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Titlebook: Calcium in Drug Actions; Peter F. Baker (Professor Sc. D., F.R.S.) Book 1988 Springer-Verlag Berlin Heidelberg 1988 ATP.ATPase.Calcium.bon

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發(fā)表于 2025-3-21 19:41:54 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
書(shū)目名稱Calcium in Drug Actions
編輯Peter F. Baker (Professor Sc. D., F.R.S.)
視頻videohttp://file.papertrans.cn/221/220805/220805.mp4
叢書(shū)名稱Handbook of Experimental Pharmacology
圖書(shū)封面Titlebook: Calcium in Drug Actions;  Peter F. Baker (Professor Sc. D., F.R.S.) Book 1988 Springer-Verlag Berlin Heidelberg 1988 ATP.ATPase.Calcium.bon
描述The Editorial Board and the Publishers of the Handbook of Experimental Pharmacology wish to express their profound grief at the untimely death of Professor Peter Baker. Aware of his international recognition as an expert on the ubiquitous role of calcium in physiological processes and their pharma- cological control, the Board was gratified when Professor Baker accepted its invitation to edit a new Handbook volume on "Calcium in Drug Actions". He went about this task with his usual energy and effectiveness so that, in the few months before his unexpected death, Professor Baker had mustered his distinguished contributors, got them to provide their manuscripts, and seen almost the entire material into the press. This achievement is all the more remarkable when one bears in mind the extraordinary number of his other commitments during the same time; they are mentioned in Sir Alan Hodgkin‘s preface to this volume. With so many other professional and personal responsibilities upon him, the Board of the Handbook wishes to record its grateful appreciation for the admirable way in which Professor Baker took on and carried out the additional work of bringing this fine book into existence; a
出版日期Book 1988
關(guān)鍵詞ATP; ATPase; Calcium; bone; lead; metabolism; proteins; smooth muscle
版次1
doihttps://doi.org/10.1007/978-3-642-71806-9
isbn_softcover978-3-642-71808-3
isbn_ebook978-3-642-71806-9Series ISSN 0171-2004 Series E-ISSN 1865-0325
issn_series 0171-2004
copyrightSpringer-Verlag Berlin Heidelberg 1988
The information of publication is updating

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發(fā)表于 2025-3-21 20:17:18 | 只看該作者
Die ,sche Algebra. Anwendungen,rs on the topic have described a detailed examination of the energetics of calcium-ligand interactions, including both thermodynamic and kinetic considerations, and of the structures of calcium complexes (L. and W. 1982 a, b). The discussion was made in the light of a detailed knowledge of model, sm
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地板
發(fā)表于 2025-3-22 06:02:24 | 只看該作者
Marc K. Peter,Martina Dalla Vecchia membrane-bound exchange proteins and ATP-driven pump proteins are responsible for excreting the Ca. into the extracellular environment or into intracellular organelles that function as calcium stores. Taken together, these proteins produce a 10 000-fold gradient of Ca. over the plasma membrane, thu
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發(fā)表于 2025-3-22 11:17:28 | 只看該作者
Frictionless Commerce und Seamless Paymentts function, is among the most fascinating. Although our knowledge of the necessity of calcium for cardiac contraction goes back to the year 1883 in which Sydney Ringer published his famous paper, the concept of voltage-sensitive calcium entry did not start until 1953. Based on the pioneering work o
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Pascal D. K?nig,Sebastian J?ckle We have reviewed mainly the literature files in our laboratory, concentrating on papers published in 1983, 1984, and 1985. There are a number of reviews in related areas, including calmodulin (CaM) (T. et al. 1984) and its drug interaction (V. 1981; W. et al. 1985; R. et al. 1983; R. 1985), regulat
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發(fā)表于 2025-3-23 01:46:12 | 只看該作者
Neue Trends in den Sozialwissenschaftenolved by which to accomplish this task. These mechanisms typically act together to maintain Ca. homeostasis, thereby preventing buildup of cytoplasmic Ca. which would be cytotoxic. There are two plasmalemmal active transport systems which directly regulate Ca. fluxes in many types of cells. The firs
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發(fā)表于 2025-3-23 08:39:34 | 只看該作者
https://doi.org/10.1007/978-3-322-99733-3ndrial metabolism and on the adverse effects of increased Ca. load on mitochondrial function. Until quite recently, it was generally believed that the function of mitochondria in cellular Ca. metabolism was to provide a sink for Ca.. This view arose principally from the relatively low affinity of th
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