To clarify the pathogenetic mechanisms in acute gastric lesions induced by vibration (VIB), the effects of VIB (3.0G, 10Hz, 90min) on changes in gastric mucosal blood flow (GMBF), plasma corticosterone (COR) and catecholamines (CA) as well as ulcer formation were compared with those of forced water immersion stress (FWI). While the VIB increased the GMBF during the exposure, the FWI decreased it during and after the stress. No difference in the severity of ulcer formation between the VIB groups was seen. Although both VIB and FWI increased the COR and CA, the degree of increased in the COR by the VIB tended to be less than that by the FWI. The truncal vagotomy inhibited the reduction of the GMBF and ulcer formation by the FWI, but promoted the reduction of the GMBF by the VIB. These results suggest that ulceration induced by VIB is caused primarily by its direct, mechanical and specific actions and not through the central nerve system.
Mapping specimens of 6 cases of ulcerative colitis included adenocarcinoma invaded into submucosa (invasive carcinoma) were made and Index value of Nucleus-Gland (ING) of invasive carcinoma, severe and moderate dysplasia in ulcerative colitis was measured and compared with one another. Large intestinal carcinoma invaded into submucosa, colonic adenoma and normal mucosa were examined as the control. Spatial relations of invasive carcinoma and dysplasia in ulcerative colitis were also examined. Severe and moderate dysplasia as well as large intestinal carcinoma invaded into submucosa showed significantly higher values of ING than adenoma (P<0.01). Invasive carcinoma and severe dysplasia of ulcerative colitis showed significantly higher values of ING than moderate dysplasia (P<0.01). Severe dysplasia was located around the portion of invasive carcinoma of ulcerative colitis. Severe dysplasia falls into the same category with invasive carcinoma of ulcerative colitis because of the same value of ING and spatial translation each other. Moderate dysplasia was defined as borderline lesion because of the mean value of ING between severe dysplasia and adenoma.
To clarify the kinetics of cell membrane and intracellular mediators in the process of auranofin (AF)-induced diarrhea, we perfused electrolyte solution containing the oral gold preparation AF, which is a treatment for rheumatoid arthritis, through the rat jejunum, and studied net water and electrolyte transport, Na+, K+-ATPase activity, and c-AMP and c-GMP concentrations in the jejunal mucosa. In addition, change in Ca++ concentration in isolated intestinal cells was evaluated using fura-2-acetoxylmethyl ester. AF significantly suppressed water and electrolyte transport. Mucosal secretion was increased due to elevation of the intracellular Ca++ concentration early in the perfusion period, then due to reduction in the Na+, K+-ATPase activity, and increase in the c-AMP concentration late in the perfusion period. Therefore, these cell membranes and intracellular mediators are considered to be involved in the mechanism of AF-induced diarrhea.
The purpose of this study was to clarify the significance of immunohistological staining for PCNA/cyclin in human colorectal lesions. Our results: The PCNA-positive cells existed at the bottom of colonal tubuli in the normal and hyperplastic conditions. In the neoplastic lesions, however, the positive cells were existed at the relatively surface of the mucosa (χ2: P<0.01) and distributed irregularly from the bottom to the top of carcinoma tissue. These results suggested that immunohistological staining for PCNA would specifically detect the cell proliferation and be beneficial for practical use and clinical application of the diagnosis of the colorectal lesions.
The relationship between recurrence of esophageal varices after endoscopic injection sclerotherapy (EIS) and changes of the blood pool of portosystemic collaterals was studied in 36 patients with liver cirrhosis. Examination of the blood pool of portosystemic collaterals was performed by single photon emission CT (SPECT). Seven hundreds and forty MBq of 99mTc-RBCs, labeled by an in vivo technique, were given intra-venously, and tomographic imaging of the intraabdominal vascular blood pool was performed. Before EIS, the blood pool images of the coronary vein was demonstrated in 34 cases (94.4%). According to changes of SPECT images, the patients were divided into 3 groups, that is, the groups showing a disappearence, decrease, and no changes of the blood pool images of the coronary vein. The recurrence rates of esophageal varices after EIS were 11.1% (1 of 9 patients), 40.0% (6 of 15 patients), and 90.0% (9 of 10 patients) in the disappeared, decreased and unchanged groups respectively. These values were significantly different between the disappeared group and the unchanged group (P<0.01), and between the decreased group and the unchanged group (P<0.05). These results indicate that the abdominal blood pool SPECT is useful for evaluating the therapeutic effectiveness of EIS.
We established a new culture method of mouse gallbladder epithelial cells. Explantation of a tiny fragment of the mouse gallbladder (microexplant) on the collagen gel allowed the epithelial cells to proliferate on the collagen gel for more than 4 weeks. The epithelial cells spreaded in a monolayer sheet from the microexplant and extended onto the surface of the collagen gel 0.31±0.02mm per day. Whereas, contaminated stromal cells proliferated under the epithelial cell layer and into the collagen gel. At the peripheral zone of epithelial sheet, the shape of the epithelial cells was squamous, and the cells were frequently positive for BrdU immunostaining, indicating the high proliferative activity. In contrast, the cells in the central part of epithelial sheet were cuboidal or low columnar in shape and showed well cell-polarity and mucus-secretory activity similar to the gallbladder epithelia in vivo. It was indicated that the cultured epithelial cells in this system preserved the morphological and functinal differentiation to the physiological gallbladder epithelia. This newly established culture method has the characteristics of both the organ and the cell culture, and might be useful for the morphological and functional studies of the gallbladder epithelia in vitro.
Collagen and non-collagen protein metabolisms in rat acute pancreatitis induced by ethionine were investigated with an incorporation study of 3H-proline to those proteins. Enhanced collagen metabolism, which may provide a basis for parenchymal cells regeneration, was observed in the initial phase of acute pancreatitis. This phenomenon was followed by the increase of non-collagen protein metabolism, and histologically mitosis of pancreatic acinar cell was detected concomitantly. Thereafter the enhancement of collagen metabolism continued to the convalescent phase of acute pancreatitis and this change was thought to be related to the resolution and the elimination of excess of collagenous materials and simultaneous increase of non-collagen protein synthesis, which may result in the maturation of acinar cell, was observed. It was thus assumed that the restoration from acute pancreatitis was initiated by the enhanced collagen metabolism with following parenchymal cell regeneration, and was finished by the maturation of acinar cells.
To better understand the mechanism underlying the inhibition induced by cholecystokinin (CCK) of phosphatidylcholine (PC) synthesis, the effects of CCK treatment on the activities of enzyme involved in PC synthesis via CDP-choline pathway were studied in isolated rat pancreatic acini. CCK treatment of acini reduced CTP: phosphocholine cytidylyltransferase activity in both cytosolic and particulate fraction. However, CCK treatment of acini did not alter the activities of choline kinase and phosphocholinetransferase in acini. When acini were labeled with [3H] myristic acid and chased, CCK8 (1nM) reduced the synthesis of [3H] myristic acid labeled-PC to 27% of control after 60min-chase period. This inhibition of PC synthesis induced by CCK was accompanied by a delayed disappearance of [3H] diacylglycerol (DAG), the radioactivity of which was 225% of control at 60 min. CCK also induced an increase in [3H] triacylglycerol and [3H] phosphatidic acid in acini. These results suggest that CCK inhibits PC synthesis by inducing the inhibition of CTP: phosphocholine cytidylyltransferase activity. The inhibition by CCK of PC synthesis may contribute to the sustained accumulation of DAG in pancreatic acinar cells.