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The antiplatelet drug clopidogrel helps prevent stent-associated thrombosis, but the antiplatelet effects are quite variable and the clinical consequences can be serious. New findings show that the variability in clopidogrel efficacy is affected by the enzyme paraoxonase-1 (PON1), which is required for clopidogrel bioactivation (pages 110–116).
Adenosine therapy for sickle cell disease has been proposed to improve blood flow, mediate cytoprotection and inhibit natural killer cell activity. Complicating this approach, adenosine signaling also induces hemoglobin S polymerization, promoting 'sickling', vasoocclusion, hemolysis and organ damage (pages 79–86).
