去甲斑蝥酸钠对耐顺铂肺腺癌A549/DDP细胞的逆转作用及机制

目的 探讨去甲斑蝥酸钠(SNCTD)对耐顺铂人肺腺癌细胞系A549/DDP的逆转作用及可能分子机制.方法 (1)采用CCK法筛选出SNCTD对A549/DDP的无毒浓度(即对细胞抑制率＜10%的药物浓度),并检测出顺铂及与无毒浓度SNCTD联合对耐药细胞株的IC50;(2)采用流式细胞仪检测无毒浓度SNCTD对细胞内罗丹明123的蓄积情况;(3)采用反转录-聚合酶链反应(RT-PCR)检测1、2倍无毒浓度SNCTD处理细胞48h后耐药相关基因mdrlmRNA,MRP1 mRNA的表达.结果 (1)SNCTD对A549/DDP的无毒浓度为5μg/ml,与顺铂联合用药降低A549/DDP的耐药性,逆转倍数为1.97;(2)无毒浓度SNCTD处理耐药细胞48h后细胞内罗丹明123荧光强度明显增强(F=36.99,P＜0.05);(3)1、2倍无毒浓度SNCTD处理耐药细胞后mdr1,MRP1mRNA表达明显减低,并具有浓度依赖性.结论 SNCTD对A549/DDP具有耐药逆转作用,其作用机制可能与下调耐药相关基因mdr1,MRP1的表达,影响膜蛋白外排泵功能有关.     

补中益气汤与siRNA对肺腺癌A549/DDP细胞耐药逆转作用的比较

目的比较补中益气汤含药血清与siRNA技术(RNA)对人肺腺癌耐顺铂细胞A549/DDP的耐药效果及对多药耐药蛋白P-gp表达的影响。方法制备补中益气汤含药血清,设计并合成针对P-gp基因对应序列的siRNA,转染A549/DDP细胞;实验分组为空白对照组、补中益气汤含药血清处理组、siRNA处理组,利用RT-PCR检测P-gp mRNA,Western印迹及免疫细胞化学法检测P-gp蛋白质的表达;MTT法检测A549/DDP细胞耐药逆转效果。结果补中益气汤含药血清和siRNA均能降低P-gp mRNA和蛋白质表达,恢复顺铂敏感性,耐药倍数分别降至2.01、2.73,具有统计学意义(P<0.05)。结论补中益气汤含药血清和siRNA均能有效逆转人肺腺癌耐药细胞A549/DDP的多药耐药。     

YAP调控肺癌A549/DDP细胞顺铂耐药性的机制分析

目的探讨Yse相关蛋白(Yes-associated protein, YAP)对A549/DDP细胞顺铂耐药性的影响及其机制。 方法采用MTS检测顺铂对肺腺癌A549细胞以及肺腺癌耐顺铂A549/DDP细胞的50%抑制浓度(IC₅₀)。使用qPCR以及Western blot检测A549和A549/DDP细胞中YAP mRNA以及蛋白的表达。Western blot检测维替泊芬(Verteporfin, VP)处理A549/DDP后YAP蛋白表达变化。将A549/DDP细胞设置为DMSO对照组、顺铂组(DDP组)、维替泊芬组(VP组)、顺铂联合维替泊芬组(DDP+VP组),采用MTS检测0、24和48 h各处理组细胞活力的变化。采用qPCR检测VP处理A549/DDP后干细胞标志物ALDHA1、CD133、OCT4、NANOG、SOX2的mRNA表达变化。 结果顺铂对A549和A549/DDP细胞的IC50分别为(4.07±0.03)μg/ml、(23.44±0.98)μg/ml,耐药指数为5.76。A549/DDP细胞中YAP显著高于A549细胞(P<0.05)。VP处理A549/DDP细胞后YAP蛋白表达水平较DMSO组明显降低。DDP+VP组较单独DDP组,其细胞活力在24 h和48 h均明显降低(P<0.05)。qPCR检测发现A549/DDP细胞经VP处理后,干细胞标志物ALDHA1、CD133、OCT4、NANOG、SOX2的mRNA均较DMSO组明显降低(P<0.05)。 结论YAP可能参与了肺癌细胞的顺铂耐药。抑制YAP可通过抑制肿瘤干细胞特性,进而发挥逆转耐药的作用。     

