9 results on '"SWISS COHORT"'
Search Results
2. Retrospective validation of the postnatal Growth and Retinopathy of Prematurity (G-ROP) criteria in a Swiss cohort
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Nithursa Vinayahalingam, Jane McDougall, Olaf Ahrens, and Andreas Ebneter
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Screening ,Retinopathy of Prematurity ,G-ROP ,Swiss Cohort ,Ophthalmology ,RE1-994 - Abstract
Abstract Background Currently used screening criteria for retinopathy of prematurity (ROP) show high sensitivity for predicting treatment-requiring ROP but low specificity; over 90% of examined infants do not develop ROP that requires treatment (type 1 ROP). A novel weight gain-based prediction model was developed by the G-ROP study group to increase the specificity of the screening criteria and keep the number of ophthalmic examinations as low as possible. This retrospective cohort study aimed to externally validate the G-ROP screening criteria in a Swiss cohort. Methods Data from 645 preterm infants in ROP screening at Inselspital Bern between January 2015 and December 2019 were retrospectively retrieved from the screening log and analysed. The G-ROP screening criteria, consisting of 6 trigger parameters, were applied in infants with complete data. To determine the performance of the G-ROP prediction model for treatment-requiring ROP, sensitivity and specificity were calculated. Results Complete data were available for 322 infants who were included in the analysis. None of the excluded infants had developed type 1 ROP. By applying the 6 criteria in the G-ROP model, 214 infants were flagged to undergo screening: among these, 14 developed type 1 ROP, 9 developed type 2 ROP, and 43 developed milder stages of ROP. The sensitivity for predicting treatment-requiring ROP was 100% (CI, 0.79–1.00), and the specificity was 41% (CI, 0.35 –0.47). Implementing the novel G-ROP screening criteria would reduce the number of infants entering ROP screening by approximately one third. Conclusions The overall prevalence of treatment-requiring ROP was low (2.15%). Previously published performance parameters for the G-ROP algorithm were reproducible in this Swiss cohort. Importantly, all treatment-requiring infants were correctly identified. By using these novel criteria, the burden of screening examinations could be significantly reduced.
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- 2022
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3. Swiss Cohort & Biobank – The White Paper
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Nicole Probst-Hensch, Murielle Bochud, Arnaud Chiolero, Luca Crivelli, Julia Dratva, Antoine Flahault, Daniel Frey, Nino Kuenzli, Milo Puhan, L. Suzanne Suggs, and Corina Wirth
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Swiss cohort ,biobank ,white paper ,public health ,health data ,personalized health ,Public aspects of medicine ,RA1-1270 - Published
- 2022
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4. Retrospective validation of the postnatal Growth and Retinopathy of Prematurity (G-ROP) criteria in a Swiss cohort.
- Author
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Vinayahalingam, Nithursa, McDougall, Jane, Ahrens, Olaf, and Ebneter, Andreas
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NEWBORN screening ,GESTATIONAL age ,RETROSPECTIVE studies ,RETROLENTAL fibroplasia ,BIRTH weight ,LONGITUDINAL method - Abstract
Background: Currently used screening criteria for retinopathy of prematurity (ROP) show high sensitivity for predicting treatment-requiring ROP but low specificity; over 90% of examined infants do not develop ROP that requires treatment (type 1 ROP). A novel weight gain-based prediction model was developed by the G-ROP study group to increase the specificity of the screening criteria and keep the number of ophthalmic examinations as low as possible. This retrospective cohort study aimed to externally validate the G-ROP screening criteria in a Swiss cohort.Methods: Data from 645 preterm infants in ROP screening at Inselspital Bern between January 2015 and December 2019 were retrospectively retrieved from the screening log and analysed. The G-ROP screening criteria, consisting of 6 trigger parameters, were applied in infants with complete data. To determine the performance of the G-ROP prediction model for treatment-requiring ROP, sensitivity and specificity were calculated.Results: Complete data were available for 322 infants who were included in the analysis. None of the excluded infants had developed type 1 ROP. By applying the 6 criteria in the G-ROP model, 214 infants were flagged to undergo screening: among these, 14 developed type 1 ROP, 9 developed type 2 ROP, and 43 developed milder stages of ROP. The sensitivity for predicting treatment-requiring ROP was 100% (CI, 0.79-1.00), and the specificity was 41% (CI, 0.35 -0.47). Implementing the novel G-ROP screening criteria would reduce the number of infants entering ROP screening by approximately one third.Conclusions: The overall prevalence of treatment-requiring ROP was low (2.15%). Previously published performance parameters for the G-ROP algorithm were reproducible in this Swiss cohort. Importantly, all treatment-requiring infants were correctly identified. By using these novel criteria, the burden of screening examinations could be significantly reduced. [ABSTRACT FROM AUTHOR]- Published
