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J	Akira, S; Uematsu, S; Takeuchi, O				Akira, S; Uematsu, S; Takeuchi, O			Pathogen recognition and innate immunity	CELL			English	Review							TOLL-LIKE RECEPTORS; NF-KAPPA-B; DOUBLE-STRANDED-RNA; PLASMACYTOID DENDRITIC CELLS; INTERFERON-ALPHA INDUCTION; IFN-BETA PROMOTER; HEPATITIS-C VIRUS; SIGNALING PATHWAY; RIG-I; ANTIVIRAL RESPONSE	Microorganisms that invade a vertebrate host are initially recognized by the innate immune system through germline-encoded pattern-recognition receptors (PRRs). Several classes of PRRs, including Toll-like receptors and cytoplasmic receptors, recognize distinct microbial components and directly activate immune cells. Exposure of immune cells to the ligands of these receptors activates intracellular signaling cascades that rapidly induce the expression of a variety of overlapping and unique genes involved in the inflammatory and immune responses. New insights into innate immunity are changing the way we think about pathogenesis and the treatment of infectious diseases, allergy, and autoimmunity.	Osaka Univ, Res Inst Microbial Dis, Dept Host Defense, Suita, Osaka 5650871, Japan; ERATO, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan	Akira, S (reprint author), Osaka Univ, Res Inst Microbial Dis, Dept Host Defense, 3-1 Yamadaoka, Suita, Osaka 5650871, Japan.	sakira@biken.osaka-u.ac.jp	Yang, Chen/G-1379-2010; Takeuchi, Osamu/D-6007-2011; Tang, Amy/L-3226-2016	Tang, Amy/0000-0002-5772-2878			Adachi K, 2001, J IMMUNOL, V167, P5928; Agrawal S, 2003, J IMMUNOL, V171, P4984; Ahmad-Nejad P, 2002, EUR J IMMUNOL, V32, P1958, DOI 10.1002/1521-4141(200207)32:7<1958::AID-IMMU1958>3.0.CO;2-U; Akira S, 2004, NAT REV IMMUNOL, V4, P499, DOI 10.1038/nri1391; Alexopoulou L, 2002, NAT MED, V8, P878, DOI 10.1038/nm732; Alexopoulou L, 2001, NATURE, V413, P732, DOI 10.1038/35099560; Andersen-Nissen E, 2005, P NATL ACAD SCI USA, V102, P9247, DOI 10.1073/pnas.0502040102; Andrejeva J, 2004, P NATL ACAD SCI USA, V101, P17264, DOI 10.1073/pnas.0407639101; Balachandran S, 2004, NATURE, V432, P401, DOI 10.1038/nature03124; 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Zhang DK, 2004, SCIENCE, V303, P1522, DOI 10.1126/science.1094351	141	5045	5354	157	1251	CELL PRESS	CAMBRIDGE	1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA	0092-8674			CELL	Cell	FEB 24	2006	124	4					783	801		10.1016/j.cell.2006.02.015		19	Biochemistry & Molecular Biology; Cell Biology	Biochemistry & Molecular Biology; Cell Biology	038RO	WOS:000237240900021	16497588	
J	Chen, WJ; Jin, WW; Hardegen, N; Lei, KJ; Li, L; Marinos, N; McGrady, G; Wahl, SM				Chen, WJ; Jin, WW; Hardegen, N; Lei, KJ; Li, L; Marinos, N; McGrady, G; Wahl, SM			Conversion of peripheral CD4(+)CD25(-) naive T cells to CD4(+)CD25(+) regulatory T cells by TGF-beta induction of transcription factor Foxp3	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article						anergy; IL-10; OVA TCR transgenic; house dust mite; asthma	GROWTH-FACTOR-BETA; IMMUNOLOGICAL SELF-TOLERANCE; ANTIGEN 4; ALLERGIC-ASTHMA; IN-VITRO; DISRUPTION; CTLA-4; MOUSE; IMMUNOSUPPRESSION; PROLIFERATION	CD4(+)CD25(+) regulatory T cells (T-reg) are instrumental in the maintenance of immunological tolerance. One critical question is whether T-reg can only be generated in the thymus or can differentiate from peripheral CD4(+)CD25(-) naive T cells. In this paper, we present novel evidence that conversion of naive peripheral CD4(+)CD25(-) T cells into anergic/suppressor cells that are CD25(+), CD45RB(-/low) and intracellular CTLA-4(+) can be achieved through costimulation with T cell receptors (TCRs) and transforming growth factor beta (TGF-beta). Although transcription factor Foxp3 has been shown recently to be associated with the development of T-reg, the physiological inducers for Foxp3 gene expression remain a mystery. TGF-beta induced Foxp3 gene expression in TCR-challenged CD4(+)CD25(-) naive T cells, which mediated their transition toward a regulatory T cell phenotype with potent immunosuppressive potential. These converted anergic/suppressor cells are not only unresponsive to TCR stimulation and produce neither T helper cell 1 nor T helper cell 2 cytokines but they also express TGF-beta and inhibit normal T cell proliferation in vitro. More importantly, in an ovalbumin peptide TCR transgenic adoptive transfer model, TGF-beta-converted transgenic CD4(+)CD25(+) suppressor cells proliferated in response to immunization and inhibited antigen-specific naive CD4(+) T cell expansion in vivo. Finally, in a murine asthma model, coadministration of these TGF-beta-induced suppressor T cells prevented house dust mite-induced allergic pathogenesis in lungs.	Natl Inst Dent & Craniofacial Res, Oral Infect & Immun Branch, Cellular Immunol Sect, NIH, Bethesda, MD 20892 USA	Chen, WJ (reprint author), Natl Inst Dent & Craniofacial Res, Oral Infect & Immun Branch, Cellular Immunol Sect, NIH, Bethesda, MD 20892 USA.		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Exp. Med.	DEC 15	2003	198	12					1875	1886		10.1084/jem.20030152		12	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	756CZ	WOS:000187449400012	14676299	
J	Bousquet, J; Khaltaev, N; Cruz, AA; Denburg, J; Fokkens, WJ; Togias, A; Zuberbier, T; Baena-Cagnani, CE; Canonica, GW; van Weel, C; Agache, I; Ait-Khaled, N; Bachert, C; Blaiss, MS; Bonini, S; Boulet, LP; Bousquet, PJ; Camargos, P; Carlsen, KH; Chen, Y; Custovic, A; Dahl, R; Demoly, P; Douagui, H; Durham, SR; van Wijk, RG; Kalayci, O; Kaliner, MA; Kim, YY; Kowalski, ML; Kuna, P; Le, LTT; Lemiere, C; Li, J; Lockey, RF; Mavale-Manuel, S; Meltzer, EO; Mohammad, Y; Mullol, J; Naclerio, R; Hehir, REO; Ohta, K; Ouedraogo, S; Palkonen, S; Papadopoulos, N; Passalacqua, G; Pawankar, R; Popov, TA; Rabe, KF; Rosado-Pinto, J; Scadding, GK; Simons, FER; Toskala, E; Valovirta, E; van Cauwenberge, P; Wang, DY; Wickman, M; Yawn, BP; Yorgancioglu, A; Yusuf, OM; Zar, H; Annesi-Maesano, I; Bateman, ED; Ben Kheder, A; Boakye, DA; Bouchard, J; Burney, P; Busse, WW; Chan-Yeung, M; Chavannes, NH; Chuchalin, A; Dolen, WK; Emuzyte, R; Grouse, L; Humbert, M; Jackson, C; Johnston, SL; Keith, PK; Kemp, JP; Klossek, JM; Larenas-Linnemann, D; Lipworth, B; Malo, JL; Marshall, GD; Naspitz, C; Nekam, K; Niggemann, B; Nizankowska-Mogilnicka, E; Okamoto, Y; Orru, MP; Potter, P; Price, D; Stoloff, SW; Vandenplas, O; Viegi, G; Williams, D				Bousquet, J.; Khaltaev, N.; Cruz, A. 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H.; Chuchalin, A.; Dolen, W. K.; Emuzyte, R.; Grouse, L.; Humbert, M.; Jackson, C.; Johnston, S. L.; Keith, P. K.; Kemp, J. P.; Klossek, J. -M.; Larenas-Linnemann, D.; Lipworth, B.; Malo, J. -L.; Marshall, G. D.; Naspitz, C.; Nekam, K.; Niggemann, B.; Nizankowska-Mogilnicka, E.; Okamoto, Y.; Orru, M. P.; Potter, P.; Price, D.; Stoloff, S. W.; Vandenplas, O.; Viegi, G.; Williams, D.			Allergic rhinitis and its impact on asthma (ARIA) 2008 update (in collaboration with the World Health Organization, GA(2)LEN and AllerGen)	ALLERGY			English	Review						ARIA; asthma; guideline; management; rhinitis	QUALITY-OF-LIFE; HOUSE-DUST-MITE; AQUEOUS NASAL SPRAY; PLACEBO-CONTROLLED TRIAL; SKIN-TEST REACTIVITY; COMMUNITY-RESPIRATORY-HEALTH; RANDOMIZED CONTROLLED-TRIAL; INTRANASAL FLUTICASONE PROPIONATE; NATURAL-RUBBER LATEX; LABORATORY-ANIMAL ALLERGY	Allergic rhinitis is a symptomatic disorder of the nose induced after allergen exposure by an IgE-mediated inflammation of the membranes lining the nose. It is a global health problem that causes major illness and disability worldwide. Over 600 million patients from all countries, all ethnic groups and of all ages suffer from allergic rhinitis. It affects social life, sleep, school and work and its economic impact is substantial. Risk factors for allergic rhinitis are well identified. Indoor and outdoor allergens as well as occupational agents cause rhinitis and other allergic diseases. The role of indoor and outdoor pollution is probably very important, but has yet to be fully understood both for the occurrence of the disease and its manifestations. In 1999, during the Allergic Rhinitis and its Impact on Asthma (ARIA) WHO workshop, the expert panel proposed a new classification for allergic rhinitis which was subdivided into 'intermittent' or 'persistent' disease. This classification is now validated. The diagnosis of allergic rhinitis is often quite easy, but in some cases it may cause problems and many patients are still under-diagnosed, often because they do not perceive the symptoms of rhinitis as a disease impairing their social life, school and work. The management of allergic rhinitis is well established and the ARIA expert panel based its recommendations on evidence using an extensive review of the literature available up to December 1999. The statements of evidence for the development of these guidelines followed WHO rules and were based on those of Shekelle et al. A large number of papers have been published since 2000 and are extensively reviewed in the 2008 Update using the same evidence-based system. Recommendations for the management of allergic rhinitis are similar in both the ARIA workshop report and the 2008 Update. In the future, the GRADE approach will be used, but is not yet available. Another important aspect of the ARIA guidelines was to consider co-morbidities. Both allergic rhinitis and asthma are systemic inflammatory conditions and often co-exist in the same patients. In the 2008 Update, these links have been confirmed. The ARIA document is not intended to be a standard-of-care document for individual countries. It is provided as a basis for physicians, health care professionals and organizations involved in the treatment of allergic rhinitis and asthma in various countries to facilitate the development of relevant local standard-of-care documents for patients.	[Bousquet, J.] Univ Hosp, Montpellier, France; [Demoly, P.] Hop Arnaud Villeneuve, INSERM, Univ Hosp Montpellier, U657, Montpellier, France; [Khaltaev, N.] GARD ARIA, Geneva, Switzerland; [Cruz, A. A.] Univ Fed Bahia, Sch Med, BR-41170290 Salvador, BA, Brazil; [Denburg, J.] McMaster Univ, AllerGen NCE, Hamilton, ON L8S 4L8, Canada; [Fokkens, W. J.] Univ Amsterdam, Acad Med Ctr, NL-1105 AZ Amsterdam, Netherlands; [Togias, A.] NIAID, Bethesda, MD 20892 USA; [Zuberbier, T.] Charite, Allergy Ctr Charite, D-13353 Berlin, Germany; [Baena-Cagnani, C. E.] WAO, Cordoba, Argentina; [Baena-Cagnani, C. E.] Catholic Univ Cordoba, Cordoba, Argentina; [Canonica, G. 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Immunology	Allergy; Immunology	271YZ	WOS:000253825900001	18331513	
J	Kalliomaki, M; Salminen, S; Arvilommi, H; Kero, P; Koskinen, P; Isolauri, E				Kalliomaki, M; Salminen, S; Arvilommi, H; Kero, P; Koskinen, P; Isolauri, E			Probiotics in primary prevention of atopic disease: a randomised placebo-controlled trial	LANCET			English	Article							GROWTH-FACTOR-BETA; ORAL TOLERANCE; 4 REGIONS; COW MILK; CHILDREN; DERMATITIS; ANTIGEN; CELLS; PREVALENCE; ALLERGY	Background Reversal of the progressive increase in frequency of atopic disease would be an important breakthrough for health care and wellbeing in western societies. In the hygiene hypothesis this increase is attributed to reduced microbial exposure in early life. Probiotics are cultures of potentially beneficial bacteria of the healthy gut microflora. We assessed the effect on atopic disease of Lactobacillus GG (which is safe at an early age and effective in treatment of allergic inflammation and food allergy). Methods In a double-blind, randomised placebo-controlled trial we gave Lactobacillus GG prenatally to mothers who had at least one first-degree relative (or partner) with atopic eczema. allergic rhinitis, or asthma, and postnatally for 6 months to their infants. Chronic recurring atopic eczema, which is the main sign of atopic disease in the first years of life, was the primary endpoint. Findings Atopic eczema was diagnosed in 46 of 132 (35%) children aged 2 years. Asthma was diagnosed in six of these children and allergic rhinitis in one. The frequency of atopic eczema in the probiotic group was half that of the placebo group (15/64 [23%] vs 31/68 [46%]; relative risk 0.51 [95% CI 0.32-0.84]). The number needed to treat was 4.5 (95% CI 2.6-15.6). Interpretations Lactobacillus GG was effective in prevention of early atopic disease in children at high risk. 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J	Bousquet, J; van Cauwenberge, P; Khaltaev, N; Ait-Khaled, N; Annesi-Maesano, I; Bachert, C; Baena-Cagnani, C; Bateman, E; Bonini, S; Canonica, GW; Carlsen, KH; Demoly, P; Durham, SR; Enarson, D; Fokkens, WJ; van Wijk, RG; Howarth, P; Ivanova, NA; Kemp, JP; Klossek, JM; Lockey, RF; Lund, V; Mackay, I; Malling, HJ; Meltzer, EO; Mygind, N; Okunda, M; Pawankar, R; Price, D; Scadding, GK; Simons, FER; Szczeklik, A; Valovirta, E; Vignola, AM; Wang, DY; Warner, JO; Weiss, KB				Bousquet, J; van Cauwenberge, P; Khaltaev, N; Ait-Khaled, N; Annesi-Maesano, I; Bachert, C; Baena-Cagnani, C; Bateman, E; Bonini, S; Canonica, GW; Carlsen, KH; Demoly, P; Durham, SR; Enarson, D; Fokkens, WJ; van Wijk, RG; Howarth, P; Ivanova, NA; Kemp, JP; Klossek, JM; Lockey, RF; Lund, V; Mackay, I; Malling, HJ; Meltzer, EO; Mygind, N; Okunda, M; Pawankar, R; Price, D; Scadding, GK; Simons, FER; Szczeklik, A; Valovirta, E; Vignola, AM; Wang, DY; Warner, JO; Weiss, KB		ARIA Workshop Grp	Allergic rhinitis and its impact on asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review							AQUEOUS NASAL SPRAY; HOUSE-DUST MITE; QUALITY-OF-LIFE; FC-EPSILON-RI; TORSADES-DE-POINTES; PLACEBO-CONTROLLED TRIAL; INTRANASAL FLUTICASONE PROPIONATE; BRONCHIAL EPITHELIAL-CELLS; DOUBLE-BLIND PLACEBO; MESSENGER-RNA EXPRESSION			Bousquet, J (reprint author), Hop Amaud Villeneuve, Serv Malad Resp, ARIA, 371 Ave Doyen Gaston Giraud, F-34295 Montpellier 5, France.		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J	Bousquet, J; Jeffery, PK; Busse, WW; Johnson, M; Vignola, AM				Bousquet, J; Jeffery, PK; Busse, WW; Johnson, M; Vignola, AM			Asthma - From bronchoconstriction to airways inflammation and remodeling	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Review							BRONCHOALVEOLAR LAVAGE FLUID; BRONCHIAL EPITHELIAL-CELLS; NECROSIS-FACTOR-ALPHA; COLONY-STIMULATING FACTOR; GROWTH-FACTOR-BETA; AIR-FLOW OBSTRUCTION; SMOOTH-MUSCLE CELLS; SEGMENTAL ANTIGEN CHALLENGE; INHALED BECLOMETHASONE DIPROPIONATE; IDIOPATHIC PULMONARY FIBROSIS		CHU Montpellier, Hop Arnaud Villeneuve, Clin Malad Resp, F-34295 Montpellier 5, France; Hop Arnaud Villeneuve, INSERM U454, Montpellier, France; Univ London Imperial Coll Sci Technol & Med, Sch Med, Natl Heart & Lung Inst, London, England; Univ Wisconsin, Dept Med, Madison, WI USA; CNR, Ist Fisiopatol Resp, Palermo, Italy	Bousquet, J (reprint author), CHU Montpellier, Hop Arnaud Villeneuve, Clin Malad Resp, F-34295 Montpellier 5, France.						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J. Respir. Crit. Care Med.	MAY	2000	161	5					1720	1745				26	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	312LU	WOS:000086945400054	10806180	
J	Braun-Fahrlander, C; Riedler, J; Herz, U; Eder, W; Waser, M; Grize, L; Maisch, S; Carr, D; Gerlach, F; Bufe, A; Lauener, RP; Schierl, R; Renz, H; Nowak, D; von Mutius, E				Braun-Fahrlander, C; Riedler, J; Herz, U; Eder, W; Waser, M; Grize, L; Maisch, S; Carr, D; Gerlach, F; Bufe, A; Lauener, RP; Schierl, R; Renz, H; Nowak, D; von Mutius, E		Allergy Endotoxin Study Team	Environmental exposure to endotoxin and its relation to asthma in school-age children	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							HOUSE-DUST ENDOTOXIN; AIRBORNE ENDOTOXIN; IMMUNE-RESPONSE; CHILDHOOD; LIFE; RISK; SENSITIZATION; ALLERGY	Background: In early life, the innate immune system can recognize both viable and nonviable parts of microorganisms. Immune activation may direct the immune response, thus conferring tolerance to allergens such as animal dander or tree and grass pollen. Methods: Parents of children who were 6 to 13 years of age and were living in rural areas of Germany, Austria, or Switzerland where there were both farming and nonfarming households completed a standardized questionnaire on asthma and hay fever. Blood samples were obtained from the children and tested for atopic sensitization; peripheral-blood leukocytes were also harvested from the samples for testing. The levels of endotoxin in the bedding used by these children were examined in relation to clinical findings and to the cytokine-production profiles of peripheral-blood leukocytes that had been stimulated with lipopolysaccharide and staphylococcal enterotoxin B. Complete data were available for 812 children. Results: Endotoxin levels in samples of dust from the child's mattress were inversely related to the occurrence of hay fever, atopic asthma, and atopic sensitization. Nonatopic wheeze was not significantly associated with the endotoxin level. Cytokine production by leukocytes (production of tumor necrosis factor (alpha), interferon-(gamma), interleukin-10, and interleukin-12) was inversely related to the endotoxin level in the bedding, indicating a marked down-regulation of immune responses in exposed children. Conclusions: A subject's environmental exposure to endotoxin may have a crucial role in the development of tolerance to ubiquitous allergens found in natural environments.	Univ Basel, Inst Social & Prevent Med, CH-4051 Basel, Switzerland; Childrens Hosp Salzburg, Salzburg, Austria; Hosp Univ Marburg, Dept Clin Chem & Mol Diagnost, Marburg, Germany; Dr von Hauner Childrens Hosp, Munich, Germany; Ruhr Univ Bochum, Dept Expt Pneumol, D-4630 Bochum, Germany; Univ Zurich, Childrens Hosp, Zurich, Switzerland; Univ Munich, Inst Occupat & Environm Med, Munich, Germany	Braun-Fahrlander, C (reprint author), Univ Basel, Inst Social & Prevent Med, Steinengraben 49, CH-4051 Basel, Switzerland.		Lauener, Roger/O-8612-2016	Lauener, Roger/0000-0002-8412-606X			AbouZeid C, 1997, INFECT IMMUN, V65, P1856; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Cleveland MG, 1996, INFECT IMMUN, V64, P1906; D'Amato G, 2000, J INVEST ALLERG CLIN, V10, P123; Delves PJ, 2000, NEW ENGL J MED, V343, P37; Douwes J, 2000, AM J RESP CRIT CARE, V162, P1348; Fearon DT, 1996, SCIENCE, V272, P50, DOI 10.1126/science.272.5258.50; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Gold DR, 2000, ENVIRON HEALTH PERSP, V108, P643, DOI 10.2307/3454400; HOLLANDER A, 1993, AM IND HYG ASSOC J, V54, P647, DOI 10.1202/0002-8894(1993)054<0647:IAEITA>2.0.CO;2; ISAAC, 1998, PHAS 2 MOD INT STUD; Kabesch M, 1999, EUR RESPIR J, V13, P577, DOI 10.1183/09031936.99.13357799; Lauener RP, 2002, LANCET, V360, P465, DOI 10.1016/S0140-6736(02)09641-1; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; *MATHS, 2000, S PLUS; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Park JH, 2000, ENVIRON HEALTH PERSP, V108, P1023, DOI 10.2307/3434953; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; RYLANDER R, 1989, AM REV RESPIR DIS, V140, P981; SAS Institute, 2001, SAS REL 8 02; Schade FU, 1996, J ENDOTOXIN RES, V3, P455; Silverman M, 1997, THORAX, V52, P936; Strachan David P., 2000, Thorax, V55, pS2, DOI 10.1136/thorax.55.suppl_1.S2; Strachan DP, 1996, BRIT MED J, V312, P1195; Tulic MK, 2000, AM J RESP CELL MOL, V22, P604; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; West MA, 2002, CRIT CARE MED, V30, pS64, DOI 10.1097/00003246-200201001-00009	27	1064	1090	16	94	MASSACHUSETTS MEDICAL SOC/NEJM	WALTHAM	WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA	0028-4793			NEW ENGL J MED	N. Engl. J. Med.	SEP 19	2002	347	12					869	877		10.1056/NEJMoa020057		9	Medicine, General & Internal	General & Internal Medicine	594GJ	WOS:000178040700002	12239255	
J	Akbari, O; DeKruyff, RH; Umetsu, DT				Akbari, O; DeKruyff, RH; Umetsu, DT			Pulmonary dendritic cells producing IL-10 mediate tolerance induced by respiratory exposure to antigen	NATURE IMMUNOLOGY			English	Article							COLONY-STIMULATING FACTOR; MOUSE BONE-MARROW; CD4(+) T-CELLS; IN-VIVO; INTERFERON-GAMMA; IMMUNE DEVIATION; TH2 RESPONSES; INDUCTION; DIFFERENTIATION; INTERLEUKIN-10	Respiratory exposure to allergen induces T cell tolerance and protection against the development of airway hyperreactivity and asthma. However, the specific mechanisms by which tolerance is induced by respiratory allergen are not clear. We report here that pulmonary dendritic cells (DCs) from mice exposed to respiratory antigen transiently produced interleukin 10 (IL-10). These phenotypically mature pulmonary DCs, which were B-7(hi) as well as producing IL-10, stimulated the development of CD4(+)T regulatory I-like cells that also produced high amounts of IL-10. In addition, adoptive transfer of pulmonary DCs from IL-10(+/+), but not IL-10(-/-), mice exposed to respiratory antigen induced antigen-specific unresponsiveness in recipient mice. These studies show that IL-10 production by DCs is critical for the induction of tolerance, and that phenotypically mature pulmonary DCs mediate tolerance induced by respiratory exposure to antigen.	Stanford Univ, Sch Med, Dept Pediat, Div Immunol & Allergy, Stanford, CA 94305 USA	Umetsu, DT (reprint author), Stanford Univ, Sch Med, Dept Pediat, Div Immunol & Allergy, Stanford, CA 94305 USA.				NHLBI NIH HHS [R01HL62348]; NIAID NIH HHS [AI24571, AI26322]		ASSENMACHER M, 1994, EUR J IMMUNOL, V24, P1097, DOI 10.1002/eji.1830240513; Borish L, 1998, J ALLERGY CLIN IMMUN, V101, P293; Chang CCJ, 2000, J IMMUNOL, V165, P3584; CHEN YH, 1994, SCIENCE, V265, P1237, DOI 10.1126/science.7520605; CHEN YH, 1995, NATURE, V376, P177, DOI 10.1038/376177a0; de Saint-Vis B, 1998, J IMMUNOL, V160, P1666; Dong HD, 1999, NAT MED, V5, P1365; Groux H, 1997, NATURE, V389, P737; Gutgemann I, 1998, IMMUNITY, V8, P667, DOI 10.1016/S1074-7613(00)80571-3; HOLT PG, 1989, CLIN EXP ALLERGY, V19, P597, DOI 10.1111/j.1365-2222.1989.tb02752.x; HOLT PG, 1988, J EXP MED, V167, P262, DOI 10.1084/jem.167.2.262; Hutloff A, 1999, NATURE, V397, P263; INABA K, 1992, J EXP MED, V176, P1693, DOI 10.1084/jem.176.6.1693; Iwasaki A, 1999, J EXP MED, V190, P229, DOI 10.1084/jem.190.2.229; John M, 1998, AM J RESP CRIT CARE, V157, P256; Jonuleit H, 2000, GENE THER, V7, P249, DOI 10.1038/sj.gt.3301077; KEARNEY ER, 1994, IMMUNITY, V1, P327, DOI 10.1016/1074-7613(94)90084-1; Khanna A, 2000, J IMMUNOL, V164, P1346; Lambrecht BN, 2000, J CLIN INVEST, V106, P551, DOI 10.1172/JCI8107; Lambrecht BN, 2000, J IMMUNOL, V164, P2937; LEVIN D, 1993, J IMMUNOL, V151, P6742; LYONS AB, 1994, J IMMUNOL METHODS, V171, P131, DOI 10.1016/0022-1759(94)90236-4; Macaulay AE, 1998, J IMMUNOL, V160, P1694; MALONEY DG, 1985, HYBRIDOMA, V4, P191, DOI 10.1089/hyb.1985.4.191; MARRACK P, 1983, J EXP MED, V158, P1635, DOI 10.1084/jem.158.5.1635; McAdam AJ, 2000, J IMMUNOL, V165, P5035; MCMENAMIN C, 1993, J EXP MED, V178, P889, DOI 10.1084/jem.178.3.889; MCMENAMIN C, 1991, INT ARCH ALLER A IMM, V94, P78; MELAMED D, 1993, EUR J IMMUNOL, V23, P935, DOI 10.1002/eji.1830230426; POLLARD AM, 1990, J EXP MED, V172, P159, DOI 10.1084/jem.172.1.159; Pulendran B, 1997, J IMMUNOL, V159, P2222; REINER SL, 1993, J IMMUNOL METHODS, V165, P37, DOI 10.1016/0022-1759(93)90104-F; SANDER B, 1991, IMMUNOL REV, V119, P65, DOI 10.1111/j.1600-065X.1991.tb00578.x; SCHEICHER C, 1992, J IMMUNOL METHODS, V154, P253, DOI 10.1016/0022-1759(92)90199-4; SEDER RA, 1992, J EXP MED, V176, P1091, DOI 10.1084/jem.176.4.1091; STOCKINGER B, 1994, INT IMMUNOL, V6, P247, DOI 10.1093/intimm/6.2.247; Stumbles PA, 1998, J EXP MED, V188, P2019, DOI 10.1084/jem.188.11.2019; Tsitoura DC, 1999, J IMMUNOL, V163, P2592; Tsitoura DC, 2000, J ALLERGY CLIN IMMUN, V106, P239; Vremec D, 1997, J IMMUNOL, V159, P565; Wills-Karp M, 1999, ANNU REV IMMUNOL, V17, P255, DOI 10.1146/annurev.immunol.17.1.255; Wu L, 1996, J EXP MED, V184, P903, DOI 10.1084/jem.184.3.903; XIA WJ, 1995, J EXP MED, V181, P1275, DOI 10.1084/jem.181.4.1275; Yoshinaga SK, 1999, NATURE, V402, P827, DOI 10.1038/45582	44	874	909	0	22	NATURE AMERICA INC	NEW YORK	345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA	1529-2908			NAT IMMUNOL	Nat. Immunol.	AUG	2001	2	8					725	731		10.1038/90667		7	Immunology	Immunology	459BN	WOS:000170230100015	11477409	
J	Eisenbarth, SC; Piggott, DA; Huleatt, JW; Visintin, I; Herrick, CA; Bottomly, K				Eisenbarth, SC; Piggott, DA; Huleatt, JW; Visintin, I; Herrick, CA; Bottomly, K			Lipopolysaccharide-enhanced, toll-like receptor 4-dependent T helper cell type 2 responses to inhaled antigen	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article						asthma; Toll-like receptor; T cell; dendritic cell; lung	EXPOSURE; ASTHMA; MOUSE; TLR4	Allergic asthma is an inflammatory lung disease initiated and directed by T helper cells type 2 (Th2). The mechanism involved in generation of Th2 responses to inert inhaled antigens, however, is unknown. Epidemiological evidence suggests that exposure to lipopolysaccharide (LPS) or other microbial products can influence the development and severity of asthma. However, the mechanism by which LPS influences asthma pathogenesis remains undefined. Although it is known that signaling through Toll-like receptors (TLR) is required for adaptive T helper cell type 1 (Th1) responses, it is unclear if TLRs are needed for Th2 priming. Here, we report that low level inhaled LPS signaling through TLR4 is necessary to induce Th2 responses to inhaled antigens in a mouse model of allergic sensitization. The mechanism by which LPS signaling results in Th2 sensitization involves the activation of antigen-containing dendritic cells. In contrast to low levels, inhalation of high levels of LPS with antigen results in Th1 responses. These studies suggest that the level of LPS exposure can determine the type of inflammatory response generated and provide a potential mechanistic explanation of epidemiological data on endotoxin exposure and asthma prevalence.	Yale Univ, Sch Med, Immunobiol Sect, New Haven, CT 06520 USA; Yale Univ, Sch Med, Dept Dermatol, New Haven, CT 06520 USA	Bottomly, K (reprint author), Yale Univ, Sch Med, Immunobiol Sect, 310 Cedar St, New Haven, CT 06520 USA.			Eisenbarth, Stephanie/0000-0002-1244-208X	NHLBI NIH HHS [HL54450, R01 HL054450]; NIAID NIH HHS [R37 AI026791, AI26791, R01 AI026791]; NIGMS NIH HHS [5T32GM07205, T32 GM007205]		Arbour NC, 2000, NAT GENET, V25, P187; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Cohn L, 1999, J EXP MED, V190, P1309, DOI 10.1084/jem.190.9.1309; Dabbagh K, 2002, J IMMUNOL, V168, P4524; Gern JE, 2000, J ALLERGY CLIN IMMUN, V105, pS497; Herrick CA, 2000, J CLIN INVEST, V105, P765, DOI 10.1172/JCI8624; Kaisho T, 2002, INT IMMUNOL, V14, P695, DOI 10.1093/intimm/dxf039; Kurt-Jones EA, 2000, NAT IMMUNOL, V1, P398, DOI 10.1038/80833; Liu AH, 2002, J ALLERGY CLIN IMMUN, V109, P379, DOI 10.1067/mai.2002.122157; Lutz MB, 1999, J IMMUNOL METHODS, V223, P77, DOI 10.1016/S0022-1759(98)00204-X; Medzhitov R, 2001, NAT REV IMMUNOL, V1, P135, DOI 10.1038/35100529; Reed CE, 2001, J ALLERGY CLIN IMMUN, V108, P157, DOI 10.1067/mai.2001.116862; Schnare M, 2001, NAT IMMUNOL, V2, P947, DOI 10.1038/ni712; Schwartz DA, 2001, AM J RESP CRIT CARE, V163, P305; Seymour BWP, 1998, J EXP MED, V187, P721, DOI 10.1084/jem.187.5.721; Tsitoura DC, 1999, J IMMUNOL, V163, P2592; Tulic MK, 2000, AM J RESP CELL MOL, V22, P604; VOGEL SN, 1994, INFECT IMMUN, V62, P4454; Wan GH, 2000, CLIN EXP ALLERGY, V30, P426	19	770	803	2	22	ROCKEFELLER UNIV PRESS	NEW YORK	1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA	0022-1007			J EXP MED	J. Exp. Med.	DEC 16	2002	196	12					1645	1651		10.1084/jem.20021340		7	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	629PP	WOS:000180058300013	12486107	
J	Kunzli, N; Kaiser, R; Medina, S; Studnicka, M; Chanel, O; Filliger, P; Herry, M; Horak, F; Puybonnieux-Texier, V; Quenel, P; Schneider, J; Seethaler, R; Vergnaud, JC; Sommer, H				Kunzli, N; Kaiser, R; Medina, S; Studnicka, M; Chanel, O; Filliger, P; Herry, M; Horak, F; Puybonnieux-Texier, V; Quenel, P; Schneider, J; Seethaler, R; Vergnaud, JC; Sommer, H			Public-health impact of outdoor and traffic-related air pollution: a European assessment	LANCET			English	Article							TERM AMBIENT CONCENTRATIONS; RESPIRATORY HEALTH; TIME-SERIES; PARTICULATE MATTER; NONSMOKING POPULATION; INHALABLE PARTICLES; HOSPITAL ADMISSIONS; ASTHMATIC-CHILDREN; SULFUR-DIOXIDE; UNITED-STATES	Background Air pollution contributes to mortality and morbidity. We estimated the impact of outdoor (total) and traffic-related air pollution on public health in Austria, France, and Switzerland. Attributable cases of morbidity and mortality were estimated. Methods Epidemiology-based exposure-response functions for a 10 mu g/m(3) increase in particulate matter (PM10) were used to quantify the effects of air pollution. Cases attributable to air pollution were estimated for mortality (adults greater than or equal to 30 years), respiratory and cardiovascular hospital admissions tall ages), incidence of chronic bronchitis (adults greater than or equal to 25 years), bronchitis episodes in children (<15 years), restricted activity days (adults greater than or equal to 20 years), and asthma attacks in adults and children. Population exposure (PM10) was modelled for each km(2). The traffic-related fraction was estimated based on PM10 emission inventories. Findings Air pollution caused 6% of total mortality or more than 40 000 attributable cases per year. About half of all mortality caused by air pollution was attributed to motorised traffic, accounting also for: more than 25 000 new cases of chronic bronchitis (adults); more than 290 000 episodes of bronchitis (children); more than 0.5 million asthma attacks; and more than 16 million person-days of restricted activities. Interpretation This assessment estimates the public-health impacts of current patterns of air pollution. Although individual health risks of air pollution are relatively small, the public-health consequences are considerable. Traffic-related air pollution remains a key target for public-health action in Europe. Our results, which have also been used for economic valuation, should guide decisions on the assessment of environmental health-policy options.	Univ Basel, Inst Sozial & Pravent Med, CH-4051 Basel, Switzerland; Natl Inst Publ Hlth Surveillance, Dept Environm Hlth, St Maurice, France; Ctr Pulm Dis, Vienna, Austria; GREQAM, Dept Econ, French Natl Ctr Sci Res, Marseille, France; BUWAL, Swiss Agcy Environm Forest & Landscape, Bern, Switzerland; Consultancy Dr Max Henry, Vienna, Austria; Univ Childrens Hosp, Vienna, Austria; Univ Paris 07, LED, Paris, France; Fed Environm Agcy, Dept Air Qual Control, Vienna, Austria; Univ Sydney, Inst Transport Studies, Sydney, NSW 2006, Australia; EUREQUA, Dept Econ, Franch Natl Ctr Sci Res, Paris, France; ECOPLAN, Econ & Environm Studies, Bern, Switzerland; ECOPLAN, Econ & Environm Studies, Altdorf, Switzerland	Kunzli, N (reprint author), Univ Basel, Inst Sozial & Pravent Med, Steinengraben 49, CH-4051 Basel, Switzerland.		Chanel, Olivier/H-6500-2013; QUENEL, PHILIPPE/J-4351-2015; Kunzli, Nino/F-7195-2014	Chanel, Olivier/0000-0002-8221-7558; QUENEL, PHILIPPE/0000-0003-3361-3623; Kunzli, Nino/0000-0001-8360-080X			ABBEY DE, 1993, ARCH ENVIRON HEALTH, V48, P33; ABBEY DE, 1995, ARCH ENVIRON HEALTH, V50, P139; Abbey DE, 1999, AM J RESP CRIT CARE, V159, P373; *AM LUNG ASS, 1998, DOLL CENTS EC HLTH B; Baldi I, 1999, EUR RESPIR J, V24, pS392; BATES DV, 1992, ENVIRON RES, V59, P336, DOI 10.1016/S0013-9351(05)80040-4; Bates DV, 2000, ENVIRON HEALTH PERSP, V108, P91, DOI 10.2307/3454504; BraunFahrlander C, 1997, AM J RESP CRIT CARE, V155, P1042; Brunekreef B, 1999, EPIDEMIOLOGY, V10, P661, DOI 10.1097/00001648-199911000-00001; *DEP HLTH AD HOC G, 1999, EC APPR HLTH EFF AIR; DOCKERY DW, 1989, AM REV RESPIR DIS, V139, P587; Dockery DW, 1996, ENVIRON HEALTH PERSP, V104, P500, DOI 10.2307/3432990; DOCKERY DW, 1993, NEW ENGL J MED, V329, P1753, DOI 10.1056/NEJM199312093292401; Dora C, 1999, BRIT MED J, V318, P1686; Dusseldorp A, 1995, AM J RESP CRIT CARE, V152, P1032; Eder W, 1998, WIEN KLIN WOCHENSCHR, V110, P669; FILLIGER P, 1999, POPULATION EXPOSURE; Gielen MH, 1997, AM J RESP CRIT CARE, V155, P2105; HAIDINGER W, 1998, SCHLUSSBERICHT ISAAC; Hiltermann TJN, 1998, EUR RESPIR J, V11, P686; Holgate ST, 1999, AIR POLLUTION HLTH; Katsouyanni K, 1997, BMJ-BRIT MED J, V314, P1658; Kunzli N, 1997, ENVIRON HEALTH PERSP, V105, P1078, DOI 10.2307/3433849; KUNZLI N., 1999, HLTH COSTS DUE ROAD; LA D, 1999, INT J EPIDEMIOL, V28, P894; McMichael AJ, 1998, INT J EPIDEMIOL, V27, P450, DOI 10.1093/ije/27.3.450; Medina S, 1997, EVALUATION RISQUES P; National Research Council, 1999, RES PRIOR AIRB PART; *NAT RES DEF COUNC, 1996, BREATH TAK PREM MORT; Neukirch F, 1998, ARCH ENVIRON HEALTH, V53, P320; OBERFELD G, 1996, 1 SALZBURGER KINDERG; Ostro B, 1996, J EXPO ANAL ENV EPID, V6, P97; Ostro B, 1998, ENVIRON RES, V76, P94, DOI 10.1006/enrs.1997.3799; OSTRO BD, 1990, RISK ANAL, V10, P421, DOI 10.1111/j.1539-6924.1990.tb00525.x; Poloniecki JD, 1997, OCCUP ENVIRON MED, V54, P535; POPE CA, 1995, AM J RESP CRIT CARE, V151, P669; Prescott GJ, 1998, OCCUP ENVIRON MED, V55, P697; ROEMER W, 1993, AM REV RESPIR DIS, V147, P118; Samet JM, 1998, AM J EPIDEMIOL, V148, P929; Segala C, 1998, EUR RESPIR J, V11, P677; Smith KR, 1999, EPIDEMIOLOGY, V10, P573, DOI 10.1097/00001648-199909000-00027; SOMMER H, HLTH COSTS DUE ROAD; Sommer H, 1999, 3 WHO MIN C ENV HLTH; STUDNICKA M, 1997, EUR RESPIR J, V10, P2257; Wilson R., 1996, PARTICLES OUR AIR CO; Wordley J, 1997, OCCUP ENVIRON MED, V54, P108; Zemp E, 1999, AM J RESP CRIT CARE, V159, P1257; Zmirou D, 1998, EPIDEMIOLOGY, V9, P495, DOI 10.1097/00001648-199809000-00005; 1998, ANN STAT REP SWITZ S	49	767	812	20	187	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	SEP 2	2000	356	9232					795	801		10.1016/S0140-6736(00)02653-2		7	Medicine, General & Internal	General & Internal Medicine	350LF	WOS:000089101800009	11022926	
J	Riedler, J; Braun-Fahrlander, C; Eder, W; Schreuer, M; Waser, M; Maisch, S; Carr, D; Schierl, R; Nowak, D; von Mutius, E				Riedler, J; Braun-Fahrlander, C; Eder, W; Schreuer, M; Waser, M; Maisch, S; Carr, D; Schierl, R; Nowak, D; von Mutius, E		ALEX Study Team	Exposure to farming in early life and development of asthma and allergy: a cross-sectional survey	LANCET			English	Article							HAY-FEVER; AUSTRIAN CHILDREN; IGE PRODUCTION; CHILDHOOD; SENSITIZATION; PREVALENCE; ATOPY; RISK; STIMULATION; CHALLENGE	Background A farming environment protects against development of asthma, hay fever, and atopic sensitisation in children. We aimed to establish whether increased exposure to microbial compounds has to occur early in life to affect maturation of the immune system and thereby reduces risk for development of allergic diseases. Methods We did a cross-sectional survey in rural areas of Austria, Germany, and Switzerland. 2618 (75%) of 3504 parents of 6-13-year-old children completed a standardised questionnaire on asthma, hay fever, and atopic eczema. Children from farming families, and a random sample of non-farmers' children, who gave consent for blood samples to be obtained for measurements of specific serum IgE antibodies to common allergens were invited to participate (n = 901). Findings Exposure of children younger than 1 year, compared with those aged 1-5 years, to stables and consumption of farm milk was associated with lower frequencies of asthma (1% [3/218] vs 11% [15/138]), hay fever (3% [7] vs 13% [18]), and atopic sensitisation (12% [27] vs 29% [40]). Protection against development of asthma was independent from effect on atopic sensitisation. Continual long-term exposure to stables until age 5 years was associated with the lowest frequencies of asthma (0.8% [1/122]), hay fever (0.8% [1]), and atopic sensitisation (8.2% [10]). Interpretation Long-term and early-life exposure to stables and farm milk induces a strong protective effect against development of asthma, hay fever, and atopic sensitisation.	Childrens Hosp, A-5020 Salzburg, Austria; Univ Basel, Inst Social & Prevent Med, Basel, Switzerland; Salzburg Univ, Dept Sociol, A-5020 Salzburg, Austria; Univ Munich, Dr von Hauner Childrens Hosp, Munich, Germany; Univ Munich, Inst Occupat & Environm Med, Munich, Germany	Riedler, J (reprint author), Childrens Hosp, Muellner Hauptstr 48, A-5020 Salzburg, Austria.						Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Ernst P, 2000, AM J RESP CRIT CARE, V161, P1563; Holt PG, 1996, J EXP MED, V183, P1297, DOI 10.1084/jem.183.4.1297; KILEWEIN G, 1994, LEITFADEN MILCHKUNDE, P83; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Klinman DM, 1999, VACCINE, V17, P19, DOI 10.1016/S0264-410X(98)00151-0; Kramer U, 1999, LANCET, V353, P450, DOI 10.1016/S0140-6736(98)06329-6; Lewis SA, 2000, CLIN EXP ALLERGY, V30, P153; MACATONIA SE, 1995, J IMMUNOL, V154, P5071; Murosaki S, 1998, J ALLERGY CLIN IMMUN, V102, P57, DOI 10.1016/S0091-6749(98)70055-7; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; RIEDLER J, 1994, AM J RESP CRIT CARE, V150, P1632; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Riedler J, 1998, EUR RESPIR J, V11, P355, DOI 10.1183/09031936.98.11020355; Sudo N, 1997, J IMMUNOL, V159, P1739; SUHREN G, 1986, MILCHWISSENSCHAFT, V41, P156; Tariq SM, 1998, J ALLERGY CLIN IMMUN, V101, P587; Tulic MK, 2000, AM J RESP CELL MOL, V22, P604; ULEVITCH RJ, 1995, ANNU REV IMMUNOL, V13, P437, DOI 10.1146/annurev.iy.13.040195.002253; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230	24	764	785	21	104	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	OCT 6	2001	358	9288					1129	1133		10.1016/S0140-6736(01)06252-3		5	Medicine, General & Internal	General & Internal Medicine	479HM	WOS:000171399000009	11597666	
J	Nierman, WC; Pain, A; Anderson, MJ; Wortman, JR; Kim, HS; Arroyo, J; Berriman, M; Abe, K; Archer, DB; Bermejo, C; Bennett, J; Bowyer, P; Chen, D; Collins, M; Coulsen, R; Davies, R; Dyer, PS; Farman, M; Fedorova, N; Fedorova, N; Feldblyum, TV; Fischer, R; Fosker, N; Fraser, A; Garcia, JL; Garcia, MJ; Goble, A; Goldman, GH; Gomi, K; Griffith-Jones, S; Gwilliam, R; Haas, B; Haas, H; Harris, D; Horiuchi, H; Huang, J; Humphray, S; Jimenez, J; Keller, N; Khouri, H; Kitamoto, K; Kobayashi, T; Konzack, S; Kulkarni, R; Kumagai, T; Lafton, A; Latge, JP; Li, WX; Lord, A; Majoros, WH; May, GS; Miller, BL; Mohamoud, Y; Molina, M; Monod, M; Mouyna, I; Mulligan, S; Murphy, L; O'Neil, S; Paulsen, I; Penalva, MA; Pertea, M; Price, C; Pritchard, BL; Quail, MA; Rabbinowitsch, E; Rawlins, N; Rajandream, MA; Reichard, U; Renauld, H; Robson, GD; de Cordoba, SR; Rodriguez-Pena, JM; Ronning, CM; Rutter, S; Salzberg, SL; Sanchez, M; Sanchez-Ferrero, JC; Saunders, D; Seeger, K; Squares, R; Squares, S; Takeuchi, M; Tekaia, F; Turner, G; de Aldana, CRV; Weidman, J; White, O; Woodward, J; Yu, JH; Fraser, C; Galagan, JE; Asai, K; Machida, M; Hall, N; Barrell, B; Denning, DW				Nierman, WC; Pain, A; Anderson, MJ; Wortman, JR; Kim, HS; Arroyo, J; Berriman, M; Abe, K; Archer, DB; Bermejo, C; Bennett, J; Bowyer, P; Chen, D; Collins, M; Coulsen, R; Davies, R; Dyer, PS; Farman, M; Fedorova, N; Fedorova, N; Feldblyum, TV; Fischer, R; Fosker, N; Fraser, A; Garcia, JL; Garcia, MJ; Goble, A; Goldman, GH; Gomi, K; Griffith-Jones, S; Gwilliam, R; Haas, B; Haas, H; Harris, D; Horiuchi, H; Huang, J; Humphray, S; Jimenez, J; Keller, N; Khouri, H; Kitamoto, K; Kobayashi, T; Konzack, S; Kulkarni, R; Kumagai, T; Lafton, A; Latge, JP; Li, WX; Lord, A; Majoros, WH; May, GS; Miller, BL; Mohamoud, Y; Molina, M; Monod, M; Mouyna, I; Mulligan, S; Murphy, L; O'Neil, S; Paulsen, I; Penalva, MA; Pertea, M; Price, C; Pritchard, BL; Quail, MA; Rabbinowitsch, E; Rawlins, N; Rajandream, MA; Reichard, U; Renauld, H; Robson, GD; de Cordoba, SR; Rodriguez-Pena, JM; Ronning, CM; Rutter, S; Salzberg, SL; Sanchez, M; Sanchez-Ferrero, JC; Saunders, D; Seeger, K; Squares, R; Squares, S; Takeuchi, M; Tekaia, F; Turner, G; de Aldana, CRV; Weidman, J; White, O; Woodward, J; Yu, JH; Fraser, C; Galagan, JE; Asai, K; Machida, M; Hall, N; Barrell, B; Denning, DW			Genomic sequence of the pathogenic and allergenic filamentous fungus Aspergillus fumigatus	NATURE			English	Article							CELL-WALL; SACCHAROMYCES-CEREVISIAE; GENE-CLUSTER; SENSITIZATION; ARSENITE; COMPOST	Aspergillus fumigatus is exceptional among microorganisms in being both a primary and opportunistic pathogen as well as a major allergen(1-3). Its conidia production is prolific, and so human respiratory tract exposure is almost constant(4). A. fumigatus is isolated from human habitats(5) and vegetable compost heaps(6,7). In immunocompromised individuals, the incidence of invasive infection can be as high as 50% and the mortality rate is often about 50% (ref. 2). The interaction of A. fumigatus and other airborne fungi with the immune system is increasingly linked to severe asthma and sinusitis(8). Although the burden of invasive disease caused by A. fumigatus is substantial, the basic biology of the organism is mostly obscure. Here we show the complete 29.4-megabase genome sequence of the clinical isolate Af293, which consists of eight chromosomes containing 9,926 predicted genes. Microarray analysis revealed temperature-dependent expression of distinct sets of genes, as well as 700 A. fumigatus genes not present or significantly diverged in the closely related sexual species Neosartorya fischeri, many of which may have roles in the pathogenicity phenotype. The Af293 genome sequence provides an unparalleled resource for the future understanding of this remarkable fungus.	Inst Genom Res, Rockville, MD 20850 USA; George Washington Univ, Sch Med, Dept Biochem & Mol Biol, Washington, DC 20037 USA; Wellcome Trust Sanger Inst, Hinxton CB10 1SA, England; Univ Manchester, Fac Life Sci, Manchester M13 9PT, Lancs, England; Univ Manchester, Sch Med, Manchester M13 9PT, Lancs, England; Univ Complutense Madrid, Dept Microbiol 2, E-28040 Madrid, Spain; Tohoku Univ, Aoba Ku, Sendai, Miyagi 9808555, Japan; Univ Nottingham, Sch Biol, Nottingham NG7 2RD, England; Tulane Univ, Dept Cell & Mol Biol, New Orleans, LA 70118 USA; European Bioinformat Inst, Hinxton CB10 1SD, England; Univ Kentucky, Dept Plant Pathol, Lexington, KY 40546 USA; Max Planck Inst Terr Microbiol, D-35043 Marburg, Germany; CSIC, Ctr Invest Biol, Madrid 28040, Spain; Univ Salamanca, Dept Genet & Microbiol, Salamanca 37007, Spain; Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, BR-05508 Sao Paulo, Brazil; Innsbruck Med Univ, Dept Mol Biol, A-6020 Innsbruck, Austria; Univ Wisconsin, Dept Plant Pathol, Madison, WI 53706 USA; Univ Tokyo, Dept Biotechnol, Tokyo 1138657, Japan; Nagoya Univ, Grad Sch Bioagr Sci, Dept Biol Mech & Funct, Nagoya, Aichi 4648601, Japan; Natl Inst Adv Ind Sci 7 Technol AIST, Computat Biol Res Ctr, Koto Ku, Tokyo 1350064, Japan; Inst Pasteur, INRA USC 2019, Unite Postulante Biol & Pathogen Fong, F-75015 Paris, France; Inst Pasteur, Unite Aspergillus, F-75015 Paris, France; Univ Texas, MD Anderson Canc Ctr, Div Pathol & Lab Med, Houston, TX 77030 USA; Univ Idaho, Ctr Reprod Biol, Dept Microbiol, Moscow, ID 83844 USA; Univ Idaho, Ctr Reprod Biol, Dept Mol Biol & Biochem, Moscow, ID 83844 USA; CHU Vaudois, Dept Dermatol, CH-1011 Lausanne, Switzerland; Univ Gottingen, Dept Bacteriol, D-37077 Gottingen, Germany; Tokyo Univ Agr & Technol, Tokyo 1830054, Japan; Univ Sheffield, Dept Mol Biol & Biotechnol, Sheffield S10 2TN, S Yorkshire, England; Univ Wisconsin, Dept Food Microbiol & Toxicol, Madison, WI 53706 USA; MIT, Broad Inst, Cambridge, MA 02139 USA; Harvard Univ, Cambridge, MA 02139 USA; Natl Inst Adv Ind Sci & Technol, Res Ctr Glycosci, Tsukuba, Ibaraki 3058566, Japan	Nierman, WC (reprint author), Inst Genom Res, Rockville, MD 20850 USA.	wnierman@tigr.org	Berriman, Matthew/A-7618-2011; mouyna, isabelle/F-3578-2011; Tekaia, Fredj/H-4553-2012; Paulsen, Ian/K-3832-2012; Hall, Neil/A-8717-2013; Goldman, Gustavo/F-1848-2013; Latge, Jean Paul/C-9846-2014; Griffiths-Jones, Sam/H-2998-2014; Vazquez de Aldana, Carlos/B-7772-2008; Rodriguez de Cordoba, Santiago/K-6727-2014; TAKEUCHI, Michio/H-6592-2013; Penalva, Miguel A/G-2295-2015; Pain, Arnab/L-5766-2015; Molina, Maria/F-7939-2015; Kobayashi, Tetsuo/I-6901-2014; Rodriguez-Pena, Jose/E-9624-2016; Abrams, Natalie/F-4845-2011; Salzberg, Steven/F-6162-2011; Arroyo, Javier/E-9308-2016; Rawlings, Neil/M-5566-2013	Paulsen, Ian/0000-0001-9015-9418; Hall, Neil/0000-0002-7995-3810; Griffiths-Jones, Sam/0000-0001-6043-807X; Vazquez de Aldana, Carlos/0000-0002-4513-3654; Rodriguez de Cordoba, Santiago/0000-0001-6401-1874; Penalva, Miguel A/0000-0002-3102-2806; Pain, Arnab/0000-0002-1755-2819; Molina, Maria/0000-0003-0074-3309; Kobayashi, Tetsuo/0000-0002-4008-454X; Rodriguez-Pena, Jose/0000-0002-8792-362X; Abrams, Natalie/0000-0001-9698-2819; Salzberg, Steven/0000-0002-8859-7432; Arroyo, Javier/0000-0002-1971-1721; Jimenez, Javier/0000-0002-0402-4427; Yates, Bethan/0000-0003-1658-1762; Wortman, Jennifer/0000-0002-8713-1227; Galagan, James/0000-0003-0542-3291; Rawlings, Neil/0000-0001-5557-7665; Denning, David/0000-0001-5626-2251; Murphy, Lee/0000-0001-6467-7449; Fraser, Claire/0000-0003-1462-2428; Hall, Neil/0000-0003-2808-0009	Biotechnology and Biological Sciences Research Council [CFB17726]; Wellcome Trust		Beffa T, 1998, MED MYCOL, V36, P137; Bentley R, 2002, MICROBIOL MOL BIOL R, V66, P250, DOI 10.1128/MMBR.66.2.250-271.2002; BLYTH W, 1977, CLIN ALLERGY, V7, P549, DOI 10.1111/j.1365-2222.1977.tb01485.x; Bok JW, 2004, EUKARYOT CELL, V3, P527, DOI 10.1128/EC.3.2.527-535.2004; Bozza S, 2002, MICROBES INFECT, V4, P1281, DOI 10.1016/S1286-4579(02)00007-2; 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J	Furuta, GT; Liacouras, CA; Collins, MH; Gupta, SK; Justinich, C; Putnam, PE; Bonis, P; Hassall, E; Straumann, A; Rothenberg, ME				Furuta, Glenn T.; Liacouras, Chris A.; Collins, Margaret H.; Gupta, Sandeep K.; Justinich, Chris; Putnam, Phil E.; Bonis, Peter; Hassall, Eric; Straumann, Alex; Rothenberg, Marc E.		FIGERS Subcommittees	Eosinophilic esophagitis in children and adults: A systematic review and consensus recommendations for diagnosis and treatment	GASTROENTEROLOGY			English	Review							GASTROESOPHAGEAL-REFLUX DISEASE; ATOPY PATCH TEST; ALLERGIC ESOPHAGITIS; RINGED ESOPHAGUS; SKIN PRICK; FLUTICASONE PROPIONATE; FOOD ALLERGY; FOLLOW-UP; ENDOSCOPIC MANIFESTATION; GASTROINTESTINAL-TRACT	During the last decade, clinical practice saw a rapid increase of patients with esophageal eosinophilia who were thought to have gastroesophageal reflux disease (GERD) but who did not respond to medical and/or surgical GERD management. Subsequent studies demonstrated that these patients had a "new" disease termed eosinophilic esophagitis (EE). As recognition of EE grew, so did confusion surrounding diagnostic criteria and treatment. To address these issues, a multidisciplinary task force of 31 physicians assembled with the goal of determining diagnostic criteria and making recommendations for evaluation and treatment of children and adults with suspected EE. Consensus recommendations were based upon a systematic review of the literature and expert opinion. EE is a clinicopathological disease characterized by (1) Symptoms including but not restricted to food impaction and dysphagia. in adults, and feeding intolerance and GERD symptoms in children; (2) 2 >= 15 eosinophils/HPF; (3) Exclusion of other disorders associated with similar clinical, histological, or endoscopic features, especially GERD. (Use of high dose proton pump inhibitor treatment or normal pH monitoring). Appropriate treatments include dietary approaches based upon eliminating exposure to food allergens, or topical corticosteroids. Since EE is a relatively new disease, the intent of this report is to provide current recommendations for care of affected patients and defining gaps in knowledge for future research studies.	Childrens Hosp, Sect Pediat Gastroenterol Hepatol & Nutr, Denver, CO 80218 USA; Univ Colorado, Sch Med, Denver, CO 80202 USA; Univ Penn, Childrens Hosp Philadelphia, Sch Med, Div Gastroenterol Hepatol & Nutr, Philadelphia, PA 19104 USA; Univ Cincinnati, Childrens Hosp, Ctr Med, Div Pathol, Cincinnati, OH 45267 USA; Indiana Univ, Sch Med, Div Pediat Gastroenterol Hepatol & Nutr, Riley Hosp Children, Indianapolis, IN 46204 USA; Queens Univ, Kingston Gen Hosp, Div Pediat Gastroenterol, Kingston, ON, Canada; Univ Cincinnati, Childrens Hosp, Coll Med, Div Pediat Gastroenterol Hepatol & Nutr,Med Ctr, Cincinnati, OH 45267 USA; Tufts Univ, Sch Med, Div Gastroenterol, Boston, MA 02111 USA; Univ British Columbia, BC Childrens Hosp, Div Gastroenterol, Vancouver, BC V5Z 1M9, Canada; Univ Basel, Univ Basel Hosp, Dept Gastroenterol, Basel, Switzerland; Univ Cincinnati, Med Ctr, Coll Med, Childrens Hosp,Div Allergy & Immunol, Cincinnati, OH 45267 USA	Furuta, GT (reprint author), Amer Gasteroenterol Assoc Inst, Clin Practice & Qual Management Committee, 4930 Del Ray Ave, Bethesda, MD 20814 USA.				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J	Barnes, PJ; Shapiro, SD; Pauwels, RA				Barnes, PJ; Shapiro, SD; Pauwels, RA			Chronic obstructive pulmonary disease: molecular and cellular mechanisms	EUROPEAN RESPIRATORY JOURNAL			English	Review						chemokine; cytokine; emphysema; macrophage; oxidative stress; protease	BRONCHIAL EPITHELIAL-CELLS; AIR-FLOW OBSTRUCTION; BRONCHOALVEOLAR LAVAGE FLUID; CHRONIC MUCUS HYPERSECRETION; RANDOMIZED CONTROLLED-TRIAL; FACTOR-KAPPA-B; SECRETORY LEUCOPROTEASE INHIBITOR; LEUKOCYTE PROTEASE INHIBITOR; LATENT ADENOVIRAL INFECTION; EXHALED BREATH CONDENSATE	Chronic obstructive pulmonary disease is a leading cause of death and disability, but has only recently been extensively explored from a cellular and molecular perspective. There is a chronic inflammation that leads to fixed narrowing of small airways and alveolar wall destruction (emphysema). This is characterised by increased numbers of alveolar macrophages, neutrophils and cytotoxic T-lymphocytes, and the release of multiple inflammatory mediators (lipids, chemokines, cytokines, growth factors). A high level of oxidative stress may amplify this inflammation. There is also increased elastolysis and evidence for involvement of several elastolytic enzymes, including serine proteases, cathepsins and matrix metalloproteinases. The inflammation and proteolysis in chronic obstructive pulmonary disease is an amplification of the normal inflammatory response to cigarette smoke. This inflammation, in marked contrast to asthma, appears to be resistant to corticosteroids, prompting a search for novel anti-inflammatory therapies that may prevent the relentless progression of the disease.	Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Sch Med, London SW3 6LY, England; Harvard Univ, Sch Med, Brigham & Womens Hosp, Boston, MA 02115 USA; State Univ Ghent Hosp, Dept Resp Dis, B-9000 Ghent, Belgium	Barnes, PJ (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Sch Med, Dovehouse St, London SW3 6LY, England.						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J	Van Eerdewegh, P; Little, RD; Dupuis, J; Del Mastro, RG; Falls, K; Simon, J; Torrey, D; Pandit, S; McKenny, J; Braunschweiger, K; Walsh, A; Liu, ZY; Hayward, B; Folz, C; Manning, SP; Bawa, A; Saracino, L; Thackston, M; Benchekroun, Y; Capparell, N; Wang, M; Adair, R; Feng, Y; Dubois, J; FitzGerald, MG; Huang, H; Gibson, R; Allen, KM; Pedan, A; Danzig, MR; Umland, SP; Egan, RW; Cuss, FM; Rorke, S; Clough, JB; Holloway, JW; Holgate, ST; Keith, TP				Van Eerdewegh, P; Little, RD; Dupuis, J; Del Mastro, RG; Falls, K; Simon, J; Torrey, D; Pandit, S; McKenny, J; Braunschweiger, K; Walsh, A; Liu, ZY; Hayward, B; Folz, C; Manning, SP; Bawa, A; Saracino, L; Thackston, M; Benchekroun, Y; Capparell, N; Wang, M; Adair, R; Feng, Y; Dubois, J; FitzGerald, MG; Huang, H; Gibson, R; Allen, KM; Pedan, A; Danzig, MR; Umland, SP; Egan, RW; Cuss, FM; Rorke, S; Clough, JB; Holloway, JW; Holgate, ST; Keith, TP			Association of the ADAM33 gene with asthma and bronchial hyperresponsiveness	NATURE			English	Article							LINKAGE DISEQUILIBRIUM; PROTEASE; PROTEINS; MARKERS; MUTATION; DOMAIN; FAMILY	Asthma is a common respiratory disorder characterized by recurrent episodes of coughing, wheezing and breathlessness. Although environmental factors such as allergen exposure are risk factors in the development of asthma, both twin and family studies point to a strong genetic component(1,2). To date, linkage studies have identified more than a dozen genomic regions linked to asthma(3). In this study, we performed a genome-wide scan on 460 Caucasian families and identified a locus on chromosome 20p13 that was linked to asthma (log(10) of the likelihood ratio (LOD), 2.94) and bronchial hyperresponsiveness (LOD, 3.93). A survey of 135 polymorphisms in 23 genes identified the ADAM33 gene 4 as being significantly associated with asthma using case-control, transmission disequilibrium and haplotype analyses (P=0.04-0.000003). ADAM proteins are membrane-anchored metalloproteases with diverse functions, which include the shedding of cell-surface proteins such as cytokines and cytokine receptors(5). The identification and characterization of ADAM33, a putative asthma susceptibility gene identified by positional cloning in an outbred population, should provide insights into the pathogenesis and natural history of this common disease.	Genome Therapeut Corp, Waltham, MA 02453 USA; Schering Plough Corp, Res Inst, Kenilworth, NJ 07033 USA; Univ Southampton, Sch Med, Resp Cell & Mol Biol Infect Inflammat & Repair Re, Southampton Gen Hosp, Southampton, Hants, England	Keith, TP (reprint author), Genome Therapeut Corp, 100 Beaver St, Waltham, MA 02453 USA.		Holloway, John/B-5424-2009; Little, Randall/O-7172-2014	Holloway, John/0000-0001-9998-0464; Dupuis, Josee/0000-0003-2871-3603			Abecasis GR, 2000, BIOINFORMATICS, V16, P182, DOI 10.1093/bioinformatics/16.2.182; Black RA, 1998, CURR OPIN CELL BIOL, V10, P654, DOI 10.1016/S0955-0674(98)80042-2; BOEHNKE M, 1991, AM J HUM GENET, V48, P22; Burney P, 1997, AM J RESP CRIT CARE, V156, P1773; Das M, 2001, PHYSIOL GENOMICS, V6, P57; Del Mastro R G, 1997, Methods Mol Biol, V68, P183; DESANCTIS GT, 1995, NAT GENET, V11, P150, DOI 10.1038/ng1095-150; DIETZ HC, 1991, NATURE, V352, P337, DOI 10.1038/352337a0; Dupuis J, 1999, GENETICS, V151, P373; EXCOFFIER L, 1995, MOL BIOL EVOL, V12, P921; Ghosh S, 1997, GENOME RES, V7, P165, DOI 10.1101/gr.7.2.165; Holgate ST, 2000, J ALLERGY CLIN IMMUN, V105, P193, DOI 10.1016/S0091-6749(00)90066-6; Howard L, 2000, BIOCHEM J, V348, P21, DOI 10.1042/0264-6021:3480021; Kruglyak L, 1996, AM J HUM GENET, V58, P1347; KRUGLYAK L, 1995, AM J HUM GENET, V57, P439; LANGE K, 1988, GENET EPIDEMIOL, V5, P471, DOI 10.1002/gepi.1370050611; Loechel F, 1999, J BIOL CHEM, V274, P13427, DOI 10.1074/jbc.274.19.13427; Los H, 2001, Twin Res, V4, P81, DOI 10.1375/1369052012191; Maquat LE, 2001, NAT GENET, V27, P5, DOI 10.1038/83759; MATISE TC, 1994, NAT GENET, V6, P384, DOI 10.1038/ng0494-384; Mullberg J, 2000, EUR CYTOKINE NETW, V11, P27; Primakoff P, 2000, TRENDS GENET, V16, P83, DOI 10.1016/S0168-9525(99)01926-5; Richter A, 2001, AM J RESP CELL MOL, V25, P385; Soares M. B., 1994, AUTOMATED DNA SEQUEN, P110; SPIELMAN RS, 1993, AM J HUM GENET, V52, P506; Stone AL, 1999, J PROTEIN CHEM, V18, P447, DOI 10.1023/A:1020692710029; Wilkinson J, 1998, GENOMICS, V53, P251, DOI 10.1006/geno.1998.5485; Wjst M, 1998, BIOINFORMATICS, V14, P827, DOI 10.1093/bioinformatics/14.9.827; YAGAMIHIROMASA T, 1995, NATURE, V377, P652, DOI 10.1038/377652a0; Yoshinaka T, 2002, GENE, V282, P227, DOI 10.1016/S0378-1119(01)00818-6	30	710	743	0	42	NATURE PUBLISHING GROUP	LONDON	MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND	0028-0836			NATURE	Nature	JUL 25	2002	418	6896					426	430		10.1038/nature00878		5	Multidisciplinary Sciences	Science & Technology - Other Topics	576MU	WOS:000177009700040	12110844	
J	Sears, MR; Greene, JM; Willan, AR; Wiecek, EM; Taylor, DR; Flannery, EM; Cowan, JO; Herbison, GP; Silva, PA; Poulton, R				Sears, MR; Greene, JM; Willan, AR; Wiecek, EM; Taylor, DR; Flannery, EM; Cowan, JO; Herbison, GP; Silva, PA; Poulton, R			A longitudinal, population-based, cohort study of childhood asthma followed to adulthood	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							RISK-FACTORS; LUNG-FUNCTION; AIRWAY HYPERRESPONSIVENESS; NEW-ZEALAND; WHEEZING ILLNESS; BIRTH COHORT; ATOPY; PREVALENCE; CHILDREN; LIFE	BACKGROUND: The outcome of childhood asthma in adults has been described in high-risk cohorts, but few population-based studies have reported the risk factors for persistence and relapse. METHODS: We assessed children born from April 1972 through March 1973 in Dunedin, New Zealand, repeatedly from 9 to 26 years of age with questionnaires, pulmonary-function tests, bronchial-challenge testing, and allergy testing. RESULTS: By the age of 26 years, 51.4 percent of 613 study members with complete respiratory data had reported wheezing at more than one assessment. Eighty-nine study members (14.5 percent) had wheezing that persisted from childhood to 26 years of age, whereas 168 (27.4 percent) had remission, but 76 (12.4 percent) subsequently relapsed by the age of 26. Sensitization to house dust mites predicted the persistence of wheezing (odds ratio, 2.41; P=0.001) and relapse (odds ratio, 2.18; P=0.01), as did airway hyperresponsiveness (odds ratio for persistence, 3.00; P<0.001; odds ratio for relapse, 3.03; P<0.001). Female sex predicted the persistence of wheezing (odds ratio, 1.71; P=0.03), as did smoking at the age of 21 years (odds ratio, 1.84; P=0.01). The earlier the age at onset, the greater the risk of relapse (odds ratio, 0.89 per year of increase in the age at onset; P<0.001). Pulmonary function was consistently lower in those with persistent wheezing than in those without persistent wheezing. CONCLUSIONS: In an unselected birth cohort, more than one in four children had wheezing that persisted from childhood to adulthood or that relapsed after remission. The factors predicting persistence or relapse were sensitization to house dust mites, airway hyperresponsiveness, female sex, smoking, and early age at onset. These findings, together with persistently low lung function, suggest that outcomes in adult asthma may be determined primarily in early childhood.	McMaster Univ, Dept Med, Hamilton, ON, Canada; McMaster Univ, Dept Clin Epidemiol & Biostat, Hamilton, ON, Canada; Univ Otago, Dept Prevent & Social Med, Dunedin, New Zealand; Univ Otago, Dunedin Multidisciplinary Hlth & Dev Res Unit, Dunedin, New Zealand	Sears, MR (reprint author), McMaster Univ & St Josephs Healthcare, Firestone Inst Resp Hlth, 50 Charlton Ave E, Hamilton, ON L8N 4A6, Canada.						Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; BRONNIMANN S, 1986, CHEST, V90, P480, DOI 10.1378/chest.90.4.480; BURNEY PGJ, 1987, CHEST, V91, P79; CHAI H, 1975, J ALLERGY CLIN IMMUN, V56, P323, DOI 10.1016/0091-6749(75)90107-4; Downs SH, 2001, ARCH DIS CHILD, V84, P20, DOI 10.1136/adc.84.1.20; FERRIS BG, 1978, AM REV RESPIR DIS, V118, P1; Grol MH, 1996, ALLERGY, V51, P855; Grol MH, 1999, AM J RESP CRIT CARE, V160, P1830; JENKINS MA, 1994, BRIT MED J, V309, P90; JONES DT, 1987, BRIT J DIS CHEST, V81, P332, DOI 10.1016/0007-0971(87)90181-1; Lowe L, 2002, LANCET, V359, P1904, DOI 10.1016/S0140-6736(02)08781-0; Oswald H, 1997, PEDIATR PULM, V23, P14, DOI 10.1002/(SICI)1099-0496(199701)23:1<14::AID-PPUL2>3.0.CO;2-P; Phelan PD, 2002, J ALLERGY CLIN IMMUN, V109, P189, DOI 10.1067/mai.2001.120951; Rhodes HL, 2001, J ALLERGY CLIN IMMUN, V108, P720, DOI 10.1067/mai.2001.119151; Rhodes HL, 2002, AM J RESP CRIT CARE, V165, P176; 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; Sears MR, 1996, ARCH DIS CHILD, V75, P392; Sears MR, 1997, EUR RESPIR J, V10, P51, DOI 10.1183/09031936.97.10010051; SEARS MR, 1994, BRIT MED J, V309, P72; Silva PA, 1996, CHILD ADULT DUNEDIN; SINCLAIR SW, 1980, NEW ZEAL MED J, V91, P1; Strachan DP, 1996, BRIT MED J, V312, P1195; Strachan DP, 1996, AM J RESP CRIT CARE, V154, P1629; Ulrik CS, 1999, EUR RESPIR J, V13, P904, DOI 10.1034/j.1399-3003.1999.13d35.x; Ulrik CS, 1996, RESP MED, V90, P623, DOI 10.1016/S0954-6111(96)90021-9; Xuan W, 2000, AM J RESP CRIT CARE, V161, P1820; Xuan W, 2002, THORAX, V57, P104, DOI 10.1136/thorax.57.2.104	28	672	685	6	31	MASSACHUSETTS MEDICAL SOC/NEJM	WALTHAM	WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA	0028-4793			NEW ENGL J MED	N. Engl. J. Med.	OCT 9	2003	349	15					1414	1422		10.1056/NEJMoa022363		9	Medicine, General & Internal	General & Internal Medicine	729JF	WOS:000185769500004	14534334	
J	Moore, WC; Meyers, DA; Wenzel, SE; Teague, WG; Li, HS; Li, XN; D'Agostino, R; Castro, M; Curran-Everett, D; Fitzpatrick, AM; Gaston, B; Jarjour, NN; Sorkness, R; Calhoun, WJ; Chung, KF; Comhair, SAA; Dweik, RA; Israel, E; Peters, SP; Busse, WW; Erzurum, SC; Bleecker, ER				Moore, Wendy C.; Meyers, Deborah A.; Wenzel, Sally E.; Teague, W. Gerald; Li, Huashi; Li, Xingnan; D'Agostino, Ralph, Jr.; Castro, Mario; Curran-Everett, Douglas; Fitzpatrick, Anne M.; Gaston, Benjamin; Jarjour, Nizar N.; Sorkness, Ronald; Calhoun, William J.; Chung, Kian Fan; Comhair, Suzy A. A.; Dweik, Raed A.; Israel, Elliot; Peters, Stephen P.; Busse, William W.; Erzurum, Serpil C.; Bleecker, Eugene R.		Natl Heart Lung Blood Inst	Identification of Asthma Phenotypes Using Cluster Analysis in the Severe Asthma Research Program	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma phenotype; definition; cluster analysis; severe asthma	EXHALED NITRIC-OXIDE; RANDOMIZED CONTROLLED-TRIAL; AIR-FLOW OBSTRUCTION; CLINICAL CHARACTERISTICS; LUNG-FUNCTION; OBESITY; ADULTS; INFLAMMATION; CHILDREN; DISEASE	Rationale The Severe Asthma Research Program cohort includes subjects with persistent asthma who have undergone detailed phenotypic characterization. Previous univariate methods compared features of mild, moderate, and severe asthma. Objectives: To identify novel asthma phenotypes using an unsupervised hierarchical cluster analysis. Methods: Reduction of the initial 628 variables to 34 core variables was achieved by elimination of redundant data and transformation of categorical variables into ranked ordinal composite variables. Cluster analysis was performed on 726 subjects. Measurements and Main Results: Five groups were identified. Subjects in Cluster 1 (n = 110) have early onset atopic asthma with normal lung function treated with two or fewer controller medications (82%) and minimal health care utilization. Cluster 2 (n = 321) consists of subjects with early-onset atopic asthma and preserved lung function but increased medication requirements (29% on three or more medications) and health care utilization. Cluster 3 (n = 59) is a unique group of mostly older obese women with late-onset non-atopic asthma, moderate reductions in FEV1, and frequent oral corticosteroid use to manage exacerbations. Subjects in Clusters 4 (n = 120) and 5 (n = 116) have severe airflow obstruction with bronchodilator responsiveness but differ in to their ability to attain normal lung function, age of asthma onset, atopic status, and use of oral corticosteroids. Conclusions: Five distinct clinical phenotypes of asthma have been identified using unsupervised hierarchical cluster analysis. All clusters contain subjects who meet the American Thoracic Society definition of severe asthma, which supports clinical heterogeneity in asthma and the need for new approaches for the classification of disease severity in asthma.	[Moore, Wendy C.; Meyers, Deborah A.; Li, Huashi; Li, Xingnan; Peters, Stephen P.; Bleecker, Eugene R.] Wake Forest Univ, Ctr Human Genom, Sch Med, Winston Salem, NC 27157 USA; [Moore, Wendy C.; Meyers, Deborah A.; Wenzel, Sally E.; Teague, W. Gerald; Castro, Mario; Curran-Everett, Douglas; Fitzpatrick, Anne M.; Gaston, Benjamin; Jarjour, Nizar N.; Sorkness, Ronald; Calhoun, William J.; Chung, Kian Fan; Comhair, Suzy A. A.; Dweik, Raed A.; Israel, Elliot; Peters, Stephen P.; Busse, William W.; Erzurum, Serpil C.; Bleecker, Eugene R.; Natl Heart Lung Blood Inst] Severe Asthma Res Program, Bethesda, MD USA	Moore, WC (reprint author), Wake Forest Univ, Ctr Human Genom, Sch Med, Med Ctr Blvd, Winston Salem, NC 27157 USA.	wmoore@wfubmc.edu	Fain, Sean/K-4260-2016; Dagostino Jr, Ralph/C-4060-2017	Fain, Sean/0000-0001-5461-0646; Dagostino Jr, Ralph/0000-0002-3550-8395; Chung, Kian Fan/0000-0001-7101-1426	National Institute of Health [HL69116, HL69130, HL69149, HL69155, HL69167, HL69170, HL69174, HL69349, M01 RR018390, M01 RR07122, M01 RR03186, HL087665]	Supported by National Institute of Health grants HL69116, HL69130, HL69149, HL69155, HL69167, HL69170, HL69174, HL69349, M01 RR018390, M01 RR07122, M01 RR03186, and HL087665.	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J	Galli, SJ; Tsai, M; Piliponsky, AM				Galli, Stephen J.; Tsai, Mindy; Piliponsky, Adrian M.			The development of allergic inflammation	NATURE			English	Review							OBSTRUCTIVE PULMONARY-DISEASE; MAST-CELL ACTIVATION; REGULATORY T-CELLS; ATOPIC-DERMATITIS; HYGIENE HYPOTHESIS; IMMUNE-RESPONSES; EPITHELIAL-CELLS; BRONCHIAL-ASTHMA; DENDRITIC CELLS; NERVOUS-SYSTEM	Allergic disorders, such as anaphylaxis, hay fever, eczema and asthma, now afflict roughly 25% of people in the developed world. In allergic subjects, persistent or repetitive exposure to allergens, which typically are intrinsically innocuous substances common in the environment, results in chronic allergic inflammation. This in turn produces long-term changes in the structure of the affected organs and substantial abnormalities in their function. It is therefore important to understand the characteristics and consequences of acute and chronic allergic inflammation, and in particular to explore how mast cells can contribute to several features of this maladaptive pattern of immunological reactivity.	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J	Barnes, PJ				Barnes, Peter J.			Immunology of asthma and chronic obstructive pulmonary disease	NATURE REVIEWS IMMUNOLOGY			English	Review							REGULATORY T-CELLS; THYMIC STROMAL LYMPHOPOIETIN; AIR-FLOW LIMITATION; PERIPHERAL AIRWAYS; GENE-EXPRESSION; DENDRITIC CELLS; INDUCED SPUTUM; ATOPIC ASTHMA; TH2 CELLS; ALLERGIC INFLAMMATION	Asthma and chronic obstructive pulmonary disease (COPD) are both obstructive airway diseases that involve chronic inflammation of the respiratory tract, but the type of inflammation is markedly different between these diseases, with different patterns of inflammatory cells and mediators being involved. As described in this Review, these inflammatory profiles are largely determined by the involvement of different immune cells, which orchestrate the recruitment and activation of inflammatory cells that drive the distinct patterns of structural changes in these diseases. However, it is now becoming clear that the distinction between these diseases becomes blurred in patients with severe asthma, in asthmatic subjects who smoke and during acute exacerbations. This has important implications for the development of new therapies.	Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW3 6LY, England	Barnes, PJ (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dovehouse St, London SW3 6LY, England.	p.j.barnes@imperial.ac.uk					Agusti A, 2003, THORAX, V58, P832, DOI 10.1136/thorax.58.10.832; Akbari O, 2006, NEW ENGL J MED, V354, P1117, DOI 10.1056/NEJMoa053614; ALEXANDER A, 1991, American Review of Respiratory Disease, V143, pA633; Allakhverdi Z, 2007, J EXP MED, V204, P253, DOI 10.1084/jem.20062211; Avila PC, 2007, ANNU REV MED, V58, P185, DOI 10.1146/annurev.med.58.061705.145252; Avni O, 2002, NAT IMMUNOL, V3, P643, DOI 10.1038/ni808; BAMES PJ, 2006, CHEST, V129, P151; Barczyk A, 2006, J ALLERGY CLIN IMMUN, V117, P1484, DOI 10.1016/j.jaci.2006.02.013; Barnes PJ, 2007, PLOS MED, V4, P779, DOI 10.1371/journal.pmed.0040112; Barnes PJ, 2006, TRENDS MOL MED, V12, P515, DOI 10.1016/j.molmed.2006.09.006; Barnes PJ, 2006, LAB INVEST, V86, P867, DOI 10.1038/labinvest.3700456; 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J	Adler, NE; Newman, K				Adler, NE; Newman, K			Socioeconomic disparities in health: Pathways and policies	HEALTH AFFAIRS			English	Article							UNITED-STATES; INCOME-DISTRIBUTION; RISK-FACTORS; US ADULTS; MORTALITY; INEQUALITIES; INSURANCE; DISEASE; ASTHMA; CARE	Socioeconomic status (SES) underlies three major determinants of health: health care, environmental exposure, and health behavior. In addition, chronic stress associated with lower SES may also increase morbidity and mortality. Reducing SES disparities in health will require policy initiatives addressing the components of socioeconomic status (income, education, and occupation) as well as the pathways by which these affect health, Lessons for U.S. policy approaches are taken from the Acheson Commission in England, which was charged with reducing health disparities in that country.	Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA; Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA; Univ Calif San Francisco, Ctr Hlth & Community, San Francisco, CA 94143 USA; Harvard Univ, John F Kennedy Sch Govt, Cambridge, MA 02138 USA; Harvard Univ, Radcliffe Inst Adv Study, Cambridge, MA 02138 USA	Adler, NE (reprint author), Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA.						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J	Christ-Crain, M; Jaccard-Stolz, D; Bingisser, R; Gencay, MM; Huber, PR; Tamm, M; Muller, B				Christ-Crain, M; Jaccard-Stolz, D; Bingisser, R; Gencay, MM; Huber, PR; Tamm, M; Muller, B			Effect of procalcitonin-guided treatment on antibiotic use and outcome in lower respiratory tract infections: cluster-randomised, single-blinded intervention trial	LANCET			English	Article							COMMUNITY-ACQUIRED PNEUMONIA; OBSTRUCTIVE PULMONARY-DISEASE; UNCOMPLICATED ACUTE BRONCHITIS; CRITICALLY ILL PATIENTS; MANAGEMENT; THERAPY; EXACERBATIONS; IMPACT; SEPSIS; RESISTANCE	Background Lower respiratory tract infections are often treated with antibiotics without evidence of clinically relevant bacterial disease. Serum calcitonin precursor concentrations, including procalcitonin, are raised in bacterial infections. We aimed to assess a procalcitonin-based therapeutic strategy to reduce antibiotic use in lower respiratory tract infections with a new rapid and sensitive assay. Methods 243 patients admitted with suspected lower respiratory tract infections were randomly assigned standard care (standard group; n=119) or procalcitonin-guided treatment (procalcitonin group; n=124). On the basis of serum procalcitonin concentrations, use of antibiotics was more or less discouraged (<0.1 &mu;g/L or <0.25 mug/L) or encouraged (greater than or equal to0.5 mug/L or greater than or equal to0.25 mug/L), respectively. Re-evaluation was possible after 6-24 h in both groups. Primary endpoint was use of antibiotics and analysis was by intention to treat. Findings Final diagnoses were pneumonia (n=87; 36%), acute exacerbation of chronic obstructive pulmonary disease (60; 25%), acute bronchitis (59; 24%), asthma (13; 5%), and other respiratory affections (24; 10%). Serological evidence of viral infection was recorded in 141 of 175 tested patients (81%). Bacterial cultures were positive from sputum in 51 (21%) and from blood in 16 (7%). In the procalcitonin group, the adjusted relative risk of antibiotic exposure was 0.49 (95% CI 0.44-0.55; p<0.0001) compared with the standard group. Antibiotic use was significantly reduced in all diagnostic subgroups. Clinical and laboratory outcome was similar in both groups and favourable in 235 (97%). Interpretation Procalcitonin guidance substantially reduced antibiotic use in lower respiratory tract infections. Withholding antimicrobial treatment did not compromise outcome. In view of the current overuse of antimicrobial therapy in often self-limiting acute respiratory tract infections, treatment based on procalcitonin measurement could have important clinical and financial implications.	Univ Basel Hosp, Dept Internal Med, CH-4031 Basel, Switzerland; Univ Basel Hosp, Div Pneumol, CH-4031 Basel, Switzerland; Univ Basel Hosp, Div Endocrinol, CH-4031 Basel, Switzerland; Univ Basel Hosp, Dept Res, CH-4031 Basel, Switzerland; Univ Basel Hosp, Dept Clin Chem, CH-4031 Basel, Switzerland	Muller, B (reprint author), Univ Basel Hosp, Dept Internal Med, Petersgraben 4, CH-4031 Basel, Switzerland.	happymiller@bluewin.ch		Bingisser, Roland/0000-0001-8223-9792			ANTHONISEN NR, 1987, ANN INTERN MED, V106, P196; ASSICOT M, 1993, LANCET, V341, P515, DOI 10.1016/0140-6736(93)90277-N; Ball P, 2002, J ANTIMICROB CHEMOTH, V49, P31, DOI 10.1093/jac/49.1.31; British Thoracic Society Standards of Care C, 2001, THORAX S4, V56, pIV1; Chen DK, 1999, NEW ENGL J MED, V341, P233, DOI 10.1056/NEJM199907223410403; Evans AT, 2002, LANCET, V359, P1648, DOI 10.1016/S0140-6736(02)08597-5; Fluckiger U, 2000, EUR J CLIN MICROBIOL, V19, P493, DOI 10.1007/s100960000306; Gonzales R, 2003, JAMA-J AM MED ASSOC, V289, P2701, DOI 10.1001/jama.289.20.2701; Gonzales R, 2000, ANN INTERN MED, V133, P981; Gonzales R, 1999, JAMA-J AM MED ASSOC, V281, P1512, DOI 10.1001/jama.281.16.1512; Guillemot D, 2001, CLIN INFECT DIS, V33, P542, DOI 10.1086/322583; HALLS GA, 1993, J ANTIMICROB CHEMOTH, V31, P985, DOI 10.1093/jac/31.6.985; Halm EA, 2002, NEW ENGL J MED, V347, P2039, DOI 10.1056/NEJMcp020499; Hament JM, 1999, FEMS IMMUNOL MED MIC, V26, P189, DOI 10.1016/S0928-8244(99)00159-5; Harbarth S, 2001, AM J RESP CRIT CARE, V164, P396; JOKINEN C, 1993, AM J EPIDEMIOL, V137, P977; Karzai W, 1997, INFECTION, V25, P329, DOI 10.1007/BF01740811; Korppi M, 2002, APMIS, V110, P515, DOI 10.1034/j.1600-0463.2002.11007801.x; MACFARLANE JT, 1993, LANCET, V341, P511, DOI 10.1016/0140-6736(93)90275-L; Marik PE, 2000, J CRIT CARE, V15, P85, DOI 10.1053/jcrc.2000.16460; Marrie TJ, 2003, EUR RESPIR J, V21, P779, DOI 10.1183/09031936.03.00095403; Meisner M, 2002, CLIN CHIM ACTA, V323, P17, DOI 10.1016/S0009-8981(02)00101-8; Muller B, 2000, CRIT CARE MED, V28, P977; Muller B, 2001, SWISS MED WKLY, V131, P595; NIEDERMAN MS, 1993, AM REV RESPIR DIS, V148, P1418; [Anonymous], 1997, NIH PUBL; Nylen E, 2003, CLIN INFECT DIS, V36, P823, DOI 10.1086/368088; Nylen ES, 1996, AM J MED SCI, V312, P12; ORTQVIST A, 1995, J ANTIMICROB CHEMOTH, V35, P205, DOI 10.1093/jac/35.1.205; Rohde G, 2003, THORAX, V58, P37, DOI 10.1136/thorax.58.1.37; Ruokonen E, 2002, ACTA ANAESTH SCAND, V46, P398, DOI 10.1034/j.1399-6576.2002.460412.x; Sethi S, 2002, NEW ENGL J MED, V347, P465, DOI 10.1056/NEJMoa012561; Sethi S, 2001, CLIN MICROBIOL REV, V14, P336, DOI 10.1128/CMR.14.2.336-363.2001; Snider RH, 1997, J INVEST MED, V45, P552; Stephenson J, 1996, JAMA-J AM MED ASSOC, V275, P175, DOI 10.1001/jama.275.3.175; Strausbaugh LJ, 2003, CLIN INFECT DIS, V36, P870, DOI 10.1086/368197; Uyeki TM, 2003, PEDIATR INFECT DIS J, V22, P164; Wenzel RP, 1999, CLIN INFECT DIS, V28, P1126, DOI 10.1086/514753	38	557	622	4	47	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	FEB 21	2004	363	9409					600	607		10.1016/S0140-6736(04)15591-8		8	Medicine, General & Internal	General & Internal Medicine	776EZ	WOS:000189104900008	14987884	
J	Akbari, O; Freeman, GJ; Meyer, EH; Greenfield, EA; Chang, TT; Sharpe, AH; Berry, G; DeKruyff, RH; Umetsu, DT				Akbari, O; Freeman, GJ; Meyer, EH; Greenfield, EA; Chang, TT; Sharpe, AH; Berry, G; DeKruyff, RH; Umetsu, DT			Antigen-specific regulatory T cells develop via the ICOS-ICOS-ligand pathway and inhibit allergen-induced airway hyperreactivity	NATURE MEDICINE			English	Article							COLONY-STIMULATING FACTOR; HEAT-KILLED LISTERIA; MOUSE BONE-MARROW; DENDRITIC CELLS; IN-VIVO; IMMUNE-RESPONSES; CO-STIMULATION; MOLECULE ICOS; INFLAMMATION; EXPRESSION	Asthma is caused by T-helper cell 2 (Th2)-driven immune responses, but the immunological mechanisms that protect against asthma development are poorly understood. T-cell tolerance, induced by respiratory exposure to allergen, can inhibit the development of airway hyperreactivity (AHR), a cardinal feature of asthma, and we show here that regulatory T (T-R) cells can mediate this protective effect. Mature pulmonary dendritic cells in the bronchial lymph nodes of mice exposed to respiratory allergen induced the development of TR cells, in a process that required T-cell costimulation via the inducible costimulator (ICOS)-ICOS-ligand pathway. The TR cells produced IL-10, and had potent inhibitory activity; when adoptively transferred into sensitized mice, TR cells blocked the development of AHR. Both the development and the inhibitory function of regulatory cells were dependent on the presence of IL-10 and on ICOS-ICOS-ligand interactions. These studies demonstrate that TR cells and the ICOS-ICOS-ligand signaling pathway are critically involved in respiratory tolerance and in downregulating pulmonary inflammation in asthma.	Stanford Univ, Dept Pediat, Sch Med, Div Immunol & Allergy, Stanford, CA 94305 USA; Stanford Univ, Dept Pathol, Sch Med, Stanford, CA 94305 USA; Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA; Harvard Univ, Sch Med, Dept Pathol, Div Immunol Res, Boston, MA USA; Harvard Univ, Sch Med, Dept Med, Boston, MA USA	Umetsu, DT (reprint author), Stanford Univ, Dept Pediat, Sch Med, Div Immunol & Allergy, Stanford, CA 94305 USA.				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Med.	SEP	2002	8	9					1024	1032		10.1038/nm745		9	Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental	Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine	589KQ	WOS:000177757900039	12145647	
J	Morgan, WJ; Crain, EF; Gruchalla, RS; O'Connor, GT; Kattan, M; Evans, RI; Stout, J; Malindzak, G; Smartt, E; Plaut, M; Walter, M; Vaughn, B; Mitchell, H				Morgan, WJ; Crain, EF; Gruchalla, RS; O'Connor, GT; Kattan, M; Evans, RI; Stout, J; Malindzak, G; Smartt, E; Plaut, M; Walter, M; Vaughn, B; Mitchell, H		Inner-City Asthma Study Grp	Results of a home-based environmental intervention among urban children with asthma	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							HOUSE-DUST-MITE; INNER-CITY CHILDREN; COCKROACH ALLERGEN EXPOSURE; RANDOMIZED CONTROLLED-TRIAL; DOUBLE-BLIND TRIAL; AVOIDANCE MEASURES; TOBACCO-SMOKE; RISK-FACTORS; LOW-INCOME; REDUCTION	Background: Children with asthma who live in the inner city are exposed to multiple indoor allergens and environmental tobacco smoke in their homes. Reductions in these triggers of asthma have been difficult to achieve and have seldom been associated with decreased morbidity from asthma. The objective of this study was to determine whether an environmental intervention tailored to each child's allergic sensitization and environmental risk factors could improve asthma-related outcomes. Methods: We enrolled 937 children with atopic asthma (age, 5 to 11 years) in seven major U.S. cities in a randomized, controlled trial of an environmental intervention that lasted one year (intervention year) and included education and remediation for exposure to both allergens and environmental tobacco smoke. Home environmental exposures were assessed every six months, and asthma-related complications were assessed every two months during the intervention and for one year after the intervention. Results: For every 2-week period, the intervention group had fewer days with symptoms than did the control group both during the intervention year (3.39 vs. 4.20 days, P<0.001) and the year afterward (2.62 vs. 3.21 days, P<0.001), as well as greater declines in the levels of allergens at home, such as Dermatophagoides farinae (Derf1) allergen in the bed (P<0.001) and on the bedroom floor (P=0.004), D. pteronyssinus in the bed (P=0.007), and cockroach allergen on the bedroom floor (P<0.001). Reductions in the levels of cockroach allergen and dust-mite allergen (Derf1) on the bedroom floor were significantly correlated with reduced complications of asthma (P<0.001). Conclusions: Among inner-city children with atopic asthma, an individualized, home-based, comprehensive environmental intervention decreases exposure to indoor allergens, including cockroach and dust-mite allergens, resulting in reduced asthma-associated morbidity.	Univ Arizona, Arizona Resp Ctr, Coll Med, Tucson, AZ 85724 USA; Albert Einstein Coll Med, Jacobi Med Ctr, Bronx, NY 10467 USA; Univ Texas, SW Med Ctr, Dallas, TX USA; Boston Univ, Sch Med, Boston, MA 02118 USA; CUNY Mt Sinai Sch Med, New York, NY 10029 USA; Childrens Mem Hosp, Chicago, IL 60614 USA; Univ Washington, Sch Med & Publ Hlth, Seattle, WA USA; NIEHS, Res Triangle Pk, NC 27709 USA; NIAID, Bethesda, MD 20892 USA; Rho, Chapel Hill, NC USA	Morgan, WJ (reprint author), Univ Arizona, Arizona Resp Ctr, Coll Med, 1501 N Campbell Ave, Tucson, AZ 85724 USA.			O'Connor, George/0000-0002-6476-3926	NCRR NIH HHS [M01 RR00533]; NIAID NIH HHS [AI-39785, AI-39761, AI-39769, AI-39776, AI-39789, AI-39900, AI-39901, AI-39902]		BANDURA A, 1986, SOCIAL FDN THOUGHT A; Bandura A., 1986, SOCIAL LEARNING THEO; CALL RS, 1992, J PEDIATR-US, V121, P862, DOI 10.1016/S0022-3476(05)80329-4; Carswell F, 1996, CLIN EXP ALLERGY, V26, P386, DOI 10.1111/j.1365-2222.1996.tb00554.x; Carter MC, 2001, J ALLERGY CLIN IMMUN, V108, P732, DOI 10.1067/mai.2001.119155; CHAPMAN MD, 1987, J ALLERGY CLIN IMMUN, V80, P184, DOI 10.1016/0091-6749(87)90128-X; CHILMONCZYK BA, 1993, NEW ENGL J MED, V328, P1665, DOI 10.1056/NEJM199306103282303; Cook DG, 1997, THORAX, V52, P1081; Crain EF, 2002, ENVIRON HEALTH PERSP, V110, P939; DORWARD AJ, 1988, THORAX, V43, P98, DOI 10.1136/thx.43.2.98; Eggleston PA, 1998, J ALLERGY CLIN IMMUN, V102, P563, DOI 10.1016/S0091-6749(98)70272-6; EHNERT B, 1992, J ALLERGY CLIN IMMUN, V90, P135, DOI 10.1016/S0091-6749(06)80024-2; Elder JP, 1999, AM J PREV MED, V17, P275, DOI 10.1016/S0749-3797(99)00094-X; Gergen PJ, 1999, J ALLERGY CLIN IMMUN, V103, P501, DOI 10.1016/S0091-6749(99)70477-X; GERGEN PJ, 1990, JAMA-J AM MED ASSOC, V264, P1688, DOI 10.1001/jama.264.13.1688; Gotzsche PC, 2001, COCHRANE DB SYST REV, V3; Hamilton RG, 1997, METHODS, V13, P53, DOI 10.1006/meth.1997.0495; Hovell MF, 2002, PEDIATRICS, V110, P946, DOI 10.1542/peds.110.5.946; Htut T, 2001, J ALLERGY CLIN IMMUN, V107, P55, DOI 10.1067/mai.2001.111240; *I MED, 2000, CLEAR AIR ASTHM IND, P124; Irvine L, 1999, BRIT MED J, V318, P1456; Jalaludin B, 1998, J ALLERGY CLIN IMMUN, V102, P382, DOI 10.1016/S0091-6749(98)70124-1; Kattan M, 1997, PEDIATR PULM, V24, P253, DOI 10.1002/(SICI)1099-0496(199710)24:4<253::AID-PPUL4>3.0.CO;2-L; Kitch BT, 2000, ENVIRON HEALTH PERSP, V108, P301, DOI 10.2307/3454347; MARKS GB, 1994, CLIN EXP ALLERGY, V24, P1078, DOI 10.1111/j.1365-2222.1994.tb02746.x; McDonald E, 2002, CHEST, V122, P1535, DOI 10.1378/chest.122.5.1535; *NAT KIDN FDN INC, 1997, DIAL OUTC QUAL IN CL, P42; Pauwels RA, 2003, LANCET, V361, P1071, DOI 10.1016/S0140-6736(03)12891-7; Platts-Mills TAE, 2003, NEW ENGL J MED, V349, P207, DOI 10.1056/NEJMp030082; Rijssenbeek-Nouwens LHM, 2002, THORAX, V57, P784, DOI 10.1136/thorax.57.9.784; 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; Szefler S, 2000, NEW ENGL J MED, V343, P1054; Terreehorst I, 2003, NEW ENGL J MED, V349, P237, DOI 10.1056/NEJMoa023171; *THOM HEALTHC, 2004, DRUG TOP RED BOOK; vanderHeide S, 1997, ALLERGY, V52, P921; Vojta PJ, 2001, ENVIRON HEALTH PERSP, V109, P815, DOI 10.2307/3454824; Wakefield M, 2002, PREV MED, V34, P58, DOI 10.1006/pmed.2001.0953; WALSHAW MJ, 1986, Q J MED, V58, P199; Warner JA, 2000, J ALLERGY CLIN IMMUN, V105, P75, DOI 10.1016/S0091-6749(00)90181-7; WEITZMAN M, 1992, JAMA-J AM MED ASSOC, V268, P2673, DOI 10.1001/jama.268.19.2673; Williams LW, 1999, J ALLERGY CLIN IMMUN, V104, P702, DOI 10.1016/S0091-6749(99)70346-5; Wood RA, 2001, ANN ALLERG ASTHMA IM, V87, P60; Woodcock A, 2003, NEW ENGL J MED, V349, P225, DOI 10.1056/NEJMoa023175; [Anonymous], 1995, AM J RESP CRIT CARE, V152, P1107	45	548	572	3	48	MASSACHUSETTS MEDICAL SOC	WALTHAM	WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA	0028-4793			NEW ENGL J MED	N. Engl. J. Med.	SEP 9	2004	351	11					1068	1080		10.1056/NEJMoa032097		13	Medicine, General & Internal	General & Internal Medicine	852CX	WOS:000223733900006	15356304	
J	Ball, TM; Castro-Rodriguez, JA; Griffith, KA; Holberg, CJ; Martinez, FD; Wright, AL				Ball, TM; Castro-Rodriguez, JA; Griffith, KA; Holberg, CJ; Martinez, FD; Wright, AL			Siblings, day-care attendance, and the risk of asthma and wheezing during childhood	NEW ENGLAND JOURNAL OF MEDICINE			English	Article; Proceedings Paper	39th Annual Meeting of the Ambulatory-Pediatric-Association	MAY 01-04, 1999	SAN FRANCISCO, CALIFORNIA	Ambulat Pediatr Assoc			RESPIRATORY-TRACT ILLNESS; HAY-FEVER; 1ST YEAR; CHILDREN; ALLERGEN; ATOPY; LIFE; SENSITIZATION; RESPONSES; DISEASE	Background: Young children with older siblings and those who attend day care are at increased risk for infections, which in turn may protect against the development of allergic diseases, including asthma. However, the results of studies examining the relation between exposure to other children and the subsequent development of asthma have been conflicting. Methods: In a study involving 1035 children followed since birth as part of the Tucson Children's Respiratory Study, we determined the incidence of asthma (defined as at least one episode of asthma diagnosed by a physician when the child was 6 to 13 years old) and the prevalence of frequent wheezing (more than three wheezing episodes during the preceding year) in relation to the number of siblings at home and in relation to attendance at day care during infancy. Results: The presence of one or more older siblings at home protected against the development of asthma (adjusted relative risk for each additional older sibling, 0.8; 95 percent confidence interval, 0.7 to 1.0; P = 0.04), as did attendance at day care during the first six months of life (adjusted relative risk, 0.4; 95 percent confidence interval, 0.2 to 1.0; P = 0.04). Children with more exposure to other children at home or at day care were more likely to have frequent wheezing at the age of 2 years than children with little or no exposure (adjusted relative risk, 1.4; 95 percent confidence interval, 1.1 to 1.8; P = 0.01) but were less likely to have frequent wheezing from the age of 6 (adjusted relative risk, 0.8; 95 percent confidence interval, 0.6 to 1.0; P = 0.03) through the age of 13 (adjusted relative risk, 0.3; 95 percent confidence interval, 0.2 to 0.5; P<0.001). Conclusions: Exposure of young children to older children at home or to other children at day care protects against the development of asthma and frequent wheezing later in childhood. (N Engl J Med 2000;343:538-43.) (C)2000, Massachusetts Medical Society.	Univ Arizona, Coll Med, Resp Sci Ctr, Tucson, AZ 85724 USA; Univ Arizona, Coll Med, Dept Pediat, Tucson, AZ 85724 USA	Wright, AL (reprint author), Univ Arizona, Coll Med, Resp Sci Ctr, 1501 N Campbell Ave,POB 245073, Tucson, AZ 85724 USA.				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Engl. J. Med.	AUG 24	2000	343	8					538	543		10.1056/NEJM200008243430803		6	Medicine, General & Internal	General & Internal Medicine	346QM	WOS:000088882600003	10954761	
J	Jutel, M; Akdis, M; Budak, F; Aebischer-Casaulta, C; Wrzyszcz, M; Blaser, K; Akdis, CA				Jutel, M; Akdis, M; Budak, F; Aebischer-Casaulta, C; Wrzyszcz, M; Blaser, K; Akdis, CA			IL-10 and TGF-beta cooperate in the regulatory T cell response to mucosal allergens in normal immunity and specific immunotherapy	EUROPEAN JOURNAL OF IMMUNOLOGY			English	Article						specific immunotherapy; T cell; IL-10; TGF-beta; regulatory T cell	GROWTH-FACTOR-BETA; GRASS-POLLEN IMMUNOTHERAPY; BEE VENOM IMMUNOTHERAPY; HUMAN LYMPHOCYTES-T; IN-VITRO; HELPER CELLS; CUTANEOUS RESPONSES; PHOSPHOLIPASE A(2); INTERFERON-GAMMA; IGE SYNTHESIS	The regulation of normal and allergic immune responses to airborne allergens in the mucosa is still poorly understood, and the mechanism of specific immunotherapy (SIT) in normalizing the allergic response to such allergens is currently not clear. Accordingly, we have investigated the immunoregulatory mechanism of both normal and allergic responses to the major house-dust mite (HDM) and birch pollen allergens - Dermatophagoides pteroynyssinus (Der p)1 and Bet v 1, respectively - as well as the immunologic basis of SIT to HDM in rhinitis and asthma patients. In normal immunity to HDM and birch pollen, an allergen-specific peripheral T cell suppression to Der p 1 and Bet v 1 was observed. The deviated immune response was characterized by suppressed proliferative T cell and Th1 (IFN-gamma) and Th2 (IL-5, IL-13) cytokine responses, and increased IL-10 and TGF-beta secretion by allergen-specific T cells. Neutralization of cytokine activity showed that T cell suppression was induced by IL-10 and TGF-beta during SIT and in normal immunity to the mucosal allergens. In addition, SIT induced an antigen-specific suppressive activity in CD4(+) CD25(+) T cells of allergic individuals. Together, these results demonstrate a deviation towards a regulatory/suppressor T cell response during SIT and in normal immunity as a key event for the healthy immune response to mucosal antigens.	Swiss Inst Allergy & Asthma Res, CH-7270 Davos, Switzerland; Med Acad Wroclaw, Wroclaw, Poland; Uludag Univ, Sch Med, Bursa, Turkey; Univ Hosp, Dept Pediat, Bern, Switzerland	Jutel, M (reprint author), Swiss Inst Allergy & Asthma Res, Obere Str 22, CH-7270 Davos, Switzerland.		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J. Immunol.	MAY	2003	33	5					1205	1214		10.1002/eji.200322919		10	Immunology	Immunology	680DM	WOS:000182961100008	12731045	
J	Olsen, J; Melbye, M; Olsen, SF; Sorensen, TIA; Aaby, P; Andersen, AMN; Taxbol, D; Hansen, KD; Juhl, M; Schow, TB; Sorensen, HT; Andresen, J; Mortensen, EL; Olesen, AW; Sondergaard, C				Olsen, J; Melbye, M; Olsen, SF; Sorensen, TIA; Aaby, P; Andersen, AMN; Taxbol, D; Hansen, KD; Juhl, M; Schow, TB; Sorensen, HT; Andresen, J; Mortensen, EL; Olesen, AW; Sondergaard, C			The Danish National Birth Cohort - its background, structure and aim	SCANDINAVIAN JOURNAL OF PUBLIC HEALTH			English	Article						cohort; pregnancy; life-course; epidemiology	IN-UTERO; REGISTER; EXPOSURE; CHILDHOOD; HEALTH; RISK; PREVENTION; WEIGHT	Background: It is well known that the time from conception to early childhood has importance for health conditions that reach into later stages of life. Recent research supports this view,, and diseases such as cardiovascular morbidity, cancer. mental illnesses. asthma. and allergy may all have component causes that act early in life. Exposures in this period, which influence fetal growth, cell divisions, and organ functioning, may have long-lasting impact on health and disease susceptibility. Methods: To investigate these issues the Danish National Birth Cohort (Better health for mother and child) was established. A large cohort of pregnant women with long-term follow-up of the offspring was the obvious choice because many of the exposures of interest cannot be reconstructed with sufficient validity back in time. The Study needs to be large, and it is aimed to recruit 100,000 women early in pregnancy, and to continue follow-up for decades. The Nordic countries are better Suited for this kind of research than most other countries because of their population-based registers on diseases, demography md social conditions, linkable at the individual level by means of the unique ID-number given to all citizens. Exposure information is mainly collected by computer-assisted telephone interviews with the women twice during pregnancy and when their children are six and 18 months old. participants are also asked to fill in a self-administered food frequency questionnaire in mid-pregnancy. Furthermore. a biological bank has been set up with blood taken from the mother twice during pregnancy and blood from the umbilical cord taken shortly after birth. Data collection started in 1996 and the project covered all regions in Denmark in 1999. By August 2000, a total of 60,000 pregnant women had been recruited to the study. It is expected that a large number of gene-environmental hypotheses need to be based on case-control analyses within a cohort like this.	Statens Serum Inst, Danish Epidemiol Sci Ctr, DK-2300 Copenhagen S, Denmark; Danish Epidemiol Sci Ctr, Aarhus, Denmark	Olsen, SF (reprint author), Statens Serum Inst, Danish Epidemiol Sci Ctr, Artillerivej 5, DK-2300 Copenhagen S, Denmark.		Andersen, Anne-Marie Nybo/E-4993-2013	Andersen, Anne-Marie Nybo/0000-0002-4296-8488			Abel EL, 1998, ALCOHOL ALCOHOLISM, V33, P417; Andersen TF, 1999, DAN MED BULL, V46, P263; Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; BARKER D J P, 1992, Journal of Epidemiology and Community Health, V46, P8, DOI 10.1136/jech.46.1.8; Barker D. J. P., 1994, MOTHERS BABIES DIS L; BARR CE, 1990, ARCH GEN PSYCHIAT, V47, P869; Bingley PJ, 2000, BRIT MED J, V321, P420, DOI 10.1136/bmj.321.7258.420; CARLSEN E, 1992, BRIT MED J, V305, P609; Christensen K, 1998, DAN MED BULL, V45, P91; Ekbom A, 1998, SEMIN CANCER BIOL, V8, P237, DOI 10.1006/scbi.1998.0073; Gaist D, 1997, DAN MED BULL, V44, P445; GIUSTI RM, 1995, ANN INTERN MED, V122, P778; GODFREY KM, AM J CLIN NUTR, V71, pS1377; Grandjean P, 1997, NEUROTOXICOL TERATOL, V19, P417, DOI 10.1016/S0892-0362(97)00097-4; Juel K, 1999, DAN MED BULL, V46, P354; Knudsen LB, 1998, DAN MED BULL, V45, P221; Kuh D, 1997, LIFE COURSE APPROACH; Kyvik KO, 1996, DAN MED BULL, V43, P467; MITTENDORF R, 1995, TERATOLOGY, V51, P435, DOI 10.1002/tera.1420510609; MunkJorgensen P, 1997, DAN MED BULL, V44, P82; Olsen J, 2000, EPIDEMIOL REV, V22, P76; REINISCH JM, 1995, JAMA-J AM MED ASSOC, V274, P1518, DOI 10.1001/jama.274.19.1518; Roed AS, 1999, DAN MED BULL, V46, P269; SHARPE RM, 1993, LANCET, V341, P1392, DOI 10.1016/0140-6736(93)90953-E; Sorensen HT, 1997, BRIT MED J, V315, P401; Sorensen HT, 1997, BRIT MED J, V315, P1137; TRICHOPOULOS D, 1990, LANCET, V335, P939; Westergaard T, 1997, J NATL CANCER I, V89, P939, DOI 10.1093/jnci/89.13.939	28	537	539	3	30	TAYLOR & FRANCIS AS	OSLO	CORT ADELERSGT 17, PO BOX 2562, SOLLI, 0202 OSLO, NORWAY	1403-4948			SCAND J PUBLIC HEALT	Scand. J. Public Health	DEC	2001	29	4					300	307		10.1177/14034948010290040201		8	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	499HY	WOS:000172566800011	11775787	
J	Bruce, N; Perez-Padilla, R; Albalak, R				Bruce, N; Perez-Padilla, R; Albalak, R			Indoor air pollution in developing countries: a major environmental and public health challenge	BULLETIN OF THE WORLD HEALTH ORGANIZATION			English	Review						air pollution, indoor-adverse effects; fossil fuels-toxicity; lung diseases; smoke inhalation injury; cataract; developing countries	PAPUA-NEW-GUINEA; BIOMASS FUEL COMBUSTION; LOWER RESPIRATORY-INFECTIONS; DOMESTIC SMOKE POLLUTION; DIFFERENT COOKING FUELS; YOUNG GAMBIAN CHILDREN; LUNG-CANCER MORTALITY; WOOD-BURNING STOVES; LOW-BIRTH-WEIGHT; RISK-FACTORS	Around 50% of people, almost all in developing countries, rely on coal and biomass in the form of wood, dung and crop residues for domestic energy. These materials are typically burnt in simple stoves with very incomplete combustion. Consequently, women and young children are exposed to high levels of indoor air pollution every clay. There is consistent evidence that indoor air pollution increases the risk of chronic obstructive pulmonary disease and of acute respiratory infections in childhood, the most important cause of death among children under 5 years of age in developing countries. Evidence also exists of associations with low birth weight, increased infant and perinatal mortality, pulmonary tuberculosis, nasopharyngeal and laryngeal cancer, cataract, and, specifically in respect of the use of coal, with lung cancer. Conflicting evidence exists with regard to asthma. All studies are observational and very few have measured exposure directly, while a substantial proportion have not dealt with confounding, As a result, risk estimates are poorly quantified and may be biased. Exposure to indoor air pollution may be responsible for nearly 2 million excess deaths in developing countries and for some 4% of the global burden of disease. Indoor air pollution is a major global public health threat requiring greatly increased efforts in the areas of research and policy-making. Research on its health effects should be strengthened, particularly in relation to tuberculosis and acute lower respiratory infections. A more systematic approach to the development and evaluation of interventions is desirable, with clearer recognition of the interrelationships between poverty and dependence on polluting fuels.	Univ Liverpool, Dept Publ Hlth, Liverpool L69 3GB, Merseyside, England; Natl Inst Resp Dis, Mexico City, DF, Mexico; Emory Univ, Rollins Sch Publ Hlth, Dept Int Hlth, Atlanta, GA 30322 USA	Bruce, N (reprint author), Univ Liverpool, Dept Publ Hlth, Whelan Bldg, Liverpool L69 3GB, Merseyside, England.						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J	Platts-Mills, T; Vaughan, J; Squillace, S; Woodfolk, J; Sporik, R				Platts-Mills, T; Vaughan, J; Squillace, S; Woodfolk, J; Sporik, R			Sensitisation, asthma, and a modified Th2 response in children exposed to cat allergen: a population-based cross-sectional study	LANCET			English	Article							INNER-CITY CHILDREN; RISK FACTOR; IGG4 ANTIBODIES; SENSITIZATION; CHILDHOOD; MITE; IGE; LYMPHOCYTES; REACTIVITY; SUBCLASS	Background Although asthma is strongly associated with immediate hypersensitivity to indoor allergens, several studies have suggested that a cat in the house can decrease the risk of asthma. We investigated the immune response to cat and mite allergens, and asthma among children with a wide range of allergen exposure. Methods We did a population-based cross-sectional study of children (aged 12-14 years), some of whom had symptoms of asthma and bronchial hyper-reactivity, Antibodies to mite (Der f 1) and cat (Fel d 1) allergens measured by isotype (IgG and IgG4) specific radioimmunoprecipitation assays were compared with sensitisation and allergen concentrations in house dust. Findings 226 children were recruited, 47 of whom had symptoms of asthma and bronchial hyper-reactivity, Increasing exposure to mite was associated with increased prevalence of sensitisation and IgG antibody to Der f 1. By contrast, the highest exposure to cat was associated with decreased sensitisation, but a higher prevalence of IgG antibody to Fel d 1, Thus, among children with high exposure, the odds of sensitisation to mite rather than cat was 4.0 (99% CI 1.49-10.00). Furthermore. 31 of 76 children with 23 mug Fel d 1 at home, who were not sensitised to cat allergen had >125 units of IgG antibody to Fel d 1. Antibodies to Fel d 1 of the IgG4 isotype were strongly correlated with IgG antibody in both allergic and non-allergic children (r=0.84 and r=0.66, respectively). Sensitisation to mite or cat allergens was the strongest independent risk factor for asthma (p<0.001). Interpretation Exposure to cat allergen can produce an IgG and IgG4 antibody response without sensitisation or risk of asthma, This modified T-helper-2 cell response should be regarded as a form of tolerance and may be the correct objective of immunotherapy. The results may also explain the observation that animals in the house can decrease the risk of asthma.	Univ Virginia, Dept Med, Asthma & Allerg Dis Ctr, Charlottesville, VA 22908 USA	Platts-Mills, T (reprint author), Univ Virginia Hlth Syst, Asthma & Allerg Dis Ctr, POB 801355, Charlottesville, VA 22908 USA.				NIAID NIH HHS [AI-20565, AI-34607]		AALBERSE RC, 1983, J IMMUNOL, V130, P722; Agresti A, 1999, INT ARCH ALLERGY IMM, V118, P279, DOI 10.1159/000024099; Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; Borish L, 1997, J ALLERGY CLIN IMMUN, V99, P161, DOI 10.1016/S0091-6749(97)70090-3; CALL RS, 1992, J PEDIATR-US, V121, P862, DOI 10.1016/S0022-3476(05)80329-4; CHAPMAN MD, 1988, J IMMUNOL, V140, P812; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Halonen M, 1997, AM J RESP CRIT CARE, V155, P1356; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; HUSSAIN R, 1992, J IMMUNOL, V148, P2731; ISHIZAKA K, 1967, J IMMUNOL, V98, P490; Jeannin P, 1998, J IMMUNOL, V160, P3555; Muller U, 1998, J ALLERGY CLIN IMMUN, V101, P747, DOI 10.1016/S0091-6749(98)70402-6; 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, 1978, J IMMUNOL, V120, P1201; Prescott SL, 1998, J IMMUNOL, V160, P4730; Ronmark E, 1999, ALLERGY, V54, P926, DOI 10.1034/j.1398-9995.1999.00044.x; Roost HP, 1999, J ALLERGY CLIN IMMUN, V104, P941, DOI 10.1016/S0091-6749(99)70072-2; 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; Schuurman J, 1999, IMMUNOLOGY, V97, P693, DOI 10.1046/j.1365-2567.1999.00845.x; Sporik R, 1999, THORAX, V54, P675; SPORIK R, 1995, AM J RESP CRIT CARE, V151, P1388; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; Squillace SP, 1997, AM J RESP CRIT CARE, V156, P1760; Strachan DP, 1996, ARCH DIS CHILD, V74, P422; von Mutius E, 2000, J ALLERGY CLIN IMMUN, V105, P9, DOI 10.1016/S0091-6749(00)90171-4; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; Wan H, 1999, J CLIN INVEST, V104, P123, DOI 10.1172/JCI5844; WHITE H, 1982, ECONOMETRICA, V50, P1, DOI 10.2307/1912526; ZHANG K, 1994, J IMMUNOL, V152, P3427	33	533	545	1	14	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	MAR 10	2001	357	9258					752	756		10.1016/S0140-6736(00)04168-4		5	Medicine, General & Internal	General & Internal Medicine	409TC	WOS:000167400900013	11253969	
J	Hammad, H; Chieppa, M; Perros, F; Willart, MA; Germain, RN; Lambrecht, BN				Hammad, Hamida; Chieppa, Marcello; Perros, Frederic; Willart, Monique A.; Germain, Ronald N.; Lambrecht, Bart N.			House dust mite allergen induces asthma via Toll-like receptor 4 triggering of airway structural cells	NATURE MEDICINE			English	Article							THYMIC STROMAL LYMPHOPOIETIN; DENDRITIC CELLS; EPITHELIAL-CELLS; ALVEOLAR MACROPHAGES; INHALED ENDOTOXIN; TYPE-2 RESPONSES; TH2 RESPONSES; LYMPH-NODES; T-CELLS; INFLAMMATION	Barrier epithelial cells and airway dendritic cells (DCs) make up the first line of defense against inhaled substances such as house dust mite (HDM) allergen and endotoxin (lipopolysaccharide, LPS). We hypothesized that these cells need to communicate with each other to cause allergic disease. We show in irradiated chimeric mice that Toll-like receptor 4 (TLR4) expression on radioresistant lung structural cells, but not on DCs, is necessary and sufficient for DC activation in the lung and for priming of effector T helper responses to HDM. TLR4 triggering on structural cells caused production of the innate proallergic cytokines thymic stromal lymphopoietin, granulocyte-macrophage colony-stimulating factor, interleukin-25 and interleukin-33. The absence of TLR4 on structural cells, but not on hematopoietic cells, abolished HDM-driven allergic airway inflammation. Finally, inhalation of a TLR4 antagonist to target exposed epithelial cells suppressed the salient features of asthma, including bronchial hyperreactivity. Our data identify an innate immune function of airway epithelial cells that drives allergic inflammation via activation of mucosal DCs.	[Hammad, Hamida; Perros, Frederic; Willart, Monique A.; Lambrecht, Bart N.] Univ Ghent, Dept Resp Med, Lab Immunoregulat & Mucosal Immunol, B-9000 Ghent, Belgium; [Chieppa, Marcello; Germain, Ronald N.] NIAID, Immunol Lab, Sect Lymphocyte Biol, US Natl Inst Hlth, Bethesda, MD 20892 USA; [Lambrecht, Bart N.] Erasmus Univ, Med Ctr, Dept Pulm Med, Rotterdam, Netherlands	Lambrecht, BN (reprint author), Univ Ghent, Dept Resp Med, Lab Immunoregulat & Mucosal Immunol, B-9000 Ghent, Belgium.	bart.lambrecht@ugent.be	Chieppa, Marcello/K-4846-2012; Hammad, Hamida/J-9391-2015; Lambrecht, Bart/K-2484-2014	Hammad, Hamida/0000-0003-3762-8603; Lambrecht, Bart/0000-0003-4376-6834	Intramural NIH HHS [ZIA AI000545-21]		Angkasekwinai P, 2007, J EXP MED, V204, P1509, DOI 10.1084/jem.20061675; Bajenoff M, 2006, IMMUNITY, V25, P989, DOI 10.1016/j.immuni.2006.10.011; Barnes PJ, 2008, NAT REV IMMUNOL, V8, P183, DOI 10.1038/nri2254; Berndt A, 2007, AM J PHYSIOL-LUNG C, V292, pL936, DOI 10.1152/ajplung.00394.2006; Beutler B, 2001, DRUG METAB DISPOS, V29, P474; BILYK N, 1993, J EXP MED, V177, P1773, DOI 10.1084/jem.177.6.1773; Boes M, 2002, NATURE, V418, P983, DOI 10.1038/nature01004; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Cates EC, 2004, J IMMUNOL, V173, P6384; Eisenbarth SC, 2002, J EXP MED, V196, P1645, DOI 10.1084/jem.20021340; Fallon PG, 2006, J EXP MED, V203, P1105, DOI 10.1084/jem.20051615; Fattouh R, 2005, AM J RESP CRIT CARE, V172, P314, DOI 10.1164/rccm.200502-198OC; Geissmann F, 2003, IMMUNITY, V19, P71, DOI 10.1016/S1074-7613(03)00174-2; Guillot L, 2004, J BIOL CHEM, V279, P2712, DOI 10.1074/jbc.M305790200; Hammad H, 2008, NAT REV IMMUNOL, V8, P193, DOI 10.1038/nri2275; Hammad H, 2007, ADV IMMUNOL, V93, P265, DOI 10.1016/S0065-2776(06)93007-7; Hammad H, 2007, J EXP MED, V204, P357, DOI 10.1084/jem.20061196; IROMPETTE A, 2009, NATURE, V457, P585; Kondo Y, 2008, INT IMMUNOL, V20, P791, DOI 10.1093/intimm/dxn037; Lambrecht BN, 1998, J IMMUNOL, V160, P4090; Lewkowich IP, 2005, J EXP MED, V202, P1549, DOI 10.1084/jem.20051506; Liu YJ, 2006, J EXP MED, V203, P269, DOI 10.1084/jem.20051745; Lorenz E, 2001, AM J PHYSIOL-LUNG C, V281, pL1106; Matute-Bello G, 2004, J IMMUNOL METHODS, V292, P25, DOI 10.1016/j.jim.2004.05.010; NATHAN AI, 2009, J ALLERGY CLIN  0127, DOI DOI 10.1016/J.JACI.2008.12; Nolte MA, 2007, J EXP MED, V204, P1487, DOI 10.1084/jem.20070325; Noulin N, 2005, J IMMUNOL, V175, P6861; Pichavant M, 2005, J ALLERGY CLIN IMMUN, V115, P771, DOI 10.1016/j.jaci.2004.11.043; Piggott DA, 2005, J CLIN INVEST, V115, P459, DOI 10.1172/JCI200522462; Poynter ME, 2003, J IMMUNOL, V170, P6257; Robays LJ, 2007, J IMMUNOL, V178, P5305; Saito T, 2005, CELL TISSUE RES, V321, P75, DOI 10.1007/s00441-005-1113-9; Schmitz J, 2005, IMMUNITY, V23, P479, DOI 10.1016/j.immuni.2005.09.015; Sha Q, 2004, AM J RESP CELL MOL, V31, P358, DOI 10.1165/rcmb.2003-03880C; Skerrett SJ, 2004, AM J PHYSIOL-LUNG C, V287, pL143, DOI 10.1152/ajplung.00030.2004; Sokol CL, 2008, NAT IMMUNOL, V9, P310, DOI 10.1038/ni1558; Reis e Sousa, 2006, NAT REV IMMUNOL, V6, P476, DOI DOI 10.1038/NRI1845; Stampfli MR, 1998, J CLIN INVEST, V102, P1704, DOI 10.1172/JCI4160; Stumbles PA, 1998, J EXP MED, V188, P2019, DOI 10.1084/jem.188.11.2019; van Rijt LS, 2004, J IMMUNOL METHODS, V288, P111, DOI 10.1016/j.jim.2004.03.004; Veres TZ, 2007, AM J RESP CELL MOL, V37, P553, DOI 10.1165/rcmb.2007-00870C; Vermaelen KY, 2001, J EXP MED, V193, P51; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; Zhou BH, 2005, NAT IMMUNOL, V6, P1047, DOI 10.1038/ni1247; Ziegler SF, 2006, NAT IMMUNOL, V7, P709, DOI 10.1038/ni1360	45	522	539	3	42	NATURE PUBLISHING GROUP	NEW YORK	75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA	1078-8956			NAT MED	Nat. Med.	APR	2009	15	4					410	416		10.1038/nm.1946		7	Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental	Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine	429RG	WOS:000264937200028	19330007	
J	Douwes, J; Thorne, P; Pearce, N; Heederik, D				Douwes, J; Thorne, P; Pearce, N; Heederik, D			Bioaerosol health effects and exposure assessment: Progress and prospects	ANNALS OF OCCUPATIONAL HYGIENE			English	Article; Proceedings Paper	5th International Conference of the International-Occupational-Hygiene-Association	JUN, 2002	BERGEN, NORWAY	Int Occupat Hygiene Assoc		asthma; beta(1,3)-glucans; bioaerosols; cancer; endotoxin; exposure assessment; infections; microorganisms	UPPER AIRWAY INFLAMMATION; WORK-RELATED SYMPTOMS; HOUSE-DUST ENDOTOXIN; LEGIONNAIRES-DISEASE; INHALED ENDOTOXIN; COTTON DUST; GRAIN DUST; HYPERSENSITIVITY PNEUMONITIS; ENVIRONMENTAL EXPOSURE; RESPONSE RELATIONSHIPS	Exposures to bioaerosols in the occupational environment are associated with a wide range of health effects with major public health impact, including infectious diseases, acute toxic effects, allergies and cancer. Respiratory symptoms and lung function impairment are the most widely studied and probably among the most important bioaerosol-associated health effects. In addition to these adverse health effects some protective effects of microbial exposure on atopy and atopic conditions has also been suggested. New industrial activities have emerged in recent years in which exposures to bioaerosols can be abundant, e.g. the waste recycling and composting industry, biotechnology industries producing highly purified enzymes and the detergent and food industries that make use of these enzymes. Dose-response relationships have not been established for most biological agents and knowledge about threshold values is sparse. Exposure limits are available for some contaminants, e.g. wood dust, subtilisins (bacterial enzymes) and flour dust. Exposure limits for bacterial endotoxin have been proposed. Risk assessment is seriously hampered by the lack of valid quantitative exposure assessment methods. Traditional culture methods to quantify microbial exposures have proven to be of limited use. Non-culture methods and assessment methods for microbial constituents [e.g. allergens, endotoxin, beta(1-->3)-glucans, fungal extracellular polysaccharides] appear more successful; however, experience with these methods is generally limited. Therefore, more research is needed to establish better exposure assessment tools and validate newly developed methods. Other important areas that require further research include: potential protective effects of microbial exposures on atopy and atopic diseases, inter-individual susceptibility for biological exposures, interactions of bioaerosols with non-biological agents and other potential health effects such as skin and neurological conditions and birth effects.	Univ Utrecht, Div Environm & Occupat Hlth, IRAS, NL-3508 TD Utrecht, Netherlands; Massey Univ, Ctr Publ Hlth Res, Wellington, New Zealand; Univ Iowa, Coll Publ Hlth, Dept Environm & Occupat Hlth, Iowa City, IA 52242 USA	Douwes, J (reprint author), Univ Utrecht, Div Environm & Occupat Hlth, IRAS, POB 80176, NL-3508 TD Utrecht, Netherlands.			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Occup. Hyg.	APR	2003	47	3					187	200		10.1093/annhyg/meg032		14	Public, Environmental & Occupational Health; Toxicology	Public, Environmental & Occupational Health; Toxicology	665KL	WOS:000182119200003	12639832	
J	Ricciardolo, FLM; Sterk, PJ; Gaston, B; Folkerts, G				Ricciardolo, FLM; Sterk, PJ; Gaston, B; Folkerts, G			Nitric oxide in health and disease of the respiratory system	PHYSIOLOGICAL REVIEWS			English	Review							AIRWAY SMOOTH-MUSCLE; OBSTRUCTIVE PULMONARY-DISEASE; GUINEA-PIG TRACHEA; VASOACTIVE-INTESTINAL-PEPTIDE; SYNTHASE GENE-EXPRESSION; BRONCHIAL EPITHELIAL-CELLS; HUMAN ALVEOLAR MACROPHAGES; PRIMARY CILIARY DYSKINESIA; NUCLEUS-TRACTUS-SOLITARII; EARLY ASTHMATIC REACTION	During the past decade a plethora of studies have unravelled the multiple roles of nitric oxide (NO) in airway physiology and pathophysiology. In the respiratory tract, NO is produced by a wide variety of cell types and is generated via oxidation Of L-arginine that is catalyzed by the enzyme NO synthase (NOS). NOS exists in three distinct isoforms: neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). NO derived from the constitutive isoforms of NOS (nNOS and eNOS) and other NO-adduct molecules (nitrosothiols) have been shown to be modulators of bronchomotor tone. On the other hand, NO derived from iNOS seems to be a proinflammatory mediator with immunomodulatory effects. The concentration of this molecule in exhaled air is abnormal in activated states of different inflammatory airway diseases, and its monitoring is potentially a major advance in the management of, e.g., asthma. Finally, the production of NO under oxidative stress conditions secondarily generates strong oxidizing agents (reactive nitrogen species) that may modulate the development of chronic inflammatory airway diseases and/or amplify the inflammatory response. The fundamental mechanisms driving the altered NO bioactivity under pathological conditions still need to be fully clarified, because their regulation provides a novel target in the prevention and treatment of chronic inflammatory diseases of the airways.	G Gaslini Inst Children, Dept Pulm, Genoa, Italy; Leiden Univ, Dept Pulmonol, Leiden, Netherlands; Univ Virginia Hlth Syst, Dept Pediat Resp Med, Charlottesville, VA USA; Univ Utrecht, Inst Pharmaceut Sci, Dept Pharmacol & Pathophysiol, Utrecht, Netherlands	Folkerts, G (reprint author), G Gaslini Inst Children, Dept Pulm, Genoa, Italy.	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Rev.	JUL	2004	84	3					731	765		10.1152/physrev.00034.2003		35	Physiology	Physiology	833RV	WOS:000222357500002	15269335	
J	Sokol, CL; Barton, GM; Farr, AG; Medzhitov, R				Sokol, Caroline L.; Barton, Gregory M.; Farr, Andrew G.; Medzhitov, Ruslan			A mechanism for the initiation of allergen-induced T helper type 2 responses	NATURE IMMUNOLOGY			English	Article							THYMIC STROMAL LYMPHOPOIETIN; DUST-MITE ALLERGEN; MAST-CELLS; TH2 DIFFERENTIATION; CYTOKINE PRODUCTION; NEMATODE PARASITES; DENDRITIC CELLS; IL-4 EXPRESSION; LYMPH-NODES; IN-VIVO	Both metazoan parasites and simple protein allergens induce T helper type 2 (T(H)2) immune responses, but the mechanisms by which the innate immune system senses these stimuli are unknown. In addition, the cellular source of cytokines that control T(H)2 differentiation in vivo has not been defined. Here we showed that basophils were activated and recruited to the draining lymph nodes specifically in response to T(H)2-inducing allergen challenge. Furthermore, we demonstrate that the basophil was the accessory cell type required for T(H)2 induction in response to protease allergens. Finally, we show that basophils were directly activated by protease allergens and produced T(H)2-inducing cytokines, including interleukin 4 and thymic stromal lymphopoietin, which are involved in T(H)2 differentiation in vivo.	[Sokol, Caroline L.; Medzhitov, Ruslan] Yale Univ, Sch Med, Immunobiol Sect, Howard Hughes Med Inst, New Haven, CT 06510 USA; [Barton, Gregory M.] Univ Calif Berkeley, Dept Mol Cell Biol, Berkeley, CA 94720 USA; [Farr, Andrew G.] Univ Washington, Dept Immunol, Seattle, WA 98195 USA	Medzhitov, R (reprint author), Yale Univ, Sch Med, Immunobiol Sect, Howard Hughes Med Inst, 333 Cedar St, New Haven, CT 06510 USA.	ruslan.medzhitov@yale.edu			NIAID NIH HHS [AI 055502, R01 AI055502]		Acosta-Rodriguez EV, 2007, NAT IMMUNOL, V8, P942, DOI 10.1038/ni1496; Al-Shami A, 2005, J EXP MED, V202, P829, DOI 10.1084/jem.20050199; Al-Shami A, 2004, J EXP MED, V200, P159, DOI 10.1084/jem.20031975; Amsen D, 2004, CELL, V117, P515, DOI 10.1016/S0092-8674(04)00451-9; Banchereau J, 1998, NATURE, V392, P245, DOI 10.1038/32588; Chambers L, 1998, BIOCHEM BIOPH RES CO, V253, P837, DOI 10.1006/bbrc.1998.9862; CHUA KY, 1988, J EXP MED, V167, P175, DOI 10.1084/jem.167.1.175; Cote-Sierra J, 2004, P NATL ACAD SCI USA, V101, P3880, DOI 10.1073/pnas.0400339101; Dillon SR, 2004, NAT IMMUNOL, V5, P752, DOI 10.1038/ni1084; Else KJ, 1998, INT J PARASITOL, V28, P1145, DOI 10.1016/S0020-7519(98)00087-3; FINKELMAN FD, 1992, PARASITOL TODAY, V8, P311, DOI 10.1016/0169-4758(92)90105-B; FRIEND SL, 1994, EXP HEMATOL, V22, P321; Gessner A, 2005, J IMMUNOL, V174, P1063; Ghaemmaghami AM, 2002, CLIN EXP ALLERGY, V32, P1468, DOI 10.1046/j.1365-2745.2002.01504.x; Gottar M, 2006, CELL, V127, P1425, DOI 10.1016/j.cell.2006.10.046; Gough L, 1999, J EXP MED, V190, P1897, DOI 10.1084/jem.190.12.1897; Grobe K, 1999, EUR J BIOCHEM, V263, P33, DOI 10.1046/j.1432-1327.1999.00462.x; Henri S, 2001, J IMMUNOL, V167, P741; Jones JDG, 2006, NATURE, V444, P323, DOI 10.1038/nature05286; Kheradmand F, 2002, J IMMUNOL, V169, P5904; Khodoun MV, 2004, J EXP MED, V200, P857, DOI 10.1084/jem.20040598; Krammer PH, 2007, NAT REV IMMUNOL, V7, P532, DOI 10.1038/nri2115; LeibundGut-Landmann S, 2007, NAT IMMUNOL, V8, P630, DOI 10.1038/ni1460; Liu YJ, 2007, ANNU REV IMMUNOL, V25, P193, DOI 10.1146/annurev.immunol.25.022106.141718; Liu ZG, 2005, J IMMUNOL, V174, P2242; Luccioli S, 2002, J ALLERGY CLIN IMMUN, V110, P117, DOI 10.1067/mai.2002.125828; Martin-Fontecha A, 2004, NAT IMMUNOL, V5, P1260, DOI 10.1038/ni1138; McKerrow JH, 2006, ANNU REV PATHOL-MECH, V1, P497, DOI 10.1146/annurev.pathol.1.110304.100151; Min B, 2004, J EXP MED, V200, P507, DOI 10.1084/jem.20040590; Mohrs K, 2005, IMMUNITY, V23, P419, DOI 10.1016/j.immuni.2005.09.006; Mohrs M, 2001, IMMUNITY, V15, P303, DOI 10.1016/S1074-7613(01)00186-8; Mowen KA, 2004, IMMUNOL REV, V202, P203, DOI 10.1111/j.0105-2896.2004.00209.x; Mukai K, 2005, IMMUNITY, V23, P191, DOI 10.1016/j.immuni.2005.06.011; Noben-Trauth N, 2000, J IMMUNOL, V165, P3620; NOVEY HS, 1979, J ALLERGY CLIN IMMUN, V63, P98, DOI 10.1016/0091-6749(79)90198-2; Oh K, 2007, BLOOD, V109, P2921, DOI 10.1182/blood-2006-07-037739; Ohshima Y, 1998, BLOOD, V92, P3338; Omori M, 2007, J IMMUNOL, V178, P1396; PARK LS, 1990, J EXP MED, V171, P1073, DOI 10.1084/jem.171.4.1073; Phillips C, 2003, J LEUKOCYTE BIOL, V73, P165, DOI 10.1189/jlb.0702356; Shakib F, 1998, IMMUNOL TODAY, V19, P313, DOI 10.1016/S0167-5699(98)01284-5; Trinchieri G, 2003, NAT REV IMMUNOL, V3, P133, DOI 10.1038/nri1001; URBAN JF, 1992, IMMUNOL REV, V127, P205, DOI 10.1111/j.1600-065X.1992.tb01415.x; Voehringer D, 2004, IMMUNITY, V20, P267, DOI 10.1016/S1074-7613(04)00026-3; Wedemeyer J, 2000, CURR OPIN IMMUNOL, V12, P624, DOI 10.1016/S0952-7915(00)00154-0; Zaph C, 2007, NATURE, V446, P552, DOI 10.1038/nature05590; Zheng WP, 1997, CELL, V89, P587, DOI 10.1016/S0092-8674(00)80240-8; Zhou BH, 2005, NAT IMMUNOL, V6, P1047, DOI 10.1038/ni1247; Zingoni A, 1998, J IMMUNOL, V161, P547	49	486	505	7	30	NATURE PUBLISHING GROUP	NEW YORK	75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA	1529-2908			NAT IMMUNOL	Nat. Immunol.	MAR	2008	9	3					310	318		10.1038/ni1558		9	Immunology	Immunology	266BQ	WOS:000253406700017	18300366	
J	Isolauri, E; Arvola, T; Sutas, Y; Moilanen, E; Salminen, S				Isolauri, E; Arvola, T; Sutas, Y; Moilanen, E; Salminen, S			Probiotics in the management of atopic eczema	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergic inflammation; atopy; breast-feeding; food allergy; infants; probiotics	GG-DERIVED ENZYMES; ASTHMA; INFANTS; PROLIFERATION; DERMATITIS; INFECTION; DISORDERS; RESPONSES; CHILDREN; DIARRHEA	Background Over the last two decades the incidence of allergic diseases has increased in industrialized countries, and consequently new approaches have to be explored. Objective The potential of probiotics to control allergic inflammation at an early age was assessed in a randomized double-blind placebo-controlled study. Methods A total of 27 infants, mean age 4.6 months, who manifested atopic eczema during exclusive breast-feeding and who have had no exposure to any infant or substitute formula were weaned to probiotic-supplemented. Bifidobacterium lactis Bb-12 or Lactobacillus strain GG (ATCC 53103), extensively hydrolysed whey formulas or to the same formula without probiotics. The extent and severity of atopic eczema, the growth and nutrition of infants, and concentrations of circulating cytokines/chemokines and soluble cell surface adhesion molecules in serum and methyl-histamine and eosinophilic protein X in urine were determined. Results The SCORAD score reflecting the extent and severity of atopic eczema was 16 (7-25) during breast-feeding, median (interquartile range). After 2 months, a significant improvement in skin condition occurred in patients given probiotic-supplemented formulas, as compared to the unsupplemented group; chi (2) = 12.27, P = 0.002. SCORAD decreased in the Bifidobacterium lactis Bb-12 group to 0 (0-3.8), and in the Lactobacillus GG group to 1 (0.1-8.7), vs unsupplemented 13.4 (4.5-18.2), median (interquartile range), in parallel with a reduction in the concentration of soluble CD4 in serum and eosinophilic protein X in urine. Conclusion The results provide the first clinical demonstration of specific probiotic strains modifying the changes related to allergic inflammation. The data further indicate that probiotics may counteract inflammatory responses beyond the intestinal milieu. The combined effects of these probiotic strains will guide infants through the weaning period, when sensitization to newly encountered antigens is initiated. The probiotic approach may thus offer a new direction in the search for future foods for allergy treatment and prevention strategies.	Univ Turku, Dept Paediat, FIN-20520 Turku, Finland; Tampere Univ Hosp, Dept Paediat, Tampere, Finland; Univ Tampere, Sch Med, Dept Pharmacol, FIN-33101 Tampere, Finland; Tampere Univ Hosp, Dept Clin Chem, Tampere, Finland; Univ Turku, Dept Biochem & Food Chem, SF-20500 Turku, Finland	Isolauri, E (reprint author), Univ Turku, Dept Paediat, FIN-20520 Turku, Finland.						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Exp. Allergy	NOV	2000	30	11					1604	1610				7	Allergy; Immunology	Allergy; Immunology	383WH	WOS:000165907100016	11069570	
J	Wright, JR				Wright, JR			Immunoregulatory functions of surfactant proteins	NATURE REVIEWS IMMUNOLOGY			English	Review							RESPIRATORY SYNCYTIAL VIRUS; INFLUENZA-A VIRUSES; PULMONARY HOST-DEFENSE; PROINFLAMMATORY CYTOKINE PRODUCTION; CARBOHYDRATE-RECOGNITION DOMAIN; HUMAN ALVEOLAR MACROPHAGES; BACILLUS-CALMETTE-GUERIN; AIRWAY DENDRITIC CELLS; GRAM-NEGATIVE BACTERIA; MANNOSE-BINDING LECTIN	Because the lungs function as the body's gas-exchange organ, they are inevitably exposed to air that is contaminated with pathogens, allergens and pollutants. Host-defence mechanisms within the lungs must facilitate clearance of inhaled pathogens and particles while minimizing an inflammatory response that could damage the thin, delicate gas-exchanging epithelium. Pulmonary surfactant is a complex of lipids and proteins that enhances pathogen clearance and regulates adaptive and innate immune-cell functions. In this article, I review the structure and functions of the surfactant proteins SP-A and SP-D in regulating host immune defence and in modulating inflammatory responses.	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J	Hunt, JF; Fang, KZ; Malik, R; Snyder, A; Malhotra, N; Platts-Mills, TAE; Gaston, B				Hunt, JF; Fang, KZ; Malik, R; Snyder, A; Malhotra, N; Platts-Mills, TAE; Gaston, B			Endogenous airway acidification - Implications for asthma pathophysiology	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							RESPIRATORY-DISTRESS-SYNDROME; EXHALED NITRIC-OXIDE; EXPIRED BREATH; SENSORY NERVES; PH; FLUID; ELECTROPHORESIS; ACETAZOLAMIDE; INFLAMMATION; EOSINOPHILS	Airway concentrations of many reactive nitrogen and oxygen species are high In asthma. The stability and bioactivities of these species are pH-dependent; however, the pH of the airway during acute asthma has not previously been studied. As with gastric and urinary acidification, asthmatic airway acidification could be expected dramatically to alter the concentrations and bioactivites/cytotoxicities of endogenous nitrogen oxides. Here, we demonstrate that the pH of deaerated exhaled airway vapor condensate is over two log orders lower in patients with acute asthma (5.23 +/- 0.21, n = 22) than in control subjects (7.65 +/- 0.20, n = 19, p < 0.001) and normalizes with corticosteroid therapy. Values are highly reproducible, unaffected by salivary or therapeutic artifact, and identical to samples taken directly from the lower airway. Further, at these low pH values the endogenous airway compound, nitrite, is converted to nitric oxide (NO) in quantities sufficient largely to account for the concentrations of NO in asthmatic expired air, and eosinophils undergo accelerated necrosis. We speculate that airway pH may be an important determinant of expired NO concentration and airway inflammation, and suggest that regulation of airway pH has a previously unsuspected role in asthma pathophysiology.	Univ Virginia Hlth Syst, Div Pediat Resp Med, Charlottesville, VA 22908 USA; Univ Virginia Hlth Syst, Div Pediat Hematol Oncol, Charlottesville, VA 22908 USA; Univ Virginia Hlth Syst, Div Allergy Asthma & Immunol, Charlottesville, VA 22908 USA	Gaston, B (reprint author), Univ Virginia Hlth Syst, Dept Pediat, Box 386, Charlottesville, VA 22908 USA.				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J	Olszak, T; An, DD; Zeissig, S; Vera, MP; Richter, J; Franke, A; Glickman, JN; Siebert, R; Baron, RM; Kasper, DL; Blumberg, RS				Olszak, Torsten; An, Dingding; Zeissig, Sebastian; Vera, Miguel Pinilla; Richter, Julia; Franke, Andre; Glickman, Jonathan N.; Siebert, Reiner; Baron, Rebecca M.; Kasper, Dennis L.; Blumberg, Richard S.			Microbial Exposure During Early Life Has Persistent Effects on Natural Killer T Cell Function	SCIENCE			English	Article							INVARIANT NKT CELLS; ULCERATIVE-COLITIS; AIRWAY INFLAMMATION; HYGIENE HYPOTHESIS; CHEMOKINE CXCL16; B-CELLS; DISEASE; ASTHMA; COLONIZATION; ANTIBIOTICS	Exposure to microbes during early childhood is associated with protection from immune-mediated diseases such as inflammatory bowel disease (IBD) and asthma. Here, we show that in germ-free (GF) mice, invariant natural killer T (iNKT) cells accumulate in the colonic lamina propria and lung, resulting in increased morbidity in models of IBD and allergic asthma as compared with that of specific pathogen-free mice. This was associated with increased intestinal and pulmonary expression of the chemokine ligand CXCL16, which was associated with increased mucosal iNKT cells. Colonization of neonatal-but not adult-GF mice with a conventional microbiota protected the animals from mucosal iNKT accumulation and related pathology. These results indicate that age-sensitive contact with commensal microbes is critical for establishing mucosal iNKT cell tolerance to later environmental exposures.	[An, Dingding; Kasper, Dennis L.] Harvard Univ, Brigham & Womens Hosp, Channing Lab, Sch Med, Boston, MA 02115 USA; [An, Dingding; Kasper, Dennis L.] Harvard Univ, Sch Med, Dept Microbiol & Immunobiol, Boston, MA 02115 USA; [Olszak, Torsten; Blumberg, Richard S.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Gastroenterol Hepatol & Endoscopy, Boston, MA 02115 USA; [Zeissig, Sebastian] Univ Med Ctr Schleswig Holstein, Dept Internal Med 1, D-24105 Kiel, Germany; [Vera, Miguel Pinilla; Baron, Rebecca M.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Pulm & Crit Care Med, Boston, MA 02115 USA; [Richter, Julia; Siebert, Reiner] Univ Kiel, Inst Human Genet, D-24105 Kiel, Germany; [Franke, Andre] Univ Kiel, Inst Clin Mol Biol, D-24105 Kiel, Germany; [Glickman, Jonathan N.] GI Pathol, Caris Diagnost, Caris Life Sci, Newton, MA 02464 USA	Kasper, DL (reprint author), Harvard Univ, Brigham & Womens Hosp, Channing Lab, Sch Med, Boston, MA 02115 USA.	dennis_kasper@hms.harvard.edu; rblumberg@partners.org	Siebert, Reiner/A-8049-2010; Zeissig, Sebastian/B-6297-2012; Franke, Andre/B-2151-2010	Franke, Andre/0000-0003-1530-5811	NIH [DK44319, DK51362, DK53056, DK88199, AI090102]; Crohn's Colitis Foundation of America; Harvard Digestive Diseases Center [DK034854]; Medizinausschuss Schleswig-Holstein, German Ministry of Education Research through the National Genome Research Network; Medical Faculty, Kiel; Deutsche Forschungsgemeinschaft (DFG) [OL 324/1-1, SZ 814/1-1, 814/4-1]; DFG Excellence Cluster "Inflammation at Interfaces"	We thank E. Troy and S. Edwards for handling of the GF mice, J. Cusick for technical assistance, E. Nieuwenhuis and K. Schneeberger for assistance with epigenetics studies, A. Bellacosa and K. Baker for helpful discussions and manuscript preparation, and the KinderKrebsInitiative Buchholz/Holm-Seppensen for providing pyrosequencing infrastructure. The work was supported by NIH grants DK44319, DK51362, DK53056, and DK88199 (R. S. B.) and AI090102 (D. L. K.); Crohn's Colitis Foundation of America Senior Research Award (D. L. K.) and Crohn's and Colitis Foundation of America Postdoctoral Fellowship Award (D. A. and S.Z.); the Harvard Digestive Diseases Center (DK034854); the Medizinausschuss Schleswig-Holstein, German Ministry of Education Research through the National Genome Research Network (A. F.); The Medical Faculty, Kiel (R. S.) and the Deutsche Forschungsgemeinschaft (DFG) (OL 324/1-1, SZ 814/1-1, 814/4-1); as well as DFG Excellence Cluster "Inflammation at Interfaces" (A.F. and S.Z.). The data reported in this manuscript are tabulated in the main paper and in the supplementary materials.	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J	Oberg, M; Jaakkola, MS; Woodward, A; Peruga, A; Pruss-Ustun, A				Oberg, Mattias; Jaakkola, Maritta S.; Woodward, Alistair; Peruga, Armando; Pruess-Ustuen, Annette			Worldwide burden of disease from exposure to second-hand smoke: a retrospective analysis of data from 192 countries	LANCET			English	Article							ENVIRONMENTAL TOBACCO-SMOKE; PASSIVE SMOKING; HEALTH; LEGISLATION; CHILDREN; IMPACT	Background Exposure to second-hand smoke is common in many countries but the magnitude of the problem worldwide is poorly described. We aimed to estimate the worldwide exposure to second-hand smoke and its burden of disease in children and adult non-smokers in 2004. Methods The burden of disease from second-hand smoke was estimated as deaths and disability-adjusted life-years (DALYs) for children and adult non-smokers. The calculations were based on disease-specific relative risk estimates and area-specific estimates of the proportion of people exposed to second-hand smoke, by comparative risk assessment methods, with data from 192 countries during 2004. Findings Worldwide, 40% of children, 33% of male non-smokers, and 35% of female non-smokers were exposed to second-hand smoke in 2004. This exposure was estimated to have caused 379 000 deaths from ischaemic heart disease, 165 000 from lower respiratory infections, 36 900 from asthma, and 21 400 from lung cancer. 603 000 deaths were attributable to second-hand smoke in 2004, which was about 1.0% of worldwide mortality. 47% of deaths from second-hand smoke occurred in women, 28% in children, and 26% in men. DALYs lost because of exposure to second-hand smoke amounted to 10.9 million, which was about 0.7% of total worldwide burden of diseases in DALYs in 2004. 61% of DALYs were in children. The largest disease burdens were from lower respiratory infections in children younger than 5 years (5 939 000), ischaemic heart disease in adults (2 836 000), and asthma in adults (1 246 000) and children (651 000). Interpretation These estimates of worldwide burden of disease attributable to second-hand smoke suggest that substantial health gains could be made by extending effective public health and clinical interventions to reduce passive smoking worldwide.	[Pruess-Ustuen, Annette] WHO, Dept Publ Hlth & Environm, CH-1211 Geneva 27, Switzerland; [Oberg, Mattias] Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; [Jaakkola, Maritta S.] Univ Oulu, Resp Med Unit, Ctr Environm & Resp Hlth Res, Oulu, Finland; [Jaakkola, Maritta S.] Univ Oulu, Inst Clin Med, Oulu, Finland; [Woodward, Alistair] Univ Auckland, Sch Populat Hlth, Auckland 1, New Zealand	Pruss-Ustun, A (reprint author), WHO, Dept Publ Hlth & Environm, 20 Ave Appia, CH-1211 Geneva 27, Switzerland.	pruessa@who.int		Oberg, Mattias/0000-0001-5377-530X; Woodward, Alistair/0000-0001-5425-6018	Swedish National Board of Health and Welfare; Bloomberg Philanthropies	We thank the Swedish National Board of Health and Welfare and the Bloomberg Philanthropies for their funding support. The authors alone are responsible for the views expressed in this publication, which do not necessarily reflect the decisions or the stated policy of WHO or of its Member States. (C) World Health Organization, 2010.	*CA EPA AIR RES BO, 2005, PROP ID ENV TOB SMOK; Centers for Disease Control and Prevention, GLOB YOUTH TOB SURV; Eriksen MP, 2008, ANNU REV PUBL HEALTH, V29, P171, DOI [10.1146/annurev.publhealth.29.020907.090920, 10.1146/annurev.publhealtb.29.020907.090920]; ETZEL RA, 1992, PEDIATRICS, V90, P228; Ezzati M, 2002, LANCET, V360, P1347, DOI 10.1016/S0140-6736(02)11403-6; Ezzati M, 2004, COMP QUANTIFICATION; Fontana L, 2007, G Ital Med Lav Ergon, V29, P484; *GALL ORG, 2009, SURV TOB AN REP; Gan Q, 2007, TOB CONTROL, V16, P417, DOI 10.1136/tc.2007.021477; *I MED, 2009, SECONDH SMOK EXP CAR; International Agency for Research on Cancer, 2009, EV EFF SMOK FREE POL; International Agency for Research on Cancer, 2004, TOB SMOK INV SMOK; International Labour Office, 2008, GLOB EMPL TRENDS WOM; Jaakkola MS, 2006, EUR RESPIR J, V28, P397, DOI 10.1183/09031936.06.00001306; Jaakkola MS, 2003, AM J PUBLIC HEALTH, V93, P2055, DOI 10.2105/AJPH.93.12.2055; Jaakkola MS, 1999, ENVIRON HEALTH PERSP, V107, P829, DOI 10.2307/3434561; Li JS, 1999, PEDIATR PULM, V27, P5, DOI 10.1002/(SICI)1099-0496(199901)27:1<5::AID-PPUL3>3.0.CO;2-5; Lightwood JM, 2009, CIRCULATION, V120, P1373, DOI 10.1161/CIRCULATIONAHA.109.870691; Lopez MJ, 2007, TOB CONTROL, V16, P373, DOI 10.1136/tc.2006.019679; McNabola A, 2009, INT J ENV RES PUB HE, V6, P741, DOI 10.3390/ijerph6020741; Menzies D, 2006, JAMA-J AM MED ASSOC, V296, P1742, DOI 10.1001/jama.296.14.1742; Musk AW, 2003, RESPIROLOGY, V8, P286, DOI 10.1046/j.1440-1843.2003.00483.x; Oberg M, 2010, 2 HAND SMOKE ASSESSI; OBERG M, GLOBAL ESTI IN PRESS; Pell JP, 2008, NEW ENGL J MED, V359, P482, DOI 10.1056/NEJMsa0706740; SCHONHERR E., 1928, ZEITSCHR KREBSFORSCH, V27, P436, DOI 10.1007/BF02125480; UN, 2009, MILL DEV GOALS REP 2; U.S. Department of Health Education and Welfare, 1972, DHEW PUBL; US Surgeon General, 2006, HLTH CONS INV EXP TO; World Health Organization, 2009, WHO FRAM CONV TOB CO; World Health Organization, 1999, INT CONS ENV TOB SMO; World Health Organisation, 2009, GLOB HLTH RISKS MORT; World Health Organization. (WHO), 2009, GLOB BURD DIS 2004 U; World Health Organization, 2009, WHO REP GLOB TOB EP; World Health Organization, 2009, GUID IMPL WHO FRAM C; World Health Organization, 2002, WORLD HLTH REP 2002; Wipfli H, 2008, AM J PUBLIC HEALTH, V98, P672, DOI 10.2105/AJPH.2007.126631; Woodward A, 2001, TOB CONTROL, V10, P383, DOI 10.1136/tc.10.4.383	38	468	479	12	109	ELSEVIER SCIENCE INC	NEW YORK	360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA	0140-6736			LANCET	Lancet	JAN 8	2011	377	9760					139	146		10.1016/S0140-6736(10)61388-8		8	Medicine, General & Internal	General & Internal Medicine	707NH	WOS:000286292800026	21112082	
J	Sigurs, N; Gustafsson, PM; Bjarnason, R; Lundberg, F; Schmidt, S; Sigurbergsson, F; Kjellman, B				Sigurs, N; Gustafsson, PM; Bjarnason, R; Lundberg, F; Schmidt, S; Sigurbergsson, F; Kjellman, B			Severe respiratory syncytial virus bronchiolitis in infancy and asthma and allergy at age 13	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						airway obstruction; atopic hypersensitivity; children; respiratory syncytial virus	RSV BRONCHIOLITIS; AIRWAY FUNCTION; INFECTION; CHILDREN; SENSITIZATION; LIFE; DISEASE; RISK; MECHANISMS; WHEEZE	We have prospectively studied wheezing disorder and allergy in 47 children hospitalized with respiratory syncytial virus (RSV) bronchiolitis in infancy and 93 matched control subjects. Subjects with at least three episodes of wheezing were defined as recurrent wheezers and as having asthma if the episodes were doctor verified. Here we report the outcome at age 13 years in 46/47 children with RSV and 92/93 control subjects. Wheezing disorder and clinical allergy were estimated using a questionnaire. Skin prick tests were performed and serum IgE antibodies measured. Spirometry was undertaken at rest, after dry air challenge, and after beta(2)-agonist inhalation. The occurrence of symptoms over the previous 12 months was significantly higher in the RSV group than among the control subjects, 43% versus 8% for asthma/recurrent wheezing and 39% versus 15% for allergic rhinoconjunctivitis. Sensitization to common inhaled allergens was more frequent in the RSV group than in the control subjects, judged by skin prick tests (50% versus 28%; p = 0.022), or by serum IgE antibodies (45% versus 26%; p = 0.038). Compared with the control subjects, the RSV group showed mild airway obstruction both at rest and after bronchodilation, and had slightly more reactive airways. RSV bronchiolitis in infancy severe enough to cause hospitalization is a risk factor for allergic asthma in early adolescence.	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J. Respir. Crit. Care Med.	JAN 15	2005	171	2					137	141		10.1164/rccm.200406-730OC		5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	886UO	WOS:000226258400009	15516534	
J	Pope, CA				Pope, CA			Epidemiology of fine particulate air pollution and human health: Biologic mechanisms and who's at risk?	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Review						air pollution; cardiopulmonary disease; health effects; life expectancy; particulate pollution; review	EMERGENCY ROOM VISITS; PEAK EXPIRATORY FLOW; OBSTRUCTIVE PULMONARY-DISEASE; TIME-SERIES ANALYSIS; RESPIRATORY HOSPITAL ADMISSIONS; HEART-RATE-VARIABILITY; NORTH-AMERICAN CHILDREN; MINNEAPOLIS ST-PAUL; LONG-TERM EXPOSURE; SANTA-CLARA COUNTY	This article briefly summarizes the epidemiology of the health effects of fine particulate air pollution, provides an early, somewhat speculative, discussion of the contribution of epidemiology to evaluating biologic mechanisms, and evaluates who's at risk or is susceptible to adverse health effects. Based on preliminary epidemiologic evidence, it is speculated that a systemic response to fine particle-induced pulmonary inflammation, including cytokine release and altered cardiac autonomic function, may be part of the pathophysiologic mechanisms or pathways linking particulate pollution with cardiopulmonary disease. The elderly, infants, and persons with chronic cardiopulmonary disease, influenza, or asthma are most susceptible to mortality and serious morbidity effects from short-term acutely elevated exposures. Others are susceptible to less serious health effects such as transient increases in respiratory symptoms, decreased lung function, or other physiologic changes. Chronic exposure studies suggest relatively broad susceptibility to cumulative effects of long-term repeated exposure to fine particulate pollution, resulting in substantive estimates of population average loss of life expectancy in highly polluted environments. Additional knowledge is needed about the specific pollutants or mix of pollutants responsible for the adverse health effects and the biologic mechanisms involved.	Brigham Young Univ, Provo, UT 84602 USA	Pope, CA (reprint author), Brigham Young Univ, 142 FOB, Provo, UT 84602 USA.						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Health Perspect.	AUG	2000	108			4			713	723		10.2307/3454408		11	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	350VH	WOS:000089121500015	10931790	
J	Homey, B; Alenius, H; Muller, A; Soto, H; Bowman, EP; Yuan, W; McEvoy, L; Lauerma, AI; Assmann, T; Bunemann, E; Lehto, M; Wolff, H; Yen, D; Marxhausen, H; To, W; Sedgwick, J; Ruzicka, T; Lehmann, P; Zlotnik, A				Homey, B; Alenius, H; Muller, A; Soto, H; Bowman, EP; Yuan, W; McEvoy, L; Lauerma, AI; Assmann, T; Bunemann, E; Lehto, M; Wolff, H; Yen, D; Marxhausen, H; To, W; Sedgwick, J; Ruzicka, T; Lehmann, P; Zlotnik, A			CCL27-CCR10 interactions regulate T cell-mediated skin inflammation	NATURE MEDICINE			English	Article							PROTEIN-COUPLED RECEPTOR-2; ALLERGIC DERMATITIS; ENDOTHELIAL-CELLS; ATOPIC-DERMATITIS; CUTTING EDGE; CHEMOKINE; PSORIASIS; EXPRESSION; ANTIGEN; BINDING	The skin-associated chemokine CCL27 (also called CTACK, ALP and ESkine) and its receptor CCR10 (GPR-2) mediate chemotactic responses of skin-homing T cells in vitro. Here we report that most skin-infiltrating lymphocytes in patients suffering from psoriasis, atopic or allergic-contact dermatitis express CCR10. Epidermal basal keratinocytes produced CCL27 protein that bound to extracellular matrix, mediated adhesion and was displayed on the surface of dermal endothelial cells. Tumor necrosis factor-alpha and interleukin-1beta induced CCL27 production whereas the glucocorticosteroid clobetasol propionate suppressed it. Circulating skin-homing CLA(+) T cells, dermal microvascular endothelial cells and fibroblasts expressed CCR10 on their cell surface. In vivo, intracutaneous CCL27 injection attracted lymphocytes and, conversely, neutralization of CCL27-CCR10 interactions impaired lymphocyte recruitment to the skin leading to the suppression of allergen-induced skin inflammation. Together, these findings indicate that CCL27-CCR10 interactions have a pivotal role in T cell-mediated skin inflammation.	DNAX Res Inst Molec & Cellular Biol Inc, Palo Alto, CA USA; Finnish Inst Occupat Hlth, Dept Ind Hyg & Toxicol, Helsinki, Finland; Univ Dusseldorf, Dept Dermatol, D-4000 Dusseldorf, Germany; Univ Dusseldorf, Dept Radiat Oncol, D-4000 Dusseldorf, Germany; Univ Helsinki, Cent Hosp, Dept Dermatol, FIN-00170 Helsinki, Finland; Finnish Inst Occupat Hlth, Dept Pathol, Helsinki, Finland; Kymenlaakso Cent Hosp, Kotka, Finland; R&D Syst, Minneapolis, MN USA	Homey, B (reprint author), DNAX Res Inst Molec & Cellular Biol Inc, Palo Alto, CA USA.		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Med.	FEB	2002	8	2					157	165		10.1038/nm0202-157		9	Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental	Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine	517FN	WOS:000173600600025	11821900	
J	Ege, MJ; Mayer, M; Normand, AC; Genuneit, J; Cookson, WOCM; Braun-Fahrlander, C; Heederik, D; Piarroux, R; von Mutius, E				Ege, Markus J.; Mayer, Melanie; Normand, Anne-Cecile; Genuneit, Jon; Cookson, William O. C. M.; Braun-Fahrlaender, Charlotte; Heederik, Dick; Piarroux, Renaud; von Mutius, Erika		GABRIELA Transregio 22 Study Grp	Exposure to Environmental Microorganisms and Childhood Asthma	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							SCHOOL-AGE-CHILDREN; IN-HOUSE DUST; ATOPIC SENSITIZATION; ALLERGIC DISEASES; FARM CHILDREN; MATTRESS DUST; ENDOTOXIN; BACTERIAL; INFLAMMATION; ASSOCIATION	BACKGROUND Children who grow up in environments that afford them a wide range of microbial exposures, such as traditional farms, are protected from childhood asthma and atopy. In previous studies, markers of microbial exposure have been inversely related to these conditions. METHODS In two cross-sectional studies, we compared children living on farms with those in a reference group with respect to the prevalence of asthma and atopy and to the diversity of microbial exposure. In one study - PARSIFAL (Prevention of Allergy - Risk Factors for Sensitization in Children Related to Farming and Anthroposophic Lifestyle) - samples of mattress dust were screened for bacterial DNA with the use of single-strand conformation polymorphism (SSCP) analyses to detect environmental bacteria that cannot be measured by means of culture techniques. In the other study - GABRIELA (Multidisciplinary Study to Identify the Genetic and Environmental Causes of Asthma in the European Community [GABRIEL] Advanced Study) - samples of settled dust from children's rooms were evaluated for bacterial and fungal taxa with the use of culture techniques. RESULTS In both studies, children who lived on farms had lower prevalences of asthma and atopy and were exposed to a greater variety of environmental microorganisms than the children in the reference group. In turn, diversity of microbial exposure was inversely related to the risk of asthma (odds ratio for PARSIFAL, 0.62; 95% confidence interval [CI], 0.44 to 0.89; odds ratio for GABRIELA, 0.86; 95% CI, 0.75 to 0.99). In addition, the presence of certain more circumscribed exposures was also inversely related to the risk of asthma; this included exposure to species in the fungal taxon eurotium (adjusted odds ratio, 0.37; 95% CI, 0.18 to 0.76) and to a variety of bacterial species, including Listeria monocytogenes, bacillus species, corynebacterium species, and others (adjusted odds ratio, 0.57; 95% CI, 0.38 to 0.86). CONCLUSIONS Children living on farms were exposed to a wider range of microbes than were children in the reference group, and this exposure explains a substantial fraction of the inverse relation between asthma and growing up on a farm. (Funded by the Deutsche Forschungsgemeinschaft and the European Commission.)	[Ege, Markus J.; von Mutius, Erika] Univ Childrens Hosp Munich, Munich, Germany; [Mayer, Melanie] Tech Univ Munich, Inst Anim Hyg, D-8050 Freising Weihenstephan, Germany; [Genuneit, Jon] Univ Ulm, Inst Epidemiol, Ulm, Germany; [Normand, Anne-Cecile] Univ Franche Comte, Chronoenvironm Lab, F-25030 Besancon, France; [Piarroux, Renaud] Assistance Publ Hop Marseille, Dept Parasitol & Mycol, Marseille, France; [Piarroux, Renaud] Univ Aix Marseille 2, Marseille, France; [Cookson, William O. C. M.] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW7 2AZ, England; [Braun-Fahrlaender, Charlotte] Swiss Trop & Publ Hlth Inst, Basel, Switzerland; [Braun-Fahrlaender, Charlotte] Univ Basel, Basel, Switzerland; [Heederik, Dick] Univ Utrecht, Inst Risk Assessment, Div Environm Epidemiol, Utrecht, Netherlands	Ege, MJ (reprint author), Univ Munich, Childrens Hosp, 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	Deutsche Forschungsgemeinschaft [SFB Transregio 22, A1]; European Commission [LSH-2004-1.2.5-1, QLRT 1999-01391]	Supported by grants from Deutsche Forschungsgemeinschaft (SFB Transregio 22 Pulmonary Allergies, Project A1) and the European Commission (LSH-2004-1.2.5-1 and QLRT 1999-01391).	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J	Wallace, DV; Dykewicz, MS; Bernstein, DI; Bernstein, IL; Blessing-Moore, J; Cox, L; Khan, DA; Lang, DM; Nicklas, RA; Oppenheimer, J; Portnoy, JM; Randolph, CC; Schuller, D; Spector, SL; Tilles, SA; May, KR; Miller, TA; Druce, HM; Baroody, FM; Bernstein, JA; Craig, TJ; Georgitis, JW; Pawankar, R; Rachelefsky, GS; Settipane, RA; Skoner, DP; Stoloff, SW				Wallace, Dana V.; Dykewicz, Mark S.; Bernstein, David I.; Bernstein, I. Leonard; Blessing-Moore, Joann; Cox, Linda; Khan, David A.; Lang, David M.; Nicklas, Richard A.; Oppenheimer, John; Portnoy, Jay M.; Randolph, Christopher C.; Schuller, Diane; Spector, Sheldon L.; Tilles, Stephen A.; May, Kathleen R.; Miller, Travis A.; Druce, Howard M.; Baroody, Faud M.; Bernstein, Jonathan A.; Craig, Timothy J.; Georgitis, John W.; Pawankar, Ruby; Rachelefsky, Gary S.; Settipane, Russell A.; Skoner, David P.; Stoloff, Stuart W.			The diagnosis and management of rhinitis: An updated practice parameter	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review							SEASONAL ALLERGIC RHINITIS; QUALITY-OF-LIFE; AQUEOUS NASAL SPRAY; PLACEBO-CONTROLLED TRIAL; HOUSE-DUST-MITE; LONG-TERM TREATMENT; DERMATOPHAGOIDES-PTERONYSSINUS EXTRACT; INTRANASAL FLUTICASONE PROPIONATE; CONJUNCTIVAL PROVOCATION TEST; RANDOMIZED CONTROLLED-TRIAL	These parameters were developed by the Joint Task Force on Practice Parameters, representing the American Academy of Allergy, Asthma & immunology; the American College of Allergy, Asthma and Immunology; and the Joint Council of Allergy, Asthma and Immunology. The American Academy of Allergy, Asthma & Immunology (AAAAI) and the American College of Allergy, Asthma and Immunology (ACAAI) have jointly accepted responsibility for establishing "The diagnosis and Management of Rhinitis: An Updated Practice Parameter" This is a complete and comprehensive document at the current time. The medical environment is a changing environment, and not all recommendations will be appropriate for all patients. Because this document incorporated the efforts of many participants, no single individual, including those who served on the Joint Task Force, is authorized to provide an official AAAAI or ACAAI interpretation of these practice parameters. Any request for information about or an interpretation of these practice parameters by the AAAAI or ACAAI should be directed to the Executive Offices of the AAAAI, the ACAAI, and the Joint Council of Allergy, Asthma and Immunology. These parameters are not designed for rise by pharmaceutical companies in drug promotion.	[Wallace, Dana V.; Cox, Linda] Nova SE Univ, Coll Osteopath Med, Davie, FL USA; [Dykewicz, Mark S.] St Louis Univ, Sch Med, Allergy & Immunol Fellowship Program, St Louis, MO USA; [Dykewicz, Mark S.] St Louis Univ, Allergy & Clin Immunol Sect, Div Immunol, St Louis, MO USA; [Bernstein, David I.] Univ Cincinnati, Coll Med, Div Allergy Immunol, Cincinnati, OH USA; [Blessing-Moore, Joann] Stanford Univ, Med Ctr, Dept Immunol, Palo Alto, CA 94304 USA; [Khan, David A.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA; [Lang, David M.] Cleveland Clin Fdn, Allergy Immunol Sect, Div Med, Cleveland, OH 44195 USA; [Lang, David M.] Cleveland Clin Fdn, Allergy & Immunol Fellowship Training, Cleveland, OH 44195 USA; [Nicklas, Richard A.] George Washington Med Ctr, Washington, DC USA; [Oppenheimer, John] Pulm & Allergy Associates, New Jersey Med Sch, Dept Internal Med, Morristown, NJ USA; [Portnoy, Jay M.] Univ Missouri, Kansas City Sch Med, Kansas City, MO 64110 USA; [Portnoy, Jay M.] Childrens Mercy Hosp, Sect Allergy Asthma & Immunol, Kansas City, MO 64108 USA; [Randolph, Christopher C.] Yale Affiliated Hosp, Ctr Allergy Asthma & Immunol, Waterbury, CT USA; [Schuller, Diane] Penn State Univ, Milton S Hershey Med Coll, Hershey, PA USA; [Spector, Sheldon L.] Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA; [Tilles, Stephen A.] Univ Washington, Sch Med, Redmond, WA USA; [May, Kathleen R.] Allegany Allergy & Asthma, Cumberland, MD USA; [Miller, Travis A.] Univ Michigan, Capital Allergy & Resp Dis Ctr, Sacramento, CA USA; [Druce, Howard M.] Univ Hosp, Morris Plains, NJ USA; [Baroody, Faud M.] Univ Chicago, Pritzker Sch Med, Chicago, IL 60637 USA; [Bernstein, Jonathan A.] Univ Cincinnati, Coll Med, Dept Internal Med, Div Immunol,Allergy Sect, Cincinnati, OH USA; [Georgitis, John W.] Lafayette Clin, Fayetteville, NC USA; [Pawankar, Ruby] Nippon Med Sch, Dept Otolaryngol, Div Rhinol & Allergy, Tokyo 113, Japan; [Rachelefsky, Gary S.] Univ Calif Los Angeles, Med Ctr, Ctr Asthma Allergy & Resp Dis, Los Angeles, CA 90024 USA; [Settipane, Russell A.] Brown Univ, Sch Med, Providence, RI 02912 USA; [Skoner, David P.] Allegheny Gen Hosp, Div Allergy Asthma & Immunol, Pittsburgh, PA 15212 USA; [Skoner, David P.] Drexel Univ, Coll Med, Pittsburgh, PA USA; [Stoloff, Stuart W.] Univ Nevada, Sch Med, Reno, NV 89557 USA	Wallace, DV (reprint author), Nova SE Univ, Coll Osteopath Med, Davie, FL USA.						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J	Arts, ICW; Hollman, PCH				Arts, ICW; Hollman, PCH			Polyphenols and disease risk in epidemiologic studies	AMERICAN JOURNAL OF CLINICAL NUTRITION			English	Article; Proceedings Paper	1st International Conference on Poplyphenols and Health	NOV 18-21, 2004	Vichy, FRANCE			review; epidemiology; polyphenols; flavonoids; flavonols; catechins; lignans; antioxidants; phytoestrogens; cancer; cardiovascular diseases; stroke	CORONARY HEART-DISEASE; BREAST-CANCER RISK; POTENTIALLY ANTICARCINOGENIC FLAVONOIDS; CARDIOVASCULAR-DISEASE; POSTMENOPAUSAL WOMEN; PHYTOESTROGEN INTAKE; DIETARY FLAVONOIDS; UNITED-STATES; MALE SMOKERS; ANTIOXIDANT FLAVONOLS	Plant polyphenols, a large group of natural antioxidants, are serious candidates in explanations of the protective effects of vegetables and fruits against cancer and cardiovascular diseases. Epidemiologic studies are useful for evaluation of the human health effects of long-term exposure to physiologic concentrations of polyphenols, but reliable data on polyphenol contents of foods are still scarce. The aim of this review is to summarize available epidemiologic data on the health effects of polyphenols, focusing on the flavonoid subclasses of flavonols, flavones, and catechins and on lignans. Data obtained to date suggest beneficial effects of both flavonoids and lignans on cardiovascular diseases but not on cancer, with the possible exception of lung cancer. There is a need for more research on stroke and lung diseases such as asthma and chronic obstructive pulmonary disease. Most studies to date have included only flavonols and flavones. With data becoming available for other polyphenols, these compounds should be included in future studies. Careful design of prospective studies is important to offset some of the major drawbacks of epidemiologic studies, including residual confounding (by smoking and other dietary factors) and exposure assessment.	Univ Wageningen & Res Ctr, RIKILT, Inst Food Safety, NL-6700 AE Wageningen, Netherlands	Arts, ICW (reprint author), Univ Wageningen & Res Ctr, RIKILT, Inst Food Safety, POB 230, NL-6700 AE Wageningen, Netherlands.	ilja.arts@wur.nl	Arts, Ilja/C-6946-2008; Hollman, Peter/I-7446-2013	Arts, Ilja/0000-0001-6462-6692; Hollman, Peter/0000-0002-7510-6809			Adlercreutz H, 1997, ANN MED, V29, P95; Arts ICW, 2002, CANCER CAUSE CONTROL, V13, P373, DOI 10.1023/A:1015290131096; Arts ICW, 2000, J AGR FOOD CHEM, V48, P1746, DOI 10.1021/jf000025h; Arts ICW, 2000, J AGR FOOD CHEM, V48, P1752, DOI 10.1021/jf000026+; Arts ICW, 2001, EPIDEMIOLOGY, V12, P668, DOI 10.1097/00001648-200111000-00015; Arts ICW, 2001, AM J CLIN NUTR, V74, P227; Arts ICW, 2001, INT J CANCER, V92, P298, DOI 10.1002/1097-0215(200102)9999:9999<::AID-IJC1187>3.0.CO;2-8; Burke V, 1997, PREV MED, V26, P724, DOI 10.1006/pmed.1997.0198; Dai Q, 2003, CANCER EPIDEM BIOMAR, V12, P497; Dai Q, 2002, CANCER EPIDEM BIOMAR, V11, P815; de Kleijn MJJ, 2001, J NUTR, V131, P1826; de Kleijn MJJ, 2002, J NUTR, V132, P276; den Tonkelaar I, 2001, CANCER EPIDEM BIOMAR, V10, P223; Geleijnse JM, 2002, AM J CLIN NUTR, V75, P880; GOLDBOHM RA, 1998, POLYPHENOLS FOOD, P159; Heinonen S, 2001, J AGR FOOD CHEM, V49, P3178, DOI 10.1021/jf010038a; HERTOG MGL, 1994, NUTR CANCER, V22, P175; Hertog MGL, 1997, AM J CLIN NUTR, V65, P1489; HERTOG MGL, 1993, LANCET, V342, P1007, DOI 10.1016/0140-6736(93)92876-U; Hertog MGL, 1997, LANCET, V349, P699, DOI 10.1016/S0140-6736(05)60135-3; HERTOG MGL, 1992, J AGR FOOD CHEM, V40, P2379, DOI 10.1021/jf00024a011; HERTOG MGL, 1993, J AGR FOOD CHEM, V41, P1242, DOI 10.1021/jf00032a015; Higdon JV, 2003, CRIT REV FOOD SCI, V43, P89, DOI 10.1080/10408690390826464; Hirvonen T, 2001, CANCER CAUSE CONTROL, V12, P789, DOI 10.1023/A:1012232008016; Hirvonen T, 2000, STROKE, V31, P2301; Hirvonen T, 2001, EPIDEMIOLOGY, V12, P62, DOI 10.1097/00001648-200101000-00011; Hollman PCH, 2001, FREE RADICAL RES, V34, P297, DOI 10.1080/10715760100300261; Hollman PCH, 2000, J SCI FOOD AGR, V80, P1081, DOI 10.1002/(SICI)1097-0010(20000515)80:7<1081::AID-JSFA566>3.0.CO;2-G; Horn-Ross PL, 2001, AM J EPIDEMIOL, V154, P434, DOI 10.1093/aje/154.5.434; Horn-Ross PL, 2002, CANCER CAUSE CONTROL, V13, P407, DOI 10.1023/A:1015786030864; Horn-Ross PL, 2003, J NATL CANCER I, V95, P1158, DOI 10.1093/jnci/djg015; Horn-Ross PL, 2002, CANCER EPIDEM BIOMAR, V11, P43; Horn-Ross PL, 2000, CANCER CAUSE CONTROL, V11, P289, DOI 10.1023/A:1008995606699; HULSHOF KFAM, 1992, J EPIDEMIOL COMMUN H, V46, P417, DOI 10.1136/jech.46.4.417; Hulten K, 2002, EUR J NUTR, V41, P168, DOI 10.1007/s00394-002-0373-3; Ingram D, 1997, LANCET, V350, P990, DOI 10.1016/S0140-6736(97)01339-1; Keli SO, 1996, ARCH INTERN MED, V156, P637, DOI 10.1001/archinte.156.6.637; Knekt P, 2002, AM J CLIN NUTR, V76, P560; Knekt P, 1997, AM J EPIDEMIOL, V146, P223; Knekt P, 1996, BRIT MED J, V312, P478; Law MR, 1998, EUR J CLIN NUTR, V52, P549, DOI 10.1038/sj.ejcn.1600603; Le Marchand L, 2000, JNCI-J NATL CANCER I, V92, P154, DOI 10.1093/jnci/92.2.154; Marshall JR, 1996, AM J EPIDEMIOL, V143, P1069; McCann SE, 2002, J NUTR, V132, P3036; McCann SE, 2003, J NUTR, V133, P1937; MCPHILLIPS JB, 1994, J AM DIET ASSOC, V94, P287, DOI 10.1016/0002-8223(94)90370-0; Milder IEJ, 2004, J AGR FOOD CHEM, V52, P4643, DOI 10.1021/jf0497556; Nesbitt PD, 1999, AM J CLIN NUTR, V69, P549; Nijveldt RJ, 2001, AM J CLIN NUTR, V74, P418; Olthof MR, 2003, J NUTR, V133, P1806; Peters U, 2001, AM J EPIDEMIOL, V154, P495, DOI 10.1093/aje/154.6.495; Pietinen P, 2001, CANCER EPIDEM BIOMAR, V10, P339; Pillow PC, 1999, NUTR CANCER, V33, P3; Riboli E., 1996, IARC SCI PUBL, P23; Rimm EB, 1996, ANN INTERN MED, V125, P384; Sesso HD, 2003, AM J CLIN NUTR, V77, P1400; Stattin P, 2002, INT J CANCER, V99, P124, DOI 10.1002/ijc.10313; Strom SS, 1999, NUTR CANCER, V33, P20; Stumpf K, 2000, ANAL BIOCHEM, V284, P153, DOI 10.1006/abio.2000.4655; Tabak C, 2001, AM J RESP CRIT CARE, V164, P61; Tjonneland A, 1999, AM J CLIN NUTR, V69, P49; Tsubono Y, 1997, PREV MED, V26, P704, DOI 10.1006/pmed.1997.0194; van der Schouw YT, 2002, ARTERIOSCL THROM VAS, V22, P1316, DOI 10.1161/01.ATV.0000027176.83618.1A; Vanharanta M, 1999, LANCET, V354, P2112, DOI 10.1016/S0140-6736(99)05031-X; Vanharanta M, 2003, ARCH INTERN MED, V163, P1099, DOI 10.1001/archinte.163.9.1099; Vanharanta M, 2002, ATHEROSCLEROSIS, V160, P465, DOI 10.1016/S0021-9150(01)00603-7; VEENSTRA J, 1993, EUR J CLIN NUTR, V47, P482; Walcott FL, 2002, NUTR CANCER, V44, P44, DOI 10.1207/S15327914NC441_6; *WORLD CANC RES FU, 1997, FOOD NUTR PREV CANC, P436; Yang CS, 2001, ANNU REV NUTR, V21, P381, DOI 10.1146/annurev.nutr.21.1.381; Yochum L, 1999, AM J EPIDEMIOL, V149, P943	71	452	469	3	59	AMER SOC CLINICAL NUTRITION	BETHESDA	9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-3300, BETHESDA, MD 20814-3998 USA	0002-9165			AM J CLIN NUTR	Am. J. Clin. Nutr.	JAN	2005	81	1		S			317S	325S				9	Nutrition & Dietetics	Nutrition & Dietetics	888VB	WOS:000226401200015		
J	Gereda, JE; Leung, DYM; Thatayatikom, A; Streib, JE; Price, MR; Klinnert, MD; Liu, AH				Gereda, JE; Leung, DYM; Thatayatikom, A; Streib, JE; Price, MR; Klinnert, MD; Liu, AH			Relation between house-dust endotoxin exposure, type 1 T cell development, and allergen sensitisation in infants at high risk of asthma	LANCET			English	Article							INTERFERON-GAMMA PRODUCTION; BLOOD MONONUCLEAR-CELLS; PERIPHERAL-BLOOD; CHILDREN; ATOPY; PREVALENCE; SENSITIZATION; ASSOCIATION; RESPONSES; INTERLEUKIN-4	Background Bacterial endotoxin is known to induce interferon gamma and interleukin 12 production, and therefore has the potential to decrease allergen sensitisation. To find out the role of early chronic endotoxin exposure in the development of allergen sensitisation and asthma, we compared concentrations of endotoxin in house dust with allergen sensitisation in infants at high risk for developing asthma. Methods 61 infants 9-24 months old with at. least three physician-documented episodes of wheezing were studied. Concentrations of house-dust endotoxin and allergens were measured in the infants' homes. Allergen sensitisation was measured by skin-prick testing with a panel of common inhalant and food allergens. In a subset of these infants, proportions of T lymphocytes producing interferon gamma, and interleukins 4, 5, and 13 were calculated by cell-surface and intracellular cytokine staining, with flow cytometry. Findings House-dust endotoxin concentrations ranged from 104 to 10 000 endotoxin units (EU) per mt (geometric mean 912 EU/mL). Concentrations did not vary significantly over a 6-month interval. Ten infants (16%) were sensitised to at least one allergen. The homes of allergen-sensitised infants contained significantly lower concentrations of house-dust endotoxin than those of non-sensitised infants (mean 468 vs 1035 EU/mL, respectively; p=0.01). Increased house-dust endotoxin concentrations correlated with increased proportions of interferon-gamma-producing CD4 T cells (p=0.01). Such concentrations did not correlate with proportions of cells that produced interleukins 4, 5, or 13. Interpretation This study may provide the first direct in-vivo evidence that indoor endotoxin exposure early in life may protect against allergen sensitisation by enhancing type 1 immunity.	Natl Jewish Med & REs Ctr, Dept Behav Sci, Denver, CO 80206 USA; Natl Jewish Med & REs Ctr, Dept Pediat, Div Pediat Allergy & Immunol, Denver, CO 80206 USA; Univ Colorado, Hlth Sci Ctr, Denver, CO USA	Liu, AH (reprint author), Natl Jewish Med & REs Ctr, Dept Pediat, Div Pediat Allergy & Immunol, Denver, CO 80206 USA.				NCRR NIH HHS [M01-RR00051]; NHLBI NIH HHS [HL-36577]; NIAID NIH HHS [R18AI41137]		Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; DANDREA A, 1992, J EXP MED, V176, P1387, DOI 10.1084/jem.176.5.1387; DONHAM K, 1989, BRIT J IND MED, V46, P31; Hamilton RG, 1997, METHODS, V13, P53, DOI 10.1006/meth.1997.0495; Hoekstra MO, 1997, CLIN EXP ALLERGY, V27, P1254; Kramer U, 1999, LANCET, V353, P450, DOI 10.1016/S0140-6736(98)06329-6; LE JM, 1986, J IMMUNOL, V136, P4525; MARTINEZ FD, 1995, J ALLERGY CLIN IMMUN, V96, P652, DOI 10.1016/S0091-6749(95)70264-4; Martinez FD, 1999, J ALLERGY CLIN IMMUN, V103, P355, DOI 10.1016/S0091-6749(99)70456-2; Martinez FD, 1999, LANCET S2, V354, pSII12; Matricardi PM, 1998, J ALLERGY CLIN IMMUN, V101, P439, DOI 10.1016/S0091-6749(98)70350-1; Matricardi PM, 1997, BRIT MED J, V314, P999; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; Milton DK, 1997, AM IND HYG ASSOC J, V58, P861; Munir AKM, 1997, J ALLERGY CLIN IMMUN, V100, P177, DOI 10.1016/S0091-6749(97)70221-5; PAUL WE, 1994, CELL, V76, P241, DOI 10.1016/0092-8674(94)90332-8; PLATTMILLS TAE, 1995, RELEVANCE INDOOR ALL, P111; PLATTSMILLS TAE, 1992, J ALLERGY CLIN IMMUN, V89, P1046, DOI 10.1016/0091-6749(92)90228-T; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; Rizzo MC, 1997, PEDIATR ALLERGY IMMU, V8, P121; RYLANDER R, 1985, AM REV RESPIR DIS, V131, P209; 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; 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; Svanes C, 1999, J ALLERGY CLIN IMMUN, V103, P415, DOI 10.1016/S0091-6749(99)70465-3; TANG MLK, 1995, CLIN EXP ALLERGY, V25, P515, DOI 10.1111/j.1365-2222.1995.tb01088.x; VANASPEREN PP, 1984, J ALLERGY CLIN IMMUN, V73, P381, DOI 10.1016/0091-6749(84)90412-3; VANNIEKERK CH, 1979, CLIN ALLERGY, V9, P319; VONMUTIUS E, 1994, AM J RESP CRIT CARE, V149, P358; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; WAITE DA, 1980, CLIN ALLERGY, V10, P71, DOI 10.1111/j.1365-2222.1980.tb02082.x; WEISS K, 1992, CHEST, V6, pS362; WOODFOLK JA, 1992, ANN ALLERGY, V69, P273	35	449	463	2	9	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	MAY 13	2000	355	9216					1680	1683		10.1016/S0140-6736(00)02239-X		4	Medicine, General & Internal	General & Internal Medicine	313CY	WOS:000086983800010	10905243	
J	Lau, S; Illi, S; Sommerfeld, C; Niggemann, B; Bergmann, R; von Mutius, E; Wahn, U				Lau, S; Illi, S; Sommerfeld, C; Niggemann, B; Bergmann, R; von Mutius, E; Wahn, U		Multicentre Allergy Study Grp	Early exposure to house-dust mite and cat allergens and development of childhood asthma: a cohort study	LANCET			English	Article							SKIN-TEST REACTIVITY; RISK FACTOR; SENSITIZATION; CHILDREN; ASSOCIATION; ALTITUDE; FEL-D-1	Background In a prospective birth-cohort study, we assessed the relevance of mite and cat allergen exposure for the development of childhood asthma up to age 7 years. Methods Of 1314 newborn infants enrolled in five German cities in 1990, follow-up data at age 7 years were available far 939 children. Assessments included repeated measurement of specific IgE to food and inhalant allergens, measurement of indoor allergen exposure at 6 months, 18 months, and 3 years of age, and yearly interviews by a paediatrician. At age 7 years, pulmonary function was tested and bronchial hyper-responsiveness was measured in 645 children. Findings At age 7, the prevalence of wheezing in the past 12 months was 10.0% (94 of 938), and 6.1% (57 of 939) parents reported a doctor's diagnosis of asthma in their children. Sensitisation to indoor allergens was associated with asthma, wheeze, and increased bronchial responsiveness. However, no relation between early indoor allergen exposure and the prevalence of asthma, wheeze, and bronchial hyper-responsiveness was seen. Interpretation Our data do not support the hypothesis that exposure to environmental allergens causes asthma in childhood, but rather that the induction of specific IgE responses and the development of childhood asthma are determined by independent factors.	Humboldt Univ, Dept Paediat Pneumol & Immunol, Berlin, Germany; Univ Munich, Childrens Hosp, D-8000 Munich, Germany	Lau, S (reprint author), Charite Virchow Klinikum, Klin Padiat Pneumol & Immunol, Augustenburger Pl 1, D-13353 Berlin, Germany.						ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Bergmann R L, 1994, Pediatr Allergy Immunol, V5, P19, DOI 10.1111/j.1399-3038.1994.tb00343.x; BURR M L, 1989, Archives of Disease in Childhood, V64, P1452; CHARPIN D, 1991, AM REV RESPIR DIS, V143, P983; Custovic A, 1998, J ALLERGY CLIN IMMUN, V101, pS81; Custovic A, 1996, J ALLERGY CLIN IMMUN, V98, P64, DOI 10.1016/S0091-6749(96)70227-0; Demissie K, 1996, THORAX, V51, P59, DOI 10.1136/thx.51.1.59; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Hide DW, 1996, ALLERGY, V51, P89, DOI 10.1111/j.1398-9995.1996.tb04563.x; Hodge L, 1998, EUR RESPIR J, V11, P361, DOI 10.1183/09031936.98.11020361; INGRAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449, DOI 10.1016/S0091-6749(95)70286-5; KUHR J, 1995, J ALLERGY CLIN IMMUN, V95, P655; KUHR J, 1994, J ALLERGY CLIN IMMUN, V94, P44; LAU S, 1989, J ALLERGY CLIN IMMUN, V84, P718, DOI 10.1016/0091-6749(89)90300-X; LAUSCHADENDORF S, 1991, J ALLERGY CLIN IMMUN, V87, P41, DOI 10.1016/0091-6749(91)90211-6; MARKS GB, 1995, J ALLERGY CLIN IMMUN, V96, P441, DOI 10.1016/S0091-6749(95)70285-7; MATTHYS H, 1993, RESPIRATION, V60, P343; Nishioka K, 1998, J ALLERGY CLIN IMMUN, V101, P28, DOI 10.1016/S0091-6749(98)70189-7; Pearce N, 2000, THORAX, V55, P424, DOI 10.1136/thorax.55.5.424; Peat JK, 1996, AM J RESP CRIT CARE, V153, P141; Peterson EL, 1999, J ALLERGY CLIN IMMUN, V104, P348, DOI 10.1016/S0091-6749(99)70378-7; PLATTSMILLS TAE, 1995, J ALLERGY CLIN IMMUN, V96, P435, DOI 10.1016/S0091-6749(95)70284-9; Roost HP, 1999, J ALLERGY CLIN IMMUN, V104, P941, DOI 10.1016/S0091-6749(99)70072-2; SCHWARTZ J, 1990, AM REV RESPIR DIS, V142, P555; SEARS MR, 1989, CLIN EXP ALLERGY, V19, P419, DOI 10.1111/j.1365-2222.1989.tb02408.x; Shaheen SO, 1996, LANCET, V347, P1792, DOI 10.1016/S0140-6736(96)91617-7; Shaheen SO, 1999, CLIN EXP ALLERGY, V29, P291; Shirakawa T, 1997, SCIENCE, V275, P77, DOI 10.1126/science.275.5296.77; Sporik R, 1999, THORAX, V54, P675; SPORIK R, 1995, AM J RESP CRIT CARE, V151, P1388; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; VONMUTIUS E, 1994, BRIT MED J, V308, P692; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; Weiland SK, 1999, EUR RESPIR J, V14, P862, DOI 10.1034/j.1399-3003.1999.14d23.x; YUNGINGER JW, 1992, AM REV RESPIR DIS, V146, P888	35	445	462	6	26	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	OCT 21	2000	356	9239					1392	1397		10.1016/S0140-6736(00)02842-7		6	Medicine, General & Internal	General & Internal Medicine	365XQ	WOS:000089976100012	11052581	
J	Brunekreef, B; Forsberg, B				Brunekreef, B; Forsberg, B			Epidemiological evidence of effects of coarse airborne particles on health	EUROPEAN RESPIRATORY JOURNAL			English	Review						air pollution; coarse particles; epidemiology; morbidity; mortality	PARTICULATE AIR-POLLUTION; SOUTHERN CALIFORNIA CHILDREN; LUNG-FUNCTION GROWTH; DAILY MORTALITY; HOSPITAL ADMISSIONS; FINE PARTICLES; URBAN AIR; RESPIRATORY-DISEASES; TIME-SERIES; ASSOCIATION	Studies on health effects of airborne particulate matter (PM) have traditionally focused on particles <10 mu m in diameter (PM10) or particles <2.5 mu m in diameter (PM2.5). The coarse fraction of PM10, particles >2.5 mu m, has only been studied recently. These particles have different sources and composition compared with PM2.5. This paper is based on a systematic review of studies that have analysed fine and coarse PM jointly and examines the epidemiological evidence for effects of coarse particles on health. Time series studies relating ambient PM to mortality have in some places provided evidence of an independent effect of coarse PM on daily mortality, but in most urban areas, the evidence is stronger for fine particles. The few long-term studies of effects of coarse PM on survival do not provide any evidence of association. In studies of chronic obstructive pulmonary disease, asthma and respiratory admissions, coarse PM has a stronger or as strong short-term effect as fine PM, suggesting that coarse PM may lead to adverse responses in the lungs triggering processes leading to hospital admissions. There is also support for an association between coarse PM and cardiovascular admissions. It is concluded that special consideration should be given to studying and regulating coarse particles separately from fine particles.	Univ Utrecht, Inst Risk Assessment Sci, NL-3508 TD Utrecht, Netherlands; Umea Univ, Dept Publ Hlth & Clin Med, Umea, Sweden	Brunekreef, B (reprint author), Univ Utrecht, Inst Risk Assessment Sci, POB 80176, NL-3508 TD Utrecht, Netherlands.	b.brunekreef@iras.uu.nl		brunekreef, bert/0000-0001-9908-0060			Anderson HR, 2005, EPIDEMIOLOGY, V16, P155, DOI 10.1097/01.ede.0000152528.22746.0f; Anderson HR, 2001, OCCUP ENVIRON MED, V58, P504, DOI 10.1136/oem.58.8.504; Becker S, 2003, EXP LUNG RES, V29, P29, DOI 10.1080/01902140390116535; Becker S, 2002, AM J RESP CELL MOL, V27, P611, DOI 10.1165/rcmb.4868; Berner A, 2004, ATMOS ENVIRON, V38, P3959, DOI 10.1016/j.atmoenv.2004.02.056; Burnett RT, 1999, ARCH ENVIRON HEALTH, V54, P130; Burnett RT, 2001, AM J EPIDEMIOL, V153, P444, DOI 10.1093/aje/153.5.444; Burnett RT, 1997, ENVIRON HEALTH PERSP, V105, P614, DOI 10.1289/ehp.97105614; Burnett RT, 2000, INHAL TOXICOL, V12, P15, DOI 10.1080/089583700750019495; Burnett R. 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J	Matricardi, PM; Rosmini, F; Riondino, S; Fortini, M; Ferrigno, L; Rapicetta, M; Bonini, S				Matricardi, PM; Rosmini, F; Riondino, S; Fortini, M; Ferrigno, L; Rapicetta, M; Bonini, S			Exposure to foodborne and orofecal microbes versus airborne viruses in relation to atopy and allergic asthma: epidemiological study	BRITISH MEDICAL JOURNAL			English	Article							FAMILY-SIZE; SERUM IGE; ASSOCIATION; INFECTIONS; PREVALENCE; CHILDHOOD; DISEASES; HYGIENE; CELLS; FLORA	Objective To investigate if markers of exposure to foodborne and orofecal microbes versus airborne viruses are associated with atopy and respiratory allergies. Design Retrospective case-control study. Participants 240 atopic cases and 240 non-atopic controls from a population sample of 1659 participants, all Italian male cadets aged 17-24. Setting Air force school in Caserta, Italy. Main outcome measures Serology for Toxoplasma gondii, Helicobacter pylori, hepatitis A virus, measles, mumps, rubella, chickenpox, cytomegalovirus, and herpes simplex virus type 1; skin sensitisation and IgE antibodies to relevant airborne allergens; total IgE concentration; and diagnosis of allergic asthma or rhinitis, Results Compared with controls there tvas a lower prevalence of T gondii (26% v 18%, P = 0.027), hepatitis A virus (30% v 16%, P = 0.004), and H pylori (18% v 15%, P = 0.325) in atopic participants. Adjusted odds ratios of atopy decreased with a gradient of exposure to H pylori, T gondii, and hepatitis A virus (none, odds ratio 1; one, 0.70; two or three, 0.37; P for trend = 0.000045) but not with cumulative exposure to the other viruses. Conversely, total IgE concentration was not independently associated with any infection. Allergic asthma was rare (1/245, 0.4%) and allergic rhinitis infrequent (16/245, 7%) among the participants (245/1659) exposed to at least two orofecal and foodborne infections (H pylori, T gondii, hepatitis A virus). Conclusion Respiratory allergy is less frequent in people heavily exposed to orofecal and foodborne microbes. Hygiene and a westernised, semisterile diet may facilitate atopy by influencing the overall pattern of commensals and pathogens that stimulate the gut associated lymphoid tissue thus contributing to the epidemic of allergic asthma and rhinitis in developed countries.	Div Aerea Studi Ric & Sperimentaz, Lab Immunol & Allergol, I-00040 Pomezia, Italy; Ist Super Sanita, Epidemiol & Biostat Lab, I-00161 Rome, Italy; Ist Super Sanita, Virol Lab, I-00161 Rome, Italy; CNR, Ist Med Sperimentale, I-00137 Rome, Italy	Matricardi, PM (reprint author), Div Aerea Studi Ric & Sperimentaz, Lab Immunol & Allergol, I-00040 Pomezia, Italy.			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Med. J.	FEB 12	2000	320	7232					412	417		10.1136/bmj.320.7232.412		6	Medicine, General & Internal	General & Internal Medicine	285EU	WOS:000085377400022	10669445	
J	Leung, DYM				Leung, DYM			Atopic dermatitis: New insights and opportunities for therapeutic intervention	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						atopic dermatitis; keratinocytes; T cells; hypersensitivity; skin; allergy; superantigens; IgE	DOSE INTRAVENOUS IMMUNOGLOBULIN; LYMPHOCYTE-ASSOCIATED ANTIGEN; EPIDERMAL LANGERHANS CELLS; COLONY-STIMULATING FACTOR; INTERFERON-GAMMA-THERAPY; HIGH-AFFINITY RECEPTOR; IN-VIVO EXPRESSION; HOUSE-DUST MITE; MEMORY T-CELLS; FC-EPSILON-RI	Atopic dermatitis (AD) is a chronic inflammatory skin disease that frequently predates the development of allergic rhinitis or asthma. It is an important skin condition with significant costs and morbidity to patients and their families; the disease affects more than 10% of children. Recent studies have demonstrated the complex interrelationship of genetic, environmental, skin barrier, pharmacologic, psychologic, and immunologic factors that contribute to the development and severity of AD. The current review will examine the cellular and molecular mechanisms that contribute to AD as well as the immunologic triggers involved in its pathogenesis. These insights provide new opportunities for therapeutic intervention in this common skin condition.	Natl Jewish Med & Res Ctr, Div Pediat Allergy Immunol, Denver, CO 80206 USA; Univ Colorado, Hlth Sci Ctr, Dept Pediat, Denver, CO 80262 USA	Leung, DYM (reprint author), Natl Jewish Med & Res Ctr, Div Pediat Allergy Immunol, 1400 Jackson St,Room K926, Denver, CO 80206 USA.				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Allergy Clin. Immunol.	MAY	2000	105	5					860	876		10.1067/mai.2000.106484		17	Allergy; Immunology	Allergy; Immunology	316TW	WOS:000087185000002	10808164	
J	Suissa, S				Suissa, Samy			Immortal time bias in pharmacoepidemiology	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						bias (epidemiology); cohort studies; databases; epidemiologic methods; pharmaceutical preparations; relative biological effectiveness; statistics; treatment outcome	OBSTRUCTIVE PULMONARY-DISEASE; ACUTE MYOCARDIAL-INFARCTION; INHALED CORTICOSTEROIDS; CARDIAC TRANSPLANTATION; ASTHMA; RISK; MORTALITY; SURVIVAL; COPD; STEROIDS	Immortal time is a span of cohort follow-up during which, because of exposure definition, the outcome under study could not occur. Bias from immortal time was first identified in the 1970s in epidemiology in the context of cohort studies of the survival benefit of heart transplantation. It recently resurfaced in pharmacoepidemiology, with several observational studies reporting that various medications can be extremely effective at reducing morbidity and mortality. These studies, while using different cohort designs, all involved some form of immortal time and the corresponding bias. In this paper, the author describes various cohort study designs leading to this bias, quantifies its magnitude under different survival distributions, and illustrates it by using data from a cohort of lung cancer patients. The author shows that for time-based, event-based, and exposure-based cohort definitions, the bias in the rate ratio resulting from misclassified or excluded immortal time increases proportionately to the duration of immortal time. The bias is more pronounced with a decreasing hazard function for the outcome event, as illustrated with the Weibull distribution compared with a constant hazard from the exponential distribution. In conclusion, observational studies of drug benefit in which computerized databases are used must be designed and analyzed properly to avoid immortal time bias.	[Suissa, Samy] McGill Univ, Dept Epidemiol & Biostat, Montreal, PQ, Canada; [Suissa, Samy] McGill Univ, Dept Med, Montreal, PQ, Canada	Suissa, S (reprint author), Royal Victoria Hosp, McGill Pharmacoepidemiol Res Unit, 687 pine Ave W,Ross 4-29, Montreal, PQ H3A 1A1, Canada.	samy.suissa@clinepi.mcgill.ca					Adams RJ, 2002, J ALLERGY CLIN IMMUN, V109, P636, DOI 10.1067/mai.2002.123237; Adams RJ, 2001, PEDIATRICS, V107, P706, DOI 10.1542/peds.107.4.706; CHERRY DK, 2002, NATL AMBULATORY MED, P1; CLARK DA, 1971, ANN INTERN MED, V75, P15; Donahue JG, 1997, JAMA-J AM MED ASSOC, V277, P887, DOI 10.1001/jama.277.11.887; DUCK BW, 1975, LANCET, V2, P1197; ELLWOOD PM, 1988, NEW ENGL J MED, V318, P1549, DOI 10.1056/NEJM198806093182329; ENTERLINE PE, 1976, J OCCUP ENVIRON MED, V18, P150, DOI 10.1097/00043764-197603000-00006; EPTSTEIN AM, 1990, NEW ENGL J MED, V323, P266; GAIL MH, 1972, ANN INTERN MED, V76, P815; Gail M. H., 2000, ENCY EPIDEMIOLOGIC M; Gelfand JM, 2005, PHARMACOEPIDEMIOLOGY, 4TH EDITION, P337; Glesby MJ, 1996, ANN INTERN MED, V124, P999; Kiri VA, 2005, AM J RESP CRIT CARE, V172, P460, DOI 10.1164/rccm.200502-210OC; Mamdani M, 2003, ARCH INTERN MED, V163, P481, DOI 10.1001/archinte.163.4.481; MANCUSO TF, 1967, JOM-J OCCUP MED, V9, P147; MANTEL N, 1974, J AM STAT ASSOC, V69, P81, DOI 10.2307/2285503; MESSMER BJ, 1969, LANCET, V1, P954; Redelmeier DA, 2001, ANN INTERN MED, V134, P955; RELMAN AS, 1988, NEW ENGL J MED, V319, P1220, DOI 10.1056/NEJM198811033191810; Robins JM, 2000, BIOMETRICS, V56, P779, DOI 10.1111/j.0006-341X.2000.00779.x; Rochon PA, 2000, LANCET, V356, P639, DOI 10.1016/S0140-6736(00)02606-4; Rothman KJ, 1998, MODERN EPIDEMIOLOGY; Samet JM, 2003, AM J RESP CRIT CARE, V168, P1, DOI 10.1164/rccm.2304004; Sin DD, 2001, AM J RESP CRIT CARE, V164, P580; Soriano JB, 2002, EUR RESPIR J, V20, P819, DOI 10.1183/09031936.02.00301302; SPITZER WO, 1992, NEW ENGL J MED, V326, P501, DOI 10.1056/NEJM199202203260801; Strom BL, 2005, PHARMACOEPIDEMIOLOGY, 4TH EDITION, P1; Suissa S, 2006, AM J RESP CRIT CARE, V173, P464; Suissa S, 2005, J ALLERGY CLIN IMMUN, V115, P714, DOI 10.1016/j.jaci.2004.12.1118; Suissa S, 2004, EUR RESPIR J, V23, P391, DOI 10.1183/09031936.04.00062504; Suissa S, 2003, AM J RESP CRIT CARE, V168, P49, DOI 10.1164/rccm.200210-1231OC; Suissa S, 2003, THORAX, V58, P43, DOI 10.1136/thorax.58.1.43; Suissa S, 2000, NEW ENGL J MED, V343, P332, DOI 10.1056/NEJM200008033430504; Suissa S, 2007, PHARMACOEPIDEM DR S, V16, P241, DOI 10.1002/pds.1357; Sylvestre MP, 2006, ANN INTERN MED, V145, P361; Szklo M, 2000, EPIDEMIOLOGY BASICS; WAGONER JK, 1976, LANCET, V2, P194; Walker AM, 1991, OBSERVATION INFERENC; Zhou Z, 2005, AM J EPIDEMIOL, V162, P1016, DOI 10.1093/aje/kwi307	40	434	434	6	34	OXFORD UNIV PRESS INC	CARY	JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA	0002-9262	1476-6256		AM J EPIDEMIOL	Am. J. Epidemiol.	FEB 15	2008	167	4					492	499		10.1093/aje/kwm324		8	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	263WC	WOS:000253246200016	18056625	
J	Moore, WC; Bleecker, ER; Curran-Everett, D; Erzurum, SC; Ameredes, BT; Bacharier, L; Calhoun, WJ; Castro, M; Chung, KF; Clark, MP; Dweik, RA; Fitzpatrick, AM; Gaston, B; Hew, M; Hussain, I; Jarjour, NN; Israel, E; Levy, BD; Murphy, JR; Peters, SP; Teague, WG; Meyers, DA; Busse, WW; Wenzel, SE				Moore, Wendy C.; Bleecker, Eugene R.; Curran-Everett, Douglas; Erzurum, Serpil C.; Ameredes, Bill T.; Bacharier, Leonard; Calhoun, William J.; Castro, Mario; Chung, Kian Fan; Clark, Melissa P.; Dweik, Raed A.; Fitzpatrick, Anne M.; Gaston, Benjamin; Hew, Mark; Hussain, Iftikhar; Jarjour, Nizar N.; Israel, Elliot; Levy, Bruce D.; Murphy, James R.; Peters, Stephen P.; Teague, W. Gerald; Meyers, Deborah A.; Busse, William W.; Wenzel, Sally E.		Natl Heart Lung Blood Inst Severe	Characterization of the severe asthma phenotype by the National Heart, Lung, and Blood Institute's Severe Asthma Research Program	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						severe asthma; definition; bronchodilator response; pathophysiology; phenotype; pneumonia	EXHALED NITRIC-OXIDE; AIR-FLOW OBSTRUCTION; NEAR-FATAL ASTHMA; TO-TREAT ASTHMA; INHALED-CORTICOSTEROIDS; RISK-FACTORS; EOSINOPHILIC INFLAMMATION; DISEASE; ADULTS; EXACERBATIONS	Background: Severe asthma causes the majority of asthma morbidity. Understanding mechanisms that contribute to the development of severe disease is important. Objective: The goal of the Severe Asthma Research Program is to identify and characterize subjects with severe asthma to understand pathophysiologic mechanisms in severe asthma. Methods: We performed a comprehensive phenotypic characterization (questionnaires, atopy and pulmonary function testing, phlebotomy, exhaled nitric oxide) in subjects with severe and not severe asthma. Results: A total of 438 subjects with asthma were studied (204 severe, 70 moderate, 164 mild). Severe subjects with asthma were older with longer disease duration (P < .0001), more daily symptoms, intense urgent health care utilization, sinusitis, and pneumonia (P < .0001). Lung function was lower in severe asthma with marked bronchodilator reversibility (P < .001). The severe group had less atopy by skin tests (P = .0007), but blood eosinophils, IgE, and exhaled nitric oxide levels did not differentiate disease severity. A reduced FEV1, history of pneumonia, and fewer positive skin tests were risk factors for severe disease. Early disease onset (age < 12 years) in severe asthma was associated with longer disease duration (P < .0001) and more urgent health care, especially intensive care (P = .002). Later disease onset (age >= 12 years) was associated with lower lung function and sinopulmonary infections (P <= .02). Conclusion: Severe asthma is characterized by abnormal lung function that is responsive to bronchodilators, a history of sinopulmonary infections, persistent symptoms, and increased health care utilization. Clinical implications: Lung function abnormalities in severe asthma are reversible in most patients, and pneumonia is a risk factor for the development of severe disease.	Wake Forest Univ, Sch Med, Ctr Human Genom, Winston Salem, NC 27157 USA; Wake Forest Univ, Sch Med, Sect Pulm Crit Care Allergy & Immunol Dis, Winston Salem, NC 27157 USA; Univ Colorado, Hlth Sci Ctr, Natl Jewish Med & Res Ctr, Denver, CO 80202 USA; Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA	Moore, WC (reprint author), Wake Forest Univ, Sch Med, Ctr Human Genom, Med Ctr Blvd, Winston Salem, NC 27157 USA.	wmoore@wfubmc.edu		Chung, Kian Fan/0000-0001-7101-1426	NCRR NIH HHS [M01 RR003186, M01 RR003186-22, M01 RR007122, M01 RR007122-14, M01 RR007122-17, M01 RR018390, M01 RR018390-03, M01 RR03186]; NHLBI NIH HHS [R01 HL069170, HL69116, HL69130, HL69149, HL69155, HL69167, HL69170, HL69174, HL69349, R01 HL069116, R01 HL069116-09, R01 HL069130, R01 HL069130-03, R01 HL069149, R01 HL069149-05, R01 HL069155, R01 HL069155-05, R01 HL069167, R01 HL069167-09, R01 HL069170-09, R01 HL069174, R01 HL069174-09, R01 HL069349, R01 HL069349-05]		Abraham B, 2003, EUR RESPIR J, V22, P470, DOI 10.1183/09031936.03.00261903; American Thoracic Society, 2005, AM J RESP CRIT CARE, V171, P912, DOI DOI 10.1164/RCCM.200406-710ST; Antonicelli L, 2004, EUR RESPIR J, V23, P723, DOI 10.1183/09031936.04.00004904; Bates CA, 2003, J ALLERGY CLIN IMMUN, V111, P256, DOI 10.1067/mai.2003.103; Bergmann MM, 2004, EUR J EPIDEMIOL, V19, P411; Bresciani M, 2001, J ALLERGY CLIN IMMUN, V107, P73, DOI 10.1067/mai.2001.111593; Bumbacea D, 2004, EUR RESPIR J, V24, P122, DOI 10.1183/09031936.04.00077803; Busse William W., 2000, Journal of Allergy and Clinical Immunology, V106, P1033; Cochrane MG, 2000, CHEST, V117, P542, DOI 10.1378/chest.117.2.542; Colice Gene L, 2004, Clin Med Res, V2, P155; Comhair SAA, 2005, AM J RESP CRIT CARE, V172, P306, DOI 10.1164/rccm.200502-180OC; Curran-Everett D, 2000, AM J PHYSIOL-REG I, V279, pR1; De Smet BD, 2006, ANN PHARMACOTHER, V40, P414, DOI 10.1345/aph.1G475; Des Roches Anne, 1996, Journal of Allergy and Clinical Immunology, V98, P522, DOI 10.1016/S0091-6749(96)70085-4; Diette GB, 2004, ANN ALLERG ASTHMA IM, V93, P546; Diette GB, 1999, ARCH INTERN MED, V159, P2697, DOI 10.1001/archinte.159.22.2697; Dolan CM, 2004, ANN ALLERG ASTHMA IM, V92, P32; Dweik RA, 2001, P NATL ACAD SCI USA, V98, P2622, DOI 10.1073/pnas.051629498; Eisner MD, 2005, J ASTHMA, V42, P315, DOI 10.1081/JAS-200062959; Godard P, 2002, EUR RESPIR J, V19, P61, DOI 10.1183/09031936.02.00232001; Griswold SK, 2005, CHEST, V127, P1579, DOI 10.1378/chest.127.5.1579; Jenkins HA, 2003, CHEST, V124, P1318, DOI 10.1378/chest.124.4.1318; Koga T, 2006, RESP MED, V100, P273, DOI 10.1016/j.rmed.2005.05.017; Lim S, 2000, THORAX, V55, P184, DOI 10.1136/thorax.55.3.184; Liou Aimee, 2003, Chest, V124, P1781, DOI 10.1378/chest.124.5.1781; Mahler DA, 1999, CHEST, V115, P957, DOI 10.1378/chest.115.4.957; Miller MK, 2005, J ALLERGY CLIN IMMUN, V116, P990, DOI 10.1016/j.jaci.2005.08.018; Miller MR, 2005, EUR RESPIR J, V26, P319, DOI 10.1183/09031936.05.00034805; Miranda C, 2004, J ALLERGY CLIN IMMUN, V113, P101, DOI 10.1016/j.jaci.2003.10.041; Mitchell I, 2002, CHEST, V121, P1407, DOI 10.1378/chest.121.5.1407; *NAT HEART LUNG BL, 2002, 023659 NHLBIWHO, P1; *NAT I HLTH NAT HE, 1997, 974051 NAT I HLTH NA; *NAT I HLTH NAT HE, 2002, 025075 NAT I HLTH NA; Ricciardolo FLM, 2004, PHYSIOL REV, V84, P731, DOI 10.1152/physrev.00034.2003; Serra-Batlles J, 1998, EUR RESPIR J, V12, P1322, DOI 10.1183/09031936.98.12061322; Silkoff PE, 2005, J ALLERGY CLIN IMMUN, V116, P1249, DOI 10.1016/j.jaci.2005.09.029; Stirling RG, 1998, THORAX, V53, P1030; Stoloff SW, 2004, J ALLERGY CLIN IMMUN, V113, P245, DOI 10.1016/j.jaci.2003.10.011; Talbot TR, 2005, NEW ENGL J MED, V352, P2082, DOI 10.1056/NEJMoa044113; ten Brinke A, 2005, EUR RESPIR J, V26, P812, DOI 10.1183/09031936.05.00037905; Turner MO, 1998, AM J RESP CRIT CARE, V157, P1804; Wenzel S, 2005, AM J RESP CRIT CARE, V172, P149, DOI 10.1164/rccm.200409-1181PP; [Anonymous], 2000, AM J RESP CRIT CARE, V162, P2341	43	434	440	0	12	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	FEB	2007	119	2					405	413		10.1016/j.jaci.2006.11.639		9	Allergy; Immunology	Allergy; Immunology	137YB	WOS:000244327900019	17291857	
J	D'Amato, G; Cecchi, L; Bonini, S; Nunes, C; Annesi-Maesano, I; Behrendt, H; Liccardi, G; Popov, T; van Cauwenberge, P				D'Amato, G.; Cecchi, L.; Bonini, S.; Nunes, C.; Annesi-Maesano, I.; Behrendt, H.; Liccardi, G.; Popov, T.; van Cauwenberge, P.			Allergenic pollen and pollen allergy in Europe	ALLERGY			English	Review						airway hypersensitivity; allergenic pollens; allergic asthma; allergic rhinitis; bronchial asthma; outdoor air-pollution; pollinosis; respiratory allergy; seasonal allergy.	RAGWEED AMBROSIA-ARTEMISIIFOLIA; RESPIRATORY HEALTH SURVEY; LONG-DISTANCE TRANSPORT; BENJAMINA WEEPING FIG; NATURAL-RUBBER LATEX; ALPHA-LINOLENIC ACID; GRASS-POLLEN; FICUS-BENJAMINA; BIRCH-POLLEN; ENVIRONMENTAL-FACTORS	The allergenic content of the atmosphere varies according to climate, geography and vegetation. Data on the presence and prevalence of allergenic airborne pollens, obtained from both aerobiological studies and allergological investigations, make it possible to design pollen calendars with the approximate flowering period of the plants in the sampling area. In this way, even though pollen production and dispersal from year to year depend on the patterns of preseason weather and on the conditions prevailing at the time of anthesis, it is usually possible to forecast the chances of encountering high atmospheric allergenic pollen concentrations in different areas.Aerobiological and allergological studies show that the pollen map of Europe is changing also as a result of cultural factors (for example, importation of plants such as birch and cypress for urban parklands), greater international travel (e.g. colonization by ragweed in France, northern Italy, Austria, Hungary etc.) and climate change. In this regard, the higher frequency of weather extremes, like thunderstorms, and increasing episodes of long range transport of allergenic pollen represent new challenges for researchers.Furthermore, in the last few years, experimental data on pollen and subpollen-particles structure, the pathogenetic role of pollen and the interaction between pollen and air pollutants, gave new insights into the mechanisms of respiratory allergic diseases.	High Special Hosp A Cardarelli, Dept Chest Dis, Div Resp & Allerg Dis, Naples, Italy; Univ Florence, Interdept Ctr Bioclimatol, Florence, Italy; Azienda Sanitaria 10 Firenze, Allerg Clin, Florence, Italy; Univ Naples 2, Naples, Italy; CNR, Inst Mol Neurobiol Med, ARTOV, Rome, Italy; Ctr Imunoalerlogia Algarve, Portimao, Portugal; INSERM, UMR S 707, EPAR, Paris, France; Univ Paris 06, UMR S 707, EPAR, Paris, France; Tech Univ Munich, Div Environm Dermatol & Allerg GSF, D-8000 Munich, Germany; Med Univ, Clin Ctr Allergol, Sofia, Bulgaria; State Univ Ghent Hosp, Dept Otorhinolaryngol, B-9000 Ghent, Belgium	D'Amato, G (reprint author), High Special Hosp A Cardarelli, Dept Chest Dis, Div Resp & Allerg Dis, Naples, Italy.		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J	van den Biggelaar, AHJ; van Ree, R; Rodrigues, LC; Lell, B; Deelder, AM; Kremsner, PG; Yazdanbakhsh, M				van den Biggelaar, AHJ; van Ree, R; Rodrigues, LC; Lell, B; Deelder, AM; Kremsner, PG; Yazdanbakhsh, M			Decreased atopy in children infected with Schistosoma haematobium: a role for parasite-induced interleukin-10	LANCET			English	Article							HUMAN LYMPHATIC FILARIASIS; ALLERGIC REACTIVITY; CYTOKINE CONTROL; CELL RESPONSES; ASTHMA; MODULATION; ACTIVATION; INDUCTION; ANTIBODY; CD4(+)	Background Most of the effort directed at understanding the role infections have in preventing allergy has focused on bacteria and viruses and their ability to divert the immune system towards T-helper-1 responses and away from proallergic T-helper-2 responses. However, helminth infections, highly prevalent in large parts of the developing world, where allergy is uncommon, stimulate strong T-helper-2 responses. We investigated the influence of chronic helminth infections on the prevalence of atopy and aimed to understand the relation at a detailed immunological level. Methods 520 Gabonese schoolchildren were tested for shin reaction to house-dust mite and other allergens, for Schistosoma haematobium eggs In urine, and for microfilariae in blood samples. Total and mite-specific IgE antibodies were measured. A subsample selected on the basis of their skin test to house-dust mite received detailed immunological investigations. Findings Children with urinary schistosomiasis had a lower prevalence of a positive skin reaction to house-dust mite than those free of this infection (odds ratio 0.32 [95% CI 0.16-0.63]). The degree of sensitisation to house-dust mite could not explain this difference in skin-prick positivity. Schistosome-antigen-specific concentrations of interleukin-10 were significantly higher in infected children, and higher specific concentrations of this anti-inflammatory cytokine were negatively associated with the outcome of skin-test reactivity to mite (0.53 [0.30-0.96]). No association between polyclonal IgE antibodies and skin-test results was found. Interpretation The anti-inflammatory cytokine, interleukin-10, induced in chronic schistosomiasis, appears central to suppressing atopy in African children.	Leiden Univ, Med Ctr, Dept Parasitol, NL-2333 ZA Leiden, Netherlands; CLB, Dept Allergy, Amsterdam, Netherlands; London Sch Hyg & Trop Med, Dept Infect & Trop Dis, London WC1, England; Univ Tubingen, Inst Trop Med, Dept Parasitol, D-72074 Tubingen, Germany; Albert Schweitzer Hosp, Res Unit, Lambarene, Gabon	Yazdanbakhsh, M (reprint author), Leiden Univ, Med Ctr, Dept Parasitol, L4-Q,Albinusdreef 2, NL-2333 ZA Leiden, Netherlands.						Akdis CA, 1998, J CLIN INVEST, V102, P98, DOI 10.1172/JCI2250; Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Borish L, 1996, J ALLERGY CLIN IMMUN, V97, P1288, DOI 10.1016/S0091-6749(96)70197-5; Cookson W, 1999, NATURE, V402, pB5; Cookson WOCM, 1997, SCIENCE, V275, P41, DOI 10.1126/science.275.5296.41; Cooper PJ, 1998, J INFECT DIS, V178, P1133, DOI 10.1086/515661; DREBORG S, 1993, ALLERGY, V48, P49, DOI 10.1111/j.1398-9995.1993.tb04756.x; Edwards-Smith CJ, 1999, HEPATOLOGY, V30, P526, DOI 10.1002/hep.510300207; GODFREY RC, 1976, NATURE, V259, P484, DOI 10.1038/259484a0; Groux H, 1997, NATURE, V389, P737; HAGEL I, 1993, PARASITE IMMUNOL, V15, P311, DOI 10.1111/j.1365-3024.1993.tb00615.x; Hirsch CS, 1996, P NATL ACAD SCI USA, V93, P3193, DOI 10.1073/pnas.93.8.3193; Holt PG, 1999, NATURE, V402, pB12; HUSSAIN R, 1992, J IMMUNOL, V148, P2731; JARRETT E, 1974, NATURE, V251, P613, DOI 10.1038/251613a0; JARRETT E, 1980, NATURE, V283, P302, DOI 10.1038/283302a0; KING CL, 1993, J CLIN INVEST, V92, P1667, DOI 10.1172/JCI116752; King CL, 1996, J IMMUNOL, V156, P4715; Lim S, 1998, LANCET, V352, P113, DOI 10.1016/S0140-6736(98)85018-6; Macaubas C, 1999, CLIN EXP ALLERGY, V29, P1223; Matricardi PM, 2000, BRIT MED J, V320, P412, DOI 10.1136/bmj.320.7232.412; Oxenius A, 1998, IMMUNITY, V9, P449, DOI 10.1016/S1074-7613(00)80628-7; Schuurman J, 1997, J ALLERGY CLIN IMMUN, V99, P545, DOI 10.1016/S0091-6749(97)70083-6; 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, V351, P1225; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; YAZDANBAKHSH M, 1993, EUR J IMMUNOL, V23, P3312, DOI 10.1002/eji.1830231238; YEMANEBERHAN H, 1997, LANCET, V350, P400	30	425	438	2	29	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	NOV 18	2000	356	9243					1723	1727		10.1016/S0140-6736(00)03206-2		5	Medicine, General & Internal	General & Internal Medicine	376MX	WOS:000165462300011	11095260	
J	Wrensch, M; Minn, Y; Chew, T; Bondy, M; Berger, MS				Wrensch, M; Minn, Y; Chew, T; Bondy, M; Berger, MS			Epidemiology of primary brain tumors: Current concepts and review of the literature	NEURO-ONCOLOGY			English	Review							CENTRAL-NERVOUS-SYSTEM; FRANCISCO BAY AREA; PETROCHEMICAL RESEARCH FACILITY; OCCUPATIONAL RISK-FACTORS; ACUTE LYMPHOBLASTIC-LEUKEMIA; INTERNATIONAL CASE-CONTROL; MAGNETIC-FIELD EXPOSURE; VINYL-CHLORIDE WORKERS; GROWTH-FACTOR RECEPTOR; CELLULAR-TELEPHONE USE	The purpose of this review is to provide a sufficiently detailed perspective on epidemiologic studies of primary brain tumors to encourage multidisciplinary etiologic and prognostic studies among surgeons, neuro-oncologists, epidemiologists, and molecular scientists. Molecular tumor markers that predict survival and treatment response are being identified with hope of even greater gains in this area from emerging array technologies. Regarding risk factors, studies of inherited susceptibility and constitutive polymorphisms in genes pertinent to carcinogenesis (for example, DNA repair and detoxification genes and mutagen sensitivity) have revealed provocative findings. Inverse associations of the history of allergies with glioma risk observed in 3 large studies and reports of inverse associations of glioma with common infections suggest a possible role of immune factors in glioma genesis or progression. Studies continue to suggest that brain tumors might result from workplace, dietary, and other personal and residential exposures, but studies of cell phone use and power frequency electromagnetic fields have found little to support a causal connection with brain tumors; caveats remain. The only proven causes of brain tumors (that is, rare hereditary syndromes, therapeutic radiation, and immune suppression giving rise to brain lymphomas) account for a small proportion of cases. Progress in understanding primary brain tumors might result from studies of well-defined histologic and molecular tumor types incorporating assessment of potentially relevant information on subject susceptibility and environmental and noninherited endogenous factors (viruses, radiation, and carcinogenic or protective chemical exposures through diet, workplace, oxidative metabolism, or other sources). Such studies will require the cooperation of researchers from many disciplines.	Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94102 USA; Univ Calif San Francisco, Dept Neurol Surg, San Francisco, CA 94102 USA; Univ Calif San Francisco, Brain Tumor Res Ctr, San Francisco, CA 94102 USA; Stanford Univ, Dept Neurol, Stanford, CA 94305 USA; Univ Texas, MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA	Wrensch, M (reprint author), Univ Calif San Francisco, Dept Epidemiol & Biostat, Box 1215,44 Page St,Suite 503, San Francisco, CA 94102 USA.		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Zheng TZ, 2001, J OCCUP ENVIRON MED, V43, P317, DOI 10.1097/00043764-200104000-00005	214	423	440	7	50	CARDEN JENNINGS PUBL CO LTD	CHARLOTTESVILLE	BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 USA	1522-8517			NEURO-ONCOLOGY	Neuro-Oncology	OCT	2002	4	4					278	299		10.1215/15228517-4-4-278		22	Oncology; Clinical Neurology	Oncology; Neurosciences & Neurology	596JP	WOS:000178161800006	12356358	
J	Chung, KF; Wenzel, SE; Brozek, JL; Bush, A; Castro, M; Sterk, PJ; Adcock, IM; Bateman, ED; Bel, EH; Bleecker, ER; Boulet, LP; Brightling, C; Chanez, P; Dahlen, SE; Djukanovic, R; Frey, U; Gaga, M; Gibson, P; Hamid, Q; Jajour, NN; Mauad, T; Sorkness, RL; Teague, WG				Chung, Kian Fan; Wenzel, Sally E.; Brozek, Jan L.; Bush, Andrew; Castro, Mario; Sterk, Peter J.; Adcock, Ian M.; Bateman, Eric D.; Bel, Elisabeth H.; Bleecker, Eugene R.; Boulet, Louis-Philippe; Brightling, Christopher; Chanez, Pascal; Dahlen, Sven-Erik; Djukanovic, Ratko; Frey, Urs; Gaga, Mina; Gibson, Peter; Hamid, Qutayba; Jajour, Nizar N.; Mauad, Thais; Sorkness, Ronald L.; Teague, W. Gerald			International ERS/ATS guidelines on definition, evaluation and treatment of severe asthma	EUROPEAN RESPIRATORY JOURNAL			English	Article							EXHALED NITRIC-OXIDE; AIR-FLOW OBSTRUCTION; RANDOMIZED CONTROLLED-TRIAL; PLACEBO-CONTROLLED TRIAL; SEVERE PERSISTENT ASTHMA; POORLY CONTROLLED ASTHMA; GENOME-WIDE ASSOCIATION; RELATIVE CORTICOSTEROID INSENSITIVITY; SPUTUM EOSINOPHIL COUNTS; ALLERGIC AIRWAYS DISEASE	Severe or therapy-resistant asthma is increasingly recognised as a major unmet need. A Task Force, supported by the European Respiratory Society and American Thoracic Society, reviewed the definition and provided recommendations and guidelines on the evaluation and treatment of severe asthma in children and adults. A literature review was performed, followed by discussion by an expert committee according to the GRADE (Grading of Recommendations, Assessment, Development and Evaluation) approach for development of specific clinical recommendations. When the diagnosis of asthma is confirmed and comorbidities addressed, severe asthma is defined as asthma that requires treatment with high dose inhaled corticosteroids plus a second controller and/or systemic corticosteroids to prevent it from becoming "uncontrolled" or that remains "uncontrolled" despite this therapy. Severe asthma is a heterogeneous condition consisting of phenotypes such as eosinophilic asthma. Specific recommendations on the use of sputum eosinophil count and exhaled nitric oxide to guide therapy, as well as treatment with anti-IgE antibody, methotrexate, macrolide antibiotics, antifungal agents and bronchial thermoplasty are provided. Coordinated research efforts for improved phenotyping will provide safe and effective biomarker-driven approaches to severe asthma therapy.	[Chung, Kian Fan; Bush, Andrew; Adcock, Ian M.] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London SW3 6LY, England; [Chung, Kian Fan; Bush, Andrew] Royal Brompton Hosp, Biomed Res Unit, London SW3 6LY, England; [Brightling, Christopher] Univ Leicester, Inst Lung Hlth, Leicester, Leics, England; [Djukanovic, Ratko] Univ Southampton, Sch Med, Southampton NIHR Resp Biomed Res Unit, Southampton, Hants, England; [Djukanovic, Ratko] Southampton Gen Hosp, Southampton SO9 4XY, Hants, England; [Wenzel, Sally E.] Univ Pittsburgh, Dept Med, Pittsburgh, PA USA; [Castro, Mario] Washington Univ, Dept Med, St Louis, MO USA; [Bleecker, Eugene R.] Wake Forest Univ, Dept Med, Winston Salem, NC 27109 USA; [Jajour, Nizar N.; Sorkness, Ronald L.] Univ Wisconsin, Dept Med, Madison, WI USA; [Teague, W. Gerald] Univ Virginia, Sch Med, Dept Paediat, Div Resp Med Allergy & Immunol, Charlottesville, VA 22903 USA; [Brozek, Jan L.] McMaster Univ, Dept Clin Epidemiol & Biostat & Med, Hamilton, ON, Canada; [Boulet, Louis-Philippe] Inst Univ Cardiol & Pneumol Quebec, Ctr Rech, Quebec City, PQ, Canada; [Hamid, Qutayba] McGill Univ, Meakins Christie Labs, Montreal, PQ, Canada; [Sterk, Peter J.; Bel, Elisabeth H.] Univ Amsterdam, Acad Med Ctr, Dept Resp Med, NL-1105 AZ Amsterdam, Netherlands; [Bateman, Eric D.] Univ Cape Town, Lung Inst, ZA-7925 Cape Town, South Africa; [Chanez, Pascal] Marseille Univ, Dept Malad Resp, Marseille, France; [Dahlen, Sven-Erik] Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; [Frey, Urs] Univ Basel, Univ Childrens Hosp UKBB, Basel, Switzerland; [Gaga, Mina] Athens Chest Hosp, Resp Dept 7, Athens, Greece; [Gaga, Mina] Athens Chest Hosp, Asthma Ctr, Athens, Greece; [Gibson, Peter] John Hunter Hosp, Hunter Med Res Inst, Newcastle, NSW, Australia; [Mauad, Thais] Univ Med Sch, Dept Pathol, Sao Paulo, Brazil	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	Mauad, Thais/G-1254-2012	Adcock, Ian/0000-0003-2101-8843; 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J	Wilson, DR; Lima, MT; Durham, SR				Wilson, DR; Lima, MT; Durham, SR			Sublingual immunotherapy for allergic rhinitis: systematic review and meta-analysis	ALLERGY			English	Reprint						allergic rhinitis; immunotherapy; sublingual; systematic review	PLACEBO-CONTROLLED EVALUATION; HOUSE-DUST-MITE; RANDOMIZED CONTROLLED-TRIAL; PARIETARIA-JUDAICA EXTRACT; GRASS-POLLEN IMMUNOTHERAPY; DOUBLE-BLIND; SWALLOW IMMUNOTHERAPY; HAY-FEVER; SEASONAL RHINITIS; RHINOCONJUNCTIVITIS	Allergic rhinitis is a common condition which, at its most severe, can significantly impair quality of life despite optimal treatment with antihistamines and topical nasal corticosteroids. Allergen injection immunotherapy significantly reduces symptoms and medication requirements in allergic rhinitis but its use is limited by the possibility of severe systemic reactions. There has therefore been considerable interest in alternative routes for delivery of allergen immunotherapy, particularly the sublingual route. The objective was to evaluate the efficacy of sublingual immunotherapy (SLIT), compared with placebo, for reductions in symptoms and medication requirements. The Cochrane Controlled Clinical Trials Register, MEDLINE (1966-2002), EMBASE (1974-2002) and Scisearch were searched, up to September 2002, using the terms (Rhin* OR hay fever) AND (immunotherap* OR desensiti*ation) AND (sublingual). All studies identified by the searches were assessed by the reviewers to identify Randomized Controlled Trials involving participants with symptoms of allergic rhinitis and proven allergen sensitivity, treated with SLIT or corresponding placebo. Data from identified studies was abstracted onto a standard extraction sheet and subsequently entered into RevMan 4.1. Analysis was performed by the method of standardized mean differences (SMD) using a random effects model. P-values < 0.05 were considered statistically significant. Subgroup analyses were performed according to the type of allergen administered, the age of participants and the duration of treatment. Twenty-two trials involving 979 patients, were included. There were six trials of SLIT for house dust mite allergy, five for grass pollen, five for parietaria, two for olive and one each for, ragweed, cat, tree and cupressus. Five studies enrolled exclusively children. Seventeen studies administered the allergen by sublingual drops subsequently swallowed, three by drops subsequently spat out and two by sublingual tablets. Eight studies involved treatment for less than 6 months, 10 studies for 6-12 months and four studies for greater than 12 months. All included studies were double-blind placebo-controlled trials of parallell group design. Concealment of treatment allocation was considered adequate in all studies and the use of identical placebo preparations was almost universal. There was significant heterogeneity, most likely due to widely differing scoring systems between studies, for most comparisons. Overall there was a significant reduction in both symptoms (SMD -0.42, 95% confidence interval -0.69 to -0.15; P = 0.002) and medication requirements [SMD -0.43 (-0.63, -0.23); P = 0.00003] following immunotherapy. Subgroup analyses failed to identify a disproportionate benefit of treatment according to the allergen administered. There was no significant reduction in symptoms and medication scores in those studies involving only children but total numbers of participants was too small to make this a reliable conclusion. Increasing duration of treatment does not clearly increase efficacy. The total dose of allergen administered may be important but insufficient data was available to analyse this factor.	Natl Heart & Lung Inst, Imperial Coll London Sch Med, London SW3 6LY, England; Univ Hosp Birmingham NHS Trust, Birmingham, W Midlands, England	Durham, SR (reprint author), Natl Heart & Lung Inst, Imperial Coll London Sch Med, Guy Scadding Bldg,Royal Brompton Campus,Dovehouse, London SW3 6LY, England.						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J	Finotto, S; Neurath, MF; Glickman, JN; Qin, SX; Lehr, HA; Green, FHY; Ackerman, K; Haley, K; Gatte, PR; Szabo, SJ; Drazen, JM; De Sanctis, GT; Glimcher, LH				Finotto, S; Neurath, MF; Glickman, JN; Qin, SX; Lehr, HA; Green, FHY; Ackerman, K; Haley, K; Gatte, PR; Szabo, SJ; Drazen, JM; De Sanctis, GT; Glimcher, LH			Development of spontaneous airway changes consistent with human asthma in mice lacking T-bet	SCIENCE			English	Article							HYPERRESPONSIVENESS; INFLAMMATION; CELLS; TH2	Human asthma is associated with airway infiltration by T helper 2 (T(H)2) lymphocytes. We observed reduced expression of the T(H)1 transcription factor, T-bet, in T cells from airways of patients with asthma compared with that in T cells from airways of nonasthmatic patients, suggesting that loss of T-bet might be associated with asthma. Mice with a targeted deletion of the T-bet gene and severe combined immunodeficient mice receiving CD4(+) cells from T-bet knockout mice spontaneously demonstrated multiple physiological and inflammatory features characteristic of asthma, Thus, T-bet deficiency, in the absence of allergen exposure, induces a murine phenotype reminiscent of both acute and chronic human asthma.	Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA; Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Pulm & Crit Care, Boston, MA 02115 USA; Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Gastroenterol, Boston, MA 02115 USA; Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA; Millenium Pharmaceut, Cambridge, MA 02138 USA; Univ Mainz, Dept Pathol, D-55131 Mainz, Germany; Univ Calgary, Dept Pathol & Lab Med, Calgary, AB T2N 4N1, Canada; Univ Mainz, Med Clin 1, D-55131 Mainz, Germany	Glimcher, LH (reprint author), Harvard Univ, Sch Publ Hlth, 665 Huntington Ave, Boston, MA 02115 USA.		Ain, Kenneth/A-5179-2012	Ain, Kenneth/0000-0002-2668-934X	NHLBI NIH HHS [HL-36110]		Abbas AK, 1996, NATURE, V383, P787, DOI 10.1038/383787a0; Cohn L, 1998, J IMMUNOL, V161, P3813; De Sanctis GT, 1999, J EXP MED, V189, P1621, DOI 10.1084/jem.189.10.1621; Drazen JM, 1999, ANNU REV PHYSIOL, V61, P593, DOI 10.1146/annurev.physiol.61.1.593; Elias JA, 1999, J CLIN INVEST, V104, P1001, DOI 10.1172/JCI8124; Finotto S, 1999, DEVELOPMENT, V126, P2935; FINOTTO S, UNPUB; GAVETT SH, 1995, J EXP MED, V182, P1527, DOI 10.1084/jem.182.5.1527; Grogan JL, 2001, IMMUNITY, V14, P205, DOI 10.1016/S1074-7613(01)00103-0; Hansen G, 1999, J CLIN INVEST, V103, P175, DOI 10.1172/JCI5155; LI XM, 1996, J IMMUNOL, V157, P2316; Mullen AC, 2001, SCIENCE, V292, P1907, DOI 10.1126/science.1059835; Papaioannou VE, 1997, TRENDS GENET, V13, P212, DOI 10.1016/S0168-9525(97)01144-X; Robinson DS, 2000, BRIT MED BULL, V56, P956, DOI 10.1258/0007142001903625; Szabo SJ, 2000, CELL, V100, P655, DOI 10.1016/S0092-8674(00)80702-3; Szabo SJ, 2002, SCIENCE, V295, P338, DOI 10.1126/science.1065543	16	418	481	2	16	AMER ASSOC ADVANCEMENT SCIENCE	WASHINGTON	1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA	0036-8075			SCIENCE	Science	JAN 11	2002	295	5553					336	338		10.1126/science.1065544		3	Multidisciplinary Sciences	Science & Technology - Other Topics	511RD	WOS:000173278600052	11786643	
J	Larche, M; Akdis, CA; Valenta, R				Larche, Mark; Akdis, Cezmi A.; Valenta, Rudolf			Immunological mechanisms of allergen-specific immunotherapy	NATURE REVIEWS IMMUNOLOGY			English	Review							GRASS-POLLEN IMMUNOTHERAPY; RANDOMIZED CONTROLLED-TRIAL; T-CELL EPITOPES; IGG MONOCLONAL-ANTIBODIES; MONOPHOSPHORYL-LIPID-A; MAJOR PEANUT ALLERGEN; HOUSE-DUST MITE; BET V 1; SUBLINGUAL IMMUNOTHERAPY; BIRCH-POLLEN	Allergen-specific immunotherapy has been carried out for almost a century and remains one of the few antigen-specific treatments for inflammatory diseases. The mechanisms by which allergen-specific immunotherapy exerts its effects include the modulation of both T-cell and B-cell responses to allergen. There is a strong rationale for improving the efficacy of allergen-specific immunotherapy by reducing the incidence and severity of adverse reactions mediated by IgE. Approaches to address this problem include the use of modified allergens, novel adjuvants and alternative routes of administration. This article reviews the development of allergen-specific immunotherapy, our current understanding of its mechanisms of action and its future prospects.	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J	DiFranza, JR; Aligne, CA; Weitzman, M				DiFranza, JR; Aligne, CA; Weitzman, M			Prenatal and postnatal environmental tobacco smoke exposure and children's health	PEDIATRICS			English	Review						environmental tobacco smoke; children; prenatal; otitis media; asthma; SIDS	LOW-BIRTH-WEIGHT; MATERNAL CIGARETTE-SMOKING; INFANT-DEATH-SYNDROME; ADOLESCENT NICOTINE EXPOSURE; RAT-BRAIN REGIONS; RESPIRATORY-TRACT ILLNESS; MIDDLE-EAR DISEASE; AGE 7 YEARS; PARENTAL SMOKING; PASSIVE SMOKING	Children's exposure to tobacco constituents during fetal development and via environmental tobacco smoke (ETS) exposure is perhaps the most ubiquitous and hazardous of children's environmental exposures. A large literature links both prenatal maternal smoking and children's ETS exposure to decreased lung growth and increased rates of respiratory tract infections, otitis media, and childhood asthma, with the severity of these problems increasing with increased exposure. Sudden infant death syndrome, behavioral problems, neurocognitive decrements, and increased rates of adolescent smoking also are associated with such exposures. Studies of each of these problems suggest independent effects of both pre- and postnatal exposure for each, with the respiratory risk associated with parental smoking seeming to be greatest during fetal development and the first several years of life.	Univ Massachusetts, Sch Med, Dept Family Med & Community Hlth, Worcester, MA 01655 USA; Univ Rochester, Sch Med & Dent, Dept Pediat, Rochester, NY 14642 USA; Amer Acad Pediat, Ctr Child Hlth Res, Rochester, NY USA	DiFranza, JR (reprint author), Univ Massachusetts, Sch Med, Dept Family Med & Community Hlth, 55 Lake Ave, Worcester, MA 01655 USA.	difranzj@ummhc.org					Adair-Bischoff CE, 1998, ARCH PEDIAT ADOL MED, V152, P127; Agabiti N, 1999, EPIDEMIOLOGY, V10, P692, DOI 10.1097/00001648-199911000-00008; Al-Delaimy WK, 2002, TOB CONTROL, V11, P176, DOI 10.1136/tc.11.3.176; Aligne CA, 1997, ARCH PEDIAT ADOL MED, V151, P648; Alm B, 1998, ARCH DIS CHILD, V78, P329; Anderson HR, 1997, THORAX, V52, P1003; ANDERSON LJ, 1988, PEDIATRICS, V82, P300; Baghurst P A, 1992, Paediatr Perinat Epidemiol, V6, P403, DOI 10.1111/j.1365-3016.1992.tb00784.x; BARROS FC, 1992, PEDIATRICS, V90, P238; BENOWITZ NL, 1998, NICOTINE SAFETY TOXI, P7; BLAND M, 1973, BR J PREV SOC MED, V27, P150; BREESEHALL C, 1984, J PEDIATR, V105, P358; Breslau N, 2000, BIOL PSYCHIAT, V47, P1005, DOI 10.1016/S0006-3223(99)00312-1; Breslau N, 2000, BIOL PSYCHIAT, V47, P71, DOI 10.1016/S0006-3223(99)00131-6; Brook JS, 2000, ARCH PEDIAT ADOL MED, V154, P381; Bush PG, 2000, PLACENTA, V21, P824, DOI 10.1053/plac.2000.0571; BUTLER NR, 1973, BRIT MED J, V4, P573; BYRD RS, 1994, PEDIATRICS, V93, P481; CAMERON P, 1967, J ALLERGY, V40, P12, DOI 10.1016/0021-8707(67)90054-8; CHARLTON A, 1984, BRIT MED J, V288, P1647; CHEN Y, 1986, BRIT MED J, V293, P303; CHEN Y, 1988, INT J EPIDEMIOL, V17, P348, DOI 10.1093/ije/17.2.348; COGHLIN J, 1989, AM J EPIDEMIOL, V130, P696; COLLEY JRT, 1974, LANCET, V2, P1031; Cook DG, 1997, THORAX, V52, P1081; Cook DG, 1998, THORAX, V53, P295; Cook DG, 1998, THORAX, V53, P884; Corbo GM, 1996, AM J RESP CRIT CARE, V154, P695; CORBO GM, 1989, BRIT MED J, V299, P1491; COURT C, 1995, BRIT MED J, V310, P7; DENSON R, 1975, CAN PSYCHIAT ASSOC J, V20, P183; DeSalvia MA, 1995, PSYCHOPHARMACOLOGY, V122, P66; DiFranza JR, 1996, PEDIATRICS, V97, P560; DIGIOVANNI V, 1993, BRAIN RES, V616, P126; DODGE R, 1982, ARCH ENVIRON HEALTH, V37, P151; Dube M. 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J	Evans, GW; Kantrowitz, E				Evans, GW; Kantrowitz, E			Socioeconomic status and health: The potential role of environmental risk exposure	ANNUAL REVIEW OF PUBLIC HEALTH			English	Review						environmental justice; income; socioeconomic status; poverty; environmental risk	HOME ENVIRONMENTS; YOUNG-CHILDREN; COCKROACH ALLERGEN; CLASS-INEQUALITY; CARBON-MONOXIDE; MENTAL-HEALTH; UNITED-STATES; AIR-POLLUTION; SOCIAL-CLASS; QUALITY	Among several viable explanations for the ubiquitous SES-health gradient is differential exposure to environmental risk. We document evidence of inverse relations between income and other indices of SES with environmental risk factors including hazardous wastes and other toxins, ambient and indoor air pollutants, water quality, ambient noise, residential crowding, housing quality, educational facilities, work environments, and neighborhood conditions. We then briefly over-view evidence that such exposures are inimical to health and well-being. 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J	Gauderman, WJ				Gauderman, WJ			Sample size requirements for association studies of gene-gene interaction	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						association; case-control studies; genetics; interaction; research design; sample size	CASE-PARENT TRIADS; CASE-CONTROL DESIGNS; ENVIRONMENT INTERACTION; LINKAGE DISEQUILIBRIUM; POWER; TESTS; EXPOSURE; MODELS	In the study of complex diseases, it may be important to test hypotheses related to gene-gene (G x G) interaction. The success of such studies depends critically on obtaining adequate sample sizes. In this paper, the author investigates sample size requirements for studies of G x G interaction, focusing on four study designs: the matched-case-control design, the case-sibling design, the case-parent design, and the case-only design. All four designs provide an estimate of interaction on a multiplicative scale, which is used as a unifying theme in the comparison of sample size requirements. Across a variety of genetic models, the case-only and case-parent designs require fewer sampling units (cases and case-parent trios, respectively) than the case-control (pairs) or case-sibling (pairs) design. For example, the author describes an asthma study of two common recessive genes for which 270 matched case-control pairs would be required to detect a G x G interaction of moderate magnitude with 80% power. By comparison, the same study would require 319 case-sibling pairs but only 146 trios in the case-parent design or 116 cases in the case-only design. A software program that computes sample size for studies of G x G interaction and for studies of gene-environment (G x E) interaction is freely available (http://hydra.usc.edu/gxe).	Univ So Calif, Sch Med, Dept Prevent Med, Los Angeles, CA 90089 USA	Gauderman, WJ (reprint author), Univ So Calif, Sch Med, Dept Prevent Med, 1540 Alcazar St,Suite 220, Los Angeles, CA 90089 USA.				NCI NIH HHS [CA 52862]; NIEHS NIH HHS [5P30 ES 07048-03, ES 10421]		Andrieu N., 2000, Genetic Epidemiology, V19, P235; Andrieu N, 2001, AM J EPIDEMIOL, V153, P265, DOI 10.1093/aje/153.3.265; Breslow N. E., 1980, IARC SCI PUBLICATION, V32; BROOKMEYER R, 1986, AM J EPIDEMIOL, V124, P693; Cotton SC, 2000, AM J EPIDEMIOL, V151, P7; Curtis D, 1997, ANN HUM GENET, V61, P319, DOI 10.1046/j.1469-1809.1998.6210089.x; Foppa I, 1997, AM J EPIDEMIOL, V146, P596; Gail MH, 1999, GENET EPIDEMIOL, V16, P15, DOI 10.1002/(SICI)1098-2272(1999)16:1<15::AID-GEPI3>3.0.CO;2-8; Garcia-Closas M, 1999, AM J EPIDEMIOL, V149, P689; Gauderman W, 2001, 157 U SO CAL DEP PRE; Gauderman W J, 1999, J Natl Cancer Inst Monogr, P31; Gauderman WJ, 2002, STAT MED, V21, P35, DOI 10.1002/sim.973; Gilliland FD, 1999, ENVIRON HEALTH PERSP, V107, P403; Goldstein AM, 1997, GENET EPIDEMIOL, V14, P1085, DOI 10.1002/(SICI)1098-2272(1997)14:6<1085::AID-GEPI87>3.0.CO;2-D; GREENLAND S, 1985, STAT MED, V4, P117, DOI 10.1002/sim.4780040203; HWANG SJ, 1994, AM J EPIDEMIOL, V140, P1029; Khoury MJ, 1996, AM J EPIDEMIOL, V144, P207; Khoury MJ, 1998, AM J EPIDEMIOL, V147, P1; Longmate JA, 2001, AM J HUM GENET, V68, P1229, DOI 10.1086/320106; Martin ER, 1997, AM J HUM GENET, V61, P439, DOI 10.1086/514860; Martin ER, 2000, GENET EPIDEMIOL, V18, P48, DOI 10.1002/(SICI)1098-2272(200001)18:1<48::AID-GEPI4>3.0.CO;2-S; Martin ER, 2000, AM J HUM GENET, V67, P146, DOI 10.1086/302957; OTTMAN R, 1990, GENET EPIDEMIOL, V7, P177, DOI 10.1002/gepi.1370070302; Ottman R, 1996, PREV MED, V25, P764, DOI 10.1006/pmed.1996.0117; PIEGORSCH WW, 1994, STAT MED, V13, P153, DOI 10.1002/sim.4780130206; ROTHMAN KJ, 1980, AM J EPIDEMIOL, V112, P467; Rothman KJ, 1998, MODERN EPIDEMIOLOGY; Schaid DJ, 1999, GENET EPIDEMIOL, V16, P261, DOI 10.1002/(SICI)1098-2272(1999)16:3<261::AID-GEPI3>3.0.CO;2-M; Schaid DJ, 1996, GENET EPIDEMIOL, V13, P423, DOI 10.1002/(SICI)1098-2272(1996)13:5<423::AID-GEPI1>3.0.CO;2-3; SELF SG, 1991, BIOMETRICS, V47, P53, DOI 10.2307/2532495; Siegmund KD, 2000, AM J HUM GENET, V67, P244, DOI 10.1086/302973; SIEMIATYCKI J, 1981, INT J EPIDEMIOL, V10, P383, DOI 10.1093/ije/10.4.383; SPIELMAN RS, 1993, AM J HUM GENET, V52, P506; Spielman RS, 1998, AM J HUM GENET, V62, P450, DOI 10.1086/301714; Umbach DH, 2000, AM J HUM GENET, V66, P251, DOI 10.1086/302707; Weinberg C, 2000, AM J EPIDEMIOL, V152, P689, DOI 10.1093/aje/152.7.689; Weinberg CR, 1998, AM J HUM GENET, V62, P969, DOI 10.1086/301802; Weinberg CR, 1999, AM J HUM GENET, V65, P229, DOI 10.1086/302466; Weinberg CR, 1999, AM J HUM GENET, V64, P1186, DOI 10.1086/302337; Wilcox AJ, 1998, AM J EPIDEMIOL, V148, P893; Witte JS, 1999, AM J EPIDEMIOL, V149, P693; Yang QH, 1999, EPIDEMIOLOGY, V10, P167, DOI 10.1097/00001648-199903000-00014	42	409	417	1	10	OXFORD UNIV PRESS INC	CARY	JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA	0002-9262			AM J EPIDEMIOL	Am. J. Epidemiol.	MAR 1	2002	155	5					478	484		10.1093/aje/155.5.478		7	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	526WX	WOS:000174153800014	11867360	
J	Hawrylowicz, CM; O'Garra, A				Hawrylowicz, CM; O'Garra, A			Potential role of interleukin-10-secreting regulatory T cells in allergy and asthma	NATURE REVIEWS IMMUNOLOGY			English	Review							GRASS-POLLEN IMMUNOTHERAPY; INDUCED AIRWAY HYPERREACTIVITY; IMMUNOLOGICAL SELF-TOLERANCE; COLONY-STIMULATING FACTOR; TRANSCRIPTION FACTOR FOXP3; GROWTH-FACTOR-BETA; HOUSE-DUST MITE; FC-EPSILON-RI; CYTOKINE PRODUCTION; IN-VIVO	Allergic diseases are caused by aberrant T-helper-2 immune responses in susceptible individuals. Both naturally occurring CD4(+)CD25(+) regulatory T cells and inducible populations of antigen-specific interleukin-10-secreting regulatory T cells inhibit these inappropriate immune responses in experimental models. This article discusses the evidence that regulatory T-cell function might be impaired in allergic and asthmatic disease and that certain therapeutic regimens might function, at least in part, to promote regulatory T-cell generation. Current research strategies seek to exploit these observations to improve the generation of allergen-specific regulatory T-cell populations with the potential to provide the safe and long-term alleviation of disease symptoms.	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Walker MR, 2003, J CLIN INVEST, V112, P1437, DOI 10.1172/JCI200319441; Wan S, 1997, ANN THORAC SURG, V63, P269; Weiner HL, 2001, IMMUNOL REV, V182, P207, DOI 10.1034/j.1600-065X.2001.1820117.x; Wildin RS, 2001, NAT GENET, V27, P18, DOI 10.1038/83707; Wills-Karp M, 2001, NAT REV IMMUNOL, V1, P69, DOI 10.1038/35095579; Wilson DR, 2003, COCHRANE DB SYST REV, V2; Xu DM, 2003, J IMMUNOL, V170, P394; Yagi H, 2004, INT IMMUNOL, V16, P1643, DOI 10.1093/intimm/dxh165; Zuany-Amorim C, 2002, NAT MED, V8, P625, DOI 10.1038/nm0602-625	188	408	455	0	22	NATURE PUBLISHING GROUP	LONDON	MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND	1474-1733			NAT REV IMMUNOL	Nat. Rev. Immunol.	APR	2005	5	4					271	283		10.1038/nri1589		13	Immunology	Immunology	912PX	WOS:000228092800011	15775993	
J	Von Ehrenstein, OS; Von Mutius, E; Illi, S; Baumann, L; Bohm, O; Von Kries, R				Von Ehrenstein, OS; Von Mutius, E; Illi, S; Baumann, L; Bohm, O; Von Kries, R			Reduced risk of hay fever and asthma among children of farmers	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article							ALLERGIC RHINOCONJUNCTIVITIS; CHILDHOOD ISAAC; SCHOOL-CHILDREN; PREVALENCE; SYMPTOMS; ATOPY; TH1; SENSITIZATION; DISEASES; RHINITIS	Background The prevalence of atopic diseases is on the rise. Traditional lifestyles may be associated with a reduced risk of atopy. Objective To test the hypothesis that children living on a farm have lower prevalences of atopic diseases. To identify differences in living conditions between farmers and other families which are associated with the development of atopic conditions. Design Cross-sectional survey among children entering school (aged 5-7 years). A written questionnaire including the ISAAC core questions and asking for exposures on a farm and elsewhere was administered to the parents. Setting: School health entry examination in two Bavarian districts with extensive farming activity. Subjects: 10 163 children. Main outcome measures The prevalence of doctor's diagnoses and symptoms of hay fever, asthma and eczema as assessed by parental report. Results Farmers' children had lower prevalences of hay fever (adjusted odds ratio = 0.52, 95% CI 0.28-0.99), asthma (0.65, 0.39-1.09), and wheeze (0.55, 0.36-0.86) than their peers not living in an agricultural environment. The reduction in risk was stronger for children whose families were running the farm on a full-time basis as compared with families with part-time farming activity. Among farmers' children increasing exposure to livestock was related to a decreasing prevalence of atopic diseases (aOR = 0.41, 95% CI 0.23-0.74). Conclusions Factors related to environmental influences on a farm such as increased exposure to bacterial compounds in stables where livestock is kept prevent the development of allergic disorders in children.	Univ Munich, Univ Childrens Hosp, Munich, Germany; Univ Munich, Inst Social Paediat & Adolescent Med, Munich, Germany	Von Ehrenstein, OS (reprint author), Univ Munich, Dr von Haunersche Kinderklin, Lindwurmstr 4, D-80337 Munich, Germany.						ANDREA S, 1988, ARCH DIS CHILD, V63, P474; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; BATSCHELET E, 1960, SCHWEIZ MED WOCHENSC, V40, P1109; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; BJORKSTEN B, 1994, ALLERGY, V49, P400, DOI 10.1111/j.1398-9995.1994.tb00831.x; Black PN, 1997, EUR RESPIR J, V10, P6, DOI 10.1183/09031936.97.10010006; Braback L, 1991, PEDIATR ALLERGY IMMU, V2, P14, DOI 10.1111/j.1399-3038.1991.tb00174.x; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; BraunFahrlander C, 1997, PEDIATR ALLERGY IMMU, V8, P75, DOI 10.1111/j.1399-3038.1997.tb00147.x; EMANUEL MB, 1988, CLIN ALLERGY, V18, P295, DOI 10.1111/j.1365-2222.1988.tb02872.x; Hilkens CMU, 1997, BLOOD, V90, P1920; Kaur B, 1998, BRIT MED J, V316, P118; LAU S, 1989, J ALLERGY CLIN IMMUN, V84, P718, DOI 10.1016/0091-6749(89)90300-X; Lewis S, 1997, NEW ZEAL MED J, V110, P286; MACATONIA SE, 1995, J IMMUNOL, V154, P5071; MARTINEZ FD, 1995, THORAX, V50, P1067, DOI 10.1136/thx.50.10.1067; Matricardi PM, 1998, J ALLERGY CLIN IMMUN, V101, P439, DOI 10.1016/S0091-6749(98)70350-1; Murosaki S, 1998, J ALLERGY CLIN IMMUN, V102, P57, DOI 10.1016/S0091-6749(98)70055-7; Nathan RA, 1997, J ALLERGY CLIN IMMUN, V99, pS808, DOI 10.1016/S0091-6749(97)80040-1; NOVAK D, 1998, ARBEITSMEDIZIN SOZIA, V6, P233; Nystad W, 1997, PEDIATR ALLERGY IMMU, V8, P35, DOI 10.1111/j.1399-3038.1997.tb00140.x; POPP W, 1989, ALLERGY, V44, P572, DOI 10.1111/j.1398-9995.1989.tb04202.x; REHSTEINER R, 1926, SCHWEIZ Z GESUNDHEIT, V1, P1; ROMAGNANI S, 1992, INT ARCH ALLERGY IMM, V98, P279; Strachan DP, 1997, PEDIATR ALLERGY IMMU, V8, P161, DOI 10.1111/j.1399-3038.1997.tb00156.x; von Mutius E, 1998, LANCET, V351, P862, DOI 10.1016/S0140-6736(97)10100-3; VONMUTIUS E, 1992, BRIT MED J, V305, P1395; VONMUTIUS E, 1994, BRIT MED J, V308, P692; VONMUTIUS E, 1996, BRIT MED J, V312, P448; WAEGEMAEKERS M, 1989, ALLERGY, V44, P142; WUTHRICH B, 1986, SCHWEIZ MED WSCHR, V116, P909; Yemaneberhan H, 1997, LANCET, V350, P85, DOI 10.1016/S0140-6736(97)01151-3	32	406	413	0	27	BLACKWELL SCIENCE LTD	OXFORD	P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	FEB	2000	30	2					187	193				7	Allergy; Immunology	Allergy; Immunology	287NF	WOS:000085511600007	10651770	
J	McCreanor, J; Cullinan, P; Nieuwenhuijsen, MJ; Stewart-Evans, J; Malliarou, E; Jarup, L; Harrington, R; Svartengren, M; Han, I; Ohman-Strickland, P; Chung, KF; Zhang, JF				McCreanor, James; Cullinan, Paul; Nieuwenhuijsen, Mark J.; Stewart-Evans, James; Malliarou, Eleni; Jarup, Lars; Harrington, Robert; Svartengren, Magnus; Han, In-Kyu; Ohman-Strickland, Pamela; Chung, Kian Fan; Zhang, Junfeng			Respiratory effects of exposure to diesel traffic in persons with asthma	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							ULTRAFINE PARTICLES; AIRWAY INFLAMMATION; EPITHELIAL-CELLS; LUNG-FUNCTION; EXHAUST; HUMANS; HEALTH; POLLUTION; SYMPTOMS	Background: Air pollution from road traffic is a serious health hazard, and people with preexisting respiratory disease may be at increased risk. We investigated the effects of short-term exposure to diesel traffic in people with asthma in an urban, roadside environment. Methods: We recruited 60 adults with either mild or moderate asthma to participate in a randomized, crossover study. Each participant walked for 2 hours along a London street (Oxford Street) and, on a separate occasion, through a nearby park (Hyde Park). We performed detailed real-time exposure, physiological, and immunologic measurements. Results: Participants had significantly higher exposures to fine particles (<2.5 mu m in aerodynamic diameter), ultrafine particles, elemental carbon, and nitrogen dioxide on Oxford Street than in Hyde Park. Walking for 2 hours on Oxford Street induced asymptomatic but consistent reductions in the forced expiratory volume in 1 second (FEV1) (up to 6.1%) and forced vital capacity (FVC) (up to 5.4%) that were significantly larger than the reductions in FEV1 and FVC after exposure in Hyde Park (P=0.04 and P=0.01, respectively, for the overall effect of exposure, and P<0.005 at some time points). The effects were greater in subjects with moderate asthma than in those with mild asthma. These changes were accompanied by increases in biomarkers of neutrophilic inflammation (sputum myeloperoxidase, 4.24 ng per milliliter after exposure in Hyde Park vs. 24.5 ng per milliliter after exposure on Oxford Street; P=0.05) and airway acidification (maximum decrease in pH, 0.04% after exposure in Hyde Park and 1.9% after exposure on Oxford Street; P=0.003). The changes were associated most consistently with exposures to ultrafine particles and elemental carbon. Conclusions: Our observations serve as a demonstration and explanation of the epidemiologic evidence that associates the degree of traffic exposure with lung function in asthma.	Univ London Imperial Coll Sci & Technol, Dept Occupat & Environm Med, Natl Heart & Lung Inst, London SW3 6LR, England; Royal Brompton Hosp, London, England; Univ London Imperial Coll Sci & Technol, Dept Epidemiol & Publ Hlth, London SW3 6LR, England; Univ Med & Dent New Jersey, Sch Publ Hlth, Piscataway, NJ USA; Karolinska Inst, Dept Publ Hlth Sci, Stockholm, Sweden	Cullinan, P (reprint author), Univ London Imperial Coll Sci & Technol, Dept Occupat & Environm Med, Natl Heart & Lung Inst, 1b Manresa Rd, London SW3 6LR, England.	p.cullinan@imperial.ac.uk	Nieuwenhuijsen, Mark/C-3914-2017	Nieuwenhuijsen, Mark/0000-0001-9461-7981			Abe S, 2000, AM J RESP CELL MOL, V22, P296; Air Quality Expert Group, 2005, PART MATT UK; Fischer H, 2002, AM J PHYSIOL-CELL PH, V282, pC736, DOI 10.1152/ajpcell.00369.2001; Goldsmith Carroll-Ann W., 1999, Reviews on Environmental Health, V14, P121; Gong Jr H, 2003, RES REP HLTH EFF I, V118; HISHAM MWM, 1990, ATMOS ENVIRON A-GEN, V24, P2523, DOI 10.1016/0960-1686(90)90344-M; Hunt JF, 2000, AM J RESP CRIT CARE, V161, P694; Ising H, 2003, Noise Health, V5, P41; Janssen NAH, 2003, ENVIRON HEALTH PERSP, V111, P1512, DOI 10.1289/ehp.6243; KAUFMAN DS, 1993, ARCH BIOCHEM BIOPHYS, V302, P245, DOI 10.1006/abbi.1993.1206; Kulkarni N, 2006, NEW ENGL J MED, V355, P21, DOI 10.1056/NEJMoa052972; Li N, 2003, CLIN IMMUNOL, V109, P250, DOI 10.1016/j.clim.2003.08.006; Manchester-Neesvig JB, 2003, J AIR WASTE MANAGE, V53, P1065; Nel A, 2005, SCIENCE, V309, P1326; Nightingale JA, 2000, AM J RESP CRIT CARE, V162, P161; Nordenhall C, 2001, EUR RESPIR J, V17, P909, DOI 10.1183/09031936.01.17509090; Nordenhall C, 2000, EUR RESPIR J, V15, P1046, DOI 10.1034/j.1399-3003.2000.01512.x; Oberdorster G, 2005, ENVIRON HEALTH PERSP, V113, P823, DOI 10.1289/ehp.7339; Penttinen P, 2001, EUR RESPIR J, V17, P428, DOI 10.1183/09031936.01.17304280; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Polosa R, 2002, ARCH ENVIRON HEALTH, V57, P188; 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; Salvi SS, 2000, AM J RESP CRIT CARE, V161, P550; *SAS I, 2006, SAS MIX MOD; Stenfors N, 2004, EUR RESPIR J, V23, P82, DOI 10.1183/09031936.03.00004603; Svartengren M, 2000, EUR RESPIR J, V15, P716, DOI 10.1034/j.1399-3003.2000.15d15.x	28	405	418	17	105	MASSACHUSETTS MEDICAL SOC	WALTHAM	WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA	0028-4793			NEW ENGL J MED	N. Engl. J. Med.	DEC 6	2007	357	23					2348	2358		10.1056/NEJMoa071535		11	Medicine, General & Internal	General & Internal Medicine	237QA	WOS:000251389200005	18057337	
J	Wormuth, M; Scheringer, M; Vollenweider, M; Hungerbuhler, K				Wormuth, M; Scheringer, M; Vollenweider, M; Hungerbuhler, K			What are the sources of exposure to eight frequently used phthalic acid esters in Europeans?	RISK ANALYSIS			English	Review						consumer exposure; consumer products; exposure modeling; exposure pathways; phthalates; plasticizers	EXPERT PANEL REPORT; N-BUTYL PHTHALATE; MALE REPRODUCTIVE DEVELOPMENT; NURSERY-SCHOOL CHILDREN; DEUTERIUM-LABELED DEHP; DI-ISONONYL PHTHALATE; IN-HOUSE DUST; DEVELOPMENTAL TOXICITY; NTP CENTER; DI(2-ETHYLHEXYL)PHTHALATE DEHP	Phthalic acid esters (phthalates) are used as plasticizers in numerous consumer products, commodities, and building materials. Consequently, phthalates are found in human residential and occupational environments in high concentrations, both in air and in dust. Phthalates are also ubiquitous food and environmental contaminants. An increasing number of studies sampling human urine reveal the ubiquitous phthalate exposure of consumers in industrialized countries. At the same time, recent toxicological studies have demonstrated the potential of the most important phthalates to disturb the human hormonal system and human sexual development and reproduction. Additionally, phthalates are suspected to trigger asthma and dermal diseases in children. To find the important sources of phthalates in Europeans, a scenario-based approach is applied here. Scenarios representing realistic exposure situations are generated to calculate the age-specific range in daily consumer exposure to eight phthalates. The scenarios demonstrate that exposure of infant and adult consumers is caused by different sources in many cases. Infant consumers experience significantly higher daily exposure to phthalates in relation to their body weight than older consumers. The use of consumer products and different indoor sources dominate the exposure to dimethyl, diethyl, benzylbutyl, diisononyl, and diisodecyl phthalates, whereas food has a major influence on the exposure to diisobutyl, dibutyl, and di-2-ethylhexyl phthalates. The scenario-based approach chosen in the present study provides a link between the knowledge on emission sources of phthalates and the concentrations of phthalate metabolites found in human urine.	ETH Honggerberg, Swiss Fed Inst Technol Zurich, Inst Chem & Bioengn, CH-8093 Zurich, Switzerland	Scheringer, M (reprint author), ETH Honggerberg, Swiss Fed Inst Technol Zurich, Inst Chem & Bioengn, HCI G127, CH-8093 Zurich, Switzerland.	martin.scheringer@chem.ethz.ch					ADAMS WC, 1993, FINAL REPORT; Afshari A, 2004, INDOOR AIR, V14, P120, DOI 10.1046/j.1600-0668.2003.00220.x; Akingbemi BT, 2004, P NATL ACAD SCI USA, V101, P775, DOI 10.1073/pnas.0305977101; Alexy U, 2003, EUR J CLIN NUTR, V57, P1331, DOI 10.1038/sj.ejcn.1601696; Alexy U, 2002, BRIT J NUTR, V87, P595, DOI [10.1079/BJNBJN/2002572, 10.1079/BJN2002572]; Andersen LF, 2003, EUR J CLIN NUTR, V57, P881, DOI 10.1038/sj.ejcn.1601621; Anderson WAC, 2001, FOOD ADDIT CONTAM, V18, P1068, DOI 10.1080/02652030110050113; Barr DB, 2003, ENVIRON HEALTH PERSP, V111, P1148, DOI 10.1289/ehp.6074; Becker K, 2004, INT J HYG ENVIR HEAL, V207, P409, DOI 10.1078/1438-4639-00309; Blount BC, 2000, ENVIRON HEALTH PERSP, V108, P979, DOI 10.1289/ehp.00108979; 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JUN	2006	26	3					803	824		10.1111/j.1539-6924.2006.00770.x		22	Public, Environmental & Occupational Health; Mathematics, Interdisciplinary Applications; Social Sciences, Mathematical Methods	Public, Environmental & Occupational Health; Mathematics; Mathematical Methods In Social Sciences	055IG	WOS:000238442900022	16834635	
J	Zheng, T; Zhu, Z; Wang, ZD; Homer, RJ; Ma, B; Riese, RJ; Chapman, HA; Shapiro, SD; Elias, JA				Zheng, T; Zhu, Z; Wang, ZD; Homer, RJ; Ma, B; Riese, RJ; Chapman, HA; Shapiro, SD; Elias, JA			Inducible targeting of IL-13 to the adult lung causes matrix metalloproteinase-and cathepsin-dependent emphysema	JOURNAL OF CLINICAL INVESTIGATION			English	Article							OBSTRUCTIVE PULMONARY-DISEASE; BRONCHOALVEOLAR LAVAGE FLUID; CHRONIC-BRONCHITIS; CYSTEINE PROTEINASES; AIRWAY HYPERRESPONSIVENESS; ALVEOLAR MACROPHAGES; T-LYMPHOCYTES; RESPONSIVENESS; SMOKERS; CELLS	Cigarette smoke exposure is the major cause of chronic obstructive pulmonary disease (COPD). However, only a minority of smokers develop significant COPD, and patients with asthma or asthma-like airway hyperresponsiveness or eosinophilia experience accelerated loss of lung function after cigarette smoke exposure. Pulmonary inflammation is a characteristic feature of lungs from patients with COPD. Surprisingly, the mediators of this inflammation and their contributions to the pathogenesis and varied natural history of COPD are not well defined. Here we show that IL-13, a critical cytokine in asthma, causes emphysema with enhanced lung volumes and compliance, mucus metaplasia, and inflammation, when inducibly overexpressed in the adult murine lung. MMP-2, -9, -12, -13, and -14 and cathepsins B, S, L, H, and K were induced by IL-13 in this setting. Zn addition, treatment with MMP or cysteine proteinase antagonists significantly decreased the emphysema and inflammation, but not the mucus in these animals. These studies demonstrate that IL-13 is a potent stimulator of MMP and cathepsin-based proteolytic pathways in the lung. They also demonstrate that IL-13 causes emphysema via a MMP- and cathepsin-dependent mechanism(s) and highlight common mechanisms that may underlie COPD and asthma.	Yale Univ, Sch Med, Dept Internal Med, Pulm & Crit Care Med Sect, New Haven, CT 06520 USA; Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06520 USA; Vet Adm Connecticut Hlth Care Syst, Pathol & Lab Med Serv, W Haven, CT USA; Harvard Univ, Boston, MA 02115 USA; Univ Calif San Francisco, Sch Med, Inst Cardiovasc Res, San Francisco, CA USA; Washington Univ, Sch Med, Dept Med, St Louis, MO USA; Washington Univ, Sch Med, Dept Cell Biol, St Louis, MO USA; Washington Univ, Sch Med, Dept Pediat, Div Allergy & Pulm Med, St Louis, MO USA	Elias, JA (reprint author), Yale Univ, Sch Med, Dept Internal Med, Pulm & Crit Care Med Sect, 333 Cedar St,105 LCI, New Haven, CT 06520 USA.				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Clin. Invest.	NOV	2000	106	9					1081	1093		10.1172/JCI10458		13	Medicine, Research & Experimental	Research & Experimental Medicine	371PE	WOS:000165186700004	11067861	
J	McConnell, R; Berhane, K; Gilliland, F; London, SJ; Islam, T; Gauderman, WJ; Avol, E; Margolis, HG; Peters, JM				McConnell, R; Berhane, K; Gilliland, F; London, SJ; Islam, T; Gauderman, WJ; Avol, E; Margolis, HG; Peters, JM			Asthma in exercising children exposed to ozone: a cohort study	LANCET			English	Article							SOUTHERN CALIFORNIA CHILDREN; AIR-POLLUTION; BRONCHIAL RESPONSIVENESS; CHILDHOOD ASTHMA; SCHOOL CHILDREN; PREVALENCE; POLLUTANTS; ASSOCIATION; SYMPTOMS; TAIWAN	Background Little is known about the effect of exposure to air pollution during exercise or time spent outdoors on the development of asthma. We investigated the relation between newly-diagnosed asthma and team sports in a cohort of children exposed to different concentrations and mixtures of air pollutants. Methods 3535 children with no history of asthma were recruited from schools in 12 communities in southern California and were followed up for up to 5 years. 265 children reported a new diagnosis of asthma during follow-up. We assessed risk of asthma in children playing team sports at study entry in six communities with high daytime ozone concentrations, six with lower concentrations, and in communities with high or low concentrations of nitrogen dioxide, particulate matter, and inorganic-acid vapour. Findings In communities with high ozone concentrations, the relative risk of developing asthma in children playing three or more sports was 3.3 (95% CI 1.9-5.8), compared with children playing no sports. Sports had no effect in areas of low ozone concentration (0.8, 0.4-1.6). Time spent outside was associated with a higher incidence of asthma in areas of high ozone (1.4, 1.0-2.1), but not in areas of low ozone. Exposure to pollutants other than ozone did not alter the effect of team sports. Interpretation Incidence of new diagnoses of asthma is associated with heavy exercise in communities with high concentrations of ozone, thus, air pollution and outdoor exercise could contribute to the development of asthma in children.	Univ So Calif, Sch Med, Dept Prevent Med, Los Angeles, CA 90089 USA; NIEHS, Res Triangle Pk, NC 27709 USA; Calif Air Resources Board, Sacramento, CA USA	McConnell, R (reprint author), Univ So Calif, Sch Med, Dept Prevent Med, 1540 Alcazar St,CHP 236, Los Angeles, CA 90089 USA.			London, Stephanie/0000-0003-4911-5290	NHLBI NIH HHS [1R01HL61768]; NIEHS NIH HHS [1PO1ES0939581-02, 5P30ES07048-05]		AINSWORTH BARBARA E., 2000, MED SCI SPORTS EXERC, P498, DOI DOI 10.1097/00005768-200009001-00009; Asher MI, 1998, EUR RESPIR J, V12, P315; Avol EL, 1998, ENVIRON SCI TECHNOL, V32, P463, DOI 10.1021/es970351m; Baldi I, 1999, EUR RESPIR J, V14, P132, DOI 10.1034/j.1399-3003.1999.14a22.x; Becklake MR, 1997, LANCET S2, V350, pS10, DOI 10.1016/S0140-6736(97)90030-1; BRUNEKREEF B, 1994, AM J RESP CRIT CARE, V150, P962; BURR ML, 1992, CLIN EXP ALLERGY, V22, P509, DOI 10.1111/j.1365-2222.1992.tb00158.x; Clark NM, 1999, ENVIRON HEALTH PERSP, V107, P421; Corrao W, 1996, CHEST, V109, P298, DOI 10.1378/chest.109.2.298; Ehrlich RI, 1995, INT J EPIDEMIOL, V24, P1138, DOI 10.1093/ije/24.6.1138; Gauderman WJ, 2000, AM J RESP CRIT CARE, V162, P1383; Guo YLL, 1999, ENVIRON HEALTH PERSP, V107, P1001; Heir T., 1995, Scandinavian Journal of Medicine and Science in Sports, V5, P94; Helenius IJ, 1998, J ALLERGY CLIN IMMUN, V101, P646; HORSTMAN DH, 1990, AM REV RESPIR DIS, V142, P1158; Jenkins HS, 1999, AM J RESP CRIT CARE, V160, P33; Kehrl HR, 1999, J ALLERGY CLIN IMMUN, V104, P1198; KOREN HS, 1995, ENVIRON HEALTH PERSP, V103, P235, DOI 10.2307/3432379; MCARDLE WD, 1996, EXERCISE PHYSL ENERG, P228; McConnell R, 1999, ENVIRON HEALTH PERSP, V107, P757, DOI 10.2307/3434662; McDonnell WF, 1999, ENVIRON RES, V80, P110, DOI 10.1006/enrs.1998.3894; Miller FJ, 1995, TOXICOL LETT, V82-3, P277, DOI 10.1016/0378-4274(95)03562-1; OSEBOLD JW, 1988, P SOC EXP BIOL MED, V188, P259; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; Rasmussen F, 2000, EUR RESPIR J, V16, P866, DOI 10.1183/09031936.00.16586600; RUPP NT, 1992, AM J DIS CHILD, V146, P941; Samet JM., 1987, CHEST, V91, P74; Sears MR, 1997, LANCET, V350, P1015, DOI 10.1016/S0140-6736(97)01468-2; SueChu M, 1996, RESP MED, V90, P99, DOI 10.1016/S0954-6111(96)90206-1; TAGER IB, 1998, RES REP HLTH EFF I, V81, P27; Wang TN, 1999, ENVIRON RES, V81, P239, DOI 10.1006/enrs.1999.3985; WICHMANN HE, 1995, ENVIRON HEALTH PERSP, V103, P29, DOI 10.2307/3432446	32	391	401	3	51	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	FEB 2	2002	359	9304					386	391		10.1016/S0140-6736(02)07597-9		6	Medicine, General & Internal	General & Internal Medicine	518UP	WOS:000173686500008	11844508	
