生活行为因素与脑梗死患者颈动脉粥样硬化的相关性研究

目的探讨脑梗死患者颈动脉粥样硬化(CAS)的发生与生活行为因素的关系以及颈动脉粥样硬化与脑梗死的关系。方法选取137例脑梗死患者(脑梗死组)和同期行健康体检者84例(对照组),采用彩色多普勒超声对2组CAS的发生、斑块的位置及超声特点进行分析,并对2组的生活行为习惯、身高、体质量进行调查。采用非条件Logistic回归分析等统计学方法处理数据。结果脑梗死组CAS的发生率显著高于对照组(67.15%vs45.23%),斑块的发生率也高于对照组(54.01%vs 35.71%),颈动脉内膜中层厚度较对照组明显增厚(P<0.05或P<0.01)。Logistic逐步回归分析显示吸烟、不良膳食习惯、肥胖、年龄是脑梗死患者发生CAS的影响因素,其OR值分别是3.89、2.17、1.03、1.06。结论吸烟、不良膳食习惯、肥胖、年龄是脑梗死患者发生CAS的独立危险因素。脑梗死患者CAS程度明显加重,重视颈动脉的超声检查对预防和治疗脑血管病具有重要意义。     

颈动脉硬化患病情况及危险因素分析

目的 探讨颈动脉硬化（CAS）的患病情况及其危险因素。 方法 将该院603例住院患者根据颈动脉彩超检查结果分为非硬化组和硬化组,计算CAS的患病率,分析比较两组临床资料及生化指标,利用多因素Logistic回归分析各危险因素与CAS的相关性。 结果 入选患者CAS的发生率为57.5%。两组年龄、糖化血红蛋白、血尿酸、甘油三酯、低密度脂蛋白胆固醇、高血压、糖尿病、吸烟差异有统计学意义（P<0.05）。Logistic回归分析显示,年龄、吸烟、高血压、糖尿病、低密度脂蛋白胆固醇为CAS的独立危险因素。 结论 年龄、吸烟、高血压、糖尿病、低密度脂蛋白胆固醇与CAS的发生具有明显相关性,合并危险因素的中老年人应尽早行颈动脉彩超检查。血尿酸与CAS的相关性有待进一步研究证实。       

超声诊断颈动脉粥样硬化斑块及其形成危险因素分析

目的应用超声对颈动脉进行筛查,探讨颈动脉粥样硬化斑块形成的危险因素。方法 150例行颈动脉超声检查的受检者,彩色多普勒超声检测出颈动脉粥样硬化斑块92例。应用Logistic回归分析筛选出差异有统计学意义的各变量及各变量发生颈动脉粥样硬化斑块的优势比(OR),评价各变量对颈动脉粥样硬化斑块形成的危险性。结果共筛选出年龄、高血压病史及糖尿病史3个具有统计学意义的特征变量,OR值从大到小依次为糖尿病史、年龄及高血压病史。结论颈动脉超声可作为反映动脉粥样硬化程度的一个"窗口",便于临床给予有效干预,减少心血管意外的发生。     

脑卒中高危人群颈动脉粥样硬化危险因素分析

目的探讨脑卒中高危人群颈动脉粥样硬化的危险因素。方法选取石家庄某社区1200例脑卒中高危人群作为研究对象,均行颈部超声检查,根据结果分为有无颈动脉内膜中层增厚组及有无斑块形成组,记录各组颈动脉粥样硬化危险因素分布情况。结果内膜中层增厚组与内膜中层厚度正常组、斑块形成组与无斑块形成组性别、年龄、受教育程度、既往病史、体育锻炼等方面比较差异均有统计学意义(P0.05)。颈动脉内膜中层增厚和斑块形成与年龄、脑卒中病史、高血压病、吸烟、糖尿病、冠心病、体育锻炼等呈明显正相关(P0.05),与受教育程度、脑卒中家族史、常吃水果等呈明显负相关(P0.05)。多因素Logistic回归分析显示,吸烟、年龄、脑卒中病史、糖尿病及体育锻炼等为脑卒中高危人群颈动脉粥样硬化发生的高危因素。结论加强体育锻炼、养成良好的生活习惯、积极控制高危因素可有效预防脑卒中高危人群颈动脉粥样硬化的发生。     

颈动脉粥样硬化预测冠状动脉病变的临床价值及其危险因素分析

目的评价颈动脉粥样硬化预测冠状动脉病变的临床价值，分析颈动脉粥样硬化的危险因素。方法105例行冠状动脉造影患者根据病变支数分为四组：正常、单支病变、二支病变及三支病变组，分别进行颈动脉超声检查，并收集相关危险因素。结果随着冠状动脉病变程度增加，其最大内中膜厚度、斑块数目、厚度积分及面积均随之增加，经统计分析均有显著意义。另经多因素回归分析显示年龄、吸烟是颈动脉粥样硬化的独立危险因子。结论颈动脉粥样硬化与冠状动脉病变之间有显著的相关性，而且二者有相似的危险因素，因此颈动脉超声检查可用以预测冠状动脉病变。     