- 2022
- Full Text
- View/download PDF
5. Anti-myelin antibodies in clinically isolated syndrome indicate the risk of multiple sclerosis in a Swiss cohort.
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Greeve, I., Sellner, J., Lauterburg, T., Walker, U., Rösler, K. M., and Mattle, H. P.
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MULTIPLE sclerosis , *IMMUNOGLOBULINS , *GLYCOPROTEINS , *BASIC proteins , *INTERFERONS - Abstract
Objectives – In patients with a clinically isolated syndrome (CIS), the time interval to convert to clinically definite multiple sclerosis (CDMS) is highly variable. Individual and geographical prognostic factors remain to be determined. Whether anti-myelin antibodies may predict the risk of conversion to CDMS in Swiss CIS patients of the canton Berne was the subject of the study. Methods – Anti-myelin oligodendrocyte glycoprotein and anti-myelin basic protein antibodies were determined prospectively in patients admitted to our department. Results – After a mean follow-up of 12 months, none of nine antibody-negative, but 22 of 30 antibody-positive patients had progressed to CDMS. β-Interferon treatment delayed the time to conversion from a mean of 7.4 to 10.9 months. Conclusions – In a Swiss cohort, antibody-negative CIS patients have a favorable short-term prognosis, and antibody-positive patients benefit from early treatment. [ABSTRACT FROM AUTHOR]
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- 2007
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6. Genes Interacting with Occupational Exposures to Low Molecular Weight Agents and Irritants on Adult-Onset Asthma in Three European Studies
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Marie-Hélène Dizier, Rachel Nadif, Orianne Dumas, Amar J. Mehta, Ismaïl Ahmed, Jan-Paul Zock, Pascale Tubert-Bitter, Juan R. González, Medea Imboden, Emmanuelle Bouzigon, Ivan Curjuric, Deborah Jarvis, Florence Demenais, Marta Rava, Nicole Probst-Hensch, Nicole Le Moual, Manolis Kogevinas, Vieillissement et Maladies chroniques : approches épidémiologique et de santé publique (VIMA), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Spanish National Cancer Research Center (CNIO), Biostatistique, Biomathématique, Pharmacoépidémiologie et Maladies Infectieuses (B2PHI), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Center for Research in Environmental Epidemiology (CREAL), Universitat Pompeu Fabra [Barcelona] (UPF)-Catalunya ministerio de salud, Variabilité Génétique et Maladies Humaines, Institut Universitaire d'Hématologie (IUH), Université Paris Diderot - Paris 7 (UPD7)-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Epidemiology & Public Health [Basel, Switzerland], Swiss Tropical and Public Health Institute [Basel]-Medical School University of Basel, Department of Environmental Health [Boston, USA], Harvard School of Public Health, Centre for Research in Environmental Epidemiology (CREAL), Universitat Pompeu Fabra [Barcelona] (UPF), Respiratory Epidemiology and Public Health Group [London, U.K.], National Heart and Lung Institute-Imperial College London, U946, Fondation Jean Dausset/CEPH, Institut National de la Santé et de la Recherche Médicale (INSERM), The genotyping of all three studies was funded by the French National Agency of Research (ANR-PRSP 2009: IAGO), and by the European Commission (contract n° 018996) (GABRIEL) and the Wellcome Trust grant (WT 084703MA), both awarded to the GABRIEL consortium (a multidisciplinary study to identify the genetic and environmental causes of asthma in the European