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.
Papers published on a yearly basis
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University of Tennessee1, Oak Ridge National Laboratory2, West Virginia University3, Umeå University4, University of British Columbia5, United States Department of Energy6, Ghent University7, Swedish University of Agricultural Sciences8, Institut national de la recherche agronomique9, Virginia Tech10, Michigan Technological University11, University of Toronto12, Pennsylvania State University13, University of Provence14, University of Georgia15, University of Florida16, University of California, Berkeley17, Lawrence Berkeley National Laboratory18, University of Arizona19, Purdue University20, Stanford University21, United States Department of Agriculture22, University of Helsinki23, University of Turku24, Massachusetts Institute of Technology25, University of Tennessee Health Science Center26, University of Tübingen27
TL;DR: The draft genome of the black cottonwood tree, Populus trichocarpa, has been reported in this paper, with more than 45,000 putative protein-coding genes identified.
Abstract: We report the draft genome of the black cottonwood tree, Populus trichocarpa. Integration of shotgun sequence assembly with genetic mapping enabled chromosome-scale reconstruction of the genome. More than 45,000 putative protein-coding genes were identified. Analysis of the assembled genome revealed a whole-genome duplication event; about 8000 pairs of duplicated genes from that event survived in the Populus genome. A second, older duplication event is indistinguishably coincident with the divergence of the Populus and Arabidopsis lineages. Nucleotide substitution, tandem gene duplication, and gross chromosomal rearrangement appear to proceed substantially more slowly in Populus than in Arabidopsis. Populus has more protein-coding genes than Arabidopsis, ranging on average from 1.4 to 1.6 putative Populus homologs for each Arabidopsis gene. However, the relative frequency of protein domains in the two genomes is similar. Overrepresented exceptions in Populus include genes associated with lignocellulosic wall biosynthesis, meristem development, disease resistance, and metabolite transport.
4,025 citations
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United Nations Environment Programme1, BirdLife International2, Zoological Society of London3, Statistics Netherlands4, University of North Carolina at Chapel Hill5, Old Dominion University6, Conservation International7, Food and Agriculture Organization8, University of Virginia9, Royal Society for the Protection of Birds10, University of Queensland11, University of Cambridge12, National Center for Atmospheric Research13, World Wide Fund for Nature14, South African National Parks15, UNESCO16, University of British Columbia17, Tata Institute of Fundamental Research18, The Nature Conservancy19, Patuxent Wildlife Research Center20, American Bird Conservancy21, Stellenbosch University22, International Union for Conservation of Nature and Natural Resources23
TL;DR: Most indicators of the state of biodiversity showed declines, with no significant recent reductions in rate, whereas indicators of pressures on biodiversity showed increases, indicating that the Convention on Biological Diversity’s 2010 targets have not been met.
Abstract: In 2002, world leaders committed, through the Convention on Biological Diversity, to achieve a significant reduction in the rate of biodiversity loss by 2010. We compiled 31 indicators to report on progress toward this target. Most indicators of the state of biodiversity (covering species' population trends, extinction risk, habitat extent and condition, and community composition) showed declines, with no significant recent reductions in rate, whereas indicators of pressures on biodiversity (including resource consumption, invasive alien species, nitrogen pollution, overexploitation, and climate change impacts) showed increases. Despite some local successes and increasing responses (including extent and biodiversity coverage of protected areas, sustainable forest management, policy responses to invasive alien species, and biodiversity-related aid), the rate of biodiversity loss does not appear to be slowing.
3,993 citations
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Washington University in St. Louis1, Brown University2, University of British Columbia3, University of North Carolina at Chapel Hill4, University of Southern California5, Massachusetts Institute of Technology6, Seattle Cancer Care Alliance7, Johns Hopkins University8, University of Texas MD Anderson Cancer Center9, Nationwide Children's Hospital10, National Institutes of Health11, SRA International12, Temple University13, University of Chicago14, University of Pennsylvania15
TL;DR: It is found that a complex interplay of genetic events contributes to AML pathogenesis in individual patients and the databases from this study are widely available to serve as a foundation for further investigations of AMl pathogenesis, classification, and risk stratification.
