刺五加皂苷对缺血性脑损伤的保护作用

目的　观察刺五加皂苷 (ASS)对缺血性脑损伤的作用。方法　采用神经元缺血性损伤模型。用流式细胞仪检测细胞凋亡率 ,用硝酸还原酶法测定细胞培养上清液中NO的含量 ,用MTT、LDH测定神经细胞活性 ,并在电镜下观察细胞形态学变化。结果　①缺血性神经元发生凋亡 ,细胞超微结构呈现凋亡样改变 ,其凋亡率与正常对照组比较有显著性差异(P <0 0 1)。ASS能减少缺血性神经元凋亡。②缺血性神经元存活率下降、LDH释放量和NO含量升高 ,与正常对照组比较有显著性差异 (P <0 0 1)。ASS能提高神经元存活率、降低LDH释放量及NO含量。结论　一定浓度的ASS对缺血性神经元凋亡有保护作用 ,ASS可能是通过抑制NO的释放及稳定细胞膜拮抗神经元凋亡     

急性脑挫伤患者血清神经元特异性烯醇化酶的动态变化及其意义

目的探讨急性脑挫伤患者血清神经元特异性烯醇化酶(NSE)在急性期的动态变化及其临床意义。方法选择28例急性脑挫伤患者,脑外伤按严重程度分为弥漫性脑挫伤组13例,局灶性脑挫伤组15例。分时抽取外周静脉血,用放射免疫法(RIA)检测急性期NSE血清水平,观察NSE与出血量和神经功能缺损的相关性。另取15位健康人作为正常对照组。结果弥漫性脑挫伤患者早期血清NSE浓度为(75．43±5．61)μg/ml,局灶性脑挫伤组为(34．61±7．52)μg/ml,对照组为(10．8l±3．21)μg/ml,脑挫伤组明显高于对照组(P＜0．05),且弥漫性脑挫伤组与局灶性脑挫伤组差异有显著性(P＜0．05)。弥漫性脑挫伤组与局灶性脑挫伤组血清NSE水平均于第3天达到高峰,随后开始下降。血清NSE水平与患者神经功能缺损程度评分之间呈正相关,与预后呈负相关。结论神经元特异性烯醇化酶可以作为判断脑挫伤急性期病情严重程度和评估预后的指标之一。     

大鼠下颌下腺颗粒曲管细胞属性的研究

用免疫组织化学ABC染色和镀银染色法研究大鼠下颌下腺颗粒曲管（GCT）细胞的属性,发现大鼠下颌下腺GCT细胞呈嗜铬粒素A和神经元特异性烯醇化酶免疫反应阳性,但镀银染色呈阴性,因此认为大鼠下颌下腺GCT细胞可归属于消化道弥散神经内分泌系统。     

Lesion of the subthalamic nucleus or globus pallidus does not cause chaotic firing patterns in basal ganglia neurons in rats

The basal ganglia appears to play an important role in behavioral selection. One model (Berns and Sejnowski’s) of basal ganglia function argues that the subthalamic nucleus plays a critical role in this selection process and predicts that the subthalamic nucleus prevents the basal ganglia and its re-entrant circuits with the thalamus and cerebral cortex from developing chaotic oscillations. We tested this prediction by generating three-dimensional sequential interval state space plots of the spike trains from 684 globus pallidus, substantia nigra pars reticulata and subthalamic neurons recorded in intact, subthalamic lesioned and globus pallidus lesioned rats, neurons which had previously been analyzed with more standard statistical methods. Only 1 neuron (a globus pallidus neuron in a subthalamic lesioned rat) of the 684 showed a chaotic attractor. In no case did subthalamic nucleus lesion induce a chaotic firing pattern elsewhere in the basal ganglia.     

Neurosteroid modulation of embryonic neuronal survival in vitro following anoxia

Neurosteroids are synthesized de novo in the brain from cholesterol or peripheral steroid precursors and modulate inhibitory γ-aminobutyric acid (GABA_A) and excitatory N-methyl-d-aspartate (NMDA) receptors. Evidence indicates that neurosteroids are neuroprotective and important during neurodevelopment. We tested the hypothesis that neurosteroids increase embryonic neuronal survival following anoxia in rat embryonic day 18 cerebral cortical cultures to examine potential neurosteroid modulation of this insult during early development. Twenty-four hours after plating in serum-free medium, cultures were exposed to DHEA, DHEAS, or allopregnanolone (10⁻¹⁰, 10⁻⁸, or 10⁻⁶ M), or vehicle, for 24 h (n=9 per treatment condition). Cultures were then subjected to anoxia for 2 h and subsequently reincubated for 24 h prior to neuron immunostaining with microtubule-associated protein 2 (MAP-2) antibody. Supernatant from DHEA and DHEAS-exposed cultures was tested for 17β-estradiol metabolite formation by radioimmunoassay. DHEA 10⁻⁶ and 10⁻⁸ M significantly increased neuron survival by 85–87% following anoxia. DHEAS 10⁻⁶ M significantly increased neuron survival by 74% following anoxia, but DHEAS 10⁻¹⁰ M decreased neuron survival after this insult. Allopregnanolone had modest effects on neuron survival that did not attain statistical significance. 17β-Estradiol concentrations were below the limit of detection in all specimens tested (sensitivity 4.7 nM). Our data indicate that pretreatment with DHEA and DHEAS at physiologically relevant concentrations promotes neuronal survival following anoxia in embryonic rat cerebral cortical cultures, and that these effects are not secondary to 17β-estradiol metabolite formation. DHEA and DHEAS modulation of anoxia in embryonic neurons may be relevant to disorders of neurodevelopment involving this insult.     

