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Your search keyword '"Van der Plaat, D. A."' showing total 28 results
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28 results on '"Van der Plaat, D. A."'

1. The Digital Archives of Queensland Architecture (DAQA) Dataset Codebook v1.0

Author

Ryan, T, van der Plaat, D, Macarthur, J, Ryan, T, van der Plaat, D, and Macarthur, J

Abstract

The digital archive of Queensland architecture offers a wealth of information on the region's design history. The archive was originally constructed as part of the Hot Modernism project and focused on the period 1945-1975. We are now expanding to include earlier and later periods. The database comprises thousands of audiovisual and textual files that allow you to explore relationships between people, projects and firms.

Published
2022

2. Impact of COVID-19 pandemic on sickness absence for mental ill health in National Health Service staff

Author

Van der Plaat, D, Edge, R, Coggon, D, Van Tongeren, M, Muiry, R, Parsons, V, Cullinan, P, and Madan, I

Abstract

Objective: To explore the patterns of sickness absence in National Health Service (NHS) staff attributable to mental ill health during the first wave of the Covid19 epidemic in March to July 2020 Design: Case-referent analysis of a secondary data set Setting: NHS Trusts in England Participants: Pseudonymised data on 959,356 employees who were continuously employed by NHS trusts during 1 January 2019 to 31 July 2020 Main Outcome Measures: Trends in the burden of sickness absence due to mental ill health from 2019 to 2020 according to demographic, regional and occupational characteristics. Results: Over the study period, 164,202 new sickness absence episodes for mental ill health were recorded in 12.5% (119,525) of the study sample. There was a spike of sickness absence for mental ill health in March-April 2020 (899,730 days lost) compared with 519,807 days in March and April 2019; the surge was driven by an increase in new episodes of long-term absence and had diminished by May and June 2020. The increase was greatest in those aged >60 years (227%) and among employees of Asian and Black ethnic origin (109%-136%). Among doctors and dentists the number of days absent declined by 12.7%. The biggest increase was in London (122%) and the smallest in the East Midlands (43.7%); the variation between regions reflected the rates of Covid19 sickness absence during the same period. Conclusion: Although the Covid19 epidemic led to an increase in sickness absence attributed to mental ill health in NHS staff, this had substantially declined by May and June 2020, corresponding with the decrease in pressures at work as the first wave of the epidemic subsided.

Published
2021

3. Occupational risks of COVID-19 in NHS workers in England

Author

Van der Plaat, D, Madan, I, Coggon, D, Van Tongeren, M, Edge, R, Muiry, R, Parsons, V, and Cullinan, P

Abstract

Objective To quantify occupational risks of Covid-19 among healthcare staff during the first wave of the pandemic in England Methods Using pseudonymised data on 902,813 individuals continuously employed by 191 National Health Service trusts during 1.1.19 to 31.7.20, we explored demographic and occupational risk factors for sickness absence ascribed to Covid-19 during 9.3.20 to 31.7.20 (n = 92,880). We estimated odds ratios (ORs) by multivariate logistic regression. Results With adjustment for employing trust, demographic characteristics, and previous frequency of sickness absence, risk relative to administrative/clerical occupations was highest in additional clinical services (a group that included care assistants) (OR 2.31), registered nursing and midwifery professionals (OR 2.28) and allied health professionals (OR 1.94), and intermediate in doctors and dentists (OR 1.55). Differences in risk were higher after the employing trust had started to care for documented Covid-19 patients, and were reduced, but not eliminated, following additional adjustment for exposure to infected patients or materials, assessed by a job-exposure matrix. For prolonged Covid-19 sickness absence (episodes lasting >14 days), the variation in risk by staff group was somewhat greater. Conclusions After allowance for possible bias and confounding by non-occupational exposures, we estimated that relative risks for Covid-19 among most patient-facing occupations were between 1.5 and 2.5. The highest risks were in those working in additional clinical services, nursing and midwifery and in allied health professions. Better protective measures for these staff groups should be a priority. Covid-19 may meet criteria for compensation as an occupational disease in some healthcare occupations.

Published
2021

4. Genetic correlation and causal relationships between cardio-metabolic traits and lung function impairment

Author

Wielscher, M. (Matthias), Amaral, A. F. (Andre F. S.), van der Plaat, D. (Diana), Wain, L. V. (Louise V.), Sebert, S. (Sylvain), Mosen-Ansorena, D. (David), Auvinen, J. (Juha), Herzig, K.-H. (Karl-Heinz), Dehghan, A. (Abbas), Jarvis, D. L. (Debbie L.), Järvelin, M.-R. (Marjo-Riitta), Wielscher, M. (Matthias), Amaral, A. F. (Andre F. S.), van der Plaat, D. (Diana), Wain, L. V. (Louise V.), Sebert, S. (Sylvain), Mosen-Ansorena, D. (David), Auvinen, J. (Juha), Herzig, K.-H. (Karl-Heinz), Dehghan, A. (Abbas), Jarvis, D. L. (Debbie L.), and Järvelin, M.-R. (Marjo-Riitta)

