枣花丹合剂对失眠症夜间慢波睡眠影响的研究

目的:观察枣花丹合剂对失眠症夜间慢波睡眠的影响。方法:选择无器质性病变,每天睡眠少于240~300min为主症者64例患者随机分为两组。枣花丹合剂组在08:00和19:00时分别服用枣花丹合剂200mL。对照组在08:00和19:00时服同量红糖水,连服4周。睡眠监测的数据包括记录时间、非快动眼睡眠期、快动眼睡眠期、睡眠时间、觉醒时间、睡眠比、觉醒比。结果:枣花丹合剂组与对照组相比,夜间睡眠Ⅰ、Ⅱ期减少,Ⅲ、Ⅳ期增加;夜间觉醒次数减少,总睡眠时间明显增加;SWS睡眠结构比改变,SWS睡眠的连续性好、周期性显著,明显优于对照组改变,差异有统计学意义(P<0.05)。结论:枣花丹合剂可以增加失眠症夜间慢波睡眠,是治疗失眠症的一种有效和较好治疗方法。     

非控制性出血性休克低压复苏治疗效果的研究

目的　应用大鼠脾损伤非控制性出血性休克模型探讨低压及低压扩容复苏治疗非控制性出血性休克的可行性。方法　雄性Wistar大鼠 5 0只 ,在大鼠脾损伤模型复制成功后随机等分为 5组 ,组 1 :假手术组 ;组 2 :休克未处理组 ;组 3:常压复苏组 (急救期控制MAP在 80mmHg以上 ) ;组 4 :低压复苏组 (急救期控制MAP在 6 0mmHg±5mmHg) ;组 5 :低压扩容复苏组 (急救期输入硝普钠 5 μg·kg- 1 ·min- 1 ,同时输液控制MAP在 6 0mmHg± 5mmHg)。结果　 1～ 5组平均存活时间 (min)分别为 1 80、73.5 0± 8.0 4、1 1 4 .30± 31 .33、1 4 6 .70± 2 8.0 7和 1 71 .6 0± 1 5 .74 ,除组1、组 5外 (P =0 .0 6 71 ) ,其余各组间比较均有统计学意义 (P <0 .0 5 ) ;2～ 5组的急救期出血量 (ml·kg- 1 )分别为 :3.79± 1 .39、1 7.4 1± 8.88、8.6 7± 4 .5 9、1 0 .33± 4 .31 ,其中组 3出血量明显高于其他各组 (P <0 .0 1 ) ;组 4、组 5与组 2比较出血量明显增多 (P <0 .0 5 )。结论　在非控制性出血性休克治疗中 ,低压及低压复合适量硝普钠扩容复苏方法可改善组织代谢 ,提高生存时间 ,是更为理想的复苏方法     

失血性休克对肠上皮细胞线粒体编码的细胞色素氧化酶mRNA表达变化的研究

目的　观察大鼠失血性休克后肠上皮细胞线粒体编码基因细胞色素氧化酶亚基 (COXⅠ、COXⅡ、COXⅢ )mRNA的表达变化。方法　采用失血性休克模型 ,分离肠上皮细胞后进行RNA的提取 ,应用RT PCR检测COXⅠ、COXⅡ、COXⅢmRNA的表达变化。结果　大鼠失血性休克 1h ,COXⅠ、COXⅡ基因表达开始增强 ,2h表达最强 ,以后随着休克时间延长 ,表达又逐渐减弱 ,失血性休克晚期 5h表达显著低于正常对照组 (P <0 .0 1)。结论　失血性休克可引起大鼠肠上皮细胞线粒体编码基因COXⅠ、COXⅡmRNA的明显改变。     

槲皮素对K562/A02细胞株热休克蛋白mRNA及蛋白质表达的影响

目的 了解槲皮素对K562／A02细胞株70kd热休克蛋白(HSP70)基因及蛋白质表达的影响。方法 热处理前后加入终浓度为10μmol／L的槲皮素，RT-PCR方法检测HSP70基因mRNA表达，Western blot方法检测HSP70蛋白表达。结果 热处理明显增加K562／A02细胞HSP70基因mRNA转录和蛋白表达；热处理前加入槲皮素，HSP70基因mRNA及蛋白表达均显著下调；热处理后加入槲皮素，HSP70基因mRNA及蛋白表达无明显变化。结论 热处理能明显增加K562／A02细胞HSP70基因转录和蛋白表达；槲皮素能抑制K562／A02细胞HSP70基因mRNA及蛋白的表达，并且抑制点早于HSP70的基因转录；槲皮素在K562／A02细胞HSP70基因转录启动后则不再有抑制作用。     

黄芪对ESWL致兔肾损伤后缺氧诱导因子-1α表达的影响

目的探讨缺氧诱导因子-1α（HIF-1α）在ESWL致肾脏损伤中的作用及黄芪是否通过调节HIF-1α的表达而发挥对肾脏的保护作用。方法45只家兔随机分为对照组、ESWL损伤组和黄芪治疗组,每组15只,除对照组外,所有动物接受ESWL处理（18kV,1 500次）。黄芪治疗组家兔于冲击前3d至后2d,每天注射黄芪注射液2.0g/kg。2周后处死家兔,取肾脏HE染色观察肾组织形态学改变,免疫组织化学染色观察HIF-1α在肾脏中的表达。结果ESWL处理后肾小管上皮细胞肿胀、脱落,小管内可见大量管型,肾间质大量炎细胞浸润;黄芪治疗组以上病变显著减轻。ESWL损伤组HIF-1α显著表达于肾小管上皮细胞及间质,黄芪能够明显抑制HIF-1α的表达。结论HIF-1α参与了ESWL对肾脏的损伤,黄芪可能通过抑制HIF-1α的表达发挥对肾脏的保护作用。     

