Institution
St George's, University of London
Education•London, United Kingdom•
About: St George's, University of London is a education organization based out in London, United Kingdom. It is known for research contribution in the topics: Population & Health care. The organization has 4953 authors who have published 11675 publications receiving 574153 citations. The organization is also known as: SGUL & St George's Hospital Medical School.
Papers published on a yearly basis
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University of Glasgow1, University of Lugano2, St George's, University of London3, Pasteur Institute4, Queen Mary University of London5, Buck Institute for Research on Aging6, National and Kapodistrian University of Athens7, Université de Montréal8, Imperial College London9, Osaka University10, Weizmann Institute of Science11, Mayo Clinic12, University of Melbourne13, University of Cambridge14, University of Minnesota15, Max Delbrück Center for Molecular Medicine16, Brown University17, Academy of Athens18, Newcastle University19, University of Florida20, Catalan Institution for Research and Advanced Studies21, University of Groningen22
TL;DR: A consensus from the International Cell Senescence Association (ICSA) is presented, defining and discussing key cellular and molecular features of senescence and offering recommendations on how to use them as biomarkers.
1,220 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
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TL;DR: In this paper, the authors investigated whether intensive-dose statin therapy is associated with increased risk of new-onset diabetes compared with moderate-dose stochastic insulin this paper.
Abstract: Context A recent meta-analysis demonstrated that statin therapy is associated with excess risk of developing diabetes mellitus. Objective To investigate whether intensive-dose statin therapy is associated with increased risk of new-onset diabetes compared with moderate-dose statin therapy. Data Sources We identified relevant trials in a literature search of MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials (January 1, 1996, through March 31, 2011). Unpublished data were obtained from investigators. Study Selection We included randomized controlled end-point trials that compared intensive-dose statin therapy with moderate-dose statin therapy and included more than 1000 participants who were followed up for more than 1 year. Data Extraction Tabular data provided for each trial described baseline characteristics and numbers of participants developing diabetes and experiencing major cardiovascular events (cardiovascular death, nonfatal myocardial infarction or stroke, coronary revascularization). We calculated trial-specific odds ratios (ORs) for new-onset diabetes and major cardiovascular events and combined these using random-effects model meta-analysis. Between-study heterogeneity was assessed using the I 2 statistic. Results In 5 statin trials with 32 752 participants without diabetes at baseline, 2749 developed diabetes (1449 assigned intensive-dose therapy, 1300 assigned moderate-dose therapy, representing 2.0 additional cases in the intensive-dose group per 1000 patient-years) and 6684 experienced cardiovascular events (3134 and 3550, respectively, representing 6.5 fewer cases in the intensive-dose group per 1000 patient-years) over a weighted mean (SD) follow-up of 4.9 (1.9) years. Odds ratios were 1.12 (95% confidence interval [CI], 1.04-1.22; I 2 = 0%) for new-onset diabetes and 0.84 (95% CI, 0.75-0.94; I 2 = 74%) for cardiovascular events for participants receiving intensive therapy compared with moderate-dose therapy. As compared with moderate-dose statin therapy, the number needed to harm per year for intensive-dose statin therapy was 498 for new-onset diabetes while the number needed to treat per year for intensive-dose statin therapy was 155 for cardiovascular events. Conclusion In a pooled analysis of data from 5 statin trials, intensive-dose statin therapy was associated with an increased risk of new-onset diabetes compared with moderate-dose statin therapy.
1,199 citations
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University of Cambridge1, Wellcome Trust Centre for Human Genetics2, King's College London3, Western General Hospital4, University of Oxford5, Newcastle University6, University of Bristol7, St George's, University of London8, Wellcome Trust Sanger Institute9, University College London10, Guy's and St Thomas' NHS Foundation Trust11
TL;DR: A genome-wide association scan in individuals with Crohn's disease by the Wellcome Trust Case Control Consortium detected strong association at four novel loci, and 37 SNPs from these and other loci were tested for association in an independent case-control sample.
Abstract: A genome-wide association scan in individuals with Crohn's disease by the Wellcome Trust Case Control Consortium detected strong association at four novel loci. We tested 37 SNPs from these and other loci for association in an independent case-control sample. We obtained replication for the autophagy-inducing IRGM gene on chromosome 5q33.1 (replication P = 6.6 x 10(-4), combined P = 2.1 x 10(-10)) and for nine other loci, including NKX2-3, PTPN2 and gene deserts on chromosomes 1q and 5p13.
1,189 citations
Authors
Showing all 5006 results
Name | H-index | Papers | Citations |
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JoAnn E. Manson | 270 | 1819 | 258509 |
Paul M. Ridker | 233 | 1242 | 245097 |
George Davey Smith | 224 | 2540 | 248373 |
Peer Bork | 206 | 697 | 245427 |
Grant W. Montgomery | 157 | 926 | 108118 |
Naveed Sattar | 155 | 1326 | 116368 |
Alan S. Verkman | 146 | 771 | 70434 |
David P. Strachan | 143 | 472 | 105256 |
Sekar Kathiresan | 141 | 479 | 98784 |
Nick C. Fox | 139 | 748 | 93036 |
Andrew Steptoe | 137 | 1003 | 73431 |
Daniel I. Chasman | 134 | 484 | 72180 |
Joel N. Hirschhorn | 133 | 431 | 101061 |
Dan M. Roden | 132 | 859 | 67578 |
Hugh Watkins | 128 | 524 | 91317 |