16 research outputs found
THE IMAGINARY LACAN SEBAGAI INSPIRASI PENCIPTAAN SKENARIO FILM PENDEK SEKUEL KEDUA FILM KOPER GENDIS MENCARI JAWAB MENAKAR TANYA
Get PDFSejauh ini teori psikologi (psikoanalisis) Lacan hanya digunakan sebagaipisau analisis, baik karya teks (sastra), pertunjukan, film maupun karya seni rupa. Berpijak dari hal tersebut, penulis menawarkan interprerstasi lain tentang aplikatif teori psikoanalisis Lacan sebagai dasar penciptaan skenario. Penelitian ini merupakan penelitian terapan berupa penciptaan skenario film pendek dengan pendekatan teori Lacan tentang the imaginary dan kelanjutan pada penciptaan film sebelumnya (sekuel kedua) dari Film Koper Gendis Mencari Jawab Menakar Tanya. Penciptaan skenario dengan pendekatan Lacan ini diharapkan menjadi alternatif baru pada ranah penciptaan skenario film.Kata kunci: The Imaginary, Lacan, skenario film, Koper GendisSo far, Lacan's psychological theory (psychoanalysis) has only beenused as a tool of analysis, whether it be text (literature), performances, films, orworks of art. The author used Lacan's psychoanalytic theory as the basis forscenario creation. This report is applied research in the form of short film scenario creation with Lacan's theory approach of the imaginary and the continuation of the previous film creation (as a second sequel) from Film Koper Gendis Mencari Jawab Menakar Tanya. This scenario creation is expected to be a new alternative in film scenario creation.Keywords: The Imaginary, Lacan, film scenario, Koper Gendi
Study on the theoretical framework of monopoly capital school and its comparison with Minsky theory
Get PDFAbstract. Global financial crisis which broke out in 2008 triggered the great recession of the global economy, making the non-mainstream Monopoly Capital School of economics rise to fame. The mainstream economics attributed the crisis to the different external shocks and policy errors. On the contrary, Monopoly Capital School focused on the process of capital accumulation under the stage of monopoly capitalism, and offered perspective on inherent instability defects of capitalism. Based on teasing out the theoretical framework of Monopoly Capital School, this paper analyzed the standpoints, views and methods of monopoly capitalism through comparing the theory with Minsky theory, not only contributing to the understanding the instability defects of capitalism, but also contributing to the thinking of the future direction of capitalism.Keywords. Monopoly capital, Capital accumulation, Economic surplus, Economic stagnation, Financialization.JEL. D42, L12
Author Correction: Green synthesis, characterization, anti-SARS-CoV-2 entry, and replication of lactoferrin-coated zinc nanoparticles with halting lung fibrosis induced in adult male albino rats
No full textRituximab versus tocilizumab in anti-TNF inadequate responder patients with rheumatoid arthritis (R4RA): 16-week outcomes of a stratified, biopsy-driven, multicentre, open-label, phase 4 randomised controlled trial
Get PDF\ua9 2021 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 licenseBackground: Although targeted biological treatments have transformed the outlook for patients with rheumatoid arthritis, 40% of patients show poor clinical response, which is mechanistically still unexplained. Because more than 50% of patients with rheumatoid arthritis have low or absent CD20 B cells—the target for rituximab—in the main disease tissue (joint synovium), we hypothesised that, in these patients, the IL-6 receptor inhibitor tocilizumab would be more effective. The aim of this trial was to compare the effect of tocilizumab with rituximab in patients with rheumatoid arthritis who had an inadequate response to anti-tumour necrosis factor (TNF) stratified for synovial B-cell status. Methods: This study was a 48-week, biopsy-driven, multicentre, open-label, phase 4 randomised controlled trial (rituximab vs tocilizumab in anti-TNF inadequate responder patients with rheumatoid arthritis; R4RA) done in 19 centres across five European countries (the UK, Belgium, Italy, Portugal, and Spain). Patients aged 18 years or older who fulfilled the 2010 American College of Rheumatology and European League Against Rheumatism classification criteria for rheumatoid arthritis and were eligible for treatment with rituximab therapy according to UK National Institute for Health and Care Excellence guidelines were eligible for inclusion in the trial. To inform balanced stratification, following a baseline synovial biopsy, patients were classified histologically as B-cell poor or rich. Patients were then