急性心肌梗死患者J波的临床研究

目的　研究心电图有 J波的急性心肌梗死 ( AMI)患者的临床情况。方法　选择住院的急性心肌梗死患者 10 2例 ,心电图有 J波者 5 0例为研究组 ,心电图无 J波者 5 2例为对照组 ,比较两组临床情况。结果　心电图有 J波组比心电图无 J波组发生胸闷 ( 3 0 /5 0∶ 2 0 /5 2 ,P<0 .0 5 )、前壁心肌梗死 ( 2 8/5 0∶ 18/5 2 ,P<0 .0 5 )、合并糖尿病 ( 14/5 0∶ 4/5 2 ,P<0 .0 5 )、超声心动图检查发生舒张功能减低 ( 2 4/5 0∶ 14/5 2 ,P<0 .0 5 )、心电图检查发现室性心动过速 ( 11/5 0∶ 1/5 1,P<0 .0 5 )者多。结论　心电图有 J波者比心电图无 J波者临床情况差 ,易于发生严重心律失常     

胆源性感染性休克兔血栓素、前列环素与血小板聚集率的变化

动态观察胆总管急性完全性梗阻并感染、继发休克兔的血浆血栓素(TXA_2)和前列环素(PGI_2)的稳定代谢产物 TXB_2和6-keto-PGF_(1α)含量及血小板聚集率的变化。结果,血浆 TXB_2呈进行性升高,20h 后(休克时)呈下降趋势,血浆6-keto-PGF_(1α)6h 升高,随后回降;血小板聚集率呈进行性下降。提示血栓素和前列环素、血小板聚集率的变化在重症急性胆管炎、胆源性感染性休克发病过程中起重要病理生理作用,与病情和预后转归有重要联系。     

内毒素、失血性休克大鼠线粒体质子跨膜转运和H~ -ATP酶的改变

目的研究内毒素、失血性休克大鼠肝线粒体质子跨膜转运和Ｈ＋－ＡＴＰ酶的变化。方法大肠杆菌内毒素休克模型和失血性休克模型。采用荧光探针ＡＣＭＡ测定质子跨膜转运。结果（１）内毒素休克５小时亚线粒体在以ＡＴＰ、ＮＡＤＨ和ｓｕｃｃｉｎａｔｅ为底物时引起的ＡＣＭＡ最大荧光淬灭值显著减少（Ｐ＜０．０５）；最大荧光淬灭时间和半数荧光淬灭时间非常显著延长（Ｐ＜０．０１）。（２）内毒素休克早期，线粒体Ｈ＋－ＡＴＰ酶活性显著升高（Ｐ＜０．０５），晚期非常显著下降。（３）内毒素休克大鼠肝线粒体膜结合ＰＬＡ２、血浆和线粒体ＭＤＡ升高（Ｐ＜０．０５）。（４）失血性休克时Ｈ＋－ＡＴＰ酶和质子转运无显著改变。结论内毒素休克时线粒体跨膜质子转运和Ｈ＋－ＡＴＰ酶活性显著下降，失血性休克时变化不大     

F wave studies after intrathecal methotrexate administration

Electrophysiological examinations were done on 20 patients aged 40–71 years with recently diagnosed high grade non-Hodgkin's lymphomas. General chemotherapy and intrathecal chemotherapy in order to prevent central nervous system (CNS) involvement were begun. On the first day of chemotherapeutic cycle patients received intrathecally methotrexate (ITMTX) and prednisolone. Electrophysiological study was carried out twice in each subject: before ITMTX injection and a day after injection. The study procedure included: a conventional nerve conduction examination (peripheral conduction velocity and compound muscle action potential amplitude), the F wave latency and amplitude measurement and F ratio (F-M-1/2M) calculation for peroneal and tibial nerve bilaterally. Results of the first and the second examinations were statistically compared by t-Student's test. No significant differences between values of estimated parameters were found. The study revealed no recent alterations in proximal, paraspinal motor conduction and motor neuron excitability due to antidromical activation after single ITMTX administration.     

The heat shock/oxidative stress connection

Involvement of free-radical oxidations in the aging process has been a topic of interest since Harman's original contribution. Because of the close association between aging and Alzheimer disease (AD) and the qualitative similarity in the neuropathology of both conditions, it has been proposed by many investigators that oxidative stress may be important in AD. If such modality of injury was indeed involved, one should expect to find markers of oxidation and heat shock (since free radicals are key mediators of heat-shock induction) in brains of patients with AD. In fact, several studies documented abnormal expression of antioxidant enzymes and heat-shock proteins (HSP) along with other markers of oxidation in AD brains. We showed that abnormally expressed antioxidant enzymes are topographically associated with senile plaques and neurofibrillary tangles, and that the activity of these enzymes is (contrary to what one would expect) markedly reduced. These findings have recently been confirmed by other investigators. Despite a large amount of evidence that suggests an association between oxidative stress and the pathogenesis of AD, it is not yet known whether oxidative stress is a cause or consequence of the disorder. Future research efforts regarding the oxidative stress hypothesis of AD should include attempts, at generating AD pathology by oxidative means in laboratory animals, determining the role and integrity of the heat-shock response in AD, as well as that of various antioxidant systems, growth factors, and hormones with antioxidant and neuroprotective properties.