Jack h botting (30 Ergebnisse)

hardcover. Zustand: Very Good. VG+ hardcover. 150 pp.

Hardcover. Zustand: Très bon. Ancien livre de bibliothèque avec équipements. Edition 1996. Ammareal reverse jusqu'à 15% du prix net de cet article à des organisations caritatives. ENGLISH DESCRIPTION Book Condition: Used, Very good. Former library book. Edition 1996. Ammareal gives back up to 15% of this item's net price to charity organizations.…

Paperback. Zustand: Very Good. 98p blue paperback, from the library of the late Cambridge Nobel Laureate Andrew Huxley with his name to endpaper, text clean and fresh, binding tight, images throughout, a good copy Language: English.

Cloth/Laminated Boards. Zustand: Very Good. Zustand des Schutzumschlags: No d/j as Published. Reprint. Type: Book This volume is the proceedings of the William Harvey Research Conference held in Cannes, France, on the 20th and 21st March, 1997. It describes the present knowledge of the structures of the cyclooxygenase isoforms and the experimental and clinical effects of selective inhibitors of cyclooxygenase-2. The pathophysiological significance of the cyclooxygenase enzymes in tumorigenesis, programmed cell death, vascular disease and asthma is also covered.150pp.…

Cloth/Laminated Boards. Zustand: Very Good. Zustand des Schutzumschlags: No d/j as Published. First Edition. Type: Book This volume is the proceedings of the William Harvey Research Conference held in Cannes, France, on the 20th and 21st March, 1997. It describes the present knowledge of the structures of the cyclooxygenase isoforms and the experimental and clinical effects of selective inhibitors of cyclooxygenase-2. The pathophysiological significance of the cyclooxygenase enzymes in tumorigenesis, programmed cell death, vascular disease and asthma is also covered.150pp.…

Cloth/Laminated Boards. Zustand: Very Good. Zustand des Schutzumschlags: No d/j as Published. Type: Book This volume of conference proceedings reviews the general pathophysiological significance of the isoforms of cyclooxygenase, and the likely value of selective COX-2 inhibitors in the treatment of rheumatoid conditions. Also covered is the possible use of antibodies against cytokines and cell adhesion receptors in the treatment of inflammatory conditions. N.B.Top edge front board slightly bumped.147pp.…

Cloth. Zustand: Like New. Zustand des Schutzumschlags: No d/j as Published. Type: Book This volume contains the proceedings of the William Harvey Conference held in London, 10-11 October, 1995. It covers the molecular biology and physiological functions of the cyclo-oxygenase enzymes, as well as the experimental and clinical aspects of the recently discovered inhibitors of the inducible cyclooxygenase. Particular attention has been directed at the discussion of the selectivity of non-steroid anti-inflammatory drugs for cyclooxygenase-2 and their propensity to cause gastric and kidney damage. 248pp.…

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Paperback. Zustand: Brand New. 150 pages. 9.45x6.30x0.37 inches. In Stock.

Paperback. Zustand: Brand New. 1996 edition. 160 pages. 9.25x6.10x0.47 inches. In Stock.

Paperback. Zustand: Brand New. reprint edition. 248 pages. 8.75x6.00x0.75 inches. In Stock.

Taschenbuch. Zustand: Neu. Selective COX-2 Inhibitors | Pharmacology, Clinical Effects and Therapeutic Potential | John R. Vane (u. a.) | Taschenbuch | ix | Englisch | 2012 | Springer | EAN 9789401060417 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu. …

