脑梗死,糖尿病患者血小板膜糖蛋白及其与纤维蛋白原结合反？…

观察脑梗死及Ⅱ型糖尿病患者血小板膜糖蛋白及纤维蛋白结合的改变,确定其在血栓及血栓前状态研究中的价值。方法应用流式细胞术测定８５例Ⅱ型糖尿病患者和２８例脑梗死患者血小板纤维蛋白原结合率及糖蛋白（ＧＰ）Ⅰｂ、ＧＰⅡｂ、ＧＰⅢａ、ＧＰⅡｂ－Ⅲａ复合物及Ｐ－选择素的表达,并与３０例健康成人所测结果进行比较。     

流式细胞术在检测血小板无力症中的意义

血小板上含有丰富的GPⅡ-Ⅲa,在血小板聚集时,GPⅡb-Ⅲa复合物上的纤维蛋白原受体与纤维蛋白原结合。血小板无力症(Glanzmann’s thrombasthenia,GT)患者是GPⅡb-Ⅲa复合物的质或量的缺陷所致血小板聚集异常。通常用聚丙烯酸胺凝胶电泳(SDS-PAGE)及Western印迹等方法检测膜糖蛋白,但操作烦琐、费时费试剂。流式细胞术(FCM)及特异性单机的应用使血小板膜GP检测有了新突破,特别是纤维蛋白原结合试验使变异型GT的诊断成为可能。我们用FCM检测12例GT患者及其家属的血小板膜GP及纤维蛋白原结合并与SDS-PAGE和Western印迹做比较,以探索FCM方法对GT诊断的价值和意义。     

活化血小板表面膜糖蛋白的异位分布

目的观察血小板活化后表面一些抗原决定簇的动态改变,探讨其在血栓性疾病研究中的意义。方法以凝血酶与腺苷二磷酸(ADP)分别在不同时间段(0~30min)诱导正常人血小板活化,应用流式细胞仪检测其血小板膜糖蛋白(GP)Ⅰb,GPⅢa及P-选择素的表达;同时用全血法测定脑梗死患者相应抗原的改变。结果凝血酶及ADP活化血小板后均可导致GPⅠb表达呈现先下降又逐渐回升的可逆性分布趋势,各时间段引起的GPⅠb改变在两者之间都具有显著差异;GPⅢa表达在活化后初期变化不明显,10min后呈现递增趋势;两种活化剂均可促使P-选择素显著升高,并维持于高水平。脑梗死患者GPⅠb表达减少,P-选择素的表达远高于对照组,GPⅢa无变化。结论凝血酶与ADP均能介导血小板活化,以时间依赖的方式促使GPⅠb与GPⅢa逆转,同时P-选择素向外释放,而血小板表面活化相关性抗原的改变是反映体内血小板活化的重要指标。     

血小板膜糖蛋白Ⅱb-Ⅲa复合体研究进展

运用凝胶电泳方法可将血小板膜糖蛋白(GP)分为若干个型和亚型。80年代初Kunilzi等用交叉免疫电泳技术证实GPⅡb和GPⅢa以钙依赖性二聚体(GPⅡb-Ⅲa)形式存在。以后许多实验结果提示GPⅡb-Ⅲa结构中含有纤维蛋白原(Fg)结合位点,在血小板聚集过程中发挥重要作用。近年来在GPⅡb-Ⅲa研究中广泛采用了单克隆抗体和电子显微镜等方法,进一步揭示了GPⅡb-Ⅲa的结构、性质硬变化规律。     

骨髓增殖性疾病病人血小板膜糖蛋白及其受体的研究

目的检测骨髓增殖性疾病(MPD)病人血小板膜糖蛋白(GP)及其受体的变化,并探讨其出血及血栓发生的可能机制.方法应用流式细胞仪(FCM)、酶联免疫吸附试验(ELISA)和Western blot 方法检测部分MPD病人血浆纤维蛋白原和vWF含量,血小板膜GP Ⅰb、GP Ⅱb/Ⅲa 以及纤维蛋白原和vWF结合位点的变化.结果MPD组血浆纤维蛋白原和vWF含量较对照组均无统计学意义(P＞0.05).血小板膜GP Ⅰb百分标记率在MPD组为60.51%±11.80%,较正常对照组75.84%±6.18%减低(P＜0.01).血小板膜GP Ⅱb/Ⅲa的百分标记率在MPD组和正常组分别为63.84%±10.92%和70.34%±9.15%(P＞0.05).血小板表面纤维蛋白原和vWF结合位点的百分标记率在疾病组及正常对照组分别为55.55%±16.15%和68.71%±5.87%(P＜0.05)和66.00%±3.34%和62.67%±3.39%(P＞0.05).Western blot 结果显示MPD组病人血小板GP Ⅱb/Ⅲa存在较大异质性,个别病例还有异常条带出现.结论MPD病人出血或血栓形成可能与血小板膜糖蛋白及其受体改变有关.     