针刺“内关”“中脘”“足三里”对背侧网状亚核神经元放电的影响

目的:观察腧穴"胃病方"即"内关"中脘"足三里"的针刺信号在背侧网状亚核传导与整合的途径。方法:选用健康成年雄性SD大鼠,10%乌拉坦腹腔注射麻醉,人工呼吸。立体定位仪固定头部,暴露菱形窝,玻璃微电极记录延脑背侧网状亚核(SRD)神经元细胞放电。首先记录30 s的神经元背景活动,然后施以手法(捻转角度120°、频率80次/min)刺激"内关"30 s,同时记录SRD神经元的反应;刺激结束,待细胞放电恢复后,再用相同手法分别刺激"中脘"与"足三里"穴。结果:刺激"内关"穴后,放电频率从(1.67±0.35)个/s增加到(17.55±1.40)个/s;刺激"中脘"穴后,放电频率从(2.35±0.43)个/s增加到(16.96±1.83)个/s;刺激"足三里"后,放电频率从(1.83±0.37)个/s增加到(17.39±1.58)个/s。结论:SRD可能为腧穴"胃病方"3穴在中枢传入信息聚合的部位之一。     

血清肿瘤标志物检测在肺癌诊断中价值

目的探讨血清中癌胚抗原（CEA）、可溶性细胞角蛋白19片段（CYFRA 21-1）、神经元特异性烯醇化酶（NSE）、鳞状细胞癌相关抗原（SCC）浓度对肺癌的诊断、病理分型及临床分期的意义。方法选择经组织学和细胞学确诊的125例肺癌患者作为观察组,125例肺部良性病变患者作为对照组,分别测定两组患者血清中CEA、CYFRA 21-1、NSE、SCC的浓度。结果（1）观察组血清中四项肿瘤标志物浓度明显高于对照组（P〈0.01）。（2）腺癌血清CEA浓度最高,鳞癌血清CYFRA 21-1、SCC浓度最高,小细胞癌（SCLC）血清NSE浓度最高（P〈0.05）。（3）血清中四项肿瘤标志物浓度随肺癌TNM临床分期越晚浓度越高（P〈0.05）。（4）联合检测诊断肺癌的敏感性和准确性明显高于单项检测（P〈0.01）,联合检测特异性下降,与CEA、CYFRA 21-1对比（P〈0.01）。结论血清中CEA、CYFRA 21-1、NSE及SCC的检测在肺癌的诊断、病理分型、判断预后有较好的临床价值,值得在临床上推广应用。     

EV71感染手足口病患儿外周血中Treg细胞、细胞因子和NSE的变化及其意义

目的 探讨EV71感染手足口病患儿外周血中Treg细胞、细胞因子和NSE的变化,分析其在EV71感染手足口病患儿发病机制中的作用及意义.方法 共采集EV71感染手足口病患儿97例(轻症组65例,重症组32例)和健康儿童50例(对照组)外周血,分别用流式细胞仪检测CD4+ CD25+ Foxp3+ Treg,ELISA法测定IL-6、IL-10、TNF-α的含量,化学发光免疫分析仪检测血清中NSE水平,采用SPSS软件对所得数值进行统计学分析.结果 与轻症组和对照组比较,重症组患儿外周血中CD4+ CD25+ Foxp3+ Treg水平显著降低(P＜0.05),IL-6、TNF-α、NSE水平显著增高(P＜0.05);重症组患儿外周血中IL-10水平高于对照组,差异具有统计学意义(P＜0.05);与对照组比较,轻症组患儿外周血中TNF-α、NSE表达水平显著升高(P＜0.05).结论 观察EV71感染手足口病患儿外周血中CD4+ CD25+ Foxp3+ Treg细胞、IL-6、IL-10、TNF-α、NSE水平的动态变化,可以为EV71型重症手足口病患儿早期鉴别诊断和治疗提供理论依据.     

血浆凝溶胶蛋白浓度对重型颅脑损伤长期预后的预测价值

目的 观察血浆凝溶胶蛋白浓度对重型颅脑损伤（STBI）6个月死亡和预后不良（格拉斯哥预后评分1～3分）的预测价值.方法 对80例重型颅脑损伤患者采用ELISA法测定血浆凝溶胶蛋白、神经元特异性烯醇化酶、S100B蛋白、髓鞘碱性蛋白和胶质纤维酸性蛋白浓度.比较格拉斯哥昏迷评分及上述生化指标对重型颅脑损伤6个月死亡和预后不良的预测价值.结果 重型颅脑损伤患者血浆凝溶胶蛋白浓度较健康体检者显著降低（P＜0.01）,血浆神经元特异性烯醇化酶（NSE）、S100B蛋白、髓鞘碱性蛋白（MBP）和胶质纤维酸性蛋白（GFAP）浓度均较健康体检者显著升高（P均＜0.01）.ROC曲线分析显示,血浆凝溶胶蛋白浓度可显著预测重型颅脑损伤患者6个月死亡和预后不良.且血浆凝溶胶蛋白的预测价值与入院时格拉斯哥昏迷评分及血浆神经元特异性烯醇化酶、S100B蛋白、髓鞘碱性蛋白和胶质纤维酸性蛋白浓度比较,均具有较好的预后预测价值.结论 血浆凝溶胶蛋白水平有助于预测重型颅脑损伤患者长期预后.     

癫痫的认知损害与神经元损伤关系的研究

癫痫的认知功能损害表现为对外部信息作出整合反应的能力下降,严重影响患者的生存质量,主要与年龄、癫痫的类型、发作的频率、程度、部位、持续及干预时间、手术及抗癫痫药物治疗等因素有关。神经元的损伤机制主要有钙内流机制、兴奋性氨基酸机制及凋亡机制。目前大量的实验可望通过神经元保护治疗改善癫痫的认知损害,提高患者的生活质量。