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Timothy D. Warner

Researcher at Queen Mary University of London

Publications -  272
Citations -  18436

Timothy D. Warner is an academic researcher from Queen Mary University of London. The author has contributed to research in topics: Platelet & Endothelin 1. The author has an hindex of 62, co-authored 263 publications receiving 17452 citations. Previous affiliations of Timothy D. Warner include Université de Sherbrooke & Northwestern University.

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Nonsteroid drug selectivities for cyclo-oxygenase-1 rather than cyclo-oxygenase-2 are associated with human gastrointestinal toxicity: A full in vitro analysis

TL;DR: This full in vitro analysis of COx-1/2 selectivities in human tissues clearly supports the theory that inhibition of COX-1 underlies the gastrointestinal toxicity of NSAIDs in man.
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Pressor effects of circulating endothelin are limited by its removal in the pulmonary circulation and by the release of prostacyclin and endothelium-derived relaxing factor.

TL;DR: In the rat, the effects of endothelin on the blood pressure vary from pressor (in pithed rats) to purely depressor in anesthetized rats where the resting blood pressure is high, and has the characteristics of a local pressor hormone, rather than a circulating one.
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Purification and characterization of particulate endothelium-derived relaxing factor synthase from cultured and native bovine aortic endothelial cells.

TL;DR: The particulate enzyme responsible for the synthesis of endothelium-derived relaxing factor has been purified from cultured and native (noncultured) bovine aortic endothelial cells and required L-arginine, NADPH, Ca2+, calmodulin, and 5,6,7,8-tetrahydrobiopterin for full activity.
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Cyclooxygenases: new forms, new inhibitors, and lessons from the clinic

TL;DR: Clinical use of COX‐2‐selective compounds has ignited strong debates regarding potential side effects, most notably those within the cardiovascular system such as myocardial infarctions, strokes, and elevation in blood pressure, and this review will discuss how the latest studies help to understand the roles ofCOX‐1 and COx‐2 and what clinically proven benefits the newer generation of CO X‐2•selective inhibitors offer.