J	Salvi, SS; Barnes, PJ				Salvi, Sundeep S.; Barnes, Peter J.			Chronic obstructive pulmonary disease in non-smokers	LANCET			English	Review							INDOOR AIR-POLLUTION; NUTRITION EXAMINATION SURVEY; CHRONIC RESPIRATORY-DISEASE; CHRONIC-BRONCHITIS; LUNG-FUNCTION; BIOMASS SMOKE; OCCUPATIONAL EXPOSURES; SOCIOECONOMIC-STATUS; DEVELOPING-COUNTRIES; VENTILATORY FUNCTION	Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. Tobacco smoking is established as a major risk factor, but emerging evidence suggests that other risk factors are important, especially in developing countries. An estimated 25-45% of patients with COPD have never smoked; the burden of non-smoking COPD is therefore much higher than previously believed. About 3 billion people, half the worldwide population, are exposed to smoke from biomass fuel compared with 1.01 billion people who smoke tobacco, which suggests that exposure to biomass smoke might be the biggest risk factor for COPD globally. We review the evidence for the association of COPD with biomass fuel, occupational exposure to dusts and gases, history of pulmonary tuberculosis, chronic asthma, respiratory-tract infections during childhood, outdoor air pollution, and poor socioeconomic status.	[Salvi, Sundeep S.] Chest Res Fdn, Pune 411014, Maharashtra, India; [Barnes, Peter J.] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London, England	Salvi, SS (reprint author), Chest Res Fdn, Pune 411014, Maharashtra, India.	ssalvi@crfindia.com			AstraZeneca; Boehringer Ingelheim; Chiesi Farmaceutici; GlaxoSmithKline; Novartis; Pfizer; Teva; Union Chimique Belge	PJB has received research funding and been a member of scientific advisory boards for AstraZeneca, Boehringer Ingelheim, Chiesi Farmaceutici, GlaxoSmithKline, Novartis, Pfizer, Teva, and Union Chimique Belge, some of which are marketing and developing treatments for COPD. SSS declares that he has no conflicts of interest.	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J	Brand, PLP; Baraldi, E; Bisgaard, H; Boner, AL; Castro-Rodriguez, JA; Custovic, A; de Blic, J; de Jongste, JC; Eber, E; Everard, ML; Frey, U; Gappa, M; Garcia-Marcos, L; Grigg, J; Lenney, W; Le Souef, P; McKenzie, S; Merkus, PJFM; Midulla, F; Paton, JY; Piacentini, G; Pohunek, P; Rossi, GA; Seddon, P; Silverman, M; Sly, PD; Stick, S; Valiulis, A; van Aalderen, WMC; Wildhaber, JH; Wennergren, G; Wilson, N; Zivkovic, Z; Bush, A				Brand, P. L. P.; Baraldi, E.; Bisgaard, H.; Boner, A. L.; Castro-Rodriguez, J. A.; Custovic, A.; de Blic, J.; de Jongste, J. C.; Eber, E.; Everard, M. L.; Frey, U.; Gappa, M.; Garcia-Marcos, L.; Grigg, J.; Lenney, W.; Le Souef, P.; McKenzie, S.; Merkus, P. J. F. M.; Midulla, F.; Paton, J. Y.; Piacentini, G.; Pohunek, P.; Rossi, G. A.; Seddon, P.; Silverman, M.; Sly, P. D.; Stick, S.; Valiulis, A.; van Aalderen, W. M. C.; Wildhaber, J. H.; Wennergren, G.; Wilson, N.; Zivkovic, Z.; Bush, A.			Definition, assessment and treatment of wheezing disorders in preschool children: an evidence-based approach	EUROPEAN RESPIRATORY JOURNAL			English	Review						asthma; episodic viral wheeze; inhaled corticosteroids; montelukast; multiple-trigger wheeze	EXHALED NITRIC-OXIDE; RESPIRATORY SYNCYTIAL VIRUS; BUDESONIDE INHALATION SUSPENSION; PLACEBO-CONTROLLED TRIAL; LEUKOTRIENE RECEPTOR ANTAGONIST; INHALED FLUTICASONE PROPIONATE; RANDOMIZED CONTROLLED-TRIAL; YOUNG ASTHMATIC-CHILDREN; EPISODIC VIRAL WHEEZE; PROSPECTIVE FOLLOW-UP	There is poor agreement on definitions of different phenotypes of preschool wheezing disorders. The present Task Force proposes to use the terms episodic (viral) wheeze to describe children who wheeze intermittently and are well between episodes, and multi pie-trigger wheeze for children who wheeze both during and outside discrete episodes. Investigations are only needed when in doubt about the diagnosis. Based on the limited evidence available, inhaled short-acting beta(2)-agonists by metered-dose inhaler/spacer combination are recommended for symptomatic relief. Educating parents regarding causative factors and treatment is useful. Exposure to tobacco smoke should be avoided; allergen avoidance may be considered when sensitisation has been established. Maintenance treatment with inhaled corticosteroids is recommended for multiple-trigger wheeze; benefits are often small. Montelukast is recommended for the treatment of episodic (viral) wheeze and can be started when symptoms of a viral cold develop. Given the large overlap in phenotypes, and the fact that patients can move from one phenotype to another, inhaled corticosteroids and montelukast may be considered on a trial basis in almost any preschool child with recurrent wheeze, but should be discontinued if there is no clear clinical benefit. Large well-designed randomised controlled trials with clear descriptions of patients are needed to improve the present recommendations on the treatment of these common syndromes.	[Brand, P. L. P.] Isala Klin, Princess Amalia Childrens Clin, NL-8000 K Zwolle, Netherlands; [de Jongste, J. C.] Sophia Childrens Univ Hosp, Erasmus Med Ctr, Dept Paediat Resp Med, Rotterdam, Netherlands; [Merkus, P. J. F. M.] Childrens Hosp, Radboud Med Ctr Nijmegen, Div Resp Med, Dept Paediat, Nijmegen, Netherlands; [van Aalderen, W. M. C.] Univ Amsterdam, Acad Med Ctr, Emma Childrens Hosp, Dept Paediat Pulm, NL-1105 AZ Amsterdam, Netherlands; [Baraldi, E.] Univ Padua, Sch Med, Neonatal Intens Care Unit,Unit Resp Med & Allergy, Dept Paediat, Padua, Italy; [Boner, A. L.; Piacentini, G.] GB Rossi Polyclin, Dept Paediat, Verona, Italy; [Midulla, F.] Univ Roma La Sapienza, Dept Paediat Emergency, Rome, Italy; [Rossi, G. A.] G Gaslini Inst Children, Pulm Dis Unit, Genoa, Italy; [Bisgaard, H.] Copenhagen Univ Hosp, Danish Paediat Asthma Ctr, Copenhagen, Denmark; [Castro-Rodriguez, J. A.] Pontificia Univ Catolica Chile, Sch Med, Santiago, Chile; [Custovic, A.] Wythenshawe Hosp, NW Lung Res Ctr, Manchester M23 9LT, Lancs, England; [Everard, M. L.] Sheffield Childrens Hosp, Univ Div Child Hlth, Sheffield, S Yorkshire, England; [Grigg, J.] Barts & London Med Sch, Inst Cell & Mol Sci, Acad Unit Paediat, London, England; [McKenzie, S.] Royal London Hosp, Barts & London NHS Trust, London E1 1BB, England; [Bush, A.] Royal Brompton Hosp, Dept Paediat, Natl Heart & Lung Inst, London, England; [Bush, A.] Univ London Imperial Coll Sci Technol & Med, London, England; [Lenney, W.] Univ Hosp N Staffordshire, Acad Dept Child Hlth, Stoke On Trent, Staffs, England; [Paton, J. Y.] Yorkhill Hosp, Univ Div Dev Med, Glasgow, Lanark, Scotland; [Seddon, P.; Silverman, M.] Royal Alexandra Childrens Hosp, Brighton, E Sussex, England; [Silverman, M.] Univ Leicester, Dept Infect Inflammat & Immunol, Leicester, Leics, England; [de Blic, J.] Necker Hosp Sick Children, Paris Publ Assistance Hosp, Paediat Pneumol & Allergol Serv, Paris, France; [Eber, E.] Med Univ Graz, Dept Paediat & Adolescent Med, Resp & Allerg Dis Div, Graz, Austria; [Frey, U.] Univ Hosp Bern, Inselspital, CH-3010 Bern, Switzerland; [Frey, U.] Univ Bern, Bern, Switzerland; [Wildhaber, J. H.] Fribourg Bertigny Hosp, Dept Paediat, Fribourg, Switzerland; [Gappa, M.] Med Univ Hanover, Dept Paediat Pulmonol & Neonatol, Hannover, Germany; [Garcia-Marcos, L.] Univ Murcia, Inst Resp Hlth, Murcia, Spain; [Stick, S.] Univ Western Australia, Ctr Asthma Allergy & Resp Res, Perth, WA 6009, Australia; [Pohunek, P.] Motol Univ Hosp, Prague, Czech Republic; [Valiulis, A.] Vilnius City Univ Hosp, Vilnius, Lithuania; [Wennergren, G.] Gothenburg Univ, Dept Paediat, Queen Silvia Childrens Hosp, Gothenburg, Sweden; [Zivkovic, Z.] Dr Dragisa Misov Med Ctr, Ctr Paediat Pulmonol, Belgrade, Serbia	Brand, PLP (reprint author), Isala Klin, Princess Amalia Childrens Clin, POB 10400, NL-8000 K Zwolle, Netherlands.	p.l.p.brand@isala.nl	Sly, Peter/F-1486-2010; Eber, Ernst/B-6381-2012; Kronow, Joern/B-1054-2011; Stick, Stephen/O-5683-2014; Merkus, P.J.F.M./L-4523-2015; Custovic, Adnan/A-2435-2012; Bisgaard, Hans/N-4761-2016; Osborne, Nicholas/N-4915-2015	Sly, Peter/0000-0001-6305-2201; Custovic, Adnan/0000-0001-5218-7071; 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J	Illi, S; von Mutius, E; Lau, S; Niggemann, B; Gruber, C; Wahn, U				Illi, Sabina; von Mutius, Erika; Lau, Susanne; Niggemann, Bodo; Grueber, Christoph; Wahn, Ulrich		Multictr Allergy Study Grp	Perennial allergen sensitisation early in life and chronic asthma in children: a birth cohort study	LANCET			English	Article							HOUSE-DUST MITE; AGE 3 YEARS; CHILDHOOD ASTHMA; LUNG-FUNCTION; INHALED CORTICOSTEROIDS; PRESCHOOL-CHILDREN; EXPOSURE; PREVALENCE; SYMPTOMS; GERMANY	Background Reduced lung function is a feature of chronic asthma, which becomes apparent at school age. Unknown factors between birth and school age determine the progressive loss of pulmonary function in children with persistent asthma. We investigated the role of allergic sensitisation and allergen exposure early in life. Methods The German Multicentre Allergy Study followed 1314 children from birth to 13 years of age. We regularly interviewed parents about their child's asthma and measured IgE levels. Allergen exposure was assessed at age 6 months, 18 months, and at 3, 4, and 5 years; lung function was assessed at 7, 10, and 13 years; post-bronchodilator response at 10 and 13 years; and a bronchial histamine challenge was done at 7 years. Results 90% of children with wheeze but no atopy lost their symptoms at school age and retained normal lung function at puberty. By contrast, sensitisation to perennial allergens (eg, house dust mite, cat and dog hair) developing in the first 3 years of life was associated with a loss of lung function at school age. Concomitant exposure to high levels of perennial allergens early in life aggravated this process: forced expiratory volume in 1 s (FEV1) to forced vital capacity (FVC) ratio was 87.4 (SD 7.4) for those sensitised and with high exposure compared with 92.6 (6.0) for those not sensitised, p<0.0001; and maximal expiratory flow at 50% (MEF50) 86.4 (25.1) for sensitised and with high exposure compared with 101.5 (23.2; p=0.0031) for those not sensitised. Such exposure also enhanced the development of airway hyper-responsiveness in sensitised children with wheeze. Sensitisation and exposure later in life had much weaker effects and sensitisation to seasonal allergens did not play a part. Interpretation The chronic course of asthma characterised by airway hyper-responsiveness and impairment of lung function at school age is determined by continuing allergic airway inflammation beginning in the first 3 years of life. However, children with a non-atopic wheezing phenotype lose their symptoms over school age and retain normal lung function at puberty.	Charite Univ Med Berlin, Dept Pediat Pneumol & Immunol, Berlin, Germany; Univ Childrens Hosp, Munich, Germany	Illi, S (reprint author), Univ Munich, Dr Von Haunerschen Kinderspital, Lindwurmstr 4, D-80337 Munich, Germany.	sabina.illi@med.uni-muenchen.de	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Bergmann R L, 1994, Pediatr Allergy Immunol, V5, P19, DOI 10.1111/j.1399-3038.1994.tb00343.x; Bisgaard H, 2006, NEW ENGL J MED, V354, P1998, DOI 10.1056/NEJMoa054692; Bisgaard H, 1997, Pediatr Pulmonol Suppl, V15, P27; Chen YZ, 2006, PEDIAT ALLERG IMM-UK, V17, P7, DOI 10.1111/j.1600-5562.2006.00379.x; Cnaan A, 1997, STAT MED, V16, P2349, DOI 10.1002/(SICI)1097-0258(19971030)16:20<2349::AID-SIM667>3.0.CO;2-E; Fedorov IA, 2005, THORAX, V60, P389, DOI 10.1136/thx.2004.030262; *GLOB IN ASTHM, 2005, GINA GUID WORKSH REP; Guilbert TW, 2006, NEW ENGL J MED, V354, P1985, DOI 10.1056/NEJMoa051378; Hirsch T, 2000, CLIN EXP ALLERGY, V30, P529, DOI 10.1046/j.1365-2222.2000.00785.x; Holt PG, 2004, NAT IMMUNOL, V5, P695, DOI 10.1038/ni0704-695; Holt PG, 2000, ALLERGY, V55, P688, DOI 10.1034/j.1398-9995.2000.00118.x; Illi S, 2001, BRIT MED J, V322, P390, DOI 10.1136/bmj.322.7283.390; Koopman LP, 2002, AM J RESP CRIT CARE, V166, P307, DOI 10.1164/rccm.2106026; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; Lowe LA, 2004, ARCH PEDIAT ADOL MED, V158, P996, DOI 10.1001/archpedi.158.10.996; Lowe LA, 2005, AM J RESP CRIT CARE, V171, P231, DOI 10.1164/rccm.200406-695OC; Morgan WJ, 2005, AM J RESP CRIT CARE, V172, P1253, DOI 10.1164/rccm.200504-525OC; Niggemann B, 2001, EUR RESPIR J, V17, P246, DOI 10.1183/09031936.01.17202460; Phelan PD, 2002, J ALLERGY CLIN IMMUN, V109, P189, DOI 10.1067/mai.2001.120951; Saglani S, 2005, AM J RESP CRIT CARE, V171, P722, DOI 10.1164/rccm.200410-14040C; Sears MR, 2003, NEW ENGL J MED, V349, P1414, DOI 10.1056/NEJMoa022363; Szefler S, 2000, NEW ENGL J MED, V343, P1054; van den Akker-van Marle ME, 2005, ALLERGY, V60, P140, DOI 10.1111/j.1398-9995.2005.00692.x; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; Wahn U, 1997, PEDIATR ALLERGY IMMU, V8, P16; Weiland SK, 1999, EUR RESPIR J, V14, P862, DOI 10.1034/j.1399-3003.1999.14d23.x; WILLIAMS H, 1969, BRIT MED J, V4, P321; Woodcock A, 2004, AM J RESP CRIT CARE, V170, P433, DOI 10.1164/rccm.200401-083OC	28	384	397	6	22	ELSEVIER SCIENCE INC	NEW YORK	360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA	0140-6736	1474-547X		LANCET	Lancet	AUG-SEP	2006	368	9537					763	770		10.1016/S0140-6736(06)69286-6		8	Medicine, General & Internal	General & Internal Medicine	080ID	WOS:000240240200028	16935687	
J	Schmidt, M; Sun, G; Stacey, MA; Mori, L; Mattoli, S				Schmidt, M; Sun, G; Stacey, MA; Mori, L; Mattoli, S			Identification of circulating fibrocytes as precursors of bronchial myofibroblasts in asthma	JOURNAL OF IMMUNOLOGY			English	Article							BRONCHOALVEOLAR LAVAGE FLUID; HUMAN-LUNG FIBROBLASTS; EPITHELIAL-CELLS; SUBEPITHELIAL FIBROSIS; IN-SITU; EXPRESSION; AIRWAY; INFLAMMATION; ENDOTHELIN-1; OBSTRUCTION	The mechanisms contributing to airway wall remodeling in asthma are under investigation to identify appropriate therapeutic targets. Bronchial myofibroblasts would represent an important target because they play a crucial role in the genesis of subepithelial fibrosis, a characteristic feature of the remodeling process, but their origin is poorly understood. We hypothesized that they originate from fibrocytes, circulating cells with the unique characteristic of expressing the hemopoietic stem cell Ag CD34 and collagen I. In this study we show that allergen exposure induces the accumulation of fibrocyte-like cells in the bronchial mucosa of patients with allergic asthma. These cells are CD34-positive; express collagen I and a-smooth muscle actin, a marker of myofibroblasts; and localize to areas of collagen deposition below the epithelium. By tracking labeled circulating fibrocytes in a mouse model of allergic asthma, we provide evidence that fibrocytes are indeed recruited into the bronchial tissue following allergen exposure and differentiate into myofibroblasts. We also show that human circulating fibrocytes acquire the myofibroblast phenotype under in vitro stimulation with fibrogenic cytokines that are produced in exaggerated quantities in asthmatic airways. These results indicate that circulating fibrocytes may function as myofibroblast precursors and may contribute to the genesis of subepithelial fibrosis in asthma.	Avail GmbH, CH-4051 Basel, Switzerland; Avail Biomed Res Inst, Basel, Switzerland	Mattoli, S (reprint author), Avail GmbH, Spalentorweg 18, CH-4051 Basel, Switzerland.		Mattoli, Sabrina/H-8211-2014	Mattoli, Sabrina/0000-0002-6866-604X			Abe R, 2001, J IMMUNOL, V166, P7556; ACKERMAN V, 1995, J ALLERGY CLIN IMMUN, V96, P618, DOI 10.1016/S0091-6749(95)70260-1; BOUSQUET J, 1992, ALLERGY, V47, P3, DOI 10.1111/j.1398-9995.1992.tb02242.x; Bousquet J, 2000, AM J RESP CRIT CARE, V161, P1720; BREWSTER CEP, 1990, AM J RESP CELL MOL, V3, P507; Brown JR, 1998, CLIN EXP IMMUNOL, V114, P137; BUCALA R, 1994, MOL MED, V1, P71; Chesney J, 2000, Curr Rheumatol Rep, V2, P501, DOI 10.1007/s11926-000-0027-5; Chesney J, 1997, P NATL ACAD SCI USA, V94, P6307, DOI 10.1073/pnas.94.12.6307; Elias JA, 1999, J CLIN INVEST, V104, P1001, DOI 10.1172/JCI8124; Fish JE, 1999, J ALLERGY CLIN IMMUN, V104, P509, DOI 10.1016/S0091-6749(99)70315-5; Gabbrielli S., 1994, Pathologica (Genoa), V86, P157; GIZYCKI MJ, 1997, AM J RESPIR CELL MOL, V3, P507; GROULS V, 1981, STAIN TECHNOL, V56, P323; HAMADA K, 1995, HISTOCHEM J, V27, P309, DOI 10.1007/BF00398973; Hashimoto S, 2001, J ALLERGY CLIN IMMUN, V107, P1001, DOI 10.1067/mai.2001.114702; Hendrikx PJ, 1996, EXP HEMATOL, V24, P129; Herrera C, 2001, BRIT J HAEMATOL, V114, P920, DOI 10.1046/j.1365-2141.2001.02974.x; Hoshino M, 1998, J ALLERGY CLIN IMMUN, V102, P783, DOI 10.1016/S0091-6749(98)70018-1; James AL, 1997, AIRWAY WALL REMODELI, P1; Krause DS, 1996, BLOOD, V87, P1; Kumar RK, 2002, AM J RESP CELL MOL, V27, P267, DOI 10.1165/rcmb.F248; Lanzkron SM, 1999, BLOOD, V93, P1916; Lemanske RF, 1993, ALLERGY PRINCIPLES P, P320; Marini M, 1996, BIOCHEM BIOPH RES CO, V220, P896, DOI 10.1006/bbrc.1996.0502; MATTOLI S, 1991, J ALLERGY CLIN IMMUN, V88, P376, DOI 10.1016/0091-6749(91)90100-3; Mori L, 1995, BIOCHEM BIOPH RES CO, V217, P817, DOI 10.1006/bbrc.1995.2845; Morishima Y, 2001, AM J RESP CELL MOL, V24, P1; OBYME PM, 1987, AM REV RESPIR DIS, V136, P740; Pare P D, 1997, Monaldi Arch Chest Dis, V52, P589; Parish CR, 1999, IMMUNOL CELL BIOL, V77, P499, DOI 10.1046/j.1440-1711.1999.00877.x; Powell DW, 1999, AM J PHYSIOL-CELL PH, V277, pC1; Redington AE, 1997, AM J RESP CRIT CARE, V156, P642; Redington AE, 1997, THORAX, V52, P310; Richter A, 2001, AM J RESP CELL MOL, V25, P385; ROBERTS CJ, 1988, J BIOL CHEM, V263, P4586; ROCHE WR, 1989, LANCET, V1, P520; Serini G, 1999, EXP CELL RES, V250, P273, DOI 10.1006/excr.1999.4543; Sun G, 1997, PEPTIDES, V18, P1449, DOI 10.1016/S0196-9781(97)00194-0; Tang WL, 1996, J CLIN INVEST, V98, P2845, DOI 10.1172/JCI119113; Teder P, 2000, AM J RESP CELL MOL, V23, P7; Vignola AM, 1997, AM J RESP CRIT CARE, V156, P591; VITTORI E, 1992, AM REV RESPIR DIS, V146, P1320; Wilson JW, 1997, CLIN EXP ALLERGY, V27, P363; Zhang S, 1996, J PATHOL, V180, P95; Zhang SL, 1999, LAB INVEST, V79, P395	46	384	413	2	15	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	JUL 1	2003	171	1					380	389				10	Immunology	Immunology	692RQ	WOS:000183674400048	12817021	
J	Atkinson, RW; Anderson, HR; Sunyer, J; Ayres, J; Baccini, M; Vonk, JM; Boumghar, A; Forastiere, F; Forsberg, B; Touloumi, G; Schwartz, J; Katsouyanni, K				Atkinson, RW; Anderson, HR; Sunyer, J; Ayres, J; Baccini, M; Vonk, JM; Boumghar, A; Forastiere, F; Forsberg, B; Touloumi, G; Schwartz, J; Katsouyanni, K			Acute effects of particulate air pollution on respiratory admissions - Results from APHEA 2 project	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						particles; respiratory admissions; heterogeneity; APHEA 2	TIME-SERIES DATA; HOSPITAL ADMISSIONS; EUROPEAN CITIES; HEALTH; ASTHMA; DISEASE; OZONE; URBAN	The APHEA 2 project investigated short-term health effects of particles in eight European cities. In each city associations between particles with an aerodynamic diameter of less than 10 mum (PM10) and black smoke and daily counts of emergency hospital admissions for asthma (0-14 and 15-64 yr), chronic obstructive pulmonary disease (COPD), and all-respiratory disease (65+ yr) controlling for environmental factors and temporal patterns were investigated. Summary PM10 effect estimates (percentage change in mean number of daily admissions per 10 mug/m(3) increase) were asthma (0-14 yr) 1.2% (95% Cl: 0.2, 2.3), asthma (15-64 yr) 1.1% (0.3, 1.8), and COPD plus asthma and all-respiratory (65+ yr) 1.0% (0.4, 1.5) and 0.9% (0.6, 1.3). The combined estimates for Black Smoke tended to be smaller and less precisely estimated than for PM10. Variability in the sizes of the PM10 effect estimates between cities was also investigated. In the 65+ groups PM10 estimates were positively associated with annual mean concentrations of ozone In the cities. For asthma admissions (0-14 yr) a number of city-specific factors, including smoking prevalence, explained some of their variability. This study confirms that particle concentrations in European cities are positively associated with increased numbers of admissions for respiratory diseases and that some of the variation in PM10 effect estimates between cities can be explained by city characteristics.	St George Hosp, Sch Med, Dept Publ Hlth Sci, London SW17 ORE, England; Inst Municipal Invest Med, Unita Recerca Resp & Ambiental, E-08003 Barcelona, Spain; Birmingham Heartlands Hosp, Birmingham B9 5ST, W Midlands, England; Univ Florence, Dept Stat, Florence, Italy; Univ Groningen, Fac Med Sci, Det Epidemiol & Stat, Groningen, Netherlands; Hlth Reg Observ, Paris, France; Agcy Publ Hlth, Lazio, Italy; Umea Univ, Dept Publ Hlth & Clin Med, Umea, Sweden; Dept Hyg Epidemiol, Athens, Greece; Harvard Sch Publ Hlth, Dept Environm Hlth, Environm Epidemiol Program, Boston, MA USA	Atkinson, RW (reprint author), St George Hosp, Sch Med, Dept Publ Hlth Sci, London SW17 ORE, England.		Katsouyanni, Klea/D-4856-2014; Forastiere, Francesco/J-9067-2016; Sunyer, J/G-6909-2014	Katsouyanni, Klea/0000-0002-0132-9575; Forastiere, Francesco/0000-0002-9162-5684; Sunyer, J/0000-0002-2602-4110			Anderson HR, 1997, EUR RESPIR J, V10, P1064, DOI 10.1183/09031936.97.10051064; BRUNEKREEF B, 1995, ENVIRON HEALTH PERSP, V103, P3, DOI 10.2307/3432443; CHAPMAN R, 1996, EPA600R95001CF US EP; Gamble JF, 1996, ENVIRON HEALTH PERSP, V104, P838, DOI 10.2307/3432938; HATCH M, 1993, ENVIRON HEALTH PERSP, V101, P49, DOI 10.2307/3431659; HOPPEL WA, 1990, ATMOS ENVIRON A-GEN, V24, P645, DOI 10.1016/0960-1686(90)90020-N; Jorres R, 1996, AM J RESP CRIT CARE, V153, P56; Katsouyanni K, 1996, J EPIDEMIOL COMMUN H, V50, pS12, DOI 10.1136/jech.50.Suppl_1.S12; KATSOUYANNI K, 1995, EUR RESPIR J, V8, P1030; McMichael AJ, 1998, INT J EPIDEMIOL, V27, P450, DOI 10.1093/ije/27.3.450; MCMURRY PH, 1983, J GEOPHYS RES-OCEANS, V88, P5101, DOI 10.1029/JC088iC09p05101; MENG ZY, 1994, AEROSOL SCI TECH, V20, P253, DOI 10.1080/02786829408959681; MOLFINO NA, 1991, LANCET, V338, P199, DOI 10.1016/0140-6736(91)90346-Q; Monn C, 2001, ATMOS ENVIRON, V35, P1, DOI 10.1016/S1352-2310(00)00330-7; Phalen RF, 1998, TOXICOL LETT, V96-7, P263, DOI 10.1016/S0378-4274(98)00081-2; Pope III CAD, 1999, AIR POLLUTION HLTH, P673; Samet JM, 2000, NATL MORBIDITY MOR 2; Schwartz J, 1996, EPIDEMIOLOGY, V7, P20, DOI 10.1097/00001648-199601000-00005; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; Schwartz J., 1997, HLTH CROSSROADS TRAN, P61; Spix C, 1998, ARCH ENVIRON HEALTH, V53, P54; Sunyer J, 1997, THORAX, V52, P760	22	382	401	3	41	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	NOV 15	2001	164	10					1860	1866				7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	502TK	WOS:000172758700023	11734437	
J	Bornehag, CG; Blomquist, G; Gyntelberg, F; Jarvholm, B; Malmberg, P; Nordvall, L; Nielsen, A; Pershagen, G; Sundell, J				Bornehag, CG; Blomquist, G; Gyntelberg, F; Jarvholm, B; Malmberg, P; Nordvall, L; Nielsen, A; Pershagen, G; Sundell, J			Dampness in buildings and health - Nordic interdisciplinary review of the scientific evidence on associations between exposure to "dampness" in buildings and health effects (NORDDAMP)	INDOOR AIR-INTERNATIONAL JOURNAL OF INDOOR AIR QUALITY AND CLIMATE			English	Review						review; dampness; exposure; health effects; allergy; asthma	HOUSE-DUST MITES; DAY-CARE-CENTERS; CHILDHOOD RESPIRATORY SYMPTOMS; ENVIRONMENTAL RISK-FACTORS; VOLATILE ORGANIC-COMPOUNDS; PRIMARY-SCHOOL CHILDREN; REPORTED HOME DAMPNESS; INDOOR AIR-QUALITY; RESIDENTIAL CHARACTERISTICS; SUBTROPICAL CLIMATE	Several epidemiological investigations concerning indoor environments have indicated that "dampness" in buildings is associated to health effects such as respiratory symptoms, asthma and allergy The aim of the present interdisciplinary review is to evaluate this association as shown in the epidemiological literature. A literature search identified 590 peer-reviewed articles of which 61 have been the foundation for this review. The review shows that "dampness" in buildings appears to increase the risk for health effects in the airways, such as cough, wheeze and asthma. Relative risks are in the range of OR 1.4-2.2. There also seems to be an association between "dampness" and other symptoms Such as tiredness, headache and airways infections. It is concluded that the evidence for a causal association between "dampness" and health effects is strong. However, the mechanisms are unknown. Several definitions of dampness have been used in the studies, but all seems to be associated with health problems. Sensitisation to mites may be one but obviously not the only mechanism. Even if the mechanisms are unknown, there is sufficient evidence to take preventive measures against dampness in buildings.	Natl Testing & Res Inst, Karlstad, Sweden; Natl Inst Working Life, Umea, Sweden; Bispebjerg Hosp, DK-2400 Copenhagen, Denmark; Umea Univ, Umea, Sweden; Natl Inst Working Life, Stockholm, Sweden; Univ Uppsala Hosp, Uppsala, Sweden; Natl Testing & Res Inst, Boras, Sweden; Karolinska Inst, Stockholm, Sweden; Tech Univ Denmark, DK-2800 Lyngby, Denmark	Bornehag, CG (reprint author), Natl Testing & Res Inst, Karlstad, Sweden.		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J. Indoor Air Qual. Clim.	JUN	2001	11	2					72	86				15	Construction & Building Technology; Engineering, Environmental; Public, Environmental & Occupational Health	Construction & Building Technology; Engineering; Public, Environmental & Occupational Health	435VC	WOS:000168902000002	11394014	
J	Trompette, A; Divanovic, S; Visintin, A; Blanchard, C; Hegde, RS; Madan, R; Thorne, PS; Wills-Karp, M; Gioannini, TL; Weiss, JP; Karp, CL				Trompette, Aurelien; Divanovic, Senad; Visintin, Alberto; Blanchard, Carine; Hegde, Rashmi S.; Madan, Rajat; Thorne, Peter S.; Wills-Karp, Marsha; Gioannini, Theresa L.; Weiss, Jerry P.; Karp, Christopher L.			Allergenicity resulting from functional mimicry of a Toll-like receptor complex protein	NATURE			English	Article							TLR4-MD-2 COMPLEX; CRYSTAL-STRUCTURE; ALLERGIC DISEASE; CELL ACTIVATION; ENDOTOXIN; MD-2; ASTHMA; LIPOPOLYSACCHARIDE; RESPONSES; EXPOSURE	Aeroallergy results from maladaptive immune responses to ubiquitous, otherwise innocuous environmental proteins(1). Although the proteins targeted by aeroallergic responses represent a tiny fraction of the airborne proteins humans are exposed to, allergenicity is a quite public phenomenon - the same proteins typically behave as aeroallergens across the human population. Why particular proteins tend to act as allergens in susceptible hosts is a fundamental mechanistic question that remains largely unanswered. The main house- dust- mite allergen, Der p 2, has structural homology with MD- 2 ( also known as LY96), the lipopolysaccharide ( LPS)- binding component of the Toll- like receptor ( TLR) 4 signalling complex(2-4). Here we show that Der p 2 also has functional homology, facilitating signalling through direct interactions with the TLR4 complex, and reconstituting LPS- driven TLR4 signalling in the absence of MD- 2. Mirroring this, airway sensitization and challenge with Der p 2 led to experimental allergic asthma in wild type and MD- 2- deficient, but not TLR4- deficient, mice. Our results indicate that Der p 2 tends to be targeted by adaptive immune responses because of its auto-adjuvant properties. The fact that other members of the MD- 2- like lipid- binding family are allergens, and that most defined major allergens are thought to be lipid- binding proteins(5), suggests that intrinsic adjuvant activity by such proteins and their accompanying lipid cargo may have some generality as a mechanism underlying the phenomenon of allergenicity.	[Trompette, Aurelien; Divanovic, Senad; Madan, Rajat; Karp, Christopher L.] Childrens Hosp, Med Ctr, Div Mol Immunol, Cincinnati, OH 45229 USA; [Blanchard, Carine] Childrens Hosp, Med Ctr, Div Allergy & Immunol, Cincinnati, OH 45229 USA; [Hegde, Rashmi S.] Childrens Hosp, Med Ctr, Div Dev Biol, Cincinnati, OH 45229 USA; [Wills-Karp, Marsha] Childrens Hosp, Med Ctr, Div Immunobiol, Cincinnati, OH 45229 USA; Univ Cincinnati, Coll Med, Cincinnati, OH 45229 USA; [Visintin, Alberto] Univ Massachusetts, Sch Med, Div Infect Dis & Immunol, Dept Med, Worcester, MA 01606 USA; [Thorne, Peter S.] Univ Iowa, Dept Occupat & Environm Med, Iowa City, IA 52241 USA; [Gioannini, Theresa L.; Weiss, Jerry P.] Univ Iowa, Inflammat Program, Dept Internal Med, Iowa City, IA 52241 USA; [Gioannini, Theresa L.; Weiss, Jerry P.] Vet Affairs Med Ctr, Iowa City, IA 52247 USA	Karp, CL (reprint author), Childrens Hosp, Med Ctr, Div Mol Immunol, Cincinnati, OH 45229 USA.	chris.karp@chmcc.org	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Karp, Christopher/0000-0002-0832-2659	Sandler Foundation for Asthma Research; National Institute of Allergy and Infectious Diseases; Veteran's Administration	We thank S. Vogel for re-purified LPS; E. Kurt-Jones and R. Finberg for HEK293 cells expressing TLR4 complex proteins, N.J. Gay for discussions, and L. Flick and J. Bohnert for technical assistance. This work was funded by grants from the Sandler Foundation for Asthma Research (C.L.K.), the National Institute of Allergy and Infectious Diseases (C.L.K., J.P.W.), and the Veteran's Administration (T.L.G.).	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J	Lemanske, RF; Jackson, DJ; Gangnon, RE; Evans, MD; Li, ZH; Shult, PA; Kirk, CJ; Reisdorf, E; Roberg, KA; Anderson, EL; Carlson-Dakes, KT; Adler, KJ; Gilbertson-White, S; Pappas, TE; DaSilva, DF; Tisler, CJ; Gern, JE				Lemanske, RF; Jackson, DJ; Gangnon, RE; Evans, MD; Li, ZH; Shult, PA; Kirk, CJ; Reisdorf, E; Roberg, KA; Anderson, EL; Carlson-Dakes, KT; Adler, KJ; Gilbertson-White, S; Pappas, TE; DaSilva, DF; Tisler, CJ; Gern, JE			Rhinovirus illnesses during infancy predict subsequent childhood wheezing	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						rhinovirus; respiratory syncytial virus; virus; asthma; wheezing illnesses; allergic sensitization; atopy; infants; children; allergic disease	RESPIRATORY SYNCYTIAL VIRUS; DISEASE SEVERITY; EARLY-LIFE; BRONCHIOLITIS; ASTHMA; INFECTION; CHILDREN; RISK; ASSOCIATION; AGE	Background: The contribution of viral respiratory infections during infancy to the development of subsequent wheezing and/ or allergic diseases in early childhood is not established. Objective: To evaluate these relationships prospectively from birth to 3 years of age in 285 children genetically at high risk for developing allergic respiratory diseases. Methods: By using nasal lavage, the relationship of timing, severity, and etiology of viral respiratory infections during infancy to wheezing in the 3rd year of life was evaluated. In addition, genetic and environmental factors that could modify risk of infections and wheezing prevalence were analyzed. Results: Risk factors for 3rd year wheezing were passive smoke exposure (odds ratio [OR] = 2.1), older siblings (OR = 2.5), allergic sensitization to foods at age 1 year (OR = 2.0), any moderate to severe respiratory illness without wheezing during infancy (OR = 3.6), and at least 1 wheezing illness with respiratory syncytial virus (RSV; OR = 3.0), rhinovirus (OR 10) and/or non-rhinovirus/RSV pathogens (OR = 3.9) during infancy. When viral etiology was considered, 1st-year wheezing illnesses caused by rhinovirus infection were the strongest predictor of subsequent 3rd year wheezing (OR = 6.6; P < .0001). Moreover, 63% of infants who wheezed during rhinovirus seasons continued to wheeze in the 3rd year of life, compared with only 20% of all other infants (OR = 6.6; P < .0001). Conclusion: In this population of children at increased risk of developing allergies and asthma, the most significant risk factor for the development of preschool childhood wheezing is the occurrence of symptomatic rhinovirus; illnesses during infancy that are clinically and prognostically informative based on their seasonal nature.	Univ Wisconsin, Dept Pediat, Madison, WI 53706 USA; Univ Wisconsin, Dept Biostat & Med Informat, Madison, WI 53706 USA; Univ Wisconsin, Dept Med, Madison, WI 53706 USA; Univ Wisconsin, Wisconsin State Lab Hyg, Madison, WI 53706 USA	Lemanske, RF (reprint author), Univ Wisconsin Hosp, K4-916,600 Highland Ave, Madison, WI 53792 USA.	rfl@medicine.wisc.edu		Evans, Michael/0000-0001-7449-3993	NHLBI NIH HHS [1P01HLPO, 1R01HL61879]		Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; Bont L, 2000, AM J RESP CRIT CARE, V161, P1518; Bont L, 2001, J INFECT DIS, V184, P355, DOI 10.1086/322035; CALHOUN WJ, 1994, J CLIN INVEST, V94, P2200, DOI 10.1172/JCI117581; Cane RS, 2000, ARCH DIS CHILD, V82, P327, DOI 10.1136/adc.82.4.327; Cane RS, 2001, ARCH DIS CHILD, V84, P31, DOI 10.1136/adc.84.1.31; Castro-Rodriguez JA, 2000, AM J RESP CRIT CARE, V162, P1403; Choi EH, 2002, J INFECT DIS, V186, P1207, DOI 10.1086/344310; Copenhaver CC, 2004, AM J RESP CRIT CARE, V170, P175, DOI 10.1164/rccm.200312-1647OC; Gern JE, 2002, PEDIATR ALLERGY IMMU, V13, P386, DOI 10.1034/j.1399-3038.2002.01093.x; Gern JE, 1997, AM J RESP CRIT CARE, V155, P1159; Guilbert TW, 2004, CONTROL CLIN TRIALS, V25, P286, DOI 10.1016/j.cct.2004.03.002; Hoebee B, 2004, J INFECT DIS, V189, P239, DOI 10.1086/380908; Hoebee B, 2003, J INFECT DIS, V187, P2, DOI 10.1086/345859; Hoffjan S, 2004, J ALLERGY CLIN IMMUN, V113, P511, DOI 10.1016/j.jaci.2003.10.044; Hull J, 2000, THORAX, V55, P1023, DOI 10.1136/thorax.55.12.1023; Hull J, 2003, J INFECT DIS, V188, P904, DOI 10.1086/377587; Illi S, 2001, BRIT MED J, V322, P390, DOI 10.1136/bmj.322.7283.390; IRELAND DC, 1993, J MED VIROL, V40, P96, DOI 10.1002/jmv.1890400204; Jartti T, 2004, EMERG INFECT DIS, V10, P1095; Korppi M, 2004, PEDIATR INFECT DIS J, V23, P995, DOI 10.1097/01.inf.0000143642.72480.53; Kotaniemi-Syrjanen A, 2003, J ALLERGY CLIN IMMUN, V111, P66, DOI 10.1067/mai.2003.33; Lahti M, 2002, PEDIATR RES, V51, P696, DOI 10.1023/01.PDR.0000015911.65104.93; Lemanske RF, 2002, PEDIATR ALLERGY IMMU, V13, P38, DOI 10.1034/j.1399-3038.13.s.15.8.x; LEMANSKE RF, 1989, J CLIN INVEST, V83, P1, DOI 10.1172/JCI113843; Lowe L, 2004, ARCH DIS CHILD, V89, P540, DOI 10.1136/adc.2003.038539; Mosser AG, 2005, AM J RESP CRIT CARE, V171, P645, DOI 10.1164/rccm.200407-970OC; Neaville WA, 2003, J ALLERGY CLIN IMMUN, V112, P740, DOI 10.1067/mai.2003.1716; Openshaw PJM, 2003, PEDIATR INFECT DIS J, V22, pS58, DOI 10.1097/00006454-200302001-00009; Papadopoulos NG, 2002, AM J RESP CRIT CARE, V165, P1285, DOI 10.1164/rccm.200112-1188C; Reijonen TM, 2000, PEDIATRICS, V106, P1406, DOI 10.1542/peds.106.6.1406; Sigurs N, 2000, AM J RESP CRIT CARE, V161, P1501; Stein R, 1999, LANCET, V354, P541, DOI 10.1016/S0140-6736(98)10321-5	33	377	393	3	19	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					571	577		10.1016/j.jaci.2005.06.024		7	Allergy; Immunology	Allergy; Immunology	017IE	WOS:000235686500016	16159626	
J	von Mutius, E; Braun-Fahrlander, C; Schierl, R; Riedler, J; Ehlermann, S; Maisch, S; Waser, M; Nowak, D				von Mutius, E; Braun-Fahrlander, C; Schierl, R; Riedler, J; Ehlermann, S; Maisch, S; Waser, M; Nowak, D			Exposure to endotoxin or other bacterial components might protect against the development of atopy	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						atopy; endotoxin; children	ALLERGIC SENSITIZATION; RESPIRATORY HEALTH; AIRBORNE ENDOTOXIN; IMMUNE-RESPONSES; DUST; CHILDHOOD; ASTHMA; INTERLEUKIN-12; COMMUNITY; CHILDREN	Background Several recent studies have shown that growing up on a farm confers significant protection against the development of atopy. These findings point particularly towards the importance of exposure to stable dust and farm animals. It has furthermore been reported that endotoxin, an intrinsic part of the outer membrane of gram negative bacteria, is abundant in environments where livestock and poultry is kept. The aim of this study was therefore to measure the level of environmental endotoxin exposure in homes of farmers' children, children with regular contact to livestock and control children with no contact to farm animals. Methods Eighty-four farming and nonfarming families were identified in rural areas in Southern Germany and Switzerland. Samples of settled and airborne dust were collected in stables, and of settled dust indoors from kitchen floors and the children's mattresses. Endotoxin concentrations were determined by a kinetic Limulus assay. Results Endotoxin concentrations were highest in stables of farming families, but were also significantly higher indoors in dust from kitchen floors (143 EU/mg vs 39 EU/mg, P < 0.001) and children's mattresses (49479 EU/m(2) vs 9383 EU/m(2), P < 0.001) as compared to control children from nonfarming families. In addition, endotoxin levels were also significantly higher in mattresses and dust from kitchen floors in households where children had regular contact to farm animals (38.6 EU/mg and 23340 EU/m(2), respectively) as compared to control subjects. Conclusion We propose that the level of environmental exposure to endotoxin and other bacterial wall components is an important protective determinant for the development of atopic diseases in childhood.	Univ Childrens Hosp, Munich, Germany; Univ Basel, Inst Social & Prevent Med, CH-4003 Basel, Switzerland; Univ Munich, Inst Occupat & Environm Med, D-80539 Munich, Germany; Childrens Hosp, Salzburg, Austria	von Mutius, E (reprint author), Univ Munich, Klinikum Innenstadt, Lindwurmstr 4, D-80337 Munich, Germany.						ABERG N, 1989, CLIN EXP ALLERGY, V19, P59, DOI 10.1111/j.1365-2222.1989.tb02345.x; AbouZeid C, 1997, INFECT IMMUN, V65, P1856; Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; BraunFahrlander C, 1997, AM J RESP CRIT CARE, V155, P1042; Cleveland MG, 1996, INFECT IMMUN, V64, P1906; DUTKIEWICZ J, 1978, ARCH ENVIRON HEALTH, V33, P250; HEEDERIK D, 1991, INT ARCH OCC ENV HEA, V62, P595, DOI 10.1007/BF00381114; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; HOLLANDER A, 1993, AM IND HYG ASSOC J, V54, P647, DOI 10.1202/0002-8894(1993)054<0647:IAEITA>2.0.CO;2; Holt PG, 1996, J EXP MED, V183, P1297, DOI 10.1084/jem.183.4.1297; Holt PG, 1997, PEDIATR ALLERGY IMMU, V8, P53, DOI 10.1111/j.1399-3038.1997.tb00145.x; International Study of Asthma and Allergies in Childhood (ISAAC) Steering Committee, 1998, PHAS 2 MOD INT STUD; Jagielo PJ, 1996, CHEST, V110, P263, DOI 10.1378/chest.110.1.263; Jahn-Schmid B, 1999, J ALLERGY CLIN IMMUN, V104, P1015; Lee SM, 1996, BLOOD, V88, P945; MACATONIA SE, 1995, J IMMUNOL, V154, P5071; MAGGI E, 1992, J IMMUNOL, V148, P2142; Martinez FD, 1999, J ALLERGY CLIN IMMUN, V103, P355, DOI 10.1016/S0091-6749(99)70456-2; MICHEL O, 1991, CLIN EXP ALLERGY, V21, P441, DOI 10.1111/j.1365-2222.1991.tb01684.x; MICHEL O, 1989, J APPL PHYSIOL, V66, P1059; Milton DK, 1997, AM IND HYG ASSOC J, V58, P861; Nicolai T, 1998, THORAX, V53, P1035; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Rietschel E T, 1982, Scand J Infect Dis Suppl, V31, P8; Shaheen SO, 1996, LANCET, V347, P1792, DOI 10.1016/S0140-6736(96)91617-7; Svanes C, 1999, J ALLERGY CLIN IMMUN, V103, P415, DOI 10.1016/S0091-6749(99)70465-3; Thedell T D, 1980, Am J Ind Med, V1, P3, DOI 10.1002/ajim.4700010103; VINZENTS P, 1992, AM IND HYG ASSOC J, V53, P237, DOI 10.1202/0002-8894(1992)053<0237:VIETDA>2.0.CO;2; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; Yeung VP, 1998, J IMMUNOL, V161, P4146	32	377	380	2	21	BLACKWELL SCIENCE LTD	OXFORD	P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	SEP	2000	30	9					1230	1234				5	Allergy; Immunology	Allergy; Immunology	348PP	WOS:000088994100008	10971468	
J	Rahman, I; Biswas, SK; Kode, A				Rahman, I; Biswas, SK; Kode, A			Oxidant and antioxidant balance in the airways and airway diseases	EUROPEAN JOURNAL OF PHARMACOLOGY			English	Review						oxidants; antioxidants; lungs; glutathione; superoxide dismutase; thioredoxin	EXTRACELLULAR-SUPEROXIDE-DISMUTASE; IDIOPATHIC PULMONARY-FIBROSIS; TUMOR-NECROSIS-FACTOR; HEME OXYGENASE-1 EXPRESSION; INDUCED LUNG INJURY; KAPPA-B ACTIVATION; GAMMA-GLUTAMYLCYSTEINE SYNTHETASE; RESPIRATORY-DISTRESS-SYNDROME; ALVEOLAR INFLAMMATORY CELLS; BRONCHIAL EPITHELIAL-CELLS	Although oxygen is a prerequisite to life, at concentrations beyond the physiological limits it may be hazardous to the cells. Since the lungs are directly exposed to very high amounts of oxygen, it is imperative for the organ to possess defences against possible oxidative challenge. The lungs are therefore endowed with an armamentarium of a battery of endogenous agents called antioxidants. The antioxidant species help the lungs ward off the deleterious consequences of a wide variety of oxidants/reactive oxygen species such as superoxide anion, hydroxyl radical, hypohalite radical, hydrogen peroxide and reactive nitrogen species such as nitric oxide, peroxynitrite, nitrite produced endogenously and sometimes accessed through exposure to the environment. The major non-enzymatic antioxidants of the lungs are glutathione, vitamins C and E, beta-carotene, uric acid and the enzymatic antioxidants are superoxide dismutases, catalase and peroxidases. These antioxidants are the first lines of defence against the oxidants and usually act at a gross level. Recent insights into cellular redox chemistry have revealed the presence of certain specialized proteins such as peroxiredoxins, thioredoxins, glutaredoxins, heme oxygenases and reductases, which are involved in cellular adaptation and protection against an oxidative assault. These molecules usually exert their action at a more subtle level of cellular signaling processes. Aberrations in oxidant: antioxidant balance can lead to a variety of airway diseases, such as asthma, chronic obstructive Pulmonary disease and idiopathic pulmonary fibrosis which is the topic of discussion in this review. (c) 2005 Elsevier B.V. All rights reserved.	Univ Rochester, Med Ctr, Dept Environm Med, Div Lung Biol & Dis, Rochester, NY 14642 USA; Dr Ambedkar Coll, Dept Biochem, Nagpur, Maharashtra, India	Rahman, I (reprint author), Univ Rochester, Med Ctr, Dept Environm Med, Div Lung Biol & Dis, 601 Elmwood Ave,Bldg 850, Rochester, NY 14642 USA.	irfan_rahman@urmc.rochester.edu			NIEHS NIH HHS [ES01247]		ADAMSON IYR, 1974, AM J PATHOL, V77, P185; Allen RG, 1999, J CELL PHYSIOL, V180, P114, DOI 10.1002/(SICI)1097-4652(199907)180:1<114::AID-JCP13>3.0.CO;2-0; Amer E.S., 2000, EUR J BIOCHEM, V267, P6102, DOI DOI 10.1046/J.1432-1327.2000.01701.X.PMID:11012661; Andoh T, 2002, J BIOL CHEM, V277, P9655, DOI 10.1074/jbc.M110701200; Antuni JD, 2000, THORAX, V55, P138, DOI 10.1136/thorax.55.2.138; Asikainen TM, 1998, AM J RESP CELL MOL, V19, P942; AVISSAR N, 1996, AM J PHYSIOL, V270, pL447; Avissar NE, 2000, AM J RESP CRIT CARE, V162, P1342; Beeh KM, 2004, CHEST, V126, P1116, DOI 10.1378/chest.126.4.1116; Behr J, 2000, AM J RESP CRIT CARE, V161, P1968; 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J. Pharmacol.	MAR 8	2006	533	1-3					222	239		10.1016/j.ejphar.2005.12.087		18	Pharmacology & Pharmacy	Pharmacology & Pharmacy	025KS	WOS:000236265400022	16500642	
J	Wilson, MS; Taylor, MD; Balic, A; Finney, CAM; Lamb, JR; Maizels, RM				Wilson, MS; Taylor, MD; Balic, A; Finney, CAM; Lamb, JR; Maizels, RM			Suppression of allergic airway inflammation by helminth-induced regulatory T cells	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article							HOUSE-DUST MITE; GROWTH-FACTOR-BETA; TOTAL SERUM IGE; IMMUNE-RESPONSES; HELIGMOSOMOIDES-POLYGYRUS; HYGIENE HYPOTHESIS; CUTTING EDGE; CHILDHOOD ASTHMA; INFECTION; DISEASE	Allergic diseases mediated by T helper type ( Th) 2 cell immune responses are rising dramatically in most developed countries. Exaggerated Th2 cell reactivity could result, for example, from diminished exposure to Th1 cell - inducing microbial infections. Epidemiological studies, however, indicate that Th2 cell - stimulating helminth parasites may also counteract allergies, possibly by generating regulatory T cells which suppress both Th1 and Th2 arms of immunity. We therefore tested the ability of the Th2 cell - inducing gastrointestinal nematode Heligmosomoides polygyrus to influence experimentally induced airway allergy to ovalbumin and the house dust mite allergen Der p 1. Inflammatory cell infiltrates in the lung were suppressed in infected mice compared with uninfected controls. Suppression was reversed in mice treated with antibodies to CD25. Most notably, suppression was transferable with mesenteric lymph node cells ( MLNC) from infected animals to uninfected sensitized mice, demonstrating that the effector phase was targeted. MLNC from infected animals contained elevated numbers of CD4(+)CD25(+)Foxp3(+) T cells, higher TGF-beta expression, and produced strong interleukin ( IL)-10 responses to parasite antigen. However, MLNC from IL-10-deficient animals transferred suppression to sensitized hosts, indicating that IL-10 is not the primary modulator of the allergic response. Suppression was associated with CD4(+) T cells from MLNC, with the CD4(+)CD25(+) marker defining the most active population. These data support the contention that helminth infections elicit a regulatory T cell population able to down-regulate allergen induced lung pathology in vivo.	Univ Edinburgh, Inst Immunol & Infect Res, Edinburgh EH9 3JT, Midlothian, Scotland; Univ Edinburgh, Ctr Inflammat Res, Edinburgh EH9 3JT, Midlothian, Scotland	Maizels, RM (reprint author), Univ Edinburgh, Inst Immunol & Infect Res, Edinburgh EH9 3JT, Midlothian, Scotland.	rick.maizels@ed.ac.uk	Taylor, Matthew/C-7973-2011; Balic, Adam/C-7718-2013		Wellcome Trust		Akbari O, 2003, CURR OPIN IMMUNOL, V15, P627, DOI 10.1016/j.coi.2003.09.012; Akdis M, 2004, J EXP MED, V199, P1567, DOI 10.1084/jem.20032058; Araujo MI, 2000, INT ARCH ALLERGY IMM, V123, P145, DOI 10.1159/000024433; Araujo MIAS, 2004, J INFECT DIS, V190, P1797, DOI 10.1086/425017; Bashir MEH, 2002, J IMMUNOL, V169, P3284; Belkaid Y, 2005, NAT IMMUNOL, V6, P353, DOI 10.1038/ni1181; Bluestone JA, 2003, NAT REV IMMUNOL, V3, P253, DOI 10.1038/nri1032; Chen WJ, 2003, J EXP MED, V198, P1875, DOI 10.1084/jem.20030152; Chiaramonte MG, 2003, J EXP MED, V197, P687, DOI 10.1084/jem.20020903; Doetze A, 2000, INT IMMUNOL, V12, P623, DOI 10.1093/intimm/12.5.623; 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Exp. Med.	NOV 7	2005	202	9					1199	1212		10.1084/jem.20042572		14	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	981UB	WOS:000233112400007	16275759	
J	Olson, TS; Ley, K				Olson, TS; Ley, K			Chemokines and chemokine receptors in leukocyte trafficking	AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY			English	Review						homing; chemoattractants; T cell; B cell; monocyte; neutrophil	MONOCYTE CHEMOATTRACTANT PROTEIN-1; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MACROPHAGE-DERIVED CHEMOKINE; CENTRAL-NERVOUS-SYSTEM; SMOOTH-MUSCLE CELLS; C-C CHEMOKINE; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; SIGNAL-TRANSDUCTION PATHWAYS; HUMAN NEUTROPHIL LEUKOCYTES; MESSENGER-RNA ACCUMULATION	Chemokines regulate inflammation, leukocyte trafficking, and immune cell differentiation. The role of chemokines in homing of naive T lymphocytes to secondary lymphatic organs is probably the best understood of these processes, and information on chemokines in inflammation, asthma, and neurological diseases is rapidly increasing. Over the past 15 years, understanding of the size and functional complexity of the chemokine family of peptide chemoattractants has grown substantially. In this review, we first present information regarding the structure, expression, and signaling properties of chemokines and their receptors. The second part is a systems physiology-based overview of the roles that chemokines play in tissue-specific homing of lymphocyte subsets and in trafficking of inflammatory cells. This review draws on recent experimental findings as well as current models proposed by experts in the chemokine field.	Univ Virginia, Dept Mol Physiol & Biol Phys, Charlottesville, VA 22908 USA; Univ Virginia, Dept Biomed Engn, Charlottesville, VA 22908 USA; Univ Virginia, Cardiovasc Res Ctr, Charlottesville, VA 22908 USA	Ley, K (reprint author), Hlth Sci Ctr, Box 800759, Charlottesville, VA 22908 USA.						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J	Higa, KD; Boone, KB; Ho, TC				Higa, KD; Boone, KB; Ho, TC			Complications of the laparoscopic Roux-en-Y gastric bypass: 1,040 patients - What have we learned?	OBESITY SURGERY			English	Article; Proceedings Paper	5th Congress of the International-Federation-for-the-Surgery-of-Obesity	SEP   22, 2000	GENOA, ITALY	Int Federat Surg Obes		morbid obesity; bariatric surgery; laparoscopy; gastric bypass	PROSPECTIVE TRIAL; FOLLOW-UP	Background: The Roux-en-Y gastric bypass (RYGBP) is one of the most common operations for morbid obesity. Laparoscopic techniques have been reported, but suffer from small numbers of patients, longer operative times and seemingly higher initial complication rates as compared to the traditional "open" procedure. The minimally invasive approach continues to be a challenge even to the most experienced laparoscopic surgeons. The purpose of this study is to describe our experience and complications of the laparoscopic Roux-en-Y gastric bypass with a totally hand-sewn gastrojejunostomy, Methods: 1,040 consecutive laparoscopic procedures were evaluated prospectively. Only patients who had a previous open gastric procedure were excluded initially, Eventually, even patients with failed "open" bariatric procedures and other gastric procedures were revised laparoscopically to the RYGBP. All patients met NIH criteria for consideration for weight reductive surgery. Results: There were no anastomotic leaks from the hand-sewn gastrojejunostomy. Early complications and open conversions were related to sub-optimal exposure and bowel fixation techniques. Several staple failures were attributed to a manufacturer redesign of an instrument, Average hospital stay was 1.9 days for all patients and 1.5 days for patients without complications, Operative times consistently approach 60 minutes. Average excess weight loss was 70% at 12 months. There were 5 deaths: perioperative pulmonary embolism (1), late pulmonary embolism (2), asthma (1), and suicide (1), Conclusions: The laparoscopic Roux-en-Y gastric bypass for morbid obesity with a totally hand-sewn gastrojejunostomy can be safely performed by the bariatric surgeon with advanced laparoscopic skills in the community setting, Fixation and closure of all potential hernia sites with non-absorbable sutures is essential. Stenosis of the hand-sewn gastrojejunal anastomosis is amenable to endoscopic balloon dilation. Meticulous attention must be paid to the operative and perioperative care of the patient.	Bariatr Surg Ctr, Fresno, CA USA	Higa, KD (reprint author), 7202 N Millbrook Ave,Suite 105, Fresno, CA 93720 USA.						Catona A, 2000, OBES SURG, V10, P15, DOI 10.1381/09608920060674049; de la Torre RA, 1999, OBES SURG, V9, P492, DOI 10.1381/096089299765552800; Doherty C, 1998, J Gastrointest Surg, V2, P102, DOI 10.1016/S1091-255X(98)80110-8; GRUNDY SM, 1991, ANN INTERN MED, V115, P956; Higa KD, 2000, ARCH SURG-CHICAGO, V135, P1029, DOI 10.1001/archsurg.135.9.1029; Miller K, 1999, OBES SURG, V9, P183, DOI 10.1381/096089299765553467; Schauer PR, 1999, J LAPAROENDOSC ADV A, V9, P101, DOI 10.1089/lap.1999.9.101; Serra C, 1999, OBES SURG, V9, P546, DOI 10.1381/096089299765552648; SUGERMAN HJ, 1987, ANN SURG, V205, P613, DOI 10.1097/00000658-198706000-00002; SUGERMAN HJ, 1995, AM J SURG, V169, P91, DOI 10.1016/S0002-9610(99)80115-9; Wittgrove AC, 2000, OBES SURG, V10, P233, DOI 10.1381/096089200321643511	11	366	379	0	9	F D-COMMUNICATIONS INC	TORONTO	3100 BAYVIEW AVE, UNIT 4, TORONTO, ONTARIO MZN 5L3, CANADA	0960-8923			OBES SURG	Obes. Surg.	DEC	2000	10	6					509	513		10.1381/096089200321593706		5	Surgery	Surgery	388DQ	WOS:000166162500005	11175957	
J	Ownby, DR; Johnson, CC; Peterson, EL				Ownby, DR; Johnson, CC; Peterson, EL			Exposure to dogs and cats in the first year of life and risk of allergic sensitization at 6 to 7 years of age	JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION			English	Article							CORD-BLOOD-IGE; HOUSE-DUST ENDOTOXIN; ASTHMATIC-CHILDREN; SERUM IGE; RESPIRATORY SYMPTOMS; BRONCHIAL HYPERRESPONSIVENESS; AUSTRALIAN SCHOOLCHILDREN; ATOPIC SENSITIZATION; PARENTAL HISTORY; MATERNAL SMOKING	Context Childhood asthma is strongly associated with allergic sensitization. Studies have suggested that animal exposure during infancy reduces subsequent allergic sensitization. Objective To evaluate the relationship between dog and cat exposure in the first year of life and allergic sensitization at 6 to 7 years of age. Design, Setting, and Subjects Prospective birth cohort study of healthy, fullterm infants enrolled in a health maintenance organization in suburban Detroit, Mich, who were born between April 15,1987, and August 31,1989, and followed up yearly to a mean age of 6.7 years. Of 835 children initially in the study at birth, 474 (57%) completed follow-up evaluations at age 6 to 7 years. Main Outcome Measures Atopy, defined as any skin prick test positivity to 6 common aeroallergens (dust mites [Dermatophagoides farinae, D pteronyssinus], dog, cat, short ragweed [Ambrosia artemisiifolia], and blue grass [Poa pratensis]); seroatopy, defined as any positive allergen-specific IgE test result for the same 6 allergens or for Alternaria species. Results The prevalence of any skin prick test positivity (atopy) at age 6 to 7 years was 33.6% with no dog or cat exposure in the first year of life, 34.3% with exposure to 1 dog or cat, and 15.4% with exposure to 2 or more dogs or cats (P = .005). The prevalence of any positive allergen-specific IgE test result (seroatopy) was 38.5% with no dog or cat exposure, 41.2% with exposure to 1 dog or cat, and 17.9% with exposure to 2 or more dogs or cats (P = .003). After adjustment for cord serum IgE concentration, sex, older siblings, parental smoking, parental asthma, bedroom dust mite allergen levels at 2 years, and current dog and cat ownership, exposure to 2 or more dogs or cats in the first year of life was associated with a significantly lower risk of atopy (adjusted odds ratio, 0.23; 95% confidence interval, 0.09-0.60) and seroatopy (adjusted odds ratio, 0.33; 95% confidence interval, 0.13-0.83). Conclusion Exposure to 2 or more dogs or cats in the first year of life may reduce subsequent risk of allergic sensitization to multiple allergens during childhood.	Med Coll Georgia, Dept Pediat, Sect Allergy & Immunol, Augusta, GA 30912 USA; Henry Ford Hlth Syst, Dept Biostat & Res Epidemiol, Detroit, MI USA; Wayne State Univ, Natl Inst Environm Hlth Sci Ctr Mol & Cellular To, Detroit, MI USA	Ownby, DR (reprint author), Med Coll Georgia, Dept Pediat, Sect Allergy & Immunol, BG-1019, Augusta, GA 30912 USA.			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Am. Med. Assoc.	AUG 28	2002	288	8					963	972		10.1001/jama.288.8.963		10	Medicine, General & Internal	General & Internal Medicine	587RM	WOS:000177656400021	12190366	
J	Bornehag, CG; Sundell, J; Weschler, CJ; Sigsgaard, T; Lundgren, B; Hasselgren, M; Hagerhed-Engman, L				Bornehag, CG; Sundell, J; Weschler, CJ; Sigsgaard, T; Lundgren, B; Hasselgren, M; Hagerhed-Engman, L			The association between asthma and allergic symptoms in children and phthalates in house dust: A nested case-control study	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; BBzP; children; DEHP; homes; phthalates	SUBCUTANEOUS INJECTION MODEL; EXPERT PANEL REPORT; NONINDUSTRIAL INDOOR ENVIRONMENTS; AIRBORNE PARTICULATE MATTER; HUMAN REFERENCE POPULATION; DI-N-BUTYL; DEVELOPMENTAL TOXICITY; HUMAN-REPRODUCTION; NTP CENTER; DI(2-ETHYLHEXYL) PHTHALATE	Global phthalate ester production has increased from very low levels at the end of World War II to approximately 3.5 million metric tons/year. The aim of the present study was to investigate potential associations between persistent allergic symptoms in children, which have increased markedly in developed countries over the past three decades, and the concentration of phthalates in dust collected from their homes. This investigation is a case-control study nested within a cohort of 10,852 children. From the cohort, we selected 198 cases with persistent allergic symptoms and 202 controls without allergic symptoms. A clinical and a technical team investigated each child and her or his environment. We found higher median concentrations of butyl benzyl phthalate (BBzP) in dust among cases than among controls (0.15 vs. 0.12 mg/g dust). Analyzing the case group by symptoms showed that BBzP was associated with rhinitis (p = 0.001) and eczema (p = 0.001), whereas di(2-ethylhexyl) phthalate (DEHP) was associated with asthma (p = 0.022). Furthermore, dose-response relationships for these associations are supported by trend analyses. This study, shows that phthalates, within the range of what is normally found in indoor environments, are associated with allergic symptoms in children. We believe that the different associations of symptoms for the three major phthalates-BBzP, DEHP, and di-n-butyl phthalate-can be explained by a combination of chemical physical properties and toxicologic potential. Given the phthalate exposures of children worldwide, the results from this study of Swedish children have global implications.	Karlstad Univ, S-65188 Karlstad, Sweden; Swedish Natl Testing & Res Inst, Boras, Sweden; Tech Univ Denmark, DK-2800 Lyngby, Denmark; Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Piscataway, NJ 08854 USA; Rutgers State Univ, Piscataway, NJ USA; Aarhus Univ, Aarhus, Denmark	Bornehag, CG (reprint author), Karlstad Univ, S-65188 Karlstad, Sweden.	carl-gustaf.bornehag@kau.se	Sundell, Jan/B-2857-2012; Weschler, Charles/A-9788-2009	Weschler, Charles/0000-0002-9097-5850; Sigsgaard, Torben/0000-0002-2043-7571			Adibi JJ, 2003, ENVIRON HEALTH PERSP, V111, P1719, DOI 10.1289/ehp.6235; Ahlbom A, 1998, INDOOR AIR, V8, P219, DOI 10.1111/j.1600-0668.1998.00003.x; Andersson K, 1997, INDOOR AIR, V7, P78, DOI 10.1111/j.1600-0668.1997.t01-2-00002.x; ATLAS E, 1981, SCIENCE, V211, P163, DOI 10.1126/science.211.4478.163; Barr DB, 2003, ENVIRON HEALTH PERSP, V111, P1148, DOI 10.1289/ehp.6074; Beasley R, 2003, PEDIATR CLIN N AM, V50, P539, DOI 10.1016/S0031-3955(03)00050-6; Blount BC, 2000, ENVIRON HEALTH PERSP, V108, P979, DOI 10.1289/ehp.00108979; Bornehag CG, 2001, INDOOR AIR, V11, P72; Bornehag CG, 2003, ALLERGY, V58, P939, DOI 10.1034/j.1398-9995.2003.00050.x; Butte W, 2001, GEFAHRST REINHALT L, V61, P19; Cadogan DF, 1996, KIRKOTHMER ENCY CHEM, V19, P258; CAUTREELS W, 1976, ATMOS ENVIRON, V10, P447, DOI 10.1016/0004-6981(76)90025-1; CAUTREELS W, 1976, WATER AIR SOIL POLL, V6, P103; *CDC, 2003, 2 CDC NAT CTR ENV HL; Clausen PA, 2003, J CHROMATOGR A, V986, P179, DOI 10.1016/S0021-9673(02)02007-1; Etzel RA, 2003, PEDIATRICS, V112, P233; Fromme H, 2004, INDOOR AIR, V14, P188, DOI 10.1046/j.1600-0668.2003.00223.x; GIAM CS, 1978, SCIENCE, V199, P419, DOI 10.1126/science.199.4327.419-a; Jaakkola JJK, 1999, AM J PUBLIC HEALTH, V89, P188, DOI 10.2105/AJPH.89.2.188; Kavlock R, 2002, REPROD TOXICOL, V16, P529, DOI 10.1016/S0890-6238(02)00032-1; Kavlock R, 2002, REPROD TOXICOL, V16, P489, DOI 10.1016/S0890-6238(02)00033-3; Kavlock R, 2002, REPROD TOXICOL, V16, P453, DOI 10.1016/S0890-6238(02)00029-1; Koch HM, 2003, INT J HYG ENVIR HEAL, V206, P77, DOI 10.1078/1438-4639-00205; Kohn M.C., 2000, ENV HLTH PERSPECT, V108, P440; Koo JW, 2002, ENVIRON HEALTH PERSP, V110, P405; Larsen ST, 2003, FOOD CHEM TOXICOL, V41, P439, DOI 10.1016/S0278-6915(02)00248-X; Larsen ST, 2002, PHARMACOL TOXICOL, V91, P264, DOI 10.1034/j.1600-0773.2002.910508.x; Larsen ST, 2001, TOXICOL LETT, V125, P11; Larsen ST, 2001, TOXICOLOGY, V169, P37, DOI 10.1016/S0300-483X(01)00484-X; Nazaroff WW, 2003, ATMOS ENVIRON, V37, P5451, DOI 10.1016/j.atmosenv.2003.09.021; *NTP, 2003, 10 NTP; Oie L, 1997, ENVIRON HEALTH PERSP, V105, P972; Palmer A., 1997, UMWELT GESUNDHEIT, V8, P79; Rudel RA, 2003, ENVIRON SCI TECHNOL, V37, P4543, DOI 10.1021/es0264596; Schneider T, 2003, INDOOR AIR, V13, P38, DOI 10.1034/j.1600-0668.2003.02025.x; Strachan DP, 2000, BRIT MED BULL, V56, P865, DOI 10.1258/0007142001903562; *UN, 2000, LEAG TABL CHILD POV; Wargocki P, 2002, INDOOR AIR, V12, P113, DOI 10.1034/j.1600-0668.2002.01145.x; WESCHLER CJ, 1984, ENVIRON SCI TECHNOL, V18, P648, DOI 10.1021/es00127a004; WESCHLER CJ, 1980, ENVIRON SCI TECHNOL, V14, P428, DOI 10.1021/es60164a008	40	362	384	9	113	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	2004	112	14					1393	1397		10.1289/ehp.7187		5	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	860JG	WOS:000224337900034	15471731	
J	Riedler, J; Eder, W; Oberfeld, G; Schreuer, M				Riedler, J; Eder, W; Oberfeld, G; Schreuer, M			Austrian children living on a farm have less hay fever, asthma and allergic sensitization	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergic sensitization; asthma; farm; hay fever	ENVIRONMENTAL-FACTORS; EAST-GERMANY; PREVALENCE; SCHOOLCHILDREN; ATOPY; STIMULATION; EXPOSURE; SYMPTOMS; IL-12; TH1	Background and objectives In some studies, the prevalence of hay fever and asthma has been found to be lower in children from rural areas than in children from an urban environment. We hypothesized that living on a farm might be protective against development of allergic sensitization and allergic diseases. Methods In a cross-sectional survey, parents of 2283 children aged 8-10 years from a mostly rural area in Austria answered a standardized questionnaire on allergic diseases and environmental factors. 1137 children performed a skin prick test to seven local allergens. Results The prevalence of hay fever (3.1 vs 10.3%, P = 0.0002), asthma (1.1 vs 3.9%, P = 0.017) and a positive skin prick reactivity to at least one of the common local allergens (18.8 vs 32.7%, P = 0.001) was significantly lower in children living on a farm than in children from a non-farming environment. In a multivariate logistic regression model, adjusting for genetic background, parent education, living and housing conditions and dietary factors did not change the odds ratio for the association of farming and allergic sensitization. Only after including 'regular contact with livestock and poultry' into the model did the odds ratio change significantly (cOR 0.48 95% CI 0.30-0.75 to aOR 0.75 95% CI 0.37-1.52) indicating an association between regular contact with farm animals and reduced risk of atopic sensitization. Conclusion Possible explanations for the lower prevalence of hay fever, asthma and allergic sensitization in children living on a farm might be the development of immunotolerance or the stimulation of TH1 cells and suppression of TH2 cells by increased exposure of farm children to microbial antigens in the stables or farmhouses.	Childrens Hosp, A-5020 Salzburg, Austria; Salzburg Univ, Dept Publ Hlth, A-5020 Salzburg, Austria; Salzburg Univ, Dept Sociol, A-5020 Salzburg, Austria	Riedler, J (reprint author), Childrens Hosp, Muellner Hauptstr 48, A-5020 Salzburg, Austria.						BJORKSTEN B, 1994, ALLERGY, V49, P400, DOI 10.1111/j.1398-9995.1994.tb00831.x; BraunFahrlander C, 1997, AM J RESP CRIT CARE, V155, P1042; BRAUNFAHRLANDER C, 1996, EPIDEMIOLOGY, V7, pS47; BURR M L, 1989, Archives of Disease in Childhood, V64, P1452; CORBO GM, 1993, J ALLERGY CLIN IMMUN, V92, P616, DOI 10.1016/0091-6749(93)90086-U; Holt PG, 1997, CURR OPIN IMMUNOL, V9, P782, DOI 10.1016/S0952-7915(97)80178-1; HOLT PG, 1995, PEDIATR ALLERGY IMMU, V6, P1, DOI 10.1111/j.1399-3038.1995.tb00250.x; *ISAAC STEER COMM, 1998, LANCET, V351, P1255; Jenmalm MC, 1998, J ALLERGY CLIN IMMUN, V102, P671, DOI 10.1016/S0091-6749(98)70286-6; Kilpelainen M., 1997, European Respiratory Journal Supplement, V10, p143S; MACATONIA SE, 1995, J IMMUNOL, V154, P5071; Murosaki S, 1998, J ALLERGY CLIN IMMUN, V102, P57, DOI 10.1016/S0091-6749(98)70055-7; NINAN TK, 1992, BRIT MED J, V304, P873; Oberfeld G., 1998, European Respiratory Journal, V12, p211S; POPP W, 1989, ALLERGY, V44, P572, DOI 10.1111/j.1398-9995.1989.tb04202.x; Riedler J, 1998, EUR RESPIR J, V11, P355, DOI 10.1183/09031936.98.11020355; ROBERTSON CF, 1991, BRIT MED J, V302, P1116; ROMAGNANI S, 1992, INT ARCH ALLERGY IMM, V98, P279; ULEVITCH RJ, 1995, ANNU REV IMMUNOL, V13, P437, DOI 10.1146/annurev.iy.13.040195.002253; von Mutius E, 1998, LANCET, V351, P862, DOI 10.1016/S0140-6736(97)10100-3; VONMUTIUS E, 1994, AM J RESP CRIT CARE, V149, P358; vonMutius E, 1996, BRIT MED J, V312, P1448; VONOHRENSTEIN V, 1998, EPIDEMIOLOGY, V9, pS118	23	360	364	4	33	BLACKWELL SCIENCE LTD	OXFORD	P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	FEB	2000	30	2					194	200				7	Allergy; Immunology	Allergy; Immunology	287NF	WOS:000085511600008	10651771	
J	Dang, JM; Leong, KW				Dang, Jiyoung M.; Leong, Kam W.			Natural polymers for gene delivery and tissue engineering	ADVANCED DRUG DELIVERY REVIEWS			English	Review						gene delivery; gene therapy; tissue engineering; natural polymers; collagen; alginate; chitosan; regenerative medicine	CHITOSAN-DNA NANOPARTICLES; MESENCHYMAL STEM-CELLS; DUST MITE ALLERGEN; IN-VIVO; PLASMID DNA; TRANSFECTION EFFICIENCY; INTRACELLULAR TRAFFICKING; CATIONIZED GELATIN; DRUG-DELIVERY; WOUND REPAIR	Although the field of gene delivery is dominated by viral vectors and synthetic polymeric or lipid gene carriers, natural polymers offer distinct advantages and may help advance the field of non-viral gene therapy. Natural polymers, such as chitosan, have been successful in oral and nasal delivery due to their mucoadhesive properties. Collagen has broad utility as gene activated matrices, capable of delivering large quantities of DNA in a direct, localized manner. Most natural polymers contain reactive sites amenable for ligand conjugation, cross-linking, and other modifications that can render the polymer tailored for a range of clinical applications. Natural polymers also often possess good cytocompatibility, making them popular choices for tissue engineering scaffolding applications. The marriage of gene therapy and tissue engineering exploits the power of genetic cell engineering to provide the biochemical signals to influence proliferation or differentiation of cells. Natural polymers with their ability to serve as gene carriers and tissue engineering scaffolds are poised to play an important role in the field of regenerative medicine. This review highlights the past and present research on various applications of natural polymers as particulate and matrix delivery vehicles for gene delivery. (c) 2006 Elsevier B.V All rights reserved.	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Drug Deliv. Rev.	JUL 7	2006	58	4					487	499		10.1016/j.addr.2006.03.001		13	Pharmacology & Pharmacy	Pharmacology & Pharmacy	062YE	WOS:000238982100003	16762443	
J	Hirschfeld, RMA; Calabrese, JR; Weissman, MM; Reed, M; Davies, MA; Frye, MA; Keck, PE; Lewis, L; McElroy, SL; McNulty, JP; Wagner, KD				Hirschfeld, RMA; Calabrese, JR; Weissman, MM; Reed, M; Davies, MA; Frye, MA; Keck, PE; Lewis, L; McElroy, SL; McNulty, JP; Wagner, KD			Screening for bipolar disorder in the community	JOURNAL OF CLINICAL PSYCHIATRY			English	Article							PSYCHIATRIC-DISORDERS; UNITED-STATES; SPECTRUM DISORDER; AMERICAN MIGRAINE; YOUNG-ADULTS; PREVALENCE; MANIA; EPIDEMIOLOGY; DIAGNOSIS; SUICIDALITY	Background: Our goal was to estimate the rate of positive screens for bipolar I and bipolar II disorders in the general population of the United States. Method: The Mood Disorder Questionnaire (MDQ), a validated screening instrument for bipolar I and II disorders, was sent to a sample of 127,800 people selected to represent the U.S. adult population by demographic variables. 85,358 subjects (66.8% response rate) that were 18 years of age or above returned the survey and had usable data. Of the nonrespondents, 3404 subjects matched demographically to the 2000 U.S. Census data completed a telephone interview to estimate nonresponse bias. Results: The overall positive screen rate for bipolar I and II disorders, weighted to match the 2000 U.S. Census demographics, was 3.4%. When adjusted for the nonresponse bias, the rate rose to 3.7%. Only 19.8% of the individuals with positive screens for bipolar I or II disorders reported that they had previously received a diagnosis of bipolar disorder from a physician, whereas 31.2% reported receiving a diagnosis of unipolar depression. An additional 49.0% reported receiving no diagnosis of either bipolar disorder or unipolar depression. Positive screens were more frequent in young adults and low income house-holds. The rates of migraine, allergies, asthma, and alcohol and drug abuse were substantially higher among those with positive screens. Conclusion: The positive MDQ screen rate of 3.7% suggests that nearly 4% of American adults may suffer from bipolar I and II disorders. Young adults and individuals with lower income are at greater risk for this largely underdiagnosed disorder.	Univ Texas, Med Branch, Dept Psychiat & Behav Sci, Galveston, TX 77555 USA; Natl Alliance Mentally Ill, Alexandria, VA USA; Depress & Bipolar Support Alliance, Chicago, IL USA; Univ Cincinnati, Coll Med, Dept Psychiat, Cincinnati, OH USA; Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA; Vedanta Associates Inc, Chapel Hill, NC USA; New York State Psychiat Inst & Hosp, New York, NY 10032 USA; Columbia Univ Coll Phys & Surg, New York, NY 10032 USA; Case Western Reserve Univ, Dept Psychiat, Cleveland, OH 44106 USA	Hirschfeld, RMA (reprint author), Univ Texas, Med Branch, Dept Psychiat & Behav Sci, 1-302 Rebecca Sealy,301 Univ Blvd, Galveston, TX 77555 USA.			Weissman, Myrna/0000-0003-3490-3075	NIMH NIH HHS [R01 MH079261]		Akiskal HS, 2000, J AFFECT DISORDERS, V59, pS5, DOI 10.1016/S0165-0327(00)00203-2; Akiskal H. 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Clin. Psychiatry	JAN	2003	64	1					53	59				7	Psychology, Clinical; Psychiatry	Psychology; Psychiatry	641PQ	WOS:000180754500010	12590624	
J	Li, N; Xia, T; Nel, AE				Li, Ning; Xia, Tian; Nel, Andre E.			The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles	FREE RADICAL BIOLOGY AND MEDICINE			English	Review						particulate matter; oxidative stress; asthma; dendritic cells; adjuvant effect; nanotoxicology; free radicals	DIESEL EXHAUST PARTICLES; AIRWAY EPITHELIAL-CELLS; RAT ALVEOLAR MACROPHAGES; EXHALED CARBON-MONOXIDE; LONG-TERM EXPOSURE; HOUSE-DUST MITE; DENDRITIC CELLS; CYTOKINE PRODUCTION; REACTIVE OXYGEN; IN-VITRO	Ambient particulate matter (PM) is an environmental factor that has been associated with increased respiratory morbidity and mortality. The major effect of ambient PM on the pulmonary system is the exacerbation of inflammation, especially in susceptible people. One of the mechanisms by which ambient PM exerts its proinflammatory effects is the generation of oxidative stress by its chemical compounds and metals. Cellular responses to PM-induced oxidative stress include activation of antioxidant defense, inflammation, and toxicity. The proinflammatory effect of PM in the lung is characterized by increased cytokine/chemokine production and adhesion molecule expression. Moreover, there is evidence that ambient PM can act as an adjuvant for allergic sensitization, which raises the possibility that long-term PM exposure may lead to increased prevalence of asthma. In addition to ambient PM, rapid expansion of nanotechnology has introduced the potential that engineered nanoparticles (NP) may also become airborne and may contribute to pulmonary diseases by novel mechanisms that could include oxidant injury. Currently, little is known about the potential adverse health effects of these particles. In this communication, the mechanisms by which particulate pollutants, including ambient PM and engineered NP, exert their adverse effects through the generation of oxidative stress and the impacts of oxidant injury in the respiratory tract will be reviewed. The importance of cellular antioxidant and detoxification pathways in protecting against particle-induced lung damage will also be discussed. (c) 2008 Elsevier Inc. All rights reserved.	[Li, Ning; Xia, Tian; Nel, Andre E.] Univ Calif Los Angeles, Dept Med, Div NanoMed, Los Angeles, CA 90095 USA; [Li, Ning; Nel, Andre E.] Univ Calif Los Angeles, Asthma & Allerg Dis Cooperat Res Ctr, Los Angeles, CA 90095 USA; [Li, Ning; Nel, Andre E.] Univ Calif Los Angeles, So Calif Particle Ctr, Los Angeles, CA 90095 USA; [Nel, Andre E.] Univ Calif Los Angeles, Calif NanoSyst Inst, Los Angeles, CA 90095 USA	Nel, AE (reprint author), Univ Calif Los Angeles, Dept Med, Div NanoMed, Los Angeles, CA 90095 USA.	anel@mednet.ucla.edu	xia, tian/C-3158-2013; Nel, Andre/J-2808-2012	xia, tian/0000-0003-0123-1305; 	NIAID NIH HHS [U19 AI070453, U19 AI070453-01]; NIEHS NIH HHS [R01 ES010553, R01 ES010553-05, R01 ES015498, R01 ES015498-02, R01 ES10553]		ADES EW, 1992, J INVEST DERMATOL, V99, P683, DOI 10.1111/1523-1747.ep12613748; Antonini JM, 2004, MOL CELL BIOCHEM, V255, P257, DOI 10.1023/B:MCBI.0000007281.32126.2c; Arimoto T, 1999, JPN J PHARMACOL, V80, P49, DOI 10.1254/jjp.80.49; Baeza-Squiban A, 1999, CELL BIOL TOXICOL, V15, P375, DOI 10.1023/A:1007653900063; 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Biol. Med.	MAY 1	2008	44	9					1689	1699		10.1016/j.freeradbiomed.2008.01.028		11	Biochemistry & Molecular Biology; Endocrinology & Metabolism	Biochemistry & Molecular Biology; Endocrinology & Metabolism	293OB	WOS:000255343500001	18313407	
J	Katz, LF; Kling, JR; Liebman, JB				Katz, LF; Kling, JR; Liebman, JB			Moving to opportunity in Boston: Early results of a randomized mobility experiment	QUARTERLY JOURNAL OF ECONOMICS			English	Article							CHILDREN; NEIGHBORHOODS; IDENTIFICATION; EXTERNALITIES; EDUCATION; COMMUNITY; PROGRAM; MATTER; CITY	We examine short-run impacts of changes in residential neighborhoods on the well-being of families residing in high-poverty public housing projects who received Section 8 housing vouchers through a random lottery. Households offered vouchers experienced improvements in multiple measures of well-being relative to a control group, including increased safety, improved health among household heads, and fewer behavior problems among boys. There were no significant short-run impacts of vouchers on the employment, earnings, or welfare receipt of household heads. Children in households offered vouchers valid only in low poverty neighborhoods also had reduced likelihood of injuries, asthma attacks, and victimizations by crime.	Harvard Univ, Cambridge, MA 02138 USA; Natl Bur Econ Res, Cambridge, MA 02138 USA; Princeton Univ, Princeton, NJ 08544 USA	Katz, LF (reprint author), Harvard Univ, Cambridge, MA 02138 USA.						Aaronson D, 1998, J HUM RESOUR, V33, P915, DOI 10.2307/146403; Angrist JD, 1996, J AM STAT ASSOC, V91, P444, DOI 10.2307/2291629; Augustyn M., 1995, CONT PEDIAT, V12, P35; BENABOU R, 1993, Q J ECON, V108, P619, DOI 10.2307/2118403; Black SE, 1999, Q J ECON, V114, P577, DOI 10.1162/003355399556070; BLOOM HS, 1984, EVALUATION REV, V8, P225, DOI 10.1177/0193841X8400800205; BORJAS GJ, 1995, AM ECON REV, V85, P365; McLoyd V., 1999, NEW HOPE PEOPLE LOW; BROCK WA, 2000, IN PRESS HDB ECONOME, V5; BROOKSGUNN J, 1993, AM J SOCIOL, V99, P353, DOI 10.1086/230268; *BUR JUST STAT, 1994, NCJ151172 US DEP JUS; Case A. 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J	Li, N; Hao, MQ; Phalen, RF; Hinds, WC; Nel, AE				Li, N; Hao, MQ; Phalen, RF; Hinds, WC; Nel, AE			Particulate air pollutants and asthma - A paradigm for the role of oxidative stress in PM-induced adverse health effects	CLINICAL IMMUNOLOGY			English	Review						antioxidant enzyme; asthma exacerbation; diesel exhaust particles; inflammation; particulate matter; polycyclic aromatic hydrocarbons; quinone; reactive oxygen species; redox cycling; stratified oxidative stress response	DIESEL EXHAUST PARTICLES; GLUTATHIONE-S-TRANSFERASE; INDUCED EOSINOPHILIC INFLAMMATION; ANTIOXIDANT RESPONSE ELEMENTS; BRONCHIAL EPITHELIAL-CELLS; EXPIRED BREATH CONDENSATE; MURINE STRAIN DIFFERENCES; EXHALED CARBON-MONOXIDE; NITRIC-OXIDE; SUPEROXIDE-DISMUTASE	Asthma is a chronic inflammatory disease, which involves a variety of different mediators, including reactive oxygen species. There is growing awareness that particulate pollutants act as adjuvants during allergic sensitization and can also induce acute asthma exacerbations. In this communication we review the role of oxidative stress in asthma, with an emphasis on the pro-oxidative effects of diesel exhaust particles and their chemicals in the respiratory tract. We review the biology of oxidative stress, including protective and injurious effects that explain the impact of particulate matter-induced oxidative stress in asthma. (C) 2003 Elsevier Inc. All rights reserved.	Univ Calif Los Angeles, Dept Med, Div Clin Immunol & Allergy, Los Angeles, CA 90095 USA; Univ Calif Irvine, Dept Community & Environm Med, Irvine, CA 92717 USA; Univ Calif Los Angeles, Sch Publ Hlth, Dept Environm Hlth Sci, Los Angeles, CA 90024 USA; So Calif Particulate Ctr & Supersite, Los Angeles, CA USA	Nel, AE (reprint author), Univ Calif Los Angeles, Dept Med, Div Clin Immunol & Allergy, 52-175 CHS,10833 Le Conte Ave, Los Angeles, CA 90095 USA.		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Immunol.	DEC	2003	109	3					250	265		10.1016/j.clim.2003.08.006		16	Immunology	Immunology	756XM	WOS:000187511100002	14697739	
J	Arbes, SJ; Gergen, PJ; Elliott, L; Zeldin, DC				Arbes, SJ; Gergen, PJ; Elliott, L; Zeldin, DC			Prevalences of positive skin test responses to 10 common allergens in the US population: Results from the Third National Health and Nutrition Examination Survey	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergens; allergic sensitization; allergy skin test; epidemiology; NHANES II; NHANES III; survey	TEST REACTIVITY; AEROALLERGENS; SMOKING; ASTHMA; LEAD; IGE	Background: Allergy skin tests were administered in the second and third National Health and Nutrition Examination Surveys (NHANES II and III) conducted in the United States from 1976 through 1980 and 1988 through 1994, respectively. Objectives: This study estimated positive skin test response rates in NHANES III and identified predictors of one or more positive test responses. Comparisons with NHANES II were also made. Methods: In NHANES III, 10 allergens and 2 controls were tested in all subjects aged 6 to 19 years and a random half-sample of subjects aged 20 to 59 years. A wheal-based definition of a positive test response was used. Results: In NHANES III, 54.3% of the population had positive test responses to 1 or more allergens. Prevalences were 27.5% for dust mite, 26.9% for perennial rye, 26.2% for short ragweed, 26.1% for German cockroach, 18.1% for Bermuda grass, 17.0% for cat, 15.2% for Russian thistle, 13.2% for white oak, 12.9% for Alternaria alternata, and 8.6% for peanut. Among those with positive test responses, the median number of positive responses was 3.0. Adjusted odds of a positive test response were higher for the following variables: age of 20 to 29 years, male sex, minority race, western region, old homes, and lower serum cotinine levels. For the 6 allergens common to NHANES II and III, prevalences were 2.1 to 5.5 times higher in NHANES III. Conclusions: The majority of the US population represented in NHANES III was sensitized to 1 or more allergens. Whether the higher prevalences observed in NHANES III reflect true changes in prevalence or methodological differences between the surveys cannot be determined with certainty.	NIEHS, NIH, Lab Resp Biol, Div Intramural Res, Res Triangle Pk, NC 27709 USA; NIAID, Div Allergy Immunol & Transplantat, NIH, Bethesda, MD 20892 USA	Zeldin, DC (reprint author), NIEHS, NIH, Lab Resp Biol, Div Intramural Res, POB 12233, Res Triangle Pk, NC 27709 USA.	zeldin@niehs.nih.gov					Arbes SJ, 2004, J ALLERGY CLIN IMMUN, V114, P111, DOI 10.1016/j.jaci.2004.04.036; Arbes SJ, 2003, J ALLERGY CLIN IMMUN, V111, P408, DOI 10.1067/mai.2003.16; BARBEE RA, 1981, J ALLERGY CLIN IMMUN, V68, P106, DOI 10.1016/0091-6749(81)90167-6; BURROWS B, 1982, J ALLERGY CLIN IMMUN, V70, P199, DOI 10.1016/0091-6749(82)90042-2; Cohn RD, 2004, J ALLERGY CLIN IMMUN, V113, P1167, DOI 10.1016/j.jaci.2003.12.592; GERGEN PJ, 1987, J ALLERGY CLIN IMMUN, V80, P669, DOI 10.1016/0091-6749(87)90286-7; GERGEN PJ, 1986, NATL CTR HIGH STAT U; GLEICH GJ, 1976, J ALLERGY CLIN IMMUN, V58, P31, DOI 10.1016/0091-6749(76)90104-4; Linneberg A, 2000, J ALLERGY CLIN IMMUN, V106, P247, DOI 10.1067/mai.2000.108312; Mannino D. M., 2002, MMWR-MORBID MORTAL W, V51, P1; NAKAGOMI T, 1994, LANCET, V343, P121, DOI 10.1016/S0140-6736(94)90854-0; *NAT CTR HLTH STAT, 1986, PUBL US DAT TAP DOC; *NAT HLTH NUTR EX, TRAIN MAN ALL COMP; Robertson CF, 2004, MED J AUSTRALIA, V180, P273; Rose G, 2001, B WORLD HEALTH ORGAN, V79, P990; SIBBALD B, 1990, BRIT J GEN PRACT, V40, P338; Sopori ML, 1998, J NEUROIMMUNOL, V83, P148, DOI 10.1016/S0165-5728(97)00231-2; Stevenson LA, 2001, J ALLERGY CLIN IMMUN, V108, P747, DOI 10.1067/mai.2001.119410; Strachan DP, 1998, THORAX, V53, P117; Verlato G, 2003, J ALLERGY CLIN IMMUN, V111, P1232, DOI 10.1067/mai.2003.1484; 1909, VITAL HLTH STAT, P1; 2001, ASTHMA PREVALENCE HL	22	351	355	0	12	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749	1097-6825		J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	AUG	2005	116	2					377	383		10.1016/j.jaci.2005.05.017		7	Allergy; Immunology	Allergy; Immunology	017ID	WOS:000235686400021	16083793	
J	Gauderman, WJ; Vora, H; McConnell, R; Berhane, K; Gilliland, F; Thomas, D; Lurmann, F; Avol, E; Kunzli, N; Jerrett, M; Peters, J				Gauderman, W. James; Vora, Hita; McConnell, Rob; Berhane, Kiros; Gilliland, Frank; Thomas, Duncan; Lurmann, Fred; Avol, Edward; Kunzli, Nino; Jerrett, Michael; Peters, John			Effect of exposure to traffic on lung development from 10 to 18 years of age: a cohort study	LANCET			English	Article							SOUTHERN CALIFORNIA COMMUNITIES; AMBIENT NITROGEN-DIOXIDE; OUTDOOR AIR-POLLUTION; PULMONARY-FUNCTION; RESPIRATORY HEALTH; FUNCTION GROWTH; CHILDHOOD ASTHMA; MAJOR HIGHWAY; PREADOLESCENT CHILDREN; ULTRAFINE PARTICLES	Background Whether local exposure to major roadways adversely affects lung-function growth during the period of rapid lung development that takes place between 10 and 18 years of age is unknown. This study investigated the association between residential exposure to traffic and 8-year lung-function growth. Methods In this prospective study, 3677 children (mean age 10 years [SD 0.44]) participated from 12 southern California communities that represent a wide range in regional air quality. Children were followed up for 8 years, with yearly lung-function measurements recorded. For each child, we identified several indicators of residential exposure to traffic from large roads. Regression analysis was used to establish whether 8-year growth in lung function was associated with local traffic exposure, and whether local traffic effects were independent of regional air quality Findings Children who lived within 500 m of a freeway (motorway) had substantial deficits in 8-year growth of forced expiratory volume in 1 s (FEV(1)-81 mL, p=0.01 [95% CI -143 to -18]) and maximum midexpiratory flow rate (MMEF, -127 mL/s, p=0.03 [-243 to -11), compared with children who lived at least 1500 m from a freeway. joint models showed that both local exposure to freeways and regional air pollution had detrimental, and independent, effects on lung-function growth. Pronounced deficits in attained lung function at age 18 years were recorded for those living within 500 m of a freeway, with mean percent-predicted 97.0% for FEV(1) (p=0.013, relative to >1500 m [95% CI 94.6-99.4]) and 93.4% for MMEF (p=0.006 [95% CI 89.1-97.7]). Interpretation Local exposure to traffic on a freeway has adverse effects on children's lung development, which are independent of regional air quality, and which could result in important deficits in attained lung function in later life.	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J	Cox, L; Nelson, H; Lockey, R; Calabria, C; Chacko, T; Finegold, I; Nelson, M; Weber, R; Bernstein, DI; Blessing-Moore, J; Khan, DA; Lang, DM; Nicklas, RA; Oppenheimer, J; Portnoy, JM; Randolph, C; Schuller, DE; Spector, SL; Tilles, S; Wallace, D				Cox, Linda; Nelson, Harold; Lockey, Richard; Calabria, Christopher; Chacko, Thomas; Finegold, Ira; Nelson, Michael; Weber, Richard; Bernstein, David I.; Blessing-Moore, Joann; Khan, David A.; Lang, David M.; Nicklas, Richard A.; Oppenheimer, John; Portnoy, Jay M.; Randolph, Christopher; Schuller, Diane E.; Spector, Sheldon L.; Tilles, Stephen; Wallace, Dana			Allergen immunotherapy: A practice parameter third update	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Allergy immunotherapy; subcutaneous immunotherapy; sublingual immunotherapy; allergic rhinitis; asthma; Hymenoptera; atopic dermatitis; anaphylaxis; epinephrine; beta-blockers; angiotensin-converting enzyme inhibitor; epicutaneous immunotherapy; intralymphatic immunotherapy; nasal immunotherapy	GRASS-POLLEN IMMUNOTHERAPY; HOUSE-DUST-MITE; DERMATOPHAGOIDES-PTERONYSSINUS EXTRACT; IMPORTED FIRE ANT; PLACEBO-CONTROLLED TRIAL; LOCAL NASAL IMMUNOTHERAPY; RAGWEED HAY-FEVER; HYMENOPTERA VENOM IMMUNOTHERAPY; BETA-ADRENERGIC-BLOCKADE; INTRADERMAL SKIN-TESTS		[Cox, Linda] Nova SE Univ, Coll Osteopath Med, Dept Med, Davie, FL USA; [Lockey, Richard] James A Haley Vet Hosp, Tampa, FL 33612 USA; [Lockey, Richard] Univ S Florida, Coll Med, Dept Internal Med, Div Allergy & Immunol, Tampa, FL 33612 USA; [Nelson, Harold] Natl Jewish Hlth, Dept Med, Denver, CO USA; [Bernstein, David I.] Univ Cincinnati, Coll Med, Dept Med & Environm Hlth, Cincinnati, OH USA; [Khan, David A.] Univ Texas SW Med Ctr Dallas, Dept Internal Med, Dallas, TX 75390 USA; [Blessing-Moore, Joann] Stanford Univ, Med Ctr, Dept Immunol, Dept Med, Palo Alto, CA 94304 USA; [Blessing-Moore, Joann] Stanford Univ, Med Ctr, Dept Immunol, Dept Pediat, Palo Alto, CA 94304 USA; [Lang, David M.] Cleveland Clin Fdn, Allergy Immunol Sect, Div Med Allergy & Immunol, Fellowship Training Program, Cleveland, OH 44195 USA; [Nicklas, Richard A.] George Washington Med Ctr, Dept Med, Washington, DC USA; [Oppenheimer, John] Univ Med & Dent New Jersey, Pulm & Allergy Associates, Dept Internal Med, Morristown, NJ USA; [Portnoy, Jay M.] Univ Missouri, Childrens Mercy Hosp, Kansas City Sch Med, Dept Pediat,Sect Allergy Asthma & Immunol, Kansas City, MO 64108 USA; [Randolph, Christopher] Yale Univ, New Haven, CT USA; [Schuller, Diane E.] Penn State Univ, Milton S Hershey Med Ctr, Dept Pediat, Hershey, PA 17033 USA; [Spector, Sheldon L.] Univ Calif Los Angeles, Sch Med, Dept Med, Los Angeles, CA 90024 USA; [Tilles, Stephen] Univ Washington, Sch Med, Dept Med, Redmond, WA USA	Cox, L (reprint author), Joint Council Allergy Asthma & Immunol, 50 N Brockway St 3-3, Palatine, IL 60067 USA.	lindaswolfcox@msn.com			Stallergenes; ALK-Abello; Department of Defense; Novartis; GlaxoSmithKline; Merck; Schering-Plough; Meda; Vanberg Family Foundation; Sellars Family Foundation; Genentech/Novartis; AstraZeneca; Genentech; US Department of Housing and Urban Development; Aventis; Pharmaxis; Boehringer Ingelheim; Johnson Johnson; Xyzal; Alcon; Centocor; Sepracor; UCB; Amgen; Capnia; IVAX; Amphastar; Astellas; Ception; Icagen; MAP Pharma; Roxane	L. Cox is a consultant for Genentech/Novartis, Hollister-Stier, and Stallergenes; is a speaker for Novartis; has received research support from Stallergenes; is on the Board of Directors for the American Board of Allergy and Immunology; and is on the US Food and Drug Administration (FDA)'s Allergenic Product Advisory Committee. H. Nelson is a consultant for Merck and Planet Biopharmaceuticals, is a Data and Safety Monitoring Board member of DBV Technologies, and has received research support from ALK-Abello. M. Nelson has received research support from the Department of Defense, is a speaker for the American College of Allergy, Asthma & Immunology (ACAAI), and is a member of the FDA's Advisory Committee on Allergic Products. R. Weber is on the speakers' bureau for AstraZeneca and Genentech, has received research support from Novartis and GlaxoSmithKline, and is Committee Chair of the ACAAI. D. I. Bernstein is a consultant and on the advisory board for ALK America, is on the advisory board for Merck, and has received research support from Merck and Schering-Plough. J. Blessing-Moore is a speaker for Merck-Schering/AstraZeneca, Novartis, TEVA, and Meda Alcon and has received research support from Meda. D. A. Khan is a speaker for AstraZeneca and Merck, has received research support from the Vanberg Family Foundation and the Sellars Family Foundation, is Conjoint Board Review Chair for the ACAAI, and is a past president of the Texas Allergy, Asthma and Immunology Society. D. M. Lang is a speaker and consultant for GlaxoSmithKline; is a speaker for AstraZeneca, Merck, TEVA, Sanofi-Aventis, and Genentech/Novartis; and has received research support from Genentech/Novartis. R. A. Nicklas is a fellow for the ACAAI. J. Oppenheimer is a consultant and has provided lectures for AstraZeneca, Merck, and GlaxoSmithKline; and has received research support from AstraZeneca, Merck, GlaxoSmithKline, and Genentech. J. M. Portnoy is a speaker for Phadia, Merck, and CSL Behring; has received research support from the US Department of Housing and Urban Development; and is a board member of the ACAAI board of regents. S. L. Spector has received research support from Genentech, GlaxoSmithKline, Schering-Plough, Aventis, Novartis, Pharmaxis, Boehringer Ingelheim, AstraZeneca, Johnson & Johnson, Xyzal, Alcon, Centocor, Sepracor, UCB, Amgen, Capnia, and IVAX. S. Tilles is a speaker for Alcon; is on the advisory board for ALK, Ista, Merck, and Stallergenes; has received research support from Alcon, Amgen, Amphastar, Astellas, Boehringer Ingelheim, Ception, Genentech, Icagen, MAP Pharma, MEDA, Merck, Novartis, Roxane, and Sepracor; is Associate Editor of Allergy Watch and Annals of Allergy; and is a task force member for the Joint Task Force for Practice Parameters. D. Wallace is a speaker and advisor for Alcon, is a speaker for Merck and Sanofi-Aventis, and is President-Elect of the ACAAI. The rest of the authors have declared that they have no conflict of interest.	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Allergy Clin. Immunol.	JAN 11	2011	127	1		1						10.1016/j.jaci.2010.09.034		55	Allergy; Immunology	Allergy; Immunology	700XW	WOS:000285779900001	21122901	
J	Kasprzak, KS; Sunderman, FW; Salnikow, K				Kasprzak, Kazimierz S.; Sunderman, F. William, Jr.; Salnikow, Konstantin			Nickel carcinogenesis	MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS			English	Review						Nickel carcinogenesis; Epigenetic toxicity; Genotoxicity; Histones; Hypoxia; Oxidative damage		Human exposure to highly nickel-polluted environments, such as those associated with nickel refining, electroplating, and welding, has the potential to produce a variety of pathologic effects. Among them are skin allergies, lung fibrosis, and cancer of the respiratory tract. The exact mechanisms of nickel-induced carcinogenesis are not known and have been the subject of numerous epidemiologic and experimental investigations. These mechanisms are likely to involve genetic and epigenetic routes. The present review provides evidence for the genotoxic and mutagenic activity of Ni(II) particularly at high doses. Such doses are best delivered into the cells by phagocytosis of sparingly soluble nickel-containing dust particles. Ni(II) genotoxicity may be aggravated through the generation of DNA-damaging reactive oxygen species (ROS) and the inhibition of DNA repair by this metal. Broad spectrum of epigenetic effects of nickel includes alteration in gene expression resulting from DNA hypermethylation and histone hypoacetylation, as well as activation or silencing of certain genes and transcription factors, especially those involved in cellular response to hypoxia. The investigations of the pathogenic effects of nickel greatly benefit from the understanding of the chemical basis of Ni(II) interactions with intracellular targets/ligands and oxidants. Many pathogenic effects of nickel are due to the interference with the metabolism of essential metals such as Fe(II), Mn(II), Ca(II), Zn(II), or Mg(II). Research in this field allows for identification of putative Ni(II) targets relevant to carcinogenesis and prediction of pathogenic effects caused by exposure to nickel. Ultimately, the investigations of nickel carcinogenesis should be aimed at the development of treatments that would inhibit or prevent Ni(II) interactions with critical target molecules and ions, Fe(II) in particular, and thus avert the respiratory tract cancer and other adverse health effects in nickel workers. (C) 2003 Elsevier B.V. All rights reserved.	[Kasprzak, Kazimierz S.; Salnikow, Konstantin] NCI, Comparat Carcinogenesis Lab, Ft Detrick, MD 21702 USA; [Sunderman, F. 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Res.-Fundam. Mol. Mech. Mutagen.	DEC 10	2003	533	1-2			SI		67	97		10.1016/j.mrfmmm.2003.08.021		31	Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology	Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology	V18WB	WOS:000208033800004	14643413	
J	Sonkoly, E; Muller, A; Lauerma, AI; Pivarcsi, A; Soto, H; Kemeny, L; Alenius, H; Dieu-Nosjean, MC; Meller, S; Rieker, J; Steinhoff, M; Hoffmann, TK; Ruzicka, T; Zlotnik, A; Homey, B				Sonkoly, E; Muller, A; Lauerma, AI; Pivarcsi, A; Soto, H; Kemeny, L; Alenius, H; Dieu-Nosjean, MC; Meller, S; Rieker, J; Steinhoff, M; Hoffmann, TK; Ruzicka, T; Zlotnik, A; Homey, B			IL-31: A new link between T cells and pruritus in atopic skin inflammation	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						IL-31; pruritus; atopic dermatitis; T cells; cytokines; superantigen	ACTIVATION-REGULATED CHEMOKINE; DISEASE-ACTIVITY; SERUM THYMUS; ONCOSTATIN-M; DERMATITIS; EXPRESSION; RECEPTOR; EOTAXIN-3/CCL26; INTERLEUKIN-31; RECRUITMENT	Background: IL-31 is a novel T-cell-derived cytokine that induces severe pruritus and dermatitis in transgenic mice, and signals through a heterodimeric receptor composed of IL-31 receptor A and oncostatin M receptor. Objective: To investigate the role of human IL-31 in pruritic and nonpruritic inflammatory skin diseases. Methods: The expression of IL-31 was analyzed by quantitative real-time PCR in skin samples of healthy individuals and patients with chronic inflammatory skin diseases. Moreover, IL-31 expression was analyzed in nonlesional skin of atopic dermatitis patients after allergen or superantigen exposure, as well as in stimulated leukocytes. The tissue distribution of the IL-31 receptor heterodimer was investigated by DNA microarray analysis. Results: IL-31 was significantly overexpressed in pruritic atopic compared with nonpruritic psoriatic skin inflammation. Highest IL-31 levels were detected in prurigo nodularis, one of the most pruritic forms of chronic skin inflammation. In vivo, staphylococcal superantigen rapidly induced IL-31 expression in atopic individuals. In vitro, staphylococcal enterotoxin B but not viruses or T(H)1 and T(H)2 cytokines induced IL-31 in leukocytes. In patients with atopic dermatitis.. activated leukocytes expressed significantly higher IL-31 levels compared with control subjects. IL-31 receptor A showed most abundant expression in dorsal root ganglia representing the site where the cell bodies of cutaneous sensory neurons reside. Conclusion: Our findings provide a new link among staphylococcal colonization, subsequent T-cell recruitment/activation, and pruritus induction in patients with atopic dermatitis. Taken together, these findings show that IL-31 may represent a novel target for antipruritic drug development.	Univ Dusseldorf, Dept Dermatol, D-40225 Dusseldorf, Germany; Univ Dusseldorf, Dept Radiat Oncol, Dusseldorf, Germany; Univ Dusseldorf, Dept Otorhinolaryngol, Dusseldorf, Germany; Helsinki Univ Hosp, Finnish Inst Occupat Hlth, Dermatol Sect, Helsinki, Finland; Helsinki Univ Hosp, Skin & Allergy Hosp, Helsinki, Finland; Univ Szeged, Dept Dermatol & Allergol, Szeged, Hungary; Neurocrine Biosci Inc, San Diego, CA USA; Finnish Inst Occupat Hlth, Dept Ind Hyd & Toxicol, Helsinki, Finland; INSERM, U255, Lab Immunol Cellulaire & Clin, Ctr Rech Biomed Cordeliers, Paris, France; Univ Hosp Munster, Dept Dermatol, Munster, Germany	Homey, B (reprint author), Univ Dusseldorf, Dept Dermatol, Moorenstr 5, D-40225 Dusseldorf, Germany.	Bemhard.Homey@uni-duesseldorf.de	Steinhoff, Martin/F-6312-2013; Lauerma, Antti/J-8180-2016	Sonkoly, Eniko/0000-0002-4909-5413; Pivarcsi, Andor/0000-0003-2196-1102; Steinhoff, Martin/0000-0002-7090-2187			Banwell ME, 2002, CYTOKINE, V17, P317, DOI 10.1006/cyto.2002.1021; BURTON JL, 1998, ROOK WILKINSON EBLIN, P629; Camp RDR, 1998, ROOK WILKINSON EBLIN, P1589; Darsow U, 2000, CLIN EXP DERMATOL, V25, P544, DOI 10.1046/j.1365-2230.2000.00695.x; Dillon SR, 2004, NAT IMMUNOL, V5, P752, DOI 10.1038/ni1084; Diveu C, 2004, EUR CYTOKINE NETW, V15, P291; Finlay AY, 2001, J AM ACAD DERMATOL, V45, pS64, DOI 10.1067/mjd.2001.117010; Ghilardi N, 2002, J BIOL CHEM, V277, P16831, DOI 10.1074/jbc.M201140200; Gombert M, 2005, J IMMUNOL, V174, P5082; Greaves MW, 2004, INT ARCH ALLERGY IMM, V135, P166, DOI 10.1159/000080898; Gunther C, 2005, J IMMUNOL, V174, P1723; Guzik TJ, 2005, CLIN EXP ALLERGY, V35, P448, DOI 10.1111/j.1365-2222.2005.02210.x; Hanifin JM, 1980, ACTA DERM-VENEREOL S, V92, P44; Hermann GE, 2005, CURR PHARM DESIGN, V11, P1391, DOI 10.2174/1381612053507828; Hijnen DJ, 2004, J ALLERGY CLIN IMMUN, V113, P334, DOI 10.1016/j.jaci.2003.12.007; Homey B, 2000, J IMMUNOL, V164, P3465; Irizarry RA, 2003, BIOSTATISTICS, V4, P249, DOI 10.1093/biostatistics/4.2.249; Kagami S, 2003, CLIN EXP IMMUNOL, V134, P309, DOI 10.1046/j.1365-2249.2003.02273.x; Kakinuma T, 2002, CLIN EXP IMMUNOL, V127, P270, DOI 10.1046/j.1365-2249.2002.01727.x; Kakinuma T, 2001, J ALLERGY CLIN IMMUN, V107, P535, DOI 10.1067/mai.2001.113237; Laouini D, 2003, J ALLERGY CLIN IMMUN, V112, P981, DOI 10.1067/mai.2003.1789; Lee HL, 2004, NEUROREPORT, V15, P2807; LEE J, 2005, FASEB J, V10, P1356; Leung DYM, 2004, J CLIN INVEST, V113, P651, DOI 10.1172/JCI200421060; Leung DYM, 2003, LANCET, V361, P151, DOI 10.1016/S0140-6736(03)12193-9; Meller S, 2005, ARTHRITIS RHEUM, V52, P1504, DOI 10.1002/art.21034; Morikawa Y, 2004, J NEUROSCI, V24, P1941, DOI 10.1523/JNEUROSCI.4975-03.2004; Nickoloff BJ, 2004, J CLIN INVEST, V113, P1664, DOI 10.1172/JCI200422147; Pivarcsi A, 2004, J IMMUNOL, V173, P5810; Roll Antonie, 2004, Curr Opin Allergy Clin Immunol, V4, P373, DOI 10.1097/00130832-200410000-00008; Rottman JB, 2001, LAB INVEST, V81, P335; Stander S, 2002, EXP DERMATOL, V11, P12, DOI 10.1034/j.1600-0625.2002.110102.x; Tamura S, 2003, EUR J NEUROSCI, V17, P2287, DOI 10.1046/j.1460-9568.2003.02681.x; WAHLGREN CF, 1990, ACTA DERM-VENEREOL, V70, P323; Wallengren J, 2004, AM J CLIN DERMATOL, V5, P85, DOI 10.2165/00128071-200405020-00003; Yamashita T, 2003, ALLERGY, V58, P261, DOI 10.1034/j.1398-9995.2003.00062_2.x; Yosipovitch G, 2003, LANCET, V361, P690, DOI 10.1016/S0140-6736(03)12570-6; Zhang N, 2005, P NATL ACAD SCI USA, V102, P4536, DOI 10.1073/pnas.0406030102	38	346	357	4	15	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	FEB	2006	117	2					411	417		10.1016/j.jaci.2005.10.033		7	Allergy; Immunology	Allergy; Immunology	017IM	WOS:000235687300023	16461142	
J	Holgate, ST				Holgate, Stephen T.			Pathogenesis of asthma	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review							NERVE GROWTH-FACTOR; AIRWAY SMOOTH-MUSCLE; KILLER T-CELLS; BRONCHIAL EPITHELIAL-CELLS; CHEMOKINE RECEPTOR-3 EXPRESSION; SUBEPITHELIAL BASEMENT-MEMBRANE; NONATOPIC INTRINSIC ASTHMATICS; THYMIC STROMAL LYMPHOPOIETIN; MESENCHYMAL TROPHIC UNIT; NECROSIS-FACTOR-ALPHA	While asthma is considered an inflammatory disorder of the conducting airways, it is becoming increasingly apparent that the disease is heterogeneous with respect to immunopathology, clinical phenotypes, response to therapies, and natural history. Once considered purely an allergic disorder dominated by Th2-type lymphocytes, IgE, mast cells, eosinophils, macrophages, and cytokines, the disease also involves local epithelial, mesenchymal, vascular and neurologic events that are involved in directing the Th2 phenotype to the lung and through aberrant injury-repair mechanisms to remodeling of the airway wall. Structural cells provide the necessary "soil" upon which the "seeds" of the inflammatory response are able to take root and maintain a chronic phenotype and upon which are superimposed acute and subacute episodes usually driven by environmental factors such as exposure to allergens, microorganisms, pollutants or caused by inadequate antiinflammatory treatment. Greater consideration of additional immunologic and inflammatory pathways are revealing new ways of intervening in the prevention and treatment of the disease. Thus increased focus on environmental factors beyond allergic exposure (such as virus infection, air pollution, and diet) are identifying targets in structural as well as immune and inflammatory cells at which to direct new interventions.						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Exp. Allergy	JUN	2008	38	6					872	897		10.1111/j.1365-2222.2008.02971.x		26	Allergy; Immunology	Allergy; Immunology	304IL	WOS:000256103100002	18498538	
J	Pajno, GB; Barberio, G; De Luca, F; Morabito, L; Parmiani, S				Pajno, GB; Barberio, G; De Luca, F; Morabito, L; Parmiani, S			Prevention of new sensitizations in asthmatic children monosensitized to house dust mite by specific immunotherapy. A six-year follow-up study.	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						asthma; children; house dust mite; new sensitizations; rhinitis; specific immunotherapy	GRASS-POLLEN IMMUNOTHERAPY; ALLERGEN IMMUNOTHERAPY; INTERFERON-GAMMA; DERMATOPHAGOIDES-PTERONYSSINUS; MESSENGER-RNA; T-LYMPHOCYTES; ONSET; CELLS; INTERLEUKIN-4; EXTRACT	Background Specific immunotherapy (SIT) is a recognized way of treating IgE-mediated respiratory diseases. The clinical outcome is usually better in allergic children than in adults. Objective To increase our knowledge of the ability of SIT to prevent the onset of new sensitizations in monosensitized subjects, so far poorly documented. Methods 134 children (age range 5-8 years), who had intermittent asthma with or without rhinitis, with single sensitization to mite allergen (skin prick test and serum-specific IgE), were enrolled. SIT was proposed to all the children's parents, but was accepted by only 75 of them (SIT Group). The remaining 63 children were treated with medication only, and were considered the Control Group. Injective SIT with mite mix was administered to the SIT Group during the first three years and all patients were followed for a total of 6 years. All patients were checked for allergic sensitization(s) by skin prick test and serum-specific IgE every year until the end of the follow-up period. Results Both groups were comparable in terms of age, sex and disease characteristics. 123 children completed the follow-up study. At the end of the study, 52 out of 69 children (75.4%) in the SIT Group showed no new sensitization, compared to 18 out of 54 children (33.3%) in the Control Group (P < 0.0002). Parietaria, Gramineae and Olea were the most common allergens responsible for the new sensitization(s). Conclusions According to our data, SIT may prevent the onset of new sensitizations in children with respiratory symptoms monosensitized to house dust mite (HDM).	Univ Messina, Policlin Univ, Ist Clin Pediat, I-98124 Messina, Italy; ALK Abello SpA, Milan, Italy	Pajno, GB (reprint author), Univ Messina, Policlin Univ, Ist Clin Pediat, Via Consolare Valeria Gazzi, I-98124 Messina, Italy.						ABRAMSON MJ, 2000, COCHRANE DATABASE SY; Akoum H, 1996, IMMUNOLOGY, V87, P593, DOI 10.1046/j.1365-2567.1996.506585.x; Bousquet J., 1998, Allergy (Copenhagen), V53, P1; DAMATO G, 1994, CLIN EXP ALLERGY, V24, P210, DOI 10.1111/j.1365-2222.1994.tb00222.x; DesRoches A, 1997, J ALLERGY CLIN IMMUN, V99, P450, DOI 10.1016/S0091-6749(97)70069-1; DESROCHES A, 1995, J ALLERGY CLIN IMMUN, V95, P309; DREBORG S, 1993, ALLERGY, V48, P49, DOI 10.1111/j.1398-9995.1993.tb04756.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; Gruber W, 1999, CLIN EXP ALLERGY, V29, P176; Hedlin G, 1999, J ALLERGY CLIN IMMUN, V103, P609, DOI 10.1016/S0091-6749(99)70232-0; *I NAZ STAT, 1996, ANN STAT IT, P308; Jacobsen L., 1996, Journal of Allergy and Clinical Immunology, V97, P232, DOI 10.1016/S0091-6749(96)80416-7; JACOBSEN L, 1995, P 16 EUR C ALL CLIN, P745; JUTEL M, 1995, J IMMUNOL, V154, P4187; Kjellman N I, 1994, Pediatr Allergy Immunol, V5, P13, DOI 10.1111/j.1399-3038.1994.tb00342.x; KUEHR J, 1995, J ALLERGY CLIN IMMUN, V95, P655, DOI 10.1016/S0091-6749(95)70168-0; Lack G, 1997, J ALLERGY CLIN IMMUN, V99, P530, DOI 10.1016/S0091-6749(97)70081-2; NELSON HS, 1985, ANN ALLERGY, V55, P441; *NIH NAT HEART LUN, 1995, PUBL NIH; OWNBY DR, 1994, J ALLERGY CLIN IMMUN, V94, P662, DOI 10.1016/0091-6749(94)90171-6; Paul K, 1998, EUR J PEDIATR, V157, P109, DOI 10.1007/s004310050780; Platts-Mills Thomas A. E., 1997, Journal of Allergy and Clinical Immunology, V100, pS1; SECRIST H, 1993, J EXP MED, V178, P2123, DOI 10.1084/jem.178.6.2123; Valovirta E, 1997, J INVEST ALLERG CLIN, V7, P369; VANASPEREN PP, 1989, ACTA PAEDIATR SCAND, V78, P239; VANBEVER HP, 1988, ALLERGY, V43, P378; WALKER SM, 1995, ALLERGY, V50, P405, DOI 10.1111/j.1398-9995.1995.tb01170.x	28	344	368	1	5	BLACKWELL SCIENCE LTD	OXFORD	P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND	0954-7894			CLIN EXP ALLERGY	Clin. Exp. Allergy	SEP	2001	31	9					1392	1397		10.1046/j.1365-2222.2001.01161.x		6	Allergy; Immunology	Allergy; Immunology	473CF	WOS:000171021400010	11591189	
J	Hammad, H; Lambrecht, BN				Hammad, Hamida; Lambrecht, Bart N.			Dendritic cells and epithelial cells: linking innate and adaptive immunity in asthma	NATURE REVIEWS IMMUNOLOGY			English	Review							THYMIC STROMAL LYMPHOPOIETIN; ALLERGIC AIRWAY INFLAMMATION; HOUSE-DUST MITE; BRONCHIAL LYMPH-NODE; REGULATORY T-CELLS; INHALED ANTIGEN; TH2 RESPONSES; MEDIATE TOLERANCE; RESPIRATORY-TRACT; PROTEASE ALLERGEN	Dendritic cells (DCs) are generally held responsible for initiating and maintaining allergic T helper 2 (TH2)-cell responses to inhaled allergens in asthma. Although the epithelium was initially considered to function solely as a physical barrier, it is now seen as a central player in the T H 2-cell sensitization process by influencing the function of DCs. 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 DCs. A better understanding of these interactions, ascertained from human and animal studies, might lead to better prevention and treatment of asthma.	[Lambrecht, Bart N.] Erasmus Univ, Dept Pulm Med, Med Ctr, Rotterdam, Netherlands; [Hammad, Hamida] State Univ Ghent Hosp, Dept Resp Dis, Lab Immunolregulat & Mucosal Immunol, Ghent, Belgium	Lambrecht, BN (reprint author), Erasmus Univ, Dept Pulm Med, Med Ctr, Rotterdam, Netherlands.	bart.lambrecht@ugent.be	Hammad, Hamida/J-9391-2015; Lambrecht, Bart/K-2484-2014; Osborne, Nicholas/N-4915-2015	Hammad, Hamida/0000-0003-3762-8603; Lambrecht, Bart/0000-0003-4376-6834; Osborne, Nicholas/0000-0002-6700-2284			Akbari O, 2001, NAT IMMUNOL, V2, P725, DOI 10.1038/90667; Akbari O, 2002, NAT MED, V8, P1024, DOI 10.1038/nm745; Akdis M, 2004, J EXP MED, V199, P1567, DOI 10.1084/jem.20032058; Al-Shami A, 2005, J EXP MED, V202, P829, DOI 10.1084/jem.20050199; Allakhverdi Z, 2007, J EXP MED, V204, P253, DOI 10.1084/jem.20062211; Angkasekwinai P, 2007, J EXP MED, V204, P1509, DOI 10.1084/jem.20061675; Antony AB, 2002, J ALLERGY CLIN IMMUN, V110, P589, DOI 10.1067/mai.2002.127798; Arora M, 2006, P NATL ACAD SCI USA, V103, P7777, DOI 10.1073/pnas.0508492103; 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J	Denning, DW; O'Driscoll, BR; Hogaboam, CM; Bowyer, P; Niven, RM				Denning, DW; O'Driscoll, BR; Hogaboam, CM; Bowyer, P; Niven, RM			The link between fungi and severe asthma: a summary of the evidence	EUROPEAN RESPIRATORY JOURNAL			English	Review						aspergillosis; asthma clinical/basic investigations; asthma epidemiology; asthma immunology; fungi	ALLERGIC BRONCHOPULMONARY ASPERGILLOSIS; HOUSE-DUST-MITE; THUNDERSTORM-ASSOCIATED ASTHMA; SKIN-TEST REACTIVITY; OCCUPATIONAL ASTHMA; ENVIRONMENTAL-FACTORS; RESPIRATORY HEALTH; AIRWAY DISEASE; CHILDHOOD ASTHMA; DIFFICULT ASTHMA	There is current evidence to demonstrate a close association between fungal sensitisation and asthma severity. Whether such an association is causal remains to be confirmed, but this is explored by means of a detailed literature review. There is evidence from two randomised controlled trials that, in the example of allergic bronchopulmonary aspergillosis (ABPA), treatment with systemic antifungal therapy can offer a therapeutic benefit to similar to 60% of patients. ABPA is only diagnosed if a combination of clinical and immunological criteria is achieved. It is not known whether such cases are a discrete clinical entity or part of a spectrum of the pulmonary allergic response to fungi or fungal products. This paper describes the epidemiological evidence that associates severity of asthma with fungi and discusses possible pathogenetic mechanisms. Many airborne fungi are involved including species of Alternaria, Aspergillus, Cladosporium and Penicillium, and exposure may be indoors, outdoors or both. The potential for a therapeutic role of antifungal agents for patients with severe asthma and fungal sensitisation is also explored. Not only are many patients with severe asthma desperately disabled by their disease, but, in the UK alone, asthma accounts for 1,500 deaths per yr. The healthcare costs of these patients are enormous and any treatment option merits close scrutiny. Within this report, the case for the consideration of a new term related to this association is put forward. The current authors propose the term "severe asthma with fungal sensitisation". However, it is recognised that enhanced and precise definition of fungal sensitisation will require improvements in diagnostic testing.	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Resp. J.	MAR	2006	27	3					615	626		10.1183/09031936.06.00074705		12	Respiratory System	Respiratory System	021CY	WOS:000235962200025	16507864	
J	Brauer, M; Hoek, G; Van Vliet, P; Meliefste, K; Fischer, PH; Wijga, A; Koopman, LP; Neijens, HJ; Gerritsen, J; Kerkhof, M; Heinrich, J; Bellander, T; Brunekreef, B				Brauer, M; Hoek, G; Van Vliet, P; Meliefste, K; Fischer, PH; Wijga, A; Koopman, LP; Neijens, HJ; Gerritsen, J; Kerkhof, M; Heinrich, J; Bellander, T; Brunekreef, B			Air pollution from traffic and the development of respiratory infections and asthmatic and allergic symptoms in children	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; allergy; respiratory infections; air pollution; vehicle emissions	NITROGEN-DIOXIDE; CHILDHOOD ASTHMA; EAST-GERMANY; PRESCHOOL-CHILDREN; EXPOSURE; INDOOR; HEALTH; PREVALENCE; OUTDOOR; DISORDERS	Despite the important contribution of traffic sources to urban air quality, relatively few studies have evaluated the effects of traffic-related air pollution on health, such as its influence on the development of asthma and other childhood respiratory diseases. We examined the relationship between traffic-related air pollution and the development of asthmatic/allergic symptoms and respiratory infections in a birth cohort (n similar to 4,000) study in The Netherlands. A validated model was used to assign outdoor concentrations of traffic-related air pollutants (nitrogen dioxide, particulate matter less than 2.5 mum in aerodynamic diameter, and "soot") at the home of each subject of the cohort. Question n a! re-derived data on wheezing, dry nighttime cough, ear, nose, and throat infections, skin rash, and physician-diagnosed asthma, bronchitis, influenza, and eczema at 2 years of age were analyzed in relation to air pollutants. Adjusted odds ratios for wheezing, physician-diagnosed asthma, ear/nose/ throat infections, and flu/serious colds indicated positive associations with air pollutants, some of which reached borderline statistical significance. No associations were observed for the other health outcomes analyzed. Sensitivity analyses generally supported these results and suggested somewhat stronger associations with traffic, for asthma that was diagnosed before I year of age. These findings are subject to confirmation at older ages, when asthma can be more readily diagnosed.	Univ British Columbia, Sch Occupat & Environm Hyg, Vancouver, BC V6T 1Z3, Canada; Univ Utrecht, Inst Risk Assessment Sci, Environm & Occupat Hlth Grp, Utrecht, Netherlands; Natl Inst Publ Hlth & Environm, RIVM, NL-3720 BA Bilthoven, Netherlands; Erasmus Univ, Dept Pediat, Rotterdam, Netherlands; Sophia Childrens Univ Hosp, Rotterdam, Netherlands; Beatrix Childrens Hosp, Groningen, Netherlands; Univ Groningen, Dept Epidemiol, Groningen, Netherlands; GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, Neuherberg, Germany; Stockholm Cty Council, Dept Environm Hlth, Stockholm, Sweden; Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden	Brauer, M (reprint author), Univ British Columbia, Sch Occupat & Environm Hyg, 2206 East Mall, Vancouver, BC V6T 1Z3, Canada.		Kerkhof, Marjan/A-8846-2008; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; brunekreef, bert/0000-0001-9908-0060; Brauer, Michael/0000-0002-9103-9343			Arlian LG, 2001, J ALLERGY CLIN IMMUN, V107, pS406, DOI 10.1067/mai.2001.113670; ARSHAD SH, 1992, LANCET, V339, P1493, DOI 10.1016/0140-6736(92)91260-F; ARSHAD SH, 1993, CLIN EXP ALLERGY, V23, P504, DOI 10.1111/j.1365-2222.1993.tb03238.x; Bellander T, 2001, EPIDEMIOLOGY, V12, pS77; Brauer M, 2001, EPIDEMIOLOGY, V12, pS71; BRAUNFAHRLANDER C, 1992, AM REV RESPIR DIS, V145, P42; Briggs DJ, 1997, INT J GEOGR INF SCI, V11, P699, DOI 10.1080/136588197242158; Briggs DJ, 2000, SCI TOTAL ENVIRON, V253, P151, DOI 10.1016/S0048-9697(00)00429-0; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; Ciccone G, 1998, OCCUP ENVIRON MED, V55, P771; Cyrys J, 2000, SCI TOTAL ENVIRON, V250, P51, DOI 10.1016/S0048-9697(00)00361-2; Duhme H, 1998, EUR RESPIR J, V11, P840, DOI 10.1183/09031936.98.11040840; EDWARDS J, 1994, ARCH ENVIRON HEALTH, V49, P223; English P, 1999, ENVIRON HEALTH PERSP, V107, P761, DOI 10.2307/3434663; Fischer PH, 2000, ATMOS ENVIRON, V34, P3713, DOI 10.1016/S1352-2310(00)00067-4; Gold DR, 2000, ENVIRON HEALTH PERSP, V108, P643, DOI 10.2307/3454400; Guo YLL, 1999, ENVIRON HEALTH PERSP, V107, P1001; Hirsch T, 1999, EUR RESPIR J, V14, P669, DOI 10.1034/j.1399-3003.1999.14c29.x; Huss K, 2001, J ALLERGY CLIN IMMUN, V107, P48, DOI 10.1067/mai.2001.111146; Janssen NAH, 2000, J AIR WASTE MANAGE, V50, P1133; Koopman LP, 2001, PEDIATRICS, V108, P943, DOI 10.1542/peds.108.4.943; Litonjua AA, 2001, J ALLERGY CLIN IMMUN, V107, P41, DOI 10.1067/mai.2001.111143; Martinez FD, 1999, J ALLERGY CLIN IMMUN, V103, P355, DOI 10.1016/S0091-6749(99)70456-2; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; NAKATSUKA H, 1991, ENVIRON INT, V17, P51, DOI 10.1016/0160-4120(91)90337-P; Nelson HS, 2000, J ALLERGY CLIN IMMUN, V105, pS628; NITTA H, 1993, ARCH ENVIRON HEALTH, V48, P53; Oosterlee A, 1996, OCCUP ENVIRON MED, V53, P241; Pershagen G, 1995, INT J EPIDEMIOL, V24, P1147, DOI 10.1093/ije/24.6.1147; Rijnders E, 2001, ENVIRON HEALTH PERSP, V109, P411, DOI 10.2307/3434789; Studnicka M, 1997, EUR RESPIR J, V10, P2275, DOI 10.1183/09031936.97.10102275; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; Venn AJ, 2001, AM J RESP CRIT CARE, V164, P2177, DOI 10.1164/rccm2106126; VONMUTIUS E, 1995, EUR RESPIR J, V8, P723; VONMUTIUS E, 2001, J ALLERGY CLIN IMMUN, V105, P9; WARDLAW AJ, 1993, CLIN EXP ALLERGY, V23, P81, DOI 10.1111/j.1365-2222.1993.tb00303.x; Weiland Stephan K., 1994, Annals of Epidemiology, V4, P243; Wijga A, 2001, CLIN EXP ALLERGY, V31, P576, DOI 10.1046/j.1365-2222.2001.01072.x; WJST M, 1993, BRIT MED J, V307, P596; Woolcock AJ, 1997, CIBA F SYMP, V206, P122; WRIGHT AL, 1989, AM J EPIDEMIOL, V129, P1232	41	343	350	19	105	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	2002	166	8					1092	1098		10.1164/rccm.200108-007OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	602YY	WOS:000178533100016	12379553	
J	Gould, HJ; Sutton, BJ; Beavil, AJ; Beavil, RL; McCloskey, N; Coker, HA; Fear, D; Smurthwaite, L				Gould, HJ; Sutton, BJ; Beavil, AJ; Beavil, RL; McCloskey, N; Coker, HA; Fear, D; Smurthwaite, L			The biology of IgE and the basis of allergic disease	ANNUAL REVIEW OF IMMUNOLOGY			English	Review						IgE; IgE receptors; immediate hypersensitivity; allergy; mucosal immunity	FC-EPSILON-RI; CLASS-SWITCH RECOMBINATION; HUMAN B-CELLS; HIGH-AFFINITY RECEPTOR; LYMPHOCYTE TERMINAL DIFFERENTIATION; IMMUNOGLOBULIN CLASS SWITCH; GERMLINE GENE TRANSCRIPTS; ANTIGEN-PRESENTING CELLS; HUMAN MAST-CELLS; HUMAN T-CELLS	Allergic individuals exposed to minute quantities of allergen experience an immediate response. Immediate hypersensitivity reflects the permanent sensitization of mucosal mast cells by allergen-specific IgE antibodies bound to their high-affinity receptors (FcepsilonRI). A combination of factors contributes to such long-lasting sensitization of the mast cells. They include the homing of mast cells to mucosal tissues, the local synthesis of IgE, the induction of FcepsilonRI expression on mast cells by IgE, the consequent downregulation of FcgammaR (through an insufficiency of the common gamma-chains), and the exceptionally slow dissociation of IgE from FcepsilonRI. To understand the mechanism of the immediate hypersensitivity phenomenon, we need explanations of why IgE antibodies are synthesized in preference to IgG in mucosal tissues and why the IgE is so tenaciously retained on mast cell-surface receptors. There is now compelling evidence that the microenvironment of mucosal tissues of allergic disease favors class switching to IgE; and the exceptionally high affinity of IgE for FcepsilonRI can now be interpreted in terms of the recently determined crystal structures of IgE-FcepsilonRI and IgG-FcgammaR complexes. The rate of local IgE synthesis can easily compensate for the rate of the antibody dissociation from its receptors on mucosal mast cells. Effective mechanisms ensure that allergic reactions are confined to mucosal tissues, thereby minimizing the risk of systemic anaphylaxis.	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J	Dolovich, MB; Ahrens, RC; Hess, DR; Anderson, P; Dhand, R; Rau, JL; Smaldone, GC; Guyatt, G				Dolovich, MB; Ahrens, RC; Hess, DR; Anderson, P; Dhand, R; Rau, JL; Smaldone, GC; Guyatt, G			Device selection and outcomes of aerosol therapy: Evidence-based guidelines	CHEST			English	Review						aerosols; bronchodilators; corticosteroids; drug delivery systems; dry powder inhalers; metaanalysis; metered-dose inhalers; nebulizers	METERED-DOSE INHALER; MECHANICALLY VENTILATED PATIENTS; AIR-FLOW OBSTRUCTION; EXERCISE-INDUCED ASTHMA; DRY-POWDER INHALER; INTERMITTENT NEBULIZED ALBUTEROL; BRONCHODILATOR DELIVERY METHODS; CHLOROFLUOROCARBON CFC INHALER; PRESSURIZED AEROSOL; COPD PATIENTS	Background: The proliferation of inhaler devices has resulted in a confusing number of choices for clinicians who are selecting a delivery device for aerosol therapy. There are advantages and disadvantages associated with each device category. Evidence-based guidelines for the selection of the appropriate aerosol delivery device in specific clinical settings are needed. Aim: (1) To compare the efficacy and adverse effects of treatment using nebulizers vs pressurized metered-dose inhalers (MDIs) with or without a spacer/bolding chamber vs dry powder inhalers (DPIs) as delivery, systems for beta-agonists, anticholinergic agents, and corticosteroids for several commonly encountered clinical settings and patient populations, and (2) to provide recommendations to clinicians to aid them in selecting a particular aerosol delivery device for their patients. Methods: A systematic review of pertinent randomized, controlled clinical trials (RCTs) was undertaken using MEDLINE, EmBase, and the Cochrane Library databases. A broad search strategy was chosen, combining terms related to aerosol devices or drugs with the diseases of interest in various patient groups and clinical settings. Only RCTs in which the same drug was administered with different devices were included. RCTs (394 trials) assessing inhaled corticosteroid, beta(2)-agonist, and anticholinergic agents delivered by an MDI, an MDI with a spacer/holding chamber, a nebulizer, or a DPI were identified for the years 1982 to 2001. A total of 254 outcomes were tabulated. Of the 131 studies that met the eligibility criteria, only 59 (primarily those that tested beta(2)-agonists) proved to have useable data. Results: None of the pooled metaanalyses showed a significant difference between devices in any efficacy, outcome in any, patient group for each of the clinical settings that was investigated. The adverse effects that were reported were minimal and were related to the increased drug dose that was delivered. Each of the delivery devices provided similar outcomes in patients using the correct technique for inhalation. Conclusions: Devices used for the delivery of bronchodilators and steroids can be equally efficacious. When selecting an aerosol delivery device for patients with asthma and COPD, the following should be considered: device/drug availability; clinical setting; patient age and the ability to use the selected device correctly; device use with multiple medications; cost and reimbursement; drug administration time; convenience in both outpatient and inpatient settings; and physician and patient preference.	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J	Eder, W; Klimecki, W; Yu, LZ; von Mutius, E; Riedler, J; Braun-Fahrlander, C; Nowak, D; Martinez, FD				Eder, W; Klimecki, W; Yu, LZ; von Mutius, E; Riedler, J; Braun-Fahrlander, C; Nowak, D; Martinez, FD		ALEX Study Team	Toll-like receptor 2 as a major gene for asthma in children of European farmers	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						farming; endotoxin; asthma; atopy; children; TLR2; TLR4; gene-environment interaction	HAY-FEVER; ALLERGIC SENSITIZATION; CELL ACTIVATION; INNATE IMMUNITY; CUTTING EDGE; EXPOSURE; LIPOPOLYSACCHARIDE; ENDOTOXIN; RECOGNITION; ATOPY	Background: The finding that the prevalence of asthma and allergies is less frequent in children raised on animal farms has led to the conjecture that exposure to microbial products modifies immune responses. The toll-like receptors (TLRs) represent an evolutionarily conserved family of innate immunity receptors with microbial molecules as ligands. Objectives: We reasoned that polymorphisms in genes encoding TLRs might modulate the protective effects observed in farming populations. Methods: Farmers' and nonfarmers' children living in rural areas in Austria and Germany and who were enrolled in the cross-sectional ALEX study were genotyped for single nucleotide polymorphisms in the TLR2 and TLR4 genes. The frequencies of asthma, allergic rhinitis, and atopic sensitization were compared between the genotypes in relation to exposure to farming and endotoxin. Results: Among farmers' children, those carrying a T allele in TLR2/-16934 compared with children with genotype AA were significantly less likely to have a diagnosis of asthma (3% vs 13%, P = .012), current asthma symptoms (3% vs 16%, P = .004), atopic sensitization (14% vs 27%, P = .023), and current hay fever symptoms (3% vs 14%, P = .01). The association between TLR2/-16934 and asthma among children of farmers was independent of atopy. No such association was found among children from the same rural communities but not living on farms. Conclusion: Our results suggest that genetic variation in TLR2 is a major determinant of the susceptibility to asthma and allergies in children of farmers.	Univ Arizona, Arizona Resp Ctr, Tucson, AZ 85724 USA; Univ Munich, Dr Von Haunerschen Kinderspital, D-80337 Munich, Germany; Childrens Hosp, Salzburg, Austria; Univ Basel, Inst Social & Prevent Med, CH-4003 Basel, Switzerland; Univ Munich, Inst Occupat & Environm Med, D-80539 Munich, Germany; Univ Munich, Outpatient Clin Occupat & Environm Med, D-80539 Munich, Germany	Martinez, FD (reprint author), Univ Arizona, Arizona Resp Ctr, 1501 N Campbell Ave,POB 245030, Tucson, AZ 85724 USA.			von Mutius, Erika/0000-0002-8893-4515	NHLBI NIH HHS [HL66800, HL67672]		Arbour NC, 2000, NAT GENET, V25, P187; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Burney P, 1997, AM J RESP CRIT CARE, V156, P1773; Caramalho I, 2003, J EXP MED, V197, P403, DOI 10.1084/jem.20021633; Clayton D., 2001, HDB STAT GENETICS, P519; DUTKIEWICZ J, 1978, ARCH ENVIRON HEALTH, V33, P250; Ernst P, 2000, AM J RESP CRIT CARE, V161, P1563; Flo TH, 2002, J BIOL CHEM, V277, P35489, DOI 10.1074/jbc.M201366200; Hirschfeld M, 2000, J IMMUNOL, V165, P618; HOLLANDER A, 1993, AM IND HYG ASSOC J, V54, P647, DOI 10.1202/0002-8894(1993)054<0647:IAEITA>2.0.CO;2; Imler JL, 2001, TRENDS CELL BIOL, V11, P304, DOI 10.1016/S0962-8924(01)02004-9; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Lauener RP, 2002, LANCET, V360, P465, DOI 10.1016/S0140-6736(02)09641-1; Lazarus R, 2002, IMMUNOL REV, V190, P9, DOI 10.1034/j.1600-065X.2002.19002.x; Lien E, 1999, J BIOL CHEM, V274, P33419, DOI 10.1074/jbc.274.47.33419; Martinez FD, 1997, AM J RESP CRIT CARE, V156, pS117; Martinez FD, 1999, LANCET S2, V354, pSII12; Means TK, 1999, J IMMUNOL, V163, P6748; MIETTINE.OS, 1974, AM J EPIDEMIOL, V99, P325; Miyake K, 2003, INT IMMUNOPHARMACOL, V3, P119, DOI 10.1016/S1567-5769(02)00258-8; Muzio M, 2000, J IMMUNOL, V164, P5998; 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; Schwandner R, 1999, J BIOL CHEM, V274, P17406, DOI 10.1074/jbc.274.25.17406; Sieling PA, 2002, CURR OPIN MICROBIOL, V5, P70, DOI 10.1016/S1369-5274(02)00288-6; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; WERNER M, 2003, J ALLERGY CLIN IMMUN, V112, P1; Yoshimura A, 1999, J IMMUNOL, V163, P1	31	338	352	1	19	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	2004	113	3					482	488		10.1016/j.jaci.2003.12.374		7	Allergy; Immunology	Allergy; Immunology	802DM	WOS:000220144200021	15007351	
J	Mishra, A; Hogan, SP; Brandt, EB; Rothenberg, ME				Mishra, A; Hogan, SP; Brandt, EB; Rothenberg, ME			An etiological role for aeroallergens and eosinophils in experimental esophagitis	JOURNAL OF CLINICAL INVESTIGATION			English	Article							GASTROESOPHAGEAL REFLUX; CHEMOKINE EOTAXIN; ANTIGEN; ASTHMA; AIRWAYS; MOUSE; INTERLEUKIN-5; INFLAMMATION; ALLERGEN; CHILDREN	Eosinophil infiltration into the esophagus is observed in diverse diseases including gastroesophageal reflux and allergic gastroenteritis, but the processes involved are largely unknown. We now report an original model of experimental esophagitis induced by exposure of mice to respiratory allergen. Allergen-challenged mice develop marked levels of esophageal eosinophils, free eosinophil granules, and epithelial cell hyperplasia, features that mimic the human disorders. Interestingly, exposure of mice to oral or intragastric allergen does not promote eosinophilic esophagitis, indicating that hypersensitivity in the esophagus occurs with simultaneous development of pulmonary inflammation. Furthermore, in the absence of eotaxin, eosinophil recruitment is attenuated, whereas in the absence of IL-5, eosinophil accumulation and epithelial hyperplasia are ablated. These results establish a pathophysiological connection between allergic hypersensitivity responses in the lung and esophagus and demonstrate an etiologic role for inhaled allergens and eosinophils in gastrointestinal inflammation.	Childrens Hosp, Med Ctr, Dept Pediat, Div Pulm Med Allergy & Clin Immunol, Cincinnati, OH 45229 USA	Rothenberg, ME (reprint author), Childrens Hosp, Med Ctr, Dept Pediat, Div Pulm Med Allergy & Clin Immunol, Cincinnati, OH 45229 USA.				NIAID NIH HHS [R01 AI045898, R01 AI42242-02, R01 AI45898-01]; NIAMS NIH HHS [R01 AR042242]		Burks AW, 1998, J PEDIATR-US, V133, P175, DOI 10.1016/S0022-3476(98)70215-X; COLLINS PD, 1995, J EXP MED, V182, P1169, DOI 10.1084/jem.182.4.1169; DISCOMBE G, 1946, Lancet, V1, P195; DONALDSON K, 1995, EXP TOXICOL PATHOL, V47, P207; DVORAK AM, 1994, HISTOL HISTOPATHOL, V9, P339; Erjefalt JS, 1999, AM J RESP CRIT CARE, V160, P304; Foster PS, 1996, J EXP MED, V183, P195, DOI 10.1084/jem.183.1.195; Furuta GT, 1998, J PEDIATR GASTR NUTR, V26, P468, DOI 10.1097/00005176-199804000-00021; FURUTA GT, 1995, CURR OPIN GASTROEN, V11, P541, DOI 10.1097/00001574-199511000-00013; GREENSPON LW, 1986, J ALLERGY CLIN IMMUN, V77, P443, DOI 10.1016/0091-6749(86)90178-8; HAMEL R, 1986, J APPL PHYSIOL, V61, P2081; Harding SM, 1999, J ALLERGY CLIN IMMUN, V104, P251, DOI 10.1016/S0091-6749(99)70360-X; Holgate ST, 1999, NATURE, V402, pB2; Huang WW, 1998, J EXP MED, V188, P1063, DOI 10.1084/jem.188.6.1063; Kelly KJ, 2000, J PEDIATR GASTR NUTR, V30, pS28, DOI 10.1097/00005176-200001001-00005; KELLY KJ, 1995, GASTROENTEROLOGY, V109, P1503, DOI 10.1016/0016-5085(95)90637-1; Lamkhioued B, 1997, J IMMUNOL, V159, P4593; Liacouras CA, 1998, J PEDIATR GASTR NUTR, V26, P380, DOI 10.1097/00005176-199804000-00004; Lukacs NW, 1999, J CLIN INVEST, V104, P995, DOI 10.1172/JCI8125; MARRETTA J, 1979, IMMUNOLOGY, V37, P609; Matthews AN, 1998, P NATL ACAD SCI USA, V95, P6273, DOI 10.1073/pnas.95.11.6273; Mishra A, 1999, J CLIN INVEST, V103, P1719, DOI 10.1172/JCI6560; Nickel R, 1999, J ALLERGY CLIN IMMUN, V104, P723; Orenstein SR, 2000, AM J GASTROENTEROL, V95, P1422; RENZ H, 1992, J ALLERGY CLIN IMMUN, V89, P1127, DOI 10.1016/0091-6749(92)90296-E; Rothenberg ME, 1997, J EXP MED, V185, P785, DOI 10.1084/jem.185.4.785; Rothenberg ME, 1998, NEW ENGL J MED, V338, P1592; Ruchelli E, 1999, PEDIATR DEVEL PATHOL, V2, P15, DOI 10.1007/s100249900084; Sampson HA, 2000, J PEDIATR GASTR NUTR, V30, pS87, DOI 10.1097/00005176-200001001-00013; Sampson HA, 1999, J ALLERGY CLIN IMMUN, V103, P717, DOI 10.1016/S0091-6749(99)70411-2; SCHUMACHER JH, 1988, J IMMUNOL, V141, P1576; Walsh SV, 1999, AM J SURG PATHOL, V23, P390, DOI 10.1097/00000478-199904000-00003; Wills-Karp M, 1999, ANNU REV IMMUNOL, V17, P255, DOI 10.1146/annurev.immunol.17.1.255; WILLSKARP MA, 1999, IN VIVO MODELS INFLA, P137; WINTER HS, 1982, GASTROENTEROLOGY, V83, P818; Xia Y, 2000, PARASITOLOGY, V120, P211, DOI 10.1017/S0031182099005363; Yang Y, 1998, BLOOD, V92, P3912	37	337	348	0	6	AMER SOC CLINICAL INVESTIGATION INC	ANN ARBOR	ROOM 4570 KRESGE I, 200 ZINA PITCHER PLACE, ANN ARBOR, MI 48109-0560 USA	0021-9738			J CLIN INVEST	J. Clin. Invest.	JAN	2001	107	1					83	90		10.1172/JCI10224		8	Medicine, Research & Experimental	Research & Experimental Medicine	389GY	WOS:000166231300014	11134183	
J	Nazaroff, WW; Weschler, CJ				Nazaroff, WW; Weschler, CJ			Cleaning products and air fresheners: exposure to primary and secondary air pollutants	ATMOSPHERIC ENVIRONMENT			English	Review						indoor air quality; hazardous air pollutants; terpenes; ozone; hydroxyl radical; nitrate radical	VOLATILE ORGANIC-COMPOUNDS; GAS-PHASE REACTIONS; MIXING HOUSEHOLD CLEANERS; OH RADICAL FORMATION; OXIDIZED D-LIMONENE; INDOOR AIR; NO3 RADICALS; RATE CONSTANTS; OCCUPATIONAL ASTHMA; BUILDING-MATERIALS	Building occupants, including cleaning personnel, are exposed to a wide variety of airborne chemicals when cleaning agents and air fresheners are used in buildings. Certain of these chemicals are listed by the state of California as toxic air contaminants (TACs) and a subset of these are regulated by the US federal government as hazardous air pollutants (HAPs). California's Proposition 65 list of species recognized as carcinogens or reproductive toxicants also includes constituents of certain cleaning products and air fresheners. In addition, many cleaning agents and air fresheners contain chemicals that can react with other air contaminants to yield potentially harmful secondary products. For example, terpenes can react rapidly with ozone in indoor air generating many secondary pollutants, including TACs such as formaldehyde. Furthermore, ozone-terpene reactions produce the hydroxyl radical, which reacts rapidly with organics, leading to the formation of other potentially toxic air pollutants. Indoor reactive chemistry involving the nitrate radical and cleaning-product constituents is also of concern, since it produces organic nitrates as well as some of the same oxidation products generated by ozone and hydroxyl radicals. Few studies have directly addressed the indoor concentrations of TACs that might result from primary emissions or secondary pollutant formation following the use of cleaning agents and air fresheners. In this paper, we combine direct empirical evidence with the basic principles of indoor pollutant behavior and with information from relevant studies, to analyze and critically assess air pollutant exposures resulting from the use of cleaning products and air fresheners. Attention is focused on compounds that are listed as HAPs, TACs or Proposition 65 carcinogens/reproductive toxicants and compounds that can readily react to generate secondary pollutants. The toxicity of many of these secondary pollutants has yet to be evaluated. The inhalation intake of airborne organic compounds from cleaning product use is estimated to be of the order of 10 mg d(-1) person(-1) in California. More than two dozen research articles present evidence of adverse health effects from inhalation exposure associated with cleaning or cleaning products. Exposure to primary and secondary pollutants depends on the complex interplay of many sets of factors and processes, including cleaning product composition, usage, building occupancy, emission dynamics, transport and mixing, building ventilation, sorptive interactions with building surfaces, and reactive chemistry. Current understanding is sufficient to describe the influence of these variables qualitatively in most cases and quantitatively in a few. (C) 2004 Elsevier Ltd. All rights reserved.	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Environ.	JUN	2004	38	18					2841	2865		10.1016/j.atmosenv.2004.02.040		25	Environmental Sciences; Meteorology & Atmospheric Sciences	Environmental Sciences & Ecology; Meteorology & Atmospheric Sciences	820XF	WOS:000221422400008		
J	Garcia-Aymerich, J; Farrero, E; Felez, MA; Izquierdo, J; Marrades, RM; Anto, JM				Garcia-Aymerich, J; Farrero, E; Felez, MA; Izquierdo, J; Marrades, RM; Anto, JM		EFRAM investigators	Risk factors of readmission to hospital for a COPD exacerbation: a prospective study	THORAX			English	Article							OBSTRUCTIVE PULMONARY-DISEASE; CHRONIC LUNG-DISEASE; QUALITY-OF-LIFE; PHYSICAL ACTIVITIES; ASTHMA; MORTALITY; QUESTIONNAIRE; EFRAM	Background: Exacerbations of chronic obstructive pulmonary disease (COPD) are a leading cause of admission to hospital among men in many countries, although the factors causing exacerbations are largely unknown. The association between readmission for a COPD exacerbation and a wide range of modifiable potential risk factors, after adjusting for sociodemographic and clinical factors, has been assessed. Methods: Three hundred and forty patients with COPD recruited during an admission for an exacerbation in four tertiary hospitals in the Barcelona area of Spain were followed for a mean period of 1.1 years. Information on potential risk factors, including clinical and functional status, medical care and prescriptions, medication adherence, lifestyle, health status, and social support, was collected at the recruitment admission. A Cox's proportional hazards model was used to obtain independent relative risks of readmission for COPD. Results: During the follow up period 63% of patients were readmitted at least once, and 29% died. The final multivariate model showed the following risk (or protective) factors: greater than or equal to3 admissions for COPD in the year before recruitment (hazard ratio (HR)= 1.66, 95% Cl 1.16 to 2.39), forced expiratory volume in 1 second (FEV1 percentage predicted (0.97, 95% Cl 0.96 to 0.99), oxygen tension (0.88, 95% Cl 0.79 to 0.98), higher levels of usual physical activity (0.54, 95% Cl 0.34 to 0.86), and taking anticholinergic drugs (1.81, 95% 1.11 to 2.94). Exposure to passive smoking was also related to an increased risk of readmission with COPD after adjustment for clinical factors (1.63, 95% Cl 1.04 to 2.57) but did not remain in the final model. Conclusions: This is the first study to show a strong association between usual physical activity and reduced risk of readmission to hospital with COPD, which is potentially relevant for rehabilitation and other therapeutic strategies.	Inst Municipal Invest Med, Resp & Environm Hlth Res Unit, E-08003 Barcelona, Spain; Univ Bellvitge, Ciutat Sanitaria, Dept Pneumol, Lhospitalet De Llobregat, Spain; Hosp del Mar, Dept Pneumol, Barcelona, Spain; Hosp Germans Trias & Pujol, Dept Pneumol, Badalona, Spain; Hosp Clin Barcelona, Dept Pneumol, Barcelona, Spain; Univ Pompeu Fabra, Dept Expt & Hlth Sci, Barcelona, Spain	Anto, JM (reprint author), Inst Municipal Invest Med, Resp & Environm Hlth Res Unit, Doctor Aiguader 80, E-08003 Barcelona, Spain.		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J	Dodd, M; Janson, S; Facione, N; Faucett, J; Froelicher, ES; Humphreys, J; Lee, K; Miaskowski, C; Puntillo, K; Rankin, S; Taylor, D				Dodd, M; Janson, S; Facione, N; Faucett, J; Froelicher, ES; Humphreys, J; Lee, K; Miaskowski, C; Puntillo, K; Rankin, S; Taylor, D			Advancing the science of symptom management	JOURNAL OF ADVANCED NURSING			English	Article						concepts/constructs related to health; symptom management model; symptom management theory	TYPE-2 DIABETES MANAGEMENT; AMERICAN MIDLIFE WOMEN; PRACTITIONER PERSPECTIVES; CONTRASTING PATIENT; PAIN; EXPERIENCE; ASTHMA; STIMULATION; EDUCATION; PATTERNS	Since the publication of the original Symptom Management Model (Larson et al. 1994), faculty and students at the University of California, San Francisco (UCSF) School of Nursing Centre for System Management have tested this model in research studies and expanded the model through collegial discussions and seminars. Aim. In this paper, we describe the evidence-based revised conceptual model, the three dimensions of the model, and the areas where further research is needed. Background/Rationale. The experience of symptoms, minor to severe, prompts millions of patients to visit their healthcare providers each year. Symptoms not only create distress, but also disrupt social functioning. The management of symptoms and their resulting outcomes often become the responsibility of the patient and his or her family members. Healthcare providers have difficulty developing symptom management strategies that can be applied across acute and home-care settings because few models of symptom management have been tested empirically. To date, the majority of research on symptoms was directed toward studying a single symptom, such as pain or fatigue, or toward evaluating associated symptoms, such as depression and sleep disturbance. While this approach has advanced our understanding of some symptoms, we offer a generic symptom management model to provide direction for selecting clinical interventions, informing research, and bridging an array of symptoms associated with a variety of diseases and conditions. Finally, a broadly-based symptom management model allows the integration of science from other fields.	Univ Calif San Francisco, Sch Nursing, San Francisco, CA 94143 USA	Dodd, M (reprint author), Univ Calif San Francisco, Sch Nursing, Box 0610, San Francisco, CA 94143 USA.				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J	Sears, MR; Greene, JM; Willan, AR; Taylor, DR; Flannery, EM; Cowan, JO; Herbison, GP; Poulton, R				Sears, MR; Greene, JM; Willan, AR; Taylor, DR; Flannery, EM; Cowan, JO; Herbison, GP; Poulton, R			Long-term relation between breastfeeding and development of atopy and asthma in children and young adults: a longitudinal study	LANCET			English	Article							CHILDHOOD ASTHMA; NEW-ZEALAND; FED INFANTS; EPIDEMIOLOGY; MICROFLORA; ALLERGY; BIRTH	Background Breastfeeding is widely advocated to reduce risk of atopy and asthma, but the evidence for such an effect is conflicting. We aimed to assess long-term outcomes of asthma and atopy related to breastfeeding in a New Zealand birth cohort. Methods Our cohort consisted of 1037 of 1139 children born in Dunedin, New Zealand, between April, 1972, and March, 1973, and residing in Otago province at age 3 years. Children were assessed every 2-5 years from ages 9 to 26 years with respiratory questionnaires, pulmonary function, bronchial challenge, and allergy skin tests. History of breastfeeding had been independently recorded in early childhood. Findings 504 (49%) of 1037 eligible children were breastfed (4 weeks or longer) and 533 (51%) were not. More children who were breastfed were atopic at all ages from 13 to 21 years to cats (p=0.0001), house dust mites (p=0.0010), and grass pollen (p<0.0001) than those who were not. More children who were breastfed reported current asthma at each assessment between age 9 (p=0.0008) and 26 years (p=0.0008) than those who were not. Breastfeeding effects were not affected by parental history of hayfever or asthma. Multifactor analysis controlling for socioeconomic status, parental smoking, birth order, and use of sheepskin bedding in infancy, showed odds ratios of 1.94 (95% Cl 1.42-2-65, p<0.0001) for any allergen positive at age 13 years, 2.40 (1-36-4.26, p=0.0003) for current asthma at 9 years, and 1.83 (1.35-2.47, p<0.0001) for current asthma at 9-26 years by repeated-measures analysis. Interpretation Breastfeeding does not protect children against atopy and asthma and may even increase the risk.	McMaster Univ, Dept Med, Hamilton, ON, Canada; McMaster Univ, Dept Clin Epidemiol & Biostat, Hamilton, ON, Canada; Univ Otago, Dunedin Sch Med, Dept Med, Dunedin, New Zealand; Univ Otago, Dunedin Sch Med, Dept Prevent & Social Med, Dunedin, New Zealand	Sears, MR (reprint author), St Josephs Healthcare & McMaster Univ, Firestone Inst Resp Hlth, 50 Charlton Ave, Hamilton, ON L8N 4A6, Canada.						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L., 1989, BRIT MED J, V299, P945; Wright AL, 1999, J ALLERGY CLIN IMMUN, V104, P589, DOI 10.1016/S0091-6749(99)70328-3; Wright AL, 2001, THORAX, V56, P192, DOI 10.1136/thorax.56.3.192	37	335	352	2	27	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	SEP 21	2002	360	9337					901	907		10.1016/S0140-6736(02)11025-7		7	Medicine, General & Internal	General & Internal Medicine	596AU	WOS:000178142200008	12354471	
J	Skoner, DR				Skoner, DR			Allergic rhinitis: Definition, epidemiology, detection, and pathophysiology, diagnosis	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergic rhinitis; IgE; mast cells; perennial rhinitis	PRACTICE PARAMETERS; NASAL-MUCOSA; DUST MITE; ASTHMA; CHILDHOOD; DISEASE; PREVALENCE; CYTOKINES; IL-4	Allergic rhinitis (AR) is a heterogeneous disorder that despite its high prevalence is often undiagnosed. It is characterized by one or more symptoms including sneezing, itching, nasal congestion, and rhinorrhea. Many causative agents have been linked to AR including pollens, molds, dust mites, and animal dander. Seasonal allergic rhinitis (SAR) is fairly easy to identify because of the rapid and reproducible onset and offset of symptoms in association with pollen exposure. Perennial AR is often more difficult to detect than SAR because of the overlap with sinusitis, respiratory infections, and vasomotor rhinitis. SAR can result in hyperresponsiveness to allergens such as cigarette smoke, once pollen season is over. Perennial AR is defined as occurring during approximately 9 months of the year. AR affects an estimated 20 to 40 million people in the United States alone, and the incidence is increasing; an estimated 20% of cases are SAR; 40% of cases are perennial rhinitis; and 40% of cases are mixed. The pathophysiology of SAR is complex. There is a strong genetic component to the allergic response, which is driven through mucosal infiltration and action on plasma cells, roast cells, and eosinophils. The allergic response occurs in two phases, which are considered the "early" and "late" phase responses. Early phase response occurs within minutes of exposure to the allergen and tends to produce sneezing, itching, and clear rhinorrhea; late phase response occurs 4 to 8 hours after allergen exposure and is characterized by congestion, fatigue, malaise, irritability, and possibly neurocognitive deficits. The key to diagnosis of AR is awareness of signs and symptoms. IgE antibody tests to detect specific allergens are the standard method used today; however, in addition, diagnosis must be confirmed with a positive history and demonstration that the symptoms are the result of IgE-mediated inflammation.	Univ Pittsburgh, Sch Med, Dept Pediat & Otolaryngol, Pittsburgh, PA 15231 USA; Childrens Hosp Pittsburgh, Pittsburgh, PA 15231 USA	Skoner, DR (reprint author), Univ Pittsburgh, Sch Med, Dept Pediat & Otolaryngol, Pittsburgh, PA 15231 USA.						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Allergy Clin. Immunol.	JUL	2001	108	1		S			S2	S8		10.1067/mai.2001.115569		7	Allergy; Immunology	Allergy; Immunology	459BU	WOS:000170230600002	11449200	
J	Lough, GC; Schauer, JJ; Park, JS; Shafer, MM; Deminter, JT; Weinstein, JP				Lough, GC; Schauer, JJ; Park, JS; Shafer, MM; Deminter, JT; Weinstein, JP			Emissions of metals associated with motor vehicle roadways	ENVIRONMENTAL SCIENCE & TECHNOLOGY			English	Article							AIRBORNE PARTICULATE MATTER; FINE ORGANIC AEROSOL; CHEMICAL-COMPOSITION; SOURCE PROFILES; LOS-ANGELES; URBAN AREAS; EXHAUST; TUNNEL; ASTHMA; CARBON	Emissions of metals and other particle-phase species from on-road motor vehicles were measured in two tunnels in Milwaukee, WI during the summer of 2000 and winter of 2001. Emission factors were calculated from measurements of fine (PM2.5) and coarse (PM10) particulate matter at tunnel entrances and exits, and effects of fleet composition and season were investigated. Cascade impactors (MOUDI) were used to obtain size-resolved metal emission rates. Metals were quantified with inductively-coupled plasma mass spectrometry (ICP-MS) and X-ray fluorescence (XRF). PM10 emission rates ranged from 38.7 to 201 mg km(-1) and were composed mainly of organic carbon (OC, 30%), inorganic ions (sulfate, chloride, nitrate, ammonium, 20%), metals (19%), and elemental carbon (EC, 9.3%). PM10 metal emissions were dominated by crustal elements Si, Fe, Ca, Na, Mg, Al, and K, and elements associated with tailpipe emissions and brake and tire wear, including Cu, Zn, Sb, Ba, Pb, and S. Metals emitted in PM2.5 were lower (11.6% of mass). Resuspension of roadway dust was dependent on weather and road surface conditions, and increased emissions were related to higher traffic volumes and fractions of heavy trucks. Emission of noble metals from catalytic converters appeared to be impacted by the presence of older vehicles. Elements related to brake wear were impacted by enriched road dust resuspension, but correlations between these elements in PM2.5 indicate that direct brake wear emissions are also important. A submicrometer particle mode was observed in the emissions of Pb, Ca, Fe, and Cu.	Univ Wisconsin, Environm Chem & Technol Program, Madison, WI 53706 USA; Univ Wisconsin, Wisconsin State Lab Hyg, Madison, WI 53706 USA; US EPA, Res Triangle Pk, NC USA	Schauer, JJ (reprint author), Univ Wisconsin, Environm Chem & Technol Program, Madison, WI 53706 USA.	jschauer@engr.wisc.edu		Lough, Glynis/0000-0002-9152-6520			Allen JO, 2001, ENVIRON SCI TECHNOL, V35, P4189, DOI 10.1021/es0015545; Aust A., 2002, PARTICLE CHARACTERIS; Cadle SH, 1997, ENVIRON SCI TECHNOL, V31, P3405, DOI 10.1021/es9700257; Cadle SH, 1999, ENVIRON SCI TECHNOL, V33, P2328, DOI 10.1021/es9810843; Chow JC, 2001, AEROSOL SCI TECH, V34, P23, DOI 10.1080/027868201300081923; Chow JC, 2003, ATMOS ENVIRON, V37, P1317, DOI 10.1016/S1352-2310(02)01021-X; Claiborn CS, 2002, ENVIRON HEALTH PERSP, V110, P547; Davis AP, 2001, CHEMOSPHERE, V44, P997, DOI 10.1016/S0045-6535(00)00561-0; Dietl C, 1997, SCI TOTAL ENVIRON, V205, P235, DOI 10.1016/S0048-9697(97)00204-0; El-Fadel M, 2001, CRIT REV ENV SCI TEC, V31, P125, DOI 10.1080/20016491089190; Fraser MP, 1998, ENVIRON SCI TECHNOL, V32, P2051, DOI 10.1021/es970916e; Fraser MP, 1999, ATMOS ENVIRON, V33, P2715, DOI 10.1016/S1352-2310(98)00311-2; Garg BD, 2000, ENVIRON SCI TECHNOL, V34, P4463, DOI 10.1021/es001108h; Gavett SH, 2001, INT ARCH ALLERGY IMM, V124, P109, DOI 10.1159/000053685; Gertler A.W., 2002, EMISSIONS DIESEL GAS; GERTLER AW, 1995, AWMA PARTICULATE HLT; Gillies JA, 2001, ENVIRON SCI TECHNOL, V35, P1054, DOI 10.1021/es991320p; Harrison RM, 1996, ENVIRON SCI TECHNOL, V30, P825, DOI 10.1021/es950252d; HILDEMANN LM, 1991, ENVIRON SCI TECHNOL, V25, P744, DOI 10.1021/es00016a021; HUANG XD, 1994, ATMOS ENVIRON, V28, P1385, DOI 10.1016/1352-2310(94)90201-1; Jaecker-Voirol A, 2000, ENVIRON MODELL SOFTW, V15, P575, DOI 10.1016/S1364-8152(00)00044-X; Kanitsar K, 2003, J ANAL ATOM SPECTROM, V18, P239, DOI 10.1039/b212218a; Kellog R., 1999, 1033 EPA; Kleeman MJ, 2000, ENVIRON SCI TECHNOL, V34, P1132, DOI 10.1021/es981276y; Kweon C. 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Sci. Technol.	FEB 1	2005	39	3					826	836		10.1021/es048715f		11	Engineering, Environmental; Environmental Sciences	Engineering; Environmental Sciences & Ecology	893IN	WOS:000226712600031	15757346	
J	Tlaskalova-Hogenova, H; Stepankova, R; Hudcovic, T; Tuckova, L; Cukrowska, B; Lodinova-Zadnikova, R; Kozakova, H; Rossmann, P; Bartova, J; Sokol, D; Funda, DP; Borovska, D; Rehakova, Z; Sinkora, J; Hofman, J; Drastich, P; Kokesova, A				Tlaskalova-Hogenova, H; Stepankova, R; Hudcovic, T; Tuckova, L; Cukrowska, B; Lodinova-Zadnikova, R; Kozakova, H; Rossmann, P; Bartova, J; Sokol, D; Funda, DP; Borovska, D; Rehakova, Z; Sinkora, J; Hofman, J; Drastich, P; Kokesova, A			Commensal bacteria (normal microflora), mucosal immunity and chronic inflammatory and autoimmune diseases	IMMUNOLOGY LETTERS			English	Review						mucosal microbiota; intestinal barrier; germ-free animal; gut inflammation; allergy; autoimmunity; probioties	GERM-FREE PIGLETS; INTESTINAL EPITHELIAL-CELLS; PROBIOTIC ESCHERICHIA-COLI; INNATE IMMUNITY; GASTROINTESTINAL MICROFLORA; CONVENTIONAL CONDITIONS; ANTIBODY-FORMATION; MOLECULAR MIMICRY; BALB/C MICE; CPG-DNA	Commensal microflora (normal microflora, indigenous microbiota) consists of those micro-organisms, which are present on body surfaces covered by epithelial cells and are exposed to the external environment (gastrointestinal and respiratory tract, vagina, skin, etc.). The number of bacteria colonising mucosal and skin surfaces exceeds the number of cells forming human body. Commensal bacteria co-evolved with their hosts, however, under specific conditions they are able to overcome protective host responses and exert pathologic effects. Resident bacteria form complex ecosystems, whose diversity is enormous. The most abundant microflora. is present in the distal parts of the gut; the majority of the intestinal bacteria are Gram-negative anaerobes. More than 50% of intestinal bacteria cannot be cultured by conventional microbiological techniques. Molecular biological methods help in analysing the structural and functional complexity of the microflora and in identifying its components. Resident microflora contains a number of components able to activate innate and adaptive immunity. Unlimited immune activation in response to signals from commensal bacteria could pose the risk of inflammation; immune responses to mucosal microbiota therefore require a precise regulatory control. The mucosal immune system has developed specialised regulatory, anti-inflammatory mechanisms for eliminating or tolerating non-dangerous, food and airborne antigens and commensal micro-organisms (oral, mucosal tolerance). However, at the same time the mucosal immune system must provide local defense mechanisms against environmental threats (e.g. invading pathogens). This important requirement is fulfilled by several mechanisms of mucosal immunity: strongly developed innate defense mechanisms ensuring appropriate function of the mucosal barrier, existence of unique types of lymphocytes and their products, transport of polymeric immunoglobulins through epithelial cells into secretions (slgA) and migration and homing of cells originating from the mucosal organised tissues in mucosae and exocrine glands. The important role of commensal bacteria in development of optimally functioning mucosal immune system was demonstrated in germ-free animals (using gnotobiological techniques). Involvement of commensal microflora and its components with strong immunoactivating properties (e.g. LPS, peptidoglycans, superantigens, bacterial DNA, Hsp) in etiopathogenetic mechanism of various complex, multifactorial and multigenic diseases, including inflammatory bowel diseases, periodontal disease, rheumatoid arthritis, atherosclerosis, allergy, multiorgan failure, colon cancer has been recently suggested. Animal models of human diseases reared in defined gnotobiotic conditions are helping to elucidate the aetiology of these frequent disorders. An improved understanding of commensal bacteria-host interactions employing germ-free animal models with selective colonisation strategies combined with modern molecular techniques could bring new insights into the mechanisms of mucosal immunity and also into pathogenetic mechanisms of several infectious, inflammatory, autoimmune and neoplastic diseases. Regulation of microflora composition (e.g. by probiotics and prebiotics) offers the possibility to influence the development of mucosal and systemic immunity but it can play a role also in prevention and treatment of some diseases. (C) 2004 Elsevier B.V. All rights reserved.	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Lett.	MAY 15	2004	93	2-3					97	108		10.1016/j.imlet.2004.02.005		12	Immunology	Immunology	828SP	WOS:000221993600001	15158604	
J	Daisey, JM; Angell, WJ; Apte, MG				Daisey, JM; Angell, WJ; Apte, MG			Indoor air quality, ventilation and health symptoms in schools: an analysis of existing information	INDOOR AIR			English	Article						allergy; asthma; microbiological contaminant; carbon dioxide concentration; formaldehyde; sick building syndrome; ventilation rate	VOLATILE ORGANIC-COMPOUNDS; BUILDING SYNDROME SYMPTOMS; DAY-CARE-CENTERS; DER-P-I; FEL-D-I; RESPIRATORY SYMPTOMS; CO2 CONCENTRATIONS; SMOOTH FLOORS; DUST; CHILDREN	We reviewed the literature on Indoor Air Quality (IAQ), ventilation, and building-related health problems in schools and identified commonly reported building-related health symptoms involving schools until 1999. We collected existing data on ventilation rates, carbon dioxide (CO(2) ) concentrations and symptom-relevant indoor air contaminants, and evaluated information on causal relationships between pollutant exposures and health symptoms. Reported ventilation and CO(2) data strongly indicate that ventilation is inadequate in many classrooms, possibly leading to health symptoms. Adequate ventilation should be a major focus of design or remediation efforts. Total volatile organic compounds, formaldehyde (HCHO) and microbiological contaminants are reported. Low HCHO concentrations were unlikely to cause acute irritant symptoms (<0.05 ppm), but possibly increased risks for allergen sensitivities, chronic irritation, and cancer. Reported microbiological contaminants included allergens in deposited dust, fungi, and bacteria. Levels of specific allergens were sufficient to cause symptoms in allergic occupants. Measurements of airborne bacteria and airborne and surface fungal spores were reported in schoolrooms. Asthma and 'sick building syndrome' symptoms are commonly reported. The few studies investigating causal relationships between health symptoms and exposures to specific pollutants suggest that such symptoms in schools are related to exposures to volatile organic compounds (VOCs), molds and microbial VOCs, and allergens.	Univ Calif Berkeley, Lawrence Berkeley Lab, Indoor Environm Dept, Berkeley, CA 94720 USA; Univ Minnesota, Minnesota Extens Serv, Indoor Air Qual Project, St Paul, MN 55108 USA	Apte, MG (reprint author), Univ Calif Berkeley, Lawrence Berkeley Lab, Indoor Environm Dept, MS 90-3058,1 Cyclotron Rd, Berkeley, CA 94720 USA.	mgapte@lbl.gov			NIAID NIH HHS [K24 AI106822, R01 AI073964]		*ACGIH, 1995, AM C GOV HYG; Apte MG, 2000, INDOOR AIR, V10, P246, DOI 10.1034/j.1600-0668.2000.010004246.x; ASHRAE, 1999, 621999 ASHRAE; Bates J.M., 1996, P IND AIR 96 7 INT C, V1, P551; BAYER CW, 1992, P IAQ 92 ENV PEOPL A, P197; BAYER CW, 1995, P ASHRAE IAQ 95 C, P101; BLACK MS, 1995, P ASHRAE IAQ 95 C, P25; BRENNAN T, 1991, P ASHRAE IAQ 91 HLTH, P228; BRUNDAGE JF, 1988, JAMA-J AM MED ASSOC, V259, P2108, DOI 10.1001/jama.259.14.2108; *CARB, 1991, FORM HOM IND AIR QUA; *CARB, 1991, FORM HOM IND AIR Q S; CASEY ME, 1995, P ENG SOL IND AIR QU; CAVALLO D, 1993, P 6 INT C IND AIR QU, V2, P45; *CDNHW, 1987, EXP GUID R ES IND AI; COUSINS DM, 1989, P ASHRAE C IAQ 87 HU, P104; Daisey J.M., 1998, LBNL41517; Dotterud LK, 1996, INDOOR AIR, V6, P71, DOI 10.1111/j.1600-0668.1996.t01-2-00002.x; DYBENDAL T, 1989, ALLERGY, V44, P401, DOI 10.1111/j.1398-9995.1989.tb04171.x; DYBENDAL T, 1992, CLIN EXP ALLERGY, V22, P1100, DOI 10.1111/j.1365-2222.1992.tb00136.x; FISHER G, 1994, RADIAT PROT DOSIM, V56, P51; FISK WJ, 2001, INDOOR AIR QUALITY H, P1; Gallup J. 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J	Lake, SL; Lyon, H; Tantisira, K; Silverman, EK; Weiss, ST; Laird, NM; Schaid, DJ				Lake, SL; Lyon, H; Tantisira, K; Silverman, EK; Weiss, ST; Laird, NM; Schaid, DJ			Estimation and tests of haplotype-environment interaction when linkage phase is ambiguous	HUMAN HEREDITY			English	Article						haplotype; association; gene-environment interaction; generalized linear model	EM ALGORITHM; MAXIMUM-LIKELIHOOD; GENOMIC CONTROL; INCOMPLETE DATA; GENE PROMOTER; INTERLEUKIN-10; ASSOCIATION; POPULATION; ASTHMA; POLYMORPHISMS	In the study of complex traits, the utility of linkage analysis and single marker association tests can be limited for researchers attempting to elucidate the complex interplay between a gene and environmental covariates. For these purposes, tests of gene-environment interactions are needed. In addition, recent studies have indicated that haplotypes, which are specific combinations of nucleotides on the same chromosome, may be more suitable as the unit of analysis for statistical tests than single genetic markers. The difficulty with this approach is that, in standard laboratory genotyping, haplotypes are often not directly observable. Instead, unphased marker phenotypes are collected. In this article, we present a method for estimating and testing haplotype-environment interactions when linkage phase is potentially ambiguous. The method builds on the work of Schaid et al. [2002] and is applicable to any trait that can be placed in the generalized linear model framework. Simulations were run to illustrate the salient features of the method. addition, the method was used to test for haplotype-smoking exposure interaction with data from the Childhood Asthma Management Program. Copyright (C) 2003 S. Karger AG, Basel.	Harvard Univ, Sch Med, Brigham & Womens Hosp, Channing Lab, Boston, MA USA; EigenStat, Brookline, MA USA; Harvard Partners Ctr Genet & Genom, Partners Hlth Care, Boston, MA USA; Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA; Mayo Clin & Mayo Fdn, Dept Hlth Sci, Rochester, MI USA; Mayo Clin & Mayo Fdn, Res Dept, Rochester, MI USA; Mayo Clin & Mayo Fdn, Dept Med Genet, Rochester, MI USA	Lake, SL (reprint author), Channing Labs, 181 Longwood Ave, Boston, MA 02115 USA.				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Hered.		2003	55	1					56	65		10.1159/000071811		10	Genetics & Heredity	Genetics & Heredity	712NT	WOS:000184804300008	12890927	
J	Glezen, WP; Greenberg, SB; Atmar, RL; Piedra, PA; Couch, RB				Glezen, WP; Greenberg, SB; Atmar, RL; Piedra, PA; Couch, RB			Impact of respiratory virus infections on persons with chronic underlying conditions	JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION			English	Article							SYNCYTIAL VIRUS; AIR-POLLUTION; DISEASE HOSPITALIZATIONS; INFLUENZA EPIDEMICS; VIRAL-INFECTIONS; ASTHMA; CHILDREN; ADULTS; ILLNESS; VACCINE	Context While hospitalization rates have declined overall, hospitalizations for acute lower respiratory tract infections have increased steadily since 1980. Development of new approaches for prevention of acute respiratory tract conditions requires studies of the etiologies of infections and quantification of the risk of hospitalization for vulnerable patients. Objective To determine the frequency of specific virus infections associated with acute respiratory tract conditions leading to hospitalization of chronically ill patients. Design Analysis of viral etiology of patients hospitalized with acute respiratory tract conditions between July 1991 and June 1995. Setting Four large clinics and related hospitals serving diverse populations representative of Harris County, Texas. Patients A total of 1029 patients who were hospitalized for pneumonia, tracheobronchitis, bronchiolitis, croup, exacerbations of asthma or chronic obstructive pulmonary disease, and/or congestive heart failure. Main Outcome Measure Virus infection, defined by culture, antigen detection, and significant rise in serum antibodies, by underlying condition; hospitalization rates by low- vs middle-income status. Results Ninety-three percent of patients older than 5 years had a chronic underlying condition; a chronic pulmonary condition was most common. Patients with chronic pulmonary disease from low-income populations were hospitalized at a rate of 398.6 per 10 000, almost 8 times higher than the rate for patients from middle-income groups (52.2 per 10 000; P<.001). Of the 403 patients (44.4% of adults and 32.3% of children) who submitted convalescent serum specimens for antibody testing, respiratory tract virus infections were detected in 181 (44.9%). influenza, parainfluenza, and respiratory syncytial virus (RSV) infections accounted for 75% of all virus infections. Conclusions Our study suggests that respiratory virus infections commonly trigger serious acute respiratory conditions that result in hospitalization of patients with chronic underlying conditions, highlighting the need for development of effective vaccines for these viruses, especially for parainfluenza and RSV.	Baylor Coll Med, Dept Microbiol & Immunol, Houston, TX 77030 USA; Baylor Coll Med, Dept Med, Houston, TX 77030 USA	Glezen, WP (reprint author), Baylor Coll Med, Dept Microbiol & Immunol, 1 Baylor Plaza, Houston, TX 77030 USA.				NIAID NIH HHS [AI15103]		ABRAMSON M, 1994, J ASTHMA, V31, P367, DOI 10.3109/02770909409061316; *ADV COMM IMM PRAC, 1998, MMWR-MORBID MORTAL W, V47, P1; AGIUS G, 1990, J MED VIROL, V30, P117, DOI 10.1002/jmv.1890300208; Atmar RL, 1998, ARCH INTERN MED, V158, P2453, DOI 10.1001/archinte.158.22.2453; BAXTER BD, 1977, J CLIN MICROBIOL, V6, P19; BRAUNFAHRLANDER C, 1992, AM REV RESPIR DIS, V145, P42; BUSSE WW, 1993, ASTHMA, P345; Dowell SF, 1996, J INFECT DIS, V174, P456; Drews AL, 1997, CLIN INFECT DIS, V25, P1421, DOI 10.1086/516137; ENGLUND JA, 1988, ANN INTERN MED, V109, P203; FALSEY AR, 1995, J INFECT DIS, V172, P389; Fleiss J. 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Am. Med. Assoc.	JAN 26	2000	283	4					499	505		10.1001/jama.283.4.499		7	Medicine, General & Internal	General & Internal Medicine	276LT	WOS:000084879800029	10659876	
J	Douwes, J; Gibson, P; Pekkanen, J; Pearce, N				Douwes, J; Gibson, P; Pekkanen, J; Pearce, N			Non-eosinophilic asthma: importance and possible mechanisms	THORAX			English	Review							ANTI-IGE ANTIBODY; PARTICULATE AIR-POLLUTION; HOUSE-DUST ENDOTOXIN; INDUCED SPUTUM; NEUTROPHILIC INFLAMMATION; AMBIENT OZONE; BRONCHIAL HYPERREACTIVITY; INHALED CORTICOSTEROIDS; MONOCLONAL-ANTIBODY; OCCUPATIONAL ASTHMA	There is increasing evidence that inflammatory mechanisms other than eosinophilic inflammation may be involved in producing the final common pathway of enhanced bronchial reactivity and reversible airflow obstruction that characterises asthma. A review of the literature has shown that, at most, only 50% of asthma cases are attributable to eosinophilic airway inflammation. It is hypothesised that a major proportion of asthma is based on neutrophilic airway inflammation, possibly triggered by environmental exposure to bacterial endotoxin, particulate air pollution, and ozone, as well as viral infections. If there are indeed two (or more) subtypes of asthma, and if non-eosinophilic (neutrophil mediated) asthma is relatively common, this would have major consequences for the treatment and prevention of asthma since most treatment and prevention strategies are now almost entirely focused on allergic/eosinophilic asthma and allergen avoidance measures, respectively. It is therefore important to study the aetiology of asthma further, including the underlying inflammatory profiles.	Univ Utrecht, IRAS, Div Environm & Occupat Hlth, NL-3508 TD Utrecht, Netherlands; John Hunter Hosp, Newcastle, NSW, Australia; Natl Publ Hlth Inst, Environm Epidemiol Unit, Kuopio, Finland; Massey Univ, Ctr Publ Hlth Res, Wellington, New Zealand	Douwes, J (reprint author), Univ Utrecht, IRAS, Div Environm & Occupat Hlth, POB 80176, NL-3508 TD Utrecht, Netherlands.			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J	McConnell, R; Berhane, K; Yao, L; Jerrett, M; Lurmann, F; Gilliland, F; Kunzli, N; Gauderman, J; Avol, E; Thomas, D; Peters, J				McConnell, R; Berhane, K; Yao, L; Jerrett, M; Lurmann, F; Gilliland, F; Kunzli, N; Gauderman, J; Avol, E; Thomas, D; Peters, J			Traffic, susceptibility, and childhood asthma	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; asthma; child; epidemiology; traffic	ENVIRONMENTAL TOBACCO-SMOKE; CHRONIC RESPIRATORY SYMPTOMS; AMBIENT NITROGEN-DIOXIDE; AIR-POLLUTION; WHEEZING ILLNESS; PARENTAL SMOKING; MATERNAL SMOKING; SCHOOL-CHILDREN; MAJOR HIGHWAY; EXPOSURE	Results from studies of traffic and childhood asthma have been inconsistent, but there has been little systematic evaluation of susceptible subgroups. In this study, we examined the relationship of local traffic-related exposure and asthma and wheeze in southern California school children (5-7 years of age). Lifetime history of doctor-diagnosed asthma and prevalent asthma and wheeze were evaluated by questionnaire. Parental history of asthma and child's history of allergic symptoms, sex, and early-life exposure (residence at the same home since 2 years of age) were examined as susceptibility factors. Residential exposure was assessed by proximity to a major road and by modeling exposure to local traffic-related pollutants. Residence within 75 in of a major road was associated with an increased risk of lifetime asthma [odds ratio (OR) = 1.29; 95% confidence interval (CI), 1.01-1.86], prevalent asthma (OR = 1.50; 95% Cl, 1.16-1-95), and wheeze (OR = 1.40; 95% Cl, 1.09-1-78). Susceptibility increased in long-term residents with no parental history of asthma for lifetime asthma (OR = 1.85; 95% Cl, 1. 11-3.09), prevalent asthma (OR = 2.46; 95% Cl, 0.48-4.09), and recent wheeze (OR = 2.74; 95% Cl, 1.71-4-39). The higher risk of asthma near a major road decreased to background rates at 150-200 in from the road. In children with a parental history of asthma and in children moving to the residence after 2 years of age, there was no increased risk associated with exposure. Effect of residential proximity to roadways was also larger in girls. A similar pattern of effects was observed with traffic-modeled exposure. These results indicate that residence near a major road is associated with asthma. The reason for larger effects in those with no parental history of asthma merits further investigation.	Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA; Sonoma Technol Inc, Petaluma, CA USA	McConnell, R (reprint author), Univ So Calif, Keck Sch Med, Dept Prevent Med, 1540 Alcazar St,CHP 236, Los Angeles, CA 90033 USA.	rmcconne@usc.edu	Kunzli, Nino/F-7195-2014	Kunzli, Nino/0000-0001-8360-080X	NHLBI NIH HHS [5R01HL61768, R01 HL061768]; NIEHS NIH HHS [P01 ES011627, 5 P01 ES009581, 5 P01 ES011627, 5P30ES007048, P01 ES009581, P30 ES007048]		Almqvist C, 2003, J ALLERGY CLIN IMMUN, V111, P800, DOI 10.1067/mai.2003.1334; Beasley R, 2001, Pediatr Pulmonol, VSuppl 23, P149; Brauer M, 2002, AM J RESP CRIT CARE, V166, P1092, DOI 10.1164/rccm.200108-007OC; Briggs DJ, 2000, SCI TOTAL ENVIRON, V253, P151, DOI 10.1016/S0048-9697(00)00429-0; BURR ML, 1992, CLIN EXP ALLERGY, V22, P509, DOI 10.1111/j.1365-2222.1992.tb00158.x; Douwes J, 2002, THORAX, V57, P643, DOI 10.1136/thorax.57.7.643; Ehrlich RI, 1995, INT J EPIDEMIOL, V24, P1138, DOI 10.1093/ije/24.6.1138; English P, 1999, ENVIRON HEALTH PERSP, V107, P761, DOI 10.2307/3434663; Gauderman WJ, 2005, EPIDEMIOLOGY, V16, P737, DOI 10.1097/01.ede.00001813087.51440.75; Gautrin D, 2003, EUR RESPIR J, V22, P551, DOI 10.1183/09031936.03.00047803; 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; 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; GORDIAN ME, 2005, J EXPO ANAL ENV EPID; Hastie T, 1990, GEN ADDITIVE MODELS; *ISAAC STEER COMM, 1998, INT STUD ASTHM ALL C; Ising H., 2002, NOISE HEALTH, V4, P13; Jaakkola JJK, 2001, ENVIRON HEALTH PERSP, V109, P579, DOI 10.2307/3455031; Janssen NAH, 2003, ENVIRON HEALTH PERSP, V111, P1512, DOI 10.1289/ehp.6243; Jenkins HS, 1999, AM J RESP CRIT CARE, V160, P33; Kehrl HR, 1999, J ALLERGY CLIN IMMUN, V104, P1198; KERSHAW CR, 1987, J ROY SOC MED, V80, P683; Kim JJ, 2004, AM J RESP CRIT CARE, V170, P520, DOI 10.1164/rccm.200403-2810C; KITANI H, 1993, ACTA MED OKAYAMA, V47, P317; Kunzli N, 2003, AM J PUBLIC HEALTH, V93, P1494, DOI 10.2105/AJPH.93.9.1494; Li N, 2003, CLIN IMMUNOL, V109, P250, DOI 10.1016/j.clim.2003.08.006; London SJ, 2001, EPIDEMIOLOGY, V12, P577, DOI 10.1097/00001648-200109000-00019; Martinez JC, 1999, PEDIATRICS, V103, P1, DOI 10.1542/peds.103.1.1; McConnell R, 2002, LANCET, V359, P386, DOI 10.1016/S0140-6736(02)07597-9; Morris SE, 2000, J EPIDEMIOL COMMUN H, V54, P75, DOI 10.1136/jech.54.1.75; Nicolai T, 2003, EUR RESPIR J, V21, P956, DOI 10.1183/09031936.03.00041103; Oosterlee A, 1996, OCCUP ENVIRON MED, V53, P241; PALMIERI M, 1990, EUR J PEDIATR, V149, P738, DOI 10.1007/BF01959535; Pearce N, 1999, THORAX, V54, P268; Peden DB, 2000, ENVIRON HEALTH PERSP, V108, P475, DOI 10.2307/3454539; Pershagen G, 1995, INT J EPIDEMIOL, V24, P1147, DOI 10.1093/ije/24.6.1147; Ross Z, 2006, J EXPO SCI ENV EPID, V16, P106, DOI 10.1038/sj.jea.7500442; Schelegle ES, 2003, TOXICOL APPL PHARM, V191, P74, DOI 10.1016/S0041-008X(03)00218-7; Shima M, 2003, J EPIDEMIOL, V13, P108; Strachan DP, 1996, BRIT MED J, V312, P1195; Strachan DP, 1998, THORAX, V53, P204; Strachan DP, 1996, AM J RESP CRIT CARE, V154, P1629; van Strien RT, 2002, ENVIRON HEALTH PERSP, V110, pA693; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; Venables WN, 2002, MODERN APPL STAT S P; 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; WALDRON G, 1995, J PUBLIC HEALTH MED, V17, P85; WJST M, 1993, BRIT MED J, V307, P596; Zhu YF, 2002, J AIR WASTE MANAGE, V52, P1032; Zmirou D, 2004, J EPIDEMIOL COMMUN H, V58, P18, DOI 10.1136/jech.58.1.18	52	314	321	4	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.	MAY	2006	114	5					766	772		10.1289/ehp.8594		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	039LZ	WOS:000237308500048	16675435	
J	Agostoni, A; Aygoren-Pursun, E; Binkley, KE; Blanch, A; Bork, K; Bouillet, L; Bucher, C; Castaldo, AJ; Cicardi, M; Davis, AE; De Carolis, C; Drouet, C; Duponchel, C; Farkas, H; Fay, K; Fekete, B; Fischer, B; Fontana, L; Fust, G; Giacomelli, R; Groner, A; Hack, CE; Harmat, G; Jakenfelds, J; Juers, M; Kalmar, L; Kaposi, PN; Karadi, I; Kitzinger, A; Kollar, T; Kreuz, W; Lakatos, P; Longhurst, HJ; Lopez-Trascasa, M; Martinez-Saguer, I; Monnier, N; Nagy, I; Nemeth, E; Nielsen, EW; Nuijens, JH; O'Grady, C; Pappalardo, E; Penna, V; Perricone, C; Perricone, R; Rauch, U; Roche, O; Rusicke, E; Spath, PJ; Szendei, G; Takacs, E; Tordai, A; Truedsson, L; Varga, L; Visy, B; Williams, K; Zanichelli, A; Zingale, L				Agostoni, Angelo; Aygoeren-Puersuen, Emel; Binkley, Karen E.; Blanch, Alvaro; Bork, Konrad; Bouillet, Laurence; Bucher, Christoph; Castaldo, Anthony J.; Cicardi, Marco; Davis, Alvin E., III; De Carolis, Caterina; Drouet, Christian; Duponchel, Christiane; Farkas, Henriette; Fay, Kalman; Fekete, Bela; Fischer, Bettina; Fontana, Luigi; Fuest, George; Giacomelli, Roberto; Groener, Albrecht; Hack, C. Erik; Harmat, George; Jakenfelds, John; Juers, Mathias; Kalmar, Lajos; Kaposi, Pal N.; Karadi, Istvan; Kitzinger, Arianna; Kollar, Timea; Kreuz, Wolfhart; Lakatos, Peter; Longhurst, Hilary J.; Lopez-Trascasa, Margarita; Martinez-Saguer, Inmaculada; Monnier, Nicole; Nagy, Istvan; Nemeth, Eva; Nielsen, Erik Waage; Nuijens, Jan H.; O'Grady, Caroline; Pappalardo, Emanuela; Penna, Vincenzo; Perricone, Carlo; Perricone, Roberto; Rauch, Ursula; Roche, Olga; Rusicke, Eva; Spaeth, Peter J.; Szendei, George; Takacs, Edit; Tordai, Attila; Truedsson, Lennart; Varga, Lilian; Visy, Beata; Williams, Kayla; Zanichelli, Andrea; Zingale, Lorenza			Hereditary and acquired angioedema: Problems and progress: Proceedings of the third C1 esterase inhibitor deficiency workshop and beyond	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						AAE; acquired angioedema; angioedema; C1 esterase inhibitor; C1-INH; HAE; HANE; HANO; hereditary angioedema; hereditary angioneurotic edema; angioneurotic edema; chemically induced angioedema; human SERPING1 protein	HORMONE REPLACEMENT THERAPY; MOLECULAR-WEIGHT KININOGEN; FACTOR-VIII CONCENTRATE; FACTOR FACTOR-XII; CONVERTING-ENZYME-ACTIVITY; OVARIAN FOLLICULAR-FLUID; PLASMA KALLIKREIN/KININ SYSTEM; HELICOBACTER-PYLORI INFECTION; NORMAL C1-INHIBITOR ACTIVITY; EPSILON AMINOCAPROIC ACID	Hereditary angioedema (HAE), a rare but life-threatening condition, manifests as acute attacks of facial, laryngeal, genital, or peripheral swelling or abdominal pain secondary to intra-abdominal edema. Resulting from mutations affecting C1 esterase inhibitor (C1-INH), inhibitor of the first complement system component, attacks are not histamine-mediated and do not respond to antihistamines or corticosteroids. Low awareness and resemblance to other disorders often delay diagnosis; despite availability of C1-INH replacement in some countries, no approved, safe acute attack therapy exists in the United States. The biennial C1 Esterase Inhibitor Deficiency Workshops resulted from a European initiative for better knowledge and treatment of HAE and related diseases. This supplement contains work presented at the third workshop and expanded content toward a definitive picture of angioedema in the absence of allergy. Most notably, it includes cumulative genetic investigations; multinational laboratory diagnosis recommendations; current pathogenesis hypotheses; suggested prophylaxis and acute attack treatment, including home treatment; future treatment options; and analysis of patient subpopulations, including pediatric patients and patients whose angioedema worsened during pregnancy or hormone administration. Causes and management of acquired angioedema and a new type of angioedema with normal C1-INH are also discussed. Collaborative patient and physician efforts, crucial in rare diseases, are emphasized. This supplement seeks to raise awareness and aid diagnosis of HAE, optimize treatment for all patients, and provide a platform for further research in this rare, partially understood disorder. (J Allergy Clin Immunol 2004;114:S51-131.)	[Cicardi, Marco] Univ Milan, Osped S Giuseppe, Dipartimento Med Interna, Milan, Italy	Agostoni, A (reprint author), Care of Williams T, Dyax Corp, 300 Technol Sq, Cambridge, MA 02139 USA.		Kalmar, Lajos/C-3040-2014; Roche, Olga/K-9342-2014; Lopez-Trascasa, Margarita/L-2699-2014; cicardi, marco/K-9219-2016	Kalmar, Lajos/0000-0003-3691-8350; Lopez-Trascasa, Margarita/0000-0001-8594-282X; cicardi, marco/0000-0003-1251-225X; Giacomelli, Roberto/0000-0003-0670-9638; Perricone, Carlo/0000-0003-4771-6981; Roche, Olga/0000-0003-1884-8256	Kallikrein, LLC; Genzyme Corporation, Cambridge, Mass	Supported by Kallikrein, LLC, a joint venture of Dyax Corp., and Genzyme Corporation, Cambridge, Mass.	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J	Krieger, J; Higgins, DL				Krieger, J; Higgins, DL			Housing and health: Time again for public health action	AMERICAN JOURNAL OF PUBLIC HEALTH			English	Review							INNER-CITY CHILDREN; RISK-FACTORS; SOCIOECONOMIC-STATUS; TUBERCULOSIS INFECTION; BRONCHIAL OBSTRUCTION; ENVIRONMENTAL-CONTROL; RESPIRATORY SYMPTOMS; HOMELESS CHILDREN; IMPACT ASSESSMENT; ALAMEDA-COUNTY	Poor housing conditions are associated with a wide range of health conditions, including respiratory infections, asthma. lead poisoning. injuries, and mental health. Addressing housing issues offers public health practitioners an opportunity to address an important social determinant of health. Public health has long been involved in housing issues, In the 19th century. health officials targeted poor sanitation, crowding, and inadequate ventilation to reduce infectious diseases as well as fire hazards to decrease injuries, Today, public health departments can employ multiple strategies to improve housing, such as developing and enforcing housing guidelines and codes, implementing ''Healthy Homes'' programs to improve indoor environmental quality, assessing housing conditions, and advocating for healthy, affordable housing, Now is the time for public health to create healthier homes by confronting substandard housing.	Publ Hlth Seattle & King Cty, EPE, Seattle, WA 98104 USA; Univ Washington, Sch Med, Seattle, WA 98195 USA; Univ Washington, Sch Publ Hlth, Seattle, WA 98195 USA; Ctr Dis Control & Prevent, Atlanta, GA USA	Krieger, J (reprint author), Publ Hlth Seattle & King Cty, EPE, 999 3rd Ave,12th Floor, Seattle, WA 98104 USA.						*AM PUBL HLTH ASS, 1971, BAS HLTH PRINC HOUS; *AM PUBL HLTH ASS, 1938, BAS PRINC HEALTHF HO; *APHA PROGR AR COM, 1969, AM J PUBLIC HEALTH, V59, P841; *ASHRAE, 1981, 621981 ANSIASHRAE; ASHRAE, 1981, 551981 ANSIASHRAE; Barr RG, 2001, AM J PUBLIC HEALTH, V91, P1487, DOI 10.2105/AJPH.91.9.1487; Bierman CW, 1996, IMMUNOL ALLERGY CLIN, V16, P753, DOI 10.1016/S0889-8561(05)70269-1; Billings C G, 1998, Monaldi Arch Chest Dis, V53, P43; Boardman B., 1993, UNHEALTHY HOUSING RE, P282; Bornehag CG, 2001, INDOOR AIR, V11, P72; Bosma H, 2001, AM J EPIDEMIOL, V153, P363, DOI 10.1093/aje/153.4.363; Brownson RC, 2001, AM J PUBLIC HEALTH, V91, P1995, DOI 10.2105/AJPH.91.12.1995; BRUNEKREEF B, 1989, AM REV RESPIR DIS, V140, P1363; Bull MJ, 2001, PEDIATRICS, V107, P1188; Burridge R., 1993, UNHEALTHY HOUSING RE, P420; BYRNE D, 1993, UNHEALTHY HOUSING RE, P41; CARP FM, 1977, GERONTOLOGIST, V17, P242; *CDCP, 2002, ABOUT LEAD; Centers for Disease Control and Prevention, 1999, MMWR-MORBID MORTAL W, V48, P143; Chadwick E., 1965, REPORT SANITARY COND; Cohen D, 2000, AM J PUBLIC HEALTH, V90, P230, DOI 10.2105/AJPH.90.2.230; Coleman William, 1982, DEATH IS SOCIAL DIS; COLLINS KJ, 1986, AGE AGEING, V15, P212, DOI 10.1093/ageing/15.4.212; Collins K., 1993, UNHEALTHY HOUSING RE, P117; CONWAY J, 1993, UNHEALTHY HOUSING RE, P283; Cook DG, 1997, THORAX, V52, P1081; *COUNC HYG PUBL HL, 1865, SAN COND CIT REP COU; Cubbin C, 2000, J EPIDEMIOL COMMUN H, V54, P517, DOI 10.1136/jech.54.7.517; Dales R. 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J. Public Health	MAY	2002	92	5					758	768		10.2105/AJPH.92.5.758		11	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	545MV	WOS:000175222200025	11988443	
J	Gale, CR; Robinson, SM; Harvey, NC; Javaid, MK; Jiang, B; Martyn, CN; Godfrey, KM; Cooper, C				Gale, C. R.; Robinson, S. M.; Harvey, N. C.; Javaid, M. K.; Jiang, B.; Martyn, C. N.; Godfrey, K. M.; Cooper, C.		Princess Anne Hosp Study Grp	Maternal vitamin D status during pregnancy and child outcomes	EUROPEAN JOURNAL OF CLINICAL NUTRITION			English	Article						pregnancy; diet; vitamin D; infant; child	D DEFICIENCY; D SUPPLEMENTATION; HYPOVITAMINOSIS-D; FETAL GROWTH; ASIAN WOMEN; BONE MASS; WEIGHT; PREVALENCE; NUTRITION; ASTHMA	Objective: To investigate whether exposure to high maternal concentrations of 25(OH)-vitamin D in pregnancy poses any risk to the child. Design: Prospective study. Setting: Princess Anne Maternity Hospital, Southampton, UK. Subjects: A group of 596 pregnant women were recruited. A total of 466 (78%) children were examined at birth, 440 (74%) at age 9 months and 178 (30%) at age 9 years. Methods: Maternal 25 (OH)-vitamin D concentrations were measured in late pregnancy. Anthropometry of the child was recorded at birth, 9 months and 9 years. At 9 months, atopic eczema was assessed. At 9 years, children had an echocardiogram and a dual energy x-ray absorptiometry scan, blood pressure, arterial compliance and carotid intima-media thickness were measured and intelligence and psychological function assessed. Results: There were no associations between maternal 25(OH)-vitamin D concentrations and the child's body size or measures of the child's intelligence, psychological health or cardiovascular system. Children whose mothers had a 25(OH)-vitamin D concentration in pregnancy 475 nmol/l had an increased risk of eczema on examination at 9 months (OR 3.26, 95% CI 1.15-9.29, P=0.025) and asthma at age 9 years (OR 5.40, 95% CI, 1.09-26.65, P=0.038) compared to children whose mothers had a concentration of <30 nmol/l. Conclusion: Exposure to maternal concentrations of 25(OH)-vitamin D in pregnancy in excess of 75 nmol/l does not appear to influence the child's intelligence, psychological health or cardiovascular system; there could be an increased risk of atopic disorders, but this needs confirmation in other studies. Sponsorship: The study was supported by the Medical Research Council and WellChild (previously known as Children Nationwide).	[Gale, C. R.; Robinson, S. M.; Harvey, N. C.; Javaid, M. K.; Jiang, B.; Martyn, C. N.; Godfrey, K. M.; Cooper, C.; Princess Anne Hosp Study Grp] Southampton Gen Hosp, MRC, Epidemiol Resource Ctr, Southampton SO16 6YD, Hants, England	Gale, CR (reprint author), Southampton Gen Hosp, MRC, Epidemiol Resource Ctr, Southampton SO16 6YD, Hants, England.	crg@mrc.soton.ac.uk	Gale, Catharine/B-1653-2012; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Godfrey, Keith/0000-0002-4643-0618; Robinson, Sian/0000-0003-1766-7269	Medical Research Council [MC_U147585827, MC_U147574237, MC_UP_A620_1014, MC_UP_A620_1015, U.1475.00.003.00010.02(74237)]		ALFAHIM M, 1995, BRIT J NUTR, V73, P881, DOI 10.1079/BJN19950093; BONNER SE, 1995, FORTSCHR BER, V107, P43; BROOKE OG, 1981, BRIT MED J, V283, P1024; BROOKE OG, 1980, BRIT MED J, V280, P751; Butland BK, 2006, THORAX, V61, P383, DOI 10.1136/thx.2005.043646; Cole TJ, 1998, STAT MED, V17, P407, DOI 10.1002/(SICI)1097-0258(19980228)17:4<407::AID-SIM742>3.0.CO;2-L; Datt S, 2002, BJOG-INT J OBSTET GY, V109, P905, DOI 10.1016/S1470-0328(02)01171-0; Dawodu A, 2003, J PEDIATR-US, V142, P169, DOI 10.1067/mpd.2003.63; *DEP HLTH, 1998, DIET REF VAL FOOD EN; *DEP HLTH, 1998, NUTR BON HLTH REP HL, V49; FRIEDMAN WF, 1966, CIRCULATION, V34, P77; Godfrey K, 1996, BRIT MED J, V312, P410; Godfrey KM, 1996, EARLY HUM DEV, V46, P129, DOI 10.1016/0378-3782(96)01752-5; GOODENDAY LS, 1971, ANN INTERN MED, V75, P807; Goodman R, 1997, J CHILD PSYCHOL PSYC, V38, P581, DOI 10.1111/j.1469-7610.1997.tb01545.x; Holick MF, 2004, AM J CLIN NUTR, V80, p1678S; HOLLIS BW, 1984, J CLIN ENDOCR METAB, V59, P652; HOLLIS BW, 2004, AM J CLIN NUTR, V79, P726; Hypponen E, 2004, ANN NY ACAD SCI, V1037, P84, DOI 10.1196/annals.1337.013; Javaid MK, 2006, LANCET, V367, P36, DOI 10.1016/S0140-6736(06)67922-1; Jiang BY, 2006, PEDIATRICS, V117, pE257, DOI 10.1542/peds.2005-1325; Mahomed K, 1999, COCHRANE DB SYST REV, DOI [10.1002/14651858.CD000228, DOI 10.1002/14651858.CD000228]; MALABANAN AO, 1998, LANCET, V351, P806; MALLET E, 1986, OBSTET GYNECOL, V68, P300; MARYA RK, 1981, GYNECOL OBSTET INVES, V12, P155; Matheu V, 2003, J ALLERGY CLIN IMMUN, V112, P585, DOI 10.1037/mai.2003.1703; Meddeb N, 2005, OSTEOPOROSIS INT, V16, P180, DOI 10.1007/s00198-004-1658-6; Nesby-O'Dell S, 2002, AM J CLIN NUTR, V76, P187; Norman P, 2002, CARDIOVASC RES, V55, P369, DOI 10.1016/S0008-6363(02)00444-3; Poon AH, 2004, AM J RESP CRIT CARE, V170, P967, DOI 10.1164/rccm.200403-412oc; Raby BA, 2004, AM J RESP CRIT CARE, V170, P1057, DOI 10.1164/rccm.200404-447OC; Robinson S, 1996, EUR J CLIN NUTR, V50, P302; Sachan A, 2005, AM J CLIN NUTR, V81, P1060; Schroth Robert J, 2005, Int J Circumpolar Health, V64, P112; Sproston K, 2003, HLTH SURVEY ENGLAND; TODA T, 1985, TOHOKU J EXP MED, V145, P303, DOI 10.1620/tjem.145.303; Wechsler D., 1999, WECHSLER ABBREVIATED; Weiler H, 2005, CAN MED ASSOC J, V172, P757, DOI 10.1503/cmaj.1040508; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P416; Wjst M, 1999, ALLERGY, V54, P757, DOI 10.1034/j.1398-9995.1999.00193.x; Zeghoud F, 1997, AM J CLIN NUTR, V65, P771	41	310	320	6	35	NATURE PUBLISHING GROUP	LONDON	MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND	0954-3007			EUR J CLIN NUTR	Eur. J. Clin. Nutr.	JAN	2008	62	1					68	77		10.1038/sj.ejcn.1602680		10	Nutrition & Dietetics	Nutrition & Dietetics	249IK	WOS:000252221300008	17311057	
J	Ley, K				Ley, K			The role of selectins in inflammation and disease	TRENDS IN MOLECULAR MEDICINE			English	Review							ADHESION-DEFICIENCY-II; ACUTE-RENAL-FAILURE; DOUBLE MUTANT MICE; ROLLING IN-VIVO; P-SELECTIN; LEUKOCYTE RECRUITMENT; APOLIPOPROTEIN-E; ENDOTHELIAL ADHESION; ISCHEMIA-REPERFUSION; ACTIVATED PLATELETS	Selectins are carbohydrate-binding molecules that bind to fucosylated and sialylated glycoprotein ligands, and are found on endothelial cells, leukocytes and platelets. They are involved in trafficking of cells of the innate immune system, T lymphocytes and platelets. An absence of selectins or selectin ligands has serious consequences in mice or humans, leading to recurrent bacterial infections and persistent disease. Selectins are involved in constitutive lymphocyte homing, and in chronic and acute inflammation processes, including post-ischemic inflammation in muscle, kidney and heart, skin inflammation, atherosclerosis, glomerulonephritis and lupus erythematosus. Selectin-neutralizing monoclonal antibodies, recombinant soluble P-selectin glycoprotein ligand 1 and small-molecule inhibitors of selectins have been tested in clinical trials on patients with multiple trauma, cardiac indications and pediatric asthma, respectively. Anti-selectin antibodies have also been successfully used in preclinical models to deliver imaging contrast agents and therapeutics to sites of inflammation. Further improvements in the efficiency, availability, specificity and pharmacokinetics of selectin inhibitors, and specialized application routes and schedules, hold promise for therapeutic indications.	Univ Virginia, Cardiovasc Res Ctr, Charlottesville, VA 22908 USA; Univ Virginia, Dept Biomed Engn, Charlottesville, VA 22908 USA; Univ Virginia, Dept Mol Physiol & Biol Phys, Charlottesville, VA 22908 USA	Ley, K (reprint author), Univ Virginia, Cardiovasc Res Ctr, MR5 Bldg,Room 1013,POB 801394, Charlottesville, VA 22908 USA.						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Med	JUN	2003	9	6					263	268		10.1016/S1471-4914(03)00071-6		6	Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental	Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine	700TD	WOS:000184126500008	12829015	
J	Aimanianda, V; Bayry, J; Bozza, S; Kniemeyer, O; Perruccio, K; Elluru, SR; Clavaud, C; Paris, S; Brakhage, AA; Kaveri, SV; Romani, L; Latge, JP				Aimanianda, Vishukumar; Bayry, Jagadeesh; Bozza, Silvia; Kniemeyer, Olaf; Perruccio, Katia; Elluru, Sri Ramulu; Clavaud, Cecile; Paris, Sophie; Brakhage, Axel A.; Kaveri, Srini V.; Romani, Luigina; Latge, Jean-Paul			Surface hydrophobin prevents immune recognition of airborne fungal spores	NATURE			English	Article							ASPERGILLUS-FUMIGATUS; CELL-WALL; INVASIVE ASPERGILLOSIS; ALVEOLAR MACROPHAGES; CLADOSPORIUM; RESPONSES; PROTEINS; ANTIGENS; CONIDIA; HOMES	The air we breathe is filled with thousands of fungal spores (conidia) per cubic metre, which in certain composting environments can easily exceed 10 9 per cubic metre. They originate from more than a hundred fungal species belonging mainly to the genera Cladosporium, Penicillium, Alternaria and Aspergillus(1-4). Although these conidia contain many antigens and allergens(5-7), it is not known why airborne fungal microflora do not activate the host innate immune cells continuously and do not induce detrimental inflammatory responses following their inhalation. Here we show that the surface layer on the dormant conidia masks their recognition by the immune system and hence prevents immune response. To explore this, we used several fungal members of the airborne microflora, including the human opportunistic fungal pathogen Aspergillus fumigatus, in in vitro assays with dendritic cells and alveolar macrophages and in in vivo murine experiments. In A. fumigatus, this surface 'rodlet layer' is composed of hydrophobic RodA protein covalently bound to the conidial cell wall through glycosylphosphatidylinositol-remnants. RodA extracted from conidia of A. fumigatus was immunologically inert and did not induce dendritic cell or alveolar macrophage maturation and activation, and failed to activate helper T-cell immune responses in vivo. The removal of this surface 'rodlet/hydrophobin layer' either chemically (using hydrofluoric acid), genetically (Delta rodA mutant) or biologically (germination) resulted in conidial morphotypes inducing immune activation. All these observations show that the hydrophobic rodlet layer on the conidial cell surface immunologically silences airborne moulds.	[Aimanianda, Vishukumar; Clavaud, Cecile; Paris, Sophie; Latge, Jean-Paul] Inst Pasteur, Unite Aspergillus, F-75015 Paris, France; [Bayry, Jagadeesh; Elluru, Sri Ramulu; Kaveri, Srini V.] Univ Paris 06, INSERM, UMR S 872, U872, F-75006 Paris, France; [Bayry, Jagadeesh; Elluru, Sri Ramulu; Kaveri, Srini V.] Univ Paris 06, Ctr Rech Cordeliers, UMR S 872, F-75006 Paris, France; [Bayry, Jagadeesh; Elluru, Sri Ramulu; Kaveri, Srini V.] Univ Paris 05, UMR S 872, F-75006 Paris, France; [Bozza, Silvia; Romani, Luigina] Univ Perugia, Dept Expt Med & Biochem Sci, I-06122 Perugia, Italy; [Perruccio, Katia] Univ Perugia, Dept Clin & Expt Med, I-06122 Perugia, Italy; [Kniemeyer, Olaf; Brakhage, Axel A.] Leibniz Inst Nat Prod Res & Infect Biol HKI, Dept Mol & Appl Microbiol, D-07745 Jena, Germany; [Kniemeyer, Olaf; Brakhage, Axel A.] Univ Jena, D-07745 Jena, Germany	Latge, JP (reprint author), Inst Pasteur, Unite Aspergillus, F-75015 Paris, France.	jplatge@pasteur.fr	Elluru, Sri Ramulu/B-1097-2009; Aimanianda, Vishukumar/E-9204-2011; Kniemeyer, Olaf/K-1253-2013; Latge, Jean Paul/C-9846-2014; Bayry, Jagadeesh/A-6589-2011; Marion-Poll, Frederic/D-8882-2011	Aimanianda, Vishukumar/0000-0001-5813-7497; Kniemeyer, Olaf/0000-0002-9493-6402; Marion-Poll, Frederic/0000-0001-6824-0180; Elluru, Sri Ramulu/0000-0001-9188-710X; Romani, Luigina/0000-0002-1356-525X	Deutsche Forschungsgemeinschaft (DFG); EU-STREP [LSHB-CT-2004-511952, MANASP LSGBH37899]; INSERM; CNRS; Universities Paris 5 and 6	We thank J. Vani, Y. Repesse and C. Galeotti for help with dendritic cell experiments; and R. Winkler, S. Behnken and M. Potsch for help with the MALDI-TOF/TOF analysis. The research of O. K. and A. A. B. was supported by the Deutsche Forschungsgemeinschaft (DFG) Priority Programme 1160, and the EU-STREP Fungwall LSHB-CT-2004-511952 and MANASP LSGBH37899 were also awarded to J.-P. L., A. A. B. and L. R. J. B and S. V. K are supported by INSERM, CNRS and Universities Paris 5 and 6.	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J	van Staa, TP; Leufkens, HGM; Abenhaim, L; Zhang, B; Cooper, C				van Staa, TP; Leufkens, HGM; Abenhaim, L; Zhang, B; Cooper, C			Oral corticosteroids and fracture risk: relationship to daily and cumulative doses	RHEUMATOLOGY			English	Article						osteoporosis; epidemiology; glucocorticoids; fracture; risk factors	BONE-MINERAL CONTENT; RHEUMATOID-ARTHRITIS; VERTEBRAL FRACTURES; OSTEOPOROSIS; THERAPY; UK; DATABASE; ASTHMA	Objective. This study examined the effects of daily and cumulative oral corticosteroid doses on the risk of fractures. Methods. Information was obtained from the General Practice Research Database, which contains medical records of general practitioners in England and Wales. The study included 244 235 oral corticosteroid users and 244 235 controls. Results. Patients taking higher doses (at least 7.5 mg daily of prednisolone or equivalent) had significantly increased risks of non-vertebral fracture [relative rate (RR) = 1.44, 95% confidence interval (CI) 1.34-1.54], hip fracture (RR = 2.21, 95% CI 1.85-2.64) and vertebral fracture (RR = 2.83, 95% CI 2.35-2.40) relative to patients using oral corticosteroids at lower doses (less than 2.5 mg per day). Fracture risk was also elevated among people with higher cumulative exposure to oral corticosteroids over the study period, but this effect was almost wholly removed by adjustment for daily dose, age, gender and other confounding variables. Conclusions. These findings suggest that the adverse skeletal effects of oral corticosteroids manifest rapidly and are related to daily dose. The level of previous exposure to oral corticosteroids was not a strong determinant of the risk of fracture. Preventive measures against corticosteroid-induced osteoporosis should therefore be instituted as soon after the commencement of glucocorticoid therapy as possible.	Univ Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton SO16 6YD, Hants, England; Univ Utrecht, Dept Pharmacoepidemiol & Pharmacotherapy, Utrecht, Netherlands; Procter & Gamble Pharmaceut, Staines, England; Sir Mortimer B Davis Jewish Gen Hosp, Ctr Clin Epidemiol & Community Studies, Montreal, PQ, Canada; McGill Univ, Dept Epidemiol & Biostat, Montreal, PQ, Canada	Cooper, C (reprint author), Univ Southampton, Southampton Gen Hosp, MRC, Environm Epidemiol Unit, Southampton SO16 6YD, Hants, England.		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J	Brehm, JM; Celedon, JC; Soto-Quiros, ME; Avila, L; Hunninghake, GM; Forno, E; Laskey, D; Sylvia, JS; Hollis, BW; Weiss, ST; Litonjua, AA				Brehm, John M.; Celedon, Juan C.; Soto-Quiros, Manuel E.; Avila, Lydiana; Hunninghake, Gary M.; Forno, Erick; Laskey, Daniel; Sylvia, Jody S.; Hollis, Bruce W.; Weiss, Scott T.; Litonjua, Augusto A.			Serum Vitamin D Levels and Markers of Severity of Childhood Asthma in Costa Rica	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							1,25-DIHYDROXYVITAMIN D-3; D DEFICIENCY; 25-HYDROXYVITAMIN-D; EPIDEMIC; EXPOSURE; CHILDREN; INSIGHTS; REALITY; 25-HYDROXYCHOLECALCIFEROL; RADIOIMMUNOASSAY	Rationale: Maternal vitamin D intake during pregnancy has been inversely associated with asthma symptoms in early childhood. However, no study has examined the relationship between measured vitamin D levels and markers of asthma severity in childhood. Objectives: To determine the relationship between measured vitamin D levels and both markers of asthma severity and allergy in childhood. Methods: We examined the relation between 25-hydroxyvitamin D levels (the major circulating form of vitamin D) and markers of allergy and asthma severity in a cross-sectional study of 616 Costa Rican children between the ages of 6 and 14 years. Linear, logistic, and negative binomial regressions were used for the univariate and multivariate analyses. Measurements and Main Results- Of the 616 children with asthma, 175 (28%) had insufficient levels of vitamin D (<30 ng/ml). In multivariate linear regression models, vitamin D levels were significantly and inversely associated with total IgE and eosinophil count. In multivariate logistic regression models, a log(10) unit increase in vitamin D levels was associated with reduced odds of any hospitalization in the previous year (odds ratio [OR], 0.05; 95% confidence interval [CI], 0.004-0.71; P = 0.03), any use of antiinflammatory medications in the previous year (OR, 0.18; 95% Cl, 0.05-0.67; P = 0.01), and increased airway responsiveness (a <= 8.58-mu mol provocative dose of methacholine producing a 20% fall in baseline FEV1 [OR, 0.15; 95% Cl, 0.024-0.97; P = 0.05]). Conclusions: Our results suggest that vitamin D insufficiency is relatively frequent in an equatorial population of children with asthma. In these children, lower vitamin D levels are associated with increased markers of allergy and asthma severity.	[Brehm, John M.; Celedon, Juan C.; Hunninghake, Gary M.; Forno, Erick; Laskey, Daniel; Sylvia, Jody S.; Weiss, Scott T.; Litonjua, Augusto A.] Brigham & Womens Hosp, Channing Lab, Dept Med, Boston, MA 02115 USA; [Brehm, John M.; Celedon, Juan C.; Hunninghake, Gary M.; Litonjua, Augusto A.] Brigham & Womens Hosp, Div Pulm Crit Care Med, Dept Med, Boston, MA 02115 USA; [Brehm, John M.; Celedon, Juan C.; Hunninghake, Gary M.; Forno, Erick; Weiss, Scott T.; Litonjua, Augusto A.] Harvard Univ, Sch Med, Boston, MA USA; [Celedon, Juan C.; Litonjua, Augusto A.] Brigham & Womens Hosp, Ctr Genom Med, Dept Med, Boston, MA 02115 USA; [Soto-Quiros, Manuel E.; Avila, Lydiana] Hosp Nacl Ninos Dr Carlos Saenz Herrera, Dept Med, Div Pediat Pulmonol, San Jose, Costa Rica; [Forno, Erick] Childrens Hosp, Div Pediat Pulmonol, Boston, MA 02115 USA; [Hollis, Bruce W.] Med Univ S Carolina, Darby Childrens Res Inst, Charleston, SC 29425 USA	Celedon, JC (reprint author), Brigham & Womens Hosp, Channing Lab, Dept Med, 181 Longwood Ave, Boston, MA 02115 USA.	juan.celedon@channing.harvard.edu		Litonjua, Augusto/0000-0003-0422-5875; Forno, Erick/0000-0001-6497-9885	National Institutes of Health [HL66289, HL089842, HL04370, T32 HL07427]	Supported by grants HL66289, HL089842, HL04370, and T32 HL07427 from the National Institutes of Health.	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J. Respir. Crit. Care Med.	MAY 1	2009	179	9					765	771		10.1164/rccm.200808-1361OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	439YX	WOS:000265665000005	19179486	
J	Holgate, ST; Polosao, R				Holgate, Stephen T.; Polosao, Riccardo			Treatment strategies for allergy and asthma	NATURE REVIEWS IMMUNOLOGY			English	Review							REGULATORY T-CELLS; HOUSE-DUST MITE; THYMIC STROMAL LYMPHOPOIETIN; PLACEBO-CONTROLLED TRIAL; KINASE INHIBITOR R112; SMOOTH-MUSCLE-CELLS; IL-5 RECEPTOR-ALPHA; MAST-CELL; AIRWAY HYPERRESPONSIVENESS; ATOPIC-DERMATITIS	Allergic diseases have reached epidemic proportions worldwide. An understanding of the cellular and soluble mediators that are involved in allergic inflammatory responses not only helps in understanding the mechanisms of current treatments, but is also important for the identification of new targets that are amenable to both small-molecule and biological interventions. There is now considerable optimism with regards to tackling the allergy epidemic in light of improvements in systemic and mucosal allergen-specific immunotherapy, the identification of key cytokines and their receptors that drive T-helper-2-cell polarization, a clearer understanding of the pathways of leukocyte recruitment and the signalling pathways that are involved in cell activation and mediator secretion, and new approaches to vaccine development.	[Holgate, Stephen T.] Southampton Gen Hosp, IIR Div, Southampton SO16 6YD, Hants, England; [Polosao, Riccardo] Univ Catania, Dipartimento Med Interna & Specialist, I-95125 Catania, Italy	Holgate, ST (reprint author), Southampton Gen Hosp, IIR Div, F Level, Southampton SO16 6YD, Hants, England.	sth@soton.ac.uk			Medical Research Council [G0800766]		Abramson M. 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J	Gilliland, FD; Li, YF; Peters, JM				Gilliland, FD; Li, YF; Peters, JM			Effects of maternal smoking during pregnancy and environmental tobacco smoke on asthma and wheezing in children	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							PARENTAL SMOKING; CHILDHOOD ASTHMA; LUNG-FUNCTION; FAMILY HISTORY; RISK-FACTORS; PREVALENCE; EXPOSURE; COMMUNITIES; TRENDS; BIRTH	The effects of maternal smoking during pregnancy and childhood environmental tobacco smoke (ETS) exposure on asthma and wheezing were investigated in 5,762 school-aged children residing in 12 Southern California communities. Responses to a self-administered questionnaire completed by parents of 4th, 7th, and 10th grade students were used to ascertain children with wheezing or physician-diagnosed asthma. Lifetime household exposures to tobacco smoke were assessed using responses about past and current smoking histories of household members and any history of maternal smoking during pregnancy. Logistic regression models were fitted to cross-sectional data to estimate the effects of in utero exposure to maternal smoking and previous and current ETS exposure on the prevalence of wheezing and physician-diagnosed asthma. In utero exposure to maternal smoking without subsequent postnatal ETS exposure was associated with increased prevalence of physician-diagnosed asthma (OR, 1.8; 95% CI, 1.1 to 2.9), asthma with current symptoms (OR, 2.3; 95% CI, 1.3 to 4.0), asthma requiring medication use in the previous 12 mo (OR, 2.1; 95% CI, 1.2 to 3.6), lifetime history of wheezing (OR, 1.8; 95% CI, 1.2 to 2.6), current wheezing with colds (OR, 2.1; 95% CI, 1.3 to 3.4) and without colds (OR, 2.5; 95% CI, 1.4 to 4.4), persistent wheezing (OR, 3.1; 95% CI, 1.6 to 6.1), wheezing with exercise (OR, 2.4 95% CI; 1.3 to 4.3), attacks of wheezing causing shortness of breath (OR, 2.4; 95% CI, 1.3 to 4.4) or awakening at night in the previous 12 mo (OR, 3.2; 95% CI, 1.7 to 5.8), and wheezing requiring medication (OR 2.1; 95% CI, 1.2 to 3.7) or emergency room visits during the previous year (OR, 3.4; 95% CI, 1.4 to 7.8). In contrast, current and previous ETS exposure was not associated with asthma prevalence, but was consistently associated with subcategories of wheezing. Current ETS exposure was associated with lifetime wheezing (OR, 1.3; 95% CI, 1.1 to 1.5), current wheezing with colds (OR, 1.6; 95% CI, 1.3 to 2.0) and without colds (OR, 1.5; 95% CI, 1.1 to 1.9), wheezing with exercise (OR, 1.7; 95% CI, 1.3 to 2.2), attacks of wheezing causing shortness of breath (OR, 1.6; 95% CI, 1.2 to 2.1) or awakening at night (OR, 1.5; 95% CI, 1.1 to 2.0), and wheezing requiring medication (OR, 1.4; 95% CI, 1.1 to 1.8) or emergency room visits within the previous year (OR, 1.9; 95% CI, 1.2 to 3.0). The effects of current ETS exposure on subcategories of wheezing were most pronounced among children exposed to two or more smokers and remained significant after adjusting for maternal smoking during pregnancy. We conclude that maternal smoking during pregnancy increases the occurrence of physician-diagnosed asthma and wheezing during childhood. In contrast, current ETS exposure is associated with wheezing, but not physician-diagnosed asthma. Taken together, our findings support the hypothesis that ETS operates as a cofactor with other insults such as intercurrent infections as a trigger of wheezing attacks, rather than as a factor that induces asthma, whereas in utero exposure acts to increase physician-diagnosed asthma.	Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA	Gilliland, FD (reprint author), Univ So Calif, Keck Sch Med, Dept Prevent Med, 1540 Alcazar St,CHP 236, Los Angeles, CA 90033 USA.		LI, YU-FEN/F-4770-2010		NHLBI NIH HHS [1R01 HL61768-01]; NIEHS NIH HHS [5P01 ES09581, 5P30 ES07048-02]; PHS HHS [R826708-01]		ANDERSON HR, 1994, BRIT MED J, V308, P1600; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; California Environmental Protection Agency (Cal EPA) Office of Environmental Health Hazard Assessment, 1997, HLTH EFF EXP ENV TOB; Carlsen KCL, 1997, EUR RESPIR J, V10, P1774; *CDC, 1997, MMWR-MORBID MORTAL W, V46, P1038; Committee on the Assessment of Asthma and Indoor Air, 2000, CLEAR AIR ASTHM IND; Cook DG, 1999, THORAX, V54, P357; Cook DG, 1997, THORAX, V52, P1081; Cook DG, 1998, THORAX, V53, P295; Cook DG, 1998, THORAX, V53, P884; CUNNINGHAM J, 1994, AM J EPIDEMIOL, V139, P1139; Cunningham J, 1996, AM J RESP CRIT CARE, V153, P218; Ebrahim SH, 2000, JAMA-J AM MED ASSOC, V283, P361, DOI 10.1001/jama.283.3.361; Ehrlich RI, 1996, AM J RESP CRIT CARE, V154, P681; FINGERHUT LA, 1990, AM J PUBLIC HEALTH, V80, P541, DOI 10.2105/AJPH.80.5.541; Forsberg B, 1997, INT J EPIDEMIOL, V26, P610, DOI 10.1093/ije/26.3.610; Gilliland FD, 2000, THORAX, V55, P271, DOI 10.1136/thorax.55.4.271; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; Holt PG, 1999, NATURE, V402, pB12; Hu FB, 1997, ANN ALLERG ASTHMA IM, V79, P80; Joad JP, 1999, TOXICOL APPL PHARM, V155, P253, DOI 10.1006/taap.1998.8612; Lackmann GM, 1999, J NATL CANCER I, V91, P459, DOI 10.1093/jnci/91.5.459; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; RAPPAPORT S, 1998, MMWR-MORBID MORTAL W, V47, P1022; Rothman K., 1986, MODERN EPIDEMIOLOGY; Samet JM, 1995, TOXICOL LETT, V82-3, P33, DOI 10.1016/0378-4274(95)03544-3; SAS INSTITUTE, 1990, SAS STAT US GUID VER, V2; *SCOTH, 2000, REP SCI COMM TOB HLT; Stick SM, 1996, LANCET, V348, P1060, DOI 10.1016/S0140-6736(96)04446-7; Strachan DP, 1998, THORAX, V53, P204; TAGER IB, 1995, AM J RESP CRIT CARE, V152, P977; Tager IB, 1998, AM J RESP CRIT CARE, V158, P349; *USEPA, 1992, EPA600690006F; World Health Organization, 1999, WHONCDTFI9910; YOUNG S, 1991, NEW ENGL J MED, V324, P1168, DOI 10.1056/NEJM199104253241704	35	296	313	1	18	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. 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J	Bacharier, LB; Boner, A; Carlsen, KH; Eigenmann, PA; Frischer, T; Goetz, M; Helms, PJ; Hunt, J; Liu, A; Papadopoulos, N; Platts-Mills, T; Pohunek, P; Simons, FER; Valovirta, E; Wahn, U; Wildhaber, J				Bacharier, L. B.; Boner, A.; Carlsen, K. -H.; Eigenmann, P. A.; Frischer, T.; Goetz, M.; Helms, P. J.; Hunt, J.; Liu, A.; Papadopoulos, N.; Platts-Mills, T.; Pohunek, P.; Simons, F. E. R.; Valovirta, E.; Wahn, U.; Wildhaber, J.		European Pediat Asthma Grp	Diagnosis and treatment of asthma in childhood: a PRACTALL consensus report	ALLERGY			English	Review						diagnosis; education; guidelines; monitoring; pediatric asthma; treatment	EXHALED-NITRIC-OXIDE; EXERCISE-INDUCED ASTHMA; SHORT-TERM GROWTH; RANDOMIZED CONTROLLED-TRIAL; HOUSE-DUST MITE; INHALED FLUTICASONE PROPIONATE; RESPIRATORY-SYNCYTIAL-VIRUS; GRASS-POLLEN IMMUNOTHERAPY; METERED-DOSE INHALER; SKIN-TEST REACTIVITY	Asthma is the leading chronic disease among children in most industrialized countries. However, the evidence base on specific aspects of pediatric asthma, including therapeutic strategies, is limited and no recent international guidelines have focused exclusively on pediatric asthma. As a result, the European Academy of Allergy and Clinical Immunology and the American Academy of Allergy, Asthma and Immunology nominated expert teams to find a consensus to serve as a guideline for clinical practice in Europe as well as in North America. This consensus report recommends strategies that include pharmacological treatment, allergen and trigger avoidance and asthma education. The report is part of the PRACTALL initiative**, which is endorsed by both academies.	Charite Univ Med Berlin, Dept Med, Berlin, Germany; Washington Univ, Dept Pediat, St Louis, MO 63130 USA; Univ Verona, Dept Pediat, I-37100 Verona, Italy; Univ Oslo, Dept Pediat, Oslo, Norway; Univ Childrens Hosp Geneva, Geneva, Switzerland; Univ Childrens Hosp Vienna, Vienna, Austria; Med Univ Vienna, Dept Paediat & Adolescent Med, Vienna, Austria; Univ Aberdeen, Dept Child Hlth, Aberdeen, Scotland; Univ Virginia, Dept Pediat, Charlottesville, VA USA; Univ Colorado, Sch Med, Dept Pediat, Natl Jewish Med & Res Ctr, Denver, CO USA; Allergy Res Ctr, Goudi, Greece; Charles Univ Prague, Univ Hosp Motol, Dept Pediat, Prague, Czech Republic; Univ Manitoba, Dept Pediat & Child Hlth, Winnipeg, MB R3T 2N2, Canada; Turku Allergy Ctr, Turku, Finland; Univ Childrens Hosp, Dept Resp Med, Zurich, Switzerland	Wahn, U (reprint author), Charite Univ Med Berlin, Augustenburger Pl 1, D-13353 Berlin, Germany.		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J	Brauer, M; Hoek, G; van Vliet, P; Meliefste, K; Fischer, P; Gehring, U; Heinrich, J; Cyrys, J; Bellander, T; Lewne, M; Brunekreef, B				Brauer, M; Hoek, G; van Vliet, P; Meliefste, K; Fischer, P; Gehring, U; Heinrich, J; Cyrys, J; Bellander, T; Lewne, M; Brunekreef, B			Estimating long-term average particulate air pollution concentrations: Application of traffic indicators and geographic information systems	EPIDEMIOLOGY			English	Article						air pollution; environmental epidemiology; particles; geographic information systems; GIS; vehicle emissions	CHRONIC RESPIRATORY SYMPTOMS; NITROGEN-DIOXIDE; HOSPITAL ADMISSIONS; SPATIAL VARIABILITY; CHILDREN; EXPOSURE; HEALTH; ASTHMA; DENSITY; OUTDOOR	Background. As part of a multicenter study relating traffic-related air pollution with incidence of asthma in three birth cohort studies (TRAPCA), we used a measurement and modelling procedure to estimate long-term average exposure to traffic-related particulate air pollution in communities throughout the Netherlands; in Munich, Germany; and in Stockholm County, Sweden. Methods. In each of the three locations, 40-42 measurement sites were selected to represent rural, urban background and urban traffic locations. At each site and fine particles and filter absorbance (a marker for diesel exhaust particles) were measured for four 2-week periods distributed over approximately 1-year periods between February 1999 and July 2000. We used these measurements to calculate annual average concentrations after adjustment for temporal variation. Traffic-related variables (eg, population density and traffic intensity) were collected using Geographic Information Systems and used in regression models predicting annual average concentrations. From these models we estimated ambient air concentrations at the home addresses of the cohort members. Results. Regression models using traffic-related variables explained 73%, 56% and 50% of the variability in annual average fine particle concentrations for the Netherlands, Munich arid Stockholm County, respectively. For filter absorbance, the regression models explained 81%, 67% and 66% of the variability in the annual average concentrations. Cross-validation to estimate the model prediction errors indicated root mean squared errors of 1.1-1.6 mug/m(3) for PM2.5 and 0.22-0.31 *10(-5)m(-1) for absorbance. Conclusions. A substantial fraction of the variability in annual average concentrations for all locations was explained by traffic-related variables. This approach can be used to estimate individual exposures for epidemiologic studies and offers advantages over alternative techniques relying on surrogate variables or traditional approaches that utilize ambient monitoring data alone.	Univ British Columbia, Sch Occupat & Environm Hyg, Vancouver, BC V6T 1Z3, Canada; Univ Utrecht, Inst Risk Assessment Sci, Environm & Occupat Hlth Grp, Utrecht, Netherlands; Natl Inst Publ Hlth & Environm, RIVM, NL-3720 BA Bilthoven, Netherlands; GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, Neuherberg, Germany; Stockholm Cty Council, Dept Environm Hlth, Stockholm, Sweden; Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden	Brauer, M (reprint author), Univ British Columbia, Sch Occupat & Environm Hyg, 2206 E Mall, Vancouver, BC V6T 1Z3, Canada.		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J	Friedman, MS; Powell, KE; Hutwagner, L; Graham, LM; Teague, WG				Friedman, MS; Powell, KE; Hutwagner, L; Graham, LM; Teague, WG			Impact of changes in transportation and commuting behaviors during the 1996 Summer Olympic Games in Atlanta on air quality and childhood asthma	JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION			English	Article							ENVIRONMENTAL-FACTORS; HOSPITAL ADMISSIONS; RESPIRATORY HEALTH; UNITED-KINGDOM; MEXICO-CITY; POLLUTION; CHILDREN; OZONE; PREVALENCE; MORTALITY	Context Vehicle exhaust is a major source of ozone and other air pollutants. Although high ground-level ozone pollution is associated with transient increases in asthma morbidity, the impact of citywide transportation changes on air quality and childhood asthma has not been studied. The alternative transportation strategy implemented during the 1996 Summer Olympic Games in Atlanta, Ga, provided such an opportunity. Objective To describe traffic changes in Atlanta, Ca, during the 1996 Summer Olympic Games and concomitant changes in air quality and childhood asthma events. Design Ecological study comparing the 17 days of the Olympic Games (July 19-August 4, 1996) to a baseline period consisting of the 4 weeks before and 4 weeks after the Olympic Games. Setting and Subjects Children aged 1 to 16 years who resided in the 5 central counties of metropolitan Atlanta and whose data were captured in 1 of 4 databases. Main Outcome Measures Citywide acute care visits and hospitalizations for asthma (asthma events) and nonasthma events, concentrations of major air pollutants, meteorological variables, and traffic counts. Results During the Olympic Games, the number of asthma acute care events decreased 41.6% (4.23 vs 2.47 daily events) in the Georgia Medicaid claims file, 44.1% (1.36 vs 0.76 daily events) in a health maintenance organization database, 11.1% (4.77 vs 4.24 daily events) in 2 pediatric emergency departments, and 19.1% (2.04 vs 1.65 daily hospitalizations) in the Georgia Hospital Discharge Database. The number of nonasthma acute care events in the 4 databases changed -3.1%, +1.3%, -2.1%, and +1.0%, respectively. In multivariate regression analysis, only the reduction in asthma events recorded in the Medicaid database was significant (relative risk, 0.48; 95% confidence interval, 0.44-0.86). Peak daily ozone concentrations decreased 27.9%, from 81.3 ppb during the baseline period to 58.6 ppb during the Olympic Games (P<.001). Peak weekday morning traffic counts dropped 22.5% (P<.001). Traffic counts were significantly correlated with that day's peak ozone concentration (average r=0.36 for all 4 roads examined). Meteorological conditions during the Olympic Games did not differ substantially from the baseline period. Conclusions Efforts to reduce downtown traffic congestion in Atlanta during the Olympic Games resulted in decreased traffic density, especially during the critical morning period. This was associated with a prolonged reduction in ozone pollution and significantly lower rates of childhood asthma events. These data provide support for efforts to reduce air pollution and improve health via reductions in motor vehicle traffic.	Georgia Div Publ Hlth, Epidem Intelligence Serv, Atlanta, GA USA; Georgia Div Publ Hlth, Chron Dis Injury & Environm Epidemiol Sect, Epidemiol & Prevent Branch, Atlanta, GA USA; Ctr Dis Control & Prevent, Epidemiol Program Off, Atlanta, GA USA; Morehouse Sch Med, Dept Pediat, Atlanta, GA 30310 USA; Egleston Childrens Hosp, Div Pediat Pulm & Crit Care, Atlanta, GA USA; Georgia Pediat Pulm Associates, Atlanta, GA USA; Emory Univ, Atlanta, GA 30322 USA	Friedman, MS (reprint author), Ctr Dis Control & Prevent, Air Pollut & Resp Hlth Branch, Natl Ctr Environm Hlth, Atlanta, GA 30333 USA.		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J	Josefowicz, SZ; Niec, RE; Kim, HY; Treuting, P; Chinen, T; Zheng, Y; Umetsu, DT; Rudensky, AY				Josefowicz, Steven Z.; Niec, Rachel E.; Kim, Hye Young; Treuting, Piper; Chinen, Takatoshi; Zheng, Ye; Umetsu, Dale T.; Rudensky, Alexander Y.			Extrathymically generated regulatory T cells control mucosal T(H)2 inflammation	NATURE			English	Article							TRANSCRIPTION FACTOR FOXP3; IN-VIVO; BOWEL-DISEASE; INDUCTION; RESPONSES; LINEAGE; FATE; GENE; MICE; HOMEOSTASIS	A balance between pro- and anti-inflammatory mechanisms at mucosal interfaces, which are sites of constitutive exposure to microbes and non-microbial foreign substances, allows for efficient protection against pathogens yet prevents adverse inflammatory responses associated with allergy, asthma and intestinal inflammation(1). Regulatory T (T-reg) cells prevent systemic and tissue-specific autoimmunity and inflammatory lesions at mucosal interfaces. These cells are generated in the thymus (tT(reg) cells) and in the periphery (induced (i)T-reg cells), and their dual origin implies a division of labour between tT(reg) and iT(reg) cells in immune homeostasis. Here we show that a highly selective blockage in differentiation of iT(reg) cells in mice did not lead to unprovoked multi-organ autoimmunity, exacerbation of induced tissue-specific autoimmune pathology, or increased pro-inflammatory responses of T helper 1 (T(H)1) and T(H)17 cells. However, mice deficient in iT(reg) cells spontaneously developed pronounced T(H)2-type pathologies at mucosal sites-in the gastrointestinal tract and lungs-with hallmarks of allergic inflammation and asthma. Furthermore, iT(reg)-cell deficiency altered gut microbial communities. These results suggest that whereas T-reg cells generated in the thymus appear sufficient for control of systemic and tissue-specific autoimmunity, extrathymic differentiation of T-reg cells affects commensal microbiota composition and serves a distinct, essential function in restraint of allergic-type inflammation at mucosal interfaces.	[Josefowicz, Steven Z.; Niec, Rachel E.; Chinen, Takatoshi; Rudensky, Alexander Y.] Howard Hughes Med Inst, New York, NY 10021 USA; [Josefowicz, Steven Z.; Niec, Rachel E.; Chinen, Takatoshi; Rudensky, Alexander Y.] Sloan Kettering Inst, Program Immunol, New York, NY 10021 USA; [Josefowicz, Steven Z.] Rockefeller Univ, Lab Chromatin Biol & Epigenet, New York, NY 10065 USA; [Kim, Hye Young; Umetsu, Dale T.] Harvard Univ, Childrens Hosp, Sch Med, Div Immunol, Boston, MA 02115 USA; [Treuting, Piper] Univ Washington, Sch Med, Dept Comparat Med, Seattle, WA 98195 USA; [Chinen, Takatoshi] Keio Univ, Dept Microbiol & Immunol, Sch Med, Tokyo 1608582, Japan; [Zheng, Ye] Salk Inst Biol Studies, Nomis Fdn Labs Immunobiol & Microbial Pathogenesi, La Jolla, CA 92037 USA	Rudensky, AY (reprint author), Howard Hughes Med Inst, New York, NY 10021 USA.	rudenska@mskcc.org	Zheng, Ye/G-4866-2015	Zheng, Ye/0000-0001-5012-4309; josefowicz, steven/0000-0001-7453-779X	NIH MSTP [GM07739]; NINDS [1F31NS073203-01]; Department of Microbiology and Immunology, Keio University School of Medicine; NIH [R37 AI034206]	We thank T. Tedder for depleting CD20 antibody, R. Tudor for assistance interpreting lung pathology, P. DeRoos for assistance with Ig ELISA assays, B. Johnson for immunohistochemical expertise, Y. Chen for assistance with airway measurements, and E. Pamer, L. Lipuma, A. Gobourne and R. Khanin for help with analysis of intestinal microbiota. This work was supported by NIH MSTP grant GM07739 and NINDS grant 1F31NS073203-01 (R.E.N.), Strategic Young Researcher Overseas Visits Program for Accelerating Brain Circulation from Department of Microbiology and Immunology, Keio University School of Medicine (T. C.) and NIH grant R37 AI034206 (A. Y. R.). A. Y. R is an investigator with the Howard Hughes Medical Institute.	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J	Breton, CV; Byun, HM; Wenten, M; Pan, F; Yang, A; Gilliland, FD				Breton, Carrie V.; Byun, Hyang-Min; Wenten, Made; Pan, Fei; Yang, Allen; Gilliland, Frank D.			Prenatal Tobacco Smoke Exposure Affects Global and Gene-specific DNA Methylation	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						DNA methylation; epigenetics; prenatal; smoke	CHILDHOOD ASTHMA; TYROSINE PHOSPHATASES; EPIGENETIC REGULATION; MATERNAL SMOKING; CIGARETTE-SMOKE; PASSIVE SMOKING; EXPRESSION; CHILDREN; SUSCEPTIBILITY	Rationale: Prenatal exposure to tobacco smoke increases the risk for diseases later in the child's life that may be mediated through alterations in DNA methylation. Objectives: To demonstrate that differences in DNA methylation patterns occur in children exposed to tobacco smoke and that variation in detoxification genes may alter these associations. Methods: Methylation of DNA repetitive elements, LINE1 and AluYb8, was measured using bisulfite conversion and pyrosequencing in buccal cells of 348 children participating in the Children's Health Study. Gene-specific CpG methylation differences associated with smoke exposure were screened in 272 participants in the Children's Health Study children using an Illumina GoldenGate panel. CpG loci that demonstrated a statistically significant difference in methylation were validated by pyrosequencing. Estimates were standardized across loci using a Z score to enable cross-comparison of results. Measurements and Main Results: DNA methylation patterns were associated with in utero exposure to maternal smoking. Exposed children had significantly lower methylation of AluYb8 (beta, -0.31; P = 0.03). Differences in smoking-related effects on LINE1 methylation were observed in children with the common GSTM1 null genotype. Differential methylation of CpG loci in eight genes was identified through the screen. Two genes, AXL and PTPRO, were validated by pyrosequencing and showed significant increases in methylation of 0.37 (P = 0.005) and 0.34 (P = 0.02) in exposed children. The associations with maternal smoking varied by a common GSTP1 haplotype. Conclusions: Life-long effects of in utero exposures may be mediated through alterations in DNA methylation. Variants in detoxification genes may modulate the effects of in utero exposure through epigenetic mechanisms.	[Breton, Carrie V.; Wenten, Made; Gilliland, Frank D.] Univ So Calif, Dept Prevent Med, Keck Sch Med, Los Angeles, CA 90033 USA; [Byun, Hyang-Min; Yang, Allen] Univ So Calif, Keck Sch Med, Dept Hematol, Los Angeles, CA 90033 USA; [Pan, Fei; Yang, Allen] Univ So Calif, Keck Sch Med, Epigenome Canc Ctr, Los Angeles, CA 90033 USA	Gilliland, FD (reprint author), Univ So Calif, Dept Prevent Med, Keck Sch Med, 1540 Alcazar St,CHP 236, Los Angeles, CA 90033 USA.	gillilan@usc.edu		Byun, Hyang-Min/0000-0002-6278-3165	NIEHS [5P01 E5009581, SP01 ES011627, 5P30 ES007048]; Hastings Foundation; American Society of Clinical Oncology Career Development Award in Geriatric Oncology	Supported by NIEHS grants 5P01 E5009581, SP01 ES011627, and 5P30 ES007048; by the Hastings Foundation; and by a American Society of Clinical Oncology Career Development Award in Geriatric Oncology (A.Y.).	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J. Respir. Crit. Care Med.	SEP 1	2009	180	5					462	467		10.1164/rccm.200901-0135OC		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	489ZW	WOS:000269467100012	19498054	
J	Jaddoe, VWV; van Duijn, CM; Franco, OH; van der Heijden, AJ; van Ijzendoorn, MH; de Jongste, JC; van der Lugt, A; Mackenbach, JP; Moll, HA; Raat, H; Rivadeneira, F; Steegers, EAP; Tiemeier, H; Uitterlinden, AG; Verhulst, FC; Hofman, A				Jaddoe, Vincent W. V.; van Duijn, Cornelia M.; Franco, Oscar H.; van der Heijden, Albert J.; van Ijzendoorn, Marinus H.; de Jongste, Johan C.; van der Lugt, Aad; Mackenbach, Johan P.; Moll, Henriette A.; Raat, Hein; Rivadeneira, Fernando; Steegers, Eric A. P.; Tiemeier, Henning; Uitterlinden, Andre G.; Verhulst, Frank C.; Hofman, Albert			The Generation R Study: design and cohort update 2012	EUROPEAN JOURNAL OF EPIDEMIOLOGY			English	Article						Cohort; Pregnancy; Child; Fetal	POPULATION-BASED COHORT; QUALITY-OF-LIFE; CHILD HEALTH QUESTIONNAIRE; GENOME-WIDE ASSOCIATION; ISCHEMIC-HEART-DISEASE; ALL-CAUSE MORTALITY; FETAL-GROWTH; BEHAVIOR QUESTIONNAIRE; PHYSICAL-ACTIVITY; COMMON VARIANTS	The Generation R Study is a population-based prospective cohort study from fetal life until adulthood. The study is designed to identify early environmental and genetic causes and causal pathways leading to normal and abnormal growth, development and health during fetal life, childhood and adulthood. The study focuses on six areas of research: (1) maternal health; (2) growth and physical development; (3) behavioural and cognitive development; (4) respiratory health and allergies; (5) diseases in childhood; and (6) health and healthcare for children and their parents. Main exposures of interest include environmental, endocrine, genetic and epigenetic, lifestyle related, nutritional and socio-demographic determinants. In total, n = 9,778 mothers with a delivery date from April 2002 until January 2006 were enrolled in the study. Response at baseline was 61 %, and general follow-up rates until the age of 6 years exceed 80 %. Data collection in mothers, fathers and children include questionnaires, detailed physical and ultrasound examinations, behavioural observations, and biological samples. A genome and epigenome wide association screen is available in the participating children. From the age of 5 years, regular detailed hands-on assessments are performed in a dedicated research center including advanced imaging facilities such as Magnetic Resonance Imaging. Eventually, results forthcoming from the Generation R Study contribute to the development of strategies for optimizing health and healthcare for pregnant women and children.	[Jaddoe, Vincent W. V.] Erasmus MC, Generat Study Grp AE006 R, NL-3000 CA Rotterdam, Netherlands; [Jaddoe, Vincent W. V.; van Duijn, Cornelia M.; Franco, Oscar H.; Tiemeier, Henning; Uitterlinden, Andre G.; Hofman, Albert] Erasmus MC, Dept Epidemiol, NL-3000 CA Rotterdam, Netherlands; [Jaddoe, Vincent W. V.; van der Heijden, Albert J.; de Jongste, Johan C.; Moll, Henriette A.] Erasmus MC, Dept Pediat, Sophia Childrens Hosp, NL-3000 CA Rotterdam, Netherlands; [van Ijzendoorn, Marinus H.] Erasmus Univ, Sch Pedag & Educ Sci, Rotterdam, Netherlands; [van der Lugt, Aad] Erasmus MC, Dept Radiol, NL-3000 CA Rotterdam, Netherlands; [Tiemeier, Henning; Verhulst, Frank C.] Erasmus MC, Dept Child & Adolescent Psychiat, Sophia Childrens Hosp, NL-3000 CA Rotterdam, Netherlands; [Steegers, Eric A. P.] Erasmus MC, Dept Obstet & Gynaecol, NL-3000 CA Rotterdam, Netherlands; [Rivadeneira, Fernando; Uitterlinden, Andre G.] Erasmus MC, Dept Internal Med, NL-3000 CA Rotterdam, Netherlands; [Mackenbach, Johan P.; Raat, Hein] Erasmus MC, Dept Publ Hlth, NL-3000 CA Rotterdam, Netherlands	Jaddoe, VWV (reprint author), Erasmus MC, Generat Study Grp AE006 R, POB 2040, NL-3000 CA Rotterdam, Netherlands.	v.jaddoe@erasmusmc.nl	Rivadeneira, Fernando/O-5385-2015	Rivadeneira, Fernando/0000-0001-9435-9441; Tiemeier, Henning/0000-0002-4395-1397	Erasmus Medical Center, Rotterdam; Erasmus University Rotterdam; Netherlands Organization for Health Research and Development (ZonMw); Netherlands Organisation for Scientific Research (NWO); Ministry of Health, Welfare and Sport; Netherlands Organization for Health Research and Development [ZonMw 907.00303, ZonMw 916.10159]	The Generation R Study is conducted by the Erasmus Medical Center in close collaboration with the School of Law and Faculty of Social Sciences of the Erasmus University Rotterdam, the Municipal Health Service Rotterdam area, Rotterdam, the Rotterdam Homecare Foundation, Rotterdam and the Stichting Trombosedienst & Artsenlaboratorium Rijnmond (STAR-MDC), Rotterdam. We gratefully acknowledge the contribution of children and parents, general practitioners, hospitals, midwives and pharmacies in Rotterdam. We thank Marjolein Kooijman, Claudia Kruithof, Natalia Loekabino, Patricia Maeijer, Ronald van den Nieuwenhof, and Karien Toebes for their study coordination. The general design of Generation R Study is made possible by financial support from the Erasmus Medical Center, Rotterdam, the Erasmus University Rotterdam, the Netherlands Organization for Health Research and Development (ZonMw), the Netherlands Organisation for Scientific Research (NWO), the Ministry of Health, Welfare and Sport. Vincent Jaddoe received an additional grant from the Netherlands Organization for Health Research and Development (ZonMw 907.00303, ZonMw 916.10159).	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J. Epidemiol.	SEP	2012	27	9					739	756		10.1007/s10654-012-9735-1		18	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	030SF	WOS:000310589700008	23086283	
J	Hiller, R; Laffer, S; Harwanegg, C; Huber, M; Schmidt, WM; Twardosz, A; Barletta, B; Becker, WM; Blaser, K; Breiteneder, H; Chapman, M; Crameri, R; Duchene, M; Ferreira, F; Fiebig, H; Hoffmann-Sommergruber, K; King, TP; Kleber-Janke, T; Kurup, VP; Lehrer, SB; Lidholm, J; Muller, U; Pini, C; Reese, G; Scheiner, O; Scheynius, A; Shen, HD; Spitzauer, S; Suck, R; Swoboda, I; Thomas, W; Tinghino, R; Van Hage-Hamsten, M; Virtanen, T; Kraft, D; Muller, MW; Valenta, R				Hiller, R; Laffer, S; Harwanegg, C; Huber, M; Schmidt, WM; Twardosz, A; Barletta, B; Becker, WM; Blaser, K; Breiteneder, H; Chapman, M; Crameri, R; Duchene, M; Ferreira, F; Fiebig, H; Hoffmann-Sommergruber, K; King, TP; Kleber-Janke, T; Kurup, VP; Lehrer, SB; Lidholm, J; Muller, U; Pini, C; Reese, G; Scheiner, O; Scheynius, A; Shen, HD; Spitzauer, S; Suck, R; Swoboda, I; Thomas, W; Tinghino, R; Van Hage-Hamsten, M; Virtanen, T; Kraft, D; Muller, MW; Valenta, R			Microarrayed allergen molecules: diagnostic gatekeepers for allergy treatment	FASEB JOURNAL			English	Article						type I allergy; IgE; microarray technology; recombinant allergen; diagnosis	GRASS PHLEUM-PRATENSE; HOUSE-DUST MITE; BIRCH POLLEN ALLERGEN; IGE-BINDING EPITOPES; AMINO-ACID-SEQUENCE; ASPERGILLUS-FUMIGATUS ALLERGENS; PENICILLIUM-CITRINUM ALLERGEN; COCKROACH BLATTELLA-GERMANICA; SURFACE DISPLAY TECHNOLOGY; ANTIGENIC CROSS-REACTIVITY	Type I allergy is an immunoglobulin E (IgE)-mediated hypersensitivity disease affecting more than 25% of the population. Currently, diagnosis of allergy is performed by provocation testing and IgE serology using allergen extracts. This process defines allergen-containing sources but cannot identify the disease-eliciting allergenic molecules. We have applied microarray technology to develop a miniaturized allergy test containing 94 purified allergen molecules that represent the most common allergen sources. The allergen microarray allows the determination and monitoring of allergic patients' IgE reactivity profiles to large numbers of disease-causing allergens by using single measurements and minute amounts of serum. This method may change established practice in allergy diagnosis, prevention, and therapy. In addition, microarrayed antigens may be applied to the diagnosis of autoimmune and infectious diseases.	Univ Vienna, Dept Pathophysiol, A-1090 Vienna, Austria; Univ Vienna, Dept Internal Med 4, Div Pulm, A-1090 Vienna, Austria; VBC GENOMICS, A-1030 Vienna, Austria; Ist Super Sanita, Immunol Lab, I-00161 Rome, Italy; Res Ctr Borstel, D-23845 Borstel, Germany; Swiss Inst Allergy & Asthma Res, CH-7270 Davos, Switzerland; Univ Virginia, Dept Internal Med, Asthma & Allerg Dis Ctr, Charlottesville, VA 22908 USA; Salzburg Univ, Dept Genet & Biol, A-5020 Salzburg, Austria; Allergopharma Joachim Ganzer KG, D-21465 Reinbek, Germany; Rockefeller Univ, New York, NY 10021 USA; Med Coll Wisconsin, Milwaukee, WI 53295 USA; Tulane Univ, Med Ctr, Dept Med, Sect Clin Immunol & Allergy, New Orleans, LA 70112 USA; Pharmacia Diagnost AB, Uppsala, Sweden; Zieglerspital Bern, Dept Internal Med, CH-3007 Bern, Switzerland; Karolinska Inst, S-17176 Stockholm, Sweden; Vet Gen Hosp, Dept Med Res & Educ, Taipei 11217, Taiwan; Univ Vienna, Inst Med & Lab Diagnost, A-1090 Vienna, Austria; Univ W Australia, TVW Telethon Inst Child Hlth Res, Perth 6872, Australia; Karolinska Hosp & Inst, Div Clin Immunol, Dept Lab Med, S-17176 Stockholm, Sweden; Univ Kuopio, Dept Clin Microbiol, FIN-70211 Kuopio, Finland	Valenta, R (reprint author), Univ Vienna, Vienna Gen Hosp AKH, Dept Pathophysiol, Waehringer Guertel 18-20, A-1090 Vienna, Austria.	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JAN	2002	16	1					414	+		10.1096/fj.01-0711fje		21	Biochemistry & Molecular Biology; Biology; Cell Biology	Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology	518FU	WOS:000173656600022	11790727	
J	Bernstein, JA; Alexis, N; Barnes, C; Bernstein, IL; Bernstein, JA; Nel, A; Peden, D; Diaz-Sanchez, D; Tarlo, SM; Williams, PB				Bernstein, JA; Alexis, N; Barnes, C; Bernstein, IL; Bernstein, JA; Nel, A; Peden, D; Diaz-Sanchez, D; Tarlo, SM; Williams, PB			Health effects of air pollution	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						outdoor air pollution; particulate matter; ozone; nitrogen dioxide; sulfur dioxide; diesel exhaust; asthma; exposure; interactions between allergens and pollutants	DIESEL EXHAUST PARTICLES; NITROGEN-DIOXIDE EXPOSURE; DAILY ASTHMA SEVERITY; MILD ALLERGIC-ASTHMA; 20 US CITIES; OZONE EXPOSURE; INHALED ALLERGEN; SULFUR-DIOXIDE; FUNGAL SPORES; INFLAMMATORY RESPONSES	The general public, especially patients with upper or lower respiratory symptoms, is aware from media reports that adverse respiratory effects can occur from air pollution. It is important for the allergist to have a current knowledge of the potential health effects of air pollution and how they might affect their patients to advise them accordingly. Specifically, the allergist-clinical immunologist should be keenly aware that both gaseous and particulate outdoor pollutants might aggravate or enhance the underlying pathophysiology of both the upper and lower airways. Epidemiologic and laboratory exposure research studies investigating the health effects of outdoor air pollution each have advantages and disadvantages. Epidemiologic studies can show statistical associations between levels of individual or combined air pollutants and outcomes, such as rates of asthma, emergency visits for asthma, or hospital admissions, but cannot prove a causative role. Human exposure studies, animal models, and tissue or cellular studies provide further information on mechanisms of response but also have inherent limitations. The aim of this rostrum is to review the relevant publications that provide the appropriate context for assessing the risks of air pollution relative to other more modifiable environmental factors in patients with allergic airways disease.	Univ Cincinnati, Coll Med, Dept Internal Med, Div Immunol,Allergy Sect, Cincinnati, OH USA; Univ N Carolina, Dept Pediat, Chapel Hill, NC USA; Childrens Mercy Hosp, Dept Pediat, Kansas City, MO 64108 USA; Univ Calif Los Angeles, Sch Med, Dept Internal Med, Los Angeles, CA USA; Toronto Western Hosp, Dept Internal Med, Toronto, ON M5T 2S8, Canada	Bernstein, JA (reprint author), 231 Albert Sabin Way,ML 563, Cincinnati, OH 45267 USA.	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Allergy Clin. Immunol.	NOV	2004	114	5					1116	1123		10.1016/j.jaci.2004.08.030		8	Allergy; Immunology	Allergy; Immunology	870HI	WOS:000225047800019	15536419	
J	Busse, WW; Morgan, WJ; Gergen, PJ; Mitchell, HE; Gern, JE; Liu, AH; Gruchalla, RS; Kattan, M; Teach, SJ; Pongracic, JA; Chmiel, JF; Steinbach, SF; Calatroni, A; Togias, A; Thompson, KM; Szefler, SJ; Sorkness, CA				Busse, William W.; Morgan, Wayne J.; Gergen, Peter J.; Mitchell, Herman E.; Gern, James E.; Liu, Andrew H.; Gruchalla, Rebecca S.; Kattan, Meyer; Teach, Stephen J.; Pongracic, Jacqueline A.; Chmiel, James F.; Steinbach, Suzanne F.; Calatroni, Agustin; Togias, Alkis; Thompson, Katherine M.; Szefler, Stanley J.; Sorkness, Christine A.			Randomized Trial of Omalizumab (Anti-IgE) for Asthma in Inner-City Children	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							SEVERE ALLERGIC-ASTHMA; MONOCLONAL-ANTIBODY; COST-EFFECTIVENESS; CHILDHOOD ASTHMA; EXACERBATIONS; VIRUSES; ADULTS; CELLS; ADOLESCENTS; RHINOVIRUS	BACKGROUND Research has underscored the effects of exposure and sensitization to allergens on the severity of asthma in inner-city children. It has also revealed the limitations of environmental remediation and guidelines-based therapy in achieving greater disease control. METHODS We enrolled inner-city children, adolescents, and young adults with persistent asthma in a randomized, double-blind, placebo-controlled, parallel-group trial at multiple centers to assess the effectiveness of omalizumab, as compared with placebo, when added to guidelines-based therapy. The trial was conducted for 60 weeks, and the primary outcome was symptoms of asthma. RESULTS Among 419 participants who underwent randomization (at which point 73% had moderate or severe disease), omalizumab as compared with placebo significantly reduced the number of days with asthma symptoms, from 1.96 to 1.48 days per 2-week interval, a 24.5% decrease (P<0.001). Similarly, omalizumab significantly reduced the proportion of participants who had one or more exacerbations from 48.8 to 30.3% (P<0.001). Improvements occurred with omalizumab despite reductions in the use of inhaled glucocorticoids and long-acting beta-agonists. CONCLUSIONS When added to a regimen of guidelines-based therapy for inner-city children, adolescents, and young adults, omalizumab further improved asthma control, nearly eliminated seasonal peaks in exacerbations, and reduced the need for other medications to control asthma.	[Busse, William W.; Gern, James E.; Sorkness, Christine A.] Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI 53719 USA; [Morgan, Wayne J.] Univ Arizona, Coll Med, Tucson, AZ USA; [Gergen, Peter J.; Togias, Alkis; Thompson, Katherine M.] NIAID, Bethesda, MD 20892 USA; [Mitchell, Herman E.; Calatroni, Agustin] Rho Fed Syst Div, Chapel Hill, NC USA; [Liu, Andrew H.; Szefler, Stanley J.] Natl Jewish Hlth, Denver, CO USA; [Liu, Andrew H.; Szefler, Stanley J.] Univ Colorado Hlth Sci, Denver, CO USA; [Gruchalla, Rebecca S.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA; [Kattan, Meyer] Columbia Univ, Coll Phys & Surg, New York, NY USA; [Teach, Stephen J.] Childrens Natl Med Ctr, Washington, DC 20010 USA; [Pongracic, Jacqueline A.] Childrens Mem Hosp, Chicago, IL 60614 USA; [Chmiel, James F.] Rainbow Babies & Childrens Hosp, Cleveland, OH USA; [Steinbach, Suzanne F.] Boston Univ, Sch Med, Boston, MA 02118 USA	Busse, WW (reprint author), Univ Wisconsin, Sch Med & Publ Hlth K4 910 CSC, MC 9988,600 Highland Ave, Madison, WI 53719 USA.	wwb@medicine.wisc.edu			National Institute of Allergy and Infectious Diseases, National Institutes of Health (NIH) [NO1-AI-25496, NO1-AI-25482]; National Center for Research Resources, NIH [M01RR00533, 1UL1RR025771, M01RR00071, 1UL1RR024156, 5M01RR020359-040]; Novartis Pharmaceuticals; Dey Pharma; Boehringer Ingelheim; Teva; Amgen; Pfizer; Genentech; AstraZeneca; GlaxoSmithKline; MedImmune; Novartis; Ception; Phadia; Vertex; Biota; Centocor; Synairgen; Merck; 3V BioSciences; EraGen Biosciences; Ross Abbott; Sandoz; ScheringPlough	Supported by contracts with the National Institute of Allergy and Infectious Diseases, National Institutes of Health (NIH) (NO1-AI-25496 and NO1-AI-25482); grants from the National Center for Research Resources, NIH (M01RR00533, 1UL1RR025771, M01RR00071, 1UL1RR024156, and 5M01RR020359-040); Novartis Pharmaceuticals, under a clinical trial agreement with the University of Wisconsin-Madison; Dey Pharma (which provided EpiPens), and SC Johnson (which provided household pest control).; Dr. Busse reports receiving board membership fees from Centocor and Merck, consulting fees from Boehringer Ingelheim, Teva, Amgen, Pfizer, and Genentech; consulting fees and grant support from AstraZeneca, GlaxoSmithKline, MedImmune, and Novartis; and grant support from Ception. Dr. Morgan reports receiving consulting fees from Novartis, lecture fees from Phadia and Vertex, royalties from Elsevier, consulting fees from Genentech, and payment to his institution for development of educational presentations from Genentech. Dr Gern reports receiving consulting fees from GlaxoSmithKline, Biota, Centocor, Synairgen, and Boehringer Ingelheim; grant support from Merck and AstraZeneca; stock options and consulting fees from 3V BioSciences; and stock payments from EraGen Biosciences. Dr. Liu reports receiving consulting fees from AstraZeneca and Novartis and lecture fees from Glaxo-SmithKline, Merck and Phadia. Dr. Teach reports receiving consulting fees from AstraZeneca. Dr. Steinbach reports providing expert testimony for Harvard Medical Institutions. Dr. Szefler reports receiving consulting fees from Schering, Boehringer Ingelheim, and Novartis, consulting fees and grant support from Merck and Genentech, and grant support from GlaxoSmithKline and Ross Abbott. Dr. Sorkness reports receiving consulting fees from GlaxoSmithKline and AstraZeneca, grant support from Pharmaxis and Sandoz, and consulting fees and grant support from ScheringPlough. No other potential conflict of interest relevant to this article was reported. Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.	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J	Vahter, M; Akesson, A; Liden, C; Ceccatelli, S; Berglund, M				Vahter, Marie; Akesson, Agneta; Liden, Carola; Ceccatelli, Sandra; Berglund, Marika			Gender differences in the disposition and toxicity of metals	ENVIRONMENTAL RESEARCH			English	Review						gender; females; males; exposure; toxicity; metabolism; susceptibility	BREAST-CANCER CELLS; ENVIRONMENTAL CADMIUM EXPOSURE; ESTROGEN-RECEPTOR-ALPHA; MERCURY-TREATED RATS; FOREARM BONE-DENSITY; WATER SUPPLY-SYSTEM; LOW-LEVEL EXPOSURE; BLOOD LEAD LEVELS; DRINKING-WATER; METHYL MERCURY	There is increasing evidence that health effects of toxic metals differ in prevalence or are manifested differently in men and women. However, the database is small. The present work aims at evaluating gender differences in the health effects of cadmium, nickel, lead, mercury and arsenic. There is a markedly higher prevalence of nickel-induced allergy and hand eczema in women compared to men, mainly due to differences in exposure. Cadmium retention is generally higher in women than in men, and the severe cadmium-induced Itai-itai disease was mainly a woman's disease. Gender differences in susceptibility at lower exposure are uncertain, but recent data indicate that cadmium has estrogenic effects and affect female offspring. Men generally have higher blood lead levels than women. Lead accumulates in bone and increased endogenous lead exposure has been demonstrated during periods of increased bone turnover, particularly in women in pregnancy and menopause. Lead and mercury, in the form of mercury vapor and methylmercury, are easily transferred from the pregnant women to the fetus. Recent data indicate that boys are more susceptible to neurotoxic effects of lead and methylmercury following exposure early in life, while experimental data suggest that females are more susceptible to immunotoxic effects of lead. Certain gender differences in the biotransformation of arsenic by methylation have been reported, and men seem to be more affected by arsenic-related skin effect than women. Experimental studies indicate major gender differences in arsenic-induced cancer. Obviously, research on gender-related differences in health effects caused by metals needs considerable more focus in the future. (c) 2006 Elsevier Inc. All rights reserved.	Karolinska Inst, Div Met & Hlth, Inst Environm Med, SE-17177 Stockholm, Sweden; Karolinska Inst, Div Toxicol & Neurotoxicol, Inst Environm Med, SE-17177 Stockholm, Sweden; Karolinska Inst, Dept Med, SE-17177 Stockholm, Sweden; Stockholm Cty Council, Stockholm, Sweden	Vahter, M (reprint author), Karolinska Inst, Div Met & Hlth, Inst Environm Med, Box 210, SE-17177 Stockholm, Sweden.	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Res.	MAY	2007	104	1					85	95		10.1016/j.envres.2006.08.003		11	Environmental Sciences; Public, Environmental & Occupational Health	Environmental Sciences & Ecology; Public, Environmental & Occupational Health	166VQ	WOS:000246409200008	16996054	
