Download e-book for iPad: Advances in Eicosanoid Research by J. R. Vane (auth.), C. N. Serhan, H. D. Perez (eds.)

By J. R. Vane (auth.), C. N. Serhan, H. D. Perez (eds.)

ISBN-10: 3662040476

ISBN-13: 9783662040478

ISBN-10: 3662040492

ISBN-13: 9783662040492

Over the previous couple of years, now we have witnessed large growth within the box of eicosanoids and their healing functions. Receptor an­ tagonists for leukotrienes were validated as anti-inflammatories and are out there as a therapy for bronchial asthma. Receptor agonists for professional­ stacyclin are being validated for the remedy of peripheral vascular dis­ ease, and selective inhibitors of cyclooxygenase kind II have been simply ap­ proved for the remedy of rheumatoid arthritis. some of these advancements are the end result of a long time and man-hours of cautious learn. the sphere has now entered an upswing that may lead to novel thera­ peutic functions in the subsequent 10 years. New molecules and me­ diators were pointed out, new enzymes and pathways elucidated and new healing methods have emerged. the idea that of ei­ cosanoids as "pro-inflammatory" molecules is being challenged, and their function as regulators is more and more famous. in reality, a few of these molecules will be very important endogenous anti inflammatory agents.

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This figure was generated using RASMOL (Sayle and Milner-White 1995) required to demonstrate that this enzyme represented a new class of PLA2S. Shortly afterward, another paper reported the cloning of group- V PLA2 from rats (Chen et al. 1994b). This enzyme was calcium dependent and had the same substrate specificity as the human group- V enzyme. These findings strengthened the notion that the group- V PLA2S are an important new class of sPLA2S found in mammals. 3 Role of Group-V PLA2 in P388DI Macrophages The discovery of the group- V enzyme required a re-evaluation of earlier studies that had attributed PLA 2 activity in non-pancreatic tissues to the group-IIA enzyme .

1987) and from the synovial fluid of arthritis patients (Stefanski et al. 1986; Kramer et al. 1989; Seilham er et al. 1989), the group-IIA enzyme has attracted considerable attention as a potential drug target due to its role in the release of arachidonic acid (AA), the precursor of several pro-inflammatory lipids. Many pharmaceut ical companies tried to develop inhibitors against this enzyme in the hope of developing therapies for inflammatory diseases. Not surprisingly, much enthusiasm accompanied the discovery of a novel group-V gene (Chen et al.

Gastrointest Endosc 42:428-433 Langenbach R, Morham, SG, Tiano HF, Loftin CD, Ghanayem BI, Chulada PC, et aI. (1995) Prostaglandin synthase I gene disruption in mice reduces arachidonic acid-induced inflammation and indomethacin-induced gastric ulceration. Cell 83:483-492 Lanza FL (1989) A review of gastric ulcer and gastroduodenal injury in normal volunteers receiving aspirin and other non-steroidal anti-inflammatory drugs. Scand J Gastroenterol Suppl 163:24-31 Lanza FL, Rack MF, Callison DA, Hubbard RC, Yu SS, Talwalker S, et aI.

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Advances in Eicosanoid Research by J. R. Vane (auth.), C. N. Serhan, H. D. Perez (eds.)


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