOI 10.1016/S1074-7613(02)00331-X; Robinson DS, 2002, CURR BIOL, V12, pR322, DOI 10.1016/S0960-9822(02)00830-8; Robinson N E, 2001, Equine Vet J, V33, P5, DOI 10.2746/042516401776767412; Rush BR, 1998, AM J VET RES, V59, P1033; Schmallenbach KH, 1998, VET IMMUNOL IMMUNOP, V66, P245, DOI 10.1016/S0165-2427(98)00202-5; Sherwood ER, 2001, CLIN SCI, V101, P541, DOI 10.1042/CS20010074; SNAPPER JR, 1986, AM REV RESPIR DIS, V133, P351; Szabo SJ, 2002, SCIENCE, V295, P338, DOI 10.1126/science.1065543; Turlej RK, 2001, THORAX, V56, P696, DOI 10.1136/thorax.56.9.696; Varma TK, 2002, CLIN DIAGN LAB IMMUN, V9, P530, DOI 10.1128/CDLI.9.3.530-543.2002; Watson DB, 1997, IEEE T DIELECT EL IN, V4, P108, DOI 10.1109/94.590877	33	81	81	0	5	ELSEVIER SCIENCE BV	AMSTERDAM	PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS	0165-2427			VET IMMUNOL IMMUNOP	Vet. Immunol. Immunopathol.	NOV 15	2003	96	1-2					83	91		10.1016/S0165-2427(03)00142-9		9	Immunology; Veterinary Sciences	Immunology; Veterinary Sciences	733CX	WOS:000185983300009	14522137	
J	Heinrich, J; Holscher, B; Douwes, J; Richter, K; Koch, A; Bischof, W; Fahlbusch, B; Kinne, RW; Wichmann, HE				Heinrich, J; Holscher, B; Douwes, J; Richter, K; Koch, A; Bischof, W; Fahlbusch, B; Kinne, RW; Wichmann, HE		INGA Study Grp	Reproducibility of allergen, endotoxin and fungi measurements in the indoor environment	JOURNAL OF EXPOSURE ANALYSIS AND ENVIRONMENTAL EPIDEMIOLOGY			English	Article						reproducibility; house dust mite; cat; allergen; endotoxin; house dust; fungi	HOUSE-DUST MITE; RESPIRATORY SYMPTOMS; EXTRACELLULAR POLYSACCHARIDES; CULTURABLE FUNGI; 2 CITIES; EXPOSURE; ASTHMA; SENSITIZATION; CHILDREN; GERMANY	Measurements of biocontaminants in settled house dust once a year are commonly used to assess long-term exposure. To examine stability over time and seasonal variation, we measured concentrations of mite and cat allergens, endotoxin and mold spores in living room floor dust in 745 German homes collected twice a year in two different seasons. The study population consisted of adults and children living in five different areas in Germany. All dust samples were collected in a standardized manner from the living room floor and taken during the years 1995 to 1998. The median interval between the two dust samplings was approximately 7 months. Mite and cat allergens were measured in settled house dust by monoclonal antibodies, endotoxin by the limulus amebocyte lysate method, and total spore counts by cultural methods. Crude Pearson's correlation coefficients between log-transformed concentrations in the first and second dust samples ranged between 0.65 and 0.75 for allergens, 0.59 for endotoxin and only 0.06 for total spore counts. The strongest and most consistent seasonal effects were observed for fungi with highest levels in July-September. Cat allergen concentrations were found consistently to be increased in January-March. Mite allergens did not show a strong and consistent seasonal pattern. We conclude that repeated measurements of mite and cat allergens and endotoxin in settled house dust improve the estimate for annual mean concentrations. However, even a single observation of these biocontaminants may be a good proxy for a 1-year exposure since repeated measures were highly correlated. However, repeated measurements of fungi levels were only weakly correlated and thus repeated observations for assessment of annual means of total spore counts are needed.	GSF, Inst Epidemiol, Natl Res Ctr Environm & Hlth, D-85758 Neuherberg, Germany; Univ Utrecht, Inst Risk Assessment Sci, Div Environm & Occupat Hlth, Utrecht, Netherlands; Grosshansdorf Hosp, Ctr Pneumol & Thorac Surg, Hamburg, Germany; Univ Jena, Dept Indoor Climatol, Erfurt, Germany; Univ Jena, Inst Immunol, D-6900 Jena, Germany; Univ Munich, Dept Epidemiol, Neuherberg, Germany	Heinrich, J (reprint author), GSF, Inst Epidemiol, Natl Res Ctr Environm & Hlth, Ingolstadter Landstr 1, D-85758 Neuherberg, Germany.			Douwes, Jeroen/0000-0003-3599-4036			Altman DG, 1991, PRACTICAL STAT MED R; BISCHOF W, 2002, INDOOR AIR, V121, P2; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; CHANYEUNG M, 1995, CLIN EXP ALLERGY, V25, P240, DOI 10.1111/j.1365-2222.1995.tb01035.x; Chew GL, 2001, INDOOR AIR, V11, P171, DOI 10.1034/j.1600-0668.2001.011003171.x; Diggle P. 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Expo. Anal. Environ. Epidemiol.	MAR	2003	13	2					152	160		10.1038/sj.jea.7500267		9	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	676HD	WOS:000182744500007	12679795	
J	Webb, JAW; Stacul, F; Thomsen, HS; Morcos, SK				Webb, JAW; Stacul, F; Thomsen, HS; Morcos, SK		Contrast Media Safety Comm ESUR	Late adverse reactions to intravascular iodinated contrast media	EUROPEAN RADIOLOGY			English	Review						iodinated contrast media; late adverse reactions	ALLERGY-LIKE REACTIONS; DELAYED-REACTIONS; INTERLEUKIN-2; HYPERSENSITIVITY; IMMEDIATE; UROGRAPHY; IOPAMIDOL; VASCULITIS; IOXAGLATE; IODIXANOL	Late adverse reactions to intravascular iodinated contrast media are defined as reactions occurring 1 h to 1 week after contrast medium injection. They have received increasing interest over the past decade, but their prevalence remains uncertain and their pathophysiology is not fully understood. The Contrast Media Safety Committee of the European Society of Urogenital Radiology decided to review the literature and to issue guidelines. An extensive literature search was carried out and summarized in a report. Based on the available information, simple guidelines have been drawn up. The report and guidelines were discussed at the 8th European Symposium on Urogenital Radiology in Genoa. Late adverse reactions after intravascular iodinated contrast medium include symptoms such as nausea, vomiting, headache, itching, skin rash, musculoskeletal pain, and fever. A significant proportion of these reactions is unrelated to the contrast medium; however, allergy-like skin reactions are well-documented side effects of contrast media with an incidence of approximately 2%. Late reactions appear to be commoner after nonionic dimers. The majority of late skin reactions after contrast medium exposure are probably T cell-mediated allergic reactions. Patients at increased risk of late skin reactions are those with a history of previous contrast medium reaction and those on interluekin-2 treatment. Most skin reactions are self-limiting and resolve within a week. Management is symptomatic and similar to the management of other drug-induced skin reactions.	Univ Copenhagen, Herlev Hosp, Dept Diagnost Radiol 54E2, DK-2730 Herlev, Denmark; Univ London St Bartholomews Hosp Med Coll, Dept Diagnost Imaging, London EC1A 7BE, England; Osped Cattinara, Inst Radiol, I-34149 Trieste, Italy; No Gen Hosp, Sheffield Teaching Hosp NHS Trust, Dept Diagnost Imaging, Sheffield S5 7AU, S Yorkshire, England	Thomsen, HS (reprint author), Univ Copenhagen, Herlev Hosp, Dept Diagnost Radiol 54E2, DK-2730 Herlev, Denmark.						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Radiol.	JAN	2003	13	1					181	184		10.1007/s00330-002-1650-5		4	Radiology, Nuclear Medicine & Medical Imaging	Radiology, Nuclear Medicine & Medical Imaging	643YK	WOS:000180891000026	12541128	
J	Gent, JF; Ren, P; Belanger, K; Triche, E; Bracken, MB; Holford, TR; Leaderer, BP				Gent, JF; Ren, P; Belanger, K; Triche, E; Bracken, MB; Holford, TR; Leaderer, BP			Levels of household mold associated with respiratory symptoms in the first year of life in a cohort at risk for asthma	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; fungi; indoor air; infants; mold; Penicillium; wheezing	FUNGAL EXTRACELLULAR POLYSACCHARIDES; CULTURABLE FUNGI; DUST MITES; INDOOR-AIR; HEALTH; CHILDREN; EXPOSURE; HOMES; DAMP; PREVALENCE	We assessed prospectively the risk of increased incidence of respiratory symptoms after exposure to particular fungal genera in a susceptible population-namely, infants (n = 880) at high risk for developing asthma. Days of wheeze or persistent cough, information on maternal allergy and asthma, socioeconomic variables, and housing characteristics were collected over the course of the infant's first year of life. Exposure to mold was assessed by airborne samples collected at one time early in the infant's life. Fungi were identified to genus level, recorded as colony-forming units per cubic meter (CFU/m(3)), and then categorized into four levels: 0 (undetectable), 1-499 CFU/m(3) (low), 500-999 CFU/m(3) (medium), and 1,000 CFU/m(3) (high). Effects of mold on wheeze and persistent cough, adjusting for potential confounding factors, were examined with Poisson regression analyses. The two most commonly found genera were Cladosporium (in 62% of the homes) and Penicillium (41%). Cladosporium was associated with reported mold (p < 0.02) and water leaks (p < 0.003). Rate of persistent cough was associated with reported mold [Rate ratio (RR) = 1.49; 95% CI, 1.18-1.88]. The highest level of Penicillium was associated with higher rates of wheeze (RR = 2.15; 95% CI, 1.34-3.46) and persistent cough (RR = 2.06; 95% CI, 1.31-3.24) in models controlling for maternal history of asthma and allergy, socioeconomic status, season of mold sample, and certain housing characteristics. We conclude that infants in this high-risk group who are exposed to high levels of Penicillium are at significant risk for wheeze and persistent cough.	Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, Yale Ctr Perinatal Pediat & Environm Epidemiol, New Haven, CT 06510 USA; New York State Dept Hlth, Albany, NY USA	Gent, JF (reprint author), Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, Yale Ctr Perinatal Pediat & Environm Epidemiol, 1 Church St,6th Floor, New Haven, CT 06510 USA.		Triche, Elizabeth/I-4986-2014		NIEHS NIH HHS [ES05410, ES07456]		Al-Doory Y., 1984, MOULD ALLERGY; Allison PD, 1999, LOGISTIC REGRESSION; BEAUMONT F, 1984, ANN ALLERGY, V53, P486; *CEC, 1994, 12 CEC COMM EUR COMM; Chew GL, 2001, INDOOR AIR, V11, P171, DOI 10.1034/j.1600-0668.2001.011003171.x; Dales RE, 1999, MYCOPATHOLOGIA, V147, P21, DOI 10.1023/A:1007096704217; Dharmage S, 2001, AM J RESP CRIT CARE, V164, P65; Dill I, 1996, PEDIATR ALLERGY IMMU, V7, P151, DOI 10.1111/j.1399-3038.1996.tb00123.x; Dillon HK, 1999, ENVIRON HEALTH PERSP, V107, P473; Douwes J, 1999, J ALLERGY CLIN IMMUN, V103, P494, DOI 10.1016/S0091-6749(99)70476-8; Garrett MH, 1998, CLIN EXP ALLERGY, V28, P459; GRAVESEN S, 1972, ACTA ALLERGOL, V27, P337, DOI 10.1111/j.1398-9995.1972.tb01433.x; Husman T, 1996, SCAND J WORK ENV HEA, V22, P5; Katz Y, 1999, CLIN EXP ALLERGY, V29, P186; Larone D. H., 1987, MED IMPORTANT FUNGI; LI CS, 1995, ARCH ENVIRON HEALTH, V50, P38; Ortega AN, 2001, ANN ALLERG ASTHMA IM, V86, P405; Peat JK, 1998, ALLERGY, V53, P120, DOI 10.1111/j.1398-9995.1998.tb03859.x; PLATT SD, 1989, BRIT MED J, V298, P1673; Ren P, 2001, ALLERGY, V56, P419, DOI 10.1034/j.1398-9995.2001.056005419.x; Ren P, 1999, J EXPO ANAL ENV EPID, V9, P560, DOI 10.1038/sj.jea.7500061; Rylander R, 1998, AM J RESP CRIT CARE, V158, P1685; *SAS I INC, 2001, VERS 8; STRACHAN DP, 1990, THORAX, V45, P382, DOI 10.1136/thx.45.5.382; Su HJ, 2001, ENVIRON RES, V85, P135, DOI 10.1006/enrs.2000.4113; Su HJJ, 2001, ARCH ENVIRON HEALTH, V56, P144; VANDERWERFF PJ, 1958, MOULD FUNGI BRONCHIA; VERHOEFF AP, 1990, ALLERGY, V45, P275, DOI 10.1111/j.1398-9995.1990.tb00496.x; Verhoeff AP, 1997, ANN ALLERG ASTHMA IM, V78, P544; VERHOEFF AP, 1995, AM J EPIDEMIOL, V141, P103; WAEGEMAEKERS M, 1989, ALLERGY, V44, P192, DOI 10.1111/j.1398-9995.1989.tb02261.x	31	81	82	1	5	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	DEC	2002	110	12					A781	A786				6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	625HG	WOS:000179810600034	12460818	
J	Booth, BW; Adler, KB; Bonner, JC; Tournier, F; Martin, LD				Booth, BW; Adler, KB; Bonner, JC; Tournier, F; Martin, LD			Interleukin-13 induces proliferation of human airway epithelial cells in vitro via a mechanism mediated by transforming growth factor-alpha	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article							FACTOR-RECEPTOR; IN-VITRO; EGF-RECEPTOR; EXPRESSION; INJURY; RATS; ASTHMA; LUNG	Remodeling of the airways, as occurs in asthmatic patients, is associated with the continual presence of inflammatory mediators and Th2 cytokines, especially interleukin (IL)-13, during cycles of epithelial injury and repair. In this study, we examined the effect of IL-13 on well-differentiated normal human bronchial epithelial (NHBE) cells maintained in air-liquid interface culture. IL-13 induced proliferation of NHBE cells after 24 h exposure, as reflected by [H-3]thymidine uptake and cell counts. The effects of IL-13 were mediated through the epidermal growth factor receptor (EGFR), as proliferation was attenuated by AG1478, an EGFR tyrosine kinase inhibitor. Proliferation appeared to be mediated by transforming growth factor (TGF)-alpha, a potent ligand for EGFR, which was released rapidly from NHBE cells in response to IL-13. Neutralizing antibody to TGF-alpha, but not antibodies against other potentially important growth factors (EGF, heparin binding epidermal growth factor-like growth factor [HB-EGF], platelet-derived growth factor [PDGF]), inhibited the mitogenic response to IL-13. This study provides the first experimental evidence that IL-13 can initiate a proliferative response of human airway epithelium in the absence of inflammatory cells or other cell types. The results are consistent with a mechanism whereby IL-13 induces release of TGF-alpha from the epithelial cells, which in turn binds via an autocrine/paracrine-type action to the EGFR, initiating proliferation. IL-13-induced airway remodeling in vivo may involve this epithelium-driven response.	N Carolina State Univ, Coll Vet Med, Dept Anat Physiol Sci & Radiol, Raleigh, NC 27606 USA; NIEHS, Res Triangle Pk, NC 27709 USA; Univ Paris 07, Lab Cytophysiol & Toxicol Cellulaire, Paris, France	Martin, LD (reprint author), N Carolina State Univ, Coll Vet Med, Dept Anat Physiol Sci & Radiol, Raleigh, NC 27606 USA.				NHLBI NIH HHS [HL66236, HL36982]		Alimam MZ, 2000, AM J RESP CELL MOL, V22, P253; Barth PJ, 2000, VIRCHOWS ARCH, V437, P648, DOI 10.1007/s004280000316; BATES SE, 1990, ENDOCRINOLOGY, V126, P596; BOOTH B, 2001, AM J RESP CRIT CARE, V163, pA738; COFFEY RJ, 1992, YALE J BIOL MED, V65, P693; Dignass AU, 1996, GUT, V38, P687, DOI 10.1136/gut.38.5.687; Druilhe A, 1998, AM J RESP CELL MOL, V19, P747; Farbman AI, 1996, J NEUROBIOL, V30, P267, DOI 10.1002/(SICI)1097-4695(199606)30:2<267::AID-NEU8>3.0.CO;2-3; Fischer BM, 1999, AM J RESP CELL MOL, V20, P413; Grunig G, 1998, SCIENCE, V282, P2261, DOI 10.1126/science.282.5397.2261; HAUGEN DRF, 1993, INT J CANCER, V55, P37, DOI 10.1002/ijc.2910550108; Huang ZW, 1996, FOLD DES, V1, P13, DOI 10.1016/S1359-0278(96)00007-7; JANKOWSKI J, 1993, DIGEST DIS, V11, P1, DOI 10.1159/000171396; Krunkosky TM, 2000, AM J RESP CELL MOL, V22, P685; Longphre M, 1999, J APPL PHYSIOL, V86, P341; MADTES DK, 1994, AM J RESP CELL MOL, V11, P540; MARTIN L, 2000, AM J RESP CRIT CARE, V161, pA779; Partik G, 1999, J CANCER RES CLIN, V125, P379, DOI 10.1007/s004320050290; Peschon JJ, 1998, SCIENCE, V282, P1281, DOI 10.1126/science.282.5392.1281; Raab G, 1997, BBA-REV CANCER, V1333, pF179, DOI 10.1016/S0304-419X(97)00024-3; Rice AB, 1999, AM J PATHOL, V155, P213, DOI 10.1016/S0002-9440(10)65115-2; Riese DJ, 1996, J BIOL CHEM, V271, P20047; SHERWOOD E, 1993, WORLD J UROL, V13, P290; Shim JJ, 2001, AM J PHYSIOL-LUNG C, V280, pL134; STRANDJORD TP, 1995, PEDIATR RES, V38, P851, DOI 10.1203/00006450-199512000-00005; Takeyama K, 1999, P NATL ACAD SCI USA, V96, P3081, DOI 10.1073/pnas.96.6.3081; Vesely KR, 1999, AM J RESP CELL MOL, V20, P699; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; Winkle LS, 1997, AM J PATHOL, V151, P443; Zhu Zhou, 1999, Journal of Clinical Investigation, V103, P779, DOI 10.1172/JCI5909; ZIOBER BL, 1993, J BIOL CHEM, V268, P691	31	81	83	0	3	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	2001	25	6					739	743				5	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	505MD	WOS:000172915800013	11726400	
J	McCall, C; Hunter, S; Stedman, K; Weber, E; Hillier, A; Bozic, C; Rivoire, B; Olivry, T				McCall, C; Hunter, S; Stedman, K; Weber, E; Hillier, A; Bozic, C; Rivoire, B; Olivry, T			Characterization and cloning of a major high molecular weight house dust mite allergen (Der f 15) for dogs	VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY			English	Article						atopic dermatitis; mite allergen; allergen; dog; IgE	DERMATOPHAGOIDES-FARINAE; IGE; CANINE; REACTIVITY; CHITINASES; EXTRACTS; PROTEIN; FAMILY; SITES	Although house dust mites (HDM(s)) are important elicitors of canine allergy, the low molecular weight molecules defined as major allergens for humans do not appear to be major allergens for dogs. Western blotting of Dermatophagoides farinae (D. farinae) extracts with sera from sensitized dogs showed that the majority of animals had IgE antibodies specific for two proteins of apparent molecular weights of 98 and 109 kDa (98/109 kDa). The N-terminal sequences of these two proteins were identical, suggesting they were very closely related, and sequencing of internal peptides showed the protein(s) to have homology with insect chitinases. A purified preparation of 98/109 kDa proteins elicited positive intradermal skin tests (IDST(s)) in a group of well-characterized atopic dogs sensitized to D. farinae, but not in normal dogs. A rabbit polyclonal antiserum raised against the purified proteins was used to immunoscreen a D. farinae cDNA library. The mature coding region of the isolated chitinase cDNA predicts a protein of 63.2 kDa; sequence analysis and glycan detection blotting suggest that the molecule is extensively O-glycosylated. Monoclonal antibodies made against the purified native protein were used to localize the chitinase in sections of whole D. farinae mites. The protein displayed an intracellular distribution in the proventriculus and intestine of the mite, suggesting that it has a digestive, rather than a moulting-related, function. The high prevalence of IgE antibodies to this antigen in canine atopic dermatitis makes it a major HDM allergen for dogs, and the protein has been formally designated Der f 15. (C) 2001 Elsevier Science B.V. All rights reserved.	Heska Corp, Ft Collins, CO 80525 USA; Ohio State Univ, Coll Vet Med, Dept Vet Clin Sci, Columbus, OH 43210 USA; N Carolina State Univ, Coll Vet Med, Dept Clin Sci, Raleigh, NC USA	McCall, C (reprint author), Heska Corp, 1825 Sharp Point Dr, Ft Collins, CO 80525 USA.		Hillier, Andrew/C-9159-2012; Olivry, Thierry/E-3289-2013				ATTSCHUL SF, 1990, J MOL BIOL, V215, P403; Baldo B.A., 1989, Advances in the Biosciences, V74, P13; Bard J., 1992, P 2 WORLD C VET DERM; BEVIER DE, 1997, CLIN ADV SUPPLEMENT, V3, P10; CHARACH M, 1993, P 9 ANN M AAVD ACVD, P50; CODNER EC, 1995, J AM VET MED ASSOC, V206, P812; de la Vega H, 1998, INSECT MOL BIOL, V7, P233; Esch RE, 1997, P ANN M AM AC VET DE, P87; Fujimura K, 1996, IEEE ROBOT AUTOM MAG, V3, P33, DOI 10.1109/100.486659; GAVEL Y, 1990, PROTEIN ENG, V3, P433, DOI 10.1093/protein/3.5.433; HANSEN JE, 1995, BIOCHEM J, V308, P801; Kramer KJ, 1997, INSECT BIOCHEM MOLEC, V27, P887, DOI 10.1016/S0965-1748(97)00078-7; Lian TM, 1998, VET IMMUNOL IMMUNOP, V66, P203, DOI 10.1016/S0165-2427(98)00199-8; Le Mao J, 1998, J ALLERGY CLIN IMMUN, V102, P631; Masuda K, 1999, VET IMMUNOL IMMUNOP, V72, P303, DOI 10.1016/S0165-2427(99)00142-7; MCCALL CA, 1997, CLIN ADV SUPPLEMENT, V3, P24; Noli C, 1996, VET IMMUNOL IMMUNOP, V52, P147, DOI 10.1016/0165-2427(96)05550-X; Reedy LM, 1997, ALLERGIC SKIN DIS DO; Rodriguez J.G., 1987, P345; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; STURE GH, 1995, VET IMMUNOL IMMUNOP, V44, P293, DOI 10.1016/0165-2427(94)05306-D; Thomas WR, 1998, ALLERGY, V53, P821, DOI 10.1111/j.1398-9995.1998.tb03987.x; TOVEY ER, 1987, J ALLERGY CLIN IMMUN, V79, P93, DOI 10.1016/S0091-6749(87)80022-2; Tsai LC, 1998, J ALLERGY CLIN IMMUN, V102, P295, DOI 10.1016/S0091-6749(98)70099-5; Wassom DL, 1998, VET DERMATOL, V9, P173; Watanabe T, 1997, ZOOL SCI, V14, P65, DOI 10.2108/zsj.14.65	26	81	84	1	8	ELSEVIER SCIENCE BV	AMSTERDAM	PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS	0165-2427			VET IMMUNOL IMMUNOP	Vet. Immunol. Immunopathol.	FEB 10	2001	78	3-4					231	247		10.1016/S0165-2427(00)00258-0		17	Immunology; Veterinary Sciences	Immunology; Veterinary Sciences	423FL	WOS:000168164700002	11292526	
J	Reijonen, TM; Kotaniemi-Syrjanen, A; Korhonen, K; Korppi, M				Reijonen, TM; Kotaniemi-Syrjanen, A; Korhonen, K; Korppi, M			Predictors of asthma three years after hospital admission for wheezing in infancy	PEDIATRICS			English	Article						asthma; atopy; budesonide; child; cromlyn sodium; follow-up study; infant; immunoglobulin E; respiratory syncytial virus; risk factors; sensitization; wheezing; virus diseases	RESPIRATORY SYNCYTIAL VIRUS; ENVIRONMENTAL RISK-FACTORS; ACUTE VIRAL BRONCHIOLITIS; FOLLOW-UP; LUNG-FUNCTION; BRONCHIAL-ASTHMA; CHILDHOOD ASTHMA; IMMUNOGLOBULIN-E; HAY-FEVER; CHILDREN	Objective. To evaluate the influence of early antiinflammatory therapy in the development of asthma 3 years after hospitalization for wheezing in infancy. In addition, the effects of allergic sensitization and respiratory syncytial virus (RSV) infection on the development of asthma were investigated. Design and Setting. A randomized, controlled follow-up study in a university hospital that provides primary hospital care for all pediatric patients in a defined area. Patients. Eighty-nine infants under 2 years of age who had been hospitalized for infection associated with wheezing and followed up for 3 years. Intervention. Early antiinflammatory therapy was given for 16 weeks; 29 patients received cromolyn sodium and 31 received budesonide. Twenty-nine control patients received no therapy. Outcome Measures. Clinical diagnosis of current asthma, defined as having at least 3 episodes of physician-diagnosed wheezing and either a wheezing episode during the preceding year or ongoing antiinflammatory medication for asthma. Results. Fourteen (48%) patients in the former cromolyn group, 15 (48%) in the former budesonide group, and 16 (55%) in the control group had current asthma. The significant predictors of asthma were age over 12 months (risk ratio [RR] 4.1; 95% confidence interval [CI] = 1.59-10.35), history of wheezing (RR 6.8; CI = 1.35-34.43), and atopic dermatitis on study entry (RR 3.4; CI = 1.17-9.39). Skin prick test positivity at the age of 16 months significantly predicted asthma (RR 9.5; CI = 2.45-36.72). In addition, all of the 18 (20%) children sensitized with furred pet developed asthma. RSV identification (RR 0.3; CI = 0.08-0.80) and early furred pet contact at home (RR 0.3; CI 0.10-0.79) were associated with the decreased occurrence of asthma. Conclusions. Antiinflammatory therapy for 4 months has no influence on the occurrence of asthma 3 years after wheezing in infancy. Early sensitization to indoor allergens, especially to pets, and atopic dermatitis predict subsequent development of asthma. RSV infection in wheezing infants may have a better outcome than other infections.	Kuopio Univ Hosp, Dept Pediat, FIN-70211 Kuopio, Finland	Reijonen, TM (reprint author), Kuopio Univ Hosp, Dept Pediat, Box 1777, FIN-70211 Kuopio, Finland.						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J	Petsonk, EL; Wang, ML; Lewis, DM; Siegel, PD; Husberg, BJ				Petsonk, EL; Wang, ML; Lewis, DM; Siegel, PD; Husberg, BJ			Asthma-like symptoms in wood product plant workers exposed to methylene diphenyl diisocyanate	CHEST			English	Article						asthma; diisocyanates; occupational asthma; respiratory protection; skin exposure; wood products	OCCUPATIONAL ASTHMA; SURVEILLANCE SYSTEM; ISOCYANATES; METHACHOLINE; POPULATION; CHALLENGE; RESPONSES; DISEASES; MDI	Background: Diisocyanates, a group of highly reactive chemicals, have frequently been associated with occupational asthma. We evaluated respiratory health in workers at a new wood products manufacturing plant that uses methylene diphenyl diisocyanate (MDI), and was designed and operated with a goal of minimizing worker exposures, Methods: Health surveys using standardized respiratory questionnaires were done prior to the initial use of diisocyanates in the plant, and semiannually thereafter for a period of 2 years. Other testing included occupational and work practice histories, serial peak flow measurements, spirometry, methacholine challenge, and measurement of specific IgE antibodies to MDI-albumin conjugate. Results: Of 214 plant employees who participated in at least one health survey, a follow-up survey was also available from 178 employees (83%). New-onset asthma-like symptoms (NAS) were reported by 15 of 56 workers (27%) in areas with the highest potential for exposures to liquid MDI monomer and prepolymer, vs 0 of 43 workers in the lowest potential exposure areas (p = 0.001). In the areas with high potential exposure, NAS developed in 47% of workers who had noted MDI skin staining, vs 19% without skin stains (p = 0.07), Working around and cleaning up liquid MDI represented a significant risk for asthma-like symptoms in both current smokers and nonsmokers; work with finished wood products did not. Asthma-like symptoms were associated with variable airflow limitation (odds ratio [OR], 5.0; confidence interval [CI], 1.4 to 18.7) and specific IgE to MDI-albumin (OR, 3.2; CI, 1.1 to 9.0), but not with skin prick tests to common aeroallergens (OR, 1.1; CI, 0.5 to 2.7), Conclusions: During the first 2 years of operation, in a plant designed and operated to control exposure to diisocyanates, the development of asthma-like symptoms was reported in a relatively high proportion of the employees who worked with liquid MDI. To prevent asthma symptoms among workers, careful control of respiratory tract exposures associated with liquid MDI is important, especially during cleanup activities. Strict limitation of skin contact with diisocyanates may also be necessary.	NIOSH, Div Resp Dis Studies, Morgantown, WV 26505 USA; NIOSH, Hlth Effects Lab Div, Morgantown, WV 26505 USA	Petsonk, EL (reprint author), NIOSH, Div Resp Dis Studies, 1095 Willowdale Rd, Morgantown, WV 26505 USA.						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J	Hofstra, WB; Neijens, HJ; Duiverman, EJ; Kouwenberg, JM; Mulder, PGH; Kuethe, MC; Sterk, PJ				Hofstra, WB; Neijens, HJ; Duiverman, EJ; Kouwenberg, JM; Mulder, PGH; Kuethe, MC; Sterk, PJ			Dose-responses over time to inhaled fluticasone propionate treatment of exercise- and methacholine-induced bronchoconstriction in children with asthma	PEDIATRIC PULMONOLOGY			English	Article						exercise-induced asthma; bronchial hyperresponsiveness; inhaled corticosteroids; fluticasone propionate; eosinophil cationic protein; randomized clinical trial; children	WORKING PARTY STANDARDIZATION; EUROPEAN RESPIRATORY SOCIETY; CATIONIC PROTEIN ECP; BRONCHIAL HYPERRESPONSIVENESS; LUNG-FUNCTION; AIRWAY RESPONSIVENESS; OFFICIAL STATEMENT; TERM TREATMENT; MILD ASTHMA; BUDESONIDE	When treating bronchial hyperresponsiveness to so-called direct and indirect stimuli, distinct pathophysiological mechanisms might require differences in dose and duration of inhaled corticosteroid therapy. To test this hypothesis in children with asthma, we investigated the time- and dose-dependent effects of 2 doses of fluticasone propionate (FP, 100 or 250 mu g bid.) in improving exercise- (EIB) and methacholine-induced bronchoconstriction during 6 months of treatment, using a placebo-controlled parallel group study design. Thirty-seven children with asthma (aged 6 to 14 years; forced expired volume in 1 sec (FEV1) greater than or equal to 70% predicted; EIB greater than or equal to 20% fall in FEV1 from baseline; no inhaled steroids during the past 4 months) participated in a double-blind, placebo-controlled, 3-arm parallel study. Children receiving placebo were rerandomized to active treatment after 6 weeks. Standardized dry air treadmill exercise testing (EIB expressed as %fall in FEV1 from baseline) and methacholine challenge using a dosimetric technique (expressed as PD20) were performed repeatedly during the study. During FP-treatment, the severity of EIB decreased significantly as compared to placebo within 3 weeks, the geometric mean % fall in FEV1 being reduced from 34.1% to 9.9% for 100 mu g FP bid, and from 35.9% to 7.6% for 250 mu g FP bid (P < 0.05). These reductions in EIB did not differ between the 2 doses and were sustained throughout the treatment period. PD20 methacholine improved significantly during the first 6 weeks as compared to placebo (P < 0.04) and steadily increased with time in both treatment limbs (P = 0.04), the difference in improvement between doses (100 mu g FP bid, 1.6 dose steps; 250 mu g FP bid, 3.3 dose steps) approaching significance after 24 weeks (P = 0.06). We conclude that in childhood asthma, the protection afforded by inhaled fluticasone propionate against methacholine-induced bronchoconstriction is time- and dose-dependent, whereas protection against EIB is not. This suggests different modes of action of inhaled steroids in protecting against these pharmacological and physiological stimuli. This has to be taken into account when monitoring asthma treatment. (C) 2000 Wiley-Liss, Inc.	Univ Groningen Hosp, Beatrix Childrens Hosp, Acad Hosp, Dept Pediat Pulm, NL-9700 RB Groningen, Netherlands; Juliana Childrens Hosp, Dept Pulm Pediat, The Hague, Netherlands; Sophia Childrens Hosp, Rotterdam, Netherlands; Erasmus Univ, Sch Med, Dept Epidemiol & Biostat, NL-3000 DR Rotterdam, Netherlands; T Lange Land Ziekenhuis Zoetermeer, Dept Pediat, Zoetermeer, Netherlands; Leiden Univ, Med Ctr, Dept Pulm Dis, Leiden, Netherlands	Duiverman, EJ (reprint author), Univ Groningen Hosp, Beatrix Childrens Hosp, Acad Hosp, Dept Pediat Pulm, POB 30-001, NL-9700 RB Groningen, Netherlands.						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Pulmonol.	JUN	2000	29	6					415	423		10.1002/(SICI)1099-0496(200006)29:6<415::AID-PPUL1>3.0.CO;2-7		9	Pediatrics; Respiratory System	Pediatrics; Respiratory System	317EZ	WOS:000087214200001	10821721	
J	Jaakkola, JJK; Verkasalo, PK; Jaakkola, N				Jaakkola, JJK; Verkasalo, PK; Jaakkola, N			Plastic wall materials in the home and respiratory health in young children	AMERICAN JOURNAL OF PUBLIC HEALTH			English	Article							BRONCHIAL OBSTRUCTION; SYMPTOMS; ASTHMA	Objectives, The relation between the presence of plastic wall materials in the home and respiratory health in children was assessed. Methods. This population-based cross-sectional study involved 2568 Finnish children aged 1 to 7 years. Results. In logistic regression models, lower respiratory tract symptoms-persistent wheezing (adjusted odds ratio [OR] = 3.42, 95% confidence interval [CI] = 1.13, 10.36), cough (OR=2.41, 95% CI = 1.04, 5.63), and phlegm (OR= 2.76, 95% Cf = 1.03, 7.41)-were strongly related to the presence of plastic wall materials, whereas upper respiratory symptoms were not. The risk of asthma (OR = 1.52, 95% CI = 0.35, 6.71) and pneumonia (OR= 1.81, 95% CI = 0.62, 5.29) was also increased in children exposed to such materials. Conclusions. Emissions from plastic materials indoors may have adverse effects on the lower respiratory tracts of small children.	Nord Sch Publ Hth, SE-402421 Gothenburg, Sweden; Univ Helsinki, Dept Publ Hlth, Helsinki, Finland; Univ Oxford, Imperial Canc Res Fund, Canc Epidemiol Unit, Oxford, England; Univ Helsinki, Dept Publ Hlth, Environm Epidemiol Unit, FIN-00014 Helsinki, Finland	Jaakkola, JJK (reprint author), Nord Sch Publ Hth, Box 12133, SE-402421 Gothenburg, Sweden.	jouni.jaakkola@nhv.se	Jaakkola, Jouni/G-4314-2012				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; LOUHIALA PJ, 1995, AM J PUBLIC HEALTH, V85, P1109, DOI 10.2105/AJPH.85.8_Pt_1.1109; Oie L, 1997, ENVIRON HEALTH PERSP, V105, P972; Oie L, 1999, EPIDEMIOLOGY, V10, P294, DOI 10.1097/00001648-199905000-00018; SAARELA K, 1989, INT CONGR SER, V860, P329; TIMONEN KL, 1995, EUR RESPIR J, V8, P1155, DOI 10.1183/09031936.95.08071155	7	81	83	0	6	AMER PUBLIC HEALTH ASSOC INC	WASHINGTON	800 I STREET, NW, WASHINGTON, DC 20001-3710 USA	0090-0036			AM J PUBLIC HEALTH	Am. J. Public Health	MAY	2000	90	5					797	799		10.2105/AJPH.90.5.797		3	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	308VN	WOS:000086733700025	10800434	
J	Thornton, EE; Looney, MR; Bose, O; Sen, D; Sheppard, D; Locksley, R; Huang, XZ; Krummel, MF				Thornton, Emily E.; Looney, Mark R.; Bose, Oishee; Sen, Debasish; Sheppard, Dean; Locksley, Richard; Huang, Xiaozhu; Krummel, Matthew F.			Spatiotemporally separated antigen uptake by alveolar dendritic cells and airway presentation to T cells in the lung	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article							TIGHT JUNCTION PROTEINS; DUST MITE ALLERGEN; IN-VIVO; IMMUNE-SYSTEM; LYMPH-NODE; 2-PHOTON MICROSCOPY; RESPIRATORY-TRACT; CHRONIC ASTHMA; ATOPIC ASTHMA; MOUSE	Asthma pathogenesis is focused around conducting airways. The reasons for this focus have been unclear because it has not been possible to track the sites and timing of antigen uptake or subsequent antigen presentation to effector T cells. In this study, we use two-photon microscopy of the lung parenchyma and note accumulation of CD11b(+) dendritic cells (DCs) around the airway after allergen challenge but very limited access of these airway-adjacent DCs to the contents of the airspace. In contrast, we observed prevalent transepithelial uptake of particulate antigens by alveolar DCs. These distinct sites are temporally linked, as early antigen uptake in alveoli gives rise to DC and antigen retention in the airway-adjacent region. Antigen-specific T cells also accumulate in the airway-adjacent region after allergen challenge and are activated by the accumulated DCs. Thus, we propose that later airway hyperreactivity results from selective retention of allergen-presenting DCs and antigen-specific T cells in airway-adjacent interaction zones, not from variation in the abilities of individual DCs to survey the lung.	[Thornton, Emily E.; Bose, Oishee; Sen, Debasish; Krummel, Matthew F.] Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94143 USA; [Looney, Mark R.] Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA; [Sheppard, Dean; Huang, Xiaozhu] Univ Calif San Francisco, Lung Biol Ctr, San Francisco, CA 94143 USA; [Looney, Mark R.; Sheppard, Dean; Huang, Xiaozhu] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA; [Locksley, Richard] Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA	Krummel, MF (reprint author), Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94143 USA.	matthew.krummel@ucsf.edu		Sen, Debasish/0000-0001-9879-8345; Thornton, Emily/0000-0002-0068-2502	National Science Foundation; Strategic Asthma Basic Research; American Asthma Foundation; National Institutes of Health [P01 HL024136]	This work was supported by the National Science Foundation graduate research fellowship program, the Strategic Asthma Basic Research, the American Asthma Foundation, and the National Institutes of Health (grant P01 HL024136).	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J	Shamji, MH; Durham, SR				Shamji, M. H.; Durham, S. R.			Mechanisms of immunotherapy to aeroallergens	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review							GRASS-POLLEN IMMUNOTHERAPY; RANDOMIZED CONTROLLED-TRIAL; REGULATORY T-CELLS; FC-EPSILON-RI; SEASONAL ALLERGIC RHINOCONJUNCTIVITIS; MESSENGER-RNA EXPRESSION; HOUSE-DUST MITES; LYMPHOCYTIC ACTIVATION MOLECULE; SYSTEMIC IMMUNOLOGICAL CHANGES; BASOPHIL HISTAMINE-RELEASE	Allergen immunotherapy is allergen-specific, allergen dose-and time-dependent and is associated with long-term clinical and immunological tolerance that persists for years after discontinuation. Successful immunotherapy is accompanied by the suppression of numbers of T-helper 2 (Th2) effector cells, eosinophils, basophils, c-kit + mast cells and neutrophils infiltration in target organs, induction of IL-10 and/or TGF-beta + Treg cells and increases in 'protective' non-inflammatory blocking antibodies, particularly IgG4 and IgA2 subclasses with inhibitory activity. These events are accompanied by a reduction and/or a redirection of underlying antigen-specific Th2-type T cell-driven hypersensitivity to the allergen(s) used for therapy. This suppression occurs within weeks or months as a consequence of the appearance of a population of regulatory T cells that exert their effects by mechanisms involving cell-cell contact, but also by the release of cytokines such as IL-10 (increases IgG4) and TGF-beta (increases specific IgA). The more delayed-in-time appearance of antigen-specific T-helper 1 responses and alternative mechanisms such as Th2 cell anergy and/or apoptosis may also be involved. The mechanisms of sublingual immunotherapy are similar to those following a subcutaneous administration of allergen, whereas it is likely that additional events following antigen presentation in the sublingual mucosa and regional lymph nodes are involved. These insights have resulted in novel approaches and portend future biomarkers that may be surrogate or predictive of the clinical response to treatment.	[Shamji, M. H.] Univ London Imperial Coll Sci Technol & Med, MRC, Allergy & Clin Immunol Sect, London SW7 2AZ, England; [Shamji, M. H.] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Fac Med, Asthma UK Ctr Allerg Mech Asthma, London SW7 2AZ, England	Shamji, MH (reprint author), Univ London Imperial Coll Sci Technol & Med, MRC, Allergy & Clin Immunol Sect, Room 365,3rd Floor,Sir Alexander Fleming Bldg,S K, London SW7 2AZ, England.	m.shamji99@imperial.ac.uk			Immune Tolerance Network; National Institutes of Health USA; Biotechnology and Biological Sciences Research Council UK (BBSRC); ALK-Abello, Horsholm, Denmark; ALK-Abello	This work was supported by grants from the Immune Tolerance Network, National Institutes of Health USA, a Biotechnology and Biological Sciences Research Council UK (BBSRC) studentship case award and ALK-Abello, Horsholm, Denmark.; Disclosure of potential conflict of interest: S. R. Durham is a member of the Immune Tolerance Network Steering Committee and has consulting arrangements with ALK-Abello and has received research support from ALK-Abello.	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Exp. Allergy	SEP	2011	41	9			SI		1235	1246		10.1111/j.1365-2222.2011.03804.x		12	Allergy; Immunology	Allergy; Immunology	808SO	WOS:000293998900008	21762223	
J	McGwin, G; Lienert, J; Kennedy, JI				McGwin, Gerald, Jr.; Lienert, Jeffrey; Kennedy, John I., Jr.			Formaldehyde Exposure and Asthma in Children: A Systematic Review	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Review						asthma; children; epidemiology; formaldehyde; meta-analysis	VOLATILE ORGANIC-COMPOUNDS; RISK-FACTORS; SCHOOL ENVIRONMENT; AIR-POLLUTANTS; UNITED-STATES; INDOOR; SYMPTOMS; SCHOOLCHILDREN; SENSITIZATION; ALLERGY	OBJECTIVE: Despite multiple published studies regarding the association between formaldehyde exposure and childhood asthma, a consistent association has not been identified. Here we report the results of a systematic review of published literature in order to provide a more comprehensive picture of this relationship. DATA SOURCES: After a comprehensive literature search, we identified seven peer-reviewed studies providing quantitative results regarding the association between formaldehyde exposure and asthma in children. Studies were heterogeneous with respect to the definition of asthma (e.g., self-report, physician diagnosis). Most of the studies were cross-sectional. DATA EXTRACTION: For each study, an odds ratio (OR) and 95% confidence interval (CI) for asthma were either abstracted from published results or calculated based on the data provided. Characteristics regarding the study design and population were also abstracted. DATA SYNTHESIS: We used fixed- and random-effects models to calculate pooled ORs and 95% Cls; measures of heterogeneity were also calculated. A fixed-effects model produced an OR of 1.03 (95% Cl, 1.02-1.04), and random effects model produced an OR of 1.17 (95% Cl, 1.01-1.36), both reflecting an increase of 10 mu g/m(3) of formaldehyde. Both the Q and I(2) statistics indicated a moderate amount of heterogeneity. CONCLUSIONS: Results indicate a significant positive association between formaldehyde exposure and childhood asthma. Given the largely cross-sectional nature of the studies underlying this meta-analysis, further well-designed prospective epidemiologic studies are needed.	[McGwin, Gerald, Jr.] Univ Alabama, Sch Publ Hlth, Dept Epidemiol, Birmingham, AL 35294 USA; [Lienert, Jeffrey] Franklin & Marshall Coll, Lancaster, PA 17604 USA; [Kennedy, John I., Jr.] Dept Vet Affairs Med Ctr, Birmingham, AL USA; [Kennedy, John I., Jr.] Univ Alabama, Dept Med, Div Pulm Allergy & Crit Care Med, Tuscaloosa, AL 35487 USA	McGwin, G (reprint author), 1922 7th Ave S,Suite 120, Birmingham, AL 35294 USA.	mcgwin@uab.edu	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Akinbami LJ, 2009, PEDIATRICS, V123, pS131, DOI 10.1542/peds.2008-2233C; Burr M L, 1999, Pediatr Pulmonol Suppl, V18, P3; Daisey JM, 2003, INDOOR AIR, V13, P53, DOI 10.1034/j.1600-0668.2003.00153.x; Delfino RJ, 2003, ENVIRON HEALTH PERSP, V111, P647, DOI 10.1289/ehp.5992; Doi S, 2003, ALLERGY, V58, P668, DOI 10.1034/j.1398-9995.2003.00044.x; Elias JA, 2003, J CLIN INVEST, V111, P291, DOI 10.1172/JCI200317748; Erdei E, 2003, ARCH ENVIRON HEALTH, V58, P337; Franklin P, 2000, AM J RESP CRIT CARE, V161, P1757; Garrett MH, 1999, ALLERGY, V54, P330, DOI 10.1034/j.1398-9995.1999.00763.x; KRZYZANOWSKI M, 1990, ENVIRON RES, V52, P117, DOI 10.1016/S0013-9351(05)80247-6; Mendell MJ, 2007, INDOOR AIR, V17, P259, DOI 10.1111/j.1600-0668.2007.00478.x; Mi YH, 2006, INDOOR AIR, V16, P454, DOI 10.1111/j.1600-0668.2006.00439.x; Moorman Jeanne E., 2007, Morbidity and Mortality Weekly Report, V56, P1; National library of medicine, 2009, PUBMED; *OSHA, 2005, THRESH LIM VAL BIOL; Pati S, 2005, EPIDEMIOLOGY, V16, pS132, DOI 10.1097/00001648-200509000-00335; Paustenbach D, 1997, J TOXICOL ENV HEALTH, V50, P217; Ronmark E, 1999, ALLERGY, V54, P926, DOI 10.1034/j.1398-9995.1999.00044.x; Rumchev KB, 2002, EUR RESPIR J, V20, P403, DOI 10.1183/09031936.02.00245002; Smedje G, 1997, CLIN EXP ALLERGY, V27, P1270, DOI 10.1111/j.1365-2222.1997.tb01171.x; Smedje G, 2001, INT J TUBERC LUNG D, V5, P1059; Stroup DF, 2000, JAMA-J AM MED ASSOC, V283, P2008, DOI 10.1001/jama.283.15.2008; SYMINGTON P, 1991, BRIT J IND MED, V48, P588; Tavernier G, 2006, J ALLERGY CLIN IMMUN, V117, P656, DOI 10.1016/j.jaci.2005.12.1311; Thompson CM, 2008, TOXICOL APPL PHARM, V233, P355, DOI 10.1016/j.taap.2008.09.011; Venn AJ, 2003, THORAX, V58, P955, DOI 10.1136/thorax.58.11.955; Wantke F, 1996, CLIN EXP ALLERGY, V26, P276; Wieslander G, 1997, INT ARCH OCC ENV HEA, V69, P115; Zhao ZH, 2008, ENVIRON HEALTH PERSP, V116, P90, DOI 10.1289/ehp.10576	29	80	83	4	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.	MAR	2010	118	3					313	317		10.1289/ehp.0901143		5	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	567LX	WOS:000275449500019	20064771	
J	Balloy, V; Chignard, M				Balloy, Viviane; Chignard, Michel			The innate immune response to Aspergillus fumigatus	MICROBES AND INFECTION			English	Review						Aspergillus fumigatus; Innate defense; Lung; Infection	INVASIVE PULMONARY ASPERGILLOSIS; COLONY-STIMULATING FACTOR; TOLL-LIKE RECEPTORS; HOST-DEFENSE; IN-VITRO; ANTIFUNGAL ACTIVITY; CANDIDA-ALBICANS; BINDING LECTIN; SYSTEMIC ASPERGILLOSIS; IMMUNOSUPPRESSED MICE	Despite the development of new treatments, the mortality due to invasive pulmonary aspergillosis remains above 50%, reaching 95% in certain situations. The battle against Aspergillus fumigatus involves several components of the pulmonary innate immune system: cells, mediators, and natural antifungal molecules involved in the recognition and elimination of the fungus, thereby preventing colonization of the respiratory system. With the 10,000-15,000 1 of air we inhale each day, the lungs are constantly exposed to a wide range of microorganisms, such as A. fumigatus. This fungus is ubiquitous in the environment and can release large numbers of spores able, due to their small size, to penetrate the respiratory tract. The spores of A. fumigatus, like any other pathogen, are then confronted with the innate immune system, a constitutive defense system that is permanently active and tightly regulated. The various elements of the pulmonary innate immune system-physical and cellular barriers and soluble mediators-are involved in the recognition and elimination of pathogens, thereby preventing colonization of the respiratory system. Consequently, the presence of spores in immunocompetent hosts is completely innocuous, because these spores are normally eliminated. However, changes in one of the components of the defense system may lead to the development of pulmonary infections. Thus, in immunocompromised individuals, the spores are able to develop and cause pulmonary mycoses. These mycoses, known as aspergillosis, are highly variable, with the range of presentations extending from an allergy-type illness, allergic bronchopulmonary aspergilloses, to a very serious generalized and frequently fatal infection: invasive pulmonary aspergillosis (IPA). (C) 2009 Elsevier Masson SAS. All rights reserved.	[Balloy, Viviane; Chignard, Michel] Inst Pasteur, Unite Def Innee & Inflammat, F-75015 Paris, France; [Balloy, Viviane; Chignard, Michel] INSERM, U874, F-75015 Paris, France	Chignard, M (reprint author), Inst Pasteur, Unite Def Innee & Inflammat, 25 Rue Dr Roux, F-75015 Paris, France.	chignard@pasteur.fr	Chignard, Michel/B-4351-2008	Chignard, Michel/0000-0003-3810-6575			AMITANI R, 1995, INFECT IMMUN, V63, P3266; Aratani Y, 2002, MED MYCOL, V40, P557, DOI 10.1080/714031156; Balloy V, 2005, INFECT IMMUN, V73, P5420, DOI 10.1128/IAI.73.9.5420-5425.2005; Balloy V, 2005, INFECT IMMUN, V73, P494, DOI 10.1128/IAI.73.1.494-503.2005; BALLOY V, 2008, J BIOL CHEM, V7, P30513; Baranger K, 2008, FEBS J, V275, P2008, DOI 10.1111/j.1742-4658.2008.06355.x; Behnsen J, 2008, INFECT IMMUN, V76, P820, DOI 10.1128/IAI.01037-07; Bellocchio S, 2004, J IMMUNOL, V172, P3059; Bochud PY, 2008, NEW ENGL J MED, V359, P1766, DOI 10.1056/NEJMoa0802629; Botterel F, 2008, BMC MICROBIOL, V8, DOI 10.1186/1471-2180-8-97; BOUCHARA JP, 1994, PATHOL BIOL, V42, P640; Braedel S, 2004, BRIT J HAEMATOL, V125, P392, DOI 10.1111/j.1365-2141.2004.04922.x; Brouard J, 2005, J INFECT DIS, V191, P1988, DOI 10.1086/429964; Cenci E, 1998, J INFECT DIS, V178, P1750, DOI 10.1086/314493; Centeno-Lima S, 2002, FEMS IMMUNOL MED MIC, V32, P167, DOI 10.1111/j.1574-695X.2002.tb00549.x; Chen L, 2009, CLIN EXP DERMATOL, V34, P55, DOI 10.1111/j.1365-2230.2008.03092.x; Chignard M, 2009, ASPERGILLUS FUMIGATU, P229; Chignard M, 2007, CLIN IMMUNOL, V124, P238, DOI 10.1016/j.clim.2007.05.004; Clemons KV, 2000, CLIN EXP IMMUNOL, V122, P186, DOI 10.1046/j.1365-2249.2000.01382.x; Da Silva CA, 2008, J IMMUNOL, V181, P4279; Dubourdeau M, 2006, J IMMUNOL, V177, P3994; Duong M, 1998, J INFECT DIS, V178, P1472, DOI 10.1086/314425; Garlanda C, 2002, NATURE, V420, P182, DOI 10.1038/nature01195; Gersuk GM, 2006, J IMMUNOL, V176, P3717; Hamilton AJ, 1999, MED MYCOL, V37, P375, DOI 10.1046/j.1365-280X.1999.00208.x; HECTOR RF, 1990, INFECT IMMUN, V58, P1476; Hogaboam CM, 2004, J LEUKOCYTE BIOL, V75, P805, DOI 10.1189/jlb.0703325; Kaur S, 2007, CLIN EXP IMMUNOL, V148, P382, DOI 10.1111/j.1365-2249.2007.03351.x; LEVITZ SM, 1985, J INFECT DIS, V152, P33; Lupetti A, 2008, EUR J CLIN MICROBIOL, V27, P1125, DOI 10.1007/s10096-008-0553-z; Luther K, 2007, CELL MICROBIOL, V9, P368, DOI 10.1111/j.1462-5822.2006.00796.x; Madan T, 2001, INFECT IMMUN, V69, P2728, DOI 10.1128/IAI.69.4.2728-2731.2001; Mambula SS, 2002, J BIOL CHEM, V277, P39320, DOI 10.1074/jbc.M201683200; Mehrad B, 2002, AM J RESP CRIT CARE, V166, P1263, DOI 10.1164/rccm.200204-367OC; Mehrad B, 1999, J IMMUNOL, V162, P1633; Meier A, 2003, CELL MICROBIOL, V5, P561, DOI 10.1046/j.1462-5822.2003.00301.x; Netea MG, 2003, J INFECT DIS, V188, P320, DOI 10.1086/376456; Neth O, 2000, INFECT IMMUN, V68, P688, DOI 10.1128/IAI.68.2.688-693.2000; Paris S, 1997, INFECT IMMUN, V65, P1510; Persat F, 2003, CLIN EXP IMMUNOL, V133, P370, DOI 10.1046/j.1365-2249.2003.02222.x; Philippe B, 2003, INFECT IMMUN, V71, P3034, DOI 10.1128/IAI.71.6.3034-3042.2003; POLAKWYSS A, 1991, MYCOSES, V34, P205; Ramaprakash H, 2009, INFECT IMMUN, V77, P108, DOI 10.1128/IAI.00998-08; Ramirez-Ortiz ZG, 2008, INFECT IMMUN, V76, P2123, DOI 10.1128/IAI.00047-08; ROBERTSON MD, 1989, J MED VET MYCOL, V27, P295; Rodriguez-Adrian LJ, 1998, CLIN INFECT DIS, V26, P1270; ROILIDES E, 1993, INFECT IMMUN, V61, P4870; Roilides E, 2001, J INFECT DIS, V183, P518, DOI 10.1086/318077; Saijo S, 2007, NAT IMMUNOL, V8, P39, DOI 10.1038/ni1425; Sainz J, 2007, IMMUNOL LETT, V109, P76, DOI 10.1016/j.imlet.2007.01.005; SCHAFFNER A, 1983, INFECT IMMUN, V42, P1109; Schelenz S, 1999, MED MYCOL, V37, P183, DOI 10.1046/j.1365-280X.1999.00219.x; Serrano-Gomez D, 2004, J IMMUNOL, V173, P5635; Simon A, 2008, ANTIMICROB AGENTS CH, V52, P1407, DOI 10.1128/AAC.00155-07; STEELE C, 2005, PLOS PATHOG, V1, P42; STURTEVANT JE, 1992, INFECT IMMUN, V60, P1913; Taylor PR, 2007, NAT IMMUNOL, V8, P31, DOI 10.1038/ni1408; Tkalcevic J, 2000, IMMUNITY, V12, P201, DOI 10.1016/S1074-7613(00)80173-9; Wang JE, 2001, INFECT IMMUN, V69, P2402, DOI 10.1128/IAI.69.4.2402-2406.2001; WASHBURN RG, 1990, INFECT IMMUN, V58, P3508; Wasylnka JA, 2003, J CELL SCI, V116, P1579, DOI 10.1242/jcs.00329; Wasylnka JA, 2002, INFECT IMMUN, V70, P3156, DOI 10.1128/IAI.70.6.3156-3163.2002; Zarember KA, 2007, J IMMUNOL, V178, P6367; Zhang HJ, 2008, ACTA PHARMACOL SIN, V29, P1202, DOI 10.1111/j.1745-7254.2008.00860.x	64	80	88	0	9	ELSEVIER SCIENCE BV	AMSTERDAM	PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS	1286-4579			MICROBES INFECT	Microbes Infect.	OCT	2009	11	12					919	927		10.1016/j.micinf.2009.07.002		9	Immunology; Infectious Diseases; Microbiology	Immunology; Infectious Diseases; Microbiology	504QI	WOS:000270631700003	19615460	
J	Litonjua, AA				Litonjua, Augusto A.			Childhood asthma may be a consequence of vitamin D deficiency	CURRENT OPINION IN ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						allergies; asthma; sun exposure; vitamin D; wheeze	REGULATORY T-CELLS; NUTRITION EXAMINATION SURVEY; IMR-90 HUMAN FIBROBLASTS; 3RD NATIONAL-HEALTH; SMOOTH-MUSCLE-CELLS; RAT LUNG EXPLANTS; D-RECEPTOR GENE; 1,25-DIHYDROXYVITAMIN D-3; 1-ALPHA,25-DIHYDROXYVITAMIN D-3; 25-HYDROXYVITAMIN D	Purpose of review Vitamin D deficiency has been rediscovered as a public-health problem worldwide. It has been postulated that vitamin D deficiency may explain a portion of the asthma epidemic. The purpose of this review is to present the evidence for a role of vitamin D in asthma. Recent findings Both animal models and studies in human fetal tissues show that vitamin D plays a role in fetal lung growth and maturation. Epidemiologic studies have also suggested that higher prenatal vitamin D intakes have a protective role against wheezing illnesses in young children. Vitamin D may protect against wheezing illnesses through its role in upregulating antimicrobial proteins or through its multiple immune effects. In addition, vitamin D may play a therapeutic role in steroid resistant asthmatics, and lower vitamin D levels have recently been associated with higher risks for asthma exacerbations. Summary Improving vitamin D status holds promise in primary prevention of asthma, in decreasing exacerbations of disease, and in treating steroid resistance. However, the appropriate level of circulating vitamin D for optimal immune functioning remains unclear. Because vitamin D deficiency is prevalent even in sun-replete areas, clinical trials are needed to definitively answer questions about the role of vitamin D in asthma.	[Litonjua, Augusto A.] Harvard Univ, Sch Med, Channing Lab, Brigham & Womens Hosp, Boston, MA 02115 USA; [Litonjua, Augusto A.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Pulm & Crit Care, Boston, MA 02115 USA	Litonjua, AA (reprint author), 181 Longwood Ave, Boston, MA 02115 USA.	augusto.litonjua@channing.harvard.edu		Litonjua, Augusto/0000-0003-0422-5875	NHLBI NIH HHS [R21 HL089842-01, R21 HL089842]		Adorini L, 2004, J STEROID BIOCHEM, V89-90, P437, DOI 10.1016/j.jsbmb.2004.03.013; Akeno N, 1997, ENDOCRINOLOGY, V138, P2233, DOI 10.1210/endo.138.6.5170; Aloia JF, 2007, EPIDEMIOL INFECT, V135, P1097; Aloia JF, 2007, EPIDEMIOL INFECT, V135, P1095; Annesi-Maesano I, 2002, PEDIATR RES, V52, P3, DOI 10.1023/01.PDR/0000017228.29635.EF; Banerjee A, 2008, BRIT J PHARMACOL, V155, P84, DOI 10.1038/bjp.2008.232; Bischoff-Ferrari HA, 2006, AM J CLIN NUTR, V84, P18; Black PN, 2005, CHEST, V128, P3792, DOI 10.1378/chest.128.6.3792; Boonstra A, 2001, J IMMUNOL, V167, P4974; Bosse Y, 2007, PHYSIOL GENOMICS, V29, P161, DOI 10.1152/physiolgenomics.00134.2006; BREHM JM, 2009, AM J RESP CRIT CARE; BRUN P, 1987, PEDIATR RES, V21, P362, DOI 10.1203/00006450-198704000-00008; BURRI PH, 1984, ANNU REV PHYSIOL, V46, P617, DOI 10.1146/annurev.ph.46.030184.003153; Camargo CA, 2007, AM J CLIN NUTR, V85, P788; Cantorna MT, 2004, AM J CLIN NUTR, V80, p1717S; Cantorna MT, 1998, J IMMUNOL, V160, P5314; Chatenoud L, 2001, IMMUNOL REV, V182, P149, DOI 10.1034/j.1600-065X.2001.1820112.x; Cippitelli M, 1998, EUR J IMMUNOL, V28, P3017, DOI 10.1002/(SICI)1521-4141(199810)28:10<3017::AID-IMMU3017>3.3.CO;2-Y; Come JM, 2002, LANCET, V359, P831; D'Ambrosio D, 1998, J CLIN INVEST, V101, P252, DOI 10.1172/JCI1050; Devereux G, 2007, AM J CLIN NUTR, V85, P853; DICKSON I, 1987, NATURE, V325, P18, DOI 10.1038/325018a0; ERKKOLA M, 2009, CLIN EXP AL IN PRESS; GALE CR, 2007, EUR J CLIN NUTR; GAULTIER C, 1984, AM REV RESPIR DIS, V130, P1108; Ginde AA, 2009, ARCH INTERN MED, V169, P384, DOI 10.1001/archinternmed.2008.560; Grant WB, 2008, PHOTOCHEM PHOTOBIOL, V84, P356, DOI 10.1111/j.1751-1097.2007.00266.x; Gregori S, 2002, DIABETES, V51, P1367, DOI 10.2337/diabetes.51.5.1367; Gregori S, 2001, J IMMUNOL, V167, P1945; Griffin MD, 2003, ANNU REV NUTR, V23, P117, DOI 10.1146/annurev.nutr.23.011702.073114; Heine G, 2002, EUR J IMMUNOL, V32, P3395, DOI 10.1002/1521-4141(200212)32:12<3395::AID-IMMU3395>3.0.CO;2-#; Herr C, 2007, EXPERT OPIN BIOL TH, V7, P1449, DOI 10.1517/14712598.7.9.1449; Holick MF, 2006, MAYO CLIN PROC, V81, P353; Holick MF, 2007, NEW ENGL J MED, V357, P266, DOI 10.1056/NEJMra070553; Hollis BW, 2007, J STEROID BIOCHEM, V103, P631, DOI 10.1016/j.jsbmb.2006.12.066; Hollis BW, 2006, AM J CLIN NUTR, V84, P273; Hollis BW, 2006, CAN MED ASSOC J, V174, P1287, DOI 10.1503/cmaj.060149; Hollis BW, 2004, AM J CLIN NUTR, V79, P717; HYATTSVILLE MD, 2004, ASTHMA PREVALENCE HE; Hypponen E, 2004, ANN NY ACAD SCI, V1037, P84, DOI 10.1196/annals.1337.013; IHO S, 1985, IMMUNOL LETT, V11, P331, DOI 10.1016/0165-2478(85)90116-6; Jackson DJ, 2008, AM J RESP CRIT CARE, V178, P667, DOI 10.1164/rccm.200802-309OC; Lamberg-Allardt C, 2006, PROG BIOPHYS MOL BIO, V92, P33, DOI 10.1016/j.pbiomolbio.2006.02.017; Lee JM, 2007, CLIN PEDIATR, V46, P42, DOI 10.1177/0009922806289311; Litonjua AA, 2007, J ALLERGY CLIN IMMUN, V120, P1031, DOI 10.1016/j.jaci.2007.08.028; Liu PT, 2007, J IMMUNOL, V179, P2060; Lunghi B, 1995, MOL CELL ENDOCRINOL, V115, P141, DOI 10.1016/0303-7207(95)03681-4; Mahon BD, 2003, J CELL BIOCHEM, V89, P922, DOI 10.1002/jcb.10580; Mannino D. 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Opin. Allergy Clin. Immunol.	JUN	2009	9	3					202	207		10.1097/ACI.0b013e32832b36cd		6	Allergy; Immunology	Allergy; Immunology	452YU	WOS:000266577900004	19365260	
J	Ozdemir, C; Akdis, M; Akdis, CA				Ozdemir, C.; Akdis, M.; Akdis, C. A.			T regulatory cells and their counterparts: masters of immune regulation	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review							GROWTH-FACTOR-BETA; IMMUNOLOGICAL SELF-TOLERANCE; ALLERGEN-SPECIFIC IMMUNOTHERAPY; TRANSCRIPTION FACTOR FOXP3; LATE ASTHMATIC REACTIONS; BEE VENOM IMMUNOTHERAPY; DENDRITIC CELLS; IN-VIVO; NK CELLS; CUTTING EDGE	The interaction of environmental and genetic factors with the immune system can lead to the development of allergic diseases. The essential step in this progress is the generation of allergen-specific CD4(+) T-helper (Th) type 2 cells that mediate several effector functions. The influence of Th2 cytokines leads to the production of allergen-specific IgE antibodies by B cells, development and recruitment of eosinophils, mucus production and bronchial hyperreactivity, as well as tissue homing of other Th2 cells and eosinophils. Meanwhile, Th1 cells may contribute to chronicity and the effector phases. T cells termed T regulatory (Treg) cells, which have immunosuppressive functions and cytokine profiles distinct from that of either Th1 or Th2 cells, have been intensely investigated during the last 13 years. Treg cell response is characterized by an abolished allergen-specific T cell proliferation and the suppressed secretion of Th1 and Th2-type cytokines. Treg cells are able to inhibit the development of allergen-specific Th2 and Th1 cell responses and therefore play an important role in a healthy immune response to allergens. In addition, Treg cells potently suppress IgE production and directly or indirectly suppress the activity of effector cells of allergic inflammation, such as eosinophils, basophils and mast cells. Currently, Treg cells represent an exciting area of research, where understanding the mechanisms of peripheral tolerance to allergens may soon lead to more rational and safer approaches for the prevention and cure of allergic diseases.	[Ozdemir, C.] Marmara Univ, Div Pediat Allergy & Immunol, Istanbul, Turkey; [Akdis, M.; Akdis, C. A.] Swiss Inst Allergy & Asthma Res, CH-7270 Davos, Switzerland	Ozdemir, C (reprint author), Obere Str 22, CH-7270 Davos, Switzerland.	akdisac@siaf.unizh.ch			Swiss National Science Foundation [SNF-32-112306/1, 32-118226]; Global Allergy; Asthma European Network (GA<SUP>2</SUP>LEN)	The authors' laboratories are funded by the Swiss National Science Foundation (grant no. SNF-32-112306/1, 32-118226) and Global Allergy and Asthma European Network (GA<SUP>2</SUP>LEN).	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Exp. Allergy	MAY	2009	39	5					626	639		10.1111/j.1365-2222.2009.03242.x		14	Allergy; Immunology	Allergy; Immunology	430ZX	WOS:000265032200003	19422105	
J	Islam, T; Berhane, K; McConnell, R; Gauderman, WJ; Avol, E; Peters, JM; Gilliland, FD				Islam, T.; Berhane, K.; McConnell, R.; Gauderman, W. J.; Avol, E.; Peters, J. M.; Gilliland, F. D.			Glutathione-S-transferase (GST) P1, GSTM1, exercise, ozone and asthma incidence in school children	THORAX			English	Article							POLYCYCLIC AROMATIC-HYDROCARBONS; SOUTHERN CALIFORNIA COMMUNITIES; AIR-POLLUTION; BRONCHIAL HYPERRESPONSIVENESS; CHILDHOOD ASTHMA; RISK-FACTORS; SUSCEPTIBILITY GENE; OXIDATIVE STRESS; DIFFERING LEVELS; DIOL EPOXIDES	Background: Because asthma has been associated with exercise and ozone exposure, an association likely mediated by oxidative stress, we hypothesised that glutathione-S-transferase (GST) P1, GSTM1, exercise and ozone exposure have interrelated effects on the pathogenesis of asthma. Methods: Associations of the well characterised null variant of GSTM1 and four single nucleotide polymorphisms (SNPs) that characterised common variation in the GSTP1 locus with new onset asthma in a cohort of 1610 school children were examined. Children's exercise and ozone exposure were classified using participation in team sports and community annual average ozone levels, respectively. Results: A two SNP model involving putatively functional variants (rs6591255, rs1695 (Ile105Va)) best captured the association between GSTP1 and asthma. The risk of asthma was lower for those with the Val allele of Ile105Val (hazard ratio (HR) 0.60, 95% CI 0.4 to 0.8) and higher for the variant allele of rs6591255 (HR 1.40, 95% CI 1.1 to 1.9). The risk of asthma increased with level of exercise among ile(105) homozygotes but not among those with at least one val(105) allele (interaction p value= 0.02). The risk was highest among ile(105) homozygotes who participated in >= 3 sports in the high ozone communities (HR 6.15, 95% CI 2.2 to 7.4). GSTM1 null was independently associated with an increased risk of asthma and showed little variation with air pollution or GSTP1 genotype. These results were consistent in two independent fourth grade cohorts recruited in 1993 and 1996. Conclusion: Children who inherit a val105 variant allele may be protected from the increased risk of asthma associated with exercise, especially in high ozone communities. GSTM1 null genotype was associated with an increased risk of asthma.	[Islam, T.; Berhane, K.; McConnell, R.; Gauderman, W. J.; Avol, E.; Peters, J. M.; Gilliland, F. 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,CHP 236, Los Angeles, CA 90033 USA.	gillilan@usc.edu	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	National Institute of Environmental Health Sciences [5P30ES007048, 5P01ES009581, R826708-01, RD831861-01, 5P01ES011627]; Environmental Protection Agency; National Heart, Lung and Blood Institute [5R01HL061768, 5R01HL076647]; Hastings Foundation	Funding: This work was supported by the Southern California Environmental Health Sciences Center (grant No 5P30ES007048) funded by the National Institute of Environmental Health Sciences; the Children's Environmental Health Center (grant Nos 5P01ES009581, R826708-01 and RD831861-01) funded by the National Institute of Environmental Health Sciences and the Environmental Protection Agency; the National Institute of Environmental Health Sciences (grant No 5P01ES011627); the National Heart, Lung and Blood Institute (grant Nos 5R01HL061768 and 5R01HL076647); and the Hastings Foundation.	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J	Holguin, F; Flores, S; Ross, Z; Cortez, M; Molina, M; Molina, L; Rincon, C; Jerrett, M; Berhane, K; Granados, A; Romieu, I				Holguin, Fernando; Flores, Silvia; Ross, Zev; Cortez, Marlene; Molina, Mario; Molina, Luisa; Rincon, Carlos; Jerrett, Michael; Berhane, Kiros; Granados, Alfredo; Romieu, Isabelle			Traffic-related exposures, airway function, inflammation, and respiratory symptoms in children	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						air pollution; traffic; asthma; exhaled nitric oxide	EXHALED NITRIC-OXIDE; CHILDHOOD ASTHMA; RESIDENTIAL EXPOSURE; NITROGEN-DIOXIDE; YOUNG-CHILDREN; POLLUTION; ROAD; HEALTH; CANADA; HOSPITALIZATION	Rationale: Traffic-related emissions have been associated with respiratory symptoms in some studies. However, there is limited information on how traffic-related emissions relate to lung function and airway inflammation. Objectives: To determine the differential association of traffic-related exposures with exhaled nitric oxide (NO) and lung volumes and symptoms in children with and without asthma. Methods: We performed a longitudinal study of 200 children from ages 6 to 12 years of whom half had physician-diagnosed asthma. Two-week NO(2) and 48-hour average levels of elemental carbon and particulate matter of less than 2.5 mu m (PM(2.5)) were measured at participating schools. Road and traffic densities were determine at schools and at each participant's house. Measurements and Main Results: In children with asthma, an inter-quartile increase in road density within the 50-, 100-, and 200-m home buffer areas was associated with increased exhaled NO (50 m: 28%; P = 0.03; 95% confidence interval [CI], 3-60; 100 m: 27%; P = 0.005; 95% Cl, 8-49; 200 m: 17%, P = 0.09, 95% Cl, -2 to 40), and reduced FEV(1) (50 m: -0.091 L; P = 0.038; 95% Cl, -0.174 to -0.007; 100 m: -0.072 L, P = -0.028, 95% Cl, -0.134 to -0.009; 200 in: -0.106L, P= 0.002,95%Cl, -0.171 to -0.041]). Exposure to NO(2) at schools was marginally associated with reduced FEV(1) (-0.020; P = 0.060; 95% Cl, -0.042 to 0.001). We did not observe significant associations with PM(2.5) or elemental carbon on exhaled NO. We did not observe significant reductions in lung volumes or changes in exhaled NO among healthy children. Conclusions: Vehicular traffic exposures are associated with increased levels of exhaled NO and reduced lung volumes in children with asthma.	[Holguin, Fernando] Emory Univ, Atlanta, GA 30322 USA; [Flores, Silvia; Cortez, Marlene; Romieu, Isabelle] Natl Inst Publ Hlth, Cuernavaca, Morelos, Mexico; [Ross, Zev] Zev Ross Spat Anal, Ithaca, NY USA; [Molina, Mario] Univ Calif San Diego, San Diego, CA 92103 USA; [Molina, Luisa] MIT, Cambridge, MA 02139 USA; [Rincon, Carlos] US EPA, Washington, DC 20460 USA; [Jerrett, Michael] Univ Calif Berkeley, Berkeley, CA 94720 USA; [Berhane, Kiros] Univ So Calif, Los Angeles, CA USA; [Granados, Alfredo] Univ Autonoma Ciudad Juarez, Juarez, Mexico	Holguin, F (reprint author), 550 Peachtree St,NE,Room 2331, Atlanta, GA 30308 USA.	fch@cdc.gov					American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Cesaroni G, 2003, EUR RESPIR J, V22, P619, DOI 10.1183/09031936.03.00091202; Ciccone G, 1998, OCCUP ENVIRON MED, V55, P771; Delfino RJ, 2006, ENVIRON HEALTH PERSP, V114, P1736, DOI 10.1289/ehp.9141; Dinakar C, 2004, CURR ALLERGY ASTHM R, V4, P454, DOI 10.1007/s11882-004-0011-7; English P, 1999, ENVIRON HEALTH PERSP, V107, P761, DOI 10.2307/3434663; Fritz GJ, 2001, INT J HYG ENVIR HEAL, V203, P235, DOI 10.1078/S1438-4639(04)70034-6; Gauderman WJ, 2007, LANCET, V369, P571, DOI 10.1016/S0140-6736(07)60037-3; GINA, 2004, GLOB STRAT ASTHM MAN; Green RS, 2004, ENVIRON HEALTH PERSP, V112, P61, DOI 10.1289/ehp.6566; Ising H, 2004, Noise Health, V6, P21; Ising H, 2003, Noise Health, V5, P41; 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; Lewis SA, 2005, AM J EPIDEMIOL, V161, P406, DOI 10.1093/aje/kwi059; Lin S, 2002, ENVIRON RES, V88, P73, DOI 10.1006/enrs.2001.4303; Lwebuga-Mukasa JS, 2004, J ASTHMA, V41, P289, DOI 10.1081/JAS-120026086; McConnell R, 2006, ENVIRON HEALTH PERSP, V114, P766, DOI 10.1289/ehp.8594; Meng Ying-Ying, 2006, Policy Brief UCLA Cent Health Policy Res, P1; Morgenstern V, 2007, OCCUP ENVIRON MED, V64, P8, DOI 10.1136/oem.2006.028241; Nicolai T, 2003, EUR RESPIR J, V21, P956, DOI 10.1183/09031936.03.00041103; O'Neill MS, 2003, ENVIRON HEALTH PERSP, V111, P1861, DOI 10.1289/ehp.6334; Oyana TJ, 2004, AM J PUBLIC HEALTH, V94, P1250, DOI 10.2105/AJPH.94.7.1250; Oyana Tonny J, 2005, Int J Health Geogr, V4, P14, DOI 10.1186/1476-072X-4-14; Reponen T, 2003, J ENVIRON MONITOR, V5, P557, DOI 10.1039/b303557c; Sahsuvaroglu T, 2006, J AIR WASTE MANAGE, V56, P1059; Slutsky AS, 1999, AM J RESP CRIT CARE, V160, P2104; Smargiassi A, 2006, J EPIDEMIOL COMMUN H, V60, P507, DOI 10.1136/jech.2005.037044; Steerenberg PA, 2001, ARCH ENVIRON HEALTH, V56, P167; Trenga CA, 2006, CHEST, V129, P1614, DOI 10.1378/chest.129.6.1614; *US EPA, 2006, US MEX BORD ENV PROG; Venables W. N., 2002, MODERN APPL STAT S; Venn A, 2000, OCCUP ENVIRON MED, V57, P152, DOI 10.1136/oem.57.3.152; Venn AJ, 2001, AM J RESP CRIT CARE, V164, P2177, DOI 10.1164/rccm2106126; Wilkinson P, 1999, THORAX, V54, P1070; Witten A, 2005, J OCCUP ENVIRON MED, V47, P1250, DOI 10.1097/01.jom.0000177081.62204.8d	36	80	83	2	19	AMER THORACIC SOC	NEW YORK	61 BROADWAY, FL 4, NEW YORK, NY 10006 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	DEC 15	2007	176	12					1236	1242		10.1164/rccm.200611-1616OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	243PZ	WOS:000251811100011	17641154	
J	Bernard, A; Carbonnelle, S; Dumont, X; Nickmilder, M				Bernard, Alfred; Carbonnelle, Sylviane; Dumont, Xavier; Nickmilder, Marc			Infant swimming practice, pulmonary epithelium integrity, and the risk of allergic and respiratory diseases later in childhood	PEDIATRICS			English	Article						chlorine; trichloramine; nitrogen trichloride; baby swimming; Clara cell protein; CC16; childhood asthma; recurrent bronchitis	CLARA CELL PROTEIN; EXHALED NITRIC-OXIDE; POOL ATTENDANCE; SERUM PNEUMOPROTEINS; ASTHMA; LUNG; CHILDREN; CC16; EXPOSURE; EXERCISE	Objective. Irritant gases and aerosols contaminating the air of indoor swimming pools can affect the lung epithelium and increase asthma risk in children. We evaluated the impact of infant swimming practice on allergic status and respiratory health later in childhood. Methods. Clara cell protein, surfactant-associated protein D, and total and aeroallergen-specific immunoglobulin E were measured in the serum of 341 schoolchildren aged 10 to 13 years, among whom 43 had followed an infant swimming program. Asthma was defined as doctor-diagnosed asthma and/or positive exercise-induced bronchoconstriction (15% decrease in postexercise forced expiratory volume). Results. There were no significant differences between the infant swimming group and the other children regarding the levels of exhaled nitric oxide and total or aeroallergen-specific serum immunoglobulin E. Children who swam as infants showed, by contrast, a significant decrease of serum Clara cell protein and of the serum Clara cell protein/surfactant-associated protein D ratio integrating Clara cell damage and permeability changes of the lung epithelial barrier. These effects were associated with higher risks of asthma and of recurrent bronchitis. Passive exposure to tobacco alone had no effect on these outcomes but seemed to interact with infant swimming practice to increase the risk of asthma or of recurrent bronchitis. Conclusions. Our data suggest that infant swimming practice in chlorinated indoor swimming pools is associated with airways changes that, along with other factors, seem to predispose children to the development of asthma and recurrent bronchitis.	Univ Catholique Louvain, Fac Med, Toxicol Unit, Dept Publ Hlth, B-1200 Brussels, Belgium	Bernard, A (reprint author), Univ Catholique Louvain, Fac Med, Toxicol Unit, Dept Publ Hlth, Ave 3 Mounier 53, B-1200 Brussels, Belgium.	alfred.bernard@uclouvain.be	Nickmilder, Marc/A-9060-2010; BERNARD, Alfred/A-6511-2010	BERNARD, Alfred/0000-0003-3171-3743			AGIBATI N, 2001, OCCUP ENVIRON MED, V58, P399; Anderson SJ, 2000, PEDIATRICS, V105, P868; BENNETT HJ, 1983, PEDIATRICS, V72, P125; BERNARD A, 1992, EUR RESPIR J, V5, P1231; Bernard A, 2005, TOXICOL APPL PHARM, V206, P185, DOI 10.1016/j.taap.2004.10.022; Bernard A, 2003, OCCUP ENVIRON MED, V60, P385, DOI 10.1136/oem.60.6.385; BERNARD A, 1992, LANCET, V339, P1620, DOI 10.1016/0140-6736(92)91891-B; Bernard A, 2006, ENVIRON HEALTH PERSP, V114, P1567, DOI 10.1289/ehp.8461; BERNARD AM, 1994, ENVIRON RES, V66, P96, DOI 10.1006/enrs.1994.1047; BERNARD AM, 1994, EUR RESPIR J, V7, P1932; Bonetto G, 2006, AM J RESP CRIT CARE, V174, P545, DOI 10.1164/rccm.200509-1392OC; Broeckaert F, 2000, CLIN EXP ALLERGY, V30, P469; Burgess JL, 2003, AM J IND MED, V44, P246, DOI 10.1002/ajim.10269; Carbonnelle S, 2002, BIOMARKERS, V7, P464, DOI 10.1080/13547500210166612; Cardinale F, 2005, PEDIATR ALLERGY IMMU, V16, P236, DOI 10.1111/j.1399-3038.2005.00265.x; Finkelstein JN, 2004, PEDIATRICS, V113, P1092; FREEDMAN FB, 2003, WATER BABIES; GOLDBERG GN, 1982, PEDIATRICS, V70, P599; Hermans C, 1999, AM J RESP CRIT CARE, V159, P646; Hermans C, 1998, CLIN CHIM ACTA, V272, P101, DOI 10.1016/S0009-8981(98)00006-0; Hermans C, 1998, EUR RESPIR J, V11, P801, DOI 10.1183/09031936.98.11040801; HERY M, 1995, ANN OCCUP HYG, V39, P427, DOI 10.1016/0003-4878(95)00013-5; *IUSE, 2004, MEAS CHLOR AIR SWIMM; JESSEN HJ, 1988, Z GESAMTE HYG, V34, P248; Johnston CJ, 1997, AM J RESP CELL MOL, V17, P147; JONES A, 1994, THORAX, V49, P757, DOI 10.1136/thx.49.8.757; Kohlhammer Y, 2006, ALLERGY, V61, P1305, DOI 10.1111/j.1398-9995.2006.01229.x; Lagerkvist BJ, 2004, ENVIRON HEALTH PERSP, V112, P1768, DOI 10.1289/ehp.7027; Lesur O, 2006, INTENS CARE MED, V32, P1167, DOI 10.1007/s00134-006-0235-1; Malinovschi A, 2006, RESP RES, V7, DOI 10.1186/1465-9921-7-92; Mattsson J, 2005, TRANSPLANTATION, V79, P1411, DOI 10.1097/01.TP.0000158354.39635.AB; MCFADDEN ER, 1994, NEW ENGL J MED, V330, P1362, DOI 10.1056/NEJM199405123301907; Nickmilder M, 2007, OCCUP ENVIRON MED, V64, P37, DOI 10.1136/oem.2005.025452; Nystad W, 2003, ACTA PAEDIATR, V92, P905, DOI 10.1080/08035250310003587; Parimon Tanyalak, 2004, Respir Care, V49, P291; Porsbjerg C, 2005, ANN ALLERG ASTHMA IM, V95, P137; Rasmussen F, 1999, THORAX, V54, P587; Robin M, 2002, EUR RESPIR J, V20, P1152, DOI 10.1183/09031936.02.02042001; Shijubo N, 1997, EUR RESPIR J, V10, P1108, DOI 10.1183/09031936.97.10051108; Shijubo N, 1999, AM J RESP CRIT CARE, V160, P930; Silkoff PE, 2004, J ALLERGY CLIN IMMUN, V114, P1241, DOI 10.1016/j.jaci.2004.08.042; Stav D, 2005, NEW ENGL J MED, V353, P1635, DOI 10.1056/NEJMc050955; Vohra R, 2006, PEDIATR EMERG CARE, V22, P254, DOI 10.1097/01.pec.0000210173.56010.c1; WHO, 2006, GUID SAF RECR WAT EN, V2	44	80	83	1	12	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	JUN	2007	119	6					1095	1103		10.1542/peds.2006-3333		9	Pediatrics	Pediatrics	174NL	WOS:000246948900008	17545376	
J	Jacobs, JH; Spaan, S; van Rooy, GBGJ; Meliefste, C; Zaat, VAC; Rooyackers, JM; Heederik, D				Jacobs, J. H.; Spaan, S.; van Rooy, G. B. G. J.; Meliefste, C.; Zaat, V. A. C.; Rooyackers, J. M.; Heederik, D.			Exposure to trichloramine and respiratory symptoms in indoor swimming pool workers	EUROPEAN RESPIRATORY JOURNAL			English	Article						occupational asthma; swimming pools; trichloramines	NITROGEN TRICHLORIDE; ASTHMA; CHLORAMINES; CHLORINE; WATER; AIR	The association between swimming pool characteristics and activities of employees and respiratory symptoms in employees was studied. Trichloramine levels were measured to evaluate relationships with pool characteristics and to estimate long-term exposure levels. Questionnaires were available from 624 pool workers and 38 swimming facilities. Chloramine levels were measured by area sampling over 2-h periods and analysed using ion chromatography. Work-related and general respiratory symptoms, and symptoms indicatiive of atopy and bronchial hyperresponsiveness were considered. Respiratory symptom prevalence among pool workers was compared with symptoms in a Dutch population sample. Chloramine levels were modelled with regression analysis. This model was used to estimate long-term average chloramine levels for each pool studied. Employees with higher exposure reported upper respiratory symptoms with greater frequency. Upper respiratory symptoms were statistically significantly associated with cumulative chloramine levels (odds ratio (OR) >1.4 for hoarseness, lost voice, sinusitis). General respiratory symptoms were significantly elevated compared with a Dutch population sample (OR ranged 1.4-7.2). An excess risk for respiratory symptoms indicative of asthma was observed in swimming pool employees. Aggravation of existing respiratory disease or interactions between irritants and allergen exposures are the most likely explanations for the observed associations.	Univ Utrecht, Div Environm Epidemiol, Inst Risk Assessment Sci, NL-3508 TD Utrecht, Netherlands; Univ Utrecht, Netherlands Expertise Ctr Occupat Resp Disorders, Utrecht, Netherlands; Univ Utrecht, Univ Med Ctr Utrecht, Utrecht, Netherlands	Jacobs, JH (reprint author), Univ Utrecht, Div Environm Epidemiol, Inst Risk Assessment Sci, POB 80-178, NL-3508 TD Utrecht, Netherlands.	j.h.jacobs@iras.uu.nl					Armstrong B, 2004, OCCUP ENVIRON MED, V61, P475, DOI 10.1136/oem.2003.011205; Bernard A, 2003, OCCUP ENVIRON MED, V60, P385, DOI 10.1136/oem.60.6.385; CHARLIER G, 2003, ETUDE QUALITE ATMOSP; DEJOODE BV, 2004, OCCUPATIONAL DREAM D; GAGNAIRE F, 1994, J APPL TOXICOL, V14, P405, DOI 10.1002/jat.2550140604; Hermans C, 1999, AM J RESP CRIT CARE, V159, P646; Hermans C, 1998, EUR RESPIR J, V11, P801, DOI 10.1183/09031936.98.11040801; HERY M, 1995, ANN OCCUP HYG, V39, P427, DOI 10.1016/0003-4878(95)00013-5; LAHL U, 1981, WATER RES, V15, P803, DOI 10.1016/0043-1354(81)90133-0; Massin N, 1998, OCCUP ENVIRON MED, V55, P258; Medina-Ramon M, 2005, OCCUP ENVIRON MED, V62, P598, DOI 10.1136/oem.2004.017640; Medina-Ramon M, 2003, THORAX, V58, P950, DOI 10.1136/thorax.58.11.950; Nemery B, 2002, EUR RESPIR J, V19, P790, DOI 10.1183/09031936.02.00308602; Preller L, 1996, EUR RESPIR J, V9, P1407, DOI 10.1183/09031936.96.09071407; PRELLER L, 1995, RESP HLTH EFFECTS PI; RIJCKEN B, 1996, EUROPEES LUCHTWEG ON; SPAAN S, 2004, BLOOTSTELLING ENDOTO; Thickett KM, 2002, EUR RESPIR J, V19, P827, DOI 10.1183/09031936.02.00232802; WHO, 2000, GUID SAF RECR WAT EN, V2; Zock JP, 2002, EUR RESPIR J, V20, P679, DOI 10.1183/09031936.02.00279702	20	80	81	1	12	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	APR	2007	29	4					690	698		10.1183/09031936.00024706		9	Respiratory System	Respiratory System	156QC	WOS:000245663100012	17107995	
J	Lu, FL; Johnston, RA; Flynt, L; Theman, TA; Terry, RD; Schwartzman, IN; Lee, A; Shore, SA				Lu, FL; Johnston, RA; Flynt, L; Theman, TA; Terry, RD; Schwartzman, IN; Lee, A; Shore, SA			Increased pulmonary responses to acute ozone exposure in obese db/db mice	AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY			English	Article						leptin; interleukin-1 beta; airway responsiveness; macrophage inflammatory protein-2; neutrophil; ventilation	BODY-MASS INDEX; NECROSIS-FACTOR-ALPHA; LEPTIN RECEPTOR; AIRWAY HYPERRESPONSIVENESS; INSULIN-RESISTANCE; WEIGHT-REDUCTION; SPLICE VARIANTS; ASTHMA SEVERITY; TNF-ALPHA; IN-VITRO	Epidemiological studies indicate the incidence of asthma is increased in obese and overweight humans. Responses to ozone (O-3), an asthma trigger, are increased in obese (ob/ob) mice lacking the satiety hormone leptin. The long form of leptin receptor (Ob-Rb) is required for satiety; mice lacking this receptor (db/db mice) are also substantially obese. Here, wild-type (WT) and db/db mice were exposed to air or O-3 (2 ppm) for 3 h. Airway responsiveness, measured by the forced oscillation technique, was greater in db/db than WT mice after air exposure. O-3-induced increases in pulmonary resistance and airway responsiveness were also greater in db/db mice. BALF eotaxin, IL-6, KC, and MIP-2 increased 4 h after O-3 exposure and subsided by 24 h, whereas protein and neutrophils continued to increase through 24 h. For each outcome, the effect of O-3 was significantly greater in db/db than WT mice. Previously published results obtained in ob/ob mice were similar except for O-3-induced neutrophils and MIP-2, which were not different from WT mice. O-3 also induced pulmonary IL-1 beta and TNF-alpha mRNA expression in db/db but not ob/ob mice. Leptin was increased in serum of db/db mice, and pulmonary mRNA expression of short form of leptin receptor (Ob-R-a) was similar in db/db and WT mice. These data confirm obese mice have innate airway hyperresponsiveness and increased pulmonary responses to O-3. Differences between ob/ob mice, which lack leptin, and db/db mice, which lack Ob-Rb but not Ob-R-a, suggest leptin, acting through Ob-R-a, can modify some pulmonary responses to O-3.	Harvard Univ, Sch Publ Hlth, Physiol Program, Dept Environm Hlth, Boston, MA 02115 USA; Natl Taiwan Univ, Natl Taiwan Univ Hosp & Med Coll, Dept Pediat, Taipei, Taiwan	Shore, SA (reprint author), Harvard Univ, Sch Publ Hlth, Physiol Program, Dept Environm Hlth, Bldg 1,Rm 311,665 Huntington Ave, Boston, MA 02115 USA.	sshore@hsph.harvard.edu	Lu, Frank/G-6196-2012	Lu, Frank/0000-0002-5225-7751	NHLBI NIH HHS [HL 33009]; NIEHS NIH HHS [ES 00002, ES 013307]		Aaron SD, 2004, CHEST, V125, P2046, DOI 10.1378/chest.125.6.2046; Akerman MJH, 2004, J ASTHMA, V41, P521, DOI 10.1081/JAS-120037651; ARSALANE K, 1995, AM J RESP CELL MOL, V13, P60; Baeuerle PA, 1996, CELL, V87, P13, DOI 10.1016/S0092-8674(00)81318-5; Bastard JP, 2002, J CLIN ENDOCR METAB, V87, P2084, DOI 10.1210/jc.87.5.2084; Bergen HT, 2002, AM J RESP CELL MOL, V27, P71; Bjorbaek C, 2001, J BIOL CHEM, V276, P4747, DOI 10.1074/jbc.M007439200; Bruno A, 2005, J IMMUNOL, V174, P8090; Brusasco V, 1998, THORAX, V53, P992; Bruun JM, 2003, EUR J ENDOCRINOL, V148, P535, DOI 10.1530/eje.0.1480535; Camargo CA, 1999, ARCH INTERN MED, V159, P2582, DOI 10.1001/archinte.159.21.2582; Castro-Rodriguez Jose A., 2001, American Journal of Respiratory and Critical Care Medicine, V163, P1344; Celedon JC, 2001, AM J RESP CRIT CARE, V164, P1835; Chen H, 1996, CELL, V84, P491, DOI 10.1016/S0092-8674(00)81294-5; Chinn S, 2002, THORAX, V57, P1028, DOI 10.1136/thorax.57.12.1028; Cho HY, 2001, AM J PHYSIOL-LUNG C, V280, pL537; COHEN MP, 1995, J CLIN INVEST, V95, P2338, DOI 10.1172/JCI117926; Considine RV, 1997, INT J BIOCHEM CELL B, V29, P1255, DOI 10.1016/S1357-2725(97)00050-2; DING DJ, 1987, J APPL PHYSIOL, V62, P1324; Faggioni R, 1997, AM J PHYSIOL-REG I, V273, pR181; Ford ES, 2005, J ALLERGY CLIN IMMUN, V115, P897, DOI 10.1016/j.jaci.2004.11.050; Gainsford T, 1996, P NATL ACAD SCI USA, V93, P14564, DOI 10.1073/pnas.93.25.14564; Ghilardi N, 1996, P NATL ACAD SCI USA, V93, P6231, DOI 10.1073/pnas.93.13.6231; Hakala K, 2000, CHEST, V118, P1315, DOI 10.1378/chest.118.5.1315; Hamada K, 2003, J IMMUNOL, V170, P1683; Hoggard N, 1997, BIOCHEM BIOPH RES CO, V232, P383, DOI 10.1006/bbrc.1997.6245; Hosoi T, 2002, BRAIN RES, V949, P139, DOI 10.1016/S0006-8993(02)02974-8; HOTAMISLIGIL GS, 1993, SCIENCE, V259, P87, DOI 10.1126/science.7678183; Hotamisligil GS, 1997, DIABETES, V46, P451, DOI 10.2337/diabetes.46.3.451; Hotta K, 2001, DIABETES, V50, P1126, DOI 10.2337/diabetes.50.5.1126; Hu E, 1996, J BIOL CHEM, V271, P10697; HUANG J, 1992, DIS MARKERS, V10, P81; Inigo C, 2004, J PHYSIOL BIOCHEM, V60, P93; Johnston RA, 2006, AM J PHYSIOL-REG I, V290, pR126, DOI 10.1152/ajpregu.00306.2005; Johnston RA, 2005, AM J PHYSIOL-LUNG C, V288, pL61, DOI 10.1152/ajplung.00101.2004; JOHNSTON RA, 2005, AM J PHYSIOL-LUNG C, V288, pL3908; Kellerer M, 1997, DIABETOLOGIA, V40, P1358, DOI 10.1007/s001250050832; Leibel RL, 1997, J BIOL CHEM, V272, P31937, DOI 10.1074/jbc.272.51.31937; Litonjua AA, 2002, THORAX, V57, P581, DOI 10.1136/thorax.57.7.581; Loffreda S, 1998, FASEB J, V12, P57; Lollmann B, 1997, BIOCHEM BIOPH RES CO, V238, P648, DOI 10.1006/bbrc.1997.7205; Luttmann-Gibson H, 2004, AM J RESP CRIT CARE, V169, pA19; Nystad W, 2004, AM J EPIDEMIOL, V160, P969, DOI 10.1093/aje/kwh303; Ouchi N, 2003, CURR OPIN LIPIDOL, V14, P561, DOI 10.1097/01.mol.0000103609.38789.96; Park JW, 2004, AM J RESP CELL MOL, V30, P830, DOI 10.1165/rcmb.2003.0373OC; Rivera-Sanchez YM, 2004, J APPL PHYSIOL, V96, P2200, DOI 10.1152/japplphysiol.00960.2003; Sahai A, 2004, AM J PHYSIOL-GASTR L, V287, pG1035, DOI 10.1152/ajpgi.00199.2004; Shore SA, 2005, J ALLERGY CLIN IMMUN, V115, P925, DOI 10.1016/j.jaci.2005.01.064; Shore SA, 2003, J APPL PHYSIOL, V95, P938, DOI 10.1152/japplphysiol.00336.2003; Shore SA, 2005, J ALLERGY CLIN IMMUN, V115, P103, DOI 10.1016/j.jaci.2004.10.007; Shore SA, 2001, AM J RESP CRIT CARE, V164, P602; SHORE SA, IN PRESS PHARM THER; Stenius-Aarniala B, 2000, BRIT MED J, V320, P827, DOI 10.1136/bmj.320.7238.827; Tankersley CG, 1998, J APPL PHYSIOL, V85, P2261; Tartaglia LA, 1997, J BIOL CHEM, V272, P6093; Thomson CC, 2003, CHEST, V124, P795, DOI 10.1378/chest.124.3.795; Tsuchiya T, 1999, EUR J PHARMACOL, V365, P273, DOI 10.1016/S0014-2999(98)00884-X; Uysal KT, 1997, NATURE, V389, P610, DOI 10.1038/39335; Varraso R, 2005, AM J RESP CRIT CARE, V171, P334, DOI 10.1164/rccm.200405-674OC; Weister MJ, 1987, Toxicol. Appl. Pharmacol, V89, P429; Zarkesh-Esfahani H, 2004, J IMMUNOL, V172, P1809; ZHANG LY, 1995, EXP LUNG RES, V21, P503, DOI 10.3109/01902149509031755	62	80	83	0	4	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.	MAY	2006	290	5					L856	L865		10.1152/ajplung.00386.2005		10	Physiology; Respiratory System	Physiology; Respiratory System	030VU	WOS:000236664000009	16373670	
J	Effros, RM; Casaburi, R; Su, J; Dunning, M; Torday, J; Biller, J; Shaker, R				Effros, RM; Casaburi, R; Su, J; Dunning, M; Torday, J; Biller, J; Shaker, R			The effects of volatile salivary acids and bases on exhaled breath condensate pH	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						acetate; ammonium; bicarbonate; buffer; exhaled breath condensate	CYSTIC-FIBROSIS; AIR-POLLUTION; ASTHMA; ACIDIFICATION; INFLAMMATION; DILUTION; CHILDREN; AMMONIA; DISEASE; COUGH	Rationale: Recent studies have reported acidification of exhaled breath condensate (EBC) in inflammatory lung diseases. This phenomenon, designated "acidopnea," has been attributed to airway inflammation. Objectives: To determine whether salivary acids and bases can influence EBC pH in chronic obstructive pulmonary disease (COPD). Methods: Measurements were made of pH, electrolytes, and volatile bases and acids in saliva and EBC equilibrated with air in 10 healthy subjects and 10 patients. Results: The average EBC pH in COPD was reduced (normal, 7.24 +/- 0.24 SEM; range, 6.11-8.34; COPD, 6.67 +/- 0.18; range, 5.74-7.64; p = 0.079). EBCs were well buffered by NH4+/NH3 and CO2/HCO3- in all but four patients, who had NH4+ concentrations under 60 mu mol/L, and acetate concentrations that approached or exceeded those of NH4+. Saliva contained high concentrations of acetate (similar to 6,000 mu mol/L) and NH4+ (similar to 12,000 mu mol/L). EBC acetate increased and EBC NH4+ decreased when salivary pH was low, consistent with a salivary source for these volatile constituents. Nonvolatile acids did not play a significant role in determining pH of condensates because of extreme dilution of respiratory droplets by water vapor (similar to 1:12,000). Transfer of both acetic acid and NH3 from the saliva to the EBC was in the gas phase rather than droplets. bConclusions: EBC acidification in COPD can be affected by the balance of volatile salivary acids and bases, suggesting that EBC pH may not be a reliable marker of airway acidification. Salivary acidification may play an important role in acidopnea.	Univ Calif Los Angeles, Los Angeles Cty Harbor Med Ctr, Inst Biomed Res, LABiomed, Torrance, CA 90502 USA; Med Coll Wisconsin, Dept Med, Milwaukee, WI 53226 USA	Effros, RM (reprint author), Univ Calif Los Angeles, Los Angeles Cty Harbor Med Ctr, Inst Biomed Res, LABiomed, 1124 W Carson St,RB2, Torrance, CA 90502 USA.	reffros@labiomed.org		Torday, John/0000-0001-9071-3052	NHLBI NIH HHS [HL074407, HL55268]; NIDDK NIH HHS [DK25731]		Borrill Z, 2005, EUR RESPIR J, V25, P269, DOI 10.1183/09031936.05.00085804; BRIDGES SR, 1992, AM J CLIN NUTR, V56, P455; Carpagnano GE, 2004, CHEST, V125, P2005, DOI 10.1378/chest.125.6.2005; Chen ZF, 2004, ARCH ORAL BIOL, V49, P863, DOI 10.1016/j.archoralbio.2004.05.002; CRAPO RO, 1981, AM REV RESPIR DIS, V123, P659; Dwyer TM, 2004, LUNG, V182, P241, DOI 10.1007/s00408-004-2506-3; Effros RM, 2002, AM J RESP CRIT CARE, V165, P663, DOI 10.1164/rccm.2101078; Effros RM, 2003, AM J RESP CRIT CARE, V168, P1500, DOI 10.1164/rccm.200307-920OC; Effros RM, 2005, J APPL PHYSIOL, V99, P1286, DOI 10.1152/japplphysiol.00362.2005; Effros RM, 2004, AM J PHYSIOL-LUNG C, V287, pL1073, DOI 10.1152/ajplung.00069.2004; EFFROS RM, 2003, AM J MED, V115, P137, DOI 10.1016/S0002-9343(03)00212-2; Gauderman WJ, 2004, NEW ENGL J MED, V351, P1057, DOI 10.1056/NEJMoa040610; Gauderman WJ, 2002, AM J RESP CRIT CARE, V166, P76, DOI 10.1164/rccm.2111021; Gessner C, 2003, RESP MED, V97, P1188, DOI 10.1016/S0954-6111(03)00225-7; HARDING SM, 2003, AM J MED, V115, P137; Hunt JF, 2000, AM J RESP CRIT CARE, V161, P694; Hunt JF, 2002, AM J RESP CRIT CARE, V165, P101; Kostikas K, 2002, AM J RESP CRIT CARE, V165, P1364, DOI 10.1164/rccm.200111-068OC; MITSUHASHI M, 1985, PEDIATRICS, V75, P855; Moloney ED, 2004, AM J RESP CRIT CARE, V169, P64, DOI 10.1164/rccm.200307.105OC; Niimi A, 2004, THORAX, V59, P608, DOI 10.1136/thx.2003.012906; NORWOOD DM, 1992, ARCH ENVIRON HEALTH, V47, P309; OJOOJC, 2005, THORAX, V60, P22; Ricciardolo FLM, 2004, J ALLERGY CLIN IMMUN, V113, P610, DOI 10.1016/j.jaci.2003.12.034; Tate S, 2002, THORAX, V57, P926, DOI 10.1136/thorax.57.11.926; Vass G, 2003, AM J RESP CRIT CARE, V167, P850, DOI 10.1164/rccm.200207-716BC; VAUGHAN J, 2003, EUR RESPIR J, V322, P889; VAUGHAN W, 2001, EUR RESPIR J, V18, pS463; Wells K, 2005, THORAX, V60, P27, DOI 10.1136/thx.2003.020602	29	80	81	1	10	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 15	2006	173	4					386	392		10.1164/rccm.200507-1059OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	012GU	WOS:000235327100006	16284109	
J	Belanger, K; Gent, JF; Triche, EW; Bracken, MB; Leaderer, BP				Belanger, K; Gent, JF; Triche, EW; Bracken, MB; Leaderer, BP			Association of indoor nitrogen dioxide exposure with respiratory symptoms in children with asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; children; gas stoves; indoor environment; nitrogen dioxide; respiratory symptoms	1ST YEAR; PERSONAL EXPOSURE; PRESCHOOL-CHILDREN; AIR CONTAMINANTS; GAS COOKING; LIFE; NO2; POLLUTION; RISK; SCHOOLCHILDREN	Rationale: Chronic exposure to indoor nitrogen dioxide (NO2) is a public health concern. Over half of U.S. households have a source of NO2, and experimental data suggest potential for adverse respiratory effects. Objective: To examine associations of indoor NO2 exposure with respiratory symptoms among children with asthma. Methods: NO2 was measured using Palmes tubes, and respiratory symptoms in the month before sampling were collected during home interviews of mothers of 728 children with active asthma. All were younger than 12 yr, lived at the sampled home for at least 2 mo, and had asthma symptoms or used maintenance medication within the previous year. Measurements: Respiratory symptoms (wheeze, persistent cough, shortness of breath, chest tightness). Results: Mean (SD) NO2 was 8.6 (9.1) ppb in homes with electric ranges and 25.9 (18.1) ppb in homes with gas stoves. In models stratified by housing type (a factor associated with socioeconomic status), gas stove presence and elevated NO2 were each significantly associated with respiratory symptoms, controlling for age, ethnicity, medication, mold/mildew, water leaks, and season of sampling. Among children in multifamily housing, exposure to gas stoves increased likelihood of wheeze (odds ratio [OR], 2.27; 95% confidence interval [95% Cl], 1.15, 4.47), shortness of breath (OR, 2.33; 95% Cl, 1.12, 5.06), and chest tightness (OR, 4.34; 95% Cl, 1.76, 10.69), whereas each 20-ppb increase in NO2 increased both likelihood of any wheeze (OR, 1.52; 95% Cl, 1.04, 2.21) or chest tightness (OR, 1.61; 95% Cl, 1.04, 2.49), and days of wheeze (rate ratio (RR), 1.33; 95% Cl, 1.05, 1.68) or chest tightness (RR, 1.51; 95% Cl, 1.18, 1.91). Conclusion: Exposure to indoor NO2 at levels well below the Environmental Protection Agency outdoor standard (53 ppb) is associated with respiratory symptoms among children with asthma in multifamily housing.	Yale Univ, Sch Med, Yale Ctr Perinatal Pediat & Environm Epidemiol, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA	Belanger, K (reprint author), Yale Univ, Sch Med, Yale Ctr Perinatal Pediat & Environm Epidemiol, Dept Epidemiol & Publ Hlth, 1 Church St,6th Floor, New Haven, CT 06510 USA.	kathleen.belanger@yale.edu	Triche, Elizabeth/I-4986-2014; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	NIEHS NIH HHS [R01 ES005410, ES07456, ES11013, ES05410, R01 ES007456, R01 ES011013]		Basu R., 1999, J ENV MED, V1, P173, DOI DOI 10.1002/JEM.28; BAUER MA, 1986, AM REV RESPIR DIS, V134, P1203; Belanger K, 2003, AM J EPIDEMIOL, V158, P195, DOI 10.1093/aje/kwg148; BERGLUND M, 1993, SKANDINAVIAN J WO S2, V19, P37; BREYSSE PN, 2005, ENVIRON RES, V95, P167; Brunekreef B, 2001, CLIN EXP ALLERGY, V31, P1170, DOI 10.1046/j.1365-2222.2001.01208.x; BRUNEKREEF B, 1987, AM J EPIDEMIOL, V125, P892; Chauhan AJ, 2003, LANCET, V361, P1939, DOI 10.1016/S0140-6736(03)13582-9; Chauhan AJ, 1999, CLIN EXP ALLERGY, V29, P1009, DOI 10.1046/j.1365-2222.1999.00648.x; DEKKER C, 1991, CHEST, V100, P922, DOI 10.1378/chest.100.4.922; Emenius G, 2004, INDOOR AIR, V14, P34, DOI 10.1046/j.1600-0668.2003.00207.x; FOLINSBEE LJ, 1992, TOXICOL IND HEALTH, V8, P273; FUHLBRIGGE A, 1997, THORAX S3, V52, P58; Garrett MH, 1998, AM J RESP CRIT CARE, V158, P891; Gent JF, 2002, ENVIRON HEALTH PERSP, V110, pA781; GENT JF, 2004, AM J RESP CRIT CARE, V170, pA162; HASSELBLAD V, 1992, J AIR WASTE MANAGE, V42, P662; HOEK G, 1984, INT ARCH OCC ENV HEA, V55, P79, DOI 10.1007/BF00378070; Jarvis D, 1999, THORAX, V54, P1054; KUHR J, 1991, SOZ PRAVENTIV MED, V36, P67, DOI 10.1007/BF01846044; LEADERER BP, 1986, AM J EPIDEMIOL, V124, P275; Levy JI, 1998, J AIR WASTE MANAGE, V48, P553, DOI 10.1080/10473289.1998.10463704; Liard R, 1999, ENVIRON RES, V81, P339, DOI 10.1006/enrs.1999.3993; Linaker CH, 2000, THORAX, V55, P930, DOI 10.1136/thorax.55.11.930; Linaker CH, 2000, OCCUP ENVIRON MED, V57, P472, DOI 10.1136/oem.57.7.472; Magnus P, 1998, INT J EPIDEMIOL, V27, P995, DOI 10.1093/ije/27.6.995; Mukala K, 2000, ARCH ENVIRON HEALTH, V55, P431; Nitschke M, 1999, INT J ENVIRON HEAL R, V9, P39, DOI 10.1080/09603129973344; PALMES ED, 1976, AM IND HYG ASSOC J, V37, P570, DOI 10.1080/0002889768507522; PILOTTO LS, 2003, INT J EPIDEMIOL, V33, P208; Ponsonby AL, 2001, CLIN EXP ALLERGY, V31, P1205, DOI 10.1046/j.1365-2222.2001.01168.x; SAMET JM, 1993, AM REV RESPIR DIS, V148, P1258; Samet JM, 2004, INT J EPIDEMIOL, V33, P215, DOI 10.1093/ije/dyh045; SAMET JM, 1990, TOXICOL IND HEALTH, V6, P247; Shima M, 2000, INT J EPIDEMIOL, V29, P862, DOI 10.1093/ije/29.5.862; Smith BJ, 2000, EUR RESPIR J, V16, P879, DOI 10.1183/09031936.00.16587900; Spengler J. D., 1996, RES REP HLTH EFFECTS, V58, P1; Strachan DP, 2000, BRIT MED BULL, V56, P865, DOI 10.1258/0007142001903562; Sunyer J, 2004, INT J EPIDEMIOL, V33, P116, DOI 10.1093/ije/dyh037; *US CENS BUR, 2000, CENS POP HOUS SUMM; U.S. Environmental Protection Agency, 2005, NAT AMB AIR QUAL STA; Utell M, 1997, COMPREHENSIVE TOXICO, P303; van Strien RT, 2004, EPIDEMIOLOGY, V15, P471, DOI 10.1097/01.ede.0000129511.61698.d8; VOLKMER RE, 1995, J PAEDIATR CHILD H, V31, P116, DOI 10.1111/j.1440-1754.1995.tb00758.x; WHO, 2000, AIR QUAL GUID EUR	45	80	84	2	15	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	FEB 1	2006	173	3					297	303		10.1164/rccm.200408-1123OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	007IJ	WOS:000234962000009	16254270	
J	Eisner, MD; Klein, J; Hammond, SK; Koren, G; Lactao, G; Iribarren, C				Eisner, MD; Klein, J; Hammond, SK; Koren, G; Lactao, G; Iribarren, C			Directly measured second hand smoke exposure and asthma health outcomes	THORAX			English	Article							ENVIRONMENTAL TOBACCO-SMOKE; QUALITY-OF-LIFE; PASSIVE SMOKING; WORK DISABILITY; NEONATAL HAIR; BETA-AGONISTS; ADULT ASTHMA; NICOTINE; RISK; COTININE	Background: Because they have chronic airway inflammation, adults with asthma could have symptomatic exacerbation after exposure to second hand smoke (SHS). Surprisingly, data on the effects of SHS exposure in adults with asthma are quite limited. Most previous epidemiological studies used self-reported SHS exposure which could be biased by inaccurate reporting. In a prospective cohort study of adult nonsmokers recently admitted to hospital for asthma, the impact of SHS exposure on asthma health outcomes was examined. Methods: Recent SHS exposure during the previous 7 days was directly measured using a personal nicotine badge (n = 189) and exposure during the previous 3 months was estimated using hair nicotine and cotinine levels (n = 138). Asthma severity and health status were ascertained during telephone interviews, and subsequent admission to hospital for asthma was determined from computerised utilisation databases. Results: Most of the adults with asthma were exposed to SHS, with estimates ranging from 60% to 83% depending on the time frame and methodology. The highest level of recent SHS exposure, as measured by the personal nicotine badge, was related to greater asthma severity (mean score increment for highest tertile of nicotine level 1.56 points; 95% CI 0.18 to 2.95), controlling for sociodemographic covariates and previous smoking history. Moreover, the second and third tertiles of hair nicotine exposure during the previous month were associated with a greater baseline prospective risk of hospital admission for asthma (HR 3.73; 95% CI 1.04 to 13.30 and HR 3.61; 95% CI 1.0 to 12.9, respectively). Conclusions: Directly measured SHS exposure appears to be associated with poorer asthma outcomes. In public health terms, these results support efforts to prohibit smoking in public places.	Univ Calif San Francisco, Dept Med, Div Environm & Occupat Med, San Francisco, CA 94117 USA; Univ Calif San Francisco, Dept Med, Div Pulm & Crit Care Med, San Francisco, CA 94117 USA; Kaiser Permanente, Div Res, Oakland, CA USA; Hosp Sick Children, Motherisk, Fetal Toxicol Lab, Toronto, ON M5G 1X8, Canada; Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA	Eisner, MD (reprint author), Univ Calif San Francisco, Dept Med, Div Environm & Occupat Med, 350 Parnassus Ave,Ste 609, San Francisco, CA 94117 USA.	eisner@itsa.ucsf.edu	Travers, Mark/C-7832-2011		NHLBI NIH HHS [K23 HL04201]		Allison P. D., 1995, SURVIVAL ANAL USING; Blanc P, 2000, CHEST, V118, P564, DOI 10.1378/chest.118.2.564; Blanc PD, 1999, AM J RESP CRIT CARE, V160, P2028; California Environmental Protection Agency, 1997, HLTH EFF EXP ENV TOB; Chan D, 2004, CLIN BIOCHEM, V37, P429, DOI 10.1016/j.clinbiochem.2004.01.01; COGHLIN J, 1989, AM J EPIDEMIOL, V130, P696; Coultas DB, 1998, THORAX, V53, P381; DimichWard H, 1997, J OCCUP ENVIRON MED, V39, P946, DOI 10.1097/00043764-199710000-00006; Eisner MD, 1998, MED CARE, V36, P1567, DOI 10.1097/00005650-199811000-00006; Eisner MD, 2002, AM J PUBLIC HEALTH, V92, P1506, DOI 10.2105/AJPH.92.9.1506; Eisner MD, 2002, THORAX, V57, P973, DOI 10.1136/thorax.57.11.973; Eisner MD, 2002, CHEST, V122, P826, DOI 10.1378/chest.122.3.826; Eisner MD, 2001, ENVIRON HEALTH PERSP, V109, P809, DOI 10.2307/3454823; Eisner MD, 2001, EUR RESPIR J, V17, P233, DOI 10.1183/09031936.01.17202330; EISNER MD, 2002, AM J RESP CRIT CARE, V165, pA121; Eliopoulos C, 1996, CLIN INVEST MED, V19, P231; ELIOPOULOS C, 1994, JAMA-J AM MED ASSOC, V271, P621, DOI 10.1001/jama.271.8.621; HAMMOND SK, 1987, ENVIRON SCI TECHNOL, V21, P494, DOI 10.1021/es00159a012; HAMMOND SK, 1995, JAMA-J AM MED ASSOC, V274, P956, DOI 10.1001/jama.274.12.956; Iribarren C, 2001, J EPIDEMIOL COMMUN H, V55, P721, DOI 10.1136/jech.55.10.721; Jaakkola MS, 1997, EUR RESPIR J, V10, P2384, DOI 10.1183/09031936.97.10102384; JINDAL SK, 1994, CHEST, V106, P746, DOI 10.1378/chest.106.3.746; Karter AJ, 2002, JAMA-J AM MED ASSOC, V287, P2519, DOI 10.1001/jama.287.19.2519; Katz PP, 1999, J CLIN EPIDEMIOL, V52, P667, DOI 10.1016/S0895-4356(99)00026-8; KLEIN J, 1994, THER DRUG MONIT, V16, P67, DOI 10.1097/00007691-199402000-00011; KLEIN J, 1993, NEW ENGL J MED, V328, P66, DOI 10.1056/NEJM199301073280116; Klein J, 1999, HUM EXP TOXICOL, V18, P279, DOI 10.1191/096032799678840048; Knight JM, 1998, J ASTHMA, V35, P113, DOI 10.3109/02770909809055412; KRIEGER N, 1992, AM J PUBLIC HEALTH, V82, P703, DOI 10.2105/AJPH.82.5.703; Lieu TA, 1999, J ASTHMA, V36, P359, DOI 10.3109/02770909909068229; MARKS GB, 1993, J CLIN EPIDEMIOL, V46, P1103, DOI 10.1016/0895-4356(93)90109-E; MARKS GB, 1992, J CLIN EPIDEMIOL, V45, P461, DOI 10.1016/0895-4356(92)90095-5; Nafstad P, 1998, AM J PUBLIC HEALTH, V88, P120, DOI 10.2105/AJPH.88.1.120; National Heart Lung and Blood Institute, 1991, J ALLERGY CLIN IMMUN, V88, P425; NILSEN T, 1994, PHARMACOL TOXICOL, V75, P136; OSBORNE ML, 1992, J CLIN EPIDEMIOL, V45, P403, DOI 10.1016/0895-4356(92)90041-K; Osman LM, 2000, AM J RESP CRIT CARE, V161, P498; OSTRO BD, 1994, AM J RESP CRIT CARE, V149, P1400; SCHOENFELD D, 1982, BIOMETRIKA, V69, P239, DOI 10.1093/biomet/69.1.239; Sippel JM, 1999, CHEST, V115, P691, DOI 10.1378/chest.115.3.691; SPITZER WO, 1992, NEW ENGL J MED, V326, P501, DOI 10.1056/NEJM199202203260801; Ware JE, 1996, MED CARE, V34, P220, DOI 10.1097/00005650-199603000-00003; Weiss ST, 1999, ENVIRON HEALTH PERSP, V107, P891, DOI 10.2307/3434571; Zahlsen K, 1996, PHARMACOL TOXICOL, V79, P183; 1999, MMWR, V48, P993	45	80	81	1	6	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	OCT	2005	60	10					814	821		10.1136/thx.2004.037283		8	Respiratory System	Respiratory System	968QS	WOS:000232177800009	16192366	
J	Comhair, SAA; Ricci, KS; Arroliga, M; Lara, AR; Dweik, RA; Song, W; Hazen, SL; Bleecker, ER; Busse, WW; Chung, KF; Gaston, B; Hastie, A; Hew, M; Jarjour, N; Moore, W; Peters, S; Teague, WG; Wenzel, SE; Erzurum, SC				Comhair, SAA; Ricci, KS; Arroliga, M; Lara, AR; Dweik, RA; Song, W; Hazen, SL; Bleecker, ER; Busse, WW; Chung, KF; Gaston, B; Hastie, A; Hew, M; Jarjour, N; Moore, W; Peters, S; Teague, WG; Wenzel, SE; Erzurum, SC		Severe Asthma Res Program National	Correlation of systemic superoxide dismutase deficiency to airflow obstruction in asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							EOSINOPHIL PEROXIDASE; IN-VIVO; OXIDATIVE STRESS; GLUTATHIONE-PEROXIDASE; ANTIOXIDANT ENZYMES; ENHANCED PRODUCTION; TYROSINE NITRATION; OXYGEN RADICALS; LUNG-DISEASES; MILD ASTHMA	Rationale: Increased oxidative stress and decreased superoxide dismutase (SOD) activity in the asthmatic airway are correlated to airflow limitation and hyperreactivity. We hypothesized that asthmatic individuals with higher levels of oxidative stress may have greater loss of SOD activity, which would be reflected systemically in loss of circulating SOD activity and clinically by development of severe asthma and/or worsening airflow limitation. Methods: To investigate this, serum SOD activity and proteins, the glutathione peroxidase/glutathione antioxidant system, and oxidatively modified amino acids were measured in subjects with asthma and healthy control subjects. Results: SOD activity, but not Mn-SOD or Cu,Zn-SOD protein, was lower in asthmatic serum as compared with control, and activity loss was significantly related to airflow limitation. Further, serum SOD activity demonstrated an inverse correlation with circulating levels of 3-bromotyrosine, a posttranslational modification of proteins produced by the eosinophil peroxidase system of eosinophils. Exposure of purified Cu,Zn-SOD to physiologically relevant levels of eosinophil peroxidase-generated reactive brominating species reactive nitrogen species, or tyrosyl radicals in vitro confirmed that eosinophil-derived oxidative pathways promote enzyme inactivation. Conclusion: These findings are consistent with greater oxidant stress in asthma leading to greater inactivation of SOD, which likely amplifies inflammation and progressive airflow obstruction.	Cleveland Clin Fdn, Dept Pathobiol, Cleveland, OH 44195 USA; Cleveland Clin Fdn, Dept Pulm, Cleveland, OH 44195 USA; Cleveland Clin Fdn, Dept Allergy, Cleveland, OH 44195 USA; Cleveland Clin Fdn, Dept Crit Care Med, Cleveland, OH 44195 USA; Cleveland Clin Fdn, Dept Cell Biol, Cleveland, OH 44195 USA; Cleveland Clin Fdn, Ctr Cardiovasc Diagnost & Prevent, Lerner Res Inst, Cleveland, OH 44195 USA	Comhair, SAA (reprint author), Cleveland Clin Fdn, Dept Pathobiol, 9500 Euclid Ave,NB40, Cleveland, OH 44195 USA.	comhais@ccf.org		Chung, Kian Fan/0000-0001-7101-1426	NCRR NIH HHS [M01 RR018390]; NHLBI NIH HHS [HL 07649, HL04265, HL61878, HL69116, HL69130, HL69155, HL69167, HL69170, HL69174, HL69349, P01/U01HL67663, U10HL74225]; NIAID NIH HHS [AI70649]		Alvarez B, 2004, FREE RADICAL BIO MED, V37, P813, DOI 10.1016/j.freeradbiomed.2004.06.006; American Thoracic Society, 2000, AM J RESP CRIT CARE, V162, P2341, DOI DOI 10.1164/AJRCCM.162.6.ATS9-00; Andreadis AA, 2003, FREE RADICAL BIO MED, V35, P213, DOI 10.1016/S0891-5849(03)00278-8; Bowler RP, 2002, J ALLERGY CLIN IMMUN, V110, P349, DOI 10.1067/mai.2002.126780; BRACCI R, 1970, BIOL NEONATE, V15, P135; Brennan ML, 2002, J BIOL CHEM, V277, P17415, DOI 10.1074/jbc.M112400200; CALHOUN WJ, 1992, AM REV RESPIR DIS, V145, P317; Chang LY, 2002, FREE RADICAL BIO MED, V33, P379, DOI 10.1016/S0891-5849(02)00919-X; Comhair SAA, 1999, AM J RESP CRIT CARE, V159, P1824; Comhair SAA, 2005, AM J PATHOL, V166, P663, DOI 10.1016/S0002-9440(10)62288-2; Comhair SAA, 2000, LANCET, V355, P624, DOI 10.1016/S0140-6736(99)04736-4; Comhair SAA, 2002, AM J PHYSIOL-LUNG C, V283, pL246, DOI 10.1152/ajplung.00491.2001; Comhair SAA, 2001, FASEB J, V15, P70, DOI 10.1096/fj.00-0085com; COMHAIR SAA, 2005, P AM THORAC SOC, V2, pA240; DEMOLY P, 1994, J ALLERGY CLIN IMMUN, V93, P108, DOI 10.1016/0091-6749(94)90239-9; DeRaeve HR, 1997, AM J PHYSIOL-LUNG C, V272, pL148; Dweik RA, 2001, P NATL ACAD SCI USA, V98, P2622, DOI 10.1073/pnas.051629498; Eiserich JP, 2002, SCIENCE, V296, P2391, DOI 10.1126/science.1106830; ERZURUM SC, 1993, J APPL PHYSIOL, V75, P1256; FLATT A, 1990, THORAX, V45, P95, DOI 10.1136/thx.45.2.95; GASTON B, 1994, AM J RESP CRIT CARE, V149, P538; Guo W, 2003, AM J PHYSIOL-HEART C, V285, pH1396, DOI 10.1152/ajpheart.00096.2003; Haahtela T, 1997, CLIN EXP ALLERGY, V27, P351; HASS MA, 1989, J CLIN INVEST, V83, P1241, DOI 10.1172/JCI114007; JARJOUR NN, 1994, J LAB CLIN MED, V123, P131; JARJOUR NN, 1992, AM REV RESPIR DIS, V146, P905; Joseph-Bowen J, 2004, J ALLERGY CLIN IMMUN, V114, P1040, DOI 10.1016/j.jaci.2004.07.051; KARLSSON K, 1988, BIOCHIM BIOPHYS ACTA, V967, P110, DOI 10.1016/0304-4165(88)90195-X; Kelly FK, 1999, LANCET, V354, P482, DOI 10.1016/S0140-6736(99)01812-7; Kinnula VL, 2003, AM J RESP CRIT CARE, V167, P1600, DOI 10.1164/rccm.200212-1479SO; LARSEN GL, 2000, AM J PHYSIOL-LUNG C, V279, P350; MacMillan-Crow LA, 2001, FREE RADICAL BIO MED, V31, P1603, DOI 10.1016/S0891-5849(01)00750-X; MacMillan-Crow LA, 1999, ARCH BIOCHEM BIOPHYS, V366, P82, DOI 10.1006/abbi.1999.1202; MacMillanCrow LA, 1996, P NATL ACAD SCI USA, V93, P11853, DOI 10.1073/pnas.93.21.11853; MacPherson JC, 2001, J IMMUNOL, V166, P5763; Majori M, 1998, EUR RESPIR J, V11, P133, DOI 10.1183/09031936.98.11010133; Mak JCW, 2004, J ALLERGY CLIN IMMUN, V114, P260, DOI 10.1016/j.jaci.2004.05.013; Mamo LB, 2004, AM J RESP CRIT CARE, V170, P313, DOI 10.1164/rccm.200309-1282OC; MASINI EVA, 2001, AM J RESP CRIT CARE, V163, pA813; Montuschi P, 1999, AM J RESP CRIT CARE, V160, P216; Nadeem A, 2003, J ALLERGY CLIN IMMUN, V111, P72, DOI 10.1067/mai.2003.17; NEBOT C, 1993, ANAL BIOCHEM, V214, P442, DOI 10.1006/abio.1993.1521; PerrinNadif R, 1996, OCCUP ENVIRON MED, V53, P41; Rahman I, 2000, THORAX, V55, P189, DOI 10.1136/thorax.55.3.189; Rubin RN, 2004, AM J RESP CRIT CARE, V169, P393, DOI 10.1164/rccm.200301-055OC; SALO DC, 1990, J BIOL CHEM, V265, P11919; SANDSTROM J, 1994, J BIOL CHEM, V269, P19163; Sanz ML, 1997, ALLERGY, V52, P417, DOI 10.1111/j.1398-9995.1997.tb01021.x; Schunemann HJ, 2001, AM J RESP CRIT CARE, V163, P1246; SHARONOV BP, 1992, BIOCHEM BIOPH RES CO, V189, P1129, DOI 10.1016/0006-291X(92)92321-N; SHULL S, 1991, J BIOL CHEM, V266, P24398; Smith LJ, 1997, FREE RADICAL BIO MED, V22, P1301, DOI 10.1016/S0891-5849(96)00550-3; SMITH LJ, 1993, AM REV RESPIR DIS, V147, P1461; VACHIER I, 1992, AM REV RESPIR DIS, V146, P1161; Wood LG, 2000, LIPIDS, V35, P967, DOI 10.1007/s11745-000-0607-x; Wu WJ, 2000, J CLIN INVEST, V105, P1455, DOI 10.1172/JCI9702; Wu WJ, 1999, J BIOL CHEM, V274, P25933, DOI 10.1074/jbc.274.36.25933; Wu WJ, 1999, BIOCHEMISTRY-US, V38, P3538, DOI 10.1021/bi982401l	58	80	82	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.	AUG 1	2005	172	3					306	313		10.1164/rccm.200502-180OC		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	949IM	WOS:000230778600007	15883124	
J	Green, BJ; Sercombe, JK; Tovey, ER				Green, BJ; Sercombe, JK; Tovey, ER			Fungal fragments and undocumented conidia function as new aeroallergen sources	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergen; Alternaria species; antigen; conidia; fragment; fungal; hyphae; germination; immunoassay; mold	ALTERNARIA; ASTHMA; GERMINATION; ALLERGENS; EXPOSURE; SPORES	Background: More than 100 genera of fungal conidia are currently recognized as sources of allergens. The contribution of other fungal genera plus airborne fungal hyphae and fragmented conidia to allergic diseases is poorly understood. Objective: We sought to investigate the expression of allergens from airborne wild-type fungi using the Halogen immunoassay, which uses allergic serum IgE to immunostain immobilized allergens extracted from individual fungal particles. Methods: Airborne fungi were collected onto mixed cellulose ester protein-binding membranes for 2.5 hours with volumetric air pumps. Collected fungi were incubated overnight in a humid chamber to promote the germination of conidia. The membranes were laminated with an adhesive cover slip and immunostained with an Altentaria species-sensitive serum IgE pool. The samples were examined by means of light microscopy, and positively immunostained fungal particles were classified and counted. Results: All air samples contained fungal hyphae that expressed soluble allergens and were significantly higher in concentration than counts of conidia of individual well-ebaracterized allergenic genera (P &LT; .05). Resultant immunostaining of fungal hyphae was heterogeneous, and approximately 25% of all hyphae expressed detectable allergen compared with nonstained hyphae (P &LT; .05). Fungal conidia of 10 genera that were previously uncharacterized as allergen sources were shown to demonstrate IgE binding to expressed antigens and accounted for 8% of the total airborne conidia count. Conclusions: Our analysis of wild-type fungi collected indoors presents a new paradigm of natural fungal exposure, which, in addition to commonly recognized species, implicates airborne hyphae, fragmented conidia, and the conidia of a much more diverse range of genera as airborne allergens.	Univ Sydney, Dept Med, Woolcock Allergen Unit, Sydney, NSW 2006, Australia	Green, BJ (reprint author), Univ Sydney, Dept Med, Woolcock Allergen Unit, Room 461,Blackburn Bldg D06, Sydney, NSW 2006, Australia.	brettg@mail.med.usyd.edu.au	Tovey, Euan/G-8604-2017	Tovey, Euan/0000-0002-1802-7266			Black PN, 2000, ALLERGY, V55, P501, DOI 10.1034/j.1398-9995.2000.00293.x; Burge HA, 2000, CURR MICROBIOL, V40, P10, DOI 10.1007/s002849910003; Delfino RJ, 1997, ENVIRON HEALTH PERSP, V105, P622; Downs SH, 2001, AM J RESP CRIT CARE, V164, P455; Gorny RL, 2002, APPL ENVIRON MICROB, V68, P3522, DOI 10.1128/AEM.68.7.3522-3531.2002; Gots RE, 2003, AIHA J-J SCI OCCUP E, V64, P427, DOI 10.1202/396.1; Green BJ, 2003, J ALLERGY CLIN IMMUN, V111, P285, DOI 10.1067/mai.2003.57; HORNER WE, 1995, CLIN MICROBIOL REV, V8, P161; Levestin E., 1995, BIOAEROSOLS, P87; Li DW, 1995, MYCOPATHOLOGIA, V131, P149, DOI 10.1007/BF01102894; Li ZJ, 2002, BIOTECHNOL LETT, V24, P1, DOI 10.1023/A:1013848325193; LICORISH K, 1985, J ALLERGY CLIN IMMUN, V76, P819, DOI 10.1016/0091-6749(85)90755-9; MARFENINA OE, 1994, MICROBIOLOGY+, V63, P603; MARK D, 1986, ANN OCCUP HYG, V30, P89, DOI 10.1093/annhyg/30.1.89; Mitakakis TZ, 2001, J ALLERGY CLIN IMMUN, V107, P388, DOI 10.1067/mai.2001.112602; Mitakakis TZ, 2000, CLIN EXP ALLERGY, V30, P1733, DOI 10.1046/j.1365-2222.2000.00966.x; PAUL GC, 1994, BIOTECHNOL BIOENG, V44, P655, DOI 10.1002/bit.260440513	17	80	82	1	5	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	MAY	2005	115	5					1043	1048		10.1016/j.jaci.2005.02.009		6	Allergy; Immunology	Allergy; Immunology	925LR	WOS:000229055100022	15867864	
J	Korppi, M; Piippo-Savolainen, E; Korhonen, K; Remes, S				Korppi, M; Piippo-Savolainen, E; Korhonen, K; Remes, S			Respiratory morbidity 20 years after RSV infection in infancy	PEDIATRIC PULMONOLOGY			English	Article						respiratory syncytial virus; bronchiolitis; pneumonia; lung function; asthma; atopy; childhood; adulthood	SYNCYTIAL VIRUS BRONCHIOLITIS; BRONCHIAL-ASTHMA; AGE; CHILDHOOD; CHILDREN; ALLERGY; HISTORY; ILLNESS; ATOPY; RISK	Epidemiological data suggest that respiratory syncytial virus (RSV) infection in early life is a risk factor for later asthma. There are no prospective studies on RSV infection starting from infancy progressing through childhood into adulthood. We followed up a cohort of children, hospitalized for RSV bronchiolitis or RSV pneumonia before age 24 months, until age 18-20 years. The aim of the study was to evaluate early RSV infection as a risk factor for asthma, bronchial reactivity, and lung function abnormalities in young adults. The participants filled in a questionnaire on asthma and asthma-like symptoms. The clinical study included flow-volume spirometry (FVS), methacholine inhalation challenge (MIC), home PEF (peak expiratory flow) monitoring, and skin prick tests (SPT) to common allergens. Asthma was present in 17-22% of 36 index subjects, depending on asthma definition, compared to 11% of 45 controls. Furthermore, FEV% and MEF25 were lower, and MEF50 tended to be lower, in index than in control subjects. One or more abnormal lung function results were found in 16 (44%) index subjects, but only in 5 (11%) controls (P < 0.01). Bronchial reactivity (PD20 <4,900 mug methacholine) was demonstrated in 16 (46%) index subjects and 14 (32%) controls (NS). At least one positive SPT result was present in 21 (60%) index subjects; 6 (29%) had asthma (NS vs. nonatopic index subjects); 13 (62%) had abnormal lung function (P < 0.05); and 14 (67%) had bronchial reactivity (P < 0.01). In the logistic regression adjusted for atopy, as defined by SPT positivity, RSV infection in infancy was an independent risk factor for lung function abnormality (one or more abnormal results in FVS; OR, 5.27; 95% Cl, 1.6017.36), and also for decreased FEV% and MEF50 when these were analyzed separately. However, RSV infection in infancy was not a significant risk factor for asthma or bronchial reactivity. In young adults, lung function abnormalities may be associated with RSV infection which required hospitalization in infancy. (C) 2004 Wiley-Liss, Inc.	Univ Kuopio, Dept Pediat, FIN-70210 Kuopio, Finland; Kuopio Univ Hosp, SF-70210 Kuopio, Finland	Korppi, M (reprint author), Univ Kuopio, Dept Pediat, FIN-70210 Kuopio, Finland.	matti.korppi@uku.fi					[Anonymous], 1993, ALLERGY, V48, P48; GASTRORODRIQUEZ J, 2000, AM J RESP CRIT CARE, V159, P1891; Guilbert T, 2003, PEDIATR CLIN N AM, V50, P523, DOI 10.1016/S0031-3955(03)00044-0; HAAHTELA T, 1979, ALLERGY, V34, P413, DOI 10.1111/j.1398-9995.1979.tb02011.x; Kneyber M, 2000, ACTA PAEDIATR, V89, P654, DOI 10.1080/080352500750043945; KORPPI M, 1993, AM J DIS CHILD, V147, P628; KORPPI M, 1986, ACTA PAEDIATR SCAND, V75, P457, DOI 10.1111/j.1651-2227.1986.tb10230.x; KORPPI M, 1994, ARCH PEDIAT ADOL MED, V148, P1079; KUIKKA L, 1994, ACTA PAEDIATR, V83, P744, DOI 10.1111/j.1651-2227.1994.tb13131.x; MACINTOSH K, 1987, PEDIAT REV, V9, P191; Martinez Fernando D, 2002, Paediatr Respir Rev, V3, P193, DOI 10.1016/S1526-0542(02)00188-4; MOK JYQ, 1982, BRIT MED J, V285, P333; MURRAY M, 1992, ARCH DIS CHILD, V67, P482; POYSA L, 1989, ACTA PAEDIATR SCAND, V78, P902, DOI 10.1111/j.1651-2227.1989.tb11172.x; PULLAN CR, 1982, BRIT MED J, V284, P1165; Remes ST, 1996, ACTA PAEDIATR, V85, P59, DOI 10.1111/j.1651-2227.1996.tb13891.x; SAMET JM, 1983, AM REV RESPIR DIS, V127, P508; SIGURS N, 1995, PEDIATRICS, V95, P500; Sigurs N, 2000, AM J RESP CRIT CARE, V161, P1501; SIMS DG, 1978, BRIT MED J, V1, P11; Stein R, 1999, LANCET, V354, P541, DOI 10.1016/S0140-6736(98)10321-5; Stein RT, 1997, THORAX, V52, P946; Strachan DP, 1996, AM J RESP CRIT CARE, V154, P1629; Taussig LM, 2003, J ALLERGY CLIN IMMUN, V111, P661, DOI 10.1067/mai.2003.162; Turner SW, 2002, ARCH DIS CHILD, V87, P417, DOI 10.1136/adc.87.5.417; Viljanen A A, 1982, Scand J Clin Lab Invest Suppl, V159, P5; Welliver R C, 1999, J Pediatr, V135, P14; Welliver RC, 2000, PEDIATR INFECT DIS J, V19, P780, DOI 10.1097/00006454-200008000-00030	28	80	85	0	3	WILEY-LISS	HOBOKEN	DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA	8755-6863			PEDIATR PULM	Pediatr. Pulmonol.	AUG	2004	38	2					155	160		10.1002/ppul.20058		6	Pediatrics; Respiratory System	Pediatrics; Respiratory System	840KM	WOS:000222857500010	15211700	
J	Shaheen, SO; Newson, RB; Henderson, AJ; Emmett, PM; Sherriff, A; Cooke, M				Shaheen, SO; Newson, RB; Henderson, AJ; Emmett, PM; Sherriff, A; Cooke, M		ALSPAC Study Team	Umbilical cord trace elements and minerals and risk of early childhood wheezing and eczema	EUROPEAN RESPIRATORY JOURNAL			English	Article						birth cohort; eczema; prenatal/foetal nutrition; trace elements/minerals; wheezing	CYTOKINE PRODUCTION; ATOPIC-DERMATITIS; IRON-DEFICIENCY; IMMUNE FUNCTION; FETAL-GROWTH; DISEASE; BIRTH; CHILDREN; ASTHMA; PREGNANCY	It has been suggested that foetal nutrition might influence the inception of wheezing and atopic disorders in childhood but specific nutrients have not been implicated. In the Avon Longitudinal Study of Parents and Children umbilical cord samples were assayed for trace elements and minerals, and mothers were asked about wheezing and eczema in their children. Associations of cord concentrations of selenium, zinc, copper, manganese, magnesium, iron, lead and mercury with wheezing at 30-42 months, with wheezing patterns defined by the presence or absence of transient infant, later onset or persistent wheezing at 0-6 months and 30-42 months, respectively (n=2,044), and with eczema at 18-30 months (n=2,173), were analysed. Cord selenium was negatively associated with persistent wheeze (adjusted odds ratio (OR) per doubling concentration: 0.67). Cord iron was negatively associated with later onset wheeze (OR: 0.86) and with eczema (OR: 0.90). Children with high cord concentrations of selenium and iron were less likely than those with low concentrations to wheeze transiently in infancy. The level of foetal exposure to selenium and iron may possibly influence the risk of wheezing and eczema in early childhood although, in view of the multiple analyses carried out, it is possible that the main findings occurred by chance.	Kings Coll London, Guys Kings & St Thomas Sch Med, Dept Publ Hlth Sci, London SE1 3QD, England; Univ London, Royal Holloway & Bedford New Coll, Ctr Chem Sci, London SE1 3QD, England; Univ Bristol, Inst Child Hlth, Unit Paediat & Perinatal Epidemiol, Bristol, Avon, England	Shaheen, SO (reprint author), Kings Coll London, Guys Kings & St Thomas Sch Med, Dept Publ Hlth Sci, Capital House,42 Weston St, London SE1 3QD, England.	seif.shaheen@kcl.ac.uk		Henderson, Alexander John/0000-0001-9650-231X; Emmett, Pauline/0000-0003-1076-4779			Akagi H, 1998, ENVIRON RES, V77, P98, DOI 10.1006/enrs.1997.3822; Benjamini Y, 2001, BEHAV BRAIN RES, V125, P279, DOI 10.1016/S0166-4328(01)00297-2; BRITTON J, 1994, LANCET, V344, P357, DOI 10.1016/S0140-6736(94)91399-4; Brock JH, 2000, P NUTR SOC, V59, P537, DOI 10.1017/S002966510000077X; Fergusson DM, 1997, CLIN EXP ALLERGY, V27, P1394, DOI 10.1046/j.1365-2222.1997.1430947.x; Gambling L, 2002, BIOL REPROD, V66, P516, DOI 10.1095/biolreprod66.2.516; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; Golding J, 2001, PAEDIATR PERINAT EP, V15, P74; Gregory A, 1999, CLIN EXP ALLERGY, V29, P330; Harding JE, 2001, INT J EPIDEMIOL, V30, P15, DOI 10.1093/ije/30.1.15; Heo Y, 1996, TOXICOL APPL PHARM, V138, P149, DOI 10.1006/taap.1996.0108; Jason J, 2001, CLIN EXP IMMUNOL, V126, P466, DOI 10.1046/j.1365-2249.2001.01707.x; KIM HY, 1991, PEDIATR RES, V29, P440, DOI 10.1203/00006450-199105010-00006; Klesges LM, 1998, AM J EPIDEMIOL, V147, P127; Kugelmas V, 2000, J TRACE ELEM EXP MED, V13, P327; Langley-Evans S, 1997, CLIN EXP ALLERGY, V27, P1377, DOI 10.1046/j.1365-2222.1997.1690965.x; Leadbitter P, 1999, THORAX, V54, P905; Levander OA, 1986, J AM COLL TOXICOL, V5, P37; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Mathews F, 1998, J HUM NUTR DIET, V11, P151; McKeever TM, 2002, AM J RESP CRIT CARE, V166, P827, DOI 10.1164/rccm.200202-158OC; Miller TE, 1998, TOXICOL SCI, V42, P129, DOI 10.1006/toxs.1998.2424; Myers GJ, 2003, LANCET, V361, P1686, DOI 10.1016/S0140-6736(03)13371-5; NISHIGAKI S, 1975, NATURE, V258, P324, DOI 10.1038/258324a0; Olesen AB, 1997, BRIT MED J, V314, P1003; Oryszczyn MP, 1999, CLIN EXP ALLERGY, V29, P334; Paeratakul S, 1998, EUR J CLIN NUTR, V52, P722, DOI 10.1038/sj.ejcn.1600633; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; Rayman MP, 1997, BRIT MED J, V314, P387; Rogers I, 1998, EUR J CLIN NUTR, V52, P246, DOI 10.1038/sj.ejcn.1600543; SCHWARTZ J, 1990, AM REV RESPIR DIS, V142, P555; Shaheen SO, 2002, THORAX, V57, P958, DOI 10.1136/thorax.57.11.958; Sherriff A, 2001, INT J EPIDEMIOL, V30, P1473, DOI 10.1093/ije/30.6.1473; Sprietsma JE, 1999, MED HYPOTHESES, V53, P6, DOI 10.1054/mehy.1999.0867; Stata, 2001, STAT STAT SOFTW REL; THIBAULT H, 1993, EUR J PEDIATR, V152, P120, DOI 10.1007/BF02072487; WEGMANN TG, 1993, IMMUNOL TODAY, V14, P353, DOI 10.1016/0167-5699(93)90235-D; Weiss G, 2002, EUR J CLIN INVEST, V32, P70, DOI 10.1046/j.1365-2362.2002.0320s1070.x; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P383, DOI 10.1111/j.1365-2133.1994.tb08530.x; Zhang ZW, 1999, EUR J CLIN NUTR, V53, P226, DOI 10.1038/sj.ejcn.1600711	40	80	81	3	8	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. 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J	Gangloff, M; Gay, NJ				Gangloff, M; Gay, NJ			MD-2: the Toll 'gatekeeper' in endotoxin signalling	TRENDS IN BIOCHEMICAL SCIENCES			English	Editorial Material							DUST-MITE ALLERGEN; CONFERS LIPOPOLYSACCHARIDE RESPONSIVENESS; N-LINKED GLYCOSYLATIONS; LPS BINDING-PROTEIN; CRYSTAL-STRUCTURE; DROSOPHILA TOLL; GM2-ACTIVATOR PROTEIN; ANGSTROM RESOLUTION; ESCHERICHIA-COLI; INNATE IMMUNITY	Lipopolysaccharide (LPS) from the outer cell wall of Gram-negative bacteria is a potent stimulator of the mammalian innate immune system. The Toll-like receptor 4 (TLR4) pathway triggers the inflammatory responses induced by LPS in a process that requires the interaction of LPS-bound myeloid differentiation-2 (MD-2) with TLR4. Here we propose two possible mechanisms for LPS recognition and signalling that take into account both the structural information available for TLR4 and MD-2, and the determinants of endotoxicity, namely, the acylation and phosphorylation patterns of LIPS. In our first model, LPS induces the association of two TLR4-MD-2 heterodimers by binding to two different molecules of MD-2 through the acyl chains of lipid A. In our second model, the binding of LPS to a single TLR4-MD-2 complex facilitates the recruitment of a second TLR4-MD-2 heterodimer. These models contrast with the activation of Drosophila Toll, where the receptor is crosslinked by a dimeric protein ligand.	Univ Cambridge, Dept Biochem, Cambridge CB2 1GA, England	Gangloff, M (reprint author), Univ Cambridge, Dept Biochem, 80 Tennis Court Rd, Cambridge CB2 1GA, England.	njg11@mole.bio.cam.ac.uk		Gangloff, Monique/0000-0001-6131-0115	Medical Research Council [G0400007, G1000133]		Akashi S, 2003, J EXP MED, V198, P1035, DOI 10.1084/jem.20031076; Beamer LJ, 1997, SCIENCE, V276, P1861, DOI 10.1126/science.276.5320.1861; Belvin MP, 1996, ANNU REV CELL DEV BI, V12, P393, DOI 10.1146/annurev.cellbio.12.1.393; Buchanan SGS, 1996, PROG BIOPHYS MOL BIO, V65, P1, DOI 10.1016/S0079-6107(96)00003-X; Correia JD, 2002, J BIOL CHEM, V277, P1845, DOI 10.1074/jbc.M109910200; DeLotto Y, 1998, MECH DEVELOP, V72, P141, DOI 10.1016/S0925-4773(98)00024-0; Derewenda U, 2002, J MOL BIOL, V318, P189, DOI 10.0000/S0022-2836(02)00027-X; DIN ZZ, 1993, BIOCHEMISTRY-US, V32, P4579, DOI 10.1021/bi00068a014; Erridge C, 2002, MICROBES INFECT, V4, P837, DOI 10.1016/S1286-4579(02)01604-0; Ferguson AD, 1998, SCIENCE, V282, P2215, DOI 10.1126/science.282.5397.2215; Ferguson AD, 2000, STRUCT FOLD DES, V8, P585; Friedland N, 2003, P NATL ACAD SCI USA, V100, P2512, DOI 10.1073/pnas.0437840100; Gangloff M, 2003, BIOCHEM SOC T, V31, P659, DOI 10.1042/BST0310659; Golenbock DT, 2001, NAT IMMUNOL, V2, P286, DOI 10.1038/86289; HAILMAN E, 1994, J EXP MED, V179, P269, DOI 10.1084/jem.179.1.269; He XLL, 2003, NEURON, V38, P177, DOI 10.1016/S0896-6273(03)00232-0; HOESS A, 1993, EMBO J, V12, P3351; Huizinga EG, 2002, SCIENCE, V297, P1176, DOI 10.1126/science.107355; Ichikawa S, 1998, J BIOL CHEM, V273, P356, DOI 10.1074/jbc.273.1.356; Imler JL, 2001, TRENDS CELL BIOL, V11, P304, DOI 10.1016/S0962-8924(01)02004-9; Inohara N, 2002, TRENDS BIOCHEM SCI, V27, P219, DOI 10.1016/S0968-0004(02)02084-4; Jack RS, 1997, NATURE, V389, P742, DOI 10.1038/39622; Janeway CA, 2002, ANNU REV IMMUNOL, V20, P197, DOI 10.1146/annurev.immunol.20.083001.084359; Liang J, 1998, PROTEIN SCI, V7, P1884; LUGTENBERG B, 1983, BIOCHIM BIOPHYS ACTA, V737, P51, DOI 10.1016/0304-4157(83)90014-X; Mancek M, 2002, BIOCHEM BIOPH RES CO, V292, P880, DOI 10.1006/bbrc.2002.6748; Medzhitov R, 1997, NATURE, V388, P394; Mizuguchi K, 1998, TRENDS BIOCHEM SCI, V23, P239, DOI 10.1016/S0968-0004(98)01216-X; MORISATO D, 1994, CELL, V76, P677, DOI 10.1016/0092-8674(94)90507-X; Mueller GA, 1998, BIOCHEMISTRY-US, V37, P12707, DOI 10.1021/bi980578+; Mueller GA, 1997, J BIOL CHEM, V272, P26893, DOI 10.1074/jbc.272.43.26893; Nagai Y, 2002, NAT IMMUNOL, V3, P667, DOI 10.1038/ni809; Ohnishi T, 2001, J IMMUNOL, V167, P3354; Parker JS, 2001, PROTEINS, V45, P71, DOI 10.1002/prot.1125; Pellegrini L, 2001, CURR OPIN STRUC BIOL, V11, P629, DOI 10.1016/S0959-440X(00)00258-X; 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; Re F, 2002, J BIOL CHEM, V277, P23427, DOI 10.1074/jbc.M202554200; Rock FL, 1998, P NATL ACAD SCI USA, V95, P588, DOI 10.1073/pnas.95.2.588; SALI A, 1993, J MOL BIOL, V234, P779, DOI 10.1006/jmbi.1993.1626; Schromm AB, 2001, J EXP MED, V194, P79, DOI 10.1084/jem.194.1.79; 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; Vigers GPA, 1997, NATURE, V386, P190, DOI 10.1038/386190a0; 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; Weber ANR, 2003, NAT IMMUNOL, V4, P794, DOI 10.1038/ni955; 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; WRIGHT SD, 1989, J EXP MED, V170, P1231, DOI 10.1084/jem.170.4.1231; WRIGHT SD, 1990, SCIENCE, V249, P1431, DOI 10.1126/science.1698311	52	80	85	0	1	ELSEVIER SCIENCE LONDON	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0968-0004			TRENDS BIOCHEM SCI	Trends Biochem.Sci.	JUN	2004	29	6					294	300		10.1016/j.tibs.2004.04.008		7	Biochemistry & Molecular Biology	Biochemistry & Molecular Biology	834KR	WOS:000222410500006	15276183	
J	Harik-Khan, RI; Muller, DC; Wise, RA				Harik-Khan, RI; Muller, DC; Wise, RA			Serum vitamin levels and the risk of asthma in children	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						adolescent; antioxidants; ascorbic acid; asthma; child	NUTRITION-EXAMINATION-SURVEY; NATIONAL-HEALTH; ASCORBIC-ACID; PULMONARY-FUNCTION; BRONCHIAL-ASTHMA; ALPHA-TOCOPHEROL; RESPONSIVENESS; ANTIOXIDANTS; CONSUMPTION; HISTAMINE	Dietary intake, especially of antioxidant vitamins A, C, E, and the carotenoids, has been linked with the presence and severity of asthma. From the Third National Health and Nutrition Examination Survey (NHANES III), conducted in the United States between 1988 and 1994, the authors selected 4,093 children (aged 6-17 years) for whom relevant medical, socioeconomic, and anthropometric data were complete. The children were 50.6% female, and 9.7% reported a diagnosis of asthma. Bivariate analyses showed that asthma diagnosis was associated with lower levels of serum vitamin C, alpha-carotene, beta-carotene, and beta-cryptoxanthin. However, antioxidant levels may be surrogate markers for socioeconomic variables such as race, poverty, tobacco exposure, or general nutritional status. In logistic models that included age, body mass index, socioeconomic variables, antioxidant levels, parental asthma, and household smoking, the only antioxidants significantly associated with asthma were vitamin C (odds ratio = 0.72 per mg/dl, 95% confidence interval = 0.55, 0.95) and alpha-carotene (odds ratio = 0.95 per mug/dl, 95% confidence interval = 0.90, 0.99). The odds ratio for asthma in the highest quintile of serum vitamin C relative to the lowest was 0.65 (p < 0.05), whereas it was 0.74 for &alpha;-carotene (p = 0.066). The authors concluded that low vitamin C and &alpha;-carotene intakes are associated with asthma risk in children.	Johns Hopkins Univ, Sch Med, Baltimore, MD 21224 USA; NIA, Clin Res Branch, NIH, Baltimore, MD USA	Wise, RA (reprint author), Johns Hopkins Univ, Sch Med, 5501 Hopkins Bayview Circle, Baltimore, MD 21224 USA.	rwise@jhmi.edu		Wise, Robert/0000-0002-8353-2349			ADERELE W I, 1985, African Journal of Medicine and Medical Sciences, V14, P115; BIELORY L, 1994, ANN ALLERGY, V73, P89; BUCCA C, 1990, ANN ALLERGY, V65, P311; BUCCA C, 1989, EUR RESPIR J, V2, P229; CHYTIL F, 1992, AM J PHYSIOL, V262, P517; Cook DG, 1997, THORAX, V52, P628; Forastiere F, 2000, THORAX, V55, P283, DOI 10.1136/thorax.55.4.283; Gray T, 2001, TOXICOLOGY, V160, P35, DOI 10.1016/S0300-483X(00)00455-8; Gunter EW, 1996, LAB PROCEDURES USED; Hatch GE, 1995, AM J CLIN NUTR S, V61, p625S; Hu GZ, 2000, AM J EPIDEMIOL, V151, P975; Kalayci O, 2000, TURKISH J PEDIATR, V42, P17; Kaur B, 2001, COCHRANE DB SYST REV; Knutsen SF, 2001, ANN EPIDEMIOL, V11, P406, DOI 10.1016/S1047-2797(01)00224-1; Mainous AG, 2000, ARCH FAM MED, V9, P241, DOI 10.1001/archfami.9.3.241; MOHSENIN V, 1983, AM REV RESPIR DIS, V127, P143; Monteleone CA, 1997, ARCH INTERN MED, V157, P23, DOI 10.1001/archinte.157.1.23; Mudway IS, 2001, FREE RADICAL BIO MED, V31, P962, DOI 10.1016/S0891-5849(01)00671-2; OGILVY CS, 1981, J ALLERGY CLIN IMMUN, V67, P363, DOI 10.1016/0091-6749(81)90081-6; Pekkanen J, 1999, EUR RESPIR J, V14, P951, DOI 10.1034/j.1399-3003.1999.14d37.x; Picado C, 2001, ALLERGY, V56, P43, DOI 10.1034/j.1398-9995.2001.00793.x; POWELL CVE, 1994, PEDIATR PULM, V18, P34, DOI 10.1002/ppul.1950180109; Romieu I, 2002, AM J RESP CRIT CARE, V166, P703, DOI 10.1164/rccm.2112074; Schock BC, 2001, PEDIATR RES, V49, P155, DOI 10.1203/00006450-200102000-00005; SCHWARTZ J, 1994, AM J CLIN NUTR, V59, P110; SCHWARTZ J, 1990, AM J EPIDEMIOL, V132, P67; SEATON A, 2000, PEDIAT ALLERGY IMM S, V13, P37; Soutar A, 1997, THORAX, V52, P166; von Mutius E, 2001, THORAX, V56, P835, DOI 10.1136/thorax.56.11.835; Weiss ST, 1997, CIBA F SYMP, V206, P244; WinklhoferRoob BM, 1997, AM J CLIN NUTR, V65, P1858; [Anonymous], 1994, VITAL HLTH STAT 1, V1, P1	32	80	83	0	0	OXFORD UNIV PRESS INC	CARY	JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA	0002-9262			AM J EPIDEMIOL	Am. J. Epidemiol.	FEB 15	2004	159	4					351	357		10.1093/aje/kwh053		7	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	774GQ	WOS:000188971800004	14769638	
J	Lehrer, SB; Ayuso, R; Reese, G				Lehrer, SB; Ayuso, R; Reese, G			Seafood allergy and allergens: A review	MARINE BIOTECHNOLOGY			English	Review						seafood; shrimp; allergy; tropomyosin; epitopes; IgE antibody reactivity	IGE-BINDING EPITOPES; GRASS-POLLEN IMMUNOTHERAPY; MUSCLE PROTEIN TROPOMYOSIN; CROSS-REACTIVE ALLERGEN; CRAB-PROCESSING WORKERS; CULTURE-OYSTER WORKERS; MAJOR SHRIMP ALLERGEN; SALMON SALMO-SALAR; OCCUPATIONAL ASTHMA; CONTACT URTICARIA	Seafoods are composed of diverse sea organisms and humans are allergic to many of them. Tropomyosin is a major allergen in many shellfish, especially crustacea and mollusks. Interestingly, tropomyosin has also been identified as an important allergen in other invertebrates including dust mites and cockroaches, and it has been proposed by some to be an invertebrate pan allergen. Different regions of shrimp tropomyosin bind IgE; 5 major IgE-binding regions have been identified in shrimp tropomyosin containing 8 epitopes. Mutations of these shrimp allergenic epitopes can reduce seafood allergenicity; methods utilizing such mutations will provide safer vaccines for more effective treatment of seafood-allergic patients, and in the future less-allergenic seafood products for consumption.	Tulane Univ, Hlth Sci Ctr, Dept Med, Clin Immunol Sect, New Orleans, LA 70112 USA	Lehrer, SB (reprint author), Tulane Univ, Hlth Sci Ctr, Dept Med, Clin Immunol Sect, Allergy & Rheumatol 1700 Perdido St,SL-57, New Orleans, LA 70112 USA.						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Biotechnol.	JUL-AUG	2003	5	4					339	348		10.1007/s10126-002-0082-1		10	Biotechnology & Applied Microbiology; Marine & Freshwater Biology	Biotechnology & Applied Microbiology; Marine & Freshwater Biology	724XG	WOS:000185513100003	14719162	
J	Packard, KA; Khan, MM				Packard, KA; Khan, MM			Effects of histamine on Th1/Th2 cytokine balance	INTERNATIONAL IMMUNOPHARMACOLOGY			English	Review						Th1/Th2; histamine; asthma	PROTEIN-KINASE-A; RECOMBINANT INTERFERON-GAMMA; ALLERGIC AIRWAY INFLAMMATION; NATURAL SUPPRESSOR CELLS; NITRIC-OXIDE SYNTHASE; HUMAN T-CELLS; IFN-GAMMA; TH2 CELLS; SIGNAL-TRANSDUCTION; IMMUNE-RESPONSE	Atopic asthma is a chronic inflammatory disorder of the airways where upon exposure to allergens, the body mounts an immune response. This disease is associated with an increase in the number of Th2 (T helper type 2) cells and Th2 cytokines and a decrease in the number of Th1 (T helper type 1) cells and Th1 cytokines. Histamine plays an important role in the pathogenesis of atopic asthma through differential regulation of T helper lymphocytes. Histamine enhances the secretion of Th2 cytokines such as IL-4 (interleukin-4), IL-5, IL-10 and IL-13 and inhibits the production of Th1 cytokines IL-2 and IFNgamma (interferon-gamma)and monokine IL-12. It has been shown that histamine can modulate the cytokine network through upregulation of PGE(2) (prostaglandin E-2) and NO (nitric oxide). Histamine also affects cytokine production via H2 receptors and through the activation of PKA (protein kinase A). We have also demonstrated that the Jak-STAT (Janus kinase-signal transducers and activators of transcription) pathway is involved in histamine-mediated regulation of Th2 cytokines IL-5, IL-10, IL-13 and Th1 cytokine IFNgamma. While standard treatment of asthma consists of beta-receptor agonists and inhaled corticosteroids, the elucidation of histamine's control over the cytokine network and the Th1/Th2 balance provides a basis for the potential use of antihistamines in the prevention and treatment of atopic asthma. Several other anti-allergic agents to modulate the Th1/Th2 balance are under current investigation based on this paradigm. These include cytokines, cytokine antagonists, anti-IgE, and vaccinations. As more advances are made in our understanding of histamine and its control over the Th1/Th2 balance, the use of new therapeutic targets such as these will play a prominent role in disease management. (C) 2003 Published by Elsevier Science B.V.	Creighton Univ, Dept Pharm Sci, Omaha, NE 68178 USA	Khan, MM (reprint author), Creighton Univ, Dept Pharm Sci, Omaha, NE 68178 USA.						*AM LUNG ASS WEBS, 2001, TRENDS ASTHM MORB MO; Arad G, 1996, CELL IMMUNOL, V170, P149, DOI 10.1006/cimm.1996.0145; Babe KS, 1996, GOODMAN GILMANS PHAR, P581; Benbernou N, 1997, IMMUNOLOGY, V91, P361, DOI 10.1046/j.1365-2567.1997.00260.x; BETZ M, 1991, J IMMUNOL, V146, P108; BOGUNIEWICZ M, 1993, CLIN EXP ALLERGY, V23, P785, DOI 10.1111/j.1365-2222.1993.tb00367.x; BORISH LC, 2001, J ALLERGY CLIN IMMUN, V107, P63; Brune M, 1996, EUR J HAEMATOL, V57, P312; BRUSSELLE GG, 1994, CLIN EXP ALLERGY, V24, P73, DOI 10.1111/j.1365-2222.1994.tb00920.x; CARLSSON R, 1985, CELL IMMUNOL, V96, P104, DOI 10.1016/0008-8749(85)90343-0; Caron G, 2001, J IMMUNOL, V167, P3682; DEFRANCE T, 1994, J EXP MED, V179, P135, DOI 10.1084/jem.179.1.135; DEVRIES JE, 1995, INT ARCH ALLERGY IMM, V106, P175; DOHLSTEN M, 1986, CELL IMMUNOL, V101, P493, DOI 10.1016/0008-8749(86)90160-7; Eigler A, 1998, J LEUKOCYTE BIOL, V63, P101; 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Immunopharmacol.	JUL	2003	3	7					909	920		10.1016/S1567-5769(02)00235-7		12	Immunology; Pharmacology & Pharmacy	Immunology; Pharmacology & Pharmacy	697MQ	WOS:000183947300001	12810348	
J	Chew, JL; Wolfowicz, CB; Mao, HQ; Leong, KW; Chua, KY				Chew, JL; Wolfowicz, CB; Mao, HQ; Leong, KW; Chua, KY			Chitosan nanoparticles containing plasmid DNA encoding house dust mite allergen, Der p 1 for oral vaccination in mice	VACCINE			English	Article						oral; chitosan nanoparticles; Der p 1	HIV ENVELOPE GLYCOPROTEIN; SYSTEMIC IMMUNE-RESPONSES; MURINE PEYERS-PATCHES; IN-VIVO UPTAKE; DER-P-I; GENE-TRANSFER; DERMATOPHAGOIDES-PTERONYSSINUS; BIODEGRADABLE MICROPARTICLES; MUCOSAL IMMUNIZATION; ANTIBODY-RESPONSES	Our previous studies indicated that intramuscular (i.m.) immunisation with full length Der p 1 cDNA induced significant humoral response to the left domain (approximately corresponding to amino acids 1-116) but not to the right domain (approximately corresponding to amino acids 117-222) of Der p I allergen. This study explored the use of chitosan-DNA nanoparticles for oral immunisation to induce immune responses specific to both the left and right domains of Der p 1. DNA constructs pDer p 1 (1-222) and pDer p 1 (114-222) were complexed with chitosan and delivered orally followed by an i.m. injection of pDer p 1 (1-222) 13 weeks later. Such approach has successfully primed Th1-skewed immune responses against both domains of Der p 1. This strategy could be further optimised for more efficacious gene vaccination for full length Der p 1. (C) 2003 Elsevier Science Ltd. All rights reserved.	Natl Univ Singapore, Fac Med, Dept Paediat, Singapore 119074, Singapore; Johns Hopkins Singapore, Tissue & Therapeut Engn Lab, Singapore 117597, Singapore; Natl Univ Singapore, Dept Mat Sci, Singapore 117543, Singapore; Johns Hopkins Univ, Sch Med, Dept Biomed Engn, Baltimore, MD 21205 USA	Chua, KY (reprint author), Natl Univ Singapore, Fac Med, Dept Paediat, Lower Kent Ridge Rd, Singapore 119074, Singapore.		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J	Anderson, SD; Brannan, JD				Anderson, SD; Brannan, JD			Methods for "indirect" challenge tests including exercise, eucapnic voluntary hyperpnea, and hypertonic aerosols	CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY			English	Review						exercise; dry air hyperpnea; mannitol; hypertonic saline	ULTRASONICALLY NEBULIZED SOLUTIONS; INHALED CORTICOSTEROID BUDESONIDE; HYPERVENTILATION-INDUCED ASTHMA; WORKING PARTY STANDARDIZATION; EUROPEAN RESPIRATORY SOCIETY; COLD-AIR HYPERVENTILATION; THERMALLY-INDUCED ASTHMA; LONG-TERM TREATMENT; INDUCED BRONCHOCONSTRICTION; BRONCHIAL RESPONSIVENESS	Bronchial provocation tests that use stimuli that act indirectly to cause airway narrowing have a high specificity for identifying people with active asthma who have the potential to respond to treatment with antiinflammatory drugs. The first test to be developed was exercise and it was used to assess the efficacy of drugs such as sodium cromoglycate. Eucapnic voluntary hyperpnea was developed later, as a surrogate test for exercise. Hypertonic aerosols were introduced to mimic the dehydrating effects of evaporative water loss that occurs during hyperpnea. A wet aerosol of 4.5% saline or a dry powder formulation of mannitol is used. At present the indirect challenge tests are becoming increasingly recognised as appropriate for monitoring treatment with inhaled steroids. Indirect tests identify those with potential for exercise-induced bronchoconstriction, an important problem for some occupations, such as the defence forces, fire fighters and the police force and for some athletic activities. The advantage in using an indirect challenges, over a direct challenge with a single pharmacological agonist, is that a positive response indicates that inflammatory cells and their mediators (prostaglandins, leukotrienes and histamine) are present in the airways in sufficient numbers and concentration to indicate that asthma is active at the time of testing. The corollary to this is that a negative test in a known asthmatic indicates good control or mild disease. Another advantage is that healthy subjects do not have significant airway narrowing to indirect challenge tests. The protocols used for challenge with indirectly acting stimuli are presented in detail.	Royal Prince Alfred Hosp, Dept Resp Med, Camperdown, NSW 2050, Australia	Anderson, SD (reprint author), Royal Prince Alfred Hosp, Dept Resp Med, E11S,Missenden Rd, Camperdown, NSW 2050, Australia.	sandya@mail.med.usyd.edu.au		Anderson, Sandra/0000-0002-6308-8770			American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; ANDERSON S, 1979, J ALLERGY CLIN IMMUN, V64, P612, DOI 10.1016/0091-6749(79)90024-1; ANDERSON SD, 1991, CHEST, V100, P1254, DOI 10.1378/chest.100.5.1254; ANDERSON SD, 1994, CHEST, V105, P673, DOI 10.1378/chest.105.3.673; 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, 1983, THORAX, V38, P284, DOI 10.1136/thx.38.4.284; ANDERSON SD, 1975, BRIT J DIS CHEST, V69, P1; ANDERSON SD, 1982, EUR J RESPIR DIS, V63, P459; Anderson SD, 1996, J ALLERGY CLIN IMMUN, V98, pS124, DOI 10.1016/S0091-6749(96)80140-0; Anderson SD, 1997, AM J RESP CRIT CARE, V156, P758; ANDERSON SD, 1992, THORAX, V47, P748, DOI 10.1136/thx.47.9.748; ANDERSON SD, 1984, AUST NZ J MED, V14, P803, DOI 10.1111/j.1445-5994.1984.tb04941.x; 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, 1984, J ALLERGY CLIN IMMUN, V73, P660, DOI 10.1016/0091-6749(84)90301-4; Anderson SD, 1995, PROVOCATION CHALLENG, P249; ANDERSON SD, 1985, CHEST, V87, P191; Anderson SD, 1985, AIRWAY RESPONSIVENES, P39; Anderson SD, 1995, SPUMS, V25, P233; 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; ARGYROS GJ, 1993, AM REV RESPIR DIS, V147, P1419; ASSOUFI BK, 1986, B EUR PHYSIOPATH RES, V22, P349; AVITAL A, 1995, THORAX, V50, P511, DOI 10.1136/thx.50.5.511; BACKER V, 1991, J ALLERGY CLIN IMMUN, V88, P68, DOI 10.1016/0091-6749(91)90302-5; Baki A, 2002, ARCH DIS CHILD, V86, P38, DOI 10.1136/adc.86.1.38; BARBEN J, 2001, EUR RESPIR J, V18, pS493; BARDAGI S, 1993, AM REV RESPIR DIS, V147, P1112; BARNES NC, 1984, THORAX, V39, P500, DOI 10.1136/thx.39.7.500; BARYISHAY E, 1983, AM REV RESPIR DIS, V127, P572; BELCHER NG, 1987, AM REV RESPIR DIS, V135, P822; BJORCK T, 1992, AM REV RESPIR DIS, V145, P1087; BLACKIE SP, 1990, AM REV RESPIR DIS, V142, P1133; Brannan JD, 1998, AM J RESP CRIT CARE, V158, P1120; Brannan JD, 2000, AM J RESP CRIT CARE, V161, P2096; Brannan JD, 2002, RESPIROLOGY, V7, P37, DOI 10.1046/j.1440-1843.2002.00357.x; Brannan JD, 2001, AM J RESP CRIT CARE, V163, P1420; BRANNAN JD, 2002, RESPIROLOGY, V7, pA16; BRANNAN JD, 2001, EUR RESPIR J, V18, pS102; BRANNAN JD, 1998, AM J RESP CRIT CARE, V157, pA407; BRUDNO DS, 1994, ANN ALLERGY, V73, P227; Carlsen KH, 1998, RESP MED, V92, P308, DOI 10.1016/S0954-6111(98)90114-7; Carlsen KH, 2000, RESP MED, V94, P750, DOI 10.1053/rmed.2000.0809; Crapo RO, 2000, AM J RESP CRIT CARE, V161, P309; CRAPO RO, 1981, AM REV RESPIR DIS, V123, P659; CUSHLEY MJ, 1983, BRIT J CLIN PHARMACO, V15, P161; Dahlen B, 2002, J ALLERGY CLIN IMMUN, V109, P789, DOI 10.1067/mai.2002.123306; Dahlen B, 2001, EUR RESPIR J, V17, P581, DOI 10.1183/09031936.01.17405810; DAXUN Z, 1989, J ALLERGY CLIN IMMUN, V83, P152, DOI 10.1016/0091-6749(89)90490-9; DEAL EC, 1980, AM REV RESPIR DIS, V121, P621; DEAL EC, 1979, J APPL PHYSIOL, V46, P476; Dessanges JF, 1999, J ALLERGY CLIN IMMUN, V104, P1155; Doull IJM, 1997, PEDIATR PULM, V23, P404, DOI 10.1002/(SICI)1099-0496(199706)23:6<404::AID-PPUL2>3.0.CO;2-I; duToit JI, 1997, ALLERGY ASTHMA PROC, V18, P7, DOI 10.2500/108854197778612817; EDMUNDS AT, 1978, AM REV RESPIR DIS, V117, P247; EGGLESTON PA, 1979, J ALLERGY CLIN IMMUN, V64, P642, DOI 10.1016/0091-6749(79)90028-9; ELIASSON AH, 1992, CHEST, V102, P347, DOI 10.1378/chest.102.2.347; FINNERTY JP, 1990, EUR RESPIR J, V3, P540; Folgering H, 1997, EUR RESP MON, V6, P51; GANDEVIA B., 1957, THORAX, V12, P290, DOI 10.1136/thx.12.4.290; Gibson PG, 1998, CLIN EXP ALLERGY, V28, P1081; GIBSON PG, 1995, CLIN EXP ALLERGY, V25, P127, DOI 10.1111/j.1365-2222.1995.tb01017.x; Gibson PG, 2000, J ALLERGY CLIN IMMUN, V105, P752, DOI 10.1067/mai.2000.105319; Godfrey S, 1999, EUR RESPIR J, V14, P659, DOI 10.1034/j.1399-3003.1999.14c28.x; Godfrey S., 1974, EXERCISE TESTING CHI; GONDA I, 1986, PHARM TECH JAPAN, V2, P883; HABY MM, 1995, EUR RESPIR J, V8, P729; HABY MM, 1994, EUR RESPIR J, V7, P43, DOI 10.1183/09031936.94.07010043; Hancox RJ, 2002, AM J RESP CRIT CARE, V165, P1068, DOI 10.1164/rccm.200111-091BC; HENRIKSEN JM, 1983, AM REV RESPIR DIS, V128, P993; Hofstra WB, 1997, THORAX, V52, P739; Holzer K, 2002, J ALLERGY CLIN IMMUN, V110, P374, DOI 10.1067/mai.2002.127784; HOLZER K, 2002, AM J RESP CRIT  1127; HURWITZ KM, 1995, CHEST, V108, P1240, DOI 10.1378/chest.108.5.1240; In 'T Veen J. 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Rev. Allergy Immunol.	FEB	2003	24	1					27	54		10.1385/CRIAI:24:1:27		28	Allergy; Immunology	Allergy; Immunology	658GV	WOS:000181714000004	12644717	
J	Matsuoka, H; Maki, N; Yoshida, S; Arai, M; Wang, J; Oikawa, Y; Ikeda, T; Hirota, N; Nakagawa, H; Ishii, A				Matsuoka, H; Maki, N; Yoshida, S; Arai, M; Wang, J; Oikawa, Y; Ikeda, T; Hirota, N; Nakagawa, H; Ishii, A			A mouse model of the atopic eczema/dermatitis syndrome by repeated application of a crude extract of house-dust mite Dermatophagoides farinae	ALLERGY			English	Article						atopic eczema/dermatitis syndrome; Dermatophagoides farinae; IgE; mast cell; mouse model	EPIDERMAL LANGERHANS CELLS; REGIONAL LYMPH-NODES; IGE HYPERPRODUCTION; NC/NGA MICE; DERMATITIS; SENSITIZATION; ANTIBODIES; POPULATION; ALLERGENS; ANTIGEN	Background: We cultured Dermatophagoides farinae (Df), one of the most common mites in house dust and the most important allergen among natural allergens. With this material, we attempted to produce an animal model of the atopic eczema/dermatitis syndrome (AEDS). Methods: We cultured Df mites in high density and prepared a crude extract of Df (DfE) together with the culture medium. We applied the extract to the back skin of NC/Nga and BALB/c mice three times per week for 8 weeks. Results: In the NC/Nga group, dryness or scaling appeared on the skin, and scratching behavior increased at the second week in the DfE-treated group. Skin erosion and hemorrhage occurred at the fourth week. The epidermis thickened and deepened into the upper dermis, in which mast cells were highly accumulated, corresponding with the skin lesion of AEDS patients. Specific IgE and IgG to DfE and total IgE were elevated in the sera. Mice treated with an extract of mite culture medium did not develop skin lesions. In the BALB/c group, mice developed specific IgE and IgG to DfE, however, no typical skin lesions appeared. Mast cells in the upper dermis did not increase. Conclusions: Repeated painting of Dermatophagoides extract produced IgE-associated AEDS-like lesions on the skin of NC mice.	Jichi Med Sch, Dept Med Zool, Minami Kawachi, Tochigi 3290498, Japan; Kanazawa Med Sch, Dept Med Zool, Kanazawa, Ishikawa, Japan; Jichi Med Sch, Dept Dermatol, Minami Kawachi, Tochigi, Japan	Matsuoka, H (reprint author), Jichi Med Sch, Dept Med Zool, 3311-1 Yakushiji, Minami Kawachi, Tochigi 3290498, Japan.			Matsuoka, Hiroyuki/0000-0001-8839-0012			ALANI M, 1970, ACTA ALLERGOL, V25, P41, DOI 10.1111/j.1398-9995.1970.tb01379.x; Bellinghausen I, 1996, J INVEST DERMATOL, V107, P582, DOI 10.1111/1523-1747.ep12582825; Bellinghausen I, 1999, J ALLERGY CLIN IMMUN, V103, P298, DOI 10.1016/S0091-6749(99)70505-1; Breuer K, 2001, ALLERGY, V56, P1034, DOI 10.1034/j.1398-9995.2001.00146.x; CARSWELL F, 1986, LANCET, V2, P13; CHAPMAN MD, 1983, J ALLERGY CLIN IMMUN, V72, P27, DOI 10.1016/0091-6749(83)90048-9; FUJUI M, 1961, JIKKEN DOBUTSU, V10, P83; Iijima OT, 2000, COMPARATIVE MED, V50, P225; Johansson SGO, 2001, ALLERGY, V56, P813, DOI 10.1034/j.1398-9995.2001.t01-1-00001.x; KRIPKE ML, 1990, J IMMUNOL, V145, P2833; LALTOO H, 1979, IMMUNOL COMMUN, V8, P1, DOI 10.3109/08820137909044702; Matsuda H, 1997, INT IMMUNOL, V9, P461, DOI 10.1093/intimm/9.3.461; MATSUOKA H, 1995, JPN J MED SCI BIOL, V48, P103; Morita E, 1999, J DERMATOL SCI, V19, P37, DOI 10.1016/S0923-1811(98)00047-4; MUDDE GC, 1990, IMMUNOLOGY, V69, P335; Okudaira H, 1989, Arerugi, V38, P296; PLATTSMILLS TAE, 1987, J ALLERGY CLIN IMMUN, V80, P755, DOI 10.1016/S0091-6749(87)80261-0; PLATTSMILLS TAE, 1983, CLIN EXP DERMATOL, V8, P233, DOI 10.1111/j.1365-2230.1983.tb01776.x; Saloga J, 2000, ALLERGY, V55, P905, DOI 10.1034/j.1398-9995.2000.00126.x; SASA M, 1970, Japanese Journal of Experimental Medicine, V40, P367; Sugiura H, 1998, ACTA DERM-VENEREOL, V78, P293; Suto H, 1999, INT ARCH ALLERGY IMM, V120, P70, DOI 10.1159/000053599; TANAKA Y, 1990, Journal of Dermatological Science, V1, P361, DOI 10.1016/0923-1811(90)90593-3; THOMPSON SJ, 1988, IMMUNOLOGY, V64, P311; YAMASHITA K, 1994, MICROBIOL IMMUNOL, V38, P567	25	80	86	0	4	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	FEB	2003	58	2					139	145		10.1034/j.1398-9995.2003.23790.x		7	Allergy; Immunology	Allergy; Immunology	652AA	WOS:000181355500007	12622745	
J	Lehtimaki, L; Kankaanranta, H; Saarelainen, S; Turjanmaa, V; Moilanen, E				Lehtimaki, L; Kankaanranta, H; Saarelainen, S; Turjanmaa, V; Moilanen, E			Inhaled fluticasone decreases bronchial but not alveolar nitric oxide output in asthma	EUROPEAN RESPIRATORY JOURNAL			English	Article						asthma; eosinophil cationic protein; eosinophil protein X; exhaled nitric oxide; inflammation; inhaled glucocorticoids	EXHALED AIR; SPUTUM EOSINOPHILS; MILD ASTHMA; INDUCTION; SYNTHASE; AIRWAYS; RESPONSIVENESS; INFLAMMATION	Exhaled nitric oxide (NO) concentration is a noninvasive measure of airway inflammation and is increased in asthma. Inhaled glucocorticoids decrease exhaled NO concentration, but the relative contributions of alveolar and bronchial levels to the decrease in exhaled NO concentration are unknown. Alveolar NO concentration and bronchial NO flux can be separately approximated by measuring exhaled NO at several exhalation flow rates. The effect of steroid treatment on alveolar and bronchial NO output in asthma was studied. Alveolar NO concentration and bronchial NO flux were assessed in 16 patients with asthma before and during treatment with inhaled fluticasone for 8 weeks and in 16 healthy controls. Before the treatment, asthmatics had increased bronchial NO flux (mean +/- SEM: 3.6 +/-0.4 versus 0.7 +/-0.1 nL.s(-1), p<0.001) but normal alveolar NO concentration (1.2<plus/minus>0.5 versus 1.0 +/-0.2 parts per billion (ppb), p>0.05) compared with controls Inhaled fluticasone decreased bronchial NO flux from 3.6 +/-0.4 to 0.7 +/-0.1 nL.s(-1)(p<0.01) but had no effect on alveolar NO concentration (before: 1.2<plus/minus>0.5; after: 1.2 +/-0.1 ppb, p>0.05). The forced expiratory volume in one second improved, whereas asthma symptom score and serum levels of eosinophil cationic protein and eosinophil protein X decreased during the treatment. In conclusion, inhaled fluticasone decreases bronchial but not alveolar nitric oxide output simultaneously with clinical improvement in patients with asthma.	Univ Tampere, Sch Med, Immunopharmacol Res Grp, FIN-33014 Tampere, Finland; Tampere Univ Hosp, Dept Clin Chem, FIN-33521 Tampere, Finland; Tampere Univ Hosp, Dept Resp Med, Tampere, Finland; Tampere Univ Hosp, Dept Clin Physiol, Tampere, Finland	Moilanen, E (reprint author), Univ Tampere, Sch Med, Immunopharmacol Res Grp, FIN-33014 Tampere, Finland.			Kankaanranta, Hannu/0000-0001-5258-0906			ALVING K, 1993, EUR RESPIR J, V6, P1368; HAMID Q, 1993, LANCET, V342, P1510, DOI 10.1016/S0140-6736(05)80083-2; Ho LP, 2000, CHEST, V118, P1327, DOI 10.1378/chest.118.5.1327; Hogman M, 2000, RESP MED, V94, P985, DOI 10.1053/rmed.2000.0872; Jatakanon A, 1999, THORAX, V54, P108; Jatakanon A, 1998, THORAX, V53, P91; Jorres RA, 2000, EUR RESPIR J, V16, P555, DOI 10.1034/j.1399-3003.2000.016003555.x; KHARITONOV SA, 1994, LANCET, V343, P133, DOI 10.1016/S0140-6736(94)90931-8; Kharitonov SA, 1996, AM J RESP CRIT CARE, V153, P454; Kharitonov SA, 2000, EUR RESPIR J, V16, P781, DOI 10.1183/09031936.00.16478100; Kleinert H, 1996, MOL PHARMACOL, V49, P15; Lehtimaki L, 2000, ANN MED, V32, P417, DOI 10.3109/07853890008995949; Lehtimaki L, 2001, AM J RESP CRIT CARE, V163, P1557; Moilanen E, 1999, INFLAMMATION BASIC P, P787; Saleh D, 1998, FASEB J, V12, P929; Silkoff PE, 2000, AM J RESP CRIT CARE, V161, P1218; Silkoff PE, 2000, CLIN CHEST MED, V21, P345, DOI 10.1016/S0272-5231(05)70271-9; Sippel JM, 2000, J ALLERGY CLIN IMMUN, V106, P645, DOI 10.1067/mai.2000.1096618; Tsoukias NM, 1998, J APPL PHYSIOL, V85, P653; van Rensen ELJ, 1999, THORAX, V54, P403	20	80	80	0	0	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	2001	18	4					635	639		10.1183/09031936.01.00000201		5	Respiratory System	Respiratory System	495EM	WOS:000172327300005	11716167	
J	Carbonell-Estrany, X; Quero, J				Carbonell-Estrany, X; Quero, J		IRIS Study Grp	Hospitalization rates for respiratory syncytial virus infection in premature infants born during two consecutive seasons	PEDIATRIC INFECTIOUS DISEASE JOURNAL			English	Article						respiratory syncytial virus; premature infants; hospitalization; epidemiology	REHOSPITALIZATION; GESTATION; CHILDREN	Objective. To collect data on hospitalization rates for respiratory syncytial virus (RSV) illness during the season of 1999 to 2000 in nonprophylaxed premature infants less than or equal to 32 weeks gestational age (GA) in Spain and compare this with previously published data collected in the season of 1998 to 1999. Methods. Children born at less than or equal to 32 weeks GA between April 1, 1999, and April 31, 2000, and discharged from the hospital before April 31, 2000, were included. Neonatal and demographic data were obtained at the initial visit. Study subjects were followed at monthly intervals throughout the respiratory season. RSV status and morbidity data were collected on patients rehospitalized for respiratory illness. Results. The 999 evaluable patients in the 2000 season were comparable to the 1999 sample, except for higher rates of family allergy history and number of multiple deliveries and a lower rate of neonatal morbidity. The hospitalization rate for RSV illness was 13.4% in the 1999 season and 13.1% in the 2000 season; 10 (8%) were RSV reinfections in the 2000 season. Significant independent prognostic variables for high risk of RSV hospital admission included: lower gestational age; chronologic age <3 months at onset of the RSV season; living with school age siblings; and exposure to tobacco smoke. Conclusions. Hospitalization rates for RSV disease in nonprophylaxed preterm infants less than or equal to 32 weeks GA were high in Spain and comparable during two consecutive RSV seasons (13%). Readmission for a second RSV infection was also common.	Hosp Clin Barcelona, Inst Clin Ginecol Obstet & Neonatol, Serv Neonatol, Unitat Integrada, Barcelona 08034, Spain; Hosp La Paz, Madrid, Spain	Carbonell-Estrany, X (reprint author), Hosp Clin Barcelona, Inst Clin Ginecol Obstet & Neonatol, Serv Neonatol, Unitat Integrada, C-Sabino Arana 1, Barcelona 08034, Spain.						ANDERSON LJ, 1991, J INFECT DIS, V163, P687; Behrendt CE, 1998, EUR J PEDIATR, V157, P215, DOI 10.1007/s004310050798; Boyce TG, 2000, J PEDIATR-US, V137, P865, DOI 10.1067/mpd.2000.110531; Carbonell-Estrany X, 2000, PEDIATR INFECT DIS J, V19, P592, DOI 10.1097/00006454-200007000-00002; Chew FT, 1998, EPIDEMIOL INFECT, V121, P121, DOI 10.1017/S0950268898008905; COCKBURN F, 1993, LANCET, V342, P193; CUNNINGHAM CK, 1991, PEDIATRICS, V88, P527; DUCOFFRE G, 1998, IPH EPIDEMIOLOGY NOV; FARSTAD T, 2000, 18 ANN M EUR SOC PAE; Gellida Royo M J, 1999, An Esp Pediatr, V50, P21; *GREEK RSV STUD GR, 2000, 18 ANN M EUR SOC PAE; Law B, 1998, Paediatr Child Health, V3, P402; LOWTHER SA, 2000, PED AC SOC AM AC PED; NAVAS L, 1992, J PEDIATR-US, V121, P348, DOI 10.1016/S0022-3476(05)90000-0; Null D, 1998, PEDIATRICS, V102, P531; Shay DK, 1999, JAMA-J AM MED ASSOC, V282, P1440, DOI 10.1001/jama.282.15.1440; Simoes EAF, 1999, LANCET, V354, P847, DOI 10.1016/S0140-6736(99)80040-3; Simoes EAF, 1999, INFECT MED, V16, P11; WANG EEL, 1995, J PEDIATR-US, V126, P212, DOI 10.1016/S0022-3476(95)70547-3; WEIGL JAI, 2000, 18 ANN M EUR SOC PAE	20	80	81	0	0	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	0891-3668			PEDIATR INFECT DIS J	Pediatr. Infect. Dis. J.	SEP	2001	20	9					874	879		10.1097/00006454-200109000-00010		6	Immunology; Infectious Diseases; Pediatrics	Immunology; Infectious Diseases; Pediatrics	472CW	WOS:000170966500009	11734767	
J	Larsson, ML; Frisk, M; Hallstrom, J; Kiviloog, J; Lundback, B				Larsson, ML; Frisk, M; Hallstrom, J; Kiviloog, J; Lundback, B			Environmental tobacco smoke exposure during childhood is associated with increased prevalence of asthma in adults	CHEST			English	Article						asthma; environmental tobacco smoke; respiratory symptoms	PASSIVE SMOKING; DISEASE; LIFE; RISK	Objective: To examine if exposure to environmental tobacco smoke (ETS) during childhood has an impact on asthma prevalence in adults, and to identify the amount of nuisance from ETS and other lower airway irritants (LAWIs) in a city population. Design: A postal survey. Setting: The municipality of Orebro, Sweden. Participants: A total of 8,008 randomly selected inhabitants aged 15 to 69 years. Measurements: Exposures, airway symptoms, and respiratory history were assessed using a questionnaire. Results: The response rate was 84%. In never-smokers with childhood ETS exposure, the prevalence of physician-diagnosed asthma was 7.6% vs 5.9% in nonexposed subjects (p = 0.036). In never-smokers without a family history of asthma, the prevalence of physician-diagnosed asthma in subjects reporting childhood ETS exposure was 6.8% vs 3.8% in nonexposed subjects (p < 0.001). Subjects with childhood ETS exposure were more likely to start smoking in adulthood. The prevalence of ever-smokers was 54.5% vs 33.8% (p < 0.0001) in nonexposed subjects. ETS was the most commonly reported LAWI in the total sample (21%), followed by exercise in cold air (20%); dust (19%), exercise (16%), perfume (15%), cold air (12%), pollen (10%), and pets (8%). All LAWIs were more frequently reported by women. Conclusions: Childhood exposure to ETS is associated with an increased prevalence of asthma among adult never-smokers, especially in nonatopic subjects. Children exposed to ETS are also more likely to become smokers. ETS is as a major LAWI.	Orebro Med Ctr Hosp, Dept Lung Med, SE-70185 Orebro, Sweden; Univ Uppsala, Dept Publ Hlth & Caring Sci, S-75105 Uppsala, Sweden; Natl Inst Working Life, Dept Occupat Med, Resp Unit, Stockholm, Sweden	Larsson, ML (reprint author), Orebro Med Ctr Hosp, Dept Lung Med, SE-70185 Orebro, Sweden.						Becklake MR, 1999, THORAX, V54, P1119; *COMM PASS SMOK BO, 1983, ENV TOB SMOK MEAS EX; Coultas DB, 1998, THORAX, V53, P381; *DEP HHS, 1994, PREV TOB US AM YOUNG; Hu FB, 1997, J ASTHMA, V34, P67, DOI 10.3109/02770909709071205; JINOT J, 1994, J CLIN EPIDEMIOL, V47, P339, DOI 10.1016/0895-4356(94)90154-6; KIVILOOG J, 1974, SCAND J RESPIR DIS, V55, P262; KNIGHT A, 1985, MED J AUSTRALIA, V142, P194; LEUENBERGER P, 1994, AM J RESP CRIT CARE, V150, P1222; LUNDBACK B, 1991, EUR RESPIR J, V4, P257; Medical Research Council, 1960, BRIT MED J, V2, P1665; NIELSEN P, 1993, PASSIV RYGNING OVERF; PEDREIRA FA, 1985, PEDIATRICS, V75, P594; Ramstrom Lars M., 1997, V28, P64; Reid DJ, 1995, TOB CONTROL, V4, P266, DOI 10.1136/tc.4.3.266; SHEPHARD RJ, 1979, ENVIRON RES, V20, P392, DOI 10.1016/0013-9351(79)90015-X; Steenland K, 1996, CIRCULATION, V94, P622; Strachan DP, 1998, THORAX, V53, P204; Thoren K, 1993, CHEST, V104, P600; WEBER A, 1984, EUR J RESPIR DIS, V68, P98; WEINBERGER M, 1997, CIGARETTES WHAT WARN, P69; WILLERS S, 1991, ALLERGY, V46, P330, DOI 10.1111/j.1398-9995.1991.tb00595.x; ZETTERSTROM O, 1981, BRIT MED J, V283, P1215	23	80	82	0	2	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	SEP	2001	120	3					711	717		10.1378/chest.120.3.711		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	472EN	WOS:000170970700009	11555497	
J	Huss, K; Naumann, PL; Mason, PJ; Nanda, JP; Huss, RW; Smith, CM; Hamilton, RG				Huss, K; Naumann, PL; Mason, PJ; Nanda, JP; Huss, RW; Smith, CM; Hamilton, RG			Asthma severity, atopic status, allergen exposure, and quality of life in elderly persons	ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY			English	Article							INNER-CITY CHILDREN; DUST MITE ALLERGENS; INDOOR ALLERGENS; INTERNATIONAL WORKSHOP; RISK FACTOR; OF-LIFE; SENSITIZATION; ADULTS; POPULATION; CHILDHOOD	Background: Although asthma can be associated with significant airflow obstruction in those over the age of 65, it is often underdiagnosed and undertreated. Objective: To describe severity of asthma, allergy skin test sensitivities, indoor allergen exposures, and the impact on quality of life (QOL) and health status in elderly persons with asthma. Methods: A cross-sectional data analysis with 80 elderly persons with asthma recruited from medical, geriatric, and allergy/immunology tertiary care centers. Asthma severity was determined by symptoms and measurements of lung function. House dust specimens were collected from mattresses and bedroom carpets and analyzed separately for the major allergens of house dust, using monoclonal antibody-based immunoenzymetric assays. QOL was measured using Juniper's Asthma Quality of Life Questionnaire. Health status was measured using the Short Form Health Survey Medical Outcome Questionnaire which included Ferrans and Powers' Quality of Life Index subscales. Results: Two-thirds of participants had either moderate or severe persistent asthma. Skin tests to a battery of common airborne allergens were positive to at least one allergen in 56 of the 75 participants tested (74.7%). Reservoir dust allergen levels were often high enough to place participants at risk of symptoms or at risk of developing sensitization. Increased asthma severity was associated with significantly lower QOL and a trend toward decreased health status. Conclusions: Asthma is a significant chronic problem in the elderly. Atopy was common. Asthma severity impacts on these participants' QOL and health status. Results support interventions aimed at identifying allergens precipitating attacks and reducing them in the home.	Johns Hopkins Univ, Sch Nursing, Baltimore, MD 21205 USA; Johns Hopkins Univ, Sch Publ Hlth, Baltimore, MD USA; Johns Hopkins Asthma & Allergy Ctr, Serum Repository, DACI Reference Lab, Baltimore, MD USA	Huss, K (reprint author), Johns Hopkins Univ, Sch Nursing, 525 N Wolfe St, Baltimore, MD 21205 USA.						BURROWS B, 1991, CHEST, V100, P935, DOI 10.1378/chest.100.4.935; *CDC, 1998, MMWR CDC SURVEILLANC, V47; CHANYEUNG M, 1995, AM J RESP CRIT CARE, V152, P1805; CHAPMAN MD, 1995, PEDIATR ALLERGY IMMU, V6, P8, DOI 10.1111/j.1399-3038.1995.tb00378.x; Crater Scott E., 1998, Current Opinion in Pediatrics, V10, P594; Dyer CAE, 1999, EUR RESPIR J, V14, P39, DOI 10.1034/j.1399-3003.1999.14a09.x; Eggleston PA, 1998, J ALLERGY CLIN IMMUN, V102, P563, DOI 10.1016/S0091-6749(98)70272-6; Enright PL, 1999, CHEST, V116, P603, DOI 10.1378/chest.116.3.603; FERRANS CE, 1985, ADV NURS SCI, V8, P15; FOLSTEIN MF, 1975, J PSYCHIAT RES, V12, P189, DOI 10.1016/0022-3956(75)90026-6; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; HAMILTON RG, 1997, MANUAL CLIN LAB IMMU, P881; HUSS K, 1992, J ALLERGY CLIN IMMUN, V89, P836, DOI 10.1016/0091-6749(92)90439-9; INGRAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449, DOI 10.1016/S0091-6749(95)70286-5; JUNIPER EF, 1993, AM REV RESPIR DIS, V147, P832; KIVITY S, 1993, J ALLERGY CLIN IMMUN, V91, P844, DOI 10.1016/0091-6749(93)90341-C; LAU S, 1989, J ALLERGY CLIN IMMUN, V84, P718, DOI 10.1016/0091-6749(89)90300-X; Marks GB, 1998, ALLERGY, V53, P108; *NAT ASTHM ED PREV, 1997, NIH PUB; NIEMEIJER NR, 1992, ALLERGY, V47, P431, DOI 10.1111/j.1398-9995.1992.tb02084.x; Peat JK, 1996, AM J RESP CRIT CARE, V153, P141; Platts-Mills TAE, 1997, J ALLERGY CLIN IMMUN, V100, pS2, DOI 10.1016/S0091-6749(97)70292-6; PLATTSMILLS TAE, 1992, J ALLERGY CLIN IMMUN, V89, P1046, DOI 10.1016/0091-6749(92)90228-T; PLATTSMILLS TAE, 1995, J ALLERGY CLIN IMMUN, V96, P435, DOI 10.1016/S0091-6749(95)70284-9; PRICE JA, 1990, LANCET, V336, P895, DOI 10.1016/0140-6736(90)92268-M; 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, 1995, AM J RESP CRIT CARE, V151, P1388; STEWART AL, 1988, MED CARE, V26, P724, DOI 10.1097/00005650-198807000-00007; Weiner P, 1998, EUR RESPIR J, V12, P564, DOI 10.1183/09031936.98.12030564; Weiss ST, 1998, J ALLERGY CLIN IMMUN, V101, P720, DOI 10.1016/S0091-6749(98)70300-8	31	80	83	1	5	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.	MAY	2001	86	5					524	530				7	Allergy; Immunology	Allergy; Immunology	433UW	WOS:000168779900006	11379803	
J	Best, NG; Ickstadt, K; Wolpert, RL				Best, NG; Ickstadt, K; Wolpert, RL			Spatial Poisson regression for health and exposure data measured at disparate resolutions	JOURNAL OF THE AMERICAN STATISTICAL ASSOCIATION			English	Article						air pollution; Bayesian hierarchical models; continuous random fields; ecological regression; environmental epidemiology; respiratory illness	AIR-POLLUTION; RESPIRATORY HEALTH; ASTHMA; CHILDREN; PREVALENCE; STATISTICS; MOTORWAYS; MORTALITY; SYMPTOMS; MODELS	Ecological regression studies are widely used to examine relationships between disease rates for small geographical areas and exposure to environmental risk factors. The raw data for such studies, including disease cases, environmental pollution concentrations, and the reference population at risk, are typically measured at various levels of spatial aggregation but are accumulated to a common geographical scale to facilitate statistical analysis. In this traditional approach, heterogeneous exposure distributions within the aggregate areas may lead to biased inference, whereas individual attributes such as age, gender, and smoking habits must either be summarized to provide area-level covariate values or used to stratify the analysis. This article presents a spatial regression analysis of the effect of traffic pollution on respiratory disorders in children. The analysis features data measured at disparate, nonnested scales, including spatially varying covariates, latent spatially varying risk factors, and case-specific individual attributes. The problem of disparate discretizations is overcome by relating all spatially varying quantities to a continuous underlying random field model. Case-specific individual attributes are accommodated by treating cases as a marked point process. Inference in these hierarchical Poisson/gamma models is based on simulated samples drawn from Bayesian posterior distributions, using Markov chain Monte Carlo methods with data augmentation.	Imperial Coll Sch Med, Dept Epidemiol & Publ Hlth, Small Area Stat Unit, London W2 1PG, England; Duke Univ, Inst Stat & Decis Sci, Durham, NC 27708 USA	Best, NG (reprint author), Imperial Coll Sch Med, Dept Epidemiol & Publ Hlth, Small Area Stat Unit, St Marys Campus, London W2 1PG, England.						Bernardinelli L, 1997, STAT MED, V16, P741, DOI 10.1002/(SICI)1097-0258(19970415)16:7<741::AID-SIM501>3.0.CO;2-1; BESAG J, 1991, ANN I STAT MATH, V43, P1, DOI 10.1007/BF00116466; BEST NG, 2000, SPATIAL EPIDEMIOLOGY, pCH22; Breslow N. 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Am. Stat. Assoc.	DEC	2000	95	452					1076	1088		10.2307/2669744		13	Statistics & Probability	Mathematics	376RJ	WOS:000165470300006		
J	Siracusa, A; Desrosiers, M; Marabini, A				Siracusa, A; Desrosiers, M; Marabini, A			Epidemiology of occupational rhinitis: prevalence, aetiology and determinants	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review							LABORATORY-ANIMAL ALLERGY; WORK-RELATED SYMPTOMS; EXPOSURE-RESPONSE RELATIONSHIPS; IGE-MEDIATED SENSITIZATION; RESPIRATORY SYMPTOMS; METHYLTETRAHYDROPHTHALIC ANHYDRIDE; ACOUSTIC RHINOMETRY; PROCESSING WORKERS; TEXTILE WORKERS; GREEN COFFEE		Univ Perugia, Dept Clin & Expt Med, I-06100 Perugia, Italy; Ctr Hosp Univ Montreal, Dept Otorhinolaryngol, Montreal, PQ, Canada	Siracusa, A (reprint author), Via E dai Pozzo, I-06126 Perugia, Italy.						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Exp. Allergy	NOV	2000	30	11					1519	1534		10.1046/j.1365-2222.2000.00946.x		16	Allergy; Immunology	Allergy; Immunology	383WH	WOS:000165907100005	11069559	
J	Chung, KF				Chung, KF			Airway smooth muscle cells: contributing to and regulating airway mucosal inflammation?	EUROPEAN RESPIRATORY JOURNAL			English	Article						airway smooth muscle; asthma; bronchial hyperresponsiveness; chemokines; proliferation	INTERCELLULAR-ADHESION MOLECULE-1; REPEATED ALLERGEN EXPOSURE; BROWN-NORWAY RATS; GROWTH-FACTOR; DNA SYNTHESIS; BRONCHOALVEOLAR LAVAGE; PASSIVE SENSITIZATION; T-HELPER-2 CYTOKINES; ASTHMATIC SUBJECTS; ICAM-1 EXPRESSION	In addition to its contractile properties, airway smooth muscle may contribute to the pathogenesis of asthma by increased proliferation, and by the expression and secretion of pro-inflammatory cytokines and mediators. Studies of airway smooth muscle cells in culture have shown that many mitogenic mediators can induce proliferation, and that these may therefore, contribute to the increase in airway smooth muscle mass observed in asthma. Other mechanisms for airway smooth muscle proliferation include the interaction with inflammatory cells such as T-cells and eosinophils. Airway smooth muscle cells may also be a source of inflammatory mediators and cytokines, in particular chemokines, thus implicating airway smooth muscle cells as contributors to the inflammatory mechanisms of asthma. The pro-activating signals for converting airway smooth muscle cells into a proliferative and secretory cell in asthma are unknown, but may include viruses and immunoglobulin E. Airway smooth muscle contractility may also be altered in response to inflammation. Airway smooth muscle cells may play an important interactive role with inflammatory and other structural cells, contributing to inflammation, injury and repair of the airways. Such a recognition makes it imperative to consider the airway smooth muscle as a target of therapeutic drugs for suppressing not only the contractile but also the proliferative and secretory effects of asthma.	Imperial Coll Sch Med & Royal Brompton Hosp, Natl Heart & Lung Inst, London SW3 6LY, England	Chung, KF (reprint author), Imperial Coll Sch Med & Royal Brompton Hosp, Natl Heart & Lung Inst, London SW3 6LY, England.			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Resp. J.	MAY	2000	15	5					961	968		10.1034/j.1399-3003.2000.15e26.x		8	Respiratory System	Respiratory System	317JH	WOS:000087221900026	10853867	
J	Robinson, MK; Gerberick, GF; Ryan, CA; McNamee, P; White, IR; Basketter, DA				Robinson, MK; Gerberick, GF; Ryan, CA; McNamee, P; White, IR; Basketter, DA			The importance of exposure estimation in the assessment of skin sensitization risk	CONTACT DERMATITIS			English	Review						skin; contact allergy; exposure; risk assessment; cosmetics; household products; dose per unit area	LYMPH-NODE ASSAY; ALLERGIC CONTACT SENSITIZATION; SODIUM LAURYL SULFATE; DOSE-RESPONSE ASSESSMENTS; KATHON BIOCIDE; GUINEA-PIGS; PATCH TESTS; AREA; PRETREATMENT; SENSITIVITY	The development of new ingredients and products for the consumer market requires a thorough assessment of their potential for skin sensitization and the possible clinical manifestation of allergic contact dermatitis. The process by which low molecular weight chemicals induce and elicit skin sensitization reactions is complex and dependent on many factors relevant to the ability of the chemical to penetrate the skin, react with protein, and trigger the cell-mediated immune response. These major factors include inherent potency, chemical dose, duration and frequency of exposure, vehicle or product matrix, and occlusion. The fact that a chemical is a contact allergen does not mean that it cannot be formulated into a consumer product at levels well tolerated by most individuals. Many common ingredients (e.g., fragrances, preservatives) are known skin allergens. However, all allergens show dose-response and threshold characteristics. Therefore, one should be able to incorporate these chemicals into products at levels that produce acceptably low incidences of skin sensitization under foreseeable conditions of exposure. The critical exposure determinant for evaluating skin sensitization risk is dose per unit area of skin exposed. Use of this parameter allows for comparative assessments from different types of skin sensitization tests (including cross-species comparisons), and, at least for known potent allergens, there is remarkable similarity in threshold dose/unit area determinations across species. The dose/unit area calculation enables a judgment of the sensitization risk for different product types. This is illustrated using the chemical preservative methylchloroisothiazoline/methylisothiazolinone (MCI/MI) as a case study.	Procter & Gamble Co, Miami Valley Labs, Cincinnati, OH 45253 USA; Rusham Pk Tech Ctr, Egham, Surrey, England; St Thomas Hosp, St Johns Inst Dermatol, London, England; Unilever, SEAC Toxicol Unit, Sharnbrook, Beds, England	Robinson, MK (reprint author), Procter & Gamble Co, Miami Valley Labs, POB 538707, Cincinnati, OH 45253 USA.			Robinson, Michael/0000-0002-6914-8543			BARRATT MD, 1992, CONTACT DERMATITIS, V27, P98, DOI 10.1111/j.1600-0536.1992.tb05217.x; Basketter D. 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J	Young, S; Sherrill, DL; Arnott, J; Diepeveen, D; LeSouef, PN; Landau, LI				Young, S; Sherrill, DL; Arnott, J; Diepeveen, D; LeSouef, PN; Landau, LI			Parental factors affecting respiratory function during the first year of life	PEDIATRIC PULMONOLOGY			English	Article						infant lung function; maternal tobacco smoking; in utero tobacco smoke exposure; maternal inheritance; infant gender; predictive equations; asthma	FLOW-VOLUME CURVES; FORCED EXPIRATORY FLOWS; PULMONARY-FUNCTION; MATERNAL SMOKING; LUNG-FUNCTION; 1ST YEAR; PASSIVE SMOKING; NORMAL INFANTS; LONGITUDINAL DATA; NEWBORN-INFANTS	In a prospective, longitudinal, population-based cohort study of familial and environmental influences on the development of wheezing respiratory illness in early childhood, we identified infant length, weight, gender, and exposure to maternal cigarette smoking as significant determinants of lung function during the first year of life. A cohort of 237 infants (106 females: 131 males) was evaluated, and 496 lung function measurements were made between the ages of 1-12 months. Respiratory function was assessed using the rapid thoracic compression technique to obtain maximum expiratory flow at functional residual capacity (V'maxFRC). Parental history of asthma and smoking habits during pregnancy were obtained by questionnaire. Data were analyzed using a longitudinal random effects model. infants with a parental history of asthma and/or in utero passive smoke exposure were compared to a reference group of infants who had no parental history of asthma and in whom neither parent smoked pre- or postnatally. Boys were found to have a consistently lower V'maxFRC (-21.05 mL.s(-1)) throughout the first year of life in comparison to girls (P < 0.05). Maternal smoking during pregnancy was associated with a lower V'maxFRG in both genders in comparison to unexposed infants (P < 0.05). V'maxFRC was unaffected by parental history of asthma. Gender-specific normative equations for V'maxFRC throughout the first year of life were derived for the infant cohort as a whole and also for subgroups of infants, based on parental asthma and smoking history. We conclude that lung function during the first year of life differs between genders and is adversely affected by in utero passive tobacco smoke exposure. Gender-specific predictive equations for V'maxFRG should be used during infancy. Pediatr Pulmonol. 2000; 29:331-340, (C) 2000 Wiley-Liss, Inc.	Princess Margaret Hosp Children, Dept Resp Med, Perth, WA, Australia; Univ Arizona, Div Resp Sci, Tucson, AZ USA	Landau, LI (reprint author), Univ Western Australia, Fac Med & Dent, Nedlands, WA 6907, Australia.						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Pulmonol.	MAY	2000	29	5					331	340		10.1002/(SICI)1099-0496(200005)29:5<331::AID-PPUL1>3.0.CO;2-A		10	Pediatrics; Respiratory System	Pediatrics; Respiratory System	308AA	WOS:000086685300001	10790244	
J	Miravitlles, M; Calle, M; Soler-Cataluna, JJ				Miravitlles, Marc; Calle, Myriam; Jose Soler-Cataluna, Juan			Clinical Phenotypes of COPD: Identification, Definition and Implications for Guidelines	ARCHIVOS DE BRONCONEUMOLOGIA			Spanish	Article						COPD; Phenotype; Asthma; Emphysema; Exacerbation; Treatment	OBSTRUCTIVE PULMONARY-DISEASE; INHALED CORTICOSTEROID TREATMENT; RESOLUTION COMPUTED-TOMOGRAPHY; RANDOMIZED CONTROLLED-TRIAL; VOLUME REDUCTION SURGERY; LUNG-FUNCTION DECLINE; AIR-FLOW OBSTRUCTION; QUALITY-OF-LIFE; DYNAMIC HYPERINFLATION; RISK-FACTORS	The term phenotype in the field of COPD is defined as "a single or combination of disease attributes that describe differences between individuals with COPD as they relate to clinically meaningful outcomes". Among all phenotypes described, there are three that are associated with prognosis and especially are associated with a different response to currently available therapies. There phenotypes are: the exacerbator, the overlap COPD-asthma and the emphysema-hyperinflation. The exacerbator is characterised by the presence of, at least, two exacerbations the previous year, and on top of long-acting bronchodilators, may require the use of antiinflammatory drugs. The overlap phenotype presents symptoms of increased variability of airflow and incompletely reversible airflow obstruction. Due to the underlying inflammatory profile, it uses to have a good therapeutic response to inhaled corticosteroids in addition to bronchodilators. Lastly, the emphysema phenotype presents a poor therapeutic response to the existing antiinflammatory drugs and long-acting bronchodilators together with rehabilitation are the treatments of choice. Identifying the peculiarities of the different phenotypes of COPD will allow us to implement a more personalised treatment, in which the characteristics of the patients, together with their severity will be key to choose the best treatment option. (c) 2011 SEPAR. Published by Elsevier Espana, S.L. All rights reserved.	[Miravitlles, Marc] Hosp Clin Barcelona, IDIBAPS, Ciber Enfermedades Resp CIBERES, Barcelona, Spain; [Calle, Myriam] Hosp Clin San Carlos, Serv Neumol, Madrid, Spain; [Jose Soler-Cataluna, Juan] Hosp Requena, Med Interna Serv, Unidad Neumol, Valencia, Spain	Miravitlles, M (reprint author), Hosp Clin Barcelona, IDIBAPS, Ciber Enfermedades Resp CIBERES, Barcelona, Spain.	marcm@separ.es	Calle Rubio, Myriam/B-9780-2017	Calle Rubio, Myriam/0000-0002-3890-2742; Miravitlles, Marc/0000-0002-9850-9520			Abroug F, 2006, AM J RESP CRIT CARE, V174, P990, DOI 10.1164/rccm.200603-380OC; Albert RK, 2011, NEW ENGL J MED, V365, P689, DOI 10.1056/NEJMoa1104623; Alfageme Inmaculada, 2010, Chron Respir Dis, V7, P135, DOI 10.1177/1479972310368692; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P77; Anderson David, 2009, Int J Chron Obstruct Pulmon Dis, V4, P321; Martinez-Garcia MA, 2011, CHEST, V140, P1130, DOI 10.1378/chest.10-1758; Barr RG, 2010, NEW ENGL J MED, V362, P217, DOI 10.1056/NEJMoa0808836; 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J	Rothers, J; Wright, AL; Stern, DA; Halonen, M; Camargo, CA				Rothers, Janet; Wright, Anne L.; Stern, Debra A.; Halonen, Marilyn; Camargo, Carlos A., Jr.			Cord blood 25-hydroxyvitamin D levels are associated with aeroallergen sensitization in children from Tucson, Arizona	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Vitamin D; IgE; aeroallergen; allergic rhinitis; asthma; children	VITAMIN-D INTAKE; CHILDHOOD ASTHMA; ALLERGIC RHINITIS; D SUPPLEMENTATION; PREGNANCY; DISEASES; RISK; IGE; DEFICIENCY; INFANTS	Background: The association between vitamin D status at birth and childhood allergic outcomes is uncertain. The desert climate of Tucson offers a unique setting for studying the health effects of higher exposure to vitamin D. Objective: To assess the relationship between cord blood 25-hydroxyvitamin D (25[OH]D) levels and allergic outcomes through age 5 years. Methods: Cord blood 25(OH)D levels were measured in 219 participants in the Tucson Infant Immune Study, a population-based birth cohort. Plasma total IgE and specific IgE levels to 6 aeroallergens were measured at 1, 2, 3, and 5 years. Skin prick test (SPT) positivity (wheal diameter >= 3 mm) and physician-diagnosed active allergic rhinitis and asthma were assessed at age 5 years. Longitudinal models were used to assess the relationship between 25(OH)D and IgE levels. Logistic regression models were used to assess the relationship of 25(OH)D level with SPT positivity, allergic rhinitis, and asthma. Results: The median cord blood 25(OH)D level was 64 nmol/L (interquartile range, 49-81 nmol/L). Relative to the reference group (50-74.9 nmol/L), both low (<50 nmol/L) and high (>= 100 nmol/L) levels were associated with increased total IgE (coefficient = 0.27, P = .006 and coefficient = 0.27, P = .04, respectively) and detectable inhalant allergen-specific IgE (odds ratio = 2.4, P = .03 and odds ratio = 4.0, P = .01, respectively) through age 5 years. High 25(OH)D levels were also associated with increased SPT positivity (odds ratio = 4.0, P = .02). By contrast, the 25(OH)D level was not significantly associated with allergic rhinitis or asthma. Conclusion: Both low and high levels of cord blood 25(OH)D were associated with increased aeroallergen sensitization. The association between vitamin D status and actual allergic diseases merits further study. (J Allergy Clin Immunol 2011;128:1093-9.)	[Wright, Anne L.] Univ Arizona, Arizona Hlth Sci Ctr, Arizona Resp Ctr, Tucson, AZ 85724 USA; [Rothers, Janet] Univ Arizona, Mel & Enid Zuckerman Coll Publ Hlth, Tucson, AZ 85724 USA; [Wright, Anne L.] Univ Arizona, Dept Pediat, Tucson, AZ 85724 USA; [Halonen, Marilyn] Univ Arizona, Dept Pharmacol, Tucson, AZ 85724 USA; [Camargo, Carlos A., Jr.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Emergency Med, Boston, MA USA; [Camargo, Carlos A., Jr.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Rheumatol Allergy & Immunol,Dept Med, Boston, MA USA	Wright, AL (reprint author), Univ Arizona, Arizona Hlth Sci Ctr, Arizona Resp Ctr, 1501 N Campbell Ave, Tucson, AZ 85724 USA.	awright@arc.arizona.edu			National Institutes of Health [AI 42268, AI 61811]	This study was funded by National Institutes of Health grants AI 42268 and AI 61811 and the Massachusetts General Hospital Center for D-receptor Activation Research.; Disclosure of potential conflict of interest: J. Rothers, A.L. Wright, and M. Halonen receive research support from the National Institutes of Health. 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					1093	U275		10.1016/j.jaci.2011.07.015		12	Allergy; Immunology	Allergy; Immunology	842FJ	WOS:000296578200024	21855975	
J	Van den Abbeele, P; Van de Wiele, T; Verstraete, W; Possemiers, S				Van den Abbeele, Pieter; Van de Wiele, Tom; Verstraete, Willy; Possemiers, Sam			The host selects mucosal and luminal associations of coevolved gut microorganisms: a novel concept	FEMS MICROBIOLOGY REVIEWS			English	Review						microbial communities; colon; symbiotic bacteria; Crohn's disease; gastrointestinal	HUMAN INTESTINAL MICROBIOTA; INFLAMMATORY-BOWEL-DISEASE; INNATE IMMUNE-SYSTEM; 16S RIBOSOMAL-RNA; GRADIENT GEL-ELECTROPHORESIS; BUTYRATE-PRODUCING BACTERIA; LACTOBACILLUS-RHAMNOSUS GG; ILEAL CROHNS-DISEASE; TOLL-LIKE RECEPTOR-3; T-CELL POLARIZATION	Along the human gastrointestinal tract, microorganisms are confronted with multiple barriers. Besides selective physical conditions, the epithelium is regularly replaced and covered with a protective mucus layer trapping immune molecules. Recent insights into host defense strategies show that the host selects the intestinal microbiota, particularly the mucosa-associated microbial community. In this context, humans coevolved with thousands of intestinal microbial species that have adapted to provide host benefits, while avoiding pathogenic behavior that might destabilize their host interaction. While mucosal microorganisms would be crucial for immunological priming, luminal microorganisms would be important for nutrient digestion. Further, we propose that the intestinal microorganisms also coevolved with each other, leading to coherently organized, resilient microbial associations. During disturbances, functionally redundant members become more abundant and are crucial for preserving community functionality. The outside of the mucus layer, where host defense molecules are more diluted, could serve as an environment where microorganisms are protected from disturbances in the lumen and from where they can recolonize the lumen after perturbations. This might explain the remarkable temporal stability of microbial communities. Finally, commensals that become renegade or a decreased exposure to essential coevolved microorganisms may cause particular health problems such as inflammatory bowel diseases, obesity or allergies.	[Van den Abbeele, Pieter; Van de Wiele, Tom; Verstraete, Willy; Possemiers, Sam] Univ Ghent, Lab Microbial Ecol & Technol LabMET, B-9000 Ghent, Belgium	Verstraete, W (reprint author), Univ Ghent, Lab Microbial Ecol & Technol LabMET, Coupure Links 653, B-9000 Ghent, Belgium.	willy.verstraete@ugent.be			FWO-Vlaanderen (Research Foundation of Flanders, Belgium); Ghent University [BOF07/GOA/002]	T.V.d.W. and S. P. are Postdoctoral Fellows and P.V.d.A. is a PhD student, all supported by FWO-Vlaanderen (Research Foundation of Flanders, Belgium). We acknowledge Erwin Zoetendal, Sahar El Aidy, Nico Boon and David van der Ha for their critical review of the manuscript. Finally, this work was financially supported by GOA (BOF07/GOA/002) project from Ghent University.	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Rev.	JUL	2011	35	4					681	704		10.1111/j.1574-6976.2011.00270.x		24	Microbiology	Microbiology	773ND	WOS:000291313100005	21361997	
J	Samoli, E; Nastos, PT; Paliatsos, AG; Katsouyanni, K; Priftis, KN				Samoli, E.; Nastos, P. T.; Paliatsos, A. G.; Katsouyanni, K.; Priftis, K. N.			Acute effects of air pollution on pediatric asthma exacerbation: Evidence of association and effect modification	ENVIRONMENTAL RESEARCH			English	Article						Air pollution; Asthma; Children; Desert dust; Time-series	4 EUROPEAN CITIES; TIME-SERIES; EMERGENCY ADMISSIONS; CASE-CROSSOVER; CHILDREN; EXPOSURE; VISITS; HEALTH; MORTALITY; PROJECT	We investigated the short-term effects of particulate matter with aerodynamic diameter < 10 mu g/m(3) (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2) and ozone (O-3) on pediatric asthma emergency admissions in Athens, Greece over the period 2001-2004. We explored effect modification patterns by season, sex, age and by the presence of desert dust transported mainly from the Sahara area. We used daily time-series data provided by the children's hospitals and the fixed monitoring stations. The associations were investigated using Poisson regression models controlling for seasonality, weather, influenza episodes, day of the week and holiday effects. A 10 mu g/m(3) increase in PM10, was associated with a 2.54% increase (95% confidence interval (Cl): 0.06%, 5.08%) in the number of pediatric asthma hospital admissions, while the same increase in SO2 was associated with a 5.98% (95% Cl: 0.88%, 11.33%) increase. O-3 was associated with a statistically significant increase in asthma admissions among older children in the summer. Our findings provide limited evidence of an association between NO2 exposure and asthma exacerbation. Statistically significant PM10 effects were higher during winter and during desert dust days, while SO2 effects occurred mainly during spring. Our study confirms previously reported PM10 effects on emergency hospital admissions for pediatric asthma and further provides evidence of stronger effects during desert dust days. We additionally report severe effects of SO2, even at today's low concentration levels. (C) 2011 Elsevier Inc. All rights reserved.	[Samoli, E.; Katsouyanni, K.] Med Sch Univ Athens, Dept Hyg Epidemiol & Med Stat, Athens 11527, Greece; [Nastos, P. T.] Univ Athens, Dept Geol & Geoenvironm, Lab Climatol & Atmospher Environm, GR-10679 Athens, Greece; [Paliatsos, A. G.] Technol Educ Inst Piraeus, Gen Dept Math, Piraeus, Greece; [Priftis, K. N.] Penteli Childrens Hosp, Allergy Pneumonol Dept, Athens, Greece	Samoli, E (reprint author), Med Sch Univ Athens, Dept Hyg Epidemiol & Med Stat, 75 Mikras Asias St, Athens 11527, Greece.	esamoli@med.uoa.gr; nastos@geol.uoa.gr; agpal@in.teipir.gr; kkatsouy@med.uoa.gr; kpriftis@otenet.gr	Katsouyanni, Klea/D-4856-2014; Nastos, Panagiotis/E-7455-2015	Katsouyanni, Klea/0000-0002-0132-9575; Nastos, Panagiotis/0000-0001-9336-6586			Abe T, 2009, AM J EMERG MED, V27, P153, DOI 10.1016/j.ajem.2008.01.013; Aekplakorn Wichai, 2003, Southeast Asian Journal of Tropical Medicine and Public Health, V34, P906; Anderson H R, 2003, Eur Respir J Suppl, V40, p39s; Anderson H.R., 2004, MET TIM SER STUD PAN; Atkinson RW, 1999, EUR RESPIR J, V13, P257, DOI 10.1183/09031936.99.13225799; Atkinson RW, 2001, AM J RESP CRIT CARE, V164, P1860; Barnett AG, 2005, AM J RESP CRIT CARE, V171, P1272, DOI 10.1164/rccm.200411-1586OC; BRUMBACK BA, 2000, J AM STAT ASSOC, V95, P16, DOI 10.2307/2669519; Brunekreef B, 2005, EUR RESPIR J, V26, P309, DOI 10.1183/09031936.05.00001805; Chauhan AJ, 2003, LANCET, V361, P1939, DOI 10.1016/S0140-6736(03)13582-9; Clougherty JE, 2010, ENVIRON HEALTH PERSP, V118, P167, DOI 10.1289/ehp.0900994; Dougherty RH, 2009, CLIN EXP ALLERGY, V39, P193, DOI 10.1111/j.1365-2222.2008.03157.x; Georgoulis LB, 2002, ATMOS ENVIRON, V36, P963, DOI 10.1016/S1352-2310(01)00473-3; Gotschi T, 2002, ENVIRON SCI TECHNOL, V36, P1191, DOI 10.1021/es010079n; Gouveia N, 2000, OCCUP ENVIRON MED, V57, P477, DOI 10.1136/oem.57.7.477; Griffin DW, 2007, CLIN MICROBIOL REV, V20, P459, DOI 10.1128/CMR.00039-06; Gyan K, 2005, INT J BIOMETEOROL, V49, P371, DOI 10.1007/s00484-005-0257-3; Halonen JI, 2008, THORAX, V63, P635, DOI 10.1136/thx.2007.091371; Halonen JI, 2010, J EPIDEMIOL COMMUN H, V64, P814, DOI 10.1136/jech.2009.087106; HOEK G, 1993, ARCH ENVIRON HEALTH, V48, P328; Holgate ST, 1999, AIR POLLUTION HLTH; Kallos G., 1997, P INT S REG WEATH PR; Kaskaoutis DG, 2008, ATMOS ENVIRON, V42, P6884, DOI 10.1016/j.atmosenv.2008.05.017; Katsouyanni K, 2001, EPIDEMIOLOGY, V12, P521, DOI 10.1097/00001648-200109000-00011; Katsouyanni K, 2009, RES REP HLTH EFF I, V142, P5; Lin M, 2003, J EPIDEMIOL COMMUN H, V57, P50, DOI 10.1136/jech.57.1.50; Middleton N, 2008, ENVIRON HEALTH-GLOB, V7, DOI 10.1186/1476-069X-7-39; Peel JL, 2005, EPIDEMIOLOGY, V16, P164, DOI 10.1097/01.ede.0000152905.42113.db; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; Priftis KN, 2007, ACTA PAEDIATR, V96, P924, DOI 10.1111/j.1651.2227.2007.00299.x; Priftis KN, 2007, RESP MED, V101, P98, DOI 10.1016/j.rmed.2006.04.008; Samet J M, 2000, Res Rep Health Eff Inst, V94, P5; Samet JM, 2000, RES REP HLTH EFF I, V94, P71; Samoli E, 2008, ENVIRON HEALTH PERSP, V116, P1480, DOI 10.1289/ehp.11345; Schildcrout JS, 2006, AM J EPIDEMIOL, V164, P505, DOI 10.1093/aje/kwj225; Strickland M.J., 2010, AM J RESP CRIT  0408; Sunyer J, 1997, THORAX, V52, P760; Sunyer J, 2003, OCCUP ENVIRON MED, V60, DOI 10.1136/oem.60.8.e2; Touloumi G, 2004, ENVIRONMETRICS, V15, P101, DOI 10.1002/env.623; WHO, 2006, AIR QUAL GUID GLOB U; Zanobetti A, 2009, ENVIRON HEALTH-GLOB, V8, DOI 10.1186/1476-069X-8-58; Zeger SL, 2000, ENVIRON HEALTH PERSP, V108, P419, DOI 10.2307/3454382	42	79	84	2	23	ACADEMIC PRESS INC ELSEVIER SCIENCE	SAN DIEGO	525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA	0013-9351			ENVIRON RES	Environ. Res.	APR	2011	111	3					418	424		10.1016/j.envres.2011.01.014		7	Environmental Sciences; Public, Environmental & Occupational Health	Environmental Sciences & Ecology; Public, Environmental & Occupational Health	743OC	WOS:000289026700014	21296347	
J	Spira-Cohen, A; Chen, LC; Kendall, M; Lall, R; Thurston, GD				Spira-Cohen, Ariel; Chen, Lung Chi; Kendall, Michaela; Lall, Ramona; Thurston, George D.			Personal Exposures to Traffic-Related Air Pollution and Acute Respiratory Health among Bronx Schoolchildren with Asthma	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						pollution; asthma; children's health; diesel; elemental carbon; personal monitoring traffic; PM2.5	EXHALED NITRIC-OXIDE; LUNG-FUNCTION; CHILDHOOD ASTHMA; SOUTH BRONX; CHILDREN; ASSOCIATION; PARTICULATE; SYMPTOMS; INFLAMMATION; COMMUNITIES	BACKGROUND: Previous studies have reported relationships between adverse respiratory health outcomes and residential proximity to traffic pollution, but have not shown this at a personal exposure level. OBJECTIVE: We compared, among inner-city children with asthma, the associations of adverse asthma outcome incidences with increased personal exposure to particulate matter mass <= 2.5 mu m in aerodynamic diameter (PM2.5) air pollution versus the diesel-related carbonaceous fraction of PM2.5. METHODS: Daily 24-hr personal samples of PM2.5, including the elemental carbon (EC) fraction, were collected for 40 fifth-grade children with asthma at four South Bronx schools (10 children per school) during approximately 1 month each. Spirometry and symptom scores were recorded several times daily during weekdays. RESULTS: We found elevated same-day relative risks of wheeze [1.45; 95% confidence interval (CI), 1.03-2.04)], shortness of breath (1.41; 95% CI, 1.01-1.99), and total symptoms (1.30; 95% CI, 1.04-1.62) with an increase in personal EC, but not with personal PM2.5 mass. We found increased risk of cough, wheeze, and total symptoms with increased 1-day lag and 2-day average personal and school-site EC. We found no significant associations with school-site PM2.5 mass or sulfur. The EC effect estimate was robust to addition of gaseous pollutants. CONCLUSION: Adverse health associations were strongest with personal measures of EC exposure, suggesting that the diesel "soot" fraction of PM2.5 is most responsible for pollution-related asthma exacerbations among children living near roadways. Studies that rely on exposure to PM mass may underestimate PM health impacts.	[Spira-Cohen, Ariel; Chen, Lung Chi; Lall, Ramona; Thurston, George D.] NYU, Sch Med, Nelson Inst Environm Med, Tuxedo Pk, NY 10987 USA; [Kendall, Michaela] Univ Exeter, European Ctr Environm & Human Hlth, Peninsula Coll Med & Dent, Truro, Cornwall, England	Thurston, GD (reprint author), NYU, Sch Med, Nelson Inst Environm Med, 57 Old Forge Rd, Tuxedo Pk, NY 10987 USA.	george.thurston@nyu.edu	Cjem, Lung-Chi/H-5030-2012	Chen, Lung Chi/0000-0003-1154-2107	Health Effects Institute; New York University-National Institute of Environmental Health Sciences Center of Excellence [5P30ES000260]; U.S. Environmental Protection Agency (EPA) [R827351, X-982152]; Science to Achieve Results graduate fellowship program	This work is supported by the Health Effects Institute, by New York University-National Institute of Environmental Health Sciences Center of Excellence grant 5P30ES000260, and by the U.S. Environmental Protection Agency (EPA) under grant R827351 (agreement X-982152) and under the Science to Achieve Results graduate fellowship program.	ASHER MI, 1995, EUR RESPIR J, V8, P463; Bailey D., 2007, EVERYONES STAT SOFTW; Balmes JR, 2009, J ALLERGY CLIN IMMUN, V123, P626, DOI 10.1016/j.jaci.2008.10.062; Bosson J, 2008, EUR RESPIR J, V31, P1234, DOI 10.1183/09031936.00078407; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; Buckeridge DL, 2002, ENVIRON HEALTH PERSP, V110, P293; Chang J, 2009, OCCUP ENVIRON MED, V66, P90, DOI 10.1136/oem.2008.039412; Claudio L, 2006, ANN EPIDEMIOL, V16, P332, DOI 10.1016/j.annepidem.2005.06.046; Dales R, 2008, ENVIRON HEALTH PERSP, V116, P1423, DOI 10.1289/ehp.10943; Delfino RJ, 2008, ENVIRON HEALTH PERSP, V116, P550, DOI 10.1289/ehp.10911; 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, 1997, J IMMUNOL, V158, P2406; English P, 1999, ENVIRON HEALTH PERSP, V107, P761, DOI 10.2307/3434663; Finkelstein JA, 2002, ARCH PEDIAT ADOL MED, V156, P562; Gauderman WJ, 2004, NEW ENGL J MED, V351, P1057, DOI 10.1056/NEJMoa040610; Gauderman WJ, 2005, EPIDEMIOLOGY, V16, P737, DOI 10.1097/01.ede.00001813087.51440.75; Gent JF, 2003, JAMA-J AM MED ASSOC, V290, P1859, DOI 10.1001/jama.290.14.1859; Holguin F, 2007, AM J RESP CRIT CARE, V176, P1236, DOI 10.1164/rccm.200611-1616OC; Kan HD, 2007, THORAX, V62, P873, DOI 10.1136/thx.2006.073015; Kim JJ, 2004, AM J RESP CRIT CARE, V170, P520, DOI 10.1164/rccm.200403-2810C; Kulkarni N, 2006, NEW ENGL J MED, V355, P21, DOI 10.1056/NEJMoa052972; Maciejczyk PB, 2004, ATMOS ENVIRON, V38, P5283, DOI 10.1016/j.atmosenv.2004.02.062; McConnell R, 2006, ENVIRON HEALTH PERSP, V114, P766, DOI 10.1289/ehp.8594; McCreanor J, 2007, NEW ENGL J MED, V357, P2348, DOI 10.1056/NEJMoa071535; Miller MR, 2005, EUR RESPIR J, V26, P319, DOI 10.1183/09031936.05.00034805; Mortimer KM, 2002, EUR RESPIR J, V19, P699, DOI 10.1183/09031936.02.00247102; NAPHTALI SZ, 2007, USING GIS EXAMINE EN; Narvaez RF, 2008, ENVIRON SCI TECHNOL, V42, P7330, DOI 10.1021/es801273h; Nicolai T, 2003, EUR RESPIR J, V21, P956, DOI 10.1183/09031936.03.00041103; Nordling E, 2008, EPIDEMIOLOGY, V19, P401, DOI [10.1097/EDE.0b013e31816a1ce3, 10.1097/EDE.0b013e31816alce3]; New York State Department of Health Center for Community Health, 2009, NEW YORK STAT ASTHM; *NY STAT DEP TRANS, 2010, TRAFF DAT VIEW; Patel MM, 2009, AM J RESP CRIT CARE, V180, P1107, DOI 10.1164/rccm.200901-0122OC; Pinhiero J., 2000, MIXED EFFECTS MODELS; Pourazar J, 2005, AM J PHYSIOL-LUNG C, V289, pL724, DOI 10.1152/ajplung.00055.2005; Rabinovitch N, 2006, AM J RESP CRIT CARE, V173, P1098, DOI 10.1164/rccm.200509-1393OC; Sawyer G, 1998, CLIN EXP ALLERGY, V28, P1565; Spira-Cohen A, 2010, J EXPO SCI ENV EPID, V20, P446, DOI 10.1038/jes.2009.34; Suglia SF, 2008, ENVIRON HEALTH PERSP, V116, P1333, DOI 10.1289/ehp.11223; Thurston GD, 2003, JAMA-J AM MED ASSOC, V290, P1915, DOI 10.1001/jama.290.14.1915; Thurston GD, 1997, AM J RESP CRIT CARE, V155, P654; Trasande L, 2005, J ALLERGY CLIN IMMUN, V115, P689, DOI 10.1016/j.jaci.2005.01.056; Trenga CA, 2006, CHEST, V129, P1614, DOI 10.1378/chest.129.6.1614; *US EPA, 2004, EPA600P99002AF NAT C; US EPA, 2008, EPA600R08047F NAT CT; von Klot S, 2002, EUR RESPIR J, V20, P691, DOI 10.1183/09031936.02.01402001	47	79	79	7	48	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765	1552-9924		ENVIRON HEALTH PERSP	Environ. Health Perspect.	APR	2011	119	4					559	565		10.1289/ehp.1002653		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	744BA	WOS:000289065900040	21216722	
J	Cecchi, L; D'Amato, G; Ayres, JG; Galan, C; Forastiere, F; Forsberg, B; Gerritsen, J; Nunes, C; Behrendt, H; Akdis, C; Dahl, R; Annesi-Maesano, I				Cecchi, L.; D'Amato, G.; Ayres, J. G.; Galan, C.; Forastiere, F.; Forsberg, B.; Gerritsen, J.; Nunes, C.; Behrendt, H.; Akdis, C.; Dahl, R.; Annesi-Maesano, I.			Projections of the effects of climate change on allergic asthma: the contribution of aerobiology	ALLERGY			English	Review						allergic diseases; climate change; environment; pollen; spores	RAGWEED AMBROSIA-ARTEMISIIFOLIA; ELEVATED ATMOSPHERIC CO2; THUNDERSTORM-ASSOCIATED ASTHMA; LONG-RANGE TRANSPORT; GRASS-POLLEN SEASONS; COMMON RAGWEED; BIRCH POLLEN; ENVIRONMENTAL-FACTORS; DIESEL EXHAUST; AIR-POLLUTION	Climate change is unequivocal and represents a possible threat for patients affected by allergic conditions. It has already had an impact on living organisms, including plants and fungi with current scenarios projecting further effects by the end of the century. Over the last three decades, studies have shown changes in production, dispersion and allergen content of pollen and spores, which may be region- and species-specific. In addition, these changes may have been influenced by urban air pollutants interacting directly with pollen. Data suggest an increasing effect of aeroallergens on allergic patients over this period, which may also imply a greater likelihood of the development of an allergic respiratory disease in sensitized subjects and exacerbation of symptomatic patients. There are a number of limitations that make predictions uncertain, and further and specifically designed studies are needed to clarify current effects and future scenarios. We recommend: More stress on pollen/spore exposure in the diagnosis and treatment guidelines of respiratory and allergic diseases; collection of aerobiological data in a structured way at the European level; creation, promotion and support of multidisciplinary research teams in this area; lobbying the European Union and other funders to finance this research.	[Cecchi, L.] Univ Florence, Interdept Ctr Bioclimatol, I-50144 Florence, Italy; [D'Amato, G.] High Special Hosp A Cardarelli, Div Resp & Allerg Dis, Dept Chest Dis, Naples, Italy; [Ayres, J. G.] Univ Birmingham, Inst Occupat & Environm Med, Birmingham, W Midlands, England; [Galan, C.] Univ Cordoba, Dept Plant Biol, E-14071 Cordoba, Spain; [Forastiere, F.] Rome E Hlth Author, Dept Epidemiol, Rome, Italy; [Forsberg, B.] Umea Univ, S-90187 Umea, Sweden; [Gerritsen, J.] Univ Groningen, Beatrix Childrens Hosp, Univ Med Ctr Groningen, NL-9700 AB Groningen, Netherlands; [Nunes, C.] Ctr Imunoalergol Algarve, Portimao, Portugal; [Behrendt, H.] KKG Umweltdermatol & Allergol GSF TUM, Munich, Germany; [Akdis, C.] Univ Zurich, Swiss Inst Allergy & Asthma Res, CH-8006 Zurich, Switzerland; [Dahl, R.] Aarhus Univ Hosp, Dept Resp Dis, DK-8000 Aarhus, Denmark; [Annesi-Maesano, I.] INSERM, EPAR, UMR S 707, Paris, France; [Annesi-Maesano, I.] UPMC Univ Paris 061, Paris, France	Cecchi, L (reprint author), Univ Florence, Interdept Ctr Bioclimatol, Piazzale Cascine 18, I-50144 Florence, Italy.	lorenzo.cecchi@unifi.it	Dahl, Ronahl/F-8170-2013; Annesi-Maesano, Isabella/D-9173-2016; Forastiere, Francesco/J-9067-2016	Forastiere, Francesco/0000-0002-9162-5684			Ahas R, 2002, INT J CLIMATOL, V22, P1727, DOI 10.1002/joc.818; Ahlholm JU, 1998, CLIN EXP ALLERGY, V28, P1384; Asero R, 2002, ALLERGY, V57, P1063, DOI 10.1034/j.1398-9995.2002.23766.x; Ayres JG, 2009, EUR RESPIR J, V34, P295, DOI 10.1183/09031936.00003409; Beggs PJ, 2004, CLIN EXP ALLERGY, V34, P1507, DOI 10.1111/j.1365-2222.2004.02061.x; BELLOMO R, 1992, MED J AUSTRALIA, V156, P834; Belmonte J, 2008, INT J BIOMETEOROL, V52, P675, DOI 10.1007/s00484-008-0160-9; Burr ML, 1999, CLIN EXP ALLERGY, V29, P735; Buters JTM, 2008, INT ARCH ALLERGY IMM, V145, P122, DOI 10.1159/000108137; CAROSSO A, 1986, ANN ALLERGY, V56, P300; Cecchi Lorenzo, 2006, Ann Allergy Asthma Immunol, V96, P86; Celenza A, 1996, BRIT MED J, V312, P604; Charpin D, 2005, ALLERGY, V60, P293, DOI 10.1111/j.1398-9995.2005.00731.x; Clot Bernard, 2003, Aerobiologia, V19, P227, DOI 10.1023/B:AERO.0000006572.53105.17; Corden JM, 2001, AEROBIOLOGIA, V17, P127, DOI 10.1023/A:1010876917512; Corden Julie M., 2003, Aerobiologia, V19, P191, DOI 10.1023/B:AERO.0000006529.51252.2f; CRONER S, 1992, ALLERGY, V47, P150, DOI 10.1111/j.1398-9995.1992.tb00956.x; Curtis PS, 1998, OECOLOGIA, V113, P299, DOI 10.1007/s004420050381; D'Amato G, 2001, RESP MED, V95, P606, DOI 10.1053/rmed.2001.1112; D'Amato G, 2008, CLIN EXP ALLERGY, V38, P1264, DOI 10.1111/j.1365-2222.2008.03033.x; D'Amato G, 2007, ALLERGY, V62, P976, DOI 10.1111/j.1398-9995.2007.01393.x; D'Amato G, 2007, ALLERGY, V62, P11, DOI 10.1111/j.1398-9995.2006.01271.x; Dales RE, 2003, CHEST, V123, P745, DOI 10.1378/chest.123.3.745; DAMATO G, 2008, J ALLERGY CLIN IMMUN, V121, P2; Delfino RJ, 1996, AM J RESP CRIT CARE, V154, P633; Dik N, 2004, CHEST, V126, P1147, DOI 10.1378/chest.126.4.1147; Emberlin J, 2002, INT J BIOMETEOROL, V46, P159, DOI 10.1007/s00484-002-0139-x; EMBERLIN J, 1994, ALLERGY, V49, P15, DOI 10.1111/j.1398-9995.1994.tb04233.x; Emberlin J, 1999, CLIN EXP ALLERGY, V29, P347; EMBERLIN J, 1993, CLIN EXP ALLERGY, V23, P911, DOI 10.1111/j.1365-2222.1993.tb00275.x; Fisk WJ, 2007, INDOOR AIR, V17, P284, DOI 10.1111/j.1600-0668.2007.00475.x; Frei T, 2008, INT J BIOMETEOROL, V52, P667, DOI 10.1007/s00484-008-0159-2; Frenguelli G, 2002, Monaldi Arch Chest Dis, V57, P141; Galan C, 2005, INT J BIOMETEOROL, V49, P184, DOI 10.1007/s00484-004-0223-5; Garcia-Mozo H, 2006, ANN AGR ENV MED, V13, P209; Gazala E, 2006, PEDIATR PULM, V41, P1125, DOI 10.1002/ppul.20442; Gehring U, 2005, ALLERGY, V60, P1079, DOI 10.1111/j.1398-9995.2005.00872.x; Girgis ST, 2000, EUR RESPIR J, V16, P3, DOI 10.1034/j.1399-3003.2000.16a02.x; Griffin D. 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J	Vassallo, MF; Camargo, CA				Vassallo, Milo F.; Camargo, Carlos A., Jr.			Potential mechanisms for the hypothesized link between sunshine, vitamin D, and food allergy in children	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Food allergy; vitamin D; vitamin D deficiency; mucosal immunity; epithelial barrier; microbial ecology; infections; sensitization; atopy	REGULATORY T-CELLS; BODY-MASS INDEX; D DEFICIENCY; ATOPIC-DERMATITIS; 1,25-DIHYDROXYVITAMIN D-3; UNITED-STATES; ORAL TOLERANCE; IMMUNE-SYSTEM; US CHILDREN; D-RECEPTOR	Epidemiologic data suggest that the incidence of food allergy (FA) is increasing among children, yet a satisfactory model of its pathogenesis remains elusive. FA is the consequence of maladaptive immune responses to common and otherwise innocuous food antigens. Concurrent with the increase in FA is an epidemic of vitamin D deficiency (VDD) caused by several factors, especially decreased sunlight/UVB exposure. There is growing appreciation of the importance of the pleiotropic hormone vitamin D in the development of tolerance, immune system defenses, and epithelial barrier integrity. We propose a "multiplehit'' model in which VDD in a developmentally critical period increases susceptibility to colonization with abnormal intestinal microbial flora and gastrointestinal infections, contributing to abnormal intestinal barrier permeability and excess and inappropriate exposure of the immune system to dietary allergens. A compounding effect (and additional "hit'') of VDD is the promotion of a pro-sensitization immune imbalance that might compromise immunologic tolerance and contribute to FA. We propose that early correction of VDD might promote mucosal immunity, healthy microbial ecology, and allergen tolerance and thereby blunt the FA epidemic in children. (J Allergy Clin Immunol 2010;126:217-22.)	[Vassallo, Milo F.; Camargo, Carlos A., Jr.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Rheumatol Allergy & Immunol,Dept Med, Boston, MA 02114 USA; [Camargo, Carlos A., Jr.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA; [Camargo, Carlos A., Jr.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA	Camargo, CA (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Rheumatol Allergy & Immunol,Dept Med, 326 Cambridge St,Suite 410, Boston, MA 02114 USA.	ccamargo@partners.org			National Institutes of Health (Bethesda, Md) [T32 AI-060548]; Massachusetts General Hospital Center for D-receptor Activation Research (Boston, Mass); Food Allergy and Anaphylaxis Network (Fairfax, Va)	M. F. V. was supported by T32 AI-060548 from the National Institutes of Health (Bethesda, Md). C. A. 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Allergy Clin. Immunol.	AUG	2010	126	2					217	222		10.1016/j.jaci.2010.06.011		6	Allergy; Immunology	Allergy; Immunology	642IL	WOS:000281203800004	20624647	
J	James, LK; Durham, SR				James, L. K.; Durham, S. R.			Update on mechanisms of allergen injection immunotherapy	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review							GRASS-POLLEN IMMUNOTHERAPY; REGULATORY T-CELLS; MESSENGER-RNA EXPRESSION; PLACEBO-CONTROLLED TRIAL; AFFINITY IGE RECEPTOR; PLASMACYTOID DENDRITIC CELLS; RANDOMIZED CONTROLLED-TRIAL; PHASE SKIN REACTIONS; HOUSE-DUST MITE; SUBLINGUAL IMMUNOTHERAPY	The incidence of allergic diseases is increasing at an alarming rate, paricularly in countries with a western lifestyle. Currently in the UK, approximately one quarter of the population suffers from seasonal allergic rhinitis. Most patients can be treated with conventional pharmacotherapy on an 'as needed' symptomatic basis whereas allergen immunotherapy represents a useful treatment approach in carefully selected patients with severe, IgE-mediated disease. Allergen immunotherapy can deliver improvements in hayfever symptoms over and above that which can be achieved by pharmacotherapy. In addition, unlike pharmacotherapy, allergen immunotherapy provides long-term clinical benefits. These include long-term disease remission, prevention of new atopic sensitisations and a reduction in disease progression from rhinitis to asthma. This review provides a comprehensive update on the mechanisms of allergen injection immunotherapy, recent data on the mechanisms of sublingual allergen immunotherapy is also included.	[James, L. K.; Durham, S. 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Exp. Allergy	JUL	2008	38	7					1074	1088		10.1111/j.1365-2222.2008.02976.x		15	Allergy; Immunology	Allergy; Immunology	325KA	WOS:000257586600003	18691292	
J	Nguyen, LP; Omoluabi, O; Parra, S; Frieske, JM; Clement, C; Ammar-Aouchiche, Z; Ho, SB; Ehre, C; Kesimer, M; Knoll, BJ; Tuvim, MJ; Dickey, BF; Bond, RA				Nguyen, Long P.; Omoluabi, Ozozoma; Parra, Sergio; Frieske, Joanna M.; Clement, Cecilia; Ammar-Aouchiche, Zoulikha; Ho, Samuel B.; Ehre, Camille; Kesimer, Mehmet; Knoll, Brian J.; Tuvim, Michael J.; Dickey, Burton F.; Bond, Richard A.			Chronic exposure to beta-blockers attenuates inflammation and mucin content in a murine asthma model	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article						beta-blockers; beta-adrenoceptor; asthma; mucin; airway inflammation	HEART-FAILURE; ADRENERGIC-BLOCKADE; AIRWAY MUCUS; GOBLET CELL; OVEREXPRESSION; ABNORMALITIES; EXPRESSION; BUCINDOLOL; SECRETION; MICE	Single-dose administration of beta-adrenoceptor agonists produces bronchodilation and inhibits airway hyperresponsiveness (AHR), and is the standard treatment for the acute relief of asthma. However, chronic repetitive administration of beta-adrenoceptor agonists may increase AHR, airway inflammation, and risk of death. Based upon the paradigm shift that occurred with the use of beta-blockers in congestive heart failure, we previously determined that chronic administration of beta-blockers decreased AHR in a murine model of asthma. To elucidate the mechanisms for the beneficial effects of beta-blockers, we examined the effects of chronic administration of several beta-adrenoceptor ligands in a murine model of allergic asthma. Administration of beta-blockers resulted in a reduction in total cell counts, eosinophils, and the cytokines IL-13, IL-10, IL-5, and TGF-beta 1 in bronchoalveolar lavage, and attenuated epithelial mucin content and morphologic changes. The differences in mucin content also occurred if the beta-blockers were administered only during the ovalbumin challenge phase, but administration of beta-blockers for 7 days was not as effective as administration for 28 days. These results indicate that in a murine model of asthma, chronic administration of beta-blockers reduces inflammation and mucous metaplasia, cardinal features of asthma that may contribute to airflow obstruction and AHR. Similar to heart failure, our results provide a second disease model in which beta-blockers producing an acutely detrimental effect may provide a therapeutically beneficial effect with chronic administration.	[Nguyen, Long P.; Knoll, Brian J.; Bond, Richard A.] Univ Houston, Coll Pharm, Dept Pharmacol & Pharmaceut Sci, Houston, TX 77204 USA; [Omoluabi, Ozozoma] Univ Houston, Coll Pharm, Dept Biol & Biochem, Houston, TX 77204 USA; [Clement, Cecilia; Ammar-Aouchiche, Zoulikha; Tuvim, Michael J.; Dickey, Burton F.] Univ Texas Houston, MD Anderson Canc Ctr, Dept Pulm Med, Houston, TX 77030 USA; [Clement, Cecilia; Ammar-Aouchiche, Zoulikha; Tuvim, Michael J.; Dickey, Burton F.] Texas A&M Univ Syst Houston Hlth Sci Ctr, Inst Biosci & Technol, Houston, TX USA; [Ho, Samuel B.] Vet Affairs San Diego Healthcare Syst, Dept Med, San Diego, CA USA; [Ho, Samuel B.] Univ Calif San Diego, San Diego, CA 92103 USA; [Ehre, Camille; Kesimer, Mehmet] Univ N Carolina, Cyst Fibrosis Pulm Res & Treatment Ctr, Chapel Hill, NC USA	Bond, RA (reprint author), Univ Houston, Coll Pharm, Dept Pharmacol & Pharmaceut Sci, 4800 Calhoun, Houston, TX 77204 USA.	RABond@uh.edu		Parra, Sergio/0000-0002-3191-0475; Dickey, Burton/0000-0002-4780-1847	NHLBI NIH HHS [R01HL72984]		Agrawal A, 2007, J APPL PHYSIOL, V102, P399, DOI 10.1152/japplphysiol.00630.2006; *AM LUNG ASS EP ST, 2002, BEST PRACT PROGR SER; Anderson JL, 2003, J CARD FAIL, V9, P266, DOI 10.1054/jcaf.2003.42; Barnes PJ, 1998, PHARMACOL REV, V50, P515; BOND RA, 1995, NATURE, V374, P272, DOI 10.1038/374272a0; Bond RA, 2003, INT CONGR SER, V1249, P27, DOI 10.1016/S0531-5131(03)00614-9; Bond RA, 2002, NAT REV DRUG DISCOV, V1, P825, DOI 10.1038/nrd918; Bond RA, 2001, TRENDS PHARMACOL SCI, V22, P273, DOI 10.1016/S0165-6147(00)01711-9; BOND RA, IN PRESS PHARM THER; Boskabady M H, 2000, Respirology, V5, P111, DOI 10.1046/j.1440-1843.2000.00236.x; Callaerts-Vegh Z, 2004, P NATL ACAD SCI USA, V101, P4948, DOI 10.1073/pnas.0400452101; Evans CM, 2004, AM J RESP CELL MOL, V31, P382, DOI 10.1165/rcmb.0060OC; Evans KLJ, 2003, J APPL PHYSIOL, V94, P245, DOI 10.1152/japplphysiol.00593.2002; Fahy JV, 2002, CHEST, V122, p320S, DOI 10.1378/chest.122.6_suppl.320S; HALL SA, 1995, J AM COLL CARDIOL, V25, P1154, DOI 10.1016/0735-1097(94)00543-Y; HANANIA NA, IN PRESS PULM PHARM; Holgate Stephen T, 2004, Proc Am Thorac Soc, V1, P93, DOI 10.1513/pats.2306034; Kuperman DA, 2002, NAT MED, V8, P885, DOI 10.1038/nm734; Kuyper LM, 2003, AM J MED, V115, P6, DOI 10.1016/S0002-9343(03)00241-9; Lechat P, 1998, CIRCULATION, V98, P1184; LIN R, IN PRESS PULM PHARM; Maack C, 2000, BRIT J PHARMACOL, V130, P1131, DOI 10.1038/sj.bjp.0703400; McGraw DW, 2000, AM J PHYSIOL-LUNG C, V279, pL379; Nelson HS, 2006, CHEST, V129, P15, DOI 10.1378/chest.129.1.15; Ordonez CL, 2001, AM J RESP CRIT CARE, V163, P517; Rogers DF, 2004, CURR OPIN PHARMACOL, V4, P241, DOI 10.1016/j.coph.2004.01.011; SHEKELS LL, 1995, BIOCHEM J, V311, P775; SINGH BN, 1976, CLIN PHARMACOL THER, V19, P493; Wang SZ, 2001, AM J PHYSIOL-LUNG C, V281, pL1303; Williams OW, 2006, AM J RESP CELL MOL, V34, P527, DOI 10.1165/rcmb.2005-0436SF; Wills-Karp M, 2004, SCIENCE, V305, P1726, DOI 10.1126/science.1104134; Witchitz S, 2000, AM J CARDIOL, V85, P1467, DOI 10.1016/S0002-9149(00)00796-7; Young HWJ, 2007, AM J RESP CELL MOL, V37, P273, DOI 10.1165/rcmb.2005-04600C; Zhen GH, 2007, AM J RESP CELL MOL, V36, P244, DOI 10.1165/rcmb.2006-0180OC	34	79	82	1	8	AMER THORACIC SOC	NEW YORK	61 BROADWAY, FL 4, NEW YORK, NY 10006 USA	1044-1549			AM J RESP CELL MOL	Am. J. Respir. Cell Mol. Biol.	MAR	2008	38	3					256	262		10.1165/rcmb.2007-0279RC		7	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	266LA	WOS:000253435500003	18096872	
