依贝沙坦对心肌梗死后大鼠心肌Smad表达及心室重构的影响

目的研究依贝沙坦对心肌梗死后大鼠心肌Smad表达及心室重构的影响.方法冠状动脉结扎建立大鼠心肌梗死(MI)模型,24 h后存活大鼠随机分为安慰剂组和依贝沙坦组,另设假手术组.8周后,测量心室重量/体重(HW/BW),非梗死区胶原含量,梗死区、非梗死区心肌转化生长因子(TGF)β1mRNA、Smad3 mRNA的表达,多普勒超声评价心脏功能.结果安慰剂组与假手术组比较HW/BW、左心室舒张末期内径(LVDd)、E/A比值、非梗死区胶原含量、梗死区及非梗死区FGFβ1 mRNA、Smad3 mBNA的表达均增加;射血分数(EF)、短轴缩短率(FS)、后壁(PW)增厚率均降低.依贝沙坦组与安慰剂组比较,上述指标显著改善.结论TGF-β-Smad传导通路可能参与MI后的心室重构,依贝沙坦可抑制Smad表达并减轻MI后左室重构.     

贝那普利及依贝沙坦对大鼠心肌纤维化的作用

目的研究血管紧张素转换酶抑制剂(angiotensin converting enzyme inhibitor,ACEI)和血管紧张素Ⅱ受体拮抗剂(angiotensin II receptor blocker,ARB)对心肌梗死(myocardial infarction,MI)后大鼠结缔组织生长因子(connective tissue growth factor,CTGF)和纤溶酶原激活抑制物-1(plasminogen activator inhibitor-1,PAI-1)表达及胶原沉积的影响。方法通过冠状动脉结扎建立wistar大鼠MI模型,分为假手术组(n=9),安慰剂组(n=6),ACEI组[贝那普利10mg/(kg.d)n=8],ARB组[依贝沙坦50mg/(kg.d),n=8]和ACEI ARB组[贝那普利10mg/(kg.d) 依贝沙坦50mg/kg.d,n=8),于术后8周处死大鼠,行心脏超声检查、检测胶原含量、分别采用逆转录多聚酶链反应和Western blot检测大鼠心肌转化生长因子β1(transforming growth factorβ1,TGFβ1)、CTGF、PAI-1mRNA和蛋白的表达。采用方差分析和Turkey's检验进行统计学分析。结果(1)与假手术组比较,安慰剂组射血分数和短轴缩短率明显降低,左室舒张末直径和E/A升高(均为P<0.01);与安慰剂组比较,ACEI组、ARB组和ACEI ARB组射血分数(P<0.01)和短轴缩短率(P<0.05)升高,左室舒张末直径和E/A降低(P<0.05)。(2)与假手术组比较,安慰剂组的心室重量/体重和胶原总量显著升高(P<0.01);与安慰剂组比较,ACEI组、ARB组和ACEI ARB组重量/体重下降(P<0.05),胶原总量明显降低(P<0.01);与ACEI组比较,ARB组和ACEI ARB组胶原总量降低更为显著(P<0.01)。(3)与假手术组比较,安慰剂组TGFβ1、CTGF、PAI-1基因mRNA、蛋白表达明显升高(mRNA为0.69±0.07,0.60±0.07和0.61±0.06,P<0.01;蛋白为9.07±0.63,0.58±0.06,1.03±0.07,P<0.01),ACEI组,ARB组和ACEI ARB组可降低这三种基因表达,联合用药较ACEI和ARB单药治疗更有效地降低mRNA基因表达;与ACEI组比较,ARB组和ACEI ARB组降低蛋白表达更为显著。结论在心肌纤维化过程中,CTGF和PAI-1对细胞外基质过量沉积起主要作用,贝那普利和依贝沙坦通过抑制此作用阻止纤维化发生。与单用贝那普利相比,依贝沙坦单独用药和二者联合应用对阻止心肌纤维化更有效。     

福辛普利和非络地平逆转原发性高血压左室肥厚的对比研究

目的 :对比研究福辛普利和非络地平逆转原发性高血压 (EH)左室肥厚的作用。方法 :将 10 4例EH伴左室肥厚的患者随机分为福辛普利组和非络地平组 ,于服药前及服药后 6个月、12个月、2 4个月分别测定左室舒张末内径 (LVDT)、舒张期室间隔厚度 (IVST)、左室后壁厚度 (LVPWT)、左室射血分数 (LVEF)、心排量 (CO)、A峰 /E峰比值 (A/E比值 )。结果 :两组治疗前后比较LVEF、CO均无变化 ,而A/E比值则明显降低 ;左室重量指数 (LVMI)、LVDd、IVST、LVPDWT在福辛普利组明显下降 ,而在非络地平组则无变化。结论 :福辛普利和非络地平均能明显改善左室舒张功能 ,但福辛普利能明显减轻左室肥厚。     

