痛风汤剂益肾养肝合剂治疗痛风性肾病33例临床观察

目的: 探讨痛风汤剂与益肾养肝合剂同用治疗痛风性肾病的临床疗效.方法: 将痛风性肾病患者58例分为两组,治疗组33例予痛风汤剂加益肾养肝合剂治疗,对照组25例只予痛风汤剂治疗.观察两组治疗前后血尿酸,肾功能,血、尿β2-微球蛋白指标的变化.结果: 治疗组在改善临床症状、肾功能,降低血尿酸、尿β2-微球蛋白(β2-MG)方面均优于对照组.结论: 对痛风性肾病患者的治疗,痛风汤剂与益肾养肝合剂同用扶正祛邪的治疗方法较好,能够改善肾小管功能.     

厄贝沙坦与黄芪注射液联合治疗肾性蛋白尿疗效观察

目的:观察厄贝沙坦与黄芪注射液联合治疗对肾性蛋白尿的影响.方法:将80例慢性肾病患者分为A组(对比组)和B组(治疗组),A组为常规治疗:低盐、低蛋白饮食、控制感染、控制血压等;B组在常规治疗的基础上,给予厄贝沙坦与黄芪注射液治疗.观察治疗1个月前后24h尿量、24h尿蛋白定量、血肌酐、血尿素和血浆白蛋白的变化.结果:B组治疗后24h尿量明显增加,P＜0.01,有非常显著差异;24h尿蛋白减少,P＜0.05,有显著差异;血浆白蛋白增加,P＜0.05,有显著差异.结论:厄贝沙坦与黄芪注射液联合治疗能明显减少尿蛋白.     

4-甲基-香豆素及4-甲基喹啉-2(1H)-酮的7位羟基、巯基与炔丙基卤代物的不同反应性

目的合成具有抗HIV活性的三环杂环化合物的关键中间体.方法 7-羟基-4-甲基-香豆素、7-羟基-4-甲基喹啉-2(1H)-酮、7-巯基-4-甲基-香豆素分别与3-氯-3-甲基-1-丁炔、3-溴丙炔反应得到相应产物,其结构经波谱确证.结果 4-甲基-香豆素的7位羟基发生正常的双分子亲核取代反应(SN2),得到炔丙基醚产物4、7和10,进一步热环合得到三环杂环化合物5、8和11;7-巯基-4-甲基-香豆素、7-巯基-4-甲基喹啉-2(1H)-酮与3-氯-3-甲基-1-丁炔反应分别得丙二烯醚双分子亲核取代反应(SN2′)产物聚集双键硫醚化合物12和14,且不能进一步热环合成三环杂环.结论 4-甲基-香豆素及4-甲基喹啉-2(1H)-酮的7位羟基、巯基与炔丙基卤代物表现出不同的反应性.     

青岛市麻疹流行病学分析与监测状况评价

目的 分析2003年青岛市麻疹流行现况及麻疹监测系统报告资料，获得青岛市麻疹的流行特点并探索麻疹发病的主要影响因素，初步评价青岛市麻疹监测系统运转情况，为改善青岛市麻疹防制和监测工作提供依据。方法 采用酶联免疫吸附试验(ELISA)检测IgM和IgG抗体。结果 青岛市2003年各区市麻疹发病以散发为主，麻疹病例相对集中的4个地区分别是位于城乡结合部的黄岛区、崂山区、李沧区和城阳区，麻疹病例占总数的66．67％，发病高峰主要为3、4月，病例多集中于15-24岁年龄段人群。结论 青岛市麻疹发病以成人为主，城乡结合部发病较集中，其中拥挤程度和人员流动性是影响青岛市麻疹发病的主要因素。今后青岛市麻疹的防制和监测工作重点应进行相应的调整，加强对成年麻疹发病的免疫干预，并进一步完善监测样本采集和流调信息的完整。     

高效液相色谱法测定灯盏花素注射液含量

目的 :建立高效液相色谱法测定灯盏花素注射液含量的方法。方法 :色谱柱 μ- Bondapak C1 8钢柱 ( 4 .6 mm×2 0 0 mm,10μm) ,流动相为甲醇 -水 ( 6 0∶ 4 0 ) ,流速为 0 .6 ml/ min,检测波长 335 nm。结果 :灯盏花素注射液在 10 .0～ 5 0 .0mg/ L浓度范围内 ,线性关系良好 ,r=0 .9996 ,平均加样回收率为 10 0 .31% ,RSD为 1.19% ( n =6 )。结论 :本法简便 ,结果准确 ,可用于灯盏花素注射液的质量控制     

秦皮总香豆素致突变作用研究

目的评价秦皮总香豆素的致突变性。方法应用Ames试验、小鼠骨髓微核试验对秦皮总香豆素进行了致突变研究。结果秦皮总香豆素在受试剂量40～20000μg/皿范围内,各剂量组各菌株与阴性对照组比较均未见回变菌落数明显增加。秦皮总香豆素三个试验剂量组微核率均在正常范围内,经卡方检验与阴性对照组比较无显著性差异(P>0.05)。结论本实验条件下秦皮总香豆素无致突变作用。     

浅论企业药品召回管理规范的制定

结合中美史克公司召回康泰克的经验,浅谈企业药品召回管理规范的制定.     