J	Martin-Morales, A; Sanchez-Cruz, JJ; de Tejada, IS; Rodriguez-Vela, L; Jimenez-Cruz, JF; Burgos-Rodriguez, R				Martin-Morales, A; Sanchez-Cruz, JJ; de Tejada, IS; Rodriguez-Vela, L; Jimenez-Cruz, JF; Burgos-Rodriguez, R			Prevalence and independent risk factors for erectile dysfunction in Spain: Results of the Epidemiologia de la Disfuncion Erectil Masculina study	JOURNAL OF UROLOGY			English	Article						impotence; questionnaires; epidemiology; risk factors	MALE SEXUAL DYSFUNCTION; INTERNATIONAL INDEX; FUNCTION DOMAIN; SELF-ASSESSMENT; IMPOTENCE; ALCOHOLISM; SMOKING	Purpose: We determined the prevalence of and risks factors for erectile dysfunction in Spain in a cross-sectional study. Materials and Methods: A total of 2,476 noninstitutionalized Spanish men 25 to 70 years old were interviewed at home and answered a self-administered questionnaire of 71 items, including 2 instruments to define erectile dysfunction, a simple self-assessment question to estimate erectile function and the International Index of Erectile Function. Data on disease, medication and toxic habits were also obtained. Results: With an overall participation rate of 75% the prevalence of erectile dysfunction according to the simple question was 12.1%. According to the erectile function domain of the International Index of Erectile Function the overall prevalence was 18.9%. Several independent risk factors were significantly associated with the probability of erectile dysfunction. Some differences arose according to the tool used to define the condition. However, there was a strong relationship of patient age with frequency or severity no matter which instrument was used to define erectile dysfunction. Diabetes (age adjusted odds ratio 4), high blood pressure (odds ratio 1.58), high cholesterol (1.63), peripheral vascular disorder (2.63), lung disease (3.11), prostate disease (2.93), cardiac problems (1.79), rheumatism (2.37) and allergy (3.08) were significantly associated with erectile dysfunction. Drug intake, which respondents called medication for nerves and sleeping pills, correlated strongly (odds ratio 2.78 and 4.27, respectively), as did tobacco use (2.5) and alcohol consumption (1.53). Conclusions: This study provides data on the prevalence of and risks factors for erectile dysfunction in Spain. The relationship of erectile dysfunction with certain risk factors, such as cardiovascular risk factors and drugs intake, are well known and our study corroborates these associations. Other associations with erectile dysfunction, such as prostate disease, allergy and rheumatism, support findings in previous reports, although to our knowledge the pathophysiological mechanisms remain unclear. Estimating the strength of the association of erectile dysfunction with distinct risk factors in terms of odds ratios enabled us to identify the factors to pursue when seeking to prevent erectile dysfunction. Furthermore, the relationship of tobacco with erectile dysfunction, which has been controversial in previous series, was well characterized in our study.	Carlos Haya Hosp, Dept Urol, Malaga, Spain; Andalusian Sch Publ Hlth, Granada, Spain; Fdn Inves & Desarrollo Androl, Madrid, Spain; Spanish Urol Assoc, Madrid, Spain	Martin-Morales, A (reprint author), Carlos Haya Hosp, Dept Urol, Malaga, Spain.						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E., 1993, SF 36 HLTH SURVEY MA; WEIN AJ, 1988, UROL CLIN N AM, V15, P23	29	278	291	1	13	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	0022-5347			J UROLOGY	J. Urol.	AUG	2001	166	2					569	574		10.1016/S0022-5347(05)65986-1		6	Urology & Nephrology	Urology & Nephrology	451KE	WOS:000169800600046	11458070	
J	Dahl, R; Kapp, A; Colombo, G; deMonchy, JGR; Rak, S; Emminger, W; Rivas, MF; Ribel, M; Durham, SR				Dahl, Ronald; Kapp, Alexander; Colombo, Giselda; deMonchy, Jan G. R.; Rak, Sabina; Emminger, Waltraud; Rivas, Montserrat Fernandez; Ribel, Mette; Durham, Stephen R.			Efficacy and safety of sublingual immunotherapy with grass allergen tablets for seasonal allergic rhinoconjunctivitis	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergy; asthma; grass pollen; immunotherapy; sublingual; rhinoconjunctivitis; tablet-based; double-blind; placebo-controlled; Phleum pratense	RANDOMIZED CONTROLLED-TRIAL; POLLEN IMMUNOTHERAPY; HAY-FEVER; RHINITIS; ASTHMA; METAANALYSIS; CHILDREN	Background: Allergen immunotherapy (desensitization) by injection is effective for seasonal allergic rhinitis and has been shown to induce long-term disease remission. The sublingual route also has potential, although definitive evidence from large randomized controlled trials has been lacking. Objective: The aim was to confirm the efficacy of a rapidly dissolving grass allergen tablet (GRAZAX, ALK-Abello, Horsholm, Denmark) compared with placebo in patients with seasonal rhinoconjunctivitis. Methods: A longitudinal, double-blind, placebo-controlled, parallel-group study that included 51 centers from 8 countries. Subjects were randomized (1:1) to receive a grass allergen tablet or placebo once daily. A total of 634 subjects with a history of grass pollen-induced rhinoconjunctivitis for at least 2 years and confirmation of IgE sensitivity (positive skin prick test and serum-specific IgE) were included in the study. Subjects commenced treatment at least 16 weeks before the grass pollen season, and treatment was continued throughout the entire season. Results: The primary efficacy analysis showed a reduction of 30% in rhinoconjunctivitis symptom score (P < .0001) and a reduction of 38% in rhinoconjunctivitis medication score (P < .0001) compared with placebo. Side effects mainly comprised mild itching and swelling in the mouth that was in general well tolerated and led to treatment withdrawal in less than 4% of participants. There were no serious local side effects and no severe systemic adverse events. Conclusion: Sublingual immunotherapy with grass allergen tablets was effective in grass pollen-induced rhinoconjunctivitis. The tablet was well tolerated with minor local side effects. Clinical implications: The grass allergen tablet represents a safe alternative to injection immunotherapy suitable for home use.	Royal Brompton Hosp,Imperial Coll, MRC & Asthma UK Ctr Allerg Mech Asthma, Allergy & Clin Immunol Sect, Natl Heart & Lung Inst, London SW3 6LY, England; Aarhus Univ Hosp, Dept Resp Dis, DK-8000 Aarhus, Denmark; Hannover Med Univ, Dept Dermatol & Allergol, Hannover, Germany; Osped San Raffaele, I-20127 Milan, Italy; Univ Groningen, Div Allergol, NL-9700 AB Groningen, Netherlands; Sahlgrenska Univ Hosp, Sect Allergy, Gothenburg, Sweden; Allergie Ambulatorium Rennweg, Vienna, Austria; Fdn Hosp Alcorcon, Madrid, Spain; ALK Abello AS, Grp Clin Dev, Horsholm, Denmark	Durham, SR (reprint author), Royal Brompton Hosp,Imperial Coll, MRC & Asthma UK Ctr Allerg Mech Asthma, Allergy & Clin Immunol Sect, Natl Heart & Lung Inst, Guy Scadding Bldg,Royal Brompton Campus,Dovehouse, London SW3 6LY, England.	s.durham@imperial.ac.uk	Dahl, Ronahl/F-8170-2013				Dahl R, 2006, ALLERGY, V61, P185, DOI 10.1111/j.1398-9995.2005.00949.x; Dahl R, 2004, RESP MED, V98, P398, DOI 10.1016/j.rmed.2003.11.015; Durham SR, 2006, J ALLERGY CLIN IMMUN, V117, P802, DOI 10.1016/j.jaci.2005.12.1358; Durham SR, 1999, NEW ENGL J MED, V341, P468, DOI 10.1056/NEJM199908123410702; Frew AJ, 2006, J ALLERGY CLIN IMMUN, V117, P319, DOI 10.1016/j.jaci.2005.11.014; JOHNSTONE DE, 1968, PEDIATRICS, V42, P793; Kleine-Tebbe J, 2006, ALLERGY, V61, P181, DOI 10.1111/j.1398-9995.2006.00959.x; Lima MT, 2002, CLIN EXP ALLERGY, V32, P507, DOI 10.1046/j.0954-7894.2002.01327.x; Malling HJ, 2002, CURR OPIN ALLERGY CL, V2, P523, DOI 10.1097/01.all.0000044538.45448.80; Moller C, 2002, J ALLERGY CLIN IMMUN, V109, P251, DOI 10.1067/mai.2002.121317; Passalacqua Giovanni, 2004, Curr Opin Allergy Clin Immunol, V4, P31, DOI 10.1097/00130832-200402000-00007; Passalacqua Giovanni, 2003, Curr Opin Allergy Clin Immunol, V3, P139, DOI 10.1097/00130832-200304000-00008; Robinson DS, 2004, J CLIN INVEST, V114, P1389, DOI 10.1172/JCI200423595; Roches Anne Des, 1997, Journal of Allergy and Clinical Immunology, V99, P450; Till SJ, 2004, J ALLERGY CLIN IMMUN, V113, P1025, DOI 10.1016/j.jaci.2004.03.024; VARNEY VA, 1991, BRIT MED J, V302, P265; 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; White P, 1998, CLIN EXP ALLERGY, V28, P266; Wilson AM, 2004, AM J MED, V116, P338, DOI 10.1016/j.amjmed.2003.10.030; Wilson DR, 2005, ALLERGY, V60, P4, DOI 10.1111/j.1398-9995.2005.00699.x	21	277	280	0	16	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					434	440		10.1016/j.jaci.2006.05.003		7	Allergy; Immunology	Allergy; Immunology	075IH	WOS:000239877700020	16890769	
J	Sicherer, SH; Sampson, HA				Sicherer, Scott H.; Sampson, Hugh A.			Food allergy: Epidemiology, pathogenesis, diagnosis, and treatment	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						Food allergy; food hypersensitivity; oral tolerance; gastrointestinal food hypersensitivity; food allergens; anaphylaxis	SKIN PRICK TEST; COWS MILK ALLERGY; RED MEAT ALLERGY; QUALITY-OF-LIFE; ARA H 2; INDUCED ENTEROCOLITIS SYNDROME; PROSPECTIVE BIRTH COHORT; LONG-TERM OUTCOMES; PEANUT ALLERGY; EGG ALLERGY	This review focuses on advances and updates in the epidemiology, pathogenesis, diagnosis, and treatment of food allergy over the past 3 years since our last comprehensive review. On the basis of numerous studies, food allergy likely affects nearly 5% of adults and 8% of children, with growing evidence of an increase in prevalence. Potentially rectifiable risk factors include vitamin D insufficiency, unhealthful dietary fat, obesity, increased hygiene, and the timing of exposure to foods, but genetics and other lifestyle issues play a role as well. Interesting clinical insights into pathogenesis include discoveries regarding gene-environment interactions and an increasing understanding of the role of nonoral sensitizing exposures causing food allergy, such as delayed allergic reactions to carbohydrate moieties in mammalian meats caused by sensitization from homologous substances transferred during tick bites. Component-resolved diagnosis is being rapidly incorporated into clinical use, and sophisticated diagnostic tests that indicate severity and prognosis are on the horizon. Current management relies heavily on avoidance and emergency preparedness, and recent studies, guidelines, and resources provide insight into improving the safety and well-being of patients and their families. Incorporation of extensively heated (heat-denatured) forms of milk and egg into the diets of children who tolerate these foods, rather than strict avoidance, represents a significant shift in clinical approach. Recommendations about the prevention of food allergy and atopic disease through diet have changed radically, with rescinding of many recommendations about extensive and prolonged allergen avoidance. Numerous therapies have reached clinical trials, with some showing promise to dramatically alter treatment. Ongoing studies will elucidate improved prevention, diagnosis, and treatment.	[Sicherer, Scott H.; Sampson, Hugh A.] Kravis Childrens Hosp, Dept Pediat, Icahn Sch Med Mt Sinai, Elliot & Roslyn Jaffe Food Allergy Inst,Div Aller, New York, NY USA	Sicherer, SH (reprint author), Mt Sinai Hosp, Div Allergy Immunol, Box 1198,One Gustave L Levy Pl, New York, NY 10029 USA.	scott.sicherer@mssm.edu			Novartis; Food Allergy Research Education; National Institute of Allergy and Infectious Diseases (NIAID); NIAID/National Institutes of Health; Allertein Therapeutics; Regeneron; Thermo Fisher Scientific; UCB; Pfizer	S. H. Sicherer is on the American Board of Allergy and Immunology; has received consultancy fees from Novartis and Food Allergy Research & Education; has received research support from the National Institute of Allergy and Infectious Diseases (NIAID) and Food Allergy Research & Education; and receives royalties from UpToDate. H. A. Sampson has received research support from the NIAID/National Institutes of Health and Food Allergy Research & Education; has received travel support as Chair of the PhARF Award review committee; has received consultancy fees from Allertein Therapeutics and Regeneron; and has received lecture fees from Thermo Fisher Scientific, UCB, and Pfizer.	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Allergy Clin. Immunol.	FEB	2014	133	2					291	+		10.1016/j.jaci.2013.11.020		22	Allergy; Immunology	Allergy; Immunology	AC3EF	WOS:000332397100001	24388012	
J	Brightling, CE; Monteiro, W; Ward, R; Parker, D; Morgan, MDL; Wardlaw, AJ; Pavord, ID				Brightling, CE; Monteiro, W; Ward, R; Parker, D; Morgan, MDL; Wardlaw, AJ; Pavord, ID			Sputum eosinophilia and short-term response to prednisolone in chronic obstructive pulmonary disease: a randomised controlled trial	LANCET			English	Article							AIR-FLOW OBSTRUCTION; INHALED CORTICOSTEROIDS; AIRWAYS OBSTRUCTION; CHRONIC-BRONCHITIS; ASTHMA; INFLAMMATION; SMOKERS; COPD; BUDESONIDE; MILD	Background Some patients wit chronic obstructive pulmonary disease (COPD) respond toe corticosteroid therapy. Whether these patients have different airway pathology from other COPD patients is unclear. We tested the hypothesis that response to prednisolone is related to the presence of eosinophilic airway inflammation. Methods We did a randomised, double-blind, crossover trial. Patients who had COPD treated with bronchodilators only were assigned placebo and 30 mg prednisolone daily for 2 weeks each, in a random order, separated by a 4-week washout period. Before and after each treatment period, we assessed patients with spirometry, symptom scores, the chronic respiratory disease questionnaire (CRQ), incremental shuttle walk test, and induced sputum. Analysis was done by intention to treat. Findings 83 patients were recruited, of whom 67 were randomised. The geometric mean sputum eosinophil count fell significantly after prednisolone (from 2.4% to 0.4%; mean difference six-fold [95% CI 3.1-11.4]) but not after placebo. Other sputum cell counts did not change. After stratification into tertiles by baseline eosinophil count, postbronchodilator forced expiratory volume in 1 s (FEV1) and total scores on the CRQ improved progressively after prednisolone from the lowest to the highest eosinophilic tertile, compared with placebo. The mean change in postbronchodilator FEV1, total CRQ score, and shuttle walk distance with prednisolone compared with placebo in the highest tertile was 0.19 L (0.06-0.32), 0.62 (0.31-0.93), and 20 m (5-35), respectively. Interpretation Our findings suggest that eosinophilic airway inflammation contributes to airflow obstruction and symptoms in some patients with COPD and that the short-term effects of prednisolone are due to modification of this feature of the inflammatory response. The possibility that sputum eosinophilia identifies a subgroup of patients who particularly respond to long-term treatment with inhaled corticosteroids should be investigated.	Glenfield Gen Hosp, Dept Resp Med, Inst Lung Hlth, Leicester LE3 9QP, Leics, England	Brightling, CE (reprint author), Glenfield Gen Hosp, Dept Resp Med, Inst Lung Hlth, Leicester LE3 9QP, Leics, England.						Barnes NC, 1998, LANCET, V351, P766, DOI 10.1016/S0140-6736(98)22011-3; Boushey HA, 1999, NEW ENGL J MED, V340, P1990, DOI 10.1056/NEJM199906243402509; Brightling CE, 1999, EUR RESPIR J, V14, P1228, DOI 10.1183/09031936.99.14512289; Brightling CE, 1999, AM J RESP CRIT CARE, V160, P406; *BRIT THOR SOC, 1997, THORAX S1, V52, P9; Burge PS, 2000, BRIT MED J, V320, P1297, DOI 10.1136/bmj.320.7245.1297; Calverley PMA, 1999, THORAX, V54, P3; Chanez P, 1997, AM J RESP CRIT CARE, V155, P1529; CLIFTON M, 1962, LANCET, V1, P1311; Confalonieri M, 1998, THORAX, V53, P583; Di Stefano A, 1998, AM J RESP CRIT CARE, V158, P1277; GUYATT GH, 1987, THORAX, V136, P1285; Hunter CJ, 1999, RESP MED, V93, P345, DOI 10.1016/S0954-6111(99)90317-7; JANOFF A, 1983, AM REV RESPIR DIS, V127, P540; Keatings VM, 1997, AM J RESP CRIT CARE, V155, P542; Keatings VM, 1996, AM J RESP CRIT CARE, V153, P530; Matsumoto K, 1998, EUR RESPIR J, V12, P387, DOI 10.1183/09031936.98.12020387; Pauwels RA, 1999, NEW ENGL J MED, V340, P1948, DOI 10.1056/NEJM199906243402503; 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 E, 1996, AM J RESP CRIT CARE, V154, P808; SAETTA M, 1994, AM J RESP CRIT CARE, V150, P1646; SHIM C, 1978, J ALLERGY CLIN IMMUN, V62, P363, DOI 10.1016/0091-6749(78)90137-9; SINGH SJ, 1992, THORAX, V47, P1019, DOI 10.1136/thx.47.12.1019; Stanescu D, 1996, THORAX, V51, P267, DOI 10.1136/thx.51.3.267; TWEEDDALE PM, 1987, THORAX, V42, P87; Vestbo J, 1999, LANCET, V353, P1819, DOI 10.1016/S0140-6736(98)10019-3; WEIR DC, 1990, THORAX, V45, P112, DOI 10.1136/thx.45.2.112	29	275	288	0	6	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	OCT 28	2000	356	9240					1480	1485		10.1016/S0140-6736(00)02872-5		6	Medicine, General & Internal	General & Internal Medicine	367NA	WOS:000090067300012	11081531	
J	Lambrecht, BN; Hammad, H				Lambrecht, Bart N.; Hammad, Hamida			The airway epithelium in asthma	NATURE MEDICINE			English	Review							HOUSE-DUST MITE; THYMIC STROMAL LYMPHOPOIETIN; RESPIRATORY SYNCYTIAL VIRUS; EPIDERMAL-GROWTH-FACTOR; PROTEASE-ACTIVATED RECEPTOR-2; INFLAMMATORY DENDRITIC CELLS; ALLERGIC LUNG INFLAMMATION; INNATE IMMUNE-RESPONSES; FACTOR-KAPPA-B; IN-VIVO	Asthma is a T lymphocyte-controlled disease of the airway wall caused by inflammation, overproduction of mucus and airway wall remodeling leading to bronchial hyperreactivity and airway obstruction. The airway epithelium is considered an essential controller of inflammatory, immune and regenerative responses to allergens, viruses and environmental pollutants that contribute to asthma pathogenesis. Epithelial cells express pattern recognition receptors that detect environmental stimuli and secrete endogenous danger signals, thereby activating dendritic cells and bridging innate and adaptive immunity. Improved understanding of the epithelium's function in maintaining the integrity of the airways and its dysfunction in asthma has provided important mechanistic insight into how asthma is initiated and perpetuated and could provide a framework by which to select new therapeutic strategies that prevent exacerbations and alter the natural course of the disease.	[Lambrecht, Bart N.; Hammad, Hamida] VIB, Dept Mol Biomed Res, Lab Immunoregulat & Mucosal Immunol, Ghent, Belgium; [Lambrecht, Bart N.] Univ Hosp, Dept Resp Med, Ghent, Belgium; [Lambrecht, Bart N.] Erasmus MC, Dept Pulm Med, Rotterdam, Netherlands	Lambrecht, BN (reprint author), VIB, Dept Mol Biomed Res, Lab Immunoregulat & Mucosal Immunol, Ghent, Belgium.	bart.lambrecht@ugent.be	Hammad, Hamida/J-9391-2015; Lambrecht, Bart/K-2484-2014	Hammad, Hamida/0000-0003-3762-8603; Lambrecht, Bart/0000-0003-4376-6834	Flemish Organization for Scientific Research (FWO); ERC; UGent; National Institutes of Health [5R21AI083690-02]	B.N.L. is a recipient of an Odysseus Grant of the Flemish Organization for Scientific Research (FWO) and recipient of an ERC Consolidator grant and a UGent Multidisciplinary Research Partnership grant (Group-ID). H.H. and B.N.L. are supported by National Institutes of Health grant 5R21AI083690-02. H.H. is a recipient of an FWO program grant.	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Med.	MAY	2012	18	5					684	692		10.1038/nm.2737		9	Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental	Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine	938WE	WOS:000303763500036	22561832	
J	Schwartz, J				Schwartz, J			Air pollution and children's health	PEDIATRICS			English	Article						asthma; particles; ozone; lung reaction	LOW-BIRTH-WEIGHT; PEAK EXPIRATORY FLOW; EXHALED NITRIC-OXIDE; LUNG-FUNCTION GROWTH; RESPIRATORY SYMPTOMS; PARTICULATE MATTER; SOUTHERN CALIFORNIA; PULMONARY-FUNCTION; INFANT-MORTALITY; CHILDHOOD ASTHMA	Children's exposure to air pollution is a special concern because their immune system and lungs are not fully developed when exposure begins, raising the possibility of different responses than seen in adults. In addition, children spend more time outside, where the concentrations of pollution from traffic, powerplants, and other combustion sources are generally higher. Although air pollution has long been thought to exacerbate minor acute illnesses, recent studies have suggested that air pollution, particularly traffic-related pollution, is associated with infant mortality and the development of asthma and atopy. Other studies have associated particulate air pollution with acute bronchitis in children and demonstrated that rates of bronchitis and chronic cough declined in areas where particle concentrations have fallen. More mixed results have been reported for lung function. Overall, evidence for effects of air pollution on children have been growing, and effects are seen at concentrations that are common today. Although many of these associations seem likely to be causal, others require and warrant additional investigation.	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J	Rennard, S; Decramer, M; Calverley, PMA; Pride, NB; Soriano, JB; Vermeire, PA; Vestbo, J				Rennard, S; Decramer, M; Calverley, PMA; Pride, NB; Soriano, JB; Vermeire, PA; Vestbo, J			Impact of COPD in North America and Europe in 2000: subjects' perspective of Confronting COPD International Survey	EUROPEAN RESPIRATORY JOURNAL			English	Article						chronic obstructive pulmonary disease; epidemiology; guidelines; management; subject perspective	OBSTRUCTIVE PULMONARY-DISEASE; ECONOMIC BURDEN; UNITED-STATES; LUNG-FUNCTION; ASTHMA; HEALTH; EPIDEMIOLOGY; ADULTS; RISK; EXACERBATIONS	To date, no international surveys estimating the burden of chronic obstructive pulmonary disease (COPD) in the general population have been published. The Confronting COPD International Survey aimed to quantify morbidity and burden in COPD subjects in 2000. From a total of 201,921 households screened by random-digit dialling in the USA, Canada, France, Italy, Germany, the Netherlands, Spain and the UK, 3,265 subjects with a diagnosis of COPD, chronic bronchitis or emphysema, or with symptoms of chronic bronchitis, were identified. The mean age of the subjects was 63.3 yrs and 44.2%) were female. Subjects with COPD in North America and Europe appear to underestimate their morbidity, as shown by the high proportion of subjects with limitations to their basic daily life activities, frequent work loss (45.3% of COPD subjects of <65 yrs reported work loss in the past year) and frequent use of health services (13.8%. of subjects required emergency care in the last year), and may be undertreated. There was a significant disparity between subjects' perception of disease severity and the degree of severity indicated by an objective breathlessness scale. Of those with the most severe breathlessness (too breathless to leave the house), 35.8%, described their condition as mild or moderate, as did 60.3% of those with the next most severe degree of breathlessness (breathless after walking a few minutes on level ground). This international survey confirmed the great burden to society and high individual morbidity associated with chronic obstructive pulmonary disease in subjects in North America and Europe.	Univ Nebraska, Med Ctr, Pulm & Crit Care Med Sect, Nebraska Med Ctr 985125, Omaha, NE 68198 USA; Univ Catholique Louvain, Div Resp, B-1348 Louvain, Belgium; Univ Liverpool, Dept Med, Ctr Clin Sci, Aintree Hosp, Liverpool L69 3BX, Merseyside, England; Imperial Coll Sch Med, Natl Heart & Lung Inst, Sch Med, London, England; GlaxoSmithKline Res & Dev, Worldwide Epidemiol, Greenford, Middx, England; Univ Antwerp, Dept Resp Med, B-2020 Antwerp, Belgium; Hvidovre Univ Hosp, Dept Resp Med, Copenhagen, Denmark	Rennard, S (reprint author), Univ Nebraska, Med Ctr, Pulm & Crit Care Med Sect, Nebraska Med Ctr 985125, Omaha, NE 68198 USA.			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J	Anderson, SD; Daviskas, E				Anderson, SD; Daviskas, E			The mechanism of exercise-induced asthma is ...	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						exercise; airway cooling; airway drying; osmolarity; respiratory water loss	CANINE PERIPHERAL AIRWAYS; THERMALLY-INDUCED ASTHMA; BRONCHIAL BLOOD-FLOW; DRY AIR; ISOCAPNIC HYPERVENTILATION; MUCOCILIARY CLEARANCE; WATER-LOSS; HYPERTONIC SALINE; RESPIRATORY-TRACT; HEALTHY-SUBJECTS	Exercise-induced asthma (EIA) refers to the transient narrowing of the airways that follows vigorous exercise. The mechanism whereby EIA occurs is thought to relate to the consequences of heating and humidifying large volumes of air during exercise. In 1978 airway cooling was identified as an important stimulus for EIA; however, severe EIA also occurred when hot dry air was inspired, and there was no abnormal cooling of the airways. In 1986 the thermal hypothesis proposed that cooling of the airways needed to be followed by rapid rewarming and that these two events caused a vasoconstriction and a reactive hyperemia of the bronchial microcirculation, together with edema of the airway wall, causing the airways to narrow after exercise. The osmotic, or airway-drying, hypothesis developed from 1982-1992 because neither airway cooling nor rewarming appeared to be necessary for EIA to occur. As water is evaporated from the airway surface liquid, it becomes hyperosmolar and provides an osmotic stimulus for water to move from any cell nearby, resulting in cell volume loss. It is proposed that the regulatory volume increase, after cell shrinkage, is the key event resulting in release of inflammatory mediators that cause airway smooth muscle to contract and the airways of asthmatic subjects to narrow. This event may or may not be associated with airway edema. The osmotic and thermal theories come together by considering that inspiration of cold air not only cools the airways but also increases the numbers of airway generations becoming dehydrated in the humidifying process.	Royal Prince Alfred Hosp, Dept Resp Med, Camperdown, NSW 2050, Australia	Anderson, SD (reprint author), Royal Prince Alfred Hosp, Dept Resp Med, Level 9,Page Chest Pavil,Missenden Rd, Camperdown, NSW 2050, Australia.			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J	Hammad, H; Plantinga, M; Deswarte, K; Pouliot, P; Willart, MAM; Kool, M; Muskens, F; Lambrecht, BN				Hammad, Hamida; Plantinga, Maud; Deswarte, Kim; Pouliot, Philippe; Willart, Monique A. M.; Kool, Mirjam; Muskens, Femke; Lambrecht, Bart N.			Inflammatory dendritic cells-not basophils-are necessary and sufficient for induction of Th2 immunity to inhaled house dust mite allergen	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article							EOSINOPHILIC AIRWAY INFLAMMATION; IN-VIVO DEPLETION; CD4(+) T-CELLS; TYPE-2 IMMUNITY; CUTTING EDGE; LYMPH-NODES; ADAPTIVE IMMUNITY; IL-4 PRODUCTION; STEADY-STATE; RESPONSES	It is unclear how Th2 immunity is induced in response to allergens like house dust mite (HDM). Here, we show that HDM inhalation leads to the TLR4/MyD88-dependent recruitment of IL-4 competent basophils and eosinophils, and of inflammatory DCs to the draining mediastinal nodes. Depletion of basophils only partially reduced Th2 immunity, and depletion of eosinophils had no effect on the Th2 response. Basophils did not take up inhaled antigen, present it to T cells, or express antigen presentation machinery, whereas a population of FceRI(+) DCs readily did. Inflammatory DCs were necessary and sufficient for induction of Th2 immunity and features of asthma, whereas basophils were not required. We favor a model whereby DCs initiate and basophils amplify Th2 immunity to HDM allergen.	[Hammad, Hamida; Plantinga, Maud; Deswarte, Kim; Pouliot, Philippe; Willart, Monique A. M.; Kool, Mirjam; Lambrecht, Bart N.] Univ Ghent, Dept Resp Dis, Lab Immunoregulat & Mucosal Immunol, B-9000 Ghent, Belgium; [Muskens, Femke; Lambrecht, Bart N.] Erasmus MC, Dept Pulm Med, NL-3000 CA Rotterdam, Netherlands	Lambrecht, BN (reprint author), Univ Ghent, Dept Resp Dis, Lab Immunoregulat & Mucosal Immunol, B-9000 Ghent, Belgium.	hamida.hammad@ugent.be; Bart.lambrecht@ugent.be	Hammad, Hamida/J-9391-2015; Lambrecht, Bart/K-2484-2014	Hammad, Hamida/0000-0003-3762-8603; Lambrecht, Bart/0000-0003-4376-6834	Flemish government; University of Ghent [GOA 01G01009]; National Institutes of Health; Ghent University; EU	Bart N. Lambrecht and Hamida Hammad were supported by an Odysseus Grant of the Flemish government and by a concerted research initiative grant (GOA 01G01009), a 4 year project grant, and a Multidisciplinary Research Initiative Grant of University of Ghent and a National Institutes of Health R21 grant. Maud Plantinga was supported by a grant of Ghent University. Mirjam Kool was supported by an EU Marie Curie Intra-european Fellowship and Philippe Pouliot was supported by a EU Marie Curie International Incoming Fellowship.	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J	Staden, U; Rolinck-Werninghaus, C; Brewe, F; Wahn, U; Niggemann, B; Beyer, K				Staden, U.; Rolinck-Werninghaus, C.; Brewe, F.; Wahn, U.; Niggemann, B.; Beyer, K.			Specific oral tolerance induction in food allergy in children: efficacy and clinical patterns of reaction	ALLERGY			English	Article						children; food allergy; specific oral tolerance induction	EXERCISE-INDUCED ANAPHYLAXIS; PEANUT ALLERGY; COWS MILK; RUSH DESENSITIZATION; EGG ALLERGY; HYPERSENSITIVITY; IMMUNOTHERAPY; POPULATION; PREVALENCE; SENSITIZATION	Background: Specific oral tolerance induction (SOTI) seems to be a promising treatment of food allergy. Specific oral tolerance induction and elimination diet were compared with respect to efficacy rate and patterns of clinical reaction. Methods: Children with challenge proven immunoglobulin E (IgE)-mediated cow's milk (CM) allergy or hen's egg (HE) allergy were randomly assigned to SOTI or elimination diet as a control group. Specific oral tolerance induction treatment was performed at home on a daily basis according to a study protocol with fresh CM or lyophilized HE protein. Re-evaluation of clinically relevant food allergy was performed by food challenge after a median of 21 months. Children in the SOTI group received a secondary elimination diet for 2 months prior to follow-up challenge to evaluate persistence of induced oral tolerance. Results: At follow-up challenge, nine of 25 children (36%) showed permanent tolerance in the SOTI group, three of 25 (12%) were tolerant with regular intake and four of 25 (16%) were partial responders. In the control group, seven of 20 children (35%) were tolerant. Allergen-specific immunoglobulin E decreased significantly both in children who developed natural tolerance during the elimination diet (P < 0.05) and in those with SOTI (P < 0.001). Conclusions: Specific oral tolerance induction seems a valid treatment option for patients with persistent food allergy. Indications may be given if avoidance cannot be guaranteed or for those who are eager to eat the food in question. Advantages of SOTI are the increased threshold dose for allergic reactions and the substantially reduced risk of severe allergic reactions after inadvertent ingestion of the allergen. However, careful monitoring during SOTI is mandatory.	Univ Childrens Hosp Charite, Dept Pediat Pneumol & Immunol, D-13353 Berlin, Germany; Childrens Hosp Osnabruck, Osnabruck, Germany	Staden, U (reprint author), Univ Childrens Hosp Charite, Dept Pediat Pneumol & Immunol, Augustenburger Pl 1, D-13353 Berlin, Germany.						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J	Hedayati, MT; Pasqualotto, AC; Warn, PA; Bowyer, P; Denning, DW				Hedayati, M. T.; Pasqualotto, A. C.; Warn, P. A.; Bowyer, P.; Denning, D. W.			Aspergillus flavus: human pathogen, allergen and mycotoxin producer	MICROBIOLOGY-SGM			English	Review							PRIMARY CUTANEOUS ASPERGILLOSIS; PARANASAL SINUS MYCOSES; HEMATOPOIETIC STEM-CELL; INTENSIVE-CARE-UNIT; IN-VITRO ACTIVITIES; AIR-BORNE FUNGI; INVASIVE ASPERGILLOSIS; AMPHOTERICIN-B; SECTION FLAVI; BRONCHOPULMONARY ASPERGILLOSIS	Aspergillus infections have grown in importance in the last years. However, most of the studies have focused on Aspergillus fumigatus, the most prevalent species in the genus. In certain locales and hospitals, Aspergillus flavus is more common in air than A. fumigatus, for unclear reasons. After A. fumigatus, A. flavus is the second leading cause of invasive aspergillosis and it is the most common cause of superficial infection. Experimental invasive infections in mice show A. flavus to be 100-fold more virulent than A. fumigatus in terms of inoculum required. Particularly common clinical syndromes associated with A. flavus include chronic granulonnatous sinusitis, keratitis, cutaneous aspergillosis, wound infections and osteomyelitis following trauma and inoculation. Outbreaks associated with A. flavus appear to be associated with single or closely related strains, in contrast to those associated with A. fumigatus. In addition, A. flavus produces aflatoxins, the most toxic and potent hepatocarcinogenic natural compounds ever characterized. Accurate species identification within Aspergillus flavus complex remains difficult due to overlapping morphological and biochemical characteristics, and much taxonomic and population genetics work is necessary to better understand the species and related species. The flavus complex currently includes 23 species or varieties, including two sexual species, Petromyces alliaceus and P. albertensis. The genome of the highly related Aspergillus oryzae is completed and available; that of A. flavus in the final stages of annotation. Our understanding of A. flavus lags far behind that of A. fumigatus. Studies of the genomics, taxonomy, population genetics, pathogenicity, allergenicity and antifungal susceptibility of A. flavus are all required.	Univ Manchester, Sch Med, Manchester M23 9PL, Lancs, England; Wythenshawe Hosp, Manchester M23 9PL, Lancs, England; Mazandaran Univ Med Sci, Sch Med, Dept Med Mycol & Parasitol, Sari, Iran	Denning, DW (reprint author), Univ Manchester, Sch Med, Southmoor Rd, Manchester M23 9PL, Lancs, England.	ddenning@manchester.ac.uk	Hedayati, Mohammad T./E-2304-2017	Hedayati, Mohammad T./0000-0001-6415-4648; Denning, David/0000-0001-5626-2251	NIAID NIH HHS [N01-AI-30041]		ABDALLA MH, 1988, MYCOPATHOLOGIA, V104, P137, DOI 10.1007/BF00437427; ACQUATI F, 1987, Giornale Italiano di Cardiologia, V17, P467; Adhikari A, 2004, SCI TOTAL ENVIRON, V326, P123, DOI 10.1016/j.scitotenv.2003.12.007; AKIYAMA K, 1987, CHEST, V91, P285, DOI 10.1378/chest.91.2.285; ALLO MD, 1987, NEW ENGL J MED, V317, P1105, DOI 10.1056/NEJM198710293171802; Alrajhi AA, 2001, AM J TROP MED HYG, V65, P83; Anaissie EJ, 2002, CLIN INFECT DIS, V34, P780, DOI 10.1086/338958; BARTOLI A, 1978, T BRIT MYCOL SOC, V71, P383; BATISTA AC, 1955, AN SOC BIOL PERNAMB, V8, P94; 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J	Cohen, D; Spear, S; Scribner, R; Kissinger, P; Mason, K; Wildgen, J				Cohen, D; Spear, S; Scribner, R; Kissinger, P; Mason, K; Wildgen, J			"Broken windows" and the risk of gonorrhea	AMERICAN JOURNAL OF PUBLIC HEALTH			English	Article							SEXUALLY-TRANSMITTED DISEASES; UNITED-STATES POPULATION; COCKROACH ALLERGEN; DRUG-USE; HEALTH; SYPHILIS; BEHAVIOR; CHILDREN; ALCOHOL; NEIGHBORHOODS	Objectives. We examined the relationships between neighborhood conditions and gonorrhea. Methods. We assessed 55 block soups by rating housing and street conditions. We mapped all cases of gonorrhea between 1994 and 1996 and calculated aggregated case rates by block group. We obtained public school inspection reports and assigned findings to the block groups served by the neighborhood schools. A "broken windows" index measured housing quality, abandoned cars, graffiti: trash and public school deterioration. Using data from the 1990 census and 1995 updates, we determined the association between "broken windows," demographic characteristics, and gonorrhea rates. Results. The broken windows index explained more of the variance in gonorrhea rates than did a poverty index measuring: income, unemployment, and low education. in high-poverty neighborhoods, block groups with high broken windows scores had significantly higher gonorrhea rates than block groups with low broken windows scores(46.6 per 1000 vs 25.8 per 1000; P<.001). Conclusions. The robust association of deteriorated physical conditions of local neighborhoods with gonorrhea rates, independent of poverty, merits an intervention trial to test whether the environment has a, causal role in influencing high-risk sexual behaviors.	Louisiana State Univ, Med Ctr, New Orleans, LA 70112 USA; Univ New Orleans, Coll Publ & Urban Affairs, New Orleans, LA 70148 USA	Cohen, D (reprint author), Louisiana State Univ, Med Ctr, 1600 Canal St, New Orleans, LA 70112 USA.						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J	Eisner, MD; Anthonisen, N; Coultas, D; Kuenzli, N; Perez-Padilla, R; Postma, D; Romieu, I; Silverman, EK; Balmes, JR				Eisner, Mark D.; Anthonisen, Nicholas; Coultas, David; Kuenzli, Nino; Perez-Padilla, Rogelio; Postma, Dirkje; Romieu, Isabelle; Silverman, Edwin K.; Balmes, John R.		Environm & Occupational Hlth	An Official American Thoracic Society Public Policy Statement: Novel Risk Factors and the Global Burden of Chronic Obstructive Pulmonary Disease	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						pulmonary disease, chronic obstructive; pulmonary emphysema; chronic bronchitis; respiratory function tests; genetics; diet; asthma; air pollution; air pollution, indoor; tobacco smoke pollution; biomass; occupational exposure; occupational diseases; diet; nutritional status; tuberculosis	AIR-FLOW OBSTRUCTION; LUNG-FUNCTION DECLINE; CHRONIC RESPIRATORY SYMPTOMS; 3RD NATIONAL-HEALTH; NUTRITION EXAMINATION SURVEY; ENVIRONMENTAL TOBACCO-SMOKE; HOGG-DUBE-SYNDROME; SEVERE ALPHA(1)-ANTITRYPSIN DEFICIENCY; RESOLUTION COMPUTED-TOMOGRAPHY; SOUTHERN CALIFORNIA CHILDREN	Rationale: Although cigarette smoking is the most important cause of chronic obstructive pulmonary disease (COPD), a substantial proportion of COPD cases cannot be explained by smoking alone. Objectives: To evaluate the risk factors for COPD besides personal cigarette smoking. Methods: We constituted an ad hoc subcommittee of the American Thoracic Society Environmental and Occupational Health Assembly. An international group of members was invited, based on their scientific expertise in a specific risk factor for COPD. For each risk factor area, the committee reviewed the literature, summarized the evidence, and developed conclusions about the likelihood of it causing COPD. All conclusions were based on unanimous consensus. Measurements and Main Results: The population-attributable fraction for smoking as a cause of COPD ranged from 9.7 to 97.9%, but was less than 80% in most studies, indicating a substantial burden of disease attributable to nonsmoking risk factors. On the basis of our review, we concluded that specific genetic syndromes and occupational exposures were causally related to the development of COPD. Traffic and other outdoor pollution, secondhand smoke, biomass smoke, and dietary factors are associated with COPD, but sufficient criteria for causation were not met. Chronic asthma and tuberculosis are associated with irreversible loss of lung function, but there remains uncertainty about whether there are important phenotypic differences compared with COPD as it is typically encountered in clinical settings. Conclusions: In public health terms, a substantive burden of COPD is attributable to risk factors other than smoking. To prevent COPD-related disability and mortality, efforts must focus on prevention and cessation of exposure to smoking and these other, less well-recognized risk factors.				Kunzli, Nino/F-7195-2014	Kunzli, Nino/0000-0001-8360-080X	Roche; NIH; State of California Tobacco-Related Disease Research Program; Flight Attendant Medical Research Institute; GlaxoSmithKline; Boehringer Ingelheim; Nycomed	M.D.E. became an employee of Genentech subsequent to submission of manuscript; he was a consultant to Genentech ($5,001-$10,000) and Novartis ($5,001-$10,000), was an expert witness for DLA Piper LLP ($5,001-$10,000), received research grants from Roche ($50,001-$100,000) and NIH (more than $100,001), and an NIH study section reviewer (up to $1,000). N.A. served on an advisory board of GlaxoSmithKline ($5,001-$10,000) and as chair of the American Lung Association asthma clinical centers research project ($15,000/year). D.C. served on advisory boards of Boehringer Ingelheim (up tp $1,000) and Pfizer (up to $1,000) and as a grant reviewer for the State of California Tobacco-Related Disease Research Program (up to $1,000) and the Flight Attendant Medical Research Institute (up to $1,000). N.K. holds stock in Roche Holding Basel ($1,001-$5,000). R.P-P. received lecture fees from GlaxoSmithKline (up to $1,000) and Boehringer Ingelheim (up to $1,000). D.P. served on advisory boards of GlaxoSmithKline (up to $1,000), AstraZeneca (up to $1,000) and Nycomed (up to $1,000); he received lecture fees from GlaxoSmithKline ($1,001-$5,000), AstraZeneca ($1,001-5,000), and Nycomed ($1,001-$5,000), and received research grants from GlaxoSmithKline (more than $100,001), AstraZeneca ($50,001-100,000) and Nycomed ($50,001-100,000). I.R. reported she had nothing to disclose relevant to this manuscript. E.K.S. was a consultant to GlaxoSmithKline ($10,001-$50,000) and AstraZeneca ($5,001-$10,000), received lecture fees from GlaxoSmithKline ($1,001-$5,000), AstraZeneca ($1,001-$5,000) and Bayer ($1,001-$5,000), and research grants from GlaxoSmithKline (more than $100,001) and NIH (more than $100,001). J.R.B. served on an advisory board of the U.S. EPA ($1,001-$5,000), chaired the California Air Resources Board ($10,001-$50,000), and received book royalties from McGraw-Hill (up to $1,000).	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J	Corbett, JJ; Winebrake, JJ; Green, EH; Kasibhatla, P; Eyring, V; Lauer, A				Corbett, James J.; Winebrake, James J.; Green, Erin H.; Kasibhatla, Prasad; Eyring, Veronika; Lauer, Axel			Mortality from ship emissions: A global assessment	ENVIRONMENTAL SCIENCE & TECHNOLOGY			English	Article							AIR-POLLUTION; OCEAN; MODEL; HEALTH	Epidemiological studies consistently link ambient concentrations of particulate matter (PM) to negative health impacts, including asthma, heart attacks, hospital admissions, and premature mortality. We model ambient PM concentrations from oceangoing ships using two geospatial emissions inventories and two global aerosol models. We estimate global and regional mortalities by applying ambient PM increases due to ships to cardiopulmonary and lung cancer concentration-risk functions and population models. Our results indicate that shipping-related PM emissions are responsible for approximately 60,000 cardiopulmonary and lung cancer deaths annually, with most deaths occurring near coastlines in Europe, East Asia, and South Asia. Under current regulation and with the expected growth in shipping activity, we estimate that annual mortalities could increase by 40% by 2012.	[Corbett, James J.] Univ Delaware, Coll Marine & Earth Studies, Newark, DE 19716 USA; [Winebrake, James J.; Green, Erin H.] Rochester Inst Technol, Dept STS Publ Policy, Rochester, NY 14623 USA; [Kasibhatla, Prasad] Duke Univ, Nicholas Sch Environm, Durham, NC USA; [Eyring, Veronika; Lauer, Axel] Deutches Zentrum Luft & Raumfahrt, Inst Phys Atmosphaere, Wessling, Germany	Corbett, JJ (reprint author), Univ Delaware, Coll Marine & Earth Studies, 305 Robinson Hall, Newark, DE 19716 USA.	jcorbett@udel.edu	Corbett, James/B-3321-2009; Kasibhatla, Prasad/A-2574-2010; Winebrake, James/D-2478-2010; Eyring, Veronika/O-9999-2016	Corbett, James/0000-0002-2588-3474; Eyring, Veronika/0000-0002-6887-4885; Kasibhatla, Prasad/0000-0003-3562-3737			*ABT ASS, 2005, BENMAP ENV BEN MAPP, P275; Anderson HR, 2004, METAANALYSIS TIME SE; Bailey D, 2004, ENVIRON IMPACT ASSES, V24, P749, DOI 10.1016/j.eiar.2004.06.005; Bey I, 2001, J GEOPHYS RES-ATMOS, V106, P23073, DOI 10.1029/2001JD000807; *CAL AIR RES BOARD, 2006, APP QUANT HLTH IMP E; *CAL AIR RES BOARD, 2006, PROP EM RED PLAN POR; Capaldo K, 1999, NATURE, V400, P743; Cofala J, 2007, FINAL REPORT ANAL PO, P74; Cohen AJ, 2005, J TOXICOL ENV HEAL A, V68, P1301, DOI 10.1080/15287390590936166; Cohen A. J., 2004, COMP QUANTIFICATION, V2, P1353; Corbett JJ, 1999, J GEOPHYS RES-ATMOS, V104, P3457, DOI 10.1029/1998JD100040; Corbett JJ, 2000, ENVIRON SCI TECHNOL, V34, P3254, DOI 10.1021/es9911768; Corbett JJ, 2003, J GEOPHYS RES-ATMOS, V108, DOI 10.1029/2003JD003751; Corbett J.J., 2007, ALLOCATION FORECASTI, P26; Davis DL, 1997, LANCET, V350, P1341, DOI 10.1016/S0140-6736(97)10209-4; Endresen O, 2003, J GEOPHYS RES D, V108; European Commission ENTECUK Limited, 2002, QUANT EM SHIPS ASS S; Eyring V, 2005, J GEOPHYS RES-ATMOS, V110, DOI DOI 10.1029/2004JD005619; Hodan W. B., 2004, EVALUATING CONTRIBUT; KAISER J, 2005, SCIENCE, V307, pA1858, DOI 10.1126/science.307.5717.1858a; Krewski D, 2000, REANALYSIS HARVARD 6; Lauer A, 2007, ATMOS CHEM PHYS, V7, P5061; Nel A, 2005, SCIENCE, V308, P804, DOI 10.1126/science.1108752; O'Neill MS, 2003, ENVIRON HEALTH PERSP, V111, P1861, DOI 10.1289/ehp.6334; Ostro B, 2004, OUTDOOR AIR POLLUTIO; Pope CA, 2002, JAMA-J AM MED ASSOC, V287, P1132; *SEDAC, 2007, GRIDD POP WORLD; Streets DG, 2000, ATMOS ENVIRON, V34, P4425, DOI 10.1016/S1352-2310(00)00175-8; Streets D. G., 2003, J GEOPHYS RES, V108; *US CENS BUR, 2006, INT DAT BAS IDB DAT; Wang CF, 2007, ENVIRON SCI TECHNOL, V41, P3226, DOI 10.1021/es060752e; World Health Organization, 2004, REV GLOB BURD DIS GB	32	264	272	10	82	AMER CHEMICAL SOC	WASHINGTON	1155 16TH ST, NW, WASHINGTON, DC 20036 USA	0013-936X			ENVIRON SCI TECHNOL	Environ. Sci. Technol.	DEC 15	2007	41	24					8512	8518		10.1021/es071686z		7	Engineering, Environmental; Environmental Sciences	Engineering; Environmental Sciences & Ecology	240JB	WOS:000251582800050	18200887	
J	Rabe, KF; Bateman, ED; O'Donnell, D; Witte, S; Bredenbroker, D; Bethke, TD				Rabe, KF; Bateman, ED; O'Donnell, D; Witte, S; Bredenbroker, D; Bethke, TD			Roflumilast - an oral anti-inflammatory treatment for chronic obstructive pulmonary disease: a randomised controlled trial	LANCET			English	Article							AIR-FLOW LIMITATION; PHOSPHODIESTERASE-4 INHIBITOR; PDE4 INHIBITOR; HEALTH-STATUS; IN-VITRO; ASTHMA; COPD; BURDEN; FLUTICASONE; SALMETEROL	Background Chronic-obstructive pulmonary disease (COPD) is characterised by progressive airflow limitation associated with chronic inflammation. There are few treatment options for the disease. This study assessed the efficacy and safety of roflumilast, a phosphodiesterase-4 inhibitor, in patients with moderate to severe COPD. Methods This phase III, multicentre, double-blind, randomised, placebo-controlled study was undertaken in an outpatient setting. 1411 patients with COPD were randomly assigned roflumilast 250 mu g (n=576), roflumilast 500 mu g (n=555), or placebo (n=280) given orally once daily for 24 weeks. Primary outcomes were postbronchodilator FEV1 and health-related quality of life. Secondary outcomes included other lung function parameters and COPD exacerbations. Analyses were by intention to treat. Findings 1157 (82%) patients completed the study; 32 (11%) withdrew from the placebo group, 100 (17%) from the roflumilast 250 mu g group, and 124 (22%) from the roflumilast 500 mu g group. Postbronchodilator FEV1 at the end of treatment significantly improved with roflumilast 250 mu g (by 74 mL [SD 18]) and roflumilast 500 mu g (by 97 mL [18]) compared with placebo (p<0.0001). Improvement in health-related quality of life was greater with roflumilast 250 mu g (-3.4 units [0.6]) and roflumilast 500 mu g (-3.5 units [0.6]) than with placebo (-1.8 units [0.8]), although the differences between treatment groups were not significant. The mean numbers of exacerbations per patient were 1.13 (2.37), 1.03 (2.33), and 0.75 (1.89) with placebo, roflumilast 250 mu g, and roflumilast 500 mu g, respectively. Most adverse events were mild to moderate in intensity and resolved during the study. Interpretation Roflumilast is a promising candidate for anti-inflammatory COPD treatment because it improved lung function and reduced exacerbations compared with placebo. Long-term studies are needed to fully assess the effect on health-related quality of life.	Leiden Univ, Med Ctr, Dept Pulmonol, NL-2333 ZA Leiden, Netherlands; Univ Cape Town, ZA-7925 Cape Town, South Africa; Kingston Gen Hosp, Kingston, ON K7L 2V7, Canada; ALTANA Pharma AG, Constance, Germany	Rabe, KF (reprint author), Leiden Univ, Med Ctr, Dept Pulmonol, C3P,Albinusdreef 2, NL-2333 ZA Leiden, Netherlands.	k.f.rabe@lumc.nl					American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Barnes PJ, 2003, EUR RESPIR J, V22, P672, DOI 10.1183/09031936.03.00040703; Barnette M S, 1999, Prog Drug Res, V53, P193; Bundschuh DS, 2001, J PHARMACOL EXP THER, V297, P280; Burge PS, 2000, BRIT MED J, V320, P1297, DOI 10.1136/bmj.320.7245.1297; Calverley P, 2003, LANCET, V361, P449, DOI 10.1016/S0140-6736(03)12459-2; Calverley PM, 2003, EUR RESPIR J, V22, P912, DOI 10.1183/09031936.03.00027003; Calverley PMA, 2003, LANCET, V362, P1053, DOI 10.1016/S0140-6736(03)14416-9; Casaburi R, 2002, EUR RESPIR J, V19, P217, DOI 10.1183/09031936.02.00269802; Compton CH, 2001, LANCET, V358, P265, DOI 10.1016/S0140-6736(01)05481-2; *CPMP, 1999, CPMPEWP56298 EUR AG; Donohue JF, 2002, CHEST, V122, P47, DOI 10.1378/chest.122.1.47; Engelstaetter R., 2005, ANN ALLERG ASTHMA IM, V94, P169; Global Initiative for Chronic Obstructive Lung Disease, 2004, GLOB STRAT DIAGN MAN; Global Initiative for Chronic Obstructive Lung Disease, 2001, NHLBI WHO WORKSH REP; Grootendorst DC, 2003, PULM PHARMACOL THER, V16, P115, DOI 10.1016/S1094-5539(02)00172-4; Halbert RJ, 2003, CHEST, V123, P1684, DOI 10.1378/chest.123.5.1684; Hansen EF, 2001, AM J RESP CRIT CARE, V163, P690; Hatzelmann A, 2001, J PHARMACOL EXP THER, V297, P267; Hogg JC, 2004, LANCET, V364, P709, DOI 10.1016/S0140-6736(04)16900-6; JONES PW, 1992, AM REV RESPIR DIS, V145, P1321; Kumar RK, 2003, J PHARMACOL EXP THER, V307, P349, DOI 10.1124/jpet.103.053819; Lipworth BJ, 2005, LANCET, V365, P167, DOI 10.1016/S0140-6736(05)17708-3; Muise ES, 2002, BIOCHEM PHARMACOL, V63, P1527, DOI 10.1016/S0006-2952(02)00903-6; Murray CJL, 1997, LANCET, V349, P1498, DOI 10.1016/S0140-6736(96)07492-2; O'Donnell DE, 1999, AM J RESP CRIT CARE, V160, P542; ODONNELL DE, 1994, CHEST, V106, P904, DOI 10.1378/chest.106.3.904; Pauwels RA, 2004, LANCET, V364, P613; Quanjer PH, 1993, EUR RESPIR J S, V16, P5, DOI 10.1183/09041950.005s1693; Swanney MP, 2000, AM J RESP CRIT CARE, V162, P917; Szafranski W, 2003, EUR RESPIR J, V21, P74, DOI 10.1183/09031936.03.00031402; Timmer W, 2002, J CLIN PHARMACOL, V42, P297, DOI 10.1177/00912700222011328; Viegi G, 2001, RESPIRATION, V68, P4, DOI 10.1159/000050456	33	264	271	1	18	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	AUG 13	2005	366	9485					563	571		10.1016/S0140-6736(05)67100-0		9	Medicine, General & Internal	General & Internal Medicine	955LL	WOS:000231227300028	16099292	
J	Barnes, PJ				Barnes, PJ			Scientific rationale for inhaled combination therapy with long-acting beta(2)-agonists and corticosteroids	EUROPEAN RESPIRATORY JOURNAL			English	Review						asthma; budesonide; fluticasone propionate; formoterol; salmeterol	AIRWAY SMOOTH-MUSCLE; LUNG MAST-CELLS; SALMETEROL/FLUTICASONE PROPIONATE COMBINATION; NK2 RECEPTOR EXPRESSION; DOWN-REGULATION; IN-VIVO; MU-G; GLUCOCORTICOID RECEPTOR; ADENOSINE-MONOPHOSPHATE; MICROVASCULAR LEAKAGE	The addition of an inhaled long-acting beta(2)-agonist (LABA) to an inhaled corticosteroid (ICS) gives optimal control of asthma in most patients and two fixed combination inhalers (salmeterol/fluticasone and formoterol/budesonide) are increasingly used as a convenient controller in patients with persistent asthma. There is a strong scientific rationale for the combination of these two drug classes. ICS suppress the chronic inflammation of asthma and reduce airway hyperresponsiveness and this is achieved at low doses in most patients. LABA act on different aspects of the pathophysiology of asthma. In addition to their bronchodilator action, LABA also inhibit mast cell mediator release, plasma exudation and may reduce sensory nerve activation. Thus these two classes of drug address complementary aspects of the pathophysiology of asthma that neither drug class is able to achieve alone. There are several positive interactions between LABA and ICS. Corticosteroids increase the expression of beta(2)-receptors by increasing gene transcription. Experimentally this protects against the loss of beta(2)-receptors in response to long-term exposure to beta(2)-agonists. While this is unlikely to be important in bronchodilator responses to beta(2)-agonists, in view of the large beta-receptor reserve, it is probably important in preventing loss of beta-agonist effects on the nonbronchodilator actions of LABA discussed earlier. beta(2)-Agonists may potentiate the molecular mechanism of corticosteroid actions, with increased nuclear localization of glucocorticoid receptors and additive or sometimes synergistic suppression of inflammatory mediator release. Thus LABA and ICS may optimize each others beneficial actions in the airways, but the low systemic effects of these drugs do not result in any increase in adverse effects. Long-acting beta(2)-agonists corticosteroid inhaler therapy is therefore a logical advance and results in effective control of asthma in the majority of patients without significant adverse effects. This simplified approach to long-term asthma therapy has a strong scientific rationale.	Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Thorac Med, London SW3 6LY, England	Barnes, PJ (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Thorac Med, Dovehouse St, London SW3 6LY, England.						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J	Mendell, MJ; Heath, GA				Mendell, MJ; Heath, GA			Do indoor pollutants and thermal conditions in schools influence student performance? A critical review of the literature	INDOOR AIR			English	Review						indoor environment; indoor air quality; performance; schools; education; children	SICK BUILDING SYNDROME; PERCEIVED AIR-QUALITY; VOLATILE ORGANIC-COMPOUNDS; SYNDROME SBS SYMPTOMS; MODERATE HEAT-STRESS; DAY-CARE-CENTERS; OFFICE WORKERS; ALLERGIC SENSITIZATION; RESPIRATORY SYMPTOMS; YOUNG-CHILDREN	To assess whether school environments can adversely affect academic performance, we review scientific evidence relating indoor pollutants and thermal conditions, in schools or other indoor environments, to human performance or attendance. We critically review evidence for direct associations between these aspects of indoor environmental quality (IEQ) and performance or attendance. Secondarily, we summarize, without critique, evidence on indirect connections potentially linking IEQ to performance or attendance. Regarding direct associations, little strongly designed research was available. Persuasive evidence links higher indoor concentrations of NO2 to reduced school attendance, and suggestive evidence links low ventilation rates to reduced performance. Regarding indirect associations, many studies link indoor dampness and microbiologic pollutants (primarily in homes) to asthma exacerbations and respiratory infections, which in turn have been related to reduced performance and attendance. Also, much evidence links poor IEQ (e.g. low ventilation rate, excess moisture, or formaldehyde) with adverse health effects in children and adults and documents dampness problems and inadequate ventilation as common in schools. Overall, evidence suggests that poor IEQ in schools is common and adversely influences the performance and attendance of students, primarily through health effects from indoor pollutants. Evidence is available to justify (i) immediate actions to assess and improve IEQ in schools and (ii) focused research to guide IEQ improvements in schools.	Univ Calif Berkeley, Lawrence Berkeley Lab, Environm Energy Technol Div, Indoor Environm Dept, Berkeley, CA 94720 USA; Univ Calif Berkeley, Energy & Resources Grp, Berkeley, CA 94720 USA	Mendell, MJ (reprint author), Univ Calif Berkeley, Lawrence Berkeley Lab, Environm Energy Technol Div, Indoor Environm Dept, 1 Cyclotron Rd,MS 90-3058, Berkeley, CA 94720 USA.	mjmendell@lbl.gov					Apte M., 1999, P IND AIR 99 8 INT C, V1, P117; Austin JK, 1998, DEV MED CHILD NEUROL, V40, P248; Bako-Biro Z, 2004, INDOOR AIR, V14, P178, DOI 10.1111/j.1600-0668.2004.00218.x; BARTLETT KH, 1999, IND AIR 99 P 8 INT C, V1, P252; BAYER CW, 2000, CAUES INDOOR AIR QUA; BERNER MM, 1993, URBAN EDUC, V28, P6, DOI 10.1177/0042085993028001002; BLONDEAU P, 2004, IN PRESS INDOOR AIR; Bornehag CG, 2001, INDOOR AIR, V11, P72; BORNEHAG CG, 2002, IND AIR 02 P 9 INT C, V3, P431; BRAGANZA E, 2000, P HLTH BUILD 2000, V1, P193; Burton WN, 2001, J OCCUP ENVIRON MED, V43, P64, DOI 10.1097/00043764-200101000-00013; BUSSING R, 1995, ARCH PEDIAT ADOL MED, V149, P565; Chaloulakou A, 2003, CHEMOSPHERE, V52, P1007, DOI 10.1016/S0045-6535(03)00263-7; CHALOULAKOU A, 2002, ATMOS ENVIRON, V36, P1169; Chen L, 2000, INHAL TOXICOL, V12, P997; Committee on the Assessment of Asthma and Indoor Air, 2000, CLEAR AIR ASTHM IND; Campbell D. 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J	Mucida, D; Kutchukhidze, N; Erazo, A; Russo, M; Lafaille, JJ; de Lafaille, MAC				Mucida, D; Kutchukhidze, N; Erazo, A; Russo, M; Lafaille, JJ; de Lafaille, MAC			Oral tolerance in the absence of naturally occurring Tregs	JOURNAL OF CLINICAL INVESTIGATION			English	Article							REGULATORY T-CELLS; TRANSCRIPTION FACTOR FOXP3; RECEPTOR TRANSGENIC MICE; GROWTH-FACTOR-BETA; IN-VIVO EXPANSION; TGF-BETA; AUTOIMMUNE ENCEPHALOMYELITIS; CUTTING EDGE; PERIPHERAL TOLERANCE; AIRWAY INFLAMMATION	Mucosal tolerance prevents pathological reactions against environmental and food antigens, and its failure results in exacerbated inflammation typical of allergies and asthma. One of the proposed mechanisms of oral tolerance is the induction of Tregs. Using a mouse model of hyper-IgE and asthma, we found that oral tolerance could be effectively induced in the absence of naturally occurring thymus-derived Tregs. Oral antigen administration prior to i.p. immunization prevented effector/memory Th2 cell development, germinal center formation, class switching to IgE, and lung inflammation. Oral exposure to antigen induced development of antigen-specific CD4(+)CD25(+)Foxp3(+)CD45RB(low) cells that were anergic and displayed suppressive activity in vivo and in vitro. Oral tolerance to the Th2 allergic response was in large part dependent on TGF-beta and independent of IL-10. Interestingly, Tregs were also induced by single i.p. immunization with antigen and adjuvant. However, unlike oral administration of antigen, which induced Tregs but not effector T cells, i.p. immunization led to the simultaneous induction of Tregs and effector Th2 cells displaying the same antigen specificity.	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J	Weingart, SN; Toth, M; Sands, DZ; Aronson, MD; Davis, RB; Phillips, RS				Weingart, SN; Toth, M; Sands, DZ; Aronson, MD; Davis, RB; Phillips, RS			Physicians' decisions to override computerized drug alerts in primary care	ARCHIVES OF INTERNAL MEDICINE			English	Article							MEDICATION ERRORS; CONTROLLED TRIAL; AMBULATORY-CARE; ORDER ENTRY; REMINDERS; SYSTEM; RECORD; EVENTS	Background: Although computerized physician order entry reduces medication errors among inpatients, little is known about the use of this system in primary care. Methods: We calculated the override rate among 3481 consecutive alerts generated at 5 adult primary care practices that use a common computerized physician order entry system for prescription writing. For detailed review, we selected a random sample of 67 alerts in which physicians did not prescribe an alerted medication and 122 alerts that resulted in a written prescription. We identified factors associated with the physicians' decisions to override a medication alert, and determined whether an adverse drug event (ADE) occurred. Results: Physicians overrode 91.2% of drug allergy and 89.4% of high-severity drug interaction alerts. In the multivariable analysis using the medical chart review sample (n=189), physicians were less likely to prescribe an alerted medication if the prescriber was a house officer (odds ratio [OR], 0.26; 95% confidence interval [CI], 0.08-0.84) and if the patient had many drug allergies (OR, 0.70; 95% CI, 0.53-0.93). They were more likely to override alerts for renewals compared with new prescriptions (OR, 17.74; 95% CI, 5.60-56.18). We found no ADEs in cases where physicians observed the alert and 3 ADEs among patients with alert overrides, a nonsignificant difference (P=.55). Physician reviewers judged that 36.5% of the alerts were inappropriate. Conclusions: Few physicians changed their prescription in response to a drug allergy or interaction alert, and there were few ADEs, suggesting that the threshold for alerting was set too low. Computerized physician order entry systems should suppress alerts for renewals of medication combinations that patients currently tolerate.	Beth Israel Deaconess Med Ctr, Div Gen Med & Primary Care, Boston, MA 02215 USA; Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA	Weingart, SN (reprint author), Beth Israel Deaconess Med Ctr, Div Gen Med & Primary Care, Rose 112,330 Brookline Ave, Boston, MA 02215 USA.				AHRQ HHS [1K08 HS 11644-01]		Abookire S A, 2000, Proc AMIA Symp, P2; Bates DW, 1998, JAMA-J AM MED ASSOC, V280, P1311, DOI 10.1001/jama.280.15.1311; Gandhi TK, 2003, NEW ENGL J MED, V348, P1556, DOI 10.1056/NEJMsa020703; GANDHI TK, 2001, J GEN INTERN MED S, V16, P133; Kuperman G J, 1996, Proc AMIA Annu Fall Symp, P704; Kuperman G J, 1994, Proc Annu Symp Comput Appl Med Care, P836; Kuperman GJ, 1999, J AM MED INFORM ASSN, V6, P512; The Leapfrog Group, FACT SHEET; *MASS COAL PREV ME, MHA BEST PRACT REC R; MCDONALD CJ, 1992, M D COMPUT, V9, P304; MCDONALD CJ, 1976, NEW ENGL J MED, V295, P1351, DOI 10.1056/NEJM197612092952405; MCDONALD CJ, 1977, AM J PUBLIC HEALTH, V67, P240, DOI 10.2105/AJPH.67.3.240; MCDONALD CJ, 1984, ANN INTERN MED, V100, P130; Overhage JM, 2001, J AM MED INFORM ASSN, V8, P361; Peterson JF, 2001, J GEN INTERN MED S, V16, P212; Raschke RA, 1998, JAMA-J AM MED ASSOC, V280, P1317, DOI 10.1001/jama.280.15.1317; RIND DM, 1994, ARCH INTERN MED, V154, P1511, DOI 10.1001/archinte.154.13.1511; Safran C, 2001, JAMA-J AM MED ASSOC, V285, P1766, DOI 10.1001/jama.285.13.1766; Schiff GD, 2000, AM J MED, V109, P494, DOI 10.1016/S0002-9343(00)00546-5; TIERNEY WM, 1993, JAMA-J AM MED ASSOC, V269, P379, DOI 10.1001/jama.269.3.379; TIERNEY WM, 1986, MED CARE, V24, P659, DOI 10.1097/00005650-198608000-00001	21	258	262	2	12	AMER MEDICAL ASSOC	CHICAGO	515 N STATE ST, CHICAGO, IL 60610 USA	0003-9926			ARCH INTERN MED	Arch. Intern. Med.	NOV 24	2003	163	21					2625	2631		10.1001/archinte.163.21.2625		7	Medicine, General & Internal	General & Internal Medicine	747TQ	WOS:000186821300010	14638563	
J	Schuster, E; Dunn-Coleman, N; Frisvad, JC; van Dijck, PWM				Schuster, E; Dunn-Coleman, N; Frisvad, JC; van Dijck, PWM			On the safety of Aspergillus niger - a review	APPLIED MICROBIOLOGY AND BIOTECHNOLOGY			English	Review							FRAGMENT-LENGTH-POLYMORPHISMS; GREEN COFFEE BEANS; BLACK ASPERGILLI; OCHRATOXIN-A; CUTANEOUS ASPERGILLOSIS; AFLATOXIN PRODUCTION; MICROBIAL ESTERASES; BIOTECHNOLOGY PLANT; STORED COTTONSEED; MOLECULAR-CLONING	Aspergillus niger is one of the most important microorganisms used in biotechnology. It has been in use already for many decades to produce extracellular (food) enzymes and citric acid. In fact, citric acid and many A. niger enzymes are considered GRAS by the United States Food and Drug Administration. In addition, A. niger is used for biotransformations and waste treatment. In the last two decades, A. niger has been developed as an important transformation host to over-express food enzymes. Being pre-dated by older names, the name A. niger has been conserved for economical and information retrieval reasons and there is a taxonomical consensus based on molecular data that the only other common species closely related to A. niger in the Aspergillus series Nigri is A. tubingensis. A. niger, like other filamentous fungi, should be treated carefully to avoid the formation of spore dust. However, compared with other filamentous fungi, it does not stand out as a particular problem concerning allergy or mycopathology. A few medical cases, e.g. lung infections, have been reported, but always in severely immunocompromised patients. In tropical areas, ear infections (otomycosis) do occur due to A. niger invasion of the outer ear canal but this may be caused by mechanical damage of the skin barrier. A. niger strains produce a series of secondary metabolites, but it is only ochratoxin A that can be regarded as a mycotoxin in the strict sense of the word. Only 3-10% of the strains examined for ochratoxin A production have tested positive under favourable conditions. New and unknown isolates should be checked for ochratoxin A production before they are developed as production organisms. It is concluded, with these restrictions, that A. niger is a safe production organism.	DSM Food Specialt, Dept Regulatory Affairs, NL-2600 MA Delft, Netherlands; Rohm GmbH, Enzyme Technol, D-64293 Darmstadt, Germany; Genencor Int Inc, Palo Alto, CA 94304 USA; Tech Univ Denmark, BioCentrum, DK-2800 Kgs Lyngby, Denmark	van Dijck, PWM (reprint author), DSM Food Specialt, Dept Regulatory Affairs, 600-0245,POB 1, NL-2600 MA Delft, Netherlands.	piet.dijck-van@dsm.com					ABARCA ML, 1994, APPL ENVIRON MICROB, V60, P2650; Abarca ML, 2001, J FOOD PROTECT, V64, P903; ABRAMSON C, 1986, J AM PODIAT MED ASSN, V76, P168; Accensi F, 1999, FEMS MICROBIOL LETT, V180, P191, DOI 10.1111/j.1574-6968.1999.tb08795.x; ALMUSSALAM A, 1980, THESIS RIJKSUNIVERSI; ANDEREGG RJ, 1976, J AM CHEM SOC, V98, P3365, DOI 10.1021/ja00427a051; BALLANCE DJ, 1983, BIOCHEM BIOPH RES CO, V112, P284, DOI 10.1016/0006-291X(83)91828-4; BARBESGAARD P, 1992, APPL MICROBIOL BIOT, V36, P569; BENNETT JW, 1989, MYCOPATHOLOGIA, V100, P3; *BER CHEM IND, 1998, MERKBL B 007; BERCOVITZ A, 1990, APPL ENVIRON MICROB, V56, P1594; Berka RM, 1992, ASPERGILLUS BIOL IND, P155; BHATIA YN, 1969, MYKOSEN, V12, P651; BINDER RE, 1982, MEDICINE, V61, P109, DOI 10.1097/00005792-198203000-00005; BLOCH F, 1973, AM POTATO J, V50, P357, DOI 10.1007/BF02851891; BULLERMAN LB, 1968, APPL MICROBIOL, V16, P1945; BUSSINK HJD, 1991, CURR GENET, V19, P467, DOI 10.1007/BF00312738; BUSSINK HJD, 1990, FEBS LETT, V273, P127, DOI 10.1016/0014-5793(90)81066-W; BUXTON FP, 1985, GENE, V37, P207, DOI 10.1016/0378-1119(85)90274-4; CAESAR F, 1969, HELV PHYSL PHARM ACT, V44, P676; CAHILL KM, 1967, ARCH DERMATOL, V96, P545, DOI 10.1001/archderm.96.5.545; CAMPBELL EI, 1989, MOL GEN GENET, V206, P71; Cole R. 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Microbiol. Biotechnol.	AUG	2002	59	4-5					426	435		10.1007/s00253-002-1032-6		10	Biotechnology & Applied Microbiology	Biotechnology & Applied Microbiology	589AF	WOS:000177734800005	12172605	
J	Humbles, AA; Lu, B; Friend, DS; Okinaga, S; Lora, J; Al-garawi, A; Martin, TR; Gerard, NP; Gerard, C				Humbles, AA; Lu, B; Friend, DS; Okinaga, S; Lora, J; Al-garawi, A; Martin, TR; Gerard, NP; Gerard, C			The murine CCR3 receptor regulates both the role of eosinophils and mast cells in allergen-induced airway inflammation and hyperresponsiveness	PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA			English	Article							GUINEA-PIG MODEL; ASTHMA MODEL; CHEMOKINE EOTAXIN; IN-VIVO; EXPRESSION; MICE; LUNG; INTERLEUKIN-5; RECRUITMENT; ACTIVATION	CCR3 is a chemokine receptor initially thought specific to eosinophils but subsequently identified on TH2 cell subsets, basophils, mast cells, neural tissue, and some epithelia. Because of the prominent role of these cells in allergic disease, including asthma, we generated mice deficient in CCR3 to determine its contribution in a model of allergic airway disease. Here we show that CCR3 is important for the basal trafficking of eosinophils to the intestinal mucosa but not the lung. In contrast, CCR3 disruption significantly curtails eosinophil recruitment to the lung after allergen challenge, with the majority of the eosinophils being arrested in the subendothelial space. Further, a role for CCR3 in mast cell homing has been identified; after sensitization and allergen challenge, we find increased numbers of intraepithelial mast cells in the trachea of knockout mice. Physiologically, we find that the net result of these complex cell fates after sensitization and allergen challenge is a paradoxical increase in airway responsiveness to cholinergic stimulation. These data underscore a more complex role for CCR3 in allergic disease than was anticipated.	Harvard Univ, Ina Sue Perlmutter Lab, Sch Med, Childrens Hosp, Boston, MA 02115 USA; Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA; Millennium Pharmaceut Inc, Dept Biol, Inflammat Div, Cambridge, MA 02139 USA; Tufts Univ, New England Med Ctr, Boston, MA 02111 USA	Gerard, C (reprint author), Harvard Univ, Ina Sue Perlmutter Lab, Sch Med, Childrens Hosp, Enders Bldg,Room 144,320 Longwood Ave, Boston, MA 02115 USA.				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Natl. Acad. Sci. U. S. A.	FEB 5	2002	99	3					1479	1484		10.1073/pnas.261462598		6	Multidisciplinary Sciences	Science & Technology - Other Topics	519YF	WOS:000173752500070	11830666	
J	Kellogg, CA; Griffin, DW				Kellogg, Christina A.; Griffin, Dale W.			Aerobiology and the global transport of desert dust	TRENDS IN ECOLOGY & EVOLUTION			English	Review							AMBIENT FUNGAL SPORES; AERIAL DISPERSAL; AIRBORNE SPREAD; MOUTH-DISEASE; AFRICAN DUST; CORAL-REEFS; ASIAN DUST; SOIL DUST; BACTERIA; DIVERSITY	Desert winds aerosolize several billion tons of soil-derived dust each year, including concentrated seasonal pulses from Africa and Asia. These transoceanic and transcontinental dust events inject a large pulse of microorganisms and pollen into the atmosphere and could therefore have a role in transporting pathogens or expanding the biogeographical range of some organisms by facilitating long-distance dispersal events. As we discuss here, whether such dispersal events are occurring is only now beginning to be investigated. Huge dust events create an atmospheric bridge over land and sea, and the microbiota contained within them could impact downwind ecosystems. Such dispersal is of interest because of the possible health effects of allergens and pathogens that might be carried with the dust.	US Geol Survey, St Petersburg, FL 33701 USA	Kellogg, CA (reprint author), US Geol Survey, 600 4th St S, St Petersburg, FL 33701 USA.	ckellogg@usgs.gov	Kellogg, Christina/B-3257-2009; MORENO-GRAU, STELLA/E-6540-2012	Kellogg, Christina/0000-0002-6492-9455			Blades E, 1998, W INDIAN MED J S2, V47, P34; Bovallius A, 1980, Ann N Y Acad Sci, V353, P186, DOI 10.1111/j.1749-6632.1980.tb18922.x; BREITMAN L, 2001, J LONGEVITY, V7, P9; Brown JKM, 2002, SCIENCE, V297, P537, DOI 10.1126/science.1072678; Buttner MP, 1997, MANUAL ENV MICROBIOL, P629; Capone DG, 2005, ASM NEWS, V71, P179; Carinanos P, 2004, ARCH ENVIRON CON TOX, V46, P141, DOI 10.1007/s00244-003-2273-9; Carlson T. 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R., 2004, Aerobiologia, V20, P119, DOI 10.1023/B:AERO.0000032949.14023.3a; Whitaker RJ, 2003, SCIENCE, V301, P976, DOI 10.1126/science.1086909; Whitfield J, 2005, SCIENCE, V310, P960, DOI 10.1126/science.310.5750.960; Wu PC, 2004, ATMOS ENVIRON, V38, P4879, DOI 10.1016/j.atmosenv.2004.05.039; Yeo HG, 2002, ATMOS ENVIRON, V36, P5437, DOI 10.1016/S1352-2310(02)00672-6	61	256	271	12	80	ELSEVIER SCIENCE LONDON	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0169-5347			TRENDS ECOL EVOL	Trends Ecol. Evol.	NOV	2006	21	11					638	644		10.1016/j.tree.2006.07.004		7	Ecology; Evolutionary Biology; Genetics & Heredity	Environmental Sciences & Ecology; Evolutionary Biology; Genetics & Heredity	105DQ	WOS:000242010000009	16843565	
J	Janssen, NAH; Brunekreef, B; van Vliet, P; Aarts, F; Meliefste, K; Harssema, H; Fischer, P				Janssen, NAH; Brunekreef, B; van Vliet, P; Aarts, F; Meliefste, K; Harssema, H; Fischer, P			The relationship between air pollution from heavy traffic and allergic sensitization, bronchial hyperresponsiveness, and respiratory symptoms in Dutch schoolchildren	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; allergy; bronchial hyperresponsiveness; children; diesel; lung function; respiratory symptoms	DIESEL EXHAUST PARTICLES; LUNG-FUNCTION; ADJUVANT ACTIVITY; CHILDHOOD ASTHMA; EXPIRATORY FLOW; CHILDREN; EXPOSURE; HEALTH; ROAD; ATOPY	Studies have suggested that children living close to busy roads may have impaired respiratory health. This study was designed to test the hypothesis that exposure to exhaust from heavy traffic in particular is related to childhood respiratory health. Children attending 24 schools located within 400 in from busy motorways were investigated. The motorways carried between 5,190 and 22,326 trucks per weekday and between 30,399 and 155,656 cars per day. Locations were chosen so that the correlation between truck and car traffic counts was low. Air pollution measurements were performed at the schools for I year. Respiratory symptoms were collected by parent-completed questionnaire. Sensitization to common allergens was measured by serum immunoglobulin E and skin prick tests. Bronchial hyperresponsiveness (BHR) was measured with a hypertonic saline challenge. Respiratory symptoms were increased near motorways with high truck but not high car traffic counts. They were also related to air pollutants that increased near motorways with high truck traffic counts. Lung function and BHR were not related to pollution. Sensitization to pollen increased in relation to truck but not car traffic counts. The relation between symptoms and measures of exposure to (truck) traffic-related air pollution were almost entirely restricted to children with BHR and/or sensitization to common allergens, indicating that these are a sensitive subgroup among all children for these effects.	Univ Utrecht, Inst Risk Assessment Sci, Dept Environm Epidemiol, NL-3508 TD Utrecht, Netherlands; Natl Inst Publ Hlth & Environm, NL-3720 BA Bilthoven, Netherlands	Brunekreef, B (reprint author), Univ Utrecht, Inst Risk Assessment Sci, Dept Environm Epidemiol, POB 80176, NL-3508 TD Utrecht, Netherlands.		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Health Perspect.	SEP	2003	111	12					1512	1518		10.1289/ehp.6243		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	733HZ	WOS:000185995500033	12948892	
J	Calverley, PMA; Burge, PS; Spencer, S; Anderson, JA; Jones, PW				Calverley, PMA; Burge, PS; Spencer, S; Anderson, JA; Jones, PW		ISOLDE Study Investigators	Bronchodilator reversibility testing in chronic obstructive pulmonary disease	THORAX			English	Article							AIR-FLOW OBSTRUCTION; CORTICOSTEROID TRIALS; COPD; MANAGEMENT; SMOKING; ASTHMA; FEV1	Background: A limited or absent bronchodilator response is used to classify chronic obstructive pulmonary disease (COPD) and can determine the treatment offered. The reliability of the recommended response criteria and their relationship to disease progression has not been established. Methods: 660 patients meeting European Respiratory Society (ERS) diagnostic criteria for irreversible COPD were studied. Spirometric parameters were measured on three occasions before and after salbutamol and ipratropium bromide sequentially or in combination over 2 months. Responses were classified using the American Thoracic Society/GOLD (ATS) and ERS criteria. Patients were followed for 3 years with post-bronchodilator FEV1 and exacerbation history recorded 3 monthly and health status 6 monthly. Results: FEV1 increased significantly with each bronchodilator, a response that was normally distributed. Mean post-bronchodilator FEV1 was reproducible between visits (intraclass correlation 0.93). The absolute change in FEV1 was independent of the pre-bronchodilator value but the percentage change correlated with pre-bronchodilator FEV1 (r=-0.44; p<0.0001). Using ATS criteria, 52.1% of patients changed responder status between visits compared with 38.2% using ERS criteria. Smoking status, atopy, and withdrawing inhaled corticosteroids were unrelated to bronchodilator response, as was the rate of decline in FEV1, decline in health status, and exacerbation rate. Conclusion: In moderate to severe COPD bronchodilator responsiveness is a continuous variable. Classifying patients as "responders" and "non-responders" can be misleading and does not predict disease progression.	Univ Liverpool, Dept Med, Liverpool L69 3BX, Merseyside, England; Birmingham Heartlands Hosp, Birmingham B9 5ST, W Midlands, England; GlaxoSmithKline R&D, Dept Med Stat, Stevenage, Herts, England; Univ London St Georges Hosp, Sch Med, London SW17 0RE, England	Calverley, PMA (reprint author), Univ Hosp Aintree, Ctr Clin Sci, Liverpool L69 7AL, Merseyside, England.		Spencer, Sally/D-6963-2013				American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; American thoracic society, 1995, AM J RESP CRIT CARE, V152, pS77; ANTHONISEN NR, 1986, AM REV RESPIR DIS, V133, P814; ANTHONISEN NR, 1986, AM REV RESPIR DIS, V133, P14; Bland M., 1987, INTRO MED STAT; BRAND PLP, 1992, THORAX, V47, P429, DOI 10.1136/thx.47.6.429; British Thoracic Society (BTS), 1997, THORAX S5, V52, pS1; Burge PS, 2000, BRIT MED J, V320, P1297, DOI 10.1136/bmj.320.7245.1297; CALLAHAN CM, 1991, ANN INTERN MED, V114, P216; Davies L, 1999, QJM-MON J ASSOC PHYS, V92, P395, DOI 10.1093/qjmed/92.7.395; DOMPELING E, 1992, EUR RESPIR J, V5, P975; ENRIGHT PL, 1991, AM REV RESPIR DIS, V143, P1215; GROSS NJ, 1989, CHEST, V96, P984, DOI 10.1378/chest.96.5.984; GROSS NJ, 1989, AM REV RESPIR DIS, V139, P1188; Hansen EF, 1999, AM J RESP CRIT CARE, V159, P1267; HAY JG, 1992, EUR RESPIR J, V5, P659; Jarad NA, 1999, RESP MED, V93, P161, DOI 10.1016/S0954-6111(99)90001-X; Jones PW, 1997, AM J RESP CRIT CARE, V155, P1283; KERSTJENS HAM, 1993, EUR RESPIR J, V6, P868; Kerstjens HAM, 1996, AM J RESP CRIT CARE, V154, pS266; Lofdahl CG, 1998, RESP MED, V92, P467, DOI 10.1016/S0954-6111(98)90293-1; NISAR M, 1992, AM REV RESPIR DIS, V146, P555; Pauwels RA, 1999, NEW ENGL J MED, V340, P1948, DOI 10.1056/NEJM199906243402503; Pauwels Romain A., 2001, American Journal of Respiratory and Critical Care Medicine, V163, P1256; Quanjer PH, 1993, EUR RESPIR J S, V16, P5, DOI 10.1183/09041950.005s1693; SIAFAKAS NM, 1995, EUR RESPIR J, V8, P1398, DOI 10.1183/09031936.95.08081398; TWEEDDALE PM, 1987, THORAX, V42, P487, DOI 10.1136/thx.42.7.487; VATHENEN AS, 1988, AM REV RESPIR DIS, V138, P850; WEIR DC, 1990, THORAX, V45, P112, DOI 10.1136/thx.45.2.112	29	256	271	0	3	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	AUG	2003	58	8					659	664		10.1136/thorax.58.8.659		6	Respiratory System	Respiratory System	705YP	WOS:000184425100006	12885978	
J	Lieu, TA; Lozano, P; Finkelstein, JA; Chi, FW; Jensvold, NG; Capra, AM; Quesenberry, CP; Selby, JV; Farber, HJ				Lieu, TA; Lozano, P; Finkelstein, JA; Chi, FW; Jensvold, NG; Capra, AM; Quesenberry, CP; Selby, JV; Farber, HJ			Racial/ethnic variation in asthma status and management practices among children in managed medicaid	PEDIATRICS			English	Article						asthma; race; race/ethnicity; health status; quality of care; processes of care; managed care	HEALTH MAINTENANCE ORGANIZATION; PATIENT-PHYSICIAN RELATIONSHIP; AFRICAN-AMERICAN CHILDREN; INNER-CITY CHILDREN; RACIAL-DIFFERENCES; ETHNIC-DIFFERENCES; CHILDHOOD ASTHMA; UNITED-STATES; RENAL-TRANSPLANTATION; CULTURAL COMPETENCE	Objective. Racial/ethnic disparities in hospitalization rates among children with asthma have been documented but are not well-understood. Medicaid programs, which serve many minority children, have markedly increased their use of managed care in recent years. It is unknown whether racial/ethnic disparities in health care use or other processes of care exist in managed Medicaid populations. This study of Medicaid-insured children with asthma in 5 managed care organizations aimed to 1) compare parent-reported health status and asthma care processes among black, Latino, and white children and 2) test the hypothesis that racial/ ethnic variations in processes of asthma care exist after adjusting for socioeconomic status and asthma status. Methods. This cross-sectional study collected data via telephone interviews with parents and computerized records for Medicaid-insured children with asthma in 5 managed care organizations in California, Washington, and Massachusetts. The American Academy of Pediatrics (AAP) Children's Health Survey for Asthma was used to measure parent-reported asthma status. We used multivariate models to evaluate associations between race/ethnicity and asthma status while controlling for other sociodemographic variables. We evaluated racial/ ethnic variations in selected processes of asthma care while controlling for other demographic variables and asthma status. Results. The response rate was 63%. Of the 1658 children in the respondent group, 38% were black, 19% were Latino, and 31% were white. Black children had worse asthma status than white children on the basis of the AAP asthma physical and emotional health scores, symptom-days, and school days missed in the past 2 weeks. Latino children had equivalent AAP scores but missed more school days than white children. On the basis of the AAP asthma physical health score, the black-white disparity persisted after adjusting for other sociodemographic variables. After adjusting for sociodemographic variables and asthma status, black and Latino children were less likely to be using inhaled antiinflammatory medication than white children (relative risk for blacks: 0.69; relative risk for Latinos: 0.58). They were more likely to have home nebulizers. Other processes of asthma care, including ratings of providers and asthma care, use of written management plans, use of preventive visits and specialists, and having no pets or smokers at home, were equal or better for minority children compared with white children. Conclusions. Black and Latino children had worse asthma status and less use of preventive asthma medications than white children within the same managed Medicaid populations. Most other processes of asthma care seemed to be equal or better for minorities in the populations that we studied. Increasing the use of preventive medications is a natural focus for reducing racial disparities in asthma.	Harvard Pilgrim Hlth Care, Dept Ambulatory Care & Prevent, Boston, MA 02215 USA; Harvard Univ, Sch Med, Boston, MA 02215 USA; Grp Hlth Cooperat Puget Sound, Ctr Hlth Studies, Seattle, WA 98101 USA; Univ Washington, Seattle, WA 98195 USA; Kaiser Permanente, Dept Pediat Vallejo, Oakland, CA USA; Kaiser Permanente, Div Res Oakland, Oakland, CA USA	Lieu, TA (reprint author), Harvard Pilgrim Hlth Care, Dept Ambulatory Care & Prevent, 126 Brookline Ave,Ste 200, Boston, MA 02215 USA.				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J	Lewkowich, IP; Herman, NS; Schleifer, KW; Dance, MP; Chen, BL; Dienger, KM; Sproles, AA; Shah, JS; Kohl, J; Belkaid, Y; Wills-Karp, M				Lewkowich, IP; Herman, NS; Schleifer, KW; Dance, MP; Chen, BL; Dienger, KM; Sproles, AA; Shah, JS; Kohl, J; Belkaid, Y; Wills-Karp, M			CD4(+) CD25(+) T cells protect against experimentally induced asthma and alter pulmonary dendritic cell phenotype and function	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article							INDUCED AIRWAY HYPERRESPONSIVENESS; TRYPTOPHAN CATABOLISM; HYGIENE HYPOTHESIS; IMMUNE-RESPONSES; ALLERGIC DISEASE; REGULATORY CELLS; CUTTING EDGE; ANTIGEN; SUPPRESSION; INDUCTION	The role of natural CD4(+)CD25(+) regulatory T ( T reg) cells in the control of allergic asthma remains poorly understood. We explore the impact of T reg cell depletion on the allergic response in mice susceptible (A/J) or comparatively resistant (C3H) to the development of allergen-induced airway hyperresponsiveness ( AHR). In C3H mice, anti-CD25-mediated T reg cell depletion before house dust mite treatment increased several features of the allergic diathesis ( AHR, eosinophilia, and IgE), which was concomitant with elevated T helper type 2 ( Th2) cytokine production. In similarly T reg cell-depleted A/J mice, we observed a moderate increase in airway eosinophilia but no effects on AHR, IgE levels, or Th2 cytokine synthesis. As our experiments suggested that T reg cell depletion in C3H mice before sensitization was sufficient to enhance the allergic phenotype, we characterized dendritic cells ( DCs) in T reg cell-depleted C3H mice. T reg cell-depleted mice had increased numbers of pulmonary myeloid DCs with elevated expression of major histocompatibility complex class II, CD80, and CD86. Moreover, DCs from T reg cell-depleted mice demonstrated an increased capacity to stimulate T cell proliferation and Th2 cytokine production, which was concomitant with reduced IL-12 expression. These data suggest that resistance to allergen-driven AHR is mediated in part by CD4(+)CD25(+) T reg cell suppression of DC activation and that the absence of this regulatory pathway contributes to susceptibility.	Childrens Hosp, Med Ctr, Div Immunobiol, Cincinnati, OH 45229 USA; Childrens Hosp, Med Ctr, Div Mol Immunol, Cincinnati, OH 45229 USA	Wills-Karp, M (reprint author), Childrens Hosp, Med Ctr, Div Immunobiol, Cincinnati, OH 45229 USA.	wildc7@cchmc.org	Koehl, Joerg/C-8531-2011	Koehl, Joerg/0000-0003-1121-3178	NHLBI NIH HHS [HL076383, HL67736, P01 HL076383, R01 HL067736, R01 HL067736-06]		Akbari O, 2002, NAT MED, V8, P1024, DOI 10.1038/nm745; Akdis M, 2004, J EXP MED, V199, P1567, DOI 10.1084/jem.20032058; Cederbom L, 2000, EUR J IMMUNOL, V30, P1538, DOI 10.1002/1521-4141(200006)30:6<1538::AID-IMMU1538>3.0.CO;2-X; Coombes JL, 2005, IMMUNOL REV, V204, P184, DOI 10.1111/j.0105-2896.2005.00250.x; de Heer HJ, 2004, J EXP MED, V200, P89, DOI 10.1084/jem.20040035; de Lafaille MAC, 2001, J EXP MED, V194, P1349, DOI 10.1084/jem.194.9.1349; Ewart SL, 2000, AM J RESP CELL MOL, V23, P537; Fallarino F, 2003, NAT IMMUNOL, V4, P1206, DOI 10.1038/ni1003; Finkelman FD, 2005, J IMMUNOL, V174, P4630; Fontenot JD, 2005, IMMUNITY, V22, P329, DOI 10.1016/j.immuni.2005.01.016; Francis JN, 2003, J ALLERGY CLIN IMMUN, V111, P1255, DOI 10.1067/mai.2003.1570; Frasca L, 2002, J IMMUNOL, V168, P1060; Greenwald RJ, 2005, ANNU REV IMMUNOL, V23, P515, DOI 10.1146/annurev.immunol.23.021704.115611; Hadeiba H, 2003, J IMMUNOL, V170, P5502; Haeryfar SMM, 2005, J IMMUNOL, V174, P3344; Jaffar Z, 2004, J IMMUNOL, V172, P3842; Julia V, 2002, IMMUNITY, V16, P271, DOI 10.1016/S1074-7613(02)00276-5; Jutel M, 2003, EUR J IMMUNOL, V33, P1205, DOI 10.1002/eji.200322919; Keane-Myers A, 1998, J IMMUNOL, V161, P919; Ling EM, 2004, LANCET, V363, P608, DOI 10.1016/S0140-6736(04)15592-X; Ma XJ, 1996, J EXP MED, V183, P147, DOI 10.1084/jem.183.1.147; McHugh RS, 2002, J IMMUNOL, V168, P5979; Mellor AL, 2004, NAT REV IMMUNOL, V4, P762, DOI 10.1038/nri1457; Min WP, 2003, J IMMUNOL, V170, P1304; Nakamura K, 2004, J IMMUNOL, V172, P834; Ostroukhova M, 2005, CURR ALLERGY ASTHM R, V5, P35, DOI 10.1007/s11882-005-0052-6; Piccirillo CA, 2004, SEMIN IMMUNOL, V16, P81, DOI 10.1016/j.smim.2003.12.003; Read S, 2000, J EXP MED, V192, P295, DOI 10.1084/jem.192.2.295; Romagnani S, 2004, IMMUNOLOGY, V112, P352, DOI 10.1111/j.1365-2567.2004.01925.x; Sakaguchi S, 2005, NAT IMMUNOL, V6, P345, DOI 10.1038/ni1178; Shimizu J, 1999, J IMMUNOL, V163, P5211; Stock P, 2004, NAT IMMUNOL, V5, P1149, DOI 10.1038/ni1122; Sundstedt A, 2003, J IMMUNOL, V170, P1240; Suto A, 2001, AM J RESP CRIT CARE, V164, P680; Thornton AM, 2004, J IMMUNOL, V172, P6519; Vermaelen K, 2004, CYTOM PART A, V61A, P170, DOI 10.1002/cyto.a.20064; Wan YSY, 2005, P NATL ACAD SCI USA, V102, P5126, DOI 10.1073/pnas.0501701102; Wills-Karp M, 2004, IMMUNOL REV, V202, P175, DOI 10.1111/j.0105-2896.2004.00215.x; Wills-Karp M, 2001, NAT REV IMMUNOL, V1, P69, DOI 10.1038/35095579; Zuany-Amorim C, 2002, NAT MED, V8, P625, DOI 10.1038/nm0602-625	40	255	286	0	9	ROCKEFELLER UNIV PRESS	NEW YORK	1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA	0022-1007			J EXP MED	J. Exp. Med.	DEC 5	2005	202	11					1549	1561		10.1084/jem.20051506		13	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	990OU	WOS:000233753900011	16314437	
J	Janes, H; Sheppard, L; Lumley, T				Janes, H; Sheppard, L; Lumley, T			Case-crossover analyses of air pollution exposure data - Referent selection strategies and their implications for bias	EPIDEMIOLOGY			English	Article							BIDIRECTIONAL CASE-CROSSOVER; PRIMARY CARDIAC-ARREST; DAILY MORTALITY; PARTICULATE MATTER; TIME-SERIES; ASTHMA HOSPITALIZATION; MYOCARDIAL-INFARCTION; RISK; DESIGNS; TAIWAN	The case-crossover design has been widely used to study the association between short-term air pollution exposure and the risk of an acute adverse health event. The design uses cases only; for each individual case, exposure just before the event is compared with exposure at other control (or "referent") times. Time-invariant confounders are controlled by making within-subject comparisons. Even more important in the air pollution setting is that time-varying confounders can also be controlled by design by matching referents to the index time. The referent selection strategy is important for reasons in addition to control of confounding. The case-crossover design makes the implicit assumption that there is no trend in exposure across the referent times. In addition, the statistical method that is used-conditional logistic regression-is unbiased only with certain referent strategies. We review here the case-crossover literature in the air pollution context, focusing on key issues regarding referent selection. We conclude with a set of recommendations for choosing a referent strategy with air pollution exposure data. Specifically, we advocate the time-stratified approach to referent selection because it ensures unbiased conditional logistic regression estimates, avoids bias resulting from time trend in the exposure series, and can be tailored to match on specific time-varying confounders.	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J	Romagnani, S				Romagnani, S			The increased prevalence of allergy and the hygiene hypothesis: missing immune deviation, reduced immune suppression, or both?	IMMUNOLOGY			English	Review						hygiene hypothesis; immune deviation; immune suppression; Th1/Th2 cells; Treg cells	REGULATORY T-CELLS; INDUCED AIRWAY HYPERRESPONSIVENESS; GRASS-POLLEN IMMUNOTHERAPY; TOLL-LIKE RECEPTOR-2; MULTIPLE-SCLEROSIS; IFN-GAMMA; INTERFERON-GAMMA; DENDRITIC CELLS; GENE-TRANSFER; HELPER-CELLS	Allergic atopic disorders, such as rhinitis, asthma, and atopic dermatitis, are the result of a systemic inflammatory reaction triggered by type 2 T helper (Th2) cell-mediated immune responses against 'innocuous' antigens (allergens) of complex genetic and environmental origin. A number of epidemiological studies have suggested that the increase in the prevalence of allergic disorders that has occurred over the past few decades is attributable to a reduced microbial burden during childhood, as a consequence of Westernized lifestyle (the 'hygiene hypothesis'). However, the mechanisms by which the reduced exposure of children to pathogenic and nonpathogenic microbes results in enhanced responses of Th2 cells are still controversial. The initial interpretation proposed a missing immune deviation of allergen-specific responses from a Th2 to a type 1 Th (Th1) profile, as a result of the reduced production of interleukin-12 and interferons by natural immunity cells which are stimulated by bacterial products via their Toll-like receptors. More recently, the role of reduced activity of T regulatory cells has been emphasized. The epidemiological findings and the experimental evidence available so far suggest that both mechanisms may be involved. A better understanding of this question is important not only from a theoretical point of view, but also because of its therapeutic implications.	Univ Florence, Ctr Res Transfer & High Educ MCIDNENT, Florence, Italy	Romagnani, S (reprint author), Viale Morgagni 85, I-50134 Florence, Italy.	s.romagnani@dmi.unifi.it					Abbas AK, 1996, NATURE, V383, P787, DOI 10.1038/383787a0; Agrawal S, 2003, J IMMUNOL, V171, P4984; Alm J. S., 1999, LANCET, V353, P1484; Annunziato F, 2001, J ALLERGY CLIN IMMUN, V108, P815; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; Blaser K, 2004, CLIN EXP ALLERGY, V34, P328, DOI 10.1111/j.1365-2222.2004.01909.x; Bluestone JA, 2003, NAT REV IMMUNOL, V3, P253, DOI 10.1038/nri1032; BOGUNIEWICZ M, 1995, J ALLERGY CLIN IMMUN, V95, P133, DOI 10.1016/S0091-6749(95)70162-1; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Brugnolo F, 2003, J ALLERGY CLIN IMMUN, V111, P380, DOI 10.1067/mai.2003.102; Campbell J. 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J	Dhabhar, FS				Dhabhar, Firdaus S.			Enhancing versus Suppressive Effects of Stress on Immune Function: Implications for Immunoprotection and Immunopathology	NEUROIMMUNOMODULATION			English	Review						Acute stress-induced enhancement; Fight-or-flight stress; Immune cell distribution; Immune function, effects of stress; Immune function, enhancing vs. suppressive effects; Immunoprotection vs. immunopathology; Innate/primary immune responses; Leukocyte trafficking; Adaptive/secondary immune responses	CELL-MEDIATED-IMMUNITY; PERIPHERAL-BLOOD LYMPHOCYTES; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; CORTICOTROPIN-RELEASING HORMONE; ACUTE PSYCHOLOGICAL STRESS; PITUITARY-ADRENAL AXIS; ACUTE-PHASE RESPONSE; INDUCED ENHANCEMENT; GLUCOCORTICOID HORMONES; LEWIS RATS	Stress is known to suppress immune function and increase susceptibility to infections and cancer. Paradoxically, stress is also known to exacerbate asthma, and allergic, autoimmune and inflammatory diseases, although such diseases should be ameliorated by immunosuppression. Moreover, the short-term fight-or-flight stress response is one of nature's fundamental defense mechanisms that enables the cardiovascular and musculoskeletal systems to promote survival, and it is unlikely that this response would suppress immune function at a time when it is most required for survival (e. g. in response to wounding and infection by a predator or aggressor). These observations suggest that stress may suppress immune function under some conditions while enhancing it under others. The effects of stress are likely to be beneficial or harmful depending on the type (immunoprotective, immunoregulatory/inhibitory, or immunopathological) of immune response that is affected. Studies have shown that several critical factors influence the direction (enhancing vs. suppressive) of the effects of stress or stress hormones on immune function: (1) Duration (acute vs. chronic) of stress: Acute or short-term stress experienced at the time of immune activation can enhance innate and adaptive immune responses. Chronic or long-term stress can suppress immunity by decreasing immune cell numbers and function and/or increasing active immunosuppressive mechanisms (e. g. regulatory T cells). Chronic stress can also dysregulate immune function by promoting proinflammatory and type-2 cytokine-driven responses. (2) Effects of stress on leukocyte distribution: Compartments that are enriched with immune cells during acute stress show immunoenhancement, while those that are depleted of leukocytes, show immunosuppression. (3) The differential effects of physiologic versus pharmacologic concentrations of glucocorticoids, and the differential effects of endogenous versus synthetic glucocorticoids: Endogenous hormones in physiological concentrations can have immunoenhancing effects. Endogenous hormones at pharmacologic concentrations, and synthetic hormones, are immunosuppressive. (4) The timing of stressor or stress hormone exposure relative to the time of activation and time course of the immune response: Immunoenhancement is observed when acute stress is experienced at early stages of immune activation, while immunosuppression may be observed at late stages of the immune response. We propose that it is important to study and, if possible, to clinically harness the immunoenhancing effects of the acute stress response, that evolution has finely sculpted as a survival mechanism, just as we study its maladaptive ramifications (chronic stress) that evolution has yet to resolve. In view of the ubiquitous nature of stress and its significant effects on immunoprotection as well as immunopathology, it is important to further elucidate the mechanisms mediating stress-immune interactions and to meaningfully translate findings from bench to bedside. Copyright (C) 2009 S. Karger AG, Basel	[Dhabhar, Firdaus S.] Stanford Univ, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA; [Dhabhar, Firdaus S.] Stanford Univ, Stanford Inst Immun Transplantat & Infect, Stanford, CA 94305 USA	Dhabhar, FS (reprint author), Stanford Univ, Dept Psychiat & Behav Sci, 300 Pasteur Dr,MC 5135, Stanford, CA 94305 USA.	dhabhar@gmail.com			NIH [AI48995, CA107498]; Dana Foundation	I wish to thank current and previous members of my laboratory, particularly, Jean Tillie, Dr. Kavitha Viswanathan, Dr. Alison Saul, Kanika Ghai, and Christine Daugherty, whose work and publications are among those discussed in this chapter. The work described here was supported by grants from the NIH (AI48995 and CA107498) and The Dana Foundation.	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J	Sydbom, A; Blomberg, A; Parnia, S; Stenfors, N; Sandstrom, T; Dahlen, SE				Sydbom, A; Blomberg, A; Parnia, S; Stenfors, N; Sandstrom, T; Dahlen, SE			Health effects of diesel exhaust emissions	EUROPEAN RESPIRATORY JOURNAL			English	Review						air pollution; allergy incidence; animal studies; asthma exacerbation; diesel; human exposure	PARTICULATE AIR-POLLUTION; BRONCHIAL EPITHELIAL-CELLS; SYSTEMIC IGE PRODUCTION; HEART-RATE-VARIABILITY; LUNG-TISSUE RESPONSES; SHORT-TERM EXPOSURE; IN-VITRO; CYTOKINE PRODUCTION; ALLERGEN CHALLENGE; PARTICLE RETENTION	Epidemiological studies have demonstrated an association between different levels of air pollution and various health outcomes including mortality, exacerbation of asthma, chronic bronchitis, respiratory tract infections, ischaemic heart disease and stroke. Of the motor vehicle generated air pollutants, diesel exhaust particles account for a highly significant percentage of the particles emitted in many towns and cities. This review is therefore focused on the health effects of diesel exhaust, and especially the particular matter components. Acute effects of diesel exhaust exposure include irritation of the nose and eyes, lung function changes, respiratory changes, headache, fatigue and nausea. Chronic exposures are associated with cough, sputum production and lung function decrements. In addition to symptoms, exposure studies in healthy humans have documented a number of profound inflammatory changes in the airways, notably, before changes in pulmonary function can be detected. It is likely that such effects may be even more detrimental in asthmatics and other subjects with compromised pulmonary function. There are also observations supporting the hypothesis that diesel exhaust is one important factor contributing to the allergy pandemic. For example, in many experimental systems, diesel exhaust particles can be shown to act as adjuvants to allergen and hence increase the sensitization response. Much of the research on adverse effects of diesel exhaust, both in vivo and in vitro, has however been conducted in animals. Questions remain concerning the relevance of exposure levels and whether findings in such models can be extrapolated into humans. It is therefore imperative to further assess acute and chronic effects of diesel exhaust in mechanistic studies with careful consideration of exposure levels. Whenever possible and ethically justified, studies should be carried out in humans.	Karolinska Inst, Natl Inst Environm Med, Unit Expt Asthma & Allergy Res, SE-17177 Stockholm, Sweden; Univ Hosp, Dept Resp Med & Allergy, Umea, Sweden; So Gen Hosp, Resp Cell & Mol Biol Res Div, Southampton, Hants, England	Dahlen, SE (reprint author), Karolinska Inst, Natl Inst Environm Med, Unit Expt Asthma & Allergy Res, SE-17177 Stockholm, Sweden.		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Resp. J.	APR	2001	17	4					733	746		10.1183/09031936.01.17407330		14	Respiratory System	Respiratory System	438JT	WOS:000169050400026	11401072	
J	Ferguson, GT; Enright, PL; Buist, AS; Higgins, MW				Ferguson, GT; Enright, PL; Buist, AS; Higgins, MW			Office spirometry for lung health assessment in adults - A consensus statement from the National Lung Health Education Program	CHEST			English	Review						COPD; risk assessment; smoking; spirometry	OBSTRUCTIVE PULMONARY-DISEASE; SMOKING CESSATION INTERVENTIONS; AIR-FLOW LIMITATION; FORCED EXPIRATORY VOLUME; CONTROLLED TRIAL; RESPIRATORY SYMPTOMS; RANDOMIZED TRIAL; REFERENCE VALUES; GENERAL-PRACTICE; NICOTINE PATCH	COPD is easily detected in its preclinical phase using spirometry, and successful smoking cessation (a cost-effective intervention) prevents further disease progression, This consensus statement recommends the widespread use of office spirometry by primary-care providers for patients greater than or equal to 45 years old who smoke cigarettes. Discussion of the spirometry results with current smokers should be accompanied by strong advice to quit smoking and referral to local smoking cessation resources. Spirometry also is recommended for patients with respiratory symptoms such as chronic cough, episodic wheezing, and exertional dyspnea in order to detect airways obstruction due to asthma or COPD, Although diagnostic-quality spirometry may be used to detect COPD, we recommend the development, validation, and implementation of a new type of spirometry-office spirometry-for this purpose in the primary-care setting, In order to encourage the widespread use of office spirometers, their specifications differ somewhat from those for diagnostic spirometers, allowing lower instrument cost, smaller size, less effort to perform the test, improved ease of calibration checks, and an improved quality-assurance program.	Botsford Pulm Associates, Framington Hills, MI USA; Oregon Hlth Sci Univ, Portland, OR 97201 USA; Univ Michigan, Ann Arbor, MI 48109 USA	Enright, PL (reprint author), Univ Arizona, Tucson, AZ 85721 USA.						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J	Litonjua, AA; Weiss, ST				Litonjua, Augusto A.; Weiss, Scott T.			Is vitamin D deficiency to blame for the asthma epidemic?	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						asthma; allergy; vitamin D; prevention	REGULATORY T-CELLS; NUTRITION EXAMINATION SURVEY; 3RD NATIONAL-HEALTH; D-RECEPTOR GENE; 1-ALPHA,25-DIHYDROXYVITAMIN D-3; 1,25-DIHYDROXYVITAMIN D-3; HYGIENE HYPOTHESIS; HYPOVITAMINOSIS-D; IGE PRODUCTION; II CELLS	In the 1960s, the prevalence of asthma and allergic diseases began to increase worldwide. Currently, the burden of the disease is more than 300 million people affected. We hypothesize that as populations grow more prosperous, more time is spent indoors, and there is less exposure to sunlight, leading to decreased cutaneous vitamin D production. Coupled with inadequate intake from foods and supplements, this then leads to vitamin D deficiency, particularly in pregnant women, resulting in more asthma and allergy in their offspring. Vitamin D has been linked to immune system and lung development in utero, and our epiderniologic studies show that higher vitamin D intake by pregnant mothers reduces asthma risk by as much as 40% in children 3 to 5 years old. Vitamin D deficiency has been associated with obesity, African American race (particularly in urban, inner-city settings), and recent immigrants to westernized countries, thus reflecting the epiderniologic patterns observed in the asthma epidemic. Providing adequate vitamin D supplementation in pregnancy may lead to significant decreases in asthma incidence in young children.	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Allergy Clin. Immunol.	NOV	2007	120	5					1031	1035		10.1016/j.jaci.2007.08.028		5	Allergy; Immunology	Allergy; Immunology	231TZ	WOS:000250973400008	17919705	
J	Brauer, M; Hoek, G; Smit, HA; de Jongste, JC; Gerritsen, J; Postma, DS; Kerkhof, M; Brunekreef, B				Brauer, M.; Hoek, G.; Smit, H. A.; de Jongste, J. C.; Gerritsen, J.; Postma, D. S.; Kerkhof, M.; Brunekreef, B.			Air pollution and development of asthma, allergy and infections in a birth cohort	EUROPEAN RESPIRATORY JOURNAL			English	Article						air pollution; allergy; asthma; respiratory infections; vehicle emissions	CHRONIC RESPIRATORY SYMPTOMS; 3 EUROPEAN AREAS; TOTAL SERUM IGE; CHILDHOOD ASTHMA; NITROGEN-DIOXIDE; PRESCHOOL-CHILDREN; SCHOOL-CHILDREN; EXPOSURE; HEALTH; ATOPY	Few studies have addressed associations between traffic-related air pollution and respiratory disease in young children. The present authors assessed the development of asthmatic/allergic symptoms and respiratory infections during the first 4 yrs of life in a birth cohort study (n=similar to 4,000). Outdoor concentrations of traffic-related air pollutants (nitrogen dioxide PM2.5, particles with a 50% cut-off aerodynamic diameter of 2.5 mu m and soot) were assigned to birthplace home addresses with a land-use regression model. They were linked by logistic regression to questionnaire data on doctor-diagnosed asthma, bronchitis, influenza and eczema and to self-reported wheeze, dry night-time cough, ear/nose/throat infections and skin rash. Total and specific immunoglobulin (Ig)E to common allergens were measured in a subgroup (n=713). Adjusted odds ratios (95% confidence intervals) per interquartile pollution range were elevated for wheeze (1.2 (1.0-1.4) for soot), doctor-diagnosed asthma (1.3 (1.0-1.7)), ear/nose/throat infections (1.2 (1.0-1.3)) and flu/serious colds (1.2 (1.0-1.4)). No consistent associations were observed for other end-points. Positive associations between air pollution and specific sensitisation to common food allergens (1.6 (1.2-2.2) for soot), but not total IgE, were found in the subgroup with IgE measurements. Traffic-related pollution was associated with respiratory infections and some measures of asthma and allergy during the first 4 yrs of life.	Univ British Columbia, Sch Occupat & Environm Hyg, Vancouver, BC V6T 1Z3, Canada; Univ Utrecht, Inst Risk Assessment Sci, NL-3508 TC Utrecht, Netherlands; Univ Utrecht, Med Ctr, Ctr Hlth Sci & Primary Care, NL-3508 TC Utrecht, Netherlands; RIVM, Ctr Prevent & Hlth Serv Res, Bilthoven, Netherlands; Erasmus Univ, Sophia Childrens Hosp, Erasmus Med Ctr, Dept Paediat,Div Resp Med, NL-3000 DR Rotterdam, Netherlands; Univ Groningen, Dept Paediat Resp Med, NL-9700 AB Groningen, Netherlands; Univ Groningen, Dept Pulmonol, NL-9700 AB Groningen, Netherlands; Univ Groningen, Dept Epidemiol, NL-9700 AB Groningen, Netherlands	Brauer, M (reprint author), Univ British Columbia, Sch Occupat & Environm Hyg, 2206 East Mall, Vancouver, BC V6T 1Z3, Canada.	brauer@interchange.ubc.ca	Kerkhof, Marjan/A-8846-2008; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; brunekreef, bert/0000-0001-9908-0060; Brauer, Michael/0000-0002-9103-9343			Brauer M, 2003, EPIDEMIOLOGY, V14, P228, DOI 10.1097/00001648-200303000-00019; Brauer M, 2002, AM J RESP CRIT CARE, V166, P1092, DOI 10.1164/rccm.200108-007OC; BRAUNFAHRLANDER C, 1992, AM REV RESPIR DIS, V145, P42; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; Brunekreef B, 2003, EUR RESPIR J, V21, P913, DOI 10.1183/09031936.03.00014903; Brussee JE, 2005, J ALLERGY CLIN IMMUN, V115, P946, DOI 10.1016/j.jaci.2005.02.035; Brussee JE, 2005, EUR RESPIR J, V25, P455, DOI 10.1183/09031936.05.00079604; Cyrys J, 2003, J EXPO ANAL ENV EPID, V13, P134, DOI 10.1038/sj.jea.7500262; EDWARDS J, 1994, ARCH ENVIRON HEALTH, V49, P223; English P, 1999, ENVIRON HEALTH PERSP, V107, P761, DOI 10.2307/3434663; Gauderman WJ, 2005, EPIDEMIOLOGY, V16, P737, DOI 10.1097/01.ede.00001813087.51440.75; Gehring U, 2002, EUR RESPIR J, V19, P690, DOI 10.1183/09031936.02.01182001; Heinrich Joachim, 2004, Curr Opin Allergy Clin Immunol, V4, P341, DOI 10.1097/00130832-200410000-00003; Hirsch T, 1999, EUR RESPIR J, V14, P669, DOI 10.1034/j.1399-3003.1999.14c29.x; Hoek G, 2002, ATMOS ENVIRON, V36, P4077, DOI 10.1016/S1352-2310(02)00297-2; Hwang BF, 2005, THORAX, V60, P467, DOI 10.1136/thx.2004.033977; Janssen NAH, 2003, ENVIRON HEALTH PERSP, V111, P1512, DOI 10.1289/ehp.6243; Kim JJ, 2004, AM J RESP CRIT CARE, V170, P520, DOI 10.1164/rccm.200403-2810C; Koopman LP, 2001, PEDIATRICS, V108, P943, DOI 10.1542/peds.108.4.943; Lau Susanne, 2002, Paediatr Respir Rev, V3, P265, DOI 10.1016/S1526-0542(02)00189-6; Lewne M, 2004, SCI TOTAL ENVIRON, V332, P217, DOI 10.1016/j.scitotenv.2004.04.014; Martinez Fernando D, 2002, Paediatr Respir Rev, V3, P193, DOI 10.1016/S1526-0542(02)00188-4; McConnell R, 2002, LANCET, V359, P386, DOI 10.1016/S0140-6736(02)07597-9; McConnell R, 2006, ENVIRON HEALTH PERSP, V114, P766, DOI 10.1289/ehp.8594; Nicolai T, 2003, EUR RESPIR J, V21, P956, DOI 10.1183/09031936.03.00041103; Oosterlee A, 1996, OCCUP ENVIRON MED, V53, P241; Pershagen G, 1995, INT J EPIDEMIOL, V24, P1147, DOI 10.1093/ije/24.6.1147; Shima M, 2003, J EPIDEMIOL, V13, P108; Sinclair D, 2004, J CLIN PATHOL, V57, P956, DOI 10.1136/jcp.2004.017681; Sunyer J, 1996, EUR RESPIR J, V9, P1880, DOI 10.1183/09031936.96.09091880; Trasande L, 2005, J ALLERGY CLIN IMMUN, V115, P689, DOI 10.1016/j.jaci.2005.01.056; Van Roosbroeck S, 2006, SCI TOTAL ENVIRON, V368, P565, DOI 10.1016/j.scitotenv.2006.03.034; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; Venn AJ, 2001, AM J RESP CRIT CARE, V164, P2177, DOI 10.1164/rccm2106126; VONMUTIUS E, 1995, EUR RESPIR J, V8, P723; VONMUTIUS E, 2001, J ALLERGY CLIN IMMUN, V105, P9; Weiland SK, 2004, EUR RESPIR J, V24, P406, DOI 10.1183/09031936.04.00090303; Weiland Stephan K., 1994, Annals of Epidemiology, V4, P243; Wichmann J, 2005, ATMOS ENVIRON, V39, P7384, DOI 10.1016/j.atmosenv.2005.09.015; Wijga A, 2001, CLIN EXP ALLERGY, V31, P576, DOI 10.1046/j.1365-2222.2001.01072.x; WJST M, 1993, BRIT MED J, V307, P596; Zmirou D, 2004, J EPIDEMIOL COMMUN H, V58, P18, DOI 10.1136/jech.58.1.18	42	253	262	9	60	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	Till, SJ; Francis, JN; Nouri-Aria, K; Durham, SR				Till, SJ; Francis, JN; Nouri-Aria, K; Durham, SR			Molecular mechanisms in allergy and clinical immunology	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						immunotherapy; allergy; IgE; IL-10; regulatory T cells	GRASS-POLLEN IMMUNOTHERAPY; REGULATORY T-CELLS; MESSENGER-RNA EXPRESSION; BEE VENOM IMMUNOTHERAPY; ANTIGEN-PRESENTING CELL; MONOPHOSPHORYL-LIPID-A; HUMAN DENDRITIC CELLS; IGG ANTIBODIES; HAY-FEVER; IN-VITRO	Specific allergen injection immunotherapy is highly effective in IgE-mediated diseases, such as allergic rhinitis and venom anaphylaxis. Immunotherapy inhibits both early and late responses to allergen exposure. Immunotherapy is accompanied by increases in allergen-specific IgG, particularly the IgG4 isotype, which blocks not only IgE-dependent histamine release from basophils but also IgE-mediated antigen presentation to T cells. Immunotherapy acts on T cells to modify peripheral and mucosal T(H)2 responses to allergen in favor of T(H)1 responses. Recent studies have identified increased IL-10 production in peripheral blood and mucosal surfaces after immunotherapy. IL-10 has numerous potential antiallergic properties, including suppression of mast cell, eosinophil, and T-cell responses, as well as acting on B cells to favor heavy chain class switching to IgG4. These IL-10-producing cells might be so-called regulatory T cells and appear to be identified by the CD4(+)CD25(+) phenotype. Studies in mice suggest that dendritic cells play a vital role in induction of regulatory T cells. Novel approaches to immunotherapy currently being explored include the use of adjuvants, such as monophosphoryl lipid A or nucleotide immunostimulatory sequences derived from bacteria that potentiate T(H)1 responses. Alternative strategies include the use of allergen-derived peptides; or modified recombinant allergen vaccines that act on T cells while minimizing the IgE-dependent mast cell activation that is dependent on the native allergen conformation.	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, Doverhouse St, London SW3 6LY, England.	stephen.till@imperial.ac.uk					Akbari O, 2001, NAT IMMUNOL, V2, P725, DOI 10.1038/90667; Akbari O, 2003, CURR OPIN IMMUNOL, V15, P627, DOI 10.1016/j.coi.2003.09.012; Akbari O, 2002, NAT MED, V8, P1024, DOI 10.1038/nm745; Akdis CA, 1998, J CLIN INVEST, V102, P98, DOI 10.1172/JCI2250; Akdis CA, 2000, FASEB J, V14, P1666; Akdis CA, 1999, FASEB J, V13, P603; Akdis CA, 1996, J CLIN INVEST, V98, P1676, DOI 10.1172/JCI118963; Bellinghausen I, 1997, EUR J IMMUNOL, V27, P1131, DOI 10.1002/eji.1830270513; Bellinghausen I, 2001, INT ARCH ALLERGY IMM, V126, P97, DOI 10.1159/000049499; Bellinghausen I, 2001, J ALLERGY CLIN IMMUN, V108, P242, DOI 10.1067/mai.2001.117177; 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; 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Allergy Clin. Immunol.	JUN	2004	113	6					1025	1034		10.1016/j.jaci.2004.03.024		10	Allergy; Immunology	Allergy; Immunology	829ZI	WOS:000222091000002	15208578	
J	Park, JH; Gold, DR; Spiegelman, DL; Burge, HA; Milton, DK				Park, JH; Gold, DR; Spiegelman, DL; Burge, HA; Milton, DK			House dust endotoxin and wheeze in the first year of life	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							LUNG-FUNCTION; LIPOPOLYSACCHARIDE LPS; RESPIRATORY ILLNESS; LIMULUS ASSAY; GRAIN DUST; ASTHMA; EXPOSURE; INHALATION; INTERLEUKIN-1; SENSITIZATION	We examined endotoxin exposure and wheezing episodes during the first year of life in a birth cohort of 499 infants with one or both parents having a history of asthma or allergy. We measured endotoxin in settled dust from the baby's bed, bedroom floor, family room, and kitchen floor within the first 3 mo after birth. The primary outcomes were any wheeze (versus no wheeze), and repeated wheeze (versus one or no report of wheeze). We found a significant univariate association of elevated endotoxin (greater than or equal to 100 EU/mg) in family room dust with increased risk of any wheeze (Relative Risk = 1.29, 95% CI = 1.03-1.62). The association was not confounded by cockroach allergen, lower respiratory illness (croup, bronchitis, bronchiolitis, and pneumonia), smoking during pregnancy, tower birth weight, maternal asthma, presence of dog, and race/ethnicity in a multivariate model; the multivariate relative risk (RR = 1.33) was marginally significant (95% CI: 1.00-1.76, p < 0.05). In a multivariate model, controlling for the above covariates, elevated endotoxin in family room dust was significantly associated with increased risk (RR = 1.56, 95% CI = 1.03-2.38) of repeated wheeze. These results suggest that home endotoxin exposure may independently increase risk of any wheeze and repeated wheeze during the first year of life for children with a familial predisposition to asthma or allergy.	Harvard Sch Publ Hlth, Occupat Hlth Program, Dept Environm Hlth, Boston, MA 02115 USA; Harvard Sch Publ Hlth, Dept Epidemiol & Biostat, Boston, MA 02115 USA; Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA; Harvard Univ, Sch Med, Boston, MA USA	Milton, DK (reprint author), Harvard Sch Publ Hlth, Occupat Hlth Program, Dept Environm Hlth, 665 Huntington Ave, Boston, MA 02115 USA.		Milton, Donald/G-3286-2010	Milton, Donald/0000-0002-0550-7834	NIAID NIH HHS [R01 AI/EHS-35786]; NIEHS NIH HHS [2P30ES00002, R01 ES-07036]		Baldini M, 1999, AM J RESP CELL MOL, V20, P976; BAYNE EK, 1986, J EXP MED, V163, P1267, DOI 10.1084/jem.163.5.1267; Busse WW, 1997, CIBA F SYMP, V206, P208; CLAPP WD, 1994, AM J RESP CRIT CARE, V150, P611; DINARELLO CA, 1984, REV INFECT DIS, V6, P51; Dodge R, 1996, J ALLERGY CLIN IMMUN, V98, P48, DOI 10.1016/S0091-6749(96)70225-7; DOUWES J, 1998, RESP HLTH EFFECTS IN, P109; Fahrmeir L., 1994, MULTIVARIATE STAT MO; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; Holt PG, 1997, CIBA F SYMP, V206, P35; HOLT PG, 1995, PEDIATR ALLERGY IMMU, V6, P1, DOI 10.1111/j.1399-3038.1995.tb00250.x; HUNT LW, 1994, AM J RESP CRIT CARE, V149, P1471; Iwasaki Y, 1998, HISTOCHEM CELL BIOL, V109, P339, DOI 10.1007/s004180050234; Jagielo PJ, 1996, CHEST, V110, P263, DOI 10.1378/chest.110.1.263; Keman S, 1998, INT ARCH OCC ENV HEA, V71, P131, DOI 10.1007/s004200050260; Martinez FD, 1999, J ALLERGY CLIN IMMUN, V103, P355, DOI 10.1016/S0091-6749(99)70456-2; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; MARTINEZ FD, 1988, NEW ENGL J MED, V319, P1112, DOI 10.1056/NEJM198810273191702; MICHEL O, 1992, AM REV RESPIR DIS, V146, P352; MICHEL O, 1992, THORAX, V47, P288, DOI 10.1136/thx.47.4.288; 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; MICHIE HR, 1988, NEW ENGL J MED, V318, P1481, DOI 10.1056/NEJM198806093182301; Milton DK, 1997, AM IND HYG ASSOC J, V58, P861; MILTON DK, 1992, ENVIRON RES, V57, P212, DOI 10.1016/S0013-9351(05)80081-7; PETERSON RD, 1964, J ALLERGY, V35, P134, DOI 10.1016/0021-8707(64)90027-9; Rizzo MC, 1997, PEDIATR ALLERGY IMMU, V8, P121; RYLANDER R, 1990, AM J IND MED, V17, P39; SANDSTROM T, 1992, EUR RESPIR J, V5, P992; SIRAGANIAN RP, 1979, J ALLERGY CLIN IMMUN, V64, P526, DOI 10.1016/0091-6749(79)90063-0; TAGER IB, 1993, AM REV RESPIR DIS, V147, P811; WILSON NM, 1994, CLIN EXP ALLERGY, V24, P522, DOI 10.1111/j.1365-2222.1994.tb00949.x; WRIGHT SD, 1990, SCIENCE, V249, P1431, DOI 10.1126/science.1698311; Zimmer S., 1996, Journal of Burn Care and Rehabilitation, V17, P491, DOI 10.1097/00004630-199611000-00004	35	253	260	0	3	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	FEB	2001	163	2					322	328				7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	403PD	WOS:000167050900008	11179100	
J	von Mutius, E; Schwartz, J; Neas, LM; Dockery, D; Weiss, ST				von Mutius, E; Schwartz, J; Neas, LM; Dockery, D; Weiss, ST			Relation of body mass index to asthma and atopy in children: the National Health and Nutrition Examination Study III	THORAX			English	Article						body mass index; obesity; atopy; asthma	OVERWEIGHT; OBESITY; WEIGHT; ASSOCIATION; CHILDHOOD; PREVALENCE; ADULTS; AGE; OLD	Background-An increase in the prevalence of obesity and asthma over recent decades has been reported in affluent societies. Both overweight and obesity have been shown to be inversely related to having been breastfed, which is also a potential protective factor against childhood atopic diseases. The aim of this analysis was to explore the relation of body mass index (BMI) to asthma and atopy in a large representative sample of the United States population. Methods-Children aged 4-17 years were included in the NHANES III survey. Prevalences of atopic diseases and potential confounding factors such as exposure to environmental tobacco smoke, birth weight, breast feeding, and household size were assessed using structured interviews with parents. Height and weight were measured, and BMI was calculated as kg/m(2) and transformed into Z scores. Children underwent skin prick tests for atopy to a battery of food and inhalant allergens. Results-The prevalence of asthma (8.7% v 9.3% v 10.3% v 14.9%, p=0.0001) and atopy (48.6% v 50.5% v 53.0% v 53.2%, p=0.05) rose significantly with increasing quartiles of BMI. After adjustment for confounders, a significant positive association between BMI and asthma remained (adjusted OR 1.77, 95% confidence interval 1.44 to 2.19 between the highest and lowest quartiles of BMI), whereas no independent relation between BMI and atopy was evident. No effect modification by sex or ethnic group was seen. Conclusions-The effects of increased BMI on asthma may be mediated by mechanical properties of the respiratory system associated with obesity or by upregulation of inflammatory mechanisms rather than by allergic eosinophilic inflammation of the airway epithelium.	Univ Munich, Childrens Hosp, D-80337 Munich, Germany; Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA; Harvard Univ, Sch Med, Brigham & Womens Hosp, Channing Lab, Boston, MA USA	von Mutius, E (reprint author), Univ Munich, Childrens Hosp, D-80337 Munich, Germany.		Neas, Lucas/J-9378-2012; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Camargo CA, 1999, ARCH INTERN MED, V159, P2582, DOI 10.1001/archinte.159.21.2582; Camargo CA, 1999, AM J RESP CRIT CARE, V159, pA150; Chen Y, 1999, AM J EPIDEMIOL, V150, P255; CHINN S, 1994, PAEDIATR PERINAT EP, V8, P90, DOI 10.1111/j.1365-3016.1994.tb00438.x; Ezzati TM, 1992, VITAL HLTH STAT, V2; Fredberg JJ, 1999, AM J RESP CRIT CARE, V159, P959; Gennuso J, 1998, ARCH PEDIAT ADOL MED, V152, P1197; GOLD DR, 1993, AM REV RESPIR DIS, V148, P10; Huang SL, 1999, CLIN EXP ALLERGY, V29, P323; Jedrychowski W, 1998, PUBLIC HEALTH, V112, P189, DOI 10.1038/sj.ph.1900438; Litonjua A, 1999, AM J RESP CRIT CARE, V159, pA131; Luder E, 1998, J PEDIATR-US, V132, P699, DOI 10.1016/S0022-3476(98)70363-4; NEGRI E, 1988, J EPIDEMIOL COMMUN H, V42, P24, DOI 10.1136/jech.42.1.24; Oddy WH, 1999, BRIT MED J, V319, P815; POSKITT EME, 1978, BRIT MED J, V1, P603; SAARINEN UM, 1995, LANCET, V346, P1065, DOI 10.1016/S0140-6736(95)91742-X; Shaheen SO, 1999, THORAX, V54, P396; Visser M, 1999, JAMA-J AM MED ASSOC, V282, P2131, DOI 10.1001/jama.282.22.2131; von Kries R, 1999, BRIT MED J, V319, P147; Von Mutius E, 1999, LUNG BIOL HEALTH DIS, V126, P1; WILKINSON PW, 1977, LANCET, V1, P350; Woolcock AJ, 1997, CIBA F SYMP, V206, P122	22	252	263	1	10	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	NOV	2001	56	11					835	838		10.1136/thorax.56.11.835		4	Respiratory System	Respiratory System	486ZZ	WOS:000171850400005	11641506	
J	Dishy, V; Sofowora, GG; Xie, HG; Kim, RB; Byrne, DW; Stein, CM; Wood, AJJ				Dishy, V; Sofowora, GG; Xie, HG; Kim, RB; Byrne, DW; Stein, CM; Wood, AJJ			The effect of common polymorphisms of the beta(2)-adrenergic receptor on agonist-mediated vascular desensitization	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							BETA-2-ADRENERGIC RECEPTOR; ADULT-POPULATION; BLOOD-PRESSURE; HYPERTENSION; VASODILATION; ASTHMA; INDIVIDUALS; CELLS	Background: With continuous exposure to beta (2)-adrenergic agonists, vascular tissue becomes desensitized to agonist-mediated vasodilatation. We studied the effects of two common polymorphisms of the beta (2)-adrenergic receptor, one at codon 16 and one at codon 27, on agonist-mediated vasodilatation and desensitization in the vascular bed. Methods: We studied 26 healthy subjects who were selected to represent three genotypes: 7 were homozygous for the alleles encoding Arg16 and GIn27, 8 were homozygous for the alleles encoding Gly16 and Gln27, and 11 were homozygous for the alleles encoding Gly16 and Glu27. Vascular responses were assessed by measuring changes in the diameter of a dorsal hand vein. A dose-response curve of the effect of the beta (2)-adrenergic-receptor agonist isoproterenol was constructed (dose range, 4 to 480 ng per minute). Desensitization was then induced by a 2-hour continuous infusion of isoproterenol, and venodilatation was measured 30, 60, 90, and 120 minutes after the start of the infusion. Results: Subjects who were homozygous for Arg16 had almost complete desensitization; venodilatation in response to isoproterenol in this group decreased from a mean (+/-SE) of 44+/-11 percent to 8+/-4 percent (P=0.006). In contrast, subjects who were homozygous for Gly16 did not have significant desensitization, irrespective of the amino acid encoded by codon 27. Subjects who were homozygous for Glu27 had higher maximal venodilatation in response to isoproterenol than those who were homozygous for Gln27 (86+/-13 percent vs. 54+/-8 percent, P=0.03). Conclusions: The Arg16 polymorphism of the beta (2)-adrenergic receptor is associated with enhanced agonist-mediated desensitization in the vasculature, and the Glu27 polymorphism is associated with increased agonist-mediated responsiveness. Therefore, polymorphisms of the beta (2)-adrenergic receptor are potentially important determinants of the vascular response to stress. (N Engl J Med 2001;345:1030-5.) Copyright (C) 2001 Massachusetts Medical Society.	Vanderbilt Univ, Sch Med, Div Clin Pharmacol, Nashville, TN 37232 USA; Vanderbilt Univ, Sch Med, Gen Clin Res Ctr, Nashville, TN 37232 USA	Wood, AJJ (reprint author), Vanderbilt Univ, Sch Med, Div Clin Pharmacol, Rm 550,Med Res Bldg 1, Nashville, TN 37232 USA.		Sofowora, Gbemiga/E-4118-2011		NHLBI NIH HHS [HL-04012, HL-56251]; NIGMS NIH HHS [GM-RR0095]		AELLIG WH, 1981, BRIT J CLIN PHARMACO, V11, P237; Black HR, 1997, ARCH INTERN MED, V157, P2413; BRISTOW MR, 1989, MOL PHARMACOL, V35, P295; BURT VL, 1995, HYPERTENSION, V25, P305; Chong LK, 2000, PHARMACOGENETICS, V10, P153, DOI 10.1097/00008571-200003000-00007; Cockcroft JR, 2000, HYPERTENSION, V36, P371; Dewar JC, 1998, CLIN EXP ALLERGY, V28, P442; Drysdale CM, 2000, P NATL ACAD SCI USA, V97, P10483, DOI 10.1073/pnas.97.19.10483; FELDMAN RD, 1990, J CLIN INVEST, V85, P647, DOI 10.1172/JCI114487; Flier J, 1996, NEW ENGL J MED, V334, P580, DOI 10.1056/NEJM199602293340907; GOLDSTEIN DS, 1983, HYPERTENSION, V5, P86; Gratze G, 1999, HYPERTENSION, V33, P1425; GREEN SA, 1993, J BIOL CHEM, V268, P23116; GREEN SA, 1995, AM J RESP CELL MOL, V13, P25; Hoit BD, 2000, AM HEART J, V139, P537, DOI 10.1067/mhj.2000.101781; Israel E, 2000, AM J RESP CRIT CARE, V162, P75; LANDAU R, 2000, ANESTHESIOLOGY S, V93, pA1053; LANG CC, 1995, NEW ENGL J MED, V333, P155, DOI 10.1056/NEJM199507203330304; NASLUND T, 1990, CLIN PHARMACOL THER, V48, P87; REIHSAUS E, 1993, AM J RESP CELL MOL, V8, P334; Schobel HP, 1996, NEW ENGL J MED, V335, P1480, DOI 10.1056/NEJM199611143352002; STEIN CM, 1995, J CLIN INVEST, V96, P579, DOI 10.1172/JCI118070; Stein CM, 2001, PHARMACOGENETICS, V11, P95, DOI 10.1097/00008571-200103000-00001; STEIN M, 1993, CLIN PHARMACOL THER, V54, P187; Tan S, 1997, LANCET, V350, P995, DOI 10.1016/S0140-6736(97)03211-X; Taylor DR, 2000, THORAX, V55, P762, DOI 10.1136/thorax.55.9.762; VINCENT J, 1992, J CARDIOVASC PHARM, V19, P447, DOI 10.1097/00005344-199203000-00023; Xie HG, 1999, PHARMACOGENETICS, V9, P511	28	252	266	1	5	MASSACHUSETTS MEDICAL SOC/NEJM	WALTHAM	WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA	0028-4793			NEW ENGL J MED	N. Engl. J. Med.	OCT 4	2001	345	14					1030	1035		10.1056/NEJMoa010819		6	Medicine, General & Internal	General & Internal Medicine	478HF	WOS:000171340400004	11586955	
J	Ege, MJ; Bieli, C; Frei, R; van Strien, RT; Riedler, J; Ublagger, E; Schram-Bijkerk, D; Brunekreef, B; van Hage, M; Scheynius, A; Pershagen, G; Benz, MR; Lauener, R; von Mutius, E; Braun-Fahrlander, C				Ege, MJ; Bieli, C; Frei, R; van Strien, RT; Riedler, J; Ublagger, E; Schram-Bijkerk, D; Brunekreef, B; van Hage, M; Scheynius, A; Pershagen, G; Benz, MR; Lauener, R; von Mutius, E; Braun-Fahrlander, C		PARSIFAL Study Team	Prenatal farm exposure is related to the expression of receptors of the innate immunity and to atopic sensitization in school-age children	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; allergy; atopic sensitization; gene expression; Toll-like receptors; CD14; farming; maternal exposure; microbial exposure	TOLL-LIKE RECEPTORS; DAY-CARE ATTENDANCE; HOUSE-DUST; EARLY-LIFE; MATERNAL HISTORY; CHILDHOOD ASTHMA; RISK; PREGNANCY; SMOKING; SCHOOLCHILDREN	Background: There is increasing evidence that environmental exposures determining childhood illnesses operate early in life. Prenatal exposure to a farming environment through the mother might also play an important role. Objective: We sought to investigate the role of maternal exposures to environments rich in microbial compounds for the development of atopic sensitization, asthma, and corresponding alterations in the innate immune system in offspring. Methods: In the children of the cross-sectional Prevention of Allergy Risk Factors for Sensitization in Children Related to Farming and Anthroposophic Life Style study, asthma and atopy were assessed by means of standardized questionnaires (n = 8263) and serum IgE measurements (n = 2086). In a subsample (n = 322) gene expression of Toil-like receptors (TLR2 and TLR4) and CD14 was assessed. Maternal exposures were defined through questionnaire information. Results: Both atopic sensitization (adjusted odds ratio, 0.58; 95% CI, 0.39-0.86) and the gene expression of receptors of innate immunity were strongly determined by maternal exposure to stables during pregnancy, whereas current exposures had much weaker or no effects. A dose-response relation was found between the extent of upregulation of these genes and the number of different farm animal species the mother had encountered in her pregnancy. Each additional farm animal species increased the expression of TLR2, TLR4, and CD14 by a factor of 1.16 (95% CI, 1.07-1.26), 1.12 (95% Cl, 1.04-1.2), and 1.10 (95% Cl, 1.03-1.23), respectively. Conclusion: Maternal exposure to an environment rich in microbial compounds might protect against the development of atopic sensitization and lead to upregulation of receptors of the innate immune system. The underlying mechanisms potentially operating through the intrauterine milieu or epigenetic inheritance await further elucidation. Clinical implications: When assessing risk factors of allergies in an infant's medical history, attention must also be paid to environmental exposures affecting the mother.	Univ Childrens Hosp Munich, Munich, Germany; Univ Basel, Inst Social & Prevent Med, CH-4003 Basel, Switzerland; Univ Zurich, Childrens Hosp, CH-8006 Zurich, Switzerland; Childrens Hosp, Schwarzach, Austria; Childrens Hosp, Salzburg, Austria; Univ Utrecht, Inst Risk Assessment Sci, NL-3508 TC Utrecht, Netherlands; Karolinska Inst, Dept Med, Clin Allergy Res Unit, Stockholm, Sweden; Univ Hosp, Stockholm, Sweden; Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden	Ege, MJ (reprint author), Univ Munich, Dr Von Haunerschen Kinderspital, Lindwurmstr 4, D-80337 Munich, Germany.	markus.ege@med.uni-muenchen.de	Lauener, Roger/O-8612-2016; van Hage, Marianne/A-9678-2017	Lauener, Roger/0000-0002-8412-606X; van Hage, Marianne/0000-0003-3091-1596; Pershagen, Goran/0000-0002-9701-1130; brunekreef, bert/0000-0001-9908-0060; Ege, Markus/0000-0001-6643-3923; von Mutius, Erika/0000-0002-8893-4515			ALFVEN T, 2006, IN PRESS ALLERGY; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; 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; Braun-Fahrlander C, 2004, EUR RESPIR J, V23, P407, DOI 10.1183/09031936.04.00074004; Celedon JC, 2003, AM J RESP CRIT CARE, V167, P1239, DOI 10.1164/rccm.200209-1063OC; Celedon JC, 2002, LANCET, V360, P781, DOI 10.1016/S0140-6736(02)09906-3; Douwes J, 1999, J ALLERGY CLIN IMMUN, V103, P494, DOI 10.1016/S0091-6749(99)70476-8; Eisenbarth SC, 2004, CURR OPIN PEDIATR, V16, P659, DOI 10.1097/01.mop.0000145920.00101.e4; Holloway JA, 2000, LANCET, V356, P1900, DOI 10.1016/S0140-6736(00)03265-7; Holt P, 2004, CHEM IMMUNOL, V84, P102; Illi S, 2001, J ALLERGY CLIN IMMUN, V108, P709, DOI 10.1067/mai.2001.118786; Iwasaki A, 2004, NAT IMMUNOL, V5, P987, DOI 10.1038/ni1112; Kihlstrom A, 2003, ALLERGY, V58, P871, DOI 10.1034/j.1398-9995.2003.00232.x; Lauener RP, 2002, LANCET, V360, P465, DOI 10.1016/S0140-6736(02)09641-1; Li YF, 2005, CHEST, V127, P1232, DOI 10.1378/chest.127.4.1232; McKeever TM, 2002, AM J RESP CRIT CARE, V166, P827, DOI 10.1164/rccm.200202-158OC; Musikacharoen T, 2003, J BIOL CHEM, V278, P9167, DOI 10.1074/jbc.M211829200; Noakes PS, 2003, ALLERGY, V58, P1053, DOI 10.1034/j.1398-9995.2003.00290.x; Piani A, 2000, EUR J IMMUNOL, V30, P3140, DOI 10.1002/1521-4141(200011)30:11<3140::AID-IMMU3140>3.0.CO;2-O; 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; Ronchetti R, 2001, EUR RESPIR J, V17, P881, DOI 10.1183/09031936.01.17508810; Schnare M, 2001, NAT IMMUNOL, V2, P947, DOI 10.1038/ni712; Schonberger HJ, 2005, PEDIATR ALLERGY IMMU, V16, P27, DOI 10.1111/j.1399-3038.2005.00243.x; Schram D, 2005, ALLERGY, V60, P611, DOI 10.1111/j.1398-9995.2005.00748.x; Shaheen SO, 2005, CLIN EXP ALLERGY, V35, P18, DOI 10.1111/j.1365-2222.2005.02151.x; Smits HH, 2005, CURR ALLERGY ASTHM R, V5, P42, DOI 10.1007/s11882-005-0053-5; Stick SM, 1996, LANCET, V348, P1060, DOI 10.1016/S0140-6736(96)04446-7; Takeda K, 2003, ANNU REV IMMUNOL, V21, P335, DOI 10.1146/annurev.immunol.21.120601.141126; TAYLOR A, 2005, MICROBES INFECT, V25, P25; Toelle BG, 2004, BRIT MED J, V328, P386, DOI 10.1136/bmj.328.7436.386; van Strien RT, 2004, J ALLERGY CLIN IMMUN, V113, P860, DOI 10.1016/j.jaci.2004.01.078; Vercelli D, 2004, J ALLERGY CLIN IMMUN, V113, P381, DOI 10.1016/j.jaci.2004.01.752; Warner JO, 2004, ARCH DIS CHILD, V89, P97, DOI 10.1136/adc.2003.013029; Waser M, 2004, CLIN EXP ALLERGY, V34, P389, DOI 10.1111/j.1365-2222.2004.01873.x	36	251	259	5	25	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	2006	117	4					817	823		10.1016/j.jaci.2005.12.1307		7	Allergy; Immunology	Allergy; Immunology	033QB	WOS:000236862800015	16630939	
J	Cox, LS; Linnemann, DL; Nolte, H; Weldon, D; Finegold, I; Nelson, HS				Cox, LS; Linnemann, DL; Nolte, H; Weldon, D; Finegold, I; Nelson, HS			Sublingual immunotherapy: A comprehensive review	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						sublingual-swallow immunotherapy; sublingual-spit immunotherapy; allergen immunotherapy; allergic asthma; allergic rhinitis	RANDOMIZED CONTROLLED-TRIAL; DOUBLE-BLIND PLACEBO; HOUSE-DUST MITES; SEASONAL ALLERGIC RHINOCONJUNCTIVITIS; STANDARDIZED 5-GRASS-POLLEN EXTRACT; GRASS-POLLEN EXTRACT; SWALLOW IMMUNOTHERAPY; SYSTEMIC REACTIONS; RESPIRATORY ALLERGY; RUSH IMMUNOTHERAPY	Sublingual immunotherapy (SLIT) has been used with increasing frequency in Europe and is viewed with increasing interest by allergists in the United States. To address this interest, a Joint Task Force of the American College of Allergy, Asthma and Immunology and the American Academy of Allergy, Asthma and Immunology's Immunotherapy and Allergy Diagnostic Committees reviewed the available literature on SLIT and prepared this report. The task force concluded that despite clear evidence that SLIT is an effective treatment, many questions remained unanswered, including effective dose, treatment schedules, and overall duration of treatment. Until these have been determined, an assessment of the cost/benefit ratio of the treatment cannot be made. SLIT does appear to be associated with few serious side effects, but it has not been administered in high-risk asthmatic patients, nor in the studies reviewed has it been administered as a mixture of non-cross-reacting allergens. Furthermore, there is currently no allergy extract approved for this use in the United States, nor is there a Current Procedural Terminology code for billing purposes. All of these factors should be given careful consideration by anyone contemplating initiating SLIT treatment for their allergic patients.	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Allergy Clin. Immunol.	MAY	2006	117	5					1021	1035		10.1016/j.jaci.2006.02.040		15	Allergy; Immunology	Allergy; Immunology	041EM	WOS:000237436300008	16675328	
J	Janson, C; Anto, J; Burney, P; Chinn, S; de Marco, R; Heinrich, J; Jarvis, D; Kuenzli, N; Leynaert, B; Luczynska, C; Neukirch, F; Svanes, C; Sunyer, J; Wjst, M				Janson, C; Anto, J; Burney, P; Chinn, S; de Marco, R; Heinrich, J; Jarvis, D; Kuenzli, N; Leynaert, B; Luczynska, C; Neukirch, F; Svanes, C; Sunyer, J; Wjst, M		European Community Resp Hlth Surve	The European Community Respiratory Health Survey: what are the main results so far?	EUROPEAN RESPIRATORY JOURNAL			English	Review						asthma; atopy; epidemiology; incidence; prevalence; risk factors	ASTHMA-LIKE SYMPTOMS; VOLATILE ORGANIC-COMPOUNDS; TOTAL SERUM IGE; YOUNG-ADULTS; BRONCHIAL HYPERRESPONSIVENESS; ATOPIC SENSITIZATION; LUNG-FUNCTION; INDIVIDUAL ALLERGENS; OCCUPATIONAL ASTHMA; REPORTED ASTHMA	The European Community Respiratory Heath Survey (ECRHS) was the first study to assess the geographical variation in asthma and allergy in adults using the same instruments and definitions. The database of the ECRHS includes information from similar to 140,000 individuals from 22 countries. The aim of this review is to summarize the results of the ECRHS to date. The ECRHS has shown that there are large geographical differences in the prevalence of asthma, atopy and bronchial responsiveness, with high prevalence rates in English speaking countries and low prevalence rates in the Mediterranean region and Eastern Europe. Analyses of risk factors have highlighted the importance of occupational exposure for asthma in adulthood. The association between sensitization to individual allergens and bronchial responsiveness was strongest for indoor allergens (mite and cat). Analysis of treatment practices has confirmed that the treatment of asthma varies widely between countries and that asthma is often undertreated. In conclusion, the European Community Respiratory Health Survey has shown that the prevalence of asthma varies widely. The fact that the geographical pattern is consistent with the distribution of atopy and bronchial responsiveness supports the conclusion that the geographical variations in the prevalence of asthma are true and most likely due to environmental factors.	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J	Canonica, GW; Bousquet, J; Casale, T; Lockey, RF; Baena-Cagnani, CE; Pawankar, R; Potter, PC; Bousquet, PJ; Cox, LS; Durham, SR; Nelson, HS; Passalacqua, G; Ryan, DP; Brozek, JL; Compalati, E; Dahl, R; Delgado, L; van Wijk, RG; Gower, RG; Ledford, DK; Filho, NR; Valovirta, EJ; Yusuf, OM; Zuberbier, T; Akhanda, W; Almarales, RC; Ansotegui, I; Bonifazi, F; Ceuppens, J; Chivato, T; Dimova, D; Dumitrascu, D; Fontana, L; Katelaris, CH; Kaulsay, R; Kuna, P; Larenas-Linnemann, D; Manoussakis, M; Nekam, K; Nunes, C; O'Hehir, R; Olaguibel, JM; Onder, NB; Park, JW; Priftanji, A; Puy, R; Sarmiento, L; Scadding, G; Schmid-Grendelmeier, P; Seberova, E; Sepiashvili, R; Sole, D; Togias, A; Tomino, C; Toskala, E; Van Beever, H; Vieths, S				Canonica, G. Walter; Bousquet, Jean; Casale, Thomas; Lockey, Richard F.; Baena-Cagnani, Carlos E.; Pawankar, Ruby; Potter, Paul C.; Bousquet, Philippe J.; Cox, Linda S.; Durham, Stephen R.; Nelson, Harold S.; Passalacqua, Giovanni; Ryan, Dermot P.; Brozek, Jan L.; Compalati, Enrico; Dahl, Ronald; Delgado, Luis; van Wijk, Roy Gerth; Gower, Richard G.; Ledford, Dennis K.; Filho, Nelson Rosario; Valovirta, Erkka J.; Yusuf, Osman M.; Zuberbier, Torsten; Akhanda, Wahiduzzaman; Almarales, Raul Castro; Ansotegui, Ignacio; Bonifazi, Floriano; Ceuppens, Jan; Chivato, Tomas; Dimova, Darina; Dumitrascu, Diana; Fontana, Luigi; Katelaris, Constance H.; Kaulsay, Ranbir; Kuna, Piotr; Larenas-Linnemann, Desiree; Manoussakis, Manolis; Nekam, Kristof; Nunes, Carlos; O'Hehir, Robyn; Olaguibel, Jose M.; Onder, Nerin Bahceciler; Park, Jung Won; Priftanji, Alfred; Puy, Robert; Sarmiento, Luis; Scadding, Glenis; Schmid-Grendelmeier, Peter; Seberova, Ester; Sepiashvili, Revaz; Sole, Dirceu; Togias, Alkis; Tomino, Carlo; Toskala, Elina; Van Beever, Hugo; Vieths, Stefan			Sub-lingual Immunotherapy: World Allergy Organization Position Paper 2009	ALLERGY			English	Review							HOUSE-DUST-MITE; GRASS-POLLEN IMMUNOTHERAPY; SUBLINGUAL-SWALLOW IMMUNOTHERAPY; PLACEBO-CONTROLLED TRIAL; RANDOMIZED CONTROLLED-TRIAL; DOUBLE-BLIND PLACEBO; FC-EPSILON-RI; STANDARDIZED 5-GRASS-POLLEN EXTRACT; SYSTEMIC IMMUNOLOGICAL CHANGES; PARIETARIA-JUDAICA EXTRACT		[Canonica, G. 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J	Gauderman, WJ; Avol, E; Lurmann, F; Kuenzli, N; Gilliland, F; Peters, J; McConnell, R				Gauderman, WJ; Avol, E; Lurmann, F; Kuenzli, N; Gilliland, F; Peters, J; McConnell, R			Childhood asthma and exposure to traffic and nitrogen dioxide	EPIDEMIOLOGY			English	Article							SOUTHERN CALIFORNIA CHILDREN; AIR-POLLUTION; BRONCHITIC SYMPTOMS; PRESCHOOL-CHILDREN; RESPIRATORY HEALTH; SCHOOL-CHILDREN; ATOPY; ROAD; PREVALENCE; PARTICLES	Background: Evidence for a causal relationship between traffic-related air pollution and asthma has not been consistent across studies, and comparisons among studies have been difficult because of the use of different indicators of exposure. Methods: We examined the association between traffic-related pollution and childhood asthma in 208 children from 10 southern California communities using multiple indicators of exposure. Study subjects were randomly selected from participants in the Children's Health Study. Outdoor nitrogen dioxide (NO2) was measured in summer and winter outside the home of each child. We also determined residential distance to the nearest freeway, traffic volumes on roadways within 150 meters, and model-based estimates of pollution from nearby roadways. Results: Lifetime history of doctor-diagnosed asthma was associated with outdoor NO2; the odds ratio (OR) was 1.83 (95% confidence interval = 1.04-3.22) per increase of 1 interquartile range (IQR = 5.7 ppb) in exposure. We also observed increased asthma associated with closer residential distance to a freeway (1.89 per IQR; 1.19-3.02) and with model-based estimates of outdoor pollution from a freeway (2.22 per IQR; 1.36-3.63). These 2 indicators of freeway exposure and measured NO2 concentrations were also associated with wheezing and use of asthma medication. Asthma was not associated with traffic volumes on roadways within 150 meters of homes or with model-based estimates of pollution from nonfreeway roads. Conclusions: These results indicate that respiratory health in children is adversely affected by local exposures to outdoor NO2 or other freeway-related pollutants.	Univ So Calif, Dept Prevent Med, Keck Sch Med, Los Angeles, CA 90089 USA; Sonoma Technol Inc, Petaluma, CA USA	Gauderman, WJ (reprint author), Univ So Calif, Dept Prevent Med, Keck Sch Med, 1540 Alcazar St,Suite 220, Los Angeles, CA 90089 USA.	jimg@use.edu	Kunzli, Nino/F-7195-2014	Kunzli, Nino/0000-0001-8360-080X	NIEHS NIH HHS [1P01ES11627, 5P30 ES07048]		Alm S, 1998, J EXPO ANAL ENV EPID, V8, P79; Avol EL, 2001, AM J RESP CRIT CARE, V164, P2067; Bascom R, 1996, AM J RESP CRIT CARE, V153, P477; BATES DV, 1995, ENVIRON HEALTH PERSP, V103, P243, DOI 10.2307/3432380; BENSEN PE, 1989, CALINE4 DISPERSION M; Brauer M, 2003, EPIDEMIOLOGY, V14, P228, DOI 10.1097/00001648-200303000-00019; Brauer M, 2002, AM J RESP CRIT CARE, V166, P1092, DOI 10.1164/rccm.200108-007OC; BURR ML, 1992, CLIN EXP ALLERGY, V22, P509, DOI 10.1111/j.1365-2222.1992.tb00158.x; Clark NM, 1999, ENVIRON HEALTH PERSP, V107, P421; EDWARDS J, 1994, ARCH ENVIRON HEALTH, V49, P223; Ehrlich RI, 1995, INT J EPIDEMIOL, V24, P1138, DOI 10.1093/ije/24.6.1138; English P, 1999, ENVIRON HEALTH PERSP, V107, P761, DOI 10.2307/3434663; Fischer PH, 2000, ATMOS ENVIRON, V34, P3713, DOI 10.1016/S1352-2310(00)00067-4; Gauderman WJ, 2000, AM J RESP CRIT CARE, V162, P1383; Gauderman WJ, 2004, NEW ENGL J MED, V351, P1057, DOI 10.1056/NEJMoa040610; Hirsch T, 1999, EUR RESPIR J, V14, P669, DOI 10.1034/j.1399-3003.1999.14c29.x; 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; Li N, 2002, INHAL TOXICOL, V14, P459, DOI 10.1080/089583701753678571; Linaker CH, 2000, THORAX, V55, P930, DOI 10.1136/thorax.55.11.930; 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; Nicolai T, 1999, Pediatr Pulmonol Suppl, V18, P9; Nicolai T, 2003, EUR RESPIR J, V21, P956, DOI 10.1183/09031936.03.00041103; PALMES ED, 1976, AM IND HYG ASSOC J, V37, P570, DOI 10.1080/0002889768507522; Peters JM, 1999, AM J RESP CRIT CARE, V159, P768; Roorda-Knape MC, 1998, ATMOS ENVIRON, V32, P1921, DOI 10.1016/S1352-2310(97)00496-2; SAMET JM, 1993, AM REV RESPIR DIS, V148, P1258; Samet JM., 1987, CHEST, V91, P74; Seaton A, 2003, THORAX, V58, P1012, DOI 10.1136/thorax.58.12.1012; Smith DH, 1997, AM J RESP CRIT CARE, V156, P787; Trainer M, 2000, ATMOS ENVIRON, V34, P2045, DOI 10.1016/S1352-2310(99)00459-8; 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; WALDRON G, 1995, J PUBLIC HEALTH MED, V17, P85; WJST M, 1993, BRIT MED J, V307, P596; Wu J, 2005, ATMOS ENVIRON, V39, P259, DOI 10.1016/j.atmosenv.2004.09.061; Zmirou D, 2004, J EPIDEMIOL COMMUN H, V58, P18, DOI 10.1136/jech.58.1.18	40	248	257	4	46	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA	1044-3983			EPIDEMIOLOGY	Epidemiology	NOV	2005	16	6					737	743		10.1097/01.ede.00001813087.51440.75		7	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	976CD	WOS:000232709500004	16222162	
J	Hellings, PW; Kasran, A; Liu, ZJ; Vandekerckhove, P; Wuyts, A; Overbergh, L; Mathieu, C; Ceuppens, JL				Hellings, PW; Kasran, A; Liu, ZJ; Vandekerckhove, P; Wuyts, A; Overbergh, L; Mathieu, C; Ceuppens, JL			Interleukin-17 orchestrates the granulocyte influx into airways after allergen inhalation in a mouse model of allergic asthma	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article							TUMOR-NECROSIS-FACTOR; NEUTROPHIL RECRUITMENT; HUMAN KERATINOCYTES; EPITHELIAL-CELLS; TNF-ALPHA; IN-VIVO; T-CELL; CHEMOTACTIC PROTEIN-2; IL-17; EXPRESSION	Interleukin (IL)-17 is produced by activated memory CD4(+) cells and induces cytokines and chemokines that stimulate neutrophil generation and recruitment. Here, we investigated the involvement of IL-17 in the bronchial influx of neutrophils in experimental allergic asthma. Inhalation of nebulized ovalbumin (OVA) by sensitized mice with bronchial eosinophilic inflammation resulting from chronic OVA exposure induced early IL-17 mRNA expression in inflamed lung tissue, concomitant with a prominent bronchial neutrophilic influx. Anti-IL-17 monoclonal antibodies (mAb) injected before allergen inhalation strongly reduced bronchial neutrophilic influx, in a manner equally as potent as the anti-inflammatory dexamethasone. Remarkably, anti-IL-17 mAb significantly enhanced IL-5 levels in both BAL fluid and serum, and aggravated allergen-induced bronchial eosinophilia. In another series of experiments, anti-IL-17 mAb were given repeatedly during the inhalatory challenge phase with OVA of sensitized mice. This treatment regimen abated bronchial neutrophilia in parallel with reduction of bone marrow and blood neutrophilia. In addition, anti-IL-17 mAb treatment elevated eosinophil counts in the bone marrow and bronchial IL-5 production, without alteration of allergen-induced bronchial hyperresponsiveness. In summary, our results demonstrate that IL-17 expression in airways is upregulated upon allergen inhalation, and constitutes the link between allergen-induced T cell activation and neutrophilic influx. Because neutrophils may be important in airway remodeling in chronic severe asthma, targeting IL-17 may hold therapeutic potential in human asthma.	Katholieke Univ Leuven, Fac Med, Univ Hosp, Lab Expt Immunol,Dept Otorhinolaryngol Head & Nec, Louvain, Belgium; Katholieke Univ Leuven, Fac Med, Univ Hosp, Hematol Lab, Louvain, Belgium; Katholieke Univ Leuven, Fac Med, Univ Hosp, Lab Mol Immunol,Rega Inst, Louvain, Belgium; Katholieke Univ Leuven, Fac Med, Univ Hosp, Lab Expt Geneeskunde & Endocrinol,Dept Internal M, Louvain, Belgium	Ceuppens, JL (reprint author), Univ Hosp Gasthuisberg, Expt Immunol Lab, Onderwijs & Navorsing, Herestr 49, B-3000 Louvain, Belgium.						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J. Respir. Cell Mol. Biol.	JAN	2003	28	1					42	50		10.1165/rcmb.4832		9	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	630VU	WOS:000180131500007	12495931	
J	Bowler, RP; Crapo, JD				Bowler, RP; Crapo, JD			Oxidative stress in allergic respiratory diseases	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						antioxidants; asthma; superoxide dismutase; oxidative stress	EXTRACELLULAR-SUPEROXIDE DISMUTASE; EXHALED HYDROGEN-PEROXIDE; OXYGEN RADICAL PRODUCTION; NITRIC-OXIDE SYNTHASE; AIRWAY SMOOTH-MUSCLE; ASTHMATIC-PATIENTS; ATOPIC-DERMATITIS; NITROTYROSINE FORMATION; ANTIOXIDANT STATUS; BREATH CONDENSATE	There is ample evidence that allergic disorders, such as asthma, rhinitis, and atopic dermatitis, are mediated by oxidative stress. Excessive exposure to reactive oxygen and nitrogen species is the hallmark of oxidative stress and leads to damage of proteins, lipids, and DNA. Oxidative stress occurs not only as a result of inflammation but also from environmental exposure to air pollution and cigarette smoke. The specific localization of antioxidant enzymes in the lung and the rapid reaction of nitric oxide with reactive oxygen species, such as superoxide, suggest that antioxidant enzymes might also function as cell-signaling agents or regulators of cell signaling. Therapeutic interventions that decrease exposure to environmental reactive oxygen species or augment endogenous antioxidant defenses might be beneficial as adjunctive therapies for allergic respiratory disorders.	Natl Jewish Med & Res Ctr, Denver, CO 80206 USA	Bowler, RP (reprint author), Natl Jewish Med & Res Ctr, K736A,1400 Jackson St, Denver, CO 80206 USA.				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Allergy Clin. Immunol.	SEP	2002	110	3					349	356		10.1067/mai.2002.126780		8	Allergy; Immunology	Allergy; Immunology	592KM	WOS:000177936900002	12209079	
J	Plantinga, M; Guilliams, M; Vanheerswynghels, M; Deswarte, K; Branco-Madeira, F; Toussaint, W; Vanhoutte, L; Neyt, K; Killeen, N; Malissen, B; Hammad, H; Lambrecht, BN				Plantinga, Maud; Guilliams, Martin; Vanheerswynghels, Manon; Deswarte, Kim; Branco-Madeira, Filipe; Toussaint, Wendy; Vanhoutte, Leen; Neyt, Katrijn; Killeen, Nigel; Malissen, Bernard; Hammad, Hamida; Lambrecht, Bart N.			Conventional and Monocyte-Derived CD11b(+) Dendritic Cells Initiate and Maintain T Helper 2 Cell-Mediated Immunity to House Dust Mite Allergen	IMMUNITY			English	Article							CHEMOKINE RECEPTOR CCR2; AIRWAY INFLAMMATION; TH2 RESPONSES; INHALED ALLERGENS; VIRAL-INFECTION; LYMPH-NODES; BONE-MARROW; URIC-ACID; T-CELLS; MICE	Dendritic cells (DCs) are crucial for mounting allergic airway inflammation, but it is unclear which subset of DCs performs this task. By using CD64 and MAR-1 staining, we reliably separated CD11b(+) monocyte-derived DCs (moDCs) from conventional DCs (cDCs) and studied antigen uptake, migration, and presentation assays of lung and lymph node (LN) DCs in response to inhaled house dust mite (HDM). Mainly CD11b(+) cDCs but not CD103(+) cDCs induced T helper 2 (Th2) cell immunity in HDM-specific T cells in vitro and asthma in vivo. Studies in Flt3l(-/-) mice, lacking all cDCs, revealed that moDCs were also sufficient to induce Th2 cell-mediated immunity but only when high-dose HDM was given. The main function of moDCs was the production of proinflammatory chemokines and allergen presentation in the lung during challenge. Thus, we have identified migratory CD11b(+) cDCs as the principal subset inducing Th2 cell-mediated immunity in the LN, whereas moDCs orchestrate allergic inflammation in the lung.	[Plantinga, Maud; Guilliams, Martin; Vanheerswynghels, Manon; Deswarte, Kim; Branco-Madeira, Filipe; Toussaint, Wendy; Vanhoutte, Leen; Neyt, Katrijn; Hammad, Hamida; Lambrecht, Bart N.] VIB, Dept Mol Biomed Res, Lab Immunoregulat & Mucosal Immunol, B-9050 Ghent, Belgium; [Plantinga, Maud; Deswarte, Kim; Branco-Madeira, Filipe; Toussaint, Wendy; Vanhoutte, Leen; Neyt, Katrijn; Hammad, Hamida; Lambrecht, Bart N.] Univ Ghent, Dept Pulm Med, B-9000 Ghent, Belgium; [Guilliams, Martin; Malissen, Bernard] Univ Aix Marseille 2, Ctr Immunol Marseille Luminy, CNRS, INSERM, F-13288 Marseille, France; [Vanhoutte, Leen] Ghent Univ Hosp, Dept Clin Genet, B-9000 Ghent, Belgium; [Killeen, Nigel] Trianni Inc, Emeryville, CA 94143 USA; [Lambrecht, Bart N.] Erasmus Univ, Med Ctr, Dept Pulm Med, NL-3015 Rotterdam, Netherlands	Lambrecht, BN (reprint author), VIB, Dept Mol Biomed Res, Lab Immunoregulat & Mucosal Immunol, B-9050 Ghent, Belgium.	bart.lambrecht@ugent.be	Hammad, Hamida/J-9391-2015; Lambrecht, Bart/K-2484-2014	Hammad, Hamida/0000-0003-3762-8603; Lambrecht, Bart/0000-0003-4376-6834; Guilliams, Martin/0000-0003-3525-7570; Malissen, Bernard/0000-0003-1340-9342	ERC consolidator grant; University of Gent MRP grant (GROUP-ID consortium); Marie Curie Career Integration Grant (CIG); BELSPO Return Grant; FWO Post-Doc Fellowship; FWO project grant	This work was supported by an ERC consolidator grant to B.N.L., by a University of Gent MRP grant (GROUP-ID consortium) to B.N.L., by a Marie Curie Career Integration Grant (CIG), a BELSPO Return Grant, and FWO Post-Doc Fellowship to M. G., and by a FWO project grant to H.H.	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J	Gibson, PG; Simpson, JL				Gibson, P. G.; Simpson, J. L.			The overlap syndrome of asthma and COPD: what are its features and how important is it?	THORAX			English	Review							AIR-FLOW OBSTRUCTION; PULMONARY-FUNCTION TESTS; LUNG-FUNCTION DECLINE; RISK-FACTORS; FOLLOW-UP; RESPIRATORY SYMPTOMS; BRONCHIAL HYPERRESPONSIVENESS; COMPUTED-TOMOGRAPHY; CIGARETTE-SMOKING; PARENTAL SMOKING	There is a need to re-evaluate the concept of asthma and chronic obstructive pulmonary disease (COPD) as separate conditions, and to consider situations when they may coexist, or when one condition may evolve into the other. Epidemiological studies show that in older people with obstructive airway disease, as many as half or more may have overlapping diagnoses of asthma and COPD (overlap syndrome). These people are typically excluded from current therapy trials, which limit the generalisability of these trials, and this presents a problem for evidence-based guidelines for obstructive airway diseases. Studying overlap syndrome may shed light on the mechanisms of COPD development. Overlap syndrome is recognised by the coexistence of increased variability of airflow in a patient with incompletely reversible airway obstruction. Patients typically have inflammatory features that resemble COPD, with increased airway neutrophilia, as well as features of airway wall remodelling. Overlap syndrome can develop when there is accelerated decline in lung function, or incomplete lung growth, or both. The risk factors for these events are shared, such that increasing age, bronchial hyper-responsiveness, tobacco smoke exposure, asthma and lower respiratory infections/exacerbations are significant risk factors for both incomplete lung growth and accelerated loss of lung function. Studying these events may offer new insights into the mechanisms and treatment of obstructive airway diseases.	[Gibson, P. G.] John Hunter Hosp, Dept Resp & Sleep Med, Hunter Mail Ctr, Newcastle, NSW 2310, Australia; [Gibson, P. G.; Simpson, J. L.] Univ Newcastle, Ctr Asthma & Resp Dis, Newcastle, NSW 2308, Australia	Gibson, PG (reprint author), John Hunter Hosp, Dept Resp & Sleep Med, Hunter Mail Ctr, Level 3 HMRI,Locked Bag 1, Newcastle, NSW 2310, Australia.	peter.gibson@hnehealth.nsw.gov.au			NHMRC Practitioner Fellowship; NHMRC Centre of Respiratory Research Excellence Fellowship	PGG holds an NHMRC Practitioner Fellowship and JLS holds am NHMRC Centre of Respiratory Research Excellence Fellowship.	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J	Kishore, U; Greenhough, TJ; Waters, P; Shrive, AK; Ghai, R; Kamran, MF; Bernal, AL; Reid, KBM; Madan, T; Chakraborty, T				Kishore, U; Greenhough, TJ; Waters, P; Shrive, AK; Ghai, R; Kamran, MF; Bernal, AL; Reid, KBM; Madan, T; Chakraborty, T			Surfactant proteins SP-A and SP-D: Structure, function and receptors	MOLECULAR IMMUNOLOGY			English	Review						surfactant; immunity; lung; allergy; infection; crystal structure	RESPIRATORY SYNCYTIAL VIRUS; GENE-TARGETED MICE; CARBOHYDRATE-RECOGNITION DOMAINS; GRAM-NEGATIVE BACTERIA; HUMAN AMNIOTIC-FLUID; EOSINOPHILIC AIRWAY INFLAMMATION; HEPATOCYTE NUCLEAR FACTOR-3-BETA; MEDIATES ENHANCED PHAGOCYTOSIS; COLONY-STIMULATING FACTOR; MANNAN-BINDING PROTEIN	Surfactant proteins. SP-A and SP-D, are collagen-containing C-type (calcium dependent) lectins called collectins, which contribute significantly to surfactant homeostasis and pulmonary immunity. These highly versatile innate immune molecules are involved in a range of immune functions including viral neutralization. clearance of bacteria, fungi and apoptotic and necrotic cells, down regulation of allergic reaction and resolution of inflammation. Their basic structures include a triple-helical collagen region and a C-terminal homotrimeric lectin or carbohydrate recognition domain (CRD). The trimeric CRDs can recognize carbohydrate or charge patterns on microbes, allergens and dying cells, while the collagen region can interact with receptor molecules present on a variety of immune cells in order to initiate clearance mechanisms. Studies involving gene knock-out mice. murine models of lung hypersensitivity and infection, and functional characterization of cell surface receptors have revealed the diverse roles of SP-A and SP-D in the control of lung inflammation. A recently proposed model based on studies with the calreticulin-CD91 complex as a receptor for SP-A and SP-D has suggested an anti-inflammatory role for SP-A and SP-D in naive lungs which would help minimise the potential damage that continual low level exposure to pathogens, allergens and apoptosis can cause. However, when the lungs are overwhelmed with exogenous insults, SP-A and SP-D can assume pro-inflammatory roles in order to complement pulmonary innate and adaptive immunity. This review is an update on the structural and functional aspects of SP-A and SP-D, with emphasis on their roles in controlling pulmonary infection, allergy and inflammation. We also try to put in perspective the controversial subject of the candidate receptor molecules for SP-A and SP-D. (c) 2005 Elsevier Ltd. All rights reserved.	Univ Oxford, John Radcliffe Hosp, Weatherall Inst Mol Med, Oxford OX3 9DS, England; Univ Giessen, Inst Med Microbiol, D-35392 Giessen, Germany; Univ Keele, Sch Life Sci, Keele ST5 5BG, Staffs, England; Univ Keele, Inst Sci & Technol Med, Keele ST5 5BG, Staffs, England; Univ Nottingham, Sch Med, Sch Biomed Sci, Queens Med Ctr, Nottingham NG7 2UH, England; St Michaels Hosp, Div Obstet & Gynecol, Bristol BS2 8EG, Avon, England; Univ Oxford, MRC, Dept Biochem, Immunochem Unit, Oxford OX1 3QU, England; Inst Genom & Integrat Biol, Council Sci & Ind Res, Delhi 110007, India	Kishore, U (reprint author), Univ Oxford, John Radcliffe Hosp, Weatherall Inst Mol Med, Oxford OX3 9DS, England.	ukishore@hotmail.com	Ganju, Shahji/F-3409-2012; Ghai, Rohit/E-7086-2012	Kishore, Uday/0000-0002-6033-6759	Medical Research Council [G0400743]		Allen MJ, 2001, INFECT IMMUN, V69, P2037, DOI 10.1128/IAI.69.4.2037-2044.2001; Atochina EN, 2003, RESPIR RES, V4, DOI 10.1186/1465-9921-4-15; Bachurski CJ, 2001, AM J PHYSIOL-LUNG C, V280, pL279; 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Immunol.	MAR	2006	43	9					1293	1315		10.1016/j.molimm.2005.08.004		23	Biochemistry & Molecular Biology; Immunology	Biochemistry & Molecular Biology; Immunology	022JT	WOS:000236052500001	16213021	
J	Raghu, G; Freudenberger, TD; Yang, S; Curtis, JR; Spada, C; Hayes, J; Sillery, JK; Pope, CE; Pellegrini, CA				Raghu, G; Freudenberger, TD; Yang, S; Curtis, JR; Spada, C; Hayes, J; Sillery, JK; Pope, CE; Pellegrini, CA			High prevalence of abnormal acid gastro-oesophageal reflux in idiopathic pulmonary fibrosis	EUROPEAN RESPIRATORY JOURNAL			English	Article						aspiration; cryptogenic fibrosing alveolitis; gastro-oesophageal reflux disease; idiopathic pulmonary fibrosis; usual interstitial pneumonia	SURGICAL THERAPY; HIATAL HERNIA; DISEASE; ASPIRATION; FREQUENCY; PRESSURE; ASTHMA	The aim of this prospective study was to determine the prevalence and characteristics of acid gastro-oesophageal reflux (GER) in patients with idiopathic pulmonary fibrosis (IPF). Sixty-five consecutive patients with well-defined IPF were subjected to 24-h pH monitoring and oesophageal manometry. A total of 133 consecutive patients with intractable asthma and symptoms of GER were used as comparisons. The prevalence of abnormal acid GER in IPF patients was 87%, with 76% and 63% demonstrating abnormal distal and proximal oesophageal acid exposures, respectively. Abnormal acid GER was significantly more common in IPF patients than asthma patients. Only 47% of IPF patients experienced classic GER symptoms. Despite treatment with standard doses of proton pump inhibitors (PPIs), 12 out of 19 patients receiving PPIs during the 24-h pH monitoring had abnormal oesophageal acid exposures by pH probe. There was no correlation between IPF severity and acid GER severity. In conclusion, abnormal acid gastro-oesophageal reflux is highly prevalent, but often clinically occult in patients with idiopathic pulmonary fibrosis. Standard doses of proton pump inhibitors may not suppress the acid gastro-oesophageal reflux in this population. Therefore, further studies are needed to determine if acid abnormal gastro-oesophageal reflux represents an important risk factor for idiopathic pulmonary fibrosis development or progression, and if optimal suppression of acid gastro-oesophageal reflux slows the progression of idiopathic pulmonary fibrosis and/or decreases episodic exacerbations of idiopathic pulmonary fibrosis.	Univ Washington, Med Ctr, Dept Med, Div Pulm & Crit Care Med, Seattle, WA 98195 USA; Univ Washington, Dept Surg, Gastrointestinal Motil Clin, Seattle, WA 98195 USA; Singapore Gen Hosp, Dept Resp & Crit Care Med, Singapore 0316, Singapore	Raghu, G (reprint author), Univ Washington, Med Ctr, Dept Med, Div Pulm & Crit Care Med, Campus Box 356522, Seattle, WA 98195 USA.	graghu@u.washington.edu					American Thoracic Society, 2000, AM J RESP CRIT CARE, V161, P646; American Thoracic Society European Respiratory Society. American Thoracic Society/European Respiratory Society international multidisciplinary consensus classification of the idiopathic interstitial pneumonias, 2002, AM J RESP CRIT CARE, V165, P277; Baumgartner KB, 2000, AM J EPIDEMIOL, V152, P307, DOI 10.1093/aje/152.4.307; Baumgartner KB, 1997, AM J RESP CRIT CARE, V155, P242; Bremner RM, 1998, AM J GASTROENTEROL, V93, P183; BRENNAN NJ, 1983, THORAX, V38, P62, DOI 10.1136/thx.38.1.62; CARRINGTON CB, 1978, NEW ENGL J MED, V298, P801, DOI 10.1056/NEJM197804132981501; COULTAS DB, 1994, AM J RESP CRIT CARE, V150, P967; DANGELO E, 1974, J APPL PHYSIOL, V37, P311; DAVIS MV, 1972, NEW YORK STATE J MED, V72, P935; DOBHAN R, 1993, AM J GASTROENTEROL, V88, P25; DUCOLONE A, 1987, AM REV RESPIR DIS, V135, P327; ElSerag HB, 1997, GASTROENTEROLOGY, V113, P755, DOI 10.1016/S0016-5085(97)70168-9; Harding SM, 2000, AM J RESP CRIT CARE, V162, P34; IRWIN RS, 1990, AM REV RESPIR DIS, V141, P640; LAM HGT, 1994, DIGEST DIS SCI, V39, P402, DOI 10.1007/BF02090215; Matsuse T, 1996, CHEST, V110, P1289, DOI 10.1378/chest.110.5.1289; MAYS EE, 1976, CHEST, V69, P512, DOI 10.1378/chest.69.4.512; MITSUHASHI T, 1985, EXP MOL PATHOL, V42, P261, DOI 10.1016/0014-4800(85)90032-2; PEARSON JEG, 1971, THORAX, V26, P300, DOI 10.1136/thx.26.3.300; PELLEGRINI CA, 1979, SURGERY, V86, P110; PERRINFAYOLLE M, 1990, CLIN REV ALLERG, V8, P457; POPE CE, 1994, NEW ENGL J MED, V331, P656, DOI 10.1056/NEJM199409083311007; POPPER H, 1986, VIRCHOWS ARCH A, V409, P105, DOI 10.1007/BF00705410; RAIHA I, 1992, AGE AGEING, V21, P250, DOI 10.1093/ageing/21.4.250; ROUSSOS CS, 1977, AM REV RESPIR DIS, V116, P457; SONTAG SJ, 1990, GASTROENTEROLOGY, V99, P613; TEABEAUT JR, 1952, AM J PATHOL, V28, P51; Tobin RW, 1998, AM J RESP CRIT CARE, V158, P1804; WIENER GJ, 1989, AM J GASTROENTEROL, V84, P1503	30	245	258	2	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. Resp. J.	JAN	2006	27	1					136	142		10.1183/09031936.06.00037005		7	Respiratory System	Respiratory System	002TT	WOS:000234635100021	16387946	
J	Fisk, WJ; Lei-Gomez, Q; Mendell, MJ				Fisk, W. J.; Lei-Gomez, Q.; Mendell, M. J.			Meta-analyses of the associations of respiratory health effects with dampness and mold in homes	INDOOR AIR			English	Article							PRIMARY-SCHOOL CHILDREN; ADULT-ONSET ASTHMA; INDOOR ENVIRONMENT; BUILDING DAMPNESS; RISK-FACTORS; PRESCHOOL-CHILDREN; CHILDHOOD ASTHMA; PARENTAL ATOPY; SYMPTOMS; EXPOSURES	The Institute of Medicine (TOM) of the National Academy of Sciences recently completed a critical review of the scientific literature pertaining to the association of indoor dampness and mold contamination with adverse health effects. In this paper, we report the results of quantitative meta-analyses of the studies reviewed in the TOM report plus other related studies. We developed point estimates and confidence intervals (CIs) of odds ratios (ORs) that summarize the association of several respiratory and asthma-related health outcomes with the presence of dampness and mold in homes. The ORs and CIs from the original studies were transformed to the log scale and random effect models were applied to the log ORs and their variance. Models accounted for the correlation between multiple results within the studies analyzed. Central estimates of ORs for the health outcomes ranged from 1.34 to 1.75. CIs (95%) excluded unity in nine of 10 instances, and in most cases the lower bound of the CI exceeded 1.2. Based on the results of the meta-analyses, building dampness and mold are associated with approximately 30-50% increases in a variety of respiratory and asthma-related health outcomes.	Lawrence Berkeley Natl Lab, Environm Energy Technol Div, Indoor Environm Dept, Berkeley, CA 94720 USA	Fisk, WJ (reprint author), Lawrence Berkeley Natl Lab, Environm Energy Technol Div, Indoor Environm Dept, 1 Cyclotron Rd 90R3058, Berkeley, CA 94720 USA.	wjfisk@lbl.gov	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			ANDRAE S, 1988, ARCH DIS CHILD, V63, P473; Bornehag CG, 2005, INDOOR AIR, V15, P48, DOI 10.1111/j.1600-0668.2005.00306.x; BRUNEKREEF B, 1992, SCI TOTAL ENVIRON, V127, P79, DOI 10.1016/0048-9697(92)90471-4; BRUNEKREEF B, 1989, AM REV RESPIR DIS, V140, P1363; CUIJPERS CEJ, 1995, ENVIRON RES, V68, P11, DOI 10.1006/enrs.1995.1003; Dales RE, 1999, ENVIRON HEALTH PERSP, V107, P481; DEKKER C, 1991, CHEST, V100, P922, DOI 10.1378/chest.100.4.922; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; Egger M, 1998, BRIT MED J, V316, P140; Emenius G, 2004, ACTA PAEDIATR, V93, P899, DOI 10.1080/08035250410025582; Engvall K, 2001, INT ARCH OCC ENV HEA, V74, P270, DOI 10.1007/s004200000218; Gent J., 2002, ENV HLTH PERSPECT, V110, P781; Gunnbjornsdottir MI, 2006, THORAX, V61, P221, DOI 10.1136/thx.2005.057430; Gunnbjornsdottir MI, 2003, RESP MED, V97, P302, DOI 10.1053/rmed.2002.1389; Haverinen U, 2001, INDOOR AIR, V11, P192, DOI 10.1034/j.1600-0668.2001.011003192.x; Institute of Medicine [IOM], 2004, DAMP IND SPAC HLTH I; Jaakkola JJK, 2005, ENVIRON HEALTH PERSP, V113, P357, DOI 10.1289/ehp.7242; JAAKKOLA JJK, 1993, J EXPO ANAL ENV EPID, V3, P129; Jaakkola MS, 2002, ENVIRON HEALTH PERSP, V110, P543; Jedrychowski W, 1998, Int J Occup Med Environ Health, V11, P19; Koskinen OM, 1999, EUR RESPIR J, V14, P1363, DOI 10.1183/09031936.99.14613639; Lee YL, 2003, PEDIATRICS, V112, pE389, DOI 10.1542/peds.112.5.e389; LEVIN H, 2005, LBNL58694; Li CS, 1997, ARCH ENVIRON HEALTH, V52, P72; Maier WC, 1997, ENVIRON HEALTH PERSP, V105, P208, DOI 10.1289/ehp.97105208; Mommers M, 2005, INT J HYG ENVIR HEAL, V208, P373, DOI 10.1016/j.ijheh.2005.04.007; Nafstad P, 1998, AM J RESP CRIT CARE, V157, P410; Norback D, 1999, INT J TUBERC LUNG D, V3, P368; Pirhonen I, 1996, EUR RESPIR J, V9, P2618, DOI 10.1183/09031936.96.09122618; Ronmark E, 2002, RESP MED, V96, P1006, DOI 10.1053/rmed.2002.1391; Simoni M, 2005, OCCUP ENVIRON MED, V62, P616, DOI 10.1136/oem.2004.018291; Skorge TD, 2005, THORAX, V60, P937, DOI 10.1136/thx.2004.025973; Slezak JA, 1998, J ASTHMA, V35, P203, DOI 10.3109/02770909809068208; Stark PC, 2005, ENVIRON HEALTH PERSP, V113, P1405, DOI 10.1289/ehp.7844; Thorn J, 2001, ALLERGY, V56, P287, DOI 10.1034/j.1398-9995.2001.00805.x; Venn AJ, 2003, THORAX, V58, P955, DOI 10.1136/thorax.58.11.955; WAEGEMAEKERS M, 1989, ALLERGY, V44, P192, DOI 10.1111/j.1398-9995.1989.tb02261.x; Williamson IJ, 1997, THORAX, V52, P229; Yang CY, 1997, ENVIRON RES, V75, P49, DOI 10.1006/enrs.1997.3774; Yang CY, 1997, PEDIATR PULM, V24, P73, DOI 10.1002/(SICI)1099-0496(199708)24:2<73::AID-PPUL1>3.3.CO;2-L; Yang CY, 1998, CHEST, V114, P393, DOI 10.1378/chest.114.2.393	41	244	249	7	48	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0905-6947			INDOOR AIR	Indoor Air	AUG	2007	17	4					284	296		10.1111/j.1600-0668.2007.00475.x		13	Construction & Building Technology; Engineering, Environmental; Public, Environmental & Occupational Health	Construction & Building Technology; Engineering; Public, Environmental & Occupational Health	201QX	WOS:000248848800004	17661925	
J	Zureik, M; Neukirch, C; Leynaert, B; Liard, R; Bousquet, L; Neukirch, F				Zureik, M; Neukirch, C; Leynaert, B; Liard, R; Bousquet, L; Neukirch, F		European Community Respiratory Hlt	Sensitisation to airborne moulds and severity of asthma: cross sectional study from European Community respiratory health survey	BRITISH MEDICAL JOURNAL			English	Article							SKIN-TEST REACTIVITY; YOUNG-ADULTS; RISK FACTOR; INDIVIDUAL ALLERGENS; LUNG-FUNCTION; CHILDREN; ASSOCIATION; SYMPTOMS; EXPOSURE; SENSITIZATION	Objective To assess whether the.. severity of asthma is associated with sensitisation to airborne moulds rather than to other seasonal or perennial allergens. Design Multicentre epidemiological survey in 30 centres. Setting European Community respiratory health survey. Participants 1132 adults. aged 20-44 years with current asthma and with skin prick test results. Main outcome measure Severity of asthma according to score based on forced expiratory volume in one second, number of asthma attacks, hospital admissions for breathing problems, and use of corticosteroids in past 12 months. Results The frequency of sensitisation to moulds (Alternaria alternata or Cladosporium herbarum, or both) increased significantly with increasing asthma severity (odds ratio 2.34 (95% confidence interval 1.56 to 3.52) for either for severe v mild asthma). This association existed in all of the study areas (gathered into regions), although there were differences in the frequency of sensitisation. There was no association between asthma severity and sensitisation to pollens or cats. Sensitisation to Dermatophagoides pteronyssinus was also positively associated with severity. In multivariable logistic regressions including sensitisation to moulds, pollens, D pteronyssinus, and cats simultaneously, the odds ratios for sensitisation to moulds were 1.48 (0.97 to 2.26) for moderate v mild asthma and 2.16 (1.37 to 3.35) for severe v mild asthma (P < 0.001 for trend)., Conclusions Sensitisation to moulds is a powerful risk factor for severe asthma in adults. This should be taken into account in primary prevention, management and patients' education.	Univ Paris 07, Natl Inst Hlth & Med Res, INSERM,U408, Unite Epidemiol, F-75870 Paris 18, France; Hop Arnaud Villeneuve, INSERM, U454, Natl Inst Hlth & Med Res, F-34295 Montpellier, France	Zureik, M (reprint author), Univ Paris 07, Natl Inst Hlth & Med Res, INSERM,U408, Unite Epidemiol, BP 416, F-75870 Paris 18, France.		bucca, caterina/C-9886-2009	bucca, caterina/0000-0002-9941-9236	NCRR NIH HHS [2 S07 RR05521-28]		Black PN, 2000, ALLERGY, V55, P501, DOI 10.1034/j.1398-9995.2000.00293.x; Burney P, 1996, EUR RESPIR J, V9, P687; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; Chinn S, 1998, THORAX, V53, P662; Cockcroft DW, 1996, J ALLERGY CLIN IMMUN, V98, P1016, DOI 10.1016/S0091-6749(96)80185-0; Codina R, 1998, J ALLERGY CLIN IMMUN, V102, P318, DOI 10.1016/S0091-6749(98)70102-2; Des Roches Anne, 1996, Journal of Allergy and Clinical Immunology, V98, P522, DOI 10.1016/S0091-6749(96)70085-4; *EUR COMM DIR GEN, 1993, PROT EUR COMM RESP H; Halonen M, 1997, AM J RESP CRIT CARE, V155, P1356; HENDERSON FW, 1995, AM J RESP CRIT CARE, V151, P1786; Hopkinson L., 1997, European Respiratory Journal Supplement, V10, p28S; INGRAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449, DOI 10.1016/S0091-6749(95)70286-5; Janson C, 1997, EUR RESPIR J, V10, P1795, DOI 10.1183/09031936.97.10081795; Janson C, 2001, EUR RESPIR J, V18, P598, DOI 10.1183/09031936.01.00205801; Jarvis D, 1998, EUR RESPIR J, V11, P651; Jarvis D, 1996, LANCET, V347, P426, DOI 10.1016/S0140-6736(96)90009-4; Liard R, 2000, EUR RESPIR J, V16, P615, DOI 10.1034/j.1399-3003.2000.16d08.x; *NAT HEART LUNG BL, 1995, NATL HEART LUNG BLOO; Neukirch C, 1999, J ALLERGY CLIN IMMUN, V103, P709, DOI 10.1016/S0091-6749(99)70247-2; Newson R, 1997, THORAX, V52, P680; OHOLLAREN MT, 1991, NEW ENGL J MED, V324, P359, DOI 10.1056/NEJM199102073240602; Peat JK, 1996, AM J RESP CRIT CARE, V153, P141; POLLART SM, 1988, J ALLERGY CLIN IMMUN, V82, P224, DOI 10.1016/0091-6749(88)91003-2; Roca J, 1998, EUR RESPIR J, V11, P1354, DOI 10.1183/09031936.98.11061354; Ronchetti R, 1997, EUR RESPIR J, V10, P1248, DOI 10.1183/09031936.97.10061248; Rosenstreich DL, 1997, NEW ENGL J MED, V336, P1356, DOI 10.1056/NEJM199705083361904; Ross MA, 2000, ALLERGY, V55, P705, DOI 10.1034/j.1398-9995.2000.00551.x; SCHWARTZ J, 1995, AM J RESP CRIT CARE, V152, P2176; SNELLER MR, 1981, ANN ALLERGY, V46, P30; SPORIK R, 1995, AM J RESP CRIT CARE, V151, P1388; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; Sunyer J, 2000, INT J EPIDEMIOL, V29, P125, DOI 10.1093/ije/29.1.125; TARGONSKI PV, 1995, J ALLERGY CLIN IMMUN, V95, P955, DOI 10.1016/S0091-6749(95)70095-1	33	244	258	1	11	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0959-535X			BRIT MED J	Br. Med. J.	AUG 24	2002	325	7361					411	414		10.1136/bmj.325.7361.411		6	Medicine, General & Internal	General & Internal Medicine	588RY	WOS:000177715500016	12193354	
J	Niederberger, V; Horak, F; Vrtala, S; Spitzauer, S; Krauth, MT; Valent, P; Reisinger, J; Pelzmann, M; Hayek, B; Kronqvist, M; Gafvelin, G; Gronlund, H; Purohit, A; Suck, R; Fiebig, H; Cromwell, O; Pauli, G; van Hage-Hamsten, M; Valenta, R				Niederberger, V; Horak, F; Vrtala, S; Spitzauer, S; Krauth, MT; Valent, P; Reisinger, J; Pelzmann, M; Hayek, B; Kronqvist, M; Gafvelin, G; Gronlund, H; Purohit, A; Suck, R; Fiebig, H; Cromwell, O; Pauli, G; van Hage-Hamsten, M; Valenta, R			Vaccination with genetically engineered allergens prevents progression of allergic disease	PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA			English	Article; Proceedings Paper	Arthur M Sackler Colloquium of the National-Academy-of-Sciences on therapeutic Vaccines	APR 01-03, 2004	Natl Acad Sci, Washington, DC		Natl Acad Sci		BIRCH POLLEN ALLERGEN; B-CELL EPITOPES; HAY-FEVER; V 1; IMMUNOTHERAPY; IGE; GENE; DERIVATIVES; CANDIDATES; RESPONSES	IgE-mediated allergy affects >25% of the population in industrialized countries. Repeated contact with the disease-eliciting allergens induces rises of allergen-specific IgE Abs and progression of the disease to more severe manifestations. Our study uses a type of vaccine that is based on genetically modified allergen derivatives to treat allergic patients. We developed hypoallergenic derivatives of the major birch pollen allergen, Bet v 1, by genetic engineering and vaccinated birch pollen-allergic patients (n = 124) in a double-blind, placebo-controlled study. Active treatment induced protective IgG Abs that inhibited allergen-induced release of inflammatory mediators. We also observed a reduction of cutaneous sensitivity as well as an improvement of symptoms in actively treated patients. Most important, rises of allergen-specific IgE induced by seasonal birch pollen exposure were significantly reduced in vaccinated patients. Vaccination with genetically engineered allergen derivatives is a therapy for allergy that not only ameliorates allergic reactions but also reduces the IgE production underlying the disease.	Univ Vienna, Vienna Gen Hosp, Dept Pathophysiol, A-1090 Vienna, Austria; Univ Vienna, Vienna Gen Hosp, Dept Otorhinolaryngol, A-1090 Vienna, Austria; Univ Vienna, Vienna Gen Hosp, Dept Med & Chem Lab Diagnost, A-1090 Vienna, Austria; Univ Vienna, Vienna Gen Hosp, Dept Hematol & Hemostaseol, A-1090 Vienna, Austria; Karolinska Univ Hosp, Dept Med, Allergy & Clin Immunol Unit, SE-17177 Stockholm, Sweden; Allergopharma Joachim Ganzer KG, D-21465 Reinbek, Germany; Hop Univ Strasbourg, Serv Pneumol, F-67000 Strasbourg, France	Valenta, R (reprint author), Univ Vienna, Vienna Gen Hosp, Dept Pathophysiol, Waehringer Guertel 18, A-1090 Vienna, Austria.	rudolf.valenta@meduniwien.ac.at	van Hage, Marianne/A-9678-2017	van Hage, Marianne/0000-0003-3091-1596; Gafvelin, Guro/0000-0003-1618-4011			Aghayan-Ugurluoglu R, 2000, J ALLERGY CLIN IMMUN, V105, P803, DOI 10.1067/mai.2000.104782; Ball T, 1999, FASEB J, V13, P1277; 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; Bousquet J, 1998, J ALLERGY CLIN IMMUN, V102, P558, DOI 10.1016/S0091-6749(98)70271-4; BREITENEDER H, 1989, EMBO J, V8, P1935; CLINTON PM, 1989, INT ARCH ALLER A IMM, V89, P43; Cromwell O, 2004, METHODS, V32, P300, DOI 10.1016/j.ymeth.2003.08.009; Drachenberg KJ, 2001, ALLERGY, V56, P498, DOI 10.1034/j.1398-9995.2001.056006498.x; Durham SR, 1997, EUR J IMMUNOL, V27, P2899, DOI 10.1002/eji.1830271123; Durham SR, 1999, NEW ENGL J MED, V341, P468, DOI 10.1056/NEJM199908123410702; HENDERSON LL, 1975, J ALLERGY CLIN IMMUN, V55, P10, DOI 10.1016/S0091-6749(75)80003-0; Kay A. B., 1997, ALLERGY ALLERGIC DIS; Kinet JP, 1999, ANNU REV IMMUNOL, V17, P931, DOI 10.1146/annurev.immunol.17.1.931; LICHTENSTEIN LM, 1973, J CLIN INVEST, V52, P472, DOI 10.1172/JCI107204; Mahler V, 2004, CLIN EXP ALLERGY, V34, P115, DOI 10.1111/j.1365-2222.2004.01857.x; MATHES N, 2003, CLIN EXP ALLERGY, V33, P1; Moverare R, 2002, ALLERGY, V57, P423, DOI 10.1034/j.1398-9995.2002.13248.x; Naclerio RM, 1997, J ALLERGY CLIN IMMUN, V100, P505; NORMAN PS, 1978, J ALLERGY CLIN IMMUN, V61, P384, DOI 10.1016/0091-6749(78)90118-5; Pauli G, 2000, CLIN EXP ALLERGY, V30, P1076; Simons FER, 1999, J ALLERGY CLIN IMMUN, V104, P534, DOI 10.1016/S0091-6749(99)70320-9; VALENT P, 1989, P NATL ACAD SCI USA, V86, P5542, DOI 10.1073/pnas.86.14.5542; Valenta R, 2004, ADV IMMUNOL, V82, P105, DOI 10.1016/S0065-2776(04)82003-0; Valenta R, 1999, CLIN EXP ALLERGY, V29, P896; Valenta R, 2002, NAT REV IMMUNOL, V2, P446, DOI 10.1038/nri824; VANHAGEHAMSTEN S, 1999, J ALLERGY CLIN IMMUN, V104, P969; Vrtala S, 1997, J CLIN INVEST, V99, P1673, DOI 10.1172/JCI119330; Vrtala S, 2001, FASEB J, V15, P2045, DOI 10.1096/fj.00-0767fje; Vrtala S, 1996, J ALLERGY CLIN IMMUN, V97, P781, DOI 10.1016/S0091-6749(96)80156-4; Wills-Karp M, 2001, NAT REV IMMUNOL, V1, P69, DOI 10.1038/35095579; Woodfolk JA, 2002, INT ARCH ALLERGY IMM, V129, P277, DOI 10.1159/000067595	31	243	253	2	18	NATL ACAD SCIENCES	WASHINGTON	2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA	0027-8424			P NATL ACAD SCI USA	Proc. Natl. Acad. Sci. U. S. A.	OCT 5	2004	101			2			14677	14682		10.1073/pnas.0404735101		6	Multidisciplinary Sciences	Science & Technology - Other Topics	861NT	WOS:000224424300020	15310844	
J	Wenzel, SE; Barnes, PJ; Bleecker, ER; Bousquet, J; Busse, W; Dahlen, SE; Holgate, ST; Meyers, DA; Rabe, KF; Antczak, A; Baker, J; Horvath, I; Mark, Z; Bernstein, D; Kerwin, E; Schlenker-Herceg, R; Lo, KH; Watt, R; Barnathan, ES; Chanez, P				Wenzel, Sally E.; Barnes, Peter J.; Bleecker, Eugene R.; Bousquet, Jean; Busse, William; Dahlen, Sven-Erik; Holgate, Stephen T.; Meyers, Deborah A.; Rabe, Klaus F.; Antczak, Adam; Baker, James; Horvath, Ildiko; Mark, Zsuzsanna; Bernstein, David; Kerwin, Edward; Schlenker-Herceg, Rozsa; Lo, Kim Hung; Watt, Rosemary; Barnathan, Elliot S.; Chanez, Pascal		T03 Asthma Investigators	A Randomized, Double-blind, Placebo-controlled Study of Tumor Necrosis Factor-alpha Blockade in Severe Persistent Asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						golimumab; asthma; tumor necrosis factor-alpha	AIR-FLOW LIMITATION; SMOOTH-MUSCLE; TNF-ALPHA; CLINICAL CHARACTERISTICS; RHEUMATOID-ARTHRITIS; MONOCLONAL-ANTIBODY; REFRACTORY ASTHMA; BRONCHIAL-ASTHMA; CANCER INCIDENCE; RISK-FACTORS	Rationale: The treatment effect of golimumab, a human monoclonal antibody against tumor necrosis factor (TNF)-alpha, in severe persistent asthma is unknown. Objectives: To assess the safety and efficacy of golimumab in a large population of patients with uncontrolled, severe persistent asthma. Methods: From 2004 to 2006, 309 patients with severe and uncontrolled asthma, despite high-dose inhaled corticosteroids and long-acting beta(2) agonists, were randomized 1:1:1:1 to monthly subcutaneous injections of placebo or golimumab (50, 100, or 200 mg) through Week 52. Coprimary endpoints were the change from baseline through Week 24 in prebronchodilator percent-predicted FEV(1) and the number of severe asthma exacerbations through Week 24. Measurements and Main Results: No significant differences were observed for the change in percent-predicted FEV(1) (least squares mean: placebo, 2.44 [95% confidence interval (CI) -0.574 to 5.461]; combined 100-mg and 200-mg, 2.91 [0.696-5.116]) or severe exacerbations (mean +/- SD: placebo, 0.5 +/- 1.07 vs. combined 100-mg and 200-mg 0.5 +/- 0.97) through week 24. Through Week 24, 2.6% of patients treated with placebo vs. 19.5% of those treated with golimumab discontinued the study agent, and 1.3% and 7.8% discontinued study participation, respectively. An unfavorable risk-benefit profile led to early discontinuation of study-agent administration after the Week-24 database lock. Through Week 76, 20.5% of patients treated with placebo and 30.3% of patients treated with golimumab experienced serious adverse events, with serious infections occurring more frequently in golimumab-treated patients. One death and all eight malignancies occurred in the active groups. Conclusions Overall, treatment with golimumab did not demonstrate a favorable risk-benefit profile in this study population of patients	[Wenzel, Sally E.] Univ Pittsburgh, Med Ctr, Div Pulm Allergy & Crit Care Med, Pittsburgh, PA 15213 USA; [Barnes, Peter J.] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Airway Dis Sect, London, England; [Bleecker, Eugene R.; Meyers, Deborah A.] Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA; [Bousquet, Jean] Hop Arnaud Villeneuve, Clin Malad Resp, Montpellier, France; [Busse, William] Univ Wisconsin, Dept Med, Sch Med & Publ Hlth, Madison, WI USA; [Dahlen, Sven-Erik] Karolinska Inst, Unit Expt Asthma & Allergy Res, Stockholm, Sweden; [Holgate, Stephen T.] Southampton Gen Hosp, AIR Div, Southampton SO9 4XY, Hants, England; [Rabe, Klaus F.] Leiden Univ, Dept Pulmonol, Med Ctr, Leiden, Netherlands; [Antczak, Adam] Prywatny Gabinet Specjalisty, Lodz, Poland; [Baker, James] Allergy Asthma & Dermatol Res Ctr LLC, Oswego, OR USA; [Horvath, Ildiko] Semmelweis Univ, Natl Koranyi TBC & Pulmonol Inst, Budapest, Hungary; [Horvath, Ildiko] Semmelweis Univ, Inst Expt Clin Res, Budapest, Hungary; [Mark, Zsuzsanna] Pulm Med Inst Torokbalint, Torokbalint, Hungary; [Bernstein, David] Bernstein Allergy Grp, Cincinnati, OH USA; [Kerwin, Edward] Clin Res Inst So Oregon PC, Medford, OR USA; [Schlenker-Herceg, Rozsa; Lo, Kim Hung; Watt, Rosemary; Barnathan, Elliot S.] Centocor Res & Dev Inc, Malvern, PA USA; [Chanez, Pascal] Hop Arnaud Villeneuve, Montpellier, France	Wenzel, SE (reprint author), Univ Pittsburgh, Med Ctr, Div Pulm Allergy & Crit Care Med, NW 628 Montefiore,3459 5th Ave, Pittsburgh, PA 15213 USA.	wenzelse@upmc.edu		Horvath, Ildiko/0000-0001-6891-1044	Centocor, Inc.; Centocor BV	Supported by Centocor, Inc. and Centocor BV.	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J. Respir. Crit. Care Med.	APR 1	2009	179	7					549	558		10.1164/rccm.200809-1512OC		10	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	425UU	WOS:000264663700007	19136369	
J	Buchanan, AD; Green, TD; Jones, SM; Scurlock, AM; Christie, L; Althage, KA; Steele, PH; Pons, L; Heim, RM; Lee, LA; Burks, AW				Buchanan, Ariana D.; Green, Todd D.; Jones, Stacie M.; Scurlock, Amy M.; Christie, Lynn; Althage, Karen A.; Steele, Pamela H.; Pons, Laurent; Heim, Rick M.; Lee, Laurie A.; Burks, A. Wesley			Egg oral immunotherapy in nonanaphylactic children with egg allergy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						egg allergy; food allergy; anaphylaxis; allergen immunotherapy; oral immunotherapy	QUALITY-OF-LIFE; FOOD ALLERGY; PEANUT ALLERGY; TOLERANCE; FAMILIES; PARENTS; FUTURE; IMPACT	Background: There is no current active treatment for food allergy. Traditional injection immunotherapy has been proved unsafe, and thus there is a need for other forms of immunotherapy. Objective: The purpose was to study the safety and immunologic effects of egg oral immunotherapy (OIT). The short-term goal was to desensitize subjects to protect against accidental ingestion reactions. The eventual goal was to induce lasting clinical and immunologic tolerance. Methods: Subjects with a history of egg allergy but without a history of anaphylaxis to egg underwent a 24-month egg OIT protocol involving modified rush, build-up, and maintenance phases. Double-blind, placebo-controlled food challenges were performed at study conclusion. Egg-specific IgE and IgG concentrations were followed. Results: Seven subjects completed the protocol. Egg-specific IgG concentrations increased significantly, whereas egg-specific IgE concentrations did not significantly change. Three subjects tolerated known or possible accidental egg ingestions while receiving OIT. During double-blind, placebo-controlled food challenges at study conclusion, all tolerated significantly more egg protein than at study onset and than that found in the typical accidental exposure. Two subjects demonstrated oral tolerance. Conclusion: This study provides proof of concept that OIT can be safely used for patients with egg allergy without a history of anaphylaxis to egg. Egg OIT does not heighten sensitivity to egg and might protect against reaction on accidental ingestion. Whether OIT will induce clinical oral tolerance cannot be concluded from this initial cohort. Clinical implications: Use of allergen-specific OIT to protect subjects with food allergy from reaction on accidental ingestion would represent a significant paradigm change in the treatment of food allergy.	Duke Univ, Med Ctr, Dept Pediat, Durham, NC 27710 USA; Univ Arkansas Med Sci, Dept Pediat, Little Rock, AR 72205 USA; Arkansas Childrens Hosp, Little Rock, AR 72202 USA; Univ Arkansas Med Sci, Dept Microbiol, Little Rock, AR 72205 USA	Burks, AW (reprint author), Duke Univ, Med Ctr, Dept Pediat, Box 2644, Durham, NC 27710 USA.	wesley.burks@duke.edu			NCRR NIH HHS [5M01-RR-000030-45]		Abramson M, 1999, ALLERGY, V54, P1022, DOI 10.1034/j.1398-9995.1999.00102.x; Altschul AS, 2001, J ALLERGY CLIN IMMUN, V108, P468, DOI 10.1067/mai.2001.117794; Bollinger ME, 2006, ANN ALLERG ASTHMA IM, V96, P415; Bousquet J, 1998, J ALLERGY CLIN IMMUN, V102, P558, DOI 10.1016/S0091-6749(98)70271-4; Boyano-Martinez T, 2002, J ALLERGY CLIN IMMUN, V110, P304, DOI 10.1067/mai.2002.126081; BURKS AW, 2003, ALLERGY, V67, P121; Canonica GW, 2003, J ALLERGY CLIN IMMUN, V111, P437, DOI 10.1067/mai.2003.129; Chehade M, 2005, J ALLERGY CLIN IMMUN, V115, P3, DOI 10.1016/j.jaci.2004.11.008; Cohen BL, 2004, J ALLERGY CLIN IMMUN, V114, P1159, DOI 10.1016/j.jaci.2004.08.007; Durham SR, 1999, NEW ENGL J MED, V341, P468, DOI 10.1056/NEJM199908123410702; Eigenmann PA, 2003, ALLERGY, V58, P1217, DOI 10.1046/j.1398-9995.2003.00303.x; FREW AJ, 2003, J ALLERGY CLIN IMMUN, V11, pS712; Gruchalla R. 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Allergy Clin. Immunol.	JAN	2007	119	1					199	205		10.1016/j.jaci.2006.09.016		7	Allergy; Immunology	Allergy; Immunology	127YL	WOS:000243622200028	17208602	
J	Togias, A				Togias, A			Rhinitis and asthma: Evidence for respiratory system integration	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						allergy; nasal function; lung function; rhinitis epidemiology; asthma epidemiology	SKIN-TEST REACTIVITY; NITRIC-OXIDE SYNTHASE; PERENNIAL ALLERGIC RHINITIS; COLONY-STIMULATING FACTOR; MESSENGER-RNA EXPRESSION; INDEPENDENT RISK FACTOR; SERUM IGE LEVELS; BRONCHIAL RESPONSIVENESS; NASAL-MUCOSA; MAST-CELL	The vast majority of patients with asthma have rhinitis, and rhinitis is a major independent risk factor for asthma in cross-sectional and longitudinal studies. The relationships between rhinitis and asthma can be viewed under the concept that the 2 conditions are manifestations of one syndrome, the chronic allergic respiratory syndrome, in 2 parts of the respiratory tract. At the low end of the syndrome's severity spectrum, rhinitis appears to be the sole manifestation, although pathologic abnormalities in the lower airways are already present. At the higher end, rhinitis is worse, and the lower airways disease becomes clinically evident. Once manifested, the 2 conditions track in parallel in terms of severity. This parallel relationship is influenced by many interactions between the nasal and the lower airways: some interactions stem from the fact that the nasal passages play a major homeostatic role by conditioning inhaled air, but perhaps even more important is the bidirectional interaction that results from the systemic inflammation that is produced after local allergic reactions. Successful management of the chronic allergic respiratory syndrome requires an integrated view of the airways and an understanding of their interactions.	Johns Hopkins Univ, Sch Med, Div Clin Immunol, Dept Med, Baltimore, MD USA; Johns Hopkins Univ, Sch Med, Div Resp & Crit Care Med, Dept Med, Baltimore, MD USA	Togias, A (reprint author), Johns Hopkins Asthma & Allergy Ctr, Unit Off 7,5501 Hopkins Bayview Circle, Baltimore, MD 21224 USA.						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Allergy Clin. Immunol.	JUN	2003	111	6					1171	1183		10.1067/mai.2003.1592		13	Allergy; Immunology	Allergy; Immunology	688FZ	WOS:000183424700001	12789212	
J	Jatakanon, A; Lim, S; Barnes, PJ				Jatakanon, A; Lim, S; Barnes, PJ			Changes in sputum eosinophils predict less of asthma control	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							EXHALED NITRIC-OXIDE; AIRWAY INFLAMMATION; RESPIRATORY-TRACT; MILD ASTHMA; EXACERBATIONS; GLUCOCORTICOIDS; PREDNISONE; BUDESONIDE; EXPOSURE; EXAMINE	Exacerbations of asthma are likely to be due to an increase in airway inflammation. We have studied noninvasive markers of airway inflammation in asthma exacerbations induced by reducing the dose of inhaled corticosteroids. Following a 2-wk run-in period, mild exacerbations were induced in subjects with stable asthma controlled with medium- to high-dose inhaled corticosteroids (beclomethasone dipropionate greater than or equal to 800 mu g or equivalent daily) by switching them to budesonide 200 mu g daily given from a dry-powder inhaler (Turbohaler). Fifteen subjects were enrolled and were seen twice weekly for 8 wk after steroid reduction. At each visit, exhaled nitric oxide (NO), and methacholine airway responsiveness were measured and spirometry and sputum induction were performed. Mild exacerbation was defined as: (1) a decrease in morning peak expiratory flow (PEF) of greater than or equal to 20% but < 30% on at least two consecutive days as compared with the mean for the last 7 d of the run-in period; (2) awakening on two consecutive nights because of asthma; or (3) increased use of a short-acting beta(2)-agonist to eight or more puffs daily. Eight subjects did not develop exacerbations during the 8-wk study, whereas seven subjects developed mild exacerbations at Week 4 (n = 1), Week 6 (n = 1), and Week 8 (n = 5). The only significant difference between these two groups at baseline was a higher baseline sputum eosinophil count in subjects with subsequent exacerbations (p < 0.05). The increases in sputum eosinophils and exhaled NO were correlated with decreases in airway function, including decreases in morning PEF and FEV1. However, multiple regression analysis suggested that the change in sputum eosinophils is a potentially useful marker in predicting loss of asthma control reflected by loss of airway function.	Natl Heart & Lung Inst, Dept Thorac Med, Imperial Coll, Sch Med, London SW3 6LY, England	Barnes, PJ (reprint author), Natl Heart & Lung Inst, Dept Thorac Med, Imperial Coll, Sch Med, Dovehouse St, London SW3 6LY, England.						BAIGELMAN W, 1983, AM J MED, V75, P929, DOI 10.1016/0002-9343(83)90871-9; BOULET LP, 1993, J ALLERGY CLIN IMMUN, V91, P883, DOI 10.1016/0091-6749(93)90346-H; British Thoracic Society, 1997, THORAX S1, V52, pS1, DOI DOI 10.1136/THX.52.2008.S1]; CHAI H, 1975, J ALLERGY CLIN IMMUN, V56, P323, DOI 10.1016/0091-6749(75)90107-4; CHOWIENCZYK PJ, 1994, BRIT MED J, V309, P1618; CLAMAN DM, 1994, J ALLERGY CLIN IMMUN, V94, P861, DOI 10.1016/0091-6749(94)90154-6; Djukanovic R, 1996, THORAX, V51, P575, DOI 10.1136/thx.51.6.575; ENRIGHT PL, 1994, AM J RESP CRIT CARE, V149, pS9; FAHY JV, 1995, J ALLERGY CLIN IMMUN, V95, P843, DOI 10.1016/S0091-6749(95)70128-1; GIBSON PG, 1992, CLIN EXP ALLERGY, V22, P525, DOI 10.1111/j.1365-2222.1992.tb00161.x; HAAHTELA T, 1994, NEW ENGL J MED, V331, P700, DOI 10.1056/NEJM199409153311103; Jatakanon A, 1998, EUR RESPIR J, V12, P1084, DOI 10.1183/09031936.98.12051084; Jatakanon A, 1999, THORAX, V54, P108; Keatings VM, 1997, AM J RESP CRIT CARE, V155, P542; 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, 1996, AM J RESP CRIT CARE, V153, P1773; Kharitonov SA, 1996, AM J RESP CRIT CARE, V153, P454; Kharitonov SA, 1996, EUR RESPIR J, V9, P196, DOI 10.1183/09031936.96.09020196; KIKUCHI Y, 1994, NEW ENGL J MED, V330, P1329, DOI 10.1056/NEJM199405123301901; Kips JC, 1998, EUR RESPIR J, V11, P529; LAITINEN LA, 1992, J ALLERGY CLIN IMMUN, V90, P32, DOI 10.1016/S0091-6749(06)80008-4; National Heart Lung and Blood Institute National Asthma Education Program, 1997, NIH PUBL; Pizzichini E, 1997, J ALLERGY CLIN IMMUN, V99, P539, DOI 10.1016/S0091-6749(97)70082-4; Pizzichini MMM, 1996, EUR RESPIR J, V9, P449, DOI 10.1183/09031936.96.09030449; Pizzichini MMM, 1997, AM J RESP CRIT CARE, V155, P1501; SMITH L, 1995, ANN ALLERG ASTHMA IM, V74, P454; Sont JK, 1996, THORAX, V51, P496, DOI 10.1136/thx.51.5.496; SPENCE DPS, 1994, AM J RESP CRIT CARE, V149, P1142; Tamaoki J, 1997, AM J RESP CRIT CARE, V155, P1235; TURNER MO, 1995, THORAX, V50, P1057, DOI 10.1136/thx.50.10.1057; VATHENEN AS, 1991, AM REV RESPIR DIS, V143, P1317	32	240	254	0	2	AMER LUNG ASSOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	JAN	2000	161	1					64	72				9	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	275KW	WOS:000084820200012	10619799	
J	Meiler, F; Zumkehr, J; Klunker, S; Ruckert, B; Akdis, CA; Akdis, M				Meiler, Flurina; Zumkehr, Judith; Klunker, Sven; Rueckert, Beate; Akdis, Cezmi A.; Akdis, Muebeccel			In vivo switch to IL-10-secreting T regulatory cells in high dose allergen exposure	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article							PHASE CUTANEOUS REACTIONS; BEE VENOM; AUTOIMMUNE-DISEASES; IMMUNE-RESPONSES; GENE-EXPRESSION; DENDRITIC CELLS; ATOPIC SUBJECTS; SELF-TOLERANCE; ORAL TOLERANCE; IL-10 RECEPTOR	High dose bee venom exposure in beekeepers by natural bee stings represents a model to understand mechanisms of T cell tolerance to allergens in healthy individuals. Continuous exposure of nonallergic beekeepers to high doses of bee venom antigens induces diminished T cell-related cutaneous late-phase swelling to bee stings in parallel with suppressed allergen-specific T cell proliferation and T helper type 1 (Th1) and Th2 cytokine secretion. After multiple bee stings, venom antigen-specific Th1 and Th2 cells show a switch toward interleukin (IL) 10-secreting type 1 T regulatory (Tr1) cells. T cell regulation continues as long as antigen exposure persists and returns to initial levels within 2 to 3 mo after bee stings. Histamine receptor 2 up-regulated on specific Th2 cells displays a dual effect by directly suppressing allergen-stimulated T cells and increasing IL-10 production. In addition, cytotoxic T lymphocyte-associated antigen 4 and programmed death 1 play roles in allergen-specific T cell suppression. In contrast to its role in mucosal allergen tolerance, transforming growth factor beta does not seem to be an essential player in skin-related allergen tolerance. Thus, rapid switch and expansion of IL-10-producing Tr1 cells and the use of multiple suppressive factors represent essential mechanisms in immune tolerance to a high dose of allergens in nonallergic individuals.	[Meiler, Flurina; Zumkehr, Judith; Klunker, Sven; Rueckert, Beate; Akdis, Cezmi A.; Akdis, Muebeccel] Univ Zurich, Swiss Inst Allergy & Asthma Res, CH-7270 Davos, Switzerland	Akdis, M (reprint author), Univ Zurich, Swiss Inst Allergy & Asthma Res, CH-7270 Davos, Switzerland.	akdism@siaf.unizh.ch			Swiss National Science Foundation [32-112306/1, 32-118226]; Global Allergy and Asthma European Network	This work was funded by the Swiss National Science Foundation (grants 32-112306/1 and 32-118226) and the Global Allergy and Asthma European Network.	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Exp. Med.	NOV 24	2008	205	12					2887	U120		10.1084/jem.20080193		18	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	378BE	WOS:000261295300021	19001136	
J	Abrahamsson, TR; Jakobsson, T; Bottcher, MF; Fredrikson, M; Jenmalm, MC; Bjorksten, B; Oldaeus, G				Abrahamsson, Thomas R.; Jakobsson, Ted; Bottcher, Malin Fageras; Fredrikson, Mats; Jenmalm, Maria C.; Bjorksten, Bengt; Oldaeus, Goran			Probiotics in prevention of IgE-associated eczema: A double-blind, randomized, placebo-controlled trial	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						children; eczema; IgE; Lactobacillus; prevention; probiotics; sensitization; skin prick test	ATOPIC-DERMATITIS; LACTOBACILLUS-REUTERI; IN-VITRO; CHILDREN; INFANTS; DISEASE; COLONIZATION; SUPPLEMENTATION; SENSITIZATION; INFECTIONS	Background: An altered microbial exposure may underlie the increase of allergic diseases in affluent societies. Probiotics may alleviate and even prevent eczema in infants. Objective: To prevent eczema and sensitization in infants with a family history of allergic disease by oral supplementation with the probiotic Lactobacillus reuteri. Methods: Double-blind, randomized, placebo-controlled trial, which comprised 232 families with allergic disease, of whom 188 completed the study. The mothers received L reuteri ATCC 55730(1 x 10(8) colony forming units) daily from gestational week 36 until delivery. Their babies then continued with the same product from birth until 12 months of age and were followed up for another year. Primary outcome was allergic disease, with or without positive skin prick test or circulating IgE to food allergens. Results: The cumulative incidence of eczema was similar, 36% in the treated versus 34% in the placebo group. The L reuteri group had less IgE-associated eczema during the second year, 8% versus 20% (P = .02), however. Skin prick test reactivity was also less common in the treated than in the placebo group, significantly so for infants with mothers with allergies, 14% versus 31% (P = .02). Wheeze and other potentially allergic diseases were not affected. Conclusion: Although a preventive effect of probiotics on infant eczema was not confirmed, the treated infants had less IgE-associated eczema at 2 years of age and therefore possibly run a reduced risk to develop later respiratory allergic disease. Clinical implication: Probiotics may reduce the incidence of IgE-associated eczema in infancy.	Linkoping Univ, Div Pediat, Div Mol & Clin Med, S-58183 Linkoping, Sweden; Linkoping Univ, Dept Mol & Clin Med, Div Environm & Occupat Med, S-58183 Linkoping, Sweden; Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; Cty Hosp Ryhov, Dept Pediat, Jonkoping, Sweden	Abrahamsson, TR (reprint author), Linkoping Univ Hosp, Div Paediat, S-58185 Linkoping, Sweden.	Thomas.Abrahamsson@lio.se	Jenmalm, Maria/C-9679-2009	Jenmalm, Maria/0000-0002-2117-5366			ADLERBERTH I, 1991, ACTA PAEDIATR SCAND, V80, P602, DOI 10.1111/j.1651-2227.1991.tb11917.x; Alfven T, 2006, ALLERGY, V61, P414, DOI 10.1111/j.1398-9995.2005.00939.x; BJORKSTEN B, 1999, CLIN EXP ALLERGY, V29, P1; Bottcher MF, 2003, CLIN EXP ALLERGY, V33, P295, DOI 10.1046/j.1365-2222.2003.01562.x; Brouwer ML, 2006, CLIN EXP ALLERGY, V36, P899, DOI 10.1111/j.1365-2222.2006.02513.x; Eom TH, 2005, KOREAN J PEDIAT, V48, P986; Guarner F, 1998, INT J FOOD MICROBIOL, V39, P237, DOI 10.1016/S0168-1605(97)00136-0; Holt PG, 1997, PEDIATR ALLERGY IMMU, V8, P53, DOI 10.1111/j.1399-3038.1997.tb00145.x; Isolauri E, 2000, CLIN EXP ALLERGY, V30, P1604, DOI 10.1046/j.1365-2222.2000.00943.x; Jacobsen CN, 1999, APPL ENVIRON MICROB, V65, P4949; Kalliomaki M, 2003, LANCET, V361, P1869, DOI 10.1016/S0140-6736(03)13490-3; Kalliomaki M, 2001, J ALLERGY CLIN IMMUN, V107, P129, DOI 10.1067/mai.2001.111237; Kalliomaki M, 2001, LANCET, V357, P1076, DOI 10.1016/S0140-6736(00)04259-8; Liu CA, 2003, J ALLERGY CLIN IMMUN, V112, P899, DOI 10.1067/mai.2003.1812; Ma DL, 2004, INFECT IMMUN, V72, P5308, DOI 10.1128/IAI.72.9.5308-5314.2004; McKeever TM, 2002, J ALLERGY CLIN IMMUN, V109, P43, DOI 10.1067/mai.2002.121016; Novembre E, 2001, ALLERGY, V56, P452, DOI 10.1034/j.1398-9995.2001.056005452.x; Pena JA, 2005, INFECT IMMUN, V73, P912, DOI 10.1128/IAI.73.2.912-920.2005; Rosenfeldt V, 2003, J ALLERGY CLIN IMMUN, V111, P389, DOI 10.1067/mai.2003.389; Sepp E, 1997, ACTA PAEDIATR, V86, P956, DOI 10.1111/j.1651-2227.1997.tb15178.x; SEYMOUR JL, 1987, J AM ACAD DERMATOL, V17, P988, DOI 10.1016/S0190-9622(87)70288-6; Shornikova AV, 1997, PEDIATR INFECT DIS J, V16, P1103, DOI 10.1097/00006454-199712000-00002; Shornikova AV, 1997, J PEDIATR GASTR NUTR, V24, P399, DOI 10.1097/00005176-199704000-00008; SIGURS N, 1994, J ALLERGY CLIN IMMUN, V94, P757, DOI 10.1016/0091-6749(94)90184-8; Smits HH, 2005, J ALLERGY CLIN IMMUN, V115, P1260, DOI 10.1016/j.jaci.2005.03.036; STALDER JF, 1993, DERMATOLOGY, V186, P23; Taylor AL, 2007, J ALLERGY CLIN IMMUN, V119, P184, DOI 10.1016/j.jaci.2006.08.036; Vaarala O, 2003, CLIN EXP ALLERGY, V33, P1634, DOI 10.1111/j.1365-2222.2003.01835.x; Valeur N, 2004, APPL ENVIRON MICROB, V70, P1176, DOI 10.1128/AEM.70.2.1176-1181.2004; Viljanen M, 2005, ALLERGY, V60, P494, DOI 10.1111/j.1398-9995.2004.00514.x; Weizman Z, 2005, PEDIATRICS, V115, P5, DOI 10.1542/peds.2004-1815; Weston S, 2005, ARCH DIS CHILD, V90, P892, DOI 10.1136/adc.2004.060673; WOLF BW, 1995, MICROB ECOL HEALTH D, V8, P41; Wolf BW, 1998, FOOD CHEM TOXICOL, V36, P1085, DOI 10.1016/S0278-6915(98)00090-8; Zeuthen L., 2005, CLIN VACCINE IMMUNOL, V13, P365	35	239	260	4	25	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. 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J	Hayashi, T; Beck, L; Rossetto, C; Gong, X; Takikawa, O; Takabayashi, K; Broide, DH; Carson, DA; Raz, E				Hayashi, T; Beck, L; Rossetto, C; Gong, X; Takikawa, O; Takabayashi, K; Broide, DH; Carson, DA; Raz, E			Inhibition of experimental asthma by indoleamine 2,3-dioxygenase	JOURNAL OF CLINICAL INVESTIGATION			English	Article							T-CELL PROLIFERATION; DENDRITIC CELLS; IMMUNOSTIMULATORY DNA; TRYPTOPHAN CATABOLISM; HYGIENE HYPOTHESIS; IN-VIVO; AIRWAY INFLAMMATION; ALLERGIC DISEASES; EPITHELIAL-CELLS; INTERFERON-GAMMA	Epidemiological evidence points to the inverse relationship between microbial exposure and the prevalence of allergic asthma and autoimmune diseases in Westernized countries. The molecular basis for this observation has not yet been completely delineated. Here we report that the administration of certain toll-like receptor (TLR) ligands, via the activation of innate immunity, induces high levels of indoleamine 2,3-dioxygenase (IDO), the rate-limiting enzyme of tryptophan catabolism in various organs. TLR9 ligand-induced pulmonary IDO activity inhibits Th2-driven experimental asthma. IDO activity expressed by resident lung cells rather than by pulmonary DCs suppressed lung inflammation and airway hyperreactivity. Our results provide a mechanistic insight into the various formulations of the hygiene hypothesis and underscore the notion that activation of innate immunity can inhibit adaptive Th cell responses.	Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA; Hokkaido Univ, Grad Sch Med, Cent Res Inst, Sapporo, Hokkaido, Japan	Raz, E (reprint author), Univ Calif San Diego, Dept Med, 9500 Gilman Dr, La Jolla, CA 92093 USA.	eraz@ucsd.edu			NIAID NIH HHS [AI40682, AI56453, P01 AI040682, U01 AI056453]; NIAMS NIH HHS [AR47360, P30 AR047360]; NIDDK NIH HHS [P01 DK035108, DK35108]		Babcock TA, 2000, CYTOKINE, V12, P588, DOI 10.1006/cyto.1999.0661; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; Barnes PJ, 2001, PULM PHARMACOL THER, V14, P329, DOI 10.1006/pupt.2000.0318; Bodaghi B, 1999, J IMMUNOL, V162, P957; Broide D, 1998, J IMMUNOL, V161, P7054; Broide DH, 2001, J CLIN IMMUNOL, V21, P175, DOI 10.1023/A:1011078930363; Caucheteux SM, 2003, IMMUNITY, V18, P169, DOI 10.1016/S1074-7613(03)00028-1; Cho JY, 2004, AM J RESP CELL MOL, V30, P651, DOI 10.1165/rcmb.2003-0066OC; Datta SK, 2003, J IMMUNOL, V170, P4102; Daubener W, 2001, INFECT IMMUN, V69, P6527, DOI 10.1128/IAI.69.10.6527-6531.2001; de Lafaille MAC, 2002, CURR OPIN IMMUNOL, V14, P771; Eisenbarth SC, 2002, J EXP MED, V196, P1645, DOI 10.1084/jem.20021340; Fallarino F, 2003, NAT IMMUNOL, V4, P1206, DOI 10.1038/ni1003; Fallarino I, 2002, CELL DEATH DIFFER, V9, P1069, DOI 10.1038/sj.cdd.4401073; Frumento G, 2002, J EXP MED, V196, P459, DOI 10.1084/jem.20020121; GODFREY DG, 1978, NATURE, V273, P600, DOI 10.1038/273600a0; Grogan JL, 2002, CURR OPIN IMMUNOL, V14, P366, DOI 10.1016/S0952-7915(02)00340-0; Grohmann U, 2002, NAT IMMUNOL, V3, P1097, DOI 10.1038/ni846; Hansen G, 1999, J CLIN INVEST, V103, P175, DOI 10.1172/JCI5155; Hayashi T, 2001, INFECT IMMUN, V69, P6156, DOI 10.1128/IAI.69.10.6156-6164.2001; HISSONG BD, 1995, CELL IMMUNOL, V160, P264, DOI 10.1016/0008-8749(95)80037-J; Horner AA, 2001, IMMUNOL REV, V179, P102, DOI 10.1034/j.1600-065X.2001.790111.x; Howarth PH, 1998, CLIN EXP ALLERGY, V28, P2; Hwu P, 2000, J IMMUNOL, V164, P3596; Ikeda RK, 2003, AM J RESP CELL MOL, V28, P655, DOI 10.1165/rcmb.4853; Kemp A, 2003, PEDIATR ALLERGY IMMU, V14, P74, DOI 10.1034/j.1399-3038.2003.00017.x; Lloyd CM, 2000, J EXP MED, V191, P265, DOI 10.1084/jem.191.2.265; Mackler AM, 2003, J IMMUNOL, V170, P823; Martinez FD, 1999, LANCET S2, V354, pSII12; Mellor AL, 2003, J IMMUNOL, V171, P1652; Mellor AL, 2001, SEMIN IMMUNOL, V13, P213, DOI 10.1006/smim.2000.0317; Munn DH, 2002, SCIENCE, V297, P1867, DOI 10.1126/science.1073514; Munn DH, 1998, SCIENCE, V281, P1191, DOI 10.1126/science.281.5380.1191; Munn DH, 1999, J EXP MED, V189, P1363, DOI 10.1084/jem.189.9.1363; Roman M, 1997, NAT MED, V3, P849, DOI 10.1038/nm0897-849; Sedlmayr P, 2002, MOL HUM REPROD, V8, P385, DOI 10.1093/molehr/8.4.385; 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; Suzuki S, 2001, BIOCHEM J, V355, P425, DOI 10.1042/0264-6021:3550425; SWANSON KA, 2003, AM J RESP CELL MOL B, V30, P311, DOI 10.1165/rcmb.2003-0268OC; Takeda K, 2003, ANNU REV IMMUNOL, V21, P335, DOI 10.1146/annurev.immunol.21.120601.141126; TAKIKAWA O, 1988, J BIOL CHEM, V263, P2041; Takikawa O, 1999, ADV EXP MED BIOL, V467, P553; Terness P, 2002, J EXP MED, V196, P447, DOI 10.1084/jem.20020052; van Kooyk Y, 2003, NAT REV IMMUNOL, V3, P697, DOI 10.1038/nri1182; Vermaelen KY, 2001, J EXP MED, V193, P51; Wakkach A, 2003, IMMUNITY, V18, P605, DOI 10.1016/S1074-7613(03)00113-4; Weiss ST, 2002, NEW ENGL J MED, V347, P930, DOI 10.1056/NEJMe020092; Wills-Karp M, 2001, NAT REV IMMUNOL, V1, P69, DOI 10.1038/35095579	50	239	255	1	11	AMER SOC CLINICAL INVESTIGATION INC	ANN ARBOR	35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA	0021-9738			J CLIN INVEST	J. 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J	Knight, DA; Holgate, ST				Knight, DA; Holgate, ST			The airway epithelium: Structural and functional properties in health and disease	RESPIROLOGY			English	Review						asthma; epithelium; human; inflammation; respiratory disease	EPIDERMAL-GROWTH-FACTOR; V BETA 3; EXTRACELLULAR-MATRIX COMPONENTS; ASTHMATIC BRONCHIAL EPITHELIUM; PROTEASE-ACTIVATED RECEPTORS; ARACHIDONIC-ACID METABOLISM; DIESEL EXHAUST PARTICLES; CELL-ADHESION RECEPTORS; NITRIC-OXIDE SYNTHASES; REPAIR IN-VIVO	The major function of the respiratory epithelium was once thought to be that of a physical barrier. However, it constitutes the interface between the internal milieu and the external environment as well as being a primary target for inhaled respiratory drugs. It also responds to changes in the external environment by secreting a large number of molecules and mediators that signal to cells of the immune system and underlying mesenchyme. Thus, the epithelium is in a unique position to translate gene-environment interactions. Normally, the epithelium has a tremendous capacity to repair itself following injury. However, evidence is rapidly accumulating to show that the air-way epithelium of asthmatics is abnormal and has increased susceptibility to injury compared to normal epithelium. Areas of detachment and fragility are a characteristic feature not observed in other inflammatory diseases such as COPD. In addition to being more susceptible to damage, normal repair processes are also compromised. Failure of appropriate growth and differentiation of airway epithelial cells will cause persistent mucosal injury. The response to traditional therapy such as glucocorticoids may also be compromised. However, whether the differences observed in asthmatic epithelium are a cause of or secondary to the development of the disease remains unanswered. Strategies to address this question include careful examination of the ontogeny of the disease in children and use of gene array technology should provide some important answers, as well as allow a better understanding of the critical role that the epithelium plays under normal conditions and in diseases such as asthma.	Sir Charles Gairdner Hosp, Asthma & Allergy Res Inst, Nedlands, WA 6009, Australia; Southampton Gen Hosp, Sch Med, Div Infect Inflammat & Repair, Brooke Lab, Southampton SO9 4XY, Hants, England; Univ Western Australia, Sch Med & Pharmacol, Crawley, WA, Australia	Knight, DA (reprint author), Sir Charles Gairdner Hosp, Asthma & Allergy Res Inst, Ground Floor,E Block,Verdun St, Nedlands, WA 6009, Australia.						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J	Soubani, AO; Chandrasekar, PH				Soubani, AO; Chandrasekar, PH			The clinical spectrum of pulmonary aspergillosis	CHEST			English	Review						allergic pulmonary aspergillosis; aspergillus; fungal diseases; immunocompromised host; pulmonary infection	ALLERGIC BRONCHOPULMONARY ASPERGILLOSIS; BONE-MARROW TRANSPLANTATION; INVASIVE FUNGAL-INFECTIONS; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; CHRONIC EOSINOPHILIC PNEUMONIA; LINKED-IMMUNOSORBENT-ASSAY; LIPOSOMAL AMPHOTERICIN-B; LATEX AGGLUTINATION-TEST; AIR CRESCENT SIGN; ACUTE-LEUKEMIA	Aspergillus is a ubiquitous fungus that causes a variety of clinical syndromes in the lung, ranging from aspergilloma in patients with lung cavities, to chronic necrotizing aspergillosis in those who are mildly immunocompromised or have chronic lung disease. Invasive pulmonary aspergillosis (IPA) is a severe and commonly fatal disease that is seen in immunocompromised patients, while allergic bronchopulmonary aspergillosis is a hypersensitivity reaction to Aspergillus antigens that mainly affects patients with asthma. In light of the increasing risk factors leading to IPA, such as organ transplantation and immunosuppressive therapy, and recent advances in the diagnosis and treatment of Aspergillus-related lung diseases, it is essential for clinicians to be familiar with the clinical presentation, diagnostic methods, and approach to management of the spectrum of pulmonary aspergillosis.	Wayne State Univ, Sch Med, Div Pulm Crit Care & Sleep Med, Detroit, MI USA; Wayne State Univ, Sch Med, Div Infect Dis, Detroit, MI USA	Soubani, AO (reprint author), Harper Univ Hosp, Div Pulm Crit Care & Sleep Med, 3990 John,R-3 Hudson, Detroit, MI 48201 USA.						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J	Peel, JL; Tolbert, PE; Klein, M; Metzger, KB; Flanders, WD; Todd, K; Mulholland, JA; Ryan, PB; Frumkin, H				Peel, JL; Tolbert, PE; Klein, M; Metzger, KB; Flanders, WD; Todd, K; Mulholland, JA; Ryan, PB; Frumkin, H			Ambient air pollution and respiratory emergency department visits	EPIDEMIOLOGY			English	Article							HOSPITAL ADMISSIONS; SIZE DISTRIBUTIONS; ONTARIO HOSPITALS; CHILDHOOD ASTHMA; HUMAN HEALTH; TIME-SERIES; ROOM VISITS; NEW-YORK; ATLANTA; EPIDEMIOLOGY	Background: A number of emergency department studies have corroborated findings from mortality and hospital admission studies regarding an association of ambient air pollution and respiratory outcomes. More refined assessment has been limited by study size and available air quality data. Methods: Measurements of 5 pollutants (particulate matter [PM10] ozone, nitrogen dioxide [NO2] carbon monoxide [CO], and sulfur dioxide [SO2]) were available for the entire study period (I January 1993 to 31 August 2000); detailed measurements of particulate matter were available for 25 months. We obtained data on 4 million emergency department visits from 31 hospitals in Atlanta. Visits for asthma, chronic obstructive pulmonary disease, upper respiratory infection, and pneumonia were assessed in relation to air pollutants using Poisson generalized estimating equations. Results: In single-pollutant models examining 3-day moving averages of pollutants (lags 0, 1, and 2): standard deviation increases of ozone, NO2, CO, and PM10 were associated with 1-3% increases in UR1 visits; a 2 mug/m(3) increase of PM2.5 organic carbon was associated with a 3% increase in pneumonia visits; and standard deviation increases of NO2 and CO were associated with 2-3% increases in chronic obstructive pulmonary disease visits. Positive associations persisted beyond 3 days for several of the outcomes, and over a week for asthma. Conclusions: The results of this study contribute to the evidence of an association of several correlated gaseous and particulate pollutants, including ozone, NO2, CO, PM, and organic carbon, with specific respiratory conditions.	Emory Univ, Rollins Sch Publ Hlth, Dept Epidemiol, Atlanta, GA 30322 USA; Emory Univ, Rollins Sch Publ Hlth, Dept Environm & Occupat Hlth, Atlanta, GA 30322 USA; Emory Univ, Sch Med, Dept Emergency Med, Atlanta, GA 30322 USA; Georgia Inst Technol, Sch Civil & Environm Engn, Atlanta, GA 30332 USA	Peel, JL (reprint author), Colorado State Univ, Dept Environm & Radiol Hlth Sci, 1681 Campus Delivery, Ft Collins, CO 80523 USA.	jennifer.peel@colostate.edu	Ryan, P. 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J	Noverr, MC; Huffnagel, GB				Noverr, MC; Huffnagel, GB			Does the microbiota regulate immune responses outside the gut?	TRENDS IN MICROBIOLOGY			English	Review							CHAIN FATTY-ACIDS; ANTHROPOSOPHIC LIFE-STYLE; PLACEBO-CONTROLLED TRIAL; INTESTINAL MICROFLORA; ORAL TOLERANCE; CANDIDA-ALBICANS; ATOPIC DISEASE; T-CELLS; PROBIOTIC BACTERIA; ALLERGIC DISEASE	Perturbations in the gastrointestinal (GI) microbiota composition that occur as a result of antibiotics and diet in 'westernized' countries are strongly associated with allergies and asthma ('hygiene hypothesis'). The microbiota ('microflora') plays a crucial role in the development of mucosal tolerance, including the airways. Significant attention has been focused on the role of the microbiota in GI development, immune adaptation and initiation of GI inflammatory diseases. This review covers the post-develop mental functions that the microbiota plays in regulating immunological tolerance to allergen exposure outside the GI tract and proposes the question: is the microbiota a major regulator of the immune system?.	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DEC	2004	12	12					562	568		10.1016/j.tim.2004.10.008		7	Biochemistry & Molecular Biology; Microbiology	Biochemistry & Molecular Biology; Microbiology	880GY	WOS:000225778200008	15539116	
J	Murray, CS; Poletti, G; Kebadze, T; Morris, J; Woodcock, A; Johnston, SL; Custovic, A				Murray, CS; Poletti, G; Kebadze, T; Morris, J; Woodcock, A; Johnston, SL; Custovic, A			Study of modifiable risk factors for asthma exacerbations: virus infection and allergen exposure increase the risk of asthma hospital admissions in children	THORAX			English	Article							ANTIGEN BRONCHOPROVOCATION; INHALED CORTICOSTEROIDS; VIRAL-INFECTIONS; RHINOVIRUS-16; PRECIPITANTS; EMERGENCY; CITY; AGE	Background: Asthma exacerbation is the most common cause of hospital admission in children. A study was undertaken to investigate the importance of allergen exposure in sensitised individuals in combination with viral infections and other potentially modifiable risk factors precipitating asthma hospital admission in children. Methods: Eighty four children aged 3 - 17 years admitted to hospital over a 1 year period with an acute asthma exacerbation (AA) were matched for age and sex with two control groups: stable asthmatics (SA) and children admitted to hospital with non-respiratory conditions (IC). Risk factors were assessed by questionnaires and determination of allergen sensitisation, home allergen exposure, pollen exposure, and respiratory virus infection. Results: Several non-modifiable factors (atopy, duration of asthma) were associated with increased risk. Among the modifiable factors, pet ownership, housing characteristics, and parental smoking did not differ between the groups. Regular inhaled corticosteroid treatment was significantly less common in the AA group than in the SA group (OR 0.2, 95% CI 0.1 to 0.6; p = 0.002). A significantly higher proportion of the AA group were virus infected ( 44%) and sensitised and highly exposed to sensitising allergen (76%) compared with the SA (18% and 48%) and IC groups (17% and 28%; both p < 0.001). In a multiple conditional logistic regression ( AA v SA), allergen sensitisation and exposure or virus detection alone were no longer independently associated with hospital admission. However, the combination of virus detection and sensitisation with high allergen exposure substantially increased the risk of admission to hospital ( OR 19.4, 95% CI 3.7 to 101.5, p < 0.001). Conclusions: Natural virus infection and real life allergen exposure in allergic asthmatic children increase the risk of hospital admission. Strategies for preventing exacerbations will need to address these factors.	Univ Manchester, S Manchester Univ Hosp NHS Trust, NW Lung Ctr, Acad Div Med & Surg S, Manchester M23 9LT, Lancs, England; S Manchester Univ Hosp NHS Trust, Dept Med Stat, Manchester M23 9LT, Lancs, England; Univ London Imperial Coll Sci Technol & Med, Fac Med, Natl Heart & Lung Inst, Dept Resp Med, London, England	Murray, CS (reprint author), Univ Manchester, S Manchester Univ Hosp NHS Trust, NW Lung Ctr, Acad Div Med & Surg S, Manchester M23 9LT, Lancs, England.	clare.murray@manchester.ac.uk	Johnston, Sebastian/I-2423-2012; Custovic, Adnan/A-2435-2012	Custovic, Adnan/0000-0001-5218-7071; Woodcock, Ashley/0000-0002-5428-8578			Bacharier LB, 2003, PEDIATRICS, V112, pE85, DOI 10.1542/peds.112.2.e85; BEASLEY R, 1988, THORAX, V43, P679, DOI 10.1136/thx.43.9.679; Bisgaard H, 1999, AM J RESP CRIT CARE, V160, P126; CALHOUN WJ, 1994, J CLIN INVEST, V94, P2200, DOI 10.1172/JCI117581; CALHOUN WJ, 1991, AM REV RESPIR DIS, V144, P1267; Campbell MJ, 1997, BRIT MED J, V315, P1012; CHAUHAN AJ, 2000, ASTHMA RESP INFECT, P221; de Kluijver Josephine, 2003, American Journal of Respiratory and Critical Care Medicine, V168, P1174, DOI 10.1164/rccm.200212-1520OC; Doull IJM, 1997, BRIT MED J, V315, P858; Doull IJM, 2003, J PEDIATR-US, V142, pS21, DOI 10.1067/mpd.2003.22; DUFF AL, 1993, PEDIATRICS, V92, P535; Freymuth F, 1999, J CLIN VIROL, V13, P131, DOI 10.1016/S1386-6532(99)00030-X; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; Green RM, 2002, BRIT MED J, V324, P763, DOI 10.1136/bmj.324.7340.763; Heymann PW, 2004, J ALLERGY CLIN IMMUN, V114, P239, DOI 10.1016/j.jaci.2004.04.006; HORN MEC, 1979, THORAX, V34, P23, DOI 10.1136/thx.34.1.23; INHAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449; JOHNSTON SL, 1995, BRIT MED J, V310, P1225; Johnston SL, 1996, AM J RESP CRIT CARE, V154, P654; KEUHR J, 1994, J ALLERGY CLIN IMMUN, V94, P44; LEMANSKE RF, 1989, J CLIN INVEST, V83, P1, DOI 10.1172/JCI113843; MINOR TE, 1974, JAMA-J AM MED ASSOC, V227, P292, DOI 10.1001/jama.227.3.292; MINOR TE, 1976, AM REV RESPIR DIS, V113, P149; NICHOLSON KG, 1993, BRIT MED J, V307, P982; pidemiology Standardization Project. 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J	Romagnani, S				Romagnani, S			Immunologic influences on allergy and theT(H)1/T(H)2 balance	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						T(H)1T(H)2 cells; immune deviation; treg cells; immune suppression; hygiene hypothesis	REGULATORY T-CELLS; IMMUNE-RESPONSE; HYGIENE HYPOTHESIS; DENDRITIC CELLS; TH2 RESPONSES; DISEASE; LYMPHOCYTES; ASTHMA; CHILDREN; IL-10	T(H)2 cell-mediated immune responses against "innocuous" antigens play a triggering role in atopic allergy. Several epidemiologic studies have clearly shown that the reduced microbial exposure of children caused by the westernized lifestyle is responsible for the increased prevalence of allergy that has occurred in the last decades in developed countries ("hygiene hypothesis"). The immunologic changes caused by the reduced exposure to pathogenic and nonpathogenic microbes during childhood are still controversial. The initial interpretation has been a lack of shift of allergen-specific responses from the T(H)2 to the T(H)1 phenotype. This is because of reduced production of IL-12 and IFNs by cells of the natural immunity stimulated by bacterial products through their Toll-like receptors (missing immune deviation). Another interpretation emphasizes the importance of reduced activity of T-regulatory cells (reduced immune suppression). However, although there are impressive amounts of data in favor of the missing immune deviation, experimental evidence supporting the role of reduced immune suppression in explaining the increased prevalence of allergy is currently weak or even contradictory. The solution to this question is very important not only from a theoretic point of view but also because of its therapeutic implications.	Univ Florence, Dept Internal Med, Sect Clin Immunol Allergy & Resp Dis, I-50134 Florence, Italy	Romagnani, S (reprint author), Univ Florence, Dept Internal Med, Sect Clin Immunol Allergy & Resp Dis, Viale Morgagni 85, I-50134 Florence, Italy.						Abbas AK, 1996, NATURE, V383, P787, DOI 10.1038/383787a0; Akdis CA, 2001, MICROBES INFECT, V3, P891, DOI 10.1016/S1286-4579(01)01449-6; Annunziato F, 2001, J ALLERGY CLIN IMMUN, V108, P815; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; Bluestone JA, 2003, NAT REV IMMUNOL, V3, P253, DOI 10.1038/nri1032; Boonstra A, 2003, J EXP MED, V197, P101, DOI 10.1084/jem.20021908; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Brugnolo F, 2003, J ALLERGY CLIN IMMUN, V111, P380, DOI 10.1067/mai.2003.102; Chatelain R, 1999, PARASITE IMMUNOL, V21, P211, DOI 10.1046/j.1365-3024.1999.00224.x; COSMI L, 2004, IN PRESS BLOOD; Eisenbarth SC, 2002, J EXP MED, V196, P1645, DOI 10.1084/jem.20021340; Finotto S, 2002, SCIENCE, V295, P336, DOI 10.1126/science.1065544; Laouini D, 2003, J CLIN INVEST, V112, P1058, DOI 10.1172/JCI200318246; Larche M, 2003, J ALLERGY CLIN IMMUN, V111, P450, DOI 10.1067/mai.2003.169; Liu NS, 2003, NAT IMMUNOL, V4, P687, DOI 10.1038/ni941; Martinez FD, 2001, RESPIR RES, V2, P129, DOI 10.1186/rr48; Pasare C, 2003, SCIENCE, V299, P1033, DOI 10.1126/science.1078231; Rengarajan J, 2000, IMMUNOL TODAY, V21, P479, DOI 10.1016/S0167-5699(00)01712-6; Renz H, 2002, J ALLERGY CLIN IMMUN, V109, P338, DOI 10.1067/mai.2002.121459; Romagnani S, 2000, ANN ALLERG ASTHMA IM, V85, P9; Romagnani S, 2000, J ALLERGY CLIN IMMUN, V105, P399, DOI 10.1067/mai.2000.104575; ROMAGNANI S, 1992, IMMUNOL TODAY, V13, P379, DOI 10.1016/0167-5699(92)90083-J; ROMAGNANI S, 1994, CURR OPIN IMMUNOL, V6, P838, DOI 10.1016/0952-7915(94)90002-7; ROMAGNANI S, 1994, ANNU REV IMMUNOL, V12, P227, DOI 10.1146/annurev.iy.12.040194.001303; ROMAGNANI S, 2004, IN PRESS NESTLE NUTR, V53; Sabroe I, 2002, CLIN EXP ALLERGY, V32, P984, DOI 10.1046/j.1365-2745.2002.01451.x; Sewell DL, 2002, IMMUNOL LETT, V82, P101, DOI 10.1016/S0165-2478(02)00025-1; Suto A, 2001, AM J RESP CRIT CARE, V164, P680; Tang LL, 1998, J ALLERGY CLIN IMMUN, V102, P428, DOI 10.1016/S0091-6749(98)70131-9; Turcanu V, 2003, J CLIN INVEST, V111, P1065, DOI 10.1172/JCI200316142; Umetsu DT, 2003, J ALLERGY CLIN IMMUN, V112, P480, DOI 10.1067/mai.2003.1717; van Roon JAG, 2002, ANN RHEUM DIS, V61, P951, DOI 10.1136/ard.61.11.951; Yazdanbakhsh M, 2002, SCIENCE, V296, P490, DOI 10.1126/science.296.5567.490	33	237	253	1	20	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	2004	113	3					395	400		10.1016/j.jaci.2003.11.025		6	Allergy; Immunology	Allergy; Immunology	802DM	WOS:000220144200006	14758340	
J	Akdis, CA; Akdis, M; Bieber, T; Bindslev-Jensen, C; Boguniewicz, M; Eigenmann, P; Hamid, Q; Kapp, A; Leung, DYM; Lipozencic, JK; Luger, TA; Muraro, A; Novak, N; Platts-Mills, TAE; Rosenwasser, L; Scheynius, A; Simons, FER; Spergel, J; Turjanmaa, K; Wahn, U; Weidinger, S; Werfel, T; Zuberbier, T				Akdis, Cezmi A.; Akdis, Mubeccel; Bieber, Thomas; Bindslev-Jensen, Carsten; Boguniewicz, Mark; Eigenmann, Philippe; Hamid, Qutayba; Kapp, Alexander; Leung, Donald Y. M.; Lipozencic, Jasna K.; Luger, Thomas A.; Muraro, Antonella; Novak, Natalija; Platts-Mills, Thomas A. E.; Rosenwasser, Lanny; Scheynius, Annika; Simons, F. Estelle R.; Spergel, Jonathan; Turjanmaa, Kristiina; Wahn, Ulrich; Weidinger, Stefan; Werfel, Thomas; Zuberbier, Torsten		European Acad Allergol, CI; Amer Acad Allergy Asthma Immunol; PRACTALL Consensus Grp	Diagnosis and treatment of atopic dermatitis in children and adults: European Academy of Allergology and Clinical Immunology/American Academy of Allergy, Asthma and Immunology/PRACTALL Consensus Report	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						atopic dermatitis; children; adults; risk factors; immunopathology; diagnosis; systemic treatment; topical treatment	RANDOMIZED CONTROLLED-TRIAL; STAPHYLOCOCCUS-AUREUS COLONIZATION; TOPICAL CALCINEURIN INHIBITORS; PIMECROLIMUS CREAM 1-PERCENT; PLASMACYTOID DENDRITIC CELLS; PLACEBO-CONTROLLED TRIAL; DUST-MITE ALLERGENS; REGULATORY T-CELLS; LONG-TERM EFFICACY; DOUBLE-BLIND	There are remarkable differences in the diagnostic and therapeutic management of atopic dermatitis practiced by dermatologists and pediatricians in different countries. Therefore, the European Academy of Allergy and Clinical Immunology and the American Academy of Allergy, Asthma and Immunology nominated expert teams who were given the task of finding a consensus to serve as a guideline for clinical practice in Europe as well as in North America. The consensus report is part of the PRACTALL initiative, which is endorsed by both academies.	Swiss Inst Allergy & Asthma Res, CH-7270 Davos, Switzerland; Univ Bonn, D-5300 Bonn, Germany; Odense Univ Hosp, DK-5000 Odense, Denmark; Natl Jewish Med & Res Ctr, Denver, CO USA; Univ Colorado, Sch Med, Denver, CO 80202 USA; Univ Geneva, Childrens Hosp, CH-1211 Geneva 4, Switzerland; McGill Univ, Montreal, PQ H3A 2T5, Canada; Hannover Med Univ, Hannover, Germany; Univ Zagreb, Zagreb Hosp Ctr, Zagreb 41000, Croatia; Univ Zagreb, Sch Med, Zagreb 41000, Croatia; Univ Munster, D-4400 Munster, Germany; Univ Padua, I-35100 Padua, Italy; Asthma & Allerg Dis Ctr, Charlottesville, VA USA; Karolinska Univ Hosp, Solna, Sweden; Univ Manitoba, Winnipeg, MB R3T 2N2, Canada; Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA; Univ Penn, Sch Med, Philadelphia, PA 19104 USA; Tampere Univ Hosp, Tampere, Finland; Univ Berlin, Charite, Berlin, Germany; Tech Univ Munich, D-8000 Munich, Germany; Hannover Med Sch, D-3000 Hannover, Germany	Wahn, U (reprint author), Univ Med Berlin, Charite, Augustenburger Pl 1, D-13353 Berlin, Germany.	ulrich.wahn@charite.de	Weidinger, Stephan/C-8461-2011; 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Allergy Clin. Immunol.	JUL	2006	118	1					152	169		10.1016/j.jaci.2006.03.045		18	Allergy; Immunology	Allergy; Immunology	065UH	WOS:000239184800019	16815151	
J	Bohle, B; Kinaciyan, T; Gerstmayr, M; Radakovics, A; Jahn-Schmid, B; Ebner, C				Bohle, Barbara; Kinaciyan, Tamar; Gerstmayr, Marianne; Radakovics, Astrid; Jahn-Schmid, Beatrice; Ebner, Christof			Sublingual immunotherapy induces IL-10-producing T regulatory cells, allergen-specific T-cell tolerance, and immune deviation	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						specific immunotherapy; sublingual immunotherapy; T-cell tolerance; immune deviation; regulatory T cells; Bet v 1; IL-10	BIRCH-POLLEN ALLERGEN; BET V 1; DUST MITE IMMUNOTHERAPY; GRASS-POLLEN; IMMUNOLOGICAL CHANGES; CROSS-REACTIVITY; ORAL TOLERANCE; MAJOR ALLERGEN; IFN-GAMMA; IN-VITRO	Background: The immunologic mechanisms underlying sublingual immunotherapy (SLIT) are still unclear, particularly the role of regulatory T cells. Objective: We sought to characterize allergen-specific T-cell responses during successful birch pollen SLIT. Methods: Proliferation of PBMCs and PBMCs depleted of CD25(+) cells obtained from 9 patients before, after 4 weeks. and after 52 weeks of SLIT was assessed in response to the major birch pollen allergen Bet v 1, the homologous apple allergen Mal d 1, or tetanus toxoid. Allergen-induced cytokine responses and FoxP3 expression of T cells were analyzed by using real-time PCR. The role of IL-10 for regulatory activity of T cells was investigated. Results: After 4 weeks, higher frequencies of circulating CD4(+)CD25(+) T cells were detected together with increased FoxP3 and IL-10 and reduced IL-4 and IFN-gamma mRNA expression levels compared with those before SLIT. Proliferation to all 3 antigens was markedly reduced but increased significantly after depletion of CD25(+) cells or addition of anti-IL-10 antibodies. After 52 weeks, proliferation in response to Mal d I or tetanus toxoid returned to pre-SLIT levels, whereas Bet v I-induced proliferation remained significantly suppressed and was enhanced by neither depletion of CD25(+) cells nor addition of anti-IL-10 antibodies. In parallel, increased IFN-gamma and reduced IL-4, IL-10, and FoxP3 mRNA expression was detected. Neither TGF-beta levels nor cell-cell contact-mediated suppression of CD4(+)CD25(+) cells changed during the course of SLIT. Conclusion: SLIT induces regulatory T-cell suppression through IL-10 during the early phase and specific nonreactivity and immune deviation of allergen-specific T cells during the later phase of therapy. Clinical implications: SLIT induces immune mechanisms comparable with subcutaneous specific immunotherapy.	Med Univ Vienna, Ctr Physiol Pathophysiol & Immunol, Dept Pathophysiol, A-1090 Vienna, Austria; Med Univ Vienna, Dept Dermatol, Div Immunol Allergy & Infect Dis, A-1090 Vienna, Austria	Bohle, B (reprint author), Med Univ Vienna, Ctr Physiol & Pathophysiol, Dept Pathophysiol, Waehringer Guertel 18, A-1090 Vienna, Austria.	barbara.bohle@meduniwien.ac.at					Akdis CA, 1998, J CLIN INVEST, V102, P98, DOI 10.1172/JCI2250; Akdis CA, 2000, FASEB J, V14, P1666; Akdis CA, 1999, FASEB J, V13, P603; Akdis M, 2004, J EXP MED, V199, P1567, DOI 10.1084/jem.20032058; Bellinghausen I, 1997, EUR J IMMUNOL, V27, P1131, DOI 10.1002/eji.1830270513; Bohle B, 2005, CLIN EXP ALLERGY, V35, P367, DOI 10.1111/j.1365-2222.2005.02180.x; Bohle B, 2006, J ALLERGY CLIN IMMUN, V118, P242, DOI 10.1016/j.jaci.2006.03.01; Bousquet J, 2005, ALLERGY, V60, P1, DOI 10.1111/j.1398-9995.2005.00700.x; BOUSQUET J, 1998, ALLERGY S, V53, P20; Bousquet J, 2006, ALLERGY, V61, P5, DOI 10.1111/j.1398-9995.2006.01183.x; BREITENEDER H, 1989, EMBO J, V8, P1935; Calderon M, 2006, J INVEST ALLERG CLIN, V16, P338; CHEN YH, 1994, SCIENCE, V265, P1237, DOI 10.1126/science.7520605; CHEN YH, 1995, NATURE, V376, P177, DOI 10.1038/376177a0; Ciprandi G, 2005, ANN ALLERG ASTHMA IM, V95, P38; Cosmi L, 2006, CLIN EXP ALLERGY, V36, P261, DOI 10.1111/j.1365-2222.2006.02429.x; EBNER C, 1991, J ALLERGY CLIN IMMUN, V88, P588, DOI 10.1016/0091-6749(91)90152-E; Ebner C, 1997, CLIN EXP ALLERGY, V27, P1007, DOI 10.1111/j.1365-2222.1997.tb01252.x; EBNER C, 1995, J IMMUNOL, V154, P1932; EBNER C, 1995, J ALLERGY CLIN IMMUN, V95, P962, DOI 10.1016/S0091-6749(95)70096-X; Eusebius NP, 2002, INT ARCH ALLERGY IMM, V127, P234, DOI 10.1159/000053868; Fanta C, 1999, INT ARCH ALLERGY IMM, V120, P218, DOI 10.1159/000024270; Francis JN, 2003, J ALLERGY CLIN IMMUN, V111, P1255, DOI 10.1067/mai.2003.1570; Fritsch R, 1998, J ALLERGY CLIN IMMUN, V102, P679, DOI 10.1016/S0091-6749(98)70287-8; Gajhede M, 1996, NAT STRUCT BIOL, V3, P1040, DOI 10.1038/nsb1296-1040; Gardner LM, 2004, CLIN EXP ALLERGY, V34, P1209, DOI 10.1111/j.1365-2222.2004.02009.x; Gardner LM, 2004, INT ARCH ALLERGY IMM, V133, P1, DOI 10.1159/000075248; Gehlhar K, 1999, CLIN EXP ALLERGY, V29, P497; Hori S, 2004, MICROBES INFECT, V6, P745, DOI 10.1016/j.micinf.2004.02.020; Jahn-Schmid B, 2005, J ALLERGY CLIN IMMUN, V116, P213, DOI 10.1016/j.jaci.2005.04.019; Jensen-Jarolim E, 1998, FASEB J, V12, P1635; Jutel M, 2003, EUR J IMMUNOL, V33, P1205, DOI 10.1002/eji.200322919; JUTEL M, 1995, J IMMUNOL, V154, P4187; Kinaciyan T, 2007, J ALLERGY CLIN IMMUN, V119, P937, DOI 10.1016/j.jaci.2006.11.010; Mirza O, 2000, J IMMUNOL, V165, P331; Nouri-Aria KT, 2004, J IMMUNOL, V172, P3252; OBrien RM, 1997, CLIN EXP ALLERGY, V27, P46, DOI 10.1046/j.1365-2222.1997.d01-424.x; Savolainen J, 2004, CLIN EXP ALLERGY, V34, P413, DOI 10.1111/j.1365-2222.2004.01823.x; SECRIST H, 1993, J EXP MED, V178, P2123, DOI 10.1084/jem.178.6.2123; Spangfort MD, 1999, ACTA CRYSTALLOGR D, V55, P2035, DOI 10.1107/S0907444999011804; van Neerven RJJ, 1999, J IMMUNOL, V163, P2944; VANEKKREBITZ M, 1995, BIOCHEM BIOPH RES CO, V214, P538, DOI 10.1006/bbrc.1995.2320; Vukmanovic-Stejic M, 2006, J CLIN INVEST, V116, P2423, DOI 10.1172/JCI28941; Wachholz PA, 2003, J ALLERGY CLIN IMMUN, V112, P915, DOI [10.1067/mai.2003.1770, 10.1016/S0091-6749(03)02022-0]; Weiner HL, 2001, IMMUNOL REV, V182, P207, DOI 10.1034/j.1600-065X.2001.1820117.x; Wilson DR, 2005, ALLERGY, V60, P4, DOI 10.1111/j.1398-9995.2005.00699.x	46	234	251	2	7	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	SEP	2007	120	3					707	713		10.1016/j.jaci.2007.06.013		7	Allergy; Immunology	Allergy; Immunology	211DV	WOS:000249505400033	17681368	
J	Beuther, DA; Weiss, ST; Sutherland, ER				Beuther, David A.; Weiss, Scott T.; Sutherland, E. Rand			Pulmonary perspective - Obesity and asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; epidemiology; inflammation; obesity; pathogenesis	BODY-MASS INDEX; ADULT-ONSET ASTHMA; ADIPOSE-TISSUE; MORBID-OBESITY; WEIGHT-LOSS; AIRWAY HYPERRESPONSIVENESS; GASTROESOPHAGEAL-REFLUX; RESPIRATORY-FUNCTION; PROSPECTIVE COHORT; CHILDHOOD ASTHMA	Asthma and obesity are prevalent disorders, each with a significant public health impact, and a large and growing body of literature suggests an association between the two. The systemic inflammatory milieu in obesity leads to metabolic and cardiovascular complications, but whether this environment alters asthma risk or phenotype is not yet known. Animal experiments have evaluated the effects of leptin and obesity on airway inflammation in response to both allergic and nonallergic exposures and suggest that airway inflammatory response is enhanced by both endogenous and exogenous leptin. Cross-sectional and prospective cohort studies of humans have shown a modest overall increase in asthma incidence and prevalence in the obese, although body mass index does not appear be a significant modifier of asthma severity. Studying the obesity-asthma relationship in large cohorts, in which self-reports are frequently used to ascertain the diagnosis of asthma, has been complicated by alterations in pulmonary physiology caused by obesity, which may lead to dyspnea or other respiratory symptoms but do not fulfill accepted physiologic criteria for asthma. Recent investigations toward elucidating a shared genetic basis for these two disorders have identified polymorphisms in specific regions of chromosomes 5q, 6p, 11q13, and 12q, each of which contains one or more genes encoding receptors relevant to asthma, inflammation, and metabolic disorders, including the beta(2)-adrenergic receptor gene ADRB2 and the glucocorticoid receptor gene NR3C1. Further research is warranted to synthesize these disparate observations into a cohesive understanding of the relationship between obesity and asthma.	Natl Jewish Med & Res Ctr, Denver, CO 80206 USA; Univ Colorado, Hlth Sci Ctr, Denver, CO USA; Harvard Univ, Sch Med, Boston, MA USA; Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA	Sutherland, ER (reprint author), Natl Jewish Med & Res Ctr, 1400 Jackson St,J220, Denver, CO 80206 USA.	sutherlande@njc.org	Sutherland, Everett/B-7666-2008		NHLBI NIH HHS [K23HL04385]		Aaron SD, 2004, CHEST, V125, P2046, DOI 10.1378/chest.125.6.2046; BARRERA F, 1973, AM REV RESPIR DIS, V108, P819; Beckett WS, 2001, AM J RESP CRIT CARE, V164, P2045; BEDELL GN, 1958, J CLIN INVEST, V37, P1049, DOI 10.1172/JCI103686; Beuther DA, 2005, J ALLERGY CLIN IMMUN, V115, P1100, DOI 10.1016/j.jaci.2004.12.1141; Bibi H, 2004, J ASTHMA, V41, P403, DOI 10.1081/JAS-120026297; Biring MS, 1999, AM J MED SCI, V318, P293, DOI 10.1097/00000441-199911000-00002; 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; Chen Y, 2002, AM J EPIDEMIOL, V155, P191, DOI 10.1093/aje/155.3.191; Chen Y, 1999, AM J EPIDEMIOL, V150, P255; Chinn S, 2002, THORAX, V57, P1028, DOI 10.1136/thorax.57.12.1028; Chinn S, 2001, THORAX, V56, P845, DOI 10.1136/thorax.56.11.845; CLEMENT K, 1995, NEW ENGL J MED, V333, P352, DOI 10.1056/NEJM199508103330605; COURNAND A, 1954, T ASSOC AM PHYSICIAN, V67, P162; Dolan CM, 2004, ANN ALLERG ASTHMA IM, V92, P32; FADELL E J, 1962, N Engl J Med, V266, P861, DOI 10.1056/NEJM196204262661704; Fantuzzi G, 2005, J ALLERGY CLIN IMMUN, V115, P911, DOI 10.1016/j.jaci.2005.02.023; Flegal KM, 1998, INT J OBESITY, V22, P39, DOI 10.1038/sj.ijo.0800541; Ford ES, 2004, EUR RESPIR J, V24, P740, DOI 10.1183/09031936.04.00088003; Ford ES, 2005, J ALLERGY CLIN IMMUN, V115, P897, DOI 10.1016/j.jaci.2004.11.050; Fredberg JJ, 1999, AM J RESP CRIT CARE, V159, P959; Gilliland FD, 2003, AM J EPIDEMIOL, V158, P406, DOI 10.1093/aje/kwg175; Gold DR, 2003, PEDIATR PULM, V36, P514, DOI 10.1002/ppul.10376; Guerra S, 2002, CHEST, V122, P1256, DOI 10.1378/chest.122.4.1256; Guler N, 2004, J ALLERGY CLIN IMMUN, V114, P254, DOI 10.1016/j.jaci.2004.03.053; Gunnbjomsdottir MI, 2004, EUR RESPIR J, V24, P116, DOI 10.1183/09031936.04.00042603; Gurkan F, 2004, ANN ALLERG ASTHMA IM, V93, P277; Hakala K, 2000, CHEST, V118, P1315, DOI 10.1378/chest.118.5.1315; HALL IP, 1995, LANCET, V345, P1213, DOI 10.1016/S0140-6736(95)91994-5; Hallstrand TS, 2005, J ALLERGY CLIN IMMUN, V116, P1235, DOI 10.1016/j.jaci.2005.09.016; Hamano N, 1998, ALLERGY ASTHMA PROC, V19, P263, DOI 10.2500/108854198778557773; Hamano N, 1998, Acta Otolaryngol Suppl, V537, P27; Hampel H, 2005, ANN INTERN MED, V143, P199; Hancox RJ, 2005, AM J RESP CRIT CARE, V171, P440, DOI 10.1164/rccm.200405-623OC; HASLER G, IN PRESS INT J OBES; HEDENSTIERNA G, 1976, ACTA ANAESTH SCAND, V20, P334; Hedley AA, 2004, JAMA-J AM MED ASSOC, V291, P2847, DOI 10.1001/jama.291.23.2847; Hellings PW, 2003, CLIN EXP ALLERGY, V33, P1457, DOI 10.1046/j.1365-2222.2003.01743.x; Huovinen E, 2003, RESP MED, V97, P273, DOI 10.1053/rmed.2003.1419; Ishiyama-Shigemoto S, 1999, DIABETOLOGIA, V42, P98, DOI 10.1007/s001250051120; Israel E, 2004, LANCET, V364, P1505, DOI 10.1016/S0140-6736(04)17273-5; KAUFMAN BJ, 1959, J CLIN INVEST, V38, P500, DOI 10.1172/JCI103827; Larsson I, 2006, AM J CLIN NUTR, V83, P252; Lilly CM, 1999, J ALLERGY CLIN IMMUN, V104, P786; Litonjua AA, 2002, THORAX, V57, P581, DOI 10.1136/thorax.57.7.581; Mai XM, 2004, PEDIATR ALLERGY IMMU, V15, P523, DOI 10.1111/j.1399-3038.2004.00195.x; Mancuso P, 2006, AM J RESP CRIT CARE, V173, P212, DOI 10.1164/rccm.200506-909OC; Mannino D. 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J. Respir. Crit. Care Med.	JUL 15	2006	174	2					112	119		10.1164/rccm.200602-231PP		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	064QR	WOS:000239104700003	16627866	
