急性心肌梗死患者血浆BNP、ET、CRP、ANP水平变化与临床观察分析

目的　观察急性心肌梗死 (AMI)患者血浆中B型钠尿肽 (BNP)、内皮素 (ET)、C 反应蛋白 (CRP)、A型钠尿肽 (ANP)水平变化 ,为治疗及预后判断提供依据。方法　应用酶联免疫法及免疫放射分析法对 4 6例AMI患者治疗前后和 30名正常对照者血浆中BNP、ET、CRP、ANP水平进行检测。结果　AMI患者血浆中BNP、ET、CRP、ANP治疗前后比较差异有显著性 (P <0 .0 0 1) ,正常对照组与AMI治疗前比较差异有显著性 (P<0 .0 0 1) ,BNP与CRP在AMI治疗前水平呈正相关 (r =0 .874 ) ,治疗后呈明显的下降趋势 (r =0 .6 5 4 ) ,AMI治疗前后ANP与ET呈正相关 ,但AMI经溶栓和相应的支持治疗后ANP基本恢复到正常水平 (P >0 .0 5 ) ,而BNP、ET、CRP水平虽然下降明显 ,但与正常组比较差异仍有显著性 (P <0 .0 5 )。结论　AMI患者血浆中BNP、ANP、ET、CRP水平的变化说明其参与了AMI的发生、发展 ,特别是冠状动脉粥样斑块的形成和 (或 )破裂及血栓形成 ,其炎症因子是主要因素。因此 ,4项指标的观察分析对AMI治疗、预后判断具有重要意义     

冠心病患者血浆内皮素血栓素B2和6-酮-前列腺素F1α变化的临床研究

目的　探讨内皮素(ET)、血栓素B2(TXB2)和6-酮-前列腺素F1α(6-keto-PGF1α)的变化在冠心病发病中的作用及临床意义。方法　采用放射免疫分析方法对不稳定性心绞痛(UA)组(n=23)、急性心肌梗死(AMI)组(n=20)、及正常对照组(n=20)血浆ET、TXB2和6-keto-PGF1α浓度同时进行测定。结果　UA组心绞痛发作期分别较终止后对照组、AMI组溶栓前分别较溶栓后及对照组ET和TXB2升高(P<001),6-keto-PGF1α降低(P<001和005);AMI组溶栓前ET和TXB2高于UA组心绞痛发作期(P<001),6-keto-PGF1α则无差异(P>005),AMI组溶栓后较UA组心绞痛终止后ET和6-keto-PGF1α无差异(P>005),UA组心绞痛终止后及AMI组溶栓后TXB2仍高于对照组(P<001),6-keto-PGF1α低于以照组(P<001和005),ET则无差异(P>005)。血浆ET浓度的升高与TXB2/6-keto-PGF1α比值呈正相关(AMI组:r=081P<001;UA组:r=068,P<001)结论　内皮素、TXB2/6-keto-PGF1α代谢失调导致了冠状动脉痉挛和血栓形成,三者共同参与了冠心病的发病,是诱发心绞痛的重要原因。内皮素和TXB2/6-keto-PGF1α可能通过相互作用加速UA向AMI的转化。     

内皮素与P-选择素在冠心病中的意义

目的研究内皮素 (endothelin 1,ET 1)、P 选择素和肌钙蛋白I(CTnI)在急性心肌梗死 (acutemyocardialinfarction ,AMI)和不稳定性心绞痛 (unstableangina ,UA)中的意义。 方法用放射免疫法测定ET 1,流式细胞仪测定P 选择素 ,Access化学发光法测定CTnI ,共检测 2 3例AMI患者 ,2 1例UA患者及 2 8例健康对照者。结果AMI组的ET 1、P 选择素和CTnI值均明显高于对照组 (P <0 .0 5— 0 .0 1) ;UA组的ET 1、P 选择素高于对照组 (P <0 .0 5 ) ;UA组的CTnI与对照组无显著性差异 (P >0 .0 5 ) ;UA组的P 选择素、CTnI低于AMI组 (P <0 .0 5 )。多元回归分析发现P 选择素与CTnI相关 ,相关系数r =0 .40 4,(P <0 .0 1)。结论ET 1、P 选择素是检测血栓前状态的敏感指标。     

