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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TL;DR: Experimental results demonstrate that the proposed edge-preserving filtering based classification method can improve the classification accuracy significantly in a very short time and can be easily applied in real applications.
Abstract: The integration of spatial context in the classification of hyperspectral images is known to be an effective way in improving classification accuracy. In this paper, a novel spectral-spatial classification framework based on edge-preserving filtering is proposed. The proposed framework consists of the following three steps. First, the hyperspectral image is classified using a pixelwise classifier, e.g., the support vector machine classifier. Then, the resulting classification map is represented as multiple probability maps, and edge-preserving filtering is conducted on each probability map, with the first principal component or the first three principal components of the hyperspectral image serving as the gray or color guidance image. Finally, according to the filtered probability maps, the class of each pixel is selected based on the maximum probability. Experimental results demonstrate that the proposed edge-preserving filtering based classification method can improve the classification accuracy significantly in a very short time. Thus, it can be easily applied in real applications.
640 citations
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TL;DR: Long-term IL-6 levels are associated with CHD risk about as strongly as are some major established risk factors, but causality remains uncertain, highlighting the potential relevance of IL- 6–mediated pathways to CHD.
Abstract: Background The relevance to coronary heart disease (CHD) of cytokines that govern inflammatory cascades, such as interleukin-6 (IL-6), may be underestimated because such mediators are short acting and prone to fluctuations. We evaluated associations of long-term circulating IL-6 levels with CHD risk (defined as nonfatal myocardial infarction [MI] or fatal CHD) in two populationbased cohorts, involving serial measurements to enable correction for within-person variability. We updated a systematic review to put the new findings in context. Methods and Findings Measurements were made in samples obtained at baseline from 2,138 patients who had a first-ever nonfatal MI or died of CHD during follow-up, and from 4,267 controls in two cohorts comprising 24,230 participants. Correction for within-person variability was made using data from repeat measurements taken several years apart in several hundred participants. The yearto-year variability of IL-6 values within individuals was relatively high (regression dilution ratios of 0.41, 95% confidence interval [CI] 0.28–0.53, over 4 y, and 0.35, 95% CI 0.23–0.48, over 12 y). Ignoring this variability, we found an odds ratio for CHD, adjusted for several established risk factors, of 1.46 (95% CI 1.29–1.65) per 2 standard deviation (SD) increase of baseline IL-6 values, similar to that for baseline C-reactive protein. After correction for within-person variability, the odds ratio for CHD was 2.14 (95% CI 1.45–3.15) with long-term average (‘‘usual’’) IL-6, similar to those for some established risk factors. Increasing IL-6 levels were associated with progressively increasing CHD risk. An updated systematic review of electronic databases and other sources identified 15 relevant previous population-based prospective studies of IL-6 and clinical coronary outcomes (i.e., MI or coronary death). Including the two current studies, the 17 available prospective studies gave a combined odds ratio of 1.61 (95% CI 1.42–1.83) per 2 SD increase in baseline IL-6 (corresponding to an odds ratio of 3.34 [95% CI 2.45–4.56] per 2 SD increase in usual [long-term average] IL-6 levels).
639 citations
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TL;DR: New candidate genes for serum urate concentration highlight the importance of metabolic control of urate production and excretion, which may have implications for the treatment and prevention of gout.
Abstract: Elevated serum urate concentrations can cause gout, a prevalent and painful inflammatory arthritis. By combining data from >140,000 individuals of European ancestry within the Global Urate Genetics Consortium (GUGC), we identified and replicated 28 genome-wide significant loci in association with serum urate concentrations (18 new regions in or near TRIM46, INHBB, SFMBT1, TMEM171, VEGFA, BAZ1B, PRKAG2, STC1, HNF4G, A1CF, ATXN2, UBE2Q2, IGF1R, NFAT5, MAF, HLF, ACVR1B-ACVRL1 and B3GNT4). Associations for many of the loci were of similar magnitude in individuals of non-European ancestry. We further characterized these loci for associations with gout, transcript expression and the fractional excretion of urate. Network analyses implicate the inhibins-activins signaling pathways and glucose metabolism in systemic urate control. New candidate genes for serum urate concentration highlight the importance of metabolic control of urate production and excretion, which may have implications for the treatment and prevention of gout.
