糖尿病患者凝血、抗凝血及纤溶功能的变化

目的探讨糖尿病患者凝血、抗凝血、纤溶系统的变化及意义.方法纤维蛋白原(Fg)采用Clauss法,纤维蛋白A肽(FPA)、血管性血友病因子(vWF)、D-二聚体(D-dimer)、抗凝血酶-Ⅲ(AT-Ⅲ)、血浆血小板α-颗粒膜蛋白140(GMP-140)采用酶联免疫吸附试验(ELISA)法,组织型纤溶酶原激活物(t-PA)、纤溶酶原激活剂抑制物(PAI)采用发色底物法.结果与对照组比较,糖尿病无并发症组Fg、FPA、vWF、GMP-140水平显著增高(P<0.05),AT-Ⅲ、D-dimer、t-PA、PAI差异无显著性;糖尿病有并发症组Fg、FPA、vWF、D-dimer、PAI、GMP-140水平显著增高(P<0.01),AT-Ⅲ、t-PA水平显著降低(P<0.01).结论糖尿病时,凝血、抗凝血、血小板、纤溶等系统发生了显著变化,因此测定上述指标,对指导临床治疗、监测病情、预防血栓形成具有一定价值.     

糖尿病患者凝血、抗凝血及纤溶功能的变化

目的 探讨糖尿病患者凝血、抗凝血、纤溶系统的变化及意义。方法 纤维蛋白原（Fg)采用Clauss法，纤维蛋白A肽（FPA）、血管性血友病因子（vWF)、D－二聚体（D－dimer)、抗凝血酶－Ⅲ（AT－Ⅲ）、血浆血小板α－颗粒膜蛋白140（GMP－140）采用酶联免疫吸附试验（ELISA）法，组织型纤溶酶原激活物（t-PA)、纤溶酶原激活剂抑制物（PAI）采用发色底物法。结果 与对照组比较，糖尿病无并发症组Fg、FPA、vWF、GMP-140水平显著增高（P＜0.05),AT-Ⅲ、D-dimer、t-PA、PAI差异无显著性；糖尿病有并发症组Fg、FPA、vWF、D-dimer、PAI、GMP－140水平显著增高（P＜0.01)，AT－Ⅲ、t-PA水平显著降低（P＜0.01)。结论 糖尿病时，凝血、抗凝血、血小板、纤溶等系统发生了显著变化，因此测定上述指标，对指导临床治疗、监测病情、预防血栓形成具有一定价值。     

H型高血压患者血栓前状态相关标志物的变化及意义

血栓前状态(prothrombotic state,PTS)是指多种因素引起的凝血纤溶系统失衡、有利于血栓形成的病理状态.研究表明:通过检测血栓前状态的一些分子标志物可反映体内高凝状态或血栓形成[1].H型高血压(HCY≥10μmol/L)是引发心脑血管疾病,尤其是脑卒中最重要的危险因素,但有关H型高血压患者血栓前状态的研究报道不多.本研究通过检测血浆血管性假性血友病因子(vWF)、血小板α颗粒膜蛋白-140(GMP-140)、纤维蛋白原(FIB)、D-二聚体(D-D)、纤溶酶原激活物抑制物-1 (PAI-1)和组织型纤溶酶原激活物(t-PA)等指标,探讨其在H型高血压患者中的变化及临床意义.     

冠心病患者止凝血与纤溶状态检测的临床价值

目的探讨冠心病(coronaryheartdisease,CHD)患者止凝血、纤溶状态检测的临床价值。方法102例冠心病患者,其中31例稳定型心绞痛(stableangina,SA),33例不稳定型心绞痛(unstableangina,UA),38例急性心肌梗死(acutemyocardialinfarction,AMI),采用酶联免疫吸附双抗体夹心法检测血浆中血管性血友病因子(vonWillebrandfactor,vWF)、血浆血小板α颗粒膜蛋白140(α-granulemembraneprotein140,GMP-140)、组织型纤溶酶原激活物(tissue-typeplasminogenactivator,t-PA)、血浆纤溶酶原激活物抑制物(plasminogenactivatorinhibitor,PAI)及D-二聚体(D-Dimer),采用Clauss法检测纤维蛋白原(fibrinogen,FIB)含量并比较各指标在CHD患者组与健康对照组的差别。结果CHD患者血浆中t-PA低于健康对照组,其他指标的含量高于健康对照组。UA组与SA组比较,vWF、t-PA、PAI、D-Dimer、FIB有显著性差异(P<0.05),而GMP-140无显著性差异(P>0.05)。AMI组与UA组比较,GMP-140和D-Dimer无显著性差异(P>0.05),其他指标有显著性差异(P<0.05)。结论CHD患者存在内皮细胞损伤、血小板活性增高而纤溶活性降低的状态,易发生血栓,并且各项指标异常程度与CHD严重程度相一致(AMI>UA>SA),有助于进行危险分层诊断。     

急性脑梗死患者血浆GMP-140、TAT、TpP、F1+2的检测

目的探讨血浆血小板膜糖蛋白140(GMP-140)、凝血酶-抗凝血酶复合物(TAT)、凝血酶原片段1 2(F1 2)和血栓前体蛋白(TpP)含量测定对急性脑梗死(ACI)患者的诊断价值。方法对发病后24h内就诊的37例急性脑梗死患者血浆分别测定GMP-140、TAT、TpP、F1 2,并与正常组比较。结果患者血浆GMP-140、TAT、TpP、F1 2增高,说明ACI患者血液处于高凝状态,其有助于早期诊断。结论血浆GMP-140、TAT、TpP、F1 2联合测定,有助于早期判断ACI患者血液是否处于高凝状态。     