补中益气汤对肺腺癌顺铂耐药细胞株与顺铂敏感细胞株荷瘤BALB/c小鼠移植瘤P-gp蛋白表达的影响

目的探讨补中益气汤对肺腺癌顺铂(DDP)耐药与敏感细胞株荷瘤BALB/c小鼠移植瘤P-gp蛋白表达的影响。方法体外培养肺腺癌顺铂耐药株A549/DDP及敏感细胞株A549,接种于BALB/c小鼠腋窝皮下,荷瘤成功后给予顺铂或顺铂联合低、中、高剂量补中益气汤治疗。实验共分为10组:A549/DDP或A549荷瘤对照组、A549/DDP或A549荷瘤+顺铂组、A549/DDP或A549荷瘤+顺铂+低剂量补中益气汤组、A549/DDP或A549荷瘤+顺铂+中剂量补中益气汤组、A549/DDP或A549荷瘤+顺铂+高剂量补中益气汤组。给药结束后,测量移植瘤体积并计算药物抑瘤率及抑瘤作用提高率,蛋白质印迹法检测移植瘤组织P-gp蛋白的表达。结果顺铂对A549/DDP移植瘤体积无显著影响(P0.05),而使A549移植瘤体积显著缩小(P0.05);联合低、中、高剂量补中益气汤的A549/DDP及A549移植瘤体积均缩小(P0.05),抑瘤率均增加(P0.05),随着中药剂量的增加,移植瘤体积随之缩小,抑瘤率随之增加,抑瘤作用提高率也随之增加;单独顺铂可上调A549/DDP移植瘤组织中P-gp蛋白表达(P0.05),下调A549移植瘤组织中P-gp蛋白表达(P0.05);联合低剂量补中益气汤并未显著下调A549/DDP及A549移植瘤组织中P-gp蛋白表达(P0.05);联合中、高剂量补中益气汤的A549/DDP及A549移植瘤组织中P-gp蛋白表达均显著下调(P0.05),两剂量间无差异(P0.05)。结论在顺铂耐药与顺铂敏感的肺腺癌移植瘤组织中,补中益气汤均有缩小移植瘤体积、提高顺铂抑瘤率、下调P-gp蛋白表达的作用,尤以中、高剂量作用最显著。     

选择性COX-2抑制剂逆转肺癌顺铂耐药作用及机制研究

目的探讨选择性环氧化酶-2(COX-2)抑制剂逆转肺癌对顺铂耐药的作用,并从分子水平研究其机制。方法 1.构建肺癌A549/DDP细胞裸鼠移植瘤模型。2.药物干预:将荷瘤裸鼠随机分为4组:对照组(腹腔注射生理盐水和胃内灌注0.5%羟甲基纤维素钠);顺铂(DDP)组(腹腔注射顺铂溶液);尼美舒利(NIM)组(胃内灌注尼美舒利溶液);NIM与DDP联合组(腹腔注射顺铂溶液和胃内灌注尼美舒利溶液)。DDP每4天腹腔注射1次,共5次,NIM连续灌胃21天。给药期间,测量瘤径及鼠重,绘制肿瘤生长曲线。3.计算抑瘤率:给药3周处死裸鼠,剥离移植瘤,检测各组移植瘤重量、体积,计算抑瘤率。4.免疫组化法检测各组肺癌A549/DDP裸鼠移植瘤细胞内耐药相关因子P-gp、LRP、MRP1的蛋白表达水平。结果 1. NIM有抑制肺癌生长的作用,瘤体积及瘤重抑瘤率分别为22.63%和15.98%。NIM与DDP联合用药后抑瘤作用更明显,瘤体体积及瘤重抑瘤率分别为60.83%和46.76%,分别明显大于NIM组、DDP组及对照组的抑瘤率,差异有统计学意义(P0.05),NIM有增强肺癌细胞对DDP敏感性的作用。2.免疫组化结果显示:P-gp、LRP、MRP1耐药基因在肺癌A549/DDP裸鼠移植瘤细胞内均呈阳性表达,在NIM与DDP联合中的阳性表达分别显著低于各自在DDP组及对照组中的表达,差异有统计学意义(P0.05)。结论 1.选择性COX-2抑制剂NIM有抑制肺癌生长的作用;2.选择性COX-2抑制剂NIM有逆转肺癌对DDP耐药的作用;3.选择性COX-2抑制剂NIM逆转肺癌对DDP耐药的机制,可能与下调肺癌细胞耐药因子P-gp、LRP、MRP1蛋白表达有关。     