J	Gruchalla, RS; Pongracic, J; Plaut, M; Evans, R; Visness, CM; Walter, M; Crain, EF; Kattan, M; Morgan, WJ; Steinbach, S; Stout, J; Malindzak, G; Smartt, E; Mitchell, H				Gruchalla, RS; Pongracic, J; Plaut, M; Evans, R; Visness, CM; Walter, M; Crain, EF; Kattan, M; Morgan, WJ; Steinbach, S; Stout, J; Malindzak, G; Smartt, E; Mitchell, H			Inner City Asthma Study: Relationships among sensitivity, allergen exposure, and asthma morbidity	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; allergen exposure; allergen sensitivity; morbidity; allergens; cockroach; dust mite; cat; dog	RISK-FACTORS; CHILDHOOD ASTHMA; INDOOR ALLERGENS; COCKROACH ALLERGEN; MANAGEMENT PROGRAM; CAT ALLERGEN; CHILDREN; SENSITIZATION; SEVERITY; MITE	Background: Asthma-associated morbidity is rising, especially in inner city children. Objective: We evaluated the allergen sensitivities, allergen exposures, and associated morbidity for participants in the Inner City Asthma Study. We also determined geographic variations of indoor allergen levels. Methods: Nine hundred thirty-seven inner city children 5 to 11 years old with moderate to severe asthma underwent allergen skin testing. Bedroom dust samples were evaluated for Der p 1, Der f 1, Bla g 1, Fel d 1, and Can f 1. Results: Skin test sensitivities to cockroach (69%), dust mites (62%), and molds (50%) predominated, with marked study site-specific differences. Cockroach sensitivity was highest in the Bronx, New York, and Dallas (81.2%, 78.7%, and 78.5%, respectively), and dust mite sensitivity was highest in Dallas and Seattle (83.7% and 78.0%, respectively). A majority of homes in Chicago, New York, and the Bronx had cockroach allergen levels greater than 2 U/g, and a majority of those in Dallas and Seattle had dust mite allergen levels greater than 2 mu g/g. Levels of both of these allergens were influenced by housing type. Cockroach allergen levels were highest in high-rise apartments, whereas dust mite allergen levels were highest in detached homes. Children who were both sensitive and exposed to cockroach allergen had significantly more asthma symptom days, more caretaker interrupted sleep, and more school days missed than children who were not sensitive or exposed. Conclusion: Geographic differences in allergen exposure and sensitivity exist among inner city children. Cockroach exposure and sensitivity predominate in the Northeast, whereas dust mite exposure and sensitivity are highest in the South and Northwest. Cockroach allergen appears to have a greater effect on asthma morbidity than dust mite or pet allergen in these children.	Univ Texas, SW Med Ctr, Dallas, TX 75390 USA; Childrens Mem Hosp, Chicago, IL 60614 USA; NIAID, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA; Rho Inc, Chapel Hill, NC USA; Albert Einstein Coll Med, Jacobi Med Ctr, Bronx, NY 10467 USA; Mt Sinai Sch Med, New York, NY USA; Univ Arizona, Coll Med, Tucson, AZ 85721 USA; Boston Univ, Sch Med, Boston, MA 02215 USA; Univ Washington, Sch Med & Publ Hlth, Seattle, WA 98195 USA; Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA	Gruchalla, RS (reprint author), Univ Texas, SW Med Ctr, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.	Rebecca.Gruchalla@utsouthwestern.edu			NCRR NIH HHS [M01 RR00533]; NIAID NIH HHS [AI-39902, AI-39761, AI-39769, AI-39776, AI-39785, AI-39789, AI-39900, AI-39901]		Arbes SJ, 2004, J ALLERGY CLIN IMMUN, V114, P111, DOI 10.1016/j.jaci.2004.04.036; Black PN, 2000, ALLERGY, V55, P501, DOI 10.1034/j.1398-9995.2000.00293.x; CALL RS, 1992, J PEDIATR-US, V121, P862, DOI 10.1016/S0022-3476(05)80329-4; Chew GL, 1999, ALLERGY, V54, P1058, DOI 10.1034/j.1398-9995.1999.00003.x; Crain EF, 2002, ENVIRON HEALTH PERSP, V110, P939; 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; GERGEN PJ, 1990, JAMA-J AM MED ASSOC, V264, P1688, DOI 10.1001/jama.264.13.1688; Green RM, 2002, BRIT MED J, V324, P1; Huss K, 2001, J ALLERGY CLIN IMMUN, V107, P48, DOI 10.1067/mai.2001.111146; Institute of Medicine, 2000, CLEAR AIR ASTHM IND, P105; INGRAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449, DOI 10.1016/S0091-6749(95)70286-5; Kattan M, 1997, PEDIATR PULM, V24, P253, DOI 10.1002/(SICI)1099-0496(199710)24:4<253::AID-PPUL4>3.0.CO;2-L; KITCH B, 2000, ENV HLTH PERSPECT, V108, P310; Lewis SA, 2002, AM J RESP CRIT CARE, V165, P961, DOI 10.1164/rccm.2103044; Nelson HS, 1999, J ALLERGY CLIN IMMUN, V104, P775; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; 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, 1999, THORAX, V54, P675; Tunnicliffe WS, 1999, EUR RESPIR J, V13, P654, DOI 10.1183/09031936.99.13365499; WEITZMAN M, 1992, JAMA-J AM MED ASSOC, V268, P2673, DOI 10.1001/jama.268.19.2673	22	233	243	0	10	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					478	485		10.1016/j.jaci.2004.12.006		8	Allergy; Immunology	Allergy; Immunology	907AN	WOS:000227687000007	15753892	
J	Prezant, DJ; Weiden, M; Banauch, GI; McGuinness, G; Rom, WN; Aldrich, TK; Kelly, KJ				Prezant, DJ; Weiden, M; Banauch, GI; McGuinness, G; Rom, WN; Aldrich, TK; Kelly, KJ			Cough and bronchial responsiveness in firefighters at the World Trade Center site	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							HIGH-RESOLUTION CT; AIRWAY RESPONSIVENESS; RESPIRATORY SYMPTOMS; OCCUPATIONAL ASTHMA; PERSISTENT ASTHMA; POPULATION-SAMPLE; METHACHOLINE; EXPOSURE; ISOCYANATES; INHALATION	Background: Workers from the Fire Department of New York City were exposed to a variety of inhaled materials during and after the collapse of the World Trade Center. We evaluated clinical features in a series of 332 firefighters in whom severe cough developed after exposure and the prevalence and severity of bronchial hyperreactivity in firefighters without severe cough classified according to the level of exposure. Methods: ``World Trade Center cough'' was defined as a persistent cough that developed after exposure to the site and was accompanied by respiratory symptoms severe enough to require medical leave for at least four weeks. Evaluation of exposed firefighters included completion of a standard questionnaire, spirometry, airway-responsiveness testing, and chest imaging. Results: In the first six months after September 11, 2001, World Trade Center cough occurred in 128 of 1636 firefighters with a high level of exposure (8 percent), 187 of 6958 with a moderate level of exposure (3 percent), and 17 of 1320 with a low level of exposure (1 percent). In addition, 95 percent had symptoms of dyspnea, 87 percent had gastroesophageal reflux disease, and 54 percent had nasal congestion. Of those tested before treatment of World Trade Center cough, 63 percent of firefighters (149 of 237) had a response to a bronchodilator and 24 percent (9 of 37) had bronchial hyperreactivity. Chest radiographs were unchanged from precollapse findings in 319 of the 332 with World Trade Center cough. Among the cohort without severe cough, bronchial hyperreactivity was present in 77 firefighters with a high level of exposure (23 percent) and 26 with a moderate level of exposure (8 percent). Conclusions: Intense, short-term exposure to materials generated during the collapse of the World Trade Center was associated with bronchial responsiveness and the development of cough. Clinical and physiological severity was related to the intensity of exposure.	Fire Dept New York City, Bur Hlth Serv, New York, NY USA; Albert Einstein Coll Med, Bronx, NY 10467 USA; Montefiore Med Ctr, Dept Med, Div Pulm Med, Bronx, NY 10467 USA; NYU, Sch Med, Dept Med, Div Pulm & Crit Care Med, New York, NY USA; NYU, Sch Med, Dept Environm Med, New York, NY USA; NYU, Sch Med, Dept Radiol, New York, NY USA	Prezant, DJ (reprint author), Montefiore Med Ctr, Div Pulm, Centennial 423, Bronx, NY 10467 USA.				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Engl. J. Med.	SEP 12	2002	347	11					806	815		10.1056/NEJMoa021300		10	Medicine, General & Internal	General & Internal Medicine	592DK	WOS:000177921300005	12226151	
J	Cork, MJ; Robinson, DA; Vasilopoulos, Y; Ferguson, A; Moustafa, M; MacGowan, A; Duff, GW; Ward, SJ; Tazi-Ahnini, R				Cork, Michael J.; Robinson, Darren A.; Vasilopoulos, Yiannis; Ferguson, Adam; Moustafa, Manar; MacGowan, Alice; Duff, Gordon W.; Ward, Simon J.; Tazi-Ahnini, Rachid			New perspectives on epidermal barrier dysfunction in atopic dermatitis: Gene-environment interactions	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						atopic dermatitis; eczema; environmental triggers; genome; proteases; protease inhibitors; skin barrier dysfunction; topical corticosteroids	CORNEUM CHYMOTRYPTIC ENZYME; MAST-CELL CHYMASE; SKIN IN-VIVO; CUTANEOUS PERMEABILITY BARRIER; CORTICOSTEROID-INDUCED ATROPHY; CLINICALLY UNINVOLVED SKIN; THIN-LAYER CHROMATOGRAPHY; HUMAN STRATUM-CORNEUM; DUST-MITE ALLERGEN; NETHERTON-SYNDROME	Atopic dermatitis (AD) is a multifactorial, chronic inflammatory skin disorder in which genetic mutations and cutaneous hyperreactivity to environmental stimuli play a causative role. Genetic mutations alone might not be enough to cause clinical manifestations of AD, and this review will propose a new perspective on the importance of epidermal barrier dysfunction in genetically predisposed individuals, predisposing them to the harmful effects of environmental agents. The skin barrier is known to be damaged in patients with AD, both in acute eczematous lesions and also in clinically unaffected skin. Skin barrier function can be impaired first by a genetic predisposition to produce increased levels of stratum corneum chymotryptic enzyme. This protease enzyme causes premature breakdown of corneodesmosomes, leading to impairment of the epidermal barrier. The addition of environmental interactions, such as washing with soap and detergents, or long-term application of topical corticosteroids can further increase production of stratum corneum chymotryptic enzyme and impair epidermal barrier function. The epidermal barrier can also be damaged by exogenous proteases from house dust mites and Staphylococcus aureus. One or more of these factors in combination might lead to a defective barrier, thereby increasing the risk of allergen penetration and succeeding inflammatory reaction, thus contributing to exacerbations of this disease.	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Allergy Clin. Immunol.	JUL	2006	118	1					3	21		10.1016/j.jaci.2006.04.042		19	Allergy; Immunology	Allergy; Immunology	065UH	WOS:000239184800001	16815133	
J	Weisglas-Kuperus, N; Patandin, S; Berbers, GAM; Sas, TCJ; Mulder, PGH; Sauer, PJJ; Hooijkaas, H				Weisglas-Kuperus, N; Patandin, S; Berbers, GAM; Sas, TCJ; Mulder, PGH; Sauer, PJJ; Hooijkaas, H			Immunologic effects of background exposure to polychlorinated biphenyls and dioxins in Dutch preschool children	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						allergic diseases; antibody levels; breast-feeding; infectious diseases; leucocyte (sub)populations; PCBs; PCDDs; PCDFs	LYMPHOCYTE SUBSETS; OTITIS-MEDIA; INFANTS; ANTIBODIES; DIBENZOFURANS; NETHERLANDS; PREVALENCE; CHILDHOOD; MEASLES; ASTHMA	Prenatal exposure to polychlorinated biphenyls (PCBs) and dioxins is associated with changes in the T-cell lymphocyte population in healthy Dutch infants. We investigated whether these changes persist into later childhood and whether background exposure to PCBs and dioxins is associated with the prevalence of infectious or allergic diseases and humoral immunity at preschool age. The total study group consisted of 207 healthy mother-infant pairs. We estimated prenatal exposure to PCBs and dioxins by the sum of PCBs 118, 138, 153, and 180 (Sigma PCB) in maternal and cord plasma and in breast-fed infants by the dioxin, planar, and mono-ortho PCB toxic equivalent (TEQ) levels in human milk At 42 months of age, current body burden was estimated by the Sigma PCB in plasma. We assessed the prevalence of infectious and allergic diseases by parent questionnaire, and measured humoral immunity by antibody levels for mumps, measles, and rubella after primary vaccination. We performed immunologic marker analyses of lymphocytes in a subgroup of 85 children. Prenatal PCB exposure was associated with an increased number of lymphocytes, T-cells, and CD3CD8(+) (cytotoxic), CD4(+)CD45RO(+) (memory), T-cell receptor (TcR) alpha beta (+), and CD3(+)HLA-DR+ (activated) T cells and lower antibody levels to mumps and measles at preschool age. Adjusted for confounders, prenatal PCB exposure was associated with less shortness of breath with wheeze, and current PCB body burden was associated with a higher prevalence of recurrent middle-ear infections and of chicken pox and a lower prevalence of allergic reactions. A higher dioxin TEQ was associated with a higher prevalence of coughing, chest congestion, and phlegm. We conclude that in Dutch preschool children the effects of perinatal background exposure to PCBs and dioxins persist into childhood and might be associated with a greater susceptibility to infectious diseases. Common infections acquired early in life may prevent the development of allergy, so PCB exposure might be associated with a lower prevalence of allergic diseases.	Univ Rotterdam Hosp, Sophia Childrens Hosp, Rotterdam, Netherlands; Erasmus Univ, Dept Paediat, Div Neonatol, Rotterdam, Netherlands; Natl Inst Publ Hlth & Environm, Dept Clin Vaccine Res, NL-3720 BA Bilthoven, Netherlands; Erasmus Univ, Inst Epidemiol & Biostat, Rotterdam, Netherlands; Erasmus Univ, Dept Immunol, NL-3000 DR Rotterdam, Netherlands	Weisglas-Kuperus, N (reprint author), Sophia Childrens Hosp, Dept Paediat, Div Neonatol, POB 2060, NL-3000 CB Rotterdam, Netherlands.						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G., 1989, HALOGENATED BIPHENYL, P295; WEISGLASKUPERUS N, 1995, PEDIATR RES, V38, P404, DOI 10.1203/00006450-199509000-00022	30	232	239	2	18	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	2000	108	12					1203	1207		10.2307/3434834		5	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	385LJ	WOS:000166005700033	11133402	
J	Buchvald, F; Baraidi, E; Carraro, S; Gaston, B; De Jongste, J; Pijnenburg, MWH; Silkoff, PE; Bisgaard, H				Buchvald, F; Baraidi, E; Carraro, S; Gaston, B; De Jongste, J; Pijnenburg, MWH; Silkoff, PE; Bisgaard, H			Measurements of exhaled nitric oxide in healthy subjects age 4 to 17 years	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						exhaled nitric oxide; children; normal values	EXERCISE-INDUCED BRONCHOCONSTRICTION; ASTHMATIC-CHILDREN; AIR; DECREASES; SENSITIZATION; RHINITIS; ONLINE; VALUES; ADULTS; ATOPY	Background: Fractional exhaled nitric oxide (FENO) is used in monitoring of asthma. Objectives: The aim of this multicenter study was to establish normal values of FENO and assess feasibility in children with a standardized method and equipment approved for clinical use. Methods: FENO was measured in healthy subjects of 4 to 17 years according to American Thoracic Society guidelines (single breath online, exhalation flow 50 mL/s) with a chemilumineseence analyzer (NIOX Exhaled Nitric Oxide Monitoring System, Aerocrine, Sweden) in 3 European and 2 US centers. Each child performed 3 acceptable nitric oxide measurements within 6 attempts and completed an extended International Study of Asthma and Allergy in Children questionnaire. Results: Measurement of FENO was attempted in 522 children. Four hundred five children completed the study according to the protocol. Geometric mean FENO in 405 children was 9.7 pph, and the upper 95% confidence limit was 25.2 pph. FENO increased significantly with age, and higher FENO was seen in children with self-reported rhinitis/conjunctivitis or hay fever. The success rate was age-dependent and improved from 40% in the children 4 years old to almost 100%, front the age of 10 years. The repeatability of 3 approved measurements was 1.6 ppb (95% CI, 1.49-1.64 ppb). Conclusion: FENO in healthy children is below 15 to 25 pph depending on age and self-reported atopy. Measurement of FENO by NIOX is simple and safe and has a good repeatability. Feasibility depends on age and may be difficult in the preschool child.	Copenhagen Univ Hosp, Danish Pediat Asthma Ctr, Studies Asthma Childhood Res Clin, DK-2900 Hellerup, Denmark; Univ Padua, Dept Pediat, Sch Med, Padua, Italy; Univ Virginia, Charlottesville, VA 22903 USA; Erasmus Med Univ Ctr, Sophia Childrens Hosp, Rotterdam, Netherlands; Natl Jewish Med & Res Ctr, Denver, CO USA	Bisgaard, H (reprint author), Copenhagen Univ Hosp, Danish Pediat Asthma Ctr, Studies Asthma Childhood Res Clin, Niels Andersensvej 79, DK-2900 Hellerup, Denmark.		Kronow, Joern/B-1054-2011; Bisgaard, Hans/N-4761-2016	Bisgaard, Hans/0000-0003-4131-7592; BARALDI, EUGENIO/0000-0002-1829-3652; silkoff, philip/0000-0001-6018-5199			ALVING K, 1993, EUR RESPIR J, V6, P1368; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Avital A, 2003, PEDIATR PULM, V36, P433, DOI 10.1002/ppul.10377; Baraldi E, 1999, AM J RESP CRIT CARE, V159, P262; Baraldi E, 2002, EUR RESPIR J, V20, P223, DOI 10.1183/09031936.02.00293102; Baraldi E, 1999, PEDIATR PULM, V27, P54, DOI 10.1002/(SICI)1099-0496(199901)27:1<54::AID-PPUL10>3.0.CO;2-V; Berlyne GS, 2000, J ALLERGY CLIN IMMUN, V106, P638, DOI 10.1067/mai.2000.109622; Bruce C, 2002, THORAX, V57, P361, DOI 10.1136/thorax.57.4.361; Buchvald F, 2003, CLIN EXP ALLERGY, V33, P1735, DOI 10.1111/j.1365-2222.2003.01822.x; Dotsch J, 1996, EUR RESPIR J, V9, P2537, DOI 10.1183/09031936.96.09122537; Franklin PJ, 1999, AM J RESP CRIT CARE, V159, P69; Gratziou C, 1999, EUR RESPIR J, V14, P897, DOI 10.1034/j.1399-3003.1999.14d28.x; Henriksen AH, 1999, EUR RESPIR J, V13, P301, DOI 10.1034/j.1399-3003.1999.13b14.x; Horvath I, 1999, CLIN EXP ALLERGY, V29, P1276; Jobsis Q, 2001, EUR RESPIR J, V17, P898, DOI 10.1183/09031936.01.17508980; Jungersten L, 1997, J APPL PHYSIOL, V82, P760; 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; Kissoon N, 2002, PEDIATR PULM, V33, P283, DOI 10.1002/ppul.10023; Latzin P, 2002, PEDIATR ALLERGY IMMU, V13, P37; Mattes J, 2002, PEDIATR RES, V51, P190, DOI 10.1203/00006450-200202000-00011; Olin AC, 2001, RESP MED, V95, P153, DOI 10.1053/rmed.2000.1010; Piacentini GL, 1998, AM J RESP CRIT CARE, V158, P1299; Pijnenburg MWH, 2002, EUR RESPIR J, V20, P919, DOI 10.1183/09031936.02.01282002; Scollo M, 2000, AM J RESP CRIT CARE, V161, P1047; Silkoff PE, 1997, AM J RESP CRIT CARE, V155, P260; Slutsky AS, 1999, AM J RESP CRIT CARE, V160, P2104; Spergel Jonathan M., 2003, Journal of Allergy and Clinical Immunology, V112, pS118, DOI 10.1016/j.jaci.2003.09.033; ten Hacken NHT, 1998, AM J RESP CRIT CARE, V158, P902; Terada A, 2001, AM J RESP CRIT CARE, V164, P1879; Togashi H, 1997, P NATL ACAD SCI USA, V94, P2676, DOI 10.1073/pnas.94.6.2676; Tsang KW, 2001, LUNG, V179, P83, DOI 10.1007/s004080000050; van Amsterdam JGC, 2003, CLIN EXP ALLERGY, V33, P187, DOI 10.1046/j.1365-2222.2003.01597.x; Van Amsterdam JGC, 1999, ARCH ENVIRON HEALTH, V54, P331; Yates DH, 2001, AM J RESP CRIT CARE, V164, P1043; Zetterquist W, 1999, EUR RESPIR J, V13, P327, DOI 10.1034/j.1399-3003.1999.13b18.x	36	231	246	0	10	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					1130	1136		10.1016/j.jaci.2005.03.020		7	Allergy; Immunology	Allergy; Immunology	935WZ	WOS:000229815400004	15940124	
J	Vozoris, NT; Tarasuk, VS				Vozoris, NT; Tarasuk, VS			Household food insufficiency is associated with poorer health	JOURNAL OF NUTRITION			English	Article						food insecurity; health status; welfare; body mass index; Canada	BODY-MASS INDEX; NUTRITION EXAMINATION SURVEY; CHILDRENS FEEDING PROGRAMS; 3RD NATIONAL-HEALTH; POPULATION HEALTH; UNITED-STATES; ATLANTIC CANADA; FAMILY INCOME; INSECURITY; HUNGER	The purposes of this study were to estimate the prevalence of household food insufficiency in Canada, to identify sociodemographic characteristics of households most likely to report food insufficiency and to examine the relationship between food insufficiency and physical, mental and social health. These objectives were achieved through an analysis of data from the 1996/1997 National Population Health Survey. An estimated 4% of Canadians, 1.1 million people, were found to be living in food-insufficient households. Single-parent families, households reporting their major source of income as welfare, unemployment insurance or workers' compensation, those who did not own their own homes and households in Western Canada were more likely to report food insufficiency. The likelihood of reporting food insufficiency increased dramatically as income adequacy deteriorated. Individuals from food-insufficient households had significantly higher odds of reporting poor/fair health, of having poor functional health, restricted activity and multiple chronic conditions, of suffering from major depression and distress, and of having poor social support. Individuals in food-insufficient households were also more likely to report heart disease, diabetes, high blood pressure and food allergies. Men in food-insufficient households were less likely to be overweight; after adjusting for potentially confounding variables, no other associations were found between food insufficiency and body mass index. These findings suggest that food insufficiency is one dimension of a more pervasive vulnerability to a range of physical, mental and social health problems among households struggling with economic constraints.	Univ Toronto, Fac Med, Dept Nutr Sci, Toronto, ON M5S 3E2, Canada	Tarasuk, VS (reprint author), Univ Toronto, Fac Med, Dept Nutr Sci, Toronto, ON M5S 3E2, Canada.						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J	Howard, TD; Koppelman, GH; Xu, JF; Zheng, SQL; Postma, DS; Meyers, DA; Bleecker, ER				Howard, TD; Koppelman, GH; Xu, JF; Zheng, SQL; Postma, DS; Meyers, DA; Bleecker, ER			Gene-gene interaction in asthma: IL4RA and IL13 in a Dutch population with asthma	AMERICAN JOURNAL OF HUMAN GENETICS			English	Article							SKIN-TEST REACTIVITY; SERUM IGE LEVELS; INTERLEUKIN-4 RECEPTOR; AIRWAY INFLAMMATION; BRONCHIAL RESPONSIVENESS; IL4-RECEPTOR GENE; ATOPIC ASTHMA; ALPHA-GENE; ASSOCIATION; IL-4	Asthma is a common respiratory disease that is characterized by variable airways obstruction caused by acute and chronic bronchial inflammation; associated phenotypes include bronchial hyperresponsiveness (BHR), elevated total serum immunoglobulin E (IgE) levels, and skin tests positive to common allergens. Binding of interleukin-13 (IL13) or interleukin-4 (IL4) to the IL4 receptor (IL4R) induces the initial response for Th2 lymphocyte polarization. Both IL13 and IL4 are produced by Th2 cells and are capable of inducing isotype class-switching of B-cells to produce IgE after allergen exposure. These cytokines also share a common receptor component, IL4R. We have investigated five IL4RA single-nucleotide polymorphisms in a population of Dutch families ascertained through a proband with asthma. By considering the probands and their spouses as an unrelated sample, we observed significant associations of atopy and asthma-related phenotypes with several IL4RA polymorphisms, including S478P and total serum IgE levels (P=.0007). A significant gene-gene interaction between S478P in IL4RA and the - 1111 promoter variation in IL13, previously shown to be associated with BHR (P = .003), was detected. Individuals with the risk genotype for both genes were at almost five times greater risk for the development of asthma compared to individuals with both nonrisk genotypes (P = .0004). These data suggest that variations in IL4RA contribute to elevated total serum IgE levels, and interaction between IL4RA and IL13 markedly increases an individual's susceptibility to asthma.	Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genome, Winston Salem, NC 27157 USA; Univ Groningen Hosp, Dept Pulmonol, Groningen, Netherlands; Beatrixoord, Dept Pulm Rehabil, Haren, Netherlands	Bleecker, ER (reprint author), Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genome, Med Ctr Blvd, Winston Salem, NC 27157 USA.				NHLBI NIH HHS [R01 HL048341, R01 HL066393, R01HL/48341, R01HL/66393]		Aman MJ, 1996, J BIOL CHEM, V271, P29265; Borish LC, 1999, AM J RESP CRIT CARE, V160, P1816; BRUSSELLE G, 1995, AM J RESP CELL MOL, V12, P254; BRUSSELLE GG, 1994, CLIN EXP ALLERGY, V24, P73, DOI 10.1111/j.1365-2222.1994.tb00920.x; BURROWS B, 1989, NEW ENGL J MED, V320, P271, DOI 10.1056/NEJM198902023200502; BURROWS B, 1995, J ALLERGY CLIN IMMUN, V95, P548, DOI 10.1016/S0091-6749(95)70317-9; Deichmann K, 1997, BIOCHEM BIOPH RES CO, V231, P696, DOI 10.1006/bbrc.1997.6115; Deichmann KA, 1998, CLIN EXP ALLERGY, V28, P151; Drazen JM, 1999, NAT GENET, V22, P168, DOI 10.1038/9680; Drysdale CM, 2000, P NATL ACAD SCI USA, V97, P10483, DOI 10.1073/pnas.97.19.10483; Gauchat JF, 1997, EUR J IMMUNOL, V27, P971, DOI 10.1002/eji.1830270425; Graves PE, 2000, J ALLERGY CLIN IMMUN, V105, P506, DOI 10.1067/mai.2000.104940; Grunig G, 1998, SCIENCE, V282, P2261, DOI 10.1126/science.282.5397.2261; Hackstein H, 2001, IMMUNOGENETICS, V53, P264, DOI 10.1007/s002510100324; Heinzmann A, 2000, HUM MOL GENET, V9, P549, DOI 10.1093/hmg/9.4.549; Henderson WR, 2000, J IMMUNOL, V164, P1086; Hershey GKK, 1997, NEW ENGL J MED, V337, P1720, DOI 10.1056/NEJM199712113372403; Howard TD, 2001, AM J RESP CELL MOL, V25, P377; Howard TD, 1999, BIOTECHNIQUES, V26, P380; Kraan TCTMV, 1999, GENES IMMUN, V1, P61; Kruse S, 1999, IMMUNOLOGY, V96, P365; Kruse S, 1999, INT IMMUNOL, V11, P1965, DOI 10.1093/intimm/11.12.1965; Liu X, 2000, J ALLERGY CLIN IMMUN, V106, P167; Mitsuyasu H, 1998, NAT GENET, V19, P119, DOI 10.1038/472; Ober C, 2000, AM J HUM GENET, V66, P517, DOI 10.1086/302781; Panhuysen CIM, 1998, AM J RESP CRIT CARE, V157, P1734; SEARS MR, 1991, NEW ENGL J MED, V325, P1067, DOI 10.1056/NEJM199110103251504; Xu JF, 2000, AM J HUM GENET, V67, P1163, DOI 10.1086/321190; ZAYKIN D, 1995, GENETICA, V96, P169, DOI 10.1007/BF01441162	29	231	253	1	3	UNIV CHICAGO PRESS	CHICAGO	1427 E 60TH ST, CHICAGO, IL 60637-2954 USA	0002-9297			AM J HUM GENET	Am. J. Hum. Genet.	JAN	2002	70	1					230	236		10.1086/338242		7	Genetics & Heredity	Genetics & Heredity	499LD	WOS:000172571900020	11709756	
J	Morgenstern, V; Zutavern, A; Cyrys, J; Brockow, I; Koletzko, S; Kramer, U; Behrendt, H; Herbarth, O; von Berg, A; Bauer, CP; Wichmann, HE; Heinrich, J				Morgenstern, Verena; Zutavern, Anne; Cyrys, Josef; Brockow, Inken; Koletzko, Sibylle; Kraemer, Ursula; Behrendt, Heidrun; Herbarth, Olf; von Berg, Andrea; Bauer, Carl Peter; Wichmann, H. -Erich; Heinrich, Joachim		GINI Study Grp; LISA Study Grp	Atopic diseases, allergic sensitization, and exposure to traffic-related air pollution in children	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						air pollution; GIS; allergic sensitization; allergy	INDIVIDUAL ESTIMATED EXPOSURE; PROSPECTIVE BIRTH COHORT; SOLID FOOD INTRODUCTION; RESPIRATORY HEALTH; SPATIAL VARIABILITY; PARTICULATE MATTER; NITROGEN-DIOXIDE; TERM EXPOSURE; SYMPTOMS; ASTHMA	Rationale: In vitro studies, animal experiments, and human exposure studies have shown how ambient air pollution increases the risk of atopic diseases. However, results derived from observational studies are inconsistent. Objectives: To assess the relationship between individual-based exposure to traffic-related air pollutants and allergic disease outcomes in a prospective birth cohort study during the first 6 years of life. Methods: We studied 2,860 children at the age of 4years and 3,061 at the age of 6 years to investigate atopic diseases and allergic sensitization. Long-term exposure to particulate matter (PM2.5), PM2.5 absorbance, and long-term exposure to nitrogen dioxide (NO2) was assessed at residential addresses using geographic information systems based regression models and air pollution measurements. The distance to the nearest main road was used as a surrogate for traffic-related air pollutants. Measurements and Main Results: Strong positive associations were found between the distance to the nearest main road and asthmatic bronchitis, hay fever, eczema, and sensitization. A distance-dependent relationship could be identified, with the highest odds ratios (ORs) for children living less than 50 m from busy streets. For PM2.5 absorbance, statistically significant effects were found for asthmatic bronchitis (OR, 1.56; 95% confidence interval [CI], 1.03-2.37), hay fever (OR, 1.59; 95% CI, 1.11-2.27), and allergic sensitization to pollen (OR, 1.40; 95% CI, 1.20-1.64). NO2 exposure was associated with eczema, whereas no association was found for allergic sensitization. Conclusions: This study provides strong evidence for increased risk of atopic diseases and allergic sensitization when children are exposed to ambient particulate matter.	[Morgenstern, Verena; Zutavern, Anne; Cyrys, Josef; Wichmann, H. -Erich; Heinrich, Joachim] Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol, D-85764 Neuherberg, Germany; [Zutavern, Anne; Koletzko, Sibylle] Univ Munich, Dr V Hauners Childrens Hosp, Munich, Germany; [Cyrys, Josef] Univ Augsburg, WZU Environm Sci Ctr, Augsburg, Germany; [Brockow, Inken; Bauer, Carl Peter] Tech Univ Munich, Childrens Hosp, Munich, Germany; [Kraemer, Ursula] Inst Umweltmed Forsch, Working Area Epidemiol, Dusseldorf, Germany; [Behrendt, Heidrun] Tech Univ Munich, Div Environm Dermatol & Allergy, ZAUM Ctr Allergy & Environm, Munich, Germany; [Herbarth, Olf] UFZ Helmholtz Ctr Environm Res, UFZ Human Exposure Res & Epidemiol, Leipzig, Germany; [Herbarth, Olf] Univ Leipzig, Fac Med Environm Med & Environm Hyg, Leipzig, Germany; [von Berg, Andrea] Marien Hosp Wesel, Wesel, Germany; [Wichmann, H. -Erich] Univ Munich, Inst Med Data Management, Munich, Germany	Heinrich, J (reprint author), Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol, Ingolstaedter Landstr 1, D-85764 Neuherberg, Germany.	joachim.heinrich@helmholtz-muenchen.de	Weidinger, Stephan/C-8461-2011; Cyrys, Josef/B-5359-2014; Osborne, Nicholas/N-4915-2015; Sack, Ulrich/J-6301-2015; Buters, Jeroen/G-5070-2011	Osborne, Nicholas/0000-0002-6700-2284; Sack, Ulrich/0000-0002-7813-0492; Cyrys, Josef/0000-0002-2105-8696; Traidl-Hoffmann, Claudia/0000-0001-5085-5179			Amann M., 2005, BASELINE SCENARIOS C; Asher MI, 2006, LANCET, V368, P733, DOI 10.1016/S0140-6736(06)69283-0; Bayer-Oglesby L, 2005, ENVIRON HEALTH PERSP, V113, P1632, DOI 10.1289/ehp.8159; Bayer-Oglesby L, 2006, AM J EPIDEMIOL, V164, P1190, DOI 10.1093/aje/kwj338; BEHRENDT H, 1992, INT ARCH ALLERGY IMM, V99, P425; Brauer M, 2007, EUR RESPIR J, V29, P879, DOI 10.1183/09031936.00083406; Brauer M, 2006, ENVIRON HEALTH PERSP, V114, P1414, DOI 10.1289/ehp.9089; Briggs DJ, 1997, INT J GEOGR INF SCI, V11, P699, DOI 10.1080/136588197242158; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; Cyrys J, 2003, J EXPO ANAL ENV EPID, V13, P134, DOI 10.1038/sj.jea.7500262; Cyrys J, 2000, SCI TOTAL ENVIRON, V250, P51, DOI 10.1016/S0048-9697(00)00361-2; de Haar C, 2006, CLIN EXP ALLERGY, V36, P1469, DOI 10.1111/j.1365-2222.2006.02586.x; Filipiak B, 2007, J PEDIATR-US, V151, P352, DOI 10.1016/j.jpeds.2007.05.01; Gehring U, 2002, EUR RESPIR J, V19, P690, DOI 10.1183/09031936.02.01182001; Gilbert NL, 2005, J AIR WASTE MANAGE, V55, P1059; Gordian ME, 2006, J EXPO SCI ENV EPID, V16, P49, DOI 10.1038/sj.jea.7500436; Heinrich J, 2005, OCCUP ENVIRON MED, V62, P517, DOI 10.1136/oem.2004.016766; Heinrich J, 2005, ENVIRON RES, V98, P240, DOI 10.1016/j.envres.2004.08.004; Heinrich Joachim, 2004, Curr Opin Allergy Clin Immunol, V4, P341, DOI 10.1097/00130832-200410000-00003; Hirsch T, 1999, EUR RESPIR J, V14, P669, DOI 10.1034/j.1399-3003.1999.14c29.x; Hochadel M, 2006, ATMOS ENVIRON, V40, P542, DOI 10.1016/j.atmosenv.2005.09.067; Hoek G, 2002, ATMOS ENVIRON, V36, P4077, DOI 10.1016/S1352-2310(02)00297-2; Holguin F, 2007, AM J RESP CRIT CARE, V176, P1236, DOI 10.1164/rccm.200611-1616OC; Janssen NAH, 2003, ENVIRON HEALTH PERSP, V111, P1512, DOI 10.1289/ehp.6243; Jerrett M, 2007, J TOXICOL ENV HEAL A, V70, P200, DOI 10.1080/15287390600883018; Krzyzanowski M., 2005, WHO HLTH EFFECTS TRA; *LAND MUNCH SA, 2001, MUN FACTS FIG; Livingstone AE, 1996, BRIT MED J, V312, P676; McConnell R, 2006, ENVIRON HEALTH PERSP, V114, P766, DOI 10.1289/ehp.8594; Morgenstern V, 2007, EPIDEMIOLOGY, V18, pS10; 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; Oftedal B, 2007, CLIN EXP ALLERGY, V37, P1632, DOI 10.1111/j.1365-2222.2007.02823.x; Penard-Morand C, 2005, CLIN EXP ALLERGY, V35, P1279, DOI 10.1111/j.1365-2222.2005.02336.x; Sagai M, 1996, FREE RADICAL BIO MED, V21, P199, DOI 10.1016/0891-5849(96)00032-9; Svartengren M, 2000, EUR RESPIR J, V15, P716, DOI 10.1034/j.1399-3003.2000.15d15.x; Traidl-Hoffmann C, 2003, INT ARCH ALLERGY IMM, V131, P1, DOI 10.1159/000070428; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; WATKISS P, 2005, CLEAN AIR EUROPE COS; Wyler C, 2000, EPIDEMIOLOGY, V11, P450, DOI 10.1097/00001648-200007000-00015; Zhu YF, 2002, J AIR WASTE MANAGE, V52, P1032; Zutavern A, 2006, PEDIATRICS, V117, P401, DOI 10.1542/peds.2004-2521	42	230	237	12	54	AMER THORACIC SOC	NEW YORK	61 BROADWAY, FL 4, NEW YORK, NY 10006 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	JUN 15	2008	177	12					1331	1337		10.1164/rccm.200701-036OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	310SE	WOS:000256549700007	18337595	
J	Ford, RA; Domeyer, B; Easterday, O; Maier, K; Middleton, J				Ford, RA; Domeyer, B; Easterday, O; Maier, K; Middleton, J			Criteria for development of a database for safety evaluation of fragrance ingredients	REGULATORY TOXICOLOGY AND PHARMACOLOGY			English	Article							IDENTIFYING CONTACT ALLERGENS; EXPERT-SYSTEM RULEBASE; GENOTOXICITY TESTS; CHEMICAL-STRUCTURE; CARCINOGENICITY; MUTAGENICITY	Over 2000 different ingredients are used in the manufacture of fragrances. The majority of these ingredients have been used for many decades. Despite this long history of use, all of these ingredients need continued monitoring to ensure that each ingredient meets acceptable safety standards. As with other large databases of existing chemicals, fulfilling this need requires an organized approach to identify the most important potential hazards. One such approach, specifically considering the dermal route of exposure as the most relevant one for fragrance ingredients, has been developed. This approach provides a rational selection of materials for review and gives guidance for determining the test data that would normally be considered necessary for the elevation of safety under intended conditions of use. As a first step, the process takes into account the following criteria: quantity of use, consumer exposure, and chemical structure. These are then used for the orderly selection of materials for review with higher quantity, higher exposure, and the presence of defined structural alerts all contributing to a higher priority for review. These structural alerts along with certain exposure and volume limits are then used to develop guidelines for determining the quality and quantity of data considered necessary to support an adequate safety evaluation of the chosen materials, taking into account existing data on the substance itself as well as on closely related analogs. This approach can be considered an alternative to testing; therefore, it is designed to be conservative but not so much so as to require excessive effort when not justified. (C) 2000 Academic Press.	Res Inst Fragrance Mat Inc, Hackensack, NJ 07601 USA; Procter & Gamble Co, Ross, OH 45061 USA; Flavors & Fragrances Inc, Union Beach, NJ 07735 USA; Haarmann & Reimer GmbH, D-37603 Holzminden, Germany; Quest Int Ltd, Ashford TN24 0LT, Kent, England	Ford, RA (reprint author), Res Inst Fragrance Mat Inc, 2 Univ Plaza,Suite 406, Hackensack, NJ 07601 USA.						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M., 1981, SPECTROMETRIC IDENTI, P305; Somogyi L. P., 1995, FLAVORS FRAGRANCES; Spielmann H, 1998, TOXICOL IN VITRO, V12, P305, DOI 10.1016/S0887-2333(98)00006-X; TENNANT RW, 1991, MUTAT RES, V257, P209, DOI 10.1016/0165-1110(91)90002-D; Vuilleumier C., 1995, International Journal of Cosmetic Science, V17, P61, DOI 10.1111/j.1467-2494.1995.tb00110.x; WINGROVE AS, 1981, SPECTROSCOPY, V1, P502	38	230	230	0	6	ACADEMIC PRESS INC	SAN DIEGO	525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA	0273-2300			REGUL TOXICOL PHARM	Regul. Toxicol. Pharmacol.	APR	2000	31	2	1				166	181		10.1006/rtph.1999.1362		16	Medicine, Legal; Pharmacology & Pharmacy; Toxicology	Legal Medicine; Pharmacology & Pharmacy; Toxicology	319AK	WOS:000087316700002	10854123	
J	McDonnell, PJ; Jacobs, MR				McDonnell, PJ; Jacobs, MR			Hospital admissions resulting from preventable adverse drug reactions	ANNALS OF PHARMACOTHERAPY			English	Article						adverse drug reaction; hospital admission	INDUCED ILLNESS; EVENTS	BACKGROUND: Adverse drug reactions (ADRs) are a significant cause of hospital admissions. These events can lead to significant morbidity and mortality and financial costs. ADRs that may be preventable might be considered a form of medication error. OBJECTIVE: To assess the potential preventability of ADRs directly related to a patient's hospital admission. METHODS: A retrospective chart review of 437 ADRs occurring during an 11-month period was conducted at a university hospital. A subset of these events leading to hospital admissions was identified for further review. Those that resulted in admission were further examined to determine probability of causality, severity, and preventability. RESULTS: Over 11 months, 158 ADRs were directly related to hospital admission. The relationship of these admissions to drug exposure was determined to be probable or highly probable in 154 (97.4%) of these cases. From this group, 96 (62.3%) of these events were considered potentially preventable, with 23 (24%) considered severe to life-threatening. Characteristics associated with these ADRs included documentation of a toxic drug concentration or abnormal laboratory value (80%), inadequate monitoring of a patient's drug therapy (67%), inappropriate dose (51%), patient noncompliance (33%), drug-drug interaction (26%), contraindication to therapy (3%), and documented allergy (1%). These ADRs resulted in 595 hospital days, with an average length of stay of 6.1 days. CONCLUSIONS: ADRs leading to hospital admissions are often preventable. Approximately 25% of these events were serious to life-threatening. Most resulted from inadequate monitoring of therapy or inappropriate dosing. Patient noncompliance and drug interactions were also common causes. Multidisciplinary prevention strategies among physicians, pharmacists, other healthcare professionals, and patients focusing on communication and education should be targeted.	Temple Univ, Sch Pharm, Philadelphia, PA 19140 USA	McDonnell, PJ (reprint author), Temple Univ, Sch Pharm, 3307 N Broad ST, Philadelphia, PA 19140 USA.						BATES DW, 1995, JAMA-J AM MED ASSOC, V274, P29, DOI 10.1001/jama.274.1.29; BOSH TK, 1992, 49 AM SOC HOSP PHARM; BURNUM JF, 1976, ANN INTERN MED, V85, P80; CARANASOS GJ, 1974, JAMA-J AM MED ASSOC, V228, P713, DOI 10.1001/jama.228.6.713; COLT HG, 1989, J AM GERIATR SOC, V37, P323; Dartnell JGA, 1996, MED J AUSTRALIA, V164, P659; EINARSON TR, 1993, ANN PHARMACOTHER, V27, P832; Institute of Medicine, 1999, ERR HUM BUILD SAF HL; JICK H, 1994, J ALLERGY CLIN IMMUN, V74, P55; JOHNSON JA, 1995, ARCH INTERN MED, V155, P1949, DOI 10.1001/archinte.155.18.1949; LAKSHMANAN MC, 1986, ARCH INTERN MED, V146, P1931, DOI 10.1001/archinte.146.10.1931; Lazarou J, 1998, JAMA-J AM MED ASSOC, V279, P1200, DOI 10.1001/jama.279.15.1200; LEAPE L, 1999, MED ERROR; MELMON KL, 1971, NEW ENGL J MED, V284, P1361; MILLER RR, 1974, ARCH INTERN MED, V134, P219, DOI 10.1001/archinte.134.2.219; NARANJO CA, 1981, CLIN PHARMACOL THER, V30, P239; PORTER J, 1977, JAMA-J AM MED ASSOC, V237, P879, DOI 10.1001/jama.237.9.879; Pouyanne P, 2000, BRIT MED J, V320, P1036, DOI 10.1136/bmj.320.7241.1036; Roughead EE, 1998, MED J AUSTRALIA, V168, P405; Schumock G T, 1992, Hosp Pharm, V27, P538; TALLEY RB, 1974, JAMA-J AM MED ASSOC, V229, P1043; 1969, WHO TECH REP SER, V426, P5	22	229	239	1	12	HARVEY WHITNEY BOOKS CO	CINCINNATI	PO BOX 42696, CINCINNATI, OH 45242 USA	1060-0280			ANN PHARMACOTHER	Ann. Pharmacother.	SEP	2002	36	9					1331	1336		10.1345/aph.1A333		6	Pharmacology & Pharmacy	Pharmacology & Pharmacy	587UA	WOS:000177660600001	12196047	
J	Kilpelainen, M; Terho, EO; Helenius, H; Koskenvuo, M				Kilpelainen, M; Terho, EO; Helenius, H; Koskenvuo, M			Farm environment in childhood prevents the development of allergies	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						allergic conjunctivitis; allergic rhinitis; asthma; atopic dermatitis; epidemiology; family size; farm environment; rural; urban	SKIN-TEST REACTIVITY; HAY-FEVER; RESPIRATORY SYMPTOMS; SIBSHIP SIZE; EAST-GERMANY; FAMILY-SIZE; ASTHMA; ATOPY; PREVALENCE; CHILDREN	Background A protective effect of infections in early life might explain the firmly reported finding of an inverse association between atopic disorders and large sibships. Objective To study the effect of childhood farm, rural non-farm and urban environment, as well as family size and other factors on the occurrence of asthma, wheezing and atopic disorders up to young adulthood. Methods Data on lifetime prevalence of physician-diagnosed asthma, allergic rhinitis and/or allergic conjunctivitis, atopic dermatitis, as well as self-reported episodic wheezing from 10 667 Finnish first-year university students aged 18-24 years were collected by a postal questionnaire. Associations of lifetime prevalence of the diseases with living on a farm, in a rural non-farm and urban environment during childhood were estimated by logistic regression analysis. Adjustment was made for potential confounding by gender, parental atopy, parental education, number of older siblings, day care outside the home and passive smoking. Results The childhood farm environment independently reduced the risk for physician-diagnosed allergic rhinitis and/or allergic conjunctivitis (adjusted odds ratio 0.63, 95% CI 0.50-0.79, P < 0.001), and for diagnosed asthma and episodic wheezing analysed together (OR 0.71, 95% CI 0.54-0.93, P < 0.05), but not for atopic dermatitis during lifetime. Urban childhood environment did not show independent increased risk when compared with rural non-farm residence. The inverse association of sibship size with the occurrence of allergic rhinitis and/or allergic conjunctivitis was found among subjects with one (OR 0.86, 95% CI 0.77-0.96, P < 0.01) or at least four older siblings (OR 0.47, 95% CI 0.26-0.84, P < 0.05). Conclusion Childhood farm environment seems to have a protective effect against allergic rhinitis and/or conjunctivitis, and more weakly against asthma and wheezing irrespective of family size. Environmental exposure to immune modulating agents, such as environmental mycobacteria and actinomycetes, favouring manifestation of a nonatopic phenotype could explain the finding.	Univ Turku, Dept Pulm Dis & Clin Allergol, SF-20500 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.						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Exp. Allergy	FEB	2000	30	2					201	208				8	Allergy; Immunology	Allergy; Immunology	287NF	WOS:000085511600009	10651772	
J	Almqvist, C; Worm, M; Leynaert, B				Almqvist, C.; Worm, M.; Leynaert, B.		Working Grp GA2 LEN WP 25 'Gender'	Impact of gender on asthma in childhood and adolescence: a GA(2)LEN review	ALLERGY			English	Review						adolescence; asthma; child; GA(2)LEN; gender	BODY-MASS INDEX; RESPIRATORY SYMPTOMS; SEX-DIFFERENCES; LUNG-FUNCTION; BIRTH COHORT; BRONCHIAL RESPONSIVENESS; EMERGENCY-DEPARTMENT; DIAGNOSED ASTHMA; SWISS CHILDREN; RISK-FACTORS	A number of studies have shown gender differences in the prevalence of wheeze and asthma. The aim of this review was to examine published results on gender differences in childhood and adolescent asthma incidence and prevalence, define current concepts and to identify new research needs. A Medline search was performed with the search words (gender OR sex) AND (child OR childhood OR adolescence) AND (asthma). Articles that reported on abscence or prescence of gender differences in asthma were included and reviewed, and cross-references were checked. Boys are consistently reported to have more prevalent wheeze and asthma than girls. In adolescence, the pattern changes and onset of wheeze is more prevalent in females than males. Asthma, after childhood, is more severe in females than in males, and is underdiagnosed and undertreated in female adolescents. Possible explanations for this switch around puberty in the gender susceptibility to develop asthma include hormonal changes and gender-specific differences in environmental exposures. This aspect needs consideration of the doctors and allergists who diagnose and treat asthmatic individuals. In conclusion, sex hormones are likely to play an important role in the development and outcome of the allergic immune response and asthma in particular. By obtaining functional data from appropriate models, the exact underlying mechanisms can be unravelled. To examine the effect of gender-specific differences in environmental exposures and changes of asthma prevalence and severity in puberty, larger populations may need to be investigated.	Astrid Lindgren Childrens Hosp, Karolinska Inst, Dept Woman & Child Hlth, SE-17176 Stockholm, Sweden; Astrid Lindgren Childrens Hosp, Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17176 Stockholm, Sweden; Univ Med Berlin, Dept Dermatol & Allergy, Allergy Ctr Charite, Berlin, Germany; INSERM, Natl Inst Hlth & Med Res, U700, Paris, France	Almqvist, C (reprint author), Astrid Lindgren Childrens Hosp, Karolinska Inst, Dept Woman & Child Hlth, Q2-05, SE-17176 Stockholm, Sweden.						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J	Monneret, G; Gravel, S; Diamond, M; Rokach, J; Powell, WS				Monneret, G; Gravel, S; Diamond, M; Rokach, J; Powell, WS			Prostaglandin D-2 is a potent chemoattractant for human eosinophils that acts via a novel DIP receptor	BLOOD			English	Article							5-OXO-6,8,11,14-EICOSATETRAENOIC ACID; PROSTANOID RECEPTORS; HUMAN NEUTROPHILS; L-SELECTIN; HUMAN-PLATELETS; HUMAN AIRWAYS; D SYNTHETASE; MAST-CELLS; INHIBITION; EXPRESSION	Prostaglandin D-2 (PGD(2)) is released following exposure of asthmatics to allergen and acts via the adenylyl cyclase-coupled receptor for PGD(2) (DID receptor). In this study, it is reported that human eosinophils possess this receptor, which would be expected to inhibit their activation. In contrast, it was found that prostaglandin D-2 is a potent stimulator of eosinophil chemotaxis, actin polymerization, CD11b expression, and L-selectin shedding. These responses are specific for eosinophils, as neutrophils display little or no response to prostaglandin D-2 They were not due to interaction with receptors for other prostanoids, as prostaglandins E-2 and F-2 alpha, U46619 (a thromboxane A(2) analogue), and carbaprostacyclin (a prostacyclin analogue) displayed little or no activity. Furthermore, they were not shared by the selective DID receptor agonist BW245C and were not prevented by the selective DID receptor antagonist BWA868C, indicating that they were not mediated by DID receptors. In contrast, the prostaglandin D2 metabolite 13,14-dihydro-15-oxoprostaglandin D-2 induced eosinophil activation but did not stimulate DID receptor-mediated adenosine 3 ' ,5 ' -cyclic monophosphate (cAMP) formation. These results indicate that in addition to the classic inhibitory DID, receptor, eosinophils possess a second, novel DP2 receptor that is associated with PGD(2)-induced cell activation. These 2 receptors appear to interact to regulate eosinophil responses to PGD(2), as blockade of DPI receptor-mediated cAMP production by BWA868C resulted in enhanced DP2 receptor-mediated stimulation of CD11b expression. The balance between DPI and DP2 receptors could determine the degree to which prostaglandin D-2 can activate eosinophils and may play a role in eosinophil recruitment in asthma.	McGill Univ, Meakins Christie Labs, Dept Med, Montreal, PQ H2X 2P2, Canada; Florida Inst Technol, Dept Chem, Melbourne, FL 32901 USA; Florida Inst Technol, Claude Pepper Inst, Melbourne, FL 32901 USA	Powell, WS (reprint author), McGill Univ, Meakins Christie Labs, Dept Med, 3626 St Urbain St, Montreal, PQ H2X 2P2, Canada.				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NW SUITE 200, WASHINGTON, DC 20036 USA	0006-4971			BLOOD	Blood	SEP 15	2001	98	6					1942	1948		10.1182/blood.V98.6.1942		7	Hematology	Hematology	471UV	WOS:000170947800047	11535533	
J	Gent, JF; Triche, EW; Holford, TR; Belanger, K; Bracken, MB; Beckett, WS; Leaderer, BP				Gent, JF; Triche, EW; Holford, TR; Belanger, K; Bracken, MB; Beckett, WS; Leaderer, BP			Association of low-level ozone and fine particles with respiratory symptoms in children with asthma	JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION			English	Article							AFRICAN-AMERICAN CHILDREN; AIR-POLLUTION; MEXICO-CITY; MEDICATION USE; AMBIENT OZONE; 1ST YEAR; PARTICULATE; EXPOSURE; SUMMER; HEALTH	Context Exposure to ozone and particulate matter of 2.5 mum or less (PM2.5) in air at levels above current US Environmental Protection Agency (EPA) standards is a risk factor for respiratory symptoms in children with asthma. Objective To examine simultaneous effects of ozone and PM2.5 at levels below EPA standards on daily respiratory symptoms and rescue medication use among children with asthma. Design, Setting, and Participants Daily respiratory symptoms and medication use were examined prospectively for 271 children younger than 12 years with physician-diagnosed, active asthma residing in southern New England. Exposure to ambient concentrations of ozone and PM2.5 from April 1 through September 30, 2001, was assessed using ozone (peak 1-hour and 8-hour) and 24-hour PM2.5. Logistic regression analyses using generalized estimating equations were performed separately for maintenance medication users (n=130) and nonusers (n=141). Associations between pollutants (adjusted for temperature, controlling for same- and previous-day levels) and respiratory symptoms and use of rescue medication were evaluated. Main Outcome Measures Respiratory symptoms and rescue medication use recorded on calendars by subjects' mothers. Results Mean (SD) levels were 59 (19) ppb (1-hour average) and 51 (16) ppb (8-hour average) for ozone and 13 (8) mug/m(3) for PM2.5. In copollutant models, ozone level but not PM2.5 was significantly associated with respiratory symptoms and rescue medication use among children using maintenance medication; a 50-ppb increase in 1-hour ozone was associated with increased likelihood of wheeze (by 35%) and chest tightness (by 47%). The highest levels of ozone (1-hour or 8-hour averages) were associated with increased shortness of breath and rescue medication use. No significant, exposure-dependent associations were observed for any outcome by any pollutant among children who did not use maintenance medication. Conclusion Asthmatic children using maintenance medication are particularly vulnerable to ozone, controlling for exposure to fine particles, at levels below EPA standards.	Yale Univ, Ctr Perinatal Pediat & Environm Epidemiol, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA; Univ Rochester, Sch Med & Dent, Dept Environm Med, Rochester, NY USA	Gent, JF (reprint author), Yale Univ, Ctr Perinatal Pediat & Environm Epidemiol, Sch Med, Dept Epidemiol & Publ Hlth, 1 Church St,6th Floor, New Haven, CT 06510 USA.		Triche, Elizabeth/I-4986-2014		NIEHS NIH HHS [ES11013, ES01247, ES05410, ES07456]		Allison PD, 1999, LOGISTIC REGRESSION; Belanger K, 2003, AM J EPIDEMIOL, V158, P195, DOI 10.1093/aje/kwg148; *COMM MASS DEP ENV, 2000, AIR QUAL REP; Delfino RJ, 1998, ENVIRON HEALTH PERSP, V106, P751, DOI 10.1289/ehp.98106751; Friedman MS, 2001, JAMA-J AM MED ASSOC, V285, P897, DOI 10.1001/jama.285.7.897; Gent JF, 2002, ENVIRON HEALTH PERSP, V110, pA781; Gielen MH, 1997, AM J RESP CRIT CARE, V155, P2105; Gold DR, 1999, EPIDEMIOLOGY, V10, P8, DOI 10.1097/00001648-199901000-00004; Hanania NA, 1998, CHEST, V114, P752, DOI 10.1378/chest.114.3.752; Kehrl HR, 1999, J ALLERGY CLIN IMMUN, V104, P1198; LIANG KY, 1986, BIOMETRIKA, V73, P13, DOI 10.1093/biomet/73.1.13; Mortimer KM, 2000, AM J RESP CRIT CARE, V162, P1838; Ostro B, 2001, EPIDEMIOLOGY, V12, P200, DOI 10.1097/00001648-200103000-00012; OSTRO BD, 1995, INHAL TOXICOL, V7, P711, DOI 10.3109/08958379509014475; Peters A, 1997, ENVIRON HEALTH PERSP, V105, P430, DOI 10.1289/ehp.97105430; Romieu I, 1997, ARCH ENVIRON HEALTH, V52, P368; Romieu I, 1996, AM J RESP CRIT CARE, V154, P300; *SAS I INC, 2001, SAS VERS 8; SILVERMAN F, 1979, ENVIRON HEALTH PERSP, V29, P131, DOI 10.2307/3429055; SPEKTOR DM, 1988, AM REV RESPIR DIS, V137, P313; *STAT CONN DEP ENV, 1999, ANN AIR QUAL SUMM; Thurston GD, 1997, AM J RESP CRIT CARE, V155, P654; Ulmer C, 1997, PEDIATR PULM, V23, P344, DOI 10.1002/(SICI)1099-0496(199705)23:5<344::AID-PPUL6>3.0.CO;2-K; *US EPA, 1996, EPA600AP93004AC US E	24	227	236	4	29	AMER MEDICAL ASSOC	CHICAGO	515 N STATE ST, CHICAGO, IL 60610 USA	0098-7484			JAMA-J AM MED ASSOC	JAMA-J. Am. Med. Assoc.	OCT 8	2003	290	14					1859	1867		10.1001/jama.290.14.1859		9	Medicine, General & Internal	General & Internal Medicine	729CB	WOS:000185752600026	14532314	
J	Briggs, DJ; de Hoogh, C; Guiliver, J; Wills, J; Elliott, P; Kingham, S; Smallbone, K				Briggs, DJ; de Hoogh, C; Guiliver, J; Wills, J; Elliott, P; Kingham, S; Smallbone, K			A regression-based method for mapping traffic-related air pollution: application and testing in four contrasting urban environments	SCIENCE OF THE TOTAL ENVIRONMENT			English	Article						air pollution; exposure assessment; road traffic; GIS; mapping	NITROGEN-DIOXIDE CONCENTRATIONS; RESPIRATORY HEALTH; UNITED-KINGDOM; CHILDREN; ASTHMA; GIS; SAMPLERS; MODELS; ROADS	Accurate, high-resolution maps of traffic-related air pollution are needed both as a basis for assessing exposures as part of epidemiological studies, and to inform urban air-quality policy and traffic management. This paper assesses the use of a GIS-based, regression mapping technique to model spatial patterns of traffic-related air pollution. The model - developed using data from 80 passive sampler sites in Huddersfield, as part of the SAVIAH (Small Area Variations in Air Quality and Health) project - uses data on traffic flows and land cover in the 300-m buffer zone around each site, and altitude of the site, as predictors of NO, concentrations. It was tested here by application in four urban areas in the UK: Huddersfield (for the year following that used for initial model development), Sheffield, Northampton, and part of London. In each case, a GIS was built in ArcInfo, integrating relevant data on road traffic, urban land use and topography. Monitoring of NO2 was undertaken using replicate passive samplers (in London, data were obtained from surveys carried out as part of the London network). In Huddersfield, Sheffield and Northampton, the model was first calibrated by comparing modelled results with monitored NO2 concentrations at 10 randomly selected sites; the calibrated model was then validated against data from a further 10-28 sites. In London, where data for only 11 sites were available, validation was not undertaken. Results showed that the model performed well in all cases. After local calibration, the model gave estimates of mean annual NO2 concentrations within a factor of 1.5 of the actual mean (approx. 70-90%) of the time and within a factor of 2 between 70 and 100% of the time. r(2) values between modelled and observed concentrations are in the range of 0.58-0.76. These results are comparable to those achieved by more sophisticated dispersion models. The model also has several advantages over dispersion modelling. It is able, for example, to provide high-resolution maps across a whole urban area without the need to interpolate between receptor points. It also offers substantially reduced costs and processing times compared to formal dispersion modelling. It is concluded that the model might thus be used as a means of mapping long-term air pollution concentrations either in support of local authority air-quality management strategies, or in epidemiological studies. (C) 2000 Elsevier Science B.V. All rights reserved.	Univ London Imperial Coll Sci Technol & Med, Dept Epidemiol & Publ Hlth, London W2 1PG, England; Univ Coll Northampton, Nene Ctr Res, Northampton NN2 7AL, England; Univ Hertfordshire, Dept Environm Sci, Hatfield AL10 9AB, Herts, England; Univ Brighton, Sch Construct Geog & Surveying, Brighton BN2 4AT, E Sussex, England	Briggs, DJ (reprint author), Univ London Imperial Coll Sci Technol & Med, Dept Epidemiol & Publ Hlth, Norfolk Pl, London W2 1PG, England.						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Total Environ.	MAY 15	2000	253	1-3					151	167		10.1016/S0048-9697(00)00429-0		17	Environmental Sciences	Environmental Sciences & Ecology	318ZU	WOS:000087315200013	10843339	
J	von Mutius, E				von Mutius, E			The environmental predictors of allergic disease	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						allergy; environment; epidemiology; atopy; asthma	RESPIRATORY SYNCYTIAL VIRUS; SKIN-TEST REACTIVITY; DIESEL EXHAUST PARTICLES; SERUM IGE LEVELS; RISK-FACTORS; PULMONARY-FUNCTION; ATOPIC DISEASE; OZONE EXPOSURE; AIR-POLLUTION; HAY-FEVER	The prevalence of allergic diseases has been on the rise for the last 200 years, when hay fever, an easy and obvious-to-recognize illness, was virtually unknown in Europe and North America. Genetic factors are unlikely to explain these rapid increases, Among the potential environmental factors, exposure to ambient air pollution has been intensely debated, Besides passive smoking, which has convincingly been shown to increase the risk for asthma and bronchial hyperresponsiveness among exposed children, the evidence to suggest that outdoor pollution to sulfur dioxide, particulate matter, diesel exhaust, and ozone is causally related with the inception of allergic diseases is poor. Rather, factors associated with the lifestyle of populations or families, such as socioeconomic status, allergen exposure, sibship size, early childhood infections, dietary habits, and growing up in anthroposophic families or a farming environment, may prove to be of greater relevance. The future challenge is to tackle the complex interplay between environmental factors and genetic determinants that will eventually contribute to a better understanding and to better prevention strategies for such multifactorial conditions as asthma and allergies.	Univ Munich, Childrens Hosp, D-8000 Munich, Germany	von Mutius, E (reprint author), Dr Von Haunerschen Kinderspital, Lindwurmstr 4, D-80337 Munich, Germany.		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Allergy Clin. Immunol.	JAN	2000	105	1	1				9	19		10.1016/S0091-6749(00)90171-4		11	Allergy; Immunology	Allergy; Immunology	278LW	WOS:000084992100002	10629447	
J	Bessac, BF; Sivula, M; Von Hehn, CA; Escalera, J; Cohn, L; Jordt, SE				Bessac, Bret F.; Sivula, Michael; Von Hehn, Christian A.; Escalera, Jasmine; Cohn, Lauren; Jordt, Sven-Eric			TRPA1 is a major oxidant sensor in murine airway sensory neurons	JOURNAL OF CLINICAL INVESTIGATION			English	Article							SENSING ION CHANNELS; GENE-RELATED PEPTIDE; AIRBORNE CHEMICALS; CHLORINE INHALATION; IRRITATION RESPONSE; HYPOCHLOROUS ACID; LONGITUDINAL DISTRIBUTION; RESPIRATORY RESPONSES; COVALENT MODIFICATION; OXIDATIVE STRESS	Sensory neurons in the airways are finely tuned to respond to reactive chemicals threatening airway function and integrity. Nasal trigeminal nerve endings are particularly sensitive to oxidants formed in polluted air and during oxidative stress as well as to chlorine, which is frequently released in industrial and domestic accidents. Oxidant activation of airway neurons induces respiratory depression, nasal obstruction, sneezing, cough, and pain. While normally protective, chemosensory airway reflexes can provoke severe complications in patients affected by inflammatory airway conditions like rhinitis and asthma. Here, we showed that both hypochlorite, the oxidizing mediator of chlorine, and hydrogen peroxide, a reactive oxygen species, activated Ca2+ influx and membrane currents in an oxidant-sensitive subpopulation of chemosensory neurons. These responses were absent in neurons from mice lacking TRPA1, an ion channel of the transient receptor potential (TRP) gene family. TRPA1 channels were strongly activated by hypochlorite and hydrogen peroxide in primary sensory neurons and heterologous cells. In tests of respiratory function, Trpa1(-/-) mice displayed profound deficiencies in hypochlorite- and hydrogen peroxide-induced respiratory depression as well as decreased oxidant-induced pain behavior. Our results indicate that TRPA1 is an oxidant sensor in sensory neurons, initiating neuronal excitation and subsequent physiological responses in vitro and in vivo.	[Bessac, Bret F.; Sivula, Michael; Von Hehn, Christian A.; Escalera, Jasmine; Jordt, Sven-Eric] Yale Univ, Sch Med, Dept Pharmacol, New Haven, CT 06510 USA; [Cohn, Lauren] Yale Univ, Sch Med, Pulm & Crit Care Med Sect, New Haven, CT 06510 USA	Bessac, BF (reprint author), Yale Univ, Sch Med, Dept Pharmacol, New Haven, CT 06510 USA.				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Clin. Invest.	MAY	2008	118	5					1899	1910		10.1172/JCI34192		12	Medicine, Research & Experimental	Research & Experimental Medicine	295QX	WOS:000255490100033	18398506	
J	Pijnenburg, MW; Bakker, EM; Hop, WC; De Jongste, JC				Pijnenburg, MW; Bakker, EM; Hop, WC; De Jongste, JC			Titrating steroids on exhaled nitric oxide in children with asthma - A randomized controlled trial	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						airway hyperresponsiveness; corticosteroids; lung function; symptoms; treatment	AIRWAY INFLAMMATION; CHILDHOOD ASTHMA; BRONCHIAL HYPERRESPONSIVENESS; LONGITUDINAL POPULATION; CLINICAL REMISSION; ALLERGIC-ASTHMA; ATOPIC ASTHMA; LUNG-FUNCTION; RISK-FACTORS; MARKERS	Rationale: Corticosteroids are the antiinflammatory treatment of choice in asthma. Treatment guidelines are mainly symptom-driven but symptoms are not closely related to airway inflammation. The fraction of nitric oxide in exhaled air (F-ENO) is a marker of airway inflammation in asthma. Objective: We evaluated whether titrating steroids on F-ENO improved asthma management in children. Methods: Eighty-five children with atopic asthma, using inhaled steroids, were allocated to a F-ENO group (n = 39) in which treatment decisions were made on both F-ENO and symptoms, or to a symptom group (n = 46) treated on symptoms only. Children were seen eve 3 months over a 1-year period. Measurements: Symptoms were scored during 2 weeks before visits and 4 weeks before the final visit. FeNO was measured at all visits, and airway hyperresponsiveness and FEV1 were measured at the start and end of the study. Primary endpoint was cumulative steroid dose. Results: Changes in steroid dose from baseline did not differ between groups. In the F-ENO group, hyperresponsiveness improved more than in the symptom group (2.5 vs. 1.1 doubling dose, p = 0.04). FEV1 in the F-ENO group improved, and the change in FEV1 was not significantly different between groups. The F-ENO group had 8 severe exacerbations versus 18 in the symptom group. The change in symptom scores did not differ between groups. F-ENO increased in the symptom group; the change in F-ENO from baseline differed between groups (p = 0.02). Conclusion: In children with asthma, 1 year of steroid titration on F-ENO did not result in higher steroid doses and did improve airway hyperresponsiveness and inflammation.	Erasmus Univ, Ctr Med, Sophia Childrens Hosp, Dept Pediat Pediat Resp Med, NL-3000 CB Rotterdam, Netherlands; Erasmus Univ, Ctr Med, Sophia Childrens Hosp, Dept Epidemiol & Biostat, NL-3000 CB Rotterdam, Netherlands	Pijnenburg, MW (reprint author), Erasmus Univ, Ctr Med, Sophia Childrens Hosp, Dept Pediat Pediat Resp Med, POB 2060, NL-3000 CB Rotterdam, Netherlands.	m.pijnenburg@erasmusmc.nl					ALVING K, 1993, EUR RESPIR J, V6, P1368; Baraldi E, 2002, EUR RESPIR J, V20, P223, DOI 10.1183/09031936.02.00293102; Barbato A, 2003, AM J RESP CRIT CARE, V168, P798, DOI 10.1164/rccm.200305-650OC; Beck-Ripp J, 2002, EUR RESPIR J, V19, P1015, DOI 10.1183/09031936.02.01582001; Berlyne GS, 2000, J ALLERGY CLIN IMMUN, V106, P638, DOI 10.1067/mai.2000.109622; Buchvald F, 2005, J ALLERGY CLIN IMMUN, V115, P1130, DOI 10.1016/j.jaci.2005.03.020; Cochrane MG, 2000, CHEST, V117, P542, DOI 10.1378/chest.117.2.542; Delgado-Corcoran Claudia, 2004, Pediatr Crit Care Med, V5, P48, DOI 10.1097/01.CCM.0000105310.00799.51; Djukanovic R, 2002, J ALLERGY CLIN IMMUN, V109, pS539, DOI 10.1067/mai.2002.124568; Green RH, 2002, LANCET, V360, P1715, DOI 10.1016/S0140-6736(02)11679-5; Grol MH, 1999, AM J RESP CRIT CARE, V160, P1830; Hunt J, 2000, J PEDIATR-US, V137, P14, DOI 10.1067/mpd.2000.107526; Kharitonov SA, 2001, AM J RESP CRIT CARE, V163, P1693; Kharitonov SA, 2001, AM J RESP CRIT CARE, V164, P727; Kharitonov SA, 1996, AM J RESP CRIT CARE, V153, P454; Nelson BV, 1997, J PEDIATR-US, V130, P423, DOI 10.1016/S0022-3476(97)70204-X; [Anonymous], 2002, NIH PUBL, V01-4913; Payne DNR, 2001, AM J RESP CRIT CARE, V164, P1376; Piacentini GL, 1999, EUR RESPIR J, V13, P1386, DOI 10.1183/09031936.99.13613919; Pijnenburg MW, 2005, THORAX, V60, P215, DOI 10.1136/thx.2004.023374; PIJNENBURG MW, 2005, P AM THORAC SOC, V2, pA690; Powell H, 2004, COCHRANE DB SYST REV; Rasmussen F, 2002, AM J RESP CRIT CARE, V165, P1480, DOI 10.1164/rccm.2108009; RIJCKEN B, 1995, AM J RESP CRIT CARE, V151, P1377; Roberts G, 2004, THORAX, V59, P752, DOI 10.1136/thx.2003.008722; Sears MR, 2003, NEW ENGL J MED, V349, P1414, DOI 10.1056/NEJMoa022363; SHERRILL D, 1992, PEDIATR PULM, V13, P78, DOI 10.1002/ppul.1950130204; Silvestri M, 2003, PEDIATR PULM, V35, P358, DOI 10.1002/ppul.10264; Smith AD, 2005, NEW ENGL J MED, V352, P2163, DOI 10.1056/NEJMoa043596; Sont JK, 1999, AM J RESP CRIT CARE, V159, P1043; Spallarossa D, 2003, J ASTHMA, V40, P301, DOI 10.1081/JAS-120018629; Strunk RC, 2003, J ALLERGY CLIN IMMUN, V112, P883, DOI 10.1067/mai.2003.1795; Tsai YG, 2001, J PEDIATR-US, V139, P433, DOI 10.1067/mpd.2001.116295; Van den Toorn LM, 2001, AM J RESP CRIT CARE, V164, P2107; van den Toorn LM, 2000, AM J RESP CRIT CARE, V162, P953; van Grunsven PM, 2001, J ASTHMA, V38, P113, DOI 10.1081/JAS-100000028; Verberne AAPH, 1997, AM J RESP CRIT CARE, V156, P688; Ward C, 2002, THORAX, V57, P309, DOI 10.1136/thorax.57.4.309; Warke TJ, 2002, EUR RESPIR J, V19, P284, DOI 10.1183/09031936.02.00882002; Xuan W, 2000, AM J RESP CRIT CARE, V161, P1820; Zacharasiewicz A, 2005, AM J RESP CRIT CARE, V171, P1077, DOI 10.1164/rccm.200409-1242OC	41	225	236	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.	OCT 1	2005	172	7					831	836		10.1164/rccm.200503-458OC		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	967UD	WOS:000232115800009	15976380	
J	Weiland, SK; Bjorksten, B; Brunekreef, B; Cookson, WOC; von Mutius, E; Strachan, DP				Weiland, SK; Bjorksten, B; Brunekreef, B; Cookson, WOC; von Mutius, E; Strachan, DP		International Study Asthma Aller	Phase II of the international study of asthma and allergies in childhood (ISAAC II): rationale and methods	EUROPEAN RESPIRATORY JOURNAL			English	Article						asthma; childhood; eczema; epidemiology; international study of asthma and allergies; in childhood phase II; rhinitis	RESPIRATORY-HEALTH-SURVEY; WORLDWIDE VARIATIONS; BLOOD-PRESSURE; ATOPIC ECZEMA; PREVALENCE; SYMPTOMS; CHILDREN; RHINOCONJUNCTIVITIS	International comparative studies, investigating whether disease incidence or prevalence rates differ between populations and, if so, which factors explain the observed differences, have made important contributions to the understanding of disease aetiology in many areas. In Phase I of the International Study of Asthma and Allergies in Childhood (ISAAC), the prevalence rates of symptoms of asthma, allergic rhinitis and atopic eczema in 13-14-yr-olds, assessed by standardised questionnaires, were found to differ >20-fold between the 155 study centres around the world. Phase II of ISAAC aims to identify determinants of these differences by studying informative populations. A detailed study protocol was developed for use in community-based random samples of children aged 9-11 yrs. The study modules include standardised questionnaires with detailed questions on the occurrence and severity of symptoms of asthma, allergic rhinitis and atopic eczema, their clinical management, and a broad range of previous and current exposure conditions. In addition, standardised protocols were applied for examination of flexural dermatitis, skin-prick testing, bronchial challenge with hypertonic saline, blood sampling for immunoglobulin E analyses and genotyping, and dust sampling for assessment of indoor exposures to allergens and endotoxin. To date, ISAAC II field work had been completed or started in 30 study centres in 22 countries. The majority of centres are in countries that participated in International Study of Asthma and Allergies in Childhood Phase I and reflect almost the full range of the observed variability in Phase I prevalence rates.	Univ Ulm, Dept Epidemiol, D-89081 Ulm, Germany; Univ Munich, Childrens Hosp, D-8000 Munich, Germany; Karolinska Inst, Ctr Allergy Res, Stockholm, Sweden; Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; Univ Utrecht, Inst Risk Assessment Sci, Utrecht, Netherlands; Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England; Univ London St Georges Hosp, Sch Med, London SW17 0RE, England	Weiland, SK (reprint author), Univ Ulm, Dept Epidemiol, Helmholzstr 22, D-89081 Ulm, Germany.	stephan.weiland@medizin.uni-ulm.de	MARTINEZ-GIMENO, ANTONIO/A-9416-2010; Ellwood, Philippa/G-7555-2015; Jones, Marcus/A-3580-2011; Forastiere, Francesco/J-9067-2016; De sario, Manuela/K-1932-2016; Osborne, Nicholas/N-4915-2015	MARTINEZ-GIMENO, ANTONIO/0000-0003-4051-1860; Ellwood, Philippa/0000-0002-1994-4023; Jones, Marcus/0000-0002-8263-1265; Forastiere, Francesco/0000-0002-9162-5684; De sario, Manuela/0000-0002-1117-2735; Osborne, Nicholas/0000-0002-6700-2284; brunekreef, bert/0000-0001-9908-0060			Asher MI, 1998, EUR RESPIR J, V12, P315; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; CHAMBLESS LE, 1985, COMMUN STAT-THEOR M, V14, P1377, DOI 10.1080/03610928508828982; *DEP EP U ULM, INT STUD ASTHM ALL C; DOUWES J, 1995, APPL ENVIRON MICROB, V61, P1763; Janson C, 2001, EUR RESPIR J, V18, P598, DOI 10.1183/09031936.01.00205801; Jarvis D, 2002, EUR RESPIR J, V20, P1071, DOI 10.1183/09031936.02.00046802; Marmot MG, 1998, LANCET, V351, P57, DOI 10.1016/S0140-6736(97)08084-7; Parkin DM, 2002, IARC SCI PUBL, VVIII, P1; Pearce N, 2000, EUR RESPIR J, V16, P420, DOI 10.1183/9031936.00.16337700; PFEFFERMANN D, 1993, INT STAT REV, V61, P317, DOI 10.2307/1403631; RIEDLER J, 1994, AM J RESP CRIT CARE, V150, P1632; Rose G., 1992, STRATEGY PREVENTION; Strachan DP, 1997, PEDIATR ALLERGY IMMU, V8, P161, DOI 10.1111/j.1399-3038.1997.tb00156.x; *U AUCKL, INT STUD ASTHM ALL C; van den Hoogen PCW, 2000, NEW ENGL J MED, V342, P1, DOI 10.1056/NEJM200001063420101; VANSTRIEN RT, 2002, ENV HLTH PERSPECT, V110, P693; Weiland SK, 1999, EUR RESPIR J, V14, P862, DOI 10.1034/j.1399-3003.1999.14d23.x; Williams H, 1999, J ALLERGY CLIN IMMUN, V103, P125, DOI 10.1016/S0091-6749(99)70536-1; Williams HC, 1995, BRIT J DERMATOL, V133, P941, DOI 10.1111/j.1365-2133.1995.tb06930.x; WILLIAMS HC, SO HOW DO I DEFINE A; Wolf-Maier K, 2003, JAMA-J AM MED ASSOC, V289, P2363, DOI 10.1001/jama.289.18.2363; ZHANG L, 1992, P NATL ACAD SCI USA, V89, P5847, DOI 10.1073/pnas.89.13.5847	25	225	234	1	15	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	SEP	2004	24	3					406	412		10.1183/09031936.04.00090303		7	Respiratory System	Respiratory System	852LS	WOS:000223757400017	15358699	
J	Holgate, ST				Holgate, Stephen T.			Epithelium dysfunction in asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						asthma; environment; epithelium; epithelial mesenchymal trophic unit; airway remodeling; origins of asthma; progression of asthma; tight junctions; impaired barrier function	RETICULAR BASEMENT-MEMBRANE; RESOLUTION COMPUTED-TOMOGRAPHY; OBSTRUCTIVE PULMONARY-DISEASE; ALLERGIC AIRWAY INFLAMMATION; LUNG-TRANSPLANT RECIPIENTS; GOBLET CELL HYPERPLASIA; GROWTH-FACTOR RECEPTOR; KILLER T-CELLS; BRONCHIAL EPITHELIUM; EOSINOPHILIC BRONCHITIS	Although asthma is an inflammatory disorder of the conducting airways involving T(H)2-type T cells, there is increasing evidence for an important role played by the epithelium in orchestrating the inflammatory response by interacting with multiple environmental factors to produce a chronic wound scenario involving tissue injury and aberrant repair. Part of this abnormal response is the consequence of impaired barrier function caused by a primary disruption of epithelial tight junctions that allows inhaled substances to pass more easily into the airway wall to interact with immune and inflammatory cells. Aberrant communication between the damaged and stressed epithelium leads to the generation of growth factors that interact with the underlying mesenchyme to promote airway remodeling responses and a more chronic and persistent inflammatory phenotype. Disordered epithelial function with reduced antioxidant defense and impaired capacity to produce primary IFNs may also account for asthmatic susceptibility to air pollution and respiratory virus infection, respectively. Considering asthma as a disease of impaired barrier function opens new opportunities for therapeutic intervention or prevention by agents that could increase the airways resistance to the inhaled environment rather than suppressing the immune or inflammatory response.	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Allergy Clin. Immunol.	DEC	2007	120	6					1233	1246		10.1016/j.jaci.2007.10.025		14	Allergy; Immunology	Allergy; Immunology	241JX	WOS:000251653800001	18073119	
J	Cockcroft, DW; Davis, BE				Cockcroft, Donald W.; Davis, Beth E.			Mechanisms of airway hyperresponsiveness	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						asthma; airway hyperresponsiveness; airway inflammation; airway smooth muscle	LATE ASTHMATIC RESPONSE; INDIRECT BRONCHIAL HYPERRESPONSIVENESS; ALLERGEN-INDUCED INCREASES; SMOOTH-MUSCLE; MONOCLONAL-ANTIBODY; INHALED BUDESONIDE; MAST-CELLS; ADENOSINE 5'-MONOPHOSPHATE; BRONCHOALVEOLAR LAVAGE; TOLUENE DIISOCYANATE	Airway hyperresponsiveness (AHR) to direct (histamine and methacholine) and indirect (exercise, cold air, hyperventilation, AMP) challenges is a universal and defining feature of asthma. One component of AHR is transient or inducible and occurs after allergen exposure, for example, and improves occasionally rapidly after inhaled corticosteroids or environmental control. This transient airway hyperresponsiveness is more marked to the indirect stimuli. There are convincing data linking this component of AHR to airway inflammation; however, the precise mechanisms linking airway inflammation and hyperresponsiveness of the airway smooth muscle are not clear. The other component of AHR is more persistent and is relatively refractory to environmental control and inhaled corticosteroids. This is likely secondary to structural airway changes, which are collectively referred to as airway remodeling, and which are a result of the chronic (rather than the acute) effects of airway inflammation. This persistent AHR is best reflected by airway hyperresponsiveness to direct stimuli such as methacholine. The mechanisms are also uncertain, but reduced airway caliber, increased airway wall thickness, increased airway smooth muscle mass, and perhaps contractility likely all play a role.	Univ Saskatchewan, Div Respirol Crit Care & Sleep Med, Dept Med, Royal Univ Hosp, Saskatoon, SK S7N 0W8, Canada	Cockcroft, DW (reprint author), Univ Saskatchewan, Div Respirol Crit Care & Sleep Med, Dept Med, Royal Univ Hosp, 103 Hosp Dr,Ellis Hall,5th Floor, Saskatoon, SK S7N 0W8, Canada.	cockcroft@sask.usask.ca					Akdis CA, 2006, EUR J PHARMACOL, V533, P69, DOI 10.1016/j.ejphar.2005.12.044; ALTOUNYAN R. E. 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Allergy Clin. Immunol.	SEP	2006	118	3					551	559		10.1016/j.jaci.2006.07.012		9	Allergy; Immunology	Allergy; Immunology	086BV	WOS:000240649000002	16950269	
J	Aalberse, RC; Schuurman, J				Aalberse, RC; Schuurman, J			IgG4 breaking the rules	IMMUNOLOGY			English	Review							FACILITATED ALLERGEN PRESENTATION; HINGE REGION; COMPLEMENT ACTIVATION; BLOCKING ANTIBODY; SEROLOGIC ASPECTS; HUMAN FILARIASIS; IMMUNOGLOBULIN-G; PLASMA-MEMBRANE; DISULFIDE BONDS; ATOPIC DISEASE	Immunoglobulin G4 (IgG4) antibodies have been known for some time to be functionally monovalent. Recently, the structural basis for this monovalency has been elucidated: the in vivo exchange of IgG half-molecules (one H-plus one L-chain) among IgG4. This process results in bispecific antibodies that in most situations will behave as functionally monovalent antibodies. The structural basis for the abnormal behaviour of IgG4 seems to be largely the result of a single amino acid change relative to human IgG1: the change of a proline in core hinge of IgG1 to serine. This results in a marked shift in the equilibrium between interchain disulphide bridges and intrachain disulphide bridges, which for IgG4 results in 25-75% absence of a covalent interaction between the H-chains. Because of strong non-covalent interactions between the CH3 domains (and possibly also between the CH1 domain and the trans-CH2 domain) IgG4 is a stable four-chain molecule and does not easily exchange half-molecules under standard physiological conditions in vitro. We postulate that the exchange is catalysed in vivo by protein disulphide isomerase (PDI) and/or FcRn (the major histocompatibility complex (MHC)-related Fc receptor) during transit of IgG4 in the endosomal pathway in endothelial cells. Because IgG4 is predominantly expressed under conditions of chronic antigen exposure, the biological relevance of this exchange of half-molecules is that it generates antibodies that are unable to form large immune complexes and therefore have a low potential for inducing immune inflammation. In contrast to monovalent immunoglobulin fragments, these scrambled immunoglobulins have a normal half-life. The significance of the ensuing bispecificity needs further evaluation, because thus will be relevant only in situations where high IgG4 responses are found to two unrelated antigens that happen to be present in the body at the same time and place. In this context the significance of IgG4 autoreactivity might have to be re-evaluated. The main function of IgG4, however, is presumably to interfere with immune inflammation induced by complement-fixing antibodies, or, in the case of helminth infection or allergy, by IgE antibodies.	Univ Amsterdam, CLB, Dept Immunopathol, Acad Med Ctr, NL-1066 CX Amsterdam, Netherlands; Univ Amsterdam, Expt & Clin Immunol Lab, Acad Med Ctr, NL-1066 CX Amsterdam, Netherlands	Aalberse, RC (reprint author), Univ Amsterdam, CLB, Dept Immunopathol, Acad Med Ctr, Plesmanlaan 125, NL-1066 CX Amsterdam, Netherlands.		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J	Christman, JW; Sadikot, RT; Blackwell, TS				Christman, JW; Sadikot, RT; Blackwell, TS			The role of nuclear factor-kappa B in pulmonary diseases	CHEST			English	Article						air pollution; ARDS; asbestosis; asthma; ozone; respiratory syncytial virus; rhinovirus; sepsis; silicosis	RESPIRATORY SYNCYTIAL VIRUS; BRONCHIAL EPITHELIAL-CELLS; DNA-BINDING ACTIVITY; TRANSCRIPTION FACTORS; ALVEOLAR MACROPHAGES; GENE-EXPRESSION; RAT LUNG; PSEUDOMONAS-AERUGINOSA; INTERLEUKIN-8 GENE; OXIDATIVE STRESS	Nuclear factor-kappa B (NF-kappa B) is a family of DNA-binding protein factors that are required for transcription of most proinflammatory molecules, including adhesion molecules, enzymes, cytokines, and chemokines. NF-kappa B activation seems to be a key early event in a variety of cell and animal model systems developed to elucidate the pathobiology of lung diseases. The purpose of this short review is to describe what is known about the molecular biology of NF-kappa B and to review information that implicates NF-kappa B in the pathogenesis of lung disease, including ARDS, systemic inflammatory response syndrome, asthma, respiratory viral infections, occupational and environmental lung disease, and cystic fibrosis.	Vanderbilt Univ, Sch Med, Div Allergy Pulm & Crit Care Med, Dept Med, Nashville, TN USA; Dept Vet Affairs Med Ctr, Nashville, TN 37212 USA	Christman, JW (reprint author), Vanderbilt Univ, Sch Med, Div Allergy Pulm & Crit Care Med, Dept Med, T-1217 MCN, Nashville, TN USA.				NHLBI NIH HHS [HL 07123, HL 61419]		Biagioli MC, 1999, FREE RADICAL BIO MED, V26, P454, DOI 10.1016/S0891-5849(98)00233-0; Bitko V, 1997, VIROLOGY, V232, P369, DOI 10.1006/viro.1997.8582; Blackwell TS, 1999, CHEST, V116, p73S, DOI 10.1378/chest.116.suppl_1.73S; Blackwell TS, 1997, AM J RESP CELL MOL, V17, P3; Bohrer H, 1997, J CLIN INVEST, V100, P972, DOI 10.1172/JCI119648; Christman JW, 1998, INTENS CARE MED, V24, P1131, DOI 10.1007/s001340050735; Christman JW, 1999, AM J RESP CRIT CARE, V159, pA382; DEMARTIN R, 1993, EMBO J, V12, P2773; DiMango E, 1998, J CLIN INVEST, V101, P2598, DOI 10.1172/JCI2865; Farver CF, 1998, CYTOKINE, V10, P868, DOI 10.1006/cyto.1998.0373; Fiedler MA, 1996, AM J PHYSIOL-LUNG C, V271, pL963; Garofalo R, 1996, J VIROL, V70, P8773; Ghio AJ, 1996, AM J RESP CRIT CARE, V154, P783; Gilmour PS, 1997, ENVIRON HEALTH PERSP, V105, P1313, DOI 10.2307/3433553; Gius D, 1999, TOXICOL LETT, V106, P93, DOI 10.1016/S0378-4274(99)00024-7; Graziano FM, 1999, ALLERGY ASTHMA PROC, V20, P141, DOI 10.2500/108854199778553055; Haddad EB, 1996, FEBS LETT, V379, P265, DOI 10.1016/0014-5793(95)01524-8; Hancox RJ, 1999, THORAX, V54, P488; Hart LA, 1998, AM J RESP CRIT CARE, V158, P1585; JANSSEN YMW, 1995, P NATL ACAD SCI USA, V92, P8458, DOI 10.1073/pnas.92.18.8458; Janssen YMW, 1997, AM J PATHOL, V151, P389; Jaspers I, 1998, J CELL PHYSIOL, V177, P313, DOI 10.1002/(SICI)1097-4652(199811)177:2<313::AID-JCP13>3.0.CO;2-A; Jaspers I, 1997, AM J PHYSIOL-LUNG C, V272, pL504; Kennedy T, 1998, AM J RESP CELL MOL, V19, P366; LEBAIL O, 1993, EMBO J, V12, P5043; Lentsch AB, 1999, AM J RESP CELL MOL, V20, P692; Li JD, 1998, P NATL ACAD SCI USA, V95, P5718, DOI 10.1073/pnas.95.10.5718; Liu SF, 1997, BRIT J PHARMACOL, V121, P1241; Luster Michael I., 1998, Toxicology Letters (Shannon), V102-103, P271, DOI 10.1016/S0378-4274(98)00321-X; Mastronarde JG, 1996, J INFECT DIS, V174, P262; Mercurio F, 1999, CURR OPIN CELL BIOL, V11, P226, DOI 10.1016/S0955-0674(99)80030-1; Papi A, 1999, J BIOL CHEM, V274, P9707, DOI 10.1074/jbc.274.14.9707; Quay JL, 1998, AM J RESP CELL MOL, V19, P98; SACHS M, 1998, BIOCHEM BIOPH RES CO, V253, P181; SCHMITZ ML, 1991, EMBO J, V10, P3805; Schwartz MD, 1996, CRIT CARE MED, V24, P1285, DOI 10.1097/00003246-199608000-00004; SIEBENLIST U, 1994, ANNU REV CELL BIOL, V10, P405, DOI 10.1146/annurev.cb.10.110194.002201; Simeonova PP, 1997, J IMMUNOL, V159, P3921; Simeonova PP, 1996, AM J RESP CELL MOL, V15, P787; Stacey MA, 1997, BIOCHEM BIOPH RES CO, V236, P522, DOI 10.1006/bbrc.1997.6997; Suyang H, 1996, MOL CELL BIOL, V16, P5444; Takizawa H, 1999, J IMMUNOL, V162, P4705; Thomas LH, 1998, J IMMUNOL, V161, P1007; Venkatakrishnan A, 1999, AM J RESP CRIT CARE, V159, pA270; Zhao QY, 1998, AM J PHYSIOL-LUNG C, V274, pL39	45	224	265	2	11	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	MAY	2000	117	5					1482	1487		10.1378/chest.117.5.1482		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	315DL	WOS:000087097300041	10807839	
J	Ito, K; Chung, KF; Adcock, IM				Ito, K; Chung, KF; Adcock, IM			Update on glucocorticoid action and resistance	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						severe asthma; steroid resistance; glucocorticoid receptor; molecular mechanisms; future therapies	NF-KAPPA-B; OBSTRUCTIVE PULMONARY-DISEASE; STEROID-INSENSITIVE ASTHMA; HISTONE DEACETYLASE ACTIVITY; COLONY-STIMULATING FACTOR; BLOOD MONONUCLEAR-CELLS; PITUITARY-ADRENAL AXIS; RECEPTOR-BETA-ISOFORM; LIGAND-BINDING DOMAIN; NECROSIS-FACTOR-ALPHA	Extensive development of inhaled and oral glucocorticoids has resulted in highly potent molecules that have been optimized to target activity to the lung and minimize systemic exposure. These have proved highly effective for most asthmatic subjects, but despite these developments, there are a number of subjects with asthma who fail to respond to even high doses of inhaled or even oral glucocorticoids. Advances in delineating the fundamental mechanisms of glucocorticoid pharmacology, especially the concepts of transactivation and transrepression and cofactor recruitment, have resulted in better understanding of the molecular mechanisms whereby glucocorticoids suppress inflammation. The existence of multiple mechanisms underlying glucocorticoid insensitivity raises the possibility that this might indeed reflect different diseases with a common phenotype, and studies examining the efficacy of potential new agents should be targeted toward subgroups of patients with severe corticosteroid-resistant asthma who clearly require effective new drugs and other approaches to improved asthma control.	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Allergy Clin. Immunol.	MAR	2006	117	3					522	543		10.1016/j.jaci.2006.01.032		22	Allergy; Immunology	Allergy; Immunology	025JY	WOS:000236263100006	16522450	
J	Chehade, M; Mayer, L				Chehade, M; Mayer, L			Oral tolerance and its relation to food hypersensitivities	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						oral tolerance; food allergy; food hypersensitivity; mucosal immunity; antigen uptake; intestine	REGULATORY T-CELLS; TRANSFORMING GROWTH FACTOR-BETA-1; TRANSEPITHELIAL ANTIGEN TRANSPORT; INFLAMMATORY-BOWEL-DISEASE; MYELIN BASIC-PROTEIN; DENDRITIC CELLS; PEYERS-PATCHES; MURINE MODEL; ACTIVE SUPPRESSION; IMMUNE TOLERANCE	The gastrointestinal tract is the largest immunologic organ in the body. It is constantly bombarded by a myriad of dietary proteins. Despite the extent of protein exposure, very few patients have food allergies because of development of oral tolerance to these antigens. Once proteins contact the intestinal surface, they are sampled by different cells and, depending on their characteristics, result in different responses. Antigens might be taken up by Microfold cells overlying Peyer's patches, dendritic cells, or epithelial cells. Different cells of the immune system participate in oral tolerance induction, with regulatory T cells being the most important. Several factors can influence tolerance induction. Some are antigen related, and others are inherent to the host. Disturbances at different steps in the path to oral tolerance have been described in food hypersensitivity. In this review we provide an overview of oral tolerance and cite data related to food hypersensitivity wherever evidence available.	CUNY Mt Sinai Sch Med, Div Allergy Immunol, Dept Pediat, New York, NY 10029 USA; CUNY Mt Sinai Sch Med, Div Gastroenterol, Dept Pediat, New York, NY 10029 USA; CUNY Mt Sinai Sch Med, Dept Med, Div Clin Immunol, New York, NY 10029 USA; CUNY Mt Sinai Sch Med, Dept Immunobiol, Div Clin Immunol, New York, NY 10029 USA	Chehade, M (reprint author), CUNY Mt Sinai Sch Med, Div Allergy Immunol, Dept Pediat, 1 Gustave L Levy Pl, New York, NY 10029 USA.	mima.chehade@mssm.edu			NIAID NIH HHS [AI 44236]		Appleman LJ, 2003, IMMUNOL REV, V192, P161, DOI 10.1034/j.1600-065X.2003.00009.x; Asano M, 1996, J EXP MED, V184, P387, DOI 10.1084/jem.184.2.387; Barone KS, 2000, CELL IMMUNOL, V199, P65, DOI 10.1006/cimm.1999.1603; BARONE KS, 1995, CELL IMMUNOL, V163, P19, DOI 10.1006/cimm.1995.1094; Bashir MEH, 2004, J IMMUNOL, V172, P6978; Bennett CL, 2001, NAT GENET, V27, P20; Berin MC, 1998, J IMMUNOL, V161, P2561; Beyer K, 2002, J ALLERGY CLIN IMMUN, V109, P707, DOI 10.1067/mai.2002.122503; BLAND PW, 1986, IMMUNOLOGY, V58, P9; 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Allergy Clin. Immunol.	JAN	2005	115	1					3	12		10.1016/j.jaci.2004.11.008		10	Allergy; Immunology	Allergy; Immunology	886XS	WOS:000226267000001	15637539	
J	Bass, JL; Corwin, M; Gozal, D; Moore, C; Nishida, H; Parker, S; Schonwald, A; Wilker, RE; Stehle, S; Kinane, TB				Bass, JL; Corwin, M; Gozal, D; Moore, C; Nishida, H; Parker, S; Schonwald, A; Wilker, RE; Stehle, S; Kinane, TB			The effect of chronic or intermittent hypoxia on cognition in childhood: A review of the evidence	PEDIATRICS			English	Review						hypoxia; cognition; development; behavior; academic achievement	OBSTRUCTIVE SLEEP-APNEA; CONGENITAL HEART-DISEASE; DEFICIT-HYPERACTIVITY DISORDER; OXYGEN-SATURATION; TERM INFANTS; RESPIRATORY INSTABILITY; ACADEMIC-PERFORMANCE; SCHOOL PERFORMANCE; PROSPECTIVE COHORT; MOTOR DEVELOPMENT	Objective. A review of the evidence concerning the effect of chronic or intermittent hypoxia on cognition in childhood was performed by using both a systematic review of the literature and critical appraisal criteria of causality. Because of the significant impact of behavioral disorders such as attention-deficit/hyperactivity disorder on certain cognitive functions as well as academic achievement, the review also included articles that addressed behavioral outcomes. Methods. Both direct and indirect evidence were collected. A structured Medline search was conducted from the years 1966-2000 by using the OVID interface. Both English- and non - English- language citations were included. Significant articles identified by the reviewers up to 2003 were also included. To be included as direct evidence, an article needed to be an original report in a peer-reviewed journal with data on cognitive, behavioral, or academic outcomes in children up to 14 years old, with clinical conditions likely to be associated with exposure to chronic or intermittent hypoxia. Indirect evidence from other reviews and publications in closely related fields, including experimental studies in adults, was used to help formulate conclusions. Two reviewers screened abstracts and titles. Each article included as direct evidence received a structured evaluation by 2 reviewers. Adjudication of differences was performed by a group of 2 reviewers and a research consultant. After this review, tables of evidence were constructed that were used as the basis for group discussion and consensus development. Indirect evidence assigned by topic to specific reviewers was also presented as part of this process. A formal procedure was used to rank the studies by design strength. The critical appraisal criteria for causation described in Evidence Based Pediatrics and Child Health (Moyer V, Elliott E, Davis R, et al, eds. London, United Kingdom: BMJ Books; 2000: 46 - 55) were used to develop consensus on causality. Results. A total of 788 literature citations were screened. For the final analysis, 55 articles met the criteria for inclusion in the direct evidence. Of these, 43 (78.2%) reported an adverse effect. Of the 37 controlled studies, 31 (83.8%) reported an adverse effect. Adverse effects were noted at every level of arterial oxygen saturation and for exposure at every age level except for premature newborns. The studies were classified into 5 clinical categories: congenital heart disease (CHD), sleep-disordered breathing (SDB), asthma, chronic ventilatory impairment, and respiratory instability in infants. Two of these categories, CHD and SDB, which accounted for 42 (76.4%) of the included articles, fulfilled the Evidence Based Pediatrics and Child Health criteria for causation. The indirect evidence included 8 reviews, 1 meta-analysis, and 10 original reports covering the fields of adult anoxia, animal research, SDB in adults, natural and experimental high-altitude studies, perinatal hypoxic-ischemic encephalopathy, anemia, and carbon-monoxide poisoning. The studies of high-altitude and carbon-monoxide poisoning provided evidence for causality. Conclusions. Adverse impacts of chronic or intermittent hypoxia on development, behavior, and academic achievement have been reported in many well-designed and controlled studies in children with CHD and SDB as well as in a variety of experimental studies in adults. This should be taken into account in any situation that may expose children to hypoxia. Because adverse effects have been noted at even mild levels of oxygen desaturation, future research should include precisely defined data on exposure to all levels of desaturation.	Harvard Univ, Sch Med, MassGen Hosp Children, Newton Wellesley Hosp,Dept Pediat, Newton, MA 02462 USA; Boston Univ, Sch Med, CareStat Inc, Boston Med Ctr,Dept Pediat, Newton, MA USA; Univ Louisville, Kosair Childrens Hosp Res Inst, Dept Pediat, Louisville, KY 40292 USA; Tokyo Womens Med Univ, Maternal & Perinatal Ctr, Tokyo, Japan; Boston Univ, Sch Med, Boston Med Ctr, Dept Pediat, Boston, MA 02118 USA; Harvard Univ, Sch Med, Childrens Hosp, Med Ctr,Dev Med Ctr, Boston, MA USA; Greater Lawrence Family Hlth Ctr, Lawrence, MA USA; Harvard Univ, Sch Med, MassGen Hosp Children, Boston, MA USA	Bass, JL (reprint author), Harvard Univ, Sch Med, MassGen Hosp Children, Newton Wellesley Hosp,Dept Pediat, 2014 Washington St, Newton, MA 02462 USA.	jbass@partners.org		Corwin, Michael/0000-0002-6591-209X			AISENBERG RB, 1982, PEDIATR CARDIOL, V3, P133; AISENBERG RB, 1977, AM J DIS CHILD, V45, P595; AISENBERG RB, 1994, AM J DIS CHILD, V128, P335; ALI NJ, 1994, ARCH DIS CHILD, V71, P74; Ali NJ, 1996, EUR J PEDIATR, V155, P56, DOI 10.1007/BF02309859; 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J	Dick, CAJ; Brown, DM; Donaldson, K; Stone, V				Dick, CAJ; Brown, DM; Donaldson, K; Stone, V			The role of free radicals in the toxic and inflammatory effects of four different ultrafine particle types	INHALATION TOXICOLOGY			English	Article							PARTICULATE AIR-POLLUTION; NF-KAPPA-B; OXIDATIVE STRESS; CARBON-BLACK; TRANSITION-METALS; INTRATRACHEAL INSTILLATION; SURFACE-AREA; EXPOSURE; LUNG; GLUTATHIONE	PM10 contains an ultrafine component, which is generally derived from combustion processes. This ultrafine fraction may be a factor in the increases in exacerbations of respiratory disease and deaths from cardiorespiratory causes associated with transient increases in levels of PM10. By using four different ultrafine particles (carbon black, cobalt, nickel, and titanium dioxide), we set out to determine the attributes of the ultrafine particle (surface area, chemical composition, particle number, or surface reactivity) that contribute most to its toxicity and proinflammatory effects both in vivo and in vitro. Instillation of 125 mug ultrafine carbon black (UFCB) and ultrafine cobalt (UFCo) particles induced a significant influx of neutrophils at both 4 and 18 h postinstillation. Accompanying the influx of neutrophils was an increase in macrophage inflammatory protein-2 (MIP-2) (at 4 h) and an increase in gamma-glutamyl transpeptidase (at 18 h) in bronchoalveolar lavage fluid (BAL). Ultrafine nickel (UFNi) did not induce a significant increase in neutrophil influx until 18 h postinstillation. The increase in neutrophils induced by UFNi at this timepoint was comparable to that induced by UFCo and UFCB. UFTi did not induce a significant increase in neutrophils following instillation into the rat lung. The levels of MIP-2 observed at 4 h and neutrophil influx at 18 h induced by the particle samples were consistent with the pattern of surface free radical generation (as measured by the plasmid scission assay) whereby UFCo, UFCB, and UFNi all cause significant increases in inflammatory markers, as well as inducing a significant depletion of supercoiled plasmid DNA, indicative of hydroxyl radical generation. A role for free radicals and reactive oxygen species (ROS) in mediating ultrafine inflammation is further strengthened by the ability of the antioxidants N-acetylcysteine (NAC) and glutathione monoethyl ester (GSHme) to block the particle induced release of tumour necrosis factor-alpha (TNF-alpha) from alveolar macrophages in vitro. The ultrafine particles in PM10 may cause adverse effects via oxidative stress, and this could have implications for susceptible individuals. Susceptible individuals, such as those with COPD or asthma, already exhibit preexisting oxidative stress and hence are in a primed state for further oxidative stress induced by occupational or environmental particles.	Napier Univ, Sch Life & Hlth Sci, Edinburgh EH14 1DJ, Midlothian, Scotland	Scottish Biomed, Todd Campus,W Scotland Sci Pk,G200X, Glasgow, Lanark, Scotland.	colin.dick@scottish-biomedical.com					Beck-Speier I, 2001, ENVIRON HEALTH PERSP, V109, P613, DOI 10.2307/3454679; Brown DM, 2001, TOXICOL APPL PHARM, V175, P191, DOI 10.1006/taap.2001.9240; Brown DM, 2000, OCCUP ENVIRON MED, V57, P685, DOI 10.1136/oem.57.10.685; Bucher JR, 1999, TOXICOL SCI, V49, P56, DOI 10.1093/toxsci/49.1.56; Carter JD, 1997, TOXICOL APPL PHARM, V146, P180, DOI 10.1006/taap.1997.8254; Costa DL, 1997, ENVIRON HEALTH PERSP, V105, P1053, DOI 10.2307/3433509; Dennekamp M, 2001, OCCUP ENVIRON MED, V58, P511, DOI 10.1136/oem.58.8.511; *DEP HLTH, 1993, ADV GROUP MED ASP AI; Donaldson K, 1998, J AEROSOL SCI, V29, P553, DOI 10.1016/S0021-8502(97)00464-3; Donaldson K, 1997, ENVIRON HEALTH PERSP, V105, P1285, DOI 10.2307/3433548; Donaldson K, 1996, TOXICOL LETT, V88, P293, DOI 10.1016/0378-4274(96)03752-6; Driscoll KE, 2000, TOXICOL LETT, V112, P177, DOI 10.1016/S0378-4274(99)00282-9; FERIN J, 1992, AM J RESP CELL MOL, V6, P535; Gilmour PS, 1997, ENVIRON HEALTH PERSP, V105, P1313, DOI 10.2307/3433553; GRATTAGLIANO I, 1995, J PHARMACOL EXP THER, V272, P484; HALLIWELL B, 1989, FREE RADICAL BIO MED, V2, P1; Jimenez LA, 2000, TOXICOL APPL PHARM, V166, P101, DOI 10.1006/taap.2000.8957; Lay JC, 1999, AM J RESP CELL MOL, V20, P631; Li XY, 1999, INHAL TOXICOL, V11, P709; Li XY, 1996, THORAX, V51, P1216, DOI 10.1136/thx.51.12.1216; Lundborg M, 1999, ENVIRON RES, V81, P309, DOI 10.1006/enrs.1999.3992; MACNEE W, 1991, AM J MED, V91, P60; NOLAN RP, 1987, BRIT J IND MED, V44, P687; Oberdorster G, 1996, PARTICUL SCI TECHNOL, V14, P135, DOI 10.1080/02726359608906690; Pahl HL, 1997, TRENDS BIOCHEM SCI, V22, P63, DOI 10.1016/S0968-0004(96)10073-6; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Rahman I, 2000, EUR RESPIR J, V16, P534, DOI 10.1034/j.1399-3003.2000.016003534.x; Rahman I, 2001, BIOCHEM PHARMACOL, V62, P787, DOI 10.1016/S0006-2952(01)00702-X; Rice TM, 2001, TOXICOL APPL PHARM, V177, P46, DOI 10.1006/taap.2001.9287; SCHRECK R, 1992, FREE RADICAL RES COM, V17, P221, DOI 10.3109/10715769209079515; SEATON A, 1995, LANCET, V345, P176, DOI 10.1016/S0140-6736(95)90173-6; Serita F, 1999, IND HEALTH, V37, P353, DOI 10.2486/indhealth.37.353; Soukup JM, 2001, TOXICOL APPL PHARM, V171, P20, DOI 10.1006/taap.2000.9096; Stone V, 1998, TOXICOL IN VITRO, V12, P649, DOI 10.1016/S0887-2333(98)00050-2; Stone V, 2000, EUR RESPIR J, V15, P297, DOI 10.1034/j.1399-3003.2000.15b13.x; Tran CL, 2000, INHAL TOXICOL, V12, P1113, DOI 10.1080/08958370050166796; Zhang QW, 1998, J TOXICOL ENV HEAL A, V53, P423; Zhang QW, 1998, J OCCUP HEALTH, V40, P171, DOI 10.1539/joh.40.171	38	223	239	4	33	TAYLOR & FRANCIS LTD	ABINGDON	2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND	0895-8378	1091-7691		INHAL TOXICOL	Inhal. Toxicol.	JAN	2003	15	1					39	52		10.1080/08958370304454		14	Toxicology	Toxicology	627CR	WOS:000179911900003	12476359	
J	Melani, AS; Bonavia, M; Cilenti, V; Cinti, C; Lodi, M; Martucci, P; Serra, M; Scichilone, N; Sestini, P; Aliani, M; Neri, M				Melani, Andrea S.; Bonavia, Marco; Cilenti, Vincenzo; Cinti, Cristina; Lodi, Marco; Martucci, Paola; Serra, Maria; Scichilone, Nicola; Sestini, Piersante; Aliani, Maria; Neri, Margherita		Grp Educ Assoc Italiana Pneumologi	Inhaler mishandling remains common in real life and is associated with reduced disease control	RESPIRATORY MEDICINE			English	Article						Asthma; COPD; MDI; DPI; Inhaler technique; Patient education	METERED-DOSE INHALER; DRY POWDER INHALERS; INHALATION TECHNIQUE; DRUG-DELIVERY; CLINICAL CONSEQUENCES; LUNG DEPOSITION; PATIENT; ASTHMA; MISUSE; VOLUMES	Proper inhaler technique is crucial for effective management of asthma and COPD. This multi-centre, cross-sectional, observational study investigates the prevalence of inhaler mishandling in a large population of experienced patients referring to chest clinics; to analyze the variables associated with misuse and the relationship between inhaler handling and health-care resources use and disease control. We enrolled 1664 adult subjects (mean age 62 years) affected mostly by COPD (52%) and asthma (42%). Respectively, 843 and 1113 patients were using MDIs and DP's at home; of the latter, the users of Aerolizer (R), Diskus (R), HandiHaler (R) and Turbuhaler (R) were 82, 467, 505 and 361. We have a total of 2288 records of inhaler technique. Critical mistakes were widely distributed among users of all the inhalers, ranging from 12% for MDIs, 35% for Diskus (R) and HandiHaler (R) and 44% for Turbuhaler (R). Independently of the inhaler, we found the strongest association between inhaler misuse and older age (p = 0.008), lower schooling (p = 0.001) and lack of instruction received for inhaler technique by health caregivers (p < 0.001). Inhaler misuse was associated with increased risk of hospitalization (p = 0.001), emergency room visits (p < 0.001), courses of oral steroids (p < 0.001) and antimicrobials (p < 0.001) and poor disease control evaluated as an ACT score for the asthmatics (p < 0.0001) and the whole population (p < 0.0001). We conclude that inhaler mishandling continues to be common in experienced outpatients referring to chest clinics and associated with increased unscheduled health-care resource use and poor clinical control. Instruction by health caregivers is the only modifiable factor useful for reducing inhaler mishandling (C) 2011 Elsevier Ltd. All rights reserved.	[Melani, Andrea S.] Azienda Osped Senese, Policlin Le Scotte, Siena, Italy; [Bonavia, Marco] Osped La Colletta, Arenzano, Ge, Italy; [Cilenti, Vincenzo] IRCCS Regina Elena, Rome, Italy; [Cinti, Cristina] Osped Bellaria, Bologna, Italy; [Lodi, Marco] Osped Copparo, Ferrara, Italy; [Martucci, Paola] Osped Antonio Cardarelli, Ctr Antifumo, Naples, Italy; [Serra, Maria] Osped Villa Scassi, Genoa, Italy; [Scichilone, Nicola] Univ Palermo, Dipartimento Med Pneumol Fisiol & Nutr Umana, I-90133 Palermo, Italy; [Sestini, Piersante] Univ Siena, Clin Malattie Apparato Resp, I-53100 Siena, Italy	Melani, AS (reprint author), Azienda Osped Senese, Policlin Le Scotte, Siena, Italy.	a.melani@ao-siena.toscana.it		Scichilone, Nicola/0000-0001-6400-6573	Chiesi; Artsana; AstraZeneca; GSK; Menarini; Novartis; Pfizer; Abbott	The study was supported from Chiesi, which does not interfere with the study design, analysis and interpretation of the results and writing of the manuscript.; Andrea S Melani has received consulting fees or for lectures from Artsana, AstraZeneca, Chiesi, GSK, Menarini, Novartis, Pfizer.; Margherita Neri has received consulting fees or for lectures from GSK, Menarini, Abbott, Chiesi, AstraZeneca, Pfizer.	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Med.	JUN	2011	105	6					930	938		10.1016/j.rmed.2011.01.005		9	Cardiac & Cardiovascular Systems; Respiratory System	Cardiovascular System & Cardiology; Respiratory System	771DG	WOS:000291136800016	21367593	
J	McConnell, R; Islam, T; Shankardass, K; Jerrett, M; Lurmann, F; Gilliland, F; Gauderman, J; Avol, E; Kunzli, N; Yao, L; Peters, J; Berhane, K				McConnell, Rob; Islam, Talat; Shankardass, Ketan; Jerrett, Michael; Lurmann, Fred; Gilliland, Frank; Gauderman, Jim; Avol, Ed; Kuenzli, Nino; Yao, Ling; Peters, John; Berhane, Kiros			Childhood Incident Asthma and Traffic-Related Air Pollution at Home and School	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; asthma; child; epidemiology; vehicular traffic	CHILDRENS RESPIRATORY HEALTH; NITROGEN-DIOXIDE; ALLERGIC SENSITIZATION; ULTRAFINE PARTICLES; SIZE DISTRIBUTION; PUBLIC-SCHOOLS; MAJOR HIGHWAY; LOS-ANGELES; BUSY ROADS; EXPOSURE	BACKGROUND: Traffic-related air pollution has been associated with adverse cardiorespiratory effects, including increased asthma prevalence. However, there has been little study of effects of traffic exposure at school on new-onset asthma. OBJECTIVES: We evaluated the relationship of new-onset asthma with traffic-related pollution near homes and schools. Methods: Parent-reported physician diagnosis of new-onset asthma (n = 120) was identified during 3 years of follow-up of a cohort of 2,497 kindergarten and first-grade children who were asthma-and wheezing-free at study entry into the Southern California Children's Health Study. We assessed traffic-related pollution exposure based on a line source dispersion model of traffic volume, distance from home and school, and local meteorology. Regional ambient ozone, nitrogen dioxide (NO(2)), and particulate matter were measured continuously at one central site monitor in each of 13 study communities. Hazard ratios (HRs) for new-onset asthma were scaled to the range of ambient central site pollutants and to the residential interquartile range for each traffic exposure metric. RESULTS: Asthma risk increased with modeled traffic-related pollution exposure from roadways near homes [HR 1.51; 95% confidence interval (CI), 1.25-1.82] and near schools (HR 1.45; 95% CI, 1.06-1.98). Ambient NO(2) measured at a central site in each community was also associated with increased risk (HR 2.18; 95% CI, 1.18-4.01). In models with both NO(2) and modeled traffic exposures, there were independent associations of asthma with traffic-related pollution at school and home, whereas the estimate for NO(2) was attenuated (HR 1.37; 95% CI, 0.69-2.71). CONCLUSIONS: Traffic-related pollution exposure at school and homes may both contribute to the development of asthma.	[McConnell, Rob] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA; [Shankardass, Ketan] St Michaels Hosp, Toronto, ON M5B 1W8, Canada; [Jerrett, Michael] Univ Calif Berkeley, Berkeley, CA 94720 USA; [Lurmann, Fred] Sonoma Technol Inc, Petaluma, CA USA; [Kuenzli, Nino] Swiss Trop & Publ Hlth Inst, Basel, Switzerland; [Kuenzli, Nino] Univ Basel, CH-4003 Basel, Switzerland; [Yao, Ling] City Hope Hosp Med Ctr, United Hlth Grp, Los Angeles, CA USA	McConnell, R (reprint author), Univ So Calif, Keck Sch Med, Dept Prevent Med, 1540 Alcazar St,CHP 236, Los Angeles, CA 90033 USA.	rmcconne@usc.edu	Kunzli, Nino/F-7195-2014	Kunzli, Nino/0000-0001-8360-080X	National Institutes of Health [5P30ES007048, 5P01ES009581, 5 P01ES011627, 1R01ES016535, 5R01ES014447, 5R03ES014046, 5R01HL61768]; U.S. Environmental Protection Agency [R826708, RD831861, R831845, R82735201]; South Coast Air Quality Management District; Hastings Foundation	This study was supported by National Institutes of Health grants 5P30ES007048, 5P01ES009581, 5 P01ES011627, 1R01ES016535, 5R01ES014447, 5R03ES014046, and 5R01HL61768; U.S. Environmental Protection Agency grants R826708, RD831861, R831845, and R82735201; the South Coast Air Quality Management District, and the Hastings Foundation.	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J	Schroeder, HW; Cavacini, L				Schroeder, Harry W., Jr.; Cavacini, Lisa			Structure and function of immunoglobulins	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Antibody structure; antibody function; immunoglobulin structure; immunoglobulin function; immunoglobulin gene rearrangement; class switching; somatic hypermutation	MONOCLONAL-ANTIBODY; SOMATIC HYPERMUTATION; IGG1 ANTIBODIES; BINDING; LOCUS; GLYCOSYLATION; DIVERSITY; SEQUENCE; REGION; GENES	Immunoglobulins are heterodimeric proteins composed of 2 heavy and 2 light chains. They can be separated functionally into variable domains that bind antigens and constant domains that specify effector functions, such as activation of complement or binding to Fc receptors. The variable domains are created by means of a complex series of gene rearrangement events and can then be subjected to somatic hypermutation after exposure to antigen to allow affinity maturation. Each variable domain can be split into 3 regions of sequence variability termed the complementarity-determining regions (CDRs) and 4 regions of relatively constant sequence termed the framework regions. The 3 CDRs of the heavy chain are paired with the 3 CDRs of the light chain to form the antigen-binding site, as classically defined. The constant domains of the heavy chain can be switched to allow altered effector function while maintaining antigen specificity. There are 5 main classes of heavy chain constant domains. Each class defines the IgM, IgG, IgA, IgD, and IgE isotypes. IgG can be split into 4 subclasses, IgG1, IgG2, IgG3, and IgG4, each with its own biologic properties, and IgA can similarly be split into IgA1 and IgA2. (J Allergy Clin Immunol 2010;125:S41-52.)	[Schroeder, Harry W., Jr.] Univ Alabama, Dept Med, Div Clin Immunol & Rheumatol, Birmingham, AL 35294 USA; [Schroeder, Harry W., Jr.] Univ Alabama, Dept Microbiol, Div Clin Immunol & Rheumatol, Birmingham, AL 35294 USA; [Schroeder, Harry W., Jr.] Univ Alabama, Dept Genet, Div Clin Immunol & Rheumatol, Birmingham, AL 35294 USA; [Cavacini, Lisa] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA	Schroeder, HW (reprint author), Univ Alabama, Dept Med, Div Clin Immunol & Rheumatol, SHEL 176,1530 3rd Ave S, Birmingham, AL 35294 USA.	hwsj@uab.edu			National Institutes of Health/National Institute of Allergy and Infectious Diseases; United States Immunodeficiency Network; NABI Pharmaceuticals	Disclosure of potential conflict of interest: H. W. Schroeder receives research support from the National Institutes of Health/National Institute of Allergy and Infectious Diseases, the United States Immunodeficiency Network, and NABI Pharmaceuticals and is a councilor for the Henry Kunkel Society. L. Cavacini is a consultant for GTC Biotherapeutics and receives research support from the National Institutes of Health.	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G., 1995, IMMUNOGLOBULIN GENES, P173, DOI 10.1016/B978-012053640-5/50011-2	52	221	224	11	103	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	FEB	2010	125	2		2			S41	S52		10.1016/j.jaci.2009.09.046		12	Allergy; Immunology	Allergy; Immunology	629CC	WOS:000280170600005	20176268	
J	Kim, JJ; Smorodinsky, S; Lipsett, M; Singer, BC; Hodgson, AT; Ostro, B				Kim, JJ; Smorodinsky, S; Lipsett, M; Singer, BC; Hodgson, AT; Ostro, B			Traffic-related air pollution near busy roads - The East Bay children's respiratory health study	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						air pollution; asthma; bronchitis; epidemiology; vehicle emissions	SOUTHERN CALIFORNIA COMMUNITIES; CHILDHOOD ASTHMA; ALLERGIC SENSITIZATION; CARBON CONCENTRATION; DIFFERING LEVELS; LUNG-FUNCTION; SYMPTOMS; EXPOSURE; PARTICLES; AMBIENT	Recent studies, primarily in Europe, have reported associations between respiratory symptoms and residential proximity to traffic; however, few have measured traffic pollutants or provided information about local air quality. We conducted a school-based, cross-sectional study in the San Francisco Bay Area in 2001. Information on current bronchitis symptoms and asthma, home environment, and demographics was obtained by parental questionnaire (n = 1,109). Concentrations of traffic pollutants (particulate matter, black carbon, total nitrogen oxides [NOX], and nitrogen dioxide [NO2]) were measured at 10 school sites during several seasons. Although pollutant concentrations were relatively low, we observed differences in concentrations between schools nearby versus those more distant (or upwind) from major roads. Using a two-stage multiple-logistic regression model, we found associations between respiratory symptoms and traffic-related pollutants. Among,those living at their current residence for at least 1 year, the adjusted odds ratio for asthma in relationship to an interquartile difference in NOX was 1.07 (95% confidence interval, 1.00-1.14). Thus, we found spatial variability in traffic pollutants and associated differences in respiratory symptoms in a region with good air quality. Our findings support the hypothesis that traffic-related pollution is associated with respiratory symptoms in children.	Calif Environm Protect Agcy, Off Environm Hlth Hazard Assessment, Oakland, CA 94612 USA; Lawrence Berkeley Lab, Dept Atmospher Sci, Berkeley, CA USA; Lawrence Berkeley Lab, Indoor Environm Dept, Environm Energy Technol Div, Berkeley, CA USA	Ostro, B (reprint author), Calif Environm Protect Agcy, Off Environm Hlth Hazard Assessment, 1515 Clay St,16th Floor, Oakland, CA 94612 USA.	bostro@oehha.ca.gov	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Bornehag CG, 2001, INDOOR AIR, V11, P72; Brauer M, 2003, EPIDEMIOLOGY, V14, P228, DOI 10.1097/00001648-200303000-00019; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; Brunekreef B, 2002, LANCET, V360, P1233, DOI 10.1016/S0140-6736(02)11274-8; *CAL DEP HLTH SERV, 2004, TOB CONTR SECT CAL T; Ciccone G, 1998, OCCUP ENVIRON MED, V55, P771; Cook DG, 1997, THORAX, V52, P1081; Delfino RJ, 2002, ENVIRON HEALTH PERSP, V110, P573; Delfino RJ, 2003, ENVIRON HEALTH PERSP, V111, P647, DOI 10.1289/ehp.5992; DOCKERY DW, 1989, AM REV RESPIR DIS, V139, P587; Dockery DW, 1996, ENVIRON HEALTH PERSP, V104, P500, DOI 10.2307/3432990; EDWARDS J, 1994, ARCH ENVIRON HEALTH, V49, P223; EDWARDS JD, 1983, ATMOS ENVIRON, V17, P2337, DOI 10.1016/0004-6981(83)90233-0; English P, 1999, ENVIRON HEALTH PERSP, V107, P761, DOI 10.2307/3434663; Fischer PH, 2000, ATMOS ENVIRON, V34, P3713, DOI 10.1016/S1352-2310(00)00067-4; Gauderman WJ, 2002, AM J RESP CRIT CARE, V166, P76, DOI 10.1164/rccm.2111021; GUNDEL LA, 1984, SCI TOTAL ENVIRON, V36, P197, DOI 10.1016/0048-9697(84)90266-3; 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; Kim JJ, 2002, EPIDEMIOLOGY, V13, pS100; Klinnert MD, 2002, AM J PUBLIC HEALTH, V92, P792, DOI 10.2105/AJPH.92.5.792; Kramer U, 2000, EPIDEMIOLOGY, V11, P64, DOI 10.1097/00001648-200001000-00014; Lin S, 2002, ENVIRON RES, V88, P73, DOI 10.1006/enrs.2001.4303; MARTINEZ FD, 1995, AM J RESP CRIT CARE, V151, P1644; Martinez FD, 1997, CIBA F SYMP, V206, P233; McConnell R, 1999, ENVIRON HEALTH PERSP, V107, P757, DOI 10.2307/3434662; Oosterlee A, 1996, OCCUP ENVIRON MED, V53, P241; Pershagen G, 1995, INT J EPIDEMIOL, V24, P1147, DOI 10.1093/ije/24.6.1147; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; Peters JM, 1999, AM J RESP CRIT CARE, V159, P768; Rijnders E, 2001, ENVIRON HEALTH PERSP, V109, P411, DOI 10.2307/3434789; Roorda-Knape MC, 1998, ATMOS ENVIRON, V32, P1921, DOI 10.1016/S1352-2310(97)00496-2; Singer BC, 2004, ATMOS ENVIRON, V38, P393, DOI 10.1016/j.atmosenv.2003.10.005; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; WARE JH, 1986, AM REV RESPIR DIS, V133, P834; Weiland Stephan K., 1994, Annals of Epidemiology, V4, P243; WJST M, 1993, BRIT MED J, V307, P596; Wyler C, 2000, EPIDEMIOLOGY, V11, P450, DOI 10.1097/00001648-200007000-00015	38	221	224	5	63	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. 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J	Gilliland, FD; Li, YF; Saxon, A; Diaz-Sanchez, D				Gilliland, FD; Li, YF; Saxon, A; Diaz-Sanchez, D			Effect of glutathione-S-transferase M1 and P1 genotypes on xenobiotic enhancement of allergic responses: randomised, placebo-controlled crossover study	LANCET			English	Article							DIESEL EXHAUST PARTICLES; AIR-POLLUTION; IN-VIVO; NASAL CHALLENGE; CYTOKINE PRODUCTION; TOBACCO-SMOKE; LUNG-CANCER; ASTHMA; EXPOSURE; CHILDREN	Background Particulate pollution is associated with the occurrence of asthma and allergy. The model pollutant, diesel exhaust particles, can participate with allergens in starting and exacerbating allergic airway diseases in part by production of reactive oxygen species. Glutathione-S-transferases (GSTs) can metabolise reactive oxygen species and detoxify xenobiotics present in diesel exhaust particles. We tested the hypothesis that null genotypes for GSTM1 and GSTT1, and GSTP1 codon 105 variants (I105 and V105) are key regulators of the adjuvant effects of diesel exhaust particles on allergic responses. Methods Patients sensitive to the ragweed allergen were challenged intranasally with allergen alone and with allergen plus diesel exhaust particles in a randomised order at separate visits. Nasal allergen-specific IgE, histamine, interleukin 4, and interferon gamma concentrations were measured before and 24 h after challenge. Findings Individuals with GSTM1 null or the GSTP1 I105 wildtype genotypes showed enhanced nasal allergic responses in the presence of diesel exhaust particles. Compared with patients with a functional GSTM1 genotype, GSTM1 null patients had a significantly larger increase in IgE (median 102.5 U/mL [range 1.0-510.5] vs 45.5 U/mL [1.5-60.6], p=0.03) and histamine (14.0 nmol/L [-0.2-24.7] vs 7.4 nmol/L [1.2-12.3], p=0.02) after diesel exhaust particles plus allergen challenge. The I105 GSTP1 genotype was associated with an increase in IgE (120.3 U/mL [6.7-510.5] vs 27.7 U/mL [-1.5-60.6], p=0.03) and histamine (13.8 nmol/L [3.1-24.7] vs 5.2 nmol/L [-0.2-19.6], p=0.01) after challenge with diesel exhaust particles and allergens. The diesel exhaust particles enhancement was largest in patients with both the GSTM1 null and GSTP1 I/I genotypes. Interpretation GSTM1 and GSTP1 modify the adjuvant effect of diesel exhaust particles on allergic inflammation.	Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA; Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Clin Immunol,Hart & Louis Lab, Los Angeles, CA USA	Gilliland, FD (reprint author), Univ So Calif, Keck Sch Med, Dept Prevent Med, 1540 Alcazar St,CHP 236, Los Angeles, CA 90033 USA.	gillilan@usc.edu	LI, YU-FEN/F-4770-2010		NHLBI NIH HHS [HL-61768]; NIAID NIH HHS [AI-40945]; NIEHS NIH HHS [ES-07048, ES-09581]		Al-Humadi NH, 2002, ENVIRON HEALTH PERSP, V110, P349; Barfknecht T R, 1982, Dev Toxicol Environ Sci, V10, P277; BASCOM R, 1991, PHARMACOGENETICS, V1, P102, DOI 10.1097/00008571-199111000-00008; BASCOM R, 1990, AM REV RESPIR DIS, V142, P594; D'Amato G, 2002, Monaldi Arch Chest Dis, V57, P136; Delfino RJ, 2002, ENVIRON HEALTH PERSP, V110, P573; Diaz-Sanchez D, 2000, CLIN IMMUNOL, V97, P140, DOI 10.1006/clim.2000.4921; 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; DiazSanchez D, 1996, J ALLERGY CLIN IMMUN, V98, P114, DOI 10.1016/S0091-6749(96)70233-6; DIAZSANCHEZ D, 1994, J CLIN INVEST, V94, P1417, DOI 10.1172/JCI117478; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; DIAZSANCHEZ D, 2000, IMMUNOLOGY, V101, P1; DOCKERY DW, 1993, NEW ENGL J MED, V329, P1753, DOI 10.1056/NEJM199312093292401; 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; 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, 2002, AM J RESP CRIT CARE, V166, P346, DOI 10.1164/rccm.2111048; Hayes JD, 1995, CRIT REV BIOCHEM MOL, V30, P445, DOI 10.3109/10409239509083491; Hiura TS, 2000, J IMMUNOL, V165, P2703; Kramer U, 2000, EPIDEMIOLOGY, V11, P64, DOI 10.1097/00001648-200001000-00014; MANCHESTER J, 2001, DETERMINATION ELEM B, P1; Mapp CE, 2002, J ALLERGY CLIN IMMUN, V109, P867, DOI 10.1067/mai.2002.123234; McConnell R, 1999, ENVIRON HEALTH PERSP, V107, P757, DOI 10.2307/3434662; Naclerio RM, 1997, J ALLERGY CLIN IMMUN, V100, P505; Nel A E, 2001, Curr Opin Pulm Med, V7, P20, DOI 10.1097/00063198-200101000-00004; Ng D, 1998, J IMMUNOL, V161, P942; Nightingale JA, 2000, AM J RESP CRIT CARE, V162, P161; OPPENHEIM JJ, 1991, ANNU REV IMMUNOL, V9, P617; Pandya RJ, 2002, ENVIRON HEALTH PERSP, V110, P103; Piirila P, 2001, PHARMACOGENETICS, V11, P437, DOI 10.1097/00008571-200107000-00007; Pope CA, 2002, JAMA-J AM MED ASSOC, V287, P1132, DOI 10.1001/jama.287.9.1132; PRESTERA T, 1995, P NATL ACAD SCI USA, V92, P8965, DOI 10.1073/pnas.92.19.8965; Sagai M, 1996, FREE RADICAL BIO MED, V21, P199, DOI 10.1016/0891-5849(96)00032-9; SAGAI M, 1998, INVOLVEMENTS SUPEROX; Samet J M, 2000, Res Rep Health Eff Inst, V94, P5; Strand V, 1997, AM J RESP CRIT CARE, V155, P881; ToFigueras J, 1997, CARCINOGENESIS, V18, P1529, DOI 10.1093/carcin/18.8.1529; Trenga CA, 1999, OCCUP ENVIRON MED, V56, P544; Wang M, 1999, CLIN IMMUNOL, V90, P47, DOI 10.1006/clim.1998.4628; Whitekus MJ, 2002, J IMMUNOL, V168, P2560; WILLIAMS PT, 1986, FUEL, V65, P1150, DOI 10.1016/0016-2361(86)90184-5; XU GB, 1987, AEROSOL SCI TECH, V7, P117, DOI 10.1080/02786828708959152	44	220	227	2	13	ELSEVIER SCIENCE INC	NEW YORK	360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA	0140-6736			LANCET	Lancet	JAN 10	2004	363	9403					119	125		10.1016/S0140-6736(03)15262-2		7	Medicine, General & Internal	General & Internal Medicine	761WV	WOS:000187939200009	14726165	
J	Landrigan, PJ; Schechter, CB; Lipton, JM; Fahs, MC; Schwartz, J				Landrigan, PJ; Schechter, CB; Lipton, JM; Fahs, MC; Schwartz, J			Environmental pollutants and disease in American children: Estimates of morbidity, mortality, and costs for lead poisoning, asthma, cancer, and developmental disabilities	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						asthma; cancer; developmental disabilities; environmental pediatrics; health economics; lead poisoning	UNITED-STATES; OCCUPATIONAL INJURY; CHILDHOOD CANCERS; AIR-POLLUTION; HEALTH; TRENDS; EXPOSURE; BENEFITS; ILLNESS; RISK	In this study, we aimed to estimate the contribution of environmental pollutants to the incidence, prevalence, mortality, and costs of pediatric disease in American children. We examined four categories of illness: lead poisoning, asthma, cancer, and neurobehavioral disorders. To estimate the proportion of each attributable to toxins in the environment, we used an environmentally attributable fraction (EAF) model. EAFs for lead poisoning, asthma, and cancer were developed by panels of experts through a Delphi process, whereas that for neurobehavioral disorders was based on data from the National Academy of Sciences. We define environmental pollutants as toxic chemicals of human origin in air, food, water, and communities. To develop estimates of costs, we relied on data from the U.S. Environmental Protection Agency, Centers for Disease Control and Prevention, National Center for Health Statistics, the Bureau of Labor Statistics, the Health Care Financing Agency, and the Practice Management Information Corporation. EAFs were judged to be 100% for lead poisoning, 30% for asthma (range, 10-35%), 5% for cancer (range, 2-10%), and 10% for neurobehavioral disorders (range, 5-20%). Total annual costs are estimated to be $54.9 billion (range $48.8-64.8 billion): $43.4 billion for lead poisoning, $2.0 billion for asthma, $0.3 billion for childhood cancer, and $9.2 billion for neurobehavioral disorders. This sum amounts to 2.8 percent of total U.S. health care costs. This estimate is likely low because it considers only four categories of illness, incorporates conservative assumptions, ignores costs of pain and Suffering, and does not include late complications for which etiologic associations are poorly quantified. The costs of pediatric environmental disease are high, in contrast with the limited resources directed to research, tracking, and prevention.	CUNY Mt Sinai Sch Med, Dept Community & Prevent Med, New York, NY 10029 USA; CUNY Mt Sinai Sch Med, Ctr Childrens Hlth & Environm, New York, NY 10029 USA; CUNY Mt Sinai Sch Med, Dept Pediat, New York, NY 10029 USA; New Sch Social Res, Ctr Hlth Policy Res, New York, NY 10011 USA; Harvard Univ, Sch Publ Hlth, Environm Epidemiol Program, Boston, MA 02115 USA	Landrigan, PJ (reprint author), CUNY Mt Sinai Sch Med, Dept Community & Prevent Med, Box 1057,1 Gustave L Levy Pl, New York, NY 10029 USA.						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Health Perspect.	JUL	2002	110	7					721	728				8	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	585VZ	WOS:000177546400033	12117650	
J	Arshad, SH; Tariq, SM; Matthews, S; Hakim, E				Arshad, SH; Tariq, SM; Matthews, S; Hakim, E			Sensitization to common allergens and its association with allergic disorders at age 4 years: A whole population birth cohort study	PEDIATRICS			English	Article						atopy; allergic diseases; asthma; eczema; rhinitis; skin-prick test	SKIN-TEST REACTIVITY; HOUSE-DUST MITE; CHILDHOOD ASTHMA; SERUM IGE; AIRWAY RESPONSIVENESS; ENVIRONMENTAL-FACTORS; INHALANT ALLERGENS; RISK-FACTORS; HAY-FEVER; ATOPY	Background. Atopy is defined as the genetic propensity to develop immunoglobulin E antibodies in response to exposure to allergens and assessed by skin prick test responses to common allergens. Although it is generally agreed that atopy is an important risk factor for allergic diseases such as asthma, rhinitis, and eczema, the extent to which atopy accounts for these diseases is controversial. Objective. We aim to describe the prevalence of sensitization to common allergens and investigate the degree of association of atopy (as defined by positive skin prick test to 1 or more common allergens) to asthma, rhinitis, and eczema in a birth cohort at the age of 4 years. Methods. A birth cohort of 1456 children was recruited over a 14-month period (1989-1990). These children have been seen previously at 1 and 2 years of age. At 4 years, 1218 children were reviewed and an interview was administered or postal questionnaire was completed for the presence of allergic diseases (asthma, rhinitis, and eczema). Additionally, in 981 children, skin prick tests with a battery of 12 common allergens were performed. Allergens were house dust mite (Dermatophagoides pteronyssimus), grass pollen mix, cat, dog, Alternaria alternata, Cladosporium herbarum, cow's milk, hen's egg, soya, cod, wheat, and peanut. A mean wheal diameter of at least 3 mm greater than the negative control was taken as positive. This analysis is confined to the 981 (67% of the original population) who also had skin prick tests to the standard battery. chi (2) tests were used to test the univariate association between each allergic disease and positive skin test. Multiple logistic regression analysis was performed to obtain the adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for the independent effect of sensitization to each allergen on allergic disease, adjusting for the effect of sensitization to other allergens. To ascertain how much of allergic disease is attributable to atopy, we estimated the population-attributable risk. This was calculated with the formula: P(R - 1) where R is the OR for the allergic disease under consideration and P is the proportion of atopy in children with that disease. Results. Children who were skin prick-tested at 4 years were similar in most characteristics to the rest of the population, except that they had a higher prevalence of allergic disease. Allergic disorders (asthma, rhinitis, and eczema) were present in 276 (28.1%) of 981. One hundred ninety-two (19.6%) children were atopic (positive reaction to 1 or more allergens). Sensitization to inhalant allergens was relatively common (19.2%) as compared with food allergens (3.5%). House dust mite (11.9%), grass pollen (7.8%), and cat (5.8%) were the most common positive reactions. A test to the 4 most common allergens (house dust mite, grass pollen, cat, and A alternata) could detect 94% of the atopic children. Sensitization to the 4 most common allergens was strongly associated with the presence of allergic disorders. There was a graded effect with the potent allergens, such as house dust mite, having the greatest impact. For example, 50% of children sensitized to house dust mite had asthma as opposed to 44% sensitized to cat, 42% sensitized to grass pollen, and 32% sensitized to A alternata. Overall, 68.4% of children sensitized to house dust mite had asthma, eczema, and/or rhinitis. The respective figures for grass pollen, cat, and A alternata were 64.9%, 66.7%, and 57.4%. The proportion of children sensitized to cat was not higher in households with cat ownership (households with cats: 5.1% [19/374]; households without cats: 6.2% [36/580]; not significant [NS]). Similarly, no difference was seen in sensitization to dog in households with and without dogs (households with dogs: 1.8% [5/282]; households without dogs: 2.8% [19/673]; NS). Boys were atopic more often than girls at this age (male: 112 of 497 [22.5%] vs female: 80 of 484 [16.5%]; OR: 1.47, 95% CI: 1.07-2.02). Male preponderance was observed with most allergens, but this was statistically significant only for house dust mite (male: 75/497 [15.1%] vs female: 42/484 [8.7%]; OR: 1.87; CI: 1.25-2.79) and grass pollen (male: 51/497 [10.3%] vs female: 26/484 [5.4%]; OR: 2.01; CI: 1.23-3.29). An independent effect of allergen sensitization on asthma was observed only with house dust mite with an OR of 8.07 (CI: 4.60-14.14). The highest independent risk for rhinitis was sensitization to grass pollen (OR: 5.02; CI: 2.21-11.41), and for eczema, sensitization to peanut (OR: 4.65; CI: 1.02-21.34). The majority of children (98/192) were sensitized to >1 allergen. A graded effect was observed with the risk of allergic disease in the child increasing with the number of positive skin prick test reactions. This effect was consistent throughout the spectrum of allergic diseases (asthma, eczema, and rhinitis). Nearly 80% of the children with positive skin test reactions to 4 or more allergens had asthma, eczema, and/or rhinitis compared with 20%, if they were nonatopic. The prevalence of atopy in asthmatic children was 44%. With an OR of 4.56, the population-attributable risk was calculated to be 35%. Fifty-five percent of children with rhinitis were atopic, and the OR of rhinitis was 5.85. Therefore, 46% of the cases of rhinitis could be attributable to atopy. The population-attributable risk of atopy for eczema was 32% (the prevalence of atopy in children with eczema: 43%; and the OR for the development of eczema: 3.86). Conclusion. Atopy is closely associated with asthma, rhinitis, and eczema at 4 years of age, with a direct and linear relationship. However, the proportion of cases of allergic disease attributable to atopy is <50%. We propose a model for the development of allergic disorders, where 30% to 40% of cases of allergic disease (asthma, eczema, and rhinitis) in early childhood are attributable to atopy and 60% to 70% of cases could be accounted for by organ-based and other factors.	St Marys Hosp, DAvid Hide Asthma & Allergy Res Ctr, Newport PO30 5TG, Wight, England	Arshad, SH (reprint author), St Marys Hosp, DAvid Hide Asthma & Allergy Res Ctr, Newport PO30 5TG, Wight, England.						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J	Monn, C				Monn, C			Exposure assessment of air pollutants: a review on spatial heterogeneity and indoor/outdoor/personal exposure to suspended particulate matter, nitrogen dioxide and ozone	ATMOSPHERIC ENVIRONMENT			English	Review						exposure assessment; particles; PM10; PM2.5; NO2; O-3; bioaerosols	VOLATILE ORGANIC-COMPOUNDS; RESIDENTIAL NO2 CHARACTERIZATION; SOUTHERN CALIFORNIA COMMUNITY; GRASS-POLLEN ALLERGEN; PERSONAL EXPOSURE; AIRBORNE PARTICLES; ENVIRONMENTAL EPIDEMIOLOGY; BIOLOGICAL MARKERS; PULMONARY-FUNCTION; MASS CONCENTRATION	This review describes databases of small-scale spatial variations and indoor, outdoor and personal measurements of air pollutants with the main focus on suspended particulate matter, and to a lesser extent, nitrogen dioxide and photochemical pollutants. The basic definitions and concepts of an exposure measurement are introduced as well as some study design considerations and implications of imprecise exposure measurements. Suspended particulate matter is complex with respect to particle size distributions, the chemical composition and its sources. With respect to small-scale spatial variations in urban areas, largest variations occur in the ultrafine (<0.1 <mu>m) and the coarse mode (PM10-2.5, resuspended dust). Secondary aerosols which contribute to the accumulation mode (0.1-2 mum) show quite homogenous spatial distribution. In general, small-scale spatial variations of PM2.5 were described to be smaller than the spatial variations of PM10. Recent studies in outdoor air show that ultrafine particle number counts have large spatial variations and that they are not well correlated to mass data. Sources of indoor particles are from outdoors and some specific indoor sources such as smoking and cooking for fine particles or moving of people (resuspension of dust) for coarse particles. The relationships between indoor, outdoor and personal levels are complex. The finer the particle size, the better becomes the correlation between indoor, outdoor and personal levels. Furthermore, correlations between these parameters are better in longitudinal analyses than in cross-sectional analyses. For NO2 and O-3 the air chemistry is important. Both have considerable small-scale spatial variations within urban areas. In the absence of indoor sources such as gas appliances, NO2 indoor/outdoor relationships are strong. For ozone, indoor levels are quite small. The study hypothesis largely determines the choice of a specific concept in exposure assessment, i.e. whether personal sampling is needed or if ambient monitoring is sufficient. Careful evaluation of the validity and improvements in precision of an exposure measure reduce error in the measurements and bias in the exposure-effect relationship. (C) 2000 Published by Elsevier Science Ltd.	ETH Zurich, Inst Hyg & Appl Physiol, CH-8092 Zurich, Switzerland	Monn, C (reprint author), ETH Zurich, Inst Hyg & Appl Physiol, Clausiusstr 25, CH-8092 Zurich, Switzerland.		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Environ.		2001	35	1					1	32		10.1016/S1352-2310(00)00330-7		32	Environmental Sciences; Meteorology & Atmospheric Sciences	Environmental Sciences & Ecology; Meteorology & Atmospheric Sciences	390YL	WOS:000166327300001		
J	von Mutius, E; Vercelli, D				von Mutius, Erika; Vercelli, Donata			Farm living: effects on childhood asthma and allergy	NATURE REVIEWS IMMUNOLOGY			English	Article							NORMAL HUMAN MONOCYTES; IFN-GAMMA PRODUCTION; SCHOOL-AGE-CHILDREN; HAY-FEVER; EARLY-LIFE; BIRTH-COHORT; ATOPIC SENSITIZATION; INVERSE ASSOCIATION; MICROBIAL EXPOSURE; DENDRITIC CELLS	Numerous epidemiological studies have shown that children who grow up on traditional farms are protected from asthma, hay fever and allergic sensitization. Early-life contact with livestock and their fodder, and consumption of unprocessed cow's milk have been identified as the most effective protective exposures. Studies of the immunobiology of farm living point to activation and modulation of innate and adaptive immune responses by intense microbial exposures and possibly xenogeneic signals delivered before or soon after birth.	[von Mutius, Erika] Univ Munich, Dr von Haunersche Kinderklin, D-80337 Munich, Germany; [Vercelli, Donata] Univ Arizona, Arizona Ctr Biol Complex Dis, Arizona Resp Ctr, Tucson, AZ 85719 USA; [Vercelli, Donata] Univ Arizona, Dept Cell Biol, Tucson, AZ 85719 USA	von Mutius, E (reprint author), Univ Munich, Dr von Haunersche Kinderklin, D-80337 Munich, Germany.	erika.von.mutius@med.lmu.de; donata@arc.arizona.edu		von Mutius, Erika/0000-0002-8893-4515			Adler A, 2005, J ALLERGY CLIN IMMUN, V115, P67, DOI 10.1016/j.jaci.2004.10.008; Alfven T, 2006, ALLERGY, V61, P414, DOI 10.1111/j.1398-9995.2005.00939.x; Amsen D, 2004, CELL, V117, P515, DOI 10.1016/S0092-8674(04)00451-9; BACH FH, 1995, NAT MED, V1, P869, DOI 10.1038/nm0995-869; Braback L, 2004, CLIN EXP ALLERGY, V34, P38, DOI 10.1111/j.1365-2222.2004.01841.x; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Chen X, 2007, J IMMUNOL, V179, P154; Chrischilles E, 2004, J ALLERGY CLIN IMMUN, V113, P66, DOI 10.1016/j.jaci.2003.09.037; 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Rev. Immunol.	DEC	2010	10	12					861	868		10.1038/nri2871		8	Immunology	Immunology	685CD	WOS:000284601100012	21060319	
J	van Odijk, J; Kull, I; Borres, MP; Brandtzaeg, P; Edberg, U; Hanson, LA; Host, A; Kuitunen, M; Olsen, SF; Skerfving, S; Sundell, J; Wille, S				van Odijk, J; Kull, I; Borres, MP; Brandtzaeg, P; Edberg, U; Hanson, LA; Host, A; Kuitunen, M; Olsen, SF; Skerfving, S; Sundell, J; Wille, S			Breastfeeding and allergic disease: a multidisciplinary review of the literature (1966-2001) on the mode of early feeding in infancy and its impact on later atopic manifestations	ALLERGY			English	Review						allergy; asthma; atopic disease; breast feeding; cow's milk formula; wheezing	COWS MILK ALLERGY; HIGH-RISK INFANTS; RESPIRATORY-TRACT INFECTIONS; PARTIAL WHEY HYDROLYSATE; PROSPECTIVE FOLLOW-UP; FAMILY HISTORY; PATHOGENETIC ROLE; PARENTAL SMOKING; CHILDHOOD ASTHMA; MATERNAL SMOKING	Background: Strategies to prevent children from developing allergy have been elaborated on the basis of state-of-the-art reviews of the scientific literature regarding pets and allergies, building dampness and health, and building ventilation and health. A similar multidisciplinary review of infant feeding mode in relation to allergy has not been published previously. Here, the objective is to review the scientific literature regarding the impact of early feeding (breast milk and/or cow's milk and/or formula) on development of atopic disease. The work was performed by a multidisciplinary group of Scandinavian researchers. Methods: The search in the literature identified 4323 articles that contained at least one of the exposure and health effect terms. A total of 4191 articles were excluded mainly because they did not contain information on both exposure and health effects. Consequently, 132 studies have been scrutinized by this review group. Results: Of the 132 studies selected, 56 were regarded as conclusive. Several factors contributed to the exclusions. The studies considered conclusive by the review group were categorized according to population and study design. Conclusions: The review group concluded that breastfeeding seems to protect from the development of atopic disease. The effect appears even stronger in children with atopic heredity. If breast milk is unavailable or insufficient, extensively hydrolysed formulas are preferable to unhydrolysed or partially hydrolysed formulas in terms of the risk of some atopic manifestations.	Odense Univ Hosp, Dept Pediat, DK-5000 Odense C, Denmark; Univ Gothenburg, Dept Clin Nutr, Sahlgrenska Acad, Gothenburg, Sweden; Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; Univ Gothenburg, Dept Woman & Child Hlth, Sahlgrenska Acad, Gothenburg, Sweden; Univ Oslo, Rikshosp, Inst Pathol, LIIPAT, Oslo, Norway; Swedish Natl Food Adm, Uppsala, Sweden; Univ Gothenburg, Dept Clin Immunol, Sahlgrenska Acad, Gothenburg, Sweden; Univ Helsinki Hosp, Skin & Allergy Hosp, Helsinki, Finland; Danish Epidemiol Sci Ctr, Copenhagen, Denmark; Lund Univ, Dept Environm & Occupat Med, Lund, Sweden; Tech Univ Denmark, Int Ctr Indoor Air & Energy, DK-2800 Lyngby, Denmark; Helsingborg Hosp, Dept Paediat, Helsingborg, Sweden	Host, A (reprint author), Odense Univ Hosp, Dept Pediat, Sdr Blvd 29, DK-5000 Odense C, Denmark.		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J	Beck, LA; Marcotte, GV; MacGlashan, D; Togias, A; Saini, S				Beck, LA; Marcotte, GV; MacGlashan, D; Togias, A; Saini, S			Omalizumab-induced reductions in mast cell Fc epsilon RI expression and function	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						mast cells; Fc epsilon RI; omalizumab; basophils	ANTI-IGE ANTIBODY; DOWN-REGULATION; IN-VIVO	Background: By design, omalizumab binds free IgE in the circulation and prevents its attachment to the surface of mast cells and basophils, thereby preventing them from responding to allergens. Previously, omalizumab rapidly reduced free IgE levels, as well as basophil high-affinity IgE receptors, leading to significant reductions in basophil mediator response to allergen. It is assumed that tissue mast cells are similarly altered in their FcepsilonRI density and function. Objective: We examined the phenotypic shift of skin mast cells in parallel to that of blood basophils in 3 subjects infused with omalizumab. Methods: Three subjects with allergic rhinitis underwent intradermal skin test titration with house dust mite antigen at days 0, 7, 70, and 196 of omalizumab treatment. As control subjects, 5 untreated subjects with allergic rhinitis were evaluated at similar time points. All subjects underwent skin biopsy 18 to 24 hours later at the site of allergen injection. Biopsy specimens were characterized by means of immunohistochemisty for tryptase and FcepsilonRIalpha immunoreactivity, as well other markers (CD3, CD45RO, CD68, cutaneous lymphocyte antigen, and major basic protein). Results: Omalizumab recipients, but not control subjects, demonstrated reductions in FcepsilonRIalpha immunoreactivity at days 70 and 196 in parallel with reductions in the acute wheal response to allergen. However, no reductions in tryptase-positive cells were noted at these time points. Conclusion: Reductions in free IgE levels by omalizumab leads to a rapid reduction in basophil FcepsilonRI receptor expression. In contrast, the time course for the decrease of FcepsilonRI expression in skin mast cells is slower and associated with decreased acute allergen wheal size.	Johns Hopkins Asthma & Allergy Ctr, Unit Off 1, Dept Med, Div Clin Immunol, Baltimore, MD 21224 USA	Saini, S (reprint author), Johns Hopkins Asthma & Allergy Ctr, Unit Off 1, Dept Med, Div Clin Immunol, 5501 Hopkins Bayview Circle, Baltimore, MD 21224 USA.	ssaini@jhmi.edu			NIAID NIH HHS [AI045839, K08 AI001564, AI01564, K08 AI001564-05, R01 AI045839]		Beck LA, 1997, J IMMUNOL, V159, P2962; Boulet LP, 1997, AM J RESP CRIT CARE, V155, P1835; Fahy JV, 1997, AM J RESP CRIT CARE, V155, P1828; Leung DYM, 2003, NEW ENGL J MED, V348, P986, DOI 10.1056/NEJMoa022613; MacGlashan DW, 1997, J IMMUNOL, V158, P1438; Ong Y., 2004, Journal of Allergy and Clinical Immunology, V113, pS84, DOI 10.1016/j.jaci.2003.12.280; PETERS MS, 1983, J INVEST DERMATOL, V81, P39, DOI 10.1111/1523-1747.ep12538380; Saini SS, 1999, J IMMUNOL, V162, P5624; Togias A, 1998, J ALLERGY CLIN IMMUN, V101, pS171	9	217	222	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.	SEP	2004	114	3					527	530		10.1016/j.jaci.2004.06.032		4	Allergy; Immunology	Allergy; Immunology	853AX	WOS:000223799600009	15356552	
J	Herrick, CA; Bottomly, K				Herrick, CA; Bottomly, K			To respond or not to respond: T cells in allergic asthma	NATURE REVIEWS IMMUNOLOGY			English	Review							INDUCED AIRWAY HYPERREACTIVITY; IFN-GAMMA PRODUCTION; DENDRITIC CELLS; TH2 RESPONSES; MURINE MODEL; CYTOKINE PRODUCTION; TRANSGENIC MICE; BRONCHIAL HYPERRESPONSIVENESS; EOSINOPHILIC INFLAMMATION; INTERLEUKIN-10 PRODUCTION	The incidence of allergic asthma has almost doubled in the past two decades. Numerous epidemiological studies have linked the recent surge in atopic disease with decreased exposure to infections in early childhood as a result of a more westernized lifestyle. However, a clear mechanistic explanation for how this might occur is still lacking. An answer might lie in the presently unfolding story of various regulatory T-cell populations that can limit adaptive immune responses, including T helper 2 (T(H)2)-cell-mediated allergic airway disease.	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J	Valenta, R				Valenta, R			The future of antigen-specific immunotherapy of allergy	NATURE REVIEWS IMMUNOLOGY			English	Editorial Material							FC-EPSILON-RI; BIRCH POLLEN ALLERGEN; HIGH-AFFINITY RECEPTOR; T-CELL EPITOPE; BEE VENOM IMMUNOTHERAPY; DUST MITE ALLERGEN; ENGINEERED HYPOALLERGENIC DERIVATIVES; QUANTITATIVE IGE INHIBITION; EPIDERMAL LANGERHANS CELLS; SITE-DIRECTED MUTAGENESIS		Univ Vienna, Sch Med, Vienna Gen Hosp AKH, Mol Immunopathol Grp,Dept Pathophysiol, A-1090 Vienna, Austria	Valenta, R (reprint author), Univ Vienna, Sch Med, Vienna Gen Hosp AKH, Mol Immunopathol Grp,Dept Pathophysiol, Waehringer Guertel 18-20, A-1090 Vienna, Austria.	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J	Sicherer, SH; Furlong, TJ; Munoz-Furlong, A; Burks, AW; Sampson, HA				Sicherer, SH; Furlong, TJ; Munoz-Furlong, A; Burks, AW; Sampson, HA			A voluntary registry for peanut and tree nut allergy: Characteristics of the first 5149 registrants	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						food allergy; anaphylaxis; peanut; tree nuts	FOOD; PREVALENCE; SENSITIZATION; CHILDREN; BIRTH; SKIN	Background: A voluntary registry of individuals with peanut and/or tree nut allergy was established in 1997 to learn more about these food allergies. Objective: The purpose of this study was to elucidate a variety of features of peanut and tree nut allergy among the first 5149 registry participants. Methods: The registry was established through use of a structured questionnaire distributed to all members of the Food Allergy and Anaphylaxis Network and to patients by allergists. Parental surrogates completed the forms for children under the age of 18 years. Results: Registrants were primarily children (89% of registrants were younger than 18 years of age: the median age was 5 years), reflecting the membership of the Network. Isolated peanut allergy was reported by 3482 registrants (68%), isolated tree nut allergy by 464 (9%), and allergy to both foods by 1203 (23%). Registrants were more likely to have been born in October, November, or December (odds ratio, 1.2; 95% CI, 1.18-1.23; P < .0001). The median age of reaction to peanut was 14 months, and the median age of reaction to tree nuts was 36 months; these represented the first known exposure for 74% and 68% of registrants, respectively. One half of the reactions involved more than 1 organ system, and more than 75% required treatment, frequently from medical personnel. Registrants with asthma were more likely than those without asthma to have severe reactions (33% vs 21%; P < .0001). In comparison with initial reactions, subsequent reactions due to accidental ingestion were more severe. more common outside the home, and more likely to be treated with epinephrine. Conclusions: Allergic reactions to peanut and tree nut are frequently severe, often occur on the first known exposure, and can become more severe over time.	CUNY Mt Sinai Sch Med, Div Allergy & Immunol, Dept Pediat, Elliot & Roslyn Jaffe Food Allergy Inst, New York, NY 10029 USA; Food Allergy & Anaphylaxis Network, Fairfax, VA USA; Univ Arkansas Med Sci, Arkansas Childrens Hosp, Little Rock, AR 72205 USA	Sicherer, SH (reprint author), CUNY Mt Sinai Sch Med, Div Allergy & Immunol, Dept Pediat, Elliot & Roslyn Jaffe Food Allergy Inst, 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 AI 01709-01]; NICHD NIH HHS [HD28822-08]		AALBERSE RC, 1992, CLIN EXP ALLERGY, V22, P1003, DOI 10.1111/j.1365-2222.1992.tb03028.x; Bock SA, 2001, J ALLERGY CLIN IMMUN, V107, P191, DOI 10.1067/mai.2001.112031; BOCK SA, 1989, J ALLERGY CLIN IMMUN, V83, P900, DOI 10.1016/0091-6749(89)90103-6; *CDCP, 2000, NATL VIT STAT REP, V48, P1; Emmett SE, 1999, ALLERGY, V54, P380, DOI 10.1034/j.1398-9995.1999.00768.x; Ewan PW, 1996, BRIT MED J, V312, P1074; Furlong TJ, 1998, J ALLERGY CLIN IMMUN, V101, pS104; Hourihane JO, 1996, BRIT MED J, V313, P518; Hourihane JO, 1997, CLIN EXP ALLERGY, V27, P634, DOI 10.1046/j.1365-2222.1997.d01-559.x; Hourihane JO, 1998, BRIT MED J, V316, P1271; KEATING MU, 1990, J ALLERGY CLIN IMMUN, V86, P41, DOI 10.1016/S0091-6749(05)80121-6; Kusunoki T, 1999, J ALLERGY CLIN IMMUN, V103, P1148, DOI 10.1016/S0091-6749(99)70191-0; Moneret-Vautrin DA, 1998, CLIN EXP ALLERGY, V28, P1113, DOI 10.1046/j.1365-2222.1998.00370.x; SAMPSON HA, 1992, NEW ENGL J MED, V327, P380, DOI 10.1056/NEJM199208063270603; Sarpong SB, 1998, J ALLERGY CLIN IMMUN, V101, P566, DOI 10.1016/S0091-6749(98)70369-0; Sicherer SH, 2000, J ALLERGY CLIN IMMUN, V106, P53, DOI 10.1067/mai.2000.108105; Sicherer SH, 2001, J PEDIATR-US, V138, P560, DOI 10.1067/mpd.2001.111821; Sicherer SH, 1998, PEDIATRICS, V102, part. no., DOI 10.1542/peds.102.1.e6; Sicherer SH, 2001, J ALLERGY CLIN IMMUN, V107, pS231; 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; Spergel JM, 2000, ANN ALLERG ASTHMA IM, V85, P473; Tariq SM, 1996, BRIT MED J, V313, P514; VANASPEREN PP, 1983, ARCH DIS CHILD, V58, P253; Vander Leek TK, 2000, J PEDIATR-US, V137, P749, DOI 10.1067/mpd.2000.109376; YUNGINGER JW, 1988, JAMA-J AM MED ASSOC, V260, P1450, DOI 10.1001/jama.260.10.1450	27	217	226	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					128	132				5	Allergy; Immunology	Allergy; Immunology	458AN	WOS:000170171200019	11447394	
J	Peng, RD; Dominici, F; Pastor-Barriuso, R; Zeger, SL; Samet, JM				Peng, RD; Dominici, F; Pastor-Barriuso, R; Zeger, SL; Samet, JM			Seasonal analyses of air pollution and mortality in 100 US cities	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						air pollution; epidemiologic methods; models; statistical; mortality; seasons	PARTICULATE MATTER; TIME-SERIES; RESPONSE RELATIONSHIPS; PHILADELPHIA; HEALTH; EXPOSURE; CHILDREN; PROJECT; MODELS; ASTHMA	Time series models relating short-term changes in air pollution levels to daily mortality counts typically assume that the effects of air pollution on the log relative rate of mortality do not vary with time. However, these short-term effects might plausibly vary by season. Changes in the sources of air pollution and meteorology can result in changes in characteristics of the air pollution mixture across seasons. The authors developed Bayesian semiparametric hierarchical models for estimating time-varying effects of pollution on mortality in multisite time series studies. The methods were applied to the database of the National Morbidity and Mortality Air Pollution Study, which includes data for 100 US cities, for the period 1987-2000. At the national level, a 10-mug/m(3) increase in particulate matter less than 10 mum in aerodynamic diameter at a 1-day lag was associated with 0.15% (95% posterior interval (PI): -0.08, 0.39), 0.14% (95% PI: -0.14, 0.42), 0.36% (95% PI: 0.11, 0.61), and 0.14% (95% PI: -0.06, 0.34) increases in mortality for winter, spring, summer, and fall, respectively. An analysis by geographic region found a strong seasonal pattern in the Northeast (with a peak in summer) and little seasonal variation in the southern regions of the country. These results provide useful information for understanding particle toxicity and guiding future analyses of particle constituent data.	Johns Hopkins Bloomberg Sch Publ Hlth, Dept Biostat, Baltimore, MD 21205 USA; Inst Salud Carlos III, Natl Ctr Epidemiol, Epidemiol & Biostat Sect, Madrid, Spain; Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA	Peng, RD (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Biostat, 615 N Wolfe St, Baltimore, MD 21205 USA.	rpeng@jhsph.edu			NHLBI NIH HHS [T32 HL 07024]; NIEHS NIH HHS [P30 ES 03819, R01 ES 012054]		Bell ML, 2004, ANNU REV PUBL HEALTH, V25, P247, DOI 10.1146/annurev.publhealth.25.102802.124329; Daniels MJ, 2000, AM J EPIDEMIOL, V152, P397, DOI 10.1093/aje/152.5.397; Dockery D., 1996, PARTICLES OUR AIR CO, P123; Dominici F, 2000, J ROY STAT SOC A STA, V163, P263, DOI 10.1111/1467-985X.00170; Dominici F, 2002, AM J EPIDEMIOL, V156, P193, DOI 10.1093/aje/kwf062; Dominici F, 2002, J AM STAT ASSOC, V97, P100, DOI 10.1198/016214502753479266; Dominici F, 2003, MORTALITY RESIDENTS, P9; Everson PJ, 2000, J ROY STAT SOC B, V62, P399, DOI 10.1111/1467-9868.00239; Hastie T., 1990, GENERALIZED ADDITIVE; Katsouyanni K, 2001, EPIDEMIOLOGY, V12, P521, DOI 10.1097/00001648-200109000-00011; Keeler GJ, 2002, ENVIRON HEALTH PERSP, V110, P173; Kelsall JE, 1997, AM J EPIDEMIOL, V146, P750; Klepeis NE, 2001, J EXPO ANAL ENV EPID, V11, P231, DOI 10.1038/sj.jea.7500165; Moolgavkar SH, 2003, INHAL TOXICOL, V15, P877, DOI 10.1080/08958370390215767; MOOLGAVKAR SH, 1995, EPIDEMIOLOGY, V6, P476, DOI 10.1097/00001648-199509000-00003; Moolgavkar SH, 1996, EPIDEMIOLOGY, V7, P420, DOI 10.1097/00001648-199607000-00014; *NATL CTR ENV ASS, 1996, OFF RES DEV NAT CTR; *NATL RES COUNC, 2004, NAT AC SCI RES PRIOR; *OFF RES DEV, 1996, EPA600P95001AF; *OFF RES DEV, 2003, EPA600P99002AD; Peng RD, 2004, R NEWS, V4, P10; POPE CA, 1995, INHAL TOXICOL, V7, P1, DOI 10.3109/08958379509014267; R Development Core Team. R, 2004, LANG ENV STAT COMP; Samet J, 1998, ENVIRON RES, V77, P9, DOI 10.1006/enrs.1997.3821; Samet JM, 2000, NEW ENGL J MED, V343, P1742, DOI 10.1056/NEJM200012143432401; Samet J.M., 2000, NATL MORBIDITY MORTA; Samoli E, 2001, ENVIRON HEALTH PERSP, V109, P349, DOI 10.2307/3454893; SCHWARTZ J, 1994, CAN J STAT, V22, P471, DOI 10.2307/3315405; SCHWARTZ J, 1994, ENVIRON HEALTH PERSP, V102, P186, DOI 10.2307/3431609; Spengler J.D., 1996, PARTICLES OUR AIR CO, P41; Stolwijk AM, 1999, J EPIDEMIOL COMMUN H, V53, P235; STYER P, 1995, ENVIRON HEALTH PERSP, V103, P490, DOI 10.2307/3432588; Touloumi G, 2004, ENVIRONMETRICS, V15, P101, DOI 10.1002/env.623; Wallace LA, 2003, ENVIRON HEALTH PERSP, V111, P1265, DOI 10.1289/ehp.6135	34	216	227	5	26	OXFORD UNIV PRESS INC	CARY	JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA	0002-9262			AM J EPIDEMIOL	Am. J. Epidemiol.	MAR 15	2005	161	6					585	594		10.1093/aje/kwi075		10	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	903DQ	WOS:000227406100010	15746475	
J	Scrivener, S; Yemaneberhan, H; Zebenigus, M; Tilahun, D; Girma, S; Ali, S; McElroy, P; Custovic, A; Woodcock, A; Pritchard, D; Venn, A; Britton, J				Scrivener, S; Yemaneberhan, H; Zebenigus, M; Tilahun, D; Girma, S; Ali, S; McElroy, P; Custovic, A; Woodcock, A; Pritchard, D; Venn, A; Britton, J			Independent effects of intestinal parasites infection and domestic allergen exposure on risk of wheeze in Ethiopia: a nested case-control study	LANCET			English	Article							EXERCISE-INDUCED BRONCHOSPASM; KENYAN SCHOOL-CHILDREN; PAPUA-NEW-GUINEA; HOUSE-DUST MITE; ASTHMA; PREVALENCE; URBAN; ATOPY; HOOKWORM; ASSOCIATION	Background Why asthma is rare in rural subsistence societies is not clear. We tested the hypotheses that the risk of asthma is reduced by intestinal parasites or hepatitis A infection, and increased by exposure to dust-mite allergen or organophosphorus insecticides in urban and rural areas of Jimma, Ethiopia. Methods From 12876 individuals who took part in a study of asthma and atopy in urban and rural Jimma in 1996, we identified all who reported wheeze in the previous 12 months, and a random subsample of controls. In 1999, we assessed parasites in faecal samples, Der p 1 levels in bedding, hepatitis A antibodies, serum cholinesterase (a marker of organophosphorus exposure), total and specific serum IgE, and skin sensitisation to Dermatophagoides pteronyssinus in 205 cases and 399 controls aged over 16 years. The effects of parasitosis, Der p 1 level, hepatitis A seropositivity, and cholinesterase concentration on risk of wheeze, and the role of IgE and skin sensitisation in these associations, were analysed by multiple logistic regression. Findings The risk of wheeze was independently reduced by hookworm infection by an odds ratio of 0.48 (95% CI 0.24-0.93, p=0.03), increased in relation to Der p 1 level (odds ratio per quartile 1.26 [1.00-1.59], p=0.05), and was unrelated to hepatitis A seropositivity or cholinesterase concentration. In the urban population, D pteronyssinus skin sensitisation was more strongly related to wheeze (9.45 [5.03-17.75]) than in the rural areas (1.95 [0.58-6.61], p for interaction=0.017), where D pteronyssinus sensitisation was common, but unrelated to wheeze in the presence of high-intensity parasite infection. Interpretation High degrees of parasite infection might prevent asthma symptoms in atopic individuals.	Univ Nottingham, City Hosp, Div Resp Med, Nottingham NG5 1PB, England; Jimma Univ, Dept Internal Med, Jima, Ethiopia; Univ Nottingham, Sch Pharmaceut Sci, Boots Sci Inst, Nottingham NG7 2RD, England; Wythenshawe Hosp, NW Lung Ctr, Manchester M23 9LT, Lancs, England	Britton, J (reprint author), Univ Nottingham, City Hosp, Div Resp Med, Nottingham NG5 1PB, England.		Britton, John/G-9705-2011; Custovic, Adnan/A-2435-2012	Custovic, Adnan/0000-0001-5218-7071; Woodcock, Ashley/0000-0002-5428-8578			Armstrong PB, 2001, TRENDS IMMUNOL, V22, P47, DOI 10.1016/S1471-4906(00)01803-2; BUCHANAN DJ, 1974, POSTGRAD MED J, V50, P680; Chow SC, 2000, PARASITE IMMUNOL, V22, P21, DOI 10.1046/j.1365-3024.2000.00270.x; CLYMER JM, SABIN I DEV HOOKWORM; Culley FJ, 2000, J IMMUNOL, V165, P6447; Dold S, 1998, J ALLERGY CLIN IMMUN, V102, P414, DOI 10.1016/S0091-6749(98)70129-0; Faniran AO, 1999, THORAX, V54, P606; GODFREY RC, 1976, NATURE, V259, P484, DOI 10.1038/259484a0; KEELEY DJ, 1991, THORAX, V46, P549, DOI 10.1136/thx.46.8.549; Matricardi PM, 2000, BRIT MED J, V320, P412, DOI 10.1136/bmj.320.7232.412; Ng'ang'a LW, 1998, THORAX, V53, P919; NUTMAN TB, 1991, MEASUREMENT IGE RESP; Odhiambo JA, 1998, EUR RESPIR J, V12, P1105, DOI 10.1183/09031936.98.12051105; Platts-Mills TAE, 2000, J ALLERGY CLIN IMMUN, V105, pS503, DOI 10.1016/S0091-6749(00)90051-4; PRITCHARD DI, 1990, PARASITOLOGY, V100, P317; Pritchard DI, 1999, PARASITE IMMUNOL, V21, P439, DOI 10.1046/j.1365-3024.1999.00238.x; QUINNELL RJ, 1993, PARASITOLOGY, V106, P379; ROACH TIA, 1988, PARASITE IMMUNOL, V10, P279, DOI 10.1111/j.1365-3024.1988.tb00221.x; Selassie FG, 2000, CLIN EXP ALLERGY, V30, P356, DOI 10.1046/j.1365-2222.2000.00706.x; SENTHILSELVAN A, 1992, AM REV RESPIR DIS, V146, P884; Strachan David P., 2000, Thorax, V55, pS2, DOI 10.1136/thorax.55.suppl_1.S2; Sunyer J, 2000, ALLERGY, V55, P762, DOI 10.1034/j.1398-9995.2000.00657.x; van den Biggelaar AHJ, 2000, LANCET, V356, P1723, DOI 10.1016/S0140-6736(00)03206-2; VANNIEKERK CH, 1979, CLIN ALLERGY, V9, P319; VENN AJ, IN PRESS AM J RESP C; WARRELL DA, 1975, Q J MED, V44, P325; Weinberg EG, 2000, J ALLERGY CLIN IMMUN, V105, P224, DOI 10.1016/S0091-6749(00)90069-1; Weiss ST, 2000, J ALLERGY CLIN IMMUN, V105, P205, DOI 10.1016/S0091-6749(00)90067-8; Yemaneberhan H, 1997, LANCET, V350, P85, DOI 10.1016/S0140-6736(97)01151-3; Yobo EODA, 1997, THORAX, V52, P161	30	216	228	2	16	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	NOV 3	2001	358	9292					1493	1499		10.1016/S0140-6736(01)06579-5		7	Medicine, General & Internal	General & Internal Medicine	490MN	WOS:000172055800011	11705561	
J	Ernst, P; Cormier, Y				Ernst, P; Cormier, Y			Relative scarcity of asthma and atopy among rural adolescents raised on a farm	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							RESPIRATORY-HEALTH-SURVEY; HAY-FEVER; ALLERGIC RHINITIS; EAST-GERMANY; PREVALENCE; CHILDHOOD; COMMUNITY; INCREASE; SCHOOLCHILDREN; ENVIRONMENT	We determined the prevalence of markers of atopy and asthma among 1,199 rural secondary school students ages 12 to 19 yr. Subjects identified as having been raised on a farm and half as many subjects without regular exposure to a farming environment from the same school class completed a respiratory symptom questionnaire and underwent allergy skin tests and a methacholine bronchoprovocation test. Current wheeze, airways hyperresponsiveness (AHR), and skin test positivity to inhaled allergens were all significantly less common among adolescents raised on the farm and these differences were especially pronounced in girls. After adjusting for gender and current smoking, the odds ratios for being raised on a farm were: 0.70 (95% CI 0.52 to 0.95) for current wheeze; 0.59 (95% CI 0.37 to 0.95) for asthma, defined as the concomitant occurrence of wheeze and AHR; and 0.58 (95% CI 0.46 to 0.75) for atopy defined as a positive reaction to any one of 24 common inhaled allergens. These associations were also not significantly altered by adjusting for the difference in the number of siblings.	Hop Laval, Ctr Pneumol, Unite Rech, Quebec City, PQ, Canada; McGill Univ, Ctr Hlth, Div Resp, Montreal, PQ, Canada	Ernst, P (reprint author), Royal Victoria Hosp, 687 Pine Ave W,R4-29, Montreal, PQ H3A 1A1, Canada.						ABERG N, 1995, CLIN EXP ALLERGY, V25, P815, DOI 10.1111/j.1365-2222.1995.tb00023.x; ABERG N, 1989, CLIN EXP ALLERGY, V19, P59, DOI 10.1111/j.1365-2222.1989.tb02345.x; American Thoracic Society, 1998, AM J RESP CRIT CARE, V158, pS1; American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P1285, DOI 10.1164/ajrccm/136.5.1285; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; BJORKSTEN B, 1997, EUR RESPIR REV, V7, P11; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; BURR M L, 1989, Archives of Disease in Childhood, V64, P1452; Butland BK, 1999, EUR RESPIR J, V13, P744, DOI 10.1034/j.1399-3003.1999.13d08.x; Helms PJ, 1999, ARCH DIS CHILD, V80, P401; Holt PG, 1997, THORAX, V52, P1; Kogevinas M, 1999, LANCET, V353, P1750, DOI 10.1016/S0140-6736(98)07397-8; MANFREDA J, 1993, CHEST, V103, P151, DOI 10.1378/chest.103.1.151; Omran M, 1996, BRIT MED J, V312, P34; SEATON A, 1994, THORAX, V49, P171, DOI 10.1136/thx.49.2.171; 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; Svanes C, 1999, J ALLERGY CLIN IMMUN, V103, P415, DOI 10.1016/S0091-6749(99)70465-3; TOELLE BG, 1992, AM REV RESPIR DIS, V146, P633; von Mutius E, 1998, LANCET, V351, P862, DOI 10.1016/S0140-6736(97)10100-3; VONMUTIUS E, 1994, AM J RESP CRIT CARE, V149, P358; vonMutius E, 1996, BRIT MED J, V312, P1448; VONMUTIUS E, 1994, BRIT MED J, V308, P692; YAN K, 1983, THORAX, V38, P760, DOI 10.1136/thx.38.10.760	26	216	218	0	6	AMER LUNG ASSOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	MAY	2000	161	5					1563	1566				4	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	312LU	WOS:000086945400029	10806155	
J	James, AL; Palmer, LJ; Kicic, E; Maxwell, PS; Lagan, SE; Ryan, GF; Musk, AW				James, AL; Palmer, LJ; Kicic, E; Maxwell, PS; Lagan, SE; Ryan, GF; Musk, AW			Decline in lung function in the Busselton Health Study - The effects of asthma and cigarette smoking	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; epidemiology; lung function tests; smoking	OBSTRUCTIVE PULMONARY-DISEASE; PERIPHERAL LEUKOCYTE COUNT; AIR-FLOW OBSTRUCTION; LONGITUDINAL DECLINE; WESTERN-AUSTRALIA; CHILDHOOD ASTHMA; MILD ASTHMA; INFLAMMATION; ADULTS; HYPERRESPONSIVENESS	Asthma in adults may be associated with chronic airflow obstruction, possibly resulting from airway disease in early life and/or a greater rate of decline in lung function in adult life compared with those with asthma. Treatment and cigarette smoking may also influence the rate of decline of lung function. The aim of this analysis was to examine the level and rate of decline in lung function in relationship to asthma and cigarette smoking in adults. Subjects (n = 9,317) had participated as adults (> 18 years) in one or more of the cross-sectional Busselton Health Surveys between 1966 and 1981 or in the follow-up study of 1994/1995. The effects of sex, doctor-diagnosed asthma, smoking status, and anthropometric data on the level and rate of decline in FEV1 were examined in a linear mixed effects model. At the age of 19 years, FEV1 was reduced in subjects with asthma but was similar in smokers and nonsmokers. Males, taller subjects, smokers, and subjects with asthma had greater declines in FEV1 with age. Smoking and asthma had additive but not multiplicative effects on decline. Thus, asthma is associated with reduced lung function at the beginning of adult life as well as an increased rate of decline during adult life.	Queen Elizabeth II Med Ctr, W Australian Sleep Disorders Res Inst, Nedlands, WA 6009, Australia; Univ Western Australia, Med Res Ctr, Sch Med & Pharmacol, Nedlands, WA 6009, Australia; Western Australia Inst Med Res, Lab Genet Epidemiol, Nedlands, WA, Australia; Sir Charles Gairdner Hosp, Dept Resp Med, Nedlands, WA 6009, Australia	James, AL (reprint author), Queen Elizabeth II Med Ctr, W Australian Sleep Disorders Res Inst, Level 5,G Block,Hosp Ave, Nedlands, WA 6009, Australia.	ajames@it.net.au	Palmer, Lyle/K-3196-2014	Palmer, Lyle/0000-0002-1628-3055			Altose MD, 2000, NEW ENGL J MED, V343, P1902; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; American Thoracic Society, 1979, AM REV RESPIR DIS, V119, P831; ANTHONISEN NR, 1994, JAMA-J AM MED ASSOC, V272, P1497, DOI 10.1001/jama.272.19.1497; BEASLEY R, 1989, AM REV RESPIR DIS, V139, P806; Brieman L., 1984, CLASSIFICATION REGRE; BROWN PJ, 1984, THORAX, V39, P131, DOI 10.1136/thx.39.2.131; BURCHFIEL CM, 1995, AM J RESP CRIT CARE, V151, P1778; Carroll N, 1997, EUR RESPIR J, V10, P292, DOI 10.1183/09031936.97.10020292; Chalmers GW, 2002, THORAX, V57, P226, DOI 10.1136/thorax.57.3.226; CHANYEUNG M, 1988, THORAX, V43, P462, DOI 10.1136/thx.43.6.462; DOMPELING E, 1993, ANN INTERN MED, V118, P770; Fletcher C, 1976, NATURAL HIST CHRONIC; James AL, 1999, EUR RESPIR J, V13, P1115, DOI 10.1034/j.1399-3003.1999.13e29.x; JAMES AL, 1998, BUSSELTON STUDY MAPP, P92; LAIRD NM, 1982, BIOMETRICS, V38, P963, DOI 10.2307/2529876; LAITINEN LA, 1988, EUR RESPIR J, V1, P488; LAITINEN LA, 1992, J ALLERGY CLIN IMMUN, V90, P32, DOI 10.1016/S0091-6749(06)80008-4; Lange P, 1998, NEW ENGL J MED, V339, P1194, DOI 10.1056/NEJM199810223391703; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Medical Research Council on the aetiology of chronic bronchitis, 1960, BRIT MED J, V2, P1965; MUSK AW, 1998, BUSSELTON HLTH STUDY, P99; OSWALD H, 1994, BRIT MED J, V309, P95; Palmer LJ, 2001, AM J RESP CRIT CARE, V163, P37; Panizza J, 1999, AM J RESP CRIT CARE, V159, pA134; PEAT JK, 1992, BRIT MED J, V305, P1326; PEAT JK, 1987, EUR J RESPIR DIS, V70, P171; PEAT JK, 1990, THORAX, V45, P32, DOI 10.1136/thx.45.1.32; SAETTA M, 1994, EUR RESPIR J, V7, P1505, DOI 10.1183/09031936.94.07081505; Sears MR, 2003, NEW ENGL J MED, V349, P1414, DOI 10.1056/NEJMoa022363; Sherrill D, 2003, EUR RESPIR J, V21, P95, DOI 10.1183/09031936.03.00017103; Sont JK, 1999, AM J RESP CRIT CARE, V159, P1043; SPARROW D, 1984, CHEST, V86, P383, DOI 10.1378/chest.86.3.383; Szefler S, 2000, NEW ENGL J MED, V343, P1054; Ulrik CS, 1999, EUR RESPIR J, V14, P892, DOI 10.1034/j.1399-3003.1999.14d27.x; ULRIK CS, 1994, AM J RESP CRIT CARE, V150, P629; Wang ML, 1999, OCCUP ENVIRON MED, V56, P837; Ward C, 2002, THORAX, V57, P309, DOI 10.1136/thorax.57.4.309	38	215	220	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.	JAN 15	2005	171	2					109	114		10.1164/rccm.200402-230OC		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	886UO	WOS:000226258400005	15486340	
S	Gold, DR; Wright, R				Gold, DR; Wright, R			Population disparities in asthma	ANNUAL REVIEW OF PUBLIC HEALTH	Annual Review of Public Health		English	Review; Book Chapter						children; hygiene hypothesis; smoking; allergens; traffic pollution; obesity	POSTTRAUMATIC-STRESS-DISORDER; DAY-CARE ATTENDANCE; SMALL-AREA ANALYSIS; INNER-CITY ASTHMA; LOWER RESPIRATORY ILLNESS; CORONARY HEART-DISEASE; BODY-MASS INDEX; TOTAL SERUM IGE; CHILDHOOD ASTHMA; UNITED-STATES	The prevalence of asthma in the United States is higher than in many other countries in the world. Asthma, the most common chronic disease of childhood in the United States, disproportionately burdens many socioeconomically disadvantaged urban communities. In this review we discuss hypotheses for between-country disparities in asthma prevalence, including differences in "hygiene" (e.g., family size, use of day care, early-life respiratory infection exposures, endotoxin and other farm-related exposures, microbial colonization of the infant bowel, exposure to parasites, and exposure to large domestic animal sources of allergen), diet, traffic pollution, and cigarette smoking. We present data on socioeconomic and ethnic disparities in asthma prevalence and morbidity in the United States and discuss environmental factors contributing to asthma disparities (e.g., housing conditions, indoor environmental exposures including allergens, traffic air pollution, disparities in treatment and access to care, and cigarette smoking). We discuss environmental influences on somatic growth (low birth weight, prematurity, and obesity) and their relevance to asthma disparities. The relevance of the hygiene hypothesis to the U.S. urban situation is reviewed. Finally, we discuss community-level factors contributing to asthma disparities.	Harvard Univ, Sch Med, Channing Lab, Brigham & Womens Hosp, Boston, MA 02467 USA	Gold, DR (reprint author), Harvard Univ, Sch Med, Channing Lab, Brigham & Womens Hosp, Boston, MA 02467 USA.	diane.gold@channing.harvard.edu; rosalind.wright@channing.harvard.edu			NHLBI NIH HHS [K08 HL04187, U10 HL72494]; NIAID NIH HHS [R01 AI 35786]; NIEHS NIH HHS [ES10932]		Acierno R, 1996, BEHAV MODIF, V20, P363, DOI 10.1177/01454455960204001; ADLER NE, 1994, AM PSYCHOL, V49, P15, DOI 10.1037/0003-066X.49.1.15; Aligne CA, 2000, AM J RESP CRIT CARE, V162, P873; ANDA RF, 1990, JAMA-J AM MED ASSOC, V264, P1541, DOI 10.1001/jama.264.12.1541; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; ATTAR BK, 1994, J CLIN CHILD PSYCHOL, V23, P391, DOI 10.1207/s15374424jccp2304_5; Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Beckett WS, 1996, AM J RESP CRIT CARE, V154, P894; BECKHAM JC, 1995, J TRAUMA STRESS, V8, P461, DOI 10.1007/BF02102970; BENSON CB, 1998, DIAGNOSTIC ULTRASOUN, P1013; BENSON V, 1998, VITAL HLTH STAT, P10; Black PN, 1997, EUR RESPIR J, V10, P6, DOI 10.1183/09031936.97.10010006; BOYCE WT, 1995, PSYCHOSOM MED, V57, P411; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; BRESLAU N, 1991, ARCH GEN PSYCHIAT, V48, P216; Britton J, 2003, AM J RESP CRIT CARE, V168, P266, DOI 10.1164/rccm.2305011; BUSSE WE, 1994, AM J RESP CRIT CARE, V151, P249; BVALDINI M, 1999, AM J RESP CELL MOL B, V20, P976; CARR W, 1992, AM J PUBLIC HEALTH, V82, P59, DOI 10.2105/AJPH.82.1.59; Castro-Rodriguez Jose A., 2001, American Journal of Respiratory and Critical Care Medicine, V163, P1344; CDC, 1998, TOB US US RAC ETHN M; Celedon JC, 2003, AM J RESP CRIT CARE, V167, P1239, DOI 10.1164/rccm.200209-1063OC; Celedon JC, 2002, LANCET, V360, P781, DOI 10.1016/S0140-6736(02)09906-3; Celedon JC, 2001, AM J RESP CRIT CARE, V164, P1835; Celedon JC, 2002, ARCH PEDIAT ADOL MED, V156, P241; Celedon JC, 2004, CHEST, V125, P85, DOI 10.1378/chest.125.1.85; Chen E, 2003, PSYCHOSOM MED, V65, P984, DOI 10.1097/01.PSY.0000097340.54195.3C; Chew GL, 1998, AM J RESP CRIT CARE, V157, P1536; *COMM UND EL RAC E, 2002, UN TREAT CONFR RAC E; CURRY SJ, 1993, AM J PREV MED, V9, P78; DEKKER C, 1991, CHEST, V100, P92; DERANT R, 1995, DEV BEHAV PEDIAT, V16, P233; DIAZSANCHEZ D, 1994, J CLIN INVEST, V94, P1417, DOI 10.1172/JCI117478; DiezRoux AV, 1997, AM J EPIDEMIOL, V146, P48; DOHRENWEND BP, 2000, SOCIAL STATUS PSYCHO; Doubilet PM, 2000, ULTRASONOGRAPHY OBST, P206; Evans GW, 2001, HANDBOOK OF HEALTH PSYCHOLOGY, P365; FEIGELMAN W, 1989, J PSYCHOACTIVE DRUGS, V21, P299; Ganz ML, 2000, AM J PUBLIC HEALTH, V90, P367, DOI 10.2105/AJPH.90.3.367; Gennuso J, 1998, ARCH PEDIAT ADOL MED, V152, P1197; GERGEN PJ, 1988, PEDIATRICS, V81, P1; Gern JE, 2004, J ALLERGY CLIN IMMUN, V113, P307, DOI 10.1016/j.jaci.2003.11.017; GOLD DR, 1993, AM REV RESPIR DIS, V148, P10; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; Gold DR, 2003, PEDIATR PULM, V36, P514, DOI 10.1002/ppul.10376; GOTTLIEB DJ, 1995, CHEST, V108, P28, DOI 10.1378/chest.108.1.28; GRAVES E, 1996, NATL CENT HLTH STAT, V13, pR1; Green RS, 2003, ENV HLTH PERSPECT, V112, P61, DOI DOI 10.1289/EHP.6566; Grischkan J, 2004, J PEDIATR-US, V144, P321, DOI 10.1016/j.jpeds.2003.11.029; HAAN M, 1987, AM J EPIDEMIOL, V125, P989; Haan M. 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Public Health		2005	26						89	113		10.1146/annurev.publhealth.26.021304.144528		25	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	924LY	WOS:000228981500005	15760282	
J	Akdis, CA; Blaser, K				Akdis, CA; Blaser, K			Mechanisms of interleukin-10-mediated immune suppression	IMMUNOLOGY			English	Review							BEE VENOM PHOSPHOLIPASE-A2; T-CELL EPITOPE; PERIPHERAL-BLOOD EOSINOPHILS; INHIBITS CYTOKINE PRODUCTION; HUMAN LYMPHOCYTES-T; PHOSPHATIDYLINOSITOL 3-KINASE; IN-VITRO; B-CELL; TYROSINE PHOSPHORYLATION; DIFFERENTIAL REGULATION	Specific immune suppression and induction of anergy are essential processes in the regulation and circumvention of immune defence. Interleukin-10 (IL-10), a suppressor cytokine of T-cell proliferative and cytokine responses, plays a key regulatory role in tolerizing exogenous antigens during specific immunotherapy (SIT) of allergy and natural exposure to antigens. Specific T-cell tolerance is directed against the T-cell epitopes of an antigen and characterized by suppressed proliferative and T helper type 1 (Th1) and type 2 (Th2) cytokine responses. IL-10 elicits tolerance in T cells by selective inhibition of the CD28 co-stimulatory pathway and thereby controls suppression and development of antigen-specific immunity. IL-10 only inhibits T cells stimulated by low numbers of triggered T-cell receptors and which therefore depend on CD28 co-stimulation. T cells receiving a strong signal from the T-cell receptor alone, and thus not requiring CD28 co-stimulation, are not affected by IL-10. IL-10 inhibits CD28 tyrosine phosphorylation, the initial step of the CD28 signalling pathway, and consequently the phosphatidylinositol 3-kinase p85 binding to CD28. Together these results demonstrate that IL-10-induced selective inhibition of the CD28 co-stimulatory pathway acts as a decisive mechanism in determining whether a T cell will contribute to an immune response or become anergic.	Swiss Inst Allergy & Asthma Res, CH-7270 Davos, Switzerland	Akdis, CA (reprint author), Swiss Inst Allergy & Asthma Res, Obere Str 22, CH-7270 Davos, Switzerland.						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J	Lack, G				Lack, Gideon			Epidemiologic risks for food allergy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						risk factors; food allergy; allergen	ATOPIC-DERMATITIS; PEANUT ALLERGY; VITAMIN-D; QUESTIONNAIRE SURVEY; ORAL TOLERANCE; NUT ALLERGY; SKIN PRICK; FOLLOW-UP; CHILDREN; INFANT	This article reviews possible risk factors and theories for the development of food allergy. It is noted that previous strategies to prevent food allergy through allergen avoidance during pregnancy, breast-feeding, and infancy have more recently been called into question. Alternative hypotheses are examined with respect to food allergy, namely the hygiene hypothesis, the dietary fat hypothesis, the antioxidant hypothesis, and the vitamin D hypotheses. An alternative hypothesis is proposed, suggesting that sensitization to allergen occurs through environmental exposure to allergen through the skin and that consumption of food allergen induces oral tolerance. This hypothesis provides a possible explanation for the close link between eczema and the development of food allergies. It also suggests novel interventional strategies to prevent the development of food allergies.	Kings Coll London, St Thomas Hosp, Childrens Allergies Dept, London SE1 7EH, England	Lack, G (reprint author), Kings Coll London, St Thomas Hosp, Childrens Allergies Dept, 2nd Floor,S Wing, London SE1 7EH, England.	gideon.lack@kcl.ac.uk					*54 WORLD HLTH ASS, 2001, PROV AG IT 1311 GLOB; ALBERTO EJC, 2008, PEDIAT ALLERGY  0116; Amoli MM, 2002, GENES IMMUN, V3, P220, DOI 10.1038/sj.gene.6363872; Bager P, 2008, CLIN EXP ALLERGY, V38, P634, DOI 10.1111/j.1365-2222.2008.02939.x; Baker SS, 2000, PEDIATRICS, V106, P346; Bergmann RL, 2002, CLIN EXP ALLERGY, V32, P205, DOI 10.1046/j.1365-2222.2002.01274.x; Black PN, 1997, EUR RESPIR J, V10, P6, DOI 10.1183/09031936.97.10010006; Camargo CA, 2007, J ALLERGY CLIN IMMUN, V120, P131, DOI 10.1016/j.jaci.2007.03.049; Cantorna MT, 2004, AM J CLIN NUTR, V80, p1717S; Cohen A, 2007, PEDIATR ALLERGY IMMU, V18, P217, DOI 10.1111/j.1399-3038.2006.00506.x; *COMM TOX CHEM FOO, 1998, CONS PROD ENV PEAN A; Derby CJ, 2005, PEDIATR ALLERGY IMMU, V16, P171, DOI 10.1111/j.1399-3038.2005.00232.x; Dioun AF, 2003, PEDIATR ALLERGY IMMU, V14, P307, DOI 10.1034/j.1399-3038.2003.00063.x; Eggesbo M, 2003, J ALLERGY CLIN IMMUN, V112, P420, DOI 10.1067/mai.2003.1610; Eigenmann PA, 2000, PEDIATR ALLERGY IMMU, V11, P95, DOI 10.1034/j.1399-3038.2000.00071.x; Greer FR, 2008, PEDIATRICS, V121, P183, DOI 10.1542/peds.2007-3022; Grundy J, 2002, J ALLERGY CLIN IMMUN, V110, P784, DOI 10.1067/mai.2002.128802; Hill DJ, 2008, CLIN EXP ALLERGY, V38, P161, DOI 10.1111/j.1365-2222.2007.02861.x; Hill DJ, 1997, ENVIRON TOXICOL PHAR, V4, P101, DOI 10.1016/S1382-6689(97)10049-7; Host A, 2008, PEDIATR ALLERGY IMMU, V19, P1, DOI 10.1111/j.1399-3038.2007.00680.x; Hourihane JO, 1996, BRIT MED J, V313, P518; Howell MD, 2007, J ALLERGY CLIN IMMUN, V120, P150, DOI 10.1016/j.jaci.2007.04.031; Hypponen E, 2004, ANN NY ACAD SCI, V1037, P84, DOI 10.1196/annals.1337.013; Karmaus W, 2002, J EPIDEMIOL COMMUN H, V56, P209, DOI 10.1136/jech.56.3.209; Kulig M, 1999, J ALLERGY CLIN IMMUN, V103, P1173, DOI 10.1016/S0091-6749(99)70195-8; Kull I, 2006, ALLERGY, V61, P1009, DOI 10.1111/j.1398-9995.2006.01115.x; Lack G, 2003, NEW ENGL J MED, V348, P977, DOI 10.1056/NEJMoa013536; LACK G, 2007, CONCEPT ORAL TOLERAN, V59, P63; Lee J, 2008, J ALLERGY CLIN IMMUN, V121, P116, DOI 10.1016/j.jaci.2007.10.043; Levy Y, 2003, ALLERGY, V58, P1206, DOI 10.1046/j.1398-9995.2003.00307.x; Liu X, 2004, J ALLERGY CLIN IMMUN, V113, P489, DOI 10.1016/j.jaci.2003.12.037; Lucas JSA, 2003, PEDIATR ALLERGY IMMU, V14, P420, DOI 10.1046/j.0905-6157.2003.00095.x; Milner JD, 2004, PEDIATRICS, V114, P27, DOI 10.1542/peds.114.1.27; Palmer CNA, 2006, NAT GENET, V38, P441, DOI 10.1038/ng1767; Perry TT, 2004, J ALLERGY CLIN IMMUN, V113, P973, DOI 10.1016/j.jaci.2004.02.035; Poole JA, 2006, PEDIATRICS, V117, P2175, DOI 10.1542/peds.2005-1803; Roberts G, 2005, J ALLERGY CLIN IMMUN, V115, P1291, DOI 10.1016/j.jaci.2005.02.038; Rona RJ, 2007, J ALLERGY CLIN IMMUN, V120, P638, DOI 10.1016/j.jaci.2007.05.026; SAARINEN UM, 1980, LANCET, V1, P166; SALOGA J, 1994, AM J RESP CRIT CARE, V149, P65; Sampson HA, 1997, J ALLERGY CLIN IMMUN, V100, P444; SAMPSON HA, 1998, PEDIATRICS, V101, pE8; Sears MR, 2002, LANCET, V360, P901, DOI 10.1016/S0140-6736(02)11025-7; Sicherer SH, 2000, J ALLERGY CLIN IMMUN, V106, P53, DOI 10.1067/mai.2000.108105; Strid J, 2004, EUR J IMMUNOL, V34, P2100, DOI 10.1002/eji.200324843; Strid J, 2004, IMMUNOLOGY, V113, P293, DOI 10.1111/j.1365-2567.2004.01989.x; Sudo N, 1997, J IMMUNOL, V159, P1739; van Reijsen FC, 1998, J ALLERGY CLIN IMMUN, V101, P207; WIST M, 2005, CLIN MOL ALLERGY, V3, P7; ZEIGER RS, 1995, J ALLERGY CLIN IMMUN, V95, P1179, DOI 10.1016/S0091-6749(95)70074-9; Zuidmeer L, 2008, J ALLERGY CLIN IMMUN, V121, P1210, DOI 10.1016/j.jaci.2008.02.019; LEAP LEARNING EARLY	52	214	226	2	25	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JUN	2008	121	6					1331	1336		10.1016/j.jaci.2008.04.032		6	Allergy; Immunology	Allergy; Immunology	313WW	WOS:000256771700005	18539191	
J	Audicana, MT; Kennedy, MW				Audicana, M. Teresa; Kennedy, Malcolm W.			Anisakis simplex: from obscure infectious worm to inducer of immune hyersensitivity	CLINICAL MICROBIOLOGY REVIEWS			English	Review							EXCRETORY-SECRETORY PRODUCTS; PSEUDOTERRANOVA-DECIPIENS NEMATODA; GASTRO-ALLERGIC ANISAKIASIS; SERINE-PROTEASE INHIBITOR; ANI S 1; MAJOR ALLERGEN; ASCARIS-SUUM; ANTIBODY REPERTOIRE; MOLECULAR-CLONING; CROSS-REACTIVITY	Infection of humans with the nematode worm parasite Anisakis simplex was first described in the 1960s in association with the consumption of raw or undercooked fish. During the 1990s it was realized that even the ingestion of dead worms in food fish can cause severe hypersensitivity reactions, that these may be more prevalent than infection itself, and that this outcome could be associated with food preparations previously considered safe. Not only may allergic symptoms arise from infection by the parasites ("gastroallergic anisakiasis"), but true anaphylactic reactions can also occur following exposure to allergens from dead worms by food-borne, airborne, or skin contact routes. This review discusses A. simplex pathogenesis in humans, coveting immune hypersensitivity reactions both in the context of a living infection and in terms of exposure to its allergens by other routes. Over the last 20 years, several studies have concentrated on A. simplex antigen characterization and innate as well as adaptive immune response to this parasite. Molecular characterization of Anisakis allergens and isolation of their encoding cDNAs is now an active field of research that should provide improved diagnostic tools in addition to tools with which to enhance our understanding of pathogenesis and controversial aspects of A. simplex allergy. We also discuss the potential relevance of parasite products such as allergens, proteinases, and proteinase inhibitors and the activation of basophils, eosinophils, and mast cells in the induction of A. simplex-related immune hypersensitivity states induced by exposure to the parasite, dead or alive.	[Audicana, M. 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J	Schwarze, PE; Ovrevik, J; Lag, M; Refsnes, M; Nafstad, P; Hetland, RB; Dybing, E				Schwarze, P. E.; Ovrevik, J.; Lag, M.; Refsnes, M.; Nafstad, P.; Hetland, R. B.; Dybing, E.			Particulate matter properties and health effects: consistency of epidemiological and toxicological studies	HUMAN & EXPERIMENTAL TOXICOLOGY			English	Review						ambient particulate matter; epidemiology; health effects; particle composition; toxicology	DIESEL EXHAUST PARTICLES; AIRWAY EPITHELIAL-CELLS; POLYCYCLIC AROMATIC-HYDROCARBONS; CORONARY-HEART-DISEASE; INSOLUBLE IRIDIUM PARTICLES; LONG-TERM EXPOSURE; NF-KAPPA-B; AMBIENT AIR; IN-VITRO; DAILY MORTALITY	Identifying the ambient particulate matter (PM) fractions or constituents, critically involved in eliciting adverse health effects, is crucial to the implementation of more cost-efficient abatement strategies to improve air quality. This review focuses on the importance of different particle properties for PM-induced effects, and whether there is consistency in the results from epidemiological and experimental studies. An evident problem for such comparisons is that epidemiological and experimental data on the effects of specific components of ambient PM are limited. Despite this, some conclusions can be drawn. With respect to the importance of the PM size-fractions experimental and epidemiological studies are somewhat conflicting, but there seems to be a certain consistency in that the coarse fraction (PM10-2.5) has an effect that should not be neglected. Better exposure characterization may improve the consistency between the results from experimental and epidemiological studies, in particular for ultrafine particles. Experimental data indicate that surface area is an important metric, but composition may play an even greater role in eliciting effects. The consistency between epidemiological and experimental findings for specific PM-components appears most convincing for metals, which seem to be important for the development of both pulmonary and cardiovascular disease. Metals may also be involved in PM-induced allergic sensitization, but the epidemiological evidence for this is scarce. Soluble organic compounds appear to be implicated in PM-induced allergy and cancer, but the data from epidemiological studies are insufficient for any conclusions. The present review suggests that there may be a need for improvements in research designs. In particular, there is a need for better exposure assessments in epidemiological investigations, whereas experimental data would benefit from an improved comparability of studies. Combined experimental and epidemiological investigations may also help answer some of the unresolved issues.	Norwegian Inst Publ Hlth, N-0403 Oslo, Norway	Schwarze, PE (reprint author), Norwegian Inst Publ Hlth, POB4404 Nydalen, N-0403 Oslo, Norway.	per.schwarze@fhi.no	Schwarze, Per/I-2080-2016				Abrahamowicz M, 2003, J TOXICOL ENV HEAL A, V66, P1625, DOI 10.1080/15287390390211676; AGATE K, 2005, IN PRESS TOXICOL IN; Anderson HR, 2004, METAANALYSIS TIME SE; Armstrong B, 2004, ENVIRON HEALTH PERSP, V112, P970, DOI 10.1289/ehp.6895; Aukrust P, 2005, ANN MED, V37, P74, DOI 10.1080/07853890510007232; Avogbe PH, 2005, CARCINOGENESIS, V26, P613, DOI 10.1093/carcin/bgh353; Barchowsky A, 2003, FREE RADICAL BIO MED, V34, P1130, DOI 10.1016/S0891-5849(03)00059-5; Bauer H, 2002, ATMOS RES, V64, P109, DOI 10.1016/S0169-8095(02)00084-4; Becher R, 2001, INHAL TOXICOL, V13, P789, DOI 10.1080/089583701316941311; Becker S, 2005, TOXICOL APPL PHARM, V203, P45, DOI 10.1016/j.taap.2004.07.007; BECKER S, 2005, IN PRESS TOXICOL APP; Binkovda B, 2003, MUTAT RES-FUND MOL M, V525, P43, DOI 10.1016/S0027-5107(02)00312-3; 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J	Reed, CE; Kita, H				Reed, CE; Kita, H			The role of protease activation of inflammation in allergic respiratory diseases	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						allergen; proteases; allergic inflammation; asthma; sinusitis	MAST-CELL TRYPTASE; AIRWAY SMOOTH-MUSCLE; DUST-MITE ALLERGEN; LUNG EPITHELIAL-CELLS; SEVERE ALPHA(1)-ANTITRYPSIN DEFICIENCY; INDUCE CYTOKINE RELEASE; FACTOR XA; ENDOTHELIAL-CELLS; DERMATOPHAGOIDES-FARINAE; ASPERGILLUS-FUMIGATUS	Extracellular endogenous proteases, as well as exogenous proteases from mites and molds, react with cell-surface receptors in the airways to generate leukocyte infiltration and to amplify the response to allergens. Stimulation leads to increased intracellular Ca++ and gene transcription. The most thoroughly investigated receptors, protease-activated receptors (PARs), are 7-transmembrane proteins coupled to G proteins. PARs are widely distributed on the cells of the airways, where they contribute to the inflammation characteristic of allergic diseases. PAR stimulation of epithelial cells opens tight junctions, causes desquamation, And produces cytokines, chemokines, and growth factors. They degranulate eosinophils and mast cells. Proteases contract bronchial smooth muscle and cause it to proliferate. PARs also promote maturation, proliferation, and collagen production of fibroblast precursors and mature fibroblasts. PAR-2, apparently the most important of the 4 PARs that have been characterized, is increased on the epithelium of patients with asthma. Trypsin, a product of injured epithelial cells, and mast cell tryptase are potent activators of PAR-2. Mast cell chymase activates PAR-I. Proteases from mites and molds appear to act through similar receptors. They amplify IgE production to allergens, degranulate eosinophils, and can generate inflammation, even in the absence of IgE. Proteases produced by Aspergillus species to support its growth are presumably responsible for the exuberant IgE, IgG, and granulomatous response of allergic bronchopulmonary aspergillosis. Similar proteases from molds germinating on the respiratory mucosa have been recently been implicated in the pathogenesis of chronic hyperplastic rhinitis and polyps and, by extension, of intrinsic asthma. Finally, proteases from mites and fungi growing in damp, water-damaged buildings might be the basis for the increased prevalence in these buildings of rhinitis, asthma, and other respiratory diseases. Future research promises to promote our understanding of the pathogenesis of allergic respiratory diseases and point the way to new therapies.	Mayo Clin, Allerg Dis Res Lab, Rochester, MN 55905 USA	Kita, H (reprint author), Mayo Clin, Allerg Dis Res Lab, Guggenheim Bldg,Room 401, Rochester, MN 55905 USA.	kita.hirohito@mayo.edu	Tang, Amy/L-3226-2016	Tang, Amy/0000-0002-5772-2878			Adam E., 2004, Journal of Allergy and Clinical Immunology, V113, pS339, DOI 10.1016/j.jaci.2004.01.730; Akers IA, 2000, AM J PHYSIOL-LUNG C, V278, pL193; ALTIERI DC, 1994, CELL IMMUNOL, V155, P372, DOI 10.1006/cimm.1994.1130; ANDO T, 1991, INT ARCH ALLER A IMM, V96, P199; ANDO T, 1993, CLIN EXP ALLERGY, V23, P777, DOI 10.1111/j.1365-2222.1993.tb00366.x; Andrade-Gordon P, 1999, P NATL ACAD SCI USA, V96, P12257, DOI 10.1073/pnas.96.22.12257; Asokananthan N, 2002, J IMMUNOL, V168, P3577; Asokananthan N, 2002, J IMMUNOL, V169, P4572; Barrios VE, 2003, BIOCHEM PHARMACOL, V66, P519, DOI 10.1016/S0006-2952(03)00292-2; Berger P, 2001, J APPL PHYSIOL, V91, P1372; Berger P, 2001, J APPL PHYSIOL, V91, P995; Blanc-Brude OP, 2001, AM J PHYSIOL-CELL PH, V281, pC681; 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Allergy Clin. Immunol.	NOV	2004	114	5					997	1008		10.1016/j.jaci.2004.07.060		12	Allergy; Immunology	Allergy; Immunology	870HI	WOS:000225047800001	15536399	
J	Thomas, WR; Smith, WA; Hales, BJ; Mills, KL; O'Brien, RM				Thomas, WR; Smith, WA; Hales, BJ; Mills, KL; O'Brien, RM			Characterization and immunobiology of house dust mite allergens	INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY			English	Review						house dust mite; allergen; IgE; T cell; recombinant mite allergens	DER-P-I; T-CELL RESPONSES; SITE-DIRECTED MUTAGENESIS; HUMAN IGE ANTIBODIES; CYSTEINE PROTEASE ACTIVITY; GLUTATHIONE-S-TRANSFERASE; MOLECULAR-WEIGHT ALLERGEN; MAJOR SECRETORY PROTEIN; ACID-BINDING PROTEINS; GROUP-III ALLERGEN	The examination of house dust mite extracts has indicated that over 30 different proteins can induce IgE antibody in patients allergic to the house dust mite. There are however dominant specificities especially the group 1 and 2 allergens which can account for much of the allergenicity of extracts. Of the 19 denominated allergens, the major IgE binding has been reported for the group 1, 2, 3, 9, 11, 14 and 15 allergens. The high-molecular-weight group 11, 14 and 15 allergens have only recently been described and although high IgE binding has been anticipated from immunoblotting, there is a need for considerable corroboration. Similarly, the study of the group 3 and 9 serine protease allergens has been incomplete. The group 4, 5, 7 and 8 allergens have shown intermediate IgE binding and the group 10 tropomyosins are of interest because of their potential cross-reactivity with allergen from disparate species. Although the progress with the production of recombinant group 1 allergens has been recent, many of the allergens can be produced as high IgE-binding polypeptides. The tertiary structure of the group 2 allergens has been determined from recombinant proteins and they are an excellent model for the investigation of modified allergens. An unexpected property of the group 1, 2 and 3 allergens has been the high degree of polymorphism found by cDNA analysis. It has however been possible to identify sequences to represent the variation in the natural allergens. The group 7 and 14 allergens show secondary modifications which vary in different extracts creating batch variation. While some estimate of the importance of allergens can be obtained from IgE binding, few analyses of T-cell responses have been made and these regulate both the development of, and the protection from sensitization. Copyright (C) 2002 S. Karger AG, Basel.	Univ Western Australia, Telethon Inst Child Hlth Res, Ctr Child Hlth Res, Perth, WA 6872, Australia; Univ Melbourne, Western Gen Hosp, Dept Med, Footscray, Vic, Australia	Thomas, WR (reprint author), Univ Western Australia, Telethon Inst Child Hlth Res, Ctr Child Hlth Res, POB 855, Perth, WA 6872, Australia.		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Arch. Allergy Immunol.	SEP	2002	129	1					1	18		10.1159/000065179		18	Allergy; Immunology	Allergy; Immunology	605YA	WOS:000178703600001	12372994	
J	Liu, AH				Liu, AH			Endotoxin exposure in allergy and asthma: Reconciling a paradox	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						allergy; asthma; therapy; prevention; endotoxin; LPS; infection; hygiene; IFN-gamma; IL-12; T(H)1	CD4(+) T-CELLS; GROWTH-FACTOR-BETA; INDUCED AIRWAY HYPERRESPONSIVENESS; STIMULATORY FACTOR INTERLEUKIN-12; INTERFERON-GAMMA PRODUCTION; GRASS-POLLEN IMMUNOTHERAPY; HAY-FEVER; MESSENGER-RNA; COLLAGEN-SYNTHESIS; INHALED ENDOTOXIN	Well-established evidence links endotoxin exposure, especially in the workplace, to airways disease. Endotoxin can increase disease severity by acting as a natural adjuvant to augment asthma and atopic inflammation. Recent studies suggest that it can even act on its own, causing a distinct endotoxic form of asthma. Other studies, however, contradict the paradigm that endotoxin's influence is solely a negative one. Epidemiologic associations of environmental endotoxin exposure with allergy and asthma prevention are consistent with hygiene hypothesis associations of other microbial exposures or infections with a lower incidence of atopic disease. Currently, microbe-derived products are being developed as potential therapies for allergy and asthma. Thus it is an ideal time to consider endotoxin as a prototype of a natural intervention with microbial components. Nature's ongoing experiment with endotoxin can provide clues for the development of effective and safe microbe-based products for disease treatment and prevention. This article will discuss (1) conventional paradigms in which endotoxin-induced immune modulation by T(H)1-type induction leads to mitigation of T(H)2-type immune development, allergen sensitization, and atopic inflammation; (2) newer concepts of T(H)1-type immune responses that may provide additional asthma-protective effects by preventing airways remodeling; (3) home and environmental features that significantly contribute to endotoxin exposure; (4) different aspects of asthma mediated by endotoxin exposure; and (5) how to understand endotoxin's paradoxical nature of serving as both friend and foe.	Natl Jewish Med & Res Ctr, Dept Pediat, Div Pediat Allergy & Immunol, Denver, CO 80206 USA; Univ Colorado, Hlth Sci Ctr, Dept Pediat, Boulder, CO 80309 USA	Liu, AH (reprint author), Natl Jewish Med & Res Ctr, Dept Pediat, Div Pediat Allergy & Immunol, 1400 Jackson St,K1023, Denver, CO 80206 USA.				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Allergy Clin. Immunol.	MAR	2002	109	3					379	392		10.1067/mai.2002.122157		14	Allergy; Immunology	Allergy; Immunology	534KW	WOS:000174586400001	11897980	
J	Sigurs, N; Aljassim, F; Kjellman, B; Robinson, PD; Sigurbergsson, F; Bjarnason, R; Gustafsson, PM				Sigurs, Nele; Aljassim, Fatma; Kjellman, Bengt; Robinson, Paul D.; Sigurbergsson, Fridrik; Bjarnason, Ragnar; Gustafsson, Per M.			Asthma and allergy patterns over 18 years after severe RSV bronchiolitis in the first year of life	THORAX			English	Article							RESPIRATORY-SYNCYTIAL-VIRUS; VENTILATION MALDISTRIBUTION; VIRAL-INFECTIONS; REFERENCE RANGES; AGE 13; INFANCY; SENSITIZATION; CHILDREN; RISK; SPIROMETRY	Background An increased prevalence of asthma/recurrent wheeze (RW), clinical allergy and allergic sensitisation up to age 13 years has previously been reported in subjects hospitalised with respiratory syncytial virus (RSV) bronchiolitis in their first year of life compared with matched controls. A study was undertaken to examine whether these features persist into early adulthood, to report longitudinal wheeze and allergy patterns, and to see how large and small airway function relates to RSV infection and asthma. Methods Follow-up at age 18 years was performed in 46 of 47 subjects with RSV and 92 of 93 controls. Assessments included questionnaire, clinical examination, skin prick tests, serum IgE antibodies to inhaled allergens, blood eosinophils, fraction of exhaled nitric oxide (FeNO), spirometry, multiple breath washout (lung clearance index, LCI) and dry air hyperventilation challenge. Results Increased prevalence of asthma/RW (39% vs 9%), clinical allergy (43% vs 17%) and sensitisation to perennial allergens (41% vs 14%) were present at age 18 in the RSV cohort compared with controls. Persistent/relapsing wheeze associated with early allergic sensitisation predominated in the RSV cohort compared with controls (30% vs 1%). Spirometric function was reduced in subjects with RSV with or without current asthma, but not in asthmatic controls. LCI was linked only to current asthma, airway hyperresponsiveness and FeNO. Conclusions Severe early RSV bronchiolitis is associated with an increased prevalence of allergic asthma persisting into early adulthood. Small airway dysfunction (LCI) is related to current asthma and airway inflammation but not to RSV bronchiolitis. Reduced spirometry after RSV may reflect airway remodelling.	[Sigurs, Nele] Boras Cent Hosp, Dept Paediat, S-50182 Boras, Sweden; [Aljassim, Fatma] Govt Dubai, Dubai Hlth Author, Alwasl Hosp, Dept Paediat, Dubai, U Arab Emirates; [Kjellman, Bengt; Gustafsson, Per M.] Cent Hosp Skovde, Dept Paediat, S-54185 Skovde, Sweden; [Aljassim, Fatma; Gustafsson, Per M.] Queen Silvia Childrens Hosp, Gothenburg, Sweden; [Robinson, Paul D.] Childrens Hosp Westmead, Dept Resp Med, Westmead, NSW, Australia; [Robinson, Paul D.] Univ Sydney, Fac Med, Discipline Paediat & Child Hlth, Childrens Hosp Westmead,Clin Sch, Sydney, NSW 2006, Australia; [Sigurbergsson, Fridrik] Landspitali Univ Hosp, Emergency Dept, Reykjavik, Iceland; [Bjarnason, Ragnar] Univ Iceland, Dept Paediat, Landspitali Univ Hosp Iceland, Reykjavik, Iceland; [Gustafsson, Per M.] Univ Gothenburg, Sahlgrenska Acad, Gothenburg, Sweden	Sigurs, N (reprint author), Boras Cent Hosp, Dept Paediat, S-50182 Boras, Sweden.	nele.sigurs@vgregion.se			Regional Health Care Authority of West Sweden; Boras Hospital; Fokus Foundation; SeBe's Fund	The study was supported by grants from the Regional Health Care Authority of West Sweden, from Boras Hospital, the Fokus Foundation and SeBe's Fund.	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J	Henderson, J; Granell, R; Heron, J; Sherriff, A; Simpson, A; Woodcock, A; Strachan, DP; Shaheen, SO; Sterne, JAC				Henderson, J.; Granell, R.; Heron, J.; Sherriff, A.; Simpson, A.; Woodcock, A.; Strachan, D. P.; Shaheen, S. O.; Sterne, J. A. C.			Associations of wheezing phenotypes in the first 6 years of life with atopy, lung function and airway responsiveness in mid-childhood	THORAX			English	Article							PRESCHOOL-CHILDREN; HIGH-RISK; ASTHMA; INFANTS; BIRTH; SENSITIZATION; PATTERNS; EXPOSURE; SOUNDS; COHORT	Background: Patterns of wheezing during early childhood may indicate differences in aetiology and prognosis of respiratory illnesses. Improved characterisation of wheezing phenotypes could lead to the identification of environmental influences on the development of asthma and airway diseases in predisposed individuals. Methods: Data collected on wheezing at seven time points from birth to 7 years from 6265 children in a longitudinal birth cohort (the ALSPAC study) were analysed. Latent class analysis was used to assign phenotypes based on patterns of wheezing. Measures of atopy, airway function ( forced expiratory volume in 1 s (FEV(1)), mid forced expiratory flow (FEF(25-75))) and bronchial responsiveness were made at 7-9 years of age. Results: Six phenotypes were identified. The strongest associations with atopy and airway responsiveness were found for intermediate onset (18 months) wheezing (OR for atopy 8.36, 95% CI 5.2 to 13.4; mean difference in dose response to methacholine 1.76, 95% CI 1.41 to 2.12 %FEV(1) per mu mol, compared with infrequent/never wheeze phenotype). Late onset wheezing (after 42 months) was also associated with atopy (OR 6.6, 95% CI 4.7 to 9.4) and airway responsiveness (mean difference 1.61, 95% CI 1.37 to 1.85 % FEV(1) per mmol). Transient and prolonged early wheeze were not associated with atopy but were weakly associated with increased airway responsiveness and persistent wheeze had intermediate associations with these outcomes. Conclusions: The wheezing phenotypes most strongly associated with atopy and airway responsiveness were characterised by onset after age 18 months. This has potential implications for the timing of environmental influences on the initiation of atopic wheezing in early childhood.	[Henderson, J.] Univ Bristol, Dept Community Based Med, Bristol, Avon, England; [Granell, R.; Heron, J.; Sherriff, A.; Sterne, J. A. C.] Univ Bristol, Dept Social Med, Bristol, Avon, England; [Simpson, A.; Woodcock, A.] Univ Manchester, North West Lung Ctr, Manchester, Lancs, England; [Strachan, D. P.] St Georges Hosp Med Sch, Dept Community Hlth Sci, London, England; [Shaheen, S. O.] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London & Resp Epidemiol & Publ Hlth Grp, London, England	Henderson, J (reprint author), ALSPAC, 24 Tyndall Ave, Bristol BS8 1TQ, Avon, England.	a.j.henderson@bris.ac.uk	Heron, Jon/D-5884-2011	Heron, Jon/0000-0001-6199-5644; Woodcock, Ashley/0000-0002-5428-8578; Simpson, Angela/0000-0003-2733-6666	Asthma UK [Senior Research Fellow]; British Lung Foundation; UK Medical Research Council; University of Bristol; Wellcome Trust	This research was specifically funded by a grant from Asthma UK to establish a research network of UK asthma birth cohorts (the STELAR network). The skin prick tests were funded by a grant from the British Lung Foundation and the measurements of lung function and airway responsiveness were supported by a grant from the UK Medical Research Council. SOS is an Asthma UK Senior Research Fellow. The UK Medical Research Council, the Wellcome Trust and the University of Bristol provide core support for ALSPAC.	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J	Holgate, ST; Polosa, R				Holgate, Stephen T.; Polosa, Riccardo			The mechanisms, diagnosis, and management of severe asthma in adults	LANCET			English	Review							LUNG-FUNCTION DECLINE; SEVERE PERSISTENT ASTHMA; NECROSIS-FACTOR-ALPHA; TO-TREAT ASTHMA; DOSE INTRAVENOUS IMMUNOGLOBULIN; PLACEBO-CONTROLLED TRIAL; GROWTH-FACTOR RECEPTOR; CHURG-STRAUSS-SYNDROME; AIRWAY SMOOTH-MUSCLE; QUALITY-OF-LIFE	There has been a recent increase in the prevalence of asthma worldwide; however, the 5-10% of patients with severe disease account for a substantial proportion of the health costs. Although most asthma cases can be satisfactorily managed with a combination of anti-inflammatory drugs and bronchodilators, patients who remain symptomatic despite maximum combination treatment represent a heterogeneous group consisting of those who are under-treated or non-adherent with their prescribed medication. After excluding under-treatment and poor compliance, corticosteroid refractory asthma can be identified as a subphenotype characterised by a heightened neutrophilic airway inflammatory response in the presence or absence of eosinophils, with evidence of increased tissue injury and remodelling. Although a wide range of environmental factors such as allergens, smoking, air pollution, infection, hormones, and specific drugs can contribute to this phenotype, other features associated with changes in the airway inflammatory response should be taken into account. Aberrant communication between an injured airway epithelium and underlying mesenchyme contributes to disease chronicity and refractoriness to corticosteroids. The importance of identifying underlying causative factors and the recent introduction of novel therapeutic approaches, including the targeting of immunoglobulin E and tumour necrosis factor a with biological agents, emphasise the need for careful phenotyping of patients with severe disease to target improved management of the individual patient's needs.	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J	Sun, G; Stacey, MA; Schmidt, M; Mori, L; Mattoli, S				Sun, G; Stacey, MA; Schmidt, M; Mori, L; Mattoli, S			Interaction of mite allergens Der P3 and Der P9 with protease-activated receptor-2 expressed by lung epithelial cells	JOURNAL OF IMMUNOLOGY			English	Article							GROUP-III ALLERGEN; DERMATOPHAGOIDES-PTERONYSSINUS; AIRWAY HYPERRESPONSIVENESS; THROMBIN RECEPTORS; GENE-EXPRESSION; ATOPIC ASTHMA; RELEASE; CLONING; KERATINOCYTES; INFLAMMATION	The respiratory epithelium represents the first barrier encountered by airborne Ags. Two major dust mite Ags, Der p3 and Der p9, are serine proteases that may activate lung epithelial cells by interaction with the protease-activated receptor 2 (PAR-2). In this study both Der p3 and Der p9 cleaved the peptide corresponding to the N terminus of PAR-2 at the activation site. Both Ags sequentially stimulated phosphoinositide hydrolysis, transient cytosolic Ca2+ mobilization, and release of GM-CSF and eotaxin in human pulmonary epithelial cells. These responses were similar to those observed with trypsin and a specific PAR-2 agonist and were related to the serine protease activity of Der p3 and Der p9. Cell exposure to the Ags resulted in a refractory period, indicating that a PAR had been cleaved. Partial desensitization to Der p3 and Der p9 by the PAR-2 agonist suggested that PAR-2 was one target of the Ags. However, PAR-2 was not the only target, because the PAR-2 agonist caused less desensitization to Der p3 and Der p9 than did trypsin. A phospholipase C inhibitor prevented the cytokine-releasing effect of the PAR-2 agonist and abolished or reduced (> 70%) the cytokine-releasing effects of Der p3 and Der p9. Our results suggest that Der p 3 and Der p9 may induce a nonallergic inflammatory response in the airways through the release of proinflammatory cytokines from the bronchial epithelium and that this effect is at least in part mediated by PAR-2.	Avail GmbH, AVAIL Biomed Res Inst, CH-4051 Basel, Switzerland	Mattoli, S (reprint author), Avail GmbH, AVAIL Biomed Res Inst, Spalentorweg 18, CH-4051 Basel, Switzerland.		Mattoli, Sabrina/H-8211-2014	Mattoli, Sabrina/0000-0002-6866-604X			ACKERMAN V, 1994, CHEST, V105, P687, DOI 10.1378/chest.105.3.687; BELLINI A, 1993, CHEST, V103, P997, DOI 10.1378/chest.103.4.997; Blackhart BD, 1996, J BIOL CHEM, V271, P16466; Bohm SK, 1996, J BIOL CHEM, V271, P22003; BROWN JR, 1998, CLIN EXP IMMUNOL, V114, P134; Cocks TM, 1999, NATURE, V398, P156, DOI 10.1038/18223; D'Andrea MR, 1998, J HISTOCHEM CYTOCHEM, V46, P157; Dery O, 1998, AM J PHYSIOL-CELL PH, V274, pC1429; DOWSE GK, 1985, J ALLERGY CLIN IMMUN, V75, P75, DOI 10.1016/0091-6749(85)90016-8; EVANS MD, 1994, AM J PHYSIOL, V266, P593; FERGUSON P, 1995, AM J RESP CRIT CARE, V151, P71; GRYNKIEWICZ G, 1985, J BIOL CHEM, V260, P3440; HEWITT CRA, 1995, J EXP MED, V182, P1537, DOI 10.1084/jem.182.5.1537; Hou L, 1998, IMMUNOLOGY, V94, P356, DOI 10.1046/j.1365-2567.1998.00528.x; Howells GL, 1997, J CELL SCI, V110, P881; Kauffman HF, 2000, J ALLERGY CLIN IMMUN, V105, P1185, DOI 10.1067/mai.2000.106210; King C, 1996, J ALLERGY CLIN IMMUN, V98, P739, DOI 10.1016/S0091-6749(96)70121-5; King C, 1998, J IMMUNOL, V161, P3645; Loew D, 2000, BIOCHEMISTRY-US, V39, P10812, DOI 10.1021/bi0003341; Madison JM, 2000, AM J RESP CELL MOL, V22, P513; Mattoli S, 1997, BIOCHEM BIOPH RES CO, V236, P299, DOI 10.1006/bbrc.1997.6958; MATTOLI S, 2001, HLTH PERSPECT S, V109; Molino M, 1997, J BIOL CHEM, V272, P11133; Molino M, 1997, J BIOL CHEM, V272, P4043; Mori L, 1995, BIOCHEM BIOPH RES CO, V217, P817, DOI 10.1006/bbrc.1995.2845; Pavord ID, 1994, LANCET, V344, P436; Pina JS, 1997, POSTGRAD MED, V101, P153; PLATTSMILLS TAE, 1992, J ALLERGY CLIN IMMUN, V89, P1046, DOI 10.1016/0091-6749(92)90228-T; Ricciardolo FLM, 2000, AM J RESP CRIT CARE, V161, P1672; Ritz Stacey A., 2000, Journal of Allergy and Clinical Immunology, V106, pS206; SEMINARIO MC, 1994, CURR OPIN IMMUNOL, V6, P860, DOI 10.1016/0952-7915(94)90005-1; Shibata Y, 1996, J IMMUNOL, V156, P772; SMITH WA, 1994, CLIN EXP ALLERGY, V24, P220, DOI 10.1111/j.1365-2222.1994.tb00223.x; SOLOPERTO M, 1991, AM J PHYSIOL, V260, pL530; Stacey MA, 1997, BIOCHEM BIOPH RES CO, V236, P522, DOI 10.1006/bbrc.1997.6997; Steinhoff M, 2000, NAT MED, V6, P151; STEWART GA, 1992, IMMUNOLOGY, V75, P29; Stewart GA, 1996, CLIN EXP ALLERGY, V26, P1020, DOI 10.1046/j.1365-2222.1996.d01-405.x; Sun G, 1997, PEPTIDES, V18, P1449, DOI 10.1016/S0196-9781(97)00194-0; Thompson PJ, 1998, CLIN EXP ALLERGY, V28, P110; Tomee JFC, 1997, J INFECT DIS, V176, P300, DOI 10.1086/517272; Vliagoftis A, 2000, J ALLERGY CLIN IMMUN, V106, P537, DOI 10.1067/mai.2000.109058; VU TKH, 1991, CELL, V64, P1057, DOI 10.1016/0092-8674(91)90261-V; Wakita H, 1997, P ASSOC AM PHYSICIAN, V109, P190; Wan H, 1999, J CLIN INVEST, V104, P123, DOI 10.1172/JCI5844; Xu WF, 1998, P NATL ACAD SCI USA, V95, P6642, DOI 10.1073/pnas.95.12.6642; Ying S, 1997, EUR J IMMUNOL, V27, P3507, DOI 10.1002/eji.1830271252	47	213	223	1	3	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	JUL 15	2001	167	2					1014	1021				8	Immunology	Immunology	471VL	WOS:000170949300050	11441110	
J	Christakis, DA; Mell, L; Koepsell, TD; Zimmerman, FJ; Connell, FA				Christakis, DA; Mell, L; Koepsell, TD; Zimmerman, FJ; Connell, FA			Association of lower continuity of care with greater risk of emergency department use and hospitalization in children	PEDIATRICS			English	Article						continuity of patient care; pediatrics; ambulatory care; emergency department; hospitalization	HEALTH-CARE; SERVICES; EXPERIENCE; SEVERITY; CHOICE; ASTHMA	Context. The benefits of continuity of pediatric care remain controversial. Objective. To determine whether there is an association between having a continuous relationship with a primary care pediatric provider and decreased risk of emergency department (ED) visitation and hospitalization. Design. Retrospective cohort study. Setting and Population. We used claims data from 46 097 pediatric patients enrolled at Group Health Cooperative, a large staff-model health maintenance organization, between January 1, 1993, and December 31, 1998, for our analysis. To be eligible, patients had to have been continuously enrolled for at least a 2-year period or since birth and to have made at least 4 visits to one of the Group Health Cooperative clinics. Main Exposure Variable. A continuity of care (COC) index that quantifies the degree to which a patient has experienced continuous care with a provider. Main Outcome Measures. ED utilization and hospitalization. Results. Compared with children with the highest COC, children with medium continuity were more likely to have visited the ED (hazard ratio [HR]: 1.28 [1.20-1.36]) and more likely to be hospitalized (HR: 1.22 [1.09-1.38]). Children with the lowest COC were even more likely to have visited the ED (HR: 1.58 [1.49-1.66]) and to be hospitalized (HR: 1.54 [1.33-1.75]). These risks were even greater for children on Medicaid and those with asthma. Conclusions. Lower continuity of primary care is associated with higher risk of ED utilization and hospitalization. Efforts to improve and maintain continuity may be warranted.	Univ Washington, Inst Child Hlth, Dept Pediat, Seattle, WA 98103 USA; Inst Child Hlth, Seattle, WA USA; Grp Hlth Cooperat Puget Sound, Seattle, WA 98121 USA; Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA; Robert Wood Johnson Clin Scholars Program, Seattle, WA USA; Univ Washington, Dept Hlth Serv, Seattle, WA 98195 USA	Christakis, DA (reprint author), Univ Washington, Inst Child Hlth, Dept Pediat, 146 N Canal St,Suite 300, Seattle, WA 98103 USA.		Zimmerman, Frederick/C-7259-2008	Zimmerman, Frederick/0000-0002-4163-9893; Mell, Loren/0000-0003-2277-6080			ALPERT JJ, 1976, PEDIATRICS, V57, P917; BECKER MH, 1974, AM J PUBLIC HEALTH, V64, P1062, DOI 10.2105/AJPH.64.11.1062; BECKER MH, 1974, J PEDIATR-US, V84, P599, DOI 10.1016/S0022-3476(74)80689-X; BICE TW, 1977, MED CARE, V15, P347, DOI 10.1097/00005650-197704000-00010; BINDMAN AB, 1995, JAMA-J AM MED ASSOC, V274, P305, DOI 10.1001/jama.274.4.305; Bodenheimer T, 1999, JAMA-J AM MED ASSOC, V281, P2045, DOI 10.1001/jama.281.21.2045; BRESLAU N, 1975, J MED EDUC, V50, P965; Chamberlain JM, 1998, ANN EMERG MED, V32, P161, DOI 10.1016/S0196-0644(98)70132-5; CHARNEY E, 1967, PEDIATRICS, V40, P188; Christakis DA, 1999, PEDIATRICS, V103, P738, DOI 10.1542/peds.103.4.738; Clayton D, 1993, STAT MODELS EPIDEMIO; EJLERTSSON G, 1984, MED CARE, V22, P231, DOI 10.1097/00005650-198403000-00006; ERIKSSON EA, 1983, MED CARE, V21, P858, DOI 10.1097/00005650-198309000-00003; Ettner SL, 1996, AM J PUBLIC HEALTH, V86, P1748, DOI 10.2105/AJPH.86.12.1748; Fishman PA, 1999, MED CARE, V37, P874, DOI 10.1097/00005650-199909000-00004; FRANKS P, 1992, NEW ENGL J MED, V327, P424, DOI 10.1056/NEJM199208063270613; FREEMAN GK, 1993, BRIT J GEN PRACT, V43, P493; GORDIS L, 1971, PEDIATRICS, V48, P766; GRAZIER KL, 1986, HEALTH SERV RES, V20, P659; Halfon N, 1996, PEDIATRICS, V98, P28; HENNEKENNS CH, 1987, EPIDEMIOLOGY MED; Kelleher KJ, 1997, ARCH PEDIAT ADOL MED, V151, P1109; Kleinbaum DG, 1998, APPL REGRESSION ANAL, P798; Krug SE, 1997, PEDIATR EMERG CARE, V13, P87, DOI 10.1097/00006565-199704000-00001; LOZANO P, 1995, JAMA-J AM MED ASSOC, V274, P469, DOI 10.1001/jama.274.6.469; McCaig LF, 1998, PUBLIC HEALTH REP, V113, P75; Rae D. W., 1970, ANAL POLITICAL CLEAV; Robinson JC, 1998, JAMA-J AM MED ASSOC, V279, P144, DOI 10.1001/jama.279.2.144; ROOS LL, 1980, MED CARE, V18, P174, DOI 10.1097/00005650-198002000-00004; SACKETT DL, 1991, CLIN EPIDEMIOLOGY BA, P307; Schaeffer HA, 1999, PEDIATRICS, V103, P1050; SHENKIN BN, 1995, JAMA-J AM MED ASSOC, V273, P1937, DOI 10.1001/jama.273.24.1937; Starfield B, 1998, PRIMARY CARE BALANCI; STARFIELD BH, 1976, MED CARE, V14, P625, DOI 10.1097/00005650-197607000-00008; STONE EL, 1995, PEDIATRICS, V96, P844; THOMPSON RS, 1995, JAMA-J AM MED ASSOC, V273, P1130; WASSON JH, 1984, JAMA-J AM MED ASSOC, V252, P2413; Weiss LJ, 1996, AM J PUBLIC HEALTH, V86, P1742, DOI 10.2105/AJPH.86.12.1742; WEITZMAN M, 1992, JAMA-J AM MED ASSOC, V268, P2673, DOI 10.1001/jama.268.19.2673; WILLNER JH, 1980, NEW ENGL J MED, V303, P138, DOI 10.1056/NEJM198007173030306	40	213	216	2	11	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	MAR	2001	107	3					524	529		10.1542/peds.107.3.524		6	Pediatrics	Pediatrics	406KW	WOS:000167216200027	11230593	
J	Marenholz, I; Nickel, R; Ruschendorf, F; Schulz, F; Esparza-Gordillo, J; Kerscher, T; Gruber, C; Lau, S; Worm, M; Keil, T; Kurek, M; Zaluga, E; Wahn, U; Lee, YA				Marenholz, Ingo; Nickel, Renate; Rueschendorf, Franz; Schulz, Florian; Esparza-Gordillo, Jorge; Kerscher, Tamara; Grueber, Christoph; Lau, Susanne; Worm, Margitta; Keil, Thomas; Kurek, Michael; Zaluga, Elisabetha; Wahn, Ulrich; Lee, Young-Ae			Filaggrin loss-of-function mutations predispose to phenotypes involved in the atopic march	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						eczema; atopic march; asthma; allergic rhinitis; atopy; filaggrin; genetic association; skin barrier	CORNIFIED ENVELOPE; DERMATITIS; ASTHMA; SKIN; ASSOCIATION; PROTEIN; SENSITIZATION; EXPOSURE; LINKAGE; MICE	Background: Childhood eczema often precedes the development of asthma and allergic rhinitis in the so-called atopic march. Recently, 2 loss-of-function mutations in the gene encoding the epidermal barrier protein filaggrin were reported to be predisposing factors for eczema and concomitant asthma, suggesting a possible role in disease transition. Objective: We aimed to assess the importance of filaggrin loss-of-function mutations in the susceptibility to eczema and associated clinical phenotypes. Methods: The filaggrin mutations were genotyped and tested for association with allergic disorders in 2 large European populations including 1092 children with eczema. Results: Highly significant association of the filaggrin null mutations with eczema and concomitant asthma was replicated. Moreover, we found that these mutations predispose to asthma, allergic rhinitis, and allergic sensitization only in the presence of eczema. We show that the presence of 2 filaggrin null alleles is an independent risk factor for asthma in children with eczema, and that the 2 investigated mutations account for about 11% of eczema cases in the German population. Conclusion: These results lend strong support to the role of filaggrin in the pathogenesis of eczema and in the subsequent progression along the atopic march. The fact that previous expression of eczema is a prerequisite for the manifestation of allergic airways disease and specific sensitization highlights the importance of the epidermal barrier in the pathogenesis of these disorders. Clinical implications: Our results suggest that the maintenance and repair of the epidermal barrier in infants with eczema may prevent the subsequent development of allergic airways disease.	Charite Univ Med, D-13353 Berlin, Germany; Charite Univ Med, Dept Dermatol & Allergy, D-13353 Berlin, Germany; Charite Univ Med, Inst Social Med Epidemiol & Hlth Econ, D-13353 Berlin, Germany; Max Delbruck Ctr Mol Med, Berlin, Germany; Pomeranian Acad Med, Dept Clin Allergol, Szczecin, Poland	Lee, YA (reprint author), Charite Univ Med, Campus Virchow Klinikum,Augustenburger Pl 1, D-13353 Berlin, Germany.	yo.lee@charite.de	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Bergmann R L, 1994, Pediatr Allergy Immunol, V5, P19, DOI 10.1111/j.1399-3038.1994.tb00343.x; Candi E, 2005, NAT REV MOL CELL BIO, V6, P328, DOI 10.1038/nrm1619; Cookson WOCM, 2001, NAT GENET, V27, P372, DOI 10.1038/86867; Ginger RS, 2005, ARCH DERMATOL RES, V297, P235, DOI 10.1007/s00403-005-0590-8; Hanifin JM, 1980, ACTA DERM-VENEREOL S, V92, P44; HENNEKENS CH, 2006, EPIDEMIOLOGY MED, P54; Hinds DA, 1996, ASPEX PACKAGE AFFECT; Hoffjan S, 2003, RESPIR RES, V4, DOI 10.1186/1465-9921-4-14; Illi S, 2004, J ALLERGY CLIN IMMUN, V113, P925, DOI 10.1016/j.jaci.2004.01.778; Koch PJ, 2000, J CELL BIOL, V151, P389, DOI 10.1083/jcb.151.2.389; Kunz B, 1997, DERMATOLOGY, V195, P10; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; Lee YA, 2000, NAT GENET, V26, P470, DOI 10.1038/82625; Leung DYM, 2004, J CLIN INVEST, V113, P651, DOI 10.1172/JCI200421060; Leung DYM, 1997, ANN ALLERG ASTHMA IM, V79, P197; Mischke D, 1996, J INVEST DERMATOL, V106, P989, DOI 10.1111/1523-1747.ep12338501; Nickel R, 2002, CLIN EXP ALLERGY, V32, P1274, DOI 10.1046/j.1365-2745.2002.01482.x; Palmer CNA, 2006, NAT GENET, V38, P441, DOI 10.1038/ng1767; Smith FJD, 2006, NAT GENET, V38, P337, DOI 10.1038/ng1743; Spergel JM, 1998, J CLIN INVEST, V101, P1614, DOI 10.1172/JCI1647; Spergel Jonathan M., 2003, Journal of Allergy and Clinical Immunology, V112, pS118, DOI 10.1016/j.jaci.2003.09.033; Spielman RS, 1996, AM J HUM GENET, V59, P983; Sugiura H, 2005, BRIT J DERMATOL, V152, P146, DOI 10.1111/J.1365-2133.2005.06352.X; Tay YK, 1999, INT J DERMATOL, V38, P689, DOI 10.1046/j.1365-4362.1999.00667.x; Weidinger S, 2006, J ALLERGY CLIN IMMUN, V118, P214, DOI 10.1016/j.jaci.2006.05.004; Zutavern A, 2005, CLIN EXP ALLERGY, V35, P1301, DOI 10.1111/j.1365-2222.2005.02350.x	27	211	222	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.	OCT	2006	118	4					866	871		10.1016/j.jaci.2006.07.026		6	Allergy; Immunology	Allergy; Immunology	097GD	WOS:000241434200013	17030239	
J	Penagos, M; Compalati, E; Tarantini, F; Baena-Cagnani, R; Huerta, J; Passalacqua, G; Canonica, GW				Penagos, Martin; Compalati, Enrico; Tarantini, Francesco; Baena-Cagnani, Rodrigo; Huerta, Jose; Passalacqua, Giovanni; Canonica, Giorgio Walter			Efficacy of sublingual immunotherapy in the treatment of allergic rhinitis in pediatric patients 3 to 18 years of age: a meta-analysis of randomized, placebo-controlled, double-blind trials	ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY			English	Review							HOUSE-DUST MITE; SWALLOW IMMUNOTHERAPY; GRASS-POLLEN; CLINICAL-EFFICACY; CHILDREN; SAFETY; ASTHMA; RHINOCONJUNCTIVITIS; QUALITY; EXTRACT	Objective: To evaluate the efficacy of sublingual immunotherapy (SLIT) in the treatment of allergic rhinitis in children. Data Sources: A comprehensive search of the EMBASE, MEDLINE, LILACS, and CINAHL databases from January 1966 to February 10, 2006, was performed. Study Selection: Randomized, double-blind, placebo-controlled trials of SLIT in the treatment of allergic rhinitis in patients 18 years or younger were selected. Outcomes measured were symptom scores and rescue medication use. Analysis was performed with standardized mean differences (SMDs) and a random-effects model. Results: Seventy articles were identified and reviewed. Ten studies, published between 1990 and 2004, fulfilled the selection criteria. Five hundred seventy-seven patients were initially included in the studies. Of these patients, 484 (245 SLIT and 239 placebo) had a final clinical evaluation and could be evaluated. A relevant heterogeneity due to widely differing scoring systems was found. Overall, there was a significant reduction in both symptoms (SMD, 0.56, 95% confidence interval, 1.01-0.10; P = .02) and medication use (SMD, 0.76; 95% confidence interval, 1.46-0.06; P = .03) after immunotherapy. The subanalyses performed for treatment duration and type of allergen showed that SLIT for more than 18 months and with pollen extracts was effective compared with SLIT courses shorter than 18 months and with mites. Conclusion: The results of this meta-analysis showed that, compared with placebo, SLIT with standardized extracts is effective in pediatric patients with allergic rhinitis.	Univ Genoa, DIMI, Allergy & Resp Dis Clin, Dept Internal Med, I-16132 Genoa, Italy; Pediat Hosp, IMSS, CMN Siglo XXI, Infants Serv, Mexico City, DF, Mexico; Natl Pediat Inst, Allergy Serv, Mexico City, DF, Mexico	Canonica, GW (reprint author), Univ Genoa, DIMI, Allergy & Resp Dis Clin, Dept Internal Med, Pad Maragliano,Lgo R Benzi 10, I-16132 Genoa, Italy.	canonica@unige.it					Alderson P., 2002, COCHRANE COLLABORATI; *AM AC PED COUNC C, 1972, PEDIATRICS, V49, P463; Bachert C, 2003, CHEM IMMUNOL, V82, P119; Baena-Cagnani CE, 2005, CURR OPIN ALLERGY CL, V5, P173, DOI 10.1097/01.all.0000162311.87178.9e; Bahceciler NN, 2001, PEDIATR PULM, V32, P49, DOI 10.1002/ppul.1088; Begg C, 1996, JAMA-J AM MED ASSOC, V276, P637, DOI 10.1001/jama.276.8.637; *BORM, 2003, DIG 1 5 7 PROGR COMP; Bousquet J, 2005, ALLERGY, V60, P1, DOI 10.1111/j.1398-9995.2005.00700.x; Bousquet J., 1998, Allergy (Copenhagen), V53, P1; Bufe A, 2004, ALLERGY, V59, P498, DOI 10.1111/j.1398-9995.2004.00457.x; Caffarelli C, 2000, ALLERGY, V55, P1142, DOI 10.1034/j.1398-9995.2000.00655.x; Canonica GW, 2003, J ALLERGY CLIN IMMUN, V111, P437, DOI 10.1067/mai.2003.129; *COCHR COLL, 2004, REVM 4 2 7 PROGR COM; Cohen J., 1988, STAT POWER ANAL BEHA; Dawson BD, 2004, BASIC CLIN BIOSTATIS, P118; Deeks J, 2001, SYSTEMATIC REV HLTH, P285, DOI 10.1002/9780470693926.ch15; DERSIMONIAN R, 1986, CONTROL CLIN TRIALS, V7, P177, DOI 10.1016/0197-2456(86)90046-2; Di Rienzo V, 2005, CLIN EXP ALLERGY, V35, P560, DOI 10.1111/j.1365-2222.2005.02219.x; Di Rienzo V, 1999, ALLERGY, V54, P1110, DOI 10.1034/j.1398-9995.1999.00267.x; Fiocchi A, 2005, ANN ALLERG ASTHMA IM, V95, P254; Gidaro GB, 2005, CLIN EXP ALLERGY, V35, P565, DOI 10.1111/j.1365-2222.2005.02240.x; Higgins JPT, 2003, BRIT MED J, V327, P557, DOI 10.1136/bmj.327.7414.557; Hirsch T, 1997, PEDIATR ALLERGY IMMU, V8, P21, DOI 10.1111/j.1399-3038.1997.tb00138.x; Ioannidis JPA, 1998, NEW ENGL J MED, V338, P59; Ippoliti F, 2003, PEDIATR ALLERGY IMMU, V14, P216, DOI 10.1034/j.1399-3038.2003.00025.x; Jadad AR, 1996, CONTROL CLIN TRIALS, V17, P1, DOI 10.1016/0197-2456(95)00134-4; Jenkins CNH, 2000, PEDIATRICS, V106, part. no., DOI 10.1542/peds.106.6.e78; Khinchi MS, 2004, ALLERGY, V59, P45, DOI 10.1046/j.1398-9995.2003.00387.x; La Rosa M, 1999, J ALLERGY CLIN IMMUN, V104, P425, DOI 10.1016/S0091-6749(99)70388-X; Litt IF, 1998, PEDIATRICS, V102, P249; Lombardi C, 2001, ALLERGY, V56, P889; MALLING H, 1993, ALLERGY, V48, pS9; MOHER D, 1995, CONTROL CLIN TRIALS, V16, P62, DOI 10.1016/0197-2456(94)00031-W; Moher D, 1999, HEALTH TECHNOL ASSES, V3, P12; Moller C, 2002, J ALLERGY CLIN IMMUN, V109, P251, DOI 10.1067/mai.2002.121317; Nelson Harold S., 2003, Journal of Allergy and Clinical Immunology, V111, pS793, DOI 10.1067/mai.2003.150; NIU CK, 2006, RESP MED        0103; Novembre E, 2004, J ALLERGY CLIN IMMUN, V114, P851, DOI 10.1016/j.jaci.2004.07.012; Olaguibel JM, 2005, J INVEST ALLERG CLIN, V15, P9; Passalacqua G, 2004, ANN ALLERG ASTHMA IM, V93, P3; Passalacqua Giovanni, 2004, Curr Opin Allergy Clin Immunol, V4, P31, DOI 10.1097/00130832-200402000-00007; Plaut M, 2005, NEW ENGL J MED, V353, P1934, DOI 10.1056/NEJMcp044141; Rodriguez Santos Olimpio, 2004, Rev Alerg Mex, V51, P177; Rolinck-Werninghaus C, 2004, ALLERGY, V59, P1285, DOI 10.1111/j.1398-9995.2004.00627.x; TARI MG, 1990, ALLERGOL IMMUNOPATH, V18, P277; Vourdas D, 1998, ALLERGY, V53, P662, DOI 10.1111/j.1398-9995.1998.tb03952.x; Wilson DR, 2005, ALLERGY, V60, P4, DOI 10.1111/j.1398-9995.2005.00699.x; Wuthrich B, 2003, J INVEST ALLERG CLIN, V13, P145	48	211	226	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.	AUG	2006	97	2					141	148				8	Allergy; Immunology	Allergy; Immunology	075AF	WOS:000239853400003	16937742	
J	Frew, AJ; Powell, RJ; Corrigan, CJ; Durham, SR				Frew, AJ; Powell, RJ; Corrigan, CJ; Durham, SR		UK Immunotherapy Study Grp	Efficacy and safety of specific immunotherapy with SQ allergen extract in treatment-resistant seasonal allergic rhinoconjunctivitis	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						immunotherapy; allergic rhinitis; efficacy; safety; quality of life; grass pollen	GRASS-POLLEN IMMUNOTHERAPY; HOUSE-DUST-MITE; CLINICAL-EFFICACY; GENERAL-PRACTICE; POSITION PAPER; HAY-FEVER; SENSITIZATIONS; RHINITIS; CHILDREN; ASTHMA	Background: Specific immunotherapy is widely used to treat allergic rhinitis, but few large-scale clinical trials have been performed. Objective: We sought to assess the efficacy and safety of specific immunotherapy with 2 doses of Alutard grass pollen in patients with moderately severe seasonal allergic rhinitis inadequately controlled with standard drug therapy. Methods: We performed a double-blind, randomized, placebo-controlled study of 410 subjects (203 randomized to 100,000 standardized quality units [SQ-U] maintenance, 104 to 10,000 SQ-U, and 103 to placebo). Three hundred forty-seven (85%) completed treatment. Groups were well matched for demographics and symptoms. Results: Across the whole pollen season, mean symptom and medication scores were 29% and 32% lower, respectively, in the 100,000-SQ-U group compared with those in the placebo group (both P < .001). Over the peak pollen season, mean symptom and medication scores were 32% and 41% lower, respectively, than those in the placebo group. The 10,000-SQ-U group had 22% less symptoms than the placebo group over the whole season (P < .01), but medication scores reduced by only 16% (P = .16). Quality-of-life measures confirmed the superiority of both doses to placebo. Local and delayed side effects were common but generally mild. Clinically significant early and delayed systemic side effects were confined to the 100,000-SQ-U group, but no life-threatening reactions occurred. Conclusions: One season of immunotherapy with Alutard grass pollen reduced symptoms and medication use and improved the quality of life of subjects with moderately severe hay fever. The 100,000-SQ-U regimen was more effective, but the 10,000-SQ-U regimen caused fewer side effects.	Univ Southampton, Sch Med, Allergy & Inflammat Res Subdiv, Southampton, Hants, England; Queens Med Ctr, Clin Immunol Unit, Nottingham, England; Guys Kings & St Thomas Sch Med, Dept Resp Med & Allergy, London, England; Royal Brompton Hosp, Dept Upper Resp Med, London, England	Frew, AJ (reprint author), Brighton Gen Hosp, Dept Resp Med, Brighton BN2 3EW, E Sussex, England.	ajf@eaaci.org					Arvidsson MB, 2002, J ALLERGY CLIN IMMUN, V109, P777, DOI 10.1067/mai.2002.123868; 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; DesRoches A, 1997, J ALLERGY CLIN IMMUN, V99, P450, DOI 10.1016/S0091-6749(97)70069-1; Durham SR, 1999, NEW ENGL J MED, V341, P468, DOI 10.1056/NEJM199908123410702; HAUGAARD L, 1993, J ALLERGY CLIN IMMUN, V91, P709, DOI 10.1016/0091-6749(93)90190-Q; JUNIPER EF, 1991, CLIN EXP ALLERGY, V21, P77, DOI 10.1111/j.1365-2222.1991.tb00807.x; MALLING HJ, 1993, ALLERGY, V48, P9; Moller C, 2002, J ALLERGY CLIN IMMUN, V109, P251, DOI 10.1067/mai.2002.121317; Pajno GB, 2001, CLIN EXP ALLERGY, V31, P1392, DOI 10.1046/j.1365-2222.2001.01161.x; Pichler CE, 2001, ALLERGY, V56, P301, DOI 10.1034/j.1398-9995.2001.00834.x; Purello-D'Ambrosio F, 2001, CLIN EXP ALLERGY, V31, P1295, DOI 10.1046/j.1365-2222.2001.01027.x; ROSS AM, 1994, BRIT MED J, V308, P897; VARNEY VA, 1991, BRIT MED J, V302, P265; 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; White P, 1998, CLIN EXP ALLERGY, V28, P266	17	210	220	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.	FEB	2006	117	2					319	325		10.1016/j.jaci.2005.11.014		7	Allergy; Immunology	Allergy; Immunology	017IM	WOS:000235687300014	16461133	
J	Asokananthan, N; Graham, PT; Stewart, DJ; Bakker, AJ; Eidne, KA; Thompson, PJ; Stewart, GA				Asokananthan, N; Graham, PT; Stewart, DJ; Bakker, AJ; Eidne, KA; Thompson, PJ; Stewart, GA			House dust mite allergens induce proinflammatory cytokines from respiratory epithelial cells: The cysteine protease allergen, Der p 1, activates protease-activated receptor (PAR)-2 and inactivates PAR-1	JOURNAL OF IMMUNOLOGY			English	Article							THROMBIN RECEPTOR; DERMATOPHAGOIDES-PTERONYSSINUS; BRONCHIAL EPITHELIUM; AIRWAY INFLAMMATION; TIGHT JUNCTIONS; CATHEPSIN-G; ASTHMA; CLEAVAGE; INTERLEUKIN-8; PERMEABILITY	In previous studies, we demonstrated that allergenic house dust mite proteases are potent inducers of proinflammatory cytokines from the respiratory epithelium, although the precise mechanisms involved were unclear. In this study, we investigated whether this was achieved through activation of protease-activated receptor (PAR)-1 or -2. Pretreatment of A549 respiratory epithelial cells with the clinically important cysteine protease allergen, Der p 1, ablated subsequent PAR-1, but not PAR-2 agonist peptide-induced IL-6 and IL-8 release. HeLa cells transfected with the plasmid coding for PAR-2, in contrast to PAR-1, released significant concentration of IL-6 after exposure to Der p 1. Exposure of HeLa cells transfected with either PAR-1/enhanced yellow fusion protein or PAR-2/enhanced yellow fusion protein to Der p 1 caused receptor internalization in the latter cells only, as judged by confocal microscopy with re-expression of the receptor within 120-min postenzyme exposure. Der p 1-induced cytokine release from both A549 and transfected HeLa cells was accompanied by changes in intracellular C2+ concentrations. Desensitization studies showed that Der p 1 pretreatment of the A549 cells resulted in the abolition of both trypsin- and PAR-2 agonist peptide-induced Ca2+ release, but not that induced by subsequent exposure to either thrombin or PAR-1 agonist peptide. These data indicate for the first time that the house dust mite allergen Der p 1-induced cytokine release from respiratory epithelial cells is, in part, mediated by activation of PAR-2, but not PAR-1.	Univ Western Australia, Sch Med & Pharmacol, Perth, WA 6009, Australia; Univ Western Australia, Asthma & Allergy Res Inst, Perth, WA 6009, Australia; Univ Western Australia, Western Australian Inst Med Res, Perth, WA 6009, Australia	Stewart, GA (reprint author), Univ Western Australia, Dept Microbiol, 35 Stirling Highway, Crawley, WA 6009, Australia.		Bakker, Anthony/B-1185-2011; Bakker, Anthony/B-8163-2014	Bakker, Anthony/0000-0002-6889-8932			Alm AK, 1999, THROMB HAEMOSTASIS, V81, P984; Asokananthan N, 2002, J IMMUNOL, V168, P3577; BAHOU WF, 1994, BLOOD, V84, P4195; Blackhart BD, 2000, MOL PHARMACOL, V58, P1178; Blackhart BD, 1996, J BIOL CHEM, V271, P16466; BRASS LF, 1994, J BIOL CHEM, V269, P2943; CHAPMAN MD, 1987, J IMMUNOL, V139, P1479; CHUA KY, 1988, J EXP MED, V167, P175, DOI 10.1084/jem.167.1.175; Cocks TM, 1999, NATURE, V398, P156, DOI 10.1038/18223; Dery O, 1999, J BIOL CHEM, V274, P18524, DOI 10.1074/jbc.274.26.18524; DEVLIN RB, 1994, AM J PHYSL, V266; ECKMANN L, 1993, INFECT IMMUN, V61, P4569; Hamilton L M, 2001, Monaldi Arch Chest Dis, V56, P48; HARTMANN T, 1994, AM J PHYSIOL, V267, pL113; HERBERT CA, 1990, LANCET, V336, P1132, DOI 10.1016/0140-6736(90)92611-K; HERBERT CA, 1995, AM J RESP CELL MOL, V12, P369; Higgins DG, 1996, METHOD ENZYMOL, V266, P383; Holgate ST, 1999, CLIN EXP ALLERGY, V29, P90, DOI 10.1046/j.1365-2222.1999.00016.x; Kalsheker NA, 1996, BIOCHEM BIOPH RES CO, V221, P59, DOI 10.1006/bbrc.1996.0544; Kauffman HF, 2000, J ALLERGY CLIN IMMUN, V105, P1185, DOI 10.1067/mai.2000.106210; King C, 1996, J ALLERGY CLIN IMMUN, V98, P739, DOI 10.1016/S0091-6749(96)70121-5; King C, 1998, J IMMUNOL, V161, P3645; Knight DA, 2001, J ALLERGY CLIN IMMUN, V108, P797; Kroeger KM, 2001, J BIOL CHEM, V276, P12736, DOI 10.1074/jbc.M011311200; Loew D, 2000, BIOCHEMISTRY-US, V39, P10812, DOI 10.1021/bi0003341; Lordan JL, 2002, J IMMUNOL, V169, P407; MARINI M, 1992, J ALLERGY CLIN IMMUN, V89, P1001, DOI 10.1016/0091-6749(92)90223-O; MOLINO M, 1995, J BIOL CHEM, V270, P11168, DOI 10.1074/jbc.270.19.11168; Nanevicz T, 1996, J BIOL CHEM, V271, P702; NOAH TL, 1993, AM J PHYSIOL, V265, P472; NYSTEDT S, 1994, P NATL ACAD SCI USA, V91, P9208, DOI 10.1073/pnas.91.20.9208; O'Brien PJ, 2001, ONCOGENE, V20, P1570, DOI 10.1038/sj.onc.1204194; PlattsMills TAE, 1997, CIBA F SYMP, V206, P173; Renesto P, 1997, BLOOD, V89, P1944; Riewald M, 2001, BLOOD, V97, P3109, DOI 10.1182/blood.V97.10.3109; Schulz O, 1997, EUR J IMMUNOL, V27, P584, DOI 10.1002/eji.1830270303; Schulz O, 1998, J CLIN PATHOL-MOL PA, V51, P222; STEWART GA, 1992, IMMUNOLOGY, V75, P29; Sun G, 2001, J IMMUNOL, V167, P1014; Thompson P. J., 2001, Clinical and Experimental Allergy Reviews, V1, P107, DOI 10.1046/j.1472-9725.2001.00018.x; Tomee JFC, 1998, J ALLERGY CLIN IMMUN, V102, P75, DOI 10.1016/S0091-6749(98)70057-0; Trejo J, 2000, J BIOL CHEM, V275, P31255, DOI 10.1074/jbc.M003770200; WADDELL WJ, 1956, J LAB CLIN MED, V48, P311; Wan H, 2000, EUR RESPIR J, V15, P1058, DOI 10.1034/j.1399-3003.2000.01514.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; YASUEDA H, 1986, INT ARCH ALLER A IMM, V81, P214; Yasuhara T, 2001, CLIN EXP ALLERGY, V31, P116, DOI 10.1046/j.1365-2222.2001.00945.x	48	210	217	1	7	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	OCT 15	2002	169	8					4572	4578				7	Immunology	Immunology	602NU	WOS:000178512000065	12370395	
J	Smith, KR				Smith, KR			National burden of disease in India from indoor air pollution	PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA			English	Review							ENVIRONMENTAL TOBACCO-SMOKE; LOWER RESPIRATORY-INFECTIONS; BIOMASS FUEL COMBUSTION; YOUNG GAMBIAN CHILDREN; WOOD-BURNING STOVES; LOW-BIRTH-WEIGHT; RISK-FACTORS; DEVELOPING-COUNTRIES; UNITED-STATES; CHRONIC-BRONCHITIS	In the last decade, a number of quantitative epidemiological studies of specific diseases have been done in developing countries that for the first time allow estimation of the total burden of disease (mortality and morbidity) attributable to use of solid fuels in adult women and young children, who jointly receive the highest exposures because of their household roles. Few such studies are available as yet for adult men or children over 5 years. This paper evaluates the existing epidemiological studies and applies the resulting risks to the more than three-quarters of all Indian households dependent on such fuels. Allowance is made for the existence of improved stoves with chimneys and other factors that may lower exposures. Attributable risks are calculated in reference to the demographic conditions and patterns of each disease in India. Sufficient evidence is available to estimate risks most confidently for acute respiratory infections (ARI), chronic obstructive pulmonary disease (COPD), and lung cancer, Estimates for tuberculosis (TB), asthma, and blindness are of intermediate confidence. Estimates for heart disease have the lowest confidence. Insufficient quantitative evidence is currently available to estimate the impact of adverse pregnancy outcomes (e.g., low birthweight and stillbirth). The resulting conservative estimates indicate that some 400-550 thousand premature deaths can be attributed annually to use of biomass fuels in these population groups. Using a disability-adjusted lost life-year approach, the total is 4-6% of the Indian national burden of disease, placing indoor air pollution as a major risk factor in the country.	East West Ctr, Honolulu, HI 96848 USA; Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA	Smith, KR (reprint author), Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA.						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Natl. Acad. Sci. U. S. A.	NOV 21	2000	97	24					13286	13293		10.1073/pnas.97.24.13286		8	Multidisciplinary Sciences	Science & Technology - Other Topics	376UZ	WOS:000165476300071	11087870	
