Institution
University of Copenhagen
Education•Copenhagen, Denmark•
About: University of Copenhagen is a education organization based out in Copenhagen, Denmark. It is known for research contribution in the topics: Population & Galaxy. The organization has 57645 authors who have published 149740 publications receiving 5903093 citations. The organization is also known as: Copenhagen University & Københavns Universitet.
Topics: Population, Galaxy, Insulin, Skeletal muscle, Diabetes mellitus
Papers published on a yearly basis
Papers
More filters
••
TL;DR: Emerald as mentioned in this paper is an object-based language and system designed for the construction of distributed programs that allows objects to freely move within the system to take advantage of distribution and dynamically changing environments.
Abstract: Emerald is an object-based language and system designed for the construction of distributed programs. An explicit goal of Emerald is support for object mobility; objects in Emerald can freely move within the system to take advantage of distribution and dynamically changing environments. We say that Emerald has fine-grained mobility because Emerald objects can be small data objects as well as process objects. Fine-grained mobility allows us to apply mobility in new ways but presents implementation problems as well. This paper discusses the benefits of tine-grained mobility, the Emerald language and run-time mechanisms that support mobility, and techniques for implementing mobility that do not degrade the performance of local operations. Performance measurements of the current implementation are included.
869 citations
••
Iris M. Heid1, Anne U. Jackson2, Joshua C. Randall3, Tthomas W. Winkler1 +352 more•Institutions (90)
TL;DR: A meta-analysis of genome-wide association studies for WHR adjusted for body mass index provides evidence for multiple loci that modulate body fat distribution independent of overall adiposity and reveal strong gene-by-sex interactions.
Abstract: Waist-hip ratio (WHR) is a measure of body fat distribution and a predictor of metabolic consequences independent of overall adiposity. WHR is heritable, but few genetic variants influencing this trait have been identified. We conducted a meta-analysis of 32 genome-wide association studies for WHR adjusted for body mass index (comprising up to 77,167 participants), following up 16 loci in an additional 29 studies (comprising up to 113,636 subjects). We identified 13 new loci in or near RSPO3, VEGFA, TBX15-WARS2, NFE2L3, GRB14, DNM3-PIGC, ITPR2-SSPN, LY86, HOXC13, ADAMTS9, ZNRF3-KREMEN1, NISCH-STAB1 and CPEB4 (P = 1.9 × 10⁻⁹ to P = 1.8 × 10⁻⁴⁰) and the known signal at LYPLAL1. Seven of these loci exhibited marked sexual dimorphism, all with a stronger effect on WHR in women than men (P for sex difference = 1.9 × 10⁻³ to P = 1.2 × 10⁻¹³). These findings provide evidence for multiple loci that modulate body fat distribution independent of overall adiposity and reveal strong gene-by-sex interactions.
869 citations
••
TL;DR: It appears that intramuscular IL‐6 is stimulated by complex signaling cascades initiated by both calcium (Ca2+) ‐dependent and ‐independent stimuli, and it also seems likely that skeletal muscle produces IL‐ 6 to aid in maintaining metabolic homeostasis during periods of altered metabolic demand such as muscular exercise or insulin stimulation.
Abstract: It has recently been demonstrated that the marked increase in the systemic concentration of cytokine interleukin-6 (IL-6) seen with exercise originates from the contracting limb and that skeletal muscle cells per se are the likely source of the production. This review summarizes the possible mechanisms for activation and biological consequences of muscle-derived IL-6. It appears that intramuscular IL-6 is stimulated by complex signaling cascades initiated by both calcium (Ca2+) -dependent and -independent stimuli. It also seems likely that skeletal muscle produces IL-6 to aid in maintaining metabolic homeostasis during periods of altered metabolic demand such as muscular exercise or insulin stimulation. It may do so via local and/or systemic effects. This review also explores the efficacy that IL-6 may be used as a therapeutic drug in treating metabolic disorders such as obesity, type 2 diabetes, and atherosclerosis.—Febbraio, M. A., Pedersen, B. K. Muscle-derived interleukin 6: mechanisms for activation ...
