阿托伐他汀预处理对心肌缺血再灌注损伤大鼠心室重构、炎症反应和氧化应激的影响

目的:研究阿托伐他汀预处理对心肌缺血再灌注损伤大鼠心室重构、炎症反应和氧化应激的影响.方法:选取90只SD级大鼠进行研究,将其随机分成假手术组、缺血再灌注组、阿托伐他汀组,每组30只.假手术组与缺血再灌注组大鼠予以生理盐水(5 mL/d)连续灌胃7d处理,阿托伐他汀组予以阿托伐他汀20 mg/(kg-d)连续灌胃7 d...     

A region of calpastatin domain L that reprimes cardiac L-type Ca2+ channels

Calpastatin, an endogenous inhibitor of calpain, is composed of domain L and four repetitive homologous domains 1-4. Domains 1-4 inhibit calpain, whereas domain L partially reprimes L-type Ca2+ channels for voltage-gated activation. In the present study, the effects on Ca2+ channel activity of four isoforms and a series of fragments of calpastatin domain L were investigated in guinea-pig ventricular myocytes with the patch-clamp method. With one exception, all the isoforms and fragment peptides that contained amino acid residues 54-64 of domain L reprimed the Ca2+ channels to comparable levels (9-15% of control activity) to those observed previously with a full-length form of calpastatin. These results suggest that the region containing amino acid residues 54-64 (EGKPKEHTEPK) is responsible for the Ca2+ channel repriming function of calpastatin domain L.     

维拉帕米对急性前壁心肌梗死行急诊PCI术患者再灌注室性心律失常的影响

目的:探讨经指引导管早期应用维拉帕米对急性前壁心肌梗死行急诊经皮冠状动脉介入治疗术(Percutaneous Coronary Intervention,PCI)患者再灌注室性心律失常的影响。方法:采用单中心、随机对照、前瞻性研究方法。选取2014年5月-2016年11月诊断为急性前壁心肌梗死并于我院行急诊PCI的患者,共纳入162例患者,按随机方法(随机数字表)分成2组,其中治疗组82例,对照组80例。治疗组患者在首次球囊扩张后早期经指引导管内给予维拉帕米(200μg),对照组患者则给予生理盐水。观察再灌注后室性心律失常发生率,PCI术后冠脉血流情况,心肌梗死相关血清指标(CK-MB,cTn I)的峰值,住院期间发生的主要不良心血管事件(MACE)。结果:维拉帕米治疗组患者再灌注心律室性失常及无复流的发生率显著低于生理盐水对照组(P0.05);维拉帕米治疗组患者cTnI和CK-MB峰值分别为(46.63±13.77)μg/L和(139.87±35.45)U/L,生理盐水组cTnI和CK-MB峰值为(54.36±12.59)μg/L和(158.34±40.18)U/L,两组比较,P均0.01。MACE事件两组间未见有统计学差异。结论:急性前壁心肌梗死患者急诊PCI术前经导管早期给予维拉帕米不但可显著减少无复流现象,还可显著减少再灌注后室性心律失常的发生,住院期间MACE事件的发生率无显著性差异。     

Kinetic Monte Carlo simulation for the striation distribution of void defects in Czochralski silicon growth

Unique crystal-originated pit (COP) distribution, similar to a striation pattern, is well matched with the oxygen profile in experimental analysis. It shows the strong relationship between oxygen concentration and COP distribution. In this paper, we study the generation of void defects and the relationship between interstitial oxygen and vacancy using the kinetic lattice Monte Carlo (KLMC) method. The KLMC method has been applied extensively in various forms to the study of micro-defects in silicon wafers. It explained well the formation of void defects such as vacancy–oxygen complex and vacancy–vacancy complex. The formation of clusters is strongly affected by oxygen concentration, which showed the relationship between COP distribution and oxygen concentration. The unique COP distribution could be correctly explained with KLMC results, and this kind of meso-scale results has not yet been reported.     

随机、平行对照评价陶瓷膜室间隔缺损封堵器安全性和有效性

目的:随机、平行对照的临床试验验证先健科技(深圳)有限公司生产的TM陶瓷膜VSD封堵器治疗室间隔缺损的安全性及有效性。方法:根据试验的要求入选术前确诊为室间隔缺损的病人42例,随机分为实验组(A组)和对照组(B组),每组各21例,对A组病人植入CeraTM陶瓷膜VSD封堵器,对B组病人植入普通镍钛合金VSD封堵器,在超声心动图下或X线下观察室间隔缺损大小、位置、形态、类型,选择合适的封堵伞,经输送系统置入封堵器闭合VSD,分别于术前、术后24小时、术后30天、90天及术后180天进行随访,主要随访内容包括临床症状和体征、超声心动图、心电图、胸片、24小时动态心电图检查等。比较这两组患者的即刻手术成功率以及随访过程中终点事件发生率的不同。结果:试验组和对照组的成功率均为100%,残余分流率分别为0和4.8%,试验组的并发症发生率与对照组未见明显差异(P0.005)。结论:试验组与对照组安全性与疗效相当,应用国产陶瓷封堵器是安全、有效的。但由于该项技术是一项新技术,临床试验样本量较少,其安全性和疗效特别是中远期疗效仍需进一步观察。     