miR-200c通过下调TUBB3基因表达逆转老年肺癌患者顺铂耐药性的机制

目的探讨miR-200c逆转肺癌细胞顺铂耐药性的作用机制。方法 miR-200c模拟物转染肺癌A549细胞后,采用实时定量PCR法检测miR-200c的表达;采用细胞活力测定(MTS)法检测miR-200c对肺癌A549细胞顺铂耐受性的影响。采用流式细胞术(FCM)检测肿瘤细胞凋亡率的变化。采用Western blotting检测肿瘤细胞耐药蛋白survivin和Bcl-2蛋白的表达。通过生物信息学分析发现miR-200c下游靶分子TUBB3表达存在差异后,构建TUBB3 3′UTR的野生型和突变型荧光素酶报告载体,然后利用双荧光素酶活性分析miR-200c对TUBB3基因表达的结合位点和调控作用。通过Western blotting检测miR-200c对TUBB3蛋白表达的调控作用以及Bcl-2蛋白和肿瘤细胞耐药蛋白survivin的表达。采用SPSS 19.0统计软件分析实验数据。结果与对照组相比,miR-200c转染肺癌细胞株后,肺癌细胞对顺铂的敏感性呈明显增加趋势[IC_(50)分别为(37.3±3.1)和(15.3±3.3)μmol/L,P0.01]。过表达miR-200c的A549/DDP组的细胞凋亡率明显高于NC组(P0.01)。而肿瘤耐药相关基因Bcl-2和survivin蛋白表达降低。转染miR-200c mimics的A549/DDP细胞中TUBB3蛋白和mRNA的表达均下调(P0.01)。双荧光素酶活性分析显示miR-200c对TUBB3基因表达具有调控作用(P0.01)。这些结果均证实TUBB3为miR-200c的下游靶基因。pcDNA-TUBB3质粒转染后,过表达miR-200c的A549/DDP细胞株survivin和Bcl-2蛋白表达较miR-200c mimics组上调。结论 miR-200c可通过下调TUBB3基因的表达逆转肺癌顺铂耐药细胞的耐药性。     

粉防己碱逆转人卵巢癌耐药细胞SKOV3/DDP耐药的逆转作用及机制

目的探讨粉防己碱（Tet）对人卵巢癌耐药细胞株SKOV3/DDP耐药的逆转作用及其作用机制。方法采用MTT法测定Tet对SKOV3/DDP的细胞毒作用,并确定其无毒剂量;同法测定无毒剂量Tet干预后SKOV3/DDP对顺铂（DDP）耐药性的变化,并计算耐药逆转倍数（RF）;用RT-PCR法检测无毒剂量Tet干预后SKOV3/DDP细胞中的MDR-1 mRNA表达情况。结果选取Tet 2μmol/L作为逆转多药耐药的实验浓度;Tet 2μmol/L联合DDP后,DDP对SKOV3/DDP细胞的IC50从6.24μg/ml降为3.89μg/ml,RF约为1.60倍;SKOV3/DDP细胞内MDR-1 mRNA表达随Tet作用时间延长呈下降趋势（P〈0.05）。结论无毒剂量的Tet能部分逆转SKOV3/DDP细胞的耐药性,其逆转机制可能与下调MDR-1 mRNA表达有关。     

LY294002逆转KB/VCR细胞多药耐药的作用及机制

目的 探讨蛋白激酶抑制剂LY294002对多药耐药细胞KB/VCR的耐药逆转作用及逆转机制.方法 采用MTT法检测LY294002对VCR和ADR的耐药逆转作用,流式细胞仪检测Rh123在KB和KB/VCR细胞内的蓄积,Western blot法检测LY294002对P-gp蛋白表达的影响,DAPI染色检测细胞凋亡.结果 LY294002对化疗药物具有协同增效作用,可以显著逆转KB/VCR的耐药性,能明显减少Rh123的外排,同时降低P-gp的表达.结论 LY294002能够逆转KB/VCR细胞的多药耐药性,不仅能够抑制P-gp功能,而且能够降低P-gp蛋白表达,使肿瘤细胞内化疗药物的浓度增加,提高化疗药物的杀伤作用.     

