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Reveals that nonsteroidal anti-inflammatory drugs disrupt intracellular signaling in neutrophils, suggesting therapeutic mechanisms beyond prostaglandin inhibition.
The ability of aspirin and related drugs to inhibit prostaglandin biosynthesis accounts for many effects of NSAIDs but does not completely explain their efficacy against inflammation. An additional mechanism may be disruption of the intracellular signal pathways responsible for activation of inflammatory cells--notably, neutrophils.
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Gerald Weissmann (1991) studied this question.
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