灵芝多糖对小鼠黑素瘤细胞的体外抑制作用

目的：探讨灵芝多糖在体外对小鼠黑素瘤B16F10细胞株的抑制作用。方法：以小鼠黑素瘤B16F10细胞株为研究对象,用MTT法检测灵芝多糖对肿瘤细胞增殖的影响,流式细胞仪检测细胞毒作用。结果：经灵芝多糖作用后黑素瘤B16F10细胞增殖活性受抑,细胞死亡增多。结论：灵芝多糖可抑制B16F10细胞的增殖,促进细胞死亡。     

前列腺增生的尿液蛋白质组学分析

目的在临床前列腺特异性抗原(prostate-specific antigen,PSA)升高的情况下,特别是前列腺特异性抗原在4μg/L至10μg/L时,前列腺增生和前列腺癌的鉴别诊断很难,本实验对前列腺增生患者、前列腺癌患者和健康对照的尿液蛋白质双向凝胶电泳图谱进行对比分析,旨在较全面的分析其成分,为临床鉴别诊断提供依据。方法用丙酮沉淀蛋白的方法对前列腺增生患者、前列腺癌患者和健康对照尿液中的蛋白质进行浓缩,再用双向凝胶电泳技术分离蛋白质样品,CANON G9照相获取图像,PDQuest2D分析软件对图像进行背景消减、斑点检测、匹配、斑点位置重复性的系统分析,寻找差异表达蛋白质。在此基础上用基质辅助激光解吸电离飞行时间质谱(MALIDI-TOF)进行肽指纹图谱鉴定,并进行生物信息学分析。结果通过前列腺增生、前列腺癌和健康对照尿液双向凝胶电泳图的对比分析,获得前列腺增生差异蛋白质点,选取其中20个做质谱和生物信息学分析,最终分离鉴定出血清白蛋白、视黄醇结合蛋白前体等17种有效蛋白。结论通过实验条件的优化,应用蛋白质组学方法分析前列腺增生患者尿液蛋白质的组成成分是可行的,为研究前列腺增生患者尿液检测特异标志物提供了基础资料,为今后鉴别前列腺增生和前列腺癌提供了有益的依据,同时也为解决临床误诊难题提供了思路。     

Drug-eluting stent implantation could be associated with long-term coronary endothelial dysfunction

Drug-eluting stent (DES) implantation may be associated with endothelial dysfunction. However, changes in long-term endothelial function based on the type of DES remain largely unknown. We assessed coronary endothelial function after DES implantation compared to bare-metal stents (BMS) and determined the differences according to DES type. Patients who had single BMS or DES implantation in the left anterior descending artery and showed no restenosis in follow-up angiography at 6 to 9 months were assigned to the BMS group (5 patients) or DES group (9 sirolimus-eluting stents, SES, and 8 paclitaxel-eluting stents, PES). Endothelium-dependent vasomotion, after intracoronary infusion of acetylcholine, was determined by quantitative coronary angiography. Also, endothelium-independent vasomotion was assessed after nitrate infusion. In the distal and far distal segments, the SES (SES versus BMS, distal: -27.6 +/- 16.3% versus -0.6 +/- 1.6%; P = 0.01, far distal: -24.8 +/- 13.2% versus -0.9 +/- 1.3%; P = 0.02) and PES groups (PES versus BMS, distal: -25.4 +/- 17.1% versus -0.6 +/- 1.6%; P = 0.01, far distal: -26.6 +/- 15.9% versus -0.9 +/- 1.3%; P = 0.01) had similar patterns showing significant vasoconstriction compared with the BMS group. In addition, the DES group showed a significant reduction of diameter in distal (SES: P = 0.001, PES: P = 0.04) and far distal segments (SES: P = 0.002, PES: P = 0.001) compared with proximal and near proximal segments. However, the BMS group did not demonstrate significantly different vasomotion between proximal and distal segments. Vasodilatation by nitrate infusion was preserved in all subjects. SES or PES implantation could be associated with the similar pattern of endothelial dysfunction identified predominantly in the long distal portion of the treated vessel.     

