GENE EXPRESSION-ENVIRONMENT LINK IN CEREBRAL ISCHEMIA

脑缺血中基因表达与环境的联系

基本信息

  • 批准号:
    7001238
  • 负责人:
  • 金额:
    $ 27.23万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2002
  • 资助国家:
    美国
  • 起止时间:
    2002-02-01 至 2008-01-31
  • 项目状态:
    已结题

项目摘要

DESCRIPTION: (provided by applicant) Cerebral ischemia (drastic reduction in blood flow to the brain) is common condition seen in traumatic brain injury, stroke, and cardiac arrest. It has been reported that some genes are activated in cerebral ischemia and that these genes play a role in influencing the processes of both cell survival and cell death. However, it is not clear how one process can be promoted over the other. Thus, the objective of the proposed study is to determine whether environmental stimulation can modulate the gene expression seen in cerebral ischemia and promote cell survival accompanied by amelioration in the cognitive and sensory motor effects of insult. This study will examine if; 1) environmental stimulation can modulate the genes activated in cerebral ischemia and possibly promote cell survival, 2) environmental stimulation can influence the processing of genes into proteins (proteins carry the message that regulates behavior), 3) gender differences exist in gene and protein expression after cerebral ischemia, and 4) cell survival following environmental stimulation is accompanied by improvement in cognitive and sensory motor functions. Adult male and female Wistar rats will receive either ischemia or sham (control) surgery. Then animals will be assigned to either one of 4 conditions: complex environment, motor learning, exercise, and social condition (control) group 2 days after recovery from cerebral ischemia. Rats will be housed in their assigned environment for 10 days. Molecular, histological, and behavior groups will be used in the study to optimize the experimental design. After environmental stimulation, the animals in the molecular group with be euthanized and the brains will be analyzed of gene expression while animals in the histological group will be euthanized and the brains will analyzed for protein expression. Gene expression will be determined by in site hybridization while immunocytochemistry and the optical dissector method will be used to assess protein expression. Animals in the behavioral group will be tested in cognitive and sensory motor function before euthanasia. Sensory motor function will be tested using rope climbing and rotating rode tests while cognitive function will be tested using the water maze. From a nursing perspective, results from this study are important clinically because memory loss is the most frequent and enduring cognitive disability resulting from cerebral ischemia and often hinders the patient's progress during rehabilitation. Additionally, the sensory motor deficit seen following ischemic damage can affect the long-term outcome of these survivors.
描述:(由申请人提供)脑缺血(急剧减少, 流向大脑的血流)是创伤性脑损伤中常见的情况, 中风和心脏骤停据报道,一些基因被激活, 在脑缺血中,这些基因在影响 细胞存活和细胞死亡的过程。然而,目前尚不清楚如何 一个过程可以比另一个过程更好。因此,建议的目标 这项研究的目的是确定环境刺激是否可以调节基因 表达见于脑缺血并促进细胞存活, 改善侮辱的认知和感觉运动效应。本研究 将检查是否; 1)环境刺激可以调节激活的基因 在脑缺血中并可能促进细胞存活,2)环境 刺激可以影响基因转化为蛋白质的过程(蛋白质携带 调节行为的信息),3)性别差异存在于基因和 脑缺血后的蛋白表达,以及4)脑缺血后的细胞存活 环境刺激伴随着认知和 感觉运动功能成年雄性和雌性Wistar大鼠将接受 局部缺血或假(对照)手术。然后动物将被分配到任何一个 4个条件:复杂的环境,运动学习,锻炼和社会 条件组(对照组)脑缺血恢复后2天。大鼠 将被安置在指定的环境中10天。分子, 组织学和行为组将用于研究,以优化 实验设计环境刺激后, 分子组被安乐死,大脑将被分析基因 而组织学组中的动物将被安乐死, 分析大脑的蛋白质表达。基因表达将被确定 原位杂交,免疫细胞化学和光学解剖 方法将用于评估蛋白质表达。动物在行为 组将在安乐死前进行认知和感觉运动功能测试。 将使用绳索攀爬和旋转杆测试感觉运动功能 测试,而认知功能将使用水迷宫测试。从 从护理的角度来看,这项研究的结果在临床上很重要,因为 记忆丧失是最常见和最持久的认知障碍, 脑缺血,并经常阻碍病人的进展, 康复活动.此外,缺血后出现感觉运动缺陷, 损伤会影响这些幸存者的长期结果。