培多普利逆转肾血管性高血压大鼠心肌肥厚及对心功能的影响

目的探讨血管紧张素转换酶抑制剂—培多普利在逆转两肾一夹高血压大鼠心肌肥厚过程中对心功能的影响。方法两肾一夹法制作肾性高血压大鼠模型,通过心脏超声和心室内插管,以射血分数(EF)和左室短轴缩短率(FS)、零负荷下等容收缩期心肌纤维收缩成分的最大缩短速度(Vmax)作为心脏收缩功能指标,以左心室舒张末压(LVEDP),等容舒张期压力下降的时间常数(T)作为心脏舒张功能指标。结果培多普利在逆转心肌肥厚同时,可使心肌肥厚时升高的LVEDP、T值下降,同时对心脏EF、FS和Vmax值无明显影响。结论培多普利在逆转两肾一夹高血压大鼠心肌肥厚同时,可改善大鼠心脏舒张功能。     

福辛普利和非络地平逆转原发性高血压左室肥厚的对比研究

目的：对比研究福辛普利和非络地平逆转原发性高血压（EH）左室肥厚的作用。方法：将104例EH伴左室肥厚的患者随机分为福辛普利组和非络地平组，于服药前及服药后6个月、12个月、24个月分别测定左室舒张末内径（LVDT）、舒张期室间隔厚度（IVST）、左室后壁厚度（LVPWT）、左室射血分数（LVEF）、心排量（CO）、A峰／E峰比值（A／E比值）。结果：两组治疗前后比较LVEF、CO均无变化，而A／E比值则明显降低；左室重量指数（LVMI）、LVDd、IVST、LVPDWT在福辛普利组明显下降，而在非络地平组则无变化。结论：福辛普利和非络地平均能明显改善左室舒张功能，但福辛普利能明显减轻左室肥厚。     

伊贝沙坦对心肌梗死后心室重塑的影响

目的观察伊贝沙坦对急性心肌梗死(AMI)后心室重塑的阻抑作用.方法将72例AMI患者随机分为常规治疗组36例、伊贝沙坦治疗组36例,并于AMI后2周、24周分别测定室间隔厚度(IVST)、左室后壁厚度(LVPWT)、左室舒张末内径(LVDd)、左室心肌重量指数(LVMI)、左室射血分数(LVEF)、心输出量(CO)、A峰/E峰比值(A/E比值)、A峰速度(PAV)和E峰速度(PEV).结果 2周时,伊贝沙坦组与常规治疗组比较,上述各参数均无变化(P＞0.05).24周时,伊贝沙坦组与常规治疗组比较,IVST、LVPWT、LVDd和LVMI均显著降低(P＜0.05,或P＜0.01),LVEF、CO、PEV均显著增加(P＜0.05,或P＜0.01),A/E比值和PAV均显著降低(P＜0.05,或P＜0.001).结论伊贝沙坦能明显减轻心肌梗死后心肌肥厚和左室重塑,改善左室功能.     

伊贝沙坦对心肌硬死后心室重塑的影响

目的：观察伊贝沙坦对急性心肌梗死（AMI）后心室重塑的阻抑作用。方法：将72例AMI患者随机分为常规治疗组36例、伊贝沙坦治疗组36例，并于AMI后2周、24周分别测定室间隔厚度（IVST）、左室后壁厚度（LVPWT）、左室舒张末内经（LVDd）、左室心肌重量指数（LVMI）、左室射血分数（LVEF）、心输出量（CO）、A峰／E峰比值（A／E比值）、A峰速度（PAV）和E峰速度（PEV）。结果：2周时，伊贝沙坦组与常规治疗组比较，上海各参数均无变化（P＞0．05）。24周时，伊贝沙坦组与常规治疗组比较，IVST、LVPWT、LVDd和LVMI均显著降低（P＜0．05，或P＜0．01），LVEF、CO、PEV均显著增加（P＜0．05，或P＜0．01），A／E比值和PAV均显著降低（P＜0．05，或P＜0．001）。结论：伊贝沙坦能明显减轻心肌梗死后心肌肥厚和左室重塑，改善左室功能。     