Abstract

Background: Associations of low lung function with features of poor cardio-metabolic health have been reported. It is, however, unclear whether these co-morbidities reflect causal associations, shared genetic heritability or are confounded by environmental factors. Methods: We performed three analyses: (1) cardio-metabolic health to lung function association tests in Northern Finland Birth cohort 1966, (2) cross-trait linkage disequilibrium score regression (LDSC) to compare genetic backgrounds and (3) Mendelian randomisation (MR) analysis to assess the causal effect of cardio-metabolic traits and disease on lung function, and vice versa (bidirectional MR). Genetic associations were obtained from the UK Biobank data or published large-scale genome-wide association studies (N > 82,000). Results: We observed a negative genetic correlation between lung function and cardio-metabolic traits and diseases. In Mendelian Randomisation analysis (MR), we found associations between type 2 diabetes (T2D) instruments and forced vital capacity (FVC) as well as FEV1/FVC. Body mass index (BMI) instruments were associated to all lung function traits and C-reactive protein (CRP) instruments to FVC. These genetic associations provide evidence for a causal effect of cardio-metabolic traits on lung function. Multivariable MR suggested independence of these causal effects from other tested cardio-metabolic traits and diseases. Analysis of lung function specific SNPs revealed a potential causal effect of FEV1/FVC on blood pressure. Conclusions: The present study overcomes many limitations of observational studies by using Mendelian Randomisation. We provide evidence for an independent causal effect of T2D, CRP and BMI on lung function with some of the T2D effect on lung function being attributed to inflammatory mechanisms. Furthermore, this analysis suggests a potential causal effect of FEV1/FVC on blood pressure. Our detailed analysis of the interplay between cardio-metabolic

Published
2021

6. Lung function changes over eight years and testosterone markers in both sexes: UK Biobank

Author

Lenoir, A, Fuertes, E, Gómez Real, F, Leynaert, B, Van der Plaat, D, and Jarvis, D

Subjects
respiratory system, respiratory tract diseases
Abstract

Higher levels of testosterone have been associated with better lung function in cross-sectional population-based studies. The role of testosterone on lung function in women, and on lung function decline in men or women is unclear. We studied 5,114 men and 5,467 women in UK Biobank with high-quality spirometry at baseline (2006-10) and 8.4 years later. We studied cross-sectional associations of total testosterone (TT), calculated free testosterone (cFT), free androgen index (FAI) and sex-hormone binding globulin (SHBG) with FEV1, FVC and FEV1/FVC using linear regression and associations of baseline markers with lung function decline using linear mixed effects regression. Men with higher levels of TT had higher FEV1 (27.56 ml per interquartile range (IQR) increase TT, 95%CI 5.43 to 49.68) and FVC (48.06 ml, 95%CI 22.07 to 74.06) at baseline. Higher cFT levels were associated with higher FEV1 and FVC among physically active men only. In women, higher FAI and cFT levels were associated with lower lung function at baseline, and higher levels of TT, cFT and FAI were associated with slightly attenuated FEV1 and FVC decline. Higher levels of SHBG were associated with better lung function in both sexes but slightly accelerated decline in men. In this population-based sample, higher levels of TT were associated with better lung function in men and higher levels of cFT with better lung function in physically active men. A small attenuation of lung function decline with higher levels of TT, cFT and FAI was seen in women only.

Published
2020

7. Epigenome-wide association study identifies DNA methylation markers for asthma remission in blood and nasal epithelium

Author

Qi, C, Vonk, J, Van der Plaat, D, Nieuwenhuis, M, Dijk, N, Aïssi, D, Siroux, V, Boezen, HM, Xu, C, and Koppelman, G

Abstract

Background: Asthma is a chronic respiratory disease which is not curable, yet some patients experience spontaneous remission. We hypothesized that epigenetic mechanisms may be involved in asthma remission. Methods: Clinical remission (ClinR) was defined as the absence of asthma symptoms and medication for at least 12 months, and complete remission (ComR) was defined as ClinR with normal lung function and absence of airway hyperresponsiveness. We analyzed differential DNA methylation of ClinR and ComR comparing to persistent asthma (PersA) in whole blood samples (n=72) and nasal brushing samples (n=97) in a longitudinal cohort of well characterized asthma patients. Significant findings of whole blood DNA methylation were tested for replication in two independent cohorts, Lifelines and EGEA. Results: We identified differentially methylated CpG sites associated with ClinR (7 CpG sites) and ComR (129 CpG sites) in whole blood. One CpG (cg13378519, Chr1) associated with ClinR was replicated and annotated to PEX11 (Peroxisomal Biogenesis Factor 11 Beta). The whole blood DNA methylation levels of this CpG were also different between ClinR and healthy subjects. One ComR-associated CpG (cg24788483, Chr10) that annotated to TCF7L2 (Transcription Factor 7 Like 2) was replicated and associated with expression of TCF7L2 gene. One out of seven ClinR-associated CpG sites and 8 out of 129 ComR-associated CpG sites identified from whole blood samples showed nominal significance (P

