电针上调δ阿片受体的表达减轻大鼠急性缺血性脑损伤

目的：探讨δ-阿片受体（delta—opioid receptor，DOR）在电针抗急性脑缺血损伤中的作用。方法：51只大鼠随机分为假手术组、假电针组、模型组、电针组、DOR拮抗剂＋电针组。除假手术组外，其余各组均用大脑中动脉线栓法致大鼠局部脑缺血并行再灌注。电针干再灌注时开始．持续30min。再灌注24h后检查神经功能缺损程度、脑梗死体积。另取12只大鼠分为假手术组、模型组、电针组和DOR拮抗剂＋电针组．蛋白印迹法检测脑组织中DOR蛋白的表达。结果：与模型组、假电针组比较，电针组脑梗死体积减小（P〈0．05），神经功能缺损评分增加（P〈0．05）。电针组60kD的DOR蛋白表达较模型组增加（P〈10．05），36kD的DOR蛋白表达有增加趋势，但差异无统计学意义。DOR拮抗剂＋电针组脑梗死体积、神经功能缺损评分与模型组和假电针组比较，差异无统计学意义．DOR蛋白表达和模型组比较。差异亦无统计学意义。结论：电针通过增加DOR的表达减轻缺血性脑梗死和神经功能缺损。     

丹参通脉胶囊治疗短暂性脑缺血发作临床研究

目的:探讨丹参通脉胶囊临床疗效.方法:选门诊短暂性脑缺血发作病例气血亏虚型、肝肾阴虚型、风阳上扰型、痰瘀互阻型共140例,随机分为治疗组踟例,对照组60例,用西药加丹双通脉胶囊治疗与单纯西药治疗作对照.结果:治疗组有效率90.0%,对照组83.3%.结论:丹参通脉胶囊可提高临床治疗短暂性脑缺血发作疗效.     

肢体抖动性短暂性脑缺血发作的研究进展

肢体抖动性短暂性脑缺血发作是一种少见的短暂性脑缺血发作类型,极易被误诊为局灶性运动性癫痫发作或锥体外系疾病.本文对肢体抖动性短暂性脑缺血发作的相关问题做一综述,以提高神经科医师对该综合征的认识.     

辛伐他汀对短暂性脑缺血发作患者颈动脉粥样硬化斑块和血脂影响的研究

目的:观察辛伐他汀对短暂性脑缺血发作(TlA)患者颈动脉粥样硬化斑块和血脂水平的影响及临床疗效。方法:66例有颈动脉粥样硬化斑块的TIA患者随机分为辛伐他汀组(简称他汀组)和对照组:他汀组口服辛伐他汀和阿斯匹林6个月,对照组仅口服阿斯匹林,治疗前、后进行颈动脉超声检查,观察颈动脉内中膜厚度(IMT)、动脉粥样硬化斑块面积,检测血脂水平,比较治疗6个月内两组患者脑血管事件的发生率。结果:治疗后他汀组血胆固醇、低密度脂蛋白、甘油三酯水平比治疗前明显下降,高密度脂蛋白水平明显升高(均P<0.01);颈动脉IMT变薄及斑块面积减少,与对照组比较差异均有显著性(P<0.05);他汀组脑血管事件的发生率为9.09%,对照组为21.21%,两组间差异无显著性(P>0.05)。结论:辛伐他汀不仅有调整血脂的作用,还具有抗脂质氧化、保护血管内皮等多种作用,并能消除或稳定TIA患者的颈动脉粥样硬化斑。     

ABR对前列地尔治疗椎基底动脉缺血性眩晕的疗效评估

目的 寻找治疗椎基底动脉短暂缺血性眩晕(vertebrobasilar transient ischemic vertigo, VBTIV)的有效药物,为前列地尔治疗VBTIV的临床应用提供客观依据.方法 VBTIV患者40例,选用丹麦Madsen公司2260型脑干诱发电位(ABR)系统测试.以短声刺激,刺激声为交替极性,扫描时间10 ms,方波脉冲0.1 ms交替短声刺激,感觉级75 dBSL,最大输出为120 dBpeSPL.叠加1 000次,增益至1 200次.滤波带通为100～2 500 Hz,分别给予11次/s的常规ABR测试和51次/s的高刺激率ABR测试.给予前列地尔静脉注射,每日1次,每次10 μg,2周后症状缓解,再用同样方法复查ABR.结果 应用前列地尔治疗14 d后,40例患者中30例完全缓解占75%.2例部分缓解,8例无缓解.以51次/s ABR与11次/s的ABR差值作为分析参数,治疗前后的组群对比和同一患者自身对比,除了波Ⅰ潜伏期两者无差异外(P＞0.05),其余的波潜伏期及波间期,治疗后较治疗前缩短,有统计学意义(P＜0.05).结论 高刺激率ABR可作为前列地尔治疗VBTIV疗效评估的一个客观指标,前列地尔是治疗VBTIV的有效药物,值得临床推广应用.     

