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Titlebook: Cell Signaling in Vascular Inflammation; Jahar Bhattacharya (Professor of Physiology and Ce Book 2005 Humana Press 2005 biology.calcium.ci

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發(fā)表于 2025-3-21 16:27:58 | 只看該作者 |倒序瀏覽 |閱讀模式
書目名稱Cell Signaling in Vascular Inflammation
編輯Jahar Bhattacharya (Professor of Physiology and Ce
視頻videohttp://file.papertrans.cn/223/222876/222876.mp4
概述Includes supplementary material:
圖書封面Titlebook: Cell Signaling in Vascular Inflammation;  Jahar Bhattacharya (Professor of Physiology and Ce Book 2005 Humana Press 2005 biology.calcium.ci
描述A comprehensive survey by leading basic and clinical researchers of the signal transduction mechanisms responsible for lung inflammation, including vascular hyperpermeability, white cell accumulation, and vascular remodeling. The authors cut across disciplines to bring together a broad-based presentation of inflammatory challenge, both in the initial phases of the inflammatory response, as well as in the more prolonged phase of genomic involvement. The book illuminates not only the processes of lung inflammation, but also the potential for developing new therapeutic strategies to combat inflammatory lung disease.
出版日期Book 2005
關鍵詞biology; calcium; circulation; clinical research; cytokine; inflammation; methylation; necrosis; nitric oxid
版次1
doihttps://doi.org/10.1007/978-1-59259-909-7
isbn_softcover978-1-61737-619-1
isbn_ebook978-1-59259-909-7
copyrightHumana Press 2005
The information of publication is updating

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Y. Shiozaki,E. Nakamura,T. Mitsuiare expressed to initiate the cell-growth response. Similar cellular responses by these vasoactive substances may be important in the production and release of cytokines, such as interleukin-6, which participate in vascular inflammation. The inflammatory responses of vasoactive substances are in need of further study.
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Y. Shiozaki,E. Nakamura,T. Mitsui) channel may function as a “flow sensor” with the ability to initiate signaling subsequent to flow cessation. This response to altered shear stress may represent a physiological attempt to promote both vasodilation and the generation of new capillaries as mechanisms to restore blood perfusion.
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,Tumor Necrosis Factor-α/Receptor Signaling Through the Akt Kinase,ons with cytoplasmic proteins that also contain death domains. Thus, a signal transduction cascade is initiated that coincidentally activates caspases that promote cell death and, additionally, anti-apoptotic events. The balance between these arms of the TNFR1 signaling cascade determines whether cells live or die.
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Y. Shiozaki,E. Nakamura,T. Mitsuiaerobic conditions by releasing cytochrome c, which results in the activation of caspases. Thus, mitochondria serve to integrate changes in environmental conditions such as changes in oxygen levels to the activation of diverse events, such as gene transcription and programmed cell death
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