红景天联合顺铂协同诱导人肺腺癌耐药细胞的凋亡

目的观察红景天联合顺铂对人肺腺癌耐顺铂细胞株A549/DDP的生长抑制和凋亡诱导作用。方法应用MTT法检测红景天、顺铂对A549/DDP细胞的生长抑制并计算IC50,采用Annexin V-FITC试剂盒、流式细胞仪定量检测凋亡率;采用Western印迹法检测各组细胞Caspase-3、聚腺苷二磷酸-核糖多聚酶(PARP)表达水平。结果 A549/DDP对顺铂具有一定耐药性;在红景天、顺铂分别作用24 h后,A549/DDP细胞凋亡率为(11.49+1.73)%、(19.87+3.65)%;显著低于联合用药组(34.88+5.62)%(P<0.05)。联合用药组Caspase-3、PARP活化程度高于红景天组、顺铂组。结论联合红景天与顺铂具有协同作用,抑制肺腺癌耐药细胞生长,促进肺腺癌耐药细胞凋亡,提示红景天在化疗耐药的肺癌治疗中有一定的应用前景。     

槲皮素逆转结肠癌耐药细胞SW480/OXP耐药性研究

目的观察槲皮素(Quercetin,Que)对结肠癌耐药细胞SW480/OXP耐药性的逆转,并探讨其可能的机制。方法体外诱导结肠癌耐药细胞SW480/OXP,用10μg/ml、20μg/ml的Que处理SW480/OXP细胞,CCK8法检测对其耐药性的影响,罗丹明123检测细胞膜泵功能,实时荧光定量PCR检测MDR1及E-cadherin mRNA的表达,Western blotting检测P-gp和E-cadherin蛋白的表达。结果 10μg/ml Que及20μg/ml Que对SW480/OXP的逆转倍数分别为2.25和3.08。经Que处理的SW480/OXP细胞中罗丹明123残余荧光强度大于SW480/OXP细胞。以10μg/ml和20μg/ml Que处理后,MDR1/P-gp mRNA及蛋白的相对表达量均下降,E-cadherin mRNA和蛋白相对表达量则上升。结论 Que可逆转SW480/OXP的耐药,可影响P-gp的功能,降低MDR1/P-gp mRNA及蛋白的表达,并可诱导耐药细胞E-cadherin mRNA和蛋白表达上升。     

胰岛素瘤的解剖分布特点分析

目的胰岛素瘤是最常见的胰腺神经内分泌肿瘤，因其临床表现多样，导致诊断困难。影像学诊断尤其是超声内镜(EUS)在胰岛素瘤的诊断中起着重要作用，拥有较高的敏感性和特异性。本研究拟通过明确胰岛素瘤的解剖分布特点，以期有助于提高影像学的诊断准确率和降低漏诊率，尤其是在教育和培训实践中对于EUS的学习者更具有指导价值。 方法回顾性分析解放军总医院第一医学中心病案资料数据库1993年1月至2019年11月经外科手术、病理确诊为胰岛素瘤的患者的临床资料，检索方法采取搜索术后病理诊断为"胰岛素瘤"的病例，通过查阅病例的方法，提取出胰岛素瘤的大小和解剖分布等数据，进一步分析其特点。 结果共检索到确诊为胰岛素瘤的患者116例，其中，男45例、女71例，年龄13～76岁，平均年龄(44.4±14.85)岁。胰岛素瘤单发110例(94.8%)、多发6例(5.2%)。位置分布：头颈部46例(39.7%)，单发45例、多发1例；体尾部68例(58.6%)，单发65例、多发3例；全胰腺多发2例(1.7%)。病变大小特点：最大径0.4～3.4 cm，平均大小(1.53±0.58)cm。≤1 cm 29例、>1 cm而≤1.5 cm41例、>1.5 cm而≤2.0 cm28例，≤3 cm 15例，>3 cm 3例。年龄与肿瘤的大小相关，≤44岁患者肿瘤平均大小为(1.36±0.51)cm、>44岁患者肿瘤平均大小为(1.70±0.60)cm，P<0.05。头颈部的肿瘤大于体尾部的肿瘤，头颈部肿瘤平均大小(1.66±0.63)cm，体尾部(1.42±0.52)cm，P<0.05。 结论胰岛素瘤在胰腺体尾部较头颈部更好发；绝大多数单发，但可以全胰腺多发；多数小于1.5 cm，肿瘤的大小与患者年龄和肿瘤的解剖分布相关。     

