標(biāo)題: Titlebook: Cell-Cycle Mechanisms and Neuronal Cell Death; Agata Copani,Ferdinando Nicoletti Book 2005 Springer-Verlag US 2005 Activation.Alzheimer.Ma [打印本頁(yè)] 作者: VIRAL 時(shí)間: 2025-3-21 18:47
書目名稱Cell-Cycle Mechanisms and Neuronal Cell Death影響因子(影響力)
書目名稱Cell-Cycle Mechanisms and Neuronal Cell Death影響因子(影響力)學(xué)科排名
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書目名稱Cell-Cycle Mechanisms and Neuronal Cell Death被引頻次
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書目名稱Cell-Cycle Mechanisms and Neuronal Cell Death讀者反饋
書目名稱Cell-Cycle Mechanisms and Neuronal Cell Death讀者反饋學(xué)科排名
作者: Anguish 時(shí)間: 2025-3-21 22:40 作者: Fermentation 時(shí)間: 2025-3-22 00:41 作者: onlooker 時(shí)間: 2025-3-22 05:45 作者: kidney 時(shí)間: 2025-3-22 08:55 作者: 牲畜欄 時(shí)間: 2025-3-22 16:17
Alzheimer Disease, of division, remain nonproliferative, and are terminally differentiated. Here, we review the provocative notion that, in Alzheimer disease, whole populations of nonstem cell neurons leave their quiescent state and re-enter into the cell cycle. However, such neuronal re-entry into the cell cycle is 作者: 牲畜欄 時(shí)間: 2025-3-22 20:20
Offending Women in Contemporary Chinaeir relationship to other cells to reorganize their connectivity according to the requirements for information processing within a cellular network. This puts neurons on the permanent risk to erroneously convert signals derived from plastic synaptic changes into positional cues that will activate th作者: 慌張 時(shí)間: 2025-3-23 00:07
Offending Women in Contemporary Chinaated as modifiers or risk factors for the disease. Although 100 years have elapsed since AD was first recognized as a separate disease entity, the last two decades have produced some of the most significant breakthroughs in our understanding of the disease. Despite this progress, the precise mechani作者: TEN 時(shí)間: 2025-3-23 05:13
https://doi.org/10.1057/9781137447180ia, and eventually die of Alzheimer’s disease. Because the gene for amyloid precursor protein (APP) resides on chromosome 21, its consequent overexpression in trisomy 21 cells presumably contributes to the development of Alzheimer’s disease in Down syndrome individuals..The connection between Down s作者: 無(wú)辜 時(shí)間: 2025-3-23 07:07 作者: cylinder 時(shí)間: 2025-3-23 13:38 作者: Adrenaline 時(shí)間: 2025-3-23 14:06
,Cell Cycle and Chromosome Segregation Defects in Alzheimer’s Disease,ia, and eventually die of Alzheimer’s disease. Because the gene for amyloid precursor protein (APP) resides on chromosome 21, its consequent overexpression in trisomy 21 cells presumably contributes to the development of Alzheimer’s disease in Down syndrome individuals..The connection between Down s作者: Curmudgeon 時(shí)間: 2025-3-23 21:35 作者: Irritate 時(shí)間: 2025-3-24 01:17 作者: PLE 時(shí)間: 2025-3-24 04:31
Cell-Cycle Mechanisms and Neuronal Cell Death978-0-387-29390-5Series ISSN 1431-0406 作者: fertilizer 時(shí)間: 2025-3-24 07:53
Offending Women in Contemporary Chinaation and survival in local neighbourhoods. Instructions from neighbouring cells can induce cell proliferation, differentiation or death. These stimuli include cell-cell and cell-ECM adhesion, growth factors, cytokines, neuropeptides and mechanical factors. Signals from G-protein-coupled receptors, 作者: menopause 時(shí)間: 2025-3-24 14:05 作者: 改變 時(shí)間: 2025-3-24 16:14 作者: SLAY 時(shí)間: 2025-3-24 19:34
https://doi.org/10.1057/9781137447180tions of the discovery had a more profound effect on biological research than anticipated at the time. We can now clearly distinguish between the activation of the cell division cycle and cell division itself. We also have closer understanding of the differences between senescence, quiescence and te作者: pester 時(shí)間: 2025-3-24 23:39 作者: 高原 時(shí)間: 2025-3-25 05:01 作者: 仇恨 時(shí)間: 2025-3-25 07:48 作者: Yourself 時(shí)間: 2025-3-25 12:47 作者: Bernstein-test 時(shí)間: 2025-3-25 18:17 作者: 安裝 時(shí)間: 2025-3-25 20:36 作者: 爭(zhēng)論 時(shí)間: 2025-3-26 00:55 作者: Factorable 時(shí)間: 2025-3-26 06:23
1431-0406 . This book serves to gain new insights into the molecular determinants of neuronal death and to establish new targets for therapeutic intervention. .978-1-4899-9835-4978-0-387-29390-5Series ISSN 1431-0406 作者: harpsichord 時(shí)間: 2025-3-26 09:20
Book 2005. Leading Authors discuss this topic in relation to the major neurological disorders, including Alzheimer’s disease, stroke and epilepsy. This book serves to gain new insights into the molecular determinants of neuronal death and to establish new targets for therapeutic intervention. .作者: oracle 時(shí)間: 2025-3-26 15:26
Offending Women in Contemporary China neurons are dying, any effort to create new nerve cells should be welcome. But these good intentions on the part of the mature neurons have unintended consequences, and in the final analysis end up paving a very famous road that leads only to a worsening of the brains condition.作者: Myelin 時(shí)間: 2025-3-26 19:27
Paved with Good Intentions, neurons are dying, any effort to create new nerve cells should be welcome. But these good intentions on the part of the mature neurons have unintended consequences, and in the final analysis end up paving a very famous road that leads only to a worsening of the brains condition.作者: 萬(wàn)花筒 時(shí)間: 2025-3-26 22:53 作者: Bricklayer 時(shí)間: 2025-3-27 03:22
1431-0406 ary material: .Cell-Cycle Mechanisms and Neuronal Cell Death examines the role of cell cycle activation in the molecular mechanisms leading to neuronal degeneration. Leading Authors discuss this topic in relation to the major neurological disorders, including Alzheimer’s disease, stroke and epilepsy作者: Canyon 時(shí)間: 2025-3-27 06:43
https://doi.org/10.1057/9781137452726ulations of nonstem cell neurons leave their quiescent state and re-enter into the cell cycle. However, such neuronal re-entry into the cell cycle is futile and ultimately leads to the neurodegeneration that typifies Alzheimer disease.作者: Emg827 時(shí)間: 2025-3-27 10:41
Alzheimer Disease,ulations of nonstem cell neurons leave their quiescent state and re-enter into the cell cycle. However, such neuronal re-entry into the cell cycle is futile and ultimately leads to the neurodegeneration that typifies Alzheimer disease.作者: 摻假 時(shí)間: 2025-3-27 16:53
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