超声心动图评价高血压病患者左心功能

目的运用超声心动图技术综合评价高血压病患者左室收缩功能和舒张功能。方法高血压病组56例和对照组36例,M-型和二维(2D)超声心动图检测:左房内径(LAd),舒张期室间隔厚度(IVST)和左室后壁厚度(PWT),左室舒张末期内径(LVDd),二尖瓣EF斜率,室间隔及左室后壁运动幅度,左室射血分数(EF),左室短轴缩短率(FS),每搏量(SV);脉冲多普勒(PW)检测二尖瓣口舒张早期充盈峰速度(VE),舒张晚期充盈峰速度(VA),E/A比值,等容舒张时间(IVRT)。结果高血压病患者左室壁与室间隔收缩期运动幅度普遍增强,与对照组比较P<0.01;左室收缩功能各项参数(EF、FS、SV)高于对照组(P<0.05),高血压病组左室舒张功能各参数异常,表现为VE减低,VA升高,E/A<1,IVRT延长,MV-EF斜率减慢,与对照组比较P<0.001;左房扩大(P<0.001)。结论超声心动图技术可反映高血压病患者左心结构和功能变化,为临床诊治提供客观依据。     

不同剂量卡维地洛对急性心肌梗死大鼠左室重构及血流动力学的影响

目的比较不同剂量卡维地洛对大鼠急性心肌梗死(AMI)后左室重构及血流动力学的影响。方法选取AMI术后存活的SD大鼠随机分为AMI组、卡维地洛大剂量组[30mg/(kg.d)]、卡维地洛小剂量组[2mg/(kg.d)]。给药6周后用导管法行血流动力学测定和心脏组织病理分析。另设正常对照组及假手术组。结果与假手术组比,AMI组左室舒张末压(LVEDP)、各心室重量均显著增加,左室内压最大收缩和舒张速率(±dp/dtmax)显著降低。与AMI组比,大、小剂量卡维地洛组的LVEDP、心室重量均显著降低,±dp/dtmax显著升高。与卡维地洛大剂量组比,小剂量组LVEDP及左心室重量下降更明显。结论卡维地洛疗能有效抑制大鼠AMI左室重构并改善血流动力学,且小剂量卡维地洛组疗效优于大剂量组。     

二维超声斑点追踪成像评估大鼠不同程度心肌损伤的应用价值

目的 探讨基于二维超声斑点追踪成像(2D-STI)技术的左心室整体环向应变及应变率参数评估急性心肌梗死大鼠不同程度心肌损伤的应用价值.方法 55只Wistar大鼠随机分为急性心肌梗死组(MI组)45只和假手术组(SO组)10只.MI组大鼠随机分为MI15组、MI30组和MI60组各15只,分别钳夹冠状动脉左前降支15 min、30 min、60 min,以建立不同梗死面积的急性心肌梗死模型.各组大鼠分别于基础状态和恢复灌注24 h后行超声心动图检查,记录左室乳头肌短轴高帧频二维图像,应用EchoPAC工作站分析获得左室乳头肌短轴整体收缩期峰值环向应变(GSc)和应变率(GSRc)值,并采用解剖M型测量左室舒张末期内径(LVIDd)和收缩末期内径(LVIDs)、短轴缩短率(FS)、射血分数(EF).实验结束后处死大鼠取出心脏行TTC染色并计算左室乳头肌短轴的梗死面积(AN).结果 ①MI15组、MI30组和MI60组的LVIDd和LVIDs测值均较基础状态和假手术组明显增加,FS和EF测值明显降低;MI60组的LVIDd和LVIDs测值均较MI15和MI30组明显增大,FS和EF测值明显降低(P<0.05);②MI15组、MI30组和MI60组GSc和GSRc测值均较假手术组明显减低;MI组的GSc和GSRc测值随缺血时间延长而显著降低(P<0.05);③GSc和GSRc与AN显著相关(P<0.01),相关系数分别为0.90和0.88;GSc和GSRe参数是AN的显著预测因子(P<0.01),标准回归系数(Beta)分别为0.558和0.491;④TTC染色显示AN随缺血时间延长而显著增加(P<0.05).结论 基于2D-STI技术的左室整体环向应变及应变率随心肌梗死面积增加而显著降低,该参数可准确评价急性心肌梗死后不同程度心肌损伤.     

Migraine and genetic and acquired vasculopathies

It is remarkable that migraine is a prominent part of the phenotype of several genetic vasculopathies, including cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL), retinal vasculopathy with cerebral leukodystrophy (RVCL) and hereditary infantile hemiparessis, retinal arteriolar tortuosity and leukoencephalopahty (HIHRATL). The mechanisms by which these genetic vasculopathies give rise to migraine are still unclear. Common genetic susceptibility, increased susceptibility to cortical spreading depression (CSD) and vascular endothelial dysfunction are among the possible explanations. The relation between migraine and acquired vasculopathies such as ischaemic stroke and coronary heart disease has long been established, further supporting a role of the (cerebral) blood vessels in migraine. This review focuses on genetic and acquired vasculopathies associated with migraine. We speculate how genetic and acquired vascular mechanisms might be involved in migraine.     