J	Kappos, AD; Bruckmann, P; Eikmann, T; Englert, N; Heinrich, U; Hoppe, P; Koch, E; Krause, GHM; Kreyling, WG; Rauchfuss, K; Rombout, P; Schulz-Klemp, V; Thiel, WR; Wichmann, HE				Kappos, AD; Bruckmann, P; Eikmann, T; Englert, N; Heinrich, U; Hoppe, P; Koch, E; Krause, GHM; Kreyling, WG; Rauchfuss, K; Rombout, P; Schulz-Klemp, V; Thiel, WR; Wichmann, HE			Health effects of particles in ambient air	INTERNATIONAL JOURNAL OF HYGIENE AND ENVIRONMENTAL HEALTH			English	Article						particulate matter; air pollution; PM10; PM2.5; ultra fine particles; health effects; review; limit values	LONG-TERM EXPOSURE; OIL FLY-ASH; NORTH-AMERICAN CHILDREN; RESPIRATORY SYMPTOMS; INFANT-MORTALITY; INFLAMMATORY RESPONSES; PARTICULATE MATTER; HUMAN VOLUNTEERS; UNITED-STATES; ACID AEROSOLS	A summary of a critical review by a working group of the German commission on Air Pollution Prevention of VDI and DIN of the actual data on exposure and health effects (excluding cancer) of fine particulate air pollution is presented. Exposure: Typical ambient particle concentrations for PM10 (PM2.5) in Germany are in the range of 10-45 (10-30) mug/m(3) as annual mean and 50-200 (40-150) mug/m(3) as maximum daily mean. The ratio Of PM2.5/PM10 generally amounts between 0.7 and 0.9. Health effects: During the past 10 years many new epidemiological and toxicological studies on health effects of particulate matter (PM) have been published. In summary, long-term exposure against PM for years or decades is associated with elevated total, cardiovascular, and infant mortality. With respect to morbidity, respiratory symptoms, lung growth, and function of the immune system are affected. Short-term studies show consistant associations of exposure to daily concentrations of PM with mortality and morbidity on the same day or the subsequent days. Patients with asthma, COPD, pneumonia, and other respiratory diseases as well as patients with cardio-vascular diseases and diabetes are especially affected. The strongest associations are found for PM2.5 followed by PM10, with no indication of a threshold value for the health effects. The data base for ultra fine particles is too small for final conclusions.	Behorde Umwelt & Gesundheit, Hamburg, Germany; Landesumweltamt NRW, Essen, Germany; Univ Giessen, Inst Hyg & Umweltmed, Giessen, Germany; Umweltbundesamt, Berlin, Germany; Fraunhofer Inst Toxicol & Expt Med, Hannover, Germany; Univ Munich, Inst Arbeitsmed, Munich, Germany; Minist Umwelt & Naturschutz, NRW, Dusseldorf, Germany; GSF Forschungszentrum Umwelt & Gesundheit, Inst Inhalat Biol, Neuherberg, Germany; Verein Deutsch Eisenhuttenleute, Dusseldorf, Germany; GSF Forschungszentrum Umwelt & Gesundheit, Inst Epidemiol, Neuherberg, Germany	Kappos, AD (reprint author), Dr Phil Nat Andreas Kappos,Im Geeren 36, D-60433 Frankfurt, Germany.	adkappos@t-online.de		Kreyling, Wolfgang/0000-0002-0702-6567			Abbey DE, 1999, AM J RESP CRIT CARE, V159, P373; AckermannLiebrich U, 1997, AM J RESP CRIT CARE, V155, P122; Avol EL, 2001, AM J RESP CRIT CARE, V164, P2067; BOBAK M, 1992, LANCET, V340, P1010, DOI 10.1016/0140-6736(92)93017-H; Bobak M, 1999, OCCUP ENVIRON MED, V56, P539; BRAND P, 1992, ATMOS ENVIRON A-GEN, V26, P2451, DOI 10.1016/0960-1686(92)90375-U; BraunFahrlander C, 1997, AM J RESP CRIT CARE, V155, P1042; *CEN, 1998, LUFTBESCHAFFENHEIT E; Clancy L, 2002, LANCET, V360, P1210, DOI 10.1016/S0140-6736(02)11281-5; Clarke RW, 2000, INHAL TOXICOL, V12, P73, DOI 10.1080/089583700196400; COSTA DL, 1997, ENV HLTH PERSPECT, V105, P1060; Dejmek J, 1999, ENVIRON HEALTH PERSP, V107, P475, DOI 10.2307/3434630; Dockery DW, 1996, ENVIRON HEALTH PERSP, V104, P500, DOI 10.2307/3432990; DOCKERY DW, 1993, NEW ENGL J MED, V329, P1753, DOI 10.1056/NEJM199312093292401; Dreher KL, 1997, J TOXICOL ENV HEALTH, V50, P285, DOI 10.1080/009841097160492; Dye JA, 2001, ENVIRON HEALTH PERSP, V109, P395, DOI 10.2307/3434787; FERIN J, 1992, AM J RESP CELL MOL, V6, P535; Ghio AJ, 2000, AM J RESP CRIT CARE, V162, P981; GODLESKI JJ, 2000, MECH MORBIDITY MORTA; GODLESKI JJ, 1996, AM J RESPIR CRIT C A, V5; *HEI, 2003, REV AN TIM SER STUD; Heinrich J., 2002, Umweltmedizin in Forschung und Praxis, V7, P91; Heinrich J, 2002, EPIDEMIOLOGY, V13, P394, DOI 10.1097/01.EDE.00000016977.59359.B6; Heinrich J, 1999, Eur J Med Res, V4, P107; Heinrich J, 2000, AM J RESP CRIT CARE, V161, P1930; Hoek G, 2002, LANCET, V360, P1203, DOI 10.1016/S0140-6736(02)11280-3; Jedrychowski W, 1999, ENVIRON HEALTH PERSP, V107, P669, DOI 10.2307/3434460; Kodavanti UP, 1997, INHAL TOXICOL, V9, P679; Kramer U, 1999, INT J EPIDEMIOL, V28, P865, DOI 10.1093/ije/28.5.865; Krewski D, 2000, REANALYSIS HARVARD 6; KREYLING WG, 2003, IN PRESS ATM ENV, V37; KUHLBUSCH TAJ, 2002, PMX MASSENKONZENTRAT; Kuschner WG, 1997, ENVIRON HEALTH PERSP, V105, P1234, DOI 10.1289/ehp.971051234; LEONARDI GS, 2000, INHAL TOXICOL, P1; Li XY, 1999, INHAL TOXICOL, V11, P709; Li XY, 1997, ENVIRON HEALTH PERSP, V105, P1279, DOI 10.2307/3433547; Li XY, 1996, THORAX, V51, P1216, DOI 10.1136/thx.51.12.1216; Lipfert FW, 2000, J AIR WASTE MANAGE, V50, P1350; Lipfert FW, 2000, INHAL TOXICOL, V12, P41, DOI 10.1080/089583700750019503; McConnell R, 1999, ENVIRON HEALTH PERSP, V107, P757, DOI 10.2307/3434662; McDonnell WF, 2000, J EXPO ANAL ENV EPID, V10, P427, DOI 10.1038/sj.jea.7500095; Muggenburg BA, 2000, INHAL TOXICOL, V12, P189, DOI 10.1080/089583700750019567; OBERDORSTER G, 1994, ENVIRON HEALTH PERSP, V102, P173, DOI 10.2307/3432080; Peters A, 1996, AM J EPIDEMIOL, V144, P570; Peters A., 2002, Umweltmedizin in Forschung und Praxis, V7, P101; Peters A, 1997, LANCET, V349, P1582, DOI 10.1016/S0140-6736(97)01211-7; PITZ M, 2001, ATMOS ENVIRON, V35, P4366; Pope CA, 1999, ENVIRON HEALTH PERSP, V107, P567; POPE CA, 1995, AM J RESP CRIT CARE, V151, P669; Pope CA, 2002, JAMA-J AM MED ASSOC, V287, P1132, DOI 10.1001/jama.287.9.1132; Raizenne M, 1996, ENVIRON HEALTH PERSP, V104, P506, DOI 10.2307/3432991; Salvi S, 1999, AM J RESP CRIT CARE, V159, P702; Samet J.M., 2000, NATL MORBIDITY MORTA; Schwartz J, 2000, ENVIRON HEALTH PERSP, V108, P563, DOI 10.2307/3454620; Tuch T, 2000, ATMOS ENVIRON, V34, P139, DOI 10.1016/S1352-2310(99)00248-4; *US EPA, 2003, 4 EXT REV DRAFT AIR, V2; *WHO, 2003, WHO WORK GROUP M BON; Wichmann HE, 2000, PHILOS T ROY SOC A, V358, P2751; WICHMANN HE, 2002, SOURCES ELEMENTAL CO; WICHMANN HE, 2000, DAILY MORTALITY FI 1, V98, P1; WICHMANN HE, 2002, WIRKUNGEN FEINSTAUB; Wiedensohler A, 2002, J AEROSOL MED, V15, P237, DOI 10.1089/089426802320282365; Bruckmann P., 2002, GUIDANCE MEMBER STAT; Woodruff TJ, 1997, ENVIRON HEALTH PERSP, V105, P608; Zemp E, 1999, AM J RESP CRIT CARE, V159, P1257	65	209	215	13	73	URBAN & FISCHER VERLAG	JENA	BRANCH OFFICE JENA, P O BOX 100537, D-07705 JENA, GERMANY	1438-4639			INT J HYG ENVIR HEAL	Int. J. Hyg. Environ. Health.	SEP	2004	207	4					399	407		10.1078/1438-4639-00306		9	Public, Environmental & Occupational Health; Infectious Diseases	Public, Environmental & Occupational Health; Infectious Diseases	857DU	WOS:000224097200012	15471105	
J	Mendell, MJ; Mirer, AG; Cheung, K; Tong, M; Douwes, J				Mendell, Mark J.; Mirer, Anna G.; Cheung, Kerry; Tong, My; Douwes, Jeroen			Respiratory and Allergic Health Effects of Dampness, Mold, and Dampness-Related Agents: A Review of the Epidemiologic Evidence	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Review						allergy; asthma; dampness; fungi; indoor air; moisture; mold	HOUSE-DUST ENDOTOXIN; ENVIRONMENTAL RISK-FACTORS; INCIDENT CASE-CONTROL; ADULT-ONSET ASTHMA; BIRTH-COHORT; CHILDHOOD ASTHMA; INDOOR MOLD; HYPERSENSITIVITY PNEUMONITIS; BRONCHIAL OBSTRUCTION; SCIENTIFIC EVIDENCE	OBJECTIVES: Many studies have shown consistent associations between evident indoor dampness or mold and respiratory or allergic health effects, but causal links remain unclear. Findings on measured microbiologic factors have received little review. We conducted an updated, comprehensive review on these topics. DATA SOURCES: We reviewed eligible peer-reviewed epidemiologic studies or quantitative meta-analyses, up to late 2009, on dampness, mold, or other microbiologic agents and respiratory or allergic effects. DATA EXTRACTION: We evaluated evidence for causation or association between qualitative/subjective assessments of dampness or mold (considered together) and specific health outcomes. We separately considered evidence for associations between specific quantitative measurements of microbiologic factors and each health outcome. DATA SYNTHESIS: Evidence from epidemiologic studies and meta-analyses showed indoor dampness or mold to be associated consistently with increased asthma development and exacerbation, current and ever diagnosis of asthma, dyspnea, wheeze, cough, respiratory infections, bronchitis, allergic rhinitis, eczema, and upper respiratory tract symptoms. Associations were found in allergic and nonallergic individuals. Evidence strongly suggested causation of asthma exacerbation in children. Suggestive evidence was available for only a few specific measured microbiologic factors and was in part equivocal, suggesting both adverse and protective associations with health. CONCLUSIONS: Evident dampness or mold had consistent positive associations with multiple allergic and respiratory effects. Measured microbiologic agents in dust had limited suggestive associations, including both positive and negative associations for some agents. Thus, prevention and remediation of indoor dampness and mold are likely to reduce health risks, but current evidence does not support measuring specific indoor microbiologic factors to guide health-protective actions.	[Mendell, Mark J.; Tong, My] Calif Dept Publ Hlth, Indoor Air Qual Sect, Environm Hlth Lab Branch, Richmond, CA 94804 USA; [Mendell, Mark J.] Univ Calif Berkeley, Lawrence Berkeley Lab, Indoor Environm Dept, Environm Energy Technol Div, Berkeley, CA 94720 USA; [Mirer, Anna G.] Univ Wisconsin Sch Med & Publ Hlth, Dept Populat Hlth Sci, Madison, WI USA; [Cheung, Kerry; Douwes, Jeroen] Massey Univ, Ctr Publ Hlth, Wellington, New Zealand	Mendell, MJ (reprint author), Calif Dept Publ Hlth, Indoor Air Qual Sect, Environm Hlth Lab Branch, 850 Marina Bay Pkwy,G365, Richmond, CA 94804 USA.	mark.mendell@cdph.ca.gov		Douwes, Jeroen/0000-0003-3599-4036	WHO Regional Office for Europe	An earlier version of this review, Chapter 4.1 in World Health Organization (WHO) Guidelines for Indoor Air Quality: Dampness and Mould (available: http://www.euro.who.int/__data/assets/pdf_file/0017/43325/E92645.pdf), was supported in part by the WHO Regional Office for Europe.	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Health Perspect.	JUN	2011	119	6					748	756		10.1289/ehp.1002410		9	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	771JC	WOS:000291152000016	21269928	
J	Grainge, CL; Lau, LCK; Ward, JA; Dulay, V; Lahiff, G; Wilson, S; Holgate, S; Davies, DE; Howarth, PH				Grainge, Christopher L.; Lau, Laurie C. K.; Ward, Jonathon A.; Dulay, Valdeep; Lahiff, Gemma; Wilson, Susan; Holgate, Stephen; Davies, Donna E.; Howarth, Peter H.			Effect of Bronchoconstriction on Airway Remodeling in Asthma	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							GROWTH-FACTOR RECEPTOR; ALLERGEN CHALLENGE; MECHANICAL-STRESS; EPITHELIAL-CELLS; MODEL; RAT; INFLAMMATION; EXPRESSION; GUIDELINES; CHILDREN	BACKGROUND Asthma is characterized pathologically by structural changes in the airway, termed airway remodeling. These changes are associated with worse long-term clinical outcomes and have been attributed to eosinophilic inflammation. In vitro studies indicate, however, that the compressive mechanical forces that arise during broncho-constriction may induce remodeling independently of inflammation. We evaluated the influence of repeated experimentally induced bronchoconstriction on airway structural changes in patients with asthma. METHODS We randomly assigned 48 subjects with asthma to one of four inhalation challenge protocols involving a series of three challenges with one type of inhaled agent presented at 48-hour intervals. The two active challenges were with either a dust-mite allergen (which causes bronchoconstriction and eosinophilic inflammation) or methacholine (which causes bronchoconstriction without eosinophilic inflammation); the two control challenges (neither of which causes bronchoconstriction) were either saline alone or albuterol followed by methacholine (to control for non-bronchoconstrictor effects of methacholine). Bronchial-biopsy specimens were obtained before and 4 days after completion of the challenges. RESULTS Allergen and methacholine immediately induced similar levels of bronchoconstriction. Eosinophilic inflammation of the airways increased only in the allergen group, whereas both the allergen and the methacholine groups had significant airway remodeling not seen in the two control groups. Subepithelial collagen-band thickness increased by a median of 2.17 mu m in the allergen group (interquartile range [IQR], 0.70 to 3.67) and 1.94 mu m in the methacholine group (IQR, 0.37 to 3.24) (P<0.001 for the comparison of the two challenge groups with the two control groups); periodic acid-Schiff staining of epithelium (mucus glands) also increased, by a median of 2.17 percentage points in the allergen group (IQR, 1.03 to 4.77) and 2.13 percentage points in the methacholine group (IQR, 1.14 to 7.96) (P=0.003 for the comparison with controls). There were no significant differences between the allergen and methacholine groups. CONCLUSIONS Bronchoconstriction without additional inflammation induces airway remodeling in patients with asthma. These findings have potential implications for management.	[Grainge, Christopher L.; Lau, Laurie C. K.; Ward, Jonathon A.; Dulay, Valdeep; Lahiff, Gemma; Wilson, Susan; Holgate, Stephen; Davies, Donna E.; Howarth, Peter H.] Univ Southampton, Sch Med, Div Infect Inflammat & Immun, Southampton, Hants, England; [Grainge, Christopher L.; Howarth, Peter H.] Wellcome Trust Clin Res Facil, Southampton, Hants, England; [Holgate, Stephen; Howarth, Peter H.] Natl Inst Hlth Res Resp Biomed Res Unit, Southampton, Hants, England	Howarth, PH (reprint author), Southampton Gen Hosp, Sir Henry Wellcome Labs, Mailpoint 810,S Block, Southampton SO16 6YD, Hants, England.	p.h.howarth@soton.ac.uk	Davies, Donna/H-2993-2012		Defence Postgraduate Medical Deanery; Medical Research Council [G0900453]	Supported by the Defence Postgraduate Medical Deanery and by a grant from the Medical Research Council (G0900453).	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Engl. J. Med.	MAY 26	2011	364	21					2006	2015				10	Medicine, General & Internal	General & Internal Medicine	768QR	WOS:000290952000005	21612469	
J	Heymann, PW; Carper, HT; Murphy, DD; Platts-Mills, TAE; Patrie, J; McLaughlin, AP; Erwin, EA; Shaker, MS; Hellems, M; Peerzada, J; Hayden, FG; Hatley, TK; Chamberlain, R				Heymann, PW; Carper, HT; Murphy, DD; Platts-Mills, TAE; Patrie, J; McLaughlin, AP; Erwin, EA; Shaker, MS; Hellems, M; Peerzada, J; Hayden, FG; Hatley, TK; Chamberlain, R			Viral infections in relation to age, atopy, and season of admission among children hospitalized for wheezing	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						wheezing; asthma; children; hospitalization; viral respiratory tract infections; rhinovirus; respiratory syncytial virus; influenza; total serum IgE; inhaled allergens	RESPIRATORY SYNCYTIAL VIRUS; POLYMERASE-CHAIN-REACTION; SERUM IGE; AIRWAY RESPONSIVENESS; INHALANT ALLERGENS; CHILDHOOD ASTHMA; GRASS-POLLEN; RISK-FACTORS; DUST MITE; EXACERBATIONS	Background: Viral respiratory tract infections and atopy are associated with attacks of wheezing during childhood. However, information about the relationship between viral infections and atopy among children whose attacks of wheezing lead to hospitalization is unclear. Objective: To evaluate the prevalence of viral respiratory tract pathogens among infants and children hospitalized for wheezing and to analyze the results in relation to the patient's age, atopic characteristics, and season of admission. Methods: This was a case-control study of children (age 2 months to 18 years) admitted for wheezing to the University of Virginia Medical Center over a period of 12 months. Children without wheezing were enrolled as controls. Nasal secretions were evaluated for viral pathogens by using cultures, PCR tests, and antigen detection. Total IgE and specific IgE antibody to common aeroallergens; was measured in serum. Results: Seventy percent of children hospitalized for wheezing before age 3 years (n = 79) were admitted between December and March, whereas 46% of children age 3 to 18 years (n = 54) were hospitalized between September and November. Among children younger than 3 years, viral pathogens were detected in 84% (66/79) of wheezing children and 55% (42/77) of controls (P < .001). Respiratory syncytial virus was the dominant pathogen during the winter months, but rhinovirus was more common during other months. Total serum IgE levels were generally low, and values from wheezing and control subjects overlapped considerably. Among children 3 years and older, 61% (33/54) of subjects admitted for wheezing tested positive for virus (predominantly rhinovirus), compared with 21% (12/ 56) of controls (P < .001). The total serum IgE values among wheezing children (geometric mean, 386 IU/mL; 95% CI, 259573) were substantially elevated compared with those of controls (geometric mean, 38 IU/mL; 95% CI, 26-56; P < .001). A significantly higher percentage of wheezing children compared with controls was sensitized to at least 1 of the inhaled allergens tested: 84% (36/43) compared with 33% (15/45; P < .001). The atopic characteristics of wheezing children who tested positive or negative for virus were similar. Conclusions: Viral infections were the dominant risk factor for wheezing among children hospitalized before 3 years of age. By comparison, a large majority of the wheezing children age 3 to 18 years had striking atopic characteristics that may be critical as a risk factor for hospitalization and an adverse response to viral infections, especially infections caused by rhinovirus.	Univ Virginia, Hlth Syst, Dept Pediat, Charlottesville, VA 22908 USA; Univ Virginia, Hlth Syst, Dept Internal Med, Charlottesville, VA 22908 USA; Univ Virginia, Hlth Syst, Dept Hlth Evaluat Sci, Charlottesville, VA 22908 USA	Heymann, PW (reprint author), Univ Virginia, Hlth Syst, Dept Pediat, POB 800386, Charlottesville, VA 22908 USA.	pwh5a@virginia.edu			NIAID NIH HHS [1P01 AI50989, AI 20565]		Agresti A, 2001, BIOMETRICS, V57, P963, DOI 10.1111/j.0006-341X.2001.00963.x; Agresti A., 1990, CATEGORICAL DATA ANA; ANDERSON HR, 1989, THORAX, V44, P614, DOI 10.1136/thx.44.8.614; ARRUDA E, 1993, MOL CELL PROBE, V7, P373, DOI 10.1006/mcpr.1993.1055; BURROWS B, 1989, NEW ENGL J MED, V320, P271, DOI 10.1056/NEJM198902023200502; Centers for Disease Control and Prevention, 2000, MMWR-MORBID MORTAL W, V49, P908; Chang MY, 2000, PEDIATR PULM, V29, P257, DOI 10.1002/(SICI)1099-0496(200004)29:4<257::AID-PPUL4>3.0.CO;2-V; Chiu SS, 2002, NEW ENGL J MED, V347, P2097, DOI 10.1056/NEJMoa020546; *CYT SOFTW CORP, 2001, STATSXACT 5 STAT SOF; DUFF AL, 1993, PEDIATRICS, V92, P535; GERGEN PJ, 2001, J ALLERGY CLIN IMMUN, V107, P445; Green RM, 2002, BRIT MED J, V324, P763, DOI 10.1136/bmj.324.7340.763; HENDERSON FW, 1979, J PEDIATR-US, V95, P183; Heymann PW, 1998, IMMUNOL ALLERGY CLIN, V18, P35, DOI 10.1016/S0889-8561(05)70345-3; HIERHOLZER JC, 1993, J CLIN MICROBIOL, V31, P1886; ISAACS D, 2002, MED J AUST S, V117, pS50; JOHNSTON SL, 1993, J CLIN MICROBIOL, V31, P111; JOHNSTON SL, 1995, BRIT MED J, V310, P1225; LAVIA WV, 1992, J PEDIATR-US, V121, P503; Lester LA, 2001, J ALLERGY CLIN IMMUN, V108, P357, DOI 10.1067/mai.2001.117796; LOYANO P, 1999, J ALLERGY CLIN IMMUN, V104, P957; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; MARTINEZ FD, 1992, PEDIATRICS, V89, P21; McCullagh P., 1989, GEN LINEAR MODELS; MORGAN WJ, 1992, PEDIATR CLIN N AM, V39, P1185; Neuzil KM, 2000, NEW ENGL J MED, V342, P225, DOI 10.1056/NEJM200001273420401; NICHOLSON KG, 1993, BRIT MED J, V307, P982; Pitkaranta A, 1998, PEDIATRICS, V102, P291, DOI 10.1542/peds.102.2.291; PLATTSMILLS TAE, 1987, J ALLERGY CLIN IMMUN, V79, P781, DOI 10.1016/0091-6749(87)90211-9; POLLART SM, 1989, J ALLERGY CLIN IMMUN, V83, P875, DOI 10.1016/0091-6749(89)90100-0; Ponsonby AL, 2002, CHEST, V121, P135, DOI 10.1378/chest.121.1.135; Rakes Gary P., 1999, American Journal of Respiratory and Critical Care Medicine, V159, P785; Rawlinson WD, 2003, J INFECT DIS, V187, P1314, DOI 10.1086/368411; SEARS MR, 1989, CLIN EXP ALLERGY, V19, P419, DOI 10.1111/j.1365-2222.1989.tb02408.x; SEARS MR, 1991, NEW ENGL J MED, V325, P1067, DOI 10.1056/NEJM199110103251504; Sherrill DL, 1999, J ALLERGY CLIN IMMUN, V104, P28, DOI 10.1016/S0091-6749(99)70110-7; Stein R, 1999, LANCET, V354, P541, DOI 10.1016/S0140-6736(98)10321-5; SUMYER J, 1996, EUR RESPIR J, V9, P1880; Thumerelle C, 2003, PEDIATR PULM, V35, P75, DOI 10.1002/ppul.10191; WELLIVER RC, 1993, PEDIATR PULM, V15, P19, DOI 10.1002/ppul.1950150104; WU TC, 1992, AM J PATHOL, V140, P991; YOUNG S, 1991, NEW ENGL J MED, V324, P1168, DOI 10.1056/NEJM199104253241704; ZUMBRANO JC, 2003, J ALLERGY CLIN IMMUN, V111, P1008	43	208	213	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.	AUG	2004	114	2					239	247		10.1016/j.jaci.2004.04.006		9	Allergy; Immunology	Allergy; Immunology	847OU	WOS:000223405600004	15316497	
J	Que, LG; Liu, LM; Yan, Y; Whitehead, GS; Gavett, SH; Schwartz, DA; Stamler, JS				Que, LG; Liu, LM; Yan, Y; Whitehead, GS; Gavett, SH; Schwartz, DA; Stamler, JS			Protection from experimental asthma by an endogenous bronchodilator	SCIENCE			English	Article							NITRIC-OXIDE SYNTHASE; PROTEIN S-NITROSYLATION; AIRWAY HYPERRESPONSIVENESS; CYSTIC-FIBROSIS; NITROGEN-OXIDES; EXHALED AIR; NITROSOTHIOLS; DISEASE; INFLAMMATION; INHIBITION	Mechanisms that protect against asthma remain poorly understood. S-nitrosoglutathione (GSNO), an endogenous bronchodilator, is depleted from asthmatic airways, suggesting a protective role. We report that, following allergen challenge, witd-type mice exhibiting airway hyperresponsivity have increased airway levels of the enzyme GSNO reductase (GSNOR) and are depleted of lung S-nitrosothiols (SNOs). In contrast, mice with genetic deletion of GSNOR exhibit increases in lung SNOs and are protected from airway hyperresponsivity. Our results indicate that endogenous SNOs, governed by GSNOR, are critical regulators of airway responsivity and may provide new therapeutic approaches to asthma.	Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA; Duke Univ, Med Ctr, Howard Hughes Med Inst, Durham, NC 27710 USA; Duke Univ, Med Ctr, Dept Biochem, Durham, NC 27710 USA; US EPA, Expt Toxicol Div, Res Triangle Pk, NC 27711 USA	Stamler, JS (reprint author), Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.	STAML001@mc.duke.edu			NHLBI NIH HHS [HL004171, K08 HL004171, K08 HL004171-05]; NIEHS NIH HHS [ES012496, P01 ES012496, P01 ES012496-010004]		ALVING K, 1993, EUR RESPIR J, V6, P1368; Cohn L, 2004, ANNU REV IMMUNOL, V22, P789, DOI 10.1146/annurev.immunol.22.012703.104716; De Sanctis GT, 1999, J EXP MED, V189, P1621, DOI 10.1084/jem.189.10.1621; Dweik RA, 2001, P NATL ACAD SCI USA, V98, P2622, DOI 10.1073/pnas.051629498; Foster MW, 2003, TRENDS MOL MED, V9, P160, DOI 10.1016/S1471-4914(03)00028-5; GASTON B, 1994, AM J RESP CRIT CARE, V149, P538; Gaston B, 1998, LANCET, V351, P1317, DOI 10.1016/S0140-6736(97)07485-0; GASTON B, 1993, P NATL ACAD SCI USA, V90, P10957, DOI 10.1073/pnas.90.23.10957; Grasemann H, 1999, J PEDIATR-US, V135, P770, DOI 10.1016/S0022-3476(99)70101-0; Grunig G, 1998, SCIENCE, V282, P2261, DOI 10.1126/science.282.5397.2261; 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; Hess DT, 2005, NAT REV MOL CELL BIO, V6, P150, DOI 10.1038/nrm1569; Jaffrey SR, 2001, NAT CELL BIOL, V3, P193, DOI 10.1038/35055104; KHARITONOV SA, 1994, LANCET, V343, P133, DOI 10.1016/S0140-6736(94)90931-8; Koarai A, 2000, PULM PHARMACOL THER, V13, P267, DOI 10.1006/pupt.2000.0254; Liu L, 2004, CELL, V116, P617, DOI 10.1016/S0092-8674(04)00131-X; Liu LM, 2001, NATURE, V410, P490, DOI 10.1038/35068596; QUE L, UNPUB; Saleh D, 1998, FASEB J, V12, P929; Snyder AH, 2002, AM J RESP CRIT CARE, V165, P922, DOI 10.1164/rccm.2105032; Whalen EJ, 2000, HYPERTENSION, V36, P376; Whitehead GS, 2003, AM J PHYSIOL-LUNG C, V285, pL32, DOI 10.1152/ajplung.00390.2002; Wills-Karp M, 1998, SCIENCE, V282, P2258, DOI 10.1126/science.282.5397.2258; Xiong YL, 1999, J IMMUNOL, V162, P445	25	207	212	2	13	AMER ASSOC ADVANCEMENT SCIENCE	WASHINGTON	1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA	0036-8075			SCIENCE	Science	JUN 10	2005	308	5728					1618	1621		10.1126/science.1108228		4	Multidisciplinary Sciences	Science & Technology - Other Topics	936BH	WOS:000229827000054	15919956	
J	Jarvis, D				Jarvis, D		European Community Resp Health Su	The European Community Respiratory Health Survey II	EUROPEAN RESPIRATORY JOURNAL			English	Article						asthma; atopy; cohort; epidemiology; European Community Respiratory Health Survey; forced expiratory volume in one second	PARTY DIAGNOSTIC-CRITERIA; SKIN-TEST REACTIVITY; LUNG-FUNCTION; ATOPIC-DERMATITIS; PULMONARY-FUNCTION; POPULATION-SAMPLE; AEROSOL OUTPUT; AIR-POLLUTION; ASTHMA; DECLINE	The European Community Respiratory Health Survey (ECRHS) II will determine the incidence of and risk factors for the development of allergic disease, atopy and rapid loss of lung function in middle-aged adults living in Europe. From 1991-1993, >18,000 individuals took part in ECRHS I and provided information on symptoms and exposure to known or suspected risk factors for asthma. Blood samples for assessment of specific immunoglobulin E to environmental allergen were taken and lung function and bronchial responsiveness to methacholine were assessed. From 1999-2001, study participants were re-contacted to determine symptom status and exposure to a variety of factors, including tobacco smoke, animals, occupational agents and air pollutants (including particulate matter). In a subsample of responders, exposure to house dust-mite allergen was assessed by analysis of dust samples taken from participants' mattresses. In addition, blood samples suitable for deoxyribonucleic acid extraction were collected and stored. Currently, European Community Respiratory Health Survey II is being conducted in 29 centres in 14 countries. At the time of writing this paper, 27 centres had begun the study and similar to12,000 participants had completed a short postal questionnaire, similar to9,000 had completed a more detailed health assessment and 3,500 participants had provided dust samples. Historical air-pollution data have been collated and the programme of monitoring particles with a 50% cut-off aerodynamic diameter of 2.5 mum has been completed in 21 centres in 10 countries.	Kings Coll London, Dept Publ Hlth Sci, London SE1 3QD, England	Jarvis, D (reprint author), Kings Coll London, Dept Publ Hlth Sci, 5th Floor,Capital House,42 Weston St, London SE1 3QD, England.	deborah.jarvis@kcl.ac.uk	de Marco, Roberto/A-5470-2008; SESM, SESM/C-1440-2008; Jarvis, Deborah/E-6494-2011				Abbey DE, 1998, AM J RESP CRIT CARE, V158, P289; ABRAMSON MJ, 1991, J ASTHMA, V28, P129, DOI 10.3109/02770909109082737; ADAMS N, 2001, INHALED BECLOMETHASO; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; BARBEE RA, 1987, J ALLERGY CLIN IMMUN, V79, P16, DOI 10.1016/S0091-6749(87)80010-6; Burney P, 1996, EUR RESPIR J, V9, P687; Burney P, 1997, J ALLERGY CLIN IMMUN, V99, P314, DOI 10.1016/S0091-6749(97)70048-4; BURNEY PGJ, 1994, EUR RESPIR J, V7, P954; BURNEY PGJ, 1987, CHEST, V91, P79; Chinn S, 1997, EUR RESPIR J, V10, P452, DOI 10.1183/09031936.97.10020452; Chinn S, 1997, EUR RESPIR J, V10, P2495, DOI 10.1183/09031936.97.10112495; DENNIS JH, 1990, THORAX, V45, P728, DOI 10.1136/thx.45.10.728; DODGE RR, 1980, AM REV RESPIR DIS, V122, P567; Gottlieb DJ, 1996, AM J RESP CRIT CARE, V153, P561; Hendrick DJ, 2001, CLIN EXP ALLERGY, V31, P1; *INT LAB OFF, 1999, INT STAND CLASS OCC; Janson C, 2001, EUR RESPIR J, V18, P598, DOI 10.1183/09031936.01.00205801; Jantunen MJ, 1998, J EXPO ANAL ENV EPID, V8, P495; JUNIPER EF, 1993, AM REV RESPIR DIS, V147, P832; Kennedy SM, 2000, OCCUP ENVIRON MED, V57, P635, DOI 10.1136/oem.57.9.635; LUCZYNSKA CM, 1989, J IMMUNOL METHODS, V118, P227, DOI 10.1016/0022-1759(89)90010-0; MATHYS P, 2001, ICP INFORMATION NEWS, V27; *NAT HEART LABI GL, 1995, GLOB STRAT ASTHM MAN; Oglesby L, 2000, AM J EPIDEMIOL, V152, P75, DOI 10.1093/aje/152.1.75; OHMAN JL, 1993, J ALLERGY CLIN IMMUN, V91, P752, DOI 10.1016/0091-6749(93)90195-L; Panhuysen CIM, 1997, AM J RESP CRIT CARE, V155, P1267; Peters JM, 1999, AM J RESP CRIT CARE, V159, P768; RIJCKEN B, 1995, AM J RESP CRIT CARE, V151, P1377; Roca J, 1998, EUR RESPIR J, V11, P1354, DOI 10.1183/09031936.98.11061354; RODRIGUEZ BL, 1994, AM J EPIDEMIOL, V140, P398; Ryan G, 1999, J EPIDEMIOL COMMUN H, V53, P230; SETTIPANE RJ, 1994, ALLERGY PROC, V15, P21, DOI 10.2500/108854194778816634; SPARROW D, 1993, AM REV RESPIR DIS, V147, P367; Strachan DP, 1996, BRIT MED J, V312, P1195; TOCKMAN MS, 1995, AM J RESP CRIT CARE, V151, P390; Tracey M, 1995, Am J Respir Crit Care Med, V151, P656; TROISI RJ, 1995, AM J RESP CRIT CARE, V152, P1183; TROISI RJ, 1995, CHEST, V108, P1557, DOI 10.1378/chest.108.6.1557; VANSCHAYCK CP, 1991, AM REV RESPIR DIS, V144, P1297; Ware JE, 1994, SF 36 PHYSICAL MENTA; Weiss ST, 1998, J ALLERGY CLIN IMMUN, V101, P720, DOI 10.1016/S0091-6749(98)70300-8; 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 HC, 1994, BRIT J DERMATOL, V131, P383, DOI 10.1111/j.1365-2133.1994.tb08530.x; YUNGINGER JW, 1992, AM REV RESPIR DIS, V146, P888	45	207	210	0	4	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	NOV	2002	20	5					1071	1079		10.1183/09031936.02.00046802		9	Respiratory System	Respiratory System	614EZ	WOS:000179176500002		
J	Penttinen, P; Timonen, KL; Tiittanen, P; Mirme, A; Ruuskanen, J; Pekkanen, J				Penttinen, P; Timonen, KL; Tiittanen, P; Mirme, A; Ruuskanen, J; Pekkanen, J			Ultrafine particles in urban air and respiratory health among adult asthmatics	EUROPEAN RESPIRATORY JOURNAL			English	Article						air pollution; asthma; particles; particle size; peak expiratory flow rate; respiratory symptoms	CYTOKINE PRODUCTION; POLLUTION; CHILDREN; PM10; ASSOCIATION; INVOLVEMENT; GENERATION; MORTALITY; EXPOSURE; SYMPTOMS	Airborne particles are associated with adverse health effects and contribute to excess mortality in epidemiological studies. A recent hypothesis proposes that the high numbers of ultrafine (<0.1 pm diameter) particles in ambient air might provoke alveolar inflammation and subsequently cause exacerbations in pre-existing cardiopulmonary diseases. To test the hypothesis adult asthmatics were followed with daily peak expiratory flow (PEF) measurements and symptom and medication diaries for sis months, while simultaneously monitoring particulate pollution in ambient air. The associations between daily health endpoints of 57 asthmatics and indicators of air pollution mere examined by multivariate regression models. Daily mean number concentration of particles, but not particle mass (PM10 (particle mass < 10 pm), PM2.5-10, PM2.5, PM1), was negatively associated with daily PEF deviations. The strongest effects were seen for particles in the ultrafine range. However, the effect of ultrafine particles could not definitely be separated from other traffic generated pollutants, namely nitric oxide, nitrogen dioxide and carbon monoxide. No associations were observed with respiratory symptoms or medication use. Particle mass measurements can be strongly influenced by mechanically produced, soil-derived particles, which may not be associated with adverse health effects. Therefore, air quality monitoring should include particle number concentrations, which mainly reflect ultrafine particles.	Natl Publ Hlth Inst, Environm Epidemiol Unit, Kuopio 70701, Finland; Univ Tartu, Inst Environm Phys, EE-2400 Tartu, Estonia; Univ Kuopio, Dept Environm Sci, Kuopio 70211, Finland	Pekkanen, J (reprint author), Natl Publ Hlth Inst, Environm Epidemiol Unit, Kuopio 70701, Finland.						Becker S, 1996, TOXICOL APPL PHARM, V141, P637, DOI 10.1006/taap.1996.0330; Buzorius G, 1999, ATMOS ENVIRON, V33, P553, DOI 10.1016/S1352-2310(98)00287-8; Carter JD, 1997, TOXICOL APPL PHARM, V146, P180, DOI 10.1006/taap.1997.8254; DOCKERY DW, 1993, NEW ENGL J MED, V329, P1753, DOI 10.1056/NEJM199312093292401; DUSSELDORP A, 1995, AM J RESP CRIT CARE, V152, P1932; Gilmour PS, 1996, OCCUP ENVIRON MED, V53, P817; HOSIOKANGAS J, 1995, J AEROSOL SCI, V26, pS423, DOI 10.1016/0021-8502(95)97119-Y; Johnston CJ, 1996, TOXICOL APPL PHARM, V140, P154, DOI 10.1006/taap.1996.0208; OBERDORSTER G, 1995, INHAL TOXICOL, V7, P111, DOI 10.3109/08958379509014275; Osier M, 1997, FUND APPL TOXICOL, V40, P220, DOI 10.1006/faat.1997.2390; Pekkanen J, 1997, ENVIRON RES, V74, P24, DOI 10.1006/enrs.1997.3750; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; POPE CA, 1991, AM REV RESPIR DIS, V144, P668; POPE CA, 1992, AM REV RESPIR DIS, V145, P1123; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; Tiittanen P, 1999, EUR RESPIR J, V13, P266, DOI 10.1034/j.1399-3003.1999.13b08.x; Timonen KL, 1997, AM J RESP CRIT CARE, V156, P546; Tuch T, 2000, ATMOS ENVIRON, V34, P139, DOI 10.1016/S1352-2310(99)00248-4; Vallius MJ, 2000, ENVIRON SCI TECHNOL, V34, P1919, DOI 10.1021/es990603e; Vedal S, 1997, J AIR WASTE MANAGE, V47, P551; Vedal S, 1998, AM J RESP CRIT CARE, V157, P1034; Venkataraman C, 1998, INHAL TOXICOL, V10, P183; Vincent R, 1997, AM J PATHOL, V151, P1563; 1997, FINNISH POLLEN B, V22	24	207	216	4	35	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146, WEST ST, STE 2.4 HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	MAR	2001	17	3					428	435		10.1183/09031936.01.17304280		8	Respiratory System	Respiratory System	437TK	WOS:000169009500017	11405521	
J	Mattes, J; Collison, A; Plank, M; Phipps, S; Foster, PS				Mattes, Joerg; Collison, Adam; Plank, Maximilian; Phipps, Simon; Foster, Paul S.			Antagonism of microRNA-126 suppresses the effector function of T(H)2 cells and the development of allergic airways disease	PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA			English	Article						animal model; asthma; inflammation; microRNA; T(H)2 cytokines	TOLL-LIKE RECEPTORS; DENDRITIC CELLS; EXPERIMENTAL ASTHMA; IMMUNE-RESPONSES; INHALED ANTIGEN; LINKING INNATE; PLASMA-CELLS; IN-VIVO; EXPRESSION; HYPERREACTIVITY	Allergic asthma is an inflammatory disease of the lung characterized by abnormal T helper-2 (T(H)2) lymphocyte responses to inhaled antigens. The molecular mechanisms leading to the generation of T(H)2 responses remain unclear, although toll-like receptors (TLRs) present on innate immune cells play a pivotal role in sensing molecular patterns and in programming adaptive T cell responses. Here we show that in vivo activation of TLR4 by house dust mite antigens leads to the induction of allergic disease, a process that is associated with expression of a unique subset of small, noncoding microRNAs. Selective blockade of microRNA (miR)-126 suppressed the asthmatic phenotype, resulting in diminished T(H)2 responses, inflammation, airways hyperresponsiveness, eosinophil recruitment, and mucus hypersecretion. miR-126 blockade resulted in augmented expression of POU domain class 2 associating factor 1, which activates the transcription factor PU. 1 that alters T(H)2 cell function via negative regulation of GATA3 expression. In summary, this study presents a functional connection between miRNA expression and asthma pathogenesis, and our data suggest that targeting miRNA in the airways may lead to anti-inflammatory treatments for allergic asthma.	[Mattes, Joerg; Collison, Adam; Plank, Maximilian] Univ Newcastle, Immunol & Resp Res Grp, Callaghan, NSW 2300, Australia; [Mattes, Joerg] Univ Newcastle, John Hunter Childrens Hosp, Callaghan, NSW 2300, Australia; [Collison, Adam; Plank, Maximilian; Phipps, Simon; Foster, Paul S.] Univ Newcastle, Fac Hlth, Sch Biomed Sci & Pharm, CARD, Callaghan, NSW 2300, Australia; Hunter Med Res Inst, Callaghan, NSW 2300, Australia	Mattes, J (reprint author), Univ Newcastle, Immunol & Resp Res Grp, Callaghan, NSW 2300, Australia.	joerg.mattes@newcastle.edu.au; paul.foster@newcastle.edu.au	Phipps, Simon/F-9170-2010; Foster, Paul/G-5057-2013	Phipps, Simon/0000-0002-7388-3612; 	National Health and Medical Research Council; Cooperative Research Centre Asthma and Airways	Wethank Prof. Akira (Osaka University, Japan) for the generous provision of MyD88-and TLR4-deficient mice, and Ana Pereira de Siqueira, Stuart Reeves, and Fiona Eyers for technical assistance. This work was supported by a National Health and Medical Research Council project grant (to J. M. and P. S. F.), a National Health and Medical Research Council Health Professional Research Fellowship (to J. M.), and the Cooperative Research Centre Asthma and Airways (J. M. and P. S. F.).	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Natl. Acad. Sci. U. S. A.	NOV 3	2009	106	44					18704	18709		10.1073/pnas.0905063106		6	Multidisciplinary Sciences	Science & Technology - Other Topics	514XM	WOS:000271429800053	19843690	
J	Schaub, B; Lauener, R; von Mutius, E				Schaub, B; Lauener, R; von Mutius, E			The many faces of the hygiene hypothesis	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						allergy; asthma; infection; innate; microbial; virus; toll	TOLL-LIKE RECEPTORS; RESPIRATORY SYNCYTIAL VIRUS; REGULATORY T-CELLS; KILLED MYCOBACTERIUM-VACCAE; DAY-CARE ATTENDANCE; BRONCHIAL EPITHELIAL-CELLS; EARLY BCG VACCINATION; SCHOOL-AGE-CHILDREN; HEPATITIS-A VIRUS; EARLY-LIFE	About 15 years have gone by since Strachan first proposed the idea that infections and unhygienic contact might confer protection against the development of allergic illnesses. The so-called hygiene hypothesis has ever since undergone numerous more or less subtle modifications by various researchers in the fields of epidemiology, clinical science, and immunology. Three major tracts have developed exploring the role of overt viral and bacterial infections, the significance of environmental exposure to microbial compounds, and the effect of both on underlying responses of the innate and adaptive immunity. To date, a truly unifying concept has not yet emerged, but various pieces of a complex interplay between immune responses of the host, characteristics of the invading microorganism, the level and variety of the environmental exposure, and the interactions between a genetic background and a range of exposures becomes apparent. These influences are discussed as determinants for a number of complex allergic illnesses in this review, while we attempt to pay attention to the importance of different phenotypes, namely of the asthma syndrome. Even if today practical implications cannot directly be deduced from these findings, there is great potential for the development of novel preventive and therapeutic strategies in the future.	Univ Munich, Univ Childrens Hosp Munich, Dr Haunersches Kinderspital, Pediat Pulm Div, D-80337 Munich, Germany; Univ Zurich, Childrens Hosp, Ctr Allergy Res, Zurich, Switzerland	Schaub, B (reprint author), Univ Munich, Univ Childrens Hosp Munich, Dr Haunersches Kinderspital, Pediat Pulm Div, Lindwurmstr 4, D-80337 Munich, Germany.	bianca.schaub@med.uni-muenchen.de	Lauener, Roger/O-8612-2016	Lauener, Roger/0000-0002-8412-606X; von Mutius, Erika/0000-0002-8893-4515			Abbas AK, 1996, NATURE, V383, P787, DOI 10.1038/383787a0; Akdis CA, 2004, ALLERGY, V59, P897, DOI 10.1111/j.1398-9995.2004.00587.x; Akdis M, 2005, J ALLERGY CLIN IMMUN, V116, P961, DOI 10.1016/j.jaci.2005.09.004; Alm JS, 1997, LANCET, V350, P400, DOI 10.1016/S0140-6736(97)02207-1; Annus T, 2004, ALLERGY, V59, P1068, DOI 10.1111/j.1398-9995.2004.00557.x; Arkwright PD, 2001, J ALLERGY CLIN IMMUN, V107, P531, DOI 10.1067/mai.20001.113081; Arshad SH, 2005, CHEST, V127, P502, DOI 10.1378/chest.127.2.502; Avila PC, 2000, J ALLERGY CLIN IMMUN, V105, P923, DOI 10.1067/mai.2000.106214; 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Immunology	Allergy; Immunology	085SF	WOS:000240624000001	16930249	
J	Spencer, S; Calverley, PMA; Burge, PS; Jones, PW				Spencer, S; Calverley, PMA; Burge, PS; Jones, PW		ISOLDE Study Grp	Health status deterioration in patients with chronic obstructive pulmonary disease	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							QUALITY-OF-LIFE; GEORGE RESPIRATORY QUESTIONNAIRE; AIR-FLOW LIMITATION; SF-36; ASTHMA; COPD	This study examined health status decline in patients with chronic obstructive pulmonary disease (COPD). Data are from the Inhaled Steroids in Obstructive Lung Disease (ISOLDE) trial. After an 8-wk run-in, 751 patients (566 male), mean age 64 yr, were randomized to receive fluticasone propionate (FP) 500 mug twice daily (376 patients) or placebo (375 patients). Mean baseline postbronchodilator FEV1 was 50 +/- 15% predicted. Patients completed the St George's Respiratory Questionnaire (SGRQ) and the Short-Form 36 (SF-36) at baseline and every 6 mo for 3 yr. FEV1 and smoking status were assessed at baseline and at 3-mo intervals. A total of 387 (212 FP) patients completed the trial. All SGRQ components (p = 0.03 to 0.004) and Physical Function, Mental Health, Energy/Vitality, and Physical Role Limitation scales of the SF-36 (p = 0.05 to 0.005) deteriorated faster in the placebo group. FEV, and SGRQ scores correlated at baseline values (r = -0.25, p < 0.0001), as did change in FEV1 and change in SGRQ (<Delta> r = -0.24, p < 0.0001). At baseline values smokers had worse SGRQ Total, Symptoms, and Impacts scores than ex-smokers. This difference was maintained throughout the study. Smoking status did not influence the rate of decline in health status. The SGRQ Total scores of FP-treated patients took 59% longer than placebo to deteriorate by a clinically significant amount. We conclude that health status decline in moderate to severe COPD can be reduced by high-dose fluticasone.	St George Hosp, Sch Med, Dept Med Physiol, London SW17 0RE, England	Spencer, S (reprint author), St George Hosp, Sch Med, Dept Med Physiol, Cranmer Terrace, London SW17 0RE, England.		Spencer, Sally/D-6963-2013				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; Bowling A., 1995, MEASURING HLTH REV Q; BRAZIER JE, 1992, BRIT MED J, V305, P160; Burge PS, 2000, BRIT MED J, V320, P1297, DOI 10.1136/bmj.320.7245.1297; Ferrer M, 1996, EUR RESPIR J, V9, P1160, DOI 10.1183/09031936.96.09061160; Goldstein H., 1995, MULTILEVEL STAT MODE; The Intermittent Positive Pressure Breathing Trial Group, 1983, ANN INTERN MED, V99, P612; Jarad NA, 1999, RESP MED, V93, P161, DOI 10.1016/S0954-6111(99)90001-X; JENKINSON C, 1993, BRIT MED J, V306, P1437; JONES PW, 1991, RESP MED, V85, P25, DOI 10.1016/S0954-6111(06)80166-6; JONES PW, 1992, AM REV RESPIR DIS, V145, P1321; Jones PW, 1997, AM J RESP CRIT CARE, V155, P1283; JONES PW, 1989, AM REV RESPIR DIS, V140, P1538; JONES PW, 1995, EUR RESPIR REV, V5, P279; Jones PW, 1994, AM J RESP CRIT CARE, V149, pA211; MAHLER DA, 1995, AM J RESP CRIT CARE, V151, P61; MEECHAMJONES DJ, 1995, AM J RESP CRIT CARE, V152, P538; NOONAN M, 1995, AM J RESP CRIT CARE, V152, P1467; Okubadejo AA, 1996, THORAX, V51, P44, DOI 10.1136/thx.51.1.44; Osman L. M., 1996, European Respiratory Journal Supplement, V9, p143S; Seemungal TAR, 1998, AM J RESP CRIT CARE, V157, P1418; SWINBURN CR, 1988, BRIT J CLIN PHARMACO, V26, P709; VANSCHAYCK CP, 1995, CHEST, V107, P1199, DOI 10.1378/chest.107.5.1199; WARE JE, 1992, MED CARE, V30, P473, DOI 10.1097/00005650-199206000-00002	25	205	209	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	2001	163	1					122	128				7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	394TV	WOS:000166540100025	11208636	
J	Lee, M; Lee, J; Carroll, MW; Choi, H; Min, S; Song, T; Via, LE; Goldfeder, LC; Kang, E; Jin, B; Park, H; Kwak, H; Kim, H; Jeon, HS; Jeong, I; Joh, JS; Chen, RY; Olivier, KN; Shaw, PA; Follmann, D; Song, SD; Lee, JK; Lee, D; Kim, CT; Dartois, V; Park, SK; Cho, SN; Barry, CE				Lee, Myungsun; Lee, Jongseok; Carroll, Matthew W.; Choi, Hongjo; Min, Seonyeong; Song, Taeksun; Via, Laura E.; Goldfeder, Lisa C.; Kang, Eunhwa; Jin, Boyoung; Park, Hyeeun; Kwak, Hyunkyung; Kim, Hyunchul; Jeon, Han-Seung; Jeong, Ina; Joh, Joon Sung; Chen, Ray Y.; Olivier, Kenneth N.; Shaw, Pamela A.; Follmann, Dean; Song, Sun Dae; Lee, Jong-Koo; Lee, Dukhyoung; Kim, Cheon Tae; Dartois, Veronique; Park, Seung-Kyu; Cho, Sang-Nae; Barry, Clifton E., III			Linezolid for Treatment of Chronic Extensively Drug-Resistant Tuberculosis	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							INTRACTABLE MULTIDRUG-RESISTANT; MYCOBACTERIUM-TUBERCULOSIS; PULMONARY TUBERCULOSIS; OXAZOLIDINONE ANTIBACTERIAL; MURINE MODEL; PHARMACOKINETICS; TOLERABILITY; MOXIFLOXACIN; OFLOXACIN; EFFICACY	BACKGROUND Linezolid has antimycobacterial activity in vitro and is increasingly used for patients with highly drug-resistant tuberculosis. METHODS We enrolled 41 patients who had sputum-culture-positive extensively drug-resistant (XDR) tuberculosis and who had not had a response to any available chemotherapeutic option during the previous 6 months. Patients were randomly assigned to linezolid therapy that started immediately or after 2 months, at a dose of 600 mg per day, without a change in their background regimen. The primary end point was the time to sputum-culture conversion on solid medium, with data censored 4 months after study entry. After confirmed sputum-smear conversion or 4 months (whichever came first), patients underwent a second randomization to continued linezolid therapy at a dose of 600 mg per day or 300 mg per day for at least an additional 18 months, with careful toxicity monitoring. RESULTS By 4 months, 15 of the 19 patients (79%) in the immediate-start group and 7 of the 20 (35%) in the delayed-start group had culture conversion (P = 0.001). Most patients (34 of 39 [87%]) had a negative sputum culture within 6 months after linezolid had been added to their drug regimen. Of the 38 patients with exposure to linezolid, 31 (82%) had clinically significant adverse events that were possibly or probably related to linezolid, including 3 patients who discontinued therapy. Patients who received 300 mg per day after the second randomization had fewer adverse events than those who continued taking 600 mg per day. Thirteen patients completed therapy and have not had a relapse. Four cases of acquired resistance to linezolid have been observed. CONCLUSIONS Linezolid is effective at achieving culture conversion among patients with treatment-refractory XDR pulmonary tuberculosis, but patients must be monitored carefully for adverse events. (Funded by the National Institute of Allergy and Infectious Diseases and the Ministry of Health and Welfare, South Korea; ClinicalTrials.gov number, NCT00727844.)	[Carroll, Matthew W.; Via, Laura E.; Goldfeder, Lisa C.; Barry, Clifton E., III] NIAID, TB Res Sect, NIH, Bethesda, MD 20892 USA; [Lee, Myungsun; Lee, Jongseok; Choi, Hongjo; Min, Seonyeong; Song, Taeksun; Kang, Eunhwa; Jin, Boyoung; Park, Hyeeun; Kwak, Hyunkyung; Kim, Hyunchul; Jeon, Han-Seung; Song, Sun Dae] Int TB Res Ctr, Chang Won, South Korea; [Jeong, Ina; Joh, Joon Sung] Natl Med Ctr, Dept Internal Med, Seoul, South Korea; [Lee, Jong-Koo] Seoul Natl Univ Hosp, Dept Family Med, Seoul 110744, South Korea; [Lee, Dukhyoung] Korea Ctr Dis Control & Prevent, Osong, South Korea; [Kim, Cheon Tae; Park, Seung-Kyu] Natl Masan Hosp, Masan, South Korea; [Cho, Sang-Nae] Yonsei Univ, Coll Med, Dept Microbiol, Seoul, South Korea; [Cho, Sang-Nae] Yonsei Univ, Coll Med, Inst Immunol & Immunol Dis, Seoul, South Korea; [Olivier, Kenneth N.] NIAID, Immunopathol Sect, NIH, Bethesda, MD 20892 USA; [Chen, Ray Y.] NIAID, Lab Clin Infect Dis, Off Global Res, NIH, Bethesda, MD 20892 USA; [Shaw, Pamela A.; Follmann, Dean] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA; [Dartois, Veronique] Novartis Inst Trop Dis, Singapore, Singapore	Barry, CE (reprint author), NIAID, TB Res Sect, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.	cbarry@niaid.nih.gov	Barry, III, Clifton/H-3839-2012	Via, Laura/0000-0001-6074-9521; Chen, Ray/0000-0001-6344-1442	National Institute of Allergy and Infectious Diseases, National Institutes of Health; Ministry of Health and Welfare, South Korea	Supported by the Intramural Research Program, National Institute of Allergy and Infectious Diseases, National Institutes of Health, and by the Ministry of Health and Welfare, South Korea.	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Engl. J. Med.	OCT 18	2012	367	16					1508	1518		10.1056/NEJMoa1201964		11	Medicine, General & Internal	General & Internal Medicine	021SA	WOS:000309904500008	23075177	
J	Beckett, WS; Jacobs, DR; Yu, XH; Iribarren, C; Williams, D				Beckett, WS; Jacobs, DR; Yu, XH; Iribarren, C; Williams, D			Asthma is associated with weight gain in females but not males, independent of physical activity	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; obesity; body mass index; African American; physical activity; epidemiology; environmental tobacco smoke; passive smoking; sex differences	BODY-MASS INDEX; RISK; CARDIA; CHILDREN; WOMEN; MEN	We tested whether asthma diagnosis is associated with weight gain and physical activity in 4,547 18 to 30-yr-old African American and white men and women, followed prospectively for up to 10 yr. Baseline asthma was most frequent in African American men. Incident asthma was more frequent in women. Incident asthma was associated with highest and lowest baseline and change in body mass index (BMI), in a J-shaped curve, after adjustment for other factors. When stratified by sex, this association was seen only in females. Subjects on average decreased physical activity and gained weight over time, but there was no significant difference in asthma prevalence by physical activity at baseline or asthma incidence by change in physical activity. Cigarette smoking in females was significantly associated with asthma incidence, but serum cotinine level at baseline among nonsmokers (reflecting environmental tobacco smoke [ETS] exposure) was not significantly associated with asthma. We conclude that gain in BMI predisposes to new asthma diagnosis In female young adults, but decreased physical activity does not explain the association of weight gain with asthma.	Univ Rochester, Sch Med & Dent, Div Pulm & Crit Care, Rochester, NY 14642 USA; Univ Rochester, Sch Med & Dent, Dept Environm Med, Rochester, NY 14642 USA; Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA; Univ Oslo, Inst Nutr Res, Oslo, Norway; Univ Alabama, Div Prevent Med, Birmingham, AL USA; Kaiser Permanente, Div Res, Oakland, CA USA	Beckett, WS (reprint author), Univ Rochester, Sch Med & Dent, Div Pulm & Crit Care, Box EHSC,575 Elmwood Ave, Rochester, NY 14642 USA.		Yu, Xinhua/D-5570-2009		NHLBI NIH HHS [N01-HC-48049, N01-HC-48048, N01-HC-48050, N01-HC-4807]; NIEHS NIH HHS [P30 ES01247]		American College of Sports Medicine position stand, 1990, MED SCI SPORTS EXERC, V22, P265; Anderssen N, 1996, AM J EPIDEMIOL, V143, P351; Beckett WS, 1996, AM J RESP CRIT CARE, V154, P894; Camargo CA, 1999, ARCH INTERN MED, V159, P2582, DOI 10.1001/archinte.159.21.2582; Chen Y, 1999, AM J EPIDEMIOL, V150, P255; FRIEDMAN GD, 1988, J CLIN EPIDEMIOL, V41, P1105, DOI 10.1016/0895-4356(88)90080-7; GUERRA S, 2001, AM J RESP CRIT CARE, V163, P138; HIGGINS M, 1991, CHEST, V99, P315, DOI 10.1378/chest.99.2.315; JACOBS DR, 1989, J CARDIOPULMONARY RE, V0009; Litonjua A, 1999, AM J RESP CRIT CARE, V159, pA131; Mannino DM, 1998, MMWR-MORBID MORTAL W, V47, P1; Platts-Mills TA, 1996, J ALLERGY CLIN IMMUN, V98, P297; Schachter LM, 2001, THORAX, V56, P4, DOI 10.1136/thorax.56.1.4; SCHWARTZ J, 1990, AM REV RESPIR DIS, V142, P555; Sporik R, 1999, THORAX, V54, P675	15	204	208	2	11	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	2001	164	11					2045	2050				6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	504CA	WOS:000172838600008	11739133	
J	Wong, CA; Walsh, LJ; Smith, CJP; Wisniewski, AF; Lewis, SA; Hubbard, R; Cawte, S; Green, DJ; Pringle, M; Tattersfield, AE				Wong, CA; Walsh, LJ; Smith, CJP; Wisniewski, AF; Lewis, SA; Hubbard, R; Cawte, S; Green, DJ; Pringle, M; Tattersfield, AE			Inhaled corticosteroid use and bone-mineral density in patients with asthma	LANCET			English	Article							BECLOMETHASONE DIPROPIONATE; REFERENCE RANGES; STEROID-THERAPY; WOMEN; RISK; BUDESONIDE; GLUCOCORTICOIDS; FLUTICASONE; METABOLISM; FRACTURE	Background Inhaled corticosteroids are absorbed into the systemic circulation, but the extent to which they have adverse effects on bone is uncertain. The question is important since 3% of the European population take an inhaled corticosteroid regularly and may do so for many years. Methods We studied the dose-response relation between cumulative inhaled corticosteroid dose and bone-mineral density at the lumbar spine and proximal femur in 196 adults (119 women) with asthma aged 20-40 years. Patients had taken an inhaled corticosteroid regularly for at least 6 months, and had had limited exposure to systemic steroids. Cumulative dose of inhaled corticosteroid was calculated from questionnaires and computerised and written general-practice records, and its effect on bone-mineral density was estimated by multiple regression analysis. Findings Median duration of inhaled corticosteroid treatment was 6 years (range 0.5-24), and median cumulative dose was 876 mg (87-4380), There was a negative association between cumulative dose of inhaled corticosteroid and bone-mineral density at the lumbar spine (L2-L4), femoral neck, Ward's triangle, and trochanter, both before and after adjustment for the effects of age and sex. A doubling in dose of inhaled corticosteroid was associated with a decrease in bone-mineral density at the lumbar spine of 0.16 SD (95% CI 0.04-0.28). Similar decreases were found at the femoral neck, Ward's triangle, and trochanter, Adjustment for potential confounding factors including physical activity and past oral, nasal, dermal, and parenteral corticosteroids did not weaken the associations. Interpretation This study provides evidence of a negative relation between total cumulative dose of inhaled corticosteroid and bone-mineral density in patients with asthma.	City Hosp, Div Resp Med, Nottingham NG5 1PB, England; City Hosp, Dept Radiol, Nottingham NG5 1PB, England; Queens Med Ctr, Dept Gen Practice, Nottingham NG7 2UH, England	Wong, CA (reprint author), City Hosp, Div Resp Med, Nottingham NG5 1PB, England.						BALFOURLYNNE L, 1987, PAEDIATRICIAN, V24, P237; BARNES PJ, 1993, AM REV RESPIR DIS, V148, pS1; Bisgaard H, 1996, EUR RESPIR J, V9, pS28; BOULET LP, 1994, J ALLERGY CLIN IMMUN, V94, P796, DOI 10.1016/0091-6749(94)90145-7; Cumming RG, 1997, NEW ENGL J MED, V337, P8, DOI 10.1056/NEJM199707033370102; EASTELL R, 1991, J BONE MINER RES, V6, P207; Ebeling PR, 1998, J BONE MINER RES, V13, P1283, DOI 10.1359/jbmr.1998.13.8.1283; Egan JJ, 1999, EUR RESPIR J, V13, P1267, DOI 10.1183/09031936.99.13612769; Garbe E, 1997, JAMA-J AM MED ASSOC, V277, P722, DOI 10.1001/jama.277.9.722; HANANIA NA, 1995, J ALLERGY CLIN IMMUN, V96, P571, DOI 10.1016/S0091-6749(95)70254-7; HERRALA J, 1994, BONE, V15, P621, DOI 10.1016/8756-3282(94)90309-3; Hughes JA, 1999, THORAX, V54, P223; IP M, 1994, CHEST, V105, P1722, DOI 10.1378/chest.105.6.1722; JAGLAL SB, 1993, AM J EPIDEMIOL, V138, P107; Lau EMC, 1998, CLIN EXP ALLERGY, V28, P1066; Luengo M, 1997, EUR RESPIR J, V10, P2110, DOI 10.1183/09031936.97.10092110; Marystone JF, 1995, AM J PUBLIC HEALTH, V85, P1693, DOI 10.2105/AJPH.85.12.1693; Mazess RB, 1997, BRIT J RADIOL, V70, P109; Packe GE, 1996, J ROY COLL PHYS LOND, V30, P128; PACKE GE, 1992, THORAX, V47, P414, DOI 10.1136/thx.47.6.414; Pauwels RA, 1999, NEW ENGL J MED, V340, P1948, DOI 10.1056/NEJM199906243402503; Petley GW, 1996, BRIT J RADIOL, V69, P655; RUSELL G, 1993, ARCH DIS CHILD, V69, P694; SAMBROOK P, 1990, J BONE MINER RES, V5, P1211; TOOGOOD JH, 1995, J ALLERGY CLIN IMMUN, V96, P157, DOI 10.1016/S0091-6749(95)70003-X; Truscott JG, 1997, BRIT J RADIOL, V70, P1245; Walsh LJ, 1999, THORAX, V54, P296; WASNICH R, 1993, AM J MED, V95, pS6, DOI 10.1016/0002-9343(93)90374-X; Wisniewski AF, 1997, THORAX, V52, P853; WOLFF AH, 1991, ANN ALLERGY, V67, P117	30	204	212	0	6	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	APR 22	2000	355	9213					1399	1403		10.1016/S0140-6736(00)02138-3		5	Medicine, General & Internal	General & Internal Medicine	310LN	WOS:000086829800010	10791523	
J	Lambrecht, BN; Hammad, H				Lambrecht, Bart N.; Hammad, Hamida			Biology of Lung Dendritic Cells at the Origin of Asthma	IMMUNITY			English	Review							HOUSE-DUST MITE; ALLERGIC AIRWAY INFLAMMATION; CD4(+) T-CELLS; RESPIRATORY SYNCYTIAL VIRUS; ANTIGEN-PRESENTING CELLS; BLOOD MONOCYTE SUBSETS; EPITHELIAL-CELLS; IMMUNE-RESPONSES; INHALED ANTIGEN; TH2 RESPONSES	Dendritic cells (DCs) initiate and maintain adaptive T helper 2 (Th2) cell responses to inhaled allergens in asthma. Various functions like antigen uptake, migration to the draining LNs, and induction of tolerance and adaptive immunity are not equally shared by all subsets of DCs, adding considerable complexity to understanding the immunology of allergic sensitization. Whereas the epithelium was initially considered solely as a physical barrier, it is now seen as a central player in controlling the function of lung DCs through release of Th2 cell-promoting cytokines. Although DCs are sufficient and necessary for induction of Th2 cell responses to many antigens, some allergens might require antigen presentation by basophils. Clinically relevant allergens, as well as environmental and genetic risk factors for allergy and asthma, often interfere directly or indirectly with the innate immune functions of airway epithelial cells, basophils, and DCs. This review summarizes the recent progress on our understanding how DCs control Th2 cell immunity in the lung.	[Lambrecht, Bart N.; Hammad, Hamida] Ghent Univ Hosp, Dept Resp Dis, Lab Immunoregulat & Mucosal Immunol, B-9000 Ghent, Belgium; [Lambrecht, Bart N.] Erasmus Univ, Med Ctr, Dept Pulm Med, NL-3015 GE Rotterdam, Netherlands	Lambrecht, BN (reprint author), Ghent Univ Hosp, Dept Resp Dis, Lab Immunoregulat & Mucosal Immunol, B-9000 Ghent, Belgium.	bart.lambrecht@ugent.be	Hammad, Hamida/J-9391-2015; Lambrecht, Bart/K-2484-2014	Hammad, Hamida/0000-0003-3762-8603; Lambrecht, Bart/0000-0003-4376-6834			Akbari O, 2001, NAT IMMUNOL, V2, P725, DOI 10.1038/90667; Akbari O, 2002, NAT MED, V8, P1024, DOI 10.1038/nm745; Al-Shami A, 2005, J EXP MED, V202, P829, DOI 10.1084/jem.20050199; Allakhverdi Z, 2007, J EXP MED, V204, P253, DOI 10.1084/jem.20062211; Angkasekwinai P, 2007, J EXP MED, V204, P1509, DOI 10.1084/jem.20061675; Barrett NA, 2009, IMMUNITY, V31, P425, DOI 10.1016/j.immuni.2009.08.014; Barrett NA, 2009, J IMMUNOL, V182, P1119; Beaty SR, 2007, J IMMUNOL, V178, P1882; Bleck B, 2006, J IMMUNOL, V176, P7431; 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J	Gilliland, FD; Li, YF; Dubeau, L; Berhane, K; Avol, E; McConnell, R; Gauderman, WJ; Peters, JM				Gilliland, FD; Li, YF; Dubeau, L; Berhane, K; Avol, E; McConnell, R; Gauderman, WJ; Peters, JM			Effects of glutathione S-transferase M1, maternal smoking during pregnancy, and environmental tobacco smoke on asthma and wheezing in children	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						In utero exposure; tobacco smoke; GSTM1; asthma; wheeze; children	PARENTAL SMOKING; CHILDHOOD ASTHMA; LUNG-FUNCTION; OXIDATIVE STRESS; FAMILY HISTORY; RESPIRATORY HEALTH; AIR-POLLUTION; RISK-FACTORS; PREVALENCE; EXPOSURE	The rise in childhood asthma prevalence suggests a role for environmental factors in the etiology of this evolving epidemic; however, genetics also influence the occurrence of asthma. Glutathione S-transferase (GST) M1 may play a role in asthma and wheezing occurrence among those exposed to tobacco smoke, as it functions in pathways involved in asthma pathogenesis such as xenobiotic metabolism and antioxidant defenses. Effects of GSTM1 genotype, maternal smoking during pregnancy, and childhood environmental tobacco smoke (ETS) exposure on asthma and wheezing were investigated in 2,950 children enrolled in 4th, 7th, and 10th grade classrooms in 12 Southern California communities. The effects of in utero exposure to maternal smoking on asthma and wheezing occurrence were largely restricted to children with GSTM1 null genotype. Among GSTM1 null children, in utero exposure was associated with increased prevalence of early onset asthma (odds ratio [OR] 1.6, 95% confidence interval [CI] 1.0-2.5), asthma with current symptoms (OR 1.7, 95% Cl 1.1-2.8), persistent asthma (OR 1.6, 95% Cl 1.1-2.4), lifetime history of wheezing (OR 1.8, 95% Cl 1.3-2.5), wheezing with exercise (OR 2.1, 95% Cl 1.3-3.3), wheezing requiring medication (OR 2.2, 95% Cl 1.4-3.4), and emergency room visits in the past year (OR 3.7, 95% Cl 1.9-7.3). Among children with GSTM1 (+) genotype, in utero exposure was not associated with asthma or wheezing. Our findings indicate that there are important long-term effects of in utero exposure in a genetically susceptible group of children.	Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA	Gilliland, FD (reprint author), Univ So Calif, Keck Sch Med, Dept Prevent Med, 1540 Alcazar St,CHP 236, Los Angeles, CA 90033 USA.		LI, YU-FEN/F-4770-2010; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	NHLBI NIH HHS [5R01 HL 61768]; NIEHS NIH HHS [1P50 ES 09581, 2P30 ES 07048]		ANDERSON HR, 1994, BRIT MED J, V308, P1600; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; California Environmental Protection Agency (Cal EPA) Office of Environmental Health Hazard Assessment, 1997, HLTH EFF EXP ENV TOB; Carlsen KCL, 1997, EUR RESPIR J, V10, P1774; *COMM ASS ASTHM IN, 2000, CLEAN AIR ASTHM IND; Cook DG, 1999, THORAX, V54, P357; Cook DG, 1997, THORAX, V52, P1081; Cook DG, 1998, THORAX, V53, P295; Cook DG, 1998, THORAX, V53, P884; Cookson WOC, 2000, HUM MOL GENET, V9, P2359, DOI 10.1093/hmg/9.16.2359; CUNNINGHAM J, 1994, AM J EPIDEMIOL, V139, P1139; Cunningham J, 1996, AM J RESP CRIT CARE, V153, P218; Ebrahim SH, 2000, JAMA-J AM MED ASSOC, V283, P361, DOI 10.1001/jama.283.3.361; Ehrlich RI, 1996, AM J RESP CRIT CARE, V154, P681; Forsberg B, 1997, INT J EPIDEMIOL, V26, P610, DOI 10.1093/ije/26.3.610; Fryer A A, 1999, IARC Sci Publ, P303; Geisler SA, 2001, AM J EPIDEMIOL, V154, P95, DOI 10.1093/aje/154.2.95; Gilliland FD, 2000, THORAX, V55, P271, DOI 10.1136/thorax.55.4.271; Gilliland FD, 1999, ENVIRON HEALTH PERSP, V107, P403; Gilliland FD, 2001, AM J RESP CRIT CARE, V163, P429; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; Hayes JD, 2000, PHARMACOLOGY, V61, P154, DOI 10.1159/000028396; Holt P.G., 1999, NATURE, V402, P12, DOI 10.1038/35037009; Howard DJ, 1998, CANCER EPIDEM BIOMAR, V7, P981; Hu FB, 1997, ANN ALLERG ASTHMA IM, V79, P80; Ivaschenko T. 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J. Respir. Crit. Care Med.	AUG 15	2002	166	4					457	463		10.1164/rccm.2112064		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	584BE	WOS:000177446700008	12186820	
J	Kogevinas, M; Zock, JP; Jarvis, D; Kromhout, H; Lillienberg, L; Plana, E; Radon, K; Toren, K; Alliksoo, A; Benke, G; Blanc, PD; Dahlman-Hoglund, A; D'Errico, A; Hery, M; Kennedy, S; Kunzli, N; Leynaert, B; Mirabelli, MC; Muniozguren, N; Norback, D; Olivieri, M; Payo, F; Villani, S; van Sprundel, M; Urrutia, I; Wieslander, G; Sunyer, J; Anto, JM				Kogevinas, Manolis; Zock, Jan-Paul; Jarvis, Debbie; Kromhout, Hans; Lillienberg, Linnea; Plana, Estel; Radon, Katja; Toren, Kjell; Alliksoo, Ada; Benke, Geza; Blanc, Paul D.; Dahlman-Hoglund, Anna; D'Errico, Angelo; Hery, Michel; Kennedy, Susan; Kunzli, Nino; Leynaert, Benedicte; Mirabelli, Maria C.; Muniozguren, Nerea; Norback, Dan; Olivieri, Mario; Payo, Felix; Villani, Simona; van Sprundel, Marc; Urrutia, Isabel; Wieslander, Gundla; Sunyer, Jordi; Anto, Josep M.			Exposure to substances in the workplace and new-onset asthma: an international prospective population-based study (ECRHS-II)	LANCET			English	Article							OCCUPATIONAL RESPIRATORY-DISEASES; AIRWAYS DYSFUNCTION SYNDROME; WORK-RELATED ASTHMA; REPORTED INCIDENCE; EPIDEMIOLOGY; SURVEILLANCE; LATEX	Background The role of exposure to substances in the workplace in new-onset asthma is not well characterised in population-based studies. We therefore aimed to estimate the relative and attributable risks of new-onset asthma in relation to occupations, work-related exposures, and inhalation accidents. Methods We studied prospectively 6837 participants from 13 countries who previously took part in the European Community Respiratory Health Survey (1990-95) and did not report respiratory symptoms or a history of asthma at the time of the first study. Asthma was assessed by methacholine challenge test and by questionnaire data on asthma symptoms. Exposures were defined by high-risk occupations, an asthma-specific job exposure matrix with additional expert judgment, and through self-report of acute inhalation events. Relative risks for new onset asthma were calculated with log-binomial models adjusted for age, sex, smoking, and study Centre. Findings A significant excess asthma risk was seen after exposure to substances known to cause occupational asthma (Relative risk=1.6, 95% CI 1.1-2.3, p=0.017). Risks were highest for asthma defined by bronchial hyper-reactivity in addition to symptoms (2.4,1.3-4.6, p=0.008). Of common occupations, a significant excess risk of asthma was seen for nursing (2.2,1.3-4.0, p=0.007). Asthma risk was also increased in participants who reported an acute symptomatic inhalation event such as fire, mixing cleaning products, or chemical spills (RR=3.3, 95% CI 1.0-11.1, p=0.051). The population-attributable risk for adult asthma due to occupational exposures ranged from 10% to 25%, equivalent to an incidence of new-onset occupational asthma of 250-300 cases per million people per year. Interpretation Occupational exposures account for a substantial proportion of adult asthma incidence. The increased risk of asthma after inhalation accidents suggests that workers who have such accidents should be monitored closely.	Municipal Inst Med Res, Ctr Res Environm Epidemiol, Barcelona 08003, Spain; Univ Crete, Sch Med, Iraklion, Greece; Univ London Imperial Coll Sci Technol & Med, Resp Epidmeiol & Publ Hlth Grp, Natl Heart & Lung Inst, London, England; Univ Utrecht, Inst Risk Assessment Sci, Div Environm Epidemiol, Utrecht, Netherlands; Sahlgrens Univ Hosp, Dept Occupat & Environm Med, Gothenburg, Sweden; Univ Munich, Inst Occupat & Environm Med, Unit Occupat & Environm Epidemiol & NetTeaching, Munich, Germany; Tartu Univ Clin, Lung Clin, Tartu, Estonia; Monash Univ, Dept Epidemiol & Prevent Med, Clayton, Vic 3168, Australia; Univ Calif San Francisco, Dept Med, Div Environm & Occupat Med, San Francisco, CA USA; Serv Reg Epidemiol, Turin, Italy; Inst Natl Rech & Secur, F-54501 Vandoeuvre Les Nancy, France; Univ British Columbia, Sch Occupat & Environm Hyg, Vancouver, BC V5Z 1M9, Canada; Univ Paris 07, INSERM, French Inst Hlth & Med Res, Unit Epidemiol 700, Paris, France; Publ Hlth Dept Bizkaia, Epidemiol Unit, Galolatao, Spain; Uppsala Univ, Dept Med Sci Occupat & Environm Med, Uppsala, Sweden; Univ Verona, Dept Med & Publ Hlth, Unit Occupat Med, I-37100 Verona, Italy; Natl Inst Silicosis, Oviedo, Spain; Univ Pavia, Dept Hlth Sci, Sect Epidemiol & Med Stat, I-27100 Pavia, Italy; Univ Antwerp, Dept Epidemiol & Community Hlth, Antwerp, Belgium; Pompeu Fabra Univ, Barcelona, Spain	Kogevinas, M (reprint author), Municipal Inst Med Res, Ctr Res Environm Epidemiol, Barcelona 08003, Spain.	kogevinas@imim.es	; Kromhout, Hans/A-9159-2008; Jarvis, Deborah/E-6494-2011; Kunzli, Nino/F-7195-2014; Sanchez-Ramos, Jose Luis/G-1259-2011; Ciccone, Giovannino/K-3136-2016; Burgos, Felip/E-5734-2015; Kogevinas, Manolis/C-3918-2017; Sunyer, J/G-6909-2014	Mirabelli, Maria/0000-0002-3540-0085; ROMANO, Canzio/0000-0001-5294-9793; Kunzli, Nino/0000-0001-8360-080X; Sanchez-Ramos, Jose Luis/0000-0001-7187-9989; Ciccone, Giovannino/0000-0001-7644-9574; Burgos, Felip/0000-0002-4938-4581; Sunyer, J/0000-0002-2602-4110; Abramson, Michael/0000-0002-9954-0538; Basagana, Xavier/0000-0002-8457-1489; Corsico, Angelo Guido/0000-0002-8716-4694; Rolla, Giovanni/0000-0001-5997-7172; Dalmasso, Paola/0000-0001-6081-6966; /0000-0003-2517-6515	NCRR NIH HHS [2 S07RR05521-28]; NHLBI NIH HHS [1 R01 HL62633-01, R01 HL62633-01]; NIEHS NIH HHS [5P30 ES07048]		Ameille J, 2003, OCCUP ENVIRON MED, V60, P136, DOI 10.1136/oem.60.2.136; Balmes J, 2003, AM J RESP CRIT CARE, V167, P787, DOI 10.1164/rccm.167.5.787; Balmes JR, 2002, CLIN CHEST MED, V23, P727, DOI 10.1016/S0272-5231(02)00031-X; Bernstein DI, 2006, ASTHMA WORKPLACE; Blanc PD, 1999, AM J MED, V107, P580, DOI 10.1016/S0002-9343(99)00307-1; BROOKS SM, 1985, CHEST, V88, P376, DOI 10.1378/chest.88.3.376; CHANYEUNG M, 1995, NEW ENGL J MED, V333, P107, DOI 10.1056/NEJM199507133330207; CONTRERAS GR, 1994, OCCUP ENVIRON MED, V51, P710; Elder D, 2004, OCCUP MED-OXFORD, V54, P395, DOI 10.1093/occmed/kqh050; Garabrant DH, 2002, J ALLERGY CLIN IMMUN, V110, pS82, DOI 10.1067/mai.2002.124967; GREENLAND S, 1993, BIOMETRICS, V49, P865, DOI 10.2307/2532206; International Labour Organization, 1991, INT STAND CLASS OCC; Karjalainen A, 2000, AM J IND MED, V37, P451, DOI 10.1002/(SICI)1097-0274(200005)37:5<451::AID-AJIM1>3.0.CO;2-U; Kennedy SM, 2000, OCCUP ENVIRON MED, V57, P635, DOI 10.1136/oem.57.9.635; Kogevinas M, 1999, LANCET, V353, P1750, DOI 10.1016/S0140-6736(98)07397-8; Lemiere C, 1997, EUR RESPIR J, V10, P241, DOI 10.1183/09031936.97.10010241; McDonald JC, 2000, OCCUP ENVIRON MED, V57, P823, DOI 10.1136/oem.57.12.823; Medina-Ramon M, 2005, OCCUP ENVIRON MED, V62, P598, DOI 10.1136/oem.2004.017640; Orriols R, 2006, OCCUP ENVIRON MED, V63, P255, DOI 10.1136/oem.2005.022525; Pekkanen J, 2006, J CLIN EPIDEMIOL, V59, P281, DOI 10.1016/j.jclinepi.2005.07.013; Rosenman KD, 1997, J OCCUP ENVIRON MED, V39, P415, DOI 10.1097/00043764-199705000-00007; Rosenman KD, 2003, J OCCUP ENVIRON MED, V45, P556, DOI 10.1097/01.jom.0000058347.05741.f9; Toren K, 1996, OCCUP ENVIRON MED, V53, P757; VANDENPLAS O, 1995, AM J RESP CRIT CARE, V151, P54; Vandenplas O, 2005, REV MAL RESPIR, V22, P421, DOI 10.1019/200530010; Venables KM, 1997, LANCET, V349, P1465, DOI 10.1016/S0140-6736(96)07219-4; Zock JP, 2002, EUR RESPIR J, V20, P679, DOI 10.1183/09031936.02.00279702	27	201	201	2	29	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	JUL-AUG	2007	370	9584					336	341		10.1016/S0140-6736(07)61164-7		6	Medicine, General & Internal	General & Internal Medicine	195QG	WOS:000248426100031	17662882	
J	Jahnsen, FL; Lund-Johansen, F; Dunne, JF; Farkas, L; Haye, R; Brandtzaeg, P				Jahnsen, FL; Lund-Johansen, F; Dunne, JF; Farkas, L; Haye, R; Brandtzaeg, P			Experimentally induced recruitment of plasmacytoid (CD123(high)) dendritic cells in human nasal allergy	JOURNAL OF IMMUNOLOGY			English	Article							ENDOTHELIAL ADHESION MOLECULES; T-CELLS; LYMPH-NODE; HUMAN BLOOD; EXPRESSION; INTERFERON; MONOCYTES; ORIGIN; MXA; LYMPHADENITIS	Recent evidence suggests that the previously enigmatic cell type designated plasmacytoid monocytes can function as dendritic cells and contribute substantially to both innate and adaptive immunity. This cell type has previously been described only in bone marrow, blood, and organized lymphoid tissue, but not at effector sites with direct Ag exposure such as the mucosae, Plasmacytoid dendritic cells (P-DCs) matured in vitro can induce T cells to produce allergy-promoting Th2 cytokines; therefore, their possible occurrence in nasal mucosa during experimentally elicited allergic rhinitis was examined. Patients with silent nasal allergy were challenged topically with relevant allergen daily for 7 days. Biopsy specimens as well as blood samples were obtained before and during such provocation, and P-DCs were identified by their high expression of CD123 (IL3R alpha-chain), together with CD45RA, Our results showed that P-DCs were present in low and variable numbers in normal nasal mucosa but increased dramatically during the allergic reaction. This accumulation concurred with the expression of the L-selectin ligand peripheral lymph node addressin on the mucosal vascular endothelium. The latter observation was particularly interesting in view of the high levels of L-selectin on circulating P-DC precursors and of previous reports suggesting that these cells ran enter organized lymphoid tissue via high endothelial venules (which express peripheral lymph node addressin constitutively). Together, our findings suggested that P-DCs are involved in the triggering of airway allergy and that they are directed to allergic lesions by adhesion molecules that normally mediate leukocyte extravasation in organized lymphoid tissue.	Univ Oslo, Rikshosp, Inst Pathol, Lab Immunohistochem & Immunopathol, N-0027 Oslo, Norway; Univ Oslo, Rikshosp, Dept Ear Nose & Throat, N-0027 Oslo, Norway; Becton Dickinson Immunocytometry Syst, San Jose, CA 95131 USA	Brandtzaeg, P (reprint author), Univ Oslo, Rikshosp, Inst Pathol, Lab Immunohistochem & Immunopathol, N-0027 Oslo, Norway.						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Immunol.	OCT 1	2000	165	7					4062	4068				7	Immunology	Immunology	357AZ	WOS:000089477500066	11034417	
J	Karjalainen, EM; Laitinen, A; Sue-Chu, M; Altraja, A; Bjermer, L; Laitinen, LA				Karjalainen, EM; Laitinen, A; Sue-Chu, M; Altraja, A; Bjermer, L; Laitinen, LA			Evidence of airway inflammation and remodeling in ski athletes with and without bronchial hyperresponsiveness to methacholine	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							CROSS-COUNTRY SKIERS; INHALED HISTAMINE; ASTHMA; RESPONSIVENESS; LYMPHOCYTES; MACROPHAGES; EOSINOPHILS; PREVALENCE; SYMPTOMS; TENASCIN	Asthma-like symptoms, methacholine hyperresponsiveness, and use of asthma medication are prevalent in elite cross-country skiers. We quantitated mucosal inflammatory cell infiltration and tenascin expression in the subepithelial basement membrane in endobronchial biopsy specimens of the proximal airways from 40 elite, competitive skiers (mean: 17.5; range: 16 to 20 yr) without a diagnosis of asthma, in 12 subjects with mild asthma, and in 12 healthy controls, through immunohistochemistry and indirect immunofluorescence, respectively. All of the subjects were nonsmokers. T-lymphocyte, macrophage, and eosinophil counts were, respectively, greater by 43-fold (p < 0.001), 26-fold (p < 0.001), and twofold (p < 0.001) in skiers, and by 70-fold (p < 0.001), 63-fold (p < 0.001), and eightfold (p < 0.001) in asthmatic subjects than in controls. In skiers, neutrophil counts were more than twofold greater than in asthmatic subjects, and mast cell counts were not significantly different than in controls. Tenascin expression (as measured through the thickness of the tenascin-specific immunoreactivity band in the basement membrane) was increased in skiers (median: 6.7 mu m; interquartile range [IQR]: 5.3 to 8.5 mu m, p < 0.001) and asthmatic subjects (mean: 8.8 mu m; IQR: 7.2 to 10.8 mu m, p < 0.001) compared with controls (mean: 0.8 mu m; IQR: 0 to 3.1 mu m) and did not correlate with inflammatory cell counts. Inflammatory changes were present irrespective of asthmalike symptoms, hyperresponsiveness, or atopy. Prolonged repeated exposure of the airways to inadequately conditioned air may induce inflammation and remodeling in competitive skiers.	Univ Helsinki, Cent Hosp, Dept Med, FIN-00290 Helsinki, Finland; Univ Helsinki, Dept Anat, Inst Biomed, Helsinki, Finland; Univ Trondheim Hosp, Dept Lung Med, N-7006 Trondheim, Norway; Univ Tartu, Dept Pulm Med, EE-50090 Tartu, Estonia	Laitinen, LA (reprint author), Univ Helsinki, Cent Hosp, Dept Med, Haartmaninkatu 4, FIN-00290 Helsinki, Finland.						Altraja A, 1996, J ALLERGY CLIN IMMUN, V98, pS58, DOI 10.1016/S0091-6749(96)80130-8; AMIRAV I, 1989, AM REV RESPIR DIS, V140, P1416; BEASLEY R, 1989, AM REV RESPIR DIS, V139, P806; BENTLEY AM, 1992, AM REV RESPIR DIS, V146, P500; Blecker E.R., 1991, J ALLERGY CLIN IMMUN, V88, P808; BRADLEY BL, 1991, J ALLERGY CLIN IMMUN, V88, P661, DOI 10.1016/0091-6749(91)90160-P; COCKCROFT DW, 1977, CLIN ALLERGY, V7, P235, DOI 10.1111/j.1365-2222.1977.tb01448.x; EMPEY DW, 1976, AM REV RESPIR DIS, V113, P131; Heir T., 1994, Scandinavian Journal of Medicine and Science in Sports, V4, P128; Laitinen A, 1997, AM J RESP CRIT CARE, V156, P951; LAITINEN LA, 1993, AM REV RESPIR DIS, V147, P697; LARSSON K, 1993, BRIT MED J, V307, P1326; MACKIE EJ, 1988, J CELL BIOL, V107, P2757, DOI 10.1083/jcb.107.6.2757; MCFADDEN ER, 1985, J APPL PHYSIOL, V58, P564; OMORI C, 1995, J APPL PHYSIOL, V78, P1043; POWER C, 1993, THORAX, V48, P1125, DOI 10.1136/thx.48.11.1125; RAMSDALE EH, 1984, THORAX, V39, P912, DOI 10.1136/thx.39.12.912; Richmond I, 1996, AM J RESP CRIT CARE, V153, P899; Sue-Chu M, 1999, EUR RESPIR J, V13, P626, DOI 10.1183/09031936.99.13362699; Sue-Chu M, 1998, AM J RESP CRIT CARE, V158, P597; SueChu M, 1996, RESP MED, V90, P99, DOI 10.1016/S0954-6111(96)90206-1; TIKKANEN HO, 1994, BRIT MED J, V309, P1087	22	201	205	0	8	AMER LUNG ASSOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	JUN	2000	161	6					2086	2091				6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	325KV	WOS:000087675500054	10852791	
J	Sicherer, SH; Sampson, HA				Sicherer, Scott H.; Sampson, Hugh A.			Peanut allergy: Emerging concepts and approaches for an apparent epidemic	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						food allergy; food hypersensitivity; peanut allergy; food allergens; anaphylaxis; treatment	TREE NUT ALLERGY; CONTROLLED FOOD CHALLENGES; COWS MILK ALLERGY; SKIN PRICK TESTS; MURINE MODEL; DOUBLE-BLIND; IN-VITRO; ANAPHYLACTIC REACTIONS; IMMUNE-RESPONSE; ORAL TOLERANCE	Peanut allergy is typically lifelong, often severe, and potentially fatal. Because reactions can occur from small amounts, the allergy presents patients with significant obstacles to avoid allergic reactions. In North America and the United Kingdom, prevalence rates among schoolchildren are now in excess of 1%, framing an increasing public health concern and raising research questions about environmental, immunologic, and genetic factors that may influence outcomes of peanut allergy. This review focuses on recent observations that continue to question the influences of maternal and infant diet on outcomes of peanut allergy, and explore how peanut may be uniquely suited to induce an allergic response. We highlight studies that affect current diagnosis, management, and the nature of advice that can be provided to patients, including the utility of diagnostic tests. doses that elicit reactions, characteristics of reactions from exposure, issues of cross-reactivity, concerns about peanut contamination of manufactured goods, and the natural course of the allergy. Clinical, molecular, and immunologic advances are reviewed, highlighting research discoveries that influence strategies for improved diagnosis, prevention, and treatment. Among the therapeutic strategies reviewed are sublingual and oral immunotherapy, anti-IgE, Chinese herbal medicine, and vaccine strategies.	CUNY Mt Sinai Sch Med, Div Allergy Immunol, Dept Pediat, Elliot & Roslyn Jaffe Food Allergy Inst, New York, NY 10029 USA	Sicherer, SH (reprint author), CUNY Mt Sinai Sch Med, Div Allergy Immunol, Dept Pediat, Elliot & Roslyn Jaffe Food Allergy Inst, Box 1198,One Gustave L Levy Pl, New York, NY 10029 USA.	scott.sicherer@mssm.edu	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			AMOLD DM, 2007, ARCH INTERN MED, V167, P853; Arbes SJ, 2005, J ALLERGY CLIN IMMUN, V116, P377, DOI 10.1016/j.jaci.2005.05.017; Astier C, 2006, J ALLERGY CLIN IMMUN, V118, P250, DOI 10.1016/j.jaci.2006.04.053; AUDIBERT F, 1975, CR ACAD SCI D NAT, V280, P1629; Baker SS, 2000, PEDIATRICS, V106, P346; Bannon GA, 2001, INT ARCH ALLERGY IMM, V124, P70, DOI 10.1159/000053672; Bashir MEH, 2004, J IMMUNOL, V172, P6978; Beyer K, 2002, J ALLERGY CLIN IMMUN, V109, pS288, DOI 10.1016/S0091-6749(02)82015-2; Beyer K, 2003, J ALLERGY CLIN IMMUN, V112, P202, DOI 10.1067/mai.2003.1621; Beyer KB, 2001, J ALLERGY CLIN IMMUN, V107, P1077, DOI 10.1067/mai.2001.115480; 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Allergy Clin. Immunol.	SEP	2007	120	3					491	503		10.1016/j.jaci.2007.07.015		13	Allergy; Immunology	Allergy; Immunology	211DV	WOS:000249505400001	17689596	
J	Kharitonov, SA; Gonio, F; Kelly, C; Meah, S; Barnes, PJ				Kharitonov, SA; Gonio, F; Kelly, C; Meah, S; Barnes, PJ			Reproducibility of exhaled nitric oxide measurements in healthy and asthmatic adults and children	EUROPEAN RESPIRATORY JOURNAL			English	Article						asthma; exhaled nitric oxide; fractional exhaled nitric oxide measurements	SPUTUM INDUCTION; ATOPIC ASTHMA; FLOW; AIR	Airway inflammation in asthma is not measured routinely in clinical practice. Fractional exhaled nitric oxide (FENO), a marker of airway inflammation, is increasingly used as an outcome measure in asthma intervention studies and yet the reproducibility of FENO measurements is unknown. The reproducibility, day-to-day, diurnal variation and perception of standardised FENO measurements were examined in 59 subjects (40 children aged 7-13 yrs and 19 adults aged 18-60 yrs), both healthy (n=30) and with mild (n=29) asthma. FENO was measured on five consecutive days (four measurements on the same day) for adults and twice on the same day for children. The coefficient of reproducibility expressed as the mean pooled standard deviation (n=59, 675 estimations) was 2.11 parts per billion (ppb) and intraclass correlation coefficient was 0.99 in both children and adults. FENO was significantly higher in asthma subjects (32.3 ppb) than in healthy subjects (16.3 ppb). There was no diurnal or day-to-day variation, or a learning effect, as the result of FEND measurements were identical at results of the beginning and at the end of the study. It was concluded that fractional exhaled nitric oxide measurements are simple, reproducible, free from diurnal and day-to-day variation, and acceptable by both healthy and asthmatic adults and children, as a part of their routine visit to a physician.	Univ London Imperial Coll Sci Technol & Med, Royal Brompton & Harefield NHS Trust, Fac Med,Natl Heart & Lung Inst, Dept Thorac Med, London, England	Kharitonov, SA (reprint author), Univ London Imperial Coll Sci Technol & Med, Dept Thorac Med, Natl Heart & Lung Inst, Dovehouse St, London SW3 6LY, England.						Ames M H, 1996, J Biopharm Stat, V6, P177, DOI 10.1080/10543409608835131; den Otter JJ, 2000, FAM PRACT, V17, P314, DOI 10.1093/fampra/17.4.314; Fahy JV, 2001, AM J RESP CRIT CARE, V163, P1470; Faul JL, 1999, AM J RESP CRIT CARE, V160, P1457; Gannon PFG, 1999, EUR RESPIR J, V14, P28, DOI 10.1034/j.1399-3003.1999.14a07.x; Godfrey S, 2001, RESPIRATION, V68, P637, DOI 10.1159/000050589; Inman MD, 1998, J ALLERGY CLIN IMMUN, V101, P342; Jatakanon A, 2000, AM J RESP CRIT CARE, V161, P64; Jones SL, 2001, AM J RESP CRIT CARE, V164, P738; Kamps AWA, 2001, THORAX, V56, P180, DOI 10.1136/thorax.56.3.180; Kharitonov S, 1997, EUR RESPIR J, V10, P1683, DOI 10.1183/09031936.97.10071683; Kharitonov SA, 2001, AM J RESP CRIT CARE, V163, P1693; Kharitonov SA, 1996, AM J RESP CRIT CARE, V153, P1773; KHARITONOV SA, 1994, LANCET, V343, P133, DOI 10.1016/S0140-6736(94)90931-8; Kharitonov SA, 2002, THORAX, V57, P889, DOI 10.1136/thorax.57.10.889; Kharitonov SA, 2001, AM J RESP CRIT CARE, V164, P727; Kharitonov SA, 1996, AM J RESP CRIT CARE, V153, P454; Kharitonov SA, 1996, EUR RESPIR J, V9, P196, DOI 10.1183/09031936.96.09020196; KHARITONOV SA, 1999, EUR RESPIR J, V9, P212; Nightingale JA, 1998, THORAX, V53, P87; O'Neill ME, 2002, BIOMETRICS, V58, P216, DOI 10.1111/j.0006-341X.2002.00216.x; Omland O, 2001, RESP MED, V95, P287, DOI 10.1053/rmed.2001.1036; Philipp L., 2002, PEDIAT ALLERGY IMMUN, V13, P37, DOI 10.1034/j.1399-3038.2002.00066.x; Purokivi M, 2000, EUR RESPIR J, V16, P242, DOI 10.1034/j.1399-3003.2000.16b10.x; Ross R, 2001, THORAX, V56, P500; Salome CM, 1999, AM J RESP CRIT CARE, V159, P911; Silkoff PE, 2001, CHEST, V119, P1322, DOI 10.1378/chest.119.5.1322; Slutsky AS, 1999, AM J RESP CRIT CARE, V160, P2104; Upton MN, 2000, PUBLIC HEALTH, V114, P353, DOI 10.1038/sj.ph.1900683; van den Toorn LM, 2000, AM J RESP CRIT CARE, V162, P953	30	200	207	0	6	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	MAR	2003	21	3					433	438		10.1183/09031936.03.00066903		6	Respiratory System	Respiratory System	655XP	WOS:000181578200010	12661997	
J	Mishra, A; Hogan, SP; Brandt, EB; Rothenberg, ME				Mishra, A; Hogan, SP; Brandt, EB; Rothenberg, ME			IL-5 promotes eosinophil trafficking to the esophagus	JOURNAL OF IMMUNOLOGY			English	Article							GASTROESOPHAGEAL REFLUX; TISSUE EOSINOPHILIA; CHEMOKINE EOTAXIN; TRANSGENIC MICE; IN-VIVO; INTERLEUKIN-5; ACID; CHILDREN; DISEASE; CORTICOSTEROIDS	Eosinophil infiltration into the esophagus occurs in a wide range of diseases; however, the underlying pathophysiological mechanisms involved are largely unknown. We now report that the Th2 cytokine, IL-5, is necessary and sufficient for the induction of eosinophil trafficking to the esophagus. We show that transgenic mice overexpressing IL-5 under the control of a T cell (CD2) or a small intestinal enterocyte (fatty acid-binding protein) promoter have markedly increased eosinophil numbers in the esophagus. For example, esophageal eosinophil levels are 1.9 +/- 0.9 and 121 +/- 14 eosinophils/mm(2) in wild-type and CD2-IL-5-transgenic mice, respectively. Consistent with this effect being mediated by a systemic mechanism, pharmacological administration of IL-5 via a miniosmotic pump in the peritoneal cavity resulted in blood and esophageal eosinophilia. To examine the role of IL-5 in oral Ag-induced esophageal eosinophilia, eosinophilic esophagitis was induced by allergen exposure in IL-5-deficient and wild-type mice. Importantly, IL-5-deficient mice were resistant to eosinophilic esophagitis. Finally, we examined the role of eotaxin when IL-5 was overproduced in vivo. Esophageal eosinophil levels in CD2-IL-5-transgenic mice were found to decrease 15-fold in the absence of the cotaxin gene; however, esophageal eosinophil numbers in eotaxin-deficient IL-5-transgenic mice still remained higher than wild-type nice. In conclusion, these studies demonstrate a central role for IL-5 in inducing eosinophil trafficking to the esophagus.	Childrens Hosp, Med Ctr, Dept Pediat, Div Allergy & Immunol, Cincinnati, OH 45229 USA; Australian Natl Univ, John Curtin Sch Med Res, Div Biochem & Mol Biol, Canberra, ACT, Australia	Rothenberg, ME (reprint author), Childrens Hosp, Med Ctr, Dept Pediat, Div Allergy & Immunol, Cincinnati, OH 45229 USA.				NIAID NIH HHS [AI 42242-03, R01 AI 45898-02]		Bochner BS, 2001, IMMUNOL REV, V179, P5, DOI 10.1034/j.1600-065X.2001.790101.x; BROWN LF, 1984, AM J SURG PATHOL, V8, P899, DOI 10.1097/00000478-198412000-00002; COLLINS PD, 1995, J EXP MED, V182, P1169, DOI 10.1084/jem.182.4.1169; DENT LA, 1990, J EXP MED, V172, P1425, DOI 10.1084/jem.172.5.1425; DISCOMBE G, 1946, Lancet, V1, P195; Faubion WA, 1998, J PEDIATR GASTR NUTR, V27, P90, DOI 10.1097/00005176-199807000-00016; Furuta GT, 1998, J PEDIATR GASTR NUTR, V26, P468, DOI 10.1097/00005176-199804000-00021; FURUTA GT, 1995, CURR OPIN GASTROEN, V11, P541, DOI 10.1097/00001574-199511000-00013; HERMISTON ML, 1995, J CELL BIOL, V129, P489, DOI 10.1083/jcb.129.2.489; Hogan SP, 2000, P NATL ACAD SCI USA, V97, P6681, DOI 10.1073/pnas.97.12.6681; Hogan SP, 2001, NAT IMMUNOL, V2, P353, DOI 10.1038/86365; Kelly KJ, 2000, J PEDIATR GASTR NUTR, V30, pS28, DOI 10.1097/00005176-200001001-00005; KELLY KJ, 1995, GASTROENTEROLOGY, V109, P1503, DOI 10.1016/0016-5085(95)90637-1; LECKIE MJ, 1999, RESP CRIT CARE MED, V159, pA624; Liacouras CA, 1998, J PEDIATR GASTR NUTR, V26, P380, DOI 10.1097/00005176-199804000-00004; Lukacs NW, 1999, J CLIN INVEST, V104, P995, DOI 10.1172/JCI8125; Matthews AN, 1998, P NATL ACAD SCI USA, V95, P6273, DOI 10.1073/pnas.95.11.6273; Mishra A, 2001, J CLIN INVEST, V107, P83, DOI 10.1172/JCI10224; Mishra A, 2000, BLOOD, V96, P1538; Mishra A, 1999, J CLIN INVEST, V103, P1719, DOI 10.1172/JCI6560; MISHRA A, 2002, IN PRESS J BIOL CHEM; Mould AW, 1997, J CLIN INVEST, V99, P1064, DOI 10.1172/JCI119234; Nicholson AG, 1997, J PATHOL, V183, P233, DOI 10.1002/(SICI)1096-9896(199710)183:2<233::AID-PATH936>3.0.CO;2-Z; Nickel R, 1999, J ALLERGY CLIN IMMUN, V104, P723; Rothenberg ME, 1999, AM J RESP CELL MOL, V21, P291; Rothenberg ME, 1997, J EXP MED, V185, P785, DOI 10.1084/jem.185.4.785; Rothenberg ME, 2001, IMMUNOL REV, V179, P139, DOI 10.1034/j.1600-065X.2001.790114.x; Rothenberg ME, 1998, NEW ENGL J MED, V338, P1592; Ruchelli E, 1999, PEDIATR DEVEL PATHOL, V2, P15, DOI 10.1007/s100249900084; Sampson HA, 2000, J PEDIATR GASTR NUTR, V30, pS87, DOI 10.1097/00005176-200001001-00013; Sampson HA, 1999, J ALLERGY CLIN IMMUN, V103, P717, DOI 10.1016/S0091-6749(99)70411-2; SANDERSON CJ, 1992, BLOOD, V79, P3101; SWEETSER DA, 1988, P NATL ACAD SCI USA, V85, P9611, DOI 10.1073/pnas.85.24.9611; SWEETSER DA, 1987, J BIOL CHEM, V262, P16060; Walsh SV, 1999, AM J SURG PATHOL, V23, P390, DOI 10.1097/00000478-199904000-00003; WINTER HS, 1982, GASTROENTEROLOGY, V83, P818	36	199	203	1	4	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	MAR 1	2002	168	5					2464	2469				6	Immunology	Immunology	524AR	WOS:000173990200049	11859139	
J	Tulic, MK; Wale, JL; Holt, PG; Sly, PD				Tulic, MK; Wale, JL; Holt, PG; Sly, PD			Modification of the inflammatory response to allergen challenge after exposure to bacterial lipopolysaccharide	AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY			English	Article							INDUCED BRONCHIAL HYPERRESPONSIVENESS; BROWN-NORWAY RATS; AIRWAY HYPERRESPONSIVENESS; HUMAN-LYMPHOCYTES; VIRAL-INFECTIONS; NITRIC-OXIDE; ASTHMA; ENDOTOXIN; IGE; CHILDHOOD	The potential role of respiratory infections in altering the development of atopy and asthma is complex. Infections have been suggested to be effective in preventing the induction of T-helper 2-polarized allergen-specific immunity in early life, but also to exacerbate asthma in older, sensitized individuals. The mechanism(s) underlying these effects are poorly defined. The aim of this work was to determine the influence of lipopolysaccharide (LPS) exposure on the development of sensitization to allergen and the response to allergen challenge in vivo. Piebald-Virol-Glaxo rats were exposed to a single aerosol of LPS 1 d before or 1, 2, 4, 6, 8, or 10 d after sensitization with ovalbumin (OVA). On Day 11 animals were exposed to 1% OVA and responses to allergen were measured 24 h later, monitoring inflammatory cell influx and microvascular leakage into bronchoalveolar lavage (BAL) fluid as well as pulmonary responses to methacholine using the forced oscillation technique. Histologic analysis was included to complement the BAL results. Single aerosol exposure to LPS 1 d before and up to 4 d after intraperitoneal injection of OVA protected against the development of OVA-specific immunoglobulin tig) E. LPS exposure 6, 8, or 10 d after sensitization further exacerbated the OVA-induced cellular influx, resulting in neutrophilia and increased Evans Blue dye leakage with no effect on serum IgE levels. In addition, LPS abolished the OVA-induced hyperresponsiveness in sensitized animals when given 18 h after OVA challenge. This study demonstrates that exposure to LPS can modify the development of allergic inflammation in vivo by two independent mechanisms. Exposure early in the sensitization process, up to Day 6 after exposure to allergen, prevented allergen sensitization. Exposure to LPS after allergen challenge in sensitized animals abolished the hyperresponsiveness and modified the inflammatory cell influx characteristic of late-phase response to allergen.	TVW Telethon Inst Child Hlth Res, Div Clin Sci, W Perth, WA 6872, Australia; Univ Western Australia, Dept Paediat, Perth, WA 6009, Australia	Tulic, MK (reprint author), TVW Telethon Inst Child Hlth Res, Div Clin Sci, POB 855, W Perth, WA 6872, Australia.		Sly, Peter/F-1486-2010; Holt, Patrick/H-1548-2011; Tulic, Meri/P-6613-2016	Sly, Peter/0000-0001-6305-2201; Holt, Patrick/0000-0003-1193-0935; 			ANDERSSON D, 1998, AM J RESP CRIT CARE, V175, pA823; Baldini M, 1999, AM J RESP CELL MOL, V20, P976; BANCHEREAU J, 1994, ANNU REV IMMUNOL, V12, P881, DOI 10.1146/annurev.immunol.12.1.881; BARNES PJ, 1995, IMMUNOL TODAY, V16, P128, DOI 10.1016/0167-5699(95)80128-6; BENTLEY AM, 1992, AM REV RESPIR DIS, V146, P500; BJORKSTEN B, 1994, ALLERGY, V49, P400, DOI 10.1111/j.1398-9995.1994.tb00831.x; Bjorksten B, 1996, Eur Respir J Suppl, V21, p22s; Bjornsson E, 1996, SCAND J INFECT DIS, V28, P63, DOI 10.3109/00365549609027152; Borish L, 1997, J ALLERGY CLIN IMMUN, V99, P161, DOI 10.1016/S0091-6749(97)70090-3; BUSSE WW, 1994, AM J RESP CRIT CARE, V150, pS77; BUSSE WW, 1989, CLIN EXP ALLERGY, V19, P1, DOI 10.1111/j.1365-2222.1989.tb02336.x; DJUKANOVIC R, 1990, AM REV RESPIR DIS, V142, P434; ELWOOD W, 1992, INT ARCH ALLERGY IMM, V99, P91; ELWOOD W, 1991, J ALLERGY CLIN IMMUN, V88, P951, DOI 10.1016/0091-6749(91)90253-K; EVANS TW, 1988, AM REV RESPIR DIS, V138, P140; HANTOS Z, 1992, J APPL PHYSIOL, V73, P427; Holt PG, 1997, CURR OPIN IMMUNOL, V9, P782, DOI 10.1016/S0952-7915(97)80178-1; Holt PG, 1997, PEDIATR ALLERGY IMMU, V8, P53, DOI 10.1111/j.1399-3038.1997.tb00145.x; HOLT PG, 1995, PEDIATR ALLERGY IMMU, V6, P1, DOI 10.1111/j.1399-3038.1995.tb00250.x; HUNT LW, 1994, AM J RESP CRIT CARE, V149, P1471; JOHNSSON P, 1995, J CARDIOTHOR VASC AN, V9, P1; KATO H, 1997, AM J RESP CRIT CARE, V156, P234; KAY AB, 1991, RESP MED, V85, P87, DOI 10.1016/S0954-6111(06)80283-0; KOBAYASHI M, 1989, J EXP MED, V170, P827, DOI 10.1084/jem.170.3.827; LARSEN GL, 1991, AM REV RESPIR DIS, V143, pS64; MARTINEZ FD, 1994, THORAX, V49, P1189, DOI 10.1136/thx.49.12.1189; MICHEL O, 1992, AM REV RESPIR DIS, V146, P352; MORRIS SC, 1994, J IMMUNOL, V152, P1047; MOSMANN TR, 1989, ANNU REV IMMUNOL, V7, P145, DOI 10.1146/annurev.immunol.7.1.145; PAUWELS RA, 1990, AM REV RESPIR DIS, V141, P540; Peat JK, 1996, EUR RESPIR J, V9, P1545, DOI 10.1183/09031936.96.09071545; PENE J, 1988, P NATL ACAD SCI USA, V85, P6880, DOI 10.1073/pnas.85.18.6880; Petak F, 1997, J APPL PHYSIOL, V82, P1479; Rylander R, 1998, MEDIAT INFLAMM, V7, P105; Schuiling M, 1998, BRIT J PHARMACOL, V123, P1450, DOI 10.1038/sj.bjp.0701738; Schwarze J, 1998, J ALLERGY CLIN IMMUN, V102, P86, DOI 10.1016/S0091-6749(98)70058-2; SEDGWICK JD, 1983, IMMUNOLOGY, V50, P625; Strachan D, 1996, TOXICOL LETT, V86, P199, DOI 10.1016/0378-4274(96)03691-0; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Sunyer J, 1996, EUR RESPIR J, V9, P1880, DOI 10.1183/09031936.96.09091880; vanHalteren AGS, 1997, J ALLERGY CLIN IMMUN, V99, P94; Verhasselt V, 1997, J IMMUNOL, V158, P2919; VONMUTIUS E, 1994, AM J RESP CRIT CARE, V149, P365; WILLIESJACOBO LJ, 1993, J ALLERGY CLIN IMMUN, V92, P630, DOI 10.1016/0091-6749(93)90090-3; YANO T, 1994, AM J RESP CRIT CARE, V149, P1348	45	199	204	0	4	AMER LUNG ASSOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019 USA	1044-1549			AM J RESP CELL MOL	Am. J. Respir. Cell Mol. Biol.	MAY	2000	22	5					604	612				9	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	Biochemistry & Molecular Biology; Cell Biology; Respiratory System	313EC	WOS:000086986500015	10783133	
J	Riedl, M; Diaz-Sanchez, D				Riedl, M; Diaz-Sanchez, D			Biology of diesel exhaust effects on respiratory function	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						air pollution; diesel exhaust particles; allergy; asthma; oxidative stress; respiratory effects	BRONCHIAL EPITHELIAL-CELLS; GLUTATHIONE-S-TRANSFERASE; PARTICULATE AIR-POLLUTION; PLACEBO-CONTROLLED TRIAL; OXIDATIVE STRESS; IN-VIVO; BRONCHOALVEOLAR LAVAGE; ASTHMATIC-PATIENTS; CHILDHOOD ASTHMA; NASAL CHALLENGE	In recent decades, clinicians and scientists have witnessed a significant increase in the prevalence of allergic rhinitis and asthma. The factors underlying this phenomenon are clearly complex; however, this rapid increase in the burden or atopic disease has undeniably occurred in parallel with rapid industrialization and urbanization in many parts or the world. Consequently, more people are exposed to air pollutants than at any point in human history. Worldwide, increases in allergic respiratory disease have mainly been observed in urban communities. Epidemiologic and clinical investigations have suggested a strong link between particulate air pollution and detrimental health effects, including cardiopulmonary morbidity and mortality. The purpose of this review is to provide an evidence-based summary of the health effects of air pollutants on asthma, focusing on diesel exhaust particles (DEPs) as a model particulate air pollutant. An overview of observational and experimental studies linking DEPs and asthma will be provided, followed by consideration of the mechanisms underlying DEP-induced inflammation and a brief discussion of future research and clinical directions.	Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Clin Immunol Allergy,Hart & Louis Lyon Lab, Los Angeles, CA 90095 USA	Diaz-Sanchez, D (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Clin Immunol Allergy,Hart & Louis Lyon Lab, 52-175 Ctr Hlth Sci, Los Angeles, CA 90095 USA.	ddiazsa@mednet.ucla.edu			NIAID NIH HHS [AI-40945]		Alam R, 1996, AM J RESP CRIT CARE, V153, P1398; Allam MF, 2004, COCHRANE DB SYST REV, V2004; Arimoto T, 1999, JPN J PHARMACOL, V80, P49, DOI 10.1254/jjp.80.49; Baulig A, 2003, TOXICOL IN VITRO, V17, P567, DOI 10.1016/S0887-2333(03)00115-2; Bayram H, 1998, J ALLERGY CLIN IMMUN, V102, P771, DOI 10.1016/S0091-6749(98)70017-X; Bowler RP, 2002, J ALLERGY CLIN IMMUN, V110, P349, DOI 10.1067/mai.2002.126780; BRABACK L, 1994, CLIN EXP ALLERGY, V24, P826, DOI 10.1111/j.1365-2222.1994.tb01805.x; Brauer M, 2002, AM J RESP CRIT CARE, V166, P1092, DOI 10.1164/rccm.200108-007OC; BraunFahrlander C, 1997, AM J RESP CRIT CARE, V155, P1042; BURNETT RT, 1994, ENVIRON RES, V65, P172, DOI 10.1006/enrs.1994.1030; 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Allergy Clin. Immunol.	FEB	2005	115	2					221	228		10.1016/j.jaci.2004.11.047		8	Allergy; Immunology	Allergy; Immunology	897YU	WOS:000227043600002	15696072	
J	Johnson, JR; Wiley, RE; Fattouh, R; Swirski, FK; Gajewska, BU; Coyle, AJ; Gutierrez-Ramos, JC; Ellis, R; Inman, MD; Jordana, M				Johnson, JR; Wiley, RE; Fattouh, R; Swirski, FK; Gajewska, BU; Coyle, AJ; Gutierrez-Ramos, JC; Ellis, R; Inman, MD; Jordana, M			Continuous exposure to house dust mite elicits chronic airway inflammation and structural remodeling	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						allergy and immunology; animal; asthma; models	MURINE MODEL; ALLERGEN DER-P-1; LUNG INFLAMMATION; EPITHELIAL-CELLS; GM-CSF; ASTHMA; HYPERRESPONSIVENESS; RESPONSIVENESS; SENSITIZATION; EOSINOPHILIA	It is now fully appreciated that asthma is a disease of a chronic nature resulting from intermittent or continued aeroallergen exposure leading to airway inflammation. To investigate responses to continuous antigen exposure, mice were exposed to either house dust mite extract (HDM) or ovalbumin intranasally for five consecutive days, followed by 2 days of rest, for up to seven consecutive weeks. Continuous exposure to HDM, unlike ovalbumin, elicited severe and persistent eosinophilic airway inflammation. Flow cytometric analysis demonstrated an accumulation of CD4(+) lymphocytes in the lung with elevated expression of inducible costimulator a marker of T cell activation, and of T1/ST2, a marker of helper T Type 2 effector cells. We also detected increased and sustained production of helper T cell Type 2-associated cytokines by splenocytes of HDM-exposecl mice on in vitro HDM recall. Histologic analysis of the lung showed evidence of airway remodeling in mice exposed to HIDM, with goblet cell hyperplasia, collagen deposition, and peribronchial accumulation of contractile tissue. In addition, HDM-exposed mice demonstrated severe airway hyperreactivity to methacholine. Finally, these responses were studied for up to 9 weeks after cessation of HDM exposure. We observed that whereas airway inflammation resolved fully, the remodeling changes did not resolve and airway hyperreactivity resolved only partly.	McMaster Univ, Firestone Inst Resp Hlth, Dept Med, Hamilton, ON, Canada; Millennium Pharmaceut, Ctr Gene Therapeut, Div Resp Dis & Allergy, Cambridge, MA USA; Millennium Pharmaceut, Ctr Gene Therapeut, Dept Pathol & Mol Med, Cambridge, MA USA	Jordana, M (reprint author), McMaster Univ, Ctr Hlth Sci, Dept Pathol & Mol Med, Room 4H17,1200 Main St, Hamilton, ON L8N 3Z5, Canada.	jordanam@mcmaster.ca					Asokananthan N, 2002, J IMMUNOL, V169, P4572; Blyth DI, 1996, AM J RESP CELL MOL, V14, P425; Boulet LP, 2000, AM J RESP CRIT CARE, V162, P1308; Busse WW, 2001, NEW ENGL J MED, V344, P350; Cates E. C., 2003, Journal of Allergy and Clinical Immunology, V111, pS81, DOI 10.1016/S0091-6749(03)80205-1; Cates EC, 2003, J ALLERGY CLIN IMMUN, V111, P1076, DOI 10.1067/mai.2003.1460; Ewart SL, 1996, AM J RESP CELL MOL, V14, P487; Fahy JV, 2001, AM J RESP CRIT CARE, V164, pS46; Fernandez-Caldas Enrique, 2002, Curr Allergy Asthma Rep, V2, P424, DOI 10.1007/s11882-002-0077-z; Fish JE, 1999, J ALLERGY CLIN IMMUN, V104, P509, DOI 10.1016/S0091-6749(99)70315-5; Gough L, 2003, CLIN EXP ALLERGY, V33, P1159, DOI 10.1046/j.1365-2222.2003.01716.x; John RJ, 2000, CLIN EXP ALLERGY, V30, P784, DOI 10.1046/j.1365-2222.2000.00840.x; JOHNSON JR, 2003, AM J RESP CRIT CARE, V167, pA453; Knight DR, 2001, IMMUNOL CELL BIOL, V79, P160, DOI 10.1046/j.1440-1711.2001.00988.x; Laprise C, 1999, EUR RESPIR J, V14, P63, DOI 10.1034/j.1399-3003.1999.14a12.x; Leigh R, 2002, AM J RESP CELL MOL, V27, P526, DOI 10.1165/rcmb.2002-0048OC; Nahm DH, 2000, ANN ALLERG ASTHMA IM, V85, P129; Stampfli MR, 1998, J CLIN INVEST, V102, P1704, DOI 10.1172/JCI4160; Sun G, 2001, J IMMUNOL, V167, P1014; Swirski FK, 2002, J IMMUNOL, V169, P3499; Temelkovski J, 1998, THORAX, V53, P849; Trifilieff A, 2001, CLIN EXP ALLERGY, V31, P934, DOI 10.1046/j.1365-2222.2001.01084.x; Tsuyuki S, 1997, J EXP MED, V185, P1671, DOI 10.1084/jem.185.9.1671; Wan H, 2000, CLIN EXP ALLERGY, V30, P685, DOI 10.1046/j.1365-2222.2000.00820.x; Wan H, 2001, CLIN EXP ALLERGY, V31, P279, DOI 10.1046/j.1365-2222.2001.00970.x; Wiley RE, 2003, AM J RESP CELL MOL, V28, P722, DOI 10.1165/rcmb.2002-0220OC	26	198	212	0	8	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	FEB 1	2004	169	3					378	385		10.1164/rccm.200308-1094OC		8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	767BA	WOS:000188417800014	14597485	
J	Crystal-Peters, J; Neslusan, C; Crown, WH; Torres, A				Crystal-Peters, J; Neslusan, C; Crown, WH; Torres, A			Treating allergic rhinitis in patients with comorbid asthma: The risk of asthma-related hospitalizations and emergency department visits	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergic rhinitis; asthma; administrative claims analysis		Background: Although asthma and allergic rhinitis commonly occur together, the nature of the association has yet to be determined. Treatments for one condition could potentially alleviate the coexisting condition. Objective: Patients with both allergic rhinitis and asthma were studied to test the hypothesis that treating allergic rhinitis reduces health care utilization for co-morbid asthma. Methods: A retrospective cohort study was carried out with 1994-1995 MarketScan claims data. The cohort was limited to patients with both allergic rhinitis and asthma, aged 12 to 60 years, who were continuously enrolled and had no evidence of chronic obstructive pulmonary disease. Allergic rhinitis treatment and asthma-related events (hospitalizations and emergency department visits) were identified. An incidence density ratio (IDR) associated with exposure to allergic rhinitis treatment was calculated. A multivariate Poisson regression was estimated, and the parameter estimates were transformed into IDRs for each explanatory variable. An allergic rhinitis treatment indicator was included in all regressions. Results: The study sample population consisted of 4944 patients with allergic asthma, approximately 73% of whom were treated for their allergic rhinitis. Asthma-related events occurred more often for the untreated group compared with the treated group, 6.6 % compared with 1.3 %. An IDR of 0.49 for the treatment group (P =.001) indicates that the risk of an asthma-related event for the treated group was about half that for the untreated group. Conclusion: In summary, those who were treated for allergic rhinitis have a significantly lower risk of subsequent asthma-related events (emergency department visits or hospitalizations) than those who were not treated.	MEDSTAT Grp, Washington, DC 20008 USA	Crystal-Peters, J (reprint author), MEDSTAT Grp, 4401 Connecticut Ave NW,Suite 400, Washington, DC 20008 USA.						ALTEMEIER WA, 2001, PEDIATR ANN, V29, P398; ALTEMEIER WA, 2001, PEDIATR ANN, V29, P391; *AM AC ALL ASTHM I, FAST FACTS STAT ASTH; Busse WW, 1998, J ALLERGY CLIN IMMUN, V101, pS424, DOI 10.1016/S0091-6749(98)70236-2; Bykowsky M, 2000, J S C Med Assoc, V96, P229; Corren J, 1998, J ALLERGY CLIN IMMUN, V101, pS352, DOI 10.1016/S0091-6749(98)70218-0; Fireman P, 2000, ALLERGY ASTHMA PROC, V21, P45, DOI 10.2500/108854100778248935; GRANT JA, 1995, J ALLERGY CLIN IMMUN, V95, P923, DOI 10.1016/S0091-6749(95)70090-0; HALPERN M, 1996, AM J RESP CRIT CARE, V153, pA860; HECKMAN JJ, 1976, ANN ECON SOC MEAS, V5, P475; Hennekens C. H., 1987, EPIDEMIOLOGY MED; HENRIKSEN JM, 1984, AM REV RESPIR DIS, V130, P1014; Lemanske RF, 1998, J ALLERGY CLIN IMMUN, V101, pS392, DOI 10.1016/S0091-6749(98)70228-3; PEDERSEN PA, 1983, ALLERGY, V38, P25, DOI 10.1111/j.1398-9995.1983.tb00852.x; RoweJones JM, 1997, ALLERGY, V52, P20; Selvin S, 1996, STAT ANAL EPIDEMIOLO; Skoner DP, 2000, J ALLERGY CLIN IMMUN, V105, pS605; Sly RM, 1999, ANN ALLERG ASTHMA IM, V82, P233, DOI 10.1016/S1081-1206(10)62603-8; Stata Corp, 1997, STAT STAT SOFTW REL; WATSON WT, 1993, J ALLERGY CLIN IMM 1, V9, P97; WELSH PW, 1987, MAYO CLIN PROC, V62, P125	21	198	209	0	2	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JAN	2002	109	1					57	62		10.1067/mai.2002.120554		6	Allergy; Immunology	Allergy; Immunology	519RM	WOS:000173739300009	11799366	
J	Kauffman, HF; Tomee, JFC; van de Riet, MA; Timmerman, AJB; Borger, P				Kauffman, HF; Tomee, JFC; van de Riet, MA; Timmerman, AJB; Borger, P			Protease-dependent activation of epithelial cells by fungal allergens leads to morphologic changes and cytokine production	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						fungal; proteases; epithelial cells; cytokines; desquamation; protease-activated receptor; asthma; sensitization	VOLUMETRIC AEROBIOLOGICAL SURVEY; HOUSE-DUST MITE; MOLD ALLERGY; NORTHEAST NETHERLANDS; CONIDIAL FUNGI; ASPERGILLUS; ASTHMA; DETACHMENT; DIAGNOSIS; SENSITIZATION	Background: Proteases in extracts of Aspergillus fumigatus cause epithelial cell desquamation and release of proinflammatory cytokines. Objective: We sought to assess protease activity in Alternaria alternata, Cladosporium herbarum, and Aspergillus fumigatus extracts and study the ability of these extracts to cause desquamation and release of proinflammatory cytokines from epithelial cells. Methods: Protease activities of the fungal extracts were quantified, Changes with respect to cell morphology, cell desquamation, and cytokine production (IL-6 and IL-8) were measured in the absence and presence of the fungal extracts in an airway-derived epithelial cell line (A549) and primary epithelial nasal cells. Results: Fungal proteases differentially induced morphologic changes, cell desquamation, and production of IL-6 and IL-8 in a dose- and time-dependent fashion. Alternaria alternata extracts induced cell shrinking and cell desquamation and strongly enhanced the production of IL-6 and IL-8 at higher concentrations. Aspergillus fumigatus extracts caused cell shrinking, cell desquamation, and production of IL-6 and IL-8, even at low concentrations. The Aspergillus fumigatus-derived extract groan on collagen medium induced a strong dose-dependent decline in cytokine production at higher concentrations. Cladosporium herbarum extracts did not induce morphologic changes or cell desquamation but enhanced IL-6 and IL-8 productions at higher concentrations. The dependence of these effects on intact protease activity was shown by their abrogation by protease inhibitors. Conclusion: Proteases present in fungal extracts interact with epithelial cells, leading to morphologic changes, cell desquamation, and induction of proinflammatory cytokines. It is proposed that these fungal proteases may activate epithelial cells through a protease-activated receptor type 2-driven mechanism.	Univ Groningen Hosp, Clin Internal Med, Lab Allergol & Pulmonol, NL-9700 RB Groningen, Netherlands	Kauffman, HF (reprint author), Univ Groningen Hosp, Clin Internal Med, Lab Allergol & Pulmonol, POB 30-001, NL-9700 RB Groningen, Netherlands.						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Allergy Clin. Immunol.	JUN	2000	105	6	1				1185	1193		10.1067/mai.2000.106210		9	Allergy; Immunology	Allergy; Immunology	327EX	WOS:000087781800021	10856154	
J	Shi, HZ; Humbles, A; Gerard, C; Jin, Z; Weller, PF				Shi, HZ; Humbles, A; Gerard, C; Jin, Z; Weller, PF			Lymph node trafficking and antigen presentation by endobronchial eosinophils	JOURNAL OF CLINICAL INVESTIGATION			English	Article							INTERCELLULAR-ADHESION MOLECULE-1; T-CELL CLONES; HLA-DR; DENDRITIC CELLS; ALVEOLAR MACROPHAGES; PRESENTING CELL; INDUCED SPUTUM; EXPRESSION; ASTHMA; LUNG	Because eosinophils recruited into the airways in allergic diseases are exposed to inhaled allergens, we evaluated whether eosinophils within the endobronchial lumen can function in vivo as antigen-presenting cells for inhaled antigens. We recovered eosinophils from the airways after aerosol antigen challenge in sensitized mice or from the peritoneal cavities of IL-5 transgenic mice and fluorescently labeled these cells ex vivo. These labeled cells, instilled intratracheally into normal mice, migrated into draining paratracheal lymph nodes and localized to T cell-rich paracortical areas. The homing of airway eosinophils to lymph nodes was not governed by eotaxin, because CCR3(-/-) and CCR3(+/+) eosinophils migrated identically. Airway eosinophils, recovered after inhalational antigen challenge in sensitized mice, expressed MHC class II and costimulatory CD80 and CD86 proteins and functioned in vitro as CD80- and CD86-dependent, antigen-specific, antigen-presenting cells. Moreover, when instilled into the airways of antigen-sensitized recipient mice, airway eosinophils recovered after inhalational antigen challenge stimulated antigen-specific CD4(+) T cell proliferation within paratracheal lymph nodes. Thus, eosinophils within the lumina of airways can process inhaled antigens, traffic to regional lymph nodes, and function in vivo as antigen-presenting cells to stimulate responses of CD4(+) T cells.	Harvard Univ, Sch Med,Charles A Dana Res Inst, Beth Israel Deaconess Med Ctr,Dept Med, Harvard Thorndike Labs, Boston, MA 02215 USA; Harvard Univ, Childrens Hosp, Sch Med,Med Ctr, Ina Sue Perlmutter Labs,Dept Pediat, Boston, MA 02115 USA	Weller, PF (reprint author), Harvard Univ, Sch Med,Charles A Dana Res Inst, Beth Israel Deaconess Med Ctr,Dept Med, Harvard Thorndike Labs, DA-617,330 Brookline Ave, Boston, MA 02215 USA.				NHLBI NIH HHS [HL46563]; NIAID NIH HHS [R01 AI022571, AI20241, AI22571, R01 AI020241, R37 AI020241]		BENTLEY AM, 1993, AM J RESP CELL MOL, V8, P35; CHELEN CJ, 1995, J CLIN INVEST, V95, P1415, DOI 10.1172/JCI117796; CROWLEY M, 1990, J EXP MED, V172, P383, DOI 10.1084/jem.172.1.383; DELPOZO V, 1992, EUR J IMMUNOL, V22, P1919; Foresi A, 1997, J ALLERGY CLIN IMMUN, V100, P58; Foster PS, 1996, J EXP MED, V183, P195, DOI 10.1084/jem.183.1.195; GOSSELIN EJ, 1992, J IMMUNOL, V149, P3477; HANSEL TT, 1992, J IMMUNOL, V149, P2130; HANSEL TT, 1991, CLIN EXP IMMUNOL, V86, P271; HARMSEN AG, 1985, SCIENCE, V230, P1277, DOI 10.1126/science.4071052; HAVENITH CEG, 1993, AM J RESP CELL MOL, V9, P484; HOLT PG, 1993, J EXP MED, V177, P397, DOI 10.1084/jem.177.2.397; IWAMOTO I, 1993, J EXP MED, V177, P573, DOI 10.1084/jem.177.2.573; Laberge S, 1997, AM J RESP CELL MOL, V17, P193; LACY P, 1997, MEM I OSWALDO CRUZ S, V92, pH125; LUCEY DR, 1989, P NATL ACAD SCI USA, V86, P1348, DOI 10.1073/pnas.86.4.1348; MacLean JA, 1996, AM J PATHOL, V148, P657; MAURER D, 1995, J IMMUNOL, V154, P6285; MAWHORTER SD, 1994, IMMUNOLOGY, V81, P584; McAdam AJ, 1998, IMMUNOL REV, V165, P231; MENGELERS HJ, 1994, AM J RESP CRIT CARE, V149, P345; Ohkawara Y, 1996, J CLIN INVEST, V97, P1761, DOI 10.1172/JCI118603; Persson CGA, 1997, LANCET, V350, P1021, DOI 10.1016/S0140-6736(96)02335-5; PIN I, 1992, AM REV RESPIR DIS, V145, P1265; PLATTSMILLS TAE, 1992, AM REV RESPIR DIS, V145, pS44; RESNICK MB, 1995, GASTROENTEROLOGY, V108, P409, DOI 10.1016/0016-5085(95)90067-5; Rothenberg ME, 1999, AM J RESP CELL MOL, V21, P291; RYTOMAA T, 1960, Acta Pathol Microbiol Scand Suppl, V50(Suppl 140), P1; SEDGWICK JB, 1992, J IMMUNOL, V149, P3710; SEMINARIO MC, 1994, CURR OPIN IMMUNOL, V6, P860, DOI 10.1016/0952-7915(94)90005-1; STELLATO C, 1995, J IMMUNOL, V155, P410; Taguchi M, 1998, J EXP MED, V187, P1927, DOI 10.1084/jem.187.12.1927; Tamura N, 1996, SCAND J IMMUNOL, V44, P229, DOI 10.1046/j.1365-3083.1996.d01-303.x; TOMINAGA A, 1991, J EXP MED, V173, P429, DOI 10.1084/jem.173.2.429; van Rooijen N, 1992, Semin Immunol, V4, P237; VANROOIJEN N, 1990, IMMUNOL TODAY, V11, P436, DOI 10.1016/0167-5699(90)90171-5; WELLER PF, 1993, J IMMUNOL, V150, P2554; WELLER PF, 1991, NEW ENGL J MED, V324, P1110; Woerly G, 1999, J EXP MED, V190, P487, DOI 10.1084/jem.190.4.487; WYSSCORAY T, 1993, EUR J IMMUNOL, V23, P3350, DOI 10.1002/eji.1830231243; XIA WJ, 1995, J EXP MED, V181, P1275, DOI 10.1084/jem.181.4.1275	41	198	204	3	4	AMER SOC CLINICAL INVESTIGATION INC	ANN ARBOR	ROOM 4570 KRESGE I, 200 ZINA PITCHER PLACE, ANN ARBOR, MI 48109-0560 USA	0021-9738			J CLIN INVEST	J. Clin. Invest.	APR	2000	105	7					945	953		10.1172/JCI8945		9	Medicine, Research & Experimental	Research & Experimental Medicine	300XW	WOS:000086279900016	10749574	
J	Brandt, EB; Strait, RT; Hershko, D; Wang, Q; Muntel, EE; Scribner, TA; Zimmermann, N; Finkelman, FD; Rothenberg, ME				Brandt, EB; Strait, RT; Hershko, D; Wang, Q; Muntel, EE; Scribner, TA; Zimmermann, N; Finkelman, FD; Rothenberg, ME			Mast cells are required for experimental oral allergen-induced diarrhea	JOURNAL OF CLINICAL INVESTIGATION			English	Article							IMMUNOGLOBULIN-E RECEPTOR; FC-GAMMA RIII; SYSTEMIC-ANAPHYLAXIS; TRICHINELLA-SPIRALIS; TRYPTASE LEVELS; T-CELL; INFLAMMATION; IGE; HISTAMINE; MICE	Gastrointestinal allergic disorders represent a diverse spectrum of inflammatory diseases that are occurring with increasing incidence and severity. An essential question concerning these disorders is to determine the specific cells and mediators responsible for specific clinical manifestations. With this in mind, we developed a murine model of oral allergen-induced intestinal inflammation accompanied by strong Th2-associated humoral and cellular responses and focused on the immunopathogenesis of allergic diarrhea. Exposure of OVA/alum-sensitized mice to repeated doses of intragastric OVA induced genetically restricted, dose-dependent, acute diarrhea associated with increased intestinal permeability, eosinophilia, and mastocytosis. Mice developed limited systemic manifestations of anaphylaxis, even though they developed marked intestinal mucosal mast cell degranulation. Notably, experiments involving mast cell depletion (with anti-c-kit mAb), anti-IgE treatment, and FcepsilonRI-deficient mice indicated a critical effector role for mast cells in mediating allergic diarrhea. Furthermore, allergic diarrhea was dependent upon synergistic signaling induced by serotonin and platelet-activating factor (PAF), but not histamine. These results demonstrate that oral allergen-induced diarrhea associated with experimental Th2 intestinal inflammation is largely mast cell, IgE, serotonin, and PAF dependent.	Cincinnati Childrens Hosp, Dept Pediat, Div Allergy & Immunol, Med Ctr, Cincinnati, OH 45229 USA; Cincinnati Childrens Hosp, Dept Pediat, Div Emergency Med, Med Ctr, Cincinnati, OH 45229 USA; Shriners Hosp Children, Cincinnati, OH USA; Univ Cincinnati, Dept Surg, Cincinnati, OH 45267 USA; Univ Cincinnati, Dept Internal Med, Div Immunol, Cincinnati, OH USA; Vet Adm Med Ctr, Cincinnati, OH 45220 USA	Rothenberg, ME (reprint author), Cincinnati Childrens Hosp, Dept Pediat, Div Allergy & Immunol, Med Ctr, 3333 Burnet Ave, Cincinnati, OH 45229 USA.				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Clin. Invest.	DEC	2003	112	11					1666	1677		10.1172/JCI19785		12	Medicine, Research & Experimental	Research & Experimental Medicine	751VY	WOS:000187111800011	14660743	
J	Beggs, PJ				Beggs, PJ			Impacts of climate change on aeroallergens: past and future	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review						allergen; carbon dioxide; climate change; distribution; mould; plant; pollen; season; spore; temperature	RAGWEED AMBROSIA-ARTEMISIIFOLIA; OUTDOOR AIR-POLLUTION; BIRCH POLLEN SEASONS; PUBLIC-HEALTH; RESPIRATORY ALLERGY; AIRBORNE POLLEN; CO2 ENRICHMENT; COMMON RAGWEED; WEATHER; EUROPE	Human activities are resulting in increases in atmospheric greenhouse gases, such as carbon dioxide, and changes in global climate. These, in turn, are likely to have had, and will continue to have, impacts on human health. While such impacts have received increasing attention in recent years, the impacts of climate change on aeroallergens and related allergic diseases have been somewhat neglected. Despite this, a number of studies have revealed potential impacts of climate change on aeroallergens that may have enormous clinical and public health significance. The purpose of this review is to synthesize this work and to outline a number of research challenges in this area. There is now considerable evidence to suggest that climate change will have, and has already had, impacts on aeroallergens. These include impacts on pollen amount, pollen allergenicity, pollen season, plant and pollen distribution, and other plant attributes. There is also some evidence of impacts on other aeroallergens, such as mould spores. There are many research challenges along the road to a more complete understanding of the impacts of climate change on aeroallergens and allergic diseases such as asthma and hayfever. It is important that public health authorities and allergy practitioners be aware of these changes in the environment, and that research scientists embrace the challenges that face further work in this area.	Macquarie Univ, Dept Phys Geog, Div Environm & Life Sci, N Ryde, NSW 2109, Australia	Beggs, PJ (reprint author), Macquarie Univ, Dept Phys Geog, Div Environm & Life Sci, N Ryde, NSW 2109, Australia.	paul.beggs@mq.edu.au	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Ahlholm JU, 1998, CLIN EXP ALLERGY, V28, P1384; ALEXANDER JB, 1991, MED VET ENTOMOL, V5, P395, DOI 10.1111/j.1365-2915.1991.tb00567.x; BEGGS P, 1997, ADV ENV CONTROL TECH, P329, DOI 10.1016/B978-088415386-3/50016-3; Behrendt H, 1997, INT ARCH ALLERGY IMM, V113, P69; Bernard SM, 2001, ENVIRON HEALTH PERSP, V109, P199, DOI 10.2307/3435010; Buckland SM, 2001, J APPL ECOL, V38, P301, DOI 10.1046/j.1365-2664.2001.00603.x; Bunyavanich S, 2003, AMBUL PEDIATR, V3, P44, DOI 10.1367/1539-4409(2003)003<0044:TIOCCO>2.0.CO;2; Burch M, 2002, INT J BIOMETEOROL, V46, P107, DOI 10.1007/s00484-002-0127-1; Corden JM, 2001, AEROBIOLOGIA, V17, P127, DOI 10.1023/A:1010876917512; Cubasch U, 2001, CLIMATE CHANGE 2001, P525; D'Amato G, 2002, EUR RESPIR J, V20, P763, DOI 10.1183/09031936.02.00401402; D'Amato G, 2000, J INVEST ALLERG CLIN, V10, P123; D'Amato G, 2000, CLIN EXP ALLERGY, V30, P628; Devalia JL, 1998, ALLERGY, V53, P335, DOI 10.1111/j.1398-9995.1998.tb03903.x; Emberlin J, 2002, INT J BIOMETEOROL, V46, P159, DOI 10.1007/s00484-002-0139-x; Emberlin J, 1997, GRANA, V36, P29; EMBERLIN J, 1994, ALLERGY, V49, P15, DOI 10.1111/j.1398-9995.1994.tb04233.x; Emberlin J, 2003, INT J BIOMETEOROL, V47, P113, DOI 10.1007/s00484-002-0154-y; Folland C K, 2001, CLIMATE CHANGE 2001, P99; Frei T, 1998, GRANA, V37, P172; Frenguelli G, 2002, Monaldi Arch Chest Dis, V57, P141; Harvell CD, 2002, SCIENCE, V296, P2158, DOI 10.1126/science.1063699; HASHIMOTO M, 1990, CLIMATE CHANGE IPCC; HJELMROOS M, 1993, GRANA, V32, P40; HJELMROOS M, 1995, INT ARCH ALLERGY IMM, V108, P368; Huynen M, 2003, WHO M ROM IT 16 17 J; Katial RK, 1997, INT J BIOMETEOROL, V41, P17, DOI 10.1007/s004840050048; Keeling CD, 2004, ATMOSPHERIC CARBON D; Klus DJ, 2001, AM J BOT, V88, P1080, DOI 10.2307/2657091; Koenig JQ, 1999, J ALLERGY CLIN IMMUN, V104, P717; LAST J, 1990, Public Health Reviews, V18, P49; LAST JM, 1993, ANNU REV PUBL HEALTH, V14, P115; Levetin E, 2001, J ALLERGY CLIN IMMUN, V107, pS172; Lindroth RL, 2001, ENVIRON POLLUT, V115, P395, DOI 10.1016/S0269-7491(01)00229-9; McCarthy J.J., 2001, CLIMATE CHANGE 2001; McMichael AJ, 2001, CLIMATE CHANGE 2001, P451; Mc Michael AJ, 2003, CLIMATE CHANGE HUMAN; McMichael A. 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Exp. Allergy	OCT	2004	34	10					1507	1513		10.1111/j.1365-2222.2004.02061.x		7	Allergy; Immunology	Allergy; Immunology	861RB	WOS:000224434800002	15479264	
J	Neugut, AI; Ghatak, AT; Miller, RL				Neugut, AI; Ghatak, AT; Miller, RL			Anaphylaxis in the United States - An investigation into its epidemiology	ARCHIVES OF INTERNAL MEDICINE			English	Review							CONTRAST-MEDIA; ADVERSE REACTIONS; LATEX ALLERGY; PREVALENCE; RISK; HYPERSENSITIVITY; WORKERS; RUBBER; PEANUT; DRUGS	Background: Anaphylaxis is a severe, life-threatening allergic reaction that affects both children and adults in the United States. However, data regarding the incidence and prevalence of anaphylaxis and the number of deaths caused by it are limited. Objective: To provide a better understanding of the magnitude of the problem of anaphylaxis in the United States. Methods: A thorough review of the current medical literature was conducted to obtain prevalence estimates on each of the 4 major subtypes of anaphylaxis (food, drugs, latex, and insect stings). We calculated an overall estimate of the risk of anaphylaxis by using only estimates that are specifically derived from epidemiologic studies measuring anaphylaxis in the general population. Results: Known rates or cases of anaphylaxis were 0.0004% for food, 0.7% to 10% for penicillin, 0.22% to 1% for radiocontrast media, and 0.5% to 5% after insect stings. There were 220 cases after latex exposure. Considering the 1999 US population of 272 million, the population at risk for anaphylaxis from food is 1099, from penicillin is 1.9 million to 27.2 million, from radiocontrast media is 22 000 to 100 000, from latex is 220, and from insect stings is 1.36 million to 13.6 million. These calculations yield a total of 1.29 million to 40.9 million individuals at risk of anaphylaxis. Conclusion: The occurrence of anaphylaxis in the US is not as rare as is generally believed. On the basis of our figures, the problem of anaphylaxis may, in fact, affect 1.21% to 15.04% of the US population.	Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA; Columbia Univ Coll Phys & Surg, Joseph L Mailman Sch Publ Hlth, New York, NY 10032 USA; DEY Corp, Napa, CA USA	Neugut, AI (reprint author), Columbia Univ Coll Phys & Surg, Dept Med, 630 W 168th St,Room PH18-127, New York, NY 10032 USA.						ANDERSON JA, 1992, JAMA-J AM MED ASSOC, V268, P2845; ANSELL G, 1980, INVESTIGATIVE RADI S, V15, P32; ARELLANO R, 1992, ANESTHESIOLOGY, V77, P905, DOI 10.1097/00000542-199211000-00011; BOCHNER BS, 1991, NEW ENGL J MED, V324, P1785; BOCK SA, 1992, J ALLERGY CLIN IMMUN, V90, P683, DOI 10.1016/0091-6749(92)90143-P; *BOST COLL DRUG SU, 1973, JAMA-J AM MED ASSOC, V224, P613; BUSH WH, 1991, AM J ROENTGENOL, V157, P1153; BUSH WH, 1990, UROLOGY, V35, P145, DOI 10.1016/0090-4295(90)80064-T; Centers for Disease Control and Prevention, 1994, DHHS PUBL; Ewan PW, 1998, BRIT MED J, V316, P1442; GREENBERGER PA, 1991, J ALLERGY CLIN IMMUN, V87, P867, DOI 10.1016/0091-6749(91)90135-B; Hollingsworth H, 1997, JAMA-J AM MED ASSOC, V277, P1196; Kagy L, 1998, PEDIATR ANN, V27, P727; KATAYAMA H, 1990, RADIOLOGY, V175, P621; KELLY KJ, 1994, J ALLERGY CLIN IMMUN, V93, P813, DOI 10.1016/0091-6749(94)90370-0; KLEIN JS, 1995, J ALLERGY CLIN IMMUN, V95, P637, DOI 10.1016/S0091-6749(95)70329-2; LANG DM, 1991, ANN INTERN MED, V115, P270; LIEBERMAN P, 1992, IMMUNOL ALLERGY CLIN, V12, P649; Liss GM, 1997, OCCUP ENVIRON MED, V54, P335; MONERETVAUTRIN DA, 1993, J ALLERGY CLIN IMMUN, V77, P905; Ownby DR, 1996, J ALLERGY CLIN IMMUN, V97, P1188, DOI 10.1016/S0091-6749(96)70183-5; SAMPSON HA, 1990, J ALLERGY CLIN IMMUN, V86, P1, DOI 10.1016/S0091-6749(05)80115-0; SAMPSON HA, 1992, JAMA-J AM MED ASSOC, V268, P2840, DOI 10.1001/jama.268.20.2840; SHEHADI WH, 1975, AM J ROENTGENOL, V124, P145; Sicherer SH, 1999, J ALLERGY CLIN IMMUN, V103, P559, DOI 10.1016/S0091-6749(99)70224-1; STARK BJ, 1986, J ALLERGY CLIN IMMUN, V78, P76, DOI 10.1016/0091-6749(86)90117-X; SUE MA, 1988, AM J EMERG MED, V6, P456, DOI 10.1016/0735-6757(88)90245-8; Sullivan TJ., 1993, ALLERGY PRINCIPLES P, P1726; SUSSMAN GL, 1995, ANN INTERN MED, V122, P43; TOOGOOD JH, 1988, J ALLERGY CLIN IMMUN, V81, P1, DOI 10.1016/0091-6749(88)90212-6; VALENTINE M, 1979, ASTHMA OTHER ALLERGI, P467; Valentine M D, 1992, JAMA, V268, P2830; Watts DN, 1998, AM J IND MED, V34, P359, DOI 10.1002/(SICI)1097-0274(199810)34:4<359::AID-AJIM9>3.0.CO;2-N; WEISS ME, 1988, CLIN ALLERGY, V18, P515, DOI 10.1111/j.1365-2222.1988.tb02904.x; World Health Organization, 1977, INT CLASS DIS; Wyatt R, 1996, POSTGRAD MED, V100, P87; Yocum MW, 1999, J ALLERGY CLIN IMMUN, V104, P452, DOI 10.1016/S0091-6749(99)70392-1; 1998, J ALLERGY CLIN IMM S, V101, pS465	38	196	202	2	7	AMER MEDICAL ASSOC	CHICAGO	515 N STATE ST, CHICAGO, IL 60610 USA	0003-9926			ARCH INTERN MED	Arch. Intern. Med.	JAN 8	2001	161	1					15	21		10.1001/archinte.161.1.15		7	Medicine, General & Internal	General & Internal Medicine	387LN	WOS:000166124200001	11146694	
J	Bashir, MEH; Louie, S; Shi, HN; Nagler-Anderson, C				Bashir, MEH; Louie, S; Shi, HN; Nagler-Anderson, C			Toll-like receptor 4 signaling by intestinal microbes influences susceptibility to food allergy	JOURNAL OF IMMUNOLOGY			English	Article							MAJOR PEANUT ALLERGEN; ENDOTOXIN EXPOSURE; BALB/C MICE; CD14 GENE; HAY-FEVER; 1ST YEAR; CPG DNA; ASTHMA; RESPONSES; SENSITIZATION	The mechanisms by which signaling by the innate immune system controls susceptibility to allergy are poorly understood. In this report, we show that intragastric administration of a food allergen with a mucosal adjuvant induces allergen-specific IgE, elevated plasma histamine levels, and anaphylactic symptoms in three different strains of mice lacking a functional receptor for bacterial LPS (Toll-like receptor 4 (TLR4)), but not in MHC-matched or congenic controls. Susceptibility to allergy correlates with a Th2-biased cytokine response in both the mucosal (mesenteric lymph node and Peyer's patch) and systemic (spleen) tissues of TLR4-mutant or -deficient mice. TLR4-mutant mice are not inherently impaired in their ability to regulate Th1 cytokine production because they respond to stimulation via TLR9. Coadministration of CpG oligodeoxynucleotides during sensitization of TLR4-mutant mice with allergen plus CT abrogates anaphylactic symptoms and Ag-specific IgE, and results in a Th1-polarized cytokine response. When the composition of the bacterial flora is reduced and altered by antibiotic administration (beginning at 2 wk of age), TLR4 wild-type mice become as susceptible to the induction of allergy as their TLR4-mutant counterparts. Both allergen-specific IgE and Th2 cytokine responses are reduced in antibiotic-treated mice in which the flora has been allowed to repopulate. Taken together, our results suggest that TLR4-dependent signals provided by the intestinal commensal flora inhibit the development of allergic responses to food Ags.	Massachusetts Gen Hosp E, Mucosal Immunol Lab, Charlestown, MA 02129 USA; Harvard Univ, Sch Med, Charlestown, MA 02129 USA	Nagler-Anderson, C (reprint author), Massachusetts Gen Hosp E, Mucosal Immunol Lab, Bldg 114,16th St, Charlestown, MA 02129 USA.	nagler_a@helix.mgh.harvard.edu			NIDDK NIH HHS [DK 40561, DK 55678, DK43551]		Akira S, 2001, NAT IMMUNOL, V2, P675, DOI 10.1038/90609; Alexopoulou L, 2001, NATURE, V413, P732, DOI 10.1038/35099560; Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Bashir MEH, 2002, J IMMUNOL, V169, P3284; Berg RD, 1996, TRENDS MICROBIOL, V4, P430, DOI 10.1016/0966-842X(96)10057-3; Bjorksten B, 2001, J ALLERGY CLIN IMMUN, V108, P516; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; Burks W, 2003, J CLIN INVEST, V111, P950, DOI 10.1172/JCI200318233; Cebra JJ, 1999, AM J CLIN NUTR, V69, p1046S; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; HOMER AA, 2002, ALLERGY S72, V57, P24; Imler JL, 2003, NAT IMMUNOL, V4, P105, DOI 10.1038/ni0203-105; Julia V, 2000, J IMMUNOL, V165, P5637; Kalliomaki M, 2001, LANCET, V357, P1076, DOI 10.1016/S0140-6736(00)04259-8; Kawai T, 2001, J IMMUNOL, V167, P5887; Koppelman GH, 2001, AM J RESP CRIT CARE, V163, P965; Koppelman SJ, 1999, J BIOL CHEM, V274, P4770, DOI 10.1074/jbc.274.8.4770; Li XM, 2000, J ALLERGY CLIN IMMUN, V106, P150, DOI 10.1067/mai.2000.107395; Liu AH, 2002, J ALLERGY CLIN IMMUN, V109, P379, DOI 10.1067/mai.2002.122157; Liu NS, 2003, NAT IMMUNOL, V4, P687, DOI 10.1038/ni941; Maleki SJ, 2000, J IMMUNOL, V164, P5844; MARINARO M, 1995, J IMMUNOL, V155, P4621; Matricardi PM, 2003, ALLERGY, V58, P461, DOI 10.1034/j.1398-9995.2003.00175.x; McCluskie MJ, 2000, VACCINE, V19, P413, DOI 10.1016/S0264-410X(00)00208-5; McCluskie MJ, 2000, MOL MED, V6, P867; McCluskie MJ, 1998, J IMMUNOL, V161, P4463; Medzhitov R, 2001, NAT REV IMMUNOL, V1, P135, DOI 10.1038/35100529; Morafo V, 2003, J ALLERGY CLIN IMMUN, V111, P1122, DOI 10.1067/mai.2003.1463; Nagler-Anderson C, 2001, NAT REV IMMUNOL, V1, P59, DOI 10.1038/35095573; Ownby DR, 2002, JAMA-J AM MED ASSOC, V288, P963, DOI 10.1001/jama.288.8.963; Poltorak A, 1998, SCIENCE, V282, P2085, DOI 10.1126/science.282.5396.2085; Qureshi ST, 1999, J EXP MED, V189, P615, DOI 10.1084/jem.189.4.615; Raby BA, 2002, AM J RESP CRIT CARE, V166, P1449, DOI 10.1164/rrcm.200207-634OC; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Sudo N, 2002, CLIN EXP ALLERGY, V32, P1112, DOI 10.1046/j.1365-2222.2002.01430.x; Sudo N, 1997, J IMMUNOL, V159, P1739; TOSCHAKOV V, 2002, NAT IMMUNOL, V3, P392	38	195	207	1	16	AMER ASSOC IMMUNOLOGISTS	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	0022-1767			J IMMUNOL	J. Immunol.	JUN 1	2004	172	11					6978	6987				10	Immunology	Immunology	822ZN	WOS:000221579600057	15153518	
J	Hanifin, JM; Cooper, KD; Ho, VC; Kang, SW; Krafchik, BR; Margolis, DJ; Schachner, LA; Sidbury, R; Whitmore, SE; Sieck, CK; Van Voorhees, AS				Hanifin, JM; Cooper, KD; Ho, VC; Kang, SW; Krafchik, BR; Margolis, DJ; Schachner, LA; Sidbury, R; Whitmore, SE; Sieck, CK; Van Voorhees, AS		Chair Guidlines Outcomes Task	Guidelines of care for atopic dermatitis	JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY			English	Review							PLACEBO-CONTROLLED TRIAL; RANDOMIZED CONTROLLED TRIAL; FLUTICASONE PROPIONATE CREAM; CHINESE HERBAL MEDICINE; LONG-TERM EFFICACY; AIR-CONDITIONED PHOTOTHERAPY; ALLERGEN-ANTIBODY COMPLEXES; FUROATE 0.1-PERCENT CREAM; INTERFERON-GAMMA-THERAPY; DOSE UVA1 PHOTOTHERAPY		Amer Acad Dermatol, Schaumburg, IL 60168 USA	Hanifin, JM (reprint author), Amer Acad Dermatol, POB 4014, Schaumburg, IL 60168 USA.			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J	Nicolai, T; Carr, D; Weiland, SK; Duhme, H; von Ehrenstein, O; Wagner, C; von Mutius, E				Nicolai, T; Carr, D; Weiland, SK; Duhme, H; von Ehrenstein, O; Wagner, C; von Mutius, E			Urban traffic and pollutant exposure related to respiratory outcomes and atopy in a large sample of children	EUROPEAN RESPIRATORY JOURNAL			English	Article						asthma; atopy; children; pollutants; respiratory; traffic	DIESEL EXHAUST PARTICLES; AIR-POLLUTION; ALLERGIC SENSITIZATION; LUNG-FUNCTION; ASTHMA; SYMPTOMS; PREVALENCE; INFLAMMATION; GERMANY; POLLEN	Conflicting results have been reported for the relationship between traffic exposure and inception of atopy. The effect of traffic on the prevalence of asthma and atopy at school age was investigated in a representative population. Random samples of schoolchildren (n = 7,509, response rate 83.7%,) were studied using the International Study of Asthma and Allergies in Childhood phase-II protocol with skin-prick tests, measurements of specific immunoglobulin E and lung function. Traffic exposure was assessed via traffic counts and by an emission model which predicted soot, benzene and nitrogen dioxide (NO2). Traffic counts were associated with current asthma, wheeze and cough. In children with tobacco-smoke exposure, traffic volume was additionally associated with a positive skin-prick test. Cough was associated with soot, benzene and NO2, current asthma with soot and benzene, and current wheeze with benzene and NO2. No pollutant was associated with allergic sensitisation. High vehicle traffic was associated with asthma, cough and wheeze, and in children additionally exposed to environmental tobacco smoke, with allergic sensitisation. However, effects of socioeconomic factors associated with living close to busy roads cannot be ruled out.	Univ Munich, Childrens Hosp, D-8000 Munich, Germany; Univ Ulm, Dept Epidemiol, Ulm, Germany; Univ Munster, Inst Epidemiol & Social Med, D-4400 Munster, Germany	Nicolai, T (reprint author), Univ Munich, Childrens Hosp, D-8000 Munich, Germany.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; BARBEE RA, 1976, ANN INTERN MED, V84, P129; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Behrendt H, 1997, INT ARCH ALLERGY IMM, V113, P69; Briggs DJ, 1997, INT J GEOGR INF SCI, V11, P699, DOI 10.1080/136588197242158; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; Carr D, 2002, ENVIRON RES, V90, P111, DOI 10.1006/enrs.2002.4393; Ciccone G, 1998, OCCUP ENVIRON MED, V55, P771; Devalia JL, 1997, ALLERGY, V52, P45; Emberlin J, 1995, CLIN EXP ALLERGY, V25, P33, DOI 10.1111/j.1365-2222.1995.tb00040.x; Gardner RM, 1987, AM REV RESPIR DIS, V136, P1285; Heinrich J, 1998, AM J PUBLIC HEALTH, V88, P1319, DOI 10.2105/AJPH.88.9.1319; Hirsch T, 1999, EUR RESPIR J, V14, P669, DOI 10.1034/j.1399-3003.1999.14c29.x; Hirsch T, 2000, J ALLERGY CLIN IMMUN, V106, P573, DOI 10.1067/mai.2000.109430; Kabesch M, 1999, EUR RESPIR J, V13, P577, DOI 10.1183/09031936.99.13357799; Knox RB, 1997, CLIN EXP ALLERGY, V27, P246; Kramer U, 2000, EPIDEMIOLOGY, V11, P64, DOI 10.1097/00001648-200001000-00014; Miyabara Y, 1998, AM J RESP CRIT CARE, V157, P1138; Oosterlee A, 1996, OCCUP ENVIRON MED, V53, P241; Pekkanen J, 1997, ENVIRON RES, V74, P24, DOI 10.1006/enrs.1997.3750; RIEDLER J, 1994, AM J RESP CRIT CARE, V150, P1632; Studnicka M, 1997, EUR RESPIR J, V10, P2275, DOI 10.1183/09031936.97.10102275; Takano H, 1997, AM J RESP CRIT CARE, V156, P36; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; von Ehrenstein OS, 2002, EUR RESPIR J, V19, P1099, DOI 10.1183/09031936.02.00104302; Weiland SK, 1999, EUR RESPIR J, V14, P862, DOI 10.1034/j.1399-3003.1999.14d23.x; Weiland Stephan K., 1994, Annals of Epidemiology, V4, P243; WILLIAMS PB, 1995, J ALLERGY CLIN IMMUN, V95, P88, DOI 10.1016/S0091-6749(95)70156-7; WJST M, 1993, BRIT MED J, V307, P596; Wyler C, 2000, EPIDEMIOLOGY, V11, P450, DOI 10.1097/00001648-200007000-00015; ZAPLETAL A, 1977, Zeitschrift fuer Erkrankungen der Atmungsorgane, V149, P343	31	195	198	1	21	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	JUN	2003	21	6					956	963		10.1183/09031936.03.00041103		8	Respiratory System	Respiratory System	685CH	WOS:000183242900009	12797488	
J	ten Brinke, A; Zwinderman, AH; Sterk, PJ; Rabe, KF; Bel, EH				ten Brinke, A; Zwinderman, AH; Sterk, PJ; Rabe, KF; Bel, EH			Factors associated with persistent airflow limitation in severe asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; severity of illness index; airway obstruction; sputum; eosinophilia	AIR-FLOW OBSTRUCTION; LONG-TERM INFLAMMATION; LUNG-FUNCTION; BRONCHIAL-ASTHMA; FOLLOW-UP; PULMONARY-FUNCTION; NATURAL-HISTORY; RISK-FACTORS; DECLINE; ADULTS	Persistent airflow limitation can develop in nonsmoking patients with asthma. However, the prevalence and risk factors for airways obstruction with incomplete reversibility in asthma are unknown. We assessed the prevalence of persistent airflow limitation (defined as postbronchodilator FEV1 or FEV1/VC < 75% predicted) in 132 nonsmoking outpatients with severe asthma visiting chest physicians in general hospitals in The Netherlands. They had used inhaled corticosteroids (greater than or equal to 1,600 mug/d) and/or daily oral prednisone and long-acting bronchodilators for > 1 yr. In addition, we examined whether persistent airways obstruction in these patients was associated with specific clinical characteristics (age at onset, smoking history, atopic status, bronchodilator reversibility, provocative concentration of histamine causing a 20% decrease in FEV1 [PC(20)histamine]) or markers of inflammation (exhaled nitric oxide [NO], blood eosinophils, total IgE; and eosinophilia or neutrophilia in induced sputum). Multiple logistic regression analyses were used to calculate adjusted odds ratios (OR). Persistent airflow limitation was observed in 49% of the patients in the study, and apart from older age and longer asthma duration, was strongly associated with a sputum eosinophils percent greater than or equal to 2% (OR = 7.7; confidence interval [CI]: 2.4 to 25), PC(20)histamine less than or equal to 1.0 mg/ml (OR = 3.9; CI: 1.2 to 13), and adult onset (greater than or equal to 18 yr) of asthma (OR = 3.3; CI: 1.2 to 9). Only sputum eosinophilia appeared to be independently associated with persistent airflow limitation (OR = 8.9; CI: 1.3 to 59). In conclusion, persistent airflow limitation is common in adult patients with severe asthma, and is associated with adult onset of the disease, airway hyperresponsiveness, and most importantly, sputum eosinophilia. These findings suggest that eosinophilic airway inflammation contributes to persistent airflow limitation in severe asthma. Whether reduction of sputum eosinophils with more vigorous treatment leads to a better prognosis in severe asthma is still an open question.	Leiden Univ, Med Ctr, Dept Pulm Dis, NL-2300 RC Leiden, Netherlands; Leiden Univ, Dept Med Stat, NL-2300 RA Leiden, Netherlands	ten Brinke, A (reprint author), Leiden Univ, Med Ctr, Dept Pulm Dis, C3-P,POB 9600, NL-2300 RC Leiden, Netherlands.						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J. Respir. Crit. Care Med.	SEP 1	2001	164	5					744	748				5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	472QQ	WOS:000170996800007	11549526	
J	Abrahamsson, TR; Jakobsson, HE; Andersson, AF; Bjorksten, B; Engstrand, L; Jenmalm, MC				Abrahamsson, Thomas R.; Jakobsson, Hedvig E.; Andersson, Anders F.; Bjorksten, Bengt; Engstrand, Lars; Jenmalm, Maria C.			Low diversity of the gut microbiota in infants with atopic eczema	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Allergic disease; Bacteroides species; diversity; eczema; hygiene hypothesis; infant; microbiota; molecular microbiology; pyrosequencing; Sutterella species	INTESTINAL MICROBIOTA; MOLECULAR ANALYSIS; REDUCED DIVERSITY; MICROFLORA; EXPOSURE; DISEASE; ALLERGY; COHORT; RISK	Background: It is debated whether a low total diversity of the gut microbiota in early childhood is more important than an altered prevalence of particular bacterial species for the increasing incidence of allergic disease. The advent of powerful, cultivation-free molecular methods makes it possible to characterize the total microbiome down to the genus level in large cohorts. Objective: We sought to assess microbial diversity and characterize the dominant bacteria in stool during the first year of life in relation to atopic eczema development. Methods: Microbial diversity and composition were analyzed with barcoded 16S rDNA 454-pyrosequencing in stool samples at 1 week, 1 month, and 12 months of age in 20 infants with IgE-associated eczema and 20 infants without any allergic manifestation until 2 years of age (ClinicalTrials.gov ID NCT01285830). Results: Infants with IgE-associated eczema had a lower diversity of the total microbiota at 1 month (P = .004) and a lower diversity of the bacterial phylum Bacteroidetes and the genus Bacteroides at 1 month (P = .02 and P = .01) and the phylum Proteobacteria at 12 months of age (P = .02). The microbiota was less uniform at 1 month than at 12 months of age, with a high interindividual variability. At 12 months, when the microbiota had stabilized, Proteobacteria, comprising gram-negative organisms, were more abundant in infants without allergic manifestation (Empirical Analysis of Digital Gene Expression in R [edgeR] test: P = .008, q = 0.02). Conclusion: Low intestinal microbial diversity during the first month of life was associated with subsequent atopic eczema. (J Allergy Clin Immunol 2012;129:434-40.)	[Abrahamsson, Thomas R.; Jenmalm, Maria C.] Linkoping Univ, Dept Clin & Expt Med, Div Pediat, S-58183 Linkoping, Sweden; [Jakobsson, Hedvig E.; Engstrand, Lars] Swedish Inst Communicable Dis Control, Dept Preparedness, Solna, Sweden; [Jakobsson, Hedvig E.; Engstrand, Lars] Karolinska Inst, Dept Microbiol Tumor & Cell Biol, Stockholm, Sweden; [Andersson, Anders F.] KTH Royal Inst Technol, Sci Life Lab, Sch Biotechnol, Stockholm, Sweden; [Bjorksten, Bengt] Univ Orebro, Sch Hlth & Med Sci, Orebro, Sweden; [Bjorksten, Bengt] Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; [Jenmalm, Maria C.] Linkoping Univ, Dept Clin & Expt Med, Unit Autoimmun & Immune Regulat, Div Clin Immunol, S-58183 Linkoping, Sweden	Abrahamsson, TR (reprint author), Linkoping Univ Hosp, Div Paediat, SE-58185 Linkoping, Sweden.	thomas.abrahamsson@lio.se	Jenmalm, Maria/C-9679-2009	Jenmalm, Maria/0000-0002-2117-5366; Andersson, Anders/0000-0002-3627-6899	BioGaia AB, Stockholm, Sweden; Ekhaga Foundation, the Heart and Lung foundation; Research Council for the South-East Sweden [F2000-106]; Olle Engqvist Foundation; Swedish Asthma and Allergy Association; Swedish Research Council; University Hospital of Linkoping; Soderberg Foundation; Vardal Foundation for Health Care Science and Allergy Research, Sweden; BioGaia AB	Supported by grants from BioGaia AB, Stockholm, Sweden; the Ekhaga Foundation, the Heart and Lung foundation; the Research Council for the South-East Sweden (grant no. F2000-106); the Olle Engqvist Foundation; the Swedish Asthma and Allergy Association; the Swedish Research Council; the University Hospital of Linkoping; the Soderberg Foundation; and the Vardal Foundation for Health Care Science and Allergy Research, Sweden.; B. Bjorksten has received research support from BioGaia AB. M. C. Jenmalm has received lecture honoraria from BioGaia AB. The rest of the authors declare that they have no relevant conflicts of interest.	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Allergy Clin. Immunol.	FEB	2012	129	2					434	U244		10.1016/j.jaci.2011.10.025		9	Allergy; Immunology	Allergy; Immunology	887TC	WOS:000299951700021	22153774	
J	Perera, F; Tang, WY; Herbstman, J; Tang, DL; Levin, L; Miller, R; Ho, SM				Perera, Frederica; Tang, Wan-yee; Herbstman, Julie; Tang, Deliang; Levin, Linda; Miller, Rachel; Ho, Shuk-mei			Relation of DNA Methylation of 5 '-CpG Island of ACSL3 to Transplacental Exposure to Airborne Polycyclic Aromatic Hydrocarbons and Childhood Asthma	PLOS ONE			English	Article								In a longitudinal cohort of similar to 700 children in New York City, the prevalence of asthma (>25%) is among the highest in the US. This high risk may in part be caused by transplacental exposure to traffic-related polycyclic aromatic hydrocarbons (PAHs) but biomarkers informative of PAH-asthma relationships is lacking. We here hypothesized that epigenetic marks associated with transplacental PAH exposure and/or childhood asthma risk could be identified in fetal tissues. Mothers completed personal prenatal air monitoring for PAH exposure determination. Methylation sensitive restriction fingerprinting was used to analyze umbilical cord white blood cell (UCWBC) DNA of 20 cohort children. Over 30 DNA sequences were identified whose methylation status was dependent on the level of maternal PAH exposure. Six sequences were found to be homologous to known genes having one or more 5'-CpG island(s) (5'-CGI). Of these, acyl-CoA synthetase long-chain family member 3 (ACSL3) exhibited the highest concordance between the extent of methylation of its 5'-CGI in UCWBCs and the level of gene expression in matched fetal placental tissues in the initial 20 cohort children. ACSL3 was therefore chosen for further investigation in a larger sample of 56 cohort children. Methylation of the ACSL3 5'-CGI was found to be significantly associated with maternal airborne PAH exposure exceeding 2.41 ng/m(3) (OR = 13.8; p<0.001; sensitivity = 75%; specificity = 82%) and with a parental report of asthma symptoms in children prior to age 5 (OR = 3.9; p<0.05). Thus, if validated, methylated ACSL3 5'CGI in UCWBC DNA may be a surrogate endpoint for transplacental PAH exposure and/or a potential biomarker for environmentally-related asthma. This exploratory report provides a new blueprint for the discovery of epigenetic biomarkers relevant to other exposure assessments and/or investigations of exposure-disease relationships in birth cohorts. The results support the emerging theory of early origins of later life disease development.		Perera, F (reprint author), Columbia Univ, Mailman Sch Publ Hlth, Columbia Ctr Childrens Environm Hlth, New York, NY 10027 USA.	shuk-mei.ho@uc.edu			NIEHS NIH HHS [ES013071, ES006096, ES008977, ES009600, ES015584, ES015905, ES016817, K99 ES016817, P01 ES009600, P01 ES009600-060005, P30 ES006096, P50 ES015905, P50 ES015905-010001, R00 ES016817, R01 ES008977, R01 ES013163, R01 ES015584, R21 ES013071]		Agarwal S, 1998, CURR OPIN IMMUNOL, V10, P345, DOI 10.1016/S0952-7915(98)80174-X; Anway MD, 2005, SCIENCE, V308, P1466, DOI 10.1126/science.1108190; Aqeilan RI, 2005, CANCER RES, V65, P6764, DOI 10.1158/0008-5472.CAN-05-1150; Beck M, 2000, ACTA PAEDIATR, V89, P279, DOI 10.1080/080352500750028401; BIRKENBIHL RP, 1992, NUCLEIC ACIDS RES, V20, P6605, DOI 10.1093/nar/20.24.6605; Bouzigon E, 2007, EUR RESPIR J, V30, P253, DOI 10.1183/09031936.00162206; Choudhry S, 2008, HUM GENET, V123, P455, DOI 10.1007/s00439-008-0495-7; Coleman RA, 2004, PROG LIPID RES, V43, P134, DOI 10.1016/S0163-7827(03)00051-1; DAS DK, 1982, LUNG, V160, P207, DOI 10.1007/BF02719294; Dolinoy DC, 2007, P NATL ACAD SCI USA, V104, P13056, DOI 10.1073/pnas.0703739104; Faergeman NJ, 1997, BIOCHEM J, V323, P1; Fujino T, 1996, J BIOL CHEM, V271, P16748; Godschalk RWL, 2003, J BIOCHEM MOL BIOL, V36, P1; Gyorffy E, 2008, MUTAGENESIS, V23, P1, DOI 10.1093/mutage/gem043; Herman JG, 1996, P NATL ACAD SCI USA, V93, P9821, DOI 10.1073/pnas.93.18.9821; Hilakivi-Clarke L, 2006, TRENDS ENDOCRIN MET, V17, P340, DOI 10.1016/j.tem.2006.09.002; Ho SM, 2007, REPROD TOXICOL, V23, P267, DOI 10.1016/j.reprotox.2007.01.004; Ho SM, 2006, CANCER RES, V66, P5624, DOI 10.1158/0008-5472.CAN-06-0516; Huang THM, 1997, CANCER RES, V57, P1030; Jedrychowski W, 2005, EUR J EPIDEMIOL, V20, P775, DOI 10.1007/s10654-005-1048-1; Jones B, 2006, EMBO J, V25, P2443, DOI 10.1038/sj.emboj.7601148; Khaled AR, 2005, J CELL BIOL, V169, P755, DOI 10.1083/jcb.200409099; Kuzmin A, 2008, GENE EXPR PATTERNS, V8, P107, DOI 10.1016/j.modgep.2007.09.005; Lee DU, 2002, IMMUNITY, V16, P649, DOI 10.1016/S1074-7613(02)00314-X; Li SF, 2003, ANN NY ACAD SCI, V983, P161; Liu J, 2008, TOXICOL SCI, V102, P76, DOI 10.1093/toxsci/kfm290; Mannino DM, 1998, MMWR-MORBID MORTAL W, V47, P1; Mashek DG, 2004, J LIPID RES, V45, P1958, DOI 10.1194/jlr.E4000002-JLR200; Mashima T, 2005, J NATL CANCER I, V97, P765, DOI 10.1093/jnci.dji133; Miller RL, 2008, AM J RESP CRIT CARE, V177, P567, DOI 10.1164/rccm.200710-1511PP; Miller RL, 2004, CHEST, V126, P1071, DOI 10.1378/chest.126.4.1071; Minekura H, 2001, GENE, V278, P185, DOI 10.1016/S0378-1119(01)00714-4; Miyazaki M, 2003, PROSTAG LEUKOTR ESS, V68, P113, DOI 10.1016/S0952-3278(02)00261-2; Mori Trevor A, 2004, Curr Atheroscler Rep, V6, P461, DOI 10.1007/s11883-004-0087-5; Nicholas SW, 2005, AM J PUBLIC HEALTH, V95, P245, DOI 10.2105/AJPH.2004.042705; Oddy WH, 2006, PEDIATR ALLERGY IMMU, V17, P4, DOI 10.1111/j.1399-3038.2005.00340.x; Padmanabhan V, 2007, REV ENDOCR METAB DIS, V8, P67, DOI 10.1007/s11154-007-9051-3; Perera FP, 2003, ENVIRON HEALTH PERSP, V111, P201, DOI 10.1289/ehp.5742; Perzanowski MS, 2006, J ALLERGY CLIN IMMUN, V117, P1082, DOI 10.1016/j.jaci.2005.12.1348; Prins GS, 2007, REPROD TOXICOL, V23, P374, DOI 10.1016/j.reprotox.2006.10.001; Selgrade MK, 2006, ENVIRON HEALTH PERSP, V114, P615, DOI 10.1289/ehp.8376; Stock W, 2000, LANCET, V355, P1351, DOI 10.1016/S0140-6736(00)02125-5; Tang WY, 2007, REV ENDOCR METAB DIS, V8, P173, DOI 10.1007/s11154-007-9042-4; TANG WY, 2008, ENDOCRINOLOGY   0731; Tomita Michiyo, 2004, Lipids Health Dis, V3, P1, DOI 10.1186/1476-511X-3-1; Tykocinski LO, 2005, J BIOL CHEM, V280, P28177, DOI 10.1074/jbc.M502038200; Van Horn CG, 2005, BIOCHEMISTRY-US, V44, P1635, DOI 10.1021/bi0477211; Weber P, 2001, BRIT J NUTR, V86, pS93, DOI 10.1079/BJN2001344; Wijga A, 2003, PEDIATR ALLERGY IMMU, V14, P156, DOI 10.1034/j.1399-3038.2003.00022.x; Woods RK, 2004, THORAX, V59, P105, DOI 10.1136/thorax.2003.009498; Wu MC, 2004, ONCOGENE, V23, P250, DOI 10.1038/sj.onc.1207076	51	194	206	3	24	PUBLIC LIBRARY SCIENCE	SAN FRANCISCO	185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA	1932-6203			PLOS ONE	PLoS One	FEB 16	2009	4	2							e4488	10.1371/journal.pone.0004488		14	Multidisciplinary Sciences	Science & Technology - Other Topics	437KF	WOS:000265485700013	19221603	
J	Green, RM; Cusotvic, A; Sanderson, G; Hunter, J; Johnston, SL; Woodcock, A				Green, RM; Cusotvic, A; Sanderson, G; Hunter, J; Johnston, SL; Woodcock, A			Synergism between allergens and viruses and risk of hospital admission with asthma: case-control study	BRITISH MEDICAL JOURNAL			English	Article							MONOCLONAL-ANTIBODIES; INDOOR ALLERGENS; EXPOSURE; CHILDREN; SENSITIZATION; RHINOVIRUS-16; EXACERBATIONS; INFLAMMATION; PURIFICATION; INFECTIONS	Objective To investigate the importance of sensitisation and exposure to allergens and viral infection in precipitating acute asthma in adults resulting in admission to hospital. Design Case-control study. Setting Large district general hospital. Participants 60 patients aged 17-50 admitted to hospital over a year with acute asthma, matched with two controls: patients with stable asthma recruited from die outpatient department and patients admitted to hospital with non-respiratory conditions (inpatient controls). Main outcome measures Atopic status (skin testing and total and specific IgE), presence of common respiratory Viruses and atypical bacteria (polymerase chain reaction), dust samples from homes, and exposure to allergens (enzyme linked immunosorbent assay (ELISA): Der p 1, Fel d 1, Can f 1, and Bla g 2). Results Viruses were detected in 31 of 177 patients. The difference in the frequency of viruses detected between the groups was significant (admitted with asthma 26%, stable asthma 18%, inpatient controls 9%; P=0.04). A significantly higher proportion of patients admitted with asthma (66%) were sensitised and exposed to either mite, cat, or dog allergen than patients with stable asthma (37%) and inpatient controls (15%; P < 0.001). Being sensitised and exposed to allergens was all independent associate of the group admitted to hospital (odds ratio 2.3, 95% confidence interval 1.0 to 5.4; P=0.05), whereas the combination of sensitisation, high exposure to one or more allergens, and viral detection considerably increased the risk of being admitted with asthma (8.4, 2.1 to 32.8; P=0.002). Conclusions Allergens and viruses may act together to exacerbate asthma.	Wythenshawe Hosp, NW Lung Ctr, Manchester M23 9LT, Lancs, England; Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Resp Med, London W2 1PG, England; Southampton Gen Hosp, Univ Med, Southampton SO9 6YD, Hants, England	Cusotvic, A (reprint author), Wythenshawe Hosp, NW Lung Ctr, Manchester M23 9LT, Lancs, England.		Johnston, Sebastian/I-2423-2012; Custovic, Adnan/A-2435-2012	Custovic, Adnan/0000-0001-5218-7071; Woodcock, Ashley/0000-0002-5428-8578			Busse WW, 1997, J ALLERGY CLIN IMMUN, V100, P147, DOI 10.1016/S0091-6749(97)70216-1; CALHOUN WJ, 1994, J CLIN INVEST, V94, P2200, DOI 10.1172/JCI117581; Campbell MJ, 1997, BRIT MED J, V315, P1012; CHAPMAN MD, 1988, J IMMUNOL, V140, P812; CHAUHAN AJ, 2001, ASTHMA RESP INFECT, P221; Custovic A, 1997, AM J RESP CRIT CARE, V155, P94; Custovic A, 1996, J ALLERGY CLIN IMMUN, V98, P64, DOI 10.1016/S0091-6749(96)70227-0; DUFF AL, 1993, PEDIATRICS, V92, P535; FRAENKEL DJ, 1995, AM J RESP CRIT CARE, V151, P879; GELBER LE, 1993, AM REV RESPIR DIS, V147, P573; Grunberg K, 1997, AM J RESP CRIT CARE, V156, P609; INGRAM JM, 1995, J ALLERGY CLIN IMMUN, V96, P449, DOI 10.1016/S0091-6749(95)70286-5; JOHNSTON SL, 1995, BRIT MED J, V310, P1225; Johnston SL, 1996, AM J RESP CRIT CARE, V154, P654; LEMANSKE RF, 1989, J CLIN INVEST, V83, P1, DOI 10.1172/JCI113843; LUCZYNSKA CM, 1989, J IMMUNOL METHODS, V118, P227, DOI 10.1016/0022-1759(89)90010-0; MILLS TAE, 1997, J ALLERGY CLIN IMMUN, V100, pS1; *NAT ASTHM CAMP, 1999, NAT ASTHM AUD 1999 2, P12; NICHOLSON KG, 1993, BRIT MED J, V307, P982; POLLART SM, 1991, J ALLERGY CLIN IMMUN, V87, P511, DOI 10.1016/0091-6749(91)90010-L; Rosenstreich DL, 1997, NEW ENGL J MED, V336, P1356, DOI 10.1056/NEJM199705083361904; Simpson A, 1999, AM J RESP CRIT CARE, V160, P45; Smith DH, 1997, AM J RESP CRIT CARE, V156, P787; Tunnicliffe WS, 1999, EUR RESPIR J, V13, P654, DOI 10.1183/09031936.99.13365499	24	194	199	1	7	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0959-535X			BRIT MED J	Br. Med. J.	MAR 30	2002	324	7340					763	766A		10.1136/bmj.324.7340.763		7	Medicine, General & Internal	General & Internal Medicine	538KY	WOS:000174816200016	11923159	
J	Wichmann, HE; Peters, A				Wichmann, HE; Peters, A			Epidemiological evidence of the effects of ultrafine particle exposure	PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES A-MATHEMATICAL PHYSICAL AND ENGINEERING SCIENCES			English	Article						ultrafine particles; fine particles; short-term effects; mortality; respiratory diseases; cardiovascular diseases	PARTICULATE AIR-POLLUTION; CORONARY HEART-DISEASE; ENVIRONMENTAL AEROSOLS; PLASMA VISCOSITY; DAILY MORTALITY; CHILDREN; ASSOCIATION; EPISODE; COHORT; NUMBER	In epidemiological studies associations have been observed consistently and coherently between ambient concentrations of particulate matter and morbidity and mortality. With improvement of measurement techniques, the effects became clearer when smaller particle sizes were considered. Therefore, it seems worthwhile to look at the smallest size fraction available today, namely ultrafine particles (UPs, diameter below 0.1 mum) and to compare their health effects with those of fine particles (FPs, diameter below 2.5 mum) However, there are only few studies available which allow such a comparison. Four panel studies with asthma patients have been performed in Germany and Finland. A decrease of peak expiratory flow and an increase of daily symptoms and medication use was found for elevated daily particle concentrations, and in three of these studies it was strongest for UPs. One large study on daily mortality is available from Germany. It showed comparable effects of fine and ultrafine particles in all sire classes considered. However, FPs showed more immediate effects while UPs showed more delayed effects with a lag of four days between particulate concentrations and mortality. Furthermore, immediate effects were clearer in respiratory cases, whereas delayed effects were clearer in cardiovascular cases. In total, the limited body of studies suggests that there are health effects, due to both UPs and FPs, which might be independent from each other. If this is confirmed in further investigations, it might have important implications for monitoring and regulation, which until now does not exist for UPs. Data from Germany show that FPs cannot be used as indicator for UPs: the time trends for FPs decreased, while UPs was stable and the smallest size fraction of UPs has continually increased since 1991/92.	GSF, Inst Epidemiol, D-85764 Neuherberg, Germany; Univ Munich, LMU, D-85764 Neuherberg, Germany	Wichmann, HE (reprint author), GSF, Inst Epidemiol, Ingolstadter Landstr 1, D-85764 Neuherberg, Germany.		Peters, Annette/A-6117-2011				Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; BATES DV, 1992, ENVIRON RES, V59, P336, DOI 10.1016/S0013-9351(05)80040-4; 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; Danesh J, 1998, JAMA-J AM MED ASSOC, V279, P1477, DOI 10.1001/jama.279.18.1477; DOCKERY DW, 1992, ENVIRON RES, V59, P362, DOI 10.1016/S0013-9351(05)80042-8; DOCKERY DW, 1994, REV PUBLIC HLTH, V15, P107; FERIN J, 1991, J AEROSOL MED, V4, P57, DOI 10.1089/jam.1991.4.57; Fuchs N.A., 1964, MECH AEROSOLS, P288; GOLD DR, 2000, IN PRESS CIRCULATION; *ICRP, 1994, ICRP PUBL, V66, P36; Katsouyanni K, 1997, BMJ-BRIT MED J, V314, P1658; Katsouyanni K., 1996, J EPIDEMIOL COMMUN S, V50, pS12; KOENIG W, 1992, ATHEROSCLEROSIS, V94, P93, DOI 10.1016/0021-9150(92)90234-8; Koenig W, 1998, ARTERIOSCL THROM VAS, V18, P768; KREYLING WG, 1999, P 3 COLL PART AIR PO; Liao DP, 1997, AM J EPIDEMIOL, V145, P696; MIRME A, 2000, UNPUB ATMOS ENV; OBERDORSTER G, 1995, INHAL TOXICOL, V7, P111, DOI 10.3109/08958379509014275; Pekkanen J, 1997, ENVIRON RES, V74, P24, DOI 10.1006/enrs.1997.3750; PEKKANEN J, 1999, ENV4CT950205 ULTRA; PEKKANEN J, 1999, AM J RESP CRIT CARE, V54, P1027; PENTTINEN P, 2000, IN PRESS AM J RESP C; Peters A, 1999, AM J EPIDEMIOL, V150, P1094; Peters A, 1997, ENVIRON HEALTH PERSP, V105, P430, DOI 10.1289/ehp.97105430; Peters A, 2000, EPIDEMIOLOGY, V11, P11, DOI 10.1097/00001648-200001000-00005; Peters A, 1997, EUR RESPIR J, V10, P872; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Peters A, 1997, LANCET, V349, P1582, DOI 10.1016/S0140-6736(97)01211-7; PETERS A, 1999, P INT INH S HAN GERM; PETERS A, 1999, P 3 COLL PART AIR PO; PITZ M, 2000, UNPUB CHANGE PARTICL; Pope CA, 1999, AM HEART J, V138, P890, DOI 10.1016/S0002-8703(99)70014-1; Pope CA, 1999, AM J RESP CRIT CARE, V159, P365; Pope III CAD, 1999, AIR POLLUTION HLTH, P673; POPE CA, 2000, IN PRESS ENV HLTH PE; RUSSKANEN J, 2000, IN PRESS ATMOS ENV; Schwartz J, 1996, J AIR WASTE MANAGE, V46, P927, DOI 10.1080/10473289.1996.10467528; SCHWARTZ J, 1994, ENVIRON RES, V64, P36, DOI 10.1006/enrs.1994.1005; Seaton A, 1999, THORAX, V54, P1027; SEATON A, 1995, LANCET, V345, P176, DOI 10.1016/S0140-6736(95)90173-6; STEARNS RC, 1994, ICEM, V13, P763; Stone PH, 1999, AM HEART J, V138, P804, DOI 10.1016/S0002-8703(99)70002-5; Tuch T, 2000, ATMOS ENVIRON, V34, P139, DOI 10.1016/S1352-2310(99)00248-4; Tuch T, 1997, ATMOS ENVIRON, V31, P4193, DOI 10.1016/S1352-2310(97)00260-4; TUCH T, 2000, UNPUB REDUCTION PART; U. S. Environmental Protection Agency, 1996, AIR QUAL CRIT PART M; UTELL MJ, 1999, J AEROSOL MED, V12, P104; VONKLOT S, 2000, P C AM THOR SOC 2000; WICHMANN H, 2000, DAILY MORTALITY FINE; WICHMANN HE, 1999, HLTH EFFECTS FINE PA, V8, P163; Willeke K., 1993, AEROSOL MEASUREMENTS	52	194	211	3	32	ROYAL SOC LONDON	LONDON	6 CARLTON HOUSE TERRACE, LONDON SW1Y 5AG, ENGLAND	1364-503X			PHILOS T ROY SOC A	Philos. Trans. R. Soc. Lond. Ser. A-Math. Phys. Eng. Sci.	OCT 15	2000	358	1775					2751	2768				18	Multidisciplinary Sciences	Science & Technology - Other Topics	368DH	WOS:000090102100025		
J	Hanski, I; von Hertzen, L; Fyhrquist, N; Koskinen, K; Torppa, K; Laatikainen, T; Karisola, P; Auvinen, P; Paulin, L; Makela, MJ; Vartiainen, E; Kosunen, TU; Alenius, H; Haahtela, T				Hanski, Ilkka; von Hertzen, Leena; Fyhrquist, Nanna; Koskinen, Kaisa; Torppa, Kaisa; Laatikainen, Tiina; Karisola, Piia; Auvinen, Petri; Paulin, Lars; Makela, Mika J.; Vartiainen, Erkki; Kosunen, Timo U.; Alenius, Harri; Haahtela, Tari			Environmental biodiversity, human microbiota, and allergy are interrelated	PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA			English	Article						biodiversity benefits; hygiene hypothesis; microbial deprivation; civilization diseases	BLOOD MONONUCLEAR-CELLS; GRAM-POSITIVE BACTERIA; IN-VITRO STIMULATION; GUT MICROBIOTA; ATOPIC ECZEMA; INTESTINAL MICROBIOTA; HYGIENE HYPOTHESIS; REDUCED DIVERSITY; IMMUNE-RESPONSES; CHILDHOOD ASTHMA	Rapidly declining biodiversity may be a contributing factor to another global megatrend-the rapidly increasing prevalence of allergies and other chronic inflammatory diseases among urban populations worldwide. According to the "biodiversity hypothesis," reduced contact of people with natural environmental features and biodiversity may adversely affect the human commensal microbiota and its immunomodulatory capacity. Analyzing atopic sensitization (i.e., allergic disposition) in a random sample of adolescents living in a heterogeneous region of 100 x 150 km, we show that environmental biodiversity in the surroundings of the study subjects' homes influenced the composition of the bacterial classes on their skin. Compared with healthy individuals, atopic individuals had lower environmental biodiversity in the surroundings of their homes and significantly lower generic diversity of gammaproteobacteria on their skin. The functional role of the Gram-negative gammaproteobacteria is supported by in vitro measurements of expression of IL-10, a key anti-inflammatory cytokine in immunologic tolerance, in peripheral blood mononuclear cells. In healthy, but not in atopic, individuals, IL-10 expression was positively correlated with the abundance of the gammaproteobacterial genus Acinetobacter on the skin. These results raise fundamental questions about the consequences of biodiversity loss for both allergic conditions and public health in general.	[Hanski, Ilkka; Torppa, Kaisa] Univ Helsinki, Dept Biosci, FI-00014 Helsinki, Finland; [von Hertzen, Leena; Makela, Mika J.; Haahtela, Tari] Univ Helsinki, Cent Hosp, Skin & Allergy Hosp, FI-00029 Helsinki, Finland; [Fyhrquist, Nanna; Karisola, Piia; Alenius, Harri] Finnish Inst Occupat Hlth, FI-00250 Helsinki, Finland; [Koskinen, Kaisa; Auvinen, Petri; Paulin, Lars] Univ Helsinki, Inst Biotechnol, FI-00014 Helsinki, Finland; [Laatikainen, Tiina; Vartiainen, Erkki] Natl Inst Hlth & Welf, FI-00271 Helsinki, Finland; [Kosunen, Timo U.] Univ Helsinki, Haartman Inst, Dept Bacteriol & Immunol, FI-00014 Helsinki, Finland	Hanski, I (reprint author), Univ Helsinki, Dept Biosci, FI-00014 Helsinki, Finland.	ilkka.hanski@helsinki.fi; tari.haahtela@hus.fi	Auvinen, Petri/D-5044-2009; Osborne, Nicholas/N-4915-2015	Auvinen, Petri/0000-0002-3947-4778; Osborne, Nicholas/0000-0002-6700-2284; Fyhrquist, Nanna Theresia/0000-0002-5408-0005; Makela, Mika/0000-0002-2933-3111	European Research Council [232826]; European Commission [261357]; Academy of Finland [131155, 138932]; Helsinki University Hospital [8361]; Juselius Foundation; Liv och Halsa Foundation	We thank T. Vlasoff and S. Lipponen for obtaining DNA and blood samples; E.-M. Turkki, K. Lipponen, and H. Kangas for technical assistance in processing the bacterial samples; and J. Corander, C. Godfray, H. Jacobs, E. von Mutius, and G. Rook for comments on the manuscript. This work was supported by European Research Council Advanced Grant 232826 (to I.H.), European Commission Seventh Framework Programme Grant Agreement 261357, the Finnish CoE Programme 2006-2011, Academy of Finland Grants 131155 and 138932, Helsinki University Hospital Research Grant 8361, the Juselius Foundation, and the Liv och Halsa Foundation.	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Natl. Acad. Sci. U. S. A.	MAY 22	2012	109	21					8334	8339		10.1073/pnas.1205624109		6	Multidisciplinary Sciences	Science & Technology - Other Topics	947QY	WOS:000304445800082	22566627	
J	de Lafaille, MAC; Kutchukhidze, N; Shen, S; Ding, Y; Yee, H; Lafaille, JJ				de Lafaille, Maria A. Curotto; Kutchukhidze, Nino; Shen, Shiqian; Ding, Yi; Yee, Herman; Lafaille, Juan J.			Adaptive Foxp3(+) regulatory T cell-dependent and -independent control of allergic inflammation	IMMUNITY			English	Article							SPONTANEOUS AUTOIMMUNE ENCEPHALOMYELITIS; TRANSCRIPTION FACTOR FOXP3; RECEPTOR TRANSGENIC MICE; MYELIN BASIC-PROTEIN; TGF-BETA; DENDRITIC CELLS; RETINOIC-ACID; IN-VIVO; AIRWAY HYPERRESPONSIVENESS; INDUCTION	Adaptive Foxp3(+) regulatory T (Treg) cells develop during induction of mucosal tolerance and after immunization. Large numbers of Foxp3(+) T cells have been found in inflamed tissues. We investigated the role of adaptive Foxp3(+) Treg cells in mucosal tolerance and in chronic allergic lung inflammation. We used two strains of mice that are devoid of naturally occurring Treg cells; one is capable of generating adaptive Foxp3+ Treg cells upon exposure to antigen, whereas the other is deficient in both naturally occurring and adaptive Foxp3(+) Treg cells. We found that adaptive Foxp3(+) Treg cells were essential for establishing mucosal tolerance and for suppressing IL-4 production and lymphoid neogenesis in chronic inflammation, whereas IL-5 production and eosinophilia. could be controlled by Foxp3-independent IFN-gamma-dependent mechanisms. Thus, whereas adaptive Foxp3(+) Treg cells regulate sensitization to allergens and the severity of chronic inflammation, IFN-gamma-producing cells can play a beneficial role in inflammatory conditions involving eosinophils.	[de Lafaille, Maria A. Curotto; Kutchukhidze, Nino; Shen, Shiqian; Ding, Yi; Lafaille, Juan J.] NYU, Sch Med, Skirball Inst, Kimmel Ctr Biol & Med,Program Mol Pathogenesis, New York, NY 10016 USA; [Ding, Yi] NYU, Sch Med, Sackler Inst Grad Biomed Sci, New York, NY 10016 USA; [de Lafaille, Maria A. Curotto; Yee, Herman; Lafaille, Juan J.] NYU, Sch Med, Dept Pathol, New York, NY 10016 USA	de Lafaille, MAC (reprint author), NYU, Sch Med, Skirball Inst, Kimmel Ctr Biol & Med,Program Mol Pathogenesis, New York, NY 10016 USA.	curotto@saturn.med.nyu.edu; lafaille@saturn.med.nyu.edu					Aloisi F, 2006, NAT REV IMMUNOL, V6, P205, DOI 10.1038/nri1786; Annacker O, 2001, J IMMUNOL, V166, P3008; Apostolou I, 2004, J EXP MED, V199, P1401, DOI 10.1084/jem.20040249; Bennett CL, 2001, NAT GENET, V27, P20; Bettelli E, 2006, NATURE, V441, P235, DOI 10.1038/nature04753; Carrier Y, 2007, J IMMUNOL, V178, P179; Chatila TA, 2000, J CLIN INVEST, V106, pR75, DOI 10.1172/JCI11679; Chen WJ, 2003, J EXP MED, V198, P1875, DOI 10.1084/jem.20030152; Cobbold SP, 2004, J IMMUNOL, V172, P6003; Cohn L, 2004, ANNU REV IMMUNOL, V22, P789, DOI 10.1146/annurev.immunol.22.012703.104716; Coombes JL, 2007, J EXP MED, V204, P1757, DOI 10.1084/jem.20070590; de Lafaille MAC, 2001, J EXP MED, V194, P1349, DOI 10.1084/jem.194.9.1349; Lafaille J. 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J	Verhasselt, V; Milcent, V; Cazareth, J; Kanda, A; Fleury, S; Dombrowicz, D; Glaichenhaus, N; Julia, V				Verhasselt, Valerie; Milcent, Valerie; Cazareth, Julie; Kanda, Akira; Fleury, Sebastien; Dombrowicz, David; Glaichenhaus, Nicolas; Julia, Valerie			Breast milk-mediated transfer of an antigen induces tolerance and protection from allergic asthma	NATURE MEDICINE			English	Article							GROWTH-FACTOR-BETA; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; T-CELLS; IMMUNE-RESPONSES; INHALED ANTIGEN; ORAL TOLERANCE; MICE; PROTEIN; ABSORPTION; EXPRESSION	Allergic asthma is a chronic disease characterized by airway obstruction in response to allergen exposure. It results from an inappropriate T helper type 2 response to environmental airborne antigens and affects 300 million individuals(1). Its prevalence has increased markedly in recent decades, most probably as a result of changes in environmental factors(2). Exposure to environmental antigens during infancy is crucial to the development of asthma(3). Epidemiological studies on the relationship between breastfeeding and allergic diseases have reached conflicting results(4-8). Here, we have investigated whether the exposure of lactating mice to an airborne allergen affects asthma development in progeny. We found that airborne antigens were efficiently transferred from the mother to the neonate through milk and that tolerance induction did not require the transfer of immunoglobulins. Breastfeeding-induced tolerance relied on the presence of transforming growth factor (TGF)-beta during lactation, was mediated by regulatory CD4(+) T lymphocytes and depended on TGF-beta signaling in T cells. In conclusion, breast milk-mediated transfer of an antigen to the neonate resulted in oral tolerance induction leading to antigen-specific protection from allergic airway disease. This study may pave the way for the design of new strategies to prevent the development of allergic diseases.	[Verhasselt, Valerie; Milcent, Valerie; Glaichenhaus, Nicolas; Julia, Valerie] Univ Nice Sophie Antipolis, U924, INSERM, F-06560 Valbonne, France; [Cazareth, Julie] Univ Nice Sophie Antipolis, UMR 6097, CNRS, F-06560 Valbonne, France; [Kanda, Akira; Fleury, Sebastien; Dombrowicz, David] Univ Lille, Inst Pasteur, INSERM, U547, F-59000 Lille, France	Verhasselt, V (reprint author), Univ Nice Sophie Antipolis, U924, INSERM, 660 Route Lucioles, F-06560 Valbonne, France.	verhasselt@unice.fr; vjulia@unice.fr	Dombrowicz, David/F-7044-2013	Dombrowicz, David/0000-0002-0485-8923			Adkins B, 2004, NAT REV IMMUNOL, V4, P553, DOI 10.1038/nri1394; Apostolou I, 2004, J EXP MED, V199, P1401, DOI 10.1084/jem.20040249; BENSCH KG, 1967, SCIENCE, V157, P1204, DOI 10.1126/science.157.3793.1204; BRALEY JF, 1978, J CLIN INVEST, V61, P1240, DOI 10.1172/JCI109040; Eder W, 2006, NEW ENGL J MED, V355, P2226, DOI 10.1056/NEJMra054308; Faria AMC, 2005, IMMUNOL REV, V206, P232, DOI 10.1111/j.0105-2896.2005.00280.x; Faria AMC, 2003, J AUTOIMMUN, V20, P135, DOI 10.1016/S0896-8411(02)00112-9; Frentsch M, 2005, NAT MED, V11, P1118, DOI 10.1038/nm1292; Friedman NJ, 2005, J ALLERGY CLIN IMMUN, V115, P1238, DOI 10.1016/j.jaci.2005.01.069; Gdalevich M, 2001, J PEDIATR-US, V139, P261, DOI 10.1067/mpd.2001.117006; Guilbert TW, 2007, AM J RESP CRIT CARE, V176, P843, DOI 10.1164/rccm.200610-1507OC; HANSON DG, 1981, J IMMUNOL, V127, P1518; Holt PG, 2005, NAT IMMUNOL, V6, P957, DOI 10.1038/ni1005-957; HOLT PG, 1981, IMMUNOLOGY, V42, P409; Julia V, 2002, IMMUNITY, V16, P271, DOI 10.1016/S1074-7613(02)00276-5; Kramer MS, 2007, BRIT MED J, V335, P815, DOI 10.1136/bmj.39304.464016.AE; Labbok MH, 2004, NAT REV IMMUNOL, V4, P565, DOI 10.1038/nri1393; LETTERIO JJ, 1994, SCIENCE, V264, P1936, DOI 10.1126/science.8009224; Lewkowich IP, 2005, J EXP MED, V202, P1549, DOI 10.1084/jem.20051506; Lucas PJ, 2000, J EXP MED, V191, P1187, DOI 10.1084/jem.191.7.1187; Masoli M, 2004, ALLERGY, V59, P469, DOI 10.1111/j.1398-9995.2004.00526.x; MILLER A, 1994, EUR J IMMUNOL, V24, P1026, DOI 10.1002/eji.1830240503; Palmer DJ, 2006, CURR OPIN CLIN NUTR, V9, P284, DOI 10.1097/01.mco.0000222113.46042.50; Penttila I, 2006, PEDIATR RES, V59, P650, DOI 10.1203/01.pdr.0000203149.75465.74; Penttila IA, 1998, PEDIATR RES, V44, P524, DOI 10.1203/00006450-199810000-00010; Robinson DS, 2004, J CLIN INVEST, V114, P1389, DOI 10.1172/JCI200423595; SAITO S, 1993, CLIN EXP IMMUNOL, V94, P220; STROBEL S, 1984, PEDIATR RES, V18, P588, DOI 10.1203/00006450-198407000-00004; van Odijk J, 2003, ALLERGY, V58, P833, DOI 10.1034/j.1398-9995.2003.00264.x; WILLOUGHBY JB, 1977, J IMMUNOL, V119, P2137	30	193	199	0	18	NATURE PUBLISHING GROUP	NEW YORK	75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA	1078-8956			NAT MED	Nat. Med.	FEB	2008	14	2					170	175		10.1038/nm1718		6	Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental	Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine	259NT	WOS:000252946700025	18223654	
J	Moingeon, P; Batard, T; Fadel, R; Frati, F; Sieber, J; Van Overtvelt, L				Moingeon, P; Batard, T; Fadel, R; Frati, F; Sieber, J; Van Overtvelt, L			Immune mechanisms of allergen-specific sublingual immunotherapy	ALLERGY			English	Review						allergy vaccine; Langerhans cells; regulatory T lymphocyte; sublingual immunotherapy	GRASS-POLLEN IMMUNOTHERAPY; REGULATORY T-CELLS; RANDOMIZED CONTROLLED-TRIAL; HOUSE-DUST MITES; PLACEBO-CONTROLLED EVALUATION; MESSENGER-RNA EXPRESSION; BLOCKING IGG ANTIBODIES; DOUBLE-BLIND; DENDRITIC CELLS; HAY-FEVER	Sublingual immunotherapy has been shown in some clinical studies to modulate allergen-specific antibody responses [with a decrease in the immunoglobulin E/immunoglobulin G4 (IgE/IgG4) ratio] and to reduce the recruitment and activation of proinflammatory cells in target mucosa. Whereas a central paradigm for successful immunotherapy has been to reorient the pattern of allergen-specific T-cell responses in atopic patients from a T helper (Th)2 to Th1 profile, there is currently a growing interest in eliciting regulatory T cells, capable of downregulating both Th1 and Th2 responses through the production of interleukin (IL)-10 and/or transforming growth factor (TGF)-beta. We discuss herein immune mechanisms involved during allergen-specific sublingual immunotherapy (SLIT), in comparison with subcutaneous immunotherapy. During SLIT, the allergen is captured within the oral mucosa by Langerhans-like dendritic cells expressing high-affinity IgE receptors, producing IL-10 and TGF-beta, and upregulating indoleamine dioxygenase (IDO), suggesting that such cells are prone to induce tolerance. The oral mucosa contains limited number of proinflammatory cells, such as mast cells, thereby explaining the well-established safety profile of SLIT. In this context, second-generation vaccines based on recombinant allergens in a native conformation formulated with adjuvants are designed to target Langerhans-like cells in the sublingual mucosa, with the aim to induce allergen-specific regulatory T cells. Importantly, such recombinant vaccines should facilitate the identification of biological markers of SLIT efficacy in humans.	Stallergenes, Res & Dev, F-92160 Antony, France; Stallergenes Italia SRL, Milan, Italy; Stallergenes GmbH & Co KG Germany, Kamp Lintfort, Germany	Moingeon, P (reprint author), Stallergenes, Res & Dev, 6 Rue Alexis de Tocqueville, F-92160 Antony, France.		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J	Nicolaou, N; Poorafshar, M; Murray, C; Simpson, A; Winell, H; Kerry, G; Harlin, A; Woodcock, A; Ahlstedt, S; Custovic, A				Nicolaou, Nicolaos; Poorafshar, Maryam; Murray, Clare; Simpson, Angela; Winell, Henric; Kerry, Gina; Haerlin, Annika; Woodcock, Ashley; Ahlstedt, Staffan; Custovic, Adnan			Allergy or tolerance in children sensitized to peanut: Prevalence and differentiation using component-resolved diagnostics	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Peanut allergy; oral food challenge; component-resolved diagnostics; Ara h 2; microarray; birth cohort	FOOD CHALLENGES; RECOMBINANT ALLERGENS; SKIN PRICK; IGE; POLLEN; IDENTIFICATION; ASSOCIATION; ADOLESCENTS; DERMATITIS; REACTIVITY	Background: Not all peanut-sensitized children develop allergic reactions on exposure. Objective: To establish by oral food challenge the proportion of children with clinical peanut allergy among those considered peanut-sensitized by using skin prick tests and/or IgE measurement, and to investigate whether component-resolved diagnostics using microarray could differentiate peanut allergy from tolerance. Methods: Within a population-based birth cohort, we ascertained peanut sensitization by skin tests and IgE measurement at age 8 years. Among sensitized children, we determined peanut allergy versus tolerance by oral food challenges. We used open challenge among children consuming peanuts (n = 45); others underwent double-blind placebo-controlled challenge (n = 34). We compared sensitization profiles between children with peanut allergy and peanut-tolerant children by using a microarray with 12 pure components (major peanut and potentially cross-reactive components, including grass allergens). Results: Of 933 children, 110 (11.8%) were peanut-sensitized. Nineteen were not challenged (17 no consent). Twelve with a convincing history of reactions on exposure, IgE >= 15 kUA/L and/or skin test >= 8mm were considered allergic without challenge. Of the remaining 79 children who underwent challenge, 7 had >= 2 objective signs and were designated as having peanut allergy. We estimated the prevalence of clinical peanut allergy among sensitized subjects as 22.4% (95% CI, 14.8% to 32.3%). By using component-resolved diagnostics, we detected marked differences in the pattern of component recognition between children with peanut allergy (n = 29; group enriched with 12 children with allergy) and peanut-tolerant children (n = 52). The peanut component Ara h 2 was the most important predictor of clinical allergy. Conclusion: The majority of children considered peanut-sensitized on the basis of standard tests do not have peanut allergy. Component-resolved diagnostics may facilitate the diagnosis of peanut allergy. Q Allergy Clin Immunol 2010;125:191-7.)	[Nicolaou, Nicolaos; Murray, Clare; Simpson, Angela; Kerry, Gina; Woodcock, Ashley; Custovic, Adnan] Univ Manchester, Univ Hosp S Manchester NHS Fdn Trust, Sch Translat Med, NIHR Translat Res Facil Resp Med, Manchester M23 9LT, Lancs, England; [Poorafshar, Maryam; Winell, Henric; Haerlin, Annika] Phadia AB, Uppsala, Sweden; [Ahlstedt, Staffan] Karolinska Inst, Natl Inst Environm Med, Ctr Allergy Res, Stockholm, Sweden	Custovic, A (reprint author), Univ Manchester, Univ Hosp S Manchester NHS Fdn Trust, Sch Translat Med, NIHR Translat Res Facil Resp Med, Manchester M23 9LT, Lancs, England.	adnan.custovic@manchester.ac.uk	Custovic, Adnan/A-2435-2012; Osborne, Nicholas/N-4915-2015	Custovic, Adnan/0000-0001-5218-7071; Osborne, Nicholas/0000-0002-6700-2284; Simpson, Angela/0000-0003-2733-6666; Woodcock, Ashley/0000-0002-5428-8578	Medical Research Council; Moulton Charitable Foundation; Grand Charity of Freemasons; National Institute for Health Research	A. Harlin, and H. Winell are employees of Phadia AB. S. Ahlstedt is a previous employee of Phadia AB. A. Simpson has received research support from the Medical Research Council, the Moulton Charitable Foundation, and the Grand Charity of Freemasons. A. Custovic has received lecture fees from GlaxoSmithKline and Phadia, is on the advisory board of ALK, and has received research support from the Medical Research Council and the National Institute for Health Research. The rest of the authors have declared that they have no conflict of interest.	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Allergy Clin. Immunol.	JAN	2010	125	1					191	197		10.1016/j.jaci.2009.10.008		7	Allergy; Immunology	Allergy; Immunology	544MG	WOS:000273660500023	20109746	
J	Bieber, T				Bieber, Thomas			Atopic Dermatitis	ANNALS OF DERMATOLOGY			English	Review						Atopic dermatitis; Pathophysiology; Proactive management; Therapy	TOPICAL CALCINEURIN INHIBITORS; RANDOMIZED CONTROLLED-TRIAL; INNATE IMMUNE-RESPONSE; SINGLE NUCLEOTIDE POLYMORPHISMS; REGULATORY T-CELLS; ANTIMICROBIAL PEPTIDES; ALLERGIC INFLAMMATION; FILAGGRIN MUTATIONS; CYTOKINE MILIEU; VACCINIA VIRUS	Atopic dermatitis (AD) is a chronic and relapsing disease affecting an increasing number of patients. Usually starting in early childhood, AD can be the initial step of the so-called atopic march, i.e. followed by allergic rhinitis and allergic asthma. AD is a paradigmatic genetically complex disease involving gene-gene and gene-environment interactions. Genetic linkage analysis as well as association studies have identified several candidate genes linked to either the epidermal barrier function or to the immune system. Stress, bacterial or viral infections, the exposure to aero- or food-allergens as well as hygienic factors are discussed to aggravate symptoms of AD. Athough generalized Th2-deviated immune response is closely linked to the condition of AD, the skin disease itself is a biphasic inflammation with an initial Th2 phase and while chronic lesions harbour Th0/Th1 cells. Regulatory T cells have been shown to be altered in AD as well as the innate immune system in the skin. The main treatment-goals include the elimination of inflammation and infection, preserving and restoring the barrier function and controlling exacerbating factors. The overall future strategy in AD will be aimed to control skin inflammation by a more proactive management in order to potentially prevent the emergence of sensitization as well as to design customized management based on genetic and pathophysiologic information. (Ann Dermatol 22(2) 125 similar to 137, 2010)	Univ Bonn, Dept Dermatol & Allergy, D-53105 Bonn, Germany	Bieber, T (reprint author), Univ Bonn, Dept Dermatol & Allergy, Sigmund Freud Str 25, D-53105 Bonn, Germany.	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J	Gehring, U; Wijga, AH; Brauer, M; Fischer, P; de Jongste, JC; Kerkhof, M; Oldenwening, M; Smit, HA; Brunekreef, B				Gehring, Ulrike; Wijga, Alet H.; Brauer, Michael; Fischer, Paul; de Jongste, Johan C.; Kerkhof, Marjan; Oldenwening, Marieke; Smit, Henriette A.; Brunekreef, Bert			Traffic-related Air Pollution and the Development of Asthma and Allergies during the First 8 Years of Life	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; allergy; air pollution; cohort; traffic	BIRTH COHORT; EXPOSURE; CHILDHOOD; CHILDREN; SYMPTOMS; SENSITIZATION; POLLUTANTS; INFECTIONS; INFANTS; MODELS	Rationale The role of air pollution exposure in the development of asthma, allergies, and related symptoms remains unclear, due in part to the limited number of prospective cohort studies with sufficiently long follow-ups addressing this problem. Objectives: We studied the association between traffic-related air pollution and the development of asthma, allergy, and related symptoms in a prospective birth cohort study with a unique 8-year follow-up. Methods: Annual questionnaire reports of asthma, hay fever, and related symptoms during the first 8 years of life were analyzed for 3,863 children. At age 8, measurements of allergic sensitization and bronchial hyperresponsiveness were performed for subpopulations (n = 1,700 and 936, respectively). Individual exposures to nitrogen dioxide (NO(2)), particulate matter (PM(2.5)), and soot at the birth address were estimated by land-use regression models. Associations between exposure to traffic-related air pollution and repeated measures of health outcomes were assessed by repeated-measures logistic regression analysis. Effects are presented for an interquartile range increase in exposure after adjusting for covariates. Measurements and Main Results: Annual prevalence was 3 to 6% for asthma and 12 to 23% for asthma symptoms. Annual incidence of asthma was 6% at age 1, and 1 to 2% at later ages. PM2.5 levels were associated with a significant increase in incidence of asthma (odds ratio [OR], 1.28; 95% confidence interval [CI], 1.10-1.49), prevalence of asthma (OR, 1.26; 95% CI, 1.04-1.51), and prevalence of asthma symptoms (OR, 1.15; 95% CI, 1.02-1.28). Findings were similar for NO(2) and soot. Associations were stronger for children who had not moved since birth. Positive associations with hay fever were found in nonmovers only. No associations were found with atopic eczema, allergic sensitization, and bronchial hyperresponsiveness. Conclusions: Exposure to traffic-related air pollution may cause asthma in children.	[Gehring, Ulrike; Oldenwening, Marieke; Brunekreef, Bert] Univ Utrecht, Inst Risk Assessment Sci, NL-3508 TD Utrecht, Netherlands; [Wijga, Alet H.; Smit, Henriette A.] Natl Inst Publ Hlth & Environm, Ctr Prevent & Hlth Serv Res, NL-3720 BA Bilthoven, Netherlands; [Brauer, Michael] Univ British Columbia, Sch Environm Hlth, Vancouver, BC V5Z 1M9, Canada; [Fischer, Paul] Natl Inst Publ Hlth & Environm, Ctr Environm Hlth Res, NL-3720 BA Bilthoven, Netherlands; [de Jongste, Johan C.] Erasmus Univ Med Ctr Sophia Childrens Hosp, Div Resp Med, Dept Pediat, Rotterdam, Netherlands; [Kerkhof, Marjan] Univ Groningen, Univ Med Ctr Groningen, Dept Epidemiol, Groningen, Netherlands; [Smit, Henriette A.; Brunekreef, Bert] Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands	Gehring, U (reprint author), Univ Utrecht, Inst Risk Assessment Sci, POB 80178, NL-3508 TD Utrecht, Netherlands.	u.gehring@uu.nl	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; brunekreef, bert/0000-0001-9908-0060; Gehring, Ulrike/0000-0003-3612-5780; Brauer, Michael/0000-0002-9103-9343	Netherlands Organization for Health Research and Development; Netherlands Organization for Scientific Research (NWO); Netherlands Asthma Fund; Netherlands Ministry of Spatial Planning, Housing, and the Environment; Netherlands Ministry of Health, Welfare, and Sport; German Academic Exchange Service (DAAD)	Supported by The Netherlands Organization for Health Research and Development; The Netherlands Organization for Scientific Research; The Netherlands Asthma Fund; The Netherlands Ministry of Spatial Planning, Housing, and the Environment; and The Netherlands Ministry of Health, Welfare, and Sport (the PIAMA Study). Ulrike Gehring was supported by research fellowships of the German Academic Exchange Service (DAAD) and the Netherlands Organization for Scientific Research (NWO).	Andersen ZJ, 2008, THORAX, V63, P710, DOI 10.1136/thx.2007.085480; Beijk R., 2008, 680704005 RIVM NAT I; Brauer M, 2007, EUR RESPIR J, V29, P879, DOI 10.1183/09031936.00083406; Brauer M, 2003, EPIDEMIOLOGY, V14, P228, DOI 10.1097/00001648-200303000-00019; Brauer M, 2002, AM J RESP CRIT CARE, V166, P1092, DOI 10.1164/rccm.200108-007OC; Brauer M, 2006, ENVIRON HEALTH PERSP, V114, P1414, DOI 10.1289/ehp.9089; Brown JS, 2007, J EXPO SCI ENV EPID, V17, pS97, DOI 10.1038/sj.jes.7500632; Brunekreef B, 2002, PEDIAT ALLERG IMM-UK, V13, P55, DOI 10.1034/j.1399-3038.13.s.15.1.x; Brunekreef B, 2003, EUR RESPIR J, V21, P913, DOI 10.1183/09031936.03.00014903; CHEN CM, CLIN EXP DE IN PRESS; Diggle P. 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J	Clifton, VL				Clifton, V. L.			Sex and the Human Placenta: Mediating Differential Strategies of Fetal Growth and Survival	PLACENTA			English	Article; Proceedings Paper	Annual Meeting of the International-Federation-of-Placenta-Associations	OCT 06-09, 2009	Adelaide, AUSTRALIA	Int Federat Placenta Assoc, Univ Adelaide, Robinson Inst, NGED		Placenta Sex; Pregnancy; Birthweight	MATERNAL ASTHMA; X-INACTIVATION; FACTOR-I; GLUCOCORTICOID EXPOSURE; ANTENATAL BETAMETHASONE; PRENATAL-DIAGNOSIS; ANDROGEN RECEPTOR; IMMUNE-RESPONSES; BLOOD-PRESSURE; EXPRESSION	There are known sex specific differences in fetal and neonatal morbidity and mortality. There are also known differences in birthweight centile with males generally being larger than females at birth. These differences are generally ignored when studying obstetric complications of pregnancy and the mechanisms that confer these differences between the sexes are unknown. Current evidence suggests sex specific adaptation of the placenta may be central to the differences in fetal growth and survival. Our research examining pregnancies complicated by asthma has reported sexually dimorphic differences in fetal growth and survival with males adapting placental function to allow for continued growth in an adverse maternal environment while females reduce growth in an attempt to survive further maternal insults. We have reported sex differences in placental cytokine expression, insulin-like growth factor pathways and the placental response to cortisol in relation to the complication of asthma during pregnancy. More recently we have identified sex specific alterations in placental function in pregnancies complicated by preterm delivery which were associated with neonatal outcome and survival. We propose the sexually dimorphic differences in growth and survival of the fetus are mediated by the sex specific function of the human placenta. This review will present evidence supporting this hypothesis and will argue that to ignore the sex of the placenta is no longer sound scientific practice. (C) 2010 Published by IFPA and Elsevier Ltd.	Univ Adelaide, Robinson Inst, Dept Paediat & Reprod Hlth, Fac Hlth Sci, Adelaide, SA 5005, Australia	Clifton, VL (reprint author), Univ Adelaide, Robinson Inst, Dept Paediat & Reprod Hlth, Fac Hlth Sci, Med N,Level 6,Frome Rd, Adelaide, SA 5005, Australia.	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J	Smith, AD; Cowan, JO; Brassett, KP; Filsell, S; McLachlan, C; Monti-Sheehan, G; Herbison, GP; Taylor, DR				Smith, AD; Cowan, JO; Brassett, KP; Filsell, S; McLachlan, C; Monti-Sheehan, G; Herbison, GP; Taylor, DR			Exhaled nitric oxide - A predictor of steroid response	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; exhaled nitric oxide; inhaled corticosteroid; symptoms; treatment response	AIR-FLOW OBSTRUCTION; INHALED CORTICOSTEROIDS; PULMONARY-DISEASE; MILD ASTHMA; RESPONSIVENESS; INFLAMMATION; CHILDREN; ADULTS; PREDNISOLONE; EOSINOPHILS	Rationale: The initial management of patients who present with persistent respiratory symptoms includes recognizing those with the potential to benefit from inhaled steroid therapy. To date, this has required undertaking a "trial of steroid" to identify responders. There is increasing evidence that steroid response is more likely in patients with eosinophilic airway inflammation, and this can be assessed indirectly using exhaled nitric oxide (FENO) measurements. Objectives: We aimed to assess the predictive accuracy of FENO to identify steroid response in 52 patients presenting with undiagnosed respiratory symptoms in a single-blind, fixed-sequence, placebo-controlled trial of inhaled fluticasone for 4 weeks. Methods: Comparisons of predictive accuracy were made between FENO, and other conventional predictors: peak flows, spirometry, bronchodilator response, and airway hyperresponsiveness measured at baseline. "Steroid response" was defined as change in symptoms, peak flows, spirometry, or airway hyperresponsiveness to adenosin,e based on established guidelines and recommendations. Results: Steroid response was significantly greater in the highest FENO tertile (> 47 ppb) for each endpoint. This outcome was independent of the diagnostic label. The predictive values for FENO were significantly greater than for almost all other baseline predictors, with an optimum cut point of 47 ppb. Conclusions: FENO measurements greater than 47 ppb provide a means of predicting steroid response in patients with undiagnosed respiratory symptoms. Assessing airway inflammation is of more practical value than diagnostic labeling when considering the potential usefulness of inhaled antiinflammatory therapy.	Univ Otago, Sch Med, Otago Resp Res Unit, Dunedin, New Zealand	Taylor, DR (reprint author), Univ Otago, Sch Med, Otago Resp Res Unit, POB 913, Dunedin, New Zealand.	robin.taylor@stonebow.otago.ac.nz					American Thoracic Society, 1991, AM REV RESPIR DIS, V144, P1202, DOI 10.1164/ajrccm/144.5.1202; American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P225, DOI DOI 10.1164/AJRCCM/136.1.225; Brightling CE, 2000, LANCET, V356, P1480, DOI 10.1016/S0140-6736(00)02872-5; Fabbri LM, 2003, AM J RESP CRIT CARE, V167, P418, DOI 10.1164/rccm.200203-183OC; HANLEY JA, 1983, RADIOLOGY, V148, P839; Jatakanon A, 1998, THORAX, V53, P91; Jones SL, 2001, AM J RESP CRIT CARE, V164, P738; Jones SL, 2002, EUR RESPIR J, V20, P601, DOI 10.1183/09031936.02.00285302; Kelly HW, 2003, J ALLERGY CLIN IMMUN, V112, P469, DOI 10.1067/mai.2003.1718; Kharitonov SA, 2003, EUR RESPIR J, V21, P433, DOI 10.1183/09031936.03.00066903; Kharitonov SA, 2002, THORAX, V57, P889, DOI 10.1136/thorax.57.10.889; Little SA, 2000, THORAX, V55, P232, DOI 10.1136/thorax.55.3.232; Meijer RJ, 2002, CLIN EXP ALLERGY, V32, P1096, DOI 10.1046/j.1365-2222.2002.01412.x; [Anonymous], 2002, NIH PUBL, V01-4913; Pavord ID, 1999, LANCET, V353, P2213, DOI 10.1016/S0140-6736(99)01813-9; Payne DNR, 2001, AM J RESP CRIT CARE, V164, P1376; POLOSA R, 1991, J ALLERGY CLIN IMMUN, V87, P939, DOI 10.1016/0091-6749(91)90415-K; Powell H, 2003, MED J AUSTRALIA, V178, P223; QUACKENBOSS JJ, 1991, AM REV RESPIR DIS, V143, P323; Slutsky AS, 1999, AM J RESP CRIT CARE, V160, P2104; Smith AD, 2005, CURR OPIN ALLERGY CL, V5, P49, DOI 10.1097/00130832-200502000-00010; Smith AD, 2004, AM J RESP CRIT CARE, V169, P473, DOI 10.1164/rccm.200310-1376OC; STERK PJ, 1993, EUR RESPIR J, V6, P53, DOI 10.1183/09041950.053s1693; Szefler SJ, 2002, J ALLERGY CLIN IMMUN, V109, P410, DOI 10.1067/mai.2002.122635; TAYLOR DR, 2001, EVIDENCE BASED ASTHM; Van den Toorn LM, 2001, AM J RESP CRIT CARE, V164, P2107; WEIR DC, 1990, THORAX, V45, P118, DOI 10.1136/thx.45.2.118; WEIR DC, 1990, THORAX, V45, P112, DOI 10.1136/thx.45.2.112; YAN K, 1983, THORAX, V38, P760, DOI 10.1136/thx.38.10.760	29	191	199	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.	AUG 15	2005	172	4					453	459		10.1164/rccm.200411-1498OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	953DL	WOS:000231056500016	15901605	
J	Canonica, GW; Passalacqua, G				Canonica, GW; Passalacqua, G			Noninjection routes for immunotherapy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						allergen immunotherapy; sublingual immunotherapy; local nasal immunotherapy; noninjection routes	LOCAL NASAL IMMUNOTHERAPY; SUBLINGUAL-SWALLOW IMMUNOTHERAPY; PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND PLACEBO; HOUSE-DUST-MITE; ALLERGEN-SPECIFIC IMMUNOTHERAPY; GRASS-POLLEN IMMUNOTHERAPY; SHORT RAGWEED EXTRACT; CD4(+) T-CELLS; PRESEASONAL INTRANASAL IMMUNOTHERAPY	Allergen specific immunotherapy, together with drugs and allergen avoidance, is a cornerstone in the management of respiratory allergy. The traditional subcutaneous route is burdened with the risk of severe adverse events; therefore, safer routes of administration (noninjection or local routes) have been investigated and developed. Controlled trials failed to demonstrate the clinical efficacy and the safety of oral and bronchial administration, and these routes have been abandoned. Local nasal immunotherapy proved effective and safe in 17 of 18 controlled trials; thus it is considered a viable route of immunotherapy. Nevertheless, nasal immunotherapy is effective in rhinitis only and requires a particular administration technique; therefore its use is slowly declining. The sublingual route is supported by numerous controlled trials showing its efficacy in asthma and rhinitis in adults and children. The safety profile, assessed in clinical trials and postmarketing surveillance studies, is satisfactory; the most frequent side effects are gastrointestinal complaints, which can be easily managed by proper dose adjusting. Sublingual immunotherapy is now accepted by the World Health Organization as a valid alternative to the subcutaneous route also in children. Although the long-lasting efficacy has been recently documented for the sublingual route, several points still need to be elucidated, including mechanisms of action, optimal dosage, cost-effectiveness, and adherence.	Univ Genoa, Dept Internal Med, Div Allergy & Resp Dis, I-16126 Genoa, Italy	Canonica, GW (reprint author), DIMI, Allergy & Resp Dis, Lgo R Benzi 10, I-16132 Genoa, Italy.						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J	Lauener, RP; Birchler, T; Adamski, J; Braun-Fahrlander, C; Bufe, A; Herz, U; von Mutius, E; Nowak, D; Riedler, J; Waser, M; Sennhauser, FH				Lauener, RP; Birchler, T; Adamski, J; Braun-Fahrlander, C; Bufe, A; Herz, U; von Mutius, E; Nowak, D; Riedler, J; Waser, M; Sennhauser, FH		ALEX Study Grp	Expression of CD14 and Toll-like receptor 2 in farmers' and nonfarmers' children	LANCET			English	Article							ASTHMA	Children of farmers are at decreased risk of developing allergies. Results of epidemiological studies suggest increased exposure to microbial compounds might be responsible for this reduced risk. Alterations in adaptive immune response are thought to be the underlying mechanism. We measured expression of receptors for microbial compounds known to trigger the innate immune response. We showed that blood cells from farmers' children express significantly higher amounts of CD14 (0.96 vs 0.43, p = 0.0013), and Toll-like receptor 2 (0.11 vs 0.04, p < 0.0001) than those from nonfarmers' children. We propose that the innate immune system responds to the microbial burden in the environment and modulates the development of allergic disease.	Univ Zurich, Childrens Hosp, CH-8032 Zurich, Switzerland; Univ Basel, Inst Social & Prevent Med, CH-4003 Basel, Switzerland; Ruhr Univ Bochum, D-4630 Bochum, Germany; Hosp Philipps Univ, Marburg, Germany; Univ Munich, Dr von Hauner Childrens Hosp, D-80539 Munich, Germany; Univ Munich, Inst Occupat & Environm Med, D-80539 Munich, Germany; Childrens Hosp Salzburg, Salzburg, Austria	Lauener, RP (reprint author), Univ Zurich, Childrens Hosp, CH-8032 Zurich, Switzerland.		Lauener, Roger/O-8612-2016	Lauener, Roger/0000-0002-8412-606X			Akira S, 2001, NAT IMMUNOL, V2, P675, DOI 10.1038/90609; Flo TH, 2001, J LEUKOCYTE BIOL, V69, P474; Martin P, 1999, APPL MICROW WIREL, V11, P12; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3	5	191	196	0	8	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	AUG 10	2002	360	9331					465	466		10.1016/S0140-6736(02)09641-1		2	Medicine, General & Internal	General & Internal Medicine	582GZ	WOS:000177342900018	12241724	
J	Kroes, R; Muller, D; Lambe, J; Lowik, MRH; van Klaveren, J; Kleiner, J; Massey, R; Mayer, S; Urieta, I; Verger, P; Visconti, A				Kroes, R; Muller, D; Lambe, J; Lowik, MRH; van Klaveren, J; Kleiner, J; Massey, R; Mayer, S; Urieta, I; Verger, P; Visconti, A			Assessment of intake from the diet	FOOD AND CHEMICAL TOXICOLOGY			English	Review						exposure assessments; risk assessment; food consumption; concentration of chemicals in food; probabilistic modelling	SUBCUTANEOUS ADIPOSE-TISSUE; TERM EXPOSURE DISTRIBUTIONS; VETERINARY DRUG RESIDUES; HEALTH-RISK ASSESSMENT; HABITUAL FOOD-INTAKE; NUTRIENT INTAKE; FATTY-ACIDS; HUMAN-URINE; VITAMIN-E; PLASMA-CONCENTRATIONS	Exposure assessment is one of the key parts of the risk assessment process. Only intake of toxicologically significant amounts can lead to adverse health effects even for a relatively toxic substance. In the case of chemicals in foods this is based on three major aspects: (i) how to determine quantitatively the presence of a chemical in individual foods and diets, including its fate during the processes within the food production chains 60 how to determine the consumption patterns of the individual foods containing the relevant chemicals, (iii) how to integrate both the likelihood of consumers eating large amounts of the given foods and of the relevant chemical being present in these foods at high levels. The techniques used for the evaluation of these three aspects have been critically reviewed in this paper to determine those areas where the current approaches provide a solid basis for assessments and those areas here improvements are needed or desirable. For those latter areas, options for improvements are being suggested, including. for example, the development of a pan-European food composition database, activities to understand better effects of processing on individual food chemicals, harmonisation of food consumption survey methods with the option of a regular pan-European survey, evaluation of probabilistic models and the development of models to assess exposure to food allergens. In all three areas, the limitations of the approaches currently used lead to uncertainties which can either cause an over- or underestimation of real intakes and thus risks, Given these imprecisions, risk assessors tend to build in additional uncertainty factors to avoid health-relevant underestimates. This is partly done by using screening methods designed to look for "worst case" situations. Such worse case assumptions lead to intake estimates that are higher than reality. These screening methods are used to screen all those chemicals with a safe intake distribution. For chemicals with a potential risk, more information is needed to allow more refined screening or even the most accurate estimation. More information and more refined methods however. require more resources. The ultimate aims are: (1) to obtain appropriate estimations for the presence and quantity of a given chemical in a food and in the diet in general: (2) to assess the consumption patterns for the foods containing these Substances, including especially those parts of the population with high consumption and thus potentially high intakes: and (3) to develop and apply tools to predict reliably the likelihood of high end consumption with the presence of high levels of the relevant substances, It has thus been demonstrated that a tiered approach at all three steps can be helpful to optimise the use of the available resources: if relatively crude tools - designed to provide a "worst case" estimate - do not suggest a toxicologically significant exposure (or a relevant deficit of a particular nutrient) it may not be necessary to use more sophisticated tools. These ill be needed if initially high intakes are indicated for at least parts of the Population, Existing pragmatic approaches are a first crude step to model food chemical intake. It is recommended to extend. refine and validate this approach in the near future. This has to result in a cost-effective exposure assessment system to be used for existing and potential categories of chemicals. This system of knowledge (with information on sensitivities. accuracy, etc.) will guide future data collection. (C) 2002 ILSL Published by Elsevier Science Ltd All rights reserved.	Int Life Sci Inst, European Branch, B-1200 Brussels, Belgium; Univ Utrecht, Fac Vet Med, Inst Risk Assessment Sci, NL-3508 TD Utrecht, Netherlands; Procter & Gamble Serv GmbH, D-65823 Schwabach, Germany; Univ Dublin Trinity Coll, Inst European Food Studies, Inst Biotechnol, IRL, Dublin 2, Ireland; TNO, Nutr & Food Res Inst, Dept Nutr Epidemiol, NL-3700 AJ Zeist, Netherlands; DLO, RIKILT, NL-6700 AE Wageningen, Netherlands; CSL, Cent Sci Lab, York YO41 1LZ, N Yorkshire, England; Red Bull GmbH, A-5330 Fuschl Am See, Austria; Gobierno Vasco, Dept Hlth, E-48010 Bilbao, Spain; INRA, Nutr Humaine & Securite Alimentaire, F-75338 Paris 07, France; CNR, Ist Tossine & Micotossine Parassiti Vegetali, I-70126 Bari, Italy	Kleiner, J (reprint author), Int Life Sci Inst, European Branch, 83 Ave E Mounier,Box 6, B-1200 Brussels, Belgium.						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Toxicol.	FEB-MAR	2002	40	2-3					327	385	PII S0278-6915(01)00113-2	10.1016/S0278-6915(01)00113-2		59	Food Science & Technology; Toxicology	Food Science & Technology; Toxicology	543LA	WOS:000175102400007	11893401	
J	Burke, H; Leonardi-Bee, J; Hashim, A; Pine-Abata, H; Chen, YL; Cook, DG; Britton, JR; McKeever, TM				Burke, Hannah; Leonardi-Bee, Jo; Hashim, Ahmed; Pine-Abata, Hembadoon; Chen, Yilu; Cook, Derek G.; Britton, John R.; McKeever, Tricia M.			Prenatal and Passive Smoke Exposure and Incidence of Asthma and Wheeze: Systematic Review and Meta-analysis	PEDIATRICS			English	Review						asthma; wheeze; passive smoking exposure; meta-analysis	PROSPECTIVE BIRTH COHORT; ENVIRONMENTAL TOBACCO-SMOKE; BODY-MASS INDEX; MATERNAL SMOKING; EARLY-CHILDHOOD; RISK-FACTORS; PARENTAL SMOKING; 1ST YEAR; ATOPIC-DERMATITIS; SOCIOECONOMIC-STATUS	OBJECTIVES: Exposure to passive smoke is a common and avoidable risk factor for wheeze and asthma in children. Substantial growth in the prospective cohort study evidence base provides an opportunity to generate new and more detailed estimates of the magnitude of the effect. A systematic review and meta-analysis was conducted to provide estimates of the prospective effect of smoking by parents or household members on the risk of wheeze and asthma at different stages of childhood. METHODS: We systematically searched Medline, Embase, and conference abstracts to identify cohort studies of the incidence of asthma or wheeze in relation to exposure to prenatal or postnatal maternal, paternal, or household smoking in subjects aged up to 18 years old. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were estimated by using random effects model. RESULTS: We identified 79 prospective studies. Exposure to pre-or postnatal passive smoke exposure was associated with a 30% to 70% increased risk of incident wheezing (strongest effect from postnatal maternal smoking on wheeze in children aged <= 2 years, OR = 1.70, 95% CI = 1.24-2.35, 4 studies) and a 21% to 85% increase in incident asthma (strongest effect from prenatal maternal smoking on asthma in children aged <= 2 years, OR = 1.85, 95% CI = 1.35-2.53, 5 studies). CONCLUSIONS: Building upon previous findings, exposure to passive smoking increases the incidence of wheeze and asthma in children and young people by at least 20%. Preventing parental smoking is crucially important to the prevention of asthma. Pediatrics 2012;129:735-744	[Burke, Hannah; Leonardi-Bee, Jo; Hashim, Ahmed; Pine-Abata, Hembadoon; Chen, Yilu; Britton, John R.; McKeever, Tricia M.] Univ Nottingham, City Hosp, Div Epidemiol & Publ Hlth, UK Ctr Tobacco Control Studies, Nottingham NG5 1PB, England; [Cook, Derek G.] St Georges Univ London, Div Populat Hlth Sci & Educ, London, England	McKeever, TM (reprint author), Univ Nottingham, City Hosp, Div Epidemiol & Publ Hlth, UK Ctr Tobacco Control Studies, Nottingham NG5 1PB, England.	tricia.mckeever@nottingham.ac.uk	Britton, John/G-9705-2011; Cook, Derek/C-3271-2008	McKeever, Tricia/0000-0003-0914-0416	Cancer Research UK [C1512/A11160]; British Heart Foundation; Economic and Social Research Council; Medical Research Council; Department of Health under UK Clinical Research Collaboration; UK Clinical Research Collaboration	Supported by project grant C1512/A11160 from Cancer Research UK and by core funding to the UK Centre for Tobacco Control Studies (http://www.ukctcs.org) from the British Heart Foundation, Cancer Research UK, Economic and Social Research Council, Medical Research Council, and the Department of Health, under the auspices of the UK Clinical Research Collaboration.	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J	Barnes, PJ; Dweik, RA; Gelb, AF; Gibson, PG; George, SC; Grasemann, H; Pavord, ID; Ratjen, F; Silkoff, PE; Taylor, DR; Zamel, N				Barnes, Peter J.; Dweik, Raed A.; Gelb, Arthur F.; Gibson, Peter G.; George, Steven C.; Grasemann, Hartmut; Pavord, Ian D.; Ratjen, Felix; Silkoff, Philip E.; Taylor, D. Robin; Zamel, Noe			Exhaled Nitric Oxide in Pulmonary Diseases A Comprehensive Review	CHEST			English	Review							RANDOMIZED CONTROLLED-TRIAL; EOSINOPHILIC AIRWAY INFLAMMATION; DOSE-RESPONSE RELATIONSHIP; CYSTIC-FIBROSIS; AXIAL DIFFUSION; ASTHMATIC-PATIENTS; HEALTHY-VOLUNTEERS; EXCHANGE DYNAMICS; CHILDHOOD ASTHMA; REFERENCE VALUES	The upregulation of nitric oxide (NO) by inflammatory cytokines and mediators in central and peripheral airway sites can be monitored easily in exhaled air. It is now possible to estimate the predominant site of increased fraction of exhaled NO (FENO) and its potential pathologic and physiologic role in various pulmonary diseases. In asthma, increased FENO reflects eosinophilic-mediated inflammatory pathways moderately well in central and/or peripheral airway sites and implies increased inhaled and systemic corticosteroid responsiveness. Recently, five randomized controlled algorithm asthma trials reported only equivocal benefits of adding measurements of FENO to usual clinical guideline management including spirometry; however, significant design issues may exist. Overall, FENO measurement at a single expiratory flow rate of 50 mL/s may be an important adjunct for diagnosis and management in selected cases of asthma. This may supplement standard clinical asthma care guidelines, including spirometry, providing a noninvasive window into predominantly large-airway-presumed eosinophilic inflammation. In COPD, large/central airway maximal NO flux and peripheral/small airway/alveolar NO concentration may be normal and the role of FENO monitoring is less clear and therefore less established than in asthma. Furthermore, concurrent smoking reduces FENO. Monitoring FENO in pulmonary hypertension and cystic fibrosis has opened up a window to the role NO may play in their pathogenesis and possible clinical benefits in the management of these diseases. CHEST 2010; 138(3):682-692	[Barnes, Peter J.] Univ London Imperial Coll Sci Technol & Med, Airway Dis Sect, Natl Heart & Lung Inst, London, England; [Pavord, Ian D.] Glenfield Hosp, Univ Hosp Leicester Trust, Dept Resp Med Allergy & Thorac Surg, Leicester, Leics, England; [Dweik, Raed A.] Cleveland Clin Fdn, Div Pulm, Dept Med, Cleveland, OH 44195 USA; [Gelb, Arthur F.] Lakewood Reg Med Ctr, Div Pulm, Dept Med, Lakewood, CA USA; [Gelb, Arthur F.] UCLA Med Ctr, Geffen Sch Med, Los Angeles, CA USA; [George, Steven C.] Univ Calif Irvine, Dept Biomed Engn & Chem Engn & Mat Sci, Irvine, CA USA; [Gibson, Peter G.] John Hunter Hosp, Woolcock Inst Med Res, Dept Resp & Sleep Med, New Lambton, NSW, Australia; [Grasemann, Hartmut; Ratjen, Felix] Hosp Sick Children, Div Resp Med, Dept Pediat & Physiol, Toronto, ON M5G 1X8, Canada; Hosp Sick Children, Res Inst, Expt Med Program, Toronto, ON M5G 1X8, Canada; [Zamel, Noe] Univ Toronto, Sch Med, Div Resp, Toronto, ON, Canada; [Silkoff, Philip E.] Drexel Univ, Div Pulm, Sch Med, Philadelphia, PA 19104 USA; [Taylor, D. Robin] Univ Otago, Dunedin Sch Med, Dunedin, New Zealand	Gelb, AF (reprint author), 3650 E South St,Ste 308, Lakewood, CA 90712 USA.	afgelb@msn.com	George, Steven/K-9359-2015	George, Steven/0000-0003-2263-1914; silkoff, philip/0000-0001-6018-5199; Pavord, Ian/0000-0002-4288-5973	GE Analytical Instruments, Inc.; Aperion Inc.; Aerocrine, Ltd.; Aerocrine, Ltd. Sweden	The authors have reported to CHEST the following conflicts of interest: Dr George has patents issued and pending that have been licensed in the past by Aerocrine, Ltd., Sweden, and have resulted in royalties. His employer, University of California, Irvine, has received NO analyzers as gifts from Aerocrine, Ltd., and currently holds the rights to the patents. Dr Silkoff has received royalties ($2,000/year) from patents that are currently licensed to GE Analytical Instruments, Inc, and Aperion.ine, manufacturers of exhaled NO monitors. He has also received consultant fees ($10,000) from GE Analytical Instruments, Inc, Aperion Inc, and Aerocrine, Ltd. He anticipates being involved in patent litigation related to measurement of exhaled NO. Dr Zamel has received royalties ($2,000/year) from patents that are currentlylicensed to Aerocrine, Ltd. and Aperion Inc, manufacturers of exhaled NO monitors. Dr Taylor has received research funding ($25,000) and lecture fees ($2,000) from Aerocrine, Ltd., Sweden. Drs Barnes, Dweik, Gelb, Gibson Grasemann, Pavord, and Ratjen have reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.	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J	Robinson, DS; Larche, M; Durham, SR				Robinson, DS; Larche, M; Durham, SR			Tregs and allergic disease	JOURNAL OF CLINICAL INVESTIGATION			English	Review							REGULATORY T-CELLS; GRASS-POLLEN IMMUNOTHERAPY; IMMUNOLOGICAL SELF-TOLERANCE; LATE ASTHMATIC REACTIONS; COWS MILK ALLERGY; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; TRANSCRIPTION FACTOR FOXP3; MYELIN BASIC-PROTEIN; HOUSE-DUST MITE; IN-VITRO	Allergic diseases such as asthma, rhinitis, and eczema are increasing in prevalence and affect up to 15% of populations in Westernized countries. The description of Tregs as T cells that prevent development of autoinumme disease led to considerable interest in whether these Tregs were also normally involved in prevention of sensitization to allergens and whether it might be possible to manipulate Tregs for the therapy of allergic disease. Current data suggest that Th2 responses to allergens are normally suppressed by both CD4(+)CD25(+) Tregs and IL-10 Tregs. Furthermore, suppression by these subsets is decreased in allergic individuals. In animal models, Tregs could be induced by high- or low-dose inhaled antigen, and prior induction of such Tregs prevented subsequent development of allergen sensitization and airway inflammation in inhaled challenge models. For many years, allergen-injection immunotherapy has been used for the therapy of allergic disease, and this treatment may induce IL-10 Tregs, leading to both suppression of Th2 responses and a switch from IgE to IgG4 antibody production. Improvements in allergen immunotherapy, such as peptide therapy, and greater understanding of the biology of Tregs hold great promise for the treatment and prevention of allergic disease.	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Clin. Invest.	NOV	2004	114	10					1389	1397		10.1172/JCI200423595		9	Medicine, Research & Experimental	Research & Experimental Medicine	871EU	WOS:000225113200005	15545986	
J	Avery, NJ; King, RM; Knight, S; Hourihane, JO				Avery, NJ; King, RM; Knight, S; Hourihane, JO			Assessment of quality of life in children with peanut allergy	PEDIATRIC ALLERGY AND IMMUNOLOGY			English	Article						quality of life; peanut allergy; children		Children with a peanut allergy (PA) are faced with food and social restrictions due to the potentially life-threatening nature of their disease, for which there is no cure or treatment. This inevitably impacts upon their quality of life (QoL). QoL of 20 children with PA and 20 children with insulin-dependent diabetes mellitus (IDDM) was measured using two disease-specific QoL questionnaires (higher scores correspond to a poorer QoL). One questionnaire was designed by us and the other was adapted from the Vespid Allergy QoL questionnaire. We gave subjects cameras to record how their QoL is affected over a 24-h period. Response rates for both questionnaires were 100%. Mean ages were 9.0 and 10.4 years for PA and IDDM subjects, respectively. Children with a PA reported a poorer quality of life than children with IDDM: mean scores were 54.85 for PA subjects and 46.40 for diabetics (p = 0.004) in questionnaire 1 and 54.30 and 34.50 (pless than or equal to0.001) in questionnaire 2. PA children reported more fear of an adverse event and more anxiety about eating, especially when eating away from home. Photographs fell into seven common categories: food, management, environment, away from home, physical activities, restaurant and people. Most photographs related to food and management issues and revealed difficulties for both groups regarding food restrictions. PA subjects felt more threatened by potential hazards within their environment, felt more restricted by their PA regarding physical activities, and worried more about being away from home. However, they felt safe when carrying epinephrine kits and were positive about eating at familiar restaurants. The QoL in children with PA is more impaired than in children with IDDM. Their anxiety may be considered useful in some situations, promoting better adherence to allergen avoidance advice and rescue plans.	Univ Southampton, Div Infect Inflammat & Repair, Southampton, Hants, England; Southampton Univ Hosp NHS Trust, Wellcome Trust Clin Res Facil, Southampton, Hants, England; Southampton Univ Hosp NHS Trust, Dept Psychol, Southampton, Hants, England	Hourihane, JO (reprint author), Univ Southampton, Southampton Univ Hosp NHS Trust, Div Infect Inflammat & Repair, Mailpoint 218,Tremona Rd, Southampton S016 6YD, Hants, England.						Bock SA, 2001, J ALLERGY CLIN IMMUN, V107, P191, DOI 10.1067/mai.2001.112031; Elberink JNGO, 2002, J ALLERGY CLIN IMMUN, V109, P162, DOI 10.1067/mai.2002.120552; Elberink JNGO, 2002, J ALLERGY CLIN IMMUN, V110, P174, DOI 10.1067/mai.2002.125827; Gardiner P., 1997, PRACTICAL DIABETES I, V14, P43, DOI 10.1002/(ISSN)1528-252X; Hourihane JO, 2002, CURR OPIN ALLERGY CL, V2, P227, DOI 10.1097/00130832-200206000-00012; McCabe M, 2001, LANCET, V357, P1531, DOI 10.1016/S0140-6736(00)04687-0; 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; Sicherer SH, 2001, ANN ALLERG ASTHMA IM, V87, P461; Sicherer SH, 2001, J ALLERGY CLIN IMMUN, V108, P128, DOI 10.1067/mai.2001.115755; Thompson AK, 2000, ANN ALLERG ASTHMA IM, V85, P338; Vander Leek TK, 2000, J PEDIATR-US, V137, P749, DOI 10.1067/mpd.2000.109376	12	190	191	5	27	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0905-6157			PEDIATR ALLERGY IMMU	Pediatr. Allergy Immunol.	OCT	2003	14	5					378	382		10.1034/j.1399-3038.2003.00072.x		5	Allergy; Immunology; Pediatrics	Allergy; Immunology; Pediatrics	736JR	WOS:000186168100007	14641608	
J	Devereux, G; Barker, RN; Seaton, A				Devereux, G; Barker, RN; Seaton, A			Antenatal determinants of neonatal immune responses to allergens	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						atopy; T helper cells; antenatal influences; smoking; birth order; vitamin E	CELL PROLIFERATIVE RESPONSES; UMBILICAL-CORD BLOOD; HOUSE-DUST-MITE; RESPIRATORY SYMPTOMS; ABERDEEN SCHOOLCHILDREN; ASTHMA; ATOPY; GAMMA; LIFE; RESPONSIVENESS	Background The environmental factors responsible for recent increases in the prevalence of asthma and atopic disease have been assumed to act after birth. Their possible effects on fetal immune development in utero have not been investigated systematically, although sensitization to allergens may occur before birth. Objective This prospective study determined whether the risk factors for asthma and atopic disease, namely family history of atopic disease, maternal smoking, birth order, or maternal dietary intake of antioxidant vitamins, exert antenatal effects on the fetal immune system that may predispose to childhood atopy. Methods The T helper (Th) cell proliferative responses of cord blood mononuclear cells (CBMC) from a sample of 223 neonates, representative of children born to a cohort of 2000 pregnant women, were measured and related to family, maternal and environmental factors associated with the pregnancy. Results The magnitude of CBMC-proliferative responses to allergens increased significantly in association with a family history of atopic disease or maternal smoking, and decreased significantly with increasing birth order and high maternal dietary intake of vitamin E. The epidemiological association between birth order and atopy may therefore be a consequence of antenatal influences rather than of protective effects of childhood infections. The association between maternal intake of vitamin E and CBMC responsiveness suggests that diet during pregnancy may influence the fetal immune system in such a way as to modulate the risk of childhood atopy. Conclusion These results provide a new insight into the aetiology of atopic disease by demonstrating that the maternal environmental risk factors for atopy, diet, birth order and smoking, influence the development of the fetal immune system. This raises the prospect of preventative public health interventions during pregnancy.	Univ Aberdeen, Sch Med, Dept Environm & Occupat Med, Aberdeen AB25 2ZD, Scotland; Univ Aberdeen, Sch Med, Dept Med & Therapeut, Aberdeen AB25 2ZD, Scotland	Seaton, A (reprint author), Univ Aberdeen, Sch Med, Dept Environm & Occupat Med, Aberdeen AB25 2ZD, Scotland.		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Exp. Allergy	JAN	2002	32	1					43	50		10.1046/j.0022-0477.2001.01267.x		8	Allergy; Immunology	Allergy; Immunology	525GV	WOS:000174061300008	12002736	
J	Maddox, L; Schwartz, DA				Maddox, L; Schwartz, DA			The pathophysiology of asthma	ANNUAL REVIEW OF MEDICINE			English	Review						atopy; cytokines; Th-2 cells; airway obstruction; bronchial hyperreactivity; lungs	GENOME-WIDE SEARCH; ENDOTOXIN EXPOSURE-RESPONSE; ALLERGEN-SPECIFIC TH1; RI-BETA GENE; BRONCHIAL HYPERRESPONSIVENESS; BETA(2)-ADRENERGIC RECEPTOR; INNATE IMMUNITY; SEGREGATION ANALYSIS; ATOPIC ASTHMA; COTTON DUST	Asthma is a chronic disorder of the airways that is characterized by reversible airflow obstruction and airway inflammation, persistent airway hyper-reactivity, and airway remodeling. The etiology of asthma is complex and multifactorial. Recent advances have demonstrated the importance of genetics in the development of asthma, particularly atopic asthma. Environmental stimuli, particularly early childhood infections, have also been associated with the development of asthma. Most current data seem to suggest that these factors drive the development of a Th-2 lymphocyte-predominant immune response, which has been associated with atopy and IgE-mediated inflammation. The concept of reversible airflow obstruction has also recently been challenged. It is now clear that chronic airway changes occur, which may contribute to progressive airflow obstruction. We discuss the important influence of genetic and environmental factors on the emergence of the asthmatic phenotype. The significance of Th-1 and Th-2 lymphocyte-mediated immunity are discussed, and the inflammatory processes leading to chronic airway inflammation are detailed.	Duke Univ, Med Ctr, Div Pulm & Crit Care, Durham, NC 27710 USA	Maddox, L (reprint author), Duke Univ, Med Ctr, Div Pulm & Crit Care, Res Dr, Durham, NC 27710 USA.				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J	Dayan, AD; Paine, AJ				Dayan, AD; Paine, AJ			Mechanisms of chromium toxicity, carcinogenicity and allergenicity: Review of the literature from 1985 to 2000	HUMAN & EXPERIMENTAL TOXICOLOGY			English	Review						chromium; toxicity; allergenicity; carcinogenicity; genotoxicity; biochemical mechanisms	SINGLE-STRAND BREAKS; HEXAVALENT CHROMIUM; ALVEOLAR MACROPHAGES; ASCORBIC-ACID; CROSS-LINKS; DNA-DAMAGE; IN-VITRO; REDUCTION; GLUTATHIONE; EXPOSURE	Laboratory and clinical reports about the pathogenesis of the carcinogenicity and allergenicity of chromium compounds published between 1985 and 2000 have been reviewed as a basis for consideration of the pathogenetic mechanisms involved. There is good evidence from the clinic and the laboratory that Cr[VI] is the ion responsible for most of the toxic actions, although much of the underlying molecular damage may be due to its intracellular reduction to the even more highly reactive and short-lived chemical species Cr[III] and Cr[V]. Exposure to Cr[VI] can result in various point mutations in DNA and to chromosomal damage, as well as to oxidative changes in proteins and to adduct formation. The relative importance of these effects of chromium ions and of the free oxidising radicals they may generate in the body in causing tumours and allergic sensitisation remain to be demonstrated. Biochemical studies of the DNA-damaging effects and of the pathogenesis of the allergic reactions to chromium ions have not kept up with advances in understanding of the molecular basis of the effects of other carcinogens and allergens.	Kings Coll London, Dept Pharm, IRG Toxicol, London SE1 9NN, England	Paine, AJ (reprint author), Kings Coll London, Dept Pharm, IRG Toxicol, Franklin Wilkins Bldg,150 Stamford St, London SE1 9NN, England.						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Exp. Toxicol.	SEP	2001	20	9					439	451		10.1191/096032701682693062		13	Toxicology	Toxicology	501DE	WOS:000172666900001	11776406	
J	Underwood, DC; Osborn, RR; Bochnowicz, S; Webb, EF; Rieman, DJ; Lee, JC; Romanic, AM; Adams, JL; Hay, DWP; Griswold, DE				Underwood, DC; Osborn, RR; Bochnowicz, S; Webb, EF; Rieman, DJ; Lee, JC; Romanic, AM; Adams, JL; Hay, DWP; Griswold, DE			SB 239063, a p38 MAPK inhibitor, reduces neutrophilia, inflammatory cytokines, MMP-9, and fibrosis in lung	AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY			English	Article						chronic obstructive pulmonary disease; interleukin-6; bleomycin; alveolar macrophage; mitogen-activated protein kinase; matrix metalloproteinase-9	OBSTRUCTIVE PULMONARY-DISEASE; ACTIVATED PROTEIN-KINASE; COR-PULMONALE; ASTHMA; PATHOPHYSIOLOGY; INTERLEUKIN-6; EXPRESSION; MACROPHAGE; RELEASE; STRESS	The effects of a second generation p38 mitogen-activated protein kinase (MAPK) inhibitor, SB 239063 [trans-1-(4-hydroxycyclohexyl)-4-(4-fluorophenyl)-5-(2-methoxypyridimidin-4-yl) imidazole; IC50 = 44 nM vs. p38 alpha], were assessed in models that represent different pathological aspects of chronic obstructive pulmonary disease (COPD) [airway neutrophilia, enhanced cytokine formation and increased matrix metalloproteinase (MMP)-9 activity] and in a model of lung fibrosis. Airway neutrophil infiltration and interleukin (IL)-6 levels, assessed by bronchoalveolar lavage 48 h after lipopolysaccharide (LPS) inhalation, were inhibited dose dependently by 3-30 mg/kg of SB 239063 given orally twice a day. In addition, SB 239063 (30 mg/kg orally) attenuated IL-6 bronchoalveolar lavage fluid concentrations (>90% inhibition) and MMP-9 activity (64% inhibition) assessed 6 h after LPS exposure. In guinea pig cultured alveolar macrophages, SB 239063 inhibited LPS-induced IL-6 production (IC50 of 362 nM). In a bleomycin-induced pulmonary fibrosis model in rats, treatment with SB 239063 (2.4 or 4.8 mg/day via osmotic pump) significantly inhibited bleomycin-induced right ventricular hypertrophy (indicative of secondary pulmonary hypertension) and increases in lung hydroxyproline synthesis (indicative of collagen synthesis and fibrosis). Therefore, SB 239063 demonstrates activity against a range of sequelae commonly associated with COPD and fibrosis, supporting the therapeutic potential of p38 MAPK inhibitors such as SB 239063 in chronic airway disease.	SmithKline Beecham Pharmaceut, Dept Pulm Pharmacol, King Of Prussia, PA 19406 USA; SmithKline Beecham Pharmaceut, Dept Bone & Cartilage Biol, King Of Prussia, PA 19406 USA; SmithKline Beecham Pharmaceut, Dept Cardiovasc Biol, King Of Prussia, PA 19406 USA; SmithKline Beecham Pharmaceut, Dept Med Chem, King Of Prussia, PA 19406 USA	Underwood, DC (reprint author), SmithKline Beecham Pharmaceut, Dept Pulm Pharmacol, UW2532,709 Swedeland Rd, King Of Prussia, PA 19406 USA.						Barnes PJ, 1999, AM J RESP CRIT CARE, V160, pS72; Barnes PJ, 1998, THORAX, V53, P137; Barnes PJ, 1998, PHARMACOL REV, V50, P515; Bochnowicz S, 2000, CLIN EXP HYPERTENS, V22, P471, DOI 10.1081/CEH-100100085; Cuzzocrea S, 1999, J LEUKOCYTE BIOL, V66, P471; Elias JA, 1999, J CLIN INVEST, V104, P1001, DOI 10.1172/JCI8124; Foltz IN, 1997, J BIOL CHEM, V272, P3296; Force T, 1999, GENE EXPRESSION, V7, P337; Griswold DE, 1996, PHARM COMMUN, V7, P323; Hashimoto S, 1999, AM J RESP CRIT CARE, V159, P634; HUNNINGHAKE GW, 1983, AM REV RESPIR DIS, V128, P833; HUTCHINS D, 1994, INT J CANCER, V58, P80, DOI 10.1002/ijc.2910580114; Jeffery PK, 1999, CLIN EXP ALLERGY, V29, P14, DOI 10.1046/j.1365-2222.1999.00004.x-i2; JEFFERY PK, 1994, AM J RESP CRIT CARE, V150, pS6; Johnson JL, 1998, J SURG RES, V76, P91, DOI 10.1006/jsre.1998.5295; Johnson S, 1999, AM J PHYSIOL-LUNG C, V277, pL1109; Kankaanranta H, 1999, J PHARMACOL EXP THER, V290, P621; Kuhn C, 2000, AM J RESP CELL MOL, V22, P289; Lee JC, 1999, PHARMACOL THERAPEUT, V82, P389, DOI 10.1016/S0163-7258(99)00008-X; Lee JC, 2000, IMMUNOPHARMACOLOGY, V47, P185, DOI 10.1016/S0162-3109(00)00206-X; Liou TG, 1996, J IMMUNOL, V157, P2624; MACNEE W, 1994, AM J RESP CRIT CARE, V150, P833; MACNEE W, 1994, AM J RESP CRIT CARE, V150, P1158; OLIVERA DL, 1992, CIRC SHOCK, V37, P301; Scott PH, 1998, AM J RESP CRIT CARE, V158, P958; Shapiro SD, 1999, AM J RESP CRIT CARE, V160, pS29; Simon C, 1998, CANCER RES, V58, P1135; SMITH RE, 1994, J IMMUNOL, V153, P4704; Tamura DY, 1998, SURGERY, V124, P403, DOI 10.1067/msy.1998.90483; Underwood DC, 2000, J PHARMACOL EXP THER, V293, P281; Underwood DC, 1996, AM J RESP CRIT CARE, V154, P850; Wanner A, 1999, AM J RESP CRIT CARE, V160, pS1	32	190	202	0	10	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.	NOV	2000	279	5					L895	L902				8	Physiology; Respiratory System	Physiology; Respiratory System	367HT	WOS:000090056200015	11053025	
J	Horwell, CJ; Baxter, PJ				Horwell, Claire J.; Baxter, Peter J.			The respiratory health hazards of volcanic ash: a review for volcanic risk mitigation	BULLETIN OF VOLCANOLOGY			English	Review						volcanic ash; respiratory; health; hazard; risk mitigation; review	MOUNT-ST-HELENS; SOUFRIERE HILLS VOLCANO; BRITISH-WEST-INDIES; PARTICULATE AIR-POLLUTION; PULMONARY TOXICITY; NEW-ZEALAND; CRYSTALLINE SILICA; LUNG-FUNCTION; MONTSERRAT; ERUPTION	Studies of the respiratory health effects of different types of volcanic ash have been undertaken only in the last 40 years, and mostly since the eruption of Mt. St. Helens in 1980. This review of all published clinical, epidemiological and toxicological studies, and other work known to the authors up to and including 2005, highlights the sparseness of studies on acute health effects after eruptions and the complexity of evaluating the long-term health risk (silicosis, non-specific pneumoconiosis and chronic obstructive pulmonary disease) in populations from prolonged exposure to ash due to persistent eruptive activity. The acute and chronic health effects of volcanic ash depend upon particle size (particularly the proportion of respirable-sized material), mineralogical composition (including the crystalline silica content) and the physicochemical properties of the surfaces of the ash particles, all of which vary between volcanoes and even eruptions of the same volcano, but adequate information on these key characteristics is not reported for most eruptions. The incidence of acute respiratory symptoms (e.g. asthma, bronchitis) varies greatly after ashfalls, from very few, if any, reported cases to population outbreaks of asthma. The studies are inadequate for excluding increases in acute respiratory mortality after eruptions. Individuals with preexisting lung disease, including asthma, can be at increased risk of their symptoms being exacerbated after falls of fine ash. A comprehensive risk assessment, including toxicological studies, to determine the long-term risk of silicosis from chronic exposure to volcanic ash, has been under-taken only in the eruptions of Mt. St. Helens (1980), USA, and Soufriere Hills, Montserrat (1995 onwards). In the Soufriere Hills eruption, a long-term silicosis hazard has been identified and sufficient exposure and toxicological information obtained to make a probabilistic risk assessment for the development of silicosis in outdoor workers and the general population. A more systematic approach to multi-disciplinary studies in future eruptions is recommended, including establishing an archive of ash samples and a website containing health advice for the public, together with scientific and medical study guidelines for volcanologists and health-care workers.	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Volcanol.	JUL	2006	69	1					1	24		10.1007/s00445-006-0052-y		24	Geosciences, Multidisciplinary	Geology	078MK	WOS:000240107700001		
J	Custovic, A; Simpson, BM; Simpson, A; Kissen, P; Woodcock, A				Custovic, A; Simpson, BM; Simpson, A; Kissen, P; Woodcock, A		NAC Manchester Asthma Allergy Stud	Effect of environmental manipulation in pregnancy and early life on respiratory symptoms and atopy during first year of life: a randomised trial	LANCET			English	Article							ALLERGEN AVOIDANCE; CONFIDENCE-INTERVALS; EARLY EXPOSURE; RISK FACTOR; ASTHMA; SENSITIZATION; CHILDREN; INFANCY; CAT; MITE	Background Asthma places huge demands on healthcare services, and its prevalence is increasing. Reduction of exposure to environmental allergens could offer a realistic chance for primary prevention. Our aim was to ascertain whether or not living in a low-allergen environment reduces the risk of asthma and atopic diseases in infants. Methods We assigned infants to four risk groups according to parental atopic status. We enrolled 291 high-risk couples (both parents atopic, no pets) into a prospective, prenatally randomised, cohort study, and allocated them to environmental manipulation, in which measures to reduce prenatal and postnatal allergen exposure were undertaken (active HRA) (n=145) or no intervention (control HRC) (n=146). Two further prospective groups were studied: 161 high-risk infants with pets in the home (HRP group) and 168 low-risk infants, whose parents were both non-atopic (LR group). The main outcome measures were signs and symptoms of atopic disease at 1 year of age. Findings 103 families dropped out or were lost to follow up. At age 1 year we followed-up 133 HRA, 118 HRC, 140 HRP, and 126 LR infants. Children in the HRA group were less likely to have respiratory symptoms during the first year of life than those in the HRC group. The most pronounced differences were in the relative risks for severe wheeze with shortness of breath (relative risk 0.44 [95% CI 0.20-1.00]), prescribed medication for the treatment of wheezy attacks (0.58 [0.36-0.95]), and wheezing after vigorous playing, crying, or exertion (0.18 [0.04-0.79]). Probability of respiratory symptoms in HRC and HRP infants was similar, whereas it was much lower in the LR than in the HRC group. Cat ownership was significantly associated with sensitisation to cats (24.6 [3.04-199.05]; p=0.003). Interpretation Environmental manipulation reduces some respiratory symptoms in the first year of life in high-risk infants. Further follow up is needed, however, to ascertain whether living in a low-allergen environment reduces allergy and asthma in later life.	Wythenshawe Hosp, NW Lung Ctr, Manchester M23 9LT, Lancs, England	Woodcock, A (reprint author), Wythenshawe Hosp, NW Lung Ctr, Manchester M23 9LT, Lancs, England.		Custovic, Adnan/A-2435-2012	Custovic, Adnan/0000-0001-5218-7071; Woodcock, Ashley/0000-0002-5428-8578; Simpson, Angela/0000-0003-2733-6666			ARSHAD SH, 1992, LANCET, V339, P1493, DOI 10.1016/0140-6736(92)91260-F; BULPITT CJ, 1987, LANCET, V1, P494; Burr ML, 1997, CLIN EXP ALLERGY, V27, P1247; Custovic A, 2000, J ALLERGY CLIN IMMUN, V105, P252, DOI 10.1016/S0091-6749(00)90073-3; Gardner M., 1989, STAT CONFIDENCE CONF; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; 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; KUEHR J, 1994, J ALLERGY CLIN IMMUN, V94, P44, DOI 10.1016/0091-6749(94)90070-1; LANGMAN MJS, 1986, BRIT MED J, V292, P716; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; Martin YC, 1998, PERSPECT DRUG DISCOV, V12, P3, DOI 10.1023/A:1017037831628; Martinez FD, 1999, J ALLERGY CLIN IMMUN, V104, pS169, DOI 10.1016/S0091-6749(99)70058-8; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Peat JK, 1999, J ALLERGY CLIN IMMUN, V103, P1, DOI 10.1016/S0091-6749(99)70517-8; pidemiology Standardization Project. II, 1978, AM REV RESP DIS S, V118, P7; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; Roost HP, 1999, J ALLERGY CLIN IMMUN, V104, P941, DOI 10.1016/S0091-6749(99)70072-2; Simpson BM, 2001, CLIN EXP ALLERGY, V31, P391, DOI 10.1046/j.1365-2222.2001.01050.x; Squillace SP, 1997, AM J RESP CRIT CARE, V156, P1760; Tovey E, 1999, J ALLERGY CLIN IMMUN, V103, P179, DOI 10.1016/S0091-6749(99)70488-4; VANTO T, 1983, ACTA PAEDIATR SCAND, V72, P571, DOI 10.1111/j.1651-2227.1983.tb09773.x; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; WARNER JA, 1991, PEDIATR ALLERGY IMMU, V1, P79	24	189	195	0	6	LANCET LTD	LONDON	84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND	0140-6736			LANCET	Lancet	JUL 21	2001	358	9277					188	193		10.1016/S0140-6736(01)05406-X		6	Medicine, General & Internal	General & Internal Medicine	454HL	WOS:000169967100011	11476835	
J	Finotto, S; De Sanctis, GT; Lehr, HA; Herz, U; Buerke, M; Schipp, M; Bartsch, B; Atreya, R; Schmitt, E; Galle, PR; Renz, H; Neurath, MF				Finotto, S; De Sanctis, GT; Lehr, HA; Herz, U; Buerke, M; Schipp, M; Bartsch, B; Atreya, R; Schmitt, E; Galle, PR; Renz, H; Neurath, MF			Treatment of allergic airway inflammation and hyperresponsiveness by antisense-induced local blockade of GATA-3 expression	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article						GATA-3 antisense DNA; asthma; T cells; Th2 cytokines	TRANSCRIPTION FACTOR GATA-3; CHRONIC INTESTINAL INFLAMMATION; DEVELOPING TH1 CELLS; CD4(+) T-CELLS; MOUSE MODEL; TH2-SPECIFIC EXPRESSION; GENE-EXPRESSION; TRANSGENIC MICE; ATOPIC ASTHMA; MURINE MODEL	Recent studies in transgenic mice have revealed that expression of a dominant negative form of the transcription factor GATA-3 in T cells can prevent T helper cell type 2 (Th2)-mediated allergic airway inflammation in mice. However, it remains unclear whether GATA-3 plays a role in the effector phase of allergic airway inflammation and whether antagonizing the expression and/or function of GATA-3 can be used for the therapy of allergic airway inflammation and hyperresponsiveness. Here, we analyzed the effects of locally antagonizing GATA-3 function in a murine model of asthma. We could suppress GATA-3 expression in interleukin (IL)-4-producing T cells in vitro and in vivo by an antisense phosphorothioate oligonucleotide overlapping the translation start site of GATA-3, whereas nonsense control oligonucleotides were virtually inactive. In a murine model of asthma associated with allergic pulmonary inflammation and hyperresponsiveness in ovalbumin (OVA)-sensitized mice, local intranasal administration of fluorescein isothiocyanate-labeled GATA-3 antisense oligonucleotides led to DNA uptake in lung cells associated with a reduction of intracellular GATA-3 expression. Such intrapulmonary blockade of GATA-3 expression caused an abrogation of signs of lung inflammation including infiltration of eosinophils and Th2 cytokine production. Furthermore, treatment with antisense but not nonsense oligonucleotides induced a significant reduction of airway hyperresponsiveness in OVA-sensitized mice to levels comparable to saline-treated control mice, as assessed by both enhanced pause (PenH) responses and pulmonary resistance determined by body plethysmography. These data indicate a critical role for GATA-3 in the effector phase of a murine asthma model and suggest that local delivery of GATA-3 antisense oligonucleotides may be a novel approach for the treatment of air-way hyperresponsiveness such as in asthma. This approach has the potential advantage of suppressing the expression of various proinflammatory Th2 cytokines simultaneously rather than suppressing the activity of a single cytokine.	Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Pulm & Crit Care Med, Boston, MA 02115 USA; Univ Marburg, Inst Lab Med, D-35033 Marburg, Germany; Univ Mainz, Inst Immunol, D-55099 Mainz, Germany; Univ Mainz, Med Clin 2, D-55099 Mainz, Germany; Univ Mainz, Inst Pathol, D-55099 Mainz, Germany; Univ Mainz, Immunol Lab, D-55099 Mainz, Germany	Finotto, S (reprint author), Brigham & Womens Hosp, Sch Med, Div Pulm & Crit Care Med, 75 Francis St, Boston, MA 02115 USA.						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Exp. Med.	JUN 4	2001	193	11					1247	1260		10.1084/jem.193.11.1247		14	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	440LV	WOS:000169177500004	11390432	
J	Wilson, RH; Whitehead, GS; Nakano, H; Free, ME; Kolls, JK; Cook, DN				Wilson, Rhonda H.; Whitehead, Gregory S.; Nakano, Hideki; Free, Meghan E.; Kolls, Jay K.; Cook, Donald N.			Allergic Sensitization through the Airway Primes Th17-dependent Neutrophilia and Airway Hyperresponsiveness	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; lung; immunity	T-CELLS; EOSINOPHILIC INFLAMMATION; LUNG INFLAMMATION; TH2 RESPONSES; SEVERE ASTHMA; ANTIGEN; INTERLEUKIN-17; DISSOCIATION; CHEMOKINE; MICE	Rationale: In humans, immune responses to inhaled aeroallergens develop in the lung and draining lymph nodes. Many animal models of asthma bypass this route and instead use intraperitoneal injections of allergen using aluminum hydroxide as an adjuvant. Objectives: We investigated whether allergic sensitization through the airway elicits immune responses qualitatively different than those arising in the peritoneum. Methods: Mice were sensitized to allergen through the airway using low-dose LIPS as an adjuvant, or through the peritoneum using aluminum hydroxide as an adjuvant. After a single allergen challenge, ELISA and flow cytometry were used to measure cytokines and leukocyte subsets. Invasive measurements of airway resistance were used to measure allergen-induced airway hyperreactivity (AHR). Measurements and Main Results: Sensitization through the peritoneum primed strong Th2 responses and eosinophilia, but not AHR, after a single allergen challenge. By contrast, allergic sensitization through the airway primed only modest Th2 responses, but strong Th17 responses. Th17 cells homed to the lung and released IL-17 into the airway on subsequent encounter with inhaled allergen. As a result, these mice developed IL-17-dependent airway neutrophilia and AHR. This AHR was neutrophil-dependent because it was abrogated in CXCR2-deficient mice and also in wild-type mice receiving a neutrophil-depleting antibody. Individually, neither IL-17 nor ongoing Th2 responses were sufficient to confer AHR, but together they acted synergistically to promote neutrophil recruitment, eosinophil recruitment and AHR. Conclusions: Allergic sensitization through the airway primes modest Th2 responses but strong Th17 responses that promote airway neutrophilia and acute AHR. These findings support a causal role for neutrophils in severe asthma.	[Cook, Donald N.] Natl Inst Environm Hlth Sci, Div Intramural Res, NIH, Lab Resp Biol, Res Triangle Pk, NC 27709 USA; [Kolls, Jay K.] Childrens Hosp Pittsburgh, Dept Pediat & Immunol, Pittsburgh, PA 15213 USA	Cook, DN (reprint author), Natl Inst Environm Hlth Sci, Div Intramural Res, NIH, Lab Resp Biol, 111 TW Alexander Dr,Bldg 101,Rm E244, Res Triangle Pk, NC 27709 USA.	usa.cookd@niehs.nih.gov			Intramural NIH HHS		Akimoto T, 1998, J EXP MED, V187, P1537, DOI 10.1084/jem.187.9.1537; Barnes PJ, 2007, J ALLERGY CLIN IMMUN, V119, P1055, DOI 10.1016/j.jaci.2007.01.015; Barnes PJ, 2007, J ALLERGY CLIN IMMUN, V119, P1063; Birrell MA, 2003, RESPIR RES, V4, DOI 10.1186/rr197; Brewer JM, 1999, J IMMUNOL, V163, P6448; Crimi E, 1998, AM J RESP CRIT CARE, V157, P4; Eisenbarth SC, 2002, J EXP MED, V196, P1645, DOI 10.1084/jem.20021340; Foley SC, 2007, J ALLERGY CLIN IMMUN, V119, P1282, DOI 10.1016/j.jaci.2007.02.006; Gereke M, 2009, AM J RESP CRIT CARE, V179, P344, DOI 10.1164/rccm.200804-592OC; Harrington LE, 2005, NAT IMMUNOL, V6, P1123, DOI 10.1038/ni1254; Herrick CA, 2003, NAT REV IMMUNOL, V3, P405, DOI 10.1038/nri1084; Holgate ST, 2009, CURR OPIN PULM MED, V15, P63, DOI 10.1097/MCP.0b013e32831da867; Hollingsworth JW, 2006, J IMMUNOL, V176, P5856; Kamachi A, 2002, EUR RESPIR J, V19, P76, DOI 10.1183/09031936.02.00208202; Kool M, 2008, J EXP MED, V205, P869, DOI 10.1084/jem.20071087; KUNG TT, 1994, INT ARCH ALLERGY IMM, V105, P83; Kuperman D, 1998, J EXP MED, V187, P939, DOI 10.1084/jem.187.6.939; Laan M, 1999, J IMMUNOL, V162, P2347; Larche M, 2003, J ALLERGY CLIN IMMUN, p[111, 464]; Lex C, 2006, AM J RESP CRIT CARE, V174, P1286, DOI 10.1164/rccm.200603-352OC; Ley K, 2006, IMMUNOL RES, V34, P229, DOI 10.1385/IR:34:3:229; Michel ML, 2007, J EXP MED, V204, P995, DOI 10.1084/jem.20061551; Molet S, 2001, J ALLERGY CLIN IMMUN, V108, P430, DOI 10.1067/mai.2001.117929; Ouyang WJ, 2008, IMMUNITY, V28, P454, DOI 10.1016/j.immuni.2008.03.004; Park H, 2005, NAT IMMUNOL, V6, P1133, DOI 10.1038/ni1261; Piggott DA, 2005, J CLIN INVEST, V115, P459, DOI 10.1172/JCI200522462; Song CW, 2008, J IMMUNOL, V181, P6117; Taube C, 2004, AM J RESP CELL MOL, V30, P837, DOI 10.1165/rcmb.2003-0395OC; Tomkinson A, 2001, AM J RESP CRIT CARE, V163, P721; Toy D, 2006, J IMMUNOL, V177, P36; Wenzel SE, 1997, AM J RESP CRIT CARE, V156, P737; Whitehead GS, 2007, AM J RESP CRIT CARE, V175, P243, DOI 10.1164/rccm.200606-839OC; XING Z, 1994, AM J RESP CELL MOL, V10, P148; Yang XXO, 2008, J EXP MED, V205, P1063, DOI 10.1084/jem.20071978; Ye P, 2001, J EXP MED, V194, P519, DOI 10.1084/jem.194.4.519	35	188	210	0	11	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	2009	180	8					720	730		10.1164/rccm.200904-0573OC		11	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	506AB	WOS:000270743100006	19661246	
