槲皮素联合survivin反义核苷酸对肝癌SMMC7721/ADM细胞MDR的逆转作用

目的 探讨槲皮素与survivin反义核苷酸(ASODN)联合应用对肝癌SMMC7721/ADM细胞多药耐药(MDR)的逆转作用.方法 选择肝癌敏感细胞株SMMC7721和MDR细胞株SMMC7721/阿霉素(ADM),观察其对四种不同化疗药物的耐药性及槲皮素、survivin反义核苷酸(ASODN)对SMMC7721/ADM细胞MDR的逆转效果.结果 槲皮素和ASODN联合时较两者单独应用时能显著降低四种化疗药物对SMMC7721/ADM细胞的半数抑制浓度(IC50) (P<0.05).槲皮素单独应用及联合ASODN时均能明显降低SMMC7721/ADM细胞的多药耐药基因1(MDR1)mRNA及p170和多药耐药相关蛋白基因(MRP)mRNA及p190的表达(P均<0.05). 结论 槲皮素与ASODN联合能明显逆转SMMC7721/ADM细胞对四种化疗药物的耐药性.槲皮素可能通过抑制MDR1 mRNA和MRP mRNA的表达使p170和p190的合成减少而发挥耐药逆转作用,ASODN不能通过该途径发挥作用.     

siRNA逆转乳腺癌细胞MDR1及MDR3介导阿霉素耐药的研究

目的探讨小分子干扰RNA(siRNA)对多药耐药基因MDR1及MDR3介导的乳腺癌MCF-7/ADR细胞耐阿霉素的逆转作用。方法pSuppressorNeoABCB1(针对MDR1的siRNA)及ABCB4(针对MDR3的siRNA)质粒转染MCF-7/ADR及MCF-7细胞(乳腺癌亲本细胞株),流式细胞术检测细胞凋亡,MTT检测MCF-7/ADR细胞对阿霉素的半数抑制浓度(IC50),RT-PCR检测MDR1及MDR3mRNA的表达。结果转染pSup-pressorNeoABCB1的MCF-7/ADR细胞凋亡率(18.21%±1.65%)高于转染pSuppressorNeoABCB4的细胞凋亡率(9.07%±2.17%),P<0.05;二者与转染空载体组的细胞凋亡率(0.2%±0.36%)相比,P均<0.01;pSuppressorNeoABCB1质粒对阿霉素的相对逆转效应高于pSuppressorNeoABCB4质粒(P<0.05);两个质粒转染组的MDR1和MDR3mRNA表达均受到明显抑制(P均<0.01)。结论针对MDR1及MDR3基因的siR-NA可逆转乳腺癌细胞对阿霉素的耐药性。     

天然药物IHA-01筛选敏感肿瘤细胞株及其对结肠癌细胞增殖的影响

目的筛选出对天然药物IHA-01的敏感肿瘤细胞,并对其抗瘤机制进行初步研究。方法体外培养12种人肿瘤细胞株,经3.125、6.25、12.5、25和50μg/ml 5个浓度IHA-01作用48 h后光镜下观察细胞株形态变化,采用CCK-8法计算IC50值（半数抑制浓度）,确认敏感细胞株及最佳作用浓度。流式细胞仪检测IHA-01最佳作用浓度下敏感细胞株细胞凋亡情况及端粒酶活性。结果 5个浓度IHA-01均能抑制12种癌细胞增殖,确定结肠癌HCT-8细胞为敏感细胞（IC50值最低）,最佳作用浓度为1.29μg/ml;鼻咽癌CNE-2细胞为不敏感细胞（IC50值最高）。1.29μg/ml的IHA-01作用后HCT-8细胞凋亡率明显高于、端粒酶活性明显低于CNE-2细胞（P均〈0.01）。结论 IHA-01对HCT-8细胞有较强的抑制作用;其机制可能为诱导肿瘤细胞凋亡及抑制细胞端粒酶活性。     