Published
2020

8. The use of two-sample methods for Mendelian randomization analyses on single large datasets

Author

Minelli, C, Fabiola Del Greco, M, Van der Plaat, D, Bowden, J, Sheehan, N, and Thompson, J

Abstract

Background With genome-wide association data for many exposures and outcomes now available from large biobanks, one-sample Mendelian randomization (MR) is increasingly used to investigate causal relationships. Many robust MR methods are available to address pleiotropy, but these assume independence between the gene-exposure and gene-outcome association estimates. Unlike in two-sample MR, in one-sample MR the two estimates are obtained from the same individuals, and the assumption of independence does not hold in the presence of confounding. Methods With simulations mimicking a typical study in UK Biobank we assessed the performance, in terms of bias and precision of the MR estimate, of the fixed-effect and (multiplicative) random-effects meta-analysis method, weighted median estimator, weighted mode estimator and MR-Egger regression, used in both one-sample and two-sample data. We considered scenarios differing for: presence/absence of a true causal effect; amount of confounding; presence and type of pleiotropy (none, balanced or directional). Results Even in the presence of substantial correlation due to confounding, all methods performed well when used in one-sample MR except for MR-Egger, which resulted in bias reflecting direction and magnitude of the confounding. Such bias was much reduced in the presence of very high variability in instrumental strength across variants (I 2 GX of 97%). Conclusions Two-sample MR methods can be safely used for one-sample MR performed within large biobanks, expect for MR-Egger. MR-Egger is not recommended for one-sample MR unless the correlation between the gene-exposure and gene-outcome estimates due to confounding can be kept low, or the variability in instrumental strength is very high. Key Messages Current availability of phenotypic and genetic data from large biobanks, such as UK Biobank, has led to increasing use of one-sample Mendelian randomization (MR) to investigate causal relationships in epidemiological research Robust MR methods have been developed to address pleiotropy, but they assume independence between the gene-exposure and gene-outcome association estimates; this holds in two-sample MR but not in one-sample MR We illustrate the practical implications, in terms of bias and precision of the MR causal effect estimate, of using robust two-sample methods in one-sample MR studies performed within large biobanks Two-sample MR methods can be safely used for one-sample MR performed within large biobanks, expect for MR-Egger regression MR-Egger is not recommended for one-sample MR unless the correlation between the gene-exposure and gene-outcome estimates due to confounding can be kept low, or the variability in instrumental strength is very high

Published
2020

11. A cross-omics integrative study of metabolic signatures of chronic obstructive pulmonary disease

Author

Prokić, I. (Ivana), Lahousse, L. (Lies), de Vries, M. (Maaike), Liu, J. (Jun), Kalaoja, M. (Marita), Vonk, J. M. (Judith M.), van der Plaat, D. A. (Diana A.), van Diemen, C. C. (Cleo C.), van der Spek, A. (Ashley), Zhernakova, A. (Alexandra), Fu, J. (Jingyuan), Ghanbari, M. (Mohsen), Ala-Korpela, M. (Mika), Kettunen, J. (Johannes), Havulinna, A. S. (Aki S.), Perola, M. (Markus), Salomaa, V. (Veikko), Lind, L. (Lars), Ärnlöv, J. (Johan), Stricker, B. H. (Bruno H. C.), Brusselle, G. G. (Guy G.), Boezen, H. M. (H. Marike), van Duijn, C. M. (Cornelia M.), Amin, N. (Najaf), Prokić, I. (Ivana), Lahousse, L. (Lies), de Vries, M. (Maaike), Liu, J. (Jun), Kalaoja, M. (Marita), Vonk, J. M. (Judith M.), van der Plaat, D. A. (Diana A.), van Diemen, C. C. (Cleo C.), van der Spek, A. (Ashley), Zhernakova, A. (Alexandra), Fu, J. (Jingyuan), Ghanbari, M. (Mohsen), Ala-Korpela, M. (Mika), Kettunen, J. (Johannes), Havulinna, A. S. (Aki S.), Perola, M. (Markus), Salomaa, V. (Veikko), Lind, L. (Lars), Ärnlöv, J. (Johan), Stricker, B. H. (Bruno H. C.), Brusselle, G. G. (Guy G.), Boezen, H. M. (H. Marike), van Duijn, C. M. (Cornelia M.), and Amin, N. (Najaf)

