Vagally innervated anral pouches were created in adult mongrel dogs, the interiors of these antral pouches were perfused with glycocholate, taurocholate, canine bile and human pancreatic juice, and antral function was investigated from the viewpoint of gastric endocrine and exocrine response. Perfusion with glycocholate and taurocholate of 20mM induced a significant increase in gastric acid secretion as well as serum gastrin secretory response. Perfusion with canine bile and human pancreatic juice induced a pronounced increase in serum gastrin levels as well as gastric acid secretion starting immediately after the beginning of perfusion, and serum gastrin secretory response also displayed a marked increase. These results demonstrated that the regurgitation into the stomach of duodenal fluid containing bile and pancreatic juice, constitutes one factor causing increased serum gastrin levels and gastric acid secretion.
Effects of ethanol and prostaglandin on the glycoprotein synthesis in the gastric mucus cells have been evaluated. The rat gastric mucosal cell were subjected to a short-term tissue culture in the presence of ethanol and prostaglandin E2 (Ornoprostil), using [3H]-proline, [3H]-palmitic acid, [3H]-galactosamine. Low concentration of ethanol (0.05-0.01M) stimulated the glycoprotein synthesis, but higher concentration of ethanol (0.5-1.5M) caused a marked reduction in the glycoprotein synthesis. Addition of prostaglandin E2, especially addition of prostaglandin prior to ethanol treatment, has improved the glycoprotein synthesis and secretion in the presence of ethanol. It was suggested that addition of prostaglandin resulted in the stabilization of the synthesis and secretion of the mucus glycoprotein in the presence of ethanol.
To better understand the mechanism of phosphatidylcholine synthesis in the stomach, [3H] choline incorporation into phosphatidylcholine in response to the drugs which have been commonly used for treating the patients with gastric ulcer was examined using isolated guinea pig gastric glands. Teprenone stimulated [3H] choline incorporation into phosphatidylcholine in gastric glands, up to 146±11% of control (n=6, P<0.05). On the other hand famotidine, ranitidine and cimetidine significantly decreased the incorporation to 73±8%, 72±11%, 67±11% of control, respectively (n=6, P<0.05, P<0.05, P<0.05). When the glands were pulsed with [3H] choline followed by incubation in the presense of teprenone or each H2RA for 180min to see the effects of the agents on the limiting step of the phosphatidylcholine synthesis, teprenone also significantly stimulated [3H] choline incorporation into phosphatidylcholine, but each H2RA did not affect phosphatidylcholine biosynthesis any more. Teprenone stimulated CTP: phosphocholine cytidylyltransferase (CTF) from a basal value of 0.92 ±0.10 to 1.69±0.39 (nmol/min/mg protein) (n=3, P<0.05). These results suggest that teprenone may stimulate phosphatidylcholine biosynthesis through the activation of CTF, a late-limiting enzyme of PC biosynthesis, and H2RA may affect phosphatidylcholine synthesis by inhibiting choline transport or choline kinase in gastric glands.
By using anti-NKH-ras and K-ras monoclonal antibodies, paraffin-embeded tissue specimens of 70 cases of colorectal cancers were immunohistologically examined. Correlation between incidence of expression of these oncogens and either of postoperative survival rate and stage of colorectal cancer were calculated. The positive rate of anti-NHK-ras and K-ras staining were correlated with maximum diameters of tumor, staging, degree of Dukes classification and depth of invasion. Positive and negative rates of between NHK-ras and K-ras staining were well coincident. The cumulative postoperative survival rate of negative casesfor anti-K-ras staining showed a significantly higher survival rate than that of the positive cases.
Using normal duodenal mucosa (28 cases), initial duodenal ulcer-associated duodenitis (IUAD, 14 cases; 3 active, 8 healing and 3 scarring or healed ulcers) and recurrent duodenal ulcer-associated duodenitis (RUAD, 16 cases; 5 active, 8 healing and 3 scarring or healed ulcers), a new histological criteria and staging of NSD was tried to be made with discriminant analysis. As a result, it is concluded that neutrophilic cell infiltration in the stroma (Ne), gastric superficial epithelial metaplasia (GM), height of villus-crypt unit (HVC) and width of villus (WV) are important factors for histological criteria of NSD (Table 7), and that number of neutrophilic cells in the stroma (NeS) and percentage of GM in the villus-crypt unit (%GM) are important factors for histological staging of NSD (Table 8).
Both humoral and cell-mediated immunity to Epstein Barr virus related antigen have recently been reported and are thought to be important for the generation of Epstein Barr virus induced human diseases. For this reason, to study immunological features in Epstein Barr virus induced hepatitis (EBH), we studied the ratio of various immunocompetent cells in peripheral blood and compared them to that of healthy control and acute hepatitis (disease control). We found that a significant elevation of CD8+CD11- cells existed in EBH patients (48.9±18.3% in EBH, 17.0±6.9% in AH and 13.6±7.0% in healty control) and atypical lymphocytes which are frequently observed in EBH are belong to CD8+CD11- cells. Regarding the study of surface expression of activated T cell markers, we found that these CD8+cells also expressed HLA-DR antigen on their cell surface. Furthermore, the percentage of CD8+CD11- cells returned to normal level with the recovery of their liver function. From these results, we can assume that activated CD8+CD11- cells may have an important roles in generation of EBH.
We evaluated the changes in the hepatic hemodynamics and blood ketone body ratio (KBR) induced by vasopressin in 40 patients with chronic liver diseases to clarify the effect of hepatic blood flow on hepatic energy charge expressed by KBR. Following infusion of vasopression, the rate of decrease in portal blood flow in liver cirrhosis (LC) was significantly lower than that in chronic hepatitis (CH). Moreover, the blood flow in the hepatic artery after vasopressin infusion was greater in LC than in CH. As a result, the total hapatic blood flow, which was the sum of the flow in the above two vessels, after vasopressin infusion was greater in LC than in CH but the decrease in the blood KBR was not significant in LC. Thus, vasopressin appearas to be hemodynamically safe in patients with LC, but caution is needed since it may decrease blood pressure, total hepatic blood flow and KBR in some LC patients.
The role of cholesterol and phosphatidylcholine on hepatic very low density lipoprotein secretion was investigated with rat hepatocytes. Hepatic very low density lipoprotein secretion (apo B, apo E, cholesterol, triglyceride, phosphatidylcholine) was decreased by the reduction of hepatic phosphatidylcholine content. However, cholesterol loading into hepatocytes did not affect hepatic very low density lipoprotein secretion. Hepatic apolipoprotein contents were constant and were not influenced by a change of hepatic cholesterol and phosphatidylcholine contents. These results suggest that lipids, which are constituents of lipoproteins, play different roles on hepatic very low density lipoprotein secretion.