肉孢子虫所致感染性肌炎1例报告

肉孢子虫病系我国少见人体寄生虫病,人肌肉内肉孢子虫病更为罕见。Jeffery(1974)收集历年世界各地的报告共28例。我国已报告5例,山东1例(冯兰州,1932)、甘肃1例(毛曼霞,1963)、西藏3例(李经邦、焦宏钧,1981),现将我们经肌活检证实的1例报告如下。

时毓民教授应用滋阴补肾法治疗小儿感染性肌炎经验

小儿感染性肌炎以受累肌肌力弱、疼痛及继发肌萎缩为临床表现,根据临床表现属于中医痿证的范畴。《内经·痿论》提出“治痿独取阳明”,时毓民教授根据小儿生理病理特点,认为热伤气阴,筋脉失养为小儿痿证的主要病机,邪热津伤是其标,脾肾亏虚为其本,采用滋阴补肾法,兼以益气活血治疗小儿感染性肌炎效果显著。本文结合病例分析,将时教授治疗小儿痿证的经验进行总结。

儿童急性良性肌炎肌电图特征

目的分析儿童急性良性肌炎的肌电图结果以提高该病临床诊断率。方法收集本院32例急性良性肌炎患儿的一般资料及肌电图结果进行回顾性分析。结果所收集患者中肌电图总异常率为82.25%,按照肌电图结果,分为运动单位(motor unit action potential,Mup)偏窄小组23例,复合肌肉动作电位(compound muscle actionpotential,CMAP)降低组3例,肌电图正常组6例。三组中,年龄、肌酸激酶(creatine kinase,CK)、肌酸激酶同工酶(creatine kinase isoenzyme MB,CK-MB)、乳酸脱氢酶(lactic dehydrogenase,LDH)、氢丁酸脱氢酶(hydrobutyrate dehydrogenase,HBDH)、谷丙转氨酶(alanin aminotransferase,ALT)、谷草转氨酶(aspartate aminotransferase,AST)无统计学差异(P>0.05)。对上下肢异常肌肉的数量进行比较分析,二者之间的差异具有独立性,且差异具有统计学意义(P=0.017)。结论肌电图是诊断急性良性肌炎的重要检查方式,其有较高的异常率,有利于有效提高急性良性肌炎的诊断率。

浮针治疗45例慢性胸壁源性胸痛患者分析

观察浮针治疗慢性胸壁源性胸痛疗效。方法:选择45例慢性胸壁源性胸痛患者,根据视觉模拟评分法,疼痛程度在3-4者有8例患者,5-6者有16例,7-8者有18例,9-10者3例。应用浮针治疗1-3次,观察止痛效果。结果:45例患者中非感染性肌筋膜炎患者17例,非特异性肋软骨炎28例。治疗有效42例,无效3例,总有效率93.3 %。其中疼痛程度在3-4者有6例有效,2例无效,有效率75%;5-6者有16例均有效,有效率100%;7-8者有18例均有效,有效率100%;9-10者2例有效,1例无效(该例患者疼痛程度有所缓解,但评分没达到有效要求)。结论:浮针疗法可有效治疗慢性胸壁源性胸痛,见效快,疗效持久,值得临床推广。

ROLE OF COXSACKIEVIRUS AND ADENOVIRUS RECEPTOR (CAR)IN CARDIOTOXICITY INFECTED BY COXSACKIEVIRUS B3

Objective To explore the role of coxsackievirus and adenovirus receptor（CAR） in cardiotoxicity infected by coxsackieviras B3. Methods A toxic cellular model was established in vitro by adding myocarditic coxsackievirus B3 （CVB3m） into the culture of neonatal mouse cardiomyocytes. 48 h later, the cardiomyocytes were divided into control, CVB3m, and CAR antibody ＋ CVB3m groups. CVB3m-mediated myocytopathic effect of above three groups was observed after further culturing for 48h. At the same time, the cardiomyocytes＇ viability of above three groups was assessed by MTT assay. Results The degree of cytopathic effect（CPE） of CAR antibody ＋ CVB3m group was significantly lower than CVB3m group （ P 〈 0. 01 ） and there was a significant increase in cell viability in CAR antibody ＋ CVB3m group compared with CVB3m group（ P 〈 0. 01 ）. No significant difference was found between CAR antibody ＋ CVB3m group and control group. Conclusion CAR antibody possesses a protective effect on CVB3m infected cardiomyoctyes, which indicates that CAR may play an important role in mediating cardiotoxicity infected by CVB3m.