匹罗卡品致(癎)大鼠海马中表达生长抑素的中间神经元数目变化及其轴突出芽

Objective To investigate the roles of somatostatin(SS)positive intemeurons in the development and compensation of temporal lobe epilepsy.Methods Piloearpine-induced epilepsy rat model was established.Immunohistochemistry method was used to detect number changes and axonal sprouting of SS positive intemeurons in different domains of the hippocampus at difierent time points.Degeneration of SS positive interneurons and their neurophils were detected by the double immunofluorescence staining with SS and Fluoro-Jade B(FJB)at 7 and 60 days after status epilepticus (SE).Results In the exoerimental rat group,the number of SS positive neurons decreased in each hippocampal domain,and it reached the lowest at 7 days post-SE(There were 11.1±3.3 in hilus,2.8±0.9 in CA1region and 1.8±0.7 in CA1region,t=13.519,9.644 and 8.808,all P<0.01).In chronic phase,the number of SS neurons gradually recovered,and exceeded the control group in CA1 area at 60 days post-SE(12.8±1.5 vs 8.8±1.3,t=-4.506,P<0.01),however,the number of SS neurons in the hilus(25.5±4.6)and CA1 area(4.8±0.8)remained significantly less than normal levels(t value were 4.691 and 3.953.both P<0.01).Increased SS positive fibers were found in the lacunosum-molecular (1m)layer and outer molecular layer of dentate gyrus after 30 days post-SE,and numerous SS positive fibers were seen threnghout the layers of area CA1 at 60 days post-SE.Double immunofluuorescence revealed that a few SS positive interneurons and fibers were also labeled by FJB in area CA1 at 7 days post-SE and in CA domain/hilus at 60 days post-SE.Conclusions SS intemeurons loss plays an important role in the development of temporal lobe epilepsy.The loss is partially caIlsed by the degeneration and death of neurons;SS positive neurophils increase within area CA1 in chronic phase may play a significant role in the generation and compensation of temporal lobe epilepsy.     

纳米粒子——协助药物透过血脑屏障的靶向载体

许多中枢神经系统药物因不能通过血脑屏障而在临床应用中受限,纳米粒子能协助药物透过血脑屏障并将其靶向有效地运载入脑内。PBCA纳米粒子运载药物的作用机制尚存在争议,似乎不适用于慢性中枢神经系统疾病的治疗。PEGPLA/PLGA纳米粒子血液循环时间长,毒性较低,具有缓释特性,在中枢神经系统药物运载的应用中体现出了极大的优越性。本文将对几种应用于中枢神经系统的纳米粒子的作用机制、性质、临床意义及研究进展进行阐述。     

匹罗卡品致(癎)大鼠海马中表达生长抑素的中间神经元数目变化及其轴突出芽

目的 探讨表达生长抑素(SS)的中间神经元在颞叶癫(癎)的发生和自我修复中的作用.方法 建立匹罗卡品致(癎)大鼠模型.免疫组织化学方法检测各时间点海马不同区域SS中间神经元的数目变化及其轴突出芽情况;结合Fluoro-Jade B(FJB)行免疫荧光双标方法特异性检测大鼠癫(癎)持续状态(status epilepticus,SE)后7 d和60 d海马不同区域SS中间神经元及其轴、树突的变性情况.结果 实验组大鼠海马各区Ss阳性神经元数目均在SE后7 d减至最低(门区11.1±3.3,CA1区2.8±0.9,CA1区1.8±0.7,t=13.519、9.644、8.808,均P<0.01),慢性期开始部分恢复,SE后60 d时CA1区SS神经元数目(12.8±1.5)超过对照组(8.8±1.3,t=-4.506,P<0.01),但门区和CA3区SS神经元数目(分别为25.5±4.6和4.8±0.8)仍明显低于正常水平(t=4.691、3.953,P<0.01);sE后30 d大鼠海马回腔隙.分子层(lacunosum-moleculare,lm)和齿状回外分子层出现大量SS染色阳性纤维,60 d时海马CA1区全层均可见大量增多的SS阳性纤维.实验组中SE后7 d的海马CA1区、60 d的CA1、CA1区和门区均可观察到少部分被FJB染色的SS中间神经元胞体及其轴、树突.结论 SS中间神经元的缺失在颞叶癫(癎)的发生中起重要作用,其缺失部分是由于神经元的变性死亡所致;慢性期CA,区SS阳性纤维大量增多,可能在颞叶癫(癎)的发生和自我修复中起重要作用.     

