利福喷丁治疗肺结核的疗效观察

目的　验证利福喷丁治疗肺结核病的疗效。方法　采用国产利福喷丁 0 .6每周 2次 ,加用 2～ 4种结核药物为治疗组 ,与利福平组对照。结果　治疗组 92例 ,有效率 85 % ,对照组 84例 ,有效率 81% ,P>0 .0 5无差别。在副作用上 ,治疗组 92例 ,有副作用 9例占 9.7% ,对照组 84例 ,有副作用 17例占 2 0 .2 % ,P<0 .0 5 ,有明显差异。结论　利福喷丁和利福平治疗效果大致相等 ,但前者副作用明显小于后者。     

缩短含利福喷丁短化方案肺结核化疗期的研究

根据治疗后逐月淡涂片检验结果，确定１０４例入选的初治涂阳肺结核使用含利福喷丁化疗方案的治疗期间，探索缩短９个月疗程的可行性。２个月时痰菌转阴率为８３．７％，５个月时痰菌转阴率为９８．１％，６个月时转阴率为１００％，平均化疗期为５．２个月，两年细菌学复发率率为２．０％。表明除少数病人外大多数病人的疗程可以缩短；短化个体化的 进一步缩短化疗期的可行途径。     

国产利福喷丁治疗结核病的系列研究

本研究对利福喷丁采用前瞻性对照研究方法，先后循序渐近地设计了疗程、用药方式和用药间隔不同的１９种方案，疗程从９个月逐步减为５个月；从每周２次用药减为２周１次用药并多角度，多方位地探索Ｌ治疗复治肺结核的作用。初复治患者分别有１４４７例和２３８例完成予定疗程，并进行了３年随访观察，初始含Ｌ组和含Ｒ组满疗程菌阴率分别达９６．１％－１００％，９８．３－１００％，病灶显效率各为６９．１－８６．２％和６９．７     

利福喷丁与利福平对嗜酒肺结核患者肝功能的影响

目的观察利福平（RFP）和利福喷丁（RFT）在治疗嗜酒肺结核患者时肝损害的情况。方法选取嗜酒肺结核患者84例分成RFP方案组（42例）和RFT方案组（42例）进行临床比较。结果84例中发生肝损害41例,其中观察组16例,对照组25例,两组肝损害发生率有显著性差异（P〈0．05）。结论含利福平（RFP）的抗结核方案引起的肝功能损害发生率明显高于含利福喷丁（RFT）的抗结核方案。     

利福喷丁与利福平对肺结核患者肝功能影响的比较

目的比较利福喷丁与利福平对肺结核患者肝功能的影响作用。方法 74例初治肺结核患者随机分为利福喷丁组和利福平组,两组均服用异烟肼,吡嗪酰胺和乙胺丁醇治疗,利福喷丁组(37例)加用利福喷丁治疗,利福平组(37例)加用利福平治疗,观察和比较两组肝功能异常发生率。结果利福平组肝功能异常发生率(18.92%)明显高于利福喷丁组(8.11%)(P<0.05)。结论肺结核患者应优先采用含利福喷丁方案进行治疗。     

国产利福喷丁在肺结核病人体内的药代动力学研究

本文用高效液相色谱法研究7例肺结核病人首剂口服国产利福喷丁600mg后的药代动力学过程.结果为:C_(max)10.63±3.76μg/ml,t~(1/2)18.09±5.53h,tm6.28±2.23h,Ke0.04±0.01h~(-1),AUC351.76±133.2μg·h/ml.临床用药3个月痰结核菌全部阴转.该药适于结核病间歇化疗,是较理想的长效,高效,抗痨新药.     

