永城市疟疾疫情分析及防治效果评价

目的对2007年永城市疟疾疫情进行分析,并对不同的防治对策进行效果评价。方法收集、分析2006年和2007年永城市疟疾疫情报告数据,分别采用间接荧光抗体方法与传统媒介调查方法评价当地人群疟疾感染水平及媒介相关数据,进一步采取针对传染源与媒介防治的措施并对其进行效果评价。结果2007年永城市疟疾发病率为0.16‰,比2006年的0.52‰下降45.02％,人群疟疾抗体阳性率与GMRT显著高于2006年;中华按蚊是永城市唯一传疟媒介,叮人率裴桥乡为5.8867只／（人·夜）,马桥乡为3.7500只／（人·夜）,经产蚊比率为54.55％,人血指数为0.6667,媒介能量与基本繁殖率为0.689和1.4536;不同的休止期治疗效果差异无统计学意义（P〉0.05）,而采用球形芽孢杆菌生物灭蚊蚴措施后,发病率较上年下降51.0％,与未实施生物灭蚊蚴措施的行政村相比,发病率差异有统计学意义（P〈0.05）。结论永城市疟疾仍处于流行之中,采取有针对性地防治对策可有效遏制疟疾疫情回升。     

当归有效成分抗缺氧损伤作用的研究进展

临床实践表明,当归注射液对脑中风患者可以起到治疗作用.经研究,当归抗低氧有效成分主要包括苯酞类、香豆素类、黄酮类、挥发油类化合物等.目前普遍认为当归可以通过抗自由基损伤、调节基因表达、激活蛋白酶、影响一氧化氮生成等方面发挥抗缺氧保护作用.我们最近的工作证明当归还可能有其他成分通过与以上机制不同的途径发挥低氧效应.有关经验教训可能对其他植物有效部位群活性研究提供借鉴.     

辐射应急内照射待积有效剂量快速计算软件的研发

目的 建立辐射应急情况下经由吸入和食入两种途径产生的内照射待积有效剂量快速计算的计算机应用软件。方法利用Visual Basic 6.0对 《Generic Procedures for Assessment and Response during a Radiological Emergency》(IAEA-TECDOC-1162)报告中经由吸入和食入产生的内照射待积有效剂量评价通用程序进行软件设计。结果按IAEA-TECDOC-1162报告建立了辐射应急情况下经吸入和食入2种途径产生的内照射待积有效剂量快速计算软件。结论本软件能够满足辐射应急情况下对吸入和食入产生的内照射待积有效剂量的快速准确计算需求,并为应急处理提供必要的剂量计算数据。     

Simulation of early after-depolarisation in non-failing human ventricular myocytes: Can this help cardiac safety pharmacology?

BackgroundIdentified as being the primary mechanism involved in the induction of torsades de pointes (TdP), early afterdepolarisation (EAD) formation is an important parameter in cardiac safety pharmacology. Easily observed experimentally at the cellular or tissue level, EAD can also be simulated by computer algorithms using animal or human models. During the last decade, confidence in these algorithms has greatly increased. We investigated the putative usefulness of EAD simulation for cardiac safety pharmacology.MethodsEAD simulations were performed in non-failing human ventricular myocytes using the O’Hara-Rudy dynamic model. The role of each cardiac current was investigated by modifying the amplitude of its activity in the model. Prediction of EAD induction by drugs was based on the ratio of their 50% inhibitory concentration values for various cardiac ionic currents to their maximal effective free therapeutic plasma concentration (EFTPC_max).ResultsIn the ventricular endocardial myocytes, EAD was only induced by at least 85% inhibition of the rapid delayed rectifier K⁺ current (I_Kr). The other currents can either induce or prevent EAD under sub- (80% I_Kr inhibition) or up-threshold conditions (87% I_Kr inhibition) of EAD. The study of the ability of drugs to induce EAD resulted in a classification which was in agreement with the Tdp risk classification.ConclusionBased on EAD computer simulation within the human situation, the present study identified the role of various cardiac currents in the EAD formation and suggested that prediction of EAD formation can be useful for early cardiac safety pharmacology.