cyclooxygenase oor Spaans
cyclooxygenase
en
(biochemistry) Any of several enzymes that catalyze the conversion of arachidonic acid into prostaglandins; their inhibition is the mode of action of aspirin and ibuprofen.
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In vitro and in vivo studies demonstrated that meloxicam inhibits cyclooxygenase-# (COX-#) to a greater extent than cyclooxygenase-# (COX
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It selectively inhibits the cyclooxygenase # enzyme (COX-#), which is responsible for pain, inflammation or fever
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The cyclooxygenase activity of PGHS is inhibited by aspirin.
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Patients who have experienced bronchospasm, acute rhinitis, nasal polyps, angioneurotic oedema, urticaria, or allergic-type reactions after taking acetylsalicylic acid or NSAIDs including COX-# (cyclooxygenase-#) inhibitors
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Based on targeted metabolomics methods developed in the project, it could clearly be shown that it is not likely that polyphenols do affect acute inflammation by modulation of cyclooxygenase-2 activity.
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The use of Dynastat, as with any medicinal product known to inhibit cyclooxygenase/prostaglandin synthesis, is not recommended in women attempting to conceive (see sections # and
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The purpose of this study was to obtain aqueous extracts of whole body of U. dermestoides and explore their potential to inhibit enzymes involved in the biosynthesis of inflammation regulators, 15-lipoxygenase (15-LOX) and cyclooxygenases COX-1 and COX-2 (COXs).
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In addition, these patients may respond well to therapy with cyclooxygenase (COX) inhibitors.
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The use of etoricoxib, as with any medicinal product known to inhibit cyclooxygenase/prostaglandin synthesis, is not recommended in women attempting to conceive (see sections #, #, and
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Cyclooxygenase is responsible for generation of prostaglandins
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Amfenac inhibits the action of prostaglandin H synthase (cyclooxygenase), an enzyme required for prostaglandin production
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Its production is inhibited indirectly by NSAIDs, which inhibit the cyclooxygenase enzymes COX1 and COX2.
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COX-2 (Section 26.6): Cyclooxygenase-2, an enzyme that catalyzes the biosynthesis of prostaglandins.
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Patients who have experienced bronchospasm, acute rhinitis, nasal polyps, angioneurotic oedema, urticaria or other allergic-type reactions after taking acetylsalicylic acid or NSAIDs including COX-# (cyclooxygenase-#) inhibitors
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The cardiovascular risks of NSAIDs, particularly the cyclooxygenase-2 (COX-2) inhibitors, are well documented.
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Aspirin ingestion is a cause in some individuals because of inhibition of the cyclooxygenase pathway.
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The vascular relaxation is reversed in the presence of methylene blue (1.0 × 10-4 M, guanylate cyclase inhibitor) and L-NAME (10-4 M, nitric oxide synthase inhibitor), and is not affected in presence of propranolol (10-6 M, beta receptor antagonist), atropine (30 × 10-5 M, muscarinic antagonist) and indomethacin (10-6 M, cyclooxygenase inhibitor).
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Cyclooxygenase converts arachidonic acid to three other eicosanoids: 1.
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In vitro and in vivo studies demonstrated that meloxicam inhibits cyclooxygenase-#(COX-#) to a greater extent than cyclooxygenase-# (COX
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One of them—cyclooxygenase—has a CH2OH group at its active site that is necessary for enzymatic activity.
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In turn, the enzyme cyclooxygenase (COX) acts on arachidonic acid to produce prostaglandins (see Fig. 12-2).
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It is a potent and selective inhibitor of the cyclooxygenase # enzyme (COX
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