佐匹克隆与盐酸曲唑酮治疗睡眠障碍的临床疗效观察

目的观察佐匹克隆与盐酸曲唑酮治疗睡眠障碍的临床疗效和安全性。方法将100例睡眠障碍患者采用随机数字表的方法分为治疗组50例和对照组50例。治疗组给予佐匹克隆治疗,对照组给予盐酸曲唑酮治疗。两组均为睡前30 min给药,疗程4周。比较两组临床治疗效果。结果治疗后,两种药品在延长患者总睡眠时间方面差异无统计学意义[(0.9±0.3)h比(0.9±0.7)h,P>0.05]。佐匹克隆治疗睡眠障碍的入睡时间评分低于盐酸曲唑酮[(0.5±0.2)分比(1.3±0.4)分,P0.05)。治疗组不良反应量表(TESS)低于对照组[(9.45±4.37)分比(12.56±4.62)分,P<0.05]。结论佐匹克隆与盐酸曲唑酮在睡眠障碍的治疗效果上疗效一致。但佐匹克隆药物不良反应更低,容易被患者接受。国家自然科学基金资助项目(81670224

CD_(39)在心肌缺血再灌注中的心脏保护作用的研究进展

腺苷循环的活化是缺血再灌注内在重要的病理生理学机制。CD_(39)[1]为膜外二三磷酸核苷水解酶.1(E.NTPDase-1),将细胞外的ATP(三磷酸腺苷)、ADP(二磷酸腺苷)水解产生AMP(一磷酸腺苷),参与腺苷循环的代谢,在缺血再灌注中如肾脏、心脏等起重要的作用。本文通过对CD_(39)的心脏保护作用的研究进展和现状作一综述,特别是在心肌缺血再灌注的发生发展中,以期能全面展示CD_(39)在心肌缺血再灌注损伤中的的应用和前景

运动性横纹肌溶解症2例诊治分析

运动性横纹肌溶解症在1971年首先被提出,主要是指由于剧烈运动后肌纤维崩解断裂从而导致肌细胞内容物释放入血液引起的一系列临床综合征,以肌肉肿痛、全身乏力、排酱油色尿及血中肌酸激酶和肌红蛋白的含量增高为主要临床特征

冠脉介入诊疗与痛风发作的相关性研究进展

冠脉介入诊疗后引起痛风的急性发作在临床工作中越来越常见,虽总体数量较少,但这一现象的出现值得引起临床工作者的重视,通过了解其产生机制及相关因素可以帮助我们识别高危患者,进而采用适当的诊疗方法,快速诊断及治疗,降低发病率,减轻患者的痛苦。国家自然科学基金资助项目(项目编号:81670224

极化液治疗急性心肌梗死研究的进展

极化液(gIk)作为调节代谢的一种溶液组合,最早是由SOdI-PAllArES等人提出用来保护缺血心肌的。有实验证实gIk可降低急性心肌梗死(AMI)患者死亡率,也有实验表明gIk对AMI患者毫无作用,甚至增加早期AMI患者死亡率。本文就gIk在AMI中的作用做一篇综述。国家自然科学基金资助项目(81170090);福建省自然科学杰出青年基金(2009D015);厦门市杰出青年科技人才创新计划项目(3502Z20116009);厦门市科技局科研基金(3502Z20094006

STUDIES ON IONIC MECHANISMS OF THE EFFECTS OF ISOPROTERENOL ON BRUGADA SYNDROME

Conference Name:22nd Great Wall International Congress of Cardiology/Asia Pacific Heart Congress (GWICC and APHF). Conference Address: Beijing, PEOPLES R CHINA. Time:OCT 13-16, 2011

