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Titlebook: Delayed Preconditioning and Adaptive Cardioprotection; G. F. Baxter,D. M. Yellon Book 1998 Springer Science+Business Media Dordrecht 1998

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書(shū)目名稱Delayed Preconditioning and Adaptive Cardioprotection
編輯G. F. Baxter,D. M. Yellon
視頻videohttp://file.papertrans.cn/265/264941/264941.mp4
叢書(shū)名稱Developments in Cardiovascular Medicine
圖書(shū)封面Titlebook: Delayed Preconditioning and Adaptive Cardioprotection;  G. F. Baxter,D. M. Yellon Book 1998 Springer Science+Business Media Dordrecht 1998
描述Interest in the ability of myocardium to adapt to ischaemicstress has continued to grow since the discovery of ischaemicpreconditioning in 1986. In 1993, two reports heralded the recognitionof a delayed preconditioning response in the heart, now commonly knownas the `second window‘ of protection. Since then, a number of studieshave described the ability of delayed preconditioning and relatedadaptive phenomena to protect against a variety of pathologies in theischaemic and reperfused myocardium. Our understanding of the cellularmechanisms of sub-acute adaptive cardioprotection has advancedconsiderably during this period. This compilation of state-of-the-artreviews by those who have made significant contributions to this fieldprovides detailed and critical analysis of this research, frommolecular basis to potential clinical relevance. The book aims toprovide an authoritative, comprehensive and thoroughly up-to-dateoverview for scientists and clinicians engaged in, or observing, thisrapidly-developing area of heart research. It will also be of interestto those engaged in research on other tissues whereischaemia-reperfusion pathology is of major concern.
出版日期Book 1998
關(guān)鍵詞adaptation; arrhythmia; endothelium; heart; tissue
版次1
doihttps://doi.org/10.1007/978-94-011-5312-6
isbn_softcover978-94-010-6231-2
isbn_ebook978-94-011-5312-6Series ISSN 0166-9842
issn_series 0166-9842
copyrightSpringer Science+Business Media Dordrecht 1998
The information of publication is updating

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Developments in Cardiovascular Medicinehttp://image.papertrans.cn/d/image/264941.jpg
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?Buffer Stocks? und Aggregationsproblematikial ischemic insult and lasts 2–3 hours, and a late (or delayed) phase, which becomes apparent 12–24 hours later and lasts for 3–4 days (reviewed in references 1 and 2). These two phases have different pathophysiology and probably different mechanisms. Since the late phase lasts much longer, it may
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https://doi.org/10.1007/978-3-663-13540-1t is the basis of adaptive modification. Adaptation involves a number of cellular and biochemical alterations including (i) changes in metabolic homeostasis and (ii) reprogramming of gene expression. Changes in metabolic pathways are generally short-lived and reversible; the consequences of reprogra
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Gesch?ftsführung und Vertretungr promoting cell injury and death. Identifying these proteins is an important first step towards understanding the molecular mechanisms underlying the stress response. As new or elevated protein synthesis can result from increased gene expression, studies of gene transcription provide a key to ident
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