食管癌幽门螺杆菌L型感染与其血管形成的关系

目的探讨食管癌Hp-L型(即球形:Hp)感染与肿瘤血管形成的相关性及Hp-L型对食管癌生长、侵袭和转移等生物学行为的影响。方法应用革兰染色、电镜和免疫组化ABC法,检测98例食管癌和30例对照组(食管癌切缘正常组织)的Hp-L型;用免疫组化SP法检测上述组织的微血管密度(MVD)值和血管内皮生长因子(VEGF)、p53表达,分析Hp-L型与MVD、VEGF、p53表达以及临床病理因素的关系。结果 食管癌组的Hp-L型阳性率为60.2％。电镜下组织中的Hp-L型有两种类型,可位于癌细胞间或癌细胞胞浆。食管癌组的Hp-L型阳性率、MVD值以及VEGF、p53表达阳性率均高于对照组(P<0.005～0.001),食管癌组中Hp-L型阳性组的MVD值、VEGF和p53表达阳性率也高于其Hp-L型阴性组(P<0.005～0.001)。Hp-L型阳性与MVD呈正相关(r=0.46,P<0.01),与VEGF、p53表达呈正相关(r=0.31,P<0.01)。食管癌组的Hp-L型阳性数与癌细胞的血管侵袭、侵袭深度、食管旁淋巴结转移及远处淋巴结转移相关,而与肿瘤大小无关。结论 Hp-L型与食管癌的血管形成密切相关,是影响食管癌生长、侵袭和转移的重要因素之一。     

食管癌VEGF与p53蛋白表达的临床意义

目的探讨食管癌VEGF与p53蛋白表达在食管癌的病理学意义及其与血管新生的关系。方法选择40例手术切除的食管癌标本,确定其病理学特点,并对其VEGF与p53蛋白和微血管进行免疫组织化学染色,明确VEGF与p53蛋白表达和血管新生的强度。结果VEGF表达阳性率为67.5％,p53蛋白表达阳性率为50.0％。MVD值为29.00±24.56。有淋巴结转移者与无淋巴结转移者VEGF表达的阳性率有明显差异(P<0.05)。VEGF表达阴性、弱阳性及强阳性者间MVD值比较均有显著差异(P值均<0.05)。p53蛋白表达阴性、弱阳性及强阳性者间MVD值比较无显著差异(P值均>0.05),与VEGF表达阳性率也无显著差异(P值均>0.05)。结论食管癌VEGF表达与血管新生密度及与淋巴结转移均有显著相关。p53蛋白表达与VEGF表达及血管新生强度均可能无密切关系。     

甲状腺乳头状癌VEGF、MMP-9及COX-2蛋白表达与淋巴道转移和血管生成的相关性

 目的 通过检测血管内皮细胞生长因子(VEGF)、基质金属蛋白酶-9(MMP -9)、环氧化酶-2(COX-2)在 甲状腺乳头状癌（PTC）细胞中的表达情况,探讨它们与PTC颈淋巴结转移的关系。 方法 采用免疫组织化学SP法检测74例PTC(有淋巴结转移者39例,无淋巴结转移者35例)中VEGF、 MMP-9、COX-2的表达,并对CD34表达阳性血管进行MVD计数。 结果 VEGF、MMP-9、COX-2的表达与MVD值在淋巴结转移组与无转移组之间的差异均具有统计学意义 (P<0.05),与PTC淋巴结转移呈正相关;VEGF、MMP-9、COX-2的表达与MVD值正相关 (P<0.05) ,VGEF、MMP-9阳性表达率与肿瘤大小密切相关（P<0.05）。 结论 甲状腺乳头状癌VEGF、MMP-9、COX-2蛋白表达与其淋巴道转移和MVD有关,检测这几种蛋白表 达将有助于判断甲状腺乳头状癌的转移潜能、血管生成能力及预后。     

