目的探讨电针足三里穴促胃动力作用机制。方法采用电生理学方法同步观察电针不同穴位后胃电的变化;采用免疫组化荧光双重标记胃电起搏区Cajal间质细胞(interstitial cells of cajal,ICCs)与缝隙连接蛋白43(CX43)、ICCs与ERK的方法 ,观...目的探讨电针足三里穴促胃动力作用机制。方法采用电生理学方法同步观察电针不同穴位后胃电的变化;采用免疫组化荧光双重标记胃电起搏区Cajal间质细胞(interstitial cells of cajal,ICCs)与缝隙连接蛋白43(CX43)、ICCs与ERK的方法 ,观察针刺足三里穴引起胃电起搏区ICCs的变化、与ICCs信息传递相关的CX43的变化、丝裂原活化蛋白激酶(MAPK)家族中的ERK的变化情况。结果电针足三里穴对胃电有明显影响。电针足三里穴可使胃电频率及波幅增高;电针足三里穴可显著激活胃ICCs表达及与ICCs信息传递密切相关的CX43的表达;电针足三里穴能促进胃ICCs调节胃运动的细胞信号转导的MAPK途径中ERK的表达。结论电针足三里穴对大鼠胃电具有明显的促进作用;电针足三里穴促进胃运动的机制可能通过激活ICCs而产生显著电生理活动,通过ICCs及SMC之间的缝隙连接蛋白传递达到平滑肌进而调节胃运动。这一作用的完成,可能是通过ICCs信号转导MAPK途径中ERK通路实现的。展开更多
Background： Among patients with Charcot-Marie-Tooth disease （CMT）, the X-linked variant （CMTX） caused by gap junction protein beta 1 （GJB1） gene mutation is the second most frequent type, accounting for approxi...Background： Among patients with Charcot-Marie-Tooth disease （CMT）, the X-linked variant （CMTX） caused by gap junction protein beta 1 （GJB1） gene mutation is the second most frequent type, accounting for approximately 90% of all CMTX. More than 400 mutations have been identified in the GJB1 gene that encodes connexin 32 （CX32）. CX32 is thought to form gap junctions that promote the diffusion pathway between cells. GJB1 mutations interfere with the formation of the functional channel and impair the maintenance of peripheral myelin, and novel mutations are continually discovered. Methods： We included 79 unrelated patients clinically diagnosed with CMT at the Department of Neurology of the Chinese People＇s Liberation Army General Hospital from December 20, 2012, to December 31, 2015. Clinical examination, nerve conduction studies, and molecular and bioinformatics analyses were performed to identify patients with CMTX 1. Results： Nine GJBI mutations （c.283G〉A, c.77C〉T, c.643C〉T, c.515C〉T, c.191G〉A, c.610C〉T, c.490C〉T, c.491G〉A, and c.44G〉A） were discovered in nine patients. Median motor nerve conduction velocities of all nine patients were 〈 38 m/s, resembling CMT Type 1. Three novel mutations, c.643C〉T, c.191G〉A, and c.610C〉T, were revealed and bioinformatics analyses indicated high pathogenicity. Conclusions： The three novel missense mutations within the GJB1 gene broaden the mutational diversity ofCMT1X. Molecular analysis of family members and bioinformatics analyses of the afflicted patients confirmed the pathogenicity of these mutations.展开更多
文摘目的探讨电针足三里穴促胃动力作用机制。方法采用电生理学方法同步观察电针不同穴位后胃电的变化;采用免疫组化荧光双重标记胃电起搏区Cajal间质细胞(interstitial cells of cajal,ICCs)与缝隙连接蛋白43(CX43)、ICCs与ERK的方法 ,观察针刺足三里穴引起胃电起搏区ICCs的变化、与ICCs信息传递相关的CX43的变化、丝裂原活化蛋白激酶(MAPK)家族中的ERK的变化情况。结果电针足三里穴对胃电有明显影响。电针足三里穴可使胃电频率及波幅增高;电针足三里穴可显著激活胃ICCs表达及与ICCs信息传递密切相关的CX43的表达;电针足三里穴能促进胃ICCs调节胃运动的细胞信号转导的MAPK途径中ERK的表达。结论电针足三里穴对大鼠胃电具有明显的促进作用;电针足三里穴促进胃运动的机制可能通过激活ICCs而产生显著电生理活动,通过ICCs及SMC之间的缝隙连接蛋白传递达到平滑肌进而调节胃运动。这一作用的完成,可能是通过ICCs信号转导MAPK途径中ERK通路实现的。
文摘Background： Among patients with Charcot-Marie-Tooth disease （CMT）, the X-linked variant （CMTX） caused by gap junction protein beta 1 （GJB1） gene mutation is the second most frequent type, accounting for approximately 90% of all CMTX. More than 400 mutations have been identified in the GJB1 gene that encodes connexin 32 （CX32）. CX32 is thought to form gap junctions that promote the diffusion pathway between cells. GJB1 mutations interfere with the formation of the functional channel and impair the maintenance of peripheral myelin, and novel mutations are continually discovered. Methods： We included 79 unrelated patients clinically diagnosed with CMT at the Department of Neurology of the Chinese People＇s Liberation Army General Hospital from December 20, 2012, to December 31, 2015. Clinical examination, nerve conduction studies, and molecular and bioinformatics analyses were performed to identify patients with CMTX 1. Results： Nine GJBI mutations （c.283G〉A, c.77C〉T, c.643C〉T, c.515C〉T, c.191G〉A, c.610C〉T, c.490C〉T, c.491G〉A, and c.44G〉A） were discovered in nine patients. Median motor nerve conduction velocities of all nine patients were 〈 38 m/s, resembling CMT Type 1. Three novel mutations, c.643C〉T, c.191G〉A, and c.610C〉T, were revealed and bioinformatics analyses indicated high pathogenicity. Conclusions： The three novel missense mutations within the GJB1 gene broaden the mutational diversity ofCMT1X. Molecular analysis of family members and bioinformatics analyses of the afflicted patients confirmed the pathogenicity of these mutations.