J	Flores, G; Tomany-Korman, SC				Flores, Glenn; Tomany-Korman, Sandra C.			Racial and ethnic disparities in medical and dental health, access to care, and use of services in US children	PEDIATRICS			English	Article						disparities; minorities; children; race; ethnicity; African Americans; Hispanics; Asians/Pacific islanders; native Americans; multiracial	UNITED-STATES; OVERWEIGHT; ADOLESCENTS; INSURANCE; AMERICAN; TRENDS; PREVALENCE; OBESITY; WEIGHT; IMPACT	BACKGROUND. Not enough is known about the national prevalence of racial/ethnic disparities in children's medical and dental care. OBJECTIVE. The purpose of this work was to examine racial/ethnic disparities in medical and oral health, access to care, and use of services in a national sample. METHODS. The National Survey of Children's Health was a telephone survey in 2003 2004 of a national random sample of parents and guardians of 102 353 children 0 to 17 years old. Disparities in selected medical and oral health and health care measures were examined for white, African American, Latino, Asian/Pacific Islander, Native American, and multiracial children. Multivariate analyses were performed to adjust for primary language at home, age, insurance coverage, income, parental education and employment, and number of children and adults in the household. Forty measures of medical and oral health status, access to care, and use of services were analyzed. RESULTS. Many significant disparities were noted; for example, uninsurance rates were 6% for whites, 21% for Latinos, 15% for Native Americans, 7% for African Americans, and 4% for Asians or Pacific Islanders, and the proportions with a usual source of care were as follows: whites, 90%; Native Americans, 61%; Latinos, 68%; African Americans, 77%; and Asians or Pacific Islanders, 87%. Many disparities persisted for >= 1 minority group in multivariate analyses, including increased odds of suboptimal health status, overweight, asthma, activity limitations, behavioral and speech problems, emotional difficulties, uninsurance, suboptimal dental health, no usual source of care, unmet medical and dental needs, transportation barriers to care, problems getting specialty care, no medical or dental visit in the past year, emergency department visits, not receiving mental health care, and not receiving prescription medications. Certain disparities were particularly marked for specific racial/ethnic groups: for Latinos, suboptimal health status and teeth condition, uninsurance, and problems getting specialty care; for African Americans, asthma, behavior problems, skin allergies, speech problems, and unmet prescription needs; for Native Americans, hearing or vision problems, no usual source of care, emergency department visits, and unmet medical and dental needs; and for Asians or Pacific Islanders, problems getting specialty care and not seeing a doctor in the past year. Multiracial children also experienced many disparities. CONCLUSIONS. Minority children experience multiple disparities in medical and oral health, access to care, and use of services. Certain disparities are particularly marked for specific racial/ethnic groups, and multiracial children experience many disparities.	[Flores, Glenn] Univ Texas SW Med Ctr Dallas, Dept Pediat, Div Gen Pediat, Dallas, TX 75390 USA; [Flores, Glenn] Childrens Med Ctr, Dept Pediat Med, Dallas, TX 75235 USA; [Tomany-Korman, Sandra C.] LLC, Signature Sci, Austin, TX USA	Flores, G (reprint author), Univ Texas SW Med Ctr Dallas, Dept Pediat, Div Gen Pediat, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.	glenn.flores@utsouthwestern.edu					*AG HEALTHC RES QU, 2006, 070012 AHRQ PUBL; Akinbami Lara, 2006, Adv Data, P1; Baruffi G, 2004, J AM DIET ASSOC, V104, P1701, DOI 10.1016/j.jada.2004.08.027; Beal AC, 2004, HEALTH AFFAIR, V23, P171, DOI 10.1377/hlthaff.23.5.171; Blumberg SJ, 2005, VITAL HLTH STAT, V1, P1; Burt CW, 2001, VITAL HLTH STAT, V13, P1; *COMM UND ELIM RAC, 2003, UN TREATM CONFR RAC, P285; Denny Clark H, 2003, MMWR Surveill Summ, V52, P1; Edelstein BL, 2002, AMBUL PEDIATR, V2, P141, DOI 10.1367/1539-4409(2002)002<0141:DIOHAA>2.0.CO;2; Eisenmann JC, 2000, INT J OBESITY, V24, P211, DOI 10.1038/sj.ijo.0801116; Elixhauser A, 2002, AMBUL PEDIATR, V2, P419, DOI 10.1367/1539-4409(2002)002<0419:HCFCAY>2.0.CO;2; Flores G, 2005, PEDIATRICS, V116, P1433, DOI 10.1542/peds.2005-0786; Flores G, 1999, AM J PUBLIC HEALTH, V89, P1066, DOI 10.2105/AJPH.89.7.1066; Flores G, 2005, PEDIATRICS, V115; Flores GF, 2005, PUBLIC HEALTH REP, V120, P418; Guevara JP, 2006, HEALTH SERV RES, V41, P532, DOI 10.1111/j.1475-6773.2005.00484.x; Harris KM, 2006, ARCH PEDIAT ADOL MED, V160, P74, DOI 10.1001/archpedi.160.1.74; Hedley AA, 2004, JAMA-J AM MED ASSOC, V291, P2847, DOI 10.1001/jama.291.23.2847; Heslin KC, 2006, ARCH OPHTHALMOL-CHIC, V124, P895, DOI 10.1001/archopht.124.6.895; JACKSON MY, 1993, J AM DIET ASSOC, V93, P1136, DOI 10.1016/0002-8223(93)91645-7; Lewis C, 2007, J AM DENT ASSOC, V138, P369; Mendoza FS, 1999, WESTERN J MED, V170, P85; Moore William E, 2006, Prev Chronic Dis, V3, pA114; NeumarkSztainer D, 1997, J AM DIET ASSOC, V97, P598, DOI 10.1016/S0002-8223(97)00154-5; NEWACHECK PW, 1989, PEDIATRICS, V84, P699; NEWACHECK PW, 1995, HEALTH AFFAIR, V14, P244, DOI 10.1377/hlthaff.14.1.244; Ogden CL, 2002, JAMA-J AM MED ASSOC, V288, P1728, DOI 10.1001/jama.2012.40; Passel JS, 2002, AMBUL PEDIATR, V2, P169, DOI 10.1367/1539-4409(2002)002<0169:DASTAT>2.0.CO;2; Stata Corporation, 2003, STAT SURV DAT REF MA; Weitzman M, 1999, PEDIATRICS, V104, P151; Williams DR, 2000, AM J PUBLIC HEALTH, V90, P1728, DOI 10.2105/AJPH.90.11.1728; Wisen AGM, 2004, CLIN PHYSIOL FUNCT I, V24, P341, DOI 10.1111/j.1475-097X.2004.00576.x; WOOD DL, 1990, PEDIATRICS, V86, P666; Yu SM, 2004, PEDIATRICS, V113, P101, DOI 10.1542/peds.113.1.101; Zephier E, 2006, ARCH PEDIAT ADOL MED, V160, P34, DOI 10.1001/archpedi.160.1.34	35	188	190	4	32	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	FEB	2008	121	2					E286	E298		10.1542/peds.2007-1243		13	Pediatrics	Pediatrics	258OQ	WOS:000252877600046	18195000	
J	Wigle, DT; Arbuckle, TE; Turner, MC; Berube, A; Yang, QY; Liu, SL; Krewski, D				Wigle, Donald T.; Arbuckle, Tye E.; Turner, Michelle C.; Berube, Annie; Yang, Qiuying; Liu, Shiliang; Krewski, Daniel			Epidemiologic evidence of relationships between reproductive and child health outcomes and environmental chemical contaminants	JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART B-CRITICAL REVIEWS			English	Review							LEVEL LEAD-EXPOSURE; ADVERSE PREGNANCY OUTCOMES; LOW-BIRTH-WEIGHT; PATERNAL OCCUPATIONAL-EXPOSURE; IN-UTERO EXPOSURE; NEURAL-TUBE DEFECTS; HAZARDOUS-WASTE LANDFILL; PORT-PIRIE COHORT; ACUTE LYMPHOBLASTIC-LEUKEMIA; TOBACCO-SMOKE EXPOSURE	This review summarizes the level of epidemiologic evidence for relationships between prenatal and/or early life exposure to environmental chemical contaminants and fetal, child, and adult health. Discussion focuses on fetal loss, intrauterine growth restriction, preterm birth, birth defects, respiratory and other childhood diseases, neuropsychological deficits, premature or delayed sexual maturation, and certain adult cancers linked to fetal or childhood exposures. Environmental exposures considered here include chemical toxicants in air, water, soil/house dust and foods (including human breast milk), and consumer products. Reports reviewed here included original epidemiologic studies (with at least basic descriptions of methods and results), literature reviews, expert group reports, meta-analyses, and pooled analyses. Levels of evidence for causal relationships were categorized as sufficient, limited, or inadequate according to predefined criteria. There was sufficient epidemiological evidence for causal relationships between several adverse pregnancy or child health outcomes and prenatal or childhood exposure to environmental chemical contaminants. These included prenatal high-level methylmercury (CH3Hg) exposure (delayed developmental milestones and cognitive, motor, auditory, and visual deficits), high-level prenatal exposure to polychlorinated biphenyls (PCBs), polychlorinated dibenzofurans (PCDFs), and related toxicants (neonatal tooth abnormalities, cognitive and motor deficits), maternal active smoking (delayed conception, preterm birth, fetal growth deficit [FGD] and sudden infant death syndrome [SIDS]) and prenatal environmental tobacco smoke (ETS) exposure (preterm birth), low-level childhood lead exposure (cognitive deficits and renal tubular damage), high-level childhood CH3Hg exposure (visual deficits), high-level childhood exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (chloracne), childhood ETS exposure (SIDS, new-onset asthma, increased asthma severity, lung and middle ear infections, and adult breast and lung cancer), childhood exposure to biomass smoke (lung infections), and childhood exposure to outdoor air pollutants (increased asthma severity). Evidence for some proven relationships came from investigation of relatively small numbers of children with high-dose prenatal or early childhood exposures, e. g., CH3Hg poisoning episodes in Japan and Iraq. In contrast, consensus on a causal relationship between incident asthma and ETS exposure came only recently after many studies and prolonged debate. There were many relationships supported by limited epidemiologic evidence, ranging from several studies with fairly consistent findings and evidence of dose-response relationships to those where 20 or more studies provided inconsistent or otherwise less than convincing evidence of an association. The latter included childhood cancer and parental or childhood exposures to pesticides. In most cases, relationships supported by inadequate epidemiologic evidence reflect scarcity of evidence as opposed to strong evidence of no effect. This summary points to three main needs: (1) Where relationships between child health and environmental exposures are supported by sufficient evidence of causal relationships, there is a need for (a) policies and programs to minimize population exposures and (b) population-based biomonitoring to track exposure levels, i.e., through ongoing or periodic surveys with measurements of contaminant levels in blood, urine and other samples. (2) For relationships suported by limited evidence, there is a need for targeted research and policy options ranging from ongoing evaluation of evidence to proactive actions. (3) There is a great need for population-based, multidisciplinary and collaborative research on the many relationships supported by inadequate evidence, as these represent major knowledge gaps. Expert groups faced with evaluating epidemiologic evidence of potential causal relationships repeatedly encounter problems in summarizing the available data. A major driver for undertaking such summaries is the need to compensate for the limited sample sizes of individual epidemiologic studies. Sample size limitations are major obstacles to exploration of prenatal, paternal, and childhood exposures during specific time windows, exposure intensity, exposure-exposure or exposure-gene interactions, and relatively rare health outcomes such as childhood cancer. Such research needs call for investments in research infrastructure, including human resources and methods development (standardized protocols, biomarker research, validated exposure metrics, reference analytic laboratories). These are needed to generate research findings that can be compared and subjected to pooled analyses aimed at knowledge synthesis.	[Wigle, Donald T.; Turner, Michelle C.; Krewski, Daniel] Univ Ottawa, McLaughlin Ctr Populat Hlth Risk Assessment, Ottawa, ON K1N 6N5, Canada; [Arbuckle, Tye E.] Hlth Canada, Healthy Environm & Consumer Safety Branch, Ottawa, ON K1A 0L2, Canada; [Berube, Annie] Hlth Canada, Vulnerable Populat Div, Safe Environm Program, Ottawa, ON K1A 0L2, Canada; [Yang, Qiuying] Univ Ottawa, Dept Obstet & Gynecol, Fac Med, OMNI Res Grp, Ottawa, ON, Canada; [Yang, Qiuying] Ottawa Hlth Res Inst, Ottawa, ON, Canada; [Liu, Shiliang] Publ Hlth Agcy Canada, Ctr Healthy Human Dev, Ottawa, ON, Canada	Wigle, DT (reprint author), Univ Ottawa, McLaughlin Ctr Populat Hlth Risk Assessment, Room 318B,1 Stewart St, Ottawa, ON K1N 6N5, Canada.	don.wigle@sympatico.ca					Abadi-Korek I, 2006, J OCCUP ENVIRON MED, V48, P165, DOI 10.1097/01.jom.0000183343.81485.7c; Abell A, 2000, SCAND J WORK ENV HEA, V26, P131; *AG TOX SUBST DIS, 1999, TOX PROF CAD; Agency for Toxic Substances and Disease Registry, 2000, TOX PROF ARS; Agency for Toxic Substances and Disease Registry, 2000, TOX PROF MANG; 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Toxicol. Env. Health-Pt b-Crit. Rev.		2008	11	5-6					373	517		10.1080/10937400801921320		145	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	319EK	WOS:000257146700001	18470797	
J	Dragonieri, S; Schot, R; Mertens, BJA; Le Cessie, S; Gauw, SA; Spanevello, A; Resta, O; Willard, NP; Vink, TJ; Rabe, KF; Bel, EH; Sterk, PJ				Dragonieri, Silvano; Schot, Robert; Mertens, Bart J. A.; Le Cessie, Saskia; Gauw, Stefanie A.; Spanevello, Antonio; Resta, Onofrio; Willard, Nico P.; Vink, Teunis J.; Rabe, Klaus F.; Bel, Elisabeth H.; Sterk, Peter J.			An electronic nose in the discrimination of patients with asthma and controls	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma mild; asthma severe; biomarkers; diagnosis; electronic nose; exhaled breath; volatile organic compounds	VOLATILE ORGANIC-COMPOUNDS; COMPOSITE VAPOR DETECTORS; LUNG-CANCER; EXHALED BREATH; CLINICAL-APPLICATION; PULMONARY-DISEASE; MARKERS; TECHNOLOGY; PNEUMONIA; DIAGNOSIS	Background: Exhaled breath contains thousands of volatile organic compounds (VOCs) that could serve as biomarkers of lung disease. Electronic noses can distinguish VOC mixtures by pattern recognition. Objective: We hypothesized that an electronic nose can discriminate exhaled air of patients with asthma from healthy controls, and between patients with different disease severities. Methods: Ten young patients with mild asthma (25.1 +/- 5.9 years; FEV1, 99.9 +/- 7.7% predicted), 10 young controls (26.8 +/- 6.4 years; FEV1, 101.9 +/- 10.3), 10 older patients with severe asthma (49.5 +/- 12.0 years; FEV1, 62.3 +/- 23.6), and 10 older controls (57.3 +/- 7.1 years; FEV1, 108.3 +/- 14.7) joined a cross-sectional study with duplicate sampling of exhaled breath with an interval of 2 to 5 minutes. Subjects inspired VOC-filtered air by tidal breathing for 5 minutes, and a single expiratory vital capacity was collected into a Tedlar bag that was sampled by electronic nose (Cyranose 320) within 10 minutes. Smellprints were analyzed by linear discriminant analysis on principal component reduction. Cross-validation values (CVVs) were calculated. Results: Smellprints of patients with mild asthma were fully separated from young controls (CVV, 100%; Mahalanobis distance [M-distance], 5.32), and patients with severe asthma could be distinguished from old controls (CVV, 90%; M-distance, 2.77). Patients with mild and severe asthma could be less well discriminated (CVV, 65%; M-distance, 1.23), whereas the 2 control groups were indistinguishable (CVV, 50%; M-distance, 1.56). The duplicate samples replicated these results. Conclusion: An electronic nose can discriminate exhaled breath of patients with asthma from controls but is less accurate in distinguishing asthma severities. Clinical implication: These findings warrant validation of electronic noses in diagnosing newly presented patients with asthma.	Univ Amsterdam, Acad Med Ctr, Dept Resp Dis, NL-1100 DE Leiden, Netherlands; Leiden Univ, Ctr Med, Dept Pulmonol, NL-2300 RA Leiden, Netherlands; Leiden Univ, Ctr Med, Dept Med Stat, NL-2300 RA Leiden, Netherlands; Univ Bari, Dept Resp Dis, I-70121 Bari, Italy; Philips Res, Eindhoven, Netherlands; Univ Amsterdam, Acad Med Ctr, Dept Resp Dis, NL-1012 WX Amsterdam, Netherlands	Sterk, PJ (reprint author), Univ Amsterdam, Acad Med Ctr, Dept Resp Dis, F5-259,POB 22700, NL-1100 DE Leiden, Netherlands.	p.j.sterk@amc.nl					American Thoracic Society, 2005, AM J RESP CRIT CARE, V171, P912, DOI DOI 10.1164/RCCM.200406-710ST; Bossuyt PM, 2003, ANN INTERN MED, V138, pW1, DOI DOI 10.7326/0003-4819-138-1-200301070-00010; BRIGHHTLING CE, 2006, CHEST, V129, P1444; Briglin SM, 2002, SENSOR ACTUAT B-CHEM, V82, P54, DOI 10.1016/S0925-4005(01)00991-1; BUCK L, 1991, CELL, V65, P175, DOI 10.1016/0092-8674(91)90418-X; Busse William W., 2003, Journal of Allergy and Clinical Immunology, V111, pS799, DOI 10.1067/mai.2003.158; Corradi M, 2004, EUR RESPIR J, V24, P1011, DOI 10.1183/09031936.04.00002404; Crameri R, 2005, ALLERGY, V60, P1227, DOI 10.1111/j.1398-9995.2005.00873.x; Davies DE, 2003, J ALLERGY CLIN IMMUN, V111, P215, DOI 10.1067/mai.2003.128; De Maesschalck R, 2000, CHEMOMETR INTELL LAB, V50, P1, DOI 10.1016/S0169-7439(99)00047-7; DRAGONIERI S, 2007, AM J RESP CRIT CARE, V175, pA330; Dutta Ritaban, 2002, Biomed Eng Online, V1, P4, DOI 10.1186/1475-925X-1-4; Fend R, 2006, J CLIN MICROBIOL, V44, P2039, DOI 10.1128/JCM.01591-05; GORDON SM, 1985, CLIN CHEM, V31, P1278; Hanson CW, 2005, ANESTHESIOLOGY, V102, P63, DOI 10.1097/00000542-200501000-00013; Hockstein NG, 2004, LARYNGOSCOPE, V114, P1701, DOI 10.1097/00005537-200410000-00005; Kharitonov SA, 2001, AM J RESP CRIT CARE, V163, P1693; Knottnerus JA, 2003, J CLIN EPIDEMIOL, V56, P1118, DOI 10.1016/S0895-4356(03)00206-3; Lai SY, 2002, LARYNGOSCOPE, V112, P975, DOI 10.1097/00005537-200206000-00007; Lewis NS, 2004, ACCOUNTS CHEM RES, V37, P663, DOI 10.1021/ar030120m; Lex C, 2006, RESP RES, V7, DOI 10.1186/1465-9921-7-63; Machado RF, 2005, AM J RESP CRIT CARE, V171, P1286, DOI 10.1164/rccm.200409-1184OC; Mertens BJA, 2006, J COMPUT BIOL, V13, P1591, DOI 10.1089/cmb.2006.13.1591; Miller MR, 2005, EUR RESPIR J, V26, P319, DOI 10.1183/09031936.05.00034805; Moser B, 2005, RESP PHYSIOL NEUROBI, V145, P295, DOI 10.1016/j.resp.2004.02.002; Paredi P, 2000, AM J RESP CRIT CARE, V162, P369; PAULING L, 1971, P NATL ACAD SCI USA, V68, P2374, DOI 10.1073/pnas.68.10.2374; Phillips M, 1999, LANCET, V353, P1930, DOI 10.1016/S0140-6736(98)07552-7; Phillips M, 2003, CHEST, V123, P2115, DOI 10.1378/chest.123.6.2115; SAVITZKY A, 1964, ANAL CHEM, V36, P1627, DOI 10.1021/ac60214a047; Sterk PJ, 1993, EUR RESPIR J S, V16, P53; Taylor DR, 2006, THORAX, V61, P817, DOI 10.1136/thx.2005.056093; Thaler ER, 2005, EXPERT REV MED DEVIC, V2, P559, DOI 10.1586/17434440.5.5.559; *WHO, 2006, GLOB IN ASTHM; WOLD S, 1987, CHEMOMETR INTELL LAB, V2, P37, DOI 10.1016/0169-7439(87)80084-9	35	188	191	2	44	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	OCT	2007	120	4					856	862		10.1016/j.jaci.2007.05.043		7	Allergy; Immunology	Allergy; Immunology	220LH	WOS:000250157700020	17658592	
J	Krieger, JW; Takaro, TK; Song, L; Weaver, M				Krieger, JW; Takaro, TK; Song, L; Weaver, M			The Seattle-King County Healthy Homes Project: A randomized, controlled trial of a community health worker intervention to decrease exposure to indoor asthma triggers	AMERICAN JOURNAL OF PUBLIC HEALTH			English	Article							LOW-INCOME CHILDREN; INNER-CITY CHILDREN; QUALITY-OF-LIFE; URBAN CHILDREN; MITE ALLERGEN; COST; CARE; OUTREACH; PROGRAM; AVOIDANCE	Objectives. We assessed the effectiveness of a community health worker intervention focused on reducing exposure to indoor asthma triggers. Methods. We conducted a randomized controlled trial with 1-year follow-up among 274 low-income households containing a child aged 4-12 years who had asthma. Community health workers provided in-home environmental assessments, education, support for behavior change, and resources. Participants were assigned to either a high-intensity group receiving 7 visits and a full set of resources or a low-intensity group receiving a single visit and limited resources. Results. The high-intensity group improved significantly more than the low-intensity group in its pediatric asthma caregiver quality-of-life score (P=.005) and asthma-related urgent health services use (P=.026). Asthma symptom days declined more in the high-intensity group, although the across-group difference did not reach statistical significance (P=.138). Participant actions to reduce triggers generally increased in the high-intensity group. The projected 4-year net savings per participant among the high-intensity group relative to the low-intensity group were $189-$721. Conclusions. Community health workers reduced asthma symptom days and urgent health services use while improving caregiver quality-of-life score. Improvement was greater with a higher-intensity intervention.	Publ Hlth Seattle & King Cty, Seattle, WA 98104 USA; Univ Washington, Sch Med, Seattle, WA USA; Univ Washington, Sch Publ Hlth & Community Med, Seattle, WA 98195 USA	Krieger, JW (reprint author), Publ Hlth Seattle & King Cty, 999 3rd Ave,Suite 1200, Seattle, WA 98104 USA.	james.krieger@metrokc.gov			NIEHS NIH HHS [5 R21 ES09095]; ODCDC CDC HHS [U48/CCU009654-07]		Baier C, 1999, CHEST, V116, p204S, DOI 10.1378/chest.116.suppl_2.204S; Balas EA, 1998, JAMA-J AM MED ASSOC, V279, P54, DOI 10.1001/jama.279.1.54; Baranowski T., 1997, HLTH BEHAV HLTH ED; BUTZ AM, 1994, CLIN PEDIATR, V33, P135, DOI 10.1177/000992289403300302; Carter MC, 2001, J ALLERGY CLIN IMMUN, V108, P732, DOI 10.1067/mai.2001.119155; CLARK NM, 1986, J ALLERGY CLIN IMMUN, V78, P108, DOI 10.1016/0091-6749(86)90122-3; *COMM ENV HLTH, 1999, HDB PED ENV HLTH; Custovic A, 2001, CLIN EXP ALLERGY, V31, P670, DOI 10.1046/j.1365-2222.2001.01092.x; Eggleston PA, 1999, ENVIRON HEALTH PERSP, V107, P439; Eggleston PA, 1998, IMMUNOL ALLERGY CLIN, V18, P75, DOI 10.1016/S0889-8561(05)70348-9; Eggleston PA, 2001, J ALLERGY CLIN IMMUN, V107, pS403, DOI 10.1067/mai.2001.113673; EHNERT B, 1992, J ALLERGY CLIN IMMUN, V90, P135, DOI 10.1016/S0091-6749(06)80024-2; Emanuel EJ, 2001, NEW ENGL J MED, V345, P915, DOI 10.1056/NEJM200109203451211; Evans R, 1999, J PEDIATR-US, V135, P332, DOI 10.1016/S0022-3476(99)70130-7; Gotzsche PC, 2001, COCHRANE DB SYST REV, V3; Greineder DK, 1998, AM J MANAG CARE, V4, P196; GUEVARA JP, 2003, BRIT MED J, V326, P308; Guyatt GH, 1998, BRIT MED J, V316, P690; Hardin J. 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M., 2002, MMWR-MORBID MORTAL W, V51, P1; Morgan WJ, 2004, NEW ENGL J MED, V351, P1068, DOI 10.1056/NEJMoa032097; National Asthma Education and Prevention Program, 1997, 2 NAT ASTHM ED PREV; *NAT I ENV HLTH SC, COMM BAS PART RES EN; NELSON H, 1995, PROVOCATIVE CHALLENG; Platts-Mills TAE, 2000, J ALLERGY CLIN IMMUN, V106, P787, DOI 10.1067/mai.2000.110548; Prochaska JO, 1997, HLTH BEHAV HLTH ED; Sarpong SB, 1997, ANN ALLERG ASTHMA IM, V79, P455; SCHNEIDER D, 2000, CHILDRENS ENV HLTH R; Stout JW, 1998, J ASTHMA, V35, P119, DOI 10.3109/02770909809055413; Stroupe KT, 1999, J ASTHMA, V36, P645, DOI 10.3109/02770909909055416; Sullivan SD, 2002, J ALLERGY CLIN IMMUN, V110, P576, DOI 10.1067/mai.2002.128009; Swider SM, 2002, PUBLIC HEALTH NURS, V19, P11, DOI 10.1046/j.1525-1446.2002.19003.x; TAKARO T, IN PRESS J EXPO ANAL; Tovey E, 1999, J ALLERGY CLIN IMMUN, V103, P179, DOI 10.1016/S0091-6749(99)70488-4; *US BUR LAB STAT, CONS PRIC IND URB CO; *US EPA, ASTHM ED OUTR PROGR; Weiss KB, 2000, J ALLERGY CLIN IMMUN, V106, P493; Wilson SR, 2001, CHEST, V120, P1709, DOI 10.1378/chest.120.5.1709; Woodcock A, 2003, NEW ENGL J MED, V349, P225, DOI 10.1056/NEJMoa023175; HLTH HOMES HLTH KIDS; HLTH HOUSE	52	188	192	4	33	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	APR	2005	95	4					652	659		10.2105/AJPH.2004.042994		8	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	911JP	WOS:000227998700025	15798126	
J	Khinchi, MS; Poulsen, LK; Carat, F; Andre, C; Hansen, AB; Malling, HJ				Khinchi, MS; Poulsen, LK; Carat, F; Andre, C; Hansen, AB; Malling, HJ			Clinical efficacy of sublingual and subcutaneous birch pollen allergen-specific immunotherapy: a randomized, placebo-controlled, double-blind, double-dummy study	ALLERGY			English	Article						allergen-specific immunotherapy; clinical efficacy; controlled study; randomized; rhinitis; side-effects; subcutaneous; sublingual	HOUSE-DUST-MITE; STANDARDIZED 5-GRASS-POLLEN EXTRACT; PARIETARIA-JUDAICA EXTRACT; HEALTH SURVEY SF-36; GRASS-POLLEN; SWALLOW IMMUNOTHERAPY; CONTROLLED TRIAL; ORAL IMMUNOTHERAPY; HAY-FEVER; RHINITIS	Background: Both sublingual allergen-specific immunotherapy (SLIT) and subcutaneous immunotherapy (SCIT) have a documented clinical efficacy, but only few comparative studies have been performed. Objective: To investigate the clinical efficacy of SLIT vs SCIT and secondary to compare SLIT and SCIT with placebo and to evaluate the relative clinical efficacy in relation to systemic side-effects. Methods: A 3-year randomized, placebo-controlled, double-blind, double-dummy study including 71 adult birch pollen hay fever patients treated for two consecutive years after a baseline year. Allocation to treatment groups was based on disease severity in the baseline season, gender and age. Results: Clinical efficacy was estimated in 58 patients completing the first treatment year by subtracting baseline data and by calculating the ratio first treatment season vs baseline. SLIT diminished the median disease severity to one-half and SCIT to one-third of placebo treatment. No statistical significant difference between the two groups was observed. Both for symptoms and medication scores actively treated patients showed statistically significant and clinical relevant efficacy compared with placebo. SLIT treatment only resulted in local mild side-effects, while SCIT resulted in few serious systemic side-effects. Conclusion: Based on the limited number of patients the clinical efficacy of SLIT was not statistically different from SCIT, and both treatments are clinically effective compared with placebo in the treatment of birch pollen rhinoconjunctivitis. The lack of significant difference between the two treatments does not indicate equivalent efficacy, but to detect minor differences necessitates investigation of larger groups. Due to the advantageous safety profile SLIT may be favored.	Natl Univ Hosp, Allergy Clin, Copenhagen, Denmark; Stallergenes SA, Antony, France	Malling, HJ (reprint author), Natl Univ Hosp, Allergy Clin 4222, Blegdamsvej 9, DK-2100 Copenhagen, Denmark.						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V., 1993, Aerobiologia, V9, P15, DOI 10.1007/BF02311366; Pradalier A, 1999, ALLERGY, V54, P819, DOI 10.1034/j.1398-9995.1999.00077.x; Purello-D'Ambrosio F, 1999, ALLERGY, V54, P968, DOI 10.1034/j.1398-9995.1999.00203.x; Quirino T, 1996, CLIN EXP ALLERGY, V26, P1253, DOI 10.1046/j.1365-2222.1996.d01-280.x; Rak S, 2001, J ALLERGY CLIN IMMUN, V108, P921, DOI 10.1067/mai.2001.119743; SABBAH A, 1994, ALLERGY, V49, P309, DOI 10.1111/j.1398-9995.1994.tb02273.x; STEWART AL, 1988, MED CARE, V26, P724, DOI 10.1097/00005650-198807000-00007; STEWART GE, 1992, J ALLERGY CLIN IMMUN, V90, P567, DOI 10.1016/0091-6749(92)90129-P; TARI MG, 1990, ALLERGOL IMMUNOPATH, V18, P277; TAUDORF E, 1987, J ALLERGY CLIN IMMUN, V80, P153, DOI 10.1016/0091-6749(87)90124-2; TAVES DR, 1974, CLIN PHARMACOL THER, V15, P443; TROISE C, 1995, J INVEST ALLERG CLIN, V5, P25; VARNEY VA, 1991, BRIT MED J, V302, P265; Voltolini S, 2001, Allergol Immunopathol (Madr), V29, P103; Vourdas D, 1998, ALLERGY, V53, P662, DOI 10.1111/j.1398-9995.1998.tb03952.x; WARE JE, 1992, MED CARE, V30, P473, DOI 10.1097/00005650-199206000-00002; Winther L, 2000, ALLERGY, V55, P818, DOI 10.1034/j.1398-9995.2000.00367.x	54	188	202	0	5	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	JAN	2004	59	1					45	53		10.1046/j.1398-9995.2003.00387.x		9	Allergy; Immunology	Allergy; Immunology	753QY	WOS:000187243100008	14674933	
J	Rundell, KW; Im, JH; Mayers, LB; Wilber, RL; Szmedra, L; Schmitz, HR				Rundell, KW; Im, JH; Mayers, LB; Wilber, RL; Szmedra, L; Schmitz, HR			Self-reported symptoms and exercise-induced asthma in the elite athlete	MEDICINE AND SCIENCE IN SPORTS AND EXERCISE			English	Article						bronchospasm; cold weather; exercise-induced asthma; exercise; pulmonary function	CROSS-COUNTRY SKIERS; INDUCED BRONCHOSPASM; AIRWAY RESPONSIVENESS; FIGURE SKATERS; COLD-AIR; CHALLENGE; CHILDREN; RUNNERS; ADULTS	Purpose: The purpose of this study was to compare self-reported symptoms for exercise-induced asthma (EIA) to postexercise challenge pulmonary function test results in elite athletes. Methods: Elite athletes (N = 158; 83 men and 75 women; age: 22 +/- 4.4 yr) performed pre- and post-exercise spirometry and were grouped according to postexercise pulmonary function decrements (PFT-positive, PFT-borderline. and PFT-normal for EIA). Before the sport/environment specific exercise challenge, subjects completed an EIA symptoms-specific questionnaire. Results: Resting FEV1 values were above predicted values (114-121%) and not different between groups. Twenty-six percent of the study population demonstrated >10% postexercise drop in FEV1 and 29% reported two or more symptoms. However, the proportion of PFT-positive and PFT-normal athletes reporting two or more symptoms was nor different (39% vs. 41%). Postrace cough was the most reported symptom, reported significantly more frequently for PFT-positive athletes (P < 0.05). Sensitivity/specificity analysis demonstrated a lack of effectiveness of self-reported symptoms to identify PFT-positive or exclude PFT-normal athletes. Postexercise lower limit reference ranges (MN-2SDs) were determined from normal athletes for FEV1, FEF25-75% and PEF to be -7%, -12.5%, and -18%, respectively. Conclusion: Although questionnaires provide reasonable estimates of ELA prevalence among elite cold-weather athletes, the use of self-reported symptoms for EIA diagnosis in this population will likely yield high frequencies Of both false positive and false negative results. Diagnosis should include spirometry using an exercise/environment specific challenge in combination with the athlete's history of asthma symptoms.	US Olymp Comm Lake Placid, Sports Sci & Technol Div, Lake Placid, NY 12946 USA	Rundell, KW (reprint author), US Olymp Comm Lake Placid, Sports Sci & Technol Div, 421 Old Mil Rd, Lake Placid, NY 12946 USA.						American Thoracic Society, 1991, AM REV RESPIR DIS, V144, P1202, DOI 10.1164/ajrccm/144.5.1202; ANDERSON SD, 1971, THORAX, V26, P396, DOI 10.1136/thx.26.4.396; AVITAL A, 1995, THORAX, V50, P511, DOI 10.1136/thx.50.5.511; BAROR O, 1983, PHYSL PRINCIPLES CLI, P88; BECK KC, 1994, AM J RESP CRIT CARE, V149, P352; CHARPIN D, 1988, ALLERGY, V43, P481, DOI 10.1111/j.1398-9995.1988.tb01624.x; DEAL EC, 1980, AM REV RESPIR DIS, V121, P621; EGGLESTON PA, 1979, J ALLERGY CLIN IMMUN, V64, P642, DOI 10.1016/0091-6749(79)90028-9; HABY MM, 1995, EUR RESPIR J, V8, P729; HABY MM, 1994, EUR RESPIR J, V7, P431; Heir T., 1994, Scandinavian Journal of Medicine and Science in Sports, V4, P128; Heir T., 1994, Scandinavian Journal of Medicine and Science in Sports, V4, P134; Helenius IJ, 1996, THORAX, V51, P628, DOI 10.1136/thx.51.6.628; Helenius IJ, 1998, BRIT J SPORT MED, V32, P125; KNUDSON RJ, 1976, AM REV RESPIR DIS, V113, P587; Larsson L., 1994, Scandinavian Journal of Medicine and Science in Sports, V4, P124; MAHLER DA, 1993, MED SCI SPORT EXER, V25, P554; Mannix ET, 1996, CHEST, V109, P312, DOI 10.1378/chest.109.2.312; MCFADDEN ER, 1994, NEW ENGL J MED, V330, P1362, DOI 10.1056/NEJM199405123301907; MORRIS JF, 1976, WESTERN J MED, V125, P110; Nystad W, 2000, MED SCI SPORT EXER, V32, P266, DOI 10.1097/00005768-200002000-00003; ProvostCraig MA, 1996, J ASTHMA, V33, P67, DOI 10.3109/02770909609077764; Rundell KW, 2000, MED SCI SPORT EXER, V32, P309, DOI 10.1097/00005768-200002000-00010; RUPP NT, 1992, AM J DIS CHILD, V146, P941; SEARS MR, 1991, ASTHMA ITS PATHOLOGY, V49, P1; SMITH L, 1999, LUNG BIOL HEALTH DIS, V130, P235; STERK PJ, 1993, EUR RESPIR J, V6, P53, DOI 10.1183/09041950.053s1693; Tan RA, 1998, SPORTS MED, V25, P1, DOI 10.2165/00007256-199825010-00001; Tikkanen H. O., 1999, Medicine and Science in Sports and Exercise, V31, pS99, DOI 10.1097/00005768-199905001-00335; VOY RO, 1986, MED SCI SPORT EXER, V18, P328, DOI 10.1249/00005768-198606000-00013; Weiler JM, 1998, J ALLERGY CLIN IMMUN, V102, P722, DOI 10.1016/S0091-6749(98)70010-7; WILBER RL, IN PRESS MED SCI SPO	32	188	193	0	6	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	0195-9131			MED SCI SPORT EXER	Med. Sci. Sports Exerc.	FEB	2001	33	2					208	213				6	Sport Sciences	Sport Sciences	399PV	WOS:000166822300006	11224807	
J	Commins, SP; Satinover, SM; Hosen, J; Mozena, J; Borish, L; Lewis, BD; Woodfolk, JA; Platts-Mills, TAE				Commins, Scott P.; Satinover, Shama M.; Hosen, Jacob; Mozena, Jonathan; Borish, Larry; Lewis, Barrett D.; Woodfolk, Judith A.; Platts-Mills, Thomas A. E.			Delayed anaphylaxis, angioedema, or urticaria after consumption of red meat in patients with IgE antibodies specific for galactose-alpha-1,3-galactose	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Anaphylaxis; urticaria; food allergy; galactose-alpha-1,3-galactose; cross-reactive carbohydrate determinant	CROSS-REACTIVE IGE; ALPHA-GAL EPITOPE; CLINICAL-RELEVANCE; CARBOHYDRATE DETERMINANTS; LINKED OLIGOSACCHARIDES; IMMUNOGLOBULIN-E; FOOD ALLERGY; SOLID-PHASE; GLYCOPROTEINS; CETUXIMAB	Background: Carbohydrate moieties are frequently encountered in food and can elicit IgE responses, the clinical significance of which has been unclear. Recent work, however, has shown that IgE antibodies to galactose-alpha-1,3-galactose (alpha-gal), a carbohydrate commonly expressed on nonprimate mammalian proteins, are capable of eliciting serious, even fatal, reactions. Objective: We sought to determine whether IgE antibodies to alpha-gal are present in sera from patients who report anaphylaxis or urticaria after eating beef, pork, or lamb. Methods: Detailed histories were taken from patients presenting to the University of Virginia Allergy Clinic. Skin prick tests (SPTs), intradermal skin tests, and serum IgE antibody analysis were performed for common indoor, outdoor, and food allergens. Results: Twenty-four patients with IgE antibodies to alpha-gal were identified. These patients described a similar history of anaphylaxis or urticaria 3 to 6 hours after the ingestion of meat and reported fewer or no episodes when following an avoidance diet. SPTs to mammalian meat produced wheals of usually less than 4 mm, whereas intradermal or fresh-food SPTs provided larger and more consistent wheal responses. CAP-RAST testing revealed specific IgE antibodies to beef, pork, lamb, cow's milk, cat, and dog but not turkey, chicken, or fish. Absorption experiments indicated that this pattern of sensitivity was explained by an IgE antibody specific for alpha-gal. Conclusion: We report a novel and severe food allergy related to IgE antibodies to the carbohydrate epitope alpha-gal. These patients experience delayed symptoms of anaphylaxis, angioedema, or urticaria associated with eating beef, pork, or lamb. (J Allergy Clin Immunol 2009;123:426-33.)	[Platts-Mills, Thomas A. E.] Univ Virginia Hlth Syst, Div Allergy, Asthma & Allerg Dis Ctr, Charlottesville, VA 22908 USA; [Mozena, Jonathan] Allergy & Asthma Associates Fredericksburg, Fredericksburg, VA USA	Platts-Mills, TAE (reprint author), Univ Virginia Hlth Syst, Div Allergy, Asthma & Allerg Dis Ctr, POB 801355, Charlottesville, VA 22908 USA.	tap2z@virginia.edu	Hosen, Jacob/F-9224-2013; Osborne, Nicholas/N-4915-2015	Hosen, Jacob/0000-0003-2559-0687; Osborne, Nicholas/0000-0002-6700-2284	National Institutes of Health [RO1 AI-20565]; American Academy of Allergy, Asthma & Immunology/GlaxoSmithKline [T32 A1007496-14];  [AI-AADCRC-U19-070364]	Supported by National Institutes of Health grant RO1 AI-20565, by AI-AADCRC-U19-070364, and by an American Academy of Allergy, Asthma & Immunology/GlaxoSmithKline fellow career development award and T32 A1007496-14 to S.P.C.	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Allergy Clin. Immunol.	FEB	2009	123	2					426	433		10.1016/j.jaci.2008.10.052		8	Allergy; Immunology	Allergy; Immunology	409GU	WOS:000263495000022	19070355	
J	Beasley, R; Clayton, T; Crane, J; von Mutius, E; Lai, CKW; Montefort, S; Stewart, A				Beasley, Richard; Clayton, Tadd; Crane, Julian; von Mutius, Erika; Lai, Christopher K. W.; Montefort, Stephen; Stewart, Alistair		ISAAC Phase Three Study Grp	Association between paracetamol use in infancy and childhood, and risk of asthma, rhinoconjunctivitis, and eczema in children aged 6-7 years: analysis from Phase Three of the ISAAC programme	LANCET			English	Article							WORLDWIDE VARIATIONS; ALLERGIC RHINOCONJUNCTIVITIS; ACETAMINOPHEN USE; LUNG-FUNCTION; EARLY-LIFE; DRUG-USE; PREVALENCE; SYMPTOMS; ASPIRIN; IBUPROFEN	Background Exposure to paracetamol during intrauterine life, childhood, and adult life may increase the risk of developing asthma. We studied 6-7-year-old children from Phase Three of the International Study of Asthma and Allergies in Childhood (ISAAC) programme to investigate the association between paracetamol consumption and asthma. Methods As part of Phase Three of ISAAC, parents or guardians of children aged 6-7 years completed written questionnaires about symptoms of asthma, rhinoconjunctivitis, and eczema, and several risk factors, including the use of paracetamol for fever in the child's first year of life and the frequency of paracetamol use in the past 12 months. The primary outcome variable was the odds ratio (OR) of asthma symptoms in these children associated with the use of paracetamol for fever in the first year of life, as calculated by logistic regression. Findings 205 487 children aged 6-7 years from 73 centres in 31. countries were included in the analysis. In the multivariate analyses, use of paracetamol for fever in the first year of life was associated with an increased risk of asthma symptoms when aged 6-7 years (OR 1.46 [95% Cl 1.36-1.56]). Current use of paracetamol was associated with a dose-dependent increased risk of asthma symptoms (1.61 [1.46-1.77] and 3.23 [2.9]-3.60] for medium and high use vs no use, respectively). Use of paracetamol was similarly associated with the risk of severe asthma symptoms, with population-attributable risks between 22% and 38%. Paracetamol use, both in the first year of life and in children aged 6-7 years, was also associated with an increased risk of symptoms of rhinoconjunctivitis and eczema. Interpretation Use of paracetamol in the first year of life and in later childhood, is associated with risk of asthma, rhinoconjunctivitis, and eczema at age 6 to 7 years. We suggest that exposure to paracetamol might be a risk factor for the development of asthma in childhood. Funding The BUPA Foundation, the Health Research Council of New Zealand, the Asthma and Respiratory Foundation of New Zealand, the Hawke's Bay Medical Research Foundation, the Waikato Medical Research Foundation, Glaxo Wellcome New Zealand, the New Zealand Lottery Board, Astra Zeneca New Zealand, and Glaxo Wellcome international Medical Affairs.	[Beasley, Richard] Med Res Inst New Zealand, Wellington 6143, New Zealand; [Clayton, Tadd] Univ Auckland, Fac Med & Hlth Sci, Auckland 1, New Zealand; [Crane, Julian] Univ Otago, Dept Med, Wellington, New Zealand; [von Mutius, Erika] Univ Munich, Dr Von Haunerschen Kinderspital, D-80337 Munich, Germany; [Lai, Christopher K. W.] Univ Hong Kong, Dept Med & Therapeut, Hong Kong, Peoples R China; [Montefort, Stephen] Univ Malta, Dept Med, Msida, Malta; [Stewart, Alistair] Univ Auckland, Sch Populat Hlth, Auckland 1, New Zealand	Beasley, R (reprint author), Med Res Inst New Zealand, POB 10055, Wellington 6143, New Zealand.	Richard.Beasley@mrinz.ac.nz	Clayton, Tadd/B-7914-2009; MARTINEZ-GIMENO, ANTONIO/A-9416-2010; Ellwood, Philippa/G-7555-2015	MARTINEZ-GIMENO, ANTONIO/0000-0003-4051-1860; Ellwood, Philippa/0000-0002-1994-4023; brunekreef, bert/0000-0001-9908-0060; Masjedi, Mohammadreza/0000-0003-4964-3851; Beasley, Richard/0000-0003-0337-406X	ISAAC International Data Centre (IIDC) is The BUPA Foundation	We thank the children and parents who participated in ISAAC Phase Three, and the school staff for their coordination and assistance. The authors also acknowledge and thank die many funding bodies throughout the world that supported the individual ISAAC centres, collaborators, and their meetings. Currently, the main source of funding for the ISAAC International Data Centre (IIDC) is The BUPA Foundation. Many funding bodies in New Zealand have contributed to support the IIDC during the periods of fieldwork arid data compilation: the Health Research Council of New Zealand, the Asthma arid Respiratory Foundation of New Zealand, the Child Health Research Foundation, the Hawke's Bay Medical Research Foundation, the Waikato Medical Research Foundation, GlaxoWellcome New Zealand, the New Zealand Lottery Board, and Astra Zeneca New Zealand. GlaxoWellcome International Medical Affairs supported the regional coordination for Phase Three and the IIDC.	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J	Di Rienzo, V; Marcucci, F; Puccinelli, P; Parmiani, S; Frati, F; Sensi, L; Canonica, GW; Passalacqua, G				Di Rienzo, V; Marcucci, F; Puccinelli, P; Parmiani, S; Frati, F; Sensi, L; Canonica, GW; Passalacqua, G			Long-lasting effect of sublingual immunotherapy in children with asthma due to house dust mite: a 10-year prospective study	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						asthma; children; long-lasting effect; respiratory allergy; rhinitis; sublingual immunotherapy	GRASS-POLLEN IMMUNOTHERAPY; DOUBLE-BLIND; SWALLOW IMMUNOTHERAPY; CONTROLLED TRIAL; ALLERGOID IMMUNOTHERAPY; MESSENGER-RNA; FOLLOW-UP; PLACEBO; RHINITIS; SENSITIZATIONS	Background Subcutaneous immunotherapy for respiratory allergy has shown a long-lasting efficacy after its discontinuation, whereas this evidence is still lacking for sublingual immunotherapy, despite the fact that it is widely used. Objective We aimed to evaluate whether a long-lasting effect of SLIT occurs, in a prospective parallel group controlled study. Methods Sixty children (mean age 8.5 years) suffering from allergic asthma/rhinitis due to mites were subdivided into two matched groups: 35 underwent a 4- to 5-year course of SLIT with standardized extract and 25 received only drug therapy. The patients were evaluated at three time points (baseline, end of SLIT and 4 to 5 years after SLIT discontinuation) regarding presence of asthma, use of anti-asthma drugs, skin prick tests and specific IgE. Results We found that in the SLIT group there was a significant difference vs. baseline for the presence of asthma (P less than or equal to 0.001) and the use of asthma medications (P less than or equal to 0.01), whereas no difference was observed in the control group. The mean peak expiratory flow result was significantly higher in the active group than in the control group after 10 years. No change was seen as far as new sensitizations were concerned. Specific IgE showed a near-significant increase (baseline vs. 10 years, P = 0.06) only in the control group. Conclusion Our study demonstrates that sublingual immunotherapy is effective in children and that it maintains the clinical efficacy for 4 to 5 years after discontinuation.	Univ Genoa, DIMI, Padigl Maragliano, I-16132 Genoa, Italy; Clin Villa Benedetta, Rome, Italy; Univ Perugia, Pediat Clin, I-06100 Perugia, Italy; ALK Abello, Milan, Italy	Passalacqua, G (reprint author), Univ Genoa, DIMI, Padigl Maragliano, Largo R Benzi 10, I-16132 Genoa, Italy.						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Exp. Allergy	FEB	2003	33	2					206	210		10.1046/j.1365-2222.2003.01587.x		5	Allergy; Immunology	Allergy; Immunology	644PN	WOS:000180927400011	12580913	
J	Mostafalou, S; Abdollahi, M				Mostafalou, Sara; Abdollahi, Mohammad			Pesticides and human chronic diseases: Evidences, mechanisms, and perspectives	TOXICOLOGY AND APPLIED PHARMACOLOGY			English	Review						Pesticides; Systematic review; Chronic diseases; Cancer; Birth defects; Reproductive toxicity; Parkinson; Alzheimer; Amyotrophic lateral sclerosis; Diabetes; Asthma; Cardiovascular disease; Nephropathy; Genetic damage; Epigenetics; Endocrine disruption; Mitochondrial dysfunction; Oxidative stress; Endoplasmic reticulum stress; Proteotoxicity	NON-HODGKINS-LYMPHOMA; AMYOTROPHIC-LATERAL-SCLEROSIS; ENDOPLASMIC-RETICULUM STRESS; ENVIRONMENTAL RISK-FACTORS; SISTER-CHROMATID EXCHANGES; SOFT-TISSUE SARCOMA; EPIGENETIC TRANSGENERATIONAL ACTIONS; PARENTAL OCCUPATIONAL-EXPOSURE; PERSISTENT ORGANIC POLLUTANTS; INDUCED OXIDATIVE STRESS	Along with the wide use of pesticides in the world, the concerns over their health impacts are rapidly growing. There is a huge body of evidence on the relation between exposure to pesticides and elevated rate of chronic diseases such as different types of cancers, diabetes, neurodegenerative disorders like Parkinson, Alzheimer, and amyotrophic lateral sclerosis (ALS), birth defects, and reproductive disorders. There is also circumstantial evidence on the association of exposure to pesticides with some other chronic diseases like respiratory problems, particularly asthma and chronic obstructive pulmonary disease (COPD), cardiovascular disease such as atherosclerosis and coronary artery disease, chronic nephropathies, autoimmune diseases like systemic lupus erythematous and rheumatoid arthritis, chronic fatigue syndrome, and aging. The common feature of chronic disorders is a disturbance in cellular homeostasis, which can be induced via pesticides' primary action like perturbation of ion channels, enzymes, receptors, etc., or can as well be mediated via pathways other than the main mechanism. In this review, we present the highlighted evidence on the association of pesticide's exposure with the incidence of chronic diseases and introduce genetic damages, epigenetic modifications, endocrine disruption, mitochondrial dysfunction, oxidative stress, endoplasmic reticulum stress and unfolded protein response (UPR), impairment of ubiquitin proteasome system, and defective autophagy as the effective mechanisms of action. (C) 2013 Elsevier Inc. All rights reserved.	[Abdollahi, Mohammad] Univ Tehran Med Sci, Fac Pharm, Dept Pharmacol & Toxicol, Tehran, Iran; Univ Tehran Med Sci, Pharmaceut Sci Res Ctr, Tehran, Iran	Abdollahi, M (reprint author), Univ Tehran Med Sci, Fac Pharm, Dept Pharmacol & Toxicol, Tehran, Iran.	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Appl. Pharmacol.	APR 15	2013	268	2					157	177		10.1016/j.taap.2013.01.025		21	Pharmacology & Pharmacy; Toxicology	Pharmacology & Pharmacy; Toxicology	117UN	WOS:000316978700008	23402800	
J	Kuitunen, M; Kukkonen, K; Juntunen-Backman, K; Korpela, R; Poussa, T; Tuure, T; Haahtela, T; Savilahti, E				Kuitunen, Mikael; Kukkonen, Kaarina; Juntunen-Backman, Kaisu; Korpela, Riitta; Poussa, Tuija; Tuure, Tuula; Haahtela, Tari; Savilahti, Erkki			Probiotics prevent IgE-associated allergy until age 5 years in cesarean-delivered children but not in the total cohort	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Allergy; prevention; high-risk infants; probiotic; prebiotic; eczema; allergic rhinitis; asthma; cesarean	PLACEBO-CONTROLLED TRIAL; 1ST 6 MONTHS; ATOPIC-DERMATITIS; DOUBLE-BLIND; INTESTINAL MICROFLORA; ECZEMA; INFANTS; RISK; LIFE; OLIGOSACCHARIDES	Background: Less microbial exposure in early childhood is associated with more allergic disease later. Allergic children have a different fecal microflora, with less lactobacilli and bifidobacteria. Beneficial effects regarding the development of allergy have been suggested to come through probiotic supplementation. Objective: We sought to study the effect of probiotic and prebiotic supplementation in preventing allergies. Methods: In a double-blinded, placebo-controlled study we randomized 1223 mothers with infants at high risk for allergy to receive a probiotic mixture (2 lactobacilli, bifidobacteria, and propionibacteria) or placebo during the last month of pregnancy and their infants to receive it from birth until age 6 months. Infants also received a prebiotic galactooligosaccharide or placebo. At 5 years, we evaluated the cumulative incidence of allergic diseases (eczema, food allergy, allergic rhinitis, and asthma) and IgE sensitization. Results: Of the 1018 intent-to-treat infants, 891 (88%) attended the 5-year visit. Frequencies of allergic and IgE-associated allergic disease and sensitization in the probiotic and placebo groups were similar: 52.6% versus 54.9% and 29.5% versus 26.6%, respectively, and 41.3% in both. No significant difference appeared in frequencies of eczema (39.3% vs 43.3%), atopic eczema (24.0% vs 25.1%), allergic rhinitis (20.7% vs 19.1%), or asthma (13.0% vs 14.1%) between groups. However, less IgE-associated allergic disease occurred in cesarean-delivered children receiving probiotics (24.3% vs 40.5%; odds ratio, 0.47; 95% CI, 0.23% to 0.96%; P = .035). Conclusions: No allergy-preventive effect that extended to age 5 years was achieved with perinatal supplementation of probiotic bacteria to high-risk mothers and children. It conferred protection only to cesarean-delivered children. (J Allergy Clin Immunol 2009;123:335-41.)	[Kuitunen, Mikael; Kukkonen, Kaarina; Juntunen-Backman, Kaisu; Haahtela, Tari] Helsinki Univ Cent Hosp, Skin & Allergy Hosp, Helsinki, Finland; [Savilahti, Erkki] Helsinki Univ Cent Hosp, Hosp Children & Adolescents, Helsinki, Finland; [Korpela, Riitta] Univ Helsinki, Inst Biomed, Helsinki, Finland; [Korpela, Riitta; Tuure, Tuula] Valio Ltd, Res & Dev, Helsinki, Finland; [Poussa, Tuija] STAT Consulting, Tampere, Finland	Kuitunen, M (reprint author), Helsinki Univ Cent Hosp, Skin & Allergy Hosp, POB 160, FIN-00029 Helsinki, Finland.	mikael.kuitunen@hus.fi					Abrahamsson TR, 2007, J ALLERGY CLIN IMMUN, V119, P1174, DOI 10.1016/j.jaci.2007.01.007; Adlerberth I, 2007, J ALLERGY CLIN IMMUN, V120, P343, DOI 10.1016/j.jaci.2007.05.018; Bjorksten B, 2001, J ALLERGY CLIN IMMUN, V108, P516; Bjorksten B, 1999, CLIN EXP ALLERGY, V29, P342; BRUIJNZEELKOOMEN C, 1995, ALLERGY, V50, P623, DOI 10.1111/j.1398-9995.1995.tb02579.x; [Anonymous], 1993, ALLERGY, V48, P48; Gronlund MM, 1999, J PEDIATR GASTR NUTR, V28, P19, DOI 10.1097/00005176-199901000-00007; Hamilton BE, 2007, PEDIATRICS, V119, P345, DOI 10.1542/peds.2006-3226; Kalliomaki M, 2003, LANCET, V361, P1869, DOI 10.1016/S0140-6736(03)13490-3; Kalliomaki M, 2001, LANCET, V357, P1076, DOI 10.1016/S0140-6736(00)04259-8; Kalliomaki M, 2007, J ALLERGY CLIN IMMUN, V119, P1019, DOI 10.1016/j.jaci.2006.12.608; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Kopp MV, 2008, PEDIATRICS, V121, pE850, DOI 10.1542/peds.2007-1492; Kukkonen K, 2007, J ALLERGY CLIN IMMUN, V119, P192, DOI 10.1016/j.jaci.2006.09.009; Lund VJ, 1994, ALLERGY S19, V49, P1; Maizels RM, 2003, NAT REV IMMUNOL, V3, P733, DOI 10.1038/nri1183; Marschan E, 2008, CLIN EXP ALLERGY, V38, P611, DOI 10.1111/j.1365-2222.2008.02942.x; Moro G, 2006, ARCH DIS CHILD, V91, P814, DOI 10.1136/adc.2006.098251; Renz-Polster H, 2005, CLIN EXP ALLERGY, V35, P1466, DOI 10.1111/j.1365-2222.2005.02356.x; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Sato A, 2003, J IMMUNOL, V171, P3684; Sepp E, 2005, CLIN EXP ALLERGY, V35, P1141, DOI 10.1111/j.1365-2222.2005.02315.x; Sudo N, 1997, J IMMUNOL, V159, P1739; SUVILAHTI E, 2008, CURR OPIN ALLERGY CL, V8, P243; Suzuki S, 2007, CLIN EXP ALLERGY, V37, P506, DOI 10.1111/j.1365-2222.2007.02676.x; Taylor AL, 2007, J ALLERGY CLIN IMMUN, V119, P184, DOI 10.1016/j.jaci.2006.08.036; van den Biggelaar AHJ, 2004, J INFECT DIS, V189, P892, DOI 10.1086/381767; Viljanen M, 2005, J ALLERGY CLIN IMMUN, V115, P1254, DOI 10.1016/j.jaci.2005.03.047; Viljanen M, 2005, PEDIATR ALLERGY IMMU, V16, P65, DOI 10.1111/j.1399-3038.2005.00224.x; Villar J, 2007, BRIT MED J, V335, P1025, DOI 10.1136/bmj.39363.706956.55; Waser M, 2007, CLIN EXP ALLERGY, V37, P661, DOI 10.1111/j.1365-2222.2006.02640.x; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P406, DOI 10.1111/j.1365-2133.1994.tb08532.x	32	186	198	6	24	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	FEB	2009	123	2					335	341		10.1016/j.jaci.2008.11.019		7	Allergy; Immunology	Allergy; Immunology	409GU	WOS:000263495000007	19135235	
J	Bush, RK; Portnoy, JM; Saxon, A; Terr, AI; Wood, RA				Bush, RK; Portnoy, JM; Saxon, A; Terr, AI; Wood, RA			The medical effects of mold exposure	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						mold; fungi; hypersensitivity; allergy; asthma	ATOPIC-DERMATITIS; FUNGAL ALLERGENS; 1ST YEAR; SYMPTOMS; HEALTH; ASTHMA; MYCOTOXINS; RISK; IGE; SPORES	Exposure to molds can cause human disease through several well-defined mechanisms. In addition, many new mold-related illnesses have been hypothesized in recent years that remain largely or completely unproved. Concerns about mold exposure and its effects are so common that all health care providers, particularly allergists and immunologists, are frequently faced with issues regarding these real and asserted mold-related illnesses. The purpose of this position paper is to provide a state-of-the-art review of the role that molds are known to play in human disease, including asthma, allergic rhinitis, allergic bronchopulmonary aspergillosis, sinusitis, and hypersensitivity pneumonitis. In addition, other purported mold-related illnesses and the data that currently exist to support them are carefully reviewed, as are the currently available approaches for the evaluation of both patients and the environment.	Univ Wisconsin, Madison, WI USA; Childrens Mercy Hosp, Kansas City, KS USA; Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA; Stanford Univ, Sch Med, Palo Alto, CA 94304 USA; Johns Hopkins Med Ctr, Dept Pediat, Baltimore, MD USA	Wood, RA (reprint author), Johns Hopkins Univ Hosp, CMSC 1102,600 N Wolfe St, Baltimore, MD 21287 USA.	rwood@jhmi.edu					*ACOEM COUNC SCI A, 2002, ADV HLTH EFF ASS MOL; Andersson M, 2003, PEDIATR ALLERGY IMMU, V14, P100, DOI 10.1034/j.1399-3038.2003.00031.x; Belanger K, 2003, AM J EPIDEMIOL, V158, P195, DOI 10.1093/aje/kwg148; Bush RK, 2005, J ALLERGY CLIN IMMUN, V115, P123, DOI 10.1016/j.jaci.2004.10.025; Bush RK, 2004, J ALLERGY CLIN IMMUN, V113, P227, DOI 10.1016/j.jaci.2003.11.023; Campbell AW, 2004, ADV APPL MICROBIOL, V55, P375, DOI 10.1016/S0065-2164(04)55015-3; *CDCP, CAS DEF CHEM POIS; McCammon J., 2001, AIR SAMPLING INSTRUM; Committee on the Assessment of Asthma and Indoor Air Division of Health Promotion and Disease Prevention IOM, 2002, CLEAR AIR ASTHM IND; Committee on Damp Indoor Spaces and Health, 2004, DAMP IND SPAC HLTH; *CTR FOOD SAF APPL, 2004, TITL 21 FOOD DRUGS; Delfino RJ, 1996, AM J RESP CRIT CARE, V154, P633; FEIGIN RD, 2003, TXB PEDIAT INFECT DI; Fung F, 2004, J TOXICOL-CLIN TOXIC, V42, P217, DOI 10.1081/CLT-120030947; Gent JF, 2002, ENVIRON HEALTH PERSP, V110, pA781; GERGEN PJ, 1992, J ALLERGY CLIN IMMUN, V90, P579, DOI 10.1016/0091-6749(92)90130-T; Gray MR, 2003, ARCH ENVIRON HEALTH, V58, P410; Greenberger PA, 2002, J ALLERGY CLIN IMMUN, V110, P685, DOI 10.1067/mai.2002.130179; Hamilton RG, 2004, J ALLERGY CLIN IMMUN, V114, P213, DOI 10.1016/j.jaci.2004.06.046; Helbling A, 1998, J ALLERGY CLIN IMMUN, V102, P853, DOI 10.1016/S0091-6749(98)70028-4; HORNER WE, 1995, CLIN MICROBIOL REV, V8, P161; Huang SW, 1997, CLIN PEDIATR, V36, P695, DOI 10.1177/000992289703601205; Katz Y, 1999, CLIN EXP ALLERGY, V29, P186; Kelman BJ, 2004, INT J TOXICOL, V23, P3, DOI 10.1080/10915810490265423; Lander F, 2001, INFLAMM RES, V50, P227, DOI 10.1007/s000110050748; Luong A, 2004, CURR ALLERGY ASTHM R, V4, P465, DOI 10.1007/s11882-004-0013-5; Macher J, 1999, BIOAEROSOLS ASSESSME; Mandell GL, 2004, PRINCIPLES PRACTICE; Monaci L, 2004, ANAL BIOANAL CHEM, V378, P96, DOI 10.1007/s00216-003-2364-5; Montealegre F, 2004, CLIN EXP ALLERGY, V34, P51, DOI 10.1111/j.1365-2222.2004.01855.x; *OSHA US DEP LAB, BRIEF GUID MOLD WORK; Pasanen AL, 1996, ANALYST, V121, P1949, DOI 10.1039/an9962101949; Pasanen AL, 1998, ENVIRON INT, V24, P703, DOI 10.1016/S0160-4120(98)00065-8; Peat JK, 1998, ALLERGY, V53, P120, DOI 10.1111/j.1398-9995.1998.tb03859.x; Reijula K, 2003, ANN ALLERG ASTHMA IM, V91, P280; Roponen M, 2002, INHAL TOXICOL, V14, P541, DOI 10.1080/089583701753678616; ROWE MS, 1986, J ALLERGY CLIN IMMUN, V77, P714, DOI 10.1016/0091-6749(86)90416-1; SALVAGGIO JE, 1994, J ALLERGY CLIN IMMUN, V94, P380; Scalabrin DMF, 1999, J ALLERGY CLIN IMMUN, V104, P1273, DOI 10.1016/S0091-6749(99)70024-2; Taskinen TM, 2002, ALLERGY, V57, P9, DOI 10.1034/j.1398-9995.2002.13154.x; Trout DB, 2004, ANN ALLERG ASTHMA IM, V92, P483; Verhoeff AP, 1997, ANN ALLERG ASTHMA IM, V78, P544; 2005, NATURE, V437, P452; [Anonymous], 2005, MMWR MORB MORTAL WKL, V54, P1018	44	186	189	0	14	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	FEB	2006	117	2					326	333		10.1016/j.jaci.2005.12.001		8	Allergy; Immunology	Allergy; Immunology	017IM	WOS:000235687300015	16514772	
J	Matricardi, PM; Rosmini, F; Panetta, V; Ferrigno, L; Bonini, S				Matricardi, PM; Rosmini, F; Panetta, V; Ferrigno, L; Bonini, S			Hay fever and asthma in relation to markers of infection in the United States	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; hay fever; hepatitis A virus; hygiene; infection; epidemiology; National Health and Nutrition Examination Survey III	ANTHROPOSOPHIC LIFE-STYLE; ATOPY; PREVALENCE; CHILDREN; CHILDHOOD; SIBLINGS; EXPOSURE; INCREASE; ALLERGY; HYGIENE	Background: The hygiene hypothesis proposes that declining exposure to infections is implicated in the rising trend of allergy, and asthma. Objective: We sought to test this hypothesis by examining the relationship of hay fever, asthma, and atopic sensitization with markers of infection in a large general population sample of the United States. Methods: We analyzed the data of 33,994 US residents recorded in a public database of a nationally representative cross-sectional survey (Third National Health and Nutrition Examination Survey, 1988-1994). The variables examined were sociodemographic information, lifetime diagnosis and age at first diagnosis of hay fever or asthma, current skin sensitization to 9 airborne allergens and peanut, and current serology for Toxoplasma gondii, herpes simplex viruses type 1 and 2, and hepatitis A, B, and C viruses. Results: Hay fever (adjusted odds ratio, 0.27; 95% CI, 0.18-0.41; P<.001) and asthma (adjusted odds ratio, 0.45; 95% CI, 0.31-0.66; P<.001) were less frequent in subjects seropositive for hepatitis A virus (HAV), T gondii, and herpes simplex virus 1 versus seronegative subjects after adjusting for age, sex, race, urban residence, census region, family size, income, an education. Skin sensitization to peanut and to all the airborne allergens examined, except for cockroach, was less frequent among HAV-seropositive versus HAV-seronegative subjects younger than 40 years of age. The prevalence of hay fever and asthma diagnosed at or before 18 years of age in HAV-seronegative subjects increased progressively from 2.7% (95% CI, 0.71%-4.7%) and 0.4% (95% CI, 0.1%-1.6%), respectively, in cohorts born before 1920 to 8.5% (95% CI, 7.3%-9.7%) and 5.8% (95% CI, 4.8%-6.8%), respectively, in cohorts born in the 1960s, whereas they remained constant at around 2% in all cohorts of HAV-seropositive subjects. Conclusion: In the United States serologic evidence of acquisition of certain infections, mainly food-borne and orofecal infection, is associated with a lower probability of having hay, fever and asthma. Third National Health and Nutrition Examination Survey data support the hypothesis that hygiene is a major factor contributing to the increase in hay fever, asthma, and atopic sensitization in westernized countries.	CNR, Inst Neurobiol & Mol Med, Rome, Italy; Ist Super Sanita, Epidemiol & Biostat Lab, I-00161 Rome, Italy	Matricardi, PM (reprint author), WHO, Chron Resp Dis & Arthrit Unit, 20 Ave Appia, CH-1211 Geneva 27, Switzerland.			Bonini, Sergio/0000-0003-0079-3031			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; Behrendt H, 1995, PROG ALLER CLIN IMM, V3, P83; Bock SA, 2001, J ALLERGY CLIN IMMUN, V107, P191, DOI 10.1067/mai.2001.112031; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Busse WW, 2001, NEW ENGL J MED, V344, P350; GUNTER EW, 1996, NCHS CDC PUBLICATION; Holgate ST, 2000, BRIT MED J, V320, P231, DOI 10.1136/bmj.320.7229.231; Holgate ST, 2000, J ALLERGY CLIN IMMUN, V105, P193, DOI 10.1016/S0091-6749(00)90066-6; Kitch BT, 2000, ENVIRON HEALTH PERSP, V108, P301, DOI 10.2307/3454347; Kramer U, 1999, LANCET, V353, P450, DOI 10.1016/S0140-6736(98)06329-6; Martinez FD, 1999, LANCET S2, V354, pSII12; Matricardi PM, 2000, BRIT MED J, V320, P412, DOI 10.1136/bmj.320.7232.412; Matricardi PM, 1999, LANCET, V354, P430, DOI 10.1016/S0140-6736(05)75853-0; Matricardi PM, 1998, J ALLERGY CLIN IMMUN, V101, P439, DOI 10.1016/S0091-6749(98)70350-1; Matricardi PM, 1997, BRIT MED J, V314, P999; McIntire JJ, 2001, NAT IMMUNOL, V2, P1109, DOI 10.1038/ni739; *PLAN OP 3 NAT HLT, 1994, VITAL HLTH STAT, V32, P1; Platts-Mills TAE, 2001, AM J RESP CRIT CARE, V164, P1107; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Snedecor G.W., 1967, STAT METHODS, p[246, 349]; Stevenson LA, 2001, J ALLERGY CLIN IMMUN, V108, P747, DOI 10.1067/mai.2001.119410; Strachan David P., 2000, Thorax, V55, pS2, DOI 10.1136/thorax.55.suppl_1.S2; STRACHAN DP, 1989, BRIT MED J, V299, P1259; VONMUTIUS E, 1994, AM J RESP CRIT CARE, V149, P358; VONMUTIUS E, 1994, BRIT MED J, V308, P692; Weiss ST, 1997, CIBA F SYMP, V206, P244; Woolcock AJ, 1995, ALLERGY, V50, P935, DOI 10.1111/j.1398-9995.1995.tb02504.x; Yazdanbakhsh M, 2002, SCIENCE, V296, P490, DOI 10.1126/science.296.5567.490	29	186	196	2	18	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	SEP	2002	110	3					381	387		10.1067/mai.2002.126658		7	Allergy; Immunology	Allergy; Immunology	592KM	WOS:000177936900006	12209083	
J	Gilliland, FD; Berhane, K; McConnell, R; Gauderman, WJ; Vora, H; Rappaport, EB; Avol, E; Peters, JM				Gilliland, FD; Berhane, K; McConnell, R; Gauderman, WJ; Vora, H; Rappaport, EB; Avol, E; Peters, JM			Maternal smoking during pregnancy, environmental tobacco smoke exposure and childhood lung function	THORAX			English	Article						maternal smoking; pregnancy; environmental tobacco smoke; lung function; children	PULMONARY-FUNCTION; PARENTAL SMOKING; FUNCTION GROWTH; CHILDREN; ASTHMA; LIFE	Background-Exposure to environmental tobacco smoke (ETS) during childhood and in utero exposure to maternal smoking are associated with adverse effects on lung growth and development. Methods-A study was undertaken of the associations between maternal smoking during pregnancy, exposure to ETS, and pulmonary function in 3357 school children residing in 12 Southern California communities. Current and past exposure to household ETS and exposure to maternal smoking in utero were assessed by at self-administered questionnaire completed by parents of 4th,7th; and 10th grade students in 1993. Standard linear regression techniques were used to estimate the effects of in utero and ETS exposure on lung function, adjusting for age, sex, race, Hispanic ethnicity, height, weight, asthma, personal smoking, and selected household characteristics. Results-In utero exposure to maternal smoking was associated with reduced peak expiratory flow rate (PEFR) (-3.0%, 95% CI -4.4 to -1.4), mean mid expiratory flow (MMEF) (-4.6%, 95% CI -7.0 to -2.3), and forced expiratory flow (FEF75) (-6.2%, 95% CI -9.1 to -3.1), but not forced expiratory volume in one second (FEV1). Adjusting for household ETS exposure did not substantially change these estimates. The reductions in flows associated with in utero exposure did not significantly vary with sex, race, grade, income, parental education, or personal smoking. Exposure to two or more current household smokers was associated with reduced MMEF (-4.1%, 95% CI -7.6 to -0.4) and FEF75 (-4.4%, 95% CI -9.0 to 0.4). Current or past maternal smoking was associated with reductions in PEFR and MMEF; however, after adjustment for in utero exposure, deficits in MMEF and FEF75 associated with all measurements of ETS were substantially reduced and were not statistically significant. Conclusions-In utero exposure to maternal smoking is independently associated with decreased lung function in children of school age, especially for small airway flows.	Univ So Calif, Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA	Gilliland, FD (reprint author), Univ So Calif, Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.				NHLBI NIH HHS [R01 HL/ES61768-01]; NIEHS NIH HHS [1PO1ESO939581-05, 5P30ES07048-02]		American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P1285, DOI 10.1164/ajrccm/136.5.1285; BURROWS B, 1980, AM REV RESPIR DIS, V122, P813; California Environmental Protection Agency, 1997, HLTH EFF EXP ENV TOB; *CDC, 1997, MMWR-MORBID MORTAL W, V46, P1038; Cook DG, 1998, THORAX, V53, P884; COULTAS DB, 1989, AM J EPIDEMIOL, V130, P338; COULTAS DB, 1990, AM REV RESPIR DIS, V142, P602; CUNNINGHAM J, 1995, AM J RESP CRIT CARE, V152, P565; CUNNINGHAM J, 1994, AM J EPIDEMIOL, V139, P1139; Cunningham J, 1996, AM J RESP CRIT CARE, V153, P218; Dezateux C, 1997, BRIT MED BULL, V53, P40; DIJKSTRA L, 1990, AM REV RESPIR DIS, V142, P1172; Hanrahan J P, 1998, Eur Respir J Suppl, V27, p46s; HANRAHAN JP, 1992, AM REV RESPIR DIS, V145, P1129; Jedrychowski W, 1997, Pneumonol Alergol Pol, V65, P605; Lodrup Carlsen K C, 1997, Eur Respir J, V10, P1774, DOI 10.1183/09031936.97.10081774; ORYSZCZYN MP, 1991, J ALLERGY CLIN IMMUN, V87, P1169, DOI 10.1016/0091-6749(91)92163-U; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; Peters JM, 1999, AM J RESP CRIT CARE, V159, P768; RONCHETTI R, 1994, EUR RESPIR J, V7, P472, DOI 10.1183/09031936.94.07030472; SHERRILL DL, 1992, AM REV RESPIR DIS, V145, P1136; SHERRILL DL, 1991, AM REV RESPIR DIS, V144, P17; Stick SM, 1996, LANCET, V348, P1060, DOI 10.1016/S0140-6736(96)04446-7; TAGER IB, 1988, AM REV RESPIR DIS, V138, P837; TAGER IB, 1995, AM J RESP CRIT CARE, V152, P977; TAGER IB, 1983, NEW ENGL J MED, V309, P699, DOI 10.1056/NEJM198309223091204; TAGER IB, 1993, AM REV RESPIR DIS, V147, P811; TAGER IB, 1987, AM REV RESPIR DIS, V136, P1366; *US DHHS, 1986, 878398 US DHHS; WANG XB, 1993, AM REV RESPIR DIS, V148, P1502; WANG XB, 1994, AM J RESP CRIT CARE, V149, P1420; Wypij D, 1996, AM J RESP CRIT CARE, V154, pS223	32	186	198	1	7	BRITISH MED JOURNAL PUBL GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	APR	2000	55	4					271	276		10.1136/thorax.55.4.271		6	Respiratory System	Respiratory System	299FK	WOS:000086185800006	10722765	
J	Thorne, PS; Kulhankova, K; Yin, M; Cohn, R; Arbes, SJ; Zeldin, DC				Thorne, PS; Kulhankova, K; Yin, M; Cohn, R; Arbes, SJ; Zeldin, DC			Endotoxin exposure is a risk factor for asthma - The National Survey of Endotoxin in United States Housing	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						airway inflammation; house dust; lipopolysaccharide; wheeze	LOWER RESPIRATORY-TRACT; DUST-INDUCED INFLAMMATION; GRAIN DUST; COTTON DUST; AIRBORNE ENDOTOXIN; ALLERGIC DISEASES; BIRTH COHORT; CHILDREN; FARM; LIPOPOLYSACCHARIDE	Background: Although research has shown that early life exposure to household endotoxin protects against development of allergies, studies are less clear on the relationship between household endotoxin exposure and prevalence of wheezing and asthma. We assayed 2,552 house dust samples in a representative nationwide sample to explore relationships between endotoxin exposures and risk factors for asthma, asthma symptoms, and medication use. Methods: House dust was vacuum-sampled from five locations within homes and assayed for endotoxin. Health, demographic, and housing information was assessed through questionnaire and on-site evaluation of 2,456 residents of 831 homes selected to represent the demographics of the United States. Results: Endotoxin concentration (EU/mg) and load (EU/m(2)) were highly correlated (r = 0.73-0.79). Geometric mean endotoxin concentrations were as follows (in EU/mg): bedroom floors, 35.3 (5th-95th percentile, 5.0-260); bedding, 18.7 (2.0-142); family room floors, 63.9 (11.5-331); sofas, 44.8 (6.4-240); and kitchen floors, 80.5 (9.8-512). Multivariate analysis demonstrated significant relationships between increasing endotoxin levels and diagnosed asthma, asthma symptoms in the past year, current use of asthma medications, and wheezing among residents of the homes. These relationships were strongest for bedroom floor and bedding dust and were observed in adults only. Modeling the joint effect of bedding and bedroom floor endotoxin on recent asthma symptoms yielded an adjusted odds ratio of 2.83 (95% confidence interval, 1.01-7.87). When stratified by allergy status, allergic subjects with higher endotoxin exposure were no more likely to have diagnosed asthma or asthma symptoms than nonallergic subjects. Conclusion: This study demonstrates that household endotoxin exposure is a significant risk factor for increased asthma prevalence.	Univ Iowa, Coll Publ Hlth, Dept Environm & Occupat Hlth, Environm Hlth Sci Res Ctr, Iowa City, IA 52242 USA; Constella Grp Inc, Durham, NC USA; NIEHS, Div Intramural Res, Res Triangle Pk, NC 27709 USA	Thorne, PS (reprint author), Univ Iowa, Coll Publ Hlth, Dept Environm & Occupat Hlth, Environm Hlth Sci Res Ctr, 100 Oakdale Campus,176 IREH, Iowa City, IA 52242 USA.	peter-thorne@uiowa.edu			Intramural NIH HHS; NIEHS NIH HHS [P30 ES05605, Z01 ES025041-08]		Bolte G, 2003, CLIN EXP ALLERGY, V33, P770, DOI 10.1046/j.1365-2222.2003.01665.x; Braun-Fahrlander C, 2002, NEW ENGL J MED, V347, P869, DOI 10.1056/NEJMoa020057; CASTELLAN RM, 1984, ANN INTERN MED, V101, P157; CAVAGNA G, 1969, BRIT J IND MED, V26, P314; Chrischilles E, 2004, J ALLERGY CLIN IMMUN, V113, P66, DOI 10.1016/j.jaci.2003.09.037; CINKOTAI FF, 1977, AM IND HYG ASSOC J, V38, P554, DOI 10.1080/0002889778507669; CLAPP WD, 1994, AM J RESP CRIT CARE, V150, P611; Deetz DC, 1997, AM J RESP CRIT CARE, V155, P254; Douwes J, 2003, ANN OCCUP HYG, V47, P187, DOI 10.1093/annhyg/meg032; 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, 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; Gioannini TL, 2003, J ENDOTOXIN RES, V9, P401, DOI 10.1179/096805103225002773; Jagielo PJ, 1996, AM J PHYSIOL-LUNG C, V270, pL1052; Jagielo PJ, 1996, CHEST, V110, P263, DOI 10.1378/chest.110.1.263; Kline JN, 1999, AM J RESP CRIT CARE, V160, P297; Klintberg B, 2001, EUR RESPIR J, V17, P1151, DOI 10.1183/09031936.01.00027301; Leynaert B, 2001, AM J RESP CRIT CARE, V164, P1829; Litonjua AA, 2002, J ALLERGY CLIN IMMUN, V110, P736, DOI 10.1067/mai.2002.128948; Merchant JA, 2005, ENVIRON HEALTH PERSP, V113, P350, DOI 10.1289/ehp.7240; 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; National Center for Health Statistics, 2002, ASTHM PREV HLTH CAR; Nomura F, 2000, J IMMUNOL, V164, P3476; Park JH, 2000, ENVIRON HEALTH PERSP, V108, P1023, DOI 10.2307/3434953; Park JH, 2001, ENVIRON HEALTH PERSP, V109, P859, DOI 10.2307/3454831; PERNIS B, 1960, Med Lav, V51, P780; PETERSON RD, 1964, J ALLERGY, V35, P134, DOI 10.1016/0021-8707(64)90027-9; RYLANDER R, 1987, AM J IND MED, V12, P687, DOI 10.1002/ajim.4700120607; SCHWARTZ DA, 1994, AM J PHYSIOL-LUNG C, V267, pL609; Thorne PS, 1999, AM J RESP CELL MOL, V20, P1155; THORNE PS, 2000, TOXICOLOGY, V152, P627; THORNE PS, 2003, AM J RESP CRIT CARE, V167, pA470; THORNE PS, 1999, ORGANIC INDOOR AIR P, P275, DOI 10.1002/9783527613663.ch20; Tobias PS, 1999, CLIN INFECT DIS, V28, P476, DOI 10.1086/515163; Vojta PJ, 2002, ENVIRON HEALTH PERSP, V110, P527; Wickens K, 2002, ALLERGY, V57, P1171, DOI 10.1034/j.1398-9995.2002.t01-1-23644.x; Wouters IM, 2000, APPL ENVIRON MICROB, V66, P627, DOI 10.1128/AEM.66.2.627-631.2000	41	185	190	0	7	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	DEC 1	2005	172	11					1371	1377		10.1164/rccm.200505-758OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	989TR	WOS:000233697300006	16141442	
J	Pijnenburg, MW; Hofhuis, W; Hop, WC; De Jongste, JC				Pijnenburg, MW; Hofhuis, W; Hop, WC; De Jongste, JC			Exhaled nitric oxide predicts asthma relapse in children with clinical asthma remission	THORAX			English	Article							AIRWAY INFLAMMATION; INHALED BUDESONIDE; CHILDHOOD ASTHMA; MILD ASTHMA; MARKERS; CORTICOSTEROIDS; REPRODUCIBILITY; BECLOMETHASONE; ADULTS	Background: Nitric oxide in exhaled air (FENO) is a marker of eosinophilic airway inflammation. A study was undertaken to determine whether FENO predicts asthma relapse in asymptomatic asthmatic children in whom inhaled corticosteroids are discontinued. Methods: Forty children ( 21 boys) of mean age 12.2 years on a median dose of 400 mg budesonide or equivalent ( range 100 - 400) were included. FENO was measured before and 2, 4, 12, and 24 weeks after withdrawal of steroids. A relapse was defined as more than one exacerbation per month, or need for beta agonist treatment on 4 days per week for at least 2 weeks, or diurnal peak flow variability of >20%. FENO measurements were performed online with an expiratory flow of 50 ml/s. Results: Nine patients relapsed. Two and 4 weeks after withdrawal of steroids geometric mean FENO in children who were about to relapse was higher than in those who did not relapse: 35.3 ppb v 15.7 ppb at 2 weeks ( ratio 2.3; 95% CI 1.2 to 4.1; p = 0.01) and 40.8 ppb v 15.9 ppb at 4 weeks ( ratio 2.6; 95% CI 1.3 to 5.1). An FENO value of 49 ppb at 4 weeks after discontinuation of steroids had the best combination of sensitivity ( 71%) and specificity ( 93%) for asthma relapse. Conclusion: FENO 2 and 4 weeks after discontinuation of steroids in asymptomatic asthmatic children may be an objective predictor of asthma relapse.	Sophia Childrens Univ Hosp, Erasmus Med Ctr, Dept Paediat Paediat Resp Med, NL-3000 CB Rotterdam, Netherlands; Sophia Childrens Univ Hosp, Erasmus Med Ctr, Dept Biostat & Epidemiol, Rotterdam, Netherlands	De Jongste, JC (reprint author), Sophia Childrens Univ Hosp, Erasmus Med Ctr, Dept Paediat Paediat Resp Med, POB 2060, NL-3000 CB Rotterdam, Netherlands.	j.c.dejongste@erasmusmc.nl					Baraldi E, 2002, EUR RESPIR J, V20, P223, DOI 10.1183/09031936.02.00293102; Baraldi E, 1997, J PEDIATR-US, V131, P381, DOI 10.1016/S0022-3476(97)80062-5; Barbee RA, 1998, J ALLERGY CLIN IMMUN, V102, pS65, DOI 10.1016/S0091-6749(98)70006-5; Beck-Ripp J, 2002, EUR RESPIR J, V19, P1015, DOI 10.1183/09031936.02.01582001; COX DR, 1972, J R STAT SOC B, V34, P187; HAMID Q, 1993, LANCET, V342, P1510, DOI 10.1016/S0140-6736(05)80083-2; Hoekstra M O, 1997, Ned Tijdschr Geneeskd, V141, P2223; Jatakanon A, 1999, THORAX, V54, P108; Jatakanon A, 2000, AM J RESP CRIT CARE, V161, P64; Jones SL, 2001, AM J RESP CRIT CARE, V164, P738; Kharitonov SA, 2001, AM J RESP CRIT CARE, V163, P1693; Kharitonov SA, 2003, EUR RESPIR J, V21, P433, DOI 10.1183/09031936.03.00066903; Kharitonov SA, 1996, EUR RESPIR J, V9, P196, DOI 10.1183/09031936.96.09020196; Leuppi JD, 2001, AM J RESP CRIT CARE, V163, P406; Lim S, 1999, AM J RESP CRIT CARE, V159, P22; LIM TK, 2001, AM J RESP CRIT CARE, V163, pA48; Silkoff PE, 2001, CHEST, V119, P1322, DOI 10.1378/chest.119.5.1322; Slutsky AS, 1999, AM J RESP CRIT CARE, V160, P2104; Strachan DP, 1999, ALLERGY, V54, P7, DOI 10.1111/j.1398-9995.1999.tb04381.x; Verberne AAPH, 1998, AM J RESP CRIT CARE, V158, P213; Zapletal A, 1987, PROGR RESPIRATION RE, V22, P114	21	185	193	0	2	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	MAR	2005	60	3					215	218		10.1136/thx.2004.023374		4	Respiratory System	Respiratory System	904BR	WOS:000227470700011	15741438	
J	Guilbert, TW; Morgan, WJ; Zeiger, RS; Bacharier, LB; Boehmer, SJ; Krawiec, M; Larsen, G; Lemanske, RF; Liu, A; Mauger, DT; Sorkness, C; Szefler, SJ; Strunk, RC; Taussig, LM; Martinez, FD				Guilbert, TW; Morgan, WJ; Zeiger, RS; Bacharier, LB; Boehmer, SJ; Krawiec, M; Larsen, G; Lemanske, RF; Liu, A; Mauger, DT; Sorkness, C; Szefler, SJ; Strunk, RC; Taussig, LM; Martinez, FD			Atopic characteristics of children with recurrent wheezing at high risk for the development of childhood asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergens; aeroallergen and food sensitization; asthma predictive index; atopy; clinical trials; earIv childhood asthma; fluticasone; glucocorticoids; intermittent wheezing; prevention of asthma; research network; skin prick test	MANAGEMENT PROGRAM CAMP; INNER-CITY ASTHMA; HOUSE-DUST MITE; BRONCHIAL HYPERRESPONSIVENESS; NATURAL-HISTORY; IGE ANTIBODIES; ALLERGENS; SENSITIZATION; EXPOSURE; DESIGN	Background: Few studies have characterized the atopic profile of toddler-aged children with recurrent wheezing at high risk of the development of persistent asthma. Objective: We sought to determine the atopic profile of toddler-aged children with frequent wheeze at high risk for the development of persistent asthma who either had a parental history of asthma, a personal history of atopic dermatitis, or both. Methods: Participants enrolled in the Prevention of Early Asthma in Kids study (n = 285) on the basis of a modified Asthma Predictive Index were characterized on the basis of allergy and asthma questionnaire responses and allergy skin puncture test results. Results: The majority of the children (60.7%, n = 148) were sensitized to either food or aeroallergens. Male children were significantly more likely to be sensitized to aeroallergens (P =.03) and to have a blood eosinophil level of 4% or greater (P =.03) and a total serum IgE level of greater than 100 IU/mL (P =.0004). Additionally, eosinophilia and total serum IgE level had the strongest correlation with aeroallergen sensitization. Conclusion: The high prevalence of aeroallergen sensitization in this high-risk cohort suggests that aeroallergens might have an important role in the early development of asthma. As such, the Prevention of Early Asthma in Kids cohort appears to he an appropriate cohort in which to test whether early intervention with an inhaled corticosteroid can significantly attenuate, or perhaps even prevent, the allergic march from the initial stages of allergic sensitization to the subsequent development of asthma in toddlers with episodic wheezing.	Univ Arizona, Div Pediat Pulm Med, Arizona Resp Ctr, Tucson, AZ 85724 USA; Univ Calif San Diego, San Diego, CA 92103 USA; Kaiser Permanente, San Diego, CA USA; Washington Univ, St Louis, MO USA; Penn State Univ, Hershey, PA USA; Univ Wisconsin, Madison, WI USA; Natl Jewish Med & Res Ctr, Denver, CO USA	Guilbert, TW (reprint author), Univ Arizona, Div Pediat Pulm Med, Arizona Resp Ctr, 1501 N Campbell Ave,POB 245073, Tucson, AZ 85724 USA.	Guilbert@arc.arizona.edu		Guilbert, Theresa/0000-0002-6932-712X	NHLBI NIH HHS [HL64313, HL004519-04, HL071742-01]		Air pollution and respiratory health Br NCEH CDC, 1996, MMWR MORB MORTAL WKL, V45, P350; Amr S, 2003, ANN ALLERG ASTHMA IM, V90, P34; Arbes SJ, 2004, J ALLERGY CLIN IMMUN, V114, P111, DOI 10.1016/j.jaci.2004.04.036; Arlian LG, 2001, ANN ALLERG ASTHMA IM, V87, P296; Castro-Rodriguez JA, 2000, AM J RESP CRIT CARE, V162, P1403; Cherniack R, 1999, CONTROL CLIN TRIALS, V20, P91; *CHILD ASTH MAN PR, 1994, CHILDH ASTHM MAN PRO; DUFF AL, 1993, PEDIATRICS, V92, P535; Guilbert TW, 2004, CONTROL CLIN TRIALS, V25, P286, DOI 10.1016/j.cct.2004.03.002; Halonen M, 1997, AM J RESP CRIT CARE, V155, P1356; HILL DJ, 1994, CLIN EXP ALLERGY, V24, P1137; Kattan M, 1997, PEDIATR PULM, V24, P253, DOI 10.1002/(SICI)1099-0496(199710)24:4<253::AID-PPUL4>3.0.CO;2-L; Kulig M, 1998, PEDIAT ALLERG IMM-UK, V9, P61, DOI 10.1111/j.1399-3038.1998.tb00305.x; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Mitchell H, 1997, PEDIATR PULM, V24, P237; Nafstad P, 2001, ALLERGY, V56, P307, DOI 10.1034/j.1398-9995.2001.00881.x; NELSON HS, 1995, ANN ALLERG ASTHMA IM, V75, P337; Nelson HS, 1999, J ALLERGY CLIN IMMUN, V104, P775; Pao CS, 2002, AM J RESP CRIT CARE, V166, P945, DOI 10.1164/rccm.200203-265OC; 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; Plaschke P, 1999, J ALLERGY CLIN IMMUN, V104, P58, DOI 10.1016/S0091-6749(99)70114-4; Platts-Mills TA, 2000, J ALLERGY CLIN IMMUN, V105, P503; PRICE GW, 1995, J ALLERGY CLIN IMMUN, V96, P266, DOI 10.1016/S0091-6749(95)70020-X; 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; SIGURS N, 1994, J ALLERGY CLIN IMMUN, V94, P757, DOI 10.1016/0091-6749(94)90184-8; Song CH, 1997, ANN ALLERG ASTHMA IM, V79, P273; SPORIK R, 1991, ARCH DIS CHILD, V66, P1050; Stein RT, 1997, THORAX, V52, P946; Strunk RC, 2002, J ALLERGY CLIN IMMUN, V110, P395, DOI 10.1067/mai.2002.127433; SULLIVAN S, 1996, AM J RESP CRIT CAR S, V154, P84; Szefler S, 2000, NEW ENGL J MED, V343, P1054; TAUSSIG LM, 1989, AM J EPIDEMIOL, V129, P1219; Withers NJ, 1998, AM J RESP CRIT CARE, V158, P352; YUNGINGER JW, 1992, AM REV RESPIR DIS, V146, P888; ZEIGER RS, 1995, J ALLERGY CLIN IMMUN, V95, P1179, DOI 10.1016/S0091-6749(95)70074-9; Zeiger RS, 1999, J ALLERGY CLIN IMMUN, V103, P376, DOI 10.1016/S0091-6749(99)70460-4; 1992, MMWR MORB MORTAL WKL, V41, P733	39	185	200	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.	DEC	2004	114	6					1282	1287		10.1016/j.jaci.2004.09.020		6	Allergy; Immunology	Allergy; Immunology	877NN	WOS:000225577400005	15577824	
J	Venn, AJ; Lewis, SA; Cooper, M; Hubbard, R; Britton, J				Venn, AJ; Lewis, SA; Cooper, M; Hubbard, R; Britton, J			Living near a main road and the risk of wheezing illness in children	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; wheezing; children; vehicular emissions	CHRONIC RESPIRATORY SYMPTOMS; TRAFFIC DENSITY; AIR-POLLUTION; ASTHMA; PREVALENCE; MOTORWAYS; EXPOSURE; EXHAUST	The effect of road vehicle traffic pollution on asthma is still not clearly understood. However, any effect is likely to be most marked among those who live within 150 m of a main road, because this is the distance within which concentrations of primary vehicle traffic pollutants are raised above ambient background levels. We have investigated the relation between proximity of the family home to the nearest main road, estimated objectively using geographical information system software, and the risk of wheeze in the past year in a case-control sample of 6,147 primary schoolchildren (age 4 to I I yr) and a random cross-sectional sample of 3,709 secondary schoolchildren (age I I to 16 yr) in Nottingham, United Kingdom. Among children living within 150 m of a main road, the risk of wheeze increased with increasing proximity by an odds ratio (OR) of 1.08 (95% confidence interval [CI] 1.00 to 1.16) per 30-m increment in primary schoolchildren, and 1.16 (1.02 to 1.32) in secondary schoolchildren. Most of the increased risk was localized to within 90 m of the roadside. Among primary schoolchildren, effects were stronger in girls than boys (P-interaction = 0.02). Living within approximately 90 m of a main road is associated with a proximity-related increase in the risk of wheezing illness in children.	Univ Nottingham, Div Resp Med, Nottingham NG7 2RD, England	Venn, AJ (reprint author), City Hosp, Div Resp Med, Clin Sci Bldg,Hucknall Rd, Nottingham NG5 1PB, England.		Britton, John/G-9705-2011; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; CARSTAIRS V, 1989, COMMUNITY MED, V11, P364; Ciccone G, 1998, OCCUP ENVIRON MED, V55, P771; *DEP TRANSP SCOTT, 1994, DES MAN ROADS BRIDG, V11; Duhme H, 1996, EPIDEMIOLOGY, V7, P578, DOI 10.1097/00001648-199611000-00003; EDWARDS J, 1994, ARCH ENVIRON HEALTH, V49, P223; FORASTIERE F, 1994, AM J RESP CRIT CARE, V149, P365; Livingstone AE, 1996, BRIT MED J, V312, P676; NITTA H, 1993, ARCH ENVIRON HEALTH, V48, P53; Oosterlee A, 1996, OCCUP ENVIRON MED, V53, P241; Pershagen G, 1995, INT J EPIDEMIOL, V24, P1147, DOI 10.1093/ije/24.6.1147; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; Venn A, 1998, EUR RESPIR J, V11, P1324, DOI 10.1183/09031936.98.11061324; Venn A, 1998, BRIT MED J, V316, P1945; Venn A, 2000, OCCUP ENVIRON MED, V57, P152, DOI 10.1136/oem.57.3.152; WALDRON G, 1995, J PUBLIC HEALTH MED, V17, P85; Weiland Stephan K., 1994, Annals of Epidemiology, V4, P243; Wilkinson P, 1999, THORAX, V54, P1070	18	185	188	1	14	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	DEC 15	2001	164	12					2177	2180		10.1164/rccm2106126		4	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	528XX	WOS:000174271400011	11751183	
J	Wolkoff, P; Nielsen, GD				Wolkoff, P; Nielsen, GD			Organic compounds in indoor air - their relevance for perceived indoor air quality?	ATMOSPHERIC ENVIRONMENT			English	Article						airway irritation; indoor air quality; OCIA; odour annoyance; TVOC; volatile organic compounds (VOCs)	SICK BUILDING SYNDROME; ENVIRONMENTAL TOBACCO-SMOKE; BIOLOGICAL EVALUATION; MATERIAL EMISSIONS; INHALED ALLERGEN; RISK-ASSESSMENT; OFFICE WORKERS; EYE IRRITATION; VOC EMISSIONS; OZONE	It is generally believed that indoor air pollution, one way or another may cause indoor air complaints. However, any association between volatile organic compounds (VOCs) concentrations and increase of indoor climate complaints, like the sick-building syndrome symptoms, is not straightforward. The reported symptom rates of, in particular, eye and upper airway irritation cannot generally be explained by our present knowledge of common chemically non-reactive VOCs measured indoors. Recently, experimental evidence has shown those chemical reactions between ozone (either with or without nitrogen dioxide) and unsaturated organic compounds (e.g. from citrus and pine oils) produce strong eye and airway irritating species. These have not yet been well characterised by conventional sampling and analytical techniques. The chemical reactions can occur indoors, and there is indirect evidence that they are associated with eye and airway irritation. However, many other volatile and non-volatile organic compounds have not generally been measured which could equally well have potent biological effects and cause an increase of complaint rates, and posses a health/comfort risk. As a consequence, it is recommended to use a broader analytical window of organic compounds than the classic VOC window as defined by the World Health Organisation. It may include hitherto not yet sampled or identified intermediary species (e.g., radicals, hydroperoxides and ionic compounds like detergents) as well as species deposited onto particles. Additionally, sampling strategies including emission testing of building products should carefully be linked to the measurement of organic compounds that are expected, based on the best available toxicological knowledge, to have biological effects at indoor concentrations. (C) 2001 Elsevier Science Ltd. All rights reserved.	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K., 1993, INDOOR AIR, V3, P283, DOI 10.1111/j.1600-0668.1993.00010.x; Wolkoff P, 1997, INDOOR AIR, V7, P92, DOI 10.1111/j.1600-0668.1997.t01-2-00003.x; Wolkoff P, 1999, SCI TOTAL ENVIRON, V227, P197, DOI 10.1016/S0048-9697(99)00019-4; Wolkoff P, 1998, SCI TOTAL ENVIRON, V215, P135, DOI 10.1016/S0048-9697(98)00110-7; Wolkoff P, 1995, INDOOR AIR, P1, DOI 10.1111/j.1600-0668.1995.tb00017.x; Wolkoff P, 1996, ATMOS ENVIRON, V30, P2679, DOI 10.1016/1352-2310(95)00323-1; Wolkoff P, 2000, INDOOR AIR, V10, P82, DOI 10.1034/j.1600-0668.2000.010002082.x; Wolkoff P., 1992, J EXPOSURE ANAL EN S, V1, P71; Wolkoff P., 1991, INDOOR AIR, V1, P389, DOI 10.1111/j.1600-0668.1991.00003.x	87	185	191	12	73	PERGAMON-ELSEVIER SCIENCE LTD	OXFORD	THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND	1352-2310			ATMOS ENVIRON	Atmos. Environ.	SEP	2001	35	26					4407	4417		10.1016/S1352-2310(01)00244-8		11	Environmental Sciences; Meteorology & Atmospheric Sciences	Environmental Sciences & Ecology; Meteorology & Atmospheric Sciences	471MK	WOS:000170933000004		
J	Kramer, U; Koch, T; Ranft, U; Ring, J; Behrendt, H				Kramer, U; Koch, T; Ranft, U; Ring, J; Behrendt, H			Traffic-related air pollution is associated with atopy in children living in urban areas	EPIDEMIOLOGY			English	Article						air pollution; traffic; atopy; child; nitrogen dioxide; living conditions; urban environment; gender	CHRONIC RESPIRATORY SYMPTOMS; NITROGEN-DIOXIDE EXPOSURE; DIESEL EXHAUST PARTICLES; AUTOMOBILE EXHAUST; ASTHMATIC-PATIENTS; ALLERGIC RHINITIS; INHALED ALLERGEN; LUNG-FUNCTION; HEALTH; PREVALENCE	Traffic emissions are a major source of air pollution in Western industrialized countries. To investigate the association between traffic-related air pollution and parameters of atopy, we studied 317 children 9 years of age living near major roads in two urban areas and one suburban area of a city in West Germany. Atopic sensitization was analyzed by skin-prick testing and determination of allergen-specific serum immunoglobulin E. Parents recorded allergic symptoms in a symptom diary, and physicians assessed allergic diseases. Personal NO2 exposure and NO2 concentrations in front of each child's home were measured. Outdoor NO2 was a good predictor for traffic exposure but a poor predictor for NO2 exposure at the personal level. Atopy was found to be related to outdoor NO2 (odds ratio for the association between symptoms of allergic rhinitis and outdoor NO2 = 1.81; 95% confidence interval = 1.02-3.21) but not to personal NO2 (odds ratio for the association between symptoms of allergic rhinitis and personal NO2 = 0.99; 95% confidence interval = 0.55-1.79). When the analysis was restricted to urban areas, we found that hay fever, symptoms of allergic rhinitis, wheezing, sensitization against pollen, house dust mites or cats, and milk or eggs were associated with outdoor NO2. The results indicate that traffic-related air pollution leads to increased prevalence of atopic sensitizations, allergic symptoms, and diseases.	Univ Dusseldorf, Med Inst Environm Hyg, D-40225 Dusseldorf, Germany; Tech Univ Munich, Dept Dermatol & Allergol, Munich, Germany; Tech Univ Munich, GSF, Natl Res Ctr Environm & Hlth, Div Environm Dermatol & Allergol, Munich, Germany	Kramer, U (reprint author), Univ Dusseldorf, Med Inst Environm Hyg, Hennekamp 50, D-40225 Dusseldorf, Germany.						Behrendt H, 1997, INT ARCH ALLERGY IMM, V113, P69; Behrendt H, 1995, PROG ALLER CLIN IMM, V3, P83; Blomberg A, 1997, AM J RESP CRIT CARE, V156, P418; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; DEVALIA JL, 1994, LANCET, V344, P1668, DOI 10.1016/S0140-6736(94)90458-8; DiazSanchez D, 1997, ALLERGY, V52, P52; DiazSanchez D, 1996, J ALLERGY CLIN IMMUN, V98, P114, DOI 10.1016/S0091-6749(96)70233-6; Duhme H, 1996, EPIDEMIOLOGY, V7, P578, DOI 10.1097/00001648-199611000-00003; EDWARDS J, 1994, ARCH ENVIRON HEALTH, V49, P223; ISHIZAKI T, 1987, ANN ALLERGY, V58, P265; Kramer U, 1998, BRIT J DERMATOL, V139, P1040; KRAMER U, 1997, NEW TRENDS ALLERGY, V4, P21; LUTTMANN H, 1994, ZBL HYG UMWELTMED, V196, P114; NAKAI S, 1995, J EXPO ANAL ENV EPID, V5, P125; NAKATSUKA H, 1991, ENVIRON INT, V17, P51, DOI 10.1016/0160-4120(91)90337-P; NITTA H, 1993, ARCH ENVIRON HEALTH, V48, P53; Oosterlee A, 1996, OCCUP ENVIRON MED, V53, P241; Pershagen G, 1995, INT J EPIDEMIOL, V24, P1147, DOI 10.1093/ije/24.6.1147; RaaschouNielsen O, 1997, ENVIRON HEALTH PERSP, V105, P964; RAFT U, 1996, P C ENV EP EUR 1995, P340; RANFT U, 1992, P 9 WORLD CLEAN AIR, V5; SCHUPP A, 1994, ALLERGOLOGIE, V17, P591; Strand V, 1997, AM J RESP CRIT CARE, V155, P881; Studnicka M, 1997, EUR RESPIR J, V10, P2275, DOI 10.1183/09031936.97.10102275; TAKAFUJI S, 1987, J ALLERGY CLIN IMMUN, V79, P639, DOI 10.1016/S0091-6749(87)80161-6; TUNNICLIFFE WS, 1994, LANCET, V344, P1733, DOI 10.1016/S0140-6736(94)92886-X; *UMW STADT DUSS, 1997, LUFTB DUSS MESSB 199; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; VONMUTIUS E, 1994, AM J RESP CRIT CARE, V149, P358; WALDRON G, 1995, J PUBLIC HEALTH MED, V17, P85; WANG JH, 1995, J ALLERGY CLIN IMMUN, V96, P669, DOI 10.1016/S0091-6749(95)70266-0; WANG JH, 1995, INT ARCH ALLERGY IMM, V107, P103; Weiland Stephan K., 1994, Annals of Epidemiology, V4, P243; World Health Organization, 1997, ENV HLTH CRIT, V188; WJST M, 1993, BRIT MED J, V307, P596	35	185	193	0	28	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	1044-3983			EPIDEMIOLOGY	Epidemiology	JAN	2000	11	1					64	70		10.1097/00001648-200001000-00014		7	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	266TH	WOS:000084316000014	10615846	
J	Clark, NA; Demers, PA; Karr, CJ; Koehoorn, M; Lencar, C; Tamburic, L; Brauer, M				Clark, Nina Annika; Demers, Paul A.; Karr, Catherine J.; Koehoorn, Mieke; Lencar, Cornel; Tamburic, Lillian; Brauer, Michael			Effect of Early Life Exposure to Air Pollution on Development of Childhood Asthma	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						administrative data; air pollution; asthma; children's health; in utero; respiratory; traffic	LAND-USE REGRESSION; RESPIRATORY HEALTH; SOUTHERN CALIFORNIA; BIRTH COHORT; PARTICULATE MATTER; PULMONARY-FUNCTION; CHILDREN; SYMPTOMS; WOODSMOKE; OUTCOMES	BACKGROUND: There is increasing recognition of the importance of early environmental exposures in the development of childhood asthma. Outdoor air pollution is a recognized asthma trigger, but it is unclear whether exposure influences incident disease. We investigated the effect of exposure to ambient air pollution in utero and during the first year of life oil risk of subsequent asthma diagnosis in a population-based nested case-control study. METHODS: We assessed all children born in southwestern British Columbia in 1999 and 2000 (n = 37,401) for incidence of asthma diagnosis tip to 3-4 years of age using outpatient and hospitalization records. Asthma cases were age- and sex-matched to five randomly chosen controls from the eligible cohort. We estimated each individual's exposure to ambient air pollution for the gestational period and first year of life using high-resolution pollution surfaces derived from regulatory monitoring data as well as land use regression models adjusted for temporal variation. We used logistic regression analyses to estimate effects of carbon monoxide, nitric oxide, nitrogen dioxide, particulate matter <= 10 mu m and < 2.5 mu m in aerodynamic diameter (PM(10) and PM(2.5)), ozone, sulfur dioxide, black carbon, woodsmoke, and proximity to roads and point sources on asthma diagnosis. RESULTS: A total of 3,482 children (9%) were classified as asthma cases. We observed a statistically significantly increased risk of asthma diagnosis with increased earl), life exposure to CO, NO, NO(2), PM(10), SO(2), and black carbon and proximity to point sources. Traffic-related pollutants were associated with the highest risks: adjusted odds ratio = 1.08 (95% confidence interval, 1.04-1.12) for a 10-mu g/m(3) increase of NO, 1.12 (1.07-1.17) for a 10-mu g/m(3) increase in NO(2), and 1.10 (1.06-1.13) for a 100-mu g/m(3) increase in CO. These data support the hypothesis that early childhood exposure to air pollutants plays a role in development of asthma.	[Demers, Paul A.; Koehoorn, Mieke; Lencar, Cornel; Brauer, Michael] Univ British Columbia, Sch Environm Hlth, Vancouver, BC V6T 1Z3, Canada; [Clark, Nina Annika; Demers, Paul A.; Koehoorn, Mieke] Univ British Columbia, Sch Populat & Publ Hlth, Vancouver, BC V6T 1Z3, Canada; [Karr, Catherine J.] Univ Washington, Dept Pediat, Seattle, WA 98195 USA; [Tamburic, Lillian] Univ British Columbia, Ctr Hlth Serv & Policy Res, Vancouver, BC V6T 1Z3, Canada	Brauer, M (reprint author), Univ British Columbia, Sch Environm Hlth, 2206 East Mall, Vancouver, BC V6T 1Z3, Canada.	brauer@interchange.ubc.ca	Wang, Linden/M-6617-2014; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Brauer, Michael/0000-0002-9103-9343	Health Canada; Centre for Health and Environment Research at the University of British Columbia; Michael Smith Foundation	The research was supported in part by Health Canada via all agreement with the British Columbia Centre for Disease Control to the Border Air Quality Study. Additional support was provided by the Centre for Health and Environment Research at the University of British Columbia, funded by the Michael Smith Foundation for Health Research. N.A.C. Was supported by the Michael Smith Foundation for Health Research Junior Graduate Trainee Award, the Canadian Institutes for Health Research Master's Award, and the Bridge Program fellowship (a Canadian Institutes for Health Research Strategic Training Program). M.K. was supported by a Michael Smith Foundation for Health Research Scholar Award.	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Health Perspect.	FEB	2010	118	2					284	290		10.1289/ehp.0900916		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	555BQ	WOS:000274482400032	20123607	
J	Castells, MC; Tennant, NM; Sloane, DE; Hsu, FI; Barrett, NA; Hong, DI; Laidlaw, TM; Legere, HJ; Nallamshetty, SN; Palis, RI; Rao, JJ; Berlin, ST; Campos, SM; Matulonis, UA				Castells, Mariana C.; Tennant, Nichole M.; Sloane, David E.; Hsu, F. Ida; Barrett, Nora A.; Hong, David I.; Laidlaw, Tanya M.; Legere, Henry J.; Nallamshetty, Samridhi N.; Palis, Ross I.; Rao, Jayanti J.; Berlin, Suzanne T.; Campos, Susana M.; Matulonis, Ursula A.			Hypersensitivity reactions to chemotherapy: Outcomes and safety of rapid desensitization in 413 cases	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						anaphylaxis; chemotherapy agents; monoclonal antibodies; rapid desensitization; hypersensitivity reactions; carboplatin; paclitaxel; adverse drug reactions	CARBOPLATIN HYPERSENSITIVITY; OVARIAN-CANCER; PROTOCOL; PACLITAXEL; SKIN; CISPLATIN; ALLERGY; TAXOL; EXPERIENCE	Background: Hypersensitivity reactions (HSRs) to chemotherapeutic drugs, including mAbs, often require that the provoking medication be discontinued, thus raising a dilemma for the caregiver: further use could precipitate a severe, even fatal, allergic reaction on re-exposure, but alternative drugs might be poorly tolerated or much less effective compared with the preferred agent. Objective: We have developed a standardized rapid desensitization protocol for achieving temporary tolerization to drug allergens. In this study we evaluate the safety and efficacy of this protocol. Methods: Ninety-eight patients who had HSRs in response to treatment with carboplatin, cisplatin, oxaliplatin, paclitaxel, liposomal doxorubicin, doxorubicin, or rituximab received rapid desensitization to these agents. A standardized 12-step protocol was used, with treatment given intravenously or intraperitoneally. Initial desensitizations occurred in the medical intensive care unit, whereas most subsequent infusions took place in an outpatient setting. Safety and efficacy of the protocol were assessed by review of treatment records. Results: Of the 413 desensitizations performed, 94% induced mild or no reactions. No life-threatening HSRs or deaths occurred during the procedure, and all patients received their full target dose. Most reactions occurred during the first desensitization. Reactions were most commonly reported at the last step of the protocol. Desensitizations through the intravenous and intraperitoneal routes were equally effective. Conclusions: Our standardized 12-step protocol for rapid drug desensitization is safe and effective and has been adopted as the standard of care at our institutions in treating patients with HSRs to chemotherapeutic drugs, including mAbs.	[Castells, Mariana C.; Tennant, Nichole M.; Sloane, David E.; Hsu, F. Ida; Barrett, Nora A.; Hong, David I.; Laidlaw, Tanya M.; Legere, Henry J.; Nallamshetty, Samridhi N.; Palis, Ross I.; Rao, Jayanti J.] Brigham & Womens Hosp, Dept Med, Div Rheumatol Immunol & Allergy, Boston, MA 02115 USA; [Berlin, Suzanne T.; Campos, Susana M.; Matulonis, Ursula A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA	Castells, MC (reprint author), 1 Jimmy Fund Way,Smith Bldg,Room 626D, Boston, MA 02115 USA.	mcastells@partners.org			Ovations for the Cure Desensitization Program; American Academy of Allergy, Asthma Immunology; National Institutes of Health; GlaxoSmithKline; Genentech; Novartis; Ortho-Biotechnology	Supported by the Ovations for the Cure Desensitization Program.; Disclosure of potential conflict of interest: D. E. Sloane has received honoraria front Genentech F. I. Hsu has served as a coinvestigator for Dyax Corporation and has received a research grant front the American Academy of Allergy, Asthma & Immunology. N. A. Barrett has served as a coinvestigator for the National Institutes of Health and has served as a primary investigator for the American Academy of Allergy, Asthma & Immunology and Altana. D. I. Hong and T M. Laidlaw have received training grant salary from the National Institutes of Health. S. N. Nallamshetty has received training grant salary front the National Institutes of Health and research grants from the American Academy of Allergy, Asthma & Immunology and GlaxoSmithKline. S. M, Campos has served as a research consultant for Genentech and has received research support from Genentech, Novartis. and Ortho-Biotechnology. The rest of the authors have declared that they have no conflict of interest.	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Allergy Clin. Immunol.	SEP	2008	122	3					574	580		10.1016/j.jaci.2008.02.044		7	Allergy; Immunology	Allergy; Immunology	348TW	WOS:000259234000020	18502492	
J	Rumchev, K; Spickett, J; Bulsara, M; Phillips, M; Stick, S				Rumchev, K; Spickett, J; Bulsara, M; Phillips, M; Stick, S			Association of domestic exposure to volatile organic compounds with asthma in young children	THORAX			English	Article							CHILDHOOD ASTHMA; INDOOR AIR; PREVALENCE; FORMALDEHYDE; POPULATION; ALLERGY; HEALTH	Aim: To investigate the association between domestic exposure to volatile organic compounds (VOCs) and asthma in young children. Methods: A population based case-control study was conducted in Perth, Western Australia in children aged between 6 months and 3 years. Cases ( n = 88) were children recruited at Princess Margaret Hospital accident and emergency department and discharged with asthma as the primary diagnosis; 104 controls consisted of children from the same age group without an asthma diagnosis identified through the Health Department of Western Australia. Information regarding the health status of the study children and characteristics of the home was collected using a standardised questionnaire. Exposure to VOCs, average temperature and relative humidity were measured in winter and summer in the living room of each participating household. Results: Cases were exposed to significantly higher VOC levels (mug/m(3)) than controls (p< 0.01). Most of the individual VOCs appeared to be significant risk factors for asthma with the highest odds ratios for benzene followed by ethylbenzene and toluene. For every 10 unit increase in the concentration of toluene and benzene (mu g/m(3)) the risk of having asthma increased by almost two and three times, respectively. Conclusions: Domestic exposure to VOCs at levels below currently accepted recommendations may increase the risk of childhood asthma. Measurement of total VOCs may underestimate the risks associated with individual compounds.	Curtin Univ Technol, Sch Publ Hlth, Perth, WA 6845, Australia; Univ Western Australia, Sch Populat Hlth, Fac Med & Dent, Crawley, WA 6009, Australia; Princess Margaret Hosp Children, Dept Resp Med, Perth, WA 6001, Australia	Rumchev, K (reprint author), Curtin Univ Technol, Sch Publ Hlth, GPO Box U1987, Perth, WA 6845, Australia.	k.rumchev@curtin.edu.au	Bulsara, Max/A-5966-2008; Stick, Stephen/O-5683-2014; Osborne, Nicholas/N-4915-2015	Bulsara, Max/0000-0002-8033-6123; Osborne, Nicholas/0000-0002-6700-2284; Stick, Stephen/0000-0002-5386-8482			ANDERSON HR, 1994, BRIT MED J, V308, P1600; *AUSTR BUR STAT, 1998, N20390 AUSTR BUR STA; BROWN SK, 1994, INDOOR AIR, V4, P123, DOI 10.1111/j.1600-0668.1994.t01-2-00007.x; BURNEY PGJ, 1990, BRIT MED J, V300, P1306; FERRIS BG, 1978, AM REV RESPIR DIS, V118, P1; Gereda JE, 2001, J ALLERGY CLIN IMMUN, V107, P790, DOI 10.1067/mai.2001.115245; HARVING H, 1991, AM REV RESPIR DIS, V143, P751; Holt PG, 1999, NATURE, V402, pB12; HYNDMAN SJ, 1994, Q J MED, V87, P367; Karol MH, 2002, TOXICOLOGY, V181, P305, DOI 10.1016/S0300-483X(02)00298-6; KOREN HS, 1992, ARCH ENVIRON HEALTH, V47, P39; LUCZYNSKA CM, 1989, J IMMUNOL METHODS, V118, P227, DOI 10.1016/0022-1759(89)90010-0; Maroni M., 1995, INDOOR AIR QUALITY C; MEINERT R, 1994, ALLERGY, V49, P526, DOI 10.1111/j.1398-9995.1994.tb01124.x; *NHMRC, 1995, 115 NHMRC SESS AUSTR; NORBACK D, 1995, OCCUP ENVIRON MED, V52, P388; Oddy WH, 2002, EUR RESPIR J, V19, P899, DOI 10.1183/09031936.02.00103602; PEAT JK, 1994, BRIT MED J, V308, P1591; Rumchev KB, 2002, EUR RESPIR J, V20, P403, DOI 10.1183/09031936.02.00245002; SAMET J, 1990, AM REV RESPIR DIS, V142, P915; WALLACE LA, 1986, TOXICOL ENVIRON CHEM, V12, P215, DOI 10.1080/02772248609357160; WALLACE LA, 1989, CELL BIOL TOXICOL, V5, P297, DOI 10.1007/BF01795358; WARE JH, 1993, AM J EPIDEMIOL, V137, P1287; Weislander G., 1997, INT ARCH OCC ENV HEA, V69, P115; Wolkoff P, 1997, INDOOR AIR, V7, P92, DOI 10.1111/j.1600-0668.1997.t01-2-00003.x; Wolkoff P, 1995, INDOOR AIR, P1, DOI 10.1111/j.1600-0668.1995.tb00017.x; Yuan W, 2003, EUR J EPIDEMIOL, V18, P763	27	184	195	4	50	B M J PUBLISHING GROUP	LONDON	BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND	0040-6376			THORAX	Thorax	SEP	2004	59	9					746	751		10.1136/thx.2003.013680		6	Respiratory System	Respiratory System	849OV	WOS:000223549100008	15333849	
J	Kheradmand, F; Kiss, A; Xu, J; Lee, SH; Kolattukudy, PE; Corry, DB				Kheradmand, F; Kiss, A; Xu, J; Lee, SH; Kolattukudy, PE; Corry, DB			A protease-activated pathway underlying Th cell type 2 activation and allergic lung disease	JOURNAL OF IMMUNOLOGY			English	Article							DUST-MITE ALLERGEN; INDUCED AIRWAY HYPERREACTIVITY; MURINE MODEL; IFN-GAMMA; PROTEOLYTIC ACTIVITY; CYSTEINE PROTEASE; GUINEA-PIG; PHYSICOCHEMICAL CHARACTERIZATION; ASPERGILLUS-FUMIGATUS; DETERGENT ENZYMES	The respiratory allergens that induce experimental. Th cell type 2-dependent allergic lung inflammation may be grouped into two functional classes. One class of allergens, in this study termed type I, requires priming with adjuvants remote from the lung to overcome airway tolerogenic mechanisms that ordinarily preclude allergic responses to inhaled Ags. In contrast, the other, or type II, allergen class requires neither remote priming nor additional adjuvants to overcome airway tolerance and elicit robust allergic lung disease. In this study, we show in an experimental model that diverse type II allergens share in common proteolytic activity that is both necessary and sufficient for overcoming airway tolerance and induction of pulmonary allergic disease. Inactivated protease and protease-free Ag fragments showed no allergenic potency, demonstrating that only active protease acting on endogenous substrates was essential. Furthermore, induction of airway tolerance could be aborted and allergic lung disease established by simply adding purified protease to a type I allergen. Thus, exogenous proteases are common to type II allergens and may be generally required to overcome the innate resistance of the airway to Th cell type 2 activation and allergic inflammation, raising concern for their potential contribution to diseases such as asthma.	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Immunol.	NOV 15	2002	169	10					5904	5911				8	Immunology	Immunology	614CG	WOS:000179170300067	12421974	
J	Wu, WJ; Samoszuk, MK; Comhair, SAA; Thomassen, MJ; Farver, CF; Dweik, RA; Kavuru, MS; Erzurum, SC; Hazen, SL				Wu, WJ; Samoszuk, MK; Comhair, SAA; Thomassen, MJ; Farver, CF; Dweik, RA; Kavuru, MS; Erzurum, SC; Hazen, SL			Eosinophils generate brominating oxidants in allergen-induced asthma	JOURNAL OF CLINICAL INVESTIGATION			English	Article							HUMAN NEUTROPHILS EMPLOY; HYDROGEN-PEROXIDE; AMINO-ACIDS; SCHISTOSOMA-MANSONI; REACTIVE ALDEHYDES; MOLECULAR-CLONING; ANTIGEN CHALLENGE; SINGLET OXYGEN; GUINEA-PIG; MYELOPEROXIDASE	Eosinophils promote tissue injury and contribute to the pathogenesis of allergen-triggered diseases like asthma, but the chemical basis of damage to eosinophil targets is unknown. We now demonstrate that eosinophil activation in vivo results in oxidative damage of proteins through bromination of tyrosine residues, a heretofore unrecognized pathway for covalent modification of biologic targets in human tissues. Mass spectrometric studies demonstrated that 3-bromotyrosine serves as a specific "molecular fingerprint" for proteins modified through the eosinophil peroxidase-H2O2 system in the presence of plasma levels of halides. We applied a localized allergen challenge to model the effects of eosinophils and brominating oxidants in human lung injury. Endobronchial biopsy specimens from allergen-challenged lung segments of asthmatic, but not healthy control, subjects demonstrated significant enrichments in eosinophils and eosinophil peroxidase, Baseline levels of 3-bromotyrosine in bronchoalveolar lavage (BAL) proteins from mildly allergic asthmatic individuals were modestly but not statistically significantly elevated over those in control subjects. After exposure to segmental allergen challenge, lung segments of asthmatics, but not healthy control subjects, exhibited a >10-fold increase in BAL 3-bromotyrosine content, but only two- to threefold increases in 3-chlorotyrosine, a specific oxidation product formed by neutrophil- and monocyte-derived myeloperoxidase. These results identify reactive brominating species produced by eosinophils as a distinct class of oxidants formed in vivo. They also reveal eosinophil peroxidase as a potential therapeutic target for allergen-triggered inflammatory tissue injury in humans.	Cleveland Clin Fdn, Lerner Res Inst, Dept Cell Biol, Cleveland, OH 44195 USA; Cleveland State Univ, Dept Chem, Cleveland, OH 44115 USA; Quest Diagnost Inc, San Juan Capistrano, CA USA; Cleveland Clin Fdn, Dept Canc Biol, Cleveland, OH 44195 USA; Cleveland Clin Fdn, Dept Pulm & Crit Care Med, Cleveland, OH 44195 USA; Cleveland Clin Fdn, Dept Anat Pathol, Cleveland, OH 44195 USA; Cleveland Clin Fdn, Dept Cardiol, Cleveland, OH 44195 USA	Hazen, SL (reprint author), Cleveland Clin Fdn, Lerner Res Inst, Dept Cell Biol, 9500 Euclid Ave,NC-10, Cleveland, OH 44195 USA.				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J	Silkoff, PE; Sylvester, JT; Zamel, N; Permutt, S				Silkoff, PE; Sylvester, JT; Zamel, N; Permutt, S			Airway nitric oxide diffusion in asthma - Role in pulmonary function and bronchial responsiveness	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							EXHALED AIR; MILD ASTHMA; SYNTHASE; HYPERREACTIVITY; INHIBITION; INDUCTION; HUMANS; LIVER; LUNG	If the nitric oxide (NO) diffusing capacity of the airways (DNO) is the quantity of NO diffusing per unit time into exhaled gas ((q) over dot) divided by the difference between the concentration of NO in the airway wall (C-w) and lumen, then DNO and C-w can be estimated from the relationship between exhaled NO concentration and expiratory flow, in 10 normal subjects and 25 asthmatic patients before and after treatment with inhaled beclomethasone, DNO averaged 6.8 +/- 1.2, 25.5 +/- 3.8, and 22.3 +/- 2.7 nl/s/ppb x 10(-3) respectively; C-w averaged 149 +/- 31.9, 255.3 +/- 46.4 and 108.3 +/- 14.3 ppb, respectively; and DNOCw (the maximal q from diffusion) averaged 1,020 +/- 157.5, 6,512 +/- 866, and 2416 +/- 208.5 nl/s x 10-3, respectively. DNO and DNOCw in the asthmatic subjects before and after steroids were greater than in normal subjects (p < 0.0001), but C-w was not different. Within asthmatic subjects, steroids caused C-w and DNOCw to fall (p < 0.0001), but DNO was Unchanged, DNOCw after steroids, presumably reflecting maximal diffusion of constitutive NO, was positively correlated with methacholine PC20 and FEV1/FVC before or after steroids. The increased DNO measured in asthmatic patients may reflect upregulation of nonadrenergic, noncholinergic, NO-producing nerves in airways in compensation for decreased sensitivity of airway smooth muscle to the relaxant effects of endogenous NO.	Natl Jewish Med & Res Ctr, Dept Med, Denver, CO 80206 USA; Johns Hopkins Asthma & Allergy Ctr, Baltimore, MD 21224 USA; Univ Toronto, Div Respirol, Toronto, ON, Canada	Silkoff, PE (reprint author), Natl Jewish Med & Res Ctr, Dept Med, 1400 Jackson St, Denver, CO 80206 USA.						ALVING K, 1993, EUR RESPIR J, V6, P1368; BARNES PJ, 1995, IMMUNOL TODAY, V16, P128, DOI 10.1016/0167-5699(95)80128-6; BELVISI MG, 1992, EUR J PHARMACOL, V210, P221, DOI 10.1016/0014-2999(92)90676-U; BLAND JM, 1995, LANCET, V346, P1085, DOI 10.1016/S0140-6736(95)91748-9; DAgostino B, 1997, LIFE SCI, V60, pPL353; deBoer J, 1996, BRIT J PHARMACOL, V119, P1109; DEFRONZO RA, 1988, DIABETES, V37, P667; Dupont LJ, 1998, AM J RESP CRIT CARE, V157, P894; Dweik RA, 1998, J CLIN INVEST, V101, P660, DOI 10.1172/JCI1378; ELLIS JL, 1992, AM REV RESPIR DIS, V146, P1543; Fischer A, 1996, AM J RESP CRIT CARE, V154, P209; HAMID Q, 1993, LANCET, V342, P1510, DOI 10.1016/S0140-6736(05)80083-2; Hogman M, 1999, AM J RESP CRIT CARE, V159, pA862; Jatakanon A, 1998, THORAX, V53, P91; Jia YL, 1996, J APPL PHYSIOL, V80, P404; JIA YL, 1995, AM J PHYSIOL-LUNG C, V269, pL85; JORRES RA, 1998, AM J RESP CRIT CARE, V157, pA612; KHARITONOV SA, 1994, LANCET, V343, P133, DOI 10.1016/S0140-6736(94)90931-8; KNOWLES RG, 1990, BIOCHEM BIOPH RES CO, V172, P1042, DOI 10.1016/0006-291X(90)91551-3; Mehta S, 1997, AM J PHYSIOL-LUNG C, V273, pL656; Miura M, 1997, AM J RESP CRIT CARE, V156, P217; PERSSON MG, 1994, LANCET, V343, P146, DOI 10.1016/S0140-6736(94)90935-0; ROHSENOW WM, 1961, HEAT MASS MOMENTUM T, P132; Schuiling M, 1998, AM J RESP CRIT CARE, V158, P1442; Silkoff PE, 1998, RESP PHYSIOL, V113, P33, DOI 10.1016/S0034-5687(98)00033-4; Silkoff PE, 1997, AM J RESP CRIT CARE, V155, P260; Taylor DA, 1998, THORAX, V53, P483; Tsoukias NM, 1998, J APPL PHYSIOL, V85, P653; Tsoukias NM, 1998, J APPL PHYSIOL, V85, P642; Weibel E, 1963, MORPHOMETRY HUMAN LU; Yates DH, 1996, AM J RESP CRIT CARE, V154, P247	31	184	184	0	0	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.	APR	2000	161	4					1218	1228				11	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	306AF	WOS:000086573400026	10764315	
J	Caceres, AI; Brackmann, M; Elia, MD; Bessac, BF; del Camino, D; D'Amours, M; Witek, JS; Fanger, CM; Chong, JA; Hayward, NJ; Homer, RJ; Cohn, L; Huang, XZ; Moran, MM; Jordt, SE				Caceres, Ana I.; Brackmann, Marian; Elia, Maxwell D.; Bessac, Bret F.; del Camino, Donato; D'Amours, Marc; Witek, JoAnn S.; Fanger, Chistopher M.; Chong, Jayhong A.; Hayward, Neil J.; Homer, Robert J.; Cohn, Lauren; Huang, Xiaozhu; Moran, Magdalene M.; Jordt, Seven-Eric			A sensory neuronal ion channel essential for airway inflammation and hyperreactivity in asthma	PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA			English	Article						airway hyperreactivity; TRP channel; TRPA1	NEUROGENIC INFLAMMATION; TRPA1; PAIN; RECEPTOR; NOCICEPTION; ACTIVATION; MECHANISMS; SENSATION; DISEASES; FIBERS	Asthma is an inflammatory disorder caused by airway exposures to allergens and chemical irritants. Studies focusing on immune, smooth muscle, and airway epithelial function revealed many aspects of the disease mechanism of asthma. However, the limited efficacies of immune-directed therapies suggest the involvement of additional mechanisms in asthmatic airway inflammation. TRPA1 is an irritant-sensing ion channel expressed in airway chemosensory nerves. TRPA1-activating stimuli such as cigarette smoke, chlorine, aldehydes, and scents are among the most prevalent triggers of asthma. Endogenous TRPA1 agonists, including reactive oxygen species and lipid peroxidation products, are potent drivers of allergen-induced airway inflammation in asthma. Here, we examined the role of TRPA1 in allergic asthma in the murine ovalbumin model. Strikingly, genetic ablation of TRPA1 inhibited allergen-induced leukocyte infiltration in the airways, reduced cytokine and mucus production, and almost completely abolished airway hyperreactivity to contractile stimuli. This phenotype is recapitulated by treatment of wild-type mice with HC-030031, a TRPA1 antagonist. HC-030031, when administered during airway allergen challenge, inhibited eosinophil infiltration and prevented the development of airway hyperreactivity. Trpa1(-/-) mice displayed deficiencies in chemically and allergen-induced neuropeptide release in the airways, providing a potential explanation for the impaired inflammatory response. Our data suggest that TRPA1 is a key integrator of interactions between the immune and nervous systems in the airways, driving asthmatic airway inflammation following inhaled allergen challenge. TRPA1 may represent a promising pharmacological target for the treatment of asthma and other allergic inflammatory conditions.	[del Camino, Donato; D'Amours, Marc; Witek, JoAnn S.; Fanger, Chistopher M.; Chong, Jayhong A.; Hayward, Neil J.; Moran, Magdalene M.] Hydra Biosci Inc, Cambridge, MA 02139 USA; [Caceres, Ana I.; Brackmann, Marian; Elia, Maxwell D.; Bessac, Bret F.; Jordt, Seven-Eric] Yale Univ, Sch Med, Dept Pharmacol, New Haven, CT 06520 USA; [Homer, Robert J.] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06520 USA; [Cohn, Lauren] Yale Univ, Sch Med, Pulm & Crit Care Med Sect, New Haven, CT 06520 USA; [Huang, Xiaozhu] Univ Calif San Francisco, Lung Biol Ctr, San Francisco, CA 94143 USA	Moran, MM (reprint author), Hydra Biosci Inc, 790 Mem Dr, Cambridge, MA 02139 USA.	mmoran@hydrabiosciences.com; sven.jordt@yale.edu	Caceres, Ana/E-5542-2012		NIEHS NIH HHS [R01 ES015056, ES015056, ES017218, U54 ES017218]; NIGMS NIH HHS [5T32GM07205, T32 GM007205]		Andersson DA, 2008, J NEUROSCI, V28, P2485, DOI 10.1523/JNEUROSCI.5369-07.2008; Andre E, 2008, J CLIN INVEST, V118, P2574, DOI 10.1172/JCI34886; Bandell M, 2004, NEURON, V41, P849, DOI 10.1016/S0896-6273(04)00150-3; Basbaum AI, 2006, SCI AM, V294, P60; Bautista DM, 2006, CELL, V124, P1269, DOI 10.1016/j.cell.2006.02.023; Bessac BF, 2008, J CLIN INVEST, V118, P1899, DOI 10.1172/JCI34192; Bessac BF, 2009, FASEB J, V23, P1102, DOI 10.1096/fj.08-117812; Bessac BF, 2008, PHYSIOLOGY, V23, P360, DOI 10.1152/physiol.00026.2008; Caterina MJ, 2000, SCIENCE, V288, P306, DOI 10.1126/science.288.5464.306; Cohn L, 2004, ANNU REV IMMUNOL, V22, P789, DOI 10.1146/annurev.immunol.22.012703.104716; Cruz-Orengo L, 2008, MOL PAIN, V4, DOI 10.1186/1744-8069-4-30; Dai Y, 2007, J CLIN INVEST, V117, P1979, DOI 10.1172/JCI3095; Dakhama A, 2002, AM J RESP CRIT CARE, V165, P1137, DOI 10.1164/rccm.2109058; DAVIS B, 1982, J APPL PHYSIOL, V53, P985; Eder W, 2006, NEW ENGL J MED, V355, P2226, DOI 10.1056/NEJMra054308; Eid SR, 2008, MOL PAIN, V4, DOI 10.1186/1744-8069-4-48; Flood-Page P, 2007, AM J RESP CRIT CARE, V176, P1062, DOI 10.1164/rccm.200701-085OC; Groneberg DA, 2004, ALLERGY, V59, P1139, DOI 10.1111/j.1398-9995.2004.00665.x; Heaney LG, 1998, THORAX, V53, P357; Jia YL, 2007, BBA-MOL BASIS DIS, V1772, P915, DOI 10.1016/j.bbadis.2007.01.013; Jordt SE, 2004, NATURE, V427, P260, DOI 10.1038/nature02282; Maddox L, 2002, ANNU REV MED, V53, P477, DOI 10.1146/annurev.med.53.082901.103921; McLeod Robbie L, 2006, Cough, V2, P10, DOI 10.1186/1745-9974-2-10; McNamara CR, 2007, P NATL ACAD SCI USA, V104, P13525, DOI 10.1073/pnas.0705924104; Petrus M, 2007, MOL PAIN, V3, DOI 10.1186/1744-8069-3-40; Redlich CA, 2002, INT IMMUNOPHARMACOL, V2, P213, DOI 10.1016/S1567-5769(01)00174-6; Shakeri MS, 2008, OCCUP MED-OXFORD, V58, P205, DOI 10.1093/occmed/kqn013; TAYLORCLARK TE, 2008, AM J RESP CELL MOL B; Trevisani M, 2007, P NATL ACAD SCI USA, V104, P13519, DOI 10.1073/pnas.0705923104; Undem Bradley J, 2002, Curr Allergy Asthma Rep, V2, P159, DOI 10.1007/s11882-002-0011-4; WEISS SJ, 1989, NEW ENGL J MED, V320, P365; White FA, 2008, CURR OPIN ANESTHESIO, V21, P580, DOI 10.1097/ACO.0b013e32830eb69d	32	183	188	3	16	NATL ACAD SCIENCES	WASHINGTON	2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA	0027-8424			P NATL ACAD SCI USA	Proc. Natl. Acad. Sci. U. S. A.	JUN 2	2009	106	22					9099	9104		10.1073/pnas.0900591106		6	Multidisciplinary Sciences	Science & Technology - Other Topics	452ZU	WOS:000266580500058	19458046	
J	Akdis, CA; Akdis, M; Bieber, T; Bindslev-Jensen, C; Boguniewicz, M; Eigenmann, P; Hamid, Q; Kapp, A; Leung, DYM; Lipozencic, J; Luger, TA; Muraro, A; Novak, N; Platts-Mills, TAE; Rosenwasser, L; Scheynius, A; Simons, FER; Spergel, J; Turjanmaa, K; Wahn, U; Weidinger, S; Werfel, T; Zuberbier, T				Akdis, C. A.; Akdis, M.; Bieber, T.; Bindslev-Jensen, C.; Boguniewicz, M.; Eigenmann, P.; Hamid, Q.; Kapp, A.; Leung, D. Y. M.; Lipozencic, J.; Luger, T. A.; Muraro, A.; Novak, N.; Platts-Mills, T. A. E.; Rosenwasser, L.; Scheynius, A.; Simons, F. E. R.; Spergel, J.; Turjanmaa, K.; Wahn, U.; Weidinger, S.; Werfel, T.; Zuberbier, T.		European Acad Allergology Clinical; Amer Acad Allergy Asthma Immunol; PRACTALL Consensus Grp	Diagnosis and treatment of atopic dermatitis in children and adults: European Academy of Allergology and Clinical Immunology/American Academy of Allergy, Asthma and Immunology/PRACTALL consensus report	ALLERGY			English	Review						atopic dermatitis; children; adults; risk factors; immunopathology; diagnosis; systemic treatment; topical treatment	RANDOMIZED CONTROLLED-TRIAL; STAPHYLOCOCCUS-AUREUS COLONIZATION; TOPICAL CALCINEURIN INHIBITORS; PIMECROLIMUS CREAM 1-PERCENT; PLASMACYTOID DENDRITIC CELLS; PLACEBO-CONTROLLED TRIAL; DUST-MITE ALLERGENS; REGULATORY T-CELLS; LONG-TERM EFFICACY; DOUBLE-BLIND	There are remarkable differences in the diagnostic and therapeutic management of atopic dermatitis practiced by dermatologists and pediatricians in different countries. Therefore, the European Academy of Allergy and Clinical Immunology and the American Academy of Allergy, Asthma and Immunology nominated expert teams who were given the task of finding a consensus to serve as a guideline for clinical practice in Europe as well as in North America. The consensus report is part of the PRACTALL initiative, which is endorsed by both academies.	Swiss Inst Allergy & Asthma Res, CH-7270 Davos, Switzerland; Univ Bonn, D-5300 Bonn, Germany; Odense Univ, Odense, Denmark; Natl Jewish Med & Res Ctr, Denver, CO USA; Univ Colorado, Sch Med, Denver, CO 80202 USA; Univ Geneva, Childrens Hosp, Geneva, Switzerland; McGill Univ, Montreal, PQ, Canada; Hannover Med Sch, Hannover, Germany; Univ Zagreb, Ctr Hosp, Zagreb 41000, Croatia; Univ Zagreb, Sch Med, Zagreb 41000, Croatia; Univ Munster, D-4400 Munster, Germany; Univ Padua, Padua, Italy; Asthma & Allerg Dis Ctr, Charlottesville, VA USA; Karolinska Univ Hosp Solna, Stockholm, Sweden; Univ Manitoba, Winnipeg, MB R3T 2N2, Canada; Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA; Univ Penn, Sch Med, Philadelphia, PA 19104 USA; Tampere Univ Hosp, Tampere, Finland; Charite Univ Berlin, Berlin, Germany; Tech Univ Munich, D-8000 Munich, Germany; Hannover Med Sch, D-3000 Hannover, Germany	Wahn, U (reprint author), Charite Univ Med Berlin, Augustenburger Pl 1, D-13353 Berlin, Germany.		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J	Noverr, MC; Huffnagle, GB				Noverr, MC; Huffnagle, GB			The 'microflora hypothesis' of allergic diseases	CLINICAL AND EXPERIMENTAL ALLERGY			English	Review							CHAIN FATTY-ACIDS; PLACEBO-CONTROLLED TRIAL; ANTHROPOSOPHIC LIFE-STYLE; ORAL TOLERANCE INDUCTION; REGULATORY T-CELLS; INTESTINAL MICROFLORA; DENDRITIC CELLS; CANDIDA-ALBICANS; EARLY-CHILDHOOD; ATOPIC DISEASE	Increasingly, epidemiologic and clinical data support the hypothesis that perturbations in the gastrointestinal (GI) microbiota because of antibiotic use and dietary differences in 'industrialized' countries have disrupted the normal microbiota-mediated mechanisms of immunological tolerance in the mucosa, leading to an increase in the incidence of allergic airway disease. The data supporting this 'microflora hypothesis' includes correlations between allergic airway disease and (1) antibiotic use early in life, (2) altered fecal microbiota and (3) dietary changes over the past two decades. Our laboratory has recently demonstrated that mice can develop allergic airway responses to allergens if their endogenous microbiota is altered at the time of first allergen exposure. These experimental and clinical observations are consistent with other studies demonstrating that the endogenous microbiota plays a significant role in shaping the development of the immune system. Data are beginning to accumulate that a 'balanced' microbiota plays a positive role in maintaining mucosal immunologic tolerance long after post-natal development. Other studies have demonstrated that even small volumes delivered to the nasopharynx largely end up in the GI tract, suggesting that airway tolerance and oral tolerance may operate simultaneously. The mechanism of microbiota modulation of host immunity is not known; however, host and microbial oxylipins are one potential set of immunomodulatory molecules that may control mucosal tolerance. The cumulative data are beginning to support the notion that probiotic and prebiotic strategies be considered for patients coming off of antibiotic therapy.	Univ Michigan, Sch Med, Dept Internal Med, Div Pulm & Crit Care Med, Ann Arbor, MI 48109 USA; Univ Michigan, Sch Med, Dept Microbiol & Immunol, Ann Arbor, MI 48109 USA	Huffnagle, GB (reprint author), Univ Michigan, Sch Med, Dept Internal Med, Div Pulm & Crit Care Med, Ann Arbor, MI 48109 USA.	ghuff@umich.edu					ADLERBERTH I, 1991, ACTA PAEDIATR SCAND, V80, P602, DOI 10.1111/j.1651-2227.1991.tb11917.x; Akbari O, 2003, CURR OPIN IMMUNOL, V15, P627, DOI 10.1016/j.coi.2003.09.012; 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; Alpan O, 2001, Curr Allergy Asthma Rep, V1, P572, DOI 10.1007/s11882-001-0067-6; Andoh A, 1999, JPEN-PARENTER ENTER, V23, pS70; Asher MI, 1998, EUR RESPIR J, V12, P315; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; ASSEMAN C, 2000, AM J RESP CRIT CARE, V162, P185; BANDEIRA A, 1990, J EXP MED, V172, P239, DOI 10.1084/jem.172.1.239; BAUER H, 1963, AM J PATHOL, V42, P471; 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Exp. Allergy	DEC	2005	35	12					1511	1520		10.1111/j.1365-2222.2005.02379.x		10	Allergy; Immunology	Allergy; Immunology	990XT	WOS:000233777400002	16393316	
J	Dobie, DJ; Kivlahan, DR; Maynard, C; Bush, KR; Davis, TM; Bradley, KA				Dobie, DJ; Kivlahan, DR; Maynard, C; Bush, KR; Davis, TM; Bradley, KA			Posttraumatic stress disorder in female veterans - Association with self-reported health problems and functional impairment	ARCHIVES OF INTERNAL MEDICINE			English	Article							QUALITY-OF-LIFE; MALE VIETNAM VETERANS; PTSD CHECKLIST; PRIMARY-CARE; SCREENING INSTRUMENT; SEXUAL VICTIMIZATION; TRAUMATIC EVENTS; AFFAIRS PATIENTS; BREAST-CANCER; DESERT-STORM	Background: The purpose of this report is to identify self-reported health problems and functional impairment associated with screening positive for posttraumatic stress disorder (PTSD) in women seen for care at a Department of Veterans Affairs (VA) medical center. Methods: A survey was mailed to all women (N = 1935) who received care at the VA Puget Sound Health Care System between October 1996 and January 1998. The survey inquired about health history and habits. It included the PTSD Checklist-Civilian Version (PCL-C) and validated screening measures for other psychiatric disorders. The veteran's version of the Medical Outcomes Study 36-Item Short-Form Health Survey (SF-36-V) was included to assess health-related quality of life. Results: Of the 1259 eligible women who completed the survey, 266 women (21%) screened positive for current PTSD (PCL-C score greater than or equal to50). In age-adjusted bivariate analyses, women who screened positive for PTSD reported more psychiatric problems, substance abuse, and lifetime exposure to domestic violence. They were significantly more likely to endorse physical health problems including obesity, smoking, irritable bowel syndrome, fibromyalgia, chronic pelvic pain, polycystic ovary disease, asthma, cervical cancer, and stroke. In fully adjusted multivariate models, a PCL-C score of 50 or greater was independently associated with scoring in the lowest quartile on SF-36-V subscales and composite scales. Conclusions: Symptoms of PTSD are common in women treated at VA facilities. In addition, PTSD is associated with self-reported mental and physical health problems and poor health-related quality of life in these patients. These findings have implications for the design of VA primary care services for the growing population of female veterans.	Univ Washington, Sch Med, Dept Psychiat, Seattle, WA USA; Univ Washington, Sch Med, Dept Behav Sci, Seattle, WA USA; Univ Washington, Sch Med, Dept Med, Seattle, WA 98195 USA; Ctr Excellence Subst Abuse Treatment & Educ, Seattle, WA USA; Hlth Serv Res & Dev, Seattle, WA USA; VA Puget Sound Hlth Care Syst, Seattle, WA USA	Dobie, DJ (reprint author), S-116 VA PSHCS,1660 S Columbian Way, Seattle, WA 98108 USA.	djdobie@u.washington.edu	Maynard, Charles/N-3906-2015	Maynard, Charles/0000-0002-1644-7814			American Psychiatric Association, 1994, DIAGN STAT MAN MENT; Andrykowski MA, 1998, J CONSULT CLIN PSYCH, V66, P586, DOI 10.1037//0022-006X.66.3.586; Andrykowski MA, 1998, J TRAUMA STRESS, V11, P189, DOI 10.1023/A:1024490718043; Asch DA, 1997, J CLIN EPIDEMIOL, V50, P1129, DOI 10.1016/S0895-4356(97)00126-1; Beckham JC, 1998, AM J PSYCHIAT, V155, P1565; Blanchard EB, 1996, BEHAV RES THER, V34, P669, DOI 10.1016/0005-7967(96)00033-2; Boscarino JA, 1999, ANN BEHAV MED, V21, P227, DOI 10.1007/BF02884839; Bradley KA, 1998, JAMA-J AM MED ASSOC, V280, P166, DOI 10.1001/jama.280.2.166; Bradley KA, 2001, PSYCHOL ADDICT BEHAV, V15, P297, DOI 10.1037//0893-164X.15.4.297; BRESLAU N, 1991, ARCH GEN PSYCHIAT, V48, P216; Breslau N, 1998, ARCH GEN PSYCHIAT, V55, P626, DOI 10.1001/archpsyc.55.7.626; Breslau N, 1997, ARCH GEN PSYCHIAT, V54, P1044; Brown RL, 1997, J FAM PRACTICE, V44, P151; Dobie DJ, 2002, GEN HOSP PSYCHIAT, V24, P367, DOI 10.1016/S0163-8343(02)00207-4; ENGEL CC, 1993, J NERV MENT DIS, V181, P683, DOI 10.1097/00005053-199311000-00006; FELITTI VJ, 1991, SOUTHERN MED J, V84, P328; Felitti VJ, 1998, AM J PREV MED, V14, P245, DOI 10.1016/S0749-3797(98)00017-8; Fontana A, 1998, PSYCHIATR SERV, V49, P658; Freund KM, 1996, J GEN INTERN MED, V11, P44, DOI 10.1007/BF02603485; Friedman M.J., 1995, NEUROBIOLOGICAL CLIN; Grossman LS, 1997, PSYCHIATR SERV, V48, P393; Hankin CS, 1999, AM J PSYCHIAT, V156, P1924; Hankin CS, 1999, J TRAUMA STRESS, V12, P601, DOI 10.1023/A:1024760900213; Hoff RA, 1998, MED CARE, V36, P1524, DOI 10.1097/00005650-199811000-00002; Kazis LE, 1998, ARCH INTERN MED, V158, P626, DOI 10.1001/archinte.158.6.626; KESSLER RC, 1995, ARCH GEN PSYCHIAT, V52, P1048; Kessler RC, 2000, J CLIN PSYCHIAT, V61, P4; Kimerling R, 2000, J TRAUMA STRESS, V13, P115, DOI 10.1023/A:1007729116133; KOSS MP, 1990, J CONSULT CLIN PSYCH, V58, P147, DOI 10.1037//0022-006X.58.2.147; LISSAU I, 1994, LANCET, V343, P324, DOI 10.1016/S0140-6736(94)91163-0; Manne SL, 1998, J PEDIATR PSYCHOL, V23, P357, DOI 10.1093/jpepsy/23.6.357; MCFALL ME, 1992, J STUD ALCOHOL, V53, P357; MCFARLANE AC, 1994, J PSYCHOSOM RES, V38, P715, DOI 10.1016/0022-3999(94)90024-8; Montrey J. 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Intern. Med.	FEB 23	2004	164	4					394	400		10.1001/archinte.164.4.394		7	Medicine, General & Internal	General & Internal Medicine	776ZE	WOS:000189148600006	14980990	
J	Samee, S; Altes, T; Powers, P; de Lange, EE; Knight-Scott, J; Rakes, G; Mugler, JP; Ciambotti, JM; Alford, BA; Brookeman, JR; Platts-Mills, TAE				Samee, S; Altes, T; Powers, P; de Lange, EE; Knight-Scott, J; Rakes, G; Mugler, JP; Ciambotti, JM; Alford, BA; Brookeman, JR; Platts-Mills, TAE			Imaging the lungs in asthmatic patients by using hyperpolarized helium-3 magnetic resonance: Assessment of response to methacholine and exercise challenge	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; helium; magnetic resonance imaging; imaging; ventilation; lungs	COMPUTED-TOMOGRAPHY; HE-3 GAS; DISEASE; AIRWAYS; HEALTH	Background: Imaging of gas distribution in the lungs of patients with asthma has been restricted because of the lack of a suitable gaseous contrast agent. Hyperpolarized helium-3 (HHe3) provides a new technique for magnetic resonance imaging of lung diseases. Objective: We sought to investigate the use of HHe3 gas to image the lungs of patients with moderate or severe asthma and to assess changes in gas distribution after methacholine and exercise challenge. Methods: Magnetic resonance imaging was performed in asthmatic patients immediately after inhalation of HHe3 gas. In addition, images were obtained before and after methacholine challenge and a standard exercise test. Results: Areas of the lung with no signal or sharply reduced HHe3 signal (ventilation defects) are common in patients with asthma, and the number of defects was inversely related to the percent predicted FEV1 (r = 0.71, P < .002). After methacholine challenge (n = 3), the number of defects increased. Similarly, imaging of the lungs after exercise (n = 6) showed increased ventilation defects in parallel with decreases in FEV1. The increase in defects after challenge in these 9 asthmatic patients was significant both for the number (P < .02) and extent (P < .02) of the defects. The variability and speed of changes in ventilation and the complete lack of signal in many areas is in keeping with a model in which the defects result from airway closure. Conclusion: HHe3 magnetic resonance provides a new technique for imaging the distribution of inhaled air in the lungs. The technique is suitable for following responses to treatment of asthma and changes after methacholine or exercise challenge.	Univ Virginia, Hlth Syst, Asthma & Allerg Dis Ctr, Dept Internal Med,Div Asthma Allergy & Immunol, Charlottesville, VA 22908 USA; Univ Virginia, Dept Radiol, Charlottesville, VA 22903 USA; Univ Virginia, Dept Biomed Engn, Charlottesville, VA 22903 USA	Platts-Mills, TAE (reprint author), Univ Virginia, Hlth Syst, Asthma & Allerg Dis Ctr, Dept Internal Med,Div Asthma Allergy & Immunol, POB 801355, Charlottesville, VA 22908 USA.		Mugler, John/B-9432-2013	Mugler, John/0000-0002-4140-308X	NHLBI NIH HHS [R44 HL 59022, R01 HL 66479]; NIAID NIH HHS [AI 20565]; NIEHS NIH HHS [P01 ES/AI 50989]		Altes TA, 2001, J MAGN RESON IMAGING, V13, P378, DOI 10.1002/jmri.1054; BARNES PJ, 1986, AM REV RESPIR DIS, V134, P1289; Bodey KJ, 1999, ALLERGY, V54, P1083, DOI 10.1034/j.1398-9995.1999.00889.x; Crapo RO, 2000, AM J RESP CRIT CARE, V161, P309; Crater SE, 1999, AM J RESP CRIT CARE, V159, P806; de Lange EE, 1999, RADIOLOGY, V210, P851; ENRIGHT PL, 1991, AM REV RESPIR DIS, V143, P1215; ENRIGHT PL, 1994, AM J RESP CRIT CARE, V149, pS9; Hunt J, 2002, J ALLERGY CLIN IMMUN, V110, P28, DOI 10.1067/mai.2002.124966; Kaminsky DA, 2000, AM J RESP CRIT CARE, V162, P179; Kauczor HU, 1997, JMRI-J MAGN RESON IM, V7, P538, DOI 10.1002/jmri.1880070314; King GG, 1999, AM J RESP CRIT CARE, V159, P992; MCFALL J, 1996, RADIOLOGY, V200, P553; MIDDLETON H, 1995, MAGNET RESON MED, V33, P271, DOI 10.1002/mrm.1910330219; National Asthma Education and Prevention Program, 1997, NIH PUBL, V97-4051; NEWMAN KB, 1994, CHEST, V106, P105, DOI 10.1378/chest.106.1.105; Parker JA, 1996, J NUCL MED, V37, P1906; WOOLCOCK AJ, 1972, AM REV RESPIR DIS, V106, P692; WOOLCOCK AJ, 1972, AUST NZ J MED, V2, P294, DOI 10.1111/j.1445-5994.1972.tb03078.x	19	183	188	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.	JUN	2003	111	6					1205	1211		10.1067/mai.2003.1544		7	Allergy; Immunology	Allergy; Immunology	688FZ	WOS:000183424700006	12789218	
J	Remes, ST; Castro-Rodriguez, JA; Holberg, CJ; Martinez, FD; Wright, AL				Remes, ST; Castro-Rodriguez, JA; Holberg, CJ; Martinez, FD; Wright, AL			Dog exposure in infancy decreases the subsequent risk of frequent wheeze but not of atopy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; wheezing; atopy; allergy; epidemiology; risk; children; cat; dog; pets; IgE	HAY-FEVER; ALLERGIC SENSITIZATION; CHILDREN; ASTHMA; ENVIRONMENT; PREVALENCE; CHILDHOOD; COMMUNITY; FARMERS; COHORT	Background: Influence of household pets in the development of childhood asthma or atopy has been controversial. Objective: The purpose of this study was to investigate whether pet exposure in early life decreases the subsequent risk of frequent wheezing and/or allergic sensitization. Methods: This was a prospective observational birth cohort study. The setting was a large health maintenance organization in Tucson, Ariz; the subjects were a population sample of 1246 newborns enrolled at birth and followed prospectively to age 13 years. The main outcome measures were as follows: time to first report of frequent wheezing (>3 episodes in the past year), skin prick test reactivity at 6 years and 11 years of age, an total serum IgE at 9 months, 6 years, and 11 years of age. Results: Children living in households with greater than or equal to1 indoor dogs at birth were less likely to develop frequent wheeze than those not having indoor dogs (P = .004). This inverse association was confined to children without parental asthma (hazard ratio = 0.47; P < .001 [Cox regression]) and was not evident for children with parental asthma (hazard ratio = 0.96; P = .87). Adjustment by potential confounders did not change the results. Indoor cat exposure was not significantly associated with the risk of frequent wheezing. Neither cat exposure in early life nor dog exposure in early life was associated with skin prick test reactivity or total serum IgE at any age. Conclusion: Dog exposure in early life might prevent the development of asthmalike symptoms, at least in low-risk children with no family history of asthma. Nevertheless, early pet exposure does not seem to significantly influence the development of allergic sensitization.	Univ Arizona, Arizona Hlth Sci Ctr, Resp Sci Ctr, Tucson, AZ 85724 USA; Natl Publ Hlth Inst, Environm Epidemiol Unit, Kuopio, Finland	Wright, AL (reprint author), Univ Arizona, Arizona Hlth Sci Ctr, Resp Sci Ctr, Tucson, AZ 85724 USA.				NHLBI NIH HHS [HL 56177, HL 14136]		ARSHAD SH, 1991, BRIT J CLIN PRACT, V45, P88; Berge M, 1998, PEDIATR ALLERGY IMMU, V9, P25, DOI 10.1111/j.1399-3038.1998.tb00296.x; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Burr ML, 1997, CLIN EXP ALLERGY, V27, P1247; HAAHTELA T, 1990, BRIT MED J, V301, P266; HALONEN M, 1991, CLIN EXP ALLERGY, V21, P235, DOI 10.1111/j.1365-2222.1991.tb00836.x; Halonen M, 1997, AM J RESP CRIT CARE, V155, P1356; Hattevig G, 1993, Pediatr Allergy Immunol, V4, P182, DOI 10.1111/j.1399-3038.1993.tb00089.x; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Lewis SA, 2000, CLIN EXP ALLERGY, V30, P153; LINDFORS A, 1995, ARCH DIS CHILD, V73, P408; Martinez FD, 1999, LANCET S2, V354, pSII12; Munir AKM, 1997, J ALLERGY CLIN IMMUN, V100, P177, DOI 10.1016/S0091-6749(97)70221-5; Peat J, 1998, EUR RESPIR J, V12, p28S; Pekkanen J, 1999, EUR RESPIR J, V14, P951, DOI 10.1034/j.1399-3003.1999.14d37.x; Prescott SL, 1999, LANCET, V353, P196, DOI 10.1016/S0140-6736(98)05104-6; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Rothman KJ, 1998, MODERN EPIDEMIOLOGY; SIGURS N, 1995, PEDIATRICS, V95, P500; StataCorp, 1999, STAT STAT SOFTW REL; Strachan D, 1998, Eur Respir J Suppl, V27, p23s; SUONIEMI I, 1981, ALLERGY, V36, P263, DOI 10.1111/j.1398-9995.1981.tb01573.x; Svanes C, 1999, J ALLERGY CLIN IMMUN, V103, P415, DOI 10.1016/S0091-6749(99)70465-3; Tariq SM, 1998, J ALLERGY CLIN IMMUN, V101, P587; TAUSSIG LM, 1989, AM J EPIDEMIOL, V129, P1219; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, J ALLERGY CLIN IMMUN, V105, P9, DOI 10.1016/S0091-6749(00)90171-4; vonMutius E, 1997, LANCET, V350, P14; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7	30	183	189	2	9	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	OCT	2001	108	4					509	515		10.1067/mai.2001.117797		7	Allergy; Immunology	Allergy; Immunology	485NK	WOS:000171760300006	11590373	
J	Stern, DA; Morgan, WJ; Halonen, M; Wright, AL; Martinez, FD				Stern, Debra A.; Morgan, Wayne J.; Halonen, Marilyn; Wright, Anne L.; Martinez, Fernando D.			Wheezing and bronchial hyper-responsiveness in early childhood as predictors of newly diagnosed asthma in early adulthood: a longitudinal birth-cohort study	LANCET			English	Article							YOUNG-ADULTS; RISK-FACTORS; FOLLOW-UP; POPULATION; LIFE; CHILDREN; ILLNESS; ALLERGEN; RATIO	Background Incidence of asthma increases during early adulthood. We aimed to estimate the contributions of sex and early life factors to asthma diagnosed in young adults. Methods 1246 healthy newborn babies were enrolled in the Tucson Children's Respiratory Study. Parental characteristics, early-life wheezing phenotypes, airway function, and bronchial hyper-responsiveness to cold dry air and sensitisation to Alternaria alternata were determined before age 6 years. Physician-diagnosed asthma, both chronic and newly diagnosed, and airway function were recorded at age 22 years. Findings Of 1246 babies enrolled, 849 had follow-up data at 22 years. Average incidence of asthma at age 16-22 years was 12.6 per thousand person-years. 49 (27%) of all 181 cases of active asthma at 22 years were newly diagnosed, of which 35 (71%) were women. Asthma remittance by 22 years was higher in men than in women (multinomial odds ratio [M-OR] 2.0, 95% CI 1.2-3.2, p=0 . 008). Age at diagnosis was linearly associated with the ratio of forced expiratory volume at 1 s to forced vital capacity at age 22 years. Factors independently associated with chronic asthma at 22 years included onset at 6 years (7.4, 3 . 9-14. 0) and persistent wheezing (14.0, 6.8-28 . 0) in early life, sensitisation to A alternata (3.6, 2.1-6.4), low airway function at age 6 years (2.1, 1.1-3.9.), and bronchial hyper-responsiveness at 6 years (4 . 5, 1.9-10 . 0). Bronchial hyper-responsiveness (6.9, 2.3-21 . 0), low airway function at 6 years (2.8, 1.1-6.9), and late-onset (4 . 6, 1.7-12 . 0) and persistent wheezing (4 . 0, 1.2-14. 0) predicted newly diagnosed asthma at age 22 years. Interpretation Asthma with onset in early adulthood has its origins in early childhood. Funding National Heart Lung and Blood Institute.	[Stern, Debra A.; Morgan, Wayne J.; Halonen, Marilyn; Wright, Anne L.; Martinez, Fernando D.] Univ Arizona, Hlth Sci Ctr, Arizona Resp Ctr, Tucson, AZ 85724 USA; [Morgan, Wayne J.; Wright, Anne L.] Univ Arizona, Dept Pediat, Tucson, AZ USA	Martinez, FD (reprint author), Univ Arizona, Hlth Sci Ctr, Arizona Resp Ctr, Tucson, AZ 85724 USA.	fernando@arc.arizona.edu			National Heart Lung and Blood Institute [HL-56177]	This work is supported by grant HL-56177 from the National Heart Lung and Blood Institute. We gratefully acknowledge the contributions of Lynn Taussig who started the Tucson Children's Respiratory Study in 1980 We thank Bruce Saul for data management and our study nurses, Marilyn Lindell and Lydia de la Ossa, for data collection and participant follow-LIP.	Anderson HR, 2007, THORAX, V62, P85, DOI 10.1136/thx.2006.066407; ANDERSON HR, 1992, THORAX, V47, P537, DOI 10.1136/thx.47.7.537; Avila L, 2005, J ASTHMA, V42, P543, DOI 10.1080/02770900500214791; Chen Y, 2002, AM J EPIDEMIOL, V155, P191, DOI 10.1093/aje/155.3.191; Guerra S, 2002, J ALLERGY CLIN IMMUN, V109, P419, DOI 10.1067/mai.2002.121701; Halonen M, 1997, AM J RESP CRIT CARE, V155, P1356; Illi S, 2006, LANCET, V368, P763, DOI 10.1016/S0140-6736(06)69286-6; King ME, 2004, PANMINERVA MED, V46, P97; LARSSON L, 1995, THORAX, V50, P260, DOI 10.1136/thx.50.3.260; Lombardi E, 1997, AM J RESP CRIT CARE, V156, P1863; Martinez FD, 2003, NEW ENGL J MED, V349, P1473, DOI 10.1056/NEJMe030041; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Moore YF, 2004, IMMUNOGENETICS, V56, P1, DOI 10.1007/s00251-004-0661-6; Morgan WJ, 2005, AM J RESP CRIT CARE, V172, P1253, DOI 10.1164/rccm.200504-525OC; Nicolai T, 2003, PEDIATR ALLERGY IMMU, V14, P280, DOI 10.1034/j.1399-3038.2003.00047.x; Ownby DR, 1996, ANN ALLERG ASTHMA IM, V77, P304; PATTEMORE PK, 1990, AM REV RESPIR DIS, V142, P549; Phelan PD, 2002, J ALLERGY CLIN IMMUN, V109, P189, DOI 10.1067/mai.2001.120951; Rasmussen F, 2002, AM J RESP CRIT CARE, V165, P1480, DOI 10.1164/rccm.2108009; Sears MR, 2003, NEW ENGL J MED, V349, P1414, DOI 10.1056/NEJMoa022363; Stein RT, 1997, THORAX, V52, P946; Strachan DP, 1996, BRIT MED J, V312, P1195; TAUSSIG LM, 1989, AM J EPIDEMIOL, V129, P1219; TOELLE BG, 1992, AM REV RESPIR DIS, V146, P633; WRIGHT AL, 1989, AM J EPIDEMIOL, V129, P1232; Wright AL, 2006, PEDIATR PULM, V41, P318, DOI 10.1002/ppul.20373; Xuan W, 2000, AM J RESP CRIT CARE, V161, P1820	27	182	187	2	16	ELSEVIER SCIENCE INC	NEW YORK	360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA	0140-6736			LANCET	Lancet	SEP 20	2008	372	9643					1058	1064		10.1016/S0140-6736(08)61447-6		7	Medicine, General & Internal	General & Internal Medicine	354OI	WOS:000259648500032	18805334	
J	Haland, G; Carlsen, KCL; Sandvik, L; Devulapalli, CS; Munthe-Kaas, MC; Pettersen, M; Carlsen, KH				Haland, Geir; Carlsen, Karin C. Lodrup; Sandvik, Leiv; Devulapalli, Chandra Sekhar; Munthe-Kaas, Monica Cheng; Pettersen, Morten; Carlsen, Kai-Hakon		ORAACLE	Reduced lung function at birth and the risk of asthma at 10 years of age	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							EXPIRATORY FLOW PATTERNS; BRONCHIAL OBSTRUCTION; AIRWAY FUNCTION; EARLY-LIFE; INFANTS; CHILDREN; MECHANICS; EXPOSURE; WHEEZE	BACKGROUND Reduced lung function in early infancy has been associated with later obstructive airway diseases. We assessed whether reduced lung function shortly after birth predicts asthma 10 years later. METHODS We conducted a prospective birth cohort study of healthy infants in which we measured lung function shortly after birth with the use of tidal breathing flow-volume loops (the fraction of expiratory time to peak tidal expiratory flow to total expiratory time [t(sub PTEF)/t(sub E)]) in 802 infants and passive respiratory mechanics, including respiratory-system compliance, in 664 infants. At 10 years of age, 616 children (77%) were reassessed by measuring lung function, exercise-induced bronchoconstriction, and bronchial hyperresponsiveness (by means of a methacholine challenge) and by conducting a structured interview to determine whether there was a history of asthma or current asthma. RESULTS As compared with children whose t(sub PTEF)/t(sub E) shortly after birth was above the median, children whose t(sub PTEF)/t(sub E) was at or below the median were more likely at 10 years of age to have a history of asthma (24.3% vs. 16.2%, P=0.01), to have current asthma (14.6% vs. 7.5%, P=0.005), and to have severe bronchial hyperresponsiveness, defined as a methacholine dose of less than 1.0 micromol causing a 20% fall in the forced expiratory volume in 1 second (FEV(sub 1)) (9.1% vs. 4.9%, P=0.05). As compared with children whose respiratory-system compliance was above the median, children with respiratory compliance at or below the median more often had a history of asthma (27.4% vs. 14.8%; P=0.001) and current asthma (15.0% vs. 7.7%, P=0.009), although this measure was not associated with later measurements of lung function. At 10 years of age, t(sub PTEF)/t(sub E) at birth correlated weakly with the maximal midexpiratory flow rate (r=0.10, P=0.01) but not with FEV(sub 1) or forced vital capacity. CONCLUSIONS Reduced lung function at birth is associated with an increased risk of asthma by 10 years of age.	Rigshosp Radiumhosp Med Ctr, Dept Pediat, Voksentoppen, N-0491 Oslo, Norway; Ullevaal Univ Hosp, Dept Pediat, Div Woman & Child, Oslo, Norway; Ullevaal Univ Hosp, Clin Res Ctr, Oslo, Norway; Univ Oslo, Fac Med, Oslo, Norway	Haland, G (reprint author), Rigshosp Radiumhosp Med Ctr, Dept Pediat, Voksentoppen, Ullveien 14, N-0491 Oslo, Norway.	haland@medisin.uio.no	Devulapalli, Chandra Sekhar/B-6170-2008				BANOVCIN P, 1995, PEDIATR RES, V38, P218, DOI 10.1203/00006450-199508000-00014; Carlsen KCL, 1997, EUR RESPIR J, V10, P1774; Carlsen KCL, 2006, ALLERGY, V61, P454, DOI 10.1111/j.1398-9995.2005.00938.x; CARLSEN KCL, 1997, EUR RESP MON, V5, P27; Carlsen KH, 2000, RESP MED, V94, P750, DOI 10.1053/rmed.2000.0809; Carlsen L, 1999, PEDIATR ALLERGY IMMU, V10, P89; Crapo RO, 2000, AM J RESP CRIT CARE, V161, P309; CUTRERA R, 1991, PEDIATR PULM, V10, P6, DOI 10.1002/ppul.1950100103; LESOUEF PN, 1984, AM REV RESPIR DIS, V129, P552; Lodrup Carlsen K C, 1994, Eur Respir J, V7, P1660, DOI 10.1183/09031936.94.07091660; LODRUP KC, 1992, PEDIATR PULM, V12, P99, DOI 10.1002/ppul.1950120208; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; MARTINEZ FD, 1991, AM REV RESPIR DIS, V143, P312; MARTINEZ FD, 1988, NEW ENGL J MED, V319, P1112, DOI 10.1056/NEJM198810273191702; MORRIS MJ, 1981, THORAX, V36, P135, DOI 10.1136/thx.36.2.135; Murray CS, 2002, THORAX, V57, P388, DOI 10.1136/thorax.57.5.388; Nystad W, 2001, EUR J EPIDEMIOL, V17, P209, DOI 10.1023/A:1017926403763; Ronmark E, 2001, PEDIATRICS, V107, DOI 10.1542/peds.107.3.e37; Seddon PC, 1996, AM J RESP CRIT CARE, V153, P1248; TAGER IB, 1993, AM REV RESPIR DIS, V147, P811; Turner SW, 2004, AM J RESP CRIT CARE, V169, P921, DOI 10.1164/rccm.200307-891OC; vanderEnt CK, 1996, AM J RESP CRIT CARE, V153, P1253; YOUNG S, 1994, J PEDIATR-US, V124, P681, DOI 10.1016/S0022-3476(05)81355-1; Young S, 2000, EUR RESPIR J, V15, P151, DOI 10.1034/j.1399-3003.2000.15a28.x; Yuksel B, 1996, THORAX, V51, P815, DOI 10.1136/thx.51.8.815	25	182	190	0	1	MASSACHUSETTS MEDICAL SOC	WALTHAM	WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA	0028-4793			NEW ENGL J MED	N. Engl. J. Med.	OCT 19	2006	355	16					1682	1689		10.1056/NEJMoa052885		8	Medicine, General & Internal	General & Internal Medicine	096DN	WOS:000241357300009	17050892	
J	Viegi, G; Pistelli, F; Sherrill, DL; Maio, S; Baldacci, S; Carrozzi, L				Viegi, G.; Pistelli, F.; Sherrill, D. L.; Maio, S.; Baldacci, S.; Carrozzi, L.			Definition, epidemiology and natural history of COPD	EUROPEAN RESPIRATORY JOURNAL			English	Review						air pollution; chronic obstructive pulmonary disease clinical/basic investigations; cor pulmonale; epidemiology of asthma/chronic obstructive pulmonary disease; smoking; spirometry	OBSTRUCTIVE PULMONARY-DISEASE; GENERAL-POPULATION SAMPLE; PARTICULATE AIR-POLLUTION; PERCUTANEOUS CORONARY INTERVENTION; DOMICILIARY OXYGEN-THERAPY; PROPORTIONAL VENN-DIAGRAM; FORCED EXPIRATORY VOLUME; PHYSICIAN-DIAGNOSED COPD; HEALTH-CARE UTILIZATION; LUNG-FUNCTION DECLINE	Chronic obstructive pulmonary disease (COPD) is the fifth cause of morbidity and mortality in the developed world and represents a substantial economic and social burden. Patients experience a progressive deterioration up to end-stage COPD, characterised by very severe airflow limitation, severely limited and declining performance status with chronic respiratory failure, advanced age, multiple comorbidities and severe systemic manifestations/ complications. COPD is frequently underdiagnosed and under-treated. Today, COPD develops earlier in life and is less gender specific. Tobacco smoking is the major risk factor for COPD, followed by occupation and air pollution. Severe deficiency for alpha(1)-antitrypsin is rare; several phenotypes are being associated with elevated risk for COPD in the presence of risk factor exposure. Any patient presenting with cough, sputum production or dyspnoea should be assessed by standardised spirometry. Continued exposure to noxious agents promotes a more rapid decline in lung function and increases the risk for repeated exacerbations, eventually leading to end-stage disease. Without major efforts in prevention, there will be an increasing proportion of end-stage patients who can live longer through long-term oxygen therapy and assisted ventilation, but with elevated suffering and huge costs. Smoking prevention and smoking cessation are the most important epidemiological measurements to counteract chronic obstructive pulmonary disease epidemics.	CNR, Inst Clin Physiol, Pulm Environm Unit, I-56126 Pisa, Italy; Univ Pisa, Cardiothorac Dept, Pisa, Italy; Univ Arizona, Arizona Clin Res Traning Program, Tucson, AZ USA; Univ Arizona, Mel & Enid Zuckerman Coll Publ Hlth, Tucson, AZ USA	Viegi, G (reprint author), CNR, Inst Clin Physiol, Pulm Environm Unit, Via Trieste 41, I-56126 Pisa, Italy.	viegig@ifc.cnr.it	Maio, Sara/K-4065-2016	Maio, Sara/0000-0001-6363-8544			Adcock IM, 2006, RESP RES, V7, DOI 10.1186/1465-9921-7-21; Ai-Ping Chua, 2005, Chest, V128, P518, DOI 10.1378/chest.128.2.518; *AM MED ASS, 1984, GUID EV PERM IMP, P85; American Thoracic Society, 2000, AM J RESP CRIT CARE, V161, P665; Anderson HR, 1997, EUR RESPIR J, V10, P1064, DOI 10.1183/09031936.97.10051064; Anthonisen NR, 2002, AM J RESP CRIT CARE, V166, P675, DOI 10.1164/rccm.2112096; *ASS NAT TRAIT DOM, 1998, OBS; Balmes J, 2003, AM J RESP CRIT CARE, V167, P787, DOI 10.1164/rccm.167.5.787; BATES DV, 1979, LUNG TRANSITION HLTH, V12, P1; Bednarek M, 2006, THORAX, V61, P869, DOI 10.1136/thx.2006.059071; 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J	Kirkpatrick, B; Fleming, LE; Squicciarini, D; Backer, LC; Clark, R; Abraham, W; Benson, J; Cheng, YS; Johnson, D; Pierce, R; Zaias, J; Bossart, GD; Baden, DG				Kirkpatrick, B; Fleming, LE; Squicciarini, D; Backer, LC; Clark, R; Abraham, W; Benson, J; Cheng, YS; Johnson, D; Pierce, R; Zaias, J; Bossart, GD; Baden, DG			Literature review of Florida red tide: implications for human health effects	HARMFUL ALGAE			English	Review						Florida red tide; red tide; neurotoxic shellfish poisoning; NSP; brevetoxins; harmful algal bloom; HAB; karenia brevis; shellfish poisoning; respiratory irritation; marine toxin diseases	NEUROTOXIC SHELLFISH TOXINS; FORMERLY GYMNODINIUM-BREVE; SENSITIVE SODIUM-CHANNELS; RAT-BRAIN SYNAPTOSOMES; MARINE ALGAL TOXINS; PTYCHODISCUS-BREVIS; NEW-ZEALAND; DINOFLAGELLATE TOXINS; CRASSOSTREA-GIGAS; MOUSE BIOASSAY	Florida red tides are a natural phenomenon caused by dense aggregations of single cell or several species Of unicellular organisms. Patches of discolored water, dead or dying fish, and respiratory irritants in the air often characterize these algal blooms. In humans, two distinct clinical entities, depending on the route of exposure, are associated with exposure to the Florida red tide toxins (particularly the brevetoxins). With the ingestion of brevetoxin-contaminated shellfish, neurotoxic shellfish poisoning (NSP) presents as a milder gastroenteritis with neurologic symptoms compared with other marine toxin diseases such as paralytic shellfish poisoning (PSP) or ciguatera fish poisoning. With the inhalation of the aerosolized red tide toxins (especially the brevetoxins) from the sea spray, respiratory irritation and possibly other health effects are reported in both humans and other mammals [Nat. Toxins Drugs (1995) 141; Fleming, L.E., Baden, D.G., 1988. Neurotoxic shellfish poisoning: public health and human health effects. White Paper for the Proceedings of the Texas Conference on Neurotoxic Shellfish Poisoning. In: Proceedings of the Texas NSP Conference, Corpus Christi, TX, pp. 27-34; Travel Med, 2 (10) (1998b) 1: Travel Med. 3 (10) (1999a) 1; Toxins Pathol. 26 (2) (1998) 276; J. Allergy Clin. Imunol. 69 (1982) 418; Arch. Intern. Med. 149 (1989) 1735; Toxicon 24 (1986) 955; Florida Med. J. 60 (11) (1773) 27; J. Nat. Toxins 4 (1995) 181; J. Nat. Toxins 4 (1995) 18 1: Sci. Ani. 271 (4) (1994) 62]. This paper reviews the literature on the known and possible human health effects of exposure to the Florida red tides and their toxins. The review includes discussion of the red tide organisms and their toxins, as well as the effects of these toxins on both wild and laboratory animals as they relate to possible human health effects and exposures. (C) 2004 Elsevier B.V. All rights reserved.	Mote Marine Lab, Sarasota, FL 34236 USA; Univ Miami, NIEHS, Marine & Freshwater Biomed Sci Ctr, Miami, FL 33149 USA; Ctr Dis Control & Prevent, Natl Ctr Environm Hlth, Atlanta, GA 30333 USA; Florida Dept Hlth, Tallahassee, FL 32399 USA; Lovelace Resp Inst, Albuquerque, NM 87108 USA; Univ N Carolina, Ctr Marine Sci, Wilmington, NC 28409 USA	Kirkpatrick, B (reprint author), Mote Marine Lab, 1600 Ken Thompson Pkwy, Sarasota, FL 34236 USA.	bkirkpat@mote.org			NIEHS NIH HHS [P01 ES010594, P01 ES010594-04]		ABRAHAM WM, 2001, INT SOC EXPOSURE ANA, V126; AHLES MD, 1974, PUBLIC HLTH BRIEFS, V64, P807; AHMED FE, 1993, ENVIRON TOXIC WATER, V8, P141, DOI 10.1002/tox.2530080203; ANDERSON DM, 1994, SCI AM, V271, P62; Anderson DM, 1993, 9302 WHOI; Anderson D. 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A., 2001, P 9 INT C HARMF ALG, P153; VIVIANI R, 1992, SCIENCE OF THE TOTAL ENVIRONMENT, SUPPLEMENT 1992, P631; Walsh JJ, 2001, J GEOPHYS RES-OCEANS, V106, P11597, DOI 10.1029/1999JC000123; WASHBURN BS, 1994, TOXICON, V32, P799, DOI 10.1016/0041-0101(94)90005-1; Washburn BS, 1996, AQUAT TOXICOL, V35, P1, DOI 10.1016/0166-445X(95)00050-E; WATANABE T, 1988, ALLERGY PRACT, V10, P185; WELLER PF, 1984, J ALLERGY CLIN IMMUN, V73, P1, DOI 10.1016/0091-6749(84)90474-3; Whitney Philip L., 1997, Natural Toxins, V5, P193; WOODCOCK AH, 1948, J MAR RES, V7, P56; Yeh HC, 1996, AEROSOL SCI TECH, V25, P134, DOI 10.1080/02786829608965386	147	181	186	9	75	ELSEVIER SCIENCE BV	AMSTERDAM	PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS	1568-9883			HARMFUL ALGAE	Harmful Algae	APR	2004	3	2					99	115		10.1016/j.hal.2003.08.005		17	Marine & Freshwater Biology	Marine & Freshwater Biology	813RY	WOS:000220925400001	20411030	
J	Kreiss, K; Gomaa, A; Kullman, G; Fedan, K; Simoes, EJ; Enright, PL				Kreiss, K; Gomaa, A; Kullman, G; Fedan, K; Simoes, EJ; Enright, PL			Clinical bronchiolitis obliterans in workers at a microwave-popcorn plant	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							POPULATION; VALUES; SAMPLE	Background In May 2000, eight persons who had formerly worked at a microwave-popcorn production plant were reported to have severe bronchiolitis obliterans. No recognized cause was identified in the plant. Therefore, we medically evaluated current employees and assessed their occupational exposures. Methods Questionnaire responses and spirometric findings in participating workers were compared with data from the third National Health and Nutrition Examination Survey, after adjustment for age and smoking status. We evaluated the relation between exposures and health-related outcomes by analyzing the rates of symptoms and abnormalities according to current and cumulative exposure to diacetyl, the predominant ketone in artificial butter flavoring and in the air at the plant. Results Of the 135 current workers at the plant, 117 (87 percent) completed the questionnaire. These 117 workers had 2.6 times the expected rates of chronic cough and shortness of breath, according to comparisons with the national data, and twice the expected rates of physician-diagnosed asthma and chronic bronchitis. Overall, the workers had 3.3 times the expected rate of airway obstruction; those who had never smoked had 10.8 times the expected rate. Workers directly involved in the production of microwave popcorn had higher rates of shortness of breath on exertion and skin problems that had developed since they started work than workers in other parts of the plant. There was a strong relation between the quartile of estimated cumulative exposure to diacetyl and the frequency and extent of airway obstruction. Conclusions The excess rates of lung disease and lung-function abnormalities and the relation between exposure and outcomes in this working population indicate that they probably had occupational bronchiolitis obliterans caused by the inhalation of volatile butter-flavoring ingredients.	NIOSH, Div Resp Dis Studies, Morgantown, WV 26505 USA; Missouri Dept Hlth & Senior Serv, Off Epidemiol, Jefferson City, MO USA	Kreiss, K (reprint author), NIOSH, Div Resp Dis Studies, H2800,1095 Willowdale Rd, Morgantown, WV 26505 USA.			Simoes, Eduardo/0000-0003-4371-4305			AKPINARELCI M, 2002, AM J RESP CRIT CARE, V165, pA526; American Thoracic Society, 1991, AM REV RESPIR DIS, V144, P1202, DOI 10.1164/ajrccm/144.5.1202; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P2185; Eller PM, 1994, DHHS NIOSH PUBLICATI; FERRIS BG, 1978, AM REV RESPIR DIS, V118, P1; Hankinson JL, 1999, AM J RESP CRIT CARE, V159, P179; HUBBS AF, 2002, TOXICOL SCI S, V66, P194; *INT BAK SERV INC, 1986, DHHS NIOSH PUBL; International Labour Office, 1980, OCC SAF HLTH SER, V22; KING TE, 1998, FISHMANS PULMONARY D, P825; Lockey J, 2002, AM J RESP CRIT CARE, V165, pA461; MILLER A, 1983, AM REV RESPIR DIS, V127, P270; MONSON RR, 1990, OCCUPATIONAL EPIDEMI, P114; MORGAN RH, 1979, AM J ROENTGENOL, V132, P803; National Center for Health Statistics, 1996, 3 NAT HLTH NUTR EX S; Parmet AJ, 2002, J OCCUP ENVIRON MED, V44, P216, DOI 10.1097/00043764-200203000-00002; SAS Institute, 1990, SAS STAT US GUID VER; [Anonymous], 2002, MMWR MORB MORTAL WKL, V51, P345	19	181	184	5	15	MASSACHUSETTS MEDICAL SOC/NEJM	WALTHAM	WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA	0028-4793			NEW ENGL J MED	N. Engl. J. Med.	AUG 1	2002	347	5					330	338		10.1056/NEJMoa020300		9	Medicine, General & Internal	General & Internal Medicine	587WC	WOS:000177665900005	12151470	
J	Huss, K; Adkinson, NF; Eggleston, PA; Dawson, C; Van Natta, ML; Hamilton, RG				Huss, K; Adkinson, NF; Eggleston, PA; Dawson, C; Van Natta, ML; Hamilton, RG			House dust mite and cockroach exposure are strong risk factors for positive allergy skin test responses in the Childhood Asthma Management Program	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						house dust mites; childhood asthma; cockroach allergy; Childhood Asthma Management Program; allergy sensitization; indoor allergens; atopy; risk factors for asthma; allergen exposure	INNER-CITY CHILDREN; CAT ALLERGEN; SENSITIZATION; HOMES; AUSTRALIA; ANTIGEN; SCHOOL; DOG	Background: Children with asthma have a high prevalence of environmental allergies, especially to indoor allergens. The relationships of exposure to indoor allergens (dust mites, cat, dog, cockroach, and molds) and other host factors to allergy sensitization have not been evaluated simultaneously in a large cohort. Objectives: We studied 1041 children aged 5 to 12 years with mild-to-moderate asthma to determine risk factors associated with having positive allergy skin test responses to indoor allergens. Also, we described, compared, and contrasted 6 allergens in the home environments of these children from 8 North American cities. Methods: Data were used from baseline visits of the Childhood Asthma Management Program. Patients' sensitivities to house dust mites (Dermatophagoides farinae and Dermatophagoides pteronyssinus), cats, dogs, cockroaches, and molds were examined for relationships to demographic variables, home dust allergen exposures, number of other positive allergy skin test responses, total serum IgE levels, and smoking in the home. Results: San Diego (78.5%) and Toronto (59.3%) had the topmost percentages of homes with moderate-to-high house dust mite levels. Boston (21.5%), St Louis (16.3%), and Baltimore (13.4%) had the highest percentages of homes with detectable levels of cockroach allergen. For house dust mites, the higher the level of allergen exposure, the more likely patients were to have positive allergy skin test responses, with relative odds of 9.0 (95% confidence interval, 5.4-15.1) for those exposed to high mite levels: (>10.0 mug/g dust) relative to those unexposed. Even exposure to low levels of mite allergen (0.020-2.0 mug/g) was found to be a significant risk factor for sensitization. For cockroach allergen, those with detectable home exposure were more likely to have positive skin test responses (relative odds, 2.2; 95% confidence interval, 1.3-3.8) than those with undetectable exposure. In contrast, levels of exposure to cat, dog, and mold allergens were not related to sensitization rates. For cat allergen, this may reflect lower rates of cat ownership among highly sensitized subjects. Furthermore, the number of allergy skin test responses that were positive, excluding the test for the outcome of interest for each model, and total serum IgE levels were strong independent predictors of sensitization. Conclusions: Levels of exposure determined by house dust analysis are important determinants of sensitization for dust mite and cockroach allergen. This relationship was not demonstrable for cat, dog, or mold allergens, possibly because of confounding factors. For all allergens studied, the degree of atopy; determined by the total number of positive skin test responses or by total serum IgE levels, is an important contributing risk factor for sensitization.	Johns Hopkins Univ, Sch Hyg & Publ Hlth, Baltimore, MD 21205 USA; Johns Hopkins Asthma & Allergy Ctr, DACI Reference Lab, Baltimore, MD USA	Huss, K (reprint author), Johns Hopkins Univ, Sch Nursing, 525 N Wolfe St,Room 416, Baltimore, MD 21205 USA.						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E., 1997, Journal of Allergy and Clinical Immunology, V100, pS1; PlattsMills TAE, 1997, NEW ENGL J MED, V336, P1382, DOI 10.1056/NEJM199705083361909; 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; SAS Institute, 1989, SAS STAT US GUID VER, V1; SPORIK R, 1995, AM J RESP CRIT CARE, V151, P1388; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; WARNER JA, 1991, PEDIATR ALLERGY IMMU, V1, P79; WITTIG HJ, 1980, J ALLERGY CLIN IMMUN, V66, P305, DOI 10.1016/0091-6749(80)90026-3	32	181	194	3	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.	JAN	2001	107	1					48	54		10.1067/mai.2001.111146		7	Allergy; Immunology	Allergy; Immunology	394PW	WOS:000166533300009	11149990	
J	Calamita, Z; Saconato, H; Pela, AB; Atallah, AN				Calamita, Z.; Saconato, H.; Pela, A. B.; Atallah, A. N.			Efficacy of sublingual immunotherapy in asthma: systematic review of randomized-clinical trials using the Cochrane Collaboration method	ALLERGY			English	Review						asthma; immunotherapy; meta-analysis; review; sublingual	PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND PLACEBO; GRASS-POLLEN EXTRACT; HOUSE-DUST MITES; STANDARDIZED 5-GRASS-POLLEN EXTRACT; SWALLOW IMMUNOTHERAPY; ALLERGIC RHINOCONJUNCTIVITIS; RESPIRATORY ALLERGY; BRONCHIAL HYPERREACTIVITY; PEDIATRIC-PATIENTS	Background: Sublingual immunotherapy (SLIT) is effective and safe in the treatment of allergic rhinitis. However, there is no meta-analysis in asthma treatment. Methods: The clinical efficacy of SLIT for asthma was evaluated through a systematic review with meta-analysis. MEDLINE (1966-2005), EMBASE (1974-2005), LILACS (1982-2005), and the Cochrane Library were searched for related literature in any language. Randomized-controlled clinical trials (RCT) on SLIT in asthma treatment for adults and children were selected. From 119 citations, 25 studies with 1706 patients were included in this meta-analysis. For each report, quality scores were assigned and data were extracted in relation to the outcomes analyzed: asthmatic symptoms, use of asthma medications, lung function, and bronchial provocation. Results: According to the Jadad quality method, 64% of the studies were assigned scores of 4 or 5. Immunotherapy was seen to significantly reduce asthma severity when parameter compositions were all analyzed by categorical outcomes. There was a nonsignificant reduction in asthma symptoms when analyzed using standardized mean differences. No severe reactions were observed. Conclusions: This meta-analysis found that SLIT is beneficial for asthma treatment albeit the magnitude of the effect is not very large. Moreover, it is a safe alternative to the subcutaneous route. More RCT with standardization of symptom scores and medications are needed in order to contribute further to this subject.	Med Sch Marilia, Div Internal Med & Allergy & Immunol, Marilia, SP, Brazil; Univ Fed Sao Paulo, Div Internal Med Urgency & Therapeut, Sch Med, Sao Paulo, Brazil; Med Sch Marilia, Div Internal Med & Allergy & Immunol, Marilia, SP, Brazil	Calamita, Z (reprint author), Med Sch Marilia, Div Internal Med & Allergy & Immunol, 648 Vicente Ferreira, Marilia, SP, Brazil.		Atallah, Alvaro/K-7182-2013				Abramson M, 1999, ALLERGY, V54, P1022, DOI 10.1034/j.1398-9995.1999.00102.x; ABRAMSON MJ, 2005, COCHRANE LIB, P1; Akdis CA, 2000, ALLERGY, V55, P522, DOI 10.1034/j.1398-9995.2000.00120.x; Allen-Diaz B, 1998, J SOIL WATER CONSERV, V53, P42; Almagro E, 1995, Allergol Immunopathol (Madr), V23, P153; Andre C, 2000, INT ARCH ALLERGY IMM, V121, P229, DOI 10.1159/000024322; Andre C, 2003, INT ARCH ALLERGY IMM, V131, P111, DOI 10.1159/000070926; Arena A, 2003, INT J IMMUNOPATH PH, V16, P277; Ariano R, 2001, Allergol Immunopathol (Madr), V29, P238; ARIANO R, 2005, ALLERG IMMUNOL PARIS, V37, P103; 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; Begg C, 1996, JAMA-J AM MED ASSOC, V276, P637, DOI 10.1001/jama.276.8.637; BELLINGHAUSEN I, 2000, ALLERGY CLIN IMMUNOL, V12, P20, DOI 10.1027/0838-1925.12.1.20; Bousquet J, 1999, ALLERGY, V54, P249, DOI 10.1034/j.1398-9995.1999.00916.x; 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MITSCH A, 1996, TW PADIATRIE, V9, P628; Mungan D, 1999, ANN ALLERG ASTHMA IM, V82, P485, DOI 10.1016/S1081-1206(10)62726-3; Mungan D., 1996, European Respiratory Journal Supplement, V9, p210S; Niu C., 2004, Journal of Allergy and Clinical Immunology, V113, pS108, DOI 10.1016/j.jaci.2003.12.377; Novembre E, 2004, J ALLERGY CLIN IMMUN, V114, P851, DOI 10.1016/j.jaci.2004.07.012; NOVEMBRE E, 1991, RIV ITAL PED, V17, P75; Olaguibel JM, 2005, J INVEST ALLERG CLIN, V15, P9; Orefice U., 2004, Journal of Allergy and Clinical Immunology, V113, pS111, DOI 10.1016/j.jaci.2003.12.390; Pajno GB, 2000, ALLERGY, V55, P842, DOI 10.1034/j.1398-9995.2000.00495.x; Pajno GB, 2005, CLIN EXP ALLERGY, V35, P551, DOI 10.1111/j.1365-2222.2005.02256.x; Pajno GB, 2004, ALLERGY, V59, P883, DOI 10.1111/j.1398-9995.2004.00578.x; Pajno GB, 2003, CLIN EXP ALLERGY, V33, P1641, DOI 10.1111/j.1365-2222.2003.01809.x; Schamann F, 2001, ALLERGOL IMMUNOPATH, V29, P60; Passalacqua G, 1999, J ALLERGY CLIN IMMUN, V104, P964, DOI 10.1016/S0091-6749(99)70076-X; Passalacqua G, 2004, ANN ALLERG ASTHMA IM, V93, P3; Passalacqua G, 1998, LANCET, V351, P629, DOI 10.1016/S0140-6736(97)07055-4; PASSALACQUA G, 2005, ALLERGY CLIN IMMUNOL, V17, P181, DOI 10.1027/0838-1925.17.5.181; Passalacqua Giovanni, 2004, Curr Opin Allergy Clin Immunol, V4, P31, DOI 10.1097/00130832-200402000-00007; Patriarca G, 2002, ANESTH ANALG, V95, P956, DOI 10.1213/01.ANE.0000028849.92989.84; PEREIRA MG, 1995, EPIDEMIOLOGIA TEORIA, P358; Pradalier A, 1999, ALLERGY, V54, P819, DOI 10.1034/j.1398-9995.1999.00077.x; Purello-D'Ambrosio F, 1999, ALLERGY, V54, P968, DOI 10.1034/j.1398-9995.1999.00203.x; PURELLODAMBROSI.F, 1996, ALLERGOL IMMUNOPATH, V24, P146; Quirino T, 1996, CLIN EXP ALLERGY, V26, P1253, DOI 10.1046/j.1365-2222.1996.d01-280.x; Rakoski J, 2001, INT ARCH ALLERGY IMM, V126, P185, DOI 10.1159/000049512; Rolinck-Werninghaus C, 2004, ALLERGY, V59, P1285, DOI 10.1111/j.1398-9995.2004.00627.x; SABBAH A, 1994, ALLERGY, V49, P309, DOI 10.1111/j.1398-9995.1994.tb02273.x; Sambugaro R, 2003, Allergol Immunopathol (Madr), V31, P329, DOI 10.1157/13055212; SANTOS OR, 2004, REV ALERG MEX, V51, P177; SCHEINMANN P, 2002, ALLERG IMMUNOL PARIS, V34, P60; Silvestri M, 2002, J INVEST ALLERG CLIN, V12, P52; Sopo SM, 2004, ARCH DIS CHILD, V89, P620, DOI 10.1136/adc.2003.030411; Tari M G, 1994, Allergol Immunopathol (Madr), V22, P209; TARI MG, 1990, ALLERGOL IMMUNOPATH, V18, P277; TePas EC, 2004, ANN ALLERG ASTHMA IM, V92, P25; Vervloet D, 2002, ALLERGY, V57, P70; Voltolini S, 2001, Allergol Immunopathol (Madr), V29, P103; Vourdas D, 1998, ALLERGY, V53, P662, DOI 10.1111/j.1398-9995.1998.tb03952.x; Wessner D, 2003, CHEM IMMUNOL, V82, P53; WILSON DC, 2005, EARTHQUAKE PREDICTIO, P1; Wilson DR, 2005, ALLERGY, V60, P4, DOI 10.1111/j.1398-9995.2005.00699.x; Wuthrich B, 2003, J INVEST ALLERG CLIN, V13, P145; Yuksel H, 1999, J INVEST ALLERG CLIN, V9, P305	87	180	195	0	4	BLACKWELL PUBLISHING	OXFORD	9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND	0105-4538			ALLERGY	Allergy	OCT	2006	61	10					1162	1172		10.1111/j.1395-9995.2006.01205.x		11	Allergy; Immunology	Allergy; Immunology	079WK	WOS:000240208400003	16942563	
J	Li, YF; Langholz, B; Salam, MT; Gilliland, FD				Li, YF; Langholz, B; Salam, MT; Gilliland, FD			Maternal and grandmaternal smoking patterns are associated with early childhood asthma	CHEST			English	Article						asthma; in utero exposure to maternal smoking; smoking cessation; transgenerational association	ENVIRONMENTAL TOBACCO-SMOKE; SOUTHERN CALIFORNIA COMMUNITIES; PARENTAL SMOKING; ALLERGIC RHINOCONJUNCTIVITIS; RESPIRATORY-FUNCTION; DIFFERING LEVELS; FAMILY-HISTORY; AIR-POLLUTION; ATOPIC ECZEMA; UNITED-STATES	Objective: To investigate the associations of maternal and grandmaternal smoking before, during, and after pregnancy with childhood asthma. Design, setting, and participants: We conducted a case-control study nested within the Children's Health Study in southern California. The case patients consisted of 338 children with asthma that had been diagnosed in the first 5 years of life, and 570 control subjects were countermatched on in utero exposure to maternal smoking within grade, sex, and community of residence. Measurements: Detailed maternal and household smoking histories and other asthma risk factor information was obtained by telephone interview. Results: The participation rates were 72.3% and S2.5%, respectively, for control subjects and case patients. In utero exposure to maternal smoking was associated with increased risk for asthma diagnosed in the first 5 years of life (odds ratio [OR], 1.5; 95% confidence interval [CI] 1.0 to 2.3), and for persistent asthma (OR, 1.5; 95% CI, 1.0 to 2.3). The associations did not differ in children with early transient asthma compared to those with early persistent asthma. Relative to never-smokers, children whose mothers smoked throughout the pregnancy had an elevated risk of asthma in the first 5 years of life (OR, 1.6; 95% CI, 1.0 to 2.6). Children of mothers who quit smoking prior to the pregnancy showed no increased risk (OR, 0.9; 95% CI, 0.5 to 1.5). We were unable to assess the association of smoking cessation during pregnancy because very few mothers were reported to have done so (15%). Asthma risk did not increase in a monotonic pattern with smoking intensity during pregnancy. Postnatal secondhand smoke exposure was not independently associated with asthma. Grandmaternal smoking during the mother's fetal period was associated with increased asthma risk in her grandchildren (OR, 2.1; 95% CI, 1.4 to 3.2). Conclusions: Maternal and grandmaternal smoking during pregnancy may increase the risk of childhood asthma.	Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA	Gilliland, FD (reprint author), Univ So Calif, Keck Sch Med, Dept Prevent Med, 1540 Alcazar St,CHP 236, Los Angeles, CA 90033 USA.	gillilan@usc.edu	LI, YU-FEN/F-4770-2010		NHLBI NIH HHS [1R01HL61768]; NIEHS NIH HHS [1P01 ES09581, 5P30 ES07048]		*AM LUNG ASS, 2003, TRENDS ASTHM MORB MO; Ansel KM, 2003, NAT IMMUNOL, V4, P616, DOI 10.1038/ni0703-616; Asher MI, 1998, EUR RESPIR J, V12, P315; Asher MI, 2001, NEW ZEAL MED J, V114, P114; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; BOTTO F, 1994, BIOCHEM BIOPH RES CO, V205, P1086, DOI 10.1006/bbrc.1994.2777; Bousquet J, 2004, ALLERGY, V59, P138, DOI 10.1046/j.1398-9995.2003.00359.x; *CDHS TOB CONTR SE, 2000, AD SMOK TRENDS CAL; CHEN Y, 1994, AM J RESP CRIT CARE, V150, P54; Cook DG, 1999, THORAX, V54, P357; Cook DG, 1998, THORAX, V53, P884; Csonka P, 2000, PEDIATR ALLERGY IMMU, V11, P225, DOI 10.1034/j.1399-3038.2000.00088.x; Cunningham J, 1996, AM J RESP CRIT CARE, V153, P218; Ebrahim SH, 2000, JAMA-J AM MED ASSOC, V283, P361, DOI 10.1001/jama.283.3.361; Ehrlich RI, 1996, AM J RESP CRIT CARE, V154, P681; Finette BA, 1998, NAT MED, V4, P1144, DOI 10.1038/2640; Floreani A A, 1999, Curr Opin Pulm Med, V5, P38, DOI 10.1097/00063198-199901000-00007; 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; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; Gold DR, 2000, ENVIRON HEALTH PERSP, V108, P643, DOI 10.2307/3454400; HANRAHAN JP, 1998, EUR RESP J S, V27; Hu FB, 1997, ANN ALLERG ASTHMA IM, V79, P80; Huberman M, 1999, AM J EPIDEMIOL, V150, P1340; Landau L I, 2001, Paediatr Respir Rev, V2, P202, DOI 10.1053/prrv.2001.0141; LANGHOLZ B, 1995, BIOMETRIKA, V82, P69; Langholz B., 2001, BIOSTATISTICS, V2, P63, DOI 10.1093/biostatistics/2.1.63; Lannero E, 2002, PEDIATR ALLERGY IMMU, V13, P182, DOI 10.1034/j.1399-3038.2002.01055.x; London SJ, 2001, EPIDEMIOLOGY, V12, P577, DOI 10.1097/00001648-200109000-00019; Lux AL, 2000, ARCH DIS CHILD, V83, P307, DOI 10.1136/adc.83.4.307; Mallol J, 2000, PEDIATR PULM, V30, P439, DOI 10.1002/1099-0496(200012)30:6<439::AID-PPUL1>3.0.CO;2-E; Peters JM, 1999, AM J RESP CRIT CARE, V159, P760; Peters JM, 1999, AM J RESP CRIT CARE, V159, P768; Pierce JP, 2001, TOB CONTROL, V10, P145, DOI 10.1136/tc.10.2.145; Pluth JM, 2000, MUTAT RES-GEN TOX EN, V465, P101, DOI 10.1016/S1383-5718(99)00217-X; Redd SC, 2002, ENVIRON HEALTH PERSP, V110, P557; Sole D, 2001, J INVEST ALLERG CLIN, V11, P123; Stein RT, 1999, AM J EPIDEMIOL, V149, P1030; Stick SM, 1996, LANCET, V348, P1060, DOI 10.1016/S0140-6736(96)04446-7; STORB U, 1983, P NATL ACAD SCI-BIOL, V80, P6642, DOI 10.1073/pnas.80.21.6642; Strachan DP, 1998, THORAX, V53, P204; U.S. Environmental Protection Agency, 1992, EPA600690006F; von Mutius E, 2002, J ALLERGY CLIN IMMUN, V109, pS525, DOI 10.1067/mai.2002.124565; Young S, 2000, PEDIATR PULM, V29, P331, DOI 10.1002/(SICI)1099-0496(200005)29:5<331::AID-PPUL1>3.0.CO;2-A	44	180	181	0	11	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	APR	2005	127	4					1232	1241		10.1378/chest.127.4.1232		10	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	915ZG	WOS:000228349900029	15821200	
J	Brunekreef, B; Smit, J; de Jongste, J; Neijens, H; Gerritsen, J; Postma, D; Aalberse, R; Koopman, L; Kerkhof, M; Wijga, A; van Strien, R				Brunekreef, B; Smit, J; de Jongste, J; Neijens, H; Gerritsen, J; Postma, D; Aalberse, R; Koopman, L; Kerkhof, M; Wijga, A; van Strien, R			The Prevention and Incidence of Asthma and Mite Allergy (PIAMA) birth cohort study: Design and first results	PEDIATRIC ALLERGY AND IMMUNOLOGY			English	Article; Proceedings Paper	Congress of the European-Academy-of-Allergy-and-Clinical-Immunology	JUN, 2001	BERLIN, GERMANY	European Acad Allergy & Clin Immunol		allergy; asthma; intervention; natural history; dust mites	HOUSE-DUST MITE; SENSITIZATION; EXPOSURE; CHILDREN; ENVIRONMENT; AVOIDANCE; CHILDHOOD; INFANCY; LIFE; RISK	The Prevention and Incidence of Asthma and Mite Allergy (PIAMA) birth cohort study was initiated in 1996. Children born to allergic mothers were enrolled in a double-blind placebo-controlled trial for evaluating the use of mite-impermeable mattress and pillow covers. Children born to allergic and non-allergic mothers were enrolled in a 'natural history' study to assess the role of environmental and dietary risk factors for the development of allergic disease in childhood. Recruitment started by distributing a validated screening questionnaire among >10,000 pregnant women during their first visit to a prenatal health clinic. Allergic mothers-to-be were invited to participate in the intervention study. Allergic, and a random sample of non-allergic, mothers-to-be were invited to participate in the 'natural history' arm of the study. In the intervention study, homes were visited before birth, 3 months after birth, and 12 months after birth for the collection of dust samples from floors and mattresses. In addition, the homes of about one-third of the children in the 'natural history' part of the study were visited for dust collection when the children were 3 months of age. The intervention study started with 855 participants and the 'natural history' study with 3,291 participants. Follow-up at 3 years of age has now been completed with satisfactory compliance (>90%,). A medical investigation and home visit at 4 years of age are nearing completion. Preliminary results show that mite-allergen levels were lower than found in previous Dutch studies, and that the intervention measure had a significant effect on mite-allergen levels, without important clinical benefits up to age 2 years old. The allergic families lived in homes with fewer 'triggers' such as pets, smoking and carpets than the non-allergic families, regardless of the intervention. The ongoing PIAMA cohort study will probably reveal useful information concerning effects of allergen load and reduction in the setting of a relatively low mite-allergen exposure, as well as other variables on the development of allergic manifestions and asthma.	Univ Utrecht, Inst Risk Assessment Sci, NL-3508 TD Utrecht, Netherlands; Natl Inst Publ Hlth & Environm, NL-3720 BA Bilthoven, Netherlands; Erasmus Univ, Med Ctr, Sophia Childrens Hosp, Dept Paediat, Rotterdam, Netherlands; Univ Groningen, Univ Groningen Hosp, Dept Paediat Resp Med, Groningen, Netherlands; Univ Groningen Hosp, Dept Pulmonol, Groningen, Netherlands; Univ Groningen, Univ Groningen Hosp, Dept Epidemiol & Stat, Groningen, Netherlands; Netherlands Red Cross, Blood Transfus Serv, Cent Lab, Amsterdam, Netherlands	Brunekreef, B (reprint author), Univ Utrecht, Inst Risk Assessment Sci, POB 80176, NL-3508 TD Utrecht, Netherlands.	b.brunekreef@iras.uu.nl	Kerkhof, Marjan/A-8846-2008	brunekreef, bert/0000-0001-9908-0060			ARSHAD SH, 1992, LANCET, V339, P1493, DOI 10.1016/0140-6736(92)91260-F; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Custovic A, 2000, J ALLERGY CLIN IMMUN, V105, P252, DOI 10.1016/S0091-6749(00)90073-3; Hide DW, 1996, ALLERGY, V51, P89, DOI 10.1111/j.1398-9995.1996.tb04563.x; Koopman LP, 2002, AM J RESP CRIT CARE, V166, P307, DOI 10.1164/rccm.2106026; Lakwijk N, 1998, CLIN EXP ALLERGY, V28, P454; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; MUNIR AKM, 1995, ALLERGY, V50, P55, DOI 10.1111/j.1398-9995.1995.tb02483.x; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; van Strien R.T., 1994, CLIN EXP ALLERGY, V24, P843, DOI 10.1111/j.1365-2222.1994.tb01807.x; STRIEN RTV, 1995, CLIN EXP ALLERGY, V25, P1184, DOI 10.1111/j.1365-2222.1995.tb03042.x; TAUSSIG LM, 1989, AM J EPIDEMIOL, V129, P1219; van Strien RT, 2002, ENVIRON HEALTH PERSP, V110, pA693; van Moerbeke D, 1997, EUROPEAN ALLERGY WHI; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; Warner JA, 1996, PEDIATR ALLERGY IMMU, V7, P98, DOI 10.1111/j.1399-3038.1996.tb00406.x; Wijga A, 2001, CLIN EXP ALLERGY, V31, P576, DOI 10.1046/j.1365-2222.2001.01072.x	17	180	181	2	15	WILEY-BLACKWELL	HOBOKEN	111 RIVER ST, HOBOKEN 07030-5774, NJ USA	0905-6157	1399-3038		PEDIAT ALLERG IMM-UK	Pediatr. Allergy Immunol.		2002	13			15			55	60		10.1034/j.1399-3038.13.s.15.1.x		6	Allergy; Immunology; Pediatrics	Allergy; Immunology; Pediatrics	638KW	WOS:000180571000012	12688626	
J	Beasley, R; Crane, J; Lai, CKW; Pearce, N				Beasley, R; Crane, J; Lai, CKW; Pearce, N			Prevalence and etiology of asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; prevalence; atopic disorders; ISAAC; etiology	RESPIRATORY-HEALTH-SURVEY; CHILDHOOD ASTHMA; INCREASING PREVALENCE; WRITTEN QUESTIONNAIRE; VIDEO QUESTIONNAIRE; CHANGING PREVALENCE; RISK FACTOR; NEW-ZEALAND; CHILDREN; ATOPY	An increased understanding of the causes of asthma is coming from the international comparisons of asthma prevalence particularly those from the European Community Respiratory Health Survey of asthma prevalence in adults and the International Study of Asthma and Allergies in Childhood. From these and other studies of asthma prevalence, it is possible to draw some tentative conclusions as to the patterns of asthma prevalence worldwide, There are five striking patterns: first, asthma prevalence is increasing worldwide; second, asthma is generally more common in Western countries and less common in developing countries; third, asthma is more prevalent in English-speaking countries; fourth, asthma prevalence is increasing in developing countries as they become more Westernized or communities become urbanized: and fifth, the prevalence of other allergic disorders may also be increasing worldwide. These five key features of the international patterns of asthma prevalence raise major questions about the role of "established" risk factors for the development of asthma, As a result, recent research has expanded to include the study of novel factors that may "program" the initial susceptibility to sensitization or contribute to the development of asthma independent of atopic sensitization. These include various exposures in utero, which are reflected in various perinatal factors measured at birth, and exposures (or lack of exposures) in the early years of life that may make the infant more susceptible to the subsequent development of asthma, These issues are now the focus of an intensive research effort worldwide, and the next few gears are likely to see exciting advances in our understanding of the causes of asthma.	Wellington Sch Med, Dept Med, Wellington Asthma Res Grp, Wellington S, New Zealand; Chinese Univ Hong Kong, Dept Med, Shatin, Hong Kong, Peoples R China	Beasley, R (reprint author), Wellington Sch Med, Dept Med, Wellington Asthma Res Grp, POB 7343, Wellington S, New Zealand.						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Allergy Clin. Immunol.	FEB	2000	105	2	2	S			S466	S472		10.1016/S0091-6749(00)90044-7		7	Allergy; Immunology	Allergy; Immunology	286JG	WOS:000085439600002	10669525	
J	Tarlo, SM; Balmes, J; Balkissoon, R; Beach, J; Beckett, W; Bernstein, D; Blanc, PD; Brooks, SM; Cowl, CT; Daroowalla, F; Harber, P; Lemiere, C; Liss, GM; Pacheco, KA; Redlich, CA; Rowe, B; Heitzer, J				Tarlo, Susan M.; Balmes, John; Balkissoon, Ronald; Beach, Jeremy; Beckett, William; Bernstein, David; Blanc, Paul D.; Brooks, Stuart M.; Cowl, Clayton T.; Daroowalla, Feroza; Harber, Philip; Lemiere, Catherine; Liss, Gary M.; Pacheco, Karin A.; Redlich, Carrie A.; Rowe, Brian; Heitzer, Julia			Diagnosis and management of work-related asthma: American College of Chest Physicians Consensus Statement	CHEST			English	Review						asthma; occupational lung; preventive medicine	EXHALED NITRIC-OXIDE; PEAK EXPIRATORY FLOW; NATURAL-RUBBER LATEX; HEALTH-CARE WORKERS; INDUCED OCCUPATIONAL ASTHMA; DIISOCYANATE-INDUCED ASTHMA; IRRITANT-INDUCED ASTHMA; VOCAL CORD DYSFUNCTION; RED CEDAR ASTHMA; NONSPECIFIC BRONCHIAL HYPERRESPONSIVENESS	Background: A previous American College of Chest Physicians Consensus Statement on asthma in the workplace was published in 1995. The current Consensus Statement updates the previous one based on additional research that has been published since then, including findings relevant to preventive measures and work-exacerbated asthma (WEA). Methods: A panel of experts, including allergists, pulmonologists, and occupational medicine physicians, was convened to develop this Consensus Document on the diagnosis and management of work-related asthma (WRA), based in part on a systematic review, that was performed by the University of Alberta/Capital Health Evidence-Based Practice and was supplemented by additional published studies to 2007. Results: The Consensus Document defined WRA to include occupational asthma (ie, asthma induced by sensitizer or irritant work exposures) and WEA (ie, preexisting or concurrent asthma worsened by work factors). The Consensus Document focuses on the diagnosis and management of NIMA (including diagnostic tests, and work and compensation issues), as well as preventive measures. WRA should be considered in all individuals with new-onset or worsening asthma, and a careful occupational history should be obtained. Diagnostic tests such as serial peak flow recordings, methacholine challenge tests, immunologic tests, and specific inhalation challenge tests, (if available), can increase diagnostic certainty. Since the prognosis is better with early diagnosis and appropriate intervention, effective preventive measures for other workers with exposure should be addressed. Conclusions: The substantial prevalence of WRA supports consideration of the diagnosis in all who present with new-onset or worsening asthma, followed by appropriate investigations and intervention including consideration of other exposed workers.	[Balmes, John; Blanc, Paul D.] Univ Calif San Francisco, San Francisco, CA 94143 USA; [Balkissoon, Ronald; Pacheco, Karin A.] Natl Jewish Med & Res Ctr, Denver, CO USA; [Beach, Jeremy; Rowe, Brian] Univ Alberta, Calgary, AB, Canada; [Beckett, William] Univ Rochester, Sch Med & Dent, Rochester, NY USA; [Bernstein, David] Univ Cincinnati, Cincinnati, OH USA; [Brooks, Stuart M.] Univ S Florida, Tampa, FL USA; [Cowl, Clayton T.] Mayo Clin, Rochester, MN USA; [Daroowalla, Feroza] SUNY Stony Brook, Stony Brook, NY 11794 USA; [Harber, Philip] Univ Calif Los Angeles, Los Angeles, CA USA; [Lemiere, Catherine] Univ Montreal, Montreal, PQ, Canada; [Redlich, Carrie A.] Yale Univ, Sch Med, New Haven, CT USA; [Heitzer, Julia] Amer Coll Chest Phys, Northbrook, IL USA; [Tarlo, Susan M.; Liss, Gary M.] Univ Toronto, Toronto, ON, Canada	Tarlo, SM (reprint author), Toronto Western Hosp, EW7-449,399 Bathurst St, Toronto, ON M5T 2S8, Canada.	susan.tarlo@utoronto.ca					Adisesh LA, 1998, CLIN EXP ALLERGY, V28, P876; Allmers H, 2000, INT ARCH OCC ENV HEA, V73, P181, DOI 10.1007/s004200050025; Allmers H, 2002, J ALLERGY CLIN IMMUN, V110, P318, DOI 10.1067/mai.2002.126461; Allmers H, 1996, DEUT MED WOCHENSCHR, V121, P823, DOI 10.1055/s-2008-1043073; Alvarez MJ, 2001, ALLERGY, V56, P185, DOI 10.1034/j.1398-9995.2001.056002185.x; ALVING K, 1993, EUR RESPIR J, V6, P1368; American Thoracic Society, 2005, AM J RESP CRIT CARE, V171, P912, DOI DOI 10.1164/RCCM.200406-710ST; American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; Ameille J, 2005, CURR OPIN ALLERGY CL, V5, P125, DOI 10.1097/01.all.0000162303.59363.b4; Ameille J, 1997, EUR RESPIR J, V10, P55, DOI 10.1183/09031936.97.10010055; ANDERTON RC, 1979, J ALLERGY CLIN IMMUN, V63, P315, DOI 10.1016/0091-6749(79)90125-8; Andreoli R, 2003, RAPID COMMUN MASS SP, V17, P637, DOI 10.1002/rcm.960; Andrianopoulos MV, 2000, J VOICE, V14, P607, DOI 10.1016/S0892-1997(00)80016-8; Anees W, 2006, THORAX, V61, P751, DOI 10.1136/thx.2005.054080; Anees W, 2002, THORAX, V57, P231, DOI 10.1136/thorax.57.3.231; Antczak Adam, 2002, Int J Occup Med Environ Health, V15, P317; ARMENTIA A, 1992, ANN ALLERGY, V69, P441; ARMENTIA A, 1990, ANN ALLERGY, V65, P265; Bachert C, 2006, CURR OPIN ALLERGY CL, V6, P29, DOI 10.1097/01.all.0000200504.54425.0e; Bagnato GF, 2000, RESPIRATION, V67, P507, DOI 10.1159/000067464; Bahima AC, 2004, J INVEST ALLERG CLIN, V14, P17; Baldwin DR, 2002, THORAX, V57, P860, DOI 10.1136/thorax.57.10.860; Balmes J, 2003, AM J RESP CRIT CARE, V167, P787, DOI 10.1164/rccm.167.5.787; BALMES JR, 1991, OCCUP MED, V6, P101; Banks Daniel E, 2003, Curr Opin Allergy Clin Immunol, V3, P101, DOI 10.1097/00130832-200304000-00003; BANKS DE, 1990, CHEST, V97, P121, DOI 10.1378/chest.97.1.121; BANKS DE, 1986, CHEST, V89, P389, DOI 10.1378/chest.89.3.389; Banks DE, 1996, CHEST, V109, P1370, DOI 10.1378/chest.109.5.1370; Barbinova L, 2006, INT ARCH OCC ENV HEA, V79, P387, DOI 10.1007/s00420-005-0051-x; Bateman ED, 2008, EUR RESPIR J, V31, P143, DOI 10.1183/09031936.00138707; BAUR X, 1995, J ALLERGY CLIN IMMUN, V96, P489, DOI 10.1016/S0091-6749(95)70292-X; Baur X, 2005, INT ARCH OCC ENV HEA, V78, P593, DOI 10.1007/s00420-005-0613-y; Baur X, 2005, EUR RESPIR J, V25, P309, DOI 10.1183/09031936.05.00021504; Baur X, 2003, ANN ALLERG ASTHMA IM, V90, P11; BEACH J, 2005, PUBLICATION AGENCY H; Beach J, 2007, CHEST, V131, P569, DOI 10.1378/chest.06-0492; Bello D, 2007, ENVIRON HEALTH PERSP, V115, P328, DOI 10.1289/ehp.9557; Bernstein DI, 2002, AM J RESP CRIT CARE, V166, P445, DOI 10.1164/rccm.2109018; Bernstein DI, 2003, J ALLERGY CLIN IMMUN, V111, P610, DOI 10.1067/mai.2003.164; Bernstein I. 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J	Pichavant, M; Goya, S; Meyer, EH; Johnston, RA; Kim, HY; Matangkasombut, P; Zhu, M; Iwakura, Y; Savage, PB; DeKruyff, RH; Shore, SA; Umetsu, DT				Pichavant, Muriel; Goya, Sho; Meyer, Everett H.; Johnston, Richard A.; Kim, Hye Y.; Matangkasombut, Ponpan; Zhu, Ming; Iwakura, Yoichiro; Savage, Paul B.; DeKruyff, Rosemarie H.; Shore, Stephanie A.; Umetsu, Dale T.			Ozone exposure in a mouse model induces airway hyperreactivity that requires the presence of natural killer T cells and IL-17	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article							NKT CELLS; EPITHELIAL-CELLS; ASTHMATIC-PATIENTS; BRONCHIAL-ASTHMA; ALLERGIC-ASTHMA; INFLAMMATION; MICE; HYPERRESPONSIVENESS; LUNG; RESPONSES	Exposure to ozone, which is a major component of air pollution, induces a form of asthma that occurs in the absence of adaptive immunity. Although ozone-induced asthma is characterized by airway neutrophilia, and not eosinophilia, it is nevertheless associated with airway hyperreactivity (AHR), which is a cardinal feature of asthma. Because AHR induced by allergens requires the presence of natural killer T (NKT) cells, we asked whether ozone-induced AHR had similar requirements. We found that repeated exposure of wild-type (WT) mice to ozone induced severe AHR associated with an increase in airway NKT cells, neutrophils, and macrophages. Surprisingly, NKT cell-deficient (CD1d(-/-) and J alpha 18(-/-)) mice failed to develop ozone-induced AHR. Further, treatment of WT mice with an anti-CD1d mAb blocked NKT cell activation and prevented ozone-induced AHR. Moreover, ozone-induced, but not allergen-induced, AHR was associated with NKT cells producing interleukin (IL)-17, and failed to occur in IL-17(-/-) mice nor in WT mice treated with anti-IL-17 mAb. Thus, ozone exposure induces AHR that requires the presence of NKT cells and IL-17 production. Because NKT cells are required for the development of two very disparate forms of AHR (ozone- and allergen-induced), our results strongly suggest that NKT cells mediate a unifying pathogenic mechanism for several distinct forms of asthma, and represent a unique target for effective asthma therapy.	[Pichavant, Muriel; Goya, Sho; Meyer, Everett H.; Kim, Hye Y.; Matangkasombut, Ponpan; DeKruyff, Rosemarie H.; Umetsu, Dale T.] Harvard Univ, Sch Med, Childrens Hosp Boston, Boston, MA 02115 USA; [Johnston, Richard A.; Zhu, Ming; Shore, Stephanie A.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA; [Iwakura, Yoichiro] Univ Tokyo, Ctr Med Expt, Inst Med Sci, Minato Ku, Tokyo 1088639, Japan; [Savage, Paul B.] Brigham Young Univ, Provo, UT 84604 USA; [Meyer, Everett H.] Stanford Univ, Stanford Immunol Program, Stanford, CA 94305 USA	Umetsu, DT (reprint author), Harvard Univ, Sch Med, Childrens Hosp Boston, Boston, MA 02115 USA.	dale.umetsu@childrens.harvard.edu	Iwakura, Yoichiro/E-5457-2011	Iwakura, Yoichiro/0000-0002-9934-5775	NHLBI NIH HHS [HL062348, R01 HL062348]; NIAID NIH HHS [AI054456, P01 AI054456, T32 AI007290]		Akbari O, 2006, NEW ENGL J MED, V354, P1117, DOI 10.1056/NEJMoa053614; Akbari O, 2003, NAT MED, V9, P582, DOI 10.1038/nm851; ARIS RM, 1993, AM REV RESPIR DIS, V148, P1363; Babin SM, 2007, ENVIRON HEALTH-UK, V6, DOI 10.1186/1476-096X-6-9; Bayram H, 2001, J ALLERGY CLIN IMMUN, V107, P287, DOI 10.1067/mai.2001.111141; Behar SM, 1999, J EXP MED, V189, P1973, DOI 10.1084/jem.189.12.1973; Bendelac A, 2007, ANNU REV IMMUNOL, V25, P297, DOI 10.1146/annurev.immunol.25.022106.141711; Brutkiewicz RR, 2006, J IMMUNOL, V177, P769; Bullens DMA, 2006, RESP RES, V7, DOI 10.1186/1465-9921-7-135; Cho HY, 2001, AM J PHYSIOL-LUNG C, V280, pL537; Cui JQ, 1997, SCIENCE, V278, P1623, DOI 10.1126/science.278.5343.1623; D'Amato G, 2005, CLIN EXP ALLERGY, V35, P1113, DOI 10.1111/j.1365-2222.2005.02328.x; DEVLIN RB, 1991, AM J RESP CELL MOL, V4, P72; Ferretti S, 2003, J IMMUNOL, V170, P2106; Gent JF, 2003, JAMA-J AM MED ASSOC, V290, P1859, DOI 10.1001/jama.290.14.1859; Gibson PG, 2001, CHEST, V119, P1329, DOI 10.1378/chest.119.5.1329; Gold DR, 2005, ANNU REV PUBL HEALTH, V26, P89, DOI 10.1146/annurev.publhealth.26.021304.144528; Hamzaoui A, 2006, MEDIAT INFLAMM, DOI 10.1155/MI/2006/71214; Hellings PW, 2003, AM J RESP CELL MOL, V28, P42, DOI 10.1165/rcmb.4832; Ivanov II, 2006, CELL, V126, P1121, DOI 10.1016/j.cell.2006.07.035; Johnston RA, 2005, AM J PHYSIOL-LUNG C, V288, pL390, DOI 10.1152/ajplung.00007.2004; Kawaguchi M, 2006, J ALLERGY CLIN IMMUN, V117, P795, DOI 10.1016/j.jaci.2005.12.1346; Kronenberg M, 2002, NAT REV IMMUNOL, V2, P557, DOI 10.1038/nri854; Kronenberg M, 2005, ANNU REV IMMUNOL, V23, P877, DOI 10.1146/annurev.immunol.23.021704.115742; Li N, 2004, J IMMUNOL, V173, P3467; Linden A, 2005, EUR RESPIR J, V25, P159, DOI 10.1183/09031936.04.00032904; Lisbonne M, 2003, J IMMUNOL, V171, P1637; Lu FL, 2006, AM J PHYSIOL-LUNG C, V290, pL856, DOI 10.1152/ajplung.00386.2005; Mercer JC, 2005, INT J BIOCHEM CELL B, V37, P1337, DOI 10.1016/j.biocel.2004.11.019; Meyer EH, 2006, P NATL ACAD SCI USA, V103, P2782, DOI 10.1073/pnas.0510282103; Michel ML, 2007, J EXP MED, V204, P995, DOI 10.1084/jem.20061551; Miyamoto M, 2003, J IMMUNOL, V170, P4665; Molet S, 2001, J ALLERGY CLIN IMMUN, V108, P430, DOI 10.1067/mai.2001.117929; Nakae S, 2002, IMMUNITY, V17, P375, DOI 10.1016/S1074-7613(02)00391-6; Nel A, 2005, SCIENCE, V308, P804, DOI 10.1126/science.1108752; Nieuwenhuis EES, 2002, NAT MED, V8, P588, DOI 10.1038/nm0602-588; Park JW, 2004, AM J RESP CELL MOL, V30, P830, DOI 10.1165/rcmb.2003.0373OC; Park SH, 2000, EUR J IMMUNOL, V30, P620, DOI 10.1002/1521-4141(200002)30:2<620::AID-IMMU620>3.0.CO;2-4; Rangasamy T, 2005, J EXP MED, V202, P47, DOI 10.1084/jem.20050538; Romieu I, 2006, EUR RESPIR J, V28, P953, DOI 10.1183/09031936.06.00114905; Ronmark E, 2005, EUR RESPIR J, V25, P282, DOI 10.1183/09031936.05.00054304; Schnyder-Candrian S, 2006, J EXP MED, V203, P2715, DOI 10.1084/jem.20061401; Sen Yang, 2005, J Immunol, V175, P4914; Shore SA, 2002, J APPL PHYSIOL, V92, P1019, DOI 10.1152/japplphysiol.00381.2001; Shore SA, 2001, AM J RESP CRIT CARE, V164, P602; Smiley ST, 1997, SCIENCE, V275, P977, DOI 10.1126/science.275.5302.977; Todokoro M, 2004, INFLAMMATION, V28, P105, DOI 10.1023/B:IFLA.0000033026.91221.ed; Tolbert PE, 2000, AM J EPIDEMIOL, V151, P798; VanderLaan PA, 2007, AM J PATHOL, V170, P1100, DOI 10.2353/ajpath.2007.060188; Voehringer D, 2006, J EXP MED, V203, P1435, DOI 10.1084/jem.20052448; Wills-Karp M, 1999, ANNU REV IMMUNOL, V17, P255, DOI 10.1146/annurev.immunol.17.1.255; Yu M, 2002, TOXICOL SCI, V68, P488, DOI 10.1093/toxsci/68.2.488	52	179	192	0	6	ROCKEFELLER UNIV PRESS	NEW YORK	1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA	0022-1007			J EXP MED	J. Exp. Med.	FEB 18	2008	205	2					385	393		10.1084/jem.20071507		9	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	263XR	WOS:000253250300016	18250191	
J	Van dn Berge, M; Meijer, RJ; Kerstjens, HAM; de Reus, DM; Koeter, GH; Kauffman, HF; Postma, DS				Van dn Berge, M; Meijer, RJ; Kerstjens, HAM; de Reus, DM; Koeter, GH; Kauffman, HF; Postma, DS			PC20 adenosine 5 '-monophosphate is more closely associated with airway inflammation in asthma than PC20 methacholine	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							EXHALED NITRIC-OXIDE; BRONCHIAL HYPERRESPONSIVENESS; ALLERGIC RHINITIS; INDUCED BRONCHOCONSTRICTION; SPUTUM EOSINOPHILS; SMOOTH-MUSCLE; DISEASE; BLOOD; RESPONSIVENESS; HYPERREACTIVITY	Inhalation of a direct stimulus such as histamine or methacholine is generally used to measure bronchial hyperresponsiveness (BHR). Provocation with adenosine 5'-monophosphate (AMP), an indirect airway challenge, has been suggested to be a better marker of airway inflammation than direct challenges. However, so far little information on this subject is available. The aim of our study was to assess whether the concentration of AMP causing the FEV1 to drop by 20% (PC20) is more closely associated with inflammatory parameters in asthma than PC20 methacholine. In 120 patients with atopic asthma (median FEV1 81% predicted [pred], median age 27 yr), PC20 methacholine and PC20 AMP as well as sputum induction, blood sampling, and measurement of nitric oxide in exhaled air were performed. PC20 methacholine was predominantly predicted by FEV1 %pred (explained variance [ev] = 18%) with the percentage of peripheral blood monocytes being a weak additional independent predictor (total ev = 23%). By contrast, PC20 AMP was predominantly predicted by the percentage of eosinophils in sputum (ev = 25%), while FEV1 %pred was only an additional independent predictor (total ev = 36%). PC20 AMP reflects more closely the extent of airway inflammation due to asthma than PC20 methacholine.	Univ Groningen Hosp, Dept Pulmonol, Groningen, Netherlands; Univ Groningen Hosp, Dept Allergol, Groningen, Netherlands	Postma, DS (reprint author), Univ Groningen Hosp, Dept Pulm Dis, Hanzepl 1, NL-9700 RB Groningen, Netherlands.						Alvarez MJ, 2000, ALLERGY, V55, P355, DOI 10.1034/j.1398-9995.2000.00312.x; ALVING K, 1993, EUR RESPIR J, V6, P1368; Benckhuijsen J, 1996, PEDIATR PULM, V22, P147, DOI 10.1002/(SICI)1099-0496(199609)22:3<147::AID-PPUL2>3.0.CO;2-M; BRAND PLP, 1991, AM REV RESPIR DIS, V143, P916; COCKCROFT DW, 1977, CLIN ALLERGY, V7, P503, DOI 10.1111/j.1365-2222.1977.tb01481.x; CRIMI N, 1992, EUR RESPIR J, V5, P560; DAHL R, 1993, ALLERGY, V48, P77, DOI 10.1111/j.1398-9995.1993.tb04704.x; DURHAM SR, 1985, CLIN ALLERGY, V15, P411, DOI 10.1111/j.1365-2222.1985.tb02290.x; FAHY JV, 1993, AM REV RESPIR DIS, V147, P1126; FINNEY MJB, 1985, BRIT J PHARMACOL, V85, P29; FRETTE C, 1991, AM REV RESPIR DIS, V143, P987; Grunberg K, 1997, AM J RESP CRIT CARE, V156, P609; Ichinose M, 2000, EUR RESPIR J, V15, P248, DOI 10.1034/j.1399-3003.2000.15b05.x; Jatakanon A, 2000, AM J RESP CRIT CARE, V161, P64; Jatakanon A, 1998, THORAX, V53, P91; KERSTJENS HAM, 1992, NEW ENGL J MED, V327, P1413, DOI 10.1056/NEJM199211123272003; KUWANO K, 1993, AM REV RESPIR DIS, V148, P1220; LAMBERT RK, 1993, J APPL PHYSIOL, V74, P2771; Lim S, 2000, THORAX, V55, P184, DOI 10.1136/thorax.55.3.184; Meijer RJ, 1999, THORAX, V54, P894; OCONNOR BJ, 1992, AM REV RESPIR DIS, V146, P560; PAUWELS RA, 1987, AM REV RESPIR DIS, V136, P374; PHILLIPS GD, 1987, THORAX, V42, P939, DOI 10.1136/thx.42.12.939; PHILLIPS GD, 1990, AM REV RESPIR DIS, V141, P9; Polosa R, 2000, EUR RESPIR J, V15, P30, DOI 10.1183/09031936.00.15103000; POLOSA R, 1995, AM J RESP CRIT CARE, V151, P624; Schmidt D, 2000, J ALLERGY CLIN IMMUN, V105, P673, DOI 10.1067/mai.2000.105705; Sont JK, 1999, AM J RESP CRIT CARE, V159, P1043; STERK PJ, 1989, EUR RESPIR J, V2, P267; TAYLOR KJ, 1987, THORAX, V42, P452, DOI 10.1136/thx.42.6.452; ULRIK CS, 1995, CLIN EXP ALLERGY, V25, P820, DOI 10.1111/j.1365-2222.1995.tb00024.x; Viksman MY, 1997, AM J RESP CRIT CARE, V155, P858; Weersink EJM, 1997, AM J RESP CRIT CARE, V155, P1241	33	179	181	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.	JUN	2001	163	7					1546	1550				5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	443JE	WOS:000169337400011	11401871	
J	Rogge, L; Bianchi, E; Biffi, M; Bono, E; Chang, SYP; Alexander, H; Santini, C; Ferrari, G; Sinigaglia, L; Seiler, M; Neeb, M; Mous, J; Sinigaglia, F; Certa, U				Rogge, L; Bianchi, E; Biffi, M; Bono, E; Chang, SYP; Alexander, H; Santini, C; Ferrari, G; Sinigaglia, L; Seiler, M; Neeb, M; Mous, J; Sinigaglia, F; Certa, U			Transcript imaging of the development of human T helper cells using oligonucleotide arrays	NATURE GENETICS			English	Article							REGULATORY FACTOR-I; SELECTIVE EXPRESSION; IMMUNE-RESPONSES; P-SELECTIN; INTERLEUKIN-12; T-HELPER-1; CYTOKINE; RECEPTOR; TYPE-1; LYMPHOCYTES	Many pathological processes, including those causing allergies and autoimmune diseases, are associated with the presence of specialized subsets of T helper cells at the site of inflammation(1) Understanding the genetic program that controls the functional properties of T helper type 1 (Th1) versus T helper type 2 (Th2) cells may provide insight into the pathophysiology of inflammatory diseases. We compared the gene-expression profiles of human Th1 and Th2 cells using high-density oligonucleotide arrays with the capacity to display transcript levels of 6,000 human genes'. Here we analyse the data sets derived from five independent experiments using statistical algorithms. This approach resulted in the identification of 215 differentially expressed genes, encoding proteins involved in transcriptional regulation, apoptosis, proteolysis, and cell adhesion and migration. A-subset of these genes was further upregulated by exposure of differentiated Th1 cells to interleukin-12 (IL-12), as confirmed by kinetic PCR analysis, indicating that IL-12 modulates the effector functions of Th1 cells in the absence of antigenic stimulation. Functional assays and in vivo expression of selected genes have validated the biological relevance of our study. Our results provide new insight into the transcriptional program controlling the functional diversity of subsets of T helper cells.	Roche Milano Ric, Milan, Italy; Ist Sci San Raffaele, DIBIT, Milan, Italy; Roche Mol Syst, Alameda, CA USA; TIGET HS Raffaele, Milan, Italy; Ist Ortoped Gaetano Pini, Chair Rheumatol, Milan, Italy; F Hoffmann La Roche & Co Ltd, PRPZB, CH-4002 Basel, Switzerland; F Hoffmann La Roche & Co Ltd, Roche Genet, CH-4002 Basel, Switzerland	Rogge, L (reprint author), Roche Milano Ric, Milan, Italy.				Telethon [TGT06S01]		Abbas AK, 1996, NATURE, V383, P787, DOI 10.1038/383787a0; Austrup F, 1997, NATURE, V385, P81, DOI 10.1038/385081a0; BERLIN C, 1993, CELL, V74, P185, DOI 10.1016/0092-8674(93)90305-A; Butcher EC, 1996, SCIENCE, V272, P60, DOI 10.1126/science.272.5258.60; Coccia EM, 1999, J BIOL CHEM, V274, P6698, DOI 10.1074/jbc.274.10.6698; Colantonio L, 1999, BLOOD, V94, P2981; Coligan J., 1991, CURRENT PROTOCOLS IM; Dolhain RJEM, 1996, ARTHRITIS RHEUM, V39, P1961, DOI 10.1002/art.1780391204; Eisen MB, 1998, P NATL ACAD SCI USA, V95, P14863, DOI 10.1073/pnas.95.25.14863; Fambrough D, 1999, CELL, V97, P727, DOI 10.1016/S0092-8674(00)80785-0; Gately MK, 1998, ANNU REV IMMUNOL, V16, P495, DOI 10.1146/annurev.immunol.16.1.495; HIGUCHI R, 1999, PCR APPL PROTOCOLS F, P263, DOI 10.1016/B978-012372185-3/50017-1; Lipshutz RJ, 1999, NAT GENET, V21, P20, DOI 10.1038/4447; Lockhart DJ, 1996, NAT BIOTECHNOL, V14, P1675, DOI 10.1038/nbt1296-1675; Lohoff M, 1997, IMMUNITY, V6, P681, DOI 10.1016/S1074-7613(00)80444-6; Maly P, 1996, CELL, V86, P643, DOI 10.1016/S0092-8674(00)80137-3; O'Garra A, 1998, IMMUNITY, V8, P275, DOI 10.1016/S1074-7613(00)80533-6; Rogge L, 1997, J EXP MED, V185, P825, DOI 10.1084/jem.185.5.825; Rogge L, 1998, J IMMUNOL, V161, P6567; ROMAGNANI S, 1994, ANNU REV IMMUNOL, V12, P227, DOI 10.1146/annurev.iy.12.040194.001303; Sallusto F, 1998, IMMUNOL TODAY, V19, P568, DOI 10.1016/S0167-5699(98)01346-2; SEDER RA, 1994, ANNU REV IMMUNOL, V12, P635, DOI 10.1146/annurev.immunol.12.1.635; SIMON AK, 1994, P NATL ACAD SCI USA, V91, P8562, DOI 10.1073/pnas.91.18.8562; Taki S, 1997, IMMUNITY, V6, P673, DOI 10.1016/S1074-7613(00)80443-4; TRINCHIERI G, 1995, ANNU REV IMMUNOL, V13, P251, DOI 10.1146/annurev.immunol.13.1.251; Van Damme J, 1999, Chem Immunol, V72, P42, DOI 10.1159/000058725; Verzeletti S, 1998, HUM GENE THER, V9, P2243, DOI 10.1089/hum.1998.9.15-2243; Xu DM, 1998, J EXP MED, V188, P1485, DOI 10.1084/jem.188.8.1485; Zheng WP, 1997, CELL, V89, P587, DOI 10.1016/S0092-8674(00)80240-8	29	179	187	0	4	NATURE AMERICA INC	NEW YORK	345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA	1061-4036			NAT GENET	Nature Genet.	MAY	2000	25	1					96	101		10.1038/75671		6	Genetics & Heredity	Genetics & Heredity	311KU	WOS:000086884000025	10802665	
J	Kouzaki, H; Iijima, K; Kobayashi, T; O'Grady, SM; Kita, H				Kouzaki, Hideaki; Iijima, Koji; Kobayashi, Takao; O'Grady, Scott M.; Kita, Hirohito			The Danger Signal, Extracellular ATP, Is a Sensor for an Airborne Allergen and Triggers IL-33 Release and Innate Th2-Type Responses	JOURNAL OF IMMUNOLOGY			English	Article							RECEPTOR ACCESSORY PROTEIN; MAST-CELLS; DENDRITIC CELLS; AIRWAY HYPERRESPONSIVENESS; INFLAMMATORY RESPONSE; ADAPTIVE IMMUNITY; TYPE-2 IMMUNITY; CYTOKINE IL-33; NK CELLS; IN-VIVO	The molecular mechanisms underlying the initiation of innate and adaptive proallergic Th2-type responses in the airways are not well understood. IL-33 is a new member of the IL-1 family of molecules that is implicated in Th2-type responses. Airway exposure of naive mice to a common environmental aeroallergen, the fungus Alternaria alternata, induces rapid release of IL-33 into the airway lumen, followed by innate Th2-type responses. Biologically active IL-33 is constitutively stored in the nuclei of human airway epithelial cells. Exposing these epithelial cells to A. alternata releases IL-33 extracellularly in vitro. Allergen exposure also induces acute extracellular accumulation of a danger signal, ATP; autocrine ATP sustains increases in intracellular Ca(2+) concentration and releases IL-33 through activation of P2 purinergic receptors. Pharmacological inhibitors of purinergic receptors or deficiency in the P2Y2 gene abrogate IL-33 release and Th2-type responses in the Alternaria-induced airway inflammation model in naive mice, emphasizing the essential roles for ATP and the P2Y2 receptor. Thus, ATP and purinergic signaling in the respiratory epithelium are critical sensors for airway exposure to airborne allergens, and they may provide novel opportunities to dampen the hypersensitivity response in Th2-type airway diseases such as asthma. The Journal of Immunology, 2011, 186: 4375-4387.	[Kita, Hirohito] Mayo Clin, Div Allerg Dis, Dept Immunol, Rochester, MN 55905 USA; [Kouzaki, Hideaki; Iijima, Koji; Kobayashi, Takao; Kita, Hirohito] Mayo Clin, Div Allerg Dis, Dept Internal Med, Rochester, MN 55905 USA; [Kouzaki, Hideaki] Shiga Univ Med Sci, Dept Otorhinolaryngol, Shiga 5250072, Japan; [O'Grady, Scott M.] Univ Minnesota, Dept Integrat Biol & Physiol, St Paul, MN 55108 USA; [O'Grady, Scott M.] Univ Minnesota, Dept Anim Sci, St Paul, MN 55108 USA	Kita, H (reprint author), Mayo Clin, Div Allerg Dis, Dept Immunol, 200 1st St SW, Rochester, MN 55905 USA.	kita.hirohito@mayo.edu			National Institutes of Health [AI34486, AI49235, DK074010, HL095811]; Mayo Foundation	This work was supported in part by National Institutes of Health Grants AI34486 and AI49235 (to H.K.) and DK074010 and HL095811 (to S.M.O.), as well as by the Mayo Foundation.	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Immunol.	APR 1	2011	186	7					4375	4387		10.4049/jimmunol.1003020		13	Immunology	Immunology	739WH	WOS:000288751200065	21357533	
J	Wright, RJ; Mitchell, H; Visness, CM; Cohen, S; Stout, J; Evans, R; Gold, DR				Wright, RJ; Mitchell, H; Visness, CM; Cohen, S; Stout, J; Evans, R; Gold, DR			Community violence and asthma morbidity: The inner-city asthma study	AMERICAN JOURNAL OF PUBLIC HEALTH			English	Article							POSTTRAUMATIC-STRESS-DISORDER; COCKROACH ALLERGEN; POLITICAL VIOLENCE; URBAN COMMUNITIES; AFRICAN-AMERICAN; LIFE EVENTS; CHILDREN; EXPOSURE; POPULATION; DISTRESS	Objectives. We examined the association between exposure to violence and asthma among urban children. Methods. We obtained reports from caretakers (n=851) of violence, negative life events, unwanted memories (rumination), caretaker-perceived stress, and caretaker behaviors (keeping children indoors, smoking, and medication adherence). Outcomes included caretaker-reported wheezing, sleep disruption, interference with play because of asthma, and effects on the caretaker (nights caretaker lost sleep because of child's asthma). Results. Increased exposure to violence predicted higher number of symptom days (P=.0008) and more nights that caretakers lost sleep (P=.02) in a graded fashion after control for socioeconomic status, housing deterioration, and negative life events. Control for stress and behaviors partially attenuated this gradient, although these variables had little effect on the association between the highest level of exposure to morbidity, which suggests there are other mechanisms. Conclusions. Mechanisms linking violence and asthma morbidity need to be further explored.	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J	Chafen, JJS; Newberry, SJ; Riedl, MA; Bravata, DM; Maglione, M; Suttorp, MJ; Sundaram, V; Paige, NM; Towfigh, A; Hulley, BJ; Shekelle, PG				Chafen, Jennifer J. Schneider; Newberry, Sydne J.; Riedl, Marc A.; Bravata, Dena M.; Maglione, Margaret; Suttorp, Marika J.; Sundaram, Vandana; Paige, Neil M.; Towfigh, Ali; Hulley, Benjamin J.; Shekelle, Paul G.			Diagnosing and Managing Common Food Allergies A Systematic Review	JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION			English	Review							COWS MILK ALLERGY; PLACEBO-CONTROLLED TRIAL; HIGH-RISK INFANTS; ATOPY PATCH TEST; BREAST-FED INFANTS; RANDOMIZED CONTROLLED-TRIAL; BRIEF NEONATAL EXPOSURE; DOUBLE-BLIND TRIAL; SKIN-PRICK TESTS; 1ST 2 YEARS	Context There is heightened interest in food allergies but no clear consensus exists regarding the prevalence or most effective diagnostic and management approaches to food allergies. Objective To perform a systematic review of the available evidence on the prevalence, diagnosis, management, and prevention of food allergies. Data Sources Electronic searches of PubMed, Cochrane Database of Systematic Reviews, Cochrane Database of Abstracts of Reviews of Effects, and Cochrane Central Register of Controlled Trials. Searches were limited to English-language articles indexed between January 1988 and September 2009. Study Selection Diagnostic tests were included if they had a prospective, defined study population, used food challenge as a criterion standard, and reported sufficient data to calculate sensitivity and specificity. Systematic reviews and randomized controlled trials (RCTs) for management and prevention outcomes were also used. For foods where anaphylaxis is common, cohort studies with a sample size of more than 100 participants were included. Data Extraction Two investigators independently reviewed all titles and abstracts to identify potentially relevant articles and resolved discrepancies by repeated review and discussion. Quality of systematic reviews and meta-analyses was assessed using the AMSTAR criteria, the quality of diagnostic studies using the QUADAS criteria most relevant to food allergy, and the quality of RCTs using the Jadad criteria. Data Synthesis A total of 12 378 citations were identified and 72 citations were included. Food allergy affects more than 1% to 2% but less than 10% of the population. It is unclear if the prevalence of food allergies is increasing. Summary receiver operating characteristic curves comparing skin prick tests (area under the curve [AUC], 0.87; 95% confidence interval [CI], 0.81-0.93) and serum food-specific IgE (AUC, 0.84; 95% CI, 0.78-0.91) to food challenge showed no statistical superiority for either test. Elimination diets are the mainstay of therapy but have been rarely studied. Immunotherapy is promising but data are insufficient to recommend use. In high-risk infants, hydrolyzed formulas may prevent cow's milk allergy but standardized definitions of high risk and hydrolyzed formula do not exist. Conclusion The evidence for the prevalence and management of food allergy is greatly limited by a lack of uniformity for criteria for making a diagnosis. JAMA. 2010; 303(18): 1848-1856	[Chafen, Jennifer J. Schneider; Bravata, Dena M.; Sundaram, Vandana] Stanford Univ, Sch Med, Ctr Primary Care & Outcomes Res, Stanford, CA 94305 USA; [Chafen, Jennifer J. Schneider; Sundaram, Vandana] VA Palo Alto Healthcare Syst, Palo Alto, CA USA; [Newberry, Sydne J.; Maglione, Margaret; Suttorp, Marika J.; Paige, Neil M.; Towfigh, Ali; Hulley, Benjamin J.; Shekelle, Paul G.] Rand Hlth, So Calif Evidence Based Practice Ctr, Santa Monica, CA USA; [Riedl, Marc A.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA; [Paige, Neil M.; Towfigh, Ali; Shekelle, Paul G.] W Los Angeles VA Med Ctr, Los Angeles, CA USA	Chafen, JJS (reprint author), Stanford Univ, Sch Med, Ctr Primary Care & Outcomes Res, 117 Encina Commons, Stanford, CA 94305 USA.	jjschnei@stanford.edu	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	National Institutes of Health [HHSN272200800065C]; National Institute of Allergy and Infectious Diseases	Funding/Support: This work was funded in part by contract HHSN272200800065C from the National Institutes of Health. This work was commissioned by National Institute of Allergy and Infectious Diseases in support of the development of practice guidelines.	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Am. Med. Assoc.	MAY 12	2010	303	18					1848	1856		10.1001/jama.2010.582		9	Medicine, General & Internal	General & Internal Medicine	594DK	WOS:000277513900026	20460624	
J	Radauer, C; Bublin, M; Wagner, S; Mari, A; Breiteneder, H				Radauer, Christian; Bublin, Merima; Wagner, Stefan; Mari, Adriano; Breiteneder, Heimo			Allergens are distributed into few protein families and possess a restricted number of biochemical functions	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergens; protein families; allergen structures; allergen databases	PLANT FOOD ALLERGENS; STRUCTURAL BIOLOGY; CROSS-REACTIVITY; POLLEN ALLERGENS; SEQUENCE; HOMOLOGS; TOOLS	Background: Existing allergen databases classify their entries by source and route of exposure, thus lacking an evolutionary, structural, and functional classification of allergens. Objective: We sought to build AllFam, a database of allergen families, and use it to extract common structural and functional properties of allergens. Methods: Allergen data from the Allergome database and protein family definitions from the Pfam database were merged into AllFam, a database that is freely accessible on the Internet at: http://www.meduniwien.ac.at/allergens/allfam/. A structural classification of allergens was established by matching Pfam families with families from the Structural Classification of Proteins database. Biochemical functions of allergens were extracted from the Gene Ontology Annotation database. Results: Seven hundred seven allergens were classified by sequence into 134 AllFam families containing 184 Pfam domains (2% of 9318 Pfam families). A random set of 707 sequences with the same taxonomic distribution contained a significantly higher number of different Pfam domains (479 +/- 17). Classifying allergens by structure revealed that 5% of 3012 Structural Classification of Proteins families contained allergens. The biochemical functions of allergens most frequently found were limited to hydrolysis of proteins, polysaccharides, and lipids; binding of metal ions and lipids; storage; and cytoskeleton association. Conclusion: The small number of protein families that contain allergens and the narrow functional distribution of most allergens confirm the existence of yet unknown factors that render proteins allergenic.	[Radauer, Christian; Bublin, Merima; Wagner, Stefan; Breiteneder, Heimo] Med Univ Vienna, Dept Pathophysiol, Ctr Physiol Pathophysiol & Immunol, A-1090 Vienna, Austria; [Mari, Adriano] IDI IRCCS, Ctr Clin & Expt Allergol, Rome, Italy; [Mari, Adriano] Allergy Data Labs, Latina, Italy	Breiteneder, H (reprint author), Med Univ Vienna, Dept Pathophysiol, Ctr Physiol Pathophysiol & Immunol, Wahringer Gurtel 18-20, A-1090 Vienna, Austria.	Heimo.Breiteneder@meduniwien.ac.at	Ferreira, Fatima/E-4889-2011	Ferreira, Fatima/0000-0003-0989-2335; Radauer, Christian/0000-0001-9920-4449			Aalberse RC, 2006, CHEM IMMUNOL ALLERGY, V91, P134; Aalberse RC, 2000, J ALLERGY CLIN IMMUN, V106, P228, DOI 10.1067/mai.2000.108434; Andersson K, 2003, INT ARCH ALLERGY IMM, V130, P87, DOI 10.1159/000069013; Andreeva A, 2004, NUCLEIC ACIDS RES, V32, pD226, DOI 10.1093/nar/gkh039; Breiteneder H, 2005, J ALLERGY CLIN IMMUN, V115, P14, DOI 10.1016/j.jaci.2004.10.022; Breiteneder H, 2004, J ALLERGY CLIN IMMUN, V113, P821, DOI 10.1016/j.jaci.2004.01.079; Chapman MD, 2007, J ALLERGY CLIN IMMUN, V119, P414, DOI 10.1016/j.jaci.2006.11.001; de Leon MP, 2007, MOL IMMUNOL, V44, P463, DOI 10.1016/j.molimm.2006.02.016; Emanuelsson C, 2007, MOL IMMUNOL, V44, P3256, DOI 10.1016/j.molimm.2007.01.019; Ferreira F, 2004, ALLERGY, V59, P243, DOI 10.1046/j.1398-9995.2003.00407.x; Finn RD, 2006, NUCLEIC ACIDS RES, V34, pD247, DOI 10.1093/nar/gkj149; Furmonaviciene R, 2007, CLIN EXP ALLERGY, V37, P231, DOI 10.1111/j.1365-2222.2007.02651.x; Jenkins JA, 2005, J ALLERGY CLIN IMMUN, V115, P163, DOI 10.1016/j.jaci.2004.10.026; Jenkins JA, 2007, J ALLERGY CLIN IMMUN, V120, P1399, DOI 10.1016/j.jaci.2007.08.019; Jeong KY, 2006, PROTEIN PEPTIDE LETT, V13, P835; Keber MM, 2005, J ENDOTOXIN RES, V11, P186, DOI 10.1179/096805105X35206; King TP, 2000, INT ARCH ALLERGY IMM, V123, P99, DOI 10.1159/000024440; Mari A, 2006, CELL IMMUNOL, V244, P97, DOI 10.1016/j.cellimm.2007.02.012; Marin-Rodriguez MC, 2002, J EXP BOT, V53, P2115, DOI 10.1093/jxb/erf089; Markovic-Housley Z, 2003, J MOL BIOL, V325, P123, DOI 10.1016/S0022-2836(02)01197-X; Menu-Bouaouiche L, 2003, BIOCHIMIE, V85, P123, DOI 10.1016/S0300-9084(03)00058-0; Page RDM, 1996, COMPUT APPL BIOSCI, V12, P357; Radauer C, 2006, CLIN EXP ALLERGY, V36, P920, DOI 10.1111/j.1365-2222.2006.02521.x; Radauer C, 2006, J ALLERGY CLIN IMMUN, V117, P141, DOI 10.1016/j.jaci.2005.09.010; Radauer C, 2007, J ALLERGY CLIN IMMUN, V120, P518, DOI 10.1016/j.jaci.2007.07.024; Robotham JM, 2005, J ALLERGY CLIN IMMUN, V115, P1284, DOI 10.1016/j.jaco.2005.02.028; Stadler MB, 2003, FASEB J, V17, P1141, DOI 10.1096/fj.02-1052fje; Thompson JD, 1997, NUCLEIC ACIDS RES, V25, P4876, DOI 10.1093/nar/25.24.4876; Wan H, 1999, J CLIN INVEST, V104, P123, DOI 10.1172/JCI5844	29	177	182	1	36	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	APR	2008	121	4					847	852		10.1016/j.jaci.2008.01.025		6	Allergy; Immunology	Allergy; Immunology	286YY	WOS:000254884000006	18395549	
J	Weinmayr, G; Weiland, SK; Bjorksten, B; Brunekreef, B; Buchele, G; Cookson, WOC; Garcia-Marcos, L; Gotua, M; Gratziou, C; van Hage, M; von Mutius, E; Riikjarv, MA; Rzehak, P; Stein, RT; Strachan, DP; Tsanakas, J; Wickens, K; Wong, GW				Weinmayr, Gudrun; Weiland, Stephan K.; Bjorksten, Bengt; Brunekreef, Bert; Buechele, Gisela; Cookson, William O. C.; Garcia-Marcos, Luis; Gotua, Maia; Gratziou, Christina; van Hage, Marianne; von Mutius, Erika; Riikjarv, Mall-Anne; Rzehak, Peter; Stein, Renato T.; Strachan, David P.; Tsanakas, John; Wickens, Kristin; Wong, Gary W.		ISAAC Phase Two Study Grp	Atopic sensitization and the international variation of asthma symptom prevalence in children	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						wheeze; ISAAC Phase Two; IgE; population attributable risk; gross national income per capita	CHILDHOOD ISAAC; RESPIRATORY SYMPTOMS; BRONCHIAL HYPERRESPONSIVENESS; ESTONIAN CHILDREN; ALLERGEN EXPOSURE; DIFFERENT PATTERN; SCHOOL-CHILDREN; SEMIRURAL AREA; RISK-FACTORS; WHEEZE	Rationale: Atopic sensitization has long been known to be related to asthma in children, but its role in determining asthma prevalence remains to be elucidated further. Objectives: To Investigate the role of atopic sensitization in the large international variation in the prevalence of childhood asthma. Methods: Cross-sectional studies of random samples of 8- to 12-yearold children (n = 1,000 per center) were performed according to the standardized methodology of Phase Two of the International Study of Asthma and Allergy in Childhood (ISAAC). Thirty study centers in 22 countries worldwide participated and reflect a wide range of living conditions, from rural Africa to urban Europe. Data were collected by parental questionnaires (n = 54,439), skin prick tests (n = 311,759), and measurements of allergen-specific IgE levels in serum (n = 8,951). Economic development was assessed by gross national income per capita (GNI). Measurements and Main Results: The prevalence of current wheeze (i.e., during the past year) ranged from 0.8% in Pichincha (Ecuador) to 25.6% in Uruguaiana (Brazil). The fraction of current wheeze attributable to atopic sensitization ranged from 0% in Ankara (Turkey) to 93.8% in Guangzhou (China). There were no correlations between prevalence rates of current wheeze and atopic sensitization, and only weak correlations of both with GNI. However, the fractions and prevalence rates of wheeze attributable to skin test reactivity correlated strongly with GNI (Spearman rank-order coefficient p = 0.50, P = 0.006, and p = 0.74, P < 0.0001, respectively). In addition, the strength of the association between current wheeze and skin test reactivity, assessed by odds ratios, increased with GNI (p = 0.47, P = 0.01). Conclusions: The link between atopic sensitization and asthma symptoms in children differs strongly between populations and increases with economic development.	Univ Ulm, Inst Epidemiol, D-89075 Ulm, Germany; Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; Univ Utrecht, Inst Risk Assessment Sci, Utrecht, Netherlands; Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands; Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England; Univ Murcia, Murcia, Spain; Ctr Allergy & Immunol, Tbilisi, Rep of Georgia; Univ Athens, Sch Med, Evgenidio Hosp, GR-11527 Athens, Greece; Karolinska Inst, Dept Med, Allergy & Clin Immunol Unit, Stockholm, Sweden; Univ Hosp, Stockholm, Sweden; Univ Munich, Childrens Hosp, Dr Von Haunerschen Univ, D-8000 Munich, Germany; Tallinn Childrens Hosp, Tallinn, Estonia; Pontificia Univ Catolica Rio Grande do Sul, Porto Alegre, RS, Brazil; St Georges Univ London, London, England; Hippokrateion Hosp, Paediat Resp Unit, Thessaloniki, Greece; Wellington Sch Med & Hlth Sci, Wellington Asthma Res Grp, Wellington, New Zealand; Chinese Univ Hong Kong, Prince Wales Hosp, Dept Paediat, Shatin, Hong Kong, Peoples R China	Weinmayr, G (reprint author), Univ Ulm, Inst Epidemiol, Helmholzstr 22, D-89075 Ulm, Germany.	gudrun.weinmayr@uni-ulm.de	van Hage, Marianne/A-9678-2017; Hatziagorou, Elpis/D-3247-2012; MARTINEZ-GIMENO, ANTONIO/A-9416-2010; Stein, Renato/K-2568-2014; Ellwood, Philippa/G-7555-2015; De sario, Manuela/K-1932-2016; Forastiere, Francesco/J-9067-2016	van Hage, Marianne/0000-0003-3091-1596; Pearce, Neil/0000-0002-9938-7852; brunekreef, bert/0000-0001-9908-0060; Braback, Lennart/0000-0001-9930-7755; MARTINEZ-GIMENO, ANTONIO/0000-0003-4051-1860; Ellwood, Philippa/0000-0002-1994-4023; De sario, Manuela/0000-0002-1117-2735; Forastiere, Francesco/0000-0002-9162-5684; Beasley, Richard/0000-0003-0337-406X; von Mutius, Erika/0000-0002-8893-4515			Alfven T, 2006, ALLERGY, V61, P414, DOI 10.1111/j.1398-9995.2005.00939.x; Asher MI, 1998, EUR RESPIR J, V12, P315; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; Bjorksten B, 2004, SPRINGER SEMIN IMMUN, V25, P257, DOI 10.1007/s00281-003-0142-2; BRABACK L, 1994, CLIN EXP ALLERGY, V24, P826, DOI 10.1111/j.1365-2222.1994.tb01805.x; 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J. Respir. Crit. Care Med.	SEP 15	2007	176	6					565	574		10.1164/rccm.200607-994OC		10	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	213DK	WOS:000249646100006	17575099	
J	Gilmour, M; Jaakkola, MS; London, SJ; Nel, AE; Rogers, CA				Gilmour, M; Jaakkola, MS; London, SJ; Nel, AE; Rogers, CA			How exposure to environmental tobacco smoke, outdoor air pollutants, and increased pollen burdens influences the incidence of asthma	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; asthma; cigarette smoke; climate change; diesel exhaust; environment; inflammation; mechanisms; ozone; particulate matter; pollen	EXHAUST PARTICLE CHEMICALS; LOWER RESPIRATORY ILLNESS; DIESEL EXHAUST; PARENTAL SMOKING; OXIDATIVE STRESS; ATMOSPHERIC CO2; ELEVATED CO2; CARBON-DIOXIDE; CLIMATE-CHANGE; HEALTH	Asthma is a multifactorial airway disease that arises from a relatively common genetic background interphased with exposures to allergens and airborne irritants. The rapid rise in asthma over the past three decades in Western societies has been attributed to numerous diverse factors, including increased awareness of the disease, altered lifestyle and activity patterns, and ill-defined changes in environmental exposures. It is well accepted that persons with asthma are more sensitive than persons without asthma to air pollutants such as cigarette smoke, traffic emissions, and photochemical smog components. It has also been demonstrated that exposure to a mix of allergens and irritants can at times promote the development phase (induction) of the disease. Experimental evidence suggests that complex organic molecules from diesel exhaust may act as allergic adjuvants through the production of oxidative stress in airway cells. It also seems that climate change is increasing the abundance of aeroallergens Such as pollen, which may result in greater incidence or severity of allergic diseases. In this review we illustrate how environmental tobacco smoke, outdoor air pollution, and climate change may act as environmental risk factors for the development of asthma and provide mechanistic explanations for how some of these effects can occur.	US EPA, Res Triangle Pk, NC 27711 USA; Univ Birmingham, Inst Occupat & Environm Med, Birmingham, AL USA; NIEHS, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA; Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA; Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA	Gilmour, M (reprint author), US EPA, Res Triangle Pk, NC 27711 USA.	gilmour.ian@epa.gov	Rogers, Christine/A-2189-2008; Nel, Andre/J-2808-2012; Osborne, Nicholas/N-4915-2015	Rogers, Christine/0000-0003-0887-9606; Osborne, Nicholas/0000-0002-6700-2284; London, Stephanie/0000-0003-4911-5290			AAAAI, 2000, ALL REP; ABBEY DE, 1995, ARCH ENVIRON HEALTH, V50, P139; ALSBERG T, 1985, ENVIRON SCI TECHNOL, V19, P43, DOI 10.1021/es00131a003; BAZZAZ FA, 1990, ANNU REV ECOL SYST, V21, P167, DOI 10.1146/annurev.es.21.110190.001123; Bornehag CG, 2001, INDOOR AIR, V11, P72; Brauer M, 2002, AM J RESP CRIT CARE, V166, P1092, DOI 10.1164/rccm.200108-007OC; California Environmental Protection Agency (Cal EPA) Office of Environmental Health Hazard Assessment, 1997, HLTH EFF EXP ENV TOB; CDC (Centers for Disease Control), 2004, MMWR-MORBID MORTAL W, V53, P145; Clot Bernard, 2003, Aerobiologia, V19, P227, DOI 10.1023/B:AERO.0000006572.53105.17; Cook DG, 1997, THORAX, V52, P1081; DALES RE, 1991, AM REV RESPIR DIS, V143, P505; Diaz-Sanchez D, 2003, CURR ALLERGY ASTHM R, V3, P146, DOI 10.1007/s11882-003-0027-4; DiazSanchez D, 1997, J IMMUNOL, V158, P2406; Drake BG, 1997, ANNU REV PLANT PHYS, V48, P609, DOI 10.1146/annurev.arplant.48.1.609; Fitter AH, 2002, SCIENCE, V296, P1689, DOI 10.1126/science.1071617; Frei T, 1998, GRANA, V37, P172; Frenguelli Giuseppe, 2002, Aerobiologia, V18, P223, DOI 10.1023/A:1021320128458; Fryer AA, 2000, AM J RESP CRIT CARE, V161, P1437; Gehring U, 2002, EUR RESPIR J, V19, P690, DOI 10.1183/09031936.02.01182001; Gilliland FD, 2004, LANCET, V363, P119, DOI 10.1016/S0140-6736(03)15262-2; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; HEINRICH J, 2004, CURR OPIN ALLERGY CL, P341; Heloma A, 2003, ADDICTION, V98, P1111, DOI 10.1046/j.1360-0443.2003.00429.x; HISADA T, 2000, EUR J PHARMACOL, V399, P299; Hiura TS, 1999, J IMMUNOL, V163, P5582; IOM. 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Health Perspect.	APR	2006	114	4					627	633		10.1289/ehp.8380		7	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	030QX	WOS:000236650500052	16581557	
J	Woodcock, A; Forster, L; Matthews, E; Martin, J; Letley, L; Vickers, M; Britton, J; Strachan, D; Howarth, P; Altmann, D; Frost, C; Custovic, A				Woodcock, A; Forster, L; Matthews, E; Martin, J; Letley, L; Vickers, M; Britton, J; Strachan, D; Howarth, P; Altmann, D; Frost, C; Custovic, A		Med Res Council Gen Practice Res	Control of exposure to mite allergen and allergen-impermeable bed covers for adults with asthma	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							INHALED STEROIDS; CONTROLLED TRIAL; OCCUPATIONAL ASTHMA; INDOOR ALLERGENS; AVOIDANCE; CHILDREN; ENCASEMENT; REDUCTION; MATTRESS	Background: The effectiveness of avoidance of house-dust-mite allergen (Dermatophagoides pteronyssinus 1 [Der p1]) in the management of asthma is uncertain. Methods: We conducted a double-blind, randomized, placebo-controlled study of allergen-impermeable bed covers involving 1122 adults with asthma. The primary outcomes were the mean morning peak expiratory flow rate over a four-week period during the run-in phase and at six months and the proportion of patients who discontinued inhaled corticosteroid therapy as part of a phased-reduction program during months 7 through 12. Der p1 was measured in mattress dust in a 10 percent random subsample of homes at entry and at 6 and 12 months. Results: The prevalence of sensitivity to dust-mite allergen was 65.4 percent in the group supplied with allergen-impermeable bed covers (active-intervention group) and 65.1 percent in the control group supplied with non-impermeable bed covers. The concentration of Der p1 in mattress dust was significantly lower in the active-intervention group at 6 months (geometric mean, 0.58 mug per gram vs. 1.71 mug per gram in the control group; P=0.01) but not at 12 months (1.05 mug per gram vs. 1.64 mug per gram; P=0.74). The mean morning peak expiratory flow rate improved significantly in both groups (from 410.7 to 419.1 liters per minute in the active-intervention group, P<0.001 for the change; and from 417.8 to 427.4 liters per minute in the control group, P<0.001 for the change). After adjustment for base-line differences (by analysis of covariance), there was no significant difference between the groups in the peak expiratory flow rate at six months (difference in means, active-intervention group vs. control group, -1.6 liters per minute [95 percent confidence interval, -5.9 to 2.7] among all patients [P=0.46] and -1.5 liters per minute [95 percent confidence interval, -6.9 to 3.9] among mite-sensitive patients [P=0.59]). There was no significant difference between the groups in the proportion in whom complete cessation of inhaled corticosteroid therapy was achieved (17.4 percent in the active-intervention group and 17.1 percent in the control group) or in the mean reduction in steroid dose, either among all patients or among mite-sensitive patients. Conclusions: Allergen-impermeable covers, as a single intervention for the avoidance of exposure to dust-mite allergen, seem clinically ineffective in adults with asthma.	Univ Manchester, NW Lung Ctr, Wythenshawe Hosp, S Manchester Acad Grp, Manchester M23 9LT, Lancs, England; MRC, Gen Practice Res Framework, London, England; Univ Nottingham, City Hosp, Div Epidemiol & Publ Hlth, Nottingham NG5 1PB, England; Univ London St Georges Hosp, Sch Med, Dept Publ Hlth Sci, London SW17 0RE, England; Univ Southampton, Gen Hosp, London, England; London Sch Hyg & Trop Med, Med Stat Unit, London WC1, England	Woodcock, A (reprint author), Univ Manchester, NW Lung Ctr, Wythenshawe Hosp, S Manchester Acad Grp, Manchester M23 9LT, Lancs, England.		Custovic, Adnan/A-2435-2012	Custovic, Adnan/0000-0001-5218-7071; Woodcock, Ashley/0000-0002-5428-8578			BURR ML, 1976, LANCET, V1, P333; Carswell F, 1996, CLIN EXP ALLERGY, V26, P386, DOI 10.1111/j.1365-2222.1996.tb00554.x; Carter MC, 2001, J ALLERGY CLIN IMMUN, V108, P732, DOI 10.1067/mai.2001.119155; Cloosterman SGM, 1999, CLIN EXP ALLERGY, V29, P1336, DOI 10.1046/j.1365-2222.1999.00627.x; Custovic A, 2002, ANN ALLERG ASTHMA IM, V88, P432; Custovic A, 2000, J ALLERGY CLIN IMMUN, V105, P252, DOI 10.1016/S0091-6749(00)90073-3; Eggleston PA, 2001, J ALLERGY CLIN IMMUN, V108, P685, DOI 10.1067/mai.2001.119569; EHNERT B, 1992, J ALLERGY CLIN IMMUN, V90, P135, DOI 10.1016/S0091-6749(06)80024-2; Gotzsche PC, 1998, BRIT MED J, V317, P1105; Green R, 2002, BRIT MED J, V324, P1131; Grootendorst DC, 2001, CLIN EXP ALLERGY, V31, P400, DOI 10.1046/j.1365-2222.2001.01022.x; Halken S, 2003, J ALLERGY CLIN IMMUN, V111, P169, DOI 10.1067/mai.2003.5; LUCZYNSKA CM, 1989, J IMMUNOL METHODS, V118, P227, DOI 10.1016/0022-1759(89)90010-0; MARKS GB, 1994, CLIN EXP ALLERGY, V24, P1078, DOI 10.1111/j.1365-2222.1994.tb02746.x; Paganelli R, 1998, ALLERGY, V53, P763; PAGGIARO PL, 1994, EUR RESPIR J, V7, P761, DOI 10.1183/09031936.94.07040761; Park HS, 1997, CLIN EXP ALLERGY, V27, P1145; Piacentini GL, 1999, J ALLERGY CLIN IMMUN, V104, P1323; Platts-Mills TAE, 1999, BRIT MED J, V318, P870; Strachan DP, 1998, BRIT MED J, V317, P1096; Terreehorst I, 2003, NEW ENGL J MED, V349, P237, DOI 10.1056/NEJMoa023171; Tunnicliffe WS, 1999, EUR RESPIR J, V13, P654, DOI 10.1183/09031936.99.13365499; vanderHeide S, 1997, EUR RESPIR J, V10, P1217, DOI 10.1183/09031936.97.10061217; Vaughan JW, 1999, J ALLERGY CLIN IMMUN, V103, P227, DOI 10.1016/S0091-6749(99)70495-1; WONG CS, 1993, CLIN EXP ALLERGY, V23, P370, DOI 10.1111/j.1365-2222.1993.tb00341.x	25	177	185	1	9	MASSACHUSETTS MEDICAL SOC/NEJM	WALTHAM	WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA	0028-4793			NEW ENGL J MED	N. Engl. J. Med.	JUL 17	2003	349	3					225	236		10.1056/NEJMoa023175		12	Medicine, General & Internal	General & Internal Medicine	701KA	WOS:000184165700006	12867606	
J	Perzanowski, MS; Ronmark, E; Platts-Mills, TAE; Lundback, B				Perzanowski, MS; Ronmark, E; Platts-Mills, TAE; Lundback, B			Effect of cat and dog ownership on sensitization and development of asthma among preteenage children	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						allergy; asthma; cat; dog; tolerance	HOUSE-DUST MITE; INNER-CITY CHILDREN; COCKROACH ALLERGEN; NORTHERN SWEDEN; RISK-FACTORS; EXPOSURE; MORBIDITY; SCHOOLS; HOMES; IGE	An inverse relationship has been proposed between exposure to high quantities of cat allergen at home and both asthma and cat allergy. First- and second-grade children from Lule (a) over circle, Kiruna, and Pite (a) over circle, Sweden participated in an asthma questionnaire study (n = 3,431) and incidence was evaluated over the next 3 years. Skin testing was performed on the children in Lule (a) over circle and Kiruna (n = 2,149). The strongest risk factor for incident cases of asthma was Type 1 allergy (relative risk [RR], 4.9 [2.9-8.4]), followed by a family history of asthma (RR, 2.83 [1.8-4.5]). Living with a cat was inversely related both to having a positive skin test to cat (1111, 0.62 [0.47-0.83]) and incidence of physician-diagnosed asthma (1111, 0.49 [0.28-0.83]). This effect on incident asthma was most pronounced among the children with a family history of asthma (RR, 0.25 [0.08-0.80]). The evidence also suggests that many of the children exposed to cats at home can develop an immune response that does not include immunoglobulin E. Weaker protective trends were seen with dog ownership. The traditional thinking that not owning cats can provide protection against developing allergy and asthma among those with a family history of allergy needs to be re-evaluated. In a community where cat sensitization was strongly associated with asthma, owning a cat was protective against both prevalent and incident asthma.	Univ Virginia, Hlth Sci Ctr, Asthma & Allerg Dis Ctr, Dept Med, Charlottesville, VA 22908 USA; Sunderby Cent Hosp Norrbotten, Dept Med, OLIN Studies, Lulea, Sweden; Umea Univ, Dept Resp Med & Allergy, S-90187 Umea, Sweden; Karolinska Inst, Natl Inst Environm Med, Unit Lung & Allergy Res, S-10401 Stockholm, Sweden	Perzanowski, MS (reprint author), Univ Virginia, Hlth Sci Ctr, Asthma & Allerg Dis Ctr, Dept Med, POB 801355, Charlottesville, VA 22908 USA.				NIAID NIH HHS [R01 AI-20565, P01 AI50989]		Aalberse RC, 2000, AM J RESP CRIT CARE, V162, pS124; Almqvist C, 1999, J ALLERGY CLIN IMMUN, V103, P1012, DOI 10.1016/S0091-6749(99)70172-7; ANDERSON HR, 1992, THORAX, V47, P537, DOI 10.1136/thx.47.7.537; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Burney P, 1996, EUR RESPIR J, V9, P687; Carter MC, 2001, J ALLERGY CLIN IMMUN, V108, P732, DOI 10.1067/mai.2001.119155; Crater DD, 2001, PEDIATRICS, V108, DOI 10.1542/peds.108.6.e97; Custovic A, 1996, CLIN EXP ALLERGY, V26, P1246, DOI 10.1046/j.1365-2222.1996.d01-278.x; Custovic A, 1996, J ALLERGY CLIN IMMUN, V98, P64, DOI 10.1016/S0091-6749(96)70227-0; Dotterud LK, 1997, CLIN EXP ALLERGY, V27, P252; Eggleston PA, 1999, J ALLERGY CLIN IMMUN, V104, P842; EVANS R, 1987, CHEST, V91, pS65; Henriksen AH, 2001, RESP MED, V95, P122, DOI 10.1053/rmed.2000.1004; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Huss K, 2001, J ALLERGY CLIN IMMUN, V107, P48, DOI 10.1067/mai.2001.111146; LAU S, 2000, LANCET, V356, P1368; Litonjua AA, 2001, J ALLERGY CLIN IMMUN, V107, P41, DOI 10.1067/mai.2001.111143; Lundback B, 1998, CLIN EXP ALLERGY, V28, P3; Melen E, 2001, ALLERGY, V56, P646, DOI 10.1034/j.1398-9995.2001.00387.x; MUNIR AKM, 1993, J ALLERGY CLIN IMMUN, V91, P1067, DOI 10.1016/0091-6749(93)90221-Z; OWNBY DR, 2001, AM J RESP CRIT CARE, V163, pA722; PEAT JK, 1994, AUST NZ J MED, V24, P270, DOI 10.1111/j.1445-5994.1994.tb02171.x; Perzanowski MS, 1999, J ALLERGY CLIN IMMUN, V103, P1018, DOI 10.1016/S0091-6749(99)70173-9; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; Platts-Mills TAE, 2000, J ALLERGY CLIN IMMUN, V106, P787, DOI 10.1067/mai.2000.110548; PLATTSMILLS TAE, 1978, J IMMUNOL, V120, P1201; 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; Roost HP, 1999, J ALLERGY CLIN IMMUN, V104, P941, DOI 10.1016/S0091-6749(99)70072-2; Rosenstreich DL, 1997, NEW ENGL J MED, V336, P1356, DOI 10.1056/NEJM199705083361904; SEARS MR, 1987, J ALLERGY CLIN IMMUN, V80, P383, DOI 10.1016/0091-6749(87)90055-8; SEARS MR, 2000, EUR RESP J S31, V16, pS555; SPORIK R, 1995, AM J RESP CRIT CARE, V151, P1388; Tovey E, 1999, J ALLERGY CLIN IMMUN, V103, P179, DOI 10.1016/S0091-6749(99)70488-4; WISSOW LS, 1988, AM J PUBLIC HEALTH, V78, P777, DOI 10.2105/AJPH.78.7.777; Woolcock AJ, 2001, MED J AUSTRALIA, V175, P141	36	177	183	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.	SEP 1	2002	166	5					696	702		10.1164/rccm.2201035		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	588ZZ	WOS:000177734100016	12204868	