Pathogenesis of carcinoma of the papilla of Vater

Most adenomas and carcinomas of the small intestine and extrahepatic bile ducts arise in the region of the papilla of Vater. In familial adenomatous polyposis (FAP) it is the main location for carcinomas after proctocolectomy. In many cases symptoms due to stenosis lead to diagnosis at an early tumor stage. In about 80%, curative intended resection is possible. Operability is the most relevant prognostic factor. Most ampullary carcinomas resp. carcinomas of the papilla of Vater develop from adenomatous or flat dysplastic precursor lesions. They can be sited in the ampulloduodenal part of the papilla of Vater, which is lined by intestinal mucosa. They also can develop in deeper parts of the ampulla, which are lined by pancreaticobiliary duct mucosa. Intestinal-type adenocarcinoma and pancreaticobiliary-type adenocarcinoma represent the main histological types of ampullary carcinoma. Furthermore, there exist unusual types and undifferentiated carcinomas. Many carcinomas of intestinal type express the immunohistochemical marker profile of intestinal mucosa (keratin 7?, keratin 20+, MUC2+). Carcinomas of pancreaticobiliary type usually show the immunohistochemical profile of pancreaticobiliary duct mucosa (keratin 7+, keratin 20?, MUC2?). Even poorly differentiated carcinomas, as well as unusual histological types, may conserve the marker profile of the mucosa they developed from. These findings underline the concept of histogenetically different carcinomas of the papilla of Vater which develop either from intestinal- or from pancreaticobiliary-type mucosa of the papilla of Vater. Molecular alterations in ampullary carcinomas are similar to those of colorectal as well as pancreatic carcinomas, although they appear at different frequencies. In future studies, molecular alterations in ampullary carcinomas should be correlated closely with the different histologic tumor types. Consequently, the histologic classification should reflect the histogenesis of ampullary tumors from the two different types of papillary mucosa.     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.     

Demonstration of the mechanism of action of biguanides

Summary Palmitic acid oxidation in rat diaphragm homogenate is depressed by biguanide concentrations that are still incapable of inhibiting oxidative phosphorylation. Glucose oxidation is not directly effected by the same biguanide concentrations: however, the inhibitory effect of palmitic acid on glucose oxidation is partly removed by biguanides. Inhibition of fatty acid oxidation, which accounts for most of the metabolic effects caused by these drugs, can be regarded as the fundamental mechanism of action of biguanides. There is some evidence suggesting that these drugs might interact with carnitine, thus preventing long-chain fatty acids from being transported across the mitochondrial membrane to the site of oxidation. Traduzione a cura degli AA.     

血吸虫童虫生长发育及其机制的研究进展

血吸虫童虫是宿主免疫系统攻击的重要靶标,包括皮肤型、肺型和肝门型童虫。宿主分子对童虫生长发育具有重要作用。童虫生长发育机制包括免疫调节、信号转导、性别发育及凋亡等。肌动蛋白、组织蛋白酶、烯醇化酶和葡萄糖基转移酶等分子为血吸虫童虫生长发育的重要分子。本文对血吸虫童虫生长发育及其机制的研究进展做一综述。     

124例耐多药结核分枝杆菌基因突变特征分析

目的对临床分离的耐多药结核分枝杆菌相关基因的突变特征进行分析。方法对124例耐多药结核分枝杆菌以及50株敏感株的耐药相关基因(包括异烟肼inh A、kat G、oxyR-ahp C间隔区以及利福平rpo B)进行序列测定,分析其基因突变情况。结果异烟肼耐药inh A基因突变率为14.5%;kat G基因突变率为70.2%(87/124),主要位于315位;oxyR-ahp C间隔区突变率为15.3%;inh A、kat G两种基因同时突变率75.0%,三种基因同时突变率为89.5%。利福平rpo B基因突变的检出率高达95.2%,突变主要发生在531、526、516位点。结论我省耐多药菌异烟肼耐药相关基因最常见突变为kat G 315、inh A C-T(-15)、axyR-ahp C间隔区(-10)C-T,利福平为rpo B531、526、516。结合MDR-TB耐药相关基因的特征分析,可以建立一种快速、准确、特异的适合于我省的检测结核菌耐多药性的新方法。     

Assessment of quality of life of parents of children with juvenile chronic arthritis