食管癌组织中p53和VEGF的表达及其与肿瘤血管生成的关系

目的探讨p53、血管内皮生长因子 (vascular endothelial growth factor,VEGF)的表达和肿瘤内微血管密度 (microvessel density,MVD)测定在食管癌中的意义.方法采用免疫组化方法,检测 45例食管癌患者手术切除标本p53、VEGF的表达,并用CD34抗体标记肿瘤组织血管内皮细胞,计算MVD.结果 p53、VEGF总阳性表达率分别为73.3%(33/45)和62.2%(28/45),MVD平均为48±20.p53的表达与临床TNM分期和淋巴结转移相关,MVD和VEGF表达与食管癌的细胞分化程度、浸润深度和临床TNM分期密切相关.p53/VEGF表达均阳性组MVD高于p53/VEGF其一阳性组和p53/VEGF均阴性组,p53、VEGF表达与MVD密切相关,并存在交互作用.p53和VEGF表达符合率为84.4%(38/45),VEGF与p53的表达有相关性(P<0.001).结论 (1)p53、VEGF的表达以及MVD的测定可作为判断食管癌恶性潜能的重要生物学指标.(2)p53、VEGF的表达对肿瘤血管形成可能起重要作用,联合检测p53、VEGF的表达对了解肿瘤血管形成的机制有一定意义.     

非小细胞肺癌组织中血管内皮生长因子的表达与微血管密度的关系

 目的　探讨非小细胞肺癌 (NSCLC)组织中血管内皮生长因子 (VEGF)表达和微血管密度(MVD)的关系。方法　采用免疫组化S P法对 76例NSCLC标本中VEGF表达和MVD进行了检测。结果　在NSCLC中鳞癌的VEGF表达阳性率显著高于腺癌 (P <0 .0 5 ) ;VEGF表达阳性率和MVD值与肿瘤组织学分化程度有关 ,低分化癌VEGF表达阳性率和MVD值显著高于中、高分化癌 (P <0 .0 5 ) ;淋巴结转移阳性组NSCLC的VEGF表达阳性率和MVD值显著高于阴性组 (P <0 .0 5 )。结论　VEGF可引起瘤内MVD增多 ,促进肿瘤的生长和转移 ;检测VEGF表达强度 ,可作为判定NSCLC转移潜能和评价预后的指标     

T-cadherin在胃癌中的表达及其与VEGF、MVD之间的关系

目的:探讨T-cadherin在胃癌组织中表达及其与VEGF、MVD之间的关系。方法:采用免疫组化SP法对80例胃癌组织及癌旁正常胃组织的T-cadherin、血管内皮生长因子(Vascularendothelialgrowthfactor,VEGF)和CD34的表达情况进行检测。结果:T-cadherin主要在胃癌细胞膜上表达,阳性率为45.0%(36/80),而癌旁正常胃组织中T-cadherin阳性率为62.5%(50/80),两者比较差异有统计学意义(P=0.026)。VEGF在癌旁正常细胞阳性率为28.75%,在胃癌中表达阳性率为71.25%,差异有统计学意义(P=0.000)。CD34阳性细胞着色部位主要是血管内皮细胞的胞膜和胞浆,胃癌中标记的微血管明显多于正常组织(54.96±7.28/HPFvs27.50±6.10/HPF,P<0.001)。T-cadherin和VEGF蛋白表达呈负相关(P=0.001);T-cadherin阳性组的MVD值明显低于阴性低表达组(P<0.001).T-cadherin、VEGF、CD343种蛋白在胃癌中的阳性表达与患者性别和年龄、肿瘤大小均无关(P>0.05),但与组织分化程度、淋巴结转移及pTNM分期显著相关(P<0.05)。结论:T-cadherin的异常表达可以作为临床评价胃癌诊断、指导治疗及判断预后的辅助指标之一。     