脑出血急性期凝血和纤溶变化的临床研究

目的探讨脑出血急性期的凝血和纤溶功能的变化.方法用酶联免疫法(ELISA)等方法定量分析脑出血患者的纤溶酶-抗纤溶酶复合物(PAP)、组织纤溶酶原激活物(t-PA)、纤溶酶原激活剂抑制物(PAI)、蛋白C(PC),用夹心酶联法定量分析凝血酶-抗凝血酶复合物(TAT),分别与对照组的凝血、纤溶各指标比较,同时对患者12h以内和24h时间段进行凝血、纤溶各指标的比较.结果脑出血的t-PA浓度明显高于对照组(P<0.05);PAI浓度低于对照组(P<0.05);PC浓度高于对照组(P<0.05);TAT浓度明显高于对照组(P<0.05);PAP浓度低于对照组(P<0.05).结论脑出血急性期有凝血和纤溶活性增强及抗凝功能的异常;有一过性TAT升高的特点.     

急性脑梗死患者血栓前状态特异性综合诊断指标探讨

目的 对急性脑梗死患者血栓前状态实验室诊断指标进行探讨。方法 收集120例急性脑梗死患者发病24h内及60例健康对照者的血浆，用酶联免疫吸附双抗体夹心法（ELISA）检测血浆D-二聚体、血管性血友病因子（vWF）、组织型纤溶酶原激活物（t-PA）、纤溶酶原激活物抑制物（PAI—1）含量；用发色底物法检测蛋白C（PC）活性、抗凝血酶Ⅲ（AT-Ⅲ）活性；并予以组间比较。结果 急性脑梗死患者血栓前状态血浆D-二聚体、vWF含量明显增高；PC、AT-Ⅲ活性明显减低；t-PA含量减低，PAI-1含量增高；与健康对照组比较差异均有显著性（均P〈0．01）。结论 急性脑梗死患者血栓前状态存在着明显的高凝状态，可将其分子标志物血浆D-二聚体、vWF、PC、AT-Ⅲ、t-PA、PAI-1的检测，作为急性脑梗死患者血栓前状态特异而敏感的诊断指标，为临床早期诊断、早期治疗提供可靠依据。     

老年冠心病患者止凝血变化的研究

本文检测老年冠心病患者的血浆凝血酶-抗凝血酶Ⅲ复合物(TAT)、血管性血友病因子抗原(vWF:Ag)、蛋白C抗原(PC:Ag)、蛋白S抗原(PS:Ag)、P-选择素(P-Selectin)、组织纤溶酶原激活物活性(t-PA:A)、纤溶酶原激活剂抑制剂活性(PAI:A)及D-二聚体(D-D),并与对照组比较.老年冠心组的TAT、vWF:Ag、P-Selectin、PS:Ag、t-PA:A、PAI:A、D-D显著升高(P＜0.05).其中,不稳定型心绞痛的TAT、t-PA:A、PAI:A、D-D升高更明显,并与稳定型心绞痛有显著差异.结果表明:老年冠心病患者主要表现为凝血系统激活、血管内皮损伤、血小板活性增加及继发性纤溶亢进.     

血栓前状态与原发性高血压关系的临床研究

目的通过观察原发性高血压患者血栓前状态（PTS）分子标志物的变化，探讨其易并发血栓性疾病的机制，为临床早期诊治提供客观依据。方法检测1000例原发性高血压患者及100例健康对照者血浆PTS分子标志物[血管性血友病因子（vWF）、血浆α-颗粒膜蛋白（GMP-140）、11-去氢血栓烷B2（11-DH-TXB：）、纤维蛋白原（FiB）、抗凝血酶（AT）]的含量，组织型纤溶酶原激活剂（t-PA）、纤溶酶原激活剂抑制物-1（PAI-1）的活性水平及血流动力学指标，并进行分析与评价。结果与正常对照组相比，高血压组患者的血浆vWF、GMP-140、11-DH-TXB，、nB含量及PAI-1活性和血粘度均明显升高，而AT含量、t-PA活性均明显下降（均为P〈0．01）。随着血压水平升高，PTS标志物水平变化越显著（P〈0．05）。结论原发性高血压燕者存在PTS，PTS与其病情进展及血栓性疾病的发生密切相关。     

冠心病患者凝血及纤溶系统功能的变化

为探讨冠心病(CHD)患者凝血及纤溶系统的变化,我们对20例稳定性心绞痛(SA),19例不稳定性心绞痛(UA),51例急性心肌梗死(AMI)患者作组织型纤溶酶原激活物(t-PA)、组织型纤溶酶原激活物抑制物(PAI)、纤溶酶原(PCG)、α_2抗纤溶酶(α_2AP)、纤维蛋白原(Fg)、D二聚体(D-Dimer)等凝血及纤溶指标的测定,结果显示与SA相比,UA及AMI患者t-PA活性、t-PA/PAI比值明显降低(P<0.05),血浆PAI活性、Fg含量及D-Dimer含量均明显增高(P<0.05),说明μA及AMI患者存在明显凝血活性增强及纤溶系统功能减退,这对冠心病的发生和发展起着重要作用。     

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.     

Physician and Nurse Practitioner Teamwork and Job Satisfaction: Gender and Profession

Designing interprofessional primary care teams composed of physicians and nurse practitioners (NPs) is a national priority. We assessed how profession and gender affect teamwork and job satisfaction among primary care physicians and NPs by using survey data from 186 physicians and 398 NPs practicing in New York State. Our regression models show profession (NP vs physician) moderates the associations of gender with teamwork and job satisfaction. Among NPs, men had higher job satisfaction than women. Among physicians, women had higher job satisfaction than men. Our results can benefit interprofessional primary care teams to optimize their professional and gender mix.