633 citations
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University of Cambridge1, University of Bristol2, University of Eastern Finland3, University of Helsinki4, University of Gothenburg5, University of Lille Nord de France6, Laval University7, Harvard University8, University of Edinburgh9, University of Sheffield10, Stanford University11, Uppsala University12, University of Pennsylvania13, Karolinska Institutet14, Pierre-and-Marie-Curie University15, University of Birmingham16, University of Michigan17, Technische Universität München18, Utrecht University19, University of Amsterdam20, University of Iceland21, National Institute for Health and Welfare22, National Institutes of Health23, Imperial College London24, Copenhagen University Hospital25, University of Copenhagen26, Clinical Trial Service Unit27, National Institute for Health Research28, deCODE genetics29, University of Oxford30
TL;DR: In this article, a functional genetic variant known to affect IL6R signalling was studied to assess whether this pathway is causally relevant to coronary heart disease, and Asp358Ala was not associated with lipid concentrations, blood pressure, adiposity, dysglycaemia, or smoking.
Abstract: Background Persistent inflammation has been proposed to contribute to various stages in the pathogenesis of cardiovascular disease. Interleukin-6 receptor (IL6R) signalling propagates downstream inflammation cascades. To assess whether this pathway is causally relevant to coronary heart disease, we studied a functional genetic variant known to affect IL6R signalling. Methods In a collaborative meta-analysis, we studied Asp358Ala (rs2228145) in IL6R in relation to a panel of conventional risk factors and inflammation biomarkers in 125 222 participants. We also compared the frequency of Asp358Ala in 51 441 patients with coronary heart disease and in 136 226 controls. To gain insight into possible mechanisms, we assessed Asp358Ala in relation to localised gene expression and to postlipopolysaccharide stimulation of interleukin 6. Findings The minor allele frequency of Asp358Ala was 39%. Asp358Ala was not associated with lipid concentrations, blood pressure, adiposity, dysglycaemia, or smoking (p value for association per minor allele >= 0.04 for each). By contrast, for every copy of 358Ala inherited, mean concentration of IL6R increased by 34.3% (95% CI 30.4-38.2) and of interleukin 6 by 14.6% (10.7-18.4), and mean concentration of C-reactive protein was reduced by 7.5% (5.9-9.1) and of fibrinogen by 1.0% (0.7-1.3). For every copy of 358Ala inherited, risk of coronary heart disease was reduced by 3.4% (1.8-5.0). Asp358Ala was not related to IL6R mRNA levels or interleukin-6 production in monocytes. Interpretation Large-scale human genetic and biomarker data are consistent with a causal association between IL6R-related pathways and coronary heart disease.
628 citations
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TL;DR: It is confirmed by explicit calculations the notion that the variation of the activation barrier with potential can be viewed as a manifestation of the Brønsted-Evans-Polanyi-type relationship between activation energy and reaction energy found throughout surface chemistry.
Abstract: We present results of density functional theory calculations on a Pt(111) slab with a bilayer of water, solvated protons in the water layer, and excess electrons in the metal surface. In this way we model the electrochemical double layer at a platinum electrode. By varying the number of protons/electrons in the double layer we investigate the system as a function of the electrode potential. We study the elementary processes involved in the hydrogen evolution reaction, 2(H+ + e−) → H2, and determine the activation energy and predominant reaction mechanism as a function of electrode potential. We confirm by explicit calculations the notion that the variation of the activation barrier with potential can be viewed as a manifestation of the Bronsted–Evans–Polanyi-type relationship between activation energy and reaction energy found throughout surface chemistry.
626 citations
Authors
Showing all 5561 results
Name | H-index | Papers | Citations |
---|---|---|---|
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 |