索拉非尼联合表阿霉素对乳腺癌MCF-7细胞增殖作用的影响及机制

目的探讨索拉非尼联合表阿霉素对乳腺癌MCF-7细胞增殖作用的影响及可能机制。方法MTT法测MCF-7细胞培养1—14d的吸光度,绘制生长曲线并在第14天检测其体外克隆形成率。于24、48、72h分别测索拉非尼及表阿霉素半数抑制浓度（IC50）值。实验分为空白对照组、索拉非尼单药组、表阿霉素单药组、联合组。根据索拉非尼及表阿霉素的IC50值设定联合给药浓度及时间,用MTT法测定72h时索拉非尼及表阿霉素单用组与联合组MCF-7细胞的增殖抑制率。结果生长曲线示MCF-7细胞在1—4d生长速度较快,之后减慢,10d后生长趋于停滞。MCF-7细胞在14d的克隆形成率为37．2％。索拉非尼24、48、72h的Ic50值分别为（7．85＋0．86）、（3．45＋0．16）、（2．10＋0．64）μmol／L,表阿霉素24、48、72h的IC50值分别为（6．52＋0．62）、（1．61＋0．82）、（1．13＋0．51）μmol／L。72h时索拉非尼组MCF-7抑制率明显低于表阿霉素组,MCF-7抑制率高于其他两组（P〈0．05）,细胞抑制率随药物浓度增加而增加（P〈0．05）。结论索拉非尼联合表阿霉素对乳腺癌细胞MCF-7细胞增殖有抑制作用;其机制可能是两药联用抑制或阻断了细胞增殖和生存相关因素的作用。     

姜黄素通过活化PI3K/Akt信号通路逆转肝癌耐药细胞株Bel7402/ADR的耐药性

目的探讨磷脂酰肌醇3激酶/蛋白激酶B(PI3K/Akt)信号通路的活化在姜黄素逆转肝癌耐药细胞株Bel7402/ADR耐药中的作用。方法采用阿霉素药物浓度递增法诱导建立肝癌耐药细胞株Bel7402/ADR;MTT法检测Bel7402/ADR细胞对阿霉素的敏感性,姜黄素对Bel7402/ADR细胞活性的影响及姜黄素对Bel7402/ADR细胞耐药逆转的作用;流式细胞仪检测细胞凋亡率;Western印迹法检测Bel7402和Bel7402/ADR细胞株中PI3K/AKT蛋白的表达水平;构建Bel7402/ADR皮下瘤模型,考察姜黄素对肿瘤生长的影响,最后通过检测小鼠体重及观察小鼠主要脏器的病理切片分析药物的在体毒性。结果 Bel7402/ADR细胞对阿霉素的半数抑制浓度(IC50)值为(1514.6±12.6)μg/ml,耐药倍数为24.3;姜黄素对Bel7402和Bel7402/ADR细胞活性均具有一定的抑制作用,IC50值分别为:(95.8±3.9)μg/ml和(101.4±3.1)μg/ml;5、10μg/ml姜黄素为Bel7402/ADR细胞无毒剂量,对Bel7402/ADR细胞的耐药逆转倍数分别为:1.97和3.51倍,并诱导细胞凋亡。姜黄素可以诱导细胞中PI3K/Akt蛋白表达水平的降低,并随着姜黄素的浓度升高而降低;姜黄素联合阿霉素可以有效抑制肿瘤生长,并表现很低的在体毒性。结论姜黄素在体和离体上可以显著逆转Bel7402/ADR的耐药性,并表现出很好的抗肿瘤效果,姜黄素的耐药逆转机制可能是抑制PI3K/Akt信号通路活化,下调PI3K/Akt蛋白表达,降低细胞对阿霉素的耐受性。     

异汉防己碱逆转白血病K562/DOX细胞多耐药性的实验研究

目的探讨中药十大功劳中异汉防己碱对白血病K562/DOX细胞多药耐药性（multidrug resistance,MDR）的逆转作用。方法采用MTT法检测异汉防己碱的内在细胞毒性及其对阿霉素（DOX）的增敏作用,并以逆转倍数（RF）值评价其逆转效果;应用免疫组化方法检测K562/DOX细胞膜上P糖蛋白（P-glycoprotein,P-gp）表达水平及异汉防己碱对P-gp表达的影响;应用流式细胞仪分析细胞内罗丹明123（rhodamine123,Rh123）和DOX浓度;以维拉帕米（verapamil,VER）为阳性对照。结果异汉防己碱在10μg/ml的无毒剂量下可明显增强DOX的细胞毒性,RF=4.86,明显高于维拉帕米（RF=2.65）的逆转活性（P〈0.05）;K562/DOX细胞膜上P-gp呈强阳性表达,但异汉防己碱对该P-gp表达水平无明显影响;异汉防己碱使细胞内Rh123和DOX的浓度明显增加。结论异汉防己碱可通过抑制P-gp功能而有效逆转白血病细胞的多药耐药性,它有望成为肿瘤多药耐药逆转剂的候选药物。     

