|
|
|
|
| LEADER |
04003nmm a2200277 u 4500 |
| 001 |
EB000718716 |
| 003 |
EBX01000000000000000571798 |
| 005 |
00000000000000.0 |
| 007 |
cr||||||||||||||||||||| |
| 008 |
140122 ||| eng |
| 020 |
|
|
|a 9789401153867
|
| 100 |
1 |
|
|a Bazan, N.
|e [editor]
|
| 245 |
0 |
0 |
|a New Targets in Inflammation
|h Elektronische Ressource
|b Inhibitors of COX-2 or Adhesion Molecules Proceedings of a conference held on April 15–16, 1996, in New Orleans, USA, supported by an educational grant from Boehringer Ingelheim
|c edited by N. Bazan, Jack H. Botting, Sir John R. Vane
|
| 250 |
|
|
|a 1st ed. 1996
|
| 260 |
|
|
|a Dordrecht
|b Springer Netherlands
|c 1996, 1996
|
| 300 |
|
|
|a IX, 147 p
|b online resource
|
| 505 |
0 |
|
|a 1 The history of anti-inflammatory drugs and their mechanism of action -- 2 Structure of prostaglandin H2 synthase-1 (COX-1) and its NSAID binding sites -- 3 Differential inhibition of cyclooxygenases 1 and 2 by NSAIDs -- 4 Blockade of inflammatory hyperalgesia and cyclooxygenase-2 -- 5 Brain COX-2 in experimental models of epilepsy and stroke: signalling pathways leading to enhanced expression -- 6 New highly selective cyclooxygenase-2 inhibitors -- 7 Characteristics of cyclooxygenase-1 and cyclooxygenase-2-deficient mice -- 8 X-ray crystal structure of human cyclooxygenase-2 -- 9 Risk of gastrointestinal side effects caused by non-steroid anti-inflammatory drugs (NSAIDs) -- 10 Expression and regulation of cyclooxygenase-2 in synovial tissues of arthritic patients -- 11 Differential target tissue presentation and COX-1/COX-2 inhibition by non-steroid anti-inflammatory drugs: a rationale for a new classification -- 12 Clinical experience with meloxicam, a selective COX-2 inhibitor -- 13 Enzymatic regulation of the prostaglandin response in a human model of inflammation -- 14 Cyclooxygenase-2 and intestinal cancer -- 15 Cytokines and adhesion molecules in the lung inflammatory response -- 16 Adhesion molecules as targets for therapy in rheumatoid arthritis
|
| 653 |
|
|
|a Pharmacology
|
| 700 |
1 |
|
|a Botting, Jack H.
|e [editor]
|
| 700 |
1 |
|
|a Vane, Sir John R.
|e [editor]
|
| 041 |
0 |
7 |
|a eng
|2 ISO 639-2
|
| 989 |
|
|
|b SBA
|a Springer Book Archives -2004
|
| 028 |
5 |
0 |
|a 10.1007/978-94-011-5386-7
|
| 856 |
4 |
0 |
|u https://doi.org/10.1007/978-94-011-5386-7?nosfx=y
|x Verlag
|3 Volltext
|
| 082 |
0 |
|
|a 615
|
| 520 |
|
|
|a 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.
|