Institution
University of Geneva
Education•Geneva, Switzerland•
About: University of Geneva is a education organization based out in Geneva, Switzerland. It is known for research contribution in the topics: Population & Planet. The organization has 26887 authors who have published 65265 publications receiving 2931373 citations. The organization is also known as: Geneva University & Universite de Geneve.
Topics: Population, Planet, Galaxy, Exoplanet, Stars
Papers published on a yearly basis
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Broad Institute1, Tehran University of Medical Sciences2, George Washington University3, European Bioinformatics Institute4, Sapienza University of Rome5, Temple University6, Tomsk State University7, University of Notre Dame8, Centre national de la recherche scientifique9, French Institute of Health and Medical Research10, Imperial College London11, James Cook University12, Massachusetts Institute of Technology13, Simon Fraser University14, University of California, Davis15, Institut de recherche pour le développement16, Kansas State University17, Foundation for Research & Technology – Hellas18, University of Perugia19, Virginia Tech20, University of Nevada, Las Vegas21, Baylor College of Medicine22, Boston College23, Harvard University24, University of Manchester25, University of California, San Francisco26, University of Cyprus27, National Health Laboratory Service28, University of Crete29, Kenya Medical Research Institute30, University of Arizona31, University of Pennsylvania32, Indian Council of Medical Research33, New Mexico State University34, Liverpool School of Tropical Medicine35, Vanderbilt University Medical Center36, Vanderbilt University37, Swiss Institute of Bioinformatics38, University of Geneva39, Texas A&M University40, Chiang Mai University41, Rio de Janeiro State University42, Oswaldo Cruz Foundation43, Indiana University44, University of Santiago de Compostela45, Wellcome Trust Sanger Institute46, Liverpool John Moores University47, University of Georgia48, Harvey Mudd College49, University of California, Irvine50, University of Groningen51, Centers for Disease Control and Prevention52, Biogen Idec53
TL;DR: The authors investigated the genomic basis of vectorial capacity and explore new avenues for vector control, sequenced the genomes of 16 anopheline mosquito species from diverse locations spanning ~100 million years of evolution Comparative analyses show faster rates of gene gain and loss, elevated gene shuffling on the X chromosome, and more intron losses, relative to Drosophila.
Abstract: Variation in vectorial capacity for human malaria among Anopheles mosquito species is determined by many factors, including behavior, immunity, and life history To investigate the genomic basis of vectorial capacity and explore new avenues for vector control, we sequenced the genomes of 16 anopheline mosquito species from diverse locations spanning ~100 million years of evolution Comparative analyses show faster rates of gene gain and loss, elevated gene shuffling on the X chromosome, and more intron losses, relative to Drosophila Some determinants of vectorial capacity, such as chemosensory genes, do not show elevated turnover but instead diversify through protein-sequence changes This dynamism of anopheline genes and genomes may contribute to their flexible capacity to take advantage of new ecological niches, including adapting to humans as primary hosts
476 citations
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TL;DR: In this article, some general features of the N = 1 supergravity, d = 4 theory were extracted as a low energy limit of the recently proposed anomaly-free superstring theories.
476 citations
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École Polytechnique Fédérale de Lausanne1, Imperial College London2, University of Cambridge3, University of Tokyo4, University of Geneva5, ETH Zurich6, National Presto Industries7, Tohoku University8, University of the Basque Country9, Korea Institute for Advanced Study10, Seoul National University11, University of Mainz12, University of California, Berkeley13, University of Paris14, University of Oxford15, Research Institute for Symbolic Computation16, Beihang University17, University of Zurich18, Polish Academy of Sciences19, Rutgers University20, Ikerbasque21
TL;DR: Wannier90 as mentioned in this paper is an open-source computer program for calculating maximally-localised Wannier functions (MLWFs) from a set of Bloch states, which is interfaced to many widely used electronic-structure codes thanks to its independence from the basis sets representing these BLoch states.
