电刺激小脑顶核促脑缺血后血管内皮生长因子表达的意义

探讨电刺激小脑顶核(FNS)对局部脑缺血后血管内皮生长因子(VEGF)表达和毛细血管新生的影响．以线栓法制成大鼠右侧大脑中动脉梗塞模型(MCAO)，大鼠随机分为假手术对照组、MCAO组、电刺激小脑顶(MCAO FNS)干预组，以免疫组织化学法检测VEGF、内皮细胞阳性表达及毛细血管记数，大脑中动脉梗塞后，缺血区神经元变性、坏死，VEGF、内皮细胞在半暗带有少量表达，毛细血管数较对照组增加，经电刺激小脑顶核干预后，VEGF、内皮细胞大量表达，毛细血管数目明显增加，有统计学差异．电刺激小脑顶核可通过促VEGF表达、内皮细胞增殖，从而促进毛细血管新生。     

Differential effects of the serotonin receptors on cultured rat cerebral cortical neurons

Effects of serotonin (5-HT) on cerebral cortical neurons were examined by patch clamp techniques. 5-HT produced a variety of responses such as outward (19/73 patches/neurons), slow inward (15/73 patches/neurons), fast inward (8/73 patches/neurons), and mixed currents (initially fast inward deflection followed by an outward response: 2/73 patches/neurons), with a latency of 12 sec, 15 sec, 0 sec, and 0 sec respectively, at a holding potential of −60 mV in whole-cell patches. The fast inward currents were again evoked by a selective 5-HT3 receptor agonist, 1-(m-chlorophenyl)-biguanide hydrochloride (CPBG). In the cell-attached patch clamp configuration, 5-HT inside the patch pipette elicited single channel currents with slope conductances of 42 pS and 132 pS (4/42 patches/neurons). CPBG inside the patch pipette evoked inward single channel currents with a lower slope conductance of 41 pS (3/23 patches/neurons). In contrast, application of 5-HT or a 5-HT₂ receptor agonist, α-methyl-5-hydroxytryptamine-maleate, outside the patch pipette induced outward single channel currents with a major slope conductance of 140 pS (8/30 patches/neurons) or 135 pS (6/20 patches/neurons), respectively. These results indicate that the outward and fast inward currents may be mediated respectively by the 5-HT₂ receptor, which is coupled to a G-protein, and by the 5-HT₃ receptor, which contains the non-selective cation channel, and that the mixed type may be caused by both the 5-HT₂ and 5-HT₃ receptors. Received 27 September 1996; received after revision 4 November 1996; accepted 7 November 1996     

刺五加对大鼠脑缺血损伤修复作用的研究

采用双侧颈总动脉结扎制作SD大鼠暂时性全脑缺血模型,手术后尾静脉分别注射药物刺五加注射液或生理盐水进行观察和神经行为学评分,制片作常规HE染色和Nestin免疫组化染色检测缺血损伤后的修复情况.神经行为学评分显示刺五加组神经功能恢复明显好于生理盐水组.脑缺血再灌注后3d时海马、室管膜和室管膜下区神经干细胞有少量Nestin阳性表达;脑缺血再灌注后5d和7d时海马、室管膜、室管膜下区和缺血区神经干细胞阳性Nestin阳性细胞数明显增加,尤其在缺血区,刺五加组Nestin阳性表达细胞数显著多于生理盐水对照组.     

优化提取与分离海兔大脑神经节蛋白质组

蓝斑背肛海兔（Notarcus Leachii cirrosus Stimpson，NLCS）属于海洋软体动物．NLCS大脑神经节（cerebral ganglion，CG）富含高丰度的脂类物质，并干扰了三氯醋酸-丙酮法沉淀CG蛋白质．本实验的目的是找到一种适合提取、分离海兔CG蛋白的方法．经各种实验方法对比后，发现超速离心法能有效分离CG破碎液中的脂类化合物，提高双向凝胶电泳法分离BG蛋白质组的分辨率，大约可检测到450个蛋白质点．     

二十二碳六烯酸乙酯对沙土鼠缺血再灌注脑损伤及水肿作用的研究

研究二十二碳六烯酸乙酯(E-DHA)对沙土鼠缺血再灌注脑损伤及其脑水肿的影响.选用雄性断奶沙土鼠灌胃给予二十二碳六烯酸乙酯(150 mg/(kg·d))或等体积溶媒10周,阻断沙土鼠双侧颈总动脉血流10 min,造成缺血再灌注模型;测定再灌注后脑组织中丙二醛(MDA)水平,还原型谷胱甘肽(GSH)含量,超歧化氧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)和钾、钠-ATP酶(Na ,K -ATPase)活性,脑水含量,钠、钾离子浓度及海马CA1区神经细胞存活百分数.结果表明:E-DHA预处理显著降低缺血再灌注沙土鼠脑组织MDA水平,阻止GSH含量、GSH-PX和Na ,K -ATPase活性下降,而对SOD的活性未表现出明显作用;E-DHA亦调节缺血再灌注沙土鼠脑组织钠、钾离子浓度,减轻缺血再灌注所致的脑水肿和神经细胞死亡.提示E-DHA对脑缺血再灌注脑损伤有显著保护作用,机制可能其与抗氧化作用有关.     

