Institution
University of Groningen
Education•Groningen, Groningen, Netherlands•
About: University of Groningen is a education organization based out in Groningen, Groningen, Netherlands. It is known for research contribution in the topics: Population & Poison control. The organization has 36346 authors who have published 69116 publications receiving 2940370 citations. The organization is also known as: Rijksuniversiteit Groningen & RUG.
Papers published on a yearly basis
Papers
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TL;DR: Extended sources of far-infrared emission superposed on the zodiacal and galactic backgrounds are found at high galactic latitudes and near the ecliptic plane as discussed by the authors.
Abstract: Extended sources of far-infrared emission superposed on the zodiacal and galactic backgrounds are found at high galactic latitudes and near the ecliptic plane. Clouds of interstellar dust at color temperatures as high as 35 K account for much of this complex structure, but the relationship to H I column density is not simple. Other features of the extended emission show the existence of warm structures within the solar system. Three bands of dust clouds at temperatures of 150-200 K appear within 10 deg on both sides of the ecliptic plane. Their ecliptic latitudes and derived distances suggest that they are associated with the main asteroid belt. A third component of the 100-micron cirrus, poorly correlated with H I, may represent cold material in the outer solar system or a new component of the interstellar medium.
448 citations
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19 Apr 2016TL;DR: The authors compared bi-LSTMs with word, character, and unicode byte embeddings for POS tagging and showed that biLSTM is less sensitive to training data size and label corruptions than previously assumed.
Abstract: Bidirectional long short-term memory (biLSTM) networks have recently proven successful for various NLP sequence modeling tasks, but little is known about their reliance to input representations, target languages, data set size, and label noise. We address these issues and evaluate bi-LSTMs with word, character, and unicode byte embeddings for POS tagging. We compare bi-LSTMs to traditional POS taggers across languages and data sizes. We also present a novel biLSTM model, which combines the POS tagging loss function with an auxiliary loss function that accounts for rare words. The model obtains state-of-the-art performance across 22 languages, and works especially well for morphologically complex languages. Our analysis suggests that biLSTMs are less sensitive to training data size and label corruptions (at small noise levels) than previously assumed.
448 citations
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Harvard University1, Broad Institute2, University of Liège3, University of Oxford4, Wellcome Trust Sanger Institute5, Montreal Heart Institute6, University of Southern Denmark7, Katholieke Universiteit Leuven8, Wellcome Trust Centre for Human Genetics9, John Radcliffe Hospital10, Karolinska Institutet11, Ikerbasque12, Illumina13, University of Kiel14, Örebro University15, Cedars-Sinai Medical Center16, Lancaster University17, University of Western Australia18, Western General Hospital19, Norwegian University of Life Sciences20, Wellcome Trust21, University Medical Center Groningen22, University of Groningen23, University of Pittsburgh24, University of the Witwatersrand25, King's College London26, Université de Montréal27, Yale University28
TL;DR: The results of this study suggest that high-resolution fine-mapping in large samples can convert many discoveries from genome-wide association studies into statistically convincing causal variants, providing a powerful substrate for experimental elucidation of disease mechanisms.
Abstract: Inflammatory bowel diseases are chronic gastrointestinal inflammatory disorders that affect millions of people worldwide. Genome-wide association studies have identified 200 inflammatory bowel disease-associated loci, but few have been conclusively resolved to specific functional variants. Here we report fine-mapping of 94 inflammatory bowel disease loci using high-density genotyping in 67,852 individuals. We pinpoint 18 associations to a single causal variant with greater than 95% certainty, and an additional 27 associations to a single variant with greater than 50% certainty. These 45 variants are significantly enriched for protein-coding changes (n = 13), direct disruption of transcription-factor binding sites (n = 3), and tissue-specific epigenetic marks (n = 10), with the last category showing enrichment in specific immune cells among associations stronger in Crohn's disease and in gut mucosa among associations stronger in ulcerative colitis. The results of this study suggest that high-resolution fine-mapping in large samples can convert many discoveries from genome-wide association studies into statistically convincing causal variants, providing a powerful substrate for experimental elucidation of disease mechanisms.