Fibrinogen and fibrin structure and functions

Fibrinogen molecules are comprised of two sets of disulfide-bridged Aalpha-, Bbeta-, and gamma-chains. Each molecule contains two outer D domains connected to a central E domain by a coiled-coil segment. Fibrin is formed after thrombin cleavage of fibrinopeptide A (FPA) from fibrinogen Aalpha-chains, thus initiating fibrin polymerization. Double-stranded fibrils form through end-to-middle domain (D:E) associations, and concomitant lateral fibril associations and branching create a clot network. Fibrin assembly facilitates intermolecular antiparallel C-terminal alignment of gamma-chain pairs, which are then covalently 'cross-linked' by factor XIII ('plasma protransglutaminase') or XIIIa to form 'gamma-dimers'. In addition to its primary role of providing scaffolding for the intravascular thrombus and also accounting for important clot viscoelastic properties, fibrin(ogen) participates in other biologic functions involving unique binding sites, some of which become exposed as a consequence of fibrin formation. This review provides details about fibrinogen and fibrin structure, and correlates this information with biological functions that include: (i) suppression of plasma factor XIII-mediated cross-linking activity in blood by binding the factor XIII A2B2 complex. (ii) Non-substrate thrombin binding to fibrin, termed antithrombin I (AT-I), which down-regulates thrombin generation in clotting blood. (iii) Tissue-type plasminogen activator (tPA)-stimulated plasminogen activation by fibrin that results from formation of a ternary tPA-plasminogen-fibrin complex. Binding of inhibitors such as alpha2-antiplasmin, plasminogen activator inhibitor-2, lipoprotein(a), or histidine-rich glycoprotein, impairs plasminogen activation. (iv) Enhanced interactions with the extracellular matrix by binding of fibronectin to fibrin(ogen). (v) Molecular and cellular interactions of fibrin beta15-42. This sequence binds to heparin and mediates platelet and endothelial cell spreading, fibroblast proliferation, and capillary tube formation. Interactions between beta15-42 and vascular endothelial (VE)-cadherin, an endothelial cell receptor, also promote capillary tube formation and angiogenesis. These activities are enhanced by binding of growth factors like fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factor (VEGF), and cytokines like interleukin (IL)-1. (vi) Fibrinogen binding to the platelet alpha(IIb)beta3 receptor, which is important for incorporating platelets into a developing thrombus. (vii) Leukocyte binding to fibrin(ogen) via integrin alpha(M)beta2 (Mac-1), which is a high affinity receptor on stimulated monocytes and neutrophils.     

Telemedicine and teleradiology technologies and applications

Summary. Telemedicine and teleradiology hold the key for improving future health care delivery. In this paper we first review current communication and computer technologies used in telemedicine and teleradiology. Five examples in teleradiology applications are given including hospital-integrated picture archiving and communication systems, tele-neuro-imaging, telemammography, university consortium teleradiology service, and teleradiology for second opinion. Parameters important to teleradiology applications like costs, image quality, system reliability, and turn around time are considered. Data security is discussed, including patient confidentiality and image authenticity-which will be a major issue in future teleradiology applications.     

创伤高血糖与感染和MODS早期诊断和干预

本文详细介绍了创伤后血糖应激适度理论,以及高血糖与感染和多器官功能不全综合征的关系;提出涉及胰岛B细胞功能不全的MODS实验诊断新方案和极化液个体化干预新措施,可早期发现创伤MODS、降低感染率及MODS发生率和病死率。     

