检测原发性肝癌血清可溶性细胞间黏附分子-1的临床价值

目的:探讨检测原发性肝癌(HCC)血清可溶性细胞间黏附分子-1(sICAM-1)水平的临床价值。方法:采用ELISA法同期检测了53例HCC患者血清sICAM-1及AFP的含量,并与肝脏良性肿瘤、慢性肝炎肝硬化及健康志愿者相比较。结果:HCC患者血清sICAM-1含量均值为(1382.5±752.3)ng/mL,显著高于各对照组(P<0.01);而肝脏良性肿瘤、肝炎肝硬化及健康志愿者之间差异无显著性(P>0.05);HCC患者血清sICAM-1含量与肿瘤大小、有无包膜及转移状态有关(P<0.05),而与肿瘤组织学分级、血清AFP水平无关(P>0.05)。结论:sICAM-1在HCC发生发展过程中起重要作用,检测血清sICAM-1对于HCC的诊断有重要价值,并有助于判断HCC患者肿瘤侵袭转移状态及病情监测。     

肝细胞癌生化标志物—血清假尿苷测定的临床意义

尿液中假尿苷(pseudouridine PU)增多可见于多种肿瘤患者。为了探讨血清PU 对肝细胞癌的诊断价值,作者应用高效液相色谱法,测定了52例肝细胞癌、42例肝硬化及25例健康人血清PU 浓度,并与AFP 做了对比分析。结果:血清PU 浓度,肝细胞癌患者3.3±1.4nmol/ml(Mean±SD)、肝硬化患者2.2±0.6nmol/ml、健康人2.2±0.4nmol/ml。可见肝硬化患者与健康     

GP73和AFP检测在肝细胞肝癌诊断中的作用

目的通过检测肝细胞肝癌、慢性肝炎、肝硬化患者及健康体检者血清中甲胎蛋白(AFP)和高尔基体蛋白73(GP73)水平,对比分析AFP和GP73的阳性检出率,探讨GP73和AFP用于诊断肝细胞肝癌的临床意义。方法收集肝细胞肝癌、慢性肝炎、肝硬化患者及健康体检者血清样本,分别采用酶联免疫吸附法和化学发光法检测AFP和GP73水平。结果在肝细胞肝癌患者血清中,GP73阳性检出率为96.00%,AFP阳性检出率为84.00%,在肝细胞肝癌患者血清中,GP73水平为(702.64±54.35)ng/mL,AFP水平为(6 772.4±1 942.3)ng/mL,均明显高于肝硬化组、肝炎组及健康对照组,差异有统计学意义(P0.01);但是GP73和AFP联合检测在灵敏度和特异度方面与单独检测比较差异无统计学意义(P0.05)。结论 GP73和AFP在肝细胞肝癌患者中的阳性检出率和水平显著高于慢性肝炎组和肝硬化组,对于肝细胞肝癌患者早期诊断有一定参考价值。     

肝病患者血清转化生长因子β_1水平及其临床意义

目的 :了解急、慢性肝炎及肝硬化患者血清转化生长因子 β1(transforminggrowthfactorβ1,TGFβ1)水平的变化 ,探讨TGFβ1在肝纤维化、肝硬化发病中的作用。方法 :采用标准的生物学方法即TGFβ1对水貂肺上皮细胞生长抑制的方法测定 89例肝病患者和 2 4例正常人血清TGFβ1含量。结果 :①急性肝炎患者血清TGFβ1水平 (1 91± 0 48ng/ml)与正常对照组 (1 6 5± 0 45ng/ml)比较无明显差异 (P >0 0 5 ) ;②慢性肝炎及肝硬化患者血清TGFβ1水平 (5 6 2± 1 0 2ng/ml,11 75± 1 0 8ng/ml)均明显高于正常对照组 (P <0 0 5 ) ,且肝硬化患者比慢性肝炎患者增高更明显 (P <0 0 5 )。结论 :慢性肝炎及肝硬化患者TGFβ1分泌增加 ,且肝硬化比慢性肝炎患者增加更明显 ;而急性肝炎患者TGFβ1分泌无明显变化。TGFβ1在一定程度上反映了肝纤维化的程度 ,在肝纤维化、肝硬化病理过程中具有重要意义。TGFβ1可望作为肝纤维化的标志物。TGFβ1拮抗剂有望成为肝纤维化治疗的重要药物。     

重型肝炎血清甲胎蛋白测定的临床意义

目的 了解重型肝炎患者血清甲胎蛋白 (AFP)的分布、与肝损害的关系以及对预后的影响。 方法 应用CHIRONDI AGNOSTICSCorporation的全自动生化荧光分析仪ACS :180测定AFP。结果 59例患者 ,AFP高于正常者45例(76.3%) ;死亡32例中AFP平均值为(44.53±18.27)ng/ml,存活27例中AFP平均值(377.81±130.98)ng/ml,明显高于死亡组 (P<0.001)。动态观察存活27例AFP ,有15例与谷丙转氨酶 (ALT)值成平行关系 ,AFP随肝功能改善于3个月内恢复正常。AFP≤400ng/ml主要分布在凝血酶原时间 (PT)≥25s者中。 结论 重型肝炎患者AFP升高反映肝细胞再生活跃 ,提示预后较好。     

