三七总皂苷抗缺氧缺糖再给氧诱导大鼠海马神经细胞凋亡的研究

目的 :以原代培养的大鼠海马神经细胞缺氧 /缺糖再给氧为模型 ,观察三七总皂苷对神经细胞凋亡的抑制作用。方法 :流式细胞仪检测凋亡细胞百分率 ,激光共聚焦扫描显微镜检测细胞内Ca²⁺浓度 ,荧光显微镜观察细胞形态学变化和坏死细胞百分率 ,同时 ,测定细胞乳酸脱氢酶 (LDH)的释放。结果 :神经细胞缺氧 /缺糖 5h后再给氧可诱导神经细胞凋亡和细胞坏死 ,并显著增加细胞内Ca²⁺浓度和LDH的释放 ,并随再给氧时间的延长而增加。三七总皂苷能降低神经细胞凋亡及坏死的百分率 ,降低细胞内Ca²⁺浓度 ,减少LDH的释放 ,三七总皂苷的作用随剂量增加而作用增强。结论 :三七总皂苷对缺血再灌注损伤后海马神经元的凋亡过程具有抑制作用 ,这种作用可能与其能降低细胞内Ca²⁺浓度有关。     

重组人生长激素治疗15例原发性扩张型心肌病的初步观察

目的　观察重组人生长激素 (rh GH)对扩张型心肌病 (DCM)患者左心室形态及功能的影响、疗效及安全性。方法　 2 8例 DCM心力衰竭患者随机分为 rh GH治疗组 (1 5例 )和对照组 (1 3例 )。两组病例均接受常规抗心衰治疗 (ACEI、利尿剂、地高辛 ) ,rh GH治疗组在常规抗心衰治疗的基础上肌肉注射 rh GH8.0 IU,每周 2～3次 ,共 3个月 ,治疗前后记录观测指标。以二维超声心动图、 X线胸片及心功能变化评价左心室形态及功能的改变。结果　 rh GH治疗组 3个月后左心室舒张末期内径 (L VED)由治疗前 (70 .0 4± 2 .2 1 ) mm缩小至治疗后 (6 0 .2 0±2 .32 ) mm ,P<0 .0 1 ;心胸比率由治疗前 0 .6 6± 0 .0 6缩小至治疗后 0 .5 5± 0 .0 5 ,P<0 .0 1 ;左心室射血分数(L VEF)由治疗前 (31 .30± 2 .89) %提高到治疗后 (4 3.32± 4 .78) % ,P<0 .0 1。结论　初步临床观察表明 ,基因重组分泌型人生长激素对 DCM心力衰竭患者左心室形态及心功能改善具有一定的作用 ,近期治疗中未发现明显不良作用     

南昌链霉菌生物合成梅岭霉素种子制备优化

以参数相关理论为指导,优化南昌链霉菌生物合成梅岭霉素种子制备工艺。结果表明,培养20～35h后,pH7.30～7.50,总糖<0.35%,pmv>10%,溶磷<100μg/ml,菌丝分化启动有利于提高梅岭霉素的发酵效价。     

Cloning and characterization of a blood coagulation factor IX-binding protein from the venom of Trimeresurus stejnegeri.

A blood coagulation factor IX-binding protein (TSV-FIX-BP) was isolated from the snake venom of Trimeresurus stejnegeri. On SDS-polyacrylamide gel electrophoresis, TSV-FIX-BP showed a single band with an apparent molecular weight of 23,000 under non-reducing conditions, and two distinct bands with apparent molecular weights of 14,800 and 14,000 under reducing conditions. cDNA clones containing the coding sequences of TSV-FIX-BP were isolated and sequenced to determine the structure of the precursors of TSV-FIX-BP subunits. The deduced amino acid sequences of two subunits of TSV-FIX-BP were confirmed by N-terminal protein sequencing and trypsin-digested peptide mass fingerprinting. TSV-FIX-BP was a non-enzymatic C-type lectin-like anti-coagulant. The anti-coagulant activity of TSV-FIX-BP was mainly caused by its dose dependent interaction with blood coagulation factor IX but not with blood coagulation factor X.     