含左氧氟沙星、利福喷丁化疗方案对复治涂阳肺结核的临床疗效研究

目的：研究含左氧氟沙星、利福喷丁化疗方案对复治涂阳肺结核的临床疗效。方法选择2013年2月至2015年12月在我院进行诊治的复治涂阳肺结核患者100例,随机分为两组。观察组采用含左氧氟沙星、利福喷丁方案治疗,对照组采用含链霉素、利福平方案治疗,比较两组的临床症状改善情况、痰结核菌阴转率及肺部结核病变吸收有效率。结果治疗后,观察组临床症状恢复情况显效41例(82.00%),有效5例(10.00%),无效4例(8.00%),有效率为92.00%;对照组显效30例(60.00%),有效10例(20.00%),无效10例(20.00%),有效率为80.00%;两组比较差异有统计学意义(P <0.05);治疗后,观察组痰结核菌阴转48例(96.00%),对照组痰结核菌阴转41例(82.00%),两组比较差异有统计学意义(P <0.05);治疗后,观察组肺部结核病变吸收显效31例(62.00%),有效14例(28.00%),无效5例(10.00%),有效率为90.00%;对照组显效22例(44.00%),有效13例(26.00%),无效1 5 例(30.00%),有效率为70.00%;两组比较差异有统计学意义(P <0.05)。结论含左氧氟沙星、利福喷丁化疗方案可以有效改善复治涂阳肺结核患者的临床症状,提高肺部结核病变吸收有效率,且不良反应发生率低。     

中国利福喷丁在香港临床研究期间的生物利用度

背景:利福喷丁在香港的临床研究。目的:评价研究中所使用的中国利福喷丁的生物利用度。设计:通过微生物学试验测定给予四批药物的287名病人血清标本中利福喷丁的含量结果:从40名病人中随机分配给西方或中国的利福喷丁所获得的首批曲线区域图对比显示:中国利福喷丁生物利用度是西方药物的74％。第二批药的生物利用度发现是西方的66％,最后二批利福喷丁的剂量由计划的600mg增至750mg或短时增至900mg,则血清中浓度同西方药获得的相类似,在每批药使用期间生物利用度没有变化。结论:通过比较开始二批和最后二批试验的结果将估价利福喷丁剂量对疗效和毒性的作用。     

汉防己甲素肺靶向微球对大鼠低氧性肺动脉高压的急性 …

目的 了解汉防己甲素（Ｔｅｔ）肺靶向微球对低氧性肺动脉高压的治疗效应及其对肺循环的选择性作用。方法 采用喷雾干燥法制备Ｔｅｔ含量为３２％的Ｔｅｔ肺靶向微球;雄性Ｗｉｓｔａｒ大鼠分为３组,每组１０只,分对照组和Ｔｅｔ水溶剂治疗组、Ｔｅｔ肺靶向微球治疗组。经低氧处理３周,分别级予Ｔｅｔ水溶剂和Ｔｅｔ肺靶向微球,观察用药前后大鼠肺动脉平均压（ｍＰＡＰ）和体循环平均压（ｍＳＢＰ）的变化。结果 低氧性肺动脉     

Magnetic targeting of microspheres in blood flow

Magnetically responsive albumin microspheres can be targeted to the vasculature of specific organs, using extracorporeal magnetic sources. Experiments have been performed on targeting these microspheres to specific regions of normal and tumorous rat tails. This paper quantitatively analyzes the relationship between magnetic forces and the observed microsphere holding. The magnetic forces are determined by the magnetic responsiveness of the microspheres, and by the spatial field of the magnet; both of these are measured. The microsphere holding is defined as that fraction of the microspheres perfusing the tail which are held at a particular site; this is measured at various positions in the tail. The holding as a function of magnetic force is thereby established. To interpret the data, the dynamics of microspheres in blood flow is considered, including motion to a vessel wall, shear forces at the wall, and intersphere attraction. Overall, the method appears favorable for targeting therapeutic drugs to tumor sites in humans.     

Reductive effect of lonazolac on lung metastasis formation in mice

The purpose of this study was to determine the antimetastatic potential of lonazolac. Intravenous inoculation of Lewis lung carcinoma (LLC) or melanoma B-16 (B-16) cells induced macroscopically detectable lung metastases on day 15 after inoculation. After pre- and post-treatment with lonazolac-Ca at oral doses of 1, 25, and 50 mg/kg, the numbers of animals with lung metastases and the score of metastases significantly decreased. Lonazolac-Ca had similar effects also on the formation of spontaneous lung metastases. After treatment with lonazolac-Ca at oral daily doses of 1, 25, and 50 mg/kg during 8 days (LLC) or 10 days (B-16) after inoculation of the tumor cells, the number of animals developing spontaneous lung metastases and the score of metastases also decreased. Intravenous injection of lonazolac natrium was effective in protecting the mice inoculated with 1 X 10(6) melanoma B-16 cells against acute pulmonary embolic death.     

