PERINATAL HYPOXIC ISCHEMIC BRAIN DAMAGE

围产期缺氧缺血性脑损伤

基本信息

批准号：
6636875
负责人：
CHARLES PALMER
金额：
$ 154.76万
依托单位：
PENNSYLVANIA STATE UNIV HERSHEY MED CTR
依托单位国家：
美国
项目类别：
财政年份：
1994
资助国家：
美国
起止时间：
1994-09-06 至 2004-12-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/6636875
关键词：
brain injury brain metabolism cerebral ischemia /hypoxia perinatal

项目摘要

The overall objective of the present Program Project proposal is to improve our understanding of the pathophysiologic mechanisms leading to hypoxic-ischemic brain damage in the human fetus and newborn infant and to develop effective strategies to prevent or minimize permanent brain damage which ultimately leads to mental retardation or developmental disability. Our specific aims include: 1) to elucidate underlying cellular and molecular mechanisms responsible for the occurrence of hypoxic-ischemic brain damage in perinatal animals; 2) to investigate mechanisms of hypoxic-ischemic neuroprotection through preconditioning and metabolic and pharmacologic manipulations; 3) to ascertain the contribution of oxidative stress and inflammatory mediators to the production of perinatal hypoxic-ischemic brain damage; 4) to study the effects of perinatal hypoxic-ischemic brain damage on short- and long-term cerebral development; and 5) to investigate the role of status epilepticus in perinatal hypoxic-ischemic brain damage. Included in the Program Project Proposals are 7 basic research projects and 3 Core projects, the latter to include an Administrative and Biostatistics Core, Neuropathology Core, and MR spectroscopy and imaging Core. The individual research project titles are: 1) Oxidative Metabolism; 2) Energy Metabolism; 3) Neuroprotective Mechanisms; 4) Inflammatory Mediators; 5) Oxidative Stress/Glia; 6 Cellular Differentiation; and 7) Status Epilepticus. Scientific disciplines represented in the Program Project include pediatric neurology, perinatology, neuroscience, neuropathology, neuroradiology, computer science and biostatistics. It is anticipated that the findings derived from the described research endeavors will have direct relevance to preventative and therapeutic interventions necessary to reduce substantially the significance and severity of mental retardation and developmental disability in developing human infants and children.

本计划项目建议的总体目标是提高我们对人类胎儿和新生婴儿缺氧缺血性脑损伤的病理生理机制的理解，并制定有效的策略，以预防或最大程度地减少永久性脑损伤，最终导致精神障碍或发育残疾。我们的具体目的包括：1）阐明导致围产期动物缺氧 - 缺血性脑损伤的潜在细胞和分子机制； 2）通过预处理和代谢和药理操作研究低氧缺血神经保护的机制； 3）确定氧化应激和炎症介质对产生围产期缺氧 - 缺血性脑损伤的贡献； 4）研究围产期缺氧缺血性脑损伤对短期和长期脑发育的影响； 5）研究状态癫痫症在围产期低氧缺氧脑损伤中的作用。计划项目建议中包括7个基础研究项目和3个核心项目，后者包括行政和生物统计学核心，神经病理学核心以及MR Spectroscopicy and Imaging Core。个别研究项目的标题是：1）氧化代谢； 2）能量代谢； 3）神经保护机制； 4）炎症介体； 5）氧化应激/神经胶质； 6个细胞分化； 7）癫痫持续状态。该计划项目中代表的科学学科包括儿科神经病学，神经科学，神经病理学，神经放射学，计算机科学和生物统计学。可以预料，从所描述的研究努力中得出的发现将与预防和治疗性干预措施直接相关，以减少对发展的人类和儿童的智力低下和发育障碍的重要性和严重性。

项目成果

期刊论文数量（48）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Pre-conditioning induces the precocious differentiation of neonatal astrocytes to enhance their neuroprotective properties.

DOI：
10.1042/an20100029
发表时间：
2011-07-26
期刊：
ASN neuro
影响因子：
4.7
作者：
Sen E;Basu A;Willing LB;Uliasz TF;Myrkalo JL;Vannucci SJ;Hewett SJ;Levison SW
通讯作者：
Levison SW

Temporal changes in mRNA expression of the brain nutrient transporters in the lithium-pilocarpine model of epilepsy in the immature and adult rat.

DOI：
10.1016/j.nbd.2011.05.007
发表时间：
2011-09
期刊：
NEUROBIOLOGY OF DISEASE
影响因子：
6.1
作者：
Leroy, Claire;Pierre, Karin;Simpson, Ian A.;Pellerin, Luc;Vannucci, Susan J.;Nehlig, Astrid
通讯作者：
Nehlig, Astrid

Experimental models of hypothermic circulatory arrest.

低温停循环的实验模型。