In injection sclerotherapy against esophageal varices, the damage of the endothelial cells of varices has been supposed to be most important for the formation of thrombi in the injected varices. Mechanisms of the destructive action of three sclerosants (ethanolamine oleate [EO], Aethoxysklerol [AS] & absolute ethanol [Et]) on endothelial cells of varices were studied by means of observation of morphological change of the cells and 51Cr release from the cells in a contact with these sclerosants using cultured human endothelial cells and culture cell line K-562 as target cells. Main mechanism for destructive action of EO on the endothelial cells was considered to be cytolysis through injury of cell membrane, since the cells disappeared immediately after addition of EO with marked release of 51Cr. The destructive action of AS on endothelial cells was considered to be mild cytolysis, since moderate destruction of the cells and moderate release of 51Cr were induced with AS. On the other hand, Et showed a fixative-destructive action on the cells without marked morphological change and with little release of 51Cr. Therefore, it was considered that EO and AS caused the damage of endothelial cells through their lytic action of the cell membrane, whereas Et caused it through the fixative action of the cell membrane.
Ursodeoxycholic acid (UDCA) has been used in the medical treatment of various gastrointestinal diseases. In this study, UDCA-supplemented rats were investigated to elucidate the role of UDCA in the pathogenesis of gastric mucosal lesions induced by water immersion restraint stress. In UDCA-administered rats, the increase of gastric mucosal lipid peroxide (LOP) and ulcer index after 2 hour's stress were prevented as compared with the rats fed on standard diet to serve as the control. In addition, the increase of serum and gastric mucosal catalase after the stress were also suppressed. These results suggested that antioxidant effect of UDCA on the lipid peroxidation may play a role in prevension of gastric lesions induced by water immersion restraint stress.
The administration of theophylline (120mg/kg•day, 14wk) to the drinking water of female BALB/c mice after treatment with 1, 2-dimethylhydrazine (DMH) (30mg/kg•sc, 1/wk, 14wk) resulted in both an increase in number of colon carcinoma and increases in ornithine decarbosylase (ODC) activities and polyamine (PA) levels in colon tissue. This increase in number of colon carcinoma was about 3-fold to mice receiving same amount of DMH and drinking water without theophylline. ODC activities (pmoles 14CO2/hr/mg prot, mean±SD) in colon tissue were 122±10.6 (n=6) in DMH with theophylline group, 28.3±2.13 (n=8) in DMH alone group, 21.3±1.67 (n=6) in control group respectively. Putrescine and spermidine levels (nmoles/g, mean±SD) were 31.0±10.5, 527±86.6 (n=11) in DMH with theophylline group, 24.0±11.4, 464±129 (n=11) in control group respectively. Thus with marked increase of ODC activities and slight increase of PA levels, theophylline has shown to significantly enhance the promoting phase of carcinogenic process with DMH.
Synthetic DNA probes were tested as hybridizaiton probes for detecting gut hormone mRNAs. When 4 gut hormones, including gastrin, somatostatin, gastrin-releasing peptide and calcitonin were examined, these probes were shown to be useful for mRNA detection in the tissues producing respective hormones. It was also revealed that there was a good correlation between the concentration of peptides determined by radioimmunoassay and the amounts of mRNAs. This methodology was applied for multiple gut hormone producing tumor with the aim to elucidate the mechanisms responsible for this phenomenon, and demonstrated that the tumor expressed a large amount of mature mRNAs encoding respective hormones. These results indicate that increase of mRNA production is one of the mechanism responsible for multiple gut hormones production by tumor.
This study was undertaken to determine the value of SLX and CA19-9 in the tissue and serum in colorectal cancer and adenoma including the relation to Lewis blood type. SLX isolated by Hakomori et al is one of sialyl SSEA-1 antigens characterized by type 2 chain lacto series glycolipids. Distribution of SLX and CA19-9 was determined in 137 specimens of colorectal cancer (107 advanced and 30 early cancer) and 20 specimens of adenoma by using immunoperoxidase (ABC) method. Serum SLX, CA19-9 and CEA levels were measured preoperatively in 58 cases with histologically proven colorectal cancer by using RIA kits. Simultaneously, Lewis blood type were determined by hemagglutination test in 31 cases. The following results were obtained; 1) SLX and CA19-9 were mostly observed in apical membrane and luminal contents, but a few in cytoplasma of cancer tissue. Positive rate of SLX and CA19-9 was 96.2% and 88.8%, respectively. 2) SLX and CA19-9 were lightly stained in the goblet cells and surface epithelium in some of the mucosa adjacent to the cancer tissue, and positive rate of SLX and CA19-9 was 24.3% and 32.7%, respectively. 3) Positive rate of SLX and CA19-9 was 60% and 50% in adenoma, and 94% and 80% in "m" cancer. Positive rate was not different due to grade of dysplasia of adenoma, but distribution of SLX or grade of the staining of CA19-9 was different between adenoma with mild and moderate dysplasia. 4) Serum SLX, CA19-9 and CEA were positive in 20.6%, 25.6% and 39.7% respectively, and were correlated to the grade of Dukes classification. There was no correlation between serum SLX and CA19-9 levels or SLX and CEA levels in each case. 5) Serum SLX level was not influenced by Lewis blood type, but serum CA19-9 level was low in all cases of Le(a-b-) type. From these results, it was considered that SLX and CA19-9 had a clinical utility for the diagnosis of colonic cancer from the finding indicating that SLX and CA19-9 were stained in most of the cancer tissue and serum SLX and CA19-9 values were related to the grade of staining in cancer tissue.