J	Wright, RJ; Cohen, S; Carey, V; Weiss, ST; Gold, DR				Wright, RJ; Cohen, S; Carey, V; Weiss, ST; Gold, DR			Parental stress as a predictor of wheezing in infancy - A prospective birth-cohort study	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						caregiver stress; wheeze; infancy; birth cohort	PSYCHOLOGICAL STRESS; BEHAVIORAL-RESPONSE; RESPIRATORY ILLNESS; ALLERGEN LEVELS; EARLY-CHILDHOOD; IMMUNE-SYSTEM; COMMON COLD; 1ST YEAR; ASTHMA; LIFE	The role of stress in the pathogenesis of childhood wheeze remains controversial. Caretaker stress might influence wheeze through stress-induced behavioral changes In caregivers (e.g., smoking, breast-feeding) or biologic processes impacting infant development (e.g., immune response, susceptibility to lower respiratory infections). The influence of caregiver stress on wheeze in infancy was studied in a genetically predisposed prospective birth-cohort (n = 496). Caregiver-perceived stress and wheeze in the children were ascertained bimonthly from the first 2 to 3 mo of life. Greater levels of caregiver-perceived stress at 2 to 3 mo was associated with increased risk of subsequent repeated wheeze among the children during the first 14 mo of life (RR, 1.6; 95% Cl, 1.3 to 1.9). Caregiver-perceived stress remained significant (RR, 1.4; 9S% Cl, 1.1 to 1.9) when controlling for factors potentially associated with both stress and wheeze (parental asthma, socioeconomic status, birth weight, and race/ethnicity) as well as mediators through which stress might influence wheeze (maternal smoking, breast-feeding, indoor allergen exposures, and lower respiratory infections). Furthermore, caregiver stress prospectively predicted wheeze In the infants, whereas wheeze In the children did not predict subsequent caregiver stress. The effect of caregiver stress on early childhood wheeze was independent of caregiver smoking and breast-feeding behaviors, as well as allergen exposure, birth weight, and lower respiratory Infections. These findings suggest a more direct mechanism may be operating between stress and wheeze In early childhood. Stress may contribute significantly to the population burden of preventable childhood respiratory illness.	Brigham & Womens Hosp, Channing Lab, Dept Med, Boston, MA 02115 USA; Beth Israel Deaconess Med Ctr, Dept Pulm & Crit Care Med, Boston, MA 02115 USA; Harvard Univ, Sch Med, Boston, MA 02115 USA; Carnegie Mellon Univ, Dept Psychol, Pittsburgh, PA 15213 USA	Wright, RJ (reprint author), Brigham & Womens Hosp, Channing Lab, Dept Med, 181 Longwood Ave, Boston, MA 02115 USA.	rosalind.wright@channing.harvard.edu		Cohen, Sheldon/0000-0003-2248-4600	NHLBI NIH HHS [K08 HL 04187]; NIAID NIH HHS [R01 AI/EH S35786]		ADER R, 1995, LANCET, V345, P99, DOI 10.1016/S0140-6736(95)90066-7; Anisman H, 1998, INT J DEV NEUROSCI, V16, P149, DOI 10.1016/S0736-5748(98)00025-2; Boyce WT, 1995, PSYCHOSOM MED, V57, P411; BUSSE WE, 1994, AM J RESP CRIT CARE, V151, P249; Chew GL, 1998, AM J RESP CRIT CARE, V157, P1536; CHROUSOS GP, 1992, JAMA-J AM MED ASSOC, V267, P1244, DOI 10.1001/jama.267.9.1244; CLOVER RD, 1989, J FAM PRACTICE, V28, P535; Coe CL, 1999, BIOL NEONATE, V76, P301, DOI 10.1159/000014172; Coe CL, 1996, BRAIN BEHAV IMMUN, V10, P221, DOI 10.1006/brbi.1996.0020; Cohen S, 1999, PSYCHOSOM MED, V61, P175; COHEN S, 1990, HEALTH PSYCHOL, V9, P466, DOI 10.1037/0278-6133.9.4.466; COHEN S, 1988, CLAR SYMP, P31; COHEN S, 1991, NEW ENGL J MED, V325, P606, DOI 10.1056/NEJM199108293250903; Cohen S, 1998, HEALTH PSYCHOL, V17, P214, DOI 10.1037//0278-6133.17.3.214; Cohen S., 1989, ADV INVESTIGATION PS, P235; Cohen S, 1995, MEASURING STRESS GUI, P3; CRONBACH LJ, 1951, PSYCHOMETRIKA, V16, P297; Elenkov IJ, 1999, BEST PRACT RES CL EN, V13, P583, DOI 10.1053/beem.1999.0045; Finn PW, 2000, J ALLERGY CLIN IMMUN, V105, P933, DOI 10.1067/mai.2000.106546; Folkerts G, 1998, AM J RESP CRIT CARE, V157, P1708; Gold DR, 1999, AM J RESP CRIT CARE, V160, P227; GUSTAFSSON PA, 1994, J PEDIATR-US, V125, P493, DOI 10.1016/S0022-3476(05)83306-2; Holgate ST, 1997, CIBA F SYMP, V206, P5; Holt PG, 1997, CIBA F SYMP, V206, P35; HOLT PG, 1995, PEDIAT ALLERG IMM-UK, V6, P59, DOI 10.1111/j.1399-3038.1995.tb00261.x; Leserman J, 1998, PSYCHOSOM MED, V60, P175; LEWIS M, 1995, DEV PSYCHOBIOL, V28, P419, DOI 10.1002/dev.420280804; LEWIS M, 1995, CHILDREN FAMILIES ST, P35; Liu D, 1997, SCIENCE, V277, P1659, DOI 10.1126/science.277.5332.1659; Martin YC, 1998, PERSPECT DRUG DISCOV, V12, P3, DOI 10.1023/A:1017037831628; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; MARTINEZ FD, 1997, ASTHMA, P121; MATTHEWS K A, 1988, Annals of Behavioral Medicine, V10, P71, DOI 10.1207/s15324796abm1002_5; McEwen BS, 1998, NEW ENGL J MED, V338, P171; MCLEAN DE, 1993, AM J PREV MED, V9, P39; MINUCHIN S, 1975, ARCH GEN PSYCHIAT, V32, P1031; Mrazek DA, 1999, PEDIATR PULM, V27, P85, DOI 10.1002/(SICI)1099-0496(199902)27:2<85::AID-PPUL4>3.0.CO;2-B; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; PATTERSON JM, 1995, CHILDREN FAMILIES ST, P11; PEARCE N, 1998, ASTHMA EPIDEMIOLOGY, P75; PRIEL B, 1999, J PEDIATR PSYCHOL, V15, P197; RAMSAY DS, 1994, CHILD DEV, V65, P1491, DOI 10.1111/j.1467-8624.1994.tb00831.x; Reyes TM, 1997, BRAIN RES, V769, P29, DOI 10.1016/S0006-8993(97)00687-2; Sandberg S, 2000, LANCET, V356, P982, DOI 10.1016/S0140-6736(00)02715-X; SHERMAN CB, 1990, AM J EPIDEMIOL, V132, P83; SILVERMAN M, 1995, CHILDHOOD ASTHMA OTH, P141; Sobrian SK, 1997, ENVIRON RES, V73, P227, DOI 10.1006/enrs.1997.3734; VALLEE M, 1997, J NEUROSCI, V17, P626; Warner JA, 1996, ALLERGY, V51, P447, DOI 10.1111/j.1398-9995.1996.tb04650.x; WRIGHT AL, 1989, AM J EPIDEMIOL, V129, P1232; Wright RJ, 1998, THORAX, V53, P1066; WRIGHT RJ, 2000, ALLERGY, P203; Yabuhara A, 1997, CLIN EXP ALLERGY, V27, P1261; ZEGER SL, 1986, BIOMETRICS, V42, P121, DOI 10.2307/2531248; ZUCKERMAN B, 1995, CHILDREN FAMILIES ST, P164	55	177	177	1	16	AMER THORACIC SOC	NEW YORK	61 BROADWAY, FL 4, NEW YORK, NY 10006 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	FEB 1	2002	165	3					358	365				8	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	517PA	WOS:000173618100011	11818321	
J	Kinney, PL; Aggarwal, M; Northridge, ME; Janssen, NAH; Shepard, P				Kinney, PL; Aggarwal, M; Northridge, ME; Janssen, NAH; Shepard, P			Airborne concentrations of PM2.5 and diesel exhaust particles on Harlem sidewalks: A community-based pilot study	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						diesel exhaust; Harlem; outdoor air pollution; PM2.5 urban	PARTICULATE AIR-POLLUTION; RESPIRATORY HOSPITAL ADMISSIONS; ELEMENTAL CARBON; EPITHELIAL-CELLS; ASTHMA; CHILDREN; MORTALITY; EXPOSURE; AEROSOL; HYDROCARBONS	Residents of the dense urban core neighborhoods of New York City (NYC) have expressed increasing concern about the potential human health impacts of diesel vehicle emissions. We measured concentrations of particulate matter less than or equal to 2.5 mu m in aerodynamic diameter (PM2.5) and diesel exhaust particles (DEP) on sidewalks in Harlem, NYC, and tested whether spatial variations in concentrations were related to local diesel traffic density. Eight-hour (1000-1800 hr) air samples for PM2.5 and elemental carbon (EC) were collected for 5 days in July 1996 on sidewalks adjacent to four geographically distinct Harlem intersections. Samples were taken using portable monitors worn by study staff. Simultaneous traffic counts for diesel trucks, buses, cars, and pedestrians were carried out at each intersection on greater than or equal to 2 of the 5 sampling days. Eight-hour diesel vehicle counts ranged from 61 to 2,467 across the four sires. Mean concentrations of PM2.5 exhibited only modest site-to-site variation (37-47 mu g/m(3)), reflecting the importance of broader regional sources of PM2.5. In contrast, EC concentrations varied 4-fold across sites (from 1.5 to 6 mu g/m(3)), and were associated with bus and truck counts on adjacent streets and, at one site, with the presence of a bus depot. A high correlation (r = 0.95) was observed between EC concentrations measured analytically and a blackness measurement based on PM2.5 filter reflectance, suggesting the utility of the tatter as a surrogate measure of DEP in future community-based studies. These results show that local diesel sources in Harlem create spatial variations in sidewalk concentrations of DEP. The study also demonstrates the feasibility of a new paradigm for community-based research involving full and active partnership between academic scientists and community-based organizations.	Columbia Univ, JL Mailman Sch Publ Hlth, Div Environm Hlth Sci, New York, NY 10032 USA; Harlem Ctr Hlth Promot & Dis Prevent, New York, NY USA; Wageningen Univ Agr, Dept Environm Sci, Environm & Occupat Hlth Grp, Wageningen, Netherlands; W Harlem Environm Act Inc, New York, NY USA	Kinney, PL (reprint author), Columbia Univ, JL Mailman Sch Publ Hlth, Div Environm Hlth Sci, 60 Haven Ave,Floor B 1, New York, NY 10032 USA.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Bayram H, 1998, AM J RESP CELL MOL, V18, P441; Bhatia R, 1998, EPIDEMIOLOGY, V9, P84, DOI 10.1097/00001648-199801000-00017; Birch ME, 1996, AEROSOL SCI TECH, V25, P221, DOI 10.1080/02786829608965393; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; Burton RM, 1996, ENVIRON SCI TECHNOL, V30, P400, DOI 10.1021/es950030f; CARR W, 1992, AM J PUBLIC HEALTH, V82, P59, DOI 10.2105/AJPH.82.1.59; CASS GR, 1995, DIESEL EXHAUST CRITI; CHOW JC, 1994, ATMOS ENVIRON, V28, P2061, DOI 10.1016/1352-2310(94)90474-X; DELUMYEA RG, 1980, ATMOS ENVIRON, V14, P647, DOI 10.1016/0004-6981(80)90047-5; DiazSanchez D, 1997, ALLERGY, V52, P52; DOCKERY DW, 1994, ANNU REV PUBL HEALTH, V15, P107, DOI 10.1146/annurev.pu.15.050194.000543; DOCKERY DW, 1993, NEW ENGL J MED, V329, P1753, DOI 10.1056/NEJM199312093292401; Duhme H, 1996, EPIDEMIOLOGY, V7, P578, DOI 10.1097/00001648-199611000-00003; EDWARDS J, 1994, ARCH ENVIRON HEALTH, V49, P223; GODLEE F, 1993, BRIT MED J, V303, P1539; GRAY HA, 1986, ENVIRON SCI TECHNOL, V20, P580, DOI 10.1021/es00148a006; Jacobs J., 1961, DEATH LIFE GREAT AM; KEELER GJ, 1990, ATMOS ENVIRON A-GEN, V24, P2795, DOI 10.1016/0960-1686(90)90166-K; Kobayashi T, 1997, FUND APPL TOXICOL, V38, P166, DOI 10.1006/faat.1997.2347; Nielsen T, 1996, ATMOS ENVIRON, V30, P3481, DOI 10.1016/1352-2310(96)00096-9; NITTA H, 1993, ARCH ENVIRON HEALTH, V48, P53; OSTRO BD, 1987, J ENVIRON ECON MANAG, V14, P87, DOI 10.1016/0095-0696(87)90008-8; PETERSON B, 1996, ANN ALLERG ASTHMA IM, V77, P262; POPE CA, 1995, AM J RESP CRIT CARE, V151, P669; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; Suh HH, 1997, ENVIRON HEALTH PERSP, V105, P826, DOI 10.2307/3433700; Suzuki T, 1996, J CLIN LAB IMMUNOL, V48, P187; Terada N, 1997, INT ARCH ALLERGY IMM, V114, P167; THURSTON GD, 1992, J EXPO ANAL ENV EPID, V2, P429; THURSTON GD, 1994, ENVIRON RES, V65, P271, DOI 10.1006/enrs.1994.1037; ULRICH E, 1992, J AEROSOL SCI, V23, pS925; *US EPA, 1999, NAT AMB AIR QUAL STA; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; WEISS KB, 1990, JAMA-J AM MED ASSOC, V264, P1683, DOI 10.1001/jama.264.13.1683; *WHO, 1996, ENV HLTH CRIT, V171; WJST M, 1993, BRIT MED J, V307, P596	36	177	180	1	38	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	2000	108	3					213	218		10.2307/3454436		6	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	296NX	WOS:000086031400029	10706526	
J	Kudo, M; Melton, AC; Chen, C; Engler, MB; Huang, KE; Ren, X; Wang, YL; Bernstein, X; Li, JT; Atabai, K; Huang, XZ; Sheppard, D				Kudo, Makoto; Melton, Andrew C.; Chen, Chun; Engler, Mary B.; Huang, Katherine E.; Ren, Xin; Wang, Yanli; Bernstein, Xin; Li, John T.; Atabai, Kamran; Huang, Xiaozhu; Sheppard, Dean			IL-17A produced by alpha beta T cells drives airway hyper-responsiveness in mice and enhances mouse and human airway smooth muscle contraction	NATURE MEDICINE			English	Article							GROWTH-FACTOR-BETA; ROR-GAMMA-T; ALLERGIC-ASTHMA; GENE POLYMORPHISMS; T(H)17 CELLS; RHO-KINASE; RECEPTOR; INFLAMMATION; INTERLEUKIN-17; ASSOCIATION	Emerging evidence suggests that the T helper 17 (T(H)17) subset of alpha beta T cells contributes to the development of allergic asthma. In this study, we found that mice lacking the alpha v beta 8 integrin on dendritic cells did not generate T(H)17 cells in the lung and were protected from airway hyper-responsiveness in response to house dust mite and ovalbumin sensitization and challenge. Because loss of T(H)17 cells inhibited airway narrowing without any obvious effects on airway inflammation or epithelial morphology, we examined the direct effects of T(H)17 cytokines on mouse and human airway smooth muscle function. Interleukin-17A (IL-17A), but not IL-17F or IL-22, enhanced contractile force generation of airway smooth muscle through an IL-17 receptor A (IL-17RA)-IL-17RC, nuclear factor kappa light-chain enhancer of activated B cells (NF-kappa B)-ras homolog gene family, member A (RhoA)-Rho-associated coiled-coil containing protein kinase 2 (ROCK2) signaling cascade. Mice lacking integrin alpha v beta 8 on dendritic cells showed impaired activation of this pathway after ovalbumin sensitization and challenge, and the diminished contraction of the tracheal rings in these mice was reversed by IL-17A. These data indicate that the IL-17A produced by T(H)17 cells contributes to allergen-induced airway hyper-responsiveness through direct effects on airway smooth muscle.	[Kudo, Makoto; Melton, Andrew C.; Chen, Chun; Huang, Katherine E.; Ren, Xin; Wang, Yanli; Bernstein, Xin; Li, John T.; Atabai, Kamran; Huang, Xiaozhu; Sheppard, Dean] Univ Calif San Francisco, Dept Med, Lung Biol Ctr, San Francisco, CA 94143 USA; [Kudo, Makoto] Yokohama City Univ, Grad Sch Med, Dept Internal Med & Clin Immunol, Kanazawa Ku, Yokohama, Kanagawa 232, Japan; [Engler, Mary B.] Univ Calif San Francisco, Dept Physiol Nursing, San Francisco, CA USA; [Li, John T.] Univ Calif San Francisco, Dept Pediat, San Francisco, CA USA; [Atabai, Kamran] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA	Sheppard, D (reprint author), Univ Calif San Francisco, Dept Med, Lung Biol Ctr, San Francisco, CA 94143 USA.	dean.sheppard@ucsf.edu			US National Institutes of Health (NIH) [HL64353, HL53949, HL083950, AI024674, U19 AI077439]; NIH Ruth L. Kirschstein National Research Service [HL095314]; American Lung Association of California; University of California, San Francisco (UCSF) Strategic Asthma Basic Research Center	This work was supported by US National Institutes of Health (NIH) grants HL64353, HL53949, HL083950, AI024674 and U19 AI077439 (to D.S.), a NIH Ruth L. Kirschstein National Research Service Award HL095314 (to A.C.M.), an American Lung Association of California Research Training Fellowship Award (to A.C.M.) and funds from the University of California, San Francisco (UCSF) Strategic Asthma Basic Research Center. Deidentified human lung was kindly provided by M. Matthay (UCSF) and P. Wolters (UCSF). IL-17RC knockout mice were kindly provided by W. Ouyang (Genentech).	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Med.	APR	2012	18	4					547	554		10.1038/nm.2684		8	Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental	Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine	923KI	WOS:000302617800031	22388091	
J	Bouzigon, E; Corda, E; Aschard, H; Dizier, MH; Boland, A; Bousquet, J; Chateigner, N; Gormand, F; Just, J; Le Moual, N; Scheinmann, P; Siroux, V; Vervloet, D; Zelenika, D; Pin, I; Kauffmann, F; Lathrop, M; Demenais, F				Bouzigon, Emmanuelle; Corda, Eve; Aschard, Hugues; Dizier, Marie-Helene; Boland, Anne; Bousquet, Jean; Chateigner, Nicolas; Gormand, Frederic; Just, Jocelyne; Le Moual, Nicole; Scheinmann, Pierre; Siroux, Valerie; Vervloet, Daniel; Zelenika, Diana; Pin, Isabelle; Kauffmann, Francine; Lathrop, Mark; Demenais, Florence			Effect of 17q21 Variants and Smoking Exposure in Early-Onset Asthma	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							ENVIRONMENTAL TOBACCO-SMOKE; CHILDHOOD ASTHMA; BRONCHIAL HYPERRESPONSIVENESS; ORMDL3 EXPRESSION; CHILDRENS HEALTH; LUNG-FUNCTION; GENE; ASSOCIATION; LIFE; POLYMORPHISM	Background: A genomewide association study has shown an association between variants at chromosome 17q21 and an increased risk of asthma. To elucidate the relationship between this locus and disease, we examined a large, family-based data set that included extensive phenotypic and environmental data from the Epidemiological Study on the Genetics and Environment of Asthma. Methods: We tested 36 single-nucleotide polymorphisms (SNPs) in the 17q21 region in 1511 subjects from 372 families for an association with asthma. We also tested for genetic heterogeneity according to the age at the onset of asthma and exposure to environmental tobacco smoke in early life. Results: Eleven SNPs were significantly associated with asthma (P<0.01), of which three (rs8069176, rs2305480, and rs4795400) were strongly associated (P<0.001). Ordered-subset regression analysis led us to select an onset at 4 years of age or younger to classify patients as having early-onset asthma. Association with early-onset asthma was highly significant (P<10(-5) for four SNPs), whereas no association was found with late-onset asthma. With respect to exposure to environmental tobacco smoke in early life, we observed a significant association with early-onset asthma only in exposed subjects (P<5 x 10(-5) for six SNPs). Under the best-fitting recessive model, homozygous status (GG) at the most strongly associated SNP (rs8069176) conferred an increase in risk by a factor of 2.9, as compared with other genotypes (AG and AA) in the group exposed to environmental tobacco smoke (P=2.8 x 10(-6); P=0.006 for the test for heterogeneity of the SNP effect on early-onset asthma between groups with tobacco exposure and those without such exposure). Conclusions: This study shows that the increased risk of asthma conferred by 17q21 genetic variants is restricted to early-onset asthma and that the risk is further increased by early-life exposure to environmental tobacco smoke. These findings provide a greater understanding of the functional role of the 17q21 variants in the pathophysiology of asthma.	[Bouzigon, Emmanuelle; Corda, Eve; Aschard, Hugues; Chateigner, Nicolas; Lathrop, Mark; Demenais, Florence] Fdn Jean Dausset, CEPH, INSERM, U794, F-75010 Paris, France; [Bouzigon, Emmanuelle; Aschard, Hugues; Chateigner, Nicolas; Demenais, Florence] Univ Evry, Evry, France; [Dizier, Marie-Helene] INSERM, U535, Villejuif, France; [Dizier, Marie-Helene; Le Moual, Nicole; Kauffmann, Francine] Univ Paris 11, Villejuif, France; [Boland, Anne; Zelenika, Diana; Lathrop, Mark] Ctr Natl Genotypage, CEA, Inst Genom, Evry, France; [Bousquet, Jean] Hop Arnaud de Villeneuve, Montpellier, France; [Gormand, Frederic] Ctr Hosp Lyon Sud, F-69310 Pierre Benite, France; [Just, Jocelyne] Hop Enfants Armand Trousseau, Paris, France; [Le Moual, Nicole; Kauffmann, Francine] INSERM, U780, Villejuif, France; [Scheinmann, Pierre] Hop Necker Enfants Malad, Paris, France; [Siroux, Valerie; Pin, Isabelle] INSERM, U823, Grenoble, France; [Vervloet, Daniel] Hop St Marguerite, Marseille, France; [Pin, Isabelle] CHU Grenoble, F-38043 Grenoble, France	Demenais, F (reprint author), Fdn Jean Dausset, CEPH, INSERM, U794, 27 Rue Juliette Dodu, F-75010 Paris, France.	demenais@inserm.fr	PIN, Isabelle/N-3020-2013; Demenais, Florence/G-3298-2013; LeMoual, Nicole/R-8976-2016; siroux, valerie/N-1865-2013	Demenais, Florence/0000-0001-8361-0936; LeMoual, Nicole/0000-0002-2723-5569; 	INSERM; French Ministry of Higher Education and Research; University of Evry; 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, ANR 06-CEBS]; European Commission as part of the Global Allergy and Asthma European Network [FOOD-CT-2004-506378]; GABRIEL consortium; Glaxo SmithKline; Stallergenes; Allerbio; Astra Zeneca; UCB	Supported by INSERM, the French Ministry of Higher Education and Research, and the University of Evry and by grants from the French Agency for Environmental and Occupational Health Safety (Afsset-APR-SE-2004), the French National Agency for Research (ANR 05-SEST-020-02/05-9-97 and ANR 06-CEBS), and the European Commission as part of the Global Allergy and Asthma European Network (FOOD-CT-2004-506378) and the GABRIEL consortium (a multidisciplinary study to identify the genetic and environmental causes of asthma in the European Community; HEALTH-LSH-2005-018996). Dr. Vervloet reports receiving lecture fees from Glaxo SmithKline, Stallergenes, and Allerbio and consulting fees from Astra Zeneca, GlaxoSmithKline, Allerbio, and UCB. No other potential conflict of interest relevant to this article was reported.	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J	Holgate, ST				Holgate, Stephen T.			The sentinel role of the airway epithelium in asthma pathogenesis	IMMUNOLOGICAL REVIEWS			English	Review						asthma; epithelium; inflammation; remodeling; environmental injury; origins; progression; phenotypes	EPIDERMAL-GROWTH-FACTOR; THYMIC STROMAL LYMPHOPOIETIN; RETICULAR BASEMENT-MEMBRANE; GOBLET CELL HYPERPLASIA; CHEMOKINE RECEPTOR 4; BRONCHIAL-ASTHMA; DENDRITIC CELLS; INCREASED EXPRESSION; CHILDHOOD ASTHMA; TIGHT JUNCTIONS	The adoption of the concept that asthma is primarily a disease most frequently associated with elaboration of T-helper 2 (Th2)-type inflammation has led to the widely held concept that its origins, exacerbation, and persistence are allergen driven. Taking aside the asthma that is expressed in non-allergic individuals leaves the great proportion of asthma that is associated with allergy (or atopy) and that often has its onset in early childhood. Evidence is presented that asthma is primarily an epithelial disorder and that its origin as well as its clinical manifestations have more to do with altered epithelial physical and functional barrier properties than being purely linked to allergic pathways. In genetically susceptible individuals, impaired epithelial barrier function renders the airways vulnerable to early life virus infection, and this in turn provides the stimulus to prime immature dendritic cells toward directing a Th2 response and local allergen sensitization. Continued epithelial susceptibility to environmental insults such as viral, allergen, and pollutant exposure and impaired repair responses leads to asthma persistence and provides the mediator and growth factor microenvironment for persistence of inflammation and airway wall remodeling. Increased deposition of matrix in the epithelial lamina reticularis provides evidence for ongoing epithelial barrier dysfunction, while physical distortion of the epithelium consequent upon repeated bronchoconstriction provides additional stimuli for remodeling. This latter response initially serves a protective function but, if exaggerated, may lead to fixed airflow obstruction associated with more severe and chronic disease. Dual pathways in the origins, persistence, and progression of asthma help explain why anti-inflammatory treatments fail to influence the natural history of asthma in childhood and only partially does so in chronic severe disease. Positioning the airway epithelium as fundamental to the origins and persistence of asthma provides a rationale for pursuit of therapeutics that increase the resistance of the airways to environmental insults rather than concentrating all effort on suppressing inflammation.	[Holgate, Stephen T.] Southampton Gen Hosp, Sch Med, Div Infect Inflammat & Immun, Southampton SO16 6YD, Hants, England; [Holgate, Stephen T.] Univ Southampton, Div Infect Inflammat & Immun, Sch Med, Southampton, Hants, England	Holgate, ST (reprint author), Southampton Gen Hosp, Sch Med, Div Infect Inflammat & Immun, MP810,Level F,South Block, Southampton SO16 6YD, Hants, England.	sth@soton.ac.uk			MSD; Novartis	Stephen Holgate is an occasional paid consultant for Novartis, MSD, Almiral, Boehringer Ingelheim and Synairgen. He was a Founder of Synairgen and serves as a non-executive board member. He has also received honoraria for lectures supported by MSD and Novartis.	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J	Simpson, A; John, SL; Jury, F; Niven, R; Woodcock, A; Ollier, WER; Custovic, A				Simpson, Angela; John, Sally L.; Jury, Francine; Niven, Rob; Woodcock, Ashley; Ollier, William E. R.; Custovic, Adrian			Endotoxin exposure, CD14, and allergic disease - An interaction between genes and the environment	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						allergy; asthma; genetics	SERUM IMMUNOGLOBULIN-E; HOUSE-DUST; PROMOTER POLYMORPHISM; SOLUBLE CD14; MANCHESTER ASTHMA; RECEPTOR CD14; IGE LEVELS; EARLY-LIFE; HAY-FEVER; ATOPY	Rationale: High endotoxin exposure may reduce the risk of allergic sensitization. Objective: To determine the relationship between a promoter polymorphism in the CD14 gene (CD14/-159 C to T) and endotoxin exposure in relation to the development of allergic sensitization, eczema, and wheeze within the setting of a birth cohort. Methods: We genotyped 442 children (CD14/-159 C to T; rs2569190). We assessed children for allergic sensitization (IgE > 0.2 kU/L to at least one of seven allergens), eczema (physical examination), and parentally reported wheeze. Endotoxin was measured in house dust. Main Results: Genotype frequencies were consistent with other populations (TT, 25%; CT, 47%; CC, 28%). Sensitization (present in 33% of children) was not associated with genotype. For children with TT and CT genotypes, there was no association between endo toxin and sensitization (odds ratio [OR], 0.95; 95% confidence interval [CI], 0.71-1.23; p = 0.7; and OR, 0.90; 95% CI, 0.77-1.04; p = 0.16, respectively) or endotoxin and eczema (OR, 0.99; 95% CI, 0.81-1.20; p = 0.89; and OR, 1.38; 95% CI, 0.83-2.30; p = 0.22, respectively). In children with the genotype CC, increasing endotoxin load was associated with a marked and significant reduction in the risk of sensitization (OR, 0.70; 95% CI, 0.55-0.89; p = 0.004) and eczema (OR, 0.73; 95% CI, 0.56-0.95; p = 0.02). However, we observed an increased risk of nonatopic wheeze with increasing endotoxin exposure in children with the CC genotype (OR, 1.42; 95% CI, 1.01-1.99; p = 0.04) but not other genotypes. No effect was seen for atopic wheeze. Conclusions: Increasing enclotoxin exposure is associated with reduced risk of allergic sensitization and eczema but with increased risk of nonatopic wheeze in children with the CC genotype at -159 of the CD14 gene. The impact of environmental enclotoxin may be enhanced in individuals with this genotype.	Wythenshawe Hosp, NW Lung Ctr, Acad Div Med & Surg S, Manchester M23 9LT, Lancs, England; Univ Manchester, Ctr Integrated Genom Med Res, Manchester, Lancs, England	Custovic, A (reprint author), Wythenshawe Hosp, NW Lung Ctr, Acad Div Med & Surg S, Manchester M23 9LT, Lancs, England.	adnan.custovic@manchester.ac.uk	Custovic, Adnan/A-2435-2012	Custovic, Adnan/0000-0001-5218-7071; Niven, Robert/0000-0003-2249-960X; Jury, Francine/0000-0003-0683-4041; Woodcock, Ashley/0000-0002-5428-8578; Simpson, Angela/0000-0003-2733-6666			Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Baldini M, 2002, ALLERGY, V57, P188, DOI 10.1034/j.1398-9995.2002.1r152.x; 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; Broadfield E, 2002, J ALLERGY CLIN IMMUN, V109, P969, DOI 10.1067/mai.2002.124772; BURR ML, 1993, ARCH DIS CHILD, V68, P724; Custovic A, 2002, PEDIATR ALLERGY IMMU, V13, P32, DOI 10.1034/j.1399-3038.13.s.15.3.x; Custovic A, 2001, LANCET, V358, P188, DOI 10.1016/S0140-6736(01)05406-X; DUFFY DL, 1990, AM REV RESPIR DIS, V142, P1351; Eder W, 2005, J ALLERGY CLIN IMMUN, V116, P601, DOI 10.1016/j.jaci.2005.05.003; Gao PS, 1999, CLIN GENET, V56, P164; 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; GOYERT SM, 1988, SCIENCE, V239, P497, DOI 10.1126/science.2448876; Heesen M, 2001, INTENS CARE MED, V27, P1770, DOI 10.1007/s001340101106; HEINZEL FP, 1994, INFECT IMMUN, V62, P4244; Hubacek JA, 1999, CIRCULATION, V99, P3218; Ito D, 2000, STROKE, V31, P2661; Kabesch M, 2004, ALLERGY, V59, P520, DOI 10.1111/j.1398-9995.2004.00439.x; Koppelman GH, 2001, AM J RESP CRIT CARE, V163, P965; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; Leung TF, 2003, PEDIATR ALLERGY IMMU, V14, P255, DOI 10.1034/j.1399-3038.2003.00048.x; LeVan TD, 2001, J IMMUNOL, V167, P5838; Litonjua AA, 2005, J ALLERGY CLIN IMMUN, V115, P1056, DOI 10.1016/j.jaci.2005.02.006; Lowe L, 2002, LANCET, V359, P1904, DOI 10.1016/S0140-6736(02)08781-0; Manukyan M, 2005, EUR J IMMUNOL, V35, P911, DOI 10.1002/eji.200425336; MARSH DG, 1994, SCIENCE, V264, P1152, DOI 10.1126/science.8178175; 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; PEARCE N, 1993, EUR RESPIR J, V6, P1455; Phipatanakul W, 2004, PEDIATRICS, V114, P13, DOI 10.1542/peds.114.1.13; PUGIN J, 1994, IMMUNITY, V1, P509, DOI 10.1016/1074-7613(94)90093-0; Sengler C, 2003, CLIN EXP ALLERGY, V33, P166, DOI 10.1046/j.1365-2222.2003.01549.x; Sharma M, 2004, IMMUNOGENETICS, V56, P544, DOI 10.1007/s00251-004-0721-y; Simpson A, 2003, CLIN EXP ALLERGY, V33, P1183, DOI 10.1046/j.1365-2745.2003.01679.x; SIMPSON A, 2004, AM J HUM GENET S, V75, P24; SIMPSON A, 2005, J ALLERGY CLIN IMMUN, V115, pS61, DOI 10.1016/j.jaci.2004.12.257; Simpson BM, 2001, CLIN EXP ALLERGY, V31, P391, DOI 10.1046/j.1365-2222.2001.01050.x; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Strachan DP, 2000, THORAX S1, V55, pS2; Tavernier GOG, 2005, INDOOR AIR, V15, P25, DOI 10.1111/j.1600-0668.2005.00354.x; Topp R, 2003, CLIN EXP ALLERGY, V33, P1659, DOI 10.1111/j.1365-2222.2003.01807.x; Trinchieri Giorgio, 1992, Progress in Growth Factor Research, V4, P355, DOI 10.1016/0955-2235(92)90016-B; Vercelli D, 2003, CLIN EXP ALLERGY, V33, P153, DOI 10.1046/j.1365-2222.2003.01606.x; Viriyakosol S, 2000, J BIOL CHEM, V275, P3144, DOI 10.1074/jbc.275.5.3144; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; Williams HC, 1996, BRIT J DERMATOL, V135, P12; Zambelli-Weiner A, 2005, J ALLERGY CLIN IMMUN, V115, P1203, DOI 10.1016/j.jaci.2005.03.001	50	174	175	0	6	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. 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J	Konig, A; Cockburn, A; Crevel, RWR; Debruyne, E; Grafstroem, R; Hammerling, U; Kimber, I; Knudsen, I; Kuiper, HA; Peijnenburg, AACM; Penninks, AH; Poulsen, M; Schauzu, M; Wal, JM				Konig, A; Cockburn, A; Crevel, RWR; Debruyne, E; Grafstroem, R; Hammerling, U; Kimber, I; Knudsen, I; Kuiper, HA; Peijnenburg, AACM; Penninks, AH; Poulsen, M; Schauzu, M; Wal, JM			Assessment of the safety of foods derived from genetically modified (GM) crops	FOOD AND CHEMICAL TOXICOLOGY			English	Article; Proceedings Paper	Conference of the European-Network-on-Safety-Assessment-of-Genetically-Modified-Food-Crops	MAY 29-30, 2003	Rome, ITALY	European Network Safety Assessment Genetically Modified Food Crops		food; plant biotechnology; genetic modification; genetic engineering; genetic manipulation; transgenic crops; novel foods; recombinant proteins; plant metabolism; regulation; safety assessment; risk analysis; molecular characterisation; toxicology; allergy; substantial equivalence; unintended effects; bioinformatics; in vitro test methods; in vivo test methods; animal testing; post market monitoring; estimated consumption; exposure assessment; compositional analysis; advanced analytical methods; profiling	SELECTABLE MARKER GENES; IN-VITRO TOXICOLOGY; BETA-LACTOGLOBULIN; RICE GENOME; INTRACHROMOSOMAL RECOMBINATION; POTENTIAL ALLERGENICITY; CONVENTIONAL COTTONSEED; SUBSTANTIAL EQUIVALENCE; PROTEIN ALLERGENICITY; CONSUMPTION SURVEYS	This paper provides guidance on how to assess the safety of foods derived from genetically modified crops (GM crops); it summarises conclusions and recommendations of Working Group I of the ENTRANSFOOD project. The paper provides an approach for adapting the test strategy to the characteristics of the modified crop and the introduced trait, and assessing potential unintended effects from the genetic modification. The proposed approach to safety assessment starts with the comparison of the new GM crop with a traditional counterpart that is generally accepted as safe based on a history of human food use (the concept of substantial equivalence). This case-focused approach ensures that foods derived from GM crops that have passed this extensive test-regime are as safe and nutritious as currently consumed plant-derived foods. The approach is suitable for current and future GM crops with more complex modifications. First, the paper reviews test methods developed for the risk assessment of chemicals, including food additives and pesticides, discussing which of these methods are suitable for the assessment of recombinant proteins and whole foods. Second, the paper presents a systematic approach to combine test methods for the safety assessment of foods derived from a specific GM crop. Third, the paper provides an overview on developments in this area that may prove of use in the safety assess-merit of GM crops, and recommendations for research priorities. It is concluded that the combination of existing test methods provides a sound test-regime to assess the safety of GM crops. Advances in our understanding of molecular biology, biochemistry, and nutrition may in future allow further improvement of test methods that will over time render the safety assessment of foods even more effective and informative. (C) 2004 Elsevier Ltd. All rights reserved.	Harvard Univ, Sch Publ Hlth, Ctr Risk Anal, Boston, MA 02115 USA; Monsanto Serv Int, Sci Affairs, Agr Sector, B-1150 Brussels, Belgium; Unilever Res Colworth, SEAC Toxicol Dept, Sharnbrook MK44 1LQ, Beds, England; Bayer CropSci, Regulatory Toxicol Herbicides & Biotechnol, F-06903 Sophia Antipolis, France; Karolinska Inst, Inst Environm Med, SE-17177 Stockholm, Sweden; Swedish Natl Food Adm, SE-751 Uppsala, Sweden; Syngenta UK, Cent Toxicol Lab, Macclesfield SK10 4TJ, Cheshire, England; Danish Vet & Food Adm, Inst Food Safety & Toxicol, DK-2860 Soborg, Denmark; Univ Wageningen & Res Ctr, Inst Food Safety, RIKILT, NL-6700 AE Wageningen, Netherlands; TNO, Nutr & Food Res, NL-3700 AJ Zeist, Netherlands; Fed Inst Risk Assessment, Ctr Novel Foods & Genet Engn, D-14195 Berlin, Germany; CEA Saclay, Serv Pharmacol & Immunol, Lab Associe INRA, CEA Immuno Allergie Alimentaire, F-91191 Gif Sur Yvette, France	Konig, A (reprint author), Harvard Univ, Sch Publ Hlth, Ctr Risk Anal, 718 Huntington Ave, Boston, MA 02115 USA.	ariane_koenig@harvard.edu					Aalberse RC, 2000, J ALLERGY CLIN IMMUN, V106, P228, DOI 10.1067/mai.2000.108434; Adel-Patient K, 2003, CLIN EXP ALLERGY, V33, P376, DOI 10.1046/j.1365-2222.2003.01613.x; Adel-Patient K, 2000, J IMMUNOL METHODS, V235, P21, DOI 10.1016/S0022-1759(99)00210-0; *ALLERGEST, 2003, QLK1CT200101239 ALLE; Astwood JD, 1996, NAT BIOTECHNOL, V14, P1269, DOI 10.1038/nbt1096-1269; Barlow SM, 2002, FOOD CHEM TOXICOL, V40, P145, DOI 10.1016/S0278-6915(01)00117-X; Barratt MD, 1998, ENVIRON HEALTH PERSP, V106, P459, DOI 10.2307/3433795; Bennetzen J, 2002, SCIENCE, V296, P60, DOI 10.1126/science.1071402; Berberich SA, 1996, J AGR FOOD CHEM, V44, P365, DOI 10.1021/jf950304i; Betz FS, 2000, REGUL TOXICOL PHARM, V32, P156, DOI 10.1006/rtph.2000.1426; Bindslev-Jensen C, 2002, ALLERGY, V57, P741, DOI 10.1034/j.1398-9995.2002.23797.x; Brake J, 1998, POULTRY SCI, V77, P648; Bredehorst R, 2001, J CHROMATOGR B, V756, P33, DOI 10.1016/S0378-4347(01)00069-X; Bufe A, 1998, INT ARCH ALLERGY IMM, V117, P215, DOI 10.1159/000024013; CBAC (Canadian Biotechnology Advisory Committee), 2002, IMPR REG GEN MOD FOO; CELLINI F, 2004, FOOD CHEM TOXICOLOGY; *CFIA, 1998, D9613 CAN FOOD INSP; CHAN MT, 1992, PLANT CELL PHYSIOL, V33, P577; CHASSY BM, 2002, BIOTECHNOLOGY SAFETY; Clark J. 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Toxicol.	JUL	2004	42	7					1047	1088		10.1016/j.fct.2004.02.019		42	Food Science & Technology; Toxicology	Food Science & Technology; Toxicology	827TW	WOS:000221924900003	15123382	
J	Delfino, RJ				Delfino, RJ			Epidemiologic evidence for asthma and exposure to air toxics: Linkages between occupational, indoor, and community air pollution research	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Review						asthma; diesel; epidemiology; toxic air pollutants; volatile organic compounds	DIESEL EXHAUST PARTICLES; ENVIRONMENTAL TOBACCO-SMOKE; VOLATILE ORGANIC-COMPOUNDS; CHRONIC RESPIRATORY SYMPTOMS; LUNG-FUNCTION GROWTH; TERM AMBIENT CONCENTRATIONS; NITROGEN-DIOXIDE EXPOSURE; BUS GARAGE WORKERS; CHILDHOOD ASTHMA; AUTOMOBILE EXHAUST	Outdoor ambient air pollutant exposures in communities are relevant to the acute exacerbation and possibly the onset of asthma. However, the complexity of pollutant mixtures and etiologic heterogeneity of asthma has made it difficult to identify causal components in those mixtures. Occupational exposures associated with asthma may yield clues to causal components in ambient air pollution because such exposures are often identifiable as single-chemical agents (e.g., metal compounds). However, translating occupational to community exposure-response relationships is limited. Of the air toxics found to cause occupational asthma, only formaldehyde has been frequently investigated in epidemiologic studies of allergic respiratory responses to indoor air, where general consistency can be shown despite lower ambient exposures. The specific volatile organic compounds (VOCs) identified in association with occupational asthma are generally not the same as those in studies showing respiratory effects of VOC mixtures on nonoccupational adult and pediatric asthma. In addition, experimental evidence indicates that airborne polycyclic aromatic hydrocarbon (PAH) exposures linked to diesel exhaust particles (DEPs) have proinflammatory effects on airways, but there is insufficient supporting evidence from the occupational literature of effects of DEPs on asthma or lung function. In contrast, nonoccupational epidemiologic studies have frequently shown associations between allergic responses or asthma with exposures to ambient air pollutant mixtures with PAH components, including black smoke, high home or school traffic density (particularly truck traffic), and environmental tobacco smoke. Other particle-phase and gaseous co-pollutants are likely causal in these associations as well. Epidemiologic research on the relationship of both asthma onset and exacerbation to air pollution is needed to disentangle effects of air toxics; from monitored criteria air pollutants such as particle mass. Community studies should focus on air toxics expected to have adverse respiratory effects based on biological mechanisms, particularly irritant and immunological pathways to asthma onset and exacerbation.	Univ Calif Irvine, Dept Med, Div Epidemiol, Irvine, CA 92697 USA	Delfino, RJ (reprint author), Univ Calif Irvine, Dept Med, Div Epidemiol, 224 Irvine Hall, Irvine, CA 92697 USA.						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Health Perspect.	AUG	2002	110			4			573	589				17	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	586ER	WOS:000177572100012	12194890	
J	Hogan, SP; Mishra, A; Brandt, EB; Royalty, MP; Pope, SM; Zimmermann, N; Foster, PS; Rothenberg, ME				Hogan, SP; Mishra, A; Brandt, EB; Royalty, MP; Pope, SM; Zimmermann, N; Foster, PS; Rothenberg, ME			A pathological function for eotaxin and eosinophils in eosinophilic gastrointestinal inflammation	NATURE IMMUNOLOGY			English	Article							MAJOR BASIC-PROTEIN; IN-VIVO; MUCOSAL EOSINOPHILS; TISSUE EOSINOPHILIA; CHEMOKINE EOTAXIN; INTERFERON-GAMMA; FOOD ALLERGY; GASTROENTERITIS; DISEASE; INTERLEUKIN-5	Although eosinophils have been implicated in the pathogenesis of gastrointestinal disorders, their function has not been established. Using a murine model of oral antigen-induced eosinophil-associated gastrointestinal disease, we report the pathological consequences of eosinophilic inflammation and the involvement of eotaxin and eosinophils, Exposure of mice to enteric-coated antigen promotes an extensive T helper 2-associated eosinophilic inflammatory response involving the esophagus, stomach, small intestine and Peyer's patches as well as the development of gastric dysmotility, gastromegaly and cachexia. Electron microscopy shows eosinophils in proximity to damaged axons, which indicated that eosinophils were mediating a pathologic response. In addition, mice deficient in eotaxin have impaired eosinophil recruitment and are protected from gastromegaly and cachexia. These results establish a critical pathological function for eotaxin and eosinophils in gastrointestinal allergic hypersensitivity.	Childrens Hosp, Med Ctr, Dept Pediat, Div Pulm Med Allergy & Clin Immunol, Cincinnati, OH 45229 USA; Australian Natl Univ, John Curtin Sch Med Res, Div Biochem & Mol Biol, Canberra, ACT 0200, Australia	Rothenberg, ME (reprint author), Childrens Hosp, Med Ctr, Dept Pediat, Div Pulm Med Allergy & Clin Immunol, Cincinnati, OH 45229 USA.		Foster, Paul/G-5057-2013		NIAID NIH HHS [R01 AI42242-02, R01 AI45898-01]		ABUGHAZALEH RI, 1989, J IMMUNOL, V142, P2393; Adamko DJ, 1999, J EXP MED, V190, P1465, DOI 10.1084/jem.190.10.1465; CELLO JP, 1979, AM J MED, V67, P1097, DOI 10.1016/0002-9343(79)90652-1; Cieslewicz G, 1999, J CLIN INVEST, V104, P301, DOI 10.1172/JCI7010; COLLINS PD, 1995, J EXP MED, V182, P1169, DOI 10.1084/jem.182.4.1169; Desreumaux P, 1996, GASTROENTEROLOGY, V110, P768, DOI 10.1053/gast.1996.v110.pm8608886; DOBBINS JW, 1977, GASTROENTEROLOGY, V72, P1312; DVORAK AM, 1993, INT ARCH ALLERGY IMM, V102, P33; Erjefalt JS, 2000, AM J RESP CRIT CARE, V161, P2074; Evans CM, 1997, J CLIN INVEST, V100, P2254, DOI 10.1172/JCI119763; FURUTA GT, 1995, CURR OPIN GASTROEN, V11, P541, DOI 10.1097/00001574-199511000-00013; GarciaZepeda EA, 1996, NAT MED, V2, P449, DOI 10.1038/nm0496-449; Gleich GJ, 1997, P NATL ACAD SCI USA, V94, P2101, DOI 10.1073/pnas.94.6.2101; GLEICH GJ, 1993, ANNU REV MED, V44, P85, DOI 10.1146/annurev.med.44.1.85; GLEICH GJ, 1979, J IMMUNOL, V123, P2925; Grimaldi JC, 1999, J LEUKOCYTE BIOL, V65, P846; Gutierrez-Ramos JC, 1999, IMMUNOL TODAY, V20, P500, DOI 10.1016/S0167-5699(99)01522-4; Hogan SP, 2000, P NATL ACAD SCI USA, V97, P6681, DOI 10.1073/pnas.97.12.6681; JAFFE JS, 1994, J CLIN IMMUNOL, V14, P299, DOI 10.1007/BF01540983; KELLY KJ, 1995, GASTROENTEROLOGY, V109, P1503, DOI 10.1016/0016-5085(95)90637-1; Kelly KJ, 2000, J PEDIAT GASTROENT S, V30, P28; KESHAVARZIAN A, 1985, GASTROENTEROLOGY, V88, P1041; KLEIN NC, 1970, MEDICINE, V49, P299; LEE RG, 1985, AM J SURG PATHOL, V9, P475, DOI 10.1097/00000478-198507000-00002; Lin S, 1997, DIGEST DIS SCI, V42, P907, DOI 10.1023/A:1018808329603; Litwin A, 1998, BIODRUGS, V9, P261, DOI 10.2165/00063030-199809040-00001; Lloyd CM, 2000, J EXP MED, V191, P265, DOI 10.1084/jem.191.2.265; Lowichik A, 1996, MODERN PATHOL, V9, P110; MESTECKY J, 1978, J CLIN INVEST, V61, P71; MICHAEL JG, 1989, IMMUNOL INVEST, V18, P1049, DOI 10.3109/08820138909030606; Mishra A, 2001, J CLIN INVEST, V107, P83, DOI 10.1172/JCI10224; Mishra A, 2000, BLOOD, V96, P1538; Mishra A, 1999, J CLIN INVEST, V103, P1719, DOI 10.1172/JCI6560; Rothenberg ME, 1999, AM J RESP CELL MOL, V21, P291; Rothenberg ME, 1997, J EXP MED, V185, P785, DOI 10.1084/jem.185.4.785; Rothenberg ME, 1998, NEW ENGL J MED, V338, P1592; Sampson HA, 1997, JAMA-J AM MED ASSOC, V278, P1888, DOI 10.1001/jama.278.22.1888; Sampson HA, 1999, J ALLERGY CLIN IMMUN, V103, P717, DOI 10.1016/S0091-6749(99)70411-2; Schleimer RP, 1998, CLIN EXP ALLERGY, V28, P15; Shi HZ, 2000, J CLIN INVEST, V105, P945, DOI 10.1172/JCI8945; Stelts D, 1998, AM J RESP CELL MOL, V18, P463; TALLEY NJ, 1990, GUT, V31, P54, DOI 10.1136/gut.31.1.54; TALLEY NJ, 1992, GASTROENTEROLOGY, V103, P137; TORPIER G, 1988, CLIN EXP IMMUNOL, V74, P404; van den Bos GAM, 1995, EUR J PUBLIC HEALTH, V5, P29, DOI 10.1093/eurpub/5.1.29; Weller P F, 1996, Eur Respir J Suppl, V22, p109s; Woerly G, 1999, J EXP MED, V190, P487, DOI 10.1084/jem.190.4.487	47	174	180	0	4	NATURE AMERICA INC	NEW YORK	345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA	1529-2908			NAT IMMUNOL	Nat. Immunol.	APR	2001	2	4					353	360		10.1038/86365		8	Immunology	Immunology	420AZ	WOS:000167982900017	11276207	
J	Bell, ML; Peng, RD; Dominici, F				Bell, ML; Peng, RD; Dominici, F			The exposure-response curve for ozone and risk of mortality and the adequacy of current ozone regulations	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						mortality; ozone; regulations; threshold	DISTRIBUTED LAG MODELS; LARGEST US CITIES; AIR-POLLUTION; PARTICULATE MATTER; AMBIENT OZONE; HEALTH; CHILDREN; ASTHMA	Time-series analyses have shown that ozone is associated with increased risk of premature mortality, but little is known about how O-3 affects health at low concentrations. A critical scientific and policy question is whether a threshold level exists below which O-3 does not adversely affect mortality. We developed and applied several statistical models to data on air pollution, weather, and mortality for 98 U.S. urban communities for the period 1987-2000 to estimate the exposure-response curve for tropospheric O-3 and risk of mortality and to evaluate whether a "safe" threshold level exists. Methods included a linear approach and subset, threshold, and spline models. All results indicate that any threshold would exist at very low concentrations, far below current U.S. and international regulations and nearing background levels. For example, under a scenario in which the U.S. Environmental Protection Agency's 8-hr regulation is met every day in each community, there was still a 0.30% increase in mortality per 10-ppb increase in the average of the same and previous days' O-3 levels (95% posterior interval, 0.15-0.45%). Our findings indicate that even low levels of tropospheric O-3 are associated with increased risk of premature mortality. Interventions to further reduce O-3 pollution would benefit public health, even in regions that meet current regulatory standards and guidelines.	Yale Univ, Sch Forestry & Environm Studies, New Haven, CT 06511 USA; Johns Hopkins Bloomberg Sch Publ Hlth, Dept Biostat, Baltimore, MD USA	Bell, ML (reprint author), Yale Univ, Sch Forestry & Environm Studies, 205 Prospect St, New Haven, CT 06511 USA.	michelle.bell@yale.edu			NIEHS NIH HHS [ES 012054-01, P30 ES 03819, P30 ES003819, R01 ES012054, R01 ES015028]		Akaike H., 1973, INT S INF THEOR, P267, DOI DOI 10.2307/2334537; American Thoracic Society, 2000, AM J RESP CRIT CARE, V161, P665; Anderson HR, 2004, META ANAL TIME SERIE; Bell ML, 2004, JAMA-J AM MED ASSOC, V292, P2372, DOI 10.1001/jama.292.19.2372; BELL ML, 2005, EPIDEMIOLOGY, V4, P436; Broeckaert F, 1999, LANCET, V353, P900, DOI 10.1016/S0140-6736(99)00540-1; Brunekreef B, 2002, LANCET, V360, P1233, DOI 10.1016/S0140-6736(02)11274-8; *CAL ENV PROT AG, 2005, CAL AD NEW OZ STAND; Canadian Council of Ministers of the Environment CCME, 2000, CAN WID STAND PART M; Chan CC, 2005, ENVIRON HEALTH PERSP, V113, P735, DOI 10.1289/ehp.7636; Daniels MJ, 2000, AM J EPIDEMIOL, V152, P397, DOI 10.1093/aje/152.5.397; DANIELS MJ, 2004, NATL MORBIDITY MORTA; Dominici F, 2000, J ROY STAT SOC A STA, V163, P263, DOI 10.1111/1467-985X.00170; Dominici F, 2002, J AM STAT ASSOC, V97, P100, DOI 10.1198/016214502753479266; *EUR COMM, 2002, DIR 2002 3 EC EUR PA; Everson PJ, 2000, J ROY STAT SOC B, V62, P399, DOI 10.1111/1467-9868.00239; FIORE A, 2004, J GEOPHYS RES ATMOS; Fiore A.M., 2003, J GEOPHYS RES ATMOS; Gent JF, 2003, JAMA-J AM MED ASSOC, V290, P1859, DOI 10.1001/jama.290.14.1859; Hoek G, 1997, ARCH ENVIRON HEALTH, V52, P455; Huang Y, 2005, ENVIRONMETRICS, V16, P547, DOI 10.1002/env.721; Hubbell BJ, 2005, ENVIRON HEALTH PERSP, V113, P73; *IHAPSS, 2006, INT BAS HLTH AIR POL; ITO K, 2005, EPIDEMIOLOGY, V4, P446; Kim SY, 2004, ENVIRON RES, V94, P113, DOI 10.1016/j.envres.2003.09.006; Knowlton K, 2004, ENVIRON HEALTH PERSP, V112, P1557, DOI 10.1289/ehp.7163; LEVY JI, 2005, EPIDEMIOLOGY, V4, P458; McConnell R, 2002, LANCET, V359, P386, DOI 10.1016/S0140-6736(02)07597-9; McCullagh P, 1989, GENERALIZED LINEAR M; Peng RD, 2005, AM J EPIDEMIOL, V161, P585, DOI 10.1093/aje/kwi075; Samet JM, 2000, NEW ENGL J MED, V343, P1742, DOI 10.1056/NEJM200012143432401; SAMET JM, 2000, HLTH EFFECTS I, V94, P1; Samet J.M., 2000, NATL MORBIDITY MORTA; *SAN JAOQ VALL AIR, 2006, OZONE; *TLNISE, 2006, 2 LEV NORM IND SAMPL; Review of the National Ambient Air Quality Standards for Particulate Matter, 2005, EPA452R05005; EPA, 2004, EPA454K04001; US EPA, 1997, FED REGISTER, V62, P38855; *US EPA, 1996, EPA600P93004ACF; Welty LJ, 2005, AM J EPIDEMIOL, V162, P80, DOI 10.1093/aje/kwi157; World Health Organization, 2000, WHO REG PUBL EUR SER, V91; World Health Organization, 1978, INT CLASS DIS; World Health Organization, 1993, INT CLASS DIS	43	173	177	6	44	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	APR	2006	114	4					532	536		10.1289/ehp.8816		5	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	030QX	WOS:000236650500036	16581541	
J	Gauvreau, GM; O'Byrne, PM; Boulet, LP; Wang, Y; Cockcroft, D; Bigler, J; FitzGerald, JM; Boedigheimer, M; Davis, BE; Dias, C; Gorski, KS; Smith, L; Bautista, E; Comeau, MR; Leigh, R; Parnes, JR				Gauvreau, Gail M.; O'Byrne, Paul M.; Boulet, Louis-Philippe; Wang, Ying; Cockcroft, Donald; Bigler, Jeannette; FitzGerald, J. Mark; Boedigheimer, Michael; Davis, Beth E.; Dias, Clapton; Gorski, Kevin S.; Smith, Lynn; Bautista, Edgar; Comeau, Michael R.; Leigh, Richard; Parnes, Jane R.			Effects of an Anti-TSLP Antibody on Allergen-Induced Asthmatic Responses	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							THYMIC STROMAL LYMPHOPOIETIN; INDUCED AIRWAY RESPONSES; HUMAN EPITHELIAL-CELLS; MAST-CELLS; INFLAMMATION; SPUTUM; REPRODUCIBILITY; RESPONSIVENESS; MEPOLIZUMAB; EXPRESSION	BACKGROUND Thymic stromal lymphopoietin (TSLP) is an epithelial-cell-derived cytokine that may be important in initiating allergic inflammation. AMG 157 is a human anti-TSLP monoclonal immunoglobulin G2 lambda that binds human TSLP and prevents receptor interaction. METHODS In this double-blind, placebo-controlled study, we randomly assigned 31 patients with mild allergic asthma to receive three monthly doses of AMG 157 (700 mg) or placebo intravenously. We conducted allergen challenges on days 42 and 84 to evaluate the effect of AMG 157 in reducing the maximum percentage decrease in the forced expiratory volume in 1 second (FEV1). We also measured the fraction of nitric oxide in exhaled air, blood and sputum eosinophils, and airway hyperresponsiveness. The primary end point was the late asthmatic response, as measured 3 to 7 hours after the allergen challenge. RESULTS AMG 157 attenuated most measures of allergen-induced early and late asthmatic responses. The maximum percentage decrease in the FEV1 during the late response was 34.0% smaller in the AMG-157 group than in the placebo group on day 42 (P=0.09) and 45.9% smaller on day 84 (P=0.02). In addition, patients receiving AMG 157 had significant decreases in levels of blood and sputum eosinophils before and after the allergen challenge and in the fraction of exhaled nitric oxide. There were 15 adverse events in the AMG-157 group, as compared with 12 in the placebo group; there were no serious adverse events. CONCLUSIONS Treatment with AMG 157 reduced allergen-induced bronchoconstriction and indexes of airway inflammation before and after allergen challenge. These findings are consistent with a key role for TSLP in allergen-induced airway responses and persistent airway inflammation in patients with allergic asthma. Whether anti-TSLP therapeutics will have clinical value cannot be determined from these data. (Funded by Amgen; ClinicalTrials.gov number, NCT01405963.)	[Gauvreau, Gail M.; O'Byrne, Paul M.] McMaster Univ, Dept Med, Firestone Inst Resp Hlth, Hamilton, ON L8N 3Z5, Canada; [Boulet, Louis-Philippe] Univ Laval, Inst Univ Cardiol & Pneumol Quebec, Quebec City, PQ, Canada; [Cockcroft, Donald; Davis, Beth E.] Univ Saskatchewan, Div Respirol Crit Care & Sleep Med, Saskatoon, SK, Canada; [FitzGerald, J. Mark] Univ British Columbia, Inst Heart & Lung Hlth, Vancouver, BC V5Z 1M9, Canada; [Leigh, Richard] Univ Calgary, Fac Med, Snyder Inst Chron Dis, Calgary, AB, Canada; [Wang, Ying; Boedigheimer, Michael; Dias, Clapton; Gorski, Kevin S.; Smith, Lynn; Bautista, Edgar; Parnes, Jane R.] Amgen Inc, Thousand Oaks, CA USA; [Bigler, Jeannette; Comeau, Michael R.] Amgen Inc, Seattle, WA USA	O'Byrne, PM (reprint author), McMaster Univ, Dept Med, HSC 3W10,1200 Main St W, Hamilton, ON L8N 3Z5, Canada.	obyrnep@mcmaster.ca		O'Byrne, Paul/0000-0003-0979-281X	Amgen; AllerGen Network of Centers of Excellence	Supported by Amgen. The AllerGen Network of Centers of Excellence provided administrative funding for the study centers.	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Engl. J. Med.	MAY 29	2014	370	22					2102	2110		10.1056/NEJMoa1402895		9	Medicine, General & Internal	General & Internal Medicine	AH9BM	WOS:000336434000008	24846652	
J	Landrigan, PJ; Lioy, PJ; Thurston, G; Berkowitz, G; Chen, LC; Chillrud, SN; Gavett, SH; Georgopoulos, PG; Geyh, AS; Levin, S; Perera, F; Rappaport, SM; Small, C				Landrigan, PJ; Lioy, PJ; Thurston, G; Berkowitz, G; Chen, LC; Chillrud, SN; Gavett, SH; Georgopoulos, PG; Geyh, AS; Levin, S; Perera, F; Rappaport, SM; Small, C		NIEHS World Trade Ctr Working Grp	Health and environmental consequences of the world trade center disaster	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; airway hyperresponsiveness; asbestos; occupational lung disease; PM2.5; PM10; small for gestational age (SGA)	NEW-YORK-CITY; FINE PARTICULATE MATTER; 11TH TERRORIST ATTACKS; CENTER SITE; MALIGNANT MESOTHELIOMA; LOWER MANHATTAN; AIR-POLLUTION; FETAL-GROWTH; CENTER COUGH; GROUND-ZERO	The attack on the World Trade Center (WTC) created an acute environmental disaster of enormous magnitude. This study characterizes the environmental exposures resulting from destruction of the WTC and assesses their effects on health. Methods include ambient air sampling; analyses of outdoor and indoor settled dust; high-altitude imaging and modeling of the atmospheric plume; inhalation studies of WTC dust in mice; and clinical examinations, community surveys, and prospective epidemiologic studies of exposed populations. WTC dust was found to consist predominantly (95%) of coarse particles and contained pulverized cement, glass fibers, asbestos, lead, polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), and polychlorinated furans and dioxins. Airborne particulate levels were highest immediately after the attack and declined thereafter. Particulate levels decreased sharply with distance from the WTC. Dust pH was highly alkaline (pH 9.0-11.0). Mice exposed to WTC dust showed only moderate pulmonary inflammation but marked bronchial hyperractivity. Evaluation of 10,116 firefighters showed exposure-related. P increases in cough and bronchial hyperreactivity. Evaluation of 183 cleanup workers showed new-onset cough (33%), wheeze (18%), and phlegm production (24%). Increased frequency of new-onset cough, wheeze, and shortness of breath were also observed in community residents. Follow-up of 182 pregnant women who were either inside or near the WTC on I I September showed a 2-fold increase in small-for-gestational-age (SGA) infants. In summary, environmental exposures after the WTC disaster were associated with significant adverse effects on health. The high alkalinity of WTC dust produced bronchial hyperreactivity, persistent cough, and increased risk of asthma. Plausible causes of the observed increase in SGA infants include maternal exposures to PAH and particulates. Future risk of mesothelioma may be increased, particularly among workers and volunteers exposed occupationally to asbestos. Continuing follow-up of all exposed populations is required to document the long-term consequences of the disaster.	CUNY Mt Sinai Sch Med, New York, NY 10029 USA; Environm & Occupat Hlth Sci Inst New Jersey, New Brunswick, NJ USA; NYU, Sch Med, Nelson Inst Environm Med, Tuxedo Pk, NY 10987 USA; Columbia Univ, Lamont Doherty Earth Observ, Palisades, NY 10964 USA; US EPA, Off Res & Dev, Res Triangle Pk, NC 27711 USA; Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA; Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD USA; Univ N Carolina, Sch Publ Hlth, Chapel Hill, NC USA	Landrigan, PJ (reprint author), CUNY Mt Sinai Sch Med, 1 Gustave L Levy Pl,Box 1057, New York, NY 10029 USA.	phil.landrigan@mssm.edu	Lioy, Paul/F-6148-2011; Cjem, Lung-Chi/H-5030-2012		NIEHS NIH HHS [P30 ES03819, P30 ES00260, P30 ES009089, P30 ES05022, P30ES09089-04S, P42ES05948, P42ES07384]		*AM THOR SOC, 1994, STAND SPIR 1994 UPD; Anderson H.A., 1982, P WORLD S ASB MONT M, P349; Bayley N., 1993, BAYLEY SCALES INFANT; Beckett WS, 2002, AM J RESP CRIT CARE, V166, P785, DOI 10.1164/rccm.2208001; Berkowitz GS, 2003, JAMA-J AM MED ASSOC, V290, P595, DOI 10.1001/jama.290.5.595-b; Bobak M, 2001, EPIDEMIOLOGY, V12, P358, DOI 10.1097/00001648-200105000-00018; Boscarino Joseph A, 2002, Int J Emerg Ment Health, V4, P143; BRENNER WE, 1976, AM J OBSTET GYNECOL, V126, P555; Camus M, 1998, NEW ENGL J MED, V338, P1565, DOI 10.1056/NEJM199805283382201; Canfield RL, 2001, INFANCY, V2, P197, DOI 10.1207/S15327078IN0202_5; Brezsnyak M. 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Health Perspect.	MAY	2004	112	6					731	739		10.1289/ehp.6702		9	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	822DD	WOS:000221514400040	15121517	
J	Mannino, DM				Mannino, DM			COPD - Epidemiology, prevalence, morbidity and mortality, and disease heterogeneity	CHEST			English	Article; Proceedings Paper	COPD 2001 International Symposium	APR, 2001	LUND, SWEDEN			COPD; epidemiology; mortality; prevalence; risk factors	OBSTRUCTIVE PULMONARY-DISEASE; AIR-FLOW OBSTRUCTION; UNITED-STATES; LUNG-DISEASE; ASTHMA; AIRWAYS; HEALTH; BURDEN; HYPERRESPONSIVENESS; NUTRITION	COPD continues to cause a heavy health and economic burden both in the United states and around the world. Some of the risk factors for COPD are well-known and include smoking, occupational exposures, air pollution, airway hyperresponsiveness, asthma, and certain genetic variations, although many questions, such as why <20% of smokers develop significant airway obstruction, remain. Precise definitions of COPD vary and are frequently dependent on an accurate diagnosis of the problem by a physician. These differences in the definition of COPD can have large effects on the estimates of COPD in the population. Furthermore, evidence that COPD represents several different disease processes with potentially different interventions continues to emerge. In most 4 the world, COPD prevalence and mortality are still increasing and likely will continue to rise in response to increases in smoking, particularly by women and adolescents. Resources aimed at smoking cessation and prevention, COPD education and early detection, and better treatment will be of the most benefit in our continuing efforts against this important cause of morbidity and mortality.	Ctr Dis Control & Prevent, Air Pollut Resp Hlth Branch, Div Environm Hazards & Hlth Effects, Natl Ctr Environm Hlth, Atlanta, GA 30333 USA	Mannino, DM (reprint author), Ctr Dis Control & Prevent, Air Pollut Resp Hlth Branch, Div Environm Hazards & Hlth Effects, Natl Ctr Environm Hlth, 1600 Clifton Rd,MS E-17, Atlanta, GA 30333 USA.			Mannino, David/0000-0003-3646-7828			[Anonymous], 1994, VITAL HLTH STAT, V32, P1; AGUILANIU B, 1992, JPEN-PARENTER ENTER, V16, P248, DOI 10.1177/0148607192016003248; American Thoracic Society, 1991, AM REV RESPIR DIS, V144, P1202, DOI 10.1164/ajrccm/144.5.1202; American Thoracic Society, 1987, AM REV RESPIR DIS, V136, P1285, DOI 10.1164/ajrccm/136.5.1285; American thoracic society, 1995, AM J RESP CRIT CARE, V152, pS77; BECKLAKE MR, 1989, AM REV RESPIR DIS, V140, pS85; Bestall JC, 1999, THORAX, V54, P581; CAMILLI AE, 1991, AM J EPIDEMIOL, V133, P795; Centers for Disease Control and Prevention, 2000, MMWR-MORBID MORTAL W, V49, P908; CHANG JT, 1995, CHEST, V108, P736, DOI 10.1378/chest.108.3.736; Dennison C, 2000, VITAL HLTH STAT 1, V39, P1; DIRKSEN A, 1991, DAN MED BULL, V38, P486; ENRIGHT PL, 1991, AM REV RESPIR DIS, V143, P1215; Hansen EF, 1999, AM J RESP CRIT CARE, V159, P1267; HEGELE RG, 1995, AM J RESP CRIT CARE, V151, P1659; Hogg J C, 2000, Semin Respir Infect, V15, P32; Hurd SS, 2000, CHEST, V117, p336S, DOI 10.1378/chest.117.5_suppl_2.336S; KANNER RE, 1994, AM J RESP CRIT CARE, V150, P956; KEELECARD G, 1993, PUBLIC HEALTH NURS, V10, P245, DOI 10.1111/j.1525-1446.1993.tb00060.x; Kraft M, 1998, AM J RESP CRIT CARE, V158, P998; Lopez AD, 1998, NAT MED, V4, P1241, DOI 10.1038/3218; Mannino DM, 2000, ARCH INTERN MED, V160, P1683, DOI 10.1001/archinte.160.11.1683; Mannino DM, 1997, AM J RESP CRIT CARE, V156, P814; McCaig LF, 2000, ADV DATA, V313, P1; Michaud CM, 2001, JAMA-J AM MED ASSOC, V285, P535, DOI 10.1001/jama.285.5.535; Murphy S L, 2000, Natl Vital Stat Rep, V48, P1; National Center for Health Statistics, 1999, VITAL HLTH STAT 2, V126, P1; Piccioni P, 1998, J CLIN EPIDEMIOL, V51, P547, DOI 10.1016/S0895-4356(98)00022-5; Popover JR, 2000, VITAL HLTH STAT 13, V148, P1; Rennard SI, 1998, CHEST, V113, p235S, DOI 10.1378/chest.113.4_Supplement.235S; Rennard SI, 2000, CHEST, V117, p360S, DOI 10.1378/chest.117.5_suppl_2.360S; SHEFFER AL, 1993, MED CARE, V31, pMS20; SIAFAKAS NM, 1995, EUR RESPIR J, V8, P1398, DOI 10.1183/09031936.95.08081398; Silverman EK, 1996, MED CLIN N AM, V80, P501; SLUSARCICK AL, 2000, ADV DATA, V317, P1; Snider G L, 1995, Monaldi Arch Chest Dis, V50, P3; SNIDER GL, 1986, AM REV RESPIR DIS, V133, P942; Sullivan SD, 2000, CHEST, V117, P5; Ulrik CS, 1999, EUR RESPIR J, V14, P892, DOI 10.1034/j.1399-3003.1999.14d27.x; ULRIK CS, 1995, CHEST, V108, P10, DOI 10.1378/chest.108.1.10; World Health Organization, 2001, GOLD GLOB STRAT MAN	41	172	183	1	12	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	MAY	2002	121	5		S			121S	126S		10.1378/chest.121.5_suppl.121S		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	554HV	WOS:000175730500003	12010839	
J	Salimi, M; Barlow, JL; Saunders, SP; Xue, LZ; Gutowska-Owsiak, D; Wang, XW; Huang, LC; Johnson, D; Scanlon, ST; McKenzie, ANJ; Fallon, PG; Ogg, GS				Salimi, Maryam; Barlow, Jillian L.; Saunders, Sean P.; Xue, Luzheng; Gutowska-Owsiak, Danuta; Wang, Xinwen; Huang, Li-Chieh; Johnson, David; Scanlon, Seth T.; McKenzie, Andrew N. J.; Fallon, Padraic G.; Ogg, Graham S.			A role for IL-25 and IL-33-driven type-2 innate lymphoid cells in atopic dermatitis	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article							IMMUNE DEFECTS; E-CADHERIN; HUMAN EOSINOPHILS; T-CELLS; INFLAMMATION; EXPRESSION; DISEASE; KERATINOCYTES; FILAGGRIN; INSIGHTS	Type 2 innate lymphoid cells (ILC2s, nuocytes, NHC) require RORA and GATA3 for their development. We show that human ILC2s express skin homing receptors and infiltrate the skin after allergen challenge, where they produce the type 2 cytokines IL-5 and IL-13. Skin-derived ILC2s express the IL-33 receptor ST2, which is up-regulated during activation, and are enriched in lesional skin biopsies from atopic patients. Signaling via IL-33 induces type 2 cytokine and amphiregulin expression, and increases ILC2 migration. Furthermore, we demonstrate that E-cadherin ligation on human ILC2 dramatically inhibits IL-5 and IL-13 production. Interestingly, down-regulation of E-cadherin is characteristic of filaggrin insufficiency, a cardinal feature of atopic dermatitis (AD). ILC2 may contribute to increases in type 2 cytokine production in the absence of the suppressive E-cadherin ligation through this novel mechanism of barrier sensing. Using Rag1(-/-) and ROR alpha-deficient mice, we confirm that ILC2s are present in mouse skin and promote AD-like inflammation. IL-25 and IL-33 are the predominant ILC2-inducing cytokines in this model. The presence of ILC2s in skin, and their production of type 2 cytokines in response to IL-33, identifies a role for ILC2s in the pathogenesis of cutaneous atopic disease.	[Salimi, Maryam; Xue, Luzheng; Gutowska-Owsiak, Danuta; Huang, Li-Chieh; Ogg, Graham S.] Univ Oxford, Human Immunol Unit, MRC, Inst Hlth Res Biomed Res Ctr,Radcliffe Dept Med, Oxford OX3 9DS, England; [Barlow, Jillian L.; Scanlon, Seth T.; McKenzie, Andrew N. J.] Univ Cambridge, Mol Biol Lab, MRC, Cambridge CB2 0QH, England; [Saunders, Sean P.; Fallon, Padraic G.] Trinity Coll Dublin, Trinity Biomed Sci Inst, Dublin 2, Ireland; [Fallon, Padraic G.] St James Hosp, Inst Mol Med, Dublin 2, Ireland; [Fallon, Padraic G.] Our Ladys Childrens Hosp, Natl Childrens Res Ctr, Dublin 12, Ireland; [Johnson, David] Oxford Univ Hosp Natl Hlth Serv Trust, John Radcliffe Hosp, Dept Plast & Reconstruct Surg, Oxford OX3 9DU, England; [Wang, Xinwen] Fourth Mil Med Univ, Sch Stomatol, Dept Periodontol & Oral Med, Xian 710032, Shaanxi, Peoples R China	McKenzie, ANJ (reprint author), Univ Cambridge, Mol Biol Lab, MRC, Cambridge CB2 0QH, England.	anm@mrc-lmb.cam.ac.uk		Scanlon, Seth Thomas/0000-0002-1792-6382; Fallon, Padraic/0000-0002-8401-7293; Saunders, Sean/0000-0003-1689-3598; Gutowska-Owsiak, Danuta/0000-0003-4503-2279	MRC; Barrie Trust; National Institute of Health Research Biomedical Research Centre Program; Comprehensive Local Research Network; Wellcome Trust; Science Foundation Ireland; National Children's Research Centre; American Asthma Foundation	We are grateful for funding from the MRC, Barrie Trust, National Institute of Health Research Biomedical Research Centre Program and Comprehensive Local Research Network. P. G. Fallon is supported by the Wellcome Trust, Science Foundation Ireland, and National Children's Research Centre. J.L. Barlow, S. T. Scanlon, and A.N.J. McKenzie were supported by the MRC and the American Asthma Foundation.	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Exp. Med.	DEC 16	2013	210	13					2939	2950		10.1084/jem.20130351		12	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	276ID	WOS:000328742600012	24323357	
J	Bartemes, KR; Iijima, K; Kobayashi, T; Kephart, GM; McKenzie, AN; Kita, H				Bartemes, Kathleen R.; Iijima, Koji; Kobayashi, Takao; Kephart, Gail M.; McKenzie, Andrew N.; Kita, Hirohito			IL-33-Responsive Lineage(-)CD25(+)CD44(hi) Lymphoid Cells Mediate Innate Type 2 Immunity and Allergic Inflammation in the Lungs	JOURNAL OF IMMUNOLOGY			English	Article							AIRWAY INFLAMMATION; CYTOKINE PRODUCTION; MAST-CELLS; T-CELLS; ASTHMA; IL-33; RESPONSES; RECEPTOR; FAMILY; ST2	Innate immunity provides the first line of response to invading pathogens and a variety of environmental insults. Recent studies identified novel subsets of innate lymphoid cells that are capable of mediating immune responses in mucosal organs. In this paper, we describe a subset of lymphoid cells that is involved in innate type 2 immunity in the lungs. Airway exposure of naive BALB/c or C57BL/6J mice to IL-33 results in a rapid (<12 h) production of IL-5 and IL-13 and marked airway eosinophilia independently of adaptive immunity. In the lungs of nonsensitized naive mice, IL-33-responsive cells were identified that have a lymphoid morphology, lack lineage markers, highly express CD25, CD44, Thy1.2, ICOS, Sca-1, and IL-7R alpha (i.e., Lin(-)CD25(+)D44(hi) lymphoid cells), and require IL-7Ra for their development. Airway exposure of naive mice to a clinically relevant ubiquitous fungal allergen, Alternaria alternata, increases bronchoalveolar lavage levels of IL-33, followed by IL-5 and IL-13 production and airway eosinophilia without T or B cells. This innate type 2 response to the allergen is nearly abolished in mice deficient in IL-33R (i.e., ST2), and the Lin(-)CD25(+)CD44(hi) lymphoid cells in the lungs are required and sufficient to mediate the response. Thus, a subset of innate immune cells that responds to IL-33 and vigorously produces Th2-type cytokines is present in mouse lungs. These cells may provide a novel mechanism for type 2 immunity in the airways and induction of allergic airway diseases such as asthma. The Journal of Immunology, 2012, 188: 1503-1513.	[Bartemes, Kathleen R.; Iijima, Koji; Kobayashi, Takao; Kephart, Gail M.; Kita, Hirohito] Mayo Clin, Div Allerg Dis, Dept Internal Med, Rochester, MN 55905 USA; [Bartemes, Kathleen R.; Kita, Hirohito] Mayo Clin, Dept Immunol, Rochester, MN 55905 USA; [McKenzie, Andrew N.] MRC, Mol Biol Lab, Cambridge CB2 0QH, England	Kita, H (reprint author), Mayo Clin, Div Allerg Dis, Dept Internal Med, 200 1st St SW, Rochester, MN 55905 USA.	kita.hirohito@mayo.edu			National Institutes of Health [AI34486, AI49235]; Mayo Foundation	This work was supported by R01 grants (AI34486 and AI49235) from the National Institutes of Health and the Mayo Foundation.	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J	Kogan, MD; Strickland, BB; Blumberg, SJ; Singh, GK; Perrin, JM; van Dyck, PC				Kogan, Michael D.; Strickland, Bonnie B.; Blumberg, Stephen J.; Singh, Gopal K.; Perrin, James M.; van Dyck, Peter C.			A National Profile of the Health Care Experiences and Family Impact of Autism Spectrum Disorder Among Children in the United States, 2005-2006	PEDIATRICS			English	Article						autism spectrum disorder; children with special health care needs; disability; national estimates; access to health care	PERVASIVE DEVELOPMENTAL DISORDERS; PARENTAL REPORT; MEDICAL HOME; NEEDS; PREVALENCE; EXPENDITURES; ACCESS; SERVICES; SUPPORT; ASTHMA	OBJECTIVES. We sought to examine the health care experiences of children with autism spectrum disorder and the impact of autism spectrum disorder on the family and to assess whether having a medical home is associated with less family impact. METHODS. We used the 2005-2006 National Survey of Children With Special Health Care Needs to compare 2088 children with special health care needs, aged 3 to 17 years, reported by their parents to have autism spectrum disorder, with children with special health care needs with "other emotional, developmental, or behavioral problems" (excluding autism spectrum disorder; n = 9534) and 26 751 other children with special health care needs. We used weighted logistic regression to examine unmet needs for specific health care and support services, delayed care, no usual care source or personal physician, difficulty receiving referrals, and financial, employment, or time problems because of child's care. RESULTS. Nationally, an estimated 535 000 children have special health care needs and autism spectrum disorder, a prevalence of 86 per 10 000 children aged 3 to 17 years. Among children with special health care needs, 5.6% have autism spectrum disorder. Compared with other children with special health care needs without emotional, developmental, or behavioral problems, children with special health care needs with autism spectrum disorder were more likely to have unmet needs for specific health care services, family support services, delayed or foregone care, difficulty receiving referrals, and care that is not family centered. Children with special health care needs with autism spectrum disorder were more likely to live in families that report financial problems, need additional income for the child's medical care, reduce or stop work because of the child's condition, spend >= 10 hours per week providing or coordinating care, and paid more than $1000 in the previous year for the child's care. The financial impacts of autism spectrum disorder were significantly more burdensome when children with special health care needs did not have a medical home. CONCLUSIONS. Children with special health care needs with autism spectrum disorder are significantly more likely to have problems regarding access to care and unmet needs, and their families have greater financial, employment, and time burdens compared with other children with special health care needs. Receipt of primary care in a medical home may reduce these burdens. 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A., 2006, Morbidity and Mortality Weekly Report, V55, P481; SCHOENBAUM SC, 2006, NO PLACE HOME; Shimabukuro TT, 2008, J AUTISM DEV DISORD, V38, P546, DOI 10.1007/s10803-007-0424-y; Strickland B, 2004, PEDIATRICS, V113, P1485; Thomas KC, 2007, J AUTISM DEV DISORD, V37, P1902, DOI 10.1007/s10803-006-0323-7; *US BUR CENS, 1997, GLOSS DEC CENS TERMS; Williams JG, 2006, ARCH DIS CHILD, V91, P8, DOI 10.1136/adc.2004.062083; Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49; [Anonymous], 2007, MMWR SURVEILL SUMM, V56, P1	61	171	171	2	22	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	DEC	2008	122	6					E1149	E1158		10.1542/peds.2008-1057		10	Pediatrics	Pediatrics	377NP	WOS:000261258200005	19047216	
J	Menzies, D; Nair, A; Williamson, PA; Schembri, S; Al-Khairalla, MZH; Barnes, M; Fardon, TC; McFarlane, L; Magee, GJ; Lipworth, BJ				Menzies, Daniel; Nair, Arun; Williamson, Peter A.; Schembri, Stuart; Al-Khairalla, Mudher Z. H.; Barnes, Martyn; Fardon, Tom C.; McFarlane, Lesley; Magee, Gareth J.; Lipworth, Brian J.			Respiratory symptoms, pulmonary function, and markers of inflammation among bar workers before and after a legislative ban on smoking in public places	JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION			English	Article							ENVIRONMENTAL TOBACCO-SMOKE; EXHALED NITRIC-OXIDE; SECONDHAND SMOKE; LUNG-FUNCTION; PASSIVE SMOKING; BRONCHIAL RESPONSIVENESS; AIRWAY INFLAMMATION; PARENTAL SMOKING; EXPOSURE; ASTHMA	Context Scotland prohibited smoking in confined public places on March 26, 2006. Objective To investigate the association of smoke-free legislation with symptoms, pulmonary function, and markers of inflammation of bar workers. Design, Setting, and Participants This prospective observational study was conducted in Tayside, Scotland from February-June 2006. One hundred five nonasthmatic and asthmatic nonsmoking bar workers were initially enrolled, of whom 77 completed the study per protocol. Main Outcome Measures Respiratory and sensory symptoms, spirometry measurements, serum cotinine levels, peripheral inflammatory cell count, asthma qualityof-life scores, and exhaled nitric oxide levels were evaluated before and after introduction of the smoking ban. Results For the per-protocol analysis, the percentage of bar workers with respiratory and sensory symptoms decreased from 79.2% (n = 61) before the smoke-free policy to 53.2% (n = 41) (total change, -26%; 95% confidence interval [CI], -13.8% to -38.1%; P < .001) and 46.8% (n = 38) (-32.5%; 95% CI, -19.8% to -45.2%; P < .001) 1 and 2 months afterward. Forced expiratory volume in the first second increased from 96.6% predicted to 104.8% (change, 8.2%; 95% CI, 3.9% to 12.4%; P , .001) and then 101.7% (change, 5.1%; 95% CI, 2.1% to 8.0%; P = .002), and serum cotinine levels decreased from 5.15 ng/mL to 3.22 ng/mL (change, -1.93 ng/mL; 95% CI, -2.83 to -1.03 ng/mL; P < .001) and then 2.93 ng/mL (-2.22 ng/mL; 95% CI, -3.10 to -1.34 ng/ mL; P < .001). The total white blood cell and neutrophil count was reduced from 7610 to 6980 cells/mu L at 2 months (-630 cells/mu L; 95% CI, - 1010 to - 260 cells/mu L; P = .002) and from 4440 to 4030 cells/mu L (-410 cells/mu L; 95% CI, - 740 to - 90 cells/mu L; P = .03), respectively. Asthmatic bar workers also had less airway inflammation, with a reduction in exhaled nitric oxide from 34.3 parts per billion (ppb) to 27.4 ppb 1 month after the ban (0.8-fold change; 95% CI, 0.67 to 0.96 ppb; P = .04), and Juniper quality-of-life scores increased from 80.2 to 87.5 points (7.3 points; 95% CI, 0.1 to 14.6 points; P = .049). Conclusions Smoke-free legislation was associated with significant early improvements in symptoms, spirometry measurements, and systemic inflammation of bar workers. Asthmatic bar workers also had reduced airway inflammation and improved quality of life.	Univ Dundee, Ninewells Hosp & Med Sch, Asthma & Allergy Res Grp, Dept Med & Therapeut, Dundee DD1 9SY, Scotland; Univ Dundee, Ninewells Hosp & Med Sch, Asthma & Allergy Res Grp, Dept Resp Med, Dundee DD1 9SY, Scotland	Menzies, D (reprint author), Univ Dundee, Ninewells Hosp & Med Sch, Asthma & Allergy Res Grp, Dept Med & Therapeut, Dundee DD1 9SY, Scotland.	d.menzies@dundee.ac.uk					Allwright S, 2005, BRIT MED J, V331, P1117, DOI 10.1136/bmj.38636.499225.55; Alving K, 2006, RESP RES, V7, DOI 10.1186/1465-9921-7-67; American Thoracic Society, 2005, AM J RESP CRIT CARE, V171, P912, DOI DOI 10.1164/RCCM.200406-710ST.PUBMED:15817806; Barnoya J, 2005, CIRCULATION, V111, P2684, DOI 10.1161/CIRCULATIONAHA.104.492215; Berry M, 2005, EUR RESPIR J, V25, P986, DOI 10.1183/09031936.05.00132404; Chaudhuri R, 2006, AM J RESP CRIT CARE, V174, P127, DOI 10.1164/rccm.200510-1589OC; Chinn S, 2005, AM J RESP CRIT CARE, V172, P956, DOI 10.1164/rccm.200503-3230C; Cook DG, 1998, THORAX, V53, P884; Crapo RO, 2000, AM J RESP CRIT CARE, V161, P309; Crook MA, 2000, EUR J CLIN INVEST, V30, P861, DOI 10.1046/j.1365-2362.2000.00738.x; Eisner MD, 1998, JAMA-J AM MED ASSOC, V280, P1909, DOI 10.1001/jama.280.22.1909; Eisner MD, 2005, THORAX, V60, P814, DOI 10.1136/thx.2004.037283; Eisner MD, 2001, ENVIRON HEALTH PERSP, V109, P809, DOI 10.2307/3454823; Fardon TC, 2004, ANN ALLERG ASTHMA IM, V93, P365; Farrelly MC, 2005, TOB CONTROL, V14, P236, DOI 10.1136/tc.2004.008839; Frohlich M, 2003, EUR HEART J, V24, P1365, DOI 10.1016/S0195-668X(03)00260-4; He J, 1999, NEW ENGL J MED, V340, P920, DOI 10.1056/NEJM199903253401204; Houston TK, 2006, BRIT MED J, V332, P1064, DOI 10.1136/bmj.38779.584028.55; Inman MD, 1998, J ALLERGY CLIN IMMUN, V101, P342; Iribarren C, 2004, NEUROEPIDEMIOLOGY, V23, P38, DOI 10.1159/000073973; Janson C, 2001, LANCET, V358, P2103, DOI 10.1016/S0140-6736(01)07214-2; Jones SL, 2002, EUR RESPIR J, V20, P601, DOI 10.1183/09031936.02.00285302; Juniper EF, 1999, EUR RESPIR J, V14, P32, DOI 10.1034/j.1399-3003.1999.14a08.x; Miller MR, 2005, EUR RESPIR J, V26, P319, DOI 10.1183/09031936.05.00034805; Moshammer H, 2006, AM J RESP CRIT CARE, V173, P1255, DOI 10.1164/rccm.200510-1552OC; Mulcahy M, 2005, TOB CONTROL, V14, P384, DOI 10.1136/tc.2005.011635; *NIH, 1995, PUBL NIH; *OFF SMOK HLTH, 2006, HLTH CONS INV EXP TO; Panagiotakos DB, 2004, AM J MED, V116, P145, DOI 10.1016/j.amjmed.2003.07.019; Quanjer PH, 1993, EUR RESPIR J S, V16, P5, DOI 10.1183/09041950.005s1693; Sargent RP, 2004, BRIT MED J, V328, P977, DOI 10.1136/bmj.38055.715683.55; Sasco AJ, 2004, LUNG CANCER-J IASLC, V45, pS3, DOI 10.1016/j.lungcan.2004.07.000; Tsoukias NM, 1998, J APPL PHYSIOL, V85, P653; Ward C, 2005, CLIN EXP ALLERGY, V35, P1565, DOI 10.1111/j.1365-2222.2005.02365.x; Willemse BWM, 2004, EUR RESPIR J, V23, P464, DOI 10.1183/09031936.01.00012704; Yates DH, 2001, AM J RESP CRIT CARE, V164, P1043	36	171	178	1	12	AMER MEDICAL ASSOC	CHICAGO	515 N STATE ST, CHICAGO, IL 60610-0946 USA	0098-7484			JAMA-J AM MED ASSOC	JAMA-J. Am. Med. Assoc.	OCT 11	2006	296	14					1742	1748		10.1001/jama.296.14.1742		7	Medicine, General & Internal	General & Internal Medicine	092NH	WOS:000241103400022	17032987	
J	Hysi, P; Kabesch, M; Moffatt, MF; Schedel, M; Carr, D; Zhang, YM; Boardman, B; von Mutius, E; Weiland, SK; Leupold, W; Fritzsch, C; Klopp, N; Musk, AW; James, A; Nunez, G; Inohara, N; Cookson, WOC				Hysi, P; Kabesch, M; Moffatt, MF; Schedel, M; Carr, D; Zhang, YM; Boardman, B; von Mutius, E; Weiland, SK; Leupold, W; Fritzsch, C; Klopp, N; Musk, AW; James, A; Nunez, G; Inohara, N; Cookson, WOC			NOD1 variation, immunoglobulin E and asthma	HUMAN MOLECULAR GENETICS			English	Article							QUANTITATIVE TRAITS; FOUNDER POPULATION; CROHNS-DISEASE; ASSOCIATION; GENE; SUSCEPTIBILITY; POLYMORPHISMS; LOCUS; IGE; RESPONSIVENESS	Asthma is a familial inflammatory disease of the airways of the lung. Microbial exposures in childhood protect against asthma through unknown mechanisms. The innate immune system is able to identify microbial components through a variety of pattern-recognition receptors (PRRs). NOD1 is an intracellular PRR that initiates inflammation in response to bacterial diaminopimelic acid (iE-DAP). The NOD1 gene is on chromosome 7p14, in a region that has been genetically linked to asthma. We carried out a systematic search for polymorphism in the gene. We found an insertion-deletion polymorphism (ND1+32656) near the beginning of intron IX that accounted for similar to 7% of the variation in IgE in two panels of families (P < 0.0005 in each). Allele*2 (the insertion) was associated with high IgE levels. The same allele was strongly associated with asthma in an independent study of 600 asthmatic children and 1194 super-normal controls [odds ratio (OR) 6.3; 95% confidence interval (CI) 1.4-28.3, dominant model]. Differential binding of the two ND1+32656 alleles was observed to a protein from nuclei of the Calu 3 epithelial cell line. In an accompanying study, the deletion allele (ND1+32656*1) was found to be associated with inflammatory bowel disease. The results indicate that intracellular recognition of specific bacterial products affects the presence of childhood asthma.	Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England; Univ Oxford, Environm Change Inst, Oxford OX3 7BN, England; Univ Childrens Hosp, Munich, Germany; Univ Ulm, Dept Epidemiol, Ulm, Germany; Univ Childrens Hosp Dresden, Dresden, Germany; Univ Childrens Hosp Leipzig, Leipzig, Germany; GSF Res Ctr Environm & Hlth, Neuherberg, Germany; Sir Charles Gairdner Hosp, Dept Resp Med & Pulm Physiol, Perth, WA, Australia; Univ Michigan, Sch Med, Dept Pathol, Ann Arbor, MI 48109 USA; Univ Michigan, Sch Med, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA	Cookson, WOC (reprint author), Univ Oxford, Wellcome Trust Ctr Human Genet, Roosevelt Dr, Oxford OX3 7BN, England.	wocc@well.ox.ac.uk		von Mutius, Erika/0000-0002-8893-4515			Abecasis GR, 2000, AM J HUM GENET, V66, P279, DOI 10.1086/302698; Abecasis GR, 2002, NAT GENET, V30, P97, DOI 10.1038/ng786; Abecasis GR, 2000, BIOINFORMATICS, V16, P182, DOI 10.1093/bioinformatics/16.2.182; Baldini M, 1999, AM J RESP CELL MOL, V20, P976; Bouma G, 2003, NAT REV IMMUNOL, V3, P521, DOI 10.1038/nri1132; Chamaillard M, 2003, NAT IMMUNOL, V4, P702, DOI 10.1038/ni945; Cordell HJ, 2002, AM J HUM GENET, V70, P124, DOI 10.1086/338007; DANIELS SE, 1996, NATURE, V383, P250; DIGNAM JD, 1983, METHOD ENZYMOL, V101, P582; Dixon MS, 1998, PLANT CELL, V10, P1915, DOI 10.1105/tpc.10.11.1915; DIZIER MH, 1995, GENET EPIDEMIOL, V12, P93, DOI 10.1002/gepi.1370120109; FRECH K, 1993, NUCLEIC ACIDS RES, V21, P1655, DOI 10.1093/nar/21.7.1655; HILL MR, 1995, BRIT MED J, V311, P776; Holt P.G., 1999, NATURE, V402, P12, DOI 10.1038/35037009; Hugot JP, 2001, NATURE, V411, P599, DOI 10.1038/35079107; Inohara N, 1999, J BIOL CHEM, V274, P14560, DOI 10.1074/jbc.274.21.14560; Inohara N, 2001, J BIOL CHEM, V276, P2551, DOI 10.1074/jbc.M009728200; Kabesch M, 2003, J ALLERGY CLIN IMMUN, V112, P893, DOI 10.1067/mai.2003.1815; Kabesch M, 2003, J ALLERGY CLIN IMMUN, V111, P813, DOI 10.1067/mai.2003.1336; Kruglyak L, 2001, NAT GENET, V27, P234, DOI 10.1038/85776; Laitinen T, 2001, NAT GENET, V28, P87, DOI 10.1038/ng0501-87; Lund O, 1997, PROTEIN ENG, V10, P1241, DOI 10.1093/protein/10.11.1241; MCGOVERN DPB, 2004, IN PRESS ASS COMPLEX; Moffatt MF, 2001, EUR J HUM GENET, V9, P341, DOI 10.1038/sj.ejhg.5200636; Monks SA, 1998, AM J HUM GENET, V63, P1507, DOI 10.1086/302104; Noel L, 1999, PLANT CELL, V11, P2099, DOI 10.1105/tpc.11.11.2099; Ober C, 2000, AM J HUM GENET, V67, P1154, DOI 10.1016/S0002-9297(07)62946-2; Ogura Y, 2001, NATURE, V411, P603, DOI 10.1038/35079114; Palmer LJ, 2000, AM J RESP CRIT CARE, V161, P1836; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; SHERRILL DL, 1995, AM J RESP CRIT CARE, V152, P98; STRACHAN DP, 1989, BRIT MED J, V299, P1259; VONMUTIUS E, 1992, BRIT MED J, V305, P1395; Weiland SK, 1999, EUR RESPIR J, V14, P862, DOI 10.1034/j.1399-3003.1999.14d23.x	34	171	178	1	5	OXFORD UNIV PRESS	OXFORD	GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND	0964-6906			HUM MOL GENET	Hum. Mol. Genet.	APR 1	2005	14	7					935	941		10.1093/hmg/ddi087		7	Biochemistry & Molecular Biology; Genetics & Heredity	Biochemistry & Molecular Biology; Genetics & Heredity	911BJ	WOS:000227975800006	15718249	
J	Woerly, G; Honda, K; Loyens, M; Papin, JP; Auwerx, J; Staels, B; Capron, M; Dombrowicz, D				Woerly, G; Honda, K; Loyens, M; Papin, JP; Auwerx, J; Staels, B; Capron, M; Dombrowicz, D			Peroxisome proliferator-activated receptors alpha and gamma down-regulate allergic inflammation and eosinophil activation	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article						nuclear receptors; asthma; eosinophils; IgE; ADCC	STEM-CELL FACTOR; FC-EPSILON-RI; NF-KAPPA-B; PPAR-GAMMA; GENE-EXPRESSION; AIRWAY HYPERRESPONSIVENESS; ENDOTHELIAL-CELLS; T-LYMPHOCYTES; MAST-CELLS; DENDRITIC CELLS	Allergic asthma is characterized by airway hyperresponsiveness, eosinophilia, and mucus accumulation and is associated with increased IgE concentrations. We demonstrate here that peroxisome proliferator-activated receptors (PPARs), PPAK-alpha and PPAR-gamma, which have been shown recently to be involved in the regulation of various cell types within the immune system, decrease antigen-induced air-way hyperresponsiveness, lung inflammation, eosinophilia, cytokine production, and GATA-3 expression as well as serum levels of antigen-specific IgE in a murine model of human asthma. In addition, we demonstrate that PPAR-alpha and -gamma are expressed in eosinophils and their activation inhibits in vitro chemotaxis and antibody-dependent cellular cytotoxicity. Thus, PPAR-alpha and -gamma (co)agonists might be of therapeutic interest for the regulation of allergic or inflammatory reactions by targeting both regulatory and effector cells involved in the immune response.	Inst Pasteur, INSERM, U547, IFR17, F-59019 Lille, France; Univ Lille 2, INSERM, U545, Inst Pasteur, F-59019 Lille, France; Univ Lille 2, Fac Pharm, F-59019 Lille, France; Univ Strasbourg 1, INSERM, CNRS, Inst Genet & Biol Mol & Cellulaire, F-67401 Illkirch Graffenstaden, France	Dombrowicz, D (reprint author), Inst Pasteur, INSERM, U547, IFR17, 1 Rue Prof Calmette BP 245, F-59019 Lille, France.		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Exp. Med.	AUG 4	2003	198	3					411	421		10.1084/jem.20021384		11	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	712TQ	WOS:000184813700005	12900517	
J	Romieu, I; Sienra-Monge, JJ; Ramirez-Aguilar, M; Tellez-Rojo, MM; Moreno-Macias, H; Reyes-Ruiz, NI; del Rio-Navarro, BE; Ruiz-Navarro, MX; Hatch, G; Slade, R; Hernandez-Avila, M				Romieu, I; Sienra-Monge, JJ; Ramirez-Aguilar, M; Tellez-Rojo, MM; Moreno-Macias, H; Reyes-Ruiz, NI; del Rio-Navarro, BE; Ruiz-Navarro, MX; Hatch, G; Slade, R; Hernandez-Avila, M			Antioxidant supplementation and lung functions among children with asthma exposed to high levels of air pollutants	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						childhood asthma; antioxidants; air pollution; Mexico	OZONE EXPOSURE; VITAMIN-E; LIPID-PEROXIDATION; PULMONARY-FUNCTION; ALPHA-TOCOPHEROL; RHESUS-MONKEYS; ASCORBIC-ACID; MILD ASTHMA; MEXICO-CITY; GLUTATHIONE	To evaluate whether acute effects of ozone, nitrogen dioxide, and particulates with mass median diameter less than 10 mum could be attenuated by antioxidant vitamin supplementation, we conducted a randomized trial using a double-blinded design. Children with asthma (n = 158) who were residents of Mexico City were randomly given a daily supplement of vitamins (50 mg/day of vitamin E and 250 mg/day of vitamin Q or a placebo and were followed from October 1998 to April 2000. Pulmonary function tests were carried out twice a week in the morning. During the follow-up observation period, the mean 1-hour maximum ozone level was 102 ppb (SD = 47), and the mean 24-hour average PM10 level was 56.7 mug/m(3) (SD = 27.4). In children with moderate and severe asthma, ozone levels 1 day before spirometry were inversely associated significantly with forced expiratory flow (FEF25-75) (-13.32 ml/ second/10 ppb; p = 0.000), FEV1 (-4.59 ml/10 ppb; p = 0.036), and peak expiratory flow (PEF) (-15.01 ml/second/10 ppb; p = 0.04) in the placebo group after adjusting for potential confounding factors. No association between ozone and lung functions was observed in the supplement group. We observed significant differences in lung function decrements between groups for FEF25-75 and PEF. Our results suggest that supplementation with antioxidants might modulate the impact of ozone exposure on the small airways of children with moderate to severe asthma.	Inst Nacl Salud Publ, Cuernavaca 62508, Morelos, Mexico; Hosp Infantil Mexico Dr Federico Gomez, Mexico City, DF, Mexico; US EPA, Durham, NC USA	Romieu, I (reprint author), Inst Nacl Salud Publ, 655 Avenida Univ,Col Santa Maria Ahuacatitlan, Cuernavaca 62508, Morelos, Mexico.						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J	Chung, KF; Pavord, ID				Chung, Kian Fan; Pavord, Ian D.			Chronic cough 1 - Prevalence, pathogenesis, and causes of chronic cough	LANCET			English	Review							GASTROESOPHAGEAL-REFLUX DISEASE; CHRONIC NONPRODUCTIVE COUGH; CHRONIC PERSISTENT COUGH; POSTNASAL-DRIP-SYNDROME; CRYPTOGENIC FIBROSING ALVEOLITIS; SOLE PRESENTING MANIFESTATION; OBSTRUCTIVE PULMONARY-DISEASE; BRONCHOALVEOLAR LAVAGE FLUID; INTERSTITIAL LUNG-DISEASE; CAPSAICIN-INDUCED COUGH	Cough is a reflex action of the respiratory tract that is used to clear the upper airways. Chronic cough lasting for more than 8 weeks is common in the community. The causes include cigarette smoking, exposure to cigarette smoke, and exposure to environmental pollution, especially particulates. Diseases causing chronic cough include asthma, eosinophilic bronchitis, gastro-oesophageal reflux disease, postnasal drip syndrome or rhinosinusitis, chronic obstructive pulmonary disease, pulmonary fibrosis, and bronchiectasis. Doctors should always work towards a clear diagnosis, considering common and rare illnesses. In some patients, no cause is identified, leading to the diagnosis of idiopathic cough. Chronic cough is often associated with an increased response to tussive agents such as capsaicin. Plastic changes in intrinsic and synaptic excitability in the brainstem, spine, or airway nerves can enhance the cough reflex, and can persist in the absence of the initiating cough event. Structural and inflammatory airway mucosal changes in non-asthmatic chronic cough could represent the cause or the traumatic response to repetitive coughing. Effective control of cough requires not only controlling the disease causing the cough but also desensitisation of cough pathways.	[Chung, Kian Fan] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Airway Dis Sect, London SW3 6LY, England; [Chung, Kian Fan] Royal Brompton Hosp, London SW3 6LY, England; [Pavord, Ian D.] Univ Hosp Leicester NHS Trust, Glenfield Gen Hosp, Dept Resp Med Allergy & Thorac Surg, Inst Lung Hlth, Leicester, Leics, England	Chung, KF (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Airway Dis Sect, Dovehouse St, London SW3 6LY, England.	f.chung@imperial.ac.uk		Pavord, Ian/0000-0002-4288-5973; Chung, Kian Fan/0000-0001-7101-1426			BALUK P, 1992, J COMP NEUROL, V319, P586, DOI 10.1002/cne.903190408; Banauch GI, 2003, AM J RESP CRIT CARE, V168, P54, DOI 10.1164/rccm.200211-1329OC; BARBEE RA, 1991, CHEST, V99, P20, DOI 10.1378/chest.99.1.20; Bayer-Oglesby L, 2006, AM J EPIDEMIOL, V164, P1190, DOI 10.1093/aje/kwj338; Benini L, 2000, GUT, V46, P762, DOI 10.1136/gut.46.6.762; BERKIN KE, 1988, BRIT MED J, V296, P1279; Birkebaek NH, 1999, CLIN INFECT DIS, V29, P1239, DOI 10.1086/313448; 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J	Marks, GB; Mihrshahi, S; Kemp, AS; Tovey, ER; Webb, K; Almqvist, C; Ampon, RD; Crisafulli, D; Belousova, EG; Mellis, CM; Peat, JK; Leeder, SR				Marks, Guy B.; Mihrshahi, Seema; Kemp, Andrew S.; Tovey, Euan R.; Webb, Karen; Almqvist, Catarina; Ampon, Rosario D.; Crisafulli, Daniel; Belousova, Elena G.; Mellis, Craig M.; Peat, Jennifer K.; Leeder, Stephen R.		Childhood Asthma Prevention Study	Prevention of asthma during the first 5 years of life: A randomized controlled trial	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergen avoidance; omega-3 fatty acids; prevention; birth cohort; house dust mite	DUST-MITE ALLERGEN; FATTY-ACID MODIFICATION; CHILDHOOD ASTHMA; ATOPIC ECZEMA; MATTRESS ENCASINGS; PREVALENCE; CHILDREN; SYMPTOMS; RISK; EXPOSURE	Background: Early life exposures may be important in the development of asthma and allergic disease. Objective: To test house dust mite (HDM) avoidance and dietary fatty acid modification, implemented throughout the first 5 years of life, as interventions to prevent asthma and allergic disease. Methods: We recruited newborns with a family history of asthma antenatally and randomized them, separately, to HDM avoidance or control and to dietary modification or control. At age 5 years, they were assessed for asthma and eczema and had skin prick tests for atopy. Results: Of 616 children randomized, 516 (84%) were evaluated at age 5 years. The HDM avoidance intervention resulted in a 61% reduction in HDM allergen concentrations (mu g/g dust) in the child's bed but no difference in the prevalence of asthma, wheeze, or atopy (P > .1). The prevalence of eczema was higher in the active HDM avoidance group (26% vs 19%; P = .06). The ratio of omega-6 to omega-3 fatty acids in plasma was lower in the active diet group (5.8 vs 7.4; P < .0001). However, the prevalence of asthma, wheezing, eczema, or atopy did not differ between the diet groups (P > .1). Conclusion: Further research is required to establish whether other interventions can be recommended for the prevention of asthma and allergic disease. Clinical implications: House dust mite avoidance measures and dietary fatty acid modification, as implemented in this trial during infancy and early childhood, did not prevent the onset of asthma, eczema, or atopy in high-risk children.	Woolcock Inst Med Res, Camperdown, NSW 2050, Australia; Univ Sydney, Sydney, NSW 2006, Australia; Childrens Hosp, Westmead, NSW, Australia	Marks, GB (reprint author), Woolcock Inst Med Res, POB M77,Missenden Rd PO, Camperdown, NSW 2050, Australia.	g.marks@unsw.edu.au	Mihrshahi, Seema/A-9877-2009; Tovey, Euan/G-8604-2017	Mihrshahi, Seema/0000-0001-6567-9884; Tovey, Euan/0000-0002-1802-7266			Arshad SH, 2003, THORAX, V58, P489, DOI 10.1136/thorax.58.6.489; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; BURNEY PGJ, 1990, BRIT MED J, V300, P1306; Chan-Yeung M, 2005, J ALLERGY CLIN IMMUN, V116, P49, DOI 10.1016/j.jaci.2005.03.029; Custovic A, 2000, J ALLERGY CLIN IMMUN, V105, P252, DOI 10.1016/S0091-6749(00)90073-3; Dunstan JA, 2003, J ALLERGY CLIN IMMUN, V112, P1178, DOI 10.1016/j.jaci.2003.09.009; Gehring U, 2001, J ALLERGY CLIN IMMUN, V108, P847, DOI 10.1067/mai.2001.119026; Haby MM, 2001, THORAX, V56, P589, DOI 10.1136/thorax.56.8.589; Hodge L, 1996, MED J AUSTRALIA, V164, P137; Horak F, 2004, CLIN EXP ALLERGY, V34, P1220, DOI 10.1111/j.1365-2222.2004.02024.x; JENKINS MA, 1994, BRIT MED J, V309, P90; Koopman LP, 2002, AM J RESP CRIT CARE, V166, P307, DOI 10.1164/rccm.2106026; KORSGAARD J, 1983, AM REV RESPIR DIS, V128, P231; MENEGHINI CL, 1982, CONTACT DERMATITIS, V8, P285, DOI 10.1111/j.1600-0536.1982.tb04231.x; Mihrshahi S, 2003, J ALLERGY CLIN IMMUN, V111, P162, DOI 10.1067/mai.2003.36; Mihrshahi S, 2003, ALLERGY, V58, P784, DOI 10.1034/j.1398-9995.2003.00194.x; Mihrshahi S, 2002, RESPIROLOGY, V7, P147, DOI 10.1046/j.1440-1843.2002.00384.x; Mihrshahi S, 2001, CONTROL CLIN TRIALS, V22, P333, DOI 10.1016/S0197-2456(01)00112-X; Peat JK, 2004, J ALLERGY CLIN IMMUN, V114, P807, DOI 10.1016/j.jaci.2004.06.057; PEAT JK, 1994, BRIT MED J, V308, P1591; PEAT JK, 1991, CLIN EXP ALLERGY, V21, P573, DOI 10.1111/j.1365-2222.1991.tb00849.x; Platts-Mills Thomas A. E., 1997, Journal of Allergy and Clinical Immunology, V100, pS1; PLATTSMILLS TAE, 1989, J ALLERGY CLIN IMMUN, V83, P416, DOI 10.1016/0091-6749(89)90128-0; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; TOELLE BG, 1992, AM REV RESPIR DIS, V146, P633; Tovey ER, 2003, ALLERGY, V58, P790, DOI 10.1034/j.1398-9995.2003.00228.x; Tovey Euan R, 2003, N Engl J Med, V349, P1668; van Strien RT, 2003, CLIN EXP ALLERGY, V33, P490, DOI 10.1046/j.1365-2222.2003.01626.x; VONMUTIUS E, 1994, AM J RESP CRIT CARE, V149, P358; Wahn U, 1997, J ALLERGY CLIN IMMUN, V99, P763, DOI 10.1016/S0091-6749(97)80009-7; WAITE DA, 1980, CLIN ALLERGY, V10, P71, DOI 10.1111/j.1365-2222.1980.tb02082.x; Warner JO, 1998, PEDIATR PULM, V25, P1; Williams H, 1999, J ALLERGY CLIN IMMUN, V103, P125, DOI 10.1016/S0091-6749(99)70536-1; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P383, DOI 10.1111/j.1365-2133.1994.tb08530.x; Woodcock A, 2004, AM J RESP CRIT CARE, V170, P433, DOI 10.1164/rccm.200401-083OC	35	170	175	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	2006	118	1					53	61		10.1016/j.jaci.2006.04.004		9	Allergy; Immunology	Allergy; Immunology	065UH	WOS:000239184800006	16815138	
J	Gehring, U; Cyrys, J; Sedlmeir, G; Brunekreef, B; Bellander, T; Fischer, P; Bauer, CP; Reinhardt, D; Wichmann, HE; Heinrich, J				Gehring, U; Cyrys, J; Sedlmeir, G; Brunekreef, B; Bellander, T; Fischer, P; Bauer, CP; Reinhardt, D; Wichmann, HE; Heinrich, J			Traffic-related air pollution and respiratory health during the first 2 yrs of life	EUROPEAN RESPIRATORY JOURNAL			English	Article						air pollution; geographic information systems; infants; respiratory symptoms; traffic	NITROGEN-DIOXIDE; EAST-GERMANY; CHILDREN; SYMPTOMS; ASTHMA; EXPOSURE; POLLUTANTS; PREVALENCE; PARTICLES; DENSITY	As part of an international collaborative study on the impact of Traffic-Related Air Pollution on Childhood Asthma (TRAPCA), the health effects associated with long-term exposure to particles with a 50% cut-off aerodynamic diameter of 2.5 mum (PM2.5), PM2.5 absorbance, and nitrogen dioxide (NO2) were analysed. The German part of the TRAPCA study used data from subpopulations of two ongoing birth cohort studies (German Infant Nutrition Intervention Programme (GIN I) and Influences of Lifestyle Related Factors on the Human Immune System and Development of Allergies in Children (LISA)) based in the city of Munich. Geographic information systems (GIS)-based exposure modelling was used to estimate traffic-related air pollutants at the birth addresses of 1,756 infants. Logistic regression was used to analyse possible health effects and potential confounding factors were adjusted for. The ranges in estimated exposures to PM2.5, PM2.5 absorbance, and NO2 were 11.9-21.9 mug.m(-3), 1.38-4.39x10(-5) m(-1), and 19.5-66.9 mug.m(3), respectively. Significant associations between these pollutants and cough without infection (odds ratio (OR) (95% confidence interval (CI): 1.34 (1.11-1.61), 1.32 (1.10-1.59), and 1.40 (1.12-1.75), respectively) and dry cough at night (OR (95% Cl): 1.31 (1.07-1.60), 1.27 (1.04-1.55), and 1.36 (1.07-1.74), respectively) in the first year of life were found. In the second year of life, these effects were attenuated. There was some indication of an association between traffic-related air pollution and symptoms of cough. Due to the very young age of the infants, it was too early to draw definitive conclusions from this for the development of asthma.	GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, D-85764 Neuherberg, Germany; Univ Munich, Chair Epidemiol, D-80539 Munich, Germany; City Munich Dept Environm & Hlth, Munich, Germany; Univ Utrecht, Inst Risk Assessment Sci, Environm & Occupat Hlth Grp, Utrecht, Netherlands; Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; RIVM Natl Inst Publ Hlth & Environm, Bilthoven, Netherlands; Tech Univ Munich, Dept Paediat, D-8000 Munich, Germany; Univ Munich, Dept Pediat, Munich, Germany	Gehring, U (reprint author), GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, Ingolstaedter Landstr 1, D-85764 Neuherberg, Germany.		Cyrys, Josef/B-5359-2014	brunekreef, bert/0000-0001-9908-0060; Gehring, Ulrike/0000-0003-3612-5780; Cyrys, Josef/0000-0002-2105-8696			BEYER U, 1998, EUR RESPIR REV, V8, P61; BraunFahrlander C, 1997, AM J RESP CRIT CARE, V155, P1042; BRAUNFAHRLANDER C, 1989, SCHWEIZ MED WSCHR, V119, P1424; BRAUNFAHRLANDER C, 1992, AM REV RESPIR DIS, V145, P42; Briggs DJ, 1997, INT J GEOGR INF SCI, V11, P699, DOI 10.1080/136588197242158; Briggs DJ, 2000, SCI TOTAL ENVIRON, V253, P151, DOI 10.1016/S0048-9697(00)00429-0; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; Ciccone G, 1998, OCCUP ENVIRON MED, V55, P771; de Marco R, 2000, AM J RESP CRIT CARE, V162, P68; DOCKERY DW, 1989, AM REV RESPIR DIS, V139, P587; DOERSHUK CF, 1974, AM REV RESPIR DIS, V109, P452; Duhme H, 1996, EPIDEMIOLOGY, V7, P578, DOI 10.1097/00001648-199611000-00003; Duhme H, 1998, EUR RESPIR J, V11, P840, DOI 10.1183/09031936.98.11040840; English P, 1999, ENVIRON HEALTH PERSP, V107, P761, DOI 10.2307/3434663; Farrow A, 1997, ARCH ENVIRON HEALTH, V52, P189; Fischer PH, 2000, ATMOS ENVIRON, V34, P3713, DOI 10.1016/S1352-2310(00)00067-4; Guo YLL, 1999, ENVIRON HEALTH PERSP, V107, P1001; Hirsch T, 1999, EUR RESPIR J, V14, P669, DOI 10.1034/j.1399-3003.1999.14c29.x; *I RISK ASS SCI UT, RISK ASS EXP TRAFF R; Kunzli N, 2000, ENVIRON HEALTH PERSP, V108, P915, DOI 10.2307/3435048; Kunzli N, 2000, LANCET, V356, P795, DOI 10.1016/S0140-6736(00)02653-2; Magnus P, 1998, INT J EPIDEMIOL, V27, P995, DOI 10.1093/ije/27.6.995; MARPLE VA, 1987, JAPCA J AIR WASTE MA, V37, P1303; NITTA H, 1993, ARCH ENVIRON HEALTH, V48, P53; Oosterlee A, 1996, OCCUP ENVIRON MED, V53, P241; Pershagen G, 1995, INT J EPIDEMIOL, V24, P1147, DOI 10.1093/ije/24.6.1147; ROEMER W, 1993, AM REV RESPIR DIS, V147, P118; Samet J M, 1993, Res Rep Health Eff Inst, P1; *STAT AMT LAND MUE, BAS JAH VERSCH BER K; Studnicka M, 1997, EUR RESPIR J, V10, P2275, DOI 10.1183/09031936.97.10102275; THURLBECK WM, 1982, THORAX, V37, P564, DOI 10.1136/thx.37.8.564; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; VONMUTIUS E, 1995, EUR RESPIR J, V8, P723; Weiland Stephan K., 1994, Annals of Epidemiology, V4, P243; Wilkinson P, 1999, THORAX, V54, P1070; WJST M, 1993, BRIT MED J, V307, P596	36	170	176	5	25	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	APR	2002	19	4					690	698		10.1183/09031936.02.01182001		9	Respiratory System	Respiratory System	541RB	WOS:000174996600017	11998999	
J	Warner, JO				Warner, JO		ETAC Study Grp	A double-blinded, randomized, placebo-controlled trial of cetirizine in preventing the onset of asthma in children with atopic dermatitis: 18 months' treatment and 18 months' posttreatment follow-up	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						atopic dermatitis; asthma; prevention; house dust mite; grass pollen; cetirizine; antihistamine; children	ALLERGIC AIRWAY DISEASE; YOUNG-CHILDREN; CAT ALLERGEN; RISK; RECRUITMENT; CHALLENGE; CHILDHOOD	Background: Because asthma is not a curable condition, the development of strategies for prevention of the disease has a high priority. Atopic dermatitis is a common precursor to the development of asthma, and 2 studies have suggested that the use of an H-1 receptor antagonist might reduce the development of asthma while the treatment is being administered, at least in subgroups with evidence of high IgE levels. However, no trial to date has conducted follow-up after the initial treatment has been stopped to establish whether the intervention has merely suppressed symptoms or truly prevented disease. Objective: We sought to establish whether the use of cetirizine compared with placebo for 18 months in infants with atopic dermatitis suppressed or truly delayed the onset of asthma, even after cessation of therapy. Methods: The Early Treatment of the Atopic Child study was a double-blinded, parallel-group, randomized trial of 0.25 mg/kg body weight cetirizine administered twice daily compared with placebo given to infants between I and 2 years of age with atopic dermatitis. After 18 months of treatment, follow-up continued for a further 18 months. This article reports the outcome over the full 3 years of follow-up and relates the outcomes to the allergic status on the basis of IgE antibody measurements at recruitment. Results: Although there was no difference in cumulative prevalence of asthma between active and placebo treatment in the intention-to-treat population (P = .7), those infants with evidence of sensitivity to house dust mite, grass pollen, or both who were treated with cetirizine were significantly less likely to have asthma compared with those treated with placebo over the 18 months of treatment (P = .005 and .002, respectively), and this effect was sustained for the grass pollen-sensitized infants over the full 36 months (P = .008). In the house dust mite-sensitized group there was a gradual narrowing of the difference between active and placebo treatment in terms of cumulative prevalence of asthma at the end of 36 months but no evidence of a rebound immediately after the treatment stopped (P = .04). In the placebo population there was a significantly higher risk of development of asthma in those sensitized at baseline to egg (relative risk, 1.4 [95% CI, 1.1-1.7]), house dust mite (relative risk, 1.6 [95% CI, 1.3-1.9%]), grass pollen (relative risk, 1.7 [95% CI, 1.4-2.1]), or cat (relative risk, 1.5 [95% CI, 1.2-1.9]). Early and persistent sensitization conferred a higher risk than transient or later sensitization. Conclusions: Cetirizine compared with placebo truly delays or, in some cases, prevents the development of asthma in a subgroup of infants with atopic dermatitis sensitized to grass pollen and, to a lesser extent, house dust mite. Further studies are required focusing specifically on sensitized groups to substantiate this finding. The study also highlights risk factors for asthma in infants with atopic dermatitis and indicates that early and persistent aeroallergen sensitization confers a higher risk than later development of sensitivity.	Univ Southampton, Sch Med, Div Infect Inflammat & Repair, Southampton S016 6YD, Hants, England	Warner, JO (reprint author), Univ Southampton, Sch Med, Div Infect Inflammat & Repair, Southampton S016 6YD, Hants, England.						Almqvist C, 1999, J ALLERGY CLIN IMMUN, V103, P1012, DOI 10.1016/S0091-6749(99)70172-7; Arnold R, 1999, CLIN EXP ALLERGY, V29, P1681, DOI 10.1046/j.1365-2222.1999.00630.x; Bergmann RL, 1998, CLIN EXP ALLERGY, V28, P965; Burr ML, 1997, CLIN EXP ALLERGY, V27, P1247; Castro-Rodriguez JA, 2000, AM J RESP CRIT CARE, V162, P1403; CIPRANDI G, 1995, J ALLERGY CLIN IMMUN, V95, P612, DOI 10.1016/S0091-6749(95)70324-1; Eriksson Nils E., 1998, Allergology International, V47, P187, DOI 10.2332/allergolint.47.187; Estelle F, 2001, J ALLERGY CLIN IMMUN, V107, P703, DOI 10.1067/mai.2001.113866; GERRITSEN J, 1989, AM REV RESPIR DIS, V140, P1325; IIKURA Y, 1992, ANN ALLERGY, V68, P233; Kulig M, 1998, PEDIAT ALLERG IMM-UK, V9, P61, DOI 10.1111/j.1399-3038.1998.tb00305.x; Marguet C, 2001, PEDIATR ALLERGY IMMU, V12, P27, DOI 10.1034/j.1399-3038.2001.012001027.x; National Heart Lung and Blood Institute, 1995, NIH PUBL, V95-3803; Orange AP, 1997, PEDIATR ALLERGY IMMU, V8, P28, DOI 10.1111/j.1399-3038.1997.tb00139.x; Oswald H, 1997, PEDIATR PULM, V23, P14, DOI 10.1002/(SICI)1099-0496(199701)23:1<14::AID-PPUL2>3.0.CO;2-P; REDIER H, 1992, J ALLERGY CLIN IMMUN, V90, P215, DOI 10.1016/0091-6749(92)90074-C; Simons FER, 1999, J ALLERGY CLIN IMMUN, V104, P433, DOI 10.1016/S0091-6749(99)70389-1; Warner JO, 1998, PEDIATR ALLERGY IMMU, V9, P116; WARNER JO, 1998, CLIN EXP ALLERGY, V28, P179; WOOD RA, 1993, CLIN EXP ALLERGY, V23, P733, DOI 10.1111/j.1365-2222.1993.tb00360.x	20	170	186	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.	DEC	2001	108	6					929	937		10.1067/mai.2001.120015		9	Allergy; Immunology	Allergy; Immunology	505WK	WOS:000172938400008	11742270	
J	Chapman, KR; Tashkin, DP; Pye, DJ				Chapman, KR; Tashkin, DP; Pye, DJ			Gender bias in the diagnosis of COPD	CHEST			English	Article						asthma; misdiagnosis; physician decision making; spirometry; underdiagnosis	OBSTRUCTIVE PULMONARY-DISEASE; INHALED CORTICOSTEROID USE; ASTHMA; DIFFERENCE; DENSITY; CARE; RISK	Background: COPD is thought to be more prevalent among men than women, a finding usually attributed to higher smoking rates and more frequent occupational exposures of significance for men. However, smoking prevalence has increased among women and there is evidence that women may be more susceptible to the adverse pulmonary function effects of smoking than men. There may also be underdiagnosis and misdiagnosis of COPD in both sexes because objective measures of lung function are underused, Objectives: We undertook the present study to determine if there is gender bias in the diagnosis of COPD, such that women are less likely than men to receive a diagnosis of COPD, We also attempted to determine if underuse of I;ng function measurements was a factor in any bias detected. Methods: We surveyed a random sample of 192 primary-care physicians (96 American and 96 Canadian; 154 men and 38 women) using a hypothetical case presentation and a structured interview. The case of cough and dyspnea in a smoker was presented in six versions differing only in the age and sex of the patient. After presentation of the history and physical findings, physicians were asked to state the most probable diagnosis and to choose the diagnostic studies needed, Physicians were then presented with spirometric findings of moderate or severe obstruction without significant bronchodilator response, and the questions repeated. Finally, the negative outcome of an oral steroid trial was described. Results: Initially, COPD was given as the most probable diagnosis significantly more often for men than women (58% vs 42%; p < 0,05), The likelihood of a COPD diagnosis increased significantly and initial differences between sexes decreased as objective information was provided. After spirometry, COPD diagnosis rates for men and women were 74% vs 66% (p = not significant); after the steroid trial 85% vs 79% (p = not significant). Only 22% of physicians would have requested spirometry after the initial presentation, Conclusions: In North America, primary-care physicians underdiagnose COPD, particularly in women. Spirometry reduces the risk of underdiagnosis and gender bias but is underused.	Univ Toronto, Dept Med, Div Resp Med, Toronto, ON, Canada; Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA; Westmount Res Consultants, Toronto, ON, Canada	Chapman, KR (reprint author), Univ Hlth Network, Asthma Ctr, Suite 4-011 ECW,399 Bathurst St, Toronto, ON M5T 2S8, Canada.						AYANIAN JZ, 1991, NEW ENGL J MED, V325, P221, DOI 10.1056/NEJM199107253250401; CELLI BR, 1995, AM J RESP CRIT CARE, V152, pS77; FRANKS P, 1995, ANN INTERN MED, V123, P548; HALL JA, 1988, MED CARE, V26, P657, DOI 10.1097/00005650-198807000-00002; HANANIA NA, 1995, J ALLERGY CLIN IMMUN, V96, P571, DOI 10.1016/S0091-6749(95)70254-7; IP M, 1994, CHEST, V105, P1722, DOI 10.1378/chest.105.6.1722; Jackevicius C, 1997, CHEST, V111, P296, DOI 10.1378/chest.111.2.296; Jackevicius CA, 1997, ANN PHARMACOTHER, V31, P160; Joyce DP, 1996, CHEST, V109, P697, DOI 10.1378/chest.109.3.697; KANNER RE, 1994, AM J RESP CRIT CARE, V150, P956; KESTEN S, 1993, CHEST, V104, P254, DOI 10.1378/chest.104.1.254; KUHN CE, 1995, PEDIATR PULM, V19, P156, DOI 10.1002/ppul.1950190303; Prescott E, 1997, EUR RESPIR J, V10, P822; REA HH, 1991, ANN ALLERGY, V66, P48; SHEFFER SL, 1992, PUBLICATION	15	170	172	1	4	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	JUN	2001	119	6					1691	1695		10.1378/chest.119.6.1691		5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	441NB	WOS:000169235500014	11399692	
J	Kouzaki, H; O'Grady, SM; Lawrence, CB; Kita, H				Kouzaki, Hideaki; O'Grady, Scott M.; Lawrence, Christopher B.; Kita, Hirohito			Proteases Induce Production of Thymic Stromal Lymphopoietin by Airway Epithelial Cells through Protease-Activated Receptor-2	JOURNAL OF IMMUNOLOGY			English	Article							NF-KAPPA-B; DUST MITE ALLERGEN; DENDRITIC CELLS; CYTOKINE PRODUCTION; ADAPTIVE IMMUNITY; HUMAN EOSINOPHILS; TYPE-2 RESPONSES; INHALED ANTIGEN; IFN-GAMMA; ASTHMA	Thymic stromal lymphopoietin (TSLP) is produced by epithelial cells and triggers dendritic cell-mediated Th2-type inflammation. Although TSLP is up-regulated in epithelium of patients with asthma, the factors that control TSLP production have not been studied extensively. Because mouse models suggest roles for protease(s) in Th2-type immune responses, we hypothesized that proteases from airborne allergens may induce TSLP production in a human airway epithelial cell line, BEAS-2B. TSLP mRNA and protein were induced when BEAS-2B cells were exposed to prototypic proteases, namely, trypsin and papain. TSLP induction by trypsin required intact protease activity and also a protease-sensing G protein-coupled receptor, protease-activated receptor (PAR)-2; TSLP induction by papain was partially dependent on PAR-2. In humans, exposure to ubiquitous airborne fungi, such as Alternaria, is implicated in the development and exacerbation of asthma. When BEAS-2B cells or normal human bronchial epithelial cells were exposed to Alternaria extract, TSLP was potently induced. The TSLP-inducing activity of Alternaria was partially blocked by treating the extract with a cysteine protease inhibitor, E-64, or by infecting BEAS-2B cells with small interfering RNA for PAR-2. Protease-induced TSLP production by BEAS-2B cells was enhanced synergistically by IL-4 and abolished by IFN-gamma. These findings demonstrate that TSLP expression is induced in airway epithelial cells by exposure to allergen-derived proteases and that PAR-2 is involved in the process. By promoting TSLP production in the airways, proteases associated with airborne allergens may facilitate the development and/or exacerbation of Th2-type airway inflammation, particularly in allergic individuals. The Journal of Immunology, 2009, 183: 1427-1434.	[Kouzaki, Hideaki; Kita, Hirohito] Mayo Clin, Dept Internal Med, Div Allerg Dis, Rochester, MN 55905 USA; [Kouzaki, Hideaki] Shiga Univ Med Sci, Dept Otorhinolaryngol, Shiga, Japan; [O'Grady, Scott M.] Univ Minnesota, Dept Integrated Biol, St Paul, MN 55108 USA; [O'Grady, Scott M.] Univ Minnesota, Dept Physiol & Anim Sci, St Paul, MN 55108 USA; [Lawrence, Christopher B.] Virginia Polytech Inst & State Univ, Virginia Bioinformat Inst, Blacksburg, VA 24061 USA; [Lawrence, Christopher B.] Virginia Polytech Inst & State Univ, Dept Biol Sci, Blacksburg, VA 24061 USA	Kita, H (reprint author), Mayo Clin, Dept Internal Med, Div Allerg Dis, Rochester, MN 55905 USA.	kita.hirohito@mayo.edu			National Institutes of Health; National Institute of Allergy and Infectious Diseases [AI49235]; Mayo Foundation	This work was supported in part by the National Institutes of Health, National Institute of Allergy and Infectious Diseases (Grant AI49235) and the Mayo Foundation.	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Immunol.	JUL 15	2009	183	2					1427	1434		10.4049/jimmunol.0900904		8	Immunology	Immunology	468JD	WOS:000267812600071	19561109	
J	Passalacqua, G; Durham, SR				Passalacqua, Giovanni; Durham, Stephen R.		Global Allergy Asthma	Allergic rhinitis and its impact on asthma update: Allergen immunotherapy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						injection immunotherapy; sublingual immunotherapy; efficacy; safety; mechanisms	GRASS-POLLEN IMMUNOTHERAPY; HOUSE-DUST-MITE; SUBLINGUAL-SWALLOW IMMUNOTHERAPY; RANDOMIZED CONTROLLED-TRIAL; MONOPHOSPHORYL-LIPID-A; PRESEASONAL-SPECIFIC IMMUNOTHERAPY; SYSTEMIC IMMUNOLOGICAL CHANGES; MESSENGER-RNA EXPRESSION; PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND	The Allergic Rhinitis and its Impact on Asthma document was first published in 2001. Since then, new data on specific immunotherapy have appeared. This review is intended as an update to the original document. MedLine (2001 to June 2006) was searched with appropriate key words, and panelists were asked to identify further relevant articles. Randomized controlled trials were considered for the evaluation of efficacy. For the evaluation of safety, and additional effects, studies with lower grades of evidence were included. The clinical efficacy of injection immunotherapy in rhinitis and asthma was confirmed, as well as the safety, provided that recommendations are followed. Studies have demonstrated the long-term efficacy and the preventive effect of immunotherapy in reducing the onset of new sensitizations. One randomized open trial demonstrated that in children with allergic rhinitis, injection immunotherapy may reduce the risk of developing asthma. There is strong evidence that sublingual immunotherapy is effective in allergic rhinitis in adults. Recent meta-analyses demonstrated its efficacy in allergic rhinitis in children and in asthma, although more definitive trials are required. Current data indicate that sublingual immunotherapy is safe and the rate of adverse reactions is not greater below 5 years of age. One randomized open trial showed that in children with allergic rhinitis, sublingual immunotherapy reduced the onset of asthma. Further studies are needed to identify the optimal maintenance dose and to elucidate the mechanism of action. Novel approaches for immunotherapy are currently under evaluation, including the use of adjuvants, peptides. and DNA-conjugated and recombinant allergens.	Univ Genoa, Dept Internal Med, I-16132 Genoa, Italy; Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London, England	Passalacqua, G (reprint author), Univ Genoa, Dept Internal Med, Padiglione Maragliano,Lgo R Benzi 10, I-16132 Genoa, Italy.	passalacqua@unige.it	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284	Medical Research Council [G9805965]		AALBERSE RC, 1983, J IMMUNOL, V130, P722; Aaronson DW, 2004, J ALLERGY CLIN IMMUN, V113, P1117, DOI 10.1016/j.jaci.2004.01.756; Abramson MJ, 2003, COCHRANE DB SYST REV, V4, DOI DOI 10.1002/14651858.CD001186; Alvarez-Cuesta E, 2006, ALLERGY, V61, P1, DOI 10.1111/j.1398-9995.2006.01219_1.x; Alvarez-Cuesta E, 2005, CLIN EXP ALLERGY, V35, P572, DOI 10.1111/j.1365-2222.2005.02245.x; Ameal A, 2005, ALLERGY, V60, P1178, DOI 10.1111/j.1398-9995.2005.00862.x; Andre C, 2003, INT ARCH ALLERGY IMM, V131, P111, DOI 10.1159/000070926; Antico A, 2006, ALLERGY, V61, P1236, DOI 10.1111/j.1398-9995.2006.01155.x; Ariano R, 2001, Allergol Immunopathol (Madr), V29, P238; 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Allergy Clin. Immunol.	APR	2007	119	4					881	891		10.1016/j.jaci.2007.01.045		11	Allergy; Immunology	Allergy; Immunology	157OK	WOS:000245729500016	17418661	
J	Johnston, NW; Johnston, SL; Duncan, JM; Greene, JM; Kebadze, T; Keith, PK; Roy, M; Waserman, S; Sears, MR				Johnston, NW; Johnston, SL; Duncan, JM; Greene, JM; Kebadze, T; Keith, PK; Roy, M; Waserman, S; Sears, MR			The September epidemic of asthma exacerbations in children: A search for etiology	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; children; viral infections; rhinovirus; school return; inhaled corticosteroid; leukotriene receptor antagonist	RESPIRATORY-INFECTIONS; RHINOVIRUS INFECTIONS; HOSPITAL ADMISSION; CHILDHOOD ASTHMA; AIR-POLLUTION; ALLERGENS; FREQUENCY; EXPOSURE; VIRUSES; SCHOOL	Background: Predictable peaks of asthma exacerbation requiring hospital treatment, of greatest magnitude in children and of uncertain etiology, occur globally after school returns. Objective: We wished to determine whether asthmatic children requiring emergency department treatment for exacerbations after school return in September were more likely to have respiratory viruses present and less likely to have prescriptions for control medications than children with equally severe asthma not requiring emergent treatment. Methods: Rates of viral detection and characteristics of asthma management in 57 (of 60) children age 5 to 15 years presenting to emergency departments with asthma in 2 communities in Canada between September 10 and 30, 2001, (cases) were compared with those in 157 age-matched volunteer children with asthma of comparable severity studied simultaneously (controls). Results: Human picornaviruses were detected in 52% of cases and 29% of controls (P=.002) and viruses of any type in 62% of cases and 41% of controls (P =.011). Cases were less likely to have been prescribed controller medication (inhaled corticosteroid, 49% vs 85%; P <.0001; leukotriene receptor antagonist, 9% vs 21%; P =.04). Conclusion: Respiratory viruses were detected in the majority of children presenting to emergency departments with asthma during the September epidemic of the disease and in a significant minority of children with asthma in the community. The latter were more likely to have anti-inflammatory medication prescriptions than children requiring emergent treatment. Such medication may reduce the risk of emergency department treatment for asthma during the September epidemic.	St Josephs Healthcare, Firestone Inst Resp Hlth, Hamilton, ON L8N 4A6, Canada; McMaster Univ, Dept Med, Hamilton, ON L8N 4A6, Canada; Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Resp Med, London, England; Brant Community Healthcare Syst, Brantford, ON, Canada	Johnston, NW (reprint author), St Josephs Healthcare, Firestone Inst Resp Hlth, 50 Charlton Ave E, Hamilton, ON L8N 4A6, Canada.	njohnsto@sympatico.ca	Johnston, Sebastian/I-2423-2012				Almqvist C, 1999, J ALLERGY CLIN IMMUN, V103, P1012, DOI 10.1016/S0091-6749(99)70172-7; Arruda E, 1997, J CLIN MICROBIOL, V35, P2864; BATES DV, 1990, ENVIRON RES, V51, P51, DOI 10.1016/S0013-9351(05)80182-3; Blaisdell CJ, 2002, J ASTHMA, V39, P567, DOI 10.1081/JAS-120014921; 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; Dales RE, 1996, EUR RESPIR J, V9, P72, DOI 10.1183/09031936.96.09010072; DEKLUIJVER J, 2002, AM J RESP CRIT CARE, V168, P1174; Fleming DM, 2000, THORAX, V55, P657, DOI 10.1136/thorax.55.8.657; Garty BZ, 1998, ANN ALLERG ASTHMA IM, V81, P563, DOI 10.1016/S1081-1206(10)62707-X; Gergen PJ, 2002, J PEDIATR-US, V141, P631, DOI 10.1067/mpd.2002.127510; Gern JE, 1999, CLIN MICROBIOL REV, V12, P9; Gern JE, 2002, AM J MED, V112, p19S; Green RM, 2002, BRIT MED J, V324, P763, DOI 10.1136/bmj.324.7340.763; Habbick BF, 1999, CAN MED ASSOC J, V160, P1824; Harju T, 1997, EUR J PEDIATR, V156, P436, DOI 10.1007/s004310050632; JOHNSTON NW, 2001, AM J RESP CRIT CARE, V163, pA359; Johnston SL, 2003, AM J RESP CRIT CARE, V168, P1145, DOI 10.1164/rccm.2309004; Johnston SL, 1996, AM J RESP CRIT CARE, V154, P654; LONGINI IM, 1984, INT J EPIDEMIOL, V13, P99, DOI 10.1093/ije/13.1.99; Makela MJ, 2003, J ALLERGY CLIN IMMUN, V112, P861, DOI 10.1067/mai.2003.1768; MAO Y, 1990, CAN J PUBLIC HEALTH, V81, P226; MELETH S, 1997, CAN RESP J, V4, P263; Message SD, 2002, BRIT MED BULL, V61, P29, DOI 10.1093/bmb/61.1.29; Monteil MA, 2000, J ASTHMA, V37, P677, DOI 10.3109/02770900009087306; Perzanowski MS, 1999, J ALLERGY CLIN IMMUN, V103, P1018, DOI 10.1016/S0091-6749(99)70173-9; POTTER PC, 1984, S AFR MED J, V15, P397; Rakes Gary P., 1999, American Journal of Respiratory and Critical Care Medicine, V159, P785; Rosas I, 1998, ALLERGY, V53, P394, DOI 10.1111/j.1398-9995.1998.tb03911.x; STORR J, 1989, ARCH DIS CHILD, V64, P103; STRACHAN D, 2002, COLLATION COMPAR DAT; Taskinen T, 1999, ACTA PAEDIATR, V88, P1373, DOI 10.1080/080352599750030112; Teichtahl H, 1997, CHEST, V112, P591, DOI 10.1378/chest.112.3.591; Thumerelle C, 2003, PEDIATR PULM, V35, P75, DOI 10.1002/ppul.10191; Tortolero SR, 2002, J SCHOOL HEALTH, V72, P33; WEISS KB, 1990, JAMA-J AM MED ASSOC, V263, P2323	36	169	172	0	10	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					132	138		10.1016/j.jaci.2004.09.025		7	Allergy; Immunology	Allergy; Immunology	886XS	WOS:000226267000019	15637559	
J	Bornehag, CG; Sundell, J; Bonini, S; Custovic, A; Malmberg, P; Skerfving, S; Sigsgaard, T; Verhoeff, A				Bornehag, CG; Sundell, J; Bonini, S; Custovic, A; Malmberg, P; Skerfving, S; Sigsgaard, T; Verhoeff, A			Dampness in buildings as a risk factor for health effects, EUROEXPO: a multidisciplinary review of the literature (1998-2000) on dampness and mite exposure in buildings and health effects	INDOOR AIR			English	Review						indoor environment; damp buildings; mite exposure; health effects; review	HOUSE-DUST-MITE; INDOOR ALLERGEN LEVELS; RESPIRATORY SYMPTOMS; ATOPIC-DERMATITIS; SCHOOL-CHILDREN; CHILDHOOD ASTHMA; AIR-POLLUTION; NASAL LAVAGE; BRONCHIAL HYPERRESPONSIVENESS; SYSTEMIC SYMPTOMS	The scientific literature on health effects from dampness in buildings, including mite exposure over the period 1998-2000 has been reviewed by a European group (EUROEXPO) of eight scientists in experience from medicine, epidemiology, toxicology and engineering. Forty studies deemed relevant have been the foundation for the conclusions. Dampness in buildings is a risk factor for health effects among atopics and non-atopics both in domestic and in public environments. However, the literature is not conclusive in respect of causative agents, e.g. mites, microbiological agents and organic chemicals from degraded building materials. There is a strong need for more multidisciplinary studies including expertise from all relevant areas. A general conclusion from the work was that there is a strong need for multidisciplinary reviews in scientific journals of articles dealing with associations between indoor environmental factors and health effects.	Swedish Natl Testing & Res Inst, Boras, Sweden; Tech Univ Denmark, Int Ctr Indoor Environm & Energy, Kongens Lyngby, Denmark; Italian Natl Res Council, Inst Neurobiol & Mol Med, Rome, Italy; Univ Naples 2, Naples, Italy; Wythenshawe Hosp, NW Lung Ctr, Manchester M23 9LT, Lancs, England; Natl Inst Working Life, Stockholm, Sweden; Lund Univ, Environm & Occupat Med Sect, Lund, Sweden; Univ Aarhus, Dept Environm & Occupat Med, Aarhus, Denmark; Municipal Hlth Serv Amsterdam, Dept Epidemiol & Hlth Promot, Amsterdam, Netherlands; Karlstad Univ, SE-65188 Karlstad, Sweden	Bornehag, CG (reprint author), Karlstad Univ, SE-65188 Karlstad, Sweden.	carl-qustaf.bornehaq@kau.se	Sundell, Jan/B-2857-2012; Verhoeff, Arnoud/F-7924-2013; Custovic, Adnan/A-2435-2012	Custovic, Adnan/0000-0001-5218-7071; Sigsgaard, Torben/0000-0002-2043-7571; Bonini, Sergio/0000-0003-0079-3031			Ahlbom A, 1998, INDOOR AIR, V8, P219, DOI 10.1111/j.1600-0668.1998.00003.x; Ahman M, 2000, INDOOR AIR, V10, P57, DOI 10.1034/j.1600-0668.2000.010001057.x; 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J	Black, PN; Udy, AA; Brodie, SM				Black, PN; Udy, AA; Brodie, SM			Sensitivity to fungal allergens is a risk factor for life-threatening asthma	ALLERGY			English	Article						asthma; fungal allergens	FATAL ASTHMA	Background: Previous studies have suggested that sensitivity to Alternaria and Cladosporium may be risk factors for life-threatening asthma. We have investigated this by studying the relationship between skin tests for fungal spores and admission to atl intensive care unit (ICU) for asthma. Methods: Skin prick tests for fungal spores (Alternaria tenuis, Cladosporium cladosporoides, Helminthosporium maydis, and Epicoccum nigrum), cat dander, house-dust mite (Dermatophagoides pteronyssinus), and a seven-grass mix were performed in three groups of patients: patients admitted to an ICU with an attack of asthma; those who had received emergency treatment for asthma but had not been admitted to an ICU, and those who had never required emergency treatment for their asthma. Results: Twenty of 37 patients (54%) admitted to the ICU had a positive skin test for one or more fungal allergens compared with 15/50 patients (30%) in each of the other groups (P=0.005). The ICU patients were no more likely to have positive skin tests for the grass mix, cat dander, or house-dust mite than the other patients. Conclusions: a positive skin test for fungal allergens is a risk factor for admission to an ICU with an acute attack of asthma.	Univ Auckland, Dept Med, Auckland, New Zealand	Black, PN (reprint author), Auckland Hosp, Dept Med, Private Bag 92024, Auckland, New Zealand.		Udy, Andrew /G-2538-2010	Udy, Andrew /0000-0002-6284-2022			ABRAMSON M, 1995, AUST N Z MED J, V25, P424; BENATAR SR, 1986, NEW ENGL J MED, V314, P423, DOI 10.1056/NEJM198602133140706; BROWN HM, 1978, CLIN ALLERGY, V7, P611; CAREY MJ, 1986, BRIT MED J, V293, P843; *COMM SKIN TEST ST, 1988, CLIN ALLERGY, V18, P305; Derrick EH, 1972, AUSTR NZ J MEDICINE, V3, P235; HASNAIN SM, 1985, NEW ZEAL MED J, V98, P342; LI DW, 1995, INT J BIOMETEOROL, V39, P74, DOI 10.1007/BF01212584; MOLFINO NA, 1994, EUR RESPIR J, V7, P981; OHOLLAREN MT, 1991, NEW ENGL J MED, V324, P359, DOI 10.1056/NEJM199102073240602; PEAT JK, 1995, MED J AUSTRALIA, V163, P22; RICHARDS GN, 1993, THORAX, V48, P1105, DOI 10.1136/thx.48.11.1105; Richerson HB, 1986, ASTHMA CLIN PHARM TH, P23; ROUX P, 1993, S AFR MED J, V83, P177; SOLOMON WR, 1993, ALLERGY PRINCIPLES P, P469; TARGONSKI PV, 1995, J ALLERGY CLIN IMMUN, V95, P955, DOI 10.1016/S0091-6749(95)70095-1	16	169	175	0	6	MUNKSGAARD INT PUBL LTD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	MAY	2000	55	5					501	504		10.1034/j.1398-9995.2000.00293.x		4	Allergy; Immunology	Allergy; Immunology	308KT	WOS:000086710800013	10843433	
J	Xiao, C; Puddicombe, SM; Field, S; Haywood, J; Broughton-Head, V; Puxeddu, I; Haitchi, HM; Vernon-Wilson, E; Sammut, D; Bedke, N; Cremin, C; Sones, J; Djukanovic, R; Howarth, PH; Collins, JE; Holgate, ST; Monk, P; Davies, DE				Xiao, Chang; Puddicombe, Sarah M.; Field, Sarah; Haywood, Joel; Broughton-Head, Victoria; Puxeddu, Ilaria; Haitchi, Hans Michael; Vernon-Wilson, Elizabeth; Sammut, David; Bedke, Nicole; Cremin, Catherine; Sones, Jody; Djukanovic, Ratko; Howarth, Peter H.; Collins, Jane E.; Holgate, Stephen T.; Monk, Phillip; Davies, Donna E.			Defective epithelial barrier function in asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Tight junction; epidermal growth factor; cigarette smoke; asthma; epithelial barrier	EPIDERMAL-GROWTH-FACTOR; TIGHT JUNCTIONS; BRONCHIAL EPITHELIUM; ULCERATIVE-COLITIS; FACTOR RECEPTOR; ERBB RECEPTORS; HEGF LEVELS; DISEASE; CELLS; EXPRESSION	Background: Asthma is a complex disease involving gene and environment interactions. Although atopy is a strong predisposing risk factor for asthma, local tissue susceptibilities are required for disease expression. The bronchial epithelium forms the interface with the external environment and is pivotally involved in controlling tissue homeostasis through provision of a physical barrier controlled by tight junction (TJ) complexes. Objectives: To explain the link between environment exposures and airway vulnerability, we hypothesized that epithelial TJs are abnormal in asthma, leading to increased susceptibility to environmental agents. Methods: Localization of TJs in bronchial biopsies and differentiated epithelial cultures was assessed by electron microscopy or immunostaining. Baseline permeability and the effect of cigarette smoke and growth factor were assessed by measurement of transepithelial electrical resistance and passage of fluorescently labeled dextrans. Results: By using immunostaining, we found that bronchial biopsies from asthmatic subjects displayed patchy disruption of TJs. In differentiated bronchial epithelial cultures, TJ formation and transepithelial electrical resistance were significantly lower (P < .05) in cultures from asthmatic donors (n = 43) than from normal controls (n = 40) and inversely correlated with macromolecular permeability. Cultures from asthmatic donors were also more sensitive to disruption by cigarette smoke extract. Epidermal growth factor enhanced basal TJ formation in cultures from asthmatic subjects (P < .01) and protected against cigarette smoke-induced barrier disruption (P < .01). Conclusions: Our results show that the bronchial epithelial barrier in asthma is compromised. This defect may facilitate the passage of allergens and other agents into the airway tissue, leading to immune activation and may thus contribute to the end organ expression of asthma. (J Allergy Clin Immunol 2011;128:549-56.)	[Davies, Donna E.] Univ Southampton, Div Infect Inflammat & Immun, Sir Henry Wellcome Labs, Sch Med,Southampton Gen Hosp, Southampton SO16 6YD, Hants, England; [Puxeddu, Ilaria; Haitchi, Hans Michael; Sammut, David; Bedke, Nicole; Djukanovic, Ratko; Howarth, Peter H.; Collins, Jane E.; Holgate, Stephen T.; Davies, Donna E.] Univ Southampton, Sch Med,Southampton Gen Hosp, Southampton NIHR Resp Biomed Res Unit, Southampton SO16 6YD, Hants, England	Davies, DE (reprint author), Univ Southampton, Div Infect Inflammat & Immun, Sir Henry Wellcome Labs, Sch Med,Southampton Gen Hosp, Level F,S Block,Mailpoint 810, Southampton SO16 6YD, Hants, England.	donnad@soton.ac.uk	Davies, Donna/H-2993-2012; Haywood, Joel/G-8311-2016	Djukanovic, Ratko/0000-0001-6039-5612	Synairgen Research Ltd; University of Southampton; National Institute of Health Research (United Kingdom); Medical Research Council; Synairgen	This work was funded by Synairgen Research Ltd and the University of Southampton. Stephen T. Holgate is a Medical Research Council Clinical Professor.; Disclosure of potential conflict of interest: C. Xiao, S. Field, J. Haywood, V. Broughton-Head, J. Sones, and P. Monk are employees of Synairgen Research Limited. R. Djukanovic is a cofounder and shareholder of and a consultant for Synairgen. P. H. Howarth has received research support from the National Institute of Health Research (United Kingdom). S. T. Holgate owns shares in and consults for Synairgen; is vice president of the British Lung Foundation; and has received research support from the Medical Research Council. D. E. Davies is a cofounder and shareholder of, is a consultant for, and has received research support from Synairgen. The rest of the authors have declared that they have no conflict of interest.	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Allergy Clin. Immunol.	SEP	2011	128	3					549	U177		10.1016/j.jaci.2011.05.038		20	Allergy; Immunology	Allergy; Immunology	812HS	WOS:000294283400013	21752437	
J	Saarinen, KM; Pelkonen, AS; Makela, M; Savilahti, E				Saarinen, KM; Pelkonen, AS; Makela, M; Savilahti, E			Clinical course and prognosis of cow's milk allergy are dependent on milk-specific IgE status	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						cow's milk allergy; IgE; sensitization; skin test; tolerance; atopy	FOLLOW-UP; ATOPIC-DERMATITIS; EGG ALLERGY; 4 REGIONS; CHILDREN; AGE; INFANTS; SENSITIZATION; TOLERANCE; FOOD	Background: Large, prospective population-based studies on clinical course, development of tolerance, and risk for other atopy in children with cow's milk allergy (CMA) are lacking. Objective: We investigated the development of tolerance and the risk for asthma, rhinoconjunctivitis, atopic dermatitis, and sensitization in children with CMA followed to school age. Methods: We followed 118 children with CMA until recovery and repeatedly measured their sensitization to cow's milk (CM). At age 8.6 years, 94 allergic subjects and 80 control subjects from the same cohort were studied for atopic diseases and sensitization. In addition, the parents of 12 allergic subjects and 26 control children returned a questionnaire on atopy, respectively. Results: IgE-mediated CMA was detected in 86 (73%) children; at age 8.6 years, 13 (15%) had persistent CMA. All children with IgE-negative CMA were tolerant by age 5.0 years (P < .0001). Risk factors for persistent CMA at age 2.0 years were sensitization to CM at age 1.6 years (odds ratio, 6.3; 95% CI, 2.6-15.2), urticaria at diagnostic challenge (odds ratio, 3.3; 95% CI, 1.4-7.8), CM exposure at the maternity hospital (odds ratio, 3.2; 95% CI, 1.4-7.8), and early sensitization to egg (odds ratio, 2.8; 95% CI, 1.2-6.6). By age 8.6 years, children with IgE-positive CMA more frequently had asthma (31% vs 13%, P <= .01), rhinoconjunctivitis (66% vs 21%, P <= .001), atopic eczema (81% vs 26%, P <= .001), and sensitization to any allergen (88% vs 39%, P <= .001) than control subjects. CMA and family history of atopy were independent risk factors for atopic diseases, and CMA was also a risk factor for sensitization to inhalant allergens. Conclusion: IgE-mediated CMA often persists to school age and is a risk factor for other atopy; non-IgE-mediated CMA, by contrast, is a benign infantile condition.	Univ Helsinki, Hosp Children & Adolescents, FIN-00029 Helsinki, Finland; Univ Helsinki, Cent Hosp, Dept Allergol Skin & Allergy Hosp, Helsinki, Finland	Savilahti, E (reprint author), Univ Helsinki, Hosp Children & Adolescents, POB 281, FIN-00029 Helsinki, Finland.	erkki.savilahti@hus.fi		Makela, Mika/0000-0002-2933-3111			Arshad SH, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.2.e33; Boyano-Martinez T, 2002, J ALLERGY CLIN IMMUN, V110, P304, DOI 10.1067/mai.2002.126081; DANNAEUS A, 1979, ACTA PAEDIATR SCAND, V68, P377, DOI 10.1111/j.1651-2227.1979.tb05023.x; de Jong MH, 2002, ARCH DIS CHILD, V86, P365, DOI 10.1136/adc.86.5.365; Garcia-Ara MC, 2004, CLIN EXP ALLERGY, V34, P866, DOI 10.1111/j.1365-2222.2004.01976.x; Gustafsson D, 2003, PEDIATR ALLERGY IMMU, V14, P448, DOI 10.1046/j.0905-6157.2003.00093.x; HATTEVIG G, 1984, CLIN ALLERGY, V14, P551, DOI 10.1111/j.1365-2222.1984.tb02243.x; HILL DJ, 1993, CLIN EXP ALLERGY, V23, P124, DOI 10.1111/j.1365-2222.1993.tb00307.x; Host A, 2002, PEDIATR ALLERGY IMMU, V13, P23, DOI 10.1034/j.1399-3038.13.s.15.7.x; HOST A, 1990, ALLERGY, V45, P587, DOI 10.1111/j.1398-9995.1990.tb00944.x; JAMES JM, 1992, J PEDIATR-US, V121, P371, DOI 10.1016/S0022-3476(05)81788-3; Jarvinen KM, 2002, J ALLERGY CLIN IMMUN, V110, P293, DOI 10.1067/mai.2002.126080; Kulig M, 1998, PEDIAT ALLERG IMM-UK, V9, P61, DOI 10.1111/j.1399-3038.1998.tb00305.x; Kulig M, 1999, J ALLERGY CLIN IMMUN, V103, P1173, DOI 10.1016/S0091-6749(99)70195-8; LINDFORS ATB, 1992, ALLERGY, V47, P207, DOI 10.1111/j.1398-9995.1992.tb00652.x; Nickel R, 1997, J ALLERGY CLIN IMMUN, V99, P613, DOI 10.1016/S0091-6749(97)70021-6; Pekkanen J, 1997, EUR RESPIR J, V10, P1787, DOI 10.1183/09031936.97.10081787; Remes ST, 1998, ALLERGY, V53, P682, DOI 10.1111/j.1398-9995.1998.tb03954.x; Saarinen KM, 1999, J ALLERGY CLIN IMMUN, V104, P457, DOI 10.1016/S0091-6749(99)70393-3; Saarinen KM, 2000, CLIN EXP ALLERGY, V30, P400, DOI 10.1046/j.1365-2222.2000.00732.x; SCHRANDER JJP, 1993, EUR J PEDIATR, V152, P640, DOI 10.1007/BF01955238; SCHRANDER JJP, 1992, EUR J PEDIATR, V151, P783, DOI 10.1007/BF01959091; Sicherer SH, 1999, CLIN EXP ALLERGY, V29, P507; Sporik R, 2000, CLIN EXP ALLERGY, V30, P1540, DOI 10.1046/j.1365-2222.2000.00928.x; Tariq SM, 2000, PEDIATR ALLERGY IMMU, V11, P162, DOI 10.1034/j.1399-3038.2000.00077.x; Vanto T, 2004, J PEDIATR-US, V144, P218, DOI 10.1016/j.jpeds.2003.10.063; Wahn U, 2001, J ALLERGY CLIN IMMUN, V107, P567, DOI 10.1067/mai.2001.112943; Weiner HL, 1997, IMMUNOL TODAY, V18, P335, DOI 10.1016/S0167-5699(97)01053-0	28	168	178	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.	OCT	2005	116	4					869	875		10.1016/j.jaci.2005.06.018		7	Allergy; Immunology	Allergy; Immunology	017IF	WOS:000235686600023	16210063	
J	Mapp, CE; Boschetto, P; Maestrelli, P; Fabbri, LM				Mapp, CE; Boschetto, P; Maestrelli, P; Fabbri, LM			Occupational asthma	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Review						asthma; management; risk; susceptibility; workplace	NATURAL-RUBBER LATEX; EXHALED NITRIC-OXIDE; WORK-RELATED ASTHMA; AIRWAYS DYSFUNCTION SYNDROME; DIISOCYANATE-INDUCED ASTHMA; HEALTH-CARE WORKERS; WESTERN RED CEDAR; EXPOSURE-RESPONSE RELATIONSHIPS; LABORATORY-ANIMAL WORKERS; ISOCYANATE-INDUCED ASTHMA	Substantial epidemiologic and clinical evidence indicates that agents inhaled at work can induce asthma. In industrialized countries, occupational factors have been implicated in 9 to 15% of all cases of adult asthma. Work-related asthma includes (1) immunologic occupational asthma (OA), characterized by a latency period before the onset of symptoms; (2) nonimmunologic OA, which occurs after single or multiple exposures to high concentrations of irritant materials; (3) work-aggravated asthma, which is preexisting or concurrent asthma exacerbated by workplace exposures; and (4) variant syndromes. Assessment of the work environment has improved, making it possible to measure concentrations of several high- and low-molecular-weight agents in the workplace. The identification of host factors, polymorphisms, and candidate genes associated with OA is in progress and may improve our understanding of mechanisms involved in OA. A reliable diagnosis of OA should be confirmed by objective testing early after its onset. Removal of the worker from exposure to the causal agent and treatment with inhaled glucocorticoids lead to a better outcome. Finally, strategies for preventing OA should be implemented and their cost-effectiveness examined.	Univ Ferrara, Sect Hyg & Occupat Med, Dept Clin & Expt Med, I-44100 Ferrara, Italy; Univ Padua, Dept Environm Med & Publ Hlth, Padua, Italy; Univ Modena, Dept Hematol & Oncol, Sect Resp Dis, I-41100 Modena, Italy	Mapp, CE (reprint author), Univ Ferrara, Sect Hyg & Occupat Med, Dept Clin & Expt Med, Via Fossato di Mortara 64-B, I-44100 Ferrara, Italy.	mapp@unipd.it	Fabbri, Leonardo/I-4055-2012	Fabbri, Leonardo/0000-0001-8894-1689			Adisesh LA, 1998, CLIN EXP ALLERGY, V28, P876; Akpinar-Elci M, 2004, CHEST, V125, P2336, DOI 10.1378/chest.125.6.2336; Alberts WM, 1996, CHEST, V109, P1618, DOI 10.1378/chest.109.6.1618; Allmers H, 2000, INT ARCH OCC ENV HEA, V73, P181, DOI 10.1007/s004200050025; Allmers H, 2002, J ALLERGY CLIN IMMUN, V110, P318, DOI 10.1067/mai.2002.126461; ALVING K, 1993, EUR RESPIR J, V6, P1368; Alwis K U, 1999, Appl Occup Environ Hyg, V14, P598; American Medical Association, 2000, GUIDES EVALUATION PE; Ameille J, 2003, OCCUP ENVIRON MED, V60, P136, DOI 10.1136/oem.60.2.136; 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J. Respir. Crit. Care Med.	AUG 1	2005	172	3					280	305		10.1164/rccm.200311-1575SO		26	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	949IM	WOS:000230778600006	15860754	
J	Ziska, LH; Gebhard, DE; Frenz, DA; Faulkner, S; Singer, BD; Straka, JG				Ziska, LH; Gebhard, DE; Frenz, DA; Faulkner, S; Singer, BD; Straka, JG			Cities as harbingers of climate change: Common ragweed, urbanization, and public health	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						global change; seasonal allergenic rhinitis; Amb a 1; common ragweed	CO2 CONCENTRATION; UNITED-STATES; PROTEIN; ALLERGY; AEROALLERGENS; QUANTITATION; NUTRITION; PROGRAM; ASSAY; USA	Background: Although controlled laboratory experiments have been conducted to demonstrate the sensitivity of allergenic pollen production to future climatic change tie, increased CO2 and temperature), no in situ data are available. Objective: The purpose of this investigation was to assess, under realistic conditions, the impact of climatic change on pollen production of common ragweed, a ubiquitous weed occurring in disturbed sites and the principal source of pollen associated with seasonal allergenic rhinitis. Methods: We used an existing temperature/CO2 gradient between urban and rural areas to examine the quantitative and qualitative aspects of ragweed growth and pollen production. Results: For 2000 and 200 1, average daily (24-hour) values of CO2 concentration and air temperature within an urban environment were 30% to 31% and 1.8degrees to 2.0degreesC (3.4degrees to 3.6degreesF) higher than those at a rural site. This result is consistent with most global change scenarios. Ragweed grew faster, flowered earlier, and produced significantly greater above-ground biomass and ragweed pollen at urban locations than at rural locations. Conclusions: Here we show that 2 aspects of future global environmental change, air temperature and atmospheric CO2, are already significantly higher in urban relative to rural areas. In general, we show that regional urbanization-induced temperature/CO2 increases similar to those associated with projected global climatic change might already have public health consequences; we suggest that urbanization, per se, might provide a low-cost alternative to current experimental methods evaluating plant responses to climate change. (J Allergy Clin Immunol 2003;111:290-5.).	USDA ARS, Alternate Crop & Syst Lab, Beltsville, MD 20705 USA; Surveillance Data Inc, St Louis Pk, MN USA; Bethesda Clin, St Paul, MN USA; Macalester Coll, Dept Biol, St Paul, MN 55105 USA	Ziska, LH (reprint author), USDA ARS, Alternate Crop & Syst Lab, 10300 Baltimore Ave, Beltsville, MD 20705 USA.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Singer, Benjamin/0000-0001-5775-8427			BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1006/abio.1976.9999; CHAPMAN JA, 1986, GRANA, V25, P235; Cifuentes L, 2001, SCIENCE, V293, P1257, DOI 10.1126/science.1063357; CONROY JP, 1992, AUST J BOT, V40, P445, DOI 10.1071/BT9920445c; DRAKE BG, 1989, FUNCT ECOL, V3, P363, DOI 10.2307/2389377; EMBERLIN J, 1994, ALLERGY, V49, P15, DOI 10.1111/j.1398-9995.1994.tb04233.x; Engvall E, 1980, Methods Enzymol, V70, P419; Fitter AH, 2002, SCIENCE, V296, P1689, DOI 10.1126/science.1071617; Frenz DA, 1996, ANN ALLERG ASTHMA IM, V76, P245; Frenz DA, 1999, ANN ALLERG ASTHMA IM, V82, P41, DOI 10.1016/S1081-1206(10)62658-0; Frenz DA, 2000, ANN ALLERG ASTHMA IM, V84, P481; Frenz DA, 2001, ANN ALLERG ASTHMA IM, V87, P390; GERGEN PJ, 1987, J ALLERGY CLIN IMMUN, V80, P669, DOI 10.1016/0091-6749(87)90286-7; HENDREY GR, 1994, AGR FOREST METEOROL, V70, P3, DOI 10.1016/0168-1923(94)90044-2; Idso CD, 2001, ATMOS ENVIRON, V35, P995, DOI 10.1016/S1352-2310(00)00412-X; LEE YS, 1979, J ALLERGY CLIN IMMUN, V63, P336, DOI 10.1016/0091-6749(79)90128-3; McCarthy J., 2001, CLIMATE CHANGE 2001, P1032; PATTERSON DT, 1995, WEED SCI, V43, P685; POORTER H, 1993, VEGETATIO, V104, P77, DOI 10.1007/BF00048146; RAYNOR GS, 1970, BNL PUBLICATION; SPECTOR T, 1978, ANAL BIOCHEM, V86, P142, DOI 10.1016/0003-2697(78)90327-5; STRAKA JG, 1991, AM J HUM GENET, V48, P72; TSANG VCW, 1983, METHOD ENZYMOL, V92, P391; United States Environmental Protection Agency (EPA), AIR QUAL PLANN STAND; 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, 2002, FUNCTIONAL PLANT BIO, V29, P1	28	168	179	3	45	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	FEB	2003	111	2					290	295		10.1067/mai.2003.53		6	Allergy; Immunology	Allergy; Immunology	644WF	WOS:000180942700011	12589347	
J	Rothenberg, ME; Mishra, A; Brandt, EB; Hogan, SP				Rothenberg, ME; Mishra, A; Brandt, EB; Hogan, SP			Gastrointestinal eosinophils	IMMUNOLOGICAL REVIEWS			English	Review							MAJOR BASIC-PROTEIN; COLONY-STIMULATING FACTOR; ACCUMULATION IN-VIVO; HUMAN CC-CHEMOKINE; AIRWAY HYPERRESPONSIVENESS; GASTROESOPHAGEAL REFLUX; TISSUE EOSINOPHILIA; ENDOTHELIAL-CELLS; CATIONIC PROTEIN; FOOD ALLERGY	The gut-associated lymphoid tissue (GALT) is composed of lymphocytes residing in Peyer's patches, lamina propria, and intraepithelial compartments. In addition to these features which distinguish GALT from other peripheral sites of the immune system, the gastrointestinal immune system is also composed of resident eosinophils. Eosinophils are generally considered to be peripheral blood leukocytes that have an important proinflammatory role in various immune disorders. Although most research concerning this cell has focused on understanding its trafficking and function in the blood and lung, recent studies have also started to elucidate its regulation and function in the gastrointestinal tract. Interestingly, eosinophil numbers in the gastrointestinal tract are substantially higher than in other tissues. At baseline (healthy conditions), most eosinophils reside in the lamina propria in the stomach and intestine. Eosinophil homing to these sites occurs during embryonic development and their levels in perinatal mice are comparable to those in adults, indicating that their homing is not dependent upon the presence of intestinal flora. Furthermore, eosinophil localization to the lamina propria at baseline is critically regulated by eotaxin, a chemokine constitutively expressed throughout the gastrointestinal tract. Although eotaxin is required for eosinophil homing, its expression in the esophagus is not sufficient for eosinophil accumulation, since this organ is devoid of eosinophils at baseline. During Th2-associated inflammatory conditions (e.g. interleukin (IL)-5 overexpression or oral allergen challenge), marked increases of eosinophils occur not only in the lamina propria but also in Peyer's patches. The accumulation of Peyer's patch eosinophils, which mainly occurs in the outer cortex and interfollicular regions, is critically regulated by IL-5 and less significantly by eotaxin, suggesting the involvement of other eosinophil chemokines in this lymphoid compartment. Preliminary investigations have shown that gastrointestinal eosinophils express the alpha4 beta7 integrin and that this molecule is responsible, in part, for eosinophil homing. In summary, eosinophils are resident cells of the gastrointestinal immune system whose levels can be induced by antigen exposure under Th2 conditions, in a manner that is critically regulated by eotaxin and IL-5. We propose that eosinophils are integral members of the gastrointestinal immune system and are likely to be important in innate, regulatory and inflammatory immune responses.	Childrens Hosp, Med Ctr, Dept Pediat, Div Pulm Med Allergy & Clin Immunol, Cincinnati, OH 45229 USA	Rothenberg, ME (reprint author), Childrens Hosp, Med Ctr, Dept Pediat, Div Pulm Med Allergy & Clin Immunol, 3333 Burnet Ave, Cincinnati, OH 45229 USA.				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J	Ciencewicki, J; Trivedi, S; Kleeberger, SR				Ciencewicki, Jonathan; Trivedi, Shweta; Kleeberger, Steven R.			Oxidants and the pathogenesis of lung diseases	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						oxidative stress; antioxidant; genetics; susceptibility; infant; reproductive outcome; premature; children; elderly; asthma; chronic obstructive pulmonary disease; ozone; pollutants; particulates; PM; acute respiratory distress syndrome; hyperoxia; SNP; single nucleotide polymorphism	OBSTRUCTIVE PULMONARY-DISEASE; RESPIRATORY-DISTRESS-SYNDROME; LOW-BIRTH-WEIGHT; EXHALED BREATH CONDENSATE; DIESEL EXHAUST PARTICLES; AMBIENT AIR-POLLUTION; SURFACTANT PROTEIN-A; ACUTE OZONE EXPOSURE; LIPID OZONATION PRODUCTS; GLUTATHIONE-S-TRANSFERASE	The increasing number of population-based and epiderniologic associations between oxidant pollutant exposures and cardiopulmonary disease exacerbation, decrements in pulmonary function, and mortality underscores the important detrimental effects of oxidants on public health. Because inhaled oxidants initiate a number of pathologic processes, including inflammation of the airways, which may contribute to the pathogenesis and/or exacerbation of airways disease, it is critical to understand the mechanisms through which exogenous and endogenous oxidants interact with molecules in the cells, tissues, and epithelial lining fluid of the lung. Furthermore, it is clear that interindividual variation in response to a given exposure also exists across an individual lifetime. Because of the potential impact that oxidant exposures may have on reproductive outcomes and infant, child, and adult health, identification of the intrinsic and extrinsic factors that may influence susceptibility to oxidants remains an important issue. In this review, we discuss mechanisms of oxidant stress in the lung, the role of oxidants in lung disease pathogenesis and exacerbation (eg, asthma, chronic obstructive pulmonary disease, and acute respiratory distress syndrome), and the potential risk factors (eg, age, genetics) for enhanced susceptibility to oxidant-induced disease.	[Ciencewicki, Jonathan; Trivedi, Shweta; Kleeberger, Steven R.] NIEHS, Lab Resp Biol, NIH, Res Triangle Pk, NC 27709 USA	Kleeberger, SR (reprint author), NIEHS, Lab Resp Biol, NIH, 111 TW Alexander Dr,Bldg 101,Rm D240, Res Triangle Pk, NC 27709 USA.	kleeber1@niehs.nih.gov			National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services.	Supported by the Division of Intramural Research at the National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services.	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Zhang HQ, 2006, AM J RESP CELL MOL, V34, P174, DOI 10.1165/rcmb.2005-0280OC	182	167	171	1	28	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	SEP	2008	122	3					456	468		10.1016/j.jaci.2008.08.004		13	Allergy; Immunology	Allergy; Immunology	348TW	WOS:000259234000002	18774381	
J	Jacobson, MZ				Jacobson, Mark Z.			Effects of ethanol (E85) versus gasoline vehicles on cancer and mortality in the United States	ENVIRONMENTAL SCIENCE & TECHNOLOGY			English	Article							EMISSIONS; FUEL; ENERGY; AIR	Ethanol use in vehicle fuel is increasing worldwide, but the potential cancer risk and ozone-related health consequences of a large-scale conversion from gasoline to ethanol have not been examined. Here, a nested global-through-urban air pollution/weather forecast model is combined with high-resolution future emission inventories, population data, and health effects data to examine the effect of converting from gasoline to E85 on cancer, mortality, and hospitalization in the United States as a whole and Los Angeles in particular. Under the base-case emission scenario derived, which accounted for projected improvements in gasoline and E85 vehicle emission controls, it was found that E85 (85% ethanol fuel, 15% gasoline) may increase ozone-related mortality, hospitalization, and asthma by about 9% in Los Angeles and 4% in the United States as a whole relative to 100% gasoline. Ozone increases in Los Angeles and the northeast were partially offset by decreases in the southeast. E85 also increased peroxyacetyl nitrate (PAN) in the U.S. but was estimated to cause little change in cancer risk. Due to its ozone effects, future E85 may be a greater overall public health risk than gasoline. However, because of the uncertainty in future emission regulations, it can be concluded with confidence only that E85 is unlikely to improve air quality over future gasoline vehicles. Unburned ethanol emissions from E85 may result in a global-scale source of acetaldehyde larger than that of direct emissions.	Stanford Univ, Dept Civil & Environm Engn, Stanford, CA 94305 USA	Jacobson, MZ (reprint author), Stanford Univ, Dept Civil & Environm Engn, Stanford, CA 94305 USA.	jacobson@stanford.edu					BARRETT R, 2004, 14 CRC ON ROAD VEH E; Black F, 1998, J AIR WASTE MANAGE, V48, P578; BLACK F, 1991, EPA600D91239; *CA AIR RES BOARD, 2004, POP VEH TRENDS REP; *CA AIR RES BOARD, 2003, ARB ALM 2003 TOX AIR; Delucchi M., 2006, LIFECYCLE ANAL BIOFU; DELUCCHI M, 1996, UCDITSRR9612; DESERVES C, 2005, 5509 AVL MTC SWED RO; *DOE, ETH 2006 RES SUMM; Energy Information Administration, 2005, HOUS VEH EN US LAT D; Farrell AE, 2006, SCIENCE, V311, P506, DOI 10.1126/science.1121416; *GEN MOT CORP, 2007, 2007 OD YEAR E8K GAS; Hammerschlag R, 2006, ENVIRON SCI TECHNOL, V40, P1744, DOI 10.1021/es052024h; Jacobson MZ, 2006, GEOPHYS RES LETT, V33, DOI 10.1029/2006GL027838; Jacobson MZ, 2004, J GEOPHYS RES-ATMOS, V109, DOI 10.1029/2004JD004945; Jacobson MZ, 2004, GEOPHYS RES LETT, V31, DOI 10.1029/2003GL018448; Jacobson MZ, 2005, SCIENCE, V308, P1901, DOI 10.1126/science.1109157; Jacobson MZ, 2001, J GEOPHYS RES-ATMOS, V106, P5385, DOI 10.1029/2000JD900560; KARMAN D, 1998, ETHANOL FUELED MOTOR; Kim S, 2005, BIOMASS BIOENERG, V28, P475, DOI 10.1016/j.biombioe.2004.11.005; Lipman TE, 2002, CLIMATIC CHANGE, V53, P477, DOI 10.1023/A:1015235211266; MACDONALD T, 2005, 15 INT S ALC FUELS S; Magnusson R, 2002, ENVIRON SCI TECHNOL, V36, P1656, DOI 10.1021/es010262g; *NREL, FACT SHEET FORD TAUR; Patzek TW, 2005, CRIT REV PLANT SCI, V24, P327, DOI 10.1080/07352680500316029; PATZEK TW, 2006, RAEL BIOFUEL CYCLE; PIMENTEL D, 2005, NAT RESOUR RES, V14, P67; Shapouri H, 2003, T ASAE, V46, P959; Thurston GD, 2001, J EXPO ANAL ENV EPID, V11, P286, DOI 10.1038/sj.jea.7500169; WHO, 2002, WORLD HLTH REP; Winebrake JJ, 2001, J AIR WASTE MANAGE, V51, P1073	31	167	172	4	53	AMER CHEMICAL SOC	WASHINGTON	1155 16TH ST, NW, WASHINGTON, DC 20036 USA	0013-936X	1520-5851		ENVIRON SCI TECHNOL	Environ. Sci. Technol.	JUN 1	2007	41	11					4150	4157		10.1021/es062085v		8	Engineering, Environmental; Environmental Sciences	Engineering; Environmental Sciences & Ecology	172ZM	WOS:000246843300052	17612204	
J	Olin, AC; Rosengren, A; Thelle, DS; Lissner, L; Bake, B; Toren, K				Olin, Anna-Carin; Rosengren, Annika; Thelle, Dag S.; Lissner, Lattren; Bake, Bjorn; Toren, Kjell			Height, age, and atopy are associated with fraction of exhaled nitric oxide in a large adult general population sample	CHEST			English	Article						asthma; epidemiology; exhaled nitric oxide; gender	AIRWAY RESPONSIVENESS; HEALTHY-CHILDREN; REFERENCE VALUES; ASTHMA; SYMPTOMS; SMOKING; SEX; SCHOOLCHILDREN; COMMUNITY; EXPOSURE	Study objectives: The fraction of exhaled nitric oxide (FENO) is elevated in subjects with asthma and atopy, and it has been proposed to be a noninvasive marker of airway inflammation. In addition to asthma and atopy, there is limited information about the determinants of FENO in a general population. Design: Cross-sectional. Setting: A random adult general population sample. Participants: A total of 2,200 subjects, 1, 111 women and 1,089 men, aged 25 to 75 years. Interventions: The subjects were examined with regard to FENO, pulmonary function, anthropometric variables, and blood samples for Ig E, and completed a respiratory questionnaire. The associations between different determinants and FENO were analyzed with multiple linear regression models. Results: The median value of FENO was 16.0 parts per billion (ppb), ranging from 2.4 to 199 ppb. Height, age, atopy, reporting of asthma symptoms in the last month, and reported use of inhaled steroids were positively associated with FENO. Current smokers had lower values of FENO. Gender was not associated with FENO. Conclusions: In this random adult population sample, height, but not gender, was associated with FENO. Furthermore, asthma symptoms in the last month, reported use of inhaled steroids, and atopy were positively and independently associated with FENO, while there was a negative association with smoking.	Sahlgrens Univ Hosp, Dept Occupat & Environm Med, SE-40530 Gothenburg, Sweden; Sahlgrens Univ Hosp, Dept Resp Med & Allergol, Gothenburg, Sweden; Sahlgrens Univ Hosp, Dept Med, S-41345 Gothenburg, Sweden; Univ Gothenburg, Sahlgrenska Acad, Dept Community Hlth & Publ Hlth, Gothenburg, Sweden; Univ Oslo, Akerhus Univ Hosp, Oslo, Norway	Olin, AC (reprint author), Sahlgrens Univ Hosp, Dept Occupat & Environm Med, Box 414, SE-40530 Gothenburg, Sweden.	Anna-Carin.Olin@amm.gu.se					Adamkiewicz G, 2004, THORAX, V59, P204, DOI 10.1136/thorax.2003.006445; ALVING K, 1993, EUR RESPIR J, V6, P1368; Avital A, 2003, PEDIATR PULM, V36, P433, DOI 10.1002/ppul.10377; Baraldi E, 1999, PEDIATR PULM, V27, P54, DOI 10.1002/(SICI)1099-0496(199901)27:1<54::AID-PPUL10>3.0.CO;2-V; Berg CM, 2005, EUR J CARDIOV PREV R, V12, P115, DOI 10.1097/00149831-200504000-00005; Berry MA, 2005, CLIN EXP ALLERGY, V35, P1175, DOI 10.1111/j.1365-2222.2005.02314.x; Buchvald F, 2005, J ALLERGY CLIN IMMUN, V115, P1130, DOI 10.1016/j.jaci.2005.03.020; D'Angelo E, 2005, J APPL PHYSIOL, V99, P433, DOI 10.1152/japplphysiol.01368.2004; Franklin PJ, 1999, AM J RESP CRIT CARE, V159, P69; Franklin PJ, 2004, CHEST, V126, P1540, DOI 10.1378/chest.126.5.1540; Franklin PJ, 2003, THORAX, V58, P1048, DOI 10.1136/thorax.58.12.1048; Gratziou C, 1999, EUR RESPIR J, V14, P897, DOI 10.1034/j.1399-3003.1999.14d28.x; Hellgren J, 2002, AM J IND MED, V42, P23, DOI 10.1002/ajim.10083; Ho LP, 2000, CHEST, V118, P1327, DOI 10.1378/chest.118.5.1327; Jilma B, 1996, LIFE SCI, V58, P469, DOI 10.1016/0024-3205(95)02311-9; Kharitonov SA, 2001, AM J RESP CRIT CARE, V163, P1693; KIISSOON N, 2000, AM J RESP CRIT CARE, V162, P539; Langhammer A, 2001, EUR RESPIR J, V18, P770, DOI 10.1183/09031936.01.00255301; Ludviksdottir D, 1999, RESP MED, V93, P552, DOI 10.1016/S0954-6111(99)90154-3; Malmberg LP, 2005, ALLERGY, V60, P464, DOI 10.1111/j.1398-9995.2005.00740.x; MATRICARDI PM, 1990, CLIN EXP ALLERGY, V20, P151, DOI 10.1111/j.1365-2222.1990.tb02660.x; Nordvall SL, 2005, ALLERGY, V60, P469, DOI 10.1111/j.1398-9995.2005.00735.x; Olin AC, 2004, CLIN EXP ALLERGY, V34, P221, DOI 10.1111/j.1365-2222.2004.01888.x; Olin AC, 2001, RESP MED, V95, P153, DOI 10.1053/rmed.2000.1010; Pedroletti C, 2003, PEDIATR RES, V54, P496, DOI 10.1203/01.PDR.0000081761.33822.36; RIISE GC, 2005, P AM THORAC SOC, V2, pA930; S. American Thoracic and S. European Respiratory, 2005, AM J RESP CRIT CARE, V171, P912; 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, 2004, EUR RESPIR J, V24, P942, DOI 10.1183/09031936.04.00044804; Tsang KW, 2001, LUNG, V179, P83, DOI 10.1007/s004080000050; van den Toorn LM, 2000, AM J RESP CRIT CARE, V162, P953; Warke TJ, 2002, THORAX, V57, P383, DOI 10.1136/thorax.57.5.383	33	167	177	0	4	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	NOV	2006	130	5					1319	1325		10.1378/chest.130.5.1319		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	106OH	WOS:000242109800009	17099006	
J	Martinez, FD				Martinez, FD			Development of wheezing disorders and asthma in preschool children	PEDIATRICS			English	Article						asthma expression; phenotypes; wheezing; atopy	MID-ADULT LIFE; CHILDHOOD ASTHMA; BRONCHIAL HYPERRESPONSIVENESS; RESPIRATORY SYMPTOMS; LUNG-FUNCTION; ATOPY; SMOKING; EXPOSURE; INFANTS; DISEASE	Recent longitudinal studies have shed light on the pathogenesis and progression of asthma. The patterns of expression of childhood asthma that persist into adult life have been explored. Distinct asthma phenotypes (transient wheezing, nonatopic wheezing, and atopy-associated asthma) have been identified. Defining which children are at risk for persistent asthma could allow for better management and, potentially, for reduced morbidity and mortality.	Univ Arizona, Tucson, AZ USA	Martinez, FD (reprint author), Arizona Resp Ctr, Box 245030,1501 N Campbell Ave,Room 2349, Tucson, AZ 85724 USA.						Ball TM, 2000, NEW ENGL J MED, V343, P538, DOI 10.1056/NEJM200008243430803; BARBEE RA, 1985, CHEST S, V87, P21; Ernst P, 2000, AM J RESP CRIT CARE, V161, P1563; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Hanrahan JP, 1996, AM J RESP CRIT CARE, V154, P670; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; KELLY WJW, 1988, AM REV RESPIR DIS, V138, P26; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Martinez FD, 1999, CLIN EXP ALLERGY, V29, P53; MORGAN W J, 1991, American Review of Respiratory Disease, V143, pA508; National Asthma Education Prevention Program (NAEPP), 1997, NIH PUBL; Nilsson L, 1999, ALLERGY, V54, P716, DOI 10.1034/j.1398-9995.1999.00896.x; OSWALD H, 1994, BRIT MED J, V309, P95; Oswald H, 1997, PEDIATR PULM, V23, P14, DOI 10.1002/(SICI)1099-0496(199701)23:1<14::AID-PPUL2>3.0.CO;2-P; PEAT JK, 1990, J ALLERGY CLIN IMMUN, V85, P65, DOI 10.1016/0091-6749(90)90223-Q; Sears MR, 2000, CLIN CHEST MED, V21, P315, DOI 10.1016/S0272-5231(05)70269-0; SOYSETH V, 1995, CHEST, V107, P389, DOI 10.1378/chest.107.2.389; Speer C P, 1998, Eur Respir J Suppl, V27, p13s; Stein R, 1999, LANCET, V354, P541, DOI 10.1016/S0140-6736(98)10321-5; Stein RT, 1997, THORAX, V52, P946; Stein RT, 1999, AM J EPIDEMIOL, V149, P1030; Stern DA, 1999, AM J RESP CRIT CARE, V159, pA148; Szefler S, 2000, NEW ENGL J MED, V343, P1054; WRIGHT AL, 1989, AM J EPIDEMIOL, V129, P1232; YUNGINGER JW, 1992, AM REV RESPIR DIS, V146, P888; Zeiger RS, 1999, J ALLERGY CLIN IMMUN, V103, P376, DOI 10.1016/S0091-6749(99)70460-4	26	167	187	0	4	AMER ACAD PEDIATRICS	ELK GROVE VILLAGE	141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA	0031-4005			PEDIATRICS	Pediatrics	FEB	2002	109			S			362	367				6	Pediatrics	Pediatrics	517FW	WOS:000173601300003	11826251	
J	Durham, SR; Emminger, W; Kapp, A; Colombo, G; de Monchy, JGR; Rak, S; Scadding, GK; Andersen, JS; Riis, B; Dahl, R				Durham, Stephen R.; Emminger, Waltraud; Kapp, Alexander; Colombo, Giselda; de Monchy, Jan G. R.; Rak, Sabina; Scadding, Glenis K.; Andersen, Jens S.; Riis, Bente; Dahl, Ronald			Long-term clinical efficacy in grass pollen-induced rhinoconjunctivitis after treatment with SQ-standardized grass allergy immunotherapy tablet	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Allergy immunotherapy tablet; disease modification; grass pollen; immunotherapy; sublingual; sustained efficacy; rhinoconjunctivitis; placebo controlled; Phleum pratense	6-YEAR FOLLOW-UP; HOUSE-DUST MITE; SUBLINGUAL IMMUNOTHERAPY; IMMUNOLOGICAL CHANGES; CONTROLLED-TRIAL; RHINITIS; SAFETY; CHILDREN; PERFORMANCE; BURDEN	Background: Sustained and disease-modifying effects of sublingual immunotherapy have never before been confirmed in a large-scale randomized, double-blind, placebo-controlled trial. Objective: We sought to investigate sustained efficacy I year after a 3-year period of daily treatment with the SQ-standardized grass allergy immunotherapy tablet Grazax (Phleum pratense 75,000 SQ-T/2,800 BAU; ALK-Abello, Horsholm, Denmark). Methods: A randomized, double-blind, placebo-controlled, phase III trial including adults with a history of moderate-to-severe grass pollen induced rhinoconjunctivitis inadequately controlled by symptomatic medications. The analysis set comprised 257 subjects at the follow-up. Efficacy end points were rhinoconjunctivitis symptom and medication scores, quality of life, and percentages of symptom and medication free days. Immunologic end points included grass pollen-specific serum IgG4 and IgE-blocking factor. Safety was assessed based on adverse events. Results: Significant improvements in efficacy were consistently shown during 3 years' treatment. One year after treatment, the active group showed sustained reductions in mean rhinoconjunctivitis symptom scores (26%, P < .001) and medication scores (29%, P = .022) when compared with placebo. This level was similar to the efficacy observed during the 3-year treatment period. The differences in percentages of symptom- and medication-free days were significant during and I year after treatment. The active group also reported sustained and significant improvements in quality of life. Sustained clinical benefit was accompanied by immunologic changes. No safety issues were identified. Conclusion: Three years of treatment with the SQ-standardized grass allergy immunotherapy tablet resulted in consistent clinical improvement and accompanying immunologic changes that were sustained I year after treatment, which is indicative of disease modification and associated long-term benefits. (J Allergy Clin Immunol 2010;125:131-38.)	[Durham, Stephen R.] Univ London Imperial Coll Sci Technol & Med, Sect Allergy & Clin Immunol, Natl Heart & Lung Inst, London SW3 6LY, England; [Durham, Stephen R.] Royal Brompton Hosp, London SW3 6LY, England; [Emminger, Waltraud] Allergie Ambulatorium Rennweg, Vienna, Austria; [Kapp, Alexander] Hannover Med Sch, Dept Dermatol & Allergol, Hannover, Germany; [Colombo, Giselda] Sci Univ Inst San Raffaele Monte Tabor, Sect Allergy, Milan, Italy; [de Monchy, Jan G. R.] Univ Groningen, Univ Med Ctr Groningen, Sect Allergol Internal Med, Groningen, Netherlands; [Rak, Sabina] Sahlgrens Univ Hosp, Sect Allergy, Gothenburg, Sweden; [Scadding, Glenis K.] Royal Natl Throat Nose & Ear Hosp, London WC1X 8DA, England; [Andersen, Jens S.; Riis, Bente] ALK Abello AS, Res & Dev, Horsholm, Denmark; [Dahl, Ronald] Aarhus Univ Hosp, Dept Resp Dis, Aarhus, Denmark	Durham, SR (reprint author), Univ London Imperial Coll Sci Technol & Med, Sect Allergy & Clin Immunol, Natl Heart & Lung Inst, Guy Scadding Bldg,Royal Brompton Campus,Dovehouse, London SW3 6LY, England.	s.durham@imperial.ac.uk	Dahl, Ronahl/F-8170-2013		Medical Research Council [G0601303]		Akdis M, 2007, J ALLERGY CLIN IMMUN, V119, P780, DOI 10.1016/j.jaci.2007.01.022; Bauchau V, 2004, EUR RESPIR J, V24, P758, DOI 10.1183/09031936.04.00013904; Bufe A, 2009, J ALLERGY CLIN IMMUN, V123, P167, DOI 10.1016/j.jaci.2008.10.044; Calderon M, 2006, J INVEST ALLERG CLIN, V16, P338; Canonica GW, 2007, ALLERGY, V62, P17, DOI 10.1111/j.1398-9995.2007.01549.x; Ciprandi G, 2007, ALLERGY ASTHMA PROC, V28, P40, DOI 10.2500/aap.2007.28.2974; Dahl R, 2006, ALLERGY, V61, P185, DOI 10.1111/j.1398-9995.2005.00949.x; Dahl R, 2004, RESP MED, V98, P398, DOI 10.1016/j.rmed.2003.11.015; Dahl R, 2008, J ALLERGY CLIN IMMUN, V121, P512, DOI 10.1016/j.jaci.2007.10.039; Dahl R, 2006, J ALLERGY CLIN IMMUN, V118, P434, DOI 10.1016/j.jaci.2006.05.003; Des Roches A., 1996, Allergy (Copenhagen), V51, P430; Di Rienzo V, 2003, CLIN EXP ALLERGY, V33, P206, DOI 10.1046/j.1365-2222.2003.01587.x; Durham SR, 2006, J ALLERGY CLIN IMMUN, V117, P802, DOI 10.1016/j.jaci.2005.12.1358; Durham SR, 1999, NEW ENGL J MED, V341, P468, DOI 10.1056/NEJM199908123410702; Durham SR, 2008, CURR OPIN ALLERGY CL, V8, P577, DOI 10.1097/ACI.0b013e3283196764; European Interoperability Framework, 2004, COAST ER EV NEED ACT, P1; *EUR MED AG, 2008, CHMPEWP185042006FINA; Jacobsen L, 1997, ALLERGY, V52, P914, DOI 10.1111/j.1398-9995.1997.tb01251.x; JUNIPER EF, 1991, CLIN EXP ALLERGY, V21, P77, DOI 10.1111/j.1365-2222.1991.tb00807.x; Kleine-Tebbe J, 2006, ALLERGY, V61, P181, DOI 10.1111/j.1398-9995.2006.00959.x; Madonini E, 2003, INT J IMMUNOPATH PH, V16, P73; Malling HJ, 2006, J INVEST ALLERG CLIN, V16, P162; Moingeon P, 2006, ALLERGY, V61, P151, DOI 10.1111/j.1398-9995.2006.01002.x; MOSBECH H, 1988, ALLERGY, V43, P523, DOI 10.1111/j.1398-9995.1988.tb01631.x; Naclerio RM, 1997, J ALLERGY CLIN IMMUN, V100, P293, DOI 10.1016/S0091-6749(97)70240-9; Nathan RA, 2007, ALLERGY ASTHMA PROC, V28, P3, DOI 10.2500/aap.2007.28.2934; Novembre E, 2004, J ALLERGY CLIN IMMUN, V114, P851, DOI 10.1016/j.jaci.2004.07.012; Ott H, 2009, ALLERGY, V64, P179, DOI 10.1111/j.1398-9995.2008.01875.x; Pajno GB, 2001, CLIN EXP ALLERGY, V31, P1392, DOI 10.1046/j.1365-2222.2001.01161.x; Petersen AB, 2004, CLIN BIOCHEM, V37, P882, DOI 10.1016/j.clinbiochem.2004.06.010; Plaut M, 2005, NEW ENGL J MED, V353, P1934, DOI 10.1056/NEJMcp044141; Schatz M, 2007, ALLERGY, V62, P9, DOI 10.1111/j.1398-9995.2007.01548.x; Sundberg R, 2007, J ADOLESCENT HEALTH, V40, P581, DOI 10.1016/j.jadohealth.2007.01.003; Valovirta E, 2008, CURR OPIN ALLERGY CL, V8, P1, DOI 10.1097/ACI.0b013e3282f3f42f; VUURMAN EFPM, 1993, ANN ALLERGY, V71, P121; Walker S, 2007, J ALLERGY CLIN IMMUN, V120, P381, DOI 10.1016/j.jaci.2007.03.034; WALKER SM, 1995, ALLERGY, V50, P405, DOI 10.1111/j.1398-9995.1995.tb01170.x; Weiss KB, 2001, J ALLERGY CLIN IMMUN, V107, P3, DOI 10.1067/mai.2001.112262; World Medical Association, 1996, DECL HELS ETH PRINC	39	166	172	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.	JAN	2010	125	1					131	138		10.1016/j.jaci.2009.10.035		8	Allergy; Immunology	Allergy; Immunology	544MG	WOS:000273660500015	20109743	
J	Mendell, MJ				Mendell, M. J.			Indoor residential chemical emissions as risk factors for-respiratory and allergic effects in children: a review	INDOOR AIR			English	Review							VOLATILE ORGANIC-COMPOUNDS; INTERIOR SURFACE MATERIALS; PEAK EXPIRATORY FLOW; 3.0 PPM FORMALDEHYDE; YOUNG-CHILDREN; HOUSE-DUST; ASTHMA SYMPTOMS; AIRWAY SYMPTOMS; MITE ALLERGEN; BUILDING CHARACTERISTICS	Most research into effects of residential exposures on respiratory health has focused on allergens, moisture/mold, endotoxin, or combustion products. A growing body of research from outside the US; however, has associated chemical emissions from common indoor materials with risk of asthma, allergies, and pulmonary infections. This review summarizes 21 studies in the epidemiologic literature on associations between indoor residential chemical emissions, or emission-related materials or activities, and respiratory health or allergy in infants or children. Associations, some strong, were reported between many risk factors and respiratory or allergic effects. Risk factors identified most frequently included formaldehyde or particleboard, phthalates or plastic materials, and recent painting. Findings for other risk factors, such as aromatic and aliphatic chemical compounds, were limited but suggestive. Elevated risks were also reported for renovation and cleaning activities, new furniture, and carpets or textile wallpaper. Reviewed studies were entirely observational, limited in size, and variable in quality, and specific risk factors identified may only be indicators for correlated, truly causal exposures. Nevertheless, overall evidence suggests a new class of residential risk factors for adverse respiratory effects, ubiquitous in modern residences, and distinct from those currently recognized. It is important to confirm and quantify any risks, to motivate and guide necessary preventive actions.	Lawrence Berkeley Natl Lab, Indoor Environm Dept, Berkeley, CA 94720 USA	Mendell, MJ (reprint author), Lawrence Berkeley Natl Lab, Indoor Environm Dept, 1 Cyclotron Rd MS 90-3058, Berkeley, CA 94720 USA.	mjmendell@lbl.gov	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			Aberg N, 1996, ALLERGY, V51, P232, DOI 10.1111/j.1398-9995.1996.tb04598.x; Andersson K, 1997, INDOOR AIR, V7, P78, DOI 10.1111/j.1600-0668.1997.t01-2-00002.x; Arts JHE, 2006, REGUL TOXICOL PHARM, V44, P144, DOI 10.1016/j.yrtph.2005.11.006; Baumann MGD, 2000, FOREST PROD J, V50, P75; Becher R, 1996, TOXICOL LETT, V86, P155, DOI 10.1016/0378-4274(96)03685-5; 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, ENVIRON HEALTH PERSP, V112, P1393, DOI 10.1289/ehp.7187; BROWN SK, 1994, INDOOR AIR, V4, P123, DOI 10.1111/j.1600-0668.1994.t01-2-00007.x; Brown SK, 2002, INDOOR AIR, V12, P55, DOI 10.1034/j.1600-0668.2002.120107.x; 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Engineering, Environmental; Public, Environmental & Occupational Health	Construction & Building Technology; Engineering; Public, Environmental & Occupational Health	201QX	WOS:000248848800002	17661923	
J	Chanan-Khan, A; Szebeni, J; Savay, S; Liebes, L; Rafique, NM; Alving, CR; Muggia, FM				Chanan-Khan, A; Szebeni, J; Savay, S; Liebes, L; Rafique, NM; Alving, CR; Muggia, FM			Complement activation following first exposure to pegylated liposomal doxorubicin (Doxil): possible role in hypersensitivity reactions	ANNALS OF ONCOLOGY			English	Article						allergy; anaphylatoxins; cancer chemotherapy; doxorubicin; liposomes; hypersensitivity reactions	PHASE-II; ANTITUMOR-ACTIVITY; OVARIAN-CANCER; CHEMOTHERAPY; PHARMACOKINETICS; PACLITAXEL; MECHANISM; TOXICITY; DISEASE	Background: Pegylated liposomal doxorubicin (Doxil(R)) has been reported to cause immediate hypersensitivity reactions (HSRs) that cannot be explained as IgE-mediated (type I) allergy. Previous in vitro and animal studies indicated that activation of the complement (C) system might play a causal role in the process, a proposal that has not been tested in humans to date. Patients and methods: Patients with solid tumors (n=29) treated for the first time with Doxil were evaluated for HSRs and concurrent C activation. HSRs were classified from mild to severe, while C activation was estimated by serial measurement of plasma C terminal complex (SC5b-9) levels. Increases in SC5b-9 were compared in patients with or without reactions, and were correlated with Doxil dose rate. Results: Moderate to severe HSRs occurred in 45% of patients. Plasma SC5b-9 at 10 min after infusion was significantly elevated in 92% of reactor patients versus 56% in the non-reactor group, and the rise was greater in reactors than in non-reactors. We found significant association between C activation and HSRs, both showing direct correlation with the initial Doxil dose rate. Conclusions: C activation may play a key role in HSRs to Doxil. However, low-level C activation does not necessarily entail clinical symptoms, highlighting the probable involvement of further, as yet unidentified, amplification factors.	Kaplan Comprehens Canc Ctr, New York, NY USA; Walter Reed Army Med Ctr, Walter Reed Army Inst Res, Dept Membrane Biochem, Washington, DC 20307 USA	Chanan-Khan, A (reprint author), Roswell Pk Canc Inst, Elm & Carlton St, Buffalo, NY 14263 USA.						*ALZA PHARM, 2000, DOX PACK INS; Brouwers AH, 2000, J DRUG TARGET, V8, P225, DOI 10.3109/10611860008997901; BUYON JP, 1992, ARTHRITIS RHEUM, V35, P1028, DOI 10.1002/art.1780350907; deMarie S, 1996, LEUKEMIA, V10, pS93; Dezube BJ, 1996, DOXIL CLIN SERIES, V1, P1; GABIZON A, 1994, CANCER RES, V54, P987; GABIZON A, 1994, ACTA ONCOL, V33, P779; Gabizon AA, 2001, CANCER INVEST, V19, P424, DOI 10.1081/CNV-100103136; Gabizon AA, 1998, LONG CIRCULATING LIP, P165; Gordon AN, 2000, J CLIN ONCOL, V18, P3093; Hubert A, 2000, ANTI-CANCER DRUG, V11, P123, DOI 10.1097/00001813-200002000-00009; Koukourakis MI, 1999, J CLIN ONCOL, V17, P3512; Lyass O, 2001, CLIN CANCER RES, V7, P3040; Lyass O, 2000, CANCER, V89, P1037, DOI 10.1002/1097-0142(20000901)89:5<1037::AID-CNCR13>3.0.CO;2-Z; Muggia F M, 2001, Curr Oncol Rep, V3, P156, DOI 10.1007/s11912-001-0016-5; Muggia FM, 2002, J CLIN ONCOL, V20, P2360, DOI 10.1200/JCO.2002.08.171; Muggia FM, 1997, J CLIN ONCOL, V15, P987; MULLEREBERHARD HJ, 1984, SPRINGER SEMIN IMMUN, V7, P93, DOI 10.1007/BF01893017; Northfelt DW, 1997, J CLIN ONCOL, V15, P653; ROSNER B, 1986, FUNDAMENTALS BIOSTAT, P424; SCULIER JP, 1986, J CLIN ONCOL, V4, P789; Skubitz KM, 1998, ANTI-CANCER DRUG, V9, P45, DOI 10.1097/00001813-199801000-00005; Szebeni J, 1998, CRIT REV THER DRUG, V15, P57; Szebeni J, 2001, INT IMMUNOPHARMACOL, V1, P721, DOI 10.1016/S1567-5769(01)00006-6; Szebeni J, 1998, J NATL CANCER I, V90, P300; Szebeni J, 1999, CIRCULATION, V99, P2302; Szebeni J, 2000, AM J PHYSIOL-HEART C, V279, pH1319; Szebeni J., 2000, J LIPOSOME RES, V10, P347; UZIELY B, 1995, J CLIN ONCOL, V13, P1777	29	166	173	5	23	OXFORD UNIV PRESS	OXFORD	GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND	0923-7534			ANN ONCOL	Ann. Oncol.	SEP	2003	14	9					1430	1437		10.1093/annonc/mdg374		8	Oncology	Oncology	723NA	WOS:000185437400015	12954584	
J	Barnes, PJ				Barnes, PJ			New concepts in chronic obstructive pulmonary disease	ANNUAL REVIEW OF MEDICINE-SELECTED TOPICS IN THE CLINICAL SCIENCES			English	Review						emphysema; bronchitis; inflammation; proteases; macrophage	RANDOMIZED CONTROLLED TRIAL; BRONCHOALVEOLAR LAVAGE FLUID; SPUTUM INFLAMMATORY MARKERS; CYSTIC-FIBROSIS SPUTUM; EXHALED NITRIC-OXIDE; AIR-FLOW LIMITATION; CHRONIC-BRONCHITIS; ALVEOLAR MACROPHAGES; LUNG-FUNCTION; INHALED BUDESONIDE	Chronic obstructive pulmonary disease (COPD) is a leading cause of death and disability but has only recently been explored from a cellular and molecular perspective. In COPD, chronic inflammation leads to fixed narrowing of small airways and alveolar wall destruction (emphysema). This is characterized by increased numbers of alveolar macrophages, neutrophils, and cytotoxic T lymphocytes, and the release of multiple inflammatory mediators (lipids, chemokines, cytokines, growth factors). There is also a high level of oxidative stress, which may amplify this inflammation. There is increased elastolysis and probable involvement of matrix metalloproteinases. The inflammation and proteolysis in COPD is an amplification of the normal inflammatory response to cigarette smoke. Unlike asthma, this inflammation appears to be resistant to corticosteroids, prompting a search for novel anti-inflammatory therapies that may prevent the relentless progression of the disease.	Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London, England	Barnes, PJ (reprint author), Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dovehouse St, London, England.						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Rev. Med.		2003	54						113	129		10.1146/annurev.med.54.101601.152209		17	Medicine, General & Internal	General & Internal Medicine	670WV	WOS:000182433600007	12359824	
J	Kharitonov, SA; Barnes, PJ				Kharitonov, SA; Barnes, PJ			Biomarkers of some pulmonary diseases in exhaled breath	BIOMARKERS			English	Review						airway inflammation; oxidative stress; nitric oxide; carbon monoxide; exhaled breath condensate; non-invasive markers; asthma; chronic obstructive pulmonary disease; cystic fibrosis; bronchiectasis; interstitial lung diseases; hydrogen peroxide; eicosanoids; products of lipid peroxidation; proteins; cytokines	NITRIC-OXIDE SYNTHASE; INCREASED CARBON-MONOXIDE; RESPIRATORY-DISTRESS SYNDROME; LEUKOTRIENE RECEPTOR ANTAGONIST; KAPPA-B ACTIVATION; CYSTIC-FIBROSIS; ASTHMATIC-PATIENTS; HYDROGEN-PEROXIDE; OXIDATIVE STRESS; AIRWAY INFLAMMATION	Analysis of various biomarkers in exhaled breath allows completely non-invasive monitoring of inflammation and oxidative stress in the respiratory tract in inflammatory lung diseases, including asthma, chronic obstructive pulmonary disease (COPD), cystic firbrosis (CF), bronchiectasis and interstitial lung diseases. The technique is simple to perform, may be repeated frequently, and can be applied to children, including neonates, and patients with severe disease in whom more invasive procedures are not possible. Several volatile chemicals can be measured in the breath (nitric oxide, carbon monoxide, ammonia), and many non-volatile molecules (mediators, oxidation and nitration products, proteins) may be measured in exhaled breath condensate. Exhaled breath analysis may be used to quantify inflammation and oxidative stress in the respiratory tract, in differential diagnosis of airway disease and in the monitoring of therapy. Most progress has been made with exhaled nitric oxide (NO), which is increased in atopic asthma, is correlated with other inflammatory indices and is reduced by treatment with corticosteroids and antileukotrienes, but not (beta (2)-agonists. In contrast, exhaled NO is normal in COPD, reduced in CF and diagnostically low in primary ciliary dyskinesia. Exhaled carbon monoxide (CO) is increased in asthma, COPD and CF. Increased concentrations of 8-isoprostane, hydrogen peroxide, nitrite and 3-nitrotyrosine are found in exhaled breath condensate in inflammatory lung diseases. Furthermore, increased levels of lipid mediators are found in these diseases, with a differential pattern depending on the nature of the disease process. In the future it is likely that smaller and more sensitive analysers will extend the discriminatory value of exhaled breath analysis and that these techniques may be available to diagnose and monitor respiratory diseases in the general practice and home setting.	Royal Brompton Hosp, Imperial Coll, Fac Med, Natl Heart & Lung Inst,Dept Thorac Med, London SW3 6LY, England	Kharitonov, SA (reprint author), Royal Brompton Hosp, Imperial Coll, Fac Med, Natl Heart & Lung Inst,Dept Thorac Med, Dovehouse St, London SW3 6LY, England.						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J	Wan, H; Winton, HL; Soeller, C; Taylor, GW; Gruenert, DC; Thompson, PJ; Cannell, MB; Stewart, GA; Garrod, DR; Robinson, C				Wan, H; Winton, HL; Soeller, C; Taylor, GW; Gruenert, DC; Thompson, PJ; Cannell, MB; Stewart, GA; Garrod, DR; Robinson, C			The transmembrane protein occludin of epithelial tight junctions is a functional target for serine peptidases from faecal pellets of Dermatophagoides pteronyssinus	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						asthma; house dust mite allergens; tight junctions; serine peptidases; adherens junctions; allergic sensitization; occludin; claudins	HOUSE-DUST MITE; DER-P-I; MEMBRANE-PROTEINS; ALLERGEN; PERMEABILITY; ASTHMA; CHILDHOOD; CLEAVAGE; RECEPTOR; DER-P-1	Background There have been only a few studies of how allergens cross the airway epithelium to cause allergic sensitization. House dust mite fecal pellets (HDMFP) contain several proteolytic enzymes. Group I allergens are cysteine peptidases, whilst those of groups 3, 6 and 9 have catalytic sites indicative of enzymes that mechanistically behave as serine peptidases. We have previously shown that the group 1 allergen Der p 1 leads to cleavage of tight junctions (TJs), allowing allergen delivery to antigen presenting cells. Objective In this study we determined whether HDMFP serine peptidases similarly compromise the airway epithelium by attacking TJs, desmosomes and adherens junctions. Methods Experiments were performed in monolayers of MDCK, Calu-3 or 16HBE14o-epithelial cells. Cell junction morphology was examined by 2-photon molecular excitation microscopy and digital image analysis. Barrier function was measured as mannitol permeability. Cleavage of cell adhesion proteins was studied by immunoblotting and mass spectrometry. Results HDMFP serine peptidases led to a progressive cleavage of TJs and increased epithelial permeability. Desmosomal puncta became more concentrated. Cleavage of TJs involved proteolysis of the TJ proteins, occludin and ZO-1. This was associated with activation of intracellular proteolysis of ZO-1. In contrast to occludin, E-cadherin of adherens junctions was cleaved less extensively. Although Calu-3 and 16HBE14o-cells expressed tethered ligand receptors for serine peptidases, these were not responsible for transducing the changes in TJs. Conclusion HDMFP serine peptidases cause cleavage of TJs. This study identifies a second general class of HDM peptidase capable of increasing epithelial permeability and thereby creating conditions that would favour transepithelial delivery of allergens.	Univ London St Georges Hosp, Sch Med, Dept Pharmacol & Clin Pharmacol, London SW17 0RE, England; Univ London Imperial Coll Sci Technol & Med, Sch Med, Clin Pharmacol Sect, London, England; Univ Calif San Francisco, Dept Lab Med, Cardiovasc Res Inst, Gene Therapy Core Ctr, San Francisco, CA 94143 USA; Univ Western Australia, Queen Elizabeth II Med Ctr, Dept Med, Nedlands, WA 6009, Australia; Univ Western Australia, Queen Elizabeth II Med Ctr, Dept Microbiol, Nedlands, WA 6009, Australia; Univ Manchester, Sch Biol Sci, Manchester, Lancs, England	Robinson, C (reprint author), Univ London St Georges Hosp, Sch Med, Dept Pharmacol & Clin Pharmacol, Cranmer Terrace, London SW17 0RE, England.		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Exp. Allergy	FEB	2001	31	2					279	294		10.1046/j.1365-2222.2001.00970.x		16	Allergy; Immunology	Allergy; Immunology	417HF	WOS:000167828900013	11251630	
J	Wang, H; Feng, Z; Shu, Y; Yu, H; Zhou, L; Zu, RQ; Huai, Y; Dong, J; Bao, CJ; Wen, LY; Wang, H; Yang, P; Zhao, W; Dong, LB; Zhou, MH; Liao, QH; Yang, HT; Wang, M; Lu, XJ; Shi, ZY; Wang, W; Gu, L; Zhu, FC; Li, Q; Yin, WD; Yang, WZ; Li, DX; Uyeki, TM; Wang, Y				Wang, Hua; Feng, Zijian; Shu, Yuelong; Yu, Hongjie; Zhou, Lei; Zu, Rongqiang; Huai, Yang; Dong, Jie; Bao, Changjun; Wen, Leying; Wang, Hong; Yang, Peng; Zhao, Wei; Dong, Libo; Zhou, Minghao; Liao, Qiaohong; Yang, Haitao; Wang, Min; Lu, Xiaojun; Shi, Zhiyang; Wang, Wei; Gu, Ling; Zhu, Fengcai; Li, Qun; Yin, Weidong; Yang, Weizhong; Li, Dexin; Uyeki, Timothy M.; Wang, Yu			Probable limited person-to-person transmission of highly pathogenic avian influenza A (H5N1) virus in China	LANCET			English	Article							HEALTH-CARE WORKERS; RECEPTOR SPECIFICITY; ANTI-H5 ANTIBODY; HONG-KONG; INFECTION; HEMAGGLUTININ; DISEASE; EPIDEMIOLOGY; RISK	Bankground in December, 2007, family cluster of two individuals infected with highly pathogenic avian influenza A (H5N1) virus was identified in Jiangsu Province, China. Field and laboratory investigations were implemented immediately by public-health authorities. Methods Epidemiological, clinical, and virological data were collected and analysed. Respiratory specimens from the patients were tested by reverse transcriptase (RT) PCR and by viral culture for the presence of H5N1 virus. Contacts of cases were monitored for symptoms of illness for 10 days. Any contacts who became ill had respiratory specimens collected for H5N1 testing by RT PCR. Sera were obtained from contacts for H5N1 serological testing by microneutralisation and horse red-blood-cell haemagglutinin inhibition assays. Findings The 24-year-old index case died, and the second case, his 52-year-old father, survived after receiving early antiviral treatment and post-vaccination plasma from a participant in an H5N1 vaccine trial. The index case's only plausible exposure to H5N1 virus was a poultry market visit 6 days before the onset of illness. The second case had substantial unprotected close exposure to his ill son. 91 contacts with close exposure to one or both cases without adequate protective equipment provided consent for serological investigation. Of these individuals, 78 (86%) received oseltamivir chemoprophylaxis and two had mild illness. Both ill contacts tested negative for H5N1 by RT PCR. All 91 close contacts tested negative for H5N1 antibodies. HSN1 viruses isolated from the two cases were genetically identical except for one non-synonymous nucleotide substitution. Interpretation Limited, non-sustained person-to-person transmission of H5N1 virus probably occurred in this family cluster. Funding Chinese Ministry of Science and Technology; US National Institute of Allergy and infectious Diseases, National Institutes of Health; China-US Collaborative Program on Emerging and Re-emerging Infectious Diseases.	[Feng, Zijian; Yu, Hongjie; Zhou, Lei; Huai, Yang; Yang, Peng; Liao, Qiaohong; Li, Qun; Yang, Weizhong; Wang, Yu] Chinese Ctr Dis Control & Prevent, Off Dis Control & Emergency Response, Beijing 100050, Peoples R China; [Wang, Hua; Zu, Rongqiang; Bao, Changjun; Zhou, Minghao; Yang, Haitao; Shi, Zhiyang; Gu, Ling; Zhu, Fengcai] Jiangsu Prov Ctr Dis Control & Prevent, Nanjing, Peoples R China; [Shu, Yuelong; Dong, Jie; Wen, Leying; Dong, Libo; Wang, Min; Wang, Wei; Li, Dexin] China CDC, State Key Lab Infect Dis Prevent & Control, Natl Inst Viral Dis Control & Prevent, Beijing, Peoples R China; [Wang, Hong] Jiangsu Prov Peoples Hosp, Nanjing, Peoples R China; [Zhao, Wei] Nanjing Secondary Peoples Hosp, Nanjing, Peoples R China; [Lu, Xiaojun] Nanjing Ctr Dis Control & Prevent, Nanjing, Peoples R China; [Yin, Weidong] Sinovac Biotech Co, Beijing, Peoples R China; [Uyeki, Timothy M.] Ctr Dis Control & Prevent, Influenza Div, Natl Ctr Immunizat & Resp Dis, Atlanta, GA USA	Wang, Y (reprint author), Chinese Ctr Dis Control & Prevent, Off Dis Control & Emergency Response, 27 Nanwei Rd, Beijing 100050, Peoples R China.	wangyu@chinacdc.cn			NIAID NIH HHS [U19 AI51915]		Abdel-Ghafar AN, 2008, NEW ENGL J MED, V358, P261; Apisarnthanarak A, 2005, CLIN INFECT DIS, V40, pE16, DOI 10.1086/427034; Auewarakul P, 2007, J VIROL, V81, P9950, DOI 10.1128/JVI.00468-07; Bridges CB, 2000, J INFECT DIS, V181, P344, DOI 10.1086/315213; Chassagne P, 1996, AM J MED, V100, P65, DOI 10.1016/S0002-9343(96)90013-3; Chiu CH, 2004, CLIN MICROBIOL REV, V17, P311, DOI 10.1128/CMR.17.2.311-322.2004; Gu J, 2007, LANCET, V370, P1137, DOI 10.1016/S0140-6736(07)61515-3; Jong M. 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J	Johnston, SL; Blasi, F; Black, PN; Martin, RJ; Farrell, DJ; Nieman, RB				Johnston, SL; Blasi, F; Black, PN; Martin, RJ; Farrell, DJ; Nieman, RB		TELICAST Investigators	The effect of telithromycin in acute exacerbations of asthma	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							IN-VITRO ACTIVITY; MYCOPLASMA-PNEUMONIAE; CHLAMYDIA-PNEUMONIAE; HMR 3647; KETOLIDE; INFECTION; TRIAL	BACKGROUND: We conducted a double-blind, randomized, placebo-controlled study to evaluate the efficacy of telithromycin in patients with acute exacerbations of asthma. METHODS: A total of 278 adults with diagnosed asthma were enrolled within 24 hours after an acute exacerbation of asthma requiring short-term medical care. The patients were randomly assigned to receive 10 days of oral treatment with telithromycin (at a dose of 800 mg daily) or placebo in addition to usual care. Primary efficacy end points were a change from baseline over the treatment period in symptoms (as recorded by patients in a diary card) and in the peak expiratory flow in the morning at home. The presence of Chlamydophila pneumoniae or Mycoplasma pneumoniae was ascertained by serologic analysis, polymerase chain reaction, and culture. RESULTS: Of the two prespecified primary outcomes, only asthma symptoms showed a significantly greater reduction among patients receiving telithromycin than among those receiving placebo. Mean (+/-SD) scores on a test of asthma symptoms (on a 7-point scale, with 0 denoting no symptoms and 6 denoting severe symptoms) were 3.0+/-1.4 at baseline and 1.7+/-1.1 at the end of treatment for the telithromycin group and 2.8+/-1.3 at baseline and 2.0+/-1.0 at the end of treatment for the placebo group. The mean decrease in symptom scores during the treatment period was 1.3 for telithromycin and 1.0 for placebo (mean difference, -0.3; 95 percent confidence interval, -0.5 to -0.1; P=0.004). There was no significant treatment effect on the other primary outcome measure, a change in morning peak expiratory flow. Nausea was more common among patients in the telithromycin group than in the placebo group (P=0.01). Although 61 percent of patients had evidence of infection with C. pneumoniae, M. pneumoniae, or both, there was no relationship between bacteriologic status and the response to asthma treatment. CONCLUSIONS: This study provides evidence of the benefit of telithromycin in patients with acute exacerbations of asthma; the mechanisms of benefit remain unclear.	Natl Heart & Lung Inst, Imperial Coll London, London W2 1PG, England; GR Micro, London, England; Univ Milan, Ist Ric & Cura Carattere Sci Policlin, Milan, Italy; Univ Auckland, Auckland 1, New Zealand; Natl Jewish Med & Res Ctr, Denver, CO USA; Sanofi Aventis, Bridgewater, NJ USA	Johnston, SL (reprint author), Natl Heart & Lung Inst, Imperial Coll London, Norfolk Pl, London W2 1PG, England.	s.johnston@imperial.ac.uk	Johnston, Sebastian/I-2423-2012	Blasi, Francesco/0000-0002-2285-9970			Ackermann G, 2003, J ANTIMICROB CHEMOTH, V51, P497, DOI 10.1093/jac/dkg123; Altman LC, 1998, J ALLERGY CLIN IMMUN, V102, P50, DOI 10.1016/S0091-6749(98)70054-5; Araujo FG, 2002, ANTIMICROB AGENTS CH, V46, P3327, DOI 10.1128/AAC.46.10.3327-3330.2002; Biscione GL, 2004, EUR RESPIR J, V24, P745, DOI 10.1183/09031936.04.00049004; Black PN, 2001, AM J RESP CRIT CARE, V164, P536; Carbon C, 2003, INFECTION, V31, P308, DOI 10.1007/s15010-003-3142-1; CLAY KD, IN PRESS ANN INTERN; Daxboeck F, 2003, CLIN MICROBIOL INFEC, V9, P263, DOI 10.1046/j.1469-0691.2003.00590.x; Dowell SF, 2001, CLIN INFECT DIS, V33, P492, DOI 10.1086/322632; *FDA, 2003, IN PRESS FDA ANT DRU, P96; FitzGerald JM, 2004, THORAX, V59, P550, DOI 10.1136/thx.2003.014936; *FOOD DRUG ADM, QUEST ANSW TEL MARK; Graham V, 2001, COCHRANE DB SYST REV, V3; Hammerschlag MR, 2001, J ANTIMICROB CHEMOTH, V48, P25; Harrison TW, 2004, LANCET, V363, P271, DOI 10.1016/S0140-6736(03)15384-6; Johnston SL, 2005, AM J RESP CRIT CARE, V172, P1078, DOI 10.1164/rccm.200412-1743PP; Kraft M, 2002, CHEST, V121, P1782, DOI 10.1378/chest.121.6.1782; National Asthma Education and Prevention Program. National Asthma Education and Prevention Program, 2002, J ALLERGY CLIN IMMUN, V110, pS141; NICOLAU DP, 2003, CLIN MICROBIOL INFEC, V9, P397; Roblin PM, 1998, ANTIMICROB AGENTS CH, V42, P1515; Santanello NC, 1997, EUR RESPIR J, V10, P646; Wark PAB, 2002, EUR RESPIR J, V20, P834, DOI 10.1183/09031936.02.00192002; Yamaguchi T, 2000, ANTIMICROB AGENTS CH, V44, P1381, DOI 10.1128/AAC.44.5.1381-1382.2000	23	165	178	0	9	MASSACHUSETTS MEDICAL SOC	WALTHAM	WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA	0028-4793			NEW ENGL J MED	N. Engl. J. Med.	APR 13	2006	354	15					1589	1600		10.1056/NEJMoa044080		12	Medicine, General & Internal	General & Internal Medicine	031WW	WOS:000236736900007	16611950	
J	Srinivasan, S; O'Fallon, LR; Dearry, A				Srinivasan, S; O'Fallon, LR; Dearry, A			Creating healthy communities, healthy homes, healthy people: Initiating a research agenda on the built environment and public health	AMERICAN JOURNAL OF PUBLIC HEALTH			English	Article							PHYSICAL-ACTIVITY; UNITED-STATES; CHILDREN; POPULATION; COCKROACH; ASTHMA; RISK; CITY	Mounting evidence suggests physical and mental health problems relate to the built environment, including human-modified places such as homes, schools, workplaces, parks, industrial areas, farms, roads and highways. The public health relevance of the built environment requires examination. Preliminary research demonstrates the health benefits of sustainable communities. However, the impact of mediating and moderating factors within the built environment on health must be explored further. Given the complexity of the built environment, understanding its influence on human health requires a community-based, multilevel, interdisciplinary research approach. The authors offer recommendations, based upon a recent conference sponsored by the National Institute of Environmental Health Sciences (NIEHS), for research and policy approaches, and suggest interagency research alliances for greater public health impact.	Natl Inst Environm Hlth Sci, Div Extramural Res, Res Triangle Pk, NC 27709 USA	Srinivasan, S (reprint author), Natl Inst Environm Hlth Sci, Div Extramural Res, 111 TW Alexander Dr,POB 12233,MD EC-21, Res Triangle Pk, NC 27709 USA.						Adler NE, 1999, ANN NY ACAD SCI, V896, P3, DOI 10.1111/j.1749-6632.1999.tb08101.x; Bashir SA, 2002, AM J PUBLIC HEALTH, V92, P733, DOI 10.2105/AJPH.92.5.733; Bell ML, 2002, ENVIRON HEALTH PERSP, V110, P1163, DOI 10.1289/ehp.021101163; BENEDICT MA, 2000, SPRAWL WATCH CLEARIN; CAPPON D, 1991, CAN J PUBLIC HEALTH, V82, P249; CLINTON WJ, 1993, EXECUTIVE ORDER 1285; Corvalan CF, 1999, EPIDEMIOLOGY, V10, P656, DOI 10.1097/00001648-199909000-00036; Cummins SK, 2001, PEDIATR CLIN N AM, V48, P1241, DOI 10.1016/S0031-3955(05)70372-2; EWING R, 2002, MEASURING SPRAWL IMP; FE K, 2001, ENVIRON BEHAV, V33, P343; Frumkin H, 2002, PUBLIC HEALTH REP, V117, P201, DOI 10.1016/S0033-3549(04)50155-3; Fullilove M T, 1998, J Am Med Womens Assoc (1972), V53, P72; Fullilove MT, 2000, AM J PUBLIC HEALTH, V90, P183, DOI 10.2105/AJPH.90.2.183; Goran MI, 2001, PEDIATR CLIN N AM, V48, P931, DOI 10.1016/S0031-3955(05)70349-7; Halpern D., 1995, MORE BRICKS MORTAR M; HANCOCK T, 2002, PUBLIC HLTH REP, V115, P151; Hancock T., 2002, CAN J PUBLIC HLTH, V93, P45; Handy SL, 2002, AM J PREV MED, V23, P64, DOI 10.1016/S0749-3797(02)00475-0; Hawe P, 2000, SOC SCI MED, V51, P871, DOI 10.1016/S0277-9536(00)00067-8; Hedge A, 2000, ERGONOMICS, V43, P1019, DOI 10.1080/001401300409198; *HLTH CAN DIV CHIL, 2002, NAT BUILT ENV; Hodgson M, 2002, ENVIRON HEALTH PERSP, V110, P663; Kawachi I, 1999, ANN NY ACAD SCI, V896, P120, DOI 10.1111/j.1749-6632.1999.tb08110.x; KILLINGSWORTH RE, 2001, URBAN LAND       JUL, P12; King AC, 2000, HEALTH PSYCHOL, V19, P354, DOI 10.1037//0278-6133.19.4.354; Kjellstrom Tord, 1995, World Health Statistics Quarterly, V48, P144; Kreiger J, 2002, AM J PUBLIC HEALTH, V92, P758; LABONTE R, 1996, AUST J PUBLIC HLTHK, V17, P4; Leaderer BP, 2002, ENVIRON HEALTH PERSP, V110, P419; Lehmann I, 2002, ALLERGY, V57, P129, DOI 10.1046/j.0105-4538.2002.00001.x; McConnell R, 2002, LANCET, V359, P386, DOI 10.1016/S0140-6736(02)07597-9; Morland K, 2002, AM J PREV MED, V22, P23, DOI 10.1016/S0749-3797(01)00403-2; *NAT I ENV HLTH SC, 2003, ENV JUST PARTN COMM; OLDEN K, 1998, SCIENTIST       0216; Pederson R M, 2000, Rev Environ Health, V15, P231; POPE CA, 2002, JAMA-J AM MED ASSOC, V287, P1131; PORRAS C, 2003, SO CALIFORNIA ENV HL; Raffestine C, 1990, J SOCIOLOGY SOCIAL W, V17, P143; Rauh VA, 2002, ENVIRON HEALTH PERSP, V110, P323; Redd SC, 2002, ENVIRON HEALTH PERSP, V110, P557; Sharfstein J, 2001, AM J PUBLIC HEALTH, V91, P1191, DOI 10.2105/AJPH.91.8.1191; SHEPARD P, 2003, NO MANHATTAN ENV JUS; Spannhake EW, 2002, ENVIRON HEALTH PERSP, V110, P665; Taylor Ralph B., 1996, PHYSICAL ENV CRIME; Thomson H, 2001, BRIT MED J, V323, P187, DOI 10.1136/bmj.323.7306.187; *US DEP HHHS, 2001, HLTH PEOPL 2010 UND; VONSCHIRNDING YE, 2002, CAN J PUBLIC HLTH, V93, P9; Wang G, 2002, PEDIATRICS, V109, P81; Weich S, 2002, BRIT J PSYCHIAT, V180, P428, DOI 10.1192/bjp.180.5.428; Wilson A., 1998, GREEN DEV INTEGRATIN; Zein SR, 1997, TRANSPORT RES REC, V1578, P3, DOI 10.3141/1578-01	51	165	167	3	41	AMER PUBLIC HEALTH ASSOC INC	WASHINGTON	1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 USA	0090-0036			AM J PUBLIC HEALTH	Am. J. Public Health	SEP	2003	93	9					1446	1450		10.2105/AJPH.93.9.1446		5	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	716KL	WOS:000185027300024	12948961	
J	Simpson, A; Tan, VYF; Winn, J; Svensen, M; Bishop, CM; Heckerman, DE; Buchan, I; Custovic, A				Simpson, Angela; Tan, Vincent Y. F.; Winn, John; Svensen, Markus; Bishop, Christopher M.; Heckerman, David E.; Buchan, Iain; Custovic, Adnan			Beyond Atopy Multiple Patterns of Sensitization in Relation to Asthma in a Birth Cohort Study	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						asthma; atopy; unsupervised clustering; Bayesian inference; machine learning in epidemiology	AGE 3 YEARS; LUNG-FUNCTION; RESPIRATORY SYMPTOMS; REVISED NOMENCLATURE; PRESCHOOL-CHILDREN; MANCHESTER ASTHMA; EARLY-LIFE; ALLERGY; CHILDHOOD; PREVALENCE	Rationale: The pattern of IgE response (over time or to specific allergens) may reflect different atopic vulnerabilities which are related to the presence of asthma in a fundamentally different way from current definition of atopy. Objectives: To redefine the atopic phenotype by identifying latent structure within a complex dataset, taking into account the timing and type of sensitization to specific allergens, and relating these novel phenotypes to asthma. Methods: In a population-based birth cohort in which multiple skin and IgE tests have been taken throughout childhood, we used a machine learning approach to cluster children into multiple atopic classes in an unsupervised way. We then investigated the relation between these classes and asthma (symptoms, hospitalizations, lung function and airway reactivity). Measurements and Main Results: A five-class model indicated a complex latent structure, in which children with atopic vulnerability were clustered into four distinct classes (Multiple Early [112/1053, 10.6%]; Multiple Late [171/1053, 16.2%]; Dust Mite [47/1053,4.5%]; and Non-dust Mite [100/1053, 9.5%]), with a fifth class describing children with No Latent Vulnerability (623/1053, 59.2%). The association with asthma was considerably stronger for Multiple Early compared with other classes and conventionally defined atopy (odds ratio [95% Cl]: 29.3 [11.1-77.2] versus 12.4 [4.8-32.2] versus 11.6 [4.8-27.9] for Multiple Early class versus Ever Atopic versus Atopic age 8). Lung function and airway reactivity were significantly poorer among children in Multiple Early class. Cox regression demonstrated a highly significant increase in risk of hospital admissions for wheeze/asthma after age 3 yr only among children in the Multiple Early class (HR 9.2 [3.5-24.0], P < 0.001). Conclusions: IgE antibody responses do not reflect a single phenotype of atopy, but several different atopic vulnerabilities which differ in their relation with asthma presence and severity.	[Simpson, Angela; Custovic, Adnan] Univ Manchester, Manchester Acad Hlth Sci Ctr, NIHR Translat Res Facil Resp Med, Univ Hosp S Manchester NHS Fdn Trust, Manchester M23 9LT, Lancs, England; [Tan, Vincent Y. F.] MIT, Stochast Syst Grp, Lab Informat & Decis Syst, Cambridge, MA 02139 USA; [Winn, John; Svensen, Markus; Bishop, Christopher M.] Microsoft Res Cambridge, Cambridge, England; [Heckerman, David E.] Microsoft Res, eSci Res Grp, Redmond, WA USA; [Buchan, Iain] Univ Manchester, NW Inst Biohlth Informat, Manchester M23 9LT, Lancs, England	Simpson, A (reprint author), Univ Manchester, Wythenshawe Hosp, ERC Bldg,2nd Floor, Manchester M23 9LT, Lancs, England.	angela.simpson@manchester.ac.uk	Custovic, Adnan/A-2435-2012	Custovic, Adnan/0000-0001-5218-7071; Simpson, Angela/0000-0003-2733-6666; Buchan, Iain/0000-0003-3392-1650	Asthma UK [04/014]; Moulton Charitable Trust; James Trust; Microsoft Research; GlaxoSmithKline; Phadia Research in industry; Pfizer; UCB Pharma; ALK; Phadia; Novartis	Supported by Asthma UK Grant 04/014, Moulton Charitable Trust, the James Trust, and Microsoft Research.; A.S. received up to $1,000 in lecture fees for CME activity from GlaxoSmithKline and $5,001 $10,000 from Phadia Research in industry-sponsored grants for collaborative research. V.Y.F.T. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. J.W. is a full-time employee of Microsoft Research and has various patents through normal course of work within Microsoft Research. M.S. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. C.M.B. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. D.E.H.'s dependent is an employee of Microsoft, has received or is pending a patent from Microsoft in algorithm patents, and holds more than $100,001 in stock ownership or options in Microsoft. I.B, received more than $100,001 from Microsoft in funding to develop methods for genetic epidemiology. A.C. received 81,001 $5,000 from Pfizer and $1,001 $5,000 from UCB Pharma in consultancy fees, $1,001 $5,000 from ALK and $1,001 $5,000 from GlaxoSmithKline in advisory board fees, $5,001 $10,000 from GlaxoSmithKline in promotional lecture fees, $1,001 $5,000 from AstraZeneca, up to $1,000 from Phadia, up to $1,000 from ALK, and up to $1,000 from Novartis in lecture fees, and $5,001 $10,000 from Phadia in collaborative industry-sponsored grants.	Bateman ED, 2008, EUR RESPIR J, V31, P143, DOI 10.1183/09031936.00138707; Broadfield E, 2002, J ALLERGY CLIN IMMUN, V109, P969, DOI 10.1067/mai.2002.124772; Chapman Martin D, 2008, Clin Allergy Immunol, V21, P47; Chinn S, 1996, J APPL STAT, V23, P395, DOI 10.1080/02664769624134; Crapo RO, 2000, AM J RESP CRIT CARE, V161, P309; Custovic A, 2003, J ALLERGY CLIN IMMUN, V111, P402, DOI 10.1067/mai.2003.55; Custovic A, 2002, PEDIATR ALLERGY IMMU, V13, P32, DOI 10.1034/j.1399-3038.13.s.15.3.x; Custovic A, 2001, LANCET, V358, P188, DOI 10.1016/S0140-6736(01)05406-X; Custovic Adnan, 2004, Pediatr Pulmonol Suppl, V26, P12; DUFFY DL, 1992, CHEST, V102, P654, DOI 10.1378/chest.102.2.654; GERGEN PJ, 1992, J ALLERGY CLIN IMMUN, V90, P579, DOI 10.1016/0091-6749(92)90130-T; Haldar P, 2008, AM J RESP CRIT CARE, V178, P218, DOI [10.1164/rccm.200711-1754OC, 10.1164/rccm.200711-17540C]; Harwanegg C, 2003, CLIN EXP ALLERGY, V33, P7, DOI 10.1046/j.1365-2222.2003.01550.x; Henderson J, 2008, THORAX, V63, P974, DOI 10.1136/thx.2007.093187; Johansson SGO, 2001, ALLERGY, V56, P813, DOI 10.1034/j.1398-9995.2001.t01-1-00001.x; Johansson SGO, 2004, J ALLERGY CLIN IMMUN, V113, P832, DOI 10.1016/j.jaci.2003.12.591; Litonjua AA, 1997, AM J RESP CRIT CARE, V156, P23; Lowe L, 2002, LANCET, V359, P1904, DOI 10.1016/S0140-6736(02)08781-0; Lowe LA, 2004, ARCH PEDIAT ADOL MED, V158, P996, DOI 10.1001/archpedi.158.10.996; Matricardi PM, 2009, CLIN EXP ALLERGY, V39, P1551, DOI 10.1111/j.1365-2222.2009.03348.x; Matricardi PM, 2009, ALLERGY, V64, P1093, DOI 10.1111/j.1398-9995.2009.02055.x; Moore WC, 2009, AM J RESP CRIT CARE, V181, P315; NICOLAOU NC, 2008, J ALLERGY CLIN IMMUN, V122; Ober C, 2006, GENES IMMUN, V7, P95, DOI 10.1038/sj.gene.6364284; RABINER LR, 1985, AT&T TECH J, V64, P1251; Reddel HK, 2009, AM J RESP CRIT CARE, V180, P59, DOI 10.1164/rccm.200801-060ST; SEARS MR, 1989, CLIN EXP ALLERGY, V19, P419, DOI 10.1111/j.1365-2222.1989.tb02408.x; Simpson A, 2005, J ALLERGY CLIN IMMUN, V116, P744, DOI 10.1016/j.jaci.2005.06.032; Simpson BM, 2001, CLIN EXP ALLERGY, V31, P391, DOI 10.1046/j.1365-2222.2001.01050.x; Smith JA, 2008, AM J RESP CRIT CARE, V177, P1358, DOI 10.1164/rccm.200709-1419OC; von Mutius E, 2007, IMMUNOBIOLOGY, V212, P433, DOI 10.1016/j.imbio.2007.03.002; Weinmayr G, 2007, AM J RESP CRIT CARE, V176, P565, DOI 10.1164/rccm.200607-994OC; Winn J, 2005, J MACH LEARN RES, V6, P661; Woodcock A, 2004, AM J RESP CRIT CARE, V170, P433, DOI 10.1164/rccm.200401-083OC; WOOLCOCK AJ, 1983, EUR J RESPIR DIS, V64, P571	35	164	168	1	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.	JUN 1	2010	181	11					1200	1206		10.1164/rccm.200907-1101OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	609NN	WOS:000278663600009	20167852	
J	Penagos, M; Passalacqua, G; Compalati, E; Baena-Cagnani, CE; Orozco, S; Pedroza, A; Canonica, GW				Penagos, Martin; Passalacqua, Giovanni; Compalati, Enrico; Baena-Cagnani, Carlos E.; Orozco, Socorro; Pedroza, Alvaro; Canonica, Giorgio Walter			Metaanalysis of the efficacy of sublingual immunotherapy in the treatment of allergic asthma in pediatric patients, 3 to 18 years of age	CHEST			English	Article						asthma; children; efficacy; metaanalysis; randomized controlled trials; sublingual immunotherapy	RANDOMIZED CONTROLLED-TRIALS; HOUSE-DUST MITE; DOUBLE-BLIND; CLINICAL-TRIALS; GRASS-POLLEN; SWALLOW IMMUNOTHERAPY; STATISTICAL POWER; RESPIRATORY ALLERGY; DOUBLE-DUMMY; CHILDREN	Background: Recent studies have documented the efficacy and safety of sublingual immunotherapy (SLIT) in patients with rhinitis, but the value of this treatment in those with asthma is still debated. We evaluated the efficacy of SLIT in the treatment of allergic asthma in children by a metaanalysis of randomized, double-blind, and placebo-controlled (DBPC) clinical trials. Methods: Electronic databases were searched up to May 31, 2006, for randomized DBPC trials assessing SLIT in pediatric cases of asthma. Effects on primary outcomes (ie, symptom scores and concomitant use of rescue medication) were calculated with standardized mean differences (SMDs) using the random-effects model. We performed the metaanalysis using a statistical software package (RevMan, 4.2.8; The Cochrane Collaboration; Oxford, UK), and we followed the recommendations of the Cochrane Collaboration and the Quality of Reporting of Metaanalyses guidelines. Results: Seventy-three articles were identified and reviewed. Nine studies, all published after 1990, fulfilled the selection criteria. A total of 441 patients had a final assessment and were included in the analysis. Two hundred thirty-two patients received SLIT, and 209 patients received placebo. The results of the present analysis demonstrated a relevant heterogeneity due to widely differing scoring systems. Overall, there was a significant reduction in both symptoms (SMD 1.14; 95% confidence interval [CI], -2.10 to -0.18; p = 0.02) and medication use (SMD, 1.63; 95% CI, -2.83 to -0.44; p = 0.007) following SLIT. Conclusion: SLIT with standardized extracts reduces both symptom scores and rescue medication use in children with allergic asthma compared with placebo.	[Penagos, Martin; Passalacqua, Giovanni; Compalati, Enrico; Canonica, Giorgio Walter] Univ Genoa, Dept Internal Med, Div Allergy & Respiratory Dis, Genoa, Italy; [Baena-Cagnani, Carlos E.] Univ Cordoba, Cordoba, Argentina; [Orozco, Socorro; Pedroza, Alvaro] Natl Pediat Inst, Mexico City, DF, Mexico	Canonica, GW (reprint author), DIMI, Largo R Benzi 10, I-16132 Genoa, Italy.	canonica@unige.it					Abramson MJ, 2003, COCHRANE DATABASE SY; Akobeng AK, 2005, ARCH DIS CHILD, V90, P837, DOI 10.1133/adc.2005.071761; Alderson P., 2002, COCHRANE COLLABORATI; *AM AC PED COUNC C, 1972, PEDIATRICS, V49, P463; Bahceciler NN, 2001, PEDIATR PULM, V32, P49, DOI 10.1002/ppul.1088; Battle M. 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J	Linneberg, A; Nielsen, NH; Frolund, L; Madsen, F; Dirksen, A; Jorgensen, T				Linneberg, A; Nielsen, NH; Frolund, L; Madsen, F; Dirksen, A; Jorgensen, T			The link between allergic rhinitis and allergic asthma: A prospective population-based study. The Copenhagen Allergy Study	ALLERGY			English	Article						allergic asthma; allergic rhinitis; epidemiology; IgE antibody; respiratory hypersensitivity	8 YEARS APART; DANISH ADULTS; SKIN-TEST; IMMUNOTHERAPY; PREVALENCE	Background: It has been hypothesized that allergic rhinitis and allergic asthma are manifestations of the same disease entity. We aimed to investigate the relationship between allergic rhinitis and allergic asthma. Methods: Participants in a population-based study of 15-69-year-olds in 1990 were invited to a follow-up in 1998. A total of 734 subjects were examined on two occasions eight years apart. Allergic rhinitis to pollen was defined as a history of nasal symptoms on exposure to pollens and IgE specific to pollen. Allergic asthma to pollen was defined as a history of lower airway symptoms on exposure to pollens and IgE specific to pollen. Similarly, diagnoses of allergic rhinitis and allergic asthma to animals or mite were defined. Results: At follow-up, all subjects with allergic asthma to pollen (n = 52) had in addition allergic rhinitis to pollen. In the longitudinal analysis, there were a total of 28 new (incident) cases of allergic asthma to pollen. They all had allergic rhinitis to pollen at baseline, or had developed allergic rhinitis to pollen at follow-up. Accordingly, allergic rhinitis to animals and mite were ubiquitous in subjects with allergic asthma to animals and mite, respectively. Conclusions: The results support the hypothesis that allergic rhinitis and allergic asthma are manifestations of the same disease entity.	Glostrup Univ Hosp, Dept Internal Med M, Ctr Prevent Med, Glostrup, Denmark; Bispebjerg Univ Hosp, Dept Dermatol, Copenhagen, Denmark; Frederiksberg Univ Hosp, Dept Internal Med B, Frederiksberg, Denmark; Gentofte Univ Hosp, Dept Resp Med Y, Gentofte, Denmark	Linneberg, A (reprint author), Glostrup Cty Hosp, Ctr Prevent Med, 57 Ndr Ringvej,Entrance 8,7th Floor, DK-2600 Glostrup, Denmark.						ABRAHAMSON MJ, 1998, COCHRANE LIB; Annesi-Maesano I, 1999, ALLERGY, V54, P7; 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; Ciprandi G, 1996, Int Arch Allergy Immunol, V111, P278; CORREN J, 1998, J ALLERGY CLIN IMMUN, V101, P352; Greisner WA, 1998, ALLERGY ASTHMA PROC, V19, P185, DOI 10.2500/108854198778557836; Grembiale RD, 2000, AM J RESP CRIT CARE, V162, P2048; Grossman J, 1997, CHEST, V111, P11; Huovinen E, 1999, CHEST, V115, P928, DOI 10.1378/chest.115.4.928; Johansson SGO, 2001, ALLERGY, V56, P813, DOI 10.1034/j.1398-9995.2001.t01-1-00001.x; Kapsali T, 1997, J ALLERGY CLIN IMMUN, V99, P138; Leynaert B, 1999, J ALLERGY CLIN IMMUN, V104, P301, DOI 10.1016/S0091-6749(99)70370-2; Leynaert B., 2000, J ALLERGY CLIN IMMUN, V106, P201; Linneberg A, 2000, ALLERGY, V55, P767, DOI 10.1034/j.1398-9995.2000.00672.x; Linneberg A, 2001, RESP MED, V95, P258, DOI 10.1053/rmed.2001.1031; Linneberg A, 2000, J ALLERGY CLIN IMMUN, V106, P247, DOI 10.1067/mai.2000.108312; LINNEBERG A, 2001, ALLERGY, V54, P328; NIELSEN NH, 1993, ALLERGY, V48, P319, DOI 10.1111/j.1398-9995.1993.tb02400.x; Passalacqua G, 2000, THORAX, V55, P26; PEDERSEN PA, 1983, ALLERGY, V38, P25, DOI 10.1111/j.1398-9995.1983.tb00852.x; Rachelefsky GS, 1999, ANN ALLERG ASTHMA IM, V82, P296, DOI 10.1016/S1081-1206(10)62612-9; Simons FER, 1999, J ALLERGY CLIN IMMUN, V104, P534, DOI 10.1016/S0091-6749(99)70320-9; Spector S. L., 1997, J ALLERGY CLIN IMMUN, V99, P773; Townley RG, 1998, ANN ALLERG ASTHMA IM, V80, P137; Valovirta E, 1997, J INVEST ALLERG CLIN, V7, P369; Vignola AM, 2001, CLIN EXP ALLERGY, V31, P674, DOI 10.1046/j.1365-2222.2001.01115.x	27	164	171	0	3	BLACKWELL MUNKSGAARD	COPENHAGEN	35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK	0105-4538			ALLERGY	Allergy	NOV	2002	57	11					1048	1052		10.1034/j.1398-9995.2002.23664.x		5	Allergy; Immunology	Allergy; Immunology	599PC	WOS:000178343400011	12359002	
J	DeRijk, RH; Schaaf, M; de Kloet, ER				DeRijk, RH; Schaaf, M; de Kloet, ER			Glucocorticoid receptor variants: clinical implications	JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY			English	Review						glucocorticoid receptor variants; clinical implications; hypothalamic-pituitary-adrenal axis	PRIMARY CORTISOL RESISTANCE; FRAGMENT-LENGTH-POLYMORPHISM; HORMONE-BINDING DOMAIN; HUMAN MULTIPLE-MYELOMA; BETA-ISOFORM; DNA-BINDING; MESSENGER-RNA; TRANSCRIPTIONAL ACTIVATION; RESPONSE ELEMENT; CUSHINGS-DISEASE	Following exposure to stress, cortisol is secreted from the adrenal cortex under the control of the hypothalamic-pituitary-adrenal axis (HPA-axis). Central in the regulation of the HPA-axis is a two tied corticosteroid-receptor system, comprised of high and low affinity receptors, the mineralocorticoid receptor (MR) and the glucocorticoid receptor (GR), respectively. In addition, these corticosteroid receptors mediate the effects of cortisol during stress on both central and peripheral targets. Cortisol modulates gene-expression of corticosteroid-responsive genes, with the effect lasting from hours to days. Mutations in the GR-gene are being associated with corticosteroid resistance and haematological malignancies, although these mutations are relatively rare and probably not a common cause of these diseases. However, several GR-gene variants and single nucleotide polymorphisms (SNP) in the GR-gene have been identified which are relatively common in the human population. The GRbeta-variant, for example, has been proposed to influence corticosteroid-sensitivity and most evidence has been derived from the immune system and in particular asthma. With respect to polymorphisms, a BclI restriction fragment polymorphism and a Asp363Ser have been described, which not only influence the regulation of the HPA-axis, but are also associated with changes in metabolism and cardiovascular control. These associations of a GR-gene polymorphism with metabolism and cardivascular control, and also with the regulation of the HPA-axis, indicates an important underlying role of cortisol in the etiology of these complex disorders. Therefore, we propose that a common underlying defect in these complex disorders is a disregulation of the HPA-axis, especially during stress. The clinical implication is that the regulation of the HPA-axis should be envisioned as a primary target of new drugs for the treatment of stress-related disorders. (C) 2002 Elsevier Science Ltd. All rights reserved.	Rijngeestgroep LUMC, Hosp Psychiat, Dept Psychiat, NL-2342 AJ Oesgstsgeest, Netherlands; NIEHS, Lab Signal Transduct, NIH, Res Triangle Pk, NC USA; LUMC, Dept Med Pharmacol, Oesgstsgeest, Netherlands	DeRijk, RH (reprint author), Rijngeestgroep LUMC, Hosp Psychiat, Dept Psychiat, Endegeesterstr Weg 5, NL-2342 AJ Oesgstsgeest, Netherlands.						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Steroid Biochem. Mol. Biol.	JUN	2002	81	2					103	122	PII S0960-0760(02)00062-6	10.1016/S0960-0760(02)00062-6		20	Biochemistry & Molecular Biology; Endocrinology & Metabolism	Biochemistry & Molecular Biology; Endocrinology & Metabolism	592MT	WOS:000177942000001	12137800	
J	O'Brien, C; Guest, PJ; Hill, SL; Stockley, RA				O'Brien, C; Guest, PJ; Hill, SL; Stockley, RA			Physiological and radiological characterisation of patients diagnosed with chronic obstructive pulmonary disease in primary care	THORAX			English	Article						chronic obstructive pulmonary disease; bronchiectasis; lung function tests; radiology	CHRONIC SPUTUM PRODUCTION; COMPUTED-TOMOGRAPHY; FUNCTION TESTS; LUNG; CHEST; EXACERBATIONS; MANAGEMENT; EMPHYSEMA; SMOKERS; COPD	Background-Chronic obstructive pulmonary disease (COPD) is common although often poorly characterised, particularly in primary care. However, application of guidelines to the management of such patients needs a clear understanding of the phenotype. In particular, the British guidelines for the management of COPD recommend that the diagnosis is based on appropriate symptoms and evidence of airflow obstruction as determined by a forced expiratory volume in one second (FEV1) of <80% of the predicted value and an FEV1/VC ratio of <70%. Methods-A study was undertaken of 110 patients aged 40-80 years who had presented to their general practitioner with an acute exacerbation of COPD. The episode was treated at home and, when patients had recovered to the stable state (two months later), they were characterised by full lung function tests and a high resolution computed tomographic (HRCT) scan of the chest. Results-There was a wide range of impairment of FEV1 which was in the normal range (greater than or equal to 80%) in 30%, mildly impaired (60-79%) in 18%, moderately impaired (40-59%) in 33%, and severely impaired (<40%) in 19% of patients. A reduced FEV1/VC ratio was present in all patients with an FEV1 of <80% predicted but also in 41% of those with an FEV1 of greater than or equal to 80% predicted. Only 5% of patients had a substantial bronchodilator response suggesting a diagnosis of asthma. Emphysema was present in 51% of patients and confined to the upper lobes in most (73% of these patients). HRCT evidence of bronchiectasis was noted in 29% of patients and was predominantly tubular; most (81%) were current or ex-smokers. A solitary pulmonary nodule was seen on 9% of scans and unsuspected lung malignancy was diagnosed in two patients. Conclusions-This study confirms that COPD in primary care is a heterogeneous condition. Some patients do not fulfil the proposed diagnostic criteria with FEV1 of greater than or equal to 80% predicted but they may nevertheless have airflow obstruction. Bronchiectasis is common in this group of patients, as is unsuspected malignancy. These findings should be considered when developing recommendations for the investigation and management of COPD in the community.	Queen Elizabeth Hosp, Dept Med, Birmingham B15 2TH, W Midlands, England; Queen Elizabeth Hosp, Dept Radiol, Birmingham B15 2TH, W Midlands, England	Stockley, RA (reprint author), Queen Elizabeth Hosp, Dept Med, Birmingham B15 2TH, W Midlands, England.						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J	Hart, PH; Gorman, S; Finlay-JonesO, JJ				Hart, Prue H.; Gorman, Shelley; Finlay-JonesO, John J.			Modulation of the immune system by UV radiation: more than just the effects of vitamin D?	NATURE REVIEWS IMMUNOLOGY			English	Review							REGULATORY-T-CELLS; ULTRAVIOLET-RADIATION; MULTIPLE-SCLEROSIS; UROCANIC ACID; INDUCED IMMUNOSUPPRESSION; HUMAN SKIN; ANTIMICROBIAL PEPTIDES; INDUCED SUPPRESSION; MAST-CELLS; INFECTIOUS-DISEASES	Humans obtain most of their vitamin D through the exposure of skin to sunlight. The immunoregulatory properties of vitamin D have been demonstrated in studies showing that vitamin D deficiency is associated with poor immune function and increased disease susceptibility. The benefits of moderate ultraviolet (UV) radiation exposure and the positive latitude gradients observed for some immune-mediated diseases may therefore reflect the activities of UV-induced vitamin D. Alternatively, other mediators that are induced by UV radiation may be more important for UV-mediated immunomodulation. Here, we compare and contrast the effects of UV radiation and vitamin D on immune function in immunopathological diseases, such as psoriasis, multiple sclerosis and asthma, and during infection.	[Hart, Prue H.; Gorman, Shelley] Univ Western Australia, Telethon Inst Child Hlth Res, Ctr Child Hlth Res, Perth, WA 6872, Australia; [Finlay-JonesO, John J.] Edith Cowan Univ, Perth, WA, Australia	Hart, PH (reprint author), Univ Western Australia, Telethon Inst Child Hlth Res, Ctr Child Hlth Res, POB 855, Perth, WA 6872, Australia.	prueh@ichr.uwa.edu.au	Finlay-Jones, John/C-2421-2013; Gorman, Shelley/E-1649-2013; Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Gorman, Shelley/0000-0002-7111-6735	Australian National Health and Medical Research Council; Cancer Council Western Australia; Asthma Foundation of Western Australia; Raine Foundation; Brightspark Foundation	The authors would like to thank M. Norval for valuable analysis of this Review and D. Damian for assistance with TABLE 1. Our research has been supported by the Australian National Health and Medical Research Council, the Cancer Council Western Australia, the Asthma Foundation of Western Australia, the Raine Foundation and the Brightspark Foundation.	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Rev. Immunol.	SEP	2011	11	9					584	596		10.1038/nri3045		13	Immunology	Immunology	811XB	WOS:000294250400002	21852793	
J	Koplin, JJ; Osborne, NJ; Wake, M; Martin, PE; Gurrin, LC; Robinson, MN; Tey, D; Slaa, M; Thiele, L; Miles, L; Anderson, D; Tan, T; Dang, TD; Hill, DJ; Lowe, AJ; Matheson, MC; Ponsonby, AL; Tang, MLK; Dharmage, SC; Allen, KJ				Koplin, Jennifer J.; Osborne, Nicholas J.; Wake, Melissa; Martin, Pamela E.; Gurrin, Lyle C.; Robinson, Marnie N.; Tey, Dean; Slaa, Marjolein; Thiele, Leone; Miles, Lucy; Anderson, Deborah; Tan, Tina; Dang, Thanh D.; Hill, David J.; Lowe, Adrian J.; Matheson, Melanie C.; Ponsonby, Anne-Louise; Tang, Mimi L. K.; Dharmage, Shyamali C.; Allen, Katrina J.			Can early introduction of egg prevent egg allergy in infants? A population-based study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Egg allergy; food allergy; solids; breast-feeding; infant diet; weaning	ATOPIC DISEASE; ORAL TOLERANCE; PEANUT ALLERGY; FOOD ALLERGY; BIRTH COHORT; CHILDREN; RISK; LIFE; SENSITIZATION; CONSUMPTION	Background: Infant feeding guidelines have long recommended delaying introduction of solids and allergenic foods to prevent allergy in high-risk infants, despite a paucity of evidence. Objective: We aimed to determine whether confirmed egg allergy in 12-month-old infants is associated with (1) duration of breast-feeding and (2) ages of introducing egg and solids. Methods: In a population-based cross-sectional study (HealthNuts) parents reported on infant feeding and potential confounding factors before skin prick testing for egg white. Egg-sensitized infants were then offered an egg oral food challenge. Multiple logistic regression was used to investigate associations between diet and egg allergy adjusted for possible confounding factors. Results: A total of 2589 infants (73% response) participated. Compared with introduction at 4 to 6 months, introducing egg into the diet later was associated with higher risks of egg allergy (adjusted odds ratios [ORs], 1.6 [95% CI, 1.0-2.6] and 3.4 [95% CI, 1.8-6.5] for introduction at 10-12 and after 12 months, respectively). These findings persisted even in children without risk factors (OR, 3.3 [95% CI, 1.1-9.9]; 10-12 months). At age 4 to 6 months, first exposure as cooked egg reduced the risk of egg allergy compared with first exposure as egg in baked goods (OR, 0.2 [95% CI, 0.06-0.71]). Duration of breast-feeding and age at introduction of solids were not associated with egg allergy. Conclusions: Introduction of cooked egg at 4 to 6 months of age might protect against egg allergy. Changes in infant feeding guidelines could have a significant effect on childhood egg allergy and possibly food allergy more generally. (J Allergy Clin Immunol 2010;126:807-13.)	[Allen, Katrina J.] Royal Childrens Hosp, Murdoch Childrens Res Inst, Parkville, Vic 3052, Australia; [Koplin, Jennifer J.; Osborne, Nicholas J.; Wake, Melissa; Martin, Pamela E.; Tan, Tina; Dang, Thanh D.; Ponsonby, Anne-Louise; Tang, Mimi L. K.; Allen, Katrina J.] Univ Melbourne, Dept Paediat, Melbourne, Vic, Australia; [Osborne, Nicholas J.; Gurrin, Lyle C.; Lowe, Adrian J.; Matheson, Melanie C.; Dharmage, Shyamali C.] Univ Melbourne, Ctr Mol Environm Genet & Analyt Epidemiol, Melbourne, Vic, Australia; [Wake, Melissa] Royal Childrens Hosp, Ctr Community Child Hlth, Parkville, Vic 3052, Australia; [Robinson, Marnie N.; Tey, Dean; Tang, Mimi L. K.; Allen, Katrina J.] Royal Childrens Hosp, Dept Allergy & Immunol, Parkville, Vic 3052, Australia	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; Osborne, Nicholas/0000-0002-6700-2284; Matheson, Melanie/0000-0002-5822-3499; Osborne, Nicholas/0000-0002-6700-2284; Tan, Hern-Tze Tina/0000-0002-8289-7573; Lowe, Adrian/0000-0002-4691-8162; Dharmage, Shyamali/0000-0001-6063-1937; Allen, Katrina/0000-0002-1921-4493	Australian National Health & Medical Research Council; Ilhan Food Allergy Foundation; AnaphylaxiStop; National Health and Medical Research Council Award; Australian Egg Corporation Limited; Australian National Health and Medical Research Council; Clifford Craig Trust; Sypkes Trust	Supported by the Australian National Health & Medical Research Council, the Ilhan Food Allergy Foundation, and AnaphylaxiStop. K. J. A. is a Viertel Senior Medical Research Fellow, and L. C. G., M. W., M. C. M., A. J. L., A.-L. P., and S. C. D. hold National Health and Medical Research Council Awards. J. J. K., P. E. M., and T. D. are Australian Postgraduate Award scholars. T. T. is a recipient of a Malaysian Government Scholarship.; Disclosure of potential conflict of interest: N. J. Osborne and K. J. Allen have received research support from the Australian Egg Corporation Limited. M. Wake and L. C. Gurrin have received research support from the Australian National Health and Medical Research Council. M. L. K. Tang is on the Medical Advisory Board for Nestle. S. C. Dharmage has received research support from the Clifford Craig Trust and the Sypkes Trust. The rest of the authors have declared that they have no conflict of interest.	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Allergy Clin. Immunol.	OCT	2010	126	4					807	813		10.1016/j.jaci.2010.07.028		7	Allergy; Immunology	Allergy; Immunology	658SP	WOS:000282510000019	20920771	
J	Bernstein, JA; Alexis, N; Bacchus, H; Bernstein, IL; Fritz, P; Horner, E; Li, N; Mason, S; Nel, A; Oullette, J; Reijula, K; Reponen, T; Seltzer, J; Smith, A; Tarlo, SM				Bernstein, Jonathan A.; Alexis, Neil; Bacchus, Hyacinth; Bernstein, I. Leonard; Fritz, Pat; Horner, Elliot; Li, Ning; Mason, Stephany; Nel, Andre; Oullette, John; Reijula, Kari; Reponen, Tina; Seltzer, James; Smith, Alisa; Tarlo, Susan M.			The health effects of nonindustrial indoor air pollution	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						indoor air pollutants; ozone; particulate matter; nitrogen dioxide; carbon monoxide; sulfur dioxide; health effects; volatile organic compounds; tobacco smoke; passive smoke exposure; cotinine; fungal allergens	ENVIRONMENTAL TOBACCO-SMOKE; VOLATILE ORGANIC-COMPOUNDS; NITROGEN-DIOXIDE EXPOSURE; RESPIRATORY SYMPTOMS; STACHYBOTRYS-CHARTARUM; PARTICULATE MATTER; OZONE EXPOSURE; SENSORY IRRITATION; INHALED ALLERGEN; OXIDATIVE STRESS	Background: There is growing public awareness regarding the risk associated with poor indoor air quality in the home and workplace. Because Americans spend approximately 22 hours every day indoors, susceptible individuals are at much greater risk of adverse health effects from chronic low levels of exposure to indoor air pollutants over time. Along with particulate matter, gases such as ozone, nitrogen dioxide, carbon monoxide, and sulfur dioxide; microbial and chemical volatile organic compounds; passive smoke; and outdoor ambient air are the most common types of air pollutants encountered indoors. Objective: To provide the allergists with necessary information that will assist them in making useful recommendations to patients seeking advice regarding indoor environmental triggers beyond traditional perennial allergens. Methods: Review of the literature pertaining to indoor exposure and health effects of gaseous and particular matter. Results: Indoor pollutants act as respiratory irritants, toxicants, and adjuvants or carriers of allergens. Conclusion: The allergist should be prepared to evaluate patient exposure to allergic and nonallergic triggers and understand how outdoor air pollution is affecting indoor environments. This requires being familiar with methodologies for monitoring and interpreting indoor air quality and interpreting results in the context of the patients exposure history and advising patients about rational environmental control interventions.	[Bernstein, Jonathan A.; Bernstein, I. Leonard] Univ Cincinnati, Div Immunol, Dept Internal Med, Allergy Sect, Cincinnati, OH 45221 USA; [Alexis, Neil] Univ N Carolina, Ctr Environm Med & Lung Biol, Chapel Hill, NC USA; [Fritz, Pat] Rensselaer Polytech Inst, Troy, NY USA; [Horner, Elliot; Mason, Stephany] Air Qual Sci Inc, Atlanta, GA USA; [Li, Ning; Nel, Andre] Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA; [Oullette, John] Adult Allergy Clin, Madison, WI USA; [Reijula, Kari] Finnish Inst Occupat Hlth, Helsinki, Finland; [Reponen, Tina] Univ Cincinnati, Ctr Environm Hlth, Cincinnati, OH 45221 USA; [Seltzer, James] Sharp Mission Pk Med Grp, Vista, CA USA; [Smith, Alisa] US EPA, Washington, DC 20460 USA; [Tarlo, Susan M.] Toronto Western Hosp, Toronto, ON, Canada	Bernstein, JA (reprint author), 231 Albert Sabin Way ML 563, Cincinnati, OH 45267 USA.	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Strand V, 1997, AM J RESP CRIT CARE, V155, P881; Taskinen T, 1997, ACTA PAEDIATR, V86, P1181, DOI 10.1111/j.1651-2227.1997.tb14841.x; Thorn A, 1998, SOC SCI MED, V47, P1307, DOI 10.1016/S0277-9536(98)00206-8; Triche EW, 2005, EPIDEMIOLOGY, V16, P377, DOI 10.1097/01.ede.0000158225.44414.85; TUNNICLIFFE WS, 1994, LANCET, V344, P1733, DOI 10.1016/S0140-6736(94)92886-X; TUNNICLIFFE WS, 2003, OCCUP ENVIRON MED, V60, pE1; van Strien RT, 2004, EPIDEMIOLOGY, V15, P471, DOI 10.1097/01.ede.0000129511.61698.d8; vanVliet P, 1997, ENVIRON RES, V74, P122, DOI 10.1006/enrs.1997.3757; Walinder R, 2005, ENVIRON HEALTH PERSP, V113, P1775, DOI 10.1289/ehp.8193; Walinder R, 1998, INT J TUBERC LUNG D, V2, P1037; Walinder R, 2001, ARCH ENVIRON HEALTH, V56, P30; Weaver LK, 2002, NEW ENGL J MED, V347, P1057, DOI 10.1056/NEJMoa013121; Weichenthal S., 2006, J EXPO SCI ENV EPID, V17, P288; Weisel CP, 2002, ENVIRON HEALTH PERSP, V110, P527; WILKIE DJ, 1995, CANCER NURS, V18, P7; Wolkoff P, 2006, INDOOR AIR, V16, P7, DOI 10.1111/j.1600-0668.2005.00393.x	76	163	168	18	70	MOSBY-ELSEVIER	NEW YORK	360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA	0091-6749	1097-6825		J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	MAR	2008	121	3					585	591		10.1016/j.jaci.2007.10.045		7	Allergy; Immunology	Allergy; Immunology	273GR	WOS:000253918900005	18155285	
J	Clark, S; Bock, SA; Gaeta, TJ; Brenner, BE; Cydulka, RK; Camargo, CA				Clark, S; Bock, SA; Gaeta, TJ; Brenner, BE; Cydulka, RK; Camargo, CA			Multicenter study of emergency department visits for food allergies	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						food allergy; emergency department; epinephrine	ANAPHYLACTIC REACTIONS; EPIDEMIOLOGY; ROOM	Background: Relatively little is known about the characteristics of patients who visit the emergency department (ED) for an acute allergic reaction. Although anaphylaxis guidelines suggest treatment with epinephrine, teaching about self-injectable epinephrine, and referral to an allergist, current ED management remains uncertain. Objective: The objective of this study was to describe the management of food-related acute allergic reactions. Methods: The Multicenter Airway Research Collaboration performed a chart review study in 21 North American EDs. Investigators reviewed a random sample of 678 charts of patients who presented with food allergy (International Classification of Diseases-ninth revision codes 693.1, 995.0, 995.3, and 995.60-995.69). Results: Patients had an average age of 29 years; the cohort was 57% female and 40% white. A variety of foods provoked the allergic reaction, including nuts (21%), crustaceans (19%), fruit (12%), and fish (10%). Although exposure to these foods can be life threatening, only 18% of patients came to the ED by ambulance. In the ED, 72% of patients received antihistamines, 48% received systemic corticosteroids, and 16% received epinephrine; 33% received respiratory treatments such as inhaled albuterol. Among patients with severe reactions (55% of total), 24% received epinephrine. Overall, 97% of patients were discharged to home. At ED discharge, 16% of patients were prescribed self-injectable epinephrine, and 12% were referred to an allergist. Conclusions: Although guidelines suggest specific approaches for the management of acute allergic reactions, ED concordance for food allergy appears low. These findings support a new collaboration between professional organizations in allergy and emergency medicine and the development of educational programs and materials for ED patients and staff.	Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA; Natl Jewish Med & Res Ctr, Denver, CO USA; New York Methodist Hosp, Dept Emergency Med, Brooklyn, NY USA; Univ Arkansas Med Sci, Dept Emergency Med, Little Rock, AR 72204 USA; Metrohlth Med Ctr, Dept Emergency Med, Cleveland, OH USA; Harvard Univ, Sch Med, Brigham & Womens Hosp, Channing Lab,Dept Med, Boston, MA USA	Clark, S (reprint author), Massachusetts Gen Hosp, Dept Emergency Med, 55 Fruit St,Clin Bldg 397, Boston, MA 02114 USA.				NIEHS NIH HHS [T32 ES07069]		Bock SA, 2001, J ALLERGY CLIN IMMUN, V107, P191, DOI 10.1067/mai.2001.112031; Brown AFT, 2001, J ALLERGY CLIN IMMUN, V108, P861, DOI 10.1067/mai.2001.119028; Burks AW, 1999, CLIN REV ALLERG IMMU, V17, P339, DOI 10.1007/BF02737615; GAETA TJ, 2001, ACAD EMERG MED, V8, P449; Hosmer DW, 1989, APPL LOGISTIC REGRES; KLEIN JS, 1995, J ALLERGY CLIN IMMUN, V95, P637, DOI 10.1016/S0091-6749(95)70329-2; KRAUSE RS, 1999, ANAPHYLAXIS; Matasar MJ, 2003, CURR ALLERGY ASTHM R, V3, P30, DOI 10.1007/s11882-003-0007-8; SAMPSON HA, 1992, NEW ENGL J MED, V327, P380, DOI 10.1056/NEJM199208063270603; SCHWARTZ HJ, 1995, ALLERGY PROC, V16, P247, DOI 10.2500/108854195778702639; Shimamoto SR, 2002, CURR OPIN ALLERGY CL, V2, P211, DOI 10.1097/00130832-200206000-00010; Sicherer SH, 1999, J ALLERGY CLIN IMMUN, V103, P559, DOI 10.1016/S0091-6749(99)70224-1; *STAT, 1985, STAT REF MAN; Stewart AG, 1996, QJM-MON J ASSOC PHYS, V89, P859; Yocum MW, 1999, J ALLERGY CLIN IMMUN, V104, P452, DOI 10.1016/S0091-6749(99)70392-1; 2000, FOOD ALLERGY ANAPHYL; 2000, SOURCEBOOK ZIP CODE; 1996, FEDERAL CENSUS DATA	18	163	164	0	13	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	FEB	2004	113	2					347	352		10.1016/j.jaci.2003.10.053		6	Allergy; Immunology	Allergy; Immunology	773EX	WOS:000188885700026	14767453	
J	Suissa, S; Ernst, P				Suissa, S; Ernst, P			Inhaled corticosteroids: Impact on asthma morbidity and mortality	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						asthma; case-control studies; cohort studies; ecologic studies; epidemiologic studies; hospitalization; inhaled glucocorticoids; mortality; registries	NEW-ZEALAND; PRESCRIBED FENOTEROL; HOSPITAL ADMISSION; CHILDHOOD ASTHMA; BETA-AGONISTS; UNITED-STATES; YOUNG-ADULTS; RISK-FACTORS; MILD ASTHMA; DEATH	Inhaled corticosteroids are now recommended as first-line therapy for asthma, Although these drugs clearly improve the symptoms of the disease and the associated physiologic abnormalities, epidemiologic studies provide important information on their effectiveness in preventing asthma morbidity and mortality. We review the evidence regarding the role of inhaled corticosteroids in the prevention of asthma fatality and hospitalization. In the process, we discuss the methodologic complexities of the nonexperimental studies and the implications of the methodologic issues on the evaluation of the impart of these drugs. Eight of the cohort and ecologic studies conducted to date strongly suggest that inhaled corticosteroids. when taken regularly, decrease the number of hospitalizations for asthma by up to 80%. For asthma death, the results of 11 investigations appear less consistent, especially those of several cohort and case-control studies whose principal objective was to examine not the benefit of inhaled corticosteroids but the adverse effects of other drug classes, Much of the inconsistency in the results, however, can be explained by weaknesses in study design and analysis-in particular, the failure to consider exposure in terms of regular use of inhaled corticosteroids. When the most recent study involving the use of the Saskatchewan databases is considered, it is evident that regular treatment with conventional or low-dose inhaled corticosteroids results in a significant reduction in fatalities due to asthma, In all, the evidence to date strongly indicates that regular use of inhaled corticosteroids, even at low doses, would prevent the major portion of asthma hospitalizations and deaths.	McGill Univ, Royal Victoria Hosp, Ctr Hlth, Div Clin Epidemiol, Montreal, PQ H3A 1A1, Canada; McGill Univ, Dept Epidemiol & Biostat, Montreal, PQ, Canada; McGill Univ, Dept Med, Montreal, PQ, Canada; McGill Univ, Ctr Hlth, Div Resp Med, Montreal, PQ, Canada	Suissa, S (reprint author), McGill Univ, Royal Victoria Hosp, Ctr Hlth, Div Clin Epidemiol, 687 Pine Ave W,Ross 4-29, Montreal, PQ H3A 1A1, Canada.						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Allergy Clin. Immunol.	JUN	2001	107	6					937	944		10.1067/mai.2001.115653		8	Allergy; Immunology	Allergy; Immunology	445JR	WOS:000169454800001	11398069	
