Lambert-Eaton肌无力综合征及其药物治疗的研究

Lambert-Eaton肌无力综合征(LEMS)是一种累及神经-肌肉接头突触前膜的自身免疫性疾病。其容易导致人体的突触前膜的乙酰胆碱释放出现严重的阻碍,从而使患者出现一系列严重发热临床症状,如四肢无力、下肢反射减弱等,本文就LEMS的临床表现、主要诊断方式做了相应的介绍,并详细介绍了该疾病的具体治疗方法。     

灯盏乙素介入IP3R-Ca2+途径抑制β淀粉样蛋白诱导的神经细胞凋亡

目的：观察灯盏乙素（Scu）对β淀粉样蛋白（Aβ）诱导的细胞模型中1，4，5-三磷酸肌醇受体（IP₃R）-Ca²⁺途径的影响，探讨其在阿尔茨海默病（AD）病程中可能发挥的积极作用。方法：选用神经母细胞瘤细胞分为对照组、Scu处理组、Aβ处理组、Aβ+Scu （高、中、低）处理组及Aβ+IP₃R拮抗剂组，用CCK-8法筛选药物浓度并检测各组细胞生存率；用酶联免疫吸附法检测各组细胞中1，4，5-三磷酸肌醇（IP₃）的含量；用蛋白印迹和实时荧光定量聚合酶链反应方法检测各组细胞IP₃R和凋亡相关因子Caspase-3、Bcl-2、Bax的蛋白及mRNA的表达水平；用激光共聚焦显微镜观察各组细胞内Ca²⁺浓度的变化；用AnnexinV/PI双染法测定各组细胞的凋亡率。结果：与对照组和Scu处理组相比，Aβ处理组细胞存活率下降，IP₃含量升高，IP₃R、Bax和Caspase-3的蛋白及mRNA表达上调，Bcl-2蛋白及mRNA的表达下调，细胞胞浆内Ca²⁺浓度及细胞凋亡率升高；Aβ+Scu处理组细胞中各检测指标的变化与Aβ处理组的结果正好相反，IP₃R通道下游指标的变化与Aβ+IP₃R拮抗剂组基本一致。结论：Scu能够下调通路蛋白IP₃、IP₃R的表达，抑制Aβ介导的Ca²⁺内流所致的细胞凋亡，可能通过对IP₃R-Ca²⁺途径的调控来影响AD病程。     

胃肠平滑肌运动的细胞信号转导机制

胃肠道功能是消化系统最主要的生理功能之一，而平滑肌是维持胃肠运动的基础，近年认为胃肠道既是多脏器功能不全综合征(MODS)的动力部位，又是靶器官。所以，胃肠平滑肌运动的细胞信号转导机制的研究有一定的实际意义。本从胃肠运动的电生理基础、钙离子和钙通道、平滑肌的收缩装置和途径、胞内信使和信息传递通路以及MODS状态下细胞因子对胃肠动力障碍的影响这五个方面对胃肠平滑肌运动的信号转导机制作一综述。     

铝致神经细胞Ca^2＋浓度升高的可能机制

本文就Ａｌ＾３＋引起神经细胞内Ｃａ６２＋浓度升高的实验依据提出了几种可能性机制，着重介绍了Ａｌ＾３＋通过信号传导系统，谷氨酸，β－淀粉样蛋白聚保，钙调蛋白以及其它机制引起胞内Ｃａ＾２＋浓度升高的过程，指出了某些尚待深入研究之处，并揭示了目前和今后的研究动向。     

硝苯地平致下肢水肿3例

硝苯地平又名心痛定，为钙离子拮抗剂，目前广泛应用于心血管病的治疗。基层医院由于地区及医生业务水平所限，在临床用药过程中，往往只重视药物作用而忽视某些副作用。如本文所述硝苯地平在我院十余年应用过程中，患者出现颜面潮红、心悸、眩晕为主，水肿未引起注意。现将我院近2年应用该药物引起患者下肢关节水肿较重3例，总结报告如下。     

12092 橡树皮灰提取物可治疗皮肤癌

橡树皮灰的提取物高浓度时，即重量超过20％，可用于治疗皮肤癌。低浓度的橡树皮提取物具有迄今尚未明了的治疗性能。例如，含有40％～80％橡树皮提取物可用于治疗急性皮肤癌溃疡。此外，含有钾离子、锌离子、钙离子的合成混合物提供许多与橡树皮提取物一样的有益性质。在某些应用中，加入铷离子（rubidium）及硫也是有益的。     