The aim of the study was to assess the quality of life (QOL) and the psychological status of parents of children with juvenile chronic arthritis (JCA). The QOL, anxiety and depression of the parents of 28 children with JCA were evaluated and compared to those of the parents of 28 healthy children. Mothers of JCA children and mothers of healthy children reported similar QOL. The reported anxiety and depression levels were similar for mothers and fathers in both groups. The parents of children with pauciarticular-type JCA reported lower QOL and higher levels of anxiety and depression than the parents of children with other types, namely polyarticular and systemic JCA. These findings may be explained by the fact that the pauciarticular patients had shorter disease duration and were less frequently seen in the outpatient clinic. The QOL of mothers of children with JCA was found to be slightly impaired in the group of children with pauciarticular JCA. Future larger studies are needed to confirm these results, as the number of subjects in the three groups was rather low. Received: 26 September 2001 / Accepted: 8 February 2002     

Numerical Simulation of the Effect of Rate of Change of Glucose on Measurement Error of Continuous Glucose Monitors

Background

A 5-day in-patient study designed to assess the accuracy of the FreeStyle Navigator® Continuous Glucose Monitoring System revealed that the level of accuracy of the continuous sensor measurements was dependent on the rate of glucose change. When the absolute rate of change was less than 1 mg•dl⁻¹•min⁻¹ (75% of the time), the median absolute relative difference (ARD) was 8.5%, with 85% of all points falling within the A zone of the Clarke error grid. When the absolute rate of change was greater than 2 mg•dl⁻¹•min⁻¹ (8% of the time), the median ARD was 17.5%, with 59% of all points falling within the Clarke A zone.

Method

Numerical simulations were performed to investigate effects of the rate of change of glucose on sensor measurement error. This approach enabled physiologically relevant distributions of glucose values to be reordered to explore the effect of different glucose rate-of-change distributions on apparent sensor accuracy.

Results

The physiological lag between blood and interstitial fluid glucose levels is sufficient to account for the observed difference in sensor accuracy between periods of stable glucose and periods of rapidly changing glucose.

Conclusions

The role of physiological lag on the apparent decrease in sensor accuracy at high glucose rates of change has implications for clinical study design, regulatory review of continuous glucose sensors, and development of performance standards for this new technology. This work demonstrates the difficulty in comparing accuracy measures between different clinical studies and highlights the need for studies to include both relevant glucose distributions and relevant glucose rate-of-change distributions.     

Angiographic diagnosis of the degree of serosal invasion of carcinoma of the colon

Angiography using Prostaglandin El^® was performed on 38 patients with carcinoma of the colon in order to diagnose the degree of serosal cancer invasion. The findings at angiography were classified into four groups:1) AG-S3, abnormal change (irregularity and/or encasement) up to marginal vessels; 2) AG-S2, abnormality up to vasa recta; 3) AG-S1, abnormality of penetrating branches of vasa recta within the wall of the colon; and 4) AG-S0, no distinct findings of abovementioned vessels. These angiographic findings were compared with both macroscopic and microscopic serosal cancer invasion. Angiographic diagnosis is in accord with the macroscopic findings in 84.2 percent of cases. Angiographic diagnosis is in accord with the microscopic findings in 32.4 percent of cases. Macroscopic findings confirm the angiographic diagnosis precisely but the conflict with microscopic findings should not be overlooked. This may be the result of inflammatory change, adhesion, and fibrosis around carcinoma of the colon.     

Study of constancy of hydrogen-consuming flora of human colon

The constancy of the hydrogen consuming flora of the human colon was studied in 15 healthy subjects via two measurements obtained 18 to 36 months apart. Hydrogen disappearance rate and the major products of H₂-consuming bacteria, methane and sulfide, were measured during incubation of fecal homogenates with excess hydrogen and sulfate. In 11/15, the hydrogen consumption rate and the predominant hydrogen-consuming pathway (methanogenesis, sulfate reduction, or neither) remained constant. However, major shifts in these pathways were observed in four subjects, with two losing and two gaining the ability to produce methane. Methanogenesis was associated with the highest hydrogen consumption rate. This study demonstrates that clinically unrecognizable, major alterations of the colonic flora occur in healthy subjects. Understanding of the factors responsible for these alterations might allow for therapeutic manipulation of the colonic flora.Supported in part by the Department of Veterans Affairs and NIDDKD RO1 DK 13309-25.