环丙沙星与氧氟沙星联用抗结核药物肝毒性比较

目的　研究环丙沙星或氧氟沙星联用抗结核药的肝毒性并探讨其机制。方法　分别测定异烟肼和利福平联合用药 (IR)组及其分别联用氧氟沙星 (IRO)或环丙沙星 (IRC)组小鼠的血清谷氨酸氨基转移酶 (ALT)、肝指数、肝匀浆丙二醛 (MDA)含量、肝微粒体细胞色素P45 0和线粒体Ca2 ATP酶活性 ,及肝病理检查 ,结果与对照组以及实验组之间进行比较。结果　与正常对照组比较 ,IR组及IRO组的血清ALT、肝细胞匀浆MDA明显增高 (P <0 .0 5 ) ,而IRC组变化不大 (P >0 .0 5 ) ;同时发现IR组和IRO组的肝微粒体细胞色素P45 0含量较高和线粒体Ca2 ATP酶活性较低 ,而IRC组则相反 ;病理检查IRO和IRC组肝细胞坏死程度稍轻但与IR组比较无明显差异。结论　氧氟沙星、环丙沙星不增加异烟肼和利福平联用肝毒性 ,且环丙沙星有一定的拮抗作用。     

女性输卵管结扎术后腰痛病机及医疗体育疗法

对女性输卵管结扎术后腰痛进行调查和病理分析 ,以中药配合医疗体育康复治疗术后腰痛 ,取得较好疗效 ,并提出预防措施。     

脂肝清对高胆固醇血症家兔模型脂质代谢影响的实验研究

目的: 明确中药脂肝清对高脂血症防治作用,探讨其作用机制。方法: 以饲喂高脂饲料复制高胆固醇血症家兔模型,观察血清和肝脂质代谢,并且采用脂肝清进行预防实验,同时与一类降脂药洛伐他汀 (Lovastatine)作对照。结果: 1)中药明显降低血清TC、LDL C、TC/HDL C比值 (P<0.01或P<0.05),降低血清氨基转移酶活力 (P<0.01).2)中药明显降低肝TC、TG及LDL C含量。结论: 脂肝清具有调整血清脂质代谢,促进肝组织中脂质的排泄及保护肝功能等作用。     

脾虚证与益气健脾治疗对T、B淋巴细胞活性影响的实验观察

为探讨脾虚证机体特异性免疫应答的变化及益气健脾中药的影响,采用利血平注射法复制脾虚证模型,观察分别代表细胞与体液免疫功能的T、B淋巴细胞活性变化、血清IgG,IgM的水平及益气健脾基本方剂四君子汤对它们的影响,结果脾虚证模型大鼠T细胞转化率及B细胞分泌的IgM水平显著降低,通过灌服四君子汤可明显预防两者的降低,因而认为脾虚证细胞与体液免疫均降低,而以细胞免疫的降低为主,益气健脾中药具有明显防治作用。     

蒙药广枣总黄酮对大鼠离体心脏功能的影响

目的：探讨广枣总黄酮(TFC)对心功能的影响。方法：采用Langendorff灌流法．用多导生理记录仪测定大鼠离体心脏的心率、心肌收缩力及心电图的变化。结果：TFC使正常灌流的大鼠离体心脏心电图的P—R问期延长．心率减慢．心肌收缩力增强;对缺氧灌流所导致的心率减慢和心脏收缩力减弱均呈明显的对抗作用。结论：TFC可改善心功能。     

临床常用药物对人体酸碱平衡的影响

目的：探讨临床常用药物对人体酸碱平衡的影响,指导临床工作。方法：用酸度计测定九种药品ｐＨ值,计算氢离子浓度。结果：偏碱性的药物有５０ｇ／Ｌ碳酸氢钠,谷氨酸钠、谷氨酸钾注射液;偏酸性的药物有盐酸精氨酸、维生素Ｃ、各种浓度葡萄糖注射液、氯化钠注射液。结论：临床上一些常用药品会影响人体的酸碱平衡,尤其在机体酸碱平衡调节发生障碍的情况下,更应谨慎。     

