细胞因子在中重度心力衰竭中的变化及其受缬沙坦的影响

目的 :探讨细胞因子在中重度心力衰竭 (CHF)中变化的触发机制及其受药物干预的反应。　　方法 :选择CHF观察组 5 0例和对照组 3 0例 ,采用放射免疫法测定血浆肿瘤坏死因子 (TNF α)、白细胞介素 1(IL 1)和白细胞介素 6(IL 6)的浓度 ;将观察组随机分为常规治疗 2 5例和加用缬沙坦 (valsartan) 2 5例 ,1个月后再测定上述指标。　　结果 :观察组 3种细胞因子血浆浓度均高于对照组 ;CHF越重 ,3种细胞因子的血浆浓度越高 (P均 <0 0 0 1) ;不同病种所致同级CHF的细胞因子浓度无明显差别 (P >0 0 5 ) ;缬沙坦能改善心功能 ,降低上述细胞因子的浓度 (P<0 0 0 1)。　　结论 :细胞因子在CHF的发展中起重要作用 ,而且与基础病无关 ;缬沙坦在改善心功能的同时 ,也降低细胞因子的血浆浓度     

心力衰竭患者炎性与抗炎性细胞因子表达的平衡失调

目的 :了解炎性与抗炎性细胞因子在充血性心力衰竭 (CHF)过程中的变化及其临床意义。方法 :用双抗体夹心ELISA法测定 12 2例CHF患者及 30例健康人血浆中肿瘤坏死因子 α(TNF α)、白细胞介素 6 (IL 6 )、白细胞介素 10 (IL 10 )的浓度。结果 :①CHF患者血浆中TNF α水平明显高于对照者 (P <0 .0 5或 <0 .0 1) ,且随着心力衰竭程度的加重 ,TNF α水平呈进行性增高 ;CHF患者血浆IL 6及IL 10水平 ,心功能Ⅲ、Ⅳ级者明显高于对照者 (P <0 .0 5或 <0 .0 1) ,而心功能Ⅱ级者与对照者相比差异无显著性意义。②TNF α与IL 6 (r =0 .6 18,P <0 .0 1)、IL 10 (r =0 .5 6 6 ,P <0 .0 1)均呈正相关 ,但TNF α与IL 10的比率 (TNF α/IL 10 )也随着心功能的恶化而升高 ,IL 10的升高与TNF α的升高相比明显不足。结论 :细胞因子的变化与心力衰竭的严重程度密切相关 ,CHF患者血中炎性细胞因子明显升高的同时伴有抗炎性细胞因子升高的相对不足 ,炎性与抗炎性细胞因子之间的平衡失调可能参与了CHF的发生发展     

充血性心力衰竭患者某些细胞因子的变化及胺碘酮对其影响的研究

检测充血性心力衰竭 (CHF)患者血清肿瘤坏死因子 α(TNF α)、白细胞介素 1β(IL 1β)和IL 6的变化 ,以及胺碘酮对培养的正常人及CHF患者单核细胞 (PBMC)分泌上述细胞因子的影响 ,以明确上述细胞因子在CHF发生过程中的作用 ,以及胺碘酮作用于CHF的免疫学机制。取 2 0例正常人和 2 0例Ⅲ～Ⅳ级的CHF患者静脉血 :①测其血清TNF α、IL 1β和IL 6含量 ;②离心取PBMC ,分别加入胺碘酮和脂多糖 (LPS)等 ,使胺碘酮的终浓度为 0 ,0 .1,1和10 μmol/ml进行培养 ,经 2 4h孵化后 ,取培养液上清 ,用酶联免疫吸附法 (ELISA)测培养上清中TNF α、IL 1β和IL 6。结果 :CHF患者血清TNF α、IL 1β和IL 6明显高于对照组 (P均 <0 .0 0 1) ,并随心衰程度的加重而增加 (P <0 .0 0 1)。TNF α与IL 1β和IL 6呈正相关 (r=0 .96 84,0 .9786 ;P均 <0 .0 0 1)。胺碘酮对两组PBMC分泌TNF α、IL 1β和IL 6均具有抑制作用 ,并呈剂量依赖性。结论 :①细胞因子TNF α、IL 1β和IL 6参与CHF的发生 ;②胺碘酮可能通过抑制细胞因子的产生 ,对心力衰竭患者产生改善心功能作用。     