J	Mitchell, CS; Zhang, JFJ; Sigsgaard, T; Jantunen, M; Lioy, PJ; Samson, R; Karol, MH				Mitchell, Clifford S.; Zhang, Junfeng Jim; Sigsgaard, Torben; Jantunen, Matti; Lioy, Paul J.; Samson, Robert; Karol, Meryl H.			Current state of the science: Health effects and indoor environmental quality	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Review						allergens; chemistry; exposure; fungi; humans; indoor air pollution; intervention; review	VOLATILE ORGANIC-COMPOUNDS; ASSESSMENT METHODOLOGY PTEAM; AIRBORNE PARTICULATE MATTER; POLYMERASE-CHAIN-REACTION; HAZARDOUS AIR-POLLUTANTS; WATER-DAMAGED BUILDINGS; HEART-RATE-VARIABILITY; OF-THE-LITERATURE; STACHYBOTRYS-CHARTARUM; TIME-SERIES	Our understanding of the relationship between human health and the indoor environment continues to evolve. Previous research on health and indoor environments has tended to concentrate on discrete pollutant sources and exposures and on specific disease processes. Recently, efforts have been made to characterize more fully the complex interactions between the health of occupants and the interior spaces they inhabit. In this article we review recent advances in source characterization, exposure assessment, health effects associated with indoor exposures, and intervention research related to indoor environments. Advances in source characterization include a better understanding of how chemicals are transported and processed within spaces and the role that other factors such as lighting and building design may play in determining health. Efforts are under way to improve our ability to measure exposures, but this remains a challenge, particularly for biological agents. Researchers are also examining the effects of multiple exposures as well as the effects of exposures on vulnerable populations such as children and the elderly. In addition, a number of investigators are also studying the effects of modifying building design, materials, and operations on occupant health. Identification of research priorities should include input from building designers, operators, and the public health community.	Johns Hopkins Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD USA; Univ Med & Dent New Jersey, Sch Publ Hlth, Dept Environm & Occupat Hlth, Piscataway, NJ USA; Univ Aarhus, Dept Environm & Occupat Med, Aarhus, Denmark; Natl Publ Hlth Inst, Dept Environm Hlth, Kuopio, Finland; Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Environm & Community Med, Piscataway, NJ 08854 USA; Centraalbur voor Schimmelcultures, Dept Serv & Appl Res, Utrecht, Netherlands; Univ Pittsburgh, Sch Publ Hlth, Dept Environm & Occupat Hlth, Pittsburgh, PA 15260 USA	Mitchell, CS (reprint author), Maryland Dept Hlth & Mental Hyg, 210 W Preston St,Rm 327, Baltimore, MD 21201 USA.	cmitchell@dhmh.state.md.us	Lioy, Paul/F-6148-2011; Mitchell, Clifford/K-3936-2015	Sigsgaard, Torben/0000-0002-2043-7571			Adgate JL, 2004, ENVIRON HEALTH PERSP, V112, P1386, DOI 10.1289/ehp.7107; Afshari A, 2005, INDOOR AIR, V15, P141, DOI 10.1111/j.1600-0668.2005.00332.x; Bell ML, 2004, ANNU REV PUBL HEALTH, V25, P247, DOI 10.1146/annurev.publhealth.25.102802.124329; 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Health Perspect.	JUN	2007	115	6					958	964		10.1289/ehp.8987		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	179HK	WOS:000247280200045	17589607	
J	Eross, E; Dodick, D; Eross, M				Eross, Eric; Dodick, David; Eross, Michael			The sinus, allergy and migraine study (SAMS)	HEADACHE			English	Article						allergy; cranial autonomic symptoms; headache; migraine; sinus	PREVALENCE; HEADACHE	Objective.-The objective of this study is to classify (according to the current International Headache Society's criteria [ICHD-II]) the headache types that those with self-diagnosed sinus headache experience and to determine barriers to correct diagnosis. Background.-The American Migraine Study II estimates that 28 million Americans suffer from migraine headache. The majority of these patients remain undiagnosed and many are erroneously diagnosed as having sinus headache. Despite this common diagnosis, the concept of sinus headache remains an enigma with a relative paucity of information in the literature. Methods.-Advertising in the greater Phoenix, U.S. metropolitan area was used to recruit 100 willing and consecutive subjects to participate in this descriptive clinical study (The Sinus, Allergy and Migraine Study [SAMS]). All patients who believed they suffered from sinus headache and were over 18 years of age were enrolled without exclusion. A detailed history and exam was performed in each patient, and patients were given headache diagnoses based on the current International Headache Society's (IHS) criteria. Results.-Of the 100 subjects with self-diagnosed headache, IHS diagnoses mistaken as sinus headache included migraine with or without aura (52%), chronic migraine associated with medication overuse versus probable medication overuse headache (11%), probable migraine (23%), cluster headache (1%), hemicrania continua (1%), headache secondary to rhinosinusitis (3%), and headaches nonclassifiable (9%). Weather changes (83%), seasonal variation (73%), exposure to allergens (62%), and changes in altitude (38%) were frequent migraine triggers. Seventy-six percent of migraine subjects reported pain in the distribution of the second division of the trigeminal nerve (either unilateral or bilateral), and 62% experienced bilateral forehead and maxillary pain with their headaches. The most common associated features included nasal congestion (56%), eyelid edema (37%), rhinorrhea (25%), conjunctival injection (22%), lacrimation (19%), and ptosis (3%). The headaches nonclassifiable were characterized by a bilateral maxillary pressure of mild to moderate intensity associated with at least one cranial autonomic symptom. Features suggestive of migraine were absent in all 9 of these nonclassifiable cases. Conclusions.-The majority of those with self-diagnosed sinus headache have migraine or probable migraine. In those patients with migraine, the most common reasons for misdiagnosis include headache triggers, pain location, and associated features ("guilt by provocation, location, and association") commonly attributed to sinus headache. The clinician must be aware of these unique presentations of migraine so that a correct diagnosis can be made and effective treatment instituted. A portion of patients with self-diagnosed sinus headache suffer from a headache type, which is unclassifiable by the current IHS criteria. These headaches are characterized by bilateral maxillary pressure, mild to moderate pain intensity, cranial autonomic symptoms, and the complete absence of migraine features.	Arizona Neurol Inst, Scottsdale Headache Ctr, Scottsdale, AZ 85255 USA; Eross Informat Serv, Suwanee, GA USA; Mayo Clin, Coll Med, Dept Neurol, Scottsdale, AZ USA	Eross, E (reprint author), Arizona Neurol Inst, Scottsdale Headache Ctr, Scottsdale, AZ 85255 USA.	ericeross@yahoo.com					*AAOHNS, 2004, STAT AM AC OT HEAD N; *ALL ASTHM FDN AM, 2004, STAT ALL ASTHM FDN A; Blumenthal HJ, 2001, HEADACHE, V41, P883, DOI 10.1046/j.1526-4610.2001.041009883.x; CADY RK, 2003, NASAL ENDOSCOPY MIGR; Goadsby PJ, 2002, NEW ENGL J MED, V346, P257; *INT CLASS HEAD DI, 2004, CEPHALALGIA, V24; Lanza DC, 1997, OTOLARYNG HEAD NECK, V117, pS1, DOI 10.1016/S0194-5998(97)70001-9; Lipton RB, 2001, HEADACHE, V41, P638, DOI 10.1046/j.1526-4610.2001.041007638.x; McAuliffe GW, 1943, RES PUBL ASSOC RES N, V23, P185; Menken M, 2000, ARCH NEUROL-CHICAGO, V57, P418, DOI 10.1001/archneur.57.3.418; REILLY JS, 1990, OTOLARYNG HEAD NECK, V103, P856; SALAM SD, 1994, J MED LIBAN, V42, P200; Schreiber CP, 2004, ARCH INTERN MED, V164, P1769, DOI 10.1001/archinte.164.16.1769; SCHREIBER CP, 2001, NEUROLOGY S, V3, pA311; SCHREIBER CP, 2001, CEPHALALGIA, V21, P298; Stammberger H, 1988, Ann Otol Rhinol Laryngol Suppl, V134, P3; STEWART WF, 1992, JAMA-J AM MED ASSOC, V267, P64, DOI 10.1001/jama.267.1.64; Tarabichi M, 2000, OTOLARYNG HEAD NECK, V122, P842, DOI 10.1016/S0194-5998(00)70011-8; Von Korff M, 1998, NEUROLOGY, V50, P1741	19	79	79	0	6	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0017-8748			HEADACHE	Headache	FEB	2007	47	2					213	224		10.1111/j.1526-4610.2006.00688.x		12	Clinical Neurology	Neurosciences & Neurology	134VP	WOS:000244112800007	17300361	
J	Jutel, M; Akdis, M; Blaser, K; Akdis, CA				Jutel, M; Akdis, M; Blaser, K; Akdis, CA			Mechanisms of allergen specific immunotherapy - T-cell tolerance and more	ALLERGY			English	Review						allergy; histamine; immunoglobulins; specific immunotherapy; T-regulatory cells; tolerance	GRASS-POLLEN IMMUNOTHERAPY; IMMUNOLOGICAL SELF-TOLERANCE; EOSINOPHIL CATIONIC PROTEIN; MESSENGER-RNA EXPRESSION; HOUSE-DUST MITES; HAY-FEVER; SUBLINGUAL IMMUNOTHERAPY; ASTHMATIC-CHILDREN; IN-VITRO; VENOM IMMUNOTHERAPY	Specific immune suppression and induction of tolerance are essential processes in the regulation and circumvention of immune defence. The balance between allergen-specific T-regulatory (Treg) cells and T helper 2 cells appears to be decisive in the development of allergic and healthy immune response against allergens. Treg cells consistently represent the dominant subset specific for common environmental allergens in healthy individuals. In contrast, there is a high frequency of allergen-specific T helper 2 cells in allergic individuals. A decrease in interleukin (IL)-4, IL-5 and IL-13 production by allergen-specific CD4(+) T cells due to the induction of peripheral T cell tolerance is the most essential step in allergen-specific immunotherapy (SIT). Suppressed proliferative and cytokine responses against the major allergens are induced by multiple suppressor factors, such as cytokines like IL-10 and transforming growth factor (TGF)-beta and cell surface molecules like cytotoxic T lymphocyte antigen-4, programmed death-1 and histamine receptor 2. There is considerable rationale for targeting T cells to increase efficacy of SIT. Such novel approaches include the use of modified allergens produced using recombinant DNA technology and adjuvants or additional drugs, which may increase the generation of allergen-specific peripheral tolerance. By the application of the recent knowledge in Treg cells and related mechanisms of peripheral tolerance, more rational and safer approaches are awaiting for the future of prevention and cure of allergic diseases.	Swiss Inst Allergy & Asthma Res, CH-7270 Davos, Switzerland; Wroclaw Med Univ, Dept Internal Med & Allergol, Wroclaw, Poland	Jutel, M (reprint author), Swiss Inst Allergy & Asthma Res, Obere Str 22, CH-7270 Davos, Switzerland.						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Immunology	Allergy; Immunology	053KW	WOS:000238305000002	16792576	
J	Peters-Golden, M; Gleason, MM; Togias, A				Peters-Golden, M; Gleason, MM; Togias, A			Cysteinyl leukotrienes: multi-functional mediators in allergic rhinitis	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review						allergic rhinitis; cysteinyl leukotrienes; CysLT(1) receptor; eosinophils; inflammation; leukotriene C4 synthase; 5-lipoxygenase	COLONY-STIMULATING FACTOR; HUMAN MAST-CELLS; PLACEBO-CONTROLLED TRIAL; VEIN ENDOTHELIAL-CELLS; HUMAN NASAL-MUCOSA; HEMATOPOIETIC PROGENITOR CELLS; ARACHIDONIC-ACID METABOLITES; PERIPHERAL-BLOOD LEUKOCYTES; GENE DISRUPTION REVEALS; C-4 SYNTHASE EXPRESSION	Cysteinyl leukotrienes (CysLTs) are a family of inflammatory lipid mediators synthesized from arachidonic acid by a variety of cells, including mast cells, eosinophils, basophils, and macrophages. This article reviews the data for the role of CysLTs as multi-functional mediators in allergic rhinitis (AR). We review the evidence that: (1) CysLTs are released from inflammatory cells that participate in AR, (2) receptors for CysLTs are located in nasal tissue, (3) CysLTs are increased in patients with AR and are released following allergen exposure, (4) administration of CysLTs reproduces the symptoms of AR, (5) CysLTs play roles in the maturation, as well as tissue recruitment, of inflammatory cells, and (6) a complex inter-regulation between CysLTs and a variety of other inflammatory mediators exists.	Div Clin Immunol & Allergy, Baltimore, MD 21224 USA; Univ Michigan, Ann Arbor, MI 48109 USA; Merck & Co Inc, West Point, PA USA; Johns Hopkins Univ, Baltimore, MD USA	Togias, A (reprint author), Div Clin Immunol & Allergy, 5501 Hopkins Bayview Circle, Baltimore, MD 21224 USA.	atogias@jhmi.edu					Akaiwa M, 2001, CYTOKINE, V13, P75, DOI 10.1006/cyto.2000.0814; Akdis CA, 2003, J ALLERGY CLIN IMMUN, V112, P15, DOI 10.1067/mai.2003.1585; Amrani Y, 2001, AM J RESP CRIT CARE, V164, P2098; Baatjes AJ, 2002, PHARMACOL THERAPEUT, V95, P63, DOI 10.1016/S0163-7258(02)00233-4; Bandeira-Melo C, 2002, J IMMUNOL, V168, P4756; Bandeira-Melo C, 2002, J ALLERGY CLIN IMMUN, V109, P975, DOI 10.1067/mai.2002.124269; BASCOM R, 1988, Journal of Allergy and Clinical Immunology, V81, P580, DOI 10.1016/0091-6749(88)90198-4; Bautz F, 2001, BLOOD, V97, P3433, DOI 10.1182/blood.V97.11.3433; Becler K, 2002, ALLERGY, V57, P1021, DOI 10.1034/j.1398-9995.2002.23620.x; Beller TC, 2004, J BIOL CHEM, V279, P46129, DOI 10.1074/jbc.M407057200; Beller TC, 2004, P NATL ACAD SCI USA, V101, P3047, DOI 10.1073/pnas.0400235101; BENTLEY AM, 1992, J ALLERGY CLIN IMMUN, V89, P877, DOI 10.1016/0091-6749(92)90444-7; BISGAARD H, 1985, ALLERGY, V40, P417, DOI 10.1111/j.1398-9995.1985.tb02680.x; BISGAARD H, 1984, PROSTAGLANDINS, V27, P369, DOI 10.1016/0090-6980(84)90196-5; BISGAARD H, 1986, CLIN ALLERGY, V16, P289, DOI 10.1111/j.1365-2222.1986.tb01960.x; Bisgaard H, 1999, AM J RESP CRIT CARE, V160, P1227; Bloemers SM, 1998, J BIOL CHEM, V273, P2249, DOI 10.1074/jbc.273.4.2249; BOEHMLER AM, 2002, BLOOD, V100; BORGEAT P, 1979, P NATL ACAD SCI USA, V76, P3213, DOI 10.1073/pnas.76.7.3213; Borish L, 2003, J ALLERGY CLIN IMMUN, V112, P1021, DOI 10.1016/j.jaci.2003.90.015; BRACCIONI F, 2001, EUR RESP SOC ANN C 2, V18; Bratton DL, 1999, PEDIATR PULM, V28, P402, DOI 10.1002/(SICI)1099-0496(199912)28:6<402::AID-PPUL3>3.0.CO;2-V; Brock TG, 1996, J IMMUNOL, V156, P2522; Busse W, 2005, CHEST, V127, P1312, DOI 10.1378/chest.127.4.1312; Busse WW, 2001, NEW ENGL J MED, V344, P350; Chibana K, 2003, J IMMUNOL, V170, P4290; CHIBANA K, 2004, AM J RESP CRIT CARE, V169, pA62; Cho SH, 2004, J IMMUNOL, V173, P624; CIFONE MG, 1995, EUR J IMMUNOL, V25, P1080, DOI 10.1002/eji.1830250433; CIPRANDI G, 2003, ALLERG IMMUNOL PARIS, V35, P295; Coffey MJ, 2002, BBA-MOL CELL BIOL L, V1584, P81, DOI 10.1016/S1388-1981(02)00286-X; Coffey MJ, 1999, BLOOD, V94, P3897; Corrigan C, 2005, J ALLERGY CLIN IMMUN, V115, P316, DOI 10.1016/j.jaci.2004.10.051; Cowburn AS, 1999, J IMMUNOL, V163, P456; CRETICOS PS, 1984, NEW ENGL J MED, V310, P1626, DOI 10.1056/NEJM198406213102502; Cyr MM, 2001, CURR OPIN IMMUNOL, V13, P727, DOI 10.1016/S0952-7915(01)00286-2; Denburg JA, 2004, IMMUNOL ALLERGY CLIN, V24, P87, DOI 10.1016/S0889-8561(03)00106-1; DENBURG JA, 1987, INT ARCH ALLER A IMM, V82, P321; Denzlinger C, 1996, CRIT REV ONCOL HEMAT, V23, P167, DOI 10.1016/1040-8428(96)00205-3; DENZLINGER C, 1990, BLOOD, V76, P1765; DONNELLY AL, 1995, AM J RESP CRIT CARE, V151, P1734; Drazen JM, 1999, NEW ENGL J MED, V340, P197; Eglite S, 2000, J IMMUNOL, V165, P2183; ELLIS JL, 1991, J PHYSIOL-LONDON, V436, P469; Espinosa K, 2003, J ALLERGY CLIN IMMUN, V111, P1032, DOI 10.1067/mai.2003.1451; Evans CM, 1997, J CLIN INVEST, V100, P2254, DOI 10.1172/JCI119763; Figueroa DJ, 2001, AM J RESP CRIT CARE, V163, P226; Figueroa DJ, 2003, CLIN EXP ALLERGY, V33, P1380, DOI 10.1046/j.1365-2222.2003.01786.x; FORDHUTCHINSON AW, 1994, ANN NY ACAD SCI, V744, P78, DOI 10.1111/j.1749-6632.1994.tb52725.x; Fregonese L, 2002, CLIN EXP ALLERGY, V32, P745, DOI 10.1046/j.1365-2222.2002.01384.x; Friedmann P. 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Exp. Allergy	JUN	2006	36	6					689	703		10.1111/j.1365-2222.2006.02498.x		15	Allergy; Immunology	Allergy; Immunology	048UX	WOS:000237973100002	16776669	
J	Bornehag, CG; Sundell, J; Hagerhed-Engman, L; Sigsgaard, T				Bornehag, CG; Sundell, J; Hagerhed-Engman, L; Sigsgaard, T			Association between ventilation rates in 390 Swedish homes and allergic symptoms in children	INDOOR AIR			English	Article						ventilation rate; homes; asthma; allergic symptoms; children	HOUSE-DUST MITE; ATOPIC-DERMATITIS; YOUNG-CHILDREN; ASTHMA; EXPOSURE; SENSITIZATION; SENSITIVITY; REDUCTION; HEALTH	The aim of the study was to test the hypothesis that a low-ventilation rate in homes is associated with an increased prevalence of asthma and allergic symptoms among children. A total of 198 cases (with at least two of three symptoms: wheezing, rhinitis, eczema) and 202 healthy controls, living in 390 homes, were examined by physicians. Ventilation rates were measured by a passive tracer gas method, and inspections were carried out in the homes. About 60% of the multi-family houses and about 80% of the single-family houses did not fulfill the minimum requirement regarding ventilation rate in the Swedish building code (0.5 air changes per hour, ach). Cases had significantly lower ventilation rates than controls and a dose-response relationship was indicated.	Karlstad Univ, SE-65188 Karlstad, Sweden; Swedish Natl Testing & Res Inst, Boras, Sweden; Tech Univ Denmark, DK-2800 Lyngby, Denmark; Univ Aarhus, Aarhus, Denmark	Bornehag, CG (reprint author), Karlstad Univ, SE-65188 Karlstad, Sweden.	carl-gustaf.bornehag@kau.se	Sundell, Jan/B-2857-2012; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Sigsgaard, Torben/0000-0002-2043-7571			Bornehag CG, 2004, ENVIRON HEALTH PERSP, V112, P1393, DOI 10.1289/ehp.7187; Bornehag CG, 2004, INDOOR AIR, V14, P59, DOI 10.1111/j.1600-0668.2004.00274.x; BORNEHAG CG, 2004, INDOOR AIR; Eggleston PA, 1998, J ALLERGY CLIN IMMUN, V102, P563, DOI 10.1016/S0091-6749(98)70272-6; Emenius G, 2004, INDOOR AIR, V14, P34, DOI 10.1046/j.1600-0668.2003.00207.x; Emenius G., 1998, Clinical and Experimental Allergy, V28, P1389; HARVING H, 1994, ALLERGY, V49, P866, DOI 10.1111/j.1398-9995.1994.tb00789.x; Holm L, 1999, ALLERGY, V54, P708, DOI 10.1034/j.1398-9995.1999.00010.x; Nahm DH, 1998, ANN ALLERG ASTHMA IM, V80, P411; Nordtest, 1997, VENT LOC MEAN AG AIR; NORLEN U, 1995, P HLTHH BUILD 95 MIL, V1, P393; Oie L, 1998, INDOOR AIR, V8, P190, DOI 10.1111/j.1600-0668.1998.t01-1-00006.x; Oie L, 1999, EPIDEMIOLOGY, V10, P294, DOI 10.1097/00001648-199905000-00018; Ricci G, 1999, BRIT J DERMATOL, V140, P651; Seppanen O, 2002, INDOOR AIR, V12, P98, DOI 10.1034/j.1600-0668.2002.01111.x; Sporik R, 1999, THORAX, V54, P675; STYMNE H, 1994, BUILD ENVIRON, V29, P373, DOI 10.1016/0360-1323(94)90037-X; SUNDELL J, 1995, ALLERGY, V50, P106; SUNDELL J, 1994, INDOOR AIR S, V2, P94; Wargocki P, 2002, INDOOR AIR, V12, P113, DOI 10.1034/j.1600-0668.2002.01145.x; Warner A, 1999, ALLERGY, V54, P681, DOI 10.1034/j.1398-9995.1999.00850.x; Warner JA, 2000, J ALLERGY CLIN IMMUN, V105, P75, DOI 10.1016/S0091-6749(00)90181-7; Weschler CJ, 2000, INDOOR AIR, V10, P92, DOI 10.1034/j.1600-0668.2000.010002092.x	23	79	82	2	22	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0905-6947			INDOOR AIR	Indoor Air	AUG	2005	15	4					275	280		10.1111/j.1600-0668.2005.00372.x		6	Construction & Building Technology; Engineering, Environmental; Public, Environmental & Occupational Health	Construction & Building Technology; Engineering; Public, Environmental & Occupational Health	939BZ	WOS:000230048500008	15982274	
J	Dakhama, A; Park, JW; Taube, C; Joetham, A; Balhorn, A; Miyahara, N; Takeda, K; Gelfand, EW				Dakhama, A; Park, JW; Taube, C; Joetham, A; Balhorn, A; Miyahara, N; Takeda, K; Gelfand, EW			The enhancement or prevention of airway hyperresponsiveness during reinfection with respiratory syncytial virus is critically dependent on the age at first infection and IL-13 production	JOURNAL OF IMMUNOLOGY			English	Article							CHILDHOOD ASTHMA; PULMONARY-FUNCTION; BALB/C MICE; BRONCHIOLITIS; INFANTS; IMMUNITY; ALLERGEN; DISEASE; RISK; SENSITIZATION	Respiratory syncytial virus (RSV) infection in early life is suspected to play a role in the development of postbronchiolitis wheezing and asthma. Reinfection is common at all ages, but factors that determine the development of altered airway function after reinfection are not well understood. This study was conducted in a mouse model to define the role of age in determining the consequences on airway function after reinfection. Mice were infected shortly after birth or at weaning and were reinfected 5 wk later, followed by assessment of airway function, airway inflammation, and lung histopathology. Infection of mice at weaning elicited a protective airway response upon reinfection. In this age group, reinfection resulted in increased airway inflammation, but without development of airway hyperresponsiveness (AHR) or eosinophilia and decreased IL-13 levels. By contrast, neonatal infection failed to protect the airways and resulted in enhanced AHR after reinfection. This secondary response was associated with the development of airway eosinophilia, increased IL-13 levels, and mucus hyperproduction. Both CD4- and CD8-positive T cells were a source of IL-13 in the lung, and inhibition of IL-13 abolished AHR and mucus production in these mice. Inoculation of UV-inactivated virus failed to elicit these divergent responses to reinfection, emphasizing the requirement for active lung infection during initial exposure. Thus, neonatal RSV infection predisposes to the development of airway eosinophilia and enhanced AHR via an IL-13-dependent mechanism during reinfection, whereas infection at a later age protects against the development of these altered airway responses after reinfection.	Natl Jewish Med & Res Ctr, Dept Pediat, Div Cell Biol, Denver, CO 80206 USA	Dakhama, A (reprint author), Natl Jewish Med & Res Ctr, Dept Pediat, Div Cell Biol, Denver, CO 80206 USA.	dakhamaa@njc.org			NHLBI NIH HHS [HL36577, HL60015]		Aberle JH, 1999, AM J RESP CRIT CARE, V160, P1263; Bont L, 2002, PEDIATR RES, V52, P363, DOI 10.1203/01.PDR.0000028458.76706.C7; Culley FJ, 2002, J EXP MED, V196, P1381, DOI 10.1084/jem.20020943; Dakhama A, 2002, AM J RESP CRIT CARE, V165, P1137, DOI 10.1164/rccm.2109058; Donaldson DD, 1998, J IMMUNOL, V161, P2317; ENGLUND JA, 1988, ANN INTERN MED, V109, P203; Gelfand EW, 2004, J IMMUNOL, V173, P1298; GLEZEN WP, 1986, AM J DIS CHILD, V140, P543; GRAHAM BS, 1991, J CLIN INVEST, V88, P1026, DOI 10.1172/JCI115362; Hall C B, 1999, J Pediatr, V135, P2; HALL CB, 1976, NEW ENGL J MED, V294, P414, DOI 10.1056/NEJM197602192940803; HALL CB, 1991, J INFECT DIS, V163, P693; HALL WJ, 1978, ANN INTERN MED, V88, P203; HENDERSON FW, 1979, NEW ENGL J MED, V300, P530, DOI 10.1056/NEJM197903083001004; Johnson TR, 1999, J VIROL, V73, P8485; KATTAN M, 1977, PEDIATRICS, V59, P683; KIMPEN JLL, 1993, CLIN EXP IMMUNOL, V91, P78; Kuperman DA, 2002, NAT MED, V8, P885, DOI 10.1038/nm734; Leader S, 2003, J PEDIATR-US, V143, pS127, DOI 10.1067/S0022-3476(03)00510-9; Legg JP, 2003, AM J RESP CRIT CARE, V168, P633, DOI 10.1164/rccm.200210-1148OC; Martinez FD, 2003, PEDIATR INFECT DIS J, V22, pS76, DOI 10.1097/00006454-200302001-00011; Miyahara N, 2004, J IMMUNOL, V172, P2549; Openshaw PJM, 2003, PEDIATR INFECT DIS J, V22, pS58, DOI 10.1097/00006454-200302001-00009; Park JW, 2003, J ALLERGY CLIN IMMUN, V112, P1078, DOI 10.1016/j.jaci.2003.08.046; PARROTT RH, 1973, AM J EPIDEMIOL, V98, P289; Pope SM, 2001, J ALLERGY CLIN IMMUN, V108, P594; Renzi PM, 1999, AM J RESP CRIT CARE, V159, P1417; Renzi PM, 1997, J PEDIATR-US, V130, P584, DOI 10.1016/S0022-3476(97)70243-9; Roman M, 1997, AM J RESP CRIT CARE, V156, P190; Schwarze J, 1997, J CLIN INVEST, V100, P226, DOI 10.1172/JCI119516; Schwarze J, 2000, AM J RESP CRIT CARE, V162, P380; Shay DK, 2001, J INFECT DIS, V183, P16, DOI 10.1086/317655; Sigurs N, 2000, AM J RESP CRIT CARE, V161, P1501; SLY PD, 1989, PEDIATR PULM, V7, P153, DOI 10.1002/ppul.1950070307; Stein R, 1999, LANCET, V354, P541, DOI 10.1016/S0140-6736(98)10321-5; Takeda K, 1997, J EXP MED, V186, P449, DOI 10.1084/jem.186.3.449; Taube C, 2002, J IMMUNOL, V169, P6482; Waris ME, 1996, J VIROL, V70, P2852; Welliver RC, 2003, J PEDIATR-US, V143, pS112, DOI 10.1067/S0022-3476(03)00508-0; Welliver RC, 2003, PEDIATR INFECT DIS J, V22, pS6, DOI 10.1097/00006454-200302001-00002; Wills-Karp M, 2003, CURR OPIN PULM MED, V9, P21, DOI 10.1097/00063198-200301000-00004	41	79	84	0	2	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	AUG 1	2005	175	3					1876	1883				8	Immunology	Immunology	989BN	WOS:000233648000062	16034131	
J	Prescott, SL; Tang, MLK				Prescott, SL; Tang, MLK			The Australasian Society of Clinical Immunology and Allergy position statement: summary of allergy prevention in children	MEDICAL JOURNAL OF AUSTRALIA			English	Editorial Material							HOUSE-DUST MITE; CHILDHOOD ASTHMA PREVENTION; PLACEBO-CONTROLLED TRIAL; FATTY-ACID MODIFICATION; FOLLOW-UP; LUNG-FUNCTION; SYMPTOMS; RISK; IMMUNOTHERAPY; SENSITIZATION	A family history of allergy and asthma identifies children at high risk of allergic disease. Dietary restrictions in pregnancy are not recommended. Avoiding inhalant allergens during pregnancy has not been shown to reduce allergic disease, and is not recommended. Breastfeeding should be recommended because of other beneficial effects, but if breast feeding is not possible, a hydrolysed formula is recommended (rather than conventional cow's milk formulas) in high-risk infants only. Maternal dietary restrictions during breastfeeding are not recommended. Soy formulas and other formulas (eg, goat's milk) are not recommended for reducing food allergy risk. Complementary foods (including normal cow's milk formulas) should be delayed until a child is aged at least 4-6 months, but a preventive effect from this measure has only been demonstrated in high-risk infants. There is no evidence that an elimination diet after age 4-6 months has a protective effect, although this needs additional investigation. Further research is needed to determine the relationship between house dust mite exposure at an early age and the development of sensitisation and disease; no recommendation can yet be made about avoidance measures for preventing allergic disease. No recommendations can be made about exposure to pets in early life and the development of allergic disease. If a family already has pets it is not necessary to remove them, unless the child develops evidence of pet allergy (as assessed by an allergy specialist). Women should be advised not to smoke while pregnant, and parents should be advised not to smoke. No recommendations can be made on the use of probiotic supplements (or other microbial agents) for preventing allergic disease at this time. Immunotherapy may be considered as a treatment option for children with allergic rhinitis, and may prevent the subsequent development of asthma.	Univ Western Australia, Sch Paediat & Child Hlth Res, Perth, WA 6001, Australia; Royal Childrens Hosp, Dept Immunol, Melbourne, Vic, Australia	Prescott, SL (reprint author), Univ Western Australia, Sch Paediat & Child Hlth Res, POB D184, Perth, WA 6001, Australia.	susanp@ichr.uwa.edu.au	Prescott, Susan/H-5665-2014				Apelberg BJ, 2001, J ALLERGY CLIN IMMUN, V107, P455, DOI 10.1067/mai.2001.113240; BURR ML, 1993, ARCH DIS CHILD, V68, P724; FALTHMAGNUSSON K, 1992, J ALLERGY CLIN IMMUN, V89, P709, DOI 10.1016/0091-6749(92)90378-F; Foucard T, 2000, ACTA PAEDIATR, V89, P71, DOI 10.1080/080352500750027439; Gdalevich M, 2001, J PEDIATR-US, V139, P261, DOI 10.1067/mpd.2001.117006; Gore C, 2004, ALLERGY, V59, P151, DOI 10.1046/j.1398-9995.2003.00358.x; HOLT PG, 1994, LANCET, V344, P456, DOI 10.1016/S0140-6736(94)91776-0; Kalliomaki M, 2003, LANCET, V361, P1869, DOI 10.1016/S0140-6736(03)13490-3; Kjellman NLM, 1998, ALLERGY, V53, P67; Koopman LP, 2002, AM J RESP CRIT CARE, V166, P307, DOI 10.1164/rccm.2106026; Kramer MS, 2003, COCHRANE DB SYST REV; KRAMER MS, 2000, COCHRANE DB SYST REV, DOI UNSP CD000132; MARTINEZ FD, 1992, PEDIATRICS, V89, P21; Mihrshahi S, 2003, J ALLERGY CLIN IMMUN, V111, P162, DOI 10.1067/mai.2003.36; Moller C, 2002, J ALLERGY CLIN IMMUN, V109, P251, DOI 10.1067/mai.2002.121317; Oddy WH, 1999, BRIT MED J, V319, P815; Osborn D. A., 2003, COCHRANE DB SYST REV, DOI DOI 10.1002/14651858.CD003664; Pajno GB, 2001, CLIN EXP ALLERGY, V31, P1392, DOI 10.1046/j.1365-2222.2001.01161.x; Peat JK, 2004, J ALLERGY CLIN IMMUN, V114, P807, DOI 10.1016/j.jaci.2004.06.057; Platts-Mills TA, 2000, J ALLERGY CLIN IMMUN, V105, P503; Ponsonby AL, 2001, CLIN EXP ALLERGY, V31, P1544, DOI 10.1046/j.1365-2222.2001.01163.x; RAM FS, 2002, COCHRANE DB SYST REV, DOI [ARTN CD003795, DOI 10.1002/14651858.CD003795]; Schoetzau A, 2002, PEDIATR ALLERGY IMMU, V13, P234, DOI 10.1034/j.1399-3038.2002.01050.x; Stick SM, 1996, LANCET, V348, P1060, DOI 10.1016/S0140-6736(96)04446-7; Woodcock A, 2004, AM J RESP CRIT CARE, V170, P433, DOI 10.1164/rccm.200401-083OC; ZEIGER R, 1995, J ALLERGY CLIN IMMUN, V96, P1179	26	79	84	0	4	AUSTRALASIAN MED PUBL CO LTD	SYDNEY	LEVEL 1, 76 BERRY ST, SYDNEY, NSW 2060, AUSTRALIA	0025-729X			MED J AUSTRALIA	Med. J. Aust.	MAY 2	2005	182	9					464	+				4	Medicine, General & Internal	General & Internal Medicine	933YA	WOS:000229667600010	15865590	
J	Lammintausta, K; Kortekangas-Savolainen, O				Lammintausta, K; Kortekangas-Savolainen, O			The usefulness of skin tests to prove drug hypersensitivity	BRITISH JOURNAL OF DERMATOLOGY			English	Article						drug hypersensitivity; patch test; skin test	GENERALIZED EXANTHEMATOUS PUSTULOSIS; TOPICAL PROVOCATION; CUTANEOUS REACTIONS; ADVERSE REACTIONS; DIAGNOSIS; CAPTOPRIL; EXPOSURE; ERUPTION; ALLERGY; IGE	Background Suspected drug hypersensitivity is common. Only a minority of cutaneous adverse drug reactions (CADRs) are allergic in origin and will reappear after the next exposure. Methods to confirm suspected CADRs are needed and skin testing could serve as one possibility. Objectives To analyse the usefulness of skin tests in revealing drug allergy. The relevance of skin test results was evaluated with drug provocation studies. Methods During 1989-2001, 947 patients with a history of suspected CADR were examined with skin tests including patch tests (PTs) (826 patients), skin prick tests (SPTs) (935 patients) and photopatch tests (12 patients). The occurrence of positive and negative test reactions to different drugs was correlated with clinical history. Drug provocation was carried out in 246 patients. Results Antimicrobial drugs were suspected and tested most often. A positive PT reaction to one or more drug was seen in 89 of 826 (10.8%), most often to beta-lactams, clindamycin and trimethoprim. A positive SPT reaction was seen in 10 of 935 (1.1%) patients. Challenge was carried out in 17 patients with positive skin test results. Thirteen of 16 (81.2%) PT positives developed exanthema, three remained negative and one SPT-positive patient developed urticaria. Among skin test negatives, 207 of 229 (90.4%) challenges were negative and 22 of 229 (9.6%) were positive, 12 with exanthema, three with fixed drug eruptions and seven with urticaria. Conclusions Skin testing, especially the PT, was a useful screening method to find a cause of CADR if the reaction was exanthema and if antimicrobial, cardiovascular or antiepileptic drugs were suspected. The SPT detected occasional positives with antimicrobials. In cases of fixed drug eruption, PTs performed at the earlier reaction site were useful. When skin tests are negative or dubious, oral challenge should be carried out to confirm the association.	Univ Turku, Cent Hosp, Dept Dermatol, FIN-20520 Turku, Finland	Lammintausta, K (reprint author), Univ Turku, Cent Hosp, Dept Dermatol, Pl 52, FIN-20520 Turku, Finland.	kaija.lammintausta@tyks.fi					Aberer W, 2003, ALLERGY, V58, P854, DOI 10.1034/j.1398-9995.2003.00279.x; ALANKO K, 1987, BRIT J DERMATOL, V116, P561, DOI 10.1111/j.1365-2133.1987.tb05879.x; Barbaud A, 2001, CONTACT DERMATITIS, V45, P321, DOI 10.1034/j.1600-0536.2001.450601.x; Barbaud A, 1998, BRIT J DERMATOL, V139, P49; Barbaud A, 2001, CONTACT DERMATITIS, V44, P373; Bedard K, 2000, BRIT J DERMATOL, V142, P253, DOI 10.1046/j.1365-2133.2000.03293.x; Bigby M, 2001, ARCH DERMATOL, V137, P765; Brockow K, 2002, ALLERGY, V57, P45; Cousin F, 2003, ANN DERMATOL VENER, V130, P321; Eaton L, 2002, BRIT MED J, V324, P8, DOI 10.1136/bmj.324.7328.8b; Friedmann PS, 2003, CLIN EXP ALLERGY, V33, P861, DOI 10.1046/j.1365-2222.2003.01718.x; Gaig P, 2001, J INVEST ALLERG CLIN, V11, P204; Galindo PA, 2002, J INVEST ALLERG CLIN, V12, P299; GHADIALLY R, 1988, J AM ACAD DERMATOL, V19, P428, DOI 10.1016/S0190-9622(88)70194-2; Gniazdowska B, 1999, CONTACT DERMATITIS, V40, P63, DOI 10.1111/j.1600-0536.1999.tb05992.x; Gruchalla RS, 2000, J ALLERGY CLIN IMMUN, V105, P637, DOI 10.1067/mai.2000.106156; Hari Y, 2001, CLIN EXP ALLERGY, V31, P1398, DOI 10.1046/j.1365-2222.2001.01164.x; Heikkila H, 1996, BRIT J DERMATOL, V134, P678, DOI 10.1111/j.1365-2133.1996.tb06969.x; Knowles S, 1998, J AM ACAD DERMATOL, V38, P201, DOI 10.1016/S0190-9622(98)70241-5; Lammintausta K, 2002, BRIT J DERMATOL, V146, P643, DOI 10.1046/j.1365-2133.2002.04665.x; Lee AY, 1998, CONTACT DERMATITIS, V38, P258, DOI 10.1111/j.1600-0536.1998.tb05739.x; Manfredi M, 2004, J ALLERGY CLIN IMMUN, V113, P155, DOI 10.1016/j.jaci.2003.09.035; Mashiah J, 2003, ARCH DERMATOL, V139, P1181, DOI 10.1001/archderm.139.9.1181; Naisbitt DJ, 2003, J ALLERGY CLIN IMMUN, V111, P1393, DOI 10.1067/mai.2003.1507; OSAWA J, 1990, Journal of Dermatology (Tokyo), V17, P235; Padial MA, 2004, BRIT J DERMATOL, V150, P139, DOI 10.1111/j.1365-2133.2004.05717.x; PASCUAL C, 1995, J ALLERGY CLIN IMMUN, V95, P668, DOI 10.1016/S0091-6749(95)70170-2; Pichler W, 2002, ALLERGY, V57, P884, DOI 10.1034/j.1398-9995.2002.02161.x; Pichler WJ, 2004, ALLERGY, V59, P809, DOI 10.1111/j.1398-9995.2004.00547.x; Rebollo S, 2001, CONTACT DERMATITIS, V45, P306, DOI 10.1034/j.1600-0536.2001.450516.x; Romano A, 1999, J ALLERGY CLIN IMMUN, V103, P1186, DOI 10.1016/S0091-6749(99)70197-1; Sandra A, 1998, CONTACT DERMATITIS, V39, P208, DOI 10.1111/j.1600-0536.1998.tb05907.x; Schnyder B, 1998, CLIN EXP ALLERGY, V28, P1412; Torres MJ, 2004, ALLERGY, V59, P219, DOI 10.1046/j.1398-9995.2003.00308.x; Watanabe K, 1996, INTERNAL MED, V35, P142, DOI 10.2169/internalmedicine.35.142; Watsky KL, 1999, ARCH DERMATOL, V135, P93, DOI 10.1001/archderm.135.1.93; Yesudian PD, 2001, CONTACT DERMATITIS, V45, P53, DOI 10.1034/j.1600-0536.2001.045001053.x	37	79	82	0	0	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0007-0963			BRIT J DERMATOL	Br. J. Dermatol.	MAY	2005	152	5					968	974		10.1111/j.1365-2133.2005.06429.x		7	Dermatology	Dermatology	924XF	WOS:000229013600018	15888154	
J	Schram, D; Doekes, G; Boeve, M; Douwes, J; Riedler, J; Ublagger, E; von Mutius, E; Budde, J; Pershagen, G; Nyberg, F; Alm, J; Braun-Fahrlander, C; Waser, M; Brunekreef, B				Schram, D; Doekes, G; Boeve, M; Douwes, J; Riedler, J; Ublagger, E; von Mutius, E; Budde, J; Pershagen, G; Nyberg, F; Alm, J; Braun-Fahrlander, C; Waser, M; Brunekreef, B		PARSIFAL Study Grp	Bacterial and fungal components in house dust of farm children, Rudolf Steiner School children and reference children - the PARSIFAL Study	ALLERGY			English	Article						beta(1,3)-glucans; anthroposophy; children; endotoxin; farm; fungal extracellular polysaccharides; house dust; microbial exposure	ANTHROPOSOPHIC LIFE-STYLE; EXTRACELLULAR POLYSACCHARIDES; ALLERGIC DISEASES; CULTURABLE FUNGI; GERMAN HOMES; HAY-FEVER; ASTHMA; ENDOTOXIN; EXPOSURE; ENVIRONMENTS	Background: Growing up on a farm and an anthroposophic lifestyle are associated with a lower prevalence of allergic diseases in childhood. It has been suggested that the enhanced exposure to endotoxin is an important protective factor of farm environments. Little is known about exposure to other microbial components on farms and exposure in anthroposophic families. Objective: To assess the levels and determinants of bacterial endotoxin, mould beta(1,3)-glucans and fungal extracellular polysaccharides (EPS) in house dust of farm children, Steiner school children and reference children. Methods: Mattress and living room dust was collected in the homes of 229 farm children, 122 Steiner children and 60 and 67 of their respective reference children in five European countries. Stable dust was collected as well. All samples were analysed in one central laboratory. Determinants were assessed by questionnaire. Results: Levels of endotoxin, EPS and glucans per gram of house dust in farm homes were 1.2- to 3.2-fold higher than levels in reference homes. For Steiner children, 1.1- to 1.6-fold higher levels were observed compared with their reference children. These differences were consistently found across countries, although mean levels varied considerably. Differences between groups and between countries were also significant after adjustment for home and family characteristics. Conclusion: Farm children are not only consistently exposed to higher levels of endotoxin, but also to higher levels of mould components. Steiner school children may also be exposed to higher levels of microbial agents, but differences with reference children are much less pronounced than for farm children. Further analyses are, however, required to assess the association between exposure to these various microbial agents and allergic and airway diseases in the PARSIFAL population.	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, Inst Environm Med, Ctr Allergy Res, Div Environm Epidemiol, S-10401 Stockholm, Sweden; AstraZeneca R&D Molndal, Molndal, Sweden; Soder Hosp, Sachs Childrens Hosp, Stockholm, Sweden; Karolinska Inst, Div Clin Immunol, Stockholm, Sweden; Univ Basel, Inst Social & Prevent Med, Basel, Switzerland	Schram, D (reprint author), Univ Utrecht, Inst Risk Assessment Sci, POB 80176, NL-3508 TD Utrecht, Netherlands.		Lauener, Roger/O-8612-2016; van Hage, Marianne/A-9678-2017	Lauener, Roger/0000-0002-8412-606X; van Hage, Marianne/0000-0003-3091-1596; Alm, Johan/0000-0002-9062-4479; Douwes, Jeroen/0000-0003-3599-4036; Pershagen, Goran/0000-0002-9701-1130; brunekreef, bert/0000-0001-9908-0060			ADACHI Y, 1994, BIOL PHARM BULL, V17, P1554; Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; Alm JS, 2002, PEDIATR ALLERGY IMMU, V13, P402, DOI 10.1034/j.1399-3038.2002.01062.x; 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; Braun-Fahrlander C, 2002, ALLERGY, V57, P1094, DOI 10.1034/j.1398-9995.2002.23644.x; Chew GL, 2001, INDOOR AIR, V11, P171, DOI 10.1034/j.1600-0668.2001.011003171.x; 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, 1998, INDOOR AIR, V8, P255, DOI 10.1111/j.1600-0668.1998.00006.x; DOUWES J, 1995, APPL ENVIRON MICROB, V61, P1763; 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; Ernst P, 2000, AM J RESP CRIT CARE, V161, P1563; Gehring U, 2001, ENVIRON HEALTH PERSP, V109, P139, DOI 10.2307/3434766; GOTO H, 1994, AM J IND MED, V25, P81, DOI 10.1002/ajim.4700250121; Hinze S, 1997, INT ARCH ALLERGY IMM, V112, P231; 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; Lauener RP, 2002, LANCET, V360, P465, DOI 10.1016/S0140-6736(02)09641-1; Leynaert B, 2001, AM J RESP CRIT CARE, V164, P1829; Omland O, 2002, ANN AGR ENV MED, V9, P119; Radon K, 2002, ANN AGR ENV MED, V9, P41; Radon K, 2000, ALLERGY, V55, P219, DOI 10.1034/j.1398-9995.2000.00461.x; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; SAKURAI T, 1994, BIOL PHARM BULL, V17, P617; Stone BA, 1992, CHEM BIOL 1 3 BETA G; SUZUKI T, 1992, J PHARMACOBIO-DYNAM, V15, P277; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; Waser M, 2004, CLIN EXP ALLERGY, V34, P389, DOI 10.1111/j.1365-2222.2004.01873.x; Wickens K, 2002, ALLERGY, V57, P1171, DOI 10.1034/j.1398-9995.2002.t01-1-23644.x; ZHANG K, 1994, J CELL BIOCHEM, V56, P225, DOI 10.1002/jcb.240560217	33	79	79	1	11	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	MAY	2005	60	5					611	618		10.1111/j.1398-9995.2005.00748.x		8	Allergy; Immunology	Allergy; Immunology	913US	WOS:000228179800007	15813805	
J	Ebeling, C; Forsythe, P; Ng, J; Gordon, JR; Hollenberg, M; Vliagoftis, H				Ebeling, C; Forsythe, P; Ng, J; Gordon, JR; Hollenberg, M; Vliagoftis, H			Proteinase-activated receptor 2 activation in the airways enhances antigen-mediated airway inflammation and airway hyperresponsiveness through different pathways	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						proteinase-activated receptor 2; allergy; rodent; airway inflammation; eosinophils; IL-13	MICROVASCULAR ENDOTHELIAL-CELLS; EPITHELIAL-CELLS; MITE ALLERGENS; MAST-CELLS; ASTHMA; HYPERREACTIVITY; TRYPTASE; RELEASE; SENSITIZATION; INDUCTION	Background: Serine proteinases such as mast cell tryptase, trypsin-like enzymes, and certain allergens are important in the pathogenesis of asthma. These proteinases can activate the proteinase-activated receptor (PAR)-2, which has been shown to be upregulated in the airways of patients with asthma. Objective: The purpose of this study was to investigate PAR-2 activation in the airways during allergen challenge and its effects on the 2 principle features of asthma, airway inflammation and airway hyperresponsiveness (AHR). Methods: Proteinase-activated receptor 2 activating peptide SLIGRL-NH2 (PAR-2 activating peptide [ap]) or control peptide LSIGRL-NH2 (PAR-2 control peptide [cp]) was administered alone or in conjunction with ovalbumin intranasally to mice, and AHR and airway inflammation were evaluated. Results: PAR2ap did not induce AHR or airway inflammation in ovalbumin-sensitized mice that had not been challenged with ovalbumin. When administered with ovalbumin, PAR-2ap enhanced AHR and airway inflammation compared with ovalbumin administered alone or with PAR-2cp. The enhanced AHR persisted for 5 days, whereas the enhancement to airway inflammation dissipated. Mice administered PAR-2ap alone during the 5 days after the final antigen challenge demonstrated an additional enhancement to airway inflammation compared with the control animals. PAR-2ap administered with allergen increased TNF and IL-5 mRNA in lung tissue and IL-13 and TNF in bronchoalveolar lavage fluid. Conclusion: Exogenous PAR-2 activation in parallel with allergen challenge enhances allergen-mediated AHR and airway inflammation through distinct mechanisms. PAR-2 activation can also enhance established airway inflammation even when dissociated from exposure to allergen. Therefore, PAR-2 activation may play a pathogenic role in the development of AHR and airway inflammation.	Univ Alberta, Pulm Res Grp, Dept Med, Edmonton, AB T6G 2S2, Canada; Univ Saskatchewan, Immunol Res Grp, Saskatoon, SK, Canada; Univ Calgary, Dept Therapeut & Pharmacol, Calgary, AB, Canada	Vliagoftis, H (reprint author), Univ Alberta, Pulm Res Grp, Dept Med, 550 HMRC, Edmonton, AB T6G 2S2, Canada.	harissios.vliagoftis@ualberta.ca	Vliagoftis, Harissios/C-6480-2013; Gordon, John/D-7621-2013				Al-Ani B, 1999, J PHARMACOL EXP THER, V290, P753; Asokananthan N, 2002, J IMMUNOL, V169, P4572; Barrios VE, 2003, BIOCHEM PHARMACOL, V66, P519, DOI 10.1016/S0006-2952(03)00292-2; Berger P, 1999, CLIN EXP ALLERGY, V29, P804; Cenac N, 2002, AM J PATHOL, V161, P1903, DOI 10.1016/S0002-9440(10)64466-5; Chow JM, 2000, BRIT J PHARMACOL, V131, P1584, DOI 10.1038/sj.bjp.0703738; Cocks TM, 1999, NATURE, V398, P156, DOI 10.1038/18223; Compton SJ, 2001, BRIT J PHARMACOL, V134, P705, DOI 10.1038/sj.bjp.0704303; Forsythe P, 2004, AM J RESP CRIT CARE, V169, P220, DOI 10.1164/rccm.200307-979OC; Gordon JR, 2000, CELL IMMUNOL, V205, P128, DOI 10.1006/cimm.2000.1714; Hamelmann E, 1997, AM J RESP CRIT CARE, V156, P766; Haraldsen G, 1996, J IMMUNOL, V156, P2558; Hewitt CRA, 1998, ALLERGY, V53, P60; Kauffman HF, 2003, CURR ALLERGY ASTHM R, V3, P430, DOI 10.1007/s11882-003-0080-z; Klarenbach SW, 2003, CIRC RES, V92, P272, DOI 10.1161/01.RES.0000057386.15390.A3; Knight DA, 2001, J ALLERGY CLIN IMMUN, V108, P797; Leynaert B, 1999, J ALLERGY CLIN IMMUN, V104, P301, DOI 10.1016/S0091-6749(99)70370-2; Lindner JR, 2000, J IMMUNOL, V165, P6504; Macfarlane SR, 2001, PHARMACOL REV, V53, P245; Miike S, 2001, J IMMUNOL, V167, P6615; Ricciardolo FLM, 2000, AM J RESP CRIT CARE, V161, P1672; Schmidlin F, 2002, J IMMUNOL, V169, P5315; Schneider AM, 2001, CELL IMMUNOL, V212, P101, DOI 10.1006/cimm.2001.1854; SCHWARTZ LB, 1990, J ALLERGY CLIN IMMUN, V86, P594, DOI 10.1016/S0091-6749(05)80222-2; SEKIZAWA K, 1989, J CLIN INVEST, V83, P175, DOI 10.1172/JCI113855; Shen HD, 1999, INT ARCH ALLERGY IMM, V119, P259, DOI 10.1159/000024202; Shpacovitch VM, 2002, J INVEST DERMATOL, V118, P380, DOI 10.1046/j.0022-202x.2001.01658.x; Steinhoff M, 2000, NAT MED, V6, P151; Sun G, 2001, J IMMUNOL, V167, P1014; Vergnolle N, 1999, BRIT J PHARMACOL, V127, P1083, DOI 10.1038/sj.bjp.0702634; Vergnolle N, 2001, NAT MED, V7, P821, DOI 10.1038/89945; Vliagoftis H, 2001, J ALLERGY CLIN IMMUN, V107, P679, DOI 10.1067/mai.2001.114245; Vliagoftis Harissios, 2000, Journal of Allergy and Clinical Immunology, V106, P537; Walter DM, 2001, J IMMUNOL, V167, P4668; Yang M, 2001, AM J RESP CELL MOL, V25, P522; Yawn BP, 1999, J ALLERGY CLIN IMMUN, V103, P54, DOI 10.1016/S0091-6749(99)70525-7	36	79	82	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.	MAR	2005	115	3					623	630		10.1016/j.jaci.2004.11.042		8	Allergy; Immunology	Allergy; Immunology	907AN	WOS:000227687000029	15753914	
J	Hubbell, BJ; Hallberg, A; McCubbin, DR; Post, E				Hubbell, BJ; Hallberg, A; McCubbin, DR; Post, E			Health-related benefits of attaining the 8-hr ozone standard	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; benefit analysis; health impact assessment; ozone; standards	MINNEAPOLIS ST-PAUL; AIR-POLLUTION; HOSPITAL ADMISSIONS; DAILY MORTALITY; EMERGENCY-DEPARTMENT; SCHOOL ABSENTEEISM; ASTHMA; VISITS; ASSOCIATIONS; PHILADELPHIA	During the 2000-2002 time period, between 36 and 56% of ozone monitors each year in the United States faded to meet the current ozone standard of 80 ppb for the fourth highest maximum 8-hr ozone concentration. We estimated the health benefits of attaining the ozone standard at these monitors using the U.S. Environmental Protection Agency's Environmental Benefits Mapping and Analysis Program. We used health impact functions based on published epidemiologic studies, and valuation functions derived from the economics literature. The estimated health benefits for 2000 and 2001 are similar in magnitude, whereas the results for 2002 are roughly twice that of each of the prior 2 years. The simple average of health impacts across the 3 years includes reductions of 800 premature deaths, 4,500 hospital and emergency department admissions, 900,000 school absences, and > 1 million minor restricted activity days. The simple average of benefits (including premature mortality) across the 3 years is $5.7 billion [90% confidence interval (0), 0.6-15-01 for the quadratic rollback simulation method and $4.9 billion (90% CI, 0.5-14.0) for the proportional rollback simulation method. Results are sensitive to the form of the standard and to assumptions about background ozone levels. If the form of the standard is based on the first highest maximum 8-hr concentration, impacts are increased by a factor of 2-3. Increasing the assumed hourly background from zero to 40 ppb reduced impacts by 30 and 60% for the proportional and quadratic attainment simulation methods, respectively.	US EPA, OAQPS, Innovat Strategies & Econ Grp, Res Triangle Pk, NC 27703 USA; ABT Associates Inc, Bethesda, MD USA	Hubbell, BJ (reprint author), US EPA, OAQPS, Innovat Strategies & Econ Grp, 4930 Old Page Rd, Res Triangle Pk, NC 27703 USA.	hubbell.bryan@epa.gov		Hubbell, Bryan/0000-0002-7963-3438			Adams PF, 1999, VITAL HLTH STAT, V10, P1; *AG HEALTHC RES QU, 2000, HCUPNET HEALTHCARE; Anderson HR, 2004, META ANAL TIME SERIE; Bell ML, 2004, JAMA-J AM MED ASSOC, V292, P2372, DOI 10.1001/jama.292.19.2372; BERGER MC, 1987, S EC J, V53, P977; Burnett RT, 2001, AM J EPIDEMIOL, V153, P444, DOI 10.1093/aje/153.5.444; *CDC, 2004, NATL HOSP AMB MED CA; *CDC, 2004, CDC WOND; *CDC, 2004, CTR DIS CONTR PREV; Chen L, 2000, INHAL TOXICOL, V12, P997; Chen LM, 2004, PROSTATE, V59, P1, DOI 10.1002/pros.10346; CODY RP, 1992, ENVIRON RES, V58, P184, DOI 10.1016/S0013-9351(05)80214-2; Dominici F., 2003, REVISED ANAL TIME SE, P9; FAIRELY D, 2003, MORTALITY AIR POLLUT, P97; FREEMAN A, 1993, MEASUREMENT ENV RES; Gilliland FD, 2001, EPIDEMIOLOGY, V12, P43, DOI 10.1097/00001648-200101000-00009; Gold C, 1997, LECT NOTES COMPUTER, V1340, P21; Hall JV, 2003, CONTEMP ECON POLICY, V21, P407, DOI 10.1093/cep/byp021; HARRINGTON W, 1987, J URBAN ECON, V22, P101, DOI 10.1016/0094-1190(87)90052-0; Ito K, 1996, J EXPO ANAL ENV EPID, V6, P79; Jaffe DH, 2003, ENVIRON RES, V91, P21, DOI 10.1016/S0013-9351(02)00004-X; Kelsall JE, 1997, AM J EPIDEMIOL, V146, P750; KINNEY PL, 1995, INHAL TOXICOL, V7, P59, DOI 10.3109/08958379509014271; Levy JI, 2001, ENVIRON HEALTH PERSP, V109, P1215, DOI 10.1289/ehp.011091215; Moolgavkar SH, 2000, ENVIRON HEALTH PERSP, V108, P777; MOOLGAVKAR SH, 1995, EPIDEMIOLOGY, V6, P476, DOI 10.1097/00001648-199509000-00003; MOOLGAVKAR SH, 1995, INHAL TOXICOL, V7, P35, DOI 10.3109/08958379509014269; Moolgavkar SH, 1997, EPIDEMIOLOGY, V8, P364, DOI 10.1097/00001648-199707000-00003; NRC (National Research Council), 2002, EST PUBL HLTH BEN PR; OSTRO BD, 1989, ENVIRON RES, V50, P238, DOI 10.1016/S0013-9351(89)80004-0; RANSOM MR, 1992, ENVIRON RES, V58, P204, DOI 10.1016/S0013-9351(05)80216-6; SAMET JM, 1997, AIR POLL WEATH MORB; SCHWARTZ J, 1994, ARCH ENVIRON HEALTH, V49, P366; SCHWARTZ J, 1995, THORAX, V50, P531, DOI 10.1136/thx.50.5.531; SCHWARTZ J, 1994, AM J RESP CRIT CARE, V150, P648; Smith DH, 1997, AM J RESP CRIT CARE, V156, P787; Stanford R, 1999, AM J RESP CRIT CARE, V160, P211; Stieb DM, 1996, ENVIRON HEALTH PERSP, V104, P1354, DOI 10.2307/3432974; Thurston GD, 2001, J EXPO ANAL ENV EPID, V11, P286, DOI 10.1038/sj.jea.7500169; TOLLEY GS, 1986, VALUING HLTH S RISKS; Touloumi G, 1997, AM J EPIDEMIOL, V146, P177; *US BUR LAB STAT, 2004, CONS PRIC IND; U.S. Census Bureau, 2001, STAT ABSTR US; *US DEP ED, 1996, COND ED 1996; *US EPA, 1996, REV NATL AMB AIR QUA; *US EPA, 2004, EPA20R04007 WASH DC; *US EPA, 2003, 454K03001 WASH DC U; *US EPA, 1999, EPA410R99001 WASH DC; *US EPA, 2004, 45203001 EPA; *US EPA, 2004, TECHN TRANSF NETW AI; *US EPA, 1996, EPA600P93004CF US EP, V3; Vingarzan R, 2004, ATMOS ENVIRON, V38, P3431, DOI 10.1016/j.atmosenv.2004.03.030; WEISEL CP, 1995, ENVIRON HEALTH PERSP, V103, P97, DOI 10.2307/3432456; World Health Organization (WHO), 2003, EUR035042688; *WOOD POOL EC INC, 2001, POP SINGL YEAR AGE C	55	79	82	1	17	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	2005	113	1					73	82				10	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	885ZQ	WOS:000226196300033	15626651	
J	Kapoor, S; Roberts, G; Bynoe, Y; Gaughan, M; Habibi, P; Lack, G				Kapoor, S; Roberts, G; Bynoe, Y; Gaughan, M; Habibi, P; Lack, G			Influence of a multidisciplinary paediatric allergy clinic on parental knowledge and rate of subsequent allergic reactions	ALLERGY			English	Article						children; education; food allergy; multidisciplinary clinic	FOOD ALLERGY; PEANUT ALLERGY; ANAPHYLACTIC REACTIONS; IGE CONCENTRATIONS; CHILDREN; MANAGEMENT; EPINEPHRINE; ADOLESCENTS; CHALLENGES; HISTORY	Background: Studies have demonstrated that families of children with food allergy have significant deficiencies in their knowledge of how to avoid allergen exposure and how to manage allergic reactions. This study aims to assess the impact of a multidisciplinary paediatric allergy clinic consultation on parental knowledge of food allergy and to determine the rate of subsequent allergic reactions. Methods: Sixty-two subjects (< 17 years) referred with food allergy were prospectively enrolled. Parental knowledge was assessed by questionnaire and EpiPen trainer. Families saw a paediatric allergist, clinical nurse specialist and dietician. Knowledge was reassessed after 3 months and rate of allergic reactions after 1 year. Results: After one visit to the paediatric allergy clinic, there was a significant improvement in parental knowledge of allergen avoidance (26.9%, P < 0.001), managing allergic reactions (185.4%, P < 0.0001) and EpiPen usage (83.3%, P < 0.001). Additionally, there was a significant reduction in allergic reactions (P < 0.001). Children with egg, milk or multiple food allergies were more likely to suffer subsequent reactions. Conclusions: A single visit to a multidisciplinary allergy clinic considerably improves families' abilities to manage allergic reactions to foods with an accompanying reduction in allergic reactions. Young children with egg, milk or multiple food allergies were at greatest risk of further reactions.	St Marys Hosp, London W2 1NY, England	Roberts, G (reprint author), St Marys Hosp, Ground Floor Salton House,Praed St, London W2 1NY, England.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P225, DOI DOI 10.1164/AJRCCM/136.1.225; BOCK SA, 1989, J ALLERGY CLIN IMMUN, V83, P900, DOI 10.1016/0091-6749(89)90103-6; Clark AT, 2003, ARCH DIS CHILD, V88, P79, DOI 10.1136/adc.88.1.79; Ewan PW, 2001, LANCET, V357, P111, DOI 10.1016/S0140-6736(00)03543-1; Gold MS, 2000, J ALLERGY CLIN IMMUN, V106, P171; Grouhi M, 1999, J ALLERGY CLIN IMMUN, V104, P190, DOI 10.1016/S0091-6749(99)70134-X; Hourihane JO, 1996, BRIT MED J, V313, P518; Huang SW, 1998, J ALLERGY CLIN IMMUN, V102, P525, DOI 10.1016/S0091-6749(98)70145-9; NICKLAS RA, 1998, J ALLERGY CLIN ALLER, V101, pS466; Primeau MN, 2000, CLIN EXP ALLERGY, V30, P1135, DOI 10.1046/j.1365-2222.2000.00889.x; Pumphrey RSH, 2000, CLIN EXP ALLERGY, V30, P1144, DOI 10.1046/j.1365-2222.2000.00864.x; Roberts G, 2000, CLIN EXP ALLERGY, V30, P1495, DOI 10.1046/j.1365-2222.2000.00960.x; Sampson HA, 1997, JAMA-J AM MED ASSOC, V278, P1888, DOI 10.1001/jama.278.22.1888; Sampson HA, 1997, J ALLERGY CLIN IMMUN, V100, P444; Sampson HA, 2001, J ALLERGY CLIN IMMUN, V107, P891, DOI 10.1067/mai.2001.114708; SAMPSON HA, 1992, NEW ENGL J MED, V327, P380, DOI 10.1056/NEJM199208063270603; Sicherer SH, 2000, PEDIATRICS, V105, P359, DOI 10.1542/peds.105.2.359; SPORIK R, 1997, J ALLERGY CLIN IMMUN, V100, P444; Vickers DW, 1997, CLIN EXP ALLERGY, V27, P898	19	79	79	0	5	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	FEB	2004	59	2					185	191		10.1046/j.1398-9995.2003.00365.x		7	Allergy; Immunology	Allergy; Immunology	771WC	WOS:000188808200010	14763932	
J	Watanabe, J; Miyazaki, Y; Zimmerman, GA; Albertine, KH; McIntyre, TM				Watanabe, J; Miyazaki, Y; Zimmerman, GA; Albertine, KH; McIntyre, TM			Endotoxin contamination of ovalbumin suppresses murine immunologic responses and development of airway hyper-reactivity	JOURNAL OF BIOLOGICAL CHEMISTRY			English	Article							HUMAN-ENDOTHELIAL-CELLS; TOLL-LIKE RECEPTOR-2; BACTERIAL LIPOPOLYSACCHARIDE; ESCHERICHIA-COLI; ALLERGIC-ASTHMA; KAPPA-B; MICE; HYPERRESPONSIVENESS; INFLAMMATION; EXPOSURE	The reversible airway hyper-reactivity (AHR) of asthma is modeled by sensitizing and challenging mice with aerosolized ovalbumin. However, the C57BL/6 murine strain does not display the large increase in circulating IgG and IgE antibodies found in human atopy and asthma. We found that commercial ovalbumin was contaminated with lipopolysaccharide (LPS) in amounts sufficient to fully activate endothelial cells in an in vitro assay of the first step of inflammation. Desensitization of TLR4 by LPS pretreatment suppressed the inflammatory effect of ovalbumin. The presence of LPS was occult, because it does not require serum presentation and, like the LPS of Salmonella minnesota, was not suppressed by polymyxin B. Purified ovalbumin did not activate endothelial cells in vitro; however, endotoxin-free ovalbumin was far more effective than commercial material in stimulating IgE production and respiratory dysfunction in a C57BL/6 murine model of AHR. Moreover, endotoxin-free ovalbumin induced lung inflammation with alveolar enlargement and destruction in a histologic pattern that differed from the changes caused by commercial, endotoxin-contaminated ovalbumin. Reconstitution of purified ovalbumin with S. minnesota LPS decreased lung inflammation, decreased changes in lung function, and suppressed anti-ovalbumin antibody production. We conclude endotoxin contaminates ovalbumin preparations and that endotoxin co-administration with the ovalbumin antigen creates a state of tolerance in a murine model of AHR. Co-exposure to endotoxin and antigen occurs in humans through organic dusts, so murine models of AHR may reflect the clinical situation, but models based on commercial ovalbumin do not accurately reflect the effect of protein antigen alone on animal physiology.	Univ Utah, Eccles Inst Human Genet 4130, Dept Pathol, Salt Lake City, UT 84112 USA; Univ Utah, Dept Med, Salt Lake City, UT 84112 USA; Univ Utah, Dept Pediat, Salt Lake City, UT 84112 USA; Univ Utah, Program Human Mol Biol & Genet, Salt Lake City, UT 84112 USA	McIntyre, TM (reprint author), Univ Utah, Eccles Inst Human Genet 4130, Dept Pathol, Salt Lake City, UT 84112 USA.				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Biol. Chem.	OCT 24	2003	278	43					42361	42368		10.1074/jbc.M307752200		8	Biochemistry & Molecular Biology	Biochemistry & Molecular Biology	733FP	WOS:000185989500098	12909619	
J	Kucharewicz, I; Kowal, K; Buczko, W; Bodzenta-Lukaszyk, A				Kucharewicz, I; Kowal, K; Buczko, W; Bodzenta-Lukaszyk, A			The plasmin system in airway remodeling	THROMBOSIS RESEARCH			English	Review						plasmin system; asthma; airway remodeling	ACTIVATOR INHIBITOR TYPE-2; INDUCED PULMONARY-FIBROSIS; BRONCHOALVEOLAR LAVAGE FLUID; NECROSIS-FACTOR-ALPHA; HUMAN MAST-CELLS; HOUSE DUST MITE; HUMAN-MONOCYTES; UROKINASE RECEPTOR; 5-LIPOXYGENASE PATHWAY; NEUTROPHIL AGGREGATION	Recent studies suggest that the plasmin system plays an active role in tissue remodeling. Plasmin degrades the extracellular matrix (ECM), either directly removing glycoproteins from ECM or by activating matrix metalloproteinases (MMPs). PAI-1 blocking MMPs may prevent ECM degradation, but inhibiting fibrinolysis leads to fibrin accumulation and fibrosis. Components of the plasmin system including tissue plasminogen activator (t-PA), urokinase plasminogen activator (u-PA), and plasminogen activator inhibitors PAI-1 and PAI-2 are synthesised by airway cells, and inflammatory mediators affect their expression. The plasmin system, in turn, actively influences the production of inflammatory mediators,and growth factors, extending pathological structural changes in the airway. Modulation of the plasmin system might be a new pharmacological strategy that could inhibit the development of airway remodeling. (C) 2003 Elsevier Ltd. All rights reserved.	Med Univ Bialystok, Dept Allergol & Internal Dis, PL-15276 Bialystok, Poland; Med Acad Bialystok, Dept Pharmacodynam, PL-15230 Bialystok, Poland	Kucharewicz, I (reprint author), Med Univ Bialystok, Dept Allergol & Internal Dis, M Sklodowska Curie St 24A, PL-15276 Bialystok, Poland.	ikuchar@poczta.onet.pl; Krzysztof.9327125@pharmanet.com; pharmdyn@amab.edu.pl; alergol@amb.edu.pl					Amin K, 2000, AM J RESP CRIT CARE, V162, P2295; Bianchi E, 1996, J CLIN INVEST, V98, P1133, DOI 10.1172/JCI118896; Buckova D, 2002, ALLERGY, V57, P446; Busse W, 1999, AM J RESP CRIT CARE, V160, P1035; CASTELLOTE JC, 1990, THROMB HAEMOSTASIS, V63, P67; CHANG WC, 1993, AM J PHYSIOL, V264, pC271; CHAPMAN HA, 1982, CELL, V28, P653, DOI 10.1016/0092-8674(82)90220-3; Chetta A, 1997, CHEST, V111, P852, DOI 10.1378/chest.111.4.852; Cho SH, 2001, J ALLERGY CLIN IMMUN, V108, P212, DOI 10.1067/mai.2001.117260; Cho SH, 2000, J IMMUNOL, V165, P3154; CHU CT, 1993, J IMMUNOL, V150, P48; Coughlin SR, 2000, NATURE, V407, P258, DOI 10.1038/35025229; 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Res.		2003	112	1-2					1	7		10.1016/j.thromres.2003.10.011		7	Hematology; Peripheral Vascular Disease	Hematology; Cardiovascular System & Cardiology	775KP	WOS:000189039700001	15013265	
J	Tomita, K; Caramori, G; Lim, S; Ito, K; Hanazawa, T; Oates, T; Chiselita, I; Jazrawi, E; Chung, KF; Barnes, PJ; Adcock, IM				Tomita, K; Caramori, G; Lim, S; Ito, K; Hanazawa, T; Oates, T; Chiselita, I; Jazrawi, E; Chung, KF; Barnes, PJ; Adcock, IM			Increased p21(CIP1/WAF1) and B cell lymphoma leukemia-x(L) expression and reduced apoptosis in alveolar macrophages from smokers	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						p21(CIP1/WAF1); monocytes/macrophages; apoptosis; cigarette smoke; epithelial cells	OXIDATIVE STRESS; CHEMOKINE RECEPTOR; CIGARETTE SMOKERS; G(1) ARREST; KAPPA-B; DEATH; DNA; P21; REPLICATION; PROTEIN	Alveolar macrophages (AMs) are the predominant defense cells in the airway, and their numbers are increased in smokers and subjects with chronic obstructive pulmonary disease. This increase may result from increased recruitment, increased proliferation, or reduced cell death. Apoptosis regulates inflammatory cell survival, and p21(CIP1/WAF1) is an important inhibitory regulator of cycle progression after oxidative stress. We have investigated whether chronic smoke exposure influences the expression and localization of cell cycle and apoptotic proteins in AM and bronchial epithelial cells in vivo. The increased numbers of AMs seen in smokers were only partially due to enhanced proliferation. p21(CIP1/WAF1) protein expression was increased in AMs and biopsies isolated from smokers and was found predominantly within the cytoplasm. In addition, B cell lymphoma leukemia (BCl)-x(L), an antiapoptotic regulator, was also highly expressed in macrophages from smokers compared with nonsmokers and subjects with asthma. Hydrogen peroxide, an oxidative stress, induced cytoplasmic expression of p21(CiP1/WAF1) and failed to induce apoptosis in an in vitro model. These results suggested that AM and bronchial epithelial cells from smokers, in contrast to those from normal subjects and subjects with asthma, have reduced cell death. Thus, oxidative stress induced by cigarette smoking may contribute to the chronicity of inflammation in the airway, through a reduction of apoptosis.	Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Thorac Med, London SW3 6LY, England	Adcock, IM (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Thorac Med, Dovehouse St, London SW3 6LY, England.			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J. Respir. Crit. Care Med.	SEP 1	2002	166	5					724	731		10.1164/rccm.2104010		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	588ZZ	WOS:000177734100020	12204872	
J	Levy, JI; Carrothers, TJ; Tuomisto, JT; Hammitt, JK; Evans, JS				Levy, JI; Carrothers, TJ; Tuomisto, JT; Hammitt, JK; Evans, JS			Assessing the public health benefits of reduced ozone concentrations	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Review						benefit-cost analysis; epidemiology; exposure assessment; monetary valuation; ozone; premature mortality	PARTICULATE AIR-POLLUTION; DAILY MORTALITY; PULMONARY-FUNCTION; AMBIENT OZONE; HOSPITAL ADMISSIONS; UNITED-STATES; LUNG-FUNCTION; BRONCHIOLAR EPITHELIUM; CARDIOVASCULAR-DISEASE; RESPIRATORY MORBIDITY	In this paper we examine scientific evidence and related uncertainties in two steps of benefit-cost analyses of ozone reduction: estimating the health improvements attributable to reductions in ozone and determining the appropriate monetary values of these improvements. Although substantial evidence exists on molecular and physiologic impacts, the evidence needed to establish concentration-response functions is somewhat limited. Furthermore, because exposure to ozone depends on factors such as air conditioning use, past epidemiologic studies may not be directly applicable in unstudied settings. To evaluate the evidence likely to contribute significantly to benefits, we focus on four health outcomes: premature mortality, chronic asthma, respiratory hospital admissions, and minor restricted activity days. We determine concentration-response functions for these health outcomes for a hypothetical case study in Houston, Texas, using probabilistic weighting reflecting our judgment of the strength of the evidence and the possibility of confounding. We make a similar presentation for valuation, where uncertainty is due primarily to the lack of willingness-to-pay data for the population affected by ozone. We estimate that the annual monetary value of health benefits from reducing ozone concentrations in Houston is approximately $10 per person per microgram per cubic meter (24-hr average) reduced (95% confidence: interval, $0.70-$40). The central estimate exceeds past estimates by approximately a factor of five, driven by the inclusion of mortality. We discuss the implications of our findings for future analyses and determine areas of research that might help reduce the uncertainties in benefit estimation.	Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Landmark Ctr, Boston, MA 02215 USA; Harvard Univ, Ctr Risk Anal, Boston, MA 02215 USA; Pharsight Corp, Mt View, CA USA; Natl Publ Hlth Inst, Dept Environm Hlth, Kuopio, Finland; Harvard Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA 02215 USA	Levy, JI (reprint author), Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Landmark Ctr, POB 15677, Boston, MA 02215 USA.		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J	Milanese, M; Crimi, E; Scordamaglia, A; Riccio, A; Pellegrino, R; Canonica, GW; Brusasco, V				Milanese, M; Crimi, E; Scordamaglia, A; Riccio, A; Pellegrino, R; Canonica, GW; Brusasco, V			On the functional consequences of bronchial basement membrane thickening	JOURNAL OF APPLIED PHYSIOLOGY			English	Article						airway responsiveness; remodeling; asthma; chronic obstructive pulmonary disease; rhinitis	SUBEPITHELIAL FIBROSIS; AIRWAY INFLAMMATION; INDUCED BRONCHOCONSTRICTION; ASTHMA; METHACHOLINE; DISEASE; HYPERRESPONSIVENESS; RESPONSIVENESS; MECHANISM; COLLAGEN	Reticular basement membrane (RBM) thickness and airway responses to inhaled methacholine (MCh) were studied in perennial allergic asthma (n = 11), perennial allergic rhinitis (n = 8), seasonal allergic rhinitis (n = 5), and chronic obstructive pulmonary disease (COPD, n = 9). RBM was significantly thicker in asthma (10.1 +/- 3.7 mum) and perennial rhinitis (11.2 +/- 4.2 mum) than in seasonal rhinitis (4.7 +/- 0.7 mum) and COPD (5.2 +/- 0.7 mum). The dose (geometric mean) of MCh causing a 20% decrease of 1-s forced expiratory volume (FEV1) was significantly higher in perennial rhinitis (1,073 mug) than in asthma (106 mug). In COPD, the slope of the linear regression of all values of forced vital capacity plotted against FEV1 during the challenge was higher, and the intercept less, than in other groups, suggesting enhanced airway closure. In asthma, RBM thickness was positively correlated (r = 0.77) with the dose (geometric mean) of MCh causing a 20% decrease of FEV1 and negatively correlated (r = -0.73) with the forced vital capacity vs. FEV1 slope. We conclude that 1) RBM thickening is not unique to bronchial asthma, and 2) when present, it may protect against airway narrowing and air trapping. These findings support the opinion that RBM thickening represents an additional load on airway smooth muscle.	Univ Genoa, Dipartimento Sci Motorie & Riabilitat & Med Inter, I-16132 Genoa, Italy; Azienda Osped S Croce & Carle, I-12100 Cuneo, Italy	Brusasco, V (reprint author), Univ Genoa, Dipartimento Sci Motorie & Riabilitat, Largo R Benzi 10, I-16132 Genoa, Italy.						American thoracic society, 1995, AM J RESP CRIT CARE, V152, pS77; Boulet LP, 1997, CHEST, V112, P45, DOI 10.1378/chest.112.1.45; BRADLEY BL, 1991, J ALLERGY CLIN IMMUN, V88, P661, DOI 10.1016/0091-6749(91)90160-P; BREWSTER CEP, 1990, AM J RESP CELL MOL, V3, P507; BURNEY PGJ, 1989, INT J EPIDEMIOL, V18, P165, DOI 10.1093/ije/18.1.165; Carroll NG, 2000, AM J RESP CRIT CARE, V161, P244; Chakir J, 1996, LAB INVEST, V75, P735; Chetta A, 1996, AM J RESP CRIT CARE, V153, P910; Chetta A, 1997, CHEST, V111, P852, DOI 10.1378/chest.111.4.852; Chu HW, 1998, AM J RESP CRIT CARE, V158, P1936; Crimi E, 2001, J APPL PHYSIOL, V91, P1029; DAVIDSON PT, 1987, AM REV RESPIR DIS, V136, P255; Gibbons WJ, 1996, AM J RESP CRIT CARE, V153, P582; Hoshino M, 1998, J ALLERGY CLIN IMMUN, V102, P783, DOI 10.1016/S0091-6749(98)70018-1; JEFFERY PK, 1989, AM REV RESPIR DIS, V140, P1745; JEFFERY PK, 1992, AM REV RESPIR DIS, V145, P890; LAMBERT RK, 1991, J APPL PHYSIOL, V71, P666; LAMBERT RK, 1993, J APPL PHYSIOL, V74, P2771; Laprise C, 1999, EUR RESPIR J, V14, P63, DOI 10.1034/j.1399-3003.1999.14a12.x; Macklem PT, 1996, AM J RESP CRIT CARE, V153, P83; MINK SN, 1983, J APPL PHYSIOL, V55, P897; MORENO RH, 1986, AM REV RESPIR DIS, V133, P1171; Palmans E, 2000, AM J RESP CRIT CARE, V161, P627; Pellegrino R, 1996, J APPL PHYSIOL, V81, P964; Roche WR, 1998, AM J RESP CRIT CARE, V157, pS191; ROCHE WR, 1989, LANCET, V1, P520; Seow CY, 2000, J APPL PHYSIOL, V88, P527; Vignola AM, 1998, AM J RESP CRIT CARE, V157, P403; WIGGS BR, 1992, AM REV RESPIR DIS, V145, P1251; Wiggs BR, 1997, J APPL PHYSIOL, V83, P1814	30	79	81	0	0	AMER PHYSIOLOGICAL SOC	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	8750-7587			J APPL PHYSIOL	J. Appl. Physiol.	SEP	2001	91	3					1035	1040				6	Physiology; Sport Sciences	Physiology; Sport Sciences	464VQ	WOS:000170552800003	11509495	
J	Corsini, E; Galli, CL				Corsini, E; Galli, CL			Epidermal cytokines in experimental contact dermatitis	TOXICOLOGY			English	Article; Proceedings Paper	7th Summer School in Immunotoxicology	SEP 14-16, 1999	ARLES, FRANCE			contact dermatitis; skin irritation; contact allergy; cytokines	TUMOR-NECROSIS-FACTOR; ACTIVATED LANGERHANS CELLS; SKIN IMMUNE-SYSTEM; FACTOR-ALPHA; IN-VIVO; HUMAN KERATINOCYTES; DENDRITIC CELLS; GUINEA-PIG; TNF-ALPHA; SENSITIZATION	Topical exposure to a variety of xenobiotics may result in irritant as well as allergic contact dermatitis both in rodents and in humans. Despite their induction by different mechanisms, they cannot be differentiated by macroscopic appearance and, by histological examination they are both generally characterized by a perivascular mononuclear cell infiltrate and capillary hyperpermeability. Recently, cytokines, a family of inducible glycoproteins that play a pivotal role in immune and inflammatory reactions, have been identified as useful tools for differentiation of irritant and allergic contact dermatitis. In this article the role of cytokines in the development and differentiation of irritant and allergic contact dermatitis is discussed. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.	Univ Milan, Inst Pharmacol Sci, Ctr Cosmet Toxicol, Toxicol Lab, I-20133 Milan, Italy	Corsini, E (reprint author), Univ Milan, Inst Pharmacol Sci, Ctr Cosmet Toxicol, Toxicol Lab, Via Balzaretti 9, I-20133 Milan, Italy.		Corsini, Emanuela/B-5602-2011	Galli, Corrado Lodovico/0000-0003-0078-5488			AIBA S, 1990, J IMMUNOL, V145, P2791; BERARDESCA E, 1994, CONTACT DERMATITIS, V31, P281, DOI 10.1111/j.1600-0536.1994.tb02019.x; BOS JD, 1993, IMMUNOL TODAY, V14, P75, DOI 10.1016/0167-5699(93)90062-P; BUEHLER EV, 1965, ARCH DERMATOL, V91, P171; Corsini E, 1996, TOXICOL APPL PHARM, V138, P268, DOI 10.1006/taap.1996.0125; Corsini E, 1997, J INVEST DERMATOL, V108, P892, DOI 10.1111/1523-1747.ep12292696; CUMBERBATCH M, 1994, IMMUNOLOGY, V81, P395; Draize JH, 1944, J PHARMACOL EXP THER, V82, P377; ENK AH, 1993, J IMMUNOL, V150, P3698; ENK AH, 1992, P NATL ACAD SCI USA, V89, P1398, DOI 10.1073/pnas.89.4.1398; GAD SC, 1986, TOXICOL APPL PHARM, V84, P93, DOI 10.1016/0041-008X(86)90419-9; Goodwin B F, 1985, Curr Probl Dermatol, V14, P201; GORDON JR, 1990, NATURE, V346, P274, DOI 10.1038/346274a0; GROVES RW, 1995, BRIT J DERMATOL, V132, P345, DOI 10.1111/j.1365-2133.1995.tb08666.x; HEUFLER C, 1988, J EXP MED, V167, P700, DOI 10.1084/jem.167.2.700; Holliday M R, 1997, Am J Contact Dermat, V8, P158, DOI 10.1016/S1046-199X(97)90097-X; Jakob T, 1998, J IMMUNOL, V160, P4067; KIMBER I, 1990, J APPL TOXICOL, V10, P173, DOI 10.1002/jat.2550100306; KIMBER I, 1996, TOXICOLOGY CONTACT H, P127; Klecak G, 1985, Curr Probl Dermatol, V14, P152; KLECAK G, 1977, J SOC COSMET CHEM, V28, P53; KOCK A, 1990, J EXP MED, V172, P1609, DOI 10.1084/jem.172.6.1609; KONDO S, 1994, LYMPHOKINE CYTOK RES, V13, P367; KUPPER TS, 1990, J CLIN INVEST, V86, P1783, DOI 10.1172/JCI114907; Kupper T. S., 1995, J INVEST DERMATOL, V105, p62S; LARRICK JW, 1989, J LEUKOCYTE BIOL, V45, P429; Luster ML, 1995, TOXICOL LETT, V82-3, P471, DOI 10.1016/0378-4274(95)03577-X; MacMillan F. S. K., 1975, ANIMAL MODELS DERMAT, P12; MAGNUSSON B, 1969, J INVEST DERMATOL, V52, P268; MAURER T, 1975, AGENTS ACTIONS, V5, P174, DOI 10.1007/BF02027360; Maurer T., 1996, TOXICOLOGY CONTACT H, P107; MCKENZIE RC, 1990, J INVEST DERMATOL, V95, P1055; MILLER K, 1984, INT ARCH ALLER A IMM, V75, P120; MIZUTANI H, 1991, J CLIN INVEST, V87, P1066, DOI 10.1172/JCI115067; [Anonymous], 1979, COSMET TOILETRIES; Muller G, 1996, Am J Contact Dermat, V7, P177, DOI 10.1016/S1046-199X(96)90009-3; Pape KA, 1997, J IMMUNOL, V159, P591; PIGUET PF, 1991, J EXP MED, V173, P673, DOI 10.1084/jem.173.3.673; POBER JS, 1990, PHYSIOL REV, V70, P427; ROUDABUSH RL, 1965, TOXICOL APPL PHARM, V7, P559, DOI 10.1016/0041-008X(65)90041-4; SHELLEY WB, 1976, NATURE, V261, P46, DOI 10.1038/261046a0; STREILEIN JW, 1989, J IMMUNOL, V143, P3925; TRINCHIERI G, 1993, IMMUNOL TODAY, V14, P335, DOI 10.1016/0167-5699(93)90230-I; WAHLBERG JE, 1996, TOXICOLOGY CONTACT H, P57; WHO, 1990, ENV HLTH CRIT, V116; Williams IR, 1996, LIFE SCI, V58, P1485, DOI 10.1016/0024-3205(96)00042-2; Yamazaki S, 1998, EXP DERMATOL, V7, P35, DOI 10.1111/j.1600-0625.1998.tb00300.x	47	79	83	0	9	ELSEVIER SCI IRELAND LTD	CLARE	CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND	0300-483X			TOXICOLOGY	Toxicology	JAN 17	2000	142	3					203	211		10.1016/S0300-483X(99)00145-6		9	Pharmacology & Pharmacy; Toxicology	Pharmacology & Pharmacy; Toxicology	275NN	WOS:000084826400006	10667891	
J	Schuijs, MJ; Willart, MA; Vergote, K; Gras, D; Deswarte, K; Ege, MJ; Madeira, FB; Beyaert, R; van Loo, G; Bracher, F; von Mutius, E; Chanez, P; Lambrecht, BN; Hammad, H				Schuijs, Martijn J.; Willart, Monique A.; Vergote, Karl; Gras, Delphine; Deswarte, Kim; Ege, Markus J.; Madeira, Filipe Branco; Beyaert, Rudi; van Loo, Geert; Bracher, Franz; von Mutius, Erika; Chanez, Pascal; Lambrecht, Bart N.; Hammad, Hamida			ALLERGY Farm dust and endotoxin protect against allergy through A20 induction in lung epithelial cells	SCIENCE			English	Article							NF-KAPPA-B; CHILDHOOD ASTHMA; AIRWAY INFLAMMATION; MITE ALLERGEN; ENZYME A20; EXPOSURE; RESPONSES; CHILDREN; IMMUNITY; ENVIRONMENT	Growing up on a dairy farm protects children from allergy, hay fever, and asthma. A mechanism linking exposure to this endotoxin (bacterial lipopolysaccharide)-rich environment with protection has remained elusive. Here we show that chronic exposure to low-dose endotoxin or farm dust protects mice from developing house dust mite (HDM)-induced asthma. Endotoxin reduced epithelial cell cytokines that activate dendritic cells (DCs), thus suppressing type 2 immunity to HDMs. Loss of the ubiquitin-modifying enzyme A20 in lung epithelium abolished the protective effect. A single-nucleotide polymorphism in the gene encoding A20 was associated with allergy and asthma risk in children growing up on farms. Thus, the farming environment protects from allergy by modifying the communication between barrier epithelial cells and DCs through A20 induction.	[Schuijs, Martijn J.; Willart, Monique A.; Vergote, Karl; Deswarte, Kim; Madeira, Filipe Branco; Lambrecht, Bart N.; Hammad, Hamida] VIB Inflammat Res Ctr, Immunoregulat Lab, Ghent, Belgium; [Schuijs, Martijn J.; Willart, Monique A.; Vergote, Karl; Deswarte, Kim; Madeira, Filipe Branco; Lambrecht, Bart N.; Hammad, Hamida] Univ Ghent, Dept Internal Med, B-9000 Ghent, Belgium; [Gras, Delphine; Chanez, Pascal] Aix Marseille Univ, Assistance Publ Hop Marseille, Dept Resp Med, UMR INSERM U1067,CNRS 7333, Marseille, France; [Ege, Markus J.; von Mutius, Erika] Univ Munich, Dr von Hauner Childrens Hosp, D-81377 Munich, Germany; [Beyaert, Rudi; van Loo, Geert] VIB Inflammat Res Ctr, Unit Mol Signal Transduct, Ghent, Belgium; [Beyaert, Rudi; van Loo, Geert] Univ Ghent, Dept Biomed Mol Biol, B-9000 Ghent, Belgium; [Bracher, Franz] Univ Munich, Dept Pharm, Ctr Drug Res, D-81377 Munich, Germany; [Lambrecht, Bart N.] Erasmus MC, Dept Pulm Med, Rotterdam, Netherlands	Lambrecht, BN (reprint author), VIB Inflammat Res Ctr, Immunoregulat Lab, Ghent, Belgium.	bart.lambrecht@ugent.be; hamida.hammad@ugent.be	van Loo, Geert/C-1505-2009; Hammad, Hamida/J-9391-2015; Lambrecht, Bart/K-2484-2014; Gras, Delphine/A-7062-2017	Hammad, Hamida/0000-0003-3762-8603; Lambrecht, Bart/0000-0003-4376-6834; 	European Union FP7 grant "MedALL" (Mechanisms in Development of Allergy); European Union Innovative Medicines Initiative grant "EUBIOPRED"; Flanders Organization for Scientific Research (FWO) program; European Research Council Consolidator grant; Ghent University Multidisciplinary Research Platform grant; ARARD; Fonds de Recherche en Sante Respiratoire; ANR "Mucocil"; European Union [GABRIEL: LSHB-CT-2006-018996, HERA: ERC2009-AdG_20090506_250268]; Gottfried-Wilhelm-Leibniz award from the German Research Council	The data reported in this manuscript are tabulated in the main paper and in the supplementary materials. M.J.E. and E.v.M have filed patent applications (EP000002361632B1, EP000001964570B1, and US020080305089A1) that relate to identifying microorganisms and derived substances in farm dust that induce protection from several inflammatory diseases. This research was supported by European Union FP7 grant "MedALL" (Mechanisms in Development of Allergy) and by a European Union Innovative Medicines Initiative grant "EUBIOPRED." H.H. and B.N.L. are recipients of several Flanders Organization for Scientific Research (FWO) program grants. B.N.L. is a recipient of a European Research Council Consolidator grant and a Ghent University Multidisciplinary Research Platform grant (Group-ID). D.G. and P.C. are supported by grants from ARARD, Fonds de Recherche en Sante Respiratoire, and ANR "Mucocil." Population analyses were supported by two European Union research grants (GABRIEL: LSHB-CT-2006-018996, HERA: ERC2009-AdG_20090506_250268). E.v.M is supported by a Gottfried-Wilhelm-Leibniz award from the German Research Council. M.J.E. and E.v.M. are members of the German Center for Lung Research (DZL).	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J	Hoff, T; Weller, W; DePuccio, M				Hoff, Timothy; Weller, Wendy; DePuccio, Matthew			The Patient-Centered Medical Home: A Review of Recent Research	MEDICAL CARE RESEARCH AND REVIEW			English	Review						health care quality; literature review; patient-centered medical home; primary care; research design	PRIMARY-CARE; HEALTH-CARE; CHILDREN; ACCESS; ASTHMA; DELIVERY; SERVICES; SYSTEM; NEEDS; MODEL	The patient-centered medical home is an important innovation in health care delivery. There is a need to assess the scope and substance of published research on medical homes. This article reviews published evaluations of medical home care for the period 2007 to 2010. Chief findings from these evaluations as a whole include associations between the provision of medical home care and improved quality, in addition to decreased utilization associated with medical home care in high-cost areas such as emergency department use. However, fewer associations were found across evaluations between medical home care and enhanced patient or family experiences. The early medical home research appears to reflect both the wide variation in how medical homes are being designed and implemented in practice and in how researchers are choosing to evaluate patient-centered medical home design and implementation. While some aspects of medical home care show promise, continued evolution of medical home evaluative research is needed.	[Hoff, Timothy] SUNY Albany, Sch Publ Hlth, Rensselaer, NY 12144 USA	Hoff, T (reprint author), SUNY Albany, Sch Publ Hlth, GEC Bldg,1 Univ Pl, Rensselaer, NY 12144 USA.	thoff@albany.edu	Webster, Susan/C-7360-2015	Webster, Susan/0000-0002-0684-4226			ANDERSEN RM, 1995, J HEALTH SOC BEHAV, V36, P1, DOI 10.2307/2137284; Barr MS, 2008, JAMA-J AM MED ASSOC, V300, P834, DOI 10.1001/jama.300.7.834; Beal A, 2009, J GEN INTERN MED, V24, P514, DOI 10.1007/s11606-009-1119-1; Berenson RA, 2008, HEALTH AFFAIR, V27, P1219, DOI 10.1377/hlthaff.27.5.1219; Bitton A, 2010, J GEN INTERN MED, V25, P584, DOI 10.1007/s11606-010-1262-8; Carrier E, 2009, MED CARE, V47, P714, DOI 10.1097/MLR.0b013e3181a469b0; Coleman K., 2010, COMMONWEALTH FUND IS, V85, P1; Coleman K, 2010, ANN FAM MED, V8, P493, DOI 10.1370/afm.1190; Cooley WC, 2009, PEDIATRICS, V124, P358, DOI 10.1542/peds.2008-2600; Davis K, 2011, J GEN INTERN MED, V26, P1201, DOI 10.1007/s11606-011-1720-y; Diedhiou A, 2010, MED CARE RES REV, V67, P450, DOI 10.1177/1077558710367735; Domino ME, 2009, MED CARE, V47, P1113, DOI 10.1097/MLR.0b013e3181adcc65; Dorr DA, 2008, J AM GERIATR SOC, V56, P2195, DOI 10.1111/j.1532-5415.2008.02005.x; Ferrante JM, 2010, J AM BOARD FAM MED, V23, P736, DOI 10.3122/jabfm.2010.06.100085; Ferrante JM, 2010, ANN FAM MED, V8, P108, DOI 10.1370/afm.1080; Friedberg Mark W, 2009, Am J Manag Care, V15, pS291; Gilfillan RJ, 2010, AM J MANAG CARE, V16, P607; Hoff T, 2010, MED CARE RES REV, V67, P383, DOI 10.1177/1077558710368550; Homer CJ, 2008, PEDIATRICS, V122, pE922, DOI 10.1542/peds.2007-3762; Jaen Carlos Roberto, 2010, Ann Fam Med, V8 Suppl 1, pS57, DOI 10.1370/afm.1121; Klitzner TS, 2010, J PEDIATR-US, V156, P1006, DOI 10.1016/j.jpeds.2009.12.012; Leff B, 2009, AM J MANAG CARE, V15, P555; McGrath Robert J, 2009, Pediatrics, V124 Suppl 4, pS443, DOI 10.1542/peds.2009-1255Q; National Academy of State Health Policy, 2011, MED HOM STAT; National Committee for Quality Assurance, 2012, PCHM 2011 CONT SCOR; Patient-Centered Primary Care Collaborative, 2012, PIL DEM JOINT PRINC; Patient-Centered Primary Care Collaborative, 2012, PIL DEM; Rankin KM, 2009, AM J MED QUAL, V24, P302, DOI 10.1177/1062860609335759; Reid RJ, 2009, AM J MANAG CARE, V27, P362; Reid RJ, 2010, HEALTH AFFAIR, V29, P835, DOI 10.1377/hlthaff.2010.0158; Rittenhouse DR, 2009, NEW ENGL J MED, V361, P2301, DOI 10.1056/NEJMp0909327; Roby DH, 2010, MED CARE RES REV, V67, P412, DOI 10.1177/1077558710368682; Romaire MA, 2010, ACAD PEDIATR, V10, P338, DOI 10.1016/j.acap.2010.06.010; ROSENSTOCK IM, 1966, MILBANK FUND Q, V44, P94, DOI 10.2307/3348967; Rosenthal TC, 2008, J AM BOARD FAM MED, V21, P427, DOI 10.3122/jabfm.2008.05.070287; Scobie Andrea, 2009, Healthc Manage Forum, V22, P47; Sidorov JE, 2008, HEALTH AFFAIR, V27, P1231, DOI 10.1377/hlthaff.27.5.1231; Starfield B, 2004, PEDIATRICS, V113, P1493; Stevens GD, 2010, J ASTHMA, V47, P1001, DOI [10.1080/02770903.2010.514636, 10.3109/02770903.2010.514636]	39	78	78	3	41	SAGE PUBLICATIONS INC	THOUSAND OAKS	2455 TELLER RD, THOUSAND OAKS, CA 91320 USA	1077-5587			MED CARE RES REV	Med. Care Res. Rev.	DEC	2012	69	6					619	644		10.1177/1077558712447688		26	Health Care Sciences & Services; Health Policy & Services	Health Care Sciences & Services	032QI	WOS:000310733600001	22645100	
J	Palmer, TM; Sterne, JAC; Harbord, RM; Lawlor, DA; Sheehan, NA; Meng, S; Granell, R; Smith, GD; Didelez, V				Palmer, Tom M.; Sterne, Jonathan A. C.; Harbord, Roger M.; Lawlor, Debbie A.; Sheehan, Nuala A.; Meng, Sha; Granell, Raquel; Smith, George Davey; Didelez, Vanessa			Instrumental Variable Estimation of Causal Risk Ratios and Causal Odds Ratios in Mendelian Randomization Analyses	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						causal inference; causality; confounding factors (epidemiology); effect modifiers (epidemiology); generalized method of moments; instrumental variables; Mendelian randomization analysis; structural models	STRUCTURAL MEAN MODELS; GENERALIZED-METHOD; INFERENCE; TRIALS; IDENTIFICATION; NONCOMPLIANCE; EPIDEMIOLOGY; EQUATION; BIAS; ENDOGENEITY	In this paper, the authors describe different instrumental variable (IV) estimators of causal risk ratios and odds ratios with particular attention to methods that can handle continuously measured exposures. The authors present this discussion in the context of a Mendelian randomization analysis of the effect of body mass index (BMI; weight (kg)/height (m)(2)) on the risk of asthma at age 7 years (Avon Longitudinal Study of Parents and Children, 19911992). The authors show that the multiplicative structural mean model (MSMM) and the multiplicative generalized method of moments (MGMM) estimator produce identical estimates of the causal risk ratio. In the example, MSMM and MGMM estimates suggested an inverse relation between BMI and asthma but other IV estimates suggested a positive relation, although all estimates had wide confidence intervals. An interaction between the associations of BMI and fat mass and obesity-associated (FTO) genotype with asthma explained the different directions of the different estimates, and a simulation study supported the observation that MSMM/MGMM estimators are negatively correlated with the other estimators when such an interaction is present. The authors conclude that point estimates from various IV methods can differ in practical applications. Based on the theoretical properties of the estimators, structural mean models make weaker assumptions than other IV estimators and can therefore be expected to be consistent in a wider range of situations.	[Palmer, Tom M.; Lawlor, Debbie A.; Smith, George Davey] Univ Bristol, Sch Social & Community Med, MRC Ctr Causal Anal Translat Epidemiol, Bristol BS8 2BN, Avon, England; [Sheehan, Nuala A.; Meng, Sha] Univ Leicester, Coll Med, Dept Hlth Sci, Leicester, Leics, England; [Sheehan, Nuala A.; Meng, Sha] Univ Leicester, Dept Genet, Coll Med, Leicester LE1 7RH, Leics, England; [Didelez, Vanessa] Univ Bristol, Sch Math, Fac Sci, Bristol BS8 2BN, Avon, England	Palmer, TM (reprint author), Univ Bristol, Sch Social & Community Med, MRC Ctr Causal Anal Translat Epidemiol, Oakfield House, Bristol BS8 2BN, Avon, England.	tom.palmer@bristol.ac.uk	Harbord, Roger/A-8699-2008; Davey Smith, George/A-7407-2013	Harbord, Roger/0000-0002-2257-8271; Davey Smith, George/0000-0002-1407-8314; Monsalve, Beatriz Elena/0000-0002-5994-866X; Palmer, Tom/0000-0003-4655-4511; Lawlor, Debbie A/0000-0002-6793-2262	Medical Research Council (MRC) [G0601625]; MRC Centre for Causal Analyses in Translational Epidemiology [G0600705]; Wellcome Trust	This work was funded by the Medical Research Council (MRC) Collaborative Project (grant G0601625). Drs. Tom M. Palmer, Debbie A. Lawlor, and George Davey Smith are employed by the MRC Centre for Causal Analyses in Translational Epidemiology, which funds Dr. Palmer's salary (MRC grant G0600705). The MRC, the Wellcome Trust, and the University of Bristol provide core funding support for the Avon Longitudinal Study of Parents and Children (ALSPAC).	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J. Epidemiol.	JUN 15	2011	173	12					1392	1403		10.1093/aje/kwr026		12	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	775UK	WOS:000291488700007	21555716	
J	Ober, C; Vercelli, D				Ober, Carole; Vercelli, Donata			Gene-environment interactions in human disease: nuisance or opportunity?	TRENDS IN GENETICS			English	Review							EARLY RESPIRATORY-INFECTIONS; GENOME-WIDE ASSOCIATION; QUANTITATIVE TRAIT LOCI; TOBACCO-SMOKE EXPOSURE; CHILDHOOD ASTHMA; AIR-POLLUTION; LUNG-FUNCTION; HAY-FEVER; OCCUPATIONAL ASTHMA; HYGIENE HYPOTHESIS	Many environmental risk factors for common, complex human diseases have been revealed by epidemiologic studies, but how genotypes at specific loci modulate individual responses to environmental risk factors is largely unknown. Gene-environment interactions will be missed in genome-wide association studies and could account for some of the 'missing heritability' for these diseases. In this review, we focus on asthma as a model disease for studying gene-environment interactions because of relatively large numbers of candidate gene-environment interactions with asthma risk in the literature. Identifying these interactions using genome-wide approaches poses formidable methodological problems, and elucidating molecular mechanisms for these interactions has been challenging. We suggest that studying gene-environment interactions in animal models, although more tractable, might not be sufficient to shed light on the genetic architecture of human diseases. Lastly, we propose avenues for future studies to find gene environment interactions.	[Ober, Carole] Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA; [Vercelli, Donata] Univ Arizona, Arizona Program Biol Complex Dis, Arizona Resp Ctr, Tucson, AZ 85719 USA; [Vercelli, Donata] Univ Arizona, Dept Cell Biol, Inst BIO5, Tucson, AZ 85719 USA	Ober, C (reprint author), Univ Chicago, Dept Human Genet, 920 E 58th St, Chicago, IL 60637 USA.	c-ober@genetics.uchicago.edu; donata@arc.arizona.edu			National Institutes of Health [HL085197, HL70831, HL101651, HL100800, HL66391, AI076715]	This work was supported by National Institutes of Health grants HL085197, HL70831, HL101651 to C.O. and HL100800, HL66391, AI076715 to D.V. The authors acknowledge S.A. Willis-Owen and W. Valdar for first using the expression 'nuisance or opportunity' in the context of GEIs in their 2009 review and F.D. Martinez, J.E. Gem, R.J. Lemanske, E. von Mutius and M. Ege for helpful discussions. The authors apologize to those investigators whose work was not cited owing to space constraints.	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J	Cheraghi, M; Salvi, S				Cheraghi, Maria; Salvi, Sundeep			Environmental tobacco smoke (ETS) and respiratory health in children	EUROPEAN JOURNAL OF PEDIATRICS			English	Review						Environmental tobacco smoke (ETS); Asthma; Respiratory tract infection; Children	INFANT-DEATH-SYNDROME; ACTIVE MATERNAL SMOKING; CHILDHOOD LUNG-FUNCTION; AGE 5 YEARS; PARENTAL SMOKING; PASSIVE SMOKING; RISK-FACTORS; 1ST YEAR; POSTNATAL EXPOSURE; FAMILY-HISTORY	Environmental tobacco smoke (ETS) is a major risk factor for poor lung health in children. Although parental smoking is the commonest source of ETS exposure to children, they are also exposed to ETS in schools, restaurants, public places and public transport vehicles. Apart from containing thousands of chemicals, the particle size in the ETS is much smaller than the main stream smoke, and therefore has a greater penetrability in the airways of children. Exposure to ETS has been shown to be associated with increased prevalence of upper respiratory tract infections, wheeze, asthma and lower respiratory tract infections. Even developing fetuses are exposed to ETS via the umbilical cord blood if the mother is exposed to tobacco smoke. The placenta also does not offer any barrier to the penetration of ETS into the fetus. The immune system in these babies is more deviated toward the allergic and asthmatic inflammatory phenotype and therefore makes them more prone to develop asthma later in life. An increased awareness of the harmful effects of ETS on children's health is warranted.	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J	Kirby, AC; Coles, MC; Kaye, PM				Kirby, Alun C.; Coles, Mark C.; Kaye, Paul M.			Alveolar Macrophages Transport Pathogens to Lung Draining Lymph Nodes	JOURNAL OF IMMUNOLOGY			English	Article							PULMONARY DENDRITIC CELLS; PNEUMOCOCCAL PNEUMONIA; IN-VIVO; B-CELLS; SUBCAPSULAR SINUS; SIGLEC-F; MOUSE; ANTIGEN; INFLAMMATION; INFECTION	The first step in inducing pulmonary adaptive immunity to allergens and airborne pathogens is Ag acquisition and transport to the lung draining lymph nodes (dLN). Dendritic cells (DC) sample the airways, and active transfer of Ag to the lung dLN is considered an exclusive property of migratory DC. However, alveolar macrophages (AM) are the first phagocytes to contact inhaled particulate matter. Although having well-defined immunoregulatory capabilities, AM are generally considered as restricted to the alveoli. We show that murine AM constitutively migrate from lung to dLN and that following exposure to Streptococcus pneumoniae, AM rapidly transport bacteria to this site. Thus AM, and not DC, appear responsible for the earliest delivery of these bacteria to secondary lymphoid tissue. The identification of this novel transport pathway has important consequences for our understanding of lung immunity and suggests more widespread roles for macrophages in the transport of Ags to lymphoid organs than previously appreciated. The Journal of Immunology, 2009, 183: 1983-1989.	[Kirby, Alun C.] Univ York, Hull York Med Sch, Ctr Immunol & Infect, York YO10 5YW, N Yorkshire, England; Univ York, Dept Biol, York YO10 5YW, N Yorkshire, England	Kirby, AC (reprint author), Univ York, Hull York Med Sch, Ctr Immunol & Infect, Wentworth Way, York YO10 5YW, N Yorkshire, England.	ak510@york.ac.uk		Kirby, Alun/0000-0001-5663-2961	Wellcome Trust; Medical Research Council	This study was funded by a Wellcome Trust grant to P.M.K. and A.C.K. and by grants from The Medical Research Council (to M.C.C. and P.M.K.).	Arredouani M, 2004, J EXP MED, V200, P267, DOI 10.1084/jem.20040731; Arredouani MS, 2005, J IMMUNOL, V175, P6058; Bellingan GJ, 1996, J IMMUNOL, V157, P2577; BILYK N, 1993, J EXP MED, V177, P1773, DOI 10.1084/jem.177.6.1773; Blumenthal RL, 2001, J ALLERGY CLIN IMMUN, V107, P258, DOI 10.1067/mai.2001.112845; Cao CZ, 2005, BLOOD, V106, P3234, DOI 10.1182/blood-2005-03-1288; Carrasco YR, 2007, IMMUNITY, V27, P160, DOI 10.1016/j.immuni.2007.06.007; CORRY D, 1984, AM J PATHOL, V115, P321; Dockrell DH, 2003, J IMMUNOL, V171, P5380; FELS AOS, 1986, J APPL PHYSIOL, V60, P353; Gays F, 2006, J IMMUNOL, V177, P5840; HARMSEN AG, 1985, SCIENCE, V230, P1277, DOI 10.1126/science.4071052; HOLT PG, 1993, J EXP MED, V177, P397, DOI 10.1084/jem.177.2.397; HULBERT WC, 1989, J ELECTRON MICR TECH, V11, P137, DOI 10.1002/jemt.1060110208; Jakubzick C, 2006, J IMMUNOL, V176, P3578; Junt T, 2007, NATURE, V450, P110, DOI 10.1038/nature06287; Kirby AC, 2006, J INFECT DIS, V193, P205, DOI 10.1086/498874; Knapp S, 2003, AM J RESP CRIT CARE, V167, P171, DOI 10.1164/rccm.200207-698OC; Legge KL, 2003, IMMUNITY, V18, P265, DOI 10.1016/S1074-7613(03)00023-2; Marriott HM, 2006, J IMMUNOL, V177, P6480; Marriott HM, 2004, FASEB J, V18, P1126, DOI 10.1096/fj.03-1450fje; McKimmie CS, 2009, BLOOD, V113, P4224, DOI 10.1182/blood-2008-08-174698; Phan TG, 2007, NAT IMMUNOL, V8, P992, DOI 10.1038/ni1494; ROSEN H, 1990, EUR J IMMUNOL, V20, P1251, DOI 10.1002/eji.1830200609; Sung SSJ, 2006, J IMMUNOL, V176, P2161; Tateno H, 2007, MOL CELL BIOL, V27, P5699, DOI 10.1128/MCB.00383-07; THEPEN T, 1989, J EXP MED, V170, P499, DOI 10.1084/jem.170.2.499; THEPEN T, 1993, ADV EXP MED BIOL, V329, P305; van Rijt LS, 2004, J IMMUNOL METHODS, V288, P111, DOI 10.1016/j.jim.2004.03.004; van Rijt LS, 2002, BLOOD, V100, P3663, DOI 10.1182/blood-2002-03-0673; Vermaelen K, 2004, CYTOM PART A, V61A, P170, DOI 10.1002/cyto.a.20064; Vermaelen KY, 2001, J EXP MED, V193, P51; Zhang JQQ, 2004, EUR J IMMUNOL, V34, P1175, DOI 10.1002/eji.200324723; Zhang M, 2007, BLOOD, V109, P4280, DOI 10.1182/blood-2006-08-039255	34	78	78	1	5	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	AUG 1	2009	183	3					1983	1989		10.4049/jimmunol.0901089		7	Immunology	Immunology	477LB	WOS:000268519500057	19620319	
J	Gent, JF; Koutrakis, P; Belanger, K; Triche, E; Holford, TR; Bracken, MB; Leaderer, BP				Gent, Janneane F.; Koutrakis, Petros; Belanger, Kathleen; Triche, Elizabeth; Holford, Theodore R.; Bracken, Michael B.; Leaderer, Brian P.			Symptoms and Medication Use in Children with Asthma and Traffic-Related Sources of Fine Particle Pollution	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						childhood asthma; fine particle pollution; PM(2.5); respiratory morbidity; source apportionment; traffic pollution	AIRBORNE PARTICULATE MATTER; AIR-POLLUTION; RESPIRATORY SYMPTOMS; SOURCE-APPORTIONMENT; LUNG-FUNCTION; EMISSION FACTORS; 1ST YEAR; ASSOCIATION; PM2.5; MORTALITY	BACKGROUND: Exposure to ambient fine particles [particulate matter <= 2.5 mu m diameter (PM(2.5))] is a potential factor in the exacerbation of asthma. National air quality particle standards consider total mass, not composition or sources, and may not protect against health impacts related to specific components. OBJECTIVE: We examined associations between daily exposure to fine particle components and sources, and symptoms and medication use in children with asthma. METHODS: Children with asthma (n = 149) 4-12 years of age were enrolled in a year-long study. We analyzed particle samples for trace elements (X-ray fluorescence) and elemental carbon (light reflectance). Using factor analysis/source apportionment, we identified particle sources (e.g., motor vehicle emissions) and quantified daily contributions. Symptoms and medication use were recorded on study diaries. Repeated measures logistic regression models examined associations between health outcomes and particle exposures as elemental concentrations and source contributions. RESULTS: More than half of mean PM(2.5) was attributed to traffic-related sources motor vehicles (42%) and road dust (12%). Increased likelihood of symptoms and inhaler use was largest for 3-day averaged exposures to traffic-related sources or their elemental constituents and ranged from a 10% increased likelihood of wheeze for each 5-mu g/m(3) increase in particles from motor vehicles to a 28% increased likelihood of shortness of breath for increases in road dust. Neither the other sources identified nor PM(2.5) alone was associated with increased health outcome risks. CONCLUSIONS: Linking respiratory health effects to specific particle pollution composition or sources is critical to efforts to protect public health. We associated increased risk of symptoms and inhaler use in children with asthma with exposure to traffic-related fine particles.	[Gent, Janneane F.; Belanger, Kathleen; Triche, Elizabeth; Holford, Theodore R.; Bracken, Michael B.; Leaderer, Brian P.] Yale Univ, Sch Med, Ctr Perinatal Pediat & Environm Epidemiol, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA; [Koutrakis, Petros] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA	Gent, JF (reprint author), Yale Univ, Sch Med, Ctr Perinatal Pediat & Environm Epidemiol, Dept Epidemiol & Publ Hlth, 1 Church St,6th Floor, New Haven, CT 06510 USA.	janneane.gent@yale.edu	Triche, Elizabeth/I-4986-2014		National Institutes of Health [ES011013, ES05410]	This study was funded by National Institutes of Health grants ES011013 and ES05410.	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Health Perspect.	JUL	2009	117	7					1168	1174		10.1289/ehp.0800335		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	465WV	WOS:000267621200039	19654929	
J	Fonseca, DE; Kline, JN				Fonseca, David E.; Kline, Joel N.			Use of CpG oligonucleotides in treatment of asthma and allergic disease	ADVANCED DRUG DELIVERY REVIEWS			English	Review						Asthma; Atopy; Inflammation; CpG oligonucleotides; Immunotherapy	DENDRITIC CELLS; MURINE MODEL; IMMUNOSTIMULATORY DNA; INDOLEAMINE 2,3-DIOXYGENASE; AIRWAY INFLAMMATION; CUTTING EDGE; OLIGODEOXYNUCLEOTIDES; MOTIFS; EXPRESSION; ANTIGEN	In the last several decades, there has been a marked increase in the prevalence of atopic disorders including asthma in "Western" societies; a relationship has been identified between lack of early-life exposure to microbes or microbial products and increased susceptibility to atopic disorders. The innate immune system is activated by early microbial exposures, many of which utilize one of the Toll-like receptors, and there has been significant interest in studying how ligation of TLRs may be therapeutically useful. CpG oligonucleotides (CpG-ODN, resembling bacterial DNA) engage TLR-9 on B-cells, dendritic cells and other cell types, resulting in a cascade that includes induction of Th1-type and T-regulatory-type immune responses. Preclinical models of asthma have demonstrated that CpG-ODN are potent inhibitors of atopic responses, suppressing Th2 cytokine and, reducing airway eosinophilia, systemic levels of IgE, and bronchial hyperreactivity-in short the critical attributes of the asthmatic phenotype. In models of chronic allergen exposure, CpG-ODN are also effective at preventing the development of airway remodeling. In established asthma, CpG-ODN can reverse manifestations of disease both when used alone or in combination with allergen immunotherapy. Early clinical trials have had mixed results, including a significant benefit when CpG-ODN were conjugated to ragweed allergen in an allergic rhinitis immunotherapy study, but only limited efficacy seen when administered prior to allergen challenge in asthmatics. Further study of CpG-ODNs for the treatment of asthma and other atopic disorders is warranted by existing data. Published by Elsevier B.V.	[Fonseca, David E.; Kline, Joel N.] Univ Iowa, Roy J & Lucille Carver Coll Med, Div Pulm Crit Care & Occupat Med, Iowa City, IA USA	Kline, JN (reprint author), C33GH UIHC, 200 Hawkins Dr, Iowa City, IA 52242 USA.	joel-kline@uiowa.edu					Chen L, 2006, J IMMUNOL, V177, P2373; Cho JY, 2004, AM J RESP CELL MOL, V30, P651, DOI 10.1165/rcmb.2003-0066OC; Chu RS, 1997, J EXP MED, V186, P1623, DOI 10.1084/jem.186.10.1623; Creticos PS, 2006, NEW ENGL J MED, V355, P1445, DOI 10.1056/NEJMoa052916; Fanucchi MV, 2004, AM J RESP CRIT CARE, V170, P1153, DOI 10.1164/rccm.200404-533OC; Gauvreau GM, 2006, AM J RESP CRIT CARE, V174, P15, DOI 10.1164/rccm.200601-057OC; GAVETT SH, 1995, J EXP MED, V182, P1527, DOI 10.1084/jem.182.5.1527; Hartmann G, 1999, P NATL ACAD SCI USA, V96, P9305, DOI 10.1073/pnas.96.16.9305; Hayashi T, 2004, J CLIN INVEST, V114, P270, DOI 10.1172/JCI200421275; Heyman K, 2008, EARLY RELEASE SELECT; Hussain I, 2002, LARYNGOSCOPE, V112, P1819, DOI 10.1097/00005537-200210000-00021; Jain VV, 2002, J ALLERGY CLIN IMMUN, V110, P867, DOI 10.1067/mai.2002.129371; JAIN VV, 2003, AM J PHYSIOL-LUNG C, V285, P1137; Jarnicki AG, 2008, J IMMUNOL, V180, P3797; Kadowaki N, 2001, J IMMUNOL, V166, P2291; Kitagaki K, 2006, CLIN EXP IMMUNOL, V143, P249, DOI 10.1111/j.1365-2249.2005.03003.x; Kitagaki K, 2002, CLIN DIAGN LAB IMMUN, V9, P1260, DOI 10.1128/CDLI.9.6.1260-1269.2002; Kline JN, 1999, J ALLERGY CLIN IMMUN, V104, P1258; Kline JN, 2002, AM J PHYSIOL-LUNG C, V283, pL170, DOI 10.1152/ajplung.00402.2001; Kline JN, 1998, J IMMUNOL, V160, P2555; Klinman DM, 1996, P NATL ACAD SCI USA, V93, P2879, DOI 10.1073/pnas.93.7.2879; KRIEG AM, 1995, NATURE, V374, P546, DOI 10.1038/374546a0; Krieg AM, 2003, NAT MED, V9, P831, DOI 10.1038/nm0703-831; Krieg AM, 2007, IMMUNOL REV, V220, P251, DOI 10.1111/j.1600-065X.2007.00572.x; Liu NS, 2003, NAT IMMUNOL, V4, P687, DOI 10.1038/ni941; Magone MT, 2000, EUR J IMMUNOL, V30, P1841, DOI 10.1002/1521-4141(200007)30:7<1841::AID-IMMU1841>3.0.CO;2-E; Mellor AL, 2003, J IMMUNOL, V171, P1652; Moseman EA, 2004, J IMMUNOL, V173, P4433; Peng SL, 2002, P NATL ACAD SCI USA, V99, P5545, DOI 10.1073/pnas.082114899; REINERO CR, 2008, IMMUNOPATHOL, V121, P241; Rhee CS, 2004, IMMUNOLOGY, V113, P106, DOI 10.1111/j.1365-2567.2004.01930.x; Ring J, 2001, CURR OPIN IMMUNOL, V13, P701, DOI 10.1016/S0952-7915(01)00282-5; ROBINSON DS, 1992, NEW ENGL J MED, V326, P298, DOI 10.1056/NEJM199201303260504; Schwartz DA, 1997, J CLIN INVEST, V100, P68, DOI 10.1172/JCI119523; Shirota H, 2000, AM J RESP CELL MOL, V22, P176; Shirota H, 2000, J IMMUNOL, V164, P5575; Simons FER, 2004, J ALLERGY CLIN IMMUN, V113, P1144, DOI 10.1016/j.jaci.2004.03.003; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Sur S, 1999, J IMMUNOL, V162, P6284; Suzuki M, 2007, OTOLARYNG HEAD NECK, V136, P246, DOI 10.1016/j.otohns.2006.09.009; Tulic MK, 2004, J ALLERGY CLIN IMMUN, V113, P235, DOI 10.1016/j.jaci.2003.11.001; Wingender G, 2006, EUR J IMMUNOL, V36, P12, DOI 10.1002/eji.200535602	42	78	86	0	8	ELSEVIER SCIENCE BV	AMSTERDAM	PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS	0169-409X			ADV DRUG DELIVER REV	Adv. Drug Deliv. Rev.	MAR 28	2009	61	3					256	262		10.1016/j.addr.2008.12.007		7	Pharmacology & Pharmacy	Pharmacology & Pharmacy	429DR	WOS:000264901500009	19167442	
J	Cox, L; Williams, B; Sicherer, S; Oppenheimer, J; Sher, L; Hamilton, R; Golden, D				Cox, Linda; Williams, Brock; Sicherer, Scott; Oppenheimer, John; Sher, Larry; Hamilton, Robert; Golden, David			Pearls and pitfalls of allergy diagnostic testing: report from the American College of Allergy, Asthma and Immunology/American Academy of Allergy, Asthma and Immunology Specific IgE Test Task Force	ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY			English	Article							NUTRITION EXAMINATION SURVEY; INTRADERMAL SKIN-TESTS; INSECT STING ALLERGY; VENOM IMMUNOTHERAPY; PRACTICE PARAMETER; ADVERSE-REACTIONS; NATIONAL-HEALTH; PEANUT ALLERGY; LUNG-FUNCTION; FOOD ALLERGY	The intended purpose of this monograph is to provide a general overview of allergy diagnostics for health care professionals who care for patients with allergic disease. For a more comprehensive review of allergy diagnostic testing, readers can refer to the Allergy Diagnostic Practice Parameters. A key message is that a positive allergy test result (skin or blood) indicates only the presence of allergen specific IgE (called sensitization). It does not necessarily mean clinical allergy (ie, allergic symptoms with exposure). It is important for this reason that the allergy evaluation be based on the patient's history and directed by a health care professional with sufficient understanding of allergy diagnostic testing to use the information obtained from his/her evaluation of the patient to determine (1) what allergy diagnostic tests to order, (2) how to interpret the allergy diagnostic test results, and (3) how to use the information obtained from the allergy evaluation to develop an appropriate therapeutic treatment plan.	[Cox, Linda] Nova SE Univ, Coll Osteopath Med, Dept Med, Davie, FL USA; [Williams, Brock] Univ Missouri, Sch Med, Kansas City, MO 64108 USA; [Sicherer, Scott] Mt Sinai Sch Med, Jaffe Food Allergy Inst, Dept Pediat, New York, NY USA; [Oppenheimer, John] Univ Med & Dent New Jersey, New Jersey Med Sch, Clin Res Pulm & Allergy Associates, Springfield, NJ USA; [Sher, Larry] Univ Calif Los Angeles, Dept Pediat, Los Angeles, CA 90024 USA; [Hamilton, Robert] Johns Hopkins Univ, Sch Med, Div Clin Immunol & Allergy, Dept Pathol & Med, Baltimore, MD USA; [Golden, David] Johns Hopkins Univ, Dept Med, Baltimore, MD USA	Cox, L (reprint author), Nova SE Univ, Coll Osteopath Med, Dept Med, 5333 N Dixie Hwy,Suite 210, Ft Lauderdale, FL 33334 USA.	lindaswolfox@msn.com					Arbes SJ, 2005, J ALLERGY CLIN IMMUN, V116, P377, DOI 10.1016/j.jaci.2005.05.017; Bernardo FP, 2004, COMP AID CH, V18, P151; Bernstein DI, 2004, J ALLERGY CLIN IMMUN, V113, P1129, DOI 10.1016/j.jaci.2004.02.006; Bernstein DI, 2003, J ALLERGY CLIN IMMUN, V111, P610, DOI 10.1067/mai.2003.164; Bernstein IL, 2008, ANN ALLERG ASTHMA IM, V100, pS1; Bodtger U, 2003, J ALLERGY CLIN IMMUN, V111, P149, DOI 10.1067/mai.2003.37; Carr WW, 2005, J ALLERGY CLIN IMMUN, V116, P341, DOI 10.1016/j.jaci.2005.03.035; Celik-Bilgili S, 2005, CLIN EXP ALLERGY, V35, P268, DOI 10.1111/j.1365-2222.2005.02150.x; Custovic A, 2005, ALLERGY, V60, P10, DOI 10.1111/j.1398-9995.2005.00851.x; Garcia-Ara C, 2001, J ALLERGY CLIN IMMUN, V107, P185, DOI 10.1067/mai.2001.111592; Gendo K, 2004, ANN INTERN MED, V140, P278; Golden DBK, 2006, ANN ALLERG ASTHMA IM, V96, pS16; Golden DBK, 2005, J ALLERGY CLIN IMMUN, V115, P439, DOI 10.1016/j.jaci.2005.01.005; Golden DBK, 2004, NEW ENGL J MED, V351, P668, DOI 10.1056/NEJMoa022952; Guilbert TW, 2004, J ALLERGY CLIN IMMUN, V114, P1282, DOI 10.1016/j.jaci.2004.09.020; Hamilton RG, 2004, J ALLERGY CLIN IMMUN, V114, P213, DOI 10.1016/j.jaci.2004.06.046; Knight AK, 2006, J ALLERGY CLIN IMMUN, V117, P842, DOI 10.1016/j.jaci.2005.12.1304; Komata T, 2007, J ALLERGY CLIN IMMUN, V119, P1272, DOI 10.1016/j.jaci.2007.01.038; Koskela H, 2003, CHEST, V124, P383, DOI 10.1378/chest.124.1.383; Langley SJ, 2003, J ALLERGY CLIN IMMUN, V112, P362, DOI 10.1067/mai.2003.1654; Leduc V, 2006, ALLERGY, V61, P349, DOI 10.1111/j.1398-9995.2006.01013.x; LOCKEY RF, 1987, J ALLERGY CLIN IMMUN, V6, P60; Lowe LA, 2004, ARCH PEDIAT ADOL MED, V158, P996, DOI 10.1001/archpedi.158.10.996; Moffitt JE, 2004, J ALLERGY CLIN IMMUN, V114, P869, DOI 10.1016/j.jaci.2004.07.046; Murray CS, 2006, THORAX, V61, P376, DOI 10.1136/thx.2005.042523; Nelson HS, 1998, J ALLERGY CLIN IMMUN, V101, P153; Nelson HS, 1996, J ALLERGY CLIN IMMUN, V97, P1193, DOI 10.1016/S0091-6749(96)70184-7; Nelson HS, 2004, J ALLERGY CLIN IMMUN, V113, P1218, DOI 10.1016/j.jaci.2004.01.566; NELSON HS, 1994, ALLERGY PROC, V15, P265, DOI 10.2500/108854194778816490; Oppenheimer J, 2006, ANN ALLERG ASTHMA IM, V96, pS6; OWNBY DR, 1982, J ALLERGY CLIN IMMUN, V69, P536, DOI 10.1016/0091-6749(82)90180-4; PASTORELLO EA, 1995, J ALLERGY CLIN IMMUN, V96, P580, DOI 10.1016/S0091-6749(95)70255-5; Perry TT, 2004, J ALLERGY CLIN IMMUN, V114, P144, DOI 10.1016/j.jaci.2004.04.009; Roberts G, 2005, J ALLERGY CLIN IMMUN, V115, P1291, DOI 10.1016/j.jaci.2005.02.038; Sampson HA, 2001, GASTROENTEROLOGY, V120, P1026, DOI 10.1053/gast.2001.23031; Sampson HA, 2001, J ALLERGY CLIN IMMUN, V107, P891, DOI 10.1067/mai.2001.114708; Sampson HA, 2000, J PEDIATR GASTR NUTR, V30, pS87, DOI 10.1097/00005176-200001001-00013; Sharma HP, 2008, J ALLERGY CLIN IMMUN, V121, P933, DOI 10.1016/j.jaci.2008.01.023; Sicherer SH, 2004, J ALLERGY CLIN IMMUN, V114, P1146, DOI 10.1016/j.jaci.2004.07.034; Simpson A, 2005, J ALLERGY CLIN IMMUN, V116, P744, DOI 10.1016/j.jaci.2005.06.032; Skolnick HS, 2001, J ALLERGY CLIN IMMUN, V107, P367, DOI 10.1067/mai.2001.112129; Stapel SO, 2008, ALLERGY, V63, P793, DOI 10.1111/j.1398-9995.2008.01705.x; Szefler S, 2000, NEW ENGL J MED, V343, P1054; TURKELTAUB PC, 1989, J ALLERGY CLIN IMMUN, V84, P886, DOI 10.1016/0091-6749(89)90384-9; Valyasevi MA, 2000, ANN ALLERG ASTHMA IM, V85, P363; Williams PB, 2000, J ALLERGY CLIN IMMUN, V105, P1221, DOI 10.1067/mai.2000.105219; Wood RA, 1999, J ALLERGY CLIN IMMUN, V103, P773, DOI 10.1016/S0091-6749(99)70419-7; Wood RA, 2007, ANN ALLERG ASTHMA IM, V99, P34; [Anonymous], 2006, ANN ALLERGY ASTHMA I, V96, pS1	49	78	86	0	8	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	2008	101	6					580	592				13	Allergy; Immunology	Allergy; Immunology	383CJ	WOS:000261651400003	19119701	
J	Mine, Y; Yang, M				Mine, Yoshinori; Yang, Marie			Recent advances in the understanding of egg allergens: Basic, industrial, and clinical perspectives	JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY			English	Review						egg allergy; ovalbumin; ovomucoid; lysozyme; food processing; allergen detection; immunotherapy; immune tolerance	OVOMUCOID 3RD DOMAIN; IMMUNOGLOBULIN-E PRODUCTION; ORAL TOLERANCE INDUCTION; AMINO-ACID-SEQUENCE; T-CELL EPITOPE; IMMUNOSTIMULATORY DNA-SEQUENCE; ANTILYSOZYME ANTIBODY HYHEL-63; LINKED-IMMUNOSORBENT-ASSAY; CHICKEN SERUM-ALBUMIN; TH2 IMMUNE-RESPONSES	The emergence of egg allergy. has had both industrial and clinical implications. In industrialized countries, egg allergy accounts for one of the most prevalent food hypersensitivities, especially in children. Atopic dermatitis represents the most common clinical manifestation in infancy; however, the range of clinical signs is broad and encompasses life-threatening anaphylaxis. The dominant egg allergens are proteins and are mainly present in the egg white, for example, ovalbumin, ovomucoid, ovotransferrin, and lysozyme. However, egg yolk also displays low-level allergenicity, for example, (x-livetin. Strict avoidance of the offending food remains the most common recommendation for egg-allergic individuals. Nevertheless, the omnipresence of egg-derived components in prepackaged or prepared foods makes it difficult. Therefore, more efficient preventive approaches are investigated to protect consumers from inadvertent exposure and ensuing adverse reactions. On the one hand, commercial kits have become readily available that allow for the detection of egg contaminants at trace levels. On the other hand, attempts to produce hypoallergenic egg-containing products through food-processing techniques have met with promising results, but the approach is limited due to its potentially undesirable effects on the unique functional and sensory attributes of egg proteins. Therefore, the development of preventive or curative strategies for egg allergy remains strongly warranted. Pilot studies have suggested that oral immunotherapy (IT) with raw or cooked preparations of egg may represent a safe alternative, immediately available to allergic subjects, but remains applicable to only nonanaphylactic patients. Due to the limitations of conventional IT, novel forms of immunotherapy are sought based on information obtained from the-molecular characterization of major egg allergens. In the past decade, promising approaches to the treatment and prevention of egg allergy have been explored and include, among others, the production of hypoallergenic recombinant egg proteins, the development of customized peptides, and bacterial-mediated immunotherapy. Nonspecific approaches have also been evaluated, and preliminary trials with the use of probiotic bacteria have yielded encouraging results. The current understanding of egg allergens offers novel approaches toward the making of food products safe for human consumption and the development of efficient immunotherapeutic strategies.	[Mine, Yoshinori; Yang, Marie] Univ Guelph, Dept Food Sci, Guelph, ON N1G 2W1, Canada	Mine, Y (reprint author), Univ Guelph, Dept Food Sci, Guelph, ON N1G 2W1, Canada.	ymine@uoguelph.ca					Aalberse RC, 2006, MOL NUTR FOOD RES, V50, P625, DOI 10.1002/mnfr.200500270; ADORINI L, 1988, P NATL ACAD SCI USA, V85, P5181, DOI 10.1073/pnas.85.14.5181; ADORINI L, 1988, J EXP MED, V168, P2091, DOI 10.1084/jem.168.6.2091; Agrawal DK, 2004, INT IMMUNOPHARMACOL, V4, P127, DOI 10.1016/j.intimp.2003.11.005; Akdis M, 2006, CHEM IMMUNOL ALLERGY, V91, P159; Akdis M, 2007, J ALLERGY CLIN IMMUN, V119, P780, DOI 10.1016/j.jaci.2007.01.022; Alessandri C, 2005, ALLERGY, V60, P128, DOI 10.1111/j.1398-9995.2004.00449.x; Allen CW, 2007, J PAEDIATR CHILD H, V43, P214, DOI 10.1111/j.1440-1754.2007.00996.x; Ando T, 2007, J ALLERGY CLIN IMMUN, V120, P916, DOI 10.1016/j.jaci.2007.05.023; ANET J, 1985, INT ARCH ALLER A IMM, V77, P364; Anibarro B, 2007, J INVEST ALLERG CLIN, V17, P168; Anibarro B, 2000, J ALLERGY CLIN IMMUN, V105, P834, DOI 10.1067/mai.2000.104547; 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Agric. Food Chem.	JUL 9	2008	56	13					4874	4900		10.1021/jf8001153		27	Agriculture, Multidisciplinary; Chemistry, Applied; Food Science & Technology	Agriculture; Chemistry; Food Science & Technology	321VU	WOS:000257335400002	18543935	
J	Johnson, LA; Prevo, R; Clasper, S; Jackson, DG				Johnson, Louise A.; Prevo, Remko; Clasper, Steven; Jackson, David G.			Inflammation-induced uptake and degradation of the lymphatic endothelial hyaluronan receptor LYVE-1	JOURNAL OF BIOLOGICAL CHEMISTRY			English	Article							NECROSIS-FACTOR-ALPHA; L-SELECTIN LIGAND; MAJOR E-SELECTIN; ENDOCYTOSIS HARE; DENDRITIC CELLS; BINDING PROTEINS; GENE-EXPRESSION; TNF-ALPHA; CD44; LYMPHANGIOGENESIS	The hyaluronan receptor LYVE-1 is selectively expressed in the endothelium of lymphatic capillaries, where it has been proposed to function in hyaluronan clearance and hyaluronan-mediated leukocyte adhesion. However, recent studies suggest that hyaluronan homeostasis is unperturbed in LYVE-1(-/-) mice and that lymphatic adhesion/transmigration may be largely mediated by ICAM-1 and VCAM-1 rather than LYVE-1. Here we have explored the possibility that LYVE-1 functions during inflammation and report that the receptor is down-regulated by pro-inflammatory cytokines. Using cultured primary lymphatic endothelial cells, we show that surface expression of LYVE-1 is rapidly and reversibly lost after exposure to tumor necrosis factor-alpha( TNF alpha) and TNF beta via internalization and degradation of the receptor in lysosomes, coupled with a shutdown in gene expression. Curiously, internalization does not result in significant uptake of hyaluronan, a process that is largely insensitive to the novel LYVE-1 adhesion blocking monoclonal antibody 3A, and proceeds almost equally in resting and inflammation-activated lymphatic endothelial cells. Finally, we show that TNF can induce down-modulation of LYVE-1 in ex vivo murine dermal tissue explants and present evidence that the process occurs in vivo, in the context of murine allergen-induced skin inflammation. These findings suggest that LYVE-1 can function independently of hyaluronan and have implications for the use of LYVE-1 as a histological marker for lymphangiogenesis in human pathology.	John Radcliffe Hosp, Weatherall Inst Mol Med, MRC, Human Immunol Unit, Oxford OX3 9DS, England	Jackson, DG (reprint author), John Radcliffe Hosp, Weatherall Inst Mol Med, MRC, Human Immunol Unit, Oxford OX3 9DS, England.	djackson@hammer.imm.ox.ac.uk			Medical Research Council [G0801186, MC_U137884182]		ANSTEE DJ, 1991, IMMUNOLOGY, V74, P197; ARUFFO A, 1990, CELL, V61, P1303, DOI 10.1016/0092-8674(90)90694-A; Baluk P, 2005, J CLIN INVEST, V115, P247, DOI 10.1172/JCI200522037; Banerji S, 1999, J CELL BIOL, V144, P789, DOI 10.1083/jcb.144.4.789; Breiteneder-Geleff S, 1999, AM J PATHOL, V154, P385, DOI 10.1016/S0002-9440(10)65285-6; Burdick MM, 2006, J BIOL CHEM, V281, P13899, DOI 10.1074/jbc.M513617200; CUMBERBATCH M, 1995, IMMUNOLOGY, V84, P31; Day AJ, 2002, J BIOL CHEM, V277, P4585, DOI 10.1074/jbc.R100036200; Dimitroff CJ, 2000, P NATL ACAD SCI USA, V97, P13841, DOI 10.1073/pnas.250484797; Dimitroff CJ, 2001, J CELL BIOL, V153, P1277, DOI 10.1083/jcb.153.6.1277; FAULKNER CB, 1995, INFECT IMMUN, V63, P4084; FRASER JRE, 1988, BIOCHEM J, V256, P153; FRASER JRE, 1989, CIBA F SYMP, V143, P41; Gale NW, 2007, MOL CELL BIOL, V27, P595, DOI 10.1128/MCB.01503-06; Gale NW, 2002, DEV CELL, V3, P411, DOI 10.1016/S1534-5807(02)00217-4; Gee K, 2003, J BIOL CHEM, V278, P37275, DOI 10.1074/jbc.M302309200; Grabbe S, 1998, IMMUNOL TODAY, V19, P37, DOI 10.1016/S0167-5699(97)01186-9; HARDINGHAM TE, 1992, FASEB J, V6, P861; Harris EN, 2007, J BIOL CHEM, V282, P2785, DOI 10.1074/jbc.M607787200; HARRISONLAVOIE KJ, 1993, EMBO J, V12, P2847; Jackson DG, 2001, TRENDS IMMUNOL, V22, P317, DOI 10.1016/S1471-4906(01)01936-6; Jackson DG, 2003, TRENDS CARDIOVAS MED, V13, P1, DOI 10.1016/S1050-1738(02)00189-5; Jackson DG, 2004, APMIS, V112, P526, DOI 10.1111/j.1600-0463.2004.apm11207-0811.x; JACKSON DG, 2004, GLYCOFORUM; Jeltsch M, 1997, SCIENCE, V276, P1423, DOI 10.1126/science.276.5317.1423; Johnson LA, 2006, J EXP MED, V203, P2763, DOI 10.1084/jem.20051759; KNUDSON CB, 1993, FASEB J, V7, P1233; Kriehuber E, 2001, J EXP MED, V194, P797, DOI 10.1084/jem.194.6.797; Levesque MC, 1999, CELL IMMUNOL, V193, P209, DOI 10.1006/cimm.1999.1456; Maiti A, 1998, SCIENCE, V282, P941, DOI 10.1126/science.282.5390.941; Meyer K, 1934, J BIOL CHEM, V107, P629; Millan J, 2006, NAT CELL BIOL, V8, P113, DOI 10.1038/ncb1356; Mishra JP, 2005, J BIOL CHEM, V280, P26825, DOI 10.1074/jbc.M500244200; Mummert DI, 2004, J INVEST DERMATOL, V122, P846, DOI 10.1046/j.0022-202X.2004.22127.x; Mummert ME, 2002, J IMMUNOL, V169, P4322; NIGHTINGALE T, 2005, HYALURONAN STRUCTURE, V2, P615; Nisato RE, 2004, AM J PATHOL, V165, P11, DOI 10.1016/S0002-9440(10)63271-3; Noble PW, 2002, MATRIX BIOL, V21, P25, DOI 10.1016/S0945-053X(01)00184-6; Pepper MS, 2001, CLIN CANCER RES, V7, P462; Prevo R, 2004, J BIOL CHEM, V279, P52580, DOI 10.1074/jbc.M406897200; Prevo R, 2001, J BIOL CHEM, V276, P19420, DOI 10.1074/jbc.M011004200; Pullinger BD, 1937, J PATHOL BACTERIOL, V45, P157, DOI 10.1002/path.1700450115; Rubbia-Brandt L, 2004, CLIN CANCER RES, V10, P6919, DOI 10.1158/1078-0432.CCR-04-0397; Sallusto F, 1998, EUR J IMMUNOL, V28, P2760, DOI 10.1002/(SICI)1521-4141(199809)28:09<2760::AID-IMMU2760>3.0.CO;2-N; STERN R, 2006, INT J CELL BIOL, V85, P699; Stessels F, 2004, BRIT J CANCER, V90, P1429, DOI 10.1038/sj.bjc.6601727; TAMMI R, 1991, J INVEST DERMATOL, V97, P126, DOI 10.1111/1523-1747.ep12478553; TAMMI R, 1994, PROG HISTOCHEM CYTOC, V29, P1; Tamura Y, 2003, J BIOL CHEM, V278, P12613, DOI 10.1074/jbc.M210211200; Termeer CC, 2000, J IMMUNOL, V165, P1863; Toole BP, 2004, NAT REV CANCER, V4, P528, DOI 10.1038/nrc1391; Van der Auwera I, 2004, CLIN CANCER RES, V10, P7965, DOI 10.1158/1078-0432.CCR-04-0063; Van Trappen PO, 2001, GYNECOL ONCOL, V82, P1, DOI 10.1006/gyno.2001.6292; VANDERAUWERA I, 2006, BE J CANC, P1; Weigel JA, 2003, J BIOL CHEM, V278, P9808, DOI 10.1074/jbc.M211462200; West D. C., 1989, CIBA F SYMP, V143, P201; Wigle JT, 1999, CELL, V98, P769, DOI 10.1016/S0092-8674(00)81511-1; Witte MH, 2006, CANCER METAST REV, V25, P159, DOI 10.1007/s10555-006-8496-2; Zhou B, 2000, J BIOL CHEM, V275, P37733, DOI 10.1074/jbc.M003030200	59	78	81	0	3	AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA	0021-9258			J BIOL CHEM	J. Biol. Chem.	NOV 16	2007	282	46							33671	10.1074/jbc.M702889200		10	Biochemistry & Molecular Biology	Biochemistry & Molecular Biology	229XP	WOS:000250840200048	17884820	
J	Ko, FWS; Tam, W; Wong, TW; Lai, CKW; Wong, GWK; Leung, TF; Ng, SSS; Hui, DSC				Ko, F. W. S.; Tam, W.; Wong, T. W.; Lai, C. K. W.; Wong, G. W. K.; Leung, T.-F.; Ng, S. S. S.; Hui, D. S. C.			Effects of air pollution on asthma hospitalization rates in different age groups in Hong Kong	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						age; air pollution; asthma; exacerbation; Hong Kong	EMERGENCY-DEPARTMENT VISITS; ACUTE RESPIRATORY SYNDROME; AMBIENT AIR; CARDIOVASCULAR-DISEASES; HEART-FAILURE; ADMISSIONS; CHILDREN; MORTALITY; CITIES; ASSOCIATIONS	Aims To assess the relationship between levels of ambient air pollutants and hospitalization rates for asthma in Hong Kong (HK). Methods This is a retrospective ecological study. Data of daily emergency hospital admissions to 15 major hospitals in HK for asthma and indices of air pollutants [sulphur dioxide (SO2), nitrogen dioxide (NO2), ozone (O-3), particulates with an aerodynamic diameter of < 10 mu m particulate matter (PM10) and 2.5 mu m (PM2.5)] and meteorological variables from January 2000 to December 2005 were obtained from several government departments. Analysis was performed by the generalized additive models with Poisson distribution. The effects of time trend, season, other cyclical factors, temperature and humidity were adjusted. Autocorrelation and overdispersion were corrected. Results Altogether, 69 716 admissions were assessed. Significant associations were found between hospital admissions for asthma and levels of NO2, O-3, PM10 and PM2.5. The relative risks (RR) for hospitalization for every 10 mu g/m(3) increase in NO2, O-3, PM10 and PM2.5 were 1.028, 1.034, 1.019 and 1.021, respectively, at a lag day that ranged from cumulative lag 0-4 to 0-5. In a multi-pollutant model, O-3 was significantly associated with increased admissions for asthma. The younger age group (0-14 years) tended to have a higher RR for each 10 mu g/m(3) increase in pollutants than those aged 15-65 years. The elderly (aged >= 65 years) had a shorter 'best' lag time to develop asthma exacerbation following exposure to pollutants than those aged < 65 years. Conclusion Adverse effects of ambient concentrations of air pollutants on hospitalization rates for asthma are evident. Measures to improve air quality in HK are urgently needed.	Chinese Univ Hong Kong, Prince Wales Hosp, Dept Med & Therapeut, Hong Kong, Hong Kong, Peoples R China; Chinese Univ Hong Kong, Prince Wales Hosp, Nethersole Sch Nursing, Hong Kong, Hong Kong, Peoples R China; Chinese Univ Hong Kong, Prince Wales Hosp, Dept Community & Family Med, Hong Kong, Hong Kong, Peoples R China; Chinese Univ Hong Kong, Prince Wales Hosp, Dept Pediat, Hong Kong, Hong Kong, Peoples R China	Hui, DSC (reprint author), Chinese Univ Hong Kong, Prince Wales Hosp, Dept Med & Therapeut, 30-32 Ngan Shing St, Hong Kong, Hong Kong, Peoples R China.	dschui@cuhk.edu.hk	Tam, Wilson/E-9887-2010; Wong, Tze Wai/K-5344-2013; Wang, Linden/M-6617-2014; Hui, David/O-2754-2015; Ko, Fanny/B-8958-2016	Ko, Fanny/0000-0001-8454-0087; Tam, Wilson/0000-0003-0641-3060			Anderson HR, 1998, THORAX, V53, P842; Arena VC, 2006, J OCCUP ENVIRON MED, V48, P38, DOI 10.1097/01.jom.0000183096.20678.f1; Asher MI, 2006, LANCET, V368, P733, DOI 10.1016/S0140-6736(06)69283-0; Atkinson RW, 2001, AM J RESP CRIT CARE, V164, P1860; Boutin-Forzano S, 2004, RESPIRATION, V71, P134, DOI 10.1159/000076673; CHANG A, 2005, AIR QUALITY HONG KON; Dominici F, 2006, JAMA-J AM MED ASSOC, V295, P1127, DOI 10.1001/jama.295.10.1127; Fusco D, 2001, EUR RESPIR J, V17, P1143, DOI 10.1183/09031936.01.00005501; Galan I, 2003, EUR RESPIR J, V22, P802, DOI 10.1183/09031936.03.00013003; Hastie T, 1995, Stat Methods Med Res, V4, P187, DOI 10.1177/096228029500400302; Hastie T., 1990, GENERALIZED ADDITIVE; *HTLH EFF I, 2004, HLTH EFF OUTD AIR PO; *HTLH EFF I, 2003, REV AN TIM SER STUD; Hui DSC, 2003, CHEST, V124, P12, DOI 10.1378/chest.124.1.12; Katsouyanni K, 2001, EPIDEMIOLOGY, V12, P521, DOI 10.1097/00001648-200109000-00011; Katsouyanni K, 2002, EPIDEMIOLOGY, V13, P742, DOI 10.1097/01.EDE.0000032424.22670.3E; Ko FWS, 2006, RESP MED, V100, P1598, DOI 10.1016/j.rmed.2005.12.007; Lee N, 2003, NEW ENGL J MED, V348, P1986, DOI 10.1056/NEJMoa030685; Lee SL, 2006, CLIN EXP ALLERGY, V36, P1138, DOI 10.1111/j.1365-2222.2006.02555.x; National Research Council, 2004, RES PRIOR AIRB PART, VIV; *NMMAPSDATA R PACK, NAT MORT MORB AIR PO; Norris G, 1999, ENVIRON HEALTH PERSP, V107, P489, DOI 10.2307/3434632; Peel JL, 2005, EPIDEMIOLOGY, V16, P164, DOI 10.1097/01.ede.0000152905.42113.db; Petroeschevsky A, 2001, ARCH ENVIRON HEALTH, V56, P37; Pope CA, 2004, CIRCULATION, V109, P71, DOI 10.1161/01.CIR.0000108927.80044.7F; Rabinovitch N, 2006, AM J RESP CRIT CARE, V173, P1098, DOI 10.1164/rccm.200509-1393OC; Rosas I, 1998, ALLERGY, V53, P394, DOI 10.1111/j.1398-9995.1998.tb03911.x; Samet JM, 2000, NEW ENGL J MED, V343, P1742, DOI 10.1056/NEJM200012143432401; Sheppard L, 1999, EPIDEMIOLOGY, V10, P23, DOI 10.1097/00001648-199901000-00006; Stieb David M, 2002, Environ Health, V1, P7, DOI 10.1186/1476-069X-1-7; Wellenius GA, 2006, AM J CARDIOL, V97, P404, DOI 10.1016/j.amjcard.2005.08.061; World Health Organization, 2006, WHOCDSNTDWHOPESGCDPP, P1; *WHO, 1977, WHO INT CLASS DIS 19; Wong GWK, 2001, CLIN EXP ALLERGY, V31, P565, DOI 10.1046/j.1365-2222.2001.01063.x; Wong TW, 2002, OCCUP ENVIRON MED, V59, P30, DOI 10.1136/oem.59.1.30; Wong TW, 1999, OCCUP ENVIRON MED, V56, P679; Yap FHY, 2004, J MED VIROL, V73, P617, DOI 10.1002/jmv.20135; 2002, STUDY AIR QUALITY PE; HONG KONG SPECIAL AD; 2005, IMPROVING AIR QUALIT, P1	40	78	83	5	22	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	SEP	2007	37	9					1312	1319		10.1111/j.1365-2222.2007.02791.x		8	Allergy; Immunology	Allergy; Immunology	207LR	WOS:000249253100008	17845411	
J	Roder, E; Berger, MY; Hop, WCJ; Bernsen, RMD; de Groot, H; van Wijk, RG				Roder, Esther; Berger, Marjolein Y.; Hop, Wim C. J.; Bernsen, Roos M. D.; de Groot, Hans; van Wijk, Roy Gerth			Sublingual immunotherapy with grass pollen is not effective in symptomatic youngsters in primary care	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						immunotherapy; sublingual; grass pollen; allergic rhinitis; child; adolescent; primary care	SEASONAL ALLERGIC RHINOCONJUNCTIVITIS; PLACEBO-CONTROLLED EVALUATION; RANDOMIZED CONTROLLED-TRIAL; HOUSE-DUST MITE; QUALITY-OF-LIFE; DOUBLE-BLIND; SWALLOW IMMUNOTHERAPY; PEDIATRIC-PATIENTS; CHILDREN; RHINITIS	Background: Sublingual immunotherapy (SLIT) is considered safer and more convenient than subcutaneous therapy and therefore has been proposed as especially suitable for children and in primary care. Most efficacy studies in children lack power to be conclusive, and all have been performed in referral centers. Objective: To investigate the efficacy of SLIT with grass pollen allergen in children and adolescents with rhinoconjunctivitis in a primary care setting. Methods: Youngsters aged 6-18 years with hay fever were enrolled from general practices and randomly assigned to receive placebo or grass pollen mix for 2 years. The primary outcome was the mean daily total symptom score (scale 0-15) comprising sneezing, itching nose, watery running nose, nasal blockage, and itching eyes during the months May-August of the second treatment year. Results: Out of 204 youngsters randomized, 168 entered the intention-to-treat analysis (91 verum, 77 placebo). The mean daily total symptom score did not differ between participants allocated to verum and those allocated to placebo (difference for verum minus placebo: -0.08, 95% CI, -0.66-0.50; P =.78). No differences were found for rescue medication-free days, disease-specific quality of life, and overall evaluation of the treatment effect. Local side effects were more frequent in the verum group (39% vs 17% of participants; P =.001). Conclusion: Sublingual immunotherapy with grass pollen in a primary care setting is not effective in children and adolescents. Clinical implications: Currently, SLIT cannot be recommended for general practitioners as a therapeutic modality in youngsters with grass pollen allergy.	Erasmus MC Univ, Med Ctr, Sect Allergol, Dept Internal Med, NL-3000 CA Rotterdam, Netherlands; Erasmus MC Univ, Med Ctr, Dept Gen Practice, NL-3000 CA Rotterdam, Netherlands; Erasmus MC Univ, Med Ctr, Dept Epidemiol & Biostat, NL-3000 CA Rotterdam, Netherlands	van Wijk, RG (reprint author), Erasmus MC Univ, Med Ctr, Sect Allergol, Dept Internal Med, POB 2040, NL-3000 CA Rotterdam, Netherlands.	r.gerthvanwijk@erasmusmc.nl					Andre C, 2000, INT ARCH ALLERGY IMM, V121, P229, DOI 10.1159/000024322; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Bahceciler NN, 2001, PEDIATR PULM, V32, P49, DOI 10.1002/ppul.1088; Bodtger U, 2003, CLIN EXP ALLERGY, V33, P496, DOI 10.1046/j.1365-2222.2003.01611.x; Bousquet J, 2006, J ALLERGY CLIN IMMUN, V117, P158, DOI 10.1016/j.jaci.2005.09.047; Bousquet J, 2001, J ALLERGY CLIN IMMUN, V108, pS147, DOI 10.1067/mai.2001.118891; Bousquet J, 1998, ALLERGY S, V53, P44; Bufe A, 2004, ALLERGY, V59, P498, DOI 10.1111/j.1398-9995.2004.00457.x; DesRoches A, 1997, J ALLERGY CLIN IMMUN, V99, P450, DOI 10.1016/S0091-6749(97)70069-1; Di Rienzo V, 1999, ALLERGY, V54, P1110, DOI 10.1034/j.1398-9995.1999.00267.x; Durham SR, 2006, J ALLERGY CLIN IMMUN, V117, P802, DOI 10.1016/j.jaci.2005.12.1358; Hirsch T, 1997, PEDIATR ALLERGY IMMU, V8, P21, DOI 10.1111/j.1399-3038.1997.tb00138.x; 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; JUNIPER EF, 1994, J ALLERGY CLIN IMMUN, V93, P413, DOI 10.1016/0091-6749(94)90349-2; Juniper EF, 1998, J ALLERGY CLIN IMMUN, V101, P163; La Rosa M, 1999, J ALLERGY CLIN IMMUN, V104, P425, DOI 10.1016/S0091-6749(99)70388-X; Lamberts H, 1987, INT CLASSIFICATION P; Malling HJ, 1998, ALLERGY, V53, P461; Moller C, 2002, J ALLERGY CLIN IMMUN, V109, P251, DOI 10.1067/mai.2002.121317; Olaguibel JM, 2005, J INVEST ALLERG CLIN, V15, P9; Pajno GB, 2003, CLIN EXP ALLERGY, V33, P1641, DOI 10.1111/j.1365-2222.2003.01809.x; Penagos M, 2006, ANN ALLERG ASTHMA IM, V97, P141; Rolinck-Werninghaus C, 2004, ALLERGY, V59, P1285, DOI 10.1111/j.1398-9995.2004.00627.x; Smith H, 2004, J ALLERGY CLIN IMMUN, V114, P831, DOI 10.1016/j.jaci.2004.06.058; TARI MG, 1990, ALLERGOL IMMUNOPATH, V18, P277; Van Hoecke H, 2006, ALLERGY, V61, P705, DOI 10.1111/j.1398-9995.2006.01057.x; Vourdas D, 1998, ALLERGY, V53, P662, DOI 10.1111/j.1398-9995.1998.tb03952.x; Wilson DR, 2003, COCHRANE DB SYST REV, V2; Winther L, 2000, ALLERGY, V55, P818, DOI 10.1034/j.1398-9995.2000.00367.x; Yuksel H, 1999, J INVEST ALLERG CLIN, V9, P305	31	78	80	0	2	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	APR	2007	119	4					892	898		10.1016/j.jaci.2006.12.651		7	Allergy; Immunology	Allergy; Immunology	157OK	WOS:000245729500017	17321581	
J	Passos, GF; Fernandes, ES; da Cunha, FM; Ferreira, J; Pianowski, LF; Campos, MM; Calixto, JB				Passos, Giselle F.; Fernandes, Elizabeth S.; da Cunha, Fernanda M.; Ferreira, Juliano; Pianowski, Luiz F.; Campos, Maria M.; Calixto, Joao B.			Anti-inflammatory and anti-allergic properties of the essential oil and active compounds from Cordia verbenacea	JOURNAL OF ETHNOPHARMACOLOGY			English	Article						essential oil; Cordia verbenacea; inflammation; allergy; TNF alpha; active compounds	CARRAGEENAN-INDUCED INFLAMMATION; CRUDE LEAF EXTRACT; PHARMACOLOGICAL ASSAY; UP-REGULATION; PLANT-ORIGIN; NITRIC-OXIDE; RAT; EDEMA; MODULATION; CYCLOOXYGENASE-2	The anti-inflammatory and anti-allergic effects of the essential oil of Cordia verbenacea (Boraginaceae) and some of its active compounds were evaluated. Systemic treatment with the essential oil of Cordia verbenacea (300-600 mg/kg, p.o.) reduced carrageenan-induced rat paw oedema, myeloperoxidase activity and the mouse oedema elicited by carrageenan, bradykinin, substance P, histamine and platelet-activating factor. It also prevented carrageenan-evoked exudation and the neutrophil influx to the rat pleura and the neutrophil migration into carrageenan-stimulated mouse air pouches. Moreover, Cordia verbenacea oil inhibited the oedema caused by Apis mellifera venom or ovalbumin in sensitized rats and ovalbumin-evoked allergic pleurisy. The essential oil significantly decreased TNF alpha, without affecting IL-1 beta production, in carrageenan-injected rat paws. Neither the PGE(2) formation after intrapleural injection of carrageenan nor the COX-1 or COX-2 activities in vitro were affected by the essential oil. Of high interest, the paw edema induced by carrageenan in mice was markedly inhibited by both sesquiterpenic compounds obtained from the essential oil: alpha-humulene and trans-caryophyllene (50 mg/kg, p.o.). Collectively, the present results showed marked anti-inflammatory effects for the essential oil of Cordia verbenacea and some active compounds, probably by interfering with TNFa production. Cordia verbenacea essential oil or its constituents might represent new therapeutic options for the treatment of inflammatory diseases. (c) 2006 Elsevier Ireland Ltd. All rights reserved.	Univ Fed Santa Catarina, Ctr Biol Sci, Dept Pharmacol, BR-88049900 Florianopolis, SC, Brazil	Calixto, JB (reprint author), Univ Fed Santa Catarina, Ctr Biol Sci, Dept Pharmacol, BR-88049900 Florianopolis, SC, Brazil.	calixto@farmaco.ufsc.br	Fernandes, Elizabeth/J-9397-2012; Ferreira, Juliano/A-9803-2013; Campos, Maria Martha/J-8829-2015; Marques da Cunha, Fernanda/G-3575-2012	Ferreira, Juliano/0000-0002-9562-0602; Campos, Maria Martha/0000-0002-1153-3633; Marques da Cunha, Fernanda/0000-0002-1583-5380; Campos, Maria/0000-0001-7738-9892			BRADLEY PP, 1982, J INVEST DERMATOL, V78, P206, DOI 10.1111/1523-1747.ep12506462; Calixto JB, 2004, PLANTA MED, V70, P93, DOI 10.1055/s-2004-815483; Calixto JB, 2003, PLANTA MED, V69, P973, DOI 10.1055/s-2003-45141; Calixto MC, 2003, INFLAMM RES, V52, P132, DOI 10.1007/s000110300026; Campos MM, 2002, BRIT J PHARMACOL, V135, P1107, DOI 10.1038/sj.bjp.0704488; CORREA CR, 1993, BRIT J PHARMACOL, V110, P193; de Carvalho PM, 2004, J ETHNOPHARMACOL, V95, P297, DOI 10.1016/j.jep.2004.07.028; DeCampos ROP, 1996, EUR J PHARMACOL, V316, P277, DOI 10.1016/S0014-2999(96)00661-9; Di Rosa M, 1971, J Pharm Pharmacol, V23, P297; DIROSA M, 1971, J PATHOL, V104, P15, DOI 10.1002/path.1711040103; EDWARDS JCW, 1981, J PATHOL, V134, P147, DOI 10.1002/path.1711340205; Faurschou M, 2003, MICROBES INFECT, V5, P1317, DOI 10.1016/j.micinf.2003.09.008; Feldmann M, 2002, NAT REV IMMUNOL, V2, P364, DOI 10.1038/nri802; GILLIGAN JP, 1994, INFLAMMATION, V18, P285, DOI 10.1007/BF01534269; HWANG SB, 1986, EUR J PHARMACOL, V120, P33, DOI 10.1016/0014-2999(86)90636-9; Ianaro A, 2000, J PHARMACOL EXP THER, V292, P156; Jorge LIF, 1998, REV BRASILEIRA FARMA, V79, P69; MARTINS MA, 1993, J LEUKOCYTE BIOL, V53, P104; Murakami M, 2004, PROG LIPID RES, V43, P3, DOI 10.1016/S0163-7827(03)00037-7; Nantel F, 1999, BRIT J PHARMACOL, V128, P853, DOI 10.1038/sj.bjp.0702866; Passos GF, 2004, J IMMUNOL, V172, P1839; Pinheiro RM, 2002, INFLAMM RES, V51, P603, DOI 10.1007/PL00012435; Portanova JP, 1996, J EXP MED, V184, P883, DOI 10.1084/jem.184.3.883; Salvemini D, 1996, BRIT J PHARMACOL, V118, P829; SEIBERT K, 1994, P NATL ACAD SCI USA, V91, P12013, DOI 10.1073/pnas.91.25.12013; SERTIE J A A, 1988, Planta Medica, V54, P7, DOI 10.1055/s-2006-962318; SERTIE JAA, 1990, PLANTA MED, V56, P36, DOI 10.1055/s-2006-960879; Sertie JAA, 2005, PHYTOMEDICINE, V12, P338, DOI 10.1016/j.phymed.2003.09.013; SERTIE JAA, 1991, J ETHNOPHARMACOL, V31, P239, DOI 10.1016/0378-8741(91)90008-2; SIN YM, 1992, ANN RHEUM DIS, V51, P112, DOI 10.1136/ard.51.1.112; STOCHLA K, 1982, AGENTS ACTIONS, V12, P201, DOI 10.1007/BF01965145; Ticli FK, 2005, TOXICON, V46, P318, DOI 10.1016/j.toxicon.2005.04.023; Tilley SL, 2001, J CLIN INVEST, V108, P15, DOI 10.1172/JCI13416; Tratsk KS, 1997, INFLAMM RES, V46, P509, DOI 10.1007/s000110050234; Van Assche G, 2000, EXPERT OPIN INV DRUG, V9, P103; VINEGAR R, 1973, P SOC EXP BIOL MED, V143, P711	36	78	86	0	15	ELSEVIER IRELAND LTD	CLARE	ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND	0378-8741			J ETHNOPHARMACOL	J. Ethnopharmacol.	MAR 21	2007	110	2					323	333		10.1016/j.jep.2006.09.032		11	Plant Sciences; Chemistry, Medicinal; Integrative & Complementary Medicine; Pharmacology & Pharmacy	Plant Sciences; Pharmacology & Pharmacy; Integrative & Complementary Medicine	154DL	WOS:000245486900013	17084568	
J	Pham-Thi, N; Scheinmann, P; Fadel, R; Combebias, A; Andre, C				Pham-Thi, Nhan; Scheinmann, Pierre; Fadel, Riad; Combebias, Anne; Andre, Claude		Study Grp	Assessment of sublingual immunotherapy efficacy in children with house dust mite-induced allergic asthma optimally controlled by pharmacologic treatment and mite-avoidance measures	PEDIATRIC ALLERGY AND IMMUNOLOGY			English	Article						asthma; corticosteroids; house dust mite; allergy; sublingual immunotherapy	RANDOMIZED CONTROLLED-TRIAL; DOUBLE-BLIND; DERMATOPHAGOIDES-PTERONYSSINUS; SWALLOW IMMUNOTHERAPY; INHALED CORTICOSTEROIDS; CLINICAL-EFFICACY; FOLLOW-UP; RHINITIS; EXTRACT; SAFETY	Although several studies have demonstrated the efficacy of subcutaneous immunotherapy in allergic asthma, few have shown the same benefit using sublingual immunotherapy (SLIT) in asthmatic patients. This study was conducted to assess the efficacy of house dust mite (HDM) SLIT in addition to allergen avoidance and standard pharmacologic treatment. A double-blind, placebo-controlled trial was performed in 111 children (aged 5-15 yr) with HDM-induced mild-to-moderate asthma. After a 4-week baseline phase, patients were randomly assigned to receive SLIT with tablets of HDM extract (n = 55) or placebo (n = 56) for 18 months. Pharmacologic treatment was adjusted every 3 months following a step-down approach. Asthma symptom scores, reduction in use of inhaled corticosteroids and inhaled beta(2)-agonists, rhinitis symptoms, lung function tests, skin sensitivity to HDM, dust mite-specific immunoglobulin (Ig) E and IgG(4), and quality of life (QoL) were assessed during the study. After 18 months of treatment, diurnal and nocturnal asthma symptoms scores did not show significant differences between SLIT and placebo groups. Inhaled corticosteroids and inhaled beta(2)-agonists use was reduced in both groups without significant differences between groups. There were no significant differences in lung function (forced expiratory volume in 1 s and peak flow rate variations) between groups. Rhinitis symptom score decreased in both groups, with no difference between the two groups. The severity dimension of QoL was significantly improved in the SLIT group (age 6-12 yr). SLIT induced a significant reduction of skin sensitivity to HDM (p < 0.01) and a significant increase in HDM-specific IgE and IgG(4) antibodies (p < 0.001) in the SLIT group compared with the placebo group. SLIT was well tolerated with mild/moderate local adverse events. No severe systemic reactions were reported. This study indicates that, when mild-moderate asthmatic children are optimally controlled by pharmacologic treatment and HDM avoidance, SLIT does not provide additional benefit, despite a significant reduction in allergic response to HDM. Under such conditions, only a complete, but ethically unfeasible, discontinuation of inhaled corticosteroid would have demonstrated a possible benefit of SLIT.	Hop Necker Enfants Malad, Dept Paediat Pneumol & Allergy, Paris, France; Stallergenes SA, Sci & Med Dept, Antony, France	Andre, C (reprint author), Stallergenes SA, Dept Med, 6 Rue Alexis de Tocqueville, F-92183 Antony, France.	candre@stallergenes.fr					Adkinson NF, 1997, NEW ENGL J MED, V336, P324, DOI 10.1056/NEJM199701303360502; Allam JP, 2003, J ALLERGY CLIN IMMUN, V112, P141, DOI 10.1067/mai.2003.1607; Andre C, 2003, INT ARCH ALLERGY IMM, V131, P111, DOI 10.1159/000070926; Bacharier LB, 2002, J ALLERGY CLIN IMMUN, V109, P916, DOI 10.1067/mai.2002.124665; Bahceciler NN, 2005, INT ARCH ALLERGY IMM, V136, P287, DOI 10.1159/000083956; 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, P147, DOI DOI 10.1067/MAI.2001.118891; Canonica GW, 2003, J ALLERGY CLIN IMMUN, V111, P437, DOI 10.1067/mai.2003.129; CHRISTIE MJ, 1993, PSYCHOSOM MED, V55, P541; Clavel R, 1998, ALLERGY, V53, P493, DOI 10.1111/j.1398-9995.1998.tb04086.x; DesRoches A, 1997, J ALLERGY CLIN IMMUN, V99, P450, DOI 10.1016/S0091-6749(97)70069-1; Gidaro GB, 2005, CLIN EXP ALLERGY, V35, P565, DOI 10.1111/j.1365-2222.2005.02240.x; Grosclaude M, 2002, INT ARCH ALLERGY IMM, V129, P248, DOI 10.1159/000066779; Gruber W, 1999, CLIN EXP ALLERGY, V29, P176; Guilbert TW, 2006, NEW ENGL J MED, V354, P1985, DOI 10.1056/NEJMoa051378; Hawkins G, 2003, BRIT MED J, V326, P1115, DOI 10.1136/bmj.326.7399.1115; Hedlin G, 1999, J ALLERGY CLIN IMMUN, V103, P609, DOI 10.1016/S0091-6749(99)70232-0; Hirsch T, 1997, PEDIATR ALLERGY IMMU, V8, P21, DOI 10.1111/j.1399-3038.1997.tb00138.x; KHINCHI M, 2004, ALLERGY, V58, P45; LIND P, 1986, ALLERGY, V41, P442, DOI 10.1111/j.1398-9995.1986.tb00325.x; Luczynska C, 2003, CLIN EXP ALLERGY, V33, P1648, DOI 10.1111/j.1365-2222.2003.01729.x; Maestrelli P, 2004, J ALLERGY CLIN IMMUN, V113, P643, DOI 10.1016/j.jaci.2003.12.586; Marcucci F, 2005, PEDIATR ALLERGY IMMU, V16, P519, DOI 10.1111/j.1399-3038.2005.00301.x; Marogna M, 2004, ALLERGY, V59, P1205, DOI 10.1111/j.1398-9995.2004.00508.x; Moingeon P, 2006, ALLERGY, V61, P151, DOI 10.1111/j.1398-9995.2006.01002.x; Moller C, 2002, J ALLERGY CLIN IMMUN, V109, P251, DOI 10.1067/mai.2002.121317; Morgan WJ, 2004, NEW ENGL J MED, V351, P1068, DOI 10.1056/NEJMoa032097; *NHLBI WHO, 1995, PUBL NHLBI WHO; Novembre E, 2004, J ALLERGY CLIN IMMUN, V114, P851, DOI 10.1016/j.jaci.2004.07.012; Olsen OT, 1997, ALLERGY, V52, P853, DOI 10.1111/j.1398-9995.1997.tb02157.x; Pajno GB, 2000, ALLERGY, V55, P842, DOI 10.1034/j.1398-9995.2000.00495.x; Pajno GB, 2001, CLIN EXP ALLERGY, V31, P1392, DOI 10.1046/j.1365-2222.2001.01161.x; Pajno Giovanni B, 2003, Paediatr Drugs, V5, P777, DOI 10.2165/00148581-200305110-00006; Passalacqua G, 2004, ANN ALLERG ASTHMA IM, V93, P3; Platts-Mills TA, 1997, J ALLERGY CLIN IMM S, V100, P2; Plaut Marshall, 2004, Clin Allergy Immunol, V18, P681; TARI MG, 1990, ALLERGOL IMMUNOPATH, V18, P277; Till SJ, 2004, J ALLERGY CLIN IMMUN, V113, P1025, DOI 10.1016/j.jaci.2004.03.024; Tonnel AB, 2004, ALLERGY, V59, P491, DOI 10.1111/j.1398-9995.2004.00456.x; WAALKENS HJ, 1993, AM REV RESPIR DIS, V148, P1252; WARNER JO, 1978, LANCET, V2, P912; Wilson DR, 2005, ALLERGY, V60, P4, DOI 10.1111/j.1398-9995.2005.00699.x	44	78	81	0	1	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0905-6157			PEDIATR ALLERGY IMMU	Pediatr. Allergy Immunol.	FEB	2007	18	1					47	57		10.1111/j.1399-3038.2006.00475.x		11	Allergy; Immunology; Pediatrics	Allergy; Immunology; Pediatrics	134CO	WOS:000244060400008	17295799	
J	Akdis, M				Akdis, Muebeccel			Healthy immune response to allergens: T regulatory cells and more	CURRENT OPINION IN IMMUNOLOGY			English	Review							IN-VIVO; BEE VENOM; AUTOIMMUNE-DISEASES; ANTIBODY-RESPONSES; ATOPIC-DERMATITIS; DENDRITIC CELLS; IMMUNOTHERAPY; IL-10; EXPRESSION; TOLERANCE	The specific immune response to allergens is decisive in the development of clinically healthy or allergic states. In healthy individuals, the B-cell response varies between there being no response and the production of IgG(4)- or IgG(1)-dominating allergen-specific antibodies in the presence or absence of low amounts of IgE. If a detectable immune response is mounted, T regulatory type 1 (Tr1) cells specific for common environmental allergens consistently represent the dominant subset in healthy individuals. Exposure to high doses of allergens leads to a high concentration of specific IgG(4), detectable IgE and a TO type of immune response. Induction of IL-10- and TGF-beta-producing TO cells, IgG(4) isotype blocking antibodies, and suppressed mast cells, basophils and eosinophils represent major components of a relatively normalized immune response after allergen-specific immunotherapy (SIT).	Swiss Inst Allergy & Asthma Res, CH-7270 Davos, Switzerland	Akdis, M (reprint author), Swiss Inst Allergy & Asthma Res, Obere Str 22, CH-7270 Davos, Switzerland.	akdism@siaf.unizh.ch					Aalberse RC, 2002, IMMUNOLOGY, V105, P9, DOI 10.1046/j.0019-2805.2001.01341.x; Akbari O, 2001, NAT IMMUNOL, V2, P725, DOI 10.1038/90667; Akdis CA, 2004, CURR OPIN IMMUNOL, V16, P717, DOI 10.1016/j.coi.2004.09.004; Akdis CA, 1998, J CLIN INVEST, V102, P98, DOI 10.1172/JCI2250; Akdis CA, 2000, FASEB J, V14, P1666; Akdis CA, 1996, J CLIN INVEST, V98, P1676, DOI 10.1172/JCI118963; Akdis CA, 2001, TRENDS IMMUNOL, V22, P175, DOI 10.1016/S1471-4906(01)01862-2; Akdis M, 2004, J EXP MED, V199, P1567, DOI 10.1084/jem.20032058; BACCHETTA R, 1994, J EXP MED, V179, P493, DOI 10.1084/jem.179.2.493; Bahceciler NN, 2005, INT ARCH ALLERGY IMM, V136, P287, DOI 10.1159/000083956; BECKER JC, 1994, INT IMMUNOL, V6, P1605, DOI 10.1093/intimm/6.10.1605; Berry MA, 2006, NEW ENGL J MED, V354, P697, DOI 10.1056/NEJMoa050580; Bettelli E, 2006, NATURE, V441, P235, DOI 10.1038/nature04753; Bilo BM, 2005, ALLERGY, V60, P1339, DOI 10.1111/j.1398-9995.2005.00963.x; CARBALLIDO JM, 1993, J IMMUNOL, V150, P3582; Chatila TA, 2000, J CLIN INVEST, V106, P75; Chen WJ, 2003, J EXP MED, V198, P1875, DOI 10.1084/jem.20030152; CHEN YH, 1994, SCIENCE, V265, P1237, DOI 10.1126/science.7520605; Cottrez F, 2000, J IMMUNOL, V165, P4848; Diebold RJ, 1995, P NATL ACAD SCI USA, V92, P12215, DOI 10.1073/pnas.92.26.12215; ENK AH, 1994, J EXP MED, V179, P1397, DOI 10.1084/jem.179.4.1397; Fontenot JD, 2003, NAT IMMUNOL, V4, P330, DOI 10.1038/ni904; Groux H, 1997, NATURE, V389, P737; Haselden BM, 1999, J EXP MED, V189, P1885, DOI 10.1084/jem.189.12.1885; Huber S, 2004, J IMMUNOL, V173, P6526; Jutel M, 2003, EUR J IMMUNOL, V33, P1205, DOI 10.1002/eji.200322919; Jutel M, 2001, NATURE, V413, P420, DOI 10.1038/35096564; Karagiannidis C, 2004, J ALLERGY CLIN IMMUN, V114, P1425, DOI 10.1016/j.jaci.2004.07.014; Karamloo F, 2005, EUR J IMMUNOL, V35, P3268, DOI 10.1002/eji.200425522; Klunker S, 2003, J IMMUNOL, V171, P1078; Kruszewski Jerzy, 1994, Archivum Immunologiae et Therapiae Experimentalis, V42, P259; Kunzmann S, 2003, FASEB J, V17, P1089, DOI 10.1096/fj.02-1008com; Kussebi F, 2005, J ALLERGY CLIN IMMUN, V115, P323, DOI 10.1016/j.jaci.2004.011.041; Larche M, 2005, NAT MED, V11, pS69, DOI 10.1038/nm1226; Levings MK, 2001, J IMMUNOL, V166, P5530; Ling EM, 2004, LANCET, V363, P608, DOI 10.1016/S0140-6736(04)15592-X; Mamura M, 2004, BLOOD, V103, P4594, DOI 10.1182/blood-2003-08-2897; Mauri C, 2003, J EXP MED, V197, P489, DOI 10.1084/jem.20021293; Mazzoni A, 2001, J CLIN INVEST, V108, P1865, DOI 10.1172/JCI13930; McCoy KD, 2006, IMMUNITY, V24, P329, DOI 10.1016/j.immuni.2006.01.013; MOSMANN TR, 1996, IMMUNOL TODAY, V17, P142; Muller U, 1998, J ALLERGY CLIN IMMUN, V101, P747, DOI 10.1016/S0091-6749(98)70402-6; Muller U, 1993, ALLERGY          S14, V48, P36; Niederberger V, 2004, P NATL ACAD SCI USA, V101, P14677, DOI 10.1073/pnas.0404735101; Nouri-Aria KT, 2004, J IMMUNOL, V172, P3252; Osna N, 2001, INT IMMUNOPHARMACOL, V1, P85, DOI 10.1016/S0162-3109(00)00268-X; Pereira EAL, 2005, ALLERGY, V60, P401, DOI 10.1111/j.1398-9995.2005.00738.x; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; PUNNONEN J, 1993, J IMMUNOL, V151, P1280; SAKAGUCHI S, 1995, J IMMUNOL, V155, P1151; SHULL MM, 1992, NATURE, V359, P693, DOI 10.1038/359693a0; Tarzi M, 2006, CLIN EXP ALLERGY, V36, P465, DOI 10.1111/j.1365-2222.2006.02469.x; TAYLOR A, 2006, IN PRESS FASEB J; VanRee R, 1997, CLIN EXP ALLERGY, V27, P68, DOI 10.1046/j.1365-2222.1997.d01-416.x; Verhagen J, 2006, J ALLERGY CLIN IMMUN, V117, P176, DOI 10.1016/j.jaci.2005.10.040; Vignola AM, 1997, AM J RESP CRIT CARE, V156, P591; Wildin RS, 2001, NAT GENET, V27, P18, DOI 10.1038/83707; Zinkernagel RM, 1997, IMMUNOL REV, V156, P199, DOI 10.1111/j.1600-065X.1997.tb00969.x	58	78	86	1	5	CURRENT BIOLOGY LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0952-7915			CURR OPIN IMMUNOL	Curr. Opin. Immunol.	DEC	2006	18	6					738	744		10.1016/j.coi.2006.06.003		7	Immunology	Immunology	105NL	WOS:000242036900016	17023149	
J	Kunzli, N; Avol, E; Wu, J; Gauderman, WJ; Rappaport, E; Millstein, J; Bennion, J; McConnell, R; Gilliland, FD; Berhane, K; Lurmann, F; Winer, A; Peters, JM				Kunzli, Nino; Avol, Ed; Wu, Jun; Gauderman, W. James; Rappaport, Ed; Millstein, Joshua; Bennion, Jonathan; McConnell, Rob; Gilliland, Frank D.; Berhane, Kiros; Lurmann, Fred; Winer, Arthur; Peters, John M.			Health effects of the 2003 Southern California wildfires on children	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						air pollution; asthma; sore throat; wheezing	AMBIENT AIR-POLLUTION; RESPIRATORY HEALTH; PARTICULATE MATTER; FOREST-FIRES; EXPOSURE; QUALITY; VISITS; ASTHMA; SMOKE	Rationale: In late October 2003, Southern California wildfires burned more than 3,000 km(2). The wildfires produced heavy smoke that affected several communities participating in the University of Southern California Children's Health Study (CHS). Objectives: To study the acute effects of fire smoke on the health of CHS participants. Methods: A questionnaire was used to assess smoke exposure and occurrence of symptoms among CHS high-school students (n = 873; age, 17-18 yr) and elementary-school children (n = 5,551; age, 6-7 yr), in a total of 16 communities. Estimates of particulate matter (PM10) concentrations during the 5 d with the highest fire activity were used to characterize community smoke level. Main Results: All symptoms (nose, eyes, and throat irritations; cough; bronchitis; cold; wheezing; asthma attacks), medication usage, and physician visits were associated with individually reported exposure differences within communities. Risks increased monotonically with the number of reported smoky days. For most outcomes, reporting rates between communities were also associated with the fire-related PM10 levels. Associations tended to be strongest among those without asthma. Individuals with asthma were more likely to take preventive action, such as wearing masks or staying indoors during the fire. Conclusions: Exposure to wildfire smoke was associated with increased eye and respiratory symptoms, medication use, and physician visits.	Inst Municipal Invest Med, E-08003 Barcelona, Spain; ICREA, Barcelona, Spain; Univ So Calif, Los Angeles, CA USA	Kunzli, N (reprint author), Inst Municipal Invest Med, C Doct Aiguader 80, E-08003 Barcelona, Spain.	kuenzli@imim.es	Kunzli, Nino/F-7195-2014	Kunzli, Nino/0000-0001-8360-080X	NIEHS NIH HHS [3P01ES011627-03S2, 5P01ES11627, 5P30 ES07048]		Boman C, 2006, EUR RESPIR J, V27, P446, DOI 10.1183/09031936.06.00000806; DUCLOS P, 1990, ARCH ENVIRON HEALTH, V45, P53; Emmanuel S C, 2000, Respirology, V5, P175, DOI 10.1046/j.1440-1843.2000.00247.x; Gilliland FD, 1999, ENVIRON HEALTH PERSP, V107, P403; Heinrich J, 2005, OCCUP ENVIRON MED, V62, P517, DOI 10.1136/oem.2004.016766; Henderson DE, 2005, J AIR WASTE MANAGE, V55, P1516, DOI 10.1080/10473289.2005.10464746; Jalaludin B, 2000, AUST NZ J PUBL HEAL, V24, P174, DOI 10.1111/j.1467-842X.2000.tb00138.x; JALALUDIN B, 2004, ENV HLTH, V4, P20; Jalaludin BB, 2004, ENVIRON RES, V95, P32, DOI 10.1016/S0013-9351(03)00038-0; Johnson J. M., 2005, MORB MORTAL WKLY R S, V54, P190; KUNZLI N, 2005, EUR RESPIR J, V26, pS385; Malilay J, 1999, HLTH GUIDELINES VEGE, P258; McConnell R, 2006, ENVIRON HEALTH PERSP, V114, P766, DOI 10.1289/ehp.8594; Mott JA, 2002, WESTERN J MED, V176, P157, DOI 10.1136/ewjm.176.3.157; Oglesby L, 2000, AM J EPIDEMIOL, V152, P75, DOI 10.1093/aje/152.1.75; Ovadnevaite J, 2006, SCI TOTAL ENVIRON, V356, P11, DOI 10.1016/j.scitotenv.2005.04.013; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; PETERS JM, 1974, NEW ENGL J MED, V291, P1320, DOI 10.1056/NEJM197412192912502; Phuleria HC, 2005, J GEOPHYS RES-ATMOS, V110, DOI 10.1029/2004JD004626; Sastry N, 2002, DEMOGRAPHY, V39, P1, DOI 10.1353/dem.2002.0009; Tan WC, 2000, AM J RESP CRIT CARE, V161, P1213; VanEeden SF, 1997, MICROCIRCULATION-LON, V4, P369, DOI 10.3109/10739689709146801; Viswanathan S, 2006, J AIR WASTE MANAGE, V56, P56; Wu J, 2006, ATMOS ENVIRON, V40, P3333, DOI 10.1016/j.atmosenv.2006.01.056; Zelikoff JT, 2002, J TOXICOL ENV HEAL B, V5, P269, DOI 10.1080/10937400290070062	25	78	79	1	23	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	DEC 1	2006	174	11					1221	1228		10.1164/rccm.200604-519OC		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	109BU	WOS:000242283700013	16946126	
J	von Mutius, E; Schmid, S				von Mutius, E; Schmid, S		PASTURE Study Grp	The PASTURE project: EU support for the improvement of knowledge about risk factors and preventive factors for atopy in Europe	ALLERGY			English	Article						allergy; asthma; atopic sensitization; farming; hygiene hypothesis; infectious disease; microbial stimuli; toll-like receptors	HOUSE-DUST ENDOTOXIN; RESPIRATORY-SYNCYTIAL-VIRUS; TOLL-LIKE RECEPTOR-2; ALLERGIC SENSITIZATION; FARMERS CHILDREN; EARLY-LIFE; HAY-FEVER; 1ST YEAR; SCHOOL-AGE; ASTHMA	Since January 2002, the European Commission is funding a large project, 'Protection against Allergy - Study in Rural Environments' (PASTURE; contract no. QLK4-2001-00250), under the Fifth Framework Program in the field of epidemiology of allergic diseases. The aim of this paper was to describe the background and design as well as the aims of the project. Asthma and allergic disorders are a major public health problem in many Western countries. The aetiology of asthma and allergic disease remains poorly understood despite considerable research. Epidemiology has the potential to add greatly to the understanding by elucidating the risk factors for asthma and allergic disease and thereby suggesting productive avenues for research into causation and prevention. Several risk factors for the development of asthma and atopic disease in children such as passive smoke exposure during pregnancy and infancy, low birth weight or high body mass index later in life have been described. Furthermore, there is consistent evidence that the prevalence of atopy increases with higher socio-economic status. Levels of air pollution such as ozone, NO2, SO2 and particles are likely to provoke acute exacerbations of pre-existent respiratory disease. Their role in the inception of asthma and allergies remains to be clarified. Allergen exposure has been linked to the development of atopic sensitization to that particular allergen in children as well as in adults with occupational exposures. Exposure to house dust mite or cat allergen is, however, unlikely to contribute to the development of childhood asthma. In turn, pet keeping in the first year of life, particularly, dog keeping, has been inversely related to the development of wheeze and atopic illnesses. Several prospective birth cohort studies found a decreased prevalence of atopic disease in children having daily contact to pets, in particular to cats and dogs, during early infancy (1, 2). The protective effect might be attributable to allergen or other exposures associated with pet ownership, but may also in part be because of the removal of pets in families with sensitized or symptomatic children or in families with a positive history for atopy at the time the child was born.	Univ Munich, Univ Childrens Hosp, PASTURE, D-80337 Munich, Germany	Schmid, S (reprint author), Univ Munich, Univ Childrens Hosp, PASTURE, Lindwurmstr 4, D-80337 Munich, Germany.						Bjorksten B, 2001, J ALLERGY CLIN IMMUN, V108, P516; Bottcher MF, 2003, CLIN EXP ALLERGY, V33, P295, DOI 10.1046/j.1365-2222.2003.01562.x; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Cardoso MRA, 2004, BMC PUBLIC HEALTH, V4, DOI 10.1186/1471-2458-4-19; Celedon JC, 2003, AM J RESP CRIT CARE, V167, P1239, DOI 10.1164/rccm.200209-1063OC; Douwes J, 1999, J ALLERGY CLIN IMMUN, V103, P494, DOI 10.1016/S0091-6749(99)70476-8; Eder W, 2004, J ALLERGY CLIN IMMUN, V113, P482, DOI 10.1016/j.jaci.2003.12.374; Eduard W, 2004, AM J IND MED, V46, P396, DOI 10.1002/ajim.20088; Eduard W, 2004, THORAX, V59, P381, DOI 10.1136/thx.2004.013326; FERRIS BG, 1978, AM REV RESPIR DIS, V188, P1; 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; Gern JE, 2000, J ALLERGY CLIN IMMUN, V106, P201; Illi S, 2001, BRIT MED J, V322, P390, DOI 10.1136/bmj.322.7283.390; Johnston SL, 1996, AM J RESP CRIT CARE, V154, P654; Kalliomaki M, 2003, LANCET, V361, P1869, DOI 10.1016/S0140-6736(03)13490-3; Kalliomaki Marko, 2003, Curr Opin Allergy Clin Immunol, V3, P15, DOI 10.1097/00130832-200302000-00003; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Korppi M, 2004, PEDIATR PULM, V38, P155, DOI 10.1002/ppul.20058; Kruisselbrink A, 2001, CLIN EXP IMMUNOL, V126, P2, DOI 10.1046/j.1365-2249.2001.01642.x; Lauener RP, 2002, LANCET, V360, P465, DOI 10.1016/S0140-6736(02)09641-1; Matricardi PM, 2002, J ALLERGY CLIN IMMUN, V110, P381, DOI 10.1067/mai.2002.126658; Noble V, 1997, ARCH DIS CHILD, V76, P315; Ownby DR, 2002, JAMA-J AM MED ASSOC, V288, P963, DOI 10.1001/jama.288.8.963; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Perzanowski MS, 2002, AM J RESP CRIT CARE, V166, P696, DOI 10.1164/rccm.2201035; Phipatanakul W, 2004, PEDIATRICS, V114, P13, DOI 10.1542/peds.114.1.13; Remes ST, 2005, CLIN EXP ALLERGY, V35, P160, DOI 10.1111/j.1365-2222.2005.02172.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; Sigurs N, 2005, AM J RESP CRIT CARE, V171, P137, DOI 10.1164/rccm.200406-730OC; Stein R, 1999, LANCET, V354, P541, DOI 10.1016/S0140-6736(98)10321-5; STRACHAN DP, 1989, BRIT MED J, V299, P1259; van Strien RT, 2004, J ALLERGY CLIN IMMUN, V113, P860, DOI 10.1016/j.jaci.2004.01.078; von Mutius E, 2004, J ALLERGY CLIN IMMUN, V113, P373, DOI 10.1016/j.jaci.2003.12.040; von Mutius E, 2000, J ALLERGY CLIN IMMUN, V105, P9, DOI 10.1016/S0091-6749(00)90171-4; Williams LK, 2004, J ALLERGY CLIN IMMUN, V113, P291, DOI 10.1016/j.jaci.2003.11.010	38	78	78	0	6	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0105-4538			ALLERGY	Allergy	APR	2006	61	4					407	413		10.1111/j.1398-9995.2006.01009.x		7	Allergy; Immunology	Allergy; Immunology	016BC	WOS:000235594500003	16512801	
J	Sunyer, J; Torrent, M; Munoz-Ortiz, L; Ribas-Fito, N; Carrizo, D; Grimalt, J; Anto, JM; Cullinan, P				Sunyer, J; Torrent, M; Munoz-Ortiz, L; Ribas-Fito, N; Carrizo, D; Grimalt, J; Anto, JM; Cullinan, P			Prenatal dichlorodiphenyldichloroethylene (DDE) and asthma in children	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; atopy; children; DDE dichlorodiphenyldichloroethylene; organochlorines	ORGANOCHLORINE COMPOUNDS; IMMUNE-SYSTEM; CORD BLOOD; EXPOSURE; HEALTH; HEXACHLOROBENZENE; ASSOCIATIONS; SUPPRESSION; INFECTIONS; CHILDHOOD	Prevalence of asthma increases with increasing dichlorodiphenyldichloroethylene (DDE) levels. However, the effect of early-life exposure, the fundamental window of exposure, is unknown. We assessed the association between prenatal DDE and other organochlorine compounds, and atopy and asthma during infancy. All women presenting for antenatal care in Menorca (Spain) over 12 months starting in mid-1997 were invited to take part in a longitudinal study; 482 children were subsequently enrolled, and 468 (97.1%) provided complete outcome data up to the fourth year of study. Prenatal exposure of organochlorine compounds was measured in cord serum in 405 (83%) children. Asthma was defined on the basis of wheezing at 4 years of age, persistent wheezing, or doctor-diagnosed asthma. We measured specific immunoglobulin-E (IgE) against house dust mite, cat, and grass in sera extracted at 4 years of age. DDE (median=1.03 ng/mL) was detected in all children, as well as hexachlorobenzene (0.68 ng/mL) and polychlorobiphenyls (0.69 ng/mL). Wheezing at 4 years of age increased with DDE concentration, particularly at the highest quartile [9% in the lowest quartile (<0.57 ng/mL) vs. 19% in the highest quartile (1.90 ng/mL); relative risk=2.63 (95% confidence interval 1.19-4.69), adjusting for maternal asthma, breast-feeding, education, social class, or other organochlorines]. The association was not modified by IgE sensitization and occurred with the same strength among nonatopic subjects and among those with persistent wheezing or diagnosed asthma. DDE was not associated with atopy alone. Prenatal exposure to DDE residues may contribute to development of asthma.	Inst Municipal Invest Med, Unitat Recerca Resp & Ambiental, E-08003 Barcelona, Catalonia, Spain; Univ Pompeu Fabra, Barcelona, Spain; IB SALUT, Area Salud Menorca, Menorca, Spain; CSIC, Barcelona, Spain; Univ London Imperial Coll Sci Technol & Med, Dept Occupat & Environm Med, London, England	Sunyer, J (reprint author), Inst Municipal Invest Med, Environm Resp Res Unit, C Doctor Aiguader 80, E-08003 Barcelona, Catalonia, Spain.	jsunyer@imim.es	Grimalt, Joan/E-2073-2011; Carrizo Gallardo, Daniel Alejandro/E-2461-2012; Sunyer, J/G-6909-2014	Grimalt, Joan/0000-0002-7391-5768; Carrizo Gallardo, Daniel Alejandro/0000-0003-1568-4591; Sunyer, J/0000-0002-2602-4110			BANARJEE BD, 1987, B ENVIRON CONTAM TOX, V39, P827; BANARJEE BD, 1987, B ENVIRON CONTAM TOX, V39, P822; Barr RG, 2004, ARCH INTERN MED, V164, P379, DOI 10.1001/archinte.164.4.379; Beard J, 2003, ENVIRON HEALTH PERSP, V111, P724, DOI 10.1289/ehp.5885; Bilrha H, 2003, ENVIRON HEALTH PERSP, V111, P1952, DOI 10.1289/ehp.6433; BOUSQUET J, 1990, NEW ENGL J MED, V323, P1033, DOI 10.1056/NEJM199010113231505; Chen A, 2003, EMERG INFECT DIS, V9, P960; Cooper GS, 2004, ENVIRON HEALTH PERSP, V112, P1080, DOI 10.1289/ehp.6892; Dallaire F, 2004, ENVIRON HEALTH PERSP, V112, P1359, DOI 10.1289/ehp.7255; Daniel V, 2002, ARCH ENVIRON HEALTH, V57, P541; Farchi S, 2003, EUR RESPIR J, V22, P772, DOI 10.1183/09031936.03.00006703; Gluckman PD, 2004, SCIENCE, V305, P1733, DOI 10.1126/science.1095292; Hoppin JA, 2002, AM J RESP CRIT CARE, V165, P683, DOI 10.1164/rccm.2106074; Jackola DR, 2003, INT ARCH ALLERGY IMM, V132, P364, DOI 10.1159/000074904; Karmaus W, 2003, PAEDIATR PERINAT EP, V17, P212, DOI 10.1046/j.1365-3016.2003.00488.x; Karmaus W, 2001, ARCH ENVIRON HEALTH, V56, P485; LAHVIS GP, 1995, ENVIRON HEALTH PERSP, V103, P62; LIBERATOS P, 1988, EPIDEMIOL REV, V10, P87; Luebke RW, 2001, TOXICOL SCI, V62, P71, DOI 10.1093/toxsci/62.1.71; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Michielsen CCPPC, 1999, ENVIRON HEALTH PERSP, V107, P783, DOI 10.2307/3434341; Nakai K, 2002, TOHOKU J EXP MED, V196, P89, DOI 10.1620/tjem.196.89; NAKANISHI Y, 1985, ENVIRON HEALTH PERSP, V59, P31, DOI 10.2307/3429870; Oddy Wendy H, 2003, J Hum Lact, V19, P250, DOI 10.1177/0890334403255516; Polk S, 2004, AM J RESP CRIT CARE, V170, P273, DOI 10.1164/rccm.200310-1348OC; REHANA T, 1992, B ENVIRON CONTAM TOX, V48, P535; Reichrtova E, 1999, ENVIRON HEALTH PERSP, V107, P895, DOI 10.2307/3454477; Rogan WJ, 2003, PEDIATRICS, V112, P247; Sala M, 2001, CHEMOSPHERE, V43, P895, DOI 10.1016/S0045-6535(00)00450-1; Salem ML, 2000, INT ARCH ALLERGY IMM, V121, P161, DOI 10.1159/000024312; SHAFER KS, 2002, J EPIDEMIOL COMMUNIT, V56, P813; Van den Heuvell RL, 2002, ENVIRON HEALTH PERSP, V110, P595; Vine MF, 2001, AM J EPIDEMIOL, V153, P53, DOI 10.1093/aje/153.1.53; WEISBAND SP, 1995, COMMUN ACM, V38, P40, DOI 10.1145/219663.219678; Weisglas-Kuperus N, 2000, ENVIRON HEALTH PERSP, V108, P1203, DOI 10.2307/3434834; Wendo C, 2004, LANCET, V363, P1376, DOI 10.1016/S0140-6736(04)16095-9	36	78	79	0	6	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.	DEC	2005	113	12					1787	1790		10.1289/ehp.8127		4	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	989ZP	WOS:000233713200054	16330365	
J	Martinez, TM; Llapur, CJ; Williams, TH; Coates, C; Gunderman, R; Cohen, MD; Howenstine, MS; Saba, O; Coxson, HO; Tepper, RS				Martinez, TM; Llapur, CJ; Williams, TH; Coates, C; Gunderman, R; Cohen, MD; Howenstine, MS; Saba, O; Coxson, HO; Tepper, RS			High-resolution computed tomography imaging of airway disease in infants with cystic fibrosis	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						airway structure; high-resolution computed tomography; lung disease	THIN-SECTION CT; PULMONARY-FUNCTION; WALL THICKNESS; YOUNG-CHILDREN; LUNG-DISEASE; ACUTE EXACERBATION; SCORING SYSTEM; ASTHMA; INFLAMMATION; EMPHYSEMA	Rationale: The development of early lung disease in patients with cystic fibrosis (CF) remains poorly defined. Objective: Determine whether asymptomatic infants with CF have evidence for changes in airway structure when assessed by high-resolution computed tomography, and whether airway structure correlates with airway function in this age group. Methods: Thirteen infants with CF (8-33 mo) and 13 control infants (7-25 mo) were evaluated. Airway wall and lumen areas were measured from three 1-mm-thick cross-sectional images obtained from upper, middle, and lower lobes during a respiratory pause with the lungs inflated to an airway pressure of 20 cm H2O. Lung tissue density was measured from images obtained during a respiratory pause at FRC. Forced expiratory flows were measured by the rapid thoracic compression technique in 11 infants with CF. Results: Airway wall area increased more per unit increase in airway size, whereas airway lumen area increased less per unit increase in airway size in the CF than in the control group. Among infants with CF, a greater ratio of wall to lumen area correlated with lower airway function. In addition, lung density at relaxed (passive) FRC was lower for infants with Cl: than for control infants (0.38 vs. 0.43 g/ml; p < 0.02). Conclusions: Our results indicate that infants with CF have thickened airway walls, narrowed airway lumens, and air trapping, when assessed by high-resolution computed tomography, and measurements of airway structure correlated with airway function.	Indiana Univ, Med Ctr, Dept Pediat Pulmonol & Crit Care, Indianapolis, IN 46204 USA; Indiana Univ, Med Ctr, Dept Radiol, Indianapolis, IN 46204 USA; Univ Iowa, Dept Radiol, Iowa City, IA 52242 USA; Vancouver Gen Hosp, Dept Radiol, Vancouver, BC, Canada; Univ British Columbia, St Pauls Hosp, James Hogg ICAPTURE Ctr Cardiovasc & Pulm Res, Vancouver, BC V5Z 1M9, Canada	Tepper, RS (reprint author), James Whitcomb Riley Hosp Children, Sect Pediat Pulmonol, Dept Pediat, 702 Barnhill Dr,Room 4270, Indianapolis, IN 46202 USA.	rtepper@iupui.edu	Coxson, Harvey/A-9861-2017	Coxson, Harvey/0000-0001-5750-9711			Armstrong DS, 1997, AM J RESP CRIT CARE, V156, P1197; Awadh N, 1998, THORAX, V53, P248; BEDROSSIAN CWM, 1976, HUM PATHOL, V7, P195, DOI 10.1016/S0046-8177(76)80023-8; BHALLA M, 1991, RADIOLOGY, V179, P783; Bonnel AS, 2004, PEDIATR PULM, V38, P396, DOI 10.1002/ppul.20091; BOULET LP, 1995, AM J RESP CRIT CARE, V152, P865; Brody AS, 2004, J PEDIATR-US, V145, P32, DOI 10.1016/j.jpeds.2004.02.038; Brody AS, 1999, PEDIATR RADIOL, V29, P731, DOI 10.1007/s002470050684; CHOW CW, 1982, EUR J PEDIATR, V139, P240, DOI 10.1007/BF00442171; Coxson HO, 1999, AM J RESP CRIT CARE, V159, P851; Coxson HO, 2004, AM J RESP CRIT CARE, V170, P748, DOI 10.1164/rccm.200405-651OC; COXSON HO, 1995, J APPL PHYSIOL, V79, P1525; de Jong PA, 2004, EUR RESPIR J, V24, P1071, DOI 10.1183/09031936.04.10099804; de Jong PA, 2004, RADIOLOGY, V231, P434, DOI 10.1148/radiol.2312021393; Demirkazik FB, 2001, EUR J RADIOL, V37, P54, DOI 10.1016/S0720-048X(00)00236-9; Goris ML, 2003, CHEST, V123, P1655, DOI 10.1378/chest.123.5.1655; Helbich TH, 1999, RADIOLOGY, V213, P537; HOGG JC, 1994, THORAX, V49, P473, DOI 10.1136/thx.49.5.473; Jones M, 2000, AM J RESP CRIT CARE, V161, P353; KHAN TZ, 1995, AM J RESP CRIT CARE, V151, P1075; King GG, 1999, AM J RESP CRIT CARE, V159, P992; Little SA, 2002, THORAX, V57, P247, DOI 10.1136/thorax.57.3.247; LLAPUR CJ, 2005, P AM THORAC SOC, pA576; Long FR, 1999, RADIOLOGY, V212, P588; Long FR, 2004, J PEDIATR-US, V144, P154, DOI 10.1016/j.jpeds.2003.09.026; Maffessanti M, 1996, J THORAC IMAG, V11, P27, DOI 10.1097/00005382-199601110-00002; MARTINEZ T, 2003, AM J RESP CRIT CARE, V167, pA41; Nakano Y, 2000, AM J RESP CRIT CARE, V162, P1102; Nakano Y, 2005, AM J RESP CRIT CARE, V171, P142, DOI 10.1164/rccm.200407-874OC; NAKANO Y, 2002, CHEST S, V122, pS275; NATHANSON I, 1991, PEDIATR PULM, V11, P81, DOI 10.1002/ppul.1950110112; Niimi A, 2000, AM J RESP CRIT CARE, V162, P1518; Okazawa M, 1996, AM J RESP CRIT CARE, V154, P1557; Ranganathan SC, 2002, AM J RESP CRIT CARE, V166, P1350, DOI 10.1164/rccm.2202041; Ranganathan SC, 2001, LANCET, V358, P1964, DOI 10.1016/S0140-6736(01)06970-7; Robinson TE, 2001, J PEDIATR-US, V138, P553, DOI 10.1067/mpd.2001.111820; Robinson TE, 2003, AM J RESP CRIT CARE, V168, P588, DOI 10.1164/rccm.200209-1093OC; ROBINSON TE, IN PRESS CHEST; Rosenfeld M, 2001, PEDIATR PULM, V32, P356, DOI 10.1002/ppul.1144; Saba OI, 2003, J APPL PHYSIOL, V95, P1063, DOI 10.1152/japplphysiol.00962.2002; Santamaria F, 1998, PEDIATRICS, V101, P908, DOI 10.1542/peds.101.5.908; SANTIS G, 1991, CLIN RADIOL, V44, P20, DOI 10.1016/S0009-9260(05)80220-X; Shah RM, 1997, AM J ROENTGENOL, V169, P375; TEPPER RS, 1993, PEDIATR PULM, V16, P96, DOI 10.1002/ppul.1950160204; TEPPER RS, 1988, PEDIATR PULM, V5, P15, DOI 10.1002/ppul.1950050105; Tepper RS, 2004, AM J RESP CRIT CARE, V170, P505, DOI 10.1164/rccm.200401-1320C; TOMASHEFSKI JF, 1986, AM REV RESPIR DIS, V133, P535	47	78	79	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 1	2005	172	9					1133	1138		10.1164/rccm.200412-1665OC		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	979UV	WOS:000232971400012	16051903	
J	Tager, IB; Balmes, J; Lurmann, F; Ngo, L; Alcorn, S; Kunzli, N				Tager, IB; Balmes, J; Lurmann, F; Ngo, L; Alcorn, S; Kunzli, N			Chronic exposure to ambient ozone and lung function in young adults	EPIDEMIOLOGY			English	Article							AIR-POLLUTION; LONG-TERM; PULMONARY-FUNCTION; NITROGEN-DIOXIDE; CHILDREN; ASSOCIATION; ASTHMA; POLLUTANTS; CALIFORNIA; MORTALITY	Background: Tropospheric ozone (O-3) is an oxidant, outdoor air pollutant. Chronic exposure has been associated with decreased lung function in children and adolescents. This study investigated the effects of long-term exposure to O-3 on lung function in college freshmen. Methods: We recruited University of California, Berkeley students (n = 255) who were lifelong residents of the Los Angeles and San Francisco Bay areas and who never smoked. Lifetime exposures to O-3, small particulate matter (PM10), and nitrogen dioxide (NO2) were based on spatial interpolation of compliance monitor measurements to all residences at which students lived. Spirometry was performed between February and May, times when students would not have had recent exposure to increased levels of O-3. Results: Lifetime exposure to O-3 was associated with decreased levels of measures of small airways ( < 2 mm) function (FEF75 and FEF25-75). There was an interaction with the FEF25-75/FVC ratio, a measure of intrinsic airway size. Subjects with a large ratio were less likely to have decreases in FEF75 and FEF25-75 for a given estimated lifetime exposure to O-3. This association was not altered by history of chronic respiratory disease, allergy, second-hand exposure to environmental tobacco smoke, exposure to PM10 and NO2, or measurement errors in exposure assessment. Conclusions: A history of increased level of lifetime exposure to ambient O-3 is associated with decreased function of airways in which O-3 deposition in the lungs is the greatest. Adolescents with intrinsically smaller airways appear to be at greatest risk. Any environmental or genetic factors that lead to reduced airway size may lead to increased susceptibility to the adverse effects of ambient ozone.	Univ Calif Berkeley, Div Epidemiol, Sch Publ Hlth, Berkeley, CA 94720 USA; Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA; Univ Calif Berkeley, Div Environm Hlth Sci, Sch Publ Hlth, Berkeley, CA 94720 USA; Sonoma Technol Inc, Petaluma, CA USA; Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90089 USA	Tager, IB (reprint author), Univ Calif Berkeley, Div Epidemiol, Sch Publ Hlth, 140 Warren Hall, Berkeley, CA 94720 USA.	ibt@berkeley.edu	Kunzli, Nino/F-7195-2014	Kunzli, Nino/0000-0001-8360-080X	NIEHS NIH HHS [P30 ES07048]; PHS HHS [R01-60689]		American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Anderson HR, 1997, EUR RESPIR J, V10, P1064, DOI 10.1183/09031936.97.10051064; Avissar NE, 2000, AM J RESP CRIT CARE, V162, P1342; Bell ML, 2004, JAMA-J AM MED ASSOC, V292, P2372, DOI 10.1001/jama.292.19.2372; Blomberg A, 1997, AM J RESP CRIT CARE, V156, P418; Burnett RT, 2001, AM J EPIDEMIOL, V153, P444, DOI 10.1093/aje/153.5.444; CHOW JC, 1993, AEROSOL SCI TECH, V18, P105, DOI 10.1080/02786829308959588; COSIO M, 1978, NEW ENGL J MED, V298, P1277, DOI 10.1056/NEJM197806082982303; Delfino RJ, 1996, AM J RESP CRIT CARE, V154, P633; DeMeo DL, 2004, THORAX, V59, P396, DOI 10.1136/thx.2003.012856; DOLISLAGER LJ, 1998, AIR WASTE MANAGEMENT, P108; Frank R, 2001, AM J RESP CRIT CARE, V164, P1253; Frischer T, 1999, AM J RESP CRIT CARE, V160, P390; FUJINAKA LE, 1985, EXP LUNG RES, V8, P167, DOI 10.3109/01902148509057520; Gauderman WJ, 2004, NEW ENGL J MED, V351, P1057, DOI 10.1056/NEJMoa040610; Geyh AS, 2000, ENVIRON HEALTH PERSP, V108, P265, DOI 10.2307/3454444; Ghio AJ, 1997, INHAL TOXICOL, V9, P255; HIGGINS ITT, 1990, AM REV RESPIR DIS, V141, P1136; HYATT RE, 1983, J APPL PHYSIOL, V55, P1; Ihorst G, 2004, EUR RESPIR J, V23, P292, DOI 10.1183/09031936.04.00021704; Kinney P L, 1998, Res Rep Health Eff Inst, P79; KINNEY PL, 1989, AM REV RESPIR DIS, V139, P56; Kinney PL, 1996, AM J RESP CRIT CARE, V154, P1430; Kinney PL, 1996, ENVIRON HEALTH PERSP, V104, P170, DOI 10.2307/3432785; KINNEY PL, 1991, ENVIRON RES, V54, P99, DOI 10.1016/S0013-9351(05)80094-5; KINNEY PL, 1998, RES REP HLTH EFF I, P109; KINNEY PL, 1992, TROPOSPHERIC OZONE E, V2, P203; Kunzli N, 1997, ENVIRON RES, V72, P8, DOI 10.1006/enrs.1996.3687; Kunzli N, 1996, J EXPO ANAL ENV EPID, V6, P289; Li N, 2003, ENVIRON HEALTH PERSP, V111, P455, DOI 10.1289/ehp.6000; Li YF, 2000, AM J RESP CRIT CARE, V162, P2097; Liu SL, 2003, ENVIRON HEALTH PERSP, V111, P1773, DOI 10.1289/ehp.6251; LOHMAN TG, 1988, ANTHROPOMETIC STANDA; McConnell R, 2002, LANCET, V359, P386, DOI 10.1016/S0140-6736(02)07597-9; McDonnell WF, 1999, ENVIRON RES, V80, P110, DOI 10.1006/enrs.1998.3894; MCMURRY P., 2004, NARSTO PARTICULATE M; MEAD J, 1980, AM REV RESPIR DIS, V121, P339; MILLER FJ, 1985, TOXICOL APPL PHARM, V79, P11, DOI 10.1016/0041-008X(85)90364-3; Motallebi N, 2003, J AIR WASTE MANAGE, V53, P1517; Mudway I. 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J	Frank, LD; Engelke, P				Frank, LD; Engelke, P			Multiple impacts of the built environment on public health: Walkable places and the exposure to air pollution	INTERNATIONAL REGIONAL SCIENCE REVIEW			English	Article						physical activity; air quality; built environment; travel behavior	PHYSICAL-ACTIVITY; URBAN FORM; LAND-USE; MYOCARDIAL-INFARCTION; CHILDHOOD ASTHMA; TRANSPORTATION; QUALITY; MORTALITY; WALKING; ATLANTA	While considerable attention has been paid to the public-health-related impacts of air pollution, relatively little research has been done to understand how other aspects of the built environment impact health. Americans are increasingly sedentary; erstwhile the rate of increase in obesity is alarming. New research suggests that increased auto dependence, and limited opportunities to walk for utilitarian purposes, has contributed to this emerging obesity, epidemic. Within socio-demographic strata, land use patterns and transportation investments collectively shape the desire to walk, drive, or to travel via other means. Mixed use and more compact community designs show significant promise for the promotion of physical activity and the reduction of regional air pollution levels. Opportunities exist to increase physical activity and improve regional air quality through more compact development. However, increased compactness, or density, often exacerbates traffic congestion and can increase exposure of harmful emissions within central areas. Therefore, strategies to reduce localized air pollution in existing and developing centers are required to enable larger health benefits from smart growth to be realized.	Univ British Columbia, Sch Community & Reg Planning, Vancouver, BC V5Z 1M9, Canada; Georgetown Univ, Dept Hist, Washington, DC 20057 USA	Frank, LD (reprint author), Univ British Columbia, Sch Community & Reg Planning, Vancouver, BC V5Z 1M9, Canada.	ldfrank@interchange.ubc.ca; poe@georgetown.edu					Bachman W, 2000, TRANSPORT RES C-EMER, V8, P205, DOI 10.1016/S0968-090X(00)00005-X; BOARNET M, 1996, URBAN STUD, V35, P1155; Brabec E, 2002, J PLAN LIT, V16, P499, DOI 10.1177/088541202400903563; Brunekreef B, 2002, LANCET, V360, P1233, DOI 10.1016/S0140-6736(02)11274-8; *CAMBR SYST, 1996, MAK LAND US TRANSP A; *CARB, 2002, MOB SOURC EM INV PRO; Center for Disease Control and Prevention, 2001, MMWR-MORBID MORTAL W, V50, P166; CERVERO R, 1988, TRANSPORT Q, V42, P429; CERVERO R, 1995, J AM PLANN ASSOC, V61, P210, DOI 10.1080/01944369508975634; *CGER, 1992, RETH OZ PROBL URB RE; Churchman A, 1999, J PLAN LIT, V13, P389, DOI DOI 10.1177/08854129922092478; Craig CL, 2002, AM J PREV MED, V23, P36, DOI 10.1016/S0749-3797(02)00472-5; DOCKERY DW, 1993, NEW ENGL J MED, V329, P1753, DOI 10.1056/NEJM199312093292401; Ewing R, 2003, AM J HEALTH PROMOT, V18, P47; Ewing R., 2001, TRANSPORTATION RES P, V35, P823; Frank LD, 2004, AM J PREV MED, V27, P87, DOI 10.1016/j.amepre.2004.04.011; Frank LD, 2005, AM J PREV MED, V28, P117, DOI 10.1016/j.amepre.2004.11.001; Frank LD, 2004, AM J PREV MED, V27, P146, DOI 10.1016/j.amepre.2004.06.018; Frank LD, 1998, J URBAN PLAN D-ASCE, V124, P11, DOI 10.1061/(ASCE)0733-9488(1998)124:1(11); Frank LD, 2000, TRANSPORT RES D-TR E, V5, P173, DOI 10.1016/S1361-9209(99)00032-2; Frank LD, 2000, J PLAN EDUC RES, V20, P6, DOI 10.1177/073945600128992564; Frank LD, 2001, J PLAN LIT, V16, P202, DOI 10.1177/08854120122093339; Frank L.D., 2003, HLTH COMMUNITY DESIG; Frank L., 1994, TRANSPORT RES REC, V1466, P44; Friedman B., 1994, TRANSPORT RES REC, V1466, P63; Friedman MS, 2001, JAMA-J AM MED ASSOC, V285, P897, DOI 10.1001/jama.285.7.897; FRUMKIN H, 2004, PUBLIC HLTH IMPACT S; Gaffield SJ, 2003, AM J PUBLIC HEALTH, V93, P1527, DOI 10.2105/AJPH.93.9.1527; Gehl J., 1996, LIFE BUILDINGS; Giles-Corti B, 2003, AM J PUBLIC HEALTH, V93, P1583, DOI 10.2105/AJPH.93.9.1583; GIULIANO G, 1989, ENVIRON PLANN A, V21, P145, DOI 10.1068/a210145; Giuliano G., 1995, ACCESS, V6, P3; GREENWALD MJ, 2001, DUANES CLIN OPHTHALM, V1, P1; GUERARD A, 1903, TENEMENT HOUSE PROBL, V1; Handy S, 2005, INT REGIONAL SCI REV, V28, P146, DOI 10.1177/0160017604273626; Handy S., 1992, BUILT ENV, V18, P253; Handy SL, 1996, J PLAN EDUC RES, V15, P183, DOI 10.1177/0739456X9601500303; Hess P. 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Reg. Sci. Rev.	APR	2005	28	2					193	216		10.1177/0160017604273853		24	Environmental Studies; Planning & Development; Urban Studies	Environmental Sciences & Ecology; Public Administration; Urban Studies	910PW	WOS:000227945100005		
J	Portengen, L; Preller, L; Tielen, M; Doekes, G; Heederik, D				Portengen, L; Preller, L; Tielen, M; Doekes, G; Heederik, D			Endotoxin exposure and atopic sensitization in adult pig farmers	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						endotoxins; hypersensitivity; IgE; allergens; adult; occupational exposure; epidemiology	RESPIRATORY SYMPTOMS; BRONCHIAL HYPERRESPONSIVENESS; ALLERGIC SENSITIZATION; LUNG-FUNCTION; HOUSE-DUST; ASTHMA; CHILDREN; POPULATION; CHILDHOOD; ENVIRONMENT	Background: Recent studies have reported a low prevalence of atopic sensitization and respiratory allergy in children growing up on farms. Objectives: We sought to evaluate the dose-response relationship between endotoxin and atopic sensitization in adult farmers and to assess the effect on respiratory health outcomes. Methods: Data on endotoxin exposure and serum IgE levels were available for 162 pig farmers from a cross-sectional, case-control study, with case selection on the basis of respiratory symptoms. Exposure to endotoxin was modeled in detail, and respiratory health effects were assessed during a medical examination. Exploratory analysis was done by using nonparametric modeling and was followed by classical parametric regression. Results: IgE to one or more common allergens was detected in sera from 28 (17%) farmers. The average (geometric mean) total serum IgE levels was 37 lU/mL (geometric SD, 4 IU/mL). A strong inverse relationship was found between endotoxin and sensitization to common allergens for exposures of 75 ng/m(3) or less, with an odds ratio of 0.03 (95% CI, 0.0-0.34) for a 2-fold increase in endotoxin. For endotoxin exposure of greater than 75 ng/m(3), the association was weak (odds ratio, 1.2 [95% Cl, 0.38-3.6]). No association was found between endotoxin exposure and total serum IgE levels. Endotoxin was associated with increased airway hyperresponsiveness to histamine and lower lung function in sensitized farmers, without evidence of a nonlinear relationship. Conclusions: The prevalence of atopic sensitization in adult pig farmers is low. Endotoxin or related exposures might protect from sensitization, even in an adult working population exposed to high levels of endotoxin, but is a risk factor for increased airway hyperresponsiveness and low lung function.	Univ Utrecht, IRAS, NL-3508 TD Utrecht, Netherlands; Univ Utrecht, Dept Herd Hlth & Reprod, NL-3508 TD Utrecht, Netherlands; TNO Chem, Food & Chem Risk Anal, Zeist, Netherlands	Portengen, L (reprint author), Univ Utrecht, IRAS, POB 80176, NL-3508 TD Utrecht, Netherlands.	L.Portengen@iras.uu.nl					BIERSTEKER K, 1974, TIJDSCHR SOC GENEESK, V52, P158; Bolte G, 2003, CLIN EXP ALLERGY, V33, P770, DOI 10.1046/j.1365-2222.2003.01665.x; Bottcher MF, 2003, CLIN EXP ALLERGY, V33, P295, DOI 10.1046/j.1365-2222.2003.01562.x; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Braun-Fahrlander C, 2003, CLIN EXP ALLERGY, V33, P409, DOI 10.1046/j.1365-2222.2003.01650.x; COCKCROFT DW, 1977, CLIN ALLERGY, V7, P235, DOI 10.1111/j.1365-2222.1977.tb01448.x; Cormier Y, 2000, EUR RESPIR J, V15, P560, DOI 10.1034/j.1399-3003.2000.15.22.x; Doekes G, 1996, OCCUP ENVIRON MED, V53, P63; Douwes J, 2002, THORAX, V57, P86, DOI 10.1136/thorax.57.1.86; Filipiak B, 2001, CLIN EXP ALLERGY, V31, P1829, DOI 10.1046/j.1365-2222.2001.01246.x; Gehring U, 2002, AM J RESP CRIT CARE, V166, P939, DOI 10.1164/rccm.200203-256OC; Hastie T., 1990, GENERALIZED ADDITIVE; Heederik D, 1999, J ALLERGY CLIN IMMUN, V103, P678, DOI 10.1016/S0091-6749(99)70242-3; HOLLANDER A, 1993, AM IND HYG ASSOC J, V54, P647, DOI 10.1202/0002-8894(1993)054<0647:IAEITA>2.0.CO;2; Houba R, 1998, AM J RESP CRIT CARE, V158, P1499; Johnson Christine Cole, 2002, Curr Opin Allergy Clin Immunol, V2, P133, DOI 10.1097/00130832-200204000-00009; Kauffmann F, 2002, CLIN EXP ALLERGY, V32, P379, DOI 10.1046/j.1365-2222.2002.01325.x; Kerkhof M, 1996, ALLERGY, V51, P770, DOI 10.1111/j.1398-9995.1996.tb04465.x; Kilpelainen M, 2002, ALLERGY, V57, P1130, DOI 10.1034/j.1398-9995.2002.23341.x; Koppelman GH, 2003, CLIN EXP ALLERGY, V33, P170, DOI 10.1046/j.1365-2222.2003.01591.x; Leynaert B, 2001, AM J RESP CRIT CARE, V164, P1829; Liu AH, 2002, J ALLERGY CLIN IMMUN, V109, P379, DOI 10.1067/mai.2002.122157; Portengen L, 2002, CLIN EXP ALLERGY, V32, P247, DOI 10.1046/j.1365-2222.2002.01310.x; Preller L, 1996, EUR RESPIR J, V9, P1407, DOI 10.1183/09031936.96.09071407; PRELLER L, 1995, ANN OCCUP HYG, V39, P545, DOI 10.1016/0003-4878(95)00024-9; Preller L, 1995, SCAND J WORK ENV HEA, V21, P504; PRELLER L, 1995, OCCUP ENVIRON MED, V52, P654; Quanjer PH, 1993, EUR RESPIR J S, V16, P5, DOI 10.1183/09041950.005s1693; 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; RIJCKEN B, 1987, AM REV RESPIR DIS, V136, P62; Roy SR, 2003, J ALLERGY CLIN IMMUN, V112, P571, DOI 10.1067/mai.2003.1711; Schwartz DA, 2001, AM J RESP CRIT CARE, V163, P305; Simpson JCG, 1999, ANN OCCUP HYG, V43, P107, DOI 10.1016/S0003-4878(98)00083-0; Vogelzang PFJ, 1997, INT ARCH OCC ENV HEA, V70, P327, DOI 10.1007/s004200050226; Vogelzang PFJ, 1998, AM J RESP CRIT CARE, V157, P15; Wahba G., 1990, SPLINE MODELS OBSERV; Wouters IM, 2002, OCCUP ENVIRON MED, V59, P106, DOI 10.1136/oem.59.2.106; Yabuhara A, 1997, CLIN EXP ALLERGY, V27, P1261; Zock JP, 1998, OCCUP ENVIRON MED, V55, P823	41	78	81	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.	APR	2005	115	4					797	802		10.1016/j.jaci.2004.11.046		6	Allergy; Immunology	Allergy; Immunology	916GM	WOS:000228373400020	15806001	
J	Currie, J				Currie, J			Health disparities and gaps in school readiness	FUTURE OF CHILDREN			English	Article							UNITED-STATES; COGNITIVE-DEVELOPMENT; MATERNAL DEPRESSION; POSTNATAL DEPRESSION; BEHAVIOR PROBLEMS; CHILDHOOD ASTHMA; IRON-DEFICIENCY; YOUNG-CHILDREN; PRIMARY-CARE; LEAD LEVELS	The author documents pervasive racial disparities in the health of American children and analyzes how and how much those disparities contribute to racial gaps in school readiness. She explores a broad sample of health problems common to U.S. children, such as attention deficit hyperactivity disorder, asthma, and lead poisoning, as well as maternal health problems and health-related behaviors that affect children's behavioral and cognitive readiness for school. If a health problem is to affect the readiness gap, it must affect many children, it must be linked to academic performance or behavior problems, and it must show a racial disparity either in its prevalence or in its effects. The author focuses not only on the black-white gap in health status but also on the poor-nonpoor gap because black children tend to be poorer than white children. The health conditions Currie considers seriously impair cognitive skills and behavior in individual children. But most explain little of the overall racial gap in school readiness. Still, the cumulative effect of health differentials summed over all conditions is significant. Curries rough calculation is that racial differences in health conditions and in maternal health and behaviors together may account for as much as a quarter of the racial gap in school readiness. Currie scrutinizes several policy steps to lessen racial and socioeconomic disparities in children's health and to begin to close the readiness gap. Increasing poor children's eligibility for Medicaid and state child health insurance is unlikely to be effective because most poor children are already eligible for public insurance. The problem is that many are not enrolled. Even increasing enrollment may not work: socioeconomic disparities in health persist in Canada and the United Kingdom despite universal public health insurance. The author finds more promise in strengthening early childhood programs with a built-in health component, like Head Start; family-based services and home visiting programs; and WIC, the federal nutrition program for women. infants, and small children. In all three, trained staff can help parents get ongoing care for their children.	Univ Calif Los Angeles, Los Angeles, CA 90024 USA	Currie, J (reprint author), Univ Calif Los Angeles, Los Angeles, CA 90024 USA.						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SPR	2005	15	1					117	138		10.1353/foc.2005.0002		22	Family Studies; Health Policy & Services; Social Sciences, Interdisciplinary	Family Studies; Health Care Sciences & Services; Social Sciences - Other Topics	985IH	WOS:000233370300008	16130544	
J	Sallusto, F; Mackay, CR				Sallusto, F; Mackay, CR			Chemoattractants and their receptors in homeostasis and inflammation	CURRENT OPINION IN IMMUNOLOGY			English	Review							LEUKOTRIENE B-4 RECEPTOR; NAIVE T-CELLS; PROTEIN-COUPLED RECEPTOR; ALLERGIC AIRWAY DISEASE; DENDRITIC CELLS; LYMPH-NODES; SPHINGOSINE 1-PHOSPHATE; CHEMOKINE RECEPTORS; CHEMOTACTIC RESPONSIVENESS; EOSINOPHIL RECRUITMENT	The study of leukocyte migration continues to provide new insights into the regulation of lymphocyte priming in secondary lymphoid organs and effector responses in inflamed tissues. Chemoattractant receptors have always been viewed as facilitators of cell movement into a tissue. This whole concept must now be revised with the discovery of sphingosine 1 phosphate receptors, which control cell exit from lymphoid tissues. The chemoattractants that regulate lymphoid tissue homing are usually different to those that regulate leukocyte recruitment to inflamed tissues. There is evidence, however, of inflammatory pathways of leukocyte recruitment in lymph nodes and, conversely of constitutive pathways in peripheral tissues. Finally, antagonists (or agonists) of chemoattractant receptors and their signalling pathways represent the most attractive strategy for the treatment of a wide range of inflammatory diseases, including allergy.	Inst Res Biomed, CH-650 Bellinzona, Switzerland; Garvan Inst Med Res, Darlinghurst, NSW 2010, Australia	Sallusto, F (reprint author), Inst Res Biomed, Via Vincenzo Vela 6, CH-650 Bellinzona, Switzerland.	federica.sallusto@irb.unisi.ch; c.mackay@garvan.org.au	Mackay, Charles/A-9673-2008	Mackay, Charles/0000-0002-6338-7340			Alcami A, 2003, NAT REV IMMUNOL, V3, P36, DOI 10.1038/nri980; ALLENDE ML, 2004, J BIOL CHEM; ANCUTA P, 2003, J EXP MED, V197, P1707; Biedermann T, 2002, EUR J IMMUNOL, V32, P3171, DOI 10.1002/1521-4141(200211)32:11<3171::AID-IMMU3171>3.0.CO;2-4; Brandes M, 2003, BLOOD, V102, P3693, DOI 10.1182/blood-2003-04-1016; Brinkmann V, 2002, J BIOL CHEM, V277, P21453, DOI 10.1074/jbc.C220176200; Cassese G, 2003, J IMMUNOL, V171, P1684; Chensue SW, 2001, J EXP MED, V193, P573, DOI 10.1084/jem.193.5.573; Chiba K, 1998, J IMMUNOL, V160, P5037; Chong BF, 2004, J IMMUNOL, V172, P1575; Chung CD, 2003, J IMMUNOL, V170, P581; Cinamon G, 2004, NAT IMMUNOL, V5, P713, DOI 10.1038/ni1083; 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Opin. Immunol.	DEC	2004	16	6					724	731		10.1016/j.coi.2004.09.012		8	Immunology	Immunology	871AY	WOS:000225102800007	15511664	
J	Becker, A; Watson, W; Ferguson, A; Dimich-Ward, H; Chan-Yeung, M				Becker, A; Watson, W; Ferguson, A; Dimich-Ward, H; Chan-Yeung, M			The Canadian asthma primary prevention study: Outcomes at 2 years of age	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; atopy; risk factors; primary prevention; environmental tobacco smoke; daycare; breast-feeding; early life	CAT ALLERGEN LEVELS; CHILDHOOD ASTHMA; HOUSE-DUST; EARLY-LIFE; MITE ALLERGEN; BIRTH COHORT; RISK-FACTORS; P-I; AVOIDANCE; EXPOSURE	Background: Avoidance of individual risk factors have not been successful in preventing the development of asthma. Objective: We sought to determine the effectiveness of a multifaceted intervention program in primary prevention of asthma in high-risk infants. Methods: We identified 545 high-risk infants on the basis of an immediate family history of asthma. Families were randomized into intervention or control groups. Intervention measures included avoidance of house dust mite, pet allergen, and environmental tobacco smoke. Breast-feeding was encouraged with formula supplementation if necessary, and introduction of solid foods was delayed. Results: At 2 years of age, 19.5% of the children had asthma, and 14.7% had atopy (positive skin test response to one or more common allergens). Significantly fewer children had asthma in the intervention group compared with in the control group (16.3% vs 23.0%), with 60% less persistent asthma at 2 years. There was a 90% reduction for recurrent wheeze in the intervention group compared with that seen in the control group. Exposure to maternal environmental tobacco smoke during pregnancy or the first year was a risk factor for asthma at 2 years of age. A positive skin test response, particularly to food, at 12 months predicted asthma at 2 years. There was no significant difference for atopy between the intervention and control groups, but daycare reduced atopy at 2 years. Conclusion: This multifaceted intervention program during a window of opportunity in the first year of life was effective in preventing asthma in high-risk children at 2 years of age. Future studies with this cohort at school age are important.	Univ Manitoba, Dept Pediat & Child Hlth, Allergy & Clin Immunol Sect, Winnipeg, MB R3E 0Z2, Canada; Univ British Columbia, Dept Pediat, Div Allergy, Vancouver, BC V5Z 1M9, Canada; Univ British Columbia, Dept Med, Div Resp, Occupat & Environm Lung Dis Unit, Vancouver, BC V5Z 1M9, Canada	Becker, A (reprint author), Univ Manitoba, Dept Pediat & Child Hlth, Allergy & Clin Immunol Sect, AE101-671 William Ave, Winnipeg, MB R3E 0Z2, Canada.						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Allergy Clin. Immunol.	APR	2004	113	4					650	656		10.1016/j.jaci.2004.01.754		7	Allergy; Immunology	Allergy; Immunology	814DY	WOS:000220956600010	15100668	
J	Auinger, P; Lanphear, BP; Kalkwarf, HJ; Mansour, ME				Auinger, P; Lanphear, BP; Kalkwarf, HJ; Mansour, ME			Trends in otitis media among children in the United States	PEDIATRICS			English	Article; Proceedings Paper	39th Annual Meeting of the Ambulatory-Pediatric-Association	MAY 01-04, 1999	SAN FRANCISCO, CALIFORNIA	Ambulatory Pediat Assoc		otitis media; early-onset otitis media; National Health and Nutrition Examination Survey; allergy; epidemiology; pediatric; children	PASSIVE SMOKE EXPOSURE; MIDDLE-EAR DISEASE; RISK-FACTORS; YOUNG-CHILDREN; LIFE; ASTHMA; PREVALENCE; INFECTIONS; OUTCOMES; VACCINE	Background. The prevalence of repeated otitis media ( OM) increased during the 1980s, but it is unknown if the increase has continued. Objectives. To determine trends in the prevalence of OM, early-onset OM, and repeated OM among US children from 1988 to 1994 and to identify factors that may explain any observed changes. Methods. The Third National Health and Nutrition Examination Survey was administered in 2 phases: phase I ( 1988 - 1991) and phase II ( 1991 - 1994), each comprising a national probability sample. OM ( ever having had OM), early-onset OM ( first episode at < 12 months of age), and repeated OM (&GE; 3 episodes) were assessed for 8261 children < 6 years of age. Results. After controlling for risk factors for OM, the prevalence of OM from phase I to phase II increased from 66.7% to 69.7% ( odds ratio [ OR] = 1.1; 95% confidence interval [ CI] = .99, 1.1), early-onset OM increased from 41.1% to 45.8% ( OR = 1.1; 95% CI = 1.03, 1.2), and repeated OM increased from 34.8% to 41.1% ( OR = 1.2; 95% CI = 1.1, 1.4). This observed increase corresponds to 561 000 and 720 000 more children having early-onset OM and repeated OM, respectively. Child care use, early breastfeeding termination, asthma, and access to health care did not significantly increase from phase I to phase II. The prevalence of early-onset OM and repeated OM was higher for affluent children, but the greatest increase in prevalence was among impoverished children. There was an increase in allergic conditions from phase I to phase II for poor children (22.6% to 30.2%). Conclusions. The prevalence of early-onset OM and repeated OM continued to increase among preschool children in the United States. Further research to investigate this increasing prevalence should explore changes in management practice and an increase in prevalence of allergic conditions among poor children.	Univ Rochester, Dept Pediat, Sch Med & Dent, Rochester, NY 14620 USA; Amer Acad Pediat Ctr Child Hlth Res, Rochester, NY USA; Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH USA	Auinger, P (reprint author), Univ Rochester, Dept Pediat, Sch Med & Dent, 1351 Mt Hope Ave,Ste 130, Rochester, NY 14620 USA.				BHP HRSA HHS [1T-32 PE-10027, 2T-32 PE-12002]		ALHO OP, 1990, AM J EPIDEMIOL, V132, P1164; Bauchner H, 1999, PEDIATRICS, V103, P395, DOI 10.1542/peds.103.2.395; Belshe RB, 2000, PEDIATR INFECT DIS J, V19, pS66, DOI 10.1097/00006454-200005001-00010; Belshe RB, 1998, NEW ENGL J MED, V338, P1405, DOI 10.1056/NEJM199805143382002; Bennett KE, 1999, ARCH DIS CHILD, V80, P28; BERMAN S, 1995, NEW ENGL J MED, V332, P1560, DOI 10.1056/NEJM199506083322307; Berman S, 1997, PEDIATRICS, V100, P585, DOI 10.1542/peds.100.4.585; Black S, 2000, PEDIATR INFECT DIS J, V19, P187, DOI 10.1097/00006454-200003000-00003; BONDY J, 2000, PEDIATRICS, V105; DALY KA, 1994, AM J EPIDEMIOL, V139, P1116; Dowell SF, 1999, PEDIATR INFECT DIS J, V18, P1, DOI 10.1097/00006454-199901000-00002; DUNCAN B, 1993, PEDIATRICS, V91, P867; Edwards DJ, 2002, ACAD EMERG MED, V9, P22, DOI 10.1111/j.1553-2712.2002.tb01162.x; Eggleston PA, 1999, ENVIRON HEALTH PERSP, V107, P439; EVANS R, 1987, CHEST, V91, pS65; EY JL, 1995, PEDIATRICS, V95, P670; HARDY AM, 1993, AM J PUBLIC HEALTH, V83, P1321, DOI 10.2105/AJPH.83.9.1321; HARSTEN G, 1989, ACTA OTO-LARYNGOL, V107, P111, DOI 10.3109/00016488909127487; HUBBARD TW, 1985, NEW ENGL J MED, V312, P1529, DOI 10.1056/NEJM198506133122401; KITCHENS GG, 1995, LARYNGOSCOPE, V105, P1, DOI 10.1288/00005537-199505001-00001; Kvaerner KJ, 1997, ACTA OTO-LARYNGOL, V117, P578, DOI 10.3109/00016489709113441; Lanphear BP, 2001, PEDIATRICS, V107, P505, DOI 10.1542/peds.107.3.505; LANPHEAR BP, 1997, PEDIATRICS, V99; LANPHEAR BP, 2001, PEDIATRICS, V107; LEVINE OS, 1999, PEDIATRICS, V103; Lieu JEC, 2002, ARCH PEDIAT ADOL MED, V156, P147; Mannino DM, 1998, MMWR-MORBID MORTAL W, V47, P1; MCCRAIG LF, 2002, JAMA-J AM MED ASSOC, V287, P3096; McCraig LG, 1995, JAMA-J AM MED ASSOC, V273, P214; National Center for Health Statistics, 1994, VITAL HLTH STAT, V1, P1; Nyquist AC, 1998, JAMA-J AM MED ASSOC, V279, P875, DOI 10.1001/jama.279.11.875; Paradise JL, 1997, PEDIATRICS, V99, P318, DOI 10.1542/peds.99.3.318; PLESS CE, 1995, ARCH PEDIAT ADOL MED, V149, P553; SCHAPPERT SM, 1992, VITAL HLTH STATISTIC, V214, P1; Shah B. 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J	Cooper, S; Oborne, J; Newton, S; Harrison, V; Coon, JT; Lewis, S; Tattersfield, A				Cooper, S; Oborne, J; Newton, S; Harrison, V; Coon, JT; Lewis, S; Tattersfield, A			Effect of two breathing exercises (Buteyko and pranayama) in asthma: a randomised controlled trial	THORAX			English	Article							ALTERNATIVE MEDICINE; YOGA	Background: Patients with asthma are interested in the use of breathing exercises but their role is uncertain. The effects of the Buteyko breathing technique, a device which mimics pranayama (a yoga breathing technique), and a dummy pranayama device on bronchial responsiveness and symptoms were compared over 6 months in a parallel group study. Methods: Ninety patients with asthma taking an inhaled corticosteroid were randomised after a 2 week run in period to Eucapnic Buteyko breathing, use of a Pink City Lung Exerciser (PCLE) to mimic pranayama, or a PCLE placebo device. Subjects practised the techniques at home twice daily for 6 months followed by an optional steroid reduction phase. Primary outcome measures were symptom scores and change in the dose of methacholine provoking a 20% fall in FEV1 (PD20) during the first 6 months. Results: Sixty nine patients (78%) completed the study. There was no significant difference in PD20 between the three groups at 3 or 6 months. Symptoms remained relatively stable in the PCLE and placebo groups but were reduced in the Buteyko group. Median change in symptom scores at 6 months was 0 (interquartile range -1 to 1) in the placebo group, -1 (-2 to 0.75) in the PCLE group, and -3 (-4 to 0) in the Buteyko group (p=0.003 for difference between groups). Bronchodilator use was reduced in the Buteyko group by two puffs/day at 6 months; there was no change in the other two groups (p=0.005). No difference was seen between the groups in FEV1, exacerbations, or ability to reduce inhaled corticosteroids. Conclusion: The Buteyko breathing technique can improve symptoms and reduce bronchodilator use but does not appear to change bronchial responsiveness or lung function in patients with asthma. No benefit was shown for the Pink City Lung Exerciser.	City Hosp Nottingham, Div Resp Med, Nottingham NG5 1PB, England	Cooper, S (reprint author), City Hosp Nottingham, Div Resp Med, Clin Sci Bldg, Nottingham NG5 1PB, England.		Cooper, Sue/A-7471-2011	Cooper, Sue/0000-0002-1994-6395			Bowler SD, 1998, MED J AUSTRALIA, V169, P575; Egbagbe E, 1997, THORAX, V52, P239; Ernst E, 1998, J ASTHMA, V35, P667, DOI 10.3109/02770909809048969; Harrison TW, 1999, THORAX, V54, P98; Hensley MJ, 1998, MED J AUSTRALIA, V169, P573; *HL SEL COMM SCI T, 2000, 6 HL SEL COMM SCI TE; JUNIPER EF, 1993, AM REV RESPIR DIS, V147, P832; Keeley D, 2001, BRIT MED J, V322, P1075, DOI 10.1136/bmj.322.7294.1075; Manocha R, 2002, THORAX, V57, P110, DOI 10.1136/thorax.57.2.110; McCarthy M, 2002, LANCET, V359, P1213, DOI 10.1016/S0140-6736(02)08253-3; Opat AJ, 2000, J ASTHMA, V37, P557, DOI 10.3109/02770900009090810; SINGH V, 1990, LANCET, V335, P1381, DOI 10.1016/0140-6736(90)91254-8; Stalmatski A., 1997, FREEDOM ASTHMA BUTEY; Thomas M, 2001, BRIT MED J, V322, P1098, DOI 10.1136/bmj.322.7294.1098; WARE JE, 1992, MED CARE, V30, P473, DOI 10.1097/00005650-199206000-00002	15	78	79	1	8	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	AUG	2003	58	8					674	679		10.1136/thorax.58.8.674		6	Respiratory System	Respiratory System	705YP	WOS:000184425100009	12885982	
J	Matricardi, PM; Bjorksten, B; Bonini, S; Bousquet, J; Djukanovic, R; Dreborg, S; Gereda, J; Malling, HJ; Popov, T; Raz, E; Renz, H; Wold, A				Matricardi, PM; Bjorksten, B; Bonini, S; Bousquet, J; Djukanovic, R; Dreborg, S; Gereda, J; Malling, HJ; Popov, T; Raz, E; Renz, H; Wold, A		EAACI Task Force 7	Microbial products in allergy prevention and therapy	ALLERGY			English	Article							MONOPHOSPHORYL-LIPID-A; IMMUNOSTIMULATORY DNA-SEQUENCES; KILLED MYCOBACTERIUM-VACCAE; GRAM-NEGATIVE BACTERIA; LACTIC-ACID BACTERIA; VAXOM OM-85 BV; INTESTINAL MICROFLORA; IN-VITRO; INFLAMMATORY RESPONSE; ENDOTOXIN EXPOSURE		IRCCS, Asthma & Allergy Res Unit, Osped Pediat Bambino Gesu, Res Inst, I-00165 Rome, Italy	Matricardi, PM (reprint author), IRCCS, Asthma & Allergy Res Unit, Osped Pediat Bambino Gesu, Res Inst, Piazza S Onofrio 4, I-00165 Rome, Italy.			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Wheeler AW, 2001, INT ARCH ALLERGY IMM, V126, P135, DOI 10.1159/000049504; Wheeler JG, 1997, ANN ALLERG ASTHMA IM, V79, P229; Wheeler JG, 1997, AM J MED SCI, V313, P120, DOI 10.1097/00000441-199702000-00011; Wills-Karp M, 2001, NAT REV IMMUNOL, V1, P69, DOI 10.1038/35095579; WYBRAN J, 1990, LUNG, V168, P720, DOI 10.1007/BF02718199; Yazdanbakhsh M, 2002, SCIENCE, V296, P490, DOI 10.1126/science.296.5567.490	88	78	80	0	1	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	JUN	2003	58	6					461	471		10.1034/j.1398-9995.2003.00175.x		11	Allergy; Immunology	Allergy; Immunology	681TK	WOS:000183051300001	12757444	
J	Rosenman, KD; Reilly, MJ; Schill, DP; Valiante, D; Flattery, J; Harrison, R; Reinisch, F; Pechter, E; Davis, L; Tumpowsky, CM; Filios, M				Rosenman, KD; Reilly, MJ; Schill, DP; Valiante, D; Flattery, J; Harrison, R; Reinisch, F; Pechter, E; Davis, L; Tumpowsky, CM; Filios, M			Cleaning products and work-related asthma	JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE			English	Article							OCCUPATIONAL ASTHMA; SURVEILLANCE SYSTEM; EXPOSURE; CLEANERS	To describe the characteristics of individuals with work-related asthma associated with exposure to cleaning products, data from the California-, Massachusetts-, Michigan-, and New Jersey state-based surveillance systems of work-related asthma were used to identify cases of asthma associated with exposure to cleaning products at work. From 1993 to 1997, 236 (12 %) of the 1915 confirmed cases of work-related asthma identfied by the four states were associated with exposure to cleaning products. Eighty Percent of the reports were of new-onset asthma and 20% were work-aggravated asthma. Among the new-onset cases, 22 % were consistent with reactive airways dysfunction syndrome. Individuals identfied were generally women (75 %), white non-Hispanic (68 %), and 45 years or older (64 %). Their most likely exposure had been in medical settings (39 %), schools (13 %), or hotels (6 %), and they were most likely to work as janitor/cleaners (22 %), nurse/nurses' aides (20 %), or clerical staff (13 %). However, cases were reported with exposure to cleaning products across a wide range of job titles. Cleaning products contain a diverse group of chemicals that are used in a wide range of industries and occupations as well as in the home. Their potential to cause or aggravate asthma has recently been recognized. Further work to characterize the specific agents and the circumstances of their use associated with asthma is needed. Additional research to investigate the frequency of adverse respiratory effects among regular users, such as housekeeping staff, is also needed. In the interim, we recommend attention to adequate ventilation, improved warning labels and Material Safety Data Sheets, and workplace training and education.	Michigan State Univ, E Lansing, MI 48824 USA; New Jersey Dept Hlth & Senior Serv, Trenton, NJ USA; Calif Dept Hlth Serv, Oakland, CA USA; Massachusetts Dept Publ Hlth, Boston, MA USA; NIOSH, Morgantown, WV USA	Rosenman, KD (reprint author), Michigan State Univ, 117 W Fee Hall, E Lansing, MI 48824 USA.						Alberts WM, 1996, CHEST, V109, P1618, DOI 10.1378/chest.109.6.1618; BARRON T, 1999, HOW SELECT USE SAFE; Bernstein IL, 1999, ASTHMA WORKPLACE; BERNSTEIN JA, 1994, J ALLERGY CLIN IMMUN, V94, P257, DOI 10.1016/0091-6749(94)90048-5; Buck RG, 2000, S AFR MED J, V90, P884; BURGE PS, 1994, THORAX, V49, P842, DOI 10.1136/thx.49.8.842; CHANYEUNG M, 1995, NEW ENGL J MED, V333, P107, DOI 10.1056/NEJM199507133330207; FLYVHOLM MA, 1993, BRIT J IND MED, V50, P1043; Henneberger P K, 1999, Int J Occup Environ Health, V5, P1; Henneberger PK, 2000, AM J IND MED, V38, P140; Hunting KL, 1995, APPL OCCUP ENV HYG, V10, P317; Jajosky R A, 1999, MMWR CDC Surveill Summ, V48, P1; Karjalainen A, 2002, EUR RESPIR J, V19, P90, DOI 10.1183/09031936.02.00201002; Kogevinas M, 1999, LANCET, V353, P1750, DOI 10.1016/S0140-6736(98)07397-8; Kreiss K., 1982, ENVIRON INT, V8, P337, DOI 10.1016/0160-4120(82)90047-2; KUJALA VM, 1995, RESP MED, V89, P693, DOI 10.1016/0954-6111(95)90137-X; LAMB VA, 1983, VIRGINIA MMWR, V32, P378; Litovitz TL, 2001, AM J EMERG MED, V19, P337, DOI 10.1053/ajem.2001.25272; Litovitz TL, 2000, AM J EMERG MED, V18, P517, DOI 10.1053/ajem.2000.9261; Lynch RM, 2000, ENVIRON HEALTH PERSP, V108, P911, DOI 10.1289/ehp.00108911; MALO JL, 1991, AM REV RESPIR DIS, V143, P528; Mapp CE, 2000, EUR RESPIR J, V16, P570, DOI 10.1034/j.1399-3003.2000.016003570.x; MATTE TD, 1990, CHEST, V98, pS173, DOI 10.1378/chest.98.5_Supplement.173S; NG TP, 1995, OCCUP MED-OXFORD, V45, P45, DOI 10.1093/occmed/45.1.45; *NIOSH, 2000, 2000105 US DEP HHS P; Purohit A, 2000, INT ARCH OCC ENV HEA, V73, P423, DOI 10.1007/s004200000162; REILLY MJ, 1995, ARCH ENVIRON HEALTH, V50, P26; Rosenman KD, 1997, J OCCUP ENVIRON MED, V39, P415, DOI 10.1097/00043764-199705000-00007; SAVONIUS B, 1994, ALLERGY, V49, P877, DOI 10.1111/j.1398-9995.1994.tb00791.x; SHELTON D, 1992, J ALLERGY CLIN IMMUN, V90, P274, DOI 10.1016/0091-6749(92)90085-G; *SWORD, 2001, OCC DIS INT NET CTR; Zock JP, 2001, SCAND J WORK ENV HEA, V27, P76	32	78	78	0	8	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	1076-2752			J OCCUP ENVIRON MED	J. Occup. Environ. Med.	MAY	2003	45	5					556	563		10.1097/01.jom.0000058347.05741.f9		8	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	679CH	WOS:000182903100016	12762081	
J	Leonardi, A; Jose, PJ; Zhan, H; Calder, VL				Leonardi, A; Jose, PJ; Zhan, H; Calder, VL			Tear and mucus eotaxin-l and eotaxin-2 in allergic keratoconjunctivitis	OPHTHALMOLOGY			English	Article							IL-4 INDUCES EOTAXIN; VERNAL KERATOCONJUNCTIVITIS; ATOPIC KERATOCONJUNCTIVITIS; CONJUNCTIVAL FIBROBLASTS; HUMAN EOSINOPHIL; MESSENGER-RNA; EYE DISEASE; TNF-ALPHA; IN-VITRO; EXPRESSION	Objective: Eotaxin-1 and eotaxin-2 are potent eosinophil chemotactic and activating peptides that may be implicated in the pathogenesis of the chronic allergic eye diseases vernal keratoconjunctivitis (VKC) and atopic keratoconjunctivitis (AKC). The purpose of this study was to measure these chemokines, in tear and mucus samples of active-disease patients and in vitro cultured conjunctival epithelial cells and fibroblasts. Design: Comparative, observational case series and in vitro study. Participants: Sixteen patients with clinically active and untreated VKC or AKC, six age-matched control patients, and five nonactive seasonal allergic conjunctivitis patients. Methods: Tears were collected from the active VKC and AKC patients, and from the normal patients. Mucus was collected from six of these VKC patients. Tears were also collected from an additional five allergic patients after obtaining a positive reaction to conjunctival allergen challenge. Conjunctival epithelial cell and conjunctival fibroblast cultures were exposed to interleukin (IL)-4, IL-13, and tumor necrosis factor-alpha (TNF-alpha), or to combinations of these cytokines. Main Outcome Measures: Levels of eotaxin-1 and eotaxin-2 in tears, mucus, and culture medium. Results: High levels of eotaxin-1 and eotaxin-2 were found in mucus of VKC patients, whereas only eotaxin-2 was found to have increased significantly in tears of VKC and AKC patients compared with those of normal patients. Mucus contained higher levels of chemokines than did tears. Both tear eotaxin-1 and eotaxin-2 were correlated significantly with the percent of eosinophils in tear fluid. Eotaxin-1 also was correlated significantly with the sum clinical score and corneal involvement in VKC patients. Conjunctival epithelial cells in culture did not produce eotaxin-1 or eotaxin-2, either at baseline or after cytokine exposure. Conjunctival fibroblasts produced eotaxin-1 only after exposure to IL-4, TNF-alpha, and the combination of IL-4 plus TNF-alpha or IL-13 plus TNF-alpha. Conclusions: Eotaxin-1 and eotaxin-2 are implicated in eosinophil recruitment and in the pathogenesis of VKC and AKC. Cytokine-stimulated conjunctival fibroblasts may be one source of eotaxin-1 in severely allergic tissues. (C) 2003 by the American Academy of Ophthalmology.	Univ Padua, Dept Ophthalmol, Padua, Italy; Univ London Imperial Coll Sci Technol & Med, London, England; UCL, Inst Ophthalmol, Dept Clin Ophthalmol, London, England	Leonardi, A (reprint author), Via Foscari 8, I-35127 Padua, Italy.	andrea-leonardi@umpd.it					ABELSON MB, 1990, ARCH OPHTHALMOL-CHIC, V108, P84; Abu El-Asrar AM, 2000, BRIT J OPHTHALMOL, V84, P1360; BONINI S, 1988, J ALLERGY CLIN IMMUN, V82, P462, DOI 10.1016/0091-6749(88)90020-6; Calder VL, 1999, CLIN EXP ALLERGY, V29, P1214; Chung KF, 1999, BRIT J PHARMACOL, V127, P1145, DOI 10.1038/sj.bjp.0702660; Culley FJ, 2000, J IMMUNOL, V165, P6447; Daugherty BL, 1996, J EXP MED, V183, P2349, DOI 10.1084/jem.183.5.2349; Dulkys Y, 2001, J INVEST DERMATOL, V116, P498, DOI 10.1046/j.1523-1747.2001.01299.x; Evans CAW, 1998, INFECT IMMUN, V66, P4522; Forssmann U, 1997, J EXP MED, V185, P2171, DOI 10.1084/jem.185.12.2171; Fukagawa K, 1999, J ALLERGY CLIN IMMUN, V103, P1220, DOI 10.1016/S0091-6749(99)70206-X; Fukagawa K, 2000, INT ARCH ALLERGY IMM, V121, P144, DOI 10.1159/000024310; JOSE PJ, 1994, J EXP MED, V179, P881, DOI 10.1084/jem.179.3.881; Kumagai N, 2000, INVEST OPHTH VIS SCI, V41, P1448; Leonardi A, 1999, INVEST OPHTH VIS SCI, V40, P3036; Leonardi A, 1999, EXP EYE RES, V68, P739, DOI 10.1006/exer.1999.0658; Leonardi A, 2000, INVEST OPHTH VIS SCI, V41, P4175; Leonardi A, 2000, AM J OPHTHALMOL, V129, P151, DOI 10.1016/S0002-9394(99)00295-0; Leonardi A, 1998, EXP EYE RES, V67, P105, DOI 10.1006/exer.1998.0499; Metz DP, 1997, J ALLERGY CLIN IMMUN, V100, P817, DOI 10.1016/S0091-6749(97)70279-3; Mochizuki M, 1998, J IMMUNOL, V160, P60; Rothenberg ME, 1996, MOL MED, V2, P334; Solomon A, 2000, INVEST OPHTH VIS SCI, V41, P1038; Terada N, 2000, CLIN EXP ALLERGY, V30, P348; Teran LM, 1999, AM J RESP CELL MOL, V20, P777; TROCME SD, 1989, AM J OPHTHALMOL, V108, P57; Trocme SD, 1997, INVEST OPHTH VIS SCI, V38, P593; TROCME SD, 1994, SURV OPHTHALMOL, V39, P241, DOI 10.1016/0039-6257(94)90197-X; Uchio E, 2000, CLIN EXP ALLERGY, V30, P103; Ying S, 1999, J IMMUNOL, V163, P6321	30	78	83	0	1	ELSEVIER SCIENCE INC	NEW YORK	360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA	0161-6420			OPHTHALMOLOGY	Ophthalmology	MAR	2003	110	3					487	492		10.1016/S0161-6420(02)01767-0		6	Ophthalmology	Ophthalmology	649XK	WOS:000181233100016	12623809	