Community). EGEA: Research funded by the French Agency of health safety, environment and work (AFSSET, EST-09-15). SAPALDIA: The Swiss National Science Foundation (grants no 33CS30-148470/1, 33CSCO-134276/1, 33CSCO-108796, 324730_135673, 3247BO-104283, 3247BO-104288, 3247BO-104284, 3247-065896, 3100-059302, 3200-052720, 3200-042532, 4026-028099, PMPDP3_129021/1, PMPDP3_141671/1), the Federal Office for the Environment, the Federal Office of Public Health, the Federal Office of Roads and Transport, the canton's government of Aargau, Basel-Stadt, Basel-Land, Geneva, Luzern, Ticino, Valais, and Zürich, the Swiss Lung League, the canton's Lung League of Basel Stadt/ Basel Landschaft, Geneva, Ticino, Valais, Graubünden and Zurich, Stiftung ehemals Bündner Heilstätten, SUVA, Freiwillige Akademische Gesellschaft, UBS Wealth Foundation, Talecris Biotherapeutics GmbH, Abbott Diagnostics.ECRHS: The co-ordination of ECRHS II was supported by the European Commission, as part of their Quality of Life program. This work was also funded by the US National Institutes of Health (NIH grant 1R01HL062633) and the Carlos III Health Institute of the Spanish Ministry of Health and Consumption (FIS grant 01/3058). The following bodies funded the local studies in ECRHS II included in this paper: Albacete: Fondo de Investigaciones Santarias (FIS) (grant code: 97/0035-01, 99/0034-01 and 99/0034-02), Hospital Universitario de Albacete, Consejeria de Sanidad, Barcelona: SEPAR, Public Health Service (grant code: R01 HL62633-01), Fondo de Investigaciones Santarias (FIS) (grant code:97/0035-01, 99/0034-01 and 99/0034-02) CIRIT (grant code: 1999SGR 00241) Red Respira ISCII, Basel: Swiss National Science Foundation, Swiss Federal Office for Education & Science, Swiss National Accident Insurance Fund (SUVA), USC NIEHS Center grant 5P30 ES07048, Bergen: Norwegian Research Council, Norwegian Asthma & Allergy Association (NAAF), Glaxo Wellcome AS, Norway Research Fund, Erfurt: GSF-National Research Centre for Environment & Health, Deutsche Forschungsgemeinschaft (DFG) (grant code FR 1526/1-1), Galdakao: Basque Health Dept, Grenoble: Programme Hospitalier de Recherche Clinique-DRC de Grenoble 2000 no. 2610, Ministry of Health, Direction de la Recherche Clinique, Ministere de l'Emploi et de la Solidarite, Direction Generale de la Sante, CHU de Grenoble, Comite des Maladies Respiratoires de l’Isere, Hamburg: GSF-National Reasearch Centre for Environment & Health, Deutsche Forschungsgemeinschaft (DFG) (grant code MA 711/4-1), Ipswich and Norwich: Asthma UK (formerly known as National Asthma Campaign), Huelva: Fondo de Investigaciones Santarias (FIS) (grant code: 97/0035-01, 99/0034-01 and 99/0034-02), Oviedo: Fondo de Investigaciones Santarias (FIS) (grant code: 97/0035-01, 99/0034-01 and 99/0034-02), Paris: Ministere de l'Emploi et de la Solidarite, Direction Generale de la Sante, UCB-Pharma (France), Aventis (France), Glaxo France, Programme Hospitalier de Recherche Clinique-DRC de Grenoble 2000 no. 2610, Ministry of Health, Direction de la Recherche Clinique, CHU de Grenoble, Tartu: Estonian Science Foundation, Umeå: Swedish Heart Lung Foundation, Swedish Foundation for Health Care Sciences & Allergy Research, Swedish Asthma & Allergy Foundation, Swedish Cancer & Allergy Foundation, Uppsala: Swedish Heart Lung Foundation, Swedish Foundation for Health Care Sciences & Allergy Research, Swedish Asthma & Allergy Foundation, Swedish Cancer & Allergy Foundation., French National Agency of Research (Francia), Unión Europea. Comisión Europea, Wellcome Trust, Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Imperial College London-National Heart and Lung Institute