Inhibition of Amiodarone‐Induced Lung Fibrosis but not Alveolitis by Angiotensin System Antagonists

Abstract: Earlier work in this laboratory showed that amiodarone induces apoptosis in alveolar epithelial cells by a mechanism inhibitable by angiotensin system antagonists. A variety of recent studies suggests a critical role for alveolar epithelial cell apoptosis in the pathogenesis of lung fibrosis. On this basis we hypothesized that amiodarone‐induced alveolar epithelial cell apoptosis and lung fibrosis in vivo might be inhibitable by the angiotensin converting enzyme inhibitor captopril or the angiotensin receptor antagonist losartan. Amiodarone‐induced lung fibrosis was induced in male Wistar rats by oral adminstration over six months. Replicate groups of rats received captopril or losartan in addition to amiodarone. Apoptosis was detected by increased total lung activity of caspase 3 and in situ end labeling (ISEL) of fragmented DNA. Collagen was localized and quantitated by the picrosirius red technique. Alveolar epithelial cell apoptosis was detected in amiodarone‐treated animals as early as three weeks after the start of amiodarone administration; by six months exposure, the incidence of alveolar epithelial cell apoptosis was significantly reduced by coadministration of captopril or losartan. Alveolar wall collagen accumulation also was significantly attenuated by captopril (100%) or losartan (74%), but neither agent blunted the accumulation of alveolar macrophages evoked by amiodarone (5.3‐fold at 6 months). Lung neutrophil content was unchanged by amiodarone treatment for three weeks or six months. These results indicate that amiodarone induces alveolar epithelial cell apoptosis in vivo that is inhibitable by angiotensin antagonists. They also support the hypothesis that blockade of angiotensin formation or function attenuates amiodarone‐induced lung fibrosis irrespective of the severity of alveolitis.     

中药不良反应及其发生因素

药品不良反应(ADR)问题越来越突出。2003年媒体关于中药ADR的大讨论引起海内外各界的强烈关注。本文从理清中药ADR概念入手，界定了中药ADR的范畴，并从药品、医生、药师、护士、病人、企业、管理因素以及其他社会因素等方面分析探讨了其发生原因，指出并澄清部分模糊认识，提出一些新观点和设想，以期服务于中药现代化和国际化。     

补肾明目冲剂抗氧化作用实验研究（Ⅱ）

探讨补肾明目冲剂处缓和预防机体组织细胞生理衰老的机理。方法：选用自然衰老的１６月龄Ｗｉｓｔａｒ大鼠，用补肾明目冲剂灌胃３０天，维生素Ｅ为阳性对照组，灌胃结束后，取大鼠心，脑，晶状体蛋白和视网膜脉络膜组织。用丙二醛法测定脂质过氧化物含量；用亚硝酸盐试剂盒检测超化物歧化酶活性；用ＤＴＮＢ法测定谷光甘肽过氧化物酶活性；用钼酸铵显色法测定过氧化氢酶活性；用Ｓｃｈｉｆｆ碱荧光法测定脂褐素含量。     

医院各区域内空气消毒效果及监测方法的探讨

目的探讨医院各区域内空气消毒效果及监测、培养所需时间.方法对3496份消毒后空气采用"平板暴露法”进行监测.第一组848份采样时平板暴露15min、置35C温箱培养48h,第二组2648份采样平板暴露5min、培养24h.结果第一组检测无菌生长率为2.6%、阳性检出率为97.4%、合格率为83.3%;第二组无菌生长率为l7.5%.阳性检出率为82.5%,合格率为88.4%.结论根据尘粒(1～10μ粒径)自然下降规律和所带细菌受损后修复需要时间,我们认为采用"平板暴露法”监测消毒后空气时以暴露15min培养48h为好.     

TUMORS INVADING PARAPHARYNGEAL SPACE : REFINED IMAGING DIAGNOSIS

ＴＵＭＯＲＳＩＮＶＡＤＩＮＧＰＡＲＡＰＨＡＲＹＮＧＥＡＬＳＰＡＣＥ：ＲＥＦＩＮＥＤＩＭＡＧＩＮＧＤＩＡＧＮＯＳＩＳＺｈｕａｎｇＱｉｘｉｎ庄奇新ＣｈｅｎｇＹｉｎｇｓｈｅｎｇ程英升ＹａｎｇＳｈｉｘｕｎ杨世埙Ｓｈａｎｇｋｅｚｈｏｎｇ尚克中ＹａｎＸｉｎｈｕａ...     

NOVA16急诊生化分析仪试剂包中A、R、H液的研制与应用

目的 研制ＮＯＶＡ１６全自动急诊生化分析仪试剂包中Ａ,Ｒ,Ｈ液。方法 根据电极法测定血浆（或全血）中Ｎａ＾＋、Ｋ＾＋、Ｃｌ＾－、ＴＣＯ２、Ｇｌｕ、Ｕｒｅａ、Ｃｒ等物质浓度（活度）和红细胞压积（Ｈｅｍａｔｏｃｒｉｔ,Ｈｃｔ）的原理及标准液配制的有关要求,配制类似血浆水的Ａ液、ＣＯ２释放液Ｈ及参比液Ｒ。结果 自配Ａ,Ｒ,Ｈ液与原装试剂的主要理化指标：ｐＨ、渗透压、电极斜率、线性范围及试剂的稳定性等方面