J	Horak, F; Stubner, UP; Zieglmayer, R; Harris, AG				Horak, F; Stubner, UP; Zieglmayer, R; Harris, AG			Effect of desloratadine versus placebo on nasal airflow and subjective measures of nasal obstruction in subjects with grass pollen-induced allergic rhinitis in an allergen-exposure unit	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						desloratadine; antihistamine; nasal obstruction; seasonal allergic rhinitis; allergen exposure; rhinomanometry	MUCOSAL BLOOD-FLOW; RECEPTOR ANTAGONISTS; ATOPIC PATIENTS; EFFICACY; CETIRIZINE; CHALLENGE; SYMPTOMS; SAFETY; LORATADINE; MANAGEMENT	Background: Unlike many antihistamines, desloratadine can reduce nasal congestion in patients with seasonal allergic rhinitis (SAR). Objective: We compared the effects of 5 mg of desloratadine and placebo on nasal airflow and SAR symptoms, including nasal congestion, in response to grass pollen in an allergen-exposure unit. Methods: In a randomized, double-blind, placebo-controlled, crossover trial, 47 subjects with histories of SAR received desloratadine or placebo every morning for 7 days and, after a 10-day washout period, were crossed over to the other treatment arm for 7 days. Subjects underwent a 6-hour allergen exposure on day 7 of each treatment period. Nasal airflow and nasal secretion weights were measured before and every 30 minutes during allergen exposure; SAR symptoms (including nasal congestion) were scored before exposure and every 15 minutes thereafter. Results: Nasal obstruction, as measured by nasal airflow, was less severe with desloratadine than with placebo (P < .02). Individual and combined SAR symptom severity scores, including nasal congestion and sneezing, were significantly lower with desloratadine than with placebo (all P less than or equal to .003). Within 30 minutes of allergen exposure, less severely decreased nasal airflow (P < .02), less nasal secretions (P < .001), and less severe symptoms, including nasal congestion (P < .002), rhinorrhea, and sneezing, occurred with desloratadine compared with placebo, and this continued throughout (0-6 hours) allergen exposure. Desloratadine was well tolerated, with an adverse event profile similar to that of placebo. Conclusion: In subjects with allergen-induced SAR symptoms, desloratadine significantly reduced the severity of nasal obstruction and accompanying complaints of nasal congestion and other SAR symptoms compared with the effects of placebo.	Univ Vienna, AKH Vienna, ENT Clin, A-1090 Vienna, Austria; Schering Plough Corp, Kenilworth, NJ 07033 USA	Horak, F (reprint author), Univ Vienna, AKH Vienna, ENT Clin, Wahringer Gurtel 18-20, A-1090 Vienna, Austria.			Harris, Alan/0000-0002-6618-2092			*AM AC ALL ASTHM I, 2001, ALL REP; ANDERSSON KE, 1984, ANN OTO RHINOL LARYN, V93, P179; Bachert C, 2001, ALLERGY, V56, P14, DOI 10.1034/j.1398-9995.2001.00102.x; BISGAARD H, 1986, CLIN ALLERGY, V16, P289, DOI 10.1111/j.1365-2222.1986.tb01960.x; BROIDE D, 1995, ALLERGY, V50, P31, DOI 10.1111/j.1398-9995.1995.tb04261.x; Day JH, 1997, ANN ALLERG ASTHMA IM, V79, P163; DOCKHORN RJ, 1987, ANN ALLERGY, V58, P407; Geha Raif S., 2001, Journal of Allergy and Clinical Immunology, V107, P751; Gentile DA, 2000, IMMUNOL ALLERGY CLIN, V20, P355, DOI 10.1016/S0889-8561(05)70152-1; HORAK F, 1993, ALLERGY, V48, P226, DOI 10.1111/j.1398-9995.1993.tb00720.x; Horak F, 2001, INT ARCH ALLERGY IMM, V125, P73, DOI 10.1159/000053799; Horak F, 1998, ALLERGY, V53, P849, DOI 10.1111/j.1398-9995.1998.tb03990.x; HORAK F, 1987, WIEN KLIN WOCHENSCHR, V99, P509; Kay AB, 2001, NEW ENGL J MED, V344, P30; Kreutner William, 2000, Arzneimittel-Forschung, V50, P345; *MED EC COMP, 2000, 2000 PHYS DESK REF N; Meltzer EO, 1998, J ALLERGY CLIN IMMUN, V102, P39, DOI 10.1016/S0091-6749(98)70053-3; Meltzer EO, 2001, CLIN DRUG INVEST, V21, P25, DOI 10.2165/00044011-200121010-00004; PIPKORN U, 1982, ALLERGY, V37, P129, DOI 10.1111/j.1398-9995.1982.tb01886.x; Schmidt BMW, 1999, J CLIN PHARMACOL, V39, P1062, DOI 10.1177/00912709922011836; SMALL P, 1991, ANN ALLERGY, V67, P520; Wang DY, 1996, ACTA OTO-LARYNGOL, V116, P91, DOI 10.3109/00016489609137720; Weiner JM, 1998, BRIT MED J, V317, P1624; Wilson AM, 2001, CLIN EXP ALLERGY, V31, P61, DOI 10.1046/j.1365-2222.2001.00964.x	24	78	81	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.	JUN	2002	109	6					956	961		10.1067/mai.2002.124657		6	Allergy; Immunology	Allergy; Immunology	566RU	WOS:000176442700010	12063524	
J	Wright, RJ; Steinbach, SF				Wright, RJ; Steinbach, SF			Violence: An unrecognized environmental exposure that may contribute to greater asthma morbidity in high risk inner-city populations	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; case series; innercity; stress; violence	POSTTRAUMATIC-STRESS-DISORDER; URBAN AFRICAN-AMERICAN; PSYCHOLOGICAL STRESS; IMMUNE INTERACTIONS; CHILDHOOD ASTHMA; LIFE EVENTS; CHILDREN; HEALTH; SMOKING; HOSPITALIZATION	In the United States, rising trends in asthma prevalence and severity, which disproportionately impact minorities and the urban poor, have not been fully explained by traditional physical environmental risk factors. Exigencies of inner-city living can increase psychosocial risk factors (e.g., stress) that confer increased asthma morbidity. In the United States, chronic exposure to violence is a unique stressor existing in many high-risk urban neighborhoods. In this paper, we describe a series of cases that exemplify a temporal association between exposure to violence and the precipitation of asthma exacerbations in four urban pediatric patients. In the first three cases, the nature of the exposure is characterized by the proximity to violence, which ranged from direct victimization (through either the threat of physical assault or actual assault) to learning of the death of a peer. The fourth case characterizes a scenario in which a child was exposed to severe parental conflict (i.e., domestic violence) in the hospital setting. Increasingly, studies have begun to explore the effect of living in a violent environment, with a chronic pervasive atmosphere of fear and the perceived or real threat of violence, on health outcomes in population-based studies. Violence exposure may contribute to environmental demands that tax both the individual and the communities in which they live to impact the inner-city asthma burden. At the individual level, intervention strategies aimed to reduce violence exposure, to reduce stress, or to counsel victims or witnesses to violence may be complementary to more traditional asthma treatment in these populations. Change in policies that address the social, economic, and political factors that contribute to crime and violence in urban America may have broader impact.	Harvard Univ, Brigham & Womens Hosp, Sch Med, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA; Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Pulm & Crit Care, Boston, MA 02115 USA; Boston Med Ctr, Dept Pediat, Boston, MA USA	Wright, RJ (reprint author), Channing Labs, 181 Longwood Ave, Boston, MA 02115 USA.				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Health Perspect.	OCT	2001	109	10					1085	1089		10.2307/3454965		5	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	487GF	WOS:000171864800031	11675274	
J	Huecas, S; Villalba, M; Rodriguez, R				Huecas, S; Villalba, M; Rodriguez, R			Ole e 9, a major olive pollen allergen is a 1,3-beta-glucanase - Isolation, characterization, amino acid sequence, and tissue specificity	JOURNAL OF BIOLOGICAL CHEMISTRY			English	Article							PATHOGENESIS-RELATED PROTEINS; DUST-MITE ALLERGEN; TREE POLLEN; EUROPEA POLLEN; E-I; BETA-1,3-GLUCANASE; TOBACCO; EXPRESSION; IDENTIFICATION; PURIFICATION	Olive pollen allergy is a clinical disorder affecting the human population of Mediterranean areas. A novel major allergen, Ole e 9, has been isolated from olive pollen by gel permeation, hydrophobic affinity, and reverse-phase high performance liquid chromatographies. It is involved in the allergic responses of 65% of patients suffering olive pollinosis. Ole e 9 (molecular mass of 46.4 kDa) displays 1,3-beta -endoglucanase activity (38.9 +/- 5.6 mg of glucose released/min x mu mol of protein at pH 4.5-6.0 using laminarin as substrate). It is the first 1,3-beta -glucanase, a member of the "pathogenesis-related" protein family, detected in pollen tissue. Seven tryptic peptides of the allergen were sequenced by Edman degradation and used for designing primers to clone the cDNA codifying the protein. Specific cDNA for Ole e 9 was synthesized from total RNA and amplified using the polymerase chain reaction. The allergen sequence showed an open reading frame of 460 amino acids comprising a putative signal peptide of 26 residues. It shows 39, 33, and 32% sequence identity including the catalytic residues when compared with 1,3-beta -glucanases from wheat, willow, and Arabidopsis thaliana, respectively. Northern blot analysis showed that Ole e 9 transcript is specifically expressed in the pollen tissue, and highly conserved counterparts were only detected in taxonomically related pollens.	Univ Complutense, Fac Quim, Dept Bioquim & Biol Mol 1, E-28040 Madrid, Spain	Rodriguez, R (reprint author), Univ Complutense, Fac Quim, Dept Bioquim & Biol Mol 1, Avda Complutense S-N, E-28040 Madrid, Spain.		Huecas, Sonia/K-1754-2014; Villalba, Mayte/K-5365-2014; RODRIGUEZ, ROSALIA/K-4993-2014	Huecas, Sonia/0000-0002-6419-441X; RODRIGUEZ, ROSALIA/0000-0002-4280-3691			ALTSCHUL SF, 1990, J MOL BIOL, V215, P403, DOI 10.1006/jmbi.1990.9999; Arruda LK, 1997, J BIOL CHEM, V272, P20907, DOI 10.1074/jbc.272.33.20907; BALDO BA, 1992, MOL IMMUNOL, V29, P1209, DOI 10.1016/0161-5890(92)90057-5; BATANERO E, 1994, MOL IMMUNOL, V31, P31, DOI 10.1016/0161-5890(94)90135-X; Batanero E, 1997, FEBS LETT, V410, P293, DOI 10.1016/S0014-5793(97)00582-6; Batanero E, 1996, EUR J BIOCHEM, V241, P772, DOI 10.1111/j.1432-1033.1996.00772.x; BLANCA M, 1983, CLIN ALLERGY, V13, P473, DOI 10.1111/j.1365-2222.1983.tb02624.x; Boluda L, 1998, J ALLERGY CLIN IMMUN, V101, P210; BOUSQUET J, 1984, CLIN ALLERGY, V14, P249, DOI 10.1111/j.1365-2222.1984.tb02204.x; Brehler R, 1997, ALLERGY, V52, P404, DOI 10.1111/j.1398-9995.1997.tb01019.x; BREITENEDER H, 1989, EMBO J, V8, P1935; BUCCIAGLIA PA, 1994, PLANT MOL BIOL, V24, P903, DOI 10.1007/BF00014444; CHEN L, 1993, J BIOL CHEM, V268, P13318; CHEN L, 1995, J BIOL CHEM, V270, P8093; CHUA KY, 1988, J EXP MED, V167, P175, DOI 10.1084/jem.167.1.175; CHYE ML, 1995, PLANT MOL BIOL, V29, P397, DOI 10.1007/BF00043663; CruzOrtega R, 1997, PLANT PHYSIOL, V114, P1453, DOI 10.1104/pp.114.4.1453; DELCAMPILLO E, 1992, PLANT PHYSIOL, V99, P1015, DOI 10.1104/pp.99.3.1015; Delp G, 1999, PLANT MOL BIOL, V39, P565, DOI 10.1023/A:1006194822666; DUDLER T, 1995, J IMMUNOL, V155, P2605; Futamura N, 2000, PLANT CELL PHYSIOL, V41, P16; Garnier J, 1996, METHOD ENZYMOL, V266, P540; Gough L, 1999, J EXP MED, V190, P1897, DOI 10.1084/jem.190.12.1897; HIRD DL, 1993, PLANT J, V4, P1023, DOI 10.1046/j.1365-313X.1993.04061023.x; Hoffmann-Sommergruber K, 2000, INT ARCH ALLERGY IMM, V122, P155, DOI 10.1159/000024392; HOJ PB, 1995, PLANT J, V7, P367, DOI 10.1046/j.1365-313X.1995.7030367.x; Huecas S, 1999, EUR J BIOCHEM, V261, P539, DOI 10.1046/j.1432-1327.1999.00307.x; Juers DH, 1999, PROTEIN SCI, V8, P122; KING TP, 1978, BIOCHEMISTRY-US, V17, P5165, DOI 10.1021/bi00617a016; KING TP, 1995, J ALLERGY CLIN IMMUN, V96, P5, DOI 10.1016/S0091-6749(95)70027-7; LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0; LAUZURICA P, 1988, MOL IMMUNOL, V25, P329, DOI 10.1016/0161-5890(88)90027-2; Ledesma A, 1998, ALLERGY, V53, P520, DOI 10.1111/j.1398-9995.1998.tb04090.x; Ledesma A, 2000, FEBS LETT, V466, P192, DOI 10.1016/S0014-5793(99)01790-1; Leubner-Metzger G, 1999, PATHOGENESIS-RELATED PROTEINS IN PLANTS, P49; LOTAN T, 1989, PLANT CELL, V1, P881; LOWRY OH, 1951, J BIOL CHEM, V193, P265; Macchia L, 1991, ALLERGENIC POLLEN PO, P87; Meins F. 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Biol. Chem.	JUL 27	2001	276	30					27959	27966		10.1074/jbc.M103041200		8	Biochemistry & Molecular Biology	Biochemistry & Molecular Biology	456QH	WOS:000170093400030	11373288	
J	Piirila, P; Wikman, H; Luukkonen, R; Kaaria, K; Rosenberg, C; Nordman, H; Norppa, H; Vainio, H; Hirvonen, A				Piirila, P; Wikman, H; Luukkonen, R; Kaaria, K; Rosenberg, C; Nordman, H; Norppa, H; Vainio, H; Hirvonen, A			Glutathione S-transferase genotypes and allergic responses to diisocyanate exposure	PHARMACOGENETICS			English	Article						allergic responses; diisocyanates; individual susceptibility; GSTs; occupational asthma; specific IgE	OCCUPATIONAL ASTHMA; TOLUENE-DIISOCYANATE; METHYL ISOCYANATE; IGE ANTIBODIES; POLYMORPHISM; ASSOCIATION; SUSCEPTIBILITY; WORKERS; LOCUS; ALLELES	Diisocyanates are the most common low molecular weight chemicals to cause occupational asthma, However, only some 5-10% of exposed workers develop asthma, which suggests an underlying genetic susceptibility, Diisocyanates and their metabolites may be conjugated with glutathione by glutathione S-transferases (GSTs). We examined whether polymorphisms in the GSTM1, GSTM3, GSTP1 and GSTT1 genes modify allergic responses to diisocyanate exposure. The study population consisted of 182 diisocyanate exposed workers, 109 diagnosed with diisocyanate-induce asthma and 73 without asthma, Lack of the GSTM1 gene (null genotype) was associated with a 1.89-fold risk of diisocyanate-induced asthma [95% confidence interval (CI) 1.01-3.52]. Moreover, among the asthma patients, the GSTM1 null genotype was associated with lack of diisocyanate-specific immunoglobulin (Ig)E antibodies [odds ratio (OR) 0.18, 95% CI 0.05-0.61] and with late reaction in the specific bronchial provocation test (OR 2.82, 95% CI 1.15-6.88). Similarly, GSTM3 AA genotype was related to late reaction in the specific bronchial provocation test (OR 3.75, 95% CI 1.26-11.2), The GSTP1 Val/Val genotype, on the other hand, was related to high total IgE levels (OR 5.46, 95% CI 1.15-26.0). The most remarkable effect was seen for the combination of GSTM1 null anti. the GSTM3 AA genotype which was strongly associated with lack of diisocyanate-specific IgE antibodies (OR 0.09, 35% CI 0.01-0.73) and with late reaction in the bronchial provocation test (OR 11.0, 95% CI 2.19-55.3). The results suggest, for the first time, that the polymorphic GSTs, especially the mu class GSTs, play an important role in inception of ill effects related to occupational exposure to diisocyanates. Pharmacogenetics 11:437-445 (C) 2001 Lippincott Williams & Wilkins.	Finnish Inst Occupat Hlth, Dept Ind Hyg & Toxicol, FIN-00250 Helsinki, Finland; Finnish Inst Occupat Hlth, Dept Occupat Med, FIN-00250 Helsinki, Finland; Finnish Inst Occupat Hlth, Dept Epidemiol, FIN-00250 Helsinki, Finland; Int Agcy Res Canc, F-69372 Lyon, France; Univ Helsinki Hosp, Lab Clin Physiol, Helsinki, Finland	Hirvonen, A (reprint author), Finnish Inst Occupat Hlth, Dept Ind Hyg & Toxicol, Topeltuksenkatu 41 AA, FIN-00250 Helsinki, Finland.			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J	Bush, RK; Portnoy, JM				Bush, RK; Portnoy, JM			The role and abatement of fungal allergens in allergic diseases	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						fungi; allergic disease; asthma; environment; exposure; abatement	NUTRITION EXAMINATION SURVEY; MAJOR ALTERNARIA ALLERGEN; SICK BUILDING SYNDROME; 2ND NATIONAL-HEALTH; SCHOOL-AGE-CHILDREN; DUST MITE; INDOOR AIR; RESIDENTIAL CHARACTERISTICS; ENVIRONMENTAL-FACTORS; RESPIRATORY SYMPTOMS	Sensitivity to a variety of fungi is known to be a factor in allergic rhinitis and asthma. In this review methods for measuring exposure to fungi in the indoor environment are evaluated. A variety of markers for the presence of fungi are also described in addition to their known relationship to either toxic or adverse immunologic effects. Key studies documenting the clinical effects of different types of fungi are also reviewed, as well as a description of abatement methods that either have been successful or need further investigation. Although many studies have shown an association between exposure to fungi and allergic disease, in many cases a direct cause-and-effect relationship has not been established. Improved knowledge of the epidemiology and mechanisms behind fungal-induced human disease will hopefully establish this causal link and suggest methods for reducing morbidity.	Univ Wisconsin, William S Middleton Mem Vet Adm Hosp, Dept Med, Madison, WI 53705 USA; Childrens Mercy Hosp, Sect Allergy Immunol, Kansas City, MO 64108 USA	Bush, RK (reprint author), Univ Wisconsin, William S Middleton Mem Vet Adm Hosp, Dept Med, 2500 OVerlook Terrace, Madison, WI 53705 USA.						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E., 1995, CLIN MICROBIOL REV, V8, P161; KAUFFMAN HF, 1995, AM J RESP CRIT CARE, V151, P2109; Kenny LC, 1999, ANN OCCUP HYG, V43, P393; LEHRER SB, 1994, ALLERGY, V49, P460, DOI 10.1111/j.1398-9995.1994.tb00840.x; Levetin E., 1995, Aerobiologia, V11, P27, DOI 10.1007/BF02136141; LEVETIN E, 1995, BIOAEROSOLS, P108; Li CS, 1997, ARCH ENVIRON HEALTH, V52, P72; Li DW, 1995, MYCOPATHOLOGIA, V131, P149, DOI 10.1007/BF01102894; LOPEZ M, 1985, CLIN REV ALLERG, V3, P183, DOI 10.1007/BF02992982; MALONEY MJ, 1987, ANN ALLERGY, V59, P192; McGrath JJ, 1999, CURR MICROBIOL, V38, P33, DOI 10.1007/PL00006768; Miller JD, 1997, AM IND HYG ASSOC J, V58, P39; Nelson RP, 1996, J ALLERGY CLIN IMMUN, V98, P258, DOI 10.1016/S0091-6749(96)70148-3; OHOLLAREN MT, 1991, NEW ENGL J MED, V324, P359, DOI 10.1056/NEJM199102073240602; PARIS S, 1991, J ALLERGY CLIN IMMUN, V88, P902, DOI 10.1016/0091-6749(91)90247-L; PEAT JK, 1993, CLIN EXP ALLERGY, V23, P812, DOI 10.1111/j.1365-2222.1993.tb00258.x; Perzanowski MS, 1998, J ALLERGY CLIN IMMUN, V101, P626; Pieckova E, 1999, ANN AGR ENV MED, V6, P1; Pirhonen I, 1996, EUR RESPIR J, V9, P2618, DOI 10.1183/09031936.96.09122618; Platts-Mills T A, 1986, Allerg Immunol (Paris), V18, P17; PLATTSMILLS TAE, 1986, J ALLERGY CLIN IMMUN, V77, P850, DOI 10.1016/0091-6749(86)90383-0; PLATTSMILLS TAE, 1982, LANCET, V2, P675; PLATTSMILLS TAE, 1983, MONOGR ALLERGY, V18, P153; PLATTSMILLS TAE, 1990, TOXICOL IND HEALTH, V6, P197; PLATTSMILLS TAE, 1987, J ALLERGY CLIN IMMUN, V79, P781, DOI 10.1016/0091-6749(87)90211-9; PORTNOY J, 1990, ANN ALLERGY, V65, P109; PORTNOY J, 1993, J ALLERGY CLIN IMMUN, V91, P773, DOI 10.1016/0091-6749(93)90197-N; Portnoy J, 1998, ANN ALLERG ASTHMA IM, V81, P59; PRAHL P, 1992, ALLERGY, V47, P362, DOI 10.1111/j.1398-9995.1992.tb02072.x; Rao CY, 1996, J AIR WASTE MANAGE, V46, P899; REISMAN RE, 1990, J ALLERGY CLIN IMMUN, V85, P1050, DOI 10.1016/0091-6749(90)90050-E; Rosas I, 1998, ALLERGY, V53, P394, DOI 10.1111/j.1398-9995.1998.tb03911.x; Rylander R, 1999, ENVIRON HEALTH PERSP, V107, P501; SALVAGGIO J, 1971, J ALLERGY CLIN IMMUN, V48, P96, DOI 10.1016/0091-6749(71)90091-1; SAMSON RA, 1992, J MED VET MYCOL, V30, P9; Shen HD, 1998, INT ARCH ALLERGY IMM, V116, P29, DOI 10.1159/000023921; Shen HD, 1997, CLIN EXP ALLERGY, V27, P682, DOI 10.1046/j.1365-2222.1997.d01-546.x; SMEDJE G, 1996, 7 INT C IND AIR QUAL, P611; SOLOMON WR, 1980, J ALLERGY CLIN IMMUN, V65, P305, DOI 10.1016/0091-6749(80)90160-8; SOLOMON WR, 1976, J ALLERGY CLIN IMMUN, V57, P46, DOI 10.1016/0091-6749(76)90078-6; SOLOMON WR, 1980, J ALLERGY CLIN IMMUN, V65, P229; Solomon W, 1998, ALLERGY PRINCIPLES P, P367; Takahashi T, 1997, MYCOPATHOLOGIA, V139, P23, DOI 10.1023/A:1006831111595; TARGONSKI PV, 1995, J ALLERGY CLIN IMMUN, V95, P955, DOI 10.1016/S0091-6749(95)70095-1; Tariq SM, 1996, CLIN EXP ALLERGY, V26, P794; vanderHeide S, 1997, EUR RESPIR J, V10, P1217, DOI 10.1183/09031936.97.10061217; VERHOEFF AP, 1990, ALLERGY, V45, P275, DOI 10.1111/j.1398-9995.1990.tb00496.x; Verhoeff AP, 1997, ANN ALLERG ASTHMA IM, V78, P544; Vijay HM, 1999, ALLERGENS ALLERGEN I, P133; YUNGINGER JW, 1976, J ALLERGY CLIN IMMUN, V57, P293, DOI 10.1016/0091-6749(76)90085-3	94	78	81	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.	MAR	2001	107	3		S			S430	S440				11	Allergy; Immunology	Allergy; Immunology	418KR	WOS:000167891800005	11242604	
J	Grootendorst, DC; Dahlen, SE; Van den Bos, JW; Duiverman, EJ; Veselic-Charvat, M; Vrijlandt, EJLE; O'Sullivan, S; Kumlin, M; Sterk, PJ; Roldaan, AC				Grootendorst, DC; Dahlen, SE; Van den Bos, JW; Duiverman, EJ; Veselic-Charvat, M; Vrijlandt, EJLE; O'Sullivan, S; Kumlin, M; Sterk, PJ; Roldaan, AC			Benefits of high altitude allergen avoidance in atopic adolescents with moderate to severe asthma, over and above treatment with high dose inhaled steroids	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergen avoidance; house dust mite; severe asthma; induced sputum; high altitude; urine; EPX; LTE4; 9 alpha 11 beta-PGF(2)	BRONCHIAL HYPERRESPONSIVENESS; CLINICAL SEVERITY; DUST MITES; CHILDREN; INFLAMMATION; GLUCOCORTICOIDS; MANAGEMENT; EXCRETION; PROTEIN	Background Some patients with severe asthma cannot be controlled with high doses of inhaled steroids (ICS), which may be related to ongoing environmental allergen exposure. Objective We investigated whether 10 weeks of high altitude allergen avoidance leads to sustained benefits regarding clinical and inflammatory markers of disease control in adolescents with persistent asthma despite treatment with high dose ICS. Methods Eighteen atopic asthmatic adolescents (12-18 yr, 500-2000 mug ICS daily) with established house dust mite allergy, participated in a parallel-group study. Quality of life (PAQL), lung function, bronchial hyperresponsiveness (BHR) to adenosine and histamine, induced sputum and urine samples were collected repeatedly from 10 patients during a 10-week admission period to the Swiss Alps (alt. 1560 m) and at 6 weeks after return to sea level. Results were compared with those in eight patients, studied in their home environment at sea level for a similar time period. Throughout the study, asthma medication remained unchanged in both groups. Results During admission to high altitude, PAQL, lung function, BHR to adenosine and histamine, and urinary levels of eosinophil protein X (U-EPX), leukotriene E-4 (U-LTE4) and 9 alpha 11 beta prostaglandin F-2 (U-9 alpha 11 beta PGF(2)) improved significantly (P < 0.05), with a similar tendency for sputum eosinophils (P < 0.07). Furthermore, the changes in PAQL and BHR to adenosine and histamine were greater in the altitude than in the control group (P < 0.05). At 6 weeks after renewed allergen exposure at sea level, the improvements in PAQL (P < 0.05), BHR to adenosine (P < 0.07) and histamine (P < 0.05), as well as U-EPX (P < 0.05) and U-LTE4 (P < 0.05) were maintained. Conclusion A short period of high altitude allergen avoidance, on top of regular treatment with ICS and long-acting beta (2)-agonists, results in improvement of asthma, as assessed by clinical and inflammatory markers of disease severity. These findings indicate that short-term, rigorous allergen avoidance can improve the long-term control of severe asthma over and above what can be achieved even by high doses of inhaled steroids.	Leiden Univ, Med Ctr, Dept Pulmonol, Lung Funct Lab C2P, NL-2300 RC Leiden, Netherlands; Dutch Asthma Ctr, Davos, Switzerland; Karolinska Inst, Natl Inst Environm Med, Stockholm, Sweden; Juliana Childrens Hosp, The Hague, Netherlands; Leiden Univ, Med Ctr, Dept Pathol, Leiden, Netherlands; Med Spectrum Twente Hosp, Enschede, Netherlands; Leijenburg Hosp, Dept Pulmonol, The Hague, Netherlands	Grootendorst, DC (reprint author), Leiden Univ, Med Ctr, Dept Pulmonol, Lung Funct Lab C2P, POB 9600, NL-2300 RC Leiden, Netherlands.						Barnes PJ, 1998, EUR RESPIR J, V12, P221, DOI 10.1183/09031936.98.12010221; Barnes PJ, 1996, RESP MED, V90, P379, DOI 10.1016/S0954-6111(96)90108-0; BONER AL, 1985, ANN ALLERGY, V54, P42; British Thoracic Society, 1997, THORAX S1, V52, pS1, DOI DOI 10.1136/THX.52.2008.S1]; Cockcroft DW, 1996, J ALLERGY CLIN IMMUN, V98, P1016, DOI 10.1016/S0091-6749(96)80185-0; Custovic A, 1998, THORAX, V53, P63; Custovic A, 1996, J ALLERGY CLIN IMMUN, V98, P64, DOI 10.1016/S0091-6749(96)70227-0; Gotzsche PC, 1998, BRIT MED J, V317, P1105; Grootendorst DC, 1999, EUR RESPIR J, V13, P647, DOI 10.1183/09031936.99.13364799; GUYATT GH, 1989, J CLIN EPIDEMIOL, V42, P913, DOI 10.1016/0895-4356(89)90105-4; Holgate ST, 1997, LANCET, V350, P5; In 'T Veen J. C. C. M., 1996, European Respiratory Journal, V9, P2441, DOI 10.1183/09031936.96.09122441; Juniper EF, 1996, QUAL LIFE RES, V5, P35, DOI 10.1007/BF00435967; KUMLIN M, 1995, CLIN EXP ALLERGY, V25, P467, DOI 10.1111/j.1365-2222.1995.tb01079.x; Lugosi E, 1997, ALLERGY, V52, P584, DOI 10.1111/j.1398-9995.1997.tb02605.x; National Heart Lung and Blood Institute National Asthma Education Program, 1997, NIH PUBL; OSHAUGHNESSY KM, 1993, AM REV RESPIR DIS, V147, P1472; OSullivan S, 1996, J ALLERGY CLIN IMMUN, V98, P421, DOI 10.1016/S0091-6749(96)70167-7; PERONI DG, 1994, AM J RESP CRIT CARE, V149, P1442; Piacentini GL, 1996, J ALLERGY CLIN IMMUN, V97, P1079, DOI 10.1016/S0091-6749(96)70261-0; QUANJER PH, 1995, PEDIATR PULM, V19, P135, DOI 10.1002/ppul.1950190209; Quanjer PH, 1993, EUR RESPIR J, V6, P16; Sont JK, 1996, THORAX, V51, P496, DOI 10.1136/thx.51.5.496; Sont JK, 1999, AM J RESP CRIT CARE, V159, P1043; Squillace SP, 1997, AM J RESP CRIT CARE, V156, P1760; STERK PJ, 1993, EUR RESPIR J, V6, P53, DOI 10.1183/09041950.053s1693; VALLETTA EA, 1995, ALLERGY, V50, P366, DOI 10.1111/j.1398-9995.1995.tb01162.x; vanVelzen E, 1996, THORAX, V51, P582, DOI 10.1136/thx.51.6.582; Verberne AAPH, 1997, AM J RESP CRIT CARE, V156, P688; VERVLOET D, 1982, J ALLERGY CLIN IMMUN, V69, P290, DOI 10.1016/S0091-6749(82)80006-7; Wenzel SE, 1997, AM J RESP CRIT CARE, V156, P737; Wisniewski AF, 1997, THORAX, V52, P853	32	78	80	0	2	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					400	408		10.1046/j.1365-2222.2001.01022.x		9	Allergy; Immunology	Allergy; Immunology	417UB	WOS:000167851600010	11260151	
J	Diette, GB; Skinner, EA; Markson, LE; Algatt-Bergstrom, P; Nguyen, TTH; Clark, RD; Wu, AW				Diette, GB; Skinner, EA; Markson, LE; Algatt-Bergstrom, P; Nguyen, TTH; Clark, RD; Wu, AW			Consistency of care with national guidelines for children with asthma in managed care	JOURNAL OF PEDIATRICS			English	Article							BETA-AGONISTS; QUALITY; THERAPY	Objective: To evaluate the consistency of pediatric asthma care with the National Asthma Education and Prevention Program Guidelines. Design: Cross-sectional survey at 2 managed care organizations in the United States (winter 1997-1998). The participants were parents of children (n = 318) age 5 to 17 years with asthma. There were no interventions. The outcome measures were indicators of care in 4 domains: (1) periodic physiologic assessment, (2) proper use of medications, (3) patient education, and (4) control of factors contributing to asthma severity. Results: Of 533 eligible patients with asthma, 318 (60%) parents responded; 59% of children were male, 76% were white, and 60% were aged 5 to 10 years. Deficiencies in care were identified in all care domains including, for patients with moderate and severe persistent symptoms, only 55% used long-term control medication daily, 49% had written instructions for handling asthma attacks, 44% had instructions for adjustment of medication before exposures, 56% had undergone allergy testing, and 54% had undergone pulmonary function testing. Conclusions: There are significant opportunities to improve the quality of care for children with asthma enrolled in managed care. A comprehensive approach to improving care may be necessary to address multiple aspects of care where opportunities exist.	Johns Hopkins Univ, Sch Med, Div Pulm & Crit Care Med, Baltimore, MD 21205 USA; Johns Hopkins Univ, Sch Med, Div Gen Med, Baltimore, MD 21205 USA; Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21205 USA; Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA; Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Hlth Policy & Management, Baltimore, MD 21205 USA; Merck & Co Inc, W Point, PA USA	Diette, GB (reprint author), Johns Hopkins Univ, Sch Med, Div Pulm & Crit Care Med, 1830 E Monument St,Room 301, Baltimore, MD 21205 USA.						Adams P., 1995, VITAL HLTH STAT, V10, P94; ALGATTBERGSTROM P, MINN J MANAGED CARE, V5, P192; Diette GB, 1999, ARCH INTERN MED, V159, P2697, DOI 10.1001/archinte.159.22.2697; Eggleston PA, 1998, PEDIATRICS, V101, P349, DOI 10.1542/peds.101.3.349; FINKELSTEIN JA, 1995, PEDIATRICS, V95, P389; Friday GA, 1997, ANN ALLERG ASTHMA IM, V78, P221; Hartert TV, 1996, AM J MED, V100, P386, DOI 10.1016/S0002-9343(97)89513-7; Homer CJ, 1996, PEDIATRICS, V98, P18; Legorreta AP, 1998, ARCH INTERN MED, V158, P457, DOI 10.1001/archinte.158.5.457; Mannino DM, 1998, MMWR-MORBID MORTAL W, V47, P1; National Heart Lung and Blood Institute National Asthma Education Program, 1997, NIH PUBL; Nestor A, 1998, ANN ALLERG ASTHMA IM, V81, P327; Pearson MG, 1996, RESP MED, V90, P539, DOI 10.1016/S0954-6111(96)90146-8; SPEIZER FE, 1968, BRIT MED J, V1, P339; SPITZER WO, 1992, NEW ENGL J MED, V326, P501, DOI 10.1056/NEJM199202203260801; STARFIELD B, 1993, PEDIATRICS, V91, P435; STEINWACHS DM, 1996, OUTCOMES MANAGEMENT; WARE JE, 1997, DIS MAN C JUN 18 NEW; Wu AW, 1999, AM J RESP CRIT CARE, V159, pA911; 1995, 12 ANN M ASS HLTH SE, P136	20	78	79	1	1	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0022-3476	1097-6833		J PEDIATR-US	J. Pediatr.	JAN	2001	138	1					59	64		10.1067/mpd.2001.109600		6	Pediatrics	Pediatrics	393PK	WOS:000166478700011	11148513	
J	Emanuel, IA; Shah, SB				Emanuel, IA; Shah, SB			Chronic rhinosinusitis: Allergy and sinus computed tomography relationships	OTOLARYNGOLOGY-HEAD AND NECK SURGERY			English	Article; Proceedings Paper	Annual Meeting of the American-Academy-of-Otolaryngology-Head-and-Neck-Surgery	SEP 26-29, 1999	NEW ORLEANS, LOUISIANA	Amer Acad Otolaryngol Head & Neck Surg			MANAGEMENT	The management of chronic or recurrent rhinosinusitis problems is multifaceted and should include consideration of contributory and potentially correctable medical and anatomic factors. To date, the relationship between allergy and rhinosinusitis has not been clearly defined. The purpose of this study is to improve understanding of the relative roles of perennial and seasonal allergens in the cause of chronic rhinosinusitis. A retrospective review of 200 consecutive patients was carried out on patients who had chronic rhinosinusitis refractory to medical therapy and who subsequently underwent functional endoscopic sinus surgery. All of these patients had allergy testing for common perennial and seasonal inhalant allergens before surgery. Each patient had sinus CT imaging before undergoing the surgery. The CT scans of each patient were staged according to a validated, standardized grading system by investigators blinded to allergic profile. Allergy testing indicated that 84% of all patients tested positive for allergies. Moreover, 60% of all patients had significant allergic sensitivity; 52% of all patients had multiple allergen sensitivities. Furthermore, there was a predominance of perennial allergens, especially house dust mite over seasonal allergens. The vast majority of our patients undergoing functional endoscopic sinus surgery had concomitant allergy. This study highlights the potential contribution of perennial allergies to the development of rhinosinusitis, Given this direction, future studies may reveal that in the care of patients with perennial allergic rhinitis, early intervention with identification of the offending allergen(s), and subsequent treatment through avoidance, pharmacotherapy, and/or immunotherapy may help in the prevention of recurrent and chronic rhinosinusitis.	Univ Calif San Francisco, San Francisco, CA 94143 USA	Emanuel, IA (reprint author), 490 Post St,1230, San Francisco, CA 94102 USA.						Benninger MS, 1997, OTOLARYNG HEAD NECK, V117, pS41, DOI 10.1016/S0194-5998(97)70006-8; BENNINGER MS, 1992, AM J RHINOL, V6, P37, DOI 10.2500/105065892781874829; CALHOUN K, 1992, OTOLARYNG HEAD NECK, V107, P850; GLICKLICH RE, 1994, AM J RHINOL, V2, P291; SHAPIRO GG, 1985, PEDIATR INFECT DIS J, V4, pS55, DOI 10.1097/00006454-198511001-00003; SLAVIN R, 1985, J ALLERGY CLIN IMMUN, V82, P950	6	78	84	2	2	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0194-5998			OTOLARYNG HEAD NECK	Otolaryngol. Head Neck Surg.	DEC	2000	123	6					687	691		10.1067/mhn.2000.110961		5	Otorhinolaryngology; Surgery	Otorhinolaryngology; Surgery	381PQ	WOS:000165772400004	11112958	
J	Tomaki, M; Zhao, LL; Lundahl, J; Sjostrand, M; Jordana, M; Linden, A; O'Byrne, P; Lotvall, J				Tomaki, M; Zhao, LL; Lundahl, J; Sjostrand, M; Jordana, M; Linden, A; O'Byrne, P; Lotvall, J			Eosinophilopoiesis in a murine model of allergic airway eosinophilia: Involvement of bone marrow IL-5 and IL-5 receptor alpha	JOURNAL OF IMMUNOLOGY			English	Article							MESSENGER-RNA; IN-VIVO; INTERLEUKIN-5 EXPRESSION; CIRCULATING EOSINOPHILS; PULMONARY INFLAMMATION; BRONCHIAL BIOPSIES; MILD ASTHMA; LUNG DAMAGE; MAST-CELLS; T-CELLS	The airway inflammation in asthma is dominated by eosinophils. The aim of this study was to elucidate the contribution of newly produced eosinophils in airway allergic inflammation and to determine mechanisms of any enhanced eosinophilopoiesis, OVA-sensitized BALB/c mice were repeatedly exposed to allergen via airway route. Newly produced cells were identified using a thymidine analog, 5-bromo-2'-deoxyuridine, which is incorporated into DNA during mitosis. Identification of IL-5-producing cells in the bone marrow was performed using FAGS. Bone marrow CD3(+) cells were enriched to evaluate IL-5-protein release in vitro. Anti-ILS-treatment (TRFK-5) was given either systemically or directly to the airways. IL-SR-bearing cells were localized by immunocytochemistry. Repeated airway allergen exposure caused prominent airway eosinophilia after three to five exposures, and increased the number of immature eosinophils in the bone marrow. Up to 78% of bronchoalveolar lavage (BAL) granulocytes were 5-bromo-2'-deoxyuridine positive. After three allergen exposures, both CD3+ and non-CD3 cells acquired from the bone marrow expressed and released IL-5-protein. Anti-IL-5 given i.p. inhibited both bone marrow and airway eosinophilia. Intranasal administration of anti-IL-5 also reduced BAL eosinophilia, partly via local effects in the airways. Bone marrow cells, but not BAL eosinophils, displayed stainable amounts of the IL-5R alpha-chain. We conclude that the bone marrow is activated by airway allergen exposure, and that newly produced eosinophils contribute to a substantial degree to the airway eosinophilia induced by allergen. Airway allergen exposure increases the number of cells expressing IL-5-protein in the bone marrow. The bone marrow, as well as the lung, are possible targets for anti-IL-5-treatment.	Gothenburg Univ, Inst Heart & Lung Dis, Dept Resp Med & Allergol, Lung Pharmacol Grp, S-41346 Gothenburg, Sweden; Karolinska Inst, Karolinska Hosp, Dept Clin Immunol, S-10401 Stockholm, Sweden; McMaster Univ, Dept Pathol & Mol Med, Hamilton, ON, Canada; McMaster Univ, Dept Med, Hamilton, ON, Canada	Lotvall, J (reprint author), Gothenburg Univ, Inst Heart & Lung Dis, Dept Resp Med & Allergol, Lung Pharmacol Grp, Guldhedsgatan 10A, S-41346 Gothenburg, Sweden.			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Immunol.	OCT 1	2000	165	7					4040	4050				11	Immunology	Immunology	357AZ	WOS:000089477500064	11034415	
J	Been, JV; Nurmatov, UB; Cox, B; Nawrot, TS; van Schayck, CP; Sheikh, A				Been, Jasper V.; Nurmatov, Ulugbek B.; Cox, Bianca; Nawrot, Tim S.; van Schayck, Constant P.; Sheikh, Aziz			Effect of smoke-free legislation on perinatal and child health: a systematic review and meta-analysis	LANCET			English	Article							ENVIRONMENTAL TOBACCO-SMOKE; PRETERM BIRTHS ANALYSIS; FREE AIR LAWS; SECONDHAND SMOKE; NONCOMMUNICABLE DISEASES; MATERNAL SMOKING; NONSMOKING YOUTH; PUBLIC PLACES; GLOBAL BURDEN; EXPOSURE	Background Smoke-free legislation has the potential to reduce the substantive disease burden associated with second-hand smoke exposure, particularly in children. We investigated the effect of smoke-free legislation on perinatal and child health. Methods We searched 14 online databases from January, 1975 to May, 2013, with no language restrictions, for published studies, and the WHO International Clinical Trials Registry Platform for unpublished studies. Citations and reference lists of articles of interest were screened and an international expert panel was contacted to identify additional studies. We included studies undertaken with designs approved by the Cochrane Effective Practice and Organisation of Care that reported associations between smoking bans in workplaces, public places, or both, and one or more predefined early-life health indicator. The primary outcomes were preterm birth, low birthweight, and hospital attendances for asthma. Effect estimates were pooled with random-effects meta-analysis. This study is registered with PROSPERO, number CRD42013003522. Findings We identified 11 eligible studies (published 2008-13), involving more than 2.5 million births and 247 168 asthma exacerbations. All studies used interrupted time-series designs. Five North American studies described local bans and six European studies described national bans. Risk of bias was high for one study, moderate for six studies, and low for four studies. Smoke-free legislation was associated with reductions in preterm birth (four studies, 1 366 862 individuals; -10.4% [95% CI -18.8 to -2.0]; p=0.016) and hospital attendances for asthma (three studies, 225 753 events: -10.1% [95% CI -15.2 to -5.0]; p=0.0001). No significant effect on low birthweight was identified (six studies, >1.9 million individuals: -1.7% [95% CI -5.1 to 1.6]; p=0.31). Interpretation Smoke-free legislation is associated with substantial reductions in preterm births and hospital attendance for asthma. Together with the health benefits in adults, this study provides strong support for WHO recommendations to create smoke-free environments.	[Been, Jasper V.; van Schayck, Constant P.; Sheikh, Aziz] Maastricht Univ, Sch Publ Hlth & Primary Care CAPHRI, NL-6202 AZ Maastricht, Netherlands; [Been, Jasper V.; Nurmatov, Ulugbek B.; van Schayck, Constant P.; Sheikh, Aziz] Univ Edinburgh, Allergy & Resp Res Grp, Ctr Populat Hlth Sci, Edinburgh, Midlothian, Scotland; [Been, Jasper V.] Maastricht Univ, Med Ctr, Dept Paediat, NL-6202 AZ Maastricht, Netherlands; [Cox, Bianca; Nawrot, Tim S.] Hasselt Univ, Ctr Environm Sci, Hasselt, Belgium; [Nawrot, Tim S.] Univ Louvain, Dept Publ Hlth, Louvain, Belgium; [Sheikh, Aziz] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Gen Internal Med & Primary Care, Boston, MA 02115 USA	Been, JV (reprint author), Maastricht Univ, Med Ctr, Dept Paediat, POB 5800, NL-6202 AZ Maastricht, Netherlands.	jasper.been@mumc.nl	Sheikh, Aziz /D-2818-2009; Cox, Bianca/A-9480-2015	Sheikh, Aziz /0000-0001-7022-3056; Cox, Bianca/0000-0001-9824-6276	Thrasher Fund; Lung Foundation Netherlands; International Paediatric Research Foundation; Maastricht University; Commonwealth Fund	Thrasher Fund, Lung Foundation Netherlands, International Paediatric Research Foundation, Maastricht University, Commonwealth Fund.	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J	Palmer, DJ; Metcalfe, J; Makrides, M; Gold, MS; Quinn, P; West, CE; Loh, R; Prescott, SL				Palmer, Debra J.; Metcalfe, Jessica; Makrides, Maria; Gold, Michael S.; Quinn, Patrick; West, Christina E.; Loh, Richard; Prescott, Susan L.			Early regular egg exposure in infants with eczema: A randomized controlled trial	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Allergy prevention; complementary feeding; eczema; egg; food allergy; oral tolerance; randomized controlled trial	ORAL IMMUNOTHERAPY; ALLERGIC DISEASES; ATOPIC-DERMATITIS; BIRTH COHORT; CHILDREN; FISH; SENSITIZATION; CHALLENGE; TOLERANCE; FORMULAS	Background: Observational studies suggest that early regular ingestion of allergenic foods might reduce the risk of food allergy. Objective: We sought to determine whether early regular oral egg exposure will reduce subsequent IgE-mediated egg allergy in infants with moderate-to-severe eczema. Methods: In a double-blind, randomized controlled trial infants were allocated to 1 teaspoon of pasteurized raw whole egg powder (n = 49) or rice powder (n = 37) daily from 4 to 8 months of age. Cooked egg was introduced to both groups after an observed feed at 8 months. The primary outcome was IgE-mediated egg allergy at 12 months, as defined based on the results of an observed pasteurized raw egg challenge and skin prick tests. Results: A high proportion (31% [15/49]) of infants randomized to receive egg had an allergic reaction to the egg powder and did not continue powder ingestion. At 4 months of age, before any known egg ingestion, 36% (24/67) of infants already had eggspecific IgE levels of greater than 0.35 kilounits of antibody (kUA)/L. At 12 months, a lower (but not significant) proportion of infants in the egg group (33%) were given a diagnosis of IgE-mediated egg allergy compared with the control group (51%; relative risk, 0.65; 95% CI, 0.38-1.11; P 5.11). Egg-specific IgG4 levels were significantly (P <.001) greater in the egg group at both 8 and 12 months. Conclusion: Induction of immune tolerance pathways and reduction in egg allergy incidence can be achieved by early regular oral egg exposure in infants with eczema. Caution needs to be taken when these high-risk infants are first exposed to egg because many have sensitization already by 4 months of age.	[Palmer, Debra J.; Metcalfe, Jessica; West, Christina E.; Prescott, Susan L.] Univ Western Australia, Sch Paediat & Child Hlth, Perth, WA 6009, Australia; [Palmer, Debra J.; Makrides, Maria] Womens & Childrens Hlth Res Inst, Adelaide, SA, Australia; [Makrides, Maria; Gold, Michael S.] Univ Adelaide, Sch Paediat & Reprod Hlth, Children Youth & Womens Hlth Serv, Adelaide, SA, Australia; [Quinn, Patrick] Children Youth & Womens Hlth Serv, Adelaide, SA, Australia; [West, Christina E.] Umea Univ, Dept Clin Sci, S-90187 Umea, Sweden; [Loh, Richard; Prescott, Susan L.] Princess Margaret Hosp, Dept Immunol, Perth, WA, Australia	Palmer, DJ (reprint author), Univ Western Australia M561, Sch Paediat & Child Hlth, 35 Stirling Highway, Crawley, WA 6009, Australia.	debbie.palmer@uwa.edu.au	Palmer, Debra /L-8554-2013; Makrides, Maria/B-6392-2014; Prescott, Susan/H-5665-2014	Makrides, Maria/0000-0003-3832-541X; 	Women's and Children's Hospital Foundation; Ilhan Food Allergy Foundation	Supported by a grant from the Women's and Children's Hospital Foundation and a grant from the Ilhan Food Allergy Foundation.	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Allergy Clin. Immunol.	AUG	2013	132	2					387	+		10.1016/j.jaci.2013.05.002		7	Allergy; Immunology	Allergy; Immunology	194KL	WOS:000322631700016	23810152	
J	Foegeding, EA; Davis, JP				Foegeding, E. Allen; Davis, Jack P.			Food protein functionality: A comprehensive approach	FOOD HYDROCOLLOIDS			English	Article						Protein; Protein functionality; Foams; Gels; Emulsions; Bioactivity; Allergenicity	EGG-WHITE PROTEIN; BOVINE BETA-LACTOGLOBULIN; PEANUT ARACHIS-HYPOGAEA; IGE-BINDING EPITOPES; AIR-WATER-INTERFACE; COWS MILK ALLERGY; COLD-SET GELS; WHEY-PROTEIN; ALPHA-LACTALBUMIN; BIOACTIVE PEPTIDES	Food protein functionality has classically been viewed from the perspective of how single molecules or protein ingredients function in solutions and form simple colloidal structures. Based on this approach, tests on protein solutions are used to produce values for solubility, thermal stability, gelation, emulsifying, foaming, fat binding and water binding to name a few. While this approach is beneficial in understanding the properties of specific proteins and ingredients, it is somewhat restricted in predicting performance in real foods where the complexities of ingredients and processing operations have a significant affect on the colloidal structures and therefore overall properties of the final food product. In addition, focusing on proteins as just biopolymers used to create food structures ignores the biological functions of proteins in the diet. These can be beneficial, as in providing amino acids for protein synthesis or bioactive peptides, or these can be detrimental, as in causing a food allergic response. This review will focus on integrating the colloidal/polymer and biological aspects of protein functionality. This will be done using foams and gels to illustrate colloidal/polymer aspects and bioactive peptides and allergenicity to demonstrate biological function. (C) 2011 Elsevier Ltd. All rights reserved.	[Foegeding, E. Allen; Davis, Jack P.] N Carolina State Univ, Dept Food Bioprocess & Nutr Sci, Raleigh, NC 27695 USA; [Davis, Jack P.] ARS, USDA, Market Qual & Handling Res Unit, Raleigh, NC USA	Foegeding, EA (reprint author), N Carolina State Univ, Dept Food Bioprocess & Nutr Sci, 236 Schaub Hall,Campus Box 7624, Raleigh, NC 27695 USA.	allen_foegeding@ncsu.edu			North Carolina Agricultural Research Service; Dairy Management Inc.	"Paper No. FSR-10-36 of the Journal Series of the Department of Food, Bioprocessing and Nutrition Science, North Carolina State University, Raleigh, NC 27695-7624. Support from the North Carolina Agricultural Research Service and Dairy Management Inc. as administered by the Dairy Research Institute are gratefully acknowledged. The authors would like to thank Ms. Paige Luck for the technical assistance in preparing the manuscript. The use of trade names in this publication does not imply endorsement by the North Carolina Agricultural Research Service of the products named nor criticism of similar ones not mentioned.	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J	Ege, MJ; Strachan, DP; Cookson, WOCM; Moffatt, MF; Gut, I; Lathrop, M; Kabesch, M; Genuneit, J; Buchele, G; Sozanska, B; Boznanski, A; Cullinan, P; Horak, E; Bieli, C; Braun-Fahrlander, C; Heederik, D; von Mutius, E				Ege, Markus J.; Strachan, David P.; Cookson, William O. C. M.; Moffatt, Miriam F.; Gut, Ivo; Lathrop, Mark; Kabesch, Michael; Genuneit, Jon; Buechele, Gisela; Sozanska, Barbara; Boznanski, Andrzej; Cullinan, Paul; Horak, Elisabeth; Bieli, Christian; Braun-Fahrlaender, Charlotte; Heederik, Dick; von Mutius, Erika		GABRIELA Study Grp	Gene-environment interaction for childhood asthma and exposure to farming in Central Europe	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Childhood asthma; atopy; GWAS; gene-by-environment interaction; candidate genes	GENOMEWIDE ASSOCIATION; GLUTAMATE; DISEASES; CHILDREN	Background: Asthma is a disease in which both genetic and environmental factors play important roles. The farming environment has consistently been associated with protection from childhood asthma and atopy, and interactions have been reported with polymorphisms in innate immunity genes. Objective: To detect gene-environment interactions for asthma and atopy in the farming environment. Methods: We performed a genome-wide interaction analysis for asthma and atopy by using 500,000 genotyped single nucleotide polymorphisms (SNPs) and farm-related exposures in 1708 children from 4 rural regions of Central Europe. We also tested selectively for interactions between farm exposures and 7 SNPs that emerged as genome-wide significant in a large meta-analysis of childhood asthma and 5 SNPs that had been reported previously as interacting with farm exposures for asthma or atopy. Results: Neither the asthma-associated SNPs nor the SNPs previously published for interactions with asthma showed significant interactions. The genome-wide interaction study did not reveal any significant interactions with SNPs within genes in the range of interacting allele frequencies from 30% to 70%, for which our study was well powered. Among rarer SNPs, we identified 15 genes with strong interactions for asthma or atopy in relation to farming, contact with cows and straw, or consumption of raw farm milk. Conclusion: Common genetic polymorphisms are unlikely to moderate the protective influence of the farming environment on childhood asthma and atopy, but rarer variants, particularly of the glutamate receptor, metabotropic 1 gene, may do so. Given the limited statistical power of our study, these findings should be interpreted with caution before being replicated in independent farm populations. (J Allergy Clin Immunol 2011;127:138-44.)	[Ege, Markus J.; von Mutius, Erika] Univ Childrens Hosp Munich, Munich, Germany; [Strachan, David P.] Univ London, Div Community Hlth Sci, London, England; [Cookson, William O. C. M.; Moffatt, Miriam F.; Cullinan, Paul] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London, England; [Gut, Ivo; Lathrop, Mark] Ctr Natl Genotypage, Inst Genom, Evry, France; [Lathrop, Mark] Fdn Jean Dausset CEPH, Paris, France; [Kabesch, Michael] Hannover Med Sch, Clin Pediat Pneumol & Neonatol, D-3000 Hannover, Germany; [Genuneit, Jon; Buechele, Gisela] Univ Ulm, Inst Epidemiol, Ulm, Germany; [Sozanska, Barbara; Boznanski, Andrzej] Wroclaw Med Univ, Dept Paediat Allergol & Cardiol 1, Wroclaw, Poland; [Horak, Elisabeth] Innsbruck Med Univ, Div Cardiol & Pulmonol, Dept Pediat & Adolescents, Innsbruck, Austria; [Bieli, Christian; Braun-Fahrlaender, Charlotte] Swiss Trop & Publ Hlth Inst, Basel, Switzerland; [Bieli, Christian; Braun-Fahrlaender, Charlotte] Univ Basel, Basel, Switzerland; [Heederik, Dick] Univ Utrecht, Inst Risk Assessment Sci, Div Environm Epidemiol, Utrecht, Netherlands	Ege, MJ (reprint author), Dr von Haunersche Kinderklin, Lindwurmstr 4, D-80337 Munich, Germany.	markus.ege@med.uni-muenchen.de	Loss, Georg/F-1557-2013; Genuneit, Jon/I-9323-2012	Genuneit, Jon/0000-0001-5764-1528; Ege, Markus/0000-0001-6643-3923; von Mutius, Erika/0000-0002-8893-4515	European Commission [018996, LSH-2004-1.2.5-1]; GABRIEL consortium; German Research Foundation (DFG); Behring-Rontgen Foundation; Wellcome Trust; Roxall; Glaxo Wellcome; Novartis; Sanofi-Aventis; MSD; Bundesministerium fur Bildung und Forschung; Airsonett; Kuhne Foundation; European Union	Supported by the European Commission as part of GABRIEL (a multidisciplinary study to identify the genetic and environmental causes of asthma in the European Community) contract number 018996 under the Integrated Program LSH-2004-1.2.5-1. M.J.E received the Stephan-Weiland Fellowship of the GABRIEL consortium.; M. J. Ege has received research support from the European Union, the German Research Foundation (DFG), and the Behring-Rontgen Foundation. I. Gut has received research support from the European Commission (through Project GABRIEL) and the Wellcome Trust. M. Kabesch has received remuneration in the form of grants, honoraria, or consulting fees from Roxall, Glaxo Wellcome, Novartis, Sanofi-Aventis, MSD, and Allergopharma and has received research support from the DFG, Bundesministerium fur Bildung und Forschung, and the European Union. D. Heederik has received research support from the European Union. E. von Mutius has consulted for Novartis, GlaxoSmithKline, Protectimmun, and UCB and has received research support from Airsonett AB. M. Depner has received research support from the European Commission. R. Lauener has received research support from the European Union and the Kuhne Foundation. J. Weber has received research support from the European Commission. The rest of the authors have declared that they have no conflict of interest.	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Allergy Clin. Immunol.	JAN	2011	127	1					138	U226		10.1016/j.jaci.2010.09.041		11	Allergy; Immunology	Allergy; Immunology	702SY	WOS:000285917300020	21211648	
J	Hochberg, NS; Hamer, DH				Hochberg, Natasha S.; Hamer, Davidson H.			Anisakidosis: Perils of the Deep	CLINICAL INFECTIOUS DISEASES			English	Article							MAJOR ALLERGEN; GASTRIC ANISAKIASIS; PARASITIC ZOONOSES; BOWEL OBSTRUCTION; EATING SUSHI; SIMPLEX; FISH; DIAGNOSIS; NEMATODA; IDENTIFICATION	Anisakidosis, human infection with nematodes of the family Anisakidae, is caused most commonly by Anisakis simplex and Pseudoterranova decipiens. Acquired by the consumption of raw or undercooked marine fish or squid, anisakidosis occurs where such dietary customs are practiced, including Japan, coastal regions of Europe, and the United States. Severe epigastric pain, resulting from larval invasion of the gastric mucosa, characterizes gastric anisakidosis; other syndromes are intestinal and ectopic. Allergic anisakidosis is a frequent cause of foodborne allergies in areas with heavy fish consumption or occupational exposure. Diagnosis and treatment of gastric disease is usually made by a compatible dietary history and visualization and removal of the larva(e) on endoscopy; serologic testing for anti-A. simplex immunoglobulin E can aid in the diagnosis of intestinal, ectopic and allergic disease. Intestinal and/or ectopic cases may require surgical removal; albendazole has been used occasionally. Preventive measures include adequately freezing or cooking fish.	[Hochberg, Natasha S.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02118 USA; [Hamer, Davidson H.] Boston Univ, Sch Publ Hlth, Dept Int Hlth, Boston, MA 02118 USA; [Hochberg, Natasha S.; Hamer, Davidson H.] Boston Univ, Sch Med, Infect Dis Sect, Dept Med, Boston, MA 02118 USA; [Hochberg, Natasha S.; Hamer, Davidson H.] Boston Med Ctr, Travel Clin, Boston, MA 02111 USA; [Hamer, Davidson H.] Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA	Hochberg, NS (reprint author), Boston Univ, Sch Publ Hlth, Dept Epidemiol, 715 Albany St,Talbot 420E, Boston, MA 02118 USA.	nhoch@bu.edu		Hochberg, Natasha/0000-0002-5449-9973; Hamer, Davidson/0000-0002-4700-1495			Abollo E, 2001, PARASITOL RES, V87, P492, DOI 10.1007/s004360100389; ADAMS AA, 1990, LANCET, V336, P1328, DOI 10.1016/0140-6736(90)93019-L; Adroher FJ, 1996, PARASITOL RES, V82, P319, DOI 10.1007/s004360050120; Akbar A, 2005, DIGEST LIVER DIS, V37, P7, DOI 10.1016/j.dld.2004.09.011; Anadon AM, 2009, CLIN EXP IMMUNOL, V156, P471, DOI 10.1111/j.1365-2249.2009.03919.x; Arilla MC, 2008, PARASITOLOGY, V135, P735, DOI 10.1017/S0031182008004332; Audicana MT, 2008, CLIN MICROBIOL REV, V21, P360, DOI 10.1128/CMR.00012-07; Audicana MT, 2002, TRENDS PARASITOL, V18, P20, DOI 10.1016/S1471-4922(01)02152-3; Caballero ML, 2002, ANN ALLERG ASTHMA IM, V89, P74; Cespedes M, 2000, ABDOM IMAGING, V25, P548, DOI 10.1007/s002610000089; Chai JY, 2005, INT J PARASITOL, V35, P1233, DOI 10.1016/j.ijpara.2005.07.013; Chen Q, 2008, PARASITOL RES, V104, P79, DOI 10.1007/s00436-008-1161-7; CHORDAUGER S, 1995, PARASITE, V2, P395; DEARDORFF TL, 1989, J WILDLIFE DIS, V25, P416; Eguia A, 2003, ORAL SURG ORAL MED O, V96, P437, DOI 10.1016/S1079-2104(03)00264-6; Foti C, 2002, ACTA DERM-VENEREOL, V82, P121, DOI 10.1080/00015550252948167; Gill CJ, 2005, CLIN INFECT DIS, V41, P1764, DOI 10.1086/498153; Gomez B, 1998, ALLERGY, V53, P1148, DOI 10.1111/j.1398-9995.1998.tb03834.x; Gorbach SL, 2004, INFECT DIS; Ishikura H., 1990, PROGR CLIN PARASITOL, V3, P43; Ito Y, 2007, ASIAN J SURG, V30, P67, DOI 10.1016/S1015-9584(09)60131-7; KAKIZOE S, 1995, AM J GASTROENTEROL, V90, P761; Kanematsu M, 1997, AM J ROENTGENOL, V168, P1114; Kanisawa Y, 2000, ENDOSCOPY, V32, pS55; KARL H, 1994, INT J FOOD SCI TECH, V29, P661; KLIKS MM, 1986, JAMA-J AM MED ASSOC, V255, P2605; Klimpel S, 2004, PARASITOL RES, V94, P1, DOI 10.1007/s00436-004-1154-0; Leuckart R., 1876, MENSCHLICHEN PARASIT; Lopez-Serrano MC, 2000, J GASTROEN HEPATOL, V15, P503, DOI 10.1046/j.1440-1746.2000.02153.x; Manfredi MT, 2000, PARASITOL RES, V86, P551, DOI 10.1007/s004360000202; McClelland G, 2002, PARASITOLOGY, V124, pS183, DOI 10.1017/S0031182002001658; Mercado R, 2001, MEM I OSWALDO CRUZ, V96, P653, DOI 10.1590/S0074-02762001000500010; MIYAZAKI I, 1991, ANISAKIASIS ILLUSTRA, P314; Moneo I, 2000, J ALLERGY CLIN IMMUN, V106, P177, DOI 10.1067/mai.2000.106732; Moore DAJ, 2002, LANCET, V360, P54, DOI 10.1016/S0140-6736(02)09333-9; Muguruma N, 1999, GASTROINTEST ENDOSC, V49, P653, DOI 10.1016/S0016-5107(99)70401-3; Muraoka A, 1996, DIGEST DIS SCI, V41, P2362, DOI 10.1007/BF02100128; Nawa Y, 2005, CLIN INFECT DIS, V41, P1297, DOI 10.1086/496920; Neto V. 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J	Frew, AJ				Frew, Anthony J.			Allergen immunotherapy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Immunotherapy; immunomodulation; rhinitis; asthma; T cell; B cell; IgE; IgG; sublingual	GRASS-POLLEN IMMUNOTHERAPY; LONG-TERM PREVENTION; HOUSE-DUST MITE; T-CELL-CLONES; DOUBLE-BLIND; BIRCH POLLEN; SUBLINGUAL IMMUNOTHERAPY; RAGWEED IMMUNOTHERAPY; CLINICAL-EFFICACY; CONTROLLED TRIAL	Specific immunotherapy (SIT) involves the administration of allergen extracts to achieve clinical tolerance of those allergens that cause symptoms in patients with allergic conditions. Immunotherapy is effective in patients with mild forms of allergic disease and also in those who do not respond well to standard drug therapy. Most SIT is given by means of injection, but there is increasing interest in performing SIT through the sublingual route. SIT remains the treatment of choice for patients with systemic allergic reactions to wasp and bee stings and should be considered as an option in patients with allergic rhinitis, asthma, or both. SIT can modify the course of allergic disease by reducing the risk of new allergic sensitizations and inhibiting the development of clinical asthma in children treated for allergic rhinitis. The precise mechanisms responsible for the beneficial effects of SIT remain a matter of research and debate. An effect on regulatory T cells seems most probable and is associated with switching of allergen-specific B cells toward IgG4 production. Few direct comparisons of SIT and drug therapy have been made. Existing data suggest that the effects of SIT take longer to develop, but once established, SIT achieves long-lasting relief of allergic symptoms, whereas the benefits of drugs only last as long as they are continued. (J Allergy Clin Immunol 2010;125:S306-13.)	Brighton Gen Hosp, Dept Resp Med, Brighton & Sussex Med Sch, Brighton BN2 3EW, E Sussex, England	Frew, AJ (reprint author), Brighton Gen Hosp, Dept Resp Med, Brighton & Sussex Med Sch, Brighton BN2 3EW, E Sussex, England.	anthony.frew@bsuh.nhs.uk			Allergy Therapeutics, Ltd; ARTU biological NV	A. J. Frew is on the Advisory Board for Allergopharma and Stallergenes; gives lectures for MSD, Schering-Plough, and Novartis; gives lectures and is on the Advisory Board for ALK-Abello, UK; has received research support from Allergy Therapeutics, Ltd, and ARTU biological NV; has provided expert witness testimony on the topic of antihistamine patents; is on the Executive Committee for the European Academy of Allergy and Clinical Immunology; and is a Council Member for the British Society for Allergy and Clinical Immunology.	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Allergy Clin. Immunol.	FEB	2010	125	2		2			S306	S313		10.1016/j.jaci.2009.10.064		8	Allergy; Immunology	Allergy; Immunology	629CC	WOS:000280170600028	20176266	
J	North, ML; Khanna, N; Marsden, PA; Grasemann, H; Scott, JA				North, Michelle L.; Khanna, Nivedita; Marsden, Philip A.; Grasemann, Hartmut; Scott, Jeremy A.			Functionally important role for arginase 1 in the airway hyperresponsiveness of asthma	AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY			English	Article						S-(2-boronoethyl)-L-cysteine; agmatinase; nitric oxide	NITRIC-OXIDE SYNTHASE; ALVEOLAR MACROPHAGES; ALLERGIC-ASTHMA; CANDIDATE GENE; MURINE MODELS; EXHALED AIR; L-ARGININE; INFLAMMATION; MICE; INHIBITION	North ML, Khanna N, Marsden PA, Grasemann H, Scott JA. Functionally important role for arginase 1 in the airway hyperresponsiveness of asthma. Am J Physiol Lung Cell Mol Physiol 296: L911-L920, 2009. First published March 13, 2009; doi: 10.1152/ajplung.00025.2009.-L-Arginine metabolism by the arginase and nitric oxide (NO) synthase (NOS) families of enzymes is important in NO production, and imbalances between these pathways contribute to airway hyperresponsiveness (AHR) in asthma. To investigate the role of arginase isozymes (ARG1 and ARG2) in AHR, we determined the protein expression of ARG1, ARG2, the NOS isozymes, and other proteins involved in L-arginine metabolism in lung tissues from asthma patients and in acute (3-wk) and chronic (12-wk) murine models of ovalbumin-induced airway inflammation. Expression of ARG1 was increased in human asthma, whereas ARG2, NOS isoforms, and the other L-arginine-related proteins (i.e., cationic amino acid transporters 1 and 2, agmatinase, and ornithine decarboxylase) were unchanged. In the acute murine model of allergic airway inflammation, augmentation of ARG1 expression was similarly the most dramatic change in protein expression. However, ARG2, NOS1, NOS2, and agmatinase were also increased, whereas NOS3 expression was decreased. Arginase inhibition in vivo with nebulized S-(2-boronoethyl)-L-cysteine attenuated the methacholine responsiveness of the central airways in mice from the acute model. Further investigations in the chronic murine model revealed an expression profile that more closely paralleled the human asthma samples: only ARG1 expression was significantly increased. Interestingly, in the chronic mouse model, which generates a remodeling phenotype, arginase inhibition attenuated methacholine responsiveness of the central and peripheral airways. The similarity in arginase expression between human asthma and the chronic model and the attenuation of AHR after in vivo treatment with an arginase inhibitor suggest the potential for therapeutic modification of arginase activity in asthma.	[North, Michelle L.; Marsden, Philip A.; Grasemann, Hartmut; Scott, Jeremy A.] Univ Toronto, Hosp Sick Children, Inst Med Sci, Toronto, ON M5G 1X8, Canada; [Scott, Jeremy A.] Univ Toronto, Hosp Sick Children, Inst Occupat & Environm Hlth Program, Dalla Lana Sch Publ Hlth,Fac Med, Toronto, ON M5G 1X8, Canada; [North, Michelle L.; Khanna, Nivedita; Scott, Jeremy A.] Univ Toronto, Hosp Sick Children, Div Occupat & Resp Med, Dept Med, Toronto, ON M5G 1X8, Canada; [North, Michelle L.; Khanna, Nivedita; Scott, Jeremy A.] Univ Toronto, Hosp Sick Children, Div Occupat & Resp Med, Fac Med, Toronto, ON M5G 1X8, Canada; [Marsden, Philip A.] Univ Toronto, Hosp Sick Children, Div Nephrol, Fac Med, Toronto, ON M5G 1X8, Canada; [Marsden, Philip A.] Univ Toronto, Hosp Sick Children, Div Nephrol, Dept Med, Toronto, ON M5G 1X8, Canada; [Grasemann, Hartmut] Univ Toronto, Hosp Sick Children, Div Physiol & Expt Med, Toronto, ON M5G 1X8, Canada; [Grasemann, Hartmut] Univ Toronto, Hosp Sick Children, Div Resp Med, Toronto, ON M5G 1X8, Canada; [North, Michelle L.; Khanna, Nivedita; Marsden, Philip A.; Scott, Jeremy A.] St Michaels Hosp, Res Ctr, Gage Occupat & Environm Hlth Unit, Toronto, ON M5B 1W8, Canada; [North, Michelle L.; Khanna, Nivedita; Marsden, Philip A.; Scott, Jeremy A.] St Michaels Hosp, Res Ctr, Keenan Res Ctr, Li Ka Shing Knowledge Inst, Toronto, ON M5B 1W8, Canada	Scott, JA (reprint author), Univ Toronto, Rm 6275A,Med Sci Bldg,1 Kings Coll Circle, Toronto, ON M5S 1A8, Canada.	jeremy.scott@utoronto.ca	Scott, Jeremy/D-2965-2009; Marsden, Philip/B-1441-2012	Scott, Jeremy/0000-0002-7513-6768; 	Ontario Thoracic Society; GlaxoSmithKline; AllerGen NCE; National Sanitarium Association; St. Michael's Hospital Research Centre; Heart and Stroke Foundation of Canada [T-5834]; Dr. Goran Enhorning Award in Pulmonary Physiology	This study was supported by an Ontario Thoracic Society/GlaxoSmithKline Grant-in-Aid of Research, AllerGen NCE, the National Sanitarium Association, St. Michael's Hospital Research Centre, and Heart and Stroke Foundation of Canada Grant T-5834. M.L. North is an Ontario Graduate Scholar in Science and Technology and recipient of the Dr. Goran Enhorning Award in Pulmonary Physiology.	ALVING K, 1993, EUR RESPIR J, V6, P1368; Belik J, 2008, AM J PHYSIOL-LUNG C, V294, pL498, DOI 10.1152/ajplung.00242.2007; Bergeron C, 2007, J ALLERGY CLIN IMMUN, V119, P391, DOI 10.1016/j.jaci.2006.10.030; Bratt JM, 2009, TOXICOL APPL PHARM, V234, P273, DOI 10.1016/j.taap.2008.10.007; Ckless K, 2008, J IMMUNOL, V181, P4255; De Sanctis GT, 1999, J EXP MED, V189, P1621, DOI 10.1084/jem.189.10.1621; Di Valentin E, 2009, AM J PHYSIOL-LUNG C, V296, pL185, DOI 10.1152/ajplung.90367.2008; Epstein MM, 2006, EXP TOXICOL PATHOL, V57, P41, DOI 10.1016/j.etp.2006.02.005; Grasemann H, 1999, CLIN EXP ALLERGY, V29, P39; Grasemann H, 2005, AM J RESP CRIT CARE, V172, P1523, DOI 10.1164/rccm.200502-253OC; Grasemann H, 2000, BIOCHEM BIOPH RES CO, V272, P391, DOI 10.1006/bbrc.2000.2794; Greene AL, 2005, TOXICOL SCI, V88, P420, DOI 10.1093/toxsci/kfi311; Hakonarson H, 2002, AM J HUM GENET, V71, P483, DOI 10.1086/342205; HAMID Q, 1993, LANCET, V342, P1510, DOI 10.1016/S0140-6736(05)80083-2; Hammermann R, 1999, AM J RESP CELL MOL, V21, P155; HANTOS Z, 1992, J APPL PHYSIOL, V72, P168; HECKER M, 1995, FEBS LETT, V359, P251, DOI 10.1016/0014-5793(95)00039-C; Hirota JA, 2006, RESP RES, V7, DOI 10.1186/1465-9921-7-120; Iyer RK, 2002, MOL GENET METAB, V75, P209, DOI 10.1006/mgme.2001.3277; Kenyon NJ, 2008, TOXICOL APPL PHARM, V230, P269, DOI 10.1016/j.taap.2008.03.004; Kenyon NJ, 2005, INFLAMM RES, V54, P57, DOI 10.1007/s00011-004-1325-6; KHARITONOV SA, 1994, LANCET, V343, P133, DOI 10.1016/S0140-6736(94)90931-8; Lara A, 2008, AM J RESP CRIT CARE, V178, P673, DOI 10.1164/rccm.200710-1542OC; Lee SK, 2003, ALLERGY ASTHMA PROC, V24, P275; Li HL, 2006, J ALLERGY CLIN IMMUN, V117, P119, DOI 10.1016/j.jaci.2005.09.026; Litonjua AA, 2008, AM J RESP CRIT CARE, V178, P688, DOI 10.1164/rccm.200709-1363OC; Maarsingh H, 2005, RESP RES, V6, DOI 10.1186/1465-9921-6-23; Maarsingh H, 2008, AM J RESP CRIT CARE, V178, P565, DOI 10.1164/rccm.200710-1588OC; Maarsingh H, 2008, EUR J PHARMACOL, V585, P375, DOI 10.1016/j.ejphar.2008.02.096; Meurs H, 2002, BRIT J PHARMACOL, V136, P391, DOI 10.1038/sj.bjp.0704725; Meurs H, 2000, BRIT J PHARMACOL, V130, P1793, DOI 10.1038/sj.bjp.0703488; Morris CR, 2004, AM J RESP CRIT CARE, V170, P148, DOI 10.1164/rccm.200309-1304OC; Satriano J, 2004, AMINO ACIDS, V26, P321, DOI 10.1007/s00726-004-0078-4; Scott JA, 2002, CRIT CARE MED, V30, P2143, DOI 10.1097/01.CCM.0000027863.16345.79; Shapiro SD, 2006, AM J RESP CRIT CARE, V174, P1171, DOI 10.1164/rccm.2609001; Takemoto K, 2007, AM J PHYSIOL-LUNG C, V293, pL1419, DOI 10.1152/ajplung.00418.2006; Taube C, 2004, INT ARCH ALLERGY IMM, V135, P173, DOI 10.1159/000080899; Tomioka S, 2002, J APPL PHYSIOL, V93, P263, DOI 10.1152/japplphysiol.01129.2001; Vercelli D, 2003, J CLIN INVEST, V111, P1815, DOI 10.1172/JCI200318908; Wechsler ME, 2000, AM J RESP CRIT CARE, V162, P2043; Wenzel S, 2006, AM J RESP CRIT CARE, V174, P1173, DOI 10.1164/rccm.2609002; Zimmermann N, 2006, EUR J PHARMACOL, V533, P253, DOI 10.1016/j.ejphar.2005.12.047; Zimmermann N, 2003, J CLIN INVEST, V111, P1863, DOI 10.1172/JCI200317912	43	77	82	1	13	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.	JUN	2009	296	6					L911	L920		10.1152/ajplung.00025.2009		10	Physiology; Respiratory System	Physiology; Respiratory System	450YQ	WOS:000266438300007	19286931	
J	Melen, E; Nyberg, F; Lindgren, CM; Berglind, N; Zucchelli, M; Nordling, E; Hallberg, J; Svartengren, M; Morgenstern, R; Kere, J; Bellander, T; Wickman, M; Pershagen, G				Melen, Erik; Nyberg, Fredrik; Lindgren, Cecilia M.; Berglind, Niklas; Zucchelli, Marco; Nordling, Emma; Hallberg, Jenny; Svartengren, Magnus; Morgenstern, Ralf; Kere, Juha; Bellander, Tom; Wickman, Magnus; Pershagen, Goeran			Interactions between glutathione S-transferase P1, tumor necrosis factor, and traffic-related air pollution for development of childhood allergic disease	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						ADRB2; air pollution; allergy; asthma; genetics; GSTP1; interaction; nitrogen oxides; polymorphism; TNF	ENVIRONMENTAL TOBACCO-SMOKE; LUNG-FUNCTION; OXIDATIVE STRESS; BRONCHIAL HYPERRESPONSIVENESS; RESPIRATORY ILLNESS; GENE POLYMORPHISM; PASSIVE SMOKING; ASTHMA; M1; ASSOCIATION	BACKGROUND: Air pollutants may induce airway inflammation and sensitization due to generation of reactive oxygen species. The genetic background to these mechanisms could be important effect modifiers. OBJECTIVE: Our goal was to assess interactions between exposure to air pollution and single nucleotide polymorphisms (SNPs) in the beta 2-adrenergic receptor (ADRB2), glutathione S-transferase P1 (GSTP1), and tumor necrosis factor (TNF) genes for development of childhood allergic disease. METHODS: In a birth cohort originally of 4,089 children, we assessed air pollution from local traffic using nitrogen oxides (traffic NOx) as an indicator based on emission databases and dispersion modeling and estimated individual exposure through geocoding of home addresses. We measured peak expiratory flow rates and specific IgE for inhalant and food allergens at 4 years of age, and selected children with asthma symptoms up to 4 years of age (n = 542) and controls (n = 542) for genotyping. RESULTS: Interaction effects on allergic sensitization were indicated between several GSTP1 SNPs and traffic NO. exposure during the first year of life (P-nominal < 0.001-0.06). Children with Ile105Val/Val105Val genotypes were at increased risk of sensitization to any allergen when exposed to elevated levels of traffic NO, (for a difference between the 5th and 95th percentile of exposure: odds ratio = 2.4; 95% confidence interval, 1.0-5.3). In children with TNF-308 GA/AA genotypes, the GSTP1-NOx interaction effect was even more pronounced. We observed no conclusive interaction effects for ADRB2. CONCLUSION: The effect of air pollution from traffic on childhood allergy appears to be modified by GSTP1 and TNF variants, supporting a role of genes controlling the antioxidative system and inflammatory response in allergy.	[Melen, Erik; Nyberg, Fredrik; Berglind, Niklas; Morgenstern, Ralf; Bellander, Tom; Wickman, Magnus; Pershagen, Goeran] Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; [Melen, Erik] Karolinska Univ Hosp, Astrid Lindgren Childrens Hosp, SE-17176 Stockholm, Sweden; [Nyberg, Fredrik] AstraZeneca R&D, Molndal, Sweden; [Lindgren, Cecilia M.; Zucchelli, Marco; Kere, Juha] Karolinska Inst, Dept Biosci Novum, Stockholm, Sweden; [Lindgren, Cecilia M.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England; [Berglind, Niklas; Nordling, Emma; Svartengren, Magnus; Bellander, Tom] Stockholm Cty Council, Dept Environm & Occupat Hlth, Stockholm, Sweden; [Zucchelli, Marco] Karolinska Inst, BEA Bioinformat Core Facil Novum, Stockholm, Sweden; [Hallberg, Jenny; Svartengren, Magnus] Karolinska Inst, Dept Publ Hlth Sci, Stockholm, Sweden; [Wickman, Magnus] Karolinska Inst, Sachs Childrens Hosp, Stockholm, Sweden	Melen, E (reprint author), Karolinska Univ Hosp, Astrid Lindgren Childrens Hosp, SE-17176 Stockholm, Sweden.	erik.melen@ki.se	Kere, Juha/A-9179-2008; Osborne, Nicholas/N-4915-2015	Kere, Juha/0000-0003-1974-0271; Osborne, Nicholas/0000-0002-6700-2284; Pershagen, Goran/0000-0002-9701-1130; Lindgren, Cecilia/0000-0002-4903-9374	Wellcome Trust [090532]		Altshuler D, 2005, NATURE, V437, P1299, DOI 10.1038/nature04226; Barrett JC, 2005, BIOINFORMATICS, V21, P263, DOI 10.1093/bioinformatics/bth457; BENJAMINI Y, 1995, J ROY STAT SOC B MET, V57, P289; Bennett BL, 2001, P NATL ACAD SCI USA, V98, P13681, DOI 10.1073/pnas.251194298; Brasch-Andersen C, 2004, HUM MUTAT, V24, P208, DOI 10.1002/humu.20074; Carroll WD, 2005, CLIN EXP ALLERGY, V35, P1155, DOI 10.1111/j.1365-2222.2005.02313.x; DEVALIA JL, 1993, AM J RESP CELL MOL, V9, P271; Forsberg L, 2001, ARCH BIOCHEM BIOPHYS, V389, P84, DOI 10.1006/abbi.2001.2295; Fryer AA, 2000, AM J RESP CRIT CARE, V161, P1437; FRYER AA, 1986, BIOCHIM BIOPHYS ACTA, V883, P448, DOI 10.1016/0304-4165(86)90283-7; Gao J, 2006, THORAX, V61, P466, DOI 10.1136/thx.2005.051284; Gilliland FD, 2002, AM J RESP CRIT CARE, V166, P457, DOI 10.1164/rccm.2112064; 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Health Perspect.	AUG	2008	116	8					1077	1084		10.1289/ehp.11117		8	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	335DE	WOS:000258270200030	18709160	
J	Jakiela, B; Brockman-Schneider, R; Amineva, S; Lee, WM; Gern, JE				Jakiela, Bogdan; Brockman-Schneider, Rebecca; Amineva, Svetlana; Lee, Wai-Ming; Gern, James E.			Basal cells of differentiated bronchial epithelium are more susceptible to rhinovirus infection	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article						airway epithelium; basal cells; rhinovirus; ICAM-1 expression	HUMAN AIRWAY EPITHELIUM; PROINFLAMMATORY CYTOKINES; ASTHMA EXACERBATIONS; TRACHEAL EPITHELIUM; BARRIER FUNCTION; TIGHT JUNCTIONS; LUNG; PERMEABILITY; MECHANISMS; SECRETION	We used an in vitro model of differentiated tracheolbronchial epithelium to analyze the susceptibility of different cell types to infection with rhinoviruses (RVs). Primary cells from control subjects were cultured in an air-liquid interface to form differentiated epithelia. Suprabasal and basal fractions were separated after trypsin digestion, and cell suspensions were infected with serotypes RV16 and RVIA. These cell fractions were analyzed for expression of viral capsid protein VP2 (flow cytometry), viral replication (real-time PCR), cytolkeratin-14, and intercellular adhesion molecule-1 (ICAM-1). Compared with suprabasal fraction, basal cells had increased percentages of cells staining positive for VP2 (RVIA: 37.8% versus 9.1%, P < 0.01; RV16: 12.0 versus 3.0%, P < 0.05). The average number of viral RNA copies per cell was also higher in basal cells (2.2- and 2.4-fold increase in RV1A- and RV16-infected cells, respectively) compared with suprabasal cells. Furthermore, ICAM-1 was expressed by 33.3% of basal cells, compared with 8.1% of suprabasal cells (P < 0.05). Finally, in culture models of epithelial injury (detached suprabasal cells or scratched surface), there was significantly greater replication of RVIA compared with intact cell layer. These findings demonstrate that basal cells are more susceptible to RV infection than suprabasal cells. For major group RV, this may be in part due to increased expression of ICAM-1; however, minor group RV also replicated more effectively in basal cells. These results suggest the possibility that epithelial cell differentiation is associated with the maturation of antiviral defense mechanisms.	[Jakiela, Bogdan] Jagiellonian Univ, Dept Med, PL-31066 Krakow, Poland; [Brockman-Schneider, Rebecca; Amineva, Svetlana; Lee, Wai-Ming; Gern, James E.] Univ Wisconsin, Madison, WI USA	Jakiela, B (reprint author), Jagiellonian Univ, Dept Med, Ul Skawinska 8, PL-31066 Krakow, Poland.	bogumil.j@poczta.fm			NHLBI NIH HHS [P01 HL70831-01]; NIAID NIH HHS [U19 AI070503]		Ahdieh M, 2001, AM J PHYSIOL-CELL PH, V281, pC2029; Bals R, 2004, EUR RESPIR J, V23, P327, DOI 10.1183/09031936.03.00098803; Benayoun L, 2003, AM J RESP CRIT CARE, V167, P1360, DOI 10.1164/rccm.200209-1030OC; Bergeron C, 2006, CHEST, V129, P1068, DOI 10.1378/chest.129.4.1068; Boers JE, 1998, AM J RESP CRIT CARE, V157, P2000; Borthwick DW, 2001, AM J RESP CELL MOL, V24, P662; Bossios A, 2005, RESP RES, V6, DOI 10.1186/1465-9921-6-114; Bruewer M, 2003, J IMMUNOL, V171, P6164; Contoli M, 2006, NAT MED, V12, P1023, DOI 10.1038/nm1462; Coyne CB, 2002, MOL BIOL CELL, V13, P3218, DOI 10.1091/mbc.E02-03-0134; Friedlander SL, 2005, J ALLERGY CLIN IMMUN, V116, P267, DOI 10.1016/j.jaci.2005.06.003; Gern JE, 1997, AM J RESP CRIT CARE, V155, P1159; Grassme H, 2005, J BIOL CHEM, V280, P26256, DOI 10.1074/jbc.M500835200; Gray TE, 1996, AM J RESP CELL MOL, V14, P104; Holgate S T, 2003, Eur Respir J Suppl, V44, p24s; Holgate Stephen T, 2004, Proc Am Thorac Soc, V1, P93, DOI 10.1513/pats.2306034; Hong KU, 2004, AM J PATHOL, V164, P577, DOI 10.1016/S0002-9440(10)63147-1; Johnston Sebastian L, 2005, Proc Am Thorac Soc, V2, P150, DOI 10.1513/pats.200502-018AW; Knight DA, 2003, RESPIROLOGY, V8, P432, DOI 10.1046/j.1440-1843.2003.00493.x; Konno S, 2002, AM J RESP CELL MOL, V26, P594; Krunkosky TM, 2000, AM J RESP CELL MOL, V22, P685; Lopez-Souza N, 2004, AM J PHYSIOL-LUNG C, V286, pL373, DOI 10.1152/ajplung.00300.2003; Mosser AG, 2005, AM J RESP CRIT CARE, V171, P645, DOI 10.1164/rccm.200407-970OC; Mosser AG, 2002, J INFECT DIS, V185, P734, DOI 10.1086/339339; Nakajima M, 1998, PATHOL INT, V48, P944; Papadopoulos NG, 2000, J INFECT DIS, V181, P1875, DOI 10.1086/315513; Puchelle Edith, 2006, Proc Am Thorac Soc, V3, P726, DOI 10.1513/pats.200605-126SF; Rawlins EL, 2006, DEVELOPMENT, V133, P2455, DOI 10.1242/dev.02407; Reed CE, 2004, J ALLERGY CLIN IMMUN, V114, P997, DOI 10.1016/j.jaci.2004.07.060; Rodriguez-Boulan E, 2005, NAT REV MOL CELL BIO, V6, P233, DOI 10.1038/nrm1593; Sachs LA, 2003, IN VITRO CELL DEV-AN, V39, P56; Savolainen Carita, 2003, Paediatr Respir Rev, V4, P91, DOI 10.1016/S1526-0542(03)00030-7; Schleimer Robert P, 2004, Proc Am Thorac Soc, V1, P222, DOI 10.1513/pats.200402-018MS; Schroth MK, 1999, AM J RESP CELL MOL, V20, P1220; Shahana S, 2005, RESP MED, V99, P429, DOI 10.1016/j.rmed.2004.08.013; Tai HY, 2006, ALLERGY, V61, P382, DOI 10.1111/j.1398-9995.2005.00958.x; Takizawa Hajime, 2005, Current Drug Targets - Inflammation and Allergy, V4, P305, DOI 10.2174/1568010054022123; Trautmann A, 2005, INT ARCH ALLERGY IMM, V138, P142, DOI 10.1159/000088436; Uchida DA, 1996, EXP LUNG RES, V22, P85, DOI 10.3109/01902149609074019; Wan H, 1999, J CLIN INVEST, V104, P123, DOI 10.1172/JCI5844; Wark PAB, 2005, J EXP MED, V201, P937, DOI 10.1084/jem.20041901; Wu R, 1997, EUR RESPIR J, V10, P2398, DOI 10.1183/09031936.97.10102398; Zabner J, 2003, J APPL PHYSIOL, V95, P394, DOI 10.1152/japplphysiol.01134.2002; Zabner J, 1996, J VIROL, V70, P6994; Zhu J, 1999, EUR RESPIR J, V13, P1318, DOI 10.1183/09031936.99.13613299	45	77	79	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	2008	38	5					517	523		10.1165/rcmb.2007-0050OC		7	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	298MV	WOS:000255692700004	18063839	
J	Kozyrskyj, AL; Mai, XM; McGrath, P; HayGlasss, KT; Becker, AB; MacNeil, B				Kozyrskyj, Anita L.; Mai, Xiao-Mei; McGrath, Patrick; HayGlasss, Kent T.; Becker, Allan B.; MacNeil, Brian			Continued exposure to maternal distress in early life is associated with an increased risk of childhood asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; child; depression; postpartum	POSTPARTUM PSYCHIATRIC-DISORDERS; PSYCHOLOGICAL STRESS; BIRTH-COHORT; DEPRESSION; CHILDREN; EXPRESSION; REACTIVITY; PREDICTOR; SYMPTOMS; CORTISOL	Rationale: Evidence is emerging that exposure to maternal distress in early life plays a causal role in the development of childhood asthma. Objectives: Because much of the data are from high-risk cohorts, we undertook a birth cohort study in a complete population of children to test this association. Methods: Using Manitoba, Canada's, health care and prescription databases, this longitudinal study assessed the association between maternal distress during the first year of life and onward, and asthma at age 7 in a 1995 birth cohort of 13,907 children. Measurements and Main Results: Maternal distress was defined on the basis of health care or prescription medication use for depression or anxiety. Asthma status was derived from health care and prescription records for asthma, using a definition validated by comparison to pediatric allergist diagnosis. Multiple logistic regression was used to determine the likelihood of asthma (odds ratio [OR], 95% confidence interval [95% CI]). Independent of wellknown asthma risk factors, our population-based study of a non-high-risk cohort demonstrated an increased risk of childhood asthma (OR, 1.25; 95% CI, 1.01-1.55) among children exposed to continued maternal distress from birth until age 7. Exposure to maternal depression and anxiety limited to the first year of life did not have a demonstrable association with subsequent asthma. Of interest, we observed that the risk of asthma associated with continued maternal distress was increased in children living in high- versus low-income households (OR, 1.44; 95% CI, 1.12-1.85). Conclusions: Maternal distress in early life plays a role in the development of childhood asthma, especially if it continues beyond the postpartum period.	[Kozyrskyj, Anita L.; Mai, Xiao-Mei] Univ Manitoba, Fac Pharm, Winnipeg, MB R3T 2N2, Canada; [Kozyrskyj, Anita L.] Univ Manitoba, Dept Community Hlth Sci, Manitoba Ctr Hlth Policy, Winnipeg, MB R3T 2N2, Canada; [Kozyrskyj, Anita L.; Becker, Allan B.] Univ Manitoba, Dept Pediat & Child Hlth, Fac Med, Winnipeg, MB R3T 2N2, Canada; [McGrath, Patrick] Dalhousie Univ, Fac Sci, Dept Psychol, Halifax, NS, Canada; [HayGlasss, Kent T.] Univ Manitoba, Dept Immunol, Fac Med, Winnipeg, MB, Canada; [MacNeil, Brian] Univ Manitoba, Sch Med Rehabil, Winnipeg, MB, Canada	Kozyrskyj, AL (reprint author), 210 Pharm Bldg, Winnipeg, MB R3T 2N2, Canada.	kozyrsk@cc.umanitoba.ca	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; MacNeil, Brian/0000-0002-2897-8049; HayGlass, Kent /0000-0002-4621-7737; McGrath, Patrick/0000-0002-9568-2571			Asher MI, 2006, LANCET, V368, P733, DOI 10.1016/S0140-6736(06)69283-0; Ball TM, 2006, J ALLERGY CLIN IMMUN, V117, P306, DOI 10.1016/j.jaci.2005.11.009; Beck CT, 1995, NURS RES, V44, P298; BOYCE WT, 1995, PSYCHOSOM MED, V57, P411; Brockington I, 2004, LANCET, V363, P303, DOI 10.1016/S0140-6736(03)15390-1; Castro-Rodriguez JA, 2000, AM J RESP CRIT CARE, V162, P1403; Chen E, 2006, J ALLERGY CLIN IMMUN, V117, P1014, DOI 10.1016/j.jaci.2006.01.036; Chida Y, 2007, AM J RESP CRIT CARE, V175, P316, DOI 10.1164/rccm.200607-898OC; Coates AO, 2004, J BEHAV HEALTH SER R, V31, P117; Collins KA, 2004, CLIN PSYCHOL REV, V24, P583, DOI 10.1016/j.cpr.2004.06.001; Diego MA, 2005, INFANT BEHAV DEV, V28, P155, DOI 10.1016/j.infbeh.2005.02.002; Essex MJ, 2002, BIOL PSYCHIAT, V52, P776, DOI 10.1016/S0006-3223(02)01553-6; Georgiopoulos AM, 1999, OBSTET GYNECOL, V93, P653, DOI 10.1016/S0029-7844(98)00543-2; Hipwell AE, 2000, DEV PSYCHOPATHOL, V12, P157, DOI 10.1017/S0954579400002030; Hornstein C, 2006, ARCH WOMEN MENT HLTH, V9, P279, DOI 10.1007/s00737-006-0148-6; Klinnert M. D., 2001, PEDIATRICS, V108, P69; Kozyrskyj AL, 2006, J ALLERGY CLIN IMMUN, V117, pS87, DOI 10.1016/j.jaci.2005.12.348; Kozyrskyj AL, 1998, ANN PHARMACOTHER, V32, P1152, DOI 10.1345/aph.18117; Kozyrskyj ALOJ., 1999, CRIT PUBLIC HLTH, V9, P197, DOI 10.1080/09581599908402932; KOZYRSKYJ AL, 2005, ALLERGY ASTHMA CLIN, V1, P108; Kozyrskyj AL, 2007, CHEST, V131, P1753, DOI 10.1378/chest.06-3008; Lin YC, 2004, CLIN EXP ALLERGY, V34, P548, DOI 10.1111/j.1365-2222.2004.1928.x; Mantymaa M, 2003, CHILD CARE HLTH DEV, V29, P181, DOI 10.1046/j.1365-2214.2003.00330.x; McLearn KT, 2006, ARCH PEDIAT ADOL MED, V160, P279, DOI 10.1001/archpedi.160.3.279; Meaney Michael J, 2005, Dialogues Clin Neurosci, V7, P103; Meaney MJ, 2001, ANNU REV NEUROSCI, V24, P1161, DOI 10.1146/annurev.neuro.24.1.1161; Mrazek DA, 1999, PEDIATR PULM, V27, P85, DOI 10.1002/(SICI)1099-0496(199902)27:2<85::AID-PPUL4>3.0.CO;2-B; Pekkanen J, 1999, EUR RESPIR J, V14, P951, DOI 10.1034/j.1399-3003.1999.14d37.x; Phipatanakul W, 2005, ALLERGY, V60, P697, DOI 10.1111/j.1398-9995.2005.00825.x; Robinson JR, 1997, MED CARE, V35, P932, DOI 10.1097/00005650-199709000-00006; Sandberg S, 2000, LANCET, V356, P982, DOI 10.1016/S0140-6736(00)02715-X; Schaub B, 2006, J ALLERGY CLIN IMMUN, V117, P969, DOI 10.1016/j.jaci.2006.03.003; Schor EL, 2003, PEDIATRICS, V111, P1541; Song D, 2004, WOMEN HEALTH, V39, P1, DOI 10.1300/J013v39n01_01; von Hertzen LC, 2002, J ALLERGY CLIN IMMUN, V109, P923, DOI 10.1067/mai.2002.124776; Wade S, 1997, PEDIATR PULM, V24, P263, DOI 10.1002/(SICI)1099-0496(199710)24:4<263::AID-PPUL5>3.0.CO;2-L; Wright RJ, 2004, J ALLERGY CLIN IMMUN, V113, P1051, DOI 10.1016/j.jaci.2004.03.032; Wright RJ, 2002, AM J RESP CRIT CARE, V165, P358; YALLOP YP, 2006, ALLERGEN ANN TRAIN W	39	77	79	2	13	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	JAN 15	2008	177	2					142	147		10.1164/rccm.200703-381OC		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	251BJ	WOS:000252345300004	17932381	
J	Macia, I; Moya, J; Ramos, R; Morera, R; Escobar, I; Saumench, J; Perna, V; Rivas, F				Macia, Ivan; Moya, Juan; Ramos, Ricard; Morera, Ricard; Escobar, Ignacio; Saumench, Josep; Perna, Valerio; Rivas, Francisco			Spontaneous pneumomediastinum: 41 cases	EUROPEAN JOURNAL OF CARDIO-THORACIC SURGERY			English	Article						spontaneous pneumomediastinum; mediastinal emphysema; dyspnea; chest pain; subcutaneous emphysema	SPONTANEOUS MEDIASTINAL EMPHYSEMA; COMPUTED-TOMOGRAPHY; EXPERIENCE; MANAGEMENT; DIAGNOSIS	Objective: Spontaneous pneumomediastinum is characterized by the presence of interstitial air in the mediastinum without any apparent precipitating factor. The purpose of this study is to review and discuss our experience with this condition. Methods: A descriptive, retrospective study of 41 cases - 34 men (83%) and 7 women (17%) - treated at our hospital for spontaneous pneumomediastinum from January 1990 through June 2006. Results: The mean age of the patients was 21 years (range, 14-35 years). Notably, 22% of patients had a prior history of asthma. No precipitating factor was identified in 51% of cases while onset was associated with physical effort in 12%. Chest pain (85%) and dyspnea (49%) were the most common symptoms. Subcutaneous emphysema, which presented in 71% of patients, was the most common sign. Pneumomediastinum was diagnosed by plain chest radiography in all cases. In certain cases, a computed tomography scan of the chest, contrast-enhanced swallow, or bronchoscopy was performed. All patients were admitted to the hospital with good progress and no instances of morbidity or mortality. Treatment included analgesia, rest, and/or initial oxygen therapy. The mean length of hospital stay was 5 days (range, 1-9 days) with only one case of early recurrence, which was resolved satisfactorily. Conclusions: Spontaneous pneumomediastinum is a benign process primarily affecting young men. Despite its tow incidence, spontaneous pneumomediastinum should be considered in the differential diagnosis of acute chest pain because it requires a high index of suspicion. Patients with spontaneous preumomediastinum respond well to medical treatment, with no recurrence in the great majority of cases. (C) 2007 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All. rights reserved.	Hosp Univ Bellvitge, Dept Thorac Surg, Hosp Llobregat, Barcelona 08907, Spain; Univ Barcelona, Hosp Llobreget, Dept Thorac Surg, Hosp Univ Bellvitge,Sch Med, Barcelona, Spain; Univ Barcelona, Hosp Llobreget, Unit Human Anat, Hosp Univ Bellvitge,Sch Med, Barcelona, Spain	Macia, I (reprint author), Hosp Univ Bellvitge, Dept Thorac Surg, Hosp Llobregat, Feixa Llarga S-N, Barcelona 08907, Spain.	ivanmacia@yahoo.com					ABOLNIK I, 1991, CHEST, V100, P93, DOI 10.1378/chest.100.1.93; Ba-Ssalamah A, 1999, EUR RADIOL, V9, P724, DOI 10.1007/s003300050742; Bejvan SM, 1996, AM J ROENTGENOL, V166, P1041; Campillo-Soto A, 2005, ARCH BRONCONEUMOL, V41, P528, DOI 10.1157/13078656; Freixinet J, 2005, RESP MED, V99, P1160, DOI 10.1016/j.rmed.2005.02.025; Gerazounis M, 2003, J THORAC CARDIOV SUR, V126, P774, DOI 10.1016/S0022-5223(03)00124-7; Hamman L, 1939, B JOHNS HOPKINS HOSP, V64, P1; Jane M, 2002, MED CLIN-BARCELONA, V118, P81; Jougon JB, 2003, ANN THORAC SURG, V75, P1711, DOI 10.1016/S0003-4975(03)00027-4; Kaneki T, 2000, RESPIRATION, V67, P408, DOI 10.1159/000029539; Koullias GJ, 2004, EUR J CARDIO-THORAC, V25, P852, DOI 10.1016/j.ejcts.2004.01.042; Macklin MT, 1944, MEDICINE, V23, P281; MAUNDER RJ, 1984, ARCH INTERN MED, V144, P1447, DOI 10.1001/archinte.144.7.1447; Newcomb AE, 2005, CHEST, V128, P3298, DOI 10.1378/chest.128.5.3298; Panacek EA, 1992, ANN EMERG MED, V21, P67; Patel A, 2000, CHEST, V117, P1809, DOI 10.1378/chest.117.6.1809; Sakai M, 2006, J COMPUT ASSIST TOMO, V30, P92, DOI 10.1097/01.rct.0000187416.07698.8d; Weissberg D, 2004, EUR J CARDIO-THORAC, V26, P885, DOI 10.1016/j.ejcts.2004.05.050	18	77	82	0	3	ELSEVIER SCIENCE BV	AMSTERDAM	PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS	1010-7940			EUR J CARDIO-THORAC	Eur. J. Cardio-Thorac. Surg.	JUN	2007	31	6					1110	1114		10.1016/j.ejcts.2007.03.008		5	Cardiac & Cardiovascular Systems; Respiratory System; Surgery	Cardiovascular System & Cardiology; Respiratory System; Surgery	179LE	WOS:000247290300027	17420139	
J	Yeatts, K; Svendsen, E; Creason, J; Alexis, N; Herbst, M; Scott, J; Kupper, L; Williams, R; Neas, L; Cascio, W; Devlin, RB; Peden, DB				Yeatts, Karin; Svendsen, Erik; Creason, John; Alexis, Neil; Herbst, Margaret; Scott, James; Kupper, Lawrence; Williams, Ronald; Neas, Lucas; Cascio, Wayne; Devlin, Robert B.; Peden, David B.			Coarse particulate matter (PM2.5-10) affects heart rate variability, blood lipids, and circulating eosinophils in adults with asthma	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; coarse PM; heart rate variability; inflammatory markers; lipids; systemic inflammation	AMBIENT AIR-POLLUTION; CARDIAC AUTONOMIC CONTROL; PHAGOCYTES IN-VIVO; INFLAMMATORY RESPONSE; HEALTHY-VOLUNTEERS; ELDERLY SUBJECTS; ENDOTOXIN; EXPOSURE; DISEASE; ASSOCIATION	INTRODUCTION: We investigated whether markers of airway and systemic inflammation, as well as heart rate variability (HRV) in asthmatics, change in response to fluctuations in ambient particulate matter (PM) in the coarse [PM with aerodynamic diameter 2.5-10 mu M (PM2.5-10)] and fine (PM2.5) size range. METHODS: Twelve adult asthmatics, living within a 30-mile radius of an atmospheric monitoring site in Chapel Hill, North Carolina, were followed over a 12-week period. Daily PM2.5-10 and PM2.5 concentrations were measured separately for each 24-hr period. Each subject had nine clinic visits, at which spirometric measures and peripheral blood samples for analysis of lipids, inflammatory cells, and coagulation-associated proteins were obtained. We also assessed HRV [SDNN24HR (standard deviation of all normal-to-normal intervals in a 24-hr recording), ASDNN5 (mean of the standard deviation in A 5-min segments of a 24-hr recording)] with four consecutive 24-hr ambulatory electrocardiogram measurements. Linear mixed models with a spatial covariance matrix structure and a 1-day lag were used to assess potential associations between PM levels and cardio- pulmonary end points. RESULTS: For a 1-mu g/m(3) increase in coarse PM, SDNN24HR, and ASDNN5 decreased 3.36% (p 0.02), and 0.77%, (p = 0.05) respectively. With a 1-mu g/m(3) increase in coarse PM, circulating eosinophils increased 0.16% (p = 0.01), triglycerides increased 4.8% (p = 0.02), and very low-density lipoprotein increased 1.15% (p = 0.01). No significant associations were found with fine PM, and none with lung function. CONCLUSION: These data suggest that small temporal increases in ambient coarse PM are sufficient to affect important cardiopulmonary and lipid parameters in adults with asthma. Coarse PM may have underappreciated health effects in susceptible populations.	Univ N Carolina, Sch Med, CEMALB, Chapel Hill, NC 27599 USA; US EPA, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA; Univ N Carolina, Sch Publ Hlth, Dept Biostat, Chapel Hill, NC USA; US EPA, Natl Exposure Res Lab, Res Triangle Pk, NC USA; E Carolina Univ, Brody Sch Med, Div Cardiol, Greenville, NC USA	Yeatts, K (reprint author), Univ N Carolina, Sch Med, CEMALB, Campus Box 7310,HSD Facil,104 Mason Farm Rd, Chapel Hill, NC 27599 USA.	Karin_Yeatts@unc.edu	Neas, Lucas/J-9378-2012; Wang, Linden/M-6617-2014; Svendsen, Erik/J-2671-2015	Svendsen, Erik/0000-0003-3941-0907	NHLBI NIH HHS [R01 HL062624, R01HL62624]; NIEHS NIH HHS [P30ES10126, P30 ES010126]		Adachi Yushi, 2006, Masui, V55, P436; Alexis N, 2001, J ALLERGY CLIN IMMUN, V107, P31, DOI 10.1067/mai.2001.111594; Alexis NE, 2006, J ALLERGY CLIN IMMUN, V117, P1396, DOI 10.1016/j.jaci.2006.02.030; Alexis NE, 2004, J ALLERGY CLIN IMMUN, V114, P1325, DOI 10.1016/j.jaci.2004.09.002; ALEXIZ NE, JACI, V115, P345; Beckwith CI, 2002, BRILLS TIBET STU LIB, V2, P27; Brunekreef B, 2005, EUR RESPIR J, V26, P309, DOI 10.1183/09031936.05.00001805; Burnett RT, 1999, ARCH ENVIRON HEALTH, V54, P130; Burnett RT, 1997, ENVIRON HEALTH PERSP, V105, P614, DOI 10.1289/ehp.97105614; Chen FL, 2007, ATMOS ENVIRON, V41, P1200, DOI 10.1016/j.atmosenv.2006.09.049; Chen LC, 2005, INHAL TOXICOL, V17, P217, DOI 10.1080/08958370590912815; Chen Y, 2004, INHAL TOXICOL, V16, P21, DOI 10.1080/0895837049258129; Chuang KJ, 2005, ENVIRON HEALTH PERSP, V113, P1693, DOI 10.1289/ehp.8145; Godin PJ, 1996, CRIT CARE MED, V24, P1117, DOI 10.1097/00003246-199607000-00009; Gold DR, 2000, CIRCULATION, V101, P1267; GOLDSTEIN B, 1995, CRIT CARE MED, V23, P1694, DOI 10.1097/00003246-199510000-00014; Gong H, 2004, INHAL TOXICOL, V16, P335, DOI 10.1080/08958370490439470; Hardardottir I, 1995, BIOCHEM SOC T, V23, P1013; Holguin F, 2003, EPIDEMIOLOGY, V14, P521, DOI 10.1097/01.ede.0000081999.1500.ae; Hudgins LC, 2003, J LIPID RES, V44, P1489, DOI 10.1194/jlr.M200440-JLR200; Koutrakis P, 2005, RES REP HLTH EFF I, V131, P1; Kunzli N, 2005, ENVIRON HEALTH PERSP, V113, P201, DOI 10.1289/ehp.7523; Levels JHM, 2003, CRIT CARE MED, V31, P1647, DOI 10.1097/01.CCM.0000063260.07222.76; Liao DP, 1999, ENVIRON HEALTH PERSP, V107, P521, DOI 10.2307/3434393; Liao DP, 2004, AM J EPIDEMIOL, V159, P768, DOI 10.1093/aje/kwh109; Lin M, 2002, ENVIRON HEALTH PERSP, V110, P575; Mar TF, 2004, INHAL TOXICOL, V16, P809, DOI 10.1080/08958370490506646; MICHEL O, 1992, AM REV RESPIR DIS, V146, P352; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; Michel O, 1997, AM J RESP CRIT CARE, V156, P1157; Mueller-Anneling L, 2004, ENVIRON HEALTH PERSP, V112, P583, DOI 10.1289/ehp.6552; *NHLBI, 2003, UPD SEL TOP 2002; O'Neill MS, 2005, CIRCULATION, V111, P2913, DOI 10.1161/CIRCULATIONAHA.104.517110; Pacheco KA, 2003, AM J RESP CRIT CARE, V167, P983, DOI 10.1164/rccm.2112062; Park SK, 2005, ENVIRON HEALTH PERSP, V113, P304, DOI 10.1289/ehp.7447; Peel JL, 2005, EPIDEMIOLOGY, V16, P164, DOI 10.1097/01.ede.0000152905.42113.db; Pekkanen J, 2002, CIRCULATION, V106, P933, DOI 10.1161/01.CIR.0000027561.41736.3C; Peters A, 2004, NEW ENGL J MED, V351, P1721, DOI 10.1056/NEJMoa040203; Pope CA, 1999, AM HEART J, V138, P890, DOI 10.1016/S0002-8703(99)70014-1; Pope CA, 2004, ENVIRON HEALTH PERSP, V112, P339, DOI 10.1289/ehp.6588; Rabinovitch N, 2005, J ALLERGY CLIN IMMUN, V116, P1053, DOI 10.1016/j.jaci.2005.08.045; Riediker M, 2004, AM J RESP CRIT CARE, V169, P934, DOI 10.1164/rccm.200310-1463OC; Ruckerl R, 2006, AM J RESP CRIT CARE, V173, P432, DOI 10.1164/rccm.200507-1123OC; Sajadieh A, 2004, EUR HEART J, V25, P363, DOI 10.1016/j.ehj.2003.12.003; Sarnat JA, 2000, J AIR WASTE MANAGE, V50, P1184; Sheppard L, 1999, EPIDEMIOLOGY, V10, P23, DOI 10.1097/00001648-199901000-00006; Soukup JM, 2001, TOXICOL APPL PHARM, V171, P20, DOI 10.1006/taap.2000.9096; Sullivan JH, 2005, THORAX, V60, P462, DOI 10.1136/thx.2004.027532; Sun QH, 2005, JAMA-J AM MED ASSOC, V294, P3003, DOI 10.1001/jama.294.23.3003; Suwa T, 2002, EXP LUNG RES, V28, P1, DOI 10.1080/019021402753355508; Thorne PS, 2005, AM J RESP CRIT CARE, V172, P1371, DOI 10.1164/rccm.200505-758OC; TIMONEN KL, 2006, J EXPO SCI ENV EPID, V16, P16332; Tomao E, 2002, ANN SAUDI MED, V22, P287; United States Environmental Protection Agency, 1990, NAT AMB AIR QUAL STA; Voss LJ, 2004, BIOL NEONATE, V86, P39, DOI 10.1159/000077452; Wheeler A, 2006, ENVIRON HEALTH PERSP, V114, P560, DOI 10.1289/ehp.8337; Williams R, 2003, ATMOS ENVIRON, V37, P5365, DOI 10.1016/j.atmosenv.2003.09.010; Williams R, 2003, ATMOS ENVIRON, V37, P5349, DOI 10.1016/j.atmosenv.2003.09.019; YUE W, 2006, INT J CARDIOL; Zeka A, 2005, OCCUP ENVIRON MED, V62, P718, DOI 10.1136/oem.2004.017012	60	77	78	0	17	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	2007	115	5					709	714		10.1289/ehp.9499		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	163KZ	WOS:000246159900029	17520057	
J	Mutti, A; Corradi, M; Goldoni, M; Vettori, MV; Bernard, A; Apostoli, P				Mutti, A; Corradi, M; Goldoni, M; Vettori, MV; Bernard, A; Apostoli, P			Exhaled metallic elements and serum pneumoproteins in asymptomatic smokers and patients with COPD or asthma	CHEST			English	Article						COPD; exhaled breath condensate; metals; pneumoproteins; trace elements	CLARA CELL PROTEIN; BREATH CONDENSATE; OXIDATIVE STRESS; TRACE-ELEMENTS; PULMONARY-DISEASE; TOBACCO-SMOKE; CADMIUM; CC16; DETERMINANTS; EMPHYSEMA	Study objectives: The aim of this study was to characterize the elemental composition of exhaled breath condensate (EBC) in order to identify new biomarkers of exposure and susceptibility in COPD patients. Serum pneumoproteins were used as lung-specific biomarkers of effect. Design: EBC was obtained from 50 healthy subjects, 30 healthy smokers, 30 asthmatics, and 50 patients with stable COPD, and was collected by cooling exhaled air. Trace elements and toxic metals in the samples were measured by means of inductively coupled plasma-mass spectrometry and electrothermal atomic absorption spectroscopy. The serum pneumoproteins were immuno-assayed. Results: The EBC of COPD subjects had higher levels of such toxic elements as lead, cadmium, and aluminum, and lower levels of iron and copper, than that of the nonsmoking control subjects. There were no between-group differences in surfactant protein (SP)-A and SP-B levels. Clara-cell protein and SP-D levels were negatively and positively influenced, respectively, by tobacco smoke. Conclusions: Our results show that toxic metals and transition elements are detectable in the EBC of studied subjects. We propose new biomarkers of exposure as a means of assessing the target tissue dose of carcinogenic and pneumotoxic substances from tobacco smoke or polluted workplaces, and the use of the transition elements involved in redox systems of oxidative stress as disease biomarkers associated with effect or susceptibility. Together with biomarkers of effect, such as serum pneumoproteins, the elemental composition of EBC may be clinically useful in distinguishing similar diseases.	Univ Parma, Lab Ind Toxicol, Dept Clin Med Nephrol & Hlth Sci, I-43100 Parma, Italy; Univ Parma, Natl Inst Occupat Safety & Prevent, I-43100 Parma, Italy; Univ Parma, Res Ctr, I-43100 Parma, Italy; Catholic Univ Louvain, Toxicol Unit, Brussels, Belgium; Univ Brescia, Lab Ind Hyg, Dept Expt & Appl Med, Brescia, Italy	Mutti, A (reprint author), Univ Parma, Lab Ind Toxicol, Dept Clin Med Nephrol & Hlth Sci, Via Gramsci 14, I-43100 Parma, Italy.	antonio.mutti@unipr.it	goldoni, matteo/E-9153-2011; BERNARD, Alfred/A-6511-2010; Mutti, Antonio/C-1095-2011	goldoni, matteo/0000-0002-1342-3921; BERNARD, Alfred/0000-0003-3171-3743; Mutti, Antonio/0000-0003-2189-3808; corradi, massimo/0000-0002-2808-4184	NHLBI NIH HHS [R01 HL072323, R01 HL72323, R01 HL072323-04]		Apostoli P, 2002, J CHROMATOGR B, V778, P63, DOI 10.1016/S0378-4347(01)00442-X; Apostoli P, 1997, J TRACE ELEM MED BIO, V11, P182; Bachelet M, 2002, FREE RADICAL RES, V36, P99, DOI 10.1080/10715760290001218; Baldi S, 2001, AM J RESP CRIT CARE, V164, P585; BERNARD A, 1992, LANCET, V339, P1620, DOI 10.1016/0140-6736(92)91891-B; CHIBA M, 1992, B WORLD HEALTH ORGAN, V70, P269; Doyle IR, 1998, AM J RESP CRIT CARE, V158, P1528; Effros RM, 2005, J APPL PHYSIOL, V99, P1286, DOI 10.1152/japplphysiol.00362.2005; Goldoni M, 2004, ENVIRON HEALTH PERSP, V112, P1293, DOI 10.1289/ehp.7108; Goldoni Matteo, 2005, BMC Pulm Med, V5, P10, DOI 10.1186/1471-2466-5-10; Hendrick DJ, 2004, THORAX, V59, P184, DOI 10.1136/thx.2003.018432; Hermans C, 1999, AM J RESP CRIT CARE, V159, P646; Hermans C, 2003, BIOMARKERS, V8, P461, DOI 10.1080/13547500310001647021; Hermans C, 1998, CLIN CHIM ACTA, V272, P101, DOI 10.1016/S0009-8981(98)00006-0; Horvath I, 2005, EUR RESPIR J, V26, P523, DOI 10.1183/09031936.05.00029705; Jiang F, 2003, BRIT J PHARMACOL, V139, P1127, DOI 10.1038/sj.bjp.0705354; Karadag F, 2004, RESPIROLOGY, V9, P33, DOI 10.1111/j.1440-1843.2003.00534.x; Kharitonov SA, 2001, AM J RESP CRIT CARE, V163, P1693; KONDO H, 1993, AM J PHYSIOL, V265, pE839; Kubala-Kukus A, 1999, NUCL INSTRUM METH B, V150, P193, DOI 10.1016/S0168-583X(98)01057-X; Leth-Larsen R, 2004, MOL HUM REPROD, V10, P149, DOI 10.1093/molehr/gah022; MacNee W, 2003, EUR RESPIR J, V21, P47; MAIER EA, 1985, CLIN CHEM, V31, P551; Mannino DM, 2004, THORAX, V59, P194, DOI 10.1136/thorax.2003.012054; Mutlu GM, 2001, AM J RESP CRIT CARE, V164, P731; Nagae H, 1997, CLIN CHIM ACTA, V266, P157, DOI 10.1016/S0009-8981(97)00124-1; National Heart Lung and Blood Institute of the National Institutes of Health (NIH) and Giovanni Lorenzini Medical Science Foundation, 2002, NIH PUBL; *NRC, 1987, ENV HLTH PERSPECT, V74, P1; Pauwels Romain A., 2001, American Journal of Respiratory and Critical Care Medicine, V163, P1256; Pellegrino R, 1997, EUR RESPIR J, V10, P468, DOI 10.1183/09031936.97.10020468; Pope III CAD, 1999, AIR POLLUTION HLTH, P673; Rahman I, 2004, REDOX REP, V9, P125, DOI 10.1179/135100004225005219; ROMEO L, 1992, SCI TOTAL ENVIRON, V120, P103, DOI 10.1016/0048-9697(92)90221-D; Rustemeier K, 2002, FOOD CHEM TOXICOL, V40, P93, DOI 10.1016/S0278-6915(01)00085-0; Saetta M, 2001, AM J RESP CRIT CARE, V163, P1304; Tatrai E, 2001, J APPL TOXICOL, V21, P479, DOI 10.1002/jat.784	36	77	84	0	14	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	MAY	2006	129	5					1288	1297		10.1378/chest.129.5.1288		10	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	043RE	WOS:000237618400026	16685021	
J	Alati, R; Al Mamun, A; O'Callaghan, M; Najman, JM; Williams, GM				Alati, R; Al Mamun, A; O'Callaghan, M; Najman, JM; Williams, GM			In utero and postnatal maternal smoking and asthma in adolescence	EPIDEMIOLOGY			English	Article							ENVIRONMENTAL TOBACCO-SMOKE; CHILDHOOD LUNG-FUNCTION; EARLY-ONSET ASTHMA; PARENTAL SMOKING; PASSIVE SMOKING; RESPIRATORY SYMPTOMS; CHILDREN; EXPOSURE; PREGNANCY; HEALTH	Background: Asthma in early childhood has been associated with maternal smoking during pregnancy and parental smoking soon after birth. However, less is known about these exposures and the development of asthma symptoms in adolescence. Methods: Data were taken from the Mater University Study, of Pregnancy, a large birth cohort study of mothers and children enrolled in Brisbane, Australia, beginning in 1981. Smoking was assessed at 2 stages during pregnancy and at the 6-month and 5-year follow-up visits. Asthma was assessed from maternal reports that were provided when the child was age 14 years. We conducted multivariable multinomial logistic regression analyses to assess the effect of maternal smoking on asthma symptoms. Results: There was a strong sex interaction such that girls whose mothers had smoked heavily (20 or more cigarettes per day) in pregnancy and at the 6-month follow up had increased odds of experiencing asthma symptoms at age 14 (odds ratio = 1.96; 95% confidence interval = 1.25-3.08). The contribution of heavy smoking during pregnancy appeared to be stronger than heavy smoking after the birth. No similar associations were seen for boys. Conclusion: Female adolescents whose mothers smoked heavily during the fetal period and the early months of life have increased risk of asthma symptoms in adolescence. In utero exposure to heavy smoking was found to have a stronger effect than postnatal environmental tobacco exposure.	Univ Queensland, Sch Populat Hlth, Brisbane, Qld 4006, Australia; Mater Childrens Hosp, Brisbane, Qld, Australia; Univ Queensland, Sch Social Sci, St Lucia, Qld, Australia	Alati, R (reprint author), Univ Queensland, Sch Populat Hlth, 1st Floor,Publ Hlth Bldg, Brisbane, Qld 4006, Australia.	r.alati@sph.uq.edu.au	Najman, Jackob/B-1527-2008; O'Callaghan, Michael/F-4414-2010; Alati, Rosa/G-2523-2010; Alati, Rosa /A-2335-2014; Mamun, Abdullah/A-4673-2011	Alati, Rosa /0000-0002-9240-3450; 			Achenbach TM, 1991, MANUAL CHILD BEHAV C; Becklake MR, 1999, THORAX, V54, P1119; Committee on the Assessment of Asthma and Indoor Air, 2000, CLEAR AIR ASTHM IND; Cook DG, 1999, THORAX, V54, P357; Coultas DB, 1998, THORAX, V53, P381; Dell S, 2001, ARCH PEDIAT ADOL MED, V155, P1261; Dezateux C, 1999, AM J RESP CRIT CARE, V159, P403; Gilliland FD, 2000, THORAX, V55, P271, DOI 10.1136/thorax.55.4.271; Gilliland FD, 2003, AM J RESP CRIT CARE, V167, P917, DOI 10.1164/rccm.200206-616OC; Gilliland FD, 2001, AM J RESP CRIT CARE, V163, P429; Hofhuis W, 2003, ARCH DIS CHILD, V88, P1086, DOI 10.1136/adc.88.12.1086; Hogan JW, 2004, STAT MED, V23, P1455, DOI 10.1002/sim.1728; Jaakkola JJK, 2004, AM J PUBLIC HEALTH, V94, P136, DOI 10.2105/AJPH.94.1.136; Janson C, 2001, LANCET, V358, P2103, DOI 10.1016/S0140-6736(01)07214-2; LEWIS S, 1995, EUR RESPIR J, V8, P349, DOI 10.1183/09031936.95.08030349; Li JS, 1999, PEDIATR PULM, V27, P5, DOI 10.1002/(SICI)1099-0496(199901)27:1<5::AID-PPUL3>3.0.CO;2-5; Lux AL, 2000, ARCH DIS CHILD, V83, P307, DOI 10.1136/adc.83.4.307; Mrazek DA, 1999, PEDIATR PULM, V27, P85, DOI 10.1002/(SICI)1099-0496(199902)27:2<85::AID-PPUL4>3.0.CO;2-B; Peat J K, 2001, Paediatr Respir Rev, V2, P207, DOI 10.1053/prrv.2001.0142; Sears MR, 2003, NEW ENGL J MED, V349, P1414, DOI 10.1056/NEJMoa022363; Sears MR, 2002, LANCET, V360, P901, DOI 10.1016/S0140-6736(02)11025-7; SHERRILL DL, 1992, AM REV RESPIR DIS, V145, P1136; Stein RT, 1999, AM J EPIDEMIOL, V149, P1030; Strachan DP, 1996, BRIT MED J, V312, P1195; Strachan DP, 1998, THORAX, V53, P204; TAGER IB, 1995, AM J RESP CRIT CARE, V152, P977	26	77	79	0	8	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	1044-3983			EPIDEMIOLOGY	Epidemiology	MAR	2006	17	2					138	144		10.1097/01.ede.0000198148.02347.33		7	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	015OX	WOS:000235561800007	16477253	
J	Winther, L; Arnved, J; Malling, HJ; Nolte, H; Mosbech, H				Winther, L; Arnved, J; Malling, HJ; Nolte, H; Mosbech, H			Side-effects of allergen-specific immunotherapy. A prospective multi-centre study	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						asthma; clinical database; immunotherapy; rhinitis; side-effects	SYSTEMIC REACTIONS; EXTRACT; SAFETY; EFFICACY	Background and objective The safety of allergen-specific immunotherapy (SIT) is a parameter of great interest in the overall assessment of the treatment. A clinical database was developed in order to obtain early warnings of changes in the frequency and severity of side-effects and sufficient data for the evaluation of possible risk factors. Methods During a 3-year period, four allergy centres in Copenhagen, Denmark, included data from all patients initiating SIT to a common database. Information on initial allergic symptoms, allergens used for treatment, treatment regimens and systemic side-effects (SSEs) during the build-up phase was collected. Results A total of 1038 patients received treatment with 1709 allergens (timothy, birch, mugwort, house dust mite (HDM), cat, and wasp and bee venom), 23 047 injections in total. Most SIT patients completed the updosing phase without side-effects, but there was a significant difference between allergens: wasp (89%), birch (82%), HDM (81%), cat (74%) and grass (70%) (P=0.004). A total of 582 SSEs were registered in 341 patients. Most side-effects were mild grade 2 reactions (78%). A difference in severity between allergens was observed (P=0.02), with grass giving most problems. The type of allergen but not patient- or centre-related parameters seemed predictive of side-effects. Conclusions Allergen extracts differ in their tendency to produce side-effects. Multi-centre studies like the present one allow more patients to be evaluated, and thereby provide a more efficient surveillance of side-effects. Online Internet-based registration to a central national database of every allergen injection would be an even more powerful tool for evaluation of risk factors and surveillance of side-effects.	Copenhagen Univ Hosp, Rigshosp, Allergy Clin, DK-2100 Copenhagen O, Denmark; Chest & Allergy Clin, Copenhagen, Denmark; Copenhagen Univ Hosp, Dept Internal Med 1, Bispebjerg, Denmark; Copenhagen Univ Hosp, Dept Internal Med B, Frederiksberg, Denmark	Winther, L (reprint author), Copenhagen Univ Hosp, Rigshosp, Allergy Clin 4222, 9 Blegdamsvej, DK-2100 Copenhagen O, Denmark.	lone.winther@dadlnet.dk					BOUSQUET J, 1989, J ALLERGY CLIN IMMUN, V83, P797, DOI 10.1016/0091-6749(89)90017-1; Bousquet J., 1998, Allergy (Copenhagen), V53, P1; Brockow K, 1997, J ALLERGY CLIN IMMUN, V100, P458; Gastaminza G, 2003, CLIN EXP ALLERGY, V33, P470, DOI 10.1046/j.1365-2222.2003.01644.x; HAUGAARD L, 1993, J ALLERGY CLIN IMMUN, V91, P709, DOI 10.1016/0091-6749(93)90190-Q; MALLING HJ, 1993, ALLERGY, V48, P9; Mellerup MT, 2000, CLIN EXP ALLERGY, V30, P1423, DOI 10.1046/j.1365-2222.2000.00910.x; Moreno C, 2004, CLIN EXP ALLERGY, V34, P527, DOI 10.1111/j.1365-2222.2004.1819.x; Mosbech H, 2000, ALLERGY, V55, P1005, DOI 10.1034/j.1398-9995.2000.00587.x; Nettis E, 2002, CLIN EXP ALLERGY, V32, P1745, DOI 10.1046/j.1365-2222.2002.01544.x; Nielsen L, 1996, J ALLERGY CLIN IMMUN, V97, P1207, DOI 10.1016/S0091-6749(96)70186-0; Winther L, 2000, ALLERGY, V55, P827, DOI 10.1034/j.1398-9995.2000.00368.x	12	77	79	0	1	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	MAR	2006	36	3					254	260		10.1111/j.1365-2222.2006.02340.		7	Allergy; Immunology	Allergy; Immunology	015YS	WOS:000235588200002	16499635	
J	Wohrl, S; Vigl, K; Zehetmayer, S; Hiller, R; Jarisch, R; Prinz, M; Stingl, G; Kopp, T				Wohrl, S; Vigl, K; Zehetmayer, S; Hiller, R; Jarisch, R; Prinz, M; Stingl, G; Kopp, T			The performance of a component-based allergen-microarray in clinical practice	ALLERGY			English	Article						allergen biochip; allergen microarray; allergy; bronchial asthma; component-resolved diagnosis; diagnosis; methodology; rhinoconjunctivitis	RECOMBINANT ALLERGENS; RESOLVED DIAGNOSIS; POLLEN ALLERGENS; IN-VITRO; MITE ALLERGENS; GRASS-POLLEN; IGE; SENSITIZATION; STANDARDIZATION; REACTIVITY	Background: Currently, the diagnosis of IgE-mediated allergy is based on allergen-specific history and diagnostic procedures using natural allergen extracts for in vivo and in vitro tests. Objective: The aim of the study was to comparatively analyse a new component-based allergen-microarray and the 'quasi-standard' ImmunoCAP((R)) for their clinical relevance in patients with allergic rhinoconjunctivitis to five aeroallergens [house dust mite (HDM), cat dander, birch, grass and mugwort pollen] in a prospective, double-centre study. Methods: We enrolled 120 subjects at the two study centres. Allergic patients were defined as having an allergen-specific history plus a concomitant positive skin-prick test (SPT) to natural allergen extracts and specific serum IgE was measured by both methods. Each allergen was analysed separately. Results: The microarray performed equally well in receiver-operating characteristic curve (ROC) analyses when compared with the CAP in cat (23 allergic vs 97 non-allergic, ROC area under the curve microarray 0.950 vs CAP 0.894, P = 0.211), birch (31/89, 0.908 vs 0.878, P = 0.483) and grass pollen (47/73, 0.923 vs 0.915, P = 0.770). It was slightly less sensitive in HDM-allergic subjects (26 allergic vs 94 non-allergic, ROC area microarray 0.808 vs CAP 0.911, P = 0.053) and displayed a reduced sensitivity in the mugwort pollen-allergic patients (17/103, 0.723 vs 0.879, P = 0.032). Conclusions: Component-based testing and the whole-allergen CAP are equally relevant in the diagnosis of grass-, birch- and cat-allergic patients. Although slightly less sensitive, the microarray is sufficient for the diagnosis of HDM-allergic patients, but needs alternative and/or additional components for detecting mugwort allergy.	Med Univ Vienna MUW, Dept Dermatol, Div Immunol Allergy & Infect Dis, A-1090 Vienna, Austria; Med Univ Vienna MUW, Core Unit Med Stat & Informat, Sect Med Stat, A-1090 Vienna, Austria; VBC GENOMICS, Vienna, Austria; FAZ Floridsdorf Allergy Ctr, Vienna, Austria; Med Univ Vienna MUW, Core Unit Med Stat & Informat, Sect Med Comp Vis, A-1090 Vienna, Austria	Wohrl, S (reprint author), Med Univ Vienna MUW, Dept Dermatol, Div Immunol Allergy & Infect Dis, Wahringer Gurtel 18-20, A-1090 Vienna, Austria.		Wohrl, Stefan/B-6954-2013	Wohrl, Stefan/0000-0002-6324-0007			Ballmer-Weber BK, 2002, J ALLERGY CLIN IMMUN, V110, P167, DOI 10.1067/mai.2002.125601; Bousquet J, 2001, J ALLERGY CLIN IMMUN, V108, P147, DOI DOI 10.1067/MAI.2001.118891; Corti V, 2005, PROTEOMICS, V5, P729, DOI 10.1002/pmic.200401038; Deinhofer K, 2004, METHODS, V32, P249, DOI 10.1016/j.ymeth.2003.08.018; DELONG ER, 1988, BIOMETRICS, V44, P837, DOI 10.2307/2531595; Dolen WK, 2003, ALLERGY, V58, P717, DOI 10.1034/j.1398-9995.2003.00281.x; DREBORG S, 1993, ALLERGY, V48, P49, DOI 10.1111/j.1398-9995.1993.tb04756.x; HARWANEGG C, 2004, PROTEIN MICROARRAYS, pCH13; Heiss S, 1999, J INVEST DERMATOL, V113, P830, DOI 10.1046/j.1523-1747.1999.00796.x; Herz U, 2004, METHODS, V32, P271, DOI 10.1016/j.ymeth.2003.08.013; Hiller R, 2002, FASEB J, V16, P414, DOI 10.1096/fj.01-0711fje; JAHNSCHMID B, 2003, CLIN EXP ALLERGY, V333, P1443; JARISCH R, 2000, WIENER GESUNDHEITSBE, P80; JensenJarolim E, 1997, ALLERGY, V52, P844, DOI 10.1111/j.1398-9995.1997.tb02156.x; Johansson SGO, 2004, EXPERT REV MOL DIAGN, V4, P273, DOI 10.1586/14737159.4.3.273; Kalogeromitros D, 2004, OCCUP ENVIRON MED, V61, P709, DOI 10.1136/oem.2003.012427; Kim TE, 2002, EXP MOL MED, V34, P152; Leonard R, 2005, J BIOL CHEM, V280, P7932, DOI 10.1074/jbc.M410407200; MALANDAIN H, 2003, IMMUNOANALYSE BIOL S, V18, P144, DOI 10.1016/S0923-2532(03)00047-4; Mari A, 2003, CLIN EXP ALLERGY, V33, P43, DOI 10.1046/j.1365-2222.2003.01569.x; Moverare R, 2002, INT ARCH ALLERGY IMM, V128, P325, DOI 10.1159/000063855; Osterballe M, 2005, ALLERGY, V60, P218, DOI 10.1111/j.1398-9995.2005.00674.x; Pittner G, 2004, CLIN EXP ALLERGY, V34, P597, DOI 10.1111/j.1365-2222.2004.1930.x; Prinz M, 2005, ST HEAL T, V116, P441; Puc M, 2003, ANN AGR ENV MED, V10, P143; Rossi RE, 2001, ALLERGY, V56, P1180, DOI 10.1034/j.1398-9995.2001.00258.x; Sanz ML, 1996, J INVEST ALLERG CLIN, V6, P152; Shreffler WG, 2004, J ALLERGY CLIN IMMUN, V113, P776, DOI 10.1016/j.jaci.2003.12.588; Thomas WR, 2002, INT ARCH ALLERGY IMM, V129, P1, DOI 10.1159/000065179; Tresch S, 2003, CLIN EXP ALLERGY, V33, P1153, DOI 10.1046/j.1365-2222.2003.01717.x; Valenta R, 1998, ALLERGY, V53, P552, DOI 10.1111/j.1398-9995.1998.tb03930.x; Valenta R, 1999, CLIN EXP ALLERGY, V29, P896; Yman L, 2001, ALLERGY, V56, P70, DOI 10.1034/j.1398-9995.2001.00921.x	33	77	82	1	6	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0105-4538			ALLERGY	Allergy	MAR	2006	61	5					633	639		10.1111/j.1398-9995.2006.01078.x		7	Allergy; Immunology	Allergy; Immunology	027CY	WOS:000236392500020	16629796	
J	Celli, BR; Halbert, RJ; Nordyke, RJ; Schau, B				Celli, BR; Halbert, RJ; Nordyke, RJ; Schau, B			Airway obstruction in never smokers: Results from the Third National Health and Nutrition Examination Survey	AMERICAN JOURNAL OF MEDICINE			English	Article						environmental exposure; obstructive lung diseases; prevalence; risk factors; socioeconomic factors; smoking	CHRONIC RESPIRATORY SYMPTOMS; PULMONARY-DISEASE; PASSIVE SMOKING; LUNG-FUNCTION; SOCIOECONOMIC-STATUS; GENERAL-POPULATION; FLOW OBSTRUCTION; RISK-FACTORS; NHANES-III; EXPOSURE	PURPOSE: Chronic obstructive pulmonary disease (COPD) is usually described as a disease of cigarette smoking. COPD is rarely considered in persons with no smoking history except in the context of another exposure. Accordingly, the disease has not been well characterized in these "never smokers." METHODS: We evaluated airway obstruction (defined as forced expiratory Volume in I second/forced vital capacity < 0.70) in US adults aged 30 to 80 years interviewed in the Third National Health and Nutrition Examination Survey with valid spirometry who had never smoked. Previously described risk factors were examined for their association with obstruction in bivariate and multivariate analyses. RESULTS: Never smokers represented 42% of the Third National Health and Nutrition Examination Survey Population aged 30 to 80 years, with obstruction prevalence of 91 per 1000. Never smokers accounted for 4.56 million cases of obstruction, or 23% of the total burden. Among these obstructed never smokers, 19% reported a prior diagnosis of asthma alone, and 12.5% reported COPD (alone or with asthma), leaving 68.5% with no prior respiratory diagnosis. After adjustment for other factors, hi, her rates of obstruction were significantly associated with increasing age, male sex. lower body mass index, and a history of allergies. CONCLUSIONS: Never smokers represent a significant proportion of airway obstruction in US adults. Only one fifth of obstruction in this group is explained by asthma. COPD may explain much of the remainder, although known risk factors were not explanatory in this dataset. Recommendations that lung health screening programs be limited to smokers should be reconsidered. (c) 2005 Elsevier Inc. All rights reserved.	Cerner Hlth Insights, Beverly Hills, CA 90212 USA; Tufts Univ, Sch Med, Caritas St Elizabeths Med Ctr, Boston, MA 02111 USA; Univ Calif Los Angeles, Sch Publ Hlth, Dept Community Hlth Sci, Los Angeles, CA 90024 USA; Boehringer Ingelheim Int GmbH, Ingelheim, Germany; Univ Calif Los Angeles, Sch Publ Hlth, Dept Hlth Serv, Los Angeles, CA 90024 USA	Halbert, RJ (reprint author), Cerner Hlth Insights, 9100 Wilshire Blvd,Suite 655E, Beverly Hills, CA 90212 USA.	rhalbert@cerner.com					Abramson M, 2002, RESPIROLOGY, V7, P325, DOI 10.1046/j.1440-1843.2002.00408.x; American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P1285, DOI 10.1164/ajrccm/136.5.1285; BAKKE PS, 1991, THORAX, V46, P863, DOI 10.1136/thx.46.12.863; BECKLAKE MR, 1985, CHEST, V88, P608, DOI 10.1378/chest.88.4.608; Berglund DJ, 1999, CHEST, V115, P49, DOI 10.1378/chest.115.1.49; Birring SS, 2002, AM J RESP CRIT CARE, V166, P1078, DOI 10.1164/rccm.200203-245OC; Calverley PMA, 2000, CHEST, V117, p365S, DOI 10.1378/chest.117.5_suppl_2.365S; Celli BR, 2004, NEW ENGL J MED, V350, P1005, DOI 10.1056/NEJMoa021322; CHEN B H, 1990, World Health Statistics Quarterly, V43, P127; Chen Y, 2000, J CLIN EPIDEMIOL, V53, P755, DOI 10.1016/S0895-4356(99)00211-5; Chinn S, 2002, THORAX, V57, P1028, DOI 10.1136/thorax.57.12.1028; Coultas DB, 2003, CURR OPIN PULM MED, V9, P96, DOI 10.1097/00063198-200303000-00002; DAYAL HH, 1994, ENVIRON RES, V65, P161, DOI 10.1006/enrs.1994.1029; Dennis RJ, 1996, CHEST, V109, P115, DOI 10.1378/chest.109.1.115; Eisner MD, 2003, OCCUP ENVIRON MED, V60, P759, DOI 10.1136/oem.60.10.759; Eisner MD, 2002, ENVIRON HEALTH PERSP, V110, P765; GILLUM RF, 1990, J NATL MED ASSOC, V82, P417; Global Initiative for Asthma, GLOB STRAT ASTHM MAN; Global Initiative for Chronic Obstructive Lung Disease, GLOB STRAT DIAGN MAN; GULSVIK A, 1979, SCAND J RESPIR DIS, V60, P286; Hardie JA, 2002, EUR RESPIR J, V20, P1117, DOI 10.1183/09031936.02.00023202; HARLOW SD, 1989, AM J EPIDEMIOL, V129, P233; HIGGINS MW, 1977, AM REV RESPIR DIS, V116, P403; Hnizdo E, 2002, AM J EPIDEMIOL, V156, P738, DOI 10.1093/aje/kwf105; Hurd SS, 2000, CHEST, V117, p336S, DOI 10.1378/chest.117.5_suppl_2.336S; Iqbal A, 2002, RESPIROLOGY, V7, P233, DOI 10.1046/j.1440-1843.2002.00399.x; JABINE TB, DATA EVALUATION METH, V2; Janson C, 2001, LANCET, V358, P2103, DOI 10.1016/S0140-6736(01)07214-2; KORN RJ, 1987, AM REV RESPIR DIS, V136, P298; Larsson ML, 2003, EUR RESPIR J, V21, P672, DOI 10.1183/09031936.03.00033702; Le Moual N, 2000, OCCUP ENVIRON MED, V57, P126, DOI 10.1136/oem.57.2.126; LEUENBERGER P, 1994, AM J RESP CRIT CARE, V150, P1222; Mannino DM, 2000, ARCH INTERN MED, V160, P1683, DOI 10.1001/archinte.160.11.1683; Melbostad E, 1997, SCAND J WORK ENV HEA, V23, P271; Meyer PA, 2002, CHEST, V122, P2003, DOI 10.1378/chest.122.6.2003; National Center for Health Statistics, 1994, DHHS PUBL, V94-1104; *NAT HEART LUNG BL, MORB MORT 2004 CHART; OXMAN AD, 1993, AM REV RESPIR DIS, V148, P38; PEAT JK, 1990, THORAX, V45, P32, DOI 10.1136/thx.45.1.32; POPE CA, 1995, ENVIRON HEALTH PERSP, V103, P472, DOI 10.2307/3432586; Prescott E, 1999, EUR RESPIR J, V13, P1109, DOI 10.1034/j.1399-3003.1999.13e28.x; *RES TRIANGL I, 2001, SUDAAN COMP PROGR; SAMET JM, 1988, AM REV RESPIR DIS, V137, P815; Samet JM, 2000, NEW ENGL J MED, V343, P1742, DOI 10.1056/NEJM200012143432401; SAS Institute Inc., 2000, SAS COMP PROGR VERS; Sethi JM, 2000, CLIN CHEST MED, V21, P67, DOI 10.1016/S0272-5231(05)70008-3; WHITTEMORE AS, 1995, AM J PUBLIC HEALTH, V85, P702, DOI 10.2105/AJPH.85.5.702; XU XP, 1995, AM J RESP CRIT CARE, V151, P41; Zuskin E, 1997, AM J IND MED, V31, P344, DOI 10.1002/(SICI)1097-0274(199703)31:3<344::AID-AJIM11>3.0.CO;2-0	49	77	77	0	0	EXCERPTA MEDICA INC	NEW YORK	650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 USA	0002-9343			AM J MED	Am. J. Med.	DEC	2005	118	12					1364	1372		10.1016/j.amjmed.2005.06.041		9	Medicine, General & Internal	General & Internal Medicine	996ER	WOS:000234157700012	16378780	
J	Ewan, PW; Clark, AT				Ewan, PW; Clark, AT			Efficacy of a management plan based on severity assessment in longitudinal and case-controlled studies of 747 children with nut allergy: proposal for good practice	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						food; nut; allergy; Management plan; anaphylaxis	PEANUT ALLERGY; ANAPHYLACTIC REACTIONS; FOOD CHALLENGES; PREVALENCE; FEATURES; SCHOOLS	There are few data on the long-term management of children with peanut/nut allergy. Advice is variable and often inadequate; further reactions are common. There is no consensus on the criteria for prescription of rescue medication, particularly adrenaline. A longitudinal prospective and case-control study in a tertiary allergy clinic. Patients/parents/school staff of 747 children with confirmed peanut or tree nut allergy received detailed verbal and written advice on nut avoidance, training in recognition and (self-) treatment of reactions and a written treatment plan. The severity of nut allergy was graded (mild-severe) and emergency medication was allocated according to our criteria: all received oral antihistamines, injected adrenaline (EpiPen) was given to those with reactions with airway narrowing, milder reactions to low-dose exposure or concomitant asthma. At annual follow-up over 25 906 patient-months (median: 39 months) retraining was given and details of further reactions (frequency, severity and treatment) were obtained. Criteria for allocation of EpiPen were evaluated. The worst reaction pre-enrolment was mild in 64% and moderate/severe in 36% (airway narrowing). Of 615 subjects followed up, 21% had a further reaction (eightfold reduction in frequency), mostly mild. There was a 60-fold reduction in the frequency of severe reactions. Of those with a moderate-severe initial reaction, 99.5% had no or a less severe follow-up reaction. No child with a mild or severe index reaction had a severe follow-up reaction. Only 1/615 (0.2%) had a severe follow-up reaction and only 2/615 (0.3%) used adrenaline, both successfully and had it available according to our criteria. Of mild-moderate reactions, 77% required oral antihistamines alone and 15% no treatment. Children who had follow-up reactions had more frequent and severe reactions pre-enrolment. The management plan greatly reduced the frequency and severity of further reactions and was successful for all children. Our criteria for selective prescription of EpiPen in the context of this management plan were appropriate. This is the first study to provide evidence on which to inform practice.	Univ Cambridge, Sch Clin, Dept Allergy, Addenbrookes NHS Trust, Cambridge CB2 2QQ, England	Clark, AT (reprint author), Univ Cambridge, Sch Clin, Dept Allergy, Addenbrookes NHS Trust, Cambridge CB2 2QQ, England.	atclark@doctors.org.uk					Bock SA, 2001, J ALLERGY CLIN IMMUN, V107, P191, DOI 10.1067/mai.2001.112031; Clark AT, 2003, CLIN EXP ALLERGY, V33, P1041, DOI 10.1046/j.1365-2745.2003.01624.x; Ewan PW, 1996, BRIT MED J, V312, P1074; Ewan PW, 2001, LANCET, V357, P111, DOI 10.1016/S0140-6736(00)03543-1; Grundy J, 2002, J ALLERGY CLIN IMMUN, V110, P784, DOI 10.1067/mai.2002.128802; Hourihane JO, 1996, BRIT MED J, V313, P518; Hourihane JO, 1997, CLIN EXP ALLERGY, V27, P634, DOI 10.1046/j.1365-2222.1997.d01-559.x; Kagan RS, 2003, J ALLERGY CLIN IMMUN, V112, P1223, DOI 10.1016/j.jaci.2003.09.026; Kapoor S, 2004, ALLERGY, V59, P185, DOI 10.1046/j.1398-9995.2003.00365.x; Moneret-Vautrin DA, 2001, ALLERGY, V56, P1071, DOI 10.1034/j.1398-9995.2001.00047.x; Pumphrey RSH, 2000, CLIN EXP ALLERGY, V30, P1144, DOI 10.1046/j.1365-2222.2000.00864.x; Roberts G, 2003, J ALLERGY CLIN IMMUN, V112, P168, DOI 10.1067/mai.2003.1569; Sampson HA, 2002, NEW ENGL J MED, V346, P1294, DOI 10.1056/NEJMcp012667; Sheikh A, 2000, BRIT MED J, V320, P1441, DOI 10.1136/bmj.320.7247.1441; Sicherer SH, 1998, PEDIATRICS, V102, part. no., DOI 10.1542/peds.102.1.e6; Sporik R, 2000, CLIN EXP ALLERGY, V30, P1540, DOI 10.1046/j.1365-2222.2000.00928.x; Tariq SM, 1996, BRIT MED J, V313, P514; Vickers DW, 1997, CLIN EXP ALLERGY, V27, P898; Watura JC, 2002, ARCH DIS CHILD, V86, P240, DOI 10.1136/adc.86.4.240; YUNGINGER JW, 1988, JAMA-J AM MED ASSOC, V260, P1450, DOI 10.1001/jama.260.10.1450	20	77	77	0	4	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	JUN	2005	35	6					751	756		10.1111/j.1365-2222.2005.02266.x		6	Allergy; Immunology	Allergy; Immunology	937WG	WOS:000229956100013	15969666	
J	Ramos-Barbon, D; Presley, JF; Hamid, QA; Fixman, ED; Martin, JG				Ramos-Barbon, D; Presley, JF; Hamid, QA; Fixman, ED; Martin, JG			Antigen-specific CD4(+) T cells drive airway in smooth muscle remodeling experimental asthma	JOURNAL OF CLINICAL INVESTIGATION			English	Article							BROWN-NORWAY RATS; REPEATED ALLERGEN EXPOSURE; DNA-SYNTHESIS; IN-VIVO; EXPRESSION; INFLAMMATION; LYMPHOCYTES; FAS; HYPERRESPONSIVENESS; TRANSDUCTION	Airway smooth muscle (ASM) growth contributes to the mechanism of airway hyperresponsiveness in asthma. Here we demonstrate that CD4(+) T cells, central to chronic airway inflammation, drive ASM remodeling in experimental asthma. Adoptive transfer of CD4(+) T cells from sensitized rats induced an increase in proliferation and inhibition of apoptosis of airway myocytes in naive recipients upon repeated antigen challenge, which resulted in an increase in ASM mass. Genetically modified CD4(+) T cells expressing enhanced GFP (EGFP) were localized by confocal microscopy in juxtaposition to ASM cells, which suggests that CD4(+) T cells may modulate ASM cell function through direct cell-cell interaction in vivo. Coculture of antigen-stimulated CD4(+) T cells with cell cycle-arrested ASM cells induced myocyte proliferation, dependent on T cell activation and direct T cell-myocyte contact. Reciprocally, direct cell contact prevented postactivation T cell apoptosis, which suggests receptor-mediated T cell-myocyte crosstalk. Overall, our data demonstrate that activated CD4(+) T cells drive ASM remodeling in experimental asthma and suggest that a direct cell-cell interaction participates in CD4(+) T cell regulation of myocyte turnover and induction of remodeling.	McGill Univ, Meakins Christie Labs, Montreal, PQ H2X 2P2, Canada; McGill Univ, Dept Anat & Cell Biol, Montreal, PQ H2X 2P2, Canada	Fixman, ED (reprint author), McGill Univ, Meakins Christie Labs, 3626 St Urbain St, Montreal, PQ H2X 2P2, Canada.	elizabeth.fixman@mcgill.ca; james.martin@mcgill.ca	RAMOS-BARBON, DAVID/C-6624-2009	RAMOS-BARBON, DAVID/0000-0002-9615-6557			Bousquet J, 2000, AM J RESP CRIT CARE, V161, P1720; Costa GL, 2000, J IMMUNOL, V164, P3581; de la Motte CA, 1999, J BIOL CHEM, V274, P30747, DOI 10.1074/jbc.274.43.30747; Elias JA, 2003, J CLIN INVEST, V111, P291, DOI 10.1172/JCI200317748; EVANS LH, 1990, J VIROL, V64, P6176; Galipeau J, 1999, CANCER RES, V59, P2384; GAVETT SH, 1995, J EXP MED, V182, P1527, DOI 10.1084/jem.182.5.1527; Geng YJ, 1997, ARTERIOSCL THROM VAS, V17, P2200; Hamann KJ, 1998, AM J RESP CELL MOL, V19, P537; Hamann KJ, 2000, AM J PHYSIOL-LUNG C, V278, pL618; JAMES AL, 1989, AM REV RESPIR DIS, V139, P242; JAMES AL, 1988, AM REV RESPIR DIS, V138, P136; LAMBERT RK, 1993, J APPL PHYSIOL, V74, P2771; Lazaar AL, 2001, J IMMUNOL, V166, P155; Lazaar AL, 1998, J IMMUNOL, V161, P3120; LAZAAR AL, 1994, J EXP MED, V180, P807, DOI 10.1084/jem.180.3.807; Lee JH, 2001, AM J RESP CELL MOL, V25, P474; Leigh R, 2002, AM J RESP CELL MOL, V27, P526, DOI 10.1165/rcmb.2002-0048OC; Panettieri Reynold A. Jr., 2002, Journal of Allergy and Clinical Immunology, V110, pS269, DOI 10.1067/mai.2002.129429; Panettieri Reynold Jr., 1998, American Journal of Physiology, V274, pL417; PATERSON DJ, 1987, MOL IMMUNOL, V24, P1281, DOI 10.1016/0161-5890(87)90122-2; Ridgway W, 1998, J IMMUNOL, V161, P714; ROBINSON DS, 1992, NEW ENGL J MED, V326, P298, DOI 10.1056/NEJM199201303260504; Salmon M, 1999, BRIT J PHARMACOL, V127, P1151, DOI 10.1038/sj.bjp.0702669; Salmon M, 2000, AM J RESP CELL MOL, V23, P618; 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; WANG CG, 1993, AM REV RESPIR DIS, V148, P413; Watanabe A, 1997, AM J RESP CELL MOL, V16, P69; WATANABE A, 1995, J CLIN INVEST, V96, P1303, DOI 10.1172/JCI118165; Weinberg AD, 1999, J IMMUNOL, V162, P1818; WIGGS BR, 1990, J APPL PHYSIOL, V69, P849; Wise JT, 1999, J IMMUNOL, V162, P5592; Ying S, 1997, J IMMUNOL, V158, P3539; Zacour ME, 1996, AM J RESP CELL MOL, V15, P590; Zimmermann N, 2003, J CLIN INVEST, V111, P1863, DOI 10.1172/JCI200317912	36	77	82	0	3	AMER SOC CLINICAL INVESTIGATION INC	ANN ARBOR	35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA	0021-9738			J CLIN INVEST	J. Clin. Invest.	JUN	2005	115	6					1580	1589		10.1172/JCI19711		10	Medicine, Research & Experimental	Research & Experimental Medicine	932ZC	WOS:000229592300032	15902312	
J	Lucarelli, M; Gatti, AM; Savarino, G; Quattroni, P; Martinelli, L; Monari, E; Boraschi, D				Lucarelli, M; Gatti, AM; Savarino, G; Quattroni, P; Martinelli, L; Monari, E; Boraschi, D			Innate defence functions of macrophages can be biased by nano-sized ceramic and metallic particles	EUROPEAN CYTOKINE NETWORK			English	Article						nanoparticles; inflammation; macrophages; TLR receptors; cytokines; innate immunity	TOLL-LIKE RECEPTORS; SIGNALING PATHWAYS; HOST-DEFENSE; INFLAMMATION; ACTIVATION; SILICA; OLIGODEOXYNUCLEOTIDES; NANOPARTICLE; DISEASE; MICE	Nano-sized particles of ceramic and metallic materials are generated by high-tech industrial activities, and can be generated from worn-out replacement and prosthetic implants. The interaction with the human body of such nanoparticles has been investigated, with a particular emphasis on innate defence mechanisms. Human macrophages (PMA-differentiated myelomonocytic U-937 cells) were exposed in vitro to non-toxic concentrations of TiO2 SiO2 ZrO2 or Co nanoparticles, and their inflammatory response (expression of TLR receptors and co-receptors, and cytokine production) was examined. Expression of TLR receptors was generally unaffected by exposure to the different nanoparticles, except for some notable cases. Exposure to nanoparticles of ZrO2 (and to a lesser extent TiO2), upregulated expression of viral TLR receptors TLR3 and TLR7. Expression of TLR10 was also increased by TiO2 and ZrO2 nanoparticles. On the other hand, TLR9 expression was decreased by SiO2 nanoparticles, and expression of the co-receptor CD14 was inhibited by Co nanoparticles. Basal and LPS-induced production of cytokines 1L-1beta, TNF-alpha, and 1L-1Ra was examined in macrophages exposed to nanoparticles. SiO2 nanoparticles strongly biased naive macrophages towards inflammation (M1 polarisation), by selectively inducing production of inflammatory cytokines IL-1beta and TNF-alpha. SiO2 nanoparticles also significantly amplified the inflammatory phenotype of LPS-polarised M1 macrophages. Other ceramic nanoparticles had little influence on cytokine production, either in resting macrophages, or in LPS-activated cells. Generally, Co nanoparticles had an overall pro-inflammatory effect on naive macrophages, by reducing anti-inflammatory IL-1Ra and inducing inflammatory TNF-alpha. However, Co nanoparticles reduced production of IL-1beta and IL-1Ra, but not TNF-alpha, in LPS-polarised M1 macrophages. Thus, exposure to different nanoparticles can modulate, in different ways, the defence/inflammatory capacities of macrophages. A thorough analysis of these biasing effects may shed light on the mechanisms of pathogensis of several diseases based on dysregulation of the immune response (allergies, autoimmunity, tumours).	CNR, Inst Biomed Technol, Unit Immunobiol, I-56124 Pisa, Italy; Univ Modena, INFM, Lab Biomat, I-41100 Modena, Italy	Boraschi, D (reprint author), CNR, CNR, Inst Biomed Technol,Area Ric S Cataldo, Unit Immunobiol & Cell Differentiat,Lab Cytokines, Via G Moruzzi 1, I-56124 Pisa, Italy.	borasc@tin.it	Monari, Emanuela/K-7743-2016	Monari, Emanuela/0000-0003-0924-4928			Alexopoulou L, 2001, NATURE, V413, P732, DOI 10.1038/35099560; Anderson KV, 2000, CURR OPIN IMMUNOL, V12, P13, DOI 10.1016/S0952-7915(99)00045-X; Arend WR, 2002, CYTOKINE GROWTH F R, V13, P323, DOI 10.1016/S1359-6101(02)00020-5; Barton GM, 2002, CURR TOP MICROBIOL, V270, P81; Beutler B, 2002, CURR TOP MICROBIOL, V270, P109; Chen Yuxiang, 2003, Current Gene Therapy, V3, P273, DOI 10.2174/1566523034578339; Dinarello C A, 1998, Int Rev Immunol, V16, P457, DOI 10.3109/08830189809043005; Dinarello CA, 1999, METHODS, V19, P121, DOI 10.1006/meth.1999.0837; DRISCOLL KE, 1991, TOXICOL APPL PHARM, V111, P201, DOI 10.1016/0041-008X(91)90024-9; Feldmann M, 2001, ANNU REV IMMUNOL, V19, P163, DOI 10.1146/annurev.immunol.19.1.163; Florence AT, 2004, J DRUG TARGET, V12, P65, DOI 10.1080/10611860410001693706; Florence AT, 2001, ADV DRUG DELIVER REV, V50, pS69, DOI 10.1016/S0169-409X(01)00184-3; Gatti AM, 1996, J BIOMED MATER RES, V31, P475, DOI 10.1002/(SICI)1097-4636(199608)31:4<475::AID-JBM6>3.0.CO;2-I; Gordon S, 2003, NAT REV IMMUNOL, V3, P23, DOI 10.1038/nri978; Heil F, 2004, SCIENCE, V303, P1526, DOI 10.1126/science.1093620; HENCH LL, 1978, BIOMATERIALS INTERFA; Hoffmann JA, 1999, SCIENCE, V284, P1313, DOI 10.1126/science.284.5418.1313; Ioannou XP, 2003, VACCINE, V21, P4368, DOI 10.1016/S0264-410X(03)00437-7; Ito T, 2002, HUM IMMUNOL, V63, P1120, DOI 10.1016/S0198-8859(02)00750-4; Mantovani A, 2002, TRENDS IMMUNOL, V23, P549, DOI 10.1016/S1471-4906(02)02302-5; McCluskie MJ, 2001, CRIT REV IMMUNOL, V21, P103; Medzhitov R, 1998, CURR OPIN IMMUNOL, V10, P12, DOI 10.1016/S0952-7915(98)80024-1; Mosser DM, 2003, J LEUKOCYTE BIOL, V73, P209, DOI 10.1189/jlb.0602325; O'Neill L, 2000, BIOCHEM SOC T, V28, P557; Okamoto Masato, 2003, Journal of Medical Investigation, V50, P9; Parks CG, 1999, ENVIRON HEALTH PERSP, V107, P793, DOI 10.2307/3434342; Perera PY, 1997, J IMMUNOL, V158, P4422; PETERS K, 2004, 7 WORLD BIOM C P, P1881; Srivastava KD, 2002, AM J RESP CRIT CARE, V165, P527, DOI 10.1164/rccm.2106009; Takeda K, 2003, ANNU REV IMMUNOL, V21, P335, DOI 10.1146/annurev.immunol.21.120601.141126; Zhang DD, 2002, EXP LUNG RES, V28, P641, DOI 10.1080/01902140290108337	31	77	78	0	12	JOHN LIBBEY EUROTEXT LTD	MONTROUGE	127 AVE DE LA REPUBLIQUE, 92120 MONTROUGE, FRANCE	1148-5493			EUR CYTOKINE NETW	Eur. Cytokine Netw.	OCT-DEC	2004	15	4					339	346				8	Biochemistry & Molecular Biology; Cell Biology; Immunology	Biochemistry & Molecular Biology; Cell Biology; Immunology	888KS	WOS:000226373400008	15627643	
J	Ward, DJ; Ayres, JG				Ward, DJ; Ayres, JG			Particulate air pollution and panel studies in children: a systematic review	OCCUPATIONAL AND ENVIRONMENTAL MEDICINE			English	Review							PEAK EXPIRATORY FLOW; CHRONIC RESPIRATORY SYMPTOMS; TIME-SERIES ANALYSIS; ASTHMATIC-CHILDREN; METHODOLOGICAL ISSUES; FINE PARTICLES; PM10 POLLUTION; MEDICATION USE; LOS-ANGELES; MEXICO-CITY	Background: Panel studies have been used to investigate the short term effects of outdoor particulate air pollution across a wide range of environmental settings. Aims: To systematically review the results of such studies in children, estimate summary measures of effect, and investigate potential sources of heterogeneity. Methods: Studies were identified by searching electronic databases to June 2002, including those where outcomes and particulate level measurements were made at least daily for greater than or equal to 8 weeks, and analysed using an appropriate regression model. Study results were compared using forest plots, and fixed and random effects summary effect estimates obtained. Publication bias was considered using a funnel plot. Results: Twenty two studies were identified, all except two reporting PM10 (24 hour mean) >50 mug. m(-3). Reported effects of PM10 on PEF were widely spread and smaller than those for PM2.5 (fixed effects summary: -0.012 v -0.063 l. min(-1) per mug. m(-3) rise). A similar pattern was evident for symptoms. Random effects models produced larger estimates. Overall, in between-study comparisons, panels of children with diagnosed asthma or pre-existing respiratory symptoms appeared less affected by PM10 levels than those without, and effect estimates were larger where studies were conducted in higher ozone conditions. Larger PM10 effect estimates were obtained from studies using generalised estimating equations to model autocorrelation and where results were derived by pooling subject specific regression coefficients. A funnel plot of PM10 results for PEF was markedly asymmetrical. Conclusions: The majority of identified studies indicate an adverse effect of particulate air pollution that is greater for PM2.5 than PM10. However, results show considerable heterogeneity and there is evidence consistent with publication bias, so limited confidence may be placed on summary estimates of effect. The possibility of interaction between particle and ozone effects merits further investigation, as does variability due to analytical differences that alter the interpretation of final estimates.	Univ Aberdeen, Dept Environm & Occupat Med, Aberdeen AB25 2ZP, Scotland; S Worcestershire Primary Care Trust, Publ Hlth Network, Worcester WR4 9RW, England	Ayres, JG (reprint author), Univ Aberdeen, Dept Environm & Occupat Med, Foresterhill Rd, Aberdeen AB25 2ZP, Scotland.	j.g.ayres@abdn.ac.uk					Atkinson RW, 2001, AM J RESP CRIT CARE, V164, P1860; Boezen HM, 1999, LANCET, V353, P874, DOI 10.1016/S0140-6736(98)06311-9; BRUNEKREEF B, 1998, EUR RESPIR REV, V8, P131; Committee on the Medical Effects of Air Pollutants, 1995, NONB PART HLTH; Committee on the Medical Effects of Air Pollutants, 1998, QUANT EFF AIR POLL H; *COMM MED EFF AIR, 1995, PAN EV STUD ASTHM OU, pCH6; Deeks J, 2001, SYSTEMATIC REV HLTH, P285, DOI 10.1002/9780470693926.ch15; Delfino RJ, 1998, ENVIRON HEALTH PERSP, V106, P751, DOI 10.1289/ehp.98106751; DOCKERY DW, 1994, ANNU REV PUBL HEALTH, V15, P107, DOI 10.1146/annurev.pu.15.050194.000543; Egger M, 2001, SYSTEMATIC REV HLTH, P211, DOI 10.1002/9780470693926.ch12; Gielen MH, 1997, AM J RESP CRIT CARE, V155, P2105; Gold DR, 1999, EPIDEMIOLOGY, V10, P8, DOI 10.1097/00001648-199901000-00004; Greenland S., 1998, MODERN EPIDEMIOLOGY, P643; Hoek G, 1998, EUR RESPIR J, V11, P1307, DOI 10.1183/09031936.98.11061307; HOEK G, 1994, ENVIRON RES, V64, P136, DOI 10.1006/enrs.1994.1012; Jalaludin B, 2000, AUST NZ J PUBL HEAL, V24, P174, DOI 10.1111/j.1467-842X.2000.tb00138.x; Jalaludin BB, 2000, INT J EPIDEMIOL, V29, P549, DOI 10.1093/ije/29.3.549; NAVIDI W, 1999, 86 HLTH EFF I; Neas LM, 1999, EPIDEMIOLOGY, V10, P550, DOI 10.1097/00001648-199909000-00015; Neas LM, 1996, AM J EPIDEMIOL, V143, P797; NEAS LM, 1995, AM J EPIDEMIOL, V141, P111; *NHS CTR REV DISS, 1996, 4 CRD U YORK NHS CTR; Ostro B, 2001, EPIDEMIOLOGY, V12, P200, DOI 10.1097/00001648-200103000-00012; Peters A, 1997, ENVIRON HEALTH PERSP, V105, P430, DOI 10.1289/ehp.97105430; Peters A, 1996, AM J EPIDEMIOL, V144, P570; Peters A, 1997, EUR RESPIR J, V10, P872; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Pope CA, 1996, AM J RESP CRIT CARE, V154, pS229; POPE CA, 1991, AM REV RESPIR DIS, V144, P668; POPE CA, 1992, AM REV RESPIR DIS, V145, P1123; Pope III CAD, 1999, AIR POLLUTION HLTH, P673; Roemer W, 1999, OCCUP ENVIRON MED, V56, P86; ROEMER W, 1993, AM REV RESPIR DIS, V147, P118; Roemer W, 1998, EUR RESPIR J, V12, P1354, DOI 10.1183/09031936.98.12061354; Roemer W, 2000, EUR RESPIR J, V15, P553, DOI 10.1034/j.1399-3003.2000.15.21.x; Roemer W, 1998, EUR RESPIR REV, V8, P125; ROEMER W, 1998, EUR RESPIR REV, V8, P4; Romieu I, 1996, AM J RESP CRIT CARE, V154, P300; Scarlett JF, 1996, THORAX, V51, P1109, DOI 10.1136/thx.51.11.1109; Schwartz J, 1996, J EPIDEMIOL COMMUN H, V50, pS3, DOI 10.1136/jech.50.Suppl_1.S3; SCHWARTZ J, 1994, AM J RESP CRIT CARE, V150, P1234; Schwartz J, 2000, EPIDEMIOLOGY, V11, P6, DOI 10.1097/00001648-200001000-00004; SCHWARTZ J, 1991, ENVIRON HEALTH PERSP, V90, P181, DOI 10.2307/3430866; Segala C, 1998, EUR RESPIR J, V11, P677; Sterne JAC, 2001, SYSTEMATIC REV HLTH, P189, DOI DOI 10.1002/9780470693926.CH11; SUTTON AJ, 1998, HLTH TECHNOLOGY ASS, V2; Tager IB, 2000, ENVIRON HEALTH PERSP, V108, P615, DOI 10.2307/3454397; van der Zee SC, 1999, OCCUP ENVIRON MED, V56, P802; Vedal S, 1998, AM J RESP CRIT CARE, V157, P1034; Vichit-Vadakan N, 2001, ENVIRON HEALTH PERSP, V109, P381, DOI 10.2307/3434785; Ward DJ, 2002, THORAX, V57, P489, DOI 10.1136/thorax.57.6.489; WHITTEMORE AS, 1980, AM J PUBLIC HEALTH, V70, P687, DOI 10.2105/AJPH.70.7.687	52	77	79	2	15	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 1	2004	61	4							e13	10.1136/oem.2003.007088		12	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	804MK	WOS:000220302600021	15031404	
J	Nave, R; Bethke, TD; van Marle, SP; Zech, K				Nave, R; Bethke, TD; van Marle, SP; Zech, K			Pharmacokinetics of [C-14]ciclesonide after oral and intravenous administration to healthy subjects	CLINICAL PHARMACOKINETICS			English	Review							TOPICAL STEROID CICLESONIDE; INHALED GLUCOCORTICOIDS; AIRWAY RESPONSIVENESS; ASTHMA; BUDESONIDE; RISK; CORTICOSTEROIDS; INHALATION	Background: Ciclesonide is a novel inhaled corticosteroid developed for the treatment of asthma. Objective: To investigate the extent of oral absorption and bioavailability of ciclesonide referenced to an intravenous infusion. This information provides an estimate for the contribution of the swallowed fraction to systemic exposure to ciclesonide after oral inhalation. Methods: In a randomised crossover study, six healthy male subjects (age range 19-40 years) received single doses of 6.9mg (oral administration) and 0.64mg (intravenous administration) of [C-14]ciclesonide, separated by a washout period of at least 14 days. Total radioactivity was determined in whole blood, plasma, urine and faeces. Serum concentrations of ciclesonide and its major metabolite, the pharmacologically active desisobutyryl-ciclesonide (des-CIC), were determined in serum by high-performance liquid chromatography with tandem mass spectrometry detection. Results: After a 10-minute intravenous infusion, the mean half-life for total radioactivity was 45.2 hours. Elimination of des-CIC was fast with a mean elimination half-life of 3.5 hours. After oral administration, the mean half-life for total radioactivity was 27.5 hours. On the basis of a comparison of dose-normalised areas under the curve of total plasma radioactivity versus time, 24.5% of orally administered [C-14]ciclesonide was absorbed. The parent compound ciclesonide was not detected in any of the serum samples after oral administration; serum concentrations of des-CIC were mostly near or below the lower limit of quantification. Thus, systemic bioavailability for des-CIC is <1 % and the absolute bioavailability of ciclesonide is even less than this. [C-14]Ciclesonide showed no retention in red blood cells. The mean cumulative excretion of total radioactivity was almost complete by 120 hours after oral and intravenous administration. Faecal excretion was the predominant route of excretion for total radioactivity after both routes of administration. Single oral and intravenous administration of ciclesonide was well tolerated. Conclusions: Because of an almost complete first-pass metabolism, ciclesonide is undetectable in serum after oral administration. Thus, any ciclesonide swallowed after oral inhalation does not contribute to systemically available ciclesonide or to its active metabolite. Drug-related metabolites are excreted mainly via the faeces, and overall recovery of administered radioactivity is virtually complete after an extended sample collection period.	ALTANA Pharma AG, D-78467 Constance, Germany; Pharma BioRes Grp BV, Zuidlaren, Netherlands	Nave, R (reprint author), ALTANA Pharma AG, Byk Gulden Str 2, D-78467 Constance, Germany.	ruediger.nave@altanapharma.com					BARNES PJ, 1995, NEW ENGL J MED, V332, P868; Barnes PJ, 1993, AM REV RESPIR DIS, V148, P1; Beasley R., 2000, J ALLERGY CLIN IMMUN, V105, P466; BLAKE KV, 2001, PHARMACOTHERAPY, V21; Busse WW, 2001, NEW ENGL J MED, V344, P350; Cumming RG, 1997, NEW ENGL J MED, V337, P8, DOI 10.1056/NEJM199707033370102; FALCOZ C, 1996, BR J CLIN PHARM, V41, P459; HALL M, 2000, XENOBIOTIC METAB D S, V15, P12; Kanniess F, 2001, PULM PHARMACOL THER, V14, P141, DOI 10.1006/pupt.2001.0288; Kumana CR, 2001, J ASTHMA, V38, P161, DOI 10.1081/JAS-100000035; LEECH JA, 1993, AM REV RESPIR DIS, V148, P113; Minto C, 2000, BRIT J CLIN PHARMACO, V50, P116, DOI 10.1046/j.1365-2125.2000.00218.x; Rohatagi S, 2004, J CLIN PHARMACOL, V44, P37, DOI 10.1177/0091270003260334; Rohatagi S, 2003, J CLIN PHARMACOL, V43, P365, DOI 10.1177/0091270002250998; RYRFELDT A, 1982, EUR J RESPIR DIS, V63, P86; Schmidt BMW, 1999, J CLIN PHARMACOL, V39, P1062, DOI 10.1177/00912709922011836; Stirling RG, 2000, BRIT MED BULL, V56, P1037, DOI 10.1258/0007142001903526; Taylor DA, 1999, AM J RESP CRIT CARE, V160, P237; van Staa TP, 2001, J BONE MINER RES, V16, P581, DOI 10.1359/jbmr.2001.16.3.581; Weinbrenner A, 2002, J CLIN ENDOCR METAB, V87, P2160, DOI 10.1210/jc.87.5.2160; Woolcock AJ, 2001, MED J AUSTRALIA, V175, P141; Yang K D, 2000, Chang Gung Med J, V23, P641	22	77	80	0	2	ADIS INTERNATIONAL LTD	AUCKLAND	41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND	0312-5963			CLIN PHARMACOKINET	Clin. Pharmacokinet.		2004	43	7					479	486		10.2165/00003088-200443070-00004		8	Pharmacology & Pharmacy	Pharmacology & Pharmacy	825VK	WOS:000221786400004	15139796	
J	Pietropaoli, AP; Frampton, MW; Hyde, RW; Morrow, PE; Oberdorster, G; Cox, C; Speers, DM; Frasier, LM; Chalupa, DC; Huang, LS; Utell, MJ				Pietropaoli, AP; Frampton, MW; Hyde, RW; Morrow, PE; Oberdorster, G; Cox, C; Speers, DM; Frasier, LM; Chalupa, DC; Huang, LS; Utell, MJ			Pulmonary function, diffusing capacity, and inflammation in healthy and asthmatic subjects exposed to ultrafine particles	INHALATION TOXICOLOGY			English	Article							PARTICULATE AIR-POLLUTION; AMBIENT FINE PARTICLES; EMERGENCY-ROOM VISITS; NASAL NITRIC-OXIDE; OXIDATIVE STRESS; ENVIRONMENTAL AEROSOLS; ADHESION MOLECULES; HUMAN VOLUNTEERS; DIESEL EXHAUST; TERM EXPOSURE	Particulate air pollution is associated with asthma exacerbations and increased morbidity and mortality from respiratory causes. Ultrafine particles (particles less than 0.1 mum in diameter) may contribute to these adverse effects because they have a higher predicted pulmonary deposition, greater potential to induce pulmonary inflammation, larger surface area, and enhanced oxidant capacity when compared with larger particles on a mass basis. We hypothesized that ultrafine particle exposure Would induce airway inflammation in susceptible humans. This hypothesis was tested in a series of randomized, double-blind studies by exposing healthy subjects and mild asthmatic subjects to carbon ultrafine particles versus filtered air. Both exposures were delivered via a mouthpiece system during rest and moderate exercise. Healthy subjects were exposed to particle concentrations of 10, 25, and 50 mug/m(3), while asthmatics were exposed to 10 mug/m(3). Lung function and airway inflammation were assessed by symptom scores, pulmonary function tests, and airway nitric oxide parameters. Airway inflammatory cells were measured via induced sputum analysis in several of the protocols. There were no differences in any of these measurements in normal or asthmatic subjects when exposed to ultrafine particles at concentrations of 10 or 25 mug/m(3). However, exposing 16 normal subjects to the higher concentration of 50 mug/m(3) caused a reduction in maximal midexpiratory flow rate (-4.34 +/- 1.78% [ultrafine particles] vs. +1.08 +/- 1.86% [air], p =.042) and carbon monoxide diffusing capacity (-1.76 +/- 0.66 ml/min/mm Hg [ultrafine particles] vs. -0.18 +/- 0.41 ml/min/mm Hg [air], p =.040) at 21 h after exposure. There were no consistent differences in symptoms, induced sputum, or exhaled nitric oxide parameters in any of these studies. These results suggest that exposure to carbon ultrafine particles results in mild small-airways dysfunction together with impaired alveolar gas exchange in normal subjects. These effects do not appear related to airway inflammation. Additional studies are required to confirm these findings in normal subjects, compare them with additional susceptible patient populations, and determine their pathophysiologic mechanisms.	Univ Rochester, Med Ctr, Sch Med & Dent, Dept Med,Pulm & Crit Care Med Unit, Rochester, NY 14642 USA; Univ Rochester, Sch Med & Dent, Dept Environm Med, Rochester, NY USA; NIH, Dept Biostat, Bethesda, MD 20892 USA; Univ Rochester, Sch Med & Dent, Dept Biostat, Rochester, NY USA	Pietropaoli, AP (reprint author), Univ Rochester, Med Ctr, Sch Med & Dent, Dept Med,Pulm & Crit Care Med Unit, 601 Elmwood Ave,Box 692, Rochester, NY 14642 USA.	Anthony_Pietropaoli@urmc.rochester.edu			NCRR NIH HHS [RR0044]; NIEHS NIH HHS [P30 ES01247, R01 ES11853]		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, 2002, INIS MONOGRAPHS, P242; Crapo RO, 2000, AM J RESP CRIT CARE, V161, P309; Elder ACP, 2000, INHAL TOXICOL, V12, P85, DOI 10.1080/089583700196419; Ghio AJ, 1999, INHAL TOXICOL, V11, P37, DOI 10.1080/089583799197258; Ghio AJ, 2000, AM J RESP CRIT CARE, V162, P981; Girgis RE, 2002, AM J RESP CRIT CARE, V165, P1587, DOI 10.1164/rccm.2104003; Gong H, 2003, INHAL TOXICOL, V15, P305, DOI 10.1080/08958370390168300; Hiltermann TJN, 1998, EUR RESPIR J, V11, P686; Holz O, 1998, THORAX, V53, P83; Huang YCT, 2003, INHAL TOXICOL, V15, P327, DOI 10.1080/08958370390187435; Hyde RW, 1997, J APPL PHYSIOL, V82, P1290; ICRP, 1994, ANN ICRP, V24, P1, DOI DOI 10.1016/0146-6453(94)90004-3; Jones B, 1989, DESIGN ANAL CROSS OV; Jorres RA, 2000, EUR RESPIR J, V16, P555, DOI 10.1034/j.1399-3003.2000.016003555.x; Kharitonov S, 1997, EUR RESPIR J, V10, P1683, DOI 10.1183/09031936.97.10071683; KITTELSON DB, 2001, 200112 MNDOT; Lee YC, 1997, J ASTHMA, V34, P405, DOI 10.3109/02770909709055382; Li N, 2003, ENVIRON HEALTH PERSP, V111, P455, DOI 10.1289/ehp.6000; Li N, 2000, J IMMUNOL, V165, P3393; Li XY, 1999, INHAL TOXICOL, V11, P709; Lipsett M, 1997, ENVIRON HEALTH PERSP, V105, P216, DOI 10.1289/ehp.97105216; MONTEFORT S, 1994, AM J RESP CRIT CARE, V149, P1149; MORRIS JF, 1971, AM REV RESPIR DIS, V103, P57; MORRIS RJ, 1980, J BIOL CHEM, V255, P8050; National Research Council, 1998, RES PRIOR AIRB PART; Nel A E, 2001, Curr Opin Pulm Med, V7, P20, DOI 10.1097/00063198-200101000-00004; Nightingale JA, 1998, THORAX, V53, P87; National Institutes of Health, 1997, NIH PUBL; OBERDORSTER G, 1995, INHAL TOXICOL, V7, P111, DOI 10.3109/08958379509014275; Oberdorster G., 2000, 96 HLTH EFF I; OHKAWARA Y, 1995, AM J RESP CELL MOL, V12, P4; Perillo IB, 2001, J APPL PHYSIOL, V91, P1931; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Pietropaoli AP, 1999, J APPL PHYSIOL, V87, P1532; Pizzichini E, 1996, EUR RESPIR J, V9, P1174, DOI 10.1183/09031936.96.09061174; Pope CA, 2002, JAMA-J AM MED ASSOC, V287, P1132, DOI 10.1001/jama.287.9.1132; ROUGHTON FJW, 1957, J APPL PHYSIOL, V11, P290; Salvi S, 1999, AM J RESP CRIT CARE, V159, P702; Samet JM, 2000, NEW ENGL J MED, V343, P1742, DOI 10.1056/NEJM200012143432401; Searle S. R., 1992, VARIANCE COMPONENTS; Shin HW, 2002, AM J RESP CRIT CARE, V165, P349; Silkoff PE, 2000, AM J RESP CRIT CARE, V161, P1218; Slutsky AS, 1999, AM J RESP CRIT CARE, V160, P2104; STEARNS RC, 1994, ICEM, V13, P763; Tolbert PE, 2000, AM J EPIDEMIOL, V151, P798; TSOUKIAS NM, 1998, J APPL PHYSIOL, V85, P658; U. S. Environmental Protection Agency, 1996, AIR QUAL CRIT PART M; *US EPA, 1998, EX SUMM PART MATT RE; UTELL MJ, 1998, INHAL TOXICOL, V10, P625; WALLENSTEIN S, 1977, BIOMETRICS, V33, P261, DOI 10.2307/2529321; Zhu YF, 2002, J AIR WASTE MANAGE, V52, P1032	57	77	82	3	12	TAYLOR & FRANCIS INC	PHILADELPHIA	325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA	0895-8378			INHAL TOXICOL	Inhal. Toxicol.		2004	16			1			59	72		10.1080/08958370490443079		14	Toxicology	Toxicology	837CQ	WOS:000222605700007	15204794	
J	Borish, L				Borish, L			Allergic rhinitis: Systemic inflammation and implications for management	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						allergic rhinitis; asthma; chronic hyperplastic eosinophilic sinusitis; eosinophils; leukotrienes; cytokines; inflammation	PLACEBO-CONTROLLED TRIAL; CHRONIC HYPERPLASTIC SINUSITIS; ADHESION MOLECULE EXPRESSION; RECEPTOR-MEDIATED MECHANISM; CHRONIC MAXILLARY SINUSITIS; MESSENGER-RNA EXPRESSION; CHRONIC-FATIGUE-SYNDROME; LATE ASTHMATIC RESPONSE; BONE-MARROW; DOUBLE-BLIND	Allergic rhinitis triggers a systemic increase of inflammation. Within minutes of allergen exposure, immune cells release histamine, proteases, cysteinyl leukotrienes, prostaglandins, and cytokines. Some produce the early symptoms, while others augment the production, systemic circulation, and subsequent infiltration of the nasal mucosa with inflammatory cells that sustain the symptoms. Systemic circulation of inflammatory cells permits their infiltration into other tissues where chemoattractant and adhesion molecules already exist. Consequently, allergic rhinitis is linked to comorbid conditions: asthma, chronic hyperplastic eosinophilic sinusitis, nasal pollyposis, and serous otitis media. Effective therapy should be directed at underlying inflammation and its systemic manifestations. It should improve the rhinitis and the comorbid conditions. Antihistamines relieve early symptoms by blocking basophil- and mast cell-generated histamine, but they do not significantly influence the pro-inflammatory loop. They are often little better than placebo. Oral corticosteroids provide the systemic anti-inflammatory efficacy, but their toxicity precludes such an approach. Intranasal corticosteroids effectively target the local inflammatory processes of rhinitis, reducing local inflammatory cells within the nares, but they do not directly access tissues involved in the comorbid conditions. Leukotriene modifiers have both systemic anti-inflammatory effects and an acceptable safety profile.	Univ Virginia, Hlth Syst, Asthma & Allerg Dis Ctr, Beirne Carter Ctr Immunol Res, Charlottesville, VA 22908 USA	Borish, L (reprint author), Univ Virginia, Hlth Syst, Asthma & Allerg Dis Ctr, Beirne Carter Ctr Immunol Res, MR-4 Bldg,Room 5041,Lane Rd, Charlottesville, VA 22908 USA.						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Allergy Clin. Immunol.	DEC	2003	112	6					1021	1031		10.1016/j.jaci.2003.90.015		11	Allergy; Immunology	Allergy; Immunology	752HC	WOS:000187154200001	14657851	
J	Martin, JG; Campbell, HR; Iijima, H; Gautrin, D; Malo, JL; Eidelman, DH; Hamid, Q; Maghni, K				Martin, JG; Campbell, HR; Iijima, H; Gautrin, D; Malo, JL; Eidelman, DH; Hamid, Q; Maghni, K			Chlorine-induced injury to the airways in mice	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						chlorine; inducible nitric oxide synthase; nitric oxide; oxidative injury	EXHALED NITRIC-OXIDE; ACUTE LUNG INJURY; LONGITUDINAL DISTRIBUTION; DYSFUNCTION SYNDROME; PROTEIN NITRATION; PERSISTENT ASTHMA; OZONE; EXPOSURE; INFLAMMATION; RATS	Exposure to chlorine gas (Cl-2) causes occupational asthma that we hypothesized occurs through the induction of airway inflammation and airway hyperresponsiveness by oxidative damage. Respiratory mechanics and airway responsiveness to methacholine were assessed in A/J mice 24 hours after a 5-minute exposure to 100, 200, 400, or 800 ppm Cl-2 and 2 and 7 days after inhalation of 400 ppm Cl-2. Airway responsiveness was higher 24 hours after 400 and 800 ppm Cl-2. Responsiveness after inhalation of 400 ppm Cl-2 returned to normal by 2 days but was again elevated at 7 days. Airway epithelial loss, patchy alveolar damage, proteinaceous exudates, and inflammatory cells within alveolar walls were observed in animals exposed to 800 ppm Cl-2. Macrophages, granulocytes, epithelial cells, and nitrate/nitrite levels increased in lung lavage fluid. Increased inducible nitric oxide synthase expression and oxidation of lung proteins were observed. Epithelial cells and alveolar macrophages from mice exposed to 800 ppm Cl-2 stained for 3-nitrotyrosine residues. Inhibition of inducible nitric oxide synthase with 1400W (1 mg/kg) abrogated the Cl-2-induced changes in responsiveness. We conclude that chlorine exposure causes functional and pathological changes in the airways associated with oxidative stress. Inducible nitric oxide synthase is involved in the induction of changes in responsiveness to methacholine.	McGill Univ, Meakins Christie Labs, Dept Med, Montreal, PQ H2X 2P2, Canada; Univ Montreal, Hop Sacre Coeur, Div Resp, Montreal, PQ, Canada	Martin, JG (reprint author), McGill Univ, Meakins Christie Labs, Dept Med, 3626 St Urbain, Montreal, PQ H2X 2P2, Canada.				NIOSH CDC HHS [1R01 OH 04058-01]		ADELSON L, 1971, AM J CLIN PATHOL, V56, P430; BARROW CS, 1977, ARCH ENVIRON HEALTH, V32, P68; Bates JHT, 1997, J APPL PHYSIOL, V82, P55; BROOKS SM, 1985, CHEST, V88, P376, DOI 10.1378/chest.88.3.376; CANNON WC, 1983, AM IND HYG ASSOC J, V44, P923, DOI 10.1202/0002-8894(1983)044<0923:TFPCAI>2.3.CO;2; CHANYEUNG M, 1994, AM J RESP CRIT CARE, V149, P1676; CHESTER EH, 1977, CHEST, V72, P247, DOI 10.1378/chest.72.2.247; Demnati R., 1995, Journal of Environmental Pathology Toxicology and Oncology, V14, P15; Demnati R, 1998, EUR RESPIR J, V11, P922, DOI 10.1183/09031936.98.11040922; DRISCOLL KE, 1993, TOXICOL APPL PHARM, V119, P306, DOI 10.1006/taap.1993.1074; Duguet A, 2001, AM J RESP CRIT CARE, V164, P1119; Eiserich JP, 1996, J BIOL CHEM, V271, P19199; Garvey EP, 1997, J BIOL CHEM, V272, P4959; Gautrin D, 1999, AM J RESP CRIT CARE, V160, P1232; Greenfield RA, 2002, AM J MED SCI, V323, P350, DOI 10.1097/00000441-200206000-00007; Henneberger PK, 1996, AM J RESP CRIT CARE, V153, P225; Iijima H, 2001, AM J RESP CRIT CARE, V163, P1233; Inoue H, 2000, AM J RESP CRIT CARE, V161, P249; Jia YL, 1996, J APPL PHYSIOL, V80, P404; Kenyon NJ, 2002, AM J PHYSIOL-LUNG C, V282, pL540; Lemiere C, 1997, EUR RESPIR J, V10, P241, DOI 10.1183/09031936.97.10010241; LEVINE RL, 1994, METHOD ENZYMOL, V233, P346; LI ZY, 1992, AM J PHYSIOL, V263, pL723; McGrogan I, 1998, AM J PHYSIOL-LUNG C, V274, pL220; Menaouar A, 1997, EUR RESPIR J, V10, P1100, DOI 10.1183/09031936.97.10051100; Nightingale JA, 1999, THORAX, V54, P1061; Nodelman V, 1999, J APPL PHYSIOL, V86, P1984; Nodelman V, 1999, J APPL PHYSIOL, V87, P2073; Olin AC, 1999, EUR RESPIR J, V14, P828, DOI 10.1034/j.1399-3003.1999.14d18.x; Schonhofer B, 1996, RESPIRATION, V63, P155; SCHUESSLER TF, 1995, IEEE T BIO-MED ENG, V42, P860, DOI 10.1109/10.412653; SHACTER E, 1994, FREE RADICAL BIO MED, V17, P429, DOI 10.1016/0891-5849(94)90169-4; STEVENS WHM, 1996, AIRWAYS SMOOTH MUSCL, P95; Tsuji C, 2000, AM J PHYSIOL-LUNG C, V278, pL719; vanderVliet A, 1997, J BIOL CHEM, V272, P7617; Wechsler ME, 2000, AM J RESP CRIT CARE, V162, P2043	36	77	79	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.	SEP 1	2003	168	5					568	574		10.1164/rccm.200201-021OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	716QC	WOS:000185039000012	12724121	
J	Remes, ST; Iivanainen, K; Koskela, H; Pekkanen, J				Remes, ST; Iivanainen, K; Koskela, H; Pekkanen, J			Which factors explain the lower prevalence of atopy amongst farmers' children?	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						atopy; children; epidemiology; farm; risk factors; skin prick test	FATTY-ACIDS; HAY-FEVER; ALLERGIC SENSITIZATION; BIRTH COHORT; ASTHMA; CHILDHOOD; ENDOTOXIN; EXPOSURE; ENVIRONMENT; COMMUNITY	Background: The inverse association between farming and atopy in children has been attributed to microbial exposure, especially through livestock. Very little is known about other potential explanatory factors. Objective: To explore potential differences in lifestyle and environmental factors between farmer and non-farmer families, and whether these factors could explain the association between farming and childhood atopy. Methods: A cross-sectional study, including 366 farmers' and 344 non-farmers' children in eastern Finland. Information regarding exposure and background characteristics was gathered by a written questionnaire. Atopy was defined as having one or more positive skin prick test reactions (> 3 mm) against the six common aeroallergens. Results: Regardless of the current farming type, atopy was less frequent among the farmers' children than the non-farmers' children (aOR 0.56, 95% CI 0.40-0.78). Remarkable differences were seen in many lifestyle factors (including diet) between the farmer and non-farmer families, but only a few of the explored factors were associated with atopy. The frequency of current livestock contacts seemed to have an inverse, dose-dependent association with atopy (aOR 0.46, 95% CI 0.22-0.97 for daily vs. no contact). Having lived on a dairy farm in infancy (aOR 0.51, 95% CI 0.28-0.93), or having had cats or dogs in infancy (aOR 0.60, 95% CI 0.42-0.85), decreased the risk of atopy at school age. The inverse association between farming and atopy was not explained by the sociodemographic factors, or by differences in conventional risk factors of atopy. Animal contacts explained partially, but not completely, the association. Conclusion Higher frequency of animal contacts is one factor, but probably not the only one, explaining the inverse association of farming and atopy in children. The importance of early life exposures may have recently been over-emphasized, and current exposures discounted, when studying the risk factors of childhood atopy.	Natl Publ Hlth Inst, Environm Epidemiol Unit, Kuopio 70701, Finland; Kuopio Univ Hosp, Dept Pediat, SF-70210 Kuopio, Finland; Kuopio Univ Hosp, Dept Resp Med, SF-70210 Kuopio, Finland	Remes, ST (reprint author), Natl Publ Hlth Inst, Environm Epidemiol Unit, POB 95, Kuopio 70701, Finland.						Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; Bischof W, 2000, P HLTH BUILDINGS, V1, P251; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; 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; Ernst P, 2000, AM J RESP CRIT CARE, V161, P1563; Fogarty A, 2000, LANCET, V356, P1573, DOI 10.1016/S0140-6736(00)03132-9; Gereda JE, 2001, J ALLERGY CLIN IMMUN, V107, P790, DOI 10.1067/mai.2001.115245; Hosmer DW, 1989, APPL LOGISTIC REGRES; Kankaanpaa P, 1999, ANN MED, V31, P282, DOI 10.3109/07853899908995891; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Klintberg B, 2001, EUR RESPIR J, V17, P1151, DOI 10.1183/09031936.01.00027301; Lewis SA, 2000, CLIN EXP ALLERGY, V30, P153; Leynaert B, 2001, AM J RESP CRIT CARE, V164, P1829; Liu AH, 2002, J ALLERGY CLIN IMMUN, V109, P379, DOI 10.1067/mai.2002.122157; PASANEN AL, 1989, AM IND HYG ASSOC J, V50, P631, DOI 10.1202/0002-8894(1989)050<0631:FCFFWI>2.0.CO;2; Pekkanen J, 2001, CLIN EXP ALLERGY, V31, P95, DOI 10.1046/j.1365-2222.2001.00930.x; 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; [Anonymous], 2001, STAT STAT SOFTW REL; Svanes C, 1999, J ALLERGY CLIN IMMUN, V103, P415, DOI 10.1016/S0091-6749(99)70465-3; Vartiainen E, 2000, INT J EPIDEMIOL, V29, P49, DOI 10.1093/ije/29.1.49; 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; Weiland SK, 1999, LANCET, V353, P2040, DOI 10.1016/S0140-6736(99)01609-8; Willet WC, 1998, MONOGRAPHS EPIDEMIOL, V30	29	77	77	0	4	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	APR	2003	33	4					427	434		10.1046/j.1365-2222.2003.01566.x		8	Allergy; Immunology	Allergy; Immunology	665BX	WOS:000182100700005	12680856	
J	Talbot-Smith, A; Fritschi, L; Divitini, ML; Mallon, DFJ; Knuiman, MW				Talbot-Smith, A; Fritschi, L; Divitini, ML; Mallon, DFJ; Knuiman, MW			Allergy, atopy, and cancer: A prospective study of the 1981 Busselton cohort	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						allergy and immunology; asthma; hypersensitivity; immediate; neoplasms; skin tests	COLORECTAL-CANCER; POPULATION; ASTHMA; RISK; PREVALENCE; MORTALITY; DISEASES	The associations among certain allergic disorders, atopy upon skin-prick testing, and specific cancers were evaluated in a prospective study. Information regarding history of asthma and hay fever was collected by questionnaire from 3,308 cancer-free participants in the 1981 Busselton Health Survey. A subset of 1,005 participants also underwent skin-prick testing. The cohort was followed for a new diagnosis of cancer or death until the end of 1999. Cox proportional hazards regression analysis was used to estimate adjusted hazard ratios (relative risks) for breast, prostate, colorectal, lung, and hematologic cancers and melanoma. Having a skin reaction to house dust mites nearly tripled the risk of prostate cancer (relative risk=2.90, 95% confidence interval: 1.26, 6.68). History of asthma and hay fever were associated with a trend toward a reduced risk of colorectal cancer and increased risk of leukemia, but these results were not statistically significant. Hay fever was associated with melanoma risk in men but not in women. No association was found between breast and lung cancers and allergic disorders or atopy.	Univ Western Australia, Sch Populat Hlth, Perth, WA 6009, Australia; Fremantle Hosp, Dept Immunol, Perth, WA, Australia; Princess Margaret Hosp, Dept Immunol, Perth, WA, Australia	Fritschi, L (reprint author), Univ Western Australia, Sch Populat Hlth, Perth, WA 6009, Australia.		Knuiman, Matthew/I-5549-2013; Fritschi, Lin /K-2096-2012	Fritschi, Lin /0000-0002-7692-3560			ALDERSON M, 1974, LANCET, V2, P1475; ALLEGRA J, 1976, CANCER RES, V36, P3225; *AUSTR BUR STAT, 1991, 43730 AUSTR BUR STAT; BERNARD SM, 1984, LEUKEMIA RES, V8, P681, DOI 10.1016/0145-2126(84)90016-X; BORISH L, 1998, ALLERGY PRINCIPLES P, P108; *BUSS POP MED RES, 2002, BUSS HLTH STUD; Clemente CG, 1996, CANCER, V77, P1303, DOI 10.1002/(SICI)1097-0142(19960401)77:7<1303::AID-CNCR12>3.0.CO;2-5; COCKCROFT DW, 1979, ANN ALLERGY, V43, P345; ERIKSSON NE, 1995, ALLERGY, V50, P718, DOI 10.1111/j.1398-9995.1995.tb01212.x; FISHERMAN E, 1960, J ALLERGY, V1, P74; FORD R, 1978, ANN ALLERGY, V49, P240; Gabriel R, 1972, Br J Clin Pract, V26, P202; GALLAGHER RP, 1983, BRIT J CANCER, V48, P853, DOI 10.1038/bjc.1983.277; HUGHES WF, 1979, ANN ALLERGY, V43, P163; JAMES A, 1992, AM REV RESPIR DIS, V146, P895; JOHNSON K, 1966, LANCET, V86, P5; KALLEN B, 1993, EUR RESPIR J, V6, P694; Kaplan DH, 1998, P NATL ACAD SCI USA, V95, P7556, DOI 10.1073/pnas.95.13.7556; Little J, 1999, EUR J CANCER PREV, V8, pS61; LOGAN J, 1953, N Z Med J, V52, P210; MACKAY WD, 1966, BRIT J CANCER, V20, P434, DOI 10.1038/bjc.1966.52; MCDUFFIE HH, 1991, CHEST, V99, P404, DOI 10.1378/chest.99.2.404; MCWORTER WP, 1988, CANCER, V62, P451; Mercader M, 2001, P NATL ACAD SCI USA, V98, P14565, DOI 10.1073/pnas.251140998; MILLS PK, 1992, AM J EPIDEMIOL, V136, P287; Naito Y, 1998, CANCER RES, V58, P3491; PENN I, 1984, TRANSPLANT P, V16, P492; PEPYS J, 1975, CLIN ASPECTS IMMUNOL, P75; RIDDELL SR, 1995, ANNU REV IMMUNOL, V13, P545; ROBINETTE CD, 1978, J CHRON DIS, V31, P619, DOI 10.1016/0021-9681(78)90022-X; ROZENCWAIG R, 1982, POSTGRAD MED, V72, P42; SEVERSON RK, 1989, J CLIN EPIDEMIOL, V42, P995, DOI 10.1016/0895-4356(89)90165-0; URE D M J, 1969, Scottish Medical Journal, V14, P51; VENA JE, 1985, AM J EPIDEMIOL, V122, P66; VESTERINEN E, 1993, INT J EPIDEMIOL, V22, P976, DOI 10.1093/ije/22.6.976; WOOLCOCK AJ, 1987, THORAX, V42, P361, DOI 10.1136/thx.42.5.361	36	77	79	1	1	OXFORD UNIV PRESS INC	CARY	JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA	0002-9262			AM J EPIDEMIOL	Am. J. Epidemiol.	APR 1	2003	157	7					606	612		10.1093/aje/kwg020		7	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	665QF	WOS:000182131600005	12672680	
J	Lanari, M; Giovannini, M; Giuffre, L; Marini, A; Rondini, G; Rossi, GA; Merolla, R; Zuccotti, GV; Salvioli, GP				Lanari, M; Giovannini, M; Giuffre, L; Marini, A; Rondini, G; Rossi, GA; Merolla, R; Zuccotti, GV; Salvioli, GP		Investigators RADAR Study Grp	Prevalence of respiratory syncytial virus infection in Italian infants hospitalized for acute lower respiratory tract infections, and association between respiratory syncytial virus infection risk factors and disease severity	PEDIATRIC PULMONOLOGY			English	Article						respiratory syncytial virus; bronchiolitis; epidemiology; wheezing; pneumonia; passive tobacco smoke; gestational age; birth order; birth weight	INVESTIGATORS COLLABORATIVE NETWORK; CANADIAN CHILDREN; VIRAL-INFECTION; BRONCHIOLITIS; REHOSPITALIZATION; MANAGEMENT; GESTATION; ILLNESSES; SMOKING; ALLERGY	This study was designed to collect data on the prevalence of respiratory syncytial virus (RSV) infection in Italy in infants hospitalized for lower respiratory tract infections, and to evaluate which of the recognized risk factors might be associated with disease severity. Thirty-two centers throughout Italy participated in the study, Over a 6-month period (November 1, 1999 to April 30, 2000), we evaluated all children < 2 years of age hospitalized for lower respiratory tract infections. All subjects were tested for RSV within 24 hr of hospitalization by using an immuno-enzymatic diagnostic test (Abbott Testpack, RSV). Logistic regression was used to identify the factors that might be associated with more severe disease or could increase the likelihood of RSV positivity in hospitalized infants. Out of a total of 1,232 children enrolled, 40.6% were found to be RSV-posftive (RSV+). The peak of the RSV epidemic occurred in February, while the lowest prevalence of RSV positivity was seen in November (P < 0.05). A high proportion of study subjects had low birth weight and low gestational age. The clinical diagnosis at hospitalization was bronchiolitis in 66.7%, pneumonia in 15.3%, and wheezy bronchitis in 18.1%. In the bronchiolitis group, a higher prevalence of RSV+ was found in patients with gestational age less than or equal to 33 weeks or 34-35 weeks, as compared to those with agestational age > 36 weeks (P < 0.04). No differences were found in the proportion of RSV+ patients in the three gestational age subgroups with pneumonia and wheezy bronchitis (P > 0.05, each comparison). Independent of the clinical diagnosis at admission, RSV infection was associated with more severe respiratory impairment. Environmental smoke exposure was higher in subjects with bronchiolitis than in those with wheezy bronchitis (P < 0.04), and RSV 4 was positively related with the birth order (P < 0.05). The presence of older siblings and birth order plays an important role in RSV infection. The collected data show that, in Italy, RSV is an important cause of lower respiratory tractinfection in infants. Gestational age, birth order, birth weight, and exposure to tobacco smoke affected the prevalence and severity of RSV-related lower respiratory tract disease. (C) Wiley-Liss, Inc.	Univ Bologna, Policlin S Orsola, Bologna, Italy; Univ Milan, Osped San Raffaele, I-20127 Milan, Italy; Univ Palermo, Ist Materno Infantile, Palermo, Italy; Univ Milan, Milan, Italy; Univ Pavia, Policlin San Matteo, I-27100 Pavia, Italy; IRCCS G Gaslini Genova, UO Pneumol, Genoa, Italy; Abbott SpA, Direzone Med, Dept Med, I-04010 Campoverde, LT, Italy	Merolla, R (reprint author), Abbott SpA, Direzone Med, Dept Med, Via Pontina Km 52, I-04010 Campoverde, LT, Italy.						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Pulmonol.	JUN	2002	33	6					458	465		10.1002/ppul.10052		8	Pediatrics; Respiratory System	Pediatrics; Respiratory System	555MJ	WOS:000175797600009	12001280	
J	Behrendt, H; Beckert, WM				Behrendt, H; Beckert, WM			Localization, release and bioavailability of pollen allergens: the influence of environmental factors	CURRENT OPINION IN IMMUNOLOGY			English	Review							PHLEUM-PRATENSE POLLEN; GRASS-POLLEN; AIR-POLLUTION; MAJOR ALLERGENS; LOLIUM-PERENNE; ELECTRON-MICROSCOPY; WALL PROTEINS; ASTHMA; PARTICLES; AEROSOL	Allergens are integral constituents of plants or animals and their normal functions and localization are being characterized. To trigger responses in humans, allergens must become bioavailable and the role of air pollutants - for example diesel-exhaust particles - in this process is causing concern. Finally, the fact that some pollen releases eicosanoid-like proinflammatory mediators may have wide implications.	Neuherberg Tech Univ Munich, GSF, Natl Res Ctr Environm & Hlth, Div Environm Dermatol & Allergy, D-80802 Munich, Germany; Res Ctr Borstel, D-23845 Borstel, Germany	Behrendt, H (reprint author), Neuherberg Tech Univ Munich, GSF, Natl Res Ctr Environm & Hlth, Div Environm Dermatol & Allergy, Biedersteiner Str 29, D-80802 Munich, Germany.						Aas K., 1997, EUROPEAN ALLERGY WHI; Anto JM, 1997, THORAX, V52, P669; BECKER WM, 1997, NEW TRENDS ALLERGY, V4, P339; Becker Wolf-Meinhard, 1996, P119; Behrendt H, 1997, INT ARCH ALLERGY IMM, V113, P69; BEHRENDT H, 1992, INT ARCH ALLERGY IMM, V99, P425; Behrendt H, 2001, INT ARCH ALLERGY IMM, V124, P121, DOI 10.1159/000053688; Behrendt H, 1999, INT ARCH ALLERGY IMM, V118, P414, DOI 10.1159/000024151; Behrendt H, 1995, PROG ALLER CLIN IMM, V3, P83; Behrendt H, 1991, NEW TRENDS ALLERGY, P467; BEHRENDT H, 1999, UMWELT GESUNDHEIT RI; BERRENS L, 1994, CLIN EXP ALLERGY, V24, P606, DOI 10.1111/j.1365-2222.1994.tb00962.x; Bufe A, 1996, PLANTA, V199, P413; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; Fischer S, 1996, J ALLERGY CLIN IMMUN, V98, P189, DOI 10.1016/S0091-6749(96)70242-7; Grobe K, 1999, EUR J BIOCHEM, V263, P33, DOI 10.1046/j.1432-1327.1999.00462.x; Grote M, 1999, INT ARCH ALLERGY IMM, V118, P1, DOI 10.1159/000024024; GROTE M, 1994, J HISTOCHEM CYTOCHEM, V42, P427; Grote M, 2000, J ALLERGY CLIN IMMUN, V105, P1140, DOI 10.1067/mai.2000.107044; HOWLETT BJ, 1973, J CELL SCI, V13, P603; HOWLETT BJ, 1981, HISTOCHEM J, V13, P461, DOI 10.1007/BF01005062; KING TP, 1995, CLIN EXP ALLERGY, V25, P27; KNOX RB, 1993, CLIN EXP ALLERGY, V23, P354, DOI 10.1111/j.1365-2222.1993.tb00339.x; KNOX RB, 1970, J CELL SCI, V6, P1; Knox RB, 1997, CLIN EXP ALLERGY, V27, P246; KNOX RB, 1975, BIOL J LINN SOC S1, V7, P177; Kramer U, 2000, EPIDEMIOLOGY, V11, P64, DOI 10.1097/00001648-200001000-00014; Marks GB, 2001, THORAX, V56, P468, DOI 10.1136/thorax.56.6.468; MARSH SGE, 1999, HLA FACTS BOOK, P61; Monn Christian, 1999, Reviews on Environmental Health, V14, P79; MUTIUS E, 1998, LANCET, V351, P862; Newson R, 1998, EUR RESPIR J, V11, P694; Rantio-Lehtimaki Auli, 1995, P387; Riediker M, 2000, CLIN EXP ALLERGY, V30, P867; Ring J, 1999, INT ARCH ALLERGY IMM, V118, P403, DOI 10.1159/000024148; Ring J, 1997, INT ARCH ALLERGY IMM, V113, P7; RISSE U, 2000, J AEROSOL SCI     S1, V31, pS27; Schappi GF, 1996, INT ARCH ALLERGY IMM, V110, P364; Schappi GF, 1999, CLIN EXP ALLERGY, V29, P633; Schappi GF, 1997, J ALLERGY CLIN IMMUN, V100, P656, DOI 10.1016/S0091-6749(97)70170-2; Schramm G, 1996, INT ARCH ALLERGY IMM, V110, P354; SPIEKSMA FTM, 1995, CLIN EXP ALLERGY, V25, P234, DOI 10.1111/j.1365-2222.1995.tb01034.x; SPIEKSMA FTM, 1990, CLIN EXP ALLERGY, V20, P273, DOI 10.1111/j.1365-2222.1990.tb02683.x; STAFF IA, 1990, HISTOCHEM J, V22, P276, DOI 10.1007/BF01387183; Stanley R. G., 1974, POLLEN BIOL BIOCH MA; Suck R, 2000, CLIN EXP ALLERGY, V30, P324, DOI 10.1046/j.1365-2222.2000.00843.x; Suphioglu C, 1998, INT ARCH ALLERGY IMM, V116, P253, DOI 10.1159/000023953; TAYLOR PE, 1994, HISTOCHEM J, V26, P392, DOI 10.1007/BF00160051; VONMUTIUS E, 1992, BRIT MED J, V305, P1395; Vrtala S, 1999, J IMMUNOL, V163, P5489; Warner JO, 1998, PEDIATR ALLERGY IMMU, V9, P116	51	77	81	1	11	CURRENT BIOLOGY LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0952-7915			CURR OPIN IMMUNOL	Curr. Opin. Immunol.	DEC	2001	13	6					709	715		10.1016/S0952-7915(01)00283-7		7	Immunology	Immunology	486BB	WOS:000171797600013	11677094	
J	Wilson, DR; Irani, AM; Walker, SM; Jacobson, MR; Mackay, IS; Schwartz, LB; Durham, SR				Wilson, DR; Irani, AM; Walker, SM; Jacobson, MR; Mackay, IS; Schwartz, LB; Durham, SR			Grass pollen immunotherapy inhibits seasonal increases in basophils and eosinophils in the nasal epithelium	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergic rhinitis; immunotherapy; immunohistochemistry; basophil; mast cell; eosinophil; neutrophil	NATURAL ALLERGEN EXPOSURE; HUMAN BLOOD BASOPHILS; MAST-CELLS; MESSENGER-RNA; INDUCED RHINITIS; HAY-FEVER; TOPICAL CORTICOSTEROIDS; METACHROMATIC CELLS; ANTIGEN CHALLENGE; T-LYMPHOCYTES	Background Symptoms of allergic rhinitis are accompanied by infiltration of the nasal mucosa with inflammatory cells, predominantly eosinophils and metachromatic cells (basophils and mast cells). Specific immunotherapy (IT) reduces mucosal eosinophilia and numbers of metachromatic cells in the epithelium. A specific marker distinguishing basophils from mast cells was recently developed. Objectives The basophil-specific manoclanal antibody 2D7 was used to determine the influence of subcutaneous IT on numbers of nasal mucosal basophils compared with the effects of IT on neutrophils, eosinophils and mast cells. Method During a randomized, placebo-controlled trial of grass pollen IT in 44 adults with severe summer hay fever, nasal biopsies were taken at baseline, out of the pollen season, and at the peak of the pollen season following 2 years treatment. Biopsies were processed for immunohistochemistry far basophils (2D7(+)), mast cells (AA1(+)), eosinophils (MBP+) and neutrophils (neutrophil elastase(+)). Results In placebo-treated (PL) patients there were significant seasonal increases in basophils (P<0.01), mast cells (P<0.05) and eosinophils (P=0.002) irt the nasal submucosa. In IT-treated patients significant increases in 2D7 cells (P<0.01) and eosinophils (P=0.01) but not AA1(+) cells (P=0.9) were observed. These differences were significant between groups for eosinophils (P<0.05). In the epithelium there were seasonal increases in AA1(+) cells and eosinophils in both groups (PL: P<0.01, IT: P<0.05 far both). The between-group difference was significant for eosinophils (P=0.05). Basophils were observed in the epithelium of six out of 17 in the placebo group and one out of 20 in the IT group (P=0.03). Neutrophil numbers remained constant in both epithelium and submucosa. Conclusion Successful grass pollen immunotherapy was associated with inhibition of seasonal increases in basophils and eosinophils, but not mast cells or neutrophils within the nasal epithelium. Immunotherapy may act, at least in part, by reducing seasonal recruitment of basophils and eosinophils into the epithelium.	Univ London Imperial Coll Sci Technol & Med, Sch Med, Natl Heart & Lung Inst, London SW3 6LY, England; Virginia Commonwealth Univ, Dept Pediat, Div Rheumatol Allergy & Immunol, Richmond, VA USA; Virginia Commonwealth Univ, Dept Internal Med, Richmond, VA USA	Durham, SR (reprint author), Univ London Imperial Coll Sci Technol & Med, Sch Med, Natl Heart & Lung Inst, Dovehouse St, London SW3 6LY, England.		Walker, Samantha/B-9740-2013	Walker, Samantha/0000-0001-5503-8258			Akdis CA, 1998, J CLIN INVEST, V102, P98, DOI 10.1172/JCI2250; BASCOM R, 1988, Journal of Allergy and Clinical Immunology, V81, P580, DOI 10.1016/0091-6749(88)90198-4; BENTLEY AM, 1992, J ALLERGY CLIN IMMUN, V89, P877, DOI 10.1016/0091-6749(92)90444-7; Bochner BS, 1996, J IMMUNOL, V157, P844; BORRES MP, 1990, ALLERGY, V45, P98, DOI 10.1111/j.1398-9995.1990.tb00465.x; BRADDING P, 1993, J IMMUNOL, V151, P3853; Durham SR, 1999, CLIN EXP ALLERGY, V29, P1490; Durham SR, 1999, NEW ENGL J MED, V341, P468, DOI 10.1056/NEJM199908123410702; Durham SR, 1996, J ALLERGY CLIN IMMUN, V97, P1356, DOI 10.1016/S0091-6749(96)70205-1; ENERBACK L, 1986, INT ARCH ALLER A IMM, V80, P44; Erel F, 2000, J INVEST ALLERG CLIN, V10, P14; FOKKENS W J, 1988, Rhinology (Utrecht), V26, P293; FOKKENS WJ, 1992, CLIN EXP ALLERGY, V22, P701, DOI 10.1111/j.1365-2222.1992.tb00194.x; FURIN MJ, 1991, J ALLERGY CLIN IMMUN, V88, P27, DOI 10.1016/0091-6749(91)90297-2; Gauvreau GM, 1999, AM J RESP CRIT CARE, V160, P640; Gauvreau GM, 2000, AM J RESP CRIT CARE, V161, P1473; HIRSCH SR, 1976, J ALLERGY CLIN IMMUN, V58, P676, DOI 10.1016/0091-6749(76)90179-2; ILIOPOULOS O, 1992, J IMMUNOL, V148, P2223; Irani AMA, 1998, J ALLERGY CLIN IMMUN, V101, P354; Jacobson MR, 1999, CLIN EXP ALLERGY, V29, P1347; Kasaian MT, 1996, INT IMMUNOL, V8, P1287, DOI 10.1093/intimm/8.8.1287; KEPLEY CL, 1995, J IMMUNOL, V154, P6548; KleinJan A, 2000, J ALLERGY CLIN IMMUN, V106, P677, DOI 10.1067/mai.2000.109621; LIU C-M, 1988, Rhinology (Utrecht), V26, P167; LOZEWICZ S, 1990, J ALLERGY CLIN IMMUN, V85, P125, DOI 10.1016/0091-6749(90)90233-T; MACGLASHAN D, 1994, J IMMUNOL, V152, P3006; Masuyama K, 1998, J ALLERGY CLIN IMMUN, V102, P610, DOI 10.1016/S0091-6749(98)70277-5; McEuen AR, 1999, LAB INVEST, V79, P27; NACLERIO RM, 1985, NEW ENGL J MED, V313, P65, DOI 10.1056/NEJM198507113130201; Ochensberger B, 1996, BLOOD, V88, P3028; OTSUKA H, 1991, CLIN EXP ALLERGY, V21, P115, DOI 10.1111/j.1365-2222.1991.tb00812.x; PIPKORN U, 1988, J ALLERGY CLIN IMMUN, V82, P1046, DOI 10.1016/0091-6749(88)90143-1; RASP G, 1993, ALLERGY, V48, P72, DOI 10.1111/j.1398-9995.1993.tb00688.x; Robinson DS, 1999, AM J RESP CELL MOL, V20, P9; Uguccioni M, 1997, J CLIN INVEST, V100, P1137, DOI 10.1172/JCI119624; VARNEY VA, 1992, AM REV RESPIR DIS, V146, P170; VIEGAS M, 1987, INT ARCH ALLER A IMM, V82, P275; Walker SM, 2001, J ALLERGY CLIN IMMUN, V107, P87, DOI 10.1067/mai.2001.112027; Winther L, 1999, ALLERGY, V54, P436, DOI 10.1034/j.1398-9995.1999.00910.x; WOODS JW, 1993, J EXP MED, V178, P1935, DOI 10.1084/jem.178.6.1935; YING S, 1994, IMMUNOLOGY, V82, P200	41	77	82	0	0	BLACKWELL SCIENCE LTD	OXFORD	P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	NOV	2001	31	11					1705	1713		10.1046/j.1365-2222.2001.01231.x		9	Allergy; Immunology	Allergy; Immunology	496XF	WOS:000172423100010	11696046	
J	Allaouchiche, B; Debon, R; Goudable, J; Chassard, D; Duflo, F				Allaouchiche, B; Debon, R; Goudable, J; Chassard, D; Duflo, F			Oxidative stress status during exposure to propofol, sevoflurane and desflurane	ANESTHESIA AND ANALGESIA			English	Article							ALVEOLAR MACROPHAGES; PROINFLAMMATORY CYTOKINES; BRONCHOALVEOLAR LAVAGE; ANTIOXIDANT STATUS; EXPIRED BREATH; RAT; EXPRESSION; ANESTHESIA; ASTHMA	We evaluated the circulating and lung oxidative status during general anesthesia established with propofol, sevoflurane, or desflurane in mechanically ventilated swines. Blood samples and bronchoalveolar lavage fluid (BAL) specimens were respectively performed via an internal jugular vein catheter and a nonbronchoscopic BAL for baseline oxidative activity measurements: malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPX). A 4-h general anesthesia was then performed in the three groups of 10 swine: the Propofol group received 8 mg(.)kg(-1.)h(-1) of IV propofol as the sole anesthetic; the Desflurane group received 1.0 minimum alveolar concentration of desflurane; and the Sevoflurane group received 1.0 minimum alveolar concentration of sevoflurane. We observed significantly larger levels of MDA in plasma and BAL during desflurane exposure than with the other anesthetics. We also observed smaller concentrations of circulating GPX and alveolar GPX We found a significant decrease for MDA measurements in the plasma and the pulmonary lavage during propofol anesthesia. We also found larger values of GPX measurements in the serum and the pulmonary lavage. No significant changes were observed when animals were exposed to sevoflurane. No significant changes were found for circulating concentrations of SOD during exposure to all anesthetics. In this mechanically ventilated swine model, desflurane seemed to induce a local and systemic oxidative stress, whereas propofol and sevoflurane were more likely to have antioxidant properties.	Hop Hotel Dieu, Dept Anesthesiol & Intens Care, F-69288 Lyon 02, France; Hop Edouard Herriot, Dept Biochem, Lyon, France	Allaouchiche, B (reprint author), Hop Hotel Dieu, Dept Anesthesiol & Intens Care, 1,Pl Hop, F-69288 Lyon 02, France.						BALDWIN SR, 1986, LANCET, V1, P11; Boya P, 1999, J HEPATOL, V31, P808, DOI 10.1016/S0168-8278(99)80281-5; De la Cruz JP, 1999, ANESTH ANALG, V89, P1050, DOI 10.1097/00000539-199910000-00043; De la Cruz JP, 1998, ANESTH ANALG, V87, P1141, DOI 10.1097/00000539-199811000-00031; DOHLMAN AW, 1993, AM REV RESPIR DIS, V148, P955; GOODE HF, 1995, CRIT CARE MED, V23, P646, DOI 10.1097/00003246-199504000-00011; HALL JC, 1991, CHEST, V99, P923, DOI 10.1378/chest.99.4.923; Kotani N, 1999, ANESTH ANALG, V89, P1250; KOTANI N, 1995, ANESTH ANALG, V81, P1255, DOI 10.1097/00000539-199512000-00023; Kotani N, 1999, ANESTHESIOLOGY, V91, P187, DOI 10.1097/00000542-199907000-00027; MARKLUND S, 1974, EUR J BIOCHEM, V47, P469, DOI 10.1111/j.1432-1033.1974.tb03714.x; McCord JM, 2000, AM J MED, V108, P652, DOI 10.1016/S0002-9343(00)00412-5; MURPHY PG, 1992, BRIT J ANAESTH, V68, P613, DOI 10.1093/bja/68.6.613; MUSACCHIO E, 1991, PHARMACOL TOXICOL, V69, P75; PAGLIA DE, 1967, J LAB CLIN MED, V70, P158; RICHARD MJ, 1992, CLIN CHEM, V38, P704; ROUBY JJ, 1989, ANESTHESIOLOGY, V71, P679, DOI 10.1097/00000542-198911000-00010; THOMPSON PJ, 1993, AM REV RESPIR DIS, V147, P164; VANVYVE T, 1992, AM REV RESPIR DIS, V146, P116	19	77	96	0	9	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	0003-2999			ANESTH ANALG	Anesth. Analg.	OCT	2001	93	4					981	985		10.1097/00000539-200110000-00036		5	Anesthesiology	Anesthesiology	476PL	WOS:000171237900033	11574369	
J	Kilpelainen, M; Terho, EO; Helenius, H; Koskenvuo, M				Kilpelainen, M; Terho, EO; Helenius, H; Koskenvuo, M			Home dampness, current allergic diseases, and respiratory infections among young adults	THORAX			English	Article						asthma; allergic rhinitis; atopic dermatitis; dampness	HOUSE-DUST MITE; HAY-FEVER; ASTHMA; CHILDREN; SENSITIZATION; CHILDHOOD; SYMPTOMS; HEALTH; MOLDS; INFLAMMATION	Background-The relation between home dampness and respiratory symptoms among adults is well confirmed, but data on specific allergic diseases and respiratory infections is more limited. Individual factors that may enhance susceptibility to the effects of home dampness are mainly unknown. Methods-The association between home dampness and current physician diagnosed asthma, allergic rhinitis, allergic conjunctivitis, atopic dermatitis, common colds, and bacterial respiratory infections was studied in a questionnaire survey of 10 667 Finnish first year university students aged 18-25 years. The dampness categories analysed were visible mould and visible mould or damp stains or water damage during the last year. In multivariate analyses adjustment was made for parental education, active and passive smoking, type and place of residence, pets, and wall to wall carpets. The interaction effect of atopic heredity and dampness was investigated. Results-Visible mould or damp stains or water damage was reported by 15.0% of the respondents. In multivariate models there was a positive association between home dampness and current asthma, allergic rhinitis, and atopic dermatitis, as well as common colds greater than or equal to4 times per year and other respiratory infections, but not between home dampness and allergic conjunctivitis. The strongest association was found between exposure to visible mould and asthma (OR 2.21, 95% CI 1.48 to 3.28) and common colds (OR 1.49, 95% CI 1.18 to 1.87). The risk of current asthma in damp homes was highest among subjects with atopic heredity. Conclusions-The risk of current asthma, allergic rhinitis, and atopic dermatitis was higher in damp homes. Of the respiratory infections, the risk of common colds was most clearly increased.	Univ Turku, Dept Pulm Dis & Clin Allergol, FIN-20520 Turku, Finland; Univ Turku, Dept Biostat, SF-20500 Turku, Finland; Univ Turku, Dept Publ Hlth, SF-20500 Turku, Finland	Kilpelainen, M (reprint author), Univ Turku, Cent Hosp, Dept Pulm Dis & Clin Allergol, Kiinamyllynkatu 4-8, FIN-20520 Turku, Finland.						Becher R, 1996, TOXICOL LETT, V86, P155, DOI 10.1016/0378-4274(96)03685-5; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; BRUNEKREEF B, 1992, ALLERGY, V47, P498, DOI 10.1111/j.1398-9995.1992.tb00672.x; Charpin D, 1999, CLIN EXP ALLERGY, V29, P1474; DALES RE, 1991, AM REV RESPIR DIS, V143, P505; Dharmage S, 1999, CLIN EXP ALLERGY, V29, P1481, DOI 10.1046/j.1365-2222.1999.00640.x; Garrett MH, 1998, CLIN EXP ALLERGY, V28, P459; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; KILPELAINEN M, 2001, IN PRESS ALLERGY; Lindfors A, 1999, J ALLERGY CLIN IMMUN, V104, P755; MARTIN CJ, 1987, BRIT MED J, V294, P1125; NEVALAINEN A, 1995, INDOOR AIR INTEGRATE, P485; Nicolai T, 1998, THORAX, V53, P1035; Norback D, 1999, INT J TUBERC LUNG D, V3, P368; Pappas G P, 2000, Int J Occup Environ Health, V6, P1; PEAT JK, 1993, CLIN EXP ALLERGY, V23, P812, DOI 10.1111/j.1365-2222.1993.tb00258.x; Pirhonen I, 1996, EUR RESPIR J, V9, P2618, DOI 10.1183/09031936.96.09122618; Plaschke P, 1999, J ALLERGY CLIN IMMUN, V104, P58, DOI 10.1016/S0091-6749(99)70114-4; PLATT SD, 1989, BRIT MED J, V298, P1673; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Rook GAW, 1998, IMMUNOL TODAY, V19, P113, DOI 10.1016/S0167-5699(97)01204-8; SAS Institute, 1996, SAS STAT SOFTW CHANG; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; SUSITAIVAL P, 1996, TUOHILAMPI QUESTIONN; Thorn J, 1998, AM J RESP CRIT CARE, V157, P1798; VERHOEFF AP, 1995, AM J EPIDEMIOL, V141, P103; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; WICKMAN M, 1992, J ALLERGY CLIN IMMUN, V89, P752, DOI 10.1016/0091-6749(92)90384-E; Williamson IJ, 1997, THORAX, V52, P229	29	77	78	0	2	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	JUN	2001	56	6					462	467		10.1136/thorax.56.6.462		6	Respiratory System	Respiratory System	438XL	WOS:000169079500010	11359962	
J	Vailes, L; Sridhara, S; Cromwell, O; Weber, B; Breitenbach, M; Chapman, M				Vailes, L; Sridhara, S; Cromwell, O; Weber, B; Breitenbach, M; Chapman, M			Quantitation of the major fungal allergens, Alt a 1 and Asp f 1, in commercial allergenic products	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Alternaria; Aspergillus; allergen exposure; recombinant allergens; fungi; asthma	SCHOOL-AGE-CHILDREN; ALTERNARIA-ALTERNATA; BRONCHIAL HYPERRESPONSIVENESS; ASPERGILLUS-FUMIGATUS; CHILDHOOD ASTHMA; A-I; SENSITIZATION; EXTRACTS; CLADOSPORIUM; ASSOCIATION	Background: Alternaria is one of the most important fungi associated with allergic disease, whereas Aspergillus fumigatus is involved in a broad spectrum of pulmonary diseases. Currently, fungal extracts used for diagnosis in the United States are unstandardized, and their allergenic content cannot be compared directly. Objective: The goal of this study was to compare the variability of major allergen levels among US allergenic products derived from fungi: specifically, Alt a 1 levels in Alternaria alternata extracts, and Asp f 1 levels in A fumigatus extracts. Methods: A novel a-site monoclonal antibody ELISA was used for measuring Alt a 1 using recombinant Alt a 1 as a standard. Asp fl was also measured by ELISA, Allergenic products produced by 8 US manufacturers over a 2-year period were compared, as were multiple lots produced by a single company, Results: Alt a 1 levels in Alternaria extracts from 8 companies produced in 1998 and 1999 ranged from less than 0.01 to 6.09 mug/mL (mean 1.4 +/- 1.6 mug/mL, n = 15), In general, Alt al levels were consistent within and between companies (1.4 +/- 1.1 mug/mL, n = 27), with 21 of 32 (66%) of all extracts tested containing 0.7 to 2 mug/mL Alt a 1, Aspergillus extracts showed much greater variability in Asp fl levels, with extracts from 8 companies containing from less than 0.1 to 64 mug/mL Asp fl (mean 16.3 +/- 23.9 mug/mL, n = 15), Overall variability was greater for Aspergillus products within and between manufacturers (22 +/- 22 mug/mL Asp f 1, a = 20), Conclusions: ELISA-based assays for specific allergens showed greater consistency among allergenic products derived from Alternaria than from Aspergillus, These assays should facilitate improved quality control and standardization of fungal allergen extracts and lead to the development of more consistent products for clinical use.	Univ Virginia, Dept Med, Asthma & Allerg Dis Ctr, Charlottesville, VA 22908 USA; Joachim Ganzer KG, Allergopharma, Reinbek, Germany; Salzburg Univ, A-5020 Salzburg, Austria	Vailes, L (reprint author), Univ Virginia, Dept Med, Asthma & Allerg Dis Ctr, Box 801355, Charlottesville, VA 22908 USA.				NIAID NIH HHS [AI 32557, AI 34607]		[Anonymous], 1997, J ALLERGY CLIN IMMUN, V99, P583; ACHATZ G, 1995, MOL IMMUNOL, V32, P213, DOI 10.1016/0161-5890(94)00108-D; ADEN E, 1999, J ALLERGY CLIN IMMUN, V103, P128; AGARWAL MK, 1982, J ALLERGY CLIN IMMUN, V70, P432, DOI 10.1016/0091-6749(82)90005-7; ALDOORY Y, 1987, MOULD HLTH WHO IS RI; ARRUDA LK, 1992, J IMMUNOL, V149, P3354; AUKRUST L, 1985, Allergy (Copenhagen), V40, P43, DOI 10.1111/j.1398-9995.1985.tb04298.x; Crameri R, 1998, INT ARCH ALLERGY IMM, V115, P99, DOI 10.1159/000023889; CURRAN IHA, 1993, INT ARCH ALLERGY IMM, V102, P267; DeVouge MW, 1996, INT ARCH ALLERGY IMM, V111, P385; GERGEN PJ, 1992, J ALLERGY CLIN IMMUN, V90, P579, DOI 10.1016/0091-6749(92)90130-T; Halonen M, 1997, AM J RESP CRIT CARE, V155, P1356; HELM RM, 1988, J ALLERGY CLIN IMMUN, V81, P651, DOI 10.1016/0091-6749(88)91035-4; HENDERSON FW, 1995, AM J RESP CRIT CARE, V151, P1786; KLEINETEBBE J, 1993, CLIN EXP ALLERGY, V23, P211, DOI 10.1111/j.1365-2222.1993.tb00884.x; Nelson HS, 1999, J ALLERGY CLIN IMMUN, V104, P775; Neukirch C, 1999, J ALLERGY CLIN IMMUN, V103, P709, DOI 10.1016/S0091-6749(99)70247-2; OHOLLAREN MT, 1991, NEW ENGL J MED, V324, P359, DOI 10.1056/NEJM199102073240602; OVSYANNIKOVA IG, 1994, J ALLERGY CLIN IMMUN, V94, P537, DOI 10.1016/0091-6749(94)90211-9; PARIS S, 1990, J ALLERGY CLIN IMMUN, V85, P941, DOI 10.1016/0091-6749(90)90081-E; PARIS S, 1990, INT ARCH ALLER A IMM, V92, P1; PEAT JK, 1993, CLIN EXP ALLERGY, V23, P812, DOI 10.1111/j.1365-2222.1993.tb00258.x; PEAT JK, 1991, CLIN EXP ALLERGY, V21, P573, DOI 10.1111/j.1365-2222.1991.tb00849.x; Perzanowski MS, 1998, J ALLERGY CLIN IMMUN, V101, P626; PLATTSMILLS TAE, 1993, AEROBIOLOGY INHALANT, P498; PORTNOY J, 1993, J ALLERGY CLIN IMMUN, V91, P930, DOI 10.1016/0091-6749(93)90351-F; Portnoy J, 1998, ANN ALLERG ASTHMA IM, V81, P59; STERINGER I, 1987, INT ARCH ALLER A IMM, V84, P190; Tariq SM, 1996, CLIN EXP ALLERGY, V26, P794; VANDERHEIDE S, 1985, ALLERGY, V40, P592; VIJAY HM, 1993, J ALLERGY CLIN IMMUN, V91, P826, DOI 10.1016/0091-6749(93)90338-G; VIJAY HM, 1984, INT ARCH ALLER A IMM, V74, P256; WAHL R, 1989, ANN ALLERGY, V63, P527; YUNGINGER JW, 1980, J ALLERGY CLIN IMMUN, V66, P138, DOI 10.1016/0091-6749(80)90061-5; ZHANG L, 1995, INT ARCH ALLERGY IMM, V108, P254	35	77	79	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.	APR	2001	107	4					641	646				6	Allergy; Immunology	Allergy; Immunology	423RG	WOS:000168190100015	11295652	
J	Piirila, PL; Nordman, H; Keskinen, HM; Luukkonen, R; Salo, SP; Tuomi, TO; Tuppurainen, M				Piirila, PL; Nordman, H; Keskinen, HM; Luukkonen, R; Salo, SP; Tuomi, TO; Tuppurainen, M			Long-term follow-up of hexamethylene diisocyanate-, biphenylmethane diisocyanate-, and toluene diisocyanate-induced asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							OCCUPATIONAL ASTHMA; NATURAL-HISTORY; ISOCYANATES; ANTIBODIES; WORKERS; IGE; REACTIVITY; DIAGNOSIS; CHALLENGE; EXPOSURE	In 1976-1992 245 new cases of asthma induced by diisocyanates were diagnosed, caused by hexamethylene diisocyanate (HDI) in 39%, diphenylmethane diisocyanate (MDI) in 39%, and toluene diisocyanate (TDI) in 17% of the cases. Our aim was to study the clinical outcome of diisocyanate-induced asthma, A questionnaire was sent to the 235 patients alive in 7995, and validated by reexamining clinically 91 of them. The study was carried out on average 10 (3-19) yr after the diagnosis. Of the patients 82% experienced symptoms of asthma, 34% used no medication, and 35% were on regular medication. The patients having displayed immunoglobulin E (IgE) antibodies to isocyanates used less medication (OR 0.273; Cl 0.098, 0.758) and had fewer symptoms of asthma (OR 0.329; Cl 0.124, 0.875) than the IgE-negative ones. They also had a significantly shorter duration of symptoms (p = 0.0025), latency period (p = 0.0249), and duration of exposure (p = 0.0008) than the IgE-negative patients. This did not, however, entirely explain the more favourable outcome of the IgE-positive patients. Patients with HDI-induced asthma used less medication (OR 0.412; Cl 0.229, 0.739) than patients with MDI- and TDI-induced asthma. The results confirm the generally rather poor medical outcome of diisocyanate-induced asthma; the persistence of symptoms and unspecific bronchial reactivity were pronounced in TDI-induced asthma. A more favourable outcome was associated with IgE mediation and HDI inducement.	Finnish Inst Occupat Hlth, FIN-00250 Helsinki, Finland; Helsinki Univ Hosp, Helsinki, Finland	Piirila, PL (reprint author), Finnish Inst Occupat Hlth, Topeliuksenkatu 41 A A, FIN-00250 Helsinki, Finland.			Piirila, Paivi/0000-0002-2535-4409			AAS K, 1973, INT ARCH ALLER A IMM, V45, P57; BAUR X, 1983, J ALLERGY CLIN IMMUN, V71, P197, DOI 10.1016/0091-6749(83)90100-8; BELIN L, 1981, European Journal of Respiratory Diseases Supplement, V62, P148; BERGLUND E, 1963, ACTA MED SCAND, V173, P185; BURGE PS, 1982, EUR J RESPIR DIS, V63, P47; CARTIER A, 1989, J ALLERGY CLIN IMMUN, V84, P507, DOI 10.1016/0091-6749(89)90364-3; DIEM JE, 1982, AM REV RESPIR DIS, V126, P420; FLETCHER C, 1977, BRIT MED J, V1, P1645; Kanerva L, 1991, EXOGENOUS DERMATOSES, P103; KAROL MH, 1981, J OCCUP ENVIRON MED, V23, P741, DOI 10.1097/00043764-198111000-00007; KESKINEN H, 1988, CLIN ALLERGY, V18, P597, DOI 10.1111/j.1365-2222.1988.tb02911.x; Keskinen H, 1996, CLIN PHYSIOL, V16, P633, DOI 10.1111/j.1475-097X.1996.tb00740.x; Laitinen L A, 1974, Scand J Respir Dis Suppl, V86, P1; LOZEWICZ S, 1987, BRIT J DIS CHEST, V81, P14, DOI 10.1016/0007-0971(87)90103-3; MAESTRELLI P, 1993, AM REV RESPIR DIS, V148, P407; MALO JL, 1992, J ALLERGY CLIN IMMUN, V90, P937, DOI 10.1016/0091-6749(92)90466-F; MAPP CE, 1988, EUR RESPIR J, V1, P273; MAPP CE, 1988, AM REV RESPIR DIS, V137, P1326; NORDMAN H, 1985, J ALLERGY CLIN IMMUN, V75, P91, DOI 10.1016/0091-6749(85)90018-1; PAGGIARO PL, 1984, CLIN ALLERGY, V14, P463, DOI 10.1111/j.1365-2222.1984.tb02230.x; PAGGIARO PL, 1993, CHEST, V103, P1123, DOI 10.1378/chest.103.4.1123; Park HS, 1997, CLIN EXP ALLERGY, V27, P1145; PEPYS J, 1975, AM REV RESPIR DIS, V112, P829; PEZZINI A, 1984, CLIN ALLERGY, V14, P453, DOI 10.1111/j.1365-2222.1984.tb02229.x; PISATI G, 1993, BRIT J IND MED, V50, P60; Quanjer Ph., 1983, B EUR PHYSIOPATHOL S, V19; Raulf-Heimsoth N, 1998, AM J IND MED, V34, P137; ROSENBERG C, 1984, AM IND HYG ASSOC J, V45, P117, DOI 10.1202/0002-8894(1984)045<0117:AIIPSP>2.3.CO;2; ROSENBERG N, 1987, CLIN ALLERGY, V17, P55, DOI 10.1111/j.1365-2222.1987.tb02319.x; SOVIJARVI ARA, 1993, CHEST, V104, P164, DOI 10.1378/chest.104.1.164; STREICHER RP, 1994, ANALYST, V119, P89, DOI 10.1039/an9941900089; TARLO SM, 1997, OCCUP ENVIRON MED, V54, P576; TAYLOR AJN, 1981, OCCUPATIONAL LUNG DI, P143; Tee RD, 1998, J ALLERGY CLIN IMMUN, V101, P709; Viljanen AA, 1982, SCAND J CLIN INVES S, V42, P1	35	77	77	0	4	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.	AUG	2000	162	2					516	522				7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	345RP	WOS:000088829200031	10934080	
J	Pope, M; Johnston, KW				Pope, M; Johnston, KW			Anaphylaxis after thrombin injection of a femoral pseudoaneurysm: Recommendations for prevention	JOURNAL OF VASCULAR SURGERY			English	Article							TOPICAL THROMBIN; COAGULATION	After the injection treatment of a femoral pseudoaneurysm, an anaphylactic reaction occurred in a patient undergoing hemodialysis who previously had repeated exposure to thrombin. Before injecting bovine thrombin in patients with a history of prior exposure, we recommend that they undergo skin prick testing to detect possible allergy.	Toronto Gen Hosp, Dept Surg, Toronto, ON M5G 2C4, Canada; Univ Toronto, Toronto, ON, Canada	Johnston, KW (reprint author), Toronto Gen Hosp, Dept Surg, Eaton 5-309,200 Elizabeth St, Toronto, ON M5G 2C4, Canada.						Brophy DP, 2000, RADIOLOGY, V214, P278; CAMBRIA RA, 2000, VASCULAR SURG, P1493; COPE C, 1986, AM J ROENTGENOL, V147, P383; Dorion RP, 1998, ARCH PATHOL LAB MED, V122, P887; GILLIS M, 1999, COMPENDIUM PHARM SPE; Liau CS, 1997, J VASC SURG, V26, P18, DOI 10.1016/S0741-5214(97)70141-1; ORTEL TL, 1994, AM J HEMATOL, V45, P128, DOI 10.1002/ajh.2830450206; Plaut Marshall, 1993, P1399; TADOKORO K, 1991, J ALLERGY CLIN IMMUN, V88, P620, DOI 10.1016/0091-6749(91)90156-I; Taylor BS, 1999, J VASC SURG, V30, P1052, DOI 10.1016/S0741-5214(99)70043-1; Tidrick RT, 1943, SURGERY, V14, P191	11	77	80	0	1	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0741-5214			J VASC SURG	J. Vasc. Surg.	JUL	2000	32	1					190	191		10.1067/mva.2000.106498		2	Surgery; Peripheral Vascular Disease	Surgery; Cardiovascular System & Cardiology	334ED	WOS:000088172500034	10876222	
J	Lambert, AL; Dong, WM; Selgrade, MJK; Gilmour, MI				Lambert, AL; Dong, WM; Selgrade, MJK; Gilmour, MI			Enhanced allergic sensitization by residual oil fly ash particles is mediated by soluble metal constituents	TOXICOLOGY AND APPLIED PHARMACOLOGY			English	Article						particulate matter; metals; adjuvant; asthma; immediate bronchoconstriction; IL-5; IL-6; IL-10; IL-13; TNF-alpha; IgE; eosinophils	PARTICULATE AIR-POLLUTION; MESSENGER-RNA EXPRESSION; DIESEL EXHAUST PARTICLES; EMERGENCY ROOM VISITS; HOUSE-DUST MITE; CYTOKINE PRODUCTION; IN-VIVO; EPITHELIAL-CELLS; IGE PRODUCTION; LEUKOCYTE ADHESION	Epidemiological studies have demonstrated an association between elevated levels of particulate matter (PM) air pollutants and exacerbation of asthma symptoms. We have shown in a Brown Norway (BN) rat model of house dust mite (HDM) allergy that preexposure to residual oil By ash (ROFA) particles enhanced the sensitization phase such that the secondary immune response and associated lung injury were increased after allergen challenge. To determine whether the metals present in ROFA mediated this effect, BN rats were intratracheally instilled with either ROFA (1000 mu g) or acidified saline + NiSO4 (105.12 mu g), VSO4 (98.2 mu g), FeSO4 (58.49 mu g), or a mixture (Mix) of each metal. HDM-specific IgE was higher in the serum of the ROFA, Ni, V, and Mix groups than in the HDM group after challenge, and antigen-induced bronchoconstriction responses were increased in the Ni group. Lymphocyte proliferation to antigen was increased in the ROFA, Ni, and V groups compared to controls. Total protein and eosinophil peroxidase levels were elevated in the Fe group, and eosinophil numbers in the bronchoalveolar lavage fluid (BALF) were increased in the ROFA and Fe groups compared to HDM control. IL-5 and IL-13 mRNA expression was also increased in the lung tissue of all metal and ROFA-treated groups, while BALF IL-10 was elevated in the Fe and Mix groups, and IL-6 and TNF-alpha were elevated in the metal and ROFA-treated groups compared to controls. These results suggest that ROFA's metallic constituents mediate enhancement of sensitization to HDM and that pulmonary inflammation may play a role in this adjuvant effect. (C) 2000 Academic Press.	US EPA, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA; Univ N Carolina, Chapel Hill, NC 27599 USA	Gilmour, MI (reprint author), US EPA, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA.						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Appl. Pharmacol.	MAY 15	2000	165	1					84	93		10.1006/taap.2000.8932		10	Pharmacology & Pharmacy; Toxicology	Pharmacology & Pharmacy; Toxicology	348RU	WOS:000089000900008	10814556	
J	Weinberg, EG				Weinberg, EG			Urbanization and childhood asthma: An African perspective	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Africa; urbanization; childhood asthma; prevalence; parasites	EXERCISE-INDUCED BRONCHOSPASM; KENYAN SCHOOL-CHILDREN; PREVALENCE; URBAN; SCHOOLCHILDREN; INFECTION; BIRTH; ATOPY	The increasing prevalence of childhood asthma in the developed world is a cause for concern. Much research is currently being conducted in an attempt to identify possible reasons for this occurrence. A so-called Western lifestyle has been the factor most commonly cited to explain this worrying increase in asthma prevalence. In essence, this implies a way of life where children are exposed from early infancy to a wide range of foods, infections, indoor and outdoor allergens, and irritants and to the effects of motor vehicle pollution, Until fairly recently, children in many African countries lived mainly in rural areas and were not exposed to the effects of a Western lifestyle, Early studies in a limited number of African countries showed a very low rural prevalence of childhood asthma, especially where children lived according to a traditional lifestyle, These same studies showed that asthma was not uncommon in urbanized African children. There has been an increasing tendency over the past 20 years for those in rural communities to move to the large urban centers. More recent childhood asthma prevalence studies, especially those from Kenya and Ghana, have confirmed the urban-rural differences but have shown a much narrower gap. In part this may be the result of exposure of rural children to agricultural pesticides and irritants as well as of an increasing tendency to adopt a more Westernized lifestyle such as the use of beds with mattresses, pillows, and blankets, These circumstances on the African continent provide a natural laboratory in the quest for factors that influence the development of asthma in susceptible children, Once more fully elucidated, it is possible that much valuable information will be available to combat the relentless increase in childhood asthma both here as well as in the developed world.	Univ Cape Town, Allergy & Asthma Clin, Red Cross Childrens Hosp & Inst Child Hlth, ZA-7700 Rondebosch, South Africa	Weinberg, EG (reprint author), Univ Cape Town, Allergy & Asthma Clin, Red Cross Childrens Hosp & Inst Child Hlth, ZA-7700 Rondebosch, South Africa.						Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Bjorksten B, 1999, CLIN EXP ALLERGY, V29, P342; BUCHANAN DJ, 1974, POSTGRAD MED J, V50, P680; CARLSEN KH, 1994, EUR RESPIR REV, V4, P5; CARSWELL GF, 1976, LANCET, V2, P706; Cookson WOCM, 1997, SCIENCE, V275, P41, DOI 10.1126/science.275.5296.41; Custovic A, 1999, CLIN EXP ALLERGY, V29, P144; DESOUZA M, 1994, E AFR MED J, V71, P473; EGBUONU L, 1982, PEDIATRICS, V69, P550; Ehrlich RI, 1995, INT J EPIDEMIOL, V24, P1138, DOI 10.1093/ije/24.6.1138; Farooqi IS, 1998, THORAX, V53, P927; GODFREY R C, 1975, Clinical Allergy, V5, P201, DOI 10.1111/j.1365-2222.1975.tb01853.x; KEELEY DJ, 1991, THORAX, V46, P549, DOI 10.1136/thx.46.8.549; KELLY YJ, 1995, THORAX, V50, P525, DOI 10.1136/thx.50.5.525; LUYT DK, 1995, S AFR MED J, V85, P999; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Matricardi PM, 1998, J ALLERGY CLIN IMMUN, V101, P439, DOI 10.1016/S0091-6749(98)70350-1; MOHAMED N, 1995, THORAX, V50, P74, DOI 10.1136/thx.50.1.74; Morley D., 1986, MY NAME IS TODAY; Ng'ang'a LW, 1998, THORAX, V53, P919; Odhiambo JA, 1998, EUR RESPIR J, V12, P1105, DOI 10.1183/09031936.98.12051105; PULLAN CR, 1982, BRIT MED J, V284, P1665; ROMAGNANI S, 1992, INT ARCH ALLERGY IMM, V98, P279; Salvi SS, 1999, CLIN EXP ALLERGY, V29, P4; SENTHILSELVAN A, 1992, AM REV RESPIR DIS, V146, P884; Shaheen SO, 1996, LANCET, V347, P1792, DOI 10.1016/S0140-6736(96)91617-7; Stein CE, 1997, THORAX, V52, P895; VANNIEKERK CH, 1979, CLIN ALLERGY, V9, P319; VANNIEKERK CH, 1979, S AFR MED J, V55, P756; VANNIEKERK CH, 1977, LANCET, V1, P96; YAMANEBERHAN H, 1997, LANCET, V350, P85; Yobo EODA, 1997, THORAX, V52, P161	32	77	82	0	9	MOSBY-YEAR BOOK INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	FEB	2000	105	2	1				224	231		10.1016/S0091-6749(00)90069-1		8	Allergy; Immunology	Allergy; Immunology	285RQ	WOS:000085402200004	10669840	
J	Allen, KJ; Koplin, JJ; Ponsonby, AL; Gurrin, LC; Wake, M; Vuillermin, P; Martin, P; Matheson, M; Lowe, A; Robinson, M; Tey, D; Osborne, NJ; Dang, T; Tan, HTT; Thiele, L; Anderson, D; Czech, H; Sanjeevan, J; Zurzolo, G; Dwyer, T; Tang, MLK; Hill, D; Dharmage, SC				Allen, Katrina J.; Koplin, Jennifer J.; Ponsonby, Anne-Louise; Gurrin, Lyle C.; Wake, Melissa; Vuillermin, Peter; Martin, Pamela; Matheson, Melanie; Lowe, Adrian; Robinson, Marnie; Tey, Dean; Osborne, Nicholas J.; Thanh Dang; Tan, Hern-Tze Tina; Thiele, Leone; Anderson, Deborah; Czech, Helen; Sanjeevan, Jeeva; Zurzolo, Giovanni; Dwyer, Terence; Tang, Mimi L. K.; Hill, David; Dharmage, Shyamali C.			Vitamin D insufficiency is associated with challenge-proven food allergy in infants	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Vitamin D; food allergy; peanut allergy; egg allergy; population; oral food challenge; eczema; epigenetic	REGULATORY T-CELLS; UNITED-STATES; BIRTH COHORT; POPULATION; PREVALENCE; CHILDREN; LATITUDE; RADIATION; EXPOSURE; SEASON	Background: Epidemiological evidence has shown that pediatric food allergy is more prevalent in regions further from the equator, suggesting that vitamin D insufficiency may play a role in this disease. Objective: To investigate the role of vitamin D status in infantile food allergy. Methods: A population sample of 5276 one-year-old infants underwent skin prick testing to peanut, egg, sesame, and cow's milk or shrimp. All those with a detectable wheal and a random sample of participants with negative skin prick test results attended a hospital-based food challenge clinic. Blood samples were available for 577 infants (344 with challenge-proven food allergy, 74 sensitized but tolerant to food challenge, 159 negative on skin prick test and food challenge). Serum 25-hydroxyvitamin D levels were measured by using liquid chromatography tandem mass spectrometry. Associations between serum 25-hydroxyvitamin D and food allergy were examined by using multiple logistic regression, adjusting for potential risk and confounding factors. Results: Infants of Australian-born parents, but not of parents born overseas, with vitamin D insufficiency (<= 50 nmol/L) were more likely to be peanut (adjusted odds ratio [aOR], 11.51; 95% CI, 2.01-65.79; P = .006) and/or egg (aOR, 3.79; 95% CI, 1.1912.08; P = .025) allergic than were those with adequate vitamin D levels independent of eczema status. Among those with Australian-born parents, infants with vitamin D insufficiency were more likely to have multiple food allergies (>= 2) rather than a single food allergy (aOR, 10.48; 95% CI, 1.60-68.61 vs aOR, 1.82; 95% CI, 0.38-8.77, respectively). Conclusions: These results provide the first direct evidence that vitamin D sufficiency may be an important protective factor for food allergy in the first year of life. (J Allergy Clin Immunol 2013; 131:1109-16.)	[Allen, Katrina J.; Koplin, Jennifer J.; Ponsonby, Anne-Louise; Gurrin, Lyle C.; Wake, Melissa; Vuillermin, Peter; Martin, Pamela; Lowe, Adrian; Osborne, Nicholas J.; Thanh Dang; Tan, Hern-Tze Tina; Thiele, Leone; Anderson, Deborah; Czech, Helen; Sanjeevan, Jeeva; Zurzolo, Giovanni; Dwyer, Terence; Tang, Mimi L. K.; Hill, David; Dharmage, Shyamali C.] Murdoch Childrens Res Inst, Parkville, Vic, Australia; [Allen, Katrina J.; Koplin, Jennifer J.; Ponsonby, Anne-Louise; Wake, Melissa; Osborne, Nicholas J.; Tang, Mimi L. K.] Univ Melbourne, Dept Paediat, Parkville, Vic 3052, Australia; [Allen, Katrina J.; Robinson, Marnie; Tey, Dean; Tang, Mimi L. K.] Royal Childrens Hosp, Dept Allergy & Immunol, Parkville, Vic 3052, Australia; [Gurrin, Lyle C.; Matheson, Melanie; Lowe, Adrian; Osborne, Nicholas J.; Dharmage, Shyamali C.] Univ Melbourne, Ctr Mol Environm Genet & Analyt Epidemiol, Parkville, Vic 3052, Australia; [Wake, Melissa] Royal Childrens Hosp, Ctr Community Child Hlth, Parkville, Vic 3052, Australia; [Vuillermin, Peter] Barwon Hlth, Child Hlth Res Unit, Geelong, Vic, Australia; [Vuillermin, Peter] Deakin Univ, Geelong, Vic 3217, Australia; [Osborne, Nicholas J.] Univ Exeter, Peninsula Coll Med & Dent, European Ctr Environm & Human Hlth, Exeter EX4 4QJ, Devon, England	Allen, KJ (reprint author), Royal Childrens Hosp, Murdoch Childrens Res Inst, Flemington Rd, Parkville, Vic 3052, Australia.	katie.allen@rch.org.au	Wake, Melissa/J-1396-2012; Osborne, Nicholas/D-2086-2011; Matheson, Melanie/O-4721-2015; Osborne, Nicholas/N-4915-2015	Wake, Melissa/0000-0001-7501-9257; Zurzolo, Giovanni/0000-0003-0230-0691; Dharmage, Shyamali/0000-0001-6063-1937; Osborne, Nicholas/0000-0002-6700-2284; Matheson, Melanie/0000-0002-5822-3499; Osborne, Nicholas/0000-0002-6700-2284; Lowe, Adrian/0000-0002-4691-8162; Tan, Hern-Tze Tina/0000-0002-8289-7573	National Health and Medical Research Council of Australia; Ilhan Food Allergy Foundation; AnaphylaxiStop; Charles and Sylvia Viertel Medical Research Foundation; Victorian Government's Operational Infrastructure Support Program; National Health and Medical Research Council; European Regional Development Fund; European Social Fund Convergence Programme; Australian Egg Corporation	This study was supported by funding from the National Health and Medical Research Council of Australia, the Ilhan Food Allergy Foundation, AnaphylaxiStop, the Charles and Sylvia Viertel Medical Research Foundation, and the Victorian Government's Operational Infrastructure Support Program.; Disclosure of potential conflict of interest: K. J. Allen is a Viertel Senior Medical Research Fellow and has received payment for lectures from Abbott, Wyeth, and Nutricia. J. J. Koplin is partly supported by a postdoctoral fellowship from a National Health and Medical Research Council Capacity Building Grant in Population Health. A.-L. Ponsonby, L. C. Gurrin, M. Wake, M. Matheson, A. Lowe, and S. C. Dharmage are supported by the National Health and Medical Research Council. D. Tey has received payment for lectures from Merck Sharp & Dohme, Abbott Nutrition, and Alphapharm. P. Martin and T. Dang are Australian Postgraduate Award PhD scholars, and H.-T. Tina Tan is a Malaysian Government PhD scholar. N. J. Osborne is supported by the European Regional Development Fund and the European Social Fund Convergence Programme, has received grants and travel support from the National Health and Medical Research Council, and has received grants from the Australian Egg Corporation. M. Tang is on the advisory board for the Nestle Nutrition Institute and Nutricia and has received speakers fees from Nutricia, Nestle Nutrition Institute, and Wyeth. The rest of the authors declare that they have no relevant conflicts of interest.	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Allergy Clin. Immunol.	APR	2013	131	4					1109	+		10.1016/j.jaci.2013.01.017		14	Allergy; Immunology	Allergy; Immunology	120QT	WOS:000317187200021	23453797	
J	Ziegler, SF				Ziegler, Steven F.			Thymic stromal lymphopoietin and allergic disease	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Thymic stromal lymphopoietin; asthma; allergy; atopic dermatitis; inflammation	OBSTRUCTIVE PULMONARY-DISEASE; NASAL EPITHELIAL-CELLS; RETINOID-X-RECEPTOR; IGM(+) B-CELLS; CD4(+) T-CELLS; ATOPIC-DERMATITIS; DENDRITIC CELLS; TSLP RECEPTOR; CUTTING EDGE; OX40 LIGAND	The importance of the epithelium in initiating and controlling immune responses is becoming more appreciated. For example, allergen contact first occurs at mucosal sites exposed to the external environment, such as the skin, airways, and gastrointestinal tract. This exposure leads to the production of a variety of cytokines and chemokines that are involved in driving allergic inflammatory responses. One such product is thymic stromal lymphopoietin (TSLP). Recent studies in both human subjects and murine models have implicated TSLP in the development and progression of allergic diseases. This review will highlight recent advances in the understanding of the role of TSLP in these inflammatory diseases. Importantly, these insights into TSLP's multifaceted role could potentially allow for novel therapeutic manipulations of these disorders. (J Allergy Clin Immunol 2012; 130:845-52.)	[Ziegler, Steven F.] Benaroya Res Inst, Program Immunol, Seattle, WA 98101 USA; [Ziegler, Steven F.] Univ Washington, Dept Immunol, Seattle, WA 98195 USA	Ziegler, SF (reprint author), Benaroya Res Inst, Program Immunol, 1201 9th Ave, Seattle, WA 98101 USA.	sziegler@benaroyaresearch.org			National Institutes of Health [AI068731, AR056113, AR055695, HL098067, HL102708, AR059058]; Asthma and Allergy Foundation of America; National Institutes of Health; American Academy of Allergy, Asthma Immunology	Support was provided by grants AI068731, AR056113, AR055695, HL098067, HL102708, and AR059058 from the National Institutes of Health and a grant from the Asthma and Allergy Foundation of America.; S.F. Ziegler has received research support from the National Institutes of Health; has received lecture fees from the American Academy of Allergy, Asthma & Immunology; and has received travel support from the Federation of Clinical Immunology Societies.	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Allergy Clin. Immunol.	OCT	2012	130	4					845	852		10.1016/j.jaci.2012.07.010		8	Allergy; Immunology	Allergy; Immunology	017MT	WOS:000309594800002	22939755	