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Male ,Health, Toxicology and Mutagenesis ,[SDV]Life Sciences [q-bio] ,05 Environmental Sciences ,Toxicology ,0302 clinical medicine ,Adult onset asthma ,Medicine ,030212 general & internal medicine ,Lung function ,Public, Environmental & Occupational Health ,biology ,CLEANING PRODUCTS ,SWISS COHORT ,NF-kappa B ,Respiratory organs diseases ,11 Medical And Health Sciences ,Middle Aged ,Local study ,3. Good health ,ENVIRONMENT INTERACTION ,LUNG-FUNCTION ,Europe ,Occupational Diseases ,Irritants ,Female ,Life Sciences & Biomedicine ,Adult ,GENETICS ,Steering committee ,Physical activity ,Environmental Sciences & Ecology ,OBSTRUCTIVE PULMONARY-DISEASE ,Polymorphism, Single Nucleotide ,Malalties de l'aparell respiratori ,03 medical and health sciences ,Administrative support ,Occupational Exposure ,Cooperative group ,Humans ,GENOME-WIDE ASSOCIATION ,Asma ,Science & Technology ,business.industry ,Research ,Public Health, Environmental and Occupational Health ,AIR-POLLUTION ,biology.organism_classification ,Asthma ,Molecular Weight ,030228 respiratory system ,Pison ,EMERGING ROLES ,Particulate Matter ,[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie ,WORKPLACE ,business ,Humanities ,Environmental Sciences - Abstract
BACKGROUND: The biological mechanisms by which cleaning products and disinfectants-an emerging risk factor-affect respiratory health remain incompletely evaluated. Studying genes by environment interactions (G × E) may help identify new genes related to adult-onset asthma. OBJECTIVES: We identified interactions between genetic polymorphisms of a large set of genes involved in the response to oxidative stress and occupational exposures to low molecular weight (LMW) agents or irritants on adult-onset asthma. METHODS: Our data came from three large European cohorts: Epidemiological Family-based Study of the Genetics and Environment of Asthma (EGEA), Swiss Cohort Study on Air Pollution and Lung and Heart Disease in Adults (SAPALDIA), and European Community Respiratory Health Survey in Adults (ECRHS). A candidate pathway-based strategy identified 163 genes involved in the response to oxidative stress and potentially related to exposures to LMW agents/irritants. Occupational exposures were evaluated using an asthma job-exposure matrix and job-specific questionnaires for cleaners and healthcare workers. Logistic regression models were used to detect G × E interactions, adjusted for age, sex, and population ancestry, in 2,599 adults (mean age, 47 years; 60% women, 36% exposed, 18% asthmatics). p-Values were corrected for multiple comparisons. RESULTS: Ever exposure to LMW agents/irritants was associated with current adult-onset asthma [OR = 1.28 (95% CI: 1.04, 1.58)]. Eight single nucleotide polymorphism (SNP) by exposure interactions at five loci were found at p < 0.005: PLA2G4A (rs932476, chromosome 1), near PLA2R1 (rs2667026, chromosome 2), near RELA (rs931127, rs7949980, chromosome 11), PRKD1 (rs1958980, rs11847351, rs1958987, chromosome 14), and PRKCA (rs6504453, chromosome 17). Results were consistent across the three studies and after accounting for smoking. CONCLUSIONS: Using a pathway-based selection process, we identified novel genes potentially involved in adult asthma by interaction with occupational exposure. These genes play a role in the NF-κB pathway, which is involved in inflammation. Citation: Rava M, Ahmed I, Kogevinas