sCD40L与急性冠脉综合征的相关性研究

目的:研究血清sCD40L水平与冠状动脉粥样硬化严重程度是否相关。方法:对不稳定型心绞痛(UA)患者进行Braunwald分级,对急性心肌梗死(AMI)患者心脏功能进行Killip分级,对冠状动脉粥样硬化病变程度按照病变支数按Gensini评分进行量化评估,用酶联免疫吸附法检测血清sCD40L水平;用SPSS13.0软件包进行统计学分析。结果:急性冠脉综合征(ACS)组sCD40L水平高于正常对照组及稳定型心绞痛组(P<0.01);AMI组sCD40L水平高于UA组(P<0.05)。冠状动脉三支及双支病变组SCD40L水平高于单支病变组(P<0.05);ACS组sCD40L水平与冠状动脉病变数量呈Pearson正相关(r=0.216,P=0.002);sCD40L与Gensini评分呈正相关(r=0.321,P=0.001)。结论:sCD40L水平可能是急性冠状动脉综合征临床识别和预测疾病严重程度的炎症指标。     

白细胞介素17、高敏C反应蛋白、白细胞计数联合检测在急性心肌梗死中的意义

目的观察白细胞介素17(IL-17)、高敏C反应蛋白(hs-CRP)、白细胞计数(WBC)在急性心肌梗死(AMI)患者血清中的水平变化及相关性,了解IL-17与AMI发病的关系。方法 95例患者分为3组:急性心肌梗死(AMI)40例,不稳定型心绞痛(UA)31例,胸痛综合征(CPS)24例。患者入院后立即留取静脉血标本离心,存于-80℃的冰箱,采用ELISA法集中检测患者血清中的IL-17、hs-CRP水平,并急诊送检白细胞计数水平。结果 AMI组外周血清IL-17水平明显高于UA组和CPS组(P<0.01);AMI组患者hs-CRP水平明显高于UA组和CPS组(P<0.05);AMI组患者WBC明显高于UA组和CPS组(P<0.01);相关性分析提示IL-17与hs-CRP(r=0.364,P<0.01)及WBC水平(r=0.302,P=0.004)均呈正相关。结论在AMI患者血清中IL-17水平明显升高,与hs-CRP、WBC呈正相关,推测IL-17与动脉粥样硬化斑块不稳定性有关,促进了AMI的发生发展。     

急性心肌梗死患者血浆BNP、ET、CRP、ANP水平变化与临床观察分析

目的观察急性心肌梗死(AMI)患者血浆中B型钠尿肽(BNP)、内皮素(ET)、C-反应蛋白(CRP)、A型钠尿肽(ANP)水平变化,为治疗及预后判断提供依据.方法应用酶联免疫法及免疫放射分析法对46例AMI患者治疗前后和30名正常对照者血浆中BNP、ET、CRP、ANP水平进行检测.结果 AMI患者血浆中BNP、ET、CRP、ANP治疗前后比较差异有显著性(P<0.001),正常对照组与AMI治疗前比较差异有显著性(P<0.001),BNP与CRP在AMI治疗前水平呈正相关(r=0.874),治疗后呈明显的下降趋势(r=0.654),AMI治疗前后ANP与ET呈正相关,但AMI经溶栓和相应的支持治疗后ANP基本恢复到正常水平(P>0.05),而BNP、ET、CRP水平虽然下降明显,但与正常组比较差异仍有显著性(P<0.05).结论 AMI患者血浆中BNP、ANP、ET、CRP水平的变化说明其参与了AMI的发生、发展,特别是冠状动脉粥样斑块的形成和(或)破裂及血栓形成,其炎症因子是主要因素.因此,4项指标的观察分析对AMI治疗、预后判断具有重要意义.     

脑梗死患者血中一氧化氮与血小板功能

目的：研究脑梗死患者血中一氧化氮（NO）含量与血小板功能之间的关系及临床意义。方法：将20例脑梗死患者分为发病初期组,缓解期组,正常对照组15例,采用硝酸还原酶法测NO含量;用血小板聚集凝血因子分析仪和流式细胞仪分别测定血小板聚集率（PAgT)和血小板α－颗粒膜蛋白（GMP－140）的含量。结果：血清中NO水平在发病初期较正常对照组明显增高（P＜0．01）。同时,血小板PAgT明显减低,与正常对照有显著差异（PADP＜0．05,PADR＜0．01）;GMP－140在发病初期和稳定期减低,较正常对照都有显著性差异（P＜0．01）。结论：实验结果表明,脑梗死患者发病初期随着血中NO水平的增高,PAgT受抑,GMP－140水平减低。认识上述病理变化对脑梗死发病机制的探讨有着重要意义。同时提示NO含量,PAgT,GMP－140测定可作为脑梗死患者诊断,治疗及预后观察的一项客观指标。     

