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 & Medicine. 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, Medicine, Galaxy, Diabetes mellitus, Cancer
Papers published on a yearly basis
Papers
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TL;DR: Fatigue or impaired performance in soccer occurs during various phases in a game, and different physiological mechanisms appear to operate in different periods of a game.
Abstract: This review describes when fatigue may develop during soccer games and the potential physiological mechanisms that cause fatigue in soccer. According to time-motion analyses and performance measures during match-play, fatigue or reduced performance seems to occur at three different stages in the game: (1) after short-term intense periods in both halves; (2) in the initial phase of the second half; and (3) towards the end of the game. Temporary fatigue after periods of intense exercise in the game does not appear to be linked directly to muscle glycogen concentration, lactate accumulation, acidity or the breakdown of creatine phosphate. Instead, it may be related to disturbances in muscle ion homeostasis and an impaired excitation of the sarcolemma. Soccer players' ability to perform maximally is inhibited in the initial phase of the second half, which may be due to lower muscle temperatures compared with the end of the first half. Thus, when players perform low-intensity activities in the interval between the two halves, both muscle temperature and performance are preserved. Several studies have shown that fatigue sets in towards the end of a game, which may be caused by low glycogen concentrations in a considerable number of individual muscle fibres. In a hot and humid environment, dehydration and a reduced cerebral function may also contribute to the deterioration in performance. In conclusion, fatigue or impaired performance in soccer occurs during various phases in a game, and different physiological mechanisms appear to operate in different periods of a game.
602 citations
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TL;DR: This article conducted a meta-analysis of genome-wide association data from 26,676 T2D case and 132,532 control subjects of European ancestry after imputation using the 1000 Genomes multiethnic reference panel.
Abstract: To characterize type 2 diabetes (T2D)-associated variation across the allele frequency spectrum, we conducted a meta-analysis of genome-wide association data from 26,676 T2D case and 132,532 control subjects of European ancestry after imputation using the 1000 Genomes multiethnic reference panel Promising association signals were followed up in additional data sets (of 14,545 or 7,397 T2D case and 38,994 or 71,604 control subjects) We identified 13 novel T2D-associated loci (P < 5 × 10-8), including variants near the GLP2R, GIP, and HLA-DQA1 genes Our analysis brought the total number of independent T2D associations to 128 distinct signals at 113 loci Despite substantially increased sample size and more complete coverage of low-frequency variation, all novel associations were driven by common single nucleotide variants Credible sets of potentially causal variants were generally larger than those based on imputation with earlier reference panels, consistent with resolution of causal signals to common risk haplotypes Stratification of T2D-associated loci based on T2D-related quantitative trait associations revealed tissue-specific enrichment of regulatory annotations in pancreatic islet enhancers for loci influencing insulin secretion and in adipocytes, monocytes, and hepatocytes for insulin action-associated loci These findings highlight the predominant role played by common variants of modest effect and the diversity of biological mechanisms influencing T2D pathophysiology
601 citations
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TL;DR: Analysis of several tumor pairs involving a CIS and an invasive cancer provided evidence that the chromosome 9 alteration may in some cases be involved in the progression of CIS to more invasive tumors, in addition to its role in the initiation of T(a) tumors.
Abstract: Noninvasive transitional cell carcinomas of the bladder can have two distinct morphologies suggesting they contain different genetic alterations. Papillary transitional cell carcinomas (T(a) tumors) are often multifocal and only occasionally progress, whereas flat tumors (carcinomas in situ, CIS), frequently progress to invasive disease. We examined 216 bladder tumors of various stages and histopathologies for two genetic alterations previously described to be of importance in bladder tumorigenesis. Loss of heterozygosity of chromosome 9 was observed in 24 of 70 (34%) T(a) tumors but was present in only 3 of 24 (12%) CIS and dysplasia lesions (P = 0.04). In contrast, only 1 of 36 (3%) T(a) tumors contained a p53 gene mutation compared to 15 of 23 (65%) CIS and dysplasias (P < 0.001), a frequency comparable to that observed in muscle invasive tumors (25 of 49; 51%). The presence of p53 mutations in CIS and dysplasia could explain their propensities to progress since these mutations are known to destabilize the genome. Analysis of several tumor pairs involving a CIS and an invasive cancer provided evidence that the chromosome 9 alteration may in some cases be involved in the progression of CIS to more invasive tumors, in addition to its role in the initiation of T(a) tumors. However, the CIS and secondary tumor were found to contain different genetic alterations in some patients suggesting divergent progression pathways. Bladder carcinogenesis may therefore proceed through two distinct genetic alteration pathways responsible for generating superficial tumors with differing morphologies and pathologies.
601 citations
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University of Leicester1, University of Warwick2, University of Cambridge3, Los Alamos National Laboratory4, University of Birmingham5, Stockholm University6, University of Copenhagen7, INAF8, Space Telescope Science Institute9, Spanish National Research Council10, Liverpool John Moores University11, Instituto Politécnico Nacional12, Cardiff University13, University of St Andrews14, Nagoya University15, Max Planck Society16, University of Iceland17, Pontifical Catholic University of Chile18, Monash University19, University of Amsterdam20, ASTRON21, Weizmann Institute of Science22
TL;DR: In this article, the authors reported the discovery and monitoring of the near-infrared counterpart (AT2017gfo) of a binary neutron-star merger event detected as a gravitational wave source by Advanced Laser Interferometer Gravitational-wave Observatory (LIGO)/Virgo (GW170817) and as a short gamma-ray burst by Fermi Gamma-ray Burst Monitor (GBM) and Integral SPI-ACS (GRB 170817A).
Abstract: We report the discovery and monitoring of the near-infrared counterpart (AT2017gfo) of a binary neutron-star merger event detected as a gravitational wave source by Advanced Laser Interferometer Gravitational-wave Observatory (LIGO)/Virgo (GW170817) and as a short gamma-ray burst by Fermi Gamma-ray Burst Monitor (GBM) and Integral SPI-ACS (GRB 170817A). The evolution of the transient light is consistent with predictions for the behavior of a "kilonova/macronova" powered by the radioactive decay of massive neutron-rich nuclides created via r-process nucleosynthesis in the neutron-star ejecta. In particular, evidence for this scenario is found from broad features seen in Hubble Space Telescope infrared spectroscopy, similar to those predicted for lanthanide-dominated ejecta, and the much slower evolution in the near-infrared ${K}_{{\rm{s}}}$-band compared to the optical. This indicates that the late-time light is dominated by high-opacity lanthanide-rich ejecta, suggesting nucleosynthesis to the third r-process peak (atomic masses $A\approx 195$). This discovery confirms that neutron-star mergers produce kilo-/macronovae and that they are at least a major—if not the dominant—site of rapid neutron capture nucleosynthesis in the universe.
600 citations
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German Cancer Research Center1, Heidelberg University2, Stanford University3, University of Copenhagen4, Centre national de la recherche scientifique5, University of Tübingen6, University of Würzburg7, Institute of Cancer Research8, University of Cambridge9, McGill University10, Necker-Enfants Malades Hospital11
TL;DR: It is shown that reduced H3K27me3 levels and DNA hypomethylation act in concert to activate gene expression in K27M mutant pHGGs, and it is demonstrated that this is caused by aberrant recruitment of the PRC2 complex to K 27M mutant H3.3.
599 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 |