紫胡皂甙的高效液相色谱分离与测定

建立了高效液相色谱法，应用反相柱，以甲醇－水（６６∶３４）为流动相，分离了柴胡中的主要有效成分柴胡皂甙ａ、ｃ、ｄ（Ｓａｉｋｏｓａｐｏｎｉｎａ，ｃ，ｄ）并用紫外法进行含量测定。     

An etiological study on fulminant viral hepatitis]

Viral markers were studied in 79 cases of viral hepatitis with hepatic failure. The results were shown as follows: 8 cases were positive for anti-HAV IgM (10.12%); 76 cases positive for HBsAg or anti-HBc IgM (96.20%) and 41 cases positive for anti-HCV antibodies (51.89%). Among those with anti-HCV positive, 35 cases were co-infected with HBV, 5 cases with HAV and/or HCV, only one was infected with HCV alone 2 cases were HD-Ag positive (2.52%) and one not identified (1.27%). With the reference of clinical findings, patients co-infected with HBV/HCV or anti-HBc IgM positive were more critical and usually entail higher mortality. In cases with HCV co-infections, the positive HBV replication markers seems to be reduced. Hepatic failure without HBV replicative markers had a high rate of hepatic coma as well as poor outcome.     

山莨菪碱防治甘油所致急性肾功能衰竭的实验研究

在１２９只ＳＤ大鼠的实验中动态观察了山莨菪碱对甘油所致急性肾功能衰竭时不同时期的Ｂｃｒ，ＢＵＮ，ｐＨ病理改变及死亡率的影响，结果表明：山莨菪碱能降低ＡＲＦ第５天大鼠死亡率以及Ｂｃｒ，ＢＵＮ水平。改善病理损害，对ＡＲＦ起到预防及治疗效果，山莨菪碱的预防效果优于治疗效果，预防是ＡＲＦ防治的关键，但山莨菪碱在治疗过程中要引起“冲刷综合征”导致洗脱性酸中毒，应引起注意。     

人乳头瘤病毒感染超微结构观察

本文对5例典型尖锐湿疣标本及10例可疑人乳头瘤病毒感染标本进行透射电子显微镜观察。结果典型尖锐湿疣标本中仅1例于细胞核内见到人乳头瘤病毒,排列规则呈结晶状。其余14例标本的细胞内均见不同程度的由病毒感染所引起的非特异性病理变化。本文对人孔头瘤病毒及受感染细胞的超微结构进行了初步探讨。     

P53基因突变、人乳头瘤病毒16，18型感染与肺鳞癌发病的关系

应用单链构象多态性分析多聚酶链反应ＥＢ染色法（ＰＣＲ－ＳＳＣＰ－ＥＢ）对４０例肺癌组织标本的Ｐ５３基因序列５～８外显子突变进行分析，同时应用ＰＣＲ方法检测上述标本及１８例肺良性疾病组织标本中ＨＰＶ１６、１８型ＤＮＡ相关序列，旨在分析二者在肺鳞癌发病中的作用及相互关系，并就肺鳞癌与Ｐ５３基因结构和功能异常的关系进行初步探讨。     

真皮下血管网岛状皮瓣抗菌力的实验研究

为研究真皮下血管网薄皮瓣用于感染创面的可行性，在家猪臀部两侧分别形成以旋髂深血管主干分支为蒂的传统岛状皮瓣和远侧５０％修薄的真皮下血管网岛状皮瓣。用细菌计数、吖啶橙荧光染色测定白细胞吞噬指数和白细胞内杀菌率，应用激光多普勒、墨汁灌注、透明标本等方法，对两种皮瓣的抗菌力作自身对照研究。结果表明，真皮下血管网岛状皮瓣的抗菌力明显降低，可能与皮瓣修薄后血供减少，白细胞功能相应降低有关。     

Thrombin regulates components of the fibrinolytic system in human mesangial cells

