人乳头瘤病毒感染与内皮缩血管肽-1、内皮缩血管肽A受体在宫颈癌发病中的作用与表达

目的 探讨人乳头瘤病毒(HPV)感染与内皮缩血管肽-1(ET-1)、内皮缩血管肽A受体(ETA-R)在宫颈癌发病机制中的作用.方法 采用免疫组化SP法对68例宫颈癌组织中的HPV及20例正常非癌变组织进行人乳头瘤病毒16/18型E6基因(HPV16/18E6)、ET-1、ETA-R免疫特异性染色.结果 宫颈癌患者中HPV16/18E6阳性率明显高于正常对照组(P<0.001).HPV阳性宫颈癌组织中ET-1、ETA-R阳性表达率100%,HPV阴性宫颈癌组织ET-1、ETA-R阳性表达率为0,对照组ET-1、ETA-R阳性表达率20%,3组ET-1、ETA-R表达差异有统计学意义(P<0.001).ET-1、ETA-R在宫颈癌中表达率与临床分期、病理分级、组织学类型无关(P>0.05).结论 HPV感染与ET-1、ETA-R自分泌环功能有关.ET-1、ETA-R自分泌环是肿瘤生长驱动器,其功能异常可能是HPV感染宫颈上皮细胞导致宫颈癌变的一种新的发病机制.     

乳腺癌患者手术外科治疗前后血清内皮素变化及其意义

[目的]探讨血清内皮素-1 (ET-1)在乳腺癌外科手术治疗前后血清中的变化及其意义.[方法]采用放射免疫分析法检测乳腺癌保乳手术与改良根治术患者,血清中ET-1的表达.[结果]保乳手术与改良根治术治疗后其ET-1水平均显著下降(P<0.01);ET-1表达水平与乳腺癌不同组织学分级、TNM分期及有无淋巴结转移密切相关(P<0.01)而与乳腺癌肿瘤大小无显著性差异(P>0.01).[结论]乳腺癌患者血清ET-1检测能够反映乳腺癌恶性程度高低,其表达水平与其临床分期呈正比,在保乳手术方面有一定参考价值,并可作为乳腺癌的一种肿瘤标志物常规检测.     

VEGF在子宫腺肌病子宫内膜-肌层界面的表达及意义

【目的】探讨子宫腺肌病患者子宫内膜-肌层界面（endometrial-myometrial interface ,EM I）血管内皮生长因子（vascular endothelial growth factor ;VEGF）的表达及意义。【方法】采用免疫组化 ElivisiongTM Super法对40例子宫腺肌病患者（观察组）子宫内膜（含部分肌层）和40例子宫肌瘤患者（对照组）子宫内膜（含部分肌层）的组织进行标记、检测并比较。【结果】观察组增生期及分泌期EMI处VEGF的表达均显著高于远肌层（ P ＜0．05）,观察组增生期、分泌期EMI处VEGF表达均显著高于对照组（ P ＜0．05）。【结论】子宫腺肌病患者EMI处VEGF的高表达,可促使异位内膜及其周围肌层血管生成,其可能在子宫腺肌病的发生发展中起重要作用。     

内皮素1及其受体在反流性食管炎及Barrett食管中的表达及意义

目的探讨内皮素1(endothelin-1,ET-1)及其受体在反流性食管炎及Barrett食管(Barrett esophagus,BE)中的表达及其意义。方法用免疫组化法及实时定量PCR方法检测内镜活检标本:正常食管上皮20例,反流性食管炎22例,长段BE14例中ET-1及其受体ET(A)R、ET(B)R的表达。结果反流性食管炎中ET-1及ET(A)RmRNA水平均显著高于正常食管上皮(3.25±1.78vs.1.10±0.71,P=0.000;2.13±1.06vs.1.12±0.64,P=0.001)。BE近侧端的ET-1mRNA水平显著高于BE远侧端(3.03±1.83vs.1.16±0.70,P=0.004)及正常食管上皮(P=0.002)。BE两端的ET(A)R及ET(B)RmRNA水平相比差异无统计学意义(P>0.05)。免疫组化法显示,ET-1在反流性食管炎中的阳性表达(51.18±30.14)显著高于正常食管上皮(21.10±18.17,P=0.000)及BE远侧端(28.02±24.92,P=0.022),近侧端BE的阳性表达(50.07±25.88)显著高于BE远侧端(P=0.030)及正常食管上皮(P=0.001)。在反流性食管炎,轻、中、重度炎症评级的ET-1表达分值分别为36.08±27.84,65.86±11.82,98.00±8.49,呈阶梯式升高,组间差异有统计学意义(P=0.003)。ET(A)R及ET(B)R在炎症及非炎症组织中表达均较弱,各组间差异均无统计学意义(P>0.05)。结论 ET-1及ET(A)R在反流性食管炎中表达增加可能与炎症有关,ET-1可能在BE的形成过程中起作用。     