Abstract: Wannier90 is an open-source computer program for calculating maximally-localised Wannier functions (MLWFs) from a set of Bloch states. It is interfaced to many widely used electronic-structure codes thanks to its independence from the basis sets representing these Bloch states. In the past few years the development of Wannier90 has transitioned to a community-driven model; this has resulted in a number of new developments that have been recently released in Wannier90 v3.0. In this article we describe these new functionalities, that include the implementation of new features for wannierisation and disentanglement (symmetry-adapted Wannier functions, selectively-localised Wannier functions, selected columns of the density matrix) and the ability to calculate new properties (shift currents and Berry-curvature dipole, and a new interface to many-body perturbation theory); performance improvements, including parallelisation of the core code; enhancements in functionality (support for spinor-valued Wannier functions, more accurate methods to interpolate quantities in the Brillouin zone); improved usability (improved plotting routines, integration with high-throughput automation frameworks), as well as the implementation of modern software engineering practices (unit testing, continuous integration, and automatic source-code documentation). These new features, capabilities, and code development model aim to further sustain and expand the community uptake and range of applicability, that nowadays spans complex and accurate dielectric, electronic, magnetic, optical, topological and transport properties of materials.
476 citations
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TL;DR: This study proposes an empirical methodology, which is called Regulatory Trait Concordance (RTC), that accounts for local LD structure and integrates eQTLs and GWAS results in order to reveal the subset of association signals that are due to cis eZTLs, and detects several potential disease-causing regulatory effects.
Abstract: The recent success of genome-wide association studies (GWAS) is now followed by the challenge to determine how the reported susceptibility variants mediate complex traits and diseases. Expression quantitative trait loci (eQTLs) have been implicated in disease associations through overlaps between eQTLs and GWAS signals. However, the abundance of eQTLs and the strong correlation structure (LD) in the genome make it likely that some of these overlaps are coincidental and not driven by the same functional variants. In the present study, we propose an empirical methodology, which we call Regulatory Trait Concordance (RTC) that accounts for local LD structure and integrates eQTLs and GWAS results in order to reveal the subset of association signals that are due to cis eQTLs. We simulate genomic regions of various LD patterns with both a single or two causal variants and show that our score outperforms SNP correlation metrics, be they statistical (r2) or historical (D'). Following the observation of a significant abundance of regulatory signals among currently published GWAS loci, we apply our method with the goal to prioritize relevant genes for each of the respective complex traits. We detect several potential disease-causing regulatory effects, with a strong enrichment for immunity-related conditions, consistent with the nature of the cell line tested (LCLs). Furthermore, we present an extension of the method in trans, where interrogating the whole genome for downstream effects of the disease variant can be informative regarding its unknown primary biological effect. We conclude that integrating cellular phenotype associations with organismal complex traits will facilitate the biological interpretation of the genetic effects on these traits.
476 citations
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TL;DR: This work mapped and examined the function of human islet cis-regulatory networks and identifies genomic sequences that are targeted by islet transcription factors to drive islet-specific gene activity and shows that most such sequences reside in clusters of enhancers that form physical three-dimensional chromatin domains.
Abstract: Type 2 diabetes affects over 300 million people, causing severe complications and premature death, yet the underlying molecular mechanisms are largely unknown. Pancreatic islet dysfunction is central in type 2 diabetes pathogenesis, and understanding islet genome regulation could therefore provide valuable mechanistic insights. We have now mapped and examined the function of human islet cis-regulatory networks. We identify genomic sequences that are targeted by islet transcription factors to drive islet-specific gene activity and show that most such sequences reside in clusters of enhancers that form physical three-dimensional chromatin domains. We find that sequence variants associated with type 2 diabetes and fasting glycemia are enriched in these clustered islet enhancers and identify trait-associated variants that disrupt DNA binding and islet enhancer activity. Our studies illustrate how islet transcription factors interact functionally with the epigenome and provide systematic evidence that the dysregulation of islet enhancers is relevant to the mechanisms underlying type 2 diabetes.
476 citations
Authors
Showing all 27203 results
Name | H-index | Papers | Citations |
---|---|---|---|
JoAnn E. Manson | 270 | 1819 | 258509 |
Joseph L. Goldstein | 207 | 556 | 149527 |
Kari Stefansson | 206 | 794 | 174819 |
David Baltimore | 203 | 876 | 162955 |
Mark I. McCarthy | 200 | 1028 | 187898 |
Michael S. Brown | 185 | 422 | 123723 |
Yang Gao | 168 | 2047 | 146301 |
Napoleone Ferrara | 167 | 494 | 140647 |
Marc Weber | 167 | 2716 | 153502 |
Alessandro Melchiorri | 151 | 674 | 116384 |
Andrew D. Hamilton | 151 | 1334 | 105439 |
David P. Strachan | 143 | 472 | 105256 |
Andrew Beretvas | 141 | 1985 | 110059 |
Rainer Wallny | 141 | 1661 | 105387 |
Josh Moss | 139 | 1019 | 89255 |