尼莫地平对急性脑梗死患者血小板活化和内皮功能的影响

目的：观察尼莫地平对急性脑梗死患者血小板活化状态和血管内皮细胞功能的影响。方法：轻、中度急性脑梗死患者，随机分为川芎嗪组和尼莫地平两组，川芎嗪组在常规治疗的基础上，加用川芎嗪120mg入液静点。尼莫地平组加用尼莫地平4mg入液静点，连用2周后，分别改为口服川芎嗪100mg，每日3次和尼莫地平30mg，每日3次，总疗程4周，于治疗前后测定血小板α颗粒膜蛋白（GMP－140）、血浆血栓调节蛋白（TM）和内皮素（ET－1）的含量。另选择30例查体健康者做为正常组。结果：治疗前，急性脑梗死患者血小板GMP－140和血浆TM、ET－1水平显著高于正常组，且与病情程度密切相关。治疗后，两治疗组GMP－140、TM和ET－1水平显著下降，尼莫地平组较川芎嗪组改善更加明显，临床疗效也显著优于川芎嗪组。相关分析表明，血浆TM、ET－1水平与血小板GMP－140显著正相关。结论：尼莫地平可显著降低急性脑梗死患者血小板GMP－140、血浆TM和ET－1水平，改善血小板活化状态和血管内皮细胞功能，对急性脑梗死患者有明显临床疗效。     

急性冠状动脉综合征患者D-Ⅱ聚体、CD62p检测的临床意义

目的　探讨急性冠状动脉综合征 (ACS)患者血中D Ⅱ聚体、血小板膜糖蛋白CD6 2p阳性表达率测定的临床意义。方法　分别测定 2 1例稳定型心绞痛 (SA)患者、 2 2例不稳定型心绞痛 (UA)患者、14例急性心肌梗塞 (AMI)患者、 2 0例对照组患者的D Ⅱ聚体、CD6 2p、肌钙蛋白 (cTnI) ,分析不同组间各检出物的水平与ACS检出的敏感度。结果　指标的检测 :UA组和AMI组D Ⅱ聚体、CD6 2p的水平与SA组及对照组相比较差异有显著性 (P <0 0 1) ;UA组与AMI组相比 ,两者含量差异有显著性 (P <0 0 5 )。cTnI含量检测 :AMI组与其余 3组比较 ,差异有显著性 (P <0 0 1) ;而SA组与对照组比较 ,差异无显著性(P >0 0 5 )。D Ⅱ聚体、CD6 2p对ACS的检出均较cTnI为敏感。结论　D Ⅱ聚体、CD6 2p可作为冠状动脉内血栓形成的指标 ,并在一定程度上反映了UA的严重程度 ,它们在cTnI的基础上加强了临床对ACS的尽早确诊     

急性脑血管病患者血浆一氧化氮和内皮素含量测定

通过观测正常人和急性脑血管病患者的血浆一氧化氮 (NO)和内皮素 (ET)水平 ,探求NO和ET在急性脑血管病发作过程中的病理生理意义。方法　用Green’s法测定血浆NO ,用放射免疫法测定血浆ET。结果　正常对照组 (A组 ) 2 4例 ,平均血浆NO 2 6 5 2± 2 5 1μmol/L ,ET 45 81± 11 2 1ng/L ;脑出血组 (B组 ) 2 7例 ,平均血浆NO 18 12± 4 14μmol/L ,ET132 41± 2 1 0 5ng/L ;脑梗死组 (C组 ) 4 2例 ,平均血浆NO 18 0 0± 3 12 μmol/L ,ET 12 9± 9 37ng/L。与A组相比较 ,B组和C组均有NO显著降低 (P <0 0 5 ) ,ET显著升高 (P <0 0 1) ;B组与C组之间无显著差异 (P >0 0 5 )。结论　在急性脑血管病发作过程中 ,血浆NO和ET的含量变化 ,可能促进了疾病的发生和发展     

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。