Institution
Clinical Trial Service Unit
About: Clinical Trial Service Unit is a based out in . It is known for research contribution in the topics: Population & Stroke. The organization has 428 authors who have published 1387 publications receiving 181920 citations.
Papers published on a yearly basis
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TL;DR: The aim was to include all unconfounded properly randomised trials of antiplatelets versus no antiplatelet therapy that could have been available for review by March 1990 in which deep venous thrombosis was systematically and unbiasedly monitored.
Abstract: Venous thromboses and pulmonary embolism remain an important cause of morbidity and mortality both in surgical patients and in immobilised medical patients.*RF 1-5* Various thromboprophylactic treatments have, therefore, been devised to prevent or limit thromboembolism. Our previous systematic overview (or meta-analysis) of randomised trials of perioperative subcutaneous heparin found that among surgical patients such treatment can roughly halve the risk not only of deep venous thrombosis but, more importantly, of pulmonary embolism6 (see fig 1). Subcutaneous heparin is now widely recommended for surgical or medical patients at high risk of venous occlusion.*RF 3-5*
The recent Antiplatelet Trialists' Collaboration overview of the thromboprophylactic effects of antiplatelet therapy used prospectively determined criteria for trial inclusion and treatment comparisons that were similar to those of the previous heparin overview.*RF 6-8* The aim was to include all unconfounded properly randomised trials of antiplatelet versus no antiplatelet therapy (or of one antiplatelet regimen versus another) that could have been available for review by March 1990 in which deep venous thrombosis was systematically and unbiasedly monitored. (Parts I and III of the previous overview report give a fuller description of the methods used.1,7 The appropriateness of using “assumption free” statistical methods rather than the “random effects” model when combining trial results, as when combining results from different centres in a multicentre trial, has been discussed in detail previously.9,10) Such randomised trials were to be included whether or not the treatment comparison was “blinded” by placebo control. This was also the case in the heparin overview, where exclusion of informative “open” trials (in particular, the important open international multicentre trials coordinated by Professor V V Kakkar11) would have been equally inappropriate. Analyses confined to placebo controlled studies, which may be less subject to treatment dependent biases in the assessment …
74 citations
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TL;DR: A systematic review and meta-analysis conducted by Kazem Rahimi and colleagues re-evaluates the hypothesis, generated in previous studies, that statins may reduce the risk of venous thromboembolic events and does not support the previous findings.
Abstract: Background: It has been suggested that statins substantially reduce the risk of venous thromboembolic events. We sought to test this hypothesis by performing a meta-analysis of both published and unpublished results from randomised trials of statins. Methods and Findings: We searched MEDLINE, EMBASE, and Cochrane CENTRAL up to March 2012 for randomised controlled trials comparing statin with no statin, or comparing high dose versus standard dose statin, with 100 or more randomised participants and at least 6 months’ follow-up. Investigators were contacted for unpublished information about venous thromboembolic events during follow-up. Twenty-two trials of statin versus control (105,759 participants) and seven trials of an intensive versus a standard dose statin regimen (40,594 participants) were included. In trials of statin versus control, allocation to statin therapy did not significantly reduce the risk of venous thromboembolic events (465 [0.9%] statin versus 521 [1.0%] control, odds ratio [OR]=0.89, 95% CI 0.78–1.01, p=0.08) with no evidence of heterogeneity between effects on deep vein thrombosis (266 versus 311, OR 0.85, 95% CI 0.72–1.01) and effects on pulmonary embolism (205 versus 222, OR 0.92, 95% CI 0.76–1.12). Exclusion of the trial result that provided the motivation for our meta-analysis (JUPITER) had little impact on the findings for venous thromboembolic events (431 [0.9%] versus 461 [1.0%], OR=0.93 [95% CI 0.82–1.07], p=0.32 among the other 21 trials). There was no evidence that higher dose statin therapy reduced the risk of venous thromboembolic events compared with standard dose statin therapy (198 [1.0%] versus 202 [1.0%], OR=0.98, 95% CI 0.80– 1.20, p=0.87). Risk of bias overall was small but a certain degree of effect underestimation due to random error cannot be ruled out. Conclusions: The findings from this meta-analysis do not support the previous suggestion of a large protective effect of statins (or higher dose statins) on venous thromboembolic events. However, a more moderate reduction in risk up to about one-fifth cannot be ruled out. Please see later in the article for the Editors’ Summary.