randomly assigned (1:1) centrally in block sizes of six and four to receive two 1000 mg rituximab infusions at an interval of 2 weeks (rituximab group) or 8 mg/kg tocilizumab infusions at 4-week intervals (tocilizumab group). To enhance the accuracy of the stratification of B-cell poor and B-cell rich patients, baseline synovial biopsies from all participants were subjected to RNA sequencing and reclassified by B-cell molecular signature. The study was powered to test the superiority of tocilizumab over rituximab in the B-cell poor population at 16 weeks. The primary endpoint was defined as a 50% improvement in Clinical Disease Activity Index (CDAI50%) from baseline. The trial is registered on the ISRCTN database, ISRCTN97443826, and EudraCT, 2012-002535-28. Findings: Between Feb 28, 2013, and Jan 17, 2019, 164 patients were classified histologically and were randomly assigned to the rituximab group (83 [51%]) or the tocilizumab group (81 [49%]). In patients histologically classified as B-cell poor, there was no statistically significant difference in CDAI50% between the rituximab group (17 [45%] of 38 patients) and the tocilizumab group (23 [56%] of 41 patients; difference 11% [95% CI −11 to 33], p=0\ub731). However, in the synovial biopsies classified as B-cell poor with RNA sequencing the tocilizumab group had a significantly higher response rate compared with the rituximab group for CDAI50% (rituximab group 12 [36%] of 33 patients vs tocilizumab group 20 [63%] of 32 patients; difference 26% [2 to 50], p=0\ub7035). Occurrence of adverse events (rituximab group 76 [70%] of 108 patients vs tocilizumab group 94 [80%] of 117 patients; difference 10% [–1 to 21) and serious adverse events (rituximab group 8 [7%] of 108 vs tocilizumab group 12 [10%] of 117; difference 3% [–5 to 10]) were not significantly different between treatment groups. Interpretation: The results suggest that RNA sequencing-based stratification of rheumatoid arthritis synovial tissue showed stronger associations with clinical responses compared with histopathological classification. Additionally, for patients with low or absent B-cell lineage expression signature in synovial tissue tocilizumab is more effective than rituximab. Replication of the results and validation of the RNA sequencing-based classification in independent cohorts is required before making treatment recommendations for clinical practice. Funding: Efficacy and Mechanism Evaluation programme from the UK National Institute for Health Research
Uncovering the complex genetics of human character
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org/licenses/by/4.0/.Human personality is 30-60% heritable according to twin and adoption studies. Hundreds of genetic variants are expected to influence its complex development, but few have been identified. We used a machine learning method for genome-wide association studies (GWAS) to uncover complex genotypic-phenotypic networks and environmental interactions. The Temperament and Character Inventory (TCI) measured the self-regulatory components of personality critical for health (i.e., the character traits of self-directedness, cooperativeness, and self-transcendence). In a discovery sample of 2149 healthy Finns, we identified sets of single-nucleotide polymorphisms (SNPs) that cluster within particular individuals (i.e., SNP sets) regardless of phenotype. Second, we identified five clusters of people with distinct profiles of character traits regardless of genotype. Third, we found 42 SNP sets that identified 727 gene loci and were significantly associated with one or more of the character profiles. Each character profile was related to different SNP sets with distinct molecular processes and neuronal functions. Environmental influences measured in childhood and adulthood had small but significant effects. We confirmed the replicability of 95% of the 42 SNP sets in healthy Korean and German samples, as well as their associations with character. The identified SNPs explained nearly all the heritability expected for character in each sample (50 to 58%). We conclude that self-regulatory personality traits are strongly influenced by organized interactions among more than 700 genes despite variable cultures and environments. These gene sets modulate specific molecular processes in brain for intentional goal-setting, self-reflection, empathy, and episodic learning and memory.The Young Finns Study has been financially supported by the Academy of Finland: grants 286284, 134309 (Eye), 126925, 121584, 124282, 129378 (Salve), 117787 (Gendi), and 41071 (Skidi); the Social