Oxalate-induced ceramide accumulation in Madin-Darby canine kidney and LLC-PK1 cells

BACKGROUND: Oxalate exposure produces oxidant stress in renal epithelial cells leading to death of some cells and adaptation of others. The pathways involved in these diverse actions remain unclear, but appear to involve activation of phospholipase A2 (PLA2) and redistribution of membrane phospholipids. The present studies examined the possibility that oxalate actions may also involve increased accumulation of ceramide, a lipid-signaling molecule implicated in a variety of pathways, including those leading to apoptotic cell death. METHODS: Ceramide accumulation was examined in renal epithelial cells from pig kidney (LLC-PK1 cells) and from dog kidney [Madin-Darby canine kidney (MDCK cells)] using the diacylglycerol kinase assay. Sphingomyelin degradation was assessed by monitoring the disappearance of 3H-sphingomyelin from cells that had been prelabeled with [3H]-choline. The effects of oxalate were compared with those of other oxidants (peroxide, xanthine/xanthine oxidase), other organic acids (formate and citrate), and a known activator of sphingomyelinase in these cells [tumor necrosis factor-alpha (TNF-alpha)]. Separate studies determined whether oxalate-induced accumulation of ceramide could be blocked by pretreatment with antioxidants [Mn (III) tetrakis (1-methyl-4-pyridyl) porphyrin (Mn TMPyP, a superoxide dismutase mimetic) or N-acetylcysteine (NAC; an antioxidant)], with an inhibitor of ceramide synthase [fumonisin B1 (FB1)] or with an inhibitor of PLA2 [arachidonyl trifluoromethylketone (AACOCF3)]. RESULTS: Oxalate exposure produced a significant time- and concentration-dependent increase in cellular ceramide. A reciprocal decrease in 3H-sphingomyelin was observed under these conditions. Increases in cellular ceramide levels were also observed after treatment with other oxidants (hydrogen peroxide, and xanthine/xanthine oxidase), activators of sphingomyelinase (TNF-alpha), exogenous sphingomyelinase, or arachidonic acid. Formate produced similar (albeit smaller) effects, and citrate did not. The oxidant-induced increases in ceramide were attenuated by pretreatment with NAC (a glutathione precursor) and MnTMPyP (a superoxide dismutase mimetic), suggesting a role for cellular redox states. The oxalate-induced increase in ceramide was also attenuated by pretreatment with AACOCF3, suggesting a role for PLA2. Pretreatment with FB1 produced a small but statistically insignificant attenuation of the response to oxalate. CONCLUSIONS: Oxalate exposure produces a marked accumulation of ceramide in renal epithelial cells by a process that is redox sensitive and mediated in part by activation of PLA2. Since cellular sphingomyelin decreased as ceramide increased, it seems likely that oxalate actions are mediated, at least in part, by an increase in sphingomyelinase activity, although alterations in ceramide synthase are also possible. Further study is required to define the steps involved in oxalate actions and to determine the extent to which ceramide signaling mediates oxalate actions.     

Recombinant human insulin-like growth factor-1 induces an anabolic response in malnourished CAPD patients

BACKGROUND: Insulin-like growth factor-1 (IGF-1) is an anabolic hormone that mediates most of the growth effects of growth hormone. This study tested the hypothesis that recombinant human IGF-1 (rhIGF-1) will induce an anabolic response in malnourished patients undergoing continuous ambulatory peritoneal dialysis (CAPD). METHODS: Six CAPD patients with protein-energy malnutrition underwent nitrogen balance studies in a clinical research center for 35 days each. Throughout the study, patients were maintained on their same CAPD regimen prior to hospitalization, and were fed a constant protein and energy intake that was similar to their diet prior to hospitalization. The first 15 hospital days were a baseline period; during the subsequent 20-day period, patients were given subcutaneous injections of rhIGF-1 (100 microg/kg/12 h), except for one patient who received 50 microg/kg/12 h for the first five days, followed by 100 microg/kg/12 h for the following 15 days. RESULTS: During the treatment with rhIGF-1, serum IGF-1 increased by about 100% (P = 0.03), and nitrogen balance became strongly positive (+2.0 g/day, P = 0.015 vs. baseline). This anabolic effect was observed within hours after commencing the rhIGF-1 treatment and was largely caused by a 20% decrease in peritoneal dialysate effluent nitrogen. There was a proportionate reduction in urine nitrogen and serum urea nitrogen. This decrease in nitrogen output was sustained during the entire 20 day of treatment with rhIGF-1. Serum phosphorus decreased significantly during the first several days of rhIGF-1 treatment, whereas serum calcium increased significantly during the rhIGF-1 treatment. Serum potassium and albumin did not change during the rhIGF-1 injections. There was no change in body weight and body composition, as assessed by anthropometry during the baseline or treatment phases of the study. Some patients exhibited minor possible adverse events that included a reduction in blood pressure and transient tachycardia. CONCLUSION: Injections of rhIGF-1 induce a strong and sustained anabolic effect, as indicated by a positive nitrogen balance in CAPD patients with protein-energy malnutrition. rhIGF-1 administration may be an effective method for treating malnutrition in maintenance dialysis patients.