噻庚啶对失血性休克兔血浆SOD活性和MDA含量的影响

３０只免随机分为噻庚啶治疗组和空白对照组各１５只。颈动脉放血至血压５．３ｋＰａ，维持９０ｍｉｎ，复制失血性休克模型。于输血输液（对照组）和给药（噻庚啶１０ｍｇ／ｋｇ）后３０ｍｉｎ分别由颈动脉采取血样，测定血ＳＯＤ活性和血清ＭＤＡ含量。结果显示，噻庚啶明显地升高ＳＯＤ活性（Ｐ＜０．０１），降低ＭＤＡ含量（Ｐ＜０．０１）。氧自由基在休克的发生发展过程中起着重要作用，巴庚啶能够清除氧自由基，进而减轻细胞损伤和多器官功能衰竭，是其抗休克作用机理之一。     

R波相关振动法血压测量

为了提高振地血压测量的准确性，提出了一咱基于心电Ｒ波与血压振动波之间相关性，识别振动信号的一种抗干扰方法＝－Ｒ波相关法，结合振动波形特征识别，该方法可有效地提取信号，消除干扰影响，该算法已在１６位８０９８单片机上实现，本文同时给出了程序的详细流程图。     

Epidemiological and pathogenic study on the outbreak of toxic shock syndrome and meningocephalitis caused by swine streptococcus

Objective: To reveal the relationship between the biological characteristics of pathogen and the pig-to-human spread of the epidemic and infectious disease in 1998 in East China. Methods: Epidemiological survey, pathological examination of pigs and patients, and pathogen isolation were performed. Results: The disease had a character of quick onset, serious symptoms, short course and high mortality. The clinical manifestations and pathological changes of the disease were high fever, sometimes with nausea, vomiting and diarrhea, then might develop to myositis, fascitis, DIC, multiple organ failure, shock and usually died in 2-3 d. Among 25 patients, 16 manifested clinically as streptococcal toxic shock syndromes and 9 streptococcal meningiocephalitis syndrome. The mortality was 81.25% and 11.11% respectively. Pathogenic bacteria isolated from diseased pigs and patients were found to have some common characteristics in morphology, staining and biological characters. Conclusion: The pathogen isolated from the blood of patients and pigs were identified as streptococci.     

左侧气胸的心电图特征及原因分析

目的探讨左侧气胸致心电图改变的特征及产生原因。方法回顾性分析50例左侧气胸患者的心电图和X线胸片资料。结果50例(100%)均呈R波逆递增,V1￣V6导联QRS波平均振幅呈V2>V3>V4>V5。左侧胸导联低电压39例(78%),而II、III、aVF导联QRS波振幅全部>0.5mV。顺钟向转位38例(76%),胸导联QRS波振幅随呼吸周期性改变31例(62%),胸导联QRS波振幅最大/最小的比值与气胸肺组织压缩程度呈正相关(p<0.05)。结论胸导联R波逆递增是左侧气胸最重要的特征性心电图改变,气胸的严重程度与胸导联QRS波振幅最大/最小的比值呈正比。     

生理信号检测中的同步工频陷波器

市电50Hz干扰一直是生理信号检测过程中最难以克服的问题之一。本文叙述了利用同步滤波器技术克服50Hz干扰的方法。同步滤波器可以自动跟踪市电频率的变化且具有极高Q值和理想的梳状滤波特性,而元件的灵敏度却很低,因而很容易获得40dB以上的陷波效果,可以从根本上克服50Hz干扰而几乎对有用信号毫无影响。     

热休克反应对大鼠油酸肺保护作用的机制研究

未研究发现，经热休克处理的大鼠注油酸后，肺组织损伤明显减轻，Ｗｅｓｔｅｒｎ印迹分析显示热休克使大鼠肺组织中ＨＳＰ７０含量明显增多；Ｎｏｒｔｈｅｒｎ印迹分析证实此乃由于ＨＳＰ７０ｍＲＮＡ转录增加所致。说明热休克处理使肺组织ＨＳＰ７０基因表达增强；提示热休克反应对大鼠油酸肺的保护作用与肺组织细胞中ＨＳＰ７０基因表达增强及与ＨＳＰ７０增多有关。     

‘Ischemic tolerance’ phenomenon detected in various brain regions

We investigated the effects of mild and non-lethal ischemic insult on neuronal death following subsequent lethal ischemic stress in various brain regions, using a gerbil model of bilateral cerebral ischemia. Single 10-min ischemia consistently caused neuronal damage in the hippocampal CA1, CA2, CA3 and CA4, layer III/IV of the cerebral cortex, dorsolateral part of the caudoputamen and ventrolateral part of the thalamus. On the other hand, in double ischemia groups, 2-min ischemic insult 2 days before 10-min ischemia exhibited significant protection in the CA1 and CA3 of the hippocampus, the cerebral cortex, the caudoputamen and the thalamus. Five-min ischemic insult 2 days before 10-min ischemia also showed protective effect in the same areas as those of 2-min ischemia except for the CA1 region of the hippocampus, while 1-min ischemic insult exhibited no protective effect in any brain regions. In the immunoblot analysis, both 2- and 5-min ischemia caused increased synthesis of heat shock protein 72 (HSP 72) in the hippocampus, but 1-min ischemia did not. The present study demonstrated that the ‘ischemic tolerance’ phenomenon was widely found in the brain and also suggested that ischemic treatment severe enough to cause HSP 72 synthesis might be needed for induction of ‘ischemic tolerance’.