Abstract

Background: Chronic obstructive pulmonary disease (COPD) is a common lung disorder characterized by persistent and progressive airflow limitation as well as systemic changes. Metabolic changes in blood may help detect COPD in an earlier stage and predict prognosis. Methods: We conducted a comprehensive study of circulating metabolites, measured by proton Nuclear Magnetic Resonance Spectroscopy, in relation with COPD and lung function. The discovery sample consisted of 5557 individuals from two large population-based studies in the Netherlands, the Rotterdam Study and the Erasmus Rucphen Family study. Significant findings were replicated in 12,205 individuals from the Lifelines-DEEP study, FINRISK and the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) studies. For replicated metabolites further investigation of causality was performed, utilizing genetics in the Mendelian randomization approach. Results: There were 602 cases of COPD and 4955 controls used in the discovery meta-analysis. Our logistic regression results showed that higher levels of plasma Glycoprotein acetyls (GlycA) are significantly associated with COPD (OR = 1.16, P = 5.6 × 10⁻⁴ in the discovery and OR = 1.30, P = 1.8 × 10⁻⁶ in the replication sample). A bi-directional two-sample Mendelian randomization analysis suggested that circulating blood GlycA is not causally related to COPD, but that COPD causally increases GlycA levels. Using the prospective data of the same sample of Rotterdam Study in Cox-regression, we show that the circulating GlycA level is a predictive biomarker of COPD incidence (HR = 1.99, 95%CI 1.52–2.60, comparing those in the highest and lowest quartile of GlycA) but is not significantly associated with mortality in COPD patients (HR = 1.07, 95%CI 0.94–1.20). Conclusions: Our study shows that circulating blood GlycA is a biomarker of early COPD pathology.

Published
2020

12. Epigenome-wide association study of lung function level and its change

Author

Imboden, M. (Medea), Wielscher, M. (Matthias), Rezwan, F. I. (Faisal I.), Amaral, A. F. (André F.S.), Schaffner, E. (Emmanuel), Jeong, A. (Ayoung), Beckmeyer-Borowko, A. (Anna), Harris, S. E. (Sarah E.), Starr, J. M. (John M.), Deary, I. J. (Ian J.), Flexeder, C. (Claudia), Waldenberger, M. (Melanie), Peters, A. (Annette), Schulz, H. (Holger), Chen, S. (Su), Sunny, S. K. (Shadia Khan), Karmaus, W. J. (Wilfried J.J.), Jiang, Y. (Yu), Erhart, G. (Gertraud), Kronenberg, F. (Florian), Arathimos, R. (Ryan), Sharp, G. C. (Gemma C.), Henderson, A. J. (Alexander John), Fu, Y. (Yu), Piirilä, P. (Päivi), Pietiläinen, K. H. (Kirsi H.), Ollikainen, M. (Miina), Johansson, A. (Asa), Gyllensten, U. (Ulf), de Vries, M. (Maaike), van der Plaat, D. A. (Diana A.), de Jong, K. (Kim), Boezen, H. M. (H. Marike), Hall, I. P. (Ian P.), Tobin, M. D. (Martin D.), Jarvelin, M.-R. (Marjo-Riitta), Holloway, J. W. (John W.), Jarvis, D. (Deborah), Probst-Hensch, N. M. (Nicole M.), Imboden, M. (Medea), Wielscher, M. (Matthias), Rezwan, F. I. (Faisal I.), Amaral, A. F. (André F.S.), Schaffner, E. (Emmanuel), Jeong, A. (Ayoung), Beckmeyer-Borowko, A. (Anna), Harris, S. E. (Sarah E.), Starr, J. M. (John M.), Deary, I. J. (Ian J.), Flexeder, C. (Claudia), Waldenberger, M. (Melanie), Peters, A. (Annette), Schulz, H. (Holger), Chen, S. (Su), Sunny, S. K. (Shadia Khan), Karmaus, W. J. (Wilfried J.J.), Jiang, Y. (Yu), Erhart, G. (Gertraud), Kronenberg, F. (Florian), Arathimos, R. (Ryan), Sharp, G. C. (Gemma C.), Henderson, A. J. (Alexander John), Fu, Y. (Yu), Piirilä, P. (Päivi), Pietiläinen, K. H. (Kirsi H.), Ollikainen, M. (Miina), Johansson, A. (Asa), Gyllensten, U. (Ulf), de Vries, M. (Maaike), van der Plaat, D. A. (Diana A.), de Jong, K. (Kim), Boezen, H. M. (H. Marike), Hall, I. P. (Ian P.), Tobin, M. D. (Martin D.), Jarvelin, M.-R. (Marjo-Riitta), Holloway, J. W. (John W.), Jarvis, D. (Deborah), and Probst-Hensch, N. M. (Nicole M.)