朱丹溪善用风药治疗血证谈

复习朱丹溪有关医学文献 ,阐发其应用风药治疗血证的机制 ,主要有 :风药直接止血 ;风药升阴散火止血 ;风药散火解毒、凉血止血 ;风药炒黑止血 ;风药振脾益气止血 ;祛除致病因素 ;其它。     

中西医结合防治围化疗期消化道损伤

目的：寻找化疗诱导胃肠粘膜损伤的保护方法。方法：对荷Ｈ２２腹水癌小鼠化疗前后分别给与健脾益气中药、肠生态制剂（以岐杆菌和地衣芽直菌）、中西医结合（中药和肠生态制剂联合）方法防治消化道损伤。检测胃肠膜病理,用流式细胞仪检测Ｈ２２腹水癌细胞凋亡,ＭＴＴ比色法检测杀伤作用,骨髓图片检测骨髓增生相。结果：中西医结合组较单纯化疗组对胃肠粘膜有保护作用明显增强化疗对Ｈ２２腹水癌细胞的杀伤和促进凋亡,减轻胃肠粘     

联合给药法治疗强直性脊柱炎

目的 采用氨甲喋呤（ＭＴＸ）、抑氮磺胺吡啶（ＳＡＳＰ） 非甾体类药（ＮＳＡＩＤｓ）“递减法”联合给药治疗７８例强直性脊柱炎（ＡＳ的临床疗效观察。方法 ＳＡＳＰ０．５ｇ,２次／日,服１周后改为０．７５ｇ,２次／日,第２周后改为１．０ｇ,２次／日,以后每周１．０ｇ,２次／日,疗程２年,ＭＴＳ５ｍｇ,１次／周,每周递增５ｍｇ,加量至１５～２０ｍｇ／周时维持０．５～１年,ＮＳＡＩＤｓ疗程为３个月左右减半量     

The cell cycle and induction of apoptosis in a hamster fibrosarcoma cell line treated with anti-cancer drugs: Its importance to solid tumour chemotherapy*

The induction of apoptosis by anticancer drugs and its relationship to stages of the cell cycle was studied in cells derived from a solid tumour; a highly malignant hamster fibrosarcoma (Met B). Asynchronously proliferating cells were treated with a wide variety of agents such as actinomycin-D, 1--D-arabinofuranosyl cytosine, camptothecin, cisplatin, cyclophosphamide, daunorubicin, 5-flurouracil, 6-mercaptopurine, hydroxyurea, ionomycin, methotrexate and vincristine. With the exception of cyclophosphamide and hydroxyurea, a 36 h exposure to these drugs resulted in inhibition of cell growth and apart from cyclophosphamide, hydroxyurea, 6-mercaptopurine and cisplatin the induction of apoptosis. Studies using a decreased concentration of drug and exp osure time (12 h) followed by examination of cells using flow cytometry indicated that most drugs were capable of affecting cell cycle progression without induction of apoptosis. However when cells were synchronised at G₀/G₁, S and G₂/M phases and then exposed to these decreased concentrations of drug apart from 6MP an HU, apoptosis was observed and for the majority of drugs it took place in the same phase in which progression through the cell cycle was blocked by the drug. Cells synchronised in G₀/G₁ phase were more susceptible to methotrexate, whereas S-phase cells were more susceptible to camptothecin and 5-flurouracil and G₂/M phase cells more susceptible to actinomycin D, 1--D-arabinofuranosyl cytosine, daunorubicin and cisplatin. In contrast, vincristine blocked cells in G₂/M phase but exerted its apoptotic effect in S-phase cells, ionomycin had no effect on the cell cycle, but G₂/M cells appeared to be more susceptible to the effect of this drug. These data indicate that entry into apoptosis by this fibrosarcoma may occur at any point in the cell cycle. They also demonstrate a correlation between the action of some anticancer drugs on the cell cycle and the subsequent induction of apoptosis which may be useful in chemotherapeutic design.