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Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - The mainstay of therapy for rheumatoid disease is the non-steroid antiinflammatory drugs (NSAIDs), despite their inherent gastrointestinal toxicity and ability to cause renal damage in susceptible patients. The theory that the beneficial and toxic effects of NSAIDs stem from a reduction in prostanoid production through inhibition of cyclooxygenase implied that particular toxicities were inevitable with NSAIDs and would always be correlated with efficacy. However, over the years, it became apparent that at therapeutic doses, some NSAIDs had greater toxic side-effects than others, a fact not explained by the general theory. A significant clarification arose from the discovery that there are two distinct isoforms of COX, a constitutive enzyme (COX-I) responsible for the production of prostanoids necessary for platelet aggregation and protection of the gastric mucosa and kidney; and an inducible enzyme (COX-2) that is newly synthesized at sites of tissue damage and produces prostaglandins that manifest pathological effects. It became clear that different NSAIDs had greater or lesser effects on COX-I when used in therapeutic doses, explaining the variation in side-effects. ' The elucidation of the crystal structure of these different enzymes and the skills of medicinal chemists have led to the synthesis of new chemicals with a selectivity for the inducible enzyme, and thus with therapeutic efficacy without those toxic effects result ing from inhibition of the constitutive enzyme.…

Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - In 1971, Vane proposed that the mechanism of action of the aspirin-like drugs was through their inhibition of prostaglandin biosynthesis. Since then, there has been intense interest in the interaction between this diverse group of inhibitors and the enzyme known as cyclooxygenase (COX). It exists in two isoforms, COX-l and COX-2 (discovered some 5 years ago). Over the last two decades several new drugs have reached the market based on COX-l enzyme screens. Elucidation of the three-dimensional structure of COX-l has provided a new understanding for the actions of COX inhibitors. The constitutive isoform of COX, COX-l has clear physiological functions. Its activation leads, for instance, to the production of prostacyclin which when released by the endothelium is anti-thrombogenic and anti-atherosclerotic, and in the gastric mucosa is cyto protective. COX-l also generates prostaglandins in the kidney, where they help to maintain blood flow and promote natriuresis. The inducible isoform, COX-2, was discovered through its activity being increased in a number of cells by pro inflammatory stimuli. A year or so later, COX-2 was identified as a distinct isoform encoded by a different gene from COX-I. COX-2 is induced by inflammatory stimuli and by cytokines in migratory and other cells. Thus the anti-inflammatory actions of non-steroid anti-inflammatory drugs (NSAIDs) may be due to the inhibition of COX-2, whereas the unwanted side-effects such as irritation of the stomach lining and toxic effects on the kidney are due to inhibition of the constitutive enzyme, COX-I.…

Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - 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.…

Taschenbuch. Zustand: Neu. Leukotrienes | New Concepts and Targets for Therapy | Ian Rodger (u. a.) | Taschenbuch | ix | Englisch | 2013 | Springer | EAN 9789401060455 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu. …

Gebunden. Zustand: New. Jack Botting is Consultant at the William Harvey Research Institute, an independent charitable foundation within Queen Mary and Westfield College of the University of London, UK. In the two decades since the elusive slow reacting substance of .

Paperback. Zustand: Brand New. 156 pages. 9.25x6.10x0.36 inches. In Stock.

Zustand: New. This volume, containing the proceedings of a conference held in 1997, covers the biosynthesis of leukotrienes, their release in pathological conditions, progress in the characterization of leukotriene receptors, and the elucidation of signal transduction mechanisms following receptor activation. Editor(s): Rodger, Ian; Botting, Jack H.; Dahlen, Sven-Erik. Num Pages: 143 pages, biography. BIC Classification: MMG. Category: (P) Professional & Vocational; (UP) Postgraduate, Research & Scholarly. Dimension: 235 x 155 x 11. Weight in Grams: 399. . 1998. Hardback. . . . . Books ship from the US and Ireland.…

Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - In the two decades since the elusive 'slow reacting substance of anaphylaxis' (SRS-A) was identified as a product of the action of the 5-lipoxygenase enzyme on arachidonic acid, it has been well established that the leukotrienes are key mediators of both alIergy and inflammation. Their release by alIergen or other challenge has been demonstrated in the lungs of asthmatic subjects, and measurement of urinary leukotriene concentrations in such patients has been shown to be a valuable, non invasive indicator. Significant progress has been made towards the characterization of the leukotriene receptor subtypes, exemplified by the cloning of the LTB4 receptor earlier this year. Coupled with this there has been a continued elucidation of signal transduction mechanisms underlying receptor activation. Consequent upon these advances has been the development of potent antagonists of the CysLT receptor, J and both these and inhibitors of leukotriene biosynthesis have entered clinical practice in the therapy of asthma. In this clinical setting antagonists of the CysLTJ receptor have been shown to be an effective therapy in chronic asthmatics, against antigen- and exercise-induced bronchoconstriction, and in aspirin-intolerant asthmatics. The advent of this new class of agents promises to change the way in which asthmatic patients are currently treated.…

