卵巢和腹壁子宫内膜异位症雌孕激素受体亚型的表达研究

目的通过检测子宫内膜位症患者正常和异位内膜中的雌孕激素受体亚型的表达,探讨其与子宫内膜异位症发病的关系。方法收集经临床和病理确认的育龄期卵巢子宫内膜异位症52例和腹壁瘢痕子宫内膜异位症6例为实验组;育龄期正常子宫内膜36例为对照组。应用免疫组织化学方法检测异位和在位子宫内膜组织中雌激素受体亚型(ERα、ERβ1、ERβ2)、孕激素受体亚型(PRA、PRB)表达。结果卵巢异位内膜腺上皮组ERβ1、PRA、PRB表达均明显低于对照组,腹壁异位子宫内膜组的ERβ1、PRB表达也明显低于对照组,差异均具有统计学意义(P0.05);此外卵巢异位内膜间质细胞ERβ1、PRB表达均明显低于对照组,腹壁异位子宫内膜组的ERβ1、ERβ2、PRB表达也明显低于对照组,差异均具有统计学意义(P0.05)。结论无论是卵巢还是腹壁子宫内膜异位,异位内膜性激素受体亚型表达与正常内膜存在明显差异,提示与内膜异位症发病有密切关系。     

子宫内膜间质肉瘤的临床病理特点和免疫表型分析

目的:探讨子宫内膜间质肉瘤(ESS)的临床病理特点、浸润生长特征和免疫表型分析。方法:分别对合并妊娠和子宫平滑肌瘤的2例子宫内膜间质肉瘤的临床资料、病理形态学和免疫组化表型进行观察。结果:合并妊娠的例1显示圆形或卵圆形的ESS瘤细胞团位于蜕膜组织和A-S腺体之间,并侵入肌壁呈条索或团块状突入淋巴管或突破脉管基底膜浸润生长;例2在子宫平滑肌瘤内有如例1相似的ESS特点,2例的免疫表型显示子宫内膜间质肉瘤细胞CD10阳性、PR阳性,间质肉瘤区内局灶性DES、SMA阳性;平滑肌瘤细胞示DES、SMA弥漫性阳性,内皮细胞示FVIII、CD34阳性;蜕膜组织为CD10阴性表达。结论:子宫内膜间质肉瘤可与妊娠相容共存,其原因可能是ESS瘤细胞颇似子宫内膜间质细胞的良性外貌。间质肉瘤细胞除直接蔓延外,还有假性脉管和真性脉管浸润性生长。CD10表达可作为ESS的鉴别诊断的重要标记。     

子宫内膜间质肉瘤17例临床病理和免疫表型分析

目的探讨子宫内膜间质肉瘤(ESS)的发病情况、临床分期、形态学特征和免疫表型特点。方法 2004年至2010年在南京江北人民医院和徐州市中心医院病理科观察到子宫体间质肿瘤2 791例,发现ESS 17例。对17例ESS的年龄、临床分期、分化程度和免疫表型进行回顾性分析。结果 17例ESS患者平均年龄为(47.0±10.6)岁,70.6%在临床Ⅰ期和Ⅱ期。14例(82.4%)为低级别ESS,3例(17.6%)为高级别或未分化ESS。17例均测定免疫组化标记物,雌激素受体(ER)阳性5例(29.4%),孕激素受体(PR)阳性9例(52.9%);表达CD10者10例(58.8%),表达p53者12例(70.6%)。结论本组ESS占同期子宫体间质肿瘤的0.61%,且大部分为低级别ESS。p53、CD10及ER、PR呈不同程度阳性表达。     

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。     

β-catenin和APC蛋白在子宫内膜腺癌中的表达及意义

目的 探讨β-catenin和APC蛋白在子宫内膜腺癌中的表达及意义.方法 采用免疫组化二步法检测β-catenin和APC蛋白在60例子宫内膜腺癌、20例子宫内膜增生症及30例正常子宫内膜组织中的表达.结果 在细胞膜上,子宫内膜腺癌β-catenin阳性表达率(36.67%,22/60)显著低于子宫内膜增生症(70.00%)及正常子宫内膜(63.33%,P<0.05);β-catenin阳性表达率与子宫内膜癌的临床分期、病理分型密切相关;子宫内膜腺癌、子宫内膜增生症可见核表达.表达率分别为(30.00%、60.00%),而正常子宫内膜核表达率为零(P<0.005).APC蛋白主要定位于细胞核上,在子宫内膜腺癌,子宫内膜增生症及正常子宫内膜组织阳性表达率分别为(63.33%、45.00%、50.00%,P>0.05).结论 在子宫内膜癌发生、发展过程中,β-catenin的改变起着主导作用.     

