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: In this article, the authors used Giddens' theory of structuration to develop the conception of entrepreneurship as an embedded socioeconomic process and found that embeddedness plays a key role in shaping and sustaining business.
1,236 citations
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International Agency for Research on Cancer1, Russian Academy2, Nofer Institute of Occupational Medicine3, Charles University in Prague4, Fred Hutchinson Cancer Research Center5, University of Liverpool6, Cancer Care Ontario7, Princess Margaret Cancer Centre8, Women's College, Kolkata9, Norwegian University of Science and Technology10, German Cancer Research Center11, University of Cambridge12, Umeå University13, University of Bremen14, French Institute of Health and Medical Research15, University of Turin16, University of Aberdeen17, University of Padua18, Newcastle University19, University of Glasgow20, Trinity College, Dublin21
TL;DR: The results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets.
Abstract: Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually. To identify genetic factors that modify disease risk, we conducted a genome-wide association study by analysing 317,139 single-nucleotide polymorphisms in 1,989 lung cancer cases and 2,625 controls from six central European countries. We identified a locus in chromosome region 15q25 that was strongly associated with lung cancer (P = 9 x 10(-10)). This locus was replicated in five separate lung cancer studies comprising an additional 2,513 lung cancer cases and 4,752 controls (P = 5 x 10(-20) overall), and it was found to account for 14% (attributable risk) of lung cancer cases. Statistically similar risks were observed irrespective of smoking status or propensity to smoke tobacco. The association region contains several genes, including three that encode nicotinic acetylcholine receptor subunits (CHRNA5, CHRNA3 and CHRNB4). Such subunits are expressed in neurons and other tissues, in particular alveolar epithelial cells, pulmonary neuroendocrine cells and lung cancer cell lines, and they bind to N'-nitrosonornicotine and potential lung carcinogens. A non-synonymous variant of CHRNA5 that induces an amino acid substitution (D398N) at a highly conserved site in the second intracellular loop of the protein is among the markers with the strongest disease associations. Our results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets.
1,226 citations
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TL;DR: ‘state of the art’ soil greenhouse gas research is highlighted, mitigation practices and potentials are summarized, gaps in data and understanding are identified and ways to close such gaps are suggested through new research, technology and collaboration.
Abstract: Soils are integral to the function of all terrestrial ecosystems and to food and fibre production. An overlooked aspect of soils is their potential to mitigate greenhouse gas emissions. Although proven practices exist, the implementation of soil-based greenhouse gas mitigation activities are at an early stage and accurately quantifying emissions and reductions remains a substantial challenge. Emerging research and information technology developments provide the potential for a broader inclusion of soils in greenhouse gas policies. Here we highlight 'state of the art' soil greenhouse gas research, summarize mitigation practices and potentials, identify gaps in data and understanding and suggest ways to close such gaps through new research, technology and collaboration.
1,221 citations
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University of Sydney1, University of Michigan2, Duke University3, University of Alabama at Birmingham4, University of Pittsburgh5, University of Florida6, Centers for Disease Control and Prevention7, University of Münster8, University of Udine9, Ankara University10, University of Wisconsin-Madison11, Paris Diderot University12, University of Arkansas for Medical Sciences13, University of Paris14, University of Lausanne15, Brown University16, Istituto Giannina Gaslini17, Carlos III Health Institute18, Uniformed Services University of the Health Sciences19, National Institutes of Health20, University of Pennsylvania21, St George's, University of London22, Heidelberg University23, University of Copenhagen24, University College London25, University of Texas MD Anderson Cancer Center26, Katholieke Universiteit Leuven27, Goethe University Frankfurt28, University of Würzburg29, Johns Hopkins University30, Monash University31, Federal University of Rio de Janeiro32, Catholic University of the Sacred Heart33, University of Texas Health Science Center at San Antonio34, Masaryk University35, RMIT University36, Radboud University Nijmegen37, University of Melbourne38, Stanford University39, University of California, Davis40, Georgia Regents University41, Cornell University42, University of Aberdeen43, University Hospital of Wales44
TL;DR: These updated definitions of IFDs should prove applicable in clinical, diagnostic, and epidemiologic research of a broader range of patients at high-risk.
Abstract: BACKGROUND: Invasive fungal diseases (IFDs) remain important causes of morbidity and mortality. The consensus definitions of the Infectious Diseases Group of the European Organization for Research and Treatment of Cancer and the Mycoses Study Group have been of immense value to researchers who conduct clinical trials of antifungals, assess diagnostic tests, and undertake epidemiologic studies. However, their utility has not extended beyond patients with cancer or recipients of stem cell or solid organ transplants. With newer diagnostic techniques available, it was clear that an update of these definitions was essential. METHODS: To achieve this, 10 working groups looked closely at imaging, laboratory diagnosis, and special populations at risk of IFD. A final version of the manuscript was agreed upon after the groups' findings were presented at a scientific symposium and after a 3-month period for public comment. There were several rounds of discussion before a final version of the manuscript was approved. RESULTS: There is no change in the classifications of "proven," "probable," and "possible" IFD, although the definition of "probable" has been expanded and the scope of the category "possible" has been diminished. The category of proven IFD can apply to any patient, regardless of whether the patient is immunocompromised. The probable and possible categories are proposed for immunocompromised patients only, except for endemic mycoses. CONCLUSIONS: These updated definitions of IFDs should prove applicable in clinical, diagnostic, and epidemiologic research of a broader range of patients at high-risk.
1,211 citations
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Christopher Newton-Cheh1, Christopher Newton-Cheh2, Toby Johnson3, Toby Johnson4 +359 more•Institutions (64)
TL;DR: In this paper, the association between systolic or diastolic blood pressure and common variants in eight regions near the CYP17A1 (P = 7 × 10(-24)), CYP1A2(P = 1 × 10-23), FGF5 (P=1 × 10 -21), SH2B3(P= 3 × 10−18), MTHFR(MTHFR), c10orf107(P), ZNF652(ZNF652), PLCD3 (P,P = 5 × 10 −9),
Abstract: Elevated blood pressure is a common, heritable cause of cardiovascular disease worldwide. To date, identification of common genetic variants influencing blood pressure has proven challenging. We tested 2.5 million genotyped and imputed SNPs for association with systolic and diastolic blood pressure in 34,433 subjects of European ancestry from the Global BPgen consortium and followed up findings with direct genotyping (N ≤ 71,225 European ancestry, N ≤ 12,889 Indian Asian ancestry) and in silico comparison (CHARGE consortium, N = 29,136). We identified association between systolic or diastolic blood pressure and common variants in eight regions near the CYP17A1 (P = 7 × 10(-24)), CYP1A2 (P = 1 × 10(-23)), FGF5 (P = 1 × 10(-21)), SH2B3 (P = 3 × 10(-18)), MTHFR (P = 2 × 10(-13)), c10orf107 (P = 1 × 10(-9)), ZNF652 (P = 5 × 10(-9)) and PLCD3 (P = 1 × 10(-8)) genes. All variants associated with continuous blood pressure were associated with dichotomous hypertension. These associations between common variants and blood pressure and hypertension offer mechanistic insights into the regulation of blood pressure and may point to novel targets for interventions to prevent cardiovascular disease.
1,205 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 |