In 41 patients with 54 lesions which were resected ans studied histopathologically, there were 14 lesions of adenomatous hyperplasias (AH) in 9 patients, 28 AHs containing hepatocellular carcinoma foci (early HCC, e-HCC) in 22 and 12 borderline lesions which fell between these two lesions in 10. The detectablity of these lesions on imagings was evaluated. Detection rates for all lesions and e-HCCs were as follows; intraoperative sonography, 70.0%, 87.5%; Portal-CT, 58.3%, 71.4%; sonography, 44.4%, 64.3%; Arterial-CT, 37.5%, 50.0%; CT, 32.7%, 57.7%; angiography, 17.0%, 30.8%; and Lipiodol-CT, 9.1%, 25.0%. On angiography, tumor stain was recognized in only 8 patients with e-HCC. Arterial-CT showed a relatively low density mass compared to non-tumorous area in 2 patients with e-HCC and one with borderline lesion. The median size of 54 lesions was 1.2±0.4cm indiameter and that of AHs was 0.8±0.3cm, the latter being significantly smaller than the other two lesions (p<0.01). Liver cirrhosis coexisted in 35 of 41 patients (85.4%). No complete necrosis occurred in 13 e-HCC lesions following therapeutic embolization or infusion chemotherapy in the hepatic artery.
Methyl tertiary butyl ether (MTBE) has been proposed as a new therapeutic material for the dissolution of pure cholesterol mixed stones. To determine the effect of solvent circulation and fragmentation on dissolution of cholesterol mixed stone in MTBE, we carried out in vitro experiments. The following results were obtained: 1) The addition of 1%EDTA and 0.5%UDCA in MTBE enhanced the dissolution of cholesterl mixed stones (56±8% of initial weight after 3 hours vs. 48±5% of intial weight after 3 hours in MTBE alone). 2) Cholesterol mixed stones withcirculation of MTBE+1%EDTA+0.5%UDCA were dissolved more rapidly than those without. 3) Under in vitro condition, when cholesterol mixed stoens were fragmented with URAT-1M stone disintegrator, fragments of stones were dissolved 96% of initial weight in solvent circulation of MTBE+1%EDTA+0.5%UDCA after 3-6 hours. In conclution, these data indicated that both fragmentation of cholesterol mixed stones and solvent circulation of MTBE+1%EDTA+0.5%UDCA considerably accelated dissolution of cholrsterol mixed stones in vitro.
We developed a specific and sensitive bioassay for measuring plasma cholecystokinin (CCK) in human and investigated CCK response after a test meal in patients with chronic pancreatitis. Treatment with cycloheximide increased the sensitivity and responsiveness of isolated rat pancreatic acini to CCK-octapeptide (CCK-8) and thus plasma levels of CCK-8 as low was 0.17pM were detectable. Fasting plasma CCK levels in normal subjects as CCK-8 equivalents were 0.75±0.25pM and rose to a peak of 6.2±0.68pM at 45min after a test meal consisting of 400ml milk and 2 boiled eggs. Basal and stimulated plasma levels of CCK-8 in patients with non-calcified chronic pancreatitis were significantly higher than those in normal subjects. In contrast, postprandial responses of plasma CCK-8 in patients with calcified chronic pancreatitis was significantly low compared to those in contraol subjects, although basal plasma levels were not significantly different from those in controls.
The potentiating effect of secretin on cholecystokinin (CCK)-stimulated exocrine pancreatic secretion was studied in anesthetized rats. Intravenous infusion of CCK-8 in three different doses of 0.03, 0.06 and 0.12μg/kg-hr increased pancreatic secretion of volume, bicarbonate, amylase and trypsin outputs dose-dependently. Simultaneous infusion of CCK-8 with secretin in a dose of 0.03CU/kg-hr produced statistically greater pancreatic secretion of volume, bicarbonate, amylase and trypsin outputs than that by CCK-8 alone, and than the sum by secretin alone and CCK-8 alone in each dose. Proglumide (600mg/kg-hr) significantly suppressed exocrine pancreatic secretion produced by CCK-8 (0.06μg/kg-hr) plus secretin (0.03CU/kg-hr), to the level induced by secretin alone. These results indicate that CCK-8 increased pancreatic secretion dose-dependently, and secretin in a physiological dose potentiates the stimulating effect of CCK-8 on exocrine pancreatic secretion in rats.
Seventeen cases with a total of eighteen insulinomas were examined by ultrasonography (US), computed tomography (CT), angiography, percutaneous transhepatic portal and pancreatic venous sampling (PTPS) and intraoperative ultrasonography (IOUS). We discussed about diagnostic accuracy of insulinomas on these diagnostic modalities. Tumor localization was achieved by US in 39%, CT in 72% and angiography in 81%. Although total 15 tumors (83%) can be correctely detected, multiple lesions were not completely ruled out. We recommended the criteria in PTPS as follows: Insulin concentration level above 200μU/ml. Or, both of insulin concentration ratio (step-up site/control) above three and elevation of the CPR concentration level on the PTPS. According to these criteria, the accuracy rate was 91%. Overall preoperative diagnostic accuracy was 100%. IOUS allowed us to detect the localization of the tumors completely.