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Titlebook: Mechanosensing Biology; Masaki Noda (Professor, Director) Book 2011 Springer 2011

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樓主
發(fā)表于 2025-3-21 18:17:34 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
書目名稱Mechanosensing Biology
編輯Masaki Noda (Professor, Director)
視頻videohttp://file.papertrans.cn/629/628802/628802.mp4
概述Most up-to-date information in the field of mechanobiology.Cutting-edge advancements in research into locomotor and circulatory diseases.Includes an exploration of mechanosensor nanoscience, gravity a
圖書封面Titlebook: Mechanosensing Biology;  Masaki Noda (Professor, Director) Book 2011 Springer 2011
描述.Mechanical stress is vital to the functioning of the body, especially for tissues such as bone, muscle, heart, and vessels. It is well known that astronauts and bedridden patients suffer muscle and bone loss from lack of use. Even the heart, in pumping blood, causes mechanical stress to itself and to vascular tissue. With the loss of mechanical stress, homeostasis becomes impaired and leads to pathological conditions such as osteopenia, muscle atrophy, and vascular tissue dysfunction. In elderly populations, such mechanical pathophysiology, as well as the mechanical activities of locomotor and cardiovascular systems, is important because skeletal and heart functions decline and cause diseases in other organs. In this monograph, mechanical stress is discussed by experts in the field with respect to molecular, cellular, and tissue aspects in relation to medicine. Covering topics such as gravity and tissues and disuse osteoporosis, the book provides the most up-to-date information on cutting-edge advancements in the field of mechanobiology and is a timely contribution to research into locomotor and circulatory diseases that are major problems in contemporary society. .
出版日期Book 2011
版次1
doihttps://doi.org/10.1007/978-4-431-89757-6
isbn_softcover978-4-431-54646-7
isbn_ebook978-4-431-89757-6
copyrightSpringer 2011
The information of publication is updating

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沙發(fā)
發(fā)表于 2025-3-21 21:05:25 | 只看該作者
板凳
發(fā)表于 2025-3-22 02:04:14 | 只看該作者
Mechanical Stress and Bone concave side and decreases it on the convex side. Under such circumstances, bone is accumulated on the concave side and is reduced on the convex side. This can be seen after angular deformity due to malunion of fractures in children where minor angular deformity could be corrected during the growth of the children.
地板
發(fā)表于 2025-3-22 05:26:49 | 只看該作者
5#
發(fā)表于 2025-3-22 10:28:30 | 只看該作者
Osteoblast Biology and Mechanosensingrole in controlling osteoblast fate, number and function in response to loading. The identification of the physiological mechanisms that mediate the anabolic effects of mechanical forces on osteoblastogenesis may contribute to the development of therapeutic strategies for the defective bone formation in disuse osteoporosis.
6#
發(fā)表于 2025-3-22 16:52:26 | 只看該作者
Osteocyte Mechanosensation and Transduction surrounding the osteocyte changes with disease and with age, these changes may influence how this cell senses and responds to mechanical loading. Key observations and concepts surrounding mechanosensation and transduction in this cell type are highlighted and emphasize the need for more information regarding osteocyte function.
7#
發(fā)表于 2025-3-22 18:17:21 | 只看該作者
Book 2011ronauts and bedridden patients suffer muscle and bone loss from lack of use. Even the heart, in pumping blood, causes mechanical stress to itself and to vascular tissue. With the loss of mechanical stress, homeostasis becomes impaired and leads to pathological conditions such as osteopenia, muscle a
8#
發(fā)表于 2025-3-23 00:11:20 | 只看該作者
9#
發(fā)表于 2025-3-23 04:48:09 | 只看該作者
Mechanobiology in Skeletal Muscle: Conversion of Mechanical Information into Molecular Signalrelated genes follows (Carson 1997). Satellite cell activation is generally thought to be a critical component for increase in muscle mass; however, it is still a debated issue whether satellite cell incorporation into hypertrophying muscle fibers is required for muscle hypertrophy (O’Connor and Pavlath 2007; McCarthy and Esser 2007).
10#
發(fā)表于 2025-3-23 08:28:42 | 只看該作者
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