868 citations
••
TL;DR: It is demonstrated that copper is needed for GH61 maximal activity and that the formation of cellodextrin and oxidized cellodesxtrin products by GH61 is enhanced in the presence of small molecule redox-active cofactors such as ascorbate and gallate.
Abstract: The enzymatic degradation of recalcitrant plant biomass is one of the key industrial challenges of the 21st century. Accordingly, there is a continuing drive to discover new routes to promote polysaccharide degradation. Perhaps the most promising approach involves the application of “cellulase-enhancing factors,” such as those from the glycoside hydrolase (CAZy) GH61 family. Here we show that GH61 enzymes are a unique family of copper-dependent oxidases. We demonstrate that copper is needed for GH61 maximal activity and that the formation of cellodextrin and oxidized cellodextrin products by GH61 is enhanced in the presence of small molecule redox-active cofactors such as ascorbate and gallate. By using electron paramagnetic resonance spectroscopy and single-crystal X-ray diffraction, the active site of GH61 is revealed to contain a type II copper and, uniquely, a methylated histidine in the copper's coordination sphere, thus providing an innovative paradigm in bioinorganic enzymatic catalysis.
867 citations
••
Technical University of Denmark1, Institut national de la recherche agronomique2, South China University of Technology3, Commissariat à l'énergie atomique et aux énergies alternatives4, University of Copenhagen5, University of Southern Denmark6, VU University Amsterdam7, Katholieke Universiteit Leuven8, Wageningen University and Research Centre9, Tokyo Institute of Technology10, King Abdulaziz University11
TL;DR: This work presents a method, based on binning co-abundant genes across a series of metagenomic samples, that enables comprehensive discovery of new microbial organisms, viruses and co-inherited genetic entities and aids assembly of microbial genomes without the need for reference sequences.
Abstract: Most current approaches for analyzing metagenomic data rely on comparisons to reference genomes, but the microbial diversity of many environments extends far beyond what is covered by reference databases. De novo segregation of complex metagenomic data into specific biological entities, such as particular bacterial strains or viruses, remains a largely unsolved problem. Here we present a method, based on binning co-abundant genes across a series of metagenomic samples, that enables comprehensive discovery of new microbial organisms, viruses and co-inherited genetic entities and aids assembly of microbial genomes without the need for reference sequences. We demonstrate the method on data from 396 human gut microbiome samples and identify 7,381 co-abundance gene groups (CAGs), including 741 metagenomic species (MGS). We use these to assemble 238 high-quality microbial genomes and identify affiliations between MGS and hundreds of viruses or genetic entities. Our method provides the means for comprehensive profiling of the diversity within complex metagenomic samples.
866 citations
Authors
Showing all 58387 results
Name | H-index | Papers | Citations |
---|---|---|---|
Michael Karin | 236 | 704 | 226485 |
Matthias Mann | 221 | 887 | 230213 |
Peer Bork | 206 | 697 | 245427 |
Ronald Klein | 194 | 1305 | 149140 |
Kenneth S. Kendler | 177 | 1327 | 142251 |
Dorret I. Boomsma | 176 | 1507 | 136353 |
Ramachandran S. Vasan | 172 | 1100 | 138108 |
Unnur Thorsteinsdottir | 167 | 444 | 121009 |
Mika Kivimäki | 166 | 1515 | 141468 |
Jun Wang | 166 | 1093 | 141621 |
Anders Björklund | 165 | 769 | 84268 |
Gerald I. Shulman | 164 | 579 | 109520 |
Jaakko Kaprio | 163 | 1532 | 126320 |
Veikko Salomaa | 162 | 843 | 135046 |
Daniel J. Jacob | 162 | 656 | 76530 |