海马

Results Compared with normal group and sham operated control groups, BrdU positive and Nestin positive cells were increased in the hippocampus, dentate subgranular zone and subependymal zone in operated groups after 24 hours of reperfusion of omni-cerebral ischemia.

结果 脑缺血再灌流24 h后，海马、齿状回和室管膜下区的BrdU阳性细胞和Nestin阳性细胞增多，7～10 d达到高峰，术后20 d仍有表达；在室管膜下区，BrdU阳性细胞和Nestin 阳性细胞有向皮质、海马迁移的现象。

Results compared with normal group and sham operated control groups, brdu positive and nestin positive cells were increased in the hippocampus, dentate subgranular zone and subependymal zone in operated groups after 24 hours of reperfusion of omni-cerebral ischemia. the expression of brdu and nestin reached a peak 7-10 days after the operation, and could still be detected 20 days after the operation. the migration of brdu positive and nestin positive cells to the cerebral cortex and hippocampus was observed in subependymal region.

结果 脑缺血再灌流24 h后，海马、齿状回和室管膜下区的brdu阳性细胞和nestin阳性细胞增多，7～10 d达到高峰，术后20 d仍有表达；在室管膜下区，brdu阳性细胞和nestin 阳性细胞有向皮质、海马迁移的现象。

Fourteen patients undertook temporal lobectomy plus hippocampectomy, 3 epileptogenic zone resection only, 2 temporal lobectomy only, 3 selective hippocampectomy, 6 epileptogenic zone resection plus multiple subpial transection , and 2 corpus callosotomy.

其中颞叶前极加海马切除14例、单纯病灶切除3例、单纯颞叶切除2例、选择性海马切除3例、病灶切除＋单纯软膜横行纤维热凝6例、胼胝体切开2例。

Then killed the animals and extracted hippocampus.The serum of TChE,SOD CAT and MDA were detected.

然后将各组剩余小鼠断髓处死，冰台上迅速取出脑组织，在预冷的生理盐水中漂洗，除去血液，分离出两侧的海马，投入4℃冰浴的玻璃匀浆器中，按1∶9于生理盐水中制成10%脑组织匀浆，在4℃下4000r/min离心10min，取上清液以检测小鼠海马组织中乙酰胆碱酯酶、超氧化物歧化酶、过氧化氢酶的活力和丙二醛的含量。

The contents of myelin basic protein in cerebrospinal; fluid , brain tissues and plasma and the MBP-mRNA expression levels in hypothalamus, hippocampus and temporoparietal grey and white matters were determined with ELISA and hybridization respectively.

结果显示：致伤后8h，低、高速组脑组织、血清、CSF中MBP含量均显著高于对照组和致伤前（P＜0.05，P＜0.01），脑组织中以丘脑下部和海马区MBP含量升高最显著（P＜0.01），血清、CSF中MBP含量与脑组织中MBP含量呈显著正相关（P＜0.05，P＜0.01）；低速组丘脑下部MBP-mRNA表达显著高于对照组（P＜0.05），高速组海马、丘脑下部MBP-mRNA表达均极显著高于对照组和低速组（P＜0.01）。

It was found that SO2 derivatives increase the amplitude of IA in CA3 neurons, and inhibit the inactivation of IA. After SO2 derivatives application, normal sensory physiology of hippocampal neurons was affected. This variation caused by SO2 could underlie the toxical modulation of sensory input to the central nervous system.

说明SO2代谢衍生物可增大大鼠海马CA3区神经元IA电流，延长A-电流的失活时间，从而影响海马神经元的膜生理感应，这可能是SO2影响神经细胞功能的机理之一。

Sections from frontal lobe, occipital lobe, striatum and hippocampus of normal subjects and sections from hippocampus of AD patients were used in hematoxylin eosin, Lox Fast blue, toluidine blue stains and ulex europaeus agglutinin immunostaining.

应用荆豆凝集素(ulex europaeus agglutinin， UEA)免疫组织化学及甲苯胺蓝等染色观察正常增龄病例额叶、枕叶、壳核、海马及AD患者海马的神经元、毛细血管形态改变，应用图像分析技术测算各部位神经元与毛细血管密度比值并分析其与年龄之间的相关性。

This implies that DNA methylation of promoter exon 1_7 may not underly the mechanism of GR up-regulation in GLP-1 -programmed rats.5 Hippocampal expression of GLP-1R and NGFI-A mRNAHippocampal GLP-1R (p =.009) and NGFI-A (p =.001) gene mRNA expression were significantly up-regulated in GP group as compared to VP group.Taken together, neonatal intramuscular injection of plasmid DNA encoding GLP-1 affects behavior and hippocampal GR expression in adolescent rats.

提示GR exon 1_7启动子区域DNA甲基化可能不参与GLP-1导致的GR转录上调。6海马GLP-1R和NGFI-A mRNA表达GP组大鼠GLP-lR(P=。009)和NGFI-A(P=。001)表达均显著高于VP组，表明肌肉注射GLP-1可能通过作用于其海马受体提高NGFI-A表达，进而调控GR表达。

In some of the kindling na- ive rats, no hippocampal sclerosis phenomenon was found during the period of mature, this illustrates that no all the prolonged seizure during the early imma- ture rats can cause the hippocampal sclerosis of mature rats, there was an indi- vidual difference, which may be largely associated with an individual genetic susceptibility.

一部分致癎幼鼠发育至成鼠后并无海马结构的神经元损害和MFS现象，说明在幼鼠早期的长时间抽搐并不都能引起成鼠后海马硬化，存在着个体差异，这可能与个体的遗传易感性有很大的关系。

The dynamic changes of the the neuron apoptosis and correlative genes in hippocampus of ACET-groups and twice-ACET-groups suggested that ACET can slower the apoptosis by inhibiting p~(53)and prolong the ascending period of p~(53) in 4 days after the seizure,this effect would weaken after 4 days.ACET may inhibit the descending of Bax,prolong its descending period and then promote its expression,in order to weaken the inhibition of the apoptosis during 4 to 10 days after seizure and then promote the apoptosis during 10 to 14 days after.This effect of ACET can be enhanced after treating again within 7 to 14 days later.

埋线组和二次埋线组大鼠海马神经元凋亡及相关基因表达的动态变化结果提示：埋线治疗在癫痫发作后的早期(4d内)可通过抑制促凋亡基因p~(53)蛋白表达、延缓其达峰值的时程，从而减缓神经元凋亡的发生，此作用在4d后减弱；埋线治疗抑制大鼠海马神经元凋亡的作用在癫痫发作后的中期(4d～10d)减弱，甚至在远期(10d～14d)出现促进凋亡的作用，可能是通过抑制Bax蛋白表达的下降、延长其降至低峰值的时程，促进Bax蛋白表达的回升的结果；在中远期(7d～14d)内予二次埋线治疗对该效应有续效叠加的作用。

This one mode pays close attention to network credence foundation of the businessman very much.

这一模式非常关注商人的网络信用基础。

Cell morphology of bacterial ghost of Pasteurella multocida was observed by scanning electron microscopy and inactivation ratio was estimated by CFU analysi.

扫描电镜观察多杀性巴氏杆菌细菌幽灵和菌落形成单位评价遗传灭活率。