KLK1基因rs3212855和rs5515多态性与 长沙地区汉族人群脑出血的关联研究

目的：分析长沙地区汉族人群脑出血与组织型激肽释放酶（tissue Kallikrein,KLK1）基因多态性的关系。方法：收集长沙地区汉族人群中273例散发性脑出血患者和140例正常对照者的外周血标本。采用多重单碱基延伸单核苷酸多态性(SNP)分型技术（Snapshot）和DNA测序法检测KLKI基因rs3212855及rs5515多态性位点在脑出血患者及正常人群中的分布情况。结果：在本研究样本中未能证实rs5515是多态性位点。脑出血组及对照组KLK1基因rs3212855多态性位点基因型分布和等位基因频率差异无统计学意义（P﹥0.05）。脑出血组rs3212855多态性位点各基因型亚组间血压水平差异无统计学意义（P﹥0.05）;对照组rs3212855位点各基因型亚组间血压水平差异无统计学意义（P﹥0.05）。结论：KLK1基因rs3212855和rs5515位点与脑出血无关。     

2005全国癫（xian）诊疗新进展研讨会通知

左旋咪唑致脱髓鞘脑病的临床与CT表现在国内已有报道，现将1995年8月～2002年8月中南大学湘雅医院神经内科确诊的32例本病患者的临床及影像学资料分析如下。     

上矢状窦血栓形成1例

脑静脉窦血栓形成大约占成年人卒中的1％～2％。磁共振影像技术的广泛应用提高了该病的诊断率，而对脑静脉窦血栓形成患者进行头CT检查时，大约20％以上的患者无异常发现。但CT检查操作简单，应用普及面广，并且可以迅速地排除其他相关疾病，因此正确全面地认识静脉窦血栓形成的早期CT特点对于该病的诊断同样具有重要的意义。     

左旋咪唑所致脱髓鞘脑病的CT、MRI评价(附35例报告)

目的 研究左旋咪唑致脱髓鞘脑病的CT、MRI表现特点,探讨CT、MRI的诊断价值。方法 分析35例左旋咪唑致脱髓鞘脑病的CT、MRI及临床资料。结果 本病在CT、MRI上显示为双侧脑室周围及额、顶、枕、颞叶白质区有多发病灶,CT为低密度影,MRI为长T1长T2信号,很少有占位效应。MRI的影像学诊断率明显高于CT。本病的主要临床表现为急性或亚急性起病的弥漫性脑损害的症状和体征。结论 CT、MRI能为左旋咪唑所致脱髓鞘脑病的临床诊断提供重要信息,且MRI优于CT。与有相似影像表现病变的鉴别应紧密结合临床资料,仅凭CT、MRI表现有一定局限性。     

氯化锂-匹罗卡品致癎大鼠的模型研究

目的:探讨氯化锂(LiCl)-匹罗卡品(PILO)致大鼠的行为学特征及海马病理改变。方法:建立改良的LiCl-PILO致大鼠模型,观察大鼠行为,尼氏染色观察不同时间点大鼠海马病理改变,FJB染色观察大鼠海马神经元及其轴突、树突变性。结果:大鼠腹腔注射LiCl-PILO后,癫持续状态(SE)诱发成功率为92.5%,死亡率21.25%;尼氏染色结果显示,实验组大鼠海马神经元于SE后7d和60d缺失最明显,与对照组相比,齿状回颗粒细胞减少(P<0.05),CA1、CA3区锥体细胞和门区神经元均显著减少(P<0.01);FJB染色结果显示,实验组大鼠海马神经元于SE后7d和60d变性最明显,主要集中在CA1、CA3区锥体细胞层和门区,SE后7d海马腔隙-分子层亦可见变性的神经元轴突和树突。结论:改良后的LiCl-PILO致模型SE诱发成功率高,死亡率低,可基本复制人类颞叶癫的发作特点及病理改变;颞叶癫海马神经元的缺失可能是由于神经元的变性死亡。     

大鼠癫持续状态后miR-21、miR-29的表达变化

目的:探讨miR-21、miR-29在癫持续状态(SE)大鼠脑组织和外周血中表达的变化及意义。方法:SD大鼠30只,随机分为SE组20只和对照组10只,SE组建立氯化锂-匹罗卡品致大鼠SE模型,对照组以生理盐水代替匹罗卡品,应用RT-PCR检测2组大鼠脑组织和外周血miR-21、miR-29的表达。结果:与对照组比较,SE组大鼠海马区脑组织和外周血中miR-21表达均下降(P0.05),miR-29表达均升高(P0.05);miR-21在外周血中的表达显著高于脑组织(P0.01),miR-29在外周血中的表达稍低于脑组织(P0.05);结论:miR-21、miR-29可能参与SE后神经元凋亡的调控过程,外周血miR-21和miR-29变化可反映脑组织中的变化趋势。     

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.     

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.     

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.