Insurance Institution of Finland; Competitive State Research Financing of the Expert Responsibility area of Kuopio, Tampere, and Turku University Hospitals (grant X51001); Juho Vainio Foundation; Paavo Nurmi Foundation; Finnish Foundation for Cardiovascular Research; Finnish Cultural Foundation; Tampere Tuberculosis Foundation; Emil Aaltonen Foundation; Yrjö Jahnsson Foundation; Signe and Ane Gyllenberg Foundation; Diabetes Research Foundation of Finnish Diabetes Association; and EU Horizon 2020 (grant 755320 for TAXINOMISIS). The American Foundation for Suicide Prevention supported the study of healthy Germans. The National Healthy Twin Family Register of Korea supported the study of healthy Koreans. The Anthropedia Foundation and the Spanish Ministry of Science and Technology TIN2012-38805 and DPI2015-69585-R supported this collaboration. We thank biostatisticians Charles Gu and Miguel Angel Rubio Escudero for advice on statistical analysis, and five anonymous reviewers for their helpful comments on the paper.Ministerio de Ciencia y Tecnología del cual soy IP: PID2021-125017OB-I00 ; RTI2018-098983-B-I00 ; DPI2015-69585-R
Corrigendum: Eligibility for clinical trials in primary Sj\uf6gren\u27s syndrome: Lessons from the UK Primary Sj\uf6gren\u27s Syndrome Registry [Rheumatology, 55, (2016) (544-552)] doi:10.1093/rheumatology/kev373
No full text\ua9 The Author 2017. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved.Further to publication of this paper the Authors have identified that although all 688 participants had a clinical diagnosis of primary Sj\uf6gren\u27s Syndrome and 668 (97.1%) fulfilled the American-European Consensus Group (AECG) classification criteria, 20 patients (2.9%) did not have sufficient features to do so. This error arose from an incorrect assumption derived from the database during analysis, for which the Authors apologize. There is no impact on the outcome or conclusions of the paper, but the methods have been amended accordingly online. The Authors also identified a small number of minor errors as follows: In the abstract the number eligible for the TEARS study is 46.3% not 31.6% (see Table 2). In Table 1: DMARD %=9.6; Pilocarpine or DMARD %=16.6; Unstimulated flow rate>1.5mls/15 mins %=15.0; Low C3%=2.0; Low C4%=17.2; Lymphoma %=4.8 (see supplementary table)
Patient-reported outcomes and safety in patients undergoing synovial biopsy: Comparison of ultrasound-guided needle biopsy, ultrasound-guided portal and forceps and arthroscopic-guided synovial biopsy techniques in five centres across Europe
Get PDF\ua9 \ua9 Author(s) (or their employer(s)) 2018. Re-use permitted under CC BY. Published by BMJ. Background We present a European multicenter study, comparing safety data and patient-reported outcomes (PRO) from patients undergoing synovial biopsy using ultrasound-guided needle biopsy (US-NB), ultrasound-guided portal and forceps (US-P&F) or arthroscopic-guided (AG) procedures. Objectives To describe safety and PRO data on joint indices of pain, stiffness and swelling before and after biopsy, procedural discomfort, joint status compared with before biopsy and willingness to undergo a second biopsy for each technique and compare the three techniques. To evaluate the impact on PRO and safety data of corticosteroid therapy as part of the biopsy procedure and sequential biopsy procedures. Methods Data were collected on the day of biopsy and 7-14 days postprocedure. Joint pain, swelling and stiffness indices were recorded as 0-100mm Visual Analogue Scale; qualitative outcome variables on five-point Likert scales. Groups were compared with linear regression, adjusting for disease activity, corticosteroid therapy and prebiopsy PRO value and accounting for repeated measurements. Results A total of 524 synovial biopsy procedures were documented (402 US-NB, 65 US-P&F and 57 AGSB). There were eight adverse events (1.5%) with no difference between biopsy methods (p=0.55). All PROs were improved 2weeks postprocedure, and there were no differences in postbiopsy change in PROs between biopsy methods. Corticosteroid administration, whether intramuscular (n=62) or intra-Articular (n=38), did not result in more adverse events (p=0.81) and was associated with reduction in postbiopsy swelling (p<0.01). Sequential biopsy procedures (n=103 patients) did not result in more adverse events (p=0.61) or worsening in PRO data. Conclusion Overall, our results do not suggest a significant difference in safety or patient tolerability between US-NB, US-P&F and AGSB sampling. Further, corticosteroid therapy as part of the biopsy procedure and sequential biopsies is safe and well tolerated in patients