Preventive effect of irbesartan on bleomycin-induced lung injury in mice

BackgroundIdiopathic pulmonary fibrosis is a specific form of chronic fibrosing interstitial pneumonia that is limited to the lung. Angiotensin receptor blockers (ARBs) and peroxisome proliferator-activated receptor (PPAR) γ ligands have anti-inflammatory and anti-fibrotic effects. We investigated the effects of irbesartan—an ARB with PPAR γ activity—on the development of bleomycin-induced pulmonary fibrosis in mice.MethodsLung injury was induced in imprinting control region (ICR) mice by intratracheal instillation of 2 mg/kg of bleomycin. The treatment group orally received 20 mg/kg of irbesartan for 5 consecutive days before instillation. The mice were sacrificed and were evaluated 14 days after bleomycin instillation.ResultsIrbesartan reduced the fluid content and hydroxyproline level in the lung and improved the pathological findings as indicated by the Ashcroft score. Total cell counts, the numbers of macrophages, neutrophils, and lymphocytes, and the levels of transforming growth factor (TGF) β1 and monocyte chemotactic protein (MCP) 1 in the bronchoalveolar lavage fluid (BALF) were decreased. Treatment with a PPARγ antagonist GW9662 reversed some of the effects of irbesartan.ConclusionsThe results of this study indicated that irbesartan attenuated the development of bleomycin-induced pulmonary fibrosis in mice by decreasing TGF-β1 and MCP-1 via blocking of ATI, by binding to CCR2b, and by PPARγ-mediated inhibition of inflammation.     

止血敏磁控缓释微球在兔胃的靶向和止血功效

目的：对自行制备的止血敏磁控缓释微球（止血敏微球）进行兔胃靶向试验，观察其靶向和止血效力。方法：用x线摄影观察止血敏微球在兔胃的分布情况，用分光光度法检测靶区的止血敏含量，观察其在兔胃的止血功效。结果：止血敏微球能有效地准确定位于胃靶区，3．0g微球在磁场强度0．49T，梯度0．23T／cm状态下可产生28cm水柱的压力；胃靶区粘摸层止血敏含量检测结果：磁控组、非磁控组和静脉组的平均含量分别为1869ug/g,108ug/g,30ug/g；磁控组是非磁控组的17倍，是静脉组的62倍。经统计学分析，P＜0．01，存在特别显差异。微球可在10min内明显控制兔胃小动脉活动性出血，对照组则需30min以上。结论：止血敏磁控缓释微球有可能成为治疗上消化道大出血的理想药物和一些新的简便而有效的非手术疗法。     

Protective effect of bicyclol on lipopolysaccharide-induced acute lung injury in mice

Bicyclol is synthesized based on schisandrin, which is one of the main active components of Chinese herb Fructus Schisandrae. The purpose of this study is to investigate whether bicyclol has a beneficial effect on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Bicyclol was given to mice by gavage for three times. ALI was induced by vena caudalis injection of LPS. The last dose of bicyclol was administrated 1 h before LPS given. Mice in each group were sacrificed at different time point after LPS administration. As revealed by survival study, pretreatment with high doses of bicyclol reduced the mortality of mice from ALI. Bicyclol pretreatment significantly improved LPS-induced lung pathological changes, inhibited myeloperoxidase (MPO) activity, and reduced lung/body and lung wet/dry weight ratios. Bicyclol also inhibited the release of TNF-α, IL-1β and HMGB1, whereas simultaneously increased the expression of IL-10. Furthermore, the phosphorylation level of NF-κB p65 was markedly decreased by bicyclol. Taken together, our study showed that bicyclol improves survival rate and attenuates LPS-induced ALI. The protective mechanism may be due to the inhibition of NF-κB activation and regulation of cytokine secretion.     

The effect of enoxaparin on bleomycin-induced lung injury in mice.

