邹城市1995～2004年细菌性痢疾的流行状况分析

细菌性痢疾是痢疾杆菌所引起的常见肠道传染病，在我国城乡时有暴发。本病历年来在邹城市传染病发病中占重要地位，为探讨邹城市细菌性痢疾的发病规律和流行特征，制定有效的防制对策，对邹城市1995～2004年细菌性痢疾发病流行情况进行分析。     

阿魏酸钠对豚鼠心室肌动作电位的影响

用普通玻璃微电极细胞内记录,观察阿魏酸钠对豚鼠心室肌细胞动作电位、有效不应期的影响,3种浓度的阿魏酸钠溶液(0.1mg/mL,0.2mg/mL,0.4mg/mL)分别灌流30min,动作电位幅值(APA)和复极20％时程(APD_(20))无明显改变,但复极90％处动作电位时程(APD_(20))与有效不应期延长,浓度在0.1mg/mL和0.2mg/mL时,药物可延长复极50％处的动作电位时程(APD_(50))。     

芬必得致双下肢水肿1例

1临床资料 患，男，60岁，因车祸致胸部疼痛伴呼吸困难半小时入院。诊断为左侧多发性肋骨骨折、左侧锁骨骨折、左侧血气胸。入院积极给予左侧锁骨切开复位克氏针内固定、左侧胸壁胶带外固定、胸腔闭式引流，注射青霉素钠抗炎、补液处理。在治疗中，因患胸痛明显，口服芬必得胶囊（天津中美史克有限公司，批号04060651）600mg，2次／d，服药后胸部疼痛减轻。第8天出现双下肢指凹性水肿，     

酒精对脑组织及胶质细胞白细胞介素—1α基因表达的影响

为了阐明酒精中毒对神经系统损害的机理，用新生CD大鼠酒精中毒模型及原代培养的神经小胶质细胞作为研究对象，用RT－PCR的方法测定酒精中霉对脑组织及体外培养细胞中IL－1α基因水平的改变作用。结果显示：酒精持续染毒11d后，大脑皮层、小脑、海马、纹状体及丘脑组织中的IL－1α基因表达都有不同程度的增加，其中海马增加程度最为明显，是对照组的2．5倍；酒精对基底神经节组织IL－1α基因表达无影响。酒精也使体外培养的小胶质细胞在染毒24h后IL－1α基因表达量开始升高，72h达到高的。体内及体外实验均表明：酒精中毒时IL－1α的基因表达水平增加，继而调控神经和免疫功能，并可能在酒们导致的大脑神经损伤中起重要的作用。     

8例中国病人茶碱代谢物的药物动力学

目的：研究病人常规剂量茶碱治疗后代谢物的动力学。方法：病人静滴茶碱（６．６μｍｏｌ·ｋｇ＾－１）。ＨＰＬＣ法测定给药前后２４ｈ茶碱及其代谢物：１，３－二甲基尿酸（ＤＭＵＡ），３－甲基黄嘌呤（３－ＭＸ），１－甲基尿酸（ＭＵＡ），中间代谢产物１－甲基黄嘌呤（１－ＭＸ）的浓度。结果：ＤＭＵＡ是代谢物中浓度最高的。３－ＭＸ的清除速率最低。１－ＭＸ很快转化成ＭＵＡ，体内浓度很低，但是，翌晨，１－ＭＸ又回升到     

Calpain-mediated regulation of NMDA receptor structure and function

Calpains have been previously shown to regulate AMPA receptor properties by producing partial truncation of the C-terminal domains of several receptor subunits. We now report that NMDA receptor subunits, in particular NR2 subunits, are also subjected to calpain-mediated truncation. Treatment of synaptic membranes with calpain I resulted in truncation of both NR1 and NR2 subunits, with the appearance of NR2 species with lower mol.wt. than native subunits, but still recognized by antibodies directed at the C-terminal domain. This treatment did not modify the binding of several ligands of the NMDA receptors, such as glutamate, glycine or TCP. Incubation of thin frozen-thawed brain sections with calcium resulted in calpain-mediated selective degradation of NR2 subunits, as truncation into smaller fragments was totally blocked by calpain inhibitors. Under the same conditions, TCP binding to sections was decreased by about 50%, an effect also blocked by calpain inhibitors. Treatment of hippocampal slices in culture with the excitotoxin, kainic acid, also produced calpain-mediated truncation of the C-terminal domain of NR2 but not NR1 subunits of the NMDA receptors. The results indicate that calpain activation produces several modifications of NMDA receptors, including the truncation of the C-terminal domain of NR2 subunits, and changes in channel binding properties. They suggest that calpain-mediated regulation of NMDA receptors might represent a feed-back regulation of the receptors which could be used to limit receptor activation.