慢性乙型肝炎患者应对方式对病耻感与自我管理行为中介作用探讨

目的 探讨慢性乙型肝炎(CHB)患者病耻感对自我管理行为的影响,及应对方式在病耻感和自我管理行为之间的中介效应,为提高患者的生活质量提供理论依据。方法 2020-03-01-2020-10-30,采用方便抽样法选取山东省千佛山医院肝病科住院的240例CHB患者为研究对象。采用一般情况调查表、慢性HBV感染者歧视测量量表、医学应对方式量表(MCMQ)、CHB患者自我管理量表对240例CHB患者进行调查。结果 CHB患者病耻感、自我管理行为得分分别为(74.43±19.16)、(89.90±20.54)分,应对方式中面对、屈服、回避得分分别为(18.98±5.28)、(10.56±2.99)、(16.46±1.91)分。Pearson相关分析结果显示,病耻感与自我管理行为、应对方式(面对)呈负相关,与应对方式中的屈服、回避呈正相关;自我管理行为与应对方式(面对)呈正相关,与应对方式中的屈服、回避呈负相关,均P<0.05。应对方式(面对、屈服)在病耻感对自我管理行为影响中的作用为部分中介,效应占比分别为18.6%、36.9%。而应对方式(回避)在病耻感与自我管理行为间的中介作用不成立。...     

头部MRI阴性的颞叶内侧癫痫患者认知功能障碍研究

目的评估头部MRI阴性颞叶内侧癫痫(MTLE)患者认知功能受损特点。方法回顾性分析27名头部MRI阴性的MTLE患者资料,其中左侧MTLE 14例(左侧MTLE组),右侧MTLE 13例(右侧MTLE组)。癫痫患者与性别、年龄和受教育程度严格匹配的14名健康对照者(对照组)均接受蒙特利尔认知评估量表(Mo CA)和失礼识别任务的测评。结果在Mo CA得分方面,两组MTLE患者的Mo CA总分及各分项测试得分均低于对照组(P 0. 05);右侧MTLE组复制立方体得分低于左侧MTLE组和对照组(P 0. 05);右侧MTLE组的画钟试验得分低于左侧MTLE组(P 0. 05);左侧MTLE组句子复述、语言流畅性测试得分低于右侧MTLE组(P 0. 05)。在失礼识别任务得分方面,两组MTLE患者得分均低于对照组(P 0. 05);左侧MTLE组比右侧MTLE组更低(P 0. 05)。结论头部MRI阴性MTLE患者的一般认知功能及高级社会认知功能均受损。     

良性成人家族性肌阵挛癫痫三家系临床特点分析

对三个良性家族性肌阵挛癫痫(BAFME)家系中的31例存活患者的临床资料进行回顾性分析.31例患者年龄为16-83岁,平均45.9岁.家系一发病年龄为14～46岁,家系二为15～39岁,家系三为31～50岁.男女发病率无明显差异.所有患者均以皮质震颤、肌阵挛伴或不伴癫痫发作为主要临床表现.28例存活者行脑电图检查,21例显示异常,主要表现为多棘波或棘慢、尖慢复合波的出现.25例存活者行体感诱发电位检查,21例可见巨大电位.丙戊酸钠能有效控制患者的肌阵挛或全身强直-阵挛发作.     

匹罗卡品致(癎)大鼠海马中表达生长抑素的中间神经元数目变化及其轴突出芽

Objective To investigate the roles of somatostatin(SS)positive intemeurons in the development and compensation of temporal lobe epilepsy.Methods Piloearpine-induced epilepsy rat model was established.Immunohistochemistry method was used to detect number changes and axonal sprouting of SS positive intemeurons in different domains of the hippocampus at difierent time points.Degeneration of SS positive interneurons and their neurophils were detected by the double immunofluorescence staining with SS and Fluoro-Jade B(FJB)at 7 and 60 days after status epilepticus (SE).Results In the exoerimental rat group,the number of SS positive neurons decreased in each hippocampal domain,and it reached the lowest at 7 days post-SE(There were 11.1±3.3 in hilus,2.8±0.9 in CA1region and 1.8±0.7 in CA1region,t=13.519,9.644 and 8.808,all P<0.01).In chronic phase,the number of SS neurons gradually recovered,and exceeded the control group in CA1 area at 60 days post-SE(12.8±1.5 vs 8.8±1.3,t=-4.506,P<0.01),however,the number of SS neurons in the hilus(25.5±4.6)and CA1 area(4.8±0.8)remained significantly less than normal levels(t value were 4.691 and 3.953.both P<0.01).Increased SS positive fibers were found in the lacunosum-molecular (1m)layer and outer molecular layer of dentate gyrus after 30 days post-SE,and numerous SS positive fibers were seen threnghout the layers of area CA1 at 60 days post-SE.Double immunofluuorescence revealed that a few SS positive interneurons and fibers were also labeled by FJB in area CA1 at 7 days post-SE and in CA domain/hilus at 60 days post-SE.Conclusions SS intemeurons loss plays an important role in the development of temporal lobe epilepsy.The loss is partially caIlsed by the degeneration and death of neurons;SS positive neurophils increase within area CA1 in chronic phase may play a significant role in the generation and compensation of temporal lobe epilepsy.     