腹膜后纤维化与肾积水发生关系的临床研究

目的：探讨腹膜后纤维化（RPF）导致肾积水的原因及诊治经验。方法：回顾分析2004年1月—2010年12月24例腹膜后纤维化致肾积水患者的诊治资料。结果：（1）RPF患者常见首发症状为腰背痛或腹痛（69.2%）;（2）红细胞沉降率（ESR）增快和血清IgG4升高最常见。超声检查仅提示上尿路积水。RPF的静脉肾盂造影（IVP）和CT尿路成像（CTU）表现具有特征性。IVP肾盂输尿管显影不良时,CTU能较清晰的显示上尿路影像。CT扫描发现腹膜后软组织肿块9例（37.5%）,优于超声检查;（3）输尿管松解和腹腔化手术治疗22例;行肾切除术1例;行输尿管置双J管术1例。最终确诊为继发性RPF8例,其中4例为术前诊断,3例为术中腹膜后软组织肿块冷冻活检证实,1例为术后病理证实;（4）特发性RPF手术后肾积水均获长期缓解,而继发性RPF的预后取决于原发疾病及其治疗方案。结论：影像学检查是诊断RPF的重要手段,CTU优于超声检查和IVP。输尿管松解和腹腔化手术可以使特发性RPF输尿管梗阻得到长期的缓解,术中对肿块进行冷冻活检有助于鉴别特发性和继发性RPF,及时调整治疗方案。     

探讨儿童慢性顽固性咳嗽与支原体感染的关系及临床治疗观察

目的探讨儿童慢性顽固性咳嗽与肺炎支原体（MP）感染的关系及临床疗效观察。方法采用回顾性研究方法对于现将2005年3月至2008年3月在我院的55例确诊慢性顽固性咳嗽患儿,主要表现为肺炎支原体感染为临床特点进行分析,并进一步临床治疗研究。结果①临床特点：在55例确诊慢性咳嗽的患儿中,以慢性顽固性咳嗽为主要症状。58％（32／55）的病例无肺部体征;②外周血：85％（47／55）的病例外周血变化不大,WBC（4—10）×10 9／L之间,嗜酸性粒细胞增多;③特别检查：47．27％（26／55）肺炎支原体IgM（MP—IgM）抗体阳性,83．64％（46／55）PeR技术检测肺炎支原体特异性DNA;④X光报告为多种形式。结论肺炎支原体（MP）感染是引起儿童慢性顽固性咳嗽的病因之一,对儿童慢性咳嗽,特别是顽固性咳嗽的诊治中应更加重视。     

Acetaminophen and acetylcysteine dose and duration: Past,present and future

Abstract

Acetylcysteine has been utilized successfully in the treatment of acetaminophen overdose since the 1970s. Although prospective trials as to efficacy and safety of acetylcysteine were conducted, there were no randomized controlled trials. This commentary addresses the reasons for this, and the background to choice of dose of acetylcysteine utilized in the oral and IV dosing regimens. Nomograms to predict possible hepatotoxicity based upon time of ingestion of acetaminophen were developed from a relatively arbitrary definition of toxicity as an aspartate aminotransferase/alanine aminotransferase (ALT/AST) greater than 1000 IU/L. While these have proved generally useful, patients still continue to develop hepatic damage after acetaminophen overdose, particularly if they present late after ingestion. The optimum management of these patients remains unclear, and one area of uncertainty is the dose and duration of acetylcysteine in various circumstances. This article discusses the issues that need to be elucidated to better target changes in acetylcysteine dose. The potential for measurements of other markers to improve treatment selection is the subject of further research.     

VEGF和NSE在良恶性嗜铬细胞瘤中的表达及意义

目的探讨肿瘤标志物血管内皮生长因子（VEGF）和神经元特异性烯醇化酶（NSE）在良、恶性嗜铬细胞瘤组织中的表达,分析其可能的临床价值及病理学意义,为临床鉴别良、恶性嗜铬细胞瘤提供辅助依据。方法应用免疫组化（SP法）检测16例恶性嗜铬细胞瘤、18例良性嗜铬细胞瘤及17例正常肾上腺髓质组织中细胞因子VEGF和NSE表达情况,显微镜下判断组织切片的染色结果。结果①恶性嗜铬细胞瘤VEGF表达明显强于正常肾上腺髓质和良性嗜铬细胞瘤（P〈0.01）。良性肿瘤和正常肾上腺髓质的VEGF表达差异无统计学意义（P〉0.05）。恶性嗜铬细胞瘤强阳性率明显高于良性嗜铬细胞瘤（P〈0.01）。②良、恶性嗜铬细胞瘤NSE表达差异有统计学意义（P〈0.05）,良性嗜铬细胞瘤NSE的表达高于正常肾上腺髓质的NSE表达（P〈0.05）。恶性嗜铬细胞瘤强阳性率高于良性嗜铬细胞瘤（P〈0.05）。③VEGF和NSE共同阳性表达在良、恶性嗜铬细胞瘤之间差异有统计学意义（P=〈0.01）。结论临床上检测VEGF和NSE可能为鉴别良、恶性嗜铬细胞瘤提供辅助依据,共同检测VEGF和NSE可能提高良、恶性嗜铬细胞瘤鉴别的敏感性。