Problemset 4

Problemset 4 - observed until several hours sometimes days...

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1) Expain the rational and mechanism behind the benefits of a low-dose aspirin regimen to reduce the risk of thrombosis. The two prostaglandins, prostacyclin (from endothelial cells) and thromboxane (from thrombocytes), have opposing effects on blood coagulation. Aspirin is an irreversible COX inhibitor, preventing synthesis of both PGs in both cell types. However, in contrast to the platelets, which are enucleated cells that can not synthesize new COX and are therefore inhibited “for life”, the ECs are able to produce new COX and are therefore able to resume prostacyclin production. Consequently, the balance is now shifted towards the anti-aggregatory prostacyclin. 2) Both glucocorticoids and NSAIDs inhibits prostaglandin synthesis. However, while NSAIDs act within <30 min, the effects of glucocorticoids can not be
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Unformatted text preview: observed until several hours, sometimes days. Why? NSAIDs act directly on COX and inhibit it. Glucocorticoidsdo not inhibit PG synthesis directly, but act by transcriptionally inducing lipocortin and inhibiting the transcription of COX2. Thus, there effect requires time (and protein synthesis). 3) Would caffeine exacerbate or counteract the effects of cholera toxin? CT causes ADP ribosylation of the G-protein G α s, “trapping” it in its active (=GTP-bound) form. Consequently, high amounts of cAMP are produced by the coupled adenylate cyclase. Caffeine as a PDE inhibitor would prevent the degradation of cAMP, thus further increasing the concentration of cAMP and worsening the symptoms of cholera....
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This note was uploaded on 04/13/2010 for the course BIMM BIMM118 taught by Professor David during the Winter '09 term at UCSD.

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