bcl-2、ER、PR在子宫内膜癌组织中的表达及其意义

目的:探讨bcl-2、雌激素受体(ER)及孕激素受体(PR)在不同类型子宫内膜组织中的表达及其与子宫内膜癌的发生、发展的关系。方法:采用免疫组织化学方法(SP法)检测55例子宫内膜癌组、13例不典型内膜增生组及11例正常子宫内膜组(对照组)的bcl-2、雌激素受体及孕激素受体的水平,行光学显微镜观察结果,进行阳性平均百分率计算,并行统计学处理。结果:bcl-2阳性表达在正常子宫内膜组最多,其阳性表达率为96.1%,不典型内膜增生组阳性表达率为78.1%,子宫内膜癌组阳性表达率为56.9%,3组比较,差异有显著性(P<0.05);雌激素阳性表达在正常子宫内膜组最多,其阳性表达率为66.1%,不典型内膜增生组阳性表达率为34.8%,子宫内膜癌组阳性表达率为20.9%,3组比较,差异有显著性(P<0.05);孕激素阳性表达在正常子宫内膜组最多,其阳性表达率为89.4%,不典型内膜增生组阳性表达率为70.9%,子宫内膜癌组阳性表达率为64.3%,3组比较,差异有显著性(P<0.05)。结论:bcl-2表达减少可能是子宫内膜癌发生过程中的早期事件。雌激素是子宫内膜癌危险因素并随病理分级的升高雌激素受体的表达逐渐减少。孕激素与雌激素相反,延缓子宫内膜癌发生与发展。     

P16、PRB在子宫内膜异位症和子宫腺肌病中的表达

目的:探讨P16、视网膜母细胞瘤蛋白质(PRB)在子宫内膜异位症和子宫腺肌病中表达的状况和意义.方法:采用免疫组化法检测25例子宫内膜异位症患者和25例子宫腺肌病患者的病变组织中P16、PRB的表达,10例正常妇女的子宫内膜为对照.结果:子宫内膜异位症标本中P16的核阳性表达率为16%,PRB核阳性表达率为32%.子宫腺肌病标本中P16蛋白的阳性表达率为36%;PRB不表达.在10例正常妇女的子宫内膜标本中P16不表达,PRB的核阳性表达率为80%.结论:(1)子宫内膜异位症是肿瘤形成过程,具有恶性转化的潜力;(2)子宫内膜异位症和子宫腺肌病的发病机制不同.     

Livin、PTEN蛋白在EMs组织中的表达及其意义

【目的】探讨Livin蛋白、PTEN蛋白在子宫内膜异位症(EMs)组织中的表达及其意义。【方法】选取2016年1月至2018年5月在本院病理科获取的术后EMs子宫内膜组织80例(EMs组)和因子宫肌瘤手术获得正常子宫内膜组织80例作为对照组,采用免疫组化法检测并比较两组标本中的Livin、PTEN蛋白表达水平,并分析其临床意义。【结果】EMs组的PTEN蛋白阳性表达率显著低于对照组(P<0.05);Livin蛋白阳性表达率显著高于对照组(P<0.05);AFS分期Ⅲ?Ⅳ期的EMs组患者Livin蛋白、PTE N蛋白阳性表达率与Ⅰ~Ⅱ期比较差异无统计学意义(P>0.05);EMs患者在位内膜的PTEN蛋白阳性表达率高于异位内膜(P<0.05),在位内膜的Livin蛋白阳性表达率低于异位内膜(P<0.05):【结论】EMs子宫内膜组织中Livin蛋白高表达、PTEN蛋白低表达,可能与EMs的发生有关。     

低度恶性子宫内膜间质肉瘤临床病理分析

目的:探讨低度恶性子宫内膜间质肉瘤(LESS)的临床病理学特征、诊断和鉴别诊断。方法:收集17例低度恶性子宫内膜间质肉瘤,复阅病历档案,进行随访,同时观察其临床病理特点,并作免疫组化染色分析。结果:患者年龄24~73岁,平均44.5岁。低度恶性子宫内膜间质肉瘤(LESS)临床上主要表现为不规则的阴道出血。光镜下观察肿瘤细胞类似增殖期子宫内膜间质细胞;呈舌状浸润肌层或弥漫浸润,肿瘤内有大量的似螺旋小动脉。3例伴有不同程度的平滑肌分化,1例伴性索样分化。结论:低度恶性子宫内膜间质肉瘤(LESS)临床少见,术前诊断困难,预后较好。确诊主要依靠组织病理学和免疫组化,诊断上应与富细胞性平滑肌瘤、静脉内平滑肌瘤病、腺肉瘤相鉴别。     

22例低度恶性子宫内膜间质肉瘤的临床病理分析

目的探讨低度恶性子宫内膜间质肉瘤(LESS)的临床病理学特征、诊断和鉴别诊断。方法收集22例低度恶性子宫内膜间质肉瘤,复阅病历档案,进行随访,同时观察其临床病理特点,并作免疫组化染色分析。结果患者年龄23～73岁,平均43岁。低度恶性子宫内膜间质肉瘤(LESS)临床上主要表现为不规则的阴道出血。光镜下观察肿瘤细胞类似增殖期子宫内膜间质细胞;呈舌状浸润肌层或弥漫浸润,肿瘤内有大量的似螺旋小动脉。3例伴有不同程度的平滑肌分化,1例伴性索样分化。结论低度恶性子宫内膜间质肉瘤(LESS)临床少见,术前诊断困难,预后较好。确诊主要依靠组织病理学和免疫组化,诊断上应与富细胞性平滑肌瘤、静脉内平滑肌瘤病、腺肉瘤相鉴别。     

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.     

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。     

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.     

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。