J	Brehm, JM; Acosta-Perez, E; Klei, L; Roeder, K; Barmada, M; Boutaoui, N; Forno, E; Kelly, R; Paul, K; Sylvia, J; Litonjua, AA; Cabana, M; Alvarez, M; Colon-Semidey, A; Canino, G; Celedon, JC				Brehm, John M.; Acosta-Perez, Edna; Klei, Lambertus; Roeder, Kathryn; Barmada, Michael; Boutaoui, Nadia; Forno, Erick; Kelly, Roxanne; Paul, Kathryn; Sylvia, Jody; Litonjua, Augusto A.; Cabana, Michael; Alvarez, Maria; Colon-Semidey, Angel; Canino, Glorisa; Celedon, Juan C.			Vitamin D Insufficiency and Severe Asthma Exacerbations in Puerto Rican Children	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						vitamin D; asthma exacerbations; Puerto Ricans; childhood	GENETIC ANCESTRY; AFRICAN ANCESTRY; LUNG-FUNCTION; INDUCTION; EXPOSURE; POPULATIONS; PREDICTORS; ADMIXTURE; MARKERS; ADULTS	Rationale: Vitamin D insufficiency (a serum 25(OH)D <30 ng/ml) has been associated with severe asthma exacerbations, but this could be explained by underlying racial ancestry or disease severity. Little is known about vitamin D and asthma in Puerto Ricans. Objectives To examine whether vitamin D insufficiency is associated with severe asthma exacerbations in Puerto Rican children, independently of racial ancestry, atopy, and time outdoors. Methods: A cross-sectional study was conducted of 560 children ages 6-14 years with (n = 287) and without (n = 273) asthma in San Juan, Puerto Rico. We measured plasma vitamin D and estimated the percentage of African racial ancestry among participants using genome-wide genotypic data. We tested whether vitamin D insufficiency is associated with severe asthma exacerbations, lung function, or atopy (greater than or equal to one positive IgE to allergens) using logistic or linear regression. Multivariate models were adjusted for African ancestry, time outdoors, atopy, and other covariates. Measurements and Main Results Vitamin D insufficiency was common in children with (44%) and without (47%) asthma. In multivariate analyses, vitamin D insufficiency was associated with higher odds of greater than or equal to one severe asthma exacerbation in the prior year (odds ratio [OR], 2.6; 95% confidence interval [CI], 1.5-4.9; P = 0.001) and atopy, and a lower FEV1/FVC in cases. After stratification by atopy, the magnitude of the association between vitamin D insufficiency and severe exacerbations was greater in nonatopic (OR, 6.2; 95% CI, 2-21.6; P = 0.002) than in atopic (OR, 2; 95% CI, 1-4.1; P = 0.04) cases. Conclusions Vitamin D insufficiency is associated with severe asthma exacerbations in Puerto Rican children, independently of racial ancestry, atopy, or markers of disease severity or control.	[Brehm, John M.; Boutaoui, Nadia; Celedon, Juan C.] UPMC, Childrens Hosp Pittsburgh, Div Pediat Pulm Med Allergy & Immunol, Dept Pediat, Pittsburgh, PA 15224 USA; [Klei, Lambertus] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Psychiat, Pittsburgh, PA USA; [Barmada, Michael] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Human Genet, Pittsburgh, PA 15261 USA; [Acosta-Perez, Edna; Alvarez, Maria; Colon-Semidey, Angel; Canino, Glorisa] Univ Puerto Rico, Behav Sci Res Inst, San Juan, PR 00936 USA; [Roeder, Kathryn] Carnegie Mellon Univ, Dept Stat, Pittsburgh, PA 15213 USA; [Forno, Erick] Univ Miami, Dept Pediat, Div Pediat Pulmonol, Miami, FL 33152 USA; [Kelly, Roxanne; Paul, Kathryn; Sylvia, Jody; Litonjua, Augusto A.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA; [Cabana, Michael] Univ Calif San Francisco, Dept Pediat, Div Gen Pediat, San Francisco, CA USA	Celedon, JC (reprint author), UPMC, Childrens Hosp Pittsburgh, Div Pediat Pulm Med Allergy & Immunol, Dept Pediat, 4401 Penn Ave, Pittsburgh, PA 15224 USA.	juan.celedon@chp.edu		acosta, edna/0000-0001-7101-3157; Barmada, M Michael/0000-0002-3604-6460; Litonjua, Augusto/0000-0003-0422-5875; Forno, Erick/0000-0001-6497-9885	National Institutes of Health [R01HL079966, K12HD052892]; Children's Hospital of Pittsburgh of the UPMC Health System	Supported by grant R01HL079966 from the National Institutes of Health. J.M.B. receives support from NIH grant K12HD052892. This project was supported in part by Children's Hospital of Pittsburgh of the UPMC Health System.	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J. Respir. Crit. Care Med.	JUL 15	2012	186	2					140	146		10.1164/rccm.201203-0431OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	974OH	WOS:000306445300009	22652028	
J	Wills-Karp, M; Rani, R; Dienger, K; Lewkowich, I; Fox, JG; Perkins, C; Lewis, L; Finkelman, FD; Smith, DE; Bryce, PJ; Kurt-Jones, EA; Wang, TC; Sivaprasad, U; Hershey, GK; Herbert, DR				Wills-Karp, Marsha; Rani, Reena; Dienger, Krista; Lewkowich, Ian; Fox, James G.; Perkins, Charles; Lewis, Lauren; Finkelman, Fred D.; Smith, Dirk E.; Bryce, Paul J.; Kurt-Jones, Evelyn A.; Wang, Timothy C.; Sivaprasad, Umasundari; Hershey, Gurjit K.; Herbert, De'Broski R.			Trefoil factor 2 rapidly induces interleukin 33 to promote type 2 immunity during allergic asthma and hookworm infection	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article							IN-VIVO; AIRWAY HYPERREACTIVITY; DENDRITIC CELLS; ACUTE SCHISTOSOMIASIS; CYTOKINE PRODUCTION; HELMINTH INFECTION; ADAPTIVE IMMUNITY; EFFECTOR FUNCTION; EPITHELIAL-CELLS; T-CELLS	The molecular mechanisms that drive mucosal T helper type 2 (T(H)2) responses against parasitic helminths and allergens remain unclear. In this study, we demonstrate in mice that TFF2 (trefoil factor 2), an epithelial cell-derived repair molecule, is needed for the control of lung injury caused by the hookworm parasite Nippostrongylus brasiliensis and for type 2 immunity after infection. TFF2 is also necessary for the rapid production of IL-33, a T(H)2-promoting cytokine, by lung epithelia, alveolar macrophages, and inflammatory dendritic cells in infected mice. TFF2 also increases the severity of allergic lung disease caused by house dust mite antigens or IL-13. Moreover, TFF2 messenger RNA expression is significantly increased in nasal mucosal brushings during asthma exacerbations in children. These experiments extend the biological functions of TFF2 from tissue repair to the initiation and maintenance of mucosal T(H)2 responses.	[Wills-Karp, Marsha; Rani, Reena; Dienger, Krista; Lewkowich, Ian; Perkins, Charles; Lewis, Lauren; Finkelman, Fred D.; Herbert, De'Broski R.] Cincinnati Childrens Hosp Med Ctr, Div Immunobiol, Cincinnati, OH 45229 USA; [Sivaprasad, Umasundari; Hershey, Gurjit K.] Cincinnati Childrens Hosp Med Ctr, Div Asthma Res, Cincinnati, OH 45229 USA; [Fox, James G.] MIT, Div Comparat Med, Cambridge, MA 02139 USA; [Finkelman, Fred D.] Univ Cincinnati, Coll Med, Div Rheumatol Allergy & Immunol, Cincinnati, OH 45267 USA; [Finkelman, Fred D.] Cincinnati Vet Affairs Med Ctr, Dept Med, Cincinnati, OH 45220 USA; [Smith, Dirk E.] Amgen Inc, Dept Inflammat Res, Seattle, WA 98119 USA; [Bryce, Paul J.] Northwestern Univ, Feinberg Sch Med, Div Allergy Immunol, Chicago, IL 60611 USA; [Kurt-Jones, Evelyn A.] Univ Massachusetts, Sch Med, Dept Med, Worcester, MA 01655 USA; [Wang, Timothy C.] Columbia Univ, Med Ctr, Dept Med, New York, NY 10032 USA	Herbert, DR (reprint author), Cincinnati Childrens Hosp Med Ctr, Div Immunobiol, Cincinnati, OH 45229 USA.	debroski.herbert@cchmc.org	Herbert, De'Broski/J-7357-2012	Herbert, De'Broski/0000-0002-2449-5365	US Department of Veterans Affairs, T.C; National Institutes of Health (NIH) [5R01DK060758]; NIH [R01AI076456, RO1 HL67736, RO1 AI1183315, U19A170235, P50ES015903];  [U19AI70235];  [R01AI095289];  [R01GM083204]	D. Finkelman is supported by a merit award from the US Department of Veterans Affairs, T.C. Wang is supported by National Institutes of Health (NIH) grant 5R01DK060758, G. K. Hershey is supported by grant U19AI70235, P.J. Bryce is supported by NIH grant R01AI076456, M. Wills- Karp is supported by NIH grants RO1 HL67736, RO1 AI1183315, U19A170235, and P50ES015903, IPL is supported by a Parker B. Francis Award, and D.R. Herbert is supported by grants R01AI095289 and R01GM083204.	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Exp. Med.	MAR 12	2012	209	3					607	622		10.1084/jem.20110079		16	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	923RH	WOS:000302635900018	22329990	
J	Cassani, B; Villablanca, EJ; Quintana, FJ; Love, PE; Lacy-Hulbert, A; Blaner, WS; Sparwasser, T; Snapper, SB; Weiner, HL; Mora, JR				Cassani, Barbara; Villablanca, Eduardo J.; Quintana, Francisco J.; Love, Paul E.; Lacy-Hulbert, Adam; Blaner, William S.; Sparwasser, Tim; Snapper, Scott B.; Weiner, Howard L.; Mora, J. Rodrigo			Gut-Tropic T Cells That Express Integrin alpha 4 beta 7 and CCR9 Are Required for Induction of Oral Immune Tolerance in Mice	GASTROENTEROLOGY			English	Article						Immune Regulation; Autoimmunity; Allergy; Intestine; Peyer's Patch	PLASMACYTOID DENDRITIC CELLS; RETINOIC-ACID; SMALL-INTESTINE; SUPPRESSION; COLITIS; ABSENCE; IL-10; TH17; INFLAMMATION; LYMPHOCYTES	BACKGROUND & AIMS: Induction of oral immune tolerance (OT) blocks proinflammatory responses to orally administered antigens and might be used to treat autoimmune conditions. We investigated whether gut-tropic T cells that express the integrin alpha 4 beta 7 and the chemokine receptor CCR9 are required for OT. METHODS: Skin delayed-type hypersensitivity and experimental autoimmune encephalomyelitis were used to monitor OT in mice. To assess the role of receptors that mediate localization of lymphocytes to the gut (gut-homing receptors) in induction of OT, we studied CCR9(-/-) and beta 7(-/-) mice and also blocked the alpha 4 beta 7 ligand MAdCAM-1 in wild-type mice. We used DEREG and Scurfy mice to assess the role of Foxp3(+) regulatory T cells (Treg) and IL-10(-/-) and IL-10R beta(-/-) mice to examine the role of interleukin (IL)-10 in induction of OT. RESULTS: OT could not be induced in CCR9(-/-) or beta 7(-/-) mice, or when MAdCAM-1 was blocked in wild-type mice, indicating that gut-homing receptors are required for oral tolerization. Consistent with the role of all-trans retinoic acid in inducing gut-homing T cells, OT could not be induced in mice depleted of vitamin A. OT was rescued in CCR9(-/-) mice following adoptive transfer of wild-type T cells, but not CCR9(-/-) or beta 7(-/-) T cells. Gut-homing T cells are therefore necessary and sufficient to induce OT. Wild-type Treg and IL-10 were required to restore OT to CCR9-/- mice, indicating that homing and functional differentiation of IL-10-producing Treg in the gut is required for OT. Conversely, transfer of CCR9(-/-) or beta 7(-/-) T cells to wild-type mice partially inhibited OT. CONCLUSIONS: Expression of CCR9 and alpha 4 beta 7 on T cells and their subsequent localization to the gut is required for induction of OT in mice. Therapies designed to block gut-homing receptors might, under some conditions, interfere with normal tolerogenic mechanisms in the intestinal mucosa.	[Cassani, Barbara; Villablanca, Eduardo J.; Mora, J. Rodrigo] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA; [Snapper, Scott B.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA; [Snapper, Scott B.] Childrens Hosp, Gastrointestinal Unit, Boston, MA 02115 USA; [Quintana, Francisco J.; Weiner, Howard L.] Brigham & Womens Hosp, Ctr Neurol Dis, Boston, MA 02115 USA; [Love, Paul E.; Lacy-Hulbert, Adam] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA; [Blaner, William S.] Columbia Univ, Dept Med, New York, NY USA; [Sparwasser, Tim] Ctr Expt & Clin Infect Res, Inst Infect Immunol, Hannover, Germany	Mora, JR (reprint author), Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.	j_rodrigo_mora@hms.harvard.edu	Villablanca, Eduardo/E-1380-2016; Cassani, Barbara/K-3871-2016	Villablanca, Eduardo/0000-0001-9522-9729; Cassani, Barbara/0000-0002-4115-8109; Lacy-Hulbert, Adam/0000-0003-2162-0156	EMBO; Crohn's & Colitis Foundation of America; National Institutes of Health [R00 AI075285-02, AI435801, NS38037, P30 AR042689, DP2 2009A054301]; National Multiple Sclerosis Society [RG4111A1]; Boston Area Diabetes Endocrinology Research Center; Cancer Research Institute; Massachusetts Life Science Center	B.C. was supported by an EMBO postdoctoral fellowship. E.J.V. was supported by a postdoctoral fellowship from the Crohn's & Colitis Foundation of America. F.J.Q. was supported by grants from the National Institutes of Health (R00 AI075285-02), National Multiple Sclerosis Society (RG4111A1), and Boston Area Diabetes Endocrinology Research Center. H.L.W. was supported by National Institutes of Health grants AI435801 and NS38037. J.R.M. was supported by grants from the Crohn's & Colitis Foundation of America, Cancer Research Institute, Massachusetts Life Science Center, National Institutes of Health Pilot Feasibility Award P30 AR042689, and National Institutes of Health Director's New Innovator Award DP2 2009A054301.	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J	Valenta, R; Linhart, B; Swoboda, I; Niederberger, V				Valenta, R.; Linhart, B.; Swoboda, I.; Niederberger, V.			Recombinant allergens for allergen-specific immunotherapy: 10 years anniversary of immunotherapy with recombinant allergens	ALLERGY			English	Review						allergy; clinical trial; immunotherapy; recombinant allergen	BIRCH-POLLEN ALLERGEN; BET V 1; DUST MITE ALLERGEN; 3-YEAR DOUBLE-BLIND; B-CELL EPITOPES; PHL P 1; IMMUNOGLOBULIN-E; IGE ANTIBODIES; SUBLINGUAL IMMUNOTHERAPY; DIAGNOSTIC GATEKEEPERS	P>The broad applicability of allergen-specific immunotherapy for the treatment and eventually prevention of IgE-mediated allergy is limited by the poor quality and allergenic activity of natural allergen extracts that are used for the production of current allergy vaccines. Today, the genetic code of the most important allergens has been deciphered; recombinant allergens equalling their natural counterparts have been produced for diagnosis and immunotherapy, and a large panel of genetically modified allergens with reduced allergenic activity has been characterized to improve safety of immunotherapy and explore allergen-specific prevention strategies. Successful immunotherapy studies have been performed with recombinant allergens and hypoallergenic allergen derivatives and will lead to the registration of the first recombinant allergen-based vaccines in the near future. There is no doubt that recombinant allergen-based vaccination strategies will be generally applicable to most allergen sources, including respiratory, food and venom allergens and allow to produce safe allergy vaccines for the treatment of the most common forms of IgE-mediated allergies.	[Valenta, R.; Swoboda, I.] Med Univ Vienna, Christian Doppler Lab Allergy Res, A-1090 Vienna, Austria; [Valenta, R.; Linhart, B.] Med Univ Vienna, Div Immunopathol, Ctr Pathophysiol Infectiol & Immunol, Dept Pathophysiol & Allergy Res, A-1090 Vienna, Austria; [Niederberger, V.] Med Univ Vienna, ENT Dept, A-1090 Vienna, Austria	Valenta, R (reprint author), Med Univ Vienna, Christian Doppler Lab Allergy Res, Waehringer Guertel 18-20, A-1090 Vienna, Austria.	rudolf.valenta@meduniwien.ac.at			Austrian Science Fund, SFB [F1815, F1818, P23350-B11]; Christian Doppler Research Association; Biomay, Vienna, Austria	This article is dedicated to my mentor Prof. Dietrich Kraft. The study was supported by the Austrian Science Fund, SFB grants F1815, F1818, grant P23350-B11, by the Christian Doppler Research Association and a research grant from Biomay, Vienna, Austria.	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ZHANG L, 1992, IMMUNOLOGY, V76, P158; ZHANG L, 1993, J IMMUNOL, V151, P791	89	76	87	0	6	WILEY-BLACKWELL	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0105-4538			ALLERGY	Allergy	JUN	2011	66	6					775	783		10.1111/j.1398-9995.2011.02565.x		9	Allergy; Immunology	Allergy; Immunology	754ZP	WOS:000289896700008	21352238	
J	Salo, PM; Calatroni, A; Gergen, PJ; Hoppin, JA; Sever, ML; Jaramillo, R; Arbes, SJ; Zeldin, DC				Salo, Paeivi M.; Calatroni, Agustin; Gergen, Peter J.; Hoppin, Jane A.; Sever, Michelle L.; Jaramillo, Renee; Arbes, Samuel J., Jr.; Zeldin, Darryl C.			Allergy-related outcomes in relation to serum IgE: Results from the National Health and Nutrition Examination Survey 2005-2006	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Allergen; allergy; allergic sensitization; serum IgE	INHALANT ALLERGENS; NATURAL-HISTORY; UNITED-STATES; RISK-FACTORS; DUST-MITE; SKIN-TEST; US HOMES; RHINITIS; PREVALENCE; ASTHMA	Background: The National Health and Nutrition Examination Survey (NHANES) 2005-2006 was the first population-based study to investigate levels of serum total and allergen-specific IgE in the general US population. Objective: We estimated the prevalence of allergy-related outcomes and examined relationships between serum IgE levels and these outcomes in a representative sample of the US population. Methods: Data for this cross-sectional analysis were obtained from NHANES 2005-2006. Study subjects aged 6 years and older (n = 8086) had blood taken for measurement of total IgE and 19 specific IgE levels against common aeroallergens, including Alternaria alternata, Aspergillus fumigatus, Bermuda grass, birch, oak, ragweed, Russian thistle, rye grass, cat dander, cockroach, dog dander, dust mite (Dermatophagoides farinae and Dermatophagoides pteronyssinus), mouse and rat urine proteins, and selected foods (egg white, cow's milk, peanut, and shrimp). Serum samples were analyzed for total and allergen-specific IgE by using the Pharmacia CAP System. Information on allergy-related outcomes and demographics was collected by questionnaire. Results: In NHANES 2005-2006, 6.6% reported current hay fever, and 23.5% had current allergies. Allergy-related outcomes increased with increasing total IgE levels (adjusted odds ratios for a 10-fold increase in total IgE level of 1.86 [95% CI, 1.44-2.41] for hay fever and 1.64 [ 95% CI, 1.41-1.91] for allergies). Increased levels of plant-, pet-, and mold-specific IgE contributed independently to allergy-related symptoms. The greatest increase in odds was observed for hay fever and plant-specific IgE (adjusted odds ratio, 4.75; 95% CI, 3.83-5.88). Conclusion: In the US population self-reported allergy symptoms are most consistently associated with increased levels of plant-, pet-, and mold-specific IgE. (J Allergy Clin Immunol 2011;127:1226-35.)	[Salo, Paeivi M.; Hoppin, Jane A.; Sever, Michelle L.; Zeldin, Darryl C.] NIEHS, NIH, Res Triangle Pk, NC 27709 USA; [Calatroni, Agustin; Arbes, Samuel J., Jr.] Rho Inc, Chapel Hill, NC USA; [Gergen, Peter J.] NIAID, NIH, Bethesda, MD 20892 USA; [Jaramillo, Renee] SRA Int Inc, Durham, NC USA	Zeldin, DC (reprint author), NIEHS, NIH, 111 TW Alexander Dr,Room A222, Res Triangle Pk, NC 27709 USA.	zeldin@niehs.nih.gov	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Sever, Michelle/0000-0002-2435-1214	National Institutes of Health, National Institute of Environmental Health Sciences	Supported by the Intramural Research Program of the National Institutes of Health, National Institute of Environmental Health Sciences.	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Allergy Clin. Immunol.	MAY	2011	127	5					1226	U527		10.1016/j.jaci.2010.12.1106		17	Allergy; Immunology	Allergy; Immunology	756NG	WOS:000290018600018	21320720	
J	Katz, Y; Goldberg, MR; Rajuan, N; Cohen, A; Leshno, M				Katz, Yitzhak; Goldberg, Michael R.; Rajuan, Nelly; Cohen, Adi; Leshno, Moshe			The prevalence and natural course of food protein-induced enterocolitis syndrome to cow's milk: A large-scale, prospective population-based study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Food protein-induced enterocolitis syndrome; oral challenge; soy allergy; skin prick test	CLINICAL-FEATURES; ALLERGY; CHALLENGE; SOY	Background: The prevalence and natural history for food protein-induced enterocolitis syndrome (FPIES) have not been determined. Objective: We sought to determine the prevalence, clinical manifestations, and rate of recovery for FPIES in a large-scale, population-based prospective study. Methods: In a prospective study the feeding history of 13,019 infants was obtained. Infants with probable adverse reactions to cow's milk protein (CMP) were clinically examined, skin prick tested, and challenged orally. Diagnostic criteria for CMP-induced FPIES included age less than 9 months, delayed recurrent vomiting (usually with nausea), and lethargy after exposure to CMP in the absence of other IgE-mediated symptoms, such as rash, urticaria, and respiratory symptoms. In addition, a positive challenge response to milk resulted in the above-mentioned gastrointestinal symptoms, removal of milk from the diet resulted in the resolution of those symptoms, or both. Results: Ninety-eight percent of the cohort participated in the study. The cumulative incidence for FPIES was 0.34% (44/13,019 patients). The most common symptoms were recurrent vomiting (100%), lethargy (77%) diarrhea (25%), pallor (14%), and bloody diarrhea (4.5%). All patients had FPIES within the first 6 months of life. By the age of 3 years, 90% of the patients had recovered. We did not detect any concomitant reaction to soy. Eight patients with FPIES had IgE-mediated cow's milk allergy (IgE-CMA). Conclusions: The prevalence of FPIES is significant, and its clinical presentation is distinct from that of IgE-CMA. Most patients with FPIES recover, although a proportion might convert to IgE-CMA. The likelihood for a cross-reactivity to soy in this population was less than previously estimated. (J Allergy Clin Immunol 2011;127:647-53.)	[Katz, Yitzhak; Goldberg, Michael R.; Cohen, Adi] Assaf Harofeh Med Ctr, Inst Allergy & Immunol, IL-70300 Zerifin, Israel; [Katz, Yitzhak; Rajuan, Nelly] Tel Aviv Univ, Dept Pediat, IL-69978 Tel Aviv, Israel; [Leshno, Moshe] Tel Aviv Univ, Sackler Fac Med, Fac Management, IL-69978 Tel Aviv, Israel	Katz, Y (reprint author), Assaf Harofeh Med Ctr, Inst Allergy & Immunol, IL-70300 Zerifin, Israel.	ykatz49@gmail.com			Israel Dairy Foundation; Israel dairy board	Supported by the Israel Dairy Foundation.; Y. Katz receives research support from the Israel dairy board. The rest of the authors have declared that they have no conflict of interest.	Bruni F, 2008, Allergy, V63, P1645, DOI 10.1111/j.1398-9995.2008.01911.x; Elizur A, 2007, ANN ALLERG ASTHMA IM, V98, P540; GRYBOSKI JD, 1967, PEDIATRICS, V40, P354; Hwang JB, 2009, ARCH DIS CHILD, V94, P425, DOI 10.1136/adc.2008.143289; Katz Y, 2010, J ALLERGY CLIN IMMUN, V126, P77, DOI 10.1016/j.jaci.2010.04.020; Levy Y, 2003, PEDIATR ALLERGY IMMU, V14, P325, DOI 10.1034/j.1399-3038.2003.00039.x; Maloney J, 2007, PEDIATR ALLERGY IMMU, V18, P360, DOI 10.1111/j.1399-3038.2007.00561.x; MEHER S, 2009, PEDIATRICS, V123, pE459; Nowak-Wegrzyn A, 2003, PEDIATRICS, V111, P829, DOI 10.1542/peds.111.4.829; Nowak-Wegrzyn A, 2009, CURR OPIN ALLERGY CL, V9, P371, DOI 10.1097/ACI.0b013e32832d6315; POWELL GK, 1978, J PEDIATR-US, V93, P553, DOI 10.1016/S0022-3476(78)80887-7; Sicherer SH, 2009, ANNU REV MED, V60, P261, DOI 10.1146/annurev.med.60.042407.205711; Sicherer SH, 2005, J ALLERGY CLIN IMMUN, V115, P149, DOI 10.1016/j.jaci.2004.09.033; Sicherer SH, 1998, J PEDIATR-US, V133, P214, DOI 10.1016/S0022-3476(98)70222-7	14	76	88	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.	MAR	2011	127	3					647	U163		10.1016/j.jaci.2010.12.1105		10	Allergy; Immunology	Allergy; Immunology	730FG	WOS:000288018400014	21377033	
J	Risnes, KR; Belanger, K; Murk, W; Bracken, MB				Risnes, Kari R.; Belanger, Kathleen; Murk, William; Bracken, Michael B.			Antibiotic Exposure by 6 Months and Asthma and Allergy at 6 Years: Findings in a Cohort of 1,401 US Children	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						anti-bacterial agents; asthma; child; cohort studies; hypersensitivity	EARLY-CHILDHOOD; HYGIENE HYPOTHESIS; 1ST YEAR; MEDICATION USE; INCREASED RISK; BIRTH COHORT; SCHOOL-AGE; EARLY-LIFE; T-CELLS; INFECTIONS	Many studies have reported that antibiotic use may be associated with increased risk of childhood asthma. Respiratory tract infections in small children may be difficult to distinguish from early symptoms of asthma, and studies may have been confounded by "protopathic" bias, where antibiotics are used to treat early symptoms of asthma. These analyses of a cohort including 1,401 US children assess the association between antibiotic use within the first 6 months of life and asthma and allergy at 6 years of age between 2003 and 2007. Antibiotic exposure was associated with increased risk of asthma (adjusted odds ratio = 1.52, 95% confidence interval (CI): 1.07, 2.16). The odds ratio if asthma was first diagnosed after 3 years of age was 1.66 (95% CI: 0.99, 2.79) and, in children with no history of lower respiratory infection in the first year of life, the odds ratio was 1.66 (95% CI: 1.12, 3.46). The adverse effect of antibiotics was particularly strong in children with no family history of asthma (odds ratio = 1.89, 95% CI: 1.00, 3.58) (P(interaction) = 0.03). The odds ratio for a positive allergy blood or skin test was 1.59 (95% CI: 1.10, 2.28). The results show that early antibiotic use was associated with asthma and allergy at 6 years of age, and that protopathic bias was unlikely to account for the main findings.	[Risnes, Kari R.; Belanger, Kathleen; Murk, William; Bracken, Michael B.] Yale Univ, Sch Publ Hlth, Ctr Perinatal Pediat & Environm Epidemiol, New Haven, CT 06510 USA; [Risnes, Kari R.; Belanger, Kathleen; Murk, William; Bracken, Michael B.] Yale Univ, Sch Med, Ctr Perinatal Pediat & Environm Epidemiol, New Haven, CT 06510 USA; [Risnes, Kari R.] St Olavs Univ Hosp, Dept Pediat, Trondheim, Norway; [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,6th Floor, New Haven, CT 06510 USA.	michael.bracken@yale.edu			National Institutes of Health [AI41040, DA05484]; Liaison Committee; Norwegian University of Science and Technology; Central Norway Regional Health Authority	This study was supported by grants AI41040 and DA05484 from the National Institutes of Health. K. R. R. 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. Epidemiol.	FEB 1	2011	173	3					310	318		10.1093/aje/kwq400		9	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	709TC	WOS:000286463300007	21190986	
J	Radulovic, S; Calderon, MA; Wilson, D; Durham, S				Radulovic, Suzana; Calderon, Moises A.; Wilson, Duncan; Durham, Stephen			Sublingual immunotherapy for allergic rhinitis	COCHRANE DATABASE OF SYSTEMATIC REVIEWS			English	Review						Administration, Sublingual; Allergens [administration & dosage]; Desensitization, Immunologic [methods]; Randomized Controlled Trials as Topic; Rhinitis, Allergic, Perennial [therapy]; Rhinitis, Allergic, Seasonal [therapy]; Humans	PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND PLACEBO; RANDOMIZED CONTROLLED-TRIAL; GRASS-POLLEN IMMUNOTHERAPY; HOUSE-DUST-MITE; STANDARDIZED 5-GRASS-POLLEN EXTRACT; PARIETARIA-JUDAICA EXTRACT; SWALLOW IMMUNOTHERAPY; CLINICAL-EFFICACY; BIRCH POLLEN	Background This is an update of a Cochrane Review first published in The Cochrane Library in Issue 2, 2003. Allergic rhinitis is a common condition which can significantly impair quality of life. Immunotherapy by injection can significantly reduce symptoms and medication use but its use is limited by the possibility of severe systemic adverse reactions. Immunotherapy by the sublingual route is therefore of considerable interest. Objectives To evaluate the efficacy and safety of sublingual immunotherapy for allergic rhinitis in adults and children. Search strategy We searched the Cochrane ENT Group Trials Register; CENTRAL (2010, Issue 3); PubMed; EMBASE; CINAHL; Web of Science; BIOSIS Previews; Cambridge Scientific Abstracts; mRCT and additional sources for published and unpublished trials. The date of the most recent search was 14 August 2009. Selection criteria Randomised, double-blind, placebo-controlled trials of sublingual immunotherapy in adults or children. Primary outcome measures were symptom and medication scores. We also collected adverse event data. Data collection and analysis Two independent authors selected studies and assessed risk of bias. One author extracted data which was rechecked by two other authors. We used the standardised mean difference (SMD) with a random-effects model to combine data. Main results We included a total of 60 randomised controlled trials in the review. Forty-nine were suitable for pooling in meta-analyses (2333 SLIT, 2256 placebo participants). Overall, we found a significant reduction in symptoms (SMD-0.49; 95% confidence interval (CI) -0.64 to -0.34, P < 0.00001) andmedication requirements (SMD -0.32; 95% CI -0.43 to -0.21, P < 0.00001) in participants receiving sublingual immunotherapy compared to placebo. None of the trials included in this review reported severe systemic reactions or anaphylaxis, and none of the systemic reactions reported required the use of adrenaline. Authors' conclusions This updated review reinforces the conclusion of the original 2003 Cochrane Review that sublingual immunotherapy is effective for allergic rhinitis and has been proven to be a safe route of administration.	[Radulovic, Suzana] St Thomas Hosp, Paediat Allergy Res Dept, LEAP Study Team, London SE1 7EH, England; [Calderon, Moises A.; Durham, Stephen] Royal Brompton Hosp, Dept Allergy & Resp Med, London SW3 6LY, England; [Wilson, Duncan] Univ Hosp Birmingham NHS Trust, Selly Oak Hosp, Birmingham, W Midlands, England	Radulovic, S (reprint author), St Thomas Hosp, Paediat Allergy Res Dept, LEAP Study Team, Lambeth Palace Rd, London SE1 7EH, England.	radulovics@yahoo.com			ITN (Immune Tolerance Network); ALK Abello, Horsholm, Denmark	The lead review author, Dr Suzana Radulovic, has received financial support from the ITN (Immune Tolerance Network) as an employee of the Paediatric Allergy Research Department at King's College London, UK.; The Department of Upper Respiratory Medicine, National Heart & Lung Institute, London, UK, headed by Professor Durham, has received financial support from ALK Abello, Horsholm, Denmark - manufacturers of allergen extracts.	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J	Daley, D; Lemire, M; Akhabir, L; Chan-Yeung, M; He, JQ; McDonald, T; Sandford, A; Stefanowicz, D; Tripp, B; Zamar, D; Bosse, Y; Ferretti, V; Montpetit, A; Tessier, MC; Becker, A; Kozyrskyj, AL; Beilby, J; McCaskie, PA; Musk, B; Warrington, N; James, A; Laprise, C; Palmer, LJ; Pare, PD; Hudson, TJ				Daley, Denise; Lemire, Mathieu; Akhabir, Loubna; Chan-Yeung, Moira; He, Jian Qing; McDonald, Treena; Sandford, Andrew; Stefanowicz, Dorota; Tripp, Ben; Zamar, David; Bosse, Yohan; Ferretti, Vincent; Montpetit, Alexandre; Tessier, Marie-Catherine; Becker, Allan; Kozyrskyj, Anita L.; Beilby, John; McCaskie, Pamela A.; Musk, Bill; Warrington, Nicole; James, Alan; Laprise, Catherine; Palmer, Lyle J.; Pare, Peter D.; Hudson, Thomas J.			Analyses of associations with asthma in four asthma population samples from Canada and Australia	HUMAN GENETICS			English	Article							TOBACCO-SMOKE EXPOSURE; ALLERGIC DISORDERS; PRIMARY PREVENTION; CHILDHOOD ASTHMA; GENETIC-VARIANTS; LUNG-FUNCTION; ORMDL3 EXPRESSION; EARLY-LIFE; HIGH-RISK; IN-UTERO	Asthma, atopy, and related phenotypes are heterogeneous complex traits, with both genetic and environmental risk factors. Extensive research has been conducted and over hundred genes have been associated with asthma and atopy phenotypes, but many of these findings have failed to replicate in subsequent studies. To separate true associations from false positives, candidate genes need to be examined in large well-characterized samples, using standardized designs (genotyping, phenotyping and analysis). In an attempt to replicate previous associations we amalgamated the power and resources of four studies and genotyped 5,565 individuals to conduct a genetic association study of 93 previously associated candidate genes for asthma and related phenotypes using the same set of 861 single-nucleotide polymorphisms (SNPs), a common genotyping platform, and relatively harmonized phenotypes. We tested for association between SNPs and the dichotomous outcomes of asthma, atopy, atopic asthma, and airway hyperresponsiveness using a general allelic likelihood ratio test. No SNP in any gene reached significance levels that survived correction for all tested SNPs, phenotypes, and genes. Even after relaxing the usual stringent multiple testing corrections by performing a gene-based analysis (one gene at a time as if no other genes were typed) and by stratifying SNPs based on their prior evidence of association, no genes gave strong evidence of replication. There was weak evidence to implicate the following: IL13, IFNGR2, EDN1, and VDR in asthma; IL18, TBXA2R, IFNGR2, and VDR in atopy; TLR9, TBXA2R, VDR, NOD2, and STAT6 in airway hyperresponsiveness; TLR10, IFNGR2, STAT6, VDR, and NPSR1 in atopic asthma. Additionally we found an excess of SNPs with small effect sizes (OR < 1.4). The low rate of replication may be due to small effect size, differences in phenotypic definition, differential environmental effects, and/or genetic heterogeneity. To aid in future replication studies of asthma genes a comprehensive database was compiled and is available to the scientific community at http://genapha.icapture.ubc.ca.	[Daley, Denise; Akhabir, Loubna; He, Jian Qing; McDonald, Treena; Sandford, Andrew; Stefanowicz, Dorota; Tripp, Ben; Zamar, David; Pare, Peter D.] Univ British Columbia, James Hogg iCAPTURE Ctr, Vancouver, BC V6Z 1Y6, Canada; [Lemire, Mathieu; Ferretti, Vincent; Montpetit, Alexandre; Tessier, Marie-Catherine; Hudson, Thomas J.] McGill Univ, Montreal, PQ, Canada; [Lemire, Mathieu; Ferretti, Vincent; Montpetit, Alexandre; Tessier, Marie-Catherine; Hudson, Thomas J.] Genome Quebec Innovat Ctr, Montreal, PQ, Canada; [Lemire, Mathieu; Ferretti, Vincent; Hudson, Thomas J.] Ontario Inst Canc Res, Toronto, ON, Canada; [Chan-Yeung, Moira] Univ British Columbia, Occupat & Environm Lung Dis Unit, Vancouver, BC V6Z 1Y6, Canada; [Bosse, Yohan] Univ Laval, Ctr Rech, Hop Laval, Inst Univ Cardiol & Pneumol, Quebec City, PQ, Canada; [Bosse, Yohan] Univ Laval, Hosp Res Ctr, CRCHUL, Quebec City, PQ, Canada; [Becker, Allan; Kozyrskyj, Anita L.] Univ Manitoba, Dept Pediat & Child Hlth, Fac Med, Winnipeg, MB R3T 2N2, Canada; [Kozyrskyj, Anita L.] Manitoba Ctr Hlth Policy, Fac Pharm, Winnipeg, MB, Canada; [Kozyrskyj, Anita L.] Manitoba Ctr Hlth Policy, Dept Community Hlth Sci, Winnipeg, MB, Canada; [Beilby, John; Musk, Bill; James, Alan] Sir Charles Gairdner Hosp, Perth, WA 6000, Australia; [McCaskie, Pamela A.; Warrington, Nicole; Palmer, Lyle J.] Univ Western Australia, Lab Genet Epidemiol, Western Australian Inst Med Res, UWA Ctr Med Res, Perth, WA 6009, Australia; [McCaskie, Pamela A.; Warrington, Nicole; Palmer, Lyle J.] Univ Western Australia, Sch Populat Hlth, Perth, WA 6009, Australia	Pare, PD (reprint author), Univ British Columbia, James Hogg iCAPTURE Ctr, 1081 Burrard St, Vancouver, BC V6Z 1Y6, Canada.	ppare@mrl.ubc.ca	Pare, Peter/C-7425-2011; Bosse, Yohan/C-7617-2012; Palmer, Lyle/K-3196-2014; Warrington, Nicole/P-4868-2014	Palmer, Lyle/0000-0002-1628-3055; Warrington, Nicole/0000-0003-4195-775X; Hudson, Thomas/0000-0002-1376-4849	AllerGen; National Centre of Excellence Network (Canada); Institutes of Gender and Health; BC Lung Association; Genome Quebec; Respiratory Health Network of the Fonds de la Recherche en Sante du Quebec (FRSQ); Michael Smith Foundation; Jacob Churg Distinguished Research Award; Burroughs Wellcome Fund; CIHR; Healthway, Western Australia; National Health and Medical Research Council of Australia; Wind-Over-Water Foundation	We thank all subjects who donated time and samples for this project, and numerous health care workers who helped with recruitment and phenotyping. Dr Paul Begin and Charles Morin for their collaboration and ascertainment of the Saguenay-Lac-Saint-Jean panel participants. Dr Louis-Philippe Boulet and Michel Laviolette for ascertainment, of the Quebec City family trios. For the Canadian Asthma Primary Prevention Study cohort we acknowledge Drs Alexander Ferguson and Wade Watson who phenotyped participants, Ms Roxanne Rousseau and Ms Marilyn Lilley who ascertained subjects and Ms Anne DyBuncio for data management. We gratefully acknowledge the assistance of James Chomin with the TaqMan genotyping of the MTHFR gene, Muriel Grenon for the assistance in recruiting subjects in the Saguenay Lac-St. Jean and Julie Park with the literature search and compiling of Supplementary Table S1. This work was supported by AllerGen, a , the Canadian Institutes of Health Research (CIHR), the Institutes of Gender and Health, BC Lung Association, Genome Quebec, and the Respiratory Health Network of the Fonds de la Recherche en Sante du Quebec (FRSQ). P. D. P was the recipient of a Michael Smith Foundation Scholarship and the Jacob Churg Distinguished Research Award. T. J. H. received a Clinician-Scientist Award in Translational Research from the Burroughs Wellcome Fund and an Investigator Award from CIHR. The 1994 Busselton follow-up study was funded by Healthway, Western Australia. A. L. J. is a recipient of a National Health and Medical Research Council of Australia Practitioner Fellowship. L. J. P. is supported by the National Health and Medical Research Council of Australia and the Wind-Over-Water Foundation. Y. Bosse and D. Daley were recipients of CIHR fellowship awards, and A. Kozyrskyj is a recipient of a New Investigator Award from the Canadian Institutes of Health Research. DD is the recipient of a Michael Smith Foundation Career Scholar Award. C. Laprise, A. Sandford and D. Daley hold Canadian Research Chair appointments.	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Genet.	MAY	2009	125	4					445	459		10.1007/s00439-009-0643-8		15	Genetics & Heredity	Genetics & Heredity	435ZX	WOS:000265383500010	19247692	
J	Rodrigues, LC; Newcombe, PJ; Cunha, SS; Alcantara-Neves, NM; Genser, B; Cruz, AA; Simoes, SM; Fiaccone, R; Amorim, L; Cooper, PJ; Barreto, ML				Rodrigues, L. C.; Newcombe, P. J.; Cunha, S. S.; Alcantara-Neves, N. M.; Genser, B.; Cruz, A. A.; Simoes, S. M.; Fiaccone, R.; Amorim, L.; Cooper, P. J.; Barreto, M. L.		SCAALA	Early infection with Trichuris trichiura and allergen skin test reactivity in later childhood	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergen skin test reactivity; asthma; atopy; immune programming; intestinal helminths; rhinitis; Trichuris trichiura	SCHOOL-AGE-CHILDREN; GEOHELMINTH INFECTIONS; GABONESE SCHOOLCHILDREN; HELMINTHIC INFECTION; HYGIENE HYPOTHESIS; ATOPY; PARASITES; ASTHMA; PREVALENCE; EXPOSURE	Background Allergic diseases cause a large and increasing burden in developed countries and in urban centres in middle-income countries. The causes of this increase are unknown and, currently, there are no interventions to prevent the development of allergic diseases. The 'hygiene hypothesis' has tried to explain the increase through a reduction in the frequency of childhood infections causing a failure to program the immune system for adequate immune regulation. Intestinal helminth parasites are prevalent in childhood in developing countries and are associated with a lower prevalence of allergen skin test reactivity and asthma. Objectives To investigate whether children who had intestinal helminth infections during early childhood have a lower prevalence of allergen skin test reactivity later in childhood. Methods We re-visited a population of 1055 children from whom stool samples had been collected for detection of intestinal helminth infections for another study, and collected new stool samples and performed allergen skin prick testing. Information on potential confounding variables was collected. Results Children with heavy infections with Trichuris trichiura in early childhood had a significantly reduced prevalence of allergen skin test reactivity in later childhood, even in the absence of T. trichiura infection at the time of skin testing in later childhood. Conclusion Early heavy infections with T. trichiura may protect against the development of allergen skin test reactivity in later childhood. Novel treatments to program immune-regulation in early childhood in a way that mimics the effects of early infections with T. trichiura may offer new strategies for the prevention of allergic disease.	[Rodrigues, L. C.; Newcombe, P. J.] London Sch Hyg & Trop Med, London WC1E 7HT, England; [Cunha, S. S.; Genser, B.; Simoes, S. M.; Barreto, M. L.] Univ Fed Bahia, Inst Saude Colet, Salvador, BA, Brazil; [Alcantara-Neves, N. M.] Univ Fed Bahia, Inst Ciencias Saude, Salvador, BA, Brazil; [Cruz, A. 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Exp. Allergy	NOV	2008	38	11					1769	1777		10.1111/j.1365-2222.2008.03027.x		9	Allergy; Immunology	Allergy; Immunology	364KH	WOS:000260334100011	18547322	
J	Bousquet, J; van Cauwenberge, P; Khaled, NA; Bachert, C; Baena-Cagnani, CE; Bouchard, J; Bunnag, C; Canonica, GW; Carlsen, KH; Chen, YZ; Cruz, AA; Custovic, A; Demoly, P; Dubakiene, R; Durham, S; Fokkens, W; Howarth, P; Kemp, J; Kowalski, ML; Kvedariene, V; Lipworth, B; Lockey, R; Lund, V; Mavale-Manuel, S; Meltzer, EO; Mullol, J; Naclerio, R; Nekam, K; Ohta, K; Papadopoulos, N; Passalacqua, G; Pawankar, R; Popov, T; Potter, P; Price, D; Scadding, G; Simons, FER; Spicak, V; Valovirta, E; Wang, DY; Yawn, B; Yusuf, O				Bousquet, J.; van Cauwenberge, P.; Khaled, N. Ait; Bachert, C.; Baena-Cagnani, C. E.; Bouchard, J.; Bunnag, C.; Canonica, G. W.; Carlsen, K. -H.; Chen, Y. -Z.; Cruz, A. A.; Custovic, A.; Demoly, P.; Dubakiene, R.; Durham, S.; Fokkens, W.; Howarth, P.; Kemp, J.; Kowalski, M. L.; Kvedariene, V.; Lipworth, B.; Lockey, R.; Lund, V.; Mavale-Manuel, S.; Meltzer, E. O.; Mullol, J.; Naclerio, R.; Nekam, K.; Ohta, K.; Papadopoulos, N.; Passalacqua, G.; Pawankar, R.; Popov, T.; Potter, P.; Price, D.; Scadding, G.; Simons, F. E. R.; Spicak, V.; Valovirta, E.; Wang, D. -Y.; Yawn, B.; Yusuf, O.			Pharmacologic and anti-IgE treatment of allergic rhinitis ARIA update (in collaboration with GA(2)LEN)	ALLERGY			English	Review						ARIA; asthma; GA(2)LEN; IgE; pharmacotherapy; rhinitis	AQUEOUS NASAL SPRAY; PLACEBO-CONTROLLED TRIAL; QUALITY-OF-LIFE; LORATADINE 10 MG; INTRANASAL FLUTICASONE PROPIONATE; ENVIRONMENTAL EXPOSURE UNIT; RANDOMIZED CONTROLLED-TRIAL; EBASTINE 20 MG; LEUKOTRIENE RECEPTOR ANTAGONISTS; ADRENAL AXIS FUNCTION	The pharmacologic treatment of allergic rhinitis proposed by ARIA is an evidence-based and step-wise approach based on the classification of the symptoms. The ARIA workshop, held in December 1999, published a report in 2001 and new information has subsequently been published. The initial ARIA document lacked some important information on several issues. This document updates the ARIA sections on the pharmacologic and anti-IgE treatments of allergic rhinitis. Literature published between January 2000 and December 2004 has been included. Only a few studies assessing nasal and non-nasal symptoms are presented as these will be discussed in a separate document.	Univ Hosp Montpellier, Montpellier, France; INSERM, U454, Montpellier, France; Univ Ghent, Ghent, Belgium; Union, Paris, France; Ghent Univ Hosp, B-9000 Ghent, Belgium; Univ Cordoba, E-14071 Cordoba, Spain; St Josephs Hosp, La Malbaie, PQ, Canada; Mahidol Univ, Dept Otolaryngol, Bangkok 10700, Thailand; Univ Genoa, Genoa, Italy; Univ Oslo, Voksentoppen BKL, N-0316 Oslo, Norway; Capital Inst Pediat, Beijing, Peoples R China; Univ Fed Bahia, Sch Med, BR-41170290 Salvador, BA, Brazil; Univ Manchester, Manchester, Lancs, England; Vilnius State Univ, Vilnius, Lithuania; Royal Brompton Hosp, London SW3 6LY, England; Univ London Imperial Coll Sci Technol & Med, London, England; Univ Amsterdam, NL-1012 WX Amsterdam, Netherlands; Univ Southampton, Southampton SO9 5NH, Hants, England; Univ Lodz, PL-90131 Lodz, Poland; Univ Dundee, Asthma & Allergy Res Grp, Dundee DD1 4HN, Scotland; Univ S Florida, Div Allergy & Immunol, Tampa, FL USA; UCL, Inst Laryngol & Otol, Ear Inst, London, England; Allergy & Asthma Med Grp & Res Ctr, San Diego, CA USA; Hosp Clin Barcelona, Barcelona, Catalonia, Spain; Otolaryngol Univ Chicago, Chicago, IL USA; Hosp Hosp Brothers, Budapest, Hungary; Teikyo Univ, Sch Med, Dept Med, Tokyo 173, Japan; Univ Athens, GR-10679 Athens, Greece; Univ Genoa, Genoa, Italy; Nippon Med Sch, Dept Otolaryngol, Tokyo 113, Japan; Med Univ Sofia, Clin Ctr Allergol, Sofia, Bulgaria; Univ Cape Town, Lung Inst, Allergy Diagnost & Clin Res Unit, ZA-7925 Cape Town, South Africa; Univ Aberdeen, Aberdeen, Scotland; Royal Natl Throat Nose & Ear Hosp, London WC1X 8DA, England; Univ Manitoba, Dept Pediat & Child Hlth, Winnipeg, MB R3T 2N2, Canada; Czech Initiat Asthma, Prague, Czech Republic; Turku Allergy Ctr, Turku, Finland; Natl Univ Singapore, Singapore 117548, Singapore; Univ Minnesota, Minneapolis, MN 55455 USA; Allergy & Asthma Clin, Islamabad, Pakistan	Bousquet, J (reprint author), CHU Montpellier, Hop Arnaud Villeneuve, Clin Malad Resp, F-34295 Montpellier 5, France.		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J	Bove, PF; van der Vliet, A				Bove, Peter F.; van der Vliet, Albert			Nitric oxide and reactive nitrogen species in airway epithelial signaling and inflammation	FREE RADICAL BIOLOGY AND MEDICINE			English	Review						guanylyl cyclase; cGMP; S-nitrosylation; NF-kappa B; asthma	NF-KAPPA-B; SOLUBLE GUANYLYL CYCLASE; PROTEIN-TYROSINE NITRATION; CILIARY BEAT FREQUENCY; S-NITROSYLATION; CYSTIC-FIBROSIS; GENE-EXPRESSION; MATRIX METALLOPROTEINASES; CYCLOOXYGENASE-2 EXPRESSION; DIFFERENTIAL SENSITIVITY	Nitric oxide (NO center dot) is produced by many diverse cell types as a cellular or intracellular signaling molecule, by the activation of nitric oxide synthases (NOSs). All three known NOS isoforms are expressed within the respiratory tract and mediate various air-way functional properties such as airway smooth muscle tone, ciliary function, epithelial electrolyte transport, and innate host defense. The respiratory epithelium is a major source of NO center dot in which it regulates normal epithelial cell function and signaling as well as signaling pathways involved in airway inflammation. In addition to its normal physiological properties, increased airway NO center dot production in inflammatory respiratory tract diseases such as asthma may activate additional signaling mechanisms to regulate inflammatory-immune pathways, and epithelial barrier (dys)function or repair. The biological actions of NO center dot are controlled at various levels, including mechanisms that regulate NOS localization and activation, and variable oxidative metabolism of NO center dot resulting in generation of bioactive reactive nitrogen species (RNS). Moreover, in addition to altered production of NO center dot or RNS, the presence of various target enzymes and/or metabolic regulators of NO center dot/RNS can be dramatically altered during airway inflammatory conditions, and contribute to alterations in W-mediated signaling pathways in disease. This review summarizes current knowledge regarding NO center dot-mediated epithelial signaling, as well as disease-related changes in airway NOS biology and target enzymes that affect NO center dot/RNS signaling mechanisms. A detailed understanding of these various changes and their impact on NO center dot signaling pathways are needed to fully appreciate the contributions of NO center dot/RNS to airway inflammation and to develop suitable therapeutic approaches based on regulating NO center dot function. (c) 2006 Elsevier Inc. All rights reserved.	Univ Vermont, Coll Med, Dept Pathol, Burlington, VT 05405 USA	van der Vliet, A (reprint author), Univ Vermont, Coll Med, Dept Pathol, Burlington, VT 05405 USA.	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Biol. Med.	AUG 15	2006	41	4					515	527		10.1016/j.freeradbiomed.2006.05.011		13	Biochemistry & Molecular Biology; Endocrinology & Metabolism	Biochemistry & Molecular Biology; Endocrinology & Metabolism	071NF	WOS:000239608200001	16863984	
J	Kim, JK; Oh, SM; Kwon, HS; Oh, YS; Lim, SS; Shin, HK				Kim, JK; Oh, SM; Kwon, HS; Oh, YS; Lim, SS; Shin, HK			Anti-inflammatory effect of roasted licorice extracts on lipopolysaccharide-induced inflammatory responses in murine macrophages	BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS			English	Article						licorice; inflammation; inducible nitric oxide synthase; prostaglandin E-2; nuclear factor-kappa B; pro-inflammatory cytokines	NF-KAPPA-B; IMMUNE-SYSTEM; ISOLIQUIRITIGENIN; EXPRESSION; COLITIS; CELLS; MICE; ACTIVATION; RESOLUTION; MEDIATORS	Licorice, the roots of Glycyrrhiza inflata, is used by practitioners of alternative medicine to treat individuals with gastric or duodenal ulcers, bronchitis, cough, arthritis, adrenal insufficiency, and allergies. We investigated the anti-inflammatory properties of 4 licorice extracts: extracts of roasted licorice obtained by ethanol (rLE) or water extraction (rLW) and extracts of raw licorice obtained by ethanol (LE) or water extraction (LW). rLE demonstrated strong anti-inflammatory activity through its ability to reduce nitric oxide and prostaglandin E-2 production in the LPS-stimulated mouse macrophage cell, RAW264.7. It also inhibited the production of pro-inflammatory cytokines and CD14 expression on the LPS-stimulated RAW264.7 cells. Further study indicated that LPS-induced degradation and phosphorylation of I kappa-B alpha, along with DNA-binding of NF-kappa B, was significantly inhibited by rLE exposure in RAW264.7 cells. In the murine model, we found that in vivo exposure to rLE-induced an increase in the survival rate, reduced plasma levels of TNF-alpha and IL-6, and increased IL-10 production in LPS-treated mice. Collectively, these data suggest that the use of rLE may be a useful therapeutic approach to various inflammatory diseases. (c) 2006 Elsevier Inc. 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Biophys. Res. Commun.	JUL 7	2006	345	3					1215	1223		10.1016/j.bbrc.2006.05.035		9	Biochemistry & Molecular Biology; Biophysics	Biochemistry & Molecular Biology; Biophysics	054AA	WOS:000238346500044	16716255	
J	Cvetkovski, RS; Zachariae, R; Jensen, H; Olsen, J; Johansen, JD; Agner, T				Cvetkovski, RS; Zachariae, R; Jensen, H; Olsen, J; Johansen, JD; Agner, T			Quality of life and depression in a population of occupational hand eczema patients	CONTACT DERMATITIS			English	Article						health-related quality of life; occupational skin disease; psychosocial factors; socioeconomic status	CONTACT-DERMATITIS; SKIN-DISEASE; INDEX DLQI; OUTPATIENTS; SEVERITY; WORKERS; IMPACT	Occupational hand eczema (OHE) is the most frequently recognized occupational disease in Denmark, and despite governmental attempts to reduce exposure to harmful occupational allergens, the number of new cases has remained almost unchanged since the mid-1990s. Some studies have indicated that OHE has considerable impact on quality of life (QoL) and may lead to depression. The aims of the study were to determine risk factors for low QoL, the frequency and severity of depression among OHE patients and changes in QoL and depression after 12 months of follow up. The study population, 758 patients, comprised all new recognized cases from the Danish National Board of Industrial Injuries Registry between October 2001 and November 2002. All patients received a questionnaire to determine impairment of QoL and depressive symptoms. A similar follow-up questionnaire was posted after 1 year. The response rate was 82% at baseline and 91% at follow up. The mean Dermatology Life Quality Index total score was 5.5 for all patients and 7.8 for severe OHE cases. Severe OHE cases and lower socioeconomic status were independently associated with low QoL. The prevalence of moderate-to-severe depression was 9%. Only minor changes in QoL and depressive symptoms were found after 12 months of follow up.	Univ Copenhagen, Gentofte Hosp, Dept Dermatol, Copenhagen, Denmark; Aarhus Univ Hosp, Psychooncol Res Univ, DK-8000 Aarhus, Denmark; Aarhus Univ, DK-8000 Aarhus, Denmark; Univ Copenhagen, Danish Epidemiol Sci Ctr, Copenhagen, Denmark; Univ Calif Los Angeles, Sch Publ Hlth, Dept Epidemiol, Los Angeles, CA 90024 USA; Gentofte Univ Hosp, Natl Allergy Res Ctr, Copenhagen, Denmark	Cvetkovski, RS (reprint author), Haderslevgade 38 4th, DK-1671 Copenhagen V, Denmark.	risk@dadlnet.dk					Adisesh A, 2002, CONTACT DERMATITIS, V46, P273, DOI 10.1034/j.1600-0536.2002.460505.x; Agner T, 1999, Am J Contact Dermat, V10, P12, DOI 10.1016/S1046-199X(99)90088-X; Anderson R T, 2001, Curr Allergy Asthma Rep, V1, P309, DOI 10.1007/s11882-001-0041-3; Antezana M, 2003, IMMUNOL ALLERGY CLIN, V23, P269, DOI 10.1016/S0889-8561(03)00027-4; Barros Aluisio J D, 2003, BMC Med Res Methodol, V3, P21, DOI 10.1186/1471-2288-3-21; BECK AT, 1961, ARCH GEN PSYCHIAT, V4, P561; Coenraads PJ, 2004, HAUTARZT, V55, P28, DOI 10.1007/s00105-003-0659-2; Coenraads PJ, 2005, BRIT J DERMATOL, V152, P296, DOI 10.1111/J.1365-2133.2004.06270.X; Cvetkovski RS, 2005, BRIT J DERMATOL, V152, P93, DOI 10.1111/J.1365-2133.2005.06415.X; Dickel H, 2002, CONTACT DERMATITIS, V46, P197, DOI 10.1034/j.1600-0536.2002.460403.x; EDMAN B, 1988, CONTACT DERMATITIS, V19, P43, DOI 10.1111/j.1600-0536.1988.tb02866.x; Finlay AY, 2005, BRIT J DERMATOL, V152, P861, DOI 10.1111/j.1365-2133.2005.06502.x; FINLAY AY, 1994, CLIN EXP DERMATOL, V19, P210, DOI 10.1111/j.1365-2230.1994.tb01167.x; Hachem JP, 2002, CONTACT DERMATITIS, V46, P220, DOI 10.1034/j.1600-0536.2002.460406.x; Hahn HB, 2001, J AM ACAD DERMATOL, V45, P44, DOI 10.1067/mjd.2001.110880; Holness DL, 2001, CONTACT DERMATITIS, V44, P80; HOLNESS DL, 1991, CONTACT DERMATITIS, V25, P296, DOI 10.1111/j.1600-0536.1991.tb01877.x; Hongbo Y, 2004, BRIT J DERMATOL, V151, P45; Hutchings CV, 2001, CONTACT DERMATITIS, V45, P17, DOI 10.1034/j.1600-0536.2001.045001017.x; JOWETT S, 1985, SOC SCI MED, V20, P425, DOI 10.1016/0277-9536(85)90021-8; Kadyk DL, 2003, J AM ACAD DERMATOL, V49, P1037, DOI 10.1016/S0190-9622(03)02112-1; MEDING B, 1990, CONTACT DERMATITIS, V23, P6, DOI 10.1111/j.1600-0536.1990.tb00076.x; MEDING B, 2005, BRIT J DERMATOL, V152, P9875; Meyer JD, 2000, OCCUP MED-OXFORD, V50, P265; NETHERCOTT JR, 1994, J AM ACAD DERMATOL, V30, P569; Niemeier V, 2002, BRIT J DERMATOL, V146, P1031, DOI 10.1046/j.1365-2133.2002.04716.x; Skoet R, 2004, CONTACT DERMATITIS, V51, P159, DOI 10.1111/j.0105-1873.2004.00423.x; Thomson KF, 2002, BRIT J DERMATOL, V146, P627, DOI 10.1046/j.1365-2133.2002.04692.x; Wallenhammar LM, 2004, J INVEST DERMATOL, V122, P1381, DOI 10.1111/j.0022-202X.2004.22604.x; Yun YH, 2005, ONCOLOGY-BASEL, V68, P107, DOI 10.1159/000085703; Zachariae R, 2000, ACTA DERM-VENEREOL, V80, P272; Zachariae R, 2004, ACTA DERM-VENEREOL, V84, P205, DOI 10.1080/00015550410023284	32	76	83	0	7	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0105-1873			CONTACT DERMATITIS	Contact Dermatitis	FEB	2006	54	2					106	111		10.1111/j.0105-1873.2006.00783.x		6	Allergy; Dermatology	Allergy; Dermatology	013OD	WOS:000235417700007	16487283	
J	Fiocchi, A; Pajno, G; La Grutta, S; Pezzuto, F; Incorvaia, C; Sensi, L; Marcucci, F; Frati, F				Fiocchi, A; Pajno, G; La Grutta, S; Pezzuto, F; Incorvaia, C; Sensi, L; Marcucci, F; Frati, F			Safety of sublingual-swallow immunotherapy in children aged 3 to 7 years	ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY			English	Article							HOUSE-DUST-MITE; DOUBLE-BLIND; ALLERGEN IMMUNOTHERAPY; THERAPEUTIC VACCINES; ASTHMATIC-CHILDREN; SYSTEMIC REACTIONS; YOUNG-CHILDREN; POSITION PAPER; EFFICACY; RHINOCONJUNCTIVITIS	Background: The minimum age to start specific immunotherapy with inhalant allergens in children has not been clearly established, and position papers discourage its use in children younger than 5 years. Objective: To assess the safety of high-dose sublingual-swallow immunotherapy (SLIT) in a group of children younger than 5 years. Methods: Sixty-five children (51 boys and 14 girls; age range, 38-80 months; mean +/- SD age, 60 +/- 10 years; median age, 60 months) were included in this observational study. They were treated with SLIT with a build-up phase of 11 days, culminating in a top dose of 300 IR (index of reactivity) and a maintenance phase of 300 IR 3 times a week. The allergens used were house dust mites in 42 patients, grass pollen in 11 patients, olive pollen in 5 patients, Parietaria pollen in 4 patients, and cypress pollen in 3 patients. All adverse reactions and changes in the treatment schedule were compared in 2 subgroups: children 38 to 60 months old and children 61 to 80 months old. Results: The average cumulative dose of SLIT was 36,900 IR. Adverse reactions were observed in 11 children, none of them severe enough to require discontinuation of immunotherapy. Six reactions occurred in the 60 months or younger age group and 7 in the older than 60 months age group, with no differences between these 2 groups. Conclusion: High-dose immunotherapy in children younger than 5 years does not cause more adverse reactions than in children aged 5 to 7 years. There is no reason to forbear studies on safety and efficacy of these preparations in young children.	Fatebenefratelli Melloni Univ Hosp, Dept Child & Maternal Med, Milan, Italy; Univ Messina, Sch Med, Dept Pediat, Messina, Italy; ARNAS, Childrens Hosp, Allergy Unit, Palermo, Italy; ASL SA2, Allergy Unit, Salerno, Italy; ICP Hosp, Allergy Rheumatol Unit, Milan, Italy; Univ Perugia, Sch Med, Dept Gynaecol Obstet & Pediat Sci, I-06100 Perugia, Italy	Fiocchi, A (reprint author), Macedonio Melloni Pediat Hosp, Via Macedonio Melloni 52, I-20121 Milan, Italy.	allerg@tin.it		Fiocchi, Alessandro/0000-0002-2549-0523			AGERTOFT L, 1994, RESP MED, V88, P373, DOI 10.1016/0954-6111(94)90044-2; Akcakaya N, 2000, ANN ALLERG ASTHMA IM, V85, P317; Bousquet J, 1998, J ALLERGY CLIN IMMUN, V102, P558, DOI 10.1016/S0091-6749(98)70271-4; Bousquet J, 2001, J ALLERGY CLIN IMMUN, V108, P147, DOI DOI 10.1067/MAI.2001.118891; Bowen T, 2004, ANN ALLERG ASTHMA IM, V93, P425; BUSINCO L, 1995, PEDIATR ALLERGY IMMU, V6, P44, DOI 10.1111/j.1399-3038.1995.tb00257.x; Cantani A, 1997, J INVEST ALLERG CLIN, V7, P90; 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; DuBuske LM, 2001, ANN ALLERG ASTHMA IM, V87, P56; Fiocchi A, 2004, ANN ALLERG ASTHMA IM, V93, P328; Frati F, 2003, ALLERG IMMUNOL PARIS, V35, P56; Guez S, 2000, ALLERGY, V55, P369, DOI 10.1034/j.1398-9995.2000.00413.x; Host A, 2003, ALLERGY, V58, P559, DOI 10.1034/j.1398-9995.2003.00238.x; Ippoliti F, 2003, PEDIATR ALLERGY IMMU, V14, P216, DOI 10.1034/j.1399-3038.2003.00025.x; Li JT, 2003, ANN ALLERG ASTHMA IM, V90, P1; MALLING HJ, 1993, ALLERGY, V48, P9; MARCUCCI F, 2001, ALLERGY, V55, P1091; Moher D, 2001, ANN INTERN MED, V134, P657; 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; OWNBY DR, 1994, J ALLERGY CLIN IMMUN, V94, P662, DOI 10.1016/0091-6749(94)90171-6; Pajno GB, 2000, ALLERGY, V55, P842, DOI 10.1034/j.1398-9995.2000.00495.x; Passalacqua G, 2004, ANN ALLERG ASTHMA IM, V93, P3; REID MJ, 1993, J ALLERGY CLIN IMMUN, V92, P6, DOI 10.1016/0091-6749(93)90030-J; Rolinck-Werninghaus C, 2004, ALLERGY, V59, P1285, DOI 10.1111/j.1398-9995.2004.00627.x; TAVES DR, 1974, CLIN PHARMACOL THER, V15, P443; Tonnel AB, 2004, ALLERGY, V59, P491, DOI 10.1111/j.1398-9995.2004.00456.x; Wilson DR, 2003, COCHRANE DB SYST REV, V2	30	76	80	1	4	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.	SEP	2005	95	3					254	258				5	Allergy; Immunology	Allergy; Immunology	966TN	WOS:000232044900010	16200816	
J	Satinover, SM; Reefer, AJ; Pomes, A; Chapman, MD; Platts-Mills, TAE; Woodfolk, JA				Satinover, SM; Reefer, AJ; Pomes, A; Chapman, MD; Platts-Mills, TAE; Woodfolk, JA			Specific IgE and IgG antibody-binding patterns to recombinant cockroach allergens	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						cockroach; asthma; allergens; troponryosin; IgE antibody; IgG antibody; multiplex	INNER-CITY CHILDREN; FLOW-CYTOMETRIC ASSAY; AMERICAN COCKROACH; HOUSE-DUST; DERMATOPHAGOIDES-PTERONYSSINUS; BLATTELLA-GERMANICA; MOLECULAR-CLONING; MAJOR ALLERGEN; RISK-FACTORS; ASTHMA	Background: The specificity of serum antibody responses to different cockroach allergens has not been studied. Objective: We sought to quantitate serum IgE and IgG antibodies to a panel of purified cockroach allergens among cockroach-sensitized subjects. Methods: IgE antibodies to recombinant cockroach allergens (rBla g 1, rBla g 2, rBla g 4, rBla g 5, and rPer a 7) were measured in sera containing IgE antibodies to Blattella germanica extract (n = 118) by using a streptavidin CAP assay and a multiplex flow cytometric assay. Specific IgG antibodies were determined by using radioimmuno-precipitation techniques. Results: Specific IgE antibodies measured by means of CAP assay and multiplex assay were strongly correlated (r = 0.8, P < .001). The sum of IgE antibodies (in international units per milliliter) against all 5 allergens equated to IgE antibodies to cockroach extract. Although the prevalence of IgE antibodies was highest for rBla g 2 (54.4%) and rBla g 5 (37.4%), patterns of IgE antibody binding were unique to each subject. Surprisingly, only 16% of cockroach-sensitized subjects with IgE antibodies to house dust mite exhibited IgE antibody binding to cockroach tropomyosin (rPer a 7). Specific IgE antibodies were associated with increased IgG antibody levels, although detection of IgG in the absence of IgE was not uncommon. Conclusion: The techniques described offer a new approach for defining the hierarchy of purified allergens. IgE antibodies directed against 5 allergens constitute the majority of the IgE antibody repertoire for cockroach. Such distinct, patterns of IgE-IgG responsiveness to different cockroach allergens highlight the complexity of B-cell responses to environmental allergens.	Univ Virginia, Asthma & Allerg Dis Ctr, Div Allergy, Charlottesville, VA 22908 USA	Woodfolk, JA (reprint author), Univ Virginia, Asthma & Allerg Dis Ctr, Div Allergy, POB 801355, Charlottesville, VA 22908 USA.	jaw4m@virginia.edu		Pomes, Anna/0000-0002-8729-1829	NIAID NIH HHS [AI 20565]		Arbes SJ, 2003, J ALLERGY CLIN IMMUN, V112, P339, DOI 10.1067/mai.2003.1597; Arruda L K, 2001, Curr Allergy Asthma Rep, V1, P466, DOI 10.1007/s11882-001-0035-1; Arruda LK, 1997, J BIOL CHEM, V272, P20907, DOI 10.1074/jbc.272.33.20907; Arruda LK, 1995, J BIOL CHEM, V270, P31196; ARRUDA LK, 1995, J BIOL CHEM, V270, P19563; Asturias JA, 1998, BBA-GENE STRUCT EXPR, V1397, P27, DOI 10.1016/S0167-4781(98)00006-2; Asturias JA, 1999, J IMMUNOL, V162, P4342; CALL RS, 1992, J PEDIATR-US, V121, P862, DOI 10.1016/S0022-3476(05)80329-4; Carter MC, 2001, J ALLERGY CLIN IMMUN, V108, P732, DOI 10.1067/mai.2001.119155; Chapman MD, 2000, J ALLERGY CLIN IMMUN, V106, P409; de Jager W, 2003, CLIN DIAGN LAB IMMUN, V10, P133, DOI 10.1128/CDLI.10.1.133-139.2003; Eggleston PA, 1998, J ALLERGY CLIN IMMUN, V102, P563, DOI 10.1016/S0091-6749(98)70272-6; Erwin EA, 2005, J ALLERGY CLIN IMMUN, V115, P74, DOI 10.1016/j.jaci.2004.10.030; ERWIN EA, 2005, IN PRESS J ALLERGY C; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; Helm R, 1996, J ALLERGY CLIN IMMUN, V98, P172, DOI 10.1016/S0091-6749(96)70240-3; HULETT AC, 1979, ANN ALLERGY, V42, P160; Jeong KY, 2003, ALLERGY, V58, P1059, DOI 10.1034/j.1398-9995.2003.00167.x; Lal G, 2004, CLIN DIAGN LAB IMMUN, V11, P272, DOI 10.1128/CDLI.11.2.272-279.2004; Lee CS, 2004, CLIN EXP ALLERGY, V34, P354, DOI 10.1111/j.1365-2222.2004.01878.x; Matsui EC, 2003, J ALLERGY CLIN IMMUN, V112, P87, DOI 10.1067/mai.2003.1588; Melen E, 1999, J ALLERGY CLIN IMMUN, V103, P859, DOI 10.1016/S0091-6749(99)70430-6; Pickering JW, 2002, CLIN DIAGN LAB IMMUN, V9, P872, DOI 10.1128/CDLI.9.4.872-876.2002; Pittner G, 2004, CLIN EXP ALLERGY, V34, P597, DOI 10.1111/j.1365-2222.2004.1930.x; Pomes A, 1998, J BIOL CHEM, V273, P30801, DOI 10.1074/jbc.273.46.30801; Pomes A, 2002, EUR J BIOCHEM, V269, P3086, DOI 10.1046/j.1432-1033.2002.02990.x; 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; Santos ABR, 1999, J ALLERGY CLIN IMMUN, V104, P329, DOI 10.1016/S0091-6749(99)70375-1; vanWijnen JH, 1997, ALLERGY, V52, P460; Wu CH, 1997, MOL IMMUNOL, V34, P1, DOI 10.1016/S0161-5890(97)00009-6; Wu CH, 1996, J BIOL CHEM, V271, P17937; Wu CH, 2000, ALLERGY, V55, P1179, DOI 10.1034/j.1398-9995.2000.00604.x; Wu CH, 1998, J ALLERGY CLIN IMMUN, V101, P832, DOI 10.1016/S0091-6749(98)70312-4	34	76	79	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.	APR	2005	115	4					803	809		10.1016/j.jaci.2005.01.018		7	Allergy; Immunology	Allergy; Immunology	916GM	WOS:000228373400021	15806002	
J	Muller, UR; Haeberli, G				Muller, UR; Haeberli, G			Use of beta-blockers during immunotherapy for Hymenoptera venom allergy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						anaphylaxis; beta-blockers; hymenoptera venom immunotherapy	FATAL ANAPHYLACTIC REACTIONS; ADRENERGIC-BLOCKADE; HEART-FAILURE; RISK; HISTAMINE; EFFICACY; THERAPY; SAFETY; DRUGS	Background: B-Blockers may aggravate anaphylactic reactions and interfere with treatment. There is therefore concern about their use in patients who have a history of anaphylaxis or are on allergen immunotherapy. Immunotherapy is the best available treatment for prevention of life-threatening anaphylaxis to Hymenoptera stings, which is often observed in elderly patients who have cardiovascular disease and therefore are on beta-blocker treatment. Objective: To analyze the risk of beta-blocker treatment during venom immunotherapy. Methods: We screened all 1682 patients with Hymenoptera venom allergy seen during a period of 34 months for immunotherapy, cardiovascular disease, and treatment with beta-blockers. Results: Of the 1389 patients in whom immunotherapy was recommended, 11.2% had cardiovascular disease, and 44 of these were on beta-blockers before immunotherapy. In 31 of those, the drug was replaced before starting treatment. In 3 with coronary heart disease and I with severe ventricular arrhythmia, the drug was continued throughout immunotherapy. In 9, it was reintroduced after reaching the maintenance dose. In an additional 12 patients, beta-blockers were newly started during immunotherapy. Of 25 patients on beta-blockers during immunotherapy, 3 (12%) developed allergic side effects, compared with 23 (16.7%) of 117 with cardiovascular disease but without beta-blockers. Systemic allergic symptoms after re-exposure by sting challenge or field sting were observed in 1 of 7 (14.3%) with and 4 of 29 (13.8%) without beta-blockade. No severe reactions to treatment or sting reexposure were observed in patients with beta-blockade. Conclusion: Combination of beta-blockers with venom immunotherapy may be indicated in heavily exposed patients with severe cardiovascular disease.	Spital Bern Ziegler, Dept Med, CH-3007 Bern, Switzerland	Muller, UR (reprint author), Spital Bern Ziegler, Dept Med, Morillonstr 75-91, CH-3007 Bern, Switzerland.	ulrich.mueller@spitalbern.ch					ASSEM ESK, 1971, BRIT J PHARMACOL, V42, P620; AWAI LE, 1984, ANN ALLERGY, V53, P48; BERKELMAN RL, 1986, ANN INTERN MED, V104, P134; Foody JM, 2002, JAMA-J AM MED ASSOC, V287, P883, DOI 10.1001/jama.287.7.883; Freemantle N, 1999, BRIT MED J, V318, P1730; Haeberli G, 2003, CLIN EXP ALLERGY, V33, P1216, DOI 10.1046/j.1365-2222.2003.01755.x; HANNAWAY PJ, 1983, NEW ENGL J MED, V308, P1536; HELBLING A, 2004, CLIN EXP ALLERGY, V34, P1; HEPNER MJ, 1990, J ALLERGY CLIN IMMUN, V86, P407, DOI 10.1016/S0091-6749(05)80105-8; Hunt SA, 2001, J AM COLL CARDIOL, V38, P2101, DOI 10.1016/S0735-1097(01)01683-7; INGALL M, 1984, JAMA-J AM MED ASSOC, V251, P1432; JACOBS RL, 1981, J ALLERGY CLIN IMMUN, V68, P125, DOI 10.1016/0091-6749(81)90170-6; KALINER M, 1972, J EXP MED, V136, P556, DOI 10.1084/jem.136.3.556; KAPLAN AP, 1989, J ALLERGY CLIN IMMUN, V84, P129, DOI 10.1016/0091-6749(89)90186-3; LANG DM, 1995, DRUG SAFETY, V12, P299; LAXENAIRE M C, 1984, Annales Francaises d'Anesthesie et de Reanimation, V3, P453, DOI 10.1016/S0750-7658(84)80146-X; Locke M, 1998, J INSECT PHYSIOL, V44, P1; MADOWITZ JS, 1979, JAMA-J AM MED ASSOC, V241, P2813, DOI 10.1001/jama.241.26.2813; MALLING HJ, 1993, ALLERGY, V48, P14; MATSUMURA Y, 1976, J ALLERGY CLIN IMMUN, V58, P387, DOI 10.1016/0091-6749(76)90119-6; Mosbech H, 2000, ALLERGY, V55, P1005, DOI 10.1034/j.1398-9995.2000.00587.x; Mueller H L, 1966, J Asthma Res, V3, P331, DOI 10.3109/02770906609106941; MULLER U, 1993, ALLERGY, V48, P37; MULLER U, 1992, J ALLERGY CLIN IMMUN, V89, P529, DOI 10.1016/0091-6749(92)90319-W; Muller U., 1990, INSECT STING ALLERGY; MULLER UR, 2003, ALLERGY S74, V58, P99; NEWMAN BR, 1981, ANN ALLERGY, V47, P35; PARRISH HM, 1963, AM J MED SCI, V245, P129; Pumphrey RSH, 1996, CLIN EXP ALLERGY, V26, P1364, DOI 10.1046/j.1365-2222.1996.d01-297.x; SAMPSON HA, 1992, NEW ENGL J MED, V327, P380, DOI 10.1056/NEJM199208063270603; SASVARY T, 1994, SCHWEIZ MED WSCHR, V124, P1887; *SCHW BUND STAT, 1998, SEKT GES TOD SCHWEIZ; Skrbic D, 1996, ALLERGOLOGIE, V19, P123; TenBrook JA, 2004, J ALLERGY CLIN IMMUN, V113, P977, DOI 10.1016/j.jaci.2004.02.043; THURNHEER U, 1983, ALLERGY, V38, P465, DOI 10.1111/j.1398-9995.1983.tb02355.x; TOOGOOD JH, 1988, J ALLERGY CLIN IMMUN, V81, P1, DOI 10.1016/0091-6749(88)90212-6; TOOGOOD JH, 1987, CAN MED ASSOC J, V136, P929	37	76	77	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	2005	115	3					606	610		10.1016/j.jsci.2004.11.012		5	Allergy; Immunology	Allergy; Immunology	907AN	WOS:000227687000026	15753911	
J	Forsberg, B; Hansson, HC; Johansson, C; Areskoug, H; Persson, K; Jarvholm, B				Forsberg, B; Hansson, HC; Johansson, C; Areskoug, H; Persson, K; Jarvholm, B			Comparative health impact assessment of local and regional particulate air pollutants in Scandinavia	AMBIO			English	Article							DAILY MORTALITY; RESPIRATORY SYMPTOMS; BACKGROUND SITES; ASTHMA SYMPTOMS; WOOD COMBUSTION; BOUNDARY-LAYER; POLLUTION; PARTICLES; URBAN; ASSOCIATION	The ongoing program Clean Air for Europe (CAFE) is an initiative from the EU Commission to establish a coordinated effort to reach better air quality in the EU. The focus is on particulate matter as it has been shown to have large impact on human health. CAFE requested that WHO make a review of the latest findings on air pollutants and health to facilitate assessments of the different air pollutants and their health effects. The WHO review project on health aspects of air pollution in Europe confirmed that exposure to particulate matter (PM), despite the lower levels we face today, still poses a significant risk to human health. Using the recommended uniform risk coefficients for health impact assessment of PM, regardless of sources, premature mortality related to long-range transported anthropogenic particles has been estimated to be about 3500 deaths per year for the Swedish population, corresponding to a reduction in life expectancy of up to about seven months. The influence of local sources is more difficult to estimate due to large uncertainties when linking available risk coefficients to exposure data, but the estimates indicate about 1800 deaths brought forward each year with a life expectancy reduction of about 2-3 months. However, some sectors of the population are exposed to quite high locally induced concentrations and are likely to suffer excessive reductions in life expectancy. Since the literature increasingly supports assumptions that combustion related particles are associated with higher relative risks, further studies may shift the focus for abatement strategies. CAFE sets out to establish a general cost effective abatement strategy for atmospheric particles. Our results, based on studies of background exposure, show that long-range transported sulfate rich particles dominate the health effects of PM in Sweden. The same results would be found for the whole of Scandinavia and many countries influenced by transboundary air pollution. However, several health studies, including epidemiological studies with a finer spatial resolution, indicate that engine exhaust particles are more damaging to health than other particles. These contradictory findings must be understood and source specific risk estimates have to be established by expert bodies, otherwise it will not be possible to find the most cost effective abatement strategy for Europe. We are not happy with today's situation where every strategy to reduce PM concentrations is estimated to have the same impact per unit change in the mass concentration. Obviously there is a striking need to introduce more specific exposure variables and a higher geographical resolution in epidemiology as well as in health impact assessments.	Umea Univ, Dept Publ Hlth & Clin Med, SE-90187 Umea, Sweden; Stockholm Univ, Dept Appl Environm Sci, SE-10691 Stockholm, Sweden; IVL Swedish Environm Res Inst, Swedish Urban Air Qual Network, SE-40014 Gothenburg, Sweden	Forsberg, B (reprint author), Umea Univ, Dept Publ Hlth & Clin Med, SE-90187 Umea, Sweden.	bertil.forsberg@envmed.umu.se; hc@itm.su.se; christer.johansson@itm.su.se; hans.areskoug@itm.su.se; karin.persson@ivi.se; bengt.jarvholm@envmed.umu.se	Johansson, Christer/C-6451-2011	Johansson, Christer/0000-0002-8459-9852			ANDERSSON J, 2001, DP010515 CONCAWE, P1; ARESKOUG H, 2004, 145 ITM LUFTL STOCKH; ARESKOUG H, 2004, 110 ITM LUFTL STOCKH; Becker S, 2003, EXP LUNG RES, V29, P29, DOI 10.1080/01902140390116535; Boman BC, 2003, SCAND J WORK ENV HEA, V29, P251; Castillejos M, 2000, INHAL TOXICOL, V12, P61, DOI 10.1080/089583700196392; Cifuentes LA, 2000, J AIR WASTE MANAGE, V50, P1287; Delfino RJ, 2003, ENVIRON HEALTH PERSP, V111, P647, DOI 10.1289/ehp.5992; DOCKERY DW, 1993, NEW ENGL J MED, V329, P1753, DOI 10.1056/NEJM199312093292401; DURING I, 2002, P 11 INT S TRANSP AI; FORSBERG B, 1993, EUR RESPIR J, V6, P1109; Garshick E, 2003, EPIDEMIOLOGY, V14, P728, DOI 10.1097/01.ede.0000082045.50073.66; Glasius M, 2001, J GEOPHYS RES-ATMOS, V106, P7415, DOI 10.1029/2000JD900676; Goldberg MS, 2001, ENVIRON RES, V86, P26, DOI 10.1006/enrs.2001.4243; Harrison RM, 2004, ATMOS ENVIRON, V38, P4531, DOI 10.1016/j.atmosenv.2004.05.022; Hedberg E, 2002, ATMOS ENVIRON, V36, P4823, DOI 10.1016/S1352-2310(02)00417-X; Hetland RB, 2000, J TOXICOL ENV HEAL A, V60, P47, DOI 10.1080/009841000156583; Hetland RB, 2004, TOXICOL IN VITRO, V18, P203, DOI 10.1016/S0887-2333(03)00142-5; Hoek G, 2000, J AIR WASTE MANAGE, V50, P1380, DOI 10.1080/10473289.2000.10464182; Hoek G, 2002, LANCET, V360, P1203, DOI 10.1016/S0140-6736(02)11280-3; Janssen NAH, 2003, ENVIRON HEALTH PERSP, V111, P1512, DOI 10.1289/ehp.6243; Janssen NAH, 2002, ENVIRON HEALTH PERSP, V110, P43; JOHANSSON C, 1999, STOCKHOLM STUDY HLTH; JOHN A, 2004, EUR AER C BUD 06 10; Katsouyanni K, 2001, EPIDEMIOLOGY, V12, P521, DOI 10.1097/00001648-200109000-00011; KITTELSON D, 2000, 2000012212 SAE, P1; KuEnzli N., 2000, LANCET, P795; Laden F, 2000, ENVIRON HEALTH PERSP, V108, P941, DOI 10.2307/3435052; Mar TF, 2000, ENVIRON HEALTH PERSP, V108, P347, DOI 10.2307/3454354; Maricq MM, 1999, ENVIRON SCI TECHNOL, V33, P2007, DOI 10.1021/es981005n; Nafstad P, 2004, ENVIRON HEALTH PERSP, V112, P610, DOI 10.1289/ehp.6684; Nicolai T, 2003, EUR RESPIR J, V21, P956, DOI 10.1183/09031936.03.00041103; OMSTEDT G, 2002, 103 SMHI; Ostro BD, 2000, J EXPO ANAL ENV EPID, V10, P412, DOI 10.1038/sj.jea.7500094; Pope AC, 2002, JAMA-J AM MED ASSOC, V287, P1132, DOI DOI 10.1001/JAMA.287.9.1132; POPE CA, 1995, AM J RESP CRIT CARE, V151, P669; QUEROL X, 2004, IN PRESS ATMOS ENV; Ristovski ZD, 1998, ENVIRON SCI TECHNOL, V32, P3845, DOI 10.1021/es980102d; Roemer WH, 2001, EPIDEMIOLOGY, V12, P649, DOI 10.1097/00001648-200111000-00012; Sakurai H, 2003, ATMOS ENVIRON, V37, P1199, DOI 10.1016/S1352-2310(02)01017-8; Schwartz J, 2002, ENVIRON HEALTH PERSP, V110, P1025; Schwarze PE, 2002, INT J HYG ENVIR HEAL, V204, P327, DOI 10.1078/1438-4639-00108; SJOBERG K, 2004, 1553 IVL B; Tunved P, 2003, ATMOS CHEM PHYS, V3, P2183; Van Dingenen R, 2004, ATMOS ENVIRON, V38, P2561, DOI 10.1016/j.atmosenv.2004.01.040; WESTERLUND KG, 2002, AIR POLLUTION 10; *WHO, 2004, EUR045046026 WHO BON; *WHO, 2003, EUR035042688 WHO BON; World Health Organization, 2000, EUR005020369 WHO REG	49	76	77	1	19	ROYAL SWEDISH ACAD SCIENCES	STOCKHOLM	PUBL DEPT BOX 50005, S-104 05 STOCKHOLM, SWEDEN	0044-7447			AMBIO	Ambio	FEB	2005	34	1					11	19		10.1639/0044-7447(2005)034[0011:CHIAOL]2.0.CO;2		9	Engineering, Environmental; Environmental Sciences	Engineering; Environmental Sciences & Ecology	894HU	WOS:000226782600002	15789513	
J	Holguin, F; Mannino, DM; Anto, J; Mott, J; Ford, ES; Teague, WG; Redd, SC; Romieu, I				Holguin, F; Mannino, DM; Anto, J; Mott, J; Ford, ES; Teague, WG; Redd, SC; Romieu, I			Country of birth as a risk factor for asthma among Mexican Americans	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; Mexican Americans; migration	BODY-MASS INDEX; NHANES-III; RESPIRATORY SYMPTOMS; SERUM IGE; US ADULTS; IMMIGRANTS; PREVALENCE; ALLERGY; HEALTH; AGE	In the United States, among Hispanics, Mexican Americans have the lowest rate of asthma. However, this population includes Mexican Americans born in the United States and in Mexico, and risk factors that might impact the prevalence of asthma differ between these groups. To determine the prevalence of and risk factors for asthma among U.S.- and Mexican-born Mexican Americans, we analyzed data from two U.S. surveys that included 4,574 persons who self-reported their ethnicity as Mexican American from the Third National Health and Nutrition Examination Survey (NHANES III) 1998-1994 and 12,980 persons who self-reported their ethnicity as Mexican American from National Health Interview Survey (NHIS) 1997-2001. U.S.-born Mexican Americans were more likely than Mexican-born Mexican Americans to report ever having asthma in both the NHANES III (7% [SE 0.5] vs. 3% [SE 0.3], p < 0.001) and NHIS surveys (8.1% [0.4] vs. 2.5% [0.2], p < 0.001). In a multivariate regression model controlling for multiple demographic variables and health care, the risk for asthma was higher among U.S.-born Mexicans in NHANES III (odds ratio 2.1, 95% confidence interval 1.4-3.3) and NHIS (odds ratio 2.7, 95% confidence interval 1.6-5.5). In conclusion, the prevalence of asthma was higher in U.S.-born than in Mexican-born Mexican Americans. This finding highlights the importance of environmental exposures in developing asthma in a migratory population.	Ctr Dis Control & Prevent, Atlanta, GA 30333 USA; Emory Univ, Sch Med, Dept Pediat, Atlanta, GA 30322 USA; Municipal Inst Med Res, Barcelona, Spain; Inst Nacl Salud Publ, Cuernavaca, Morelos, Mexico	Holguin, F (reprint author), Ctr Dis Control & Prevent, 1600 Clifton Rd,NE,Mailstop E-17, Atlanta, GA 30333 USA.	fch5@cdc.gov	Osborne, Nicholas/N-4915-2015; Anto, J/H-2676-2014	Osborne, Nicholas/0000-0002-6700-2284; Anto, J/0000-0002-4736-8529; Mannino, David/0000-0003-3646-7828			Arif AA, 2003, EUR RESPIR J, V21, P827, DOI 10.1183/09031936.03.00054103; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; Ballin A, 1998, MED HYPOTHESES, V51, P281, DOI 10.1016/S0306-9877(98)90047-0; BARBEE RA, 1987, J ALLERGY CLIN IMMUN, V79, P919, DOI 10.1016/0091-6749(87)90241-7; BOTMAN S, DHHS PUBLICATION; BURNEY PGJ, 1989, EUR RESPIR J, V2, P940; *CONS NAC POBL, MIGR MEX EST UN, P20; Crespo CJ, 2001, AM J PUBLIC HEALTH, V91, P1254, DOI 10.2105/AJPH.91.8.1254; Dervaderics M, 2002, IMMUNOL INVEST, V31, P29, DOI 10.1081/IMM-120003220; Documet Patricia I, 2004, J Immigr Health, V6, P5, DOI 10.1023/B:JOIH.0000014638.87569.2e; English P., 1998, PAN AM J PUBLIC HLTH, V3, P392, DOI 10.1590/S1020-49891998000600005; Gibson PG, 2003, PEDIATR PULM, V36, P209, DOI 10.1002/ppul.10323; Hjern A, 1999, PEDIATR ALLERGY IMMU, V10, P101, DOI 10.1034/j.1399-3038.1999.00023.x; HOLGUIN F, 2004, AM J RESP CRIT CARE, V169, pA625; KALYONCU AF, 1992, ALLERGY, V47, P277, DOI 10.1111/j.1398-9995.1992.tb02053.x; Kuczmarski MF, 2001, J AM DIET ASSOC, V101, P28, DOI 10.1016/S0002-8223(01)00008-6; Kuczmarski RJ, 1997, OBES RES, V5, P542; LEUNG RC, 1994, MED J AUSTRALIA, V161, P418; Liu Andrew H., 2003, Journal of Allergy and Clinical Immunology, V111, pS785, DOI 10.1067/mai.2003.148; Mannino D. M., 2002, MMWR-MORBID MORTAL W, V51, P1; NAHMIAS J, 1993, ISRAEL J MED SCI, V29, P338; *NAT CTR ENV HLTH, BEH RISK FACT SURV S; *NAT HEART LUNG BL, 2004, ASTHM DAT SURV; Ormerod LP, 1999, RESP MED, V93, P16, DOI 10.1016/S0954-6111(99)90071-9; Powell CVE, 1999, ARCH DIS CHILD, V81, P159; Rosenberg R, 1999, Fam Med, V31, P276; Singh GK, 2002, HUM BIOL, V74, P83, DOI 10.1353/hub.2002.0011; Sundquist J, 1999, AM J PUBLIC HEALTH, V89, P723, DOI 10.2105/AJPH.89.5.723; Sundquist J, 2000, INT J EPIDEMIOL, V29, P470, DOI 10.1093/ije/29.3.470; Sunyer J, 2000, AM J RESP CRIT CARE, V162, P930; Tedeschi A, 2003, CLIN EXP ALLERGY, V33, P449, DOI 10.1046/j.1365-2222.2003.01628.x; Tobias A, 2001, EUR RESPIR J, V18, P459, DOI 10.1183/09031936.01.00026501; TOREN K, 1993, CHEST, V104, P600, DOI 10.1378/chest.104.2.600; *US DHHS, 1994, NATL CTR HLTH STAT P; Ventura MT, 2004, ALLERGY, V59, P632, DOI 10.1111/j.1398-9995.2004.00448.x; Wernette D.R., 1992, EPA J, V18, P16; Wong GWK, 2004, CURR OPIN PULM MED, V10, P62, DOI 10.1097/00063198-200401000-00011; 2003, ATLAS SALUD	38	76	77	2	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.	JAN 15	2005	171	2					103	108		10.1164/rccm.200402-143OC		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	886UO	WOS:000226258400004	15516539	
J	Moreno, C; Cuesta-Herranz, J; Fernandez-Tavora, L; Alvarez-Cuesta, E				Moreno, C; Cuesta-Herranz, J; Fernandez-Tavora, L; Alvarez-Cuesta, E			Immunotherapy safety: a prospective multi-centric monitoring study of biologically standardized therapeutic vaccines for allergic diseases	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						asthma; compliance; immunotherapy; mite; pollen; rhinitis; safety; side-effects	SYSTEMIC REACTIONS; ASTHMA; FATALITIES; EXTRACTS	Background The fear of side-effects has led to strict regulations preventing a more widespread use of specific immunotherapy (SIT) in some countries, in spite of the low risk of systemic reactions (SRs) reported in well-controlled studies. The goal of the study was to carry out a prospective and multi-centric trial to evaluate the safety, risk factors and compliance degree of commercially available SIT. Materials and methods The study was carried out in 14 allergy departments from Spain. Four-hundred and eighty-eight patients with rhinitis and/or asthma were submitted to treatment with biologically standardized allergen extracts commercially available. They were administered following the European Academy of Allergy and Clinical Immunology guidelines. Results Four hundred and twenty-three patients (86.7%) completed the treatment and remained under control at the end of the trial. Out of 17 526 administered doses, 17 368 doses (99.1%) were not associated with a reaction. Eighteen patients (3.7%) experienced 53 (0.3% of the doses) SRs. All immediate SRs were mild or moderate and responded well to ordinary treatment measures. There were no fatal reactions, anaphylactic shock or life-threatening reactions. A higher ratio of SRs was found among asthmatic and dust mite allergic patients, although multi-variable logistic analysis did not demonstrate any risk factor associated with SRs. There was also a subgroup of patients at risk for recurrent reactions, and therefore 40% of SRs had been avoided if the maximal number of SRs had been previously limited to only three SRs. Conclusions This multi-centric study showed that SIT was a safe treatment with a very good compliance. Future guidelines of SIT should limit the maximal number of SRs.	Fdn Jimenez Diaz, Dept Allergy, E-28040 Madrid, Spain; Hosp Reina Sofia, Dept Allergy, Cordoba, Spain; Hosp Virgen de la Cinta, Allergy Unit, Huelva, Spain; Hosp Ramon y Cajal, Dept Allergy, E-28034 Madrid, Spain	Cuesta-Herranz, J (reprint author), Fdn Jimenez Diaz, Dept Allergy, Avda Reyes Catolicos 2, E-28040 Madrid, Spain.	icuesta@fid.es					Abramson M, 1999, ALLERGY, V54, P1022, DOI 10.1034/j.1398-9995.1999.00102.x; BOUSQUET J, 1998, ALLERGY S1, V44, P2; Donahue JG, 1999, ANN ALLERG ASTHMA IM, V82, P339; Dreborg S, 1993, ALLERGY          S14, V48, P48, DOI DOI 10.1111/J.1398-9995.1993.TB04698.X; DuBuske LM, 2001, ANN ALLERG ASTHMA IM, V87, P56; Finegold I, 2001, ANN ALLERG ASTHMA IM, V87, P33; Frew AJ, 1999, LUNG BIOL HEALTH DIS, V136, P199; HEJJAOUI A, 1992, J ALLERGY CLIN IMMUN, V89, P925, DOI 10.1016/0091-6749(92)90214-M; HEPNER MJ, 1990, J ALLERGY CLIN IMMUN, V86, P407, DOI 10.1016/S0091-6749(05)80105-8; Hutchinson DR, 1997, TRIAL INVESTIGATORS; Lamson R., 1924, JAMA-J AM MED ASSOC, V82, P1090; LOCKEY RF, 1987, J ALLERGY CLIN IMMUN, V79, P660, DOI 10.1016/S0091-6749(87)80164-1; Lockey RF, 2001, ANN ALLERG ASTHMA IM, V87, P47; LOWER T, 1993, ANN ALLERGY, V70, P480; Malling HJ, 2000, DRUG SAFETY, V23, P323, DOI 10.2165/00002018-200023040-00005; MALLING HJ, 1993, ALLERGY          S14, V48, P1; *NHLBI, 1995, NHLBI PUBL; REID MJ, 1993, J ALLERGY CLIN IMMUN, V92, P6, DOI 10.1016/0091-6749(93)90030-J; Salkind AR, 2001, JAMA-J AM MED ASSOC, V285, P2498, DOI 10.1001/jama.285.19.2498; SETTIPANE GA, 1983, AM J MED, V74, P102, DOI 10.1016/0002-9343(83)90537-5; TABAR AI, 1993, ALLERGY, V48, P450, DOI 10.1111/j.1398-9995.1993.tb00743.x; Theodoropoulos DS, 2000, ALLERGY ASTHMA PROC, V21, P159, DOI 10.2500/108854100778149007; TINKELMAN D, 1995, ANN ALLERG ASTHMA IM, V74, P241	23	76	91	0	3	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	APR	2004	34	4					527	531		10.1111/j.1365-2222.2004.1819.x		5	Allergy; Immunology	Allergy; Immunology	812RQ	WOS:000220857000006	15080803	
J	Joachim, RA; Quarcoo, D; Arck, PC; Herz, U; Renz, H; Klapp, BF				Joachim, RA; Quarcoo, D; Arck, PC; Herz, U; Renz, H; Klapp, BF			Stress enhances airway reactivity and airway inflammation in an animal model of allergic bronchial asthma	PSYCHOSOMATIC MEDICINE			English	Article						sonic stress; allergic asthma; airway inflammation; airway hyperreactivity; mouse model	M-2 RECEPTOR DYSFUNCTION; PSYCHOSOCIAL STRESS; HUMAN EOSINOPHILS; PSYCHOLOGICAL STRESS; CYTOKINE PRODUCTION; TRIGGERED ABORTION; ATOPIC-DERMATITIS; BREAST-CANCER; GUINEA-PIGS; MICE	Objective: Despite the long-standing clinical assumption that stress and asthma morbidity are associated, convincing experimental evidence on mechanisms has been unavailable. A wide range of immunological, endocrinological, and neuronal pathways are known to mediate and modulate a systemic stress response. Interestingly, most of these mediators play a crucial role in initiating and perpetuating symptoms associated with bronchial asthma. To explore potential mechanisms linking stress to asthma exacerbation we developed an animal model that combines allergic airway inflammation and exposure to stress. Methods: CBA/J mice were sensitized by intraperitoneal injection of ovalbumin (OVA) and challenged with OVA aerosol via the airways. Additionally, some mice were stressed by exposure to an ultrasonic stressor. Airway hyperreactivity (AHR) was measured in vitro by electric field stimulation (EFS) of tracheal smooth muscle elements. Bronchoalveolar lavage fluid (BAL) was obtained and cell numbers determined. Cytokine levels of IL-4, IL-5, and IFN-gamma in BAL were determined by ELISA. Results: Our findings demonstrate that exogenously applied stress dramatically enhances airway reactivity in OVA-sensitized and challenged mice. Further, stress significantly increases allergen-induced airway inflammation identified by increased leukocyte (ie, eosinophil) numbers in bronchoalveolar lavage fluids. Conclusions: We found further evidence that stress can indeed exacerbate airway hyperreactivity and airway inflammation in an animal model of allergic bronchial asthma and now introduce a novel murine model to identify stress-triggered pathways, including mediators as neurohormones, neuropeptides, and markers of inflammation.	Humboldt Univ, Dept Internal Med, Berlin, Germany; Humboldt Univ, Dept Pediat, Berlin, Germany; Univ Marburg, Dept Clin Chem & Mol Diagnost, Marburg, Germany	Joachim, RA (reprint author), Forschungszentrum, Biomed, Charite Campus Virchow,R 2-0594,Augustenburger Pl, D-13353 Berlin, Germany.		Arck, Petra/D-7094-2013	Quarcoo, David/0000-0001-6398-2118			Ackerman KD, 1998, PSYCHOSOM MED, V60, P484; ADER R, 1995, LANCET, V345, P99, DOI 10.1016/S0140-6736(95)90066-7; Andersen BL, 1998, J NATL CANCER I, V90, P30, DOI 10.1093/jnci/90.1.30; ARCK PC, 1995, AM J REPROD IMMUNOL, V33, P74; ARCK PC, 2001, FASEB J; AZZAWI M, 1990, AM REV RESPIR DIS, V142, P1407; BEASLEY R, 1989, AM REV RESPIR DIS, V139, P806; BUCKLEY TL, 1994, AM J RESP CRIT CARE, V149, P400; BuskeKirschbaum A, 1997, PSYCHOSOM MED, V59, P419; Chrousos George P., 2000, Journal of Allergy and Clinical Immunology, V106, pS275; CLARK DA, 1993, AM J REPROD IMMUNOL, V29, P141; Costello RW, 1998, BRIT J PHARMACOL, V124, P267, DOI 10.1038/sj.bjp.0701822; Coyle AJ, 1996, J IMMUNOL, V156, P2680; Crimi E, 1998, AM J RESP CRIT CARE, V157, P4; DURHAM SR, 1989, J ALLERGY CLIN IMMUN, V84, P931, DOI 10.1016/0091-6749(89)90391-6; Evans CM, 2001, AM J RESP CRIT CARE, V163, P1484; Evans CM, 2000, AM J PHYSIOL-LUNG C, V279, pL477; GREENE BR, 1994, BEHAV RES THER, V32, P217, DOI 10.1016/0005-7967(94)90114-7; Hamelmann E, 1997, AM J RESP CRIT CARE, V156, P766; Herz U, 1998, CLIN EXP ALLERGY, V28, P625; HUANG SK, 1995, J IMMUNOL, V155, P2688; Iwakabe K, 1998, IMMUNOL LETT, V62, P39, DOI 10.1016/S0165-2478(98)00021-2; Jacoby DB, 2001, J ALLERGY CLIN IMMUN, V107, P211, DOI 10.1067/mai.2001.112940; Kang DH, 2000, ANN BEHAV MED, V22, P276, DOI 10.1007/BF02895663; Kang DH, 2001, RES NURS HEALTH, V24, P245, DOI 10.1002/nur.1027; Koning H, 1997, CYTOKINE, V9, P427, DOI 10.1006/cyto.1996.0185; KUNG TT, 1994, INT ARCH ALLERGY IMM, V105, P83; LARSEN GL, 1992, J CLIN INVEST, V89, P747, DOI 10.1172/JCI115651; Leonard C, 1997, AM J RESP CELL MOL, V17, P368; LEVENSTEIN S, 1994, AM J GASTROENTEROL, V89, P1219; LEVY SM, 1990, PSYCHOSOM MED, V52, P73; Liu LY, 2002, AM J RESP CRIT CARE, V165, P1062, DOI 10.1164/rccm.2109065; LOPEZ AF, 1988, J EXP MED, V167, P219, DOI 10.1084/jem.167.1.219; LUNDGREN R, 1988, EUR RESPIR J, V1, P883; Maes M, 1998, CYTOKINE, V10, P313, DOI 10.1006/cyto.1997.0290; MAKKER HK, 1993, J ALLERGY CLIN IMMUN, V92, P82, DOI 10.1016/0091-6749(93)90041-D; MATSUSE T, 1991, AM REV RESPIR DIS, V144, P368; MINETTE PAH, 1989, J APPL PHYSIOL, V67, P2461; OBYRNE PM, 1988, J ALLERGY CLIN IMMUN, V81, P119, DOI 10.1016/0091-6749(88)90230-8; OHASHI Y, 1992, AM REV RESPIR DIS, V145, P1469; Qiu BS, 1999, NAT MED, V5, P1178; Ritz T, 2000, PSYCHOSOM MED, V62, P401; ROBINSON DS, 1992, NEW ENGL J MED, V326, P298, DOI 10.1056/NEJM199201303260504; Sandberg S, 2000, LANCET, V356, P982, DOI 10.1016/S0140-6736(00)02715-X; SCHLEIMER RP, 1992, J IMMUNOL, V148, P1086; Schmid-Ott G, 2001, J ALLERGY CLIN IMMUN, V107, P171, DOI 10.1067/mai.2001.111850; SCHWEIZER RC, 1994, BLOOD, V83, P3697; Undem BJ, 1999, INT ARCH ALLERGY IMM, V118, P150, DOI 10.1159/000024053; WALSH GM, 1990, IMMUNOLOGY, V71, P258; WARRINGA RAJ, 1992, AM J RESP CELL MOL, V7, P631; YAMAGUCHI Y, 1988, J EXP MED, V167, P43, DOI 10.1084/jem.167.1.43	51	76	79	2	2	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	0033-3174			PSYCHOSOM MED	Psychosom. Med.	SEP-OCT	2003	65	5					811	815		10.1097/01.PSY.0000088582.50468.A3		5	Psychiatry; Psychology; Psychology, Multidisciplinary	Psychiatry; Psychology	727QQ	WOS:000185670300014	14508025	
J	Bolte, G; Bischof, W; Borte, M; Lehmann, I; Wichmann, HE; Heinrich, J				Bolte, G; Bischof, W; Borte, M; Lehmann, I; Wichmann, HE; Heinrich, J			Early endotoxin exposure and atopy development in infants: results of a birth cohort study	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergy; asthma; hygiene hypothesis	HOUSE-DUST ENDOTOXIN; INFLAMMATORY RESPONSE; INHALED ENDOTOXIN; EARLY-LIFE; ASTHMA; CHILDREN; ALLERGY; SENSITIZATION; RISK; PETS	Background Exposure to endotoxin in childhood is currently discussed to protect from the development of allergic diseases. Objective To study the effect of early endotoxin exposure on incidence of atopic sensitization, atopic dermatitis and wheezing until the age of 2 years in infants with different risk status in terms of parental atopy. Methods Data of 1942 infants of an ongoing birth cohort study were analysed by logistic regression. Endotoxin was measured in settled dust of the mothers' mattresses at infants' age of 3 months. Data on allergic symptoms and physicians' diagnoses were gathered by questionnaire. Sensitization to common food and inhalant allergens was assessed by specific serum IgE. Results High endotoxin levels increased the risk of repeated wheeze [adjusted odds ratio (OR) for 4th exposure quartile ((Q4)) 1.52, 95% confidence interval (CI) 1.08-2.14], but were associated with neither sensitization to food allergens nor atopic dermatitis. Stratification by parental atopy showed that there was an association of endotoxin exposure with incidence of repeated wheeze as well as with sensitization to inhalant allergens (P for trend = 0.008 and 0.044, respectively) only in infants with parental atopy, with the highest risk in the 4th exposure quartile (repeated wheeze: ORQ4 1.77, 95% CI 1.14-2.73; sensitization to inhalant allergens: ORQ4 1.69, 95% CI 0.70-4.11). Conclusion Early endotoxin exposure in terms of mattress dust endotoxin levels seemed to increase the risk of atopic reactions to inhalant allergens at the age of 2 years, especially in infants at risk due to parental atopy. Our data disagree with an early protective effect of endotoxin on atopy development until the age of 2 years.	GSF Natl Res Ctr Environm & Hlth, Inst Epidemiol, D-85764 Neuherberg, Germany; Univ Ulm, Dept Epidemiol, Ulm, Germany; Univ Jena, Dept Indoor Climatol, Erfurt, Germany; Univ Leipzig, Dept Pediat, Leipzig, Germany; Hall Ltd, UFZ Ctr Environm Res Leipzig, Dept Human Exposure Res & Epidemiol, D-7010 Leipzig, Germany	Heinrich, J (reprint author), GSF Natl Res Ctr Environm & Hlth, Inst Epidemiol, Ingolstaedter Landstr 1, D-85764 Neuherberg, Germany.	joachim.heinrich@gsf.de					Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Bolte G, 2002, J ALLERGY CLIN IMMUN, V110, P634, DOI 10.1067/mai.2002.128652; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Christiani DC, 2001, AM J RESP CRIT CARE, V163, P847; Dubin W, 1996, AM J PHYSIOL-LUNG C, V270, pL736; Eldridge MW, 2000, J ALLERGY CLIN IMMUN, V105, P475, DOI 10.1067/mai.2000.104552; Fahlbusch B, 1999, ALLERGY, V54, P1215, DOI 10.1034/j.1398-9995.1999.00196.x; Gehring U, 2001, J ALLERGY CLIN IMMUN, V108, P847, DOI 10.1067/mai.2001.119026; Gehring U, 2002, AM J RESP CRIT CARE, V166, P939, DOI 10.1164/rccm.200203-256OC; GEHRING U, 2002, J ALLERGY CLIN IMMUN, V109, P648; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Hansen G, 1999, J CLIN INVEST, V103, P175, DOI 10.1172/JCI5155; Heinrich J, 2001, CLIN EXP ALLERGY, V31, P1839, DOI 10.1046/j.1365-2222.2001.01220.x; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Holt PG, 1997, PEDIATR ALLERGY IMMU, V8, P53, DOI 10.1111/j.1399-3038.1997.tb00145.x; Holt PG, 2000, AM J RESP CRIT CARE, V162, pS91; Lehmann I, 2002, ALLERGY, V57, P129, DOI 10.1046/j.0105-4538.2002.00001.x; 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; Martinez FD, 2002, PEDIATRICS, V109, P362; Martinez FD, 1999, LANCET S2, V354, pSII12; MICHEL O, 1992, AM REV RESPIR DIS, V146, P352; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; Michel O, 1997, AM J RESP CRIT CARE, V156, P1157; Nafstad P, 2001, ALLERGY, V56, P307, DOI 10.1034/j.1398-9995.2001.00881.x; Nelde A, 2001, INT ARCH ALLERGY IMM, V124, P461, DOI 10.1159/000053781; Nightingale JA, 1998, THORAX, V53, P563; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Rizzo MC, 1997, PEDIATR ALLERGY IMMU, V8, P121; Silva JRL, 2000, TOXICOLOGY, V152, P31; Tariq SM, 1998, J ALLERGY CLIN IMMUN, V101, P587; Tulic MK, 2000, AM J RESP CELL MOL, V22, P604; Vogelzang PFJ, 1998, AM J RESP CRIT CARE, V157, P15; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; Wan GH, 2000, CLIN EXP ALLERGY, V30, P426	36	76	76	0	3	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	JUN	2003	33	6					770	776		10.1046/j.1365-2222.2003.01665.x		7	Allergy; Immunology	Allergy; Immunology	688QA	WOS:000183445800010	12801311	
J	Fireman, P				Fireman, P			Symposium: Understanding asthma pathophysiology	ALLERGY AND ASTHMA PROCEEDINGS			English	Article; Proceedings Paper	Eastern Allergy Conference	MAY, 2001	NAPLES, FLORIDA				AIRWAY SMOOTH-MUSCLE; INFLAMMATION; HYPERRESPONSIVENESS; ADULTS; LIFE	Asthma is best described as a chronic disease that involves inflammation of the pulmonary airways and bronchial hyperresponsiveness that results in the clinical expression of a lower airway obstruction that usually is reversible. Physiologically, bronchial hyperresponsiveness is documented by decreased bronchial airflow after bronchoprovocation with methacholine or histamine. Other triggers that provoke airway obstruction include cold air, exercise, viral upper respiratory infection, cigarette smoke, and respiratory allergens. Bronchial provocation with allergen induces a prompt early phase immunoglobulin E (IgE)-mediated decrease in bronchial airflow (forced expiratory volume in 1 second) followed in many patients by a late-phase IgE-mediated reaction with a decrease in bronchial airflow for 4-8 hours. The gross pathology of asthmatic airways displays lung hyperinflation, smooth muscle hypertrophy, lamina reticularis thickening, mucosal edema, epithelial cell sloughing, cilia cell disruption, and mucus gland hypersecretion. Microscopically, asthma is characterized by the presence of increased numbers of eosinophils, neutrophils, lymphocytes, and plasma cells in the bronchial tissues, bronchial secretions, and mucus. Initially, there is recruitment of leukocytes from the bloodstream to the airway by activated CD, T-lymphocytes. The activated T-lymphocytes also direct the release of inflammatory mediators from eosinophils, mast cells, and lymphocytes. In addition, the subclass 2 helper T-lymphocytes subset of activated T-lymphocytes produces interleukin (IL)-4, IL-5, and IL-13. IL-4 in conjunction with IL-13 signals the switch from IgM to IgE antibodies. The cross-linkage of two IgE molecules by allergen causes mast cells to degranulate, releasing histamine, leukotrienes, and other mediators that perpetuate the airway inflammation. IL-5 activates the recruitment and activation of eosinophils. The activated mast cells and eosinophils also generate their cytokines that help to perpetuate the inflammation. Regardless of the triggers of asthma, the repeated cycles of inflammation in the lungs with injury to the pulmonary tissues followed by repair may produce long-term structural changes ("remodeling") of the airways. This review will discuss in greater detail the relationships of inflammation and airway hyperresponsiveness to the pathophysiology of asthma.	Univ Pittsburgh, Sch Med, Dept Allergy & Immunol, Pittsburgh, PA 15213 USA; Childrens Hosp Pittsburgh, Pittsburgh, PA 15213 USA	Fireman, P (reprint author), Univ Pittsburgh, Sch Med, Dept Allergy & Immunol, 3705 5th Ave, Pittsburgh, PA 15213 USA.						Banchereau J, 2000, ANNU REV IMMUNOL, V18, P767, DOI 10.1146/annurev.immunol.18.1.767; Bousquet J, 2000, AM J RESP CRIT CARE, V161, P1720; Brusasco V, 1998, THORAX, V53, P992; CADE JF, 1971, CLIN SCI, V40, P361; DAVIS RS, 1983, J ALLERGY CLIN IMMUN, V72, P393, DOI 10.1016/0091-6749(83)90505-5; Djukanovic R, 2002, J ALLERGY CLIN IMMUN, V109, pS539, DOI 10.1067/mai.2002.124568; DONCET C, 1998, J CLIN INVEST, V101, P2129; ELLIS JL, 1994, PULM PHARMACOL, V7, P205, DOI 10.1006/pulp.1994.1024; Holgate ST, 2000, CLIN EXP ALLERGY, V30, P28; Holgate ST, 2000, J ALLERGY CLIN IMMUN, V105, P193, DOI 10.1016/S0091-6749(00)90066-6; Lacy P, 2000, CHEM IMMUNOL, V76, P134; Lange P, 1998, NEW ENGL J MED, V339, P1194, DOI 10.1056/NEJM199810223391703; Lemanske RF, 2002, J ALLERGY CLIN IMMUN, V109, pS521, DOI 10.1067/mai.2002.124564; LEVIN ER, 1995, NEW ENGL J MED, V333, P355; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; MCFADDEN ER, 1980, SEMIN RESPIR MED, V1, P287, DOI 10.1055/s-2007-1012133; *NAT HEART LUNG BL, 1991, 913042 NAT HEART LUN; Peat JK, 1999, J ALLERGY CLIN IMMUN, V103, P1, DOI 10.1016/S0091-6749(99)70517-8; PERSSON MG, 1994, LANCET, V343, P146, DOI 10.1016/S0140-6736(94)90935-0; PROBST SM, 2000, J IMMUNOL, V165, P2214; Romagnani S, 2000, J ALLERGY CLIN IMMUN, V105, P399, DOI 10.1067/mai.2000.104575; Solway J, 1997, AM J RESP CELL MOL, V17, P144; Stein R, 1999, LANCET, V354, P541, DOI 10.1016/S0140-6736(98)10321-5; Szefler S, 2000, NEW ENGL J MED, V343, P1054; Walley AJ, 2001, GENOMICS, V72, P15, DOI 10.1006/geno.2000.6435	25	76	81	2	17	OCEAN SIDE PUBLICATIONS INC	PROVIDENCE	95 PITMAN ST, PROVIDENCE, RI 02906 USA	1088-5412			ALLERGY ASTHMA PROC	Allergy Asthma Proc.	MAR-APR	2003	24	2					79	83				5	Allergy	Allergy	675GQ	WOS:000182685900001	12776439	
J	Carney, AS; Powe, DG; Huskisson, RS; Jones, NS				Carney, AS; Powe, DG; Huskisson, RS; Jones, NS			Atypical nasal challenges in patients with idiopathic rhinitis: more evidence for the existence of allergy in the absence of atopy?	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergy; idiopathic rhinitis; non-allergic rhinitis; allergen challenge; rhinomanometry; vasomotor rhinitis	LOCAL IGE PRODUCTION; SYSTEMATIC EVALUATION; NONALLERGIC RHINITIS; PRELIMINARY CRITERIA; ACOUSTIC RHINOMETRY; CLINICAL-PARAMETERS; PERENNIAL RHINITIS; PROVOCATION TEST; SKIN-TESTS; AIR-FLOW	Background The pathophysiology of idiopathic rhinitis is unknown although evidence is accumulating to suggest that many patients may have a localized form of allergic rhinitis in the absence of other atopic symptoms and markers. This study compares detailed nasal challenge results obtained from patients with idiopathic rhinitis to those of atopic and normal controls. Methods Patients with idiopathic rhinitis (n = 23), perennial allergic rhinitis (n = 8) and normal controls (n = 8) underwent a normal saline challenge to exclude hyper-reactivity and then bilateral nasal allergen challenges. Nasal patency was assessed by anterior active rhinomanometry. Results All of the patients with atopic rhinitis demonstrated positive bilateral allergen challenges. All normal control subjects had bilateral negative challenges. Two patients in the idiopathic group tested positively to saline and were excluded from further study with 62% of the remainder testing positive to allergens. Of the idiopathic patients testing positive, 85% were sensitive to house dust mite. Conclusion A significant proportion of patients with idiopathic rhinitis have positive nasal challenges, the vast majority to house dust mite allergen. These findings add to the weight of evidence that suggests 'localized allergy' may exist in the absence of systemic atopic markers.	Queens Med Ctr, Dept Otolaryngol Head & Neck Surg, Nottingham NG7 2UH, England; Queens Med Ctr, Dept Clin Lab Sci, Nottingham NG7 2UH, England	Carney, AS (reprint author), Flinders Med Ctr, Dept Otolaryngol Head & Neck Surg, Adelaide, SA 5042, Australia.						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Exp. Allergy	OCT	2002	32	10					1436	1440				5	Allergy; Immunology	Allergy; Immunology	601ZJ	WOS:000178479300009	12372122	
J	Eagan, TML; Eide, GE; Gulsvik, A; Bakke, PS				Eagan, TML; Eide, GE; Gulsvik, A; Bakke, PS			Nonresponse in a community cohort study - Predictors and consequences for exposure-disease associations	JOURNAL OF CLINICAL EPIDEMIOLOGY			English	Article						cohort study; questionnaire; response bias; odds ratio; asthma; respiratory symptoms; smoking	MAIL SURVEY RESPONSE; CARDIOVASCULAR-DISEASE; RESPIRATORY SYMPTOMS; QUESTIONNAIRE; SMOKING; HEALTH; BIAS; POPULATION; RESPONDENTS; SWEDEN	We have assessed predictors for response in a Norwegian community cohort study, with an 11-year follow-up. We also examined to what extent the association of gender, age, and smoking to the incidence of respiratory symptoms and asthma differed if the analyses were based on the 65% (n = 2,079) initial responders, or were based on the 89% (n = 2,819) who responded after three reminders. The associations between the six symptoms/asthma and the gender, age, and smoking groups amounted to 42 odds ratios. The adjusted odds ratio for responding at follow-up was 1.39 (95% CI: 1.01, 1.90) for those being middle aged at baseline compared to younger subjects. The adjusted odds ratios for responding at follow-up for those being students, unemployed, or retired at baseline were 0.50 (95% CI: 0.35, 0.73), 0.29 (95% CI: 0.16, 0.55), 0.21 (95% CI: 0.13, 0.36), respectively, compared to being employed. Of the 42 odds ratios mentioned above, 25 differed less than 10% when comparing the initial and all respondents. Twelve differed 10-20% and five differed 20-45%. The study indicates that to ensure a high participation rate in a follow-up study one should pay special attention to those being late responders, unemployed, retired, or students at baseline. No overt differences were observed in the gender, age, and, smoking associations to the respiratory disorders when the analyses were based on the initial compared to all respondents. (C) 2002 Elsevier Science Inc. All rights reserved.	Haukeland Univ Hosp, Dept Thorac Med, N-5021 Bergen, Norway; Univ Bergen, Sect Med Stat, Bergen, Norway; Haukeland Univ Hosp, Clin Res Ctr, N-5021 Bergen, Norway	Eagan, TML (reprint author), Haukeland Univ Hosp, Dept Thorac Med, N-5021 Bergen, Norway.		Eagan, Tomas/P-3554-2014	Eagan, Tomas/0000-0001-8725-9960			BAKKE P, 1990, J EPIDEMIOL COMMUN H, V44, P316, DOI 10.1136/jech.44.4.316; BARTON J, 1980, AM J PUBLIC HEALTH, V70, P823, DOI 10.2105/AJPH.70.8.823; BECK GJ, 1982, AM REV RESPIR DIS, V125, P375; Bjartveit K, 1979, Acta Med Scand Suppl, V634, P1; BOSTROM G, 1993, SCAND J SOC MED, V21, P77; Cohen BB, 1987, VITAL HLTH STAT, V1, P1; CRIQUI MH, 1979, J CHRON DIS, V32, P633, DOI 10.1016/0021-9681(79)90093-6; CRIQUI MH, 1978, AM J EPIDEMIOL, V108, P367; Doll R, 1999, B WORLD HEALTH ORGAN, V77, P84; FORTHOFER RN, 1983, AM J EPIDEMIOL, V117, P507; FOSS OP, 1986, SCAND J CLIN LAB INV, V46, P245, DOI 10.3109/00365518609083666; GREENLAND S, 1977, AM J EPIDEMIOL, V106, P184; GULSVIK A, 1979, SCAND J RESPIR DIS, V60, P275; GULSVIK A, 1991, EUR RESPIR REV, V1, P436; Hill A, 1997, J PUBLIC HEALTH MED, V19, P203; JACOBSEN BK, 1988, SCAND J SOC MED, V16, P101; JANZON L, 1986, J EPIDEMIOL COMMUN H, V40, P174, DOI 10.1136/jech.40.2.174; LIBERATOS P, 1988, EPIDEMIOL REV, V10, P87; Lund E, 1998, SCAND J SOC MED, V26, P154, DOI 10.1177/14034948980260020401; MACERA CA, 1990, J CLIN EPIDEMIOL, V43, P1427, DOI 10.1016/0895-4356(90)90112-3; PIETILA AM, 1995, SCAND J SOC MED, V23, P129; Ronmark E, 1997, ALLERGY, V52, P1071, DOI 10.1111/j.1398-9995.1997.tb00178.x; Ronmark E, 1999, EUR J EPIDEMIOL, V15, P293, DOI 10.1023/A:1007582518922; SELTZER CC, 1974, AM J EPIDEMIOL, V100, P453; SHEIKH K, 1981, J EPIDEMIOL COMMUN H, V35, P293, DOI 10.1136/jech.35.4.293; SMITH C, 1990, Health Education Research, V5, P381, DOI 10.1093/her/5.3.381; SPRY VM, 1989, AM J EPIDEMIOL, V130, P166; van den Akker M, 1998, FAM PRACT, V15, P261, DOI 10.1093/fampra/15.3.261; VESTERINEN E, 1988, THORAX, V43, P534, DOI 10.1136/thx.43.7.534; YAMMARINO FJ, 1991, PUBLIC OPIN QUART, V55, P613, DOI 10.1086/269284	30	76	78	1	9	PERGAMON-ELSEVIER SCIENCE LTD	OXFORD	THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND	0895-4356			J CLIN EPIDEMIOL	J. Clin. Epidemiol.	AUG	2002	55	8					775	781	PII S0895-4356(02)00431-6	10.1016/S0895-4356(02)00431-6		7	Health Care Sciences & Services; Public, Environmental & Occupational Health	Health Care Sciences & Services; Public, Environmental & Occupational Health	594FD	WOS:000178037500006	12384191	
J	Krieger, J; Takaro, TK; Allen, C; Song, L; Weaver, M; Chai, S; Dickey, P				Krieger, J; Takaro, TK; Allen, C; Song, L; Weaver, M; Chai, S; Dickey, P			The Seattle-King County Healthy Homes Project: Implementation of a comprehensive approach to improving indoor environmental quality for low-income children with asthma	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Review						asthma; children; community health workers; Healthy Homes; indoor environmental quality; inner city; interventions	HOUSE-DUST MITE; INNER-CITY CHILDREN; CHILDHOOD ASTHMA; RISK-FACTORS; URBAN CHILDREN; TOBACCO-SMOKE; MECHANICAL VENTILATION; SOCIOECONOMIC-FACTORS; ALLERGEN REDUCTION; PATIENT COMPLIANCE	Pediatric asthma is a growing public health issue, disproportionately affecting low-income people and people of color. Exposure to indoor asthma triggers plays an important role in the development and exacerbation of asthma. We describe the implementation of the Seattle-King County Healthy Homes Project, a randomized, controlled trial of an outreach/education intervention to improve asthma-related health status by reducing exposure to allergens and irritants in the home. We randomly assigned 274 low-income children with asthma ages 4-12 to either a high- or a low-intensity group. In the high-intensity group, community health workers called Community Home Environmental Specialists (CHES) conducted initial home environmental assessments, provided individualized action plans, and made additional visits over a 12-month period to provide education and social support, encouragement of participant actions, provision of materials to reduce exposures (including bedding encasements), assistance with roach and rodent eradication, and advocacy for improved housing conditions. Members of the low-intensity group received the initial assessment, home action plan, limited education during the assessment visit, and bedding encasements. We describe the recruitment and training of CHES and challenges they faced and explain the assessment and exposure reduction protocols addressing dust mites, mold, tobacco smoke, Pets, cockroaches, rodents, dust, moisture, and toxic or hazardous chemicals. We also discuss the gap between the practices recommended in the literature and what is feasible in the home. We accomplished home interventions and participants found the project very useful. The project was limited in resolving structural housing quality issues that contributed to exposure to indoor triggers.	Publ Hlth Seattle & King Cty, Seattle, WA 98104 USA; Univ Washington, Sch Publ Hlth & Community Med, Seattle, WA 98195 USA; Univ Washington, Sch Med, Seattle, WA USA; Seattle Partners Healthy Communities, Seattle, WA USA; Washington Tox Coalit, Seattle, WA USA	Krieger, J (reprint author), Publ Hlth Seattle & King Cty, 999 3rd Ave,Ste 1200, Seattle, WA 98104 USA.				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Health Perspect.	APR	2002	110			2			311	322				12	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	542WE	WOS:000175066600025	11929743	
J	Smedje, G; Norback, D				Smedje, G; Norback, D			Incidence of asthma diagnosis and self-reported allergy in relation to the school environment - a four-year follow-up study in schoolchildren	INTERNATIONAL JOURNAL OF TUBERCULOSIS AND LUNG DISEASE			English	Article						cat allergen; dust; formaldehyde; moulds	RISK FACTOR; NORTHERN SWEDEN; NASAL PATENCY; CAT ALLERGEN; DOG CAN-F-1; CHILDREN; DUST; SENSITIZATION; CLASSROOMS; EXPOSURE	SETTING: In schools, the indoor air quality is often poor and there is growing concern about its impact on the pupils' health. OBJECTIVE: To study the incidence of asthma diagnosis and self-reported allergy in schoolchildren in relation to the school environment. DESIGN: Data on asthma and allergies were collected through a postal questionnaire answered in 1993 and 1997 by 1347 (78%) pupils (initially aged 7-13 years) in 39 randomly chosen schools. Indoor pollutants were measured in about 100 classrooms in 1993 and 1995. Relationships between indoor pollutants and incidence of asthma diagnosis and self-reported allergy were studied by multiple logistic regression, adjusting for age, sex, atopy and smoking. RESULTS: The incidence of asthma diagnosis was higher in pupils attending schools with more settled dust and more cat allergen (Fel d 1) in this dust. Incidence of self-reported furry pet allergy was higher in schools with more respirable particles. Among children without a history of atopy, a new asthma diagnosis was more common at higher concentrations of formaldehyde and total moulds in the classroom air. CONCLUSION: A school environment with more dust, cat allergen, formaldehyde and moulds may affect the incidence of asthma and sensitivity to furry pets in schoolchildren.	Uppsala Univ, Dept Med Sci Occupat & Environm Med, Uppsala, Sweden	Smedje, G (reprint author), Univ Uppsala Hosp, Dept Occupat & Environm Med, S-75185 Uppsala, Sweden.						ABERG N, 1990, ACTA PAEDIATR SCAND, V79, P206, DOI 10.1111/j.1651-2227.1990.tb11440.x; 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, 2001, AM J RESP CRIT CARE, V163, P694; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Berge M, 1998, PEDIATR ALLERGY IMMU, V9, P25, DOI 10.1111/j.1399-3038.1998.tb00296.x; BJORNSSON E, 1995, CLIN EXP ALLERGY, V25, P423, DOI 10.1111/j.1365-2222.1995.tb01073.x; BraunFahrlander C, 1997, PEDIATR ALLERGY IMMU, V8, P75, DOI 10.1111/j.1399-3038.1997.tb00147.x; BRUNEKREEF B, 1992, INT J EPIDEMIOL, V21, P338, DOI 10.1093/ije/21.2.338; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; Custovic A, 1996, CLIN EXP ALLERGY, V26, P1246, DOI 10.1046/j.1365-2222.1996.d01-278.x; Dharmage S, 2001, AM J RESP CRIT CARE, V164, P65; DODGE R, 1993, J ALLERGY CLIN IMMUN, V92, P744, DOI 10.1016/0091-6749(93)90018-B; Dotterud LK, 1995, J EUR ACAD DERMATOL, V5, P240, DOI 10.1111/j.1468-3083.1995.tb00112.x; DYBENDAL T, 1994, ALLERGY, V49, P210, DOI 10.1111/j.1398-9995.1994.tb02651.x; GEBSKI V, 1992, SPIDA USERS MANUAL; GRAVESEN S, 1986, ALLERGY, V41, P520, DOI 10.1111/j.1398-9995.1986.tb00337.x; Janssen NAH, 1999, OCCUP ENVIRON MED, V56, P482; Jenkins MA, 1996, INT J EPIDEMIOL, V25, P609, DOI 10.1093/ije/25.3.609; KUEHR J, 1995, J ALLERGY CLIN IMMUN, V95, P655, DOI 10.1016/S0091-6749(95)70168-0; LARSSON L, 1995, THORAX, V50, P260, DOI 10.1136/thx.50.3.260; Lee SC, 1999, INDOOR AIR, V9, P134, DOI 10.1111/j.1600-0668.1999.t01-2-00008.x; MUNIR AKM, 1993, J ALLERGY CLIN IMMUN, V91, P1067, DOI 10.1016/0091-6749(93)90221-Z; Norback D, 2000, ALLERGY, V55, P163, DOI 10.1034/j.1398-9995.2000.00353.x; Ormstad H, 1998, CLIN EXP ALLERGY, V28, P702; Patchett K, 1997, J ALLERGY CLIN IMMUN, V100, P755, DOI 10.1016/S0091-6749(97)70269-0; QUACKENBOSS JJ, 1989, ENVIRON INT, V15, P169, DOI 10.1016/0160-4120(89)90023-8; Ronmark E, 1998, RESP MED, V92, P316, DOI 10.1016/S0954-6111(98)90115-9; Ronmark E, 1999, ALLERGY, V54, P926, DOI 10.1034/j.1398-9995.1999.00044.x; Rylander R, 1998, AM J RESP CRIT CARE, V158, P1685; Smedje G, 1997, CLIN EXP ALLERGY, V27, P1270, DOI 10.1111/j.1365-2222.1997.tb01171.x; Taskinen T, 1997, ACTA PAEDIATR, V86, P1181, DOI 10.1111/j.1651-2227.1997.tb14841.x; VANMOERBEKE D, 1997, BRAINE ALLEUD; Walinder R, 1999, SCAND J WORK ENV HEA, V25, P137; Wantke F, 1996, CLIN EXP ALLERGY, V26, P276	35	76	79	1	4	INT UNION AGAINST TUBERCULOSIS LUNG DISEASE (I U A T L D)	PARIS	68 BOULEVARD SAINT-MICHEL,, 75006 PARIS, FRANCE	1027-3719			INT J TUBERC LUNG D	Int. J. Tuberc. Lung Dis.	NOV	2001	5	11					1059	1066				8	Infectious Diseases; Respiratory System	Infectious Diseases; Respiratory System	489WD	WOS:000172014700012	11716342	
J	Peat, JK; Toelle, BG; Marks, GB; Mellis, CM				Peat, JK; Toelle, BG; Marks, GB; Mellis, CM			Continuing the debate about measuring asthma in population studies	THORAX			English	Article						asthma; atopy; population studies	HOUSE-DUST MITE; NEW-SOUTH-WALES; ALLERGIC DISORDERS; CHILDHOOD ASTHMA; BRONCHIAL RESPONSIVENESS; CLIMATIC REGIONS; CHILDREN; PREVALENCE; ATOPY; SENSITIZATION	The reasons for measuring atopy and airway hyperresponsiveness (AHR) and the methods of validating measurements of asthma in population studies continue to be debated. The debate has centred around standards against which to validate asthma measurements but the absence of a "gold standard" makes the criterion validation of measurements difficult. Questionnaires will always be useful but cannot be validated against a doctor diagnosis because of self-selection and recall biases. In practice, measurements should be selected on the merits of what they measure rather than being regarded as validated or non-validated alternatives. The measurement of AHR is invaluable because it is reliable, not influenced by variations in symptom perception or diagnostic trends, and is closely related to the underlying mechanisms of asthma. The value of AHR lies in its high specificity (rate of true negatives) and low sensitivity (rate of false positives) against asthma symptoms which gives additional information about symptomatic subjects. Atopy is also a useful test and, in quantifying its association with asthma, we should not place any currency on ecological evidence. Atopy is a strong risk factor for asthma in the presence of regionally specific allergens and ecological analyses that ignore these effects are diversionary rather than productive. For preventing asthma, we need to identify the group at greatest risk of developing it, measure the risk factors with precision, and develop interventions that are effective in changing environmental exposures and homogenous outcomes. This is the only approach that has the potential to lead to significant public health benefits.	Childrens Hosp, Dept Pediat & Child Hlth, Clin Epidemiol Unit, Westmead, NSW 2145, Australia; Cooperat Res Ctr Asthma, Camperdown, NSW 2050, Australia; Inst Resp Med, Camperdown, NSW 2050, Australia	Peat, JK (reprint author), Childrens Hosp, Dept Pediat & Child Hlth, Clin Epidemiol Unit, Westmead, NSW 2145, Australia.		Toelle, Brett/B-1531-2008	Toelle, Brett/0000-0002-7375-0019			ARSHAD SH, 1993, CLIN EXP ALLERGY, V23, P504, DOI 10.1111/j.1365-2222.1993.tb03238.x; Asher MI, 1998, EUR RESPIR J, V12, P315; BEASLEY R, 1997, INT TRENDS ASTHMA MO, P140; BRITTON J, 1994, EUR RESPIR J, V7, P881; Burney P, 1996, EUR RESPIR J, V9, P687; BURROWS B, 1995, J ALLERGY CLIN IMMUN, V95, P548, DOI 10.1016/S0091-6749(95)70317-9; Chan-Yeung M, 2000, ARCH PEDIAT ADOL MED, V154, P657; Duhme H, 1998, EUR RESPIR J, V11, P840, DOI 10.1183/09031936.98.11040840; Gislason D, 1999, ALLERGY, V54, P1160, DOI 10.1034/j.1398-9995.1999.00093.x; Gotzsche PC, 1998, BRIT MED J, V317, P1105; Halonen M, 1997, AM J RESP CRIT CARE, V155, P1356; Jogi R, 1998, CLIN EXP ALLERGY, V28, P1072; LUYT DK, 1993, BRIT MED J, V306, P1386; Pearce N, 2000, THORAX, V55, P424, DOI 10.1136/thorax.55.5.424; Pearce N, 2000, THORAX, V55, P352, DOI 10.1136/thorax.55.5.352; Pearce N, 1999, THORAX, V54, P268; PEAT JK, 1994, EUR RESPIR J, V7, P1805, DOI 10.1183/09031936.94.07101805; Peat JK, 1999, J ALLERGY CLIN IMMUN, V103, P1, DOI 10.1016/S0091-6749(99)70517-8; PEAT JK, 1993, CLIN EXP ALLERGY, V23, P812, DOI 10.1111/j.1365-2222.1993.tb00258.x; Peat JK, 1996, AM J RESP CRIT CARE, V153, P141; PEAT JK, 1995, MED J AUSTRALIA, V163, P22; Peat JK, 2000, J ALLERGY CLIN IMMUN, V106, pS144, DOI 10.1067/mai.2000.109420; PEAT JK, 1991, AM REV RESPIR DIS, V144, P338; Pekkanen J, 1999, EUR RESPIR J, V14, P951, DOI 10.1034/j.1399-3003.1999.14d37.x; RONA RJ, 1995, THORAX, V50, P992, DOI 10.1136/thx.50.9.992; SEARS MR, 1989, CLIN EXP ALLERGY, V19, P419, DOI 10.1111/j.1365-2222.1989.tb02408.x; TOELLE BG, 1992, AM REV RESPIR DIS, V146, P633; TOELLE BG, 2000, RESPIROLOGY, V5, pA6; VONMUTIUS E, 1992, BRIT MED J, V305, P1395	29	76	77	1	1	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	MAY	2001	56	5					406	411		10.1136/thorax.56.5.406		6	Respiratory System	Respiratory System	427LN	WOS:000168405800016	11312411	
J	Katelaris, CH; Carrozzi, FM; Burke, TV; Byth, K				Katelaris, CH; Carrozzi, FM; Burke, TV; Byth, K			A springtime Olympics demands special consideration for allergic athletes	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						pollen counts; athletes; allergic rhinoconjunctivitis; olympics; paralympics; asthma	QUALITY-OF-LIFE; HAY-FEVER; QUESTIONNAIRE; ASTHMA	Background: The Sydney Olympic and Paralympic Games will be held in September-October 2000, which is early to midspring in the southern hemisphere. Pollen-sensitive athletes may encounter problems with allergic symptoms triggered by pollen exposure, thus compromising their ability to attain peak performance. Objective: We sought to monitor pollen levels at the major Olympic venues to provide information for allergic athletes and their team doctors in order to adequately prepare them for Olympic competition. Methods: We performed aerobiologic monitoring of the major Olympic venues to provide a profile of the most prevalent pollen species appearing during the spring. In the second part of this study, we surveyed a population of elite Australian athletes from Olympic sports to ascertain the prevalence of allergic rhinoconjunctivitis, to investigate the major allergens involved in sensitization, and to conduct a pilot study to assess the effect of allergic rhinoconjunctivitis on quality of life. Results: The pollen counts obtained at the 3 major sites were high over the period of Olympic competition. Tree pollens appeared from July, and grasses appeared from early September and peaked in the second week of October, the beginning of Paralympic competition. A relatively small number of pollen varieties comprise the majority of the total pollen count. Two hundred fourteen athletes (61% male; mean age, 21 +/- 16 years) representing 12 Olympic sports participated in the study. Fifty-six percent gave a symptom history consistent with allergic rhinoconjunctivitis, 41% had symptoms of allergic rhinoconjunctivitis and a positive test response to any one allergen, and 29% had seasonal allergic rhinoconjunctivitis (a positive history and at least one positive skin prick test response to a seasonal allergen). Athletes from aquatic sports were more likely to have symptoms than those from other sports, Symptom scores were higher and quality of life ratings were poorer in allergic compared with nonallergic athletes over the spring period, Conclusion: Olympic team managers and medical officers need to adequately prepare Olympic athletes for the possibility of exposure to high pollen levels in the weeks leading up to this most important sporting event. Symptoms of pollen sensitivity, such as rhinoconjunctivitis and exacerbation of asthma, could be devastating to athletes expecting peak performance, Potential Olympic athletes should be screened for the possibility of pollen allergy and have medical programs with permitted medication tailored to meet their needs. This may involve preventative therapy with meditation, such as intranasal corticosteroid sprays or immunotherapy programs, if symptoms are particularly severe. The newer nonsedating antihistamines are the treatment of choice fur acute intermittent symptoms, Appropriate management will ensure that the allergic athlete will safely perform to maximum ability with permitted medication during the Spring 2000 Olympic Games in Sydney.	Westmead Hosp, ICPMR, Dept Clin Immunol & Allergy, Sydney, NSW 2145, Australia; Westmead Hosp, Westmead Millennium Inst, Sydney, NSW 2145, Australia	Katelaris, CH (reprint author), Westmead Hosp, ICPMR, Dept Clin Immunol & Allergy, Sydney, NSW 2145, Australia.						BOUSQUET J, 1994, J ALLERGY CLIN IMMUN, V94, P182, DOI 10.1016/0091-6749(94)90038-8; Carrozzi FM, 1998, ASIAN PAC J ALLERGY, V16, P149; CONNELL JT, 1969, J ALLERGY, V43, P33, DOI 10.1016/0021-8707(69)90018-5; DAVIES R R, 1973, Clinical Allergy, V3, P263, DOI 10.1111/j.1365-2222.1973.tb01332.x; FITCH KD, 1984, J ALLERGY CLIN IMMUN, V73, P722, DOI 10.1016/0091-6749(84)90314-2; HELBLING A, 1990, SCHWEIZ MED WSCHR, V120, P231; Helenius IJ, 1998, J ALLERGY CLIN IMMUN, V101, P646; HOPPER JL, 1995, AUST J PUBLIC HEALTH, V19, P120; JUNIPER EF, 1994, J ALLERGY CLIN IMMUN, V93, P413, DOI 10.1016/0091-6749(94)90349-2; TAUDORF E, 1988, INT ARCH ALLER A IMM, V86, P225; ZEGER SL, 1986, BIOMETRICS, V42, P121, DOI 10.2307/2531248; 1994, ALLERGY S19, V49, P5	12	76	77	1	5	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	AUG	2000	106	2					260	266				7	Allergy; Immunology	Allergy; Immunology	343NH	WOS:000088708100007	10932068	
J	Dambuza, IM; Brown, GD				Dambuza, Ivy M.; Brown, Gordon D.			C-type lectins in immunity: recent developments	CURRENT OPINION IN IMMUNOLOGY			English	Review							HOUSE-DUST MITE; DENDRITIC CELL-RECEPTOR; FUNGAL BETA-GLUCANS; CANDIDA-ALBICANS; HOST-DEFENSE; AIRWAY INFLAMMATION; ANTIFUNGAL IMMUNITY; INNATE IMMUNITY; DAMAGED CELLS; CORD FACTOR	C-type lectin receptors (CLRs) comprise a large superfamily of proteins, which recognise a diverse range of ligands, and are defined by the presence of at least one C-type lectin-like domain (CTLD). Of particular interest are the single extracellular CTLD-containing receptors of the 'Dectin-1' and 'Dectin-2' clusters, which associate with signalling adaptors or possess integral intracellular signalling domains. These CLRs have traditionally been associated with the recognition of fungi, but recent discoveries have revealed diverse and unexpected functions. In this review, we describe their newly identified roles in anti-microbial host defence, homeostasis, autoimmunity, allergy and their functions in the recognition and response to dead and cancerous cells.	[Dambuza, Ivy M.; Brown, Gordon D.] Univ Aberdeen, Inst Med Sci, Div Appl Med, Aberdeen Fungal Grp,Immun Infect & Inflammat Prog, Aberdeen AB25 2ZD, Scotland	Brown, GD (reprint author), Univ Aberdeen, Inst Med Sci, Div Appl Med, Aberdeen Fungal Grp,Immun Infect & Inflammat Prog, Aberdeen AB25 2ZD, Scotland.	gordon.brown@abdn.ac.uk			Wellcome Trust [102705]; Wellcome Trust Strategic Award in Medical Mycology and Fungal Immunology [97377]	We thank the Wellcome Trust (Grant No. 102705) and Wellcome Trust Strategic Award in Medical Mycology and Fungal Immunology (Grant No. 97377) for funding. We apologise to our many colleagues whose recent work we were unable to cite due to space constraints.	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J	Macy, E; Contreras, R				Macy, Eric; Contreras, Richard			Health care use and serious infection prevalence associated with penicillin "allergy" in hospitalized patients: A cohort study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Adverse drug reaction; antibiotics; Clostridium difficile; electronic medical record; hospital use; methicillin-resistant Staphylococcus aureus; multiple drug intolerance syndrome; penicillin allergy; prevalence; vancomycin-resistant Enterococcus species	GROUP-B STREPTOCOCCUS; CLOSTRIDIUM-DIFFICILE; ANTIMICROBIAL STEWARDSHIP; PREGNANT-WOMEN; VANCOMYCIN USE; HISTORY; MANAGEMENT; ANTIBIOTICS; COSTS	Background: Penicillin is the most common drug "allergy" noted at hospital admission, although it is often inaccurate. Objective: We sought to determine total hospital days, antibiotic exposures, and the prevalence rates of Clostridium difficile, methicillin-resistant Staphylococcus aureus (MRSA), and vancomycin-resistant Enterococcus (VRE) in patients with and without penicillin "allergy" at hospital admission. Methods: We performed a retrospective, matched cohort study of subjects admitted to Kaiser Foundation hospitals in Southern California during 2010 through 2012. Results: It was possible to match 51,582 (99.6% of all possible cases) unique hospitalized subjects with penicillin "allergy" to 2 unique discharge diagnosis category-matched, sex-matched, age-matched, and date of admission-matched control subjects each. Cases with penicillin "allergy" averaged 0.59 (9.9%; 95% CI, 0.47-0.71) more total hospital days during 20.1 +/- 10.5 months of follow-up compared with control subjects. Cases were treated with significantly more fluoroquinolones, clindamycin, and vancomycin (P < .0001) for each antibiotic compared with control subjects. Cases had 23.4% (95% CI, 15.6% to 31.7%) more C difficile, 14.1% (95% CI, 7.1% to 21.6%) more MRSA, and 30.1% (95% CI, 12.5% to 50.4%) more VRE infections than expected compared with control subjects. Conclusions: A penicillin "allergy" history, although often inaccurate, is not a benign finding at hospital admission. Subjects with a penicillin "allergy" history spend significantly more time in the hospital. Subjects with a penicillin "allergy" history are exposed to significantly more antibiotics previously associated with C difficile and VRE. Drug "allergies" in general, but most those notably to penicillin, are associated with increased hospital use and increased C difficile, MRSA, and VRE prevalence.	[Macy, Eric] So Calif Permanente Med Grp, Dept Allergy, San Diego Med Ctr, San Diego, CA 92120 USA; [Contreras, Richard] Kaiser Permanente Hlth Care Program, Dept Res & Evaluat, Pasadena, CA USA	Macy, E (reprint author), Kaiser Permanente, Dept Allergy, 7060 Clairemont Mesa Blvd, San Diego, CA 92111 USA.	eric.m.macy@kp.org			Kaiser Permanente Health Care Program; ALK-Abello	Supported by the Kaiser Permanente Health Care Program and ALK-Abello.	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Allergy Clin. Immunol.	MAR	2014	133	3					790	796		10.1016/j.jaci.2013.09.021		7	Allergy; Immunology	Allergy; Immunology	AC3EK	WOS:000332397600022	24188976	
J	Reponen, T; Lockey, J; Bernstein, DI; Vesper, SJ; Levin, L; Hershey, GKK; Zheng, S; Ryan, P; Grinshpun, SA; Villareal, M; LeMasters, G				Reponen, Tiina; Lockey, James; Bernstein, David I.; Vesper, Stephen J.; Levin, Linda; Hershey, Gurjit K. Khurana; Zheng, Shu; Ryan, Patrick; Grinshpun, Sergey A.; Villareal, Manuel; LeMasters, Grace			Infant origins of childhood asthma associated with specific molds	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Asthma; molds; speciation; infants; Environmental Relative Moldiness Index	QUANTITATIVE PCR ANALYSIS; RELATIVE MOLDINESS INDEX; 1ST YEAR; ALTERNARIA-ALTERNATA; HOUSE-DUST; US HOMES; CHILDREN; COHORT; SYMPTOMS; EXPOSURE	Background: The specific cause or causes of asthma development must be identified to prevent this disease. Objective: Our hypothesis was that specific mold exposures are associated with childhood asthma development. Methods: Infants were identified from birth certificates. Dust samples were collected from 289 homes when the infants were 8 months of age. Samples were analyzed for concentrations of 36 molds that comprise the Environmental Relative Moldiness Index (ERMI) and endotoxin, house dust mite, cat, dog, and cockroach allergens. Children were evaluated at age 7 years for asthma based on reported symptoms and objective measures of lung function. Host, environmental exposure, and home characteristics evaluated included a history of parental asthma, race, sex, upper and lower respiratory tract symptoms, season of birth, family income, cigarette smoke exposure, air conditioning, use of a dehumidifier, presence of carpeting, age of home, and visible mold at age 1 year and child's positive skin prick test response to aeroallergens and molds at age 7 years. Results: Asthma was diagnosed in 24% of the children at age 7 years. A statistically significant increase in asthma risk at age 7 years was associated with high ERMI values in the child's home in infancy (adjusted relative risk for a 10-unit increase in ERMI value, 1.8; 95% CI, 1.5-2.2). The summation of levels of 3 mold species, Aspergillus ochraceus, Aspergillus unguis, and Penicillium variabile, was significantly associated with asthma (adjusted relative risk, 2.2; 95% CI, 1.8-2.7). Conclusion: In this birth cohort study exposure during infancy to 3 mold species common to water-damaged buildings was associated with childhood asthma at age 7 years. (J Allergy Clin Immunol 2012;130:639-44.)	[Reponen, Tiina; Lockey, James; Levin, Linda; Zheng, Shu; Ryan, Patrick; Grinshpun, Sergey A.; LeMasters, Grace] Univ Cincinnati, Dept Environm Hlth, Cincinnati, OH 45267 USA; [Lockey, James; Bernstein, David I.; Villareal, Manuel] Univ Cincinnati, Dept Internal Med, Cincinnati, OH 45267 USA; [Vesper, Stephen J.] US EPA, Cincinnati, OH 45268 USA; [Hershey, Gurjit K. Khurana; Ryan, Patrick] Cincinnati Childrens Hosp, Ctr Med, Cincinnati, OH USA	Reponen, T (reprint author), Univ Cincinnati, Dept Environm Hlth, POB 670056, Cincinnati, OH 45267 USA.	Tiina.Reponen@uc.edu	Ryan, Patrick /L-7062-2015; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Khurana Hershey, Gurjit/0000-0001-6663-977X	US Department of Housing and Urban Development [OHLHH0226-10]; National Institute of Environmental Health Sciences (NIEHS) [RO1 ES11170]; US Environmental Protection Agency (EPA) through its Office of Research and Development; US Housing and Urban Development; Mycometrics; EMSL; TestAmerica; Forensics Analytical; Roche; Aemtek; Microbial Insight; National Institute of Environmental Health Sciences	Supported in part by US Department of Housing and Urban Development grant no. OHLHH0226-10 and National Institute of Environmental Health Sciences (NIEHS) grant no. RO1 ES11170 awarded to the University of Cincinnati. The US Environmental Protection Agency (EPA), through its Office of Research and Development, partially funded and collaborated in the research described here. It has been subjected to the Agency's peer review and has been approved as an EPA publication. Mention of trade names or commercial products does not constitute endorsement or recommendation by the EPA for use. Commercial use of the Environmental Relative Moldiness Index technology can provide royalties to the EPA.; T. Reponen has received research support from US Housing and Urban Development. J. Lockey and G. LeMasters are involved in the Diesel, Allergens and Gene Interaction and Child Atopy study. S. J. Vesper has received royalties from Mycometrics, EMSL, TestAmerica, Forensics Analytical, Roche, Aemtek, and Microbial Insight. P. Ryan has received research support from the National Institute of Environmental Health Sciences. The rest of the authors declare that they have no relevant conflicts of interest.	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J	Hackett, TL; Singhera, GK; Shaheen, F; Hayden, P; Jackson, GR; Hegele, RG; Van Eeden, S; Bai, TR; Dorscheid, DR; Knight, DA				Hackett, Tillie-Louise; Singhera, Gurpreet K.; Shaheen, Furquan; Hayden, Patrick; Jackson, George R.; Hegele, Richard G.; Van Eeden, Stephan; Bai, Tony R.; Dorscheid, Delbert R.; Knight, Darryl A.			Intrinsic Phenotypic Differences of Asthmatic Epithelium and Its Inflammatory Responses to Respiratory Syncytial Virus and Air Pollution	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article						airway epithelium; asthma; inflammation and repair; RSV; particulate matter	EPIDERMAL-GROWTH-FACTOR; ACTIVATED PROTEIN-KINASES; FINE PARTICULATE MATTER; BRONCHIAL EPITHELIUM; CYTOKINE PRODUCTION; FACTOR RECEPTOR; ALVEOLAR MACROPHAGES; DYSREGULATED REPAIR; SIGNAL TRANSDUCER; MAPK ACTIVATION	A substantial proportion of healthcare cost associated with asthma is attributable to exacerbations of the disease. Within the airway, the epithelium forms the mucosal immune barrier, the first structural cell defense against common environmental insults such as respiratory syncytial virus (RSV) and particulate matter. We sought to characterize the phenotype of differentiated asthmatic-derived airway epithelial cultures and their intrinsic inflammatory responses to environmental challenges. Air-liquid interface (ALI) cultures were generated from asthmatic (n = 6) and nonasthmatic (n = 6) airway epithelial cells. Airway tissue and ALI cultures were analyzed by immunohistochemistry for cytokeratin-5, E-cadherin, Ki67, Muc5AC, NF-kappa B, the activation of p38, and apoptosis. ALI cultures were exposed to RSV (4 x 10(6) plaque forming unit/ml), particulate matter collected by Environmental Health Canada (EHC-93, 100 mu g/ml), or mechanically wounded for 24, 48, and 96 hours and basolateral supernatants analyzed for inflammatory cytokines, using Luminex and ELISA. The airway epithelium in airway sections of patients with asthma as well as in vitro ALI cultures demonstrated a less differentiated epithelium, characterized by elevated numbers of basal cells marked by the expression of cytokeratin-5, increased phosphorylation of p38 mitogen-activated protein kinase, and less adherens junction protein E-cadherin. Transepithelial resistance was not different between asthmatic and nonasthmatic cultures. In response to infection with RSV, exposure to EHC-93, or mechanical wounding, asthmatic ALI cultures released greater concentrations of IL-6, IL-8, and granulocyte macrophage colony-stimulating factor, compared with nonasthmatic cultures (P < 0.05). This parallel ex vivo and in vitro study of the asthmatic epithelium demonstrates an intrinsically altered phenotype and aberrant inflammatory response to common environmental challenges, compared with nonasthmatic epithelium.	[Hackett, Tillie-Louise; Singhera, Gurpreet K.; Shaheen, Furquan; Van Eeden, Stephan; Bai, Tony R.; Dorscheid, Delbert R.; Knight, Darryl A.] Univ British Columbia, James Hogg Res Ctr, St Pauls Hosp, Vancouver, BC V6Z 1Y6, Canada; [Hackett, Tillie-Louise; Knight, Darryl A.] Univ British Columbia, Dept Anesthesiol Pharmacol & Therapeut, Vancouver, BC V6Z 1Y6, Canada; [Bai, Tony R.; Dorscheid, Delbert R.] Univ British Columbia, Div Resp, Vancouver, BC V6Z 1Y6, Canada; [Bai, Tony R.; Dorscheid, Delbert R.] Univ British Columbia, Div Crit Care Med, Dept Med, Vancouver, BC V6Z 1Y6, Canada; [Hayden, Patrick; Jackson, George R.] MatTek Corp, Ashland, MA USA; [Hegele, Richard G.] Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON, Canada	Hackett, TL (reprint author), Univ British Columbia, James Hogg Res Ctr, St Pauls Hosp, 1081 Burrard St,Room 165, Vancouver, BC V6Z 1Y6, Canada.	Tillie.Hackett@hli.ubc.ca			Allergen-National Centre for Excellence/Canadian Institutes for Health Research [79632]; CIHR/Canadian Lung Association/GlaxoSmithKline; Michael Smith Foundation for Health Research	This work was supported by Allergen-National Centre for Excellence/Canadian Institutes for Health Research grant 79632. T.-L. H. is a recipient of a CIHR/Canadian Lung Association/GlaxoSmithKline, Integrated and Mentored Pulmonary and Cardiovascular Training strategic training, and a Michael Smith Foundation for Health Research postdoctoral fellowship. D. A. K. is a Canada Research Chair in Airway Disease and Michael Smith Foundation for Health Research Career Investigator. D. R. D. is a CIHR New Investigator and Michael Smith Foundation for Health Research Career Investigator. S. V. E. is a senior scholar with the Michael Smith Foundation for Health Research and a CIHR/GSK Professor in Chronic Obstructive Pulmonary Disease.	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J	Mackie, A; Macierzanka, A				Mackie, Alan; Macierzanka, Adam			Colloidal aspects of protein digestion	CURRENT OPINION IN COLLOID & INTERFACE SCIENCE			English	Review						Interface; Protein; Digestion; Biosurfactant; Enzyme; Emulsion	IN-VITRO DIGESTIBILITY; SIMULATED GASTROINTESTINAL PROTEOLYSIS; INTRAGASTRIC ACID STABILITY; AIR-WATER-INTERFACE; BETA-LACTOGLOBULIN; FOOD ALLERGENS; ENZYMATIC-HYDROLYSIS; PANCREATIC LIPASE; EMULSIFIER TYPE; BILE-ACIDS	The increase in food related health issues has sparked an interest in research on the digestion processes of the gastrointestinal tract. Because of the difficulty and expense of undertaking human trials or even animal experiments, much of the current research uses in vitro models that simulate various aspects of digestion. The results of this research indicate that the rate and extent of protein digestion is governed by accessibility of the cleavage sites to enzymes and local flexibility of the substrate molecule. However, results have also shown that digestion of an allergenic protein to small fragments does not necessarily mean that it will no longer be immunologically active. Other factors are also important. For example, adsorption to an interface increased rates of digestion as did the presence of bile acids. In fact, interaction with a range of physiological surfactants has been shown to be extremely important in protein digestion. When protein is adsorbed to an emulsified food it can be displaced by the surfactants in either the stomach or the small intestine. Lipid interaction with the protein in solution has been demonstrated to be important in effecting rates of proteolysis and phospholipids in particular have provided a protective effect for some milk proteins. Conversely the presence of specific proteins has been shown to affect rates of lipid digestion. The number of such colloidal interactions that we now know may play a role in protein digestion highlights the importance of this area to understanding how we can produce food that optimises nutrition for the consumer. (C) 2009 Elsevier Ltd. All rights reserved.	[Mackie, Alan; Macierzanka, Adam] Inst Food Res, Norwich NR4 7UA, Norfolk, England	Mackie, A (reprint author), Inst Food Res, Norwich Res Pk, Norwich NR4 7UA, Norfolk, England.	alan.mackie@bbsrc.ac.uk	Mackie, Alan/B-3753-2015	Mackie, Alan/0000-0002-5681-0593	BBSRC	The authors would like to acknowledge funding of this work by the BBSRC through an Institute Strategic Programme grant.	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Opin. Colloid Interface Sci.	APR	2010	15	1-2					102	108		10.1016/j.cocis.2009.11.005		7	Chemistry, Physical	Chemistry	567WF	WOS:000275477400016		
J	Shore, SA				Shore, Stephanie A.			Obesity, airway hyperresponsiveness, and inflammation	JOURNAL OF APPLIED PHYSIOLOGY			English	Review						mice; leptin; adiponectin; tumor necrosis factor-alpha; adipokines	BODY-MASS INDEX; ADIPOSE-TISSUE HYPOXIA; NECROSIS-FACTOR-ALPHA; DIET-INDUCED OBESITY; EXERCISE-INDUCED BRONCHOSPASM; INDUCED INSULIN-RESISTANCE; ACUTE OZONE EXPOSURE; MURINE ASTHMA MODEL; HIGH-FAT DIET; PULMONARY-FUNCTION	Shore SA. Obesity, airway hyperresponsiveness, and inflammation. J Appl Physiol 108: 735-743, 2010. First published October 29, 2009; doi: 10.1152/japplphysiol.00749.2009.-Epidemiological data indicate that obesity is a risk factor for asthma, but the mechanistic basis for this relationship is not established. Here we review data from human subjects and animal models investigating the relationship between obesity and airway hyperresponsiveness, a characteristic feature of asthma. We discuss obesity as a state of chronic systemic inflammation resulting from interactions between adipocytes and adipose tissue macrophages that are recruited to obese adipose tissue. Finally, we focus on the possibility that aspects of this inflammation, particularly obesity-related changes in TNF-alpha, leptin, and adiponectin, may contribute to airway hyperresponsiveness in obesity. Determining how obesity promotes asthma may uncover novel therapeutic strategies that are effective in the obese asthmatic subject.	Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA	Shore, SA (reprint author), Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, 665 Huntington Ave, Boston, MA 02115 USA.	sshore@hsph.harvard.edu			National Institute of Environmental Health Sciences [ES-013307, ES-000002]; National Heart, Lung, and Blood Institute [HL-084044]	This work was supported by National Institute of Environmental Health Sciences Grants ES-013307 and ES-000002 and National Heart, Lung, and Blood Institute Grant HL-084044.	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Appl. Physiol.	MAR	2010	108	3					735	743		10.1152/japplphysiol.00749.2009		9	Physiology; Sport Sciences	Physiology; Sport Sciences	570JK	WOS:000275670400039	19875711	
J	Allen, RW; Davies, H; Cohen, MA; Mallach, G; Kaufman, JD; Adar, SD				Allen, Ryan W.; Davies, Hugh; Cohen, Martin A.; Mallach, Gary; Kaufman, Joel D.; Adar, Sara D.			The spatial relationship between traffic-generated air pollution and noise in 2 US cities	ENVIRONMENTAL RESEARCH			English	Article						Air pollution; Noise; Traffic; Confounding; Cardiovascular	AMBIENT NITROGEN-DIOXIDE; MAJOR HIGHWAY; MYOCARDIAL-INFARCTION; ULTRAFINE PARTICLES; HEART-DISEASE; LOS-ANGELES; EXPOSURE; ASTHMA; MORTALITY; ASSOCIATION	Traffic-gene rated air pollution and noise have both been linked to cardiovascular morbidity. Since traffic is a shared source, there is potential for correlated exposures that may lead to confounding in epidemiologic studies. As part of the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air), 2-week NO and NO(2) concentrations were measured at up to 105 locations, selected primarily to characterize gradients near major roads, in each of 9 US communities. We measured 5-min A-weighted equivalent continuous sound pressure levels (L(eq)) and ultrafine particle (UFP) counts at a subset of these NO/NO(2) monitoring locations in Chicago, IL (N = 69 in December 2006; N = 36 in April 2007) and Riverside County, CA (N = 46 in April 2007). L(eq) and UFP were measured during non-"rush hour" periods (10:00-16:00) to maximize comparability between measurements. We evaluated roadway proximity exposure surrogates in relation to the measured levels, estimated noise-air pollution correlation coefficients, and evaluated the impact of regional-scale pollution gradients, wind direction, and roadway proximity on the correlations. Five-minute L(eq) measurements in December 2006 and April 2007 were highly correlated (r = 0.84), and measurements made at different times of day were similar (coefficients of variation: 0.5-13%), indicating that 5-min measurements are representative of long-term L(eq), Binary and continuous roadway proximity metrics characterized L(eq) as well or better than NO or NO(2). We found strong regional-scale gradients in NO and NO(2), particularly in Chicago, but only weak regional-scale gradients in L(eq) and UFP. L(eq) was most consistently correlated with NO, but the correlations were moderate (0.20-0.60). After removing the influence of regional-scale gradients the correlations generally increased (L(eq)-NO: r = 0.49-0.62), and correlations downwind of major roads (L(eq)-NO: r = 0.53-0.74) were consistently higher than those upwind (0.35-0.65). There was not a consistent effect of roadway proximity on the correlations. In conclusion, roadway proximity variables are not unique exposure surrogates in studies of endpoints hypothesized to be related to both air pollution and noise. Moderate correlations between traffic-generated air pollution and noise suggest the possibility of confounding, which might be minimized by considering regional pollution gradients and/or prevailing wind direction(s) in epidemiologic studies. (C) 2009 Elsevier Inc. All rights reserved.	[Allen, Ryan W.; Mallach, Gary] Simon Fraser Univ, Fac Hlth Sci, Burnaby, BC V5A 1S6, Canada; [Davies, Hugh] Univ British Columbia, Sch Environm Hlth, Vancouver, BC V5Z 1M9, Canada; [Cohen, Martin A.; Kaufman, Joel D.] Univ Washington, Dept Environm & Occupat Hlth Sci, Seattle, WA 98195 USA; [Kaufman, Joel D.; Adar, Sara D.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA	Allen, RW (reprint author), Simon Fraser Univ, Fac Hlth Sci, 8888 Univ Dr, Burnaby, BC V5A 1S6, Canada.	allenr@sfu.ca	Kaufman, Joel/B-5761-2008; Adar, Sara/L-2278-2016	Kaufman, Joel/0000-0003-4174-9037; Adar, Sara/0000-0001-8383-485X	Simon Fraser University President's Research; US Environmental Protection Agency [R831697]; National Institute of Environmental Health Sciences [K24ES013195]	Funding Sources: Funding for this work was provided by the Simon Fraser University President's Research Grant and the US Environmental Protection Agency (Grant R831697). Joel Kaufman was supported by the National Institute of Environmental Health Sciences through grant K24ES013195.	Adar SD, 2007, INHAL TOXICOL, V19, P135, DOI 10.1080/08958370701496012; Ainslie B, 2008, ATMOS ENVIRON, V42, P2394, DOI 10.1016/j.atmosenv.2007.12.021; Alberola J, 2005, APPL ACOUST, V66, P1180, DOI 10.1016/j.apacoust.2005.03.001; ALLEN R, 2009, EPIDEMIOLOG IN PRESS, DOI DOI 10.1097/EDE.0B013E31819644CC; Babisch W, 2002, NOISE HEALTH, V4, P1; Babisch WF, 2005, EPIDEMIOLOGY, V16, P33, DOI 10.1097/01.ede.0000147104.84424.24; Babisch Wolfgang, 2006, Noise Health, V8, P1; Beckerman B, 2008, ATMOS ENVIRON, V42, P275, DOI 10.1016/j.atmosenv.2007.09.042; Beelen R, 2009, OCCUP ENVIRON MED, V66, P243, DOI 10.1136/oem.2008.042358; Bluhm GL, 2007, OCCUP ENVIRON MED, V64, P122, DOI 10.1136/oem.2005.025866; Brauer M, 2007, EUR RESPIR J, V29, P879, DOI 10.1183/09031936.00083406; Calixto A, 2003, CITIES, V20, P23, DOI 10.1016/S0264-2751(02)00093-8; Chen E, 2008, ENVIRON HEALTH PERSP, V116, P970, DOI 10.1289/ehp.11076; Clougherty JE, 2007, ENVIRON HEALTH PERSP, V115, P1140, DOI 10.1289/ehp.9863; DAVIES HW, 2009, OCCUPATIONA IN PRESS, DOI DOI 10.1136/OEM.2008.041764; de Kluizenaar Y, 2007, J OCCUP ENVIRON MED, V49, P484, DOI 10.1097/JOM.0013618058a9ff; Dominici F, 2008, EPIDEMIOLOGY, V19, P558, DOI 10.1097/EDE.0b013e31817307dc; Finkelstein MM, 2004, AM J EPIDEMIOL, V160, P173, DOI 10.1093/aje/kwh181; Gauderman WJ, 2005, EPIDEMIOLOGY, V16, P737, DOI 10.1097/01.ede.00001813087.51440.75; Gilbert NL, 2007, ATMOS ENVIRON, V41, P2670, DOI 10.1016/j.atmosenv.2006.12.007; Gilbert NL, 2003, SCI TOTAL ENVIRON, V312, P43, DOI 10.1016/S0048-9697(03)00228-6; Gordian ME, 2006, J EXPO SCI ENV EPID, V16, P49, DOI 10.1038/sj.jea.7500436; Hoek G, 2002, LANCET, V360, P1203, DOI 10.1016/S0140-6736(02)11280-3; Hoffmann B, 2007, CIRCULATION, V116, P489, DOI 10.1161/CIRCULATIONAHA.107.693622; Hoffmann B, 2006, EUR HEART J, V27, P2696, DOI 10.1093/eurheartj/ehl278; HOTHERSALL DC, 1987, J SOUND VIB, V115, P459, DOI 10.1016/0022-460X(87)90290-2; ISING H, 2004, NOISE HLTH, V6, P23; 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; Klaeboe R, 2000, ATMOS ENVIRON, V34, P4727; Kunzli N, 2005, ENVIRON HEALTH PERSP, V113, P201, DOI 10.1289/ehp.7523; MacLehose RF, 2007, EPIDEMIOLOGY, V18, P199, DOI 10.1097/01.ede.0000256320.30737.c0; Maheswaran R, 2003, STROKE, V34, P2776, DOI 10.1161/01.STR.0000101750.77547.11; Maschke C, 2000, INT J HYG ENVIR HEAL, V203, P45, DOI 10.1078/S1438-4639(04)70007-3; Pleijel H, 2004, SCI TOTAL ENVIRON, V332, P261, DOI 10.1016/j.scitotenv.2004.03.020; Roorda-Knape MC, 1998, ATMOS ENVIRON, V32, P1921, DOI 10.1016/S1352-2310(97)00496-2; Schwela D, 2005, Noise Health, V7, P41; SELANDER J, 2009, EPIDEMIOLOG IN PRESS, DOI DOI 10.1097/EDE.0B013E31819463BD; Su JG, 2008, SCI TOTAL ENVIRON, V390, P520, DOI 10.1016/j.scitotenv.2007.10.032; Thomas DC, 2007, EPIDEMIOLOGY, V18, P186, DOI 10.1097/01.ede.0000254682.47697.70; Tobias A, 2001, EUR J EPIDEMIOL, V17, P765, DOI 10.1023/A:1015663013620; Tonne C, 2007, ENVIRON HEALTH PERSP, V115, P53, DOI 10.1289/ehp.9587; van Kempen EEMM, 2002, ENVIRON HEALTH PERSP, V110, P307; Zhu YF, 2006, ENVIRON SCI TECHNOL, V40, P2531, DOI 10.1021/es0516514; Zhu YF, 2006, AEROSOL SCI TECH, V40, P422, DOI 10.1080/02786820600643321; Zhu YF, 2002, J AIR WASTE MANAGE, V52, P1032	46	75	75	1	35	ACADEMIC PRESS INC ELSEVIER SCIENCE	SAN DIEGO	525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA	0013-9351			ENVIRON RES	Environ. Res.	APR	2009	109	3					334	342		10.1016/j.envres.2008.12.006		9	Environmental Sciences; Public, Environmental & Occupational Health	Environmental Sciences & Ecology; Public, Environmental & Occupational Health	426JT	WOS:000264704800018	19193368	
J	Jyrkka, J; Enlund, H; Korhonen, MJ; Sulkava, R; Hartikainen, S				Jyrkka, Johanna; Enlund, Hannes; Korhonen, Maarit J.; Sulkava, Raimo; Hartikainen, Sirpa			Patterns of Drug Use and Factors Associated with Polypharmacy and Excessive Polypharmacy in Elderly Persons Results of the Kuopio 75+Study: A Cross-Sectional Analysis	DRUGS & AGING			English	Article							HEALTH-CARE UTILIZATION; MEDICATION USE; OLDER-PEOPLE; MANAGED CARE; RISK-FACTORS; PRESCRIPTION; EVENTS; HOME; POPULATION; PHYSICIANS	Background: Although the increasing use of drugs in elderly persons has raised many concerns in recent years, the process leading to polypharmacy (PP) and excessive polypharmacy (EPP) remains largely unknown. Objective: To describe the number and type of drugs used and to evaluate the role of different factors associated with PP (i.e. 6-9 drugs) and EPP (i.e. >= 10 drugs), with special reference to the number and type of medical diagnoses and symptoms, in a population of home-dwelling elderly persons aged >= 75 years. Methods: The study was a cross-sectional analysis of a population-based cohort in 1998. The population consisted of home-dwelling elderly persons aged >= 75 years in the city of Kuopio, Finland. The data for the analysis were obtained from the Kuopio 75+ Study, which drew a random sample of 700 elderly residents aged >= 75 years living in the city of Kuopio from the population register. Of these, 601 attended a structured clinical examination and an interview carried out by a geriatrician and a trained nurse in 1998. For this analysis, all home-dwelling elderly participants (n=523) were included. Study data were expressed as proportions and means with standard deviations. The factors associated with PP and EPP were examined by multinomial logistic regression. Results: The most commonly used drugs were cardiovascular drugs (97% in EPP, 94% in PP and 59% in non-PP group) and analgesics (89%, 76% and 54%), respectively. Use of psychotropics was markedly higher in the EPP group (77%) than in the PP (42%) and non-PP groups (20%). The mean number of drugs per diagnosis was 3.6 in the EPP group, 2.6 in the PP group and 1.6 in the non-PP group. Factors associated only with EPP were moderate self-reported health (odds ratio [OR] 2.05; 95% CI 1.08, 3.89), female gender (OR 2.43; 95% CI 1.27, 4.65) and age >= 85 years (OR 2.84; 95% CI 1.41, 5.72). Factors that were associated with both PP and EPP included poor self-reported health (PP: OR 2.15; 95% CI 1.01, 4.59 and EPP: OR 6.02; 95% CI 2.55, 14.20), diabetes mellitus (PP: OR 2.28; 95% CI 1.26, 4.15 and EPP: OR 2.07; 95% CI 1.03, 4.18), depression (PP: OR 2.13; 95% CI 1.16, 3.90 and EPP: OR 2.93; 95% CI 1.51, 5.66), pain (PP: OR 2.69; 95% CI 1.68, 4.30 and EPP: OR 2.74; 95% CI 1.56, 4.82), heart disease (PP: OR 2.51; 95% CI 1.54, 4.08 and EPP: OR 4.63; 95% CI 2.45, 8.74) and obstructive pulmonary disease (including asthma or chronic obstructive pulmonary disease) [PP: OR 2.79; 95% CI 1.24, 6.25 and EPP: OR 6.82; 95% CI 2.87, 16.20]. Conclusions: The study indicates that the factors associated with PP and EPP are not uniform. Age >= 85 years, female gender and moderate self-reported health were factors associated only with EPP, while poor self-reported health and several specific disease states were associated with both PP and EPP. The high number of drugs per diagnosis observed in this study calls for a thorough assessment of the need for and outcomes associated with use of these drugs.	[Jyrkka, Johanna; Korhonen, Maarit J.; Sulkava, Raimo] Univ Kuopio, Sch Publ Hlth & Clin Nutr, FIN-70211 Kuopio, Finland; [Jyrkka, Johanna] Univ Kuopio, Dept Social Pharm, FIN-70211 Kuopio, Finland; [Jyrkka, Johanna; Korhonen, Maarit J.; Hartikainen, Sirpa] Univ Kuopio, Kuopio Res Ctr Geriatr Care, FIN-70211 Kuopio, Finland; [Enlund, Hannes] Kuwait Univ, Dept Pharm Practice, Kuwait, Kuwait; [Hartikainen, Sirpa] Univ Kuopio, Fac Pharm, FIN-70211 Kuopio, Finland; [Hartikainen, Sirpa] Leppavirta Hlth Ctr, Leppavirta, Finland	Jyrkka, J (reprint author), Univ Kuopio, Sch Publ Hlth & Clin Nutr, POB 1627, FIN-70211 Kuopio, Finland.	johanna.jyrkka@uku.fi			Nordic Red Feather of the Lions; Kuopio University Pharmacy Fund; Social Insurance of Finland; Jenny and Antti Wihuri Foundation; Orion-Farmos Research Foundation	The authors have no conflicts of interest that are directly relevant to the content of this study.	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J	Reibman, J; Marmor, M; Filner, J; Fernandez-Beros, ME; Rogers, L; Perez-Perez, GI; Blaser, MJ				Reibman, Joan; Marmor, Michael; Filner, Joshua; Fernandez-Beros, Maria-Elena; Rogers, Linda; Perez-Perez, Guillermo I.; Blaser, Martin J.			Asthma Is Inversely Associated with Helicobacter pylori Status in an Urban Population	PLOS ONE			English	Article								Background: Microbial exposures have been suggested to confer protection from allergic disorders and reduced exposures to gastrointestinal microbiota have been proposed as an explanation for the increase in asthma prevalence. Since the general prevalence of Helicobacter pylori has been decreasing, we hypothesized that H. pylori serostatus would be inversely related to the presence of asthma. Methods: Adults were recruited to participate in the New York University (NYU)/Bellevue Asthma Registry in New York City. Adult asthma cases (N = 318) and controls (N = 208) were identified and serum IgG antibodies to H. pylori whole cell antigens or the immunodominant CagA antigen were measured. Results: As expected, the asthma cases and controls differed with respect to atopy and lung function. Seropositivity to H. pylori or CagA antigen was present in 47.1% of the total case and control study population. Asthma was inversely associated with CagA seropositivity (=OR = 0.57, 95% CI = 0.36-0.89). Median age of onset of asthma (doctor's diagnosis) was older ( 21 years) among individuals with CagA+ strains than among H. pylori-individuals (11 years) (p = 0.006). Conclusion: These data are consistent with the hypothesis that colonization with CagA+ H. pylori strains is inversely associated with asthma and is associated with an older age of asthma onset in an urban population. The data suggest H. pylori as a marker for protection.	[Marmor, Michael; Filner, Joshua; Fernandez-Beros, Maria-Elena; Rogers, Linda; Perez-Perez, Guillermo I.; Blaser, Martin J.] NYU, Sch Med, Dept Med, New York, NY 10003 USA; [Reibman, Joan; Marmor, Michael] NYU, Sch Med, Dept Environm Med, New York, NY USA	Reibman, J (reprint author), NYU, Sch Med, Dept Med, New York, NY 10003 USA.	reibmj01@gcrc.med.nyu.edu		Marmor, Michael/0000-0001-6605-2661; Reibman, Joan/0000-0001-7878-1511; Perez Perez, Guillermo /0000-0002-0131-5798	Colton Family Foundation; Diane Belfer Program in Human Microbial Ecology; Senior Scholar Award of the Ellison Medical Foundation;  [MO 1RR00096];  [ES 000260];  [RO1 GM63270]	MO 1RR00096, ES 000260 (JR, MM), RO1 GM63270 (MB), Colton Family Foundation, The Diane Belfer Program in Human Microbial Ecology, Senior Scholar Award of the Ellison Medical Foundation (MB). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.	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J	Williams, MA; Rangasamy, T; Bauer, SM; Killedar, S; Karp, M; Kensler, TW; Yamamoto, M; Breysse, P; Biswal, S; Georas, SN				Williams, Marc A.; Rangasamy, Tirumalai; Bauer, Stephen M.; Killedar, Smruti; Karp, Matthew; Kensler, Thomas W.; Yamamoto, Masayuki; Breysse, Patrick; Biswal, Shyam; Georas, Steve N.			Disruption of the transcription factor Nrf2 promotes pro-oxidative dendritic cells that stimulate Th2-like immunoresponsiveness upon activation by ambient particulate matter	JOURNAL OF IMMUNOLOGY			English	Article							HEME OXYGENASE-1 EXPRESSION; EXHAUST PARTICLE CHEMICALS; AIRWAY INFLAMMATION; IN-VIVO; T-CELLS; ALLERGIC INFLAMMATION; COSTIMULATORY MOLECULES; ENHANCES SUSCEPTIBILITY; GLUTATHIONE DEPLETION; CYTOKINE PRODUCTION	Oxidative stress is important in dendritic cell (DC) activation. Environmental particulate matter (PM) directs pro-oxidant activities that may alter DC function. Nuclear erythroid 2 p45-related factor 2 (Nrf2) is a redox-sensitive transcription factor that regulates expression of antioxidant and detoxification genes. Oxidative stress and defective antioxidant responses may contribute to the exacerbations of asthma. We hypothesized that PM would impart differential responses by Nrf2 wild-type DCs as compared with Nrf2(-/-) DCs. We found that the deletion of Nrf2 affected important constitutive functions of both bone marrow-derived and highly purified myeloid lung DCs such as the secretion of inflammatory cytokines and their ability to take up exogenous Ag. Stimulation of Nrf2(-/-) DCs with PM augmented oxidative stress and cytokine production as compared with resting or Nrf2(+/+) DCs. This was associated with the enhanced induction of Nrf2-regulated antioxidant genes. In contrast to Nrf2(+/+) DCs, coincubation of Nrf2(-/-) DCs with PM and the antioxidant N-acetyl cysteine attenuated PM-induced up-regulation of CD80 and CD86. Our studies indicate a previously underappreciated role of Nrf2 in innate immunity and suggest that deficiency in Nrf2-dependent pathways may be involved in susceptibility to the adverse health effects of air pollution in part by promoting Th2 cytokine responses in the absence of functional Nrf2. Moreover, our studies have uncovered a hierarchal response to oxidative stress in terms of costimulatory molecule expression and cytokine secretion in DCs and suggest an important role of heightened oxidative stress in proallergic Th2-mediated immune responses orchestrated by DCs.	[Williams, Marc A.; Rangasamy, Tirumalai; Bauer, Stephen M.; Killedar, Smruti; Karp, Matthew; Georas, Steve N.] Univ Rochester, Sch Med, Div Pulm & Crit Care Med, Rochester, NY 14642 USA; [Williams, Marc A.; Georas, Steve N.] Univ Rochester, Sch Med, Dept Environm Med, Rochester, NY 14642 USA; [Kensler, Thomas W.; Breysse, Patrick; Biswal, Shyam] Johns Hopkins Univ, Sch Med, Dept Environm Hlth Sci, Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD 21205 USA; [Biswal, Shyam] Johns Hopkins Univ, Sch Med, Div Pulm & Crit Care Med, Baltimore, MD 21205 USA; [Yamamoto, Masayuki] Univ Tsukuba, Ctr Tsukuba Adv Res Alliance, Tsukuba, Ibaraki, Japan	Williams, MA (reprint author), Univ Rochester, Sch Med, Div Pulm & Crit Care Med, 601 Elmwood Ave,Box 692, Rochester, NY 14642 USA.	marc_williams@urmc.rochester.edu; steve_georas@urmc.rochester.edu	Yamamoto, Masayuki/A-4873-2010; Kensler, Thomas/D-8686-2014	Kensler, Thomas/0000-0002-6676-261X	National Institute of Environmental Health Sciences (NIEHS); U.S. Environmental Protection Agency [PO1ES09606]; Department of Medicine, University of Rochester School of Medicine and Dentistry; National Institutes of Health (NIH) [R01 HL073952, HL071933, P50 HL084945, CA 94076]; NIH NIEHS [P30 ES03819, P30 ES001247]	This research was supported in pari by a New Investigator Project from the Center for Childhood Asthma in the Urban Environment (funded by National Institute of Environmental Health Sciences (NIEHS) and U.S. Environmental Protection Agency Grant PO1ES09606 to S.N.G. and M.A.W.) as well as by the Department of Medicine, University of Rochester School of Medicine and Dentistry (Rochester, NY). The research was also supported by National Institutes of Health (NIH) Research Grants R01 HL073952 and HL071933 (to S.N.G.), COPD SCCOR P50 HL084945 and CA 94076 (to T.W.K.) and by NIH NIEHS Pilot Project Grants P30 ES03819 and P30 ES001247 (to M.A.W.).	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Immunol.	OCT 1	2008	181	7					4545	4559				15	Immunology	Immunology	356CG	WOS:000259755700017	18802057	
J	Romieu, I; Barraza-Villarreal, A; Escamilla-Nunez, C; Almstrand, AC; Diaz-Sanchez, D; Sly, PD; Olin, AC				Romieu, Isabelle; Barraza-Villarreal, Albino; Escamilla-Nunez, Consuelo; Almstrand, Ann-Charlotte; Diaz-Sanchez, David; Sly, Peter D.; Olin, Anna-Carin			Exhaled breath malondialdehyde as a marker of effect of exposure to air pollution in children with asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; clinical immunology; environment; epidemiology; pediatrics	OXIDATIVE STRESS; MEXICO-CITY; DNA-DAMAGE; OZONE EXPOSURE; IN-VIVO; CONDENSATE; LUNG; ANTIOXIDANT; GLUTATHIONE; ALDEHYDES	Background: Assessment of the adverse effects of oxidative stress related to air pollution is limited by the lack of biological markers of dose to the lungs. Objective: We evaluated the use of exhaled breath condensate (EBC) malondialdehyde as a biomarker of exposure to traffic-related pollution in children with asthma as part of a panel study in Mexico City. Methods: Standard spirometry and collection of EBC and nasal lavage were performed. Environmental monitoring sites were located within 5 km of the children's homes and schools. Data were analyzed by using generalized estimating equations. Results: A total of 480 samples of malondialdehyde were obtained from 107 patients with asthma, with a median level of 18.7 (interquartile range [IQR], 12.4-28.7) nmol. Ambient particulates less than 2.5 mu g/m(3) and ozone levels on the day of sampling were significantly associated with higher malondialdehyde levels. A 14.2-mu g/m(3) (IQR) increase in 8-hour moving average particulates less than 2.5 mu g/m(3) in size was associated with a 1.12-nmol increase in malondialdehyde and 4 15.9-ppb (IQR) increase in 8-hour moving average ozone with a 1.16-nmol increase in malondialdehyde. Malondialdehyde levels were inversely associated with forced vital capacity and FEV(1) and positively associated with IL-8 levels in nasal lavage. Conclusion: Exhaled breath condensate malondialdehyde was related to both air pollution exposure and changes in lung function and inflammatory markers.	[Romieu, Isabelle; Barraza-Villarreal, Albino; Escamilla-Nunez, Consuelo] Inst Nacl Salud Publ, Cuernavaca 62508, Morelos, Mexico; [Almstrand, Ann-Charlotte; Olin, Anna-Carin] Sahlgrens Univ Hosp, Dept Occupat & Environm Med, S-41345 Gothenburg, Sweden; [Diaz-Sanchez, David] Univ Calif Los Angeles, Los Angeles, CA USA; [Sly, Peter D.] Curtin Univ Technol, WHO, Collaborating Ctr Res Child Environm Hlth, Perth, WA 6001, Australia; [Sly, Peter D.] Univ Western Australia, Ctr Child Hlth Res, Perth, WA 6009, Australia	Romieu, I (reprint author), Inst Nacl Salud Publ, 655 Avendia Univ,Col Santa Maria Ahuacatitlan, Cuernavaca 62508, Morelos, Mexico.	iromieu@correo.insp.mx	Sly, Peter/F-1486-2010	Sly, Peter/0000-0001-6305-2201			ANEMIYA T, 1973, ECONOMETRICA, V41, P997; Arbak P, 2004, J OCCUP HEALTH, V46, P281, DOI 10.1539/joh.46.281; Behndig AF, 2006, EUR RESPIR J, V27, P359, DOI 10.1183/09031936.06.00136904; Borm PJA, 2007, OCCUP ENVIRON MED, V64, P73, DOI 10.1136/oem.2006.029090; Bowler RP, 2002, J ALLERGY CLIN IMMUN, V110, P349, DOI 10.1067/mai.2002.126780; BROWN RK, 1994, PEDIATR RES, V36, P487, DOI 10.1203/00006450-199410000-00013; Corradi M, 2003, AM J RESP CRIT CARE, V167, P395, DOI 10.1164/rccm.200206-507OC; Frampton MW, 1999, AM J RESP CRIT CARE, V159, P1134; Goldoni M, 2004, ENVIRON HEALTH PERSP, V112, P1293, DOI 10.1289/ehp.7108; Halliwell B, 2000, AM J CLIN NUTR, V72, P1082; Isik B, 2005, INHAL TOXICOL, V17, P695, DOI 10.1080/08958370500189883; Kadiiska MB, 1997, CHEM RES TOXICOL, V10, P1104, DOI 10.1021/tx970049r; Kelly FJ, 2003, OCCUP ENVIRON MED, V60, P612, DOI 10.1136/oem.60.8.612; Kostikas K, 2002, AM J RESP CRIT CARE, V165, P1364, DOI 10.1164/rccm.200111-068OC; Larstad M, 2002, J CHROMATOGR B, V766, P107, DOI 10.1016/S0378-4347(01)00437-6; Li XY, 1996, THORAX, V51, P1216, DOI 10.1136/thx.51.12.1216; LIANG KY, 1986, BIOMETRIKA, V73, P132; Marnett LJ, 2002, TOXICOLOGY, V181, P219, DOI 10.1016/S0300-483X(02)00448-1; Orman A, 2005, TOXICOLOGY, V207, P15, DOI 10.1016/j.tox.2004.07.021; OSIAS PP, 2004, PEDIATR ALLERGY IMMU, V15, P4; Pekkanen J, 1997, ENVIRON RES, V74, P24, DOI 10.1006/enrs.1997.3750; Perez-Padilla R, 2003, PEDIATR PULM, V35, P177, DOI 10.1002/ppul.10232; Profita M, 2006, J ALLERGY CLIN IMMUN, V118, P1068, DOI 10.1016/j.jaci.2006.07.028; RAMIREZAGUILAR M, 2004, PERSONAL EXPOSURE AS, P26; Risom L, 2005, MUTAT RES-FUND MOL M, V592, P119, DOI 10.1016/j.mrfmmm.2005.06.012; Romieu I, 2006, EUR RESPIR J, V28, P953, DOI 10.1183/09031936.06.00114905; Romieu I, 2004, THORAX, V59, P8; Saxon A, 2005, NAT IMMUNOL, V6, P223, DOI 10.1038/ni0305-223; Sorensen M, 2003, ENVIRON HEALTH PERSP, V111, P161, DOI 10.1289/ehp.5646; *STAT CORP, 1996, STAT SOFTW REL 5 0; Takizawa Hajime, 2004, Curr Opin Allergy Clin Immunol, V4, P355, DOI 10.1097/00130832-200410000-00005; *US DEP HHS NIH NH, 1998, NIH PUBL; Vega E, 2004, J AIR WASTE MANAGE, V54, P786; Zar JH, 1996, BIOSTATISTICAL ANAL	34	75	78	3	18	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	APR	2008	121	4					903	909		10.1016/j.jaci.2007.12.004		7	Allergy; Immunology	Allergy; Immunology	286YY	WOS:000254884000014	18234317	
J	Van Overtvelt, L; Wambre, E; Maillere, B; von Hofe, E; Louise, A; Balazuc, AM; Bohle, B; Ebo, D; Leboulaire, C; Garcia, G; Moingeon, P				Van Overtvelt, Laurence; Wambre, Erik; Maillere, Bernard; von Hofe, Eric; Louise, Anne; Balazuc, Anne Marie; Bohle, Barbara; Ebo, Didier; Leboulaire, Christophe; Garcia, Gilles; Moingeon, Philippe			Assessment of Bet v 1-specific CD4(+) T cell responses in allergic and nonallergic individuals using MHC class II peptide tetramers	JOURNAL OF IMMUNOLOGY			English	Article							BIRCH POLLEN ALLERGEN; BET-V-I; SUBLINGUAL IMMUNOTHERAPY; REGULATORY-CELLS; IMMUNE DEVIATION; DENDRITIC CELLS; GRASS-POLLEN; TGF-BETA; MECHANISMS; INDUCTION	In this study, we used HLA-DRB1*0101, DRB1*0401, and DRBI*1501 peptide tetramers combined with cytokine surface capture assays to characterize CD4(+) T cell responses against the immunodominant T cell epitope (peptide 141-155) from the major birch pollen allergen Bet v 1, in both healthy and allergic individuals. We could detect Bet v I-specific T cells in the PBMC of 20 birch pollen allergic patients, but also in 9 of 9 healthy individuals tested. Analysis at a single-cell level revealed that allergen-specific CD4(+) T cells from healthy individuals secrete IFN-gamma and IL-10 in response to the allergen, whereas cells from allergic patients are bona fide Th2 cells (producing mostly IL-5, some IL-10, but no IFN-gamma), as corroborated by patterns of cytokines produced by T cell clones. A fraction of Bet v 1-specific cells isolated from healthy, but not allergic, individuals also expresses CTLA-4, glucocorticoid-induced TNF receptor, and Foxp 3, indicating that they represent regulatory T cells. In this model of seasonal exposure to allergen, we also demonstrate the tremendous dynamics of T cell responses in both allergic and nonallergic individuals during the peak pollen season, with an expansion of Bet v 1-specific precursors from 10(-6) to 10(-3) among circulating CD4(+) T lymphocytes. Allergy vaccines should be designed to recapitulate such naturally protective Th1/regulatory T cell responses observed in healthy individuals.	[Van Overtvelt, Laurence; Wambre, Erik; Moingeon, Philippe] Stallergenes SA, Rech & Dev, F-92183 Antony, France; [Maillere, Bernard] Commissariat Energie Atom, Serv Ingn Mol Prot, Gif Sur Yvette, France; [Louise, Anne; Balazuc, Anne Marie] Inst Pasteur, Paris, France; [Leboulaire, Christophe] Beckman Coulter, Marseille, France; [Garcia, Gilles] Hop Antoine Beclere, Dept Pneumol, Clamart, France; [von Hofe, Eric] Antigen Express, Worcester, MA 01605 USA; [Bohle, Barbara] Med Univ Vienna, Dept Pathophysiol, Vienna, Austria; [Ebo, Didier] Univ Antwerp, Dept Immunol Allergy & Rheumatology, Antwerp, Belgium	Moingeon, P (reprint author), Stallergenes SA, Rech & Dev, 6 Rue Alexis Tocqueville, F-92183 Antony, France.	pmoingeon@stallergenes.fr	EBO, Didier/H-4894-2016	EBO, Didier/0000-0003-0672-7529			Ahern DJ, 2005, CURR OPIN ALLERGY CL, V5, P531, DOI 10.1097/01.all.0000191239.20632.ab; Akdis CA, 2006, CHEM IMMUNOL ALLERGY, V91, P195; Akdis M, 2004, J EXP MED, V199, P1567, DOI 10.1084/jem.20032058; AKKERDAAS JH, 1995, ALLERGY, V50, P215, DOI 10.1111/j.1398-9995.1995.tb01136.x; Bacchetta R, 2007, J ALLERGY CLIN IMMUN, V120, P227, DOI 10.1016/j.jaci.2007.06.023; Bakker AH, 2005, CURR OPIN IMMUNOL, V17, P428, DOI 10.1016/j.coi.2005.06.008; Batard T, 2005, INT ARCH ALLERGY IMM, V136, P239, DOI 10.1159/000083950; Bateman EAL, 2006, J ALLERGY CLIN IMMUN, V118, P1350, DOI 10.1016/j.jaci.2006.07.040; Bohle B, 2007, J ALLERGY CLIN IMMUN, V120, P707, DOI 10.1016/j.jaci.2007.06.013; Bullens DMA, 2005, CLIN EXP ALLERGY, V35, P1535, DOI 10.1111/j.1365-2222.2005.02352.x; Campbell J. 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Immunol.	APR 1	2008	180	7					4514	4522				9	Immunology	Immunology	324GT	WOS:000257506700022	18354173	
J	Zhao, ZH; Zhang, Z; Wang, ZH; Ferm, M; Liang, YL; Norback, D				Zhao, Zhuohui; Zhang, Zheng; Wang, Zhuanhua; Ferm, Martin; Liang, Yanling; Norback, Dan			Asthmatic symptoms among pupils in relation to winter indoor and outdoor air pollution in schools in Taiyuan, China	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; asthma; China; formaldehyde; indoor; nitrogen dioxide; ozone; outdoor; school; sulfur dioxide	SICK BUILDING SYNDROME; VOLATILE ORGANIC-COMPOUNDS; RESPIRATORY SYMPTOMS; ALLERGEN LEVELS; HONG-KONG; HEALTH; PREVALENCE; SMOKING; ENVIRONMENT; POLLUTANTS	BACKGROUND: There are few studies on associations between children's respiratory heath and air pollution in schools in China. The industrial development and increased traffic may affect the indoor exposure to air pollutants in school environment. Moreover, there is a need to study respiratory effects of environmental tobacco smoke (ETS) and emissions from new building materials in homes in China. OBJECTIVES: We studied the associations between pupils' asthmatic symptoms and indoor and Outdoor air pollution in schools, as well as selected home exposures, in a coal-burning city in north China. METHODS: A questionnaire survey was administered to pupils (11-15 years of age) in 10 schools in urban Taiyuan, collecting data on respiratory health and selected home environmental factors. Indoor and outdoor school air pollutants and climate factors were measured in winter. RESULTS: A total of 1,993 pupils (90.2%) participated; 1.8% had cumulative asthma, 8.4% wheezing, 29.8% had daytime attacks of breathlessness, The indoor average concentrations of sulfur dioxide, nitrogen dioxide, ozone, and formaldehyde by class were 264.8, 39.4, 10.1, and 2.3 mu g/m(3), respectively. Outdoor levels were two to three times higher. Controlling for possible confounders, either wheeze or daytime or nocturnal attacks of breathlessness were positively associated with SO2, NO2, or formaldehyde. In addition, ETS and new furniture at home were risk factors for wheeze, daytime breathlessness, and respiratory infections. CONCLUSIONS: Indoor chemical air pollutants of mainly outdoor origin could be risk factors for pupils' respiratory symptoms at school, and home exposure to ETS and chemical emissions from new furniture could affect pupils' respiratory health.	[Zhao, Zhuohui; Norback, Dan] Univ Uppsala Hosp, Dept Occupat & Environm Med, SE-75185 Uppsala, Sweden; [Zhao, Zhuohui; Norback, Dan] Uppsala Univ, SE-75185 Uppsala, Sweden; [Zhang, Zheng; Wang, Zhuanhua] Shanxi Univ, Inst Biotechnol, Taiyuan, Shanxi Province, Peoples R China; [Liang, Yanling] Inst High Sch Student Hlth Care, Taiyuan, Shanxi Province, Peoples R China	Zhao, ZH (reprint author), Univ Uppsala Hosp, Dept Occupat & Environm Med, SE-75185 Uppsala, Sweden.	zhuohui.zhao@medsci.uu.se		Norback, Dan/0000-0002-5174-6668			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; Aunan K, 2004, SCI TOTAL ENVIRON, V329, P3, DOI 10.1016/j.scitotenv.2004.03.008; Bruce N, 2000, B WORLD HEALTH ORGAN, V78, P1078; 蔡丽, 2002, [卫生毒理学杂志, Journal of Health Toxicology], V16, P48; Chen BH, 2004, TOXICOLOGY, V198, P291, DOI 10.1016/j.tox.2004.02.005; CHEN Y, 1988, INT J EPIDEMIOL, V17, P348, DOI 10.1093/ije/17.2.348; Chen Yu-zhi, 2004, Zhonghua Jiehe He Huxi Zazhi, V27, P112; Cheng Yibin, 2002, Wei Sheng Yan Jiu, V31, P266; Cooley JD, 1998, OCCUP ENVIRON MED, V55, P579; Daisey JM, 2003, INDOOR AIR, V13, P53, DOI 10.1034/j.1600-0668.2003.00153.x; Douwes J, 2002, INT J EPIDEMIOL, V31, P1098, DOI 10.1093/ije/31.6.1098; Garcia-Marcos L, 1999, PEDIATR ALLERGY IMMU, V10, P96, DOI 10.1034/j.1399-3038.1999.00024.x; GOLDSTEIN IF, 1986, ENVIRON RES, V40, P332, DOI 10.1016/S0013-9351(86)80108-6; HOLGUIN F, 2007, AM J RESP CRIT CARE, DOI DOI 10.1164/RCCM.200611-16160C; Hugg TT, 2008, EUR J PUBLIC HEALTH, V18, P55, DOI 10.1093/eurpub/ckm053; Janson C, 2001, EUR RESPIR J, V18, P598, DOI 10.1183/09031936.01.00205801; Janssen NAH, 2003, ENVIRON HEALTH PERSP, V111, P1512, DOI 10.1289/ehp.6243; Kim JL, 2007, INDOOR AIR, V17, P122, DOI 10.1111/j.1600-0668.2006.00460.x; Kim JJ, 2004, AM J RESP CRIT CARE, V170, P520, DOI 10.1164/rccm.200403-2810C; Kim S, 2005, INDOOR AIR, V15, P317, DOI 10.1111/j.1600-0668.2005.00368.x; Lee SL, 2006, CLIN EXP ALLERGY, V36, P1138, DOI 10.1111/j.1365-2222.2006.02555.x; Lee SC, 2000, CHEMOSPHERE, V41, P109, DOI 10.1016/S0045-6535(99)00396-3; Mendell MJ, 2005, INDOOR AIR, V15, P27, DOI 10.1111/j.1600-0668.2004.00320.x; Mestl HES, 2003, AIR QUALITY ESTIMATE; Mi YH, 2006, INDOOR AIR, V16, P454, DOI 10.1111/j.1600-0668.2006.00439.x; Morgenstern V, 2007, OCCUP ENVIRON MED, V64, P8, DOI 10.1136/oem.2006.028241; NORBACK D, 1990, BRIT J IND MED, V47, P733; Norback Dan, 1992, INDOOR AIR, V2, P58, DOI 10.1111/j.1600-0668.1992.07-21.x; Ooi PL, 1998, OCCUP ENVIRON MED, V55, P188; Qian Z, 2007, INDOOR AIR, V17, P135, DOI 10.1111/j.1600-0668.2006.00463.x; RASBABSH J, 2005, USERS GUIDE MLWIN VE; Schneider D, 2001, ARCH ENVIRON HEALTH, V56, P103; SKOV P, 1990, SCAND J WORK ENV HEA, V16, P363; Smedje G, 1997, CLIN EXP ALLERGY, V27, P1270, DOI 10.1111/j.1365-2222.1997.tb01171.x; Sundell J, 1996, SCAND J WORK ENV HEA, V22, P5; *TAIYUAN URB PLANN, 2007, URB TRAFF PLANN MAP; Tanaka K, 2007, ANN EPIDEMIOL, V17, P1004, DOI 10.1016/j.annepidem.2007.07-108; Venners SA, 2001, AM J RESP CRIT CARE, V164, P973; Watts J, 2006, LANCET, V368, P719, DOI 10.1016/S0140-6736(06)69267-2; World Health Organization (WHO), 1987, WHO REG PUBL EUR SER, V23; WHO, 2005, WHO AIR QUAL GUID GL; Wieslander G, 1997, INT ARCH OCC ENV HEA, V69, P115; Wilkins CK, 2001, ENVIRON HEALTH PERSP, V109, P937, DOI 10.2307/3454995; Yang GH, 1999, JAMA-J AM MED ASSOC, V282, P1247, DOI 10.1001/jama.282.13.1247; Zhang YH, 2006, ENVIRON HEALTH PERSP, V114, P1227, DOI 10.1289/ehp.9014; ZHAO R, 1991, Zhonghua Yufang Yixue Zazhi, V25, P149; Zhao ZH, 2006, INDOOR AIR, V16, P404, DOI 10.1111/j.1600-0668.2006.00433.x	48	75	79	3	45	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765	1552-9924		ENVIRON HEALTH PERSP	Environ. Health Perspect.	JAN	2008	116	1					90	97		10.1289/ehp.10576		8	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	248GZ	WOS:000252142100030	18197305	
J	Shore, SA				Shore, Stephanie A.			Obesity and asthma: lessons from animal models	JOURNAL OF APPLIED PHYSIOLOGY			English	Review						mice; leptin; adiponectin; tumor necrosis factor-alpha; interleukin-6; adipokines	BODY-MASS INDEX; NECROSIS-FACTOR-ALPHA; INTERLEUKIN-6 RECEPTOR GENE; INDUCED AIRWAY INFLAMMATION; INDUCED LUNG INFLAMMATION; APPARENTLY HEALTHY-MEN; EMERGENCY-ROOM VISITS; ACUTE-PHASE REACTANTS; ACUTE OZONE EXPOSURE; DIET-INDUCED OBESITY	Epidemiological data indicate that obesity is a risk factor for asthma. These data are supported by observations in several murine models of obesity. Ob/ob, db/db, and Cpe(fat) mice each exhibit innate airway hyperresponsiveness, a characteristic feature of asthma. These mice also respond more vigorously to common asthma triggers, including ozone. Here we discuss the implications of these data with respect to several mechanisms proposed to explain the relationship between obesity and asthma: 1) common etiologies; 2) comorbidities; 3) mechanical factors; and 4) adipokines. We focus on the role of adipokines, especially TNF-alpha, IL-6, leptin, and adiponectin. Understanding the mechanistic basis for the relationship between obesity and asthma may lead to novel therapeutic strategies for treatment of the obese asthmatic subject.	Harvard Univ, Sch Publ Hlth, Program Mol & Integrat Physiol Sci, Boston, MA 02115 USA	Shore, SA (reprint author), Harvard Univ, Sch Publ Hlth, Program Mol & Integrat Physiol Sci, 665 Huntington Ave, Boston, MA 02115 USA.	sshore@hsph.harvard.edu			NHLBI NIH HHS [HL-33009]; NIEHS NIH HHS [ES-00002, ES-013307]		Akerman MJH, 2004, J ASTHMA, V41, P521, DOI 10.1081/JAS-120037651; Al-Shawwa B, 2006, J ASTHMA, V43, P231, DOI 10.1080/02770900600567056; Bastard JP, 2006, EUR CYTOKINE NETW, V17, P4; Bastard JP, 2002, J CLIN ENDOCR METAB, V87, P2084, DOI 10.1210/jc.87.5.2084; Beckett WS, 2001, AM J RESP CRIT CARE, V164, P2045; Bennett WD, 2006, P AM THORAC SOC, V3, pA550; Berg AH, 2005, CIRC RES, V96, P939, DOI 10.1161/01.RES.0000163635.62927.34; Bergen HT, 2002, AM J RESP CELL MOL, V27, P71; Bergeron C, 2005, J ALLERGY CLIN IMMUN, V115, P1102, DOI 10.1016/j.jaci.2005.03.018; Berry MA, 2006, NEW ENGL J MED, V354, P697, DOI 10.1056/NEJMoa050580; Breslow MJ, 1999, AM J PHYSIOL-ENDOC M, V276, pE443; 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Appl. Physiol.	FEB	2007	102	2					516	528		10.1152/japplphysiol.00847.2006		13	Physiology; Sport Sciences	Physiology; Sport Sciences	133SM	WOS:000244033500006	17053103	
J	You, DH; Becnel, D; Wang, K; Ripple, M; Daly, M; Cormier, SA				You, Dahui; Becnel, David; Wang, Kai; Ripple, Michael; Daly, Melissa; Cormier, Stephania A.			Exposure of neonates to Respiratory Syncytial Virus is critical in determining subsequent airway response in adults	RESPIRATORY RESEARCH			English	Article							BRONCHIOLITIS; INFECTION; INFANCY; DISEASE; ALLERGY; ASTHMA; AGE; HYPERRESPONSIVENESS; INFLAMMATION; ENHANCEMENT	Background: Respiratory syncytial virus (RSV) is the most common cause of acute bronchiolitis in infants and the elderly. Furthermore, epidemiological data suggest that RSV infection during infancy is a potent trigger of subsequent wheeze and asthma development. However, the mechanism by which RSV contributes to asthma is complex and remains largely unknown. A recent study indicates that the age of initial RSV infection is a key factor in determining airway response to RSV rechallenge. We hypothesized that severe RSV infection during neonatal development significantly alters lung structure and the pulmonary immune micro-environment; and thus, neonatal RSV infection is crucial in the development of or predisposition to allergic inflammatory diseases such as asthma. Methods: To investigate this hypothesis the present study was conducted in a neonatal mouse model of RSV-induced pulmonary inflammation and airway dysfunction. Seven-day-old mice were infected with RSV (2 x 10(5) TCID50/g body weight) and allowed to mature to adulthood. To determine if neonatal RSV infection predisposed adult animals to enhanced pathophysiological responses to allergens, these mice were then sensitized and challenged with ovalbumin. Various endpoints including lung function, histopathology, cytokine production, and cellularity in bronchoalveolar lavage were examined. Results: RSV infection in neonates alone led to inflammatory airway disease characterized by airway hyperreactivity, peribronchial and perivascular inflammation, and subepithelial fibrosis in adults. If early RSV infection was followed by allergen exposure, this pulmonary phenotype was exacerbated. The initial response to neonatal RSV infection resulted in increased TNF-alpha levels in bronchoalveolar lavage. Interestingly, increased levels of IL-13 and mucus hyperproduction were observed almost three months after the initial infection with RSV. Conclusion: Neonatal RSV exposure results in long term pulmonary inflammation and exacerbates allergic airways disease. The early increase in TNF-alpha in the bronchoalveolar lavage implicates this inflammatory cytokine in orchestrating these events. Finally, the data presented emphasize IL-13 and TNF-alpha as potential therapeutic targets for treating RSV induced-asthma.	Louisiana State Univ, Dept Biol Sci, Baton Rouge, LA 70803 USA	Cormier, SA (reprint author), Louisiana State Univ, Dept Biol Sci, Baton Rouge, LA 70803 USA.	dyou1@lsu.edu; dbecne1@lsu.edu; kwang@lsu.edu; mrippl1@lsu.edu; mdaly2@lsu.edu; scormier@lsu.edu			NCRR NIH HHS [P20 RR020159, P20 RR020159-020003, P20 RR020159-037537, P20 RR020159-047695]		Becnel D, 2005, RESP RES, V6, DOI 10.1186/1465-9921-6-122; Bell S, 2000, LANCET, V355, P858, DOI 10.1016/S0140-6736(99)00442-0; Culley FJ, 2002, J EXP MED, V196, P1381, DOI 10.1084/jem.20020943; Dakhama A, 2005, J IMMUNOL, V175, P1876; Hussell T, 2001, EUR J IMMUNOL, V31, P2566, DOI 10.1002/1521-4141(200109)31:9<2566::AID-IMMU2566>3.0.CO;2-L; Kalina W V, 2004, Clin Dev Immunol, V11, P113, DOI 10.1080/10446670410001722131; KARBER G., 1931, ARCH EXP PATHOL PH, V162, P480, DOI 10.1007/BF01863914; Kuperman DA, 2002, NAT MED, V8, P885, DOI 10.1038/nm734; Leader S, 2002, PEDIATR INFECT DIS J, V21, P629, DOI 10.1097/01.inf.0000019891.59210.1c; Lovell DJ, 2000, NEW ENGL J MED, V342, P763, DOI 10.1056/NEJM200003163421103; MCCONNOCHIE KM, 1984, PEDIATRICS, V74, P1; MOK JYQ, 1984, ARCH DIS CHILD, V59, P306; MURRAY M, 1992, ARCH DIS CHILD, V67, P482; Noble V, 1997, ARCH DIS CHILD, V76, P315; Openshaw PJM, 2005, CLIN MICROBIOL REV, V18, P541, DOI 10.1128/CMR.18.3.541-555.2005; Peebles RS, 2000, J INFECT DIS, V182, P671; Peebles RS, 2001, J INFECT DIS, V184, P1374; Peschon JJ, 1998, J IMMUNOL, V160, P943; PULLAN CR, 1982, BRIT MED J, V284, P1665; Rutigliano JA, 2004, J IMMUNOL, V173, P3408; Schwarze J, 2004, AM J RESP CRIT CARE, V169, P801, DOI 10.1164/rccm.200308-1203OC; Sigurs N, 2005, AM J RESP CRIT CARE, V171, P137, DOI 10.1164/rccm.200406-730OC; Sigurs N, 2000, AM J RESP CRIT CARE, V161, P1501; SIMS DG, 1978, BRIT MED J, V1, P11; SORKNESS R, 1991, J APPL PHYSIOL, V70, P375; Spearman C, 1908, BRIT J PSYCHOL, V2, P227; Taube C, 2002, J IMMUNOL, V169, P6482; Uhl EW, 1996, AM J RESP CRIT CARE, V154, P1834; Wills-Karp M, 2003, CURR OPIN PULM MED, V9, P21, DOI 10.1097/00063198-200301000-00004	29	75	76	0	1	BIOMED CENTRAL LTD	LONDON	MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND	1465-9921			RESP RES	Respir. Res.	AUG 7	2006	7								107	10.1186/1465-9921-7-107		10	Respiratory System	Respiratory System	083VF	WOS:000240485600001	16893457	
J	Cunha, BA				Cunha, BA			The atypical pneumonias: clinical diagnosis and importance	CLINICAL MICROBIOLOGY AND INFECTION			English	Review						atypical pneumonias; clinical diagnosis of legionnaire's disease; community-acquired pneumonia; doxycycline; legionnaire's disease; Mycoplasma pneumonia; Chlamydia pneumonia; quinolones; review; telithromycin; therapy of Legionella	COMMUNITY-ACQUIRED PNEUMONIA; RESPIRATORY-TRACT INFECTIONS; CHLAMYDIA-PNEUMONIAE; MYCOPLASMA-PNEUMONIAE; MULTIPLE-SCLEROSIS; EARLY-SWITCH; LEGIONELLA-PNEUMONIA; LEGIONNAIRES-DISEASE; AMBULATORY PATIENTS; THERAPY	The most common atypical pneumonias are caused by three zoonotic pathogens, Chlamydia psittaci (psittacosis), Francisella tularensis (tularemia), and Coxiella burnetii (Q fever), and three nonzoonotic pathogens, Chlamydia pneumoniae, Mycoplasma pneumoniae, and Legionella. These atypical agents, unlike the typical pathogens, often cause extrapulmonary manifestations. Atypical CAPs are systemic infectious diseases with a pulmonary component and may be differentiated clinically from typical CAPs by the pattern of extrapulmonary organ involvement which is characteristic for each atypical CAP. Zoonotic pneumonias may be eliminated from diagnostic consideration with a negative contact history. The commonest clinical problem is to differentiate legionnaire's disease from typical CAP as well as from C. pneumoniae or M. pneumonia infection. Legionella is the most important atypical pathogen in terms of severity. It may be clinically differentiated from typical CAP and other atypical pathogens by the use of a weighted point system of syndromic diagnosis based on the characteristic pattern of extrapulmonary features. Because legionnaire's disease often presents as severe CAP, a presumptive diagnosis of Legionella should prompt specific testing and empirical anti-Legionella therapy such as the Winthrop-University Hospital Infectious Disease Division's weighted point score system. Most atypical pathogens are difficult or dangerous to isolate and a definitive laboratory diagnosis is usually based on indirect, i.e., direct flourescent antibody (DFA), indirect flourescent antibody (IFA). Atypical CAP is virtually always monomicrobial; increased IFA IgG tests indicate past exposure and not concurrent infection. Anti-Legionella antibiotics include macrolides, doxycycline, rifampin, quinolones, and telithromycin. The drugs with the highest level of anti-Legionella activity are quinolones and telithromycin. Therapy is usually continued for 2 weeks if potent anti-Legionella drugs are used. In adults, M. pneumoniae and C. pneumoniae may exacerbate or cause asthma. The importance of the atypical pneumonias is not related to their frequency (similar to 15% of CAPs), but to difficulties in their diagnosis, and their nonresponsiveness to beta-lactam therapy. Because of the potential role of C. pneumoniae in coronary artery disease and multiple sclerosis (MS), and the role of M. pneumoniae and C. pneumoniae in causing or exacerbating asthma, atypical CAPs also have public health importance.	Winthrop Univ Hosp, Div Infect Dis, Mineola, NY 11501 USA; SUNY Stony Brook, Sch Med, Stony Brook, NY 11794 USA	Cunha, BA (reprint author), Winthrop Univ Hosp, Div Infect Dis, Mineola, NY 11501 USA.						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Microbiol. Infect.	MAY	2006	12			3			12	24		10.1111/j.1469-0691.2006.01393.x		13	Infectious Diseases; Microbiology	Infectious Diseases; Microbiology	032VE	WOS:000236803100003	16669925	
J	Merchant, JA; Naleway, AL; Svendsen, ER; Kelly, KM; Burmeister, LF; Stromquist, AM; Taylor, CD; Thorne, PS; Reynolds, SJ; Sanderson, WT; Chrischilles, EA				Merchant, JA; Naleway, AL; Svendsen, ER; Kelly, KM; Burmeister, LF; Stromquist, AM; Taylor, CD; Thorne, PS; Reynolds, SJ; Sanderson, WT; Chrischilles, EA			Asthma and farm exposures in a cohort of rural Iowa children	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						agricultural occupational exposures; ammonia; animal feeding operations; asthma; asthma diagnosis and treatment; asthma health care policy; asthma school screening; asthma underdiagnosis; asthma undertreatment; children; chronic wheeze; cough with exercise; farming; genetic selection; hydrogen sulfide; hygiene hypothesis; odor; rural	ALLERGIC SENSITIZATION; EARLY-CHILDHOOD; EARLY-LIFE; HAY-FEVER; ENDOTOXIN; HEALTH; PREVALENCE; DISEASES; ATOPY; RISK	Epidemiologic studies of farm children are of international interest because farm children are less often atopic, have less allergic disease, and often have less asthma than do nonfarm children-findings consistent with the hygiene hypothesis. We studied a cohort of rural Iowa children to determine the association between farm.and other environmental risk factors with four asthma outcomes: doctor-diagnosed asthma, doctor-diagnosed asthma/medication for wheeze, current wheeze, and cough with exercise. Doctor-diagnosed asthma prevalence was 12%, but at least one of these four health outcomes was found in more than a third of the cohort. Multivariable models of the four health outcomes found independent associations between male sex (three asthma outcomes), age (three asthma outcomes), a personal history of allergies (four asthma outcomes), family history of allergic disease (two asthma outcomes), premature birth (one asthma outcome), early respiratory infection (three asthma outcomes), high-risk birth (two asthma outcomes), and farm exposure to raising swine and adding antibiotics to feed (two asthma outcomes). The high prevalence of rural childhood asthma and asthma symptoms underscores the need for asthma screening programs and improved asthma diagnosis and treatment. The high prevalence of asthma health outcomes among farm children living on farms that raise swine (44.1 %, p = 0.01) and raise swine and add antibiotics to feed (55.8%, p = 0.013), despite lower rates of atopy and personal histories of allergy, suggests the need for awareness and prevention measures and more population-based studies to further assess environmental and genetic determinants of asthma among farm children.	Univ Iowa, Coll Publ Hlth, Dept Environm & Occupat Hlth, Iowa City, IA 52242 USA; Univ Iowa, Coll Publ Hlth, Dept Epidemiol, Iowa City, IA 52242 USA; Kaiser Permanente NW, Ctr Hlth Res, Portland, OR USA; US EPA, Natl Hlth & Environm Effects Res Lab, Human Studies Div, Epidemiol & Biomarkers Branch, Res Triangle Pk, NC 27711 USA; Univ Iowa, Coll Publ Hlth, Dept Biostat, Iowa City, IA USA; Colorado State Univ, Coll Vet Med & Biomed Sci, Dept Environm & Radiol Hlth Sci, Ft Collins, CO 80523 USA	Merchant, JA (reprint author), Univ Iowa, Coll Publ Hlth, Gen Hosp, E220H1, Iowa City, IA 52242 USA.	james-merchant@uiowa.edu	Kelly, Kevin/E-2716-2013; Svendsen, Erik/J-2671-2015	Kelly, Kevin/0000-0002-9177-1454; Svendsen, Erik/0000-0003-3941-0907; Naleway, Allison/0000-0001-5747-4643	ODCDC CDC HHS [5 R01/CCR714364, U07/CCU706145]		American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Anto JM, 1998, CLIN EXP ALLERGY, V28, P13; Arbour NC, 2000, NAT GENET, V25, P187; Asher MI, 1998, EUR RESPIR J, V12, P315; Bauer EJ, 1999, J SCHOOL HEALTH, V69, P12; Bolte G, 2003, CLIN EXP ALLERGY, V33, P770, DOI 10.1046/j.1365-2222.2003.01665.x; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Campagna D, 2004, J EXPO ANAL ENV EPID, V14, P180, DOI 10.1038/sj.jea.7500313; Chrischilles E, 2004, J ALLERGY CLIN IMMUN, V113, P66, DOI 10.1016/j.jaci.2003.09.037; Contreras JP, 2003, J ALLERGY CLIN IMMUN, V112, P1072, DOI 10.1016/j.jaci.2003.08.036; Crapo RO, 2000, AM J RESP CRIT CARE, V161, P309; Douwes J, 2001, AM J IND MED, V39, P608, DOI 10.1002/ajim.1060; DOUWES J, 2003, AM C GOVNM IND HYG, P219; 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; Gilliland FD, 2004, LANCET, V363, P119, DOI 10.1016/S0140-6736(03)15262-2; Hamscher G, 2003, ENVIRON HEALTH PERSP, V111, P1590, DOI 10.1289/ehp.6288; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Leynaert B, 2001, AM J RESP CRIT CARE, V164, P1829; Merchant JA, 2002, J RURAL HEALTH, V18, P521, DOI 10.1111/j.1748-0361.2002.tb00919.x; MUST A, 1991, AM J CLIN NUTR, V53, P839; *NAT AC SCI, 2003, AIR EM AN FEED OP CU; Niven R, 2003, CLIN EXP ALLERGY, V33, P273, DOI 10.1046/j.1365-2745.2003.01618.x; Park Hyesook, 2003, Appl Occup Environ Hyg, V18, P418, DOI 10.1080/10473220301425; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; Reynolds K D, 1997, J Cardiovasc Risk, V4, P1; Reynolds S. J., 1997, Journal of Agromedicine, V4, P37, DOI 10.1300/J096v04n01_06; Reynolds SJ, 1996, AM J IND MED, V29, P33, DOI 10.1002/(SICI)1097-0274(199601)29:1<33::AID-AJIM5>3.0.CO;2-#; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Salam MT, 2004, ENVIRON HEALTH PERSP, V112, P760, DOI 10.1289/ehp.6662; Schenker MB, 1998, AM J RESP CRIT CARE, V158, pS1; SCHWARTZ DA, 1995, AM J RESP CRIT CARE, V151, P47; Schwartz DA, 2001, AM J RESP CRIT CARE, V163, P305; SVEDSEN ER, 2003, AM J RESP CRIT CARE, V167, pA155; Thu K., 1997, Journal of Agricultural Safety and Health, V3, P13; VONEHRENSTEIN GS, 2000, CLIN EXP ALLERGY, V30, P187; VONMUTIUS E, 1993, J PEDIATR-US, V123, P223, DOI 10.1016/S0022-3476(05)81692-0; Wickens K, 1999, CLIN EXP ALLERGY, V29, P766; Wickens K, 2002, ALLERGY, V57, P1171, DOI 10.1034/j.1398-9995.2002.t01-1-23644.x; Wing S, 2000, ENVIRON HEALTH PERSP, V108, P233, DOI 10.2307/3454439	43	75	80	0	13	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	MAR	2005	113	3					350	356		10.1289/ehp.7240		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	903MM	WOS:000227430100047	15743727	
J	van der Woude, HJ; Zaagsma, J; Postma, DS; Winter, TH; van Hulst, M; Aalbers, R				van der Woude, HJ; Zaagsma, J; Postma, DS; Winter, TH; van Hulst, M; Aalbers, R			Detrimental effects of beta-blockers in COPD - A concern for nonselective beta-blockers	CHEST			English	Article						airway hyperresponsiveness; beta-blockers; COPD	OBSTRUCTIVE PULMONARY-DISEASE; AIR-FLOW OBSTRUCTION; WORKING PARTY STANDARDIZATION; EUROPEAN RESPIRATORY SOCIETY; LUNG-FUNCTION; SEVERE BRONCHOCONSTRICTION; OFFICIAL STATEMENT; CHRONIC-BRONCHITIS; METHACHOLINE; RESPONSIVENESS	Introduction: beta-Blockers are known to worsen FEV1 and airway hyperresponsiveness (AHR) in patients with asthma. Both characteristics determine the outcome of COPD, a disease with frequent cardiac comorbidity requiring beta-blocker treatment. Design: A double-blind, placebo-controlled, randomized, cross-over study. Setting: An ambulatory, hospital outpatient clinic of pulmonary diseases. Patients: Patients with mild-to-moderate irreversible COPD and AHR. Intervention: Fifteen patients received propranolol (80 mg), metoprolol (100 mg), celiprolol (200 mg), or placebo for 4 days, followed by a washout period >= 3 days. On day 4 of treatment, FEV1 and PC20 were assessed. Immediately hereafter, formoterol (12 mu g) was administered and FEV1 was measured for up to 30 min. Results: PC20 was significantly lower (p < 0.01) with propranolol and metoprolol treatment (geometric means, 2.06 mg/mL and 2.02 mg/mL, respectively) than with placebo (3.16 mg/mL) or celiprolol (3.41 mg/mL). FEV1 deteriorated only after propranolol treatment (2.08 +/- 0.31 L) [mean +/- SD] compared with placebo (2.24 +/- 0.37 L). The fast bronchodilating effect of formoterol was hampered by propranolol (mean increase in FEV1 at 3 min, 6.7 +/- 8.9%) but was unaffected by the other beta-blockers (16.9 +/- 9.8%, 22 +/- 11.6%, and 16.9 +/- 9.0% for placebo, metoprolol, and celiprolol, respectively). Conclusions: Pulmonary effects did not occur by celiprolol. Only propranolol reduced FEV1 and the bronchodilating effect of formoterol. Both metoprolol and propranolol increased AHR. Thus, different classes of beta-blockers have different pulmonary effects. The anticipated beneficial cardiovascular effects of a P-blocker must be weighted against the putative detrimental pulmonary effects, ie, effect on FEV1 AHR, and response to additional beta(2)-agonists.	Martini Hosp, Dept Pulm Dis, NL-9721 SW Groningen, Netherlands; Martini Hosp, Dept Clin Pharm & Toxicol, NL-9721 SW Groningen, Netherlands; Univ Ctr Pharm, Groningen, Netherlands; Univ Groningen Hosp, Dept Pulm Dis, Groningen, Netherlands	van der Woude, HJ (reprint author), Martini Hosp, Dept Pulm Dis, Van Ketwich Verschuurlaan 82, NL-9721 SW Groningen, Netherlands.	jvbhw@home.nl					Aalbers R, 2002, EUR RESPIR J, V19, P936, DOI 10.1183/09031936.02.00240902; American thoracic society, 1995, AM J RESP CRIT CARE, V152, pS77; Calverley PMA, 2003, THORAX, V58, P659, DOI 10.1136/thorax.58.8.659; Cazzola M, 2002, CHEST, V121, P230, DOI 10.1378/chest.121.1.230; Cazzola M, 2001, PULM PHARMACOL THER, V14, P41, DOI 10.1006/pupt.2000.0267; CLAGUE HW, 1984, EUR J CLIN PHARMACOL, V27, P517, DOI 10.1007/BF00556885; [Anonymous], 1997, THORAX S5, V52, pS1; Dart RA, 2003, CHEST, V123, P222, DOI 10.1378/chest.123.1.222; Gross NJ, 2003, THORAX, V58, P647, DOI 10.1136/thorax.58.8.647; Hancox RJ, 1999, EUR RESPIR J, V14, P283, DOI 10.1034/j.1399-3003.1999.14b08.x; Hansen EF, 1999, AM J RESP CRIT CARE, V159, P1267; Hospers JJ, 2000, LANCET, V356, P1313, DOI 10.1016/S0140-6736(00)02815-4; Kendall MJ, 1999, HEART, V82, P5; Kendall MJ, 1997, AM J CARDIOL, V80, p15J; MACDONALD AG, 1967, BRIT J ANAESTH, V39, P919, DOI 10.1093/bja/39.12.919; Murray CJL, 1997, LANCET, V349, P1498, DOI 10.1016/S0140-6736(96)07492-2; *NIH, 2001, PUBL; NORRIS RJ, 1988, AM J CARDIOL, V61, pC14, DOI 10.1016/0002-9149(88)90479-1; PERKS WH, 1978, BRIT J CLIN PHARMACO, V5, P101; Politiek MJ, 1999, EUR RESPIR J, V13, P988, DOI 10.1034/j.1399-3003.1999.13e10.x; POSTMA DS, 1986, AM REV RESPIR DIS, V134, P276; QUANJER PH, 1993, EUR RESPIR J, V6, P5; RAMSDALE EH, 1984, THORAX, V39, P912, DOI 10.1136/thx.39.12.912; RAMSDALE EH, 1985, THORAX, V40, P422, DOI 10.1136/thx.40.6.422; Salpeter SR, 2003, RESP MED, V97, P1094, DOI 10.1016/S0954-6111(03)00168-9; Salpeter SR, 2002, ANN INTERN MED, V137, P715; SIAFAKAS NM, 1995, EUR RESPIR J, V8, P1398, DOI 10.1183/09031936.95.08081398; Sterk PJ, 1993, EUR RESPIR J S, V16, P53; Tashkin DP, 1996, AM J RESP CRIT CARE, V153, P1802; van der Woude HJ, 2001, THORAX, V56, P529, DOI 10.1136/thorax.56.7.529; 2004, FARMOCOTHERAPEUTISCH	31	75	82	3	3	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	MAR	2005	127	3					818	824		10.1378/chest.127.3.818		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	908HG	WOS:000227777500024	15764762	
J	Erwin, EA; Wickens, K; Custis, NJ; Siebers, R; Woodfolk, J; Barry, D; Crane, J; Platts-Mills, TAE				Erwin, EA; Wickens, K; Custis, NJ; Siebers, R; Woodfolk, J; Barry, D; Crane, J; Platts-Mills, TAE			Cat and dust mite sensitivity and tolerance in relation to wheezing among children raised with high exposure to both allergens	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; cat; mite; tolerance; high exposure	MODIFIED TH2 RESPONSE; CHILDHOOD ASTHMA; ATOPIC-DERMATITIS; IMMUNE-RESPONSE; NEW-ZEALAND; SENSITIZATION; ANTIBODIES; DETERMINANTS; PREVALENCE; ENDOTOXIN	Background: Recent evidence has suggested that high exposure to cat allergens is associated with decreased prevalence of sensitization to cat and, in some studies, decreased asthma. Objective: Our objective was to study antibodies to cat and mite allergens and their relationship to wheezing in a country with high exposure to both allergens. Methods: Sera from 112 wheezing and 112 control children aged 10 to 11 years in a nested case-control study in New Zealand were assayed for specific IgE antibody, as well as IgG antibody and IgG4 antibody, to Der p 1 and Fel d 1. Results: IgE antibody to both mite (99/224) and cat (41/224) were strongly associated with wheezing (odds ratios, 5.2 and 6.5, respectively). Children who had ever lived with a cat were less likely to have IgE antibody to cat (20/141 vs 21/83, P <.04); however, cat ownership had no effect on IgE antibody to mite (67/141 vs 32/83, P =.23). Among sensitized children, cat ownership was associated with a lower prevalence of IgE antibody to cat (28% vs 66%, P <.001), and this analysis remained significant after exclusion of children whose families had chosen not to own a cat. Among sensitized subjects, the mean titer of IgE antibody to cat (1.7 IU/mL) was 10-fold lower than for mite (22.1 IU/mL). A cat in the home had no significant effect on endotoxin or mite allergen in house dust, whereas cat allergen was much higher (40.8 vs 3.3 mug/g). Conclusion: The response to these 2 allergens was distinct on the basis of the prevalence of sensitization, the titer of IgE antibody, and the effect of cat ownership. The results suggest that induction of tolerance to cat allergen is an allergen-specific phenomenon that cannot be attributed to endotoxin or family choice. The strength of the IgE antibody response to dust mite in humid climates could contribute to the increased prevalence and severity of asthma.	Univ Virginia, Asthma & Allerg Dis Ctr, Charlottesville, VA 22908 USA; Wellington Sch Med & Hlth Sci, Wellington Asthma Res Grp, Wellington, New Zealand; Healthcare Hawkes Bay, Hastings, New Zealand	Platts-Mills, TAE (reprint author), Univ Virginia, Asthma & Allerg Dis Ctr, POB 801355, Charlottesville, VA 22908 USA.	tap2z@virginia.edu	Siebers, Robert/A-4102-2009	Siebers, Robert/0000-0002-6359-3144	NIAID NIH HHS [P01-AI-50989, AI-20565]		Asher MI, 1998, EUR RESPIR J, V12, P315; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; BURR ML, 1994, INT J EPIDEMIOL, V23, P341, DOI 10.1093/ije/23.2.341; Carneiro R, 2004, J INVEST DERMATOL, V122, P927, DOI 10.1111/j.0022-202X.2004.22407.x; Custis NJ, 2003, CLIN EXP ALLERGY, V33, P986, DOI 10.1046/j.1365-2222.2003.01706.x; Custovic A, 2001, J ALLERGY CLIN IMMUN, V108, P537, DOI 10.1067/mai.2001.118599; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Jeannin P, 1998, J IMMUNOL, V160, P3555; Kaiser L, 2003, J BIOL CHEM, V278, P37730, DOI 10.1074/jbc.M304740200; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; Mandal AK, 2004, J EXP MED, V199, P1317, DOI 10.1084/jem.20031666; Oh JW, 2002, J ALLERGY CLIN IMMUN, V110, P460, DOI 10.1067/mai.2002.127512; OWMBY DR, 2002, JAMA-J AM MED ASSOC, V288, P963; Peat JK, 1996, AM J RESP CRIT CARE, V153, P141; 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, 2003, J ALLERGY CLIN IMMUN, V111, P123, DOI 10.1067/mai.2003.10; PLATTSMILLS TAE, 1976, J CLIN INVEST, V57, P1041, DOI 10.1172/JCI108346; Portengen L, 2004, CLIN EXP ALLERGY, V34, P1243, DOI 10.1111/j.1365-2222.2004.02025.x; Reefer AJ, 2004, J IMMUNOL, V172, P2763; 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; Sawyer G, 1998, J ALLERGY CLIN IMMUN, V102, P765, DOI 10.1016/S0091-6749(98)70016-8; Schulz O, 1998, J EXP MED, V187, P271, DOI 10.1084/jem.187.2.271; SEARS MR, 1989, CLIN EXP ALLERGY, V19, P419, DOI 10.1111/j.1365-2222.1989.tb02408.x; Shao L, 2001, SEMIN IMMUNOL, V13, P163, DOI 10.1006/smim.2000.0311; SPORIK R, 1995, AM J RESP CRIT CARE, V151, P1388; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; Wan H, 1999, J CLIN INVEST, V104, P123, DOI 10.1172/JCI5844; Wickens K, 1997, CLIN EXP ALLERGY, V27, P1077, DOI 10.1111/j.1365-2222.1997.tb01260.x; Woodfolk JA, 2002, INT ARCH ALLERGY IMM, V129, P277, DOI 10.1159/000067595	32	75	79	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.	JAN	2005	115	1					74	79		10.1016/j.jaci.2004.10.030		6	Allergy; Immunology	Allergy; Immunology	886XS	WOS:000226267000010	15637550	
J	Sherriff, A; Farrow, A; Golding, J; Henderson, J				Sherriff, A; Farrow, A; Golding, J; Henderson, J		ALSPAC Study Team	Frequent use of chemical household products is associated with persistent wheezing in pre-school age children	THORAX			English	Article							VOLATILE ORGANIC-COMPOUNDS; RESPIRATORY SYMPTOMS; CHANGING PREVALENCE; SCHOOL ENVIRONMENT; MATERNAL SMOKING; ASTHMA; RISK; SCHOOLCHILDREN; CLEANERS; INDOOR	Background: In the UK and other developed countries the prevalence of asthma symptoms has increased in recent years. This is likely to be the result of increased exposure to environmental factors. A study was undertaken to investigate the association between maternal use of chemical based products in the prenatal period and patterns of wheeze in early childhood. Methods: In the population based Avon Longitudinal Study of Parents and Children (ALSPAC), the frequency of use of 11 chemical based domestic products was determined from questionnaires completed by women during pregnancy and a total chemical burden (TCB) score was derived. Four mutually exclusive wheezing patterns were defined for the period from birth to 42 months based on parental questionnaire responses ( never wheezed, transient early wheeze, persistent wheeze, and late onset wheeze). Multinomial logistic regression models were used to assess the relationship between these wheezing outcomes and TCB exposure while accounting for numerous potential confounding variables. Complete data for analysis was available for 7019 of 13 971 (50%) children. Results: The mean (SD) TCB score was 9.4 (4.1), range 0 - 30. Increased use of domestic chemical based products was associated with persistent wheezing during early childhood ( adjusted odds ratio ( OR) per unit increase of TCB 1.06 (95% confidence interval (CI) 1.03 to 1.09)) but not with transient early wheeze or late onset wheeze. Children whose mothers had high TCB scores (>90th centile) were more than twice as likely to wheeze persistently throughout early childhood than children whose mothers had a low TCB score (<10th centile) ( adjusted OR 2.3 (95% CI 1.2 to 4.4)). Conclusion: These findings suggest that frequent use of chemical based products in the prenatal period is associated with persistent wheezing in young children. Follow up of this cohort is underway to determine whether TCB is associated with wheezing, asthma, and atopy at later stages in childhood.	Univ Bristol, Unit Paediat & Perinatal Epidemiol, Div Child Hlth, Bristol BS8 1BR, Avon, England; Brunel Univ, Dept Hlth & Social Care, Isleworth TW7 5DU, Middx, England	Sherriff, A (reprint author), Univ Bristol, Unit Paediat & Perinatal Epidemiol, Div Child Hlth, Bristol BS8 1BR, Avon, England.	Andrea.Sherriff@bris.ac.uk		Golding, Jean/0000-0003-2826-3307			ANDERSON HR, 1994, BRIT MED J, V308, P1600; Arif AA, 2002, OCCUP ENVIRON MED, V59, P505, DOI 10.1136/oem.59.8.505; Becher R, 1996, TOXICOL LETT, V86, P155, DOI 10.1016/0378-4274(96)03685-5; BURR M L, 1989, Archives of Disease in Childhood, V64, P1452; Delfino RJ, 2002, ENVIRON HEALTH PERSP, V110, P573; Dezateux C, 1999, AM J RESP CRIT CARE, V159, P403; Farrow A, 1997, ENVIRON TECHNOL, V18, P605, DOI 10.1080/09593331808616578; FARROW A, 2004, IN PRESS ARCH ENV HL; GERSTMAN BB, 1993, PEDIATRICS, V81, P1; Golding J, 2001, PAEDIATR PERINAT EP, V15, P74; Institute of Medicine, 2000, CLEAR AIR ASTHM IND; Karjalainen A, 2002, EUR RESPIR J, V19, P90, DOI 10.1183/09031936.02.00201002; Kogevinas M, 1999, LANCET, V353, P1750, DOI 10.1016/S0140-6736(98)07397-8; Lemus R., 1998, Reviews on Environmental Health, V13, P91; Lewis S, 1996, THORAX, V51, P670, DOI 10.1136/thx.51.7.670; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Medina-Ramon M, 2003, THORAX, V58, P950, DOI 10.1136/thorax.58.11.950; Millqvist E, 1999, ALLERGY, V54, P495, DOI 10.1034/j.1398-9995.1999.00031.x; Murphy JFA, 1998, IRISH MED J, V91, P76; Nielsen J, 1999, OCCUP MED-OXFORD, V49, P291, DOI 10.1093/occmed/49.5.291; NINAN TK, 1992, BRIT MED J, V304, P873; NORBACK D, 1995, OCCUP ENVIRON MED, V52, P388; OMRAN M, 1996, BRIT MED J, V3, P12; PEAT JK, 1994, BRIT MED J, V308, P1591; Ross DJ, 1998, OCCUP MED-OXFORD, V48, P481, DOI 10.1093/occmed/48.8.481; Sherriff A, 2001, INT J EPIDEMIOL, V30, P1473, DOI 10.1093/ije/30.6.1473; Sly RM, 1999, ANN ALLERG ASTHMA IM, V82, P233, DOI 10.1016/S1081-1206(10)62603-8; Smedje G, 1997, CLIN EXP ALLERGY, V27, P1270, DOI 10.1111/j.1365-2222.1997.tb01171.x; Smedje G, 2001, INT J TUBERC LUNG D, V5, P1059; Stick SM, 1996, LANCET, V348, P1060, DOI 10.1016/S0140-6736(96)04446-7; Venn AJ, 2003, THORAX, V58, P955, DOI 10.1136/thorax.58.11.955; Zock JP, 2002, EUR RESPIR J, V20, P679, DOI 10.1183/09031936.02.00279702; Zock JP, 2001, SCAND J WORK ENV HEA, V27, P76	33	75	76	1	13	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	JAN	2005	60	1					45	49		10.1136/thx.2004.021154		5	Respiratory System	Respiratory System	882TB	WOS:000225960100012	15618582	
J	Harris, J; Mason, DE; Li, J; Burdick, KW; Backes, BJ; Chen, T; Shipway, A; Van Heeke, G; Gough, L; Ghaemmaghami, A; Shakib, F; Debaene, F; Winssinger, N				Harris, J; Mason, DE; Li, J; Burdick, KW; Backes, BJ; Chen, T; Shipway, A; Van Heeke, G; Gough, L; Ghaemmaghami, A; Shakib, F; Debaene, F; Winssinger, N			Activity profile of dust mite allergen extract using substrate libraries and functional proteomic microarrays	CHEMISTRY & BIOLOGY			English	Article							CYSTEINE PROTEASE ACTIVITY; DERMATOPHAGOIDES-PTERONYSSINUS; ENHANCES ALLERGENICITY; PROTEOLYTIC ACTIVITY; SERINE HYDROLASES; MASS-SPECTROMETRY; DER-P-1; SPECIFICITY; INHIBITOR; PROTEINASES	Enzymatic activity in the fecal droppings from the house dust mite has been postulated to contribute to the elicited allergic response. Screening dust mite extracts through 137,180 tetrapeptide fluorogenic substrates allowed for the characterization of proteolytic substrate specificity from the potential cysteine and serine proteases in the extract. The extract was further screened against a 4000 member peptide nucleic acid (PNA) encoded inhibitor library designed to target cysteine proteases using microarray detection. Affinity chromatography coupled with mass spectrometry identified Der p 1 as one of the proteases targeted by the PNA inhibitors in the dust mite lysate. A phenotypic readout of Der p 1 function in allergy progression was demonstrated by the inhibition of CD25 cleavage from T cells by dust mite extract that had been treated with the Der p I inhibitor identified from the PNA-encoded inhibitor library.	Scripps Res Inst, Dept Mol Biol, San Diego, CA 92121 USA; Genom Inst Novartis Res Fdn, Dept Chem, San Diego, CA 92121 USA; Novartis Inst Biomed Res, Horsham RH12 5AB, W Sussex, England; Univ Nottingham, Inst Infect Immun & Inflammat, Ctr Biomol Sci, Nottingham NG7 2RD, England; Univ Louis Pasteur Strasbourg 1, Inst Sci & Ingn Supramol, F-67000 Strasbourg, France	Winssinger, N (reprint author), Scripps Res Inst, Dept Mol Biol, 10550 N Torrey Pines Rd, San Diego, CA 92121 USA.	harris@scripps.edu; winssinger@isis-ulp.org	Winssinger, Nicolas/B-6710-2017	Winssinger, Nicolas/0000-0003-1636-7766; Fairclough, Lucy/0000-0003-4581-9741			Aebersold R, 2001, CHEM REV, V101, P269, DOI 10.1021/cr990076h; Andersen JS, 2000, FEBS LETT, V480, P25, DOI 10.1016/S0014-5793(00)01773-7; ARTHUR RP, 1955, J INVEST DERMATOL, V25, P341, DOI 10.1038/jid.1955.138; Asturias JA, 1998, BBA-GENE STRUCT EXPR, V1397, P27, DOI 10.1016/S0167-4781(98)00006-2; Backes BJ, 2000, NAT BIOTECHNOL, V18, P187; BAGAROZZI DA, 1997, PHYTOCHEMISTRY, V47, P593; Baxter SM, 2004, MOL CELL PROTEOMICS, V3, P209, DOI 10.1074/mcp.M300082-MCP200; Debaene F, 2004, TETRAHEDRON, V60, P8677, DOI 10.1016/j.tet.2004.05.107; FURKA A, 1991, INT J PEPT PROT RES, V37, P487; 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, 2003, CLIN EXP ALLERGY, V33, P1159, DOI 10.1046/j.1365-2222.2003.01716.x; Gough L, 1999, J EXP MED, V190, P1897, DOI 10.1084/jem.190.12.1897; Greenbaum DC, 2002, CHEM BIOL, V9, P1085, DOI 10.1016/S1074-5521(02)00238-7; Griffin TJ, 1998, ANAL BIOCHEM, V260, P56, DOI 10.1006/abio.1998.2686; Harris JL, 2000, P NATL ACAD SCI USA, V97, P7754, DOI 10.1073/pnas.140132697; Harris JL, 2001, CHEM BIOL, V8, P1131, DOI 10.1016/S1074-5521(01)00080-1; HERBERT CA, 1993, BRIT J PHARMACOL, V110, P840; Jeffery DA, 2003, CURR OPIN BIOTECH, V14, P87, DOI 10.1016/S0958-1669(02)00010-1; Jessani N, 2004, CURR OPIN CHEM BIOL, V8, P54, DOI 10.1016/j.cbpa.2003.11.004; John RJ, 2000, CLIN EXP ALLERGY, V30, P784, DOI 10.1046/j.1365-2222.2000.00840.x; KAM CM, 1993, BIOCONJUGATE CHEM, V4, P560, DOI 10.1021/bc00024a021; Kawamoto S, 2002, J BIOSCI BIOENG, V94, P285, DOI 10.1263/jbb.94.285; Kozarich JW, 2003, CURR OPIN CHEM BIOL, V7, P78, DOI 10.1016/S1367-5931(02)00013-3; KRANTZ A, 1991, BIOCHEMISTRY-US, V30, P4678, DOI 10.1021/bi00233a007; Licklider LJ, 2002, ANAL CHEM, V74, P3076, DOI 10.1021/ac025529o; Liu YS, 1999, P NATL ACAD SCI USA, V96, P14694, DOI 10.1073/pnas.96.26.14694; Lockhart DJ, 2000, NATURE, V405, P827, DOI 10.1038/35015701; MacBeath G, 2000, SCIENCE, V289, P1760; Maly DJ, 2002, J ORG CHEM, V67, P910, DOI 10.1021/jo016140o; MORRISON JF, 1988, ADV ENZYMOL RAMB, V61, P201; OMARI TI, 1992, CLIN EXP PHARMACOL P, V19, P785; PlattsMills TAE, 1997, NEW ENGL J MED, V336, P1382, DOI 10.1056/NEJM199705083361909; PLATTSMILLS TAE, 1983, CLIN EXP DERMATOL, V8, P233, DOI 10.1111/j.1365-2230.1983.tb01776.x; Ring PC, 2000, CLIN EXP ALLERGY, V30, P1085; Schulz O, 1999, CLIN EXP ALLERGY, V29, P439; 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; Shakib F, 1998, IMMUNOL TODAY, V19, P313, DOI 10.1016/S0167-5699(98)01284-5; SPORIK R, 1992, CLIN EXP ALLERGY, V22, P897, DOI 10.1111/j.1365-2222.1992.tb02062.x; Thomberry N. A., 1997, J BIOL CHEM, V272, P17907; Wan H, 1999, J CLIN INVEST, V104, P123, DOI 10.1172/JCI5844; Winssinger N, 2002, P NATL ACAD SCI USA, V99, P11139, DOI 10.1073/pnas.172286899; Winssinger N, 2001, ANGEW CHEM INT EDIT, V40, P3152, DOI 10.1002/1521-3773(20010903)40:17<3152::AID-ANIE3152>3.0.CO;2-P; Yang CY, 2000, BBA-GENE STRUCT EXPR, V1517, P153, DOI 10.1016/S0167-4781(00)00235-9	44	75	75	0	6	CELL PRESS	CAMBRIDGE	1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA	1074-5521			CHEM BIOL	Chem. Biol.	OCT	2004	11	10					1361	1372		10.1016/j.chembiol.2004.08.008		12	Biochemistry & Molecular Biology	Biochemistry & Molecular Biology	864YH	WOS:000224668700008	15489163	