Buch. Zustand: Neu. Neuware - Preface. 1. The History of Anti-Inflammatory Drugs and Their Mechanism of Action; J.R. Vane, R.M. Botting. 2. Structure of Prostaglandin H2synthase-1 (COX-1) and its NSAID Binding Sites; P.J. Loll. 3. Differential Inhibition of Cyclooxygenases 1 and 2 by NSAIDs; M. Pairet, et al. 4. Blockade of Inflammatory Hyperalgesia and Cyclooxygenase-2; S.H. Ferreira. 5. Brain COX-2 in Experimental Models of Epilepsy and Stroke: Signalling Pathways Leading to Enhanced Expression; N.G. Bazan, et al. 6. New Highly Selective Cyclooxygenase-2 Inhibitors; A.W. Ford-Hutchinson. 7. Characteristics of Cyclooxygenase-1 and Cyclooxygenase-2-Deficient Mice; S.G. Morham, R. Langenbach. 8. X-Ray Crystal Structure of Human Cyclooxygenase-2; M. Browner. 9. Risk of Gastrointestinal Side Effects Caused by Non-Steroid Anti-Inflammatory Drugs (NSAIDs); H. Jick. 10. Expression and Regulation of Cyclooxygenase-2 in Synovial Tissues of Arthritic Patients; L.J. Crofford. 11. Differential Target Tissue Presentation and COX-1/COX-2 Inhibition by Non-Steroid Anti-Inflammatory Drugs: A Rationale for a New Classification; H. Fenner. 12. Clinical Experience with Meloxicam, a Selective COX-2 Inhibitor; W. Bolten. 13. Enzymatic Regulation of the Prostaglandin Response in a Human Model of Inflammation; B.F. Adam, G.A. Fitzgerald. 14. Cyclooxygenase-2 and Intestinal Cancer; R.N. DuBois, et al. 15. Cytokines and Adhesion Molecules in the Lung Inflammatory Response; P.A. Ward. 16. Adhesion Molecules as Targets for Therapy in Rheumatoid Arthritis; P.E. Lipsky, et al. Index. …

Buch. Zustand: Neu. Neuware - Preface. 1. Mechanism of Action of Anti-Inflammatory Drugs: An Overview; J.R. Vane, R.M. Botting. 2. The Structure of Human COX-2 and Selective Inhibitors; M.F. Browner. 3. Differential Inhibition of COX-1 and COX-2 by NSAIDs: A Summary of Results Obtained Using Various Test Systems; M. Pairet, et al. 4. COX-2 in Brain and Retina: Role in Neuronal Survival; N.G. Bazan, et al. 5. COX-2 and Apoptosis: NSAIDs as Effectors of Programmed Cell Death; D.L. Simmons, et al. 6. Inhibition of Intestinal Tumorigenesis via Selective Inhibition of COX-2; R.N. DuBois, et al. 7. Cyclooxygenase Enzymes in Human Vascular Disease; C. Patrono, et al. 8. Gastrointestinal Effects of NSAIDs; C.J. Hawkey. 9. Renal Side-Effects of NSAIDs: Role of COX-1 and COX-2; J.C. Frolich, D.O. Stichtenoth. 10. Aspirin-Induced Asthma and Cyclooxygenases; R.J. Gryglewski. 11. New Classification of Aspirin-like Drugs; H. Fenner. 12. New Highly Selective COX-2 Inhibitors; A.W. Ford-Hutchinson. 13. Specific COX-2 Inhibitors: From Bench to Bedside; P. Isakson, et al. 14. Meloxicam: Selective COX-2 Inhibition in Clinical Practice; D.E. Furst. Index.…