T-cadherin在胃癌中的表达及其与VEGF、MVD之间的关系

目的:探讨T-cadherin在胃癌组织中表达及其与VEGF、MVD之间的关系。方法:采用免疫组化SP法对80例胃癌组织及癌旁正常胃组织的T-cadherin、血管内皮生长因子(Vascularendothelialgrowthfactor,VEGF)和CD34的表达情况进行检测。结果:T-cadherin主要在胃癌细胞膜上表达,阳性率为45.0%(36/80),而癌旁正常胃组织中T-cadherin阳性率为62.5%(50/80),两者比较差异有统计学意义(P=0.026)。VEGF在癌旁正常细胞阳性率为28.75%,在胃癌中表达阳性率为71.25%,差异有统计学意义(P=0.000)。CD34阳性细胞着色部位主要是血管内皮细胞的胞膜和胞浆,胃癌中标记的微血管明显多于正常组织(54.96±7.28/HPFvs27.50±6.10/HPF,P<0.001)。T-cadherin和VEGF蛋白表达呈负相关(P=0.001);T-cadherin阳性组的MVD值明显低于阴性低表达组(P<0.001).T-cadherin、VEGF、CD343种蛋白在胃癌中的阳性表达与患者性别和年龄、肿瘤大小均无关(P>0.05),但与组织分化程度、淋巴结转移及pTNM分期显著相关(P<0.05)。结论:T-cadherin的异常表达可以作为临床评价胃癌诊断、指导治疗及判断预后的辅助指标之一。     

食管癌中p53、VEGF-C的表达与MVD相关性研究

目的探讨p53、VEGF-C及MVD与食管病变及食管鳞癌的生物学行为的相关性。方法应用S-P免疫组化染色法对20例正常组织、20例食管炎症、35例基底细胞增生、35例非典型增生、25例原位癌及80例浸润癌进行了p53、VEGF-C标记分析及微血管密度(MVD)计数。结果80例食管浸润癌中p53、VEGF-C的阳性表达率分别为47·5%和45%,明显高于其他食管病变的阳性率;MVD为44·6±10·6,显著高于食管其他病变的微血管密度(P<0·05),且p53,VEGF-C及MVD与食管癌的病理分级,淋巴结转移有关,而与肿瘤的浸润深度无关;p53及VEGF-C阳性表达的病例其MVD明显高于p53及VEGF-C阴性表达的病例。p53,VEGF-C与MVD呈正相关。结论p53、VEGF-C,MVD与食管病变及食管癌的侵袭转移密切相关,对估计患者预后具有重要价值,并有可能做为食管癌临床生物治疗的参考指标。     

人肝癌组织中iNOS、VEGF的表达及微血管密度的病理意义

背景与目的:诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)和血管内皮生长因子(vascular endothelial growth factor,VEGF)被认为是诱导和调节肿瘤血管生成,进而影响肿瘤病理进展和预后的重要相关因子。本研究检测人肝细胞癌(hepatocellular carcinoma,HCC)及相应癌旁组织中iNOS、VEGF的表达,探讨其与血管生成的关系,为临床诊治HCC及判断其预后提供理论依据。方法:应用组织芯片技术,采用原位杂交和免疫组化法分析147例HCC组织及癌旁组织中iNOS、VEGF的表达,并用CD34标记免疫组化法检测微血管密度(microvessel density,MVD)。结果:iNOS、VEGF在癌旁组织中的阳性率分别为33.33%和40.82%,而在癌组织中的阳性率分别为86.39%和78.91%,癌组织与癌旁组织比较差异有显著性(P<0.01)。癌组织的MVD值为56.5±12.8,癌旁组织的MVD值为8.4±3.6,两者差异有显著性(P<0.01)。iNOS的表达与肿瘤大小、乙型肝炎表面抗原(HBsAg)相关(P<0.05),而与转移和肿瘤分化程度无关(P>0.05)。VEGF的表达及MVD值与肿瘤大小、转移相关(P<0.05),而与HBsAg和肿瘤分化程度无关(P>0.05)。在癌组织中MVD与VEGF、iNOS的表达呈正相关,VEGF和iNOS之间亦存在正相关关系(P<0.01)。结论:HCC中iNOS及VEGF的表达与肿瘤血管生成有关。癌组     

