丁苯酞对脑缺血再灌注大鼠炎症介质和神经细胞超微结构的影响

目的:研究丁苯酞预处理对脑缺血再灌注大鼠炎症介质(IL-1β)和神经细胞超微结构的影响。方法:将160只实验大鼠随机分成:Sham组(假手术组)、IR组(缺血再灌注组)、低NBP组、中NBP组和高NBP组,每组32只。通过Longa改良线栓法制备大鼠缺血再灌注模型,NBP预处理组给予NBP灌胃,IR及Sham组作为对照组,予等量的生理盐水灌胃。行神经功能缺损评分,检测皮质IL-1β水平,并观察大鼠的神经细胞、皮层的超微结构改变。结果:5组大鼠的神经功能缺损评分组间比较具有显著性差异(F=52.46,P<0.01),Sham组最低,IR组最高;五组大鼠的IL-1β水平组间具有显著性差异(F=30.19,P<0.01),IR组IL-1β水平最高,Sham组水平最低。结论:NBP在大鼠缺血再灌注的模型中能够通过抑制炎症反应,改善再灌注所致的损伤,对神经有保护作用。     

Sliding window averaging in normal and pathological motor unit action potential trains

Objective

To evaluate the performance of a recently proposed motor unit action potential (MUAP) averaging method based on a sliding window, and compare it with relevant published methods in normal and pathological muscles.

Ethanol modulates GABA(B) receptor expression in cortex and hippocampus of the adult rat brain

Using in situ hybridization, RNase protection assay and Western blot, we studied the effects of ethanol on the expression levels of GABA(B) receptor mRNA and protein in the cortex and hippocampus from adult rat brain. The results showed that ethanol significantly increased GABA(B1) and GABA(B2) receptor protein expression in the cortex, whereas only GABA(B2) was increased in the hippocampus. GABA(B) receptor agonist baclofen could partially reverse the effect of ethanol. Further studies of the mRNA levels defined that GABA(B1) mRNA levels were significantly increased in the hippocampus, with no significant changes of GABA(B2) mRNA levels. Moreover, GABA(B1) and GABA(B2) receptor mRNA levels were increased on 3-week ethanol treatment. Finally, GABA(B) agonist baclofen and antagonist phaclofen showed significant decreasing effects on GABA(B1) receptor mRNA levels in the cortex, but not in the hippocampus. These results were further confirmed by in situ hybridization. Thus, the present results showed the effects of ethanol on GABA(B) receptors in the cortex and hippocampus, implying the possible role of GABA(B) receptor in ethanol effects. The effects of GABA(B) receptor agonist and antagonist suggested that the possible mechanisms underlying that GABA(B) receptor modulated the behavioral effect induced by ethanol.     

监护仪血压参数准确性的讨论

本文介绍了血压的溯源、设计原理、引起测量值误差的原因，分析了监护仪血压测量的准确性问题，并提出相应策略。     

丁苯酞对癫痫小鼠脑内氨基酸的影响

目的 观察丁苯酞对癫痫小鼠脑内氨基酸含量的影响.方法 小鼠腹腔注射丁苯酞溶液30 min后制作急性癫痫模型,对癫痫小鼠脑内的4种氨基酸(天冬氨酸、γ-氨基丁酸、谷氨酸、甘氨酸)的含量变化进行观察.结果 丁苯酞能降低兴奋性氨基酸谷氨酸的含量,并能降低Glu/GABA的比值(模型组38.78;丁苯酞高剂量组5.52),与模型组比较差异均有统计学意义(P＜0.05).结论 丁苯酞可以调节大脑中兴奋/抑制系统的平衡,从而可能缓解癫痫的发作.     

2-(α-羟基戊基)苯甲酸钾反复给药对大鼠的毒性研究

目的观察Ⅰ类抗脑缺血新药2-(α-羟基戊基)苯甲酸钾[potassium 2-(1-hydroxypentyl)-benzoate,dl-PHPB]反复给药对大鼠的毒性反应。方法SD大鼠,雌、雄各半,根据给药剂量分为10,30,90 mg/kg组及溶剂对照组,尾静脉反复给药30 d,停药后恢复期观察21 d。检测指标包括动物一般状况、体重、进食量、血液常规、血液生化、尿10项和病理组织学检查等。结果 SD大鼠连续静脉注射dl-PHPB 30 d,可剂量依赖性地引起肝脏重轻度增加、血清球蛋白升高、凝血酶时间(TT)延长。30,90 mg/kg剂量组尿潜血阳性及90 mg/kg剂量组尿蛋白升高。这些改变停药后均可恢复。在90 mg/kg剂量、药物质量浓度为45 g/L时,可见明显的血管刺激性,恢复期结束时血管病变仍然存在,但已开始修复。结论SD大鼠静脉注射dl-PHPB 30 d,其无毒反应剂量为30 mg/kg(相当于药效剂量的10倍);90 mg/kg(相当于药效剂量的30倍)时可见轻度毒性反应,主要为可逆性的肝脏、肾脏损伤及血管刺激性。上述研究结果为dl-PHPB的临床安全合理应用提供了参考。     

DL-3-n-Butylphthalide protects rat bone marrow stem cells against hydrogen peroxide-induced cell death through antioxidation and activation of PI3K-Akt pathway

Bone marrow stem cells (BMSCs) have been one of the most important cell sources for cell replacement therapy (CRT) in cerebral infarction. However, long-lasting oxidative stress during stroke, which plays an important role in neuron damage, deteriorates the microenvironment for cell survival, differentiation and removal. Thus the outcome of CRT in ischemic diseases was poor. DL-3-n-Butylphthalide (NBP) has protective effects on ischemic brain tissue through multiple mechanisms and has been used for stroke treatment in China for several years. In this study, hydrogen peroxide (H(2)O(2)) was used to induce oxidative stress injury to rat bone marrow stem cells (rBMSCs), imitating the microenvironment surrounding transplanted cells in the ischemic brain in vitro. The protective effects of NBP on rBMSCs against apoptosis induced by oxidative stress were investigated. Our results indicated that NBP could protect rBMSCs against apoptosis due to antioxidative properties and modulation of PI3K/Akt pathway. NBP could be used in combination with BMSCs for the treatment of cerebral infarction by improving the oxidative stress microenvironments and cell survival, however, further studies remain warranted.     

恩必普改善血管性痴呆患者认知功能的系统评价

目的评价恩必普治疗血管性痴呆的临床疗效和安全性。方法检索CNKI、VIP、CBM、PubMed等数据库,对公开发表的恩必普治疗血管性痴呆的相关研究进行检索,运用RevMan 5.0软件对数据进行Meta分析,绘制森林图。结果共纳入10个研究。恩必普在改善血管性痴呆患者简易精神状态检查量表(MMSE)和日常生活能力量表(ADL)评分值方面要优于对照组(P<0.05);在不良反应发生概率方面,试验组与对照组相似,差异无统计学意义(P>0.05)。结论恩必普治疗血管性痴呆的疗效肯定,不良反应轻微;但由于纳入研究数目较少,上述结论需谨慎对待,期待日后有高质量、长期、大样本的试验进一步验证上述结论。