Abstract

Previous reports link differential DNA methylation (DNAme) to environmental exposures that are associated with lung function. Direct evidence on lung function DNAme is, however, limited. We undertook an agnostic epigenome-wide association study (EWAS) on pre-bronchodilation lung function and its change in adults. In a discovery–replication EWAS design, DNAme in blood and spirometry were measured twice, 6—15 years apart, in the same participants of three adult population-based discovery cohorts (n=2043). Associated DNAme markers (p<5×10−7) were tested in seven replication cohorts (adult: n=3327; childhood: n=420). Technical bias-adjusted residuals of a regression of the normalised absolute β-values on control probe-derived principle components were regressed on level and change of forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and their ratio (FEV1/FVC) in the covariate-adjusted discovery EWAS. Inverse-variance-weighted meta-analyses were performed on results from discovery and replication samples in all participants and never-smokers. EWAS signals were enriched for smoking-related DNAme. We replicated 57 lung function DNAme markers in adult, but not childhood samples, all previously associated with smoking. Markers not previously associated with smoking failed replication. cg05575921 (AHRR (aryl hydrocarbon receptor repressor)) showed the statistically most significant association with cross-sectional lung function (FEV1/FVC: pdiscovery=3.96×10−21 and pcombined=7.22×10−50). A score combining 10 DNAme markers previously reported to mediate the effect of smoking on lung function was associated with lung function (FEV1/FVC: p=2.65×10−20). Our results reveal that lung function-associated methylation signals in adults are predominantly smoking related, and possibly of clinical utility in identifying poor lung function and accelerated decline. Larger studies with more repeat time-points are needed to identify lung function DNAme in never-s

Published
2019

13. Occupational exposure to gases/fumes and mineral dust affect DNA methylation levels of genes regulating expression

Author

van Der Plaat, D., Vonk, J.M. (Judith), Terzikhan, N. (Natalie), de Jong, K., Boersma - de Vries, M., la Bastide-van Gemert, S, Boezen, H.M. (Marike), van Der Plaat, D., Vonk, J.M. (Judith), Terzikhan, N. (Natalie), de Jong, K., Boersma - de Vries, M., la Bastide-van Gemert, S, and Boezen, H.M. (Marike)

Abstract

Many workers are daily exposed to occupational agents like gases/fumes, mineral dust or biological dust, which could induce adverse health effects. Epigenetic mechanisms, such as DNA methylation, have been suggested to play a role. We therefore aimed to identify differentially methylated regions (DMRs) upon occupational exposures in never-smokers and investigated if these DMRs associated with gene expression levels. To determine the effects of occupational exposures independent of smoking, 903 never-smokers of the LifeLines cohort study were included. We performed three genome-wide methylation analyses (Illumina 450 K), one per occupational exposure being gases/fumes, mineral dust and biological dust, using robust linear regression adjusted for appropriate confounders. DMRs were identified using comb-p in Python. Results were validated in the Rotterdam Study (233 never-smokers) and methylation-expression associations were assessed using Biobank-based Integrative Omics Study data (n = 2802). Of the total 21 significant DMRs, 14 DMRs were a

Published
2019
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14. Meta-analysis of epigenome-wide association studies in neonates reveals widespread differential DNA methylation associated with birthweight

