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Titlebook: Experimental Models of Multiple Sclerosis; Ehud Lavi,Cris S. Constantinescu Book 2005 Springer-Verlag US 2005 Antigen.Chemokine.Nervous Sy

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發(fā)表于 2025-3-21 18:52:45 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
書目名稱Experimental Models of Multiple Sclerosis
編輯Ehud Lavi,Cris S. Constantinescu
視頻videohttp://file.papertrans.cn/319/318883/318883.mp4
概述This is the only title on experimental models of multiple sclerosis
圖書封面Titlebook: Experimental Models of Multiple Sclerosis;  Ehud Lavi,Cris S. Constantinescu Book 2005 Springer-Verlag US 2005 Antigen.Chemokine.Nervous Sy
描述.Multiple Sclerosis (MS) is an enigmatic immune mediated disease of the central nervous system that affects about 350,000 individuals in the US, and many more around the world. The mechanism of this disease is largely unknown and there is no cure for it. However, there are several well-characterized experimental animal models that help us understand and speculate about potential mechanisms of pathology in this disease. Many of the experimental therapies designed for this disease rely on testing the drugs in animal models before using it in clinical trials. This book combines for the first time the different experimental models for MS (including immune-mediated and viral) under one roof, and highlights aspects that are different or shared among these experimental models. It’s aim is to improve our understanding of this devastating disease and help us think about potential additional therapies for it..
出版日期Book 2005
關(guān)鍵詞Antigen; Chemokine; Nervous System; autoimmune disease; interferon; neurons
版次1
doihttps://doi.org/10.1007/b135502
isbn_ebook978-0-387-25518-7
copyrightSpringer-Verlag US 2005
The information of publication is updating

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The Role of Complement in EAE seen in multiple sclerosis. Deposition of complement proteins correlates with areas of demyelination and axonal loss observed in EAE and complement inhibition ameliorates disease. However, the precise mechanisms underlying complement-mediated damage are still largely unknown. The recent use of tran
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Topics in Algebraic Coding Theorycomplex allotypes, which in EAE is in response to induction with certain myelin antigens. Both are complex polygenic diseases where disease traits are controlled by a number of polymorphic genes which individually exhibiting modest effect on disease course. A number of as yet largely unknown genes,
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https://doi.org/10.1007/978-3-642-49903-6 in combination with different types of adjuvant. The second approach of inducing EAE consists in adoptive transfer of activated T cells that are specific for myelin-associated autoantigens of the central nervous system (CNS). This chapter presents an overview of some useful strategies and protocols
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