Institution
University of Aberdeen
Education•Aberdeen, United Kingdom•
About: University of Aberdeen is a education organization based out in Aberdeen, United Kingdom. It is known for research contribution in the topics: Population & Health care. The organization has 21174 authors who have published 49962 publications receiving 2105479 citations. The organization is also known as: Aberdeen University.
Papers published on a yearly basis
Papers
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TL;DR: A new five-item CRIB II score is developed with data from a UK-wide sample of infants admitted to neonatal intensive care in 1998-99, and how mortality after neonatalintensive care has fallen in the past 12 years is shown.
434 citations
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TL;DR: This review focuses on the CB1-selective antagonists, SR141716A, AM251, AM281 and LY320135, and discusses possible mechanisms by which these ligands produce their inverse effects.
434 citations
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University of Bonn1, Cardiff University2, Eli Lilly and Company3, Harvard University4, State University of New York Upstate Medical University5, NorthShore University HealthSystem6, University of California, San Diego7, National Institutes of Health8, Stanford University9, University of North Carolina at Chapel Hill10, Trinity College, Dublin11, Radboud University Nijmegen12, University of Pennsylvania13, University of St Andrews14, University of Western Australia15, University of California, Los Angeles16, Washington University in St. Louis17, University of Pittsburgh18, Johns Hopkins University19, Icahn School of Medicine at Mount Sinai20, University of Illinois at Urbana–Champaign21, University of Helsinki22, Université de Montréal23, University of Washington24, University of Toronto25, Vanderbilt University26, McMaster University27, University of Oslo28, University of Edinburgh29, University of Michigan30, University College London31, GlaxoSmithKline32, Indiana University33, Virginia Commonwealth University34, VU University Amsterdam35, University of Iowa36, University of California, San Francisco37, Howard University38, Institute of Physics39, QIMR Berghofer Medical Research Institute40, Columbia University41, Pfizer42, Rush University Medical Center43, Mayo Clinic44, Georgetown University45, Karolinska Institutet46, National Institute for Health and Welfare47, University of Queensland48, University of Aberdeen49, North Carolina State University50
TL;DR: GWAS methods have detected a remarkable number of robust genetic associations for dozens of common diseases and traits, leading to new pathophysiological hypotheses, although only small proportions of genetic variance have been explained thus far and therapeutic applications will require substantial further effort.
Abstract: Objective: The authors conducted a review of the history and empirical basis of genomewide association studies (GWAS), the rationale for GWAS of psychiatric disorders, results to date, limitations, and plans for GWAS meta-analyses. Method: A literature review was carried out, power and other issues discussed, and planned studies assessed. Results: Most of the genomic DNA sequence differences between any two people are common (frequency >5%) single nucleotide polymorphisms (SNPs). Because of localized patterns of correlation (linkage disequilibrium), 500,000 to 1,000,000 of these SNPs can test the hypothesis that one or more common variants explain part of the genetic risk for a disease. GWAS technologies can also detect some of the copy number variants (deletions and duplications) in the genome. Systematic study of rare variants will require large-scale resequencing analyses. GWAS methods have detected a remarkable number of robust genetic associations for dozens of common diseases and traits, leading to new pathophysiological hypotheses, although only small proportions of genetic variance have been explained thus far and therapeutic applications will require substantial further effort. Study design issues, power, and limitations are discussed. For psychiatric disorders, there are initial significant findings for common SNPs and for rare copy number variants, and many other studies are in progress. Conclusions: GWAS of large samples have detected associations of common SNPs and of rare copy number variants with psychiatric disorders. More findings are likely, since larger GWAS samples detect larger numbers of common susceptibility variants, with smaller effects. The Psychiatric GWAS Consortium is conducting GWAS meta-analyses for schizophrenia, bipolar disorder, major depressive disorder, autism, and attention deficit hyperactivity disorder. Based on results for other diseases, larger samples will be required. The contribution of GWAS will depend on the true genetic architecture of each disorder.
434 citations
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TL;DR: All photographs courtesy of Addenbrooke’s Hospital, Cambridge, NIBSC, South Mimms, University of Aberdeen.
Abstract: Trevor Baglin, Elaine Gray, Mike Greaves, Beverley J. Hunt, David Keeling, Sam Machin, Ian Mackie, Mike Makris, Tim Nokes, David Perry, R. C. Tait, Isobel Walker and Henry Watson Addenbrooke’s Hospital, Cambridge, NIBSC, South Mimms, University of Aberdeen, Aberdeen, Guy’s and St Thomas’, London, Churchill Hospital, Oxford, University College Hospital, London, Royal Hallamshire Hospital, Sheffield, Derriford Hospital, Plymouth, Glasgow Royal Infirmary, Glasgow and Aberdeen Royal Infirmary, UK
434 citations
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TL;DR: The possible biological roles of this protein in mammals are considered, which include participation in cell proliferation and apoptosis, homeostasis of essential metals, cellular free radical scavenging, and metal detoxification.
Abstract: MTs are small cysteine-rich metal-binding proteins found in many species and, although there are differences between them, it is of note that they have a great deal of sequence and structural homology. Mammalian MTs are 61 or 62 amino acid polypeptides containing 20 conserved cysteine residues that underpin the binding of metals. The existence of MT across species is indicative of its biological demand, while the conservation of cysteines indicates that these are undoubtedly central to the function of this protein. Four MT isoforms have been found so far, MT-1, MT-2, MT-3, and MT-4, but these also have subtypes with 17 MT genes identified in man, of which 10 are known to be functional. Different cells express different MT isoforms with varying levels of expression perhaps as a result of the different function of each isoform. Even different metals induce and bind to MTs to different extents. Over 40 years of research into MT have yielded much information on this protein, but have failed to assign to it a definitive biological role. The fact that multiple MT isoforms exist, and the great variety of substances and agents that act as inducers, further complicates the search for the biological role of MTs. This article reviews the current knowledge on the biochemistry, induction, regulation, and degradation of this protein in mammals, with a particular emphasis on human MTs. It also considers the possible biological roles of this protein, which include participation in cell proliferation and apoptosis, homeostasis of essential metals, cellular free radical scavenging, and metal detoxification.
434 citations
Authors
Showing all 21424 results
Name | H-index | Papers | Citations |
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Paul M. Thompson | 183 | 2271 | 146736 |
Feng Zhang | 172 | 1278 | 181865 |
Ian J. Deary | 166 | 1795 | 114161 |
Peter A. R. Ade | 162 | 1387 | 138051 |
David W. Johnson | 160 | 2714 | 140778 |
Pete Smith | 156 | 2464 | 138819 |
Naveed Sattar | 155 | 1326 | 116368 |
John R. Hodges | 149 | 812 | 82709 |
Ruth J. F. Loos | 142 | 647 | 92485 |
Alan J. Silman | 141 | 708 | 92864 |
Michael J. Keating | 140 | 1169 | 76353 |
David Price | 138 | 1687 | 93535 |
John D. Scott | 135 | 625 | 83878 |
Aarno Palotie | 129 | 711 | 89975 |
Rajat Gupta | 126 | 1240 | 72881 |