J	Murr, LE; Bang, JJ; Esquivel, EV; Guerrero, PA; Lopez, A				Murr, LE; Bang, JJ; Esquivel, EV; Guerrero, PA; Lopez, A			Carbon nanotubes, nanocrystal forms, and complex nanoparticle aggregates in common fuel-gas combustion sources and the ambient air	JOURNAL OF NANOPARTICLE RESEARCH			English	Article						carbon nanotubes; aggregates; methane; propane; natural gas; transmission electron microscopy; health risks; home environment	ULTRAFINE PARTICLES; MORTALITY; CLIMATE; AEROSOL; HEALTH; SIZE	Aggregated multiwall carbon nanotubes (with diameters ranging from similar to3 to 30 nm) and related carbon nanocrystal forms ranging in size from 0.4 to 2 mum (average diameter) have been collected in the combustion streams for methane/ air, natural gas/air, and propane gas/air flames using a thermal precipitator. Individual particle aggregates were collected on carbon/formvar-coated 3 mm nickel grids and examined in a transmission electron microscope, utilizing bright-field imaging, selected-area electron diffraction analysis, and energy-dispersive X-ray spectrometry techniques. The natural gas and propane gas sources were domestic (kitchen) stoves, and similar particle aggregates collected in the outdoor air were correspondingly identified as carbon nanocrystal aggregates and sometimes more complex aggregates of silica nanocrystals intermixed with the carbon nanotubes and other carbon nanocrystals. Finally, and in light of the potential for methane-series gas burning as major sources of carbon nanocrystal aggregates in both the indoor and outdoor air, data for natural gas consumption and corresponding asthma deaths and incidence are examined with a degree of speculation regarding any significance in the correlations.	Univ Texas, Dept Met & Mat Engn, El Paso, TX 79968 USA	Murr, LE (reprint author), Univ Texas, Dept Met & Mat Engn, M-201,500 W Univ Ave, El Paso, TX 79968 USA.	fekberg@utep.edu		Murr, Lawrence/0000-0001-5942-8376			Bang JJ, 2003, J AIR WASTE MANAGE, V53, P227; Bang JJ, 2002, J MATER SCI LETT, V21, P361, DOI 10.1023/A:1014994815240; BANG JJ, 2004, IN PRESS J NANOSCI N; BANG JJ, 2002, 5428 JOM; Buseck PR, 1999, P NATL ACAD SCI USA, V96, P3372, DOI 10.1073/pnas.96.7.3372; Chameides WL, 2002, SCIENCE, V297, P2214, DOI 10.1126/science.1076866; Chianelli RR, 1998, J HAZARDOUS SUB RES, V1, P1; Dagani R, 2003, CHEM ENG NEWS, V81, P30, DOI 10.1021/cen-v081n017.p030; ESQUIVEL EV, 2004, IN PRESS MAT CHARACT; GLADNEY ES, 1976, ATMOS ENVIRON, V10, P1071, DOI 10.1016/0004-6981(76)90116-5; Harris P., 2003, CARBON NANOTUBES REL; HAYES BS, 1980, BER BUNSEN PHYS CHEM, V84, P499; IIJIMA S, 1991, NATURE, V354, P56, DOI 10.1038/354056a0; KATRINAK KA, 1993, ENVIRON SCI TECHNOL, V27, P539, DOI 10.1021/es00040a013; Lighty JS, 2000, J AIR WASTE MANAGE, V50, P1565; Molina MJ, 1996, ANNU REV PHYS CHEM, V47, P327, DOI 10.1146/annurev.physchem.47.1.327; Momarca S., 1997, SCI TOTAL ENVIRON, V205, P137; Murr LE, 2004, J MATER SCI, V39, P2199, DOI 10.1023/B:JMSC.0000017787.53545.b7; MURR LE, 2004, IN PRESS J MAT SCI L; Murr L.E., 1991, ELECT ION MICROSCOPY; OBERDORSTER G, 1995, INHAL TOXICOL, V7, P111, DOI 10.3109/08958379509014275; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Schwartz J, 1999, ENVIRON HEALTH PERSP, V107, P339, DOI 10.2307/3434536; Smith BW, 2000, CHEM PHYS LETT, V321, P169, DOI 10.1016/S0009-2614(00)00307-9; UGARTE D, 1992, NATURE, V359, P707, DOI 10.1038/359707a0	25	75	75	2	21	KLUWER ACADEMIC PUBL	DORDRECHT	VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS	1388-0764			J NANOPART RES	J. Nanopart. Res.	JUN	2004	6	2-3					241	251		10.1023/B:NANO.0000034651.91325.40		11	Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials Science, Multidisciplinary	Chemistry; Science & Technology - Other Topics; Materials Science	837EF	WOS:000222610500011		
J	Ryan, CA; Gildea, LA; Hulette, BC; Dearman, RJ; Kimber, I; Gerberick, GF				Ryan, CA; Gildea, LA; Hulette, BC; Dearman, RJ; Kimber, I; Gerberick, GF			Gene expression changes in peripheral blood-derived dendritic cells following exposure to a contact allergen	TOXICOLOGY LETTERS			English	Article						contact allergy; dendritic cells; gene expression; in vitro method; dinitrobenzenesulfonic acid	EPIDERMAL LANGERHANS CELLS; LYMPHOCYTIC ACTIVATION MOLECULE; E-CADHERIN EXPRESSION; CLASS-II MOLECULES; COSTIMULATORY MOLECULES; HLA-DR; MATURATION; CYTOKINES; HAPTENS; SENSITIZERS	A critical step in the induction of allergic contact allergy is the activation and subsequent migration of Langerhans cells (LC), an important antigen presenting dendritic cell (DC) of the skin. As the Langerhans cells migrate, they undergo a maturation process. It has been proposed that contact allergen exposure can induce DC maturation. While changes in DC gene expression profiles induced by various maturation stimuli have been explored, there are no published reports describing genomic-scale analysis of the changes induced by chemical allergen exposure. Therefore, to explore the concept of chemical allergen-induced DC maturation and to identify genes that are regulated by exposure to allergens we examined, at the transcriptional level, the effects of exposure to a contact allergen on DC. Peripheral blood-derived DC were exposed for 24 h to either 1 mM or 5 mM dinitrobenzenesulfonic acid (DNBS). Changes in gene expression were analyzed using Affymetrix U95Av2 GeneChip(R). Comparison of mean signal values from replicate cultures revealed 173 genes that were significantly different (P less than or equal to 0.001) between 1 mM DNBS treated and untreated control DC and 1249 significant gene changes between 5 mM DNBS treated and control DC. Real-time reverse-transcriptase polymerase chain reaction (RT-PCR) was used to evaluate the observed transcript changes for selected genes in DC derived from a second donor. Comparison of the fold-changes in transcript levels between the two platforms and donors revealed a good correlation in both direction and magnitude. RT-PCR analysis was also used to assess the allergen specificity of a selected number of genes in DC derived from a third donor. Many of the gene expression changes were found to be induced only by exposure to the allergen, DNBS, and not by exposure to a structurally similar non-allergen, benzenesulfonic acid. A number of gene expression changes induced by allergen exposure were found to be consistent with what is known of the DC maturation process, and thus provide support for the theory of contact allergen-induced DC maturation. Additionally, it is hoped that some of the transcript changes identified through this approach will be shown to be suitable for use in the development of an in vitro predictive assay for contact sensitization. (C) 2004 Elsevier Ireland Ltd. All rights reserved.	Procter & Gamble Co, Cent Prod Safety Dept, Miami Valley Labs, Cincinnati, OH 45253 USA; Syngenta Cent Toxicol Lab, Macclesfield SK10 4TJ, Cheshire, England	Ryan, CA (reprint author), Procter & Gamble Co, Cent Prod Safety Dept, Miami Valley Labs, POB 538707, Cincinnati, OH 45253 USA.	ryan.ca@pg.com; gildea.la@pg.com; hulette.bc@pg.com; rebecca.dearman@syngenta.com; ian.kimber@syngenta.com; gerberick.gf@pg.com					Aiba S, 2003, J INVEST DERMATOL, V120, P390, DOI 10.1046/j.1523-1747.2003.12065.x; AIBA S, 1990, J IMMUNOL, V145, P2791; Aiba S, 1997, EUR J IMMUNOL, V27, P3031, DOI 10.1002/eji.1830271141; Aiba S, 2000, IMMUNOLOGY, V101, P68, DOI 10.1046/j.1365-2567.2000.00087.x; ALLEN RS, 2003, SCIENCE, V301, P1925; Banchereau J, 2000, ANNU REV IMMUNOL, V18, P767, DOI 10.1146/annurev.immunol.18.1.767; Banchereau J, 1998, NATURE, V392, P245, DOI 10.1038/32588; Becker D, 1997, J IMMUNOL METHODS, V203, P171, DOI 10.1016/S0022-1759(97)00024-0; BECKER D, 1992, J INVEST DERMATOL, V99, P545, DOI 10.1111/1523-1747.ep12667308; BECKER D, 1992, J INVEST DERMATOL, V98, P700, DOI 10.1111/1523-1747.ep12499912; Bleharski JR, 2001, J IMMUNOL, V167, P3174; Chen Z, 2002, BIOCHEM BIOPH RES CO, V290, P66, DOI 10.1006/bbrc.2001.6147; 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; Degwert J, 1997, TOXICOL IN VITRO, V11, P613, DOI 10.1016/S0887-2333(97)00053-2; Dietz AB, 2000, BIOCHEM BIOPH RES CO, V275, P731, DOI 10.1006/bbrc.2000.3372; ENK AH, 1992, P NATL ACAD SCI USA, V89, P1398, DOI 10.1073/pnas.89.4.1398; GIROLOMONI G, 1990, J INVEST DERMATOL, V94, P753, DOI 10.1111/1523-1747.ep12874611; Higashi N, 2002, J BIOL CHEM, V277, P20686, DOI 10.1074/jbc.M202104200; Huang Q, 2001, SCIENCE, V294, P870, DOI 10.1126/science.294.5543.870; Hulette BC, 2002, TOXICOL APPL PHARM, V182, P226, DOI 10.1006/taap.2002.9447; Imai T, 1996, J BIOL CHEM, V271, P21514; KIMBER I, 1992, TOXICOL APPL PHARM, V117, P137, DOI 10.1016/0041-008X(92)90230-P; Kruse M, 2001, J IMMUNOL, V167, P1989; Kuhn U, 1998, J IMMUNOL, V160, P667; Le Naour F, 2001, J BIOL CHEM, V276, P17920, DOI 10.1074/jbc.M100156200; Lockhart DJ, 1996, NAT BIOTECHNOL, V14, P1675, DOI 10.1038/nbt1296-1675; Manome H, 1999, IMMUNOLOGY, V98, P481, DOI 10.1046/j.1365-2567.1999.00916.x; MAURER D, 1999, DENDRITIC CELLS, P111; McColl SR, 2002, IMMUNOL CELL BIOL, V80, P489, DOI 10.1046/j.1440-1711.2002.01113.x; Messmer D, 2003, INT IMMUNOL, V15, P491, DOI 10.1093/intimm/dxg052; Moschella F, 2001, BRIT J HAEMATOL, V114, P444, DOI 10.1046/j.1365-2141.2001.02953.x; Naciff JM, 2003, TOXICOL SCI, V72, P314, DOI 10.1093/toxsci/kfg037; Ozawa H, 1996, J INVEST DERMATOL, V106, P441, DOI 10.1111/1523-1747.ep12343589; Pichowski JS, 2001, J APPL TOXICOL, V21, P115, DOI 10.1002/jat.742; Sallusto F, 1998, EUR J IMMUNOL, V28, P2760, DOI 10.1002/(SICI)1521-4141(199809)28:09<2760::AID-IMMU2760>3.0.CO;2-N; 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; Schwarzenberger K, 1996, J INVEST DERMATOL, V106, P553, DOI 10.1111/1523-1747.ep12344019; Shortman K, 2002, NAT REV IMMUNOL, V2, P151, DOI 10.1038/nri746; Tuschl H, 2000, TOXICOL IN VITRO, V14, P541, DOI 10.1016/S0887-2333(00)00051-5; Verhasselt V, 1997, J IMMUNOL, V158, P2919; Verrier AC, 1999, INT ARCH ALLERGY IMM, V120, P56, DOI 10.1159/000024220; Wang BH, 2002, J IMMUNOL, V168, P3303	43	75	81	1	2	ELSEVIER SCI IRELAND LTD	CLARE	CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND	0378-4274			TOXICOL LETT	Toxicol. Lett.	MAY 2	2004	150	3					301	316		10.1016/j.toxlet.2004.02.002		16	Toxicology	Toxicology	822CY	WOS:000221513600007	15110082	
J	Waser, M; Schierl, R; Von mutius, E; Maisch, S; Carr, D; Riedler, J; Eder, W; Schreuer, M; Nowak, D; Braun-Fahrlander, C				Waser, M; Schierl, R; Von mutius, E; Maisch, S; Carr, D; Riedler, J; Eder, W; Schreuer, M; Nowak, D; Braun-Fahrlander, C		ALEX Study Team	Determinants of endotoxin levels in living environments of farmers' children and their peers from rural areas	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergy; children; exposure assessment; farm animals and pets; farming; house and stable dust; indoor endotoxin; living room floor; mattress	IN-HOUSE DUST; HAY-FEVER; ALLERGIC SENSITIZATION; EXPOSURE; ASTHMA; ATOPY; CONTAMINANTS; PROTECT; LIFE; HOME	Background Lower frequencies of asthma and hayfever have been observed in children with contact to livestock. At school age, the amount of endotoxin measured in the dust of children's mattresses is inversely related to the occurrence of atopic asthma, hayfever and atopic sensitization both in children from farming and non-farming households. Objective The aim of the present study was to investigate which home and lifestyle characteristics of farm and non-farm families contribute to endotoxin levels measured in different indoor home environments. Methods In the framework of the Allergy and Endotoxin (ALEX) Study, endotoxin was measured in dust samples from the living room floor and the child's mattress of 319 farmers' families and 493 non-farming families, and in settled dust from stables. Endotoxin content of all dust samples was determined by a kinetic Limulus assay (Limulus-Amebocyte-Lysate test). Information about the child's activities on farms, home characteristics and cleaning behaviours was obtained from parental questionnaires. Results Endotoxin levels in stables did not predict the amount of endotoxin measured in floors or mattresses. However, a dose-dependent association between the child's activity on the farm and indoor home endotoxin levels was observed, both in farm and non-farm children. In non-farm children pet keeping and the frequency of floor cleaning were additionally associated with endotoxin levels, whereas in farm children parental farm activities, study area, time since last cleaning, the mattress type as well as younger age of the children contributed to increased microbial exposure. Conclusion These results demonstrate that regular contact to farm animals increases indoor home endotoxin concentrations, both in farm and non-farm children, and might thus explain the protective effect of contact to livestock on atopic outcomes. To assess children's individual exposure to a microbial environment, measures of mattress dust exposure are needed as stable endotoxin concentrations were not associated with indoor home levels.	Univ Basel, Inst Social & Prevent Med, Environm & Hlth Dept, CH-4051 Basel, Switzerland; Univ Munich, Inst Occupat & Environm Med, D-80539 Munich, Germany; Univ Munich, Dr Von Hauner Childrens Hosp, D-80539 Munich, Germany; Childrens Hosp Salzburg, Dept Paediat Pulmonol & Allergol, Salzburg, Austria; Salzburg Univ, Dept Sociol, A-5020 Salzburg, Austria	Waser, M (reprint author), Univ Basel, Inst Social & Prevent Med, Environm & Hlth Dept, Steinengraben 49, CH-4051 Basel, Switzerland.	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Exp. Allergy	MAR	2004	34	3					389	397		10.1111/j.1365-2222.2004.01873.x		9	Allergy; Immunology	Allergy; Immunology	801LY	WOS:000220098600011	15005732	
J	Green, RS; Smorodinsky, S; Kim, JJ; McLaughlin, R; Ostro, B				Green, RS; Smorodinsky, S; Kim, JJ; McLaughlin, R; Ostro, B			Proximity of California public schools to busy roads	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; children's health; environmental justice; ethnicity; schools; socioeconomic status; traffic	TRAFFIC DENSITY; AIR-POLLUTION; LOS-ANGELES; ENVIRONMENTAL JUSTICE; ULTRAFINE PARTICLES; CHILDHOOD-CANCER; MAJOR HIGHWAY; CHILDREN; ASTHMA; HEALTH	Residential proximity to busy roads has been associated with adverse health Outcomes, and school location may also be an important determinant of children's exposure to traffic-related pollutants. The goal of this study was to examine the characteristics of public schools (grades K-12) in California (n = 7,460) by proximity to major roads. We determined maximum daily traffic counts for all roads within 150 m of the school using a statewide road network and a geographic information system. Statewide, 173 schools (2.3%) with a total enrollment of 150,323 students were located within 150 m of high-traffic roads (greater than or equal to 50,000 vehides/day); 536 schools (7.2%) were within 150 m of medium-traffic roads (25,000-49,999 vehicles/day). Traffic exposure was related to race/ethnicity. For example, the overall percentage of nonwhite students was 78% at the schools located near high-traffic roads versus 60% at the schools with very low exposure (no streets with counted traffic data within 150 m). As the traffic exposure of schools increased, the percentage of both non-Hispanic black and Hispanic students attending the schools increased substantially. Traffic exposure was also related to school-based and census-tract-based socioeconomic indicators, including English language learners. The median percentage of children enrolled in free or reduced-price meal programs increased from 40.7% in the group with very low exposure to 60.5% in the highest exposure group. In summary, a substantial number of children in California attend schools dose to major roads with very high traffic counts, and a disproportionate number of those students are economically disadvantaged and nonwhite.	Off Environm Hlth Hazard Assessment, Calif Environm Protect Agcy, Oakland, CA 94612 USA; Environm Hlth Invest Branch, Calif Dept Hlth Serv, Oakland, CA USA	Ostro, B (reprint author), Off Environm Hlth Hazard Assessment, Calif Environm Protect Agcy, 1515 Clay St,16th Fl, Oakland, CA 94612 USA.	bostro@oehha.ca.gov					Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; *CAL AIR RES BOARD, 2003, AIR CLEAN DEV HOM; *CALT DIV TRANSP S, 1997, HIGHW PERF MON SYST; *CDE, 2000, DEM DAT FIL; Ciccone G, 1998, OCCUP ENVIRON MED, V55, P771; Delfino RJ, 2002, ENVIRON HEALTH PERSP, V110, P573; Duhme H, 1996, EPIDEMIOLOGY, V7, P578, DOI 10.1097/00001648-199611000-00003; EDWARDS J, 1994, ARCH ENVIRON HEALTH, V49, P223; English P, 1999, ENVIRON HEALTH PERSP, V107, P761, DOI 10.2307/3434663; FUNIER RB, 2003, J EXPO ANAL ENV EPID, V13, P240; Hitchins J, 2000, ATMOS ENVIRON, V34, P51, DOI 10.1016/S1352-2310(99)00304-0; Langholz B, 2002, ANN EPIDEMIOL, V12, P482, DOI 10.1016/S1047-2797(01)00317-9; Maantay J, 2002, ENVIRON HEALTH PERSP, V110, P161; Morello-Frosch R, 2002, ANN AM ACAD POLIT SS, V584, P47, DOI 10.1177/000271602237427; Morello-Frosch R, 2002, ENVIRON HEALTH PERSP, V110, P149; Pearson RL, 2000, J AIR WASTE MANAGE, V50, P175; Raaschou-Nielsen O, 2001, AM J EPIDEMIOL, V153, P433, DOI 10.1093/aje/153.5.433; Reynolds P, 2002, CANCER CAUSE CONTROL, V13, P665, DOI 10.1023/A:1019579430978; *SAN DIEG ASS GOV, 2001, LOC STREET DAIL VEH; SAVITZ DA, 1989, SCAND J WORK ENV HEA, V15, P360; Selvin S, 1996, STAT ANAL EPIDEMIOLO; *STAT CAL LEG COUN, 2003, OFF CAL LEG INF; *US CENS BUR, 2002, AM FACTF; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; Venn A, 2000, OCCUP ENVIRON MED, V57, P152, DOI 10.1136/oem.57.3.152; Venn AJ, 2001, AM J RESP CRIT CARE, V164, P2177, DOI 10.1164/rccm2106126; Weiland Stephan K., 1994, Annals of Epidemiology, V4, P243; Wilhelm M, 2003, ENVIRON HEALTH PERSP, V111, P207, DOI 10.1289/ehp.5688; WJST M, 1993, BRIT MED J, V307, P596; Zhu YF, 2002, J AIR WASTE MANAGE, V52, P1032; Zhu YF, 2002, ATMOS ENVIRON, V36, P4323, DOI 10.1016/S1352-2310(02)00354-0	31	75	75	1	11	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	JAN	2004	112	1					61	66		10.1289/ehp.6566		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	761NH	WOS:000187914500041	14698932	
J	Guerra, S; Lohman, IC; Halonen, M; Martinez, FD; Wright, AL				Guerra, S; Lohman, IC; Halonen, M; Martinez, FD; Wright, AL			Reduced interferon gamma production and soluble CD14 levels in early life predict recurrent wheezing by 1 year of age	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						wheezing; asthma; IFN gamma; CD14 antigen; LPS receptor	RESPIRATORY SYNCYTIAL VIRUS; HOUSE-DUST ENDOTOXIN; BLOOD MONONUCLEAR-CELLS; DAY-CARE ATTENDANCE; IFN-GAMMA; 1ST YEAR; PERIPHERAL-BLOOD; RISK FACTOR; ASTHMA; CHILDREN	It is unknown whether reduced production of IFNgamma in early life, before any lower respiratory tract illness, is a risk factor for recurrent wheezing in infancy. We followed 238 infants prospectively from birth to I year of age. At birth and at 3 months of age, IFNgamma production from polyclonally stimulated peripheral blood mononuclear cells and soluble CD14 (sCD14) levels in plasma were measured. The odds of developing recurrent wheezing (assessed by questionnaire) in the first year of life were up to 4.5 times higher for children in the lowest quartile of IFNgamma production at 3 months (p = 0.0005) and 3.2 times higher for children in the lowest quartile of sCD14 levels at birth (p = 0.004) as compared with children in the other 3 combined quartiles of IFNgamma and sCD14, respectively. Findings were confirmed in the multivariate analysis. IFNgamma production at 3 months and sCD14 levels at birth were correlated (r = 0.188, p = 0.031). Our findings from a longitudinal cohort suggest that impaired IFNgamma production at 3 months and reduced plasmasCD14 levels at birth significantly increase the risk of developing recurrent wheezing in the first year of life.	Univ Arizona, Arizona Resp Ctr, Coll Med, Tucson, AZ 85724 USA	Wright, AL (reprint author), Univ Arizona, Arizona Resp Ctr, Coll Med, 1501 N Campbell Ave,POB 245030, Tucson, AZ 85724 USA.				NHLBI NIH HHS [HL61892, HL67672]; NIAID NIH HHS [AI44697, AI42268]		Aberle JH, 1999, AM J RESP CRIT CARE, V160, P1263; Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Brown H, 1999, APPL MIXED MODELS ME; Dubin W, 1996, AM J PHYSIOL-LUNG C, V270, pL736; 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; Guerra S, 2002, ALLERGY, V57, P41; HALONEN M, 1992, AM REV RESPIR DIS, V146, P866; Halonen M, 1997, CLIN EXP ALLERGY, V27, P1234; Hoekstra MO, 1997, CLIN EXP ALLERGY, V27, P1254; Koning H, 1997, CYTOKINE, V9, P416, DOI 10.1006/cyto.1996.0184; Kuehni CE, 2001, LANCET, V357, P1821, DOI 10.1016/S0140-6736(00)04958-8; Kurt-Jones EA, 2000, NAT IMMUNOL, V1, P398, DOI 10.1038/80833; LANDMANN R, 1995, J INFECT DIS, V171, P639; Leech SC, 2000, ALLERGY, V55, P74, DOI 10.1034/j.1398-9995.2000.00222.x; Liao SY, 1996, CLIN EXP ALLERGY, V26, P397, DOI 10.1111/j.1365-2222.1996.tb00555.x; Lien E, 1998, BLOOD, V92, P2084; Litonjua AA, 2002, J ALLERGY CLIN IMMUN, V110, P736, DOI 10.1067/mai.2002.128948; Marbury MC, 1997, AM J RESP CRIT CARE, V155, P156; MARTINEZ FD, 1995, J ALLERGY CLIN IMMUN, V96, P652, DOI 10.1016/S0091-6749(95)70264-4; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; MARTINEZ FD, 1992, AM J EPIDEMIOL, V136, P1258; Martinez FD, 1999, LANCET S2, V354, pSII12; Nockher WA, 1999, J NEUROIMMUNOL, V101, P161, DOI 10.1016/S0165-5728(99)00141-1; Oddy WH, 2002, EUR RESPIR J, V19, P899, DOI 10.1183/09031936.02.00103602; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; 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; Roman M, 1997, AM J RESP CRIT CARE, V156, P190; Sears MR, 2000, CLIN CHEST MED, V21, P315, DOI 10.1016/S0272-5231(05)70269-0; Sherriff A, 2001, INT J EPIDEMIOL, V30, P1473, DOI 10.1093/ije/30.6.1473; TANG MLK, 1994, LANCET, V344, P983, DOI 10.1016/S0140-6736(94)91641-1; van Schaik SM, 2000, J MED VIROL, V62, P257, DOI 10.1002/1096-9071(200010)62:2<257::AID-JMV19>3.0.CO;2-M; van Schaik SM, 1999, J ALLERGY CLIN IMMUN, V103, P630, DOI 10.1016/S0091-6749(99)70235-6; WRIGHT AL, 1989, AM J EPIDEMIOL, V129, P1232	37	75	79	0	2	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	JAN 1	2004	169	1					70	76		10.1164/rccm.200304-499OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	757PK	WOS:000187570500016	14525803	
S	Walton, SF; Holt, DC; Currie, BJ; Kemp, DJ		Baker, JR; Muller, R; Rollinson, D		Walton, SF; Holt, DC; Currie, BJ; Kemp, DJ			Scabies: New future for a neglected disease	ADVANCES IN PARASITOLOGY, VOL 57	Advances in Parasitology		English	Review							HOUSE-DUST MITE; CROTAMITON 10-PERCENT CREAM; MITOCHONDRIAL-DNA SEQUENCES; CRUSTED NORWEGIAN SCABIES; IMMUNOSORBENT-ASSAY ELISA; TREATMENT AVAILABLE SOON; CDNA EXPRESSION LIBRARY; GROUP-III ALLERGEN; TEA-TREE OIL; SARCOPTES-SCABIEI	Scabies is a disease of global proportions in both human and animal populations, resulting from infestation of the skin with the "itch" mite Sarcoptes scabiei. Despite the availability of effective chemotherapy the intensely itching lesions engender significant morbidity primarily due to secondary sepsis and post-infective complications. Some patients experience an extreme form of the disease, crusted scabies, in which many hundreds of mites may infest the skin causing severe crusting and hyperkeratosis. Overcrowded living conditions and poverty have been identified as significant confounding factors in transmission of the mite in humans. Control is hindered by difficulties with diagnosis, the cost of treatment, evidence for emerging resistance and lack of effective vaccines. Historically research on scabies has been extremely limited because of the difficulty in obtaining sufficient quantities of the organism. Recent molecular approaches have enabled considerable advances in the study of population genetics and transmission dynamics of S. scabiei. However, the most exciting and promising development is the potential exploitation of newly available data from S. scabiei cDNA libraries and EST projects. Ultimately this knowledge may aid early identification of disease, novel forms of chemotherapy, vaccine development and new treatment possibilities for this important but neglected parasite.	Charles Darwin Univ, Menzies Sch Hlth Res, Darwin, NT 0811, Australia; Queensland Inst Med Res, Brisbane, Qld 4029, Australia; Australian Ctr Int & Trop Hlth & Nutr, Brisbane, Qld 4029, Australia; Univ Queensland, Brisbane, Qld 4029, Australia; Flinders Univ No Terr Clin Sch, Royal Darwin Hosp, Darwin, NT 0810, Australia	Walton, SF (reprint author), Charles Darwin Univ, Menzies Sch Hlth Res, Darwin, NT 0811, Australia.	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J	Vermaelen, K; Pauwels, R				Vermaelen, K; Pauwels, R			Accelerated airway dendritic cell maturation, trafficking, and elimination in a mouse model of asthma	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article							NECROSIS-FACTOR-ALPHA; CD4(+) T-CELLS; INHALED ANTIGEN; CLASS-II; IN-VIVO; ICOS; INFLAMMATION; RESPONSES; MICE; APOPTOSIS	Pulmonary dendritic cells (DC) can induce both tolerogenic as well as inflammatory immune responses in the lung. Conversely, little is known about the impact of ongoing airway inflammation on pulmonary DC biology. In noninflammatory conditions, expression of T cell costimulatory molecules on mouse airway DCs is low and only upregulated after homing into draining thoracic lymph nodes. In this study, we reveal that ongoing allergic airway inflammation induces a premature upregulation of the T cell costimulatory molecules CD40, B7-2 and intercellular adhesion molecule 1 on DCs still present in the airways. In contrast, high surface expression of inducible costimulator ligand, involved in respiratory tolerance induction is restricted to DCs from noninflamed lungs. In addition, during inflammation the migratory flux of allergen-transporting airway DCs toward draining thoracic nodes increases both in amplitude as well as in speed. Remarkably, migratory DCs from inflamed airways are short-lived in the draining lymph nodes, a finding that is temporally associated with a marked loss of the antiapoptotic protein Bcl-2 in these cells. This study demonstrates the profound effects of ongoing allergen-driven airway inflammation on the dynamics of pulmonary DC physiology, a knowledge that could be exploited in the development of novel DC-based immunotherapies.	State Univ Ghent Hosp, Dept Resp Dis, B-9000 Ghent, Belgium	Vermaelen, K (reprint author), State Univ Ghent Hosp, Dept Resp Dis, 7K12ie,De Pintelaan 185, B-9000 Ghent, Belgium.						Akbari O, 2002, NAT MED, V8, P1024, DOI 10.1038/nm745; AKHARI O, 2001, NAT IMMUNOL, V2, P725; Bjorck P, 1997, INT IMMUNOL, V9, P365, DOI 10.1093/intimm/9.3.365; BRUSSELLE G, 1995, AM J RESP CELL MOL, V12, P254; Cochand L, 1999, AM J RESP CELL MOL, V21, P547; Coyle AJ, 2000, IMMUNITY, V13, P95, DOI 10.1016/S1074-7613(00)00011-X; Cumberbatch M, 1999, ARCH DERMATOL RES, V291, P453, DOI 10.1007/s004030050437; Gajewska BU, 2001, AM J RESP CELL MOL, V25, P326; Gonzalo JA, 2001, NAT IMMUNOL, V2, P597, DOI 10.1038/89739; Granucci F, 2001, NAT IMMUNOL, V2, P882, DOI 10.1038/ni0901-882; Ingulli E, 1997, J EXP MED, V185, P2133, DOI 10.1084/jem.185.12.2133; Iwai H, 2002, J IMMUNOL, V169, P4332; Julia V, 2002, IMMUNITY, V16, P271, DOI 10.1016/S1074-7613(02)00276-5; Keatings VM, 1996, AM J RESP CRIT CARE, V153, P530; Kellermann SA, 1999, J IMMUNOL, V162, P3859; Krupa WM, 2002, AM J PATHOL, V161, P1815, DOI 10.1016/S0002-9440(10)64458-6; Lambrecht BN, 2000, J CLIN INVEST, V106, P551, DOI 10.1172/JCI8107; Lambrecht BN, 1998, J IMMUNOL, V160, P4090; Langenkamp A, 2002, EUR J IMMUNOL, V32, P2046, DOI 10.1002/1521-4141(200207)32:7<2046::AID-IMMU2046>3.0.CO;2-M; MACPHERSON GG, 1995, J IMMUNOL, V154, P1317; Matsue H, 1999, J IMMUNOL, V162, P5287; McLellan A, 2000, EUR J IMMUNOL, V30, P2612, DOI 10.1002/1521-4141(200009)30:9<2612::AID-IMMU2612>3.0.CO;2-G; Nopora A, 2002, J IMMUNOL, V169, P3006; PUGH CW, 1983, J EXP MED, V157, P1758, DOI 10.1084/jem.157.6.1758; SCHONHEGRAD MA, 1991, J EXP MED, V173, P1345, DOI 10.1084/jem.173.6.1345; Soumelis V, 2002, NAT IMMUNOL, V3, P673, DOI 10.1038/ni805; van Rijt LS, 2002, BLOOD, V100, P3663, DOI 10.1182/blood-2002-03-0673; Vermaelen KY, 2001, J EXP MED, V193, P51; Yoshinaga SK, 2000, INT IMMUNOL, V12, P1439, DOI 10.1093/intimm/12.10.1439; Yoshinaga SK, 1999, NATURE, V402, P827, DOI 10.1038/45582	30	75	78	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.	SEP	2003	29	3	1				405	409		10.1165/rcmb.2003-0008OC		5	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	717NE	WOS:000185095400016	12702544	
J	Lee, YL; Shaw, CK; Su, HJ; Lai, JS; Ko, YC; Huang, SL; Sung, FC; Guo, YL				Lee, YL; Shaw, CK; Su, HJ; Lai, JS; Ko, YC; Huang, SL; Sung, FC; Guo, YL			Climate, traffic-related air pollutants and allergic rhinitis prevalence in middle-school children in Taiwan	EUROPEAN RESPIRATORY JOURNAL			English	Article						air pollution; allergic rhinitis; children; climate; factor analysis	RESPIRATORY HEALTH; SUBTROPICAL CLIMATE; NITROGEN-DIOXIDE; HAY-FEVER; ASTHMA; SYMPTOMS; EPIDEMIOLOGY; ATOPY; POLLUTION; EXPOSURE	The prevalence of allergic rhinitis, a common respiratory disorder, may be rapidly increasing. Epidemiological studies, however, indicate little about its association with climatic factors and air pollution. The relationship between traffic-related air pollutants and allergic rhinitis in middle-school students was therefore investigated. In a nationwide survey of middle-school students in Taiwan conducted in 1995/1996, the lifetime prevalence of physician-diagnosed allergic rhinitis and typical symptoms of allergic rhinitis were compared with air-monitoring station data on temperature, relative humidity, sulphur dioxide (SO2), nitrogen oxides (NOx), ozone (03), carbon monoxide (CO) and particulate matter with a 50% cut-off aerodynamic diameter of 10 PM (PM10). A total of 331,686 nonsmoking children attended schools located within 2 km of 55 stations. Mean (range) annual exposures were: CO 853 (381-1,610) parts per billion (ppb), NOx 35.1 (10.2-72.4) ppb, SO2 7.57 (0.88-21.2) ppb, PM10 69.2 (40.1-116.2) mug.m(-3), O-3 21.3 (12.4-34.1) ppb, temperature 22.9 (19.6-25.1)degreesC, and relative humidity 76.2 (64.8-86.2)%. The prevalence of physician-diagnosed allergic rhinitis was 28.6 and 19.5% in males and females, respectively, with prevalence of questionnaire-determined allergic rhinitis 42.4 and 34.0%. After adjustment for age, parental education and history of atopic eczema, physician-diagnosed allergic rhinitis was found to be associated with higher nonsummer (September-May) warmth and traffic-related air pollutants, including CO, NOx and O-3. Questionnaire-determined allergic rhinitis correlated only with traffic-related air pollutants. Nonsummer warmth and traffic-related air pollution, probably mediated through exposure to common allergens such as dust mites, are possible risk factors for allergic rhinitis in middle-school-aged children.	Natl Cheng Kung Univ, Dept Environm & Occupat Hlth, Tainan 704, Taiwan; Natl Cheng Kung Univ, Dept Internal Med, Tainan 704, Taiwan; Natl Cheng Kung Univ, Inst Basic Med Sci, Tainan 704, Taiwan; Tzu Chi Univ, Dept Publ Hlth, Hualien, Taiwan; China Med Coll, Dept Occupat Safety & Hlth, Taichung, Taiwan; Kaohsiung Med Univ, Dept Publ Hlth, Kaohsiung, Taiwan; Natl Yang Ming Univ, Inst Environm Hlth Sci, Taipei 112, Taiwan; Natl Taiwan Univ, Inst Environm Hlth, Taipei 10764, Taiwan	Guo, YL (reprint author), Natl Cheng Kung Univ, Dept Environm & Occupat Hlth, 138 Sheng Li Rd, Tainan 704, Taiwan.		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Resp. J.	JUN	2003	21	6					964	970		10.1183/09031936.03.00094602		7	Respiratory System	Respiratory System	685CH	WOS:000183242900010	12797489	
J	Ravindra, K; Mor, S; Kaushik, CP				Ravindra, K; Mor, S; Kaushik, CP			Short-term variation in air quality associated with firework events: A case study	JOURNAL OF ENVIRONMENTAL MONITORING			English	Article							SULFUR-DIOXIDE; AMBIENT AIR; HOSPITAL ADMISSIONS; DAILY MORTALITY; LUNG-FUNCTION; POLLUTION; EXPOSURE; CHILDREN; BIRMINGHAM; ASTHMA	The effect of fireworks on air quality as assessed from the ambient concentrations of various air pollutants (SO2, NO2, PM10 and TSP) during Diwali festival in Hisar city (India). in November 1999, The extensive use of fireworks as found to be related to short-term variation in air quality. During the festival the concentration of SO2 was observed to be increased similar to 10-fold at few sites. whereas the concentrations of NO2, PM10 and TSP increased 2-3 times. compared to the data collected on a typical winter day in December 1999. The maximum NO2 concentration was observed a day after the festival. The diurnal pattern of the above pollutants showed a slight increase in the night. The levels of these Pollutants observed during Diwali were found to be moderately high, which can be associated with. serious health impacts.	Guru Jambheshwar Univ, Dept Environm Sci & Engn, Hisar 125001, Haryana, India	Ravindra, K (reprint author), Univ Antwerp, Dept Chem, Micro & Trace Anal Ctr, Univ Pl 1, B-2610 Antwerp, Belgium.						Ackermann-Liebrich U., 1999, AIR POLLUTION HLTH, P559; *AM THOR SOC COMM, 1996, AM J RESP CRIT CARE, V131, P133; Attri AK, 2001, NATURE, V411, P1015, DOI 10.1038/35082634; Babu SS, 2001, CURR SCI INDIA, V81, P1208; BACH W, 1975, INT J ENVIRON STUD, V7, P183, DOI 10.1080/00207237508709692; Bakke B, 2001, SCAND J WORK ENV HEA, V27, P250; BALMES JR, 1987, AM REV RESPIR DIS, V136, P1117; BATES DV, 1987, ENVIRON RES, V43, P317, DOI 10.1016/S0013-9351(87)80032-4; Bates DV, 1995, SCAND J WORK ENV HEA, V21, P405; Bates DV, 1996, THORAX, V51, pS3, DOI 10.1136/thx.51.Suppl_2.S3; Becker JM, 2000, ANN ALLERG ASTHMA IM, V85, P512; BRUNEKREEF B, 1995, ENVIRON HEALTH PERSP, V103, P3, DOI 10.2307/3432443; Bull MJ, 2001, PEDIATRICS, V108, P190; Carranza JE, 2001, SPECTROCHIM ACTA B, V56, P851, DOI 10.1016/S0584-8547(01)00183-5; *CENTR POLL CONTR, 2000, NAT AMB QUAL STAT IN; CHAUHAN AJ, 1998, REV ENV HLTH, V13, P91; Clark H, 1997, ATMOS ENVIRON, V31, P2893, DOI 10.1016/S1352-2310(97)88278-7; DOCKERY DW, 1992, ENVIRON RES, V59, P362, DOI 10.1016/S0013-9351(05)80042-8; DOCKERY DW, 1993, NEW ENGL J MED, V329, P1753, DOI 10.1056/NEJM199312093292401; Dyke P, 1997, CHEMOSPHERE, V34, P1191, DOI 10.1016/S0045-6535(97)00418-9; Fischer P, 2001, EPIDEMIOLOGY, V12, pS98; Fleischer O, 1999, CHEMOSPHERE, V39, P925, DOI 10.1016/S0045-6535(99)00019-3; Gong H, 1995, TOXICOL IND HEALTH, V11, P467; Hoek G, 1998, EUR RESPIR J, V11, P1307, DOI 10.1183/09031936.98.11061307; HOLMES HH, 1983, ENCY AM, V11, P263; Lodge Jr J. P., 1989, METHODS AIR SAMPLING, P403; Michie CA, 2000, PEDIATR RES, V47, p479A; PONKA A, 1994, ENVIRON RES, V65, P207, DOI 10.1006/enrs.1994.1032; POPE CA, 1992, ARCH ENVIRON HEALTH, V47, P211; Ravindra K, 2001, REV ENV HLTH, V16, P169; RAVINDRA K, 1999, THESIS GJ U HISAR; Schindler C, 1998, EPIDEMIOLOGY, V9, P405, DOI 10.1097/00001648-199807000-00010; SCHWARTZ J, 1993, AM J EPIDEMIOL, V137, P1136; Schwela D, 2000, Rev Environ Health, V15, P13; SEATON A, 1995, LANCET, V345, P176, DOI 10.1016/S0140-6736(95)90173-6; SUKUMAR A, 1992, SCI TOTAL ENVIRON, V114, P161, DOI 10.1016/0048-9697(92)90422-O; TAKIGUCHI SA, 2000, CRIT CARE MED, V28, P527; WALTERS S, 1994, THORAX, V49, P133, DOI 10.1136/thx.49.2.133; *WHO, 1999, WHO REG PUBL EUR SER, V23; World Health Organization (WHO), 1987, WHO REG PUBL EUR SER, V23; WHO, 2000, GUID AIR QUAL; World Health Organization, 1997, ENV HLTH CRIT, V188	42	75	82	0	19	ROYAL SOC CHEMISTRY	CAMBRIDGE	THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS, ENGLAND	1464-0325			J ENVIRON MONITOR	J. Environ. Monit.	APR	2003	5	2					260	264		10.1039/b211943a		5	Chemistry, Analytical; Environmental Sciences	Chemistry; Environmental Sciences & Ecology	670DT	WOS:000182392700020	12729265	
J	Yoshida, Y; Sakaguchi, H; Ito, Y; Okuda, M; Suzuki, H				Yoshida, Y; Sakaguchi, H; Ito, Y; Okuda, M; Suzuki, H			Evaluation of the skin sensitization potential of chemicals using expression of co-stimulatory molecules, CD54 and CD86, on the naive THP-1 cell line	TOXICOLOGY IN VITRO			English	Article						CD54; CD86; THP-1 cell line; in vitro sensitization test	EPIDERMAL LANGERHANS CELLS; VITRO PRIMARY SENSITIZATION; HUMAN DENDRITIC CELLS; IN-VITRO; T-CELLS; CONTACT SENSITIVITY; MESSENGER-RNA; HAPTENS; PHENOTYPE; INDUCTION	It has been known that dendritic cells (DCs) including Langerhans cells (LCs) play a critical role in the skin sensitization process. Many attempts have been made to develop in vitro sensitization tests that employ DCs derived from peripheral blood mononuclear cells (PBMC-DC) or CD34 + hematopoietic progenitor cells (CD34 + HPC) purified from cord blood or bone marrow. However, the use of the DCs in in vitro methods has been difficult due to the nature of these cells such as low levels in the source and/or donor-to-donor variability. In our studies, we employed the human monocytic leukemia cell line, THP-1, in order to avoid some of these difficulties. At the start, we examined whether treatment of the cells with various cytokines could produce DCs from THP-1. Treatment of THP-1 cells with cytokines such as GM-CSF, IL-4, TNF-alpha, and/or PMA did induce some phenotypic changes in THP-1 cells that were characteristic of DCs. Subsequently, responses to a known sensitizer, dinitrochlorobenzene (DNCB), and a non-sensitizer, dimethyl sulfoxide (DMSO) or sodium lauryl sulfate (SLS), on the expression of co-stimulatory molecules, CD54 and CD86, were examined between the naive cells and the cytokine-treated cells. Interestingly, the naive THP-1 cells responded only to DNCB and the response to the sensitizer was more distinct than cytokine-treated THP-1 cells. Similar phenomena were also observed in the human myeloid leukemia cell line, KG-l. Furthermore, with treatment of DNCB, naive THP-1 cells showed augmented expression of HLA, CD80 and secretion of IL-1beta. The response of THP-1 cells to a sensitizer was similar to that of LCs/DCs. Upon demonstrating the differentiation of monocyte cells in our system, we then evaluated a series of chemicals, including known sensitizers and non-sensitizers, for their potential to augment CD54 and CD86 expression on naive THP-1 cells. Indeed, known sensitizers such as PPD and 2-MBT significantly augmented CD54 and CD86 expression in a dose-dependent manner while non-sensitizers, such as SLS and methyl salicylate (MS), did not. To note, the metal allergens such as (NH4)(2)[PtCl4], NiSO4 and CoSO4 augmented significantly only CD54 expression. Taking advantage of a cultured cell line, measurement of the co-stimulatory molecules, CD54 and CD86, on naive THP-1 cells following chemical exposure shows promise for the development of a simple, short-term in vitro sensitization test. (C) 2003 Elsevier Science Ltd. All rights reserved.	Kao Corp, Safety & Microbial Control Res Ctr, Tochigi 3213497, Japan	Yoshida, Y (reprint author), Kao Corp, Safety & Microbial Control Res Ctr, 2606 Akabane Ichikai Machi Haga Gun, Tochigi 3213497, Japan.						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Vitro	APR	2003	17	2					221	228		10.1016/S0887-2333(03)00006-7		8	Toxicology	Toxicology	665YY	WOS:000182149900012	12650676	
J	Bottcher, MF; Bjorksten, B; Gustafson, S; Voor, T; Jenmalm, MC				Bottcher, MF; Bjorksten, B; Gustafson, S; Voor, T; Jenmalm, MC			Endotoxin levels in Estonian and Swedish house dust and atopy in infancy	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						atopy; childhood; endotoxin	HAY-FEVER; BACTERIAL LIPOPOLYSACCHARIDE; ALLERGIC SENSITIZATION; RESPIRATORY SYMPTOMS; CELL-DEVELOPMENT; ASTHMA; EXPOSURE; PREVALENCE; CHILDREN; ECZEMA	Background Immune responses, including those to allergens, may be T helper (Th)2 skewed in newborns. In order to redress the fetal Th1/Th2 imbalance, Th1-stimulating factors, such as bacterial endotoxin, may be required. The increasing prevalence and severity of atopic diseases in industrialized countries, which are in marked contrast with the low prevalence of allergy among children in the formerly socialist countries of Europe, have been suggested to be caused by a reduced microbial stimulation. Aim To relate the endotoxin levels in house dust from two countries with a low (Estonia) and a high (Sweden) prevalence of allergy to the development of atopic disease and sensitization in the children during the first 2 years of life. Methods The study included 108 children from Tartu, Estonia and 111 children from Linkoping, Sweden. Skin prick tests were performed at 3, 6, 12 and 24 months of age, and questionnaires were distributed to the families. At 24 months, a paediatrician examined the children. Dust samples were collected from mattresses and carpets and the endotoxin concentration was determined by a chromogenic Limulus assay. Results The endotoxin levels were higher in Estonian than in Swedish house dust (median levels 29 (range 0.25-280) and 14 (range 0.25-99) EU/mg dust, respectively, P < 0.001). Furthermore, the levels were inversely related to the development of atopic disease and sensitization in the Swedish, but not in the Estonian, children. Conclusions The low prevalence of atopic disease in Estonia may, at least in part, be related to the high endotoxin levels in this country. The findings support that high levels of endotoxin, or other bacterial products with Th1-stimulating properties, might protect children from developing atopic disease.	Linkoping Univ, Dept Mol & Clin Med, Div Paediat, S-58183 Linkoping, Sweden; Linkoping Univ, Fac Hlth Sci, Clin Res Ctr, S-58183 Linkoping, Sweden; Karolinska Inst, Ctr Allergy Res, Stockholm, Sweden; Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; Tartu Univ Clin, Childrens Clin, Tartu, Estonia	Bottcher, MF (reprint author), Linkoping Univ Hosp, Div Paediat, S-58185 Linkoping, Sweden.		Jenmalm, Maria/C-9679-2009	Jenmalm, Maria/0000-0002-2117-5366			ABERG N, 1995, CLIN EXP ALLERGY, V25, P815, DOI 10.1111/j.1365-2222.1995.tb00023.x; Adkins P, 2001, J IMMUNOL, V166, P918; Bjorksten B, 1998, EUR RESPIR J, V12, P432, DOI 10.1183/09031936.98.12020432; BRABACK L, 1995, ARCH DIS CHILD, V72, P487; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; BURR M L, 1989, Archives of Disease in Childhood, V64, P1452; Butland BK, 1997, BRIT MED J, V315, P717; Corinti S, 2001, J IMMUNOL, V166, P4312; Eldridge MW, 2000, J ALLERGY CLIN IMMUN, V105, P475, DOI 10.1067/mai.2000.104552; Ernst P, 2000, AM J RESP CRIT CARE, V161, P1563; 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; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; HOLT PG, 1995, PEDIATR ALLERGY IMMU, V6, P1, DOI 10.1111/j.1399-3038.1995.tb00250.x; Johnson CC, 2000, J ALLERGY CLIN IMMUN, V105, pS80, DOI 10.1016/S0091-6749(00)90673-0; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Koulis A, 2000, CLIN EXP ALLERGY, V30, P747; MANETTI R, 1993, J EXP MED, V177, P1199, DOI 10.1084/jem.177.4.1199; Matricardi PM, 2000, BRIT MED J, V320, P412, DOI 10.1136/bmj.320.7232.412; Matricardi PM, 2000, CLIN EXP ALLERGY, V30, P1506, DOI 10.1046/j.1365-2222.2000.00994.x; Prescott SL, 1998, J IMMUNOL, V160, P4730; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Riikjarv MA, 2000, EUR RESPIR J, V16, P86, DOI 10.1034/j.1399-3003.2000.16a15.x; Rogge L, 1998, J IMMUNOL, V161, P6567; Roost HP, 1999, J ALLERGY CLIN IMMUN, V104, P941, DOI 10.1016/S0091-6749(99)70072-2; 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; VONMUTIUS E, 1992, BRIT MED J, V305, P1395; Yang LP, 1995, EUR J IMMUNOL, V25, P3517, DOI 10.1002/eji.1830251247	32	75	76	0	0	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	MAR	2003	33	3					295	300		10.1046/j.1365-2222.2003.01562.x		6	Allergy; Immunology	Allergy; Immunology	651QA	WOS:000181330600006	12614441	
J	Hovell, MF; Meltzer, SB; Wahlgren, DR; Matt, GE; Hofstetter, R; Jones, JA; Meltzer, EO; Bernert, JT; Pirkle, JL				Hovell, MF; Meltzer, SB; Wahlgren, DR; Matt, GE; Hofstetter, R; Jones, JA; Meltzer, EO; Bernert, JT; Pirkle, JL			Asthma management and environmental tobacco smoke exposure reduction in Latino children: A controlled trial	PEDIATRICS			English	Article						environmental tobacco smoke; passive smoking; coaching; Latino; women; children; asthma; cotinine	PASSIVE SMOKING; SOCIOECONOMIC-FACTORS; YOUNG-CHILDREN; RELIABILITY; COTININE; INCOME; CALIFORNIA; VALIDITY; HEALTH; HOSPITALIZATION	Objectives. This study tested the efficacy of coaching to reduce environmental tobacco smoke (ETS) exposure among asthmatic Latino children. Design. After asthma management education, families were randomly assigned to no additional service (control condition) or to coaching for ETS exposure reduction (experimental condition). Setting. The study was conducted in San Diego, California. Participants. Two hundred four Latino children (ages 3-17 years) with asthma participated. Intervention. Approximately 1.5 hours of asthma management education was provided; experimental families also obtained 7 coaching sessions (similar to45 minutes each) to reduce ETS exposure. Outcome Measures. Reported ETS exposure and children's urine cotinine were measured. Results. Parents in the coached condition reported their children exposed to significantly fewer cigarettes than parents of control children by 4 months (postcoaching). Reported prevalence of exposed children decreased to 52% for the coached families, but only to 69% for controls. By month 4, mean cotinine levels decreased among coached and increased among control children. Cotinine prevalence decreased from 54% to 40% among coached families, while it increased from 43% to 49% among controls. However, cotinine levels decreased among controls to the same level achieved by coached families by the 13-month follow-up. Conclusions. Asthma management education plus coaching can reduce ETS exposure more than expected from education alone, and decreases in the coached condition may be sustained for about a year. The delayed decrease in cotinine among controls is discussed.	San Diego State Univ, Grad Sch Publ Hlth, Ctr Behav Epidemiol & Community Hlth, San Diego, CA 92182 USA; San Diego State Univ, Dept Psychol, San Diego, CA 92182 USA; San Diego State Univ, Dept Polit Sci, San Diego, CA 92182 USA; Allergy & Asthma Med Grp & Res Ctr, San Diego, CA USA; Ctr Dis Control & Prevent, Div Sci Lab, Natl Ctr Environm Hlth, Atlanta, GA USA	Hovell, MF (reprint author), C-BEACH,9245 Sky Pk Ct,Suite 230, San Diego, CA 92123 USA.				NHLBI NIH HHS [HL52835, R01 HL052835]		ADAMS EK, COSTS ENV TOBACCO SM; ANDERSEN RM, 1986, PUBLIC HEALTH REP, V101, P238; Benowitz NL, 1996, EPIDEMIOL REV, V18, P188; BERMAN BA, IN PRESS ADDICT BEHA; Bernert JT, 1997, CLIN CHEM, V43, P2281; Brown E. 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A., 1996, FINDING SOLUTIONS SO; MURRAY DM, 1987, ADDICT BEHAV, V12, P7, DOI 10.1016/0306-4603(87)90003-7; *NAT COAL HISP HLT, 1996, OTOLARYNGOL HEAD NEC, V114, P256; National Health and Medical Research Council, 1997, HLTH EFF PASS SMOK; National Institutes of Health, 1995, NIH PUBL, V95-2754; Pirkle JL, 1996, JAMA-J AM MED ASSOC, V275, P1233; Ray NF, 1998, CHEST, V113, P1277, DOI 10.1378/chest.113.5.1277; SCHAUFFLER H, 1999, STATE HLTH INSURANCE; Schmier JK, 1998, J ASTHMA, V35, P585, DOI 10.3109/02770909809048961; SOBELL MB, 1986, ADDICT BEHAV, V11, P149, DOI 10.1016/0306-4603(86)90040-7; SOLIS JM, 1990, AM J PUBLIC HEALTH, V80, P11, DOI 10.2105/AJPH.80.Suppl.11; *STAT CA DEP FIN, 1998, COUNT POP PROJ AG SE; Stata Statistical Software, 2000, STAT STAT SOFTW REL; Traynor MP, 1996, J HEALTH POLIT POLIC, V21, P543, DOI 10.1215/03616878-21-3-543; *US CDCP, 1997, MMWR-MORBID MORTAL W, V46, P1038; US Census Bureau, CENS 2000 DAT STAT C; *US DHHS, 2000, STRAT RES PLAN RED U; *US DHHS, 1993, NIH PUBL; U.S. Environmental Protection Agency, 1992, EPA PUBL; Wahlgren DR, 1997, CHEST, V111, P81, DOI 10.1378/chest.111.1.81; Weinhardt LS, 1998, ANN BEHAV MED, V20, P25, DOI 10.1007/BF02893805; World Health Organization, 2000, WHO REG PUBL EUR SER, V91; World Health Organization, 1999, INT CONS ENV TOB SMO; Wilson SR, 2001, CHEST, V120, P1709, DOI 10.1378/chest.120.5.1709; WOOD PR, 1993, PEDIATRICS, V91, P62; 1999, PHYS SMOK FREE CAN O	68	75	77	1	4	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	NOV	2002	110	5					946	956		10.1542/peds.110.5.946		11	Pediatrics	Pediatrics	610QK	WOS:000178971800030	12415035	
J	Bernstein, DI; Cartier, A; Cote, J; Malo, JL; Boulet, LP; Wanner, M; Milot, J; L'Archeveque, J; Trudeau, C; Lummus, Z				Bernstein, DI; Cartier, A; Cote, J; Malo, JL; Boulet, LP; Wanner, M; Milot, J; L'Archeveque, J; Trudeau, C; Lummus, Z			Diisocyanate antigen-stimulated monocyte chemoattractant protein-1 synthesis has greater test efficiency than specific antibodies for identification of diisocyanate asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						occupational asthma; diisocyanate; MCP-1; antibody	HISTAMINE-RELEASING FACTORS; INDUCED OCCUPATIONAL ASTHMA; HUMAN SERUM-ALBUMIN; HEXAMETHYLENE DIISOCYANATE; DIPHENYLMETHANE DIISOCYANATE; IMMUNE-RESPONSES; EXPOSURE; ISOCYANATES; WORKERS; REACTIVITY	We previously reported that diisocyanate-human serum albumin (DIISO-HSA) stimulated production of monocyte chemoattractant protein-1 (MCP-1) by peripheral blood mononuclear cells is significantly associated with a clinical diagnosis of diisocyanate asthma (DA). Others have reported that antibodies for DIISO-HSA are specific but insensitive markers of DA. This study was performed to evaluate test characteristics of the in vitro MCP-1 assay compared with DIISO-HSA-specific immunoglobulin (Ig) G and IgE in identifying workers with DA. MCPA was quantitated in peripheral blood mononuclear cell supernatants 48 hours after incubation with DIISO-HSA antigens. Assay results were compared with outcomes of specific inhalation challenge (SIC) testing. Nineteen of 54 (35%) workers assayed for antibodies and MCPA stimulation had SIC-confirmed DA. Mean MCP-1 produced by SIC-positive workers was greater than SIC-negative workers (p less than or equal to 0.001). Diagnostic sensitivity, specificity, and test efficiency for specific IgG were 47%, 74%, and 65%, respectively, and for specific IgE were 21%, 89%, and 65%, respectively. Sensitivity, specificity, and test efficiency of the MCPA test were 79%, 91%, and 87%, respectively. This study indicates that the MCP-1 stimulation assay has greater sensitivity and specificity than the specific antibody assays in correctly identifying DA.	Univ Cincinnati, Coll Med, Dept Internal Med, Div Immunol, Cincinnati, OH 45267 USA; Hop Sacre Coeur, Lab Pneumol Res, Montreal, PQ H4J 1C5, Canada; Univ Laval, Hop Laval, Inst Cardiol & Pneumol, St Foy, PQ G1K 7P4, Canada	Bernstein, DI (reprint author), Univ Cincinnati, Coll Med, Dept Internal Med, Div Immunol, 231 Albert Sabin Way, Cincinnati, OH 45267 USA.				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J. Respir. Crit. Care Med.	AUG 15	2002	166	4					445	450		10.1164/rccm.2109018		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	584BE	WOS:000177446700006	12186818	
J	Rasmussen, F; Taylor, DR; Flanneryb, EM; Cowan, JO; Greene, JM; Herbison, GP; Sears, MR				Rasmussen, F; Taylor, DR; Flanneryb, EM; Cowan, JO; Greene, JM; Herbison, GP; Sears, MR			Risk factors for hospital admission for asthma from childhood to young adulthood: A longitudinal population study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; hospital admission; risk factors; allergy; longitudinal population study; epidemiology	HOUSE-DUST MITE; BRONCHIAL HYPERRESPONSIVENESS; INDOOR ALLERGENS; ECONOMIC BURDEN; SCHOOL ABSENCE; CHILDREN; EMERGENCY; SENSITIZATION; PREVALENCE; EXPOSURE	Background: Predictors of hospital admissions for asthma in children and young adults in a general population are not well defined, because most studies have used selected subpopulations. Objective: The purpose of this investigation was to determine risk factors for single and multiple hospital admissions for asthma. Methods: The members of a population-based, unselected birth cohort of 1037 New Zealanders answered questionnaires and underwent lung function, airway responsiveness, and allergy testing on 7 occasions to the age of 26 years. Results: Among the 766 study members (74% of the cohort) who reported wheezing symptoms ever by the age of 26 years, 136 hospitalizations were reported by 62 individuals (8.3% of those at risk, 6.2% of the total cohort). Only 55 of these 136 admissions involved children less than 9 years of age; admissions continued to occur between the ages of 9 and 18 years (40 admissions) and at >18 years (41 admissions). Those admitted were predominantly male, had earlier ages of onset of symptoms, were more atopic, and had more airway hyperresponsiveness to methacholine than those not admitted. Frequent symptoms and low lung function were evident among the 45 study members with single admissions and even more evident among the 17 study members with multiple (2-10) admissions. Conclusions: A surprisingly large fraction of this unselected population experienced hospitalization for asthma during the 26-year follow-up, many being admitted in later childhood, adolescence, and early adulthood. Clinical characteristics and markers of severity, including frequent respiratory symptoms, airway hyperresponsiveness, atopy, and low lung function, identify those at high risk for hospitalization for asthma, particularly with respect to multiple admissions.	St Josephs Healthcare, Firestone Inst Respiratory Hlth, Hamilton, ON L8N 4A6, Canada; Univ Otago, Dunedin Sch Med, Dept Prevent & Social Med, Dunedin, New Zealand; Univ Otago, Dunedin Sch Med, Dept Med, Dunedin, New Zealand; McMaster Univ, Hamilton, ON, Canada	Sears, MR (reprint author), St Josephs Healthcare, Firestone Inst Respiratory Hlth, 50 Charlton Ave E, Hamilton, ON L8N 4A6, Canada.						ANDERSON HR, 1989, THORAX, V44, P614, DOI 10.1136/thx.44.8.614; ANDERSON HR, 1983, ARCH DIS CHILD, V58, P777; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Blais L, 1998, THORAX, V53, P1025; CAMPBELL DA, 1995, THORAX, V50, P254, DOI 10.1136/thx.50.3.254; CHAI H, 1975, J ALLERGY CLIN IMMUN, V56, P323, DOI 10.1016/0091-6749(75)90107-4; Clough JB, 1998, CLIN EXP ALLERGY, V28, P22; DALES RE, 1995, THORAX, V50, P520, DOI 10.1136/thx.50.5.520; EISNER MD, 2000, RESPIR RES, V2, P53; ELLEY WB, 1976, NEW ZEAL J EDUC STUD, V11, P25; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; Gergen PJ, 2001, J ALLERGY CLIN IMMUN, V107, pS445, DOI 10.1067/mai.2001.114992; JENKINS MA, 1994, BRIT MED J, V309, P90; LI D, 1995, AM J RESP CRIT CARE, V151, P647; Lozano P, 1999, J ALLERGY CLIN IMMUN, V104, P957; MILES J, 1995, CLIN EXP ALLERGY, V25, P1074; Newacheck PW, 2000, ARCH PEDIAT ADOL MED, V154, P287; OSWALD H, 1994, BRIT MED J, V309, P95; PATTEMORE PK, 1990, AM REV RESPIR DIS, V142, P549; POLLART SM, 1989, J ALLERGY CLIN IMMUN, V83, P875, DOI 10.1016/0091-6749(89)90100-0; Rabbat A, 1996, INTENS CARE MED, V22, P530; Ray NF, 1998, CHEST, V113, P1277, DOI 10.1378/chest.113.5.1277; Sarpong SB, 1997, ANN ALLERG ASTHMA IM, V79, P455; Schaubel D, 1996, J ASTHMA, V33, P97, DOI 10.3109/02770909609054537; SEARS MR, 1993, CLIN EXP ALLERGY, V23, P941, DOI 10.1111/j.1365-2222.1993.tb00279.x; SEARS MR, 1986, THORAX, V41, P283, DOI 10.1136/thx.41.4.283; SEARS MR, 1989, CLIN EXP ALLERGY, V19, P419, DOI 10.1111/j.1365-2222.1989.tb02408.x; Singh AK, 1999, ARCH INTERN MED, V159, P1237, DOI 10.1001/archinte.159.11.1237; SKOBELOFF EM, 1992, JAMA-J AM MED ASSOC, V268, P3437, DOI 10.1001/jama.268.24.3437; Smith DH, 1997, AM J RESP CRIT CARE, V156, P787; Spee-van der Wekke J, 1998, J EPIDEMIOL COMMUN H, V52, P359; SPITZER WO, 1992, NEW ENGL J MED, V326, P501, DOI 10.1056/NEJM199202203260801; SPORIK R, 1993, CLIN EXP ALLERGY, V23, P740, DOI 10.1111/j.1365-2222.1993.tb00361.x; SPRINGETT VH, 1969, BMJ-BRIT MED J, V1, P402; *STAT CAN CAN I HL, 82570XIE STAT CAN CA; *US DEP HHS, 1991, 9150212 PHS US DEP H; WEISS KB, 1992, NEW ENGL J MED, V326, P862, DOI 10.1056/NEJM199203263261304	37	75	79	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.	AUG	2002	110	2					220	227	UNSP 1/81/125295	10.1067/mai.2002.125295		8	Allergy; Immunology	Allergy; Immunology	585DY	WOS:000177509800005	12170261	
J	Bengtsson, AA; Rylander, L; Hagmar, L; Nived, O; Sturfelt, G				Bengtsson, AA; Rylander, L; Hagmar, L; Nived, O; Sturfelt, G			Risk factors for developing systemic lupus erythematosus: a case-control study in southern Sweden	RHEUMATOLOGY			English	Article						SLE; risk factors; smoking; alcohol; drug allergy; hypertension; family history	ORAL-CONTRACEPTIVES; DEFINED POPULATION; DISEASE; HISTORY; THERAPY; STRESS	Objective. To explore the risk factors that have been suggested to be associated with the development of SLE. Methods. A case-control study was performed and a questionnaire was developed to obtain the data. Consecutive female incident cases diagnosed between 1981 and 1999 in a defined,geographical area in southern Sweden were included. Controls, matched for calendar year of birth, were selected randomly from the same area. In total, 85 cases and 205 controls agreed to participate. The questionnaire included questions about formal education, body weight and height, medical history, family history of autoimmune diseases, exposure to ultraviolet radiation, animals, hair-colouring dyes, alfalfa (lucerne) sprouts, smoking and alcohol habits, history of physical traumata, blood transfusion, silicone breast implants, exogenous oestrogens, other medication, and significant negative life events. Results. Using a multivariate model, a history of hypertension [odds ratio (OR)=3.7, 95% confidence interval (CI) 1.4-9.8], drug allergy (OR=3.6, 95% CI 1.4-9.5), a type I/II sun-reactive Skin type (OR=2.3, 95% CI 1.1-4.8) and a family history of SLE (OR=6.8, 95% CI 1.4-32) were all significantly associated with an increased risk of developing SLE, whereas consumption of alcohol was inversely associated with the risk of SLE (use of alcohol very seldom, OR=1.0; 1-150 g/month, OR=0.4, 95% CI 0.2-1.0; > 150 g/month, OR=0.2, 95% CI 0.1-0.5). A suggested association with increased SLE risk was seen for smoking (OR=1.8, 95% CI 0.9-3.6) and blood transfusions (OR=23, 95% CI 0.9-5.8). Neither exposure to exogenous oestrogen nor exposure to hair-colouring dyes was associated with SLE. Conclusions. Risk factors of both exogenous and endogenous origin were identified in this population-based series of SLE patients.	Univ Lund Hosp, Dept Rheumatol, S-22185 Lund, Sweden; Univ Lund Hosp, Dept Occupat & Environm Med, S-22185 Lund, Sweden	Bengtsson, AA (reprint author), Univ Lund Hosp, Dept Rheumatol, S-22185 Lund, Sweden.						ADAMS LE, 1991, DRUG SAFETY, V6, P431; Cooper GS, 1998, ARTHRITIS RHEUM, V41, P1714, DOI 10.1002/1529-0131(199810)41:10<1714::AID-ART3>3.0.CO;2-U; FITZPATRICK TB, 1988, ARCH DERMATOL, V124, P869, DOI 10.1001/archderm.124.6.869; FRENITITULAER LWJ, 1989, AM J EPIDEMIOL, V130, P404; FRITZLER MJ, 1994, LUPUS, V3, P455, DOI 10.1177/096120339400300605; GEIRSSON AJ, 1987, ANN RHEUM DIS, V46, P727, DOI 10.1136/ard.46.10.727; GINSBURG KS, 1992, ARTHRITIS RHEUM, V35, P776, DOI 10.1002/art.1780350711; GRIMES DA, 1985, AM J OBSTET GYNECOL, V153, P179; Hardy CJ, 1999, LUPUS, V8, P541, DOI 10.1191/096120399678840800; Hardy CJ, 1998, ANN RHEUM DIS, V57, P451, DOI 10.1136/ard.57.8.451; Hosmer DW, 1989, APPL LOGISTIC REGRES; JONES DRE, 1992, LANCET, V339, P1378, DOI 10.1016/0140-6736(92)91197-G; JONSSON H, 1990, BRIT J RHEUMATOL, V29, P185; JONSSON H, 1989, MEDICINE, V68, P141; MALINOW MR, 1981, LANCET, V1, P615; Manzi S, 2000, RHEUMATOLOGY, V39, P353, DOI 10.1093/rheumatology/39.4.353; MCALINDON T, 2000, ARTHRITIS RHEUM, V43, P237; MCALINDON T, 1997, ARTHRITIS RHEUM, V40, P162; Meier CR, 1998, J RHEUMATOL, V25, P1515; NAGATA C, 1995, INT J DERMATOL, V34, P333, DOI 10.1111/j.1365-4362.1995.tb03614.x; NIVED O, 1992, J INTERN MED, V232, P461; Panush RS, 2000, J RHEUMATOL, V27, P287; PETRI M, 1992, ARTHRITIS RHEUM, V35, P625, DOI 10.1002/art.1780350605; REIDENBERG MM, 1993, ARTHRITIS RHEUM, V36, P971, DOI 10.1002/art.1780360714; REIDENBERG MM, 1983, AM J MED, V75, P365, DOI 10.1016/0002-9343(83)91219-6; REIDENBERG MM, 1983, AM J MED, V75, P1037, DOI 10.1016/0002-9343(83)90885-9; SanchezGuerrero J, 1997, ARTHRITIS RHEUM, V40, P804, DOI 10.1002/art.1780400505; SANCHEZGUERRERO J, 1995, ANN INTERN MED, V122, P430; SanchezGuerrero J, 1996, ARTHRITIS RHEUM, V39, P657, DOI 10.1002/art.1780390418; SCHWARTZ RS, 1975, NEW ENGL J MED, V293, P132; Sontheimer RD, 1996, PHOTOCHEM PHOTOBIOL, V63, P583, DOI 10.1111/j.1751-1097.1996.tb05660.x; STROM BL, 1994, AM J EPIDEMIOL, V140, P632; STURFELT G, 1985, CLIN EXP RHEUMATOL, V3, P303; THERNLUND GM, 1995, DIABETES CARE, V18, P1323, DOI 10.2337/diacare.18.10.1323; WALLACE DJ, 1994, BAILLIERE CLIN RHEUM, V8, P149, DOI 10.1016/S0950-3579(05)80229-8; WINSA B, 1991, LANCET, V338, P1475, DOI 10.1016/0140-6736(91)92298-G	36	75	81	0	4	OXFORD UNIV PRESS	OXFORD	GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND	1462-0324			RHEUMATOLOGY	RHEUMATOLOGY	MAY	2002	41	5					563	571		10.1093/rheumatology/41.5.563		9	Rheumatology	Rheumatology	555QQ	WOS:000175805100015	12011382	
J	Kosunen, TU; Hook-Nikanne, J; Salomaa, A; Sarna, S; Aromaa, A; Haahtela, T				Kosunen, TU; Hook-Nikanne, J; Salomaa, A; Sarna, S; Aromaa, A; Haahtela, T			Increase of allergen-specific immunoglobulin E antibodies from 1973 to 1994 in a Finnish population and a possible relationship to Helicobacter pylori infections	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article; Proceedings Paper	12th International Workshop on Gastroduodenal Pathology and Helicobacter Pylori	SEP, 1999	HELSINKI, FINLAND			allergy; allergen-specific IgE; atopy; Helicobacter pylori antibodies; prevalence rates	ADULT-POPULATION; ATOPY; IGE; PREVALENCE; CHILDREN; ASTHMA; VACCINATION; ADOLESCENTS; EXPOSURE; COHORT	Background The prevalence of atopic diseases - hayfever, asthma and eczema - has increased over the past decades. The increase may be associated with decreased rates of infections such as measles., hepatitis A, tuberculosis, toxoplasmosis, and, as recently suggested, Helicobacter pylori gastritis. Objective Since the increase of atopy has been mainly based on clinical studies. we wanted to study the prevalence of allergen-specific Immunoglobulin (Ig)E antibodies in two cross-sectional, adult population-based serum samples two decades apart. Since the sera had been tested for H. pylori antibodies, we also had a chance to look for a possible relationship between these two findings. Methods We determined the prevalence rate of allergen-specific serum IgE antibodies against birch and timothy pollen, and cat and dog epithelium allergens by the radioallergosorbent test in a 15-54-years-old Finnish population using 326 sera collected in 1973 and 319 sera collected in 1994 from randomly selected subjects. Results From 1973 to 1994 allergen-specific IgE prevalence rates and IgE antibody levels rose. In 1994, the prevalence rate of positive findings in 15-24-year-old population had increased from I I to 38% (3.5-fold increase, P=0.0001, OR 5.12, Cl 95% 2.32-11.3). In older 10-year age groups similar trends did not reach significance, but the overall change was significant with all three cut-off levels of allergen-specific IgE analysed. The percentage of IgE-positive persons rose mainly in the subgroup with no H. pylori antibodies. In 1994 21% of the H. pylori-negative subjects had IgE antibodies compared with 5% of the H. pylori-positive subjects (in 1973 11% in both subgroups). Conclusions IgE-based evidence for an increase in IgE-mediated allergy was uncovered. The increase occurred mainly in the subgroup with no antibodies to H. pylori, which support the hypothesis that H, pylori could be one of the microbes counteracting atopy.	Univ Helsinki, Dept Bacteriol & Immunol, Haartman Inst, FIN-00014 Helsinki, Finland; Univ Helsinki, Cent Hosp, Div Allergy, Helsinki, Finland; Vammala Hlth Ctr, Vammala, Finland; Univ Helsinki, Dept Publ Hlth, Helsinki, Finland; Social Insurance Inst, Helsinki, Finland; Natl Publ Hlth Inst, Helsinki, Finland	Kosunen, TU (reprint author), Univ Helsinki, Dept Bacteriol & Immunol, Haartman Inst, POB 21, FIN-00014 Helsinki, Finland.			Sarna, Seppo/0000-0003-3458-1627			Alm JS, 1997, LANCET, V350, P400, DOI 10.1016/S0140-6736(97)02207-1; BARBEE RA, 1987, J ALLERGY CLIN IMMUN, V79, P919, DOI 10.1016/0091-6749(87)90241-7; Bodner C, 2000, THORAX, V55, P383, DOI 10.1136/thorax.55.5.383; *CENTR STAT OFF FI, 1975, STAT YB FINL 1974; *CENTR STAT OFF FI, 1995, STAT YB FINL 1994; *CYT SOFTW CORP, 1998, STATX 4 STAT SOFTW; Gassner M, 1992, Schweiz Rundsch Med Prax, V81, P426; HAAHTELA T, 1990, BRIT MED J, V301, P266; HAAHTELA T, 1980, ALLERGY, V35, P425, DOI 10.1111/j.1398-9995.1980.tb01789.x; Henderson CE, 1998, J IMMUNOL METHODS, V213, P99, DOI 10.1016/S0022-1759(98)00014-3; Henderson J, 1999, BRIT MED J, V318, P1173; Howarth PH, 1998, CLIN EXP ALLERGY, V28, P2; Kosunen TU, 1997, EPIDEMIOL INFECT, V119, P29, DOI 10.1017/S0950268897007565; Linneberg A, 2000, J ALLERGY CLIN IMMUN, V106, P247, DOI 10.1067/mai.2000.108312; Matricardi PM, 2000, BRIT MED J, V320, P412, DOI 10.1136/bmj.320.7232.412; Matricardi PM, 1997, BRIT MED J, V314, P999; NAKAGOMI T, 1994, LANCET, V343, P121, DOI 10.1016/S0140-6736(94)90854-0; Paganelli R, 1998, ALLERGY, V53, P763; POHJANPELTO P, 1984, SCAND J INFECT DIS, V16, P229, DOI 10.3109/00365548409070394; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; Rehnberg-Laiho L, 1998, PEDIATR INFECT DIS J, V17, P796, DOI 10.1097/00006454-199809000-00009; Shaheen S, 1997, BRIT MED J, V314, P987; 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, 1989, BRIT MED J, V299, P1259; Talley Nicholas J., 1993, P63; von Hertzen L, 1999, J ALLERGY CLIN IMMUN, V104, P1211	27	75	78	0	0	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	MAR	2002	32	3					373	378		10.1046/j.1365-2222.2002.01330.x		6	Allergy; Immunology	Allergy; Immunology	541QB	WOS:000174994300010	11940066	
J	Lack, G				Lack, G			Pediatric allergic rhinitis and comorbid disorders	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergic rhinitis; asthma; cough variant rhinitis; postnasal drip; sinusitis	INTERCELLULAR-ADHESION MOLECULE-1; EUSTACHIAN-TUBE OBSTRUCTION; NASAL EPITHELIAL-CELLS; OTITIS-MEDIA; POLLEN EXPOSURE; DOSE-RESPONSE; ASTHMA; CHILDREN; CHALLENGE; HISTAMINE	Allergic rhinitis (AR) is rarely found in isolation and needs to be considered in the context of systemic allergic disease associated with numerous comorbid disorders, including asthma, chronic middle ear effusions, sinusitis, lymphoid hypertrophy with obstructive sleep apnea, disordered sleep, and consequent behavioral and educational effects. The coexistence of AR and asthma is complex. First, the diagnosis of asthma may be confounded by symptoms of cough caused by rhinitis and postnasal drip. This may lead to either inaccurate diagnosis of asthma or inappropriate assessment of asthma severity with over treatment of the patient. The term "cough variant rhinitis" is therefore proposed to describe rhinitis that manifests itself primarily as cough that results from postnasal drip. AR, however, also has a causal role in asthma; it appears both to be responsible for exacerbating asthma and to have a role in its pathogenesis. Postnasal drip with nasopharyngeal inflammation leads to a number of other conditions. Thus sinusitis is a frequent extension of rhinitis and is one of the most frequently missed diagnoses In children. Allergen exposure in the nasopharynx with release of histamine and other mediators can cause Eustachian tube obstruction possibly leading to middle car effusions. Chronic allergic inflammation of the upper airway causes lymphoid hypertrophy with prominence of adenoidal and tonsillar tissue. This may be associated with poor appetite, poor growth, and obstructive sleep apnea. AR is therefore part of a spectrum of allergic disorders that can profoundly affect the well being and quality of life of a child. Prospective cohort studies are required to assess the disease burden caused by AR in childhood and to further assess the potential educational impairment that may result. Because AR is part of a systemic disease process, its management requires a coordinated approach rather than a fragmented, organ-based approach.	St Marys Hosp, Dept Pediat Allergy & Immunol, London W2 1NY, England	Lack, G (reprint author), St Marys Hosp, Dept Pediat Allergy & Immunol, Praed St, London W2 1NY, England.						BAKER BM, 1982, ANN OTO RHINOL LARYN, V91, P277; Baram Y, 1998, NEURAL PROCESS LETT, V8, P1, DOI 10.1023/A:1009611427303; BAROODY FM, 1995, ARCH OTOLARYNGOL, V121, P1396; Bernstein JM, 1996, OTOLARYNG HEAD NECK, V114, P562, DOI 10.1016/S0194-5998(96)70247-4; BLUESTONE CD, 1983, J ALLERGY CLIN IMMUN, V72, P242, DOI 10.1016/0091-6749(83)90027-1; CAUWENBERGE PV, 1997, EUR RESPIR REV, V7, P286; CIPRANDI G, 1994, AM J RESP CRIT CARE, V150, P1653; Ciprandi G, 1995, J ALLERGY CLIN IMMUN, V96, P971, DOI 10.1016/S0091-6749(95)70235-0; CIPRANDI G, 1994, J ALLERGY CLIN IMMUN, V94, P738, DOI 10.1016/0091-6749(94)90182-1; COREY JP, 1994, AM J OTOLARYNG, V15, P138, DOI 10.1016/0196-0709(94)90063-9; Craig TJ, 1998, J ALLERGY CLIN IMMUN, V101, P633; DOYLE WJ, 1990, J ALLERGY CLIN IMMUN, V86, P924, DOI 10.1016/S0091-6749(05)80156-3; Faniran AO, 1998, ARCH DIS CHILD, V79, P411; FRIEDMAN RA, 1983, J ALLERGY CLIN IMMUN, V71, P442, DOI 10.1016/0091-6749(83)90459-1; GAMBLE J E, 1992, Ear Nose and Throat Journal, V71, P397; HANNAWAY PJ, 1982, JAMA-J AM MED ASSOC, V247, P206, DOI 10.1001/jama.247.2.206; IRVIN CG, 1992, J ALLERGY CLIN IMMUN, V90, P521, DOI 10.1016/0091-6749(92)90179-6; KATO M, 1995, CLIN EXP ALLERGY, V25, P744, DOI 10.1111/j.1365-2222.1995.tb00012.x; KAUFMAN J, 1969, AM REV RESPIR DIS, V100, P626; KNIGHT LC, 1992, CLIN OTOLARYNGOL, V17, P308, DOI 10.1111/j.1365-2273.1992.tb01002.x; Koskela H, 1995, EUR RESPIR J, V8, P2088, DOI 10.1183/09031936.95.08122088; Matsuzaki Z, 1996, IMMUNOLOGY, V88, P565, DOI 10.1046/j.1365-2567.1996.d01-687.x; McColley SA, 1997, CHEST, V111, P170, DOI 10.1378/chest.111.1.170; MIGLETS A, 1973, LARYNGOSCOPE, V83, P1355, DOI 10.1288/00005537-197309000-00001; Mogi G, 1992, Acta Otolaryngol Suppl, V493, P155; MONTEFORT S, 1992, AM J RESP CELL MOL, V7, P393; MULLARKEY MF, 1980, J ALLERGY CLIN IMMUN, V65, P122, DOI 10.1016/0091-6749(80)90196-7; OSUR SL, 1989, ALLERGY PROC, V10, P133, DOI 10.2500/108854189778961071; RACHELEFSKY GS, 1978, J ALLERGY CLIN IMMUN, V61, P310, DOI 10.1016/0091-6749(78)90052-0; SETTIPANE RJ, 1994, ALLERGY PROC, V15, P21, DOI 10.2500/108854194778816634; SHAPIRO GG, 1985, PEDIATR INFECT DIS J, V4, P55; SIBBALD B, 1991, THORAX, V46, P895, DOI 10.1136/thx.46.12.895; SKONER DP, 1986, ARCH OTOLARYNGOL, V112, P840; SKONER DP, 1987, J ALLERGY CLIN IMMUN, V79, P27, DOI 10.1016/S0091-6749(87)80012-X; SKONER DP, 1991, ANN ALLERGY, V67, P619; VUURMAN EFPM, 1993, ANN ALLERGY, V71, P121; WATSON WTA, 1993, J ALLERGY CLIN IMMUN, V91, P97, DOI 10.1016/0091-6749(93)90301-U; WRIGHT AL, 1994, PEDIATRICS, V94, P895; Yumoto E, 1991, Nihon Jibiinkoka Gakkai Kaiho, V94, P534	39	75	78	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.	JUL	2001	108	1		S			S9	S15		10.1067/mai.2001.115562		7	Allergy; Immunology	Allergy; Immunology	459BU	WOS:000170230600003	11449201	
J	Mari, A				Mari, A			Multiple pollen sensitization: A molecular approach to the diagnosis	INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY			English	Article						asthma; IgE; pollens; recombinant allergens; skin tests	REACTIVE CARBOHYDRATE DETERMINANTS; IN-VITRO DIAGNOSTICS; BIRCH POLLEN; BRONCHIAL HYPERRESPONSIVENESS; ALLERGIC DISEASES; MAJOR ALLERGEN; IGE-BINDING; TREE POLLEN; IDENTIFICATION; IMMUNOTHERAPY	Background: Sensitization to multiple pollen species is a frequent diagnostic event. Several allergenic molecules with a high level of homology have been identified in divergent pollen families and named panallergens. Methods: We sought to define the criteria to evaluate the prevalence of the multiple pollen sensitization, to identify specific markers of this condition, and to correlate them with the underlying allergic disease. Patients presenting an allergic respiratory disease underwent skin testing with 23 pollens. Patients fulfilling predefined selection criteria were grouped and classified as having multiple pollen sensitization. Patients in each subgroup were tested for IgE to rBet v 2, rJun o 2, rBet v 1, rPhl p 5 and bromelain. Demographical, allergological and clinical data were recorded in the subgroup of patients with multiple pollen sensitization. Results: Seventeen percent of the pollen-sensitized patients formed the multiple pollen-sensitized subgroup. These subjects were positive for most of the pollen species tested regardless of known exposure to them. None of the subjects sensitized to less than six pollen species were positive to panallergens, whereas 55% of the sera of the multiple pollen-sensitized group were positive to rBet v 2, and 15% to rJun o 2. IgE to rBet v 1 and rPhl p 5 were found positive in all the subgroups. Age, gender, bronchial asthma, oral allergy syndrome, skin test reactivity and previous specific immunotherapy differed significantly when these two subsets were considered. Conclusions: Allergy diagnosis based on allergenic molecules is crucial in the patient with multiple pollen sensitization. This condition appears to be determined by the sensitization to defined allergenic components (panallergens) rather than by pollen of multiple species as such. Detection of IgE to nonpanallergenic molecules allows to identify more relevant allergenic sources. Clinical aspects of the underlying allergic disease (e.g. asthma and oral allergy syndrome) seem to be differently related to IgE reactivity to panallergens. Ccpyright (C) 2001 S. Karger AG, Basel	Natl Hlth Serv, Allergy Unit, Rome, Italy	Mari, A (reprint author), Via Malipiero 28, I-04100 Latina, Italy.						Aalberse RC, 1997, CLIN REV ALLERG IMMU, V15, P375, DOI 10.1007/BF02737733; BARLETTA B, 2000, J ALLERGY CLIN IMMUN, V105, pS36; Batanero E, 1999, J ALLERGY CLIN IMMUN, V103, P147, DOI 10.1016/S0091-6749(99)70538-5; BRITTON WJ, 1986, INT J EPIDEMIOL, V15, P202, DOI 10.1093/ije/15.2.202; BURROWS B, 1989, NEW ENGL J MED, V320, P271, DOI 10.1056/NEJM198902023200502; DAmato G, 1991, ALLERGENIC POLLEN PO; Elfman L, 1997, INT ARCH ALLERGY IMM, V113, P249; Fritsch R, 1997, CLIN REV ALLERG IMMU, V15, P397, DOI 10.1007/BF02737735; Heiss S, 1996, J ALLERGY CLIN IMMUN, V98, P938, DOI 10.1016/S0091-6749(96)80010-8; Hirschwehr R, 1998, J ALLERGY CLIN IMMUN, V101, P196; Hoffmann-Sommergruber K, 1999, CLIN EXP ALLERGY, V29, P840, DOI 10.1046/j.1365-2222.1999.00529.x; Karamloo F, 1999, J ALLERGY CLIN IMMUN, V104, P991, DOI 10.1016/S0091-6749(99)70080-1; LAFFER S, 1994, J ALLERGY CLIN IMMUN, V94, P689, DOI 10.1016/0091-6749(94)90176-7; Liebers V, 1996, CLIN EXP ALLERGY, V26, P494, DOI 10.1046/j.1365-2222.1996.d01-343.x; Malling HJ, 1993, ALLERGY          S14, V48, P55; Mari A, 1999, J ALLERGY CLIN IMMUN, V103, P1005, DOI 10.1016/S0091-6749(99)70171-5; Mari A, 1996, J ALLERGY CLIN IMMUN, V98, P21, DOI 10.1016/S0091-6749(96)70222-1; Niederberger V, 1998, J ALLERGY CLIN IMMUN, V101, P258; Niederberger V, 1998, J ALLERGY CLIN IMMUN, V102, P579, DOI 10.1016/S0091-6749(98)70273-8; *NIH NAT HEAT LUNG, 1995, 953659 NIH NHLBIWHO; PASTORELLO EA, 1997, FOOD ALLERGY ADVERSE, P137; PEAT JK, 1992, EUR RESPIR J, V5, P921; Pignatti S., 1982, FLORA ITALIA; Schafer T, 1997, ALLERGY, V52, P14; Solomon W, 1998, ALLERGY PRINCIPLES P, P367; Stewart GA, 1996, CLIN EXP ALLERGY, V26, P1020, DOI 10.1046/j.1365-2222.1996.d01-405.x; Tinghino R, 1998, J ALLERGY CLIN IMMUN, V101, P772, DOI 10.1016/S0091-6749(98)70306-9; Tutin T. G., 1980, FLORA EUROPEA; VALENTA R, 1992, J EXP MED, V175, P377, DOI 10.1084/jem.175.2.377; VALENTA R, 1991, SCIENCE, V253, P557, DOI 10.1126/science.1857985; Valenta R, 1999, CLIN EXP ALLERGY, V29, P896; Valenta R, 1998, INT ARCH ALLERGY IMM, V117, P160, DOI 10.1159/000024005; van Ree R, 1998, J ALLERGY CLIN IMMUN, V102, P184, DOI 10.1016/S0091-6749(98)70084-3; van Ree R, 1999, CLIN EXP ALLERGY, V29, P848, DOI 10.1046/j.1365-2222.1999.00521.x; vanderVeen MJ, 1997, J ALLERGY CLIN IMMUN, V100, P327, DOI 10.1016/S0091-6749(97)70245-8; vanRee R, 1996, ALLERGY, V51, P108; Varela S, 1997, J ALLERGY CLIN IMMUN, V100, P748, DOI 10.1016/S0091-6749(97)70268-9	37	75	77	0	0	KARGER	BASEL	ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND	1018-2438			INT ARCH ALLERGY IMM	Int. Arch. Allergy Immunol.	MAY	2001	125	1					57	65		10.1159/000053797		9	Allergy; Immunology	Allergy; Immunology	437CQ	WOS:000168973000008	11385289	
J	Bayram, H; Sapsford, RJ; Abdelaziz, MM; Khair, OA				Bayram, H; Sapsford, RJ; Abdelaziz, MM; Khair, OA			Effect of ozone and nitrogen dioxide on the release of proinflammatory mediators from bronchial epithelial cells of nonatopic nonasthmatic subjects and atopic asthmatic patients in vitro	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						atopic asthma; ozone; nitrogen dioxide; bronchial epithelial cells; cytokines; soluble intercellular adhesion molecule 1	INFLAMMATORY MEDIATORS; INHALED ALLERGEN; AIR-POLLUTION; IN-VITRO; RESPONSES; CYTOKINES	Background: Although studies have suggested that ozone (O-3) and nitrogen dioxide (NO2) may play a role in the pathogenesis of asthma, the underlying mechanisms are not clear. Objective: We aimed to investigate the effects of O-3 and NO2 on the release of IL-8, GM-CSF, RANTES, and soluble intercellular adhesion molecule 1 (sICAM-1) from human bronchial epithelial cells (HBF,Cs) of nonatopic nonasthmatic subjects (nonasthmatic subjects) and atopic subjects with mild asthma (asthmatic subjects) in vitro. Methods: We cultured HBECs from bronchial biopsy specimens of nonasthmatic and asthmatic subjects; exposed these for 6 hours to air, 10 to 100 ppb O-3, or 100 to 400 ppb NO2; and analyzed the release of IL-8, GM-CSF, RANTES, and sICAM-1 after 24 hours' incubation. Results: There was no significant difference between the constitutive release of IL-8, GM-CSF; and sICAM-1 from HBECs of asthmatic and nonasthmatic subjects, RANTES was detected only in HBECs derived from asthmatic subjects. Exposure of HBECs of asthmatic subjects to both 50 to 100 ppb O-3 and 200 to 400 ppb NO2 significantly increased the release of IL-8, GM-CSF, RANTES, and sICAM-1 from these cells after 24 hours of incubation. However, 50 to 100 ppb O-3 and 200 to 400 ppb NO2 led to a significant increase in release of only IL-8 and sICAM-1 from HBECs of nonasthmatic subjects after 24 hours' incubation. A comparison between the pollutant-induced release of mediators demonstrated that 100 ppb O-3. induced release of GM-CSF and sICAM-1 was significantly greater in HBECs of asthmatic subjects (medians, 0.59 and 27.4 pg/mug cellular protein, respectively) than in HBECs of nonasthmatic subjects (medians, 0.27 and 14.4 pg/mug cellular protein, respectively; P<.02). Conclusion: These results suggest that O-3 and NO2 may modulate airway diseases, such as asthma, by increasing the release of inflammatory mediators from bronchial epithelial cells and that the cells of asthmatic subjects may be more susceptible to the adverse effects of these pollutants.	Univ Dicle, Sch Med, Dept Resp Med, TR-21280 Diyarbakir, Turkey; St Bartholomews & Royal London Sch Med & Dent, Acad Resp Med Dept, London, England; Royal Liverpool Univ Hosp, Dept Resp Med, Liverpool, Merseyside, England; City Hosp NHS Trust, Birmingham, W Midlands, England	Bayram, H (reprint author), Univ Dicle, Sch Med, Dept Resp Med, TR-21280 Diyarbakir, Turkey.						Atkinson RW, 1999, EUR RESPIR J, V13, P257, DOI 10.1183/09031936.99.13225799; Balmes J. R., 1997, RES REP HLTH EFF I, V78, P1; Bayram H, 1998, J ALLERGY CLIN IMMUN, V102, P771, DOI 10.1016/S0091-6749(98)70017-X; Bayram H, 1999, J ALLERGY CLIN IMMUN, V104, P93, DOI 10.1016/S0091-6749(99)70119-3; Bloemen PGM, 1997, CLIN EXP ALLERGY, V27, P128; Borish L, 1996, J ALLERGY CLIN IMMUN, V97, P719, DOI 10.1016/S0091-6749(96)80146-1; BOUSQUET J, 1990, NEW ENGL J MED, V323, P1033, DOI 10.1056/NEJM199010113231505; Calderon MA, 1997, J ALLERGY CLIN IMMUN, V99, P65, DOI 10.1016/S0091-6749(97)81046-9; DEVALIA JL, 1993, AM J RESP CELL MOL, V9, P271; DEVALIA JL, 1990, RESP MED, V84, P303, DOI 10.1016/S0954-6111(08)80058-3; DEVALIA JL, 1994, LANCET, V344, P1668, DOI 10.1016/S0140-6736(94)90458-8; DEVLIN RB, 1994, AM J PHYSIOL, V266, pL612; Devlin RB, 1999, INHAL TOXICOL, V11, P89, DOI 10.1080/089583799197195; DEVLIN RB, 1991, AM J RESP CELL MOL, V4, P72; Gormand F, 1995, PULM PHARMACOL, V8, P107, DOI 10.1006/pulp.1995.1013; Hakonarson H, 1998, J CLIN INVEST, V102, P1732, DOI 10.1172/JCI4141; HURD SZ, 1991, J ALLERGY CLIN IMMUN, V88, P808; JORRES R, 1995, EUR RESPIR J, V8, P416, DOI 10.1183/09031936.95.08030416; LOWRY OH, 1951, J BIOL CHEM, V193, P265; MOLFINO NA, 1991, LANCET, V338, P199, DOI 10.1016/0140-6736(91)90346-Q; Peden DB, 1997, J ALLERGY CLIN IMMUN, V100, P802, DOI 10.1016/S0091-6749(97)70277-X; Peters JM, 1999, AM J RESP CRIT CARE, V159, P768; Rusznak C, 1996, EUR RESPIR J, V9, P2296; Scannell C, 1996, AM J RESP CRIT CARE, V154, P24; SPRINGER TA, 1990, NATURE, V346, P425, DOI 10.1038/346425a0; TAKAHASHI N, 1994, AM J RESP CRIT CARE, V150, P704; TUNNICLIFFE WS, 1994, LANCET, V344, P1733, DOI 10.1016/S0140-6736(94)92886-X; Wang JH, 1997, EUR RESPIR J, V10, P834	28	75	79	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.	FEB	2001	107	2					287	294		10.1067/mai.2001.111141		8	Allergy; Immunology	Allergy; Immunology	403YV	WOS:000167071400015	11174195	
J	Wisnewski, AV; Srivastava, R; Herick, C; Xu, L; Lemus, R; Cain, H; Magoski, NM; Karol, MH; Bottomly, K; Redlich, CA				Wisnewski, AV; Srivastava, R; Herick, C; Xu, L; Lemus, R; Cain, H; Magoski, NM; Karol, MH; Bottomly, K; Redlich, CA			Identification of human lung and skin proteins conjugated with hexamethylene diisocyanate in vitro and in vivo	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							GLUCOSE-REGULATED PROTEIN; OCCUPATIONAL ASTHMA; GUINEA-PIGS; ISOCYANATE; EXPOSURE; ADDUCTS; IGE; ASSOCIATION; EXPRESSION; ANTIBODIES	Diiisocyanates are asthma-causing chemicals used in the commercial production of polyurethane. We have previously shown that human lung epithelial cell proteins can become conjugated with hexamethylene diisocyanate (HDI) and may be biologically important in diisocyanate-induced asthma. The objective of this study was to identify specific human lung and skin proteins that become conjugated with diisocyanate after in vitro and in vivo exposure. Following in vitro exposure of human airway epithelial cells (A549), keratin 18, the 78-kD glucose-regulated protein, trans-1,2-dihyrobenzene-1,2-diol dehydrogenase, and actin were identified as prominent diisocyanate-conjugated proteins through use of a combination of immunocytochemical and mass spectrometric techniques. Following in vivo inhalation of an HDI aerosol, keratin 18 was also identified as the predominant diisocyanate-conjugated protein in human endobronchial biopsy samples, whereas albumin was the predominant diisocyanate-conjugated protein in bronchoalveolar lavage fluid. Keratin was also identified as a predominant diisocyanate-conjugated protein in human skin biopsy samples after epicutaneous exposure to liquid-phase HDI, although the major skin diisocyanate-conjugated protein (56-kD) differed from the predominant lung diisocyanate-conjugated keratin (47-kD). The data from this study identify keratin and other proteins as potential "carriers" for diisocyanates in vivo, and suggest that HDI conjugation of these proteins may play a role in the pathogenesis of diisocyanate-induced asthma.	Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06520 USA; Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT 06520 USA; Univ Pittsburgh, Dept Environm & Occupat Hlth, Pittsburgh, PA USA	Wisnewski, AV (reprint author), Yale Univ, Sch Med, Dept Internal Med, 333 Cedar St,LCI-105, New Haven, CT 06520 USA.				NHLBI NIH HHS [K08HL03129, P01HL56389, R01 HL062622, R01 HL062622-01, R01 HL062622-02, R01HL62622]		AVERY SB, 1969, CLIN EXP IMMUNOL, V4, P585; BAUR X, 1983, J ALLERGY CLIN IMMUN, V71, P197, DOI 10.1016/0091-6749(83)90100-8; Bernstein JA, 1997, J ALLERGY CLIN IMMUN, V99, P245, DOI 10.1016/S0091-6749(97)70104-0; BERTORELLI G, 1998, CLIN EXP ALLERGY, V28, P527; BUTCHER BT, 1982, J ALLERGY CLIN IMMUN, V69, pS123; CARTIER A, 1989, J ALLERGY CLIN IMMUN, V84, P507, DOI 10.1016/0091-6749(89)90364-3; Cullinan P, 1998, CLIN EXP ALLERGY, V28, P668; Day BW, 1997, CHEM RES TOXICOL, V10, P424, DOI 10.1021/tx960201+; ELLGARD L, 1999, SCIENCE, V286, P1805; HENDERSHOT LM, 1988, MOL CELL BIOL, V8, P4250; Jamora C, 1996, P NATL ACAD SCI USA, V93, P7690, DOI 10.1073/pnas.93.15.7690; JIN RZ, 1993, CHEM RES TOXICOL, V6, P906, DOI 10.1021/tx00036a023; KAROL MH, 1994, AM J RESP CRIT CARE, V149, P611; KENNEDY AL, 1993, FUND APPL TOXICOL, V20, P57, DOI 10.1006/faat.1993.1007; Lange RM, 1999, TOXICOL SCI, V50, P64, DOI 10.1093/toxsci/50.1.64; Liao JA, 1997, FEBS LETT, V417, P316, DOI 10.1016/S0014-5793(97)01315-X; Magin TM, 1998, J CELL BIOL, V140, P1441, DOI 10.1083/jcb.140.6.1441; Malo JL, 1999, AM J RESP CRIT CARE, V159, P1879; MOLOWA DT, 1986, J BIOL CHEM, V261, P2624; MYER HE, 1993, AM IND HYG ASSOC J, V54, P663, DOI 10.1202/0002-8894(1993)054<0663:ASOAHH>2.0.CO;2; Rao KS, 1996, CELL BIOL INT, V20, P261; RATTRAY NJ, 1994, TOXICOLOGY, V88, P15, DOI 10.1016/0300-483X(94)90108-2; Redlich CA, 1997, SCAND J WORK ENV HEA, V23, P227; SEPAI O, 1995, CARCINOGENESIS, V16, P2583, DOI 10.1093/carcin/16.10.2583; Shiraishi H, 1998, BIOCHEM J, V334, P399; Shiraishi H, 1999, ADV EXP MED BIOL, V463, P539; TYNER AL, 1985, P NATL ACAD SCI USA, V82, P4683, DOI 10.1073/pnas.82.14.4683; Ulrich H., 1996, CHEM TECHNOLOGY ISOC; WASS U, 1989, J ALLERGY CLIN IMMUN, V83, P126, DOI 10.1016/0091-6749(89)90487-9; Wisnewski AV, 1999, J ALLERGY CLIN IMMUN, V104, P341, DOI 10.1016/S0091-6749(99)70377-5	30	75	77	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.	DEC	2000	162	6					2330	2336				7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	381ZV	WOS:000165794700061	11112159	
J	Pinkerton, KE; Green, FHY; Saiki, C; Vallyathan, V; Plopper, CG; Gopal, V; Hung, D; Bahne, EB; Lin, SS; Menache, MG; Schenker, MB				Pinkerton, KE; Green, FHY; Saiki, C; Vallyathan, V; Plopper, CG; Gopal, V; Hung, D; Bahne, EB; Lin, SS; Menache, MG; Schenker, MB			Distribution of particulate matter and tissue remodeling in the human lung	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; California; fibrosis; lung pathology; PM2.5; PM10; particulate matter; pigmentation	SAN-JOAQUIN VALLEY; SMALL AIRWAYS; CIGARETTE-SMOKING; DISEASES; PNEUMOCONIOSIS; POPULATION; PARENCHYMA; PARTICLES; EXPOSURE	We examined the relationship between intrapulmonary particle distribution of carbonaceous and mineral dusts and remodeling of the airways along anatomically distinct airway paths in the lungs of Hispanic males from the central valley of California. Lung autopsy specimens from the Fresno County Coroner's Office were prepared by intratracheal instillation of 2% glutaraldehyde at 30 cm H2O pressure. Two distinct airway paths into the apico-posterior and apico-anterior portions of the left upper lung lobe were followed. Tissue samples for histologic analysis were generally taken from the intrapulmonary second, fourth, sixth, and ninth airway generations. Parenchymal tissues beyond the 12th airway generation of each airway path were also analyzed. There was little evidence of visible particle accumulation in the larger conducting airways (generations 2-6), except in bronchial-associated lymphoid tissues and within peribronchial connective tissue. In contrast, terminal and respiratory bronchioles arising from each pathway revealed varying degrees of wall thickening and remodeling. Walls with marked thickening contained moderate to heavy amounts of carbonaceous and mineral dusts. Wall thickening was associated with increases in collagen and interstitial inflammatory cells, including dust-laden macrophages. These changes were significantly greater in first-generation respiratory bronchioles compared to second- and third-generation respiratory bronchioles. These findings suggest that accumulation of carbonaceous and mineral dust in the lungs is significantly affected by lung anatomy with the greatest retention in centers of lung acini. Furthermore, there is significant remodeling of this transitional zone in humans exposed to ambient particulate matter.	Univ Calif Davis, Dept Anat Physiol & Cell Biol, Sch Vet Med, Davis, CA 95616 USA; Univ Calif Davis, Dept Epidemiol & Prevent Med, Sch Med, Davis, CA 95616 USA; Univ Calgary, Dept Pathol & Lab Med, Fac Med, Calgary, AB T2N 1N4, Canada; NIOSH, Morgantown, WV USA; Fresno Med Coroners Off, Fresno, CA USA; Univ New Mexico, Sch Med, Dept Pediat, Albuquerque, NM 87131 USA	Pinkerton, KE (reprint author), Univ Calif Davis, Dept Anat Physiol & Cell Biol, Sch Vet Med, 1321 Haring Hall, Davis, CA 95616 USA.				NCRR NIH HHS [RR00169]; NIEHS NIH HHS [ES05707]		ADESINA AM, 1991, AM REV RESPIR DIS, V143, P144; ALEXIS A, 1999, 1999 CALIFORNIA ALMA, P271; CHOW JC, 1992, ATMOS ENVIRON A-GEN, V26, P3335, DOI 10.1016/0960-1686(92)90350-T; CHOW JC, 1993, AEROSOL SCI TECH, V18, P105, DOI 10.1080/02786829308959588; Churg A, 1997, AM J RESP CRIT CARE, V155, P2109; CHURG A, 1990, EXP LUNG RES, V16, P159, DOI 10.3109/01902149009108838; CHURG A, 1992, SEMIN RESPIR MED, V13, P140, DOI 10.1055/s-2007-1006266; Churg A, 1999, J ENV MED, V1, P39, DOI 10.1002/(SICI)1099-1301(199901/03)1:1<39::AID-JEM6>3.3.CO;2-X; COSIO MG, 1980, AM REV RESPIR DIS, V122, P265; CRAIGHEAD JE, 1982, ARCH PATHOL LAB MED, V106, P544; CRAIGHEAD JE, 1988, ARCH PATHOL LAB MED, V112, P673; Darquenne C, 1996, J APPL PHYSIOL, V80, P1401; FEDERSPIEL WJ, 1988, J APPL PHYSIOL, V64, P2614; Fisher LD, 1993, BIOSTATISTICS METHOD, P256; Green FHY, 1998, PATHOLOGY OCCUPATION, P403; GREEN FHY, 1998, PATHOLOGY OCCUPATION, P209; HAHN FF, 1997, TOXICOLOGY RESP SYST, V3, P187; HARKEMA JR, 1993, AM J PATHOL, V143, P857; KLEINERMAN J, 1979, ARCH PATHOL LAB MED, V103, P375; LIPPMANN M, 1980, BRIT J IND MED, V37, P337; NEIUWENHUIJSEN MJ, 1998, AM J IND HYG ASS, V58, P34; NEIUWENHUIJSEN MJ, 1998, AM J IND HYG ASS J, V59, P9; NIEWOEHNER DE, 1974, NEW ENGL J MED, V291, P755, DOI 10.1056/NEJM197410102911503; Oberdorster G., 1988, J AEROSOL MED, V1, P289, DOI DOI 10.1089/JAM.1988.1.289; Plopper C, 1990, MODELS LUNG DISEASE, P537; Plopper Chalres G., 1994, P15; SHERWIN RP, 1979, LAB INVEST, V40, P576; Thun MJ, 1997, J NATL CANCER I, V89, P1580, DOI 10.1093/jnci/89.21.1580; THURLBECK WM, 1974, AM REV RESPIR DIS, V109, P239; TSUDA A, 1995, J APPL PHYSIOL, V79, P1055; TSUDA S, 1984, FUND APPL TOXICOL, V4, P378, DOI 10.1016/0272-0590(84)90195-7; WRIGHT JL, 1992, AM REV RESPIR DIS, V146, P240	32	75	81	2	7	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	NOV	2000	108	11					1063	1069		10.1289/ehp.001081063		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	373XP	WOS:000165315600028	11102298	
J	van Zijverden, M; van der Pijl, A; Bol, M; van Pinxteren, FA; de Haar, C; Penninks, AH; van Loveren, H; Pieters, R				van Zijverden, M; van der Pijl, A; Bol, M; van Pinxteren, FA; de Haar, C; Penninks, AH; van Loveren, H; Pieters, R			Diesel exhaust, carbon black, and silica particles display distinct Th1/Th2 modulating activity	TOXICOLOGY AND APPLIED PHARMACOLOGY			English	Article						particulate air pollution; immunotoxicology; Th1/Th2; popliteal lymph node; diesel exhaust particles; carbon black; silica	SYSTEMIC IGE PRODUCTION; ADJUVANT ACTIVITY; AIR-POLLUTION; ANTIBODY-PRODUCTION; FINE PARTICLES; IN-VITRO; ASTHMA; MICE; PREVALENCE; CHILDREN	Certain particulate air pollutants may play an important role in the increasing prevalence of respiratory allergy by stimulating T helper 2 cell (Th2)-mediated immune responses to common antigens. The study described here examined different particles, diesel exhaust particles (DEP), carbon black particles (CBP), and silica particles (SIP) for their immunomodulating capacity in both primary and secondary immune responses in female BALB/C mice. The primary response was studied after subcutaneous injection of 1 mg of particle together with 10 mug of reporter antigen TNP-OVA (2,4,6-trinitrophenyl coupled to ovalbumin) into the hind paw. Interferon-gamma (IFN-gamma) and interleukin 4 (IL-4) production was assessed in the popliteal lymph node (PLN) at Day 2 and Day 5 after injection by flow cytometry and ELISA. The number of IL-4-containing CD4(+) T cells increased between Day 2 and Day 5 in DEP- and CBP-exposed mice, in contrast to SIP-treated animals. IL-4 production by cultured PLN cells was also significantly increased for DEP- and CBP-treated animals. The secondary response was studied in different organs after an intranasal challenge with TNP-OVA (50 mug), which was given 4 weeks after the initial subcutaneous injection. Five days after challenge the number of antibody-forming cells (AFCs) was assessed in peribronchial lymph nodes (PBLN), spleen, bone marrow, and PLN, and antibody levels were determined in weekly obtained blood samples. It appeared that all particles acted as adjuvant, but the different particles stimulated distinct types of immune responses to TNP-OVA. DEP-treated animals show high IgG1 and IgE levels in serum and high IgG1 and IgE-forming AFC numbers in PBLN, bone marrow, and spleen. CBP-treated animals show even higher IgG1 and IgE levels and AFC numbers, and in addition display IgG2a production. SIP-injected animals display predominantly IgG2a responses. It is concluded that DEP are able to skew the immune response toward the T helper 2 (Th2) side, whereas SIP stimulate a Th1 response and CBP have a mixed activity, stimulating both Th1 and Th2 responses in this model, (C) 2000 Academic Press.	Univ Utrecht, RITOX Immunotoxicol, NL-3508 TD Utrecht, Netherlands; TNO, Nutr & Food Res Inst, Utrecht, Netherlands; RIVM, Natl Inst Publ Hlth & Environm, Utrecht, Netherlands	van Zijverden, M (reprint author), Univ Utrecht, RITOX Immunotoxicol, POB 80176, NL-3508 TD Utrecht, Netherlands.						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Appl. Pharmacol.	OCT 15	2000	168	2					131	139		10.1006/taap.2000.9013		9	Pharmacology & Pharmacy; Toxicology	Pharmacology & Pharmacy; Toxicology	371YQ	WOS:000165207200006	11032768	
J	Martin, JG; Duguet, A; Eidelman, DH				Martin, JG; Duguet, A; Eidelman, DH			The contribution of airway smooth muscle to airway narrowing and airway hyperresponsiveness in disease	EUROPEAN RESPIRATORY JOURNAL			English	Article						airways responsiveness; airway smooth muscle; asthma; mechanics; modelling	BROWN-NORWAY RATS; ANTIGEN CHALLENGE; GUINEA-PIGS; ASTHMA; BRONCHOCONSTRICTION; MECHANICS; MODEL; ORIENTATION; PRESSURE; EXPOSURE	Airway hyperresponsiveness (AHR), the exaggerated response to constrictor agonists in asthmatic subjects, is incompletely understood. Changes in either the quantity or properties of airway smooth muscle (ASM) are possible explanations for AHR. Morphometric analyses demonstrate structural changes in asthmatic airways, including subepithelial fibrosis, gland hyperplasia/hypertrophy, neovascularization and an increase in ASM mass. Mathematical modelling of airway narrowing suggests that, of all the changes in structure, the increase in ASM mass is the most probable cause of AHR. An increase in ASM mass in the large airways is more closely associated with a greater likelihood of dying from asthma than increases in ASM mass in other locations within the airway tree. ASM contraction is opposed by the elastic recoil of the lungs and airways, which appears to limit the degree of bronchoconstriction in vivo. The cyclical nature of tidal breathing applies stresses to the airway wall that enhance the bronchodilating influence of the lung tissues on the contracting ASR;I, in all probability by disrupting cross-bridges. However, the increase in ASM mass in asthma may overcome the limitation resulting from the impedances to ASM shortening imposed by the lung parenchyma and airway wall tissues. Additionally, ASM with the capacity to shorten rapidly may achieve shorter lengths and cause a greater degree of bronchoconstriction when stimulated to contract than slower ASM. Changes in ASM properties are induced by the process of sensitization and allergen-exposure such as enhancement of phospholipase C activity and inositol phosphate turnover, and increases in myosin Light chain kinase activity, Whether changes in ASM mass or biochemical/biomechanical properties form the basis for asthma remains to be determined.	McGill Univ, Meakins Christie Labs, Dept Med, Montreal, PQ H2X 2P2, Canada	Martin, JG (reprint author), McGill Univ, Meakins Christie Labs, Dept Med, 3626 St Urbain St, Montreal, PQ H2X 2P2, Canada.						An SS, 1999, AM J PHYSIOL-LUNG C, V277, pL968; ANTONISSEN LA, 1979, J APPL PHYSIOL, V46, P681; BATES JHT, 1990, J APPL PHYSIOL, V69, P995; Blyth DI, 1996, AM J RESP CELL MOL, V14, P425; Brown RH, 1997, J APPL PHYSIOL, V83, P366; BROWN RH, 1995, J APPL PHYSIOL, V79, P1242; CARROLL N, 1993, AM REV RESPIR DIS, V147, P405; Chung KF, 2000, EUR RESPIR J, V15, P961, DOI 10.1034/j.1399-3003.2000.15e26.x; DING DJ, 1987, J APPL PHYSIOL, V62, P1324; Duguet A, 2000, AM J RESP CRIT CARE, V161, P839; Fredberg JJ, 1997, AM J RESP CRIT CARE, V156, P1752; Fredberg JJ, 1999, AM J RESP CRIT CARE, V159, P959; Gillis HL, 1999, J APPL PHYSIOL, V86, P2001; GUNST SJ, 1988, J APPL PHYSIOL, V64, P2522; Hai CM., 1988, AM J PHYSIOL, V254, P99; HAKONARSON H, 1995, AM J PHYSIOL-LUNG C, V269, pL645; Halayko AJ, 1999, AM J PHYSIOL-LUNG C, V276, pL197; James A, 2000, EUR RESPIR J, V15, P782, DOI 10.1034/j.1399-3003.2000.15d25.x; JAMES AL, 1989, AM REV RESPIR DIS, V139, P242; JIANG H, 1992, J APPL PHYSIOL, V72, P39; JIANG H, 1992, AM J RESP CELL MOL, V7, P567; John M, 1997, J IMMUNOL, V158, P1841; LAMBERT RK, 1993, J APPL PHYSIOL, V74, P2771; Lei M, 1997, J APPL PHYSIOL, V82, P70; Macklem PT, 1996, AM J RESP CRIT CARE, V153, P83; MACKLEM PT, 1987, CHEST, V91, pS189, DOI 10.1378/chest.91.6.189S; Mehta D, 1996, AM J PHYSIOL-CELL PH, V270, pC243; MORENO RH, 1986, AM REV RESPIR DIS, V133, P1171; MORENO RH, 1993, J APPL PHYSIOL, V75, P738; PADRID P, 1995, AM J RESP CRIT CARE, V151, P184; SALARI H, 1992, J ALLERGY CLIN IMMUN, V90, P918, DOI 10.1016/0091-6749(92)90464-D; 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; SASAKI H, 1978, J APPL PHYSIOL, V45, P858; SKLOOT G, 1995, J CLIN INVEST, V96, P2393, DOI 10.1172/JCI118296; Solway J, 1997, AM J RESP CELL MOL, V17, P144; Tao FC, 1999, AM J RESP CRIT CARE, V160, P446; Thomson RJ, 1996, AM J RESP CRIT CARE, V154, P749; Thorpe CW, 1997, J APPL PHYSIOL, V82, P1616; WANG CG, 1993, AM REV RESPIR DIS, V148, P413; WANG ZL, 1995, AM J RESP CRIT CARE, V152, P2097; Wiggs BR, 1997, J APPL PHYSIOL, V83, P1814; YAGER D, 1991, AM REV RESPIR DIS, V143, pS52; YOO J, 1994, AM J PHYSIOL-CELL PH, V267, pC1657	44	75	83	0	4	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0903-1936			EUR RESPIR J	Eur. Resp. J.	AUG	2000	16	2					349	354		10.1034/j.1399-3003.2000.16b25.x		6	Respiratory System	Respiratory System	346EF	WOS:000088857300025	10968513	
J	Cade, A; Brownlee, KG; Conway, SP; Haigh, D; Short, A; Brown, J; Dassu, D; Mason, SA; Phillips, A; Eglin, R; Graham, M; Chetcuti, A; Chatrath, M; Hudson, N; Thomas, A; Chetcuti, PAJ				Cade, A; Brownlee, KG; Conway, SP; Haigh, D; Short, A; Brown, J; Dassu, D; Mason, SA; Phillips, A; Eglin, R; Graham, M; Chetcuti, A; Chatrath, M; Hudson, N; Thomas, A; Chetcuti, PAJ			Randomised placebo controlled trial of nebulised corticosteroids in acute respiratory syncytial viral bronchiolitis	ARCHIVES OF DISEASE IN CHILDHOOD			English	Article						acute viral bronchiolitis; respiratory syncytial virus; inhaled corticosteroids	VIRUS BRONCHIOLITIS; LUNG-FUNCTION; BUDESONIDE; CHILDREN; INFANTS; ASTHMA; DEXAMETHASONE; INFECTION; AGE	Objective--To evaluate short and long term effects of giving nebulised budesonide early in respiratory syncytial viral (RSV) bronchiolitis. Design--A multicentre randomised double blind placebo controlled trial. Subjects--Infants admitted to hospital with their first episode of RSV positive bronchiolitis. Intervention-Randomised to receive either 1 mg of nebulised budesonide (Bud) or placebo (Pla) twice daily from admission until 2 weeks after discharge. Follow up was for 12 months. Main outcome measures--Duration of hospital admission, time taken to become symptom free, re-admission rates, general practitioner consultation rates, and use of antiwheeze medication during follow up. Results--161 infants were studied. Both arms were similar with respect to initial clinical severity, age, sex, socioeconomic class, and tobacco exposure, Median time from first nebulisation to discharge: Bud and Pla, 2 days. Median number of days for 50% of infants to be symptom free for 48 hours: Bud, 10 days; Ma, 12 days. Respiratory re-admission rates in the 12 month follow up: Bud, 16%; Pla, 18%; median difference (95% confidence interval (Cl)), -2 (-14 to 10). Median respiratory related general practitioner attendances: Bud, 4.0; Pla, 4.5; median difference (95% CI), -1 (-2 to 0). Percentage of infants recieving at least one prescription for antiwheeze medication during follow up, corticosteroids: Bud, 50%; Pla, 60%; difference (95% CI), -10 (-26 to 6);bronchodilators: Bud, 60%; Pla, 67%; difference (95% CI), -7 (-22 to 8). Conclusions--There are no short or long term clinical benefits from the administration of nebulised corticosteroids in the acute phase of RSV bronchiolitis.	Gen Infirm, Dept Paediat & Child Hlth, Leeds, W Yorkshire, England; St James Univ Hosp, Leeds LS9 7TF, W Yorkshire, England; Seacroft Hosp, Leeds LS14 6UH, W Yorkshire, England; St Lukes Hosp, Bradford BD5 0NA, W Yorkshire, England; Huddersfield Royal Infirm, Huddersfield HO3 3AE, W Yorkshire, England; No & Yorkshire Clin Trials & Res Unit, Leeds LS16 6QB, W Yorkshire, England	Cade, A (reprint author), Gen Infirm, Dept Paediat & Child Hlth, Clarendor Wing,Belmont Grove, Leeds, W Yorkshire, England.						CARLSEN K, 1988, ARCH DIS CHILD, V63, P1428; CARLSEN KCL, 1992, ARCH DIS CHILD, V67, P1077; DABBOUS IA, 1966, PEDIATRICS, V37, P477; DAUGBJERG P, 1993, ACTA PAEDIATR, V82, P547, DOI 10.1111/j.1651-2227.1993.tb12750.x; EVERARD ML, 1994, ARCH DIS CHILD, V71, P428; Gardner M. J., 1989, STAT CONFIDENCE; GOODWIN A, 1995, BR J CLIN RES, V6, P113; Klassen TP, 1997, J PEDIATR-US, V130, P191, DOI 10.1016/S0022-3476(97)70342-1; KUIKKA L, 1994, ACTA PAEDIATR, V83, P744, DOI 10.1111/j.1651-2227.1994.tb13131.x; LEER JA, 1969, AM J DIS CHILD, V117, P495; MARTINEZ FD, 1991, AM REV RESPIR DIS, V143, P312; MCKENZIE S, 1992, FORFAR ARNEILS TXB P, P638; MURRAY M, 1992, ARCH DIS CHILD, V67, P482; NAHATA MC, 1994, J CLIN PHARM THER, V19, P117, DOI 10.1111/j.1365-2710.1994.tb01122.x; Parmar MKB, 1995, SURVIVAL ANAL PRACTI; PULLAN CR, 1982, BRIT MED J, V284, P1665; Reijonen T, 1996, ARCH PEDIAT ADOL MED, V150, P512; Richter H, 1998, J PEDIATR-US, V132, P849, DOI 10.1016/S0022-3476(98)70316-6; ROONEY JC, 1971, J PEDIATR-US, V79, P744, DOI 10.1016/S0022-3476(71)80385-2; Roosevelt G, 1996, LANCET, V348, P292, DOI 10.1016/S0140-6736(96)02285-4; SAMMARTINO L, 1995, J PAEDIATR CHILD H, V31, P61; SIGURS N, 1995, PEDIATRICS, V95, P500; SIMS DG, 1978, BRIT MED J, V1, P11; SPRINGER C, 1990, PEDIATR PULM, V9, P181, DOI 10.1002/ppul.1950090311; STOKES GM, 1981, J PEDIATR-US, V98, P871, DOI 10.1016/S0022-3476(81)80577-X; van Woensel JBM, 1997, THORAX, V52, P634; Wong J., 1997, European Respiratory Journal Supplement, V10, p430S; YOUNG S, 1995, ARCH DIS CHILD, V72, P16	28	75	87	1	1	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0003-9888			ARCH DIS CHILD	Arch. Dis. Child.	FEB	2000	82	2					126	130		10.1136/adc.82.2.126		5	Pediatrics	Pediatrics	281HH	WOS:000085152500009	10648365	
J	Goleva, E; Jackson, LP; Harris, JK; Robertson, CE; Sutherland, ER; Hall, CF; Good, JT; Gelfand, EW; Martin, RJ; Leung, DYM				Goleva, Elena; Jackson, Leisa P.; Harris, J. Kirk; Robertson, Charles E.; Sutherland, E. Rand; Hall, Clifton F.; Good, James T., Jr.; Gelfand, Erwin W.; Martin, Richard J.; Leung, Donald Y. M.			The Effects of Airway Microbiome on Corticosteroid Responsiveness in Asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						microbiome; asthma; corticosteroids	STEROID-RESISTANT ASTHMA; GLUCOCORTICOID-INSENSITIVE ASTHMA; PROTEIN-KINASE PHOSPHATASE-1; FIBEROPTIC BRONCHOSCOPY; COMMENSAL BACTERIA; RECEPTOR-BETA; LIPID-A; DISEASE; LIPOPOLYSACCHARIDES; MACROPHAGES	Rationale: The role of airway microbiome in corticosteroid response in asthma is unknown. Objectives: To examine airway microbiome composition in patients with corticosteroid-resistant (CR) asthma and compare it with patients with corticosteroid-sensitive (CS) asthma and normal control subjects and explore whether bacteria in the airways of subjects with asthma may direct alterations in cellular responses to corticosteroids. Methods: 16S rRNA gene sequencing was performed on bronchoalveolar lavage(BAL) samples of 39 subjects with asthma and 12 healthy control subjects. In subjects with asthma, corticosteroid responsiveness was characterized, BAL macrophages were stimulated with pathogenic versus commensal microorganisms, and analyzed by real-time polymerase chain reaction for the expression of corticosteroid-regulated genes and cellular p38 mitogen-activated protein kinase (MAPK) activation. Measurements and Main Results: Of the 39 subjects with asthma, 29 were CR and 10 were CS. BAL microbiome from subjects with CR and CS asthma did not differ in richness, evenness, diversity, and community composition at the phylum level, but did differ at the genus level, with distinct genus expansions in 14 subjects with CR asthma. Preincubation of asthmatic airway macrophages with Haemophilus parainfluenzae, a uniquely expanded potential pathogen found only in CR asthma airways, resulted in p38 MAPK activation, increased IL-8 (P < 0.01), mitogen-activated kinase phosphatase 1 mRNA (P < 0.01) expression, and inhibition of corticosteroid responses (P < 0.05). This was not observed after exposure to commensal bacterium Prevotella melaninogenica. Inhibition of transforming growth factor-beta-associated kinase-1 (TAK1), upstream activator of MAPK, but not p38 MAPK restored cellular sensitivity to corticosteroids. [GRAPHICS] Conclusions: A subset of subjects with CR asthma demonstrates airway expansion of specific gram-negative bacteria, which trigger TAK1/MAPK activation and induce corticosteroid resistance. TAK1 inhibition restored cellular sensitivity to corticosteroids.	[Goleva, Elena; Jackson, Leisa P.; Hall, Clifton F.; Gelfand, Erwin W.; Leung, Donald Y. M.] Natl Jewish Hlth, Dept Pediat, Denver, CO 80206 USA; [Sutherland, E. Rand; Good, James T., Jr.; Martin, Richard J.] Natl Jewish Hlth, Dept Med, Denver, CO 80206 USA; [Harris, J. Kirk; Gelfand, Erwin W.; Leung, Donald Y. M.] Univ Colorado Denver, Dept Pediat, Aurora, CO USA; [Robertson, Charles E.] Univ Colorado, Dept Mol Cellular & Dev Biol, Boulder, CO 80309 USA	Leung, DYM (reprint author), Natl Jewish Hlth, 1400 Jackson St,K926I, Denver, CO 80206 USA.	leungd@njhealth.org		ROBERTSON, CHARLES/0000-0002-4136-4121	NIAID; NHLBI of the National Institutes of Health [AI070140, 2R56AI070140, HL37260]; Edelstein Family Foundation	Supported by NIAID and NHLBI of the National Institutes of Health under Award Numbers AI070140, 2R56AI070140, and HL37260. The authors acknowledge The Edelstein Family Foundation for their generous support of this work.	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J. Respir. Crit. Care Med.	NOV 15	2013	188	10					1193	1201		10.1164/rccm.201304-0775OC		9	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	251WO	WOS:000326963600011	24024497	
J	Ziello, C; Sparks, TH; Estrella, N; Belmonte, J; Bergmann, KC; Bucher, E; Brighetti, MA; Damialis, A; Detandt, M; Galan, C; Gehrig, R; Grewling, L; Bustillo, AMG; Hallsdottir, M; Kockhans-Bieda, MC; De Linares, C; Myszkowska, D; Paldy, A; Sanchez, A; Smith, M; Thibaudon, M; Travaglini, A; Uruska, A; Valencia-Barrera, RM; Vokou, D; Wachter, R; de Weger, LA; Menzel, A				Ziello, Chiara; Sparks, Tim H.; Estrella, Nicole; Belmonte, Jordina; Bergmann, Karl C.; Bucher, Edith; Brighetti, Maria Antonia; Damialis, Athanasios; Detandt, Monique; Galan, Carmen; Gehrig, Regula; Grewling, Lukasz; Gutierrez Bustillo, Adela M.; Hallsdottir, Margret; Kockhans-Bieda, Marie-Claire; De Linares, Concepcion; Myszkowska, Dorota; Paldy, Anna; Sanchez, Adriana; Smith, Matthew; Thibaudon, Michel; Travaglini, Alessandro; Uruska, Agnieszka; Valencia-Barrera, Rosa M.; Vokou, Despoina; Wachter, Reinhard; de Weger, Letty A.; Menzel, Annette			Changes to Airborne Pollen Counts across Europe	PLOS ONE			English	Article							AMBROSIA-ARTEMISIIFOLIA L.; CLIMATE-CHANGE; PUBLIC-HEALTH; ALLERGENIC POLLEN; ATMOSPHERIC CO2; COMMON RAGWEED; AEROALLERGENS; URBANIZATION; IMPACTS; SEASONS	A progressive global increase in the burden of allergic diseases has affected the industrialized world over the last half century and has been reported in the literature. The clinical evidence reveals a general increase in both incidence and prevalence of respiratory diseases, such as allergic rhinitis (common hay fever) and asthma. Such phenomena may be related not only to air pollution and changes in lifestyle, but also to an actual increase in airborne quantities of allergenic pollen. Experimental enhancements of carbon dioxide (CO2) have demonstrated changes in pollen amount and allergenicity, but this has rarely been shown in the wider environment. The present analysis of a continental-scale pollen data set reveals an increasing trend in the yearly amount of airborne pollen for many taxa in Europe, which is more pronounced in urban than semi-rural/rural areas. Climate change may contribute to these changes, however increased temperatures do not appear to be a major influencing factor. Instead, we suggest the anthropogenic rise of atmospheric CO2 levels may be influential.	[Ziello, Chiara; Sparks, Tim H.; Estrella, Nicole; Sanchez, Adriana; Menzel, Annette] Tech Univ Munich, Chair Ecoclimatol, Freising Weihenstephan, Germany; [Sparks, Tim H.; Estrella, Nicole; Menzel, Annette] Tech Univ Munich, Inst Adv Study, D-8046 Garching, Germany; [Sparks, Tim H.] Poznan Univ Life Sci, Inst Zool, Poznan, Poland; [Belmonte, Jordina; De Linares, Concepcion] Univ Autonoma Barcelona, Bot Unit, Bellaterra, Spain; [Belmonte, Jordina; De Linares, Concepcion] Univ Autonoma Barcelona, Inst Environm Sci & Technol ICTA, Bellaterra, Spain; [Bergmann, Karl C.] Charite, Allergie Ctr Charite, D-13353 Berlin, Germany; [Bucher, Edith] Agenzia Prov Ambiente, Biol Lab, Laives, BZ, Italy; [Brighetti, Maria Antonia; Travaglini, Alessandro] Univ Roma Tor Vergata, Dipartimento Biol, I-00173 Rome, Italy; [Damialis, Athanasios; Vokou, Despoina] Aristotle Univ Thessaloniki, Sch Biol, Dept Ecol, GR-54006 Thessaloniki, Greece; [Detandt, Monique] Sci Inst Publ Hlth, Sect Mycol & Aerobiol, Brussels, Belgium; [Galan, Carmen] Univ Cordoba, Dept Bot Ecol & Plant Physiol, Cordoba, Spain; [Gehrig, Regula] Fed Off Meteorol & Climatol MeteoSwiss, Zurich, Switzerland; [Grewling, Lukasz] Adam Mickiewicz Univ, Lab Aeropalynol, Poznan, Poland; [Gutierrez Bustillo, Adela M.] Univ Complutense Madrid, Dept Plant Biol 2, Madrid, Spain; [Hallsdottir, Margret] Iceland Inst Nat Hist, Gardabaer, Iceland; [Kockhans-Bieda, Marie-Claire] Ctr Hosp Luxembourg, Stn Aerobiol, Luxembourg, Luxembourg; [Myszkowska, Dorota] Jagiellonian Univ, Coll Med, Dept Clin & Environm Allergol, Krakow, Poland; [Paldy, Anna] Natl Inst Environm Hlth, Dept Biol, Budapest, Hungary; [Smith, Matthew] Univ Worcester, Natl Pollen & Aerobiol Res Unit, Worcester, England; [Thibaudon, Michel] Reseau Natl Surveillance Aerobiol, Brussieu, France; [Uruska, Agnieszka] Univ Gdansk, Lab Palaeoecol & Archaeobot, PL-80952 Gdansk, Poland; [Valencia-Barrera, Rosa M.] Univ Leon, Dept Biodivers & Environm Management, E-24071 Leon, Spain; [Wachter, Reinhard] Polleninformat Dienst Deutschland PID, Ganderkesee, Germany; [de Weger, Letty A.] Leiden Univ, Med Ctr, Dept Pulmonol, Leiden, Netherlands	Ziello, C (reprint author), Tech Univ Munich, Chair Ecoclimatol, Freising Weihenstephan, Germany.	ziello@wzw.tum.de	Damialis, Athanasios/C-6109-2013; Gutierrez-Bustillo, Adela Montserrat/L-7250-2014; Smith, Matt/C-3911-2014; De Linares, Concepcion/F-9313-2016; Menzel, Annette/B-1105-2013	Damialis, Athanasios/0000-0001-6400-384X; Gutierrez-Bustillo, Adela Montserrat/0000-0002-6782-0527; Smith, Matt/0000-0002-4170-2960; De Linares, Concepcion/0000-0002-2047-3337; Menzel, Annette/0000-0002-7175-2512; Belmonte, Jordina/0000-0002-6419-9595; Valencia-Barrera, Rosa M/0000-0002-6014-9961; Damialis, Athanasios/0000-0003-2917-5667; Sparks, Tim/0000-0003-4382-7051	Technische Universitat Munchen - Institute for AdvancedStudy; German Excellence Initiative; Bavarian State Ministry of the Environment and Public Health [U119]	This study is supported by the Technische Universitat Munchen - Institute for AdvancedStudy, funded by the German Excellence Initiative. The Ph.D. project of the first author is supported by Grant U119 from Bavarian State Ministry of the Environment and Public Health. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.	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J	Hinz, D; Bauer, M; Roder, S; Olek, S; Huehn, J; Sack, U; Borte, M; Simon, JC; Lehmann, I; Herberth, G				Hinz, D.; Bauer, M.; Roeder, S.; Olek, S.; Huehn, J.; Sack, U.; Borte, M.; Simon, J. C.; Lehmann, I.; Herberth, G.		LINA Study Grp	Cord blood Tregs with stable FOXP3 expression are influenced by prenatal environment and associated with atopic dermatitis at the age of one year	ALLERGY			English	Article						birth cohort; cord blood; environmental exposure; FOXP3; regulatory T cells	REGULATORY T-CELLS; IMMUNE-RESPONSES; PERIPHERAL-BLOOD; MATERNAL SMOKING; DNA METHYLATION; LINEAGE; INDUCTION; PREGNANCY; CHILDREN; DISEASE	Background: Regulatory T cells (Tregs) with stable FOXP3 expression are characterized by a specific demethylated region in the FOXP3 gene (Treg-specific demethylated region, TSDR). The aim of this study was to analyse the influence of prenatal factors on cord blood Treg numbers, as detected by changes in the TSDR demethylation, and the subsequent risk for allergic diseases. Methods: Analyses were performed within the LINA study in blood samples from pregnant women (34th gestational week) and in cord blood (n = 346 mother-child pairs). Treg numbers were detected via DNA demethylation in the FOXP3 TSDR. At age 1, total and specific IgE was measured in children's blood. In addition, maternal cytokine production (Th1/ Th2/ Th17) was analysed. Exposure and disease outcomes were assessed by questionnaires. Results: Boys had lower Treg numbers compared with girls (P < 0.001). Parental atopy history, particularly maternal hay fever and paternal asthma were related to lower Treg numbers in cord blood (adj. MR = 0.81, 95% CI = 0.68-0.97; adj. MR = 0.60, 95% CI = 0.45-0.81). Maternal cytokines (IL-13, IL-17E and IFN-gamma) and maternal smoking/ exposure to tobacco smoke during pregnancy were also associated with decreased cord blood Treg numbers (adj. MR = 0.89, 95% CI = 0.97-1.00). Children with lower Treg numbers at birth had a higher risk to develop atopic dermatitis (adj. OR = 1.55, 95% CI = 1.00-2.41) and sensitization to food allergens (adj. OR = 1.55, 95% CI = 1.06-2.25) during the first year of life. Conclusions: These results indicate that both genetic and environmental factors presumably influence the development of foetal Tregs. Low cord blood Treg numbers may predict early atopic dermatitis.	[Hinz, D.; Bauer, M.; Lehmann, I.; Herberth, G.] UFZ Helmholtz Ctr Environm Res, Dept Environm Immunol, D-04318 Leipzig, Germany; [Hinz, D.] Univ Klinikum, Klin Dermatol Venerol & Allergol, Leipzig, Germany; [Roeder, S.] UFZ Helmholtz Ctr Environm Res, Core Facil Studies, D-04318 Leipzig, Germany; [Olek, S.] Epiontis GmbH, Berlin, Germany; [Huehn, J.] Helmholtz Ctr Infect Res, Dept Expt Immunol, Braunschweig, Germany; [Sack, U.] Univ Leipzig, Inst Clin Immunol, Leipzig, Germany; [Borte, M.] Univ Leipzig, Acad Teaching Hosp, Municipal Hosp St Georg, Childrens Hosp, Leipzig, Germany	Lehmann, I (reprint author), UFZ Helmholtz Ctr Environm Res, Dept Environm Immunol, Permoserstr 15, D-04318 Leipzig, Germany.	irina.lehmann@ufz.de	Sack, Ulrich/J-6301-2015	Sack, Ulrich/0000-0002-7813-0492	Helmholtz Interdisciplinary Graduate School for Environmental Research (HIGRADE); German Research Foundation [KFO250]	We cordially thank the participants of the LINA study as well as Beate Fink and Anne Hain for their excellent technical assistance. The authors are grateful to Neil Jones and Sonja Nakasian for the careful revision of the manuscript. This work was partially supported by the Helmholtz Impulse and Networking Fund through Helmholtz Interdisciplinary Graduate School for Environmental Research (HIGRADE) and by the German Research Foundation (KFO250).	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J	Kirkham, PA; Caramori, G; Casolari, P; Papi, AA; Edwards, M; Shamji, B; Triantaphyllopoulos, K; Hussain, F; Pinart, M; Khan, Y; Heinemann, L; Stevens, L; Yeadon, M; Barnes, PJ; Chung, KF; Adcock, IM				Kirkham, Paul A.; Caramori, Gaetano; Casolari, Paolo; Papi, Alberto A.; Edwards, Matt; Shamji, Betty; Triantaphyllopoulos, Kostas; Hussain, Farhana; Pinart, Mariona; Khan, Younis; Heinemann, Lucy; Stevens, Laurie; Yeadon, Mike; Barnes, Peter J.; Chung, Kian F.; Adcock, Ian M.			Oxidative Stress-induced Antibodies to Carbonyl-modified Protein Correlate with Severity of Chronic Obstructive Pulmonary Disease	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						COPD; autoimmunity; oxidative stress; carbonyl	LIPID-PEROXIDATION PRODUCTS; CIGARETTE-SMOKE; INDUCED EMPHYSEMA; T-CELLS; COPD; AUTOANTIBODIES; AUTOIMMUNITY; MICE; AUTOANTIGENS; INFLAMMATION	Rationale: There is increasing evidence for the presence of autoantibodies in chronic obstructive pulmonary disease (COPD). Chronic oxidative stress is an essential component in COPD pathogenesis and can lead to increased levels of highly reactive carbonyls in the lung, which could result in the formation of highly immunogenic carbonyl adducts on "self" proteins. Objectives: To determine the presence of autoantibodies to carbonyl-modified protein in patients with COPD and in a murine model of chronic ozone exposure. To assess the extent of activated immune responses toward carbonyl-modified proteins. Methods: Blood and peripheral lung were taken from patients with COPD, age-matched smokers, and nonsmokers with normal lung function, as well as patients with severe persistent asthma. Mice were exposed to ambient air or ozone for 6 weeks. Antibody titers were measured by ELISA, activated compliment deposition by immunohistochemistry, and cellular activation by ELISA and fluorescence-activated cell sorter. Measurements and Main Results: Antibody titer against carbonyl-modified self-protein was significantly increased in patients with Global Initiative for Chronic Obstructive Lung Disease stage III COPD compared with control subjects. Antibody levels inversely correlated with disease severity and showed a prevalence toward an IgG1 isotype. Deposition of activated complement in the vessels of COPD lung as well as autoantibodies against endothelial cells were also observed. Ozone-exposed mice similarly exhibited increased antibody titers to carbonyl-modified protein, as well as activated antigen-presenting cells in lung tissue and splenocytes sensitized to activation by carbonyl-modified protein. Conclusions: Carbonyl-modified proteins, arising as a result of oxidative stress, promote antibody production, providing a link by which oxidative stress could drive an autoimmune response in COPD.	[Kirkham, Paul A.; Triantaphyllopoulos, Kostas; Hussain, Farhana; Pinart, Mariona; Khan, Younis; Heinemann, Lucy; Stevens, Laurie; Yeadon, Mike; Barnes, Peter J.; Chung, Kian F.; Adcock, Ian M.] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW3 6LY, England; [Kirkham, Paul A.; Edwards, Matt; Shamji, Betty] Novartis Inst Biomed Res, Horsham, W Sussex, England; [Caramori, Gaetano; Casolari, Paolo; Papi, Alberto A.] Univ Ferrara, Sect Resp Dis, I-44100 Ferrara, Italy; [Caramori, Gaetano; Casolari, Paolo; Papi, Alberto A.] Univ Ferrara, CEMICEF, I-44100 Ferrara, Italy; [Barnes, Peter J.; Chung, Kian F.; Adcock, Ian M.] Royal Brompton Resp Biomed Res Unit, London, England	Kirkham, PA (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dovehouse St, London SW3 6LY, England.	p.kirkham@imperial.ac.uk	Triantaphyllopoulos, Kostas/F-5182-2013; Pinart, Mariona/L-1931-2015	Pinart, Mariona/0000-0002-8223-1325; Adcock, Ian/0000-0003-2101-8843; Chung, Kian Fan/0000-0001-7101-1426; PAPI, ALBERTO/0000-0002-6924-4500	Royal Society; Associazione per la Ricerca e la Cura dell'Asma (ARCA, Padova, Italy); Wellcome Trust; Novartis Institutes for Biomedical Research; Novartis Institutes for Biomedical Research for research consumables; Consorzio Ferrara Ricerche; Novartis; Medical Research Council (MRC); British Lung Foundation; Engineering and Physical Sciences Research Council; Pfizer, UK; Chiesi Farmaceutici; Novartis, UK; Merck Sharp & Dohme (MSD), Italy; AZ; GSK; MSD; Boehringer Ingelheim (BI); Pfizer; Nycomed; Teva Pharmaceuticals; Chiesi; Daiichi-Sankyo; Cempra; Kyorin; Asthma UK	Supported by The Royal Society, Associazione per la Ricerca e la Cura dell'Asma (ARCA, Padova, Italy), The Wellcome Trust, and the Novartis Institutes for Biomedical Research. P.A.K. was a Royal Society Industry Fellow, and received additional support from the Novartis Institutes for Biomedical Research for research consumables. This work was also partly supported by Wellcome Trust grants to I.M.A. and K.F.C. G.C. was provided with support from Associazione per la Ricerca e la Cura dell'Asma (ARCA, Padova, Italy) and Consorzio Ferrara Ricerche.; P.A.K. received institutional grant support from the Royal Society, Novartis, the Medical Research Council (MRC), the British Lung Foundation, and the Engineering and Physical Sciences Research Council. He is employed by and owns stocks in Novartis. G.C. received institutional grant support from Pfizer, UK; Chiesi Farmaceutici; and Novartis, UK; and he received lecture fees from Merck Sharp & Dohme (MSD), Italy. P.C. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. A.A.P. is a Board member of Chiesi Farmaceutici, AstraZeneca (AZ), GlaxoSmithKline (GSK), Mundipharma, Novartis, Teva Pharmaceuticals, ProtAffin Biotechnologie, and Nycomed. He was a consultant for Chiesi Farmaceutici, GSK, Sunovion, and Zambon. He received institutional grant support from Chiesi Farmaceutici, AZ, GSK, MSD, Novartis, Boehringer Ingelheim (BI), and Pfizer. He received lecture fees from AZ, Chiesi Farmaceutici, GSK, BI, MSD, Novartis, Pfizer, and Nycomed. M.E. and B.S. are employed by the Novartis Institute for Biomedical Research. K.T. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. F.H. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. M.P. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. Y.K. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. L.H. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. L.S. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. M.Y. is employed by Pfizer. P.J.B. is a Board member of AZ, BI, Chiesi, Teva Pharmaceuticals, and Novartis. He received lecture fees from AZ, BI, Teva Pharmaceuticals, and Chiesi, and he was an expert witness for BI and Teva Pharmaceuticals. He received grant support from GSK, AZ, Novartis, Daiichi-Sankyo, and Cempra. K.F.C. is on the Advisory Board of GSK, Novartis, and Merck. He received lecture fees from Novartis and GSK. He received travel accommodations from BI and Novartis. I.M.A. was a consultant for GSK, Chiesi, Novartis, Pfizer, and Merck. He was on the Advisory Board for Chiesi and GSK. He received lecture fees from Kyorin, AZ, and GSK and received grant support from Pfizer, GSK, AZ, Novartis, the MRC, and Asthma UK.	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J. Respir. Crit. Care Med.	OCT 1	2011	184	7					796	802		10.1164/rccm.201010-1605OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	827DM	WOS:000295407300012	21965015	
J	Rappold, AG; Stone, SL; Cascio, WE; Neas, LM; Kilaru, VJ; Carraway, MS; Szykman, JJ; Ising, A; Cleve, WE; Meredith, JT; Vaughan-Batten, H; Deyneka, L; Devlin, RB				Rappold, Ana G.; Stone, Susan L.; Cascio, Wayne E.; Neas, Lucas M.; Kilaru, Vasu J.; Carraway, Martha Sue; Szykman, James J.; Ising, Amy; Cleve, William E.; Meredith, John T.; Vaughan-Batten, Heather; Deyneka, Lana; Devlin, Robert B.			Peat Bog Wildfire Smoke Exposure in Rural North Carolina Is Associated with Cardiopulmonary Emergency Department Visits Assessed through Syndromic Surveillance	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						cardiopulmonary health effects; satellite data; syndromic surveillance; wildfire smoke exposure	PARTICULATE AIR-POLLUTION; SOUTHERN CALIFORNIA WILDFIRES; CONGESTIVE-HEART-FAILURE; FOREST-FIRES; HOSPITAL ADMISSIONS; UNITED-STATES; ROOM VISITS; URBAN AREA; QUALITY; MORTALITY	BACKGROUND: In June 2008, burning peat deposits produced haze and air pollution far in excess of National Ambient Air Quality Standards, encroaching on rural communities of eastern North Carolina. Although the association of mortality and morbidity with exposure to urban air pollution is well established, the health effects associated with exposure to wildfire emissions are less well understood. OBJECTIVE: We investigated the effects of exposure on cardiorespiratory outcomes in the population affected by the fire. METHODS: We performed a population-based study using emergency department (ED) visits reported through the syndromic surveillance program NC DETECT (North Carolina Disease Event Tracking and Epidemiologic Collection Tool). We used aerosol optical depth measured by a satellite to determine a high-exposure window and distinguish counties most impacted by the dense smoke plume from surrounding referent counties. Poisson log-linear regression with a 5-day distributed lag was used to estimate changes in the cumulative relative risk (RR). RESULTS: In the exposed counties, significant increases in cumulative RR for asthma [1.65 (95% confidence interval, 1.25-2.1)], chronic obstructive pulmonary disease [1.73 (1.06-2.83)], and pneumonia and acute bronchitis [1.59 (1.07-2.34)] were observed. ED visits associated with cardiopulmonary symptoms [1.23 (1.06-1.43)] and heart failure [1.37 (1.01-1.85)] were also significantly increased. CONCLUSIONS: Satellite data and syndromic surveillance were combined to assess the health impacts of wildfire smoke in rural counties with sparse air-quality monitoring. This is the first study to demonstrate both respiratory and cardiac effects after brief exposure to peat wildfire smoke.	[Rappold, Ana G.; Stone, Susan L.; Cascio, Wayne E.; Neas, Lucas M.; Carraway, Martha Sue; Devlin, Robert B.] US EPA, Environm Publ Hlth Div, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA; [Kilaru, Vasu J.] US EPA, Natl Exposure Res Lab, Res Triangle Pk, NC 27711 USA; [Szykman, James J.] US EPA, Environm Sci Div, Natl Exposure Res Lab, NASA Langley Res Ctr, Hampton, VA USA; [Ising, Amy] Univ N Carolina, Sch Med, Dept Emergency Med, Chapel Hill, NC USA; [Cleve, William E.] Pitt Cty Mem Hosp, Greenville, NC USA; [Meredith, John T.] E Carolina Univ, Brody Sch Med, Dept Cardiovasc Sci, Greenville, NC USA; [Meredith, John T.] E Carolina Heart Inst, Greenville, NC USA; [Vaughan-Batten, Heather; Deyneka, Lana] N Carolina Dept Hlth & Human Serv, N Carolina Div Publ Hlth, Raleigh, NC USA; [Rappold, Ana G.; Stone, Susan L.; Cascio, Wayne E.; Neas, Lucas M.; Carraway, Martha Sue; Devlin, Robert B.] US EPA, Environm Publ Hlth Div, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA	Rappold, AG (reprint author), US EPA, Environm Publ Hlth Div, Natl Hlth & Environm Effects Res Lab, MD 58B,109 TW Alexander Dr, Res Triangle Pk, NC 27711 USA.	rappold.ana@epa.gov	Neas, Lucas/J-9378-2012; Xiongfei, Zhao/G-7690-2015		U.S. Environmental Protection Agency (EPA)	This work was supported by internal funding by the U.S. Environmental Protection Agency (EPA).	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Health Perspect.	OCT	2011	119	10					1415	1420		10.1289/ehp.1003206		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	827CA	WOS:000295402400026	21705297	
J	Chung, KF; Caramori, G; Adcock, IM				Chung, Kian Fan; Caramori, Gaetano; Adcock, Ian M.			Inhaled corticosteroids as combination therapy with beta-adrenergic agonists in airways disease: present and future	EUROPEAN JOURNAL OF CLINICAL PHARMACOLOGY			English	Review						Asthma; Chronic obstructive pulmonary disease; Corticosteroids; Beta-adrenergic agonists; Inflammation	OBSTRUCTIVE PULMONARY-DISEASE; RANDOMIZED CONTROLLED-TRIAL; HISTONE DEACETYLASE ACTIVITY; MILD PERSISTENT ASTHMA; BONE-MINERAL DENSITY; LONG-TERM TREATMENT; AIR-FLOW OBSTRUCTION; NITRIC-OXIDE LEVELS; LOW-DOSE BUDESONIDE; REGULATORY T-CELLS	Inhaled corticosteroid (ICS) therapy in combination with long-acting beta-adrenergic agonists represents the most important treatment for chronic airways diseases such as asthma and chronic obstructive pulmonary disease (COPD). ICS therapy forms the basis for treatment of asthma of all severities, improving asthma control, lung function and preventing exacerbations of disease. Use of ICS has also been established in the treatment of COPD, particularly symptomatic patients, who experience useful gains in quality of life, likely from an improvement in symptoms such as breathlessness and in reduction in exacerbations, and an attenuation of the yearly rate of deterioration in lung function. The addition of long-acting beta-agonist (LABA) therapy with ICS increases the efficacy of ICS effects in moderate-to-severe asthma. Thus, a 800 mu g daily dose of the ICS budesonide reduced severe exacerbation rates by 49% compared to a low dose of 200 mu g daily, and addition of the LABA formoterol to budesonide (800 mu g) led to a 63% reduction. In COPD, the effects of ICS are less prominent but there are beneficial effects on the decline in FEV(1) and the rate of exacerbations. A reduction in the rate of decline in FEV(1) of 16 ml/year with a 25% reduction in exacerbation rate has been reported with the salmeterol and fluticasone combination. A non-significant 17.5% reduction in all-cause mortality rate with ICS and LABA is reported. Chronic inflammation is a feature of both asthma and COPD, although there are site and characteristic differences. ICS targets this inflammation although this effect of ICS is less effective in patients with severe asthma and with COPD; however, addition of LABA may potentiate the anti-inflammatory effects of ICS. An important consideration is the presence of corticosteroid insensitivity in these patients. Currently available ICS have variably potent binding activities to specific glucocorticoid receptors, leading to inhibition of gene expression by either binding to DNA and inducing anti-inflammatory genes or by repressing the induction of pro-inflammatory mediators. Local side effects of ICS include oral candidiasis, hoarseness and dysphonia, while systemic side effects, such as easy bruising and reduction in growth velocity or bone mineral densitometry, are usually restricted to doses above maximally recommended doses. Use of LABA alone in patients with asthma increases the risk of asthma-related events including deaths, but this is less observed with the combination of ICS and LABA. Therefore, use of LABA alone is not recommended for asthma therapy. Future progress in ICS development will be characterised by the introduction of ICS with greater efficacy with a limited side-effect profile, and by longer-acting ICS that can be used in combination with once-daily LABAs. Other agents that could improve the efficacy of corticosteroids or reverse corticosteroid insensitivity may be added to ICS. ICS in combination with LABAs will continue to remain the main focus of treatment of airways diseases.	[Chung, Kian Fan; Caramori, Gaetano; Adcock, Ian M.] Univ London Imperial Coll Sci Technol & Med, Airway Dis Sect, Natl Heart & Lung Inst, London SW3 6LY, England; [Caramori, Gaetano] Univ Ferrara, Dept Asthma & COPD, I-44100 Ferrara, Italy	Chung, KF (reprint author), Univ London Imperial Coll Sci Technol & Med, Airway Dis Sect, Natl Heart & Lung Inst, Dovehouse St, London SW3 6LY, England.	f.chung@imperial.ac.uk		Chung, Kian Fan/0000-0001-7101-1426			Adams NP, 2006, RESP MED, V100, P1297, DOI 10.1016/j.rmed.2006.04.015; Adams NP, 2008, COCHRANE DB SYST REV, DOI 10.1002/14651858.CD003534.pub3; Adcock IM, 2008, LANCET, V372, P1073, DOI 10.1016/S0140-6736(08)61449-X; Adcock IM, 2008, CHEST, V134, P394, DOI 10.1378/chest.08-0440; Adcock Ian M., 2002, Journal of Allergy and Clinical Immunology, V110, pS261, DOI 10.1067/mai.2002.129705; ADELROTH E, 1990, AM REV RESPIR DIS, V142, P91; Ahmad T, 2008, CURR OPIN INVEST DR, V9, P470; Altose MD, 2000, NEW ENGL J MED, V343, P1902; Barnes NC, 2006, AM J RESP CRIT CARE, V173, P736, DOI 10.1164/rccm.200508-1321OC; 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J. Clin. Pharmacol.	SEP	2009	65	9					853	871		10.1007/s00228-009-0682-z		19	Pharmacology & Pharmacy	Pharmacology & Pharmacy	486ID	WOS:000269188700001	19557399	
J	Mylonas, KJ; Nair, MG; Prieto-Lafuente, L; Paape, D; Allen, JE				Mylonas, Katie J.; Nair, Meera G.; Prieto-Lafuente, Lidia; Paape, Daniel; Allen, Judith E.			Alternatively Activated Macrophages Elicited by Helminth Infection Can Be Reprogrammed to Enable Microbial Killing	JOURNAL OF IMMUNOLOGY			English	Article							ANTIGEN-PRESENTING CELLS; CD4(+) T-CELLS; TUMOR-INFILTRATING MACROPHAGES; LEISHMANIA-MEXICANA INFECTION; OXIDE-SYNTHESIZING PATHWAY; SYNTHASE ARGINASE BALANCE; SELECTIVE UP-REGULATION; IN-VIVO; PERITONEAL-MACROPHAGES; MURINE MACROPHAGES	The prime function of classically activated macrophages (activated by Th1-type signals, such as IFN-gamma) is microbial destruction. Alternatively activated macrophages (activated by Th2 cytokines, such as IL-4 and IL-13) play important roles in allergy and responses to helminth infection. We utilize a murine model of filarial infection, in which adult nematodes are surgically implanted into the peritoneal cavity of mice, as an in vivo source of alternatively activated macrophages. At 3 wk postinfection, the peritoneal exudate cell population is dominated by macrophages, termed nematode-elicited macrophages (NeM phi), that display IL-4-dependent features such as the expression of arginase 1, RELM-alpha (resistin-like molecule alpha), and Ym1. Since increasing evidence suggests that macrophages show functional adaptivity, the response of NeM phi to proinflammatory Th1-activating signals was investigated to determine whether a switch between alternative and classical activation could occur in macrophages differentiated in an in vivo infection setting. Despite the long-term exposure to Th2 cytokines and antiinflammatory signals in vivo, we found that NeM phi were not terminally differentiated but could develop a more classically activated phenotype in response to LPS and IFN-gamma. This was reflected by a switch in the enzymatic pathway for arginine metabolism from arginase to inducible NO synthase and the reduced expression of RELM-alpha and Ym1. Furthermore, this enabled NeM phi to become antimicrobial, as LPS/IFN-gamma-treated NeM phi produced NO that mediated killing of Leishmania mexicana. However, the adaptation to antimicrobial function did not extend to key regulatory pathways, such as IL-12 production, which remained unaltered. The Journal of Immunology, 2009, 182: 3084-3094.	[Mylonas, Katie J.; Nair, Meera G.; Prieto-Lafuente, Lidia; Paape, Daniel; Allen, Judith E.] Univ Edinburgh, Inst Immunol & Infect Res, Edinburgh EH9 3JT, Midlothian, Scotland	Allen, JE (reprint author), Univ Edinburgh, Inst Immunol & Infect Res, W Mains Rd, Edinburgh EH9 3JT, Midlothian, Scotland.	j.allen@ed.ac.uk	Allen, Judith/C-9198-2011; Paape, Daniel/G-1665-2015	Allen, Judith/0000-0002-3829-066X; Paape, Daniel/0000-0003-4355-8058	Wellcome Trust and the Medical Research Council, United Kingdom	This work was supported by the Wellcome Trust and the Medical Research Council, United Kingdom.	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Immunol.	MAR 1	2009	182	5					3084	3094		10.4049/jimmunol.0803463		11	Immunology	Immunology	411MG	WOS:000263653100060	19234205	
J	Caceres, M; Ali, SZ; Braud, R; Weiman, D; Garrett, HE				Caceres, Manuel; Ali, Syed Z.; Braud, Rebecca; Weiman, Darryl; Garrett, H. Edward, Jr.			Spontaneous pneumomediastinum: A comparative study and review of the literature	ANNALS OF THORACIC SURGERY			English	Review							ADULT PATIENTS; EXPERIENCE	Background. Spontaneous pneumomediastinum (SPM) is an unusual occurrence with few cases reported. It is seen after intrathoracic pressure changes leading to alveolar rupture and dissection of air along the tracheobronchial tree. This study was undertaken to provide a thorough clinical and radiologic analysis of this patient population. Methods. A retrospective comparative analysis was performed on patients with SPM over 12 years. Patient demographics, clinical presentation, and radiographic and diagnostic studies were recorded. A clinical and radiologic comparison was performed with secondary pneumomediastinum. Results. Seventy-four patients were identified with a diagnosis of pneumomediastinum. A total of 28 patients with SPM were identified. The major initial complaints were chest pain (54%), shortness of breath (39%), and subcutaneous emphysema (32%). The main triggering events were emesis (36%) and asthma flare-ups (21%). No apparent triggering event was noted in 21% of patients. Chest radiograph was diagnostic in 69%; computed tomography was required in 31%. Esophagram, esophagoscopy, and bronchoscopy were performed on an individual basis and were invariably negative. When compared with secondary pneumomediastinum, SPM is more likely to be discovered by chest radiography, has a lower incidence of pneumothorax and pleural effusion, requires a shorter hospital stay, and has no associated mortality. Conclusions. Spontaneous pneumomediastinum is a benign condition that often presents with chest pain or dyspnea. It can develop without a triggering event and with no findings on chest radiography. Treatment is expectant and recurrence is low. Secondary causes must be ruled out to avoid an unfavorable outcome.	Appalachian Regional Healthcare, Dept Cardiothorac Surg, Hazard, KY USA; Univ Tennessee HSC, Dept Cardiothorac Surg, Memphis, TN USA; Louisiana State Univ, Baton Rouge, LA 70803 USA; Baptist Mem Hosp, Dept Cardiothorac Surg, Memphis, TN 38146 USA	Garrett, HE (reprint author), 6029 Walnut Grove Rd,Suite 401, Memphis, TN 38120 USA.	egarrettmd@cvsclinic.com					ABOLNIK I, 1991, CHEST, V100, P93, DOI 10.1378/chest.100.1.93; Campillo-Soto A, 2005, ARCH BRONCONEUMOL, V41, P528, DOI 10.1157/13078656; Gerazounis M, 2003, J THORAC CARDIOV SUR, V126, P774, DOI 10.1016/S0022-5223(03)00124-7; HALPERIN AK, 1985, N C MED J, V46, P21; Ito S, 1989, Kokyu To Junkan, V37, P1359; Jougon JB, 2003, ANN THORAC SURG, V75, P1711, DOI 10.1016/S0003-4975(03)00027-4; Kaneki T, 2000, RESPIRATION, V67, P408, DOI 10.1159/000029539; Koullias GJ, 2004, EUR J CARDIO-THORAC, V25, P852, DOI 10.1016/j.ejcts.2004.01.042; Macia I, 2007, EUR J CARDIO-THORAC, V31, P1110, DOI 10.1016/j.ejcts.2007.03.008; MECKLIN CC, 1979, ARCH INTERN MED, V64, P913; Mihos P, 2004, ANN THORAC SURG, V78, P983, DOI 10.1016/.j.athorascur.2004.03.017; Miura Hiroyuki, 2003, Ann Thorac Cardiovasc Surg, V9, P188; Mondello B, 2007, LUNG, V185, P9, DOI 10.1007/s00408-006-0002-7; Nemet D, 2004, EUR J EMERG MED, V11, P105, DOI 10.1097/01.mej.0000114644.63700.7d; Newcomb AE, 2005, CHEST, V128, P3298, DOI 10.1378/chest.128.5.3298; PANACEK EA, 1992, ANN EMERG MED, V21, P1222, DOI 10.1016/S0196-0644(05)81750-0; Praski Arkadiusz, 2007, Ginekol Pol, V78, P329; Shindo Y, 1995, J EXP CLIN MED, V20, P1; Weissberg D, 2004, EUR J CARDIO-THORAC, V26, P885, DOI 10.1016/j.ejcts.2004.05.050; YELLIN A, 1983, THORAX, V38, P383, DOI 10.1136/thx.38.5.383	20	74	79	0	3	ELSEVIER SCIENCE INC	NEW YORK	360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA	0003-4975			ANN THORAC SURG	Ann. Thorac. Surg.	SEP	2008	86	3					962	966		10.1016/j.athoracsur.2008.04.067		5	Cardiac & Cardiovascular Systems; Respiratory System; Surgery	Cardiovascular System & Cardiology; Respiratory System; Surgery	340AT	WOS:000258619100037	18721592	
J	Noss, I; Wouters, IM; Visser, M; Heederik, DJJ; Thorne, PS; Brunekreef, B; Doekes, G				Noss, Ilka; Wouters, Inge M.; Visser, Maaike; Heederik, Dick J. J.; Thorne, Peter S.; Brunekreef, Bert; Doekes, Gert			Evaluation of a low-cost electrostatic dust fall collector for indoor air endotoxin exposure assessment	APPLIED AND ENVIRONMENTAL MICROBIOLOGY			English	Article							HOUSE-DUST; AIRBORNE ENDOTOXIN; SAMPLING METHODS; ALLERGEN; MITE; CAT; COMPONENTS; CHILDREN; HOMES	Exposure to endotoxin in home environments has become a key issue in asthma and allergy research. Most studies have analyzed floor or mattress dust endotoxin, but its validity as a proxy for airborne exposure is unknown, while active airborne dust sampling is not feasible in large-scale population studies because of logistic and financial limitations. We therefore developed and evaluated a simple passive airborne dust collection method for airborne endotoxin exposure assessment. We explored an electrostatic dust fall collector (EDC), consisting of a 42- by 29.6-cm-sized folder with four electrostatic cloths exposed to the air. The EDC was tested during two 14-day periods in seven nonfarm and nine farm homes and in farm stables. In parallel, active airborne dust sampling was performed with Harvard impactors and floor dust collected by vacuuming, using nylon sampling socks. The endotoxin levels could be measured in all EDC cloth extracts. The levels (in EU/m(2)) between EDCs used simultaneously or in different sampling periods in the same home correlated strongly (r > 0.8). EDC endotoxin also correlated moderately to strongly (r = 0.6 to 0.8) with the endotoxin measured by active airborne dust sampling and living room floor dust sampling and-in farm homes-with the endotoxin captured by the EDC in stables. In contrast, endotoxin levels measured by floor dust sampling showed only a poor correlation with the levels measured by active airborne dust sampling. We therefore conclude that measuring endotoxin levels with the EDC is a valid measure of average airborne endotoxin exposure, while reproducibility over time is at least equivalent to that of reservoir dust analyses.	[Noss, Ilka; Wouters, Inge M.; Visser, Maaike; Heederik, Dick J. J.; Brunekreef, Bert; Doekes, Gert] Univ Utrecht, Inst Risk Assessment Sci, Utrecht, Netherlands; [Thorne, Peter S.] Univ Iowa, Environm Hlth Sci Res Ctr, Iowa City, IA USA	Noss, I (reprint author), POB 80178, NL-3508 TD Utrecht, Netherlands.	i.noss@uu.nl		brunekreef, bert/0000-0001-9908-0060	European Commission [018996]; NIH [P30 ES05605]	This work was supported by the European Commission as part of GABRIEL, contract number 018996 under the Integrated Program LSH-2004-1.2.5-1. This work was also supported by the EU FP6-funded network of excellence GA<SUP>2</SUP>LEN. Peter S. Thorne was supported by NIH P30 ES05605.; We thank the participants of this validation study for their cooperation and James A. Deddens, University of Cincinnati, for his help with the statistical analysis.	Antens CJM, 2006, CLIN EXP ALLERGY, V36, P1525, DOI 10.1111/j.1365-2222.2006.02603.x; Custis NJ, 2003, CLIN EXP ALLERGY, V33, P986, DOI 10.1046/j.1365-2222.2003.01706.x; Custovic A, 1999, ALLERGY, V54, P612, DOI 10.1034/j.1398-9995.1999.00062.x; Fahlbusch B, 2003, ALLERGY, V58, P150, DOI 10.1034/j.1398-9995.2003.00036.x; Heinrich J, 2003, J EXPO ANAL ENV EPID, V13, P152, DOI 10.1038/sj.jea.7500267; Hyvarinen A, 2006, INDOOR AIR, V16, P20, DOI 10.1111/j.1600-0668.2005.00392.x; Janssen NAH, 1998, J EXPO ANAL ENV EPID, V8, P37; Karlsson AS, 2002, CLIN EXP ALLERGY, V32, P1776, DOI 10.1046/j.1365-2222.2002.01553.x; Karlsson AS, 2002, ALLERGY, V57, P164, DOI 10.1034/j.1398-9995.2002.1s3297.x; Krop EJM, 2007, OCCUP ENVIRON MED, V64, P267, DOI 10.1136/oem.2006.028845; Park JH, 2000, ENVIRON HEALTH PERSP, V108, P1023, DOI 10.2307/3434953; Park JH, 2001, ENVIRON HEALTH PERSP, V109, P859, DOI 10.2307/3454831; Platts-Mills JA, 2005, J ALLERGY CLIN IMMUN, V116, P384, DOI 10.1016/j.jaci.2005.05.012; PLATTSMILLS TAE, 1992, J ALLERGY CLIN IMMUN, V89, P1046, DOI 10.1016/0091-6749(92)90228-T; Renstrom A, 2002, J ENVIRON MONITOR, V4, P619, DOI 10.1039/b202756a; Schram D, 2005, ALLERGY, V60, P611, DOI 10.1111/j.1398-9995.2005.00748.x; Schram-Bijkerk D, 2006, INDOOR AIR, V16, P414, DOI 10.1111/j.1600-0668.2006.00435.x; Sotiriou M, 2008, ENVIRON MONIT ASSESS, V137, P351, DOI 10.1007/s10661-007-9770-7; Thorne PS, 2005, ANN OCCUP HYG, V49, P401, DOI 10.1093/annhyg/mei002; THORNE PS, 2007, AM J RESP CRIT CARE, V175, pA538; Tovey ER, 2003, ALLERGY, V58, P790, DOI 10.1034/j.1398-9995.2003.00228.x; Vissers M, 2001, CLIN EXP ALLERGY, V31, P1577, DOI 10.1046/j.1365-2222.2001.01204.x; Waser M, 2004, CLIN EXP ALLERGY, V34, P389, DOI 10.1111/j.1365-2222.2004.01873.x; Wurtz H, 2005, INDOOR AIR, V15, P33, DOI 10.1111/j.1600-0668.2005.00342.x	24	74	74	2	15	AMER SOC MICROBIOLOGY	WASHINGTON	1752 N ST NW, WASHINGTON, DC 20036-2904 USA	0099-2240			APPL ENVIRON MICROB	Appl. Environ. Microbiol.	SEP	2008	74	18					5621	5627		10.1128/AEM.00619-08		7	Biotechnology & Applied Microbiology; Microbiology	Biotechnology & Applied Microbiology; Microbiology	345SR	WOS:000259017400004	18676704	
J	Andersen, ZJ; Wahlin, P; Raaschou-Nielsen, O; Ketzel, M; Scheike, T; Loft, S				Andersen, Z. J.; Wahlin, P.; Raaschou-Nielsen, O.; Ketzel, M.; Scheike, T.; Loft, S.			Size distribution and total number concentration of ultrafine and accumulation mode particles and hospital admissions in children and the elderly in Copenhagen, Denmark	OCCUPATIONAL AND ENVIRONMENTAL MEDICINE			English	Article							PARTICULATE AIR-POLLUTION; CORONARY-HEART-DISEASE; 5 EUROPEAN CITIES; MYOCARDIAL-INFARCTION; EXPOSURE ASSESSMENT; URBAN AIR; FINE; AMBIENT; HEALTH; INDOOR	Objectives: To study the association between short-term exposure to ultrafine particles and morbidity in Copenhagen, Denmark. Methods: We studied the association between urban background levels of the total number concentration of particles (NCtot, 6-700 nm in diameter) measured at a single site (15 May 2001 to 31 December 2004) and hospital admissions due to cardiovascular (CVD) and respiratory disease (RD) in the elderly (age >= 65 years), and due to asthma in children (age 5-18 years). We examined these associations in the presence of PM10, PM2.5 (particulate matter < 10 and 2.5 mu m in diameter, respectively) and ambient gasses. We utilised data on size distribution to calculate NCtot for four modes with median diameters 12, 23, 57 and 212 nm, and NC100 (number concentration of particles < 100 nm in diameter) and examined their associations with health outcomes. We used a time series Poisson generalised additive model adjusted for overdispersion, season, day of the week, public holidays, school holidays, influenza, pollen and meteorology, with up to 5 days' lagged exposure. Results and conclusions: The adverse health effects of particulate matter on CVD and RD hospital admissions in the elderly were mainly mediated by PM10 and accumulation mode particles with lack of effects for NC100. For paediatric asthma, accumulation mode particles, NC100 and nitrogen oxides (mainly from traffic related sources) were relevant, whereas PM10 appeared to have little effect. Our results suggest that particle volume/mass from long-range transported air pollution is relevant for CVD and RD admissions in the elderly, and possibly particle numbers from traffic sources for paediatric asthma.	[Andersen, Z. J.; Scheike, T.] Univ Copenhagen, Inst Publ Hlth, Dept Biostat, DK-1014 Copenhagen K, Denmark; [Andersen, Z. J.; Loft, S.] Univ Copenhagen, Dept Environm & Occupat Hlth, Copenhagen, Denmark; [Wahlin, P.; Ketzel, M.] Aarhus Univ, Natl Environm Res Inst, Dept Atmospher Environm, Aarhus, Denmark; [Raaschou-Nielsen, O.] Inst Canc Epidemiol, Danish Canc Soc, Copenhagen, Denmark	Andersen, ZJ (reprint author), Univ Copenhagen, Inst Publ Hlth, Dept Biostat, 5 Entr,POB 2099, DK-1014 Copenhagen K, 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; Scheike, Thomas/0000-0002-2148-4740; Loft, Steffen/0000-0001-9552-8518			Aalto P, 2005, J AIR WASTE MANAGE, V55, P1064; Andersen ZJ, 2007, J EXPO SCI ENV EPID, V17, P625, DOI 10.1038/sj.jes.7500546; Brunekreef B, 2002, LANCET, V360, P1233, DOI 10.1016/S0140-6736(02)11274-8; Buzorius G, 1999, ATMOS ENVIRON, V33, P553, DOI 10.1016/S1352-2310(98)00287-8; Chalupa DC, 2004, ENVIRON HEALTH PERSP, V112, P879, DOI 10.1289/ehp.6851; Daigle CC, 2003, INHAL TOXICOL, V15, P539, DOI 10.1080/08958370390205065; de Hartog JJ, 2003, AM J EPIDEMIOL, V157, P613, DOI 10.1093/aje/kwg021; Delfino RJ, 2005, ENVIRON HEALTH PERSP, V113, P934, DOI 10.1289/ehp.7938; Donaldson K, 2001, OCCUP ENVIRON MED, V58, P211, DOI 10.1136/oem.58.3.211; Donaldson Ken, 2003, Ann Ist Super Sanita, V39, P405; Forastiere F, 2005, AM J RESP CRIT CARE, V172, P1549, DOI 10.1164/rccm.200412-1726OC; Gauderman WJ, 2004, NEW ENGL J MED, V351, P1057, DOI 10.1056/NEJMoa040610; Hastie T, 1990, GEN ADDITIVE MODELS; Hussein T, 2005, ATMOS ENVIRON, V39, P3697, DOI 10.1016/j.atmosenv.2005.03.011; Ibald-Mulli A, 2004, ENVIRON HEALTH PERSP, V112, P369, DOI 10.1289/ehp.6523; Ketzel M, 2003, ATMOS ENVIRON, V37, P2735, DOI 10.1016/S1352-2310(03)00245-0; Lanki T, 2006, OCCUP ENVIRON MED, V63, P844, DOI 10.1136/oem.2005.023911; Li N, 2003, ENVIRON HEALTH PERSP, V111, P455, DOI 10.1289/ehp.6000; McConnell R, 2006, ENVIRON HEALTH PERSP, V114, P766, DOI 10.1289/ehp.8594; Nemmar A, 2002, CIRCULATION, V105, P411, DOI 10.1161/hc0402.104118; Oberdorster G, 2005, ENVIRON HEALTH PERSP, V113, P823, DOI 10.1289/ehp.7339; Palmgren F, 2003, PHYS CHEM EARTH, V28, P327, DOI 10.1016/S1474-7065(03)00053-6; Pekkanen J, 2004, SCAND J WORK ENV HEA, V30, P9; Pekkanen J, 1997, ENVIRON RES, V74, P24, DOI 10.1006/enrs.1997.3750; Pekkanen J, 2002, CIRCULATION, V106, P933, DOI 10.1161/01.CIR.0000027561.41736.3C; PEKKANEN J, 2000, ULTRA EXPOSURE RISK; Penttinen P, 2001, EUR RESPIR J, V17, P428, DOI 10.1183/09031936.01.17304280; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; R Development Core Team, 2006, R LANG ENV STAT COMP; Ruuskanen J, 2001, ATMOS ENVIRON, V35, P3729, DOI 10.1016/S1352-2310(00)00373-3; Schlesinger RB, 2006, INHAL TOXICOL, V18, P95, DOI 10.1080/08958370500306016; Schneider T, 2004, ATMOS ENVIRON, V38, P6349, DOI 10.1016/j.atmosenv.2004.08.002; Schwartz J, 2004, PEDIATRICS, V113, P1037; Sioutas C, 2005, ENVIRON HEALTH PERSP, V113, P947, DOI 10.1289/ehp.7939; Stolzel M., 2007, Journal of Exposure Science and Environmental Epidemiology, V17, P458, DOI 10.1038/sj.jes.7500538; Timonen KL, 2006, J EXPO SCI ENV EPID, V16, P332, DOI 10.1038/sj.jea.7500460; Timonen KL, 2004, OCCUP ENVIRON MED, V61, P908, DOI 10.1136/oem.2004.012849; Vinzents PS, 2005, ENVIRON HEALTH PERSP, V113, P1485, DOI 10.1289/ehp.7562; von Klot S, 2005, CIRCULATION, V112, P3073, DOI 10.1161/CIRCULATIONAHA.105.548743; von Klot S, 2002, EUR RESPIR J, V20, P691, DOI 10.1183/09031936.02.01402001; WAHLIN P, 2004, NAT ENV SCI, V172, P142; WHO, 2000, EUR SER, V91; World Health Organization, 1992, INT STAT CLASS DIS R; Tuch T, 2000, RES REP HLTH EFF I, V98, P5	44	74	78	3	23	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	1351-0711			OCCUP ENVIRON MED	Occup. Environ. Med.	JUL	2008	65	7					458	466		10.1136/oem.2007.033290		9	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	315OU	WOS:000256890100005	17989204	
J	Yang, IA; Fong, KM; Zimmerman, PV; Holgate, ST; Holloway, JW				Yang, I. A.; Fong, K. M.; Zimmerman, P. V.; Holgate, S. T.; Holloway, J. W.			Genetic susceptibility to the respiratory effects of air pollution	THORAX			English	Review							BRONCHIAL EPITHELIAL-CELLS; DIESEL EXHAUST PARTICLES; ACUTE LUNG INJURY; OBSTRUCTIVE PULMONARY-DISEASE; BRONCHOALVEOLAR LAVAGE FLUID; REPEATED OZONE EXPOSURES; S-TRANSFERASE M1; OXIDATIVE STRESS; NITROGEN-DIOXIDE; PARTICULATE AIR	There is large variation between individuals in their response to air pollutants. This review summarises the existing evidence that genetic factors influence the mechanisms of lung injury caused by air pollutants. Genetic association studies have compared the adverse effects of air pollutants between subjects with specific genotypes in biologically relevant genes. In human studies of ozone exposure, polymorphisms in oxidative stress genes (NQO1, GSTM1, GSTP1) modify respiratory symptoms, lung function, biomarkers and risk of asthma. Inflammatory gene polymorphisms (TNF) influence the lung function response to ozone, and the effect of different levels of ozone on the development of asthma. Polymorphisms in oxidative stress genes (GSTM1, GSTP1) alter the response to combined exposure to ragweed pollen and diesel exhaust particles. Importantly, polymorphisms in an oxidative stress gene (GSTM1) have predicted patients with asthma who benefit from antioxidant supplementation in Mexico City, which has chronically high ozone exposure. Genetic linkage studies of families have not been feasible for studying the effects of air pollution in humans, but some progress has been made with pedigrees of specially bred mice, in identifying chromosomal regions linked to effects of ozone or particles. A high priority now, in addition to avoiding exposure in the most susceptible people, is to clearly identify the most effective and safe chemopreventive agents for individuals who are genetically susceptible to the adverse effects of air pollution (eg, antioxidants to be taken during high ozone levels).	[Yang, I. A.; Fong, K. M.; Zimmerman, P. V.] Prince Charles Hosp, Dept Thorac Med, Brisbane, Qld 4032, Australia; [Yang, I. A.; Fong, K. M.; Zimmerman, P. V.] Univ Queensland, Prince Charles Hosp, Sch Med, Brisbane, Qld, Australia; [Holgate, S. T.; Holloway, J. W.] Univ Southampton, Inflammat & Repair Div, Southampton, Hants, England; [Holloway, J. W.] Univ Southampton, Sch Med, Div Human Genet, Southampton, Hants, England	Yang, IA (reprint author), Prince Charles Hosp, Dept Thorac Med, Rode Rd, Brisbane, Qld 4032, Australia.	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J	Alm, B; Erdes, L; Mollborg, P; Pettersson, R; Norvenius, SG; Aberg, N; Wennergren, G				Alm, Bernt; Erdes, Laslo; Moellborg, Per; Pettersson, Rolf; Norvenius, S. Gunnar; Aberg, Nils; Wennergren, Goeran			Neonatal antibiotic treatment is a risk factor for early wheezing	PEDIATRICS			English	Article						antibiotics; cohort studies; infant; wheezing	TOBACCO-SMOKE EXPOSURE; EARLY-CHILDHOOD; 1ST YEAR; BIRTH COHORT; ALLERGIC DISEASE; ASTHMA; LIFE; INFANCY; AGE; INFECTIONS	OBJECTIVE. The use of antibiotics in infancy and subsequent changes in the intestinal bacterial flora have been discussed as risk factors for the development of asthma. However, it has been difficult to exclude the possibility that antibiotics have been given in early episodes of wheezing. As a result, there has been a risk of reverse causation. To minimize the risk of reverse causation, we have focused on the effect of antibiotics that are already administered on the neonatal ward. METHODS. In a cohort study of infants born in western Sweden in 2003, we studied the development of wheezing. The families of the infants were randomly selected and sent a questionnaire at child ages 6 and 12 months. The response rate was 68.5% to the 6-month questionnaire and 68.9% to the 12-month questionnaire. RESULTS. At 12 months, 20.2% of infants had had 1 or more episodes of wheezing, and 5.3% had had 3 or more episodes. Inhaled corticosteroids had been taken by 4.1% of the infants. Independent risk factors for wheezing disorder treated with inhaled corticosteroids were neonatal antibiotic treatment, male gender, gestational age of <37 weeks, having a mother with asthma, having a sibling with asthma or eczema, and breastfeeding for <5 months. CONCLUSIONS. Treatment with antibiotics in the neonatal period was an independent risk factor for wheezing that was treated with inhaled corticosteroids at 12 months of age. These results indirectly support the hypothesis that an alteration in the intestinal flora can increase the risk of subsequent wheezing.	[Alm, Bernt; Norvenius, S. Gunnar; Aberg, Nils; Wennergren, Goeran] Univ Gothenburg, Dept Pediat, Gothenburg, Sweden; [Erdes, Laslo] Pediat Outpatient Clin, Skene, Sweden; [Moellborg, Per] Uddevalla Cent Hosp, Cent Infant Welf Bur, Uddevalla, Sweden; [Pettersson, Rolf] Skaraborg Hosp, Dept Pediat, Skovde, Sweden	Alm, B (reprint author), Univ Gothenburg, Queen Silvia Childrens Hosp, Dept Pediat, SE-41685 Gothenburg, Sweden.	bernt.alm@medfak.gu.se		Alm, Bernt/0000-0002-3557-2995			Alm B, 2006, ARCH DIS CHILD, V91, P915, DOI 10.1136/adc.2005.088328; Altman M, 2006, ACTA PAEDIATR, V95, P1228, DOI 10.1080/08035250600589058; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; Bjorksten B, 2001, J ALLERGY CLIN IMMUN, V108, P516; Celedon JC, 2004, CLIN EXP ALLERGY, V34, P1011, DOI 10.1111/j.1365-2222.2004.01994.x; Celedon JC, 2002, AM J RESP CRIT CARE, V166, P72, DOI 10.1164/rccm.2109074; Cohet C, 2004, J EPIDEMIOL COMMUN H, V58, P852, DOI 10.1136/jech.2003.019182; Droste JHJ, 2000, CLIN EXP ALLERGY, V30, P1547; Illi S, 2001, BRIT MED J, V322, P390, DOI 10.1136/bmj.322.7283.390; Lux AL, 2000, ARCH DIS CHILD, V83, P307, DOI 10.1136/adc.83.4.307; Marra F, 2006, CHEST, V129, P610, DOI 10.1378/chest.129.3.610; Matricardi PM, 2000, BRIT MED J, V320, P412, DOI 10.1136/bmj.320.7232.412; McKeever TM, 2002, AM J RESP CRIT CARE, V166, P827, DOI 10.1164/rccm.200202-158OC; Murray CS, 2004, PEDIATR PULM, V37, P492, DOI 10.1002/ppul.20019; NORTH K, 1999, PEDIATRICS, V103; Norusis M.J., 2005, SPSS 13 0 GUIDE DATA; Penders J, 2007, GUT, V56, P661, DOI 10.1136/gut.2006.100164; Penders J, 2006, PEDIATRICS, V118, P511, DOI 10.1542/peds.2005-2824; PERSSON B, 2005, NATL HEALTHCARE QUAL; RYLANDER E, 1993, EUR J EPIDEMIOL, V9, P517; Stone KN, 2000, EARLY HUM DEV, V60, P137; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Thomas M, 2006, PEDIATR ALLERGY IMMU, V17, P184, DOI 10.1111/j.1399-3038.2006.00389.x; Wickens K, 1999, CLIN EXP ALLERGY, V29, P766; Wickman M, 2003, ALLERGY, V58, P742, DOI 10.1034/j.1398-9995.2003.00078.x; Wjst M, 2001, EUR J MED RES, V6, P263; WRIGHT AL, 1989, AM J EPIDEMIOL, V129, P1232; 2002, INFORM SWEDISH MED P, V13, P4	28	74	81	0	7	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	APR	2008	121	4					697	702		10.1542/peds.2007-1232		6	Pediatrics	Pediatrics	282OJ	WOS:000254576800006	18381533	
J	Andersen, ZJ; Wahlin, P; Raaschou-Nielsen, O; Scheike, T; Loft, S				Andersen, Zorana J.; Wahlin, Peter; Raaschou-Nielsen, Ole; Scheike, Thomas; Loft, Steffen			Ambient particle source apportionment and daily hospital admissions among children and elderly in Copenhagen	JOURNAL OF EXPOSURE SCIENCE AND ENVIRONMENTAL EPIDEMIOLOGY			English	Article						pM(10); source apportionment; hospital admissions; cardiovascular; respiratory; asthma	PM SOURCE APPORTIONMENT; PARTICULATE AIR-POLLUTION; DAILY MORTALITY; FINE PARTICLES; RESPIRATORY-DISEASES; CHILDHOOD ASTHMA; EUROPEAN CITIES; RECEPTOR MODEL; HEALTH; ASSOCIATIONS	An association between particulate air pollution and morbidity and mortality is well established. However, little is known about which sources of particulate matter contribute most to the adverse health effects. Identification of responsible sources would merit more effficient control. For a 6-year period ( 01 January 1999 to 31 December 2004), we examined associations between urban background PM10 in the presence of gaseous pollutants ( CO, NO2) and hospital admissions due to cardiovascular and respiratory disease in the elderly (age >= 65), and asthma in children (age 5-18) in Copenhagen, Denmark. We further studied associations between fractions of PM10 assigned to six sources (biomass, secondary, oil, crustal, sea salt, and vehicle) and admissions during a 11/2 -year campaign. We used Poisson generalized additive time-series model adjusted for season, day of the week, public holidays, influenza epidemics, grass pollen, school holidays, and meteorology, with up to 5 days lagged air pollution exposure. We found positive associations between PM10 and the three health outcomes, with strongest associations for asthma. The PM10 effect remained robustin the presence of CO and NO2. We found different PM10 sources to be variably associated with different outcomes: crustal and secondary sources showed strongest associations with cardiovascular, biomass with respiratory, and vehicle with asthma admissions. These novel results may merit future research of potential mechanism, whereas at present, no single PM10 source can be attributed to all morbidity.	Univ Copenhagen, Inst Publ Hlth, Dept Biostat, Copenhagen 1014, Denmark; Univ Copenhagen, Dept Environm & Occupat Hlth, Copenhagen 1014, Denmark; Natl Environm Res Inst, Dept Atmospher Environm, Roskilde, Denmark; Inst Canc Epidemiol, Danish Canc Soc, Copenhagen, Denmark	Andersen, ZJ (reprint author), Univ Copenhagen, Inst Publ Hlth, Dept Biostat, Oster Farimagsgade 5 entr,B PO Box 2099, Copenhagen 1014, Denmark.	zojo@biostat.ku.dk	Andersen, Zorana /P-4983-2014	Andersen, Zorana /0000-0003-4138-9828; Scheike, Thomas/0000-0002-2148-4740; Loft, Steffen/0000-0001-9552-8518			AKAIKE H, 1974, IEEE T AUTOMAT CONTR, VAC19, P716, DOI 10.1109/TAC.1974.1100705; Anderson HR, 2005, EPIDEMIOLOGY, V16, P155, DOI 10.1097/01.ede.0000152528.22746.0f; Atkinson RW, 2001, AM J RESP CRIT CARE, V164, P1860; BOMAN BC, 2003, SCAND J WORK ENV HEA, V29, P309; Brunekreef B, 2005, EUR RESPIR J, V26, P309, DOI 10.1183/09031936.05.00001805; Brunekreef B, 2002, LANCET, V360, P1233, DOI 10.1016/S0140-6736(02)11274-8; Dominici F, 2006, JAMA-J AM MED ASSOC, V295, P1127, DOI 10.1001/jama.295.10.1127; Englert N, 2004, TOXICOL LETT, V149, P235, DOI 10.1016/j.toxlet.2003.12.035; Gauderman WJ, 2005, EPIDEMIOLOGY, V16, P737, DOI 10.1097/01.ede.00001813087.51440.75; Guo YLL, 1999, ENVIRON HEALTH PERSP, V107, P1001; Hastie T., 1990, GENERALIZED ADDITIVE; *HEI, 2003, REV AN TIM SER STUD; Hopke PK, 2006, J EXPO SCI ENV EPID, V16, P275, DOI 10.1038/sj.jea.7500458; Ito K, 2006, J EXPO SCI ENV EPID, V16, P300, DOI 10.1038/sj.jea.7500464; Janssen NAH, 2002, ENVIRON HEALTH PERSP, V110, P43; Katsouyanni K, 2001, EPIDEMIOLOGY, V12, P521, DOI 10.1097/00001648-200109000-00011; Kunzli N, 2000, LANCET, V356, P795, DOI 10.1016/S0140-6736(00)02653-2; Laden F, 2000, ENVIRON HEALTH PERSP, V108, P941, DOI 10.2307/3435052; Lanki T, 2006, ENVIRON HEALTH PERSP, V114, P655, DOI 10.1289/ehp.8578; Le Tertre A, 2002, J EPIDEMIOL COMMUN H, V56, P773, DOI 10.1136/jech.56.10.773; Lippmann M, 2005, ENVIRON HEALTH PERSP, V113, P1575, DOI 10.1289/ehp.8091; Mar TF, 2000, ENVIRON HEALTH PERSP, V108, P347, DOI 10.2307/3454354; Mar TF, 2006, J EXPO SCI ENV EPID, V16, P311, DOI 10.1038/sj.jea.7500465; McConnell R, 2006, ENVIRON HEALTH PERSP, V114, P766, DOI 10.1289/ehp.8594; McConnell R, 1999, ENVIRON HEALTH PERSP, V107, P757, DOI 10.2307/3434662; Metzger KB, 2004, EPIDEMIOLOGY, V15, P46, DOI 10.1097/01.EDE.0000101748.28283.97; ORZOCCOLEVI M, 2006, EUR RESPIR J, V27, P446; OZKAYNAK H, 1987, RISK ANAL, V7, P449, DOI 10.1111/j.1539-6924.1987.tb00482.x; PAATERO P, 1994, ENVIRONMETRICS, V5, P111, DOI 10.1002/env.3170050203; Penttinen P, 2006, INHAL TOXICOL, V18, P191, DOI 10.1080/08958370500434230; R Development Core Team, 2006, R LANG ENV STAT COMP; SAMET JM, 2000, HLTH EFFECTS I RES 2, V94, P5; Schwartz J, 2004, PEDIATRICS, V113, P1037; Schwartz J, 2000, EPIDEMIOLOGY, V11, P320, DOI 10.1097/00001648-200005000-00016; SCHWARTZ J, 1994, AM J EPIDEMIOL, V139, P589; Spix C, 1998, ARCH ENVIRON HEALTH, V53, P54; Studnicka M, 1997, EUR RESPIR J, V10, P2275, DOI 10.1183/09031936.97.10102275; Sverdrup H.U., 1942, OCEANS; Wahlin P, 2006, ATMOS ENVIRON, V40, P2151, DOI 10.1016/j.atmosenv.2005.11.049; Wahlin P, 2003, ATMOS ENVIRON, V37, P4861, DOI 10.1016/j.atmosenv.2003.08.032; WATSON JG, 1984, ATMOS ENVIRON, V18, P1347, DOI 10.1016/0004-6981(84)90043-X; World Health Organization, 2005, EFF AIR POLL CHILDR; *WHO, 2004, MET AN TIM SER STUD	43	74	76	2	23	NATURE PUBLISHING GROUP	NEW YORK	75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA	1559-0631			J EXPO SCI ENV EPID	J. Expo. Sci. Environ. Epidemiol.	NOV	2007	17	7					625	636		10.1038/sj.jes.7500546		12	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	231RJ	WOS:000250966400004	17495872	
J	Johnston, RA; Zhu, M; Rivera-Sanchez, YM; Lu, FL; Theman, TA; Flynt, L; Shore, SA				Johnston, Richard A.; Zhu, Ming; Rivera-Sanchez, Yadira M.; Lu, Frank L.; Theman, Todd A.; Flynt, Lesley; Shore, Stephanie A.			Allergic airway responses in obese mice	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						airway responsiveness; eosinophil; immunoglobulin E; interleukin-13; pulmonary resistance	BODY-MASS INDEX; NECROSIS-FACTOR-ALPHA; ACUTE OZONE EXPOSURE; C-REACTIVE PROTEIN; RESPIRATORY SYMPTOMS; PULMONARY RESPONSES; INSULIN-RESISTANCE; WEIGHT-REDUCTION; ASTHMA; INFLAMMATION	Rationale: Epidemiologic data indicate an increased incidence of asthma in the obese. Objectives: To determine whether obese mice exhibit augmented pulmonary responses after allergen sensitization and challenge. Methods: Lean, wild-type (C57BL/6), obese ob/ob, and obese db/db mice were sensitized to ovalbumin (OVA), and then challenged with aerosolized OVA or phosphate-buffered saline (PBS). Changes in total pulmonary resistance (RL) induced by intravenous methacholine were measured by forced oscillation. Blood was collected, bronchoalveolar lavage (BAL) was performed, and lungs were harvested for measurement of cytokine expression by real-time reverse transcription-polymerase chain reaction. Measurements and Main Results: OVA challenge increased baseline R-L in ob/ob, but not wild-type, mice, and airway responsiveness was greater in ob/ob than wild-type mice, regardless of the challenge. Compared with PBS, OVA challenge caused an increase in the number of BAL fluid (BALF) cells, an increase in lung Th2 cytokine expression, and an increase in serum IgE. Significantly fewer BALF cells were recovered from OVA-challenged ob/ob versus wild-type mice, whereas serum IgE levels were elevated significantly more in ob/ob versus wild-type mice. BALIF and lung Th2 cytokine expression was not different in ob/ob versus wild-type mice. Airway responsiveness was greater in db/db versus wild-type mice, regardless of the challenge, and OVA caused airway hyperresponsiveness in db/db but not wild-type mice, despite reduced BALF cells in OVA-challenged db/db versus wild-type mice. Conclusions: These results demonstrate that obesity enhances OVA-induced changes in pulmonary resistance and serum IgE and that these changes are not the result of increased Th2 type airway inflammation.	Univ Texas, Med Branch, Dept Internal Med, Div Allergy Pulm Immunol Crit Care & Sleep, Galveston, TX 77555 USA; Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Mol & Integrat Physiol Sci Program, Boston, MA 02115 USA; Natl Taiwan Univ, Coll Med, Taipei 10764, Taiwan; Natl Taiwan Univ Hosp, Dept Pediat, Taipei 100, Taiwan	Johnston, RA (reprint author), Univ Texas, Med Branch, Dept Internal Med, Div Allergy Pulm Immunol Crit Care & Sleep, 301 Univ Blvd,Room 8-104A,Med Res Bldg, Galveston, TX 77555 USA.	rajohnst@utmb.edu	Lu, Frank/G-6196-2012	Lu, Frank/0000-0002-5225-7751	NHLBI NIH HHS [HL-33009]; NIEHS NIH HHS [ES-013307, ES-00002]		Aaron SD, 2004, CHEST, V125, P2046, DOI 10.1378/chest.125.6.2046; Amrani Y, 1998, THORAX, V53, P713; Back M, 2007, CIRC RES, V100, P946, DOI 10.1161/01.RES.0000264498.60702.0d; Bastard JP, 2002, J CLIN ENDOCR METAB, V87, P2084, DOI 10.1210/jc.87.5.2084; Bellmeyer A, 2007, AM J RESP CRIT CARE, V175, P587, DOI 10.1164/rccm.200603-312OC; Brewer JP, 1999, AM J RESP CRIT CARE, V160, P1150; 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J. Respir. Crit. Care Med.	OCT 1	2007	176	7					650	658		10.1164/rccm.200702-323OC		9	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	215SP	WOS:000249829600006	17641156	
J	Stranger, M; Potgieter-Vermaak, SS; Van Grieken, R				Stranger, M.; Potgieter-Vermaak, S. S.; Van Grieken, R.			Comparative overview of indoor air quality in Antwerp, Belgium	ENVIRONMENT INTERNATIONAL			English	Article						indoor air quality; PM1; PM2.5; PM10; gaseous pollutants	SUSPENDED PARTICLE EXPOSURES; ENVIRONMENTAL TOBACCO-SMOKE; PEAK EXPIRATORY FLOW; LONG-TERM EXPOSURE; HONG-KONG; PARTICULATE MATTER; RESPIRATORY SYMPTOMS; NITROGEN-DIOXIDE; INDOOR/OUTDOOR RELATIONSHIPS; ELEMENTAL COMPOSITION	This comprehensive study, a first in Belgium, aimed at characterizing the residential and school indoor air quality of subgroups that took part in the European Community Respiratory Health Survey and the International Study of Asthma and Allergy in Childhood [Masoli M, Fabian D, Holt S, Beasley R. Global Burden of Asthma, Medical Research Institute of New Zealand, University of Southampton; 2004.] questionnaire-based asthma and related illnesses studies. The principal aim was to perform a base-line study to assess the indoor air quality in Antwerp in terms of various gaseous and particulate pollutants. Secondly, it aimed to establish correlations between these pollutants investigated, the pollutant levels in the indoor and outdoor micro-environments, findings of the previous questionnaire-based studies and an epidemiological study which ran in conjunction with this study. Lastly, these results were compared and evaluated with current indoor and ambient guidelines in various countries This paper presents selected results on PM1, PM2.5 and PM 10 mass concentrations and elemental C estimates as black smoke, as well as gaseous NO, SO2, O-3 and BTEX concentrations of 18 residences and 27 schools. These are related to current guidelines of Flanders, Germany, Norway, China and Canada and evaluated with reference to selected similar studies. It was found that indoor sources such as tobacco smoking and carpets, the latter causing re-suspension of dust, are responsible for elevated indoor respirable particulate matter and place school children and residents at risk. Both PM2.5 and PM10 equalled or exceeded the current guidelines adopted by Flanders, noting that 12-h and 24-h PM2.5 were compared with an annual limit value. Indoor and ambient NO2 concentrations in the school campaign were higher than the annual EU ambient norm. The other studied pollutant levels were below the current guidelines. (c) 2007 Elsevier Ltd. All rights reserved.	Univ Witwatersrand, Sch Chem, Inst Mol Sci, ZA-2050 Wits, South Africa; Univ Antwerp, Dept Chem, B-2610 Antwerp, Belgium; Univ Coll Antwerp, Higher Inst Prod Dev Design Sci, B-2000 Antwerp, Belgium	Potgieter-Vermaak, SS (reprint author), Univ Witwatersrand, Sch Chem, Inst Mol Sci, Private Bag X3, ZA-2050 Wits, South Africa.	sanjap@chem.wits.ac.za					Asher MI, 1998, EUR RESPIR J, V12, P315; Boezen HM, 1999, LANCET, V353, P874, DOI 10.1016/S0140-6736(98)06311-9; Breysse PN, 2005, ENVIRON RES, V98, P167, DOI 10.1016/j.envres.2004.07.018; BRUNEKREEF B, 2005, HLTH EFF I, P127; Burnett RT, 2001, AM J EPIDEMIOL, V153, P444, DOI 10.1093/aje/153.5.444; CARRER P, 2002, THADE PROJECT HLTH A; Chao CY, 2002, ATMOS ENVIRON, V36, P265, DOI 10.1016/S1352-2310(01)00411-3; Farhat SCL, 2005, BRAZ J MED BIOL RES, V38, P227, DOI 10.1590/S0100-879X2005000200011; Franchi M, 2006, ALLERGY, V61, P864, DOI 10.1111/j.1398-9995.2006.01106.x; FRANCHI M, 2006, THADE REPORT; Gallelli G, 2002, SCI TOTAL ENVIRON, V287, P31, DOI 10.1016/S0048-9697(01)00990-1; GODISH T, 1990, AIR QUALITY; Goldberg MS, 2001, ENVIRON RES, V86, P26, DOI 10.1006/enrs.2001.4243; Grontoft T, 2004, ATMOS ENVIRON, V38, P533, DOI 10.1016/j.atmosenv.2003.10.010; Haller L, 1999, J AIR WASTE MANAGE, V49, P161, DOI 10.1080/10473289.1999.10463788; Hiltermann TJN, 1998, EUR RESPIR J, V11, P686; Ho KF, 2004, ATMOS ENVIRON, V38, P6327, DOI 10.1016/j.atmosenv.2004.08.007; Hoek G, 1998, EUR RESPIR J, V11, P1307, DOI 10.1183/09031936.98.11061307; Jones NC, 2000, ATMOS ENVIRON, V34, P2603, DOI 10.1016/S1352-2310(99)00489-6; KUOSA A, 2001, ATMOS ENVIRON, V35, P3405; Lai HK, 2004, ATMOS ENVIRON, V38, P6399, DOI 10.1016/j.atmosenv.2004.07.013; Lee K, 2002, ENVIRON HEALTH PERSP, V110, P145; Lee SC, 2000, CHEMOSPHERE, V41, P109, DOI 10.1016/S0045-6535(99)00396-3; Lee SC, 1997, ENVIRON INT, V23, P791, DOI 10.1016/S0160-4120(97)00091-3; Liu YS, 2004, ENVIRON INT, V30, P189, DOI 10.1016/S0160-4120(03)00173-9; Masoli M., 2004, GLOBAL BURDEN ASTHMA; Monn C, 1998, SCI TOTAL ENVIRON, V215, P243, DOI 10.1016/S0048-9697(98)00124-7; Monn C, 1997, SCI TOTAL ENVIRON, V208, P15, DOI 10.1016/S0048-9697(97)00271-4; Monn C, 2001, ATMOS ENVIRON, V35, P1, DOI 10.1016/S1352-2310(00)00330-7; Peacock JL, 2003, OCCUP ENVIRON MED, V60, P82, DOI 10.1136/oem.60.2.82; Peters A, 1996, AM J EPIDEMIOL, V144, P570; Phillips K, 1999, ATMOS ENVIRON, V33, P1889, DOI 10.1016/S1352-2310(98)00205-2; Phillips K, 2001, ENVIRON INT, V27, P69, DOI 10.1016/S0160-4120(01)00057-5; Phillips K, 1998, ENVIRON INT, V24, P851, DOI 10.1016/S0160-4120(98)00072-5; Pikhart H, 2001, INT ARCH OCC ENV HEA, V74, P574; Pope CA, 2002, JAMA-J AM MED ASSOC, V287, P1132, DOI 10.1001/jama.287.9.1132; Ramadour M, 2000, ALLERGY, V55, P1163, DOI 10.1034/j.1398-9995.2000.00637.x; Roemer W, 1998, EUR RESPIR J, V12, P1354, DOI 10.1183/09031936.98.12061354; Roemer W, 2000, EUR RESPIR J, V15, P553, DOI 10.1034/j.1399-3003.2000.15.21.x; Sawant AA, 2004, ATMOS ENVIRON, V38, P6269, DOI 10.1016/j.atmosenv.2004.08.043; Schneider P, 2001, SCI TOTAL ENVIRON, V267, P41, DOI 10.1016/S0048-9697(00)00766-X; Schwartz J, 2001, ENVIRON HEALTH PERSP, V109, P1001, DOI 10.2307/3454953; STRANGER M, IN PRESS ATM ENV; Wickman M, 2003, ALLERGY, V58, P570, DOI 10.1034/j.1398-9995.2003.00179.x; Wieringa MH, 2001, EUR RESPIR J, V17, P422, DOI 10.1183/09031936.01.17304220; Wieringa MH, 1998, INT J EPIDEMIOL, V27, P630, DOI 10.1093/ije/27.4.630; Wieringa MH, 1997, EUR RESPIR J, V10, P1460, DOI 10.1183/09031936.97.10071460	47	74	79	10	35	PERGAMON-ELSEVIER SCIENCE LTD	OXFORD	THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND	0160-4120			ENVIRON INT	Environ. Int.	AUG	2007	33	6					789	797		10.1016/j.envint.2007.02.014		9	Environmental Sciences	Environmental Sciences & Ecology	193KU	WOS:000248273700010	17399789	
J	Almqvist, C; Garden, F; Xuan, W; Mihrshahi, S; Leeder, SR; Oddy, W; Webb, K; Marks, GB				Almqvist, Catarina; Garden, Frances; Xuan, Wei; Mihrshahi, Seema; Leeder, Steve R.; Oddy, Wendy; Webb, Karen; Marks, Guy B.		CAPS Team	Omega-3 and omega-6 fatty acid exposure from early life does not affect atopy and asthma at age 5 years	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; allergy and immunology; birth cohort; child; eczema; omega-3 fatty acids; omega-6 fatty acids; primary prevention	CHILDHOOD ASTHMA; CHILDREN; DIETARY; ADULTS; RISK; PREVENTION; TRIAL; FISH	Background: The Childhood Asthma Prevention Study was a randomized controlled trial conducted in children with a family history of asthma in whom omega-3 fatty acid supplementation and restriction of dietary omega-6 fatty acids did not prevent asthma, eczema, or atopy at age 5 years. Objective: We sought to examine the relation of all measures of omega-3 and omega-6 polyunsaturated fatty acids with outcomes at age 5 years in the whole birth cohort, regardless of randomization group. Methods: Plasma fatty acids were measured at 18 months, 3 years, and 5 years. Compliance with the fatty acid supplements was estimated every 6 months. Dietary intake was assessed at 18 months by means of weighed-food record and at 3 years by means of food-frequency questionnaire. At age 5 years, 516 children were examined for wheeze and eczema (questionnaire) and atopy (skin prick tests, n = 488). Multiple logistic regression was used to evaluate associations between exposures and outcomes. Results: Plasma levels of omega-3 or omega-6 fatty acids were not associated with wheeze, eczema, or atopy at age 5 years (P = .11-.96). Overall, fatty acid exposure, measured as plasma levels, dietary intake, and compliance with supplements, was not associated with any respiratory or allergic outcomes (P =.35-.59). Conclusion: This observational analysis of the cohort, using the full range of observed variation in omega-3 and omega-6 fatty acid exposure, supports the negative findings of the randomized controlled trial. Clinical implications: Modification of dietary polyunsaturated fatty acids in early childhood is not helpful in preventing atopy and asthma.	Woolcock Inst Med Res, Sydney, NSW, Australia; Univ Sydney, Fac Med, Sydney, NSW 2006, Australia; Karolinska Inst, Astrid Lindgren Childrens Hosp, Dept Woman & Child Hlth, Stockholm, Sweden; New S Wales Dept Hlth, Sydney, NSW, Australia; Childrens Hosp Westmead, Sydney, NSW, Australia; Curtin Univ Technol, Telethon Inst Child Hlth Res, Perth, WA 6001, Australia	Almqvist, C (reprint author), Woolcock Inst Med Res, PO Box M77,Missenden Rd, Camperdown, NSW 2050, Australia.	calmqvist@woolcock.org.au	Mihrshahi, Seema/A-9877-2009	Mihrshahi, Seema/0000-0001-6567-9884			ARM J P, 1988, Thorax, V43, P84, DOI 10.1136/thx.43.2.84; Bolte G, 2006, CLIN EXP ALLERGY, V36, P293, DOI 10.1111/j.1365-2222.2006.02441.x; Broadfield EC, 2004, CLIN EXP ALLERGY, V34, P1232, DOI 10.1111/j.1365-2222.2004.02032.x; Department of Health and Ageing National Health and Medical Research Council Ministry of Health, 2006, NUTR REF VAL AUSTR N; Haby MM, 2001, THORAX, V56, P589, DOI 10.1136/thorax.56.8.589; Hodge L, 1996, MED J AUSTRALIA, V164, P137; Hodge L, 1998, EUR RESPIR J, V11, P361, DOI 10.1183/09031936.98.11020361; KIRSCH CM, 1988, CLIN ALLERGY, V18, P177, DOI 10.1111/j.1365-2222.1988.tb02857.x; Mann N. J., 2003, Nutrition & Dietetics, V60, P42; Marks GB, 2006, J ALLERGY CLIN IMMUN, V118, P53, DOI 10.1016/j.jaci.2006.04.004; Mihrshahi S, 2001, CONTROL CLIN TRIALS, V22, P333, DOI 10.1016/S0197-2456(01)00112-X; Nagakura T, 2000, EUR RESPIR J, V16, P861, DOI 10.1183/09031936.00.16586100; PEAT JK, 1992, EUR RESPIR J, V5, P921; Trak-Fellermeier MA, 2004, EUR RESPIR J, V23, P575, DOI 10.1183/09031936.04.00074404; WEBB K, 2005, NUTR DIETETICS, V62, P189; Woods RK, 2004, THORAX, V59, P105, DOI 10.1136/thorax.2003.009498; Woods RK, 2002, COCHRANE DB SYST REV, DOI DOI 10.1002/14651858	17	74	76	0	5	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	2007	119	6					1438	1444		10.1016/j.jaci.2007.01.046		7	Allergy; Immunology	Allergy; Immunology	178PO	WOS:000247232800020	17379291	
J	Heederik, D; Sigsgaard, T; Thorne, PS; Kline, JN; Avery, R; Bonlokke, JH; Chrischilles, EA; Dosman, JA; Duchaine, C; Kirkhorn, SR; Kulhankova, K; Merchant, JA				Heederik, Dick; Sigsgaard, Torben; Thorne, Peter S.; Kline, Joel N.; Avery, Rachel; Bonlokke, Jakob H.; Chrischilles, Elizabeth A.; Dosman, James A.; Duchaine, Caroline; Kirkhorn, Steven R.; Kulhankova, Katarina; Merchant, James A.			Health effects of airborne exposures from concentrated animal feeding operations	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air quality; asthma; biological agents; endotoxin; inflammation; odor; poultry; swine	SWINE CONFINEMENT BUILDINGS; IN-HOUSE DUST; ENDOTOXIN EXPOSURE; LUNG-FUNCTION; OCCUPATIONAL ASTHMA; RESPIRATORY HEALTH; HAY-FEVER; ENVIRONMENTAL ENDOTOXIN; ALLERGIC SENSITIZATION; FARMERS CHILDREN	Toxic gases, vapors, and particles are emitted from concentrated animal feeding operations (CAFOs) into the general environment. These include ammonia, hydrogen sulfide, carbon dioxide, malodorous vapors, and particles contaminated with a wide range of microorganisms. Little is known about the health risks of exposure to these agents for people living in the surrounding areas. Malodor is one of the predominant concerns, and there is evidence that psychophysiologic changes may occur as a result of exposure to malodorous compounds. There is a paucity of data regarding community adverse health effects related to low-level gas and particulate emissions. Most information comes from studies among workers in CAFO installations. Research over the last decades has shown that microbial exposures, especially endotoxin exposure, are related to deleterious respiratory health effects, of which cross-shift lung function decline and accelerated decline over time are the most pronounced effects. Studies in naive subjects and workers have shown respiratory inflammatory responses related to the microbial load. This working group, which was part of the Conference on Environmental Health Impacts of Concentrated Animal Feeding Operations: Anticipating Hazards-Searching for Solutions, concluded that there is a great need to evaluate health effects from exposures to the toxic gases, vapors, and particles emitted into the general environment by CAFOs. Research should focus not only on nuisance and odors but also on potential health effects from microbial exposures, concentrating on susceptible subgroups, especially asthmatic children and the elderly, since these exposures have been shown to be related to respiratory health effects among workers in CAFOs.	Univ Iowa, Coll Publ Hlth, Iowa City, IA 52242 USA; Univ Utrecht, Utrecht, Netherlands; Univ Aarhus, DK-8000 Aarhus C, Denmark; Univ N Carolina, Chapel Hill, NC USA; Univ Saskatchewan, Saskatoon, SK, Canada; Univ Laval, Quebec City, PQ, Canada; Natl Farm Med Ctr, Marshfield, WI USA	Thorne, PS (reprint author), Univ Iowa, Coll Publ Hlth, 100 Oakdale Campus,176 IREH, Iowa City, IA 52242 USA.	peter-thorne@uiowa.edu		Sigsgaard, Torben/0000-0002-2043-7571; Bonlokke, Jakob/0000-0002-8247-6576	NIEHS NIH HHS [P30 ES005605, P30 ES05605-14S]		ATTWOOD P, 1987, AM IND HYG ASSOC J, V48, P745, DOI 10.1202/0002-8894(1987)048<0745:ASOTRB>2.0.CO;2; Avery RC, 2004, ARCH ENVIRON HEALTH, V59, P101, DOI 10.3200/AEOH.59.2.101-108; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; BROUWER R, 1990, AM J IND MED, V17, P96; CORMIER Y, 1991, SCAND J WORK ENV HEA, V17, P269; CROOK B, 1991, AM IND HYG ASSOC J, V52, P271, DOI 10.1202/0002-8894(1991)052<0271:ADAMAA>2.0.CO;2; Donham KJ, 2000, J OCCUP ENVIRON MED, V42, P260, DOI 10.1097/00043764-200003000-00006; DONHAM KJ, 1984, ARCH ENVIRON HEALTH, V39, P96; Douwes J, 2000, AM J RESP CRIT CARE, V162, P1348; Douwes J, 2002, THORAX, V57, P86, DOI 10.1136/thorax.57.1.86; Douwes J, 1998, INDOOR AIR, V8, P255, DOI 10.1111/j.1600-0668.1998.00006.x; Douwes J, 1997, INT J OCCUP ENV HEAL, V3, pS26; 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; Ernst P, 2000, AM J RESP CRIT CARE, V161, P1563; Fishwick D, 1997, OCCUP ENVIRON MED, V54, P301; 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; Gioannini TL, 2003, J ENDOTOXIN RES, V9, P401, DOI 10.1179/096805103225002773; HARRIES MG, 1982, BRIT MED J, V284, P867; Jagielo PJ, 1996, CHEST, V110, P263, DOI 10.1378/chest.110.1.263; KATILA ML, 1981, BRIT J IND MED, V38, P334; KEIKHAEFER MS, 1995, ANN AGR ENV MED, V2, P37; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; KIMPBELLDUNN M, 1999, AM J IND MED, V35, P51; Kline JN, 1999, AM J RESP CRIT CARE, V160, P297; Kline JN, 1998, J IMMUNOL, V160, P2555; Klintberg B, 2001, EUR RESPIR J, V17, P1151, DOI 10.1183/09031936.01.00027301; Kogevinas M, 1999, LANCET, V353, P1750, DOI 10.1016/S0140-6736(98)07397-8; Kruger T, 2004, CYTOKINE, V25, P73, DOI 10.1016/j.cyto.2003.10.001; Kullman GJ, 1998, AM IND HYG ASSOC J, V59, P403, DOI 10.1202/0002-8894(1998)059<0403:ODEFWI>2.0.CO;2; Liu AH, 2000, CLIN EXP ALLERGY, V30, P1535, DOI 10.1046/j.1365-2222.2000.01012.x; Martinez FD, 1999, LANCET S2, V354, pSII12; Melbostad E, 1998, SCAND J WORK ENV HEA, V24, P262; MERCHANT JA, 2005, ENV HLTH PERSPECT, V113, P3350; MICHEL O, 1991, CLIN EXP ALLERGY, V21, P441, DOI 10.1111/j.1365-2222.1991.tb01684.x; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; Michel O, 1997, AM J RESP CRIT CARE, V156, P1157; NEIJARI C, 1996, RESP MED, V90, P401; Omland O, 1999, EUR RESPIR J, V13, P31, DOI 10.1183/09031936.99.13103199; PETERSON RD, 1964, J ALLERGY, V35, P134, DOI 10.1016/0021-8707(64)90027-9; Portengen L, 2005, J ALLERGY CLIN IMMUN, V115, P797, DOI 10.1016/j.jaci.2004.11.046; Portengen L, 2002, CLIN EXP ALLERGY, V32, P247, DOI 10.1046/j.1365-2222.2002.01310.x; RADON K, 2005, BIOMETRICS EPID 0915; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; RYLANDER R, 1989, SCAND J WORK ENV HEA, V15, P309; Rylander R, 1997, INT J OCCUP ENV HEAL, V3, pS32; SANDSTROM T, 1992, EUR RESPIR J, V5, P992; Schenker MB, 1998, AM J RESP CRIT CARE, V158, pS1; Shirakawa T, 1997, SCIENCE, V275, P77, DOI 10.1126/science.275.5296.77; Thorne PS, 2005, AM J RESP CRIT CARE, V172, P1371, DOI 10.1164/rccm.200505-758OC; TOREN K, 1991, BRIT J IND MED, V48, P323; Vogelzang PFJ, 1998, AM J RESP CRIT CARE, V157, P15; Vogelzang PFJ, 1999, EUR RESPIR J, V13, P187, DOI 10.1034/j.1399-3003.1999.13a34.x; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; Von Essen S, 2003, J Agric Saf Health, V9, P185; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; Yazdanbakhsh M, 2002, SCIENCE, V296, P490, DOI 10.1126/science.296.5567.490; Zhiping Wang, 1996, American Journal of Respiratory and Critical Care Medicine, V154, P1261	60	74	75	8	49	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	2007	115	2					298	302		10.1289/ehp.8835		5	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	132ML	WOS:000243946800043	17384782	
J	Fleming, LE; Kirkpatrick, B; Backer, LC; Beam, JA; Wanner, A; Reich, A; Zaias, J; Cheng, YS; Pierce, R; Naar, J; Abraham, WM; Baden, DG				Fleming, Lora E.; Kirkpatrick, Barbara; Backer, Lorraine C.; Beam, Judy A.; Wanner, Adam; Reich, Andrew; Zaias, Julia; Cheng, Yung Sung; Pierce, Richard; Naar, Jerome; Abraham, William M.; Baden, Daniel G.			Aerosolized red-tide toxins (brevetoxins) and asthma	CHEST			English	Article						asthma; brevetoxins; harmful algal blooms; Karenia brevis; red tides; sensitive populations; spirometry	AIR-POLLUTION; MARINE AEROSOL; HUMAN EXPOSURE; FLORIDA; POPULATION; SHELLFISH; EVENTS; BREVIS; HEALTH	Background: With the increasing incidence of asthma, there is increasing concern over environmental exposures that may trigger asthma exacerbations. Blooms of the marine microalgae, Karenia brevis, cause red titles (or harmful algal blooms) annually throughout the Gulf of Mexico. K brevis produces higlily potent natural polyether toxins, called brevetoxins, which are sodium channel blockers, and possibly histamine activators. In experimental animals, brevetoxins cause significant bronchoconstriction. In humans, a significant increase in self-reported respiratory symptoms has been described after recreational and occupational exposures to Florida red-tide aerosols, particularly among individuals with asthma. Methods: Before and after 1 h spent on beaches with and without an active K brevis red-tide exposure, 97 persons 12 years of age with physician-diagnosed asthma were evaluated by questionnaire and spirometry. Concomitant environmental monitoring, water and air sampling, and personal monitoring for brevetoxins were performed. Results: Participants were significantly more likely to report respiratory symptoms after K brevis red-tide aerosol exposure than before exposure. Participants demonstrated small, but statistically significant, decreases in FEV1, midexpiratory phase of forced expiratory, flow, and peak expiratory flow after exposure, particularly among those participants regularly using asthma medications. No significant differences were detected when there was no Florida red tide (ie, during nonexposure periods). Conclusions: This study demonstrated objectively measurable adverse changes in lung function from exposure to aerosolized Florida red-tide toxins in asthmatic subjects, particularly among those requiring regular therapy with asthma medications. Future studies will assess these susceptible subpopulations in more deptb,as well as the possible long-term effects of these toxins.	Univ Miami, Dept Epidemiol & Publ Hlth, Sch Med, Miami, FL 33136 USA; Univ Miami, Rosenstiel Sch Marine & Atmospher Sci, Miami, FL 33149 USA; Univ Miami, Natl Inst Environm Hlth Sci Marine, Miami, FL 33149 USA; Univ Miami, Freshwater Biomed Sci Ctr, Miami, FL 33149 USA; Mote Marine Lab, Sarasota, FL USA; Ctr Dis Control & Prevent, Natl Ctr Environm Hlth, Atlanta, GA 30341 USA; Childrens Hosp, Med Ctr, Cincinnati, OH 45229 USA; Univ Cincinnati, Cincinnati, OH USA; Florida Dept Hlth, Tallahassee, FL USA; Lovelace Resp Res Inst, Albuquerque, NM USA; Univ N Carolina, Marine Sci Res Ctr, Wilmington, NC 28401 USA	Fleming, LE (reprint author), Univ Miami, Dept Epidemiol & Publ Hlth, Sch Med, 1801 NW 9th Ave,Highland Profess Bldg,Suite 200,R, Miami, FL 33136 USA.	lfleming@med.miami.edu			NIEHS NIH HHS [P01 ES010594, P01 ES 10594, P01 ES010594-06A1]		Abraham WM, 2005, AM J RESP CRIT CARE, V171, P26, DOI 10.1164/rccm.200406-735OC; ABRAHAM WM, 2005, ENV HLTH PERSPECT, V112, P632; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; ASAI S, 1982, J ALLERGY CLIN IMMUN, V69, P418, DOI 10.1016/0091-6749(82)90116-6; Backer LC, 2005, ENVIRON HEALTH PERSP, V113, P644, DOI 10.1289/ehp.7502; Backer LC, 2003, HARMFUL ALGAE, V2, P19, DOI 10.1016/S1568-9883(03)00005-2; Baden D., 1995, HDB CLIN NEUROLOGY 2, P141; Baden Daniel G., 1993, P49; BENSON JM, 2005, ENV HLTH PERSPECT, V112, P626; Bourdelais AJ, 2004, CELL MOL NEUROBIOL, V24, P553, DOI 10.1023/B:CEMN.0000023629.81595.09; Chan-Yeung M, 2000, INT J TUBERC LUNG D, V4, P633; Cheng YS, 2005, ENVIRON SCI TECHNOL, V39, P3443, DOI 10.1021/es048680j; Cheng YS, 2005, HARMFUL ALGAE, V4, P87, DOI 10.1016/j.hal.2003.12.002; CHENG YS, 2005, ENV HLTH PERSPECT, V13, P638; Desqueyroux H, 2002, ENVIRON RES, V89, P29, DOI 10.1006/enrs.2002.4357; Eisen EA, 1997, AM J IND MED, V31, P671; Fleming LE, 2005, ENVIRON HEALTH PERSP, V113, P650, DOI 10.1289/ehp.7500; Fleming LE, 2005, ENVIRON HEALTH PERSP, V113, P618, DOI 10.1289/ehp.7501; Fleming L. E., 2001, SEAFOOD ENV TOXINS, P287; Gold DR, 2005, ANNU REV PUBL HEALTH, V26, P89, DOI 10.1146/annurev.publhealth.26.021304.144528; Kirkpatrick B, 2004, HARMFUL ALGAE, V3, P99, DOI 10.1016/j.hal.2003.08.005; Henry M., 2001, HARMFUL ALGAL BLOOMS, P447; Kirkpatrick B, 2006, HARMFUL ALGAE, V5, P526, DOI 10.1016/j.hal.2005.09.004; KLEINBAUM DG, 1982, EPIDEMIOLOGIC RES, P388; Koh YI, 2002, RESPIRATION, V69, P38, DOI 10.1159/000049368; Milton B, 2004, CHILD CARE HLTH DEV, V30, P711, DOI 10.1111/j.1365-2214.2004.00486.x; MORRIS PD, 1991, AM J PUBLIC HEALTH, V81, P471, DOI 10.2105/AJPH.81.4.471; Music S I, 1973, JFMA, V60, P27; Naar J, 2002, ENVIRON HEALTH PERSP, V110, P179; *NIOSH, 1997, NIOSH SPIR TRAIN GUI; Peden DB, 2005, J ALLERGY CLIN IMMUN, V115, P213, DOI 10.1016/j.jaci.2004.12.003; Pierce RH, 2005, HARMFUL ALGAE, V4, P965, DOI 10.1016/j.hal.2004.11.004; Pierce RH, 2003, B ENVIRON CONTAM TOX, V70, P161, DOI 10.1007/s00128-002-0170-y; Pierce RH, 2001, ENVIRON TOXICOL CHEM, V20, P107, DOI 10.1897/1551-5028(2001)020<0107:ITFHAT>2.0.CO;2; Poli MA, 2000, TOXICON, V38, P981, DOI 10.1016/S0041-0101(99)00191-9; Steidinger K.A., 1984, P201; Trasande L, 2005, J ALLERGY CLIN IMMUN, V115, P689, DOI 10.1016/j.jaci.2005.01.056; WOODCOCK AH, 1948, J MAR RES, V7, P56	38	74	75	5	22	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	JAN	2007	131	1					187	194		10.1378/chest.06-1830		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	126XF	WOS:000243548100029	17218574	
J	Campo, P; Kalra, HK; Levin, L; Reponen, T; Olds, R; Lummus, ZL; Cho, SH; Hershey, GKK; Lockey, J; Villareal, M; Stanforth, S; LeMasters, G; Bernstein, DI				Campo, Paloma; Kalra, Harpinder K.; Levin, Linda; Reponen, Tiina; Olds, Rolanda; Lummus, Zana L.; Cho, Seung-Hyun; Hershey, Gurjit K. Khurana; Lockey, James; Villareal, Manuel; Stanforth, Sherry; LeMasters, Grace; Bernstein, David I.			Influence of dog ownership and high endotoxin on wheezing and atopy during infancy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						endotoxin; birth cohort; wheeze; house dust; pet ownership	HOUSE-DUST ENDOTOXIN; HAY-FEVER; ALLERGIC SENSITIZATION; WRITTEN QUESTIONNAIRE; DECREASED PREVALENCE; ASTHMATIC-CHILDREN; RESPIRATORY HEALTH; CHILDHOOD ISAAC; TOBACCO-SMOKE; BIRTH COHORT	Background: Increased exposure to microbial products early in life may protect from development of atopic disorders in childhood. Few studies have examined the relationship of endotoxin exposure and pet ownership on atopy and wheezing during infancy. Objective: Evaluate relationships among high endotoxin exposure, pet ownership, atopy, and wheezing in high-risk infants. Methods: Infants (n = 532; mean age, 12.5 +/- 0.8 months) with at least 1 parent with confirmed atopy were recruited. A complete medical history and skin prick testing to foods and aeroallergens were performed at age 1 year. House dust samples were analyzed for endotoxin. Results: Prevalences of wheezing were not independently associated with dog or cat ownership or endotoxin levels. Percutaneous reactivity to at least 1 allergen was observed in 28.6% of infants. Univariate analyses showed significant associations of any wheezing, recurrent wheezing, and recurrent wheezing with an event with daycare attendance, number of siblings, respiratory infections, maternal smoking, and history of parental asthma. Logistic regression adjusting for the latter variables showed that recurrent wheezing (odds ratio, 0.4; 95% CI, 0.1-0.9) as well as 2 other wheeze outcomes were significantly reduced in homes with high endotoxin exposure in the presence of 2 or more dogs. Conclusion: Pet ownership or endotoxin did not independently modify aeroallergen sensitization or wheezing during infancy. However, high endotoxin exposure in the presence of multiple dogs was associated with reduced wheezing in infants. Clinical implications: A home environment with many dogs and high levels of endotoxin may be conducive to reduced wheezing in infancy.	Univ Cincinnati, Dept Internal Med, Div Immunol, Cincinnati, OH 45267 USA; Univ Cincinnati, Dept Environm Hlth, Cincinnati, OH 45267 USA	Bernstein, DI (reprint author), Univ Cincinnati, Dept Internal Med, Div Immunol, POB 670563, Cincinnati, OH 45267 USA.	bernstdd@ucmail.uc.edu		Khurana Hershey, Gurjit/0000-0001-6663-977X	NIEHS NIH HHS [1-R01-ES11170-04, R01 ES011170, R01 ES011170-04]		Adler A, 2005, J ALLERGY CLIN IMMUN, V115, P67, DOI 10.1016/j.jaci.2004.10.008; Almqvist C, 2003, CLIN EXP ALLERGY, V33, P1190, DOI 10.1046/j.1365-2222.2003.01764.x; Arlian LG, 1999, J ALLERGY CLIN IMMUN, V104, P707, DOI 10.1016/S0091-6749(99)70349-0; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Bjorksten B, 1999, J ALLERGY CLIN IMMUN, V104, P1119; Bolte G, 2003, CLIN EXP ALLERGY, V33, P770, DOI 10.1046/j.1365-2222.2003.01665.x; Bottcher MF, 2003, CLIN EXP ALLERGY, V33, P295, DOI 10.1046/j.1365-2222.2003.01562.x; Celedon JC, 1999, PEDIATRICS, V104, P495, DOI 10.1542/peds.104.3.495; CHO SH, 2006, IN PRESS ANN ALLERGY; D'Amato G, 2002, Monaldi Arch Chest Dis, V57, P161; Ernst P, 2000, AM J RESP CRIT CARE, V161, P1563; Farooqi IS, 1998, THORAX, V53, P927; Gehring U, 2001, J ALLERGY CLIN IMMUN, V108, P847, DOI 10.1067/mai.2001.119026; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Gern JE, 2004, J ALLERGY CLIN IMMUN, V113, P307, DOI 10.1016/j.jaci.2003.11.017; Heinrich J, 2001, CLIN EXP ALLERGY, V31, P1839, DOI 10.1046/j.1365-2222.2001.01220.x; Helsel DR, 2005, ENVIRON SCI TECHNOL, V39, p419A, DOI 10.1021/es053368a; Holt PG, 1997, THORAX, V52, P1; Hopkin JM, 1999, CLIN EXP ALLERGY, V29, P733; *INS CORP, 2000, S PLUS UN; Jaakkola JJK, 2002, SCAND J WORK ENV HEA, V28, P71; Jenkins MA, 1996, INT J EPIDEMIOL, V25, P609, DOI 10.1093/ije/25.3.609; Kuehni CE, 2001, LANCET, V357, P1821, DOI 10.1016/S0140-6736(00)04958-8; LEMASTERS GK, 2003, AM J RESP CRIT CARE, V167, pA335; Lindfors A, 1999, J ALLERGY CLIN IMMUN, V104, P755; Litonjua AA, 2002, J ALLERGY CLIN IMMUN, V110, P736, DOI 10.1067/mai.2002.128948; Mannino D. 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Allergy Clin. Immunol.	DEC	2006	118	6					1271	1278		10.1016/j.jaci.2006.08.008		8	Allergy; Immunology	Allergy; Immunology	117NP	WOS:000242880300010	17157656	
J	Turner, MC; Chen, Y; Krewski, D; Ghadirian, P				Turner, MC; Chen, Y; Krewski, D; Ghadirian, P			An overview of the association between allergy and cancer	INTERNATIONAL JOURNAL OF CANCER			English	Review							NON-HODGKINS-LYMPHOMA; ACUTE LYMPHOBLASTIC-LEUKEMIA; FRANCISCO BAY AREA; CHRONIC ANTIGENIC-STIMULATION; CHRONIC LYMPHOCYTIC-LEUKEMIA; POPULATION-BASED COHORT; PREVIOUS LUNG-DISEASE; KILLER-CELL-ACTIVITY; PRIOR MEDICATION USE; ADULT BRAIN-TUMOR	Numerous epidemiological studies have evaluated some aspect of the association between a history of allergy and cancer occurrence. In this article, an overview of the epidemiological evidence is presented with a discussion of a number of methodological issues important in this area of study. Literature searches were conducted using the MEDLINE database from 1966 through to August 2005 to identify articles that explored a personal history of allergic disorders as a risk factor for cancer. Although it is difficult to draw conclusions between allergy and cancer at many sites because of insufficient evidence or a lack of consistency both within and among studies completed to date, strong inverse associations have been reported for pancreatic cancer and glioma, whereas lung cancer was positively associated with asthma. Additional studies are needed to confirm these finding and to address the limitations of previous studies, including the validity and reliability of exposure measures and control for confounding. Further, large prospective studies using cancer incidence would be particularly useful, including studies using biological markers of allergic status to reduce potential misclassification and to confirm the results of previous studies based on self-report. There is also a need for further basic research to clarify a potential mechanism, should an association exist. (c) 2006 Wiley-Liss, Inc.	Univ Ottawa, Inst Populat Hlth, McLaughlin Ctr Populat Hlth Risk Assessment, Ottawa, ON K1N 6N5, Canada; Univ Ottawa, Dept Epidemiol & Community Med, Ottawa, ON K1N 6N5, Canada; Univ Montreal, Ctr Rech, CHUM, Unite Rech Epidemiol, Montreal, PQ H3C 3J7, Canada	Turner, MC (reprint author), Univ Ottawa, Inst Populat Hlth, McLaughlin Ctr Populat Hlth Risk Assessment, Ottawa, ON K1N 6N5, Canada.	mturner@uottawa.ca					Adami H. 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J	Bryce, PJ; Mathias, CB; Harrison, KL; Watanabe, T; Geha, RS; Oettgen, HC				Bryce, PJ; Mathias, CB; Harrison, KL; Watanabe, T; Geha, RS; Oettgen, HC			The H1 histamine receptor regulates allergic lung responses	JOURNAL OF CLINICAL INVESTIGATION			English	Article							INDUCED AIRWAY INFLAMMATION; T-CELL; INTERFERON-GAMMA; BRONCHIAL HYPERRESPONSIVENESS; BRONCHOALVEOLAR LAVAGE; EOSINOPHIL CHEMOTAXIS; CYTOKINE PRODUCTION; ANTIGEN RECEPTOR; EPITHELIAL-CELLS; DENDRITIC CELLS	Histamine, signaling via the type 1 receptor (H1R), has been shown to suppress Th2 cytokine production by in vitro cultured T cells. We examined the role of H1R in allergic inflammation in vivo using a murine asthma model. Allergen-stimulated splenic T cells from sensitized H1R(-/-) mice exhibited enhanced Th2 cytokine production. Despite this Th2 bias, allergen-challenged H1R(-/-) mice exhibited diminished lung Th2 cytokine mRNA levels, airway inflammation, goblet cell metaplasia, and airway hyperresponsiveness (AHR). Restoration of pulmonary Th2 cytokines in H1R(-/-) mice by intranasal IL-4 or IL-13 restored inflammatory lung responses and AHR Further investigation revealed that histamine acts as a T cell chemotactic factor and defective T cell trafficking was responsible for the absence of lung inflammation. Cultured T cells migrated in response to histamine in vitro, but this was ablated by blockade of H1R but not H2R In vivo, allergen-specific WT but not H1R(-/-) CD4(+) T cells were recruited to the lungs of naive recipients following inhaled allergen challenge. H1R(-/-) cells failed to confer airway inflammation or AHR observed after transfer of WT T cells. Our data establish a role for histamine and H1R in promoting the migration of Th2 cells into sites of allergen exposure.	Northwestern Univ, Feinburg Sch Med, Chicago, IL 60611 USA; Harvard Univ, Sch Med, Childrens Hosp, Div Immunol, Boston, MA 02115 USA; RIKEN, Inst Phys & Chem Res, Res Ctr Allergy & Immunol, Yokohama, Japan	Bryce, PJ (reprint author), Northwestern Univ, Feinburg Sch Med, McGaw M315,240 E Huron St, Chicago, IL 60611 USA.	p-bryce@northwestern.edu		Mathias, Clinton/0000-0002-0223-4842	NIAID NIH HHS [5R01AI054471, R01 AI047417, R01 AI054471]; NIAMS NIH HHS [R01 AR047417]		Banu Y, 1999, J EXP MED, V189, P673, DOI 10.1084/jem.189.4.673; Blaeser F, 2003, J EXP MED, V198, P1189, DOI 10.1084/jem.20030471; Blumchen K, 2004, CLIN EXP ALLERGY, V34, P1124, DOI 10.1111/j.1365-2222.2004.01974.x; BROIDE DH, 1991, J ALLERGY CLIN IMMUN, V88, P637, DOI 10.1016/0091-6749(91)90158-K; Bryce PJ, 2003, J ALLERGY CLIN IMMUN, V112, P149, DOI 10.1067/mai.2003.1616; CARLSSON R, 1985, CELL IMMUNOL, V96, P104, DOI 10.1016/0008-8749(85)90343-0; Caron G, 2001, J IMMUNOL, V167, P3682; CASALE TB, 1987, J CLIN INVEST, V79, P1197, DOI 10.1172/JCI112937; CENTER DM, 1983, J IMMUNOL, V131, P1854; CIPRANDI G, 1995, J ALLERGY CLIN IMMUN, V95, P612, DOI 10.1016/S0091-6749(95)70324-1; CORRIGAN CJ, 1990, AM REV RESPIR DIS, V141, P970; Couillin I, 2004, J IMMUNOL, V173, P3281; Dy M, 2004, CYTOKINE GROWTH F R, V15, P393, DOI 10.1016/j.cytogfr.2004.06.003; Elliott KA, 2001, INT IMMUNOPHARMACOL, V1, P1923, DOI 10.1016/S1567-5769(01)00117-5; FINKELMAN FD, 1988, J IMMUNOL, V141, P2335; Finotto S, 2002, SCIENCE, V295, P336, DOI 10.1126/science.1065544; Gantner F, 2002, J PHARMACOL EXP THER, V303, P300, DOI 10.1124/jpet.102.036939; Gelfand EW, 2002, J ALLERGY CLIN IMMUN, V110, P85, DOI 10.1067/mai.2002.124770; Hirata N, 1999, J ALLERGY CLIN IMMUN, V103, P944, DOI 10.1016/S0091-6749(99)70443-4; Hofstra CL, 2003, J PHARMACOL EXP THER, V305, P1212, DOI 10.1124/jpet.102.046581; Hogan SP, 1998, AM J RESP CRIT CARE, V157, P210; Inoue I, 1996, P NATL ACAD SCI USA, V93, P13316, DOI 10.1073/pnas.93.23.13316; Jinquan Tan, 1995, Journal of Allergy and Clinical Immunology, V95, P979, DOI 10.1016/S0091-6749(95)70098-6; Jutel M, 2001, NATURE, V413, P420, DOI 10.1038/35096564; Kayasuga R, 2002, INT IMMUNOPHARMACOL, V2, P745, DOI 10.1016/S1567-5769(02)00010-3; Koarai A, 2003, AM J RESP CRIT CARE, V167, P758, DOI 10.1164/rccm.200206-619OC; Kozma GT, 2003, INT IMMUNOL, V15, P963, DOI 10.1093/intimm/dxg095; Krouwels FH, 1998, AM J RESP CELL MOL, V18, P721; Kuperman DA, 2002, NAT MED, V8, P885, DOI 10.1038/nm734; Lagier B, 1997, CLIN EXP IMMUNOL, V108, P545, DOI 10.1046/j.1365-2249.1997.3791276.x; Lee JS, 1997, J FOOD DRUG ANAL, V5, P185; Ling P, 2004, BRIT J PHARMACOL, V142, P161, DOI 10.1038/sj.bjp.0705729; Ma RLZ, 2002, SCIENCE, V297, P620, DOI 10.1126/science.1072810; MARRACK P, 1983, J EXP MED, V158, P1077, DOI 10.1084/jem.158.4.1077; Matsubara M, 2005, BIOCHEM PHARMACOL, V69, P433, DOI 10.1016/j.bcp.2004.10.006; Mazzoni A, 2001, J CLIN INVEST, V108, P1865, DOI 10.1172/JCI13930; Miyahara N, 2004, NAT MED, V10, P865, DOI 10.1038/nm1081; Nakane H, 2004, INFLAMM RES, V53, P324, DOI 10.1007/s00011-004-1264-2; Nori M, 2003, CLIN EXP ALLERGY, V33, P1544, DOI 10.1046/j.1365-2222.2003.01701.x; OKADA C, 1994, INT ARCH ALLERGY IMM, V103, P384; Papi A, 2001, J ALLERGY CLIN IMMUN, V108, P221, DOI 10.1067/mai.2001.116861; ROBINSON D, 1993, J ALLERGY CLIN IMMUN, V92, P313, DOI 10.1016/0091-6749(93)90175-F; ROBINSON DS, 1992, NEW ENGL J MED, V326, P298, DOI 10.1056/NEJM199201303260504; SCHMIDT J, 1994, AGENTS ACTIONS, V42, P81, DOI 10.1007/BF01983469; Schroeder JT, 2001, CLIN EXP ALLERGY, V31, P1369, DOI 10.1046/j.1365-2222.2001.01130.x; Seto Y, 2003, J IMMUNOL, V170, P1077; Sirois J, 2000, J IMMUNOL, V164, P2964; Smits Agnis, 1999, Agricultural and Forest Entomology, V1, P19, DOI 10.1046/j.1461-9563.1999.00004.x; Takahashi H, 2003, CLIN EXP IMMUNOL, V133, P22, DOI 10.1046/j.1365-2249.2003.02182.x; Tamaoki J, 1997, J ALLERGY CLIN IMMUN, V99, P233, DOI 10.1016/S0091-6749(97)70102-7; Temann UA, 2002, J CLIN INVEST, V109, P29, DOI 10.1172/JCI13696; Togias Alkis, 2003, Journal of Allergy and Clinical Immunology, V112, pS60, DOI 10.1016/S0091-6749(03)01878-5; Venkayya R, 2002, AM J RESP CELL MOL, V26, P202; Warner JO, 2001, J ALLERGY CLIN IMMUN, V108, P929, DOI 10.1067/mai.2001.120015; WHITE MV, 1990, J ALLERGY CLIN IMMUN, V86, P599, DOI 10.1016/S0091-6749(05)80223-4; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; Yang M, 2001, AM J RESP CELL MOL, V25, P522	57	74	79	0	3	AMER SOC CLINICAL INVESTIGATION INC	ANN ARBOR	35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA	0021-9738			J CLIN INVEST	J. Clin. Invest.	JUN	2006	116	6					1624	1632		10.1172/JCI26150		9	Medicine, Research & Experimental	Research & Experimental Medicine	048XL	WOS:000237979700024	16680192	
J	Kim, JL; Elfman, L; Mi, Y; Johansson, M; Smedje, G; Norback, D				Kim, JL; Elfman, L; Mi, Y; Johansson, M; Smedje, G; Norback, D			Current asthma and respiratory symptoms among pupils in relation to dietary factors and allergens in the school environment	INDOOR AIR			English	Article						asthma; cat allergen (Fel d 1); dietary factors; dog allergen (Can f 1); horse allergen (Equ cx); school environment	CHILDHOOD ASTHMA; CAT ALLERGEN; SWEDISH SCHOOLCHILDREN; ATOPIC SENSITIZATION; FISH CONSUMPTION; HEALTH-SURVEY; YOUNG-ADULTS; RISK-FACTORS; AIR-QUALITY; NEW-ZEALAND	The aim was to study asthma and allergy in relation to diet and the school environment. Pupils (5-14 years) in eight schools received a questionnaire, 1014 participated (68%). Settled dust was collected on ALK-filters and analyzed for allergens from cat (Fel d 1), dog (Can f 1), horse (Equ cx), house dust mites (Der p 1, Der f 1), and cockroach (Bla g 1) by ELISA. In total, 6.8% reported cat allergy, 4.8% dog allergy, 7.7% doctor's diagnosed asthma and 5.9% current asthma, and 7.8% reported wheeze. Current asthma was less common among those consuming more fresh milk (P < 0.05) and fish (P < 0.01). Poly-unsaturated fatty acids was associated with more wheeze (P < 0.05), olive oil was associated with less doctors' diagnosed asthma (P < 0.05). Totally, 74% of the classrooms had mean CO2 < 1000 ppm. The median concentration per gram dust was 860 ng/g Fel d 1, 750 ng/g Can f 1 and 954 U/g Equ cx. Horse allergen was associated with more wheeze (P < 0.05), daytime breathlessness (P < 0.05), current asthma (P < 0.05) and atopic sensitization (P < 0.05). Dog allergen was associated with wheeze (P < 0.05) and daytime breathlessness (P < 0.05). The associations between allergens and respiratory symptoms were more pronounced among those consuming margarine, not consuming butter, and with a low intake of milk. In conclusion, cat, dog and horse allergens in schools could be a risk factor for asthma and atopic sensitization, and dietary factors may interact with the allergen exposure.	Uppsala Univ, Dept Med Sci, SE-75185 Uppsala, Sweden; Univ Hosp, SE-75185 Uppsala, Sweden	Kim, JL (reprint author), Uppsala Univ, Dept Med Sci, SE-75185 Uppsala, Sweden.	jeong-lim.kim@medsci.uu.se		Norback, Dan/0000-0002-5174-6668			ABERG N, 1995, CLIN EXP ALLERGY, V25, P815, DOI 10.1111/j.1365-2222.1995.tb00023.x; ABERG N, 1990, ACTA PAEDIATR SCAND, V79, P206, DOI 10.1111/j.1651-2227.1990.tb11440.x; *AFS, 1993, VENT AIR QUAL, P5; Almqvist C, 1999, J ALLERGY CLIN IMMUN, V103, P1012, DOI 10.1016/S0091-6749(99)70172-7; Amr S, 2003, ANN ALLERG ASTHMA IM, V90, P34; ANDERSSON K, 1981, SCAND J WORK ENV HEA, V7, P282; ANUNDI H, 1992, P 41 NORD M WORK ENV; Apter AJ, 2003, J ALLERGY CLIN IMMUN, V111, P938, DOI 10.1067/mai.2003.1417; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Bolte G, 2001, AM J RESP CRIT CARE, V163, P277; BRABACK L, 1994, CLIN EXP ALLERGY, V24, P826, DOI 10.1111/j.1365-2222.1994.tb01805.x; BRUNEKREEF B, 1992, INT J EPIDEMIOL, V21, P338, DOI 10.1093/ije/21.2.338; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; Daisey JM, 2003, INDOOR AIR, V13, P53, DOI 10.1034/j.1600-0668.2003.00153.x; Denny SI, 2003, CURR ALLERGY ASTHM R, V3, P130, DOI 10.1007/s11882-003-0025-6; Dotterud LK, 1995, J EUR ACAD DERMATOL, V5, P240, DOI 10.1111/j.1468-3083.1995.tb00112.x; Elfman L., 2000, P HLTH BUILDINGS, V1, P341; Emenius G, 2001, ALLERGY, V56, P771, DOI 10.1034/j.1398-9995.2001.056008771.x; FARCHI S, 2003, EUR RESPIR J, V22, P719; Fluge O, 1998, EUR RESPIR J, V12, P336, DOI 10.1183/09031936.98.12020336; 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; GEBSKI V, 1992, SPIDA USERS MANUAL V; HATTEVIG G, 1987, ACTA PAEDIATR SCAND, V76, P349, DOI 10.1111/j.1651-2227.1987.tb10473.x; Helm Ricki M, 2004, Curr Opin Allergy Clin Immunol, V4, P125, DOI 10.1097/00130832-200404000-00010; Hijazi N, 2000, THORAX, V55, P775, DOI 10.1136/thorax.55.9.775; Hodge L, 1996, MED J AUSTRALIA, V164, P137; Janson C, 2001, EUR RESPIR J, V18, P598, DOI 10.1183/09031936.01.00205801; Karlsson AS, 2002, ALLERGY, V57, P164, DOI 10.1034/j.1398-9995.2002.1s3297.x; Kiviranta H, 2003, CHEMOSPHERE, V50, P1201, DOI 10.1016/S0045-6535(02)00481-2; LARSSON L, 1995, THORAX, V50, P260, DOI 10.1136/thx.50.3.260; Lee SC, 2000, CHEMOSPHERE, V41, P109, DOI 10.1016/S0045-6535(99)00396-3; Meyer HW, 2004, INDOOR AIR, V14, P65, DOI 10.1046/j.1600-0668.2003.00213.x; MI YH, 2002, P 9 INT C IND AIR QU, V2, P449; Mickleborough TD, 2003, AM J RESP CRIT CARE, V168, P1181, DOI 10.1164/rccm.200303-373OC; MORGAN WJ, 1992, PEDIATR CLIN N AM, V39, P1185; MUNIR AKM, 1993, J ALLERGY CLIN IMMUN, V91, P1067, DOI 10.1016/0091-6749(93)90221-Z; Nafstad P, 2003, J ASTHMA, V40, P343, DOI 10.1081/JAS-120018633; Patchett K, 1997, J ALLERGY CLIN IMMUN, V100, P755, DOI 10.1016/S0091-6749(97)70269-0; PEAT JK, 1992, EUR RESPIR J, V5, P921; Perzanowski MS, 1999, J ALLERGY CLIN IMMUN, V103, P1018, DOI 10.1016/S0091-6749(99)70173-9; Plaschke PP, 2000, AM J RESP CRIT CARE, V162, P920; Ritz BR, 2002, ALLERGY, V57, P357, DOI 10.1034/j.1398-9995.2002.1s3404.x; Romieu I, 2001, EPIDEMIOL REV, V23, P268; RONNMARK E, 1998, RESP MED, V92, P316; Ruotsalainen R., 1995, P INDOOR AIR QUALITY, P489; Schneider D, 2001, ARCH ENVIRON HEALTH, V56, P103; SIMOPOULOS AP, 2002, J AM COLL NUTR, V6, P495; Simpson Angela, 2003, Curr Opin Allergy Clin Immunol, V3, P7, DOI 10.1097/00130832-200302000-00002; Smedje G, 1997, CLIN EXP ALLERGY, V27, P1270, DOI 10.1111/j.1365-2222.1997.tb01171.x; Smedje G, 2000, ARCH ENVIRON HEALTH, V55, P18; Smedje G, 2001, INT J TUBERC LUNG D, V5, P1059; Soutar A, 1997, THORAX, V52, P166; Strachan DP, 1996, BRIT MED J, V312, P1195; Takemura Y, 2002, PREV MED, V34, P221, DOI 10.1006/pmed.2001.0978; Taskinen T, 1997, ACTA PAEDIATR, V86, P1181, DOI 10.1111/j.1651-2227.1997.tb14841.x; Tortolero SR, 2002, J SCHOOL HEALTH, V72, P33; VONMUTIUS E, 2000, J ALLERGY CLIN IMMUN, V105, P1; 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	61	74	76	1	2	BLACKWELL MUNKSGAARD	FREDERIKSBERG C	1 ROSENORNS ALLE, DK-1970 FREDERIKSBERG C, DENMARK	0905-6947			INDOOR AIR	Indoor Air	JUN	2005	15	3					170	182		10.1111/j.1600-0668.2005.00334.x		13	Construction & Building Technology; Engineering, Environmental; Public, Environmental & Occupational Health	Construction & Building Technology; Engineering; Public, Environmental & Occupational Health	921GF	WOS:000228751500004	15865617	
