J
John R. Vane
Researcher at St Bartholomew's Hospital
Publications - 145
Citations - 32772
John R. Vane is an academic researcher from St Bartholomew's Hospital. The author has contributed to research in topics: Prostaglandin & Nitric oxide. The author has an hindex of 74, co-authored 145 publications receiving 32138 citations. Previous affiliations of John R. Vane include Westfield College & University College Hospital.
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Journal ArticleDOI
Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs
TL;DR: Experiments with guinea-pig lung suggest that some of the therapeutic effects of sodium salicylate and aspirin-like drugs are due to inhibition of the synthesis of prostaglandins.
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Inducible isoforms of cyclooxygenase and nitric-oxide synthase in inflammation
John R. Vane,Jane A. Mitchell,I. Appleton,Annette Tomlinson,David Bishop-Bailey,Jamie J. Croxtall,Derek A. Willoughby +6 more
TL;DR: The rise in COX and NOS activities in the skin during the acute phase reinforces the proinflammatory role for prostanoids and suggests one also for nitric oxide and there may be differential regulation of these enzymes, perhaps due to the changing pattern of cytokines during the inflammatory response.
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The mechanism of action of aspirin.
John R. Vane,Renia Botting +1 more
TL;DR: In 1971, Vane proved that aspirin and other non-steroid anti-inflammatory drugs (NSAIDs) inhibit the activity of the enzyme now called cyclooxygenase (COX) which leads to the formation of prostaglandins (PGs) that cause inflammation, swelling, pain and fever.
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Indomethacin and aspirin abolish prostaglandin release from the spleen.
TL;DR: The action of these two anti-inflammatory agents provides further support for the suggestion that some of their therapeutic effects depend on the inhibition of the production of prostaglandin.
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Human arterial and venous tissues generate prostacyclin (prostaglandin x), a potent inhibitor of platelet aggregation
TL;DR: It is postulated that prostacyclin is important for prevention of deposition of platelets on the vessel wall and that the inhibition or prevention of the generation of prostacycliffe is important in the genesis of diseases, especially those in which increased lipid peroxidation occurs, such as atherosclerosis.