心力衰竭患者血清白细胞介素6及其可溶性受体变化与意义

目的 :观察充血性心力衰竭 ( CHF)患者血清白细胞介素 6( IL- 6)和可溶性白细胞介素 6受体 ( s IL-6R)水平的变化 ,探讨其与 CHF患者的病因和心功能的关系。方法 :用 EL ISA法检测 5 3例治疗前的 CHF患者( CHF组 )血清中 IL - 6和 s IL - 6R水平 ,并和 2 0例健康者 (对照组 )比较。结果 :CHF组血清 IL - 6和 s IL - 6R水平显著高于对照组 ( P <0 .0 1) ,且随心功能不全的恶化逐渐升高 ,心功能 ～ 级各亚组间差异有非常显著性意义( P <0 .0 1)。 IL - 6和 s IL - 6R水平分别与左室射血分数呈显著负相关 ( r =- 0 .81,P <0 .0 1和 r=- 0 .83 ,P <0 .0 1) ,s IL - 6R和 IL - 6水平呈显著正相关 ( r =0 .91,P <0 .0 1)。不同病因组间的 IL - 6及 s IL - 6R水平差异无显著性意义。结论 :CHF患者血清 IL- 6及 s IL- 6R显著升高 ,且与心力衰竭程度明显相关 ,与心力衰竭病因无关。测定 IL- 6和 s IL- 6R水平可作为 CHF诊断的实验指标 ,提示 IL- 6及 s IL- 6R参与 CHF的发生、发展过程     

充血性心力衰竭患者TNF-α和IL-6变化及临床意义

目的 :探讨充血性心力衰竭患者肿瘤坏死因子 (TNF α) ,白细胞介素 6 (IL 6 )的变化及意义。方法 :56例充血性心力衰竭患者和 30例健康体检者为研究对象 ,采用酶联免疫双抗体夹心法测定血清TNF α ,IL 6浓度 ,用二维心脏超声测定左室射血分数 (LVEF)。结果 :1 血清IL 6、TNF α、去甲肾上腺素 (NE)在CHF各组均升高 ,但心功能Ⅱ级组与对照组比较差异不显著 (P >0 0 5) ;心功能Ⅲ级 ,Ⅳ级组IL 6 ,TNF α ,NE明显高于心功能Ⅱ级和对照组 (P均 <0 0 5)。IL 6、TNF α、NE与LVEF呈高度负相关(r=- 0 6 3,P <0 0 1 ;r=- 0 54,P <0 0 5;r=- 0 58,P <0 0 1 )。 2 随心衰程度加重 ,血清TNF α、IL 6和NE浓度越高。TNF α与NE ,IL 6与NE呈明显正相关 (r =0 57,P <0 0 1 ;r =0 51 ,P <0 0 5)。 3 随心衰程度加重 ,血清IL 6与TNF α浓度越高 ,且二者呈正相关 (r =0 39,P <0 0 5)。结论 :CHF患者血清TNF α和IL 6浓度升高 ,尤其中重度CHF患者更加明显 ,并与LVEF呈负相关 ,提示血清IL 6、TNF α水平可作为CHF严重程度的判断与预后指标。     

慢性心力衰竭患者氧化应激与细胞因子的变化及卡维地洛的影响

目的　观察慢性心力衰竭患者 (CHF)氧化应激与细胞因子的变化及卡维地洛对其影响。方法　选择 6 7例CHF患者 ,随机分为对照组 (33例 )及卡维地洛组 (34例 ) ,后者在常规治疗基础上合用卡维地洛 5～ 2 0mg/d ,疗程12w。心脏多普勒超声测定左室射血分数 (LVEF)、左室收缩末期容量指数 (LVESVI) ,并测血浆丙二醛 (MDA)、血清超氧化物歧化酶 (SOD)、肿瘤坏死因子 -α(TNF -α)、白细胞介素- 6 (IL - 6 )及基质金属蛋白酶 - 9(MMP - 9)。结果　随着NYHA心功能分级增加 ,CHF患者MDA、TNF -α、IL - 6及MMP - 9显著增高 ,SOD显著降低 (P <0 0 1)。卡维地洛使血浆MDA、TNF -α、IL - 6及MMP - 9明显降低 (P <0 0 1) ,SOD、LVEF增加、LVESVI降低 (P <0 0 5 ) ,LVEF增加与MDA、TNF -α、IL - 6及MMP - 9降低负相关 (γ =- 0 4 0 ,- 0 36 ,- 0 38,- 0 4 3,P <0 0 5 ) ,与SOD增加正相关 (γ =0 38;P <0 0 5 )。结论　卡维地洛改善CHF患者心功能 ,可能与降低氧化应激与细胞因子水平有关。     