J	Hollingsworth, JW; Chen, BJ; Brass, DM; Berman, K; Gunn, MD; Cook, DN; Schwartz, DA				Hollingsworth, JW; Chen, BJ; Brass, DM; Berman, K; Gunn, MD; Cook, DN; Schwartz, DA			The critical role of hematopoietic cells in lipopolysaccharide-induced airway inflammation	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						innate immunity; lipopolysaccharide; macrophage; neutrophil; toll-like receptor	TOLL-LIKE RECEPTOR-4; ACUTE LUNG INJURY; NEUTROPHIL RECRUITMENT; BRONCHIAL REACTIVITY; ENDOTOXIN EXPOSURE; INHALED ENDOTOXIN; EPITHELIAL-CELLS; MICE; ASTHMA; TLR4	Rapid and selective recruitment of neutrophils into the airspace in response to LPS facilitates the clearance of bacterial pathogens. However, neutrophil infiltration can also participate in the development and progression of environmental airway disease. Previous data have revealed that Toll-like receptor 4 (tlr4) is required for neutrophil recruitment to the lung after either inhaled or systemically administrated LPS from Escherichia coli. Although many cell types express tlr4, endothelial cell expression of tlr4 is specifically required to sequester neutrophils in the lung in response to systemic endotoxin. To identify the cell types requiring trl4 expression for neutrophil recruitment after inhaled LPS, we generated chimeric mice separately expressing tlr4 on either hematopoietic cells or on structural lung cells. Neutrophil recruitment into the airspace was completely restored in tlr4-deficient mice receiving wild-type bone marrow. By contrast, wild-type animals receiving tlr4-deficient marrow had dramatically reduced neutrophil recruitment. Moreover, adoptive transfer of wild-type alveolar macrophages also restored the ability of tlr4-deficient recipient mice to recruit neutrophils to the lung. These data demonstrate the critical role of hematopoietic cells and alveolar macrophages in initiating LPS-induced neutrophil recruitment from the vascular space to the airspace.	Duke Univ, Med Ctr, Div Pulm Allergy & Crit Care Med, Durham, NC 27710 USA; Duke Univ, Med Ctr, Div Cellular Therapy, Durham, NC 27710 USA; Duke Univ, Med Ctr, Div Cardiol, Durham, NC 27710 USA; Vet Adm Med Ctr, Durham, NC USA	Hollingsworth, JW (reprint author), Duke Univ, Med Ctr, Div Pulm Allergy & Crit Care Med, Box 3221, Durham, NC 27710 USA.	holli017@mc.duke.edu		Gunn, Michael/0000-0003-4602-0667	NHLBI NIH HHS [HL74538]; NIAID NIH HHS [AI-51445]; NIEHS NIH HHS [ES7031, ES011961, ES07498, ES11375, ES12496, ES12717]		Alves-Rosa F, 2003, BRIT J HAEMATOL, V121, P130, DOI 10.1046/j.1365-2141.2003.04259.x; Andonegui G, 2003, J CLIN INVEST, V111, P1011, DOI 10.1172/JCI200316510; Arbour NC, 2000, NAT GENET, V25, P187; Balmes JR, 1996, AM J RESP CRIT CARE, V153, P904; BERG JT, 1993, J APPL PHYSIOL, V74, P2812; Brass DM, 2003, AM J PHYSIOL-LUNG C, V285, pL755, DOI 10.1152/ajplung.00001.2003; Deetz DC, 1997, AM J RESP CRIT CARE, V155, P254; Drazen JM, 1999, ANNU REV PHYSIOL, V61, P593, DOI 10.1146/annurev.physiol.61.1.593; FAHY JV, 1995, J ALLERGY CLIN IMMUN, V95, P843, DOI 10.1016/S0091-6749(95)70128-1; FOLINSBEE LJ, 1994, AM J RESP CRIT CARE, V149, P98; Foster WM, 2000, J APPL PHYSIOL, V89, P1804; Fournier P, 2002, CANCER RES, V62, P6538; Gibbs DF, 1999, AM J RESP CELL MOL, V20, P1145; Guillot L, 2004, J BIOL CHEM, V279, P2712, DOI 10.1074/jbc.M305790200; Hamelmann E, 1997, AM J RESP CRIT CARE, V156, P766; Heikkila P, 2003, J SURG RES, V111, P45, DOI 10.1016/S0022-4804(03)00000-0; Heikkila P, 2002, ANTI-CANCER DRUG, V13, P245, DOI 10.1097/00001813-200203000-00006; Hollingsworth JW, 2004, AM J RESP CRIT CARE, V170, P126, DOI 10.1164/rccm.200311-1499OC; Hoshino K, 1999, J IMMUNOL, V162, P3749; Kline JN, 1999, AM J RESP CRIT CARE, V160, P297; Kline JN, 2000, J APPL PHYSIOL, V89, P1172; Koay MA, 2002, AM J RESP CELL MOL, V26, P572; Lee W L, 2001, Curr Opin Crit Care, V7, P1, DOI 10.1097/00075198-200102000-00001; Li QL, 2002, CELL, V111, P635, DOI 10.1016/S0092-8674(02)01079-6; Malcolm KC, 2003, AM J PHYSIOL-LUNG C, V284, pL663, DOI 10.1152/ajplung.00094.2002; Maus UA, 2003, J IMMUNOL, V170, P3273; 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, 1989, J APPL PHYSIOL, V66, P1059; Miyamoto M, 2003, J IMMUNOL, V170, P4665; MOTUSKY H, 1995, INTUITIVE BIOSTATIST; Poltorak A, 1998, BLOOD CELL MOL DIS, V24, P340, DOI 10.1006/bcmd.1998.0201; Poltorak A, 1998, SCIENCE, V282, P2085, DOI 10.1126/science.282.5396.2085; Quinton LJ, 2004, AM J PHYSIOL-LUNG C, V286, pL465, DOI 10.1152/ajplung.00153.2003; Qureshi ST, 1999, J EXP MED, V189, P615, DOI 10.1084/jem.189.4.615; Savov JD, 2002, AM J PHYSIOL-LUNG C, V283, pL952, DOI 10.1152/ajplung.00420.2001; Schilling JD, 2003, P NATL ACAD SCI USA, V100, P4203, DOI 10.1073/pnas.0736473100; Schwartz DA, 1994, AM J PHYSIOL, V267, P609; Schwarze J., 1996, Journal of Allergy and Clinical Immunology, V97, P293, DOI 10.1016/S0091-6749(96)80662-2; SHA Q, 2004, AM J RESP CELL MOL B, V10, P10; Skerrett SJ, 2004, AM J PHYSIOL-LUNG C, V287, pL143, DOI 10.1152/ajplung.00030.2004; Slegers TPAM, 2003, GRAEF ARCH CLIN EXP, V241, P432, DOI 10.1007/s00417-003-0665-1; SUR S, 1993, AM REV RESPIR DIS, V148, P713; Taube C, 2003, CHEST, V123, p410S, DOI 10.1378/chest.123.3_suppl.410S; Weighardt H, 2004, EUR J IMMUNOL, V34, P558, DOI 10.1002/eji.200324714; Wenzel SE, 1997, AM J RESP CRIT CARE, V156, P737; Whitehead GS, 2003, AM J PHYSIOL-LUNG C, V285, pL32, DOI 10.1152/ajplung.00390.2002; Wohlford-Lenane CL, 1999, AM J PHYSIOL-LUNG C, V276, pL736; Zarember KA, 2002, J IMMUNOL, V168, P554	50	74	74	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	2005	171	8					806	813		10.1164/rccm.200407.953OC		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	916VP	WOS:000228414800003	15618460	
S	Kleeberger, SR; Peden, D				Kleeberger, SR; Peden, D			Gene-environment interactions in asthma and other respiratory diseases	ANNUAL REVIEW OF MEDICINE	Annual Review of Medicine		English	Review; Book Chapter						pollutant; allergen; polymorphism; linkage analysis	OBSTRUCTIVE PULMONARY-DISEASE; NECROSIS-FACTOR-ALPHA; S-TRANSFERASE M1; CHRONIC BERYLLIUM DISEASE; DIESEL EXHAUST PARTICLES; CLASS-II ALLELES; CHILDHOOD LUNG-FUNCTION; HOUSE-DUST ENDOTOXIN; LINKAGE ANALYSIS; AIR-POLLUTION	It is generally agreed that many lung diseases such as asthma and chronic obstructive pulmonary disease (COPD) have polygenic inheritance, and that the association of a specific genotype or genotypes with the disease is likely to vary between populations. Furthermore, it is recognized that the etiology of many lung diseases involves a complex interplay between genetic background and exposure to multiple environmental stimuli, and understanding the mechanisms through which genes and environment interact represents a major challenge for pulmonary researchers. We discuss experimental approaches and challenges that must be overcome to identify disease genes for asthma, COPD and chronic bronchitis, and occupational lung diseases. In particular, common polymorphisms in CD14, glutathione S-transferase, and tumor necrosis factor alpha have been found to be important in gene-environment interaction and asthma pathogenesis. An understanding of gene-environment interactions in complex lung diseases is essential to the development of new strategies for lung disease prevention and treatment.	Natl Inst Environm Hlth Sci, Lab Resp Biol, Environm Genet Grp, NIH, Res Triangle Pk, NC 27709 USA; Ctr Environm Med Asthma & Lung Biol, Div Immunol & Infect Dis, Dept Pediat, Chapel Hill, NC 27599 USA	Kleeberger, SR (reprint author), Natl Inst Environm Hlth Sci, Lab Resp Biol, Environm Genet Grp, NIH, Res Triangle Pk, NC 27709 USA.	kleeber1@niehs.nih.gov			NHLBI NIH HHS [HL6262404, R01-HL66559]		Albuquerque RV, 1998, CLIN EXP ALLERGY, V28, P578; Alexis N, 2001, J ALLERGY CLIN IMMUN, V107, P31, DOI 10.1067/mai.2001.111594; ARIS RM, 1993, AM REV RESPIR DIS, V148, P1363; Barnes PJ, 2002, NAT REV DRUG DISCOV, V1, P437, DOI 10.1038/nrd820; Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; Bastain TM, 2003, CLIN IMMUNOL, V109, P130, DOI 10.1016/S1521-6616(03)00168-2; Bergamaschi E, 2001, AM J RESP CRIT CARE, V163, P1426; BIGNON JS, 1994, AM J RESP CRIT CARE, V149, P71; Borm P J, 2001, Eur Respir J Suppl, V32, p127s; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; 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Thurston GD, 1997, AM J RESP CRIT CARE, V155, P654; Timonen KL, 1997, AM J RESP CRIT CARE, V156, P546; Ueki A, 2001, IMMUNOBIOLOGY, V204, P458, DOI 10.1078/0171-2985-00055; Vedal S, 1998, AM J RESP CRIT CARE, V157, P1034; Vercelli D, 2002, J ALLERGY CLIN IMMUN, V109, P14, DOI 10.1067/mai.2002.121015; WEINMANN GG, 1995, AM J RESP CRIT CARE, V151, P33; Woo JG, 2003, J ALLERGY CLIN IMMUN, V112, P438, DOI 10.1067/mai.2003.1634; Yucesoy B, 2001, TOXICOL APPL PHARM, V172, P75, DOI 10.1006/taap.2001.9124; Zhai RH, 1998, AM J IND MED, V34, P318, DOI 10.1002/(SICI)1097-0274(199810)34:4<318::AID-AJIM4>3.0.CO;2-O; Zhou W, 2002, CANCER RES, V62, P1377; Zhu SK, 2000, AM J RESP CRIT CARE, V161, P1655; ZIEGLERHEITBROCK HWL, 1993, IMMUNOL TODAY, V14, P121, DOI 10.1016/0167-5699(93)90212-4	107	74	79	1	5	ANNUAL REVIEWS	PALO ALTO	4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA	0066-4219		978-0-8243-0556-7	ANNU REV MED	Annu. Rev. Med.		2005	56						383	400		10.1146/annurev/med.56.062904.144908		18	Medicine, General & Internal	General & Internal Medicine	904ND	WOS:000227504100021	15660518	
J	Hong, SJ; Lee, MS; Sohn, MH; Shim, JY; Han, YS; Park, KS; Ahn, YM; Son, BK; Lee, HB				Hong, SJ; Lee, MS; Sohn, MH; Shim, JY; Han, YS; Park, KS; Ahn, YM; Son, BK; Lee, HB		Korean ISAAC Study Grp	Self-reported prevalence and risk factors of asthma among Korean adolescents: 5-year follow-up study, 1995-2000	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						adolescent; asthma; middle-school children; prevalence; risk factor	BODY-MASS INDEX; CHILDHOOD ASTHMA; CHILDREN; SYMPTOMS; TRENDS; ISAAC; HOSPITALIZATION; QUESTIONNAIRE; ASSOCIATION; SMOKING	Objectives The International Study of Asthma and Allergies in Childhood (ISAAC) questionnaires have shown that the prevalence of childhood asthma is increasing worldwide. Although Asian countries used to have lower prevalence rates of allergic disease than Western countries, this prevalence is increasing in several Asian countries. To determine whether the prevalence of childhood asthma is changing in Korean adolescents, we compared findings from nationwide cross-sectional surveys in 1995 and 2000 on populations of middle-school children using the Korean version of the ISAAC questionnaire. Methods We developed Korean versions of the ISAAC written (WQ) and video (AVQ) questionnaires for allergic diseases. In 1995, the enrolled population consisted of 15 481 children, ages 12-15, and encompassing all three grades in middle school, selected from 34 schools across the nation; the response rate was 97.3%. In 2000, 15 894 children were selected from 31 of the same schools, and the response rate was 96.4%. The SAS system version 8.0 was utilized for all statistical analyses. Results The WQ showed that the lifetime and 12-month prevalence of wheeze did not change from 1995 to 2000. While the 12-month prevalence rates of sleep disturbed by wheezing and night cough increased, the rates of severe attack of wheezing and exercise-induced wheeze did not change, over this period of time. The lifetime prevalence of asthma diagnosis, however, increased significantly, from 2.7% in 1995 to 5.3% in 2000, as did the 12-month prevalence of asthma treatment, from 1.0% in 1995 to 1.9% in 2000. The AVQ also showed increases in the lifetime and 12-month prevalence rates of wheeze at rest, exercise-induced wheeze, nocturnal wheeze, nocturnal cough, and severe wheeze over this period of time. These were especially because of significant increases in the Provincial cities of Korea. Interestingly, the 12-month prevalence of wheeze was consistently high in Cheju with low air pollution indices, whereas this rate was low in Ulsan and Ansan with very high air pollution indices. Risk factor analysis showed that body mass index (BMI), passive smoking, and living with a dog or cat, but not air pollution, were associated with higher risk of wheeze. Conclusions In the 5-year period from 1995 to 2000, the prevalence of asthma symptoms has increased in Korean adolescents, much of it because of increases in Provincial Centers. BMI, passive smoking, and living with a dog or cat are important risk factors. Environmental factors other than air pollution may be associated with increases in asthma, especially in Provincial Centers.	Univ Ulsan, Dept Pediat, Ulsan 680749, South Korea; Univ Ulsan, Dept Prevent Med, Ulsan 680749, South Korea; Yonsei Univ, Dept Pediat, Seoul 120749, South Korea; Sungkyunkwan Univ, Dept Pediat, Seoul, South Korea; Chungbuk Univ, Dept Pediat, Cheongju, South Korea; Presbyterian Med Ctr, Dept Pediat, Philadelphia, PA USA; Kangnam Gen Hosp, Dept Pediat, Seoul, South Korea; Inha Univ, Dept Pediat, Inchon, South Korea; Hanyang Univ, Dept Pediat, Seoul, South Korea; Korean Acad Pediat Allergy & Resp Dis, Seoul, South Korea	Lee, HB (reprint author), Hanyang Univ, Dept Pediat, Coll Med, 17 Haengdang Dong, Seoul 133792, South Korea.	hablee@hanyang.ac.kr					AKINBAMI LJ, 2002, PEDIATRICS, V100, P315; Asher MI, 1998, EUR RESPIR J, V12, P315; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Beasley R., 2000, J ALLERGY CLIN IMMUN, V105, P466; Crane J., 1996, European Respiratory Journal Supplement, V9, p230S; CRATER DD, 2001, PEDIATRICS, V108, P1; Downs SH, 2001, ARCH DIS CHILD, V84, P20, DOI 10.1136/adc.84.1.20; Eggleston PA, 1999, ENVIRON HEALTH PERSP, V107, P439; Ehrlich RI, 1996, AM J RESP CRIT CARE, V154, P681; Evans R, 1987, CHEST S, V91, P65; GERGEN PJ, 1990, JAMA-J AM MED ASSOC, V264, P1688, DOI 10.1001/jama.264.13.1688; Guerra S, 2002, CHEST, V122, P1256, DOI 10.1378/chest.122.4.1256; HALFON N, 1986, AM J PUBLIC HEALTH, V76, P1308, DOI 10.2105/AJPH.76.11.1308; Hong SJ, 2003, J KOREAN MED SCI, V18, P48; Huang SL, 1999, CLIN EXP ALLERGY, V29, P323; Jarvis D, 2000, ASTHMA RHINITIS, P17; Kim YY, 1997, CLIN EXP ALLERGY, V27, P761, DOI 10.1046/j.1365-2222.1997.710839.x; LEE HR, 1983, KOREAN MED J, V26, P254; Lee SI, 2001, J KOREAN MED SCI, V16, P155; Luder E, 1998, J PEDIATR-US, V132, P699, DOI 10.1016/S0022-3476(98)70363-4; MORKJAROENPONG V, 2002, J ALLERGY CLIN IMMUN, V100, P147; Pearce N, 2000, THORAX, V55, P352, DOI 10.1136/thorax.55.5.352; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; Senthilselvan A, 1998, CHEST, V114, P388, DOI 10.1378/chest.114.2.388; Shin TS, 1990, KOREAN J ALLERGY, V10, P201; SLY RM, 1984, ANN ALLERGY, V53, P20; Vollmer WM, 1998, AM J RESP CRIT CARE, V157, P1079; von Kries R, 1999, BRIT MED J, V319, P147; von Mutius E, 2001, THORAX, V56, P835, DOI 10.1136/thorax.56.11.835; Weinberg EG, 2000, J ALLERGY CLIN IMMUN, V105, P224, DOI 10.1016/S0091-6749(00)90069-1; Weiss KB, 2000, J ALLERGY CLIN IMMUN, V106, P493; WEITZMAN M, 1990, PEDIATRICS, V85, P505; WOOLCOCK AJ, 1991, EUR RESPIR REV, V1, P243	33	74	76	0	0	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	OCT	2004	34	10					1556	1562		10.1111/j.1365-2222.2004.02084.x		7	Allergy; Immunology	Allergy; Immunology	861RB	WOS:000224434800008	15479270	
J	Heine, G; Schnuch, A; Uter, W; Worm, M				Heine, G; Schnuch, A; Uter, W; Worm, M			Frequency of contact allergy in German children and adolescents patch tested between 1995 and 2002: results from the Information Network of Departments of Dermatology and the German Contact Dermatitis Research Group	CONTACT DERMATITIS			English	Article						allergic contact dermatitis; children; clinical epidemiology; contact allergy; patch testing	SENSITIZATION; THIMEROSAL; IVDK; EPIDEMIOLOGY; ADULTS; DKG; SEX; AGE	Allergic contact dermatitis (ACD) affects approximately 7% of the general population. To evaluate the frequency of ACD in children, we analysed patch test results collected by the Information Network of Departments of Dermatology between 1995 and 2002. Data of 285 children (6-12 year) and 2175 adolescent patients (13-18 year) were analysed to determine the frequency of sensitization to the 30 most common contact allergens, adjusting for age and sex. As control group, we defined adult patients (60-66 year, n = 7904). The top allergens in children were thimerosal, gentamicin sulphate, nickel-II-sulphate, ammoniated mercury, cobalt-II-chloride, fragrance mix, bufexamac, Compositae mix, propylene glycol and turpentine. The overall proportion of sensitized patients according to the patch test results was 52.6% in the children group compared to 49.7% in the adolescent group. These findings were similar in the adult group at 52.2%. The detailed analysis regarding sex, occupation, atopy, site of eczema and age showed distinct patterns in each group indicating age-specific exposures. Atopy-related diseases were more common in children compared to adults. On the basis of the data of this study, the relationship between atopy and the risk of development of ACD, at least in children, needs further investigation.	Charite Univ Med Berlin, Klin Dermatol Venerol & Allergol, D-10117 Berlin, Germany; Univ Gottingen, Informat Network, Dept Dermatol, D-3400 Gottingen, Germany; Univ Erlangen Nurnberg, Dept Med Informat Biometry & Epidemiol, Erlangen, Germany	Worm, M (reprint author), Charite Univ Med Berlin, Klin Dermatol Venerol & Allergol, Campus Charite Mitte,Schumannstr 20-21, D-10117 Berlin, Germany.	margitta.worm@charite.de	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Uter, Wolfgang/0000-0002-4498-3710			ABERER W, 1991, CONTACT DERMATITIS, V24, P6, DOI 10.1111/j.1600-0536.1991.tb01621.x; Akhavan A, 2003, CLIN DERMATOL, V21, P158, DOI 10.1016/S0738-081X(02)00372-3; Brasch J, 1997, CONTACT DERMATITIS, V37, P286, DOI 10.1111/j.1600-0536.1997.tb02466.x; Brasch J, 1998, HAUTARZT, V49, P184, DOI 10.1007/s001050050725; Brehler R, 1995, DTSCH DERMATOLOGE, V43, P688; Bruckner A L, 2002, Skin Therapy Lett, V7, P3; Kay AB, 2001, NEW ENGL J MED, V344, P30; KWANGSUKSTITH C, 1995, CONTACT DERMATITIS, V33, P289, DOI 10.1111/j.1600-0536.1995.tb02041.x; LOCHNER J, 2001, DERMATOL BERUF UMWEL, V49, P228; MAZIAK M, 2003, ALLERGY, V58, P572; Niggemann B, 2003, ALLERGY, V58, P707, DOI 10.1034/j.1398-9995.2003.00219.x; Patrizi A, 1999, CONTACT DERMATITIS, V40, P94, DOI 10.1111/j.1600-0536.1999.tb05998.x; Schafer T, 2001, ALLERGY, V56, P1192, DOI 10.1034/j.1398-9995.2001.00086.x; Schnuch A, 1997, CONTACT DERMATITIS, V37, P200, DOI 10.1111/j.1600-0536.1997.tb02435.x; Schnuch A, 2002, CONTACT DERMATITIS, V47, P32, DOI 10.1034/j.1600-0536.2002.470107.x; Schnuch A, 2001, HAUTARZT, V52, P864, DOI 10.1007/s001050170048; Schnuch A, 2003, CONTACT DERMATITIS, V49, P107, DOI 10.1111/j.0105-1873.2003.0128f.x; Die Schnuch A., 1994, MANUALE ALLERGOLOGIC, V16.2, P1; Schnuch A, 1997, DIAGNOSTISCHE VERFAH, P99; SCHULZ KH, 1990, MANUALE ALLERGOLOGIC, V4, P2; Shah M, 1997, J AM ACAD DERMATOL, V37, P964, DOI 10.1016/S0190-9622(97)70073-2; Spiewak R, 2002, ALLERGOLOGIE, V25, P374; Suneja T, 2001, J AM ACAD DERMATOL, V45, P23, DOI 10.1067/mjd.2001.113473; Vender R B, 2002, Skin Therapy Lett, V7, P4; Wesley NO, 2003, FOOD CHEM TOXICOL, V41, P857, DOI 10.1016/S0278-6915(03)00036-X; Weston William L., 1997, Current Opinion in Pediatrics, V9, P372, DOI 10.1097/00008480-199708000-00012; Weston WL, 2000, PEDIATR CLIN N AM, V47, P897, DOI 10.1016/S0031-3955(05)70247-9; Westphal GA, 2003, CONTACT DERMATITIS, V48, P93, DOI 10.1034/j.1600-0536.2003.480208.x; Wohrl S, 2003, PEDIATR DERMATOL, V20, P119, DOI 10.1046/j.1525-1470.2003.20204.x	29	74	75	1	2	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-1873			CONTACT DERMATITIS	Contact Dermatitis	SEP	2004	51	3					111	117		10.1111/j.0105-1873.2004.00411.x		7	Allergy; Dermatology	Allergy; Dermatology	861QZ	WOS:000224434600002	15479199	
J	Adhikari, A; Sen, MM; Gupta-Bhattacharya, S; Chanda, S				Adhikari, A; Sen, MM; Gupta-Bhattacharya, S; Chanda, S			Air-borne viable, non-viable, and allergenic fungi in a rural agricultural area of India: a 2-year study at five outdoor sampling stations	SCIENCE OF THE TOTAL ENVIRONMENT			English	Article						airborne fungi; bioaerosol; allergy; rural area; aerobiology; air microbiology	DIFFERENT SITES; AIRBORNE; SPORES; SYMPTOMS; ASTHMA; MICROORGANISMS; ENVIRONMENTS; ENUMERATION; DUSTS	The information on airborne allergenic fungal flora in rural agricultural areas is largely lacking. Adequate information is not available to the bioaerosol researchers regarding the choice of single versus multiple sampling stations for the monitoring of both viable and non-viable airborne fungi. There is no long-term study estimating the ratios of viable and non-viable fungi in the air and earlier studies did not focus on the fractions of airborne allergenic fungi with respect to the total airborne fungal load. To fill these knowledge gaps, volumetric paired assessments of airborne viable and non-viable fungi were performed in five outdoor sampling stations during two consecutive years in a rural agricultural area of India. Samples were collected at 10-day intervals by the Burkard Personal Slide Sampler and the Andersen Two-Stage Viable Sampler. The data on the concentrations of total and individual fungal types from five stations and 2 different years were analyzed and compared by statistical methods. The allergenicity of the prevalent airborne viable fungi was estimated by the skin-prick tests of > 100 rural allergy patients using the antigenic fungal extracts from isolates collected with the Andersen sampler. The ranges of total fungal spore concentration were 82-2365 spores per cubic meter of air (spores/m(3)) in the first sampling year and 156-2022 spores/m(3) in the second sampling year. The concentration ranges of viable fungi were 72-1796 colony-forming units per cubic meter of air (CFU/m(3)) in the first sampling year and 155-1256 CFU/m(3) in the second sampling year. No statistically significant difference was observed between the total spore data of the 2 years, however, the data between five stations showed a significant difference (P<0.0001). No statistically significant difference existed between stations and years with respect to the concentration of viable fungi. When the data of individual allergenic fungal concentrations were compared between stations and years, no statistically significant difference was observed in all cases except for Aspergillus japonicus and Rhizopus nigricans, which showed significant difference in case of stations and years, respectively. The ratios between the total fungal spores collected by the Burkard sampler and the viable fungi collected by the Andersen sampler from all sampling stations ranged between 0.29 and 7.61. The antigenic extracts of eight prevalent viable airborne fungi (A. flavus, A. japonicus, A. fumigatus, Alternaria alternata, Cladosporium cladosporioides, Curvularia pallescens, Fusarium roseum, and R. nigricans) demonstrated > 60% positive reactions in the skin prick test. These selected allergenic fungi collectively represented 31.7-63.2% of the total airborne viable fungi in different stations. The study concluded that: (i) a rich fungal airspora existed in the rural study area, (ii) to achieve representative information on the total airborne fungal spores of an area, the monitoring in multiple sampling stations is preferable over a single sampling station; for viable fungi, however, one station can be considered, (iii) the percentage of airborne fungal viability is higher in rural agricultural areas, and (iv) approximately 52% of the viable airborne fungi in the rural study area were allergenic. (C) 2003 Elsevier B.V. All rights reserved.	Univ S Florida, Dept Internal Med, Div Allergy & Immunol, Joy McCann Culverhouse Airway Dis Ctr, Tampa, FL 33612 USA; Ctr Study Man & Environm, Kolkata 700091, W Bengal, India; Bose Inst, Dept Bot, Div Palynol & Environm Biol, Kolkata 700009, W Bengal, India	Adhikari, A (reprint author), Univ Cincinnati, Ctr Hlth Related Aerosol Studies, Dept Environm Hlth, 3223 Eden Ave,POB 67056, Cincinnati, OH 45267 USA.	adhikaa@email.uc.edu					ABDELHAFEZ SII, 1990, J BASIC MICROB, V30, P467, DOI 10.1002/jobm.3620300702; Aizenberg V, 2000, AIHAJ, V61, P855, DOI 10.1202/0002-8894(2000)061<0855:POAOCB>2.0.CO;2; Al-Suwaine A. 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P., 1991, The fungal spore and disease initiation in plants and animals., P379; LONG DL, 1972, J ALLERGY CLIN IMMUN, V49, P255, DOI 10.1016/0091-6749(72)90093-0; Macher J.M., 1997, APPL OCCUP ENV HYG, V12, P730, DOI 10.1080/1047322X.1997.10387755; MALLING HJ, 1986, ALLERGY, V41, P342, DOI 10.1111/j.1398-9995.1986.tb00311.x; Mitakakis TZ, 2001, GRANA, V40, P230, DOI 10.1080/001731301317223268; Mitakakis TZ, 2001, AEROBIOLOGIA, V17, P171, DOI [10.1023/A:1011028412526, DOI 10.1023/A:1011028412526]; Nayak B. K., 1998, AEROBIOLOGIA, V14, P59, DOI 10.1007/BF02694596; PALMAS F, 1990, GRANA, V29, P87; Rosas I, 1997, AEROBIOLOGIA, V13, P23, DOI 10.1007/BF02694787; Spiewak R, 2001, ANN AGR ENV MED, V8, P255; STRACHAN DP, 1988, BRIT MED J, V297, P1223; Takahashi T, 1997, MYCOPATHOLOGIA, V139, P23, DOI 10.1023/A:1006831111595; TARGONSKI PV, 1995, J ALLERGY CLIN IMMUN, V95, P709; Terr AI, 1994, BASIC CLIN IMMUNOL, P314; VITTAL BPR, 1988, INDIA ANN ALLERGY, V60, P99; Waisel Y., 1997, AEROBIOLOGIA, V13, P281, DOI 10.1007/BF02694496; Wathes C. M., 1995, P547	44	74	84	3	11	ELSEVIER SCIENCE BV	AMSTERDAM	PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS	0048-9697	1879-1026		SCI TOTAL ENVIRON	Sci. Total Environ.	JUN 29	2004	326	1-3					123	141		10.1016/j.scitotenv.2003.12.007		19	Environmental Sciences	Environmental Sciences & Ecology	824YL	WOS:000221723000010	15142771	
J	Taube, C; Wei, XD; Swasey, CH; Joetham, A; Zarini, S; Lively, T; Takeda, K; Loader, J; Miyahara, N; Kodama, T; Shultz, LD; Donaldson, DD; Hamelmann, EH; Dakhama, A; Gelfand, EW				Taube, C; Wei, XD; Swasey, CH; Joetham, A; Zarini, S; Lively, T; Takeda, K; Loader, J; Miyahara, N; Kodama, T; Shultz, LD; Donaldson, DD; Hamelmann, EH; Dakhama, A; Gelfand, EW			Mast cells, Fc epsilon RI, and IL-13 are required for development of airway hyperresponsiveness after aerosolized allergen exposure in the absence of adjuvant	JOURNAL OF IMMUNOLOGY			English	Article							N-TERMINAL KINASE; C-KIT LIGAND; DEFICIENT MICE; PULMONARY EOSINOPHILIA; BRONCHIAL RESPONSIVENESS; CYTOKINE PRODUCTION; PHASE-SEPARATION; IGE PRODUCTION; TRITON X-114; ASTHMA MODEL	In certain models of allergic airway disease, mast cells facilitate the development of inflammation and airway hyper-responsiveness (AHR). To define the role of the high affinity IgE receptor (Fcis an element ofRI) in the development of AHR, mice with a disruption of the a subunit of the high affinity IgE receptor (Fcis an element ofRI(-/-)) were exposed on 10 consecutive days to nebulized OVA. Forty-eight hours after the last nebulization, airway responsiveness was monitored by the contractile response of tracheal smooth muscle to electrical field. stimulation (EFS). After the 10-day OVA challenge protocol, wild-type mice demonstrated increased responsiveness to EFS, whereas similarly challenged Fcis an element ofRI(-/-) mice showed a low response to EFS, similar to nonexposed animals. Further, allergen-challenged Fcis an element ofRI(-/-) mice showed less airway inflammation, goblet cell hyperplasia, and lower levels of IL-13 in lung homogenates compared with the controls. IL-13-deficient mice failed to develop an increased response to EFS or goblet cell hyperplasia after the 10-day OVA challenge. We transferred bone marrow-derived mast cells from wild-type mice to Fcis an element ofRI(-/-) mice 1 day before initiating the challenge protocol. After the 10-day OVA challenge, recipient Fcis an element ofRI(-/-) mice demonstrated EFS-induced responses similar to those of challenged wild-type mice. Transferred mast cells could be detected in tracheal preparations. These results show that Fcis an element ofRI is important for the development of AHR after an aerosolized allergen sensitization protocol and that this effect is mediated through Fcis an element ofRI on mast cells and production of IL-13 in the lung.	Natl Jewish Med & Res Ctr, Dept Pediat, Div Cell Biol, Denver, CO 80206 USA; Wyeth Inst, Cambridge, MA 02140 USA; Jackson Lab, Bar Harbor, ME 04609 USA	Gelfand, EW (reprint author), Natl Jewish Med & Res Ctr, Dept Pediat, Div Cell Biol, 1400 Jackson St, Denver, CO 80206 USA.	gelfande@njc.org			NHLBI NIH HHS [HL36577, HL61005]; NIAID NIH HHS [AI42246, AI30389]		AIDA Y, 1990, J IMMUNOL METHODS, V132, P191, DOI 10.1016/0022-1759(90)90029-U; Akbari O, 2003, NAT MED, V9, P582, DOI 10.1038/nm851; Alimam MZ, 2000, AM J RESP CELL MOL, V22, P253; BOCHNER BS, 1995, J IMMUNOL, V154, P799; BORDIER C, 1981, J BIOL CHEM, V256, P1604; BOULET LP, 1983, J ALLERGY CLIN IMMUN, V71, P399, DOI 10.1016/0091-6749(83)90069-6; Brightling CE, 2002, NEW ENGL J MED, V346, P1699, DOI 10.1056/NEJMoa012705; BRUSSELLE GG, 1994, CLIN EXP ALLERGY, V24, P73, DOI 10.1111/j.1365-2222.1994.tb00920.x; BURD PR, 1995, J EXP MED, V181, P1373, DOI 10.1084/jem.181.4.1373; BURROWS B, 1989, NEW ENGL J MED, V320, P271, DOI 10.1056/NEJM198902023200502; CARTIER A, 1982, J ALLERGY CLIN IMMUN, V70, P170, DOI 10.1016/0091-6749(82)90038-0; Chayama K, 2001, P NATL ACAD SCI USA, V98, P4599, DOI 10.1073/pnas.081021898; Dombrowicz D, 1997, J CLIN INVEST, V99, P915, DOI 10.1172/JCI119256; DOMBROWICZ D, 1993, CELL, V75, P969, DOI 10.1016/0092-8674(93)90540-7; Donaldson DD, 1998, J IMMUNOL, V161, P2317; DVORAK AM, 1994, AM J PATHOL, V144, P160; Garrington TP, 2000, EMBO J, V19, P5387, DOI 10.1093/emboj/19.20.5387; Grunig G, 1998, SCIENCE, V282, P2261, DOI 10.1126/science.282.5397.2261; GRUNSTEIN M, 2002, AM J PHYSIOL, V281, pL520; Haczku A, 2000, AM J RESP CRIT CARE, V161, P952; Hamelmann E, 1999, AM J RESP CRIT CARE, V160, P934; Hamelmann E, 1999, ALLERGY, V54, P297, DOI 10.1034/j.1398-9995.1999.00085.x; Hamelmann E, 1997, P NATL ACAD SCI USA, V94, P1350, DOI 10.1073/pnas.94.4.1350; Hoshino T, 1999, J Immunol, V162, P51; Ishizuka T, 1999, J IMMUNOL, V162, P2087; KARASUYAMA H, 1988, EUR J IMMUNOL, V18, P97, DOI 10.1002/eji.1830180115; Kinet JP, 1999, ANNU REV IMMUNOL, V17, P931, DOI 10.1146/annurev.immunol.17.1.931; Kobayashi T, 2000, J IMMUNOL, V164, P3855; Kraneveld AD, 2002, J IMMUNOL, V169, P2044; KUNG TT, 1995, AM J RESP CELL MOL, V12, P404; Kuperman DA, 2002, NAT MED, V8, P885, DOI 10.1038/nm734; LARSEN GL, 1992, J CLIN INVEST, V89, P747, DOI 10.1172/JCI115651; Larsen GL, 1994, AM J PHYSIOL, V266, P263; Marietta EV, 1996, EUR J IMMUNOL, V26, P49, DOI 10.1002/eji.1830260108; Masuda A, 2002, J IMMUNOL, V169, P3801; Mayr SI, 2002, J IMMUNOL, V169, P2061; McKenzie GJ, 1998, IMMUNITY, V9, P423, DOI 10.1016/S1074-7613(00)80625-1; Mehlhop PD, 1997, P NATL ACAD SCI USA, V94, P1344, DOI 10.1073/pnas.94.4.1344; Metcalfe DD, 1997, PHYSIOL REV, V77, P1033; Nagai H, 1996, CLIN EXP ALLERGY, V26, P642, DOI 10.1111/j.1365-2222.1996.tb00590.x; NAKANO T, 1985, J EXP MED, V162, P1025, DOI 10.1084/jem.162.3.1025; NOGAMI M, 1990, AM REV RESPIR DIS, V141, P1289; Ogawa K, 1999, INT ARCH ALLERGY IMM, V120, P15, DOI 10.1159/000053586; OTSU K, 1987, J EXP MED, V165, P615, DOI 10.1084/jem.165.3.615; Peat JK, 1996, AM J RESP CRIT CARE, V153, P141; QURESHI R, 1988, J IMMUNOL, V141, P2090; RENZ H, 1994, J IMMUNOL, V152, P351; RENZ H, 1992, J ALLERGY CLIN IMMUN, V89, P1127, DOI 10.1016/0091-6749(92)90296-E; ROTTEM M, 1993, J IMMUNOL, V151, P4950; Schaefer BC, 2001, CELL IMMUNOL, V214, P110, DOI 10.1006/cimm.2001.1895; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; Stassen M, 2001, J IMMUNOL, V166, P4391; Takeda K, 1997, J EXP MED, V186, P449, DOI 10.1084/jem.186.3.449; Taube C, 2002, J IMMUNOL, V169, P6482; Tomkinson A, 2001, J IMMUNOL, V166, P5792; Walter DM, 2001, J IMMUNOL, V167, P4668; WERSHIL BK, 1987, J IMMUNOL, V139, P2605; Williams CMM, 2000, J EXP MED, V192, P455, DOI 10.1084/jem.192.3.455; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; Zhu Zhou, 1999, Journal of Clinical Investigation, V103, P779, DOI 10.1172/JCI5909; ZURAWSKI G, 1994, IMMUNOL TODAY, V15, P19, DOI 10.1016/0167-5699(94)90021-3	61	74	76	0	4	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	MAY 15	2004	172	10					6398	6406				9	Immunology	Immunology	818XD	WOS:000221276900076	15128831	
J	Prescott, SL; Calder, PC				Prescott, SL; Calder, PC			N-3 polyunsaturated fatty acids and allergic disease	CURRENT OPINION IN CLINICAL NUTRITION AND METABOLIC CARE			English	Review						n-3 polyunsaturated fatty acids; fish oil; docosahexaenoic acid; arachidonic acid; allergic disease; atopy; eicosapentaenoic acid; asthma	TUMOR-NECROSIS-FACTOR; HOUSE-DUST MITE; TYPE-2 CYTOKINE PRODUCTION; FISH-OIL SUPPLEMENTATION; PLACEBO-CONTROLLED TRIAL; T-HELPER TYPE-1; BRONCHIAL-ASTHMA; DIETARY SUPPLEMENTATION; ATOPIC-DERMATITIS; CHILDHOOD ASTHMA	Purpose of review With escalating rates of allergic disease, it is vital to explore novel causal pathways. This review examines the evidence for a potential role of changing dietary intake of omega-3 polyunsaturated fatty acids in the development, treatment and prevention of allergic diseases. Recent findings Although it is difficult to determine the contribution of altered (decreased) dietary intake of omega-3 polyunsaturated fatty acids to the recent rise in the incidence of allergic disease, there is growing evidence that these nutrients have antiinflammatory properties and may modulate immune responses. These fatty acids have few side effects, and may be of some benefit in established allergic diseases (such as asthma and atopic dermatitis), although these effects are not strong. Because of this limited efficacy in established disease, the focus has shifted to the potential benefits of these immune modulators in earlier life for disease prevention. Two recent preliminary reports in infants suggest that dietary omega-3 polyunsaturated fatty acid supplements in pregnancy or in the early postnatal period could have immunomodulatory properties and associated clinical effects, although more studies are now needed. Novel synthetic polyunsaturated fatty acids with more potent and selective antiinflammatory effects may also provide safe therapeutic and preventive strategies in the future. Summary Dietary factors are important but still under-explored candidates in the search for environmental strategies to reduce the enormous impact of allergic diseases in modernized societies. There is an ongoing need for further research into the role of omega-3 polyunsaturated fatty acids in allergic disease, particularly in early life before atopy is established.	Univ Western Australia, Sch Paediat & Child Hlth, Perth, WA 6009, Australia; Univ Southampton, Inst Human Nutr, Southampton, Hants, England	Prescott, SL (reprint author), Princess Margaret Hosp, Sch Pediat & Child Hlth, POB D184, Perth, WA 6001, Australia.	susanp@ichr.uwa.edu.au	Calder, Philip/E-9739-2013; Prescott, Susan/H-5665-2014	Calder, Philip/0000-0002-6038-710X; 			ARM J P, 1988, Thorax, V43, P84, DOI 10.1136/thx.43.2.84; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; BERTHJONES J, 1993, LANCET, V341, P1557, DOI 10.1016/0140-6736(93)90697-F; BETZ M, 1991, J IMMUNOL, V146, P108; BJORNEBOE A, 1987, BRIT J DERMATOL, V117, P463, DOI 10.1111/j.1365-2133.1987.tb04926.x; Black PN, 1997, EUR RESPIR J, V10, P6, DOI 10.1183/09031936.97.10010006; Broughton KS, 1997, AM J CLIN NUTR, V65, P1011; Calder PC, 2003, LIPIDS, V38, P343, DOI 10.1007/s11745-003-1068-y; Calder PC, 2002, BRIT J NUTR, V87, pS31, DOI [10.1079/BJN2001455, 10.1079/BJN2001482]; Calder PC, 2001, LIPIDS, V36, P1007, DOI 10.1007/s11745-001-0812-7; Caughey GE, 1996, AM J CLIN NUTR, V63, P116; Costabile M, 2001, J IMMUNOL, V167, P3980; Curtis CL, 2002, ARTHRITIS RHEUM, V46, P1544, DOI 10.1002/art.10305; Curtis CL, 2000, J BIOL CHEM, V275, P721, DOI 10.1074/jbc.275.2.721; DRY J, 1991, INT ARCH ALLER A IMM, V95, P156; Dunder T, 2001, ALLERGY, V56, P425, DOI 10.1034/j.1398-9995.2001.056005425.x; DUNSTAN J, IN PRESS EUR J CLIN; DUNSTAN J, IN PRESS CLIN IMMUNO; Dunstan JA, 2003, CLIN EXP ALLERGY, V33, P442, DOI 10.1046/j.1365-2222.2003.01590.x; Dunstan JA, 2003, J ALLERGY CLIN IMMUN, V112, P1178, DOI 10.1016/j.jaci.2003.09.009; Ellwood P, 2001, EUR RESPIR J, V17, P436, DOI 10.1183/09031936.01.17304360; ENDRES S, 1989, NEW ENGL J MED, V320, P265, DOI 10.1056/NEJM198902023200501; Foitzik T, 2002, JPEN-PARENTER ENTER, V26, P351, DOI 10.1177/0148607102026006351; Gewirtz AT, 2002, ADV EXP MED BIOL, V507, P229; GIBNEY MJ, 1993, EUR J CLIN NUTR, V47, P255; Gorelova Zh. Yu., 1999, Voprosy Pitaniya, V68, P31; Haby MM, 2001, THORAX, V56, P589, DOI 10.1136/thorax.56.8.589; Harizi H, 2003, J IMMUNOL, V170, P139; Hashimoto N, 1997, Nihon Kyobu Shikkan Gakkai Zasshi, V35, P634; HILKENS CMU, 1995, EUR J IMMUNOL, V25, P59, DOI 10.1002/eji.1830250112; Hodge L, 1996, MED J AUSTRALIA, V164, P137; Hodge L, 1998, EUR RESPIR J, V11, P361, DOI 10.1183/09031936.98.11020361; Hughes DA, 1996, BIOCHEM SOC T, V24, pS389; Hughes DA, 1997, CLIN EXP IMMUNOL, V110, P516, DOI 10.1046/j.1365-2249.1997.4351455.x; Jones AC, 1996, PEDIATR ALLERGY IMMU, V7, P109, DOI 10.1111/j.1399-3038.1996.tb00117.x; Kalinski P, 1997, J IMMUNOL, V159, P28; Kankaanpaa P, 1999, ANN MED, V31, P282, DOI 10.3109/07853899908995891; KATAMURA K, 1995, INT ARCH ALLERGY IMM, V106, P101; Kimura M, 2002, INT ARCH ALLERGY IMM, V127, P191, DOI 10.1159/000053863; KIRSCH CM, 1988, ARCH INTERN MED, V148, P1023; LEE TH, 1985, NEW ENGL J MED, V312, P1217, DOI 10.1056/NEJM198505093121903; Levy BD, 2001, NAT IMMUNOL, V2, P612, DOI 10.1038/89759; Lewis S, 1998, LANCET, V351, P1220, DOI 10.1016/S0140-6736(98)22017-4; Machura E, 1996, Pediatr Pol, V71, P97; Masuev KA, 1997, TERAPEVT ARKH, V69, P31; Masuev KA, 1997, TERAPEVT ARKH, V69, P33; Mayser P, 2002, JPEN-PARENTER ENTER, V26, P151, DOI 10.1177/0148607102026003151; MCDONALD CF, 1990, EFFECT FISH OIL DERI; MEYDANI SN, 1991, J NUTR, V121, P547; Mihrshahi S, 2003, J ALLERGY CLIN IMMUN, V111, P162, DOI 10.1067/mai.2003.36; Miles EA, 2003, CLIN EXP ALLERGY, V33, P624, DOI 10.1046/j.1365-2222.2003.01637.x; Mosmann TR, 1996, IMMUNOL TODAY, V17, P138, DOI 10.1016/0167-5699(96)80606-2; Nagakura T, 2000, EUR RESPIR J, V16, P861, DOI 10.1183/09031936.00.16586100; Ng TW, 2002, ALLERGY, V57, P207, DOI 10.1034/j.1398-9995.2002.1o3369.x; Obata T, 1999, CLIN EXP ALLERGY, V29, P1129; Okamoto M, 2000, INTERNAL MED, V39, P107, DOI 10.2169/internalmedicine.39.107; Petursdottir DH, 2002, J NUTR, V132, P3740; Prescott SL, 1998, J IMMUNOL, V160, P4730; Prescott Susan L, 2003, Curr Opin Allergy Clin Immunol, V3, P125, DOI 10.1097/00130832-200304000-00006; ROMAGNANI S, 1991, IMMUNOL TODAY, V12, P256, DOI 10.1016/0167-5699(91)90120-I; ROPER RL, 1995, J IMMUNOL, V154, P162; Sakakibara H, 1995, Nihon Kyobu Shikkan Gakkai Zasshi, V33, P395; Sanderson P, 1997, J LEUKOCYTE BIOL, V62, P771; Simopoulos AP, 1999, AM J CLIN NUTR, V70, p560S; Smart JM, 2002, CLIN EXP ALLERGY, V32, P796, DOI 10.1046/j.1365-2222.2002.01391.x; SNIJDEWINT FGM, 1993, J IMMUNOL, V150, P5321; SPERLING RI, 1993, J CLIN INVEST, V91, P651, DOI 10.1172/JCI116245; STENIUSAARNIALA B, 1989, ANN ALLERGY, V62, P534; Surette ME, 2003, CLIN THER, V25, P972, DOI 10.1016/S0149-2918(03)80117-0; Takemura Y, 2002, PREV MED, V34, P221, DOI 10.1006/pmed.2001.0978; THIEN FCK, 1993, AM REV RESPIR DIS, V147, P1138; Vachier I, 2002, BIOCHEM BIOPH RES CO, V290, P219, DOI 10.1006/bbrc.2001.6155; Villani F, 1998, RESPIRATION, V65, P265, DOI 10.1159/000029274; Wills-Karp M, 2001, NAT REV IMMUNOL, V1, P69, DOI 10.1038/35095579; WOODS RK, 2003, DIETARY MARINE FATTY; ZEIGER R, 1995, J ALLERGY CLIN IMMUN, V96, P1179	76	74	78	0	8	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	1363-1950			CURR OPIN CLIN NUTR	Curr. Opin. Clin. Nutr. Metab. Care	MAR	2004	7	2					123	129		10.1097/00075197-200403000-00004		7	Endocrinology & Metabolism; Nutrition & Dietetics	Endocrinology & Metabolism; Nutrition & Dietetics	804MT	WOS:000220303500003	15075701	
J	Lee, SL; Wong, W; Lau, YL				Lee, SL; Wong, W; Lau, YL			Increasing prevalence of allergic rhinitis but not asthma among children in Hong Kong from 1995 to 2001 (Phase 3 International Study of Asthma and Allergies in Childhood)	PEDIATRIC ALLERGY AND IMMUNOLOGY			English	Article						trend prevalence; asthma; allergic rhinitis; eczema; children; Hong Kong	ATOPIC ECZEMA; WORLDWIDE VARIATIONS; CRITICAL-APPRAISAL; SCHOOL-CHILDREN; BIRTH COHORT; RISK-FACTORS; SYMPTOMS; SENSITIZATION; ISAAC; RHINOCONJUNCTIVITIS	There is a worldwide belief that the prevalence of asthma and other allergic diseases is increasing but the measures used in many studies are susceptible to systematic errors. We examined the trend of asthma, allergic rhinitis and eczema prevalence in school children aged 6-7 years in Hong Kong from 1995 to 2001 using standardized ISAAC methodology. There were 4448 and 3618 children participating in 2001 and 1995, respectively. The prevalence of life-time rhinitis (42.4% vs. 38.9%, p < 0.01), current rhinitis (37.4% vs. 35.1%, p < 0.03), current rhinoconjunctivitis (17.2 vs. 13.6 %, p < 0.01) and life-time eczema (30.7% vs. 28.1%, p = 0.01) increased significantly. There was no significant change in prevalence of life-time asthma, life-time wheeze and current wheeze albeit a significant increase in severe asthma symptoms. We investigated a number of potential risk factors including sex, family history of atopy, sibship size, birth weight, respiratory tract infections, pet ownership and exposure to tobacco smoke. However, the increases in prevalence of rhinitis and eczema could not be entirely explained by the change of prevalence of these risk factors. The odds ratio OR for the study period remained significantly associated with current rhinitis (OR 1.31, 95% confidence intervals CI 1.17-1.46), current rhinoconjunctivitis (OR 1.63, 95% Cl 1.41-1.87) and life-time eczema (OR 1.30, 95% CI 1.16-1.45) after adjustment for these confounding variables using logistic regression model. Further study is warranted to elucidate the factors contributing to the observable change in the prevalence of rhinitis in our population.	Univ Hong Kong, Queen Mary Hosp, Dept Paediat & Adolescent Med, Hong Kong, Hong Kong, Peoples R China	Lau, YL (reprint author), Univ Hong Kong, Queen Mary Hosp, Dept Paediat & Adolescent Med, Hong Kong, Hong Kong, Peoples R China.	lauylung@hkucc.hku.hk	Lau, Yu Lung/C-4322-2009				Arshad SH, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.2.e33; Asher MI, 1998, EUR RESPIR J, V12, P315; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Chan HH, 2001, CLIN EXP ALLERGY, V31, P903, DOI 10.1046/j.1365-2222.2001.01089.x; Corne JM, 2001, AM J RESP CRIT CARE, V163, P1101; del Giudice MM, 2002, ALLERGY, V57, P169, DOI 10.1034/j.1398-9995.2002.1s3252.x; *ENV PROT DEP HONG, AIR QUAL HONG KONG 2; Kalyoncu AF, 1999, PEDIATR ALLERGY IMMU, V10, P261; Lau YL, 1998, J PAEDIATR CHILD H, V34, P47, DOI 10.1046/j.1440-1754.1998.00217.x; Magnus P, 1997, BRIT MED J, V314, P1795; Mitchell EA, 2001, EUR J EPIDEMIOL, V17, P667, DOI 10.1023/A:1015500508261; PEAT JK, 1994, BRIT MED J, V308, P1591; Pekkanen J, 1999, EUR RESPIR J, V14, P951, DOI 10.1034/j.1399-3003.1999.14d37.x; Rhodes HL, 2002, AM J RESP CRIT CARE, V165, P176; Schafer T, 1999, J ALLERGY CLIN IMMUN, V104, P1280, DOI 10.1016/S0091-6749(99)70025-4; Soto-Quiros ME, 2002, PEDIATR ALLERGY IMMU, V13, P342, DOI 10.1034/j.1399-3038.2002.02035.x; Strachan DP, 1998, THORAX, V53, P117; Strachan DP, 1997, PEDIATR ALLERGY IMMU, V8, P161, DOI 10.1111/j.1399-3038.1997.tb00156.x; Ulrik CS, 2000, ALLERGY, V55, P1019, DOI 10.1034/j.1398-9995.2000.00630.x; von Mutius E, 2000, J ALLERGY CLIN IMMUN, V105, P9, DOI 10.1016/S0091-6749(00)90171-4; von Mutius E, 1998, LANCET, V351, P862, DOI 10.1016/S0140-6736(97)10100-3; Wieringa MH, 2001, CLIN EXP ALLERGY, V31, P1553, DOI 10.1046/j.1365-2222.2001.01188.x; Williams H, 1999, J ALLERGY CLIN IMMUN, V103, P125, DOI 10.1016/S0091-6749(99)70536-1; Zhao TB, 2000, J PAEDIATR CHILD H, V36, P128, DOI 10.1046/j.1440-1754.2000.00457.x	24	74	83	0	0	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0905-6157			PEDIATR ALLERGY IMMU	Pediatr. Allergy Immunol.	FEB	2004	15	1					72	78		10.1046/j.0905-6157.2003.00109.x		7	Allergy; Immunology; Pediatrics	Allergy; Immunology; Pediatrics	803ST	WOS:000220251500010	14998385	
J	Delfino, RJ; Gong, H; Linn, WS; Hu, Y; Pellizzari, ED				Delfino, RJ; Gong, H; Linn, WS; Hu, Y; Pellizzari, ED			Respiratory symptoms and peak expiratory flow in children with asthma in relation to volatile organic compounds in exhaled breath and ambient air	JOURNAL OF EXPOSURE ANALYSIS AND ENVIRONMENTAL EPIDEMIOLOGY			English	Article						epidemiology; panel study; exposure biomarkers; hazardous air pollutants; air pollution	ANTIINFLAMMATORY MEDICATION USE; POLLUTANTS; POLLUTION; EXPOSURE; SEVERITY; INDOOR; MODELS; EXACERBATIONS; ASSOCIATIONS; FORMALDEHYDE	Indoor volatile organic compounds (VOCs) have been associated with asthma, but there is little epidemiologic work on ambient exposures, and no data on relationships between respiratory health and exhaled breath VOCs, which is a biomarker of VOC exposure. We recruited 26 Hispanic children with mild asthma in a Los Angeles community with high VOC levels near major freeways and trucking routes. Two dropped out, three had invalid peak expiratory flow (PEF) or breath VOC data, leaving 21. Children filled out symptom diaries and performed PEF maneuvers daily, November 1999 January 2000. We aimed to collect breath VOC samples on asthma episode and baseline symptom-free days, but six subjects only gave samples on symptom-free days. We analyzed 106 breath samples by GC-MS. Eight VOCs were quanti. able in >75% of breath samples (benzene, methylene chloride, styrene, tetrachloroethylene, toluene, m,p-xylene, o-xylene, and p-dichlorobenzene). Generalized estimating equation and mixed linear regression models for VOC exposure-response relationships controlled for temperature and respiratory infections. We found marginally positive associations between bothersome or more severe asthma symptoms and same day breath concentrations of benzene [odds ratio ( OR) 2.03, 95% confidence interval (CI) 0.80, 5.11] but not other breath VOCs. Ambient petroleum-related VOCs measured on the same person-days as breath VOCs showed notably stronger associations with symptoms, including toluene, m,p-xylene, o-xylene, and benzene (OR 5.93, 95% CI 1.64, 21.4). On breath sample days, symptoms were also associated with 1-h ambient NO2, OR 8.13 (1.52, 43.4), and SO2, OR 2.36 (1.16, 4.81). Consistent inverse relationships were found between evening PEF and the same ambient VOCs, NO2, and SO2. There were no associations with O-3. Given the high traffic density of the region, stronger associations for ambient than for breath VOCs suggest that ambient VOC measurements were better markers for daily exposure to combustion-related compounds thought to be causally related to acute asthma. Alternatively, the low sample size of symptom responses (5-21 responses per 108 breath samples) may have led to the nonsignificant results for breath VOCs.	Univ Calif Irvine, Coll Med, Dept Med, Div Epidemiol, Irvine, CA 92697 USA; Univ So Calif, Keck Sch Med, Dept Prevent Med, Downey, CA 90242 USA; Los Amigos Res & Educ Inst, Environm Hlth Serv, Downey, CA 90242 USA; Res Triangle Inst, Analyt & Chem Sci & Exposure Anal Res Program, Res Triangle Pk, NC 27709 USA	Delfino, RJ (reprint author), Univ Calif Irvine, Coll Med, Dept Med, Div Epidemiol, 224 Irvine Hall, Irvine, CA 92697 USA.				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Expo. Anal. Environ. Epidemiol.	SEP	2003	13	5					348	363		10.1038/sj.jea.7500287		16	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	721UD	WOS:000185335400003	12973363	
J	Leung, TF; Tang, NLS; Sung, YM; Li, AM; Wong, GWK; Chan, IHS; Lam, CWK				Leung, TF; Tang, NLS; Sung, YM; Li, AM; Wong, GWK; Chan, IHS; Lam, CWK			The C-159T polymorphism in the CD14 promoter is associated with serum total IgE concentration in atopic Chinese children	PEDIATRIC ALLERGY AND IMMUNOLOGY			English	Article						atopy; CD14; Chinese; immunoglobulin E	IMMUNOGLOBULIN-E; ASTHMA; GENE; ENDOTOXIN; CHILDHOOD; EXPOSURE; LINKAGE; MARKERS; SUSCEPTIBILITY; PREVALENCE	Activation of macrophages through CD14 by microbes is crucial in inducing immunity by type 1 T helper cells. A C-to-T polymorphism at position -159 of CD14 was associated with serum total IgE level in Caucasians but not in Japanese subjects. The objective of this study is to determine whether this polymorphic marker is associated with atopy and asthma phenotypes in Chinese children. Restriction fragment length polymorphism was used to characterize CD14/-159 genotypes. Microparticle immunoassay was used to measure serum total IgE level; fluorescent enzyme immunoassay was performed to measure serum concentrations of specific IgE to aeroallergens; and enzyme-linked immunosorbent assay was used to measure serum levels of soluble CD14 (sCD14). Lung function in asthmatics was assessed by spirometry. Two hundred and fifty-eight patients and 92 control children were recruited. Their mean serum total IgE concentrations were 331 and 74 kIU/l, respectively (p < 0.0001). Atopy, defined as the presence of at least one allergen-specific IgE in serum, was found in 220 (85%) patients and in 41 (45%) controls (p < 0.0001). Serum sCD14 levels were significantly associated with CD14/-159 genotypes (p = 0.004). Atopic subjects with CC genotype in CD14/-159 had the highest serum total IgE levels compared with CT and TT genotypes, with the respective mean values being 661, 427 and 380 kIU/l (p = 0.015). Similarly, a higher proportion of subjects with CC genotype had increased serum total IgE concentration (p = 0.039). This polymorphic marker was not associated with asthma or aeroallergen sensitization in our cohort. Our results suggest that the C-159T of CD14 was associated with serum total IgE concentration in atopic Chinese children.	Chinese Univ Hong Kong, Prince Wales Hosp, Dept Paediat, Shatin, Hong Kong, Peoples R China; Chinese Univ Hong Kong, Prince Wales Hosp, Dept Chem Pathol, Shatin, Hong Kong, Peoples R China	Leung, TF (reprint author), Chinese Univ Hong Kong, Prince Wales Hosp, Dept Paediat, 6-F Clin Sci Bldg, Shatin, Hong Kong, Peoples R China.			Tang, Nelson/0000-0002-3607-5819			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; Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; BURROWS B, 1989, NEW ENGL J MED, V320, P271, DOI 10.1056/NEJM198902023200502; Doull IJM, 1996, AM J RESP CRIT CARE, V153, P1280; Gao PS, 1999, CLIN GENET, V56, P164; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; GOYERT SM, 1988, SCIENCE, V239, P497, DOI 10.1126/science.2448876; Graves PE, 2000, J ALLERGY CLIN IMMUN, V105, P506, DOI 10.1067/mai.2000.104940; Heinzmann A, 2000, HUM MOL GENET, V9, P549, DOI 10.1093/hmg/9.4.549; 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; LAM KK, 1983, BRIT J DIS CHEST, V77, P390, DOI 10.1016/S0007-0971(83)80076-X; Leung TF, 2001, CLIN EXP ALLERGY, V31, P1515, DOI 10.1046/j.1365-2222.2001.01212.x; MARSH DG, 1994, SCIENCE, V264, P1152, DOI 10.1126/science.8178175; 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; PUNNONEN J, 1993, P NATL ACAD SCI USA, V90, P3730, DOI 10.1073/pnas.90.8.3730; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Romagnani S, 2000, J ALLERGY CLIN IMMUN, V105, P399, DOI 10.1067/mai.2000.104575; SENGLER C, 2002, J ALLERGY CLIN IMMUN, V109, pA670; Shek LPC, 2001, ALLERGY, V56, P749, DOI 10.1034/j.1398-9995.2001.056008749.x; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Ulevitch RJ, 1999, CURR OPIN IMMUNOL, V11, P19, DOI 10.1016/S0952-7915(99)80004-1; Vercelli D, 2002, J ALLERGY CLIN IMMUN, V109, P14, DOI 10.1067/mai.2002.121015; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; VONMUTIUS E, 1994, AM J RESP CRIT CARE, V149, P358; Wong GWK, 2001, CLIN EXP ALLERGY, V31, P1225, DOI 10.1046/j.1365-2222.2001.01140.x; ZAMBELLIWEINER A, 2002, J ALLERGY CLIN IMMUN, V109, P672	30	74	74	0	3	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0905-6157			PEDIATR ALLERGY IMMU	Pediatr. Allergy Immunol.	AUG	2003	14	4					255	260		10.1034/j.1399-3038.2003.00048.x		6	Allergy; Immunology; Pediatrics	Allergy; Immunology; Pediatrics	711HB	WOS:000184732600003	12911501	
J	Beard, J; Sladden, T; Morgan, G; Berry, G; Brooks, L; McMichael, A				Beard, J; Sladden, T; Morgan, G; Berry, G; Brooks, L; McMichael, A			Health impacts of pesticide exposure in a cohort of outdoor workers	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; cohort study; DDT; diabetes; leukemia; neoplasms; pancreatic cancer; pesticides	PANCREATIC-CANCER; ORGANOCHLORINE COMPOUNDS; DIABETES-MELLITUS; RISK-FACTORS; MORTALITY; SERUM; LEUKEMIA; MEN; DDT	We compared mortality of 1,999 outdoor staff working as part of an insecticide application program during 1935-1996 with that of 1,984 outdoor workers not occupationally exposed to insecticides, and with the Australian population. Surviving subjects also completed a morbidity questionnaire. Mortality was significantly higher in both exposed and control subjects compared with the Australian population. The major cause was mortality from smoking-related diseases. Mortality was also significantly increased in exposed subjects for a number of conditions that do not appear to be the result of smoking patterns. Compared with the general Australian population, mortality over the total study period was increased for asthma [standardized mortality ratio (SMR) = 3.45; 95% confidence interval (CI), 1.39-7.10] and for diabetes (SMR = 3.57; 95% CI, 1.16-8.32 for subjects working < 5 years). Mortality from pancreatic cancer was more frequent in subjects exposed to 1,1,1-trichloro-2,2-bis (p-chlorophenyl) ethane (SMR = 5.27; 95% CI, 1.09-15.40 for subjects working < 3 years). Compared with the control population, mortality from leukemia was increased in subjects working with more modern chemicals (standardized incidence ratio = 20.90; 95% CI, 1.54-284.41 for myeloid leukemia in the highest exposure group). There was also an increase in self-reported chronic illness and asthma, and lower neuropsychologic functioning scores among surviving exposed subjects when compared with controls. Diabetes was reported more commonly by subjects reporting occupational use of herbicides. These findings lend weight to other studies suggesting an association between adverse health effects and exposure to pesticides.	Univ Sydney, No Rivers Univ Dept Rural Hlth, Lismore, NSW 2480, Australia; So Cross Univ, So Cross Inst Hlth Res, Lismore, NSW, Australia; Univ Sydney, Sch Biostat, Lismore, NSW 2480, Australia; Australian Natl Univ, Natl Ctr Epidemiol & Populat Hlth, Canberra, ACT 2601, Australia	Beard, J (reprint author), Univ Sydney, No Rivers Univ Dept Rural Hlth, POB 498, Lismore, NSW 2480, Australia.		Beard, John/K-9621-2014	Beard, John/0000-0002-8557-0242			ALBERGHINI V, 1991, Medicina del Lavoro, V82, P18; Au WW, 1999, ENVIRON HEALTH PERSP, V107, P501; AXELSON O, 1988, AM J IND MED, V13, P105, DOI 10.1002/ajim.4700130107; BLAIR A, 1988, AM J IND MED, V13, P3; Blondell J M, 1990, Med Lav, V81, P524; Breslow N. 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Health Perspect.	MAY	2003	111	5					724	730		10.1289/ehp.5885		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	677CB	WOS:000182788400030	12727601	
J	Arbes, SJ; Cohn, RD; Yin, M; Muilenberg, ML; Burge, HA; Friedman, W; Zeldin, DC				Arbes, SJ; Cohn, RD; Yin, M; Muilenberg, ML; Burge, HA; Friedman, W; Zeldin, DC			House dust mite allergen in US beds: Results from the first National Survey of Lead and Allergens in Housing	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article; Proceedings Paper	97th International Conference of the American-Thoracic-Society	MAY 18-23, 2001	SAN FRANCISCO, CALIFORNIA	Amer Thorac Soc		house dust mite allergen; indoor allergens; surveys; epidemiology	REDUCING RELATIVE-HUMIDITY; DER-P-I; INDOOR ALLERGENS; RISK FACTOR; AVOIDANCE MEASURES; SEASONAL-VARIATION; ASTHMATIC-PATIENTS; CHILDHOOD ASTHMA; GRASS-POLLEN; EXPOSURE	Background: Although exposure to house dust mite allergen is a major risk factor for allergic sensitization and asthma, nationwide estimates of dust mite allergen levels in US homes have not been reported. Objective: The purpose of this study was to estimate the prevalence of dust mite allergen in beds of US homes and to identify predictors of dust mite allergen concentration. Methods: Data were obtained from the first National Survey of Lead and Allergens in Housing, a cross-sectional survey of 831 permanently occupied noninstitutional housing units that permitted resident children. Dust mite allergen concentration (Der f 1 plus Der p 1) was determined from a dust sample collected from a bed. The percentages of homes with concentrations at or greater than detection, 2.0 mug/g bed dust, and 10.0 mug/g bed dust were estimated. Independent predictors of allergen concentration were assessed with multivariable linear regression. Results: The percentages of US homes with dust mite allergen concentrations at or greater than detection, 2.0 mug/g, and 10.0 mug/g were 84.2% (SE, 1.73), 46.2% (SE, 2.0), and 24.2% (SE, 2.1), respectively. Independent predictors of higher levels were older homes, non-West census regions, single-family homes, no resident children, lower household income, heating sources other than forced air, musty or mildew odor, and higher bedroom humidity. Conclusion: Most US homes have detectable levels of dust mite allergen in a bed. Levels previously associated with allergic sensitization and asthma are common in US bedrooms. Predictors can be used to identify conditions under which homes are more likely to have increased dust mite allergen levels.	NIEHS, Div Intramural Res, NIH, Res Triangle Pk, NC 27709 USA; Analyt Sci, 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, Div Intramural Res, NIH, 111 Alexander Dr,Mail Drop D2-01, Res Triangle Pk, NC 27709 USA.						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Allergy Clin. Immunol.	FEB	2003	111	2					408	414		10.1067/mai.2003.16		7	Allergy; Immunology	Allergy; Immunology	644WF	WOS:000180942700028	12589364	
J	Hillert, L; Berglind, N; Arnetz, BB; Bellander, T				Hillert, L; Berglind, N; Arnetz, BB; Bellander, T			Prevalence of self-reported hypersensitivity to electric or magnetic fields in a population-based questionnaire survey	SCANDINAVIAN JOURNAL OF WORK ENVIRONMENT & HEALTH			English	Article						allergy; cross-sectional; hypersensitivity to electricity; symptoms	CHEMICAL ODOR INTOLERANCE; VISUAL-DISPLAY UNITS; SENSITIVITY; SYMPTOMS; INDIVIDUALS	Objectives The prevalence of medically unexplained symptoms attributed to exposure to electromagnetic fields is still largely unknown. Previous studies have investigated reported hypersensitivity to electricity in selected groups recruited from workplaces or outpatient clinics. The aim of this study was to estimate the prevalence of self-reported hypersensitivity to electric or magnetic fields in the general population and to describe characteristics of the group reporting such hypersensitivity with regard to demographics, other complaints, hypersensitivities, and traditional allergies. Methods A cross-sectional questionnaire survey was conducted in 1997 among 15 000 men and women between 19 and 80 years of age in Stockholm County. The response rate was 73%. Results One and a half percent of the respondents reported hypersensitivity to electric or magnetic fields. Prevalence was highest among women and in the 60- to 69-year age group. The hypersensitive group reported all symptoms, allergies, and other types of hypersensitivities included in the survey (as well as being disturbed by various factors in the: home) to a significantly greater extent than the rest of the respondents. No specific symptom profile set off the hypersensitive group from the rest of the respondents. Conclusions The results should be interpreted with caution. But they suggest that there is widespread concern among the general population about risks to health posed by electric and magnetic fields. More research is warranted to explore ill health among people reporting hypersensitivity to electric or magnetic fields.	Norrbacka Karolinska Hosp, Dept Environm Hlth, SE-17176 Stockholm, Sweden; Karolinska Inst, Dept Publ Hlth Sci, Div Occupat Med, S-10521 Stockholm, Sweden; Uppsala Univ, Dept Publ Hlth & Caring Sci, Sect Social Med, Uppsala, Sweden; Karolinska Inst, Inst Environm Med, Div Environm Epidemiol, S-10401 Stockholm, Sweden	Hillert, L (reprint author), Norrbacka Karolinska Hosp, Dept Environm Hlth, SE-17176 Stockholm, Sweden.						Arnetz BB, 1999, SCAND J WORK ENV HEA, V25, P569; Baldwin CM, 1999, TOXICOL IND HEALTH, V15, P403, DOI 10.1177/074823379901500314; Bell IR, 1997, ARCH ENVIRON HEALTH, V52, P6; BERG M, 1992, J OCCUP ENVIRON MED, V34, P698; BERGDAHL J, 1995, ACTA ODONTOL SCAND, V53, P304, DOI 10.3109/00016359509005992; BERGDAHL J, 1994, SCAND J DENT RES, V102, P41; Bergqvist U, 1997, ARBETE HALSA, P19; Davidoff AL, 1996, ARCH ENVIRON HEALTH, V51, P201; Feighery C, 1999, BRIT MED J, V319, P236; Fiedler N, 1997, ENVIRON HEALTH PERSP, V105, P409; FRANSSON K, 1996, ELOVERKANSLIGHET BLA; Furhoff AK, 1998, SCAND J PRIM HEALTH, V16, P247, DOI 10.1080/028134398750003043; Hillert L, 1999, J PSYCHOSOM RES, V47, P429, DOI 10.1016/S0022-3999(99)00048-3; Hillert L, 1997, J PSYCHOSOM RES, V42, P427, DOI 10.1016/S0022-3999(96)00374-1; Kreutzer R, 1999, AM J EPIDEMIOL, V150, P1; Langworth S, 1997, SCAND J WORK ENV HEA, V23, P65; MAYOU R, 1993, PSYCHOTHER PSYCHOSOM, V59, P69; PORTIER CJ, 1998, NIH PUBLICATIONS; Sandstrom M, 1997, J OCCUP ENVIRON MED, V39, P15, DOI 10.1097/00043764-199701000-00006; WANG T, 1994, COST 244 M EL HYP GR, P123; *WHO, 1983, WHO EURO REP STUD, P78	21	74	86	0	9	SCAND J WORK ENV HEALTH	HELSINKI	TOPELIUKSENKATU 41A, SF-00250 HELSINKI, FINLAND	0355-3140			SCAND J WORK ENV HEA	Scand. J. Work Environ. Health	FEB	2002	28	1					33	41				9	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	524GU	WOS:000174005500006	11871850	
J	Redlich, CA; Karol, MH				Redlich, CA; Karol, MH			Diisocyanate asthma: clinical aspects and immunopathogenesis	INTERNATIONAL IMMUNOPHARMACOLOGY			English	Review						diisocyanate; asthma; adduct; airway hyperreactivity; immunopathogenesis; thiol reactions; occupational	INDUCED OCCUPATIONAL ASTHMA; ISOCYANATE-INDUCED ASTHMA; NONSPECIFIC BRONCHIAL HYPERRESPONSIVENESS; DYSFUNCTION SYNDROME RADS; PEAK EXPIRATORY FLOW; HUMAN SERUM-ALBUMIN; HLA CLASS-II; TOLUENE-DIISOCYANATE; HEXAMETHYLENE-DIISOCYANATE; GUINEA-PIGS	Diisocyanates, highly reactive chemicals used in the production of polyurethanes, are currently the most frequently reported cause of chemically induced occupational asthma and their use continues to rise. The prevalence of diisocyanate asthma among exposed workers is estimated to range from 5% to 15%. Routes of exposure include the respiratory tract and skin. Workplace exposures are difficult to quantify and control, and there is no simple diagnostic test for the disease. This review considers recent concepts in exposure, clinical aspects and pathogenesis of the disease. The pathogenesis of diisocyanate asthma remains unclear, with evidence supporting both immunological and noninummological mechanisms. Knowledge of the chemical reactivity of diisocyanates, the target biomolecules, and the cellular sites of reaction are fundamental to understanding diisocyanate toxicity and disease. Recent findings of chemical interactions with biological nucleophiles will be described. The importance of diisocyanate-adducted biomolecules will be emphasized and their potential contributions: to pathogenesis discussed. It is anticipated that greater understanding of the immunopathogenesis of diisocyanate asthma, including the initial cell/diisocyanate reactions, should lead to clinically useful markers of exposure and early disease. (C) 2002 Elsevier Science B.V. All rights reserved.	Univ Pittsburgh, Dept Environm & Occupat Hlth, Pittsburgh, PA 15261 USA; Yale Univ, Occupat & Environm Med Program, New Haven, CT USA	Karol, MH (reprint author), Univ Pittsburgh, Dept Environm & Occupat Hlth, 130 DeSoto St, Pittsburgh, PA 15261 USA.				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Immunopharmacol.	FEB	2002	2	2-3					213	224		10.1016/S1567-5769(01)00174-6		12	Immunology; Pharmacology & Pharmacy	Immunology; Pharmacology & Pharmacy	513DA	WOS:000173361600007	11811926	
J	Gautrin, D; Ghezzo, H; Infante-Rivard, C; Malo, JL				Gautrin, D; Ghezzo, H; Infante-Rivard, C; Malo, JL			Natural history of sensitization, symptoms and occupational diseases in apprentices exposed to laboratory animals	EUROPEAN RESPIRATORY JOURNAL			English	Article						asthma; immunological sensitization; occupational asthma	DETERMINANTS; METHACHOLINE; ASTHMA; AGENTS; VOLUME; ATOPY; TESTS	The natural history of the development of sensitization and disease due to high-molecular-weight allergens is not well characterized. This study describes the timecourse of the incidence of work-related symptoms, skin reactivity and occupational rhinoconjunctivitis (RC) and asthma (OA); and assesses the predictive value of skin testing and RC symptoms in apprentices exposed to laboratory animals, in a 3-4-yr programme. Four-hundred and seventeen apprentices at five institutions were assessed prospectively with questionnaire, skin-testing with animal-derived allergens, spirometry and airway responsiveness (n = 373). Depending on the school, students were seen 8 (n = 136), 20 (n = 345), 32 (n = 355) and 44 (n = 98) months after starting the programme. At all visits, the incidence was greater for work-related RC symptoms followed in order by skin reactivity, occupational RC, and, almost equally, OA and work-related respiratory symptoms. The incidence-density figures were comparable for each followup period and for most indices up to 32 months after entry into the study and then tended to decrease. The positive predictive values (PPVs) of skin reactivity to work-related allergens for the development of work-related RC and respiratory symptoms were 30% and 9.0%, respectively, while the PPVs of work-related RC for the development of OA was 11.4%. Sensitization, symptoms and diseases occur maximally in the first 2-3 yrs after starting exposure to laboratory animals. Skin reactivity to work-related allergens and rhinoconjuctivitis symptoms have low positive predictive values.	Hop Sacre Coeur, Dept Chest Med, Montreal, PQ H4J 1C5, Canada; McGill Univ, Joint Dept Epidemiol & Biostat & Occupat Hlth, Montreal, PQ H3A 2T5, Canada	Gautrin, D (reprint author), Hop Sacre Coeur, Dept Chest Med, 5400 Gouin Blvd W, Montreal, PQ H4J 1C5, Canada.						American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; BURNEY PGJ, 1989, EUR RESPIR J, V2, P940; Cullinan P, 1999, EUR RESPIR J, V13, P1139, DOI 10.1034/j.1399-3003.1999.13e33.x; DEHAUT P, 1983, THORAX, V38, P516, DOI 10.1136/thx.38.7.516; Gautrin D, 2000, AM J RESP CRIT CARE, V162, P1222; Gautrin D, 1997, AM J RESP CRIT CARE, V155, P1841; Gautrin D, 2001, AM J RESP CRIT CARE, V163, P899; GORDON S, 1999, ASTHMA WORKPLACE, P399; KNUDSON RJ, 1983, AM REV RESPIR DIS, V127, P725; Malo JL, 1997, EUR RESPIR J, V10, P1513, DOI 10.1183/09031936.97.10071513; MALO JL, 1983, AM REV RESPIR DIS, V128, P8; MALO JL, 1993, LUNG BIOL HLTH DIS, V68, P117; MALO JL, 1999, EUR RESP MON, V11, P106; Monso E, 2000, AM J RESP CRIT CARE, V161, P1508; STERK PJ, 1993, EUR RESPIR J, V6, P53, DOI 10.1183/09041950.053s1693; Troyanov S, 2000, EUR RESPIR J, V16, P9, DOI 10.1034/j.1399-3003.2000.16a03.x	16	74	76	0	0	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146, WEST ST, STE 2.4 HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	MAY	2001	17	5					904	908		10.1183/09031936.01.17509040		5	Respiratory System	Respiratory System	458RU	WOS:000170209000012	11488324	
J	Hajat, S; Haines, A; Atkinson, RW; Bremner, SA; Anderson, HR; Emberlin, J				Hajat, S; Haines, A; Atkinson, RW; Bremner, SA; Anderson, HR; Emberlin, J			Association between air pollution and daily consultations with general practitioners for allergic rhinitis in London, United Kingdom	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						air pollutants; air pollution; family practice; ozone; primary health care; rhinitis; sulfur dioxide	TIME-SERIES; HAY-FEVER; PREVALENCE; DISORDERS; COMPUTER; ASTHMA	Few published studies have looked at the health effects of air pollution in the primary care setting, and most have concentrated on lower rather than upper respiratory diseases, The authors investigated the association of daily consultations with general practitioners for allergic rhinitis with air pollution in London, United Kingdom. Generalized additive models were used to regress time series of daily numbers of patients consulting for allergic rhinitis against 1992-1994 measures of air pollution, after control for possible confounders and adjustment for overdispersion and serial correlation. In children, a 10th-90th percentile increase in sulfur dioxide (SO(3)) levels 4 days prior to consultation (13-31 mug/m(3)) was associated with a 24.5% increase in consultations (95% confidence interval: 14.6, 35.2; p < 0.00001); a 10th-90th percentile increase in averaged ozone (O(3)) concentrations on the day of consultation and the preceding 3 days (6-29 parts per billion) was associated with a 37.6% rise (95% confidence interval: 23,3, 53.5; p < 0,00001). For adults, smaller effect sizes were observed for SO(3) and O(3). The association with SO(3) remained highly significant in the presence of other pollutants. This study suggests that air pollution worsens allergic rhinitis symptoms, leading to substantial increases in consultations. SO(3) and O(3) seem particularly responsible, and both seem to contribute independently.	Univ Coll Worcester, Natl Pollen Res Unit, Worcester, MA USA; Univ London St Georges Hosp, Sch Med, Dept Publ Hlth Sci, London SW17 0RE, England; UCL Royal Free & Univ Coll, Sch Med, Dept Primary Care & Populat Sci, London, England	Hajat, S (reprint author), Univ London London Sch Hyg & Trop Med, Dept Epidemiol & Populat Hlth, Keppel St, London WC1E 7HT, England.	Shakoor.Hajat@lshtm.ac.uk	Bremner, Stephen/R-4038-2016; CPRD, CPRD/B-9594-2017	Bremner, Stephen/0000-0003-0790-7070; 			BASCOM R, 1990, AM REV RESPIR DIS, V142, P594; BOWER JS, 1995, AEARAMP200150011 NAT; BUCK SF, 1960, J ROY STAT SOC B, V22, P302; CHELL M, 1993, LONDON ENERGY STUDY; De Swert LFA, 1999, EUR J PEDIATR, V158, P89, DOI 10.1007/s004310051024; FINN R, 1992, LANCET, V340, P1453; Hajat S, 1999, THORAX, V54, P597; ISHIZAKI T, 1987, ANN ALLERGY, V58, P265; Katsouyanni K, 1996, J EPIDEMIOL COMMUN H, V50, pS12, DOI 10.1136/jech.50.Suppl_1.S12; *MATHS INC, 1997, S PLUS VERS 4; MURANAKA M, 1986, J ALLERGY CLIN IMMUN, V77, P616, DOI 10.1016/0091-6749(86)90355-6; NAKAGOMI T, 1994, LANCET, V343, P121, DOI 10.1016/S0140-6736(94)90854-0; NAZARETH I, 1993, BRIT MED J, V307, P32; ROSS AM, 1994, BRIT MED J, V308, P897; Ross AM, 1996, BRIT J GEN PRACT, V46, P451; Shusterman DJ, 1998, J ALLERGY CLIN IMMUN, V101, P732, DOI 10.1016/S0091-6749(98)70302-1; VARJONEN E, 1992, ALLERGY, V47, P243, DOI 10.1111/j.1398-9995.1992.tb00657.x; VONMUTIUS E, 1992, BRIT MED J, V305, P1395; ZEGER SL, 1988, BIOMETRIKA, V75, P621	19	74	79	3	10	OXFORD UNIV PRESS INC	CARY	JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA	0002-9262			AM J EPIDEMIOL	Am. J. Epidemiol.	APR 1	2001	153	7					704	714		10.1093/aje/153.7.704		11	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	419CD	WOS:000167931000013	11282799	
J	Lanphear, BP; Aligne, CA; Auinger, P; Weitzman, M; Byrd, RS				Lanphear, BP; Aligne, CA; Auinger, P; Weitzman, M; Byrd, RS			Residential exposures associated with asthma in US children	PEDIATRICS			English	Article						NHANES; children; pediatric; prevention; epidemiology; allergic rhinitis; medical costs; day care; housing; pets and environment	CHILDHOOD ASTHMA; PARENTAL SMOKING; RISK-FACTORS; RESPIRATORY SYMPTOMS; INDOOR ALLERGENS; SENSITIZATION; HEALTH; PREVALENCE; MORBIDITY; TOBACCO	Objective. Residential exposures are recognized risk factors for childhood asthma, but the relative contribution of specific risk factors and the overall contribution of housing to asthma in US children is unknown. The objective of this study was to identify risk factors and estimate the population attributable risk of residential exposures for doctor-diagnosed asthma for US children. Methods. A cross-sectional survey was conducted from 1988 to 1994. Survey participants were 8257 children who were <6 years old and who participated in the Third National Health and Nutrition Examination Survey, a survey of the health and nutritional status of children and adults in the United States. The main outcome measure was doctor-diagnosed asthma, as reported by the parent. Results. Six percent of children had doctor-diagnosed asthma. The prevalence of asthma was higher among boys (6.7%) than girls (5.1%) and was higher among black children (8.9%) than white children (5.2%). Risk factors for doctor-diagnosed asthma included a family history of atopy (odds ratio [OR]: 2.2; 95% confidence interval [CI]: 1.5, 3.1), child's history of allergy to a pet (OR: 24.2; 95% CI: 8.4, 69.5), exposure to environmental tobacco smoke (OR: 1.8; 95% CI: 1.2-2.6), use of a gas stove or oven for heat (OR: 1.8; 95% CI: 1.02-3.2), and presence of a dog in the household (OR: 1.6; 95% CI: 1.1, 2.3). The population attributable risk of <greater than or equal to>1 residential exposure for doctor-diagnosed asthma in US children <6 years old was 39.2%, or an estimated 533 000 excess cases, whereas having a family history of atopy accounted for 300 000. The attributable cost of asthma as a result of residential exposures for children <6 years old was $402 million (95% CI: $296-$507 million) annually. Conclusions. The elimination of identified residential risk factors, if causally associated with asthma, would result in a 39% decline in doctor-diagnosed asthma among US children <6 years old.	Childrens Hosp, Med Ctr, Cincinnati, OH 45229 USA; Univ Rochester, Sch Med, Dept Pediat, Rochester, NY 14642 USA; Amer Acad Pediat Ctr Child Hlth Res, Rochester, NY USA; Univ Calif Davis, Dept Pediat, Sacramento, CA 95817 USA	Lanphear, BP (reprint author), Childrens Hosp, Med Ctr, 3333 Burnet Ave, Cincinnati, OH 45229 USA.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	BHP HRSA HHS [1T-32 PE-10027, 2T-32 PE-12002]		Aligne CA, 1997, ARCH PEDIAT ADOL MED, V151, P648; Burr ML, 1999, THORAX, V54, P27; Centers for Disease Control and Prevention, 1997, MMWR-MORBID MORTAL W, V46, P1221; Centers for Disease C Prevention, 1996, MMWR-MORBID MORTAL W, V45, P350; CHILMONCZYK BA, 1993, NEW ENGL J MED, V328, P1665, DOI 10.1056/NEJM199306103282303; Committee on the Assessment of Asthma and Indoor Air, 2000, CLEAR AIR ASTHM IND; COUGHLIN SS, 1994, EPIDEMIOL REV, V16, P51; CRONER S, 1992, ALLERGY, V47, P150, DOI 10.1111/j.1398-9995.1992.tb00956.x; DUFF AL, 1993, PEDIATRICS, V92, P535; Garrett MH, 1998, AM J RESP CRIT CARE, V158, P891; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; GERGEN PJ, 1998, PEDIATRICS, V101; HALFON N, 1993, PEDIATRICS, V91, P56; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; INFANTERIVARD C, 1993, AM J EPIDEMIOL, V137, P834; INGRAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449, DOI 10.1016/S0091-6749(95)70286-5; Lanphear BP, 1998, SCIENCE, V281, P1617, DOI 10.1126/science.281.5383.1617; 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, 1992, PEDIATRICS, V89, P21; Pirkle JL, 1998, ENVIRON HEALTH PERSP, V106, P745, DOI 10.1289/ehp.98106745; Plaschke P, 1999, J ALLERGY CLIN IMMUN, V104, P58, DOI 10.1016/S0091-6749(99)70114-4; PLATTSMILLS TAE, 1995, J ALLERGY CLIN IMMUN, V96, P435, DOI 10.1016/S0091-6749(95)70284-9; Pollock D A, 1988, MMWR CDC Surveill Summ, V37, P13; Pope A. 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J	Hannuksela, ML; Ellahham, S				Hannuksela, ML; Ellahham, S			Benefits and risks of sauna bathing	AMERICAN JOURNAL OF MEDICINE			English	Review							HIGH AMBIENT-TEMPERATURE; SUDDEN CORONARY DEATH; PLASMA-RENIN ACTIVITY; FINNISH SAUNA; HEAT EXPOSURE; THERMAL-STRESS; HYPERTENSIVE PATIENTS; BETA-ENDORPHIN; TRIPLOCHITON SCLEROXYLON; MATERNAL HYPERTHERMIA	Although sauna bathing causes various acute, transient cardiovascular and hormonal changes, it is well tolerated by most healthy adults and children. Sauna bathing does not influence fertility and is safe during the uncomplicated pregnancies of healthy women. Some studies have suggested that long-term sauna bathing may help lower blood pressure in patients with hypertension and improve the left ventricular ejection fraction in patients with chronic congestive heart failure, but additional data are needed to confirm these findings. The transient improvements in pulmonary function that occur in the sauna may provide some relief to patients with asthma and chronic bronchitis. Sauna bathing may also alleviate pain and improve joint mobility in patients with rheumatic disease. Although sauna bathing does not cause drying of the skin-and may even benefit patients with psoriasis-sweating may increase itching in patients with atopic dermatitis. Contraindications to sauna bathing include unstable angina pectoris, recent myocardial infarction, and severe aortic stenosis. Sauna bathing is safe, however, for most people with coronary heart disease with stable angina pectoris or old myocardial infarction. Very few acute myocardial infarctions and sudden deaths occur in saunas, but alcohol consumption during sauna bathing increases the risk of hypotension, arrhythmia, and sudden death, and should be avoided. (C) 2001 by Excerpta Medica, Inc.	Univ Oulu, Dept Internal Med, FIN-90220 Oulu, Finland; Univ Oulu, Bioctr Oulu, FIN-90220 Oulu, Finland; Washington Hosp Ctr, Div Cardiol, Washington, DC 20010 USA	Hannuksela, ML (reprint author), Univ Oulu, Dept Internal Med, Kajaanintie 50, FIN-90220 Oulu, Finland.						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J. Med.	FEB 1	2001	110	2					118	126		10.1016/S0002-9343(00)00671-9		9	Medicine, General & Internal	General & Internal Medicine	398NA	WOS:000166761500007	11165553	
J	Olin, AC; Aldenbratt, A; Ekman, A; Ljungkvist, G; Jungersten, L; Alving, K; Toren, K				Olin, AC; Aldenbratt, A; Ekman, A; Ljungkvist, G; Jungersten, L; Alving, K; Toren, K			Increased nitric oxide in exhaled air after intake of a nitrate-rich meal	RESPIRATORY MEDICINE			English	Article						nitric oxide; nasal nitric oxide; nitrate; nitrite; L-arginine; breath analysis	L-ARGININE; HUMAN-SALIVA; ASTHMA; NASAL; GENERATION; RHINITIS; MASS	Exhaled and nasal NO (ENO, NNO) have been suggested as markers for inflammation in lower and upper respiratory tract respectively. It is still unknown how a number of factors, apart from airway inflammation, can influence NO levels. The aim of this study was to determine the effect of a nitrate-rich meal on ENO and NNO. Sixteen healthy subjects were observed during 1 week on normal diet before a nitrate-restricted diet was introduced in the next. On day 3 of the second week they were made to ingest a nitrate rich meal. ENO, NNO, plasma nitrate and plasma L-arginine were followed before the meal and afterwards for 3 h. ENO and NNO as well as plasma nitrate and plasma L-arginine were significantly elevated after the nitrate-rich meal. The median maximal increase of ENO and NNO was 47% and 13% respectively. We found a moderate but significant correlation between the rise in plasma nitrate and ENO (r(s)=0.57, P=0.027) but none between plasma nitrate and NNO (r(s)=-0.02, P=0.95). As nitrate in the diet seems to substantially influence the levels of ENO it is important either to restrictor register the intake of nitrate-rich food prior to measuring ENO.	Sahlgrenska Univ Hosp, Dept Occupat & Environm Med, S-41266 Gothenburg, Sweden; Sahlgrenska Univ Hosp, Dept Clin Physiol, Gothenburg, Sweden; Karolinska Inst, Dept Physiol & Pharmacol, Stockholm, Sweden; Sahlgrenska Univ Hosp, Sect Resp Med & Allergol, Gothenburg, Sweden	Olin, AC (reprint author), Sahlgrenska Univ Hosp, Dept Occupat & Environm Med, St Sigfridsgatan 85 B, S-41266 Gothenburg, Sweden.			Alving, Kjell/0000-0003-0784-0443			Altman DG, 1991, PRACTICAL STAT MED R; ALVING K, 1993, EUR RESPIR J, V6, P1368; BERGLUND E, 1963, ACTA MED SCAND, V173, P185; BOER P, 1984, AM J PHYSIOL, V247, pF632; Byrnes CA, 1997, EUR RESPIR J, V10, P1021, DOI 10.1183/09031936.97.10051021; de Gouw HWFM, 1999, THORAX, V54, P1033; DUNCAN C, 1995, NAT MED, V1, P546, DOI 10.1038/nm0695-546; EISENBRAND G, 1980, ONCOLOGY, V37, P227; GRANLI T, 1989, FOOD CHEM TOXICOL, V27, P675, DOI 10.1016/0278-6915(89)90122-1; Jungersten L, 1996, CLIN PHYSIOL, V16, P369, DOI 10.1111/j.1475-097X.1996.tb00726.x; Kharitonov S, 1997, EUR RESPIR J, V10, P1683, DOI 10.1183/09031936.97.10071683; KHARITONOV SA, 1995, CLIN SCI, V88, P135; KHARITONOV SA, 1994, LANCET, V343, P133, DOI 10.1016/S0140-6736(94)90931-8; Kharitonov SA, 1997, J ALLERGY CLIN IMMUN, V99, P58; LUNDBERG JON, 1994, GUT, V35, P1543, DOI 10.1136/gut.35.11.1543; Lundberg JON, 1996, EUR RESPIR J, V9, P1344, DOI 10.1183/09031936.96.09071344; LUNDBERG JON, 1995, NAT MED, V1, P370, DOI 10.1038/nm0495-370; Martin U, 1996, J ALLERGY CLIN IMMUN, V97, P768, DOI 10.1016/S0091-6749(96)80154-0; MASSARO AF, 1995, AM J RESP CRIT CARE, V152, P800; Massaro AF, 1999, AM J RESP CRIT CARE, V159, pA860; MATRICARDI PM, 1990, CLIN EXP ALLERGY, V20, P151, DOI 10.1111/j.1365-2222.1990.tb02660.x; Nagase S, 1997, BIOCHEM BIOPH RES CO, V233, P150, DOI 10.1006/bbrc.1997.6428; OLIN AC, 1998, EUR RESPIR J, V12, pS249; Slutsky AS, 1999, AM J RESP CRIT CARE, V160, P2104; SPACKMAN DH, 1958, ANAL CHEM, V30, P1190, DOI 10.1021/ac60139a006; TANNENBAUM SR, 1976, FOOD COSMET TOXICOL, V14, P549, DOI 10.1016/S0015-6264(76)80006-5; ten Hacken NHT, 1998, AM J RESP CRIT CARE, V158, P902; TESCH JW, 1976, J CHROMATOGR, V126, P743, DOI 10.1016/S0021-9673(01)84117-0; WENNMALM A, 1993, CIRC RES, V73, P1121; Zetterquist W, 1999, EUR RESPIR J, V13, P327, DOI 10.1034/j.1399-3003.1999.13b18.x	30	74	77	0	3	W B SAUNDERS CO LTD	LONDON	24-28 OVAL RD, LONDON NW1 7DX, ENGLAND	0954-6111			RESP MED	Respir. Med.	FEB	2001	95	2					153	158		10.1053/rmed.2000.1010		6	Cardiac & Cardiovascular Systems; Respiratory System	Cardiovascular System & Cardiology; Respiratory System	401BH	WOS:000166906700008	11217912	
J	Rylander, R; Lin, RH				Rylander, R; Lin, RH			(1 -> 3)-beta-D-glucan - relationship to indoor air-related symptoms, allergy and asthma	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		moulds; airways inflammation; respiratory symptoms; (1 -> 3)-beta-D-glucan	AIRWAYS INFLAMMATION; ENDOTOXIN; GLUCAN; (1->3)-BETA-D-GLUCAN; INTERLEUKIN-1; INHALATION; AIRBORNE; ATOPY	(1 --> 3)-beta -D-glucan is a polyglucose structure in the cell wall of moulds, some bacteria and plants. Due to its unique (1 --> 3)-beta linkage it binds to specific receptors on phagocytosing cells and induces changes in their metabolism. Under realistic environmental concentrations, available data suggest that these changes express themselves as alterations of the defense mechanisms to other agents. Inhalation of (I --> 3)-beta -D-glucan in humans causes symptoms from the upper respiratory tract and induction of cytokines in blood monocytes. (1 --> 3)-beta -D-glucan can be used as a marker of mould biomass in field studies. Relationships between the amount of (1 --> 3)-beta -D-glucan and the extent of symptoms as well as lung function changes and inflammatory markers have been described. In view of the mechanisms involved in the normal development of the immune system, children seem to be a particular group at risk due to (I --> 3)-beta -D-glucan exposure. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.	Univ Gothenburg, Dept Environm Med, S-40530 Gothenburg, Sweden; Natl Taiwan Univ, Coll Med, Grad Inst Immunol, Taipei, Taiwan	Rylander, R (reprint author), Univ Gothenburg, Dept Environm Med, Box 414, S-40530 Gothenburg, Sweden.	ragnar.rylander@envmed.gu.se					ABEL G, 1992, INT J IMMUNOPHARMACO, V14, P1363, DOI 10.1016/0192-0561(92)90007-8; ADACHI Y, 1999, PHARM PHARM LETT, V1, P17; ADACHI Y, 1999, CARBOHYD RES, V316, P225; BEIJER L, 1998, P 22 COTT OTH ORG DU, P251; COOK JA, 1980, CIRC SHOCK, V7, P225; DEROCHEMONTEIXGALVE B, 1991, INFECT IMMUN, V59, P3646; DOUEWES J, 1997, MEDIAT INFLAMM, V6, P257; DOUWES J, 2000, UNPUB GLUCAN ENDOTOX; FOGEL DB, 1994, IEEE T NEURAL NETWOR, V1, P3; FOGELMARK B, 1992, AGENTS ACTIONS, V35, P50, DOI 10.1007/BF01990951; Fogelmark B, 1997, INDOOR BUILT ENVIRON, V6, P291, DOI 10.1177/1420326X9700600506; FOGELMARK B, 2000, UNPUB AGENTS ACTIONS; GRAVESEN S, 1994, MICROFUNGI MUNKSGAAR, P53; Holt PG, 1999, ENVIRON HEALTH PERSP, V107, P485; Ohno N, 1999, CARBOHYD RES, V316, P161, DOI 10.1016/S0008-6215(99)00049-X; RYLANDER R, 1989, INT CONGR SER, V860, P219; Rylander R, 1997, ARCH ENVIRON HEALTH, V52, P281; Rylander R, 1998, MEDIAT INFLAMM, V7, P105; Rylander R, 1998, AM J RESP CRIT CARE, V158, P1685; Rylander R, 1999, ENVIRON HEALTH PERSP, V107, P501; RYLANDER R, 1996, INDOOR BUILT ENVIRON, V5, P106, DOI 10.1177/1420326X9600500206; RYLANDER R, 1995, 16 EUR C ALL CLIN IM, P409; Rylander R, 1992, INDOOR ENVIRON, V1, P263, DOI 10.1177/1420326X9200100502; SHERWOOD ER, 1987, INT J IMMUNOPHARMACO, V9, P261, DOI 10.1016/0192-0561(87)90049-X; STONE BA, 1998, CHEM BIOL 1 ARROW 3, P1; TAMURA H, 1994, CLIN CHIM ACTA, V226, P109, DOI 10.1016/0009-8981(94)90110-4; Thorn J, 1998, AM J RESP CRIT CARE, V157, P1798; Wan GH, 1999, ARCH ENVIRON HEALTH, V54, P172; Wan GH, 1999, EUR J IMMUNOL, V29, P2491, DOI 10.1002/(SICI)1521-4141(199908)29:08<2491::AID-IMMU2491>3.3.CO;2-I	29	74	75	0	1	ELSEVIER IRELAND LTD	CLARE	ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND	0300-483X			TOXICOLOGY	Toxicology	NOV 2	2000	152	1-3					47	52		10.1016/S0300-483X(00)00291-2		6	Pharmacology & Pharmacy; Toxicology	Pharmacology & Pharmacy; Toxicology	379EC	WOS:000165627100007	11090939	
J	Coreno, A; Skowronski, M; Kotaru, C; McFadden, ER				Coreno, A; Skowronski, M; Kotaru, C; McFadden, ER			Comparative effects of long-acting beta(2)-agonists, leukotriene receptor antagonists, and a 5-lipoxygenase inhibitor on exercise-induced asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						exercise-induced asthma; beta(2)-agonist; leukotriene receptor antagonist; 5-lipoxygenase inhibitor	INDUCED BRONCHOCONSTRICTION; INDUCED BRONCHOSPASM; REFRACTORY PERIOD; MONTELUKAST; SALMETEROL; CHILDREN; ZAFIRLUKAST; PROTECTION; DURATION	Background: Exercise-induced asthma (EIA) is a common problem that can be controlled with long-acting beta-agonists and leukotriene-modifying compounds. There is, however, limited information on the comparative effectiveness of the two classes of drugs, as well as the relative potencies of the antileukotriene agents. Objective: The purpose of the present study was to provide data on the above issues. Methods: We performed a random-order, blinded, double-dummy, placebo-controlled trial in 10 patients with EIA. Each subject received standard single doses of salmeterol, montelukast, zafirlukast, zileuton, and placebo on separate days. The participants performed 4 minutes of cycle ergometry while breathing frigid air 1, 4, 8, and 12 hours after administration of the test agents. The primary endpoint was the extent of the decrement in the FEV1 10 minutes after exertion. Results: With placebo, symptomatic airway narrowing developed at all times (mean +/- SE decrease in FEV1 ranged between 21% +/- 5% and 26% +/- 5%). Salmeterol acted quickly and significantly blunted the obstructive response for 12 hours (Delta FEV1 first hour: 8% +/- 3%; Delta FEV1 twelfth hour: 8% +/- 3%; P < .0001 vs placebo and P = .72 vs time). The leukotriene-modifying agents produced effects within 1 hour of ingestion. Like salmeterol, montelukast and zafirlukast also offered long-lasting protection, and there were no significant differences between them (montelukast Delta FEV1 twelfth hour: 9% +/- 4%; zafirlukast Delta FEV1 twelfth hour: 11% +/- 2%; P = .75) or the beta(2)-agonist (montelukast vs salmeterol: P = .72; zafirlukast vs salmeterol: P = .48). Zileuton provided equivalent prophylaxis for the first 4 hours (Delta FEV1 fourth hour: 11% +/- 2%); however, by 8 hours, it was less efficacious than all of the other active compounds, and by 12 hours it did not differ from placebo (Delta FEV1 twelfth hour: 19% +/- 4%; P = .33). Conclusions: Single doses of the currently available leukotriene receptor antagonists provide prompt effective and persistent defense against EIA that equals that seen with a long-acting beta(2)-agonist. The synthesis inhibitor zileuton affords a comparable magnitude of prophylaxis but has a considerably shorter duration of action.	Univ Hosp Cleveland, Div Pulm & Crit Care Med, Cleveland, OH 44106 USA; Univ Hosp Cleveland, Airway Dis Ctr, Cleveland, OH 44106 USA; Case Western Reserve Univ, Sch Med, Dept Med, Cleveland, OH 44106 USA	McFadden, ER (reprint author), Univ Hosp Cleveland, Div Pulm & Crit Care Med, 11100 Euclid Ave, Cleveland, OH 44106 USA.				NCRR NIH HHS [MO 1 RR 00080]; NHLBI NIH HHS [HL-33791, HL-07288]		Adelroth E, 1997, J ALLERGY CLIN IMMUN, V99, P210, DOI 10.1016/S0091-6749(97)70098-8; Bronsky EA, 1997, CLIN PHARMACOL THER, V62, P556, DOI 10.1016/S0009-9236(97)90051-5; Calhoun WJ, 1998, AM J RESP CRIT CARE, V157, pS238; DEAL EC, 1979, J APPL PHYSIOL, V46, P467; Edelman JM, 2000, ANN INTERN MED, V132, P97; EDMUNDS AT, 1978, AM REV RESPIR DIS, V117, P247; FINNERTY JP, 1992, AM REV RESPIR DIS, V145, P746; GILBERT IA, 1988, J APPL PHYSIOL, V64, P2167; KEMP JP, 1994, AM J RESP CRIT CARE, V150, P1612; Kemp JP, 1998, J PEDIATR-US, V133, P424, DOI 10.1016/S0022-3476(98)70281-1; Leff JA, 1998, NEW ENGL J MED, V339, P147, DOI 10.1056/NEJM199807163390302; MCFADDEN ER, 1986, J CLIN INVEST, V78, P18, DOI 10.1172/JCI112549; MCFADDEN ER, 1994, NEW ENGL J MED, V330, P1362, DOI 10.1056/NEJM199405123301907; Meltzer SS, 1996, AM J RESP CRIT CARE, V153, P931; Nelson JA, 1998, NEW ENGL J MED, V339, P141, DOI 10.1056/NEJM199807163390301; PATESSIO A, 1991, EUR RESPIR J, V4, P296; Pearlman DS, 1999, J PEDIATR-US, V134, P273, DOI 10.1016/S0022-3476(99)70449-X; Reiss TF, 1997, THORAX, V52, P1030; ROSSING TH, 1982, J APPL PHYSIOL, V52, P1119; SILVERMAN M, 1972, ARCH DIS CHILD, V47, P882; STEARNS DR, 1981, J APPL PHYSIOL, V50, P503; Villaran C, 1999, J ALLERGY CLIN IMMUN, V104, P547, DOI 10.1016/S0091-6749(99)70322-2; Zar JH, 1984, BIOSTATISTICAL ANAL	23	74	74	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.	SEP	2000	106	3					500	506				7	Allergy; Immunology	Allergy; Immunology	356YN	WOS:000089471900013	10984370	
J	Schuller, HM; Jull, BA; Sheppard, BJ; Plummer, HK				Schuller, HM; Jull, BA; Sheppard, BJ; Plummer, HK			Interaction of tobacco-specific toxicants with the neuronal or, nicotinic acetylcholine receptor and its associated mitogenic signal transduction pathway: potential role in lung carcinogenesis and pediatric lung disorders	EUROPEAN JOURNAL OF PHARMACOLOGY			English	Article; Proceedings Paper	Congress on Neuronal Nicotinic Receptors - From Structure to Therapeutics	OCT 01-04, 1999	VENICE, ITALY	Dept Pharmacol, Univ Milan, CNR Ctr Molec & Cellular Pharmacol, European Comm & Munichs VerUm Fdn		alpha 7 nicotinic receptor; nicotine; nicotine-derived nitrosamine; small cell lung carcinoma; pulmonary neuroendocrine cell; mitogenic signal transduction	INFANT-DEATH-SYNDROME; PULMONARY NEUROENDOCRINE CELLS; GASTRIN-RELEASING PEPTIDE; MATERNAL SMOKING; FUNCTIONAL EXPRESSION; CARCINOMA CELLS; ENDOCRINE-CELLS; CALCIUM-CHANNEL; CARBON-DIOXIDE; RISK-FACTORS	Pulmonary neuroendocrine cells function as hypoxia-sensitive chemoreceptors, and they release peptides and biogenic amines that are important mediators of pulmonary neonatal adaptation. Some of these products additionally act as autocrine growth factors. Increased numbers of pulmonary neuroendocrine cells have been observed in several smoking-associated pediatric lung disorders such as bronchopulmonary dysplasia, cystic fibrosis, sudden infant death syndrome, and asthma. Disturbed pulmonary neuroendocrine function has been implicated in the etiology of this disease complex. One of the most common smoking-associated lung cancer types, small cell lung carcinoma, expresses phenotypic and functional features of pulmonary neuroendocrine cells. We, as well as others, have shown that the release of the autocrine growth factors 5-hydroxytryptamine (5-HT, serotonin) and mammalian bombesisn/gastrin releasing peptide (MB/GRP) by cell lines derived from human small cell lung carcinoma or fetal hamster pulmonary neuroendocrine cells are regulated by a neuronal nicotinic acetylcholine receptor comprised of alpha(7) subunits. In radio-receptor assays, nicotine and the nicotine-derived carcinogenic nitrosamines N'-nictrosonornicotine (NNN) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) bound with high affinity to this receptor with affinitites NNK > nicotine > NNN. Binding of nicotine or NNK to the alpha(7) receptor resulted in calcium influx and overexpression and activation of the serine-threonine protein kinase Raf-1. In turn, this event lead to overexpression and activation of the mitogen activated (MAP) kinases extracellular signal regulated kinase 1 (ERK1) and extracellular signal regulated kinase 2 (ERK2) and stimulation of DNA synthesis accompanied by an increase in cell numbers in fetal pulmonary neuroendocrine cells and small cell carcinoma cells. Exposure of fetal pulmonary neuroendocrine cells for 6 days to NNK caused a prominant up-regulation of Raf-1. Our findings suggest that chronic exposure to nicotine and NNK in pregnant women who smoke may up-regulate the alpha(7) nicotinic receptor as well as components of its associated mitogenic signal transduction pathway, thus increasing the susceptibilities of the infants for the development of pediatric lung disorders. Similarly, up-regulation of one or several components of this nicotinic receptor pathway in smokers may be an important factor for the development of small cell lung carcinoma. (C) 2000 Elsevier Science B.V. All rights reserved.	Univ Tennessee, Coll Vet Med, Carcinogenesis & Dev Therapeut Program, Knoxville, TN 37909 USA	Schuller, HM (reprint author), Univ Tennessee, Coll Vet Med, Carcinogenesis & Dev Therapeut Program, 2407 River Dr, Knoxville, TN 37909 USA.				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J. Pharmacol.	MAR 30	2000	393	1-3			SI		265	277		10.1016/S0014-2999(00)00094-7		13	Pharmacology & Pharmacy	Pharmacology & Pharmacy	306GQ	WOS:000086589300033	10771023	
J	Kiel, MA; Roder, E; van Wijk, RG; Al, MJ; Hop, WCJ; Rutten-van Molken, MPMH				Kiel, Menno A.; Roder, Esther; van Wijk, Roy Gerth; Al, Maiwenn J.; Hop, Wim C. J.; Rutten-van Molken, Maureen P. M. H.			Real-life compliance and persistence among users of subcutaneous and sublingual allergen immunotherapy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Allergic rhinitis; specific allergen immunotherapy; subcutaneous; sublingual; subcutaneous allergen immunotherapy; sublingual allergen immunotherapy; persistence; compliance; adherence; cost	TERM CLINICAL-EFFICACY; QUANTITATIVE ASSESSMENT; SLIT FORMULATION; EASY PROJECT; RHINITIS; ADHERENCE; ASTHMA; MEDICATION; CHILDREN; IMPACT	Background: Subcutaneous allergen immunotherapy (SCIT) and sublingual allergen immunotherapy (SLIT) are safe and effective treatments of allergic rhinitis, but high levels of compliance and persistence are crucial to achieving the desired clinical effects. Objective: Our objective was to assess levels and predictors of compliance and persistence among grass pollen, tree pollen, and house dust mite immunotherapy users in real life and to estimate the costs of premature discontinuation. Methods: We performed a retrospective analysis of a community pharmacy database from The Netherlands containing data from 6486 patients starting immunotherapy for 1 or more of the allergens of interest between 1994 and 2009. Two thousand seven hundred ninety-six patients received SCIT, and 3690 received SLIT. Time to treatment discontinuation was analyzed and included Cox proportional hazard models with time-dependent covariates, where appropriate. Results: Overall, only 18% of users reached the minimally required duration of treatment of 3 years (SCIT, 23%; SLIT, 7%). Median durations for SCIT and SLIT users were 1.7 and 0.6 years, respectively (P < .001). Other independent predictors of premature discontinuation were prescriber, with patients of general practitioners demonstrating longer persistence than those of allergologists and other medical specialists; single-allergen immunotherapy, lower socioeconomic status; and younger age. Of the persistent patients, 56% were never late in picking up their medication from the pharmacy. Direct medication costs per nonpersistent patient discontinuing in the third year of treatment were (sic)3800, an amount that was largely misspent. Conclusion: Real-life persistence is better in SCIT users than in SLIT users, although it is low overall. There is an urgent need for further identification of potential barriers and measures that will enhance persistence and compliance.	[Kiel, Menno A.; Al, Maiwenn J.; Rutten-van Molken, Maureen P. M. H.] Erasmus Univ, Inst Med Technol Assessment, Dept Hlth Econ iMTA, NL-3000 DR Rotterdam, Netherlands; [Kiel, Menno A.; Roder, Esther; van Wijk, Roy Gerth] Erasmus MC Univ Med Ctr, Dept Internal Med, Sect Allergol, Rotterdam, Netherlands; [Hop, Wim C. J.] Erasmus MC Univ Med Ctr, Dept Biostat, Rotterdam, Netherlands	Kiel, MA (reprint author), Inst Med Technol Assessment iMTA, Dept Hlth Econ, Rm W-J5-69,50 Burg Oudlaan,POB 1738, NL-3000 DR Rotterdam, Netherlands.	kiel@bmg.eur.nl	Al, Maiwenn/E-3272-2014; Rutten-van Molken, Maureen/G-8481-2014	Al, Maiwenn/0000-0001-9763-0436; Rutten-van Molken, Maureen/0000-0001-8706-3159	ZonMw (NWO); ALK-Abello; GlaxoSmithKline; HAL; Meda Pharma; Novartis; Phadia; Stallergenes; Allergopharma	E. Roder has received research support from ZonMw (NWO), and her thesis was financially supported by ALK-Abello, GlaxoSmithKline, HAL, Meda Pharma, Novartis, Phadia, and Stallergenes. R. Gerth van Wijk has received consultancy fees from Allergopharma, has received research support from ZonMw (NWO), and has participated in European Academy of Allergology and Clinical Immunology immunotherapy task forces. The rest of the authors declare they have no relevant conflicts of interest.	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J	Oliphant, CJ; Barlow, JL; McKenzie, ANJ				Oliphant, Chris J.; Barlow, Jillian L.; McKenzie, Andrew N. J.			Insights into the initiation of type 2 immune responses	IMMUNOLOGY			English	Review						allergens; interleukin-25; interleukin-33; innate lymphoid cells; nuocytes; T helper type 2 cells; thymic stromal lymphopoietin; type 2 responses	THYMIC STROMAL LYMPHOPOIETIN; INFLAMMATORY DENDRITIC CELLS; DUST-MITE ALLERGEN; CD4(+) T-CELLS; CYTOKINE-DEPENDENT IMMUNITY; HUMAN EPITHELIAL-CELLS; IN-VITRO DEVELOPMENT; NALP3 INFLAMMASOME; ADAPTIVE IMMUNITY; IL-4 PRODUCTION	Type 2 immune responses, characterized by the differentiation of CD4(+) T helper type 2 (Th2) cells and the production of the type 2 cytokines interleukin-4 (IL-4), IL-5, IL-9 and IL-13, are associated with parasitic helminth infections and inflammatory conditions such as asthma and allergies. Until recently the initiating factors associated with type 2 responses had been poorly understood. This review addresses the recent advances in identifying the diverse range of antigens/allergens associated with type 2 responses and the function, expression and sources of type-2-initiating cytokines (thymic stromal lymphopoietin, IL-25 and IL-33). We also discuss the latest findings regarding innate lymphoid cells, such as nuocytes, as early sources of type 2 cytokines and their importance in protective immunity to helminth infections. These developments represent major breakthroughs in our understanding of type 2 immunity, and highlight the increased complexity existing between the innate and adaptive arms of these responses. These additional steps in the type 2 immune pathway also offer potential targets for therapeutic intervention.	[Oliphant, Chris J.; Barlow, Jillian L.; McKenzie, Andrew N. J.] MRC, Mol Biol Lab, Cambridge CB2 2QH, England	Oliphant, CJ (reprint author), MRC, Mol Biol Lab, Hills Rd, Cambridge CB2 2QH, England.	oliphant@mrc-lmb.cam.ac.uk			American Asthma Foundation; Centocor	We thank Dr J. Walker for critical reading of and helpful suggestions to the manuscript. ANM and CJO are supported by the American Asthma Foundation, and ANM and JLB are supported by Centocor funding.	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J	Kearley, J; Erjefalt, JS; Andersson, C; Benjamin, E; Jones, CP; Robichaud, A; Pegorier, S; Brewah, Y; Burwell, TJ; Bjermer, L; Kiener, PA; Kolbec, R; Lloyd, CM; Coyle, AJ; Humbles, AA				Kearley, Jennifer; Erjefalt, Jonas S.; Andersson, Cecilia; Benjamin, Ebony; Jones, Carla P.; Robichaud, Annette; Pegorier, Sophie; Brewah, Yambasu; Burwell, Timothy J.; Bjermer, Leif; Kiener, Peter A.; Kolbec, Roland; Lloyd, Clare M.; Coyle, Anthony J.; Humbles, Alison A.			IL-9 Governs Allergen-induced Mast Cell Numbers in the Lung and Chronic Remodeling of the Airways	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						IL-9; mast cells; asthma; airway remodeling; AHR	FIBROBLAST-GROWTH-FACTOR; TRANSGENIC MICE; PULMONARY INFLAMMATION; SMOOTH-MUSCLE; INTERLEUKIN 9; MILD ASTHMA; TGF-BETA; HYPERRESPONSIVENESS; CHALLENGE; EXPRESSION	Rationale: IL-9 is a pleiotropic cytokine that has multiple effects on structural as well as numerous hematopoietic cells, which are central to the pathogenesis of asthma. Objectives: The contribution of IL-9 to asthma pathogenesis has thus far been unclear, due to conflicting reports in the literature. These earlier studies focused on the role of IL-9 in acute inflammatory models; here we have investigated the effects of IL-9 blockade during chronic allergic inflammation. Methods: Mice were exposed to either prolonged ovalbumin or house dust mite allergen challenge to induce chronic inflammation and airway remodeling. Measurements and Main Results: We found that IL-9 governs allergen-induced mast cell (MC) numbers in the lung and has pronounced effects on chronic allergic inflammation. Anti-IL-9 antibody-treated mice were protected from airway remodeling with a concomitant reduction in mature MC numbers and activation, in addition to decreased expression of the profibrotic mediators transforming growth factor-beta 1, vascular endothelial growth factor, and fibroblast growth factor-2 in the lung. Airway remodeling was associated with impaired lung function in the peripheral airways and this was reversed by IL-9 neutralization. In human asthmatic lung tissue, we identified MCs as the main IL-9 receptor expressing population and found them to be sources of vascular endothelial growth factor and fibroblast growth factor-2. Conclusions: Our data suggest an important role for an IL-9-MC axis in the pathology associated with chronic asthma and demonstrate that an impact on this axis could lead to a reduction in chronic inflammation and improved lung function in patients with asthma.	[Kearley, Jennifer; Benjamin, Ebony; Brewah, Yambasu; Burwell, Timothy J.; Kiener, Peter A.; Kolbec, Roland; Coyle, Anthony J.; Humbles, Alison A.] MedImmune LLC, Dept Resp Inflammat & Autoimmun, Gaithersburg, MD 20878 USA; [Erjefalt, Jonas S.; Andersson, Cecilia; Bjermer, Leif] Lund Univ, Dept Expt Med Sci, Unit Airway Inflammat, Lund, Sweden; [Jones, Carla P.; Pegorier, Sophie; Lloyd, Clare M.] Univ London Imperial Coll Sci Technol & Med, Leukocyte Biol Sect, Natl Heart & Lung Inst, Fac Med, London, England; [Robichaud, Annette] Sci Resp Equipment Inc, Montreal, PQ, Canada	Humbles, AA (reprint author), MedImmune LLC, Dept Resp Inflammat & Autoimmun, 1 MedImmune Way, Gaithersburg, MD 20878 USA.	humblesa@medimmune.com		Lloyd, Clare/0000-0001-8977-6726	MedImmune	Funded by MedImmune.	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J. Respir. Crit. Care Med.	APR 1	2011	183	7					865	875		10.1164/rccm.200909-1462OC		11	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	747KN	WOS:000289318800012	20971830	
J	Muller, T; Robaye, B; Vieira, RP; Ferrari, D; Grimm, M; Jakob, T; Martin, SF; Di Virgilio, F; Boeynaems, JM; Virchow, JC; Idzko, M				Mueller, T.; Robaye, B.; Vieira, R. P.; Ferrari, D.; Grimm, M.; Jakob, T.; Martin, S. F.; Di Virgilio, F.; Boeynaems, J. -M.; Virchow, J. C.; Idzko, M.			The purinergic receptor P2Y(2) receptor mediates chemotaxis of dendritic cells and eosinophils in allergic lung inflammation	ALLERGY			English	Article						asthma; ATP; chemotaxis; dendritic cells; eosinophils	OXYGEN RADICAL PRODUCTION; PHARMACOLOGICAL CHARACTERIZATION; NUCLEOTIDE RECEPTORS; INTERNATIONAL UNION; TISSUE DISTRIBUTION; CAPACITY; RELEASE; ASTHMA; IDENTIFICATION; EXPRESSION	Background: Extracellular ATP contributes to the pathogenesis of asthma via signalling at purinergic receptors. However, the precise purinergic receptors subtypes mediating the pro-asthmatic effects of ATP have not been identified, yet. Methods: In vivo studies were performed using the OVA-alum model. Functional expression of the P2Y(2) purinergic receptor subtype on human monocyte-derived dendritic cells and eosinophils was investigated using real-time PCR, migration assays, and production of reactive oxygen species. Results: Compared to wild-type animals P2Y(2)-/- mice showed reduced allergic airway inflammation which can be explained by defective migration of blood myeloid DCs towards ATP in vitro and in vivo, whereas the influence of ATP on maturation and cytokine production was not changed. Additionally, ATP failed to induce migration of bone marrow-derived eosinophils from P2Y(2)R-deficient animals. The relevance of our findings for humans was confirmed in functional studies with human monocyte-derived DCs and eosinophils. Interestingly, stimulation of human DCs derived from allergic individuals with house dust mite allergen induced functional up-regulation of the P2Y(2)R subtype. Furthermore, eosinophils isolated from asthmatic individuals expressed higher levels of P2Y(2)R compared to healthy controls. This was of functional relevance as these eosinophils were more sensitive to ATP-induced migration and production of reactive oxygen metabolites. Conclusions: In summary, P2Y(2)R appears to be involved in asthmatic airway inflammation by mediating ATP-triggered migration of mDCs and eosinophils, as well as reactive oxygen species production. Together our data suggest that targeting P2Y(2)R might be a therapeutic option for the treatment of asthma.	[Mueller, T.; Vieira, R. P.; Grimm, M.; Idzko, M.] Univ Med Ctr Freiburg, Dept Pneumol, D-79106 Freiburg, Germany; [Robaye, B.; Boeynaems, J. -M.] Univ Libre Bruxelles, IRIBHM, Brussels, Belgium; [Robaye, B.; Boeynaems, J. -M.] Univ Libre Bruxelles, Erasme Hosp, Brussels, Belgium; [Ferrari, D.; Di Virgilio, F.] Univ Ferrara, Dept Gen Pathol, I-44100 Ferrara, Italy; [Jakob, T.; Martin, S. F.] Univ Med Ctr Freiburg, Allergy Res Grp, D-79106 Freiburg, Germany; [Virchow, J. C.] Univ Med Ctr Rostock, Dept Pneumol, Rostock, Germany	Muller, T (reprint author), Univ Med Ctr Freiburg, Dept Pneumol, Killianstr 5, D-79106 Freiburg, Germany.	marco.idzko@uniklinink-freiburg.de	Vieira, Rodolfo/E-9315-2011; Jakob, Thilo/J-1621-2012; Ferrari, Davide/F-5644-2015	Vieira, Rodolfo/0000-0001-6379-1143; Ferrari, Davide/0000-0002-5727-9204	German Research Foundation (DFG [7/4-1]	This work was supported by a grant to M.I. from the German Research Foundation (DFG, ID 7/4-1).	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J	Pare, G; Moqadem, K; Pineau, G; St-Hilaire, C				Pare, Guy; Moqadem, Khalil; Pineau, Gilles; St-Hilaire, Carole			Clinical Effects of Home Telemonitoring in the Context of Diabetes, Asthma, Heart Failure and Hypertension: A Systematic Review	JOURNAL OF MEDICAL INTERNET RESEARCH			English	Review						Home telemonitoring; information technology; chronic illnesses; clinical effects	RANDOMIZED CONTROLLED-TRIAL; BLOOD-PRESSURE CONTROL; URBAN AFRICAN-AMERICANS; MONITORING-SYSTEM; GLYCEMIC CONTROL; FOLLOW-UP; HIGH-RISK; MANAGEMENT; TELEMEDICINE; CARE	Background: Home telemonitoring figures among the various solutions that could help attenuate some of the problems associated with aging populations, rates of chronic illness, and shortages of health professionals. Objective: The primary aim of this study was to further our understanding of the clinical effects associated with home telemonitoring programs in the context of chronic diseases. Methods: We conducted a systematic review which covered studies published between January 1966 and December 2008. MEDLINE, The Cochrane Library, and the INAHTA (International Network of Agencies for Health Technology Assessment) database were consulted. Our inclusion criteria consisted of: (I) English language publications in peer-reviewed journals or conference proceedings and (2) studies involving patients with diabetes, asthma, heart failure, or hypertension, and presenting results on the clinical effects of home telemonitoring. Results: In all, 62 empirical studies were analyzed. The results from studies involving patients with diabetes indicated a trend toward patients with home telemonitoring achieving better glycemic control. In most trials in which patients with asthma were enrolled, results showed significant improvements in patients' peak expiratory flows, significant reductions in the symptoms associated with this illness, and improvements in perceived quality of life. Virtually all studies involving patients with hypertension demonstrated the ability of home telemonitoring to reduce systolic and/or diastolic blood pressure. Lastly, due to the equivocal nature of current findings of home telemonitoring involving patients with heart failure, larger trials are still needed to confirm the clinical effects of this technology for these patients. Conclusions: Although home telemonitoring appears to be a promising approach to patient management, designers of future studies should consider ways to make this technology more effective as well as controlling possible mediating variables.	[Pare, Guy] HEC Montreal, Montreal, PQ H3T 2A7, Canada; [Moqadem, Khalil; Pineau, Gilles; St-Hilaire, Carole] Agence Evaluat Technol & Modes Intervent Sante, Quebec Dept Hlth, Montreal, PQ, Canada	Pare, G (reprint author), HEC Montreal, 3000 Cote Ste Catherine Rd, Montreal, PQ H3T 2A7, Canada.	guy.pare@hec.ca			AETMIS; Canada Research Chairs Program	The authors would like to thank the Editor, Gunther Eysenbach, and the three anonymous reviewers for their helpful comments and suggestions on an earlier version of this manuscript. Further, the AETMIS and the Canada Research Chairs Program are gratefully acknowledged for providing financial support for this research.	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K., 2002, J CARD FAIL S1, V8, P98	86	73	74	1	24	JMIR PUBLICATIONS, INC	TORONTO	59 WINNERS CIRCLE, TORONTO, ON M4L 3Y7, CANADA	1438-8871			J MED INTERNET RES	J. Med. Internet Res.	APR-JUN	2010	12	2							e21	10.2196/jmir.1357		15	Health Care Sciences & Services; Medical Informatics	Health Care Sciences & Services; Medical Informatics	611YK	WOS:000278860800012	20554500	
J	Delfino, RJ; Staimer, N; Tjoa, T; Gillen, D; Kleinman, MT; Sioutas, C; Cooper, D				Delfino, Ralph J.; Staimer, Norbert; Tjoa, Thomas; Gillen, Dan; Kleinman, Michael T.; Sioutas, Constantinos; Cooper, Dan			Personal and ambient air pollution exposures and lung function decrements in children with asthma	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; epidemiology; forced expiratory flow rates; longitudinal data analysis; nitrogen dioxide; panel study; particulate air pollution	ANTIINFLAMMATORY MEDICATION USE; NITROGEN-DIOXIDE EXPOSURE; PEAK EXPIRATORY FLOW; PARTICULATE AIR; ULTRAFINE PARTICLES; POLLUTANTS; SYMPTOMS; HEALTH; ASSOCIATION; MASS	BACKGROUND: Epidemiologic studies have shown associations between asthma outcomes and outdoor air pollutants such as nitrogen dioxide and particulate matter mass < 2.5 mu m in diameter (PM2.5). Independent effects of specific pollutants have been difficult to detect because most studies have relied on highly correlated central-site measurements. OBJECTIVES: This study was designed to evaluate the relationship of daily changes in percent-predicted forced expiratory volume in 1 see (FEV1) with personal and ambient air pollutant exposures. METHODS: For 10 days each, we followed 53 subjects with asthma who were 9-18 years of age and living in the Los Angeles, California, air basin. Subjects self-administered home spirometry in the morning, afternoon, and evening. We measured personal hourly PM2.5 mass, 24-hr PM2.5 elemental and organic carbon (EC-OC), and 24-hr NO2, and the same 24-hr average outdoor central-site (ambient) exposures. We analyzed data with transitional mixed models controlling for personal temperature and humidity, and as-needed beta(2)-agonist inhaler use. RESULTS: FEV1 decrements were significantly associated with increasing hourly peak and daily average personal PM2.5, but not ambient PM2.5. Personal NO2 was also inversely associated with FEV1. Ambient NO2 was more weakly associated. We found stronger associations among 37 subjects not taking controller bronchodilators as follows: Personal EC-OC was inversely associated with morning FEV1; for an interquartile increase of 71 mu g/m(3) 1-hr maximum personal PM2.5, overall percent-predicted FEV1 decreased by 1.32% [95% confidence interval (CI), -2.00 to -0.65%]; and for an interquartile increase of 16.8 ppb 2-day average personal NO2, overall percent-predicted FLV1 decreased by 2.45% (95% CI, -3.57 to -1.33%). Associations of both personal PM2.5 and NO2 with FEV1 remained when co-regressed, and both confounded ambient NO2. CONCLUSIONS: Independent pollutant associations with lung function might be missed using ambient data alone. Different sets of causal components are suggested by independence of FEV1 associations with personal PM2.5 mass from associations with personal NO2.	[Delfino, Ralph J.; Staimer, Norbert; Tjoa, Thomas] Univ Calif Irvine, Sch Med, Dept Epidemiol, Irvine, CA 92617 USA; [Gillen, Dan] Univ Calif Irvine, Sch Informat & Comp Sci, Dept Stat, Irvine, CA 92617 USA; [Kleinman, Michael T.] Univ Calif Irvine, Sch Med, Dept Community & Environm Med, Irvine, CA 92617 USA; [Cooper, Dan] Univ Calif Irvine, Sch Med, Dept Pediat, Irvine, CA 92617 USA; [Sioutas, Constantinos] Univ So Calif, Sch Engn, Dept Civil & Environm Engn, Los Angeles, CA USA	Delfino, RJ (reprint author), Univ Calif Irvine, Sch Med, Dept Epidemiol, 100 Theory,Suite 100, Irvine, CA 92617 USA.	rdelfino@uci.edu	Wang, Linden/M-6617-2014		NCRR NIH HHS [M01 RR000827, MO1-RR00827]; NICHD NIH HHS [HD048721, P01 HD048721]; NIEHS NIH HHS [ES11615, R01 ES011615]		Aekplakorn W, 2003, INT J EPIDEMIOL, V32, P854, DOI 10.1093/ije/dyg237; Becklake MR, 1999, THORAX, V54, P1119; Belanger K, 2006, AM J RESP CRIT CARE, V173, P297, DOI 10.1164/rccm.200408-1123OC; Biswas S, 2007, ATMOS ENVIRON, V41, P3479, DOI 10.1016/j.atmosenv.2006.11.059; Chakrabarti B, 2004, ATMOS ENVIRON, V38, P3329, DOI 10.1016/j.atmosenv.2004.03.007; Chauhan AJ, 2003, LANCET, V361, P1939, DOI 10.1016/S0140-6736(03)13582-9; Cyrys J, 2003, J EXPO ANAL ENV EPID, V13, P134, DOI 10.1038/sj.jea.7500262; Delfino RJ, 2006, ENVIRON HEALTH PERSP, V114, P1736, DOI 10.1289/ehp.9141; 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, 2003, ENVIRON HEALTH PERSP, V111, P647, DOI 10.1289/ehp.5992; Delfino RJ, 2002, ENVIRON HEALTH PERSP, V110, pA607; Diggle P, 2002, ANAL LONGITUDINAL DA; Fujita EM, 2007, J AIR WASTE MANAGE, V57, P721, DOI 10.3155/1047-3289.57.6.721; Fung K, 2002, J AIR WASTE MANAGE, V52, P1333; Giannini D, 1997, J ASTHMA, V34, P105, DOI 10.3109/02770909709075654; Hankinson JL, 1999, AM J RESP CRIT CARE, V159, P179; Jerrett M, 2005, J EXPO ANAL ENV EPID, V15, P185, DOI 10.1038/sj.jea.7500388; Kim JJ, 2004, AM J RESP CRIT CARE, V170, P520, DOI 10.1164/rccm.200403-2810C; Koenig JQ, 2005, ENVIRON HEALTH PERSP, V113, P499, DOI 10.1289/ehp.7511; Kraft M, 2005, INT J HYG ENVIR HEAL, V208, P305, DOI 10.1016/j.ijheh.2005.04.002; Levy JI, 1998, J AIR WASTE MANAGE, V48, P553, DOI 10.1080/10473289.1998.10463704; Lewis TC, 2005, ENVIRON HEALTH PERSP, V113, P1068, DOI 10.1289/ehp.7533; Li N, 2003, CLIN IMMUNOL, V109, P250, DOI 10.1016/j.clim.2003.08.006; *NAT I OCC SAF HLT, 1994, DHHS PUBL NAT I OCC; Persinger RL, 2002, MOL CELL BIOCHEM, V234, P71, DOI 10.1023/A:1015973530559; Rabinovitch N, 2006, AM J RESP CRIT CARE, V173, P1098, DOI 10.1164/rccm.200509-1393OC; Rabinovitch N, 2004, J ALLERGY CLIN IMMUN, V114, P1131, DOI 10.1016/j.jaci.2004.08.026; *RAND CAL, 2007, RAND CAL POP DENS ST; Sarnat JA, 2005, EPIDEMIOLOGY, V16, P385, DOI 10.1097/01.ede.0000155505.04775.33; Sarnat JA, 2007, CURR OPIN PULM MED, V13, P63, DOI 10.1097/MCP.0b013e3280117d25; Schauer JJ, 2000, ENVIRON SCI TECHNOL, V34, P1821, DOI 10.1021/es981312t; Schildcrout JS, 2006, AM J EPIDEMIOL, V164, P505, DOI 10.1093/aje/kwj225; Schwartz J, 2000, EPIDEMIOLOGY, V11, P320, DOI 10.1097/00001648-200005000-00016; Seaton A, 2003, THORAX, V58, P1012, DOI 10.1136/thorax.58.12.1012; Sheppard L, 2005, J EXPO ANAL ENV EPID, V15, P366, DOI 10.1038/sj.jea.7500413; Sioutas C, 2005, ENVIRON HEALTH PERSP, V113, P947, DOI 10.1289/ehp.7939; SPENGLER J, 1994, J AIR WASTE MANAGE, V44, P39; Staimer N, 2005, ANAL BIOANAL CHEM, V383, P955, DOI 10.1007/s00216-005-0086-6; Thiadens HA, 1999, THORAX, V54, P1055; Thompson R, 2006, PEDIATR PULM, V41, P819, DOI 10.1002/ppul.20449; Trasande L, 2005, J ALLERGY CLIN IMMUN, V115, P689, DOI 10.1016/j.jaci.2005.01.056; Trenga CA, 2006, CHEST, V129, P1614, DOI 10.1378/chest.129.6.1614; U.S. EPA (U.S. Environmental Protection Agency), 2008, NAT AMB AIR QUAL STA; Molenberghs G, 2001, LINEAR MIXED MODELS; Ward DJ, 2004, OCCUP ENVIRON MED, V61, DOI 10.1136/oem.2003.007088	46	73	77	3	24	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	2008	116	4					550	558				9	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	282KL	WOS:000254566500041	18414642	
J	Kovesi, T; Kulka, R; Dales, R				Kovesi, Thomas; Kulka, Ryan; Dales, Robert			Exhaled nitric oxide concentration is affected by age, height, and race in healthy 9-to 12-year-old children	CHEST			English	Article						Asian continental ancestry group; asthma; breath tests; child; continental population groups; growth; nitric oxide; reference values	BODY-MASS INDEX; CHINESE CHILDREN; REFERENCE VALUES; SCHOOL-AGE; ASTHMA; AIR; SCHOOLCHILDREN; ADOLESCENTS; MARKER	Background: The fractional concentration of exhaled nitric oxide (FENO) is a useful indicator of airway inflammation in children and adults with asthma. Methods: We determined the range of FENO concentrations and the factors affecting it in a large sample of healthy school children attending grades 4 through 6, in Windsor, ON, Canada. Results: FENO was measured in 657 children between 9.1 and 12.9 years of age. The range of FENO concentrations in healthy school children was 12.7 parts per billion (ppb) [95% confidence interval (0), 11.8 to 13.7 ppb] in whites and 22.8 ppb [95% CI, 17.9 to 27.7 ppb] in Asian-Canadian children (p < 0.001). FENO values also appeared to be higher in African-Canadian children than in whites, although the CI was wide because of the small number of African-Canadian children sampled. FENO rose slightly but significantly with age (p = 0.007) and with height (p = 0.023). Body mass index and gender did not significantly alter the measured FENO. FVC had a nonsignificant effect on FENO. Participation in physical activity during the same day had a borderline-significant effect on measured FENO, but a reported history of a respiratory tract infection in the preceding 2 weeks did not. Conclusions: FENO concentrations in healthy school-aged children appeared to be affected by race, and, to a lesser extent, by age and height. These factors should be taken into consideration when interpreting clinical results.	[Kovesi, Thomas] Childrens Hosp Eastern Ontario, Dept Pediat, Ottawa, ON K1H 8L1, Canada; [Kulka, Ryan] Hlth Canada, Air Hlth Effects Div, Ottawa, ON, Canada; [Dales, Robert] Hlth Canada, Biostat & Epidemiol Div, Ottawa, ON, Canada	Kovesi, T (reprint author), Childrens Hosp Eastern Ontario, Dept Pediat, 401 Smyth Rd, Ottawa, ON K1H 8L1, Canada.	kovesi@cheo.on.ca		Kovesi, Thomas/0000-0002-0521-8936			American Thoracic Society, 1991, AM REV RESPIR DIS, V144, P1202, DOI 10.1164/ajrccm/144.5.1202; American Thoracic Society, 2005, AM J RESP CRIT CARE, V171, P912, DOI DOI 10.1164/RCCM.200406-710ST; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Baraldi E, 2005, AM J RESP CRIT CARE, V171, P68, DOI 10.1164/rccm.200403-298Oc; Buchvald F, 2005, J ALLERGY CLIN IMMUN, V115, P1130, DOI 10.1016/j.jaci.2005.03.020; DALES RE, 2007, WINDSOR CHILDRENS CH; de Winter-de Groot KM, 2005, J ALLERGY CLIN IMMUN, V115, P419, DOI 10.1016/j.jaci.2004.11.025; Delfino RJ, 2006, ENVIRON HEALTH PERSP, V114, P1736, DOI 10.1289/ehp.9141; FERRIS BG, 1978, AM REV RESPIR DIS, V118, P1; Franklin P, 2000, AM J RESP CRIT CARE, V161, P1757; Franklin PJ, 1999, AM J RESP CRIT CARE, V159, P69; Gabriele C, 2005, PEDIATR ALLERGY IMMU, V16, P243, DOI 10.1111/j.1399-3038.2005.00255.x; Ip MSM, 2000, AM J RESP CRIT CARE, V162, P424; Kazaks A, 2005, J ALLERGY CLIN IMMUN, V116, P929, DOI 10.1016/j.jaci.2005.06.005; KHARITONOV SA, 1995, EUR RESPIR J, V8, P295, DOI 10.1183/09031936.95.08020295; Kharitonov SA, 2003, EUR RESPIR J, V21, P433, DOI 10.1183/09031936.03.00066903; Leung TF, 2005, CLIN EXP ALLERGY, V35, P1288, DOI 10.1111/j.1365-2222.2005.02342.x; MALMBERG LP, 2006, PEDIAT PULMONOL, V41, P435; Mieskonen ST, 2002, PEDIATR PULM, V33, P347, DOI 10.1002/ppul.10084; MOSTELLER RD, 1987, NEW ENGL J MED, V317, P1098; Olin AC, 2006, CHEST, V130, P1319, DOI 10.1378/chest.130.5.1319; Olivieri M, 2006, RESP RES, V7, DOI 10.1186/1465-9921-7-94; Pellegrino R, 2005, EUR RESPIR J, V26, P948, DOI 10.1183/09031936.05.00035205; POLGAR C, 1971, STANDARD VALUES PULM, P87; Rolla G, 2004, CHEST, V126, P1546, DOI 10.1378/chest.126.5.1546; Saito J, 2004, J ALLERGY CLIN IMMUN, V114, P512, DOI 10.1016/j.jaci.2004.05.033; Santamaria F, 2005, J ALLERGY CLIN IMMUN, V116, P1163, DOI 10.1016/j.jaci.2005.07.018; Sartori C, 1999, AM J RESP CRIT CARE, V160, P879; Verges S, 2006, J SPORT SCI, V24, P1157, DOI 10.1080/02640410500457364; Wong GWK, 2005, CLIN EXP ALLERGY, V35, P889, DOI 10.1111/j.1365-2222.2005.02263.x	30	73	83	2	11	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	JAN	2008	133	1					169	175		10.1378/chest.07-1177		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	251PL	WOS:000252385600029	17925422	
J	Villeneuve, PJ; Chen, L; Rowe, BH; Coates, F				Villeneuve, Paul J.; Chen, Li; Rowe, Brian H.; Coates, Frances			Outdoor air pollution and emergency department visits for asthma among children and adults: A case-crossover study in northern Alberta, Canada	ENVIRONMENTAL HEALTH			English	Article							SOUTHERN CALIFORNIA CHILDREN; RESPIRATORY HOSPITAL ADMISSIONS; LUNG-FUNCTION GROWTH; CHILDHOOD ASTHMA; ROOM VISITS; NITROGEN-DIOXIDE; TIME-SERIES; SAINT-JOHN; ASSOCIATION; OZONE	Background: Recent studies have observed positive associations between outdoor air pollution and emergency department (ED) visits for asthma. However, few have examined the possible confounding influence of aeroallergens, or reported findings among very young children. Methods: A time stratified case-crossover design was used to examine 57,912 ED asthma visits among individuals two years of age and older in the census metropolitan area of Edmonton, Canada between April 1, 1992 and March 31, 2002. Daily air pollution levels for the entire region were estimated from three fixed-site monitoring stations. Similarly, daily levels of aeroallergens were estimated using rotational impaction sampling methods for the period between 1996 and 2002. Odds ratios and their corresponding 95% confidence intervals were estimated using conditional logistic regression with adjustment for temperature, relative humidity and seasonal epidemics of viral related respiratory disease. Results: Positive associations for asthma visits with outdoor air pollution levels were observed between April and September, but were absent during the remainder of the year. Effects were strongest among young children. Namely, an increase in the interquartile range of the 5-day average for NO(2) and CO levels between April and September was associated with a 50% and 48% increase, respectively, in the number of ED visits among children 2-4 years of age (p < 0.05). Strong associations were also observed with these pollutants among those 75 years of age and older. Ozone and particulate matter were also associated with asthma visits. Air pollution risk estimates were largely unchanged after adjustment for aeroallergen levels. Conclusion: Our findings, taken together, suggest that exposure to ambient levels of air pollution is an important determinant of ED visits for asthma, particularly among young children and the elderly.	[Villeneuve, Paul J.; Chen, Li] Hlth Canada, Biostat & Epidemiol Div, Ottawa, ON, Canada; [Rowe, Brian H.] Univ Alberta Hosp, Edmonton, AB T6G 2B7, Canada; [Coates, Frances] Aerobiol Res Labs, Ottawa, ON, Canada	Villeneuve, PJ (reprint author), Hlth Canada, Biostat & Epidemiol Div, Ottawa, ON, Canada.	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Health	DEC 24	2007	6								40	10.1186/1476-069X-6-40		15	Environmental Sciences; Public, Environmental & Occupational Health	Environmental Sciences & Ecology; Public, Environmental & Occupational Health	272MP	WOS:000253863800001	18157917	
J	Weckmann, M; Collison, A; Simpson, JL; Kopp, MV; Wark, PAB; Smyth, MJ; Yagita, H; Matthaei, KI; Hansbro, N; Whitehead, B; Gibson, PG; Foster, PS; Mattes, J				Weckmann, Markus; Collison, Adam; Simpson, Jodie L.; Kopp, Matthias V.; Wark, Peter A. B.; Smyth, Mark J.; Yagita, Hideo; Matthaei, Klaus I.; Hansbro, Nicole; Whitehead, Bruce; Gibson, Peter G.; Foster, Paul S.; Mattes, Joerg			Critical link between TRAIL and CCL20 for the activation of T(H)2 cells and the expression of allergic airway disease	NATURE MEDICINE			English	Article							APOPTOSIS-INDUCING LIGAND; DENDRITIC CELLS; IN-VIVO; EXPERIMENTAL ASTHMA; TUMOR-METASTASIS; INHALED ANTIGEN; ATOPIC ASTHMA; HYPERREACTIVITY; INFLAMMATION; IL-13	The role of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in immune responses mediated by T-helper 2 (T(H)2) lymphocytes is unknown. Here we characterize the development of allergic airway disease in TRAIL-deficient (Tnfsf10(-/-)) mice and in mice exposed to short interfering RNA targeting TRAIL. We show that TRAIL is abundantly expressed in the airway epithelium of allergic mice and that inhibition of signaling impairs production of the chemokine CCL20 and homing of myeloid dendritic cells and T cells expressing CCR6 and CD4 to the airways. Attenuated homing limits TH2 cytokine release, inflammation, airway hyperreactivity and expression of the transcriptional activator STAT6. Activation of STAT6 by interleukin-13 restores airway hyperreactivity in Tnfsf10(-/-) mice. Recombinant TRAIL induces pathognomic features of asthma and stimulates the production of CCL20 in primary human bronchial epithelium cells. TRAIL is also increased in sputum of asthmatics. The function of TRAIL in the airway epithelium identifies this molecule as a target for the treatment of asthma.	Univ Freiburg, Dept Paediat & Adolescent Med, D-79106 Freiburg, Germany; Univ Newcastle, Fac Hlth, Sch Biomed Sci, CARD, Newcastle, NSW 2301, Australia; Hunter Med Res Inst, Newcastle, NSW 2301, Australia; Hunter Med Res Inst, Dept Resp & Sleep Med, Newcastle, NSW 2305, Australia; Peter MacCallum Canc Ctr, Canc Immunol Program, Melbourne, Vic 3002, Australia; Juntendo Univ, Sch Med, Dept Immunol, Tokyo 1138421, Japan; Australian Natl Univ, John Curtin Sch Med Res, Div Mol Biosci, Canberra, ACT 2601, Australia; John Hunter Childrens Hosp, Dept Paediat, Newcastle, NSW 2305, Australia	Mattes, J (reprint author), Univ Freiburg, Dept Paediat & Adolescent Med, D-79106 Freiburg, Germany.	joerg.mattes@newcastle.edu.au	Klaus, Matthaei/D-8691-2011; Foster, Paul/G-5057-2013; Smyth, Mark/H-8709-2014	Smyth, Mark/0000-0001-7098-7240; Wark, Peter/0000-0001-5676-6126			Aggarwal Bharat B., 2002, Current Drug Targets - Inflammation and Allergy, V1, P327, DOI 10.2174/1568010023344571; Akbari O, 2002, NAT MED, V8, P1024, DOI 10.1038/nm745; Begue B, 2006, GASTROENTEROLOGY, V130, P1962, DOI 10.1053/j.gastro.2006.03.022; BENTLEY AM, 1993, AM J RESP CELL MOL, V8, P35; Bousquet J, 2005, B WORLD HEALTH ORGAN, V83, P548; Busse WW, 1998, J ALLERGY CLIN IMMUN, V102, pS17, DOI 10.1016/S0091-6749(98)70002-8; Contoli M, 2006, NAT MED, V12, P1023, DOI 10.1038/nm1462; Corry DB, 1996, J EXP MED, V183, P109, DOI 10.1084/jem.183.1.109; Daigle I, 2001, SWISS MED WKLY, V131, P231; Dieu-Nosjean MC, 2000, J EXP MED, V192, P705, DOI 10.1084/jem.192.5.705; Foster PS, 1996, J EXP MED, V183, P195, DOI 10.1084/jem.183.1.195; Grunig G, 1998, SCIENCE, V282, P2261, DOI 10.1126/science.282.5397.2261; Kay AB, 2001, NEW ENGL J MED, V344, P30; Kayagaki N, 1999, J IMMUNOL, V163, P1906; Kohl J, 2006, J CLIN INVEST, V116, P783, DOI 10.1172/JCI26582; Kroegel C, 1996, EUR RESPIR J, V9, P899, DOI 10.1183/09031936.96.09050899; Kuperman DA, 2002, NAT MED, V8, P885, DOI 10.1038/nm734; Lambrecht BN, 2000, J CLIN INVEST, V106, P551, DOI 10.1172/JCI8107; Lambrecht BN, 2003, NAT REV IMMUNOL, V3, P994, DOI 10.1038/nri1249; Lambrecht BN, 1998, J IMMUNOL, V160, P4090; Lamhamedi-Cherradi SE, 2003, NAT IMMUNOL, V4, P255, DOI 10.1038/ni894; Le Borgne M, 2006, IMMUNITY, V24, P191, DOI 10.1016/j.immuni.2006.01.005; Lewkowich IP, 2005, J EXP MED, V202, P1549, DOI 10.1084/jem.20051506; Locksley RM, 2001, CELL, V104, P487, DOI 10.1016/S0092-8674(01)00237-9; Lukacs NW, 2001, J EXP MED, V194, P551, DOI 10.1084/jem.194.4.551; Lundy SK, 2005, J IMMUNOL, V174, P2054; Mattes J, 2002, J EXP MED, V195, P1433, DOI 10.1084/jem.20020009; Mattes J, 2001, J IMMUNOL, V167, P1683; Mattes J, 1999, EUR RESPIR J, V13, P1391, DOI 10.1183/09031936.99.13613969; Reibman J, 2003, AM J RESP CELL MOL, V28, P648, DOI 10.1165/rcmb.2002-00950C; Robertson NM, 2002, J IMMUNOL, V169, P5986; ROBINSON DS, 1992, NEW ENGL J MED, V326, P298, DOI 10.1056/NEJM199201303260504; Smyth MJ, 2001, J EXP MED, V193, P661, DOI 10.1084/jem.193.6.661; Takeda K, 2002, J EXP MED, V195, P161, DOI 10.1084/jem.20011171; Takeda K, 2001, NAT MED, V7, P94, DOI 10.1038/83416; Taube C, 2002, J IMMUNOL, V169, P6482; Temann UA, 1998, J EXP MED, V188, P1307, DOI 10.1084/jem.188.7.1307; Thorley AJ, 2005, AM J RESP CELL MOL, V32, P262, DOI 10.1165/rcmb.2004-0196OC; van Rift LS, 2004, J ALLERGY CLIN IMMUN, V114, P166, DOI 10.1016/j.jaci.2004.03.044; van Rijt LS, 2005, J EXP MED, V201, P981, DOI 10.1084/jem.20042311; Venkayya R, 2002, AM J RESP CELL MOL, V26, P202; Walczak H, 1999, NAT MED, V5, P157; Walter DM, 2001, J IMMUNOL, V167, P4668; Wiley SR, 1995, IMMUNITY, V3, P673, DOI 10.1016/1074-7613(95)90057-8; Wills-Karp M, 1999, ANNU REV IMMUNOL, V17, P255, DOI 10.1146/annurev.immunol.17.1.255; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; Yuan BB, 2004, NUCLEIC ACIDS RES, V32, pW130, DOI 10.1093/nar/gkh366; Zhang XR, 2003, CELL DEATH DIFFER, V10, P203, DOI 10.1038/sj.cdd.4401138; Zhang YY, 2004, J NATL CANCER I, V96, P201, DOI 10.1093/jnci/djh024; [Anonymous], 1987, AM REV RESP DIS, V136, P225	50	73	77	0	4	NATURE PUBLISHING GROUP	NEW YORK	75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA	1078-8956			NAT MED	Nat. Med.	NOV	2007	13	11					1308	1315		10.1038/nm1660		8	Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental	Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine	228NP	WOS:000250736900023	17934471	
J	Buckley, DA				Buckley, D. A.			Fragrance ingredient labelling in products on sale in the UK	BRITISH JOURNAL OF DERMATOLOGY			English	Article						allergic contact dermatitis; consumer products; fragrance; labelling; limonene; linalool	PATCH-TEST POPULATION; ALLERGY; PERFUMES; CHLOROATRANOL; SENSITIZATION; LINALOOL; LYRAL(R); MIX	Background The seventh amendment of the European Union (EU) Cosmetics Directive (March 2005) and the Detergents Regulations of the EU (October 2005) are now legal requirements in Europe. Cosmetic products and detergents must be labelled for 26 individual named fragrances, when present at concentrations of > 10 parts per million (p.p.m.) in leave-on products and > 100 p.p.m. in rinse-off products. Objectives To make an assessment of the exposure pattern to fragrance of the U.K. consumer and to determine the frequency with which the constituent fragrances of fragrance mix I (FM I) and fragrance mix II (FM II) are included in products currently sold in the U.K. Methods A study of perfumed cosmetic and household products available on the shelves of U.K. retailers was carried out in January 2006. Products were included if 'parfum' or 'aroma' was listed among the ingredients. Three hundred products were surveyed and any of the 26 listed fragrances named on the label were recorded. Results The top six most frequently labelled fragrances were linalool (190; 63%), limonene (189; 63%), citronellol (145; 48%), geraniol (126; 42%), butyl phenyl methyl propional (Lilial((TM))) (126; 42%) and hexyl cinnamal (125; (42%). One of these, geraniol, is present in FM I and two others, citronellol and hexyl cinnamal, in FM II, thus tested as part of the British Standard patch test series. The frequencies of other constituents of FM I were as follows: eugenol, 80 (27%); hydroxycitronellal, 52 (17%); isoeugenol, 27 (9%); cinnamic alcohol, 25 (8%); amyl cinnamal, 22 (7%); cinnamal, 17 (6%); Evernia prunastri (oak moss absolute), 13 (4%). The other constituents of FM II occurred as follows: coumarin, 90 (30%); hydroxyisohexyl-3-cyclohexene carboxaldehyde (Lyral((TM))), 88 (29%); citral, 74 (25%); farnesol, 23 (8%). Linalool (n = 46; 66%) was the most frequently found fragrance in 70 personal care products (soap, shampoo, shower gel). Linalool (n = 47; 80%) and limonene (n = 45; 76%) were the most frequent in 59 products for men (e.g. aftershave). Limonene (n = 29; 51%) predominated in 57 household products (washing-up liquid, detergent). Limonene (n = 43; 98%) and linalool (n = 42; 95%) were the most frequent fragrances in 44 perfumes for women. Alpha-isomethyl ionone (n = 28; 72%) was the most frequent in 39 cosmetics (foundation, lipstick, etc). Citronellol predominated (n = 15; 88%) in 17 deodorants and limonene (n = 9; 64%) was the commonest in 14 dental products (toothpaste and mouthwash). Thirty-four products (11%) contained none of the listed fragrances but were labelled as containing 'parfum' or 'aroma'. Conclusions There is ongoing consumer exposure to the most frequent sensitizers in FM I: E. prunastri, isoeugenol and the cinnamon fragrances cinnamal and cinnamic alcohol. Hydroxyisohexyl-3-cyclohexene carboxaldehyde (Lyral((TM))) is present at significant concentrations in almost one-third of products. Linalool and limonene, fragrance terpenes which are significant allergens in their oxidized state, are the most frequent fragrances encountered by individuals living in the U.K. The current exposure pattern of the U.K. consumer suggests that we should add oxidized limonene and oxidized linalool to the test series for patients suspected to have fragrance allergy.	Great Western Hosp, Dept Dermatol, Swindon SN3 6BB, Wilts, England	Buckley, DA (reprint author), Great Western Hosp, Dept Dermatol, Marlborough Rd, Swindon SN3 6BB, Wilts, England.	dbuckley@doctors.org.uk					Basketter DA, 2002, CONTACT DERMATITIS, V47, P161, DOI 10.1034/j.1600-0536.2002.470307.x; Baxter KF, 2003, CONTACT DERMATITIS, V48, P117, DOI 10.1034/j.1600-0536.2003.480212_4.x; Buckley DA, 2006, BRIT J DERMATOL, V154, P885, DOI 10.1111/j.1365-2133.2006.07170.x; Buckley DA, 2000, BRIT J DERMATOL, V142, P279, DOI 10.1046/j.1365-2133.2000.03298.x; Frosch PJ, 2005, CONTACT DERMATITIS, V52, P216, DOI 10.1111/j.0105-1873.2005.00563.x; 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; Giusti F, 2001, CONTACT DERMATITIS, V44, P37; Heydorn S, 2003, CONTACT DERMATITIS, V48, P317, DOI 10.1034/j.1600-0536.2003.00133.x; Johansen JD, 2003, CONTACT DERMATITIS, V49, P180, DOI 10.1111/j.0105-1873.2003.0214.x; Johansen J. P., 2006, CONTACT DERMATITIS, P507, DOI 10.1007/3-540-31301-X_31; Larsen W, 1996, Am J Contact Dermat, V7, P77, DOI 10.1016/S1046-199X(96)90078-0; Matura M, 2005, CONTACT DERMATITIS, V52, P320, DOI 10.1111/j.0105-1873.2005.00605.x; Matura M, 2002, J AM ACAD DERMATOL, V47, P709, DOI 10.1067/mjd.2002.124817; Murphy LA, 2003, CONTACT DERMATITIS, V49, P52; NIELSEN NH, 1992, ACTA DERM-VENEREOL, V72, P456; Rastogi SC, 2004, CONTACT DERMATITIS, V50, P367, DOI 10.1111/j.0105-1873.2004.00379.x; Rastogi SC, 2003, CONTACT DERMATITIS, V48, P130, DOI 10.1034/j.1600-0536.2003.00035.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; Schnuch A, 2004, CONTACT DERMATITIS, V50, P65, DOI 10.1111/j.0105-1873.2004.00302.x; Skold M, 2002, CONTACT DERMATITIS, V46, P267, DOI 10.1034/j.1600-0536.2002.460504.x; WHITE JML, 2007, IN PRESS BR J DERMAT	23	73	74	1	16	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0007-0963			BRIT J DERMATOL	Br. J. Dermatol.	AUG	2007	157	2					295	300		10.1111/j.1365-2133.2007.08018.x		6	Dermatology	Dermatology	196WJ	WOS:000248513200011	17573873	
J	Cao, DS; Bromberg, PA; Samet, JM				Cao, Dongsun; Bromberg, Philip A.; Samet, James M.			COX-2 expression induced by diesel particles involves chromatin modification and degradation of HDAC1	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article						diesel exhaust particles; COX-2; HDAC; airway epithelial cells	BRONCHIAL EPITHELIAL-CELLS; CYCLOOXYGENASE-2 PROMOTER ACTIVATION; ENDOPEROXIDE SYNTHASE-2 GENE; EXHAUST PARTICLES; HISTONE DEACETYLASE-1; REGULATING CYCLOOXYGENASE-2; TRANSCRIPTIONAL ACTIVATION; INFLAMMATORY MEDIATORS; OXIDATIVE STRESS; RESPONSE ELEMENT	Cyclooxygenase-2 (COX-2) plays an important role in the inflammatory response induced by physiologic and stress stimuli. Exposure to diesel exhaust particulate matter (DEP) has been shown to induce pulmonary inflammation and exacerbate asthma and chronic obstructive pulmonary disease. DEP is a potent inducer of inflammatory reponses in human airway epithelial cells. The mechanism through which DEP inhalation induces inflammatory mediator expression is not understood. In this report, we demonstrate that DEP can induce the expression of COX-2 gene in a human bronchial epithelial cell line (BEAS-2B) at both transcriptional and protein levels. The induction of COX-2 gene expression involves chromatin modification, in particular acetylation and deacetylation of histones. We show that exposure to DEP increases the acetylation of histone H4 associated with the COX-2 promoter and causes degradation of histone deacetylase 1 (HDAC1). Further, we establish that HDAC1 plays a pivotal role in mediating the transcriptional activation of the COX-2 gene in BEAS-2B cells exposed to DEP, supported by evidence that the down-regulation of HDAC1 using siRNA leads to activation of COX-2 gene expression, whereas overexpression of HDAC1 results in its repression. Finally, DEP exposure induced recruitment of histone acetyltransferase (HAT) p300 to the promoter of the COX-2 gene, suggesting that acetylation is also important in regulating its expression in response to DEP exposure. These results show for the first time acetylation via selective degradation of HDAC1, and that recruitment of HAT plays an important role in DEP-induced expression of the COX-2 gene.	Natl Hlth & Environm Effects Res Lab, Human Studies Div, Res Triangle Pk, NC 27711 USA; Univ N Carolina, Ctr Environm Med Asthma & Lung Biol, Res Triangle Pk, NC USA	Samet, JM (reprint author), Natl Hlth & Environm Effects Res Lab, Human Studies Div, Res Triangle Pk, NC 27711 USA.	samet.james@epa.gov					APPLEBY SB, 1994, BIOCHEM J, V302, P723; Ashburner BP, 2001, MOL CELL BIOL, V21, P7065, DOI 10.1128/MCB.21.20.7065-7077.2001; AYER DE, 1995, CELL, V80, P767, DOI 10.1016/0092-8674(95)90355-0; Barnes PJ, 2005, EUR RESPIR J, V25, P552, DOI 10.1183/09031936.05.00117504; BARRY CC, 1994, ENVIRONMENT, V36, P5; Bayram H, 1998, AM J RESP CELL MOL, V18, P441; Bertos NR, 2001, BIOCHEM CELL BIOL, V79, P243, DOI 10.1139/bcb-79-3-243; Bonner JC, 2002, AM J PATHOL, V161, P459, DOI 10.1016/S0002-9440(10)64202-2; Cao DS, 2005, MOL CELL BIOL, V25, P364, DOI 10.1128/MCB.25.1.364-376.2004; Colombo R, 2002, EMBO REP, V3, P1062, DOI 10.1093/embo-reports/kvf213; Dangond F, 1998, BIOCHEM BIOPH RES CO, V247, P833, DOI 10.1006/bbrc.1998.8891; David G, 2002, J BIOL CHEM, V277, P23658, DOI 10.1074/jbc.M203690200; Deng WG, 2004, BLOOD, V103, P2135, DOI 10.1182/blood-2003-09-3131; Deng WG, 2003, J BIOL CHEM, V278, P4770, DOI 10.1074/jbc.M209286200; Diaz-Sanchez D, 2000, CLIN IMMUNOL, V97, P140, DOI 10.1006/clim.2000.4921; Fasanaro P, 2006, FASEB J, V20, P1242, DOI 10.1096/fj.05-4695fje; Fischle W, 1999, J BIOL CHEM, V274, P11713, DOI 10.1074/jbc.274.17.11713; Galasinski SC, 2002, J BIOL CHEM, V277, P19618, DOI 10.1074/jbc.M201174200; Gavett SH, 1999, J CLIN INVEST, V104, P721, DOI 10.1172/JCI6890; Grunstein M, 1997, NATURE, V389, P349, DOI 10.1038/38664; Hofer TPJ, 2004, J LEUKOCYTE BIOL, V75, P856, DOI 10.1189/jlb.0803387; INOUE H, 1995, J BIOL CHEM, V270, P24965; INOUE H, 1994, FEBS LETT, V350, P51, DOI 10.1016/0014-5793(94)00731-4; Inoue K, 2004, J APPL TOXICOL, V24, P415, DOI 10.1002/jat.984; Ito K, 2000, MOL CELL BIOL, V20, P6891, DOI 10.1128/MCB.20.18.6891-6903.2000; Ito K, 2004, BIOCHEM BIOPH RES CO, V315, P240, DOI 10.1016/j.bbrc.2004.01.046; Ito K, 2002, AM J RESP CRIT CARE, V166, P392, DOI 10.1164/rccm.2110060; Jones PL, 2003, CURR TOP MICROBIOL, V274, P237; Kamei Y, 1996, CELL, V85, P403, DOI 10.1016/S0092-8674(00)81118-6; Karagiannis TC, 2006, ONCOGENE, V25, P3885, DOI 10.1038/sj.onc.1209417; Karagiannis TC, 2006, CELL CYCLE, V5, P288, DOI 10.4161/cc.5.3.2421; Kawasaki S, 2001, AM J RESP CELL MOL, V24, P419; Lander HM, 1997, FASEB J, V11, P118; Li XF, 2004, J BIOL CHEM, V279, P34201, DOI 10.1074/jbc.M405179200; Marks PA, 2001, NAT REV CANCER, V1, P194, DOI 10.1038/35106079; Mosley AL, 2003, J BIOL CHEM, V278, P19660, DOI 10.1074/jbc.M212375200; Ogryzko VV, 1996, CELL, V87, P953, DOI 10.1016/S0092-8674(00)82001-2; Pope CA, 2004, CIRCULATION, V109, P71, DOI 10.1161/01.CIR.0000108927.80044.7F; SAGAI M, 1993, FREE RADICAL BIO MED, V14, P37, DOI 10.1016/0891-5849(93)90507-Q; SAMET JM, 1998, AM J PHYSIOL, V275, P551; SEIBERT K, 1994, P NATL ACAD SCI USA, V91, P12013, DOI 10.1073/pnas.91.25.12013; Seigneurin-Berny D, 2001, MOL CELL BIOL, V21, P8035, DOI 10.1128/MCB.21.23.8035-8044.2001; Shringarpure R, 2003, J BIOL CHEM, V278, P311, DOI 10.1074/jbc.M206279200; Smith WL, 1996, J BIOL CHEM, V271, P33157; Sydbom A, 2001, EUR RESPIR J, V17, P733, DOI 10.1183/09031936.01.17407330; Takizawa H, 1999, J IMMUNOL, V162, P4705; Tsatsanis C, 2006, INT J BIOCHEM CELL B, V38, P1654, DOI 10.1016/j.biocel.2006.03.021; Vanden Berghe W, 1999, J BIOL CHEM, V274, P32091, DOI 10.1074/jbc.274.45.32091; Yang WM, 1996, P NATL ACAD SCI USA, V93, P12845, DOI 10.1073/pnas.93.23.12845; Zhou Q, 2000, J BIOL CHEM, V275, P35256, DOI 10.1074/jbc.M003106200	50	73	78	0	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.	AUG	2007	37	2					232	239		10.1165/rcmb.2006-0449OC		8	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	196RF	WOS:000248499000013	17395887	
J	Vesper, S; McKinstry, C; Haugland, R; Wymer, L; Bradham, K; Ashley, P; Cox, D; Dewalt, G; Friedman, W				Vesper, Stephen; McKinstry, Craig; Haugland, Richard; Wymer, Larry; Bradham, Karen; Ashley, Peter; Cox, David; Dewalt, Gray; Friedman, Warren			Development of an environmental relative moldiness index for US homes	JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE			English	Article							QUANTITATIVE PCR ANALYSIS; AIRBORNE FUNGI; OUTDOOR AIR; ASTHMA; PROPAGULES; BUILDINGS; DUSTBORNE; CHILDREN; WATER; DUST	Objective: The objective of this study, was to establish a national relative moldiness index for homes in the United States. Methods: As part of the Housing and Urban Development's American Healthy Homes Survey, dust samples were collected by vacuuming 2 m(2) in the bedrooms plus 2 m(2) in the living rooms from a nationally, representative 1096 homes in the United States using the Mitest sampler. Five milligrams of sieved (300 mu m pore, nylon mesh) dust was analyzed by mold-specific quantitative polymerase chain reaction for the 36 indicator species in 1096 samples. Results: On the basis of this standardized national sampling and analysis, an "Environmental Relative Moldiness Index" was created with values ranging from about -10 to 20 or above (lowest to highest). vi Conclusions: The Environmental Relative Moldiness Index scale may be useful for home mold-burden estimates in epidemiological studies.	US EPA, Natl Exposure Res Lab, Cincinnati, OH 45268 USA; Pacific NW Natl Lab, Richland, WA 99352 USA; US EPA, Natl Exposure Res Lab, Res Triangle Pk, NC 27711 USA; Dept Housing & Urban Dev, Washington, DC USA; Quan Tech, Arlington, VA USA	Vesper, S (reprint author), US EPA, Natl Exposure Res Lab, 26 W ML King Dr, Cincinnati, OH 45268 USA.	vesper.stephen@epa.gov					Brinkman NE, 2003, APPL ENVIRON MICROB, V69, P1775, DOI 10.1128/AEM.69.3.1775-1782.2003; Chao HJ, 2002, MYCOPATHOLOGIA, V154, P93, DOI 10.1023/A:1015592224368; Chew GL, 2003, ALLERGY, V58, P13, DOI 10.1034/j.1398-9995.2003.00013.x; Collett D., 2003, MODELING SURVIVAL DA; GODISH T, 2006, INDOOR ENV QUALITY P; Haugland RA, 2004, SYST APPL MICROBIOL, V27, P198, DOI 10.1078/072320204322881826; Haugland RA, 2002, J MICROBIOL METH, V50, P319, DOI 10.1016/S0167-7012(02)00037-4; HAUGLAND RA, 2005, BIOAEROSOLS FUNGI BA, P327; Helsel D, 2005, NONDETECTS DATA ANAL; Kercsmar CM, 2006, ENVIRON HEALTH PERSP, V114, P1574, DOI 10.1289/ehp.8742; Meklin T, 2004, J ENVIRON MONITOR, V6, P615, DOI 10.1039/b400250d; Melkin T., 2007, SCI TOTAL ENVIRON, V382, P130; O'Connor GT, 2004, J ALLERGY CLIN IMMUN, V114, P599, DOI 10.1016/j.jaci.2004.05.064; Shelton BG, 2002, APPL ENVIRON MICROB, V68, P1743, DOI 10.1128/AEM.68.4.1743-1753.2002; Spicer R, 2005, J OCCUP ENVIRON HYG, V2, P257, DOI 10.1080/15459620590946401; VERHOEFF AP, 1992, ALLERGY, V47, P83; Vesper SJ, 2004, J OCCUP ENVIRON MED, V46, P596, DOI 10.1097/01.jom.0000128160.17144.6e; Vesper SJ, 2007, J EXPO SCI ENV EPID, V17, P88, DOI 10.1038/sj.jes.7500528; Vesper SJ, 2006, J OCCUP ENVIRON MED, V48, P852, DOI 10.1097/01.jom.0000224736.52780.2f	19	73	73	2	18	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA	1076-2752	1536-5948		J OCCUP ENVIRON MED	J. Occup. Environ. Med.	AUG	2007	49	8					829	833		10.1097/JOM.0b013e3181255e98		5	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	200OF	WOS:000248772000002	17693779	
J	Hunninghake, GM; Soto-Quiros, ME; Avila, L; Ly, NP; Liang, C; Sylvia, JS; Klanderman, BJ; Silverman, EK; Celedon, JC				Hunninghake, Gary M.; Soto-Quiros, Manuel E.; Avila, Lydiana; Ly, Ngoc P.; Liang, Catherine; Sylvia, Jody S.; Klanderman, Barbara J.; Silverman, Edwin K.; Celedon, Juan C.			Sensitization to Ascaris lumbricoides and severity of childhood asthma in Costa Rica	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Ascaris; helminth; atopy; exacerbation; severity; asthma; Costa Rica	IMMUNOGLOBULIN-E; GEOHELMINTH INFECTIONS; ALLERGIC SENSITIZATION; ANTHELMINTIC TREATMENT; IGE ANTIBODIES; RURAL AREA; CHILDREN; ATOPY; REACTIVITY; PARASITES	Background: Little is known about sensitization (defined as a positive IgE) to helminths and disease severity in patients with asthma. Objectives: To examine the relationship between sensitization (defined as a positive IgE) to Ascaris lumbricoides and measures of asthma morbidity and severity in a Costa Rican population with low prevalence of parasitic infection but high prevalence of parasitic exposure. Methods: Cross-sectional study of 439 children (ages 6 to 14 years) with asthma. Linear regression and logistic regression were used for the multivariate statistical analysis. Results: After adjustment for parental education and other covariates, sensitization to Ascaris lumbricoides was associated with having at least 1 positive skin test to allergens (odds ratio, 5.15; 95% CI, 2.36-11.21; P < .001), increased total serum IgE and eosinophils in peripheral blood, reductions in FEV1 and FEV1/forced vital capacity, increased airway responsiveness and bronchodilator responsiveness, and hospitalizations for asthma in the previous year (odds ratio, 3.08; 95% Cl, 1.23-7.68; P = .02). Conclusion: Sensitization to Ascaris lumbricoides is associated with increased severity and morbidity of asthma among children in Costa Rica. This association is likely mediated by an increased degree of atopy among children with asthma who are sensitized to Asearis. Clinical implications: In areas with a low prevalence of helminthiasis such as Costa Rica, Ascaris sensitization may be an important marker of severe atopy and disease morbidity in children with asthma.	Channing Labs, Boston, MA 02115 USA; Brigham & Womens Hosp, Div Pulm & Crit Care Med, Boston, MA 02115 USA; Harvard Univ, Sch Med, Boston, MA 02115 USA; Hosp Nacl Ninos Dr Carlos Saenz Herrera, Div Pediat Pulmonol, San Jose, Costa Rica; Massachusetts Gen Hosp, Pediat Pulm Div, Boston, MA 02114 USA	Celedon, JC (reprint author), Channing Labs, 181 Longwood Ave, Boston, MA 02115 USA.	juan.celedon@channing.harvard.edu			NHLBI NIH HHS [F32 HL083634, F32 HL083634-01, HL04370, HL66289]		Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Bernardini R, 2005, INT J IMMUNOPATH PH, V18, P671; BLUMENTHAL MN, 1995, CLIN EXP ALLERGY, V25, P29, DOI 10.1111/j.1365-2222.1995.tb00416.x; [Anonymous], 1995, NORM AT INT SAL PRIM, P13; Camara AA, 2004, J ALLERGY CLIN IMMUN, V113, P551, DOI 10.1016/j.jaci.2003.11.027; Carroll WD, 2006, ARCH DIS CHILD, V91, P405, DOI 10.1136/adc.2005.088278; CHAN MS, 1994, PARASITOLOGY, V109, P373; CHATHAM M, 1982, AM REV RESPIR DIS, V126, P235; COOPER E, 1999, TROPICAL INFECT DIS; Cooper PJ, 2004, PARASITE IMMUNOL, V26, P455, DOI 10.1111/j.0141-9838.2004.00728.x; Cooper PJ, 2006, LANCET, V367, P1598, DOI 10.1016/S0140-6736(06)68697-2; Cooper PJ, 2004, J INFECT DIS, V190, P1338, DOI 10.1086/423944; Cooper PJ, 2003, J ALLERGY CLIN IMMUN, V111, P995, DOI 10.1067/mai.2003.1348; Cooper PJ, 2004, CLIN REV ALLERG IMMU, V26, P5, DOI 10.1385/CRIAI:26:1:5; Cooper PJ, 2003, AM J RESP CRIT CARE, V168, P313, DOI 10.1164/rccm.200211-1320OC; Dold S, 1998, J ALLERGY CLIN IMMUN, V102, P414, DOI 10.1016/S0091-6749(98)70129-0; Escamilla MA, 1996, AM J MED GENET, V67, P244, DOI 10.1002/(SICI)1096-8628(19960531)67:3<244::AID-AJMG2>3.0.CO;2-N; Fernandes J, 2003, CLIN EXP ALLERGY, V33, P956, DOI 10.1046/j.1365-2222.2003.01722.x; GYORKOS TW, 1989, AM J EPIDEMIOL, V130, P976; Karadag B, 2006, ALLERGY, V61, P996, DOI 10.1111/j.1398-9995.2006.01107.x; Khuroo MS, 1996, GASTROENTEROL CLIN N, V25, P553, DOI 10.1016/S0889-8553(05)70263-6; Leonardi-Bee J, 2006, AM J RESP CRIT CARE, V174, P514, DOI 10.1164/rccm.200603-331OC; LYNCH NR, 1993, J ALLERGY CLIN IMMUN, V92, P404, DOI 10.1016/0091-6749(93)90119-Z; Lynch NR, 1998, J ALLERGY CLIN IMMUN, V101, P217; Lynch NR, 1997, AM J RESP CRIT CARE, V156, P50; Maizels RM, 2003, NAT REV IMMUNOL, V3, P733, DOI 10.1038/nri1183; *MIN SAL, 1997, ENC NAC NUTR 1996; MORALES MT, 1997, ACTA PEDIAT COSTARRI, V11, P106; MORRIS AJ, 1992, J CLIN MICROBIOL, V30, P3213; Obihara CC, 2006, CLIN EXP ALLERGY, V36, P640, DOI 10.1111/j.1365-2222.2006.02479.x; Palmer LJ, 2002, AM J RESP CRIT CARE, V165, P1489, DOI 10.1164/rccm.2107020; Ponsonby AL, 2002, CHEST, V121, P135, DOI 10.1378/chest.121.1.135; Ramsay CE, 1999, HUM GENET, V104, P269, DOI 10.1007/s004390050947; REVOLTELLA R, 1980, INT ARCH ALLER A IMM, V62, P23; Scrivener S, 2001, LANCET, V358, P1493, DOI 10.1016/S0140-6736(01)06579-5; Siroux V, 2003, CLIN EXP ALLERGY, V33, P746, DOI 10.1046/j.1365-2222.2003.01674.x; Soto-Quiros ME, 1998, ALLERGY, V53, P499, DOI 10.1111/j.1398-9995.1998.tb04087.x; TURNER KJ, 1980, AUST J EXP BIOL MED, V58, P249, DOI 10.1038/icb.1980.25; van den Biggelaar AHJ, 2004, J INFECT DIS, V189, P892, DOI 10.1086/381767; Weiland SK, 2004, EUR RESPIR J, V24, P406, DOI 10.1183/09031936.04.00090303; [Anonymous], 1995, AM J RESP CRIT CARE, V152, P1107	41	73	74	0	1	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	2007	119	3					654	661		10.1016/j.jaci.2006.12.609		8	Allergy; Immunology	Allergy; Immunology	146HL	WOS:000244925000019	17336615	
J	Perros, F; Dorfmuller, P; Souza, R; Durand-Gasselin, I; Mussot, S; Mazmanian, M; Herve, P; Emilie, D; Simonneau, G; Humbert, M				Perros, F.; Dorfmuller, P.; Souza, R.; Durand-Gasselin, I.; Mussot, S.; Mazmanian, M.; Herve, P.; Emilie, D.; Simonneau, G.; Humbert, M.			Dendritic cell recruitment in lesions of human and experimental pulmonary hypertension	EUROPEAN RESPIRATORY JOURNAL			English	Article						dendritic cells; immunopathology; inflammation; monocrotaline; pulmonary arterial hypertension	ARTERIAL-HYPERTENSION; IMATINIB MESYLATE; PERIPHERAL-BLOOD; TUMOR; PRECURSORS; ANTIBODIES; DISEASES; ASTHMA	In the present study, the hypothesis that dendritic cells (DCs), key players in immunity and tolerance, might be involved in the immunopathology of idiopathic pulmonary arterial hypertension (IPAH) was tested. The phenotype and localisation of DCs were characterised by immunohistochemistry and double-labelling immunofluorescence in lung samples from controls, human IPAH patients and an experimental pulmonary hypertension model (monocrotaline-exposed rats). As compared with controls, morphometric analysis demonstrated increased numbers of dendritic cell-specific intercellular adhesion molecule-grabbing nonintegrin (DC-SIGN)-positive cells in muscular pulmonary arteries in IPAH and OX-62-positive DCs in monocrotaline-induced pulmonary hypertension. In human samples, the mean +/- SEM number of DC-SIGN-positive cells(.)artery(-1) of 100-300 mu m diameter was 1.4 +/- 0.4 in controls versus 26.4 +/- 2.7 in IPAH. In rats, the number of OX-62-positive cells(.)artery(-1) of 50-150 mu m diameter was 0.5 +/- 0.2 in controls, and 0.7 +/- 0.5, 3.1 +/- 0.5 and 8.4 +/- 0.6 at day 7, 14 and 28 after monocrotaline exposure, respectively. Human complex lesions of muscular pulmonary arteries showed transmural DC infiltration. Phenotyping revealed an immature DC profile in human and experimental pulmonary hypertension. The results support the concept that immature dendritic cells accumulate in remodelled pulmonary vessels and hence could be involved in the immunopathology of pulmonary hypertension.	Univ Paris 11, UPRES EA2705, Serv Pneumol,Assistance Publ Hop Paris, Ctr Natl Reference Hypertens Arterielle Pulm, Paris, France; INSERM, U764, Inst Federat Rech 13, Clamart, France; Univ Paris Sud, Ctr Chirurg Marie Lannelongue, Chirurg Expt Lab, UPRES EA2705, Le Plessis Robinson, France	Humbert, M (reprint author), Hop Antoine Beclere, Serv Pneumol & Reanimat Resp, 157 Rue Porte de Trivaux, F-92140 Clamart, France.	marc.humbert@abc.aphp.fr	Souza, Rogerio/I-3584-2013	Souza, Rogerio/0000-0003-2789-9143; Dorfmuller, Peter/0000-0003-2499-6829			Appel S, 2005, STEM CELLS, V23, P1082, DOI 10.1634/stemcells.2005-0069; Appel S, 2004, BLOOD, V103, P538, DOI 10.1182/blood-2003-03-0975; Ardavin Carlos, 2004, Immunity, V20, P17, DOI 10.1016/S1074-7613(03)00352-2; Balabanian K, 2002, AM J RESP CRIT CARE, V165, P1419, DOI 10.1164/rccm.2106007; Bowers R, 2004, AM J RESP CRIT CARE, V169, P764, DOI 10.1164/rccm.200301-147OC; BRENAN M, 1992, J EXP MED, V175, P1457, DOI 10.1084/jem.175.6.1457; Cambi A, 2005, CELL MICROBIOL, V7, P481, DOI 10.1111/j.1462-5822.2005.00506.x; Cochand L, 1999, AM J RESP CELL MOL, V21, P547; Conejo-Garcia JR, 2004, NAT MED, V10, P950, DOI 10.1038/nm1097; D'hulst AI, 2005, RESP RES, V6, DOI 10.1186/1465-9921-6-147; Demedts IK, 2005, AM J RESP CELL MOL, V32, P177, DOI 10.1165/rcmb.2004-0279OC; Dorfmuller P, 2003, EUR RESPIR J, V22, P358, DOI 10.1183/09031936.03.00038903; Dorfmuller P, 2002, AM J RESP CRIT CARE, V165, P534, DOI 10.1164/rccm.2012112; Frid MG, 2006, AM J PATHOL, V168, P659, DOI 10.2353/ajpath.2006.050599; Gabrilovich D, 1998, BLOOD, V92, P4150; Ghofrani HA, 2005, NEW ENGL J MED, V353, P1412, DOI 10.1056/NEJMc051946; HUMBERT M, 1995, AM J RESP CRIT CARE, V151, P1628; Lambrecht BN, 2003, NAT REV IMMUNOL, V3, P994, DOI 10.1038/nri1249; Millonig G, 2001, ARTERIOSCL THROM VAS, V21, P503; Mohty M, 2004, BLOOD, V103, P4666, DOI 10.1182/blood-2003-09-3220; Montani D, 2005, EUR RESPIR J, V26, P969, DOI 10.1183/09031936.05.00133904; Morelli AE, 2000, CURR OPIN NEPHROL HY, V9, P607, DOI 10.1097/00041552-200011000-00004; Mouthon L, 2005, EUR RESPIR J, V26, P986, DOI 10.1183/09031936.05.00112105; Nicolls MR, 2005, EUR RESPIR J, V26, P1110, DOI 10.1183/09031936.05.00045705; Ota M, 2004, THORAX, V59, P408, DOI 10.1136/thx.2003.006049; Palucka AK, 2005, P NATL ACAD SCI USA, V102, P3372, DOI 10.1073/pnas.0408506102; Patterson KC, 2006, ANN INTERN MED, V145, P152; Pietra GG, 2004, J AM COLL CARDIOL, V43, p25S, DOI 10.1016/j.jacc.2004.02.033; Quan TE, 2004, INT J BIOCHEM CELL B, V36, P598, DOI 10.1016/j.biocel.2003.10.005; Reddy A, 1997, BLOOD, V90, P3640; Sanchez O, 2006, CHEST, V130, P182, DOI 10.1378/chest.130.1.182; Schermuly RT, 2005, J CLIN INVEST, V115, P2811, DOI 10.1172/JCI24838; Smyth MJ, 2006, NEW ENGL J MED, V354, P2282, DOI 10.1056/NEJMcibr061878; Soilleux EJ, 2002, J LEUKOCYTE BIOL, V71, P445; Souza R, 2006, THORAX, V61, P736, DOI 10.1136/thx.2006.064097; Taieb J, 2006, NAT MED, V12, P214, DOI 10.1038/nm1356; Tamby MC, 2006, EUR RESPIR J, V28, P799, DOI 10.1183/09031936.06.00152705; Tamby MC, 2005, THORAX, V60, P765, DOI 10.1136/thx.2004.029082; Todate A, 2000, AM J RESP CRIT CARE, V162, P148; Trinite B, 2005, J IMMUNOL, V175, P2408; Van Rijt LS, 2005, CLIN EXP ALLERGY, V35, P1125, DOI 10.1111/j.1365-2222.2005.02321.x	41	73	76	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. 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J	Bai, N; Khazaei, M; van Eeden, SF; Laher, I				Bai, Ni; Khazaei, Majid; van Eeden, Stephan F.; Laher, Ismail			The pharmacology of particulate matter air pollution-induced cardiovascular dysfunction	PHARMACOLOGY & THERAPEUTICS			English	Review						particulate matter air pollution; inflammation; cardiovascular effect; reactive oxygen species; endothelial dysfunction	C-REACTIVE PROTEIN; DIESEL EXHAUST PARTICLES; HEART-RATE-VARIABILITY; CORONARY-ARTERY-DISEASE; ULTRAFINE CARBON-BLACK; BRONCHIAL EPITHELIAL-CELLS; HUMAN ALVEOLAR MACROPHAGES; HUMAN ENDOTHELIAL-CELLS; SMOOTH-MUSCLE-CELLS; SOUTH-POLAR-PLATEAU	Since the London fog of 1952, in which more than 4000 people were killed in 4 days, the combined efforts of scientists from several disciplines, including those from the environmental health, clinical and biomedical disciplines, have raised serious concerns about the impact of air pollutants on human health. These environmental pollutants are rapidly being recognized as important and independent risk factors for several diseases such as asthma, chronic obstructive pulmonary disease, lung cancer, atherosclerosis, ischemic heart disease and stroke. Although the relative effects of particulate matter air pollution (aerodynamic diameter < 10 mu m, or PM10) are greater for respiratory than for cardiovascular deaths, the number of deaths attributable to PM10 is much larger for cardiovascular than for respiratory reasons due to the higher prevalence of cardiovascular disease in the general population. This review summarizes current understanding of the mechanisms underlying the associations between PM10 exposure and cardiovascular morbidity and mortality. (c) 2006 Elsevier Inc. All rights reserved.	Univ British Columbia, Dept Pharmacol & Therapeut, Fac Med, Vancouver, BC V6T 1Z3, Canada; Univ British Columbia, St Pauls Hosp, James Hogg iCAPTURE Ctr Cardiovasc & Pulm Res, Vancouver, BC V5Z 1M9, Canada	Laher, I (reprint author), Univ British Columbia, Dept Pharmacol & Therapeut, Fac Med, 2176 Hlth Sci Mall, Vancouver, BC V6T 1Z3, Canada.	ilaher@interchange.ubc.ca	Khazaei, Majid/E-7533-2012; Laher, Ismail/L-3947-2013	Laher, Ismail/0000-0002-3917-4417			Albert CM, 2002, CIRCULATION, V105, P2595, DOI 10.1161/01.CIR.0000017493.03108.1C; Bagate K, 2004, INHAL TOXICOL, V16, P431, DOI 10.1080/08958370490439588; Bai YS, 2001, FREE RADICAL BIO MED, V30, P555, DOI 10.1016/S0891-5849(00)00499-8; BALLOU SP, 1992, CYTOKINE, V4, P361, DOI 10.1016/1043-4666(92)90079-7; Barna BP, 1996, J LEUKOCYTE BIOL, V59, P397; Barnes PJ, 1997, NEW ENGL J MED, V336, P1066; Batalha JRF, 2002, ENVIRON HEALTH PERSP, V110, P1191; BATH PMW, 1991, ARTERIOSCLER THROMB, V11, P254; Bayram H, 1998, AM J RESP CELL MOL, V18, P441; BECKMAN JS, 1990, P NATL ACAD SCI USA, V87, P1620, DOI 10.1073/pnas.87.4.1620; BERK BC, 1990, AM J CARDIOL, V65, P168, DOI 10.1016/0002-9149(90)90079-G; Bermudez EA, 2002, ARTERIOSCL THROM VAS, V22, P1668, DOI 10.1161/01.ATV.0000029781.31325.66; Bonetti PO, 2003, ARTERIOSCL THROM VAS, V23, P168, DOI 10.1161/01.ATV.0000051384.43104.FC; Bouthillier L, 1998, AM J PATHOL, V153, P1873, DOI 10.1016/S0002-9440(10)65701-X; Brook RD, 2002, CIRCULATION, V105, P1534, DOI 10.1161/01.CIR.0000013838.94747.64; Brown DM, 2004, AM J PHYSIOL-LUNG C, V286, pL344, DOI 10.1152/ajplung.00139.2003; Brown DM, 2000, OCCUP ENVIRON MED, V57, P685, DOI 10.1136/oem.57.10.685; Burnett RT, 1999, ARCH ENVIRON HEALTH, V54, P130; Calderon-Garciduenas L, 2002, TOXICOL PATHOL, V30, P373, DOI 10.1080/01926230252929954; Carr MJ, 2001, ENVIRON HEALTH PERSP, V109, P567, DOI 10.2307/3454671; Carter AM, 1997, CIRCULATION, V96, P1424; CASTELL JV, 1989, FEBS LETT, V242, P237, DOI 10.1016/0014-5793(89)80476-4; CERMAK J, 1993, BLOOD, V82, P513; Cheng TJ, 2003, ENVIRON HEALTH PERSP, V111, P147; Cheng YW, 1999, J TOXICOL ENV HEAL A, V57, P75, DOI 10.1080/009841099157791; Conway DSG, 2004, J AM COLL CARDIOL, V43, P2075, DOI 10.1016/j.jacc.2003.11.062; Costa DL, 1997, ENVIRON HEALTH PERSP, V105, P1053, DOI 10.2307/3433509; Creason J, 2001, J EXPO ANAL ENV EPID, V11, P116, DOI 10.1038/sj.jea.7500154; CUSHING SD, 1990, P NATL ACAD SCI USA, V87, P5134, DOI 10.1073/pnas.87.13.5134; Cuzzocrea S, 2004, FASEB J, V18, P94, DOI 10.1096/fj.03-0428com; DOCKERY DW, 1993, NEW ENGL J MED, V329, P1753, DOI 10.1056/NEJM199312093292401; Dolmetsch RE, 1998, NATURE, V392, P933; Dominici F, 2003, AM J EPIDEMIOL, V157, P1055, DOI 10.1093/aje/kwg087; Donaldson K, 2001, ENVIRON HEALTH PERSP, V109, P523, DOI 10.2307/3454663; FERIN J, 1992, AM J RESP CELL MOL, V6, P535; Foresti R, 1999, BIOCHEM J, V339, P729, DOI 10.1042/0264-6021:3390729; FOWLER MB, 1986, CIRCULATION, V74, P1290; Fujii T, 2002, AM J RESP CELL MOL, V27, P34; Fujii T, 2001, AM J RESP CELL MOL, V25, P265; FURUYAMA A, 2005, ARCH TOXICOL, V23, P1; GALVEDEROCHEMONTEIX B, 1993, J LEUKOCYTE BIOL, V53, P439; GARG UC, 1989, J CLIN INVEST, V83, P1774, DOI 10.1172/JCI114081; Ghio AJ, 2003, INHAL TOXICOL, V15, P1465, DOI 10.1080/08958370390249111; Ghio AJ, 2000, AM J RESP CRIT CARE, V162, P981; Gibbons GH, 1997, AM J CARDIOL, V79, P3, DOI 10.1016/S0002-9149(97)00122-7; Gilmour PS, 2005, OCCUP ENVIRON MED, V62, P164, DOI 10.1136/oem.2004.014951; Gilmour PS, 1996, OCCUP ENVIRON MED, V53, P817; Gilmour PS, 2001, AM J PHYSIOL-LUNG C, V281, pL598; Gimbrone MA, 1999, THROMB HAEMOSTASIS, V82, P722; Godleski J. 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Ther.	JAN	2007	113	1					16	29		10.1016/j.pharmthera.2006.06.005		14	Pharmacology & Pharmacy	Pharmacology & Pharmacy	129FE	WOS:000243713100002	16920197	
J	Matsubara, S; Li, GM; Takeda, K; Loader, JE; Pine, P; Masuda, ES; Miyahara, N; Miyahara, S; Lucas, JJ; Dakhama, A; Gelfand, EW				Matsubara, S; Li, GM; Takeda, K; Loader, JE; Pine, P; Masuda, ES; Miyahara, N; Miyahara, S; Lucas, JJ; Dakhama, A; Gelfand, EW			Inhibition of spleen tyrosine kinase prevents mast cell activation and airway hyperresponsiveness	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						airway hyperresponsiveness; eosinophils; goblet cell metaplasia; mast cells; spleen tyrosine kinase	AFFINITY IGE RECEPTOR; FC-EPSILON-RI; CD8(+) T-CELLS; PASSIVE TRANSFER; TERMINAL KINASE; ALLERGIC-ASTHMA; SMOOTH-MUSCLE; INFLAMMATION; SYK; PROTEIN	Rationale: Spleen tyrosine kinase (Syk) is important for Fc and B-cell receptor-mediated signaling. Objective: To determine the activity of a specific Syk inhibitor (11406) on mast cell activation in vitro and on the development of allergen-induced airway hyperresponsiveness (AHR) and inflammation in vivo. Methods: AHR and inflammation were induced after 10 d of allergen (ovalbumin [OVA]) exposure exclusively via the airways and in the absence of adjuvant. This approach was previously established to be IgE, Fc epsilon RI, and mast cell dependent. Alternatively, mice were passively sensitized with OVA-specific IgE, followed by limited airway challenge. In vitro, the inhibitor was added to cultures of IgE-sensitized bone marrow-derived mast cells (BMMCs) before crosslinking with allergen. Results: The inhibitor prevented OVA-induced degranulation of passively IgE-sensitized murine IBMMCs and inhibited the production of interieukin (IL)-13, tumor necrosis factor a, IL-2, and IL-6 in these sensitized BMMCs. When administered in vivo, R406 inhibited AHR, which developed in BALB/c mice exposed to aerosolized 1% OVA for 10 consecutive d (20 min/d), as well as pulmonary eosinophilia and goblet cell metaplasia. A similar inhibition of AHR was demonstrated in mice passively sensitized with OVA-specific IgE and exposed to limited airway challenge. Conclusion: This study delineates a functional role for Syk in the development of mast cell- and IgE-mediated AHR and airway inflammation, and these results indicate that inhibition of Syk may be a target in the treatment of allergic asthma.	Natl Jewish Med & Res Ctr, Dept Pediat, Div Cell Biol, Denver, CO 80206 USA; Rigel Pharmaceut Inc, San Francisco, CA USA	Gelfand, EW (reprint author), Natl Jewish Med & Res Ctr, Dept Pediat, Div Cell Biol, 1400 Jackson St, Denver, CO 80206 USA.	gelfande@njc.org			NHLBI NIH HHS [HL-36577, HL-42246, HL-61005, P01 HL036577, P01 HL036577-21A15977]		Bang LM, 2004, BIODRUGS, V18, P415, DOI 10.2165/00063030-200418060-00007; BENHAMOU M, 1993, J BIOL CHEM, V268, P23318; Blank U, 2004, TRENDS IMMUNOL, V25, P266, DOI 10.1016/j.it.2004.03.005; Brightling CE, 2002, NEW ENGL J MED, V346, P1699, DOI 10.1056/NEJMoa012705; Busse WW, 2001, NEW ENGL J MED, V344, P350; Chayama K, 2001, P NATL ACAD SCI USA, V98, P4599, DOI 10.1073/pnas.081021898; Costello PS, 1996, ONCOGENE, V13, P2595; DARBY C, 1994, J IMMUNOL, V152, P5429; Garrington TP, 2000, EMBO J, V19, P5387, DOI 10.1093/emboj/19.20.5387; GREENBERG S, 1994, J BIOL CHEM, V269, P3897; Gurish MF, 2001, J EXP MED, V194, pF1, DOI 10.1084/jem.194.1.F1; Hamelmann E, 1999, AM J RESP CELL MOL, V21, P480; HUTCHCROFT JE, 1992, P NATL ACAD SCI USA, V89, P9107, DOI 10.1073/pnas.89.19.9107; HUTCHCROFT JE, 1992, J BIOL CHEM, V267, P8613; Ishizuka T, 1999, J IMMUNOL, V162, P2087; Ishizuka T, 1997, P NATL ACAD SCI USA, V94, P6358, DOI 10.1073/pnas.94.12.6358; Ishizuka T, 1996, J BIOL CHEM, V271, P12762; Kim Y, 2001, J IMMUNOL, V166, P5183; KUNG TT, 1995, AM J RESP CELL MOL, V12, P404; LARSEN GL, 1992, J CLIN INVEST, V89, P747, DOI 10.1172/JCI115651; Larsen GL, 1994, AM J PHYSIOL, V266, P263; Luskova P, 2004, CURR PHARM DESIGN, V10, P1727, DOI 10.2174/1381612043384538; Luster AD, 2004, NAT REV IMMUNOL, V4, P711, DOI 10.1038/nri1438; Macedo-Soares MF, 2004, J ALLERGY CLIN IMMUN, V114, P97, DOI 10.1016/j.jaci.2004.03.033; MATSUBARA S, 2005, P AM THORAC SOC, V2, pA754; Mayr SI, 2002, J IMMUNOL, V169, P2061; Miyahara N, 2005, J IMMUNOL, V174, P4979; Miyahara N, 2004, NAT MED, V10, P865, DOI 10.1038/nm1081; Mocsai A, 2002, IMMUNITY, V16, P547, DOI 10.1016/S1074-7613(02)00303-5; Oshiba A, 1996, J CLIN INVEST, V97, P1398, DOI 10.1172/JCI118560; Robinson DS, 2004, J ALLERGY CLIN IMMUN, V114, P58, DOI 10.1016/j.jaci.2004.03.034; Sedlik C, 2003, J IMMUNOL, V170, P846; Seow CJ, 2002, EUR J PHARMACOL, V443, P189, DOI 10.1016/S0014-2999(02)01534-0; Siraganian R.P., 1999, SIGNAL TRANSDUCTION, P115; Stenton GR, 2002, J IMMUNOL, V169, P1028; Takeda K, 1997, J EXP MED, V186, P449, DOI 10.1084/jem.186.3.449; Taube C, 2004, J IMMUNOL, V172, P6398; Tomkinson A, 2001, J IMMUNOL, V166, P5792; WEISS A, 1994, CELL, V76, P263, DOI 10.1016/0092-8674(94)90334-4; Williams CMM, 2000, J EXP MED, V192, P455, DOI 10.1084/jem.192.3.455; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; Wong BR, 2004, EXPERT OPIN INV DRUG, V13, P743, DOI 10.1517/13543784.13.7.743; Yamamoto N, 2003, J PHARMACOL EXP THER, V306, P1174, DOI 10.1124/jpet.103.052316; Yang GY, 2004, CYTOKINE, V28, P224, DOI 10.1016/j.cyto.2004.08.007; Zhang J, 1996, J EXP MED, V184, P71, DOI 10.1084/jem.184.1.71	45	73	77	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.	JAN 1	2006	173	1					56	63		10.1164/rccm.200503-361OC		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	001GA	WOS:000234520400010	16192454	
J	Kattan, M; Stearns, SC; Crain, EF; Stout, JW; Gergen, PJ; Evans, R; Visness, CM; Gruchalla, RS; Morgan, WJ; O'Connor, GT; Mastin, JP; Mitchell, HE				Kattan, M; Stearns, SC; Crain, EF; Stout, JW; Gergen, PJ; Evans, R; Visness, CM; Gruchalla, RS; Morgan, WJ; O'Connor, GT; Mastin, JP; Mitchell, HE			Cost-effectiveness of a home-based environmental intervention for inner-city children with asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; inner city; cost-effectiveness; asthma intervention; allergen mitigation	UNITED-STATES; ILLNESS; TRENDS	Background: Exposure to indoor allergens contributes to increased asthma morbidity. The Inner-City Asthma Study, a randomized trial involving home environmental allergen and irritant remediation among children aged 6 through 11 years with moderate-to-severe asthma, successfully reduced asthma symptoms. A cost-effectiveness analysis can help stakeholders to evaluate the potential costs and benefits of adopting such a program. Objective: We sought to assess the cost-effectiveness of the environmental intervention of the Inner-City Asthma Study. Methods: Incremental cost-effectiveness ratios for a 2-year study period were calculated. Health outcome was measured as symptom-free days. Resource use measures included ambulatory visits, hospitalizations, and pharmaceutical use. CIs were obtained by using bootstrapping. Results: The intervention, which cost $1469 per family, led to statistically significant reductions in symptom days, unscheduled clinic visits, and use of beta-agonist inhalers. Over the year of the intervention and a year of follow-up, the intervention cost was $27.57 per additional symptom-free day (95% CI, $7.46-$67.42). Subgroup analysis showed that targeting the intervention to selected high-risk subgroups did not reduce the incremental cost-effectiveness ratio. Conclusions: A targeted home-based environmental intervention improved health and reduced service use in inner-city children with moderate-to-severe asthma. The intervention is cost-effective when the aim is to reduce asthma symptom days and the associated costs.	Mt Sinai Sch Med, Dept Pediat, New York, NY 10029 USA; Univ N Carolina, Dept Hlth Policy & Adm, Chapel Hill, NC USA; Albert Einstein Coll Med, Jacobi Med Ctr, Dept Pediat Emergency Med, Bronx, NY 10467 USA; Univ Washington, Sch Med, Dept Pediat, Seattle, WA 98195 USA; NIAID, Asthma Allergy Inflammat Branch, Div Allergy Immunol Transplantat, NIH, Bethesda, MD 20892 USA; Northwestern Univ, Sch Med, Dept Pediat, Chicago, IL 60611 USA; Northwestern Univ, Sch Med, Dept Med, Chicago, IL 60611 USA; Rho Inc, Chapel Hill, NC USA; Univ Texas, SW Med Ctr Dallas, Dept Med, Dallas, TX 75235 USA; Univ Texas, SW Med Ctr Dallas, Dept Pediat, Dallas, TX 75235 USA; Univ Arizona, Coll Med, Resp Sci Ctr, Tucson, AZ USA; Boston Univ, Sch Med, Boston, MA 02215 USA; Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA	Kattan, M (reprint author), Mt Sinai Sch Med, Dept Pediat, Box 1202B,1 Gustave L Levy Pl, New York, NY 10029 USA.	meyer.kattan@mssm.edu		O'Connor, George/0000-0002-6476-3926	NIAID NIH HHS [AI-39900, AI-39761, AI-39769, AI-39776, AI-39785, AI-39789, AI-39901, AI-39902]		Chaudhary MA, 1996, STAT MED, V15, P1447; Crain EF, 2002, ENVIRON HEALTH PERSP, V110, P939; Kattan M, 1997, PEDIATR PULM, V24, P253, DOI 10.1002/(SICI)1099-0496(199710)24:4<253::AID-PPUL4>3.0.CO;2-L; Krahn MD, 1996, CAN MED ASSOC J, V154, P821; Morgan WJ, 2004, NEW ENGL J MED, V351, P1068, DOI 10.1056/NEJMoa032097; Newacheck PW, 2000, ARCH PEDIAT ADOL MED, V154, P287; Paltiel AD, 2001, J ALLERGY CLIN IMMUN, V108, P39; Rosenstreich DL, 1997, NEW ENGL J MED, V336, P1356, DOI 10.1056/NEJM199705083361904; STEIN REK, 1987, LANCET, V2, P1506; Sullivan SD, 2003, J ALLERGY CLIN IMMUN, V112, P1229, DOI 10.1016/j.jaci.2003.09.025; Sullivan SD, 2002, J ALLERGY CLIN IMMUN, V110, P576, DOI 10.1067/mai.2002.128009; Wang Li Yan, 2005, Prev Chronic Dis, V2, pA11; Weiss KB, 2000, J ALLERGY CLIN IMMUN, V106, P493; WEISS KB, 1992, NEW ENGL J MED, V326, P862, DOI 10.1056/NEJM199203263261304	14	73	76	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.	NOV	2005	116	5					1058	1063		10.1016/j.jaci.2005.07.032		6	Allergy; Immunology	Allergy; Immunology	017IG	WOS:000235686700017	16275376	
J	Tauchi, M; Hida, A; Negishi, T; Katsuoka, F; Noda, S; Mimura, J; Hosoya, T; Yanaka, A; Aburatani, H; Fujii-Kuriyama, Y; Motohashi, H; Yamamoto, M				Tauchi, M; Hida, A; Negishi, T; Katsuoka, F; Noda, S; Mimura, J; Hosoya, T; Yanaka, A; Aburatani, H; Fujii-Kuriyama, Y; Motohashi, H; Yamamoto, M			Constitutive expression of aryl hydrocarbon receptor in keratinocytes causes inflammatory skin lesions	MOLECULAR AND CELLULAR BIOLOGY			English	Article							POLYCYCLIC AROMATIC-HYDROCARBONS; DIESEL EXHAUST PARTICLES; CONTACT HYPERSENSITIVITY; 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN TCDD; POLYAROMATIC HYDROCARBONS; ATOPIC-DERMATITIS; DIOXIN RECEPTOR; TRANSGENIC MICE; IGE; INDUCTION	Occupational and environmental exposure to polycyclic aromatic hydrocarbons (PAHs) has been suggested to provoke inflammatory and/or allergic disorders, including asthma, rhinitis, and dermatitis. The molecular mechanisms of this PAH-mediated inflammation remain to be clarified. Previous studies implied the involvement of PAHs as irritants and allergens, with the reactive oxygen species generated from the oxygenated PAHs believed to be an exacerbating factor. It is also possible that PAHs contribute to the pathogenesis through activation of aryl-hydrocarbon receptor (AhR)-mediated transcription, since PAHs are potent inducers of the AhR. To address this point, we generated transgenic mouse lines expressing the constitutive active form of the AhR in keratinocytes. In these lines of mice, the AhR activity was constitutively enhanced in the absence of ligands, so that any other direct effects of PAHs and their metabolites could be ignored. At birth, these transgenic mice were normal, but severe skin lesions with itching developed postnatally. The skin lesions were accompanied by inflammation and immunological imbalance and resembled typical atopic dermatitis. We demonstrate that constitutive activation of the AhR pathway causes inflammatory skin lesions and suggests a new mechanism for the exacerbation of inflammatory diseases after exposure to occupational and environmental xenobiotics.	Univ Tsukuba, Ctr TARA, Tsukuba, Ibaraki 3058577, Japan; Univ Tsukuba, Grad Sch Comprehens Human Sci, Tsukuba, Ibaraki 3058577, Japan; Mochida Pharmaceut Co Ltd, Pharmaceut Res Ctr, Jimba, Gotemba 4128524, Japan; Japan Sci & Technol Corp, ERATO, Environm Response Project, Tsukuba, Ibaraki 3058577, Japan; Univ Tokyo, Res Ctr Adv Sci & Technol, Tokyo 1538904, Japan; Japan Sci & Technol Corp, SORST, Kawaguchi 3320012, Japan	Motohashi, H (reprint author), Univ Tsukuba, Ctr TARA, 1-1-1 Tennoudai, Tsukuba, Ibaraki 3058577, Japan.	hozumim@tara.tsukuba.ac.jp	Mimura, Junsei/E-7893-2013				ANDERSON C, 1995, J IMMUNOL, V155, P3530; Andersson P, 2002, P NATL ACAD SCI USA, V99, P9990, DOI 10.1073/pnas.152906299; Arruda LK, 2005, CURR OPIN ALLERGY CL, V5, P153, DOI 10.1097/01.all.0000162308.89857.6c; Bonvallot V, 2001, AM J RESP CELL MOL, V25, P515; Casale GP, 2000, MOL CARCINOGEN, V27, P125, DOI 10.1002/(SICI)1098-2744(200002)27:2<125::AID-MC8>3.0.CO;2-0; COENRAADS PJ, 1994, DERMATOL CLIN, V12, P569; DAVILA DR, 1995, J TOXICOL ENV HEALTH, V45, P101; DiazSanchez D, 1997, ALLERGY, V52, P52; Frazer IH, 1998, EUR J IMMUNOL, V28, P2791, DOI 10.1002/(SICI)1521-4141(199809)28:09<2791::AID-IMMU2791>3.0.CO;2-B; Fujimaki H, 2002, TOXICOL SCI, V66, P117, DOI 10.1093/toxsci/66.1.117; GUO LF, 1993, EMBO J, V12, P973; HANKINSON O, 1995, ANNU REV PHARMACOL, V35, P307, DOI 10.1146/annurev.pharmtox.35.1.307; Heo Y, 2001, TOXICOLOGY, V159, P143, DOI 10.1016/S0300-483X(00)00418-2; KARRAS JG, 1995, TOXICOL LETT, V75, P225, DOI 10.1016/0378-4274(94)03185-A; Kepley CL, 2003, CLIN IMMUNOL, V107, P10, DOI 10.1016/S1521-6616(03)00004-4; KLEMME JC, 1987, CANCER RES, V47, P6074; Konishi H, 2002, P NATL ACAD SCI USA, V99, P11340, DOI 10.1073/pnas.152337799; Leung D, 1999, J ALLERGY CLIN IMMUN, V104, P99; Leung DYM, 2003, LANCET, V361, P151, DOI 10.1016/S0140-6736(03)12193-9; Li N, 2003, ENVIRON HEALTH PERSP, V111, P455, DOI 10.1289/ehp.6000; Mastrangelo G, 2003, INT J IMMUNOPATH PH, V16, P145; Matikainen T, 2001, NAT GENET, V28, P355, DOI 10.1038/ng575; Mimura J, 1997, GENES CELLS, V2, P645, DOI 10.1046/j.1365-2443.1997.1490345.x; Moennikes O, 2004, CANCER RES, V64, P4707, DOI 10.1158/0008-5472.CAN-03-0875; Nakayama T, 2001, INT IMMUNOL, V13, P95, DOI 10.1093/intimm/13.1.95; Nickoloff BJ, 1999, J CLIN INVEST, V104, P1161, DOI 10.1172/JCI8633; NOHARA XK, 2005, J IMMUNOL, V174, P2770; Ohtake F, 2003, NATURE, V423, P545, DOI 10.1038/nature01606; Pei XH, 2002, CYTOKINE, V19, P236, DOI 10.1006/cyto.2002.1967; Pereira LV, 2000, GENE, V255, P363, DOI 10.1016/S0378-1119(00)00313-9; Rydzynski K, 2004, TOXICOLOGY, V198, P75, DOI 10.1016/j.tox.2004.01.020; Saxon A, 2000, IMMUNOPHARMACOLOGY, V48, P325, DOI 10.1016/S0162-3109(00)00234-4; Sjogren M, 1996, MUTAT RES-FUND MOL M, V358, P97, DOI 10.1016/0027-5107(96)00175-3; TAKENAKA H, 1995, J ALLERGY CLIN IMMUN, V95, P103, DOI 10.1016/S0091-6749(95)70158-3; Tohyama M, 2001, J DERMATOL SCI, V27, P130, DOI 10.1016/S0923-1811(01)00127-X; Walker DB, 2004, TOXICOLOGY, V197, P57, DOI 10.1016/j.tox.2003.12.012; Wu MT, 2003, J OCCUP ENVIRON MED, V45, P1034, DOI 10.1097/01.jom.0000088876.25970.96; Yamamoto O, 2003, J DERMATOL SCI, V32, P85, DOI 10.1016/S0923-1811(03)00097-5	38	73	76	1	2	AMER SOC MICROBIOLOGY	WASHINGTON	1752 N ST NW, WASHINGTON, DC 20036-2904 USA	0270-7306			MOL CELL BIOL	Mol. Cell. Biol.	NOV	2005	25	21					9360	9368		10.1128/MCB.25.21.9360-9368.2005		9	Biochemistry & Molecular Biology; Cell Biology	Biochemistry & Molecular Biology; Cell Biology	976SW	WOS:000232754600018	16227587	
J	Jarvis, D; Luczynska, C; Chinn, S; Potts, J; Sunyer, J; Janson, C; Svanes, C; Kunzli, N; Leynaert, B; Heinrich, J; Kerkhof, M; Ackermann-Liebrich, U; Anto, MM; Cerveri, I; de Marco, R; Gislason, T; Neukirch, F; Vermeire, P; Wjst, M; Burney, P				Jarvis, D; Luczynska, C; Chinn, S; Potts, J; Sunyer, J; Janson, C; Svanes, C; Kunzli, N; Leynaert, B; Heinrich, J; Kerkhof, M; Ackermann-Liebrich, U; Anto, MM; Cerveri, I; de Marco, R; Gislason, T; Neukirch, F; Vermeire, P; Wjst, M; Burney, P			Change in prevalence of IgE sensitization and mean total IgE with age and cohort	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						ECRHS; atopy; total IgE; cohort	RESPIRATORY-HEALTH-SURVEY; SKIN-TEST REACTIVITY; 8 YEARS APART; HAY-FEVER; SERUM IGE; IMMUNOGLOBULIN-E; INCREASING PREVALENCE; COPENHAGEN ALLERGY; ASTHMA; ATOPY	Background: Cross-sectional studies show that the prevalence of IgE sensitization is lower in older age groups than younger age groups. This could reflect either a decrease in sensitization with aging or a higher prevalence of sensitization in more recent birth cohorts. Objective: To assess change in IgE sensitization and mean total IgE in young adults as they age. Methods: Serum specific IgE to common allergens and total IgE were measured on 2 occasions about 9 years apart in 6371 young adults living in 28 centers, mainly in Western Europe, who took part in the European Community Respiratory Health Survey II. Outcomes were analyzed by using generalized estimating equations, and adjustments were made for differences between laboratory measures on the 2 occasions. Results: Overall, there was no net change in the prevalence of sensitization to at least 1 of house dust mite, grass, or cat (net change per 10 years of follow-up, -0.1%; 95% CI, -1.7% to 1.5%), although there was a fall in mean total IgE (ratio of geometric mean total IgE, 0.86; 95% CI, 0.79 to 0.93). There was evidence that sensitization to at least 1 allergen was higher in more recent cohorts, and this was largely explained by a higher prevalence of sensitization to grass. Conclusion: The disease burden associated with IgE sensitization in adults, and particularly with IgE sensitization to grass, is likely to continue to increase for some time despite current evidence that the increase in allergy seen in children may have ceased.	Univ London Kings Coll, Dept Publ Hlth Sci, London SE1 3QD, England; Univ Pompeu Fabra, Inst Municipal Invest Med, Barcelona, Spain; Univ Uppsala, S-75105 Uppsala, Sweden; Haukeland Hosp, Dept Med, Dept Thorac Med, Bergen, Norway; Univ So Calif, Keck Sch Med, Div Environm Hlth, Dept Prevent Med, Los Angeles, CA 90089 USA; Inst Natl Sante & Rech Med Epidemiol, Paris, France; GSF Natl Res Ctr Environm & Hlth, Inst Epidemiol, Neuherberg, Germany; Univ Groningen, Dept Hlth Sci, Groningen, Netherlands; Univ Basel, Int Social & Prevent Med, CH-4003 Basel, Switzerland; Univ Pavia, Ist Ricovero & Curea Carattere Sci San Matteo, Div Resp Dis, Pavia, Italy; Univ Verona, Div Epidemiol & Stat, Dept Med & Publ Hlth, I-37100 Verona, Italy; Univ Hosp, Dept Allergy Resp Med & Sleep, Reykjavik, Iceland; Univ Antwerp, Antwerp, Belgium	Jarvis, D (reprint author), Univ London Kings Coll, Dept Publ Hlth Sci, 42 Weston St, London SE1 3QD, England.	deborah.jarvis@kcl.ac.uk	de Marco, Roberto/A-5470-2008; Kerkhof, Marjan/A-8846-2008; SESM, SESM/C-1440-2008; Jarvis, Deborah/E-6494-2011; Kunzli, Nino/F-7195-2014; Sunyer, J/G-6909-2014	Kunzli, Nino/0000-0001-8360-080X; Sunyer, J/0000-0002-2602-4110	NCRR NIH HHS [2 S07 RR05521-28]		Anderson HR, 2004, BRIT MED J, V328, P1052, DOI 10.1136/bmj.38057.583727.47; BARBEE RA, 1987, J ALLERGY CLIN IMMUN, V79, P919, DOI 10.1016/0091-6749(87)90241-7; BARBEE RA, 1987, J ALLERGY CLIN IMMUN, V79, P16, DOI 10.1016/S0091-6749(87)80010-6; Braun-Fahrlander C, 2004, EUR RESPIR J, V23, P407, DOI 10.1183/09031936.04.00074004; Broadfield E, 2002, J ALLERGY CLIN IMMUN, V109, P969, DOI 10.1067/mai.2002.124772; 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; BURROWS B, 1981, AM REV RESPIR DIS, V124, P523; CRIQUI MH, 1990, ANN ALLERGY, V64, P308; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; Downs SH, 2001, ARCH DIS CHILD, V84, P20, DOI 10.1136/adc.84.1.20; Gassner-Bachmann M, 2000, DEUT MED WOCHENSCHR, V125, P924, DOI 10.1055/s-2000-6778; GERRARD JW, 1980, ANN ALLERGY, V44, P261; Jarvis D, 2002, EUR RESPIR J, V20, P1071, DOI 10.1183/09031936.02.00046802; Jarvis D, 1999, J ALLERGY CLIN IMMUN, V104, P934, DOI 10.1016/S0091-6749(99)70071-0; Kosunen TU, 2002, CLIN EXP ALLERGY, V32, P373, DOI 10.1046/j.1365-2222.2002.01330.x; Krause TG, 2002, LANCET, V360, P691, DOI 10.1016/S0140-6736(02)09841-0; Linneberg A, 2002, CLIN EXP ALLERGY, V32, P1702, DOI 10.1046/j.1365-2222.2002.01537.x; Linneberg A, 2000, ALLERGY, V55, P767, DOI 10.1034/j.1398-9995.2000.00672.x; Linneberg A, 2000, J ALLERGY CLIN IMMUN, V106, P247, DOI 10.1067/mai.2000.108312; Matricardi PM, 1998, J ALLERGY CLIN IMMUN, V101, P439, DOI 10.1016/S0091-6749(98)70350-1; NAKAGOMI T, 1994, LANCET, V343, P121, DOI 10.1016/S0140-6736(94)90854-0; OMENAAS E, 1994, CLIN EXP ALLERGY, V24, P530, DOI 10.1111/j.1365-2222.1994.tb00950.x; ORYSZCZYN M, 1990, ANN ALLERGY, V67, P355; ORYSZCZYN MP, 1995, AM J RESP CRIT CARE, V151, P663; Ronchetti R, 2003, CLIN EXP ALLERGY, V33, P1232, DOI 10.1046/j.1365-2222.2003.01746.x; Ronchetti R, 2001, EUR RESPIR J, V17, P881, DOI 10.1183/09031936.01.17508810; StataCorp, 2003, STAT STAT SOFTW REL; Sunyer J, 1999, EUR RESPIR J, V14, P885, DOI 10.1034/j.1399-3003.1999.14d26.x; von Mutius E, 1998, LANCET, V351, P862, DOI 10.1016/S0140-6736(97)10100-3; VONMUTIUS E, 1994, BRIT MED J, V308, P692	31	73	73	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.	SEP	2005	116	3					675	682		10.1016/j.jaci.2005.05.009		8	Allergy; Immunology	Allergy; Immunology	017IE	WOS:000235686500032	16159642	
J	Johnson, CC; Ownby, DR; Alford, SH; Havstad, SL; Williams, LK; Zoratti, EM; Peterson, EL; Joseph, CLM				Johnson, CC; Ownby, DR; Alford, SH; Havstad, SL; Williams, LK; Zoratti, EM; Peterson, EL; Joseph, CLM			Antibiotic exposure in early infancy and risk for childhood atopy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergy; antibiotics; atopy; children; IgE; skin testing	PRACTICE RESEARCH DATABASE; ALLERGIC DISEASE; INFECTIOUS-DISEASES; BIRTH COHORT; SERUM IGE; 1ST YEAR; ASTHMA; LIFE; AGE; CHILDREN	Background: The increase in pediatric allergy and asthma parallels the increase in use of antibiotics. Antibiotics disturb the flora of the gastrointestinal tract, possibly perturbing the developing immune system. Objective: We evaluated whether antibiotic use during early infancy increased the risk for atopy. Methods: Antibiotic prescriptions documented in medical records were collected from a birth cohort born from 1987 through 1989 (n=725). At 6 to 7 years of age, 448 were followed by means of examination, including skin prick tests and serum IgE measurements to common allergens. Results: Adjusted odds ratios (aORs) and 95% CIs were calculated comparing children with any versus those with no antibiotic use in the first 6 months and the outcomes of atopy (any positive skin test response), seroatopy (any positive specific IgE test result), either atopy or seroatopy, and both atopy and seroatopy. Atopy increased with antibiotic use approaching statistical significance (aOR, 1.48, 95% Cl, 0.94-2.34; P =.09)., however, the risk was concentrated among children with less than 2 pets in the home (aOR, 1.73; 95% Cl, 1.07-2.80; P=.024) and children breast-fed for 4 or more months (aOR, 3.02; 95% CI, 1.27-7.17; P=.013). The aORs were generally in the same direction for seroatopy and the combined categories. Conclusion: Antibiotic use in early life appears to contribute to increased risk for atopy in certain subgroups of children.	Henry Ford Hlth Syst, Dept Biostat & Res Epidemiol, Detroit, MI 48202 USA; Henry Ford Hlth Syst, Ctr Hlth Serv Res, Detroit, MI USA; Henry Ford Hlth Syst, Div Gen Med, Dept Internal Med, Detroit, MI USA; Henry Ford Hlth Syst, Sect Allergy & Immunol, Div Pulm Crit Care Allergy Immunol & Sleep Med, Detroit, MI USA; Wayne State Univ, Environm Hlth Sci Ctr Mol & Cellular Toxicol Huma, Detroit, MI 48202 USA; Med Coll Georgia, Sect Allergy Immunol, Augusta, GA USA	Johnson, CC (reprint author), Henry Ford Hlth Syst, Dept Biostat & Res Epidemiol, 1 Ford Pl,5C, Detroit, MI 48202 USA.	cjohnso1@hfhs.org		Johnson, Christine Cole/0000-0002-6864-6604	NHLBI NIH HHS [HL 67427]; NIAID NIH HHS [AI 50681, AI 24156]; NIEHS NIH HHS [P03 ES 06639]		Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; Beasley R, 2000, J ALLERGY CLIN IMMUN, V105, pS466, DOI 10.1016/S0091-6749(00)90044-7; Bremner SA, 2003, CLIN EXP ALLERGY, V33, P1518, DOI 10.1046/j.1365-2222.2003.01794.x; Celedon JC, 2002, AM J RESP CRIT CARE, V166, P72, DOI 10.1164/rccm.2109074; Cullinan P, 2004, THORAX, V59, P11; Dowell SF, 1998, PEDIATRICS, V101, P163; Droste JHJ, 2000, CLIN EXP ALLERGY, V30, P1547; Farooqi IS, 1998, THORAX, V53, P927; Finkelstein JA, 2003, PEDIATRICS, V112, P620, DOI 10.1542/peds.112.3.620; Foliaki S, 2004, INT J EPIDEMIOL, V33, P558, DOI 10.1093/ije/dyh031; Holt PG, 1997, PEDIATR ALLERGY IMMU, V8, P53, DOI 10.1111/j.1399-3038.1997.tb00145.x; Illi S, 2001, BRIT MED J, V322, P390, DOI 10.1136/bmj.322.7283.390; Johnson CC, 2004, J ALLERGY CLIN IMMUN, V114, P105, DOI 10.1016/j.jaci.2004.04.007; Levy J, 2000, AM J GASTROENTEROL, V95, pS8, DOI 10.1016/S0002-9270(99)00808-4; McKeever TM, 2002, J ALLERGY CLIN IMMUN, V109, P43, DOI 10.1067/mai.2002.121016; Noverr MC, 2004, INFECT IMMUN, V72, P4996, DOI 10.1128/IAI.72.9.4996-5003.2004; Ownby DR, 2002, JAMA-J AM MED ASSOC, V288, P963, DOI 10.1001/jama.288.8.963; OWNBY DR, 1991, J ALLERGY CLIN IMMUN, V88, P555, DOI 10.1016/0091-6749(91)90148-H; Oyama N, 2001, J ALLERGY CLIN IMMUN, V107, P153, DOI 10.1067/mai.2001.111142; Remes ST, 2001, J ALLERGY CLIN IMMUN, V108, P509, DOI 10.1067/mai.2001.117797; Strachan DP, 2000, THORAX S1, V55, pS2; von Mutius E, 1999, EUR RESPIR J, V14, P4, DOI 10.1034/j.1399-3003.1999.14a03.x; Wickens K, 1999, CLIN EXP ALLERGY, V29, P766; Williams LK, 2004, J ALLERGY CLIN IMMUN, V113, P291, DOI 10.1016/j.jaci.2003.11.010; Wjst M, 2001, EUR J MED RES, V6, P263; Wright AL, 1999, J ALLERGY CLIN IMMUN, V104, P589, DOI 10.1016/S0091-6749(99)70328-3	27	73	75	1	5	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUN	2005	115	6					1218	1224		10.1016/j.jaci.2005.04.020		7	Allergy; Immunology	Allergy; Immunology	935WZ	WOS:000229815400017	15940137	
J	Cristaudo, A; Sera, F; Severino, V; De Rocco, M; Di Lella, E; Picardo, M				Cristaudo, A; Sera, F; Severino, V; De Rocco, M; Di Lella, E; Picardo, M			Occupational hypersensitivity to metal salts, including platinum, in the secondary industry	ALLERGY			English	Article						hypersensitivity; iridium; occupational; palladium; platinum group elements; platinum salts; rhodium; skin test	REFINERY WORKERS; MEDICAL SURVEILLANCE; PROSPECTIVE COHORT; ALLERGY; EXPOSURE; ASTHMA	Background: Exposure to platinum group elements (PGEs) - platinum (Pt), palladium (Pd), rhodium (Rh) and iridium (Ir) - may cause acute toxicity or hypersensitivity with respiratory symptoms, urticaria and (less frequently) contact dermatitis. Our aim was to determine the prevalence and the clinical characteristics of hypersensitivity to platinum salts and to other elements of the platinum group. Methods: A total of 153 subjects working in a catalyst manufacturing and recycling factory were examined. The examination consisted of a work exposure and medical questionnaire, physical examination, skin prick test for PGEs and other common aeroallergens, and patch tests for PGEs. Skin prick tests and patch tests were performed with H-2[PtCl6], K-2[PtCl4], Na-2[PtCl6], IrCl3, RhCl3, PdCl2, aqueous solutions at different concentrations. Results: Positive prick test reactions to Pt-salts at various concentrations were found in 22 (14.4%) of 153 workers; eight had simultaneous reactions to all Pt-salts tested; seven had positive responses to H-2[PtCl6] only; four had simultaneous positive reactions to both H-2[PtCl6] and K-2[PtCl4]; three had positive reactions to H-2[PtCl6] and Na-2[PtCl6]. Three of 22 had positive reactions to H-2[PtCl6] and IrCl3 solutions, two of these had positive reactions to H-2[PtCl6], IrCl3 and RhCl3 solutions. Positive patch test reactions to platinum salts at day 2 were seen in two of 153 subjects. Conclusions: The results of this study demonstrate that Pt-salts are important allergens in the catalyst industry and that the clinical manifestations involve both the respiratory system and the skin. Hexachloroplatinic acid should be considered the most important salt to use for skin prick tests.	Ist S Maria & S Gallicano, Serv Allergol, IRCCS, I-0144 Rome, Italy; IRCCS, IDI, Lab Epidemiol, Rome, Italy	Cristaudo, A (reprint author), Ist S Maria & S Gallicano, Serv Allergol, IRCCS, Via Elio Chianesi 53, I-0144 Rome, Italy.		Sera, Francesco/C-8176-2011; Picardo, Mauro/A-6978-2011; Cristaudo, Antonio/K-5944-2016	Picardo, Mauro/0000-0003-4899-6639; Cristaudo, Antonio/0000-0002-0737-983X			BAKER DB, 1990, AM J IND MED, V18, P653, DOI 10.1002/ajim.4700180604; BOLMAUDORFF U, 1992, INT ARCH OCC ENV HEA, V64, P257, DOI 10.1007/BF00378283; BURROWS D, 1999, OCCUPATIONAL SKIN DI; CALVERLEY AE, 1995, OCCUP ENVIRON MED, V52, P661; Cotton F. A., 1988, ADV INORGANIC CHEM; GUY HR, 1999, METALS SKIN TOPIC EF; HUGHES EG, 1980, J SOC OCCUP MED, V30, P27; *INT PROGR CHEM SA, 1991, ENV HLTH CRIT PLAT, P125; Johansson SGO, 2001, ALLERGY, V56, P813, DOI 10.1034/j.1398-9995.2001.t01-1-00001.x; LOEBENSTEIN JR, 1988, US BUREAU MINES MINE, V1, P689; MERGET R, 1991, BRIT J IND MED, V48, P830; Merget R, 2000, J ALLERGY CLIN IMMUN, V105, P364, DOI 10.1016/S0091-6749(00)90089-7; Merget R, 2001, SCI TOTAL ENVIRON, V270, P165, DOI 10.1016/S0048-9697(00)00788-9; Merget R, 2001, J ALLERGY CLIN IMMUN, V107, P707; Niezborala M, 1996, OCCUP ENVIRON MED, V53, P252; Quirce S, 1998, ALLERGY, V53, P633, DOI 10.1111/j.1398-9995.1998.tb03949.x; Santucci B, 2000, CONTACT DERMATITIS, V43, P333, DOI 10.1034/j.1600-0536.2000.043006333.x; Schuppe HC, 1997, INT ARCH ALLERGY IMM, V112, P125; SPSS Inc, 2001, SPSS WIND REL 11 0 1; WEDEPOHL KH, 1995, GEOCHIM COSMOCHIM AC, V59, P1217	20	73	75	0	6	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	FEB	2005	60	2					159	164		10.1111/j.1398-9995.2004.00521.x		6	Allergy; Immunology	Allergy; Immunology	887VF	WOS:000226332900005	15647035	
J	Nygaard, UC; Samuelsen, M; Aase, A; Lovik, M				Nygaard, UC; Samuelsen, M; Aase, A; Lovik, M			The capacity of particles to increase allergic sensitization is predicted by particle number and surface area, not by particle mass	TOXICOLOGICAL SCIENCES			English	Article						PM; particle size; adjuvant effect; allergy; mice; IgE	DIESEL EXHAUST PARTICLES; CARBON-BLACK; PARTICULATE MATTER; AIR-POLLUTION; ULTRAFINE PARTICLES; URBAN AIR; RESPIRATORY HEALTH; ADJUVANT ACTIVITY; OXIDATIVE STRESS; IMMUNE-RESPONSES	Particle exposure has traditionally been monitored as mass concentration of PM10 (particles with an aerodynamic diameter less than 10 mum), more recently also as PM2.5. The mass concentration is strongly influenced by the large particles. Therefore, particle mass is a poor measure for characterizing the amount of the small, possibly more biologically potent particles. We used polystyrene particles (PSP) ranging in diameter from 0.0588 to 11.14 mum, carbon black (CB), and diesel exhaust particles (DEP), to study the adjuvant effect of particles on the immune response to the allergen ovalbumin (OVA) after sc injection into the footpad of BALB/cA mice. At a given mass dose, the small particles (0.0588 and 0.202 mum PSP, CB, and DEP) increased the allergen-specific IgE serum levels to a substantially higher degree than the larger particles (1.053, 4.64, and 11.14 mum PSP). Further, in the draining lymph node during the primary response, the fine particles (0.202 mum) with OVA increased cell numbers, expression of surface markers (CD19, MHC class II, CD86, and CD23) and ex vivo production of IL-4 and IL-10, whereas the largest (11.14 mum) particles did not. Linear regression analyses indicated that the IgE response was not predicted by particle mass (R-2 = 0.06), but was predicted by the total particle surface area (R-2 = 0.64), number of particles (R-2 = 0.62), and particle diameter (R-2 = 0.58). In conclusion, we found that fine particles exerted stronger adjuvant effects on allergic responses than larger particles at equal mass doses. Consequently, the dose described as total particle surface area or particle number predicts the adjuvant effect of particles better than the currently used particle mass.	Norwegian Inst Publ Hlth, Div Environm Med, NO-0403 Oslo, Norway; Norwegian Inst Publ Hlth, Div Infect Dis Control, NO-0403 Oslo, Norway	Nygaard, UC (reprint author), Norwegian Inst Publ Hlth, Div Environm Med, POB 4404 Nydalen, NO-0403 Oslo, Norway.	unni.cecilie.nygaard@fhi.no					Al-Humadi NH, 2002, EXP LUNG RES, V28, P333, DOI 10.1080/01902140290091976; Becker S, 2003, EXP LUNG RES, V29, P29, DOI 10.1080/01902140390116535; Brown DM, 2001, TOXICOL APPL PHARM, V175, P191, DOI 10.1006/taap.2001.9240; Churg A, 1997, AM J RESP CRIT CARE, V155, P2109; Daigle CC, 2003, INHAL TOXICOL, V15, P539, DOI 10.1080/08958370390205065; Donaldson K, 2003, FREE RADICAL BIO MED, V34, P1369, DOI 10.1016/S0891-5849(03)00150-3; Donaldson K, 2000, PHILOS T ROY SOC A, V358, P2741; Dreher KL, 2000, INHAL TOXICOL, V12, P45, DOI 10.1080/08958378.2000.11463230; 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; Granum B, 2001, TOXICOLOGY, V156, P149, DOI 10.1016/S0300-483X(00)00375-9; Granum B, 2000, INHAL TOXICOL, V12, P365, DOI 10.1080/08958378.2000.11463247; Harrison RM, 2000, PHILOS T ROY SOC A, V358, P2567; Heo Y, 2001, TOXICOLOGY, V159, P143, DOI 10.1016/S0300-483X(00)00418-2; Junker M, 2000, ATMOS ENVIRON, V34, P3171, DOI 10.1016/S1352-2310(99)00372-6; Lambert AL, 2000, TOXICOL APPL PHARM, V165, P84, DOI 10.1006/taap.2000.8932; Lighty JS, 2000, J AIR WASTE MANAGE, V50, P1565; Lison D, 1997, ARCH TOXICOL, V71, P725, DOI 10.1007/s002040050453; LOVDAL T, 2003, TOXICOL SCI S, V72, P593; Lovik M, 1997, TOXICOLOGY, V121, P165, DOI 10.1016/S0300-483X(97)00075-9; Maynard AD, 2002, ATMOS ENVIRON, V36, P5561, DOI 10.1016/S1352-2310(02)00743-4; Moshammer H, 2003, ATMOS ENVIRON, V37, P1737, DOI 10.1016/S1352-2310(03)00073-6; Murphy SAM, 1999, OCCUP ENVIRON MED, V56, P813; Nel AE, 1998, J ALLERGY CLIN IMMUN, V102, P539, DOI 10.1016/S0091-6749(98)70269-6; NYGAARD UC, IN PRESS TOXICOLOGY; OBERDORSTER G, 1994, ENVIRON HEALTH PERSP, V102, P173, DOI 10.2307/3432080; Ormstad H, 1998, CLIN EXP ALLERGY, V28, P702; Ormstad H, 1998, TOXICOLOGY, V129, P227, DOI 10.1016/S0300-483X(98)00079-1; Osornio-Vargas AR, 2003, ENVIRON HEALTH PERSP, V111, P1289, DOI 10.1289/ehp.5913; Penttinen P, 2001, ENVIRON HEALTH PERSP, V109, P319, DOI 10.2307/3454889; Penttinen P, 2001, EUR RESPIR J, V17, P428, DOI 10.1183/09031936.01.17304280; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Schins RPF, 2004, TOXICOL APPL PHARM, V195, P1, DOI 10.1016/j.taap.2003.10.002; Schwartz J, 2000, EPIDEMIOLOGY, V11, P6, DOI 10.1097/00001648-200001000-00004; Siegel PD, 2004, J TOXICOL ENV HEAL A, V67, P221, DOI 10.1080/15287390490266891; Soukup JM, 2001, TOXICOL APPL PHARM, V171, P20, DOI 10.1006/taap.2000.9096; TILNEY NL, 1971, J ANAT, V109, P369; TOEWS GB, 1997, PULMONARY DEFENCES, P197; Tran CL, 2000, INHAL TOXICOL, V12, P1113, DOI 10.1080/08958370050166796; Tuschl H, 2002, TOXICOLOGY, V172, P35, DOI 10.1016/S0300-483X(01)00583-2; van Zijverden M, 2000, TOXICOL APPL PHARM, V168, P131, DOI 10.1006/taap.2000.9013; VANZIJVERDEN M, 2002, TOXICOL APPL PHARM, V178, P144; Veronesi B, 2002, INHAL TOXICOL, V14, P159, DOI 10.1080/089583701753403971; Zanobetti A, 2003, ENVIRON HEALTH PERSP, V111, P1188, DOI 10.1289/ehp.5712	44	73	76	3	15	OXFORD UNIV PRESS	OXFORD	GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND	1096-6080			TOXICOL SCI	Toxicol. Sci.	DEC	2004	82	2					515	524		10.1093/toxsci/kfh287		10	Toxicology	Toxicology	873AY	WOS:000225252300019	15456925	
J	Lee, YL; Lin, YC; Lee, YC; Wang, JY; Hsiue, TR; Guo, YL				Lee, YL; Lin, YC; Lee, YC; Wang, JY; Hsiue, TR; Guo, YL			Glutathione S-transferase P1 gene polymorphism and air pollution as interactive risk factors for childhood asthma	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						air pollution; asthma; children; gene-environmental interaction; GSTP1 polymorphism	GENOME-WIDE SEARCH; BRONCHIAL HYPERRESPONSIVENESS; RESPIRATORY SYMPTOMS; ENVIRONMENTAL EXPOSURES; SUSCEPTIBILITY LOCI; PULMONARY-FUNCTION; IMMUNOGLOBULIN-E; SCHOOL-CHILDREN; GSTP1 LOCUS; ATOPY	Background Polymorphisms at the glutathione S-transferase (GST) P1 locus were associated with asthma-related phenotypes and bronchial hyper-responsiveness. Objective This study investigated whether GSTP1 genotypes and outdoor air pollution were interactive risk factors on childhood asthma. Methods Four hundred and thirty-six subjects were recruited for oral mucosa samplings from 2853 fourth- to ninth-grade schoolchildren from three districts with different air pollution levels in southern Taiwan. PCR-based assays were performed by oral mucosa DNA to determine GSTP1 genotypes. We also conducted a nested case-control study comprising 61 asthmatic children and 95 controls confirmed by International Study of Asthma and Allergies in Childhood questionnaire results and methacholine challenge test. Multiple logistic regression was used to adjust for potential confounding factors. Results All participants were homozygous at the Ala-114 locus. Although only a marginally significant association existed between the frequency of homozygosity at the Ile-105 locus and asthma when air pollution was not considered, we found a significant gene-environmental interaction between GSTP1-105 alleles and air pollution after adjusting for confounders (P=0.035). Specifically, we found that compared with participants carrying any Val-105 allele in low air pollution, those who are Ile-105 homozygotes in high air pollution district had a significantly increased risk of asthma (adjusted odds ratio (AOR)=5.52, 95% confidence interval (CI)=1.64-21.25). Compared with participants carrying any Val-105 allele, in high air pollution district, children with Ile-105 homozygotes had a significantly increased risk of asthma (AOR=3.79, 95% CI=1.01-17.08), but those who carried two Ile-105 alleles in low or moderate air pollution districts did not show similar tendencies. The risk of asthma also revealed a clear dose-response relationship with outdoor air pollution in children with Ile-105 homozygotes. Conclusion Our result suggests a gene-environmental interaction between GSTP1-105 genotypes and outdoor air pollution on childhood asthma.	Natl Cheng Kung Univ, Coll Med, Dept Environm & Occupat Hlth, Tainan 704, Taiwan; Natl Cheng Kung Univ, Coll Med, Inst Basic Med Sci, Tainan 704, Taiwan; Natl Cheng Kung Univ Hosp, Dept Internal Med, Tainan 70428, Taiwan; Kaohsiung Med Univ, Coll Dent Med, Kaohsiung, Taiwan; Natl Cheng Kung Univ Hosp, Dept Pediat, Tainan 70428, Taiwan	Guo, YL (reprint author), Natl Cheng Kung Univ, Coll Med, Dept Environm & Occupat Hlth, 138 Sheng Li Rd, Tainan 704, Taiwan.	leonguo@mail.ncku.edu.tw		Lin, Ying-Chu/0000-0002-2499-8632; GUO, Yue Leon/0000-0002-8530-4809; LEE, YUNG-LING/0000-0002-2234-9479			41st World Medical Assembly, 1990, B PAN AM HLTH ORG, V24, P606; American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P1285, DOI 10.1164/ajrccm/136.5.1285; ATS statement, 1979, AM REV RESPIR DIS, V119, P831; BARNES PJ, 1990, FREE RADICAL BIO MED, V9, P235, DOI 10.1016/0891-5849(90)90034-G; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Bleecker ER, 1997, AM J RESP CRIT CARE, V156, pS113; BOARD PG, 1989, ANN HUM GENET, V53, P205, DOI 10.1111/j.1469-1809.1989.tb01786.x; Boezen HM, 1999, LANCET, V353, P874, DOI 10.1016/S0140-6736(98)06311-9; Brauer M, 2002, AM J RESP CRIT CARE, V166, P1092, DOI 10.1164/rccm.200108-007OC; CONSTANTIN D, 1994, ENVIRON HEALTH PERSP, V102, P161, DOI 10.2307/3431947; Daniels SE, 1996, NATURE, V383, P247, DOI 10.1038/383247a0; Delfino RJ, 2003, ENVIRON HEALTH PERSP, V111, P647, DOI 10.1289/ehp.5992; Doull IJM, 1996, AM J RESP CRIT CARE, V153, P1280; Fryer AA, 2000, AM J RESP CRIT CARE, V161, P1437; FRYER AA, 1986, BIOCHIM BIOPHYS ACTA, V883, P448, DOI 10.1016/0304-4165(86)90283-7; Fusco D, 2001, EUR RESPIR J, V17, P1143, DOI 10.1183/09031936.01.00005501; GILL P, 1985, NATURE, V318, P577, DOI 10.1038/318577a0; Gilliland FD, 2004, LANCET, V363, P119, DOI 10.1016/S0140-6736(03)15262-2; GREENE LS, 1995, J AM COLL NUTR, V14, P317; Guo YLL, 1999, ENVIRON HEALTH PERSP, V107, P1001; 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; Hill MR, 1996, HUM MOL GENET, V5, P959, DOI 10.1093/hmg/5.7.959; Hu X, 1997, BIOCHEM BIOPH RES CO, V238, P397, DOI 10.1006/bbrc.1997.7311; Ishibe N, 1998, CANCER RES, V58, P667; Kauffmann F, 1999, CLIN EXP ALLERGY, V29, P17; Lee YL, 2003, PEDIATRICS, V112, pE389, DOI 10.1542/peds.112.5.e389; Lin YC, 2004, CLIN EXP ALLERGY, V34, P548, DOI 10.1111/j.1365-2222.2004.1928.x; Lin YC, 2002, CHEST, V121, P347, DOI 10.1378/chest.121.2.347; Marsh DG, 1997, NAT GENET, V15, P389; Martinez J, 1996, ARCH BIOCHEM BIOPHYS, V336, P191, DOI 10.1006/abbi.1996.0549; Pikhart H, 2001, INT ARCH OCC ENV HEA, V74, P574; Sandford A, 1996, AM J RESP CRIT CARE, V153, P1749; Slaughter JC, 2003, ANN ALLERG ASTHMA IM, V91, P346; Sotir M, 2003, ENVIRON HEALTH PERSP, V111, P657, DOI 10.1289/ehp.5824; Soutar A, 1997, THORAX, V52, P166; SPARROW D, 1987, AM REV RESPIR DIS, V135, P1255; Spiteri MA, 2000, ALLERGY, V55, P15, DOI 10.1034/j.1398-9995.2000.00502.x; Strange RC, 1999, METABOLIC POLYMORPHI, P231; Tolbert PE, 2000, AM J EPIDEMIOL, V151, P798	40	73	76	0	4	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	NOV	2004	34	11					1707	1713		10.1111/j.1365-2222.2004.02099.x		7	Allergy; Immunology	Allergy; Immunology	870TF	WOS:000225080300009	15544594	
J	Strid, J; Thomson, M; Hourihane, J; Kimber, I; Strobel, S				Strid, J; Thomson, M; Hourihane, J; Kimber, I; Strobel, S			A novel model of sensitization and oral tolerance to peanut protein	IMMUNOLOGY			English	Article						sensitization; oral tolerance; peanut; allergy	IMMUNE-RESPONSES; T-CELLS; ATOPIC-DERMATITIS; SUPPRESSION; ALLERGEN; PREVALENCE; ANTIGENS; IDENTIFICATION; INDUCTION; OVALBUMIN	The prevalence of food allergic diseases is rising and poses an increasing clinical problem. Peanut allergy affects around 1% of the population and is a common food allergy associated with severe clinical manifestations. The exact route of primary sensitization is unknown although the gastrointestinal immune system is likely to play an important role. Exposure of the gastrointestinal tract to soluble antigens normally leads to a state of antigen-specific systemic hyporesponsiveness (oral tolerance). A deviation from this process is thought to be responsible for food-allergic diseases. In this study, we have developed a murine model to investigate immunoregulatory processes after ingestion of peanut protein and compared this to a model of oral tolerance to chicken egg ovalbumin (OVA). We demonstrate that oral tolerance induction is highly dose dependent and differs for the allergenic proteins peanut and OVA. Tolerance to peanut requires a significantly higher oral dose than tolerance to OVA. Low doses of peanut are more likely to induce oral sensitization and increased production of interleukin-4 and specific immunoglobulin E upon challenge. When tolerance is induced both T helper 1 and 2 responses are suppressed. These results show that oral tolerance to peanut can be induced experimentally but that peanut proteins have a potent sensitizing effect. This model can now be used to define regulatory mechanisms following oral exposure to allergenic proteins on local, mucosal and systemic immunity and to investigate the immunomodulating effects of non-oral routes of allergen exposure on the development of allergic sensitization to peanut and other food allergens.	UCL, Inst Child Hlth, Immunobiol Unit, London WC1N 1EH, England; Southampton Univ Hosp NHS Trust, Wellcome Trust Clin Res Facil, Southampton, Hants, England; Syngenta, Cent Toxicol Lab, Macclesfield, Cheshire, England; Peninsula Postgrad Hlth Inst, Plymouth, Devon, England	Strid, J (reprint author), UCL, Inst Child Hlth, Immunobiol Unit, 30 Guilford St, London WC1N 1EH, England.	j.strid@ich.ucl.ac.uk	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Strid, Jessica/0000-0003-3690-2201			Afuwape AO, 2004, CLIN EXP IMMUNOL, V136, P40, DOI 10.1111/j.1365-2249.2004.02400.x; Armitage P., 1971, STAT METHODS MED RES; AROEIRA LS, 1995, SCAND J IMMUNOL, V41, P319, DOI 10.1111/j.1365-3083.1995.tb03573.x; Asseman C, 1999, J EXP MED, V190, P995, DOI 10.1084/jem.190.7.995; Bock SA, 2001, J ALLERGY CLIN IMMUN, V107, P191, DOI 10.1067/mai.2001.112031; BRUIJNZEELKOOMEN C, 1995, ALLERGY, V50, P623, DOI 10.1111/j.1398-9995.1995.tb02579.x; BURKS AW, 1992, J ALLERGY CLIN IMMUN, V90, P962, DOI 10.1016/0091-6749(92)90469-I; BURKS AW, 1991, J ALLERGY CLIN IMMUN, V88, P172, DOI 10.1016/0091-6749(91)90325-I; CHEN YH, 1994, SCIENCE, V265, P1237, DOI 10.1126/science.7520605; CHEN YH, 1995, NATURE, V376, P177, DOI 10.1038/376177a0; deJong EC, 1996, J ALLERGY CLIN IMMUN, V98, P73, DOI 10.1016/S0091-6749(96)70228-2; FREED DLJ, 2002, FOOD ALLERGY INTOLER, P837; GARSIDE P, 1995, J IMMUNOL, V154, P5649; Grundy J, 2002, J ALLERGY CLIN IMMUN, V110, P784, DOI 10.1067/mai.2002.128802; Kagan RS, 2003, J ALLERGY CLIN IMMUN, V112, P1223, DOI 10.1016/j.jaci.2003.09.026; Kolopp-Sarda MN, 2001, CLIN EXP ALLERGY, V31, P47, DOI 10.1046/j.1365-2222.2001.733/ca1804.x; Koppelman SJ, 2001, ALLERGY, V56, P132, DOI 10.1034/j.1398-9995.2001.056002132.x; Li XM, 2000, J ALLERGY CLIN IMMUN, V106, P150, DOI 10.1067/mai.2000.107395; MacDonald TT, 1998, CURR OPIN IMMUNOL, V10, P620, DOI 10.1016/S0952-7915(98)80079-4; Mayer L, 2000, CLIN IMMUNOL, V94, P1, DOI 10.1006/clim.1999.4791; MELAMED D, 1994, EUR J IMMUNOL, V24, P1974, DOI 10.1002/eji.1830240906; MILLER SD, 1979, J IMMUNOL, V123, P2344; MOWAT AM, 1987, IMMUNOL TODAY, V8, P93, DOI 10.1016/0167-5699(87)90853-X; Powrie F, 1996, J EXP MED, V183, P2669, DOI 10.1084/jem.183.6.2669; RACIOPPI L, 1993, J EXP MED, V177, P1047, DOI 10.1084/jem.177.4.1047; Sicherer SH, 2003, J ALLERGY CLIN IMMUN, V112, P1203, DOI 10.1016/S0091-6749(03)02026-8; Smith KM, 2000, AM J RESP CRIT CARE, V162, pS175; Strobel S, 1998, IMMUNOL TODAY, V19, P173, DOI 10.1016/S0167-5699(97)01239-5	28	73	75	0	0	WILEY-BLACKWELL	MALDEN	COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA	0019-2805			IMMUNOLOGY	Immunology	NOV	2004	113	3					293	303		10.1111/j.1365-2567.2004.01989.x		11	Immunology	Immunology	864LC	WOS:000224634000002	15500615	
J	Beyer, M; Bartz, H; Horner, K; Doths, S; Koerner-Rettberg, C; Schwarze, J				Beyer, M; Bartz, H; Horner, K; Doths, S; Koerner-Rettberg, C; Schwarze, J			Sustained increases in numbers of pulmonary dendritic cells after respiratory syncytial virus infection	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						respiratory syncytial virus; antigen-presenting cells; dendritic cells; CD11c antigen; airway inflammation; mice; virus-induced asthma	COLONY-STIMULATING FACTOR; ANTIGEN-PRESENTING CELLS; T-CELLS; AIRWAY SENSITIZATION; ALLERGIC SENSITIZATION; IMMUNE-RESPONSE; MICE; MACROPHAGE; HYPERRESPONSIVENESS; EXPRESSION	Background: Respiratory syncytial virus (RSV) bronchiolitis in infants can lead to wheezing and early allergic sensitization. In mice, RSV infection enhances allergic airway inflammation and airway hyperresponsiveness. Dendritic cells are critical in inducing T-cell responses to both viruses and allergens and could be pivotal in regulating interactions between these. Objective: This study addresses the effects of RSV infection on phenotype and function of pulmonary dendritic cells. Methods: BALB/c mice were infected with RSV, and expression of CD11c, MHC II, and CD86 on lung and spleen cells was monitored by flow cytometry for 21 days after infection. CD11c(+) cells were isolated to assess their phagocytic capacity and their ability to induce proliferation in allogenic T cells. Results: Numbers of pulmonary CD11c(+) MHC IIhi cells increased 13-fold starting from day 6 after RSV infection. This was associated with increased CD86 expression, reduced phagocytosis, and increased allogenic T-cell stimulatory capacity in CD11c(+) cells. These changes in the lung outlasted acute infection and were not observed in spleens. Conclusion: RSV infection results in sustained increases in numbers of mature dendritic cells in the lung. These might well contribute to the development of intense airway inflammation and airway hyperresponsiveness after RSV infection and to enhancement of subsequent responses to allergen exposure.	Univ London Imperial Coll Sci Technol & Med, Fac Med, Natl Heart & Lung Inst, Dept Resp Med, London W2 1PG, England; Ruhr Univ Bochum, St Josef Hosp, Klin Kinder & Jugendmed, D-4630 Bochum, Germany	Schwarze, J (reprint author), Univ London Imperial Coll Sci Technol & Med, Fac Med, Natl Heart & Lung Inst, Dept Resp Med, Norfolk Pl, London W2 1PG, England.		Schwarze, Jurgen/F-7396-2011	Schwarze, Jurgen/0000-0002-6899-748X			ANDERSON JJ, 1990, J GEN VIROL, V71, P1561, DOI 10.1099/0022-1317-71-7-1561; Brimnes MK, 2003, J EXP MED, V198, P133, DOI 10.1084/jem.20030266; Bukreyev A, 2001, J VIROL, V75, P12128, DOI 10.1128/JVI.75.24.12128-12140.2001; CHRISTENSEN PJ, 1995, AM J RESP CELL MOL, V13, P426; Cochand L, 1999, AM J RESP CELL MOL, V21, P547; Constant SL, 2002, J CLIN INVEST, V110, P1441, DOI 10.1172/JC1200216109; Foster S, 2003, IMMUNOLOGY, V108, P109, DOI 10.1046/j.1365-2567.2003.01539.x; Gajewska BU, 2001, AM J RESP CELL MOL, V25, P326; GRAHAM BS, 1991, J CLIN INVEST, V88, P1026, DOI 10.1172/JCI115362; HOLT PG, 1988, J EXP MED, V167, P262, DOI 10.1084/jem.167.2.262; Julia V, 2002, IMMUNITY, V16, P271, DOI 10.1016/S1074-7613(02)00276-5; KEIZER GD, 1987, J IMMUNOL, V138, P3130; Lin YL, 2003, EUR J IMMUNOL, V33, P2736, DOI 10.1002/eji.200324087; Lutz MB, 1999, J IMMUNOL METHODS, V223, P77, DOI 10.1016/S0022-1759(98)00204-X; Masten BJ, 1999, J IMMUNOL, V162, P1310; Masten BJ, 1997, AM J RESP CELL MOL, V16, P335; Matsuse H, 2000, J IMMUNOL, V164, P6583; McWilliam AS, 1996, J EXP MED, V184, P2429, DOI 10.1084/jem.184.6.2429; Moller GM, 1996, CLIN EXP ALLERGY, V26, P517, DOI 10.1046/j.1365-2222.1996.d01-337.x; NOAH TL, 1993, AM J PHYSIOL, V265, P472; OPENSHAW PJ, 1995, AM J RESP CRIT CARE, V152, P59; Ruedl C, 1996, EUR J IMMUNOL, V26, P1801, DOI 10.1002/eji.1830260821; Schauer U, 2002, EUR RESPIR J, V20, P1277, DOI 10.1183/09031936.02.00019902; Schwarze J, 1999, J IMMUNOL, V163, P5729; Schwarze J, 1999, J IMMUNOL, V162, P4207; Schwarze J, 1997, J CLIN INVEST, V100, P226, DOI 10.1172/JCI119516; Sigurs N, 2000, AM J RESP CRIT CARE, V161, P1501; Smyth RL, 1999, LANCET, V354, P1997, DOI 10.1016/S0140-6736(05)76769-6; Spender LC, 1998, J GEN VIROL, V79, P1751; Stampfli MR, 1998, J CLIN INVEST, V102, P1704, DOI 10.1172/JCI4160; Stein R, 1999, LANCET, V354, P541, DOI 10.1016/S0140-6736(98)10321-5; Stumbles PA, 1998, J EXP MED, V188, P2019, DOI 10.1084/jem.188.11.2019; Vremec D, 2000, J IMMUNOL, V164, P2978; Vremec D, 1997, J IMMUNOL, V159, P565; Ward C, 2001, J HEART LUNG TRANSPL, V20, P1064, DOI 10.1016/S1053-2498(01)00319-9; Yamamoto N, 2000, EUR J IMMUNOL, V30, P316, DOI 10.1002/1521-4141(200001)30:1<316::AID-IMMU316>3.0.CO;2-0; Yamamoto N, 2001, J VIROL, V75, P499, DOI 10.1128/JVI.75.1.499-505.2001	37	73	80	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.	JAN	2004	113	1					127	133		10.1016/j.jaci.2004.10.057		7	Allergy; Immunology	Allergy; Immunology	760MP	WOS:000187837900017	14713917	
