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David E. Newby
Researcher at University of Edinburgh
Publications - 902
Citations - 45577
David E. Newby is an academic researcher from University of Edinburgh. The author has contributed to research in topics: Myocardial infarction & Coronary artery disease. The author has an hindex of 98, co-authored 805 publications receiving 35865 citations. Previous affiliations of David E. Newby include NHS Lothian & Queen's University.
Papers
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Cardiovascular PET-CT imaging: A new frontier?
TL;DR: A brief overview of the current state of cardiovascular PET-CT and the likely direction of future developments is provided.
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Comparison of Correction Techniques for the Spillin Effect in Emission Tomography
Mercy I. Akerele,Nicolas A. Karakatsanis,Daniel Deidda,Jacobo Cal-Gonzalez,Rachael O. Forsythe,Marc R. Dweck,Maaz Syed,David E. Newby,Robert G. Aykroyd,Steven Sourbron,Charalampos Tsoumpas +10 more
TL;DR: In this paper, the authors evaluated and compared the performance of various recently developed spill-in correction techniques, namely, background correction (BC), local projection (LP), and hybrid kernelized [hybrid kernel expectation maximization (HKEM)] methods.
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Heat and haze: a forecast for myocardial infarction?
TL;DR: In this article, the effect of air pollution exposure can be modified by many factors, including temperature, geographical area and social deprivation, and investigations of the effects attributable to meteorological variables are also susceptible to confounding by exposure to ambient air pollutants.
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Exosite 1 thrombin inhibition with JNJ-64179375 inhibits thrombus formation in a human translational model of thrombosis.
TL;DR: Exosite 1 inhibition with JNJ-9375 caused prolongation of blood coagulation, selective inhibition of thrombin-mediated platelet activation, and reductions in ex vivo thrombosis driven by a decrease in fibrin-rich thrombus formation.
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Toxicity of inhaled traffic related particulate matter
TL;DR: Data from these three studies suggest that exposure to traffic related PM can mediate changes in the vasculature and brain of healthy rats, to what extent these changes may contribute to chronic neurodegenerative or vascular diseases is at present unclear.