Stomachs with multiple submucosal glands keep our attention because of their high risk for having gastric carcinomas, but little is known about the relationship between submucosal glands and occurring cancers. So we investigated the structure of submucosal glands including location of proliferating cells. We labeled proliferating cells of three stomachs with cancerous lesions by circulating artificial blood through the isolated organs with bromodeoxyuridine (BrdU). Serial sections of submucosal glands were stained with hematoxylin eosin, periodic acid Schiff, Alcian blue, high iron diamine-Alcian blue, concanavalin A paradox, galactose oxydase Schiff as well as anti-BrdU immunohistochemically. Results showed that most of submucosal glands were composed of functionally maturated cells and these cells made regular structure just like those of mucosal layer. Labeling index of BrdU of these submucosal glands were low (0.2%-0.7%). Two atypical glands were seen, and labeling index were 2.6% and 22.2% respectively. In conclusion, submucosal glands of the stomachs were thought to be made by moving proliferating cells from mucosal layer to submucosal layer. So we saw these submucosal glands paracancerous lesions rather than recancerous ones. But we couldn't deny the possibility to occur cancerous lesions from atypical glands in submucosal glands.
Six severe and 7 moderately severe ulcerative colitis patients were treated by pulsed steroid therapy. For one course of the therapy, either 0.5 or 1 gram of hydrocortisone-21 sodium succinate or methylprednisolone sodium succinate was given once a day intravenously for 3 consecutive days, following 4 days with no infusion. The patients were treated for 3 to 6 courses. Ten patients entered clinical remission, 1 patient improved, and therapy failed for 2 patients. Judged endoscopically, 5 patients achieved remission. Six patients improved and 2 patients did not improve. Severe side effect was not noted as to stop the medication. One patient had hyperglycemia for a few days after the start of the first course, this patient received total parenteral nutrition. Three patients showed moon face. Steroid withdrawal syndrome did not develop.
We investigated the effect of cimetidine and histamine on splanchnic circulation in the dogs. Hepatic artery, superior mesenteric artery and portal vein were cannulated to measure each blood pressure. Each blood flow was evaluated utilizing electromagnetic blood flowmetry. And vascular resistances were calculated by measured blood pressure and blood flow. Cimetidine, histamine, 2-PEA (H1-agonist), dimaprit (H2-agonist) and mepyramine maleate (H1-antagonist) were given by intravenous bolus to the dogs. Histamine caused vasodilation of hepatic artery but vasoconstriction of superior mesenteric artery and these effects were similar to the effect of 2-PEA. These hemodynamic responses to histimine were inhibited by H1-antagonist but not inhibited by H2-antagonist. Cimetidie produced dilatation of hepatic artery but constriction of portal vein, superior mesenteric artery and reduced total hepatic blood flow. These effects were not inhibited by H1-antagonist. We concluded that cimetidine did not stimulated H1, H2receptors rather than had the own effects and that H1-receptor was superior to H2-receptor on splanchnic circulation in the dogs.
We retrospectively analyzed the prognostic factors associated with survival in HCC patients (113 cases, male 95, female 18, mean age 62.1±8.2yr.) treated only by TAE. Univariate analysis revealed that following factors significantly correlated with survival, such as T. Bil, tumor type, Vp factor, the response to the first TAE and the best response to TAE attained within 6 months after the first therapy. Also, multivariate analysis proved that T. Bil, ICGR15' and the best response to TAE during the initial 6 months were significant. Even if the first response to TAE was "no-change (NC)", the cumulative survival rate of patients would be improved when the responses to the second or the third therapy became " partial response (PR)" within 6 months after the first one. There were no significant differences between patients with which the best response to TAE within the initial 6 months were PR and those with NC in clinical backgrounds, dose of anti-cancer drugs, and dose of lipiodol used in the therapies. However, the mean interval between the first and the second TAE performed within 6 months 70 days. These results implied the importance of getting "PR" state no later than 6 months after the first intervention for the long survival in HCC patients. To accomplish this, repetitive treatments between short periods were recommended.
In order to clarify the effect of somatostatin of the ductal secretion of the exocrine pancreas, we measured pancreatic juice and protein secretion stimulated with 10pM secretin and/or 10pM cholecystokinin (CCK) in the presence or absence of somatostatin analogue, SMS 201-995 (SMS) utilizing the isolated perfused pancreas of rats. SMS significantly inhibited both pancreatic juice flow and protein output elicited by 10pM secretin without affecting basal secretion. The inhibitory effect of SMS was dose-dependent and maximal inhibition was observed with 1-10nM. Half-inhibitory dose of SMS for juice secretion was 140pM. Because CCK is thought to potentiate secretin action on the ductal system, we examined the effect of SMS on pancreatic secretory response to 10pM secretin in combination with 10pM CCK. In the experimental system we used, the amounts of pancreatic juice and protein secreted during a 30-min stimulation with secretin and CCK were additive. SMS inhibited both pancreatic juice and protein secretion to the livel comparable with that obtained with either stimulus and SMS. SMS had no effect on CCK-stimulated pancreatic juice secretion but significantly inhibited protein output. The present study demonstrated, therefore, that SMS inhibits ductal secretion in response to physiological concentration of secretin.