J	Simonte, SJ; Ma, SH; Mofidi, S; Sicherer, SH				Simonte, SJ; Ma, SH; Mofidi, S; Sicherer, SH			Relevance of casual contact with peanut butter in children with peanut allergy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						peanut allergy; inhalation; skin contact	TREE-NUT-ALLERGY; NATURAL-HISTORY; FOOD ALLERGIES; IGE; IMMUNOTHERAPY; REGISTRY; TESTS	Background: Casual skin contact or inhalation of peanut butter fumes is reported and feared to cause allergic reactions in highly sensitive children with peanut allergy but has not been systematically studied. Objective: We sought to determine the clinical relevance of exposure to peanut butter by means of inhalation and skin contact in children with peanut allergy. Methods: Children with significant peanut allergy (recent peanut-specific IgE antibody concentration >50 kIU/L or evidence of peanut-specific IgE antibody and one of the following: clinical anaphylaxis, a reported inhalation-contact reaction, or positive double-blind, placebo-controlled oral challenge result to peanut) underwent double-blind, placebo-controlled, randomized exposures to peanut butter by means of contact with intact skin (0.2 mL pressed flat for 1 minute) and inhalation (surface area of 6.3 square inches 12 inches from the face for 10 minutes). Placebo challenges were performed by using soy butter mixed with histamine (contact), and scent was masked with soy butter, tuna, and mint (inhalation). Results: Thirty children underwent the challenges (median age, 7.7 years; median peanut IgE level, >100 kIU/L; 13 with prior history of contact and 11 with inhalation reactions). None experienced a systemic or respiratory reaction. Erythema (3 subjects), pruritus without erythema (5 subjects), and wheat-and-flare reactions (2 subjects) developed only at the site of skin contact with peanut butter. From this number of participants, it can be stated with 96% confidence that at least 90% of highly sensitive children with peanut allergy would not experience a systemic-respiratory reaction from casual exposure to peanut butter. Conclusions: Casual exposure to peanut butter is unlikely to elicit significant allergic reactions. The results cannot be generalized to larger exposures or to contact with peanut in other forms (flour and roasted peanuts).	Mt Sinai Sch Med, Dept Pediat, Div Allergy & Immunol, Elliot & Roslyn Jaffe Food Allergy Inst, New York, NY 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]		Baker SS, 2000, PEDIATRICS, V106, P346; CARLSTON JA, 1988, ANN ALLERGY, V61, P80; CRESPO JF, 1995, ALLERGY, V50, P257, DOI 10.1111/j.1398-9995.1995.tb01143.x; Devenney I, 2000, Ann Allergy Asthma Immunol, V85, P457; Hallett R, 2002, NEW ENGL J MED, V346, P1833, DOI 10.1056/NEJM200206063462320; Hourihane JO, 1997, J ALLERGY CLIN IMMUN, V100, P596, DOI 10.1016/S0091-6749(97)70161-1; Jones R. T., 1996, Journal of Allergy and Clinical Immunology, V97, P423, DOI 10.1016/S0091-6749(96)81179-1; Kalogeromitros D, 1996, ANN ALLERG ASTHMA IM, V77, P480; LOCKEY RF, 1987, J ALLERGY CLIN IMMUN, V79, P660, DOI 10.1016/S0091-6749(87)80164-1; Polasani R, 1997, ANN ALLERG ASTHMA IM, V78, P35; Rance F, 2002, J ALLERGY CLIN IMMUN, V109, P1027, DOI 10.1067/mai.2002.124775; Roberts G, 2002, ALLERGY, V57, P713, DOI 10.1034/j.1398-9995.2002.03366.x; Sicherer SH, 2001, J PEDIATR-US, V138, P560, DOI 10.1067/mpd.2001.111821; 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; Skolnick HS, 2001, J ALLERGY CLIN IMMUN, V107, P367, DOI 10.1067/mai.2001.112129; Tan BM, 2001, ANN ALLERG ASTHMA IM, V86, P583; Valyasevi MA, 1999, ANN ALLERG ASTHMA IM, V83, P132, DOI 10.1016/S1081-1206(10)62624-5; Vander Leek TK, 2000, J PEDIATR-US, V137, P749, DOI 10.1067/mpd.2000.109376; Wensing M, 2002, J ALLERGY CLIN IMMUN, V110, P915, DOI 10.1067/mai.2002.129235	21	73	74	0	6	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUL	2003	112	1					180	182		10.1067/mai.2003.1486		3	Allergy; Immunology	Allergy; Immunology	698QQ	WOS:000184010600027	12847496	
J	Dunphy, JL; Barcham, GJ; Bischof, RJ; Young, AR; Nash, A; Meeusen, ENT				Dunphy, JL; Barcham, GJ; Bischof, RJ; Young, AR; Nash, A; Meeusen, ENT			Isolation and characterization of a novel eosinophil-specific galectin released into the lungs in response to allergen challenge	JOURNAL OF BIOLOGICAL CHEMISTRY			English	Article							SITE-DIRECTED MUTAGENESIS; THYMIC EPITHELIAL-CELLS; RECOMBINANT GALECTIN-1; EXTRACELLULAR-MATRIX; MOLECULAR-CLONING; ENDOGENOUS LECTIN; GENE-EXPRESSION; IN-VIVO; APOPTOSIS; BINDING	A novel galectin cDNA (galectin-14) was cloned from ovine eosinophil-rich leukocytes by low stringency reverse transcriptase-PCR and cDNA library screening. Data base searches indicate that this gene encodes a novel prototype galectin that contains one putative carbohydrate recognition domain and exhibits most identity to galectin-9/ecalectin, a potent eosinophil chemoattractant. The sugar binding properties of the recombinant molecule were confirmed by a hemagglutination assay and lactose inhibition. The mRNA and protein of galectin-14 are expressed at high levels in eosinophil-rich cell populations. Flow cytometry and cytospot staining demonstrate that the protein localizes to the cytoplasmic, but not the granular, compartment of eosinophils. In contrast, galectin-14 mRNA and protein were not detected in neutrophils, macrophages, or lymphocytes. Western blot analysis of bronchoalveolar lavage fluid indicates that galectin-14 is released from eosinophils into the lumen of the lungs after challenge with house dust mite allergen. The restricted expression of this novel galectin to eosinophils and its release into the lumen of the lung in a sheep asthma model indicates that it may play an important role in eosinophil function and allergic inflammation.	Univ Melbourne, Sch Vet Sci, Ctr Anim Biotechnol, Parkville, Vic 3010, Australia; AMRAD Operat Pty Ltd, Burnley, Vic 3121, Australia	Meeusen, ENT (reprint author), Univ Melbourne, Sch Vet Sci, Ctr Anim Biotechnol, Parkville, Vic 3010, Australia.						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Biol. Chem.	APR 26	2002	277	17					14916	14924		10.1074/jbc.M200214200		9	Biochemistry & Molecular Biology	Biochemistry & Molecular Biology	545EH	WOS:000175203000073	11839756	
J	Keeler, GJ; Dvonch, JT; Yip, FY; Parker, EA; Israel, BA; Marsik, FJ; Morishita, M; Barres, JA; Robins, TG; Brakefield-Caldwell, W; Sam, M				Keeler, GJ; Dvonch, JT; Yip, FY; Parker, EA; Israel, BA; Marsik, FJ; Morishita, M; Barres, JA; Robins, TG; Brakefield-Caldwell, W; Sam, M			Assessment of personal and community-level exposures to particulate matter among children with asthma in Detroit, Michigan, as part of Community Action Against Asthma (CAAA)	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						ambient PM; childhood asthma; community-based participatory research; particulate matter; personal exposure; urban air quality	EMERGENCY ROOM VISITS; DUST MITE ALLERGENS; AIR-POLLUTION; HOSPITAL ADMISSIONS; CHILDHOOD ASTHMA; RESPIRATORY-DISEASE; MATERNAL SMOKING; SULFUR-DIOXIDE; PUBLIC-HEALTH; MORBIDITY	We report on the research conducted by the Community Action Against Asthma (CAAA) in Detroit, Michigan, to evaluate personal and community-level exposures to particulate matter (PM) among children with asthma living in an urban environment. CAAA is a community-based participatory research collaboration among academia, health agencies, and community-based organizations. CAAA investigates the effects of environmental exposures on the residents of Detroit through a participatory process that engages participants from the affected communities in all aspects of the design and conduct of the research; disseminates the results to all parties involved; and uses the research results to design, in collaboration with all partners, interventions to reduce the identified environmental exposures. The CAAA PM exposure assessment includes four seasonal measurement campaigns each year that are conducted for a 2-week duration each season. In each seasonal measurement period, daily ambient measurements of PM2.5 and PM10 (particulate matter with a mass median aerodynamic diameter less than 2.5 mum and 10 mum, respectively) are collected at two elementary schools in the eastside and southwest communities of Detroit. Concurrently, indoor measurements Of PM2.5 and PM10 are made at the schools as well as inside the homes of a subset of 20 children with asthma. Daily personal exposure measurements of PM10 are also collected for these 20 children with asthma. Results from the first Five seasonal assessment periods reveal that mean personal PM10 (68.4 +/- 39.2 mug/m(3)) and indoor home PM10 (52.2 +/- 30.6 mug/m(3)) exposures are significantly greater (p < 0.05) than the outdoor PM10 concentrations (25.8 +/- 11.8 mug/m(3)). The same was also found for PM2.5 (indoor PM2.5 = 34.4 21.7 mug/m(3); outdoor PM2.5 = 15.6 +/- 8.2 mug/m(3)). In addition, significant differences (p < 0.05) in community-level exposure to both PM10 and PM2.5 are observed between the two Detroit communities (southwest PM10 = 28.9 +/- 14.4 mug/m(3), PM2.5 = 17.0 +/- 9.3 mug/m(3), eastside PM10 = 23.8 +/- 12.1 mug/m(3), PM2.5 = 15.5 +/- 9.0 mug/m(3)). The increased levels in the southwest Detroit community are likely due to the proximity to heavy industrial pollutant point sources and interstate motorways. Trace element characterization of filter samples collected over the 2-year period will allow a more complete assessment of the PM components. When combined with other project measures, including concurrent seasonal twice-daily peak expiratory flow and forced expiratory volume at 1 sec and daily asthma symptom and medication dairies for 300 children with asthma living in the two Detroit communities, these data will allow not only investigations into the sources of PM in the Detroit airshed with regard to PM exposure assessment but also the role of air pollutants in exacerbation of childhood asthma.	Univ Michigan, Air Qual Lab, Dept Environm Hlth Sci, Ann Arbor, MI 48109 USA; Univ Michigan, Dept Hlth Behav & Hlth Educ, Ann Arbor, MI 48109 USA; Community Act Asthma, Detroit, MI USA; Detroit Hlth Dept, Div Environm Hlth, Detroit, MI USA	Keeler, GJ (reprint author), Univ Michigan, Air Qual Lab, Dept Environm Hlth Sci, 109 S Observ St, Ann Arbor, MI 48109 USA.		Dvonch, Joseph/K-3632-2013		NIEHS NIH HHS [1-P01-ES09589-01]		ABBEY DE, 1993, ARCH ENVIRON HEALTH, V48, P33; *AM LUNG ASS, 1998, TRENDS ASTHM MORB MO; *AM LUNG ASS, 1998, MIN AIR POLL FACT SH; ARRUDA LK, 1991, CLIN EXP ALLERGY, V21, P433, DOI 10.1111/j.1365-2222.1991.tb01683.x; Barber K, 1996, ANN ALLERG ASTHMA IM, V76, P427; BATES DV, 1995, ENVIRON HEALTH PERSP, V103, P243, DOI 10.2307/3432380; BEGGS PJ, 1995, ARCH ENVIRON HEALTH, V50, P87; Brauer M, 2000, J EXPO ANAL ENV EPID, V10, P478, DOI 10.1038/sj.jea.7500136; Bryant B. 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Health Perspect.	APR	2002	110			2			173	181				9	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	542WE	WOS:000175066600008	11929726	
J	Michalec, L; Choudhury, BK; Postlethwait, E; Wild, JS; Alam, R; Lett-Brown, M; Sur, S				Michalec, L; Choudhury, BK; Postlethwait, E; Wild, JS; Alam, R; Lett-Brown, M; Sur, S			CCL7 and CXCL10 orchestrate oxidative stress-induced neutrophilic lung inflammation	JOURNAL OF IMMUNOLOGY			English	Article							OZONE-INDUCED INFLAMMATION; OBSTRUCTIVE PULMONARY-DISEASE; AIR-POLLUTION; ASTHMATIC SUBJECTS; CHEMOATTRACTANT CINC; GENE-EXPRESSION; INDUCED SPUTUM; IFN-GAMMA; CHEMOKINES; HYPERRESPONSIVENESS	Oxidative stress from ozone (03) exposure augments airway neutrophil recruitment and chemokine production. We and others have shown that severe and sudden asthma is associated with airway neutrophilia, and that 03 oxidative stress is likely to augment neutrophilic airway inflammation in severe asthma. However, very little is known about chemokines that orchestrate oxidative stress-induced neutrophilic airway inflammation in vivo. To identify these chemokines, three groups of BALB/c mice were exposed to sham air, 0.2 ppm O-3, or 0.8 ppm O-3 for 6 h. Compared with sham air, 0.8 ppm O-3, but not 0.2 ppm O-3, induced pronounced neutrophilic airway inflammation that peaked at 18 h postexposure. The 0.8 ppm 03 up-regulated lung mRNA of CXCL1,2,3 (mouse growth-related oncogene-a and macrophage-inflammatory protein-2), CXCL10 (IFN-gamma-inducible protein-10), CCL3 (macrophage-inflammatory protein-1alpha), CCL7 (monocyte chemoattractant protein-3), and CCL11 (eotaxin) at 0 h postexposure, and expression of CXCL10, CCL3, and CCL7 mRNA was sustained 18 h postexposure. 03 increased lung protein levels of CXCL10, CCL7, and CCR3 (CCL7R). The airway epithelium was identified as a source of CCL7. The role of up-regulated chemokines was determined by administering control IgG or IgG Abs against six murine chemokines before 03 exposure. As expected, anti-mouse growth-related oncogene-a inhibited neutrophil recruitment. Surprisingly, Abs to CCL7 and CXCL10 also decreased neutrophil recruitment by 63 and 72%, respectively. These findings indicate that CCL7 and CXCL10, two chemokines not previously reported to orchestrate neutrophilic inflammation, play a critical role in mediating oxidative stress-induced neutrophilic airway inflammation. These observations may have relevance in induction of neutrophilia in severe asthma.	NIH, Asthma & Allerg Dis Res Ctr, Galveston, TX 77555 USA; Univ Texas, Med Branch, Dept Internal Med, Div Allergy & Immunol, Galveston, TX 77555 USA; Univ Texas, Med Branch, Dept Prevent Med & Community Hlth, Galveston, TX 77555 USA	Sur, S (reprint author), NIH, Asthma & Allerg Dis Res Ctr, Galveston, TX 77555 USA.						Anderson HR, 1998, THORAX, V53, P842; Bless NM, 2000, J IMMUNOL, V164, P2650; Bonecchi R, 1999, J IMMUNOL, V162, P474; Chang MMJ, 1998, AM J PHYSIOL-LUNG C, V275, pL524; DRISCOLL KE, 1987, J TOXICOL ENV HEALTH, V21, P27; FOLINSBEE LJ, 1994, AM J RESP CRIT CARE, V149, P98; Foster WM, 2000, J APPL PHYSIOL, V89, P1804; Gasperini S, 1999, J IMMUNOL, V162, P4928; Gonzalo JA, 1998, J EXP MED, V188, P157, DOI 10.1084/jem.188.1.157; Haddad EB, 1996, FEBS LETT, V379, P265, DOI 10.1016/0014-5793(95)01524-8; Haraguchi M, 1999, AM J RESP CRIT CARE, V159, P1005; Hiltermann TJN, 1998, FREE RADICAL BIO MED, V24, P952, DOI 10.1016/S0891-5849(97)00381-X; Horvath I, 1998, THORAX, V53, P668; Jatakanon A, 1999, AM J RESP CRIT CARE, V160, P1532; Johnston CJ, 1999, EXP LUNG RES, V25, P81, DOI 10.1080/019021499270448; Keatings VM, 1996, AM J RESP CRIT CARE, V153, P530; KLEEBERGER SR, 1993, AM J PHYSIOL, V264, pL15; KLEEBERGER SR, 1990, AM J PHYSIOL, V258, pL313; KLEEBERGER SR, 1993, AM J PHYSIOL, V264, pL21; Koto H, 1997, AM J RESP CRIT CARE, V156, P234; Michelson PH, 1999, OTOLARYNG HEAD NECK, V120, P225, DOI 10.1016/S0194-5998(99)70411-0; Montuschi P, 1999, AM J RESP CRIT CARE, V160, P216; Nightingale JA, 1999, THORAX, V54, P1061; Ordonez CL, 2000, AM J RESP CRIT CARE, V161, P1185; Peden DB, 1997, J ALLERGY CLIN IMMUN, V100, P802, DOI 10.1016/S0091-6749(97)70277-X; Peters JM, 1999, AM J RESP CRIT CARE, V159, P768; Romieu I, 1996, AM J RESP CRIT CARE, V154, P300; Sallusto F, 1998, J EXP MED, V187, P875, DOI 10.1084/jem.187.6.875; Sallusto F, 1997, SCIENCE, V277, P2005, DOI 10.1126/science.277.5334.2005; Stafford S, 1997, J IMMUNOL, V158, P4953; Struyf S, 2001, BLOOD, V97, P2197, DOI 10.1182/blood.V97.8.2197; SUR S, 1993, AM REV RESPIR DIS, V148, P713; Thurston GD, 1997, AM J RESP CRIT CARE, V155, P654; Vagaggini B, 1999, EUR RESPIR J, V13, P274, DOI 10.1034/j.1399-3003.1999.13b09.x; Ward SG, 1998, IMMUNITY, V9, P1, DOI 10.1016/S1074-7613(00)80583-X; Wenzel SE, 1997, AM J RESP CRIT CARE, V156, P737; Zhao QY, 1998, AM J PHYSIOL-LUNG C, V274, pL39	37	73	76	0	2	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	JAN 15	2002	168	2					846	852				7	Immunology	Immunology	510DP	WOS:000173193700038	11777981	
J	Vandenplas, O; Jamart, J; Delwiche, JP; Evrard, G; Larbanois, A				Vandenplas, O; Jamart, J; Delwiche, JP; Evrard, G; Larbanois, A			Occupational asthma caused by natural rubber latex: Outcome according to cessation or reduction of exposure	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; disability; latex; occupational lung disease	HEALTH-CARE WORKERS; BRONCHIAL HYPERRESPONSIVENESS; TOLUENE DIISOCYANATE; GLOVES; DISABILITY; WORKPLACE; IMPACT; CEDAR	Background: The long-term effects of reducing exposure to latex in subjects with latex-induced asthma remain unknown. Objective: The purpose of this study was to compare the health and socioeconomic outcomes of subjects with latex-induced asthma before and after reduction or cessation of exposure to latex. Methods: Thirty-six subjects with latex-induced asthma as ascertained by specific inhalation challenges were investigated after a median follow-up of 56 months (range, 12 to 92 months). Initial and follow-up visits included use of a detailed questionnaire and measurement of the concentration of histamine causing a 20% fall in FEV1 (PC20). At follow-up, information on employment, financial status, and quality of life was collected. Results: At follow-up, 16 subjects were no longer exposed to latex, whereas 20 subjects had reduced exposure. In the subjects who avoided exposure, asthma severity decreased from a median score of 8.5 to 3.5 (P = .001) and the median histamine PC20 value increased from 0.4 mg/mL to 2.3 mg/mL (P = .002). In the subjects who reduced their exposure, asthma-severity score improved from 6.5 to 2.5 (P < .001) and PC20 values rose from 0.5 mg/mL to 2.4 mg/mL (P < .001). Cessation of exposure to latex was associated with asthma-related work disability (69%) and loss of income (62%) more frequently than was reduction of exposure (35% and 30%, respectively). Conclusion: Reduction of exposure to latex should be considered a reasonably safe alternative that is associated with fewer socioeconomic consequences than removal from exposure.	Univ Catholique Louvain, Clin Univ Mont Godinne, Serv Pneumol, B-5530 Yvoir, Belgium; Univ Catholique Louvain, Clin Univ Mont Godinne, Ctr Biostat & Documentat Med, B-5530 Yvoir, Belgium; Fons Malad Profess, Brussels, Belgium	Vandenplas, O (reprint author), Univ Catholique Louvain, Clin Univ Mont Godinne, Serv Pneumol, B-5530 Yvoir, Belgium.						Allmers H, 1998, J ALLERGY CLIN IMMUN, V102, P841, DOI 10.1016/S0091-6749(98)70026-0; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; BLANC PD, 1993, CHEST, V104, P1371, DOI 10.1378/chest.104.5.1371; Blanc PD, 1999, AM J RESP CRIT CARE, V160, P2028; CHANYEUNG M, 1995, CHEST, V108, P1084, DOI 10.1378/chest.108.4.1084; COCKCROFT DW, 1977, CLIN ALLERGY, V7, P235, DOI 10.1111/j.1365-2222.1977.tb01448.x; COTE J, 1990, AM REV RESPIR DIS, V141, P373; European Community for Coal and Steel, 1983, B EUR PHYSIOPATHO S5, V19, P45; GRAMMER LC, 1993, AM REV RESPIR DIS, V148, P54; Hamilton RG, 2000, J ALLERGY CLIN IMMUN, V105, P839, DOI 10.1067/mai.2000.105224; Heilman DK, 1996, J ALLERGY CLIN IMMUN, V98, P325, DOI 10.1016/S0091-6749(96)70157-4; JUNIPER EF, 1993, AM REV RESPIR DIS, V147, P832; Laoprasert N, 1998, J ALLERGY CLIN IMMUN, V102, P998, DOI 10.1016/S0091-6749(98)70338-0; Lin FJ, 1996, OCCUP ENVIRON MED, V53, P753; Merget R, 1999, INT ARCH OCC ENV HEA, V72, P33, DOI 10.1007/s004200050331; PAGGIARO PL, 1993, CHEST, V103, P1123, DOI 10.1378/chest.103.4.1123; PISATI G, 1993, BRIT J IND MED, V50, P60; Poley GE, 2000, J ALLERGY CLIN IMMUN, V105, P1054, DOI 10.1067/mai.2000.106925; Ross DJ, 1999, CLIN EXP ALLERGY, V29, P750; Sussman GL, 1998, J ALLERGY CLIN IMMUN, V101, P171; TARLO SM, 1994, J ALLERGY CLIN IMMUN, V93, P985, DOI 10.1016/S0091-6749(94)70045-1; Vandenplas O, 1996, THORAX, V51, P472, DOI 10.1136/thx.51.5.472; VANDENPLAS O, 1995, AM J RESP CRIT CARE, V151, P54; Vandenplas O, 2001, J ALLERGY CLIN IMMUN, V107, P542, DOI 10.1067/mai.2001.113519; VANDENPLAS O, 1995, AM J RESP CRIT CARE, V151, P887; Vandenplas O, 1999, ASTHMA WORKPLACE, P425	26	73	76	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.	JAN	2002	109	1					125	130		10.1067/mai.2002.120760		6	Allergy; Immunology	Allergy; Immunology	519RM	WOS:000173739300021	11799378	
J	Gwynn, RC; Thurston, GD				Gwynn, RC; Thurston, GD			The burden of air pollution: Impacts among racial minorities	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article; Proceedings Paper	Workshop on Inhaled Environmental/Occupational Irritants and Allergens - Mechanisms of Cardiovascular and Systemic Responses	MAR 31-APR 02, 2000	SCOTTSDALE, ARIZONA	Amer Thorac Soc		acidic aerosols; air pollution; epidemiology; ethnicity; ozone; particulate matter; poverty; race; respiratory hospital admissions; socioeconomic status; sulfate; time-series techniques	CHILDHOOD ASTHMA; NEW-YORK; SOCIOECONOMIC-FACTORS; HEALTH; RACE; HOSPITALIZATION; PREVALENCE; MORTALITY; POVERTY; MATTER	Various epidemiologic investigations have shown that ambient air pollution levels are associated with acute increases in hospital admissions and mortality in the United States and abroad. The objectives of this investigation were a) to determine if racial minorities are more adversely affected by ambient air pollution than their white counterparts and b) to assess the contribution of socioeconomic status to any observed racial differences in pollution effect. Time-series regression methods were conducted to investigate these hypotheses for daily respiratory hospital admissions in New York City, New York. Pollutants considered included mean daily levels of particulate matter with a mass median aerodynamic diameter less than 10 mum (PM10), ozone (O-3), strong aerosol acidity (H+), and sulfates (SO42). The relative risk for respiratory hospital admission was calculated for each pollutant for a maximum minus mean increment in mean daily pollutant concentration. The greatest difference between the white and nonwhite subgroups was observed for O-3, where the white relative risk (RR) was 1.032 [95% confidence interval (Cl): 0.977-1.089] and the nonwhite RR was 1.122 (95% Cl: 1.074-1.172). Although not statistically different from each other, the various pollutants' RR estimates for the Hispanic nonwhite category in New York City were generally larger in magnitude than those for the non-Hispanic white group. When these analyses incorporated differences in the underlying respiratory hospitalization rates across races (that for nonwhites, was roughly twice that for whites), the disparities in attributable risks from pollution (in terms of excess admissions per day per million persons) were even larger for nonwhites versus whites. However, when insurance status was used as an indicator of socioeconomic/health coverage status, higher RRs were indicated for the poor/working poor (i.e., those on Medicaid and the uninsured) than for those who were economically better off (i.e., the privately insured), even among non-Hispanic whites. Thus, although potential racial differences in pollution exposures could not be explored as a factor, within-race analyses suggested that most of the apparent differences in air pollutant effects found across races were explained by socioeconomic and/or health care disparities.	NYU, Sch Med, Nelson Inst Environm Med, Tuxedo Pk, NY 10987 USA; Ctr Dis Control & Prevent, Atlanta, GA USA	Thurston, GD (reprint author), NYU, Sch Med, Nelson Inst Environm Med, 57 Old Forge Rd, Tuxedo Pk, NY 10987 USA.				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Health Perspect.	AUG	2001	109			4			501	506		10.2307/3454660		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	467KG	WOS:000170700500005	11544154	
J	Bredehorst, R; David, K				Bredehorst, R; David, K			What establishes a protein as an allergen?	JOURNAL OF CHROMATOGRAPHY B			English	Review						food allergy; proteins	HOUSE-DUST MITE; IGE-BINDING EPITOPES; BOVINE BETA-LACTOGLOBULIN; LIPID TRANSFER PROTEIN; BIRCH POLLEN PROFILIN; T-CELL EPITOPES; DER-P-I; MAJOR ALLERGEN; CROSS-REACTIVITY; X-RAY	There is little known about the factors that determine the allergenicity of food proteins. Apparently, the ability of a food protein to induce an allergic response requires its presence in substantial amounts in the food supply, its durability during food processing, and its resistance to digestion in the gastrointestinal tract. In addition to the mode and degree of exposure, structural characteristics appear to play an important, role for the capacity of a protein to modulate the immune response towards allergic reactions. Until now, however, there has been no indication for common structural characteristics of linear T cell or linear IgE (B cell) epitopes and the knowledge of structural characteristics of conformational IgE binding sites is very limited. Experimental data point only to certain surface areas of allergenic proteins which are important for IgE binding. Therefore, it is not possible to suggest any structural motif or conformational sequence pattern common to all allergenic proteins. Furthermore, glycosylation appears not to be a common critical determinant of allergenicity since food allergens comprise both glycoproteins and nonglycosylated proteins. Based on the few published three-dimensional structures of allergenic proteins including food proteins, one unifying feature of allergens appears to be their spherical shape. The three-dimensional structures of many more allergens have to be determined, however, to allow for a better understanding of the molecular basis of allergenicity. Most recently, new ideas have been introduced as to why certain biochemical or biologic functions such as enzymatic activities may predispose a protein to become an allergen. Proteolytically active allergens have been demonstrated to irritate the human mucosal surface, to enhance their own transmucosal uptake, and to augment IgE production. Therefore, the functional activity of some allergens may play a role among other factors in the process of sensitization and allergic responses. (C) 2001 Elsevier Science B.V. All rights reserved.	Univ Hamburg, Inst Biochem & Food Chem, D-20146 Hamburg, Germany	Bredehorst, R (reprint author), Univ Hamburg, Inst Biochem & Food Chem, Martin Luther King Pl 6, D-20146 Hamburg, Germany.						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Chromatogr. B	MAY 25	2001	756	1-2					33	40		10.1016/S0378-4347(01)00069-X		8	Biochemical Research Methods; Chemistry, Analytical	Biochemistry & Molecular Biology; Chemistry	435PG	WOS:000168889400005	11419725	
J	D'Urzo, AD; De Salvo, MC; Ramirez-Rivera, A; Almeida, J; Sichletidis, L; Rapatz, G; Kottakis, J				D'Urzo, AD; De Salvo, MC; Ramirez-Rivera, A; Almeida, J; Sichletidis, L; Rapatz, G; Kottakis, J		FOR-INT-03 Study Grp	In patients with COPD, treatment with a combination of formoterol and ipratropium is more effective than a combination of salbutamol and ipratropium - A 3-week, randomized, double-blind, within-patient, multicenter study	CHEST			English	Article						beta(2)-agonist; COPD; formoterol; ipratropium; salbutamol	OBSTRUCTIVE PULMONARY-DISEASE; AIR-FLOW LIMITATION; SEVERE ASTHMA; STABLE COPD; SALMETEROL; BROMIDE; MANAGEMENT; DURATION; AGONIST; THERAPY	Study objectives: To compare the efficacy of adding formoterol or salbutamol to regular ipratropium bromide treatment in COPD patients whose conditions were suboptimally controlled with ipratropium bromide alone. Design: A randomized, double-blind, double-dummy, two-period, crossover clinical trial. Setting: Twenty-four clinics and university medical centers in nine countries. Patients: One hundred seventy-two patients with baseline FEV1, less than or equal to 65% predicted, with FEV, reversibility to salbutamol not exceeding the normal variability of the measurement, and symptomatic despite regular treatment with ipratropium bromide. Interventions: Each patient received two treatments in random order: either inhaled formoterol dry powder, 12 mug bid, in addition to ipratropium bromide, 40 mug qid for 3 weeks, followed by salbutamol, 200 mug qid, in addition to ipratropium, 40 mug qid for 3 weeks, or vice versa. Measurements and results: Efficacy end points included morning premedication peak expiratory now (PEF) during the last week of treatment (primary end point), the area under the curve (AUC) for FEV, measured for 6 h after morning dose on the last day of treatment, and symptom scores (from daily diary recordings). Morning PEF and the AUC for FEV,were significantly better for formoterol/ipratropium than for salbutamol/ipratropium (p = 0.0003 and p < 0.0001, respectively). The formoterol/ipratropium combination also induced a greater improvement in mean total symptom scores (p = 0.0042), The safety profile of the two treatments was comparable. Conclusions: In COPD patients requiring combination bronchodilator treatment, the addition of formoterol to regular ipratropium treatment is more effective than the addition of salbutamol.	Novartis Pharmaceut, Novartis HRC, Horsham RH12 5AB, W Sussex, England; Primary Care Asthma Clin, Toronto, ON, Canada; Hosp Gen Agudis E Tornu, Buenos Aires, DF, Argentina; Hosp Enfermedades Cardiovasc & Torax, IMSS, Monterrey, Mexico; Hosp Sao Joaa, Serv Pneumol, Porto, Portugal; Univ Thessaloniki, Papanicolaou Hosp, Pneumol Clin, GR-54006 Salonika, Greece	Kottakis, J (reprint author), Novartis Pharmaceut, Novartis HRC, Wimblehurst Rd, Horsham RH12 5AB, W Sussex, England.						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J	Caffarelli, C; Sensi, LG; Marcucci, F; Cavagni, G				Caffarelli, C; Sensi, LG; Marcucci, F; Cavagni, G			Preseasonal local allergoid immunotherapy to grass pollen in children: a double-blind, placebo-controlled, randomized trial	ALLERGY			English	Article						asthma; children; grass pollen; local immunotherapy; rhinitis	EOSINOPHIL CATIONIC PROTEIN; HOUSE DUST MITE; SUBLINGUAL IMMUNOTHERAPY; MONOCLONAL-ANTIBODIES; STANDARDIZED GRASS; HAY-FEVER; RHINITIS; ASTHMA; EFFICACY; EXTRACT	Background: We assessed the efficacy of preseasonal local allergoid immunotherapy in a group of children with asthma and/or rhinitis and/or rhinoconjunctivitis due to grass pollen. Methods: We randomly assigned 24 children allergic to grass pollen to receive local allergoid immunotherapy for 3 months before the pollen season and 24 such patients to receive identically appearing placebo. The immunotherapy consisted of tablets of monomeric allergoid grass pollen allergens held in the mouth until they dissolved and then swallowed. The study was double-blind. Symptoms and medications were scored on diary cards during the pollen season. Nasal eosinophil cationic protein levels were measured by the monoclonal antibodies EG1 and EG2 outside the pollen season and at low and at high pollen concentration during the pollen season. Results: The active-treatment group had a statistically significant reduction of total symptoms (P < 0.05), especially bronchial symptoms (P < 0.05), in comparison with the placebo group. Immunotherapy was well tolerated and compliance was good. Nasal levels of EG2 and EG1 increased significantly during the pollen season, but there was no difference between groups. EG2/EGI increased significantly only in the placebo group during natural allergen exposure (P < 0.01). Conclusions: Our results suggest that this immunotherapy is effective for the treatment of asthma due to grass pollen in children.	Univ Parma, Dept Pediat, I-43100 Parma, Italy; Dept Pediat, Perugia, Italy; Pediat Dept Modena Sud, Sassuolo, Italy	Caffarelli, C (reprint author), Pediat Clin, Via Gramsci 14, I-43100 Parma, Italy.						Bagnasco M, 1997, J ALLERGY CLIN IMMUN, V100, P122; 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; *EEC, 1991, III359391EN EEC; Fanta C, 1999, INT ARCH ALLERGY IMM, V120, P218, DOI 10.1159/000024270; Feliziani V, 1995, Allergol Immunopathol (Madr), V23, P224; Giannarini L, 1998, CLIN EXP ALLERGY, V28, P404; GIOVANE AL, 1994, CLIN EXP ALLERGY, V24, P53, DOI 10.1111/j.1365-2222.1994.tb00917.x; Holt PG, 1998, LANCET, V351, P613, DOI 10.1016/S0140-6736(05)78425-7; HOLT PG, 1994, LANCET, V344, P456, DOI 10.1016/S0140-6736(94)91776-0; HOLT PG, 1988, CLIN ALLERGY, V18, P229, DOI 10.1111/j.1365-2222.1988.tb02864.x; Klimek L, 1999, J ALLERGY CLIN IMMUN, V103, P47, DOI 10.1016/S0091-6749(99)70524-5; Malling HJ, 1998, ALLERGY, V53, P933, DOI 10.1111/j.1398-9995.1998.tb03793.x; MALLING HJ, 1993, ALLERGY, V48, P9; Mistrello G, 1996, ALLERGY, V51, P8, DOI 10.1111/j.1398-9995.1996.tb04543.x; MOQBEL R, 1992, CLIN EXP ALLERGY, V22, P265, DOI 10.1111/j.1365-2222.1992.tb03082.x; Nakajima H, 1999, J LEUKOCYTE BIOL, V66, P447; NOVEMBRE E, 1991, RIV ITAL PED, V17, P75; 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; Quirino T, 1996, CLIN EXP ALLERGY, V26, P1253, DOI 10.1046/j.1365-2222.1996.d01-280.x; SABBAH A, 1994, ALLERGY, V49, P309, DOI 10.1111/j.1398-9995.1994.tb02273.x; SCADDING GK, 1986, CLIN ALLERGY, V16, P483, DOI 10.1111/j.1365-2222.1986.tb01983.x; Sensi LG, 1997, CLIN EXP ALLERGY, V27, P270; SVENSSON C, 1990, J ALLERGY CLIN IMMUN, V85, P828, DOI 10.1016/0091-6749(90)90064-B; TARI MG, 1990, ALLERGOL IMMUNOPATH, V18, P277; TROISE C, 1995, J INVEST ALLERG CLIN, V5, P25; VANNIEKERK CH, 1987, CLIN ALLERGY, V17, P507; Vourdas D, 1998, ALLERGY, V53, P662, DOI 10.1111/j.1398-9995.1998.tb03952.x; YMAN L, 1975, DEV BIOL STAND, V1, P51; 1998, ALLERGY S44, V53, P1	31	73	74	0	0	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	DEC	2000	55	12					1142	1147		10.1034/j.1398-9995.2000.00655.x		6	Allergy; Immunology	Allergy; Immunology	375QH	WOS:000165412400005	11117271	
J	Leynadier, F; Herman, D; Vervloet, D; Andre, C				Leynadier, F; Herman, D; Vervloet, D; Andre, C			Specific immunotherapy with a standardized latex extract versus placebo in allergic healthcare workers	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						latex; urticaria; rhinoconjunctivitis; asthma; anaphylactic shock; specific immunotherapy	NATURAL-RUBBER LATEX; CROSS-REACTIVITY; SYSTEMIC REACTIONS; HYPERSENSITIVITY; ANTIBODIES; CHILDREN; ANTIGENS; ASTHMA; BANANA	Background: The prevalence of allergy to natural rubber latex proteins has increased over recent years among healthcare professionals but also in children undergoing multiple operations. Exposure to the antigen mainly occurs through the respiratory mucosa and the percutaneous route. Clinical manifestations range from urticaria to angioedema, rhinoconjunctivitis, bronchial asthma, or anaphylactic shock. Preventive measures have been proposed to reduce the risk of sensitization by using only powder-free or synthetic gloves and latex-free material in operating units, but this is not always possible. Objective: The aim of this study was to investigate the efficacy and safety of specific immunotherapy in sensitized workers. Methods: Seventeen patients with latex skin allergy and rhinitis (9 of whom also had asthma) were included in this randomized, double-blind, placebo-controlled trial (9 in the active group and 8 in the placebo group) for 1 year. Treatment started with a 2-day course of rush immunotherapy in hospital. Treatment efficacy was assessed after 6 and 12 months by means of symptom and medication scores recorded on diary cards. Conjunctival provocation tests were also performed. Results: Patients in the active treatment group had a significantly tower total rhinitis score after 6 (P < .04) and 12 months (P < .05), conjunctivitis score after 6 months (P < .02), and cutaneous score after 12 months (P < .03) than in the placebo group, Asthma symptoms after 6 or 12 months of treatment were not significantly different between the two groups after adjustment for baseline values. The global medication score was markedly decreased in the latex-treated group. A significant difference in conjunctival reactivity was observed in favor of the active group: the number of patients for whom the threshold dose was increased after 12 months of treatment was significantly greater in the active group than in the placebo group (P < .02). Most injections were well tolerated, but several adverse effects, including hypotension, urticaria, wheezing, and pharyngeal edema, were observed. Conclusion: The clinical benefits observed during the present study included a significant improvement of rhinitis, conjunctivitis, and cutaneous symptoms. Immunotherapy also decreased allergen-specific conjunctival reactivity. Latex-specific immunotherapy may allow sensitized personnel to remain at work, but further trials need to be conducted in a larger number of patients.	Stallergenes SA, Sci & Med Dept, F-92183 Antony, France; Hop Rothschild, F-75571 Paris, France; Hop Bichat, Serv Med Interne, Ctr Allergie, F-75877 Paris, France; Hop St Marguerite, Dept Malad Resp, Marseille, France	Andre, C (reprint author), Stallergenes SA, Sci & Med Dept, 6 Rue Alexis de Tocqueville, F-92183 Antony, France.						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Allergy Clin. Immunol.	SEP	2000	106	3					585	590				6	Allergy; Immunology	Allergy; Immunology	356YN	WOS:000089471900025	10984382	
J	Bisgaard, H; Nielsen, KG				Bisgaard, H; Nielsen, KG			Bronchoprotection with a leukotriene receptor antagonist in asthmatic preschool children	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							EXERCISE-INDUCED BRONCHOCONSTRICTION; COLD DRY AIR; CONTROLLED TRIAL; LUNG-FUNCTION; INHALED CORTICOSTEROIDS; FLUTICASONE PROPIONATE; NEBULIZED BUDESONIDE; 14-YEAR-OLD CHILDREN; MONTELUKAST; CHALLENGE	We hypothesized that a leukotriene receptor antagonist (LTRA) could provide bronchoprotection against the cold, dry air-induced response in asthmatic preschool children. In a randomized, double-blind, placebo-controlled crossover study, we examined the effect of the specific LTRA montelukast at 5 mg/d for 2 d on the bronchoconstriction induced by hyperventilation of cold, dry air in 13 asthmatic children 3 to 5 yr old. The bronchoconstriction was measured as the specific airway resistance (sRaw) in a whole-body plethysmograph before and 4 min after challenge with cold, dry air. The repeatability of the bronchoprotection was examined by repeating the placebo-controlled study in six of the 13 children. sRaw increased by an average of 46% (95% confidence interval [CI]: 30 to 63%) after placebo treatment and 17% (95% CI: 3 to 31%) after montelukast (p < 0.01). Eight of the children were receiving regular treatment with budesonide delivered by an inhaler with a spacer in a mean daily dose of 350 mu g, but the bronchoprotection provided by montelukast was independent of concurrent steroid treatment. There was no convincing evidence of failure to respond, and the protective effect of montelukast was consistent upon repeated testing (p = 0.02). We conclude that the LTRA montelukast provided clinically significant bronchoprotection against the effect of hyperventilation of cold dry air in asthmatic children 3 to 5 yr old. The bronchoprotection appeared to be homogeneous among the children, and seemed independent of steroid treatment. This suggests that LTRAs may be of therapeutic use in limiting clinical symptoms of asthma in young children.	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			ARGYROS GJ, 1993, AM REV RESPIR DIS, V147, P1419; 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, 1995, EUR RESPIR J, V8, P2067, DOI 10.1183/09031936.95.08122067; Bisgaard H, 1999, AM J RESP CRIT CARE, V160, P1227; CONNETT GJ, 1993, ARCH DIS CHILD, V69, P351; deBlic J, 1996, J ALLERGY CLIN IMMUN, V98, P14, DOI 10.1016/S0091-6749(96)70221-X; DWORSKI R, 1994, AM J RESP CRIT CARE, V149, P953; Fischer AR, 1997, THORAX, V52, P1074; ILANGOVAN P, 1993, ARCH DIS CHILD, V68, P356; ISRAEL E, 1990, NEW ENGL J MED, V323, P1740, DOI 10.1056/NEJM199012203232505; KANENGISER S, 1994, PEDIATR PULM, V18, P144, DOI 10.1002/ppul.1950180305; Kemp JP, 1998, J PEDIATR-US, V133, P424, DOI 10.1016/S0022-3476(98)70281-1; KLUB G, 1996, EUR RESPIR J, V10, P1599; 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; Knorr B, 1998, JAMA-J AM MED ASSOC, V279, P1181, DOI 10.1001/jama.279.15.1181; Leff JA, 1998, NEW ENGL J MED, V339, P147, DOI 10.1056/NEJM199807163390302; Lofdahl CG, 1999, BRIT MED J, V319, P87; Malmstrom K, 1999, ANN INTERN MED, V130, P487; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; MCFADDEN ER, 1987, CHEST, V91, pS151, DOI 10.1378/chest.91.6.151S; Nielsen KG, 2000, AM J RESP CRIT CARE, V161, P1805; OSHAUGHNESSY KM, 1993, AM REV RESPIR DIS, V147, P1472; Pizzichini E, 1999, EUR RESPIR J, V14, P12, DOI 10.1034/j.1399-3003.1999.14a04.x; Reiss TF, 1997, THORAX, V52, P45; SLY PD, 1990, J ASTHMA, V27, P137, DOI 10.3109/02770909009073314; 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	31	73	78	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.	JUL	2000	162	1					187	190				4	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	333JH	WOS:000088126800031	10903240	
J	Rowe, J; Macaubas, C; Monger, TM; Holt, BJ; Harvey, J; Poolman, JT; Sly, PD; Holt, PG				Rowe, J; Macaubas, C; Monger, TM; Holt, BJ; Harvey, J; Poolman, JT; Sly, PD; Holt, PG			Antigen-specific responses to diphtheria-tetanus-acellular pertussis vaccine in human infants are initially Th2 polarized	INFECTION AND IMMUNITY			English	Article							CELL-MEDIATED-IMMUNITY; BORDETELLA-PERTUSSIS; WHOLE-CELL; EARLY-CHILDHOOD; T-CELLS; ENVIRONMENTAL ALLERGENS; NEONATAL TOLERANCE; HOUSEHOLD EXPOSURE; INHALANT ALLERGEN; CONTROLLED TRIAL	Immune responses to exogenous antigens in infant experimental animals display various degrees of Th2 polarization. Preliminary evidence from small human studies suggest a similar age-dependent response pattern to vaccines, but detailed investigations on vaccine immunity during infancy have not yet been undertaken. We report below the results of a comprehensive prospective study on responses to the tetanus component of the diphtheria, tetanus, acellular pertussis (DTaP) vaccine in a cohort of 55 healthy children, employing peripheral blood mononuclear cells (PBMC) collected at the 2-, 4-, and 6-month vaccinations and at 12 months. Antigen-specific production of interleukin-4 (IL-4), IL-5, IL-6, IL-9, IL-10, IL-13, and gamma interferon (IFN-gamma) was determined at each sample point, in parallel with polyclonal (phytohemagglutinin PHA-induced) cytokine responses. Our results indicate early and persistent Th2 responses to the vaccine, in contrast to a more delayed and transient pattern of IFN-gamma production, This initial disparity between the Th1 and Th2 components of the vaccine response was mirrored by patterns of polyclonally induced cytokine production, suggesting that the delayed maturation of the Th1 component of the vaccine response during infancy is secondary to developmental processes occurring within the overall Th cell system.	TVW Telethon Inst Child Hlth Res, Div Cell Biol, W Perth, WA 6872, Australia; Univ Western Australia, Dept Microbiol, Perth, WA 6009, Australia; Univ Western Australia, Dept Paediat, Perth, WA 6009, Australia; SmithKline Beecham Pharmaceut, Rixensart, Belgium	Holt, PG (reprint author), TVW Telethon Inst Child Hlth Res, Div Cell Biol, POB 855, W Perth, WA 6872, Australia.		Sly, Peter/F-1486-2010; Holt, Patrick/H-1548-2011	Sly, Peter/0000-0001-6305-2201; Holt, Patrick/0000-0003-1193-0935			*AD HOC STUD GROUP, 1988, LANCET, V31, P955; Ausiello CM, 1999, INFECT IMMUN, V67, P4064; Ausiello CM, 1997, INFECT IMMUN, V65, P2168; Barrios C, 1996, EUR J IMMUNOL, V26, P2666, DOI 10.1002/eji.1830261118; Barrios C, 1996, EUR J IMMUNOL, V26, P1489, DOI 10.1002/eji.1830260713; Chen NX, 1995, TRANSPLANTATION, V60, P1187; CHEN NX, 1995, TRANSPLANTATION, V59, P933, DOI 10.1097/00007890-199504150-00002; Cherry JD, 1998, VACCINE, V16, P1901, DOI 10.1016/S0264-410X(98)00226-6; Cooper PJ, 1998, J INFECT DIS, V178, P1133, DOI 10.1086/515661; ELGHAZALI GEB, 1993, EUR J IMMUNOL, V23, P2740, DOI 10.1002/eji.1830231103; Greco D, 1996, NEW ENGL J MED, V334, P341, DOI 10.1056/NEJM199602083340601; Gustafsson L, 1996, NEW ENGL J MED, V334, P349, DOI 10.1056/NEJM199602083340602; Holt PG, 1997, CURR OPIN IMMUNOL, V9, P782, DOI 10.1016/S0952-7915(97)80178-1; Macaubas C, 1999, CLIN EXP ALLERGY, V29, P1223; Mahon BP, 1996, INFECT IMMUN, V64, P5295; Marchant A, 1999, J IMMUNOL, V163, P2249; MILLS KHG, 1993, INFECT IMMUN, V61, P399; Prescott SL, 1998, J IMMUNOL, V160, P4730; PRESCOTT SL, 1999, LANCET, V353, P96; Ridge JP, 1996, SCIENCE, V271, P1723, DOI 10.1126/science.271.5256.1723; Ryan M, 1998, IMMUNOLOGY, V93, P1; Schmitt HJ, 1996, JAMA-J AM MED ASSOC, V275, P37, DOI 10.1001/jama.275.1.37; Singh RR, 1996, J EXP MED, V183, P1613, DOI 10.1084/jem.183.4.1613; Storsaeter J, 1998, VACCINE, V16, P1907, DOI 10.1016/S0264-410X(98)00227-8; UPHAM JW, 1995, CLIN EXP ALLERGY, V25, P634, DOI 10.1111/j.1365-2222.1995.tb01111.x; WEGMANN TG, 1993, IMMUNOL TODAY, V14, P353, DOI 10.1016/0167-5699(93)90235-D; Yabuhara A, 1997, CLIN EXP ALLERGY, V27, P1261; Zepp F, 1996, INFECT IMMUN, V64, P4078	28	73	74	0	0	AMER SOC MICROBIOLOGY	WASHINGTON	1752 N ST NW, WASHINGTON, DC 20036-2904 USA	0019-9567			INFECT IMMUN	Infect. Immun.	JUL	2000	68	7					3873	3877		10.1128/IAI.68.7.3873-3877.2000		5	Immunology; Infectious Diseases	Immunology; Infectious Diseases	326AT	WOS:000087710200012	10858197	
J	Peden, DB				Peden, DB			Development of atopy and asthma: Candidate environmental influences and important periods of exposure	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; atopy; immunoglobulin E (IgE); immunoglobulin G (IgG); T-helper cell type 1 (Th1); T-helper cell type 2 (Th2)	INTERFERON-GAMMA PRODUCTION; SERUM IGE LEVELS; DIESEL-EXHAUST; IN-VIVO; ALLERGIC SENSITIZATION; ADJUVANT ACTIVITY; IMMUNE-RESPONSES; RISK FACTOR; MICE; ASSOCIATION	Atopy is a major risk factor for the development of asthma. immune processes that lead to the development of antigen-specific IgE are essential to the development of atopy. This review examines the immune processes that are candidate targets for modulation by environmental agents; environmental and lifestyle factors that have been suggested as modulators of the development of atopy; and the impact of known environmental agents on atopic processes in the airway. The most important periods of immune development with regard to expression of atopy are likely during gestation and early childhood. A better understanding of which environmental agents are important, as well as the period of life during which these agents may exert an important effect, is essential to devising rational environmental avoidance strategies for at-risk populations.	Univ N Carolina, Sch Med, Ctr Environm Med & Lung Biol, Chapel Hill, NC 27599 USA; Univ N Carolina, Sch Med, Dept Pediat, Chapel Hill, NC 27599 USA	Peden, DB (reprint author), Univ N Carolina, Sch Med, Ctr Environm Med & Lung Biol, 104 Mason Farm Rd,CB 7310, Chapel Hill, NC 27599 USA.						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Health Perspect.	JUN	2000	108			3			475	482		10.2307/3454539		8	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	326RK	WOS:000087748400018	10852847	
J	Eldridge, MW; Peden, DB				Eldridge, MW; Peden, DB			Allergen provocation augments endotoxin-induced nasal inflammation in subjects with atopic asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						endotoxin; dust mite; antigen; asthma; eosinophils; neutrophils; allergy	AIR-POLLUTION; OZONE; MORTALITY; CHALLENGE; RESPONSES; EXPOSURE; WORKERS; HEALTH	Background: Recent epidemiologic and in vivo studies have suggested that inhaled endotoxin plays an important role in asthma pathogenesis. Objective: The present study examines the effect of nasal allergen provocation on subsequent endotoxin challenge in subjects with atopic asthma. Methods: By using a split-nose randomized crossover design, individual nares of 12 asthmatic subjects underwent challenge and lavage as follows, Immediately after a baseline nasal lavage, one nares received normal saline, and the other received dust mite antigen, Four hours later both nares were exposed to either saline or endotoxin. Dust mite antigen (Dermatophagoides farinae) and endotoxin (Escherichia roll 026:B6) doses were 100 AU and 1000 ng, respectively. Postchallenge lavages were done at 8 and 24 hours after the initial challenge. The subjects then returned a minimum of 3 weeks later for crossover to the study arm. Nasal lavage fluid was analyzed for total and differential cell counts, IL-8, IL-6, intercellular adhesion molecule 1, GM-CSF, eosinophil cationic protein, myeloperoxidase, and soluble CD14. Results: A significant increase in the total inflammatory cell count was seen at 8 hours for the dust mite/endotoxin exposure compared with the saline/saline and saline/endotoxin exposures. Differential cell counts revealed a similar neutrophilic and eosinophilic inflammation for the dust mite/endotoxin exposure at 8 hours. Conclusions: These data demonstrate an interaction between allergen and endotoxin exposure in asthmatic subjects, suggesting that a prior allergen challenge significantly augments the endotoxin-induced inflammation. Moreover, these data provide further evidence that concomitant exposure to allergen and endotoxin may he an important factor in asthma pathogenesis.	Univ N Carolina, Sch Med, Ctr Environm Med & Lung Biol, Chapel Hill, NC 27599 USA; Univ N Carolina, Sch Med, Dept Pediat, Div Pulm Med & Allergy, Chapel Hill, NC 27599 USA; Univ N Carolina, Sch Med, Gen Clin Res Ctr, Chapel Hill, NC 27599 USA; Natl Inst Environm Hlth Sci, Chapel Hill, NC USA	Eldridge, MW (reprint author), Univ N Carolina, Sch Med, Ctr Environm Med & Lung Biol, 104 Mason Farm Rd,CB 7310, Chapel Hill, NC 27599 USA.				NHLBI NIH HHS [1RO1HL62624-01]; NIEHS NIH HHS [N01-ES-35356]		ATS, 1987, AM REV RESPIR DIS, V136, P1285, DOI 10.1164/ajrccm/136.5.1285; Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; BASHA MA, 1994, CHEST, V106, P1757, DOI 10.1378/chest.106.6.1757; COCKCROFT DW, 1987, ANN ALLERGY, V59, P89; Cook DG, 1997, THORAX, V52, P1081; DONHAM K, 1989, BRIT J IND MED, V46, P31; Dubin W, 1996, AM J PHYSIOL-LUNG C, V270, pL736; HALLSWORTH M, 1994, EUR RESPIR J, V44, P1096; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; McFadden ER, 1997, ANN INTERN MED, V127, P142; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; MICHEL O, 1989, J APPL PHYSIOL, V66, P1059; Michelson PH, 1999, OTOLARYNG HEAD NECK, V120, P225, DOI 10.1016/S0194-5998(99)70411-0; Peden DB, 1996, REGUL TOXICOL PHARM, V24, pS76, DOI 10.1006/rtph.1996.0081; Peden DB, 1997, ALLERGY, V52, P37; PEDEN DB, 1995, AM J RESP CRIT CARE, V151, P1336; Peden DB, 1999, J ALLERGY CLIN IMMUN, V104, P388, DOI 10.1016/S0091-6749(99)70383-0; Peden DB, 1996, OTOLARYNG HEAD NECK, V114, P242, DOI 10.1016/S0194-5998(96)70175-4; Peden DB, 1997, ALLERGY S38, V52, P57; RYLANDER R, 1985, AM REV RESPIR DIS, V131, P209; Saitou M, 1997, Fukushima J Med Sci, V43, P75; SALOMONSSON P, 1992, AM REV RESPIR DIS, V146, P1535; Scannell C, 1996, AM J RESP CRIT CARE, V154, P24; STERK PJ, 1993, EUR RESPIR J, V6, P53, DOI 10.1183/09041950.053s1693; Sunyer J., 1997, European Respiratory Journal, V10, P2490, DOI 10.1183/09031936.97.10112490; Virchow JC, 1998, EUR RESPIR J, V11, P317, DOI 10.1183/09031936.98.11020317; WEISS KB, 1990, JAMA-J AM MED ASSOC, V264, P1683, DOI 10.1001/jama.264.13.1683	27	73	75	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.	MAR	2000	105	3					475	481		10.1067/mai.2000.104552		7	Allergy; Immunology	Allergy; Immunology	347UC	WOS:000088946700012	10719296	
J	Braun, JM; Sathyanarayana, S; Hauser, R				Braun, Joseph M.; Sathyanarayana, Sheela; Hauser, Russ			Phthalate exposure and children's health	CURRENT OPINION IN PEDIATRICS			English	Review						children; endocrine disruption; epidemiology; phthalates	IN-UTERO EXPOSURE; BODY TOPICAL APPLICATION; PERSONAL CARE PRODUCTS; SCHOOL-AGE-CHILDREN; NEW-YORK-CITY; URINARY CONCENTRATIONS; PRENATAL EXPOSURE; BISPHENOL-A; DIETHYLHEXYL PHTHALATE; DI(2-ETHYLHEXYL)PHTHALATE DEHP	Purpose of review Phthalates are multifunctional chemicals used in personal care products, medications, and plastics. We reviewed the epidemiological literature examining the relationship between early life phthalate exposure and pediatric health outcomes. Recent findings Five studies from Asia, Europe, and the United States suggest that childhood exposure to di-2-ethylhexyl phthalate (DEHP) and butylbenzyl phthalate (BBzP) may increase the risk of allergic diseases including asthma and eczema. Six studies from four different prospective cohorts report that gestational BBzP, DEHP, di-butyl phthalate (DBP), and di-ethyl phthalate (DEP) exposures are associated with alterations in infant/toddler physical development as well as parent-reported externalizing, internalizing, and autistic-like child behavior. However, there are inconsistencies related to the specific phthalates and behavioral domains. Two small studies report shorter anogenital distance among male infants with higher gestational phthalate exposure. Summary Several epidemiological studies suggest fetal and childhood exposure to some phthalates may perturb normal development, with several studies consistently reporting increased risk of allergic diseases with DEHP and BBzP exposure. Although anticipatory guidance is not evidence-based at this time, providers can counsel concerned patients to reduce phthalate exposures in order to protect the developing fetus and child from potential adverse health outcomes.	[Braun, Joseph M.] Brown Univ, Dept Epidemiol, Providence, RI 02912 USA; [Sathyanarayana, Sheela] Univ Washington, Dept Pediat, Seattle Childrens Res Inst, Seattle, WA 98195 USA; [Hauser, Russ] Harvard Univ, Massachusetts Gen Hosp, Sch Med,Fertil Ctr, Dept Obstet & Gynecol,Div Reprod Endocrinol & Inf, Boston, MA USA; [Hauser, Russ] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA; [Hauser, Russ] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA	Braun, JM (reprint author), Brown Univ, Dept Epidemiol, Box G-S121-2, Providence, RI 02912 USA.	joseph_braun_1@brown.edu	Braun, Joseph/H-8649-2014		NIEHS [K99 ES020346, R01 ES021357, R01 ES009718]	J.M.B. was supported by NIEHS grants K99 ES020346 and R01 ES021357. R. H. is supported by NIEHS grant R01 ES009718.	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OPIN. PEDIATR.	APR	2013	25	2					247	254		10.1097/MOP.0b013e32835e1eb6		8	Pediatrics	Pediatrics	105YV	WOS:000316109500015	23429708	
J	Donovan, GH; Butry, DT; Michael, YL; Prestemon, JP; Liebhold, AM; Gatziolis, D; Mao, MY				Donovan, Geoffrey H.; Butry, David T.; Michael, Yvonne L.; Prestemon, Jeffrey P.; Liebhold, Andrew M.; Gatziolis, Demetrios; Mao, Megan Y.			The Relationship Between Trees and Human Health Evidence from the Spread of the Emerald Ash Borer	AMERICAN JOURNAL OF PREVENTIVE MEDICINE			English	Article							PHYSICAL-ACTIVITY; STREET TREES; GREEN SPACE; ASTHMA; INEQUALITIES; MORTALITY; EXPOSURE; DISEASE; FOREST; AREAS	Background: Several recent studies have identified a relationship between the natural environment and improved health outcomes. However, for practical reasons, most have been observational, cross-sectional studies. Purpose: A natural experiment, which provides stronger evidence of causality, was used to test whether a major change to the natural environment-the loss of 100 million trees to the emerald ash borer, an invasive forest pest-has influenced mortality related to cardiovascular and lower-respiratory diseases. Methods: Two fixed-effects regression models were used to estimate the relationship between emerald ash borer presence and county-level mortality from 1990 to 2007 in 15 U. S. states, while controlling for a wide range of demographic covariates. Data were collected from 1990 to 2007, and the analyses were conducted in 2011 and 2012. Results: There was an increase in mortality related to cardiovascular and lower-respiratory-tract illness in counties infested with the emerald ash borer. The magnitude of this effect was greater as infestation progressed and in counties with above-average median household income. Across the 15 states in the study area, the borer was associated with an additional 6113 deaths related to illness of the lower respiratory system, and 15,080 cardiovascular-related deaths. Conclusions: Results suggest that loss of trees to the emerald ash borer increased mortality related to cardiovascular and lower-respiratory-tract illness. This finding adds to the growing evidence that the natural environment provides major public health benefits. (Am J Prev Med 2013; 44(2): 139-145) Published by Elsevier Inc. on behalf of American Journal of Preventive Medicine	[Donovan, Geoffrey H.; Gatziolis, Demetrios; Mao, Megan Y.] US Forest Serv, USDA, PNW Res Stn, Portland, OR 97205 USA; [Butry, David T.] NIST, Gaithersburg, MD 20899 USA; [Michael, Yvonne L.] Drexel Univ, Dept Epidemiol & Biostat, Philadelphia, PA 19104 USA; [Prestemon, Jeffrey P.] US Forest Serv, USDA, So Res Stn, Res Triangle Pk, NC USA; [Liebhold, Andrew M.] US Forest Serv, No Res Stn, USDA, Morgantown, WV USA	Donovan, GH (reprint author), US Forest Serv, USDA, PNW Res Stn, 620 SW Main,Suite 400, Portland, OR 97205 USA.	gdonovan@fs.fed.us	Liebhold, Andrew/C-1423-2008	Liebhold, Andrew/0000-0001-7427-6534			ANGRIST JD, 1995, J AM STAT ASSOC, V90, P431, DOI 10.2307/2291054; Baum CF, 2001, STATA J, V1, P101; CDC, 2009, LEAD CAUS DEATH; Dadvand P., 2012, ENVIRON INT, V44, P3; Donovan GH, 2011, HEALTH PLACE, V17, P390, DOI 10.1016/j.healthplace.2010.11.004; Donovan GH, 2010, LANDSCAPE URBAN PLAN, V94, P77, DOI 10.1016/j.landurbplan.2009.07.019; Donovan GH, 2009, ENERG BUILDINGS, V41, P662, DOI 10.1016/j.enbuild.2009.01.002; Everson-Rose SA, 2005, ANNU REV PUBL HEALTH, V26, P469, DOI 10.1146/annurev.publhealth.26.021304.144542; Feng J, 2012, PLOS ONE, V7, DOI 10.1371/journal.pone.0033385; Frumkin Howard, 2001, American Journal of Preventive Medicine, V20, P234, DOI 10.1016/S0749-3797(00)00317-2; Fry J. 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J. Prev. Med.	FEB	2013	44	2					139	145		10.1016/j.amepre.2012.09.066		7	Public, Environmental & Occupational Health; Medicine, General & Internal	Public, Environmental & Occupational Health; General & Internal Medicine	077ZJ	WOS:000314067600009	23332329	
J	Huffman, JA; Prenni, AJ; DeMott, PJ; Pohlker, C; Mason, RH; Robinson, NH; Frohlich-Nowoisky, J; Tobo, Y; Despres, VR; Garcia, E; Gochis, DJ; Harris, E; Mueller-Germann, I; Ruzene, C; Schmer, B; Sinha, B; Day, DA; Andreae, MO; Jimenez, JL; Gallagher, M; Kreidenweis, SM; Bertram, AK; Poschl, U				Huffman, J. A.; Prenni, A. J.; DeMott, P. J.; Poehlker, C.; Mason, R. H.; Robinson, N. H.; Froehlich-Nowoisky, J.; Tobo, Y.; Despres, V. R.; Garcia, E.; Gochis, D. J.; Harris, E.; Mueller-Germann, I.; Ruzene, C.; Schmer, B.; Sinha, B.; Day, D. A.; Andreae, M. O.; Jimenez, J. L.; Gallagher, M.; Kreidenweis, S. M.; Bertram, A. K.; Poeschl, U.			High concentrations of biological aerosol particles and ice nuclei during and after rain	ATMOSPHERIC CHEMISTRY AND PHYSICS			English	Article							NUCLEATION-ACTIVE BACTERIA; MINERAL DUST PARTICLES; FUNGAL SPORES; PSEUDOMONAS-SYRINGAE; ATMOSPHERIC AEROSOLS; THUNDERSTORM ASTHMA; SIZE DISTRIBUTIONS; AIRBORNE BACTERIA; SPLASH DISPERSAL; UV-APS	Bioaerosols are relevant for public health and may play an important role in the climate system, but their atmospheric abundance, properties, and sources are not well understood. Here we show that the concentration of airborne biological particles in a North American forest ecosystem increases significantly during rain and that bioparticles are closely correlated with atmospheric ice nuclei (IN). The greatest increase of bioparticles and IN occurred in the size range of 2-6 mu m, which is characteristic for bacterial aggregates and fungal spores. By DNA analysis we found high diversities of airborne bacteria and fungi, including groups containing human and plant pathogens (mildew, smut and rust fungi, molds, Enterobacteriaceae, Pseudomonadaceae). In addition to detecting known bacterial and fungal IN (Pseudomonas sp., Fusarium sporotrichioides), we discovered two species of IN-active fungi that were not previously known as biological ice nucleators (Isaria farinosa and Acremonium implicatum). Our findings suggest that atmospheric bioaerosols, IN, and rainfall are more tightly coupled than previously assumed.	[Huffman, J. A.] Univ Denver, Dept Chem & Biochem, Denver, CO 80208 USA; [Huffman, J. A.; Poehlker, C.; Froehlich-Nowoisky, J.; Harris, E.; Mueller-Germann, I.; Ruzene, C.; Schmer, B.; Sinha, B.; Andreae, M. O.; Poeschl, U.] Max Planck Inst Chem, D-55020 Mainz, Germany; [Prenni, A. J.; DeMott, P. J.; Tobo, Y.; Garcia, E.; Kreidenweis, S. M.] Colorado State Univ, Dept Atmospher Sci, Ft Collins, CO 80523 USA; [Mason, R. H.; Bertram, A. K.] Univ British Columbia, Dept Chem, Vancouver, BC V6T 1Z1, Canada; [Robinson, N. H.; Gallagher, M.] Univ Manchester, Ctr Atmospher Sci, Manchester M13 9PL, Lancs, England; [Despres, V. R.] Johannes Gutenberg Univ Mainz, Inst Gen Bot, D-55099 Mainz, Germany; [Gochis, D. J.] Natl Ctr Atmospher Res, Boulder, CO 80307 USA; [Sinha, B.] IISER Mohali, Dept Earth & Environm Sci, Sect 81, Sas Nagar 140306, India; [Day, D. A.; Jimenez, J. L.] Univ Colorado, Cooperat Inst Res Environm Sci, Boulder, CO 80309 USA; [Day, D. A.; Jimenez, J. L.] Univ Colorado, Dept Chem & Biochem, Boulder, CO 80309 USA	Huffman, JA (reprint author), Univ Denver, Dept Chem & Biochem, 2190 E Illif Ave, Denver, CO 80208 USA.	alex.huffman@du.edu; anthony.prenni@colostate.edu; bertram@chem.ubc.ca; u.poschl@mpic.de	; Tobo, Yutaka/D-9158-2013; Huffman, J. Alex/A-7449-2010; Andreae, Meinrat/B-1068-2008; Robinson, Niall/I-8063-2013; Jimenez, Jose/A-5294-2008; Sinha, Baerbel/H-1250-2012; Poschl, Ulrich/A-6263-2010; Robinson, Niall/B-7865-2013; Froehlich, Janine/D-6227-2015; Mason, Ryan/K-1450-2015; Pohlker, Christopher/S-5207-2016; Kreidenweis, Sonia/E-5993-2011	Gallagher, Martin/0000-0002-4968-6088; Harris, Eliza/0000-0002-7102-8305; Tobo, Yutaka/0000-0003-0951-3315; Huffman, J. Alex/0000-0002-5363-9516; Andreae, Meinrat/0000-0003-1968-7925; Jimenez, Jose/0000-0001-6203-1847; Sinha, Baerbel/0000-0001-8614-7473; Poschl, Ulrich/0000-0003-1412-3557; Froehlich, Janine/0000-0002-1278-0054; Mason, Ryan/0000-0003-2942-3608; Kreidenweis, Sonia/0000-0002-2561-2914	ETBC (Emerging Topics in Biogeochemical Cycles); University of Colorado; Colorado State University; Penn State University [NSF ATM-0919189]; University of Denver; Max Planck Society; Max Planck Graduate Center; Johannes Gutenberg University Mainz; Geocycles Cluster Mainz (LEC Rheinland-Pfalz); German Research Foundation [DFG PO1013/5-1, FOR 1525 INUIT]; National Sciences and Engineering Research Council of Canada; Japanese Society for the Promotion of Science (JSPS); NSF [ATM-0919042, AGS-1036028]; U.S. DOE (BER, ASR program) [DE-SC0006035]	The BEACHON-RoMBAS campaign was partially supported by an ETBC (Emerging Topics in Biogeochemical Cycles) grant to the National Center for Atmospheric Research (NCAR), the University of Colorado, Colorado State University, and Penn State University (NSF ATM-0919189). J. A. Huffman acknowledges internal faculty funding from the University of Denver. The Mainz team acknowledges financial support from the Max Planck Society (MPG), the Max Planck Graduate Center with the Johannes Gutenberg University Mainz (MPGC), the Geocycles Cluster Mainz (LEC Rheinland-Pfalz), and the German Research Foundation (DFG PO1013/5-1, FOR 1525 INUIT). R. H. Mason and A. K. Bertram acknowledge financial support from the the National Sciences and Engineering Research Council of Canada. Y. Tobo acknowledges the Japanese Society for the Promotion of Science (JSPS) Postdoctoral Fellowships for Research Abroad. CFDC measurements and analysis were funded by NSF (ATM-0919042, AGS-1036028). J. L. Jimenez and D. A. Day acknowledge U.S. DOE (BER, ASR program) DE-SC0006035. N. H. Robinson and M. Gallagher thank Defence Science and Technology Laboratory (DSTL) for loan of WIBS-4 instrument. The authors wish to thank: the USFS, NCAR, R. Oakes, A. Guenther, and J. 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Phys.		2013	13	13					6151	6164		10.5194/acp-13-6151-2013		14	Meteorology & Atmospheric Sciences	Meteorology & Atmospheric Sciences	182TL	WOS:000321767200003		
J	Bacharier, LB; Cohen, R; Schweiger, T; Yin-DeClue, H; Christie, C; Zheng, J; Schechtman, KB; Strunk, RC; Castro, M				Bacharier, Leonard B.; Cohen, Rebecca; Schweiger, Toni; Yin-DeClue, Huiquing; Christie, Chandrika; Zheng, Jie; Schechtman, Kenneth B.; Strunk, Robert C.; Castro, Mario			Determinants of asthma after severe respiratory syncytial virus bronchiolitis	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Bronchiolitis; respiratory syncytial virus; asthma; prospective cohort; CCL5	LONGITUDINAL BIRTH-COHORT; DAY-CARE ATTENDANCE; EARLY-CHILDHOOD; EARLY-LIFE; RSV BRONCHIOLITIS; ALLERGIC SENSITIZATION; PARENTAL HISTORY; DIAGNOSED ASTHMA; YOUNG-CHILDREN; 1ST YEAR	Background: The development of asthma after respiratory syncytial virus (RSV) bronchiolitis has been demonstrated in case-control studies, although the determinants of post-RSV asthma remain undefined. Objectives: We sought to evaluate the potential determinants of physician-diagnosed asthma after severe RSV bronchiolitis during infancy. Methods: We enrolled 206 children during an initial episode of severe RSV bronchiolitis at 12 months of age or less in a prospective cohort study and followed these children for up to 6 years. In a subset of 81 children, we analyzed CCL5 (RANTES) mRNA expression in upper airway epithelial cells. Results: Forty-eight percent of children had physician-diagnosed asthma before the seventh birthday. Independent determinants significantly associated with increased risk for physician-diagnosed asthma by the seventh birthday included maternal asthma (odds ratio [OR], 5.2; 95% CI, 1.7-15.9; P = .004), exposure to high levels of dog allergen (OR, 3.2; 95% CI, 1.3-7.7; P = .012), aeroallergen sensitivity at age 3 years (OR, 10.7; 95% CI, 2.1-55.0; P = .005), recurrent wheezing during the first 3 years of life (OR, 7.3; 95% CI, 1.2-43.3; P = .028), and CCL5 expression in nasal epithelia during acute RSV infection (OR, 3.8; 95% CI, 1.2-2.4; P < .001). White children (OR, 0.19; 95% CI, 0.04-0.93; P = .041) and children attending day care (OR, 0.18; 95% CI, 0.04-0.84; P = .029) had a decreased risk of physician-diagnosed asthma. Conclusions: Approximately 50% of children who experience severe RSV bronchiolitis have a subsequent asthma diagnosis. The presence of increased CCL5 levels in nasal epithelia at the time of bronchiolitis or the development of allergic sensitization by age 3 years are associated with increased likelihood of subsequent asthma. (J Allergy Clin Immunol 2012;130:91-100.)	[Cohen, Rebecca; Schweiger, Toni; Yin-DeClue, Huiquing; Christie, Chandrika; Castro, Mario] Washington Univ, Sch Med, Dept Internal Med, Div Pulm & Crit Care Med, St Louis, MO 63110 USA; [Bacharier, Leonard B.; Strunk, Robert C.] Washington Univ, Sch Med, Dept Pediat, Div Pediat Allergy Immunol & Pulm Med, St Louis, MO 63110 USA; [Zheng, Jie; Schechtman, Kenneth B.] Washington Univ, Sch Med, Dept Biostat, St Louis, MO 63110 USA; [Zheng, Jie; Schechtman, Kenneth B.] St Louis Childrens Hosp, St Louis, MO 63178 USA	Castro, M (reprint author), Washington Univ, Sch Med, Dept Internal Med, Div Pulm & Crit Care Med, Campus Box 8052,660 S Euclid, St Louis, MO 63110 USA.	castrom@wustl.edu		ZHENG, JIE/0000-0003-4958-2091	National Institutes of Health [HL 61895]; Asthmatx; Amgen; Ception/Cephalon; Genentech; MedImmune; Merck; National Institutes of Health; Novartis; GlaxoSmithKline	Supported by National Institutes of Health grant HL 61895.; Disclosure of potential conflict of interest: L. B. Bacharier is on the advisory board for AstraZeneca, has received honoraria from GlaxoSmithKline, and is on the advisory board and has received honoraria from Merck. M. Castro is a consultant and speaker for Asthmatx; is on the advisory board and is a speaker for Genentech; is a speaker for AstraZeneca, Merck, and GlaxoSmithKline; has received research support from Asthmatx, Amgen, Ception/Cephalon, Genentech, MedImmune, Merck, the National Institutes of Health, Novartis, and GlaxoSmithKline; and has received royalties from Elsevier. The rest of the authors declare that they have no relevant conflicts of interest.	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Allergy Clin. Immunol.	JUL	2012	130	1					91	+		10.1016/j.jaci.2012.02.010		13	Allergy; Immunology	Allergy; Immunology	977GN	WOS:000306644800012	22444510	
J	Dimitroulopoulou, C				Dimitroulopoulou, C.			Ventilation in European dwellings: A review	BUILDING AND ENVIRONMENT			English	Review						Ventilation; Rates; Regulations; Health	VOLATILE ORGANIC-COMPOUNDS; INDOOR AIR-QUALITY; HOUSE-DUST; BUILDING CHARACTERISTICS; MECHANICAL VENTILATION; ALLERGIC SENSITIZATION; CATALAN DWELLINGS; YOUNG-CHILDREN; MITE ALLERGEN; LONG-TERM	Adequate ventilation is essential for the health and comfort of building occupants. This review examines, first of all, why residential ventilation is an issue of concern in Europe and how is related to the human health. A review of the current status of residential ventilation standards and regulations in Europe is also provided, as a reference. Finally, a review of measurements of ventilation rates in European dwellings is provided, where the compatibility with the European standards/regulations is examined. The review shows that ventilation is increasingly becoming recognised as an important component of a healthy dwelling. Ventilation requirements receive major attention in building regulations, across Europe. However, ventilation measurements across Europe show that ventilation is in practice often poor, resulting in reduced ventilation rates (lower than 0.5 h(-1), which is currently a standard in many European countries), increased concentrations of indoor pollutants and hence exposure to health risk. Surveys showed that although occupants generally think that ventilation is important, their understanding of the ventilation systems in their own houses is low, resulting to under-ventilated homes. (C) 2011 Elsevier Ltd. All rights reserved.	[Dimitroulopoulou, C.] Univ W Macedonia, Dept Mech Engn, Sialvera, Kozani, Greece; [Dimitroulopoulou, C.] Univ W Macedonia, Dept Mech Engn, Bakola, Kozani, Greece	Dimitroulopoulou, C (reprint author), Univ W Macedonia, Dept Mech Engn, Sialvera, Kozani, Greece.	sanidimi@gmail.com			European Union	This work was carried out as part of the EPHECT project. EPHECT is a European collaborative action, which has received funding from the European Union, in the framework of the Health Programme. The author would like to thank Prof. Peder Wolkoff, NCRWE, Denmark, for his constructive comments and for providing material for this review and Prof. Eduardo de Oliveira Fernandes, IDMEC-FEUP, Portugal, for his valuable comments.	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Environ.	JAN	2012	47						109	125		10.1016/j.buildenv.2011.07.016		17	Construction & Building Technology; Engineering, Environmental; Engineering, Civil	Construction & Building Technology; Engineering	830MW	WOS:000295662100014		
J	Kuhlthau, KA; Bloom, S; Van Cleave, J; Knapp, AA; Romm, D; Klatka, K; Homer, CJ; Newacheck, PW; Perrin, JM				Kuhlthau, Karen A.; Bloom, Sheila; Van Cleave, Jeanne; Knapp, Alixandra A.; Romm, Diane; Klatka, Kirsten; Homer, Charles J.; Newacheck, Paul W.; Perrin, James M.			Evidence for Family-Centered Care for Children With Special Health Care Needs: A Systematic Review	ACADEMIC PEDIATRICS			English	Review						children with special health care needs; family-centered care	MEDICAL HOME; NATIONAL-SURVEY; MENTAL-HEALTH; ASTHMA; SERVICES; OUTCOMES; SATISFACTION; PHYSICIANS; INSURANCE; EDUCATION	OBJECTIVE: Family-centered care (FCC) has received widespread endorsement for use in care in the United States. In this study, we conducted a systematic review of evidence for FCC focusing specifically on family-provider partnership as the activity that constitutes FCC. METHODS: We found and reviewed articles from the medical, nursing, psychology, and sociology literature spanning 1986 to 2010. We also reviewed articles obtained through related references and through recommendations from key informants. Four sets of terms were used to search, including FCC, child/adolescent, children with special health care needs (CSHCN, defined broadly or by condition), and a relevant outcome. RESULTS: Twenty-four studies met the review criteria. Eight were cross-sectional studies from the National Survey of Children With Special Health Care Needs, and 7 were reports of randomized, controlled trials. Of the 24 articles reviewed, 13 examined populations of CSHCN or similar populations, 6 examined children with asthma, and the remaining studied children with other specific conditions. We found positive associations of FCC with improvements in efficient use of services, health status, satisfaction, access to care, communication, systems of care, family functioning, and family impact/cost. There was little available evidence, however, for some outcomes, including cost and transition. CONCLUSIONS: The available evidence suggests that FCC is associated with improved outcomes for CSHCN. With positive findings for most of the studies reviewed here and the compelling arguments for FCC, we recommend the use of this approach by individuals and organizations.	[Kuhlthau, Karen A.; Bloom, Sheila; Van Cleave, Jeanne; Knapp, Alixandra A.; Romm, Diane; Klatka, Kirsten; Perrin, James M.] MassGen Hosp Children, Ctr Child & Adolescent Hlth Policy, Boston, MA 02114 USA; [Kuhlthau, Karen A.; Van Cleave, Jeanne; Perrin, James M.] Harvard Univ, Sch Med, Boston, MA USA; [Homer, Charles J.] Natl Initiat Child Healthcare Qual, Boston, MA USA; [Newacheck, Paul W.] Univ Calif San Francisco, Inst Hlth Policy Studies, San Francisco, CA 94143 USA; [Newacheck, Paul W.] Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA	Kuhlthau, KA (reprint author), MassGen Hosp Children, Ctr Child & Adolescent Hlth Policy, 50 Staniford St,Ste 901, Boston, MA 02114 USA.	kkuhlthau@partners.org			Maternal and Child Health Bureau [5 U53MC04473-03-00]	We thank our funders at the Maternal and Child Health Bureau, cooperative agreement 5 U53MC04473-03-00, members of our advisory group, and Jill Hurson.	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Pediatr.	MAR-APR	2011	11	2					136	143				8	Pediatrics	Pediatrics	736WO	WOS:000288525900012	21396616	
J	Wilson, KM; Klein, JD; Blumkin, AK; Gottlieb, M; Winickoff, JP				Wilson, Karen M.; Klein, Jonathan D.; Blumkin, Aaron K.; Gottlieb, Mark; Winickoff, Jonathan P.			Tobacco-Smoke Exposure in Children Who Live in Multiunit Housing	PEDIATRICS			English	Article						secondhand smoke; passive smoking; environmental tobacco smoke; multiunit housing; apartment	SECONDHAND SMOKE; THIRDHAND-SMOKE; UNITED-STATES; US CHILDREN; NICOTINE; ASSOCIATION; ASTHMA; HOME; ADOLESCENTS; DUST	OBJECTIVE: There is no safe level of secondhand tobacco-smoke exposure, and no previous studies have explored multiunit housing as a potential contributor to secondhand tobacco-smoke exposure in children. We hypothesized that children who live in apartments have higher cotinine levels than those who live in detached homes, when controlling for demographics. METHODS: We analyzed data from the 2001-2006 National Health and Nutrition Examination Survey. The housing types we included in our study were detached houses (including mobile homes), attached houses, and apartments. Our study subjects were children between the ages of 6 and 18 years. Cotinine levels were used to assess secondhand tobacco-smoke exposure, and those living with someone who smoked inside the home were excluded. chi(2) tests, t tests, and Tobit regression models were used in Stata. Sample weights accounted for the complex survey design. RESULTS: Of 5002 children in our study, 73% were exposed to secondhand tobacco smoke. Children living in apartments had an increase in cotinine of 45% over those living in detached houses. This increase was 212% (P < .01) for white residents and 46% (P < .03) for black residents, but there was no significant increase for those of other races/ethnicities. At every cutoff level of cotinine, children in apartments had higher rates of exposure. The exposure effect of housing type was most pronounced at lower levels of cotinine. CONCLUSIONS: Most children without known secondhand tobacco-smoke exposure inside the home still showed evidence of tobacco-smoke exposure. Children in apartments had higher mean cotinine levels than children in detached houses. Potential causes for this result could be seepage through walls or shared ventilation systems. Smoking bans in multiunit housing may reduce children's exposure to tobacco smoke. Pediatrics 2011;127:85-92	[Wilson, Karen M.; Klein, Jonathan D.; Blumkin, Aaron K.] Univ Rochester, Dept Pediat, Rochester, NY 14642 USA; [Wilson, Karen M.; Klein, Jonathan D.; Gottlieb, Mark; Winickoff, Jonathan P.] Amer Acad Pediat, Julius B Richmond Ctr Excellence, Elk Grove Village, IL USA; [Gottlieb, Mark] Northeastern Univ, Publ Hlth Advocacy Inst, Sch Law, Boston, MA 02115 USA; [Winickoff, Jonathan P.] Harvard Univ, Sch Med, Dept Pediat, Massachusetts Gen Hosp Children, Boston, MA 02115 USA	Wilson, KM (reprint author), Univ Rochester, Dept Pediat, 601 Elmwood Ave,Box 777, Rochester, NY 14642 USA.	karen_wilson@urmc.rochester.edu		Gottlieb, Mark/0000-0001-8679-307X	Julius B. Richmond Center of Excellence of the American Academy of Pediatrics through Flight Attendant Medical Research Institute; Julius B. Richmond Center of Excellence, American Academy of Pediatrics; Flight Attendant Medical Research Institute; Legacy Foundation	This study was funded by the Julius B. Richmond Center of Excellence of the American Academy of Pediatrics through a grant from the Flight Attendant Medical Research Institute. Drs Wilson, Klein, Winickoff, and Gottlieb receive support from the Julius B. Richmond Center of Excellence, American Academy of Pediatrics; the Flight Attendant Medical Research Institute; and from the Legacy Foundation. All of the authors contributed substantially to this work and approved of the final draft as submitted. Mr Blumkin is the programmer/analyst for the study and had full access to all the data provided by the NHANES; and Dr Wilson is the lead author of the study. They both take full responsibility for the accuracy of the data analysis.	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J	Uller, L; Leino, M; Bedke, N; Sammut, D; Green, B; Lau, L; Howarth, PH; Holgate, ST; Davies, DE				Uller, Lena; Leino, Marina; Bedke, Nicole; Sammut, David; Green, Ben; Lau, Laurie; Howarth, Peter H.; Holgate, Stephen T.; Davies, Donna E.			Double-stranded RNA induces disproportionate expression of thymic stromal lymphopoietin versus interferon-beta in bronchial epithelial cells from donors with asthma	THORAX			English	Article							MEDIATED ALLERGIC INFLAMMATION; TOLL-LIKE RECEPTOR-3; RHINOVIRUS INFECTION; VIRAL-INFECTIONS; PROTEIN-KINASE; IN-VITRO; EXACERBATIONS; CHEMOKINES; DISEASE; PHENOTYPE	Background Thymic stromal lymphopoietin (TSLP) is an epithelial cell-derived cytokine that strongly activates dendritic cells and can initiate allergic inflammation. Since exposure to rhinovirus or double-stranded (ds) RNA (a surrogate of viral infection) induces TSLP expression in bronchial epithelial cells (BECs), this cytokine may link innate antiviral responses and the type 2 adaptive immune response. Objective As BECs from donors with asthma have a deficient interferon (IFN) response to rhinovirus infection, a study was undertaken to test the hypothesis that their antiviral response shows a bias towards TSLP production. Methods Primary BECs were grown from subjects with asthma and healthy volunteers. After exposure to dsRNA, interleukin (IL)-8, IFN beta and TSLP mRNA and protein expression were measured by RT-qPCR and ELISA, respectively. Results dsRNA dose-dependently increased IL-8 expression in BECs with no significant difference between the groups. However, BECs from subjects with asthma expressed less IFN beta and more TSLP mRNA and protein in response to dsRNA than BECs from those without asthma (median (IQR) 57 (38-82) pg/ml vs 106 (57-214) pg/ml for IFN beta (p<0.05) and 114 (86-143) pg/ml vs 65 (32-119) pg/ml for TSLP (p<0.05) in response to 10 mu g/ml dsRNA for 24 h). Induction of TSLP mRNA by dsRNA was blocked by Toll-like receptor 3 or protein kinase inhibitors or by preventing de novo protein synthesis, but not by neutralisation of type I IFN receptors. Conclusion BECs from subjects with asthma are biased towards higher TSLP and lower IFN beta production in response to dsRNA, suggesting that viral infection in asthma may lead to an altered mediator profile that biases towards a Th2 immune response.	[Uller, Lena; Leino, Marina; Bedke, Nicole; Sammut, David; Green, Ben; Lau, Laurie; Howarth, Peter H.; Holgate, Stephen T.; Davies, Donna E.] Univ Southampton, Sch Med, Div Infect Inflammat & Repair, Brooke Labs, Southampton, Hants, England	Uller, L (reprint author), Southampton Gen Hosp, Sir Henry Wellcome Labs, Brooke Labs, Mailpoint 810,Level F,South Block, Southampton SO16 6YD, Hants, England.	lena.uller@med.lu.se	Davies, Donna/H-2993-2012		Medical Research Council (MRC) UK; Swedish Medical Research Council; Swedish Heart-Lung Foundation; VINNOVA	Medical Research Council (MRC) UK, Swedish Medical Research Council, Swedish Heart-Lung Foundation and VINNOVA.	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J	Midoro-Horiuti, T; Tiwari, R; Watson, CS; Goldblum, RM				Midoro-Horiuti, Terumi; Tiwari, Ruby; Watson, Cheryl S.; Goldblum, Randall M.			Maternal Bisphenol A Exposure Promotes the Development of Experimental Asthma in Mouse Pups	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						airway hyperresponsiveness; asthma; bisphenol A; environmental estrogen; eosinophilia; experimental asthma; IgE; maternal exposure; perinatal sensitization	TANDEM MASS-SPECTROMETRY; SOLID-PHASE EXTRACTION; T-CELL RESPONSES; BREAST-MILK; EARLY-LIFE; ENDOCRINE DISRUPTORS; IMMUNE-SYSTEM; CORD-BLOOD; ER-ALPHA; MICE	BACKGROUND: We recently reported that various environmental estrogens induce mast cell degranulation and enhance IgE-mediated release of allergic mediators in vitro. OBJECTIVES: We hypothesized that environmental estrogens Would enhance allergic sensitization as well as bronchial inflammation and responsiveness. To test this hypothesis, we exposed fetal and neonatal mice to the common environmental estrogen bisphenol A (BPA) via maternal loading and assessed the pups' response to allergic sensitization and bronchial challenge. METHODS: Female BALB/c mice received 10 mu g/mL BPA in their drinking water from I week before impregnation to the end of the study. Neonatal mice were given a single 5 mu g intraperitoneal dose of ovalbumin (OVA) with aluminum hydroxide on postnatal day 4 and 3% OVA by nebulization for 10 ruin on days 13, 14, and 15. Forty-eight hours after the last nebulization, we assessed serum IgE antibodies to OVA by enzyme-linked immunosorbent assay (ELISA) and airway inflammation and hyperresponsiveness by enumerating eosinophils in bronchoalveolar lavage fluid, whole-body barometric plethysmography, and a forced oscillation technique. RESULTS: Neonates from BPA-exposed mothers responded to this "suboptimal" sensitization with higher serum IgE anti-OVA concentrations compared with those from unexposed mothers (p < 0.05), and eosinophilic inflammation in their airways was significantly greater. Airway responsiveness of the OVA-sensitized neonates from BPA-treated mothers was enhanced compared with those from unexposed mothers (P < 0.05). CONCLUSIONS: Perinatal exposure to BPA enhances allergic sensitization and bronchial inflammation and responsiveness in a Susceptible animal model of asthma.	[Midoro-Horiuti, Terumi; Tiwari, Ruby; Goldblum, Randall M.] Univ Texas Med Branch, Child Hlth Res Ctr, Dept Pediat, Galveston, TX 77555 USA; [Midoro-Horiuti, Terumi; Watson, Cheryl S.; Goldblum, Randall M.] Univ Texas Med Branch, Dept Biochem & Mol Biol, Galveston, TX 77555 USA	Midoro-Horiuti, T (reprint author), Univ Texas Med Branch, Child Hlth Res Ctr, Childrens Hosp, Room 2-300,301 Univ Blvd, Galveston, TX 77555 USA.	tmidoro@utmb.edu			National Institute of Environmental Health Sciences [R21 ES016428]; National Institute of Allergy and Infectious Diseases [K08 AI1055792, R01 AI1052428]	This project was supported by grain R21 ES016428 from the National Institute of Environmental Health Sciences (T.M.H.) and by grants K08 AI1055792 (T. M. H.) and R01 AI1052428 (R.M.G.) front the National Institute of Allergy and Infectious Diseases.	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Health Perspect.	FEB	2010	118	2					273	277		10.1289/ehp.0901259		5	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	555BQ	WOS:000274482400030	20123615	
J	Boulet, LP				Boulet, L-P.			Influence of comorbid conditions on asthma	EUROPEAN RESPIRATORY JOURNAL			English	Review						Asthma comorbidities; gastro-oesophageal reflux disease; glottic dysfunction; obesity; obstructive sleep apnoea; rhinitis/sinusitis	QUALITY-OF-LIFE; OBSTRUCTIVE PULMONARY-DISEASE; ALLERGIC RHINITIS; AIRWAY INFLAMMATION; SLEEP-APNEA; FOLLOW-UP; ATOPIC-DERMATITIS; INCIDENT ASTHMA; LUNG-FUNCTION; GASTROESOPHAGEAL-REFLUX	Various conditions such as rhinosinusitis, gastro-oesophageal reflux disease, psychological disturbances, chronic Infections and obstructive sleep apnoea are often observed In asthmatic patients and may affect asthma control and outcomes. These comorbidities may change the asthma phenotype, be part of the same pathophysiological process, act as confounding factors In the diagnosis or assessment of control of asthma, and/or result from specific environmental exposures. The Influences of these conditions on asthma are variable and for many of them still uncertain; nevertheless, they may alter asthma responses to current therapy. A systematic evaluation and an appropriate treatment of asthma-associated comorbid conditions should be part of asthma management, particularly for severe disease. With regard to clinical research, associated conditions may Influence the results of trials and should be taken Into account in the subjects' Inclusion criteria and analysis of data.	Univ Laval, Inst Univ Cardiol & Pneumol, Ste Foy, PQ G1V 4G5, Canada	Boulet, LP (reprint author), Univ Laval, Inst Univ Cardiol & Pneumol, 2725 Chemin, Ste Foy, PQ G1V 4G5, Canada.	lpboulet@med.ulaval.ca	panduru, mihaela/H-2411-2011				Aaron SD, 2004, CHEST, V125, P2046, DOI 10.1378/chest.125.6.2046; Abramson M, 2002, RESPIROLOGY, V7, P325, DOI 10.1046/j.1440-1843.2002.00408.x; Ahmad T, 2008, CURR OPIN INVEST DR, V9, P470; American Thoracic Society, 2000, AM J RESP CRIT CARE, V162, P2341, DOI DOI 10.1164/AJRCCM.162.6.ATS9-00; Baiardini I, 2008, ALLERGY, V63, P660, DOI 10.1111/j.1398-9995.2008.01649.x; Bateman ED, 2004, AM J RESP CRIT CARE, V170, P836, DOI 10.1164/rccm.200401-033OC; Bilodeau L, 2007, AM J RESP CRIT CARE, V175, pA198; Boulet LP, 2007, CAN RESPIR J, V14, P217; Boulet LP, 2007, RESP MED, V101, P2240, DOI 10.1016/j.rmed.2007.06.031; Boulet Louis-Philippe, 2006, Can Respir J, V13 Suppl A, P5; Boulet Louis-Philippe, 2007, Can Respir J, V14, P201; Boulet LP, 2006, CHEST, V129, P661, DOI 10.1378/chest.129.3.661; Bousquet J, 2008, ALLERGY, V63, P8, DOI 10.1111/j.1398-9995.2007.01620.x; Braunstahl GJ, 2000, AM J RESP CRIT CARE, V161, P2051; Braunstahl GJ, 2003, CURR OPIN PULM MED, V9, P46, DOI 10.1097/00063198-200301000-00008; Braunstahl GJ, 2001, J ALLERGY CLIN IMMUN, V107, P469, DOI 10.1067/mai.2001.113046; Brenner BE, 2005, THORAX, V60, P806, DOI 10.1136/thx.2004.033928; Bresciani M, 2001, J ALLERGY CLIN IMMUN, V107, P73, DOI 10.1067/mai.2001.111593; BRESLAU N, 1993, ARCH GEN PSYCHIAT, V50, P31; Ceylan E, 2007, RESPIROLOGY, V12, P272, DOI 10.1111/j.1440-1843.2006.00964.x; Chanez P, 2007, J ALLERGY CLIN IMMUN, V119, P1337, DOI 10.1016/j.jaci.2006.11.702; Chapman KR, 2008, EUR RESPIR J, V31, P320, DOI 10.1183/09031936.00039707; Chaudhuri R, 2006, AM J RESP CRIT CARE, V174, P127, DOI 10.1164/rccm.200510-1589OC; Chen Y, 2006, AM J RESP CELL MOL, V34, P192, DOI 10.1165/rcmb.2004-0417OC; Coughlan JL, 2001, THORAX, V56, P198, DOI 10.1136/thorax.56.3.198; Crystal-Peters J, 2002, J ALLERGY CLIN IMMUN, V109, P57, DOI 10.1067/mai.2002.120554; DAHLEM NW, 1977, J ALLERGY CLIN IMMUN, V60, P295, DOI 10.1016/0091-6749(77)90108-7; Denning DW, 2006, EUR RESPIR J, V27, P615, DOI 10.1183/09031936.06.00074705; Devouassoux G, 2007, J ALLERGY CLIN IMMUN, V119, P597, DOI 10.1016/j.jaci.2006.11.638; Dixon AE, 2008, LUNG, V186, P361, DOI 10.1007/s00408-008-9119-1; Dixon AE, 2006, CHEST, V130, P429, DOI 10.1378/chest.130.2.429; ELHAI H, 1999, ANN ALLERG ASTHMA IM, V82, P574; Eneli IU, 2008, THORAX, V63, P671, DOI 10.1136/thx.2007.086470; Feldman JM, 2005, PSYCHOSOM MED, V67, P989, DOI 10.1097/01.psy.0000188556.97979.13; Field SK, 1999, CHEST, V116, P766, DOI 10.1378/chest.116.3.766; FitzGerald JM, 2006, THORAX, V61, P992, DOI 10.1136/thx.2005.045195; Forbes L, 2007, THORAX, V62, P855, DOI 10.1136/thx.2006.058362; Galli E, 2007, ALLERGY ASTHMA PROC, V28, P540, DOI 10.2500/aap2007.28.3048; Gaugris S, 2006, J ASTHMA, V43, P1, DOI 10.1080/027700500446823; Coughlan J. 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J	Cooper, PJ; Rodrigues, LC; Cruz, AA; Barreto, ML				Cooper, P. J.; Rodrigues, L. C.; Cruz, A. A.; Barreto, M. L.			Asthma in Latin America: a public health challenge and research opportunity	ALLERGY			English	Review						asthma; allergy; Latin America; urbanization	SCHISTOSOMA-MANSONI INFECTION; BODY-MASS INDEX; CHILDHOOD ASTHMA; RISK-FACTORS; SCHOOL-CHILDREN; ALLERGIC SENSITIZATION; ASCARIS-LUMBRICOIDES; COSTA-RICA; RURAL AREA; BRONCHIAL RESPONSIVENESS	Asthma has emerged as an important public health problem in many Latin American countries over the past decade. In Brazil and Costa Rica, the prevalence of asthma and associated morbidity is as great or greater as reported in traditional high prevalence countries such as the US, but remains neglected as a public health priority. Asthma in Latin America is associated particularly with underprivileged populations living in cities but remains relatively rare in many rural populations. The causes of asthma in Latin America are likely to be associated with urbanization, migration, and the adoption of a modern 'Westernized' lifestyle and environmental changes that follow these processes that include changes in diet, physical activity, hygiene, and exposures to allergens, irritants, and outdoor and indoor pollutants. Because of the enormous social, genetic, and environmental contrasts within and between Latin American countries, and the large differences in prevalence associated with these differences, the investigation of asthma in Latin America provides important research opportunities to identify the social and biological mechanisms that underlie asthma development. Asthma in Latin America poses enormous challenges for health policy makers, health services, and researchers to respond to and alleviate the growing burden of asthma disability, particularly among marginalized urban populations.	[Cooper, P. J.] Ctr Invest FEPIS, Quininde, Ecuador; [Cooper, P. J.] Univ San Francico Quito, Inst Microbiol, Quito, Ecuador; [Rodrigues, L. C.] London Sch Hyg & Trop Med, London WC1, England; [Cooper, P. J.] Univ London St Georges Hosp, Ctr Infect, London, England; [Cruz, A. A.] WHO, CH-1211 Geneva, Switzerland; [Barreto, M. L.] Univ Fed Bahia, Inst Saude Colet, BR-41170290 Salvador, BA, Brazil	Cooper, PJ (reprint author), Casilla 17-14-39, Carcelen, Quito, Ecuador.		Cruz, Alvaro/I-1676-2012	Cruz, Alvaro/0000-0002-7403-3871; Barreto, Mauricio/0000-0002-0215-4930	Wellcome Trust [074679/Z/04/Z]; The Wellcome Trust Latin American Centres of Excellence Programme [072405/Z/03/Z]	PJC is supported by Wellcome Trust, Grant No. 074679/Z/04/Z. MLB, PJC, AAC, and LCR are involved in the SCAALA-Social Change Allergy and Asthma in Latin America-programme that is funded by The Wellcome Trust Latin American Centres of Excellence Programme, Grant No. 072405/Z/03/Z.	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J	Johnston, RA; Theman, TA; Lu, FL; Terry, RD; Williams, ES; Shore, SA				Johnston, Richard A.; Theman, Todd A.; Lu, Frank L.; Terry, Raya D.; Williams, Erin S.; Shore, Stephanie A.			Diet-induced obesity causes innate airway hyperresponsiveness to methacholine and enhances ozone-induced pulmonary inflammation	JOURNAL OF APPLIED PHYSIOLOGY			English	Article						bronchoalveolar lavage fluid; chemokine; leptin; lung elastance; resistance	HIGH-FAT DIET; NECROSIS-FACTOR-ALPHA; INDUCED LUNG INFLAMMATION; BODY-MASS INDEX; INSULIN-RESISTANCE; TISSUE MECHANICS; DEFICIENT MICE; C57BL/6J MICE; ASTHMA; RESPONSES	We previously reported that genetically obese mice exhibit innate airway hyperresponsiveness (AHR) and enhanced ozone (O-3)-induced pulmonary inflammation. Such genetic deficiencies in mice are rare in humans, and they may not be representative of human obesity. Thus the purpose of this study was to determine the pulmonary phenotype of mice with diet-induced obesity (DIO), which more closely mimics the cause of human obesity. Therefore, wild-type C57BL/6 mice were reared from the time of weaning until at least 30 wk of age on diets in which either 10 or 60% of the calories are derived from fat in the form of lard. Body mass was similar to 40% greater in mice fed 60 vs. 10% fat diets. Baseline airway responsiveness to intravenous methacholine, measured by forced oscillation, was greater in mice fed 60 vs. 10% fat diets. We also examined lung permeability and inflammation after exposure to room air or O-3 (2 parts/million for 3 h), an asthma trigger. Four hours after the exposure ended, O-3-induced increases in bronchoalveolar lavage fluid protein, interleukin-6, KC, macrophage inflammatory protein-2, interferon-gamma-inducible protein-10, and eotaxin were greater in mice fed 60 vs. 10% fat diets. Innate AHR and augmented responses to O-3 were not observed in mice raised from weaning until 20-22 wk of age on a 60% fat diet. These results indicate that mice with DIO exhibit innate AHR and enhanced O3-induced pulmonary inflammation, similar to genetically obese mice. However, mice with DIO must remain obese for an extended period of time before this pulmonary phenotype is observed.	[Johnston, Richard A.; Theman, Todd A.; Lu, Frank L.; Terry, Raya D.; Williams, Erin S.; Shore, Stephanie A.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Mol & Integrat Physiol Sci Program, Boston, MA 02115 USA; [Lu, Frank L.] Natl Taiwan Univ, Dept Pediat, Natl Taiwan Univ Hosp, Taipei 10764, Taiwan; [Lu, Frank L.] Natl Taiwan Univ, Dept Pediat, Natl Taiwan Univ Hosp, Coll Med, Taipei 10764, Taiwan	Johnston, RA (reprint author), Univ Texas Med Branch, Dept Internal Med, Div Allergy Pulm Immunol Crit Care & Sleep, Rm 8-104A,Med Res Bldg,301 Univ Blvd, Galveston, TX 77555 USA.	rajohnst@utmb.edu	Lu, Frank/G-6196-2012	Lu, Frank/0000-0002-5225-7751	NHLBI NIH HHS [HL-084044, R01 HL084044]; NIEHS NIH HHS [ES-013307, ES00002, R01 ES013307]		Bastard JP, 2002, J CLIN ENDOCR METAB, V87, P2084, DOI 10.1210/jc.87.5.2084; Bhalla DK, 1999, J TOXICOL ENV HEAL B, V2, P31, DOI 10.1080/109374099281232; Bhalla DK, 1999, J TOXICOL ENV HEAL A, V57, P329, DOI 10.1080/009841099157647; Black BL, 1998, METABOLISM, V47, P1354, DOI 10.1016/S0026-0495(98)90304-3; 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Appl. Physiol.	JUN	2008	104	6					1727	1735		10.1152/japplphysiol.00075.2008		9	Physiology; Sport Sciences	Physiology; Sport Sciences	309BI	WOS:000256434700025	18323466	
J	Kapoor, R; Menon, C; Hoffstad, O; Bilker, W; Leclerc, P; Margolis, DJ				Kapoor, Roger; Menon, Chandrakala; Hoffstad, Ole; Bilker, Warren; Leclerc, Patricia; Margolis, David J.			The prevalence of atopic triad in children with physician-confirmed atopic dermatitis	JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY			English	Article							FOLLOW-UP; ASTHMA; CHILDHOOD; PREDISPOSE; MUTATIONS; ALLERGIES; EXPOSURE; CRITERIA; ECZEMA; ISAAC	Background: Atopic dermatitis (AD) is often associated with comorbidities such as allergic rhinitis and asthma. Objective: We sought to describe the frequency of these comorbidities in children with AD Methods: We conducted a cross-sectional study of the first 2270 children with physician-confirmed AD enrolled in a large postmarketing cohort. All were queried for information on comorbidities using a questionnaire from the International Study of Asthma and Allergies in Childhood. Results: In all, 71.3% reported at least one additional form of atopy (symptoms of asthma or allergic rhinitis). A total of 33.3% reported only symptoms of asthma or allergic rhinitis whereas 38.0% reported I symptoms of asthma and allergic rhinitis. By age 3 years, nearly 66% reported at least one additional form of atopy. A statistically significant trend toward poorer disease control was observed for those with additional atopic illnesses (P <.001). Limitations: This is a cross-sectional study Conclusion: Individuals with AD exhibit a predisposition to additional atopic illnesses by age 3 years and in turn the presence of these illnesses correlates with poor disease control.	[Menon, Chandrakala; Hoffstad, Ole; Bilker, Warren; Margolis, David J.] Univ Penn, Sch Med, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA; [Bilker, Warren] Univ Penn, Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA; [Margolis, David J.] Univ Penn, Sch Med, Dept Dermatol, Philadelphia, PA 19104 USA; [Leclerc, Patricia] Novartis Pharmaceut Corp, E Hanover, NJ USA; [Kapoor, Roger] George Washington Univ, Sch Med, Washington, DC USA	Margolis, DJ (reprint author), Univ Penn, Sch Med, Dept Biostat & Epidemiol, 815 Blockley Hall,423 Guardian Dr, Philadelphia, PA 19104 USA.	margo@med.mail.upenn.edu	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Abramovits W, 2005, J AM ACAD DERMATOL, V53, pS86, DOI 10.1016/j.jaad.2005.04.034; Akdis CA, 2006, ALLERGY, V61, P969, DOI 10.1111/j.1398-9995.2006.01153.x; Asher MI, 2006, LANCET, V368, P733, DOI 10.1016/S0140-6736(06)69283-0; BUFFUM WP, 1966, AM J DIS CHILD, V112, P214; Callen J, 2007, BRIT J DERMATOL, V156, P203, DOI 10.1111/j.1365-2133.2006.07538x; Cookson W, 2004, NAT REV IMMUNOL, V4, P978, DOI 10.1038/nri1500; Cookson WOCM, 2001, NAT GENET, V27, P372, DOI 10.1038/86867; Diepgen TL, 1996, J CLIN EPIDEMIOL, V49, P1031, DOI 10.1016/0895-4356(96)00119-9; Ellwood P, 2005, INT J TUBERC LUNG D, V9, P10; Fiset PO, 2006, J ALLERGY CLIN IMMUN, V118, P287, DOI 10.1016/j.jaci.2006.03.046; Gustafsson D, 2000, ALLERGY, V55, P240, DOI 10.1034/j.1398-9995.2000.00391.x; Hanifin JM, 2004, J AM ACAD DERMATOL, V50, P391, DOI 10.1016/j.jaad.2003.08.003; Lau S, 2005, ALLERGY, V60, P766, DOI 10.1111/j.1398-9995.2005.00781.x; Lau Susanne, 2002, Paediatr Respir Rev, V3, P265, DOI 10.1016/S1526-0542(02)00189-6; Leung Donald Y M, 2003, J Allergy Clin Immunol, V112, pS117, DOI 10.1016/j.jaci.2003.09.034; Leung DYM, 2003, LANCET, V361, P151, DOI 10.1016/S0140-6736(03)12193-9; MALDONADO G, 1993, AM J EPIDEMIOL, V138, P923; Marenholz I, 2006, J ALLERGY CLIN IMMUN, V118, P866, DOI 10.1016/j.jaci.2006.07.026; Morar N, 2006, J ALLERGY CLIN IMMUN, V118, P24, DOI 10.1016/j.jaci.2006.03.037; Nafstad P, 2001, ALLERGY, V56, P307, DOI 10.1034/j.1398-9995.2001.00881.x; Nomura Ichiro, 2003, Journal of Allergy and Clinical Immunology, V112, P1195, DOI 10.1016/j.jaci.2003.08.049; Purvis DJ, 2005, BRIT J DERMATOL, V152, P742, DOI 10.1111/j.1365-2133.2005.06540.x; Rhodes HL, 2002, AM J RESP CRIT CARE, V165, P176; Sandilands A, 2006, J INVEST DERMATOL, V126, P1770, DOI 10.1038/sj.jid.5700459; Spergel Jonathan M., 2003, Journal of Allergy and Clinical Immunology, V112, pS118, DOI 10.1016/j.jaci.2003.09.033; Tay YK, 1999, INT J DERMATOL, V38, P689, DOI 10.1046/j.1365-4362.1999.00667.x; Voigt LF, 2003, AM J EPIDEMIOL, V157, P66, DOI 10.1093/aje/kwf185; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P383, DOI 10.1111/j.1365-2133.1994.tb08530.x; Williams HC, 2000, CLIN EXP DERMATOL, V25, P522, DOI 10.1046/j.1365-2230.2000.00698.x	29	72	76	0	4	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0190-9622			J AM ACAD DERMATOL	J. Am. Acad. Dermatol.	JAN	2008	58	1					68	73		10.1016/j.jaad.2007.06.041		6	Dermatology	Dermatology	250GG	WOS:000252287400009	17692428	
J	Leggat, PA; Kedjarune, U; Smith, DR				Leggat, Peter A.; Kedjarune, Ureporn; Smith, Derek R.			Occupational health problems in modern dentistry: A review	INDUSTRIAL HEALTH			English	Review						dentistry; infectious diseases; dermatitis; musculoskeletal pain	GENERAL DENTAL PRACTITIONERS; MUSCULOSKELETAL DISORDERS; SOUTHERN THAILAND; BACTERIAL AEROSOLS; HAND DERMATITIS; LATEX; PERSONNEL; PREVALENCE; ALLERGY; INFECTION	Despite numerous technical advances in recent years, many occupational health problems still persist in modern dentistry. These include percutaneous exposure incidents (PEI); exposure to infectious diseases (including bioaerosols), radiation, dental materials, and noise; musculoskeletal disorders; dermatitis and respiratory disorders; eye injuries; and psychological problems. PEI remain a particular concern, as there is an almost constant risk of exposure to serious infectious agents. Strategies to minimise PEI and their consequences should continue to be employed, including sound infection control practices, continuing education and hepatitis B immunisation. As part of any infection control protocols, dentists should continue to utilise personal protective measures and appropriate sterilisation or other high-level disinfection techniques. Aside from biological hazards, dentists continue to suffer a high prevalence of musculoskeletal disorders (MSD), especially of the back, neck and shoulders. To fully understand the nature of these problems, further studies are needed to identify causative factors and other correlates of MSD. Continuing education and investigation of appropriate interventions to help reduce the prevalence of MSD and contact dermatitis are also needed. For these reasons, it is therefore important that dentists remain constantly informed regarding up-to-date measures on how to deal with newer technologies and dental materials.	James Cook Univ N Queensland, Anton Breinl Ctr Publ Hlth & Trop Med, Townsville, Qld 4811, Australia; Prince Songkla Univ, Fac Dent, Dept Oral Biol & Occlus, Hat Yai 90112, Songkla, Thailand; NIOSH, Int Ctr Res Promot & Informat, Tama Ku, Kawasaki, Kanagawa 2148585, Japan	Leggat, PA (reprint author), James Cook Univ N Queensland, Anton Breinl Ctr Publ Hlth & Trop Med, Townsville, Qld 4811, Australia.		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Health	OCT	2007	45	5					611	621		10.2486/indhealth.45.611		11	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	227HB	WOS:000250646700003	18057804	
J	Hagvall, L; Backtorp, C; Svensson, S; Nyman, G; Borje, A; Karlberg, AT				Hagvall, Lina; Backtorp, Carina; Svensson, Sophie; Nyman, Gunnar; Borje, Anna; Karlberg, Ann-Therese			Fragrance compound geraniol forms contact allergens on air exposure. Identification and quantification of oxidation products and effect on skin sensitization	CHEMICAL RESEARCH IN TOXICOLOGY			English	Article							OXIDIZED D-LIMONENE; LYMPH-NODE ASSAY; DERMATITIS; HYDROPEROXIDES; ALDEHYDES; CAPACITY; LINALOOL; POTENCY; COMMON	Fragrances are common causes of contact allergy. Geraniol (trans-3,7-dimethyl-2,6-octadiene-1-ol) is an important fragrance terpene. It is considered a weak contact allergen and is used for fragrance allergy screening among consecutive dermatitis patients. Analogous to other monoterpenes studied, such as limonene and linalool, geraniol has the potential to autoxidize on air exposure and form highly allergenic compounds. The aim of the present study was to investigate and propose a mechanism for the autoxidation of geraniol at room temperature. To investigate whether allergenic compounds are formed, the sensitizing potency of geraniol itself, air-exposed geraniol, and its oxidation products was determined using the local lymph node assay in mice. The results obtained show that the allylic alcohol geraniol follows an oxidation pattern different from those of linalool and limonene, which autoxidize forming hydroperoxides as the only primary oxidation products. The autoxidation of geraniol follows two paths, originating from allylic hydrogen abstraction near the two double bonds. From geraniol, hydrogen peroxide is primarily formed together with aldehydes geranial and neral from a hydroxyhydroperoxide. In addition, small amounts of a hydroperoxide are formed, analogous to the formation of the major linalool hydroperoxide. The autoxidation of geraniol greatly influenced the sensitizing effect of geraniol. The oxidized samples had moderate sensitizing capacity, quite different from that of pure geraniol. The hydroperoxide formed is believed to be the major contributor to allergenic activity, together with the aldehydes geranial and neral. On the basis of the present study and previous experience, we recommend that the possibility of autoxidation and the subsequent formation of contact allergenic oxidation products are considered in risk assessments performed on fragrance terpenes.	Univ Gothenburg, Dept Chem Dermatochem & Skin Allergy, SE-41296 Gothenburg, Sweden; Univ Gothenburg, Dept Chem, SE-41296 Gothenburg, Sweden; Sahlgrens Acad, SE-40530 Gothenburg, Sweden; Univ Hosp, SE-40530 Gothenburg, Sweden	Karlberg, AT (reprint author), Univ Gothenburg, Dept Chem Dermatochem & Skin Allergy, SE-41296 Gothenburg, Sweden.	karlberg@chem.gu.se	Nyman, Gunnar/B-1705-2009; Borje, Anna/A-7581-2010; Karlberg, Ann-Therese/A-7706-2010				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; BECKE AD, 1993, J CHEM PHYS, V98, P5648, DOI 10.1063/1.464913; Bergh M, 1999, J PHARM SCI, V88, P483, DOI 10.1021/js980210y; Bergstrom MA, 2006, CHEM RES TOXICOL, V19, P760, DOI 10.1021/tx060006n; Bezard M, 1997, CHEM RES TOXICOL, V10, P987, DOI 10.1021/tx970014r; BOLLAND JL, 1949, Q REV CHEM SOC, V3, P1, DOI 10.1039/qr9490300001; DeGroot AC, 1997, CONTACT DERMATITIS, V36, P57; DEROCH IS, 1968, BELG CHEM IND, V33, P994; Frisch MJ, 2004, GAUSSIAN 03; FROSCH PJ, 1995, CONTACT DERMATITIS, V33, P333, DOI 10.1111/j.1600-0536.1995.tb02048.x; Guengerich FP, 2001, CHEM RES TOXICOL, V14, P611, DOI 10.1021/tx0002583; Heinmoller P, 1998, ANAL CHEM, V70, P1437, DOI 10.1021/ac970867o; Jensen F., 1999, INTRO COMPUTATIONAL; 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, 1997, CONTACT DERMATITIS, V36, P201, DOI 10.1111/j.1600-0536.1997.tb00270.x; Kimber I, 2003, FOOD CHEM TOXICOL, V41, P1799, DOI 10.1016/S0278-6915(03)00223-0; Kimber I, 1995, TOXICOLOGY, V103, P63, DOI 10.1016/0300-483X(95)03114-U; Knapp H, 1998, J AGR FOOD CHEM, V46, P1966, DOI 10.1021/jf970987x; LEE CT, 1988, PHYS REV B, V37, P785, DOI 10.1103/PhysRevB.37.785; Liang CP, 2004, MOL NUTR FOOD RES, V48, P308, DOI 10.1002/mnfr.200400027; MAIR RD, 1964, ANAL CHEM, V36, P194, DOI 10.1021/ac60207a061; Matura M, 2005, CONTACT DERMATITIS, V52, P320, DOI 10.1111/j.0105-1873.2005.00605.x; Matura M, 2002, J AM ACAD DERMATOL, V47, P709, DOI 10.1067/mjd.2002.124817; Mutterer V, 2000, CHEM RES TOXICOL, V13, P1028, DOI 10.1021/tx9901433; Parejo I, 2000, J PHARMACOL TOXICOL, V43, P183, DOI 10.1016/S1056-8719(00)00085-X; PARLANT C, 1964, B SOC CHIM FR, P3161; Patlewicz G, 2001, CONTACT DERMATITIS, V44, P331, DOI 10.1034/j.1600-0536.2001.044006331.x; Patlewicz GY, 2002, CONTACT DERMATITIS, V47, P219, DOI 10.1034/j.1600-0536.2002.470406.x; PATLEWICZ GY, 2004, CONTACT DERMATITIS, V50, P891; Pedersen LK, 2004, CONTACT DERMATITIS, V50, P265, DOI 10.1111/j.0105-1873.2004.00342.x; Rastogi SC, 1996, CONTACT DERMATITIS, V34, P423, DOI 10.1111/j.1600-0536.1996.tb02246.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; SANTUCCI B, 1987, CONTACT DERMATITIS, V16, P93, DOI 10.1111/j.1600-0536.1987.tb01386.x; Schnuch A, 2004, CONTACT DERMATITIS, V50, P65, DOI 10.1111/j.0105-1873.2004.00302.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; Svensson S, 2004, J CHROMATOGR B, V809, P199, DOI 10.1016/j.jchromb.2004.06.027	40	72	72	3	19	AMER CHEMICAL SOC	WASHINGTON	1155 16TH ST, NW, WASHINGTON, DC 20036 USA	0893-228X	1520-5010		CHEM RES TOXICOL	Chem. Res. Toxicol.	MAY	2007	20	5					807	814		10.1021/tx700017v		8	Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology	Pharmacology & Pharmacy; Chemistry; Toxicology	169GT	WOS:000246581400012	17428070	
J	D'Amato, G; Liccardi, G; Frenguelli, G				D'Amato, G.; Liccardi, G.; Frenguelli, G.			Thunderstorm-asthma and pollen allergy	ALLERGY			English	Review						allergic asthma; bronchial asthma; bronchial hyperreactivity; climate changes; environment and allergy; pollen allergy; pollinosis; respiratory allergy; thunderstorm-asthma	GRASS-POLLEN; ENVIRONMENTAL-FACTORS; AIR-POLLUTION; HAY-FEVER; EPIDEMICS; RISK; SENSITIZATION; COMMUNITY; ORBICULES; OUTBREAK	Thunderstorms have been linked to asthma epidemics, especially during the pollen seasons, and there are descriptions of asthma outbreaks associated with thunderstorms, which occurred in several cities, prevalently in Europe (Birmingham and London in the UK and Napoli in Italy) and Australia (Melbourne and Wagga Wagga). Pollen grains can be carried by thunderstorm at ground level, where pollen rupture would be increased with release of allergenic biological aerosols of paucimicronic size, derived from the cytoplasm and which can penetrate deep into lower airways. In other words, there is evidence that under wet conditions or during thunderstorms, pollen grains may, after rupture by osmotic shock, release into the atmosphere part of their content, including respirable, allergen-carrying cytoplasmic starch granules (0.5-2.5 mu m) or other paucimicronic components that can reach lower airways inducing asthma reactions in pollinosis patients. The thunderstorm-asthma outbreaks are characterized, at the beginning of thunderstorms by a rapid increase of visits for asthma in general practitioner or hospital emergency departments. Subjects without asthma symptoms, but affected by seasonal rhinitis can experience an asthma attack. No unusual levels of air pollution were noted at the time of the epidemics, but there was a strong association with high atmospheric concentrations of pollen grains such as grasses or other allergenic plant species. However, subjects affected by pollen allergy should be informed about a possible risk of asthma attack at the beginning of a thunderstorm during pollen season.	High Special Hosp A Cardarelli, Dept Resp Dis, Div Pneumol & Allergol, I-80121 Naples, Italy; Univ Perugia, Dept Plant Biol, I-06100 Perugia, Italy	D'Amato, G (reprint author), High Special Hosp A Cardarelli, Dept Resp Dis, Div Pneumol & Allergol, Via Rione Sirignano 10, I-80121 Naples, Italy.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; FRENGUELLI, Giuseppe/0000-0002-6282-2814			Anto JM, 1997, THORAX, V52, P669; ANTO JM, 2002, MONOGRAPH EUROPEAN R, P108; ANTO JM, 1999, DIFFICULT ASTHMA, P333; Bauman A, 1996, BRIT MED J, V312, P590; BELLOMO R, 1992, MED J AUSTRALIA, V156, P834; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Burney P, 1997, J ALLERGY CLIN IMMUN, V99, P314, DOI 10.1016/S0091-6749(97)70048-4; Celenza A, 1996, BRIT MED J, V312, P604; D'Amato G, 1998, ALLERGY, V53, P567, DOI 10.1111/j.1398-9995.1998.tb03932.x; D'Amato G, 2005, CLIN EXP ALLERGY, V35, P1113, DOI 10.1111/j.1365-2222.2005.02328.x; D'Amato G, 2002, ALLERGY, V57, P30, DOI 10.1034/j.1398-9995.57.s72.5.x; D'Amato G, 2001, ALLERGY, V56, P1109, DOI 10.1034/j.1398-9995.2001.00317.x; DAmato G, 1991, ALLERGENIC POLLEN PO, P113; D'Amato G, 2005, BMJ; Davidson AC, 1996, BRIT MED J, V312, P601; ElGhazaly G, 1995, GRANA, V34, P300; Girgis ST, 2000, EUR RESPIR J, V16, P3, DOI 10.1034/j.1399-3003.2000.16a02.x; KNOX RB, 1993, CLIN EXP ALLERGY, V23, P354, DOI 10.1111/j.1365-2222.1993.tb00339.x; Marks GB, 2001, THORAX, V56, P468, DOI 10.1136/thorax.56.6.468; MURRAY V, 1994, BRIT MED J, V309, P131; Newson R, 1998, EUR RESPIR J, V11, P694; Newson R, 1997, THORAX, V52, P669; PACKE GE, 1985, LANCET, V2, P199; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Rosas I, 1998, ALLERGY, V53, P394, DOI 10.1111/j.1398-9995.1998.tb03911.x; Schappi GF, 1999, ALLERGY, V54, P478, DOI 10.1034/j.1398-9995.1999.00838.x; SUPHIOGLU C, 1992, LANCET, V339, P569, DOI 10.1016/0140-6736(92)90864-Y; Taylor PE, 2004, CLIN EXP ALLERGY, V34, P1591, DOI 10.1111/j.1365-2222.2004.02078.x; Taylor PE, 2002, J ALLERGY CLIN IMMUN, V109, P51, DOI 10.1067/mai.2002.120759; Thommen AA, 1930, NY STATE J MED, P437; Traidl-Hoffmann C, 2003, INT ARCH ALLERGY IMM, V131, P1, DOI 10.1159/000070428; Venables KM, 1997, CLIN EXP ALLERGY, V27, P725, DOI 10.1046/j.1365-2222.1997.790893.x; Vinckier S, 2001, ALLERGY, V56, P1129, DOI 10.1034/j.1398-9995.2001.00172.x; Wallis D. N., 1995, European Respiratory Journal, V8, p500S; Wardman A E Dennis, 2002, Can Respir J, V9, P267	35	72	73	4	18	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0105-4538			ALLERGY	Allergy	JAN	2007	62	1					11	16		10.1111/j.1398-9995.2006.01271.x		6	Allergy; Immunology	Allergy; Immunology	113YQ	WOS:000242634300003	17156336	
J	Kikuchi, Y; Takai, T; Kuhara, T; Ota, M; Kato, T; Hatanaka, H; Ichikawa, S; Tokura, T; Akiba, H; Mitsuishi, K; Ikeda, S; Okumura, K; Ogawa, H				Kikuchi, Yuko; Takai, Toshiro; Kuhara, Takatoshi; Ota, Mikiko; Kato, Takeshi; Hatanaka, Hideki; Ichikawa, Saori; Tokura, Tomoko; Akiba, Hisaya; Mitsuishi, Kouichi; Ikeda, Shigaku; Okumura, Ko; Ogawa, Hideoki			Crucial commitment of proteolytic activity of a purified recombinant major house dust mite allergen der p1 to sensitization toward IgE and IgG responses	JOURNAL OF IMMUNOLOGY			English	Article							CYSTEINE PROTEASE ACTIVITY; DER-F-I; DERMATOPHAGOIDES-PTERONYSSINUS; CRYSTAL-STRUCTURE; SEQUENCE POLYMORPHISMS; ENHANCES ALLERGENICITY; POTENTIAL ALLERGENS; ANTIBODY-RESPONSE; HEAT DENATURATION; GROUP-1 ALLERGEN	The major proteolytic allergen derived from the house dust mite Dermatophagoides pteronyssinus, Der Ill, is one of the most clinically relevant allergens worldwide. In the present study, we evaluate the contribution of the proteolytic activity and structure of a highly purified rDer p 1 to immune responses. Mice were i.p. immunized with three forms of rDer p I adsorbed to Alum: one enzymatically active, one treated with an irreversible cysteine protease-specific inhibitor, E-64, and one heat denatured. Immunization with E-64-treated or heat-denatured rDer p I elicited much less production of serum total IgE and not only rDer p 1-specific IgE but also IgGs compared with immunization with active rDer p 1. Assays for Ab-binding and its inhibition and structural analyses indicated that E-64-treated rDer p I retained its global structure and conformational B cell epitopes. A proliferative response and production of IL-5 by spleen cells restimulated with rDer p I were observed on immunization with the active rDer p 1 but not E-64-treated rDer p 1. The cells from mice immunized with heat-denatured rDer p I exhibited the highest levels of proliferation and production of IL-5 and IFN-gamma. The results indicate that the proteolytic activity of the highly purified rDer p I crucially commits to the sensitization process, including both IgE and IgG responses. Additionally, we demonstrated immunogenic differences by functional or structural manipulations of the rDer p 1. The findings have implications for sensitization to this relevant allergen in humans and for the design of modified allergen-vaccines for future allergen-specific immunotherapy.	Juntendo Univ, Sch Med, Atopy Res Ctr, Bunkyo Ku, Tokyo 1138421, Japan; Juntendo Univ, Sch Med, Dept Dermatol, Tokyo 1138421, Japan; Juntendo Univ, Sch Med, Dept Immunol, Tokyo 1138421, Japan; Univ Tokyo, Fac Pharmaceut Sci, Dept Hyg Chem, Chiba, Japan; Kyushu Univ, Grad Sch Syst Life Sci, Fukuoka 812, Japan; Japan Womens Univ, Fac Sci, Dept Mat & Biol Sci, Tokyo 112, Japan	Takai, T (reprint author), Juntendo Univ, Sch Med, Atopy Res Ctr, Bunkyo Ku, 2-1-1 Hongo, Tokyo 1138421, Japan.	t-takai@med.juntendo.ac.jp	Takai, Toshiro/K-5690-2013				ANDO T, 1991, INT ARCH ALLER A IMM, V96, P199; Asokananthan N, 2002, J IMMUNOL, V169, P4572; Brown A, 2003, AM J RESP CELL MOL, V29, P381, DOI 10.1165/rcmb.2003-0060OC; Chambers L, 1998, BIOCHEM BIOPH RES CO, V253, P837, DOI 10.1006/bbrc.1998.9862; CHAPMAN MD, 1983, J ALLERGY CLIN IMMUN, V72, P27, DOI 10.1016/0091-6749(83)90048-9; CHAPMAN MD, 1980, J IMMUNOL, V125, P587; CHUA KY, 1993, INT ARCH ALLERGY IMM, V101, P364; CHUA KY, 1988, J EXP MED, V167, P175, DOI 10.1084/jem.167.1.175; 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Immunol.	AUG 1	2006	177	3					1609	1617				9	Immunology	Immunology	065DT	WOS:000239140300035	16849469	
J	Lusuardi, M; De Benedetto, F; Paggiaro, P; Sanguinetti, CM; Brazzola, G; Ferri, P; Donner, CF				Lusuardi, M; De Benedetto, F; Paggiaro, P; Sanguinetti, CM; Brazzola, G; Ferri, P; Donner, CF			A randomized controlled trial on office spirometry in asthma and COPD in standard general practice - Data from spirometry in asthma and COPD: a comparative evaluation Italian study	CHEST			English	Article						asthma; COPD; general practice; office spirometry	OBSTRUCTIVE PULMONARY-DISEASE; PRIMARY-CARE; PERSISTENT COUGH; POPULATION; PROGRAM	Study objectives: To evaluate whether office spirometry by general practitioners (GPs) is feasible and may improve the diagnosis of asthma and COPD. Methods: A prospective, randomized, comparative trial was planned involving 57 Italian pulmonology centers and 570 GPs who had to enroll consecutive subjects aged IS to 65 years with symptoms of asthma or COPD without a previous diagnosis. Patients were randomized 1:1 into two groups with an interactive voice responding system: conventional evaluation alone vs conventional evaluation and spirometry. Office spirometry was performed by GPs who were trained by reference specialists using a portable electronic spirometer (Spirobank Office; MIR; Home, Italy). Diagnosis was confirmed by the reference specialist center in blind fashion. Results: Seventy-four GPs complied to the trial. Of :333 patients enrolled, 136 nonrandom violators completed the protocol. Per-protocol analysis showed a concordant diagnosis between GPs and specialists in 78.6% of cases in the conventional evaluation-plus-spirometry group vs 69.2% in the conventional evaluation group (p = 0.35). In the intention-to-treat analysis, the respective percentages of concordant diagnosis were 57.9 and 56.7 (p = 0.87). Conclusions: Office spirometry by GPs is feasible, but frequent protocol violation and inadequate sample size did not allow us to prove a significant advantage of office spirometry in improving the diagnosis of asthma and COPD in standard general practice as organized at present in Italy, thus reinforcing the need for close cooperation between GPs and specialists in respiratory medicine.	AUSL Reggio Emilia, S Sebastiano Hosp, Cardiopulm Rehabil, I-42015 Correggio, RE, Italy; San Camillo Hosp, Dept Resp Med, Chieti, Italy; Univ Pisa, Cardiothorac Dept, I-56100 Pisa, Italy; S Filippo Neri Hosp, Dept Resp Med, Rome, Italy; SIMESA, Astra Zeneca Grp, Milan, Italy; IRCCS, Salvatore Maugeri Fdn, Div Pulm Dis, Veruno, Italy	Lusuardi, M (reprint author), AUSL Reggio Emilia, S Sebastiano Hosp, Cardiopulm Rehabil, Via Mandriolo 11, I-42015 Correggio, RE, Italy.	lusuardimi@ausl.re.it	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Bolton CE, 2005, RESP MED, V99, P493, DOI 10.1016/j.rmed.2004.09.015; Buffels J, 2004, CHEST, V125, P1394, DOI 10.1378/chest.125.4.1394; Chan B, 1997, CAN MED ASSOC J, V156, P169; Dowson L J, 1999, Monaldi Arch Chest Dis, V54, P186; Eaton T, 1999, CHEST, V116, P416, DOI 10.1378/chest.116.2.416; Ferguson GT, 2000, CHEST, V117, P1146, DOI 10.1378/chest.117.4.1146; Griffiths C, 1999, RESP MED, V93, P903, DOI 10.1016/S0954-6111(99)90057-4; Hankinson JL, 1999, CHEST, V116, P276, DOI 10.1378/chest.116.2.276; NIH National Institutes of Health, 2006, NIH PUBL, V07-4518; Pinnock H, 1999, ASTHMA GEN PRACT, V7, P23; Schermer T, 2003, EUR RESPIR J, V22, P725, DOI 10.1183/0903196.03.00075203; Schermer TR, 2003, THORAX, V58, P861, DOI 10.1136/thorax.58.10.861; Takahashi TU, 2003, RESPIROLOGY, V8, P504, DOI 10.1046/j.1440-1843.2003.00501.x; Thiadens HA, 1999, THORAX, V54, P1055; Thiadens HA, 1998, BRIT MED J, V316, P1286; van den Boom G, 1998, AM J RESP CRIT CARE, V158, P1730; Voelkel NF, 2000, CHEST, V117, p372S, DOI 10.1378/chest.117.5_suppl_2.372S; Vrijhoef HJM, 2003, J CLIN NURS, V12, P366; 2001, AM J RESPIR CRIT CAR, V163, P1256	19	72	72	2	4	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	APR	2006	129	4					844	852		10.1378/chest.129.4.844		9	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	034CB	WOS:000236901000007	16608929	
J	Magnusson, LL; Olesen, AB; Wennborg, H; Olsen, J				Magnusson, LL; Olesen, AB; Wennborg, H; Olsen, J			Wheezing, asthma, hayfever, and atopic eczema in childhood following exposure to tobacco smoke in fetal life	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						atopic diseases; prenatal; smoke exposure; tobacco; wheezing	CORD-SERUM IGE; PERINATAL RISK-FACTORS; MATERNAL SMOKING; PARENTAL SMOKING; LUNG-FUNCTION; ALLERGIC SENSITIZATION; BRONCHIAL HYPERRESPONSIVENESS; REPRODUCTIVE HEALTH; RESPIRATORY ILLNESS; FAMILY-HISTORY	Prenatal maternal smoking has been associated with adverse respiratory effects in childhood such as lung deficits and wheezing, but results concerning asthma, hayfever, and atopic eczema are inconsistent. In the present study, we investigate the effects of maternal smoking in pregnancy on asthma, hayfever, atopic eczema, and wheezing in the offspring up to the age of 14-18. The study was based on a cohort of mothers enrolled during midwife visits around the 36th week of gestation in Odense and Aalborg, Denmark, 1984-1987. Singleton, live born children (n=11 144) were followed-up in 2002 to obtain a childhood history of atopic diseases, by means of questionnaires to the parents. Multivariate logistic regression analyses for medical diagnoses of asthma, hayfever, atopic eczema, and symptoms of wheezing before the age of 3, were carried out on 7844 children. After adjustment for confounders, late prenatal smoke exposure was associated with wheezing, with an odds ratio (OR) of 1.2, and a 95% confidence interval (CI) of 1.1-1.5. Furthermore, slightly reduced estimates for hayfever (OR 0.8, CI 0.7-1.0) and atopic eczema (OR 0.8, CI 0.7-0.9) were obtained for children exposed in late pregnancy compared with non-exposed. Late gestational smoke exposure was associated with wheezing but not with asthma, while null or even protective estimates were indicated for hayfever and atopic eczema. However, lack of control options for hereditary factors may have affected the results.	Karolinska Inst, Dept Biosci, Novum, S-14157 Huddinge, Sweden; Aarhus Univ Hosp, Danish Epidemiol Sci Ctr, DK-8000 Aarhus, Denmark; Aarhus Univ Hosp, Dept Dermatol, DK-8000 Aarhus, Denmark; Univ Calif Los Angeles, Sch Publ Hlth, Dept Epidemiol, Los Angeles, CA 90024 USA	Magnusson, LL (reprint author), Karolinska Inst, Dept Biosci, Novum, S-14157 Huddinge, Sweden.	linda.magnusson@biosci.ki.se	Magnusson Hanson, Linda/D-2435-2017	Magnusson Hanson, Linda/0000-0002-2908-1903			*ARB, 1979, DANKS FAG KOD; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Atici A, 1995, PEDIATR ALLERGY IMMU, V6, P213, DOI 10.1111/j.1399-3038.1995.tb00288.x; Bel EH, 2004, CURR OPIN PULM MED, V10, P44, DOI 10.1097/00063198-200401000-00008; BERGMANN RL, 1995, ALLERGY, V50, P65, DOI 10.1111/j.1398-9995.1995.tb02484.x; Braback L, 1998, CLIN EXP ALLERGY, V28, P936; Burr ML, 1997, CLIN EXP ALLERGY, V27, P1247; [California Environmental Protection Agency (Cal EPA) Office of Environmental Health Hazard Assessment], 1997, HLTH EFF EXP ENV TOB; 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; Dempsey DA, 2001, DRUG SAFETY, V24, P277, DOI 10.2165/00002018-200124040-00005; Dezateux C, 1999, AM J RESP CRIT CARE, V159, P403; Ehrlich RI, 1996, AM J RESP CRIT CARE, V154, P681; Frey U, 2004, AM J RESP CRIT CARE, V170, P260, DOI 10.1164/rccm.200307-1002OC; Gilliland FD, 2001, AM J RESP CRIT CARE, V163, P429; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; Gupta R, 2004, CLIN EXP ALLERGY, V34, P520, DOI 10.1111/j.1365-2222.2004.1935.x; HANRAHAN JP, 1992, AM REV RESPIR DIS, V145, P1129; Heinrich J, 2002, EUR RESPIR J, V19, P1040, DOI 10.1183/09031936.02.00261802; Hernan MA, 2002, AM J EPIDEMIOL, V155, P176, DOI 10.1093/aje/155.2.176; Hjern A, 2001, CLIN EXP ALLERGY, V31, P908, DOI 10.1046/j.1365-2222.2001.01096.x; Hu FB, 1997, ANN ALLERG ASTHMA IM, V79, P80; Jaakkola JJK, 2004, AM J PUBLIC HEALTH, V94, P136, DOI 10.2105/AJPH.94.1.136; Kerkhof M, 2003, CLIN EXP ALLERGY, V33, P1336, DOI 10.1046/j.1365-2222.2003.01751.x; Kramer U, 2004, BRIT J DERMATOL, V150, P111, DOI 10.1111/j.1365-2133.2004.05710.x; Kulig M, 1998, CLIN EXP ALLERGY, V28, P1397, DOI 10.1046/j.1365-2222.1998.00439.x; Kuyucu S, 2004, PEDIATR ALLERGY IMMU, V15, P62, DOI 10.1046/j.0905-6157.2003.00115.x; Landau L I, 2001, Paediatr Respir Rev, V2, P202, DOI 10.1053/prrv.2001.0141; LEWIS S, 1995, EUR RESPIR J, V8, P349, DOI 10.1183/09031936.95.08030349; Lewis SA, 1998, RESP MED, V92, P1237, DOI 10.1016/S0954-6111(98)90427-9; Lindbohm ML, 2002, SCAND J WORK ENV HEA, V28, P84; Lux AL, 2000, ARCH DIS CHILD, V83, P307, DOI 10.1136/adc.83.4.307; MAGNUSSON CGM, 1986, J ALLERGY CLIN IMMUN, V78, P898, DOI 10.1016/0091-6749(86)90237-X; MARTINEZ FD, 1988, NEW ENGL J MED, V319, P1112, DOI 10.1056/NEJM198810273191702; Melen E, 2004, CLIN EXP ALLERGY, V34, P839, DOI 10.1111/j.1365-2222.2004.01957.x; MORGAN WJ, 1992, PEDIATR CLIN N AM, V39, P1185; Murray CS, 2004, PEDIATR PULM, V37, P492, DOI 10.1002/ppul.20019; NEUSPIEL DR, 1989, AM J PUBLIC HEALTH, V79, P168, DOI 10.2105/AJPH.79.2.168; O'Connell EJ, 2004, ALLERGY, V59, P7, DOI 10.1111/j.1398-9995.2004.00563.x; Olesen AB, 1997, BRIT MED J, V314, P1003; Olesen AB, 2001, ACTA DERM-VENEREOL, V81, P277, DOI 10.1080/00015550152572921; OLSEN J, 1993, SCAND J SOC MED, V21, P90; Olsen J, 2000, EPIDEMIOL REV, V22, P76; OLSEN J, 1989, SCAND J SOC MED, V17, P277; ORYSZCZYN MP, 1991, J ALLERGY CLIN IMMUN, V87, P1169, DOI 10.1016/0091-6749(91)92163-U; OWNBY DR, 1991, J ALLERGY CLIN IMMUN, V88, P555, DOI 10.1016/0091-6749(91)90148-H; RONA RJ, 1993, BRIT MED J, V306, P817; Schafer T, 1997, J AM ACAD DERMATOL, V36, P550, DOI 10.1016/S0190-9622(97)70242-1; Schultz Larsen F, 1992, Acta Derm Venereol Suppl (Stockh), V176, P7; Sekhon HS, 2004, EUR RESPIR J, V23, P906, DOI 10.1183/09031936.04.00069604; Sekhon HS, 2001, AM J RESP CRIT CARE, V164, P989; SOYSETH V, 1995, CHEST, V107, P389, DOI 10.1378/chest.107.2.389; StataCorp, 2003, STAT STAT SOFTW REL; Stein RT, 1999, AM J EPIDEMIOL, V149, P1030; Stick SM, 1996, LANCET, V348, P1060, DOI 10.1016/S0140-6736(96)04446-7; Stocks J, 2003, RESPIROLOGY, V8, P266, DOI 10.1046/j.1440-1843.2003.00478.x; Strachan DP, 1998, THORAX, V53, P117; Strachan DP, 1996, BRIT MED J, V312, P1195; Strachan DP, 1998, THORAX, V53, P204; Tariq SM, 2000, POSTGRAD MED J, V76, P694, DOI 10.1136/pmj.76.901.694; TAYLOR B, 1984, LANCET, V2, P1255; Upton MN, 2000, BRIT MED J, V321, P88, DOI 10.1136/bmj.321.7253.88; Vonk JM, 2004, J ALLERGY CLIN IMMUN, V114, P270, DOI 10.1016/j.jaci.2004.03.051; WILLIAMS HC, 1996, SO D I DEFINE ATOPIC; Yuan W, 2002, INT J EPIDEMIOL, V31, P1240, DOI 10.1093/ije/31.6.1240	66	72	76	0	4	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	DEC	2005	35	12					1550	1556				7	Allergy; Immunology	Allergy; Immunology	990XT	WOS:000233777400006	16393320	
J	Kang, CM; Jang, AS; Ahn, MH; Shin, LA; Kim, JH; Choi, YS; Rhim, TY; Park, CS				Kang, CM; Jang, AS; Ahn, MH; Shin, LA; Kim, JH; Choi, YS; Rhim, TY; Park, CS			Interleukin-25 and interieukin-13 production by alveolar macrophages in response to particles	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article						cytokines; inflammation; lung; macrophages	PARTICULATE AIR-POLLUTION; IN-VIVO; DIESEL EXHAUST; CHEMOKINE EXPRESSION; CYTOKINE PRODUCTION; PULMONARY-FUNCTION; TITANIUM-DIOXIDE; CELL-FUNCTION; RAT LUNG; MATTER	Particle inhalation-induced lung inflammation acts as an adjuvant to allergens or respiratory viral infection in a process that is mediated by macrophages and epitheliums. The production of interleukin (IL)-4 and IL-13 by activated T cells is involved in the augmentation of Th2-type immune responses to particles, and IL-25 induces the synthesis of 11-4 and IL-13. However, whether IL-13 and IL-25 are directly regulated by particle instillation in the lung has not been studied. The aim of this study was to reveal particle induction of IL-13 and IL-25 in the lung. TiO2 instillation potently induced the mRNA expression for IL-25 and IL-13 in lung tissue extracts 24 h after treatment, as compared with the sham group. Immunostaining for IL-25 and IL-13 showed strong positivity for macrophages in the inflammatory lung lesions of TiO2-treated rats. The alveolar macrophages expressed IL-25 and IL-13 24h after in vitro stimulation with TiO2 particles in dose- and time-dependent manners, with maximal induction at 24 and 48 h after stimulation, respectively. The sequence of the rat IL-25 gene is 95% homologous with the mouse IL-25 gene. These findings indicate that alveolar macrophages play an important role in particle-induced lung inflammation via direct induction of IL-13 and IL-25 production.	Soonchunhyang Univ Hosp, Dept Internal Med, Div Allergy & Resp Dis, Gyeonggido 420767, South Korea; Soonchunhyang Univ Hosp, Genome Res Ctr Allergy & Resp Dis, Puchon, South Korea; Soonchunhyang Univ Hosp, Div Allergy & Resp Dis, Puchon, South Korea	Park, CS (reprint author), Soonchunhyang Univ Hosp, Dept Internal Med, Div Allergy & Resp Dis, 1174 Jung Dong, Gyeonggido 420767, South Korea.	mdcspark@unitel.co.kr					Becker S, 1996, TOXICOL APPL PHARM, V141, P637, DOI 10.1006/taap.1996.0330; BRODY AR, 1992, J LEUKOCYTE BIOL, V51, P640; BURD PR, 1995, J EXP MED, V181, P1373, DOI 10.1084/jem.181.4.1373; Churg A, 1999, AM J PHYSIOL-LUNG C, V277, pL975; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; DOCKERY DW, 1993, NEW ENGL J MED, V329, P1753, DOI 10.1056/NEJM199312093292401; Driscoll KE, 1995, TOXICOL LETT, V82-3, P483, DOI 10.1016/0378-4274(95)03578-8; Fahy O, 2002, J IMMUNOL, V168, P5912; Fernvik E, 2002, J TOXICOL ENV HEAL A, V65, P1025, DOI 10.1080/00984100290071108; Fort MM, 2001, IMMUNITY, V15, P985, DOI 10.1016/S1074-7613(01)00243-6; Fujieda S, 1998, AM J RESP CELL MOL, V19, P507; Fujii T, 2001, AM J RESP CELL MOL, V25, P265; GARABRANT DH, 1987, SCAND J WORK ENV HEA, V13, P47; Ghio AJ, 2001, AM J RESP CRIT CARE, V164, P704; Grunig G, 1998, SCIENCE, V282, P2261, DOI 10.1126/science.282.5397.2261; Hamilton RF, 2004, EXP LUNG RES, V30, P147, DOI 10.1080/01902140490266439; Hoshino T, 1999, J Immunol, V162, P51; Hurst SD, 2002, J IMMUNOL, V169, P443; Ikeda K, 2003, BLOOD, V101, P3594, DOI 10.1182/blood-2002-09-2817; Lanone S, 2002, J CLIN INVEST, V110, P463, DOI 10.1172/JCI200214136; Lee J, 2001, J BIOL CHEM, V276, P1660, DOI 10.1074/jbc.M008289200; Lentsch AB, 1999, J IMMUNOL, V162, P1071; Li HM, 1996, J IMMUNOL, V156, P4833; Li N, 2003, ENVIRON HEALTH PERSP, V111, P455, DOI 10.1289/ehp.6000; Li XY, 1996, THORAX, V51, P1216, DOI 10.1136/thx.51.12.1216; Lindroos PM, 1997, AM J RESP CELL MOL, V16, P283; MCKENZIE ANJ, 1993, P NATL ACAD SCI USA, V90, P3735, DOI 10.1073/pnas.90.8.3735; Miyabara Y, 1998, J ALLERGY CLIN IMMUN, V102, P805, DOI 10.1016/S0091-6749(98)70021-1; Pagan I, 2003, J TOXICOL ENV HEAL A, V66, P1087, DOI 10.1080/15287390390213908; Peden DB, 2002, ENVIRON HEALTH PERSP, V110, P565; POPE CA, 1993, AM REV RESPIR DIS, V147, P1336; ROBERTS JR, 2003, J TOXICOL ENV HEAL A, V67, P251; Ruth JH, 2000, CYTOKINE, V12, P432, DOI 10.1006/cyto.1999.0595; Sahoo SK, 2002, J CONTROL RELEASE, V82, P105, DOI 10.1016/S0168-3659(02)00127-X; Salvi S, 1999, CLIN EXP ALLERGY, V29, P1187; Schafer T, 1997, ALLERGY, V52, P14; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; SEATON A, 1995, LANCET, V345, P176, DOI 10.1016/S0140-6736(95)90173-6; SOZZANI P, 1995, J BIOL CHEM, V270, P5084; TEMPLETON DM, 1994, HDB METALS CLIN ANAL, P627; van Zijverden M, 2000, TOXICOL APPL PHARM, V168, P131, DOI 10.1006/taap.2000.9013; Ward PA, 2002, MOL CELL BIOCHEM, V234, P225, DOI 10.1023/A:1015944709177; Wills-Karp M, 2003, CURR OPIN PULM MED, V9, P21, DOI 10.1097/00063198-200301000-00004; Zelikoff JT, 2003, INHAL TOXICOL, V15, P131, DOI 10.1080/08958370390168201	44	72	78	0	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.	SEP	2005	33	3					290	296		10.1165/rcmb.2005-0003OC		7	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	961VI	WOS:000231689500011	15961726	
J	Sepp, E; Julge, K; Mikelsaar, M; Bjorksten, B				Sepp, E; Julge, K; Mikelsaar, M; Bjorksten, B			Intestinal microbiota and immunoglobulin E responses in 5-year-old Estonian children	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergy; bacteroides; bifidobacteria; children; clostridia; gut microbiota; IgE	ATOPIC DISEASES; ALLERGY; MICROFLORA; CHILDHOOD; INFANTS; EXPOSURE; BIFIDOBACTERIA; SENSITIZATION; PREVALENCE; ANTIBODIES	Background Over the last few decades, several studies from different parts of the world have indicated an increasing prevalence of allergic diseases. This has been related to environmental factors, like changes of microbial pressure. Our previous studies have demonstrated differences in the intestinal microbiota between allergic and non-allergic children. Aim To test the hypothesis that the intestinal microbiota and IgE response are related, both in allergic and non-allergic 5-year-old Estonian children. Methods The study group comprised 19 allergic and 19 non-allergic 5-year-old children, selected from a larger group who had been followed from birth. The diagnosis of allergy was based on clinical examination of the children and on data obtained from the questionnaires. The faecal microbiota were quantified by seeding serial dilutions on nine different media for incubation in different environment. The composition of the gut microbiota was expressed both as absolute counts of the various species and their relative share among the total counts of identified microbiota. Results Bifidobacteria were less commonly detected in children with allergic diseases than in healthy children and clostridia comprised a higher proportion among their gut microbes. Children with specific IgE antibodies to defined allergens had higher counts of clostridia and the counts of clostridia correlated with the level of serum IgE, but only so in allergic children. In non-allergic children, the serum IgE levels showed a positive correlation with the counts of bacteroides. Conclusion The development of allergic diseases seems to be associated with the composition of the gut microbial ecosystem. High counts of potential pathogens, such as clostridia, are associated with clinical manifestations of allergy and IgE antibody formation.	Univ Tartu, Dept Microbiol, EE-50411 Tartu, Estonia; Tartu Univ Clin, Childrens Clin, Tartu, Estonia; Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden	Sepp, E (reprint author), Univ Tartu, Dept Microbiol, Ravila St 19, EE-50411 Tartu, Estonia.	epp.sepp@ut.ee	Sepp, Epp/H-6798-2015				APPELT DM, 1993, J STRUCT BIOL, V111, P85, DOI 10.1006/jsbi.1993.1039; Balows A, 1991, MANUAL CLIN MICROBIO; Bjorksten B, 2001, J ALLERGY CLIN IMMUN, V108, P516; BJORKSTEN B, 1994, ALLERGY, V49, P400, DOI 10.1111/j.1398-9995.1994.tb00831.x; Bjorksten B, 1999, CLIN EXP ALLERGY, V29, P342; Bottcher MF, 2000, CLIN EXP ALLERGY, V30, P1590; Brandtzaeg P, 2002, ANN NY ACAD SCI, V964, P13; BRANDTZAEG P, 1989, GASTROENTEROLOGY, V97, P1562; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Butel MJ, 1998, J MED MICROBIOL, V47, P391; Dunder T, 2001, ALLERGY, V56, P425, DOI 10.1034/j.1398-9995.2001.056005425.x; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; HALLER D, 2003, J BIOL CHEM, V26, P23851; Hentges DJ, 1989, ANAEROBIC INFECT HUM, P37; Holt PG, 1997, PEDIATR ALLERGY IMMU, V8, P53, DOI 10.1111/j.1399-3038.1997.tb00145.x; JANSSENS S, 2003, CLIN MICR REV, P637; Julge K, 2001, CLIN EXP ALLERGY, V31, P1854, DOI 10.1046/j.1365-2222.2001.01235.x; Kalliomaki M, 2001, J ALLERGY CLIN IMMUN, V107, P129, DOI 10.1067/mai.2001.111237; Karlsson H, 2002, INFECT IMMUN, V70, P6688, DOI 10.1128/IAI.70.12.6688-6696.2002; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Kimura K, 1997, APPL ENVIRON MICROB, V63, P3394; Linneberg A, 2003, J ALLERGY CLIN IMMUN, V111, P847, DOI 10.1067/mai.2003.1335; Macfarlane G T, 1997, Scand J Gastroenterol Suppl, V222, P3, DOI 10.1080/00365521.1997.11720708; Mackie R I, 1999, Am J Clin Nutr, V69, p1035S; MARLER LM, 1992, J CLIN MICROBIOL, V30, P514; Matsuki T, 1999, APPL ENVIRON MICROB, V65, P4506; Matsumoto Mitsuharu, 2004, Microbial Ecology in Health and Disease, V16, P13, DOI 10.1080/08910600310026167; Mayer L, 2003, PEDIATRICS, V111, P1595; Mikelsaar M, 1993, LACTIC ACID BACTERIA, P237; NORHAGEN G, 1990, Microbial Ecology in Health and Disease, V3, P269; Norin Elisabeth, 2004, Microbial Ecology in Health and Disease, V16, P8, DOI 10.1080/08910600410026364; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; ROLFE RD, 1990, OLD HERBORN U SEMINA, P48; Sepp E, 1997, ACTA PAEDIATR, V86, P956, DOI 10.1111/j.1651-2227.1997.tb15178.x; Strachan David P., 2000, Thorax, V55, pS2, DOI 10.1136/thorax.55.suppl_1.S2; Strannegard O, 2001, ALLERGY, V56, P91, DOI 10.1034/j.1398-9995.2001.056002091.x; VANDERWAAIJ D, 1983, INFECTION S2, V11, P90; VOLLAARD EJ, 1994, ANTIMICROB AGENTS CH, V38, P409; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; WATANABE S, 2001, J ALLERGY CLIN IMMUN, V111, P587; Wold AE, 1998, ALLERGY, V53, P20; YASUI H, 1995, J INFECT DIS, V172, P403	42	72	80	0	3	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	SEP	2005	35	9					1141	1146		10.1111/j.1365-2222.2005.02315.x		6	Allergy; Immunology	Allergy; Immunology	964SX	WOS:000231901900004	16164439	
J	Choudhry, S; Avila, PC; Nazario, S; Ung, N; Kho, J; Rodriguez-Santana, JR; Casal, J; Tsai, HJ; Torres, A; Ziv, E; Toscano, M; Sylvia, JS; Alioto, M; Salazar, M; Gomez, I; Fagan, JK; Salas, J; Lilly, C; Matallana, H; Castro, RA; Selman, M; Weiss, ST; Ford, JG; Drazen, JM; Rodriguez-Cintron, W; Chapela, R; Silverman, EK; Burchard, EG				Choudhry, S; Avila, PC; Nazario, S; Ung, N; Kho, J; Rodriguez-Santana, JR; Casal, J; Tsai, HJ; Torres, A; Ziv, E; Toscano, M; Sylvia, JS; Alioto, M; Salazar, M; Gomez, I; Fagan, JK; Salas, J; Lilly, C; Matallana, H; Castro, RA; Selman, M; Weiss, ST; Ford, JG; Drazen, JM; Rodriguez-Cintron, W; Chapela, R; Silverman, EK; Burchard, EG		Genet Asthma Latino Amer Study	CD14 tobacco gene-environment interaction modifies asthma severity and Immunoglobulin E levels in Latinos with asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma genetics; CD14; gene-environment interaction; IgE; Latinos; tobacco	MENTHOL CIGARETTE USE; PUERTO-RICAN; PROMOTER POLYMORPHISMS; CHILDHOOD ASTHMA; ATOPIC DISEASES; PASSIVE SMOKING; SOLUBLE CD14; CHILDREN; IGE; ASSOCIATION	Background: A recent family-based genomewide screen revealed linkage between the 5q31 region and the diagnosis of asthma, but only in those exposed to environmental tobacco smoke (ETS). Among the candidate genes in this region is CD14. Methods: To determine whether polymorphisms in the CD14 gene are related to this gene-by-environment interaction in Latinos, we used both family-based and cross-sectional cohort analysis to test for interactions between CD14 genotypes/haplotypes, exposure to ETS, and asthma-related phenotypes in 659 Mexican and Puerto Rican families. Results: We identified 21 single nucleotide polymorphisms (SNPs) in the CD14 gene by sequencing 72 Puerto Ricans, Mexicans, and African Americans with asthma. Three SNPs, -810, -159, and +1437, were further genotyped in families with asthma. Among all subjects with asthma exposed to ETS, without regard to ethnicity, CD14 +1437 genotypes were associated with asthma severity. SNP +1437 GG or GC genotypes were significantly associated with lower baseline FEV1, using both family-based (p = 0.0009) and cross-sectional cohort (p 0.03) analyses. Subjects with asthma with the GG or GC genotypes who were exposed to ETS had mean baseline FEV1 (% predicted) values 8.6% lower than subjects not exposed to ETS (p = 0.03). As previously observed in whites, we found an interaction between plasma IgE levels, SNP -159 genotypes, and ETS exposure (p = 0.0002). The lowest IgE levels were in those subjects with the TT genotype and who were exposed to ETS regardless of ethnicity. Conclusions: Our data suggest a gene-by-environment interaction between CD14 genotypes and ETS, which affects pulmonary function and IgE levels among Latinos with asthma.	Univ Calif San Francisco, San Francisco Gen Hosp, Lung Biol Ctr, San Francisco, CA 94110 USA; Univ Puerto Rico, Sch Med, San Juan Vet Affairs Med Ctr, San Juan, PR 00936 USA; Pediat Pulm Program San Juan, San Juan, PR USA; Brigham & Womens Hosp, Boston, MA 02115 USA; Harlem Hosp Med Ctr, Harlem Lung Ctr, New York, NY USA; Columbia Univ, New York, NY USA; Inst Nacl Enfermedades Resp, Mexico City, DF, Mexico	Burchard, EG (reprint author), Univ Calif San Francisco, San Francisco Gen Hosp, Lung Biol Ctr, Bldg 30,5th Floor,Room 3501H,1001 Potrero Ave, San Francisco, CA 94110 USA.	esteban.burchard@ucsf.edu	Tsai, Hui-Ju /E-3937-2010; Ziv, Elad/L-5396-2014				American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Buckova D, 2003, ALLERGY, V58, P1023, DOI 10.1034/j.1398-9995.2003.00271.x; Burchard EG, 2004, AM J RESP CRIT CARE, V169, P386, DOI 10.1164/rccm.200309-1239OC; Burchard EG, 2003, NEW ENGL J MED, V348, P1170, DOI 10.1056/NEJMsb025007; CARTERPOKRAS OD, 1993, AM J PUBLIC HEALTH, V83, P580, DOI 10.2105/AJPH.83.4.580; Chen XN, 1999, GENOME RES, V9, P492; Colilla S, 2003, J ALLERGY CLIN IMMUN, V111, P840, DOI 10.1067/mai.2003.170; ENRIGHT PL, 1991, AM REV RESPIR DIS, V143, P1215; Enright PL, 1994, AM J RESP CRIT CAR S, V149, P9; FERRIS BG, 1978, AM REV RESPIR DIS, V118, P1; Fuhlbrigge AL, 2001, J ALLERGY CLIN IMMUN, V107, P61, DOI 10.1067/mai.2001.111590; Gardiner PS, 2004, NICOTINE TOB RES, V6, pS55, DOI 10.1080/1462220310001649478; Gilliland FD, 2002, AM J RESP CRIT CARE, V166, P457, DOI 10.1164/rccm.2112064; Giovino GA, 2004, NICOTINE TOB RES, V6, pS67, DOI 10.1080/14622203710001649696; Hankinson JL, 1999, AM J RESP CRIT CARE, V159, P179; Hasday JD, 1999, CHEST, V115, P829, DOI 10.1378/chest.115.3.829; Heinzmann A, 2003, EUR J IMMUNOGENET, V30, P345, DOI 10.1046/j.1365-2370.2003.00414.x; Hoffjan S, 2003, RESPIR RES, V4, DOI 10.1186/1465-9921-4-14; Hoffjan S, 2002, CURR OPIN IMMUNOL, V14, P709, DOI 10.1016/S0952-7915(02)00393-X; HOGG JC, 1968, NEW ENGL J MED, V278, P1355, DOI 10.1056/NEJM196806202782501; Holt PG, 1997, PEDIATR ALLERGY IMMU, V8, P53, DOI 10.1111/j.1399-3038.1997.tb00145.x; Homa DM, 2000, AM J RESP CRIT CARE, V161, P504; Horvath S, 2001, EUR J HUM GENET, V9, P301, DOI 10.1038/sj.ejhg.5200625; Kabesch M, 2004, ALLERGY, V59, P520, DOI 10.1111/j.1398-9995.2004.00439.x; Kimata H, 2003, EUR J CLIN INVEST, V33, P1024, DOI 10.1046/j.1365-2362.2003.01250.x; Kitch BT, 2004, CHEST, V126, P1875, DOI 10.1378/chest.126.6.1875; Koppelman GH, 2001, AM J RESP CRIT CARE, V163, P965; Laird NM, 2000, GENET EPIDEMIOL, V19, P36; Larsson L, 2004, INDOOR AIR, V14, P421, DOI 10.1111/j.1600-0668.2004.00290.x; Leung TF, 2003, PEDIATR ALLERGY IMMU, V14, P255, DOI 10.1034/j.1399-3038.2003.00048.x; LeVan TD, 2005, AM J RESP CRIT CARE, V171, P773, DOI 10.1164/rccm.200404-530OC; Mackay J, 2002, TOBACCO ATLAS; O'Connell JR, 1998, AM J HUM GENET, V63, P259, DOI 10.1086/301904; O'Donnell AR, 2004, AM J RESP CRIT CARE, V169, P615, DOI 10.1164/rccm.200302-278OC; Ober C, 2000, AM J HUM GENET, V67, P1154, DOI 10.1016/S0002-9297(07)62946-2; Ott J, 1999, ANAL HUMAN GENETIC L; Paull K, 2005, PEDIATR PULM, V39, P311, DOI 10.1002/ppul.20161; Perez-Stable EJ, 2001, AM J PUBLIC HEALTH, V91, P1424, DOI 10.2105/AJPH.91.9.1424; SEARS MR, 1991, NEW ENGL J MED, V325, P1067, DOI 10.1056/NEJM199110103251504; Sengler C, 2003, CLIN EXP ALLERGY, V33, P166, DOI 10.1046/j.1365-2222.2003.01549.x; Sopori M, 2002, NAT REV IMMUNOL, V2, P372, DOI 10.1038/nri803; SPIELMAN RS, 1993, AM J HUM GENET, V52, P506; Strachan DP, 1998, THORAX, V53, P204; TAGER IB, 1989, CHEST, V96, P1161, DOI 10.1378/chest.96.5.1161; Tulic MK, 2000, AM J RESP CELL MOL, V22, P604; Vercelli D, 2004, J ALLERGY CLIN IMMUN, V113, P381, DOI 10.1016/j.jaci.2004.01.752; Wells AJ, 1998, AM J PUBLIC HEALTH, V88, P1503, DOI 10.2105/AJPH.88.10.1503; Ziv E, 2003, PHARMACOGENOMICS, V4, P431, DOI 10.1517/phgs.4.4.431.22758; [Anonymous], 1999, NAT GENET, V22, P1	51	72	74	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.	JUL 15	2005	172	2					173	182		10.1164/rccm.200409-1232OC		10	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	943QG	WOS:000230368400005	15879416	
J	Wang, JL; Visness, CM; Sampson, HA				Wang, JL; Visness, CM; Sampson, HA			Food allergen sensitization in inner-city children with asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; food allergy; sensitization; IgE; inner-city children	MANIFESTATIONS	Background: Asthma continues to be an increasing cause of morbidity in the pediatric population, and studies have shown an association between food sensitivity and asthma. Objective: We investigated the degree of food allergen sensitization in inner-city patients with asthma. Methods: Five hundred four random serum samples from the National Cooperative Inner City Asthma Study were evaluated for specific IgE (UniCap) to 6 common food allergens (egg, milk, soy, peanut, wheat, and fish). Statistical analyses were performed to determine food sensitization prevalence and its association with asthma morbidity. Results: Forty-five percent of patients had evidence of sensitization (food-specific IgE &GE; 0.35 kU/L) to at least 1 food. Nineteen percent had IgE levels at &GE; 50% positive predictive value for clinical reactivity to at least 1 food, with 4% of patients having levels &GT; 95% positive predictive value for food allergy. Children sensitized to foods had higher rates of asthma hospitalization (P &LT; .01) and required more steroid medications (P = .025). Sensitization to foods also correlated with sensitization to more indoor and outdoor aeroallergens (P &LT; .001). Conclusion: Food allergen sensitization is highly prevalent in the inner-city population with asthma, and it is associated with increased asthma healthcare and medication use. Therefore, food allergen sensitivity may be a marker for increased asthma severity.	Mt Sinai Sch Med, Dept Pediat, Div Allergy & Immunol, New York, NY 10029 USA; Rho Fed Syst Div Inc, Chapel Hill, NC USA	Sampson, HA (reprint author), Mt Sinai Sch Med, Dept Pediat, Div Allergy & Immunol, Box 1198,1 Gustave L Levy Pl, New York, NY 10029 USA.	hugh.sampson@mssm.edu	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	NIAID NIH HHS [AI030779, AI-30752, AI-30756, AI-30772, AI-30773-01, AI-30777, AI-30780, N01-AI-15105, U0I AI-30751]		BOCK SA, 1989, J ALLERGY CLIN IMMUN, V83, P900, DOI 10.1016/0091-6749(89)90103-6; Bock SA, 1992, PEDIATR ALLERGY IMMU, V3, P188, DOI 10.1111/j.1399-3038.1992.tb00048.x; DEY AN, 2004, VITAL HLTH STAT, V10, P3; Heiss S, 1996, J ALLERGY CLIN IMMUN, V98, P938, DOI 10.1016/S0091-6749(96)80010-8; HILL DJ, 1986, J PEDIATR-US, V109, P270, DOI 10.1016/S0022-3476(86)80384-5; JAMES JM, 1994, AM J RESP CRIT CARE, V149, P59; James JM, 2003, PEDIATRICS, V111, P1625; JONES SM, 1995, J ALLERGY CLIN IMMUN, V96, P341, DOI 10.1016/S0091-6749(95)70053-6; Kattan M, 1997, PEDIATR PULM, V24, P253, DOI 10.1002/(SICI)1099-0496(199710)24:4<253::AID-PPUL4>3.0.CO;2-L; Mannino DM, 1998, MMWR-MORBID MORTAL W, V47, P1; Mitchell H, 1997, PEDIATR PULM, V24, P237; NOVEMBRE E, 1988, J ALLERGY CLIN IMMUN, V81, P1059, DOI 10.1016/0091-6749(88)90181-9; OEHLING A, 1980, ALLERGOL IMMUNOPATH, V8, P7; ONORATO J, 1986, J ALLERGY CLIN IMMUN, V78, P1139, DOI 10.1016/0091-6749(86)90263-0; Roberts G, 2003, J ALLERGY CLIN IMMUN, V112, P168, DOI 10.1067/mai.2003.1569; Roberts Graham, 2003, Paediatr Respir Rev, V4, P205, DOI 10.1016/S1526-0542(03)00058-7; Sampson HA, 2001, J ALLERGY CLIN IMMUN, V107, P891, DOI 10.1067/mai.2001.114708; SAMPSON HA, 1992, NEW ENGL J MED, V327, P380, DOI 10.1056/NEJM199208063270603	18	72	74	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					1076	1080		10.1016/j.jaci.2005.02.014		5	Allergy; Immunology	Allergy; Immunology	925LR	WOS:000229055100027	15867869	
J	Matsui, EC; Simons, E; Rand, C; Butz, A; Buckley, TJ; Breysse, P; Eggleston, PA				Matsui, EC; Simons, E; Rand, C; Butz, A; Buckley, TJ; Breysse, P; Eggleston, PA			Airborne mouse allergen in the homes of inner-city children with asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						mouse allergen; inner-city asthma; particulate matter; Mus m 1	SKIN-TEST SENSITIVITY; EXPOSURE; SENSITIZATION; PREVALENCE; CATS	Background: Airborne mouse allergen has not previously been measured in inner-city homes, and its relationship to settled dust mouse allergen levels is unknown. Objective: To quantify airborne and settled dust Mus m 1 levels in homes of inner-city patients with asthma and to identify risk factors for mouse allergen exposure. Methods: One hundred inner-city school-age children with asthma in Baltimore underwent skin testing to a panel of aeroallergens, and their homes were inspected by a trained technician. Air and settled dust were sampled in the child's bedroom. Mus m 1, particulate matter smaller than 10 microns (PM10), and particulate matter smaller than 2.5 microns were quantified in air samples, and Mus m 1 was quantified in settled dust samples. Results: Mus m 1 was detected in settled dust samples from 100% of bedrooms. Airborne mouse allergen was detected in 48 of 57 (84%) bedrooms, and the median airborne mouse allergen concentration was 0.03 ng/m(3). The median PM10 concentration was 48 mug/m(3). Airborne and settled dust mouse allergen levels were moderately correlated (r = .52; P < .0001), and airborne Mus m 1 and PM10 levels were weakly correlated (r =.29; P = .03). Having cracks or holes in doors or walls, evidence of food remains in the kitchen, and mouse infestation were all independently associated with having detectable airborne mouse allergen. Conclusion: Airborne mouse allergen concentrations in many inner-city homes may be similar to those found in animal facilities, where levels are sufficiently high to elicit symptoms in sensitized individuals. Exposed food remains, cracks and holes in doors or walls, and evidence of mouse infestation appear to be risk factors for having detectable airborne Mus m 1.	Johns Hopkins Univ, Sch Med, Baltimore, MD 21218 USA; Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD 21218 USA	Matsui, EC (reprint author), Johns Hopkins Univ Hosp, Dept Pediat, 600 N Wolfe St,CMSC 1102, Baltimore, MD 21287 USA.	ematsui@jhmi.edu			NHLBI NIH HHS [HL058942]; NIEHS NIH HHS [ES09606]		Bollinger ME, 1996, J ALLERGY CLIN IMMUN, V97, P907, DOI 10.1016/S0091-6749(96)80064-9; 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; Eggleston PA, 1998, J ALLERGY CLIN IMMUN, V102, P563, DOI 10.1016/S0091-6749(98)70272-6; Korpi A, 2004, J ALLERGY CLIN IMMUN, V113, P677, DOI 10.1016/j.jaci.2003.11.039; Lewis RD, 1998, AM IND HYG ASSOC J, V59, P606, DOI 10.1202/0002-8894(1998)059<0606:FATROD>2.0.CO;2; LUCZYNSKA CM, 1990, AM REV RESPIR DIS, V141, P361; Matsui EC, 2004, ANN ALLERG ASTHMA IM, V93, P171; Matsui EC, 2004, J ALLERGY CLIN IMMUN, V113, P910, DOI 10.1016/j.jaci.2004.02.034; Mitchell H, 1997, PEDIATR PULM, V24, P237; OHMAN JL, 1994, J ALLERGY CLIN IMMUN, V94, P810, DOI 10.1016/0091-6749(94)90147-3; Phipatanakul W, 2000, J ALLERGY CLIN IMMUN, V106, P1070, DOI 10.1067/mai.2000.110796; Phipatanakul W, 2000, J ALLERGY CLIN IMMUN, V106, P1075; SCHUMACHER MJ, 1981, J ALLERGY CLIN IMMUN, V68, P310, DOI 10.1016/0091-6749(81)90157-3; Swartz LJ, 2004, ENVIRON RES, V95, P156, DOI 10.1016/j.envres.2003.08.003; Wood RA, 2001, ANN ALLERG ASTHMA IM, V87, P60	16	72	72	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.	FEB	2005	115	2					358	363		10.1016/j.jaci.2004.11.007		6	Allergy; Immunology	Allergy; Immunology	897YU	WOS:000227043600024	15696095	
J	Fulkerson, PC; Zimmermann, N; Hassman, LM; Finkelman, FD; Rothenberg, ME				Fulkerson, PC; Zimmermann, N; Hassman, LM; Finkelman, FD; Rothenberg, ME			Pulmonary chemokine expression is coordinately regulated by STAT1, STAT6, and IFN-gamma	JOURNAL OF IMMUNOLOGY			English	Article							SOCS-1 GENE-EXPRESSION; AIRWAY INFLAMMATION; T-CELLS; EOSINOPHILIC INFLAMMATION; EXPERIMENTAL ASTHMA; EOTAXIN EXPRESSION; EPITHELIAL-CELLS; MUCUS PRODUCTION; TNF-ALPHA; TH2 CELLS	The expression of distinct chemokines within the asthmatic lung suggests that specific regulatory mechanisms may mediate various stages of asthmatic disease. Global transcript expression profiling was used to define the spectrum and kinetics of chemokine involvement in an experimental murine model of asthma. Seventeen chemokines were induced in the lungs of allergen-inoculated mice, as compared with saline-treated mice. Two (CXCL13 and CCL9) of the 17 identified chemokines have not previously been associated with allergic airway disease. Seven (7 of 17; CCL2, CCL7, CCL9, CCL11, CXCL1, CXCL5, CXCL10) of the allergen-induced chemokines were induced early after allergen challenge and remained induced throughout the experimental period. Three chemokines (CXCL2, CCL3, and CCL17) were induced only during the early phase of the inflammatory response after the initial allergen challenge, while seven chemokines (CCL6, CCL8, CCL12, CCL22, CXCL9, CXCL12, and CXCL13) were increased only after a second allergen exposure. Unexpectedly, expression of only three chemokines, CCL11, CCL17, and CCL22, was STAT6 dependent, and many of the identified chemokines were overexpressed in STAT6-deficient mice, providing an explanation for the enhanced neutrophilic inflammation seen in these mice. Notably, IFN-gamma and STAT1 were shown to contribute to the induction of two STAT6-independent chemokines, CXCL9 and CXCL10. Taken together, these results show that only a select panel of chemokines (those targeting Th2 cells and eosinophils) is positively regulated by STAT6; instead, many of the allergen-induced chemokines are negatively regulated by STAT6. Collectively, we demonstrate that allergen-induced inflammation involves coordinate regulation by STAT1, STAT6, and IFN-gamma.	Univ Cincinnati, Coll Med, Cincinnati Childrens Hosp, Ctr Med,Div Allergy & Immunol, Cincinnati, OH 45229 USA; Univ Cincinnati, Coll Med, Dept Mol Genet, Cincinnati, OH 45257 USA; Univ Cincinnati, Coll Med, Dept Biochem & Mol Biol, Cincinnati, OH 45257 USA; Univ Cincinnati, Coll Med, Dept Internal Med, Div Immunol, Cincinnati, OH 45257 USA	Rothenberg, ME (reprint author), Univ Cincinnati, Coll Med, Cincinnati Childrens Hosp, Ctr Med,Div Allergy & Immunol, 3333 Burnet Ave, Cincinnati, OH 45229 USA.	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Immunol.	DEC 15	2004	173	12					7565	7574				10	Immunology	Immunology	878RT	WOS:000225665100056	15585884	
J	Moorcroft, AJ; Dodd, ME; Morris, J; Webb, AK				Moorcroft, AJ; Dodd, ME; Morris, J; Webb, AK			Individualised unsupervised exercise training in adults with cystic fibrosis: a 1 year randomised controlled trial	THORAX			English	Article							PULMONARY-FUNCTION; LUNG-FUNCTION; CHILDREN; PROGRAM; TOLERANCE; CAPACITY; ASTHMA	Background: Short term studies of exercise training have shown benefits in cystic fibrosis. Transferring exercise programmes to the community and sustaining them long term is a challenge for the patient. The effectiveness of an individualised unsupervised home based exercise programme was examined in adults with cystic fibrosis over a 1 year period. Methods: Subjects were randomised to undertake three sessions per week of upper and lower body exercise based on individualised preferences (n = 30) or to a control group ( n = 18). They were evaluated at baseline and at 12 months. The primary outcome measure was improved fitness as assessed by change in blood lactate concentration at the end of an identical constant work rate for both arm and leg ergometric testing. Secondary outcome measurements were heart rate and pulmonary function. Results: For leg exercise, significant differences were seen at 12 months between the active and control groups in the mean (SE) change in blood lactate levels (-0.38 (0.23) mmol/l v 0.45 (0.25) mmol/l, p<0.05) and heart rate (-4.8 (2.5) bpm v 3.4 (2.5) bpm, p<0.05), confirming a training effect. For arm ergometry there was no change in lactate levels at 12 months but there was a significant difference in forced vital capacity (46 (72) ml v -167 (68) ml, p<0.05). Conclusions: A training effect, as measured by a reduction in lactate levels and heart rate, can be achieved with unsupervised individualised home exercise in adults with cystic fibrosis. A benefit to pulmonary function was observed and together these findings suggest that exercise programmes should be encouraged as an important component of care in cystic fibrosis.	Univ S Manchester Hosp NHS Trust, Manchester Adult CF Ctr, Wythenshawe Hosp, Manchester M23 9LT, Lancs, England; Royal Shrewsbury Hosp, Shrewsbury SY3 8XQ, Salop, England; Wythenshawe Hosp, Manchester M23 9LT, Lancs, England	Webb, AK (reprint author), Univ S Manchester Hosp NHS Trust, Manchester Adult CF Ctr, Wythenshawe Hosp, Manchester M23 9LT, Lancs, England.	the5webbs@hotmail.com					Abbott J, 1996, THORAX, V51, P1233, DOI 10.1136/thx.51.12.1233; ABBOTT J, 1994, THORAX, V49, P115, DOI 10.1136/thx.49.2.115; ANDREASSON B, 1987, ACTA PAEDIATR SCAND, V76, P70, DOI 10.1111/j.1651-2227.1987.tb10417.x; BLOMQUIST M, 1986, ARCH DIS CHILD, V61, P362; BORG GAV, 1982, MED SCI SPORT EXER, V14, P377, DOI 10.1249/00005768-198205000-00012; CASSABURI R, 1991, AM REV RESPIR DIS, V143, P9; CERNY FJ, 1984, AM J DIS CHILD, V138, P261; CERNY FJ, 1982, AM REV RESPIR DIS, V126, P217; COATES AL, 1980, ACTA PAEDIATR SCAND, V69, P353, DOI 10.1111/j.1651-2227.1980.tb07092.x; COREY M, 1976, AM REV RESPIR DIS, V114, P1085; Cote J, 1998, CHEST, V113, P968, DOI 10.1378/chest.113.4.968; DEJONG W, 1994, CHEST, V105, P463, DOI 10.1378/chest.105.2.463; EDLUND LD, 1986, AM J DIS CHILD, V140, P80; FRANKLIN BA, 1985, SPORTS MED, V2, P100; GODFREY S, 1971, ARCH DIS CHILD, V46, P144; Gulmans VAM, 1999, PEDIATR PULM, V28, P39, DOI 10.1002/(SICI)1099-0496(199907)28:1<39::AID-PPUL7>3.0.CO;2-8; Heijerman H G, 1992, Int J Rehabil Res, V15, P252, DOI 10.1097/00004356-199209000-00011; HOLZER FJ, 1984, AUST PAEDIATR J, V20, P297; Jones NL, 1988, CLIN EXERCISE TESTIN; KEREM E, 1992, NEW ENGL J MED, V326, P1187, DOI 10.1056/NEJM199204303261804; KNUDSON RJ, 1983, AM REV RESPIR DIS, V127, P725; LANDS LC, 1992, CLIN SCI, V83, P391; LEWIN LO, 1990, J CLIN EPIDEMIOL, V43, P125; Mahadeva R, 1998, BRIT MED J, V316, P1771; MARCOTTE JE, 1986, PEDIATR PULM, V2, P274, DOI 10.1002/ppul.1950020505; Milla CE, 1998, CHEST, V113, P1230, DOI 10.1378/chest.113.5.1230; NIXON PA, 1992, NEW ENGL J MED, V327, P1785, DOI 10.1056/NEJM199212173272504; ONEILL PA, 1987, BRIT J DIS CHEST, V81, P62, DOI 10.1016/0007-0971(87)90109-4; ORENSTEIN DM, 1981, CHEST, V80, P392, DOI 10.1378/chest.80.4.392; PENKETH ARL, 1987, THORAX, V42, P526, DOI 10.1136/thx.42.7.526; SALH W, 1989, THORAX, V44, P1006, DOI 10.1136/thx.44.12.1006; SCHNEIDERMANWALKER, 2000, J PEDIATR, V136, P304; STRAUSS GD, 1987, CHEST, V92, P273, DOI 10.1378/chest.92.2.273; ZACH MS, 1981, LANCET, V2, P1201	34	72	72	1	11	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	DEC	2004	59	12					1074	1080		10.1136/thx.2003.015313		7	Respiratory System	Respiratory System	874NV	WOS:000225358000016	15563708	
J	Newson, RB; Shaheen, SO; Henderson, AJ; Emmett, PM; Sherriff, A; Calder, PC				Newson, RB; Shaheen, SO; Henderson, AJ; Emmett, PM; Sherriff, A; Calder, PC		ALSPAC Study Team	Umbilical cord and maternal blood red cell fatty acids and early childhood wheezing and eczema	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						n-3/n-6 Fatty acids; wheezing; eczema; birth cohort; prenatal	AIRWAY RESPONSES; ATOPIC DISEASE; BIRTH-WEIGHT; CHILDREN; PROSTAGLANDIN-E2; ALLERGY; LYMPHOCYTES; PREGNANCY; GAMMA; RISK	Background: Few studies have explored whether fetal exposure to n-6 and n-3 fatty acids influences the inception of atopic disease. Objective: To assess prenatal fatty acid exposures as predictors of early childhood wheezing and eczema. Methods: In the Avon Longitudinal Study of Parents and Children, late pregnancy maternal blood samples and umbilical cord blood samples were assayed for n-6 and n-3 fatty acids (percentage of total red cell phospholipid), and mothers were asked about wheezing and eczema in their children. We measured associations of 11 n-6 and n-3 fatty acid exposures with wheezing at 30 to 42 months, with wheezing patterns defined by presence (+) or absence (-) of wheezing during 2 periods, 0 to 6 months and 30 to 42 months (transient infant, +/-; later-onset, -/+; persistent, +/+; n = 1191 and n = 2764 for cord and maternal analyses, respectively), and with eczema at 18 to 30 months (n = 1238 and n = 2945 for cord and maternal analyses, respectively). Results: In cord blood red cells, the ratio of arachidonic:eicosapentaenoic acid was positively associated with eczema (adjusted odds ratio [OR] per doubling, 1.14; 95% CI, 1.00-1.31; P = .044), the ratio of linoleic acid: a-linolenic acid was positively associated with later-onset wheeze (OR, 1.30; CI, 1.04-1.61; P = .019), and the ratio of a-linolenic acid:n-3 products was negatively associated with later-onset wheeze (OR, 0.86; CI, 0.75-0.99; P = .040). However, these associations were no longer significant after adjusting for multiple comparisons. Conclusions: It seems unlikely that fetal exposure to n-6 and n-3 fatty acids is an important determinant of early childhood wheezing and atopic disease.	Kings Coll London, Guys Kings & St Thomas Sch Med, Dept Publ Hlth Sci, London SE1 3QD, England; Univ Bristol, Inst Child Hlth, Unit Paediat & Perinatal Epidemiol, Bristol, Avon, England; Univ Southampton, Inst Human Nutr, Southampton, Hants, England	Shaheen, SO (reprint author), Kings Coll London, Guys Kings & St Thomas Sch Med, Dept Publ Hlth Sci, Capital House,42 Weston St, London SE1 3QD, England.	seif.shaheen@kcl.ac.uk	Calder, Philip/E-9739-2013	Calder, Philip/0000-0002-6038-710X; Henderson, Alexander John/0000-0001-9650-231X; Emmett, Pauline/0000-0003-1076-4779			Benbernou N, 1997, IMMUNOLOGY, V91, P361, DOI 10.1046/j.1365-2567.1997.00260.x; Benjamini Y, 2001, BEHAV BRAIN RES, V125, P279, DOI 10.1016/S0166-4328(01)00297-2; BETZ M, 1991, J IMMUNOL, V146, P108; Black PN, 1997, EUR RESPIR J, V10, P6, DOI 10.1183/09031936.97.10010006; Calder PC, 2000, PEDIATR ALLERGY IMMU, V11, P29, DOI 10.1034/j.1399-3038.2000.00508.x; Duchen K, 2000, PEDIATR ALLERGY IMMU, V11, P29, DOI 10.1034/j.1399-3038.2000.00052.x; Dunstan JA, 2003, CLIN EXP ALLERGY, V33, P442, DOI 10.1046/j.1365-2222.2003.01590.x; Elias SL, 2001, AM J CLIN NUTR, V73, P807; GALLI E, 1994, BRIT J DERMATOL, V130, P752, DOI 10.1111/j.1365-2133.1994.tb03413.x; Gauvreau GM, 1999, AM J RESP CRIT CARE, V159, P31; Golding J, 2001, PAEDIATR PERINAT EP, V15, P74; HORROBIN DF, 2000, AM J CLIN NUTR S, V71, pS72; MANKU MS, 1982, PROSTA LEUKOTR MED, V9, P615, DOI 10.1016/0262-1746(82)90019-1; Martin JG, 2002, J IMMUNOL, V169, P3963; MATLOFF SM, 1983, J ALLERGY CLIN IMMUN, V72, P359, DOI 10.1016/0091-6749(83)90500-6; PAVORD ID, 1995, LANCET, V345, P436, DOI 10.1016/S0140-6736(95)90409-3; 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; Rump P, 2001, AM J CLIN NUTR, V73, P797; Sherriff A, 2001, INT J EPIDEMIOL, V30, P1473, DOI 10.1093/ije/30.6.1473; SNIJDEWINT FGM, 1993, J IMMUNOL, V150, P5321; [Anonymous], 2001, STAT STAT SOFTW REL; University of Bristol, AV LONG STUD PAR CHI; Wijendran V, 1999, AM J CLIN NUTR, V70, P53; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P383, DOI 10.1111/j.1365-2133.1994.tb08530.x; WRIGHT S, 1990, OMEGA 6 ESSENTIAL FA, P55; Yu G, 1998, PEDIATR ALLERGY IMMU, V9, P133, DOI 10.1111/j.1399-3038.1998.tb00359.x; Yu G, 1998, EUR J PEDIATR, V157, P298, DOI 10.1007/s004310050815; Yu G, 1996, ACTA PAEDIATR, V85, P679, DOI 10.1111/j.1651-2227.1996.tb14124.x	29	72	73	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.	SEP	2004	114	3					531	537		10.1016/j.jaci.2004.05.010		7	Allergy; Immunology	Allergy; Immunology	853AX	WOS:000223799600010	15356553	
J	Wong, GWK; Ko, FWS; Hui, DSC; Fok, TF; Carr, D; von Mutius, E; Zhong, NS; Chen, YZ; Lai, CKW				Wong, GWK; Ko, FWS; Hui, DSC; Fok, TF; Carr, D; von Mutius, E; Zhong, NS; Chen, YZ; Lai, CKW			Factors associated with difference in prevalence of asthma in children from three cities in China: multicentre epidemiological survey	BRITISH MEDICAL JOURNAL			English	Article							RESPIRATORY SYMPTOMS; CHILDHOOD ASTHMA; HOME-ENVIRONMENT; LUNG-FUNCTION; YOUNG-ADULTS; SCHOOLCHILDREN; POPULATION; RISK	Objective To determine the factors associated with difference in prevalence of asthma in children in different regions of China. Design Multicentre epidemiological survey. Setting Three cities in china. Participants 10 902 schoolchildren aged 10 years. Main outcome measures Asthma and atopic symptoms, atopic sensitisation, and early and current exposure to environmental factors. Results Children from Hong Kong had a significantly higher prevalence of wheeze in the past year than those from Guangzhou and Beijing (odds ratio 1.64, 95% confidence interval 1.35 to 1.99). Factors during the first year of life and currently that were significantly associated with wheeze were cooking with gas (odds ratio 2.04, 1.34 to 3.13), foam pillows (2.58, 1.66 to 3.99), and damp housing (1.89,1.26 to 2.83). Factors protecting against wheeze were cotton quilts and the consumption of fruit and raw vegetables. Conclusion Environmental factors and diet may explain the differences in prevalence of asthma between children living in different regions of China.	Chinese Univ Hong Kong, Dept Paediat, Hong Kong, Hong Kong, Peoples R China; Chinese Univ Hong Kong, Dept Med & Therapeut, Hong Kong, Hong Kong, Peoples R China; Univ Childrens Hosp, Munich, Germany; Guangzhou Inst Resp Dis, Guangzhou, Peoples R China; Capital Inst Paediat, Clin & Educ Ctr Asthma, Beijing, Peoples R China	Wong, GWK (reprint author), Chinese Univ Hong Kong, Dept Paediat, Hong Kong, Hong Kong, Peoples R China.	wingkunvong@cuhk.edu.hk	Hui, David/O-2754-2015; Ko, Fanny/B-8958-2016	Ko, Fanny/0000-0001-8454-0087			ABERG N, 1995, CLIN EXP ALLERGY, V25, P815, DOI 10.1111/j.1365-2222.1995.tb00023.x; ANDRAE S, 1988, ARCH DIS CHILD, V63, P473; BRUNEKREEF B, 1989, AM REV RESPIR DIS, V140, P1363; Burr ML, 1999, THORAX, V54, P27; BURR ML, 1989, ARCH DIS CHILD, V64, P1118; D'Agostino RB, 1998, STAT MED, V17, P2265, DOI 10.1002/(SICI)1097-0258(19981015)17:19<2265::AID-SIM918>3.0.CO;2-B; DEKKER C, 1991, CHEST, V100, P922, DOI 10.1378/chest.100.4.922; Goren AI, 1997, EUR RESPIR J, V10, P2279, DOI 10.1183/09031936.97.10102279; Greenland S., 1998, MODERN EPIDEMIOLOGY; HSIEH KH, 1988, J ASTHMA, V25, P73, DOI 10.3109/02770908809071357; The International Study of Asthma and Allergies in Childhood (ISAAC) Steering Committee, 1998, LANCET, V351, P1125; Jarvis D, 1996, LANCET, V347, P426, DOI 10.1016/S0140-6736(96)90009-4; Leung R, 1997, EUR RESPIR J, V10, P354, DOI 10.1183/09031936.97.10020354; Pearce N, 1999, THORAX, V54, P268; Ponsonby AL, 2001, CLIN EXP ALLERGY, V31, P1544, DOI 10.1046/j.1365-2222.2001.01163.x; Shaheen SO, 2001, AM J RESP CRIT CARE, V164, P1823; SHAW RA, 1990, ARCH DIS CHILD, V65, P1319; Strachan D, 1997, BRIT MED J, V314, P518; STRACHAN DP, 1995, BRIT MED J, V311, P1053; Williamson IJ, 1997, THORAX, V52, P229; Wong GWK, 2002, EUR RESPIR J, V19, P288, DOI 10.1183/09031936.02.002319.02; Wong GWK, 2001, CLIN EXP ALLERGY, V31, P1225, DOI 10.1046/j.1365-2222.2001.01140.x; Woods RK, 2003, AM J CLIN NUTR, V78, P414	23	72	74	0	8	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0959-535X			BRIT MED J	Br. Med. J.	AUG 28	2004	329	7464					486	488B		10.1136/bmj.329.7464.486		5	Medicine, General & Internal	General & Internal Medicine	851KS	WOS:000223684600014	15331473	
J	Polk, S; Sunyer, J; Munoz-Ortiz, L; Barnes, M; Torrent, M; Figueroa, C; Harris, J; Vall, O; Anto, JM; Cullinan, P				Polk, S; Sunyer, J; Munoz-Ortiz, L; Barnes, M; Torrent, M; Figueroa, C; Harris, J; Vall, O; Anto, JM; Cullinan, P			A prospective study of Fel d1 and Der p1 exposure in infancy land childhood wheezing	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						allergens cohort; infants; wheezing	HOUSE-DUST MITE; ENVIRONMENTAL RISK-FACTORS; ALLERGEN EXPOSURE; CAT ALLERGEN; ASTHMA; CHILDREN; SENSITIZATION; LIFE; SYMPTOMS; FEL-D-1	The impact of domestic exposure to cat allergen (Fel d1) and house dust mite (Der p1) on wheezing from birth to the age of 4 years was investigated in a multicenter prospective birth cohort; 1,611 mothers were recruited before delivery in Ashford, England, and Barcelona and Menorca, Spain. Exposures were gathered via dust sample collection at children's home in their first year of life. Families provided complete outcome data (wheezing status in all 4 years) for 1,289 children. Domestic allergen levels varied substantially between centers. Six hundred three (47%) children never wheezed during their first 4 years of life. Der p1 did not correlate with any type of wheezing outcome. Fel d1 significantly increased the risk of wheezing in 3- and 4-year-olds in comparison to 1-year-olds. Distinct risk profiles were found for wheezing at different ages. Multivariate analysis revealed an interaction between Fel d1 and maternal asthma among children who wheeze in Year 4 (relative risk = 2.77; 95% confidence interval = 1.19-6.46). Our data support the idea that several patterns of wheezing with different risk profiles exist among young children. The effect of Fel d1 exposure varied according to age and maternal asthma.	Inst Municipal Invest Med, Environm Resp Res Unit, E-08003 Barcelona, Spain; Univ Pompeu Fabra, Barcelona, Spain; Hosp del Mar, Serv Pediat, Barcelona, Spain; IB SALUT, Area Salud Menorca, Menorca, Spain; Univ London Imperial Coll Sci Technol & Med, Dept Occupat & Environm Med, London SW7 2AZ, England	Sunyer, J (reprint author), Inst Municipal Invest Med, Environm Resp Res Unit, C Doctor Aiguader 80, E-08003 Barcelona, Spain.	jsunyer@imim.es	vall, oriol/G-2980-2010; Anto, J/H-2676-2014; Sunyer, J/G-6909-2014	Anto, J/0000-0002-4736-8529; Sunyer, J/0000-0002-2602-4110			Atkinson W, 1999, EUR RESPIR J, V13, P583, DOI 10.1183/09031936.99.13358599; Basagana X, 2002, PEDIATR ALLERGY IMMU, V13, P412, DOI 10.1034/j.1399-3038.2002.02081.x; BRUNEKREEF B, 1992, INT J EPIDEMIOL, V21, P338, DOI 10.1093/ije/21.2.338; Carter PM, 2003, ANN ALLERG ASTHMA IM, V90, P41; Celedon JC, 2002, LANCET, V360, P781, DOI 10.1016/S0140-6736(02)09906-3; Diggle P. J., 1994, OXFORD STAT SCI SERI, V13; Douwes J, 2002, INT J EPIDEMIOL, V31, P1098, DOI 10.1093/ije/31.6.1098; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; Halonen M, 1999, AM J RESP CRIT CARE, V160, P564; Heinrich J, 2003, J EXPO ANAL ENV EPID, V13, P152, DOI 10.1038/sj.jea.7500267; Heissenhuber A, 2003, ALLERGY, V58, P154, DOI 10.1034/j.1398-9995.2003.00037.x; HENDERSON FW, 1995, AM J RESP CRIT CARE, V151, P1786; HOLT PG, 1999, NATURE, V402, pR12; INGRAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449, DOI 10.1016/S0091-6749(95)70286-5; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; Lindfors A, 1999, J ALLERGY CLIN IMMUN, V104, P755; LINDFORS A, 1995, ARCH DIS CHILD, V73, P408; Litonjua AA, 1998, AM J RESP CRIT CARE, V158, P176; Martin YC, 1998, PERSPECT DRUG DISCOV, V12, P3, DOI 10.1023/A:1017037831628; Melen E, 2001, ALLERGY, V56, P646, DOI 10.1034/j.1398-9995.2001.00387.x; PALMES ED, 1976, AM IND HYG ASSOC J, V37, P570, DOI 10.1080/0002889768507522; 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; PERZANOWSKI MS, 1999, J ALLERGY CLIN IMMUN, V103, P1002; Pichini S, 2000, ENVIRON HEALTH PERSP, V108, P1079, DOI 10.1289/ehp.001081079; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; RITZ BR, 2001, ALELRGY, V57, P357; Rusconi F, 1999, AM J RESP CRIT CARE, V160, P1617; Sandford AJ, 2000, AM J RESP CRIT CARE, V161, pS202; Sherrill DL, 1999, J ALLERGY CLIN IMMUN, V104, P28, DOI 10.1016/S0091-6749(99)70110-7; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; Sunyer J, 2001, CLIN EXP ALLERGY, V31, P1352, DOI 10.1046/j.1365-2222.2001.01187.x; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; Wright AL, 2002, CLIN REV ALLERG IMMU, V22, P33, DOI 10.1385/CRIAI:22:1:033	34	72	74	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.	AUG 1	2004	170	3					273	278		10.1164/rccm.200310-1348OC		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	841DX	WOS:000222910600018	15117746	
J	Tiemessen, MM; Van Leperen-Van Dijk, AG; Bruijnzeel-Koomen, CAFM; Garssen, J; Knol, EF; Van Hoffen, E				Tiemessen, MM; Van Leperen-Van Dijk, AG; Bruijnzeel-Koomen, CAFM; Garssen, J; Knol, EF; Van Hoffen, E			Cow's milk-specific T-cell reactivity of children with and without persistent cow's milk allergy: Key role for IL-10	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						antigen-specific T cells; cow's milk; food allergy; tolerance; IL-10	HOUSE-DUST MITE; ATOPIC-DERMATITIS; LYMPHOCYTE-RESPONSES; PERIPHERAL-BLOOD; DIETARY ANTIGEN; FOOD ALLERGY; INTERLEUKIN-10; EXPRESSION; TOLERANCE; ASTHMA	Background: The role of antigen-specific T cells in the mechanism of food allergy or maintenance of tolerance toward an innocuous antigen, such as cow's milk, is not yet fully understood. Objective: The cow's milk-specific T-cell response of donors with various allergic backgrounds was investigated. Methods: Cow's milk-specific T-cell clones (TCCs) were generated from the blood of children with persistent cow's milk allergy (CMA) and the blood of cow's milk-tolerant allergic and nonallergic control subjects. The TCCs were characterized by their antigen-specific proliferation, cytokine production, and activation status. Results: Cow's milk-specific TCCs of children with persistent CMA were T(H)2 skewed, and the production of IL-4 and IL-13 was significantly correlated with the expression of the activation marker CD25. TCCs of the allergic control subjects were characterized by a high production of IL-10, which was positively correlated with the production of IL-4 and IFN-gamma and with the expression of CD25. TCCs derived from nonallergic control subjects had an attenuated response toward cow's milk in that they did not produce high levels of cytokines nor did they express high levels of surface markers. As in the allergic control subjects, in the nonallergic control subjects IL-10 production was positively correlated with the expression of CD25. Conclusion: The activation status of T cells derived from persistent donors with CMA was associated with the production of IL-4 and IL-13, whereas activated TCCs of cow's milk-tolerant control subjects were characterized by the production of IL-10 and, to a lesser extent, IFN-gamma. These findings suggest that activated CD4(+) T cells (characterized by a high CD25 expression) might contribute to the tolerogenic immune response toward an antigen, such as cow's milk, through the production of IL-10.	Univ Utrecht, Med Ctr, Dept Dermatol Allergol, NL-3508 GA Utrecht, Netherlands; Numico Res, Wageningen, Netherlands	Tiemessen, MM (reprint author), Univ Utrecht, Med Ctr, Dept Dermatol Allergol, G02-124,POB 85-500, NL-3508 GA Utrecht, Netherlands.	e.vanhoffen@azu.nl	garssen, johan/I-7159-2016				Akdis CA, 1998, J CLIN INVEST, V102, P98, DOI 10.1172/JCI2250; Bashir MEH, 2002, J IMMUNOL, V169, P3284; Borish L, 1996, J ALLERGY CLIN IMMUN, V97, P1288, DOI 10.1016/S0091-6749(96)70197-5; deJong EC, 1996, J ALLERGY CLIN IMMUN, V98, P73, DOI 10.1016/S0091-6749(96)70228-2; GURKA G, 1989, J ALLERGY CLIN IMMUN, V83, P945, DOI 10.1016/0091-6749(89)90110-3; HAMID Q, 1991, J CLIN INVEST, V87, P1541, DOI 10.1172/JCI115166; HIGGINS JA, 1995, IMMUNOLOGY, V84, P91; Jarvinen KM, 2002, J ALLERGY CLIN IMMUN, V110, P293, DOI 10.1067/mai.2002.126080; Jutel M, 2003, EUR J IMMUNOL, V33, P1205, DOI 10.1002/eji.200322919; Katsuki T, 1996, INT ARCH ALLERGY IMM, V109, P344; Kitani A, 2003, J EXP MED, V198, P1179, DOI 10.1084/jem.20030917; Lagging E, 1998, IMMUNOL LETT, V60, P45, DOI 10.1016/S0165-2478(97)00130-2; Nagata S, 2000, J IMMUNOL, V165, P5315; Neumann C, 1996, J MOL MED-JMM, V74, P401, DOI 10.1007/BF00210634; Ng TW, 2002, ALLERGY, V57, P207, DOI 10.1034/j.1398-9995.2002.1o3369.x; Oh JW, 2002, J ALLERGY CLIN IMMUN, V110, P460, DOI 10.1067/mai.2002.127512; Perez-Machado MA, 2003, EUR J IMMUNOL, V33, P2307, DOI 10.1002/eji.200323308; Sampson HA, 1999, J ALLERGY CLIN IMMUN, V103, P717, DOI 10.1016/S0091-6749(99)70411-2; Schade RP, 2003, CLIN EXP ALLERGY, V33, P725, DOI 10.1046/j.1365-2222.2003.01655.x; Schade RP, 2000, J ALLERGY CLIN IMMUN, V106, P1155, DOI 10.1067/mai.2000.110802; Schade RR, 2002, J ALLERGY CLIN IMMUN, V109, P357, DOI 10.1067/mai.2002.121457; Sicherer SH, 1999, CLIN EXP ALLERGY, V29, P507; Smart V, 2003, J IMMUNOL, V171, P2116; Torres MJ, 2003, BLOOD CELL MOL DIS, V30, P124, DOI 10.1016/S1079-9796(03)00004-4; Turcanu V, 2003, J CLIN INVEST, V111, P1065, DOI 10.1172/JCI200316142; van den Biggelaar AHJ, 2000, LANCET, V356, P1723, DOI 10.1016/S0140-6736(00)03206-2; Vila L, 2001, CLIN EXP ALLERGY, V31, P1599, DOI 10.1046/j.1365-2222.2001.01218.x; Werfel T, 1996, CLIN EXP ALLERGY, V26, P1380, DOI 10.1046/j.1365-2222.1996.d01-294.x; YSSEL H, 1984, J IMMUNOL METHODS, V72, P219, DOI 10.1016/0022-1759(84)90450-2; Zemann Barbara, 2003, J Allergy Clin Immunol, V111, P1069	30	72	74	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.	MAY	2004	113	5					932	939		10.1016/j.jaci.2003.12.016		8	Allergy; Immunology	Allergy; Immunology	818UC	WOS:000221269000017	15131577	
J	Clifton, VL; Murphy, VE				Clifton, VL; Murphy, VE			Maternal asthma as a model for examining fetal sex-specific effects on maternal physiology and placental mechanisms that regulate human fetal growth	PLACENTA			English	Article; Proceedings Paper	9th Annual Meeting of the International-Federation-of-Placenta-Associations	SEP 24-28, 2003	Mainz, GERMANY	Int Federat Placenta Assoc			11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-2; GLUCOCORTICOID EXPOSURE; ALVEOLAR MACROPHAGES; INTRAUTERINE GROWTH; BLOOD MONOCYTES; HUMAN-PREGNANCY; ATOPIC DISEASE; MESSENGER-RNA; IMMUNE-SYSTEM; T-CELLS	Studying the effect of maternal asthma during pregnancy on placental function and fetal development has highlighted that there is a strong interaction between mother, placenta and fetus and these interactions appear to be sex-specific. This work has found that the female fetus alters maternal asthma during pregnancy by upregulating maternal inflammatory pathways. When asthma-associated inflammatory pathways are not treated with inhaled steroids during pregnancy, the female fetus has reduced growth and adrenal function due to alterations in placental glucocorticold metabolism. When the mother uses inhaled steroid for the treatment of her asthma during pregnancy, female fetal growth and placental function are comparable to the control population. The growth of the male fetus appears to be unaffected by asthma or inhaled steroid use. These findings indicate there may be different mechanisms regulating placental glucocorticoid and immune mechanisms depending on fetal sex in both asthmatic and non-asthmatic pregnancies. (C) 2004 IFPA and Elsevier Ltd. All rights reserved.	John Hunter Hosp, Hunter Med Res Inst, Mothers & Babies Res Ctr, Dept Endocrinol, Newcastle, NSW 2310, Australia	Clifton, VL (reprint author), John Hunter Hosp, Hunter Med Res Inst, Mothers & Babies Res Ctr, Dept Endocrinol, Locked Bag 1,HRMC, Newcastle, NSW 2310, Australia.	vclifton@mail.newcastle.edu.au	Clifton, Vicki/A-1445-2012	Clifton, Vicki/0000-0002-4892-6748			ACKERMAN V, 1994, CHEST, V105, P687, DOI 10.1378/chest.105.3.687; Andres R L, 2000, Semin Neonatol, V5, P231, DOI 10.1053/siny.2000.0025; Beecroft N, 1998, BRIT MED J, V317, P856; BENEDIKTSSON R, 1993, LANCET, V341, P339, DOI 10.1016/0140-6736(93)90138-7; Benediktsson R, 1997, CLIN ENDOCRINOL, V46, P161, DOI 10.1046/j.1365-2265.1997.1230939.x; BURTON PJ, 1994, J ENDOCRINOL, V143, P505, DOI 10.1677/joe.0.1430505; Clifton VL, 2001, AM J RESP CRIT CARE, V164, P546; Condon J, 1997, MOL CELL ENDOCRINOL, V127, P121, DOI 10.1016/S0303-7207(97)04000-8; Da Silva JAP, 1999, ANN NY ACAD SCI, V876, P102; Da Silva JA, 1999, ANN NY ACAD SCI, V876, P117; DAYNES RA, 1989, EUR J IMMUNOL, V19, P2319, DOI 10.1002/eji.1830191221; Dayyani F, 2003, J LEUKOCYTE BIOL, V74, P33, DOI 10.1189/jlb.1202612; Dean F, 1999, BRAIN RES, V846, P253, DOI 10.1016/S0006-8993(99)02064-8; DeKruyff R, 1998, J IMMUNOL, V160, P2231; Dodds L, 1999, BRIT MED J, V318, P1011; DOUCETTE JT, 1993, EPIDEMIOLOGY, V4, P143, DOI 10.1097/00001648-199303000-00010; FITZSIMONS R, 1986, J ALLERGY CLIN IMMUN, V78, P349, DOI 10.1016/S0091-6749(86)80088-4; Fonager K, 1998, AM J GASTROENTEROL, V93, P2426, DOI 10.1016/S0002-9270(98)00579-6; French NP, 1999, AM J OBSTET GYNECOL, V180, P114, DOI 10.1016/S0002-9378(99)70160-2; Gosset P, 2001, J ALLERGY CLIN IMMUN, V107, P114, DOI 10.1067/mai.2001.111126; Hennebold JD, 1997, INT IMMUNOL, V9, P105, DOI 10.1093/intimm/9.1.105; Jana N, 1995, J Obstet Gynaecol (Tokyo 1995), V21, P227; Johnson CC, 1996, CLIN EXP ALLERGY, V26, P624, DOI 10.1111/j.1365-2222.1996.tb00588.x; KELLY YJ, 1995, THORAX, V50, P525, DOI 10.1136/thx.50.5.525; Kovar J, 2001, PEDIATR PULM, V32, P8, DOI 10.1002/ppul.1082; KUEHR J, 1993, CLIN EXP ALLERGY, V23, P600, DOI 10.1111/j.1365-2222.1993.tb00900.x; Lim S, 2000, ALLERGY, V55, P489; LOUIS R, 1994, CHEST, V106, P1094, DOI 10.1378/chest.106.4.1094; Magee MH, 2001, J CLIN PHARMACOL, V41, P1180, DOI 10.1177/00912700122012733; Mathy NL, 2000, IMMUNOLOGY, V100, P63, DOI 10.1046/j.1365-2567.2000.00997.x; Mazzarella G, 2000, ALLERGY, V55, P36, DOI 10.1034/j.1398-9995.2000.00505.x; McKay LI, 1999, ENDOCR REV, V20, P435, DOI 10.1210/er.20.4.435; Murphy VE, 2003, AM J RESP CRIT CARE, V168, P1317, DOI 10.1164/rccm.200303-374OC; Murphy VE, 2002, J CLIN ENDOCR METAB, V87, P1660, DOI 10.1210/jc.87.4.1660; PAPAGEORGIOU AN, 1981, PEDIATRICS, V67, P614; Prescott SL, 1998, CLIN EXP ALLERGY, V28, P1313; Quinlivan JA, 2002, J PERINAT MED, V30, P209, DOI 10.1515/JPM.2002.029; Ramirez F, 1998, Dev Immunol, V6, P233, DOI 10.1155/1998/73401; Raven PW, 1996, ENDOCR RES, V22, P751; REINISCH JM, 1978, SCIENCE, V202, P436, DOI 10.1126/science.705336; Rivera DL, 1998, FASEB J, V12, P189; Schatz M, 1999, J ALLERGY CLIN IMMUN, V103, pS330, DOI 10.1016/S0091-6749(99)70258-7; SCHATZ M, 1990, CHEST, V98, P389, DOI 10.1378/chest.98.2.389; Shams M, 1998, HUM REPROD, V13, P799, DOI 10.1093/humrep/13.4.799; SIITERI PK, 1966, J CLIN ENDOCR METAB, V26, P751; SIMMONS D, 1994, BIOL NEONATE, V65, P287; Smith JT, 2000, ENDOCRINOLOGY, V141, P2422, DOI 10.1210/en.141.7.2422; Tang CB, 1998, AM J RESP CRIT CARE, V157, P1120; Tang CB, 1998, J ALLERGY CLIN IMMUN, V102, P368, DOI 10.1016/S0091-6749(98)70122-8; Terpigorev SA, 2003, B EXP BIOL MED+, V135, P582, DOI 10.1023/A:1025489604819; von Hertzen LC, 2002, J ALLERGY CLIN IMMUN, V109, P923, DOI 10.1067/mai.2002.124776; WEGMANN TG, 1993, IMMUNOL TODAY, V14, P353, DOI 10.1016/0167-5699(93)90235-D; Welberg LAM, 2000, EUR J NEUROSCI, V12, P1047, DOI 10.1046/j.1460-9568.2000.00958.x; Wendel PJ, 1996, AM J OBSTET GYNECOL, V175, P150, DOI 10.1016/S0002-9378(96)70265-X; Zhu YK, 2001, J ALLERGY CLIN IMMUN, V108, P989, DOI 10.1067/mai.2001.120193	55	72	73	0	6	W B SAUNDERS CO LTD	LONDON	32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND	0143-4004			PLACENTA	Placenta	APR	2004	25			A			S45	S52		10.1016/j.placenta.2004.01.004		8	Developmental Biology; Obstetrics & Gynecology; Reproductive Biology	Developmental Biology; Obstetrics & Gynecology; Reproductive Biology	824NN	WOS:000221693400007	15033307	
J	Topilski, I; Flaishon, L; Naveh, Y; Harmelin, A; Levo, Y; Shachar, I				Topilski, I; Flaishon, L; Naveh, Y; Harmelin, A; Levo, Y; Shachar, I			The anti-inflammatory effects of 1,25-dihydroxyvitamin D3 on Th2 cells in vivo are due in part to the control of integrin-mediated T lymphocyte homing	EUROPEAN JOURNAL OF IMMUNOLOGY			English	Article						CD4 T cells; Th2 cells; vitamin D; asthma; cytoskeleton rearrangement; migration	HIGH ENDOTHELIAL VENULES; DENDRITIC CELLS; IFN-GAMMA; RECEPTOR EXPRESSION; IMMUNE-RESPONSE; B-CELLS; D-3; ACTIVATION; MICE; INHIBITION	The fat soluble vitamin D3 metabolite 1,25-dihydroxyvitamin D3 [1,25(OH)(2)D-3], and its nuclear receptor play an important role in regulating immune responses. While 1,25(OH)(2)D-3 is known to inhibit transcription of cytokine genes that are required for Th1 differentiation or are products of differentiated Th1 cells, its role in regulating differentiation of Th2 cells is less clear. In this study, we show that 1,25(OH)(2)D-3 has anti-inflammatory effects in an in vivo Th2-dependent asthma model. In addition, we demonstrate that 1,25(OH)(2)D-3 down-regulates the cytoskeleton rearrangement required for promoting integrin-mediated adhesion of naive and effector CD4(+) T cells. Finally, 1,25(OH)(2)D-3 inhibits chemokine-induced migration of naive cells and their homing to the lymph nodes. Thus, in addition to its regulation of cytokine transcription, 1,25(OH)(2)D-3 regulates migration of cells and thus controls the skewing of various Th subsets in the secondary lymphoid organs and inhibits Th function at sites of inflammation.	Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel; Sourasky Med Ctr, Tel Aviv, Israel; Weizmann Inst Sci, Expt Anim Ctr, IL-76100 Rehovot, Israel	Shachar, I (reprint author), Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel.	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J. Immunol.	APR	2004	34	4					1068	1076		10.1002/eji.200324532		9	Immunology	Immunology	812JA	WOS:000220834600017	15048717	
J	Jaakkola, JJK; Piipari, R; Jaakkola, MS				Jaakkola, JJK; Piipari, R; Jaakkola, MS			Occupation and asthma: A population-based incident case-control study	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						asthma; case-control studies; occupational diseases; occupations	MALODOROUS SULFUR-COMPOUNDS; KARELIA AIR-POLLUTION; ADULT-ONSET ASTHMA; RESPIRATORY SYMPTOMS; GENERAL-POPULATION; EXPOSURE; COMMUNITY; SAMPLE; RISK	The authors assessed the relations between occupation and risk of developing asthma in adulthood in a 1997-2000 population-based incident case-control study of 521 cases and 932 controls in south Finland. The occupations were classified according to potential exposure to asthma-causing inhalants. Asthma risk was increased consistently for both men and women in the chemical (adjusted odds ratio (OR) = 5.69, 95% confidence interval (CI): 1.08, 29.8), rubber and plastic (OR = 2.61, 95% CI: 0.92, 7.42), and wood and paper (OR = 1.72, 95% CI: 0.71, 4.17) industries. Risk in relation to occupation was increased only for men-for bakers and food processors (OR = 8.62, 95% CI: 0.86, 86.5), textile workers (OR = 4.70, 95% CI: 0.29, 77.1), electrical and electronic production workers (OR 2.83, 95% CI: 0.82, 6.93), laboratory technicians (OR = 1.66, 95% CI: 0.17, 16.6), and storage workers (OR 1.57, 95% CI: 0.40, 6.19). Of the predominantly men's occupations, metal (OR = 4.52, 95% CI: 2.35, 8.70) and forestry (OR = 6.00, 95% CI: 0.96, 37.5) work were the strongest determinants of asthma. For women, asthma risk increased for waiters (OR = 3.03, 95% CI: 1.10, 8.31), cleaners (OR = 1.42, 95% CI: 0.81, 2.48), and dental workers (OR = 4.74, 95% CI: 0.48, 46.5). Results suggest an increased asthma risk both in traditional industries and forestry and in several nonindustrial occupations.	Univ Birmingham, Inst Occupat Hlth, Birmingham B15 2TT, W Midlands, England; Univ Helsinki, Dept Publ Hlth, Environm Epidemiol Unit, Helsinki, Finland; Finnish Inst Occupat Hlth, Helsinki, Finland	Jaakkola, JJK (reprint author), Univ Birmingham, Inst Occupat Hlth, Birmingham B15 2TT, W Midlands, England.		Jaakkola, Jouni/G-4314-2012				BAKKE P, 1991, EUR RESPIR J, V4, P273; Balmes J, 2003, AM J RESP CRIT CARE, V167, P787, DOI 10.1164/rccm.167.5.787; Blanc PD, 1999, AM J MED, V107, P580, DOI 10.1016/S0002-9343(99)00307-1; CHANYEUNG M, 1995, NEW ENGL J MED, V333, P107, DOI 10.1056/NEJM199507133330207; *COMM NAT ASTHM PR, 1994, MIN SOC AFF HLTH PUB, V16; Cullinan P, 1997, CLIN EXP ALLERGY, V27, P41, DOI 10.1111/j.1365-2222.1997.tb01825.x; delaHoz RE, 1997, AM J IND MED, V31, P195, DOI 10.1002/(SICI)1097-0274(199702)31:2<195::AID-AJIM9>3.0.CO;2-Z; Fishwick D, 1997, OCCUP ENVIRON MED, V54, P301; FLODIN U, 1995, EPIDEMIOLOGY, V6, P503, DOI 10.1097/00001648-199509000-00007; Forastiere F, 1998, AM J RESP CRIT CARE, V157, P1864; GREER JR, 1993, J OCCUP ENVIRON MED, V35, P909, DOI 10.1097/00043764-199309000-00014; JAAKKOLA JJK, 1995, AM J EPIDEMIOL, V141, P755; Jaakkola JJK, 2002, J ALLERGY CLIN IMMUN, V109, P784, DOI 10.1067/mai.2002.123870; JAAKKOLA JJK, 1990, AM REV RESPIR DIS, V142, P1344; Jaakkola MS, 1999, AM J EPIDEMIOL, V150, P1223; Jaakkola MS, 2002, ENVIRON HEALTH PERSP, V110, P543; JAAKKOLA MS, 2002, SCAND J WORK ENV S2, V28, P54; JAAKKOLA MS, 2001, EUR RESPIR J, V14, pP1906; Johnson AR, 2000, AM J RESP CRIT CARE, V162, P2058; Karjalainen A, 2002, EUR RESPIR J, V19, P90, DOI 10.1183/09031936.02.00201002; Karjalainen A, 2001, AM J RESP CRIT CARE, V164, P565; Kogevinas M, 1996, AM J RESP CRIT CARE, V154, P137; Kogevinas M, 1999, LANCET, V353, P1750, DOI 10.1016/S0140-6736(98)07397-8; Monso E, 1998, ARCH ENVIRON HEALTH, V53, P93; NG TP, 1994, AM J IND MED, V25, P709, DOI 10.1002/ajim.4700250510; ParttiPellinen K, 1996, ARCH ENVIRON HEALTH, V51, P315; VIEGI G, 1991, AM REV RESPIR DIS, V143, P510; XU XP, 1993, CHEST, V104, P1364, DOI 10.1378/chest.104.5.1364	28	72	73	0	3	OXFORD UNIV PRESS INC	CARY	JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA	0002-9262			AM J EPIDEMIOL	Am. J. Epidemiol.	NOV 15	2003	158	10					981	987		10.1093/aje/kwg238		7	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	742XV	WOS:000186544200009	14607806	
J	Medina-Ramon, M; Zock, JP; Kogevinas, M; Sunyer, J; Anto, JM				Medina-Ramon, M; Zock, JP; Kogevinas, M; Sunyer, J; Anto, JM			Asthma symptoms in women employed in domestic cleaning: a community based study	THORAX			English	Article							OCCUPATIONAL ASTHMA; EXPOSURE; RISK; WORK; CLEANERS	Background: Epidemiological studies have shown an association between cleaning work and asthma, but the risk factors are uncertain. The aim of this study was to assess the risk of asthma in women employed in domestic cleaning. Methods: A cross sectional study was conducted in 4521 women aged 30 to 65 years. Information on respiratory symptoms and cleaning work history was obtained using a postal questionnaire with telephone follow up. Asthma was defined as reported symptoms in the last year or current use of drugs to treat asthma. Odds ratios (OR) with 95% confidence intervals (CI) for asthma in different cleaning groups were estimated using adjusted unconditional logistic regression models. Results: 593 women (13%) were currently employed in domestic cleaning work. Asthma was more prevalent in this group than in women who had never worked in cleaning (OR 1.46 (95% CI, 1.10 to 1.92)). Former domestic cleaning work was reported by 1170 women (26%), and was strongly associated with asthma (OR 2.09 (1.70 to 2.57)). Current and former non-domestic cleaning work was not significantly associated with asthma. Consistent results were obtained for other respiratory symptoms. Twenty five per cent of the asthma cases in the study population were attributable to domestic cleaning work. Conclusions: Employment in domestic cleaning may induce or aggravate asthma. This study suggests that domestic cleaning work has an important public health impact, probably involving not only professional cleaners but also people undertaking cleaning tasks at home.	Inst Municipal Invest Med, Resp & Environm Hlth Res Unit, E-08003 Barcelona, Spain; Pompeu Fabra Univ, Dept Expt & Hlth Sci, Barcelona, Spain	Anto, JM (reprint author), Inst Municipal Invest Med, Resp & Environm Hlth Res Unit, Dr Aiguader 80, E-08003 Barcelona, Spain.		Kogevinas, Manolis/C-3918-2017; Anto, J/H-2676-2014; Sunyer, J/G-6909-2014	Anto, J/0000-0002-4736-8529; Sunyer, J/0000-0002-2602-4110			BERNSTEIN JA, 1994, J ALLERGY CLIN IMMUN, V94, P257, DOI 10.1016/0091-6749(94)90048-5; Blanc PD, 1999, AM J MED, V107, P580, DOI 10.1016/S0002-9343(99)00307-1; BURGE PS, 1994, THORAX, V49, P842, DOI 10.1136/thx.49.8.842; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; Chan-Yeung M., 1999, ASTHMA WORKPLACE, P129; Checkoway H., 1989, RES METHODS OCCUPATI, P72; Fishwick D, 1997, AM J RESP CRIT CARE, V156, P1440; Forastiere F, 1998, AM J RESP CRIT CARE, V157, P1864; Galobardes B, 1998, J CLIN EPIDEMIOL, V51, P875, DOI 10.1016/S0895-4356(98)00063-8; Jajosky R A, 1999, MMWR CDC Surveill Summ, V48, P1; Karjalainen A, 2002, EUR RESPIR J, V19, P90, DOI 10.1183/09031936.02.00201002; Karjalainen A, 2001, AM J RESP CRIT CARE, V164, P565; Kogevinas M, 1999, LANCET, V353, P1750, DOI 10.1016/S0140-6736(98)07397-8; MEREDITH S, 1993, J EPIDEMIOL COMMUN H, V47, P459, DOI 10.1136/jech.47.6.459; PEPYS J, 1999, ASTHMA WORKPLACE, P5; Quirce S, 2000, J ASTHMA, V37, P267, DOI 10.3109/02770900009055449; REILLY MJ, 1995, ARCH ENVIRON HEALTH, V50, P26; Reinisch F, 2001, AM J IND MED, V39, P72; Symanski E, 1998, OCCUP ENVIRON MED, V55, P300; Venables KM, 1997, LANCET, V349, P1465, DOI 10.1016/S0140-6736(96)07219-4; Wolkoff P, 1998, SCI TOTAL ENVIRON, V215, P135, DOI 10.1016/S0048-9697(98)00110-7; Zock JP, 2002, EUR RESPIR J, V20, P679, DOI 10.1183/09031936.02.00279702; Zock JP, 2001, SCAND J WORK ENV HEA, V27, P76	23	72	72	0	3	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	NOV 1	2003	58	11					950	954		10.1136/thorax.58.11.950		5	Respiratory System	Respiratory System	737PU	WOS:000186241600011	14586047	
J	Cookson, W				Cookson, W			Genetics and genomics of asthma and allergic diseases	IMMUNOLOGICAL REVIEWS			English	Review							FC-EPSILON-RI; CHRONIC LYMPHOCYTIC-LEUKEMIA; INFLAMMATORY BOWEL-DISEASE; IMMUNOGLOBULIN-E RESPONSES; CALCIUM-BINDING PROTEIN; MAJOR SUSCEPTIBILITY LOCUS; ATOPIC-DERMATITIS; WIDE SEARCH; BETA-SUBUNIT; RHEUMATOID-ARTHRITIS	Asthma and eczema (atopic dermatitis) are characterized by a number of unexplained phenomena: the familial aggregation of disease, the initiation of disease by apparently trivial exposure to allergens, the preferential transmission of disease from affected mothers and the large increase in prevalence of disease in Westernized societies in the last century. A number of genes and chromosomal regions have been identified that consistently show linkage to asthma and its related phenotypes. Known loci modify the strength of the atopic response, nonspecific inflammation, the ability to respond to particular allergens and nonspecific airway reactivity. Eczema has been shown to be due to a different set of genetic loci that are shared with other skin diseases such as psoriasis and leprosy. Genetic and genomic studies both provide evidence that epithelial surfaces are active in the induction of allergic disease.	Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England	Cookson, W (reprint author), Univ Oxford, Wellcome Trust Ctr Human Genet, Roosevelt Dr, Oxford OX3 7BN, England.						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J	Douwes, J; Pearce, N				Douwes, J; Pearce, N			Asthma and the westernization 'package'	INTERNATIONAL JOURNAL OF EPIDEMIOLOGY			English	Review							EARLY BCG VACCINATION; MODIFIED TH2 RESPONSE; HUMAN IMMUNE-SYSTEM; IN-HOUSE DUST; HAY-FEVER; INTESTINAL MICROFLORA; ATOPIC DISEASE; YOUNG-ADULTS; ENVIRONMENTAL ALLERGENS; INFECTIOUS-DISEASES		Massey Univ, Ctr Publ Hlth Res, Wellington, New Zealand; Univ Utrecht, IRAS, Div Environm & Occupat Hlth, NL-3508 TC Utrecht, Netherlands	Douwes, J (reprint author), Massey Univ, Ctr Publ Hlth Res, Wellington Campus,Private Box 756, Wellington, New Zealand.			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Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; Warner I, 1998, J NURS ADMIN, V28, P3; Warner JA, 1996, PEDIATR ALLERGY IMMU, V7, P98, DOI 10.1111/j.1399-3038.1996.tb00406.x; Weiss KB, 1992, CHEST, V101, P362; Yuan W, 2002, INT J EPIDEMIOL, V31, P1240, DOI 10.1093/ije/31.6.1240	88	72	74	2	6	OXFORD UNIV PRESS	OXFORD	GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND	0300-5771			INT J EPIDEMIOL	Int. J. Epidemiol.	DEC	2002	31	6					1098	1102		10.1093/ije/31.6.1098		5	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	650TJ	WOS:000181279100003	12540698	
J	de Marco, R; Poli, A; Ferrari, M; Accordini, S; Giammanco, G; Bugiani, M; Villani, S; Ponzio, M; Bono, R; Carrozzi, L; Cavallini, R; Cazzoletti, L; Dallari, R; Ginesu, F; Lauriola, P; Mandrioli, P; Perfetti, L; Pignato, S; Pirina, P; Struzzo, P				de Marco, R; Poli, A; Ferrari, M; Accordini, S; Giammanco, G; Bugiani, M; Villani, S; Ponzio, M; Bono, R; Carrozzi, L; Cavallini, R; Cazzoletti, L; Dallari, R; Ginesu, F; Lauriola, P; Mandrioli, P; Perfetti, L; Pignato, S; Pirina, P; Struzzo, P		ISAYA Study Grp	The impact of climate and traffic-related NO2 on the prevalence of asthma and allergic rhinitis in Italy	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergic rhinitis; asthma; climate; outdoor NO2 pollution; traffic-related pollution	RESPIRATORY HEALTH SURVEY; DIESEL EXHAUST PARTICLES; LONG-TERM EXPOSURE; AIR-POLLUTION; CHILDHOOD ASTHMA; LUNG-FUNCTION; INDOOR ALLERGENS; NEW-ZEALAND; SYMPTOMS; POLLUTANTS	Background Environmental factors are likely to be involved in explaining the wide geographical variation in asthma and atopic diseases that has been documented in many recent epidemiological studies. Aim To evaluate to what extent climate and outdoor NO2 pollution can explain the geographical variation in the prevalence of asthma and allergic rhinitis, and to estimate the relative risk for exposure to different levels of these two factors. Methods The impact of climate and long-term exposure to nitrogen dioxide (NO2) pollution on asthma and allergic rhinitis was assessed in a cross-sectional study, carried out during 1998 to 2000 on young adults aged 20 to 44 years (n = 18 873), living in 13 areas from two different Italian climatic regions (subcontinental and Mediterranean). Results Mediterranean areas had a significantly higher prevalence of asthma-like symptoms (P < 0.001), higher annual mean temperature (16.2 degreesC vs. 12.9 degreesC), lower temperature range (16.0 Cdegrees vs. 22.1 Cdegrees) and lower NO2 levels (31.46 mug/m(3) vs. 57.99 mug/m(3)) than subcontinental ones. Mediterranean climate was associated with an increased risk of wheeze (OR = 1.23; 95% CI 1.13 to 1.35), tightness in the chest (OR = 1.21; 95% CI 1.11 to 1.33), shortness of breath (OR = 1.21; 95% CI 1.08 to 1.36) and asthma attacks (OR = 1.19; 95% CI 1.07 to 1.31). After adjusting for climate, an increase of 18.3 mug/m(3) in NO2 levels moderately increased the risk of asthma attacks (OR = 1.13; 95% CI 0.98 to 1.32), tightness in the chest (OR = 1.11; 95% CI 0.98 to 1.26) and wheeze (OR = 1.11; 95% CI 0.96 to 1.28). When the levels of outdoor NO2 exposure rose, the prevalence of allergic rhinitis increased significantly in the Mediterranean region (OR = 1.38; 95% CI 1.12 to 1.69), but not in the subcontinental one (OR = 1.03; 95% CI 0.83 to 1.28). Conclusion Our results show that the prevalence of asthma increases when annual mean temperature increases and temperature range decreases. Furthermore, climate interacts with NO2 outdoor exposure, increasing the risk for allergic rhinitis in people exposed to high stable temperatures. A long-term role for the effect of traffic pollution on asthma is also suggested.	Univ Verona, Inst Biol 2, Dipartimento Med & Sanit Pubbl, Sez Epidemiol & Stat Med,Unit Epidemiol & Med Sta, I-37134 Verona, Italy; Univ Verona, Unit Hyg & Prevent Environm & Occupat Med, I-37134 Verona, Italy; Univ Verona, Dept Biomed & Surg Sci, Sect Internal Med, I-37134 Verona, Italy; Univ Catania, Inst Hyg & Prevent Med, Catania, Italy; Natl Hlth Serv, CPA ASL Unit Resp Med 4, Turin, Italy; Univ Pavia, Fac Med, Dept Appl Hlth Sci, I-27100 Pavia, Italy; Univ Turin, Dept Microbiol & Publ Hlth, Turin, Italy; Univ Pisa, CNR, Inst Clin Physiol, Cardiopulm Dept, I-56100 Pisa, Italy; Hosp Pisa, Pisa, Italy; AUSL Modena, Natl Hlth Serv, Hosp Sassuolo, Unit Pulmonol, Modena, Italy; Univ Sassari, Inst Resp Dis, I-07100 Sassari, Italy; ARPA Emilia Romogna Agenzia Reg Prevent & Ambient, Environm Epidemiol Unit, Modena, Italy; CNR, Inst Atmospher & Ocean Sci, Bologna, Italy; Ctr Pavia, Salvatore Maugeri Fdn, Allergy & Clin Immunol Unit, Pavia, Italy; Municipal Udine, Udine, Italy	de Marco, R (reprint author), Univ Verona, Inst Biol 2, Dipartimento Med & Sanit Pubbl, Sez Epidemiol & Stat Med,Unit Epidemiol & Med Sta, Strada le Grazie 8, I-37134 Verona, Italy.		de Marco, Roberto/A-5470-2008; SESM, SESM/C-1440-2008; bucca, caterina/C-9886-2009; Bono, Roberto/J-8954-2012; Struzzo, Pierluigi/I-7502-2012; Osborne, Nicholas/N-4915-2015	bucca, caterina/0000-0002-9941-9236; Struzzo, Pierluigi/0000-0003-0570-3103; Osborne, Nicholas/0000-0002-6700-2284; Bono, Roberto/0000-0002-2471-6594			Accorsi CA, 1990, AEROBIOLOGIA, V6, P9; AckermannLiebrich U, 1997, AM J RESP CRIT CARE, V155, P122; Alvarez MJ, 1997, J INVEST ALLERG CLIN, V7, P572; Bernard SM, 2001, ENVIRON HEALTH PERSP, V109, P199, DOI 10.2307/3435010; BraunFahrlander C, 1997, AM J RESP CRIT CARE, V155, P1042; BRAUNFAHRLANDER C, 1992, AM REV RESPIR DIS, V145, P42; 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; CHARPIN D, 1991, AM REV RESPIR DIS, V143, P983; Chinn S, 1997, EUR RESPIR J, V10, P2495, DOI 10.1183/09031936.97.10112495; Cross S, 1997, Community Nurse, V3, P25; D'Amato G, 1998, ALLERGY, V53, P567, DOI 10.1111/j.1398-9995.1998.tb03932.x; D'Amato G, 2000, J INVEST ALLERG CLIN, V10, P123; de Marco R, 1999, EUR RESPIR J, V14, P1044, DOI 10.1183/09031936.99.14510449; DEMARCO R, 1995, ALLERGY, V50, P755; Diaz-Sanchez D, 2000, J ALLERGY CLIN IMMUN, V106, P1140, DOI 10.1067/mai.2000.111144; Diaz-Sanchez D, 1999, J ALLERGY CLIN IMMUN, V104, P1183; Estela LBL, 1998, INT J BIOMETEOROL, V42, P77; *EUR COMM RESP HLT, 1994, MED HLTH; Dunn G., 1991, APPL MULTIVARIATE DA; Fleiss J. L., 1981, STAT METHODS RATES P; Gluck U, 2000, ORL J OTO-RHINO-LARY, V62, P68, DOI 10.1159/000027720; Goldstein H., 1995, MULTILEVEL STAT MODE; GREER JR, 1993, J OCCUP ENVIRON MED, V35, P909, DOI 10.1097/00043764-199309000-00014; Guo YLL, 1999, ENVIRON HEALTH PERSP, V107, P1001; Hales S, 1998, ENVIRON HEALTH PERSP, V106, P607, DOI 10.1289/ehp.98106607; Hirsch T, 1999, EUR RESPIR J, V14, P669, DOI 10.1034/j.1399-3003.1999.14c29.x; Hosmer DW, 1989, APPL LOGISTIC REGRES; *I NAZ STAT, 1998, ANN STAT MET; Jarvis D, 1996, LANCET, V347, P426, DOI 10.1016/S0140-6736(96)90009-4; Kunzli N, 1997, ENVIRON RES, V72, P8, DOI 10.1006/enrs.1996.3687; LAOR A, 1993, BRIT MED J, V307, P841; Lim T O, 1991, Med J Malaysia, V46, P230; Millqvist E, 2000, CLIN PHYSIOL, V20, P212; NISHINO N, 1996, EPIDEMIOLOGY, V7, pS31; PEARCE N, 1993, EUR RESPIR J, V6, P1455; PEAT JK, 1993, CLIN EXP ALLERGY, V23, P812, DOI 10.1111/j.1365-2222.1993.tb00258.x; PEAT JK, 1995, MED J AUSTRALIA, V163, P22; PIAZZA A, 1988, ANN HUM GENET, V52, P203, DOI 10.1111/j.1469-1809.1988.tb01098.x; PICCOLO MC, 1988, ANN ALLERGY, V60, P107; Rasbash J, 2000, USERS GUIDE MLWIN VE; SCHWARTZ J, 1989, ENVIRON RES, V50, P309, DOI 10.1016/S0013-9351(89)80012-X; Steerenberg PA, 1999, INHAL TOXICOL, V11, P1109; Studnicka M, 1997, EUR RESPIR J, V10, P2275, DOI 10.1183/09031936.97.10102275; Tenias JM, 1998, OCCUP ENVIRON MED, V55, P541; Thurston GD, 1999, AIR POLLUTION HLTH, P485, DOI 10.1016/B978-012352335-8/50097-1; Verlato G, 2002, ARCH ENVIRON HEALTH, V57, P48; WANG JH, 1995, J ALLERGY CLIN IMMUN, V96, P669, DOI 10.1016/S0091-6749(95)70266-0; Warner AM, 1996, PEDIATR ALLERGY IMMU, V7, P61, DOI 10.1111/j.1399-3038.1996.tb00108.x	49	72	72	0	12	BLACKWELL PUBLISHING LTD	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	OCT	2002	32	10					1405	1412		10.1046/j.1365-2745.2002.01466.x		8	Allergy; Immunology	Allergy; Immunology	601ZJ	WOS:000178479300004	12372117	
J	Lewis, SA; Weiss, ST; Platts-Mills, TAE; Burge, H; Gold, DR				Lewis, SA; Weiss, ST; Platts-Mills, TAE; Burge, H; Gold, DR			The role of indoor allergen sensitization and exposure in causing morbidity in women with asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						home allergens; cockroach; cat; sensitization; asthma morbidity	INNER-CITY CHILDREN; RISK-FACTORS; COCKROACH ALLERGEN; DETERMINANTS; EOSINOPHILIA; PREDICTORS; AVOIDANCE; ANTIGEN; HOMES; AREA	Longitudinal evidence that indoor allergen exposure causes morbidity in sensitized individuals with asthma is scarce. We evaluated the association of allergen sensitization and home exposure to short and long-term morbidity in 140 women with asthma and to asthma prevalence in 458 women from metropolitan Boston. Cockroach (Blattella germanica), dust mite (Dermatophagoides farinae), and cat (Felis domesticus) allergens in home dust samples, and specific immunoglobulln E antibodies were measured at outset, and doctor-diagnosed asthma and markers of asthma morbidity were ascertained by questionnaire during a 4-year follow-up. Cat- and cockroach-sensitive (immunoglobulin E immunocap [Cap] class greater than or equal to 1) women with asthma reported greater morbidity in the past year at the start, and during follow-up, if high levels of the relevant allergen were found. Women with asthma sensitized to cat allergen and with concentrations at 8 mug/g or greater were more likely to have used steroid (adjusted odds ratio [95% confidence interval] 2.7 [1.2-6.2]) and wheezed without a cold (odds ratio 6.8 [3.314.0]) during follow-up. Those sensitized and exposed to cockroach (Bla g I or 2 greater than or equal to 2 U/g) were at least three times more likely to have used steroid and to have attended a hospital emergency room; the size of the effect upon steroid use was maintained, but the precision was reduced and the 95% confidence interval included one (p = 0.07), with adjustment for race and poverty. We conclude that cockroach and cat allergens may contribute to asthma morbidity in sensitized women.	Univ Nottingham, Div Med Res, City Hosp, Nottingham NG5 1PB, England; Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA; Univ Virginia, Dept Med, Div Asthma Allergy & Immunol, Charlottesville, VA USA; Harvard Univ, Sch Publ Hlth, Sch Med, Boston, MA 02115 USA	Lewis, SA (reprint author), Univ Nottingham, Div Med Res, City Hosp, Clin Sci Bldg,Hucknall Rd, Nottingham NG5 1PB, England.				NCEH CDC HHS [R01 A1/EHS35786]; PHS HHS [A120565]		Arshad SH, 1998, AM J RESP CRIT CARE, V157, P1900; 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; COCKCROFT DW, 1979, AM REV RESPIR DIS, V120, P1053; Committee on the Assessment of Asthma and Indoor Air, 2000, CLEAR AIR ASTHM IND; Eggleston PA, 1998, J ALLERGY CLIN IMMUN, V102, P563, DOI 10.1016/S0091-6749(98)70272-6; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; KANG B, 1976, J ALLERGY CLIN IMMUN, V58, P357, DOI 10.1016/0091-6749(76)90115-9; Kitch BT, 2000, ENVIRON HEALTH PERSP, V108, P301, DOI 10.2307/3454347; Litonjua AA, 1999, PEDIATR PULM, V28, P394, DOI 10.1002/(SICI)1099-0496(199912)28:6<394::AID-PPUL2>3.0.CO;2-6; MORRISON SJ, 1981, PRACTITIONER, V225, P1663; O'Connor G T, 1999, Environ Health Perspect, V107, P243; PERONI DG, 1994, AM J RESP CRIT CARE, V149, P1442; PLATTSMILLS TAE, 1982, LANCET, V2, P675; 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; Shaver JR, 1997, AM J RESP CRIT CARE, V155, P442; Sicherer SH, 1997, J ALLERGY CLIN IMMUN, V99, P798, DOI 10.1016/S0091-6749(97)80014-0; SIMON HU, 1994, PEDIATR PULM, V17, P304, DOI 10.1002/ppul.1950170507; SUONIEMI I, 1981, ALLERGY, V36, P263, DOI 10.1111/j.1398-9995.1981.tb01573.x; WARNER JA, 1991, PEDIATR ALLERGY IMMU, V1, P79; ZEGER SL, 1986, BIOMETRICS, V42, P121, DOI 10.2307/2531248	23	72	74	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.	APR 1	2002	165	7					961	966		10.1164/rccm.2103044		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	536ZA	WOS:000174730700016	11934722	
J	Anees, W; Huggins, V; Pavord, ID; Robertson, AS; Burge, PS				Anees, W; Huggins, V; Pavord, ID; Robertson, AS; Burge, PS			Occupational asthma due to low molecular weight agents: eosinophilic and non-eosinophilic variants	THORAX			English	Article							EXHALED NITRIC-OXIDE; RED CEDAR ASTHMA; INDUCED SPUTUM; AIRWAY INFLAMMATION; BRONCHIAL RESPONSIVENESS; FLOW-RATE; DIAGNOSIS; SEVERITY; COUNTS	Background: Despite having a work related deterioration in peak expiratory flow (PEF), many workers with occupational asthma show a low degree of within day diurnal variability atypical of non-occupational asthma. It was hypothesised that these workers would have a neutrophilic rather than an eosinophilic airway inflammatory response. Methods: Thirty eight consecutive workers with occupational asthma induced by low molecular weight agents underwent sputum induction and assessment of airway physiology while still exposed at work. Results: Only 14 (36.8%) of the 38 workers had sputum eosinophilia (>2.2%). Both eosinophilic and non-eosinophilic groups had sputum neutrophilia (mean (SD) 59.5 (19.6)% and 55.1 (18.8)%, respectively). The diurnal variation and magnitude of fall in PEF during work periods was not significantly different between workers with and without sputum eosinophilia. Those with eosinophilia had a lower forced expiratory volume in 1 second (FEV1; 61.4% v 83% predicted, mean difference 21.6, 95% confidence interval (CI) 9.2 to 34.1 p=0.001) and greater methacholine reactivity (geometric mean PD20 253 mug v 1401 mug, p=0.007), hey also had greater bronchodilator reversibility (397 ml v 161 ml, mean difference 236, 95% Cl of difference 84 to 389, p=0.003) which was unrelated to differences in baseline FEV1. The presence of sputum eosinophilia did not relate to the causative agent, duration of exposure, atopy, or lack of treatment. Conclusions: Asthma caused by low molecular weight agents can be separated into eosinophilic and non-eosinophilic pathophysiological variants with the latter predominating. Both groups had evidence of sputum neutrophilia. Sputum eosinophilia was associated with more severe disease and greater bronchodilator reversibility but no difference in PEF response to work exposure.	Birmingham Heartlands Hosp, Occupat Lung Dis Unit, Birmingham B9 5SS, W Midlands, England; Glenfield Gen Hosp, Dept Resp Med, Leicester LE3 9QP, Leics, England	Anees, W (reprint author), Birmingham Heartlands Hosp, Occupat Lung Dis Unit, Birmingham B9 5SS, W Midlands, England.						AMIN K, 2001, AM J RESP CRIT CARE, V62, P2295; Belda J, 2000, AM J RESP CRIT CARE, V161, P475; Burge PS, 1999, OCCUP ENVIRON MED, V56, P758; BURGE PS, 1979, THORAX, V34, P317, DOI 10.1136/thx.34.3.317; Chan-Yeung M, 1999, AM J RESP CRIT CARE, V159, P1434; COTE J, 1990, J ALLERGY CLIN IMMUN, V85, P592, DOI 10.1016/0091-6749(90)90098-O; Di Franco A, 1998, RESP MED, V92, P550; Fahy JV, 1998, EUR RESPIR J, V11, P1240, DOI 10.1183/09031936.98.11061240; Gibson PG, 2001, CHEST, V119, P1329, DOI 10.1378/chest.119.5.1329; Jatakanon A, 1999, AM J RESP CRIT CARE, V160, P1532; JONES P, 1992, AM REV RESPIR DIS, V145, P132; Kharitonov S, 1997, EUR RESPIR J, V10, P1683, DOI 10.1183/09031936.97.10071683; Lemiere C, 1999, EUR RESPIR J, V13, P482, DOI 10.1183/09031936.99.13348299; Louis R, 2000, AM J RESP CRIT CARE, V161, P9; MILLER MR, 1992, THORAX, V47, P904, DOI 10.1136/thx.47.11.904; Obata H, 1999, EUR RESPIR J, V13, P489, DOI 10.1183/09031936.99.13348999; Park HS, 1998, CLIN EXP ALLERGY, V28, P724; Pavord ID, 1997, THORAX, V52, P498; PERRIN B, 1992, EUR RESPIR J, V5, P40; Pizzichini E, 1997, J ALLERGY CLIN IMMUN, V99, P539, DOI 10.1016/S0091-6749(97)70082-4; Spanevello A, 2000, AM J RESP CRIT CARE, V162, P1172; Vyas A, 2000, OCCUP ENVIRON MED, V57, P752, DOI 10.1136/oem.57.11.752; Wenzel SE, 1999, AM J RESP CRIT CARE, V160, P1001; YAN K, 1983, THORAX, V38, P760, DOI 10.1136/thx.38.10.760	24	72	77	0	0	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	MAR	2002	57	3					231	236		10.1136/thorax.57.3.231		6	Respiratory System	Respiratory System	529TM	WOS:000174314700008	11867827	
J	Warman, KL; Silver, EJ; Stein, REK				Warman, KL; Silver, EJ; Stein, REK			Asthma symptoms, morbidity, and antiinflammatory use in inner-city children	PEDIATRICS			English	Article; Proceedings Paper	38th Annual Meeting of the Ambulatory-Pediatric-Association	MAY 01-08, 1998	NEW ORLEANS, LOUISIANA	Ambulatory Pediat Assoc		inner-city children; asthma severity; persistent asthma; guidelines; morbidity; antiinflammatory therapy; inhaled steroids; symptom days	AIRWAY INFLAMMATION; PULMONARY-FUNCTION; LUNG-FUNCTION; SEVERITY	Background. Asthma is a major cause of morbidity that disproportionately affects inner-city children. For children with persistent asthma, defined as having asthma symptoms 3 or more days per week or 3 or more nights per month, national guidelines recommend the use of daily antiinflammatory agents. Despite these recommendations, antiinflammatory agents remain underused, particularly in inner-city children with high asthma morbidity. Objectives. The objectives of our study were to determine: 1) whether persistent asthma symptoms in inner-city children are related to acute care utilization and to the frequency of acute exacerbations; 2) whether children with persistent asthma are receiving recommended daily antiinflammatory agents; and 3) whether antiinflammatory medication use relates to sociodemographic factors, caretaker self-efficacy, the frequency of primary care visits, and/or measures of quality asthma care. Design and Methods. A 64-item telephone survey was administered between July 1996 and June 1997 to 219 parental caretakers of 2- to 12-year-old children who had been hospitalized with asthma at an inner-city medical center between January 1995 and February 1996. Persistent asthma symptoms were assessed by inquiring about the frequency of daily and nocturnal asthma symptoms over the last 4 weeks. Children's asthma severity was classified by applying the 1997 National Asthma Education and Prevention Program (NAEPP) Asthma Guidelines' severity classification scheme based on the frequency of asthma symptoms. Asthma morbidity was defined as the frequency of acute asthma exacerbations, emergency department visits and hospitalizations. Daily antiinflammatory medication use was compared by sociodemographic factors, caretaker self-efficacy, frequency of primary care visits, and measures of quality asthma home management. Results. In this sample, quantifying persistent asthma symptoms and applying the NAEPP symptom criteria identified 17% of the children with mild intermittent asthma, 27% with mild persistent asthma and 56% with moderate to severe persistent asthma. There were no differences in the age of the children in the 3 groups (mean age: 6 years). Asthma morbidity, as measured by the number of asthma exacerbations in the last 6 months, was significantly higher in the children with moderate to severe persistent asthma compared with children with mild intermittent asthma (9.8 vs 3.5) or mild persistent asthma (9.8 vs 4.5). In addition, there were significantly more emergency department visits in the moderate to severe group than in the mild persistent (3.05 vs 1.69) or mild intermittent group (3.05 vs 1.76). Lastly, as asthma symptom frequency increased, there were trends toward more hospitalizations and more days hospitalized. Overall, 35% of the 219 families reported giving daily antiinflammatory medications to their child (mostly cromolyn sodium). Of the 181 children (83%) who met NA-EPP symptom criteria for persistent asthma, only 39% were receiving daily antiinflammatory treatment. Of the children with symptoms of moderate to severe asthma, only 15% were receiving inhaled steroids in contrast to the guidelines' recommendations. Use of antiinflammatory agents was not related to caretaker sociodemographic factors or self-efficacy scores. Measures of quality asthma home management, which included use of mattress covers, written plans, and peak flow meters, correlated positively with use of antiinflammatory agents. Children whose families reported using daily antiinflammatory medications had more primary care visits in the last 6 months than those children not receiving antiinflammatory medications. Conclusion. Questioning parents about the frequency of their child's asthma symptoms is an important, inexpensive, and readily accessible bedside and office tool that may aid in the detection of persistent symptoms and help direct therapy. Our study suggests that classifying asthma severity by quantifying persistent asthma symptoms, as defined in the NAEPP Guidelines, is a clinically useful tool that relates to asthma morbidity. In our sample of previously hospitalized children with asthma, 83% met 1997 NAEPP symptom criteria for persistent asthma, and yet only 35% were receiving daily antiinflammatory agents. Use of antiinflammatory agents correlated positively with other indicators of quality asthma home management. Additional work is necessary to increase appropriate use of antiinflammatory agents in this population, and in particular, to increase inhaled steroid use for children with moderate or severe symptoms.	Albert Einstein Coll Med, Dept Pediat, Bronx, NY 10467 USA	Warman, KL (reprint author), Childrens Hosp Montefiore, Albert Einstein Coll Med, Dept Pediat, 1621 Eastchester Rd, Bronx, NY 10461 USA.						AAS K, 1981, ALLERGY, V36, P3, DOI 10.1111/j.1398-9995.1981.tb01818.x; AGERTOFT L, 1994, RESP MED, V88, P373, DOI 10.1016/0954-6111(94)90044-2; Berg A O, 1992, J Am Board Fam Pract, V5, P629; BUSSE WW, 1993, AM REV RESPIR DIS, V147, pS20; Clark NM, 1998, PEDIATRICS, V101, P831, DOI 10.1542/peds.101.5.831; Colice GL, 1999, AM J RESP CRIT CARE, V160, P1962; CRAIN EF, 1994, PEDIATRICS, V94, P356; DJUKANOVIC R, 1990, AM REV RESPIR DIS, V142, P434; Droste JHJ, 1999, PEDIATR PULM, V27, P260, DOI 10.1002/(SICI)1099-0496(199904)27:4<260::AID-PPUL6>3.0.CO;2-6; Goodman DC, 1999, PEDIATRICS, V104, P187, DOI 10.1542/peds.104.2.187; ILFELD FW, 1978, ARCH GEN PSYCHIAT, V35, P716; LAITINEN LA, 1992, J ALLERGY CLIN IMMUN, V90, P32, DOI 10.1016/S0091-6749(06)80008-4; Lang DM, 1997, ARCH INTERN MED, V157, P1193, DOI 10.1001/archinte.157.11.1193; Louis R, 2000, AM J RESP CRIT CARE, V161, P9; *NAEPP WHO, 1995, NIH PUBL; *NAT ASTHM ED PREV, 1997, NIH PUBL, V2; ROCHE WR, 1991, CLIN EXP ALLERGY, V21, P545, DOI 10.1111/j.1365-2222.1991.tb00845.x; SVENDSEN UG, 1987, J ALLERGY CLIN IMMUN, V80, P68; VANESSENZANDVLIET EE, 1992, AM REV RESPIR DIS, V146, P547; WARMAN KL, 1999, 39 ANN M AMB PED ASS	20	72	73	0	22	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	AUG	2001	108	2					277	282		10.1542/peds.108.2.277		6	Pediatrics	Pediatrics	458TZ	WOS:000170211800028	11483788	