血清GDF-15、GP73、AFP对肝细胞癌的诊断价值研究

目的 探讨血清生长分化因子15(GDF-15)、血清高尔基体蛋白73(GP73)、甲胎蛋白(AFP)对肝细胞癌的诊断价值.方法 将2019年1-12月该院收治经病理确诊为肝细胞癌的140例患者设为研究组,另选取同期该院收治经病理确诊为慢性肝炎150例(慢性肝炎组)、肝硬化120例患者(肝硬化组)和体检健康者100例(健康对照组)作为对照.所有研究对象均采用电化学发光法检测AFP、GDF-15、GP73水平,比较研究组与慢性肝炎组、肝硬化组及健康对照组,以及研究组不同分期患者的各项指标水平,分析AFP、GDF-15、GP73单项及联合检测对肝细胞癌诊断的灵敏度和特异度等.结果 研究组的AFP、GDF-15、GP73水平较肝硬化组、慢性肝炎组及健康对照组更高,同时肝硬化组、慢性肝炎组AFP、GDF-15、GP73水平较健康对照组更高(P<0.05).研究组不同分期患者GP73水平比较,差异无统计学意义(P>0.05);C期及D期患者的AFP、GDF-15水平明显高于其他期患者(P<0.05),但B期以下AFP、GDF-15水平比较差异无统计学意义(P>0.05).GP73、GDF-15和AFP 3项联合检测诊断肝细胞癌的灵敏度显著高于单项或2项联合检测(P<0.05),但特异度未见明显增加.GP73、GDF-15和AFP单项诊断肝细胞癌的受试者工作特征曲线下面积分别为0.651、0.760、0.816;而GP73+GDF-15、GP73+AFP、GDF-15+AFP、GP73+GDF-15+AFP诊断肝细胞癌的ROC曲线下面积分别为0.852、0.894、0.839、0.925.结论 联合检测血清GDF-15、GP73与AFP水平能早期诊断肝细胞癌,提高诊断的灵敏度,对治疗和预后有重要作用.     

放射免疫测定血清铁蛋白在原发性肝癌诊断中的价值

用放射免疫分析法对60例正常成人、66例原发性肝癌患者血清铁蛋白浓度进行了测定,肝癌患者同时测定了 AFP 含量。正常人血清铁蛋白浓度为94.1±28.2ng/ml(±SD),原发性肝癌患者为533.6±51.7ng/ml(±SD)。两组均值具有显著性差异(p<0.001),可见放射免疫测定血清铁蛋白浓度对原发性肝癌的诊断具有重要的临床价值。     

临床各型病毒性肝炎血清肿瘤坏死因子检测及意义

目的 :探讨血清肿瘤坏死因子 (TNF α)在不同临床分型的病毒性肝炎患者血清中的含量及临床意义。方法 :采用双抗体夹心酶联免疫吸附试验检测 175例病毒性肝炎患者血清TNF α水平。结果 :175例肝炎病人中 ,急性重型肝炎 15例 ,TNF α平均含量 8.0 9± 1.85ng/ml;慢性肝炎 76例 ,其临床分型及TNF α平均含量分别是 :2 2例重度慢性肝炎 5 .94± 1.87ng/ml,2 4例中度慢性肝炎 5 .5 2± 1.6 7ng/ml,30例轻度慢性肝炎 3.0 3± 1.0 2ng/ml;肝炎肝硬化 14例 4.71± 1.2 7ng/ml;急性肝炎40例 1.0 2± 0 .35ng/ml;无症状乙肝病毒携带者 30例 0 .90± 0 .2 1ng/ml。结论 :除乙肝病毒携带者及急性肝炎的检测结果与对照组相比较无差异外 ,其余临床各型病毒性肝炎 (慢性肝炎、肝硬化、急性重型肝炎 )均有显著差异 ,在与其它检测指标配合下 ,血清TNF α活性检测对监测各型肝炎的进行性损害程度及预后可提供一个辅助性指标     

肝硬化患者血清神经元特异性烯醇化酶的检测及临床意义

目的 :探讨神经元特异性烯醇化酶 (neuron specificenolase ,NSE)在肝硬化患者中的意义。方法 :以ELISA法对 47例肝硬化患者的血清NSE进行检测 ,并对各Child Pugh肝功能分级及不同程度食管静脉曲张组患者NSE水平进行了比较分析。结果 :肝硬化组NSE[( 2 6 .45 2± 1 0 .5 81 )ng/ml]显著高于慢性肝炎组 [( 1 2 .1 2 7± 5 .6 73)ng/ml]及对照组[( 1 0 .1 96± 3.2 37)ng/ml];肝硬化患者肝功能愈差 ,食管静脉曲张程度愈重者NSE水平愈高。 结论 :肝硬化患者NSE水平明显升高 ,且与肝功能损害程度、门体分流程度有关。     

肝细胞癌血清铁蛋白测定的临床意义

甲胎蛋白(AFP)是肝细胞癌血清学诊断的一项有价值的指标,但在有些肝细胞癌病人中并不增高。所以必需寻找具有高敏感性和特异性的一些新的肿瘤指标。本文报告343例肝病病人血清铁蛋白测定的结果,以估价其对肝细胞癌诊断的临床意义。343例受检者中肝炎24例,肝硬化150例,肝癌132例,转移性肝癌37例,正常人35例。采用放射免疫测定技术检查空腹时血清铁蛋白。同时测定AFP。几乎全部病人亦测定了SGOT,SGPT,血清铁。结果肝病中的血清铁蛋白水平:正常人血清铁蛋白水平男性为59±11ng/ml,女性27±6ng/ml。肝硬化为168±14ng/ml,肝癌423±37ng/ml,转移性肝癌441±143ng/ml,肝炎病人最高,为969±326ng/ml,与SGOT和SGPT有明显的相关     

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。