447 citations
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University of Pittsburgh1, University of Birmingham2, University of Edinburgh3, Princess Alexandra Hospital4, Royal Free Hospital5, University of Groningen6, University of Gothenburg7, Kyoto University8, University of Chicago9, Harvard University10, University of California, Los Angeles11, Stanford University12, Rikshospitalet–Radiumhospitalet13, University of Vienna14, Yale University15, University of Patras16, Toronto General Hospital17, Mayo Clinic18, St James's University Hospital19
447 citations
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Medical Research Council1, Harvard University2, Lund University3, University of Minnesota4, Duke University5, University of Oulu6, Novo Nordisk7, Technische Universität München8, University College London9, University of Lausanne10, University of Eastern Finland11, National University of Singapore12, King's College London13, University of Bristol14, George Washington University15, National Institutes of Health16, University of Bergen17, University of Michigan18, University of North Carolina at Chapel Hill19, University of Groningen20, Utrecht University21, University of Copenhagen22, Erasmus University Rotterdam23, University of Tübingen24, Harokopio University25, Washington University in St. Louis26, University of Maryland, Baltimore27, University of Granada28, Complutense University of Madrid29, University of Turku30, University of Southern Denmark31, Umeå University32, University of Gothenburg33, Laval University34, University of London35, Pennington Biomedical Research Center36, Lille University of Science and Technology37, Newcastle University38, University of Iceland39, Danube University Krems40, Broad Institute41, University of California, Los Angeles42, Hammersmith Hospital43, University of Cambridge44, National Institute for Health and Welfare45
TL;DR: In this paper, a meta-analysis of data from 45 studies of adults and nine studies of children and adolescents was conducted to confirm or refute unambiguously whether physical activity attenuates the association of FTO with obesity risk.
Abstract: Background: The FTO gene harbors the strongest known susceptibility locus for obesity. While many individual studies have suggested that physical activity (PA) may attenuate the effect of FTO on obesity risk, other studies have not been able to confirm this interaction. To confirm or refute unambiguously whether PA attenuates the association of FTO with obesity risk, we meta-analyzed data from 45 studies of adults (n=218,166) and nine studies of children and adolescents (n=19,268). Methods and Findings: All studies identified to have data on the FTO rs9939609 variant (or any proxy [r(2)>0.8]) and PA were invited to participate, regardless of ethnicity or age of the participants. PA was standardized by categorizing it into a dichotomous variable (physically inactive versus active) in each study. Overall, 25% of adults and 13% of children were categorized as inactive. Interaction analyses were performed within each study by including the FTOxPA interaction term in an additive model, adjusting for age and sex. Subsequently, random effects meta-analysis was used to pool the interaction terms. In adults, the minor (A-) allele of rs9939609 increased the odds of obesity by 1.23-fold/allele (95% CI 1.20-1.26), but PA attenuated this effect (p(interaction) = 0.001). More specifically, the minor allele of rs9939609 increased the odds of obesity less in the physically active group (odds ratio = 1.22/allele, 95% CI 1.19-1.25) than in the inactive group (odds ratio = 1.30/allele, 95% CI 1.24-1.36). No such interaction was found in children and adolescents. Conclusions: The association of the FTO risk allele with the odds of obesity is attenuated by 27% in physically active adults, highlighting the importance of PA in particular in those genetically predisposed to obesity.
447 citations
Authors
Showing all 36692 results
Name | H-index | Papers | Citations |
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Ronald C. Kessler | 274 | 1332 | 328983 |
Nicholas J. Wareham | 212 | 1657 | 204896 |
André G. Uitterlinden | 199 | 1229 | 156747 |
Lei Jiang | 170 | 2244 | 135205 |
Brenda W.J.H. Penninx | 170 | 1139 | 119082 |
Richard H. Friend | 169 | 1182 | 140032 |
Panos Deloukas | 162 | 410 | 154018 |
Jerome I. Rotter | 156 | 1071 | 116296 |
Christopher M. Dobson | 150 | 1008 | 105475 |
Dirk Inzé | 149 | 647 | 74468 |
Scott T. Weiss | 147 | 1025 | 74742 |
Dieter Lutz | 139 | 671 | 67414 |
Wilmar B. Schaufeli | 137 | 513 | 95718 |
Cisca Wijmenga | 136 | 668 | 86572 |
Arnold B. Bakker | 135 | 506 | 103778 |