We have evaluated the effect of enoxaparin, a potent antithrombotic drug, on bleomycin (Bleo)-induced pulmonary inflammation in mice. Pulmonary injury was induced by a single intratracheal (i.t.) instillation of Bleo. Four groups of female C57BL/6 mice, each received one of four treatments: (1) i.t. Bleo and daily intraperitoneal (i.p.) injections of enoxaparin (EN) starting one day before i.t. instillation of Bleo (Bleo-EN); (2) i.t. Bleo and i.p. injections of saline (Bleo-Sal); (3) i.t. saline and i.p. enoxaparin (Sal-EN); (4) i.t. saline and i.p. saline (Sal-Sal). Animals were sacrificed 14 days after i.t. treatment. Lung injury was evaluated by analysis of bronchoalveolar lavage fluid and histologically by an overall semiquantitative index of lung injury and a quantitative image analysis assessing alveolar wall area fraction and fibrosis fraction. Treatment of mice with enoxaparin did not ameliorate Bleo-induced lung injury. Our study does not establish a critical role of procoagulant activity in the evolution of Bleo-induced lung injury and does not support the use of antithrombotic therapy for the prevention of pulmonary fibrosis.     

苯基乙酰对小鼠移植性肺癌的抑制作用及其机制

目的观察苯基乙酰(PG)对肺癌的抑制作用,并探讨其作用机制。方法选择C57BL/6小鼠40只,尾静脉注射肺癌LLC细胞建立肺癌模型。随机将成模小鼠分为PG组、PBS组各20只,PG组腹腔内注射800 mg/kg PG,PBS组腹腔内注射等量PBS,连续10天。两组各随机取5只,计数肺肿瘤个数、测量肿瘤最大直径;各随机取5只,采用Western blotting法观察肺癌组织Bcl-2、Bcl-XL、细胞凋亡抑制蛋白1(c IAP1)、Survivin、增殖细胞核抗原(PCNA)表达。剩余小鼠收集支气管肺泡灌洗液(BALF),取5只小鼠的BALF,检测炎症细胞(包括WBC总数及分类)及炎症因子(TNF-α、IL-6、趋化因子);剩余小鼠的BALF,采用电泳迁移位移试验观察NF-κB DNA结合活力。结果与PBS组比较,PG组肺肿瘤个数和肿瘤最大直径明显减少或降低(P均<0.05)。Western blotting结果显示,PG组Bcl-2、BclXL、c IAP1、Survivin及PCNA表达均明显下调,BALF中巨噬细胞中NF-κB与靶DNA结合活性明显被抑制。与PBS组比较,PG组可显著降低BALF中各种炎性细胞数量及炎症因子水平(P均<0.05)。结论 PG能明显抑制小鼠肺癌的生长,其机制与诱导肿瘤细胞凋亡、抑制巨噬细胞中NF-κB活性、减轻肺部炎症反应有关。     

Cardiac-specific inducible and conditional gene targeting in mice

Mouse genetic engineering has revolutionized our understanding of the molecular and genetic basis of heart development and disease. This technology involves conditional tissue-specific and temporal transgenic and gene targeting approaches, as well as introduction of polymorphisms into the mouse genome. These approaches are increasingly used to elucidate the genetic pathways underlying tissue homeostasis, physiology, and pathophysiology of adult heart. They have also led to the development of clinically relevant models of human cardiac diseases. Here, we review the technologies and their limitations in general and the cardiovascular research community in particular.     

Embryogenesis and gene targeting of coagulation factors in mice

Genetic or acquired thrombophilia of the pregnant mother has been associated with the occurrence of gestational vascular disease and recurrent fetal loss and may contribute to the aetiology of pre-eclampsia. This chapter reviews insights into this link between thrombophilia and pregnancy complications that were gained from the study of genetically altered mice. These studies strongly support the notion of a cause-effect relationship between altered function of the thrombomodulin-protein C pathway and adverse pregnancy outcome. Analysis of the mouse models highlights unique aspects of vascular structure and function at the feto-maternal interface, and exposes new biological functions of natural anticoagulant pathways in pregnancy. These roles are unrelated to the maintenance of vascular patency and may be mediated through specific signalling pathways activated by coagulation factors. Abnormal signalling by placental trophoblasts at the feto-maternal interface is suggested as a hitherto unrecognized mechanism that may underlie adverse pregnancy outcome associated with haemostatic disorders.