Institution
University of Iceland
Education•Reykjavik, 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 published on a yearly basis
Papers
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Technical University of Madrid1, Carlos III Health Institute2, Ghent University3, University of Zaragoza4, University of Copenhagen5, University of Tromsø6, Harokopio University7, Robert Koch Institute8, Medical Research Council9, Medical University of Graz10, VU University Amsterdam11, University of Iceland12, National Institutes of Health13, University of Helsinki14, Loyola University Chicago15, University College Cork16
TL;DR: Vitamin D deficiency is evident throughout the European population at prevalence rates that are concerning and that require action from a public health perspective, and what direction these strategies take will depend on European policy.
830 citations
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University of British Columbia1, Grand Valley State University2, University of Gothenburg3, University of Sheffield4, Royal Swedish Academy of Sciences5, St. John's University6, University of Tromsø7, VU University Amsterdam8, Arizona State University9, American Museum of Natural History10, United States Forest Service11, Agricultural University of Iceland12, University of California, Berkeley13, University of Alberta14, University of Melbourne15, University of Iceland16, Norwegian University of Life Sciences17, Colorado State University18, Hokkaido University19, University of Copenhagen20, Florida International University21, University of Saskatchewan22, Pennsylvania State University23, University of Manchester24, Aarhus University25, Marine Biological Laboratory26, Finnish Forest Research Institute27, La Trobe University28, Michigan State University29, University of Alaska Anchorage30, University of Stirling31
TL;DR: In this article, a synthesis of 61 experimental warming studies, of up to 20 years duration, in tundra sites worldwide, was used to understand the sensitivity of tundras vegetation to climate warming and to forecast future biodiversity and vegetation feedbacks to climate.
Abstract: 35 Abstract Understanding the sensitivity of tundra vegetation to climate warming is critical to forecasting future biodiversity and vegetation feedbacks to climate. In situ warming experiments accelerate climate change on a small scale to forecast responses of local plant communities. Limitations of this approach include the apparent site-specificity of results and uncertainty about the power of short-term studies to anticipate longer term change. We address these issues with a synthesis of 61 experimental warming studies, of up to 20 years duration, in tundra sites worldwide. The response of plant groups to warming often differed with ambient summer temperature, soil moisture and experimental duration. Shrubs increased with warming only where ambient temperature was high, whereas graminoids increased primarily in the coldest study sites. Linear increases in effect size over time were frequently observed. There was little indication of saturating or accelerating effects, as would be predicted if negative or positive vegetation feedbacks were common. These results indicate that tundra vegetation exhibits strong regional variation in response to warming, and that in vulnerable regions, cumulative effects of long-term warming on tundra vegetation - and associated ecosystem consequences - have the potential to be much greater than we have observed to date.
830 citations
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University of Maryland, Baltimore1, Washington University in St. Louis2, Johns Hopkins University3, MedStar Washington Hospital Center4, National Institutes of Health5, Boston Children's Hospital6, University of Iceland7, United States Department of Veterans Affairs8, University of Michigan9, Harvard University10, Boston University11, Pacific Biosciences12, University of Washington13, Broad Institute14, Wake Forest University15
TL;DR: In this article, a fixed-effects meta-analysis of genome-wide association (GWA) results between CT hepatic steatosis and 2.4 million imputed or genotyped SNPs in 7,176 individuals from the Old Order Amish, Age, Gene/Environment Susceptibility-Reykjavik study (AGES), Family Heart, and Framingham Heart Studies (n = 880 to 3,070).
