细胞间黏附分子-1在实验性自身免疫性脑脊髓炎大鼠中表达的动态变化及作用

目的探讨细胞间黏附分子-1(ICAM-1)在实验性自身免疫性脑脊髓炎(EAE)大鼠中表达的动态变化及其作用。方法分别取免疫后第4、6、8、10、12、14、16、18、20天EAE大鼠脑和脊髓制成石蜡切片,行HE染色和ICAM-1半定量免疫组化分析。结果免疫后第8天ICAM-1表达即出现明显上调,早于临床症状的发生;随免疫后时间的延长,ICAM-1表达呈逐渐增高后缓慢下降的变化趋势,并且与EAE大鼠病情评分呈显著正相关(r=0.57,P=0.003)。结论ICAM-1的表达上调可能在EAE发病中具重要作用。     

MBP对PBMC产生IFN-γ和NO的影响

目的探讨T细胞非特异性活化在CNS脱髓鞘性疾病中的作用。方法分离实验性自身免疫性脑脊髓炎(EAE)易感性BALB/c小鼠外周血单个核细胞(PBMC),采用体外细胞培养方法在体外与碱性髓鞘蛋白(MBP)共培养,测定培养上清液中IFN-γ、NO水平。结果经MBP刺激的PBMC产生IFN-γ[(43.83±6.06)pg/mL]和NO[(180.76±20.75)μmol/L]明显增加,与对照组产生的IFN-γ[(28.52±2.18)pg/mL]和NO[(95.61±13.09)μmol/L]相比差异有统计学意义(P<0.01)。结论在CNS脱髓鞘性疾病发病过程中,活化的T细胞、单核细胞等分泌致炎细胞因子和其他有害物质增多。     

广龙昊膏药对大鼠腰椎间盘突出模型细胞因子IL-1、NO及组织胺的影响

为探讨IL-1、NO及组织胺在腰椎间盘突出中的作用及广龙昊膏药的治疗效果，将60只大鼠造模并随机分为正常组（A组）、造模组（B组）、广龙昊膏药组（C组）和奇正止痛膏组（D组），观察其神经根周围局部组织中IL-1、NO及组织胺的含量。结果显示，B组中的IL-1、NO及组织胺较A组显著升高（P〈0．01）。C组、D组较B组明显下降（P〈0．01）。表明大鼠腰椎间盘突出模型中细胞因子IL-1、NO及组织胺明显增加可能是腰椎间盘突出中的潜在始动或促进因素，而C组能显著降低神经根局部中IL-1、NO及组织胺的含量，说明广龙昊膏药作用部分是通过抑制炎性细胞因子的活性实现的。     

Therapeutic effect of antimicrobial drugs against experimental infections due toYersinia pestis in mice

Although there are effective antibacterial agents against plague, newer antibacterial agents have been developed which show more potent activity against other bacterial organisms, but have not been tested againstYersinia pestis. A strain ofYersinia pestis was selected (no. 22; National Institute of Infectious Diseases, Tokyo, Japan) that caused a systemic infection in mice.Y. pestis no. 22 was intraperitoneally inoculated into DDY-strain mice, and 13 oral or 6 injectable antibacterial drugs given to the infected mice at varying doses 1 and 24 hours after infection. Levofloxacin, sparfloxacin and ofloxacin were the most effective oral agents against the infection, and prulifloxacin and pazufloxacin were also effective but to a lesser extent. Also, gentamicin and arbekacin were the most potent injectable antibacterial agents againstY. pestis. These results suggest that there are several new drugs, both oral and injectable, which exert excellent in vivo antibacterial activity against a mouse infection model and may be useful for the clinical treatment of plague.     

Dostoevsky's epilepsy: A case report and comparison

The Russian writer Dostoevsky (1821–1881) suffered from a rare form of temporal lobe epilepsy termed “ec-static epilepsy.” Dostoevsky used his epileptic experiences to create Prince Myshkin, the protagonist of The Idiot. The recent case of a patient who experienced ecstatic epilepsy as a result of a temporal lobe brain tumor is presented and compared with that of Prince Myshkin. Reading Dostoevsky can give the contemporary physician an insight into the inner life of an epileptic patient — an example of how art can directly benefit medical practice.     

放射性肝纤维化过程的定量研究

经＾６０Ｃｏγ线照射大鼠肝区，通过光镜、电镜和图像分析仪、宣研究了照后１年肝脏的病理改变。结果表明，３０Ｇｙ组在照射后１年内逐渐发生了放射性肝纤维化病变。在肝纤维化发生过程中，肝细胞内糖原颗凿含量进行性减少，间质中胶原纤维含量进行性增加，网状纤维于照射１－３个月呈进行性增加。     

颞叶癫痫手术时的皮质脑电描记

提要报告1980年10月至1992年6月间,在皮质脑电描记下手术治疗颞叶癫痫55例,前颞叶切除50例,杏仁核、海马切除5例。皮质脑电描记结果说明,颞叶癫痫的痫灶绝大多数来源于颞叶外侧皮质和颞叶内侧结构。术中皮质脑电描记可提供痫灶的精确部位和范围。     

Molecular basis of severe myoclonic epilepsy in infancy

Severe myoclonic epilepsy (SMEI) or Dravet syndrome is caused by mutations of the SCN1A gene that encodes voltage-gated sodium channel alpha-1 subunit. Recently, we generated and characterized a knock-in (KI) mice with an SCN1A nonsense mutation that appeared in three independent SMEI patients. The SCN1A-KI mice well reproduced the SMEI disease phenotypes. Both homozygous and heterozygous knock-in mice developed epileptic seizures within the first postnatal month. In heterozygous knock-in mice, trains of evoked action potentials in inhibitory neurons exhibited pronounced spike amplitude decrement late in the burst but not in pyramidal neurons. We further showed that in wild-type mice the Nav1.1 protein is expressed dominantly in axons and moderately in somata of parbalbumin (PV) – positive inhibitory interneurons. Our immunohistochemical observations of the Nav1.1 are clearly distinct to the previous studies, and our findings has corrected the view of the Nav1.1 protein distribution. The data indicate that Nav1.1 plays critical roles in the spike output from PV interneurons and further, that the specifically altered function of these inhibitory circuits may contribute to epileptic seizures in the mice. These information should contribute to the understanding of molecular pathomechanism of SMEI and to develop its effective therapies.     

Angular bundle kindling is accelerated in rats with a genetic predisposition to acoustic stimulus-induced seizures

Limbic kindling was examined in genetically epilepsy-prone (GEPR) and non-epileptic control rats. The early stage of kindling development was accelerated in both groups of GEPR rats compared to controls. Later stages of kindling were accelerated in GEPR-9 but not GEPR-3 rats. These results indicate that GEPR rats have an enhanced susceptibility to limbic kindling and suggest that limbic brain alterations may contribute to acceleration of the early stage kindling development in GEPR rats.