诊断超声波对人中孕胎儿大脑皮质神经细胞超微结构影响的初步研究

目的；研究B超定点扫描是否对人中孕胎儿大脑皮质神经细胞超微结构造成影响。方法：将8名健康因避孕失败而自愿要求引产的单胎中孕妊娠（18～25周）的妇女随机分成两组，每组各4例，行水囊引产术，对照组在引产前不作B眼扫描；实验组在引产前30min用频率3.5MHz70%的输出B超（I-SPTA=124.1mW/cm^2）经孕双腹部定点扫描胎儿大脑颞叶皮质10min，引产术后胎儿娩出即取大脑颞叶皮质作透射电镜标本的常规制备与观察。结果：与对照组相比，B超定点扫描10min，胎儿大脑皮质神经细胞的主要变化：（1）细胞核染色质分布不均，成团块状浓缩或边聚；（2）核周质（胞质）内糖原与游离核糖体稀疏；（3）部分线粒体肿胀，呈空泡化；（4）次级溶酶体多见。结论：B超定点扫描10min，胎儿大脑皮质细胞开始有变性改变，由于受损神经细胞不易再生，因此，B超用于产前胎儿颅脑检查尤其早，中孕检查时不应超过10min为宜。     

灯盏花素葡萄糖注射液的药效学研究

目的验证灯盏花素葡萄糖注射液的临床前药效学作用;方法选择不同的药理学指标对灯盏花素葡萄糖注射液的药效学作用进行评价;结果灯盏花素葡萄糖注射液对实验性大鼠急性脑缺血具有显著的保护作用,可使大鼠血液中纤维蛋白溶解酶活性明显增加,对大鼠血液血栓形成具有明显的抑制作用,可使小鼠血液凝血时间显著性延长,对小鼠肠系膜微循环具有明显的改善作用,具有明显抑制血小板聚集的功能,亦可显著性降低家兔脑血管阻力,改善脑循环;结论试验结果证明了灯盏花素葡萄糖注射液具有良好的活血化瘀作用,对改善脑血循环、增加脑血流量、降低脑血管阻力、急性脑缺血改善、增加血液纤溶酶活性、防治血液血栓形成等功效显著;讨论研究结果与文献相关报道基本一致,为其临床广泛应用提供了有力的科学依据.     

利手与注意偏向对双耳分听汉字大脑功能优势的影响

对24名左利手和24名右利手被试在三种注意条件（刺激驱动、注意左耳和注意右耳）下进行双耳分听汉字测验,检查中国人利手与汉字听觉词汇加工大脑两半球功能优势的关系,同时考察被试的注意偏向对优势效应的影响.结果表明：（1）汉语母语左利手被试加工汉字听觉词汇的大脑功能偏侧化组织明显不同于右利手;（2）右利手被试在刺激驱动条件下的右耳（左半球）优势易受注意偏向的调节出现明显波动;（3）注意偏向对左利手被试的影响主要表现为优势的左耳（右半球）成绩的下降与非优势的右耳（左半球）成绩的提高,这暗示汉语母语左利手者可能存在汉字听觉词汇加工的潜在两半球表征.     

Pathogenesis of Plasmodium falciparum malaria: the roles of parasite adhesion and antigenic variation

Malaria results in up to 2.5 million deaths annually, with young children and pregnant women at greatest risk. The great majority of severe disease is caused by Plasmodium falciparum. A characteristic feature of infection with P. falciparum is the accumulation or sequestration of parasite-infected red blood cells (RBCs) in various organs, such as the brain, lung and placenta, and together with other factors is important in the pathogenesis of severe forms of malaria. Sequestration results from adhesive interactions between parasite-derived proteins expressed on the surface of infected RBCs and a number of host molecules on the surface of endothelial cells, placental cells and uninfected RBCs. Some receptors for parasite adhesion have been implicated in particular malaria syndromes, such as intercellular adhesion molecule 1 in cerebral malaria and chondroitin sulfate A and hyaluronic acid in placental infection. The principal parasite ligand and antigen on the RBC surface, P. falciparum erythrocyte membrane protein 1 encoded by a multigene family termed var, is clonally variant, enabling evasion of specific immune responses. An understanding of these host-parasite interactions in the context of clinical disease and immunity may reveal potential targets to prevent or treat severe forms of malaria. Received 25 June 2001; received after revision 22 August 2001; accepted 24 August 2001