Pain and depression are associated with both physical and mental fatigue independently of comorbidities and medications in primary Sj\uf6gren\u27s syndrome
Get PDF\ua9 Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. Objectives To report on fatigue in patients from the United Kingdom primary Sj\uf6gren\u27s syndrome (pSS) registry identifying factors associated with fatigue and robust to assignable causes such as comorbidities and medications associated with drowsiness. Methods From our cohort (n = 608), we identified those with comorbidities associated with fatigue, and those taking medications associated with drowsiness. We constructed dummy variables, permitting the contribution of these potentially assignable causes of fatigue to be assessed. Using multiple regression analysis, we modelled the relationship between Profile of Fatigue and Discomfort physical and mental fatigue scores and potentially related variables. Results Pain, depression and daytime sleepiness scores were closely associated with both physical and mental fatigue (all p ≤ 0.0001). In addition, dryness was strongly associated with physical fatigue (p ≤ 0.0001). These effects were observed even after adjustment for comorbidities associated with fatigue or medications associated with drowsiness. Conclusions These findings support further research and clinical interventions targeting pain, dryness, depression and sleep to improve fatigue in patients with pSS. This finding is robust to both the effect of other comorbidities associated with fatigue and medications associated with drowsiness
Short-term efficacy and safety of rituximab therapy in refractory systemic lupus erythematosus: results from the British Isles Lupus Assessment Group Biologics Register
No full text\ua9 The Author 2017. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. Objectives. To describe the baseline characteristics of SLE patients requiring biologic therapy in the UK and to explore short term efficacy and infection rates associated with rituximab (RTX) use. Methods. Patients commencing biologic therapy for refractory SLE and who consented to join BILAG-BR were analysed. Baseline characteristics, disease activity (BILAG 2004/SLEDAI-2K) and rates of infection over follow-up were analysed. Response was defined as loss of all A and B BILAG scores to41 B score with no new A/B scores in other organ systems at 6 months. Results. Two hundred and seventy SLE patients commenced biologic therapy from September 2010 to September 2015, most commonly RTX (n = 261). Two hundred and fifty (93%) patients were taking glucocorticoids at baseline at a median [interquartile range (IQR)] oral dose of 10mg (5-20 mg) daily. Response rates at 6 months were available for 68% of patients. The median (IQR) BILAG score was 15 (10-23) at baseline and 3 (2-12) at 6 months (P<0.0001). The median (IQR) SLEDAI-2K reduced from 8 (5-12) to 4 (0-7) (P<0.001). Response was achieved in 49% of patients. There was also a reduction in glucocorticoid use to a median (IQR) dose of 7.5mg (5-12 mg) at 6 months (P< 0.001). Serious infections occurred in 26 (10%) patients, being more frequent in the first 3 months post-RTX therapy. A higher proportion of early infections were non-respiratory (odds ratio = 1.98, 95% CI: 0.99, 3.9; P = 0.049). Conclusion. RTX is safe and is associated with improvement in disease activity in refractory SLE patients with concomitant reductions in glucocorticoid use. Early vigilance for infection post-infusion is important to further improve treatment risks and benefits
Sixteen new lung function signals identified through 1000 Genomes Project reference panel imputation
No full textIncludes supplementary materials for the online appendix.Lung function measures are used in the diagnosis of chronic obstructive pulmonary disease. In 38,199 European ancestry individuals, we studied genome-wide association of forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC with 1000 Genomes Project (phase 1)-imputed genotypes and followed up top associations in 54,550 Europeans. We identify 14 novel loci (P<5 × 10−8) in or near ENSA, RNU5F-1, KCNS3, AK097794, ASTN2, LHX3, CCDC91, TBX3, TRIP11, RIN3, TEKT5, LTBP4, MN1 and AP1S2, and two novel signals at known loci NPNT and GPR126, providing a basis for new understanding of the genetic determinants of these traits and pulmonary diseases in which they are altered.The research undertaken by M.D.T., M.S.A. and L.V.W. was partly funded by the National Institute for Health Research (NIHR). The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health. M.D.T. holds a Medical Research Council Senior Clinical Fellowship (G0902313). This research used the ALICE High Performance Computing Facility at the University of Leicester. The Universities of Leicester and Nottingham acknowledge receipt of a Collaborative Research and Development grant from the Healthcare and Bioscience iNet, a project funded by the East Midlands Development Agency, part-financed by the European Regional Development Fund and delivered by Medilink East Midlands. I.P.H. holds a Medical Research Council programme grant (G1000861). We acknowledge the use of phenotype and genotype data from the British 1958 Birth Cohort DNA collection, funded by the Medical Research Council grant G0000934 and the Wellcome Trust grant 068545/Z/02 (http://www.b58cgene.sgul.ac.uk/). Genotyping for the B58C-WTCCC subset was funded by the Wellcome Trust grant 076113/B/04/Z. The B58C-T1DGC genotyping utilized resources provided by the Type 1 Diabetes Genetics Consortium, a collaborative clinical study sponsored by the National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Allergy and Infectious Diseases, National Human Genome Research Institute, National Institute of Child Health and Human Development and Juvenile Diabetes Research Foundation International and supported by U01 DK062418. B58C-T1DGC GWAS data were deposited by the Diabetes and Inflammation Laboratory, Cambridge Institute for Medical Research (CIMR), University of Cambridge, which is funded by Juvenile Diabetes Research Foundation International, the Wellcome Trust and the National Institute for Health Research Cambridge Biomedical Research Centre; the CIMR is in receipt of a Wellcome Trust Strategic Award (079895). The B58C-GABRIEL genotyping was supported by a contract from the European Commission Framework Programme 6 (018996) and grants from the French Ministry of Research. The Busselton Health Study (BHS) acknowledges the generous support for the 1994/5 follow-up study from Healthway, Western Australia and the numerous Busselton community volunteers who assisted with data collection and the study participants from the Shire of Busselton. The BHS is supported by The Great Wine Estates of the Margaret River region of Western Australia. GWAS genotyping was supported by a research collaboration with Pfizer. The CROATIA study was supported through grants from the Medical Research Council UK, the Ministry of Science, Education and Sport in the Republic of Croatia (number 216-1080315-0302), Croatian Science Foundation (grant number 8875) and the European Union framework program 6 EUROSPAN project (contract no. LSHG-CT-2006-018947). SNP genotyping for CROATIA-Vis was performed by the Wellcome Trust Clinical Research Facility (WTCRF) at the Western General Hospital, Edinburgh, UK. CROATIA-Korcula was genotyped by Helmholz Zentrum München, GmbH, Neuherberg, Germany and CROATIA-Split by AROS Applied Biotechnology, Aarhus, Denmark. We would like to acknowledge the invaluable contributions of the recruitment teams in Croatia (including those from the Institute of Anthropological Research in Zagreb and the Croatian Centre for Global Health at the University of Split), the administrative teams in Croatia and Edinburgh and the people of Korcula, Vis and Split. The EPIC Norfolk Study is funded by program grants from the Medical Research Council UK and Cancer Research UK, and by additional support from the European Union, Stroke Association, British Heart Foundation, Department of Health, Food Standards Agency and the Wellcome Trust. GS:SFHS is funded by the Scottish Executive Health Department, Chief Scientist Office, grant number CZD/16/6. Exome array genotyping for GS:SFHS was funded by the Medical Research Council UK and performed at the Wellcome Trust Clinical Research Facility Genetics Core at Western General Hospital, Edinburgh, UK. We acknowledge the invaluable contributions of the families who took part in the Generation Scotland: Scottish Family Health Study, the general practitioners and Scottish School of Primary Care for their help in recruiting them and the whole Generation Scotland team, which includes academic researchers, IT staff, laboratory technicians, statisticians and research managers. This study was financially supported by the Medical Research Fund of the Tampere University Hospital. S.R. was supported by the Academy of Finland (251217 and 255847), Center of Excellence in Complex Disease Genetics, EU FP7 projects ENGAGE (201413) and BioSHaRE (261433), the Finnish Foundation for Cardiovascular Research, Biocentrum Helsinki