血清ET-1、hs-CRP对颅脑损伤合并神经源性肺水肿检测的诊断价值

[目的]探讨血清内皮素-1（ET-1）、超敏C反应蛋白（hs-CRP）对于颅脑损伤合并神经源性肺水肿早期诊断的临床意义.[方法]选取2010年1月至2012年6月河北医科大学附属邢台市人民医院重症医学科收治的重症颅脑损伤患者64例,其中神经源性肺水肿（NPE组）34例,非神经源性肺水肿（非NPE组）30例,同时选取同期健康体检中心健康体检人员20例作为正常对照组.对上述受试者采用酶联免疫法（ELISA）测定血清ET-1水平,采用免疫比浊法测定hs CRP水平并进行比较.[结果]颅脑损伤患者血清ET-1、hsCRP水平均高于正常对照组,且差异均有显著性（P＜0.05）;NPE组血清ET-1水平明显高于非NPE组,且差异有显著性（P＜0.05）;NPE组血清hs-CRP水平与非NPE组相比较,差异无显著性（P＞0.05）.[结论]检测血清ET-1、hs-CRP水平,能够在颅脑损伤患者早期发现肺损伤,有利于指导临床治疗.     

EGFR、cyclinD1和CD31在子宫内膜腺癌的表达及其临床意义

目的探讨EGFR、cyclin D1、CD31在子宫内膜腺癌组织中的表达及临床病理学意义。方法采用免疫组织化学检测20例正常增生期子宫内膜、30例子宫内膜不典型增生、71例子宫内膜腺癌组织中EGFR、cyclin D1和CD31蛋白表达,并计算微血管密度(MVD)。结果 EGFR、cyclin D1在子宫内膜腺癌组的阳性表达率及MVD明显高于正常增生期子宫内膜组和子宫内膜不典型增生组(P<0.05);EGFR的阳性表达率在子宫内膜不典型增生组比正常增生期子宫内膜组高(P<0.05);EGFR、cyclin D1的过表达在子宫内膜腺癌组明显比不典型增生组高(P<0.01),正常增生期子宫内膜组无过表达;EGFR的阳性表达与子宫内膜腺癌的临床分期和淋巴结转移有关(P<0.05);cyclin D1的阳性表达与子宫内膜腺癌的组织病理学分级、临床分期有关(P<0.05);MVD与子宫内膜腺癌的临床分期、组织病理学分级和淋巴结转移有高度相关(P<0.01);EGFR的阳性表达在子宫内膜腺癌MVD>x组比MVD≤x组高(P<0.05),EGFR与cyclin D1阳性表达呈正相关(P<0.01)。结论 EGFR、cyclin D1在子宫内膜腺癌组织中高表达及高MVD可促进子宫内膜腺癌的发生与发展;EGFR可通过微血管生成,加速子宫内膜腺癌的侵袭和转移。     