VEGF、p53和MVD在胃癌中的表达及临床意义

目的:检测胃癌组织和血清中VEGF、组织的p53、MVD的表达,并观察其与胃癌生物学行为之间的关系,以及三者的相关性.方法:应用酶联免疫技术(ABC-ELISA方法)检测73例胃癌患者术前血清和20例健康体检者血清中的VEGF表达水平,同时应用免疫组织化学染色方法检测癌组织和癌旁组织中VEGF、P53和CD34的表达.结果:胃癌患者术前血清VEGF表达水平明显高于健康体检者(VEGF:101.8±53.3ng/Lvs 16.1±22.5 ng/L,P＜0.05).胃癌患者术前血清VEGF表达水平随浸润深度、TNM分期、淋巴结转移、远处转移而增高(P＜0.05),而与年龄、性别及病理类型无关.胃癌组织VEGF的阳性表达率为71.2%,癌旁组织中VEGF 未见阳性表达,P＜0.05;胃癌组织VEGF表达水平与胃癌浸润深度、TNM分期、淋巴结转移、远处转移有关(P＜0.05),而与年龄、性别及病理类型无关.胃癌患者术前血清VEGF的表达水平与组织VEGF的表达呈正相关(r=0.346,P＜0.01).胃癌组织中p53的阳性表达率明显高于癌旁组织,P＜0.05.p53在胃癌组织中的表达与性别、年龄、病理类型、浸润深度无关(P＞0.05),与淋巴结转移、TNM分期、远处转移有关,P＜0.05.MVD值在胃癌组织中明显高于胃癌癌旁组织,并与性别、年龄、病理类型无关(P＞0.05),与浸润深度、淋巴结转移、TNM分期、无远处转移有关(P＜0.05).胃癌患者术前血清与组织VEGF表达水平分别与p53的表达水平呈正相关(r=0.316,P＜0.01;r=0.290,P＜0.05);胃癌患者术前血清与组织VEGF表达水平分别与MVD的表达水平呈正相关(r=0.434,P＜0.01;r=O.512,P＜0.01);胃癌患者p53与MVD的表达水平呈正相关(r=0.431,P＜0.01).结论:胃癌患者VEGF、p53与MVD胃癌的发生、发展、转移及预后起着重要的作用,有望成为胃癌术前诊断、判断转移危险的新的肿瘤标志物.     

Selenium, lycopene, alpha-tocopherol, beta-carotene, retinol, and subsequent bladder cancer

To examine the association between serum nutrients and the development of bladder cancer we measured selenium, alpha-tocopherol, lycopene, beta-carotene, retinol, and retinol-binding protein in serum collected from 25,802 persons in Washington County, MD, in 1974. Serum samples were kept frozen at -70 degrees C. In the subsequent 12-year period, 35 cases of bladder cancer developed among participants. Comparisons of serum levels in 1974 among cases and two matched controls for each case showed that selenium was significantly lower among cases than controls (P = 0.03), lycopene was lower among cases at a borderline level of significance (P = 0.07), and alpha-tocopherol was nonsignificantly lower (P = 0.13). For selenium there was a nearly linear increase in risk with decreasing serum levels (P = 0.03). When examined by tertiles, the odds ratio associated with the lowest tertile of selenium compared to the highest tertile was 2.06. Serum levels of retinol, retinol-binding protein, and beta-carotene were similar among cases and controls. These results support a role for selenium in the prevention of bladder cancer.     