小G蛋白在心肌钠通道蛋白转运中的作用

目的研究小G蛋白Sar1和Arf1对钠通道蛋白(Nav1.5)转运的调控作用。方法以HEK293细胞作为宿主细胞,将人SCN5A基因转染到HEK293细胞中,通过G418筛选稳定表达SCN5A基因的细胞系;为了检测小G蛋白对Nav1.5的调节效应,野生型或突变型的小G蛋白Sar1和ARF1分别瞬转到HEK293-Nav1.5细胞。利用免疫印迹对目标蛋白进行定量,应用免疫荧光对细胞内的目标蛋白进行定位。结果过表达突变的Sar1减少了细胞膜上Nav1.5的表达和抑制了Nav1.5转运到细胞膜上。另外,过表达ARF1对于Nav1.5在细胞的表达及定位无明显影响。结论小G蛋白Sar1可能参与调节Nav1.5在细胞内的运输。福建省自然科学基金资助项目(2015J01563

Human Cytomegalovirus Linked to Stroke in a Chinese Population

National Natural Science Foundation of China [81170244, 81170090]; Beijing Nova Program [2009B39]; Beijing Natural Science Foundation [7102057]; Science Foundation for Distinguished Young Scholars of Fujian Province [2009D015]; Science Foundation for Distinguished Young Scholars of Xiamen [3502Z20116009]Aim: Human cytomegalovirus (HCMV) is implicated in several cardiovascular disorders, including atherosclerosis, coronary heart disease, and cardiac transplant arteriopathy. We aimed to evaluate the relationship between HCMV and stroke. Methods: Real-time polymerase chain reaction (PCR) and ELISA were performed on plasma samples isolated from 200 patients diagnosed with stroke and 200 controls. All participants belonged to the Stroke Hypertension Investigation in Genetics (SHINING) study. Results: HCMV seropositivity was higher in the stroke group than in controls (55.0% vs. 23.5%; P < 0.0001). The presence of HCMV DNA increased the risk of stroke (unadjusted odds ratio [OR], 3.98; 95% confidence interval [CI], 2.59 to 6.11; P < 0.0001). Risks were also increased for the subtypes ischemic stroke (unadjusted OR, 4.01; 95% CI, 2.576.24; P < 0.0001) and hemorrhagic stroke (unadjusted OR, 3.80; 95% CI, 1.648.78; P= 0.0018). Increased risk with HCMV remained significant after adjustment for age, sex, body mass index, hypertension, and smoking (ischemic stroke: adjusted OR, 4.07; 95% CI, 2.526.32; P < 0.0001; hemorrhagic stroke: adjusted OR, 3.88; 95% CI, 1.619.36; P= 0.0026). Conclusions: We demonstrate a novel link between HCMV infection and stroke. These findings may provide important insights into the pathogenesis of stroke

Effects of Simvastatin on Glucose Metabolism in Mouse MIN6 Cells

Chinese National Science Foundation [81170090]The aim of this study was to investigate the effects of simvastatin on insulin secretion in mouse MIN6 cells and the possible mechanism. MIN6 cells were, respectively, treated with 0 mu M, 2 mu M, 5 mu M, and 10 mu M simvastatin for 48 h. Radio immunoassay was performed to measure the effect of simvastatin on insulin secretion in MIN6 cells. Luciferase method was used to examine the content of ATP in MIN6 cells. Real-time PCR and western blotting were performed to measure the mRNA and protein levels of inward rectifier potassium channel 6.2 (Kir6.2), voltage-dependent calcium channel 1.2 (Ca(v)1.2), and glucose transporter-2 (GLUT2), respectively. ATP-sensitive potassium current and L-type calcium current were recorded by whole-cell patch-clamp technique. The results showed that high concentrations of simvastatin (5 mu M and 10 mu M) significantly reduced the synthesis and secretion of insulin compared to control groups in MIN6 cells (P < 0.05). ATP content in simvastatin-treated cells was lower than in control cells (P < 0.05). Compared with control group, the mRNA and protein expression of Kir6.2 increased with treatment of simvastatin (P < 0.05), and mRNA and protein expression of Ca(v)1.2 and GLUT2 decreased in response to simvastatin (P < 0.05). Moreover, simvastatin increased the ATP-sensitive potassium current and reduced the L-type calcium current. These results suggest that simvastatin inhibits the synthesis and secretion of insulin through a reduction in saccharometabolism in MIN6 cells