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Titlebook: New Targets in Inflammation; Inhibitors of COX-2 Nicolas Bazan,Jack Botting,John Vane Conference proceedings 1996 Springer Science+Busines

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書目名稱New Targets in Inflammation
副標(biāo)題Inhibitors of COX-2
編輯Nicolas Bazan,Jack Botting,John Vane
視頻videohttp://file.papertrans.cn/666/665791/665791.mp4
圖書封面Titlebook: New Targets in Inflammation; Inhibitors of COX-2  Nicolas Bazan,Jack Botting,John Vane Conference proceedings 1996 Springer Science+Busines
描述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 c
出版日期Conference proceedings 1996
關(guān)鍵詞Prostaglandin; cancer; cytokine; inflammation; research
版次1
doihttps://doi.org/10.1007/978-94-011-5386-7
isbn_softcover978-94-010-6265-7
isbn_ebook978-94-011-5386-7
copyrightSpringer Science+Business Media Dordrecht 1996
The information of publication is updating

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Adhesion molecules as targets for therapy in rheumatoid arthritis,enules and mononuclear cells in the circulation, mediated by a variety of adhesion molecules, govern the entry of inflammatory cells into the tissues.. Interference with these interactions, therefore, might be effective in the therapy of RA.
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atory 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-
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Cyclooxygenase-2 and intestinal cancer,exhibit chemoprotective effects as judged by a reduction in the frequency and number of premalignant and malignant lesions. Recently, Jacoby et al.. reported a decrease in tumour number in Min (multiple intestinal neoplasia) mice treated with piroxicam.
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Structure of prostaglandin H2 synthase-1 (COX-1) and its NSAID binding sites,c acid to form the intermediate PGG., and a peroxidase activity which reduces the hydroperoxide moiety of PGG. to the corresponding alcohol and produces PGH... This PGН. is acted upon by other enzymes to produce the final hormone product, which is secreted from the cell.
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