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Institution

University of Iceland

EducationReykjavik, Suðurnes, Iceland
About: University of Iceland is a education organization based out in Reykjavik, Suðurnes, Iceland. It is known for research contribution in the topics: Population & Genome-wide association study. The organization has 5423 authors who have published 16199 publications receiving 694762 citations. The organization is also known as: Háskóli Íslands.


Papers
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Journal ArticleDOI
TL;DR: The Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium and collaborating non-member studies or consortia provide an excellent framework for the identification of the genetic determinants of risk factors, subclinical-disease measures, and clinical events.
Abstract: Background— The primary aim of genome-wide association studies is to identify novel genetic loci associated with interindividual variation in the levels of risk factors, the degree of subclinical disease, or the risk of clinical disease. The requirement for large sample sizes and the importance of replication have served as powerful incentives for scientific collaboration. Methods— The Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium was formed to facilitate genome-wide association studies meta-analyses and replication opportunities among multiple large population-based cohort studies, which collect data in a standardized fashion and represent the preferred method for estimating disease incidence. The design of the Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium includes 5 prospective cohort studies from the United States and Europe: the Age, Gene/Environment Susceptibility—Reykjavik Study, the Atherosclerosis Risk in Communities Study, the Cardiovascular Health Study, the Framingham Heart Study, and the Rotterdam Study. With genome-wide data on a total of about 38 000 individuals, these cohort studies have a large number of health-related phenotypes measured in similar ways. For each harmonized trait, within-cohort genome-wide association study analyses are combined by meta-analysis. A prospective meta-analysis of data from all 5 cohorts, with a properly selected level of genome-wide statistical significance, is a powerful approach to finding genuine phenotypic associations with novel genetic loci. Conclusions— The Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium and collaborating non-member studies or consortia provide an excellent framework for the identification of the genetic determinants of risk factors, subclinical-disease measures, and clinical events. Received October 17, 2008; accepted December 17, 2008.

596 citations

Journal ArticleDOI
TL;DR: The full public release of all data from the TNG100 and TNG300 simulations of the IllustrisTNG project is presented in this article, which includes a comprehensive model for galaxy formation physics, and each TNG simulation selfconsistently solves for the coupled evolution of dark matter, cosmic gas, luminous stars, and supermassive black holes from early time to the present day.
Abstract: We present the full public release of all data from the TNG100 and TNG300 simulations of the IllustrisTNG project. IllustrisTNG is a suite of large volume, cosmological, gravo-magnetohydrodynamical simulations run with the moving-mesh code Arepo. TNG includes a comprehensive model for galaxy formation physics, and each TNG simulation self-consistently solves for the coupled evolution of dark matter, cosmic gas, luminous stars, and supermassive black holes from early time to the present day, $z=0$ . Each of the flagship runs—TNG50, TNG100, and TNG300—are accompanied by halo/subhalo catalogs, merger trees, lower-resolution and dark-matter only counterparts, all available with 100 snapshots. We discuss scientific and numerical cautions and caveats relevant when using TNG. The data volume now directly accessible online is ∼750 TB, including 1200 full volume snapshots and ∼80,000 high time-resolution subbox snapshots. This will increase to ∼1.1 PB with the future release of TNG50. Data access and analysis examples are available in IDL, Python, and Matlab. We describe improvements and new functionality in the web-based API, including on-demand visualization and analysis of galaxies and halos, exploratory plotting of scaling relations and other relationships between galactic and halo properties, and a new JupyterLab interface. This provides an online, browser-based, near-native data analysis platform enabling user computation with local access to TNG data, alleviating the need to download large datasets.

