血管内皮生长因子在胰腺癌中的表达及意义

目的探讨血管内皮生长因子(VEGF)表达在胰腺癌中的变化以及与胰腺癌临床病理间的关系.方法应用免疫组化法分析36例胰腺癌、12例正常胰腺组织中的VEGF表达.结果胰腺癌组织中VEGF阳性表达率为75% ,显著高于癌旁组织23.5%(P<0.01) 及正常胰腺组织16.7%(P<0.01),淋巴结转移组VEGF阳性表达率为87.5%,显著高于无转移组60.0%(P<0.05)及正常胰腺组4 1.7%(P<0.05),而VEGF与分化程度及TNM分期无关.结论 VEGF表达高低可作为判断胰腺癌淋巴结转移预后的关系.     

Ang-2和VEGF在大肠癌血管生成中的作用及与其临床病理特征的关系

[目的]探讨促血管生成素-2(Ang-2)及血管内皮生长因子(VEGF)在大肠癌组织肿瘤血管生成中的作用及与其临床病理特征的关系.[方法]采用免疫组织化学方法检测Ang-2及VEGF蛋白在62例大肠癌组织中的表达水平,计数微血管密度(MVD).[结果]肠癌组织中Ang-2与MVD呈正相关(r=0.7011,P<0.05);VEGF阳性表达组Ang-2和MVD明显高于阴性组(P<0.01);浸润浆膜、淋巴结转移肠癌组织中Ang-2、VEGF水平均高于无浆膜浸润、无淋巴结转移者(P<0.05);大肠癌各Dukes分期中,(C D)期Ang-2水平和VEGF阳性表达率均高于(A B)期(P<0.05).[结论]Ang-2、VEGF及其相互作用对促进大肠癌血管生成,在大肠癌的侵袭和转移中可能起到重要作用.     

SPARC和VEGF在胃癌组织中的表达及与血管生成的关系

目的探讨SPARC和VEGF在胃癌组织中的表达及其与胃癌血管生成的关系。方法用免疫组化方法检测80例胃癌组织和30例癌旁正常组织中SPARC和VEGF的表达,用CD34标记胃癌组织的微血管密度(MVD)。结果①胃癌组织中,SPARC、VEGF和MVD均显著高于正常胃黏膜(P<0.05)。②胃癌组织中,SPARC主要表达于间质纤维母细胞的胞质,VEGF主要表达于癌细胞的胞质,且均与胃癌的分化程度、临床分期、Lauren分型及淋巴结转移显著相关(P<0.05);③胃癌组织中的MVD与分化程度、临床分期、Lauren分型、浸润深度及淋巴结转移显著相关(P<0.05);④胃癌组织中,SPARC与VEGF的表达呈反比(P<0.01),且随着MVD的增高,SPARC逐渐减少,而VEGF则逐渐增加。结论 SPARC和VEGF的表达与胃癌的血管生成关系密切,SPARC抑制胃癌的血管生成,而VEGF则促进胃癌的血管生成。     

大肠癌中pAkt、VEGF和MVD的检测及其临床意义

目的 检测大肠癌组织磷酸化丝氨酸/苏氨酸激酶(pAkt)、血管内皮生长因子(VEGF)的表达和微血管密度(MVD)及其临床意义.方法 应用免疫组化SP法检测76例大肠癌的pAkt、VEGF和MVD.结果 大肠癌pAkt 和VEGF的阳性表达率分别为73.7%(56/76)和85.5%(65/76).pAkt的阳性表达与肿瘤浸润深度、临床分期和淋巴结转移(P<0.05)及其MVD(P<0.01)显著相关.pAkt阳性组的MVD明显高于阴性组.VEGF的阳性表达与大肠癌的临床分期显著相关(P<0.05).pAkt蛋白表达与VEGF蛋白表达密切相关(P<0.05).结论 pAkt和VEGF与大肠癌发生、发展和转移密切相关,提示阻断pI3K/Akt信号传导通路将对大肠癌的治疗提供新的靶点.     

血小板源性生长因子及血管内皮生长因子与食管鳞状细胞癌肿瘤血管生成的关系研究

目的探讨血小板源性生长因子(PDGF)、血管内皮生长因子(VEGF)与食管鳞状细胞癌(ESCC)肿瘤血管生成的关系。方法 2013年9月至2015年8月于该院行ESCC根除术的患者93例,以手术切除的食管癌组织作为观察组,以30例正常食管上皮组织作为对照组。采用免疫组化法检测食管组织PDGF、VEGF表达,计算微血管密度(MVD),分析PDGF、VEGF表达与ESCC病理特征及MVD的关系。结果观察组PDGF、VEGF表达阳性率及MVD水平高于对照组(P0.05)。PDGF、VEGF的表达与ESCC分化程度、淋巴结转移、浸润深度等病理特征相关,MVD与ESCC肿瘤直径、肿瘤淋巴结转移(TNM)分期、浸润深度等病理特征相关(P0.05)。ESCC组织PDGF、VEGF的表达与MVD呈正相关(P0.05)。结论 PDGF、VEGF可能参与了ESCC肿瘤血管生成,对ESCC发生、发展有重要作用。     

