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Pathophysiological and behavioral deficits in developing mice following rotational acceleration-deceleration traumatic brain injury 期刊论文

编号：

8085db6a-f2d4-4b36-bfde-fa55395c7ab9
作者：

Wang, Guoxiang#^[1,2]Zhang, Yi Ping^[3];Gao, Zhongwen(高忠文)^[2,4]Shields, Lisa B. E.^[3];Li, Fang^[2,5];Chu, Tianci^[2];Lv, Huayi(吕华毅)^[6]Moriarty, Thomas^[3];Xu, XiaoMing^[7]Yang, Xiaoyu(杨小玉)*^[1]Shields, Christopher B.*^[3,8]Cai, Jun*^[1,2,9]
语种：

英文
期刊：

DISEASE MODELS & MECHANISMS ISSN：1754-8403 2018 年 11 卷 1 期 ; JAN
收录：
摘要：

Abusive head trauma (AHT) is the leading cause of death from trauma in infants and young children. An AHT animal model was developed on 12-day-old mice subjected to 90 degrees head extension-flexion sagittal shaking repeated 30, 60, 80 and 100 times. The mortality and time until return of consciousness were dependent on the number of repeats and severity of the injury. Following 60 episodes of repeated head shakings, the pups demonstrated apnea and/or bradycardia immediately after injury. Acute oxygen desaturation was observed by pulse oximetry during respiratory and cardiac suppression. The cerebral blood perfusion was assessed by laser speckle contrast analysis (LASCA) using a PeriCam PSI system. There was a severe reduction in cerebral blood perfusion immediately after the trauma that did not significantly improve within 24 h. The injured mice began to experience reversible sensorimotor function at 9 days postinjury (dpi), which had completely recovered at 28 dpi. However, cognitive deficits and anxiety-like behavior remained. Subdural/subarachnoid hemorrhage, damage to the brain-blood barrier and parenchymal edema were found in all pups subjected to 60 insults. Proinflammatory response and reactive gliosis were upregulated at 3 dpi. Degenerated neurons were found in the cerebral cortex and olfactory tubercles at 30 dpi. This mouse model of repetitive brain injury by rotational head acceleration-deceleration partially mimics the major pathophysiological and behavioral events that occur in children with AHT. The resultant hypoxia/ischemia suggests a potential mechanism underlying the secondary rotational acceleration-deceleration-induced brain injury in developing mice.
推荐引用方式
GB/T 7714：

Wang Guoxiang,Zhang Yi Ping,Gao Zhongwen, et al. Pathophysiological and behavioral deficits in developing mice following rotational acceleration-deceleration traumatic brain injury [J].DISEASE MODELS & MECHANISMS,2018,11(1).
APA：

Wang Guoxiang,Zhang Yi Ping,Gao Zhongwen,Shields Lisa B. E.,&Cai Jun.(2018).Pathophysiological and behavioral deficits in developing mice following rotational acceleration-deceleration traumatic brain injury .DISEASE MODELS & MECHANISMS,11(1).
MLA：

Wang Guoxiang, et al. "Pathophysiological and behavioral deficits in developing mice following rotational acceleration-deceleration traumatic brain injury" .DISEASE MODELS & MECHANISMS 11,1(2018).
入库时间：

12/4/2019 7:16:23 PM
更新时间：

12/4/2019 7:16:23 PM
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