J	Flaherman, V; Rutherford, GW				Flaherman, V; Rutherford, GW			A meta-analysis of the effect of high weight on asthma	ARCHIVES OF DISEASE IN CHILDHOOD			English	Article							BODY-MASS INDEX; UNITED-STATES; BIRTH-WEIGHT; FETAL-GROWTH; RISK-FACTORS; NUTRITION EXAMINATION; CHILDHOOD ASTHMA; NATIONAL-HEALTH; LUNG-FUNCTION; YOUNG-ADULTS	Background: Prevalence rates for both overweight and asthma have been increasing among children in developed countries over the past two decades. Some recent studies have postulated a causal relation between these but have lacked power to form a definitive conclusion. Aim: To estimate the effect of high body weight in childhood on the future risk of asthma. Methods: Medline search ( 1966 to October 2004), supplemented by manual search of reference lists and grey literature. Cohort studies that examined high body weight at birth or during childhood and future outcome of asthma were included. Data from each study were extracted on exposure status, clinical outcome, and study characteristics. Results: A total of 402 studies were initially identified, of which 12 met the inclusion criteria. The combined results from four studies that examined the effect of high body weight during middle childhood on the outcome of subsequent asthma showed a 50% increase in relative risk (RR 1.5, 95% CI 1.2 to 1.8). The combined results from nine studies that examined the effect of high birth weight on subsequent asthma had a pooled RR of 1.2 ( 95% CI 1.1 to 1.3). There was consistency among the results in sensitivity analyses examining studies containing only estimates of odds ratios, studies containing only the outcome of physician diagnosis of asthma, and studies including all definitions of high body weight. Conclusions: Children with high body weight, either at birth or later in childhood, are at increased risk for future asthma. Potential biological mechanisms include diet, gastro-oesophageal reflux, mechanical effects of obesity, atopy, and hormonal influences. Further research might elucidate the causal pathway, which could improve our understanding of the pathophysiology of asthma and perhaps lead to knowledge of potential preventive interventions.	Univ Calif San Francisco, Dept Family & Community Med, Sch Med, San Francisco, CA 94143 USA; Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA	Flaherman, V (reprint author), Univ Calif San Francisco, Dept Family & Community Med, Sch Med, 3333 Calif St,Box 0503, San Francisco, CA 94143 USA.	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J	Marsland, BJ; Soos, TJ; Spath, G; Littman, DR; Kopf, M				Marsland, BJ; Soos, TJ; Spath, G; Littman, DR; Kopf, M			Protein kinase C theta is critical for the development of in vivo T helper (Th)2 cell but not Th1 cell responses	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article						PKC-theta; asthma; Leishmania; nippostrongylus; Th2 cell	NF-KAPPA-B; ALLERGIC AIRWAY INFLAMMATION; PKC-THETA; IMMUNOLOGICAL SYNAPSE; INTERFERON-GAMMA; CUTANEOUS LEISHMANIASIS; T(H)2 DIFFERENTIATION; ACTIVATION; INTERLEUKIN-4; EXPRESSION	The serine/threonine-specific protein kinase C (PKC)-theta is predominantly expressed in T cells and localizes to the center of the immunological synapse upon T cell receptor (TCR) and CD28 signaling. T cells deficient in PKC-theta exhibit reduced interleukin (IL)-2 production and proliferative responses in vitro, however, its significance in vivo remains unclear. We found that pkc-theta(-/-) mice were protected from pulmonary allergic hypersensitivity responses such as air-way hyperresponsiveness, eosinophilia, and immunoglobulin E production to inhaled allergen. Furthermore, T helper (Th)2 cell immune responses against Nippostrongylus brasiliensis were severely impaired in pkc-theta(-/-) mice. In striking contrast, pkc-theta(-/-) mice on both the C57BL/6 background and the normally susceptible BALB/c background mounted protective Th1 immune responses and were resistant against infection with Leishmania major. Using in vitro TCR transgenic T cell-dendritic cell coculture systems and antigen concentration-dependent Th polarization, PKC-theta-deficient T cells were found to differentiate into Th1 cells after activation with high concentrations of specific peptide, but to have compromised Th2 development at low antigen concentration. The addition of IL-2 partially reconstituted Th2 development in pkc-theta(-/-) T cells, consistent with an important role for this cytokine in Th2 polarization. Taken together, our results reveal a central role for PKC-theta signaling during Th2 responses.	Swiss Fed Inst Technol, CH-8952 Zurich, Switzerland; NYU, Sch Med, Howard Hughes Med Inst, New York, NY 10016 USA; NYU, Sch Med, Skirball Inst Biomol Med, Mol Pathogenesis Program, New York, NY 10016 USA; NYU, Sch Med, Dept Med & Mol Parasitol, New York, NY 10016 USA	Kopf, M (reprint author), Swiss Fed Inst Technol, Wagistr 27, CH-8952 Zurich, Switzerland.	Manfred.Kopf@ethz.ch	Spaeth, Gerald/B-1393-2014		NIAID NIH HHS [T32-AI0732, Z01 AI000732]		Altman A, 2000, IMMUNOL TODAY, V21, P567, DOI 10.1016/S0167-5699(00)01749-7; Artis D, 2002, J IMMUNOL, V169, P4481; Baier G, 2003, IMMUNOL REV, V192, P64, DOI 10.1034/j.1600-065X.2003.00018.x; BAIER G, 1993, J BIOL CHEM, V268, P4997; Bauer B, 2001, J BIOL CHEM, V276, P31627, DOI 10.1074/jbc.M103098200; BENSASSON SZ, 1990, P NATL ACAD SCI USA, V87, P1421, DOI 10.1073/pnas.87.4.1421; Bi K, 2001, NAT IMMUNOL, V2, P556, DOI 10.1038/88765; Bromley SK, 2001, ANNU REV IMMUNOL, V19, P375, DOI 10.1146/annurev.immunol.19.1.375; Cote-Sierra J, 2004, P NATL ACAD SCI USA, V101, P3880, DOI 10.1073/pnas.0400339101; Das J, 2001, NAT IMMUNOL, V2, P45, DOI 10.1038/83158; DENT LA, 1990, J EXP MED, V172, P1425, DOI 10.1084/jem.172.5.1425; Fowell DJ, 1999, IMMUNITY, V11, P399, DOI 10.1016/S1074-7613(00)80115-6; Grakoui A, 1999, SCIENCE, V285, P221, DOI 10.1126/science.285.5425.221; HEINZEL FP, 1989, J EXP MED, V169, P59, DOI 10.1084/jem.169.1.59; HEINZEL FP, 1993, J IMMUNOL, V150, P3924; Huang JY, 2002, P NATL ACAD SCI USA, V99, P9369, DOI 10.1073/pnas.142298399; Kane LP, 2001, NAT IMMUNOL, V2, P37, DOI 10.1038/83144; Korn T, 2003, J NEUROIMMUNOL, V139, P17, DOI 10.1016/S0165-5728(03)00128-0; LEBMAN DA, 1988, J EXP MED, V168, P853, DOI 10.1084/jem.168.3.853; LEGROS G, 1990, J EXP MED, V172, P921, DOI 10.1084/jem.172.3.921; Li BY, 1999, EMBO J, V18, P420, DOI 10.1093/emboj/18.2.420; Liu YH, 2000, J BIOL CHEM, V275, P3603, DOI 10.1074/jbc.275.5.3603; Monks CRF, 1998, NATURE, V395, P82; Pfeifhofer C, 2003, J EXP MED, V197, P1525, DOI 10.1084/jem.20020234; POWERS GD, 1988, J IMMUNOL, V140, P3352; REINER SL, 1995, ANNU REV IMMUNOL, V13, P151, DOI 10.1146/annurev.immunol.13.1.151; Rengarajan J, 2002, NAT IMMUNOL, V3, P48, DOI 10.1038/ni744; Ruedl C, 2000, EUR J IMMUNOL, V30, P2056, DOI 10.1002/1521-4141(200007)30:7<2056::AID-IMMU2056>3.0.CO;2-S; SADICK MD, 1986, J IMMUNOL, V136, P655; SCOTT P, 1988, J EXP MED, V168, P1675, DOI 10.1084/jem.168.5.1675; Sica A, 1997, J BIOL CHEM, V272, P30412, DOI 10.1074/jbc.272.48.30412; Sun ZM, 2000, NATURE, V404, P402, DOI 10.1038/35006090; TITUS RG, 1985, PARASITE IMMUNOL, V7, P545, DOI 10.1111/j.1365-3024.1985.tb00098.x; Villalba M, 2000, IMMUNITY, V12, P151, DOI 10.1016/S1074-7613(00)80168-5; Walter DM, 2001, J IMMUNOL, V167, P4668; YAMAGUCHI Y, 1988, J EXP MED, V167, P43, DOI 10.1084/jem.167.1.43; Yang LY, 1998, J EXP MED, V188, P1739, DOI 10.1084/jem.188.9.1739; YAO L, 1994, P NATL ACAD SCI USA, V91, P9175, DOI 10.1073/pnas.91.19.9175; Yoshida H, 1998, IMMUNITY, V8, P115, DOI 10.1016/S1074-7613(00)80464-1; Yoshimoto T, 1997, EUR J IMMUNOL, V27, P3461, DOI 10.1002/eji.1830271247	40	162	171	0	0	ROCKEFELLER UNIV PRESS	NEW YORK	1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA	0022-1007			J EXP MED	J. Exp. Med.	JUL 19	2004	200	2					181	189		10.1084/jem.20032229		9	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	841JL	WOS:000222926000006	15263025	
J	Dabbagh, K; Dahl, ME; Stepick-Biek, P; Lewis, DB				Dabbagh, K; Dahl, ME; Stepick-Biek, P; Lewis, DB			Toll-like receptor 4 is required for optimal development of Th2 immune responses: Role of dendritic cells	JOURNAL OF IMMUNOLOGY			English	Article							LEISHMANIA-MAJOR INFECTION; HOUSE-DUST ENDOTOXIN; IFN-GAMMA PRODUCTION; T-CELLS; ADAPTIVE IMMUNITY; SIGNALING PATHWAY; ALLERGIC-ASTHMA; CUTTING EDGE; MAST-CELLS; B7-2 CD86	LPS potently induces dendritic cell maturation and the production of proinflammatory cytokines, such as IL-12, by activation of Toll-like receptor 4 (TLR4). Since IL-12 is important for the generation and maintenance of Th1 responses and may also inhibit Th2 cell generation from naive CD4 T cell precursors, it has been inferred that TLR4 signaling would have similar effects via the induction of IL-12 secretion. Surprisingly, we found that TLR4-defective mice subjected to sensitization and pulmonary challenge with a protein allergen had reductions in airway inflammation with eosinophils, allergen-specific IgE levels, and Th2 cytokine production, compared with wild-type mice. These reduced responses were attributable, at least in part, to decreased dendritic cell function: Dendritic cells from TLR4-defective mice expressed lower levels of CD86, a costimulatory molecule important for The responses. They also induced less Th2 cytokine production by antigenically naive CD4 T cells in vitro and mediated diminished CD4 T cell Ag-specific pulmonary inflammation in vivo. These results indicate that TLR4 is required for optimal Th2 responses to Ags from nonpathogenic sources and suggest a role for TLR4 ligands, such as LPS derived from commensal bacteria or endogenously derived ligands, in maturation of the innate immune system before pathogen exposure.	Stanford Univ, Sch Med, Dept Pediat & Immunol Program, Palo Alto, CA 94304 USA	Lewis, DB (reprint author), Stanford Univ, Sch Med, Dept Pediat & Immunol Program, Ctr Clin Sci Res Bldg Rm 2115b 269 Campus Dr, Palo Alto, CA 94304 USA.				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Immunol.	MAY 1	2002	168	9					4524	4530				7	Immunology	Immunology	546FP	WOS:000175263000036	11970998	
J	Durham, SR; Emminger, W; Kapp, A; de Monchy, JGR; Rak, S; Scadding, GK; Wurtzen, PA; Andersen, JS; Tholstrup, B; Riis, B; Dahl, R				Durham, Stephen R.; Emminger, Waltraud; Kapp, Alexander; de Monchy, Jan G. R.; Rak, Sabina; Scadding, Glenis K.; Wurtzen, Peter A.; Andersen, Jens S.; Tholstrup, Bente; Riis, Bente; Dahl, Ronald			SQ-standardized sublingual grass immunotherapy: Confirmation of disease modification 2 years after 3 years of treatment in a randomized trial	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Allergy immunotherapy tablet; disease modification; grass pollen; immunotherapy; sublingual; sustained efficacy; placebo-controlled; Phleum pratense; rhinoconjunctivitis; rhinoconjunctivitis quality of life	ALLERGIC RHINITIS; FOLLOW-UP; RHINOCONJUNCTIVITIS; EFFICACY; TABLET; CHILDREN; ASTHMA; SAFETY; PREVALENCE; MECHANISMS	Background: The main aim of specific immunotherapy is sustained effect due to changes in the immune system that can be demonstrated only in long-term trials. Objective: To investigate sustained efficacy and disease modification in a 5-year double-blind, placebo-controlled trial, including 2 years of blinded follow-up after completion of a 3-year period of treatment, with the SQ-standardized grass allergy immunotherapy tablet, Grazax (Phleum pratense 75,000 SQ-T/2,800 BAU,* ALK, Denmark) or placebo. Methods: A randomized, double-blind, placebo-controlled, multinational, phase III trial included adults with a history of moderate-to-severe grass pollen-induced allergic rhinoconjunctivitis, with or without asthma, inadequately controlled by symptomatic medications. Two hundred thirty-eight participants completed the trial. End points included rhinoconjunctivitis symptom and medication scores, combined scores, asthma symptom and medication scores, quality of life, days with severe symptoms, immunologic end points, and safety parameters. Results: The mean rhinoconjunctivitis daily symptom score was reduced by 25% to 36% (P <= .004) in the grass allergy immunotherapy tablet group compared with the placebo group over the 5 grass pollen seasons covered by the trial. The rhinoconjunctivitis DMS was reduced by20% to45%(P <= .022 for seasons 1-4; P = .114 for season 5), and the weighted rhinoconjunctivitis combined score was reduced by 27% to 41% (P <= .003) in favor of active treatment. The percentage of days with severe symptoms during the peak grass pollen exposure was in all seasons lower in the active group than in the placebo group, with relative differences of 49% to 63% (P <= .0001). Efficacy was supported by long-lasting significant effects on the allergen-specific antibody response. No safety issues were identified. Conclusion: The results confirm disease modification by SQ-standardized grass allergy immunotherapy tablet in addition to effective symptomatic treatment of allergic rhinoconjunctivitis. (J Allergy Clin Immunol 2012; 129: 717-25.)	[Durham, Stephen R.] Univ London Imperial Coll Sci Technol & Med, Allergy & Clin Immunol Sect, Natl Heart & Lung Inst, London SW3 6LY, England; [Durham, Stephen R.] Royal Brompton Hosp, London SW3 6LY, England; [Emminger, Waltraud] Allergie Ambulatorium Rennweg, Vienna, Austria; [Kapp, Alexander] Hannover Med Sch, Dept Dermatol & Allergy, D-3000 Hannover, Germany; [de Monchy, Jan G. R.] Univ Groningen, Univ Med Ctr Groningen, Sect Allergol Internal Med, NL-9713 AV Groningen, Netherlands; [Rak, Sabina] Sahlgrens Univ Hosp, Sect Allergy, Gothenburg, Sweden; [Scadding, Glenis K.] Royal Natl Throat Nose & Ear Hosp, London WC1X 8DA, England; [Wurtzen, Peter A.; Andersen, Jens S.; Tholstrup, Bente; Riis, Bente] ALK, Res & Dev, Horsholm, Denmark; [Dahl, Ronald] Aarhus Univ Hosp, Dept Resp Dis, DK-8000 Aarhus, Denmark	Durham, SR (reprint author), Univ London Imperial Coll Sci Technol & Med, Allergy & Clin Immunol Sect, Natl Heart & Lung Inst, Guy Scadding Bldg,Royal Brompton Campus,Dovehouse, London SW3 6LY, England.	s.durham@imperial.ac.uk	Dahl, Ronahl/F-8170-2013		ALK; Novartis; Astellas; UCB; DPC; Swedish Asthma and Allergy Association; GlaxoSmithKline; Boehringer Ingelheim; AstraZeneca; Stallergenes; Pfizer; ALK, Denmark; AllergoPharma; Allergenes; Airsonett; MSD; Vectura; Elevation; Roche; Norpharma	The trial was sponsored by ALK, Denmark. S. R. D. has received consultancy and lecture fees and grant support from ALK. A. Kapp has consultant arrangements with DPC; has received grant support from Novartis, Astellas, UCB, ALK, and DPC; and is on the speakers' bureau for Novartis, Astellas, UCB, and ALK. J. G. R. d. M. has received a grant from ALK. S. R. has received grant support from the Swedish Asthma and Allergy Association. R. D. has been on advisory boards for Nycomed, Boehringer Ingelheim, Novartis, TEVA, Oxagen, and Vectura and has received grant support from GlaxoSmithKline, Boehringer Ingelheim, Novartis, AstraZeneca, ALK, Stallergenes, and Pfizer. G. K. S. has been on advisory boards and is on the speakers' bureau for ALK and is advisor and speaker for Merck. P. A. W., J. S. A., B. T., and B. R. are employed by ALK.; S. R. Durham has received honoraria for lectures and consulting from ALK, Denmark, and Merck; has received research support from ALK, Denmark; and is head of the Allergy Consortium Immune Tolerance Network/National Institute of Allergy and Infectious Disease. W. Emminger, J. G. R. de Monchy, and G. K. Scadding have received research support from ALK. A. Kapp has provided consultation services for ALK. S. Rak has received consultation fees from AllergoPharma, lecture honoraria from Stallergenes, and research support from AllergoPharma and Allergenes, and has provided consultation services/expert witness testimony on the topic of sublingual immunotherapy. P. A. Wurtzen is a shareholder in ALK and a member of the Lundbeck Foundation Board of Directors. B. Tholstrup is a shareholder in ALK. B. Riis is a shareholder in ALK Abello. R. Dahl has received lecture fees or is on the advisory board for Boehringer-Ingelheim, AstraZeneca, ALK, Airsonett, MSD, Novartis, Vectura, Elevation, Roche, and Norpharma; has received research support from ALK, Stalleren, Pfizer, Boehringer Ingelheim, AstraZeneca, Novartis, Airsonett, and GlaxoSmithKline; is Chairman of the Danish Respiratory Society; is Vice-chair of the Global Alliance against Chronic Respiratory Diseases; and is past president of Interasma. The rest of the authors declare that they have no relevant conflicts of interest.	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Allergy Clin. Immunol.	MAR	2012	129	3					717	U184		10.1016/j.jaci.2011.12.973		14	Allergy; Immunology	Allergy; Immunology	904IW	WOS:000301189300017	22285278	
J	Conrad, ML; Ferstl, R; Teich, R; Brand, S; Blumer, N; Yildirim, AO; Patrascan, CC; Hanuszkiewicz, A; Akira, S; Wagner, H; Holst, O; von Mutius, E; Pfefferle, PI; Kirschning, CJ; Garn, H; Renz, H				Conrad, Melanie L.; Ferstl, Ruth; Teich, Rene; Brand, Stephanie; Bluemer, Nicole; Yildirim, Ali Oe.; Patrascan, Cecilia C.; Hanuszkiewicz, Anna; Akira, Shizuo; Wagner, Hermann; Holst, Otto; von Mutius, Erika; Pfefferle, Petra I.; Kirschning, Carsten J.; Garn, Holger; Renz, Harald			Maternal TLR signaling is required for prenatal asthma protection by the nonpathogenic microbe Acinetobacter lwoffii F78	JOURNAL OF EXPERIMENTAL MEDICINE			English	Article							ALLERGIC SENSITIZATION; AIRWAY INFLAMMATION; DENDRITIC CELLS; EXPOSURE; CHILDREN; RISK; FARM; LIPOPOLYSACCHARIDE; RECOGNITION; EXPRESSION	The pre- and postnatal environment may represent a window of opportunity for allergy and asthma prevention, and the hygiene hypothesis implies that microbial agents may play an important role in this regard. Using the cowshed-derived bacterium Acinetobacter lwoffii F78 together with a mouse model of experimental allergic airway inflammation, this study investigated the hygiene hypothesis, maternal (prenatal) microbial exposure, and the involvement of Toll-like receptor (TLR) signaling in prenatal protection from asthma. Maternal intranasal exposure to A. lwoffii F78 protected against the development of experimental asthma in the progeny. Maternally, A. lwoffii F78 exposure resulted in a transient increase in lung and serum proinflammatory cytokine production and up-regulation of lung TLR messenger RNA. Conversely, suppression of TLRs was observed in placental tissue. To investigate further, the functional relevance of maternal TLR signaling was tested in TLR2/3/4/7/9(-/-) knockout mice. The asthma-preventive effect was completely abolished in heterozygous offspring from A. lwoffii F78-treated TLR2/3/4/7/9(-/-) homozygous mother mice. Furthermore, the mild local and systemic inflammatory response was also absent in these A. lwoffii F78-exposed mothers. These data establish a direct relationship between maternal bacterial exposures, functional maternal TLR signaling, and asthma protection in the progeny.	[Conrad, Melanie L.; Teich, Rene; Brand, Stephanie; Bluemer, Nicole; Yildirim, Ali Oe.; Patrascan, Cecilia C.; Pfefferle, Petra I.; Garn, Holger; Renz, Harald] Univ Marburg, Dept Clin Chem & Mol Diagnost, D-35043 Marburg, Germany; [Ferstl, Ruth; Wagner, Hermann] Tech Univ Munich, Inst Med Microbiol Immunol & Hyg, D-81675 Munich, Germany; [Hanuszkiewicz, Anna; Holst, Otto] Leibniz Ctr Med & Biosci, Res Ctr Borstel, Div Struct Biochem, D-23845 Borstel, Germany; [Akira, Shizuo] Osaka Univ, Microbial Dis Res Inst, Dept Host Def, Suita, Osaka 5650871, Japan; [von Mutius, Erika] Univ Munich, Univ Childrens Hosp, D-80337 Munich, Germany; [Kirschning, Carsten J.] Univ Duisburg Essen, Inst Med Microbiol, D-45147 Essen, Germany	Renz, H (reprint author), Univ Marburg, Dept Clin Chem & Mol Diagnost, D-35043 Marburg, Germany.	renzh@med.uni-marburg.de	Akira, Shizuo/C-3134-2009	Yildirim, Ali Onder/0000-0003-1969-480X; von Mutius, Erika/0000-0002-8893-4515	Deutsche Forschungsgemeinschaft [SFB/TR22]; Stiftung P. E. Kempkes, Marburg [10/07]	This work was supported by the Deutsche Forschungsgemeinschaft (SFB/TR22) and Stiftung P. E. Kempkes, Marburg (10/07).	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Exp. Med.	DEC 21	2009	206	13					2869	2877		10.1084/jem.20090845		9	Immunology; Medicine, Research & Experimental	Immunology; Research & Experimental Medicine	535RE	WOS:000272987500004	19995952	
J	Lloyd, CM; Hawrylowicz, CM				Lloyd, Clare M.; Hawrylowicz, Catherine M.			Regulatory T Cells in Asthma	IMMUNITY			English	Review							INDUCED AIRWAY HYPERREACTIVITY; VITAMIN-D SUPPLEMENTATION; TGF-BETA; IMMUNE DYSREGULATION; INHALED ANTIGEN; ALLERGIC-ASTHMA; DENDRITIC CELLS; IN-VIVO; PEPTIDE IMMUNOTHERAPY; ALVEOLAR MACROPHAGES	Asthma is characterized by T helper cell 2 (Th2) type inflammation, leading to airway hyperresponsiveness and tissue remodeling. Th2 cell-driven inflammation is likely to represent an abnormal response to harmless airborne particles. These reactions are normally suppressed by regulatory T cells, which maintain airway tolerance. The anti-inflammatory cytokine IL-10 is likely to play a central role. The role of the cytokine transforming growth factor beta (TGF-beta) is more complex, with evidence for immune suppression and remodeling in the airways. In asthmatic individuals there is a breakdown in these regulatory mechanisms. There is emerging evidence that early life events, including exposure to allergen and infections, are critical in programming effective regulatory pathways to maintain pulmonary homeostasis. In this review we examine the clinical and experimental evidence for T regulatory cell function in the lung and discuss the events that might influence the functioning of these cells. Ultimately, the ability to enhance regulatory function in affected individuals may represent an effective treatment for asthma.	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J	Homer, CJ; Klatka, K; Romm, D; Kuhlthau, K; Bloom, S; Newacheck, P; Van Cleave, J; Perrin, JM				Homer, Charles J.; Klatka, Kirsten; Romm, Diane; Kuhlthau, Karen; Bloom, Sheila; Newacheck, Paul; Van Cleave, Jeanne; Perrin, James M.			A review of the evidence for the medical home for children with special health care needs	PEDIATRICS			English	Review						medical home; special needs children; systematic review; family-centered care	PEDIATRIC-ASTHMA-CARE; OUTCOMES-RESEARCH-TEAM; QUALITY IMPROVEMENT; PATIENT-OUTCOMES; CHRONIC ILLNESS; COORDINATED CARE; NATIONAL-SURVEY; FAMILY; EMERGENCY; ACCESS	CONTEXT. The receipt of health care in a medical home is increasingly touted as a fundamental basis for improved care for persons with chronic conditions, yet the evidence for this claim has not been systematically assessed. OBJECTIVE. Our goal was to determine the evidence for the federal Maternal and Child Health Bureau recommendation that children with special health care needs receive ongoing comprehensive care within a medical home. METHODS. We searched the nursing and medical literature, references of selected articles, and requested expert recommendations. Search terms included children with special health care needs, medical home-related interventions, and health-related outcomes. Articles that met defined criteria (eg, children with special health care needs, United States-based, quantitative) were selected. We extracted data, including design, population characteristics, sample size, intervention, and findings from each article. RESULTS. We selected 33 articles that reported on 30 distinct studies, 10 of which were comparison-group studies. None of the studies examined the medical home in its entirety. Although tempered by weak designs, inconsistent definitions and extent of medical home attributes, and inconsistent outcome measures, the preponderance of evidence supported a positive relationship between the medical home and desired outcomes, such as better health status, timeliness of care, family centeredness, and improved family functioning. CONCLUSIONS. The evidence provides moderate support for the hypothesis that medical homes provide improved health-related outcomes for children with special health care needs. Additional studies with comparison groups encompassing all or most of the attributes of the medical home need to be undertaken.	[Klatka, Kirsten; Romm, Diane; Kuhlthau, Karen; Bloom, Sheila] Massachusetts Gen Hosp, Ctr Child & Adolescent Hlth Policy, Boston, MA 02114 USA; [Homer, Charles J.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA; [Homer, Charles J.] Natl Initiat Childrens Healthcare Qual, Cambridge, MA USA; [Kuhlthau, Karen; Van Cleave, Jeanne; Perrin, James M.] Harvard Univ, Sch Med, Boston, MA USA; [Newacheck, Paul; Van Cleave, Jeanne; Perrin, James M.] Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA; [Newacheck, Paul; Van Cleave, Jeanne; Perrin, James M.] Univ Calif San Francisco, Inst Hlth Policy Studies, San Francisco, CA 94143 USA	Klatka, K (reprint author), Massachusetts Gen Hosp, Ctr Child & Adolescent Hlth Policy, 50 Staniford St,Suite 901, Boston, MA 02114 USA.	kklatka@partners.org	eshaghian, azam/Q-8826-2016	eshaghian, azam/0000-0001-7918-2895	MCHB [U53MC04473-03-00]	We thank our funders at the MCHB (Cooperative Agreement 5 U53MC04473-03-00) for support.	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J	Israel, BA; Parker, EA; Rowe, Z; Salvatore, A; Minkler, M; Lopez, J; Butz, A; Mosley, A; Coates, L; Lambert, G; Potito, PA; Brenner, B; Rivera, M; Romero, H; Thompson, B; Coronado, G; Halstead, S				Israel, BA; Parker, EA; Rowe, Z; Salvatore, A; Minkler, M; Lopez, J; Butz, A; Mosley, A; Coates, L; Lambert, G; Potito, PA; Brenner, B; Rivera, M; Romero, H; Thompson, B; Coronado, G; Halstead, S			Community-based participatory research: Lessons learned from the Centers for Children's Environmental Health and Disease Prevention Research	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						children's health; collaborative research; community-based participatory research; partnership	PARTICULATE AIR-POLLUTION; INNER-CITY CHILDREN; PUBLIC-HEALTH; PESTICIDE EXPOSURE; TOBACCO-SMOKE; ASTHMA; PARTNERSHIP; ASSOCIATION; POPULATION; POLLUTANTS	Over the past several decades there has been growing evidence of the increase in incidence rates, morbidity, and mortality for a number of health problems experienced by children. The causation and aggravation of these problems are complex and multifactorial. The burden of these health problems and environmental exposures is borne disproportionately by children from low-income communities and communities of color. Researchers and funding institutions have called for increased attention to the complex issues that affect the health of children living in marginalized communities-and communities more broadly and have suggested greater community involvement in processes that shape research and intervention approaches, for example, through community-based participatory research (CBPR) partnerships among academic, health services, public health, and community-based organizations. Centers for Children's Environmental Health and Disease Prevention Research (Children's Centers) funded by the National Institute of Environmental Health Sciences and U.S. Environmental Protection Agency, were required to include a CBPR project. The purpose of this article is to provide a definition and set of CBPR principles, to describe the rationale for and major benefits of using this approach, to draw on the experiences of six of the Children's Centers in using CBPR, and to provide lessons learned and recommendations for how to successfully establish and maintain CBPR partnerships aimed at enhancing our understanding and addressing the multiple determinants of children's health.	Univ Michigan, Sch Publ Hlth, Ann Arbor, MI 48109 USA; Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA; Calif Rural Legal Assistance, Salinas, CA USA; Johns Hopkins Univ, Sch Med, Dept Gen Pediat, Baltimore, MD USA; Off Commun Hlth, Baltimore, MD USA; Dr Bernard Harris Sr Elementary Sch, Baltimore, MD USA; Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Ctr Childhood Neurotoxicol & Exposure Assessment, Piscataway, NJ 08854 USA; COSAC, Ewing, NJ USA; Mt Sinai Sch Med, Mt Sinai Ctr Childrens Environm Hlth & Dis Preven, Dept Community & Prevent Med, New York, NY USA; Boriken Neighborhood Hlth Ctr, New York, NY USA; Univ Washington, Fred Hutchinson Canc Res Ctr, Seattle, WA 98195 USA; US EPA, Prosser, WA USA	Israel, BA (reprint author), Univ Michigan, Sch Publ Hlth, 1420 Washington Heights, Ann Arbor, MI 48109 USA.	samanj@umich.edu			NIEHS NIH HHS [P01 ES011256, ES009584, ES009601, ES009605, ES009606, ES011256, ES09589, P01 ES009584, P01 ES009589, P01 ES009601, P01 ES009605, P01 ES009606]		ARNSTEIN SR, 1969, J AM I PLANNERS, V35, P216, DOI 10.1080/01944366908977225; Balcazar FE, 2004, APA DECADE BEHAV VOL, P17, DOI 10.1037/10726-001; Baldi I, 2001, ENVIRON HEALTH PERSP, V109, P839, DOI 10.2307/3454828; Barone S, 2000, NEUROTOXICOLOGY, V21, P15; Becker A, 2005, METHODS COMMUNITY BA, P52; Buchdahl R, 2000, OCCUP ENVIRON MED, V57, P86, DOI 10.1136/oem.57.2.86; Canfield RL, 2003, NEW ENGL J MED, V348, P1517, DOI 10.1056/NEJMoa022848; Daniels JL, 1997, ENVIRON HEALTH PERSP, V105, P1068, DOI 10.1289/ehp.971051068; Delfino RJ, 2002, ENVIRON HEALTH PERSP, V110, pA607; Edgren Katherine K, 2005, Health Promot Pract, V6, P263, DOI 10.1177/1524839903260696; Eggleston PA, 2000, CLIN REV ALLERG IMMU, V18, P311, DOI 10.1385/CRIAI:18:3:311; Eng E, 1990, Int Q Community Health Educ, V11, P93, DOI 10.2190/W8MU-5H9X-PQW1-LV38; Eskenazi B, 2004, ENVIRON HEALTH PERSP, V112, P1116, DOI 10.1289/ehp.6789; Evans GW, 2002, ANNU REV PUBL HEALTH, V23, P303, DOI 10.1146/annurev.publhealth.23.112001.112349; Gergen PJ, 1998, PEDIATRICS, V101, part. no., DOI 10.1542/peds.101.2.e8; Gold DR, 2000, ENVIRON HEALTH PERSP, V108, P643, DOI 10.2307/3454400; Green LW, 2001, AM J PUBLIC HEALTH, V91, P1926, DOI 10.2105/AJPH.91.12.1926; GREEN LW, 2003, COMMUNITY BASED PART, P27; Heron J., 2001, HDB ACTION RES PARTI, P179; Israel B A, 2001, J Public Health Manag Pract, V7, P1; Israel BA, 1998, ANNU REV PUBL HEALTH, V19, P173, DOI 10.1146/annurev.publhealth.19.1.173; Israel B. 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J	Trasande, L; Thurston, GD				Trasande, L; Thurston, GD			The role of air pollution in asthma and other pediatric morbidities	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Review						asthma; particulate matter; lead; sulfur dioxide; carbon monoxide; nitrogen oxides; children's environmental health	DIESEL EXHAUST PARTICLES; LOW-BIRTH-WEIGHT; EMERGENCY-ROOM VISITS; TRADE-CENTER DISASTER; SOUTHERN CALIFORNIA; CHILDHOOD ASTHMA; INFANT-MORTALITY; SULFUR-DIOXIDE; RESPIRATORY SYMPTOMS; HOSPITAL ADMISSIONS	A growing body of research supports the role of outdoor air pollutants in acutely aggravating chronic diseases in children, and suggests that the pollutants may have a role in the development of these diseases. This article reviews the biologic basis of children's unique vulnerability to highly prevalent outdoor air pollutants, with a special focus on ozone, respirable particulate matter (PM2.5 [< 2.5 mu m in diameter] and PM10 [< 10 mu m in diameter]), lead, sulfur dioxide, carbon monoxide, and nitrogen oxides. We also summarize understanding regarding health effects and molecular mechanisms of action. Practitioners can significantly reduce morbidity in children and other vulnerable populations by advising families to minimize pollutant exposures to children with asthma, or at a broader level by educating policymakers about the need to act to reduce pollutant emissions. Management of children with asthma must expand beyond preventing exposures to agents that directly cause allergic reactions (and therefore can be diagnosed by means of skin tests) and must focus more attention on agents that cause a broad spectrum of nonspecific, generalized inflammation, such as air pollution.	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A., 1991, STUDY CHILDRENS ACTI; Wiley J.A., 1991, ACTIVITY PATTERNS CA; Windham GC, 1999, PAEDIATR PERINAT EP, V13, P35; Woodruff TJ, 1997, ENVIRON HEALTH PERSP, V105, P608; Xu XP, 1995, ARCH ENVIRON HEALTH, V50, P407	102	161	164	3	44	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					689	699		10.1016/j.jaci.2005.01.056		11	Allergy; Immunology	Allergy; Immunology	916GM	WOS:000228373400005	15805986	
J	Gehring, U; Bischof, W; Fahlbusch, B; Wichmann, HE; Heinrich, J				Gehring, U; Bischof, W; Fahlbusch, B; Wichmann, HE; Heinrich, J			House dust endotoxin and allergic sensitization in children	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						endotoxin; house dust; atopy; school children	HAY-FEVER; EARLY-LIFE; EXPOSURE; ASTHMA; ATOPY; CHILDHOOD; FARM; RISK; CAT; ENVIRONMENT	A higher exposure to endotoxin was hypothesized to contribute to lower prevalence of allergic sensitization and hay fever in children growing up on a farm. We studied the association between house dust endotoxin and allergic sensitization. We randomly selected 740 children, aged between 5 and 10 years, from a group of children who participated in two cross-sectional surveys performed in Saxony-Anhalt, Germany, from 1992 to 1993 and from 1995 to 1996, such that 50% of the children were atopic or had a diagnosis of asthma. From 1996 to 1998, we collected living-room floor dust in the homes of 454 of these children (61%). The content of endotoxin in house dust was quantified using a chromogenic kinetic limulus amoebocyte lysate test and was related with health outcomes measured in the preceding cross-sectional surveys. Multiple logistic regression analyses adjusted for place of residence, sex, age, parental education, parental atopy, and pet ownership showed a negative association between exposure to endotoxin and sensitization to one or more allergens (aOR [95% CI] 0.95 [0.83; 1.10]) and two or more allergens (aOR [95% CI] 0.80 [0.67, 0.97]) using 0.35 kU/L as the cutoff value for sensitization. The protective effect was strengthened with increasing degree of sensitization. In conclusion, exposure to higher levels of house dust endotoxin is associated with lower prevalence of allergic sensitization in children.	GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, D-85764 Neuherberg, Germany; Univ Munich, Inst Med Data Management Biometr & Epidemiol, Chair Epidemiol, D-80539 Munich, Germany; Univ Jena, Inst Occupat Social & Environm Med, Dept Indoor Climatol Ark, Erfurt, Germany; Univ Jena, Inst Clin Immunol, D-6900 Jena, Germany	Gehring, U (reprint author), GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, Ingolstaedter Landstr 1, D-85764 Neuherberg, Germany.			Gehring, Ulrike/0000-0003-3612-5780			Bischof W, 2000, P HLTH BUILDINGS, V1, P251; Braback L, 2001, PEDIATR ALLERGY IMMU, V12, P4, DOI 10.1034/j.1399-3038.2001.012001004.x; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Douwes J, 2000, AM J RESP CRIT CARE, V162, P1348; Douwes J, 2002, THORAX, V57, P86, DOI 10.1136/thorax.57.1.86; 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; Fahlbusch B, 1999, ALLERGY, V54, P1215, DOI 10.1034/j.1398-9995.1999.00196.x; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Hastie T, 1990, GEN ADDITIVE MODELS; Heinrich J, 2001, CLIN EXP ALLERGY, V31, P1839, DOI 10.1046/j.1365-2222.2001.01220.x; Heinrich J, 2002, EUR RESPIR J, V19, P1040, DOI 10.1183/09031936.02.00261802; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Hosmer DW, 1989, APPL LOGISTIC REGRES; Kilpelainen M, 2000, CLIN EXP ALLERGY, V30, P201; Leynaert B, 2001, AM J RESP CRIT CARE, V164, P1829; Martinez FD, 1999, LANCET S2, V354, pSII12; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; MICHEL O, 1989, J APPL PHYSIOL, V66, P1059; Nafstad P, 2001, ALLERGY, V56, P307, DOI 10.1034/j.1398-9995.2001.00881.x; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Park JH, 2000, ENVIRON HEALTH PERSP, V108, P1023, DOI 10.2307/3434953; Platts-Mills T, 2001, LANCET, V357, P752, DOI 10.1016/S0140-6736(00)04168-4; Platts-Mills TAE, 2001, AM J RESP CRIT CARE, V164, P1107; Riedler J, 2001, LANCET, V358, P1129, DOI 10.1016/S0140-6736(01)06252-3; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Rizzo MC, 1997, PEDIATR ALLERGY IMMU, V8, P121; Roost HP, 1999, J ALLERGY CLIN IMMUN, V104, P941, DOI 10.1016/S0091-6749(99)70072-2; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Svanes C, 1999, J ALLERGY CLIN IMMUN, V103, P415, DOI 10.1016/S0091-6749(99)70465-3; Tariq SM, 1998, J ALLERGY CLIN IMMUN, V101, P587; Tulic MK, 2000, AM J RESP CELL MOL, V22, P604; Von Ehrenstein OS, 2000, CLIN EXP ALLERGY, V30, P187; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; VONMUTIUS E, 2001, AM J RESP CRIT CARE, V164, P116	35	161	166	0	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.	OCT 1	2002	166	7					939	944		10.1164/rccm.200203-256OC		6	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	599YJ	WOS:000178362600010	12359650	
J	Eggesbo, M; Botten, G; Halvorsen, R; Magnus, P				Eggesbo, M; Botten, G; Halvorsen, R; Magnus, P			The prevalence of allergy to egg: a population-based study in young children	ALLERGY			English	Article						adverse reactions; DBPCFC; egg; egg hypersensitivity; epidemiology; food hypersensitivity; prevalence; prospective	COWS MILK ALLERGY; CONTROLLED FOOD CHALLENGES; SKIN-TEST REACTIVITY; DOUBLE-BLIND; CLINICAL MANIFESTATIONS; ATOPIC-DERMATITIS; ADVERSE REACTIONS; HYPERSENSITIVITY; CHILDHOOD; INFANCY	Background: The aim of the present study was to estimate the prevalence of adverse reactions to egg, as population-based prevalence estimates based on objective diagnostic procedures are lacking. Methods: The parents of 2721 children in a population-based birth cohort completed questionnaires on the occurrence of any reaction to food at 12, 18, and 24 months of age. Children with parentally reported reactions to eggs at the age of 2 years were selected for further examination. A stepwise diagnostic procedure was developed that included diet trials at home, skin prick tests, and open and double-blind, placebo-controlled food challenges. The mean age of the children at the time of the examination was 2.5 years (CI 2.5-2.6). A sample of children without perceived reactions to egg was also selected for assessment of unrecognized reactions. Results: The estimated point prevalence of allergy to egg in children aged 2 1/2 years was 1.6% (CI 1.3-2.0%), with an upper estimate of the cumulative incidence by this age calculated roughly at 2.6% (CI 1.6-3.6). Almost all reactions were IgE mediated. In general, two-thirds of the parentally perceived reactions were verified. However, the positive predictive value of a parentally perceived reaction depended on the number of times it had been reported, and increased from 50% to 100%, for reactions reported one and three times, respectively. Unrecognized reactions were infrequent. Conclusions: This study confirms that allergy to egg is frequent in a child population.	Natl Inst Publ Hlth, Dept Populat Hlth Sci, Epidemiol Sect, N-0403 Oslo, Norway; Univ Oslo, Natl Hosp, Ctr Hlth Adm, Oslo 3, Norway; Univ Hosp Oslo, Voksentoppen Ctr Asthma Allergy & Chron Lung Dis, Oslo, Norway	Eggesbo, M (reprint author), Natl Inst Publ Hlth, Dept Populat Hlth Sci, Epidemiol Sect, Post Box 4404, N-0403 Oslo, Norway.		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J	Sunyer, J; Schwartz, J; Tobias, A; Macfarlane, D; Garcia, J; Anto, JM				Sunyer, J; Schwartz, J; Tobias, A; Macfarlane, D; Garcia, J; Anto, JM			Patients with chronic obstructive pulmonary disease are at increased risk of death associated with urban particle air pollution: A case-crossover analysis	AMERICAN JOURNAL OF EPIDEMIOLOGY			English	Article						air pollution; lung diseases; obstructive; mortality	EMERGENCY ROOM ADMISSIONS; HOSPITAL ADMISSIONS; PARTICULATE MATTER; EUROPEAN CITIES; APHEA PROJECT; MORTALITY; ASTHMA; DEPOSITION; GENDER	The authors assessed the acute association between particulate air pollution and mortality among subjects suffering from chronic obstructive pulmonary disease by using a case-crossover analysis. This design avoided the common concerns about the methods used to assess the acute effects of air pollution. The 1,845 men and the 460 women included were residents of Barcelona, Spain, who were over age 35 years, had died during the period 1990-1995, and had visited emergency rooms because of a chronic obstructive pulmonary disease exacerbation during the period 1985-1989. Particle levels (measured as black smoke at the city monitoring stations) were associated with mortality for all causes (odds ratio (OR) for an increase of 20 mu g/m(3), the interquartile change, adjusted for temperature, humidity, and influenza = 1.112, 95 percent confidence interval (CI): 1.017, 1.215). The association was stronger for respiratory causes (OR = 1.182, 95 percent CI: 1.025, 1.365), but was not significant for cardiovascular causes (OR = 1.077, 95 percent CI: 0.917, 1.264). Older women, patients admitted to intensive care units, and patients with a higher rate of emergency room visits were at greater risk of dying associated with black smoke. The results reinforced the deleterious role of urban pollution and provided information on factors possibly conferring susceptibility to the acute role of air pollution.	Inst Municipal Invest Med, Unit Resp & Environm Res, E-08003 Barcelona, Catalonia, Spain; Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Environm Epidemiol Program, Boston, MA 02115 USA; Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Channing Lab, Boston, MA 02115 USA	Sunyer, J (reprint author), Inst Municipal Invest Med, Unit Resp & Environm Res, E-08003 Barcelona, Catalonia, Spain.		Anto, J/H-2676-2014; Sunyer, J/G-6909-2014	Anto, J/0000-0002-4736-8529; Sunyer, J/0000-0002-2602-4110			Anderson HR, 1997, EUR RESPIR J, V10, P1064, DOI 10.1183/09031936.97.10051064; ANTO JM, 1990, CHEST, V98, pS185, DOI 10.1378/chest.98.5_Supplement.185S; AYRES JG, 1998, EUR RESPIR REV, V8, P135; AYRES JG, 1998, EUR RESPIR REV, V8, P53; Bagley S. T., 1996, RES REP HLTH EFF I, V76, P1; Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; BATESON T, 1999, EPIDEMIOLOGY, V54, P596; Bennett WD, 1996, AM J RESP CRIT CARE, V153, P1641; Brunekreef B, 1997, EPIDEMIOLOGY, V8, P298, DOI 10.1097/00001648-199705000-00012; Burnett RT, 1997, ENVIRON HEALTH PERSP, V105, P614, DOI 10.1289/ehp.97105614; de Hartog J J, 1997, Ned Tijdschr Geneeskd, V141, P1814; Gilmour PS, 1996, OCCUP ENVIRON MED, V53, P817; GOLD DR, 1998, AM J RESP CRIT CARE, V157, P261; HIGGINS MW, 1989, CLIN EPIDEMIOLOGY CH; Katsouyanni K, 1997, BMJ-BRIT MED J, V314, P1658; Kim CS, 1997, AM J RESP CRIT CARE, V155, P899; LAWTHER PJ, 1970, THORAX, V25, P525, DOI 10.1136/thx.25.5.525; Li XY, 1996, THORAX, V51, P1216, DOI 10.1136/thx.51.12.1216; MACLURE M, 1991, AM J EPIDEMIOL, V133, P144; MARTINEZ F, 1993, EUR RESPIR J, V6, P337; Ministry of Health, 1954, MORT MORB LOND FOG D; NEAS LM, 1995, EPIDEMIOLOGY, V6, pS56; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Peters A, 1997, LANCET, V349, P1582, DOI 10.1016/S0140-6736(97)01211-7; Rahman I, 1996, AM J RESP CRIT CARE, V154, P1055; SALVI S, 1997, AM J RESP CRIT CARE, V155, P425; SCHWARTZ J, 1990, AM J EPIDEMIOL, V131, P185; SCHWARTZ J, 1994, AM J RESP CRIT CARE, V150, P648; SCHWARTZ J, 1994, AM J EPIDEMIOL, V139, P589; SCHWARTZ J, 1998, AM J RESP CRIT CARE, V157, P879; STYER P, 1995, ENVIRON HEALTH PERSP, V103, P490, DOI 10.2307/3432588; SUNYER J, 1993, AM J EPIDEMIOL, V137, P701; Sunyer J, 1998, AM J RESP CRIT CARE, V158, P851; *WHO, 1977, INT CLASS DIS MAN IN; XU X, 1994, EUR RESPIR J, V7, P1056	35	161	170	0	7	JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH	BALTIMORE	111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 USA	0002-9262			AM J EPIDEMIOL	Am. J. Epidemiol.	JAN 1	2000	151	1					50	56				7	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	271KV	WOS:000084593500005	10625173	
J	Lambrecht, BN; Hammad, H				Lambrecht, Bart N.; Hammad, Hamida			The immunology of asthma	NATURE IMMUNOLOGY			English	Review							INNATE LYMPHOID-CELLS; ALLERGIC AIRWAY INFLAMMATION; HOUSE-DUST MITE; PLASMACYTOID DENDRITIC CELLS; REGULATORY T-CELLS; FC-EPSILON-RI; NATURAL HELPER-CELLS; THYMIC STROMAL LYMPHOPOIETIN; RESPIRATORY VIRAL-INFECTION; AFFINITY IGE RECEPTOR	Asthma is a common disease that affects 300 million people worldwide. Given the large number of eosinophils in the airways of people with mild asthma, and verified by data from murine models, asthma was long considered the hallmark T helper type 2 (T(H)2) disease of the airways. It is now known that some asthmatic inflammation is neutrophilic, controlled by the T(H)17 subset of helper T cells, and that some eosinophilic inflammation is controlled by type 2 innate lymphoid cells (ILC2 cells) acting together with basophils. Here we discuss results from in-depth molecular studies of mouse models in light of the results from the first clinical trials targeting key cytokines in humans and describe the extraordinary heterogeneity of asthma.	[Lambrecht, Bart N.; Hammad, Hamida] Univ Ghent, VIB, Inflammat Res Ctr, B-9000 Ghent, Belgium; [Lambrecht, Bart N.; Hammad, Hamida] Univ Hosp Ghent, Dept Resp Med, Ghent, Belgium; [Lambrecht, Bart N.] Erasmus MC, Dept Pulm Med, Rotterdam, Netherlands	Lambrecht, BN (reprint author), Univ Ghent, VIB, Inflammat Res Ctr, B-9000 Ghent, Belgium.	bart.lambrecht@ugent.be; hamida.hammad@ugent.be	Hammad, Hamida/J-9391-2015; Lambrecht, Bart/K-2484-2014	Hammad, Hamida/0000-0003-3762-8603; Lambrecht, Bart/0000-0003-4376-6834	European Union European Research Council; European Union Framework Programme 7 (MedALL and EUBIOPRED); University of Ghent Multidisciplinary Research Platform (Group-ID); Fonds Wetenschappelijk Onderzoek Vlaanderen	Supported by the European Union European Research Council (B.N.L.), the European Union Framework Programme 7 (MedALL and EUBIOPRED to B.N.L.), the University of Ghent Multidisciplinary Research Platform (Group-ID, to B.N.L.) and Fonds Wetenschappelijk Onderzoek Vlaanderen (B.N.L. and H.H.).	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J	Karner, AA; Eisinger, DS; Niemeier, DA				Karner, Alex A.; Eisinger, Douglas S.; Niemeier, Deb A.			Near-Roadway Air Quality: Synthesizing the Findings from Real-World Data	ENVIRONMENTAL SCIENCE & TECHNOLOGY			English	Review							CHILDRENS RESPIRATORY HEALTH; AIRBORNE PARTICULATE MATTER; SCALE SPATIAL VARIABILITY; ULTRAFINE PARTICLES; SIZE DISTRIBUTION; NITROGEN-DIOXIDE; CHILDHOOD ASTHMA; MAJOR HIGHWAY; TRAFFIC DENSITY; LOS-ANGELES	Despite increasing regulatory attention and literature linking roadside air pollution to health outcomes, studies on near roadway air quality have not yet been well synthesized. We employ data collected from 1978 as reported in 41 roadside monitoring studies, encompassing more than 700 air pollutant concentration measurements, published as of June 2008. Two types of normalization, background and edge-of-road, were applied to the observed concentrations. Local regression models were specified to the concentration-distance relationship and analysis of variance was used to determine the statistical significance of trends. Using an edge-of-road normalization, almost all pollutants decay to background by 115-570 m from the edge of road; using the more standard background normalization, almost all pollutants decay to background by 160-570 m from the edge of road. Differences between the normalization methods arose due to the likely bias inherent in background normalization, since some reported background values tend to underpredict (be lower than) actual background. Changes in pollutant concentrations with increasing distance from the road fell into one of three groups: at least a 50% decrease in peak/edge-of-road concentration by 150 m, followed by consistent but gradual decay toward background (e.g., carbon monoxide, some uttrafine particulate matter number concentrations); consistent decay or change over the entire distance range (e.g., benzene, nitrogen dioxide); or no trend with distance (e.g., particulate matter mass concentrations).	[Karner, Alex A.; Eisinger, Douglas S.; Niemeier, Deb A.] Univ Calif Davis, Dept Civil & Environm Engn, UC Davis Caltrans Air Qual Project, Davis, CA 95616 USA	Niemeier, DA (reprint author), Univ Calif Davis, Dept Civil & Environm Engn, UC Davis Caltrans Air Qual Project, 1 Shields Ave, Davis, CA 95616 USA.	dniemeier@ucdavis.edu			UC Davis-Caltrans Air Quality Project; Caltrans Division of Research and Innovation	Support for this research was partially provided by the UC Davis-Caltrans Air Quality Project (http://AQP.engr.ucdavis.edu/) and the Caltrans Division of Research and Innovation. Dr. Song Bai provided valuable statistical assistance.	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Sci. Technol.	JUL 15	2010	44	14					5334	5344		10.1021/es100008x		11	Engineering, Environmental; Environmental Sciences	Engineering; Environmental Sciences & Ecology	623NF	WOS:000279747100008	20560612	
J	Fox, AT; Sasieni, P; du Toit, G; Syed, H; Lack, G				Fox, Adam T.; Sasieni, Peter; du Toit, George; Syed, Huma; Lack, Gideon			Household peanut consumption as a risk factor for the development of peanut allergy	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Allergy; children; food allergy; peanut allergy; sensitization; peanut consumption; cutaneous exposure; environmental exposure	FOOD CHALLENGES; NUT ALLERGY; FOLLOW-UP; CHILDREN; EXPOSURE; ANTIGEN; IGE; AVOIDANCE; CHILDHOOD; FEATURES	Background: Most children with peanut allergy (PA) react on first known oral exposure to peanut. Recent data suggest cutaneous exposure as a route of sensitization. Objectives: This study aimed to establish the relevant route of peanut exposure in the development of allergy. Methods: Questionnaires were administered to children with PA and to high-risk controls (with egg allergy) and controls without allergy. Questionnaires were completed before subjects were aware of their PA status, avoiding recall bias. Questionnaires recorded maternal peanut consumption during pregnancy, breast-feeding, and the first year of life. Peanut consumption was determined among all household members, allowing quantification of environmental household exposure (household peanut). Results: Median weekly household peanut in the 133 PA cases was significantly elevated (18.8 g) compared with 150 controls without allergy (6.9 g) and 160 high-risk controls (1.9 g). There were no differences in infant peanut consumption between groups. Differences in maternal peanut consumption during pregnancy (and lactation) were significant but become nonsignificant after adjusting for household peanut. A dose-response relationship was observed between environmental (nonoral) peanut exposure and the development of PA, which was strongest for peanut butter. Early oral exposure to peanut in infants with high environmental peanut exposure may have had a protective effect against the development of PA. Conclusions: High levels of environmental exposure to peanut during infancy appear to promote sensitization, whereas low levels may be protective in atopic children. No effect of maternal peanut consumption during pregnancy or lactation is observed, supporting the hypothesis that peanut sensitization occurs as a result of environmental exposure. (J Allergy Clin Immunol 2009;123:417-23.)	[Fox, Adam T.; du Toit, George; Lack, Gideon] Kings Coll London, MRC, London, England; [Sasieni, Peter; Syed, Huma] Queen Mary Univ London, Wolfson Inst Prevent Med, Barts & London Sch Med, London, England	Lack, G (reprint author), St Thomas Hosp, Dept Pediat Allergy, Lambeth Palace Rd, London SE1 7EH, England.	gideon.lack@kel.ac.uk	Osborne, Nicholas/N-4915-2015; Fox, Adam/O-3547-2015	Osborne, Nicholas/0000-0002-6700-2284; Fox, Adam/0000-0002-3533-9798	Food Standards Agency [T07043]; Aimwell Foundation	Supported by it research grant from the Food Standards Agency (United Kingdom; T07043). This grant supported the project costs, including the salary of A.T.F. over the study duration. G.L.'s salary was supported in part by the Aimwell Foundation.	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Allergy Clin. Immunol.	FEB	2009	123	2					417	423		10.1016/j.jaci.2008.12.014		7	Allergy; Immunology	Allergy; Immunology	409GU	WOS:000263495000020	19203660	
J	Weidinger, S; Gieger, C; Rodriguez, E; Baurecht, H; Mempel, M; Klopp, N; Gohlke, H; Wagenpfeil, S; Ollert, M; Ring, J; Behrendt, H; Heinrich, J; Novak, N; Bieber, T; Kraemer, U; Berdel, D; von Berg, A; Bauer, CP; Herbarth, O; Koletzko, S; Prokisch, H; Mehta, D; Meitinger, T; Depner, M; von Mutius, E; Liang, L; Moffatt, M; Cookson, W; Kabesch, M; Wichmann, HE; Illig, T				Weidinger, Stephan; Gieger, Christian; Rodriguez, Elke; Baurecht, Hansjoerg; Mempel, Martin; Klopp, Norman; Gohlke, Henning; Wagenpfeil, Stefan; Ollert, Markus; Ring, Johannes; Behrendt, Heidrun; Heinrich, Joachim; Novak, Natalija; Bieber, Thomas; Kraemer, Ursula; Berdel, Dietrich; von Berg, Andrea; Bauer, Carl Peter; Herbarth, Olf; Koletzko, Sibylle; Prokisch, Holger; Mehta, Divya; Meitinger, Thomas; Depner, Martin; von Mutius, Erika; Liang, Liming; Moffatt, Miriam; Cookson, William; Kabesch, Michael; Wichmann, H. -Erich; Illig, Thomas			Genome-Wide Scan on Total Serum IgE Levels Identifies FCER1A as Novel Susceptibility Locus	PLOS GENETICS			English	Article							IMMUNOGLOBULIN-E CONCENTRATIONS; TH2 CYTOKINE LOCUS; EPSILON-RI-BETA; CONTROL REGION; JAPANESE POPULATION; ATOPIC-DERMATITIS; ASTHMA; ASSOCIATION; GENE; DISEASE	High levels of serum IgE are considered markers of parasite and helminth exposure. In addition, they are associated with allergic disorders, play a key role in anti-tumoral defence, and are crucial mediators of autoimmune diseases. Total IgE is a strongly heritable trait. In a genome-wide association study (GWAS), we tested 353,569 SNPs for association with serum IgE levels in 1,530 individuals from the population-based KORA S3/F3 study. Replication was performed in four independent population-based study samples (total n = 9,769 individuals). Functional variants in the gene encoding the alpha chain of the high affinity receptor for IgE (FCER1A) on chromosome 1q23 (rs2251746 and rs2427837) were strongly associated with total IgE levels in all cohorts with P values of 1.85 x 10(-20) and 7.08 x 10(-19) in a combined analysis, and in a post-hoc analysis showed additional associations with allergic sensitization (P = 7.78 x 10(-4) and P = 1.95 x 10(-3)). The "top'' SNP significantly influenced the cell surface expression of FCER1A on basophils, and genome-wide expression profiles indicated an interesting novel regulatory mechanism of FCER1A expression via GATA-2. Polymorphisms within the RAD50 gene on chromosome 5q31 were consistently associated with IgE levels (P values 6.28 x 10(-7) -4.46 x 10(-8)) and increased the risk for atopic eczema and asthma. Furthermore, STAT6 was confirmed as susceptibility locus modulating IgE levels. In this first GWAS on total IgE FCER1A was identified and replicated as new susceptibility locus at which common genetic variation influences serum IgE levels. In addition, variants within the RAD50 gene might represent additional factors within cytokine gene cluster on chromosome 5q31, emphasizing the need for further investigations in this intriguing region. Our data furthermore confirm association of STAT6 variation with serum IgE levels.	[Weidinger, Stephan; Mempel, Martin; Ollert, Markus; Ring, Johannes] Tech Univ Munich, Dept Dermatol & Allergy, Munich, Germany; [Weidinger, Stephan; Rodriguez, Elke; Baurecht, Hansjoerg; Mempel, Martin] Helmholtz Zentrum Munchen, Div Environm Dermatol & Allergy, Neuherberg, Germany; [Weidinger, Stephan; Rodriguez, Elke; Baurecht, Hansjoerg; Mempel, Martin] Tech Univ Munich, ZAUM Ctr Allergy & Environm, Munich, Germany; [Gieger, Christian; Klopp, Norman; Gohlke, Henning; Heinrich, Joachim; Wichmann, H. -Erich] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Epidemiol, Neuherberg, Germany; [Gieger, Christian; Wichmann, H. -Erich] Univ Munich, Inst Med Informat Biometry & Epidemiol, Munich, Germany; [Baurecht, Hansjoerg; Wagenpfeil, Stefan] Tech Univ Munich, Inst Med Stat & Epidemiol, Munich, Germany; [Wagenpfeil, Stefan] Tech Univ Munich, GSISH, Munich, Germany; [Novak, Natalija; Bieber, Thomas] Univ Bonn, Dept Dermatol & Allergy, D-5300 Bonn, Germany; [Kraemer, Ursula] Univ Dusseldorf, IUF, Dusseldorf, Germany; [Berdel, Dietrich; von Berg, Andrea] Marien Hosp, Wesel, Germany; [Bauer, Carl Peter] Tech Univ Munich, Dept Pediat, Munich, Germany; [Herbarth, Olf] UFZ Helmholtz Ctr Environm Res, Dept Human Exposure Res & Epidemiol, Leipzig, Germany; [Koletzko, Sibylle] Univ Munich, Univ Childrens Hosp, Munich, Germany; [Prokisch, Holger; Mehta, Divya; Meitinger, Thomas] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Human Genet, Neuherberg, Germany; [Prokisch, Holger; Mehta, Divya; Meitinger, Thomas] Tech Univ Munich, Klinikum Rechts Isar, Inst Human Genet, D-8000 Munich, Germany; [Liang, Liming] Univ Michigan, Sch Publ Hlth, Dept Biostat, Ctr Stat Genet, Ann Arbor, MI 48109 USA; [Moffatt, Miriam; Cookson, William] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London, England	Weidinger, S (reprint author), Tech Univ Munich, Dept Dermatol & Allergy, Munich, Germany.	weidinger@lrz.tum.de	Rodriguez, Elke/C-4259-2013; Prokisch, Holger/N-8964-2013; Meitinger, Thomas/O-1318-2015; Weidinger, Stephan/C-8461-2011; Baurecht, Hansjoerg/C-4035-2013	Mehta, Divya/0000-0001-7971-7255; Gieger, Christian/0000-0001-6986-9554; von Mutius, Erika/0000-0002-8893-4515; Meitinger, Thomas/0000-0002-8838-8403; 	German Ministry of Education and Research (BMBF); National Genome Research Network (NGFN); Wellcome Trust; European Commission; Genetic Epidemiological Modelling Center Munich (GEM Munich); Helmholtz Zentrum Munchen; German Research Center for Environmental Health, Neuherberg, Germany; German Federal Ministry of Education and Research (BMBF); Munich Center of Health Sciences (MC Health); BMU (for IUF) [FKZ 20462296]; Federal Ministry for Education, Science, Research, and Technology [01 EG 9705/2, 01EG9732, 01 EE 9401-4]; Stiftung Kindergesundheit (Child Health Foundation); University Hospital Rechts der Isar [KKF-07/04]; Technische Universitat Munchen [KKF-27/05]; Wilhelm-Vaillant-Stiftung	The study was funded by the German Ministry of Education and Research (BMBF) as part of the National Genome Research Network (NGFN), the Wellcome Trust, the German Ministry of Education and Research (BMBF), and the European Commission as part of GABRIEL (a multidisciplinary study to identify the genetic and environmental causes of asthma in the European Community). Furthermore the study was supported by the Genetic Epidemiological Modelling Center Munich (GEM Munich). The MONICA/KORA Augsburg studies were financed by the Helmholtz Zentrum Munchen, German Research Center for Environmental Health, Neuherberg, Germany and supported by grants from the German Federal Ministry of Education and Research (BMBF). The research was supported within the Munich Center of Health Sciences (MC Health) as part of LMUinnovativ. The GINI/LISA studies were funded by grants of the BMU (for IUF, FKZ 20462296), and Federal Ministry for Education, Science, Research, and Technology (No. 01 EG 9705/2 and 01EG9732; No. 01 EE 9401-4) and additional financial support from the Stiftung Kindergesundheit (Child Health Foundation). S. Weidinger and S. Wagenpfeil are supported by research grants KKF-07/04 and KKF-27/05 of the University Hospital Rechts der Isar, Technische Universitat Munchen. The first author in addition is supported by a grant from the Wilhelm-Vaillant-Stiftung.	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AUG	2008	4	8							e1000166	10.1371/journal.pgen.1000166		9	Genetics & Heredity	Genetics & Heredity	365MN	WOS:000260410800016	18846228	
J	Kielhorn, J; Melber, C; Keller, D; Mangelsdorf, I				Kielhorn, J; Melber, C; Keller, D; Mangelsdorf, I			Palladium - A review of exposure and effects to human health	INTERNATIONAL JOURNAL OF HYGIENE AND ENVIRONMENTAL HEALTH			English	Review						palladium; exposure; health effects; dental alloys; sensitization; nickel; allergy; auto catalytic converters; catalysts; lewellery	PLATINUM-GROUP ELEMENTS; DENTAL-CASTING ALLOYS; CELL-CULTURE MEDIUM; CONTACT-DERMATITIS; CROSS-REACTIVITY; IN-VITRO; ALLERGY DIAGNOSIS; METAL-COMPOUNDS; NICKEL SULFATE; EXHAUST FUMES	Palladium is a metal the output and use of which has more than doubled in the past ten years. It is used in dental appliances, chemical catalysts, electrical appliances and jewellery, but the greatest increase in I'd demand has been in automotive emission control catalysts. Studies on I'd concentrations in ancient ice and recent snow samples reflect the increase in mining, smelting and use of palladium in the last decades. Increases of palladium in the environment have been shown in air and dust samples. There is no data as yet available to assess the effect of this exposure. A major source of health concern is the sensitization risk of Pd as very low doses are sufficient to cause allergic reactions in susceptible individuals. Persons with known nickel allergy may be especially susceptible. Workers occupationally exposed to Pd include miners, dental technicians and chemical workers. The latter are exposed mainly to I'd salts several of which may cause primary skin and eye irritations. It. is advised that persons with known Pd allergy should not work with I'd compounds. The general population may come into contact with palladium mainly through mucosal contact with dental restorations and jewellery containing palladium and possibly via emissions from Pd catalysts. Protection of the public from related adverse effects may be achieved by the use of alloys with high corrosion stability and thus minimal release of palladium. In general, in dental patients who are sensitive to Pd, restorations using Pd-containing materials should not be used although I'd has been used without allergic effects in some of these individuals. Further, those patients who have an allergy to nickel should be informed that use of Pd-containing dental materials may cause I'd allergy, though this risk appears to be low.	Fraunhofer Inst Toxicol& Aerosol Res Drug Res & C, D-30625 Hannover, Germany; Beiersdorf AG, Hamburg, Germany	Fraunhofer Inst Toxicol& Aerosol Res Drug Res & C, Nikolai Fuchs Str 1, D-30625 Hannover, Germany.	kielhorn@ita.fhg.de					ABBASI SA, 1987, ANAL LETT, V20, P1013; ABERER W, 1993, CONTACT DERMATITIS, V28, P163, DOI 10.1111/j.1600-0536.1993.tb03379.x; Adachi Atsuko, 1997, Journal of Dermatology (Tokyo), V24, P12; Akiya Osamu, 1996, Bulletin of Tokyo Dental College, V37, P35; Augthun M, 1991, Dtsch Zahnarztl Z, V46, P519; Augthun M, 1990, Dtsch Zahnarztl Z, V45, P480; Barbante C, 2001, ENVIRON SCI TECHNOL, V35, P835, DOI 10.1021/es000146y; Begerow J, 1997, ANAL CHIM ACTA, V340, P277, DOI 10.1016/S0003-2670(96)00486-2; Begerow J, 1997, FRESEN J ANAL CHEM, V359, P427, DOI 10.1007/s002160050603; Begerow J, 1999, BIOMARKERS, V4, P27, DOI 10.1080/135475099230976; Begerow J, 1999, ZBL HYG UMWELTMED, V202, P411; Begerow J., 1998, UMWELTMEDIZIN FORSCH, V3, P257; BIAGINI RE, 1985, J ALLERGY CLIN IMMUN, V76, P794, DOI 10.1016/0091-6749(85)90750-X; 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J. Hyg. Environ. Health.	OCT	2002	205	6					417	432		10.1078/1438-4639-00180		16	Public, Environmental & Occupational Health; Infectious Diseases	Public, Environmental & Occupational Health; Infectious Diseases	612YV	WOS:000179103800001	12455264	
J	Gareau, MG; Wine, E; Rodrigues, DM; Cho, JH; Whary, MT; Philpott, DJ; MacQueen, G; Sherman, PM				Gareau, Melanie G.; Wine, Eytan; Rodrigues, David M.; Cho, Joon Ho; Whary, Mark T.; Philpott, Dana J.; MacQueen, Glenda; Sherman, Philip M.			Bacterial infection causes stress-induced memory dysfunction in mice	GUT			English	Article							IRRITABLE-BOWEL-SYNDROME; CITROBACTER-RODENTIUM INFECTION; MURINE COLONIC HYPERPLASIA; CHRONIC PSYCHOLOGICAL STRESS; INTESTINAL BARRIER FUNCTION; MATERNAL SEPARATION; ESCHERICHIA-COLI; SYNAPTIC PLASTICITY; SPATIAL MEMORY; C-FOS	Background The brainegut axis is a key regulator of normal intestinal physiology; for example, psychological stress is linked to altered gut barrier function, development of food allergies and changes in behaviour. Whether intestinal events, such as enteric bacterial infections and bacterial colonisation, exert a reciprocal effect on stress-associated behaviour is not well established. Objective To determine the effects of either acute enteric infection or absence of gut microbiota on behaviour, including anxiety and non-spatial memory formation. Methods Behaviour was assessed following infection with the non-invasive enteric pathogen, Citrobacter rodentium in both C57BL/6 mice and germ-free Swiss-Webster mice, in the presence or absence of acute water avoidance stress. Whether daily treatment with probiotics normalised behaviour was assessed, and potential mechanisms of action evaluated. Results No behavioural abnormalities were observed, either at the height of infection (10 days) or following bacterial clearance (30 days), in C rodentium-infected C57BL/6 mice. When infected mice were exposed to acute stress, however, memory dysfunction was apparent after infection (10 days and 30 days). Memory dysfunction was prevented by daily treatment of infected mice with probiotics. Memory was impaired in germ-free mice, with or without exposure to stress, in contrast to conventionally reared, control Swiss-Webster mice with an intact intestinal microbiota. Conclusions The intestinal microbiota influences the ability to form memory. Memory dysfunction occurs in infected mice exposed to acute stress, while in the germ-free setting memory is altered at baseline.	[Sherman, Philip M.] Univ Toronto, Hosp Sick Children, Res Inst, Cell Biol Program, Toronto, ON M5G 1X8, Canada; [Wine, Eytan] Univ Alberta, Div Gastroenterol & Nutr, Dept Pediat, Edmonton, AB T6G 2M7, Canada; [Cho, Joon Ho; Philpott, Dana J.] Univ Toronto, Dept Immunol, Toronto, ON, Canada; [Whary, Mark T.] MIT, Div Comparat Med, Cambridge, MA 02139 USA; [MacQueen, Glenda] Univ Calgary, Dept Psychiat, Calgary, AB T2N 1N4, Canada	Sherman, PM (reprint author), Univ Toronto, Hosp Sick Children, Res Inst, Cell Biol Program, 555 Univ Ave,Rm 8409, Toronto, ON M5G 1X8, Canada.	philip.sherman@sickkids.ca		Sherman, Philip/0000-0002-4733-6690	Crohn's and Colitis Foundation of Canada St. Clair Avenue East Toronto [ON M4T 1N5]; Crohn's and Colitis Foundation of Canada; CCFC/CAG/CIHR; Canada Research Chair in Gastrointestinal Disease; Institut-Rosell Lallemand Inc, Montreal, Quebec, Canada	Crohn's and Colitis Foundation of Canada 600-60 St. Clair Avenue East Toronto, ON M4T 1N5. This work was provided by a Faye Shapiro Cutler Grant-In-Aid from the Crohn's and Colitis Foundation of Canada (PMS). CCFC/CAG/CIHR fellowship (MGG); Canada Research Chair in Gastrointestinal Disease (PMS).; Portions of this work were funded by a research contract with Institut-Rosell Lallemand Inc, Montreal, Quebec, Canada.	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J	Henderson, J; Northstone, K; Lee, SP; Liao, HH; Zhao, YW; Pembrey, M; Mukhopadhyay, S; Smith, GD; Palmer, CNA; McLean, WHI; Irvine, AD				Henderson, John; Northstone, Kate; Lee, Simon P.; Liao, Haihui; Zhao, Yiwei; Pembrey, Marcus; Mukhopadhyay, Somnath; Smith, George Davey; Palmer, Colin N. A.; McLean, W. H. Irwin; Irvine, Alan D.			The burden of disease associated with filaggrin mutations: A population-based, longitudinal birth cohort study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						eczema; atopic dermatitis; asthma; skin barrier; filaggrin; birth cohort; atopy	ATOPIC-DERMATITIS; BRONCHIAL RESPONSIVENESS; BARRIER; METHODOLOGY; PHENOTYPES; CHILDREN; ALSPAC; ASTHMA; ECZEMA; GENE	Background: Atopic disease is a major health problem. Mutations in the filaggrin gene (FLG) confer major susceptibility to eczema and related asthma. Objective: We sought to determine the natural history and burden of atopic disease conferred by the 2 most common FLG mutations in a large, population-based birth cohort study. Methods: We analyzed the effect of the most common null alleles (R501X and 2282del4) on several atopic phenotypes in a cohort of approximately 7000 English children born in 1990-1991. Results: FLG null alleles associated strongly with eczema; eczema associated with these mutations presents in early life and is more persistent (hazard ratio for eczema resolution for those with FLG mutations to FLG wild type, 0.67; 95% CI, 0.58-0.77; P = 5 x 10(-8)). FLG mutations conferred a population asthma risk of 1.80 (95% CI, 1.34-2.41; P = .00019); asthma risk was especially high in the context of eczema (odds ratio, 3.16; 95% CI, 2.25-4.43; P = 1.4 x 10(-11)). Strong associations were identified with sensitization to grass, house dust mite, and cat dander and sensitization to multiple allergens (odds ratio, 2.12; 95% CI, 1.03-4.37; P = 5.42 x 10(-27)). Conclusion: FLG mutations are strong genetic determinants of eczema, early wheeze, asthma in the context of eczema, and atopic sensitization. They confer risk of a particular trajectory for eczema, with increased duration of disease and greater risk of asthma and multiple allergic sensitizations. FLG alleles help define the risk profile of children with eczema and help define the "eczema plus early wheeze" and "eczema plus asthma" phenotypes.	[Irvine, Alan D.] Our Ladys Childrens Hosp Crumlin, Dept Paediat Dermatol, Dublin 12, Ireland; [Henderson, John] Univ Bristol, Dept Community Based Med, Bristol BS8 1TH, Avon, England; [Northstone, Kate] Univ Bristol, Dept Social Med, Bristol BS8 1TH, Avon, England; [Smith, George Davey] Univ Bristol, MRC, Ctr Causal Anal Translat Epidemiol, Bristol BS8 1TH, Avon, England; [Lee, Simon P.; Palmer, Colin N. A.] Univ Dundee, Populat Pharmacogenet Grp, Biomed Res Ctr, Dundee DD1 4HN, Scotland; [Mukhopadhyay, Somnath] Univ Dundee, Childrens Asthma & Allergy Res Unit, Dundee DD1 4HN, Scotland; [Liao, Haihui; Zhao, Yiwei; McLean, W. H. Irwin] Univ Dundee, Epithelial Genet Grp, Human Genet Unit, Div Pathol & Neurosci, Dundee DD1 4HN, Scotland; [Pembrey, Marcus] UCL, Inst Child Hlth, London WC1E 6BT, England	Irvine, AD (reprint author), Our Ladys Childrens Hosp Crumlin, Dept Paediat Dermatol, Dublin 12, Ireland.	irvinea@tcd.ie	Palmer, Colin/C-7053-2008; McLean, William/C-6352-2009; Northstone, Kate/A-8165-2011; Osborne, Nicholas/N-4915-2015; Davey Smith, George/A-7407-2013	Palmer, Colin/0000-0002-6415-6560; Northstone, Kate/0000-0002-0602-1983; Osborne, Nicholas/0000-0002-6700-2284; Davey Smith, George/0000-0002-1407-8314; McLean, William Henry Irwin/0000-0001-5539-5757; Monsalve, Beatriz Elena/0000-0002-5994-866X; Irvine, Alan/0000-0002-9048-2044	Medical Research Council [G0700314, G0600705, G9815508]; Wellcome Trust		ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Baurecht H, 2007, J ALLERGY CLIN IMMUN, V120, P1406, DOI 10.1016/j.jaci.2007.08.067; Candi E, 2005, NAT REV MOL CELL BIO, V6, P328, DOI 10.1038/nrm1619; Chinn S, 1998, THORAX, V53, P984; Golding J, 2001, PAEDIATR PERINAT EP, V15, P74; He R, 2007, P NATL ACAD SCI USA, V104, P15817, DOI 10.1073/pnas.0706942104; Illi S, 2004, J ALLERGY CLIN IMMUN, V113, P925, DOI 10.1016/j.jaci.2004.01.778; Irvine AD, 2007, J INVEST DERMATOL, V127, P504, DOI 10.1038/sj.jid.5700695; Irvine AD, 2006, J INVEST DERMATOL, V126, P1200, DOI 10.1038/sj.jid.5700365; Johansson SGO, 2004, J ALLERGY CLIN IMMUN, V113, P832, DOI 10.1016/j.jaci.2003.12.591; Jones RW, 2000, EUR J HUM GENET, V8, P653, DOI 10.1038/sj.ejhg.5200502; Kondo H, 1998, EUR J IMMUNOL, V28, P769, DOI 10.1002/(SICI)1521-4141(199803)28:03<769::AID-IMMU769>3.0.CO;2-H; Marenholz I, 2006, J ALLERGY CLIN IMMUN, V118, P866, DOI 10.1016/j.jaci.2006.07.026; Palmer CNA, 2006, NAT GENET, V38, P441, DOI 10.1038/ng1767; Sandilands A, 2007, NAT GENET, V39, P650, DOI 10.1038/ng2020; Smith GD, 2003, INT J EPIDEMIOL, V32, P1, DOI 10.1093/ije/dyg070; Virtanen H, 2007, J ALLERGY CLIN IMMUN, V120, P1464, DOI 10.1016/j.jaci.2007.08.021; Wadonda-Kabondo N, 2003, BRIT J DERMATOL, V149, P1023, DOI 10.1111/j.1365-2133.2003.05605.x; WILLIAMS HC, 1994, BRIT J DERMATOL, V131, P383, DOI 10.1111/j.1365-2133.1994.tb08530.x; YAN K, 1983, THORAX, V38, P760, DOI 10.1136/thx.38.10.760	20	159	165	2	9	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					872	877		10.1016/j.jaci.2008.01.026		6	Allergy; Immunology	Allergy; Immunology	286YY	WOS:000254884000010	18325573	
J	Guarner, F; Bourdet-Sicard, R; Brandtzaeg, P; Gill, HS; McGuirk, P; van Eden, W; Versalovic, J; Weinstock, JV; Rook, GAW				Guarner, Francisco; Bourdet-Sicard, Raphaelle; Brandtzaeg, Per; Gill, Harsharnjit S.; McGuirk, Peter; van Eden, Willem; Versalovic, James; Weinstock, Joel V.; Rook, Graham A. W.			Mechanisms of disease: the hygiene hypothesis revisited	NATURE CLINICAL PRACTICE GASTROENTEROLOGY & HEPATOLOGY			English	Review						microbiota; probiotics; prebiotics; regulatory T cells; tolerance	REGULATORY T-CELLS; INFLAMMATORY-BOWEL-DISEASE; ACTIVE ULCERATIVE-COLITIS; PLACEBO-CONTROLLED TRIAL; TRICHURIS-SUIS THERAPY; BORDETELLA-PERTUSSIS; MULTIPLE-SCLEROSIS; CROHNS-DISEASE; TRANSCRIPTIONAL REGULATION; INTESTINAL MICROFLORA	In industrialized countries the incidence of diseases caused by immune dysregulation has risen. Epidemiologic studies initially suggested this was connected to a reduction in the incidence of infectious diseases; however, an association with defects in immunoregulation is now being recognized. Effector T(H)1 and T(H)2 cells are controlled by specialized subsets of regulatory T cells. Some pathogens can induce regulatory cells to evade immune elimination, but regulatory pathways are homeostatic and mainly triggered by harmless microorganisms. Helminths, saprophytic mycobacteria, bifidobacteria and lactobacilli, which induce immunoregulatory mechanisms in the host, ameliorate aberrant immune responses in the setting of allergy and inflammatory bowel disease. These organisms cause little, if any, harm, and have been part of human microecology for millennia; however, they are now less frequent or even absent in the human environment of westernized societies. Deficient exposure to these 'old friends' might explain the increase in immunodysregulatory disorders. The use of probiotics, prebiotics, helminths or microbe-derived immunoregulatory vaccines might, therefore, become a valuable approach to disease prevention.	Univ Hosp Valle Hebron, Digest Syst Res Unit, E-08035 Barcelona, Spain; Danone Vitapole, Palaiseau, France; Univ Oslo, LIIPAT Inst Pathol, Oslo, Norway; Univ Dublin Trinity Coll, Immune Regulat Res Grp, Dublin 2, Ireland; Dept Infect Dis & Immunol, Utrecht, Netherlands; Baylor Coll Med, Houston, TX 77030 USA; Texas Childrens Hosp, Houston, TX 77030 USA; Tufts Univ New England Med Ctr, Boston, MA USA; UCL Royal Free Univ Coll, Sch Med, Ctr Infect Dis & Int Hlth, Windeyer Inst Med Sci, London, England	Guarner, F (reprint author), Univ Hosp Valle Hebron, Digest Syst Res Unit, Passeig Vall Hebron 119-129, E-08035 Barcelona, Spain.	fguarnera@medynet.com		Guarner, Francisco/0000-0002-4051-0836; Rook, Graham/0000-0002-8041-8110			Adams VC, 2004, EUR J IMMUNOL, V34, P631, DOI 10.1002/eji.200324659; Arif S, 2004, J CLIN INVEST, V113, P451, DOI 10.1172/JCI200419585; Arshad SH, 2005, CHEST, V127, P502, DOI 10.1378/chest.127.2.502; Bach JF, 2002, NEW ENGL J MED, V347, P911, DOI 10.1056/NEJMra020100; 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J	Wenzel, S				Wenzel, S			Severe asthma in adults	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Review						asthma; inflammation; physiology; phenotypes; remodeling; treatment	NEAR-FATAL ASTHMA; STEROID-RESISTANT ASTHMA; LIFE-THREATENING ASTHMA; AIR-FLOW OBSTRUCTION; GLUCOCORTICOID-RECEPTOR; PERSISTENT ASTHMA; LUNG-FUNCTION; CLINICAL CHARACTERISTICS; CHILDHOOD ASTHMA; BRONCHIAL-ASTHMA	Severe asthma remains poorly understood and frustrating to care for, partly because it is a heterogeneous disease. Patients with severe asthma disproportionately consume health care resources related to asthma. Severe asthma may develop over time, or shortly after onset of the disease. The genetic and environmental elements that may be most important in the development of severe disease are poorly understood, but likely include both allergic and nonallergic elements. Physiologically, these patients often have air trapping, airway collapsibility, and a high degree of methacholine hyper-responsiveness. Specific phenotypes of severe asthma are only beginning to be defined. However, describing severe asthma by age at onset (early- vs. late-onset) appears to describe two phenotypes that differ at immunologic, physiologic, epidemiologic, and pathologic levels. In particular, early-onset severe asthma is a more allergic-associated disease than late-onset severe asthma. In addition, patients with severe asthma can be defined on the basis of presence and type of inflammation. Severe asthma with persistent eosinophilia (of either early or late onset) is more symptomatic and has more near-fatal events. However, at least 50% of patients with severe asthma have very little identifiable inflammation. Thus, "steroid resistance" may occur at numerous levels, not all of which are caused by a lack of effect of steroids on inflammation. Treatment remains problematic, with corticosteroids remaining the most effective therapy. However, 5-lipoxygenase inhibitors, anti-IgE, and immunomodulatory drugs are also likely to have a place in treatment. Improving therapy in this disease will require a better understanding of the phenotypes involved.	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Wenzel SE, 2002, AM J MED, V112, P627, DOI 10.1016/S0002-9343(02)01095-1; Wenzel S, 2000, AM J RESP CRIT CARE, V162, P2341; WENZEL SE, 2004, COLL INT ALL BORN DE; WOOLCOCK AJ, 1968, AM REV RESPIR DIS, V98, P788; WOOLCOCK AJ, 1971, AM REV RESPIR DIS, V104, P703; Wraight JM, 2002, RESPIROLOGY, V7, P133, DOI 10.1046/j.1440-1843.2002.00374.x	120	159	166	0	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.	JUL 15	2005	172	2					149	160		10.1164/rccm.200409-1181PP		12	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	943QG	WOS:000230368400002	15849323	
J	Chalupa, DC; Morrow, PE; Oberdorster, G; Utell, MJ; Frampton, MW				Chalupa, DC; Morrow, PE; Oberdorster, G; Utell, MJ; Frampton, MW			Ultrafine particle deposition in subjects with asthma	ENVIRONMENTAL HEALTH PERSPECTIVES			English	Article						air pollution; asthma; deposition; dosimetry; inhalation; ultrafine particles	PARTICULATE AIR-POLLUTION; BREATHING PATTERNS; RESPIRATORY-TRACT; LUNG DEPOSITION; FINE PARTICLES; DISEASE; HEALTHY; MORTALITY; EXPOSURE; NUMBER	Ambient air particles in the ultrafine size range (diameter < 100 nm) may contribute to the health effects of particulate matter. However, there are few data on ultrafine particle deposition during spontaneous breathing, and none in people with asthma. Sixteen subjects with mild to moderate asthma were exposed for 2 hr, by mouthpiece, to ultrafine carbon particles with a count median diameter (CMD) of 23 nm and a geometric standard deviation of 1.6. Deposition was measured during spontaneous breathing at rest (minute ventilation, 13.3 +/- 2.0 L/min) and exercise (minute ventilation, 41.9 +/- 9.0 L/min). The mean SD fractional deposition was 0.76 +/- 0.05 by particle number and 0.69 +/- 0.07 by particle mass concentration. The number deposition fraction increased as particle size decreased, reaching 0.84 +/- 0.03 for the smallest particles (midpoint CMD = 8.7 nm). No differences between sexes were observed. The deposition fraction increased during exercise to 0.86 +/- 0.04 and 0.79 +/- 0.05 by particle number and mass concentration, respectively, and reached 0.93 +/- 0.02 for the smallest particles. Experimental deposition data exceeded model predictions during exercise. The deposition at rest was greater in these subjects with asthma than in previously studied healthy subjects (0.76 +/- 0.05 vs. 0.65 +/- 0.10, p < 0.001). The efficient respiratory deposition of ultrafine particles increases further in subjects with asthma.	Univ Rochester, Sch Med, Rochester, NY 14642 USA; Univ Rochester, Sch Med & Dent, Dept Med, Rochester, NY 14642 USA; Univ Rochester, Sch Med & Dent, Dept Environm Med, Rochester, NY 14642 USA	Frampton, MW (reprint author), Univ Rochester, Sch Med, 601 Elmwood Ave,Box 692, Rochester, NY 14642 USA.	mark_frampton@urmc.rochester.edu			NCRR NIH HHS [RR 00044]; NIEHS NIH HHS [P30 ES 01247]		ANDERSON PJ, 1990, CHEST, V97, P1115, DOI 10.1378/chest.97.5.1115; Bennett WD, 1997, INHAL TOXICOL, V9, P1; BROWN BW, 1980, BIOMETRICS, V36, P69, DOI 10.2307/2530496; Brown JS, 2002, AM J RESP CRIT CARE, V166, P1240, DOI 10.1164/rccm.00205-399OC; Chalupa DC, 2002, CRUCIAL ISSUES INHAL, P241; 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; DEVLIN RB, 2000, RELATONSHIPS ACUTE C, P159; Frampton MW, 2001, ENVIRON HEALTH PERSP, V109, P529, DOI 10.2307/3454664; FRAMPTON MW, 2000, PARTICLE LUNG INTERA, P653; Gavett SH, 2001, INT ARCH ALLERGY IMM, V124, P109, DOI 10.1159/000053685; International Commission on Radiological Protection, 1994, ICRP PUBL, V66; Jaques PA, 2000, INHAL TOXICOL, V12, P715; Karol MH, 2002, TOXICOLOGY, V181, P305, DOI 10.1016/S0300-483X(02)00298-6; Kim CS, 1997, AM J RESP CRIT CARE, V155, P899; MORRIS JF, 1971, AM REV RESPIR DIS, V103, P57; *NCRP, 1997, 125 NCRP NAT COUNC R; OBERDORSTER G, 1995, INHAL TOXICOL, V7, P111, DOI 10.3109/08958379509014275; PAEK D, 1992, J APPL PHYSIOL, V73, P887; Penttinen P, 2001, ENVIRON HEALTH PERSP, V109, P319, DOI 10.2307/3454889; Peters A, 1997, AM J RESP CRIT CARE, V155, P1376; Pope CA, 2004, CIRCULATION, V109, P71, DOI 10.1161/01.CIR.0000108927.80044.7F; Roth C., 1994, ANN OCCUP HYG     S1, V38, P101; Schiller C. F., 1988, ANN OCCUP HYG, V32, P41; SVARTENGREN M, 1991, J APPL PHYSIOL, V71, P2238; TOBIN MJ, 1983, CHEST, V84, P286, DOI 10.1378/chest.84.3.286; Utell MJ, 2000, INHAL TOXICOL, V12, P37, DOI 10.1080/089583700196365; WICHMANN HE, 2000, 98 HEI, P1; WILSON FJ, 1985, J APPL PHYSIOL, V58, P223	29	159	165	3	23	US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE	RES TRIANGLE PK	NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA	0091-6765			ENVIRON HEALTH PERSP	Environ. Health Perspect.	JUN	2004	112	8					879	882		10.1289/ehp.6851		4	Environmental Sciences; Public, Environmental & Occupational Health; Toxicology	Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology	829BO	WOS:000222018200037	15175176	
J	Fujiwara, D; Inoue, S; Wakabayashi, H; Fujii, T				Fujiwara, D; Inoue, S; Wakabayashi, H; Fujii, T			The anti-allergic effects of lactic acid bacteria are strain dependent and mediated by effects on both Th1/Th2 cytokine expression and balance	INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY			English	Article						lactic acid bacteria; IgE; Th1; Th2; Lactobacillus paracasei strain KW3110	LIPOTEICHOIC ACID; DENDRITIC CELLS; INTERFERON-GAMMA; STAPHYLOCOCCUS-AUREUS; IFN-GAMMA; INTERLEUKIN-12; ACTIVATION; INDUCTION; RECEPTOR; IL-12	Background: There is growing interest in the immune-stimulating effect and in particular, the anti-allergic effect, of lactic acid bacteria (LAB). However, no comprehensive studies have been done that compare the immune-stimulating potential of LAB strains. Methods: The in vitro immune-stimulating effects on Th1/Th2 balance of more than 100 LAB strains were compared in splenocytes from ovalbumin-sensitized Th2-polarized mice. The in vivo anti-allergic ability of strain KW3110 was studied in the Th2-polarized model by detecting serum IgE concentration, Th1/Th2 cytokine secretion from splenocytes, and the expression of co-stimulatory molecules on macrophages. Results: In vitro studies from Th2-polarized splenocytes, using IL-12 as a Th1 parameter and IL-4 secretion as a Th2 parameter revealed a wide variety of IL-12- inducing and IL-4-repressing activities, depending on the strain of LAB, not depending on the species. However, evaluation of individual strains in vivo revealed that after exposure to Lactobacillus paracasei KW3110 strain, the serum IgE elevation elicited by repeated OVA injection of mice was strongly inhibited. Cytokine secretion from splenocytes 20 weeks after KW3110 administration showed increased IL-12 and decreased IL-4 expression. Both CD40 and B7-1 expression on macrophages was upregulated by administration of KW3110. Conclusions: Improving the consequences of the Th1/Th2 imbalance by administration of LAB was dependent upon the LAB strain rather than the LAB species. Oral KW3110 administration in the mouse allergy model directed the Th1/Th2 balance toward Th1 through the maturation of APCs and inhibition of serum IgE elevation. Copyright (C) 2004 S. Karger AG, Basel.	Kirin Brewery Co Ltd, Cent Lab Key Technol, Kanagawa 2360004, Japan	Fujiwara, D (reprint author), Kirin Brewery Co Ltd, Cent Lab Key Technol, 1-13-5 Fukuura, Kanagawa 2360004, Japan.	d-fujiwara@kirin.co.jp					Ahrne S, 1998, J APPL MICROBIOL, V85, P88; BHAKDI S, 1991, INFECT IMMUN, V59, P4614; Cella M, 1996, J EXP MED, V184, P747, DOI 10.1084/jem.184.2.747; Chiaramonte MG, 2000, J IMMUNOL, V164, P973; Christensen HR, 2002, J IMMUNOL, V168, P171; Fujimoto T, 1997, J IMMUNOL, V158, P5619; Ginsburg I, 2002, LANCET INFECT DIS, V2, P171, DOI 10.1016/S1473-3099(02)00226-8; Gupta D, 1999, J BIOL CHEM, V274, P14012, DOI 10.1074/jbc.274.20.14012; Haller D, 2000, GUT, V47, P79, DOI 10.1136/gut.47.1.79; HATCHER GE, 1993, J DAIRY SCI, V76, P2485; Kato I, 1999, INT J IMMUNOPHARMACO, V21, P121, DOI 10.1016/S0192-0561(98)00072-1; Klinman DM, 1996, P NATL ACAD SCI USA, V93, P2879, DOI 10.1073/pnas.93.7.2879; Maassen CBM, 2000, VACCINE, V18, P2613, DOI 10.1016/S0264-410X(99)00378-3; MACATONIA SE, 1993, INT IMMUNOL, V5, P1119, DOI 10.1093/intimm/5.9.1119; McDyer JF, 1998, J IMMUNOL, V160, P1701; Moore KW, 2001, ANNU REV IMMUNOL, V19, P683, DOI 10.1146/annurev.immunol.19.1.683; Morath S, 2001, J EXP MED, V193, P393, DOI 10.1084/jem.193.3.393; MURPHY TL, 1995, MOL CELL BIOL, V15, P5258; Nagura T, 2002, BRIT J NUTR, V88, P421, DOI [10.1079/BJN2002666, 10.1079/BJNBJN2002561]; PENE J, 1988, P NATL ACAD SCI USA, V85, P6880, DOI 10.1073/pnas.85.18.6880; PEREYRA BS, 1993, NUTR RES, V13, P1127; Platts-Mills T. A., 2001, AM J RESP CRIT CARE, V164, P1; Rescigno M, 2001, NAT IMMUNOL, V2, P361, DOI 10.1038/86373; Schroder NWJ, 2003, J BIOL CHEM, V278, P15587, DOI 10.1074/jbc.M212829200; Schwandner R, 1999, J BIOL CHEM, V274, P17406, DOI 10.1074/jbc.274.25.17406; SELDEN RF, 1995, SHORT PROTOCOLS MOL; SHAHANI KM, 1983, J FOOD PROTECT, V46, P385; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Takagi A, 2001, CARCINOGENESIS, V22, P599, DOI 10.1093/carcin/22.4.599; Takeuchi O, 1999, IMMUNITY, V11, P443, DOI 10.1016/S1074-7613(00)80119-3; Veckman V, 2003, J LEUKOCYTE BIOL, V74, P395, DOI 10.1189/jlb.0402212	31	159	170	1	7	KARGER	BASEL	ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND	1018-2438			INT ARCH ALLERGY IMM	Int. Arch. Allergy Immunol.		2004	135	3					205	215		10.1159/000081305		11	Allergy; Immunology	Allergy; Immunology	880CD	WOS:000225765100003	15467373	
J	Norman, GR; Sridar, FG; Guyatt, GH; Walter, SD				Norman, GR; Sridar, FG; Guyatt, GH; Walter, SD			Relation of distribution- and anchor-based approaches in interpretation of changes in health-related quality of life	MEDICAL CARE			English	Article						effect size; NNT (number needed to treat)	OBSTRUCTIVE PULMONARY-DISEASE; OF-LIFE; IMPORTANT DIFFERENCE; RHEUMATOID-ARTHRITIS; CLINICAL-TRIALS; REHABILITATION; QUESTIONNAIRE; ASTHMA; HOME	Background. Approaches to interpretation of quality of life changes in clinical trials have fallen into two camps: those that rely on the distribution of changes and the Effect Size (ES), and those that use some external anchor, such as patient judgments of change, which is then used to compute a Minimally Important Difference (MID), the proportion benefiting from treatment, p(B), and the Number Needed to Treat (NNT). OBJECTIVE. To examine the relationship between the ES and p(B), and the impact of the MID on this relationship. METHODS. Simulation was used based on a normal distribution to compute the proportion of patients benefiting in both parallel group and crossover designs, for various values of the ES and the MID. The agreement of the simulation with empirical data from four studies of asthma and respiratory disease was assessed. The effect of skewness in the distributions of change scores on the relationship between ES and p(B) was also examined. RESULTS. The simulation showed a near-linear relationship between ES and p(B), which was nearly independent of the value of the MID. Agreement of the simulation with the empirical data were excellent. Although the curves differed for crossover and parallel group designs, the general form was similar. Introducing moderate skew into the distributions had minimal impact on the relationship. CONCLUSIONS. The proportion of patients who will benefit from treatment can be directly estimated from the ES, and is nearly independent of the choice of MID. Effect size and anchor based approaches provide equivalent information in this situation.	McMaster Univ, Hlth Sci Ctr, Dept Clin Epidemiol & Biostat, Hamilton, ON L8N 3Z5, Canada	Norman, GR (reprint author), McMaster Univ, Hlth Sci Ctr, Dept Clin Epidemiol & Biostat, Room 2C14,1200 Main St W, Hamilton, ON L8N 3Z5, Canada.						Cohen J., 1969, STAT POWER ANAL BEHA; Dalton GW, 2000, PHYS THER, V80, P1214; GOLDSMITH CH, 1993, J RHEUMATOL, V20, P561; GOLDSTEIN RS, 1994, LANCET, V344, P1394, DOI 10.1016/S0140-6736(94)90568-1; Guell R, 1998, EUR RESPIR J, V11, P55, DOI 10.1183/09031936.98.11010055; Guyatt GH, 1998, BRIT MED J, V316, P690; GUYATT GH, 1987, THORAX, V42, P773, DOI 10.1136/thx.42.10.773; GUYATT GH, 1993, ANN INTERN MED, V118, P622; JACOBSON NS, 1991, J CONSULT CLIN PSYCH, V59, P12, DOI 10.1037//0022-006X.59.1.12; JAESCHKE R, 1989, CONTROL CLIN TRIALS, V10, P407, DOI 10.1016/0197-2456(89)90005-6; JUNIPER EF, 1995, AM J RESP CRIT CARE, V151, P66; Juniper EF, 1996, QUAL LIFE RES, V5, P35, DOI 10.1007/BF00435967; KAZIS LE, 1989, MED CARE, V27, pS178, DOI 10.1097/00005650-198903001-00015; Norman GR, 1997, J CLIN EPIDEMIOL, V50, P869, DOI 10.1016/S0895-4356(97)00097-8; Redelmeier DA, 1996, J CLIN EPIDEMIOL, V49, P1215, DOI 10.1016/S0895-4356(96)00206-5; SENN S, 1998, BRIT MED J, V316, P690; Stratford PW, 1998, PHYS THER, V78, P1186; WELLS GA, 1993, J RHEUMATOL, V20, P557; WIJKSTRA PJ, 1994, EUR RESPIR J, V7, P269, DOI 10.1183/09031936.94.07020269; WIJKSTRA PJ, 1995, THORAX, V50, P824, DOI 10.1136/thx.50.8.824; Wyrwich KW, 1999, MED CARE, V37, P469, DOI 10.1097/00005650-199905000-00006	21	159	160	0	9	LIPPINCOTT WILLIAMS & WILKINS	PHILADELPHIA	530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA	0025-7079			MED CARE	Med. Care	OCT	2001	39	10					1039	1047		10.1097/00005650-200110000-00002		9	Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health	Health Care Sciences & Services; Public, Environmental & Occupational Health	477KT	WOS:000171283300002	11567167	
J	Plaschke, PP; Janson, C; Norrman, E; Bjornsson, E; Ellbjar, S; Jarvholm, B				Plaschke, PP; Janson, C; Norrman, E; Bjornsson, E; Ellbjar, S; Jarvholm, B			Onset and remission of allergic rhinitis and asthma and the relationship with atopic sensitization and smoking	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							SWEDISH SCHOOLCHILDREN; CHRONIC-BRONCHITIS; CAT; SYMPTOMS; IGE; SWEDEN; ADULTS; AREAS; HOMES; PETS	The aim of this study was to assess the influence of some risk factors for onset and remission of allergic rhinitis and asthma in Swedish adults. A random sample of 1,370 subjects, age 20 to 44 yr was investigated by means of postal questionnaires in 1990 and 1993. Skin prick tests were conducted in 1991-1992. The association between risk factors and onset or remission of allergic rhinitis and asthma was estimated using multivariate logistic regression analysis. Onset of allergic rhinitis was associated with sensitization to birch (odds ratio [OR] = 6.5), Parietaria (OR = 7.4); and pets (OR = 3.0) and with female sex (OR = 1.9). Onset of asthma was associated with allergic rhinitis (OR = 4.9), sensitization to pets (OR = 2.4); and with smoking (OR = 3.0). Onset of asthma was strongly associated with allergic rhinitis among atopics (OR = 5.7), but onset of asthma and rhinitis also tended to be related among nonatopics (OR = 3.5). A strong association between smoking and onset of asthma was found among nonatopics (OR = 5.7). In conclusion, sensitization to pollens and pets were risk factors for onset of allergic rhinitis, whereas allergic rhinitis, sensitization to pets, and smoking were risk factors for onset of asthma.	Copenhagen Univ Hosp, Amager Hosp, Dept Med, DK-2300 Copenhagen S, Denmark; Sahlgrens Univ Hosp, Dept Resp Med & Allergol, S-41345 Gothenburg, Sweden; Akad Sjukhuset, Dept Med Sci Resp Med & Allergol, Uppsala, Sweden; Akad Sjukhuset, Asthma Res Ctr, Uppsala, Sweden; Univ Hosp No Sweden, Dept Pulm Med & Allergol, Umea, Sweden; Umea Univ, Dept Publ Hlth & Clin Med, Umea, Sweden	Plaschke, PP (reprint author), Copenhagen Univ Hosp, Amager Hosp, Dept Med, Italiensvej 1, DK-2300 Copenhagen S, Denmark.						ABERG N, 1995, CLIN EXP ALLERGY, V25, P815, DOI 10.1111/j.1365-2222.1995.tb00023.x; AUGUSTO A, 1997, AM J RESP CRIT CARE, V156, P23; BELIN L, 1985, ALLERGY S4, V40, P60; Berge M, 1998, PEDIATR ALLERGY IMMU, V9, P25, DOI 10.1111/j.1399-3038.1998.tb00296.x; BERGGREN B, 1993, POLLENSASONGEN 1993; BJORNSSON E, 1994, EUR RESPIR J, V7, P2146, DOI 10.1183/09031936.94.07122146; Bollinger ME, 1996, J ALLERGY CLIN IMMUN, V97, P907, DOI 10.1016/S0091-6749(96)80064-9; BURNEY PGJ, 1989, EUR RESPIR J, V2, P940; BURNEY PGJ, 1992, ASTHMA, P254; BURNEY PGJ, 1987, CHEST, V91, P79; BURROWS B, 1989, NEW ENGL J MED, V320, P271, DOI 10.1056/NEJM198902023200502; COGSWELL JJ, 1987, ARCH DIS CHILD, V62, P338; Corren J, 1997, J ALLERGY CLIN IMMUN, V100, P781, DOI 10.1016/S0091-6749(97)70274-4; DAmato G, 1991, ALLERGENIC POLLEN PO, P113; Dreborg S, 1989, ALLERGY S10, V44, P1; Egmar AC, 1998, PEDIATR ALLERGY IMMU, V9, P31, DOI 10.1111/j.1399-3038.1998.tb00297.x; FLODIN U, 1995, EPIDEMIOLOGY, V6, P503, DOI 10.1097/00001648-199509000-00007; HIGGINS MW, 1977, AM REV RESPIR DIS, V116, P403; Kaplan BA, 1997, J ASTHMA, V34, P219, DOI 10.3109/02770909709068192; KRZYANOWSKI M, 1992, EUR RESPIR J, V5, P1; LARSSON L, 1995, THORAX, V50, P260, DOI 10.1136/thx.50.3.260; Leynaert B, 1999, J ALLERGY CLIN IMMUN, V104, P301, DOI 10.1016/S0091-6749(99)70370-2; LIN RY, 1993, ANN ALLERGY, V71, P33; Norrman E, 1998, ALLERGY, V53, P28, DOI 10.1111/j.1398-9995.1998.tb03770.x; Plaschke P, 1999, J ALLERGY CLIN IMMUN, V104, P58, DOI 10.1016/S0091-6749(99)70114-4; Plaschke P, 1996, ALLERGY, V51, P461, DOI 10.1111/j.1398-9995.1996.tb04652.x; SETTIPANE RJ, 1994, ALLERGY PROC, V15, P21, DOI 10.2500/108854194778816634; Spitzauer S, 1997, J ALLERGY CLIN IMMUN, V99, P100, DOI 10.1016/S0091-6749(97)81050-0; Strachan DP, 1996, BRIT MED J, V312, P1195; Sunyer J., 1997, European Respiratory Journal, V10, P2490, DOI 10.1183/09031936.97.10112490; TROISI RJ, 1995, CHEST, V108, P1557, DOI 10.1378/chest.108.6.1557; VESTERINEN E, 1988, THORAX, V43, P534, DOI 10.1136/thx.43.7.534	32	159	164	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.	SEP	2000	162	3					920	924				5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	355AM	WOS:000089363500029	10988106	
J	Arnold, IC; Dehzad, N; Reuter, S; Martin, H; Becher, B; Taube, C; Muller, A				Arnold, Isabelle C.; Dehzad, Nina; Reuter, Sebastian; Martin, Helen; Becher, Burkhard; Taube, Christian; Mueller, Anne			Helicobacter pylori infection prevents allergic asthma in mouse models through the induction of regulatory T cells	JOURNAL OF CLINICAL INVESTIGATION			English	Article							AIRWAY INFLAMMATION; PROTECT; MICE	Atopic asthma is a chronic disease of the airways that has taken on epidemic proportions in the industrialized world. The increase in asthma rates has been linked epidemiologically to the rapid disappearance of Helicobacter pylori, a bacterial pathogen that persistently colonizes the human stomach, from Western societies. In this study, we have utilized mouse models of allergic airway disease induced by ovalbumin or house dust mite allergen to experimentally examine a possible inverse correlation between H. pylori and asthma. H. pylori infection efficiently protected mice from airway hyperresponsiveness, tissue inflammation, and goblet cell metaplasia, which are hallmarks of asthma, and prevented allergen-induced pulmonary and bronchoalveolar infiltration with eosinophils, Th2 cells, and Th17 cells. Protection against asthma was most robust in mice infected neonatally and was abrogated by antibiotic eradication of H. pylori. Asthma protection was further associated with impaired maturation of lung-infiltrating dendritic cells and the accumulation of highly suppressive Tregs in the lungs. Systemic Treg depletion abolished asthma protection; conversely, the adoptive transfer of purified Treg populations was sufficient to transfer protection from infected donor mice to uninfected recipients. Our results thus provide experimental evidence for a beneficial effect of H. pylori colonization on the development of allergen-induced asthma.	[Arnold, Isabelle C.; Mueller, Anne] Univ Zurich, Inst Mol Canc Res, CH-8057 Zurich, Switzerland; [Dehzad, Nina; Reuter, Sebastian; Martin, Helen; Taube, Christian] Johannes Gutenberg Univ Mainz, Med Clin 3, D-55101 Mainz, Germany; [Becher, Burkhard] Univ Zurich, Inst Expt Immunol, CH-8057 Zurich, Switzerland	Muller, A (reprint author), Univ Zurich, Inst Mol Canc Res, Winterthurerstr 190, CH-8057 Zurich, Switzerland.	taube@3-med.klinik.uni-mainz.de; mueller@imcr.uzh.ch	Reuter, Sebastian/L-1804-2013	Becher, Burkhard/0000-0002-1541-7867	Swiss National Science Foundation; Zurich University; Deutsches Forschungsgemeinschaft (DFG) [Ta 275/4-1, Ta 275/5-1]; Research Center for Immunology of the University of Mainz	This study was funded by grants from Swiss National Science Foundation and the Zurich University Research Priority Program - Systems Biology to A. Muller. Additional funding was obtained from Deutsches Forschungsgemeinschaft (DFG) (Ta 275/4-1 and Ta 275/5-1) and the Research Center for Immunology of the University of Mainz (to C. Taube).	Arnold IC, 2011, GASTROENTEROLOGY, V140, P199, DOI 10.1053/j.gastro.2010.06.047; BANATVALA N, 1993, J INFECT DIS, V168, P219; Blaser MJ, 2008, GUT, V57, P561, DOI 10.1136/gut.2007.133462; Blaser MJ, 2009, NAT REV MICROBIOL, V7, P887, DOI 10.1038/nrmicro2245; Busse WW, 2001, NEW ENGL J MED, V344, P350; Chang YJ, 2011, J CLIN INVEST, V121, P57, DOI 10.1172/JCI44845; Chen Y, 2008, J INFECT DIS, V198, P553, DOI 10.1086/590158; Chen Y, 2007, ARCH INTERN MED, V167, P821, DOI 10.1001/archinte.167.8.821; Eder W, 2006, NEW ENGL J MED, V355, P2226, DOI 10.1056/NEJMra054308; Harris PR, 2008, GASTROENTEROLOGY, V134, P491, DOI 10.1053/j.gastro.2007.11.006; Kitagaki K, 2006, J IMMUNOL, V177, P1628; Onishi Y, 2008, P NATL ACAD SCI USA, V105, P10113, DOI 10.1073/pnas.0711106105; Reibman J, 2008, PLOS ONE, V3, DOI 10.1371/journal.pone.0004060; Reuter S, 2008, EUR RESPIR J, V31, P773, DOI 10.1183/09031936.00058907; Robinson DS, 2009, CLIN EXP ALLERGY, V39, P1314, DOI 10.1111/j.1365-2222.2009.03301.x; Steinman RM, 2003, ANN NY ACAD SCI, V987, P15; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Wakashin H, 2008, AM J RESP CRIT CARE, V178, P1023, DOI 10.1164/rccm.200801-086OC; Wilson MS, 2005, J EXP MED, V202, P1199, DOI 10.1084/jem.20042572	19	158	174	4	23	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.	AUG	2011	121	8					3088	3093		10.1172/JCI45041		6	Medicine, Research & Experimental	Research & Experimental Medicine	802FU	WOS:000293495500019	21737881	
J	Weiland, SK; Husing, A; Strachan, DP; Rzehak, P; Pearce, N				Weiland, SK; Husing, A; Strachan, DP; Rzehak, P; Pearce, N		ISAAC Phase One Study Grp	Climate and the prevalence of symptoms of asthma, allergic rhinitis, and atopic eczema in children	OCCUPATIONAL AND ENVIRONMENTAL MEDICINE			English	Article							HOUSE-DUST MITES; CHILDHOOD ISAAC; WORLDWIDE VARIATIONS; RESPIRATORY HEALTH; EXPOSURE; SENSITIZATION; AREAS; HOME; RHINOCONJUNCTIVITIS; ADOLESCENTS	Aims: To investigate the association between climate and atopic diseases using worldwide data from 146 centres of the International Study of Asthma and Allergies in Childhood (ISAAC). Methods: Between 1992 and 1996, each centre studied random samples of children aged 13 - 14 and 6 - 7 years (approx. 3000 per age group and centre) using standardised written and video questionnaires on symptoms of asthma, allergic rhinoconjunctivitis, and atopic eczema during the past 12 months. Data on long term climatic conditions in the centres were abstracted from one standardised source, and mixed linear regression models calculated to take the clustering of centres within countries into account. Results: In Western Europe ( 57 centres in 12 countries), the prevalence of asthma symptoms, assessed by written questionnaire, increased by 2.7% ( 95% CI 1.0% to 4.5%) with an increase in the estimated annual mean of indoor relative humidity of 10%. Similar associations were seen for the video questionnaire and the younger age group. Altitude and the annual variation of temperature and relative humidity outdoors were negatively associated with asthma symptoms. The prevalence of eczema symptoms correlated with latitude ( positively) and mean annual outdoor temperature ( negatively). Conclusions: Results suggest that climate may affect the prevalence of asthma and atopic eczema in children.	Univ Ulm, Dept Epidemiol, D-89081 Ulm, Germany; Ruhr Univ Bochum, Dept Med Informat Biometr & Epidemiol, Bochum, Germany; Univ London St Georges Hosp, Sch Med, London SW17 0RE, England; Massey Univ, Wellington, New Zealand	Weiland, SK (reprint author), Univ Ulm, Dept Epidemiol, Helmholzstr 22, D-89081 Ulm, Germany.	stephan.weiland@medizin.uni-ulm.de	Clayton, Tadd/B-7914-2009; Ellwood, Philippa/G-7555-2015	Ellwood, Philippa/0000-0002-1994-4023; Pearce, Neil/0000-0002-9938-7852			ALLEGRA L, 1995, EUR RESPIR J, V8, P1842, DOI 10.1183/09031936.95.08111842; ARLIAN LG, 1992, EXP APPL ACAROL, V16, P15, DOI 10.1007/BF01201490; Asher MI, 1998, EUR RESPIR J, V12, P315; ASHER MI, 1995, EUR RESPIR J, V8, P483, DOI 10.1183/09031936.95.08030483; Asher MI, 1998, CLIN EXP ALLERGY, V28, P52; Beasley R, 1998, LANCET, V351, P1225, DOI 10.1016/S0140-6736(97)07302-9; BJORNSSON E, 1994, EUR RESPIR J, V7, P2146, DOI 10.1183/09031936.94.07122146; CAREY MJ, 1986, BRIT MED J, V293, P843; Celenza A, 1996, BRIT MED J, V312, P604; CHARPIN D, 1988, CHEST, V93, P758, DOI 10.1378/chest.93.4.758; CHARPIN D, 1991, AM REV RESPIR DIS, V143, P983; CULLEN KJ, 1972, BRIT MED J, V4, P65; Dales RE, 1996, EUR RESPIR J, V9, P72, DOI 10.1183/09031936.96.09010072; EberleinKonig B, 1996, ACTA DERM-VENEREOL, V76, P447; ECHECHIPIA S, 1995, ALLERGY, V50, P478, DOI 10.1111/j.1398-9995.1995.tb01182.x; Epton MJ, 1997, THORAX, V52, P528; Gibson PG, 2000, CLIN EXP ALLERGY, V30, P1181; GOLDSTEIN H, 1995, KENDALLS ADV THEORY; Hales S, 1998, ENVIRON HEALTH PERSP, V106, P607, DOI 10.1289/ehp.98106607; Harju T, 1998, EUR RESPIR J, V12, P1362, DOI 10.1183/09031936.98.12061362; LARSSON K, 1993, BRIT MED J, V307, P1326; Lau S, 2000, LANCET, V356, P1392, DOI 10.1016/S0140-6736(00)02842-7; LINTNER TJ, 1993, J ALLERGY CLIN IMMUN, V91, P862, DOI 10.1016/0091-6749(93)90343-E; Lipsett M, 1997, ENVIRON HEALTH PERSP, V105, P216, DOI 10.1289/ehp.97105216; Little RC, 1996, SAS SYSTEM MIXED MOD; McNally NJ, 2000, BRIT J DERMATOL, V142, P712, DOI 10.1046/j.1365-2133.2000.03416.x; MUNIR AKM, 1995, ALLERGY, V50, P55, DOI 10.1111/j.1398-9995.1995.tb02483.x; Newson R, 1997, THORAX, V52, P680; Newson R, 1998, EUR RESPIR J, V11, P694; Nicolai T, 1998, THORAX, V53, P1035; PATZ JA, 2002, BRIT MED J, V25, P1094; Pearce E. A., 1984, WORLD WEATHER GUIDE; Pearce N, 2000, THORAX, V55, P424, DOI 10.1136/thorax.55.5.424; PEAT JK, 1991, CLIN EXP ALLERGY, V21, P573, DOI 10.1111/j.1365-2222.1991.tb00849.x; PEAT JK, 1995, MED J AUSTRALIA, V163, P22; Peat JK, 1998, ALLERGY, V53, P120, DOI 10.1111/j.1398-9995.1998.tb03859.x; POYSA L, 1991, ALLERGY, V46, P161, DOI 10.1111/j.1398-9995.1991.tb00564.x; ROEDEL W, 1994, PHYS UNSERER UMWELT, P186; Schultz Larsen F, 1996, J Am Acad Dermatol, V34, P760; Stewart AW, 2001, INT J EPIDEMIOL, V30, P173, DOI 10.1093/ije/30.1.173; Strachan DP, 1997, PEDIATR ALLERGY IMMU, V8, P161, DOI 10.1111/j.1399-3038.1997.tb00156.x; Tanaka H, 1998, EUR RESPIR J, V11, P1301, DOI 10.1183/09031936.98.11061301; Tromp S W, 1968, Rev Allergy, V22, P1027; Verlato G, 2002, ARCH ENVIRON HEALTH, V57, P48; Williams H, 1999, J ALLERGY CLIN IMMUN, V103, P125, DOI 10.1016/S0091-6749(99)70536-1	45	158	168	3	16	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	2004	61	7					609	615		10.1136/oem.2002.006809		7	Public, Environmental & Occupational Health	Public, Environmental & Occupational Health	830QC	WOS:000222136700007	15208377	
J	ten Brinke, A; Grootendorst, DC; Schmidt, JT; de Bruine, FT; van Buchem, MA; Sterk, PJ; Rabe, KF; Bel, EH				ten Brinke, A; Grootendorst, DC; Schmidt, JT; de Bruine, FT; van Buchem, MA; Sterk, PJ; Rabe, KF; Bel, EH			Chronic sinusitis in severe asthma is related to sputum eosinophilia	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; severity-of-illness index; age of onset; inflammation; nasal mucosa; eosinophils; sputum; computed tomography; human	NASAL; INFLAMMATION; RHINITIS; AIRWAYS	Background: Chronic rhinosinusitis and asthma are conditions that frequently coexist, particularly in severe asthma. The precise mechanism of the relationship between upper and lower airway, inflammation is still a matter of debate. We hypothesized that the extent of inflammation in the nasal mucosa is related to lung function and inflammation in the bronchial mucosa in patients with severe asthma. Objective: We sought to investigate the relationship between sinonasal inflammation as assessed on computed tomography (CT) scanning, lung function, sputum eosinophilia, and nitric oxide (NO) in exhaled air in patients with severe asthma. Methods: Eighty-nine nonsmoking outpatients with severe asthma (29 men and 60 women; mean age 45 years; age range, 18-74 years) were included in this study. CT scans were scored (0-30) by a blinded investigator using a validated method. Lung function, NO in exhaled air, and sputum eosinophils were measured by using standard procedures. Results: CT scans showed abnormalities in 84% of patients. Extensive sinus disease (score 12-30) was found in 24% of patients. There was a significant positive correlation between CT scores and eosinophils in peripheral blood (R-s = 0.46) and induced sputum (R-s = 0.40) and level of exhaled NO (R-s = 0.45, P < .01). CT scores were also positively related to functional residual capacity and inversely, related to diffusion capacity, particularly in patients with adult-onset asthma (R-s = 0.47 and R-s = -0.53, respectively). Conclusions: The results of this study show a direct relationship between sinonasal mucosa thickness and bronchial inflammation in severe asthma, particularly in patients with adult-onset disease. Whether sinus disease directly affects the intensity of bronchial inflammation is still an unanswered question.	Leiden Univ, Med Ctr, Dept Pulm Dis, NL-2300 RC Leiden, Netherlands; Leiden Univ, Med Ctr, Dept Otorhinolaryngol, NL-2300 RC Leiden, Netherlands; Leiden Univ, Med Ctr, Dept Radiol, NL-2300 RC Leiden, Netherlands; Med Ctr Leeuwarden, Dept Pulm Dis, Leeuwarden, Netherlands	Bel, EH (reprint author), Leiden Univ, Med Ctr, Dept Pulm Dis, C3-P,POB 9600, NL-2300 RC Leiden, Netherlands.						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M., 2000, American Journal of Respiratory and Critical Care Medicine, V161, P1902; Kepley CL, 2001, AM J RESP CRIT CARE, V164, P1053; Leynaert Benedicte, 2000, Journal of Allergy and Clinical Immunology, V106, pS201; MCFADDEN ER, 1986, J ALLERGY CLIN IMMUN, V78, P1, DOI 10.1016/0091-6749(86)90106-5; Minshall EM, 1997, AM J RESP CELL MOL, V17, P683; Nakamura H, 1999, ACTA OTO-LARYNGOL, V119, P592; NEWMAN LJ, 1994, JAMA-J AM MED ASSOC, V271, P363, DOI 10.1001/jama.271.5.363; Quanjer PH, 1993, EUR RESPIR J S, V16, P5, DOI 10.1183/09041950.005s1693; Senior BA, 1996, ANN ALLERG ASTHMA IM, V77, P6; SLAVIN RG, 1992, J ALLERGY CLIN IMMUN, V90, P534, DOI 10.1016/0091-6749(92)90180-A; STERK PJ, 1993, EUR RESPIR J, V6, P53, DOI 10.1183/09041950.053s1693; SZEZCKLIK A, 2000, THORAX S2, V55, pS42; TAHA RA, 1999, J ALLERGY CLIN IMMUN, V10, P47; ten Brinke A, 2001, AM J RESP CRIT CARE, V164, P744; ten Brinke A, 2001, AM J RESP CRIT CARE, V164, P749; TENBRINKE A, 2001, EUR RESPIR J, V18, pS66; ZINREICH SJ, 1990, OTOLARYNG HEAD NECK, V103, P863	33	158	162	3	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.	APR	2002	109	4					621	626		10.1067/mai.2002.122458		6	Allergy; Immunology	Allergy; Immunology	543YZ	WOS:000175132600008	11941310	
J	Soukup, JM; Becker, S				Soukup, JM; Becker, S			Human alveolar macrophage responses to air pollution particulates are associated with insoluble components of coarse material, including particulate endotoxin	TOXICOLOGY AND APPLIED PHARMACOLOGY			English	Article						human macrophage; endotoxin; air pollution PM10 and PM2.5; phagocytosis; apoptosis; cytokines	NECROSIS-FACTOR-ALPHA; FINE PARTICLES; HOSPITAL ADMISSIONS; RESPIRATORY HEALTH; OXIDATIVE BURST; BLOOD MONOCYTES; CHILDREN; ASTHMA; LIPOPOLYSACCHARIDE; PHAGOCYTOSIS	Inhalation of particulate matter in the ambient air has been shown to cause pulmonary morbidity and exacerbate asthma. Alveolar macrophage (AIM) are essential for effective removal of inhaled particles and microbes in the lower airways. While some particles minimally effect AM function others inhibit antimicrobial activity or cause cytokine and growth factor production leading to inflammation and tissue remodeling. This study has investigated the effects of water soluble (s) and insoluble (is) components of Chapel Hill, North Carolina ambient particulate matter in the size ranges 0.1-2.5 Ccm (PM2.5) and 2.5-10 mum (PM10) diameter, on human AM IL-6, TNF alpha, and MCP-1 cytokine production and host defense mechanisms including phagocytosis and oxidant production. Cytokines were found to be induced by isPM10 to a much higher extent (>50-fold) than sPM10, which in turn stimulated production better than isPM2.5, while sPM2.5 was inactive. Previous studies have indicated that endotoxin (ETOX) is a component of sPM10 responsible for cytokine production. Here, it is shown that inhibition of isPM10-induced cytokine production was partially achieved with polymyxin B and LPS-binding protein (LBP), but not with a metal chelator, implicating ETOX as a cytokine-inducing moiety also in isPM10. In addition to inducing cytokines, exposure to isPM10, but not the other PM fractions, also inhibited phagocytosis and oxidant generation in response to yeast. This inhibition was ETOX independent. The decrease in host defenses may be the result of apoptosis in the AM population, which was also found to be specifically caused by isPM10. These results show that the functional capacity of AM is selectively modulated by insoluble components of coarse PM, including the biocontaminant ETOX.	US EPA, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA	Soukup, JM (reprint author), US EPA, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA.						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Appl. Pharmacol.	FEB 15	2001	171	1					20	26		10.1006/taap.2000.9096		7	Pharmacology & Pharmacy; Toxicology	Pharmacology & Pharmacy; Toxicology	407JE	WOS:000167267800003	11181108	
J	Nurmatov, U; Devereux, G; Sheikh, A				Nurmatov, Ulugbek; Devereux, Graham; Sheikh, Aziz			Nutrients and foods for the primary prevention of asthma and allergy: Systematic review and meta-analysis	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						Allergy; antioxidants; asthma; atopy; diet; foods; nutrients	VITAMIN-D INTAKE; MEDITERRANEAN DIET; CHILDHOOD ASTHMA; SCHOOL-CHILDREN; 5-YEAR-OLD CHILDREN; RISK-FACTORS; RESPIRATORY SYMPTOMS; ANTIOXIDANT VITAMINS; FRUIT CONSUMPTION; WHEEZING SYMPTOMS	Background: Epidemiologic studies suggest that deficiencies of the nutrients selenium; zinc; vitamins A, C, D, and E; and low fruit and vegetable intake may be associated with the development of asthma and allergic disorders. Objectives: To investigate the evidence that nutrient and food intake modifies the risk of children developing allergy. Methods: We systematically searched 11 databases. Studies were critically appraised, and meta-analyses were undertaken. Results: We identified 62 eligible reports. There were no randomized controlled trials. Studies used cohort (n = 21), case-control (n 5 15), or cross-sectional (n 5 26) designs. All studies were judged to be at moderate to substantial risk of bias. Meta-analysis revealed that serum vitamin A was lower in children with asthma compared with controls (odds ratio [OR], 0.25; 95% CI, 0.10-0.40). Meta-analyses also showed that high maternal dietary vitamin D and E intakes during pregnancy were protective for the development of wheezing outcomes (OR, 0.56, 95% CI, 0.42-0.73; and OR, 0.68, 95% CI, 0.52-0.88, respectively). Adherence to a Mediterranean diet was protective for persistent wheeze (OR, 0.22; 95% CI, 0.08-0.58) and atopy (OR, 0.55; 95% CI, 0.31-0.97). Seventeen of 22 fruit and vegetable studies reported beneficial associations with asthma and allergic outcomes. Results were not supportive for other allergic outcomes for these vitamins or nutrients, or for any outcomes in relation to vitamin C and selenium. Conclusion: The available epidemiologic evidence is weak but nonetheless supportive with respect to vitamins A, D, and E; zinc; fruits and vegetables; and a Mediterranean diet for the prevention of asthma. Experimental studies of these exposures are now warranted. (J Allergy Clin Immunol 2011;127:724-33.)	[Nurmatov, Ulugbek; Sheikh, Aziz] Univ Edinburgh, Sch Med, Ctr Populat Hlth Sci, Allergy & Resp Res Grp, Edinburgh EH8 9AG, Midlothian, Scotland; [Devereux, Graham] Univ Aberdeen, Royal Aberdeen Childrens Hosp, Dept Child Hlth, Aberdeen, Scotland	Sheikh, A (reprint author), Univ Edinburgh, Sch Med, Ctr Populat Hlth Sci, Allergy & Resp Res Grp, Teviot Pl, Edinburgh EH8 9AG, Midlothian, Scotland.	aziz.sheikh@ed.ac.uk	Sheikh, Aziz /D-2818-2009	Sheikh, Aziz /0000-0001-7022-3056	Chief Scientist's Office of the Scottish Government Health Department [CZG/2/396]	This project was supported in its entirety by a project grant awarded by the Chief Scientist's Office of the Scottish Government Health Department (CZG/2/396).	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Allergy Clin. Immunol.	MAR	2011	127	3					724	U359		10.1016/j.jaci.2010.11.001		40	Allergy; Immunology	Allergy; Immunology	730FG	WOS:000288018400027	21185068	
J	Spergel, JM				Spergel, Jonathan M.			From atopic dermatitis to asthma: the atopic march	ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY			English	Review							OF-FUNCTION MUTATIONS; MAJOR RISK-FACTOR; FOLLOW-UP; INHALED CORTICOSTEROIDS; AIRWAY INFLAMMATION; RUSSIAN KARELIA; YOUNG-CHILDREN; PEANUT ALLERGY; PHASE-III; FILAGGRIN	Objective: To examine the mechanisms whereby allergen exposure through the epidermis could initiate systemic allergy and predispose individuals to the development of 1 or more atopic diseases via the so-called atopic march. Data Sources: PubMed databases from 1950 to the present were searched for relevant articles pertaining to epidemiologic and genetic evidence of the progression of the atopic march. Study Selection: Articles concerning pathophysiologic conditions that link atopic dermatitis, allergic rhinitis, and asthma were examined. Results: The data suggest that a sequence of atopic manifestations occurs, typically atopic dermatitis in infancy followed by allergic rhinitis and/or asthma in later stages. Reduced filaggrin expression is implicated as a major predisposing factor for atopy in multiple lines of evidence, including genome-wide analysis and microarray investigations. Other gene products have an important role. Cross-sectional and longitudinal studies provide preliminary epidemiologic support for the sequential development of allergic diseases. Conclusion: The mechanisms by which allergen exposure through the epidermis can initiate systemic allergy and predispose individuals to atopic dermatitis, allergic rhinitis, and asthma have become clearer in recent years. Longitudinal studies of individuals carrying loss-of-function filaggrin gene mutations are needed to further define the risks associated with epidermal barrier dysfunction and potentially identify specific targets for barrier repair and prevention of atopic dermatitis and other atopic disease. The effects of preventive and treatment strategies have been inconsistent across studies, and further research is warranted before any definitive recommendations can be made. Ann Allergy Asthma Immunol. 2010; 105:99-106.	Univ Penn, Sch Med, Childrens Hosp Philadelphia, Div Allergy & Immunol, Philadelphia, PA 19104 USA	Spergel, JM (reprint author), Univ Penn, Sch Med, Childrens Hosp Philadelphia, Div Allergy & Immunol, Wood 5314,34th St & Civic Ctr Blvd, Philadelphia, PA 19104 USA.	spergel@email.chop.edu	Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284; Spergel, Jonathan/0000-0002-4658-5353	Novartis Pharmaceuticals Corporation; Ception Therapeutics; AstraZeneca Pharmaceuticals LP; GlaxoSmithKline; Astellas Pharma US Inc.; National Institute of Allergy and Infectious Disease [R01-AI062698]	Dr Spergel has indicated that in the last 12 months he has received grant support and speaker fees from Novartis Pharmaceuticals Corporation, grant support from Ception Therapeutics, and consultant and speaking fees from AstraZeneca Pharmaceuticals LP, GlaxoSmithKline, and Astellas Pharma US Inc.; Funding for editorial assistance was provided by Novartis Pharmaceuticals Corporation. This study was supported by National Institute of Allergy and Infectious Disease grant R01-AI062698.	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J	Agarwal, R				Agarwal, Ritesh			Allergic Bronchopulmonary Aspergillosis	CHEST			English	Review						allergic bronchopulmonary aspergillosis; Aspergillus; bronchial asthma; cystic fibrosis; prevalence	CYSTIC-FIBROSIS PATIENTS; TERM FOLLOW-UP; INVASIVE PULMONARY ASPERGILLOSIS; REGULATOR GENE-MUTATIONS; HIGH-ATTENUATION MUCUS; FUNGAL DISEASE; RECOMBINANT ALLERGENS; FUMIGATUS ALLERGENS; ASTHMATIC-PATIENTS; SERUM IGE	Allergic bronchopulmonary aspergillosis (ABPA) is air immunologic pulmonary disorder caused by hypersensitivity to Aspergillus fumigatus. Clinically, a patient presents with chronic asthma, recurrent pulmonary infiltrates, and bronchiectasis. The population prevalence of ABPA is not clearly known, but the prevalence in asthma clinics is reported to be around 13%. The disorder needs to be detected before bronchiectasis has developed because the occurrence of bronchiectasis is associated with poorer outcomes. Because many patients with ABPA may be minimally symptomatic or asymptomatic, a high index of suspicion for ABPA should be maintained while managing any patient with bronchial asthma whatever the severity or the level of control. This underscores the need for routine screening of all patients with asthma with an Aspergillus skin test. Finally, there is a need to update and revise the criteria for the diagnosis of ABPA. This review summarizes the advances in the diagnosis and management of ABPA using a systematic search methodology. 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Yoshida N, 1992, Nihon Kyobu Shikkan Gakkai Zasshi, V30, P2123; ZEASKE R, 1988, J ALLERGY CLIN IMMUN, V82, P73, DOI 10.1016/0091-6749(88)90054-1; [Anonymous], 1979, BR J DIS CHEST, V73, P349	242	157	176	1	15	AMER COLL CHEST PHYSICIANS	NORTHBROOK	3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA	0012-3692			CHEST	Chest	MAR	2009	135	3					805	826		10.1378/chest.08-2586		22	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	420SW	WOS:000264310500030	19265090	
J	Barnett, AG; Williams, GM; Schwartz, J; Neller, AH; Best, TL; Petroeschevsky, AL; Simpson, RW				Barnett, AG; Williams, GM; Schwartz, J; Neller, AH; Best, TL; Petroeschevsky, AL; Simpson, RW			Air pollution and child respiratory health - A case-crossover study in Australia and new Zealand	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						air pollutants; Australasia; meta-analysis; respiration disorders	INFANT-MORTALITY; UTAH VALLEY; ASSOCIATION; DISEASE; METAANALYSIS; POLLUTANTS; ADMISSIONS; PARTICLES; SELECTION; ASTHMA	Rationale: The strength of the association between outdoor air pollution and hospital admissions in children has not yet been well defined. Objectives: To estimate the impact of outdoor air pollution on respiratory morbidity in children after controlling for the confounding effects of weather, season, and other pollutants. Methods: The study used data on respiratory hospital admissions in children (three age groups: < 1, 1-4, and 5-14years) for five cities in Australia and two in New Zealand. Time series of daily numbers of hospital admissions were analyzed using the case-crossover method; the results from cities were combined using a random-effects meta-analysis. Measurements and Main Results: Significant increases across the cities were observed for hospital admissions in children for pneumonia and acute bronchitis (0, 1-4 years), respiratory disease (0, 1-4, 5-14 years), and asthma (5-14 years). These increases were found for particulate matter with a diameter less than 2.5 mu m (PM2.5) and less than 10 mu m (PM10), nephelometry, NO2, and SO2. The largest association found was a 6.0% increase in asthma admissions (5-14years) in relation to a 5.1-ppb increase in 24-hour NO2. Conclusions: This study found strong and consistent associations between outdoor air pollution and short-term increases in childhood hospital admissions. A number of different pollutants showed significant associations, and these were distinct from any temperature (warm or cool) effects.	Univ Sunshine Coast, Fac Sci Hlth & Educ, Maroochydore DC, Qld 4558, Australia; Univ Queensland, Sch Populat Hlth, Herston, Qld, Australia; Harvard Univ, Sch Publ Hlth, Exposure Epidemiol & Risk Program, Boston, MA 02115 USA	Simpson, RW (reprint author), Univ Sunshine Coast, Fac Sci Hlth & Educ, Maroochydore DC, Qld 4558, Australia.	rsimpson@usc.edu.au	Barnett, Adrian/I-9850-2012; Wang, Linden/M-6617-2014	Barnett, Adrian/0000-0001-6339-0374			ANDERSON H, 2004, EUR045042688; Atkinson RW, 2001, AM J RESP CRIT CARE, V164, P1860; Bateson TF, 2001, EPIDEMIOLOGY, V12, P654, DOI 10.1097/00001648-200111000-00013; Bernstein JA, 2004, J ALLERGY CLIN IMMUN, V114, P1116, DOI 10.1016/j.jaci.2004.08.030; Binkova B, 2004, EFFECTS AIR POLLUTIO; Braga A. L. F., 1999, Journal of Environmental Medicine, V1, P95, DOI 10.1002/(SICI)1099-1301(199904/06)1:2<95::AID-JEM16>3.0.CO;2-S; BraunFahrlander C, 1997, AM J RESP CRIT CARE, V155, P1042; Chauhan AJ, 2003, BRIT MED BULL, V68, P95, DOI 10.1093/bmb/ldg022; Chew FT, 1999, ALLERGY, V54, P320, DOI 10.1034/j.1398-9995.1999.00012.x; DOCKERY DW, 1989, AM REV RESPIR DIS, V139, P587; Gauderman WJ, 2000, AM J RESP CRIT CARE, V162, P1383; Ha EH, 2003, PEDIATRICS, V111, P284, DOI 10.1542/peds.111.2.284; Higgins JPT, 2002, STAT MED, V21, P1539, DOI 10.1002/sim.1186; Katsouyanni K, 2003, BRIT MED BULL, V68, P143, DOI 10.1093/bmb/ldg028; Levy D, 2001, EPIDEMIOLOGY, V12, P186, DOI 10.1097/00001648-200103000-00010; Loomis D, 1999, EPIDEMIOLOGY, V10, P118, DOI 10.1097/00001648-199903000-00006; MACLURE M, 1991, AM J EPIDEMIOL, V133, P144; Mathieu-Nolf M, 2002, J TOXICOL-CLIN TOXIC, V40, P483; McConnell R, 2003, AM J RESP CRIT CARE, V168, P790, DOI 10.1164/rccm.200304-466OC; Neas LM, 1999, ENVIRON HEALTH PERSP, V107, P629, DOI 10.2307/3434453; Normand SLT, 1999, STAT MED, V18, P321, DOI 10.1002/(SICI)1097-0258(19990215)18:3<321::AID-SIM28>3.0.CO;2-P; Ostro BD, 1999, ENVIRON HEALTH PERSP, V107, P69, DOI 10.2307/3434291; POPE CA, 1991, ARCH ENVIRON HEALTH, V46, P90; POPE CA, 1989, AM J PUBLIC HEALTH, V79, P623, DOI 10.2105/AJPH.79.5.623; RANSOM MR, 1992, ENVIRON RES, V58, P204, DOI 10.1016/S0013-9351(05)80216-6; Schwartz J, 2004, ENVIRON HEALTH PERSP, V112, P557; Schwartz J, 2004, PEDIATRICS, V113, P1037; SIMPSON R, 2004, EPIDEMIOLOGY, V106, pS54; Sunyer J, 2000, AM J EPIDEMIOL, V151, P50; Woodruff TJ, 1997, ENVIRON HEALTH PERSP, V105, P608	30	157	168	3	43	AMER THORACIC SOC	NEW YORK	1740 BROADWAY, NEW YORK, NY 10019-4374 USA	1073-449X			AM J RESP CRIT CARE	Am. J. Respir. Crit. Care Med.	JUN 1	2005	171	11					1272	1278		10.1164/rccm.200411-1586OC		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	930JB	WOS:000229410800013	15764722	
J	Muraro, A; Dreborg, S; Halken, S; Host, A; Niggemann, B; Aalberse, R; Arshad, SH; von Berg, A; Carlsen, KH; Duschen, K; Eigenmann, P; Hill, D; Jones, C; Mellon, M; Oldeus, G; Oranje, A; Pascual, C; Prescott, S; Sampson, H; Svartengren, M; Vandenplas, Y; Wahn, U; Warner, JA; Warner, JO; Wickman, M; Zeiger, RS				Muraro, A; Dreborg, S; Halken, S; Host, A; Niggemann, B; Aalberse, R; Arshad, SH; von Berg, A; Carlsen, KH; Duschen, K; Eigenmann, P; Hill, D; Jones, C; Mellon, M; Oldeus, G; Oranje, A; Pascual, C; Prescott, S; Sampson, H; Svartengren, M; Vandenplas, Y; Wahn, U; Warner, JA; Warner, JO; Wickman, M; Zeiger, RS			Dietary prevention of allergic diseases in infants and small children - Part III: Critical review of published peer-reviewed observational and interventional studies and final recommendations	PEDIATRIC ALLERGY AND IMMUNOLOGY			English	Article						breast feeding; cow's milk allergy; food allergy; prevention; review; statements of evidence	HIGH-RISK INFANTS; PARTIAL WHEY HYDROLYSATE; BRIEF NEONATAL EXPOSURE; BREAST-FED INFANTS; COWS MILK FORMULA; ATOPIC DISEASE; FOLLOW-UP; 1ST YEAR; CONTROLLED-TRIAL; PRETERM INFANTS	The role of primary prevention of allergic diseases has been a matter of debate for the last 40 years. In order to shed some light on this issue, a group of experts of the Section of Pediatrics EAACI reviewed critically the existing literature on the subject. An analysis of published peer-reviewed observational and interventional studies was performed following the statements of evidence as defined by WHO. The results of the analysis indicate that breastfeeding is highly recommended for all infants irrespective of atopic heredity. A dietary regimen is unequivocally effective in the prevention of allergic diseases in high-risk children. In these patients breastfeeding combined with avoidance of solid food and cow's milk for at least 4-6 months is the most effective preventive regimen. In the absence of breast milk, formulas with documented reduced allergenicity for at least 4-6 months should be used.	Univ Padua, Dept Pediat, I-35128 Padua, Italy; ESPACI, Lerum, Sweden; Sonderborg Hosp, Dept Pediat, Sonderborg, Denmark; Odense Univ Hosp, Dept Pediat, DK-5000 Odense, Denmark; Humboldt Univ, Univ Childrens Hosp Charite, Dept Pneumol & Immunol, Berlin, Germany; Dept Allergy CLB, Amsterdam, Netherlands; St Marys Hosp, Clin Allergy Res Unit, Newport, Isle Of Wight, England; Marien Hosp, Abt Kinderheilkunde, Wesel, Germany; Voksentoppen Natl Ctr Asthma Allergy & Chron Lung, Oslo, Norway; Linkoping Univ Hosp, Dept Paediat, S-58185 Linkoping, Sweden; Univ Geneva, Geneva, Switzerland; Royal Childrens Hosp, Dept Allergy, Melbourne, Vic, Australia; Southampton Gen Hosp, Southampton SO9 4XY, Hants, England; Kaiser Permanente San Diego, San Diego, CA USA; Cty Hosp Ryhov, Dept Paediat, Jonkoping, Sweden; Univ Hosp Sophia Rotterdam, Dept Dermatol & Venerol, Rotterdam, Netherlands; Hosp Infantil Univ La Paz, Serv Alergia, Madrid, Spain; Univ Western Australia, Dept Paediat, Subiaco, WA, Australia; 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Allergy Immunol.	AUG	2004	15	4					291	307		10.1111/j.1399-3038.2004.00127.x		17	Allergy; Immunology; Pediatrics	Allergy; Immunology; Pediatrics	843RE	WOS:000223101400002	15305938	
J	Bush, RK; Prochnau, JJ				Bush, RK; Prochnau, JJ			Alternaria-induced asthma	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						alternaria; asthma; allergens; aerobiology	HUMANIZED MONOCLONAL-ANTIBODY; NUTRITION EXAMINATION SURVEY; SCHOOL-AGE-CHILDREN; 2ND NATIONAL-HEALTH; HOUSE-DUST MITE; FUNGAL ALLERGENS; CHILDHOOD ASTHMA; MOLECULAR-CLONING; IGE ANTIBODY; RISK-FACTOR	Acute, severe asthma attacks can be precipitated by a variety of stimuli including exposure to aeroallergens, viral respiratory infections, pollutants, and occupational chemicals. Alternaria is a major aeroallergen in many parts of the world. Sensitivity to Alternaria has been increasingly recognized as a risk factor for the development and persistence of asthma, asthma severity, and potentially fatal asthma exacerbations. We present the case of a patient with IgE-mediated sensitivity to Alternaria who developed an acute, life-threatening asthma attack during the peak Alternaria season. We describe the aerobiology, pathophysiobiology, diagnosis, and treatment options for patients with Alternaria-induced asthma.	William S Middleton VA Hosp, Madison, WI 53705 USA; Univ Wisconsin, Dept Med, Madison, WI 53706 USA	Bush, RK (reprint author), William S Middleton VA Hosp, 2500 Overlook Terrace, Madison, WI 53705 USA.						ACHATZ G, 1995, MOL IMMUNOL, V32, P213, DOI 10.1016/0161-5890(94)00108-D; Adelroth E, 2000, J ALLERGY CLIN IMMUN, V106, P253, DOI 10.1067/mai.2000.108310; Barnes C, 2000, ANN ALLERG ASTHMA IM, V84, P47, DOI 10.1016/S1081-1206(10)62740-8; Bernardis P, 1996, J INVEST ALLERG CLIN, V6, P55; Black PN, 2000, ALLERGY, V55, P501, DOI 10.1034/j.1398-9995.2000.00293.x; Breitenbach M, 1997, INT ARCH ALLERGY IMM, V113, P114; BRUCE CA, 1977, J ALLERGY CLIN IMMUN, V59, P449, DOI 10.1016/0091-6749(77)90009-4; Bush RK, 2002, MED CLIN N AM, V86, P1113, DOI 10.1016/S0025-7125(02)00036-6; Bush RK, 2001, J ALLERGY CLIN IMMUN, V107, pS430, DOI 10.1067/mai.2001.113669; Bush RK, 1999, J ALLERGY CLIN IMMUN, V104, P665, DOI 10.1016/S0091-6749(99)70340-4; BUSH RK, 2001, ENV ASTHMA, P69; Busse W, 2001, J ALLERGY CLIN IMMUN, V108, P184, DOI 10.1067/mai.2001.117880; Busse WW, 2003, MIDDLETONS ALLERGY P, P1175; CANTANI A, 1988, ALLERGOL IMMUNOPATH, V16, P1; Casale TB, 1997, J ALLERGY CLIN IMMUN, V100, P110; Dales RE, 2000, AM J RESP CRIT CARE, V162, P2087; DAmato G, 1997, ALLERGY, V52, P711, DOI 10.1111/j.1398-9995.1997.tb01227.x; Delfino RJ, 1996, AM J RESP CRIT CARE, V154, P633; Downs SH, 2001, AM J RESP CRIT CARE, V164, P455; Eggleston PA, 1998, J ALLERGY CLIN IMMUN, V102, P563, DOI 10.1016/S0091-6749(98)70272-6; Esch R, 2003, MIDDLETONS ALLERGY P, P539; Floyer J., 1745, VIOLENT ASTHMA VISIT; GERGEN PJ, 1987, J ALLERGY CLIN IMMUN, V80, P669, DOI 10.1016/0091-6749(87)90286-7; 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; Halonen M, 1999, AM J RESP CRIT CARE, V160, P564; HENDERSON FW, 1995, AM J RESP CRIT CARE, V151, P1786; HEWITT CRA, 1995, J EXP MED, V182, P1537, DOI 10.1084/jem.182.5.1537; Hopkins JG, 1930, J AMER MED ASSOC, V94, P6; HORST M, 1990, J ALLERGY CLIN IMMUN, V85, P460, DOI 10.1016/0091-6749(90)90156-X; JARJOUR NN, 2003, MIDDLETONS ALLERGY P, P1257; Kauffman HF, 2000, J ALLERGY CLIN IMMUN, V105, P1185, DOI 10.1067/mai.2000.106210; Kenyon N, 2001, CLIN REV ALLERG IMMU, V20, P271, DOI 10.1385/CRIAI:20:3:271; Kheradmand F, 2002, J IMMUNOL, V169, P5904; LOPEZ M, 1985, CLIN REV ALLERG, V3, P183, DOI 10.1007/BF02992982; Milgrom H, 1999, NEW ENGL J MED, V341, P1966, DOI 10.1056/NEJM199912233412603; Nelson HS, 1999, J ALLERGY CLIN IMMUN, V104, P775; Nelson RP, 1996, J ALLERGY CLIN IMMUN, V98, P258, DOI 10.1016/S0091-6749(96)70148-3; 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; 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; 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; Seear M, 1997, AM J RESP CRIT CARE, V155, P364; Soler M, 2001, EUR RESPIR J, V18, P254, DOI 10.1183/09031936.01.00092101; TARGONSKI PV, 1995, J ALLERGY CLIN IMMUN, V95, P955, DOI 10.1016/S0091-6749(95)70095-1; VIJAY HM, 1999, ALLERGENS ALLERGEN I, P113; 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; Werner HA, 2001, CHEST, V119, P1913, DOI 10.1378/chest.119.6.1913	51	157	161	0	11	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	FEB	2004	113	2					227	234		10.1016/j.jaci.2003.11.023		8	Allergy; Immunology	Allergy; Immunology	773EX	WOS:000188885700007	14767434	
J	Trupin, L; Earnest, G; San Pedro, M; Balmes, JR; Eisner, MD; Yelin, E; Katz, PP; Blanc, PD				Trupin, L; Earnest, G; San Pedro, M; Balmes, JR; Eisner, MD; Yelin, E; Katz, PP; Blanc, PD			The occupational burden of chronic obstructive pulmonary disease	EUROPEAN RESPIRATORY JOURNAL			English	Article						Airflow limitation; chronic bronchitis; chronic obstructive pulmonary disease; emphysema; occupational health; work-related	CHRONIC RESPIRATORY SYMPTOMS; LUNG-FUNCTION; CHRONIC-BRONCHITIS; GENERAL-POPULATION; EXPOSURES; ADULTS; PREVALENCE; COMMUNITY; ASTHMA; MINERS	Although chronic obstructive pulmonary disease (COPD) is attributed predominantly to tobacco smoke, occupational exposures are also suspected risk factors for COPD. Estimating the proportion of COPD attributable to occupation is thus an important public health need. A randomly selected sample of 2,061 US residents aged 55-75 yrs completed telephone interviews covering respiratory health, general health status and occupational history. Occupational exposure during the longest-held job was determined by self-reported exposure to vapours, gas, dust or fumes and through a job exposure matrix. COPD was defined by self-reported physician's diagnosis. After adjusting for smoking status and demography, the odds ratio for COPD related to self-reported occupational exposure was 2.0 (95% confidence interval (Cl) 1.6-2.5), resulting in an adjusted population attributable risk (PAR) of 20% (95% Cl 13-27%). The adjusted odds ratio based on the job exposure matrix was 1.6 (95% Cl 1.1-2.5) for high and 1.4 (95% Cl 1.1-1.9) for intermediate probability of occupational dust exposure; the associated PAR was 9% (95% Cl 3-15%). A narrower definition of COPD, excluding chronic bronchitis, was associated with a PAR based on reported occupational exposure of 31% (95% Cl 19-41%). Past occupational exposures significantly increased the likelihood of chronic obstructive pulmonary disease, independent of the effects of smoking. Given that one in five cases of chronic obstructive pulmonary disease may be attributable to occupational exposures, clinicians and health policy-makers should address this potential avenue of chronic obstructive pulmonary disease causation and its prevention.	Univ Calif San Francisco, Div Rheumatol, San Francisco, CA 94143 USA; Univ Calif San Francisco, Div Environm & Occupat Med, San Francisco, CA 94143 USA; Univ Calif San Francisco, Div Pulm & Crit Care, San Francisco, CA 94143 USA; Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA	Trupin, L (reprint author), Univ Calif San Francisco, Div Rheumatol, Box 0920, San Francisco, CA 94143 USA.				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J	Ayuso, R; Reese, G; Leong-Kee, S; Plante, M; Lehrer, SB				Ayuso, R; Reese, G; Leong-Kee, S; Plante, M; Lehrer, SB			Molecular basis of arthropod cross-reactivity: IgE-binding cross-reactive epitopes of shrimp, house dust mite and cockroach tropomyosins	INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY			English	Article						shrimp; dust mite; cockroach; allergens; cross-reactivity	MUSCLE PROTEIN TROPOMYOSIN; MAJOR ALLERGEN; FOOD HYPERSENSITIVITY; OCCUPATIONAL ASTHMA; MUTATIONAL ANALYSIS; IDENTIFICATION; IMMUNOTHERAPY; POLLEN; LOBSTER; SENSITIZATION	Background. Shrimp may cross-react with other crustaceans and mollusks and nonedible arthropods such as insects (cockroach and chironomids), arachnids (house dust mites) and even nematodes. Since the muscle protein tropomyosin has been implicated as a possible cross-reacting allergen, this study characterized the IgE-binding epitopes in shrimp tropomyosin, Pen a 1, that cross-react with other allergenic invertebrate tropomyosins in house dust mites (Der p 10, Der f 10) and cockroaches (Per a 7). Pen a 1-reactive sera from shrimp-allergic subjects were used to evaluate the effect on IgE binding of different amino acid substitutions in Pen a 1 epitopes based on homologous sequences in Per a 7 and Der p 10/Der f 10. Methods: Peptides were synthesized spanning the length of Pen a 1 IgE-binding epitopes and amino acid substitutions were performed based on homologous amino acid sequences from Per a 7 and Der p 10/Der f 10. Results: 7/8 individually recognized Pen a 1 epitopes (2, 3a, 3b, 4, 5a, 5b and 56 had an identical amino acid sequence with lobster allergen, Hom a 1, 4/8 (3a, 3b, 4 and 5a) with Der p 10 and Derf 10, and 5/8 (2, 3a, 3b, 4 and 5a) with Per a 7. In addition, even homologous regions of other arthropod tropomyosins that differ in one or more amino acids from the sequences of Pen a 1 epitopes are still recognized by shrimp-allergic IgE antibodies. In total, shrimp-allergic sera recognize 6/8 peptides homologous to Pen a 1 epitopes in Per a 7, 7/8 in Der p 10/Der f 10, and 7/8 epitopes in Hom a 1. Conclusions: The IgE recognition by shrimp-allergic individuals of identified and/or similar amino acid sequences homologous to Pen a 1 epitopes in mite, cockroach and lobster tropomyosins are the basis of the in vitro cross-reactivity among invertebrate species. Based on amino acid sequence similarity and epitope reactivity, lobster tropomyosin has the strongest and cockroach the least cross-reactivity with shrimp. The clinical relevance of these cross-reactivities in developing allergic reactions to different arthropods needs to be determined. Copyright (C) 2002 S. Karger AG, Basel.	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Arch. Allergy Immunol.	SEP	2002	129	1					38	48		10.1159/000065172		11	Allergy; Immunology	Allergy; Immunology	605YA	WOS:000178703600004	12372997	
J	Milgrom, H; Berger, W; Nayak, A; Gupta, N; Pollard, S; McAlary, M; Taylor, AF; Rohane, P				Milgrom, H; Berger, W; Nayak, A; Gupta, N; Pollard, S; McAlary, M; Taylor, AF; Rohane, P			Treatment of childhood asthma with anti-immunoglobulin E antibody (omalizumab)	PEDIATRICS			English	Article						asthma; child; omalizumab; rhuMAb-E25; anti-IgE; beclomethasone dipropionate; steroid-sparing; inhaled corticosteroid; asthma exacerbation	IGE MONOCLONAL-ANTIBODY; AIRWAY HYPERRESPONSIVENESS; FLUTICASONE PROPIONATE; PULMONARY-FUNCTION; ALLERGIC RHINITIS; COMPLEX-FORMATION; SENSITIZATION; ASSOCIATION; CHILDREN; EXPOSURE	Background and Objective. There seems to be a strong causal relationship between allergy and the origins of asthma. Susceptibility to both is determined by a combination of genetics and environment acting through a complex network of cytokines. Nearly 90% of affected children have positive skin tests indicating the presence of specific immunoglobulin E (IgE), with sensitivity to house dust mite, Alternaria, cockroach, cat, and dog most closely linked to the disease. Greater exposure to house dust mite during infancy leads to earlier onset of wheezing, and elevated serum IgE levels correlate with the appearance of asthma symptoms. Specific IgE binds to high-affinity (Fc epsilon RI) receptors on mast cells and basophils. The IgE-mediated reactions that follow exposure of sensitized mast cells to an allergen are designated early- and late-phase asthmatic responses (EAR and LAR). EAR is characterized by release of histamine and other preformed mediators within 1 hour of allergen exposure. It is often followed by LAR, an infiltration of the airways by inflammatory cells associated with an episode of more prolonged, and usually more severe airflow obstruction, 4 to 8 hours after antigen exposure. Chronic airway symptoms result from persistent LAR caused by continuous allergen exposure. IgE antibodies are capable of passive transfer of both EAR and LAR sensitivity. IgE-mediated mast cell activation contributes to chronic tissue eosinophilia and airway remodeling, with permanent loss in pulmonary function. Omalizumab (rhuMAb-E25) is a recombinant, humanized, monoclonal anti-IgE antibody of mouse origin developed for the treatment of IgE-mediated diseases. Omalizumab binds to free IgE at the same site as the high-affinity receptor. Although it attaches to free IgE, it does not bind to IgA, IgG, or cell-bound IgE. It therefore does not induce cross-linking of cell-bound IgE, which would lead to the release of allergic mediators. It has been reported to decrease serum IgE levels in a dose-dependent manner, inhibit EAR and LAR, and cause a down-regulation of Fc epsilon RI receptors on basophils. Omalizumab has been reported to be safe and effective in improving asthma control and reducing the requirement for oral and inhaled corticosteroids. This double-blind, randomized, placebo-controlled study evaluated the safety, steroid-sparing effects, and impact on disease exacerbations of omalizumab in the treatment of childhood asthma. Methods. Participants were 334 males and premenarchal females aged 6 to 12 years, with moderate to severe allergic asthma requiring treatment with inhaled corticosteroids. During a run-in phase, all children were switched to equivalent doses of beclomethasone dipropionate (BDP), and the dose was adjusted to assure maintenance of asthma control achieved with previous corticosteroid treatment. Children were randomized to subcutaneously administered placebo (N = 109) or omalizumab (N = 225) at a dose based on body weight and initial serum IgE (0.016 mg/kg/IgE [IU/mL] per 4 weeks). BDP dose (initial range 168-420 mug/d) was kept stable for 16 weeks (stable-steroid phase), reduced over 8 weeks to the minimum effective dose (steroid-reduction phase), and maintained constant for the final 4 weeks. Results. More participants in the omalizumab group decreased their BDP dose, and their reduction was greater than that of the placebo group (median reduction 100% vs 66.7%). BDP was withdrawn completely in 55% of the omalizumab group versus 39% of the placebo group. The incidence and the frequency of asthma exacerbations requiring treatment with doubling of BDP dose or systemic corticosteroids were lower in the omalizumab group. The treatment differences were statistically significant during the steroid-reduction phase, during which fewer participants in the omalizumab group had asthma exacerbation episodes (18.2% vs 38.5%), and the mean number of episodes per patient was smaller than with placebo (0.42 vs 2.72). Five asthma exacerbations requiring hospitalization all occurred in the placebo group. Participants' and investigators' global evaluations of treatment effectiveness were more favorable for omalizumab than placebo. Investigators rated effectiveness excellent for 31.5% of the omalizumab group versus 16.3% of the placebo group and good for 44.7% of the omalizumab group versus 32.7% of the placebo group. There was little change in asthma symptom scores or spirometry measurements during either the stable-steroid or steroid dose-reduction phase, with minimal differences between the treatment groups. The requirement for rescue medication in the omalizumab group during both the stable-steroid and steroid dose-reduction phases was consistently lower than at baseline. At week 28, the median number of puffs of rescue medication taken daily was 0 in the omalizumab group and 0.46 in the placebo group. The change from baseline was significant in favor of omalizumab. Over the entire treatment period, patients in the omalizumab group missed a mean of 0.65 school days, compared with a mean of 1.21 days in the placebo group. The mean number of unscheduled medical contacts attributable to asthma-related medical problems was significantly smaller in the omalizumab group than in the placebo group throughout the treatment period (0.15 vs 5.35). Median reduction in serum free IgE was 95% to 99% among omalizumab patients. Median free IgE ranged from 133 to 790 IU/mL at baseline and was in the range of 6 to 9 IU/mL during the treatment period. The dosing scheme used in the trial therefore effectively reduced serum IgE in patients with initial concentrations as high as 1300 IU/mL. There was no reduction in free IgE in the placebo group. Omalizumab treatment was well tolerated. There were no serious treatment-related adverse events. The frequency and types of all adverse events were similar in the omalizumab and placebo groups. The majority of adverse events were mild to moderate in severity. No adverse events suggestive of serum sickness or immune complex formation were observed. Study-drug-related adverse events occurred more frequently in the omalizumab group than in the placebo group (6.2% vs 0.9%). Urticaria was reported in 9 omalizumab patients (4%) compared with 1 (0.9%) placebo patient and was mild or moderate in nearly all cases. Conclusion. Treatment with omalizumab is safe in children with asthma. It reduces the requirement for inhaled corticosteroids while protecting against disease exacerbation.	Natl Jewish Med & Res Ctr, Denver, CO 80206 USA; So Calif Res Ctr, Mission Viejo, CA USA; Univ Illinois, Peoria, IL USA; Novartis Pharmaceut, E Hanover, NJ USA; Allergy & Asthma Res Inst, Louisville, KY USA; Schering Plough Corp, Kenilworth, NJ 07033 USA	Milgrom, H (reprint author), Natl Jewish Med & Res Ctr, 1400 Jackson St, Denver, CO 80206 USA.						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J	Papi, A; Romagnoli, M; Baraldo, S; Braccioni, F; Guzzinati, I; Saetta, M; Ciaccia, A; Fabbri, LM				Papi, A; Romagnoli, M; Baraldo, S; Braccioni, F; Guzzinati, I; Saetta, M; Ciaccia, A; Fabbri, LM			Partial reversibility of airflow limitation and increased exhaled NO and sputum eosinophilia in chronic obstructive pulmonary disease	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article							ENDOGENOUS NITRIC-OXIDE; CORTICOSTEROID-THERAPY; RESPIRATORY-TRACT; SINGLE-BREATH; ASTHMA; COPD; INFLAMMATION; AIRWAY; BRONCHITIS	We investigated the relationship between the reversibility of airflow limitation, the concentration of nitric oxide (NO) in exhaled air, and the inflammatory cells in the sputum of patients with stable chronic obstructive pulmonary disease (COPD). We examined nine normal healthy control subjects and 20 nonatopic patients with COPD. Ten patients had no reversibility of airflow limitation (increase in FEV1 of < 12% and < 200 ml after 200 mug of inhaled salbutamol), and 10 patients had partial reversibility of airflow limitation (increase in FEV1 of < 12% but > 200 ml after 200 mug of inhaled salbutamol). Exhaled NO levels were higher in COPD patients with partial reversibility of airflow limitation than in those with no reversibility of airflow limitation (median 24 [interquartile range 15.3 to 32] ppb versus 8.9 [4.6 to 14.7] ppb; p < 0.01). Compared with healthy control subjects, only COPD patients with partial reversibility of airflow limitation had increased concentrations of sputum eosinophils. We conclude that, in patients with stable COPD, even a partial bronchodilator response to inhaled salbutamol is associated with increased exhaled NO and sputum eosinophilia, suggesting that these patients may have a different response to treatment than do those without reversible airflow limitation.	Univ Modena, Dept Pulm Dis, I-41100 Modena, Italy; Univ Ferrara, Res Ctr Asthma, I-44100 Ferrara, Italy; Univ Ferrara, COPD, I-44100 Ferrara, Italy; Univ Padua, Inst Occupat Med, Padua, Italy	Fabbri, LM (reprint author), Univ Modena, Dept Pulm Dis, Via Pozzo 71, I-41100 Modena, Italy.		Fabbri, Leonardo/I-4055-2012	Fabbri, Leonardo/0000-0001-8894-1689; PAPI, ALBERTO/0000-0002-6924-4500			American Thoracic Society, 1995, AM J RESP CRIT CARE, V152, P1107; ANTHONISEN NR, 1986, AM REV RESPIR DIS, V133, P814; Barnes PJ, 1996, THORAX, V51, P233, DOI 10.1136/thx.51.3.233; CALLAHAN CM, 1991, ANN INTERN MED, V114, P216; CELLI BR, 1995, AM J RESP CRIT CARE, V152, pS77; Chanez P, 1997, AM J RESP CRIT CARE, V155, P1529; Clini E, 1998, THORAX, V53, P881; Corradi M, 1999, THORAX, V54, P572; CRAPO RO, 1991, AM REV RESPIR DIS, V143, P1212; Fujimoto K, 1999, CHEST, V115, P697, DOI 10.1378/chest.115.3.697; Hedenstierna G, 1998, EUR RESPIR J, V12, P1248, DOI 10.1183/09031936.98.12061248; Hogman M, 1997, ACTA PHYSIOL SCAND, V159, P345, DOI 10.1046/j.1365-201X.1997.00101.x; Jatakanon A, 1998, THORAX, V53, P91; Kanazawa H, 1998, CLIN EXP ALLERGY, V28, P1244; Keatings VM, 1997, AM J RESP CRIT CARE, V155, P542; KERSTJENS HAM, 1992, NEW ENGL J MED, V327, P1413, DOI 10.1056/NEJM199211123272003; Kharitonov S, 1997, EUR RESPIR J, V10, P1683, DOI 10.1183/09031936.97.10071683; Kharitonov SA, 1996, AM J RESP CRIT CARE, V153, P1773; LACOSTE JY, 1993, J ALLERGY CLIN IMMUN, V92, P537, DOI 10.1016/0091-6749(93)90078-T; MAESTRELLI P, 1995, AM J RESP CRIT CARE, V152, P1926; Maziak W, 1998, AM J RESP CRIT CARE, V157, P998; *NAT I HLTH, 1997, PUBLICATION; Peleman RA, 1999, EUR RESPIR J, V13, P839, DOI 10.1034/j.1399-3003.1999.13d24.x; Pizzichini E, 1998, AM J RESP CRIT CARE, V158, P1511; Quanjer PH, 1993, EUR RESPIR J S, V16, P5, DOI 10.1183/09041950.005s1693; Robbins RA, 1996, AM J RESP CRIT CARE, V153, P1631; RODRIGUEZROISIN R, 1998, MANAGEMENT CHRONIC O, P107; Rogge L, 1999, J IMMUNOL, V162, P3926; Rutgers SR, 1998, EUR RESPIR J, V12, P816, DOI 10.1183/09031936.98.12040816; Rutgers SR, 1999, THORAX, V54, P576; Saetta M, 1997, EUR RESPIR REV, V7, P29; Saetta M, 1998, MANAGEMENT CHRONIC O, P92; Saleh D, 1998, FASEB J, V12, P929; SIAFAKAS NM, 1995, EUR RESPIR J, V8, P1398, DOI 10.1183/09031936.95.08081398; van Rensen ELJ, 1999, THORAX, V54, P403	35	157	165	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.	NOV	2000	162	5					1773	1777				5	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	371WU	WOS:000165202900031	11069811	
J	Hunninghake, GM; Cho, MH; Tesfaigzi, Y; Soto-Quiros, ME; Avila, L; Lasky-Su, J; Stidley, C; Melen, E; Soderhall, C; Hallberg, J; Kull, I; Kere, J; Svartengren, M; Pershagen, G; Wickman, M; Lange, C; Demeo, DL; Hersh, CP; Klanderman, BJ; Raby, BA; Sparrow, D; Shapiro, SD; Silverman, EK; Litonjua, AA; Weiss, ST; Celedon, JC				Hunninghake, Gary M.; Cho, Michael H.; Tesfaigzi, Yohannes; Soto-Quiros, Manuel E.; Avila, Lydiana; Lasky-Su, Jessica; Stidley, Chris; Melen, Erik; Soderhall, Cilla; Hallberg, Jenny; Kull, Inger; Kere, Juha; Svartengren, Magnus; Pershagen, Goran; Wickman, Magnus; Lange, Christoph; Demeo, Dawn L.; Hersh, Craig P.; Klanderman, Barbara J.; Raby, Benjamin A.; Sparrow, David; Shapiro, Steven D.; Silverman, Edwin K.; Litonjua, Augusto A.; Weiss, Scott T.; Celedon, Juan C.			MMP12, Lung Function, and COPD in High-Risk Populations	NEW ENGLAND JOURNAL OF MEDICINE			English	Article							OBSTRUCTIVE PULMONARY-DISEASE; AIR-FLOW OBSTRUCTION; CHILDHOOD ASTHMA; POLYMORPHISMS; EMPHYSEMA; GENE; SMOKERS; DECLINE; GROWTH; ASSOCIATION	BACKGROUND Genetic variants influencing lung function in children and adults may ultimately lead to the development of chronic obstructive pulmonary disease ( COPD), particularly in high-risk groups. METHODS We tested for an association between single-nucleotide polymorphisms (SNPs) in the gene encoding matrix metalloproteinase 12 (MMP12) and a measure of lung function (prebronchodilator forced expiratory volume in 1 second [FEV(1)]) in more than 8300 subjects in seven cohorts that included children and adults. Within the Normative Aging Study (NAS), a cohort of initially healthy adult men, we tested for an association between SNPs that were associated with FEV(1) and the time to the onset of COPD. We then examined the relationship between MMP12 SNPs and COPD in two cohorts of adults with COPD or at risk for COPD. RESULTS The minor allele ( G) of a functional variant in the promoter region of MMP12 (rs2276109 [-82A -> G]) was positively associated with FEV1 in a combined analysis of children with asthma and adult former and current smokers in all cohorts (P=2x10(-6)). This allele was also associated with a reduced risk of the onset of COPD in the NAS cohort (hazard ratio, 0.65; 95% confidence interval [CI], 0.46 to 0.92; P = 0.02) and with a reduced risk of COPD in a cohort of smokers ( odds ratio, 0.63; 95% CI, 0.45 to 0.88; P = 0.005) and among participants in a family-based study of early-onset COPD (P = 0.006). CONCLUSIONS The minor allele of a SNP in MMP12 (rs2276109) is associated with a positive effect on lung function in children with asthma and in adults who smoke. This allele is also associated with a reduced risk of COPD in adult smokers.	[Hunninghake, Gary M.; Cho, Michael H.; Lasky-Su, Jessica; Melen, Erik; Lange, Christoph; Demeo, Dawn L.; Hersh, Craig P.; Klanderman, Barbara J.; Raby, Benjamin A.; Silverman, Edwin K.; Litonjua, Augusto A.; Weiss, Scott T.; Celedon, Juan C.] Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA; [Hunninghake, Gary M.; Cho, Michael H.; Lasky-Su, Jessica; Melen, Erik; Lange, Christoph; Demeo, Dawn L.; Hersh, Craig P.; Klanderman, Barbara J.; Raby, Benjamin A.; Silverman, Edwin K.; Litonjua, Augusto A.; Weiss, Scott T.; Celedon, Juan C.] Brigham & Womens Hosp, Ctr Genom Med, Boston, MA 02115 USA; [Hunninghake, Gary M.; Cho, Michael H.; Demeo, Dawn L.; Hersh, Craig P.; Raby, Benjamin A.; Silverman, Edwin K.; Litonjua, Augusto A.; Celedon, Juan C.] Brigham & Womens Hosp, Div Pulm & Crit Care Med, Boston, MA 02115 USA; [Hunninghake, Gary M.; Cho, Michael H.; Lasky-Su, Jessica; Melen, Erik; Demeo, Dawn L.; Hersh, Craig P.; Klanderman, Barbara J.; Raby, Benjamin A.; Silverman, Edwin K.; Litonjua, Augusto A.; Weiss, Scott T.; Celedon, Juan C.] Harvard Univ, Sch Med, Boston, MA USA; [Lange, Christoph] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA; [Sparrow, David] Boston Univ, Sch Med, VA Normat Aging Study, VA Healthcare Syst, Boston, MA 02118 USA; [Sparrow, David] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA; [Tesfaigzi, Yohannes; Stidley, Chris] Lovelace Resp Res Inst, Albuquerque, NM USA; [Soto-Quiros, Manuel E.; Avila, Lydiana] Hosp Nacl Ninos Dr Carlos Saenz Herrera, Div Pediat Pulmonol, San Jose, Costa Rica; [Melen, Erik; Kull, Inger; Pershagen, Goran; Wickman, Magnus] Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden; [Soderhall, Cilla; Kere, Juha] Karolinska Inst, Novum, Dept Biosci, S-10401 Stockholm, Sweden; [Svartengren, Magnus] Karolinska Inst, Dept Publ Hlth Sci, S-10401 Stockholm, Sweden; [Wickman, Magnus] Karolinska Inst, Ctr Allergy Res, S-10401 Stockholm, Sweden; [Melen, Erik] Karolinska Univ Hosp, Astrid Lindgren Childrens Hosp, Stockholm, Sweden; [Hallberg, Jenny; Wickman, Magnus] Karolinska Inst, Sachs Childrens Hosp, Stockholm, Sweden; [Shapiro, Steven D.] Univ Pittsburgh, Dept Med, Pittsburgh, PA USA	Celedon, JC (reprint author), Brigham & Womens Hosp, Channing Lab, 181 Longwood Ave, Boston, MA 02115 USA.	juan.celedon@channing.harvard.edu	Kere, Juha/A-9179-2008; Soderhall, Cilla/E-3940-2012	Kere, Juha/0000-0003-1974-0271; Soderhall, Cilla/0000-0002-8397-3080; Litonjua, Augusto/0000-0003-0422-5875; Pershagen, Goran/0000-0002-9701-1130; Kull, Inger/0000-0001-6096-3771	National Heart, Lung, and Blood Institute (NHLBI) [K08 HL092222, K12 HL089990, K08 HL72918, K08 HL074193, R37 HL66289, K01 HL04370, U01 HL065899, U01 HL075419, P01 HL083069, R01 HL086601, R01 HL075478, N01HR76101, N01HR76102, N01HR76103, N01HR76104, N01HR76105, N01HR76106, N01HR76107, N01HR76108, N01HR76109, N01HR76110]; Swedish Research Council, Stockholm County Council, Center for Allergy Research, Karolinska Institutet; State of New Mexico; Cooperative Studies Program-Epidemiology Research and Information Center of the U. S. Department of Veterans Affairs and is a component of the Massachusetts Veterans Epidemiology Research and Information Center, Boston; Medical Research Council [G0000934]; Wellcome Trust [068545/Z/02]; AstraZeneca; Merck; Johnson Johnson; Golden Helix; Novartis Pharmaceuticals; GlaxoSmithKline; Sandvik Hard Materials; Sepracor; Genentech; Phadia; Merck Sweden	Supported by grants from the National Heart, Lung, and Blood Institute (NHLBI) (K08 HL092222, to Dr. Hunninghake; K12 HL089990, to Dr. Cho; K08 HL72918, to Dr. Demeo; and K08 HL074193, to Dr. Raby). The Genetics of Asthma in Costa Rica Study (GACRS) was supported by grants from the NHLBI (R37 HL66289 and K01 HL04370); the Childhood Asthma Management Program ( CAMP) Genetics Ancillary Study was supported by grants from the NHLBI (U01 HL065899, U01 HL075419, P01 HL083069, and R01 HL086601); the Children, Allergy, Milieu, Stockholm, Epidemiological Survey (BAMSE) was supported by the Swedish Research Council, Stockholm County Council, Center for Allergy Research, Karolinska Institutet, and Swedish Heart Lung Foundation; the Boston Early- Onset COPD (eoCOPD) study was supported by a grant from the NHLBI (R01 HL075478); the National Emphysema Treatment Trial ( NETT) was supported by contracts from the NHLBI (N01HR76101, N01HR76102, N01HR76103, N01HR76104, N01HR76105, N01HR76106, N01HR76107, N01HR76108, N01HR76109, N01HR76110, N01HR76111, N01HR76112, N01HR76113, N01HR76114, N01HR76115, N01HR76116, N01HR76118, and N01HR76119), Centers for Medicare and Medicaid Services, and Agency for Healthcare Research and Quality, and the NETT Genetics Ancillary Study was supported by grants from the NHLBI ( R01 HL71393 and R01 HL084323); the Lovelace Smokers Cohort was supported by funding from the State of New Mexico; and the Normative Aging Study (NAS) was supported by the Cooperative Studies Program-Epidemiology Research and Information Center of the U. S. Department of Veterans Affairs and is a component of the Massachusetts Veterans Epidemiology Research and Information Center, Boston. The British 1958 Birth Cohort DNA collection, from which genotype data were used, was funded by grants from the Medical Research Council (G0000934) and the Wellcome Trust (068545/Z/02). Dr. Avila reports receiving lecture fees from AstraZeneca and Merck; Dr. Kere, grant support from Johnson & Johnson; Dr. Lange, consulting fees from Golden Helix; Dr. Raby, lecture fees from Novartis Pharmaceuticals; Dr. Silverman, consulting and lecture fees from AstraZeneca and consulting fees and grant support from GlaxoSmithKline; Dr. Soto-Quiros, lecture fees from AstraZeneca, GlaxoSmithKline, and Merck; Dr. Svartengren, lecture fees from Sandvik Hard Materials; Dr. Tesfaigzi, grant support from Sepracor; Dr. Weiss, consulting fees from Genentech; and Dr. Wickman, lecture fees from Phadia and Merck Sweden. No other potential conflict of interest relevant to this article was reported.	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Engl. J. Med.	DEC 31	2009	361	27					2599	2608		10.1056/NEJMoa0904006		10	Medicine, General & Internal	General & Internal Medicine	538JV	WOS:000273181300007	20018959	
J	Mothes, N; Heinzkill, M; Drachenberg, KJ; Sperr, WR; Krauth, MT; Majlesi, Y; Semper, H; Valent, P; Niederberger V; Kraft, D; Valenta, R				Mothes, N; Heinzkill, M; Drachenberg, KJ; Sperr, WR; Krauth, MT; Majlesi, Y; Semper, H; Valent, P; Niederberger, V; Kraft, D; Valenta, R			Allergen-specific immunotherapy with a monophosphoryl lipid A-adjuvanted vaccine: reduced seasonally boosted immunoglobulin E production and inhibition of basophil histamine release by therapy-induced blocking antibodies	CLINICAL AND EXPERIMENTAL ALLERGY			English	Article						blocking antibodies; immunotherapy; recombinant grass pollen allergens	GRASS-POLLEN ALLERGEN; HEPATITIS-B-VACCINE; IGE; IGG2; IMMUNOGENICITY; IMMUNIZATION; EPITOPES; EFFICACY; DEFECTS; SAFETY	Background Allergen-specific immunotherapy represents a causal form of treatment for IgE-mediated allergies. The allergen extract-based analyses of immunotherapy-induced effects yielded highly controversial results regarding a beneficial role of therapy-induced IgG antibodies. Objective We analysed allergen-specific IgE, IgG subclass, and IgM responses in patients treated with a grass pollen allergy vaccine adjuvanted with monophosphoryl lipid A (MPL), a Th1-inducing agent, and in a placebo group using recombinant timothy grass pollen allergen molecules (rPhl p 1, rPhl p 2, rPhl p 5). Results The strong induction of allergen-specific IgG(1) and IgG(4) antibodies observed only in the actively treated group was associated with significant clinical improvement. Therapy-induced allergen-specific IgM and IgG(2) responses were also noted in several actively treated patients. An inhibition of allergen-dependent basophil histamine release was only obtained with sera containing therapy-induced allergen-specific IgG, but not with sera obtained before therapy or from placebo-treated patients. Moreover, patients with therapy-induced allergen-specific IgG antibodies showed a reduced induction of allergen-specific IgE responses during seasonal grass pollen exposure. Conclusion Successful immunotherapy with the MPL-adjuvanted grass pollen allergy vaccine is associated with the production of allergen-specific IgG antibodies. These blocking antibodies may have protective effects by inhibiting immediate-type reactions and systemic increases of IgE responses caused by seasonal allergen exposure.	Univ Vienna, Sch Med, Vienna Gen Hosp,Mol Immunopathol Grp, Dept Pathophysiol,Div Immunopathol, A-1090 Vienna, Austria; Bencard Allergie GmbH, Munich, Germany; Univ Vienna, Vienna Gen Hosp, Div Hematol & Hemostaseol, Vienna, Austria; Univ Vienna, Vienna Gen Hosp, Dept Otorhinolaryngol, Vienna, Austria	Valenta, R (reprint author), Univ Vienna, Sch Med, Vienna Gen Hosp,Mol Immunopathol Grp, Dept Pathophysiol,Div Immunopathol, Waehringer Gurtel 18-20, A-1090 Vienna, Austria.						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Exp. Allergy	SEP	2003	33	9					1198	1208		10.1046/j.1365-2222.2003.01699.x		11	Allergy; Immunology	Allergy; Immunology	727UC	WOS:000185678400006	12956739	
J	Rumchev, KB; Spickett, JT; Bulsara, MK; Phillips, MR; Stick, SM				Rumchev, KB; Spickett, JT; Bulsara, MK; Phillips, MR; Stick, SM			Domestic exposure to formaldehyde significantly increases the risk of asthma in young children	EUROPEAN RESPIRATORY JOURNAL			English	Article						asthma; children; formaldehyde; indoor air quality	VOLATILE ORGANIC-COMPOUNDS; LONGITUDINAL DATA-ANALYSIS; CHILDHOOD; ASSOCIATION; ALLERGENS; DIOXIDE	Concern has arisen in recent years about indoor air pollution as a risk factor for asthma. Formaldehyde exposure vas examined in relation to asthma among young children (between 6 months and 3 yrs old) in a population-based control study carried out in Perth, Western Australia, between 1997-1999. An association between exposure to formaldehyde and asthma in young children has been suggested. Cases (n=88), whose parents were recruited at Princess Margaret Hospital Accident and Emergency Dept (Perth, Western Australia), were children discharged with asthma as the primary diagnosis. Controls (n=104), who were children in the same age group without asthma diagnosed by a doctor, were identified from birth records through the Health Dept of Western Australia (Perth, Western Australia). Health outcomes for the children were studied using a respiratory questionnaire and skin-prick tests. Formaldehyde, average temperature and relative humidity were measured on two occasions, winter (July-September 1998) and summer (December 1998-March 1999) in the child's bedroom and in the living room. The study found seasonal differences in formaldehyde levels in the children's bedrooms and living rooms with significantly greater formaldehyde exposure during the summer period for case and control subjects. The generalised estimating equation model showed that children exposed to formaldehyde levels of greater than or equal to60 mug.m(-3) are at increased risk of having asthma. The results suggest that domestic exposure to formaldehyde increases the risk of childhood asthma.	Curtin Univ Technol, Sch Publ Hlth, Perth, WA 6001, Australia; Princess Margaret Hosp Children, Dept Resp Med, Perth, WA, Australia	Rumchev, KB (reprint author), Curtin Univ Technol, Sch Publ Hlth, GPO Box U1987, Perth, WA 6001, Australia.		Bulsara, Max/A-5966-2008; Stick, Stephen/O-5683-2014; Osborne, Nicholas/N-4915-2015	Bulsara, Max/0000-0002-8033-6123; Osborne, Nicholas/0000-0002-6700-2284; Stick, Stephen/0000-0002-5386-8482			Anderson SD, 2000, J ALLERGY CLIN IMMUN, V106, P419, DOI 10.1067/mai.2000.108914; BURROWS B, 1989, NEW ENGL J MED, V320, P271, DOI 10.1056/NEJM198902023200502; CHILMONCZYK BA, 1993, NEW ENGL J MED, V328, P1665, DOI 10.1056/NEJM199306103282303; CZAP C, 1993, EUR RESPIR J, V6, pS235; FERRIS BG, 1978, AM REV RESPIR DIS, V188, P1; Franklin P, 2000, AM J RESP CRIT CARE, V161, P1757; Garrett M.H., 1996, P 7 INT C IND AIR QU, V1, P617; HASSELBLAD V, 1992, J AIR WASTE MANAGE, V42, P662; HELWIG H, 1977, DEUT MED WOCHENSCHR, V102, P1612; Hosmer DW, 1989, APPL LOGISTIC REGRES; INFANTERIVARD C, 1993, AM J EPIDEMIOL, V137, P834; KRZYZANOWSKI M, 1990, ENVIRON RES, V52, P117, DOI 10.1016/S0013-9351(05)80247-6; LEVIN JO, 1985, ANAL CHEM, V57, P1032, DOI 10.1021/ac00283a016; LIANG KY, 1986, BIOMETRIKA, V73, P13, DOI 10.1093/biomet/73.1.13; Magnus P, 1997, BRIT MED J, V314, P1795; Maroni M., 1995, AIR QUALITY MONOGRAP, V3; McFadden ER, 1999, AM J RESP CRIT CARE, V160, P221; MEINERT R, 1994, ALLERGY, V49, P526, DOI 10.1111/j.1398-9995.1994.tb01124.x; *NAT HLTH MRC, 1995, 115 NHMRC SESS 1995; *NAT HLTH MRC AUST, 1996, AUSTR 93 SESS NAT HL; NORBACK D, 1995, OCCUP ENVIRON MED, V52, P388; Pendergast JF, 1996, INT STAT REV, V64, P89, DOI 10.2307/1403425; QUACKENBOSS JJ, 1989, ENVIRON INT, V15, P169, DOI 10.1016/0160-4120(89)90023-8; SCHENKER MB, 1983, AM REV RESPIR DIS, V128, P1038; SHERMAN CB, 1990, AM J EPIDEMIOL, V132, P83; SPORIK R, 1990, NEW ENGL J MED, V323, P502, DOI 10.1056/NEJM199008233230802; WHO, 1989, FORM ENV HLTH CRIT; Wieslander G, 1997, INT ARCH OCC ENV HEA, V69, P115; Woodcock A, 1998, BRIT MED J, V316, P1075; ZEGER SL, 1986, BIOMETRICS, V42, P121, DOI 10.2307/2531248	30	156	169	2	22	EUROPEAN RESPIRATORY SOC JOURNALS LTD	SHEFFIELD	146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND	0903-1936			EUR RESPIR J	Eur. Resp. J.	AUG	2002	20	2					403	408		10.1183/09031936.02.00245002		6	Respiratory System	Respiratory System	587LE	WOS:000177641400026	12212974	
J	Pastuszka, JS; Paw, UKT; Lis, DO; Wlazlo, A; Ulfig, K				Pastuszka, JS; Paw, UKT; Lis, DO; Wlazlo, A; Ulfig, K			Bacterial and fungal aerosol in indoor environment in Upper Silesia, Poland	ATMOSPHERIC ENVIRONMENT			English	Article						bioaerosol; bacteria; fungi; indoor air; mold problem	RESPIRATORY SYMPTOMS; MOLD PROBLEMS; AIR-QUALITY; HOMES; PREVALENCE; KATOWICE; DAMP; SCHOOLCHILDREN; BIOAEROSOLS; PARTICLES	The purpose of this study was to find the typical concentration levels of bacterial and fungal bioaerosol in healthy and moldy homes as well as in office rooms in Upper Silesia Industrial Zone. Airborne bacteria and fungi were collected using the 6-stage Andersen impactor inside and outside of buildings. It was found that the typical level of bacterial aerosol indoors is about 10(3) CFU m(-3) in horncs and 10(2) CFU m(-3) in offices, Only Micrococcus spp was present in all homes studied, constituting 36% of the bacterial genera. The second most common was Staphylococcus epidermidis, present in 76% of homes and constituting 14% of the total. The concentration of fungal aerosol in winter ranged from 10 to 102 CFU m-3 in healthy homes and from 10 to 103 CFU m-3 in homes with mold problems. In summer these values were elevated reaching 10(3) CFU m(-3) in healthy homes and 10(3)-10(4) CFU m-3 in moldy buildings. In healthy homes the relative concentration of observed species, including Penicillium, ranged from 3 to about 50% while in moldy homes the highest concentration of Penicillium accounted for 90% of the total fungi. However, the differences between viable fungal species as well as concentrations observed in moldy and healthy homes seem to be too small to be a reason of significantly higher risk for allergic asthma symptoms in any group of buildings. Comparison of the respirable fraction of airborne bacteria and Fungi with literature data suggests that the percentage of respirable fungi and bacteria is generally not dependent on the type of home, building material, geographical factors and particulate air pollution. (C) 2000 Elsevier Science Ltd. All rights reserved.	Univ Calif Davis, Davis, CA 95616 USA; Inst Occupat Med & Enviromm Hlth, PL-41200 Sosnowiec, Poland; Inst Ecol Ind Areas, PL-40832 Katowice, Poland	Pastuszka, JS (reprint author), Univ Calif Davis, Hoagland Hall,1 Shields Ave, Davis, CA 95616 USA.		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J	Finkelman, FD; Hogan, SP; Hershey, GKK; Rothenberg, ME; Wills-Karp, M				Finkelman, Fred D.; Hogan, Simon P.; Hershey, Gurjit K. Khurana; Rothenberg, Marc E.; Wills-Karp, Marsha			Importance of Cytokines in Murine Allergic Airway Disease and Human Asthma	JOURNAL OF IMMUNOLOGY			English	Review							NECROSIS-FACTOR-ALPHA; IL-5 MESSENGER-RNA; THYMIC STROMAL LYMPHOPOIETIN; RECEPTOR ANTAGONIST GENE; SINGLE-NUCLEOTIDE POLYMORPHISM; DENDRITIC CELL MATURATION; COLONY-STIMULATING FACTOR; CHILDHOOD ATOPIC ASTHMA; DUST-MITE EXPOSURE; SERUM IGE LEVELS	Asthma is a common, disabling inflammatory respiratory disease that has increased in frequency and severity in developed nations. We review studies of murine allergic airway disease (MAAD) and human asthma that evaluate the importance of Th2 cytokines, Th2 response-promoting cytokines, IL-17, and proinflammatory and anti-inflammatory cytokines in MAAD and human asthma. We discuss murine studies that directly stimulate airways with specific cytokines or delete, inactivate, neutralize, or block specific cytokines or their receptors, as well as controversial issues including the roles of IL-5, IL-17, and IL-13R alpha 2 in MAAD and IL-4R alpha expression by specific cell types. Studies of human asthmatic cytokine gene and protein expression, linkage of cytokine polymorphisms to asthma, cytokine responses to allergen stimulation, and clinical responses to cytokine antagonists are discussed as well. Results of these analyses establish the importance of specific cytokines in MAAD and human asthma and have therapeutic implications. The journal of Immunology, 2010, 184: 1663-1674.	[Finkelman, Fred D.] Cincinnati Vet Affairs Med Ctr, Dept Med, Cincinnati, OH 45220 USA; [Finkelman, Fred D.] Univ Cincinnati, Coll Med, Div Immunol, Cincinnati, OH 45267 USA; [Finkelman, Fred D.; Wills-Karp, Marsha] Cincinnati Childrens Hosp, Med Ctr, Div Immunobiol, Cincinnati, OH 45229 USA; [Hogan, Simon P.; Rothenberg, Marc E.] Cincinnati Childrens Hosp, Med Ctr, Div Allergy Res, Cincinnati, OH 45229 USA; [Hershey, Gurjit K. Khurana] Cincinnati Childrens Hosp, Med Ctr, Div Asthma Res, Cincinnati, OH 45229 USA	Finkelman, FD (reprint author), Cincinnati Vet Author Med Ctr, 3200 Vine St, Cincinnati, OH 45220 USA.	ffinkelman@pol.net		Khurana Hershey, Gurjit/0000-0001-6663-977X	U.S. Department for Veterans Affairs; National Institutes of Health [P01 HL076383, R01 HL097360]	The work was supported by the U.S. Department for Veterans Affairs and the National Institutes of Health (P01 HL076383 and R01 HL097360).	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J	Frohlich-Nowoisky, J; Pickersgill, DA; Despres, VR; Poschl, U				Froehlich-Nowoisky, Janine; Pickersgill, Daniel A.; Despres, Viviane R.; Poeschl, Ulrich			High diversity of fungi in air particulate matter	PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA			English	Article						atmospheric aerosol; bioaerosol; DNA analysis; fungal spores	HIGH-ALPINE AIR; ENVIRONMENTAL-SAMPLES; ATMOSPHERIC PROCESSES; ENDOPHYTIC FUNGI; DNA-POLYMERASES; AIRBORNE FUNGI; AEROSOLS; SPORES; URBAN; PRECIPITATION	Fungal spores can account for large proportions of air particulate matter, and they may potentially influence the hydrological cycle and climate as nuclei for water droplets and ice crystals in clouds, fog, and precipitation. Moreover, some fungi are major pathogens and allergens. The diversity of airborne fungi is, however, not well-known. By DNA analysis we found pronounced differences in the relative abundance and seasonal cycles of various groups of fungi in coarse and fine particulate matter, with more plant pathogens in the coarse fraction and more human pathogens and allergens in the respirable fine particle fraction (<3 mu m). Moreover, the ratio of Basidiomycota to Ascomycota was found to be much higher than previously assumed, which might also apply to the biosphere.	[Froehlich-Nowoisky, Janine; Pickersgill, Daniel A.; Despres, Viviane R.; Poeschl, Ulrich] Max Planck Inst Chem, Biogeochem Dept, D-55128 Mainz, Germany; [Froehlich-Nowoisky, Janine] Johannes Gutenberg Univ Mainz, Inst Geosci, D-55128 Mainz, Germany; [Despres, Viviane R.] Johannes Gutenberg Univ Mainz, Inst Gen Bot, D-55128 Mainz, Germany	Despres, VR (reprint author), Max Planck Inst Chem, Biogeochem Dept, Johann Joachim Becher Weg 27, D-55128 Mainz, Germany.	despres@mpch-mainz.mpg.de; poeschl@mpch-mainz.mpg.de	Poschl, Ulrich/A-6263-2010; Froehlich, Janine/D-6227-2015	Poschl, Ulrich/0000-0003-1412-3557; Froehlich, Janine/0000-0002-1278-0054; Pickersgill, Daniel/0000-0002-3983-506X	Max Planck Society; German Research Foundation [DE1161/2-1]; Landesexzellenzcluster Geocycles [494]	We thank J. Cimbal and I. Germann for technical assistance; M. O. Andreae, W. Elbert, H. Paulsen, and D. Begerow for helpful discussions and support; U. Kampe for providing air quality data; and the Max Planck Institute for Plant Breeding Research for DNA sequencing. This work was supported by the Max Planck Society, German Research Foundation Grant DE1161/2-1, and Landesexzellenzcluster Geocycles Contribution No. 494.	Adhikari A, 2006, ENVIRON POLLUT, V140, P16, DOI 10.1016/j.envpol.2005.07.004; Adhikari A, 2004, SCI TOTAL ENVIRON, V326, P123, DOI 10.1016/j.scitotenv.2003.12.007; Andreae MO, 2008, EARTH-SCI REV, V89, P13, DOI 10.1016/j.earscirev.2008.03.001; Andreae MO, 1997, SCIENCE, V276, P1052, DOI 10.1126/science.276.5315.1052; Arnold A. 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Natl. Acad. Sci. U. S. A.	AUG 4	2009	106	31					12814	12819		10.1073/pnas.0811003106		6	Multidisciplinary Sciences	Science & Technology - Other Topics	479NT	WOS:000268667600047	19617562	
J	Nicholson, PJ; Cullinan, P; Taylor, AJN; Burge, PS; Boyle, C				Nicholson, PJ; Cullinan, P; Taylor, AJN; Burge, PS; Boyle, C			Evidence based guidelines for the prevention, identification, and management of occupational asthma	OCCUPATIONAL AND ENVIRONMENTAL MEDICINE			English	Review							PEAK EXPIRATORY FLOW; DIISOCYANATE-INDUCED ASTHMA; LABORATORY-ANIMAL ALLERGY; NATURAL-RUBBER LATEX; ISOCYANATE-INDUCED ASTHMA; WORK-RELATED SYMPTOMS; HEALTH-CARE WORKERS; EXPOSURE-RESPONSE RELATIONSHIPS; IMMUNOLOGICAL LUNG-DISEASE; CRAB-PROCESSING WORKERS	Background: Occupational asthma is the most frequently reported work related respiratory disease in many countries. This work was commissioned by the British Occupational Health Research Foundation to assist the Health and Safety Executive in achieving its target of reducing the incidence of occupational asthma in Great Britain by 30% by 2010. Aim: The guidelines aim to improve the prevention, identification, and management of occupational asthma by providing evidence based recommendations on which future practice can be based. Methods: The literature was searched systematically using Medline and Embase for articles published in all languages up to the end of June 2004. Evidence based statements and recommendations were graded according to the Royal College of General Practitioner's star system and the revised Scottish Intercollegiate Guidelines Network grading system. Results: A total of 474 original studies were selected for appraisal from over 2500 abstracts. The systematic review produced 52 graded evidence statements and 22 recommendations based on 223 studies. Discussion: Evidence based guidelines have become benchmarks for practice in healthcare and the process used to prepare them is well established. This evidence review and its recommendations focus on interventions and outcomes to provide a robust approach to the prevention, identification, and management of occupational asthma, based on and using the best available medical evidence. The most important action to prevent cases of occupational asthma is to reduce exposure at source. Thereafter surveillance should be performed for the early identification of symptoms, including occupational rhinitis, with additional functional and immunological tests where appropriate. Effective management of workers suspected to have occupational asthma involves the identification and investigation of symptoms suggestive of asthma immediately they occur. Those workers who are confirmed to have occupational asthma should be advised to avoid further exposure completely and early in the course of their disease to offer the best chance of recovery.	British Occupat Hlth Res Fdn, London NW1 4LB, England; Procter & Gamble Co, Surrey, England; Natl Heart & Lung Inst, London, England; Birmingham Heartlands Hosp, Birmingham B9 5ST, W Midlands, England; Hlth & Safety Execut, Bootle, England	Nicholson, PJ (reprint author), British Occupat Hlth Res Fdn, 6 St Andrews Pl,Regents Pk, London NW1 4LB, England.	nicholson.pj@pg.com					AGRUP G, 1986, BRIT J IND MED, V43, P192; ALLARD C, 1989, CHEST, V96, P1046, DOI 10.1378/chest.96.5.1046; Allmers H, 2002, J ALLERGY CLIN IMMUN, V110, P318, DOI 10.1067/mai.2002.126461; Ameille J, 2003, OCCUP ENVIRON MED, V60, P136, DOI 10.1136/oem.60.2.136; Ameille J, 1997, EUR RESPIR J, V10, P55, DOI 10.1183/09031936.97.10010055; Anees W, 2002, THORAX, V57, P231, DOI 10.1136/thorax.57.3.231; AXON EJ, 1995, OCCUP MED-OXFORD, V45, P109, DOI 10.1093/occmed/45.2.109; BAKER DB, 1990, AM J IND MED, V18, P653, DOI 10.1002/ajim.4700180604; Balboni A, 1996, EUR RESPIR J, V9, P207, DOI 10.1183/09031936.96.09020207; Baldwin DR, 2002, THORAX, V57, P860, DOI 10.1136/thorax.57.10.860; 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J	Kull, I; Almqvist, C; Lilja, G; Pershagen, G; Wickman, M				Kull, I; Almqvist, C; Lilja, G; Pershagen, G; Wickman, M			Breast-feeding reduces the risk of asthma during the first 4 years of life	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						allergy; asthma; sensitization; breast-fieeding; children; primary prevention; prospective studies; BAMSE	BIRTH COHORT; ATOPIC DISEASE; NONALLERGIC MOTHERS; FOLLOW-UP; CHILDREN; CHILDHOOD; PREVALENCE; MILK; ASSOCIATION; CONTROVERSY	Background: The evidence for a preventive effect of breast-feeding on asthma and other allergic diseases in childhood is inconclusive. Objective: The aim of this study was to investigate the effect of breast-feeding on asthma and sensitization to airborne allergens among children up to 4 years of age. Methods: A birth cohort of 4089 children was followed. Exposure data were collected at 2 months and 1 year of age. The total dose of breast milk was estimated by combining periods of exclusive and partial breast-feeding. Outcomes data were collected at 1, 2, and 4 years of age. The response rate at 4 years was 90%, and 73% participated in a clinical investigation, including blood sampling for analysis of specific IgE and lung function testing. Children with onset of wheeze during lactation (n = 217) were excluded in some of the analyses to avoid disease-related modification of exposure. Results: Exclusive breast-feeding for 4 months or more reduced the risk of asthma at the age of 4 years (odds ratio [OR], 0.72; 95% CI, 0.53-0.97), irrespective of sensitization to common airborne allergens (P = .72). Excluding children with wheeze during lactation tended to strengthen the risk estimate (OR, 0.64; 95% CI, 0.46-0.88). A duration of 3 months or more of partial breast-feeding seemed to offer additional protection; exclusive breast-feeding for 3 to 4 months combined with partial breast-feeding for 3 months or more resulted in an OR of 0.44 (95% CI, 0.21-0.87). The effects tended to be stronger in children without heredity for allergy (P interaction = .36). Conclusion: Breast-feeding reduces the risk of asthma during the first 4 years of life.	Stockholm Cty Council, Dept Environm & Occupat Hlth, S-10726 Stockholm, Sweden; Astrid Lindgren Childrens Hosp, Karolinska Inst, Dept Women & Child Hlth, Stockholm, Sweden; Sachs Childrens Hosp, Inst Sodersjukhuset, Karolinska Inst, Stockholm, Sweden; Karolinska Inst, Natl Inst Environm Med, Stockholm, Sweden; Karolinska Inst, Ctr Allergy Res, Stockholm, Sweden	Kull, I (reprint author), Karolinska Hosp, Dept Environm & Occupat Hlth, SE-17176 Stockholm, Sweden.	inger.kull@smd.sll.se		Pershagen, Goran/0000-0002-9701-1130; Kull, Inger/0000-0001-6096-3771			ALMQVIST C, 2003, J ALLERGY CLIN IMMUN, V11, P800; Bergmann RL, 2002, CLIN EXP ALLERGY, V32, P205, DOI 10.1046/j.1365-2222.2002.01274.x; Bottcher MF, 2002, CLIN EXP ALLERGY, V32, P159, DOI 10.1046/j.1365-2222.2002.01343.x; Bottcher MF, 2000, PEDIATR RES, V47, P157; Chulada PC, 2003, J ALLERGY CLIN IMMUN, V111, P328, DOI 10.1067/mai.2003.127; FIDLER N, 2000, EUR J NUTR, V39, P321; Gdalevich M, 2001, J PEDIATR-US, V139, P261, DOI 10.1067/mpd.2001.117006; Hanson LA, 2003, ANN ALLERG ASTHMA IM, V90, P59; Hoppu U, 2001, ALLERGY, V56, P23, DOI 10.1034/j.1398-9995.2001.00908.x; Kerkhof M, 2003, CLIN EXP ALLERGY, V33, P1336, DOI 10.1046/j.1365-2222.2003.01751.x; KRAMER MS, 1988, J PEDIATR-US, V112, P181, DOI 10.1016/S0022-3476(88)80054-4; Kull I, 2002, ARCH DIS CHILD, V87, P478, DOI 10.1136/adc.87.6.478; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Miyake Y, 2003, CLIN EXP ALLERGY, V33, P312, DOI 10.1046/j.1365-2222.2003.t01-1-01607.x; Oddy WH, 2002, J ALLERGY CLIN IMMUN, V110, P65, DOI 10.1067/mai.2002.125296; Oddy WH, 1999, BRIT MED J, V319, P815; Peat JK, 2003, PEDIATR PULM, V35, P331, DOI 10.1002/ppul.10276; Quanjer PH, 1997, EUR RESPIR J, V10, pS2; Rothman KJ, 1998, MODERN EPIDEMIOLOGY; Rust GS, 2001, J NATL MED ASSOC, V93, P139; SAARINEN UM, 1995, LANCET, V346, P1065, DOI 10.1016/S0140-6736(95)91742-X; Sears MR, 2002, LANCET, V360, P901, DOI 10.1016/S0140-6736(02)11025-7; Siltanen M, 2003, ALLERGY, V58, P524, DOI 10.1034/j.1398-9995.2003.00150.x; Tariq SM, 1998, J ALLERGY CLIN IMMUN, V101, P587; van Odijk J, 2003, ALLERGY, V58, P833, DOI 10.1034/j.1398-9995.2003.00264.x; Wickman M, 2003, ALLERGY, V58, P742, DOI 10.1034/j.1398-9995.2003.00078.x; Wickman M, 2002, PEDIATR ALLERGY IMMU, V13, P11, DOI 10.1034/j.1399-3038.13.s.15.10.x; Wijga A, 2003, PEDIATR ALLERGY IMMU, V14, P156, DOI 10.1034/j.1399-3038.2003.00022.x; Wilson AC, 1998, BRIT MED J, V316, P21; Wright AL, 2001, ADV EXP MED BIOL, V501, P249; Wright AL, 2001, THORAX, V56, P192, DOI 10.1136/thorax.56.3.192	31	155	158	1	12	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	OCT	2004	114	4					755	760		10.1016/j.jaci.2004.07.036		6	Allergy; Immunology	Allergy; Immunology	861SO	WOS:000224439100006	15480312	
J	Dakin, CJ; Numa, AH; Wang, H; Morton, JR; Vertzyas, CC; Henry, RL				Dakin, CJ; Numa, AH; Wang, H; Morton, JR; Vertzyas, CC; Henry, RL			Inflammation, infection, and pulmonary function in infants and young children with cystic fibrosis	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						cystic fibrosis; infants; respiratory function tests	1ST 5 YEARS; BRONCHOALVEOLAR LAVAGE; PSEUDOMONAS-AERUGINOSA; RESPIRATORY MECHANICS; AIRWAY INFLAMMATION; VENTILATED INFANTS; LUNG INFLAMMATION; RESIDUAL CAPACITY; WASHOUT; RESPONSIVENESS	Our aim was to study the effect of lower airway infection on clinical parameters, pulmonary function tests, and inflammation in clinically stable infants and young children with cystic fibrosis (CF). To accomplish this goal, a prospective cohort of screened CF patients under 4 years of age were studied, using elective anesthesia and intubation for: passive respiratory mechanics (single breath occlusion passive deflation) and lung volumes (nitrogen washout), under neuromuscular blockade; and bronchoalveolar lavage (BAL) of 3 main bronchi for cytology, cytokine interleukin (IL)-8, and quantitative microbiology. There were 22 children studied, with a mean age of 23.2 months (6.7-44 months). A greater relative risk of lower airway pathogens was associated with prior respiratory admission (3.60, 95% confidence interval [CI] 2.87-4.51), history of asthma (1.75, 95% Cl 1.52-2.03), and chronic symptoms (1.50, 95% Cl 1.23-1.83), especially wheeze (1.88, 95% Cl 1.61-2.19). Lower respiratory pathogens (greater than or equal to 10 cfu/ml BAL) were found in 14 out of 22, and greater than 10(5) cfu/ml in 8 out of 22 subjects. The level of pathogens in BAL (log(10) cfu/ml) explained 78% of the variability in percent neutrophils and 34% of the variability in IL-8 levels. Pathogen level also correlated with pulmonary function tests of specific respiratory system compliance (r -0.49, p = 0.02) and functional residual capacity over total lung capacity (r 0.49, p = 0.03). We conclude that the presence of pathogens in the lower airways correlated with levels of inflammation, respiratory system compliance, and degree of air trapping.	Sydney Childrens Hosp, Dept Resp Med, Sydney, NSW, Australia; Sydney Childrens Hosp, Intens Care Unit, Sydney, NSW, Australia; Univ New S Wales, Sch Pediat, Sydney, NSW, Australia; S Eastern Area Lab Serv, Dept Microbiol, Sydney, NSW, Australia	Dakin, CJ (reprint author), Starship Childrens Hosp, Level 6,Pk Rd,Private Bag 92024, Auckland 1, New Zealand.		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J. Respir. Crit. Care Med.	APR 1	2002	165	7					904	910		10.1164/rccm.2010139		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	536ZA	WOS:000174730700006	11934712	
J	McKeever, TM; Lewis, SA; Smith, C; Collins, J; Heatlie, H; Frischer, M; Hubbard, R				McKeever, TM; Lewis, SA; Smith, C; Collins, J; Heatlie, H; Frischer, M; Hubbard, R			Early exposure to infections and antibiotics and the incidence of allergic disease: A birth cohort study with the West Midlands General Practice Research Database	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						asthma; eczema; hay fever; infections; siblings; antibiotics; cohort	RESPIRATORY SYNCYTIAL VIRUS; HAY-FEVER; ATOPIC DISORDER; GUINEA-BISSAU; FAMILY-SIZE; ASTHMA; CHILDREN; MEASLES; RISK; PREVALENCE	Background: It has been suggested that the rise in prevalence of allergic disease in westernized countries is due in part to a decrease in exposure to infections and an increase in the use of antibiotics early in life. Objective: The purpose of this investigation was to quantify the relationships between (1) exposure to personal infections, infections in siblings, and use of antibiotics in early life and (2) the incidence of allergic disease. Methods: Using the West Midlands section of the UK General Practice Research Database, we established a historical birth cohort of children (N = 29,238). For each child, we identified all personal infections and infections in siblings and determined the use of antibiotics in early life; we also noted incident diagnoses of asthma, eczema, and hay fever. The data were analyzed through use of Cox regression. Results: There was no clear protective effect of exposure to either personal infections or infections in siblings with respect to the incidence of allergic disease. Antibiotic exposure was associated with an increased risk of developing allergic disease in a dose-related manner: having 4 or more courses of antibiotics in the first year of life was associated with an increased incidence of asthma (hazard ratio [HR), 3.13; 95% CI, 2.75-3.57), eczema (HR, 1.48; 95% CI, 1.31-1.68), and hay fever (HR, 2.12; 95% CI, 1.68-2.66). However, adjusting for consulting behavior reduced these effects (adjusted HR [95% CI]: asthma, 1.99 [1.72-2.31]; eczema, 1.01 [0.88-1.17]; hay fever, 1.14 [0.88-1.47]). Conclusions: We found no evidence that exposure to infections reduced the incidence of allergic disease, and infections did not explain the previous findings of a strong birth order effect in this cohort. The use of antibiotics might be associated with early diagnoses of allergic disease.	Univ Nottingham, Div Resp Med, Nottingham NG7 2RD, England; Univ Keele, Dept Med Management, Keele ST5 5BG, Staffs, England	McKeever, TM (reprint author), City Hosp, Div Resp Med, Clin Sci Bldg,Hucknall Rd, Nottingham NG5 1PB, England.		Research Datalink, Clinical Practice/H-2477-2013	McKeever, Tricia/0000-0003-0914-0416			Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1; Bjorksten B, 1999, CLIN EXP ALLERGY, V29, P342; Bodner C, 1998, THORAX, V53, P28; Droste JHJ, 2000, CLIN EXP ALLERGY, V30, P1547; Farooqi IS, 1998, THORAX, V53, P927; Illi S, 2001, BRIT MED J, V322, P390, DOI 10.1136/bmj.322.7283.390; Kalliomaki M, 2001, J ALLERGY CLIN IMMUN, V107, P129, DOI 10.1067/mai.2001.111237; Lewis SA, 1998, CLIN EXP ALLERGY, V28, P1493; Matricardi PM, 2000, BRIT MED J, V320, P412, DOI 10.1136/bmj.320.7232.412; Matricardi PM, 1997, BRIT MED J, V314, P999; McKeever TM, 2001, THORAX, V56, P758, DOI 10.1136/thorax.56.10.758; *OFF NAT STAT, 1996, GEN PRACT RES DAT IN; Shaheen SO, 1996, LANCET, V347, P1792, DOI 10.1016/S0140-6736(96)91617-7; Shaheen SO, 1996, BRIT MED J, V313, P969; Shirakawa T, 1997, SCIENCE, V275, P77, DOI 10.1126/science.275.5296.77; Sigurs N, 2000, AM J RESP CRIT CARE, V161, P1501; Stein R, 1999, LANCET, V354, P541, DOI 10.1016/S0140-6736(98)10321-5; Strachan David P., 2000, Thorax, V55, pS2, DOI 10.1136/thorax.55.suppl_1.S2; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Strachan DP, 1996, ARCH DIS CHILD, V74, P422; Sudo N, 1997, J IMMUNOL, V159, P1739; von Hertzen L, 1999, J ALLERGY CLIN IMMUN, V104, P1211; von Mutius E, 1999, EUR RESPIR J, V14, P4, DOI 10.1034/j.1399-3003.1999.14a03.x; Walley T, 1997, LANCET, V350, P1097, DOI 10.1016/S0140-6736(97)04248-7; Wickens KL, 1999, EPIDEMIOLOGY, V10, P699, DOI 10.1097/00001648-199911000-00009	25	155	163	0	3	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	JAN	2002	109	1					43	50		10.1067/mai.2002.121016		8	Allergy; Immunology	Allergy; Immunology	519RM	WOS:000173739300007	11799364	
J	Jakobsson, HE; Abrahamsson, TR; Jenmalm, MC; Harris, K; Quince, C; Jernberg, C; Bjorksten, B; Engstrand, L; Andersson, AF				Jakobsson, Hedvig E.; Abrahamsson, Thomas R.; Jenmalm, Maria C.; Harris, Keith; Quince, Christopher; Jernberg, Cecilia; Bjoerksten, Bengt; Engstrand, Lars; Andersson, Anders F.			Decreased gut microbiota diversity, delayed Bacteroidetes colonisation and reduced Th1 responses in infants delivered by Caesarean section	GUT			English	Article							INTESTINAL MICROBIOTA; IMMUNE-RESPONSES; FECAL SAMPLES; T-CELLS; BACTERIA; ALLERGY; ASTHMA; CHILDREN; ECZEMA; MODE	important stimuli for immune development, and a reduced microbial exposure as well as caesarean section (CS) has been associated with the development of allergic disease. Here we address how microbiota development in infants is affected by mode of delivery, and relate differences in colonisation patterns to the maturation of a balanced Th1/Th2 immune response. Design The postnatal intestinal colonisation pattern was investigated in 24 infants, born vaginally (15) or by CS (nine). The intestinal microbiota were characterised using pyrosequencing of 16S rRNA genes at 1 week and 1, 3, 6, 12 and 24 months after birth. Venous blood levels of Th1- and Th2-associated chemokines were measured at 6, 12 and 24 months. Results Infants born through CS had lower total microbiota diversity during the first 2 years of life. CS delivered infants also had a lower abundance and diversity of the Bacteroidetes phylum and were less often colonised with the Bacteroidetes phylum. Infants born through CS had significantly lower levels of the Th1-associated chemokines CXCL10 and CXCL11 in blood. Conclusions CS was associated with a lower total microbial diversity, delayed colonisation of the Bacteroidetes phylum and reduced Th1 responses during the first 2 years of life.	[Jakobsson, Hedvig E.; Jernberg, Cecilia] Swedish Inst Communicable Dis Control, Dept Preparedness, Solna, Sweden; [Jakobsson, Hedvig E.; Engstrand, Lars] Karolinska Inst, Dept Microbiol Tumor & Cell Biol, Stockholm, Sweden; [Abrahamsson, Thomas R.] Linkoping Univ, Div Pediat, Dept Clin & Expt Med, Linkoping, Sweden; [Jenmalm, Maria C.] Linkoping Univ, Div Inflammat Med, Dept Clin & Expt Med, Linkoping, Sweden; [Harris, Keith; Quince, Christopher] Univ Glasgow, Sch Engn, Glasgow, Lanark, Scotland; [Bjoerksten, Bengt] Karolinska Inst, Inst Environm Med, Stockholm, Sweden; [Bjoerksten, Bengt] Univ Orebro, Sch Hlth & Med Sci, SE-70182 Orebro, Sweden; [Andersson, Anders F.] KTH Royal Inst Technol, Sci Life Lab, Sch Biotechnol, Div Gene Technol, SE-17121 Solna, Sweden	Andersson, AF (reprint author), KTH Royal Inst Technol, Sci Life Lab, Sch Biotechnol, Div Gene Technol, POB 1031, SE-17121 Solna, Sweden.	lars.engstrand@ki.se; andersson@scilifelab.se	Jenmalm, Maria/C-9679-2009	Jenmalm, Maria/0000-0002-2117-5366; Andersson, Anders/0000-0002-3627-6899	Ekhaga Foundation and the Soderbergs Foundation; Swedish Research Council [K2011-56X-21854-01-06]; Research Council for the South-East Sweden; Swedish Asthma and Allergy Association; Olle Engkvist Foundation; Vardal Foundation-for Health Care Sciences and Allergy Research; Swedish Research Councils VR [621-2011-5689]; FORMAS [215-2009-1174]; Unilever	This work was supported by the Ekhaga Foundation and the Soderbergs Foundation to LE and by the Swedish Research Council (K2011-56X-21854-01-06), the Research Council for the South-East Sweden, the Swedish Asthma and Allergy Association, the Olle Engkvist Foundation, the Vardal Foundation-for Health Care Sciences and Allergy Research to MJ and by the Swedish Research Councils VR (621-2011-5689) and FORMAS (215-2009-1174) to AA. KH was funded through a direct grant from Unilever.	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J	Sundell, J; Levin, H; Nazaroff, WW; Cain, WS; Fisk, WJ; Grimsrud, DT; Gyntelberg, F; Li, Y; Persily, AK; Pickering, AC; Samet, JM; Spengler, JD; Taylor, ST; Weschler, CJ				Sundell, J.; Levin, H.; Nazaroff, W. W.; Cain, W. S.; Fisk, W. J.; Grimsrud, D. T.; Gyntelberg, F.; Li, Y.; Persily, A. K.; Pickering, A. C.; Samet, J. M.; Spengler, J. D.; Taylor, S. T.; Weschler, C. J.			Ventilation rates and health: multidisciplinary review of the scientific literature	INDOOR AIR			English	Article						Outdoor air supply rate; Indoor air quality; Offices; Schools; Homes	SICK-BUILDING-SYNDROME; INDOOR AIR-QUALITY; SYNDROME SBS SYMPTOMS; HOUSE-DUST MITES; OFFICE BUILDINGS; CO2 CONCENTRATIONS; EXCHANGE-RATE; RESPIRATORY-DISEASES; CARBON-DIOXIDE; YOUNG-CHILDREN	P>The scientific literature through 2005 on the effects of ventilation rates on health in indoor environments has been reviewed by a multidisciplinary group. The group judged 27 papers published in peer-reviewed scientific journals as providing sufficient information on both ventilation rates and health effects to inform the relationship. Consistency was found across multiple investigations and different epidemiologic designs for different populations. Multiple health endpoints show similar relationships with ventilation rate. There is biological plausibility for an association of health outcomes with ventilation rates, although the literature does not provide clear evidence on particular agent(s) for the effects. Higher ventilation rates in offices, up to about 25 l/s per person, are associated with reduced prevalence of sick building syndrome (SBS) symptoms. The limited available data suggest that inflammation, respiratory infections, asthma symptoms and short-term sick leave increase with lower ventilation rates. Home ventilation rates above 0.5 air changes per hour (h-1) have been associated with a reduced risk of allergic manifestations among children in a Nordic climate. The need remains for more studies of the relationship between ventilation rates and health, especially in diverse climates, in locations with polluted outdoor air and in buildings other than offices. Practical Implications Ventilation with outdoor air plays an important role influencing human exposures to indoor pollutants. This review and assessment indicates that increasing ventilation rates above currently adopted standards and guidelines should result in reduced prevalence of negative health outcomes. Building operators and designers should avoid low ventilation rates unless alternative effective measures, such as source control or air cleaning, are employed to limit indoor pollutant levels.	[Levin, H.] Bldg Ecol Res Grp, Santa Cruz, CA USA; [Sundell, J.] Tsinghua Univ, Beijing 100084, Peoples R China; [Cain, W. S.] Univ Calif San Diego, San Diego, CA 92103 USA; [Fisk, W. J.] Univ Calif Berkeley, Lawrence Berkeley Lab, Berkeley, CA 94720 USA; [Gyntelberg, F.] Bispebjerg Hosp, DK-2400 Copenhagen, Denmark; [Li, Y.] Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China; [Persily, A. K.] Natl Inst Stand & Technol, Gaithersburg, MD 20899 USA; [Samet, J. M.] Univ So Calif, Los Angeles, CA USA; [Spengler, J. D.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA; [Taylor, S. T.] Taylor Engineers, Alameda, CA USA; [Weschler, C. J.] Rutgers State Univ, Piscataway, NJ USA; [Weschler, C. J.] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Piscataway, NJ 08854 USA; [Sundell, J.] Tech Univ Denmark, DK-2800 Lyngby, Denmark; [Grimsrud, D. T.] Univ Minnesota, Minneapolis, MN 55455 USA; [Pickering, A. C.] Wythenshawe Hosp, Manchester M23 9LT, Lancs, England	Levin, H (reprint author), Bldg Ecol Res Grp, Santa Cruz, CA USA.	hal.levin@buildingecology.com	Sanders, Susan/G-1957-2011; Sundell, Jan/B-2857-2012; Li, Yuguo/A-9469-2010; Nazaroff, William/C-4106-2008; Weschler, Charles/A-9788-2009	Li, Yuguo/0000-0002-2281-4529; Nazaroff, William/0000-0001-5645-3357; Weschler, Charles/0000-0002-9097-5850	American Society of Heating, Refrigerating, and Air-Conditioning Engineers, Inc. (ASHRAE); National Center for Energy Management and Building Technology (NCEMBT)	The authors gratefully acknowledge the assistance of Gina Bendy and Shela Ray of the Indoor Air Institute, Inc., for their assistance in the literature review. Funding was provided by the American Society of Heating, Refrigerating, and Air-Conditioning Engineers, Inc. (ASHRAE) and the National Center for Energy Management and Building Technology (NCEMBT). The Indoor Air Institute was the project contractor.	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J	Stenfors, N; Nordenhall, C; Salvi, SS; Mudway, I; Soderberg, M; Blomberg, A; Helleday, R; Levin, JO; Holgate, ST; Kelly, FJ; Frew, AJ; Sandstrom, T				Stenfors, N; Nordenhall, C; Salvi, SS; Mudway, I; Soderberg, M; Blomberg, A; Helleday, R; Levin, JO; Holgate, ST; Kelly, FJ; Frew, AJ; Sandstrom, T			Different airway inflammatory responses in asthmatic and healthy humans exposed to diesel	EUROPEAN RESPIRATORY JOURNAL			English	Article						airway inflammation; asthma; cytokines; diesel; pollution	EXHAUST PARTICLES; POLLUTION; INTERLEUKIN-10; CELLS	Particulate matter (PM) pollution adversely affects the airways, with asthmatic subjects thought to be especially sensitive. The authors hypothesised that exposure to diesel exhaust (DE), a major source of PM, would induce airway neutrophilia in healthy subjects, and that either these responses would be exaggerated in subjects with mild allergic asthma, or DE would exacerbate pre-existent allergic airways. Healthy and mild asthmatic subjects were exposed for 2 h to ambient levels of DE (particles with a 50% cut-off aerodynamic diameter of 10 mum (PM10) 108 mug(.)m(-3)) and lung function and airway inflammation were assessed. Both groups showed an increase in airway resistance of similar magnitude after DE exposure. Healthy subjects developed airway inflammation 6 h after DE exposure, with airways neutrophilia and lymphocytosis together with an increase in interleukin-8 (IL-8) protein in lavage fluid, increased IL-8 messenger ribonucleic acid expression in the bronchial mucosa and upregulation of the endothelial adhesion molecules. In asthmatic subjects, DE exposure did not induce a neutrophilic response or exacerbate their preexisting eosinophilic airway inflammation. Epithelial staining for the cytokine IL-10 was increased after DE in the asthmatic group. Differential effects on the airways of healthy subjects and asthmatics of particles with a 50% cut-off aerodynamic diameter of 10 mum at concentrations below current World Health Organisation air quality standards have been observed in this study. Further work is required to elucidate the significance of these differential responses.	Umea Univ Hosp, Dept Resp Med & Allergy, SE-90185 Umea, Sweden; Southampton Gen Hosp, Resp Cell & Mol Biol Res Div, Southampton SO9 4XY, Hants, England; St Thomas Hosp, Rayne Inst, London SE1 7EH, England; Natl Inst Working Life, Umea, Sweden	Sandstrom, T (reprint author), Umea Univ Hosp, Dept Resp Med & Allergy, SE-90185 Umea, Sweden.	Thomas.sandstrom@lung.umu.se	Kelly, Frank/C-6125-2009	Kelly, Frank/0000-0003-2558-8392; Blomberg, Anders/0000-0002-2452-7347; Stenfors, Nikolai/0000-0002-1684-1301			Barnes PJ, 1998, MOL MED TODAY, V4, P452, DOI 10.1016/S1357-4310(98)01335-5; Bascom R, 1996, AM J RESP CRIT CARE, V153, P3; Boezen M, 1998, AM J RESP CRIT CARE, V158, P1848; Borish L, 1996, J ALLERGY CLIN IMMUN, V97, P1288, DOI 10.1016/S0091-6749(96)70197-5; DiazSanchez D, 1997, ALLERGY, V52, P52; Jeannin P, 1998, J IMMUNOL, V160, P3555; Knox RB, 1997, CLIN EXP ALLERGY, V27, P246; MONTEFORT S, 1994, J CLIN INVEST, V93, P1411, DOI 10.1172/JCI117118; Nightingale JA, 2000, AM J RESP CRIT CARE, V162, P161; *NIH NAT HEART LAB, 1995, GLOB STRAT ASTHM MAN; RUDELL B, 1994, INT ARCH OCC ENV HEA, V66, P77, DOI 10.1007/BF00383361; Rudell B, 1990, J AEROSOL SCI     S1, V21, P411; Salvi S, 1999, AM J RESP CELL MOL, V20, P984; Salvi S, 1999, AM J RESP CRIT CARE, V159, P702; Salvi SS, 2000, AM J RESP CRIT CARE, V161, P550; Sanchez-Guerrero I, 1997, Allergol Immunopathol (Madr), V25, P98; SCHROEDER WH, 1987, JAPCA J AIR WASTE MA, V37, P1267; SCHWARTZ J, 1993, AM REV RESPIR DIS, V147, P826; Takanashi S, 1999, EUR RESPIR J, V14, P309, DOI 10.1034/j.1399-3003.1999.14b12.x; THOMPSONSNIPES LA, 1991, J EXP MED, V173, P507, DOI 10.1084/jem.173.2.507	20	154	159	2	10	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.	JAN	2004	23	1					82	86		10.1183/09031936.03.00004603		5	Respiratory System	Respiratory System	763KA	WOS:000188083000017	14738236	
J	Untersmayr, E; Scholl, I; Swoboda, I; Beil, WJ; Forster-Waldl, E; Walter, F; Riemer, A; Kraml, G; Kinaciyan, T; Spitzauer, S; Boltz-Nitulescu, G; Scheiner, O; Jensen-Jarolim, E				Untersmayr, E; Scholl, I; Swoboda, I; Beil, WJ; Forster-Waldl, E; Walter, F; Riemer, A; Kraml, G; Kinaciyan, T; Spitzauer, S; Boltz-Nitulescu, G; Scheiner, O; Jensen-Jarolim, E			Antacid medication inhibits digestion of dietary proteins and causes food allergy: A fish allergy model in Balb/c mice	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						food allergy; caviar; parvalbumin; IgE; nutrition; antacids; digestion; animal model	PEANUT; HYPERSENSITIVITY; DIGESTIBILITY; EPIDEMIOLOGY; INTOLERANCE; PREVALENCE; POPULATION; RESPONSES; EPITOPES; EXPOSURE	Background: Digestible proteins were supposed to be irrelevant for oral sensitization and induction of food allergy. Approximately 10% of the adult population uses antacids for the treatment of dyspeptic disorders, drugs that hinder peptic digestion. In these patients, proteins that are normally degradable might act as food allergens. Objective: We aimed to study the influence of antacid intake on the allergenicity of dietary proteins, taking sturgeon caviar and parvalbumin, the major fish allergen, as examples. Methods: Caviar proteins and recombinant parvalbumin from carp, rCyp c 1, were applied for intragastric feedings with or without the antacids sucralfate, ranitidine or omeprazole, using a Balb/c mouse model. Results: Both caviar proteins and parvalbumin were rapidly degraded in an in vitro digestion assay at pH 2.0, but not at pH 5.0, imitating the effect of antacids. The groups fed with caviar in combination with ranitidine hydrochloride intramuscularly or sucralfate orally had significant levels of caviar-specific IgE antibodies (P < .01), T-cell reactivity, and elevated counts of gastrointestinal eosinophils and mast cells. Food allergy in these groups was further evidenced by oral provocation tests and positive immediate-type skin reactivity. In contrast, feedings with caviar alone led to antigen-specific T-cell tolerance. None of the groups showed immune reactivity against the daily mouse diet. As a proof of the principle, feeding mice with parvalbumin in combination with ranitidine or omeprazole intramuscularly induced allergen-specific IgE antibodies (P < .05). Conclusions: When antacid medication impairs the gastric digestion, IgE synthesis toward novel dietary proteins is promoted, leading to food allergy.	Univ Vienna, Dept Pathophysiol, A-1090 Vienna, Austria; Univ Vienna, Dept Clin Chem & Lab Med, Vienna, Austria; Univ Vienna, Dept Pathol, Vienna, Austria; Univ Vienna, Dept Pediat & Juvenile Med, Vienna, Austria; Univ Vienna, Dept Dermatol, Vienna, Austria; Tech Univ Vienna, A-1060 Vienna, Austria	Jensen-Jarolim, E (reprint author), Univ Vienna, Dept Pathophysiol, AKH-3Q,Waehringer Guertel 18-20, A-1090 Vienna, Austria.		Osborne, Nicholas/N-4915-2015	Osborne, Nicholas/0000-0002-6700-2284			AAS K, 1969, J ALLERGY, V44, P333, DOI 10.1016/0021-8707(69)90025-2; AMLOT PL, 1987, CLIN ALLERGY, V17, P33, DOI 10.1111/j.1365-2222.1987.tb02317.x; Astwood JD, 1996, NAT BIOTECHNOL, V14, P1269, DOI 10.1038/nbt1096-1269; Beil Waltraud J., 1997, Histochemical Journal, V29, P759, DOI 10.1023/A:1026421303260; BERNHISELBROADBENT J, 1992, J ALLERGY CLIN IMMUN, V89, P730, DOI 10.1016/0091-6749(92)90381-B; Bindslev-Jensen C, 2001, ALLERGY, V56, P75, DOI 10.1034/j.1398-9995.2001.00922.x; Bischoff SC, 1997, GUT, V40, P745; BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1006/abio.1976.9999; Brewer JM, 1999, J IMMUNOL, V163, P6448; BRUIJNZEELKOOMEN C, 1995, ALLERGY, V50, P623, DOI 10.1111/j.1398-9995.1995.tb02579.x; Dearman RJ, 2002, FOOD CHEM TOXICOL, V40, P625, DOI 10.1016/S0278-6915(01)00132-6; Dearman RJ, 2001, TOXICOLOGY, V167, P217, DOI 10.1016/S0300-483X(01)00462-0; Fu TT, 2002, J AGR FOOD CHEM, V50, P7154, DOI 10.1021/jf020599h; Furu K, 1999, J CLIN EPIDEMIOL, V52, P509, DOI 10.1016/S0895-4356(99)00020-7; GARNETT W R, 1982, Clinical Pharmacy, V1, P307; Hong SJ, 1999, J ALLERGY CLIN IMMUN, V104, P473, DOI 10.1016/S0091-6749(99)70396-9; JANSEN JJN, 1994, J ALLERGY CLIN IMMUN, V93, P446; Jensen-Jarolim E, 1999, FASEB J, V13, P1586; Jensen-Jarolim E, 1999, CLIN EXP ALLERGY, V29, P1075, DOI 10.1046/j.1365-2222.1999.00592.x; JensenJarolim E, 1997, CLIN EXP ALLERGY, V27, P1299, DOI 10.1046/j.1365-2222.1997.1580956.x; Kelly KJ, 2000, J PEDIAT GASTROENT S, V30, P28; LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0; Maleki SJ, 2000, J IMMUNOL, V164, P5844; PEDEN NR, 1979, LANCET, V1, P690; PRICHARD PJ, 1985, GASTROENTEROLOGY, V88, P64; Sampson HA, 1996, PEDIAT ALLERG IMM-UK, V7, P42, DOI 10.1111/j.1399-3038.1996.tb00394.x; Schafer T, 2001, ALLERGY, V56, P1172, DOI 10.1034/j.1398-9995.2001.00196.x; SCHOLL I, 2002, CLIN EXP ALLERGY, V323, P1583; Sicherer SH, 1999, J ALLERGY CLIN IMMUN, V103, P559, DOI 10.1016/S0091-6749(99)70224-1; Straumann A, 2001, J ALLERGY CLIN IMMUN, V108, P954, DOI 10.1067/mai.2001.119917; Svensson L, 2003, IMMUNOLOGY, V108, P98, DOI 10.1046/j.1365-2567.2003.01561.x; Swoboda I, 2002, J IMMUNOL, V168, P4576; TOWBIN H, 1979, P NATL ACAD SCI USA, V76, P4350, DOI 10.1073/pnas.76.9.4350; Untersmayr E, 2002, J ALLERGY CLIN IMMUN, V109, P1034, DOI 10.1067/mai.2002.124893; Valenta R, 1996, J ALLERGY CLIN IMMUN, V97, P893, DOI 10.1016/S0091-6749(96)80062-5; Wiedermann U, 1998, CLIN EXP IMMUNOL, V111, P144; Yagami T, 2000, J ALLERGY CLIN IMMUN, V106, P752, DOI 10.1067/mai.2000.109171; Zivny JH, 2001, CLIN IMMUNOL, V101, P158, DOI 10.1006/clim.2001.5103	38	154	159	1	17	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	SEP	2003	112	3					616	623		10.1016/mai.2003.1681		8	Allergy; Immunology	Allergy; Immunology	719XW	WOS:000185231200024	13679824	
J	Gehring, U; Bolte, G; Borte, M; Bischof, W; Fahlbusch, B; Wichmann, HE; Heinrich, J				Gehring, U; Bolte, G; Borte, M; Bischof, W; Fahlbusch, B; Wichmann, HE; Heinrich, J		LISA Study Grp	Exposure to endotoxin decreases the risk of atopic eczema in infancy: A cohort study	JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY			English	Article						endotoxin; house dust; atopic eczema; infections; wheezing; infancy	HOUSE-DUST; HAY-FEVER; ALLERGIC SENSITIZATION; ASTHMA; CHILDREN; DERMATITIS; CHILDHOOD; ENVIRONMENT; COMMUNITY; SYMPTOMS	Background: Previous studies have shown a protective effect of early exposure to cats and dogs on the development of atopic eczema, asthma, allergic rhinitis, and atopic sensitization in later life. In particular, a higher microbial exposure to endotoxin in early childhood might contribute to this effect. Objective: We examined the associations between bacterial endotoxin in house dust and atopic eczema, infections, and wheezing during the first year of life in an ongoing birth cohort study (LISA). Methods: Data of 1884 term and normal-weight neonates with complete information on exposure to biocontaminants and confounding variables were analyzed. House dust from the mothers' and the children's mattresses was sampled 3 months after birth. Endotoxin content was quantified by using a chromogenic kinetic limulus amoebocyte lysate test. Results: During the first 6 months of life, the risk of atopic eczema was significantly decreased by endotoxin exposure in dust from mothers' mattresses in the fifth quintile (odds ratio [OR], 0.50; 95% CI, 0.28-0.88), whereas the risk was increased for respiratory infections (OR, 1.69; 95% CI, 1.25-2.28) and cough with respiratory infection, bronchitis, or both (OR, 1.73; 95% CI, 1.28-2.33). The risk of wheezing was also significantly increased during the first 6 months of life (OR, 2.37; 95% CI, 1.40-4.03). For the entire first year of life, these associations attenuated, except for the risk of wheezing, which remained significant (OR, 1.60; 95% CI, 1.10-2.30). Conclusion: Our findings support the hygiene hypothesis that exposure to high concentrations of endotoxin very early in life might protect against the development of atopic eczema within the first 6 months of life, along with an increased prevalence of nonspecific respiratory diseases.	GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, D-85764 Neuherberg, Germany; Univ Munich, Inst Med Data Management Biometr & Epidemiol, Chair Epidemiol, Munich, Germany; Univ Leipzig, Dept Pediat, D-7010 Leipzig, Germany; Univ Jena, Inst Clin Immunol, D-6900 Jena, Germany; Univ Jena, Inst Occupat Social & Enviornm Med, Dept Indoor Climatol Ark, Erfurt, Germany	Gehring, U (reprint author), GSF, Natl Res Ctr Environm & Hlth, Inst Epidemiol, Ingolstaedter Landstr 1, D-85764 Neuherberg, Germany.			Gehring, Ulrike/0000-0003-3612-5780			Asher MI, 1998, EUR RESPIR J, V12, P315; Bergmann RL, 1998, CLIN EXP ALLERGY, V28, P965; Bischof W, 2000, P HLTH BUILDINGS, V1, P251; Bjorksten B, 1999, P NUTR SOC, V58, P729, DOI 10.1017/S0029665199000956; Bonifazi E, 1989, Acta Derm Venereol Suppl (Stockh), V144, P20; Braun-Fahrlander C, 1999, CLIN EXP ALLERGY, V29, P28; Burney P, 1996, EUR RESPIR J, V9, P687; Douwes J, 2000, AM J RESP CRIT CARE, V162, P1348; 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; Gereda JE, 2000, LANCET, V355, P1680, DOI 10.1016/S0140-6736(00)02239-X; Gereda JE, 2001, J ALLERGY CLIN IMMUN, V107, P790, DOI 10.1067/mai.2001.115245; GUILLET G, 1992, ARCH DERMATOL, V128, P187, DOI 10.1001/archderm.128.2.187; HEINRICH J, IN PRESS CLIN EXP AL; Hesselmar B, 1999, CLIN EXP ALLERGY, V29, P611; Holgate ST, 1999, NATURE, V402, pB2; 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; Kaliomaki M, 2001, LANCET, V357, P1076; Kimpen JLL, 2000, AM J RESP CRIT CARE, V162, pS108; KJELLMAN B, 1994, ACTA PAEDIATR, V83, P229, DOI 10.1111/j.1651-2227.1994.tb13057.x; MARTINEZ FD, 1995, NEW ENGL J MED, V332, P133, DOI 10.1056/NEJM199501193320301; Martinez FD, 1999, LANCET S2, V354, pSII12; Michel O, 1996, AM J RESP CRIT CARE, V154, P1641; MICHEL O, 1989, J APPL PHYSIOL, V66, P1059; Nafstad P, 2001, ALLERGY, V56, P307, DOI 10.1034/j.1398-9995.2001.00881.x; Park JH, 2001, AM J RESP CRIT CARE, V163, P322; Queille-Roussel C, 1985, Acta Derm Venereol Suppl (Stockh), V114, P87; Riedler J, 2000, CLIN EXP ALLERGY, V30, P194; Rizzo MC, 1997, PEDIATR ALLERGY IMMU, V8, P121; STRACHAN DP, 1989, BRIT MED J, V299, P1259; Svanes C, 1999, J ALLERGY CLIN IMMUN, V103, P415, DOI 10.1016/S0091-6749(99)70465-3; Tulic MK, 2000, AM J RESP CELL MOL, V22, P604; von Mutius E, 2000, CLIN EXP ALLERGY, V30, P1230; WRIGHT AL, 1989, AM J EPIDEMIOL, V129, P1232; YATES VM, 1983, BRIT J DERMATOL, V108, P633, DOI 10.1111/j.1365-2133.1983.tb01074.x	36	154	155	0	9	MOSBY, INC	ST LOUIS	11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA	0091-6749			J ALLERGY CLIN IMMUN	J. Allergy Clin. Immunol.	NOV	2001	108	5					847	854		10.1067/mai.2001.119026		8	Allergy; Immunology	Allergy; Immunology	498RG	WOS:000172523800029	11692114	
J	Miller, RL; Ho, SM				Miller, Rachel L.; Ho, Shuk-mei			Environmental epigenetics and asthma - Current concepts and call for studies	AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE			English	Article						epigenetics; asthma; DNA methylation; gene-environment interactions	SCHOOL-AGE-CHILDREN; LOW-BIRTH-WEIGHT; SERUM IGE LEVELS; IFN-GAMMA GENE; CHILDHOOD ASTHMA; LUNG-FUNCTION; TOBACCO-SMOKE; ALLERGIC DISEASE; MATERNAL SMOKING; DNA METHYLATION	Recent studies suggest that epigenetic regulation (heritable changes in gene expression that occur in the absence of alterations in DNA sequences) may in part mediate the complex gene-by-environment interactions that can lead to asthma. The variable natural history of asthma (i.e., incidence and remission of symptoms) may be a result of epigenetic changes, such as DNA methylation, covalent histone modifications, microRNA changes, and chromatin alterations, after early or later environmental exposures. Findings from multiple epidemiologic and experimental studies indicate that asthma risk may be modified by epigenetic regulation. One study suggested that the transmission of asthma risk may occur across multiple generations. Experimental studies provide substantial in vitro data indicating that DNA methylation of genes critical to T-helper cell differentiation may induce polarization toward or away from an allergic phenotype. Despite this initial progress, fundamental questions remain that need to be addressed by well-designed research studies. Data generated from controlled experiments using in vivo models and/or clinical specimens collected after environmental exposure monitoring are limited. Importantly, cohort-driven epigenetic research has the potential to address key questions, such as those concerning the influence of timing of exposure, dose of exposure, diet, and ethnicity on susceptibility to asthma development. There is immense promise that the study of environmental epigenetics will help us understand a theoretically preventable environmental disease.	[Miller, Rachel L.] Columbia Univ Coll Phys & Surg, Dept Med, Div Pulm Allergy & Crit Care Med, New York, NY 10032 USA; [Ho, Shuk-mei] Univ Cincinnati, Coll Med, Dept Environm Hlth, Cincinnati, OH 45267 USA; [Ho, Shuk-mei] Univ Cincinnati, Coll Med, Ctr Canc, Cincinnati, OH 45267 USA	Miller, RL (reprint author), Columbia Univ Coll Phys & Surg, Dept Med, Div Pulm Allergy & Crit Care Med, PH8E,630 W 168th St, New York, NY 10032 USA.	rlm14@columbia.edu			NIEHS NIH HHS [ES006096, ES013071, ES013163, ES015584, ES015905, P30 ES006096, P50 ES015905, P50 ES015905-010001, R01 ES013163, R01 ES013163-01A1, ES013063, R01 ES013163-05]		Agarwal S, 1998, IMMUNITY, V9, P765, DOI 10.1016/S1074-7613(00)80642-1; Alati R, 2006, EPIDEMIOLOGY, V17, P138, DOI 10.1097/01.ede.0000198148.02347.33; Anand D, 2003, ARCH DIS CHILD, V88, P135, DOI 10.1136/adc.88.2.135; BARKER DJP, 1991, BRIT MED J, V303, P671; Barr RG, 2001, CHEST, V120, P1474, DOI 10.1378/chest.120.5.1474; Bernstein DI, 2006, ANN ALLERG ASTHMA IM, V97, P800; 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J. Respir. Crit. Care Med.	MAR 15	2008	177	6					567	573		10.1164/rccm.200710-1511PP		7	Critical Care Medicine; Respiratory System	General & Internal Medicine; Respiratory System	272IB	WOS:000253852000004	18187692	
J	Chauhan, AJ; Inskip, HM; Linaker, CH; Smith, S; Schreiber, J; Johnston, SL; Holgate, ST				Chauhan, AJ; Inskip, HM; Linaker, CH; Smith, S; Schreiber, J; Johnston, SL; Holgate, ST			Personal exposure to nitrogen dioxide (NO2) and the severity of virus-induced asthma in children	LANCET			English	Article							RESPIRATORY SYMPTOMS; AIR-POLLUTION; RISK-FACTORS; IN-VITRO; ASSOCIATION; INFECTION; COOKING; ADULTS; CELLS; GAS	Background A link between exposure to the air pollutant nitrogen dioxide (NO2) and respiratory disease has been suggested. Viral infections are the major cause of asthma exacerbations. We aimed to assess whether there is a relation between NO2 exposure and the severity of asthma exacerbations caused by proven respiratory viral infections in children. Methods A cohort of 114 asthmatic children aged between 8 and 11 years recorded daily upper and lower respiratory-tract symptoms, peak expiratory flow (PEF), and measured personal NO2 exposures every week for up to 13 months. We took nasal aspirates during reported episodes of upper respiratory-tract illness and tested for infection by common respiratory viruses and atypical bacteria with RT-PCR assays. We used generalised estimating equations to assess the relation between low (<7.5 &mu;g/m(3) medium (7.5-14 &mu;g/m(3)), and high (>14 mug/m(3)) tertiles of NO2 exposure in the week before or after upper respiratory-tract infection and the severity of asthma exacerbation in the week after the start of an infection. Findings One or more viruses were detected in 78% of reported infection episodes, and the medians of NO2 exposure were 5 (IQR 3.6-6.3), 10 (8.7-12.0), and 21 mug/m(3) (16.8-42.9) for low, medium, and high tertiles, respectively. There were significant increases in the severity of lower respiratory-tract symptom scores across the three tertiles (0.6 for all viruses [p=0.05] and >2 for respiratory syncytial virus [p=0.01]) and a reduction in PEF of more than 12 L/min for picornavirus (p=0.04) for high compared with low NO2 exposure before the start of the virus-induced exacerbation. Interpretation High exposure to NO2 in the week before the start of a respiratory viral infection, and at levels within current air quality standards, is associated with an increase in the severity of a resulting asthma exacerbation.	Univ Southampton, Resp Cell & Mol Biol Res Div, Southampton, Hants, England; Univ Southampton, MRC, Environm Epidemiol Unit, Southampton, Hants, England; Natl Heart & Lung Inst, London, England; Univ London Imperial Coll Sci Technol & Med, Wright Fleming Inst Infect & Immun, London, England	Chauhan, AJ (reprint author), St Marys Hosp, Portsmouth PO3 6AD, Hants, England.		Johnston, Sebastian/I-2423-2012	Inskip, Hazel/0000-0001-8897-1749			*ADV GROUP MED ASP, 1993, 3 DEP HLTH ADV GROUP, P29; Ando M, 2001, ARCH ENVIRON HEALTH, V56, P227; Boezen HM, 1999, LANCET, V353, P874, DOI 10.1016/S0140-6736(98)06311-9; BRUNEKREEF B, 1982, INT ARCH OCC ENV HEA, V50, P299, DOI 10.1007/BF00378091; CARSON JL, 1993, AM J RESP CELL MOL, V9, P264; Chauhan A. 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J	Tomioka, S; Bates, JHT; Irvin, CG				Tomioka, S; Bates, JHT; Irvin, CG			Airway and tissue mechanics in a murine model of asthma: alveolar capsule vs. forced oscillations	JOURNAL OF APPLIED PHYSIOLOGY			English	Article						airway resistance; tissue elastance; lung impedance; antigen challenge; inflammation	RESPIRATORY SYSTEM MECHANICS; INDUCED CONSTRICTION; LUNG-MECHANICS; DRY AIR; RATS; BRONCHOCONSTRICTION; HISTAMINE; IMPEDANCE; PRESSURE; BEHAVIOR	To better address the functional consequences of inflammation on bronchial responsiveness, we studied two groups of BALB/c mice: a nonimmunized control group (n = 8) and a group immunized and challenged with inhaled ovalbumin (n = 8). An alveolar capsule (AC) measured airway resistance (Raw(AC)) and lung elastance (EL). A forced oscillation (FO) technique independently estimated airway resistance (RawFO) and a parameter H-ti related to tissue elastance. Ovalbumin-immunized and -challenged mice had increased numbers of eosinophils in bronchoalveolar lavage and increased responsiveness to methacholine (MCh). Corresponding parameters from the AC and FO techniques were correlated: RawAC vs. RawFO (r = 0.76) and EL vs. H-ti (r = 0.88, P < 0.0001 in all cases). AC and FO techniques showed significant increases in tissue elastance in response to MCh but no significant increases in airway resistance. These results demonstrated that the AC and FO techniques yield essentially equivalent results in mice, even when the lung is inhomogeneous, and that the bronchoconstrictive responses to MCh and inflammation in mice are predominantly located in the lung periphery.	Univ Vermont, Dept Med, Fletcher Allen Hlth Care, Vermont Lung Ctr, Burlington, VT 05405 USA	Irvin, CG (reprint author), Univ Vermont, Dept Med, Fletcher Allen Hlth Care, Vermont Lung Ctr, Burlington, VT 05405 USA.				NHLBI NIH HHS [HL-62746, HL-67273]; PHS HHS [P01 15557]		CARROLL N, 1993, AM REV RESPIR DIS, V147, P405; Duguet A, 2000, AM J RESP CRIT CARE, V161, P839; FREDBERG JJ, 1984, J APPL PHYSIOL, V57, P788; FREDBERG JJ, 1985, J APPL PHYSIOL, V58, P1914; Gomes RFM, 2000, J APPL PHYSIOL, V89, P908; HANTOS Z, 1987, J APPL PHYSIOL, V63, P36; HANTOS Z, 1995, J APPL PHYSIOL, V79, P1440; HANTOS Z, 1992, J APPL PHYSIOL, V72, P168; Hirai T, 1999, J APPL PHYSIOL, V86, P16; Homma T, 1999, EUR RESPIR J, V13, P313, DOI 10.1034/j.1399-3003.1999.13b16.x; IRVIN CG, 1984, J APPL PHYSIOL, V57, P168; Irvin CG, 1997, AM J PHYSIOL-LUNG C, V272, pL1053; KAMINSKY DA, 1995, AM J RESP CRIT CARE, V152, P1784; Kaminsky DA, 1997, AM J RESP CRIT CARE, V155, P1260; Kaminsky DA, 2000, AM J RESP CRIT CARE, V162, P179; Kraft M, 1996, AM J RESP CRIT CARE, V154, P1505; LAUZON AM, 1991, J APPL PHYSIOL, V71, P1159; LAUZON AM, 1995, RESP PHYSIOL, V99, P139, DOI 10.1016/0034-5687(94)00087-G; LUDWIG MS, 1987, J APPL PHYSIOL, V62, P807; LUDWIG MS, 1989, J APPL PHYSIOL, V67, P1220; Lutchen KR, 1996, J APPL PHYSIOL, V80, P1841; LUTCHEN KR, 1994, J APPL PHYSIOL, V77, P373; MISHIMA M, 1994, J APPL PHYSIOL, V77, P2140; MORENO RH, 1986, AM REV RESPIR DIS, V133, P1171; NAGASE T, 1994, J APPL PHYSIOL, V76, P830; Nagase T, 1996, J APPL PHYSIOL, V81, P2373; NAGASE T, 1994, AM J RESP CRIT CARE, V150, P218; NAGASE T, 1992, J APPL PHYSIOL, V73, P1900; Persson CGA, 1997, TRENDS PHARMACOL SCI, V18, P465; Petak F, 1998, J APPL PHYSIOL, V84, P1680; Petak F, 1997, J APPL PHYSIOL, V82, P1479; PETAK F, 1993, J APPL PHYSIOL, V75, P513; Phillips CG, 1995, RESP PHYSIOL, V102, P303, DOI 10.1016/0034-5687(95)00056-9; RODARTE JR, 1985, J APPL PHYSIOL, V58, P164; SCHUESSLER TF, 1995, IEEE T BIO-MED ENG, V42, P860, DOI 10.1109/10.412653; SHARDONOFSKY FR, 1993, J APPL PHYSIOL, V75, P2506; SIMILOWSKI T, 1991, EUR RESPIR J, V4, P353; Takeda K, 1997, J EXP MED, V186, P449, DOI 10.1084/jem.186.3.449; TU YP, 1995, EUR RESPIR REV, V5, P224	39	153	157	0	5	AMER PHYSIOLOGICAL SOC	BETHESDA	9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA	8750-7587			J APPL PHYSIOL	J. Appl. Physiol.	JUL	2002	93	1					263	270		10.1152/japplphysiol.01129.2001		8	Physiology; Sport Sciences	Physiology; Sport Sciences	563JV	WOS:000176253300034	12070213	
J	Wargocki, P; Sundell, J; Bischof, W; Brundrett, G; Fanger, PO; Gyntelberg, F; Hanssen, SO; Harrison, P; Pickering, A; Seppanen, O; Wouters, P				Wargocki, P; Sundell, J; Bischof, W; Brundrett, G; Fanger, PO; Gyntelberg, F; Hanssen, SO; Harrison, P; Pickering, A; Seppanen, O; Wouters, P			Ventilation and health in non-industrial indoor environments: report from a European Multidisciplinary Scientific Consensus Meeting (EUROVEN)	INDOOR AIR			English	Review						ventilation; outdoor air supply rate; ventilation system; non-industrial indoor environments; offices; schools; homes; health; EUROVEN	SICK-BUILDING-SYNDROME; AIR-EXCHANGE-RATE; VOLATILE ORGANIC-COMPOUNDS; SYNDROME SBS SYMPTOMS; FACIAL SKIN SYMPTOMS; OFFICE BUILDINGS; PERSONAL FACTORS; CASE-REFERENT; CO2 CONCENTRATIONS; RISK INDICATORS	Scientific literature on the effects of ventilation on health, comfort, and productivity in non-industrial indoor environments (offices, schools, homes, etc.) has been reviewed by a multidisciplinary group of European scientists, called EUROVEN, with expertise in medicine, epidemiology, toxicology, and engineering. The group reviewed 105 papers published in peer-reviewed scientific journals and judged 30 as conclusive, providing sufficient information on ventilation, health effects, data processing, and reporting, 14 as providing relevant background information on the issue, 43 as relevant but non-informative or inconclusive, and 18 as irrelevant for the issue discussed. Based on the data in papers judged conclusive, the group agreed that ventilation is strongly associated with comfort (perceived air quality) and health [Sick Building Syndrome (SBS) symptoms, inflammation, infections, asthma, allergy, short-term sick leave], and that an association between ventilation and productivity (performance of office work) is indicated. The group also concluded that increasing outdoor air supply rates in non-industrial environments improves perceived air quality; that outdoor air supply rates below 25 l/s per person increase the risk of SBS symptoms, increase short-term sick leave, and decrease productivity among occupants of office buildings; and that ventilation rates above 0.5 air changes per hour (h(-1) ) in homes reduce infestation of house dust mites in Nordic countries. The group concluded additionally that the literature indicates that in buildings with air-conditioning systems there may be an increased risk of SBS symptoms compared with naturally or mechanically ventilated buildings, and that improper maintenance, design, and functioning of air-conditioning systems contributes to increased prevalence of SBS symptoms.	Tech Univ Denmark, Int Ctr Indoor Environm & Energy, DK-2800 Lyngby, Denmark; Univ Jena, Erfurt, Germany; Royal Soc Hlth, London, England; Bispebjerg Hosp, DK-2400 Copenhagen, Denmark; Norwegian Univ Sci & Technol, N-7034 Trondheim, Norway; MRC, Inst Environm & Hlth, Leicester, Leics, England; Wythenshawe Hosp, Manchester M23 9LT, Lancs, England; Helsinki Univ Technol, FIN-02150 Espoo, Finland; Belgian Bldg Res Inst, Brussels, Belgium	Wargocki, P (reprint author), Tech Univ Denmark, Int Ctr Indoor Environm & Energy, Bldg 402, DK-2800 Lyngby, Denmark.		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J	Wayne, P; Foster, S; Connolly, J; Bazzaz, F; Epstein, P				Wayne, P; Foster, S; Connolly, J; Bazzaz, F; Epstein, P			Production of allergenic pollen by ragweed (Ambrosia artemisiifolia L.) is increased in CO2-enriched atmospheres	ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY			English	Article							ELEVATED CO2; GROWTH; CLIMATE; PLANTS; REPRODUCTION; METAANALYSIS; ASTERACEAE; BIOLOGY; GENDER; HEALTH	Background: The potential effects of global climate change on allergenic pollen production are still poorly understood. Objective: To study the direct impact of rising atmospheric CO2 concentrations on ragweed (Ambrosia artemisiifolia L.) pollen production and growth. Methods: In environmentally controlled greenhouses, stands of ragweed plants were grown from seed through flowering stages at both ambient and twice-ambient CO2 levels (350 vs 700 muL L-1). Outcome measures included stand-level total pollen production and end-of-season measures of plant mass,, height, and seed production. Results: A doubling of the atmospheric CO2 concentration stimulated ragweed-pollen production by 61% (P = 0.005). Conclusions: These results suggest that there may be significant increases in exposure to allergenic pollen under the present scenarios of global warming. Further studies may enable public health groups to more accurately evaluate the future risks of hay fever and respiratory diseases (eg, asthma) exacerbated by allergenic pollen, and to develop strategies to mitigate them.	Harvard Univ, Dept Organism & Evolutionary Biol, Cambridge, MA 02138 USA; Univ Coll Dublin, Dept Stat, Dublin 2, Ireland; Harvard Univ, Sch Med, Ctr Hlth & Global Environm, Boston, MA USA	Wayne, P (reprint author), New England Sch Acupuncture, Dept Res, Watertown, MA 02472 USA.	pwayne@nesa.edu					ABULFATIH HA, 1979, NEW PHYTOL, V83, P829, DOI 10.1111/j.1469-8137.1979.tb02314.x; ACKERLY DD, 1995, GLOB CHANGE BIOL, V1, P199, DOI 10.1111/j.1365-2486.1995.tb00021.x; ACKERLY DD, 1990, OECOLOGIA, V82, P474, DOI 10.1007/BF00319788; Amthor J. S., 1997, Advances in carbon dioxide effects research. Proceedings of a symposium, Cincinnati, Ohio, USA, 7-12 November 1993., P35; ARRIGHI HM, 1995, ANN ALLERG ASTHMA IM, V74, P321; BASSETT IJ, 1975, CAN J PLANT SCI, V55, P463; BAZZAZ FA, 1982, OECOLOGIA, V54, P313, DOI 10.1007/BF00379999; BAZZAZ FA, 1990, ANNU REV ECOL SYST, V21, P167, DOI 10.1146/annurev.es.21.110190.001123; CONROY JP, 1994, AUST J PLANT PHYSIOL, V21, P741; Curtis PS, 1998, OECOLOGIA, V113, P299, DOI 10.1007/s004420050381; Curtis PS, 1996, PLANT CELL ENVIRON, V19, P127, DOI 10.1111/j.1365-3040.1996.tb00234.x; DAMATO G, 1994, CLIN EXP ALLERGY, V24, P566, DOI 10.1111/j.1365-2222.1994.tb00954.x; Emberlin J, 1997, GRANA, V36, P29; EMBERLIN J, 1994, ALLERGY, V49, P15, DOI 10.1111/j.1398-9995.1994.tb04233.x; Epstein PR, 1999, SCIENCE, V285, P347, DOI 10.1126/science.285.5426.347; EPSTEIN PR, 1995, AM J PUBLIC HEALTH, V85, P168, DOI 10.2105/AJPH.85.2.168; FARNSWORTH EJ, 1995, OECOLOGIA, V104, P454, DOI 10.1007/BF00341343; Fitzpatrick Thomas B., 1996, Journal of Dermatology (Tokyo), V23, P816; GRIFFITH IJ, 1991, INT ARCH ALLER A IMM, V96, P296; Houghton JT, 1996, CLIMATE CHANGE 1995; HUNTLEY B, 1991, ANN BOT-LONDON, V67, P15; Jaeger S, 1996, GRANA, V35, P171, DOI [10.1080/00173139609429078, DOI 10.1080/00173139609429078]; Lewis W. H., 1983, AIRBORNE ALLERGENIC; LOEVINSOHN ME, 1994, LANCET, V343, P714, DOI 10.1016/S0140-6736(94)91586-5; MCKONE MJ, 1986, OECOLOGIA, V70, P63, DOI 10.1007/BF00377111; Naclerio RM, 1997, J ALLERGY CLIN IMMUN, V100, P293, DOI 10.1016/S0091-6749(97)70240-9; NICHOLLS N, 1993, LANCET, V342, P1284, DOI 10.1016/0140-6736(93)92368-4; [Anonymous], 1993, NIH PUBL; PAYNE WW, 1963, AM J BOT, V50, P872, DOI 10.2307/2439774; POORTER H, 1993, VEGETATIO, V104, P77, DOI 10.1007/BF00048146; RAYNAL DJ, 1973, ECOLOGY, V54, P1335, DOI 10.2307/1934196; REEKIE JYC, 1994, CAN J BOT, V72, P533; TYREE MT, 1993, VEGETATIO, V104, P47, DOI 10.1007/BF00048144; WUTHRICH B, 1991, ALLERGY CLIN IMMUNOL, V3, P41; ZISKA LH, 2000, WORLD RESOURCE REV, V12, P449	35	153	159	0	21	ELSEVIER SCIENCE INC	NEW YORK	360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA	1081-1206			ANN ALLERG ASTHMA IM	Ann. Allergy Asthma Immunol.	MAR	2002	88	3					279	282				4	Allergy; Immunology	Allergy; Immunology	532ZX	WOS:000174505900006	11926621	
J	Pajno, GB; Morabito, L; Barberio, G; Parmiani, S				Pajno, GB; Morabito, L; Barberio, G; Parmiani, S			Clinical and immunologic effects of long-term sublingual immunotherapy in asthmatic children sensitized to mites: a double-blind, placebo-controlled study	ALLERGY			English	Article						asthma; dust-mite allergy; sublingual immunotherapy (SLIT)	HOUSE-DUST MITE; DERMATOPHAGOIDES-PTERONYSSINUS EXTRACT; CONTROLLED TRIAL; POLLEN EXTRACT; SWALLOW IMMUNOTHERAPY; EFFICACY; RHINITIS; RHINOCONJUNCTIVITIS; INFLAMMATION	Background: Immunotherapy through local routes is thought to be a valuable therapeutic option for respiratory allergy. We investigated the clinical efficacy and immunologic effects of sublingual immunotherapy (SLIT) in asthmatic children with mite-induced respiratory allergy. Methods: Twenty-four patients (age range 8-15 years), suffering from mild to moderate asthma, with single sensitization to mite allergen, were enrolled. After a 1-year observation phase, patients were randomly allocated to one of two groups, and were given SLIT (sublingual-spit) as drops for 2 years according to a double-blind, placebo-controlled (DBPC) design. Symptoms/medication scores (diary card), visual analog scale, and immunologic parameters (house-dust-mite [HDM]-specific IgE, and total HDM-specific IgG and IgG4) were determined during the observation phase and during the DBPC treatment period. Results: Twenty-one patients completed the study. At the beginning of the treatment, no difference in environmental allergenic pressure could be shown between the groups. After 2 years of therapy, there was a significant decrease ill asthmatic symptoms (P = 0.0001) and medication use (P = 0.0001) in the active group compared to the placebo group. The visual analog score on overall asthma symptoms improved in the SLIT group (P = 0.0001), but not in the placebo group. Nevertheless, the immunologic results did not show significant differences in HDM-specific IgE and total HDM-specific IgG or IgG4 between the active and placebo groups (P = NS). No relevant side-effects were recorded throughout the study. Conclusions: Our results suggest that treatment for 2 years with SLIT is clinically safe and effective in significantly decreasing respiratory symptoms in children with mild to moderate asthma sensitized to HDM. On the other hand, the lack of changes of the immunologic parameters calls for further investigations with special reference to kinetics and mechanism(s) of action of this mode of treatment.	Univ Messina, Policlin Univ, Ist Clin Pediat, I-98124 Messina, Italy; ALK Abello SpA, Milan, Italy	Pajno, GB (reprint author), Univ Messina, Policlin Univ, Ist Clin Pediat, Via Consolare Valeria,Gazzi, I-98124 Messina, Italy.						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J	Cabana, MD; Ebel, BE; Cooper-Patrick, L; Powe, NR; Rubin, HR; Rand, CS				Cabana, MD; Ebel, BE; Cooper-Patrick, L; Powe, NR; Rubin, HR; Rand, CS			Barriers pediatricians face when using asthma practice guidelines	ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE			English	Article; Proceedings Paper	Annual Conference of the Society-for-Medical-Decision-Making	OCT 24-28, 1998	BOSTON, MASSACHUSETTS	Soc Med Decis Making			CLINICAL-PRACTICE GUIDELINES; INNER-CITY CHILDREN; PHYSICIANS ATTITUDES; RANDOMIZED TRIAL; CARE; IMPLEMENTATION; EDUCATION; INTERVENTION; MANAGEMENT; PARENTS	Objective: To describe barriers to the successful use of the 1997 National Heart, Lung, and Blood Institute (NHLBI) asthma guidelines. Methods; We conducted 3 focus groups to understand barriers to the use of 4 recommendations within the NHLBI guidelines (prescription of inhaled corticosteroids, recommendation of daily peak flowmeter use, smoking cessation screening and counseling, and allergen exposure counseling). Participants: Twenty-one pediatricians and 1 nurse practitioner, who each followed an average of 47 patients with asthma, participated. Six participants (27%) had a faculty or adjunct appointment at a medical school. Nineteen (90%) of the 21 pediatricians were board certified. Results: We identified 171 comments about barriers to adherence. Type of recommendation and physician year of graduation from medical school were related to which barrier was prominent. For corticosteroid prescription, senior physicians mentioned lack of agreement, whereas younger physicians described lack of confidence in dosing or recognizing contraindications. For peak flowmeter use, senior physicians emphasized lack of training. Only senior physicians described the inertia of previous practice as a barrier. All groups mentioned time limitations. Conclusions: Efforts to improve adherence to asthma guidelines should consider the range of barriers that pediatricians face, such as lack of awareness, familiarity, or agreement, and external barriers owing to environmental, guideline, or patient factors. In addition, this study documents barriers not previously considered, such as lack of self-efficacy, lack of outcome expectancy, and inertia of previous practice, that prevent adherence, Be cause type of recommendation and physician demographics are related to which barriers are prominent, interventions to improve NHLBI guideline adherence should be tailored to these factors.	Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21205 USA; Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA; Johns Hopkins Sch Med, Robert Wood Johnson Clin Scholars Program, Baltimore, MD USA; Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Hlth Policy & Management, Baltimore, MD USA; Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Epidemiol, Baltimore, MD USA	Cabana, MD (reprint author), Univ Michigan, Dept Pediat & Communicable Dis, Div Gen Pediat, D3202 Med Profess Bldg,1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA.		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J	Darsow, U; Laifaoui, J; Kerschenlohr, K; Wollenberg, A; Przybilla, B; Wuthrich, B; Borelli, S; Giusti, F; Seidenari, S; Drzimalla, K; Simon, D; Disch, R; Borelli, S; Devillers, ACA; Oranje, AP; De Raeve, L; Hachem, JP; Dangoisse, C; Blondeel, A; Song, M; Breuer, K; Wulf, A; Werfel, T; Roul, S; Taieb, A; Bolhaar, S; Bruijnzeel-Koomen, C; Bronnimann, M; Braathen, LR; Didierlaurent, A; Andre, C; Ring, J				Darsow, U; Laifaoui, J; Kerschenlohr, K; Wollenberg, A; Przybilla, B; Wuthrich, B; Borelli, S; Giusti, F; Seidenari, S; Drzimalla, K; Simon, D; Disch, R; Borelli, S; Devillers, ACA; Oranje, AP; De Raeve, L; Hachem, JP; Dangoisse, C; Blondeel, A; Song, M; Breuer, K; Wulf, A; Werfel, T; Roul, S; Taieb, A; Bolhaar, S; Bruijnzeel-Koomen, C; Bronnimann, M; Braathen, LR; Didierlaurent, A; Andre, C; Ring, J			The prevalence of positive reactions in the atopy patch test with aeroallergens and food allergens in subjects with atopic eczema: a European multicenter study	ALLERGY			English	Article						aeroallergens; atopic eczema; atopy patch test; European multicenter	HOUSE-DUST MITE; EPIDERMAL LANGERHANS CELLS; DERMATITIS PATIENTS; DOUBLE-BLIND; SKIN; FREQUENCY; AVOIDANCE; INDUCTION; EXTRACTS; CHILDREN	Background: The atopy patch test (APT) was proposed to evaluate IgE-mediated sensitizations in patients with atopic eczema (AE). Objective: The prevalence and agreement with clinical history and specific IgE (sIgE) of positive APT reactions was investigated in six European countries using a standardized method. Methods: A total of 314 patients with AE in remission were tested in 12 study centers on clinically uninvolved, non-abraded back skin with 200 index of reactivity (IR)/g of house dust mite Dermatophagoides pteronyssinus, cat dander, grass, and birch pollen allergen extracts with defined major allergen contents in petrolatum. Extracts of egg white, celery and wheat flour with defined protein content were also patch tested. APT values were evaluated at 24, 48, and 72 h according to the European Task Force on Atopic Dermatitis (ETFAD) guidelines. In addition, skin-prick test (SPT) and sIgE and a detailed history on allergen-induced eczema flares were obtained. Results: Previous eczema flares, after contact with specific allergens, were reported in 1% (celery) to 34% (D. pteronyssinus) of patients. The frequency of clear-cut positive APT reactions ranged from 39% with D. pteronyssinus to 9% with celery. All ETFAD intensities occured after 48 and 72 h. Positive SPT (16-57%) and elevated sIgE (19-59%) results were more frequent. Clear-cut positive APT with all SPT and sIgE testing negative was seen in 7% of the patients, whereas a positive APT without SPT or sIgE for the respective allergen was seen in 17% of the patients. APT, SPT and sIgE results showed significant agreement with history for grass pollen and egg white (two-sided Pr > \Z\ less than or equal to 0.01). In addition, SPT and sIgE showed significant agreement with history for the other aeroallergens. With regard to clinical history, the APT had a higher specificity (64-91% depending on the allergen) than SPT (50-85%) or sIgE (52-85%). Positive APT were associated with longer duration of eczema flares and showed regional differences. In 10 non-atopic controls, no positive APT reaction was seen. Conclusion: Aeroallergens and food allergens are able to elicit eczematous skin reactions after epicutaneous application. As no gold standard for aeroallergen provocation in AE exists, the relevance of aeroallergens for AE flares may be evaluated by APT in addition to SPT and sIgE. The data may contribute to the international standardization of the APT.	Tech Univ Munich, Klin & Poliklin Dermatol & Allergol Biederstein, Dept Dermatol & Allergy Biederstein, D-80802 Munich, Germany; GSF TUM, Div Environm Dermatol & Allergy, Munich, Germany; Univ Munich, Dept Dermatol & Allergy, Munich, Germany; Univ Zurich Hosp, Dept Dermatol, CH-8091 Zurich, Switzerland; Univ Modena & Reggio Emilia, Dept Dermatol, Modena, Italy; Clin Dermatol & Allergy Davos, Davos, Switzerland; Ersamus MC Sophia Childrens Hosp, Rotterdam, Netherlands; Free Univ Brussels, Dept Dermatol, Brussels, Belgium; Queen Fabiola Childrens Univ Hosp, Brussels, Belgium; Hannover Med Sch, Dept Dermatol, D-3000 Hannover, Germany; Childrens Hosp Pellegrin, Dept Pediat Dermatol, Bordeaux, France; Univ Utrecht Hosp, Dept Dermatol, Utrecht, Netherlands; Univ Bern, Dept Dermatol, Bern, Switzerland; Stallergenes SA, Antony, France	Darsow, U (reprint author), Tech Univ Munich, Klin & Poliklin Dermatol & Allergol Biederstein, Dept Dermatol & Allergy Biederstein, Biedersteiner Str 29, D-80802 Munich, Germany.						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