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Titlebook: Inflammation Protocols; Paul G. Winyard,Derek A. Willoughby Book 2003 Humana Press 2003

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發(fā)表于 2025-3-21 19:47:09 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
書目名稱Inflammation Protocols
編輯Paul G. Winyard,Derek A. Willoughby
視頻videohttp://file.papertrans.cn/465/464669/464669.mp4
概述Includes supplementary material:
叢書名稱Methods in Molecular Biology
圖書封面Titlebook: Inflammation Protocols;  Paul G. Winyard,Derek A. Willoughby Book 2003 Humana Press 2003
描述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 compl
出版日期Book 2003
版次1
doihttps://doi.org/10.1385/1592593747
isbn_softcover978-1-61737-282-7
isbn_ebook978-1-59259-374-3Series ISSN 1064-3745 Series E-ISSN 1940-6029
issn_series 1064-3745
copyrightHumana Press 2003
The information of publication is updating

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1064-3745 pdated 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 no
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Inflammatory Joint Diseaseand hormonal influences (.–.). Moreover, the mechanisms responsible for the development of SCW-arthritis are susceptible to regulation by pharmacologic agents and biological response modifiers and as such, this model is considered a valid preclinical model of RA.
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Key Stages in the Acute Inflammatory Response and Their Relevance as Therapeutic Targetsy response. For the reader who is unfamiliar with the field of inflammation, it is perhaps helpful to summarize and contextualize some of the key events of the inflammatory response, as it is these that may be reproduced in the form of in vitro model systems by using the protocols that follow.
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Screening for Inhibitors of Transcription Factors Using Luciferase Reporter Gene Expression in Trans of TF function offers an innovative approach to disease therapies. TF modulation holds particular promise in diseases where several proteins contribute simultaneously to the pathology, such as in autoimmune disease, where a plethora of cytokines, destructive enzymes, and cell-adhesion molecules combine to enhance disease progression.
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Book 2003 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
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