uPA、VEGF和微血管密度在卵巢恶性生殖细胞肿瘤中表达及其临床意义研究

目的:探讨激酶型纤溶酶原激活物 (urokinase-type plasminogen activator,uPA)和血管内皮生长因子(vascular endothelial growth factor,VEGF)及微血管密度(microvascular density,MVD)在卵巢恶性生殖细胞肿瘤(malignant ovarian germ cell tumor,MOGCT)侵袭转移中的作用及其预后价值.方法:应用免疫组织化学方法检测43例MOGCT及10例正常卵巢组织中uPA和VEGF蛋白的表达情况,同时标记CD34肿瘤新生血管,计算MVD.结果:uPA和 VEGF的阳性表达率及MVD值在MOGCT患者不同年龄、不同病理类型、不同腹腔积液程度、有无网膜转移、有无肝转移上差异无统计学意义(P>0.05);uPA和VEGF的阳性表达率、表达强度及MVD值在不同FIGO分期、有无淋巴结转移上差异有统计学意义(P<0.05).Kaplan-Meier生存曲线显示uPA蛋白阳性表达者的生存期较阴性表达者明显缩短,uPA与MOGCT的总生存期有关(P<0.05);Cox比例风险模型分析提示,uPA蛋白表达越强、MVD值越高患者预后越差,二者可影响患者的生存期.结论:uPA,VEGF的表达及MVD值与MOGCT的侵袭转移密切相关;uPA和MVD可作为判断MOGCT的预后指标.     

环氧化酶-2在乳腺癌中的表达及与血管生成的关系

[目的]检测环氧化酶-2(COX-2)在乳腺癌组织中的表达,研究其与乳腺癌临床病理特征及微血管密度(MVD)、血管内皮生长因子(VEGF)之间的关系.探讨COX-2对乳腺癌血管生成的作用和意义.[方法]应用免疫组化法检测73例乳腺癌标本中COX-2、VEGF的表达和0D34标记的MVD值.[结果]73例病例中57例COX-2表达阳性,表达率为78.1%(57/73),而中度以上表达率为47.9%(35/73);COX-2表达程度与患者年龄、肿瘤直径及HER-2/neu表达程度无关(P>0.05),但与腋淋巴结转移状况和肿瘤分期有关(P<0.01);COX-2表达程度与VEGF表达程度及MVD值明显相关,高表达组的MVD明显高于低表达组,两组差异有显著性(P<0.01).[结论]COX-2能促进乳腺癌新生血管的形成,进而影响乳腺癌的发展和转归.     

环氧化酶-2、血管内皮生长因子、微血管密度与胃癌侵袭转移的相关性研究

目的探讨环氧化酶-2(COX-2)、血管内皮生长因子(VEGF)、微血管密度(MVD)与胃癌侵袭转移的相关性。方法采用SP免疫组化技术对82例胃癌组织、26例正常胃黏膜进行上述3个指标的检测。结果胃癌组织中COX-2、VEGF的表达及MVD计数明显高于对照组(P<0.01),3个指标的高表达与胃癌淋巴结转移、浸润深度、TNM分期显著相关(P<0.05),而与肿瘤大小、分化程度无关。COX-2阳性组MVD高于COX-2阴性组,COX-2与VEGF呈显著正相关性。结论COX-2与胃癌的发生及侵袭、转移有关,可能是通过参与胃癌的血管生成而起作用。     

甲状腺乳头状腺癌VEGF和P53蛋白表达与淋巴结转移和微血管密度的关系

目的探讨甲状腺乳头状腺癌中血管内皮生长因子(VEGF)和p53蛋白表达与微血管密度(MVD)以及颈淋巴结癌转移的关系.方法应用免疫组化技术对37例甲状腺乳头状腺癌VEGF和p53蛋白的表达进行检测,用FⅧRAg显示MVD,行相对定量研究.结果甲状腺乳头状腺癌VEGF和p53蛋白的表达率明显高于对照组(P＜0.01);颈淋巴结癌转移组的VEGF表达率高于无癌转移组(P＜0.05);而p53蛋白的表达率在前述两组间差异无显著性意义(P＞0.05).颈淋巴结癌转移组的MVD高于无癌转移组(P＜0.05).VEGF表达与MVD呈显著正相关(P＜0.01); p53表达与MVD无关(P＞0.05).结论甲状腺乳头状腺癌VEGF的表达与颈淋巴结转移有一定关系,还与其MVD相一致,提示VEGF的表达和MVD可作为判断甲状腺乳头状腺癌预后的一项重要参考指标.     

血管内皮生长因子和微血管密度与乳腺浸润性导管癌生物学行为的关系

目的探讨血管内皮生长因子和微血管密度与乳腺浸润性导管癌生物学行为的关系。方法应用免疫组化方法检测55例术前未作过化疗的乳腺浸润性导管癌组织中血管内皮生长因子(VEGF)、微血管密度(MVD)的表达,与乳腺癌的临床分期、淋巴结转移等生物学行为进行统计学分析。结果 (1)乳腺浸润性导管癌组织中MVD值与淋巴结转移、临床分期密切相关(P0.05);(2)VEGF主要表达于肿瘤细胞胞浆或胞膜,与乳腺浸润性导管癌淋巴结转移、临床分期有关(P0.05);(3)乳腺浸润性导管癌VEGF表达与MVD值密切相关(P0.05)。结论 VEGF表达与乳腺浸润性导管癌的血管生成和侵袭转移关系密切。MVD和VEGF的检测可以用于乳腺浸润性导管癌的预后判断。     

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.