Trarable ischemic neuronal damage
可治疗的缺血性神经元损伤
基本信息
- 批准号:61570706
- 负责人:
- 金额:$ 1.28万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for General Scientific Research (C)
- 财政年份:1986
- 资助国家:日本
- 起止时间:1986 至 1987
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Brier transient forbrain ischemia in to Mongolian gearbil produces a selective neuronal damage in the hippocampus. Immeciately follwing ishemia, prentobarbvtal,diazapem, or nizotenone were given in gerbils. The neuronal density in the CA1 sector showed a significant inforease in the treated goups. when froug administration was delayed fro longer than 15 minutes, however, no definite eccets were found. The mechanism of selective vulnerability of ischemia is not fully understood. An experiment of cerbellar ischemia was done in order to compare thr pathological change with that og thr hippocampus. %cerebella purkinje cells showed ishiemic cell damage following 10 min of comression ischemia. The alteration was, however, much faster than taht in the hippocampus. The underlying mechanism seems to be different. Focal cetebral ischiemia is more frequently sdeen in clinical case. To tsudy the reversibility of neurons in focal ischema, rats were subjected to permanent unilatearal middle cerebral artery occtusion. In ischemic region, rapid prograssion in infaction was noticed and slow process as is seen in the hippocampus was not recognized. On the other hand, in the distant areas of the brain, such as the thalamus, and substntia nigra, a slow buyt proufnd morphological changes were obsearved. Transizent focal cerebral ischemia in the rat is now being studeid in order to examine the possibility of reversible neuronal change following brief focal ischemia.
短暂性脑缺血对蒙古大鼠海马区产生选择性神经元损伤。沙土鼠一般给予缺血、巴比妥钠、安定、尼唑酮等治疗。治疗组大鼠CA1区神经元密度明显减少。然而,当弗劳格给药延迟超过15分钟时,没有发现明确的瘀斑。目前对脑缺血选择性易损性的机制尚不完全清楚。进行了小脑缺血实验,并与海马区的病理改变进行了比较。压迫性缺血10min,小脑浦肯野细胞出现缺血性细胞损伤。然而,这种变化要比海马体的变化快得多。潜在的机制似乎有所不同。局灶性脑缺血多见于临床病例。为研究局灶性脑缺血神经元的可逆性,采用永久性单侧大脑中动脉闭塞模型。在缺血区,可观察到脑梗塞的快速突起,而不能识别海马区的缓慢过程。另一方面,在大脑的远端区域,如丘脑和黑质,观察到了缓慢的购买和形态变化。为了研究短暂性局灶性脑缺血后神经元可逆性改变的可能性,目前正在对大鼠短暂性局灶性脑缺血进行研究。
项目成果
期刊论文数量(10)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
藤江和貴,桐野高明,田村晃,佐野圭司: 医学のあゆみ.
Kazutaka Fujie、Takaaki Kirino、Akira Tamura、Keiji Sano:医学史。
- DOI:
- 发表时间:
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- 影响因子:0
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- 通讯作者:
桐野高明,田村晃,戸向則子,佐野圭司: 脳神経. 38. 1157-1163 (1986)
Takaaki Kirino、Akira Tamura、Noriko Tomukai、Keiji Sano:神经病学。 38. 1157-1163 (1986)
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- 影响因子:0
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Kirino T;Tamura A;Sano K.: Stroke. 17. 455-459 (1986)
Kirino T;Tamura A;Sano K.:中风。
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- 影响因子:0
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KIRINO Takaaki其他文献
KIRINO Takaaki的其他文献
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{{ truncateString('KIRINO Takaaki', 18)}}的其他基金
Genome-wide expression analysis of ischemic neuronal injury based on functional genomics and proteomics
基于功能基因组学和蛋白质组学的缺血性神经元损伤的全基因组表达分析
- 批准号:
13307042 - 财政年份:2001
- 资助金额:
$ 1.28万 - 项目类别:
Grant-in-Aid for Scientific Research (A)
Elucidation of the Mechanisms for Glutamate Release in Ischemic Neuronal Injury
阐明缺血性神经元损伤中谷氨酸释放的机制
- 批准号:
11470283 - 财政年份:1999
- 资助金额:
$ 1.28万 - 项目类别:
Grant-in-Aid for Scientific Research (B).
The role of ubiquitin in neuronal apoptosis
泛素在神经细胞凋亡中的作用
- 批准号:
09470290 - 财政年份:1997
- 资助金额:
$ 1.28万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Stress Response in Cerebral Ischemia and the Role of Ubiquitin
脑缺血的应激反应和泛素的作用
- 批准号:
07457305 - 财政年份:1995
- 资助金额:
$ 1.28万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Mechanism of Neuronal Cell Death following Cerebral Ischemia
脑缺血后神经细胞死亡的机制
- 批准号:
05404049 - 财政年份:1993
- 资助金额:
$ 1.28万 - 项目类别:
Grant-in-Aid for General Scientific Research (A)