血小板膜糖蛋白Ⅱb/Ⅲa受体在房颤患者中的检测及临床意义

目的 :研究心房颤动 (房颤 )患者中血小板膜糖蛋白Ⅱb/Ⅲa受体的变化及其临床意义。方法 :采用全血法流式细胞术分别测定房颤患者 (16例 )、非房颤窦性心律患者以下称非房颤患者 (2 8例 )及正常对照组 (17例 )血小板膜上活化糖蛋白Ⅱb/Ⅲa复合物水平 ,比较房颤患者与非房颤患者及正常对照组血小板膜糖蛋白Ⅱb/Ⅲa受体变化情况。结果 :房颤患者GPⅡb/Ⅲa测得值显著高于非房颤患者 (P <0 .0 5 )及正常对照组 (P <0 .0 5 ) ;非房颤患者GPⅡb/Ⅲa也显著高于正常对照组 (P <0 .0 5 )。结论 :房颤患者处于血栓前状态 ,引起血小板激活 ,GPⅡb/Ⅲa高表达可能与房颤患者易发生血栓栓塞并发症有关 ,检测GPⅡb/Ⅲa对评估房颤患者的血栓栓塞危险性及指导抗凝、减少栓塞并发症有一定的临床意义。     

一种具有超大颗粒的遗传性巨血小板减少症初步报告

目的研究具有异常超微结构的遗传性巨血小板减少症的血小板形态与功能。方法采集患者外周静脉血，分离富血小板血浆，用流式细胞术结合多种抗血小板膜糖蛋白（GP）单克隆抗体测定血小板膜GPⅠb、GPⅡb、GPⅢa、p-选择素和CD63的表达；分别以常规超薄切片术和免疫电镜技术检测患者血小板及其异常超微结构的性质；用荧光分光光度法测定血小板5-羟色胺含量。结果患者及其父亲血小板表面GPⅠb、GPⅡb和GPⅢa的表达正常，阳性细胞百分数及平均荧光强度与正常对照基本相同，但P-选择素和CD63的表达较高；两者血小板内均有数量不等的高电子密度大颗粒，有膜包裹，且有胞吐现象。该颗粒P-选择素、CD63反应均阴性，不是异常的α颗粒或溶酶体；患者及其父亲血小板5-羟色胺含量正常。结论报道一种具有异常超微结构的遗传性血小板减少症，血小板内异常的高电子密度非特异性超大颗粒可能代表了一种新的遗传性血小板病。     

ITP患者二磷酸腺苷激活前后血小板活化指标表达对患者出血风险的预测作用研究

目的:研究原发免疫性血小板减少症(ITP)患者二磷酸腺苷激活前后血小板活化指标表达对患者出血风险的预测作用。方法:选择我院2017年1月-2018年10月住院治疗的ITP患者89例为ITP组,采用ITP特异性出血评价工具(ITP-BAT)进行出血评分及出血程度分级。根据出血程度分为4个亚组:无出血症状组(19例),轻度出血组(32例),中度出血组(27例),大量及严重出血组(11例)。选择同期健康体检者22例为对照组,所有受检者均以二磷酸腺苷(ADP)为激活剂,应用流式细胞术检测激活前后血小板膜糖蛋白(GP)Ⅰb、Ⅱb/Ⅲa和P选择素表达,分析GPⅠb、GPⅡb/Ⅲa、P选择素表达。采用Pearson多重线性相关性分析ADP激活前后ITP患者出血程度与GPⅠb、GPⅡb/Ⅲa、P选择素表达水平的相关性。结果:对照组、无症状组、轻度症状组ADP激活后GPⅠb表达水平显著下降,GPⅡb/Ⅲa、P选择素表达水平显著升高;中度症状组、重度症状组ADP激活后GPⅠb表达水平显著升高,GPⅡb/Ⅲa表达水平显著降低,差异均有统计学意义(P0.05)。中度症状组、重度症状组ADP激活前后P选择素表达水平差异无统计学意义(P0.05)。ADP激活前ITP各亚组GPⅠb表达水平低于对照组,GPⅡb/Ⅲa表达水平高于对照组,中度症状组、重度症状组P选择素表达水平高于对照组,差异均有统计学意义(P0.05)。ADP激活后ITP各亚组GPⅠb、P选择素表达水平均低于对照组,GPⅡb/Ⅲa表达水平高于对照组,差异均有统计学意义(P0.05)。ITP各亚组比较显示,ADP激活前中度症状组、重度症状组GPⅠb表达水平低于无症状组、轻度症状组;GPⅡb/Ⅲa、P选择素表达水平高于无症状组、轻度症状组,差异均有统计学意义(P0.05)。ADP激活后中度症状组、重度症状组GPⅠb表达水平高于无症状组、轻度症状组;GPⅡb/Ⅲa、P选择素表达水平低于无症状组、轻度症状组,差异均有统计学意义(P0.05)。相关分析显示,ADP激活前GPⅠb、GPⅡb/Ⅲa表达水平与出血风险呈正相关(r=0.483,0.504);P-选择素与出血风险不相关(r=0.000);ADP激活后GPⅠb、GPⅡb/Ⅲa和P-选择素表达水平与出血风险呈负相关(r=-0.627,-0.406,-0.108)。结论:ADP激活前后血小板活化指标表达水平对预防ITP患者出血风险有一定的价值,可以作为治疗和疗效观察的参考指标。     

GPⅡb/Ⅲa抑制剂抗血小板机理及临床应用进展

GPⅡb/Ⅲa糖蛋白复合物在血小板聚集过程中起关键作用,GPⅡb/Ⅲa抑制剂也逐渐开始应用于血栓性疾病的预防和治疗。本文着重综述GPⅡb/Ⅲa在血小板聚集中的作用及GPⅡb/Ⅲa抑制剂在抗血小板聚集的临床应用。     

血小板糖蛋白Ⅱb/Ⅲa受体抑制剂在急性冠状动脉综合征中的应用

血小板膜糖蛋白Ⅱb/Ⅲa(GPⅡb/Ⅲa)受体抑制剂,主要抑制纤维蛋白原与血小板膜GPⅡb/Ⅲa受体的结合,是血小板聚集的终末环节抑制剂。目前主要静脉制剂包括abciximab、tirofiban和eptifibatide。本文就3种药物在急性冠状动脉综合征(ACS)治疗中的应用进展综述如下。1在非ST段抬高A     

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。