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New Targets in Inflammation - Inhibitors of COX-2 or Adhesion Molecules Proceedings of a conference held on April 15-16, 1996, in New Orleans, USA, supported by an educational grant from Boehringer Ingelheim (Paperback, Softcover reprint of the original 1st ed. 1996)
Loot Price: R2,750
Discovery Miles 27 500
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New Targets in Inflammation - Inhibitors of COX-2 or Adhesion Molecules Proceedings of a conference held on April 15-16, 1996, in New Orleans, USA, supported by an educational grant from Boehringer Ingelheim (Paperback, Softcover reprint of the original 1st ed. 1996)
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Total price: R2,760
Discovery Miles: 27 600
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For the past 100 years the mainstay of therapy for rheumatoid
arthritis (RA) has been aspirin or other drugs of the non-steroid
anti-inflammatory group. In 1971 Vane pro posed that both the
beneficial and toxic actions of these drugs was through inhibition
of prostaglandin synthesis. The recent discovery that
prostaglandins responsible for pain and other symptoms at
inflammatory foci are synthesized by an inducible cyclooxygenase
(COX-2) that is encoded by a gene distinct from that of the consti
tutive enzyme (COX-I) provided a new target for therapy of RA. A
drug that would selectively inhibit COX-2 would hopefully produce
the symptomatic benefit provided by existing NSAIDs without the
gastrointestinal and renal toxicity due to the inhibition of COX-I.
Drugs selective for COX-2 are now available. Experimental studies
have shown them to be effective with minimal toxicity, and in
clinical trials gastric and renal toxicities are less. Highly
selective COX-2 inhibitors, perhaps designed with knowledge of the
crystal structures of COX-I and COX-2, are also available. Other
experimental studies, including those in animals lacking effective
genes for COX-lor COX-2 and in experimental carcinomas, suggest
there is still much to be learned of the pathophysiological
functions of these enzymes. The inflammatory response is a complex
reaction involving many mediators that derive from white blood
cells, endothelial cells and other tissues. Preliminary data have
revealed that inhibitors of the cytokines and adhesion molecules
that play a crucial role in the migration of white cells to
inflammatory sites may be useful in RA.
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