Abstract: Nonalcoholic fatty liver disease (NAFLD) clusters in families, but the only known common genetic variants influencing risk are near PNPLA3. We sought to identify additional genetic variants influencing NAFLD using genome-wide association (GWA) analysis of computed tomography (CT) measured hepatic steatosis, a non-invasive measure of NAFLD, in large population based samples. Using variance components methods, we show that CT hepatic steatosis is heritable (,26%– 27%) in family-based Amish, Family Heart, and Framingham Heart Studies (n = 880 to 3,070). By carrying out a fixed-effects meta-analysis of genome-wide association (GWA) results between CT hepatic steatosis and ,2.4 million imputed or genotyped SNPs in 7,176 individuals from the Old Order Amish, Age, Gene/Environment Susceptibility-Reykjavik study (AGES), Family Heart, and Framingham Heart Studies, we identify variants associated at genome-wide significant levels (p,5610 28 ) in or near PNPLA3, NCAN, and PPP1R3B. We genotype these and 42 other top CT hepatic steatosis-associated SNPs in 592 subjects with biopsy-proven NAFLD from the NASH Clinical Research Network (NASH CRN). In comparisons with 1,405 healthy controls from the Myocardial Genetics Consortium (MIGen), we observe significant associations with histologic NAFLD at variants in or near NCAN, GCKR, LYPLAL1, and PNPLA3, but not PPP1R3B. Variants at these five loci exhibit distinct patterns of association with serum lipids, as well as glycemic and anthropometric traits. We identify common genetic variants influencing CT–assessed steatosis and risk of NAFLD. Hepatic steatosis associated variants are not uniformly associated with NASH/fibrosis or result in abnormalities in serum lipids or glycemic and anthropometric traits, suggesting genetic heterogeneity in the pathways influencing these traits.
821 citations
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TL;DR: It is suggested that triglyceride-rich lipoproteins causally influence risk for CAD, and the strength of a polymorphism's effect on triglyceride levels is correlated with the magnitude of its effect on CAD risk.
Abstract: Triglycerides are transported in plasma by specific triglyceride-rich lipoproteins; in epidemiological studies, increased triglyceride levels correlate with higher risk for coronary artery disease (CAD). However, it is unclear whether this association reflects causal processes. We used 185 common variants recently mapped for plasma lipids (P < 5 × 10(-8) for each) to examine the role of triglycerides in risk for CAD. First, we highlight loci associated with both low-density lipoprotein cholesterol (LDL-C) and triglyceride levels, and we show that the direction and magnitude of the associations with both traits are factors in determining CAD risk. Second, we consider loci with only a strong association with triglycerides and show that these loci are also associated with CAD. Finally, in a model accounting for effects on LDL-C and/or high-density lipoprotein cholesterol (HDL-C) levels, the strength of a polymorphism's effect on triglyceride levels is correlated with the magnitude of its effect on CAD risk. These results suggest that triglyceride-rich lipoproteins causally influence risk for CAD.
817 citations
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Alisa K. Manning1, Alisa K. Manning2, Alisa K. Manning3, Robert A. Scott +240 more•Institutions (69)
TL;DR: Six previously unknown loci associated with fasting insulin at P < 5 × 10−8 in combined discovery and follow-up analyses of 52 studies comprising up to 96,496 non-diabetic individuals are presented.
Abstract: Recent genome-wide association studies have described many loci implicated in type 2 diabetes (T2D) pathophysiology and β-cell dysfunction but have contributed little to the understanding of the genetic basis of insulin resistance. We hypothesized that genes implicated in insulin resistance pathways might be uncovered by accounting for differences in body mass index (BMI) and potential interactions between BMI and genetic variants. We applied a joint meta-analysis approach to test associations with fasting insulin and glucose on a genome-wide scale. We present six previously unknown loci associated with fasting insulin at P < 5 × 10(-8) in combined discovery and follow-up analyses of 52 studies comprising up to 96,496 non-diabetic individuals. Risk variants were associated with higher triglyceride and lower high-density lipoprotein (HDL) cholesterol levels, suggesting a role for these loci in insulin resistance pathways. The discovery of these loci will aid further characterization of the role of insulin resistance in T2D pathophysiology.
811 citations
Authors
Showing all 5561 results
Name | H-index | Papers | Citations |
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Albert Hofman | 267 | 2530 | 321405 |
Kari Stefansson | 206 | 794 | 174819 |
Ronald Klein | 194 | 1305 | 149140 |
Eric Boerwinkle | 183 | 1321 | 170971 |
Unnur Thorsteinsdottir | 167 | 444 | 121009 |
Vilmundur Gudnason | 159 | 837 | 123802 |
Hakon Hakonarson | 152 | 968 | 101604 |
Bernhard O. Palsson | 147 | 831 | 85051 |
Andrew T. Hattersley | 146 | 768 | 106949 |
Fernando Rivadeneira | 146 | 628 | 86582 |
Rattan Lal | 140 | 1383 | 87691 |
Jonathan G. Seidman | 137 | 563 | 89782 |
Christine E. Seidman | 134 | 519 | 67895 |
Augustine Kong | 134 | 237 | 89818 |
Timothy M. Frayling | 133 | 500 | 100344 |