Susceptibility of Ureaplasma urealyticum to Tetracycline,Doxycycline, Erythromycin,Roxithromycin, Clarithromycin,Azithromycin, Levofloxacin and Moxifloxacin

Abstract

The in vitro activity of tetracycline, doxycycline, erythromycin, roxithromycin, clarithromycin, azithromycin, levofloxacin and moxifloxacin was tested against 63 clinical isolates of Ureaplasma urealyticum. The minimal inhibitory concentrations (MICs) and the minimal bactericidal concentrations (MBCs) were determined by the broth microdilution method in A7 medium. The miC50 and miC90 of the tested agents after 24 h of incubation were as follows: Tetracycline, 0.5 and 2.0 μg/ml; doxycycline, 0.125 and 0.25 μg/ml; erythromycin, 2.0 and 8.0 μg/ml; roxithromycin, 2.0 and 4.0 μg/ml; clarithromycin, 0.25 and 1.0 μg/ml; azithromycin, 2.0 and 4.0 μg/ml; levofloxacin, 1.0 and 2.0 μg/ml; and moxifloxacin, 0.5 and 0.5 μg/ml, respectively. The MIC values after 24 h and 48 h incubation differed by no more than one dilution for all the agents with the exception of doxycycline (two dilution difference for MIC₉₀). Overall, moxifloxacin was the most active agent in vitro against U. Urealyticum, with the narrowest difference between MIC and MBC values, followed closely by levofloxacin. Clarithromycin was the most active macrolide.     

80岁以上合并肠梗阻的结直肠癌患者的外科治疗

目的 探讨80岁以上合并肠梗阻的结直肠癌患者的外科治疗策略。方法 回顾性分析中国医学科学院结直肠外科2007年1月—2018年12月行结直肠癌手术且术前合并肠梗阻的77例80岁以上患者的临床病理资料,按照手术方式分为根治组（n=58）与非根治组（n=19）,比较两组患者临床病理特征、围手术期相关指标和预后。采用Kaplan-Meier法进行生存分析,Log rank检验进行生存时间比较;应用Cox比例风险模型进行多因素分析,对影响预后的因素进行分析。结果 根治组TNM分期为Ⅳ期患者的比例明显低于非根治组（8.6% vs. 57.9%, P<0.001）。根治组患者的5年生存率明显高于非根治组（65.5% vs. 26.3%, P<0.001）。单因素分析显示TNM分期和是否行根治性手术与合并肠梗阻的老年结直肠癌患者预后相关。多因素分析表明是否行根治性手术是影响80岁以上合并肠梗阻的结直肠癌患者预后的独立因素。结论 是否行根治性手术是影响80岁以上合并肠梗阻的结直肠癌患者预后的独立因素。     

Cholesterol, weight, height, Quetelet's index, and colon cancer recurrence

The association of low serum cholesterol with colon cancer mortality suggests that low serum cholesterol promotes colon cancer recurrence. We compared cumulative 5-year recurrence-free rates of 279 colon cancer patients in relation to serum cholesterol, weight, height, and Quetelet's index. The median value for each variable was used to divide patients into those above the median, or at the median and below. Patients with median and lower serum cholesterol exhibited an 11% lower disease-free rate at 5 years. Patients above median weight were at significantly increased risk of recurrence in both sexes (76 vs 54%, z = 3.0026, p = 0.003). Progressively decreasing weight was noted with advancing stage in males but not in females. Women above median Quetelet's index were also at significantly greater risk of recurrence (74 vs 52%, z = 2.6109, p = 0.009). Patients above median height were at insignificantly increased risk of recurrence. This study indicates that body weight is a significant prognostic factor for patients with colon cancer.     

SCLC: Epidemiology,Risk Factors,Genetic Susceptibility,Molecular Pathology,Screening, and Early Detection

We review research regarding the epidemiology, risk factors, genetic susceptibility, molecular pathology, and early detection of SCLC, a deadly tumor that accounts for 14% of lung cancers. We first summarize the changing incidences of SCLC globally and in the United States among males and females. We then review the established risk factor (i.e., tobacco smoking) and suspected nonsmoking-related risk factors for SCLC, and emphasize the importance of continued effort in tobacco control worldwide. Review of genetic susceptibility and molecular pathology suggests different molecular pathways in SCLC development compared with other types of lung cancer. Last, we comment on the limited utility of low-dose computed tomography screening in SCLC and on several promising blood-based molecular biomarkers as potential tools in SCLC early detection.