and the Sigrid Juselius Foundation. The KORA authors acknowledge all members of field staffs who were involved in the planning and conduction of the KORA Augsburg studies, as well as all KORA study participants. The KORA research platform (KORA, Cooperative Health Research in the Region of Augsburg) was initiated and financed by the Helmholtz Zentrum München—German Research Center for Environmental Health, which is funded by the German Federal Ministry of Education and Research and by the State of Bavaria. The KORA-Age project was financed by the German Federal Ministry of Education and Research (BMBF FKZ 01ET0713 and 01ET1003A) as part of the ‘Health in old age’ program. Furthermore, KORA research was supported within the Munich Center of Health Sciences (MC Health), Ludwig-Maximilians-Universität, as part of LMUinnovativ. Further support was provided by the Competence Network ASCONET, subnetwork COSYCONET (FKZ 01GI0882). We thank the cohort participants who contributed to this study. Genotyping was supported by the UK’s Biotechnology and Biological Sciences Research Council (BBSRC) (ref. BB/F019394/1). Phenotype collection was supported by Research Into Ageing (continues as part of Age UK’s The Disconnected Mind project). The work was undertaken by The University of Edinburgh Centre for Cognitive Ageing and Cognitive Epidemiology, part of the cross council Lifelong Health and Wellbeing Initiative (MR/K026992/1). Funding from the BBSRC and Medical Research Council (MRC) is gratefully acknowledged. We thank the late Professor Paula Rantakallio (launch of NFBC1966), and Ms Outi Tornwall and Ms MinttuJussila (DNA biobanking). NFBC1966 received financial support from the Academy of Finland (project grants 104781, 120315, 129269, 1114194 and 24300796), University Hospital Oulu, Biocenter, University of Oulu, Finland (75617), NHLBI grant 5R01HL087679-02 through the STAMPEED program (1RL1MH083268-01), NIH/NIMH (5R01MH63706:02), EU FP7 (HEALTH-F4-2007-201413), EU FP8 (277849) and Medical Research Council, UK (G0500539, G1002319 and G0600705). U.G. acknowledges Swedish Medical Research Council (K2007-66X-20270-01-3, 2012-2884), Foundation for Strategic Research (SSF) and European Commission FP6 STRP (LSHG-CT-2006-01947). Å.J. acknowledges Swedish Society for Medical Research. The ORCADES study was funded by the Chief Scientist Office of the Scottish Government, the Royal Society and the MRC Human Genetics Unit. DNA extraction was performed at the Wellcome Trust Clinical Research Facility in Edinburgh. Genotyping was funded by the European Union Framework Programme 6 EUROSPAN project. Study directorate: NM 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), Felber Dietrich D. (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) and 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) and M. Tsai (exp); (a) allergology, (c) cardiology, (cc) clinical chemistry, (e) epidemiology, (exp) exposure, (g) genetic and molecular biology, (m) meteorology, (n) nutrition, (o) occupational health, (p) pneumology, (pa) physical activity, (pd) pediatrics and (s) statistic. The study could not have been done without the help of the study participants, technical and administrative support and the medical teams and field workers at the local study sites. Local field workers: Aarau: S. Brun, G. Giger, M. Sperisen and M. Stahel; Basel: C. Bürli, C. Dahler, N. Oertli, I. Harreh, F. Karrer, G. Novicic and N. Wyttenbacher; Davos: A. Saner, P. Senn and R. Winzeler; Geneva: F. Bonfils, B. Blicharz, C. Landolt and J. Rochat; Lugano: S. Boccia, E. Gehrig, M.T. Mandia, G. Solari and B. Viscardi; Montana: A.P. Bieri, C. Darioly and M. Maire; Payerne: F. Ding and P. Danieli A. Vonnez; Wald: D. Bodmer, E. Hochstrasser, R. Kunz, C. Meier, J. Rakic, U. Schafroth and A. Walder. Administrative staff: N. Bauer Ott, C. Gabriel, R. Gutknecht. Funding: The Swiss National Science Foundation (grants nos 33CS30-148470/1, 33CSCO-134276/1, 33CSCO-108796, 3247BO-104283, 3247BO-104288, 3247BO-104284, 3247-065896, 3100-059302, 3200-052720, 3200-042532, 4026-028099, PMPDP3_129021/1 and 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, European Commission 018996 (GABRIEL), and Wellcome Trust WT 084703MA. SHIP is part of the Community Medicine Research net of the University of Greifswald, Germany, which is funded by the Federal Ministry of Education and Research, the Ministry of Cultural Affairs as well as the Social Ministry of the Federal State of Mecklenburg-West Pomerania, and the network ‘Greifswald Approach to Individualized Medicine (GANI_MED)’ funded by the Federal Ministry of