PAX2在子宫内膜癌中的表达及其与ERα的相关性

目的:探讨PAX2在子宫内膜癌组织中的表达情况,分析PAX2和子宫内膜癌临床病理参数的关系及其与ERα的相关性。方法:采用免疫组化法检测60例子宫内膜癌、20例子宫内膜不典型增生及30例正常子宫内膜组织中PAX2与ERα的表达情况。结果:(1)PAX2在正常子宫内膜组织、子宫内膜不典型增生、子宫内膜癌3组中的阳性表达率比较差异均有显著性(P<0.05)。PAX2的高表达与子宫内膜癌的病理类型、手术病理分期、肌层浸润深度及淋巴结转移有明显关系,与组织分化程度无明显相关(P>0.05)。(2)在ERα阳性的子宫内膜癌患者中,PAX2阳性表达率为75%,而在ERα阴性的子宫内膜癌患者中,PAX2阳性表达率为50%,两者相比有统计学意义(P<0.05)。结论:PAX2可作为判断子宫内膜癌预后的一种新指标,在子宫内膜癌中PAX2的表达可能与ERα密切相关。     

血清CA125在子宫腺肌病及子宫肌瘤中的诊断价值

【目的】探讨血清CA125对子宫腺肌病及子宫肌瘤的诊断价值。【方法】术前采用放射免疫法测定75例子宫腺肌病患者及93例子宫肌瘤患者的血清CA125值。【结果】在增生期子宫腺肌病及子宫肌瘤血清CA125的阳性率分别为89.36%和3.39%,分泌期分别为78.57%和2.94%,上述两组血清CA125平均水平在增生期分别为(90.70±54.71)kU/L和(13.16±72.99)kU/L,在分泌期为(108.81±69.72)kU/L和(15.14±13.10)kU/L。不论在增生期还是分泌期,子宫肌瘤组血清CA125阳性率及平均水平均显著低于腺肌病组,且差异有显著性(P<0.05)。【结论】测定血清CA125水平,对子宫腺肌病有重要的辅助诊断价值,且有助于与子宫肌瘤的鉴别诊断。     

基质金属蛋白酶-9在子宫内膜癌中的表达及其意义

目的:探讨基质金属蛋白酶-9(MMP-9)在正常子宫内膜、子宫内膜不典型增生、子宫内膜癌中的表达,及其与临床病理参数间的关系.方法:应用免疫组化S-P法检测14例正常子宫内膜、10例子宫内膜不典型增生及50例子宫内膜癌中MMP-9的表达情况.结果:在正常子宫内膜、子宫内膜不典型增生及子宫内膜癌中,MMP-9阳性表达率分别为14.3%、30.0%、62.0%,各组差异具有显著性(P＜0.05).在子宫内膜癌组织中,MMP-9表达与组织学分级、肌层浸润深度、手术病理分期、淋巴结转移均相关(P＜0.05).结论:MMP-9高表达与子宫内膜癌的发生发展密切相关.     

组织标本中组蛋白去乙酰化酶6蛋白水平与子宫内膜癌患者临床病理特征的关系

[目的]探讨组织标本中组蛋白去乙酰化酶6(HDAC6)蛋白水平与子宫内膜癌患者临床病理特征的关系.[方法]选取2018年3月至2020年3月在本院手术治疗的90例子宫内膜癌患者作为研究对象,取所有患者手术后癌组织与癌旁正常组织标本,采用免疫组织化学染色法测定组织标本中HDAC6蛋白表达情况,比较所有患者癌组织和癌旁正常组织中HDAC6蛋白阳性检出率及不同临床病理特征的子宫内膜癌患者癌组织中HDAC6蛋白表达情况.[结果]子宫内膜癌患者癌组织中HDAC6蛋白阳性检出率显著高于癌旁组织(P<0.05).不同年龄、病理分型、组织学分级及是否宫颈累及的子宫内膜癌患者癌组织中HDAC6蛋白阳性检出率比较差异无统计学意义(P>0.05);Ⅲ～Ⅳ期患者HDAC6蛋白阳性检出率显著高于Ⅰ～Ⅱ期患者(P<0.05);淋巴结转移患者HDAC6蛋白阳性检出率显著高于非淋巴结转移患者(P<0.05);肌层浸润≥1/2患者HDAC6蛋白阳性检出率显著高于肌层浸润<1/2患者(P<0.05).[结论]子宫内膜癌患者癌组织中HDAC6蛋白表达上调,其表达水平与患者FIGO分期、淋巴结转移、肌层浸润深度密切相关.     

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。