Titlebook: Inducible Enzymes in the Inflammatory Response; Derek A. Willoughby,Annette Tomlinson Book 1999 Springer Basel AG 1999 clinic.enzyme.infla

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iNOS and COX-2 in atherosclerosis,n the Western world today [1, 2]. The disease is regulated by a large number of different factors which partly explains why the aetiology and pathogenesis of atherosclerosis remain incompletely defined. Since the discovery of prostacyclin in the 1970s [3] and nitric oxide in the 1980s [4] considerab

Infinitesimal

The role of the inducible enzymes cyclooxygenase-2, nitric oxide synthase and heme oxygenase in ang quiescent and endothelial cell turnover may be measured in terms of years. However, it is an essential component of a variety of normal functions such as embryogenesis, normal tissue growth and the menstrual cycle. It also plays a role in the pathology of a variety of disease states and this led Ju

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Neuroinflammation,atomically tight interface between blood vessel wall and the neural parenchyma, the so called blood-brain (BBB) and blood-nerve barrier (BNB), respectively, form a strict separation between the systemic immune compartment and the nervous system, and that (b) other immunologic mechanisms such as the

Dictation

Inducible enzymes in inflammation: advances, interactions and conflicts,tion has focused on inducible nitric oxide synthase (iNOS), the enzyme which catalyses L-argininine to L-citrulline and nitric oxide (NO), and on the recently discovered second isoform of cyclooxygenase (COX-2), which converts arachidonic acid to bioac-tive prostanoids.

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The role of the inducible enzymes cyclooxygenase-2, nitric oxide synthase and heme oxygenase in angature; these include many of the chronic inflammatory diseases such as rheumatoid arthritis [2]. In these latter diseases, the neovasculature not only acts as a route for the increased nutrient supply required by the developing tissue, but also provides a greatly exaggerated area of activated endoth

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Neuroinflammation,egulating the immunologic machinery in the nervous system. The model in which an aberrant immune response as a causative mechanism in neurologic diseases has been extensively studied, is known as experimental autoimmune encephalomyelitis (EAE). While it reproduces essential aspects of the pathogenes

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Michael P. Seed,Derek Gilroy,Mark Paul-Clark,Paul R. Colville-Nash,Dean Willis,Annette Tomlinson,Der