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Titlebook: Cellular Ageing and Replicative Senescence; Suresh I.S. Rattan,Leonard Hayflick Book 2016 The Editor(s) (if applicable) and The Author(s),

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發(fā)表于 2025-3-21 19:43:17 | 只看該作者 |倒序瀏覽 |閱讀模式
書目名稱Cellular Ageing and Replicative Senescence
編輯Suresh I.S. Rattan,Leonard Hayflick
視頻videohttp://file.papertrans.cn/223/222965/222965.mp4
概述Provides a review of historical development of ideas in cellular ageing and replicative senescence.Presents a discussion of ageing and cancer in cell proliferation regulation.Explains usage of the cel
叢書名稱Healthy Ageing and Longevity
圖書封面Titlebook: Cellular Ageing and Replicative Senescence;  Suresh I.S. Rattan,Leonard Hayflick Book 2016 The Editor(s) (if applicable) and The Author(s),
描述This book covers the origins and subsequent history of research results in which attempts have been made to clarify issues related to cellular ageing, senescence, and age-related pathologies including cancer. .Cellular Ageing and Replicative Senescence. revisits more than fifty-five years of research based on the discovery that cultured normal cells are mortal and the interpretation that this phenomenon is associated with the origins of ageing. The mortality of normal cells and the immortality of cancer cells were also reported to have?.in vivo. counterparts. Thus began the field of cytogerontology..Cellular Ageing and Replicative Senescence. is organized into five sections: history and origins; serial passaging and progressive ageing; cell cycle arrest and senescence; system modulation; and recapitulation and future expectations. These issues are discussed by leading thinkers and researchers in biogerontology and cytogerontology. This collection of articles provides state-of-the-art information, and will encourage students, teachers, health care professionals and others interested in the biology of ageing to explore?the fascinating and challenging question of why and how our cells
出版日期Book 2016
關(guān)鍵詞Ageing; Cancer; Cell cycle regulation; Longevity; Stress; cytogenetics
版次1
doihttps://doi.org/10.1007/978-3-319-26239-0
isbn_softcover978-3-319-79912-4
isbn_ebook978-3-319-26239-0Series ISSN 2199-9007 Series E-ISSN 2199-9015
issn_series 2199-9007
copyrightThe Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerl
The information of publication is updating

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發(fā)表于 2025-3-21 23:36:48 | 只看該作者
Influence of Donor Age and Species Longevity on Replicative Cellular Senescence when strains are obtained from different individuals. This variability is probably due to both technical issues and heterogeneity inside the tissues. Notwithstanding these limitations, many scientists searched for an inverse relationship of proliferative potential and donor age. Reviewing this lite
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發(fā)表于 2025-3-22 01:02:48 | 只看該作者
Ageing of the Stem Cells: The Conjoined Twosome Growing Old: Stem Cell and Its Nicheed, the stem cell and the niche are subject to aging. Potent mechanisms of biological aging are control of cellular metabolism, the action of aging genes, epigenetic drift and inflammation, which also modulate the cellular age of stem cells. A common feature of aged stem cells is however hyperactiva
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發(fā)表于 2025-3-22 12:56:10 | 只看該作者
Modeling Cellular Aging: An Introduction – Mathematical and Computational Approachesing. We find that there are a large array of methods from discrete to continuous and from deterministic to stochastic. This chapter is not meant to be a comprehensive coverage of all of the modeling efforts but rather a buffet introduction to what has been done in the field over the last 50–60?years
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發(fā)表于 2025-3-22 18:08:30 | 只看該作者
Cell Cycle Checkpoints and Senescenceageing studies. In a sharp contrast to cancer cells, it is firmly regulated by cell cycle checkpoints that ensure evasion of stressed and genetically modified cells, limiting their expansion and serve as an innate check to carcinogenesis. Tumour suppressors and their regulatory proteins play key rol
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發(fā)表于 2025-3-22 22:50:18 | 只看該作者
Mitochondrial Reactive Oxygen Species in Cellular SenescenceMitochondrial dysfunction is the principle cause of increased levels of reactive oxygen species (ROS) and oxidative stress, which is a key mediator of aging. The cell responds to this stressful stimulus by the induction of the cellular aging-stress response, cellular senescence. Here, we discuss the
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發(fā)表于 2025-3-23 03:19:49 | 只看該作者
Cellular Aging and Tumor Regulationcell, senescence can be one driving force of such diseases. In contrast, cancer is, on the one hand, associated with age as well, but can be seen as a gain of function disease. Cellular senescence can act to prevent cell proliferation and is believed to inhibit cancer growth. Interestingly, this tum
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發(fā)表于 2025-3-23 06:11:05 | 只看該作者
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