M, Le Moual N, Bouzigon E, Curjuric I, Dizier MH, Dumas O, Gonzalez JR, Imboden M, Mehta AJ, Tubert-Bitter P, Zock JP, Jarvis D, Probst-Hensch NM, Demenais F, Nadif R. 2017. Genes interacting with occupational exposures to low molecular weight agents and irritants on adult-onset asthma in three European studies. Environ Health Perspect 125:207-214; http://dx.doi.org/10.1289/EHP376. We thank all study members and staff involved in data collections in each cohort: EGEA: We thank the Epidemiological Study on Genetics and Environment of Asthma (EGEA) cooperative group members as follows. Coordination: V. Siroux [epidemiology, principal investigator (PI) since 2013]; F. Demenais (genetics); I. Pin (clinical aspects); R. Nadif (biology); F. Kauffmann (PI 1992–2012). Respiratory epidemiology: Inserm U 700, Paris: M. Korobaeff (EGEA1), F. Neukirch (EGEA1); Inserm U 707, Paris: I. Annesi-Maesano (EGEA1–2); Inserm U1168 (ex-CESP/U 1018), Villejuif: F. Kauffmann, N. Le Moual, R. Nadif, M.P. Oryszczyn (EGEA1–2), R. Varraso; Inserm U 823, Grenoble: V. Siroux. Genetics: Inserm U 393, Paris: J. Feingold; Inserm U 946, Paris: E. Bouzigon, F. Demenais, M.H. Dizier; CNG, Evry: I. Gut (now CNAG, Barcelona, Spain), M. Lathrop (now McGill University, Montreal, Canada). Clinical centers: Grenoble: I. Pin, C. Pison; Lyon: D. Ecochard (EGEA1), F. Gormand, Y. Pacheco; Marseille: D. Charpin (EGEA1), D. Vervloet (EGEA1–2); Montpellier: J. Bousquet; Paris Cochin: A. Lockhart (EGEA1), R. Matran (now in Lille); Paris Necker: E. Paty (EGEA1–2), P. Scheinmann (EGEA1–2); Paris Trousseau: A. Grimfeld (EGEA1–2), J. Just. Data and quality management: Inserm ex-U155 (EGEA1): J. Hochez; Inserm U1168 (ex-CESP/U 1018), Villejuif: N. Le Moual; Inserm ex-U780: C. Ravault (EGEA1–2); Inserm ex-U794: N. Chateigner (EGEA1–2); Grenoble: J. Quentin-Ferran (EGEA1–2). SAPALDIA: We thank the team of the Swiss study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA). Study directorate: N.M. Probst-Hensch (PI; e/g); T. Rochat (p), C. Schindler (s), N. Künzli (e/exp), J.M. Gaspoz (c). Scientific team: J.C. Barthélémy (c), W. Berger (g), R. Bettschart (p), A. Bircher (a), C. Brombach (n), P.O. Bridevaux (p), L. Burdet (p), D. Felber Dietrich (e), M. Frey (p), U. Frey (pd), M.W. Gerbase (p), D. Gold (e), E. de Groot (c), W. Karrer (p), F. Kronenberg (g), B. Martin (pa), A. Mehta (e), D. Miedinger (o), M. Pons (p), F. Roche (c), T. Rothe (p), P. Schmid- Grendelmeyer (a), D. Stolz (p), A. Schmidt-Trucksäss (pa), J. Schwartz (e), A. Turk (p), A. von Eckardstein (cc), E. Zemp Stutz (e). Scientific team at coordinating centers: M. Adam (e), I. Aguilera (exp), S. Brunner (s), D. Carballo (c), S. Caviezel (pa), I. Curjuric (e), A. Di Pascale (s), J. Dratva (e), R. Ducret (s), E. Dupuis Lozeron (s), M. Eeftens (exp), I. Eze (e), E. Fischer (g), M. Foraster (e), M. Germond (s), L. Grize (s), S. Hansen (e), A. Hensel (s), M. Imboden (g), A. Ineichen (exp), A. Jeong (g), D. Keidel (s), A. Kumar (g), N. Maire (s), A. Mehta (e), R. Meier (exp), E. Schaffner (s), T. Schikowski (e), M. Tsai (exp). Abbreviations: (a) allergology, (c) cardiology, (cc) clinical chemistry, (e) epide - miology, (exp) exposure, (g) genetic and molecular biology, (m) meteorology, (n) nutrition, (o) occupational health, (p) pneumology, (pa) physical activity, (pd) pediatrics, (s) statistics. The study could not have been done without the help of the study partici - pants, technical and administrative support and the medical teams and field workers at the local study sites. Local fieldworkers: Aarau: S. Brun, G. Giger, M. Sperisen, M. Stahel; Basel: C. Bürli, C. Dahler, N. Oertli, I. Harreh, F. Karrer, G. Novicic, N. Wyttenbacher; Davos: A. Saner, P. Senn, R. Winzeler; Geneva: F. Bonfils, B. Blicharz, C. Landolt, J. Rochat; Lugano: S. Boccia, E. Gehrig, M.T. Mandia, G. Solari, B. Viscardi; Montana: A.P. Bieri, C. Darioly, M. Maire; Payerne: F. Ding, P. Danieli, A. Vonnez; Wald: D. Bodmer, E. Hochs, R. Kunz, C. Meier, J. Rakic, U. Schafroth, A. Walder. Administrative staff: N. Bauer Ott, C. Gabriel, R. Gutknecht. ECRHS: The ECRHS data incorporated in this analysis would not have been available without the collaboration of the following individuals and their research teams. ECRHS Co-ordinating Centre. P. Burney, D. Jarvis, S. Chinn, J. Knox (ECRHS II), C. Luczynska†, J. Potts. Steering Committee for ECRHS II. P. Burney, D. Jarvis, S. Chinn, U. Ackermann-Liebrich, J.M. Anto, I. Cerveri, R. deMarco†, T. Gislason, J. Heinrich, C. Janson, N. Kunzli, B. Leynaert, F. Neukirch, J. Schouten, J. Sunyer; C. Svanes, P. Vermeire†, M. Wjst. Principal Investigators and Senior Scientific Teams for ECRHS II centers within this analysis: Estonia: Tartu (R. Jogi, A. Soon); France: Paris (F. Neukirch, B. Leynaert, R. Liard, M. Zureik), Grenoble (I. Pin, J. Ferran-Quentin); Germany: Erfurt (J. Heinrich, M. Wjst, C. Frye, I. Meyer), Hamburg (K. Richter, D. Nowak); Norway: Bergen (A. Gulsvik, E. Omenaas, C. Svanes, B. Laerum); Spain: Barcelona (J.M. Anto, J. Sunyer, M. Kogevinas, J.P. Zock, X. Basagana, A. Jaen, F. Burgos), Huelva (J. Maldonado, A. Pereira, J.L. Sanchez), Albacete (J. Martinez-Moratalla Rovira, E. Almar), Galdakao (N. Muniozguren, I. Urritia), Oviedo (F. Payo); Sweden: Uppsala (C. Janson, G. Boman, D. Norback, M. Gunnbjornsdottir), Umeå (E. Norrman, M. Soderberg, K. Franklin, B. Lundback, B. Forsberg, L. Nystrom); Switzerland: Basel (N. Kunzli, B. Dibbert, M. Hazenkamp, M. Brutsche, U. Ackermann-Liebrich); United Kingdom: Norwich (D. Jarvis, B. Harrison), Ipswich (D. Jarvis, R. Hall, D. Seaton). Sí
- Published
- 2016
7. HMOX1 and GST variants modify attenuation of FEF25-75% decline due to PM10 reduction
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Exposure to particles with a 50% cut-off aerodynamic diameter of 10 mu m ,GENERAL-POPULATION ,SWISS COHORT ,lung function decline ,RESPIRATORY-HEALTH-SURVEY ,AIR-POLLUTION ,general population sample ,S-TRANSFERASE P1 ,forced expiratory flow at 25-75% of forced vital capacity ,LUNG-FUNCTION DECLINE ,GLUTATHIONE ,haem oxygenase-1 ,SAPALDIA ,HEME OXYGENASE-1 ,glutathione S-transferase ,HAPLOTYPE RECONSTRUCTION - Abstract
Reduced exposure to particulate matter with a 50% cut-off aerodynamic diameter of 10 mu m (PM(10)) attenuated age-related lung function decline in our cohort, particularly in the small airways. We hypothesised that polymorphisms in glutathione S-transferase (GST) and haem oxygenase-1 (HMOX1) genes, important for oxidative stress defence, modify these beneficial effects.A population-based sample of 4,365 adults was followed up after 11 yrs, including questionnaire, spirometry and DNA blood sampling. PM(10) exposure was estimated by dispersion modelling and temporal interpolation. The main effects on annual decline in forced expiratory flow at 25-75% of forced vital capacity (FEF(25-75%)) and interactions with PM(10) reduction were investigated for polymorphisms HMOX1 rs2071746 (T/A), rs735266 (T/A) and rs5995098 (G/C), HMOX1 (GT)(n) promoter repeat, GSTM1 and GSTT1 deletions, and GSTP1 p.lle105Val, using mixed linear regression models.HMOX1 