Institution
University of British Columbia
Education•Vancouver, British Columbia, Canada•
About: University of British Columbia is a education organization based out in Vancouver, British Columbia, Canada. It is known for research contribution in the topics: Population & Health care. The organization has 89939 authors who have published 209679 publications receiving 9226862 citations. The organization is also known as: UBC & The University of British Columbia.
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Hobart Corporation1, University of Évora2, University of Copenhagen3, Spanish National Research Council4, Conservation International5, University of Wollongong6, University of Hong Kong7, National Cheng Kung University8, Umeå University9, James Cook University10, Commonwealth Scientific and Industrial Research Organisation11, Stellenbosch University12, University of Cape Town13, National Oceanic and Atmospheric Administration14, Monash University15, Yale University16, University of Tasmania17, University of Picardie Jules Verne18, Southern Cross University19, University of Western Australia20, University of Eastern Finland21, University of Queensland22, Zoological Society of London23, National Oceanography Centre24, University of Florida25, University of California, Irvine26, La Trobe University27, University of British Columbia28, Academia Sinica29, University of New South Wales30
TL;DR: The negative effects of climate change cannot be adequately anticipated or prepared for unless species responses are explicitly included in decision-making and global strategic frameworks, and feedbacks on climate itself are documented.
Abstract: Distributions of Earth’s species are changing at accelerating rates, increasingly driven by human-mediated climate change. Such changes are already altering the composition of ecological communities, but beyond conservation of natural systems, how and why does this matter? We review evidence that climate-driven species redistribution at regional to global scales affects ecosystem functioning, human well-being, and the dynamics of climate change itself. Production of natural resources required for food security, patterns of disease transmission, and processes of carbon sequestration are all altered by changes in species distribution. Consideration of these effects of biodiversity redistribution is critical yet lacking in most mitigation and adaptation strategies, including the United Nation’s Sustainable Development Goals.
1,917 citations
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TL;DR: Tarin et al. as discussed by the authors described the process of epithelial-mesenchymal transition (EMT) as a defining structural feature of organ development and discussed its role in cancer and fibrosis, as well as identifying new markers to facilitate the observation of EMT in vivo.
Abstract: The conversion of an epithelial cell to a mesenchymal cell is critical to metazoan embryogenesis and a defining structural feature of organ development. Current interest in this process, which is described as an epithelial-mesenchymal transition (EMT), stems from its developmental importance and its involvement in several adult pathologies. Interest and research in EMT are currently at a high level, as seen by the attendance at the recent EMT meeting in Vancouver, Canada (October 1-3, 2005). The meeting, which was hosted by The EMT International Association, was the second international EMT meeting, the first being held in Port Douglas, Queensland, Australia in October 2003. The EMT International Association was formed in 2002 to provide an international body for those interested in EMT and the reverse process, mesenchymal-epithelial transition, and, most importantly, to bring together those working on EMT in development, cancer, fibrosis, and pathology. These themes continued during the recent meeting in Vancouver. Discussion at the Vancouver meeting spanned several areas of research, including signaling pathway activation of EMT and the transcription factors and gene targets involved. Also covered in detail was the basic cell biology of EMT and its role in cancer and fibrosis, as well as the identification of new markers to facilitate the observation of EMT in vivo. This is particularly important because the potential contribution of EMT during neoplasia is the subject of vigorous scientific debate (Tarin, D., E.W. Thompson, and D.F. Newgreen. 2005. Cancer Res. 65:5996-6000; Thompson, E.W., D.F. Newgreen, and D. Tarin. 2005. Cancer Res. 65:5991-5995).
1,912 citations
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University of Washington1, Harvard University2, University of Texas Southwestern Medical Center3, University of Cambridge4, Stanford University5, Lawrence Berkeley National Laboratory6, North-West University7, University of the Free State8, University of Graz9, Medical University of Graz10, University of Victoria11, University of British Columbia12, University of California, Berkeley13
TL;DR: In this article, a three-track network is proposed to combine information at the one-dimensional (1D) sequence level, the 2D distance map level, and the 3D coordinate level.