74 citations
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TL;DR: Vascular disease and left ventricular hypertrophy are prevalent among patients with chronic kidney disease not requiring dialysis, and other features of the uremic syndrome such as anemia, hyperhomocysteinemia, and inflammation may contribute.
73 citations
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TL;DR: The rationale for individual patient data reviews is discussed and some of the features will add to the analyses that can be performed and the reviewer allows the reviewer to overcome many of the problems associated with a reliance on published data alone.
Abstract: Systematic reviews help people to make well-informed decisions about health care by bringing together the relevant evidence, appraising it and, where appropriate, combining it in a meta-analysis. The ultimate aim for a systematic review should be to present all relevant data on all participants in all research judged to be eligible for the review. In reviews of the effects of interventions, this ultimate aim would be met through the collection and analyses of the results of all relevant randomized trials. Reviews that use individual patient data achieve this by the central collection and analyses of data on each participant in the trials. It allows the reviewer to overcome many of the problems associated with a reliance on published data alone, and some of the problems associated with using aggregate data supplied by the trialist, and will add to the analyses that can be performed. This chapter discusses the rationale for individual patient data reviews and describes some of their features.
72 citations
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University of Surrey1, Imperial College London2, University of Cambridge3, University College London4, Erasmus University Rotterdam5, Boston Children's Hospital6, University of Queensland7, University of Western Australia8, University of London9, University of Eastern Finland10, Children's Hospital of Philadelphia11, University of Helsinki12, Ludwig Maximilian University of Munich13, University of Bristol14, University of Oulu15, University of Pennsylvania16, Statens Serum Institut17, Aarhus University18, Agency for Science, Technology and Research19, Southampton General Hospital20, University Hospital Southampton NHS Foundation Trust21, University of Copenhagen22, Harvard University23, Technische Universität München24, Paris Descartes University25, University of Canterbury26, National Institutes of Health27, Royal Devon and Exeter Hospital28, National Institute for Health Research29, University of Lincoln30, University of Southampton31, University of South Australia32, Great Ormond Street Hospital33, Karolinska Institutet34, University of Oxford35, Stanford University36, Clinical Trial Service Unit37, University of Adelaide38, University of Auckland39, King's College London40, Kingston University41, Brunel University London42, John Radcliffe Hospital43
TL;DR: A robust overlap is found between the genetics of child and adult body mass index (BMI), with variants associated with adult BMI acting as early as 4 to 6 years old, and a completely distinct genetic makeup for peak BMI during infancy is demonstrated, influenced by variation at the LEPR/LEPROT locus.
Abstract: Early childhood growth patterns are associated with adult health, yet the genetic factors and the developmental stages involved are not fully understood. Here, we combine genome-wide association studies with modeling of longitudinal growth traits to study the genetics of infant and child growth, followed by functional, pathway, genetic correlation, risk score, and colocalization analyses to determine how developmental timings, molecular pathways, and genetic determinants of these traits overlap with those of adult health. We found a robust overlap between the genetics of child and adult body mass index (BMI), with variants associated with adult BMI acting as early as 4 to 6 years old. However, we demonstrated a completely distinct genetic makeup for peak BMI during infancy, influenced by variation at the LEPR/LEPROT locus. These findings suggest that different genetic factors control infant and child BMI. In light of the obesity epidemic, these findings are important to inform the timing and targets of prevention strategies.
72 citations
Authors
Showing all 428 results
Name | H-index | Papers | Citations |
---|---|---|---|
Salim Yusuf | 231 | 1439 | 252912 |
Richard Peto | 183 | 683 | 231434 |
Cornelia M. van Duijn | 183 | 1030 | 146009 |
Rory Collins | 162 | 489 | 193407 |
Naveed Sattar | 155 | 1326 | 116368 |
Timothy J. Key | 146 | 808 | 90810 |
John Danesh | 135 | 394 | 100132 |
Andrew J.S. Coats | 127 | 820 | 94490 |
Valerie Beral | 114 | 471 | 53729 |
Mike Clarke | 113 | 1037 | 164328 |
Robert Clarke | 111 | 512 | 90049 |
Robert U. Newton | 109 | 753 | 42527 |
Richard Gray | 109 | 808 | 78580 |
Braxton D. Mitchell | 102 | 558 | 49599 |
Naomi E. Allen | 101 | 364 | 37057 |