rs5995098, HMOX1 haplotype TTG and GSTP1 showed significant genetic main effects. Interactions with PM(10) reduction were detected: a 10 mu g.m(-3) reduction significantly attenuated annual FEF(25-75%) decline by 15.3 mL.s(-1) only in the absence of HMOX1 haplotype ATC. Similarly, carriers of long (GT)(n) promoter repeat alleles or the GSTP1 Val/Val genotype profited significantly more from a 10 mu g.m(-3) reduction (26.5 mL.s(-1) and 27.3 mL.s(-1) respectively) than non-carriers.Benefits of a reduction in PM(10) exposure are not equally distributed across the population but are modified by the individual genetic make-up determining oxidative stress defence.
- Published
- 2010
8. Land use regression models for crustal and traffic-related PM2.5 constituents in four areas of the SAPALDIA study
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Christian Schindler, Nicole Probst-Hensch, Regina E. Ducret-Stich, Harish C. Phuleria, Inmaculada Aguilera, Reto Meier, Ming-Yi Tsai, Alex Ineichen, Nino Künzli, and Marloes Eeftens
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Light absorbance ,Fine particulate ,Air pollution ,medicine.disease_cause ,Atmospheric sciences ,Land use regression ,Source Apportionment ,Biochemistry ,Ambient Air ,Association ,Land Use Regression ,chemistry.chemical_compound ,Pm2.5 ,medicine ,Air-Pollution Exposure ,Nitrogen dioxide ,General Environmental Science ,Exposure assessment ,Vehicle Emissions ,Pm Source Apportionment ,Mass ,Explained variation ,Sapaldia ,Europe ,Particles ,chemistry ,13. Climate action ,Environmental science ,Regression Analysis ,Spatial variability ,Particulate Matter ,Factor Analysis ,Daily Mortality ,Swiss Cohort - Abstract
Many studies have documented adverse health effects of long-term exposure to fine particulate matter (PM2.5), but there is still limited knowledge regarding the causal relationship between specific sources of PM2.5 and such health effects. The spatial variability of PM2.5 constituents and sources, as a exposure assessment strategy for investigating source contributions to health effects, has been little explored so far. Between 2011 and 2012, three measurement campaigns of PM and nitrogen dioxide (NO2) were performed in 80 sites across four areas of the Swiss Study on Air Pollution and Lung and heart Diseases in Adults (SAPALDIA). Reflectance analysis and energy dispersive X-ray fluorescence (XRF) were performed on PM2.5 filter samples to estimate light absorbance and trace element concentrations, respectively. Three air pollution source factors were identified using principal-component factor analysis: vehicular, crustal, and long-range transport. Land use regression (LUR) models were developed for temporally-adjusted scores of each factor, combining the four study areas. Model performance was assessed using two cross-validation methods. Model explained variance was high for the vehicular factor (R-2 = 0.76), moderate for the crustal factor (R-2 = 0.46), and low for the long-range transport factor (R-2 = 0.19). The cross-validation methods suggested that models for the vehicular and crustal factors moderately accounted for both the between and within-area variability, and therefore can be applied to the four study areas to estimate long-term exposures within the SAPALDIA study population. The combination of source apportionment techniques and LUR modelling may help in identifying air pollution sources and disentangling their contribution to observed health effects in epidemiologic studies. (C) 2015 Elsevier Inc. All rights reserved.
