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Molecular pathways for formation of eicosanoids and prostanoids. E.M. Antman, Circulation 2005; 112: 759-770. The 9 chemical groupings of NSAIDs are shown, along with key compounds in each class. Relative degree of COX-1 vs COX-2 selectivity is shown at the bottom of the figure.
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Molecular pathways for formation of eicosanoids and prostanoids E.M. Antman, Circulation 2005; 112: 759-770
The 9 chemical groupings of NSAIDs are shown, along with key compounds in each class. Relative degree of COX-1 vs COX-2 selectivity is shown at the bottom of the figure E.M. Antman, Circulation 2005; 112: 759-770
Comparison of COX-1 and COX-2 Enzymes E.M. Antman, Circulation 2005; 112: 759-770
Structural determinants of inhibition of arachidonic acid binding to COXs E.M. Antman, Circulation 2005; 112: 759-770
Consequences of COX inhibition for prostacyclin and thromboxane A2 production in normal and atherosclerotic arteries Endothelial cells are shown as a source of prostacyclin (PGI2) and platelets as a source of thromboxane A2 (TxA2) E.M. Antman, Circulation 2005; 112: 759-770
Relationships between vascular eicosanoids and NO under normal conditions (A) and in inflammatory states (B) E.M. Antman, Circulation 2005; 112: 759-770
Biostatistical considerations in a trial of a coxib vs placebo. Left, Main findings of the APC trialRight, A 2x2 table is used to arrange the data for the calculation of statistical tests of treatment effect E.M. Antman, Circulation 2005; 112: 759-770
Detection of harm with coxibs. Factors related to trial design (top) and to the patient and drug being investigated (bottom) are shown E.M. Antman, Circulation 2005; 112: 759-770
Number needed to harm E.M. Antman, Circulation 2005; 112: 759-770