利尿钠肽和其受体在内耳的研究进展

内耳是听觉、位置觉感受器官，含有内外淋巴系统，其液体容量、离子分布、局部血流调节及声音传导的机制尚未阐释清楚，推测内耳中存在的多种激素与上述机制有一定的关系。利尿钠肽（natriureticpeptides，NPs）即是其中一种激素。NPs是与液体稳态、血压等的调节有关的内源性多肽，是分子结构相似、基因来源不同的激素家族。它们与其特异的受体结合后发挥生物学作用。目前已发现三种利尿钠肽受体（NPRs）。NPs和NPRs在内耳分布广泛．它们对内耳环境的生理病理影响一直在探求中。本文就近年来的研究现状作一综述。     

幽门螺杆菌对多巴胺能细胞系SH-SY5Y损伤作用的体外研究

目的探讨幽门螺杆菌(HP)对多巴胺能细胞系SH-SY5Y的损伤作用及其机制。方法体外培养多巴胺能细胞系SH-SY5Y细胞分别加入HP上清蛋白(HP组)、1-甲基-4-苯基-吡啶离子(MPP+)(PD组)和培养液(对照组),用噻唑蓝(MTT)染色法检测细胞存活率,用共聚焦显微镜、分光光度仪检测细胞内活性氧(ROS)和线粒体呼吸链酶复合体活性。结果HP组和PD组细胞的存活率明显下降,高浓度HP组细胞生存率明显低于中、低浓度HP组(均P<0.05)。与对照组比较,HP组和PD组细胞内ROS水平明显减少、线粒体呼吸链酶复合体活性下降(均P<0.05)。结论HP分泌成分对多巴胺能细胞有与MPP+相似的损伤作用,氧化应激反应及线粒体功能受损可能是其导致多巴胺能细胞损伤的机制。     

QDs-SA和Cy3荧光标记阿尔茨海默病细胞模型β淀粉样蛋白的比较研究

目的：观察利用量子点（QDs）标记的链霉亲和素复合物（QDs—SA）和传统荧光染料Cy3分别标记的阿尔茨海默病（AD）转基因细胞模型β淀粉样蛋白（AD）在荧光强度和抗光漂白性能的差异。方法：将pcDNA3．1／APP质粒转染至HEK293细胞建立稳定表达株,Western blot法检测转染细胞APP蛋白的表达,细胞免疫荧光检测AD蛋白生成。建立AD转基因细胞模型,分别应用QDs—SA和Cy3细胞免疫荧光染色技术靶向标记转基因细胞模型的Aβ蛋白,激光共聚焦显微镜下对荧光强度和抗光漂白特性进行检测。结果：Western blot法在稳定转染pcDNA3．1／APP质粒的细胞中检测到APP目的蛋白谱带,而未转染的空载体转染组细胞未见APP蛋白表达。共聚焦荧光显微镜下观察到：①APP基因转染后能够生成大量Aβ蛋白;②QDs—SA特异标记的Aβ蛋白主要分布在细胞膜和胞质,显现出均匀分布的高密度橙红色强荧光;③Cy3特异标记AD蛋白荧光强度较QDs—SA标记弱,且细胞膜染色不均匀,部分细胞膜区域有染料少量团聚;④QDs—SA相较于传统Cy3荧光染料的平均荧光强度值更大（P〈0．05）,488nm激发光连续激发12min,QDs—SA荧光标记的Aβ蛋白仍发射较强的橙红色荧光,荧光强度下降了29．25％,而传统荧光染料Cy3荧光强度下降幅度达76．82％。结论：QDs—SA能有效识别AD转基因细胞模型中AD蛋白,且在光稳定性和荧光强度等方面均优于传统的Cy3荧光染料标记的免疫荧光成像。