项目成果

期刊论文数量(8)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Dysregulation in myelination mediated by persistent neuroinflammation: possible mechanisms in chemotherapy-related cognitive impairment.
  • DOI:
    10.1016/j.bbi.2013.07.175
  • 发表时间:
    2014-01
  • 期刊:
  • 影响因子:
    15.1
  • 作者:
    Briones, Teresita L.;Woods, Julie
  • 通讯作者:
    Woods, Julie
Chemotherapy-induced cognitive impairment is associated with decreases in cell proliferation and histone modifications.
  • DOI:
    10.1186/1471-2202-12-124
  • 发表时间:
    2011-12-09
  • 期刊:
  • 影响因子:
    2.4
  • 作者:
    Briones TL;Woods J
  • 通讯作者:
    Woods J
Decrease in age-related tau hyperphosphorylation and cognitive improvement following vitamin D supplementation are associated with modulation of brain energy metabolism and redox state.
  • DOI:
    10.1016/j.neuroscience.2013.12.064
  • 发表时间:
    2014-03-14
  • 期刊:
  • 影响因子:
    3.3
  • 作者:
    Briones TL;Darwish H
  • 通讯作者:
    Darwish H
Chronic binge-like alcohol consumption in adolescence causes depression-like symptoms possibly mediated by the effects of BDNF on neurogenesis.
  • DOI:
    10.1016/j.neuroscience.2013.09.031
  • 发表时间:
    2013-12-19
  • 期刊:
  • 影响因子:
    3.3
  • 作者:
    Briones TL;Woods J
  • 通讯作者:
    Woods J
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TERESITA L BRIONES其他文献

TERESITA L BRIONES的其他文献

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{{ truncateString('TERESITA L BRIONES', 18)}}的其他基金

GENE EXPRESSION-ENVIRONMENT LINK IN CEREBRAL ISCHEMIA
脑缺血中基因表达与环境的联系
  • 批准号:
    6435535
  • 财政年份:
    2002
  • 资助金额:
    $ 27.23万
  • 项目类别:
GENE EXPRESSION-ENVIRONMENT LINK IN CEREBRAL ISCHEMIA
脑缺血中基因表达与环境的联系
  • 批准号:
    6846875
  • 财政年份:
    2002
  • 资助金额:
    $ 27.23万
  • 项目类别:
GENE EXPRESSION-ENVIRONMENT LINK IN CEREBRAL ISCHEMIA
脑缺血中基因表达与环境的联系
  • 批准号:
    6696736
  • 财政年份:
    2002
  • 资助金额:
    $ 27.23万
  • 项目类别:
GENE EXPRESSION-ENVIRONMENT LINK IN CEREBRAL ISCHEMIA
脑缺血中基因表达与环境的联系
  • 批准号:
    6621650
  • 财政年份:
    2002
  • 资助金额:
    $ 27.23万
  • 项目类别:
A THERAPEUTIC MODEL FOR CEREBRAL ISCHEMIA
脑缺血的治疗模型
  • 批准号:
    6393084
  • 财政年份:
    2000
  • 资助金额:
    $ 27.23万
  • 项目类别:
A THERAPEUTIC MODEL FOR CEREBRAL ISCHEMIA
脑缺血的治疗模型
  • 批准号:
    6639293
  • 财政年份:
    2000
  • 资助金额:
    $ 27.23万
  • 项目类别:
A THERAPEUTIC MODEL FOR CEREBRAL ISCHEMIA
脑缺血的治疗模型
  • 批准号:
    6539416
  • 财政年份:
    2000
  • 资助金额:
    $ 27.23万
  • 项目类别:
A THERAPEUTIC MODEL FOR CEREBRAL ISCHEMIA
脑缺血的治疗模型
  • 批准号:
    6186917
  • 财政年份:
    2000
  • 资助金额:
    $ 27.23万
  • 项目类别:
BETA-AMYLOID PRECURSOR PROTEIN AND BRAIN DAMAGE
β-淀粉样前体蛋白与脑损伤
  • 批准号:
    2777665
  • 财政年份:
    1999
  • 资助金额:
    $ 27.23万
  • 项目类别:
BETA-AMYLOID PRECURSOR PROTEIN AND BRAIN DAMAGE
β-淀粉样前体蛋白与脑损伤
  • 批准号:
    6078207
  • 财政年份:
    1999
  • 资助金额:
    $ 27.23万
  • 项目类别:

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记忆获取、巩固和检索所需的神经系统的行为遗传学
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