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(Stroke. 2009;40:e50.)
© 2009 American Heart Association, Inc.
Comments, Opinions, and Reviews |
From the Centre for Clinical Brain Sciences (M.R.M., E.S.S.), University of Edinburgh, UK; the Department of Neurology, University of Massachusetts Medical School (M.F.), Worcester, Mass, USA; the National Stroke Research Institute & University of Melbourne Department of Medicine (V.O., E.S.S., G.A.D., D.W.H.), Austin Health, Melbourne, Australia; the Charité Department for Experimental Neurology & Center for Stroke Research (U.D.), Berlin, Germany; the Stroke Trials Unit (P.M.W.B.), University of Nottingham, UK; the Acute Stroke Program (A.B.), Nuffield Department of Medicine, John Radcliffe Hospital, Oxford, UK; the Department of Neurology (H.B.v.d.W.), Rudolf Magnus Institute of Neuroscience, University Medical Center, Utrecht, The Netherlands; the University of Colorado Denver (R.T.), Anschutz Medical Campus, Aurora, Colo, USA; and the Cerebrovascular Division (K.M.), Department of Medicine, National Cardiovascular Center, Osaka, Japan.
Correspondence to David Howells, National Stroke Research Institute, Austin Health, Studley Rd, Heidelberg, Victoria 3084, Australia. E-mail david.howells{at}unimelb.edu.au
Background and Purpose— As a research community, we have failed to demonstrate that drugs which show substantial efficacy in animal models of cerebral ischemia can also improve outcome in human stroke.
Summary of Review— Accumulating evidence suggests this may be due, at least in part, to problems in the design, conduct and reporting of animal experiments which create a systematic bias resulting in the overstatement of neuroprotective efficacy.
Conclusions— Here, we set out a series of measures to reduce bias in the design, conduct and reporting of animal experiments modeling human stroke.
Key Words: animal models basic science drug trials education experimental outcomes preventing bias translational research
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