Besides its procoagulant activity, thrombin has been shown to stimulate cell proliferation and to regulate the fibrinolytic pathway. We report here the effect of purified human alpha thrombin on the synthesis of tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1) by cultured human mesangial cells. Thrombin (0 to 2.5 U/ml) increased in a time- and dose-dependent manner the production of t-PA and PAI-1 (2- to 3-fold increase of secreted t-PA and PAI-1 release during a 24 hour incubation). This effect was associated with a twofold increase in DNA synthesis measured by 3H-thymidine incorporation. Zymographic analysis and reverse fibrin autography showed that thrombin also increased the level of the 110 Kd t-PA-PAI-1 complex, whereas PAI-1 was present as a free 50 Kd form in the culture medium conditioned by unstimulated and thrombin-stimulated cells. Free t-PA was never observed. Both membrane binding and catalytic activity of thrombin were required since the effects of 1 U/ml thrombin were inhibited by addition 2 U/ml hirudin, which inhibits the membrane binding and catalytic activity of thrombin, and since DFP-inactivated thrombin, which has the ability to bind but which has no enzymatic activity, did not induce t-PA or PAI-1. Gamma thrombin, which does not bind to thrombin receptor, did not increase t-PA and PAI-1 releases. The effects of thrombin were probably mediated by protein kinase C activation since H7, an inhibitor of protein kinases, inhibited significantly thrombin effects on t-PA and PAI-1 production, and since addition of an activator of protein kinase A, 8-bromocyclic AMP (100 microM), induced a significant inhibition of the thrombin effect. The effects of thrombin were also suppressed by 1.25 micrograms/ml alpha amanitin, suggesting a requirement of de novo RNA synthesis. Northern blot analysis indicated that thrombin induced an increase in the mRNA levels of t-PA and of PAI-1. We conclude that thrombin increases DNA synthesis in human mesangial cells and enhances the synthesis of both t-PA and PAI-1. The latter is released in a large excess as compared to t-PA. Hence, thrombin may have a role in provoking a localized hypofibrinolytic state and may contribute to the persistence of glomerular fibrin deposits during proliferative glomerulonephritis.     

胚胎颅骨骨膜移植修复髋关节软骨大面积缺损

１９９０年５月～１９９４年４月，对４２例（４７个髋）关节软骨全厚缺损患者采用冷冻保存胚胎颅骨骨膜移植进行修复，其中１４例股骨头骨质Ⅳ期坏死者，同时施行带旋髂深血管蒂髂骨植骨。对３４例（３８个髋）进行了２年～６年（平均４０个月）随访。结果表明，按照吴之康髋关节人工置换术后疗效评定标准，优良２５例，很好５例，好３例，尚可１例。认为，与自体移植物修复关节软骨大面积缺损相比，这种方法无附加损伤，具有移植材料、形态与股骨头相似等特点，是治疗髋关节软骨大面积缺损的一种有效方法。     

Sideropenic Dysphagia综合征膜性蹼26例分析

目的 :研究SideropenicDysphagla (S -D)综合征膜性蹼产生的机制。方法 :回顾分析S -D综合征2 6例的临床资料。结果 :影像学检查显示膜性蹼在颈段食道前壁呈 2mm深的模样陷凹。血液学检查为缺铁性低血红蛋白性贫血改变。结论 :缺铁性贫血是S -D综合征的原因 ,铁剂治疗有效     

Deletion of aldose reductase leads to protection against cerebral ischemic injury.

Previously, we reported that transgenic mice overexpressing endothelin-1 in astrocytes showed more severe neurological deficits and increased infarct after transient focal ischemia. In those studies, we also observed increased level of aldose reductase (AR), the first and rate-limiting enzyme of the polyol pathway, which has been implicated in osmotic and oxidative stress. To further understand the involvement of the polyol pathway, the mice with deletion of enzymes in the polyol pathway, AR, and sorbitol dehydrogenase (SD), which is the second enzyme in this pathway, were challenged with similar cerebral ischemic injury. Deletion of AR-protected animals from severe neurological deficits and large infarct, whereas similar protection was not observed in mice with SD deficiency. Most interestingly, AR(-/-) brains showed lowered expression of transferrin and transferrin receptor with less iron deposition and nitrotyrosine accumulation. The protection against oxidative stress in AR(-/-) brain was also associated with less poly(adenosine diphosphate-ribose) polymerase (PARP) and caspase-3 activation. Pharmacological inhibition of AR by Fidarestat also protected animals against cerebral ischemic injury. These findings are the first to show that AR contributes to iron- and transferrin-related oxidative stress associated with cerebral ischemic injury, suggesting that inhibition of AR but not SD may have therapeutic potential against cerebral ischemic injury.