影响侧脑室脑膜瘤手术疗效的多因素分析

目的：探讨影响侧脑室脑膜瘤手术疗效的因素,从而更好的促进侧脑室脑膜瘤的手术治疗。方法：回顾性分析侧脑室脑膜瘤显微手术30例的临床病理特征与顸后情况,其中KPS〉70分表示为预后良好,KP懿70分表示为预后不良。对各性别、年龄、部位、肿瘤大小、病理分型及术后有无并发症因素与预后进行χ^2检验与用Logistic回归分析其影响因素。结果：单因素分析表明肿瘤部位、病理分型及术后有无并发症对侧脑室脑膜瘤的预后有明显影响,P〈0．05,差异有统计学意义。经Logistic回归分析,最终进入模型的影响因素有2个,它们分别是肿瘤部位和术后有无并发症,其P值均小于0．05。结论：在显微手术下,侧脑室脑膜瘤大部分可以全切并取得了较好的远期疗效。肿瘤部位和术后有无并发症是影响预后的一个重要因素,及时处理并发症能显著地改善预后。     

富士Ⅱ玻璃离子充填材料修复楔状缺损的临床疗效观察

目的：比较富士Ⅱ玻璃离子与普通玻璃离子充填材料修复楔状缺损的临床疗效：方法：58例患者324颗楔状缺损患牙随机分为2组,分别用富士Ⅱ玻璃离子（实验组）和普通玻璃离子材（对照组）进行修复,观察修复后半年、一年和两年的充填效果。结果：富士Ⅱ玻璃离子和普通玻璃离子充填材料的成功率0．5年分别为98．15％、87．04％;1年分别为93．83％、71．25％;2年分别为89．38％、58．60％,修复后0．5年、1年、2年相比差异均有有显著性,（P〈0．01）。结论：富士Ⅱ玻璃离子充填材料修复楔状缺损效果好,是充填楔状缺损较理想的材料。     

Mechanisms of the acute ischemia-induced arrhythmogenesis--a simulation study

The underlying ionic mechanisms of ischemic-induced arrhythmia were studied by the computer simulation method. To approximate the real situation, ischemic cells were simulated by considering the three major component conditions of acute ischemia (elevated extracellular K(+) concentration, acidosis and anoxia) at the level of ionic currents and ionic concentrations, and a round ischemic zone was introduced into a homogeneous healthy sheet to avoid sharp angle of the ischemic tissue. The constructed models were solved using the operator splitting and adaptive time step methods, and the perturbation finite difference (PFD) scheme was first used to integrate the partial differential equations (PDEs) in the model. The numerical experiments showed that the action potential durations (APDs) of ischemic cells did not exhibited rate adaptation characteristic, resulting in flattening of the APD restitution curve. With reduction of sodium channel availability and long recovery of excitability, refractory period of the ischemic tissue was significantly prolonged, and could no longer be considered as same as APD. Slope of the conduction velocity (CV) restitution curve increased both in normal and ischemic region when pacing cycle length (PCL) was short, and refractory period dispersion increased with shortening of PCL as well. Therefore, dynamic changes of CV and dispersion of refractory period rather than APD were suggested to be the fundamental mechanisms of arrhythmia in regional ischemic myocardium.     

CLASP Mediates Microtubule Repair by Restricting Lattice Damage and Regulating Tubulin Incorporation

1. Download : Download high-res image (225KB)
2. Download : Download full-size image

     

Inhibition of proliferation and differentiation and promotion of apoptosis by cyclin L2 in mouse embryonic carcinoma P19 cells

Cyclin L2 (CCNL2) is a novel member of the cyclin gene family. In a previous study, we demonstrated that CCNL2 expression was upregulated in ventricular septum tissues from patients with ventricular septal defect compared to healthy controls. In the present study, we established a stable CCNL2-overexpressing P19 cell line that can differentiate to myocardial cells when treated with 1% dimethyl sulfoxide (DMSO). Our data showed that stable CCNL2-overexpressing P19 cells were less differentiated after treatment with 1% DMSO and that expression of myocardial cell differentiation-related genes (such as cardiac actin, GATA4, Mef2C, Nkx2.5, and BNP) were reduced compared to vector-only transfected P19. Moreover, P19 cells overexpressing the CCNL2 gene had a reduced growth rate and a remarkably decreased S phase. We also found that these cells underwent apoptosis, as detected by two different apoptosis assays. The anti-apoptotic Bcl-2 protein was also downregulated in these cells. In addition, real-time PCR analysis revealed that expression of Wnt and β-catenin was suppressed and GSK3β was induced in the CCNL2-overexpressing P19 cells. These data suggest that overexpression of CCNL2 inhibited proliferation and differentiation of mouse embryonic carcinoma P19 cells and induced them to undergo apoptosis, possibly through the Wnt signal transduction pathway.