Overview
- Editors:
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Paul G. Winyard
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William Harvey Research Institute, London, UK
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Derek A. Willoughby
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William Harvey Research Institute, London, UK
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Table of contents (36 protocols)
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In Vivo Models of Inflammation
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- Paul Colville-Nash, Toby Lawrence
Pages 181-189
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- Nicole S. Wayman, Michelle C. McDonald, Prabal K. Chatterjee, Christoph Thiemermann
Pages 199-208
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- Brendan J. R. Whittle, Maryan Cavicchi, Dominique Lamarque
Pages 209-222
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- Prabal K. Chatterjee, Christoph Thiemermann
Pages 223-237
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- Isabelle Binet, Kathryn J. Wood
Pages 239-248
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- Annette Tomlinson, Mark W. J. Ferguson
Pages 249-260
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Pharmacodynamic Endpoints in Experimental Models and In Clinical Studies in Humans
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Front Matter
Pages 261-261
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- David R. Blake, Gordon J. Taylor
Pages 263-268
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- Diane Marshall, Dorian O. Haskard
Pages 273-282
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- Zoltan Szekanecz, Alisa E. Koch
Pages 283-290
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- Daniela Salvemini, Harry Ischiropoulos, Salvatore Cuzzocrea
Pages 291-303
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- Claire A. Davies, Sophie A. Rocks, Meg C. O’ Shaughnessy, David Perrett, Paul G. Winyard
Pages 305-320
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- Nitin K. Gopaul, Erik E. Änggård
Pages 329-342
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- Robert F. Ritchie, Thomas B. Ledue
Pages 343-352
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- Jon B. Catterall, Tim E. Cawston
Pages 353-364
About this book
Inflammation has been described as the basis of many pathologies of human disease. When one considers the updated signs of inflammation, they would be vasodilation, cell migration, and, in the case of chronic inflam- tion, cell proliferation, often with an underlying autoimmune basis. Gen- ally, inflammation may be divided into acute, chronic, and autoimmune, - though the editors believe that most, if not all, chronic states are often the result of an autoimmune response to an endogenous antigen. Thus, a proper understanding of the inflammatory basis may provide clues to new therap- tic targets not only in classical inflammatory diseases, but atherosclerosis, cancer, and ischemic heart disease as well. The lack of advances in classical inflammatory diseases, such as rh- matoid arthritis, may in part arise from a failure to classify the disease into different forms. That different forms exist is exemplified in patients with d- fering responses to existing antiinflammatory drugs, ranging from nonresponders to very positive responders for a particular nonsteroidal an- inflammatory drug (NSAID). Though researchers have progressively unr- eled the mechanisms, the story is far from complete. It should also be noted that the inflammatory response is part of the innate immune response, or to use John Hunter’s words in 1795, “inflammation is a salutary response.” That may be applied in particular to the defensive response to invading micro- ganisms.