J	Gutgesell, C; Heise, S; Seubert, S; Seubert, A; Domhof, S; Brunner, E; Neumann, C				Gutgesell, C; Heise, S; Seubert, S; Seubert, A; Domhof, S; Brunner, E; Neumann, C			Double-blind placebo-controlled house dust mite control measures in adult patients with atopic dermatitis	BRITISH JOURNAL OF DERMATOLOGY			English	Article						acaricides; atopic dermatitis; clinical trial; house dust mite; mattress encasing	PATCH TEST; ALLERGEN AVOIDANCE; CONTROLLED TRIAL; EXPOSURE; ASTHMA; ECZEMA	Background Avoidance of allergens has been shown to be of benefit in patients with atopic asthma sensitized to indoor allergens. In atopic dermatitis, there is so far little information about the effect of house dust mite elimination strategies. Objectives We therefore performed a randomized controlled study of house dust mite control in patients with this disease. Methods Twenty adult patients with moderate to severe atopic dermatitis were included. Inclusion criteria were a positive RAST to house dust mite antigen (CAP class > 3) and a concentration of > 2 mug g(-1) of the house dust mite antigen Der p1 in the patient's mattress dust. Patients were randomized to either the active treatment group (allergen-impermeable mattress encasing, acaricide spray containing tannic acid and benzylbenzoate) or a control group (allergen-permeable encasing, spray containing water and traces of ethanol). Severity of disease was estimated every 2 months by an established score (SCORAD), and eosinophil cationic protein (ECP) in the serum was determined by enzyme-linked immunosorbent assay. Furthermore, the use of topical steroids was quantified. Patients assessed daytime pruritus and pruritus-induced sleeplessness weekly on a visual analogue scale. The study lasted 1 year. Results At the end of the study, the active treatment group showed a statistically significant reduction in Der p1 exposure as compared with the control group. However, when comparing the change from the start to the end of the study, there was no statistically significant difference between active treatment and control groups as measured by the SCORAD score and by ECP levels in the serum. Some patients in the active treatment group reported less pruritus-induced sleeplessness, but there was no statistically significant difference between the two treatment groups. Conclusions For adult patients with atopic dermatitis it was shown that 1 year of house dust mite avoidance reduced the allergen exposure, but an improvement of overall disease activity was not demonstrated.	Univ Gottingen, Dept Dermatol, D-37075 Gottingen, Germany; Univ Gottingen, Dept Med Stat, D-37075 Gottingen, Germany	Gutgesell, C (reprint author), Univ Gottingen, Dept Dermatol, Von Siebold Str 3, D-37075 Gottingen, Germany.						Brunner E, 2000, BIOMETRICAL J, V42, P663, DOI 10.1002/1521-4036(200010)42:6<663::AID-BIMJ663>3.0.CO;2-7; BRUNNER E, 1999, NICHTPARAMETRISCHE A; Cameron MM, 1997, BRIT J DERMATOL, V137, P1; COLLOFF MJ, 1989, BRIT J DERMATOL, V121, P199, DOI 10.1111/j.1365-2133.1989.tb01799.x; Ebata T, 1999, BRIT J DERMATOL, V141, P82; Gotzsche PC, 1998, BRIT MED J, V317, P1105; Gutgesell C, 1999, CLIN EXP ALLERGY, V29, P920, DOI 10.1046/j.1365-2222.1999.00553.x; HENDERSON AJW, 1990, ALLERGY, V45, P445, DOI 10.1111/j.1398-9995.1990.tb01095.x; Marks GB, 1998, ALLERGY, V53, P108; MITCHELL EB, 1982, LANCET, V1, P127; Pichler CE, 1999, ALLERGOLOGIE, V22, P171; Ricci G, 2000, BRIT J DERMATOL, V143, P379, DOI 10.1046/j.1365-2133.2000.03666.x; Ring J, 1997, INT ARCH ALLERGY IMM, V113, P379; SAGER N, 1992, J ALLERGY CLIN IMMUN, V89, P801, DOI 10.1016/0091-6749(92)90434-4; SANDA T, 1992, J ALLERGY CLIN IMMUN, V89, P653, DOI 10.1016/0091-6749(92)90370-H; STALDER JF, 1993, DERMATOLOGY, V186, P23; Tan BB, 1996, LANCET, V347, P15, DOI 10.1016/S0140-6736(96)91556-1; Thepen T, 1996, J ALLERGY CLIN IMMUN, V97, P828, DOI 10.1016/S0091-6749(96)80161-8	18	72	74	0	2	BLACKWELL SCIENCE LTD	OXFORD	P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND	0007-0963			BRIT J DERMATOL	Br. J. Dermatol.	JUL	2001	145	1					70	74		10.1046/j.1365-2133.2001.04283.x		5	Dermatology	Dermatology	452UX	WOS:000169879000011	11453909	
J	Li, XM; Kleiner, G; Huang, CK; Lee, SY; Schofield, B; Soter, NA; Sampson, HA				Li, XM; Kleiner, G; Huang, CK; Lee, SY; Schofield, B; Soter, NA; Sampson, HA			Murine model of atopic dermatitis associated with food hypersensitivity	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						atopic dermatitis; eczema; food hypersensitivity; murine model; T(H)2-like cytokines; IgE-mediated hypersensitivity	POLYMERASE CHAIN-REACTION; ALOPECIA-AREATA; T-CELLS; INTESTINAL PERMEABILITY; ALLERGIC DERMATITIS; IGE HYPERPRODUCTION; AEROSOLIZED ANTIGEN; MESSENGER-RNA; C3H/HEJ MICE; NC/NGA MICE	Background: Atopic dermatitis (AD) is an eczematous skin eruption that generally begins in early infancy and affects up to 126 of the population. The cause of this disorder is not fully understood, although it is frequently the first sign of atopic disease and is characterized by an elevated serum IgE level, eosinophilia, and histologic tissue changes characterized early by spongiosis and a CD4(+) T(H)2 cellular infiltrate. Hypersensitivity to foods has been implicated as one causative factor in up to 40% of children with moderate-to-severe AD. Objective: The purpose of this study was to establish a murine model of food-induced AD. Methods: Female C3H/HeJ mice were sensitized orally to cow's milk or peanut with a cholera toxin adjuvant and then subjected to low-grade allergen exposure. Histologic examination of skin lesions, allergen-specific serum Ig levels, and allergen-induced T-cell proliferation and cytokine production were examined. Results: An eczematous eruption developed in approximately one third of mice after low-grade exposure to milk or peanut proteins. Peripheral blood eosinophilia and elevated serum IgE levels were noted. Histologic examination of the Lesional skin revealed spongiosis and a cellular infiltrate consisting of CD4(+) lymphocytes, eosinophils, and mast cells, IL-5 and IL-13 mRNA expression was elevated only in the skin of mice with the eczematous eruption. Treatment of the eruption with topical corticosteroids led to decreased pruritus and resolution of the cutaneous eruption. Conclusion: This eczematous eruption resembles AD in human subjects and should provide a useful model for studying immunopathogenic mechanisms of food hypersensitivity in AD.	CUNY Mt Sinai Sch Med, Dept Pediat, New York, NY 10029 USA; NYU, Sch Med, Ronald O Perelman Dept Dermatol, New York, NY USA; Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD USA	Sampson, HA (reprint author), CUNY Mt Sinai Sch Med, Dept Pediat, Box 1198,1 Gustave L Levy Pl, New York, NY 10029 USA.		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Allergy Clin. Immunol.	APR	2001	107	4					693	702		10.1067/mai.2001.114110		10	Allergy; Immunology	Allergy; Immunology	423RG	WOS:000168190100023	11295660	
J	Thorn, J; Brisman, J; Toren, K				Thorn, J; Brisman, J; Toren, K			Adult-onset asthma is associated with self-reported mold or environmental tobacco smoke exposures in the home	ALLERGY			English	Article						asthma; epidemiology; home environment; questionnaire	RISK-FACTORS; OCCUPATIONAL EXPOSURES; RESPIRATORY SYMPTOMS; CHILDHOOD ASTHMA; BRONCHIAL HYPERREACTIVITY; HEALTH; DAMPNESS; CHILDREN; POPULATION	Background: In recent years, we have gained better knowledge about the influence of indoor environments on respiratory symptoms and asthma. The purpose of this study was to examine certain exposures in the home environment and the risk of adult-onset asthma. Methods: A nested case-referent study of adult-onset asthma was performed in a random population sample (n = 15 813), aged 20-50 years. Cases for the study included subjects reporting "physician-diagnosed" asthma (n = 174). The referents (n = 870) were randomly selected from the whole population sample. The case-referent sample was investigated with a comprehensive mailed questionnaire about exposures in the home environment, asthma, respiratory symptoms, smoking habits, and atopy. Odds ratios (OR) with 95% confidence intervals (CI) were calculated while controlling for age, sex, smoking, and atopy. Results: Increased adjusted OR for asthma were associated with exposure to molds (OR 2.2, 95% CI 1.4-3.5), environmental tobacco smoke (OR 2.4, 95% CI 1.4-4.1), and the presence of a wood stove (OR 1.7, 95% CI 1.2-2.5). Conclusions: This population-based case-referent study indicates that self-reported domestic exposures to molds or environmental tobacco smoke can be associated with adult-onset asthma.	Univ Gothenburg, Dept Environm Med, S-40530 Gothenburg, Sweden; Sahlgrens Univ Hosp, Dept Occupat & Environm Med, S-41345 Gothenburg, Sweden; Sahlgrens Univ Hosp, Dept Resp Med & Allergol, S-41345 Gothenburg, Sweden	Thorn, J (reprint author), Univ Gothenburg, Dept Environm Med, Box 414, S-40530 Gothenburg, Sweden.			Brisman, Jonas/0000-0003-2333-3273			ANDRAE S, 1988, ARCH DIS CHILD, V63, P473; BRUNEKREEF B, 1992, ALLERGY, V47, P498, DOI 10.1111/j.1398-9995.1992.tb00672.x; Dales RE, 1997, INT J EPIDEMIOL, V26, P120, DOI 10.1093/ije/26.1.120; DALES RE, 1991, AM REV RESPIR DIS, V143, P505; Dales RE, 1999, ENVIRON HEALTH PERSP, V107, P481; DIJKSTRA L, 1990, AM REV RESPIR DIS, V142, P1172; Ehrlich RI, 1996, AM J RESP CRIT CARE, V154, P681; FAGBULE D, 1994, ANN TROP PAEDIATR, V14, P15; Flodin U, 1996, SCAND J WORK ENV HEA, V22, P451; Forsberg B, 1997, INT J EPIDEMIOL, V26, P610, DOI 10.1093/ije/26.3.610; Fritschi L, 1996, AM J EPIDEMIOL, V144, P521; Garrett MH, 1998, CLIN EXP ALLERGY, V28, P459; Gergen PJ, 1998, PEDIATRICS, V101, part. no., DOI 10.1542/peds.101.2.e8; GREER JR, 1993, J OCCUP ENVIRON MED, V35, P909, DOI 10.1097/00043764-199309000-00014; Hu FB, 1997, J ASTHMA, V34, P67, DOI 10.3109/02770909709071205; LEUENBERGER P, 1994, AM J RESP CRIT CARE, V150, P1222; LINDFORS A, 1995, ARCH DIS CHILD, V73, P408; MARTIN CJ, 1987, BRIT MED J, V294, P1125; Nicolai T, 1998, THORAX, V53, P1035; Norback D, 1999, INT J TUBERC LUNG D, V3, P368; STRACHAN DP, 1986, FAM PRACT, V3, P137, DOI 10.1093/fampra/3.3.137; TESCHKE K, 1994, AM J IND MED, V26, P327, DOI 10.1002/ajim.4700260306; TOREN K, 1993, CHEST, V104, P600, DOI 10.1378/chest.104.2.600; Toren K, 1999, INT J TUBERC LUNG D, V3, P192; Toren K, 1999, SCAND J WORK ENV HEA, V25, P430; VERHOEFF AP, 1995, AM J EPIDEMIOL, V141, P103; Williamson IJ, 1997, THORAX, V52, P229	27	72	73	0	3	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	APR	2001	56	4					287	292		10.1034/j.1398-9995.2001.00805.x		6	Allergy; Immunology	Allergy; Immunology	415DR	WOS:000167706000004	11284794	
J	Mitakakis, TZ; Barnes, C; Tovey, ER				Mitakakis, TZ; Barnes, C; Tovey, ER			Spore germination increases allergen release from Alternaria	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Editorial Material						allergen; Alt a 1; Alternaria; germination; Halogen; immunoassay	ASPERGILLUS-FUMIGATUS	Allergen released from individual spores of the fungus Alternaria has not been investigated. Germination of spores has been suggested to increase allergen release. This study examined allergen released from individual spores and the effect of germination on allergen availability. Allergen release was determined with the Halogen (Inhalix, Sydney, Australia) immunoassay, by use of serum IgE from Alternaria-sensitized subjects and 3 Alt a 1-specific antibodies. Not all spores released allergen. Germination of the spores significantly increased the proportion that released allergen (P < .0001 for all antibodies). Alt a 1 may be a minor contributor to the total allergen released from spores except when spores have germinated. How these results reflect the allergen content of spores in the air that we breathe requires investigation.	Univ Sydney, Sch Biol Sci, Inst Resp Med, Allergen Unit, Sydney, NSW 2006, Australia; Royal Prince Alfred Hosp, Inst Resp Med, Sydney, NSW, Australia; Childrens Mercy Hosp, Kansas City, MO 64108 USA	Mitakakis, TZ (reprint author), Univ Sydney, Sch Biol Sci, Inst Resp Med, Allergen Unit, Room 461,Blackburn Bldg D06, Sydney, NSW 2006, Australia.		Tovey, Euan/G-8604-2017	Tovey, Euan/0000-0002-1802-7266			DeVouge MW, 1996, INT ARCH ALLERGY IMM, V111, P385; Halonen M, 1997, AM J RESP CRIT CARE, V155, P1356; MORRISON VA, 1993, CLIN INFECT DIS, V16, P265; PORTNOY J, 1993, J ALLERGY CLIN IMMUN, V91, P930, DOI 10.1016/0091-6749(93)90351-F; Razmovski V, 2000, J ALLERGY CLIN IMMUN, V105, P725, DOI 10.1067/mai.2000.105222; REIJULA KE, 1991, J ALLERGY CLIN IMMUN, V87, P683, DOI 10.1016/0091-6749(91)90389-6; SALVAGGIO JE, 1994, J ALLERGY CLIN IMMUN, V94, P304, DOI 10.1016/0091-6749(94)90090-6; SPORIK RB, 1993, CLIN EXP ALLERGY, V23, P326, DOI 10.1111/j.1365-2222.1993.tb00330.x; VIJAY HM, 1993, J ALLERGY CLIN IMMUN, V91, P826, DOI 10.1016/0091-6749(93)90338-G	9	72	72	1	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.	FEB	2001	107	2					388	390		10.1067/mai.2001.112602		3	Allergy; Immunology	Allergy; Immunology	403YV	WOS:000167071400030	11174210	
J	Schelegle, ES; Gershwin, LJ; Miller, LA; Fanucchi, MV; Van Winkle, LS; Gerriets, JP; Walby, WF; Omlor, AM; Buckpitt, AR; Tarkington, BK; Wong, VJ; Joad, JP; Pinkerton, KB; Wu, R; Evans, MJ; Hyde, DM; Plopper, CG				Schelegle, ES; Gershwin, LJ; Miller, LA; Fanucchi, MV; Van Winkle, LS; Gerriets, JP; Walby, WF; Omlor, AM; Buckpitt, AR; Tarkington, BK; Wong, VJ; Joad, JP; Pinkerton, KB; Wu, R; Evans, MJ; Hyde, DM; Plopper, CG			Allergic asthma induced in rhesus monkeys by house dust mite (Dermatophagoides farinae)	AMERICAN JOURNAL OF PATHOLOGY			English	Article							LYMPHOCYTE-T ACTIVATION; ANTIGEN CHALLENGE; MEDIATOR RELEASE; MACACA-MULATTA; AIRWAY; HISTAMINE; PROSTAGLANDINS; PRIMATES; DISEASE; CELLS	To establish whether allergic asthma could be induced experimentally in a nonhuman primate using a common human allergen, three female rhesus mon keys (Macaca mulatta) were sensitized with house dust mite (Dermatophagoides farinae) allergen (HDMA) by subcutaneous injection, followed by four intranasal sensitizations, and exposure to allergen aerosol 3 hours per day, 3 days per week for up to 13 weeks. Before aerosol challenge, all three monkeys skin-tested positive for HDMA, During aerosol challenge with HDMA, sensitized monkeys exhibited cough and rapid shallow breathing and increased airway resistance,which was reversed by albuterol aerosol treatment. Compared to nonsensitized monkeys, there was a fourfold reduction in the dose of histamine aerosol necessary to produce a 150% increase in airway resistance in sensitized monkeys, After aerosol challenge, serum levels of histamine were elevated in sensitized monkeys, Sensitized monkeys exhibited increased levels of HDMA-specific IgE in serum, numbers of eosinophils and exfoliated cells within lavage, and elevated CD25 expression on circulating CD4(+) lymphocytes, Intrapulmonary bronchi of sensitized monkeys had focal mucus tell hyperplasia, interstitial infiltrates of eosinophils, and thickening of the basement membrane zone, We conclude that a model of allergic asthma can be induced in rhesus monkeys using a protocol consisting of subcutaneous injection, intranasal instillation, and aerosol challenge with HDMA.	Univ Calif Davis, Sch Vet Med, Dept Anat Physiol & Cell Biol, Davis, CA 95616 USA; Univ Calif Davis, Sch Vet Med, Dept Pathol Microbiol & Immunol, Davis, CA 95616 USA; Univ Calif Davis, Sch Vet Med, Dept Mol Biosci, Davis, CA 95616 USA; Univ Calif Davis, Sch Vet Med, Calif Reg Primate Res Ctr, Exposure Facil, Davis, CA 95616 USA; Univ Calif Davis, Sch Med, Dept Pediat, Davis, CA 95616 USA	Univ Calif Davis, Sch Vet Med, Dept Anat Physiol & Cell Biol, 1 Shields Ave, Davis, CA 95616 USA.	esschelegle@ucdavis.edu			NCI NIH HHS [P01 CA095616]; NCRR NIH HHS [P51 RR000169, RR00169]; NIEHS NIH HHS [ES 05707, F32 ES005707, P01 ES000628, P01 ES0628, P30 ES005707]		BLEECKER ER, 1986, AM J MED, V81, P93, DOI 10.1016/0002-9343(86)90470-5; CARTIER A, 1982, J ALLERGY CLIN IMMUN, V70, P170, DOI 10.1016/0091-6749(82)90038-0; COCKCROFT DW, 1987, ANN ALLERGY, V59, P405; CORRIGAN CJ, 1990, AM REV RESPIR DIS, V141, P970; CORRIGAN CJ, 1988, LANCET, V1, P1129; Csendes T., 1988, Acta Cybernetica, V8, P361; DUBOIS AB, 1956, J APPL PHYSIOL, V8, P587; DVORAK AM, 1983, AM REV RESPIR DIS, V128, P49; GERSHWIN LJ, 1985, J IMMUNOL METHODS, V76, P39, DOI 10.1016/0022-1759(85)90479-X; GUNDEL RH, 1991, AM REV RESPIR DIS, V144, P76; HINNERS RG, 1968, ARCH ENVIRON HEALTH, V16, P194; LIU MC, 1990, AM REV RESPIR DIS, V142, P126; Madwed JB, 1997, J APPL PHYSIOL, V83, P1690; MCFADDEN ER, 1968, NEW ENGL J MED, V278, P1027, DOI 10.1056/NEJM196805092781901; Mercer T. T., 1970, J AEROSOL SCI, V1, P9, DOI 10.1016/0021-8502(70)90024-8; MIADONNA A, 1990, J ALLERGY CLIN IMMUN, V85, P906, DOI 10.1016/0091-6749(90)90076-G; Miller LA, 1998, AM J RESP CELL MOL, V19, P892; *NIH, 1997, GUID DIAGN MAN ASTHM, P1; OZOLS J, 1990, METHOD ENZYMOL, V182, P587; Ozwara H, 1997, J MED PRIMATOL, V26, P164; PARE PD, 1976, J APPL PHYSIOL, V41, P668; PESLIN R, 1985, J APPL PHYSIOL, V59, P492; PLOPPER CG, 1986, ANAT EMBRYOL, V174, P167, DOI 10.1007/BF00824332; PLOPPER CG, 1986, AM J ANAT, V175, P59, DOI 10.1002/aja.1001750107; PLOPPER CG, 1992, CHEST, V101, P2; Plopper C, 1990, MODELS LUNG DISEASE, P537; REIMANN KA, 1994, CYTOMETRY, V17, P102, DOI 10.1002/cyto.990170113; SHORE PA, 1959, J PHARMACOL EXP THER, V127, P182; STGEORGE JA, 1986, ANAT REC, V216, P60, DOI 10.1002/ar.1092160111; TEAGUE SV, 1978, HEALTH PHYS, V35, P392; WELLS E, 1986, J IMMUNOL, V137, P3933; Yasue M, 1998, INT ARCH ALLERGY IMM, V115, P303, DOI 10.1159/000069461	32	72	76	1	2	ELSEVIER SCIENCE INC	NEW YORK	360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA	0002-9440	1525-2191		AM J PATHOL	Am. J. Pathol.	JAN	2001	158	1					333	341		10.1016/S0002-9440(10)63973-9		9	Pathology	Pathology	390XV	WOS:000166325800038	11141508	
J	Meding, B				Meding, B			Differences between the sexes with regard to work-related skin disease	CONTACT DERMATITIS			English	Review						females; differences between the sexes; hand eczema; high-risk occupation; males; occupational skin disease; prevalence; prevention; risk factor; wet work	HAND DERMATITIS; ALLERGENIC ACTIVITY; ECZEMA; HAIRDRESSERS; SURFACTANTS; OCCUPATION; POPULATION; OXIDATION; BAKERS; ATOPY	Work-related skin disease is common and usually presents as hand eczema. From the Occupational Injury Information System in Sweden, as well as from registers of industrial injuries in other countries, it is evident that females report skin disease more often than males. Epidemiological studies of hand eczema also show that women are more often affected than men, in particular young women. The most common type of hand eczema is irritant contact dermatitis, which is often caused by wet work. Many female-dominated occupations involve extensive wet work, e.g., hairdressing, catering, cleaning and health-care work. These occupations are also high-risk occupations for hand eczema. Experimental studies of skin irritation have not confirmed differences between the sexes; thus, the higher prevalence of irritant contact dermatitis among females is most likely due to exposure, occupational and non-occupational. Nickel allergy is the most common contact allergy, which is most frequent in young females, and in 30-40% results over time in hand eczema. Hand eczema has an impact on quality of life and females seem to report a higher degree of discomfort than males. To achieve the optimal effect of preventive efforts regarding occupational skin disease, the focus for prevention should aim at reducing wet exposure.	Natl Inst Working Life, S-11279 Stockholm, Sweden; Karolinska Inst, Dept Med Occupat & Environm Dermatol, Stockholm, Sweden	Meding, B (reprint author), Natl Inst Working Life, S-11279 Stockholm, Sweden.						Agner T, 1992, Acta Derm Venereol Suppl (Stockh), V173, P1; Agrup G, 1969, ACTA DERM VENERE S61, V49, P1; Bergh M, 1998, J PHARM SCI, V87, P276, DOI 10.1021/js9704036; Bergh M, 1997, CONTACT DERMATITIS, V37, P9, DOI 10.1111/j.1600-0536.1997.tb00368.x; Bergh M, 1998, CONTACT DERMATITIS, V39, P14, DOI 10.1111/j.1600-0536.1998.tb05805.x; Brisman J, 1998, OCCUP ENVIRON MED, V55, P750; CHERRY NM, 1994, DHHS NIOSH PUBLICATI, P608; Conde-Salazar L, 1995, AM J CONTACT DERMATI, V6, P19, DOI 10.1016/1046-199X(95)90064-0; De Groot A.C., 1994, PATCH TESTING TEST C; DIEPGEN T, 1991, Z HAUTKRANKHEITEN, V66, P935; FROSCH PJ, 1993, CONTACT DERMATITIS, V28, P180, DOI 10.1111/j.1600-0536.1993.tb03383.x; Halkier-Sorensen L, 1996, Contact Dermatitis, V35, P1; HANSEN KS, 1983, CONTACT DERMATITIS, V9, P343, DOI 10.1111/j.1600-0536.1983.tb04426.x; HEDLIN M, 1994, 10 NAT BOARD OCC SAF; LAMMINTAUSTA K, 1993, ACTA DERM-VENEREOL, V73, P119; LAMMINTAUSTA K, 1981, CONTACT DERMATITIS, V7, P301, DOI 10.1111/j.1600-0536.1981.tb04085.x; LARSSONSTYMNE B, 1985, CONTACT DERMATITIS, V13, P289, DOI 10.1111/j.1600-0536.1985.tb02580.x; Lidegaard O, 1997, CNS DRUGS, V7, P1; Liden C, 1996, BRIT J DERMATOL, V134, P193; MARKLUND S, 1997, RISK FRISK FAKTORER, V6, P118; Meding B, 1990, Acta Derm Venereol Suppl (Stockh), V153, P1; MEDING B, 1994, 43 NORD ARB LOEN NOR, P81; MellstrOm GA, 1994, PROTECTIVE GLOVES OC, P39; Menne T, 1979, Derm Beruf Umwelt, V27, P129; Menne T., 1989, NICKEL SKIN IMMUNOLO, P109; *NAT BOARD OCC SAF, 1995, ARB ARB 1993; Nielsen J, 1996, CONTACT DERMATITIS, V34, P284; NIELSEN NH, 1992, ACTA DERM-VENEREOL, V72, P456; NILSSON E, 1985, CONTACT DERMATITIS, V13, P216, DOI 10.1111/j.1600-0536.1985.tb02553.x; ROSDAHL I, 1996, 1 U LINK LEAD EQ ORG, P61; RYSTEDT I, 1985, ACTA DERM-VENEREOL, V65, P305; Schultz Larsen F, 1993, J Am Acad Dermatol, V28, P719; SMIT HA, 1993, INT J EPIDEMIOL, V22, P288, DOI 10.1093/ije/22.2.288; STINGENI L, 1995, CONTACT DERMATITIS, V33, P172, DOI 10.1111/j.1600-0536.1995.tb00540.x; TACKE J, 1995, CONTACT DERMATITIS, V33, P112, DOI 10.1111/j.1600-0536.1995.tb00511.x; *TRGS, 1996, 531 TRGS; Turjanmaa K, 1996, ALLERGY, V51, P593, DOI 10.1111/j.1398-9995.1996.tb04678.x; *US DEP HHS, 1997, DHHS PUBLICATION P 3, P48; VANDERWALLE HB, 1994, CONTACT DERMATITIS, V30, P217	39	72	76	1	8	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-1873			CONTACT DERMATITIS	Contact Dermatitis	AUG	2000	43	2					65	71		10.1034/j.1600-0536.2000.043002065.x		7	Allergy; Dermatology	Allergy; Dermatology	339JB	WOS:000088473000001	10945743	
J	Omenaas, E; Jentoft, HF; Vollmer, WM; Buist, AS; Gulsvik, A				Omenaas, E; Jentoft, HF; Vollmer, WM; Buist, AS; Gulsvik, A			Absence of relationship between tuberculin reactivity and atopy in BCG vaccinated young adults	THORAX			English	Article						atopy; asthma; tuberculosis; immunisation; BCG vaccination	INFECTION; RESPONSES; DISORDER; CHILDREN	Background-An inverse association between tuberculin responses and atopy has been observed in Japanese children, indicating that BCG immunisation, subclinical exposure to Mycobacterium tuberculosis without clinical disease, or host characteristics may influence the T helper (Th) lymphocyte balance with decreased atopy as a result. This study was undertaken to determine whether tuberculin reactivity is inversely related to atopy in young adults vaccinated with BCG at the age of 14. Methods-Men and women aged 20-44 years were tested using the adrenaline-Pirquet test with Norwegian produced synthetic medium tuberculin (n = 891). In addition, their serum total and specific IgE antibodies against mite, cat, timothy grass, mould and birch were measured. Results-Of the 574 subjects with complete examinations, 64% had a positive adrenaline-Pirquet tuberculin test (greater than or equal to 4 mm) and 27% exhibited IgE antibodies (greater than or equal to 0.35 kU/l) to one or more of the five specific allergens. The geometric mean of total serum IgE in the population was 30.2 kU/l. Tuberculin reactivity and log IgE were not correlated (r = 0.043, p 0.30). The mean tuberculin reactivity was 4.6 mm, 4.9 mm, and 5.0 mm in the lower, middle and upper tertile of IgE distribution (< 14 kU/l, 14-61 kU/l, > 61 kU/l). The prevalence of atopy, as assessed by either the presence of any of the five specific IgE antibodies or by each specific IgE antibody separately, did not differ between subjects with a positive and those with a negative tuberculin test. These results persisted after adjustment for age, sex, and smoking status in multivariate logistic regression analyses. Conclusions-In this young adult population, BCG vaccinated at the age of 14, no significant relationship between a positive tuberculin reaction and atopy was observed. If a true relationship had been found, our study suggests that it may be limited to populations immunised in early childhood when a substantial modulation of the immune system can occur.	Univ Bergen, Dept Thorac Med, N-5020 Bergen, Norway; Kaiser Permanente Ctr Hlth Res, Oakland, CA 94612 USA; Oregon Hlth Sci Univ, Portland, OR 97201 USA	Omenaas, E (reprint author), Haukeland Univ Hosp, Dept Thorac Med, N-5021 Bergen, Norway.						Alm JS, 1997, LANCET, V350, P400, DOI 10.1016/S0140-6736(97)02207-1; BJARTVEIT K, 1996, CONTROL TUBERCULOSIS; BJERKEDAL T, 1967, AM J EPIDEMIOL, V85, P157; BJORLO R, 1985, PREPARATION SYNTHETI; 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; COOKSON OCM, 1997, SCIENCE, V275, P41; DIXON JD, 1990, BMDP STAT SOFTWARE; EILERTSEN E, 1964, ACTA TUB PNEUM S S60, V34, P84; Farooqi IS, 1998, THORAX, V53, P927; HANSEN OG, 1937, ACTA TUBERC SCAND, V6, P130; JENTOFT H, 1999, INT J TUBERC LUNG D, V4, P326; Jentoft H. F., 1996, European Respiratory Journal Supplement, V9, p203S; Martinati LC, 1997, ALLERGY, V52, P1036; OMENAAS E, 1994, CLIN EXP ALLERGY, V24, P530, DOI 10.1111/j.1365-2222.1994.tb00950.x; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; ROMAGNANI S, 1992, IMMUNOL TODAY, V13, P379, DOI 10.1016/0167-5699(92)90083-J; Shirakawa T, 1997, SCIENCE, V275, P77, DOI 10.1126/science.275.5296.77; Silverman M, 1997, LANCET, V350, P380, DOI 10.1016/S0140-6736(05)64130-X; Strannegard IL, 1998, ALLERGY, V53, P249, DOI 10.1111/j.1398-9995.1998.tb03884.x; von Pirquet C., 1907, BERL KLIN WSCHR, V48, P699; WAALER H, 1975, B INT UNION TUBERC, V1, P5	22	72	73	0	2	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	JUN	2000	55	6					454	458		10.1136/thorax.55.6.454		5	Respiratory System	Respiratory System	319WP	WOS:000087367100005	10817791	
J	Lams, BEA; Sousa, AR; Rees, PJ; Lee, TH				Lams, BEA; Sousa, AR; Rees, PJ; Lee, TH			Subepithelial immunopathology of the large airways in smokers with and without chronic obstructive pulmonary disease	EUROPEAN RESPIRATORY JOURNAL			English	Article						airway; chronic obstructive pulmonary disease; eosinophils; inflammation; lymphocytes; neutrophils	AIR-FLOW OBSTRUCTION; CHRONIC-BRONCHITIS; BRONCHOALVEOLAR LAVAGE; PERIPHERAL AIRWAYS; CELL-POPULATIONS; INDUCED SPUTUM; T-LYMPHOCYTES; INFLAMMATION; ASTHMA; BIOPSIES	Previous work has shown an increase in CD8+ T-cells, neutrophils and eosinophils in small airway subepithelium in smokers, The authors have now investigated whether similar changes occur in the large airways. Immunohistochemistry on frozen sections of bronchial biopsies were obtained at bronchoscopy in 11 nonsmokers, eight asymptomatic smokers and 11 smokers with chronic bronchitis and chronic obstructive pulmonary disease (COPD). There was an increase in the number of CD8+ cells infiltrating the bronchial subepithelium in the COPD group compared to the asymptomatic smokers (305 (109-400) versus 92 (41-550) cells.mm(-2), p=0.030). There was a negative correlation between the number of CD8+ cells and the forced expiratory volume in one second (FEV1) %predicted (p=0.005, r=-0.62), and a positive correlation between the number of CD8+ cells and the number of pack years smoked (p=0.017, r=0.42). There was a negative correlation between the activated/total eosinophils ratio and the FEV1 % pred (p=0.017, r=-0.51). There was a negative correlation between pack years smoked and the number of neutrophils (p=0.022, r=-0.36). Smokers who develop chronic obstructive pulmonary disease have increased numbers of CD8+ T-cells in large airways when compared to asymptomatic smokers. Airway obstruction was associated with an increase in the proportion of eosinophils that were activated.	Guys Kings Coll & St Thomas Hosp, Sch Med & Dent, Dept Resp Med & Allergy, London, England	Lee, TH (reprint author), Guys Hosp, Dept Allergy & Resp Med, 5th Floor,Thomas Guy House, London SE1 9RT, England.						AMADORI A, 1995, NAT MED, V1, P1279, DOI 10.1038/nm1295-1279; BOSKEN CH, 1992, AM REV RESPIR DIS, V145, P911; BOUSQUET J, 1991, INT ARCH ALLER A IMM, V94, P227; *BTS, 1997, THORAX S5, V52, P1; CANNON MJ, 1988, J EXP MED, V168, P1163, DOI 10.1084/jem.168.3.1163; COSTABEL U, 1992, RESPIRATION, V59, P17; COYLE AJ, 1995, J EXP MED, V181, P1229, DOI 10.1084/jem.181.3.1229; DiStefano A, 1996, AM J RESP CRIT CARE, V153, P629; DOLL R, 1976, BRIT MED J, V2, P1525; FINKELSTEIN R, 1995, AM J RESP CRIT CARE, V152, P1666; FLETCHER C, 1977, BRIT MED J, V1, P1645; FOURNIER M, 1989, AM REV RESPIR DIS, V140, P737; GESSER B, 1995, BIOCHEM BIOPH RES CO, V210, P660, DOI 10.1006/bbrc.1995.1711; Keatings VM, 1997, THORAX, V52, P372; Keatings VM, 1996, AM J RESP CRIT CARE, V153, P530; LACOSTE JY, 1993, J ALLERGY CLIN IMMUN, V92, P537, DOI 10.1016/0091-6749(93)90078-T; Lams BEA, 1998, AM J RESP CRIT CARE, V158, P1518; LUSUARDI M, 1994, THORAX, V49, P1211, DOI 10.1136/thx.49.12.1211; MARTIN TR, 1985, AM REV RESPIR DIS, V132, P254; Mueller R, 1996, RESP MED, V90, P79, DOI 10.1016/S0954-6111(96)90202-4; Nasser SMS, 1996, AM J RESP CRIT CARE, V153, P90; OShaughnessy TC, 1997, AM J RESP CRIT CARE, V155, P852; Pesci A, 1998, RESP MED, V92, P863, DOI 10.1016/S0954-6111(98)90389-4; 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; Stanescu D, 1996, THORAX, V51, P267, DOI 10.1136/thx.51.3.267; THOMPSON AB, 1989, AM REV RESPIR DIS, V140, P1527	28	72	74	0	0	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					512	516		10.1034/j.1399-3003.2000.15.14.x		5	Respiratory System	Respiratory System	295JG	WOS:000085962500014	10759445	
J	Hammad, H; Lambrecht, BN				Hammad, H.; Lambrecht, B. N.			Dendritic cells and airway epithelial cells at the interface between innate and adaptive immune responses	ALLERGY			English	Review						allergens; asthma; dendritic cells; epithelium	HOUSE-DUST MITE; THYMIC STROMAL LYMPHOPOIETIN; REGULATORY T-CELLS; HELPER TYPE-2 RESPONSE; BRONCHIAL LYMPH-NODE; IN-VIVO; ALLERGIC INFLAMMATION; INHALED ANTIGEN; RESPIRATORY-TRACT; TH2 RESPONSES	P>Because they can recognize and sample inhaled allergens, dendritic cells (DC) have been shown to be responsible for the initiation and maintenance of adaptive Th2 responses in asthma. It is increasingly clear that DC functions are strongly influenced by a crosstalk with neighboring cells like epithelial cells. Whereas the epithelium was initially considered only as a barrier, it is now seen as a central player in controlling the function of lung DCs through release of innate cytokines-promoting Th2 responses. Clinically relevant allergens, as well as known environmental and genetic risk factors for allergy and asthma, often interfere directly or indirectly with the innate immune functions of airway epithelial cells and DC. A better understanding of these interactions might lead to a better prevention and ultimately to new treatments for asthma.	[Hammad, H.] Univ Ghent, Dynam Imaging Unit, Immunoregulat Lab, B-9000 Ghent, Belgium	Hammad, H (reprint author), Univ Ghent, Dynam Imaging Unit, Immunoregulat Lab, Blok B Ground Floor,Pintelaan 185, B-9000 Ghent, Belgium.	hamida.hammad@ugent.be	Hammad, Hamida/J-9391-2015; Lambrecht, Bart/K-2484-2014	Hammad, Hamida/0000-0003-3762-8603; Lambrecht, Bart/0000-0003-4376-6834			Akbari O, 2001, NAT IMMUNOL, V2, P725, DOI 10.1038/90667; Akbari O, 2002, NAT MED, V8, P1024, DOI 10.1038/nm745; Al-Ramli W, 2009, J ALLERGY CLIN IMMUN, V123, P1185, DOI 10.1016/j.jaci.2009.02.024; Al-Shami A, 2005, J EXP MED, V202, P829, DOI 10.1084/jem.20050199; Angkasekwinai P, 2007, J EXP MED, V204, P1509, DOI 10.1084/jem.20061675; Asokananthan N, 2002, J IMMUNOL, V169, P4572; Ballantyne SJ, 2007, J ALLERGY CLIN IMMUN, V120, P1324, DOI 10.1016/j.jaci.2007.07.051; Barrett NA, 2009, J IMMUNOL, V182, P1119; Beaty SR, 2007, J IMMUNOL, V178, P1882; BENSASSON SZ, 1990, P NATL ACAD SCI USA, V87, P1421, DOI 10.1073/pnas.87.4.1421; 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J	Ronmark, EP; Ekerljung, L; Lotvall, J; Toren, K; Ronmark, E; Lundback, B				Ronmark, Erik P.; Ekerljung, Linda; Lotvall, Jan; Toren, Kjell; Ronmark, Eva; Lundback, Bo			Large scale questionnaire survey on respiratory health in Sweden: Effects of late- and non-response	RESPIRATORY MEDICINE			English	Article						Asthma; Allergy; Questionnaire; Non-response; Epidemiology	POSTAL SURVEY; RISK-FACTORS; YOUNG-ADULTS; SYMPTOMS; ASTHMA; PREVALENCE; POPULATION; EXPOSURE; DISEASE; COHORT	Background: Participation rates in epidemiologic studies conducted with postal questionnaires have steadily declined since 1970s. This can lead to an increased risk for selection bias. The aim of this study was to examine cause and effect of non-response in a large cross sectional study assessing respiratory health in western Sweden. Methods: The study sample was 29,218. The response rate to the initial postal. questionnaire was 33%. The response rates to subsequent postal reminders were 15%, 7% and 7% of eligible participants totalling a participation of 62%. Of those who did not respond to the postal survey, a random sample of 400 subjects were identified and contacted for interview by telephone. Results: Non-responders did not differ significantly in prevalence of airway diseases or symptoms when compared with responders. Mate sex, young age and smokers were underestimated among non-responders. No clear trends in prevalence of respiratory symptoms and report of asthma were found with delayed response to the postal. survey. The proportion of smokers and men increased with increasing number of reminders. Letters reminding subjects about the study did increase the participation rate but did not alter the risk estimates. Conclusion: We conclude that with a response rate of 62%, our estimate of disease and symptom prevalence was not biased in this Swedish population. However, smoking was underestimated. No general. trend for late-responders was seen and therefore we conclude that extrapolation of results to non-responders is not possible in our study. Causes of non-response were mainly due to circumstantial factors. (C) 2009 Elsevier Ltd. All rights reserved.	[Ronmark, Erik P.] Univ Gothenburg, VBG Grp, Ctr Asthma & Allergy Res, Dept Internal Med,Sahlgrenska Acad,LFG Lab, SE-41346 Gothenburg, Sweden; [Toren, Kjell] Univ Gothenburg, VBG Grp, Ctr Asthma & Allergy Res, Dept Environm & Occupat Med,Sahlgrenska Acad, SE-41346 Gothenburg, Sweden; [Ronmark, Eva; Lundback, Bo] Sunderby Cent Hosp Norrbotten, Dept Med, OLIN Studies, Lulea, Sweden; [Ronmark, Eva] Umea Univ, Dept Publ Hlth & Clin Med, Div Environm & Occupat Med, Umea, Sweden	Ronmark, EP (reprint author), Univ Gothenburg, VBG Grp, Ctr Asthma & Allergy Res, Dept Internal Med,Sahlgrenska Acad,LFG Lab, Guldhedsgatan 10A, SE-41346 Gothenburg, Sweden.	erik.ronmark@gu.se		Lotvall, Jan/0000-0001-9195-9249	Herman Krefting Foundation; Swedish Heart Lung Foundation	The Herman Krefting Foundation for Asthma and Allergy Research is greatly acknowledged for funding the study. Additional funding was provided by the Swedish Heart Lung Foundation and the health authorities of the Vastra Gotaland Region. The authors thank the assistants Eva-Marie Romell and Madeleine Ahrnens, Gothenburg, for help with collecting the data and associate professor Matthew Perzanowski, Columbia University, New York, for valuable comments and language revision of the paper.	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Med.	DEC	2009	103	12					1807	1815		10.1016/j.rmed.2009.07.014		9	Cardiac & Cardiovascular Systems; Respiratory System	Cardiovascular System & Cardiology; Respiratory System	526FK	WOS:000272272900005	19695859	
J	Schuttelaar, MLA; Kerkhof, M; Jonkman, MF; Koppelman, GH; Brunekreef, B; de Jongste, JC; Wijga, A; McLean, WHI; Postma, DS				Schuttelaar, M. L. A.; Kerkhof, M.; Jonkman, M. F.; Koppelman, G. H.; Brunekreef, B.; de Jongste, J. C.; Wijga, A.; McLean, W. H. I.; Postma, D. S.			Filaggrin mutations in the onset of eczema, sensitization, asthma, hay fever and the interaction with cat exposure	ALLERGY			English	Article						asthma; atopy; children; eczema; filaggrin	ATOPIC-DERMATITIS; ICHTHYOSIS VULGARIS; RARE MUTATIONS; PREDISPOSE; GENE; POPULATION; EXPRESSION; VALIDATION; PREVALENT; CHILDREN	Background: Filaggrin gene (FLG) mutations contribute to the development of eczema and asthma, but their contribution to sensitization and hay fever remains unclear. Methods: FLG mutations R501X, 2282del4 and R2447X were genotyped in the Prevention and Incidence of Asthma and Mite Allergy birth cohort (n = 934) to evaluate longitudinally, for up to 8 years, their association with eczema, sensitization, asthma, hay fever and their interaction with cat exposure. Results: The combined FLG mutations were significantly associated with eczema at all ages when occurring in the first year of life (OR = 2.0; 95% CI: 1.4-2.8). Combined FLG mutations were associated with both atopic and nonatopic eczema, as well as asthma (OR = 3.7; 95% CI: 1.8-7.5). When the FLG 2282del4 mutation was analysed separately, it was significantly associated with the development of eczema during the first year, having eczema up to 8 years and sensitization at the age of 8 years, which was enhanced by early-life cat exposure (ORs being 8.2; 95% CI: 2.6-25.9, 6.0; 95% CI: 3.2-11.3 and 5.4; 95% CI: 1.2-23.6 respectively). FLG 2282del4 was significantly associated with hay fever from the age 5 years onwards (OR = 3.9; 95% CI: 1.5-10.5). Conclusions: FLG mutations are associated both with atopic and nonatopic eczema starting in the first year of life. FLG mutations combined with eczema in the first year of life are associated with a later development of asthma and hay fever, a clear example of the atopic march. We confirm that cat exposure enhances the effect of a FLG mutation on the development of eczema and sensitization.	[Schuttelaar, M. L. A.; Jonkman, M. F.] Univ Groningen, Univ Med Ctr Groningen, Dept Dermatol, NL-9700 RB Groningen, Netherlands; [Kerkhof, M.] Univ Groningen, Univ Med Ctr Groningen, Dept Epidemiol, NL-9700 RB Groningen, Netherlands; [Koppelman, G. H.] Univ Groningen, Univ Med Ctr Groningen, Dept Pediat Pulmonol & Pediat Allergol, NL-9700 RB Groningen, Netherlands; [Brunekreef, B.] Univ Med Ctr Utrecht, Inst Risk Assessment Sci, Utrecht, Netherlands; [Brunekreef, B.] Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands; [de Jongste, J. C.] Erasmus Univ, Sophia Childrens Hosp, Dept Pediat, Med Ctr, Rotterdam, Netherlands; [Wijga, A.] Natl Inst Publ Hlth & Environm, RIVM, NL-3720 BA Bilthoven, Netherlands; [McLean, W. H. I.] Univ Dundee, Epithelial Genet Grp, Human Genet Unit, Div Pathol & Neurosci, Dundee, Scotland; [Postma, D. S.] Univ Groningen, Univ Med Ctr Groningen, Dept Pulmonol, NL-9700 RB Groningen, Netherlands	Schuttelaar, MLA (reprint author), Univ Groningen, Univ Med Ctr Groningen, Dept Dermatol, POB 30-001, NL-9700 RB Groningen, Netherlands.		McLean, William/C-6352-2009	McLean, William Henry Irwin/0000-0001-5539-5757; brunekreef, bert/0000-0001-9908-0060	Netherlands Asthma Foundation; Ministry of the Environment, ZorgOnderzoek Nederland; National Institute of Public Health and the Environment; J.P. Nater Fund	The PIAMA study was supported by the Netherlands Asthma Foundation, the Ministry of the Environment, ZorgOnderzoek Nederland and the National Institute of Public Health and the Environment. M.L.A. Schuttelaar was supported by the J.P. Nater Fund. We thank all the members of the PIAMA study group as well as the children and their parents for their participation in our study.	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D., 2003, APPL LONGITUDINAL DA; Spergel Jonathan M., 2003, Journal of Allergy and Clinical Immunology, V112, pS118, DOI 10.1016/j.jaci.2003.09.033; Weidinger S, 2006, J ALLERGY CLIN IMMUN, V118, P214, DOI 10.1016/j.jaci.2006.05.004; Weidinger S, 2008, J ALLERGY CLIN IMMUN, V121, P1203, DOI 10.1016/j.jaci.2008.02.014; Weidinger S, 2007, J INVEST DERMATOL, V127, P724, DOI 10.1038/sj.jid.5700630; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P406, DOI 10.1111/j.1365-2133.1994.tb08532.x; Williams H, 2006, J ALLERGY CLIN IMMUN, V118, P209, DOI 10.1016/j.jaci.2006.04.043; Ying S, 2006, J ALLERGY CLIN IMMUN, V118, P1386, DOI 10.1016/j.jaci.2006.08.030	27	71	74	0	2	WILEY-BLACKWELL	HOBOKEN	111 RIVER ST, HOBOKEN 07030-5774, NJ USA	0105-4538	1398-9995		ALLERGY	Allergy	DEC	2009	64	12					1758	1765		10.1111/j.1398-9995.2009.02080.x		8	Allergy; Immunology	Allergy; Immunology	516CT	WOS:000271520000008	19839980	
J	Taubel, M; Rintala, H; Pitkaranta, M; Paulin, L; Laitinen, S; Pekkanen, J; Hyvarinen, A; Nevalainen, A				Taubel, Martin; Rintala, Helena; Pitkaranta, Miia; Paulin, Lars; Laitinen, Sirpa; Pekkanen, Juha; Hyvarinen, Anne; Nevalainen, Aino			The occupant as a source of house dust bacteria	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Microbial markers; mattress dust; floor dust; indoor; microbial exposure; bacteria; sequencing; endotoxin; LPS; muramic acid	ENDOTOXIN EXPOSURE; SCHOOL-CHILDREN; FARM CHILDREN; BIRTH COHORT; DIVERSITY; CULTURE; RISK; DETERMINANTS; ENVIRONMENT; COMPONENTS	Background: Markers for microbial groups are commonly measured in house dust samples to assess indoor exposure to microbes in studies on asthma and allergy. However, little is known about the sources of different microbes. A better understanding of the nature and origin of microbes present in the immediate environment of human beings is crucial if one wants to elucidate protective as well as adverse effects on human health. Objective: To determine the extent to which the bacterial composition of mattress and floor dust reflects the presence of the human body in relation to other environmental sources. Methods: House dust and skin surface swab samples of occupants in 4 homes were collected and analyzed for their bacterial content, using a culture-independent methodology. Bacterial sequences analyzed from the different house dusts and skin surface swabs represented random samples of bacteria present in a given sample. Highly similar sequences were grouped to assess biodiversity and to draw conclusions about the sources of bacteria. Results: The bacterial flora in the house dust samples was found to be highly diverse and dominated by gram-positive bacteria. To a considerable extent, the presence of different bacterial groups was attributed to human sources. In the individuals' mattress dust samples, 69% to 88% of the bacterial sequences analyzed were associated with human origins. The respective percentages for the individual floor dusts ranged from 45% to 55%. Conclusion: Our study indicates that human-derived bacteria account for a large part of the mainly gram-positive bacterial content in house dust. (J Allergy Clin Immunol 2009;124:834-40.)	[Taubel, Martin; Rintala, Helena; Pekkanen, Juha; Hyvarinen, Anne; Nevalainen, Aino] Natl Inst Hlth & Welf, Dept Environm Hlth, FIN-70701 Kuopio, Finland; [Pitkaranta, Miia; Paulin, Lars] Univ Helsinki, Inst Biotechnol, FIN-00014 Helsinki, Finland; [Laitinen, Sirpa] Finnish Inst Occupat Hlth, Kuopio, Finland; [Pekkanen, Juha] Univ Kuopio, Sch Publ Hlth & Clin Nutr, FIN-70211 Kuopio, Finland	Taubel, M (reprint author), Natl Inst Hlth & Welf, Dept Environm Hlth, POB 95, FIN-70701 Kuopio, Finland.	martin.taubel@thl.fi			Academy of Finland [106103, 111177]	Supported by the Academy of Finland with grant nos. 106103 and 111177.	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Allergy Clin. Immunol.	OCT	2009	124	4					834	840		10.1016/j.jaci.2009.07.045		7	Allergy; Immunology	Allergy; Immunology	506UV	WOS:000270802800031	19767077	
J	Inomata, N				Inomata, Naoko			Wheat allergy	CURRENT OPINION IN ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						allergen; exercise-induced anaphylaxis; food-dependent; gliadin; IgE; wheat allergy	EXERCISE-INDUCED ANAPHYLAXIS; CONTROLLED FOOD CHALLENGE; OMEGA-5 GLIADIN; IGE-ANTIBODIES; ATOPIC-DERMATITIS; MAJOR ALLERGEN; 4-YEAR-OLD CHILDREN; PROTEOMIC ANALYSIS; CEREAL-GRAINS; DOUBLE-BLIND	Purpose of review This review describes the diverse clinical manifestations of IgE-mediated allergy to ingested wheat and summarizes recent advances in characterization of clinically significant allergens and diagnostic workup. Recent findings Recent population-based studies have shown the prevalence of wheat allergy and sensitization more precisely than past studies among small populations and in hospital settings. Intensive research has demonstrated the diverse profile of both water/salt-soluble and insoluble allergens involved in clinical types of wheat allergies determined depending on the patient age, the sensitization route, and the protein state during the exposure. Consequently, some new allergens, including nonspecific lipid transfer protein (Tri a 14), have been identified. For diagnosis, the role of water/salt-insoluble gliadins, particularly omega-5 gliadin, a major allergen of wheat-dependent, exercise-induced anaphylaxis, was assessed as compared with the results of oral challenges. The mechanisms of eliciting anaphylactic symptoms by exercise in wheat-de pendent, exercise-induced anaphylaxis were speculated upon; one is the allergenicity strengthened by activated tissue transglutaminase and another is the increased absorption of allergens through the gastrointestinal tract. Summary Findings of the recent studies show potential for more precise diagnosis in each clinical type of wheat allergies.	Yokohama City Univ Med, Dept Dermatol, Kanazawa Ku, Yokohama, Kanagawa 2360004, Japan	Inomata, N (reprint author), Yokohama City Univ Med, Dept Dermatol, Kanazawa Ku, 3-9 Fukuura, Yokohama, Kanagawa 2360004, Japan.	ninomata@med.yokohama-cu.ac.jp					Agostoni C, 2008, J PEDIATR GASTR NUTR, V46, P99; Akagawa M, 2007, J AGR FOOD CHEM, V55, P6863, DOI 10.1021/jf070843a; Battais F, 2005, ALLERGY, V60, P815, DOI 10.1111/j.1398-9995.2005.00795.x; Benhamou AH, 2007, ALLERGY, V62, P1471, DOI 10.1111/j.1398-9995.2007.01484.x; Beyer K, 2008, J ALLERGY CLIN IMMUN, V122, P419, DOI 10.1016/j.jaci.2008.06.006; Bodinier M, 2008, INT ARCH ALLERGY IMM, V146, P307, DOI 10.1159/000121465; Chiang WC, 2007, CLIN EXP ALLERGY, V37, P1055, DOI 10.1111/j.1365-2222.2007.02752.x; Crespo JF, 2003, ALLERGY, V58, P98, DOI 10.1034/j.1398-9995.2003.02170.x; Du Toit G, 2007, PEDIATR ALLERGY IMMU, V18, P455, DOI 10.1111/j.1399-3038.2007.00599.x; Harada S, 2001, BRIT J DERMATOL, V145, P336, DOI 10.1046/j.1365-2133.2001.04329.x; Imamura T, 2008, PEDIATR ALLERGY IMMU, V19, P270, DOI 10.1111/j.1399-3038.2007.00621.x; Ito K, 2008, ALLERGY, V63, P1536, DOI 10.1111/j.1398-9995.2008.01753.x; Jacquenet S, 2008, INT ARCH ALLERGY IMM, V149, P74; James JM, 1997, J ALLERGY CLIN IMMUN, V99, P239, DOI 10.1016/S0091-6749(97)70103-9; Johansson S. 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Opin. Allergy Clin. Immunol.	JUN	2009	9	3					238	243		10.1097/ACI.0b013e32832aa5bc		6	Allergy; Immunology	Allergy; Immunology	452YU	WOS:000266577900010	19318930	
J	Marenholz, I; Kerscher, T; Bauerfeind, A; Esparza-Gordillo, J; Nickel, R; Keil, T; Lau, S; Rohde, K; Wahn, U; Lee, YA				Marenholz, Ingo; Kerscher, Tamara; Bauerfeind, Anja; Esparza-Gordillo, Jorge; Nickel, Renate; Keil, Thomas; Lau, Susanne; Rohde, Klaus; Wahn, Ulrich; Lee, Young-Ae			An interaction between filaggrin mutations and early food sensitization improves the prediction of childhood asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Genetic prediction; interaction; asthma; eczema; food sensitization; filaggrin; mutations; subphenotype; prevention; pulmonary function	1ST 6 YEARS; ATOPIC-DERMATITIS; ALLERGIC RHINITIS; NATURAL COURSE; DUST-MITE; FOLLOW-UP; RISK; LIFE; DISEASE; COHORT	Background: Asthma prediction in early infancy is essential for the development of new preventive strategies. Loss-of-function mutations in the filaggrin gene (FLG) were identified as risk factors for eczema and associated asthma. Objective: We evaluated the utility of the FLG mutations for the prediction of asthma. Methods: Eight hundred seventy-one individuals of the prospective German Multicenter Allergy Study cohort were genotyped for 3 FLG mutations. Information on asthma, eczema, and food sensitization was available from birth to 13 years of age. Pulmonary function was measured from 7 to 13 years of age. The predictive value of the FLG mutations and of atopic phenotypes in infancy was assessed for asthma. Results: In infants with eczema and sensitization to food allergens, the FLG mutations predicted childhood asthma with a positive predictive value of 100% (95% CI, 65.5% to 100%). This subgroup was characterized by a significant decrease in pulmonary function until puberty and represented 8.1% of all asthmatic children and 19.1% of patients with asthma after infantile eczema. We found a strong synergistic interaction between the FLG-null alleles and early food sensitization in the disease transition from eczema to asthma (relative excess risk due to interaction, 2.64; 95% CI, 1.70-3.98; P = .00040). Conclusion: FLG mutations and food sensitization represent 2 distinct mechanisms interacting in the pathogenesis of asthma. In infants with eczema and food sensitization, genotyping of the FLG mutations allows the prediction of asthma before the onset of symptoms. Our findings might facilitate the development of early subgroup-specific interventions to prevent the progression from eczema to asthma. (J Allergy Clin Immunol 2009;123:911-6.)	[Keil, Thomas; Lee, Young-Ae] Charite Univ Med Berlin, Inst Social Med Epidemiol & Hlth Econ, D-13353 Berlin, Germany; [Marenholz, Ingo; Kerscher, Tamara; Bauerfeind, Anja; Esparza-Gordillo, Jorge; Rohde, Klaus; Lee, Young-Ae] Max Delbruck Ctr Mol Med, Berlin, Germany	Lee, YA (reprint author), Charite Univ Med Berlin, Inst Social Med Epidemiol & Hlth Econ, D-13353 Berlin, Germany.	yolee@mdc-berlin.de	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	German Ministry for Education and Research through the Clinical Research Group for Allergy; German National Genome Research Network; European Union; Global Allergy and Asthma European Network	Supported by grants from the German Ministry for Education and Research through the Clinical Research Group for Allergy and the German National Genome Research Network, the European Union through a Marie-Curie fellowship to J.E.-G., and the Global Allergy and Asthma European Network.	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Allergy Clin. Immunol.	APR	2009	123	4					911	916		10.1016/j.jaci.2009.01.051		6	Allergy; Immunology	Allergy; Immunology	431JW	WOS:000265058600020	19348926	
J	Alm, B; Aberg, N; Erdes, L; Mollborg, P; Pettersson, R; Norvenius, SG; Goksor, E; Wennergren, G				Alm, B.; Aberg, N.; Erdes, L.; Mollborg, P.; Pettersson, R.; Norvenius, S. G.; Goksor, E.; Wennergren, G.			Early introduction of fish decreases the risk of eczema in infants	ARCHIVES OF DISEASE IN CHILDHOOD			English	Article							ATOPIC-DERMATITIS; BIRTH COHORT; 1ST YEAR; INTESTINAL MICROFLORA; ALLERGY DEVELOPMENT; PRESCHOOL-CHILDREN; CHILDHOOD ASTHMA; LIFE; SENSITIZATION; ASSOCIATION	Background: Atopic eczema in infants has increased in western societies. Environmental factors and the introduction of food may affect the risk of eczema. Aims: To investigate the prevalence of eczema among infants in western Sweden, describe patterns of food introduction and assess risk factors for eczema at 1 year of age. Methods: Data were obtained from a prospective, longitudinal cohort study of infants born in western Sweden in 2003; 8176 families were randomly selected and, 6 months after the infant's birth, were invited to participate and received questionnaires. A second questionnaire was sent out when the infants were 12 months old. Both questionnaires were completed and medical birth register data were obtained for 4921 infants (60.2% of the selected population). Results: At 1 year of age, 20.9% of the infants had previous or current eczema. Median age at onset was 4 months. In multivariable analysis, familial occurrence of eczema, especially in siblings (OR 1.87; 95% confidence interval (CI) 1.50 to 2.33) or the mother (OR 1.54; 95% CI 1.30 to 1.84), remained an independent risk factor. Introducing fish before 9 months of age (OR 0.76; 95% CI 0.62 to 0.94) and having a bird in the home (OR 0.35; 95% CI 0.17 to 0.75) were beneficial. Conclusions: One in five infants suffer from eczema during the first year of life. Familial eczema increased the risk, while early fish introduction and bird keeping decreased it. Breast feeding and time of milk and egg introduction did not affect the risk.	[Alm, B.; Aberg, N.; Norvenius, S. G.; Goksor, E.; Wennergren, G.] Univ Gothenburg, Dept Paediat, Queen Silvia Childrens Hosp, SE-41685 Gothenburg, Sweden; [Mollborg, P.] Uddevalla Cent Hosp, Cent Infant Welf Unit, Uddevalla, Sweden; [Erdes, L.] Skene Hosp, Paediat Outpatient Clin, Skene, Sweden; [Pettersson, R.] Skaraborg Hosp, Dept Paediat, Skovde, Sweden	Alm, B (reprint author), Univ Gothenburg, Dept Paediat, Queen Silvia Childrens Hosp, SE-41685 Gothenburg, Sweden.	bernt.alm@medfak.gu.se		Alm, Bernt/0000-0002-3557-2995	Sahlgrenska Academy at the University of Gothenburg; Research Foundation of the Swedish Asthma and Allergy Association; Swedish Foundation for Health Care Sciences and Allergy Research; Health & Medical Care Committee of the Region Vastra Gotaland	The study was supported by the Sahlgrenska Academy at the University of Gothenburg, the Research Foundation of the Swedish Asthma and Allergy Association, the Swedish Foundation for Health Care Sciences and Allergy Research, and the Health & Medical Care Committee of the Region Vastra Gotaland.	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J	Bhalla, DK; Hirata, F; Rishi, AK; Gairola, CG				Bhalla, Deepak K.; Hirata, Fusao; Rishi, Arun K.; Gairola, C. Gary			Cigarette Smoke, Inflammation, and Lung Injury: A Mechanistic Perspective	JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART B-CRITICAL REVIEWS			English	Review							NECROSIS-FACTOR-ALPHA; ENVIRONMENTAL TOBACCO-SMOKE; NF-KAPPA-B; INDUCED PULMONARY INFLAMMATION; BRONCHIAL EPITHELIAL-CELLS; CONNECTIVE-TISSUE BREAKDOWN; GROWTH-FACTOR-BETA; INTERCELLULAR-ADHESION MOLECULE-1; BRONCHOALVEOLAR LAVAGE FLUID; INHIBITS CYTOKINE PRODUCTION	Inflammation is a common feature in the pathogenesis of cigarette smoke-associated diseases. The recruitment of inflammatory cells into the lung following cigarette smoke exposure presents a risk of tissue damage through the release of toxic mediators, including proteolytic enzymes and reactive oxygen species. This review represents a toxicological approach to investigation of cigarette smoke-induced lung injury, with a focus on laboratory studies and an emphasis on inflammatory mechanisms. The studies discussed in this review analyze the role of inflammation and inflammatory mediators in the development of injury. In cases where information relating to cigarette smoke is limited, examples are taken from other models of lung injury applicable to cigarette smoke. The primary aim of the review is to summarize published work so as to permit (1) an evaluation of chronic lung injury and inflammatory responses in animal models, (2) a discussion of inflammatory mediators in the development of chronic injury, and (3) identification of immunological mechanisms of injury. These studies discuss the currently understood roles of cytokines, cell adhesion molecules, and oxidative stress in inflammatory reactions and lung injury. A role for lipocortin 1 (annexin 1), a naturally occurring defense factor against inflammation, is discussed because of the possibility that impaired synthesis and degradation of lipocortin 1 will influence immune responses in animals exposed to cigarette smoke either by augmenting T helper cell Th1 response or by shifting Th1 to Th2 response. While Th1 augmentation will increase the risk for development of emphysema, Th1 to Th2 shift will favor development of asthma.	[Bhalla, Deepak K.; Hirata, Fusao] Wayne State Univ, Dept Pharmaceut Sci, Eugene Applebaum Coll Pharm & Hlth Sci, Detroit, MI 48202 USA; [Rishi, Arun K.] Wayne State Univ, Dept Internal Med, Detroit, MI 48202 USA; [Rishi, Arun K.] Wayne State Univ, Karmanos Canc Inst, Detroit, MI 48202 USA; [Gairola, C. Gary] Univ Kentucky, Grad Ctr Toxicol, Lexington, KY USA	Bhalla, DK (reprint author), Wayne State Univ, Dept Pharmaceut Sci, Eugene Applebaum Coll Pharm & Hlth Sci, 259 Mack Ave, Detroit, MI 48202 USA.	ad6268@wayne.edu			Susan G. Komen Breast Cancer Foundation; V. A. Merit Award	Partly supported by a grant from the Susan G. Komen Breast Cancer Foundation (F. Hirata) and a V. A. Merit Award (A.K.Rishi).	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Wright JL, 2004, AM J RESP CELL MOL, V31, P501, DOI 10.1165/rcmb.2004-0051OC; Yamashiro S, 2000, BLOOD, V96, P3958; Yang SR, 2008, AM J RESP CELL MOL, V38, P689, DOI 10.1165/rcmb.2007-0379OC; Yang SR, 2006, AM J PHYSIOL-LUNG C, V291, pL46, DOI 10.1152/ajplung.00241.2005; Yu M, 2002, TOXICOL SCI, V65, P99, DOI 10.1093/toxsci/65.1.99; Zhu Z, 2002, J IMMUNOL, V168, P2953; Zhu Zhou, 1999, Journal of Clinical Investigation, V103, P779, DOI 10.1172/JCI5909; ZUANYAMORIM C, 1995, J CLIN INVEST, V95, P2644, DOI 10.1172/JCI117966	207	71	74	0	15	TAYLOR & FRANCIS INC	PHILADELPHIA	325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA	1093-7404	1521-6950		J TOXICOL ENV HEAL B	J. Toxicol. Env. Health-Pt b-Crit. Rev.		2009	12	1					45	64	PII 907306217	10.1080/10937400802545094		20	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	389ZF	WOS:000262133400003	19117209	
J	Sackesen, C; Ercan, H; Dizdar, E; Soyer, O; Gumus, P; Tosun, BN; Buyuktuncer, Z; Karabulut, E; Besler, T; Kalayci, O				Sackesen, Cansin; Ercan, Hulya; Dizdar, Evrim; Soyer, Ozge; Gumus, Pinar; Tosun, Berat Nursal; Bueyuektuncer, Zebra; Karabulut, Erdem; Besler, Tanju; Kalayci, Omer			A comprehensive evaluation of the enzymatic and nonenzymatic antioxidant systems in childhood asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						amino acid; antioxidant; ascorbic acid; asthma; glutathione; glutathione peroxidase; lycopene; malondialdehyde; oxidative stress; superoxide dismutase; alpha-tocopherol; beta-carotene	EXTRACELLULAR-SUPEROXIDE-DISMUTASE; OXIDATIVE STRESS; AMINO-ACIDS; PROTEIN OXIDATION; CYSTEINE KINETICS; PLASMA LYCOPENE; FREE-RADICALS; GLUTATHIONE; CHILDREN; SERUM	Background: Even though there is ample evidence on the oxidative stress in asthma, there is limited information on the antioxidant defense systems. Objectives: To conduct a comprehensive evaluation of various components of both enzymatic and nonenzymatic antioxidants in a large group of children with asthma. Methods: A total of 164 children with mild asthma and 173 healthy children were included in the study. Levels of the enzymes glutathione peroxidase and superoxide dismutase were measured by using ELISA, whereas reduced glutathione, ascorbic acid, alpha-tocopherol, lycopene, beta-carotene, amino acids participating in glutathione synthesis, and amino acids susceptible to oxidation were measured by HPLC. All comparisons were adjusted for atopy, body mass index, smoke exposure, and pet ownership. Results: Levels of the enzymes glutathione peroxidase and superoxide dismutase and of the nonenzymatic components of the antioxidant system including reduced glutathione, ascorbic acid, alpha-tocopherol, lycopene, and beta-carotene were significantly lower in children with asthma compared with healthy controls (P <.001 for each). Of the amino acids contributing to glutathione synthesis, glycine and glutamine were significantly lower in children with asthma (P <.001). The majority of the amino acid susceptible to oxidative stress displayed lower levels in children with asthma (P <.05). Conclusion: Childhood asthma is associated with significant decreases in various components of both enzymatic and nonenzymatic antioxidant defenses.	[Karabulut, Erdem] Hacettepe Univ, Sch Med, Dept Biostat, TR-06100 Ankara, Turkey; [Sackesen, Cansin; Ercan, Hulya; Dizdar, Evrim; Soyer, Ozge; Gumus, Pinar; Kalayci, Omer] Hacettepe Univ, Sch Med, Pediat Allergy & Asthma Unit, TR-06100 Ankara, Turkey; [Tosun, Berat Nursal; Bueyuektuncer, Zebra; Besler, Tanju] Hacettepe Univ, Sch Hlth Technol, Dept Nutr & Dietet, TR-06100 Ankara, Turkey	Sackesen, C (reprint author), Hacettepe Univ, Sch Med, Pediat Allergy & Asthma Unit, TR-06100 Ankara, Turkey.	csackesen@yahoo.com	Karabulut, Erdem/E-9242-2013; BESLER, HALIT TANJU/I-9965-2013	BESLER, HALIT TANJU/0000-0002-6523-7995			Andreadis AA, 2003, FREE RADICAL BIO MED, V35, P213, DOI 10.1016/S0891-5849(03)00278-8; ARNAUD J, 1991, J CHROMATOGR-BIOMED, V572, P103, DOI 10.1016/0378-4347(91)80476-S; Atmaca G, 2004, YONSEI MED J, V45, P776; BAKER MA, 1990, ANAL BIOCHEM, V190, P360, DOI 10.1016/0003-2697(90)90208-Q; BARNES PJ, 1990, FREE RADICAL BIO MED, V9, P235, DOI 10.1016/0891-5849(90)90034-G; Berlett BS, 1997, J BIOL CHEM, V272, P20313, DOI 10.1074/jbc.272.33.20313; Besler HT, 2003, NUTR NEUROSCI, V6, P189, DOI 10.1080/1028415031000115945; CANTIN AM, 1987, J APPL PHYSIOL, V63, P152; CEBALLOSPICOT I, 1992, CLIN CHEM, V38, P66; COMMITTEE IS, 1998, PHASE 2 MODULES INT, P11; Deneke S.M., 1989, AM J PHYSIOL, V257, P163; Ercan H, 2006, J ALLERGY CLIN IMMUN, V118, P1097, DOI 10.1016/j.jaci.2006.08.012; Fang YZ, 2002, NUTRITION, V18, P872, DOI 10.1016/S0899-9007(02)00916-4; Fogarty A, 2004, EUR RESPIR J, V23, P565, DOI 10.1183/09031936.04.00090404; Folz RJ, 1999, J CLIN INVEST, V103, P1055, DOI 10.1172/JCI3816; Ford ES, 2004, J ASTHMA, V41, P179, DOI 10.1081/JAS-120026075; Fukagawa NK, 1996, AM J PHYSIOL-ENDOC M, V270, pE209; HALLIWELL B, 1988, HUM TOXICOL, V7, P7; Harik-Khan RI, 2004, AM J EPIDEMIOL, V159, P351, DOI 10.1093/aje/kwh053; Heber D, 2002, EXP BIOL MED, V227, P920; HIRAMATSU T, 1994, AM J CLIN NUTR, V60, P525; JONES DP, 2000, DETOXIFICATION PROTE; Kalayci O, 2006, ALLERGY, V61, P97, DOI 10.1111/j.1398-9995.2006.00979.x; Kim YG, 2003, LIFE SCI, V72, P1171, DOI 10.1016/S0024-3205(02)02366-4; KINNULA VL, 1995, LAB INVEST, V73, P3; Levine RL, 2001, EXP GERONTOL, V36, P1495, DOI 10.1016/S0531-5565(01)00135-8; Maier CM, 2002, NEUROSCIENTIST, V8, P323; MARKLUND SL, 1984, J CLIN INVEST, V74, P1398, DOI 10.1172/JCI111550; MEISTER A, 1983, ANNU REV BIOCHEM, V52, P711, DOI 10.1146/annurev.bi.52.070183.003431; Misso NLA, 2005, EUR RESPIR J, V26, P257, DOI 10.1183/09031936.05.00006705; Mizuno Y, 2006, PEDIATR INT, V48, P261, DOI 10.1111/j.1442-200X.2006.02200.x; Nadeem A, 2003, J ALLERGY CLIN IMMUN, V111, P72, DOI 10.1067/mai.2003.17; OBLED C, 2004, SULFUR CONTAINING AM; OWEN S, 1991, NEW ENGL J MED, V325, P586; Park EM, 1998, FREE RADICAL BIO MED, V25, P79, DOI 10.1016/S0891-5849(98)00041-0; Rahman I, 2000, EUR RESPIR J, V16, P534, DOI 10.1034/j.1399-3003.2000.016003534.x; Rahman I, 2006, EUR J PHARMACOL, V533, P222, DOI 10.1016/j.ejphar.2005.12.087; Rahman I, 1999, AM J PHYSIOL, V277, P1067; Riccioni G, 2007, J ASTHMA, V44, P429, DOI 10.1080/02770900701421880; Riccioni G, 2006, ALLERGY, V61, P1371, DOI 10.1111/j.1398-9995.2006.01100.x; Rubin RN, 2004, AM J RESP CRIT CARE, V169, P393, DOI 10.1164/rccm.200301-055OC; Sackesen C, 2005, ALLERGY, V60, P1485, DOI 10.1111/j.1398-9995.2005.00874.x; Saraclar Y, 2003, ANN ALLERG ASTHMA IM, V91, P477; Stadtman ER, 2006, FREE RADICAL RES, V40, P1250, DOI 10.1080/10715760600918142; Stadtman ER, 2003, AMINO ACIDS, V25, P207, DOI 10.1007/s00726-003-0011-2; STIPANUK MH, 1992, J NUTR, V122, P420; van der Vliet A, 1999, AM J PHYSIOL-LUNG C, V276, pL289; Wood LG, 2005, J AM COLL NUTR, V24, P448; Yilmaz T, 2004, OTOLARYNG HEAD NECK, V131, P797, DOI 10.1016/j.otohns.2004.07.001; Yilmaz T, 2004, INT J PEDIATR OTORHI, V68, P1053, DOI 10.1016/j.ijporl.2004.04.003	50	71	72	0	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.	JUL	2008	122	1					78	85		10.1016/j.jaci.2008.03.035		8	Allergy; Immunology	Allergy; Immunology	325RD	WOS:000257605100013	18485467	
J	Bell, ML; Levy, JK; Lin, Z				Bell, M. L.; Levy, J. K.; Lin, Z.			The effect of sandstorms and air pollution on cause-specific hospital admissions in Taipei, Taiwan	OCCUPATIONAL AND ENVIRONMENTAL MEDICINE			English	Article							DUST STORM EVENTS; DAILY STROKE ADMISSIONS; LONG-RANGE TRANSPORT; DAILY MORTALITY; CARDIOVASCULAR-DISEASE; AMBIENT AIR; PARTICLES; QUALITY; PARTICULATE; KAOHSIUNG	Objective: Relatively little research exists focusing on the impact of air pollution on hospital admissions in Asia compared to the extensive work conducted in the USA and Europe. The issue is of particular importance because of the frequency, intensity and health effects of Asian sandstorms. This work investigates the relation between cause-specific hospital admissions and sandstorms and air pollution in Taipei, Taiwan's capital. Methods: Time-series analyses of asthma, pneumonia, ischaemic heart disease and cerebrovascular disease hospital admissions were performed for Taipei. An eight-year time period (1995-2002) was considered for various indicators of sandstorms and the pollutants NO2, CO, ozone, SO2, PM10, and PM2.5. Pollution effects based on single-day lags of 0, 1, 2 and 3 days were explored, along with the average of the same day and previous three days (L03). Results: The risk of ischaemic heart disease admissions was associated with several sandstorm metrics, including indicators of high PM10 levels in the Taipei area, indicators of high PM10 at a monitor designed to measure background pollution, the PM coarse fraction, and the ratio of PM10 to PM2.5. However, the lag structure of effect was not consistent across sandstorm indicators. Hospital admissions for this disease were 16-21% higher on sandstorm days compared to other days. This cause was also associated with transportation-related pollutants, NO2, CO and PM2.5. Asthma admissions rose 4.48% (95% CI 0.71% to 8.38%) per 28 mu g/m(3) increase in L03 PM10 levels and 7.60% (95% CI 2.87% to 12.54%) per 10 ppb increase in L03 ozone. Cerebrovascular disease admissions were associated with PM10 and CO, both at lag 3 days. SO2 exhibited no relation with admissions. Conclusions: Risk of hospital admissions in Taipei may be increased by air pollution and sandstorms. Additional research is needed to clarify the lag structure and magnitude of such effects.	[Bell, M. L.] Yale Univ, Sch Forestry & Environm Studies, New Haven, CT 06511 USA; [Levy, J. K.] Western Washington Univ, Dept Environm Studies, Bellingham, WA 98225 USA; [Lin, Z.] Chinese Acad Sci, Inst Atmospher Phys, Beijing, Peoples R China	Bell, ML (reprint author), Yale Univ, Sch Forestry & Environm Studies, 205 Prospect St, New Haven, CT 06511 USA.	michelle.bell@yale.edu					BELL ML, 2005, ENVIRON SCI POLICY, V85, P525; Bennett CM, 2006, SCI TOTAL ENVIRON, V366, P918, DOI 10.1016/j.scitotenv.2005.12.025; Brunekreef B, 2005, EUR RESPIR J, V26, P309, DOI 10.1183/09031936.05.00001805; Burnett RT, 1999, ARCH ENVIRON HEALTH, V54, P130; Chan CC, 2006, EUR HEART J, V27, P1238, DOI 10.1093/eurheartj/ehi835; Chang CC, 2006, J TOXICOL ENV HEAL A, V69, P229, DOI 10.1080/15287390500227415; Chang CC, 2005, ENVIRON RES, V98, P114, DOI 10.1016/j.envres.2004.07.005; Chang G.Q, 2003, CHINESE J SCH DOCTOR, V17, P295; Chang SC, 2007, ENVIRON MONIT ASSESS, V127, P87, DOI 10.1007/s10661-006-9262-1; Chen CH, 2006, J ASTHMA, V43, P287, DOI 10.1080/02770900600622935; Chen YS, 2005, J TOXICOL ENV HEAL A, V68, P1457, DOI 10.1080/15287390590967388; Chen YS, 2004, ENVIRON RES, V95, P151, DOI 10.1016/j.envres.2003.08.008; Cheng MT, 2005, CHEMOSPHERE, V61, P1439, DOI 10.1016/j.chemosphere.2005.04.120; Cheng TM, 2003, HEALTH AFFAIR, V22, P61, DOI 10.1377/hlthaff.22.3.61; Chou CCK, 2004, TERR ATMOS OCEAN SCI, V15, P881; Dominici F, 2006, JAMA-J AM MED ASSOC, V295, P1127, DOI 10.1001/jama.295.10.1127; Dong J W, 1996, Zhonghua Liu Xing Bing Xue Za Zhi, V17, P13; Fang GC, 2002, SCI TOTAL ENVIRON, V287, P141, DOI 10.1016/S0048-9697(01)00996-2; KALKSTEIN LS, 1986, B AM METEOROL SOC, V67, P842, DOI 10.1175/1520-0477(1986)067<0842:AEOSDI>2.0.CO;2; Kan HD, 2007, ENVIRON INT, V33, P376, DOI 10.1016/j.envint.2006.12.001; Kuo HW, 2002, ARCH ENVIRON HEALTH, V57, P194; Kwon HJ, 2002, ENVIRON RES, V90, P1, DOI 10.1006/enrs.2002.4377; Lee HC, 2004, TERR ATMOS OCEAN SCI, V15, P1035; Lin CY, 2005, ATMOS ENVIRON, V39, P6066, DOI 10.1016/j.atmosenv.2005.06.046; Park JW, 2005, RESPIROLOGY, V10, P470, DOI 10.1111/j.1440-1843.2005.00728.x; *TEPA, 2006, ENV PROT DAT TAIW; Tsai SS, 2006, INHAL TOXICOL, V18, P549, DOI 10.1080/0895837006866176; Tsai SS, 2003, STROKE, V34, P2612, DOI 10.1161/01.STR.0000095564.33543.64; Tzeng GH, 2002, J ENVIRON MANAGE, V65, P109, DOI 10.1006/jema.2001.0527; USEPA, 2004, AIR QUAL CRIT PART M; WHO, 2005, WHO AIR QUAL GUID GL; XIAO HP, 1990, CHINESE J PUBLIC HLT, V66, P195; Xie SD, 2005, SCI TOTAL ENVIRON, V345, P153, DOI 10.1016/j.scitotenv.2004.10.013; XU XP, 1995, ARCH ENVIRON HEALTH, V50, P214; XU XP, 1995, ENVIRON HEALTH PERSP, V103, P286; Yang CY, 2005, ENVIRON RES, V99, P79, DOI 10.1016/j.envres.2004.12.009; Yang CY, 2005, INHAL TOXICOL, V17, P817, DOI 10.1080/08958370500241254; Yang CY, 2004, J TOXICOL ENV HEAL A, V67, P483, DOI 10.1080/15287390490276502; Zhang RJ, 2003, POWDER TECHNOL, V137, P77, DOI 10.1016/j.powtec.2003.08.056; Zhou Y. R., 1997, J MOD PREV MED, V24, P43	40	71	77	3	20	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	1351-0711			OCCUP ENVIRON MED	Occup. Environ. Med.	FEB	2008	65	2					104	111		10.1136/oem.2006.031500		8	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	254QF	WOS:000252601700005	17626134	
J	Pijnenburg, MWH; De Jongste, JC				Pijnenburg, M. W. H.; De Jongste, J. C.			Exhaled nitric oxide in childhood asthma: a review	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review							PRIMARY CILIARY DYSKINESIA; BRONCHIOLITIS OBLITERANS SYNDROME; EXPERIMENTAL RHINOVIRUS INFECTION; RESPIRATORY SYNCYTIAL VIRUS; AIRWAY EPITHELIAL-CELLS; GRASS-POLLEN EXPOSURE; SCHOOL-AGE-CHILDREN; CYSTIC-FIBROSIS; LUNG-FUNCTION; HEALTHY-CHILDREN	As an 'inflammometer', the fraction of nitric oxide in exhaled air (FENO) is increasingly used in the management of paediatric asthma. FENO provides us with valuable, additional information regarding the nature of underlying airway inflammation, and complements lung function testing and measurement of airway hyper-reactivity. This review focuses on clinical applications of FENO in paediatric asthma. First, FENO provides us with a practical tool to aid in the diagnosis of asthma and distinguish patients who will benefit from inhaled corticosteroids from those who will not. Second, FENO is helpful in predicting exacerbations, and predicting successful steroid reduction or withdrawal. In atopic asthmatic children FENO is beneficial in adjusting steroid doses, discerning those patients who require additional therapy from those whose medication dose could feasibly be reduced. In pre-school children FENO may be of help in the differential diagnosis of respiratory symptoms, and may potentially allow for better targeting and monitoring of anti-inflammatory treatment.	[Pijnenburg, M. W. H.; De Jongste, J. 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Exp. Allergy	FEB	2008	38	2					246	259		10.1111/j.1365-2222.2007.02897.x		14	Allergy; Immunology	Allergy; Immunology	253CB	WOS:000252495200003	18076708	
J	Hernandez-Diaz, S; Van Marter, LJ; Werler, MM; Louik, C; Mitchell, AA				Hernandez-Diaz, Sonia; Van Marter, Linda J.; Werler, Martha M.; Louik, Carol; Mitchell, Allen A.			Risk factors for persistent pulmonary hypertension of the newborn	PEDIATRICS			English	Article						pulmonary hypertension; newborn; PPHN; epidemiology; race; BMI; Cesarean section	EXTRACORPOREAL MEMBRANE-OXYGENATION; NEONATAL RESPIRATORY MORBIDITY; ELECTIVE CESAREAN-SECTION; BIRTH-DEFECTS; NITRIC-OXIDE; DELIVERY; LABOR; PREGNANCY; TERM; EXPOSURE	Objective. Persistent pulmonary hypertension of the newborn, a clinical syndrome that results from the failure of the normal fetal-to-neonatal circulatory transition, is associated with substantial infant mortality and morbidity. We performed a case-control study to determine possible antenatal and perinatal predictors of persistent pulmonary hypertension of the newborn. Methods. Between 1998 and 2003, the Slone Epidemiology Center enrolled 377 mothers of infants with persistent pulmonary hypertension of the newborn and 836 mothers of matched control subjects. Within 6 months of delivery, study nurses interviewed participants regarding demographic, medical, and obstetric characteristics. Results. Factors that were independently associated with an elevated risk for persistent pulmonary hypertension of the newborn were infant male gender and black or Asian maternal race compared with white race. High prepregnancy BMI (> 27 vs < 20) was also associated with persistent pulmonary hypertension of the newborn, as were diabetes and asthma. Compared with infants who were delivered vaginally, the risk for persistent pulmonary hypertension of the newborn was higher for those who were born by cesarean section. Compared with infants who were born within 37 to 41 gestational weeks, the risk was higher for those who were born between 34 and 37 completed weeks and for those born beyond 41 weeks. Compared with infants within the 10th and 90th percentiles of birth weight for gestational age distribution, the risk was higher for infants above the 90th percentile. Conclusions. Our findings suggest an increased risk for persistent pulmonary hypertension of the newborn associated with cesarean delivery; late preterm or postterm birth; being large for gestational age; and maternal black or Asian race, overweight, diabetes, and asthma. It remains unclear whether some of these factors are direct causes of persistent pulmonary hypertension of the newborn or simply share common causes with it; however, clinicians should be alert to the increased need for monitoring and intervention among pregnancies with these risk factors.	Boston Univ, Slone Epidemiol Ctr, Boston, MA 02215 USA; Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA; Harvard Univ, Sch Med, Childrens Hosp, Div Newborn Med, Boston, MA 02115 USA; Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Newborn Med, Boston, MA 02115 USA	Mitchell, AA (reprint author), Boston Univ, Slone Epidemiol Ctr, 1010 Commonwealth Ave, Boston, MA 02215 USA.	amitchell@slone.bu.edu		Louik, Carol/0000-0001-5429-5084; Werler, Martha/0000-0003-3392-6814; Mitchell, Allen/0000-0003-0950-6799	NHLBI NIH HHS [HL50763]		Abman S H, 1999, Pediatr Pulmonol Suppl, V18, P201; Anderson JL, 2005, EPIDEMIOLOGY, V16, P87, DOI 10.1097/01.ede.0000147122.97061.bb; Bearer C, 1997, ENVIRON HEALTH PERSP, V105, P202; BROWN MJ, 1983, J PHYSIOL-LONDON, V344, P137; Clark Reese H, 2003, J Perinatol, V23, P300, DOI 10.1038/sj.jp.7210908; Clark RH, 2000, NEW ENGL J MED, V342, P469, DOI 10.1056/NEJM200002173420704; Dakshinamurti S, 2005, PEDIATR PULM, V39, P492, DOI 10.1002/ppul.20201; Farrow KN, 2005, SEMIN PERINATOL, V29, P8, DOI 10.1053/j.sempert.2005.02.003; Fricker J, 1996, LANCET, V347, P1397, DOI 10.1016/S0140-6736(96)91029-6; GERSONY WM, 1969, CIRCULATION S3, V39, P87; GLASS P, 1995, J PEDIATR-US, V127, P447, DOI 10.1016/S0022-3476(95)70082-X; GOLDBERG SJ, 1971, PEDIATRICS, V48, P528; HAGEMAN JR, 1984, AM J DIS CHILD, V138, P592; HALES KA, 1993, INT J GYNECOL OBSTET, V43, P35, DOI 10.1016/0020-7292(93)90271-W; HERITAGE CK, 1985, AM J OBSTET GYNECOL, V152, P627; Hernan MA, 2002, AM J EPIDEMIOL, V155, P176, DOI 10.1093/aje/155.2.176; Hook B, 1997, PEDIATRICS, V100, P348, DOI 10.1542/peds.100.3.348; Jaillard S, 2003, J PERINAT MED, V31, P538, DOI 10.1515/JPM.2003.084; KESZLER M, 1992, PEDIATRICS, V89, P670; Levine EM, 2001, OBSTET GYNECOL, V97, P439, DOI 10.1016/S0029-7844(00)01150-9; McMahon MJ, 1996, NEW ENGL J MED, V335, P689, DOI 10.1056/NEJM199609053351001; MITCHELL AA, 1981, JAMA-J AM MED ASSOC, V245, P2311; MITCHELL AA, 1986, AM J EPIDEMIOL, V123, P670; MORRISON JJ, 1995, BRIT J OBSTET GYNAEC, V102, P101, DOI 10.1111/j.1471-0528.1995.tb09060.x; REECE EA, 1987, OBSTET GYNECOL, V70, P696; Ros HS, 1998, AM J EPIDEMIOL, V147, P1062; Sorof JM, 2003, PEDIATRICS, V111, P61, DOI 10.1542/peds.111.1.61; van den Berg A, 2001, EUR J OBSTET GYN R B, V98, P9, DOI 10.1016/S0301-2115(01)00292-5; VanMarter LJ, 1996, PEDIATRICS, V97, P658; Visser M, 1999, JAMA-J AM MED ASSOC, V282, P2131, DOI 10.1001/jama.282.22.2131; Walsh-Sukys MC, 2000, PEDIATRICS, V105, P14, DOI 10.1542/peds.105.1.14; WALSHSUKYS MC, 1993, CLIN PERINATOL, V20, P127; WHITE E, 1985, AM J EPIDEMIOL, V121, P651	33	71	76	0	5	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	AUG	2007	120	2					E272	E282		10.1542/peds.2006-3037		11	Pediatrics	Pediatrics	196SY	WOS:000248503500049	17671038	
J	Bourdin, A; Neveu, D; Vachier, I; Paganin, F; Godard, P; Chanez, P				Bourdin, Arnaud; Neveu, Dorine; Vachier, Isabelle; Paganin, Fabrice; Godard, Philippe; Chanez, Pascal			Specificity of basement membrane thickening in severe asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; COPD; remodeling; basement membrane; ROC	AIR-FLOW OBSTRUCTION; SUBEPITHELIAL FIBROSIS; COLLAGEN DEPOSITION; BRONCHIAL-ASTHMA; WALL THICKNESS; LUNG-FUNCTION; EXPRESSION; MATRIX-METALLOPROTEINASE-9; INFLAMMATION; TRANSITION	Background: Reticular basement membrane (RBM) thickness is considered a hallmark for airway remodeling in airway diseases such as asthma. It is still unclear whether this measurement could be associated with disease severity or apply to chronic obstructive pulmonary disease (COPD). A wide range of results, at baseline or after therapeutic intervention, have been reported using different measurement methods. Objective: To determine whether increased RBM thickness could be associated specifically with severe asthma and in COPD in large samples. Methods: We blindly measured RBM thickness in endobronchial biopsies from 50 patients with severe asthma (mean age, 53 years; FEV1 66% predicted, inhaled steroids >= 1500 mu g and 20 mg daily dose of oral corticosteroids, lifelong nonsmokers), 50 untreated patients with mild asthma mean age, 33 years; FEV, 93%pred, lifelong nonsmokers), 50 patients with COPD (mean age, 57 years; FEV1 53%pred, all current smokers), and 18 control subjects using 2 different validated quantitative and computer-assisted methods (repeated multiple point-to-point vs area by length ratio). Results: Reticular basement membrane thickness was higher in severe asthma compared with mild asthma and COPD (P =.0053). On the basis of receiver operating characteristic curves, RBM thickness was effective in differentiating severe asthma from other groups (sensitivity and specificity, 98% and 95%, respectively, above a threshold of 5 mu m vs control, 70% and 75% at 7 mu m vs mild, 83% and 68% at 6 mu m vs COPD). Conclusion: Increased RBM thickness was specifically associated with severe asthma, whereas surprisingly, COPD and mild asthma had similar remodeling features. Clinical implications: Reticular basement membrane thickness can be considered a hallmark of severe asthma.	CHU Montpellier, Hop Arnaud De Villeneuve, Serv Malad Resp, Montpellier, France; CHU Montpellier, Hop Arnaud De Villeneuve, Dept Med Informat, Montpellier, France	Chanez, P (reprint author), Hop Arnaud De Villeneuve, F-34295 Montpellier 5, France.	chanez@montp.inserm.fr		Vachier, Isabelle/0000-0003-2730-5165			American Thoracic Society, 2000, AM J RESP CRIT CARE, V162, P2341, DOI DOI 10.1164/AJRCCM.162.6.ATS9-00; Bel EH, 2004, CURR OPIN PULM MED, V10, P44, DOI 10.1097/00063198-200401000-00008; Benayoun L, 2003, AM J RESP CRIT CARE, V167, P1360, DOI 10.1164/rccm.200209-1030OC; BLAND JM, 1986, LANCET, V1, P307; BOULET LP, 1995, AM J RESP CRIT CARE, V152, P865; BREWSTER CEP, 1990, AM J RESP CELL MOL, V3, P507; Chetta A, 2003, AM J RESP CRIT CARE, V167, P751, DOI 10.1164/rccm.200207.710OC; Chu HW, 1998, AM J RESP CRIT CARE, V158, P1936; Corsico A, 2003, J APPL PHYSIOL, V95, P441, DOI 10.1152/japplphysiol.01018.2002; Deykin A, 2002, AM J RESP CRIT CARE, V165, P1597, DOI 10.1164/rccm.2201081; Elston WJ, 2004, EUR RESPIR J, V24, P375, DOI 10.1183/09031936.04.00063003; Fabbri LM, 2003, AM J RESP CRIT CARE, V167, P418, DOI 10.1164/rccm.200203-183OC; Ferrando RE, 2003, J ALLERGY CLIN IMMUN, V112, P1243, DOI 10.1016/j.jaci.2003.09.038; Fouty B, 2006, EUR RESPIR J, V27, P1160, DOI 10.1183/09031936.06.00078605; HANLEY JA, 1982, RADIOLOGY, V143, P29; Hoshino M, 1999, J ALLERGY CLIN IMMUN, V104, P356, DOI 10.1016/S0091-6749(99)70379-9; Hoshino M, 1998, J ALLERGY CLIN IMMUN, V102, P783, DOI 10.1016/S0091-6749(98)70018-1; James AL, 2002, AM J RESP CRIT CARE, V166, P1590, DOI 10.1164/rccm.2108069; Jeffery P, 2003, AM J RESP CRIT CARE, V168, pS1, DOI 10.1164/rccm.200202-150WS; Jeffery Peter K, 2004, Proc Am Thorac Soc, V1, P176, DOI 10.1513/pats.200402-009MS; KIDA K, 1983, AM REV RESPIR DIS, V128, P125; Little SA, 2002, THORAX, V57, P247, DOI 10.1136/thorax.57.3.247; Milanese M, 2001, J APPL PHYSIOL, V91, P1035; Minshall EM, 1997, AM J RESP CELL MOL, V17, P326; *NIH, 2001, NHLBI WHO WORKSH BET; *NIH, 2002, NHLBI WHO WORKSH BET; ROCHE WR, 1989, LANCET, V1, P520; Saglani S, 2006, EUR RESPIR J, V28, P505, DOI 10.1183/09031936.06.00056405; Sont JK, 1999, AM J RESP CRIT CARE, V159, P1043; Sullivan P, 1998, EUR RESPIR J, V12, P811, DOI 10.1183/09031936.98.12040811; Ward C, 2005, J HEART LUNG TRANSPL, V24, P533, DOI 10.1016/j.healun.2004.02.018; Wilson JW, 1997, CLIN EXP ALLERGY, V27, P363; YOUDEN WJ, 1950, CANCER, V3, P32, DOI 10.1002/1097-0142(1950)3:1<32::AID-CNCR2820030106>3.0.CO;2-3	33	71	76	0	0	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUN	2007	119	6					1367	1374		10.1016/j.jaci.2007.01.055		8	Allergy; Immunology	Allergy; Immunology	178PO	WOS:000247232800011	17481707	
J	Locke, NR; Royce, SG; Wainewright, JS; Samuel, CS; Tang, ML				Locke, Natasha R.; Royce, Simon G.; Wainewright, Jacquetta S.; Samuel, Chrishan S.; Tang, Mimi L.			Comparison of airway remodeling in acute, subacute, and chronic models of allergic airways disease	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article						asthma; fibrosis; inflammation; mice	MURINE MODEL; MOUSE MODEL; EXPERIMENTAL ASTHMA; CHILDHOOD ASTHMA; BRONCHIAL-ASTHMA; ATOPIC ASTHMA; ANIMAL-MODELS; INFLAMMATION; FIBROSIS; EXPRESSION	The relationship between airway inflammation and structural changes of airway remodeling, and their relative effects on airway function, are poorly understood. Remodeling is thought to result from chronic repetitive injury to the airway wall caused by airway inflammation; however, the mechanisms regulating remodeling changes have not been clearly defined. We examined the sequence of events in remodeling using three commonly used mouse models of allergic airways disease in which mice are exposed to nebulized ovalbumin for four consecutive days (acute), seven consecutive days (subacute), or three times a week for 6 wk (chronic). Surprisingly, we found that a very short period of exposure to ovalbumin was sufficient to elicit early changes of remodeling. Goblet cell hyperplasia and epithelial thickening were evident after just 4 d. In chronically challenged mice, these changes persisted and, in addition, subepithelial Collagen deposition was significantly increased. This Collagen deposition was associated with a failure to upregulate matrix metalloproteinase (MIMP)-2, in conjunction with increased transforming growth factor-beta and MMP-9 expression. The relationship between inflammation, remodeling changes, and airway hyperresponsiveness (AHR) were examined. The acute and subacute models exhibited marked airway inflammation, whereas the chronic model had very modest inflammation. Conversely, airway fibrosis was only evident in the chronic model. AHR was present in all three models; however, it was significantly higher in the chronic model compared with the acute (P < 0.05) and subacute (P < 0.05) models. These data demonstrate that both airway inflammation and airway fibrosis may contribute to AHR, with airway fibrosis leading to the greatest increases in AHR.	Royal Childrens Hosp, Dept Allergy & Immunol, Murdoch Childrens Res Inst, Parkville, Vic 3052, Australia; Univ Melbourne, Howard Florey Inst Expt Physiol & Med, Parkville, Vic 3052, Australia	Tang, ML (reprint author), Royal Childrens Hosp, Dept Allergy & Immunol, Murdoch Childrens Res Inst, Flemington Rd, Parkville, Vic 3052, Australia.	mimi.tang@rch.org.au					Barbato A, 2003, AM J RESP CRIT CARE, V168, P798, DOI 10.1164/rccm.200305-650OC; Blyth DI, 1998, AM J RESP CELL MOL, V19, P38; Blyth DI, 1996, AM J RESP CELL MOL, V14, P425; Chetta A, 1997, CHEST, V111, P852, DOI 10.1378/chest.111.4.852; Chiappara G, 2001, Curr Opin Allergy Clin Immunol, V1, P85, DOI 10.1097/00130832-200102000-00015; Cockcroft DW, 2006, J ALLERGY CLIN IMMUN, V118, P551, DOI 10.1016/j.jaci.2006.07.012; Davies DE, 2003, J ALLERGY CLIN IMMUN, V111, P215, DOI 10.1067/mai.2003.128; Epstein MM, 2004, INT ARCH ALLERGY IMM, V133, P84, DOI 10.1159/000076131; Fahy JV, 2001, AM J RESP CRIT CARE, V164, pS46; Foster PS, 2000, LAB INVEST, V80, P655; Foster PS, 1996, J EXP MED, V183, P195, DOI 10.1084/jem.183.1.195; GALLOP PM, 1975, PHYSIOL REV, V55, P418; Holgate ST, 2000, J ALLERGY CLIN IMMUN, V105, P193, DOI 10.1016/S0091-6749(00)90066-6; JAMES AL, 1989, AM REV RESPIR DIS, V139, P242; Kenyon NJ, 2003, TOXICOL APPL PHARM, V186, P90, DOI 10.1016/S0041-008X(02)00025-X; Keramidaris E, 2001, J ALLERGY CLIN IMMUN, V107, P734, DOI 10.1067/mai.2001.114050; Kumar RK, 2002, LAB INVEST, V82, P495; Kumar RK, 2001, IMMUNOL CELL BIOL, V79, P141, DOI 10.1046/j.1440-1711.2001.00981.x; Lee CG, 2004, J EXP MED, V200, P377, DOI 10.1084/jem.20040104; Leigh R, 2002, AM J RESP CELL MOL, V27, P526, DOI 10.1165/rcmb.2002-0048OC; Leung SY, 2004, CLIN EXP ALLERGY, V34, P213, DOI 10.1111/j.1365-2222.2004.01870.x; MAKINO S, 1995, ALLERGY PROC, V16, P13, DOI 10.2500/108854195778690110; McParland BE, 2003, J APPL PHYSIOL, V95, P426, DOI 10.1152/japplphysiol.00159.2003; Minshall EM, 1997, AM J RESP CELL MOL, V17, P326; MORENO RH, 1986, AM REV RESPIR DIS, V133, P1171; Nagao K, 2003, AM J RESP CELL MOL, V29, P314, DOI 10.1165/rcmb.2003-0035OC; Palmans E, 2000, AM J RESP CRIT CARE, V161, P627; Pohunek P, 1997, EUR RESPIR J, V10, P160; Ramos-Barbon D, 2004, CLIN REV ALLERG IMMU, V27, P3, DOI 10.1385/CRIAI:27:1:003; Rankin JA, 1996, P NATL ACAD SCI USA, V93, P7821, DOI 10.1073/pnas.93.15.7821; Richter A, 2001, AM J RESP CELL MOL, V25, P385; ROCHE WR, 1989, LANCET, V1, P520; Sakai K, 2001, INT ARCH ALLERGY IMM, V126, P126, DOI 10.1159/000049503; SAMUEL CS, 1996, ENDOCRINOLOGY, V137, P3384; Scherf W, 2005, EUR J IMMUNOL, V35, P198, DOI 10.1002/eji.200425209; Shinagawa K, 2003, AM J RESP CRIT CARE, V168, P959, DOI 10.1164/rccm.200210-1188OC; Shirakawa I, 2000, Immunol Today, V21, P60; Takeda S, 2001, J NON-CRYST SOLIDS, V281, P1, DOI 10.1016/S0022-3093(00)00422-1; Temelkovski J, 1998, THORAX, V53, P849; VANESSENZANDVLIET EE, 1994, EUR RESPIR J, V7, P63, DOI 10.1183/09031936.94.07010063; Vercelli D, 2003, CURR OPIN IMMUNOL, V15, P609, DOI 10.1016/j.coi.2003.09.005; Wegmann M, 2005, E SCHERING RES FDN W, V50, P69; WIGGS BR, 1990, J APPL PHYSIOL, V69, P849; Wiggs BR, 1992, AM REV RESPIR DIS, V145, P1249; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; Wilson JW, 1997, CLIN EXP ALLERGY, V27, P363; Zhu Zhou, 1999, Journal of Clinical Investigation, V103, P779, DOI 10.1172/JCI5909	47	71	82	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	2007	36	5					625	632		10.1165/rcmb.2006-0083OC		8	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	162BW	WOS:000246062500014	17237192	
J	Leggat, PA; Smith, DR; Kedjarune, U				Leggat, Peter A.; Smith, Derek R.; Kedjarune, Ureporn			Surgical applications of cyanoacrylate adhesives: A review of toxicity	ANZ JOURNAL OF SURGERY			English	Review						cyanoacrylate; medical; occupational allergy; occupational asthma; occupational skin disease; surgery; toxic effect	CELL-CULTURE METHOD; TISSUE ADHESIVE; ISOBUTYL CYANOACRYLATE; CAROTID-ARTERY; CYTO-TOXICITY; SURGERY; GLUE; 2-CYANOACRYLATE; CYTOTOXICITY; MANAGEMENT	Cyanoacrylate (CA) and its homologues have a variety of medical and commercial applications as biological adhesives and sealants. Homologues of CA are being widely promoted in surgery as a tissue adhesive to replace traditional suturing techniques. Potential benefits of using CA adhesives include better cosmetic results, more rapid wound closure, and perhaps most significantly, the potential for significant reductions in percutaneous injuries from suture needles, which would in turn also reduce the risk of transmission of infectious diseases. Nevertheless, certain concerns have been raised regarding the potential toxicity of CA within patients, as well as among health professionals who are occupationally exposed when using CA compounds. Reported toxicity of CA in the workplace may result in dermatological, allergic and respiratory conditions. To help reduce the occupational burden, therefore, medical staff using CA adhesives should avoid direct contact with the compound and use appropriate personal protective measures at all times. Maintaining higher levels of humidity, optimizing room ventilation and using special air conditioning filters in surgical suites and operating theatres may also be useful in minimizing the exposure to volatile CA adhesives.	James Cook Univ N Queensland, Anton Breinl Ctr Publ Hlth & Trop Med, Townsville, Qld 4811, Australia; NIOSH, Int Ctr Res Promot & Informat, Kawasaki, Kanagawa, Japan; Prince Songkla Univ, Fac Dent, Dept Oral Biol & Occlus, Hat Yai, Thailand	Leggat, PA (reprint author), James Cook Univ N Queensland, Anton Breinl Ctr Publ Hlth & Trop Med, Townsville, Qld 4811, Australia.	peter.leggat@jcu.edu.au	Smith, Derek/F-4844-2010	Smith, Derek/0000-0002-8202-2523			Agarwal A, 1998, BRIT J NEUROSURG, V12, P213, DOI 10.1080/02688699845014; ANDERSEN M, 1982, MUTAT RES, V102, P373, DOI 10.1016/0165-1218(82)90100-8; APPLEBAUM JS, 1993, ANN EMERG MED, V22, P1190, DOI 10.1016/S0196-0644(05)80988-6; BELSITO DV, 1987, CONTACT DERMATITIS, V17, P234, DOI 10.1111/j.1600-0536.1987.tb02719.x; BENSON AL, 1975, AM IND HYG ASSOC J, V36, P741, DOI 10.1080/0002889758507333; CARY R, 2001, METHYL CYANOACRYLATE; Causton B. 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Surg.	APR	2007	77	4					209	213		10.1111/j.1445-2197.2007.04020.x		5	Surgery	Surgery	144KA	WOS:000244793700004	17388821	
J	Ueda, T; Niimi, A; Matsumoto, H; Takemura, M; Hirai, T; Yamaguchi, M; Matsuoka, H; Jinnai, M; Muro, S; Chin, K; Mishima, M				Ueda, Tetsuya; Niimi, Akio; Matsumoto, Hisako; Takemura, Masaya; Hirai, Toyohiro; Yamaguchi, Masafumi; Matsuoka, Hirofumi; Jinnai, Makiko; Muro, Shigeo; Chin, Kazuo; Mishima, Michiaki			Role of small airways in asthma: Investigation using high-resolution computed tomography	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; small airways; high-resolution computed tomography; lung density; airway responsiveness; airway inflammation; airway remodeling; air trapping	OBSTRUCTIVE PULMONARY-DISEASE; LOW-ATTENUATION AREAS; CT LUNG DENSITOMETRY; WALL THICKNESS; SPUTUM INDUCTION; FATAL ASTHMA; DISTAL LUNG; INFLAMMATION; EMPHYSEMA; HYDROFLUOROALKANE	Background: Small airways may have an important role in asthma but are more difficult to assess pathologically than central airways. Computed tomographic indices of lung density are assumed to reflect air trapping and may be a useful noninvasive measure of small airways disease, but their pathophysiological relevance remains undetermined. Objective: To evaluate lung density on high-resolution computed tomography and examine its correlations with clinical and physiologic variables in 29 patients with stable asthma. Methods: Both lungs were scanned at full-inspiratory and fullexpiratory phases to quantify percentage of lung field occupied by low attenuation area (LAA%; < -960 Hounsfield units) and mean lung density. Asthma severity, pulmonary function, methacholine airway sensitivity and reactivity, and sputum eosinophil counts were evaluated. Results: The mean lung density increased and LAA% decreased in all patients at expiratory phase compared with inspiratory phase. The inspiratory density indices and expiratory mean lung density correlated only with FEV1/forced vital capacity (FVC). Expiratory LAA% correlated more strongly than other variables with FEV1/FVC and with indices of peripheral airflow obstruction. Expiratory/inspiratory ratios of LAA% and mean lung density correlated, the former more strongly, with disease severity, residual volume/total lung capacity, and airway sensitivity, as well as with indices of global (FEV1 and FEV1/FVC) and peripheral airflow obstruction. Conclusion: Expiratory/inspiratory high-resolution computed tomography is useful for assessing small airways disease in asthma. Small airways involvement is associated with airflow obstruction, airway hypersensitivity, and more severe disease. Clinical implications: Small airways are an important therapeutic target in asthma.	Kyoto Univ, Dept Resp Med, Grad Sch Med, Sakyo Ku, Kyoto 6068507, Japan; Kyoto Univ, Dept Phys Thearpy Resp Med, Kyoto, Japan	Niimi, A (reprint author), Kyoto Univ, Dept Resp Med, Grad Sch Med, Sakyo Ku, Kyoto 6068507, Japan.	niimi@kuhp.kyoto-u.ac.jp		Matsuoka, Hirofumi/0000-0001-5219-7501			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; Balzar S, 2005, AM J RESP CRIT CARE, V171, P431, DOI 10.1164/rccm.200407-949OC; Bateman ED, 2004, AM J RESP CRIT CARE, V170, P836, DOI 10.1164/rccm.200401-033OC; Beigelman-Aubry C, 2002, RADIOLOGY, V223, P181, DOI 10.1148/radiol.2231010779; Bergeron C, 2005, J ALLERGY CLIN IMMUN, V116, P983, DOI 10.1016/j.jaci.2005.07.029; Biernacki W, 1997, EUR RESPIR J, V10, P2455, DOI 10.1183/09031936.97.10112455; Bousquet J, 2000, AM J RESP CRIT CARE, V161, P1720; CARROLL N, 1993, AM REV RESPIR DIS, V147, P405; de Blic J, 2005, J ALLERGY CLIN IMMUN, V116, P750, DOI 10.1016/j.jaci.2005.07.009; Eda S, 1997, AM J RESP CRIT CARE, V155, P1290; FAHY JV, 1995, AM J RESP CRIT CARE, V152, P53; GELB AF, 1973, NEW ENGL J MED, V288, P395, DOI 10.1056/NEJM197302222880805; Gershman NH, 1999, J ALLERGY CLIN IMMUN, V104, P322, DOI 10.1016/S0091-6749(99)70374-X; Gevenois PA, 1996, AM J ROENTGENOL, V167, P1169; Goldin JG, 1999, J ALLERGY CLIN IMMUN, V104, pS258; Goldin JG, 1998, RADIOLOGY, V208, P321; Gono H, 2003, EUR RESPIR J, V22, P965, DOI 10.1183/09031936.03.00085302; Guckel C, 1999, J APPL PHYSIOL, V86, P701; Hamid Q, 1997, J ALLERGY CLIN IMMUN, V100, P44; Hansell DM, 2001, EUR RESPIR J, V17, P1294, DOI 10.1183/09031936.01.00206101; Hauber HP, 2003, J ALLERGY CLIN IMMUN, V112, P58, DOI 10.1067/mai.2003.1612; in 't Veen Johannes C. 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M., 2000, American Journal of Respiratory and Critical Care Medicine, V161, P1902; JAMES AL, 1989, AM REV RESPIR DIS, V139, P242; Kasahara K, 2002, THORAX, V57, P242, DOI 10.1136/thorax.57.3.242; Ketai L, 2005, J ASTHMA, V42, P667, DOI 10.1080/02770900500264978; King GG, 1999, AM J RESP CRIT CARE, V159, P992; Kraft M, 1999, AM J RESP CRIT CARE, V159, P228; Kraft M, 1999, EUR RESPIR J, V14, P1403, DOI 10.1183/09031936.99.14614039; Kubo K, 1998, AM J RESP CRIT CARE, V158, P979; Little SA, 2002, THORAX, V57, P247, DOI 10.1136/thorax.57.3.247; Matsumoto H, 2005, THORAX, V60, P277, DOI 10.1136/thx.2004.028936; Mauad T, 2004, AM J RESP CRIT CARE, V170, P857, DOI 10.1164/rccm.200403-305OC; MCFADDEN ER, 1972, AM J MED, V52, P725, DOI 10.1016/0002-9343(72)90078-2; McParland BE, 2003, J APPL PHYSIOL, V95, P426, DOI 10.1152/japplphysiol.00159.2003; Mishima M, 1999, J COMPUT ASSIST TOMO, V23, P380, DOI 10.1097/00004728-199905000-00011; Mishima M, 1999, P NATL ACAD SCI USA, V96, P8829, DOI 10.1073/pnas.96.16.8829; Mitsunobu F, 2003, AM J RESP CRIT CARE, V167, P411, DOI 10.1164/rccm.2112070; Mitsunobu F, 2001, J ASTHMA, V38, P413; Mitsunobu F, 2001, THORAX, V56, P851, DOI 10.1136/thorax.56.11.851; Nakano Y, 2000, AM J RESP CRIT CARE, V162, P1102; NEWMAN KB, 1994, CHEST, V106, P105, DOI 10.1378/chest.106.1.105; Niimi A, 2004, CLIN REV ALLERG IMMU, V27, P45, DOI 10.1385/CRIAI:27:1:045; Niimi A, 2000, AM J RESP CRIT CARE, V162, P1518; Niimi A, 2003, AM J RESP CRIT CARE, V168, P983, DOI 10.1164/rccm.200211.1268OC; Niimi A, 2004, AM J MED, V116, P725, DOI 10.1016/j.amjmed.2003.11.026; SAKAI N, 1994, CHEST, V106, P1319, DOI 10.1378/chest.106.5.1319; Sutherland ER, 2004, J ALLERGY CLIN IMMUN, V113, P1046, DOI 10.1016/j.jaci.2004.03.016; Takemura M, 2004, CHEST, V125, P1352, DOI 10.1378/chest.125.4.1352; TAKISHIMA T, 1981, CHEST, V80, P600, DOI 10.1378/chest.80.5.600; Zeidler MR, 2006, EUR RESPIR J, V27, P307, DOI 10.1183/09031936.06.00005605; 2004, GLOBAL STRATEGY ASTH	52	71	75	0	2	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	NOV	2006	118	5					1019	1025		10.1016/j.jaci.2006.07.032		7	Allergy; Immunology	Allergy; Immunology	137GY	WOS:000244282300004	17088124	
J	Lue, KH; Lin, YH; Sun, HL; Lu, KH; Hsieh, JC; Chou, MC				Lue, Ko-Huang; Lin, Yung-Hsiang; Sun, Hai-Lun; Lu, Ko-Hsiu; Hsieh, Jie-Cheng; Chou, Ming-Chih			Clinical and immunologic effects of sublingual immunotherapy in asthmatic children sensitized to mites: a double-blind, randomized, placebo-controlled study	PEDIATRIC ALLERGY AND IMMUNOLOGY			English	Article						sublingual immunotherapy; house dust mite; asthma; IgG4	HOUSE-DUST MITE; ALLERGEN-SPECIFIC IMMUNOTHERAPY; CONTROLLED-TRIAL; ANTIBODY-LEVELS; EFFICACY; RHINITIS; EXTRACT; SAFETY; SLIT; IGG	Immunotherapy through oral routes is thought to be a valuable therapeutic option for asthma. The clinical and immunologic effects of sublingual immunotherapy (SLIT) in children with asthma caused by mites were evaluated in a double-blind, placebo-controlled study for 6 months. Patients (aged 6-12 yr) with mild-to-moderate asthma, with single sensitization to mite allergen, received either SLIT or placebo with a standardized Dermatophagoides pteronyssinus (D.p.)/D. farinae (D.f.) 50/50 extract. The cumulative dose was around 41824 IR, equivalent to 1.7 mg of D.p. and 3.0 mg of D.f. allergen. Symptom and medication scores were assessed throughout the study. Serum total immunoglobulin (Ig)E, eosinophil count, eosinophil cationic protein, specific IgE, specific IgG4, and skin sensitivity were evaluated before starting the treatment and after the treatment period. Twenty patients completed the study. At the beginning of the treatment, no differences were observed between the groups for symptom and medication scores, skin sensitivity, or immunologic parameters. After 6 months of treatment, there was a significant difference in nighttime asthma symptom scores and specific IgG4 (p < 0.05) in the SLIT group compared with the placebo group. Daytime symptom and medication scores, total IgE, eosinophil count, forced expiratory volume in 1 s, and mean evening peak expiratory flow rate reached significant differences in the SLIT group during the treatment period (p < 0.05). No severe adverse effects were reported. Our results revealed that treatment for 6 months with SLIT is clinically effective in decreasing asthmatic symptoms and medication use in children with mild-to-moderate asthma because of mite sensitivity. The clinical usefulness of this form of immunotherapy and the mechanism underlying its immunologic effects deserve further studies.	Chung Shan Med Univ Hosp, Dept Pediat, Taichung 402, Taiwan; Chung Shan Med Univ, Inst Med, Taichung, Taiwan	Lue, KH (reprint author), Chung Shan Med Univ Hosp, Dept Pediat, 110,Sect 1,Chien Kuo N Rd, Taichung 402, Taiwan.	cshy095@csh.org.tw					Bahceciler NN, 2005, INT ARCH ALLERGY IMM, V136, P287, DOI 10.1159/000083956; Bahceciler NN, 2001, PEDIATR PULM, V32, P49, DOI 10.1002/ppul.1088; Bodtger U, 2003, ALLERGY, V58, P1180, DOI 10.1046/j.1398-9995.2003.00323.x; Bodtger U, 2002, ALLERGY, V57, P297, DOI 10.1034/j.1398-9995.2002.1o3532.x; Bousquet J, 1999, ALLERGY, V54, P249, DOI 10.1034/j.1398-9995.1999.00916.x; Bousquet J, 1998, J ALLERGY CLIN IMMUN, V102, P558, DOI 10.1016/S0091-6749(98)70271-4; DJURUP R, 1985, ALLERGY, V40, P469, DOI 10.1111/j.1398-9995.1985.tb00253.x; Feliziani V, 1995, Allergol Immunopathol (Madr), V23, P224; Hirsch T, 1997, PEDIATR ALLERGY IMMU, V8, P21, DOI 10.1111/j.1399-3038.1997.tb00138.x; LIN KL, 1991, ANN ALLERGY, V67, P63; Lu FM, 1998, ANN ALLERG ASTHMA IM, V80, P419; Madonini E, 2000, INT J IMMUNOPATH PH, V13, P77; Malling HJ, 1998, ALLERGY, V53, P933, DOI 10.1111/j.1398-9995.1998.tb03793.x; Marcucci F, 2003, ALLERGY, V58, P657, DOI 10.1034/j.1398-9995.2003.00193.x; Marcucci F, 2001, ALLERGY, V56, P1091, DOI 10.1034/j.1398-9995.2001.00226.x; MCHUGH SM, 1990, J ALLERGY CLIN IMMUN, V86, P521, DOI 10.1016/S0091-6749(05)80208-8; NELSON HS, 1993, J ALLERGY CLIN IMMUN, V92, P229, DOI 10.1016/0091-6749(93)90166-D; Pajno GB, 2000, ALLERGY, V55, P842, DOI 10.1034/j.1398-9995.2000.00495.x; Pajno Giovanni B, 2003, Paediatr Drugs, V5, P777, DOI 10.2165/00148581-200305110-00006; Passalacqua G, 1998, LANCET, V351, P629, DOI 10.1016/S0140-6736(97)07055-4; SABBAH A, 1994, ALLERGY, V49, P309, DOI 10.1111/j.1398-9995.1994.tb02273.x; TARI MG, 1990, ALLERGOL IMMUNOPATH, V18, P277; TROISE C, 1995, J INVEST ALLERG CLIN, V5, P25	23	71	77	0	2	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0905-6157			PEDIATR ALLERGY IMMU	Pediatr. Allergy Immunol.	SEP	2006	17	6					408	415		10.1111/j.1399-3038.2006.00443.x		8	Allergy; Immunology; Pediatrics	Allergy; Immunology; Pediatrics	076FG	WOS:000239941800003	16925685	
J	Beisswenger, C; Kandler, K; Hess, C; Garn, H; Felgentreff, K; Wegmann, M; Renz, H; Vogelmeier, C; Bals, R				Beisswenger, Christoph; Kandler, Kerstin; Hess, Christian; Garn, Holger; Felgentreff, Kerstin; Wegmann, Michael; Renz, Harald; Vogelmeier, Claus; Bals, Robert			Allergic airway inflammation inhibits pulmonary antibacterial host defense	JOURNAL OF IMMUNOLOGY			English	Article							INNATE IMMUNE-RESPONSE; ANTIMICROBIAL PEPTIDES; ATOPIC-DERMATITIS; LUNG INFLAMMATION; RISK-FACTORS; ASTHMA; PNEUMONIA; POLARIZATION; PATHOGENESIS; EPITHELIUM	The innate immune system of the lung is a multicomponent host defense system and in addition has an instructing role in regulating the quality and quantity of the adaptive immune response. When the interaction between innate and adaptive immunity is disturbed, pathological conditions such as asthma can develop. It was the aim of the study to investigate the effect of the allergic inflammation of the lung on the innate host defense during bacterial infection. Human bronchial epithelial cells were preinculvated with Th2 cytokines and infected with Pseudomonas aeruginosa. The effect of the Th2 cytokines on the mRNA levels of antimicrobial peptides and the antimicrobial activity of HBEC was determined. To investigate the influence of an allergic inflammation on pulmonary host defense in vivo, mice sensitized and challenged with OVA were infected with P. aeruginosa, and the number of viable bacteria in the lungs was determined together with markers of inflammation like cytokines and antimicrobial peptides. Exposure of airway epithelial cells to Th2 cytokines resulted in a significantly decreased antimicrobial activity of the cells and in suppressed mRNA levels of the antimicrobial peptide human beta-defensin 2. Furthermore, mice with allergic airway inflammation had significantly more viable bacteria in their lungs after infection. This was consistent with reduced levels of proinflammatory cytokines and of the antimicrobial peptide cathelin-related antimicrobial peptide. These results show that an allergic airway inflammation suppresses the innate antimicrobial host defense. The adaptive immune system modulates the functions of the pulmonary innate immune system.	Univ Marburg, Dept Internal Med, Div Pulm Dis, D-3550 Marburg, Germany; Univ Marburg, Dept Clin Chem & Mol Diagnost, D-3550 Marburg, Germany	Bals, R (reprint author), Hosp Univ Marburg, Dept Internal Med, Div Pulmonol, Baldingerstr 1, D-35043 Marburg, Germany.	bals@mailer.uni-marburg.de					Bals R, 2004, EUR RESPIR J, V23, P327, DOI 10.1183/09031936.03.00098803; Bals Robert, 2004, J Cyst Fibros, V3 Suppl 2, P49, DOI 10.1016/j.jcf.2004.05.010; Beisswenger Christoph, 2005, V86, P55; Diamond G, 2000, IMMUNOL REV, V173, P27, DOI 10.1034/j.1600-065X.2000.917304.x; Eisenbarth SC, 2004, CURR OPIN PEDIATR, V16, P659, DOI 10.1097/01.mop.0000145920.00101.e4; Jackson ML, 2004, CLIN INFECT DIS, V39, P1642, DOI 10.1086/425615; Kapsenberg ML, 2003, NAT REV IMMUNOL, V3, P984, DOI 10.1038/nri1246; Knight DA, 2003, RESPIROLOGY, V8, P432, DOI 10.1046/j.1440-1843.2003.00493.x; KOIVULA I, 1994, AM J MED, V96, P313, DOI 10.1016/0002-9343(94)90060-4; Lambrecht BN, 2003, NAT REV IMMUNOL, V3, P994, DOI 10.1038/nri1249; Lee SW, 2002, J KOREAN MED SCI, V17, P7; Lemanske RF, 2003, CHEST, V123, p385S, DOI 10.1378/chest.123.3_suppl.385S-a; Mahalanabis D, 2002, EPIDEMIOL INFECT, V129, P65, DOI 10.1017/S0950268802006817; Neurath MF, 2002, NAT MED, V8, P567, DOI 10.1038/nm0602-567; Nomura I, 2003, J IMMUNOL, V171, P3262; Ohmori Y, 2000, J BIOL CHEM, V275, P38095, DOI 10.1074/jbc.M006227200; Ong PY, 2002, NEW ENGL J MED, V347, P1151, DOI 10.1056/NEJMoa021481; Piggott DA, 2005, J CLIN INVEST, V115, P459, DOI 10.1172/JCI200522462; Rodriguez D, 2003, J IMMUNOL, V171, P1001; Selsted ME, 2005, NAT IMMUNOL, V6, P551, DOI 10.1038/ni1206; Singh PK, 1998, P NATL ACAD SCI USA, V95, P14961, DOI 10.1073/pnas.95.25.14961; Sur S, 1999, J IMMUNOL, V162, P6284; Zanetti M, 2005, CURR ISSUES MOL BIOL, V7, P179; Zasloff M, 2002, NATURE, V415, P389, DOI 10.1038/415389a	24	71	74	0	1	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	AUG 1	2006	177	3					1833	1837				5	Immunology	Immunology	065DT	WOS:000239140300060	16849494	
J	Chan, RCF; Wang, MY; Li, N; Yanagawa, Y; Onoe, K; Lee, JJ; Nel, AE				Chan, Ray Chun-Fai; Wang, Meiying; Li, Ning; Yanagawa, Yoshiki; Onoe, Kazunori; Lee, James J.; Nel, Andre E.			Pro-oxidative diesel exhaust particle chemicals inhibit LPS-induced dendritic cell responses involved in T-helper differentiation	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						dendritic cells; T(H)1/T(H)2 cells; LPS; cell differentiation	NF-KAPPA-B; ANTIGEN-PRESENTING CELLS; AIRWAY INFLAMMATION; EPITHELIAL-CELLS; DEPOSITION PATTERNS; HEME OXYGENASE-1; INHALED ANTIGEN; TH2 RESPONSES; MURINE MODEL; ACTIVATION	Background: Epidemiologic studies show that exposure to ambient particulate matter leads to asthma exacerbation. Diesel exhaust particles (DEPs), a model pollutant, act as an adjuvant for allergic sensitization. Increasing evidence shows that this effect could be mediated by an effect on dendritic cells (DCs). Objective: Our aim was to elucidate the mechanism by which pro-oxidative DEP chemicals change DC function so that these antigen-presenting cells strengthen the immune response to an experimental allergen. Methods: We exposed murine bone marrow-derived DCs and a homogeneous myeloid DC line, BC1, to DEPs and organic extracts made from these particles to determine how the induction of oxidative stress affects cellular maturation, cytokine production, and activation of antigen-specific T cells. Results: DEP extracts induced oxidative stress in DCs. This change in redox equilibrium interfered in the ability of Toll-like receptor agonists to induce the expression of maturation receptors (eg, CD86, CD54, and I-A(d)) and IL-12 production. This perturbation of DC function was accompanied by decreased IFN-gamma and increased IL-10 induction in antigen-specific T cells. The molecular basis for the perturbation of DC function is the activation of a nuclear factor-erythroid 2 (NF-E2)-related factor 2-mediated signaling pathway that suppresses IL-12 production. NF-E2-related factor 2 deficiency abrogates the perturbation of DC function by DEPs. Conclusion: These data provide the first report that prooxidative DEP chemicals can interfere in T(H)1-promoting response pathways in a homogeneous DC population and provide a novel explanation for the adjuvant effect of DEPs on allergic inflammation.	Univ Calif Los Angeles, Div Clin Immunol & Allergy, Dept Med, Los Angeles, CA 90095 USA; Hokkaido Univ, Div Immunobiol, Inst Med Genet, Sapporo, Hokkaido, Japan; Mayo Clin, Div Pulm Med, Scottsdale, AZ USA	Nel, AE (reprint author), Univ Calif Los Angeles, Div Clin Immunol & Allergy, Dept Med, Los Angeles, CA 90095 USA.	anel@mednet.ucla.edu	Nel, Andre/J-2808-2012		NIAID NIH HHS [U19 AI 070453]; NIEHS NIH HHS [R01 ES 12053, R01 ES 013432, R01 ES 10553]		Akdis M, 2006, CHEM IMMUNOL ALLERGY, V91, P159; Amsen D, 2004, CELL, V117, P515, DOI 10.1016/S0092-8674(04)00451-9; An HZ, 2002, IMMUNOLOGY, V106, P38, DOI 10.1046/j.1365-2567.2002.01401.x; Balashazy I, 2000, HEALTH PHYS, V78, P147; Banning A, 2005, ANTIOXID REDOX SIGN, V7, P889, DOI 10.1089/ars.2005.7.889; Bengtsson A, 2001, CLIN EXP IMMUNOL, V123, P350, DOI 10.1046/j.1365-2249.2001.01453.x; Chan KM, 1999, P NATL ACAD SCI USA, V96, P12731, DOI 10.1073/pnas.96.22.12731; Chan RCF, 2004, BRIT J CANCER, V90, P1636, DOI 10.1038/sj.bjc.6601706; Chapman TJ, 2005, VIROLOGY, V340, P296, DOI 10.1016/j.virol.2005.06.023; Choi AMK, 1996, AM J RESP CELL MOL, V15, P9; Chvatchko Y, 1996, J EXP MED, V184, P2353, DOI 10.1084/jem.184.6.2353; Devouassoux G, 2002, J ALLERGY CLIN IMMUN, V109, P847, DOI 10.1067/mai.2002.122843; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; Eisenbarth SC, 2002, J EXP MED, V196, P1645, DOI 10.1084/jem.20021340; Finkelman FD, 2004, J IMMUNOL, V172, P3808; Gao XQ, 2004, P NATL ACAD SCI USA, V101, P10446, DOI 10.1073/pnas.0403886101; Geiser M, 2005, ENVIRON HEALTH PERSP, V113, P1555, DOI 10.1289/ehp.8006; Hao MQ, 2003, J ALLERGY CLIN IMMUN, V112, P905, DOI 10.1067/mai.2003.1780; Hiura TS, 1999, J IMMUNOL, V163, P5582; Hoshino A, 2003, EUR J IMMUNOL, V33, P861, DOI 10.1002/eji.200323455; HOSKEN NA, 1995, J EXP MED, V182, P1579, DOI 10.1084/jem.182.5.1579; Justice JP, 2001, AM J PHYSIOL-LUNG C, V280, pL363; Kantengwa S, 2003, AM J RESP CRIT CARE, V167, P431, DOI 10.1164/rccm.200205-425OC; Kaye SR, 2000, J AEROSOL SCI, V31, P849, DOI 10.1016/S0021-8502(99)00565-0; Khoshnan A, 1999, J IMMUNOL, V163, P5444; Kobayashi M, 2005, ANTIOXID REDOX SIGN, V7, P385, DOI 10.1089/ars.2005.7.385; Lambrecht BN, 2000, J CLIN INVEST, V106, P551, DOI 10.1172/JCI8107; Lambrecht BN, 2005, ALLERGY, V60, P271, DOI 10.1111/j.1398-9995.2005.00708.x; Laouini D, 2003, J CLIN INVEST, V112, P1058, DOI 10.1172/JCI200318246; Li N, 2004, J IMMUNOL, V173, P3467; Li N, 2003, CLIN IMMUNOL, V109, P250, DOI 10.1016/j.clim.2003.08.006; Li N, 2002, J IMMUNOL, V169, P4531; Miyabara Y, 1998, J ALLERGY CLIN IMMUN, V102, P805, DOI 10.1016/S0091-6749(98)70021-1; Nel AE, 1998, J ALLERGY CLIN IMMUN, V102, P539, DOI 10.1016/S0091-6749(98)70269-6; Ohtani T, 2005, J IMMUNOL, V174, P2412; Peterson JD, 1998, P NATL ACAD SCI USA, V95, P3071, DOI 10.1073/pnas.95.6.3071; Phalen RF, 2006, TOXICOL SCI, V92, P126, DOI 10.1093/toxsci/kfj182; Reider N, 2002, J ALLERGY CLIN IMMUN, V109, P89, DOI 10.1067/mai.2002.120556; Soares MP, 2004, J IMMUNOL, V172, P3553; Stancovski I, 1997, CELL, V91, P299, DOI 10.1016/S0092-8674(00)80413-4; Takeda K, 2004, SEMIN IMMUNOL, V16, P3, DOI 10.1016/j.smim.2003.10.003; Trinchieri G, 2003, NAT REV IMMUNOL, V3, P133, DOI 10.1038/nri1001; Winzler C, 1997, J EXP MED, V185, P317, DOI 10.1084/jem.185.2.317; Xiao GG, 2003, J BIOL CHEM, V278, P50781, DOI 10.1074/jbc.M306423200; Yanagawa Y, 2002, J LEUKOCYTE BIOL, V71, P125	45	71	72	1	8	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	AUG	2006	118	2					455	465		10.1016/j.jaci.2006.06.006		11	Allergy; Immunology	Allergy; Immunology	075IH	WOS:000239877700023	16890772	
J	Sahsuvaroglu, T; Arain, A; Kanaroglou, P; Finkelstein, N; Newbold, B; Jerrett, M; Beckerman, B; Brook, J; Finkelstein, M; Gilbert, NL				Sahsuvaroglu, Talar; Arain, Altaf; Kanaroglou, Pavlos; Finkelstein, Norm; Newbold, Bruce; Jerrett, Michael; Beckerman, Bernardo; Brook, Jeffrey; Finkelstein, Murray; Gilbert, Nicolas L.			A land use regression model for predicting ambient concentrations of nitrogen dioxide in Hamilton, Ontario, Canada	JOURNAL OF THE AIR & WASTE MANAGEMENT ASSOCIATION			English	Article							PARTICULATE AIR-POLLUTION; EXPOSURE ASSESSMENT; PERSONAL EXPOSURE; ENVIRONMENTAL JUSTICE; SPATIAL VARIABILITY; CHILDHOOD ASTHMA; MAJOR HIGHWAY; URBAN AREA; CHILDREN; MORTALITY	This paper reports on the development of a land use regression (LUR) model for predicting the intraurban variation of traffic-related air pollution in Hamilton, Ontario, Canada, an industrial city at the western end of Lake Ontario. Although land use regression has been increasingly used to characterize exposure gradients within cities, research to date has yet to test whether this method can produce reliable estimates in an industrialized location. Ambient concentrations of nitrogen dioxide (NO,) were measured for a 2-week period in October 2002 at > 100 locations across the city and subsequently at 30 of these locations in May 2004 to assess seasonal effects. Predictor variables were derived for land use types, transportation, demography, and, physical geography using geographic information systems. The LUR model explained 76% of the variation in NO2. Traffic density, proximity to a highway, and industrial land use were all positively correlated with NO, concentrations, whereas open land use and distance from the lake were negatively correlated with NO2. Locations downwind of a major highway resulted in higher NO2 levels. Cross-validation of the results confirmed model stability Over different seasons. Our findings demonstrate that land use regression can effectively predict NO, variation at the intraurban scale in an industrial setting. Models predicting exposure within smaller areas may lead to improved detection of health effects in epidemiologic studies.	McMaster Univ, Sch Geog & Earth Sci, Div Biostat, Dept Prevent Med, Hamilton, ON L8S 4K1, Canada; Univ So Calif, Dept Prevent Med, Div Biostat, Los Angeles, CA 90089 USA; Environm Canada, Meteorol Serv Canada, Toronto, ON M3H 5T4, Canada; Mt Sinai Hosp, Family Med Ctr, Toronto, ON M5G 1X5, Canada; Hlth Canada, Air Hlth Effects Div, Ottawa, ON K1A 0L2, Canada	Sahsuvaroglu, T (reprint author), McMaster Univ, Sch Geog & Earth Sci, Div Biostat, Dept Prevent Med, 1280 Main St W, Hamilton, ON L8S 4K1, Canada.	sahsuvt@mcmaster.ca		Gilbert, Nicolas/0000-0001-6985-8046; Arain, M. Altaf/0000-0002-1433-5173	NIEHS NIH HHS [5P01 ES011627, 5P30 ES07048]		Brauer M, 2003, EPIDEMIOLOGY, V14, P228, DOI 10.1097/00001648-200303000-00019; Briggs DJ, 1997, INT J GEOGR INF SCI, V11, P699, DOI 10.1080/136588197242158; Briggs DJ, 2000, SCI TOTAL ENVIRON, V253, P151, DOI 10.1016/S0048-9697(00)00429-0; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; Buzzelli M, 2003, ANN ASSOC AM GEOGR, V93, P557, DOI 10.1111/1467-8306.9303003; CHOW GC, 1960, ECONOMETRICA, V28, P591, DOI 10.2307/1910133; Cyrys J, 2005, ENVIRON HEALTH PERSP, V113, P987, DOI 10.1289/ehp.7662; English P, 1999, ENVIRON HEALTH PERSP, V107, P761, DOI 10.2307/3434663; FERGUSON E, 2004, INT J HEALTH GEOGR, V3, P24, DOI 10.1186/1476-072X-3-24; Finkelstein MM, 2003, CAN MED ASSOC J, V169, P397; Finkelstein MM, 2004, AM J EPIDEMIOL, V160, P173, DOI 10.1093/aje/kwh181; Fischer PH, 2000, ATMOS ENVIRON, V34, P3713, DOI 10.1016/S1352-2310(00)00067-4; Gauderman WJ, 2004, NEW ENGL J MED, V351, P1057, DOI 10.1056/NEJMoa040610; Gauderman WJ, 2005, EPIDEMIOLOGY, V16, P737, DOI 10.1097/01.ede.00001813087.51440.75; Gauvin S, 2001, ARCH ENVIRON HEALTH, V56, P336; GETIS A, 1995, US CANADA LAND PEOPL; Gilbert NL, 2003, SCI TOTAL ENVIRON, V312, P43, DOI 10.1016/S0048-9697(03)00228-6; Gilbert NL, 2005, J AIR WASTE MANAGE, V55, P1059; Griffith D.A., 1987, SPATIAL AUTOCORRELAT; Harrison RM, 2002, OCCUP ENVIRON MED, V59, P671, DOI 10.1136/oem.59.10.671; HEWITT CN, 1991, ATMOS ENVIRON B-URB, V25, P429; *HLTH CAN, REG REL HLTH AIR QUA; Hoek G, 2002, LANCET, V360, P1203, DOI 10.1016/S0140-6736(02)11280-3; HUBBE J, 1997, J APPL METEOROL, V66, P1221; Isaaks EH, 1989, INTRO APPL GEOSTATIS; Jerrett M, 2005, EPIDEMIOLOGY, V16, P727, DOI 10.1097/01.ede.0000181630.15826.7d; Jerrett M, 2001, ENVIRON PLANN A, V33, P955, DOI 10.1068/a33137; JERRETT M, 2006, IN PRESS J TOXICOL E; Kanaroglou PS, 2005, ATMOS ENVIRON, V39, P2399, DOI 10.1016/j.atmosenv.2004.06.049; KANAROGLU P, 2003, P TRANSP AIR POLL C; Kramer U, 2000, EPIDEMIOLOGY, V11, P64, DOI 10.1097/00001648-200001000-00014; Lebret E, 2000, ATMOS ENVIRON, V34, P177, DOI 10.1016/S1352-2310(99)00292-7; Linaker CH, 2000, OCCUP ENVIRON MED, V57, P472, DOI 10.1136/oem.57.7.472; Lynn P. 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Air Waste Manage. Assoc.	AUG	2006	56	8					1059	1069				11	Engineering, Environmental; Environmental Sciences; Meteorology & Atmospheric Sciences	Engineering; Environmental Sciences & Ecology; Meteorology & Atmospheric Sciences	070WJ	WOS:000239556300001	16933638	
J	Brightling, CE				Brightling, CE			Chronic cough due to nonasthmatic eosinophilic bronchitis - ACCP evidence-based clinical practice guidelines	CHEST			English	Article						airway smooth muscle; asthma; cough; eosinophilic bronchitis; eosinophils; mast cells	CHRONIC NONPRODUCTIVE COUGH; AIR-FLOW OBSTRUCTION; INDUCED SPUTUM; VARIANT ASTHMA; ATOPIC COUGH; INFLAMMATION; FREQUENCY; SPECTRUM; THERAPY; DISEASE	Objectives: Nonasthmatic eosinophilic bronchitis is a newly recognized cause of chronic cough. Our objective was to review the pathogenesis, natural history, diagnosis, and treatment of this condition. Methods: The current literature was reviewed using an Ovid MEDLINE and PubMed literature review for all studies published in the English language from 1963 to December 2004 using the medical subject heading term "eosinophilic bronchitis." Results: Nonasthmatic eosinophilic bronchitis is a common cause of chronic cough. it is characterized by the presence of eosinophilic airway inflammation, similar to that seen in asthma. However, in contrast to asthma, nonasthmatic eosinophilic bronchitis is not associated with variable airflow limitation or airway hyperresponsiveness. The differences in functional association are related to differences in the localization of mast cells within the airway wall, with airway smooth muscle infiltration occurring in patients with asthma, and epithelial infiltration in patients with nonasthmatic eosinophilic bronchitis. Diagnosis is made by the confirmation of eosinophilic airway inflammation usually with induced sputum analysis after the exclusion of other causes for chronic cough on clinical, radiologic, and lung function assessment. The cough usually responds well to treatment with inhaled corticosteroids. The dose and duration of treatment differ between patients. The condition can be transient, episodic, or persistent unless treated, and occasionally patients may require long-term prednisone treatment. Conclusions: Further study of this condition may improve our understanding of airway inflammation and airway responsiveness, leading to novel targets for therapeutic agents for the treatment of both asthma and nonasthmatic eosinophilic bronchitis.	Univ Hosp Leicester NHS Trust, Glenfield Gen Hosp, Inst Lung Hlth, Leicester LE3 9QP, Leics, England	Brightling, CE (reprint author), Univ Hosp Leicester NHS Trust, Glenfield Gen Hosp, Inst Lung Hlth, Groby Rd, Leicester LE3 9QP, Leics, England.	ceb17@le.ac.uk					Ayik SO, 2003, RESP MED, V97, P695, DOI 10.1053/rmed.2003.1503; Belda J, 2000, AM J RESP CRIT CARE, V161, P475; Berlyne GS, 2000, J ALLERGY CLIN IMMUN, V106, P638, DOI 10.1067/mai.2000.109622; Berry MA, 2005, CLIN EXP ALLERGY, V35, P598, DOI 10.1111/j.1365-2222.2005.02222.x; 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, 2003, THORAX, V58, P528, DOI 10.1136/thorax.58.6.528; Brightling CE, 1999, AM J RESP CRIT CARE, V160, P406; Brightling CE, 2000, CLIN EXP ALLERGY, V30, P4; Brightling CE, 2002, NEW ENGL J MED, V346, P1699, DOI 10.1056/NEJMoa012705; Brightling Christopher E., 2000, American Journal of Respiratory and Critical Care Medicine, V162, P878; Carney IK, 1997, AM J RESP CRIT CARE, V156, P211; Efthimiadis A, 2002, EUR RESPIR J, V37, p19s; Fujimura M, 2003, CLIN EXP ALLERGY, V33, P588, DOI 10.1046/j.1365-2222.2003.01658.x; Fujimura M, 2003, THORAX, V58, P14, DOI 10.1136/thorax.58.1.14; Fujimura M, 2000, CLIN EXP ALLERGY, V30, P41; GIBSON PG, 1989, LANCET, V1, P1346; Gibson PG, 1998, J ALLERGY CLIN IMMUN, V101, P320; GIBSON PG, 1995, CLIN EXP ALLERGY, V25, P127, DOI 10.1111/j.1365-2222.1995.tb01017.x; Hancox RJ, 2001, LANCET, V358, P1104, DOI 10.1016/S0140-6736(01)06224-9; IRWIN RS, 1990, AM REV RESPIR DIS, V141, P640; IRWIN RS, 1981, AM REV RESPIR DIS, V123, P413; Keatings VM, 1997, THORAX, V52, P372; Lemiere C, 1997, J ALLERGY CLIN IMMUN, V100, P852, DOI 10.1016/S0091-6749(97)70286-0; McGarvey LPA, 1998, THORAX, V53, P738; Paggiaro PL, 2002, EUR RESPIR J, V37, P3; Pavord ID, 1999, LANCET, V353, P2213, DOI 10.1016/S0140-6736(99)01813-9; 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	31	71	78	1	4	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	JAN	2006	129	1		S			116S	121S		10.1378/chest.129.1_suppl.116S		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	009BT	WOS:000235086800015	16428700	
J	van Neerven, RJ; Knoll, EF; Ejrnaes, A; Wurtzen, PA				van Neerven, R. J.; Knoll, E. F.; Ejrnaes, A.; Wurtzen, P. A.			IgE-mediated allergen presentation and blocking antibodies: Regulation of T-Cell activation in allergy	INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY			English	Review						allergen presentation; blocking antibodies; IgE immunotherapy	FC-EPSILON-RI; GRASS-POLLEN IMMUNOTHERAPY; LOW-AFFINITY RECEPTOR; EPIDERMAL LANGERHANS CELLS; BASOPHIL HISTAMINE-RELEASE; LATE ASTHMATIC RESPONSE; ANTIGEN-SPECIFIC IGE; HAY-FEVER PATIENTS; IN-VIVO; SERUM-IGE	it is well established that both the production of IgE by B lymphocytes and the maturation and recruitment of eosinophils in late-phase reactions are dependent on the activation of allergen-specific type-2 T-helper cells. What is less well known is the fact that efficient activation of allergen-specific T cells upon low-dose exposure to allergens is critically dependent on IgE-mediated or -facilitated allergen presentation. In fact, changes in the level of IgE-mediated allergen presentation may account for many of the immunological effects described for specific immunotherapy or anti-IgE treatment. This review aims to summarize the current knowledge, and will discuss the clinical relevance of blocking IgG antibodies induced by specific immunotherapy and anti-IgE monoclonal antibodies that both interfere with IgE-mediated allergen presentation. Copyright (c) 2006 S. Karger AG, Basel.	Univ Utrecht, Med Ctr, Dept Dermatol & Allergol, NL-3584 CX Utrecht, Netherlands; Bioceros BV, Utrecht, Netherlands; ALK Abello AS, Dept Biol Allergy Res, Horsholm, Denmark	van Neerven, RJ (reprint author), Univ Utrecht, Med Ctr, Dept Dermatol & Allergol, Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands.	jneerven@umcutrecht.nl					ADKINSON NF, 1979, J IMMUNOL, V122, P965; Akdis CA, 1998, J CLIN INVEST, V102, P98, DOI 10.1172/JCI2250; Akdis CA, 1999, FASEB J, V13, P603; Ball T, 1999, EUR J IMMUNOL, V29, P2026, DOI 10.1002/(SICI)1521-4141(199906)29:06<2026::AID-IMMU2026>3.0.CO;2-2; Barata LT, 1998, J ALLERGY CLIN IMMUN, V101, P222; BEHRENS BL, 1984, AM REV RESPIR DIS, V130, P1134; BERNSTEIN IL, 1979, INT ARCH ALLER A IMM, V58, P30; BIEBER T, 1992, J EXP MED, V175, P1285, DOI 10.1084/jem.175.5.1285; Bolhaar STHP, 2004, CLIN EXP ALLERGY, V34, P761, DOI [10.1111/j.1365-2222.2004.1939.x, 10.1111/j.1365-2222.2004.01939.x]; BOUSQUET J, 1987, J ALLERGY CLIN IMMUN, V79, P947, DOI 10.1016/0091-6749(87)90245-4; Bousquet J, 1998, J ALLERGY CLIN IMMUN, V102, P558, DOI 10.1016/S0091-6749(98)70271-4; BUJANOWSKIWEBER J, 1989, IMMUNOLOGY, V66, P505; Carballido JM, 1997, EUR J IMMUNOL, V27, P515, DOI 10.1002/eji.1830270224; Casale TB, 2006, J ALLERGY CLIN IMMUN, V117, P134, DOI 10.1016/j.jaci.2005.09.036; CONNELL JT, 1970, J ALLERGY, V45, P115; Cooke RA, 1935, J EXP MED, V62, P733, DOI 10.1084/jem.62.6.733; CORRIGAN CJ, 1992, IMMUNOL TODAY, V13, P501, DOI 10.1016/0167-5699(92)90026-4; Coyle AJ, 1996, J EXP MED, V183, P1303, DOI 10.1084/jem.183.4.1303; DELARA JMT, 1994, ANN NY ACAD SCI, V725, P50; DELPRETE GF, 1993, EUR J IMMUNOL, V23, P1445, DOI 10.1002/eji.1830230707; Denepoux S, 2000, FEBS LETT, V465, P39, DOI 10.1016/S0014-5793(99)01703-2; Des RA, 1997, J ALLERGY CLIN IMMUN, V99, P450; DEUSCHL H, 1977, CLIN ALLERGY, V7, P315, DOI 10.1111/j.1365-2222.1977.tb01459.x; DEVEY ME, 1976, CLIN ALLERGY, V6, P227, DOI 10.1111/j.1365-2222.1976.tb01901.x; Djukanovic R, 2004, AM J RESP CRIT CARE, V170, P583, DOI 10.1164/rccm.200312-1651OC; DJURUP R, 1987, CLIN ALLERGY, V17, P459, DOI 10.1111/j.1365-2222.1987.tb02040.x; Durham SR, 1998, J ALLERGY CLIN IMMUN, V102, P157, DOI 10.1016/S0091-6749(98)70079-X; Durham SR, 1996, J ALLERGY CLIN IMMUN, V97, P1356, DOI 10.1016/S0091-6749(96)70205-1; Ebner C, 1997, CLIN EXP ALLERGY, V27, P1007, DOI 10.1111/j.1365-2222.1997.tb01252.x; Ejrnaes AM, 2006, CLIN EXP ALLERGY, V36, P273, DOI 10.1111/j.1365-2222.2006.02442.x; Ejrnaes AM, 2004, MOL IMMUNOL, V41, P471, DOI 10.1016/j.molimm.2004.04.018; Fahy JV, 1997, AM J RESP CRIT CARE, V155, P1828; Flicker S, 2003, INT ARCH ALLERGY IMM, V132, P13, DOI 10.1159/000073260; Francis JN, 2003, J ALLERGY CLIN IMMUN, V111, P1255, DOI 10.1067/mai.2003.1570; FREW AJ, 1988, J IMMUNOL, V141, P4158; FUJIWARA H, 1994, P NATL ACAD SCI USA, V91, P6835, DOI 10.1073/pnas.91.15.6835; FURIN MJ, 1991, J ALLERGY CLIN IMMUN, V88, P27, DOI 10.1016/0091-6749(91)90297-2; Getahun A, 2005, J IMMUNOL, V175, P1473; GLEICH G J, 1975, Clinical Allergy, V5, P79, DOI 10.1111/j.1365-2222.1975.tb01838.x; GOLDEN DBK, 1992, J ALLERGY CLIN IMMUN, V90, P386, DOI 10.1016/S0091-6749(05)80019-3; Gould HJ, 2003, ANNU REV IMMUNOL, V21, P579, DOI 10.1146/annurev.immunol.21.120601.141103; GUSTAVSSON S, 1994, J IMMUNOL, V152, P4793; Hamelmann E, 1997, AM J RESP CELL MOL, V16, P674; Hamid QA, 1997, J ALLERGY CLIN IMMUN, V99, P254, DOI 10.1016/S0091-6749(97)70106-4; Harris N, 1997, J EXP MED, V185, P177, DOI 10.1084/jem.185.1.177; Haselden BM, 1999, J EXP MED, V189, P1885, DOI 10.1084/jem.189.12.1885; Hauber HP, 2004, INT ARCH ALLERGY IMM, V134, P79, DOI 10.1159/000078384; HEYMAN B, 1993, EUR J IMMUNOL, V23, P1739, DOI 10.1002/eji.1830230754; Holgate S, 2005, J ALLERGY CLIN IMMUN, V115, P459, DOI 10.1016/j.jaci.2004.11.053; HUSSAIN R, 1992, J IMMUNOL, V148, P2731; Jacobsen L, 1997, ALLERGY, V52, P914, DOI 10.1111/j.1398-9995.1997.tb01251.x; JAROLIM E, 1990, J ALLERGY CLIN IMMUN, V85, P996, DOI 10.1016/0091-6749(90)90043-4; Jutel M, 2003, EUR J IMMUNOL, V33, P1205, DOI 10.1002/eji.200322919; JUTEL M, 1995, J IMMUNOL, V154, P4187; Kay AB, 2001, NEW ENGL J MED, V344, P30; Kay AB, 2001, NEW ENGL J MED, V344, P109; Keatings VM, 1997, J ALLERGY CLIN IMMUN, V99, P693, DOI 10.1016/S0091-6749(97)70032-0; KEHRY MR, 1989, P NATL ACAD SCI USA, V86, P7556, DOI 10.1073/pnas.86.19.7556; Kepley CL, 2000, J ALLERGY CLIN IMMUN, V106, P337, DOI 10.1067/mai.2000.107931; Krinzman SJ, 1996, J CLIN INVEST, V98, P2693, DOI 10.1172/JCI119093; Langeveld-Wildschut EG, 2000, J ALLERGY CLIN IMMUN, V105, P1008, DOI 10.1067/mai.2000.106544; Lantz CS, 1997, J IMMUNOL, V158, P2517; LARSEN JN, 2000, ALLERGY S, V55, P177; Leckie MJ, 2000, LANCET, V356, P2144, DOI 10.1016/S0140-6736(00)03496-6; Lessof M H, 1977, Monogr Allergy, V12, P253; LESSOF MH, 1978, JOHNS HOPKINS MED J, V142, P1; Leung Donald Y. 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Arch. Allergy Immunol.		2006	141	2					119	129		10.1159/000094714		11	Allergy; Immunology	Allergy; Immunology	086NC	WOS:000240679300004	16864979	
J	Brasel, TL; Martin, JM; Carriker, CG; Wilson, SC; Straus, DC				Brasel, TL; Martin, JM; Carriker, CG; Wilson, SC; Straus, DC			Detection of airborne Stachybotrys chartarum macrocyclic trichothecene mycotoxins in the indoor environment	APPLIED AND ENVIRONMENTAL MICROBIOLOGY			English	Article							SICK BUILDING SYNDROME; PULMONARY HEMOSIDEROSIS; SATRATOXIN-G; CONTAMINATION; EXPOSURE; FUNGI; MICE; ATRA; ANGUIDINE; SAMPLERS	The existence of airborne mycotoxins in mold-contaminated buildings has long been hypothesized to be a potential occupant health risk. However, little work has been done to demonstrate the presence of these compounds in such environments. The presence of airborne macrocyclic trichothecene mycotoxins in indoor environments with known Stachybotrys chartarum contamination was therefore investigated. In seven buildings, air was collected using a high-volume liquid impaction bioaerosol sampler (SpinCon PAS 450-10) under static or disturbed conditions. An additional building was sampled using an Andersen GPS-1 PUF sampler modified to separate and collect particulates smaller than conidia. Four control buildings (i.e., no detectable S. chartarum growth or history of water damage) and outdoor air were also tested. Samples were analyzed using a macrocyclic trichothecene-specific enzyme-linked immunosorbent assay (ELISA). ELISA specificity was tested using phosphate-buffered saline extracts of the fungal genera Aspergillus, Chaetomium, Cladosporium, Fusarium, Memnoniella, Penicillium, Rhizopus, and Trichoderma, five Stachybotrys strains, and the indoor air allergens Can f 1, Der p 1, and Fel d 1. For test buildings, the results showed that detectable toxin concentrations increased with the sampling time and short periods of air disturbance. Trichothecene values ranged from < 10 to > 1,300 pg/m(3) of sampled air. The control environments demonstrated statistically significantly (P < 0.001) lower levels of airborne trichothecenes. ELISA specificity experiments demonstrated a high specificity for the trichothecene-producing strain of S. chartarum. Our data indicate that airborne macrocyclic trichothecenes can exist in Stachybotrys-contaminated buildings, and this should be taken into consideration in future indoor air quality investigations.	Texas Tech Univ, Hlth Sci Ctr, Dept Microbiol & Immunol, Lubbock, TX 79430 USA	Straus, DC (reprint author), Texas Tech Univ, Hlth Sci Ctr, Dept Microbiol & Immunol, 3601 4th St, Lubbock, TX 79430 USA.	david.straus@ttuhsc.edu					Andersson MA, 1997, APPL ENVIRON MICROB, V63, P387; Barnes C, 2002, ANN ALLERG ASTHMA IM, V89, P29; Barnes C, 2000, ANN ALLERG ASTHMA IM, V84, P47, DOI 10.1016/S1081-1206(10)62740-8; BRASEL TL, 2004, APPL ENVIRON MICROB, V71, P114; Cage BR, 1996, ANN ALLERG ASTHMA IM, V77, P401; Chao H. 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G., 2002, Mycopathologia, V156, P119, DOI 10.1023/A:1022920205355; RAO CY, 2000, INDOOR AIR QUALITY H; Revankar SG, 2003, AM J MED SCI, V325, P262; Scheel CM, 2001, ARCH ENVIRON HEALTH, V56, P413; SCHICK MR, 1987, J IMMUNOL, V138, P3419; Shoeib M, 2002, ENVIRON SCI TECHNOL, V36, P4142, DOI 10.1021/es020635t; SMORAGIEWICZ W, 1993, INT ARCH OCC ENV HEA, V65, P113, DOI 10.1007/BF00405729; SORENSON WG, 1987, APPL ENVIRON MICROB, V53, P1370; Germaine G., 1996, IDENTIFYING FILAMENT; Sutton D. A., 1998, GUIDE CLIN SIGNIFICA; Tuomi T, 1998, ANALYST, V123, P1835, DOI 10.1039/a803813i; Wannemacher R, 1997, TXB MILITARY MED 1, P655; Wilkins CK, 1998, PHARMACOL TOXICOL, V83, P112; Wilson SC, 2004, J OCCUP ENVIRON HYG, V1, P442, DOI 10.1080/15459620490462823	50	71	72	1	18	AMER SOC MICROBIOLOGY	WASHINGTON	1752 N ST NW, WASHINGTON, DC 20036-2904 USA	0099-2240			APPL ENVIRON MICROB	Appl. Environ. Microbiol.	NOV	2005	71	11					7376	7388		10.1128/AEM.71.11.7376-7388.2005		13	Biotechnology & Applied Microbiology; Microbiology	Biotechnology & Applied Microbiology; Microbiology	983IN	WOS:000233225000111	16269780	
J	Fang, ZG; Ouyang, ZY; Hu, LF; Wang, XK; Zheng, H; Lin, XQ				Fang, ZG; Ouyang, ZY; Hu, LF; Wang, XK; Zheng, H; Lin, XQ			Culturable airborne fungi in outdoor environments in Beijing, China	SCIENCE OF THE TOTAL ENVIRONMENT			English	Article						culturable airborne fungi; bioaerosol; aerobiology; size distribution pattern	CONTROL CHILDREN; INDOOR AIR; BIOAEROSOLS; RESIDENCES; BUILDINGS; ALLERGENS; MICROBES; STATIONS; ASTHMA	Airborne fungi are being proposed as a cause of adverse health effects. They may adversely affect human health through allergy, infection, and toxicity. Moreover, they have a great influence on urban air quality in Beijing. In this study, a systematical survey on the culturable airborne fungi was carried out for I year in Beijing urban area. Fungal samples were collected for 3 min, three times each day, and continued for three consecutive days of each month with FA-1 sampler from three sampling sites. Results showed that the culturable fungal concentrations ranged from 24 CFU (Colony forming units) /m(3) to 13960 CFU/m(3), and the mean and median was 1165 CFU/m(3) and 710 CFU/m(3), respectively. Fungal concentrations in the greener area around the Research Center for Eco-Environmental Sciences (RCEES) and Beijing Botanical Garden (BBG) were significantly higher than in the densely urban and highly trafficked area of Xizhimen (XZM) (***P < 0.001), but no significant difference was found between RCEES and BBG (P > 0.05). The variation of fungal concentrations in different seasons was significant in RCEES and BBG, where the concentrations were higher in Summer and Autumn, and lower in Spring and Winter. However, there were no significant differences in fungal concentrations between the Spring and the Winter for three sampling sites (P > 0.05). Fourteen genera, including 40 species of culturable fungi, were identified in this study. Penicillium, with the most abundant species, which comprised more than 50% of the total isolated fungal species. Cladosporium were the most dominant fungal group, and contributed to more than one third of the total fungal concentration, followed by non-sporing isolates, Alternaria, Pencillium and Asperigillus. The concentration percentage of Cladosporium was significantly higher in RCEES than in XZM (*P < 0.05), and the concentration percentages of Penicillium (**P < 0.01) and Aspergillus (*P < 0.05) were higher in XZM than in RCEES and in BBG. For other groups' concentration percentages, no significant differences were observed among the sampling sites.	Chinese Acad Sci, Key Lab Syst Ecol, Res Ctr Ecoenvironm Sci, Beijing 100085, Peoples R China; Hunan Agr Univ, Coll Biosafety Sci & Technol, Changsha 410128, Peoples R China	Ouyang, ZY (reprint author), Chinese Acad Sci, Key Lab Syst Ecol, Res Ctr Ecoenvironm Sci, POB 2871, Beijing 100085, Peoples R China.	zyouyang@mail.rcees.ac.cn					Adhikari A, 2004, SCI TOTAL ENVIRON, V326, P123, DOI 10.1016/j.scitotenv.2003.12.007; Al-Suwaine A. 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Total Environ.	NOV 1	2005	350	1-3					47	58		10.1016/j.scitotenv.2005.01.032		12	Environmental Sciences	Environmental Sciences & Ecology	983IQ	WOS:000233225300005	16227072	
J	Arruda, LK; Sole, D; Baena-Cagnani, CE; Naspitz, CK				Arruda, LK; Sole, D; Baena-Cagnani, CE; Naspitz, CK			Risk factors for asthma and atopy	CURRENT OPINION IN ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						allergen sensitization; asthma; gene-environment interactions; respiratory viral infections; risk factors for asthma	CHILDHOOD ASTHMA; SEX-DIFFERENCES; BRONCHIAL HYPERRESPONSIVENESS; ALLERGIC RHINITIS; INDOOR ALLERGENS; VIRAL-INFECTIONS; MATERNAL SMOKING; IMMUNOGLOBULIN-E; BIRTH COHORT; BREAST-MILK	Purpose of review The aim of this article is to provide information on risk factors associated with the development of atopy and asthma in childhood. Recent findings Several gene polymorphisms have been associated with susceptibility to asthma and allergy; complex gene-environmental interactions, however, appear to play a key role in the development of the disease. Early life sensitization to aeroallergens, presence of atopic dermatitis or allergic rhinitis, maternal smoking during pregnancy and children's environmental exposure to tobacco smoke, lower respiratory tract infections with respiratory syncytial virus and potentially with other viruses including rhinovirus and metapneumovirus, exposure to air pollutants, several perinatal factors other than maternal smoking, are among factors associated with an increased risk for development of chronic asthma. Summary The prevalence of asthma and allergic diseases is increasing progressively. Those who are involved in the care of young children should be prepared to recognize risk factors for development of these diseases and to appreciate the role of gene-environment interactions. Preventive measures established at an early age may modify the natural history of asthma and other allergic diseases.	Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Internal Med, Div Clin Immunol, Sao Paulo, Brazil; Univ Fed Sao Paulo, Div Pediat Allergy Immunol & Rheumatol, Paulista Sch Med, Sao Paulo, Brazil; Catholic Univ Cordoba, Cordoba, Argentina	Arruda, LK (reprint author), USP, Fac Med Ribeirao Preto, Dept Clin Med, Av Bandeirantes 3900, BR-14049900 Ribeirao Preto, Brazil.	karla@fmrp.usp.br	Arruda, L. Karla /D-5845-2013; Sole, Dirceu/D-7789-2013	Arruda, L. 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Opin. Allergy Clin. Immunol.	APR	2005	5	2					153	159		10.1097/01.all.0000162308.89857.6c		7	Allergy; Immunology	Allergy; Immunology	970GJ	WOS:000232293000008	15764906	
J	Reibman, J; Lin, S; Hwang, SAA; Gulati, M; Bowers, JA; Rogers, L; Berger, KI; Hoerning, A; Gomez, M; Fitzgerald, EF				Reibman, J; Lin, S; Hwang, SAA; Gulati, M; Bowers, JA; Rogers, L; Berger, KI; Hoerning, A; Gomez, M; Fitzgerald, EF			The World Trade Center residents' respiratory health study: New-onset respiratory symptoms and pulmonary function	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; environmental; disasters; environmental hazards; reactive airways dysfunction; World Trade Center	AIRWAYS DYSFUNCTION SYNDROME; FINE PARTICULATE MATTER; PERSISTENT ASTHMA; LOWER MANHATTAN; SYNDROME RADS; QUESTIONNAIRE; FIREFIGHTERS; SEPTEMBER-11; GUIDELINES; VALIDITY	The destruction of the World Trade Center (WTC) on 11 September 2001 in New York City resulted in the massive release of pulverized dust and combustion products. The dust and smoke settled in the surrounding area, which encompassed a large residential community. We hypothesized that previously normal residents in the community surrounding the former WTC would have an increased incidence of persistent respiratory symptoms and abnormalities in screening spirometry. A hybrid cross-sectional and retrospective cohort study using a symptom-based questionnaire and onsite screening spirometry in residents in an exposed area and in a control area was performed 12 +/- 4 months after the collapse. Surveys were analyzed from 2,812 residents. New-onset respiratory symptoms were described by 55.8% of residents in the exposed area, compared with 20.1% in the control area after the event. Persistent new-onset symptoms were identified in 26.4 versus 7.5% of residents in the exposed area versus control area, respectively. No differences in screening spirometry between the groups were detected. A small pilot study suggested the possibility of an increase in bronchial hyperresponsiveness in exposed participants with persistent symptoms. The data demonstrate an increased rate of new-onset and persistent respiratory health effects in residents near the former WTC compared with a control population.	NYU, Sch Med, Dept Med, Div Pulm & Crit Care Med, New York, NY 10016 USA; New York State Dept Hlth, Albany, NY USA	Reibman, J (reprint author), NYU, Sch Med, Dept Med, Div Pulm & Crit Care Med, 550 1st Ave,Room NB7N24, New York, NY 10016 USA.	reibmj01@gcrc.med.nyu.edu	Fitzgerald, Edward/F-4087-2010	Lin, Shao/0000-0002-5535-7504	NCRR NIH HHS [M01RR00096]; NIEHS NIH HHS [P30 ES00260]; ODCDC CDC HHS [U1Q/CCU221059]		ABRAMSON MJ, 1991, J ASTHMA, V28, P129, DOI 10.3109/02770909109082737; Alberts WM, 1996, CHEST, V109, P1618, DOI 10.1378/chest.109.6.1618; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Banauch GI, 2003, AM J RESP CRIT CARE, V168, P54, DOI 10.1164/rccm.200211-1329OC; Bardana EJ, 1999, ANN ALLERG ASTHMA IM, V83, P583, DOI 10.1016/S1081-1206(10)62876-1; BROOKS S, 1998, ENV OCCUPATIONAL MED, P481; 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, 1989, EUR RESPIR J, V2, P940; CHANYEUNG M, 1994, AM J RESP CRIT CARE, V149, P1676; Crapo RO, 2000, AM J RESP CRIT CARE, V161, P309; Demeter SL, 2001, SCI TOTAL ENVIRON, V270, P49, DOI 10.1016/S0048-9697(00)00786-5; Fagan J, 2003, PSYCHOSOM MED, V65, P993, DOI 10.1097/01.PSY.0000097334.48556.5F; Fagan J, 2002, MMWR-MORBID MORTAL W, V51, P781; Feldman DM, 2004, CHEST, V125, P1256, DOI 10.1378/chest.125.4.1256; Gavett SH, 2003, ENVIRON HEALTH PERSP, V111, P981, DOI 10.1289/ehp.5931; Hankinson JL, 1999, AM J RESP CRIT CARE, V159, P179; KIPEN HM, 1994, J OCCUP ENVIRON MED, V36, P1133, DOI 10.1097/00043764-199410000-00017; Lioy PJ, 2002, ENVIRON HEALTH PERSP, V110, P703; McGee JK, 2003, ENVIRON HEALTH PERSP, V111, P972, DOI 10.1289/ehp.5930; *NAT HEART LUNG BL, 2002, NIH PUBL, V2; Offenberg JH, 2003, ENVIRON SCI TECHNOL, V37, P502, DOI 10.1021/es025730g; Payne JP, 2004, J OCCUP ENVIRON MED, V46, P420, DOI 10.1097/01.jom.0000126021.25149.64; Prezant DJ, 2002, NEW ENGL J MED, V347, P806, DOI 10.1056/NEJMoa021300; Ravault C, 2001, INT J TUBERC LUNG D, V5, P191; Service RF, 2003, SCIENCE, V301, P1649, DOI 10.1126/science.301.5640.1649; Stellman J.M., 1998, ENCY OCCUPATIONAL HL; *US CENS BUR, 2000, CENS 2000 RESP RAT D	28	71	73	3	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.	APR	2005	113	4					406	411				6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	913NO	WOS:000228158900038	15811830	
J	Tan, WC				Tan, WC			Viruses in asthma exacerbations	CURRENT OPINION IN PULMONARY MEDICINE			English	Article						exacerbations of asthma; viruses; epidemiology	RHINOVIRUS RESPIRATORY-INFECTIONS; EPITHELIAL-CELLS; INFLUENZA VACCINATION; TRACT INFECTION; INDUCED SPUTUM; ATOPIC ASTHMA; RISK-FACTORS; CHILDREN; LUNG; EXPRESSION	Purpose of review Respiratory viruses are well recognized as major triggers of acute exacerbations of asthma in children and adults, resulting in frequent outpatients visits and hospitalizations, Clinical and epidemiologic evidence supports this association. The application of molecular diagnostic methods has improved understanding of viral epidemiology and the pathophysiological mechanisms involved in viral induced acute asthma. This article reviews publications since October 2002 for an update of the role of viruses in exacerbations of asthma. Recent findings Respiratory viruses are present in most patients hospitalized for life-threatening asthma and acute nonlife-threatening asthma. Rhinovirus is the most common, but coinfection with other viruses may be important. Patients with asthma are not more susceptible to upper respiratory tract rhinovirus infections than healthy people but suffer from more severe consequences of the lower respiratory tract infection. Recent epidemiologic studies suggest that viruses provoke asthma attacks by additive or synergistic interactions with allergen exposure or with air pollution. An impaired antiviral immunity to rhinovirus may lead to impaired viral clearance and hence prolonged symptoms. Respiratory viral infections cause asthmatic exacerbations by triggering recruitment of T(H)2-type cells into the lungs, There is no specific antiviral strategy for prevention of respiratory-triggered asthma exacerbations, although clinical trials of potential antiviral agents are ongoing. Indirect prevention strategies focus on the reduction of overall airway inflammation to reduce the severity of the host response to respiratory viral infections. Summary Respiratory viral infections are a major cause of morbidity and mortality in asthma. There is a lack of specific antiviral strategies in the prevention or reduction of viral-triggered asthma exacerbations. Recent advances in understanding of the epidemiology and immunopathogenesis of respiratory viral infection in asthma provide opportunities or identification of specific targets for antiviral agents and strategies for management and prevention.	Natl Univ Singapore Hosp, Dept Med, Singapore 119074, Singapore	Tan, WC (reprint author), Natl Univ Singapore Hosp, Dept Med, Lower Kent Ridge Rd, Singapore 119074, Singapore.	mdctanwc@nus.edu.sg					ABRAMSON MJ, 1995, MED J AUSTRALIA, V163, P542; Akazawa Shiho, 2004, Nihon Kokyuki Gakkai Zasshi, V42, P353; Anzueto A, 2003, CHEST, V123, P1664, DOI 10.1378/chest.123.5.1664; Avila PC, 2000, J ALLERGY CLIN IMMUN, V105, P923, DOI 10.1067/mai.2000.106214; BIANCO A, 2002, MONALDI ARCH CHEST D, V7, P188; Bisgaard H, 2003, AM J RESP CRIT CARE, V167, P379, DOI 10.1164/rccm.200207-747OC; Bossios A, 2004, INT ARCH ALLERGY IMM, V134, P223, DOI 10.1159/000078769; Brooks GD, 2003, AM J RESP CRIT CARE, V168, P1091, DOI 10.1164/rccm.200306-737OC; Bueving HJ, 2004, AM J RESP CRIT CARE, V169, P488, DOI 10.1164/rccm.200309-1251OC; Camara AA, 2004, J ALLERGY CLIN IMMUN, V113, P551, DOI 10.1016/j.jaci.2003.11.027; Cates CJ, 2003, COCHRANE LIB; Chauhan AJ, 2003, LANCET, V361, P1939, DOI 10.1016/S0140-6736(03)13582-9; Corne JM, 2002, LANCET, V359, P831, DOI 10.1016/S0140-6736(02)07953-9; de Kluijver J, 2003, CLIN EXP ALLERGY, V33, P1415, DOI 10.1046/j.1365-2222.2003.01770.x; de Kluijver Josephine, 2003, American Journal of Respiratory and Critical Care Medicine, V168, P1174, DOI 10.1164/rccm.200212-1520OC; DOULL IJ, 2003, J PEDIAT S, V142, pS24; Doull IJM, 2003, J PEDIATR-US, V142, pS21, DOI 10.1067/mpd.2003.22; Duits LA, 2003, FEMS IMMUNOL MED MIC, V38, P59, DOI 10.1016/S0928-8244(03)00106-8; EMPEY DW, 1976, AM REV RESPIR DIS, V113, P131; Ferreira A, 2002, RESPIRATION, V69, P136, DOI 10.1159/000056316; Gern JE, 2003, J PEDIATR-US, V142, pS9, DOI 10.1067/mpd.2003.20; Gern JE, 2002, AM J MED, V112, p19S; Greenberg SB, 2003, ARCH INTERN MED, V163, P278, DOI 10.1001/archinte.163.3.278; Grunberg K, 1999, AM J RESP CRIT CARE, V160, P1375; Grunberg K, 2000, CLIN EXP ALLERGY, V30, P1015; Ieki K, 2004, CLIN EXP ALLERGY, V34, P745, DOI 10.1111/j.1365-2222.2004.01941.x; JOHNSTON SL, 1993, THORAX, V48, P1055; Johnston SL, 2003, AM J RESP CRIT CARE, V168, P1145, DOI 10.1164/rccm.2309004; JOHNSTON SL, 1995, BRIT MED J, V310, P1225; Kramarz P, 2000, VACCINE, V18, P2288, DOI 10.1016/S0264-410X(99)00551-4; Lemanske RF, 2003, CHEST, V123, p385S, DOI 10.1378/chest.123.3_suppl.385S-a; Lemanske RF, 2003, J PEDIATR-US, V142, pS3, DOI 10.1067/mpd.2003.19; LEMANSKE RF, 2003, J PEDIAT S, V142, pS7; Lemanske Robert F. 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J	Spahn, JD; Cherniack, R; Paull, K; Gelfand, EW				Spahn, JD; Cherniack, R; Paull, K; Gelfand, EW			Is forced expiratory volume in one second the best measure of severity in childhood asthma?	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Editorial Material							AIR-FLOW OBSTRUCTION; TO-MODERATE ASTHMA; LUNG-FUNCTION; INHALED CORTICOSTEROIDS; MANAGEMENT PROGRAM; CHILDREN; RESPONSIVENESS; BECLOMETHASONE; POPULATION; PLACEBO		Univ Colorado, Hlth Sci Ctr, Natl Jewish Med & Res Ctr, Denver, CO 80206 USA; Univ Colorado, Hlth Sci Ctr, Ira J & Jacqueline Neimark Lab Clin Pharmacol Ped, Denver, CO 80206 USA; Univ Colorado, Hlth Sci Ctr, Div Clin Pharmacol, Denver, CO 80206 USA; Univ Colorado, Hlth Sci Ctr, Div Pulm Med, Denver, CO 80206 USA; Univ Colorado, Hlth Sci Ctr, Dept Med & Allergy Clin Immunol, Denver, CO 80206 USA; Univ Colorado, Hlth Sci Ctr, Dept Pediat, Denver, CO 80206 USA	Spahn, JD (reprint author), Univ Colorado, Hlth Sci Ctr, Natl Jewish Med & Res Ctr, 1400 Jackson St, Denver, CO 80206 USA.	spahnj@njc.org					Bacharier LB, 2002, J ALLERGY CLIN IMMUN, V109, pS266, DOI 10.1016/S0091-6749(02)81946-7; BROWN PJ, 1984, THORAX, V39, P131, DOI 10.1136/thx.39.2.131; Covar RA, 2003, J PEDIATR-US, V142, P469, DOI 10.1067/mpd.2003.187; Fuhlbrigge AL, 2001, J ALLERGY CLIN IMMUN, V107, P61, DOI 10.1067/mai.2001.111590; Galant SP, 1996, ANN ALLERG ASTHMA IM, V77, P112; Jenkins HA, 2003, CHEST, V124, P1318, DOI 10.1378/chest.124.4.1318; Lange P, 1998, NEW ENGL J MED, V339, P1194, DOI 10.1056/NEJM199810223391703; Malmstrom K, 1999, ANN INTERN MED, V130, P487; MAROTTA A, 2003, J ALLERGY CLIN IMMUN, V112, P17; National Asthma Education and Prevention Program, 2002, NIH PUBL; [Anonymous], 2002, NIH PUBL, V01-4913; PEAT JK, 1987, EUR J RESPIR DIS, V70, P171; Rasmussen F, 2002, AM J RESP CRIT CARE, V165, P1480, DOI 10.1164/rccm.2108009; Sharek PJ, 2002, PEDIATRICS, V110, P797, DOI 10.1542/peds.110.4.797; Simons FER, 1997, NEW ENGL J MED, V337, P1659, DOI 10.1056/NEJM199712043372304; Szefler S, 2000, NEW ENGL J MED, V343, P1054; Szefler SJ, 2002, J ALLERGY CLIN IMMUN, V109, P410, DOI 10.1067/mai.2002.122635; Ulrik CS, 1999, EUR RESPIR J, V14, P892, DOI 10.1034/j.1399-3003.1999.14d27.x; VANESSENZANDVLIET EE, 1992, AM REV RESPIR DIS, V146, P547; Weiss ST, 2000, AM J RESP CRIT CARE, V162, P50; Zeiger RS, 1999, J ALLERGY CLIN IMMUN, V103, P376, DOI 10.1016/S0091-6749(99)70460-4	21	71	74	0	0	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	APR 1	2004	169	7					784	786		10.1164/rccm.200309-1234OE		3	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	807IB	WOS:000220494100006	14754761	
J	Eisenbarth, SC; Piggott, DA; Bottomly, K				Eisenbarth, SC; Piggott, DA; Bottomly, K			The master regulators of allergic inflammation: dendritic cells in Th2 sensitization	CURRENT OPINION IN IMMUNOLOGY			English	Review							T-HELPER-CELL; EOSINOPHILIC AIRWAY INFLAMMATION; TOLL-LIKE RECEPTORS; IN-VIVO; INHALED ANTIGEN; CUTTING EDGE; IMMUNE-RESPONSES; MURINE MODEL; TYPE-2 TH2; DIFFERENTIATION	The development of Th2 responses to inhaled proteins represents a malfunction of the adaptive immune system in that protein antigens are not microbial in nature and should not elicit an adaptive immune reaction. This derailing of the immune system may result from false alarms generated by the innate immune system, resulting in unexpected dendritic cell (DC) maturation after exposure to allergens. Conditions in the local microenvironment during DC maturation may also result in the preferential induction of Th2 responses. Recent progress has been made in our understanding of the role of DCs in both Th2 sensitization to aeroallergens and the regulation of Th2 and Th1 immunity.	Yale Univ, Dept Immunobiol, New Haven, CT 06510 USA	Eisenbarth, SC (reprint author), Yale Univ, Dept Immunobiol, 300 Cedar St, New Haven, CT 06510 USA.						Akira S, 2003, IMMUNOL LETT, V85, P85, DOI 10.1016/S0165-2478(02)00228-6; Arestides RSS, 2002, EUR J IMMUNOL, V32, P2874, DOI 10.1002/1521-4141(2002010)32:10<2874::AID-IMMU2874>3.0.CO;2-4; Barton GM, 2002, CURR OPIN IMMUNOL, V14, P380, DOI 10.1016/S0952-7915(02)00343-6; Becker S, 2002, AM J RESP CELL MOL, V27, P611, DOI 10.1165/rcmb.4868; Belladonna ML, 2002, J IMMUNOL, V168, P5448; Boonstra A, 2003, J EXP MED, V197, P101, DOI 10.1084/jem.20021908; Bozza S, 2002, J IMMUNOL, V168, P1362; Cyster JG, 1999, J EXP MED, V189, P447, DOI 10.1084/jem.189.3.447; d'Ostiani CF, 2000, J EXP MED, V191, P1661, DOI 10.1084/jem.191.10.1661; DABBAGH K, 2002, J IMMUNOL, V168, P4525; de Jong EC, 2002, J IMMUNOL, V168, P1704; De Smedt T, 2002, J IMMUNOL, V168, P661; Diehl S, 2002, MOL IMMUNOL, V39, P531, DOI 10.1016/S0161-5890(02)00210-9; Dodge IL, 2003, J IMMUNOL, V170, P4457; Drouin SM, 2002, J IMMUNOL, V169, P5926; Edwards AD, 2002, J IMMUNOL, V169, P3652; Eisenbarth SC, 2002, J EXP MED, V196, P1645, DOI 10.1084/jem.20021340; Fort MM, 2001, IMMUNITY, V15, P985, DOI 10.1016/S1074-7613(01)00243-6; Ghaemmaghami AM, 2002, CLIN EXP ALLERGY, V32, P1468, DOI 10.1046/j.1365-2745.2002.01504.x; Graffi SJ, 2002, CLIN IMMUNOL, V103, P176, DOI 10.1006/clim.2002.5190; Greenwald RJ, 2002, J IMMUNOL, V168, P991; Grewal IS, 1998, ANNU REV IMMUNOL, V16, P111, DOI 10.1146/annurev.immunol.16.1.111; Gutzmer R, 2002, J ALLERGY CLIN IMMUN, V109, P524, DOI 10.1067/mai.2002.121944; Hammad H, 2002, J IMMUNOL, V169, P1524; HOSHINO A, 2003, EUR J IMMUNOL, V33, P661; Hurst SD, 2002, J IMMUNOL, V169, P443; Idzko M, 2002, J ALLERGY CLIN IMMUN, V109, P839, DOI 10.1067/mai.2002.124044; Jahnsen FL, 2001, THORAX, V56, P823, DOI 10.1136/thorax.56.11.823; Jember AGH, 2001, J EXP MED, V193, P387, DOI 10.1084/jem.193.3.387; Julia V, 2002, IMMUNITY, V16, P271, DOI 10.1016/S1074-7613(02)00276-5; Kadowaki N, 2001, J EXP MED, V194, P863, DOI 10.1084/jem.194.6.863; Kalinski P, 1999, IMMUNOL TODAY, V20, P561, DOI 10.1016/S0167-5699(99)01547-9; KeaneMyers A, 1997, J IMMUNOL, V158, P2042; Lambrecht B N, 2001, Curr Opin Allergy Clin Immunol, V1, P51, DOI 10.1097/00130832-200102000-00010; Lambrecht BN, 2000, J CLIN INVEST, V106, P551, DOI 10.1172/JCI8107; Lambrecht BN, 1998, J IMMUNOL, V160, P4090; MacDonald AS, 2002, J IMMUNOL, V168, P4643; MacDonald AS, 2002, J IMMUNOL, V168, P537; Manickasingham SR, 2003, EUR J IMMUNOL, V33, P101, DOI 10.1002/immu.200390001; Masten BJ, 1999, J IMMUNOL, V162, P1310; Medzhitov R, 2000, NEW ENGL J MED, V343, P338; Pasare C, 2003, SCIENCE, V299, P1033, DOI 10.1126/science.1078231; Pflanz S, 2002, IMMUNITY, V16, P779, DOI 10.1016/S1074-7613(02)00324-2; Pulendran B, 1999, P NATL ACAD SCI USA, V96, P1036, DOI 10.1073/pnas.96.3.1036; Reider N, 2002, J ALLERGY CLIN IMMUN, V109, P89, DOI 10.1067/mai.2002.120556; Rissoan MC, 1999, SCIENCE, V283, P1183, DOI 10.1126/science.283.5405.1183; Shortman K, 2002, NAT REV IMMUNOL, V2, P151, DOI 10.1038/nri746; Soumelis V, 2002, NAT IMMUNOL, V3, P673, DOI 10.1038/ni805; Stumbles PA, 1998, J EXP MED, V188, P2019, DOI 10.1084/jem.188.11.2019; Takeda A, 2003, J IMMUNOL, V170, P4886; Tanaka H, 2000, J EXP MED, V192, P405, DOI 10.1084/jem.192.3.405; Trinchieri G, 2003, NAT REV IMMUNOL, V3, P133, DOI 10.1038/nri1001; Vieira PL, 2000, J IMMUNOL, V164, P4507; Whelan M, 2000, J IMMUNOL, V164, P6453; XIA WJ, 1995, J EXP MED, V181, P1275, DOI 10.1084/jem.181.4.1275	55	71	75	0	0	CURRENT BIOLOGY LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0952-7915			CURR OPIN IMMUNOL	Curr. Opin. Immunol.	DEC	2003	15	6					620	626		10.1016/j.coi.2003.09.003		7	Immunology	Immunology	748LB	WOS:000186862400005	14630194	
J	Al-Ghamdi, SM; Akbar, HO; Qari, YA; Fathaldin, OA; Al-Rashed, RS				Al-Ghamdi, SM; Akbar, HO; Qari, YA; Fathaldin, OA; Al-Rashed, RS			Pattern of admission to hospitals during muslim pilgrimage (Hajj)	SAUDI MEDICAL JOURNAL			English	Article							SAUDI-ARABIA; MENINGOCOCCAL DISEASE; AL-MUNAWARAH; HEATSTROKE; MANAGEMENT; OUTBREAK; MAKKAH	Objectives: The pattern of medical conditions necessitating admission differs according to the weather condition in that particular year. Previous studies had been conducted during the hot weather, none over the last 10 years, were carried out during, the milder weather we are experiencing. The aim of this study is to establish the pattern of admission during this mild weather and to elucidate the possible risk factors. Methods: A prospective study was performed in 4 hospitals in 2 different locations in Al-Mashaer, Kingdom of Saudi Arabia. Data were collected during one working shift in 2 hospitals in Arafat on the 9th of Dhul Hijjah 1422, corresponding to 21st of February 2002, and another working shift in 2 hospitals in Mina on the 10th of Dhul Hijjah 1422, corresponding to 22nd of February 2002. Results: A cohort of 76 patients from Arafat hospitals and 84 patients from Mina' hospitals were included (total 160 patients). Males constituted 62% and females 38% with the median age of 60 +/- 15years. The respiratory system was the most commonly affected (57%), followed by cardiovascular system (19.4%), and gastrointestinal tract (GIT) in 6.3% of cases. There were only 3 cases of heat-related admissions with only one confirmed case of heat stroke. Similarly, only one case of meningitis was confirmed in this cohort. Pneumonia was encountered in 63 cases (39.4%) and exacerbation of asthma and chronic obstructive pulmonary diseases (COPD) in 23 cases (14.4%). Pre-existing co-morbid medical conditions had included bronchial asthma and COPD (22.5%), hypertension (17.5%), and Diabetes mellitus (15%). Short-term follow up (24-48 hours) identified 2 deaths (1.3%), 94 patients (59%) were transferred to other secondary or tertiary care facilities and 64 (40%) were discharged home. Conclusion: Hospital admission during Hajj is related to old age and occurs in patients with associated co-morbid conditions. During this mild weather lower respiratory tract infections and exacerbation of bronchial asthma and COPD are the most commonly encountered diseases during Hajj.	King Abdulaziz Univ Hosp, Dept Med, Fac Med, Jeddah 80215, Saudi Arabia; King Saud Univ, Fac Med, Dept Med, Riyadh, Saudi Arabia	Al-Ghamdi, SM (reprint author), King Abdulaziz Univ Hosp, Dept Med, Fac Med, POB 80215, Jeddah 80215, Saudi Arabia.						Aguilera JF, 2002, EMERG INFECT DIS, V8, P761; ALASKA A, 1987, ANN SAUDI MED, V7, P135; ALASKA AK, 1987, LANCET, V1, P381; ALHARTHI SS, 1986, SAUDI MED J, V7, P369; El Bushra HE, 2000, EPIDEMIOL INFECT, V125, P555, DOI 10.1017/S0950268800004805; ELHASSAN OM, 1990, SAUDI MED J, V11, P290; GHAZNAWI HI, 1987, ANN SAUDI MED, V7, P323; GHAZNAWI HI, 1988, SAUDI MED J, V9, P274; KHOGALI M, 1983, INT J EPIDEMIOL, V12, P267, DOI 10.1093/ije/12.3.267; Memish ZA, 2002, SAUDI MED J, V23, P259; Memish ZA, 2002, CLIN INFECT DIS, V34, P84, DOI 10.1086/323403; MOORE PS, 1988, JAMA-J AM MED ASSOC, V260, P2686, DOI 10.1001/jama.260.18.2686; Rahman MM, 1999, ANN PLAS SURG, V43, P154; YAQUB BA, 1986, Q J MED, V59, P523; Yousuf M, 1995, ANN SAUDI MED, V15, P619	15	71	74	0	0	SAUDI MED J	RIYADH	ARMED FORCES HOSPITAL, PO BOX 7897,, RIYADH 11159, SAUDI ARABIA	0379-5284			SAUDI MED J	Saudi Med. J.	OCT	2003	24	10					1073	1076				4	Medicine, General & Internal	General & Internal Medicine	745BC	WOS:000186666500008	14578971	
J	Etzel, RA				Etzel, RA			How environmental exposures influence the development and exacerbation of asthma	PEDIATRICS			English	Article						asthma; indoor air pollution; outdoor air pollution	HOUSE-DUST MITE; OUTDOOR AIR-POLLUTION; EMERGENCY ROOM VISITS; CHILDHOOD ASTHMA; PASSIVE SMOKING; PULMONARY-FUNCTION; EPIDEMIC ASTHMA; RESPIRATORY HEALTH; NORMAL-CHILDREN; ORLEANS ASTHMA	Environmental exposures may increase a child's risk of developing asthma and also may increase the risk of asthma exacerbations. This article reviews several environmental exposures and suggests whether they contribute to asthma prevalence, asthma exacerbations, or both. Outdoor air exposures and violence are not likely to cause the increase in asthma prevalence. Exposure to outdoor air pollutants primarily leads to increased exacerbations, sometimes manifested as asthma clusters. Clinicians should be alert for space-time clusters of asthma exacerbations in the community, because these clusters may suggest a modifiable point-source exposure. Indoor air exposures are more strongly linked to the increase in asthma prevalence. Exposure to dust mites and tobacco smoke are risk factors for the development of asthma and may also exacerbate existing asthma. Effective measures to prevent exposures to these pollutants are available. With proper management, the amount of environmental exposures can be decreased. Whether decreasing these exposures will result in decreases in asthma prevalence and exacerbations is not yet documented.	George Washington Univ, Dept Environm & Occupat Hlth, Sch Publ Hlth & Hlth Serv, Washington, DC USA	Etzel, RA (reprint author), 4320 Diplomacy Dr,Ste 2630, Anchorage, AK 99508 USA.						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J	Andre, C; Perrin-Fayolle, M; Grosclaude, M; Couturier, P; Basset, D; Cornillon, J; Piperno, D; Girodet, B; Sanchez, R; Vallon, C; Bellier, P; Nasr, M				Andre, C; Perrin-Fayolle, M; Grosclaude, M; Couturier, P; Basset, D; Cornillon, J; Piperno, D; Girodet, B; Sanchez, R; Vallon, C; Bellier, P; Nasr, M			A double-blind placebo-controlled evaluation of sublingual immunotherapy with a standardized ragweed extract in patients with seasonal rhinitis - Evidence for a dose-response relationship	INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY			English	Article						sublingual-swallow immunotherapy; ragweed; seasonal rhinitis	HOUSE-DUST MITE; ALLERGIC RHINOCONJUNCTIVITIS; SWALLOW IMMUNOTHERAPY; CLINICAL EFFICACY; CONTROLLED TRIAL; POLLEN EXTRACT; CHILDREN; ASTHMA; SENSITIZATIONS	Background: There is a growing consensus on the benefits of sublingual-swallow immunotherapy in the treatment of allergic diseases. Methods: This randomized, double-blind placebo-controlled study was undertaken to assess the efficacy and safety of sublingual immunotherapy with standardized ragweed pollen extract tablets, in patients with an allergic rhinitis. A total of 110 outpatients were randomized (immunotherapy [I]: 55; placebo [P]: 55), of whom 99 were analyzable for efficacy (I: 48; P: 51) and 106 analyzable for safety (I: 53; P: 53). After a 28-day progression phase, the patients received a maintenance treatment during 6.5 months. Efficacy variables included a global assessment of efficacy (patient/investigator), symptoms and medication scores as well as the frequency of asthma attacks. Results: In the active treatment group, 43 patients completed the study, versus 49 on placebo. During the whole period of pollination, the difference favoring immunotherapy was highly significant for the global assessment by the patient (p = 0.004) and by the investigator (p = 0.005). Adverse reactions were reported more often in the active treatment but mild or moderate, and they abated after dose adjustment. A subgroup analysis of those patients receiving the highest dose of immunotherapy (3 tablets 3 times a week) showed a highly significant response for rhinitis and conjunctivitis total scores by comparison to lower dosages. Conclusion: This study confirms the efficacy and safety of sublingual immunotherapy and strongly suggests a dose-response relationship. Copyright (C) 2003 S. Karger AG, Basel	Stallergenes SA, Dept Sci & Med, F-92183 Antony, France; Ctr Hosp Lyon Sud, Dept Pneumol & Immunol Clin, Lyon, France; Clin Rhone Moyen, Grp Allergol & Immunol, Lyon, France; Grp Lyonnais Allergol, Lyon, France; PAROT, Ctr Med, Lyon, France	Andre, C (reprint author), Stallergenes SA, Dept Sci & Med, 6 Rue Alexis Tocqueville, F-92183 Antony, France.						Bousquet J, 1998, ALLERGY S, V53, P44; Bousquet J, 2001, J ALLERGY CLIN IMMUN, V108, P147, DOI DOI 10.1067/MAI.2001.118891; Clavel R, 1998, ALLERGY, V53, P493, DOI 10.1111/j.1398-9995.1998.tb04086.x; DesRoches A, 1997, J ALLERGY CLIN IMMUN, V99, P450, DOI 10.1016/S0091-6749(97)70069-1; Feliziani V, 1995, Allergol Immunopathol (Madr), V23, P224; GOLDEN DBK, 1981, J ALLERGY CLIN IMMUN, V67, P370, DOI 10.1016/0091-6749(81)90082-8; HAUGAARD L, 1993, J ALLERGY CLIN IMMUN, V91, P709, DOI 10.1016/0091-6749(93)90190-Q; JOHNSTONE D, 1961, PEDIATRICS, V27, P39; JOHNSTONE DE, 1957, AMA J DIS CHILD, V94, P1; KHINCHI MS, 2000, ALLERGY S, V55, P24; La Rosa M, 1999, J ALLERGY CLIN IMMUN, V104, P425, DOI 10.1016/S0091-6749(99)70388-X; Malling HJ, 1998, ALLERGY, V53, P461; Moller C, 2002, J ALLERGY CLIN IMMUN, V109, P251, DOI 10.1067/mai.2002.121317; Noirey N, 2000, J ALLERGY CLIN IMMUN, V105, P1194, DOI 10.1067/mai.2000.106545; Noon L, 1911, LANCET, V1, P1572; Pajno GB, 2001, CLIN EXP ALLERGY, V31, P1392, DOI 10.1046/j.1365-2222.2001.01161.x; SABBAH A, 1994, ALLERGY, V49, P309, DOI 10.1111/j.1398-9995.1994.tb02273.x; TROISE C, 1995, J INVEST ALLERG CLIN, V5, P25; Vourdas D, 1998, ALLERGY, V53, P662, DOI 10.1111/j.1398-9995.1998.tb03952.x	19	71	74	0	2	KARGER	BASEL	ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND	1018-2438			INT ARCH ALLERGY IMM	Int. Arch. Allergy Immunol.	JUN	2003	131	2					111	118		10.1159/000070926		8	Allergy; Immunology	Allergy; Immunology	696PG	WOS:000183894800006	12811019	
J	Chu, HW; Honour, JM; Rawlinson, CA; Harbeck, RJ; Martin, RJ				Chu, HW; Honour, JM; Rawlinson, CA; Harbeck, RJ; Martin, RJ			Effects of respiratory Mycoplasma pneumoniae infection on allerizen-induced bronchial hyperresponsiveness and lung inflammation in mice	INFECTION AND IMMUNITY			English	Article							HOUSE-DUST ENDOTOXIN; CHLAMYDIA-PNEUMONIAE; IMMUNE-RESPONSE; CHRONIC ASTHMA; MURINE MODEL; DISEASE; ADULTS; SENSITIZATION; CHILDREN; EXPOSURE	Airway mycoplasma infection may be associated with asthma pathophysiology. However, the direct effects of mycoplasma infection on asthma remain unknown. Using a murine allergic-asthma model, we evaluated the effects of different timing of airway Mycoplasma pneumoniae infection on bronchial hyperresponsiveness (BHR), lung inflammation, and the protein levels of Th1 (gamma interferon [IFN-gamma]) and Th2 (interleukin 4 [IL-4]) cytokines in bronchoalveolar lavage fluid. When mycoplasma infection occurred 3 days before allergen (ovalbumin) sensitization and challenge, the infection reduced the BHR and inflammatory-cell influx into the lung. This was accompanied by a significant induction of Th1 responses (increased IFN-gamma and decreased IL-4 production). Conversely, when mycoplasma infection occurred 2 days after allergen sensitization and challenge, the infection initially caused a temporary reduction of BHR and then increased BHR, lung inflammation, and IL-4 levels. Our data suggest that mycoplasma infection could modulate both physiological and immunological responses in the murine asthma model. Our animal models may also provide a new means to understand the role of infection in asthma pathogenesis and give evidence for the asthma hygiene hypothesis.	Natl Jewish Med & Res Ctr, Dept Med, Denver, CO 80206 USA; Univ Colorado, Hlth Sci Ctr, Denver, CO 80202 USA	Martin, RJ (reprint author), Natl Jewish Med & Res Ctr, Dept Med, 1400 Jackson St,Room B116, Denver, CO 80206 USA.						Busse WW, 2001, NEW ENGL J MED, V344, P350; Chan ED, 1999, CHEST, V115, P1188, DOI 10.1378/chest.115.4.1188; CIMOLAI N, 1992, MICROBIOL IMMUNOL, V36, P465; Cook PJ, 1998, THORAX, V53, P254; Dorigo-Zetsma JW, 2001, J CLIN MICROBIOL, V39, P1184, DOI 10.1128/JCM.39.3.1184-1186.2001; Esposito S, 2000, EUR RESPIR J, V16, P1142, DOI 10.1034/j.1399-3003.2000.16f21.x; Fayon M, 1999, ACTA PAEDIATR, V88, P1216, DOI 10.1080/080352599750030310; Ford JG, 2001, J IMMUNOL, V167, P1769; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; GIL JC, 1993, ANN ALLERGY, V70, P23; Hardy RD, 2002, INFECT IMMUN, V70, P649, DOI 10.1128/IAI.70.2.649-654.2002; Kalliomaki M, 2001, LANCET, V357, P1076, DOI 10.1016/S0140-6736(00)04259-8; Koh YI, 2001, J CLIN IMMUNOL, V21, P51, DOI 10.1023/A:1006745116360; Kraft M, 1998, AM J RESP CRIT CARE, V158, P998; Kraft M, 2002, CHEST, V121, P1782, DOI 10.1378/chest.121.6.1782; Kraft M, 2000, CLIN CHEST MED, V21, P301, DOI 10.1016/S0272-5231(05)70268-9; Martin RJ, 2001, AM J RESP CELL MOL, V24, P577; Martin RJ, 2001, J ALLERGY CLIN IMMUN, V107, P595; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Snedecor G. W., 1989, STAT METHODS, P177; Stampfli MR, 1998, CLIN EXP ALLERGY, V28, P1581; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Takeda K, 2001, AM J PHYSIOL-LUNG C, V281, pL394; Walzl G, 2000, J EXP MED, V192, P1317, DOI 10.1084/jem.192.9.1317; Yamamoto N, 2001, J VIROL, V75, P499, DOI 10.1128/JVI.75.1.499-505.2001; YANO T, 1994, AM J RESP CRIT CARE, V149, P1348	26	71	78	0	5	AMER SOC MICROBIOLOGY	WASHINGTON	1752 N ST NW, WASHINGTON, DC 20036-2904 USA	0019-9567			INFECT IMMUN	Infect. Immun.	MAR	2003	71	3					1520	1526		10.1128/IAI.71.3.1520-1526.2003		7	Immunology; Infectious Diseases	Immunology; Infectious Diseases	650NU	WOS:000181270900059	12595471	
J	Schuller, HM; Plummer, HK; Jull, BA				Schuller, HM; Plummer, HK; Jull, BA			Receptor-mediated effects of nicotine and its nitrosated derivative NNK on pulmonary neuroendocrine cells	ANATOMICAL RECORD PART A-DISCOVERIES IN MOLECULAR CELLULAR AND EVOLUTIONARY BIOLOGY			English	Article; Proceedings Paper	Experimental Biology 2002 Meeting	APR 20-24, 2002	NEW ORLEANS, LOUISIANA			PNEC; SCLC; alpha(7)nAChR; asthma; nicotine; NNK	TOBACCO-SPECIFIC CARCINOGEN; LUNG-CANCER; N-NITROSAMINES; NEUROEPITHELIAL BODIES; ACETYLCHOLINE-RECEPTOR; AIRWAY CHEMORECEPTORS; DNA METHYLATION; POINT MUTATIONS; CARBON-DIOXIDE; NEVER-SMOKERS	Pulmonary neuroendocrine cells (PNECs) have been implicated in the development of small cell lung carcinoma (SCLC) and pediatric asthma, and smoking is a risk factor for both diseases. We as well as others have shown that the alpha(7) nicotinic acetylcholine receptor (alpha(7) nAChR) regulates the release of 5-hydroxytryptamine (5-HT, serotonin) in PNECs and SCLC. Serotonin is an autocrine growth factor for PNECs and SCLC and acts as bronchoconstrictor. We found that nicotine and its nitrosated carcinogenic derivative 4.(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) bind to the alpha(7) nAChR in SCLC and PNECs, resulting in the influx of Ca2+, release of 5-HT, and activation of a mitogenic pathway mediated by protein kinase C (PKC), Raf-1, mitogen activated protein kinase (MAPK) and c-myc. Exposure to 10% CO2 acted synergistically. Unstimulated SCLC cells from smokers demonstrated high base levels of 5-HT release and of individual downstream signaling components in comparison to PNECs. Subchronic exposure of PNECs to NNK up-regulated the alpha(7) nAChR and its associated serotonergic mitogenic pathway in PNECs, an effect that may contribute to the development of SCLC in smokers and pediatric asthma in children of mothers who smoke. (C) 2003 Wiley-Liss, Inc.	Univ Tennessee, Coll Vet Med, Dept Pathol, Expt Oncol Lab, Knoxville, TN 37996 USA	Schuller, HM (reprint author), Univ Tennessee, Coll Vet Med, Dept Pathol, Expt Oncol Lab, 2407 River Dr, Knoxville, TN 37996 USA.						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Rec. Part A	JAN	2003	270A	1					51	58		10.1002/ar.a.10019		8	Anatomy & Morphology	Anatomy & Morphology	670ML	WOS:000182412500007	12494489	
J	Iwasaki, M; Nagata, K; Takano, S; Takahashi, K; Ishii, N; Ikezawa, Z				Iwasaki, M; Nagata, K; Takano, S; Takahashi, K; Ishii, N; Ikezawa, Z			Association of a new-type prostaglandin D2 receptor CRTH2 with circulating T helper 2 cells in patients with atopic dermatitis	JOURNAL OF INVESTIGATIVE DERMATOLOGY			English	Article						cell surface receptors; chemotaxis; flow cytometry; human; T lymphocyte subsets	LYMPHOCYTE-ASSOCIATED ANTIGEN; CHEMOKINE RECEPTORS; TH2 CELLS; IN-SITU; SELECTIVE EXPRESSION; CYTOKINE PATTERN; T-HELPER-2 CELLS; SURFACE-MOLECULE; HOMING RECEPTOR; HUMAN CD4(+)	Prostaglandin D-2 is known to be the major prostanoid produced by allergen-activated mast cells, but its role in the formation of allergic diseases is not well established because of complexity of its receptor system and lack of appropriate inhibitors. We have recently identified a new-type prostaglandin D2 receptor, named CRTH2. Studies with normal subjects have shown that CRTH2 appears to be selectively expressed by T helper 2 cells but not T helper 1 cells among circulating CD4(+) lymphocytes. The exact correlation between CRTH2 and T helper 2 cells in various disease settings and the impact of CRTH2-mediated prostaglandin D-2 activities on various T helper 2 responses in vivo still remain to be elucidated, however. In this study, we investigated the correlation between CRTH2 and T helper 2 cells among circulating CD4+ lymphocytes in normal adults and patients with atopic dermatitis, a T-helper-2-involving disease. The results showed that virtually all CRTH2(+)CD4(+) lymphocytes had a pure T helper 2 phenotype and formed not all but a large proportion of circulating T helper 2 cells for both normal and atopic dermatitis subjects. In chemotaxis assays, peripheral blood CRTH2(+)CD4(+) lymphocytes were significantly attracted by prostaglandin D2 as well as by a typical T-helper-2-attracting chemokine, thymus and activation regulated chemokine, whereas they showed little chemotactic migration toward typical T-helper-1-attracting chemokines, macrophage inflammatory protein 1beta and interferon-gamma inducible protein 10. Furthermore, in atopic dermatitis patients, a preferential increase of CRTH2(+) cells was noted within the disease-related cutaneous lymphocyte-associated antigen-positive, but not the cutaneous lymphocyte-associated antigen-negative, CD4(+) lymphocyte compartment. Our results suggest the involvement of the prostaglandin D-2/CRTH2 system in both normal and pathogenic T helper 2 responses.	BML, R&D Ctr, Kawagoe, Saitama 3501101, Japan; Toho Univ, Sch Med, Dept Biol Mol, Tokyo, Japan; Yokohama City Univ, Sch Med, Dept Dermatol, Kanagawa, Japan; Natl Inst Infect Dis, Leprosy Res Ctr, Dept Bioregulat, Tokyo, Japan	Nagata, K (reprint author), BML, R&D Ctr, 1361-1 Matoba, Kawagoe, Saitama 3501101, Japan.						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Invest. Dermatol.	SEP	2002	119	3					609	616		10.1046/j.1523-1747.2002.01862.x		8	Dermatology	Dermatology	592RV	WOS:000177951400010	12230502	
J	Herrick, CA; Xu, L; Wisnewski, AV; Das, J; Redlich, CA; Bottomly, K				Herrick, CA; Xu, L; Wisnewski, AV; Das, J; Redlich, CA; Bottomly, K			A novel mouse model of diisocyanate-induced asthma showing allergic-type inflammation in the lung after inhaled antigen challenge	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; diisocyanate; skin; airway; lung; eosinophils; T(H)2; IL-4; IL-13; IFN-gamma	HUMAN SERUM-ALBUMIN; TOLUENE DIISOCYANATE; OCCUPATIONAL ASTHMA; NONATOPIC ASTHMA; BRONCHIAL-MUCOSA; INTERFERON-GAMMA; EXPOSURE; WORKERS; IL-4; ISOCYANATES	Background: Exposure to diisocyanates, a group of highly reactive, low-molecular-weight compounds, is a major cause of occupational asthma. In contrast to mouse models of atopic asthma, previous mouse models of diisocyanate-induced asthma have failed to show lung inflammation with characteristics of human disease. Objective: Our goal was to establish a novel mouse model of diisocyanate-induced asthma in which lung inflammation reminiscent of that seen in human asthma is generated after inhaled antigen challenge. Methods: BALB/c mice were epicutaneously sensitized to hexamethylene diisocyanate (HDI) and then challenged with an HDI-protein conjugate administered by means of an intranasal droplet. Results: HDI sensitization resulted in development of contact hypersensitivity and HDI-specific antibody production. Most importantly, however, vigorous inflammatory responses with characteristics of human asthma were generated in the lung after inhaled HDI challenge. Challenge of sensitized, but not unsensitized, mice resulted in airway eosinophilia, mucus hypersecretion, and production of T(H)1-type (IFN-gamma) and T(H)2 type (IL-4, IL-5, and IL-13) cytokines by lung inflammatory cells. Despite the mixed T(H)1/T(H)2 response induced by HDI sensitization, use of cytokine-dericient mice revealed that airway eosinophilia was mediated by T(H)2 cytokines and not by IFN-gamma. Conclusion: We report a novel mouse model of diisocyanate-induced asthma that, in contrast to previous models, demonstrates antigen-induced lung inflammation with characteristics of human disease. This model will allow investigation of the immunopathogenesis of diisocyanate-induced asthma and should provide insight into this common form of occupational disease.	Yale Univ, Sch Med, Dept Dermatol, New Haven, CT 06520 USA; Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT 06520 USA; Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06520 USA	Herrick, CA (reprint author), Yale Univ, Sch Med, Dept Dermatol, 333 Cedar St,POB 208059, New Haven, CT 06520 USA.				NHLBI NIH HHS [R01-HL65209, R01 HL062622, P50-HL56389, R01 HL062622-01, R01-HL62622, R01 HL062622-02]; NIEHS NIH HHS [K24-ES00355]		Amin K, 2000, AM J RESP CRIT CARE, V162, P2295; BAUR X, 1984, J ALLERGY CLIN IMMUN, V73, P610, DOI 10.1016/0091-6749(84)90520-7; BENTLEY AM, 1992, J ALLERGY CLIN IMMUN, V89, P821, DOI 10.1016/0091-6749(92)90437-7; BENTLEY AM, 1994, J INVEST ALLERG CLIN, V4, P222; Bernstein JA, 1996, TOXICOLOGY, V111, P181, DOI 10.1016/0300-483X(96)03375-6; Busse WW, 2001, NEW ENGL J MED, V344, P350; CARTIER A, 1989, J ALLERGY CLIN IMMUN, V84, P507, DOI 10.1016/0091-6749(89)90364-3; CHANYEUNG M, 1995, NEW ENGL J MED, V333, P107, DOI 10.1056/NEJM199507133330207; Cohn L, 2001, J IMMUNOL, V166, P2760; Ebino K, 1999, INHAL TOXICOL, V11, P171, DOI 10.1080/089583799197131; FABBRI LM, 1987, AM REV RESPIR DIS, V136, P36; Herrick CA, 2000, J CLIN INVEST, V105, P765, DOI 10.1172/JCI8624; Hnizdo E, 2001, CLIN EXP ALLERGY, V31, P32, DOI 10.1046/j.1365-2222.2001.00981.x; Humbert M, 1996, AM J RESP CRIT CARE, V154, P1497; Lee Millina, 1998, Journal of Korean Medical Science, V13, P459; Lilly CM, 2001, AM J RESP CRIT CARE, V163, P1669; Lushniak BD, 1998, AM J IND MED, V33, P471, DOI 10.1002/(SICI)1097-0274(199805)33:5<471::AID-AJIM6>3.0.CO;2-V; Maestrelli P, 1997, CLIN EXP ALLERGY, V27, P1292; MAESTRELLI P, 1994, SCAND J WORK ENV HEA, V20, P376; Maestrelli P, 1997, CLIN EXP ALLERGY, V27, P47, DOI 10.1111/j.1365-2222.1997.tb01826.x; Matheson JM, 2001, CLIN EXP ALLERGY, V31, P1067, DOI 10.1046/j.1365-2222.2001.01125.x; PAGGIARO PL, 1994, EUR RESPIR J, V7, P761, DOI 10.1183/09031936.94.07040761; Park HS, 1999, J ALLERGY CLIN IMMUN, V104, P847; Petsonk EL, 2000, CHEST, V118, P1183, DOI 10.1378/chest.118.4.1183; RATTRAY NJ, 1994, TOXICOLOGY, V88, P15, DOI 10.1016/0300-483X(94)90108-2; Scheerens H, 1999, AM J RESP CRIT CARE, V159, P1074; Scheerens H, 1996, AM J RESP CRIT CARE, V154, P858; TSE KS, 1985, ALLERGY, V40, P314, DOI 10.1111/j.1398-9995.1985.tb00242.x; Vandebriel RJ, 2000, TOXICOL APPL PHARM, V162, P77, DOI 10.1006/taap.1999.8841; VANDENPLAS O, 1993, BRIT J IND MED, V50, P213; Wisnewski AV, 1999, AM J RESP CRIT CARE, V159, pA234	31	71	71	0	1	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	MAY	2002	109	5					873	878		10.1067/mai.2002.123533		6	Allergy; Immunology	Allergy; Immunology	553QW	WOS:000175687800020	11994714	
J	Vally, H; Thompson, PJ				Vally, H; Thompson, PJ			Role of sulfite additives in wine induced asthma: Single dose and cumulative dose studies	THORAX			English	Article						asthma; wine; sulfite additives	METABISULFITE-INDUCED BRONCHOCONSTRICTION; SODIUM METABISULFITE; CHALLENGE; RESPONSES	Background-Wine appears to be a significant trigger for asthma. Although sulfite additives have been implicated as a major cause of wine induced asthma, direct evidence is limited. Two studies were undertaken to assess sulfite reactivity in wine sensitive asthmatics. The first study assessed sensitivity to sulfites in wine using a single dose sulfited wine challenge protocol followed by a double blind, placebo controlled challenge. In the second study a cumulative dose sulfited wine challenge protocol was employe to establish if wine sensitive asthmatics as a group have an increased sensitivity to sulfites. Methods-In study 1, 24 asthmatic patients with a strong history of wine induced asthma were screened. Subjects showing positive responses to single blind high sulfite (300 ppm) wine challenge were rechallenged on separate days in a double blind, placebo controlled fashion with wines of varying sulfite levels to characterise their responses to these drinks. In study 2, wine sensitive asthmatic patients (n=12) and control asthmatics (n=6) were challenged cumulatively with wine containing increasing concentrations of sulfite in order to characterise further their sensitivity to sulfites in wine. Results-Four of the 24 self-reporting wine sensitive asthmatic patients were found to respond to sulfite additives in wine when challenged in a single dose fashion (study 1). In the double blind dose-response study all four had a significant fall in forced expiratory volume in one second (FEV) (> 15% from baseline) following exposure to wine containing 300 ppm sulfite, but did not respond to wines containing 20, 75 or 150 ppm sulfite. Responses were maximal at 5 minutes (mean (SD) maximal decline in FEV, 28.7 (13)%) and took 15-60 minutes to return to baseline levels. In the cumulative dose-response study (study 2) no significant difference was observed in any of the lung function parameters measured (FEV,, peak expiratory flow (PEF), mid phase forced expiratory flow (FEF25-75)) between wine sensitive and normal asthmatic subjects. Conclusions-Only a small number of wine sensitive asthmatic patients responded to a single dose challenge with sulfited wine under laboratory conditions. This may suggest that the role of sulfites and/or wine in triggering asthmatic responses has been overestimated. Alternatively, cofactors or other components in wine may play an important role in wine induced asthma. Cumulative sulfite dose challenges did not detect an increased sensitivity to sulfite in wine sensitive asthmatics and an alternative approach to identifying sulfite/wine sensitive asthma may be required.	Univ Western Australia, Dept Med, Perth, WA 6009, Australia; Asthma & Allergy Res Inst Inc, Perth, WA, Australia	Vally, H (reprint author), Sir Charles Gairdner Hosp, Asthma & Allergy Res Inst Inc, Ground Floor,E Block, Nedlands, WA 6009, Australia.						BAKER GJ, 1982, AUST NZ J MED, V12, P213; DAHL R, 1986, J ALLERGY CLIN IMMUN, V78, P1126, DOI 10.1016/0091-6749(86)90261-7; DELOHERY J, 1984, AM REV RESPIR DIS, V130, P1027; DIXON C M S, 1988, American Review of Respiratory Disease, V137, P238; GERSHWIN ME, 1985, J ALLERGY CLIN IMMUN, V75, P411, DOI 10.1016/0091-6749(85)90080-6; HALPERN GM, 1985, ANN ALLERGY, V55, P686; Lazarus SC, 1997, AM J RESP CRIT CARE, V156, P1725; MANSOUR E, 1992, J APPL PHYSIOL, V72, P1831; NICHOL GM, 1989, THORAX, V44, P1009, DOI 10.1136/thx.44.12.1009; NICHOL GM, 1990, AM REV RESPIR DIS, V142, P576; OCONNOR BJ, 1994, THORAX, V49, P307, DOI 10.1136/thx.49.4.307; PAVORD ID, 1994, EUR RESPIR J, V7, P50, DOI 10.1183/09031936.94.07010050; RANKINE B, 1962, AUST WINE BREW SPIRI, V80, P14; SAKAMOTO T, 1994, AM J RESP CRIT CARE, V149, P387; SEALE JP, 1988, ANN ALLERGY, V61, P209; SUN J, 1995, THORAX, V50, P875, DOI 10.1136/thx.50.8.875; Vally H, 2000, J ALLERGY CLIN IMMUN, V105, P462, DOI 10.1067/mai.2000.104548; Vally H, 1999, J ALLERGY CLIN IMMUN, V103, P41, DOI 10.1016/S0091-6749(99)70523-3; *W AUSTR FOOD MON, 1992, SULF DIOX FOODS; WALL PJ, 1998, USAGE SULFUR DIOXIDE; Wang M, 1996, THORAX, V51, P799, DOI 10.1136/thx.51.8.799; WRIGHT W, 1990, AM REV RESPIR DIS, V141, P1400	22	71	74	1	15	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	OCT	2001	56	10					763	769		10.1136/thorax.56.10.763		7	Respiratory System	Respiratory System	477NB	WOS:000171289100006	11562514	
J	Annesi-Maesano, I; Moreau, D; Strachan, D				Annesi-Maesano, I; Moreau, D; Strachan, D			In utero and perinatal complications preceding asthma	ALLERGY			English	Article						asthma; birth weight; family history; in utero; in utero exposure to smoking; labor; malpresentation of fetus; passive smoking; perinatal; pregnancy; risk factors; threatened labor	CHILDHOOD ASTHMA; RISK FACTOR; RESPIRATORY-DISEASE; BRONCHIAL-ASTHMA; PREGNANCY; BIRTH; EPIDEMIOLOGY; PREMATURITY; MORBIDITY; EXPOSURE	Background: It has been suggested that pregnancy and early life may influence the development of asthma in the offspring, but published studies have not carefully controlled for potential biases. Methods: In a large British birth cohort of 4065 natural children of 2583 mothers, we investigated whether in utero and perinatal influences contribute to the development and the severity of asthma in childhood, allowing for possible confounders of the relationship, and considering the nonindependence of familial data. Results: Child asthma (10.1%) was more frequently reported by mothers when there had been health complications during pregnancy (prevalence = 14.3%; adjusted odds ratio [ORadj] = 2.01; 95% confidence interval, 1.52-2.67), labor, or delivery (19.3%, ORadj = 1.35, 1.01-1.81); child illness or health complications during the first week of life (22.6%, ORadj = 1.35, 1.01-1.82); and birth weight of < 2.5 kg (7.0%, ORadj = 1.57, 1.10-2.25). Specific causes of health complications during pregnancy which significantly related to asthma were early or threatened labor (ICD: 644) (4.8%, ORadj = 1.58, 1.03-2.40) and the malposition or malpresentation of the fetus (ICD: 652) (1.6%, ORadj = 3.63, 1.47-8.91). Conclusions: The results provide further evidence that in utero and perinatal factors may increase the risk of developing asthma.	INSERM, U472, Dept Toxicol & Environm Epidemiol, Epidemiol & Biostat Unit, F-94807 Villejuif, France; Univ London St Georges Hosp, Sch Med, Dept Publ Hlth Sci, London SW17 0RE, England	Annesi-Maesano, I (reprint author), INSERM, U472, Dept Toxicol & Environm Epidemiol, Epidemiol & Biostat Unit, 16 Ave PV Couturier, F-94807 Villejuif, France.		Annesi-Maesano, Isabella/D-9173-2016				ANNESI I, 1994, REV MAL RESPIR, V11, P325; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; BAHNA SL, 1972, ACTA ALLERGOL, V27, P397, DOI 10.1111/j.1398-9995.1972.tb01439.x; BERTRAND JM, 1985, NEW ENGL J MED, V312, P742, DOI 10.1056/NEJM198503213121202; DOUCETTE JT, 1993, EPIDEMIOLOGY, V4, P143, DOI 10.1097/00001648-199303000-00010; Fergusson DM, 1997, CLIN EXP ALLERGY, V27, P1394, DOI 10.1046/j.1365-2222.1997.1430947.x; GLUCK JC, 1976, ANN ALLERGY, V37, P164; GORDON M, 1970, AM J OBSTET GYNECOL, V106, P421; HALKEN S, 1995, ALLERGY, V50, P97; HARLOW SD, 1989, AM J EPIDEMIOL, V129, P233; INFANTERIVARD C, 1995, EPIDEMIOLOGY, V6, P178, DOI 10.1097/00001648-199503000-00016; Jones CA, 1998, CLIN EXP ALLERGY, V28, P655; KELLY YJ, 1995, THORAX, V50, P525, DOI 10.1136/thx.50.5.525; Landau LI, 1996, PEDIATR PULM, V22, P314, DOI 10.1002/(SICI)1099-0496(199611)22:5<314::AID-PPUL4>3.0.CO;2-K; Langley-Evans S, 1997, CLIN EXP ALLERGY, V27, P1377, DOI 10.1046/j.1365-2222.1997.1690965.x; LAO TT, 1990, EUR J OBSTET GYN R B, V35, P1983; LIANG KY, 1986, BIOMETRIKA, V73, P13, DOI 10.1093/biomet/73.1.13; Oryszczyn MP, 1999, CLIN EXP ALLERGY, V29, P334; ORYSZCZYN MP, 1991, J ALLERGY CLIN IMMUN, V87, P1169, DOI 10.1016/0091-6749(91)92163-U; SALK L, 1974, AM J DIS CHILD, V127, P30; Schatz M, 1997, CLIN PERINATOL, V24, P407; SCHATZ M, 1995, AM J RESP CRIT CARE, V151, P1170; SCHATZ M, 1993, ALLERGY PRINCIPLES P, P1301; Schaubel D, 1996, J ASTHMA, V33, P255, DOI 10.3109/02770909609055366; Sears MR, 1997, LANCET, V350, P1015, DOI 10.1016/S0140-6736(97)01468-2; SILVERMAN M, 1993, THORAX, V48, P1200, DOI 10.1136/thx.48.12.1200; Stein RT, 1997, THORAX, V52, P946; Strachan DP, 1996, BRIT MED J, V312, P1195; STRACHAN DP, 1994, CLIN EXP ALLERGY, V24, P603, DOI 10.1111/j.1365-2222.1994.tb00961.x; Svanes C, 1998, EUR RESPIR J, V12, P1366, DOI 10.1183/09031936.98.12061366; SYUTKINA EV, 1995, CLIN DRUG INVEST, V9, P354, DOI 10.2165/00044011-199509060-00006; VanReempts PJ, 1996, AM J PERINAT, V13, P277, DOI 10.1055/s-2007-994342; VONMUTIUS E, 1993, J PEDIATR-US, V123, P223, DOI 10.1016/S0022-3476(05)81692-0	33	71	71	0	4	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	JUN	2001	56	6					491	497		10.1034/j.1398-9995.2001.056006491.x		7	Allergy; Immunology	Allergy; Immunology	443HR	WOS:000169336200005	11421892	
J	Wilson, DR; Nouri-Aria, KT; Walker, SM; Pajno, GB; O'Brien, F; Jacobson, MR; Mackay, IS; Durham, SR				Wilson, DR; Nouri-Aria, KT; Walker, SM; Pajno, GB; O'Brien, F; Jacobson, MR; Mackay, IS; Durham, SR			Grass pollen immunotherapy: Symptomatic improvement correlates with reductions in eosinophils and IL-5 mRNA expression in the nasal mucosa during the pollen season	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergic rhinitis; eosinophils; IL-5; immunotherapy	RECOMBINANT HUMAN INTERLEUKIN-5; NATURAL ALLERGEN EXPOSURE; COLONY-STIMULATING FACTOR; MESSENGER-RNA EXPRESSION; MAST-CELLS; TISSUE EOSINOPHILIA; INDUCED RHINITIS; HAY-FEVER; ASTHMA; INFLAMMATION	Background: Tissue eosinophilia and infiltration by T(H)2-type T tells are characteristic features of allergic rhinitis both after allergen challenge and during natural allergen exposure. Specific immunotherapy inhibits allergen-induced nasal eosinophilia. Objectives: We sought to assess, in the context of a randomized trial, the relationships between symptomatic improvement after immunotherapy and eosinophil numbers and IL-5 expression in the nasal mucosa during the pollen season. Methods: Nasal biopsy specimens were taken from 37 adults with severe summer hay fever at baseline (out of season) and at peak season after 2 years of treatment with a depot grass pollen extract or placebo. Biopsy specimens were processed for immunohistochemistry by using mAbs against eosinophils (EG2), T cells (CD3), and IL-2 receptor-positive cells (CD25), as well as for in situ hybridization by using a sulfur 35-labeled antisense riboprobe directed against IL-5. Results: Immunotherapy significantly reduced symptoms (49%, P = .01) and medication requirements (80%, P = .007) compared with placebo. There was a 400% increase (P = .004) in eosinophils during the pollen season in placebo-treated patients, which was inhibited in the immunotherapy group (20% increase, P = .04 between groups). Seasonal increases were also observed for CD25(+) cells (P = .002), CD3(+) cells (P = .02), and IL-5 mRNA-expressing cells (P = .03) in the placebo group but not in the immunotherapy group. A significant correlation was observed between eosinophils and IL-5 expression (r = 0.5, P < .05). Both eosinophils (r = 0.6, P < .02) and IL-5 (r = 0.6, P < .02) correlated with symptoms after immunotherapy. Conclusion: Improvement in symptoms after grass pollen immunotherapy may result, at least in part, from inhibition of IL-5-dependent tissue eosinophilia during the pollen season. Conclusion: Improvement in symptoms after grass pollen immunotherapy may result, at least in part, from inhibition of IL-5-dependent tissue eosinophilia during the pollen season.	Natl Heart & Lung Inst, Imperial Coll, Sch Med, Dept Upper Resp Med, London SW3 6LY, England	Durham, SR (reprint author), Natl Heart & Lung Inst, Imperial Coll, Sch Med, Dept Upper Resp Med, Dovehouse St, London SW3 6LY, England.		Walker, Samantha/B-9740-2013	Walker, Samantha/0000-0001-5503-8258; Jacobson, Mikila/0000-0002-2921-6169			Akdis CA, 1998, J CLIN INVEST, V102, P98, DOI 10.1172/JCI2250; BENTLEY AM, 1992, J ALLERGY CLIN IMMUN, V89, P877, DOI 10.1016/0091-6749(92)90444-7; Bousquet J., 1998, Allergy (Copenhagen), V53, P1; BROIDE DH, 1992, J CLIN INVEST, V90, P1414, DOI 10.1172/JCI116008; Cameron L, 2000, J IMMUNOL, V164, P1538; COLLINS PD, 1995, J EXP MED, V182, P1169, DOI 10.1084/jem.182.4.1169; DJURUP R, 1984, ALLERGY, V39, P472; Durham SR, 1999, CLIN EXP ALLERGY, V29, P1490; DURHAM SR, 1992, J IMMUNOL, V148, P2390; Durham SR, 1999, NEW ENGL J MED, V341, P468, DOI 10.1056/NEJM199908123410702; Durham SR, 1996, J ALLERGY CLIN IMMUN, V97, P1356, DOI 10.1016/S0091-6749(96)70205-1; FOKKENS W J, 1988, Rhinology (Utrecht), V26, P293; Foster PS, 1996, J EXP MED, V183, P195, DOI 10.1084/jem.183.1.195; Fujisawa T, 1997, INT ARCH ALLERGY IMM, V114, P81; FURIN MJ, 1991, J ALLERGY CLIN IMMUN, V88, P27, DOI 10.1016/0091-6749(91)90297-2; HAMID Q, 1991, J CLIN INVEST, V87, P1541, DOI 10.1172/JCI115166; HISAMATSU K, 1990, J ALLERGY CLIN IMMUN, V86, P52, DOI 10.1016/S0091-6749(05)80123-X; Ishihara K, 2000, INT ARCH ALLERGY IMM, V122, P36, DOI 10.1159/000053630; Kaminuma O, 1997, INT ARCH ALLERGY IMM, V114, P10; Kita H, 2000, J ALLERGY CLIN IMMUN, V106, P521, DOI 10.1067/mai.2000.108430; Leckie MJ, 2000, LANCET, V356, P2144, DOI 10.1016/S0140-6736(00)03496-6; LOPEZ AF, 1988, J EXP MED, V167, P219, DOI 10.1084/jem.167.1.219; Masuyama K, 1998, J ALLERGY CLIN IMMUN, V102, P610, DOI 10.1016/S0091-6749(98)70277-5; MOQBEL R, 1995, J IMMUNOL, V155, P4939; MOSMANN TR, 1986, J IMMUNOL, V136, P2348; Mould AW, 1997, J CLIN INVEST, V99, P1064, DOI 10.1172/JCI119234; Robinson DS, 1999, INT ARCH ALLERGY IMM, V118, P98, DOI 10.1159/000024039; Robinson DS, 1999, AM J RESP CELL MOL, V20, P9; Roboz G J, 1999, Curr Opin Hematol, V6, P164, DOI 10.1097/00062752-199905000-00007; Romagnani S, 1998, ALLERGY, V53, P12; ROTHENBERG ME, 1989, J IMMUNOL, V143, P2311; TERADA N, 1992, J ALLERGY CLIN IMMUN, V90, P160, DOI 10.1016/0091-6749(92)90067-C; VALENT P, 1994, J ALLERGY CLIN IMMUN, V94, P1177, DOI 10.1016/0091-6749(94)90329-8; VARNEY VA, 1992, AM REV RESPIR DIS, V146, P170; VARNEY VA, 1991, BRIT MED J, V302, P265; Walker C, 1998, J IMMUNOL, V161, P1962; WALKER SM, 1995, ALLERGY, V50, P405, DOI 10.1111/j.1398-9995.1995.tb01170.x; Walker SM, 2001, J ALLERGY CLIN IMMUN, V107, P87, DOI 10.1067/mai.2001.112027; WALSH GM, 1990, IMMUNOLOGY, V71, P258; WANG JM, 1989, EUR J IMMUNOL, V19, P701, DOI 10.1002/eji.1830190420; YING S, 1993, AM J RESP CELL MOL, V9, P356	41	71	74	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.	JUN	2001	107	6					971	976		10.1067/mai.2001.115483		6	Allergy; Immunology	Allergy; Immunology	445JR	WOS:000169454800006	11398073	
J	Arlian, LG; Neal, JS; Morgan, MS; Vyszenski-Moher, DL; Rapp, CM; Alexander, AK				Arlian, LG; Neal, JS; Morgan, MS; Vyszenski-Moher, DL; Rapp, CM; Alexander, AK			Reducing relative humidity is a practical way to control dust mites and their allergens in homes in temperate climates	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						house dust mites; relative humidity; dehumidification; allergen; Der p 1; Der f 1; dermatophagoides species	DERMATOPHAGOIDES-FARINAE ACARI; MECHANICAL VENTILATION; WATER-BALANCE; HOUSE; PYROGLYPHIDAE; AIR; PTERONYSSINUS; REDUCTION; PREVALENCE; EFFICACY	Background: Maintaining a relative humidity [RH) of less than 50% is one recommendation fur reducing numbers of house dust mites and their allergens in homes, Objective: The purpose of this study was to determine whether, in a humid temperate climate, indoor RH could be sufficiently lowered to control dust mites and their allergens. Methods: During a period spanning 2 humid summers (May 1998 to October 1999), dust mite and allergen densities were determined in 3 groups of homes. One group (low RH group, n = 23) maintained an RN of less than 51%, Most of these homes used a high-efficiency dehumidifier and air conditioning. A second group of homes (group A) used air conditioning only (n = 19) or air conditioning and dehumidification (n = 5) but did not maintain an RH of less than 51%, A third group of homes (group C, n = 24) controlled climate by opening windows and had an RH of greater than 51%. Normal housecleaning was maintained in all homes during the study, Results: The low RH group homes started in June with a mean +/- SE of 401 +/- 124 live mites and 17 +/- 3 mug of total Der 1 allergen per gram of dust. After 17 months of maintaining an RH of less than 51%, these declined significantly to 8 +/- 3 live mites per gram LP =.004) and 4 +/- 1 mug of Der 1 per gram of dust (P <.001). In contrast, group A and C homes exhibited seasonal peaks of 500 to 1000 mites and 40 to 70 <mu>g of Der 1 per gram of dust At all time points after the baseline sample, the low RH group homes had significantly less (P <.001) allergen than the group A and C homes, After 17 months, allergen levels were more than 10 Limes lo,Per in low Rfi homes compared with humid homes, Conclusion: This study showed that it is practical to maintain an indoor RH of less than 51% during the humid summer season in a temperate climate, and this resulted in significant reductions in mite and allergen levels.	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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Allergy Clin. Immunol.	JAN	2001	107	1					99	104		10.1067/mai.2001.112119		6	Allergy; Immunology	Allergy; Immunology	394PW	WOS:000166533300018	11149998	
J	Diaz-Sanchez, D; Jyrala, M; Ng, D; Nel, A; Saxon, A				Diaz-Sanchez, D; Jyrala, M; Ng, D; Nel, A; Saxon, A			In vivo nasal challenge with diesel exhaust particles enhances expression of the CC chemokines rantes, MIP-1 alpha, and MCP-3 in humans	CLINICAL IMMUNOLOGY			English	Article						diesel; pollution; chemokines; allergy; inflammation	IN-VIVO; MESSENGER-RNA; ALLERGIC INFLAMMATION; CYTOKINE PRODUCTION; MONONUCLEAR-CELLS; RAGWEED ALLERGEN; IGE PRODUCTION; RESPONSES; EOTAXIN; EOSINOPHILS	Diesel exhaust particles (DEP) enhance allergic inflammation by increasing in vivo IgE and cytokine production in the human upper respiratory mucosa. CC chemokines have been shown to play an important role in inflammation. We examined whether DEP could alter the production of CC chemokines by cells residing in the human nasal mucosa. At both 6 and 24 h following intranasal DEP challenge, the levels of nasal RANTES, MIP-1 alpha, and MCP-3 were significantly elevated compared to baseline. In contrast, DEP did not enhance levels of Eotaxin at any time, demonstrating that the action of DEP was not simply a global effect on all CC chemokines. Challenge with saline resulted in no significant change in expression of any chemokine at any time. Challenge with DEP also resulted in an increase in total cell counts in nasal lavage fluids. Increases in lymphocyte, monocyte/macrophage, and neutrophil cells were observed but there was no change in eosinophil cell numbers. In contrast, there was a significant enhancement of ECP protein levels in washes performed 6 to 24 h after DEP challenge. Elevated specific nasal chemokine expression following exposure to DEP likely participates in the inflammation, cellular infiltration, and increase in IgE observed in the absence of allergen. (C) 2000 Academic Press.	Univ Calif Los Angeles, Sch Med, Dept Med,Hart & Louise Lyon Lab, Div Clin Immunol Allergy, Los Angeles, CA 90095 USA; Univ Calif Los Angeles, Sch Med, Jonsson Comprehens Canc Ctr Inst, Los Angeles, CA 90095 USA; Univ Calif Los Angeles, Sch Med, Inst Mol Biol, Los Angeles, CA 90095 USA	Diaz-Sanchez, D (reprint author), Univ Calif Los Angeles, Sch Med, Dept Med,Hart & Louise Lyon Lab, Div Clin Immunol Allergy, Los Angeles, CA 90095 USA.		Nel, Andre/J-2808-2012		NIAID NIH HHS [AI-34567]		Alam R, 1997, J ALLERGY CLIN IMMUN, V99, P273, DOI 10.1016/S0091-6749(97)70042-3; ALAM R, 1992, J EXP MED, V176, P781, DOI 10.1084/jem.176.3.781; Bartels J, 1996, BIOCHEM BIOPH RES CO, V225, P1045, DOI 10.1006/bbrc.1996.1292; Bazan JF, 1997, NATURE, V385, P640, DOI 10.1038/385640a0; Berkman N, 1996, AM J RESP CRIT CARE, V154, P1804; BUSSE WW, 1993, AM REV RESPIR DIS, V147, pS20; Diaz-Sanchez D, 1999, CLIN IMMUNOL, V90, P313, DOI 10.1006/clim.1998.4676; Diaz-Sanchez D, 1999, J ALLERGY CLIN IMMUN, V104, P1183; DiazSanchez D, 1996, J ALLERGY CLIN IMMUN, V98, P114, DOI 10.1016/S0091-6749(96)70233-6; DIAZSANCHEZ D, 1994, J CLIN INVEST, V94, P1417, DOI 10.1172/JCI117478; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; Fahy O, 1999, J ALLERGY CLIN IMMUN, V103, P1115, DOI 10.1016/S0091-6749(99)70187-9; Gilmour MI, 1995, TOXICOLOGY, V105, P335, DOI 10.1016/0300-483X(95)03230-D; GRIFFITHSJOHNSON DA, 1993, BIOCHEM BIOPH RES CO, V197, P1167, DOI 10.1006/bbrc.1993.2599; Homey B, 1999, CURR OPIN IMMUNOL, V11, P626, DOI 10.1016/S0952-7915(99)00028-X; ISHIZAKI T, 1987, ANN ALLERGY, V58, P265; Kimata H, 1996, J EXP MED, V183, P2397, DOI 10.1084/jem.183.5.2397; Kita H, 1996, J EXP MED, V183, P2421, DOI 10.1084/jem.183.6.2421; Kramer U, 2000, EPIDEMIOLOGY, V11, P64, DOI 10.1097/00001648-200001000-00014; Lilly CM, 1997, J CLIN INVEST, V99, P1767, DOI 10.1172/JCI119341; MURANAKA M, 1986, J ALLERGY CLIN IMMUN, V79, P639; OPDENAKKER G, 1994, GENOMICS, V21, P403, DOI 10.1006/geno.1994.1283; OPPENHEIM JJ, 1991, ANNU REV IMMUNOL, V9, P617; Pasmans SGMA, 1996, J ALLERGY CLIN IMMUN, V98, P962, DOI 10.1016/S0091-6749(96)80013-3; PEDEN DB, 1995, AM J RESP CRIT CARE, V151, P1336; RUSZNAK C, 1994, ALLERGY, V49, P21, DOI 10.1111/j.1398-9995.1994.tb04234.x; Schroder JM, 1996, J LEUKOCYTE BIOL, V59, P1; SIM TC, 1995, AM J RESP CRIT CARE, V152, P927; TAKAFUJI S, 1987, J ALLERGY CLIN IMMUN, V79, P639, DOI 10.1016/S0091-6749(87)80161-6	29	71	73	1	2	ACADEMIC PRESS INC	SAN DIEGO	525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA	1521-6616			CLIN IMMUNOL	Clin. Immunol.	NOV	2000	97	2					140	145		10.1006/clim.2000.4921		6	Immunology	Immunology	375BX	WOS:000165380600008	11027454	
J	Nafstad, P; Magnus, P; Jaakkola, JJK				Nafstad, P; Magnus, P; Jaakkola, JJK			Risk of childhood asthma and allergic rhinitis in relation to pregnancy complications	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						pregnancy complications; prenatal conditions; asthma; allergic rhinitis; childhood	ATOPIC DISEASE; MATERNAL SMOKING; EARLY-LIFE; INFECTIONS; CHILDREN; ILLNESS; COHORT	Background: Events occurring during Fetal life may affect the development of the immune and respiratory systems and increase the risk of asthma and allergic diseases. Objectives: We sought to elaborate the relations between the occurrence of pregnancy complications and other pregnancy-related conditions and the risk of bronchial obstruction during the first 2 years of life and the occurrence of asthma and allergic rhinitis by the age of 4 years. Pregnancy complications were considered both as predictors of the health outcomes and as possible effects caused by other prenatal factors. Methods: A population-based, l-year, cohort study was carried out involving 2531 children horn in Oslo, Norway. We collected information on maternally related (hyperemesis, hypertension, and preeclampsia) and uterus-related complications in pregnancy (antepartum hemorrhage, preterm contractions, insufficient placenta, and restricted growth of the uterus) and the child's health and environmental exposures at birth and at 6, 12, 18, and 24 months and 4 years of age. The outcomes of interest were bronchial obstruction during the first 2 years and asthma and allergic rhinitis at the age of 4 years. Results: In a logistic regression analysis adjusting for potential confounders, uterus-related, but not other pregnancy-related, complications increased the risk of bronchial obstruction (odds ratio [OR], 2.1; 95% confidence interval [CI], 1,3-3.4), asthma (OR, 3.0; 95% CI, 1.8-5.4), and allergic rhinitis (OR, 2.9; 95% CI, 1.6-5.2). These relations were similar in children of atopic and nonatopic parents. Conclusions: Uterus-related complications in pregnancy increase the risk of having asthma and allergic rhinitis in childhood.	Natl Inst Publ Hlth, Dept Populat Hlth Sci, Epidemiol Sect, N-0403 Oslo, Norway; Nord Sch Publ Hlth, Gothenburg, Sweden	Nafstad, P (reprint author), Natl Inst Publ Hlth, Dept Populat Hlth Sci, Epidemiol Sect, POB 4404, N-0403 Oslo, Norway.		Jaakkola, Jouni/G-4314-2012				ABERG N, 1990, ACTA PAEDIATR SCAND, V79, P206, DOI 10.1111/j.1651-2227.1990.tb11440.x; BJORKSTEN B, 1994, ALLERGY, V49, P400, DOI 10.1111/j.1398-9995.1994.tb00831.x; Bjorksten B, 1999, J ALLERGY CLIN IMMUN, V104, P1119; Braback L, 1998, CLIN EXP ALLERGY, V28, P936; Fergusson DM, 1997, CLIN EXP ALLERGY, V27, P1394, DOI 10.1046/j.1365-2222.1997.1430947.x; *ISAAC STEER COMM, 1998, PHASE 2 MODULES INT; *ISAAC STEER COMM, 1993, ISAAC INT STUD ASTHM; Leadbitter P, 1999, THORAX, V54, P905; MARTINEZ FD, 1992, PEDIATRICS, V89, P21; Martinez FD, 1997, CIBA F SYMP, V206, P233; Nafstad P, 1999, PEDIATRICS, V103, P753, DOI 10.1542/peds.103.4.753; Nafstad P, 1996, EUR RESPIR J, V9, P2623, DOI 10.1183/09031936.96.09122623; Nafstad P, 1997, EPIDEMIOLOGY, V8, P293, DOI 10.1097/00001648-199705000-00011; Nafstad P, 2000, PEDIATRICS, V106, DOI 10.1542/peds.106.3.e38; NILSSON L, 1997, PEDIATR ALLERGY IMMU, V3, P134; Pekkanen J, 1999, ACTA PAEDIATR, V88, P710; Ponsonby AL, 1999, THORAX, V54, P664; Sears MR, 1997, LANCET, V350, P1015, DOI 10.1016/S0140-6736(97)01468-2; Stein R, 1999, LANCET, V354, P541, DOI 10.1016/S0140-6736(98)10321-5; Strachan DP, 1996, BRIT MED J, V312, P1195; Tariq SM, 1998, J ALLERGY CLIN IMMUN, V101, P587; Tomeo CA, 1999, EPIDEMIOLOGY, V10, P774, DOI 10.1097/00001648-199911000-00022; von Mutius E, 2000, J ALLERGY CLIN IMMUN, V105, P9, DOI 10.1016/S0091-6749(00)90171-4; von Mutius E, 1999, EUR RESPIR J, V14, P4, DOI 10.1034/j.1399-3003.1999.14a03.x; WEITZMAN M, 1990, PEDIATRICS, V85, P505; Xu B, 1999, ALLERGY, V54, P829, DOI 10.1034/j.1398-9995.1999.00117.x; Xu BZ, 1999, INT J EPIDEMIOL, V28, P723, DOI 10.1093/ije/28.4.723	27	71	72	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.	NOV	2000	106	5					867	873		10.1067/mai.2000.110558		7	Allergy; Immunology	Allergy; Immunology	417ZK	WOS:000167865200010	11080708	
J	Smith, CK; Moore, CA; Elahi, EN; Smart, ATS; Hotchkiss, SAM				Smith, CK; Moore, CA; Elahi, EN; Smart, ATS; Hotchkiss, SAM			Human skin absorption and metabolism of the contact allergens, cinnamic aldehyde, and cinnamic alcohol	TOXICOLOGY AND APPLIED PHARMACOLOGY			English	Article						cinnamic aldehyde; alcohol; acid; human; skin; metabolism; absorption; pyrazole; dehydrogenase; enzyme	GLUTATHIONE S-TRANSFERASES; DEHYDROGENASE GENE FAMILY; EUROPEAN STANDARD SERIES; PERCUTANEOUS-ABSORPTION; RAT SKIN; FRAGRANCE MATERIALS; BENZYL ACETATE; SENSITIZATION; DERMATITIS; CINNAMALDEHYDE	trans-Cinnamaldehyde and trans-cinnamic alcohol have been commonly reported to cause allergic contact dermatitis (ACD) in humans. Cinnamaldehyde is a more potent skin sensitizer than cinnamic alcohol. It has been hypothesized that cinnamic alcohol is a "prohapten" that requires metabolic activation, presumably by oxidoreductase enzymes such as alcohol dehydrogenase (ADH) or cytochrome P450 2E1 (CYP2E1), to the protein-reactive cinnamaldehyde (a hapten). In this study, the in vitro percutaneous absorption and metabolism of cinnamaldehyde and cinnamic alcohol (78 mu mol dose) has been examined using freshly excised, metabolically viable, full-thickness breast and abdomen skin from six female donors. Penetration rates and total cumulative recoveries of cinnamic compounds that were present in receptor fluid, extracted from within the skin, evaporated from the skin surface, or remained unabsorbed on the skin surface after 24 h were quantified by reversed-phase high-performance liquid chromatography. Biotransformation of cinnamaldehyde to both cinnamic alcohol and cinnamic acid was observed. Topically applied cinnamic alcohol was converted to cinnamaldehyde (found on the skin surface only) and cinnamic acid. To establish whether these biotransformations were enzymatic, experiments were performed in the absence and presence of varying concentrations (80-320 mu mol) of the ADH/CYP2E1 inhibitors pyrazole: or 4-methylpyrazole. The observation that pyrazole significantly reduced (p < 0.05) the total penetration of cinnamic metabolites into receptor fluid, following either cinnamaldehyde or cinnamic alcohol treatment, but did not significantly affect parent chemical penetration, suggests that we are measuring cutaneous metabolic products of ADH activity. The skin absorption and metabolism of cinnamaldehyde and cinnamic alcohol will play an important role in the manifestation of ACD following topical exposure to these compounds. (C) 2000 Academic Press.	Univ London Imperial Coll Sci Technol & Med, Sch Med, Div Biomed Sci, Sect Mol Toxicol, London SW7 2AZ, England	Smith, CK (reprint author), Univ London Imperial Coll Sci Technol & Med, Sch Med, Div Biomed Sci, Sect Mol Toxicol, Sir Alexander Fleming Bldg, London SW7 2AZ, England.						Albert M R, 1998, Am J Contact Dermat, V9, P207, DOI 10.1016/S1046-199X(98)90030-6; ASHCROFT JA, 1997, HUM EXP TOXICOL, V17, P400; Bangha E, 1996, DERMATOLOGY, V193, P17; Barry B. 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J	Szepfalusi, Z; Pichler, J; Elsasser, S; van Duren, K; Ebner, C; Bernaschek, G; Urbanek, R				Szepfalusi, Z; Pichler, J; Elsasser, S; van Duren, K; Ebner, C; Bernaschek, G; Urbanek, R			Transplacental priming of the human immune system with environmental allergens can occur early in gestation	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						cord blood cells; allergen; T-cell proliferation; diaplacentral transfer; sensitization	CELL PROLIFERATIVE RESPONSES; BLOOD MONONUCLEAR-CELLS; RESPIRATORY-TRACT; DENDRITIC CELLS; BIRCH-POLLEN; T-CELLS; ANTIGENS; MEMORY; IMMUNIZATION; TOLERANCE	Background: Allergen-specific T cells play an important role in the allergic immune response to various environmental allergens. In vitro studies have shown that T-cell responses to these allergens do occur prenatally. Some allergens (milk proteins) appear to lead more often to fetal T-cell priming than others (house dust mite allergen, ovalbumin, and birch and grass pollen allergens). Objective: We sought to determine the window of opportunity for prenatal T-cell priming with inhalant and nutritive allergens. Methods: The T-cell reactivity of cord blood cells derived through cordocentesis from unborn (n = 62) and term babies (n = 114) in response to inhalant allergens (birch pollen major allergen, recombinant Bet v 1, and timothy grass major allergen, recombinant Phl p 1) was investigated. Results: The results demonstrate that allergen-specific T-cell reactivity is as common in preterm as in term infants (Bet v 1, 8% and 5%, respectively; Phl p 1, 20% and 25%, respectively). Conclusions: Our data support the hypothesis that differential handling of the allergenic proteins by the feto-placental barrier and possibly by antigen-presenting cells may directly modulate the ensuing T-cell immune response.	Univ Vienna, AKH, Dept Pediat, A-1090 Vienna, Austria; Univ Vienna, Inst Gen & Expt Pathol, A-1090 Vienna, Austria; Univ Vienna, Dept Gynecol & Obstet, A-1090 Vienna, Austria	Szepfalusi, Z (reprint author), Univ Vienna, AKH, Dept Pediat, Wahringer Gurtel 18-20, A-1090 Vienna, Austria.						AASE JM, 1972, NEW ENGL J MED, V286, P1379, DOI 10.1056/NEJM197206292862603; BACH JF, 1978, DEFINITION IMMUNOLOG; BAKER CJ, 1988, NEW ENGL J MED, V319, P1180, DOI 10.1056/NEJM198811033191802; BJORKSTEN F, 1980, CLIN ALLERGY, V10, P585, DOI 10.1111/j.1365-2222.1980.tb02140.x; FERREIRA FD, 1993, J BIOL CHEM, V268, P19574; HAHNZORIC M, 1992, PEDIATR RES, V32, P150, DOI 10.1203/00006450-199208000-00005; Hara T, 1996, P NATL ACAD SCI USA, V93, P5136, DOI 10.1073/pnas.93.10.5136; Holt PG, 1990, PEDIATR ALLERGY IMMU, V1, P3, DOI 10.1111/j.1399-3038.1990.tb00002.x; Jones AC, 1996, PEDIATR ALLERGY IMMU, V7, P109, DOI 10.1111/j.1399-3038.1996.tb00117.x; Kondo N, 1998, CLIN EXP ALLERGY, V28, P1340; KONDO N, 1992, ARCH DIS CHILD, V67, P1003; Kopp MV, 2000, PEDIATR ALLERGY IMMU, V11, P4, DOI 10.1034/j.1399-3038.2000.00053.x; Malhotra I, 1997, J CLIN INVEST, V99, P1759, DOI 10.1172/JCI119340; Miles EA, 1996, CLIN EXP ALLERGY, V26, P780, DOI 10.1046/j.1365-2222.1996.d01-383.x; NELSON DJ, 1995, J IMMUNOL, V155, P3517; NELSON DJ, 1994, J EXP MED, V179, P203, DOI 10.1084/jem.179.1.203; PIASTRA M, 1994, INT ARCH ALLERGY IMM, V104, P358; PICINNI MP, 1993, INT ARCH ALLERGY IMM, V102, P301; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; Prescott SL, 1997, INT ARCH ALLERGY IMM, V113, P75; Prescott SL, 1998, J IMMUNOL, V160, P4730; RAWLE FC, 1984, J IMMUNOL, V133, P195; Ridge JP, 1996, SCIENCE, V271, P1723, DOI 10.1126/science.271.5256.1723; Singh RR, 1996, J EXP MED, V183, P1613, DOI 10.1084/jem.183.4.1613; Szepfalusi Z, 1997, CLIN EXP ALLERGY, V27, P28, DOI 10.1046/j.1365-2222.1997.d01-417.x; Szepfalusi Z, 1998, J ALLERGY CLIN IMMUN, V101, P514, DOI 10.1016/S0091-6749(98)70359-8; TANG MLK, 1994, LANCET, V344, P983, DOI 10.1016/S0140-6736(94)91641-1; Van Duren-Schmidt K, 1997, PEDIATR RES, V41, P1; WIERENGA EA, 1990, J IMMUNOL, V144, P4651; Yabuhara A, 1997, CLIN EXP ALLERGY, V27, P1261	30	71	74	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.	SEP	2000	106	3					530	536				7	Allergy; Immunology	Allergy; Immunology	356YN	WOS:000089471900017	10984374	
