It has been well established that reflux of gastroduodenal contents causes reflux esophagitis. Experimental model of reflux esophagitis in rats was devised by 24hrs ligature on both lower portion of duodenum and most of forestomach. Erosion of esophageal mucosa and thickening of esophageal wall developed in macroscopic findings. Histologically, many neutrophils were found from lamina propria to muscular layer, mainly in lamina propria. Edema and thickening of submucosal layer developed in cases with 24hrs ligature. These severe inflammatory changes in submucosal layer suggested that it caused thickening of esophageal wall. Bile reflux was found in gastric contents of this model. No mucosal lesions were found in cases with ligature on lower portion of duodenum. Findings in this experimental model of reflux esophagitis suggested significant roles of gastric juice and bile acids in the pathogenesis of reflux esophagitis. This model was thought to be useful for studies of pathophysiology of reflux esophagitis caused by reflux of gastroduodenal contents.
The mucin phenotypic expression of gastric differentiated adenocarcinoma was investigated by mucin histochemical method. Seventy-nine advanced gastric carcinomas, which showed histologically differentiated type (well and moderately differentiated type) in the mucosa, were classified into four types ; gastric type (30.4%), intestinal type (19.0%), combined type with both gastric and intestinal phenotype (45.6%) and lack of mucin type (5.1%). Moreover, differentiated adenocarcinoma of gastric type were subclassified into foveolar (F) type (37.5%), pyloric gland (P) type (37.5%) and mixed (M) type with foveolar and pyloric type (25.0%). Both gastric type and intestinal type differentiated adenocarcinoma were apt to change to undifferentiated type in the invasive lesion below the submucosa. On the contrary, carcinoma of combined type changed to undifferentiated type with significantly lower incidence than the former two type. F-type differentiated adenocarcinoma tended to develop scirrhous or non-solid type infiltration and carcinoma of P-type showed medullary or solid growth with significantly higher incidence than the other type. Mucin phenotypic expressions of differentiated adenocarcinoma had much to do with the mode of growth and infiltration of cancer in the gastric wall below the submucosal layer.
The relationship between titrated acidity and pH was studied using the 3206 samples of human gastric juice, which were collected by the intragastric tube in the basal and gastrin stimulated conditions. The pH of samples subjected to the present study ranged from 0.95 and 6.9. The results showed that a certain value of pH did not always indicate an identical value of titrated acidity, and that the coefficient of variation was greater as pH value rose. As a whole, however, the acidity became lower with the increase of pH value. Thus, the relationship between pH and titrated acidity could be expressed closely as “Y=369.19-424.09X + 203.66X2 - 48.29X3 + 5.57X4 - 0.25X5), where X = pH and Y= acidity. The conversion table from pH to acidity, which was calculated by this expression, was presented for the clinical use.
Intramucosal growth patterns of minute superficial colorectal carcinomas removed by endoscopic surgery were analyzed on these microscopic views by using two dimension morphometrical system. Superficial colorectal carcinomas were classified into 2 types based on endoscopic findings ; superficial elevated type 21 cases and superficial depressed type 30 cases. Main factors determining growth pattern in mucosa depended on size in superficial elevated type and ratio of transmucosal growth in superficial depressed type. PG type and NPG type showed the same growth pattern in terms of ratio of transmucosal growth and mucosal thickness of central depressive area to the horizontal size. Accordingly, intramucosal growth patterns were different between superficial elevated type and superficial depressed type in minute lesions. And, PG type and NPG type could be included as superficial depressed type.
Intraductal ultrasonography (IDUS) were performed in patients with extrahepatic bile duct cancer and compared to other diagnostic modalities and to resected specimens. Endoscopic ultrasonography (EUS) is a non-invasive diagnostic method useful for screening patients with bile duct cancers and determining whether they are resectable or not. While, EUS was not useful for the differential diagnosis of advanced and early tumors, and less useful in case of bile duct tumors located at the hilus hepatis. IDUS proved useful without blind spot even in case of bile duct cancers at the hilus hepatis. IDUS was especially useful for the differential diagnosis of advanced and early tumors. IDUS is the very accurate diagnostic modality which make up for EUS and essential to determine the appropriate operation plan.
The effects of exogenous and endogenous prostaglandin on rat pancreatic exocrine function were investigated in vivo and in vitro. Under stimulation by endogenous CCK or exogenous caerulein, protein output was significantly reduced by intravenous drip infusion of 16, 16-dimethyl prostaglandin E2 (DMPGE2), and under stimulation by exogenous secretin, volume and bicarbonate output were markedly reduced by DMPGE2. Amylase release from isolated pancreatic acini was significantly reduced by DMPGE2 under stimulation by 10-11-3×10-11M CCK-8, and was not influenced by DMPGE2 under stimulation by secretin or by indomethacin under stimulation by caerulein. Basal amylase release was not influenced by DMPGE2 or indomethacin. Basal cellular cyclic AMP and cyclic GMP contents were not influenced by DMPGE2, and elevated cyclic GMP content under stimulation by caerulein was significantly reduced by DMPGE2. These findings suggest that pancreatic enzyme secretion is reduced by DMPGE2 under stimulation by physiological or pharmacological concentration of CCK, and one of which mechanism is direct effect of DMPGE2 on pancreatic acini, may be coupling with phosphatidylinositol breakdown system and without cyclic AMP.
National surveillance studies on alcoholic liver disease (ALD) in Japan were performed in 1978 and 1985, by a previous Japanese study group for ALD (Takeuchi group). In the present study, a subsequent nationwide surveillance study was performed from 1986 to 1991 and the results were compared with the previous two studies. In order to clarify the etiological relationships between hepatitis C virus (HCV) infection and ALD, an analysis was also done according to the new diagnostic criteria of ALD which was proposed by this group (Takada group). By the criteria of the Takeuchi group, the incidence of ALD was not significantly different during 1986 to 1991. However, the incidence of hepatocellular carcinoma (HCC) in alcoholic cirrhosis (AL-LC) clearly increased during this period. The analysis including the results of the previous study indicate that incidence of ALD reached a plateau in 1980 and then features of ALD in Japan entered a stable stage. However, HCC in AL-LC continued to show a linear increase from 1976 to 1991. Analysis with the new criteria of the Takada group was done in cases of 1990 and 1991. Approximately 2 out of 3 cases of ALD were caused by alcohol alone, and the remaining cases were caused by a combination of alcohol and HCV. Cases caused only by HCV were very rare. The main etiology in patients with alcoholic hepatitis and fibrosis was alcohol alone and that in chronic hepatitis of heavy drinkers was a combination of alcohol and HCV. In half of the patients with AL-LC, the etiology was alcohol alone and in the other half patients, it was a combination of both factors. In most patients with HCC, the etiology was a combination of alcohol and HCV, indicating that HCV infection may be important for the development of HCC in alcoholics.