Author

Kupers, L. K. (Leanne K.), Monnereau, C. (Claire), Sharp, G. C. (Gemma C.), Yousefi, P. (Paul), Salas, L. A. (Lucas A.), Ghantous, A. (Akram), Page, C. M. (Christian M.), Reese, S. E. (Sarah E.), Wilcox, A. J. (Allen J.), Czamara, D. (Darina), Starling, A. P. (Anne P.), Novoloaca, A. (Alexei), Lent, S. (Samantha), Roy, R. (Ritu), Hoyo, C. (Cathrine), Breton, C. V. (Carrie, V), Allard, C. (Catherine), Just, A. C. (Allan C.), Bakulski, K. M. (Kelly M.), Holloway, J. W. (John W.), Everson, T. M. (Todd M.), Xu, C.-J. (Cheng-Jian), Huang, R.-C. (Rae-Chi), van der Plaat, D. A. (Diana A.), Wielscher, M. (Matthias), Merid, S. K. (Simon Kebede), Ullemar, V. (Vilhelmina), Rezwan, F. I. (Faisal, I), Lahti, J. (Jari), van Dongen, J. (Jenny), Langie, S. A. (Sabine A. S.), Richardson, T. G. (Tom G.), Magnus, M. C. (Maria C.), Nohr, E. A. (Ellen A.), Xu, Z. (Zongli), Duijts, L. (Liesbeth), Zhao, S. (Shanshan), Zhang, W. (Weiming), Plusquin, M. (Michelle), DeMeo, D. L. (Dawn L.), Solomon, O. (Olivia), Heimovaara, J. H. (Joosje H.), Jima, D. D. (Dereje D.), Gao, L. (Lu), Bustamante, M. (Mariona), Perron, P. (Patrice), Wright, R. O. (Robert O.), Hertz-Picciotto, I. (Irva), Zhang, H. (Hongmei), Karagas, M. R. (Margaret R.), Gehring, U. (Ulrike), Marsit, C. J. (Carmen J.), Beilin, L. J. (Lawrence J.), Vonk, J. M. (Judith M.), Jarvelin, M.-R. (Marjo-Riitta), Bergstrom, A. (Anna), Ortqvist, A. K. (Anne K.), Ewart, S. (Susan), Villa, P. M. (Pia M.), Moore, S. E. (Sophie E.), Willemsen, G. (Gonneke), Standaert, A. R. (Arnout R. L.), Haberg, S. E. (Siri E.), Sorensen, T. I. (Thorkild I. A.), Taylor, J. A. (Jack A.), Raikkonen, K. (Katri), Yang, I. V. (Ivana, V), Kechris, K. (Katerina), Nawrot, T. S. (Tim S.), Silver, M. J. (Matt J.), Gong, Y. Y. (Yun Yun), Richiardi, L. (Lorenzo), Kogevinas, M. (Manolis), Litonjua, A. A. (Augusto A.), Eskenazi, B. (Brenda), Huen, K. (Karen), Mbarek, H. (Hamdi), Maguire, R. L. (Rachel L.), Dwyer, T. (Terence), Vrijheid, M. (Martine), Bouchard, L. (Luigi), Baccarelli, A. A. (Andrea A.), Croen, L. A. (Lisa A.), Karmaus, W. (Wilfried), Anderson, D. (Denise), de Vries, M. (Maaike), Sebert, S. (Sylvain), Kere, J. (Juha), Karlsson, R. (Robert), Arshad, S. H. (Syed Hasan), Hamalainen, E. (Esa), Routledge, M. N. (Michael N.), Boomsma, D. I. (Dorret, I), Feinberg, A. P. (Andrew P.), Newschaffer, C. J. (Craig J.), Govarts, E. (Eva), Moisse, M. (Matthieu), Fallin, M. D. (M. Daniele), Melen, E. (Erik), Prentice, A. M. (Andrew M.), Kajantie, E. (Eero), Almqvist, C. (Catarina), Oken, E. (Emily), Dabelea, D. (Dana), Boezen, H. M. (H. Marike), Melton, P. E. (Phillip E.), Wright, R. J. (Rosalind J.), Koppelman, G. H. (Gerard H.), Trevisi, L. (Letizia), Hivert, M.-F. (Marie-France), Sunyer, J. (Jordi), Munthe-Kaas, M. C. (Monica C.), Murphy, S. K. (Susan K.), Corpeleijn, E. (Eva), Wiemels, J. (Joseph), Holland, N. (Nina), Herceg, Z. (Zdenko), Binder, E. B. (Elisabeth B.), Smith, G. D. (George Davey), Jaddoe, V. W. (Vincent W. V.), Lie, R. T. (Rolv T.), Nystad, W. (Wenche), London, S. J. (Stephanie J.), Lawlor, D. A. (Debbie A.), Relton, C. L. (Caroline L.), Snieder, H. (Harold), Felix, J. F. (Janine F.), Kupers, L. K. (Leanne K.), Monnereau, C. (Claire), Sharp, G. C. (Gemma C.), Yousefi, P. (Paul), Salas, L. A. (Lucas A.), Ghantous, A. (Akram), Page, C. M. (Christian M.), Reese, S. E. (Sarah E.), Wilcox, A. J. (Allen J.), Czamara, D. (Darina), Starling, A. P. (Anne P.), Novoloaca, A. (Alexei), Lent, S. (Samantha), Roy, R. (Ritu), Hoyo, C. (Cathrine), Breton, C. V. (Carrie, V), Allard, C. (Catherine), Just, A. C. (Allan C.), Bakulski, K. M. (Kelly M.), Holloway, J. W. (John W.), Everson, T. M. (Todd M.), Xu, C.-J. (Cheng-Jian), Huang, R.-C. (Rae-Chi), van der Plaat, D. A. (Diana A.), Wielscher, M. (Matthias), Merid, S. K. (Simon Kebede), Ullemar, V. (Vilhelmina), Rezwan, F. I. (Faisal, I), Lahti, J. (Jari), van Dongen, J. (Jenny), Langie, S. A. (Sabine A. S.), Richardson, T. G. (Tom G.), Magnus, M. C. (Maria C.), Nohr, E. A. (Ellen A.), Xu, Z. (Zongli), Duijts, L. (Liesbeth), Zhao, S. (Shanshan), Zhang, W. (Weiming), Plusquin, M. (Michelle), DeMeo, D. L. (Dawn L.), Solomon, O. (Olivia), Heimovaara, J. H. (Joosje H.), Jima, D. D. (Dereje D.), Gao, L. (Lu), Bustamante, M. (Mariona), Perron, P. (Patrice), Wright, R. O. (Robert O.), Hertz-Picciotto, I. (Irva), Zhang, H. (Hongmei), Karagas, M. R. (Margaret R.), Gehring, U. (Ulrike), Marsit, C. J. (Carmen J.), Beilin, L. J. (Lawrence J.), Vonk, J. M. (Judith M.), Jarvelin, M.-R. (Marjo-Riitta), Bergstrom, A. (Anna), Ortqvist, A. K. (Anne K.), Ewart, S. (Susan), Villa, P. M. (Pia M.), Moore, S. E. (Sophie E.), Willemsen, G. (Gonneke), Standaert, A. R. (Arnout R. L.), Haberg, S. E. (Siri E.), Sorensen, T. I. (Thorkild I. A.), Taylor, J. A. (Jack A.), Raikkonen, K. (Katri), Yang, I. V. (Ivana, V), Kechris, K. (Katerina), Nawrot, T. S. (Tim S.), Silver, M. J. (Matt J.), Gong, Y. Y. (Yun Yun), Richiardi, L. (Lorenzo), Kogevinas, M. (Manolis), Litonjua, A. A. (Augusto A.), Eskenazi, B. (Brenda), Huen, K. (Karen), Mbarek, H. (Hamdi), Maguire, R. L. (Rachel L.), Dwyer, T. (Terence), Vrijheid, M. (Martine), Bouchard, L. (Luigi), Baccarelli, A. A. (Andrea A.), Croen, L. A. (Lisa A.), Karmaus, W. (Wilfried), Anderson, D. (Denise), de Vries, M. (Maaike), Sebert, S. (Sylvain), Kere, J. (Juha), Karlsson, R. (Robert), Arshad, S. H. (Syed Hasan), Hamalainen, E. (Esa), Routledge, M. N. (Michael N.), Boomsma, D. I. (Dorret, I), Feinberg, A. P. (Andrew P.), Newschaffer, C. J. (Craig J.), Govarts, E. (Eva), Moisse, M. (Matthieu), Fallin, M. D. (M. Daniele), Melen, E. (Erik), Prentice, A. M. (Andrew M.), Kajantie, E. (Eero), Almqvist, C. (Catarina), Oken, E. (Emily), Dabelea, D. (Dana), Boezen, H. M. (H. Marike), Melton, P. E. (Phillip E.), Wright, R. J. (Rosalind J.), Koppelman, G. H. (Gerard H.), Trevisi, L. (Letizia), Hivert, M.-F. (Marie-France), Sunyer, J. (Jordi), Munthe-Kaas, M. C. (Monica C.), Murphy, S. K. (Susan K.), Corpeleijn, E. (Eva), Wiemels, J. (Joseph), Holland, N. (Nina), Herceg, Z. (Zdenko), Binder, E. B. (Elisabeth B.), Smith, G. D. (George Davey), Jaddoe, V. W. (Vincent W. V.), Lie, R. T. (Rolv T.), Nystad, W. (Wenche), London, S. J. (Stephanie J.), Lawlor, D. A. (Debbie A.), Relton, C. L. (Caroline L.), Snieder, H. (Harold), and Felix, J. F. (Janine F.)