Abstract: DeepMind presented notably accurate predictions at the recent 14th Critical Assessment of Structure Prediction (CASP14) conference. We explored network architectures that incorporate related ideas and obtained the best performance with a three-track network in which information at the one-dimensional (1D) sequence level, the 2D distance map level, and the 3D coordinate level is successively transformed and integrated. The three-track network produces structure predictions with accuracies approaching those of DeepMind in CASP14, enables the rapid solution of challenging x-ray crystallography and cryo-electron microscopy structure modeling problems, and provides insights into the functions of proteins of currently unknown structure. The network also enables rapid generation of accurate protein-protein complex models from sequence information alone, short-circuiting traditional approaches that require modeling of individual subunits followed by docking. We make the method available to the scientific community to speed biological research.
1,907 citations
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TL;DR: It is found that nitric oxide synthase activity and NAD PH diaphorase copurify to homogeneity and that both activities could be immunoprecipitated with an antibody recognizing neuronal NADPH diaphirase.
Abstract: NADPH diaphorase histochemistry selectively labels a number of discrete populations of neurons throughout the nervous system. This simple and robust technique has been used in a great many experimental and neuropathological studies; however, the function of this enzyme has remained a matter of speculation. We, therefore, undertook to characterize this enzyme biochemically. With biochemical and immunochemical assays, NADPH diaphorase was purified to apparent homogeneity from rat brain by affinity chromatography and anion-exchange HPLC. Western (immunoblot) transfer and immunostaining with an antibody specific for NADPH diaphorase labeled a single protein of 150 kDa. Nitric oxide synthase was recently shown to be a 150-kDa, NADPH-dependent enzyme in brain. It is responsible for the calcium/calmodulin-dependent synthesis of the guanylyl cyclase activator nitric oxide from L-arginine. We have found that nitric oxide synthase activity and NADPH diaphorase copurify to homogeneity and that both activities could be immunoprecipitated with an antibody recognizing neuronal NADPH diaphorase. Furthermore, nitric oxide synthase was competitively inhibited by the NADPH diaphorase substrate, nitro blue tetrazolium. Thus, neuronal NADPH diaphorase is a nitric oxide synthase, and NADPH diaphorase histochemistry, therefore, provides a specific histochemical marker for neurons producing nitric oxide.
1,904 citations
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TL;DR: A genome-wide association meta-analysis of individuals with clinically assessed or self-reported depression identifies 44 independent and significant loci and finds important relationships of genetic risk for major depression with educational attainment, body mass, and schizophrenia.
Abstract: Major depressive disorder (MDD) is a common illness accompanied by considerable morbidity, mortality, costs, and heightened risk of suicide. We conducted a genome-wide association meta-analysis based in 135,458 cases and 344,901 controls and identified 44 independent and significant loci. The genetic findings were associated with clinical features of major depression and implicated brain regions exhibiting anatomical differences in cases. Targets of antidepressant medications and genes involved in gene splicing were enriched for smaller association signal. We found important relationships of genetic risk for major depression with educational attainment, body mass, and schizophrenia: lower educational attainment and higher body mass were putatively causal, whereas major depression and schizophrenia reflected a partly shared biological etiology. All humans carry lesser or greater numbers of genetic risk factors for major depression. These findings help refine the basis of major depression and imply that a continuous measure of risk underlies the clinical phenotype.
1,898 citations
Authors
Showing all 90682 results
Name | H-index | Papers | Citations |
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Gordon H. Guyatt | 231 | 1620 | 228631 |
John C. Morris | 183 | 1441 | 168413 |
Douglas Scott | 178 | 1111 | 185229 |
John R. Yates | 177 | 1036 | 129029 |
Deborah J. Cook | 173 | 907 | 148928 |
Richard A. Gibbs | 172 | 889 | 249708 |
Evan E. Eichler | 170 | 567 | 150409 |
James F. Sallis | 169 | 825 | 144836 |
Michael Snyder | 169 | 840 | 130225 |
Jiawei Han | 168 | 1233 | 143427 |
Michael Kramer | 167 | 1713 | 127224 |
Bruce L. Miller | 163 | 1153 | 115975 |
Peter A. R. Ade | 162 | 1387 | 138051 |
Marc W. Kirschner | 162 | 457 | 102145 |
Kaj Blennow | 160 | 1845 | 116237 |