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。     

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。     

南蛇藤乙酸乙酯提取物诱导HepG2细胞凋亡的实验研究

目的探讨南蛇藤乙酸乙酯提取物对HepG2细胞增殖和诱导凋亡的机制。方法采用CCK-8法检测细胞增殖;使用流式细胞仪检测细胞周期和细胞凋亡;采用分光光度计检测凋亡细胞胞浆caspase-3的活性变化。结果不同浓度的南蛇藤提取物能抑制HepG2细胞增殖,呈剂量效应和时间效应关系;药物作用24h时,其IC50为111.8μg/ml,作用48h时,其IC50为99.7μg/ml,作用72h时,其IC50为43.0μg/ml;药物干预24h时,HepG2细胞停滞在G0-G1期,并产生细胞凋亡亚二倍峰。在药物为15μg/ml、30μg/ml和60μg/ml时,细胞凋亡率分别为44.91%、31.95%和21.94%,与对照组比较,均有显著性差异（F=5.449,P〈0.05）;在药物浓度为30μg/ml、60μg/ml和120μg/ml并分别作用24h和48h时,Caspase-3活性逐渐增强。结论南蛇藤乙酸乙酯提取物抑制HepG2细胞增殖和诱导细胞凋亡的作用可能与其增强Caspase-3活性有关。     

异常黑胆质成熟剂总酚与顺铂、多西他赛联用对宫颈癌HeLa细胞增殖和凋亡的影响

目的观察异常黑胆质成熟剂总酚（简称总酚）与顺铂、多西他赛联用对体外培养的人宫颈癌HeLa细胞增殖和凋亡的影响。方法取对数生长期HeLa细胞接种于96孔板,加入0、50、75、100、125μg/ml总酚,然后加入0.1、1、5μg/ml顺铂或5、10、20μg/ml多西他赛,培养24、48、72 h,每孔设只加相同浓度顺铂或多西他赛的对照孔和只加培养液的对照孔。用MTT法检测细胞增殖抑制率。取对数生长期的HeLa细胞接种到培养瓶中,分别加入5μg/ml顺铂、20μg/ml多西他赛、50μg/ml总酚、5μg/ml顺铂＋50μg/ml总酚、20μg/ml多西他赛＋50μg/ml总酚,并设对照组,培养48 h后采用流式细胞术检测细胞凋亡率,荧光倒置显微镜下观察细胞生长情况。结果用总酚联合顺铂、多西他赛培养的HeLa细胞与相同浓度顺铂、多西他赛培养者相比,细胞增殖抑制率和凋亡率更高（P均〈0.05）,形态学改变更明显。结论总酚与顺铂、多西他赛联用能显著抑制HeLa细胞的增殖,促进其凋亡。总酚与顺铂、多西他赛联用有协同作用。     

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.     

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.     

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.     

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。     

氯硝柳胺悬浮剂的毒性评价

目的评价氯硝柳胺悬浮剂的毒性，为现场大规模应用灭螺提供依据。方法按照中华人民共和国国家标准GB 15670-1995《农药登记毒理学试验方法》和鱼类毒性试验方法进行。结果经口、经皮肤的LDso雌、雄性大鼠均>5 000 mg/kg，经呼吸道的LCso雌、雄性大鼠均>5 000mg/m3，该药经口、经皮肤、经呼吸道毒性均属微毒类药物；兔眼用药后，观察期内无不良反应，对眼无刺激性；皮肤用药后对皮肤无刺激性。与氯硝柳胺原药、氯硝柳胺乙醇胺盐原药和氯硝柳胺乙醇胺盐可湿性粉剂相比，氯硝柳胺悬浮剂对鱼急性毒性最低。结论氯硝柳胺悬浮剂属微毒类药物，对鱼的毒性低于其乙醇胺盐可湿性粉剂，适合于现场应用。     

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.