颈动脉粥样硬化斑块危险因素分析

目的探讨颈动脉粥样硬化斑块形成的相关危险因素。方法 142例意识清楚的脑梗死患者和78例非脑血管病患者(对照组)的颈动脉行彩色Doppler超声检查。结果脑梗死组颈动脉粥样硬化斑块检出率64.8%,对照组检出率28.0%(P<0.01)。Logistic回归分析显示,年龄、高血压、糖尿病与颈动脉粥样硬化斑块形成相关(P<0.01)。结论颈动脉粥样硬化斑块形成是脑梗死的危险因素,年龄、高血压、糖尿病与颈动脉粥样硬化斑块形成有关。     

颈动脉粥样硬化与冠状动脉粥样硬化性心脏病的相关性研究进展

颈动脉粥样硬化（CAS）与冠状动脉粥样硬化（CAAS）同为动脉粥样硬化（AS）的最常见表现形式,二者具有相同的致病因素和病理机制。由于颈动脉位置表浅,超声显像的颈动脉血管结构清晰,可以辨别出有无内中膜增厚及斑块数量、性质等。因此,颈动脉超声检测可作为了解冠状动脉病变的一个“窗口”。AS过去被认为是老年退行性病变,现在认为是多因素共同作用引起的疾病。CAS和CHD的发生有许多共同的危险因素如高血压,、高血脂、糖尿病、吸烟、高龄等。现将上述致病因素的相关研究分别综述如下。     

脑梗死伴颈动脉狭窄患者的血清尿酸水平及其临床意义

目的:探索脑梗死伴颈动脉狭窄患者的血清尿酸水平及其临床意义。方法:脑梗死患者181例,根据颈动脉超声检查结果分为无斑块组57例,稳定斑块组50例,易损斑块组74例。检测各组血液尿酸浓度、血脂、空腹血糖(FBG)糖化血红蛋白(Hb A1c)。结果:3组的年龄、糖尿病比例差异有统计学意义(P<0.05);3组Hb A1c、尿酸浓度及颈动脉内膜中层厚度(IMT)差异有统计学意义(P<0.05);Logistic回归分析结果显示,年龄、饮酒、冠心病、血脂、Hb Alc、颈动脉IMT、性别、吸烟、糖尿病、FBG及血清尿酸含量是颈动脉粥样硬化斑块发生的独立危险因素。结论:血清尿酸的含量可能对脑梗死患者的颈动脉粥样硬化斑块的发生、发展和预后有关。     

颈动脉粥样硬化与缺血性脑血管病及相关因素研究

颈动脉粥样硬化（CAS）斑块形成及颈动脉狭窄是缺血性脑血管病（ICVD）发病的重要危险因素。CAS与脑血管病的其它危险因素如年龄、高血压、糖尿病、血脂异常、纤维蛋白原（Fbg）水平等亦有密切关系。本研究应用彩色多普勒超声检测CAS,并与缺血性脑血管病（ICVD）及相关因素的关系进行观察,现作如下报告。     

超声检测颈动脉粥样硬化与冠心病心脏事件的关系

目的　探讨颈动脉粥样硬化与冠状动脉粥样硬化的相关性 ,评价超声检测颈动脉粥样硬化对冠心病心脏事件预测的可能性。方法　将 2 33例疑是冠心病和心肌梗死患者行选择性冠状动脉造影及颈动脉超声检查 ,同时随访其心脏事件发生情况。分析颈动脉内中膜厚度 (IMT)及斑块与冠心病、冠心病危险因素及冠心病心脏事件发生情况的相关性。结果　 2 33例患者有 14 0例颈动脉超声阳性即IMT≥ 0 .8mm(6 0 .1% ) ,颈动脉超声阳性与性别、年龄、体重指数、糖尿病、高血压、痛风、吸烟、家族史、不稳定型心绞痛、心肌梗死、经皮冠状动脉腔内成形术、冠状动脉搭桥术、冠状动脉造影二支病变、冠状动脉造影三支病变、超声心动图异常、运动平板试验异常、异常Q波、ST段改变呈正相关 (P <0 .0 5 ) ;2 33例随访率为 94 .8% ,有 4 6例患者发生 4 8件心脏事件 ,其发生与体重指数、不稳定型心绞痛、冠状动脉造影阳性、冠状动脉造影二支病变、冠状动脉造影三支病变、颈动脉超声阳性、颈动脉斑块呈正相关 ,且关系密切 (P <0 .0 5 ) ;多因素非条件Logistic回归分析排除混杂因素影响 ,显示颈动脉超声阳性与阴性患者的心脏事件差别有统计学意义 (P <0 .0 5 )。结论　颈动脉粥样硬化与冠心病及冠心病危险因素之间关系密切 ,颈动脉超声     

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。