- Published
- 2014
9. HMOX1 and GST variants modify attenuation of FEF25-75% decline due to PM10 reduction
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I, Curjuric, M, Imboden, C, Schindler, S H, Downs, M, Hersberger, S L J, Liu, G, Matyas, E W, Russi, J, Schwartz, G A, Thun, D S, Postma, T, Rochat, N M, Probst-Hensch, Groningen Research Institute for Asthma and COPD (GRIAC), and University of Zurich
- Subjects
Adult ,Male ,610 Medicine & health ,Maximal Midexpiratory Flow Rate ,RESPIRATORY-HEALTH-SURVEY ,Airway Remodeling/*genetics ,Polymorphism, Single Nucleotide ,general population sample ,forced expiratory flow at 25-75% of forced vital capacity ,540 Chemistry ,LUNG-FUNCTION DECLINE ,GLUTATHIONE ,Particulate Matter/*adverse effects ,Humans ,haem oxygenase-1 ,Genetic Predisposition to Disease ,Promoter Regions, Genetic ,10038 Institute of Clinical Chemistry ,Aged ,Glutathione Transferase ,glutathione S-transferase ,HAPLOTYPE RECONSTRUCTION ,ddc:616 ,Exposure to particles with a 50% cut-off aerodynamic diameter of 10 mu m ,GENERAL-POPULATION ,Glutathione Transferase/genetics ,SWISS COHORT ,lung function decline ,AIR-POLLUTION ,Middle Aged ,S-TRANSFERASE P1 ,Glutathione S-Transferase pi ,Haplotypes ,2740 Pulmonary and Respiratory Medicine ,Glutathione S-Transferase pi/*genetics ,Airway Remodeling ,Female ,Particulate Matter ,SAPALDIA ,HEME OXYGENASE-1 ,Heme Oxygenase-1/*genetics ,Follow-Up Studies - Abstract
Reduced exposure to particulate matter with a 50% cut-off aerodynamic diameter of 10 microm (PM(10)) attenuated age-related lung function decline in our cohort, particularly in the small airways. We hypothesised that polymorphisms in glutathione S-transferase (GST) and haem oxygenase-1 (HMOX1) genes, important for oxidative stress defence, modify these beneficial effects. A population-based sample of 4,365 adults was followed up after 11 yrs, including questionnaire, spirometry and DNA blood sampling. PM(10) exposure was estimated by dispersion modelling and temporal interpolation. The main effects on annual decline in forced expiratory flow at 25-75% of forced vital capacity (FEF(25-75%)) and interactions with PM(10) reduction were investigated for polymorphisms HMOX1 rs2071746 (T/A), rs735266 (T/A) and rs5995098 (G/C), HMOX1 (GT)(n) promoter repeat, GSTM1 and GSTT1 deletions, and GSTP1 p.Ile105Val, using mixed linear regression models. HMOX1 rs5995098, HMOX1 haplotype TTG and GSTP1 showed significant genetic main effects. Interactions with PM(10) reduction were detected: a 10 microg.m(-3) reduction significantly attenuated annual FEF(25-75%) decline by 15.3 mL.s(-1) only in the absence of HMOX1 haplotype ATC. Similarly, carriers of long (GT)(n) promoter repeat alleles or the GSTP1 Val/Val genotype profited significantly more from a 10 microg.m(-3) reduction (26.5 mL.s(-1) and 27.3 mL.s(-1) respectively) than non-carriers. Benefits of a reduction in PM(10) exposure are not equally distributed across the population but are modified by the individual genetic make-up determining oxidative stress defence.
- Published
- 2010
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