Education and Research, and the German Asthma and COPD Network (COSYCONET) (grant nos 01ZZ9603, 01ZZ0103, 01ZZ0403, 03IS2061A and BMBF 01GI0883). Genome-wide data have been supported by the Federal Ministry of Education and Research and a joint grant from Siemens Healthcare, Erlangen, Germany and the Federal State of Mecklenburg-West Pomerania (grant no. 03ZIK012). The University of Greifswald is a member of the ‘Center of Knowledge Interchange’ program of the Siemens AG and the Caché Campus program of the InterSystems GmbH. We acknowledge the Academy of Finland (126925, 121584 and 124282), Academy of Finland (Eye) (134309), Academy of Finland (Salve) (129378), Academy of Finland (Gendi) (117787), Academy of Finland (Skidi) (41071), Social Insurance Institution of Finland,Tampere University Hospital Medical Funds (X51001 for T.L.), Kuopio University Hospital Medical Funds, Turku University Hospital Medical Funds, Juho Vainio Foundation, Paavo Nurmi Foundation, Finnish Foundation of Cardiovascular Research (T.L.), Finnish Cultural Foundation, Tuberculosis Foundation (T.L.), Emil Aaltonen Foundation (T.L.) and Yrjö Jahnsson Foundation (T.L.). We are extremely grateful to all the families who took part in the study, the midwives for their help in recruiting them and the whole ALSPAC team, which includes interviewers, computer and laboratory technicians, clerical workers, research scientists, volunteers, managers, receptionists and nurses. The UK Medical Research Council and the Wellcome Trust (grant ref: 092731) and the University of Bristol provide core support for ALSPAC. This publication is the work of the authors and D.M.E. will serve as guarantor for the contents of this paper. This work was funded by a Medical Research Council (MRC) strategic award to M.D.T., I.P.H., D.P.S. and L.V.W. (MC_PC_12010). This research has been conducted using the UK Biobank Resource. M.D.T. has been supported by MRC fellowships G0501942 and G0902313. I.P.H. is supported by an MRC programme grant (G1000861). J.M. is funded by an ERC Consolidator Grant (617306). This article presents independent research funded partially by the NIHR. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health. We would like to acknowledge all members of the UK Biobank Array Design Group. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health. Peter Donnelly (chair) (University of Oxford), Jeff Barrett (Wellcome Trust Sanger Institute), Jose Bras (University College London), Adam Butterworth (University of Cambridge), Richard Durbin (Wellcome Trust Sanger Institute), Paul Elliott (Imperial College London), Ian Hall (University of Nottingham), John Hardy (University College London), Mark McCarthy (University of Oxford), Gil McVean (University of Oxford), Tim Peakman (UK Biobank), Nazneen Rahman (The Institute of Cancer Research), Nilesh Samani (University of Leicester), Martin Tobin (University of Leicester), Hugh Watkins (University of Oxford). We acknowledge EU funding (GABRIEL Grant Number: 018996, ECRHS II Coordination Number: QLK4-CT-1999-01237). A.P.M. acknowledges the Wellcome Trust (WT098017,WT064890 and WT090532). The PIVUS study acknowledges The Swedish Foundation for Strategic Research (ICA08-0047), The Swedish Research Council (2012-1397), The Swedish Heart-Lung Foundation (20120197), The Swedish Society of Medicine and Uppsala University. The computations were performed on resources provided by SNIC through Uppsala Multidisciplinary Center for Advanced Computational Science (UPPMAX) under Project p2013056. A.P.M. is a Wellcome Trust Senior Research Fellow in Basic Biomedical Science (grant number WT098017). This cohort received funding from the Wellcome Trust; the European Community’s Seventh Framework Programme (FP7/2007-13); US National Institutes of Health/National Eye Institute (1RO1EY018246); NIH Center for Inherited Disease Research; the NIHR- funded BioResource, Clinical Research Facility and Biomedical Research Centre based at Guy’s and St Thomas’ NHS Foundation Trust in partnership with King’s College London. We thank the research staff at the Respiratory Health Network Tissue Bank of the FRQS for collecting lung specimens for the lung eQTL study at the Laval University. The Lung Tissue eQTL study was funded by Merck Research Laboratories. M.O. is a Postdoctoral Fellow of the Michael Smith Foundation for Health Research and the Canadian Institute for Health Research Integrated and Mentored Pulmonary and Cardiovascular Training program (IMPACT). Y.B. is the recipient of a Junior 2 Research Scholar award from the Fonds de recherche Québec—Santé (FRQS)