[Ca^2＋]i change in hippocampal neurons influenced by preconditioning of etomidate fat emulsion following cerebral ischemia in rats

BACKGROUND: It is known that intravenous anesthetic etomidate fat emulsion has cerebral protection. Now many scholars focus on the research of its cerebral protection from molecular biology, but the mechanism of cerebral protection is still fully unclear. OBJECTIVE: To observe the influence of etomidate fat emulsion on the [Ca2+]i in hippocampal neurons during the transient cerebral ischemia injury in rats. DESIGN: Randomized controlled observation. SETTING: Weifang Medical College. MATERIALS: This study was carried out in the functional laboratory of Weifang Medical College between October 2005 and March 2006. Twenty-four male healthy Wistar rats, aged 3 to 4 months, were involved. Etomidate fat emulsion was provided by the limited company of En-hua Medical Bloc in Jiangsu Province (code of H20020511) and the other agents and materials were provided by Laboratory Center of Weifang Medical College. METHODS: The 24 Wistar rats were randomized into 3 groups: sham-operation group, model group and etomidate preconditioning group, with 8 rats in each. Rat models of transient cerebral ischemia injury were made by the ligation of bilateral carotid arteries combined with descending blood pressure in the latter two groups. Before ischemia (ligation of bilateral common carotid artery), rats in the etomidate preconditioning group were intraperitoneally injected with 12 mg/kg etomidate fat emulsion and then persistently intraperitoneally injected with etomidate fat emulsion at 1.0 mg/kg per minute. Rats in the model group were not administrated. Rats in the sham-operation group were only performed bilateral common carotid artery isolation. When rats were modeled, their brain tissues were quickly taken out and detected. MAIN OUTCOME MEASURES: Change of the fluorescence pixel value of the [Ca2+]i in each group by the laser scanning confocal microscope. RESULTS: Twenty-four rats were involved in the final analysis. Fluorescence pixel value in the sham-operation group was in the low level. Fluorescence pixel value in the model group was significantly higher than that in the sham-operation group (P < 0.01). Fluorescence pixel value in the etomidate preconditioning group was significantly lower than that in the model group (P < 0.01). CONCLUSION: The protection of etomidate fat emulsion to the transient cerebral ischemic injury in rats is associated with the inhibition to the increase of [Ca2+]i to some extent.     

Protective Effects of Calcium Antagonists on Cadmium—induced Toxicity in Rats

INTRODUCTIONCadmium,oneoftheimPOrtantenvironmentalpollutants,isknowntocausere-nal,hepatic,neurologicandtesticulardisorders.ThemechanismofheavymetaItoxi-cityremainsunclearalthoughmuchresearchhasbeendonesincethe192Os.Anditwasreportedthatthemetalchelatorsusedinthetherapyofsuchheavymeta1induceddiseasesmaycausesideeffectsonthepatients(Knandelwaletal.,l987).Recently,anewhypothesissuggestedthatcalmodulin(CaM),theuniquemodulatorproteinofcalciumdependentfunctions,mightbethefirsttargetmoleculefo…     

尼莫地平在治疗神经系统疾病中的应用

尼莫地平是一种选择性钙通道阻滞剂,能抑制病理性过量钙离子向细胞内流入,阻止因细胞内钙离子超载所引起的细胞水肿、坏死和死亡,抑制血管的持续收缩,降低血粘度而保护脑组织。本品对脑血管痉挛、脑梗塞、偏头痛、外伤性脑水肿有较好疗效。亦有人将本品用于治疗癫痫、病毒性脑炎、脑复苏的病人。本品毒副反应小。     

神经降压素的肝细胞保护作用与Ca~（2＋）的关系

观察了神经降压素（ＮＴ）的肝细胞保护作用与Ｃａ２＋的关系。结果显示，醋氨酚使肝细胞Ｃａ２＋内流和肝脏钙含量增加，但对于线粒体Ｃａ２＋摄取及其钙含量无明显影响，表明细胞可能出现胞质Ｃａ２＋超载。若在醋氨酚之前给予ＮＴ则使肝细胞Ｃａ２＋内流明显减少，肝脏Ｃａ２＋含量有降低趋势，但线粒体钙含量显著增加。这些结果提示，ＮＴ通过减少Ｃａ２＋内流，增强线粒体贮存Ｃａ２＋的能力，部分缓解醋氨酚所致胞质Ｃａ２＋超载从而减轻细胞损伤。