588 citations

Journal ArticleDOI
Thomas W. Winkler1, Anne E. Justice2, Mariaelisa Graff2, Llilda Barata3  +435 moreInstitutions (106)
TL;DR: In this paper, the authors performed meta-analyses of 114 studies with genome-wide chip and/or Metabochip data by the Genetic Investigation of Anthropometric Traits (GIANT) Consortium.
Abstract: Genome-wide association studies (GWAS) have identified more than 100 genetic variants contributing to BMI, a measure of body size, or waist-to-hip ratio (adjusted for BMI, WHRadjBMI), a measure of body shape. Body size and shape change as people grow older and these changes differ substantially between men and women. To systematically screen for age- and/or sex-specific effects of genetic variants on BMI and WHRadjBMI, we performed meta-analyses of 114 studies (up to 320,485 individuals of European descent) with genome-wide chip and/or Metabochip data by the Genetic Investigation of Anthropometric Traits (GIANT) Consortium. Each study tested the association of up to ~2.8M SNPs with BMI and WHRadjBMI in four strata (men ≤50y, men >50y, women ≤50y, women >50y) and summary statistics were combined in stratum-specific meta-analyses. We then screened for variants that showed age-specific effects (G x AGE), sex-specific effects (G x SEX) or age-specific effects that differed between men and women (G x AGE x SEX). For BMI, we identified 15 loci (11 previously established for main effects, four novel) that showed significant (FDR<5%) age-specific effects, of which 11 had larger effects in younger (<50y) than in older adults (≥50y). No sex-dependent effects were identified for BMI. For WHRadjBMI, we identified 44 loci (27 previously established for main effects, 17 novel) with sex-specific effects, of which 28 showed larger effects in women than in men, five showed larger effects in men than in women, and 11 showed opposite effects between sexes. No age-dependent effects were identified for WHRadjBMI. This is the first genome-wide interaction meta-analysis to report convincing evidence of age-dependent genetic effects on BMI. In addition, we confirm the sex-specificity of genetic effects on WHRadjBMI. These results may provide further insights into the biology that underlies weight change with age or the sexually dimorphism of body shape.

584 citations

Journal ArticleDOI
17 Dec 2009-Nature
TL;DR: It is shown that for 38,167 Icelanders genotyped using single nucleotide polymorphism (SNP) chips, the parental origin of most alleles can be determined and a novel association between the SNP rs2334499 at 11p15 and type 2 diabetes is observed.
Abstract: Effects of susceptibility variants may depend on from which parent they are inherited. Although many associations between sequence variants and human traits have been discovered through genome-wide associations, the impact of parental origin has largely been ignored. Here we show that for 38,167 Icelanders genotyped using single nucleotide polymorphism (SNP) chips, the parental origin of most alleles can be determined. For this we used a combination of genealogy and long-range phasing. We then focused on SNPs that associate with diseases and are within 500 kilobases of known imprinted genes. Seven independent SNP associations were examined. Five-one with breast cancer, one with basal-cell carcinoma and three with type 2 diabetes-have parental-origin-specific associations. These variants are located in two genomic regions, 11p15 and 7q32, each harbouring a cluster of imprinted genes. Furthermore, we observed a novel association between the SNP rs2334499 at 11p15 and type 2 diabetes. Here the allele that confers risk when paternally inherited is protective when maternally transmitted. We identified a differentially methylated CTCF-binding site at 11p15 and demonstrated correlation of rs2334499 with decreased methylation of that site.

582 citations


Authors

Showing all 5561 results

NameH-indexPapersCitations
Albert Hofman2672530321405
Kari Stefansson206794174819
Ronald Klein1941305149140
Eric Boerwinkle1831321170971
Unnur Thorsteinsdottir167444121009
Vilmundur Gudnason159837123802
Hakon Hakonarson152968101604
Bernhard O. Palsson14783185051
Andrew T. Hattersley146768106949
Fernando Rivadeneira14662886582
Rattan Lal140138387691
Jonathan G. Seidman13756389782
Christine E. Seidman13451967895
Augustine Kong13423789818
Timothy M. Frayling133500100344
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202377
2022210
20211,222
20201,118
20191,140
20181,070