Hepatic vena cava disease: Etiologic relation to bacterial infection

Aim: Hepatic vena cava disease is a primary obliterative disease of the hepatic portion of the inferior vena cava (IVC) that often causes liver cirrhosis and hepatocellular carcinoma. Its geographic prevalence is inversely related to the standard of community hygiene. The disease is endemic in Nepal and is commonly associated with bacterial infection. The cause of the disease is not known. It was previously thought to be congenital. Thrombosis due to hypercoagulable condition is suggested as a possible cause of the disease. This study looks at the relation of the disease to bacterial infection. Methods: Ultrasonography is sensitive and specific for the diagnosis of acute and chronic lesions of hepatic vena cava disease. Patients attending the Liver Clinic with pyrexia with and without bacteremia were examined by ultrasonography for acute "thrombophlebitic" lesion of the IVC, and five patients with bacterial infection with acute lesion in the hepatic portion of the IVC were followed. Results: Sixty eight percent of the patients with bacteremia had ultrasonographic evidence of acute lesion in the hepatic portion of the IVC, compared to 18% patients without bacteremia. A follow-up study of five patients showed transformation of the acute lesion into chronic obliterative lesion - stenosis or complete obstruction. Conclusion: Bacterial infection is probably the cause of hepatic vena cava disease seen in developing countries.     

Effect of adding sitagliptin, a dipeptidyl peptidase-4 inhibitor, to metformin on 24-h glycaemic control and beta-cell function in patients with type 2 diabetes

AIM: The aim of this study was to assess the effect of sitagliptin, a dipeptidyl peptidase-4 inhibitor, on 24-h glucose control when added to the regimen of patients with type 2 diabetes who had inadequate glycaemic control on metformin therapy. METHODS: In a double-blind, randomized, placebo-controlled, two-period crossover study, patients with type 2 diabetes with inadequate glycaemic control on metformin monotherapy (i.e. on a stable dose of > or = 1500 mg/day for > or = 6 weeks prior to the screening visit and an haemoglobin A(1c) (HbA(1c)) > or = 6.5% and <10% and fasting plasma glucose (FPG) < or = 240 mg/dl) were recruited for participation. A total of 28 patients (baseline HbA(1c) range = 6.5-9.6%) receiving metformin were randomized into one of two treatment sequences: the addition of placebo for 4 weeks followed by the addition of sitagliptin 50 mg twice daily (b.i.d.) for 4 weeks, or vice versa. At the end of each treatment period, patients were domiciled for frequent blood sampling over 24 h. The primary endpoint was 24-h weighted mean glucose (WMG) and secondary endpoints included change in FPG, mean of 7 daily self-blood glucose measurements (MDG) and fructosamine. beta-cell function was assessed from glucose and C-peptide concentrations were measured during the 5-h period after a standard breakfast meal by using the C-peptide minimal model. RESULTS: Despite a carryover effect from period 1 to period 2, the combined period 1 and period 2 results for glycaemic endpoints were statistically significant for sitagliptin relative to placebo when added to ongoing metformin therapy. To account for the carryover effect, the period 1 results were also compared between the groups. Following period 1, there were significant least-squares (LS) mean reductions in 24-h WMG of 32.8 mg/dl, significant LS mean reduction from baseline in MDG of 28 mg/dl, FPG of 20.3 mg/dl and fructosamine of 33.7 mmol/l in patients treated with sitagliptin relative to placebo (p < 0.05). When added to ongoing metformin therapy, parameters of beta-cell function were significantly improved with sitagliptin compared with placebo. No weight gain or increases in gastrointestinal adverse events or hypoglycaemia events were observed with sitagliptin relative to placebo during this study. CONCLUSIONS: In this study, the addition of sitagliptin 50 mg b.i.d. to ongoing metformin therapy improved 24-h glycaemic control and beta-cell function, and was generally well tolerated in patients with type 2 diabetes.