目的探讨经颅直流电刺激(tDCS)联合感知水平唤醒对颅脑损伤意识障碍(DOC)患者预后的影响。方法选取河南科技大学第一附属医院2018年9月至2020年9月期间收治的113例颅脑损伤DOC患者作为研究对象,按随机数字表法分为对照组和观察组,对照...目的探讨经颅直流电刺激(tDCS)联合感知水平唤醒对颅脑损伤意识障碍(DOC)患者预后的影响。方法选取河南科技大学第一附属医院2018年9月至2020年9月期间收治的113例颅脑损伤DOC患者作为研究对象,按随机数字表法分为对照组和观察组,对照组56例给予感知水平唤醒干预,观察组57例给予感知水平唤醒干预联合tDCS,对比两组患者的意识水平、神经功能和诱发动作电位潜伏期。结果观察组干预后的JFK昏迷恢复量表(The JFK Coma Recovery Scale-Revise,CRS-R)各项得分均高于对照组(P<0.05),观察组干预后的格拉斯哥昏迷量表(GCS)得分、脑电图(EEG)得分均高于对照组,功能障碍评分(DFS)得分低于对照组(P<0.05),双耳潜伏期(PL)的Ⅰ波、Ⅲ波、Ⅴ波均低于对照组(P<0.05)。结论基于感知水平的听觉诱导唤醒干预可通过缩短颅脑损伤DOC患者的动作电位潜伏期进而改善神经功能,有助于患者觉醒。展开更多
Background Urotensin Ⅱ （Ull）,a potent vasoconstrictive peptide,is able to stimulate phenotypic differentiation of adventitial fibroblasts.This study aimed to determine the effect of UII on monocyte chemoattractant ...Background Urotensin Ⅱ （Ull）,a potent vasoconstrictive peptide,is able to stimulate phenotypic differentiation of adventitial fibroblasts.This study aimed to determine the effect of UII on monocyte chemoattractant protein-1 （MCP1） expression in rat aortic adventitial fibroblasts,so as to explore possible mechanisms in the development of vascular inflammation.Methods Growth-arrested adventitial fibroblasts were incubated in serum-free medium with UII （1010-10-7 mol/L） and inhibitors of signal transduction pathways for 1 to 24 hours.MCP-1 mRNA and protein expression and secretion were determined by RT-PCR,Western blotting analysis and enzyme-linked immunosorbent assay （ELISA）,respectively.Results UII dose-and time-dependently promoted MCP-1 mRNA and protein expression and secretion in cells,with maximal effect at 10-8 mol/L at 3 hours for mRNA expression,24 hours for protein expression in the cells,and 12 hours for protein secretion from the cells.Furthermore,the UII effects were significantly inhibited by treatment with its receptor antagonist SB710411,Rho kinase inhibitor Y27632,protein kinase C （PKC） inhibitor H7,mitogen-activated protein kinase inhibitor PD98059,calcineurin inhibitor cyclosporine A,and the Ca2＋channel blocker nicardipine.Conclusion UII may stimulate MCP-1 expression in rat aortic adventitial fibroblasts through its receptor and Rho kinase,PKC,mitogen-activated protein kinase,calcineurin and Ca2＋ channel signal transduction,thus contributing to adventitial inflammation.展开更多
文摘目的探讨经颅直流电刺激(tDCS)联合感知水平唤醒对颅脑损伤意识障碍(DOC)患者预后的影响。方法选取河南科技大学第一附属医院2018年9月至2020年9月期间收治的113例颅脑损伤DOC患者作为研究对象,按随机数字表法分为对照组和观察组,对照组56例给予感知水平唤醒干预,观察组57例给予感知水平唤醒干预联合tDCS,对比两组患者的意识水平、神经功能和诱发动作电位潜伏期。结果观察组干预后的JFK昏迷恢复量表(The JFK Coma Recovery Scale-Revise,CRS-R)各项得分均高于对照组(P<0.05),观察组干预后的格拉斯哥昏迷量表(GCS)得分、脑电图(EEG)得分均高于对照组,功能障碍评分(DFS)得分低于对照组(P<0.05),双耳潜伏期(PL)的Ⅰ波、Ⅲ波、Ⅴ波均低于对照组(P<0.05)。结论基于感知水平的听觉诱导唤醒干预可通过缩短颅脑损伤DOC患者的动作电位潜伏期进而改善神经功能,有助于患者觉醒。
基金This project was supported by grants from National Natural Science Foundation of China （No. 30971273 and No. 81270223） and Natural Science Foundation of Guangdong Province of China （No. 9151051501000016 and No. S2011010000450）.
文摘Background Urotensin Ⅱ （Ull）,a potent vasoconstrictive peptide,is able to stimulate phenotypic differentiation of adventitial fibroblasts.This study aimed to determine the effect of UII on monocyte chemoattractant protein-1 （MCP1） expression in rat aortic adventitial fibroblasts,so as to explore possible mechanisms in the development of vascular inflammation.Methods Growth-arrested adventitial fibroblasts were incubated in serum-free medium with UII （1010-10-7 mol/L） and inhibitors of signal transduction pathways for 1 to 24 hours.MCP-1 mRNA and protein expression and secretion were determined by RT-PCR,Western blotting analysis and enzyme-linked immunosorbent assay （ELISA）,respectively.Results UII dose-and time-dependently promoted MCP-1 mRNA and protein expression and secretion in cells,with maximal effect at 10-8 mol/L at 3 hours for mRNA expression,24 hours for protein expression in the cells,and 12 hours for protein secretion from the cells.Furthermore,the UII effects were significantly inhibited by treatment with its receptor antagonist SB710411,Rho kinase inhibitor Y27632,protein kinase C （PKC） inhibitor H7,mitogen-activated protein kinase inhibitor PD98059,calcineurin inhibitor cyclosporine A,and the Ca2＋channel blocker nicardipine.Conclusion UII may stimulate MCP-1 expression in rat aortic adventitial fibroblasts through its receptor and Rho kinase,PKC,mitogen-activated protein kinase,calcineurin and Ca2＋ channel signal transduction,thus contributing to adventitial inflammation.