Abstract

Birthweight is associated with health outcomes across the life course, DNA methylation may be an underlying mechanism. In this meta-analysis of epigenome-wide association studies of 8,825 neonates from 24 birth cohorts in the Pregnancy And Childhood Epigenetics Consortium, we find that DNA methylation in neonatal blood is associated with birthweight at 914 sites, with a difference in birthweight ranging from −183 to 178 grams per 10% increase in methylation (PBonferroni < 1.06 x 10−7). In additional analyses in 7,278 participants, <1.3% of birthweight-associated differential methylation is also observed in childhood and adolescence, but not adulthood. Birthweight-related CpGs overlap with some Bonferroni-significant CpGs that were previously reported to be related to maternal smoking (55/914, p = 6.12 x 10−74) and BMI in pregnancy (3/914, p = 1.13x10−3), but not with those related to folate levels in pregnancy. Whether the associations that we observe are causal or explained by confounding or fetal growth influencing DNA methylation (i.e. reverse causality) requires further research.

Published
2019

15. Occupational exposure to gases/fumes and mineral dust affect DNA methylation levels of genes regulating expression

Author

van Der Plaat, D, Vonk, JM, Terzikhan, Natalie, Jong, K, Boersma - de Vries, M, la Bastide-van Gemert, S, Lahousse, Lies, Brusselle, Guy, Prokic, Ivana, Amin, Najaf, Duijn, Cornelia, Boezen, HM, van Der Plaat, D, Vonk, JM, Terzikhan, Natalie, Jong, K, Boersma - de Vries, M, la Bastide-van Gemert, S, Lahousse, Lies, Brusselle, Guy, Prokic, Ivana, Amin, Najaf, Duijn, Cornelia, and Boezen, HM