磁共振弥散加权成像对短暂性脑缺血发作的半定量研究

目的探讨短暂性脑缺血发作（TIA）患者相关责任病灶在常规MRI和弥散加权磁共振成像（DWI）的影像表现,着重探讨DWI阳性的TIA责任病灶体积、平均ADC值、平均信号强度（AI）等半定量特点。方法前瞻性对39例资料完整的TIA患者进行了常规MRI和DWI检查,MRI检查均在TIA发作5 d内进行。运用Functool2.6.6i对其中15例在DWI表现为阳性的责任病灶进行半定量分析,计算病灶平均体积、平均ADC值、平均AI,并和健侧进行配对比较研究。结果TIA阳性责任病灶在DWI上表现为点状的异常高信号,病灶平均体积（1.29±0.38）cm3,平均ADC值较健侧下降（25.8±9.01）%,AI较健侧升高（59.9±12.9）%,患、健侧比较差异有高度统计学意义（P〈0.0001）。结论DWI序列对TIA责任病灶的检出率较常规MRI序列明显升高,TIA患者的责任病灶的体积较小,ADC值轻度下降而AI较健侧明显升高。DWI序列有利于对TIA的早期诊断,对预防脑梗死的发生有较大价值。     

Long-term treatment with fish oil prevents memory impairments but not hippocampal damage in rats subjected to transient,global cerebral ischemia

Cerebral ischemia leads to neurodegeneration and cognitive impairment. Fish oil (FO) constitutes a rich dietary source of ω-3 polyunsaturated fatty acids especially docosahexaenoic acid (DHA). The objective of the present study was to investigate whether long-term treatment with commercial, high concentration DHA-containing FO could be effective in alleviating both the cognitive and neurodegenerative deficits caused by transient, global cerebral ischemia (TGCI) in rats. Naive rats were trained for 10 days in an 8-arm radial maze task and then subjected to TGCI for 15 minutes (4-VO model) 3 days later (day 13). Retention of the previously acquired cognition (ie, memory) was assessed weekly on days 20, 27, 34, 41, 48, and 55 and measured by 3 behavioral parameters as follows: (i) latency to find the goal box, (ii) number of reference memory errors, and (iii) number of working memory errors. The extent of pyramidal cell death in the hippocampus was examined at the end of the behavioral analysis on day 43. Fish oil (300 mg/kg DHA, gavage) administration occurred once daily beginning 3 days before TGCI (the last day of training) and continued until day 41. Transient, global cerebral ischemia markedly disrupted memory performance measured by all 3 parameters (P < .0001 vs sham). This amnesic effect of ischemia persisted until the end of the behavioral analysis. Treatment with FO progressively reversed the TGCI-induced retention deficit until rats achieved control levels. This protective effect of FO on learning/memory function was clearly observed after both daily and cumulative data analysis (P < .001-0.01 vs vehicle). Such memory improvements remained statistically significant, even after cessation of FO treatment, indicating a sustained effect of FO. In contrast, FO failed to prevent ischemia-induced hippocampal damage in areas CA1, CA2, or CA4. Therefore, the present findings suggest that long-term FO treatment is able to facilitate functional recovery after ischemic brain damage, an effect that was distinct from hippocampal damage.     

混凝土路面板脱空检测的研究

本文介绍了有关混凝土路面板脱空检测的现有方法,着重阐述了利用瞬态冲击法进行路面板脱空检测的理论基础,并通过一模型试验进行脱空检测的模拟,其结果证明了该方法在理论、试验上是可行的;并在实际路面板上做了相应的试验,得出的结果和模型试验的结果相一致。文章最后对今后的研究工作做出了展望。     

Hydrogen peroxide reduces lower esophageal sphincter tone in human esophagitis

BACKGROUND & AIMS: We have previously used the normal lower esophageal sphincter (N-LES) of human organ donors to examine the physiologic signal transduction of lower esophageal sphincter (LES) circular muscle. Now, for the first time, we have obtained a human LES specimen with esophagitis (E-LES) and characterized its pathophysiologic mechanical and inflammatory profiles. METHODS: E-LES was examined histologically, and its in vitro circular muscle contraction and production of inflammatory mediators were compared with those of N-LES. RESULTS: E-LES exhibited scattered erosions and displayed inflammatory cells in the epithelial layer, basal zone hyperplasia, and elongation of lamina propria papillae, characteristic of chronic reflux esophagitis. E-LES muscle strips developed lower in vitro tone (0.78 g) than N-LES (3.3 +/- 0.2 g). E-LES tone was essentially restored to normal by the H2O2 scavenger catalase, suggesting that H2O2 was responsible for reduction of tone. NOX5 cDNA was higher and H2O2 levels were 4 times higher in E-LES circular muscle (0.85 nmol/mg protein) than in N-LES (0.19 +/- 0.05 nmol/mg protein). When N-LES smooth muscle was incubated in H2O2 (70 micromol/L, 2 hours), platelet activating factor (PAF), prostaglandin E2 (PGE2), and F2-isoprostane increased 2.5, 5.2, and 36 times, respectively. In E-LES, levels of PAF, PGE2, and F2-isoprostane were 4, 6, and 40 times, respectively, higher than in N-LES. PAF, PGE2, and F2 isoprostane produced dose-dependent reductions in tone of N-LES muscle strips. CONCLUSIONS: We conclude that an excessive production of H2O2 triggers an increased production of PAF, PGE2, and F2-isoprostane, which are responsible for reducing LES tone in human esophagitis.