心力衰竭患者血浆细胞因子的变化及其临床意义

目的　探讨充血性心力衰竭 (心衰 ,CHF)患者血中肿瘤坏死因子 α(TNF α)和白细胞介素 6(IL 6)的变化及其临床意义。方法　双抗体夹心ELISA法测定 12 2例CHF患者及 3 0例健康人血浆中TNF α和IL 6的浓度。超声心动图测量左心室射血分数及左心室舒张末期内径 ,X线胸片测心胸比。结果　CHF患者血浆中TNF α水平明显高于对照组 (P <0 .0 5 ) ,且随着心衰程度的加重 ,TNF α水平呈进行性增高 ;IL 6水平仅在心功能Ⅲ级、Ⅳ级组中明显高于对照组 (P <0 .0 5 )。TNF α、IL 6与左心室射血分数呈负相关 (r =-0 .5 13 ,r =-0 .45 3 ,P <0 .0 1) ,与心胸比呈正相关 (r =0 .5 0 1,r =0 .43 8,P <0 .0 1) ;与左心室舒张末期内径呈正相关 (r =0 .3 42 ,r =0 .3 0 4,P<0 .0 1)。结论　CHF患者TNF α和IL 6升高可能是心功能恶化的免疫学标志之一 ,提示炎症机制参与心力衰竭的进程     

心力衰竭患者血清白细胞介素10和肿瘤坏死因子α的变化及意义

目的　探讨白细胞介素 10 (IL- 10 )和肿瘤坏死因子 α(TNF- α)在充血性心力衰竭 (CHF)中的作用和地位。方法　采用双抗体夹心 ABC- EL ISA法 ,测定 4 3例不同病因和心功能的 CHF患者和 16例正常对照组受试者血清IL - 10和 TNF-α浓度。结果　与对照组比 ,CHF患者血清 IL - 10浓度无显著性变化 (P>0 .0 5 ) ,并且不同心功能分级之间也无显著性差异 (P>0 .0 5 )。而血清 TNF-α浓度在 CHF组显著升高 (P<0 .0 1) ,且随着心功能分级增加 ,TNF-α浓度呈进行性增加 (P<0 .0 5 )。相关分析显示 IL - 10与 TNF-α、心功能分级及 6 m in步行距离均无相关性 (P>0 .0 5 ) ,与心力衰竭病程显著性正相关 (相关系数为 0 .33,P<0 .0 5 )。TNF- α与 6 m in步行距离及心功能分级有相关性 (相关系数分别为 - 0 .39,0 .6 4 ,P<0 .0 5 )。结论　心力衰竭时炎性细胞因子增加 ,抗炎性细胞因子不增加 ,细胞因子网络平衡紊乱可能参与 CHF的发生、发展。     

培哚普利对老年充血性心力衰竭患者血清炎性细胞因子的影响

目的 观察培哚普利对老年充血性心力衰竭(CHF)患者血清中肿瘤坏死因子(TNF—α)、白细胞介素—1(IL-1β)、白细胞介素-6(IL-6)的影响．方法 放免法检测53例老年CHF患者(培哚普利组28例，常规治疗组25例)治疗前后及25例健康老年人血清中TNF-α、IL-1β、IL—6水平．结果 老年CHF患者血清中TNF—α、IL-1β、IL—6水平显著高于对照组(P＜0．01)，且随着心功能损害程度加重而升高，TNF—α、IL—6水平在心功能各组间比较有显著性差异(P＜0．05)，IL—1β水平在心功Ⅳ级显著高于心功能Ⅱ、Ⅲ级(P＜0．05)．培哚普利组与常规治疗组老年CHF治疗后血清炎性细胞因子浓度均有明显降低，但培哚普利组TNF—α、IL-1β、IL—6水平下降更为明显(P＜0．05)。结论 血清中TNF—α、IL—1β、IL-6水平可反映心力衰竭的程度；培哚普利可明显降低老年CHF患者血清TNF—α、IL-1β、IL—6水平，从而保护和改善心脏功能．     

缬沙坦联合依那普利对充血性心力衰竭患者促炎细胞因子的影响

目的　观察缬沙坦与依那普利联合应用对充血性心力衰竭 (CHF)患者促炎细胞因子的影响。方法　入选CHF患者 82例 ,平均年龄 (5 2± 9)岁 ,随机分为治疗组 5 2例 ,对照组 30例。治疗组应用缬沙坦 4 0～ 80 m g/d加依那普利 10 mg/d,其余治疗同对照组 ,治疗观察共 8周。两组均于治疗前后分别测定血清肿瘤坏死因子 α(TNF- α)、白介素 6 (IL - 6 )和白介素 2 (IL - 2 )的水平。结果　两组治疗后促炎细胞因子的水平均降低 (P<0 .0 1) ,但治疗组与对照组比较降低更为明显 (P<0 .0 1)。结论　缬沙坦与依那普利联合应用可降低 CHF患者促炎细胞因子的血清水平 ,可能与其改善心功能和抑制促炎细胞因子生成有关 ,两药合用对控制 CHF的发生发展可能发挥更好的治疗作用。     

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.