Published
2019

17. Multi-omics approach to assess genetic susceptibility of COPD in never-smokers

Author

van der Plaat, D. A., Vonk, J. M., Lahousse, L., de Jong, K., Faiz, A., Nedeljkovic, I., Amin, N., van Diemen, C. C., Brusselle, G. G., Bosse, Y., Brandsma, C., Hao, K., Pare, P. D., van Duijn, C. M., Postma, D. S., Boezen, H., Groningen Research Institute for Asthma and COPD (GRIAC), and Life Course Epidemiology (LCE)

Published
2018

18. Epigenomewide association study identifies DNA methylation markers for asthma remission

Author

Xu, C., van der Plaat, D. A., Qi, C., Boezen, H. M., Vonk, J. M., Koppelman, G. H., Groningen Research Institute for Asthma and COPD (GRIAC), and Life Course Epidemiology (LCE)

Subjects
Science & Technology, Critical Care Medicine, General & Internal Medicine, Respiratory System, 11 Medical And Health Sciences, Life Sciences & Biomedicine
Published
2018

20. Occupational exposure to pesticides is associated with differential DNA methylation

Author

van der Plaat, D A, Jong, K, Vries, M, van Diemen, CC, Prokic, Ivana, Amin, Najaf, Kromhout, H, Vermeulen, R, Postma, DS, Duijn, CM, Boezen, HM, Vonk, JM, van der Plaat, D A, Jong, K, Vries, M, van Diemen, CC, Prokic, Ivana, Amin, Najaf, Kromhout, H, Vermeulen, R, Postma, DS, Duijn, CM, Boezen, HM, and Vonk, JM

Published
2018

21. A Genome-Wide Linkage Study for Chronic Obstructive Pulmonary Disease in a Dutch Genetic Isolate Identifies Novel Rare Candidate Variants

Author

Prokic, Ivana, Terzikhan, Natalie, Vonk, JM, van der Plaat, D A, Lahousse, Lies, van Diemen, CC, Hobbs, BD, Qiao, D, Cho, MH, Brusselle, Guy, Postma, DS, Boezen, HM, Duijn, Cornelia, Amin, Najaf, Prokic, Ivana, Terzikhan, Natalie, Vonk, JM, van der Plaat, D A, Lahousse, Lies, van Diemen, CC, Hobbs, BD, Qiao, D, Cho, MH, Brusselle, Guy, Postma, DS, Boezen, HM, Duijn, Cornelia, and Amin, Najaf

Published
2018

22. COPD GWAS variant at 19q13.2 in relation with DNA methylation and gene expression

Author

Prokic, Ivana, Lahousse, Lies, Carnero Montoro, Elena, Faiz, A, Vonk, JM, Jong, K, van der Plaat, D A, van Diemen, CC, Berge, M, Obeidat, M, Bosse, Y, Nickle, DC, Uitterlinden, André, van Meurs, Joyce, Stricker, Bruno, Brusselle, Guy, Postma, DS, Boezen, HM, Duijn, Cornelia, Amin, Najaf, Prokic, Ivana, Lahousse, Lies, Carnero Montoro, Elena, Faiz, A, Vonk, JM, Jong, K, van der Plaat, D A, van Diemen, CC, Berge, M, Obeidat, M, Bosse, Y, Nickle, DC, Uitterlinden, André, van Meurs, Joyce, Stricker, Bruno, Brusselle, Guy, Postma, DS, Boezen, HM, Duijn, Cornelia, and Amin, Najaf

Published
2018

23. Long-term Air Pollution Exposure, Genome-wide DNA Methylation and Lung Function in the LifeLines Cohort Study

Author

Lichtenfels, A, van der Plaat, D A, Jong, K, van Diemen, CC, Postma, DS, Prokic, Ivana, Duijn, Cornelia, Amin, Najaf, la Bastide-van Gemert, S, Vries, M, Ward-Caviness, CK, De Wolf, K, Waldenberger, M, Peters, A, Stolk, RP, Brunekreef, B, Boezen, HM, Vonk, JM, Lichtenfels, A, van der Plaat, D A, Jong, K, van Diemen, CC, Postma, DS, Prokic, Ivana, Duijn, Cornelia, Amin, Najaf, la Bastide-van Gemert, S, Vries, M, Ward-Caviness, CK, De Wolf, K, Waldenberger, M, Peters, A, Stolk, RP, Brunekreef, B, Boezen, HM, and Vonk, JM

Published
2018

25. Identification Of Novel Genes Related To Obstruction Of The Small Airways In Adult Never-Smokers

Author

Van Der Plaat, D. A., De Jong, K., Faiz, A., Vonk, Judith, Van Diemen, C. C., Nedeljkovic, I., Amin, N., Brandsma, Corry-Anke, Bosse, Y., Sin, D. D., Nickle, D. C., Van Duijn, C. M., Boezen, H., Postma, D. S., Groningen Research Institute for Asthma and COPD (GRIAC), Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI), and Life Course Epidemiology (LCE)

Published
2016

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