Abstract: BACKGROUND—Many mutations that contribute to the pathogenesis of acute myeloid leukemia (AML) are undefined The relationships between patterns of mutations and epigenetic phenotypes are not yet clear METHODS—We analyzed the genomes of 200 clinically annotated adult cases of de novo AML, using either whole-genome sequencing (50 cases) or whole-exome sequencing (150 cases), along with RNA and microRNA sequencing and DNA-methylation analysis RESULTS—AML genomes have fewer mutations than most other adult cancers, with an average of only 13 mutations found in genes Of these, an average of 5 are in genes that are recurrently mutated in AML A total of 23 genes were significantly mutated, and another 237 were mutated in two or more samples Nearly all samples had at least 1 nonsynonymous mutation in one of nine categories of genes that are almost certainly relevant for pathogenesis, including transcriptionfactor fusions (18% of cases), the gene encoding nucleophosmin (NPM1) (27%), tumorsuppressor genes (16%), DNA-methylation–related genes (44%), signaling genes (59%), chromatin-modifying genes (30%), myeloid transcription-factor genes (22%), cohesin-complex genes (13%), and spliceosome-complex genes (14%) Patterns of cooperation and mutual exclusivity suggested strong biologic relationships among several of the genes and categories CONCLUSIONS—We identified at least one potential driver mutation in nearly all AML samples and found that a complex interplay of genetic events contributes to AML pathogenesis in individual patients The databases from this study are widely available to serve as a foundation for further investigations of AML pathogenesis, classification, and risk stratification (Funded by the National Institutes of Health) The molecular pathogenesis of acute myeloid leukemia (AML) has been studied with the use of cytogenetic analysis for more than three decades Recurrent chromosomal structural variations are well established as diagnostic and prognostic markers, suggesting that acquired genetic abnormalities (ie, somatic mutations) have an essential role in pathogenesis 1,2 However, nearly 50% of AML samples have a normal karyotype, and many of these genomes lack structural abnormalities, even when assessed with high-density comparative genomic hybridization or single-nucleotide polymorphism (SNP) arrays 3-5 (see Glossary) Targeted sequencing has identified recurrent mutations in FLT3, NPM1, KIT, CEBPA, and TET2 6-8 Massively parallel sequencing enabled the discovery of recurrent mutations in DNMT3A 9,10 and IDH1 11 Recent studies have shown that many patients with
3,980 citations
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Health Effects Institute1, University of British Columbia2, Health Canada3, St George's, University of London4, Institute for Health Metrics and Evaluation5, Sri Ramachandra University6, Utrecht University7, Public Health Foundation of India8, Auckland University of Technology9, United States Environmental Protection Agency10, University of Bath11, Fudan University12, University of Queensland13, Emory University14, Dalhousie University15, Queensland University of Technology16, Brigham Young University17, International Agency for Research on Cancer18
TL;DR: In this paper, the authors explored spatial and temporal trends in mortality and burden of disease attributable to ambient air pollution from 1990 to 2015 at global, regional, and country levels, and estimated the relative risk of mortality from ischaemic heart disease, cerebrovascular disease, chronic obstructive pulmonary disease, lung cancer, and lower respiratory infections from epidemiological studies using nonlinear exposure-response functions spanning the global range of exposure.
3,960 citations
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Pierre-and-Marie-Curie University1, University of British Columbia2, University of Pittsburgh3, French Institute of Health and Medical Research4, University of California, Los Angeles5, University of California, San Diego6, McGill University7, University of Kentucky8, Tohoku University9, Brown University10, NewYork–Presbyterian Hospital11, VU University Medical Center12
TL;DR: The NINCDS-ADRDA and DSM-IV-TR criteria for Alzheimer's disease (AD) are the prevailing diagnostic standards in research; however, they have now fallen behind the unprecedented growth of scientific knowledge as discussed by the authors.
Abstract: The NINCDS-ADRDA and the DSM-IV-TR criteria for Alzheimer's disease (AD) are the prevailing diagnostic standards in research; however, they have now fallen behind the unprecedented growth of scientific knowledge. Distinctive and reliable biomarkers of AD are now available through structural MRI, molecular neuroimaging with PET, and cerebrospinal fluid analyses. This progress provides the impetus for our proposal of revised diagnostic criteria for AD. Our framework was developed to capture both the earliest stages, before full-blown dementia, as well as the full spectrum of the illness. These new criteria are centred on a clinical core of early and significant episodic memory impairment. They stipulate that there must also be at least one or more abnormal biomarkers among structural neuroimaging with MRI, molecular neuroimaging with PET, and cerebrospinal fluid analysis of amyloid beta or tau proteins. The timeliness of these criteria is highlighted by the many drugs in development that are directed at changing pathogenesis, particularly at the production and clearance of amyloid beta as well as at the hyperphosphorylation state of tau. Validation studies in existing and prospective cohorts are needed to advance these criteria and optimise their sensitivity, specificity, and accuracy.
3,951 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 |