1-乙基-6-氟-1,4-二氢-4-氧代-7-(4-芳酰硫代氨甲酰基-1-哌嗪基)-3-喹啉羧酸的合成及抗菌作用

Thirteen new 1-ethyl-6-fluoro-1,4-dihydro-4-oxo-7-(4-aroyl-thiocarbamoyl- 1 piperazinyl)-3-quinoline carboxylic acids were prepared, Their structures were characterized by elemental analysis, IR, HNMR and MS spectra.Preliminary pharmacological tests indicated that some of compounds Ia～m possess strong inhibiting activity against Escherichia coli, Bacillus subtilis and Proteus at concentration of 100 μg/ml.     

大狼毒三萜类化学成分的研究

自大戟科(Euphorbiaceae)植物大狼毒(Euphorbia nematocypha Hand—Mazz)根的乙醇提取物的苯溶解部分,经20%AgNO₃硅胶层析,分离得到七个三萜类成分。根据光谱(IR,EIMS,¹H—NMR和¹³C—NMR)和化学方法,确定其中一个化合物为新化合物,命名为大狼毒醇(nematocyphol,Ⅳa),其它化合物为已知物:印度荆芥醇乙酸酯(nepehinol acetate Ⅰ),日尔曼醇乙酸酯(germanicol acetate Ⅱ),大戟醇(euphol,Ⅲ),蒲公英醇(taraxasterol,Ⅴa),24-亚甲基环阿尔廷醇(24-methylenecycloartanol,Ⅴa)和印度荆芥醇(nepehinol,Ⅶa)。这些化合物均为首次从大狼毒中得到。     

亮氨酸脑啡肽的电子结构及构效关系研究

对亮氨酸脑啡肽进行了量子化学(INDO)计算,研究其电子结构特征,讨论其活性部位、作用机理及构效关系。同吗啡和R31833进行了活性部位的电子结构与空间结构比较,推断它们的活性药效结构具有共同特点,与阿片受体相互作用时作用方式相同,作用部位有对应关系,因而具有相同的药理性质。     

神经肌电检测对单侧喉返神经损伤预后的评价

目的 探讨喉神经肌电位综合指标对声带麻痹预后的估价作用。方法 检测91例甲状腺手术单侧声带麻痹患者的喉神经电图及肌电位,按病程分成4组;分析各组恢复与未恢复声带运动的患者喉神经肌电位特征,以“95％可信区间”计算神经肌电位预后评估标准。结果 病程2个月内组最大诱发电位幅度明显低于2个月以上的其他各组,差异具有显著性意义(P<0.05),而2-4个月与4-6个月组的组间差异无显著性(P>0.05),故将病程2-6个月计为一组。2个月内组自然恢复与未恢复患者分别为2、11例,以引出诱发电位且无错向再生电位作为预后良好判断指标,准确率为92％(12/13)。2-6个月组恢复与未恢复患者各为11、48例,恢复者最大诱发电位幅度明显大于未恢复者,差异有显著性意义(P<0.01)。以引出诱发电位且电位幅度大于26.4％作为预后良好的判断标准,准确率90％(53/59);结合无错向再生电位综合判断预后,准确率为93％(55/59)。6个月以上组19例无论神经肌电位检查结果如何,声带运动均无恢复。结论 将神经肌电位进行综合分析,分别判断不同病程的声带麻痹的预后,可提高预后判断的准确率。     

Inhibition of myeloperoxidase by synovial fluid and serum.

An inhibitor of myeloperoxidase has been identified in the synovial fluids and sera from patients with rheumatoid arthritis and sera from normal subjects. Initially, these fluids were found to inhibit stimulus induced degranulation of polymorphonuclear leucocytes independently of the stimulating agent. Subsequently, the fluids were shown to inhibit the released enzyme rather than the degranulation response of polymorphonuclear leucocytes. Both rheumatoid and normal serum samples contained high concentrations of the inhibitor but the concentrations were lower in rheumatoid synovial fluids. The inhibitory activity seemed to be specific for peroxidase as the fluids did not inhibit beta-glucuronidase activity. A protein of relative molecular mass (Mr) 150 kd was purified from synovial fluid by affinity chromatography on myeloperoxidase-Sepharose. It is concluded that serum and synovial fluid contain a novel myeloperoxidase inhibitor, which acts by binding to myeloperoxidase and thereby prevents myeloperoxidase releasing oxidative products in serum.