Katsuhisa Kawamoto

Healing Process of Experimental Esophageal Ulcers Induced by Acetic Acid in Rats

We studied the healing of acetic acid-induced esophageal ulcers in rats with respect to the cellular kinetics. Esophageal ulcers were induced by topical application of acetic acid to the serosal surface. Well-demarcated circular or elliptical ulcers had developed by day 3 after the acid treatment. These ulcers began to decrease in size from day 7 and had healed by day 14. Histological and cellular kinetic findings, with bromodeoxyuridine (BrdU), were degeneration of the esophageal mucosa on day 1 and ulcer formation on day 3, with an increase in the number of BrdU-labeled cells in the esophageal mucosa around the ulcer. On day 7, regenerated epithelium was found to extend towards the ulcer base and the regenerated epithelium had become thicker, with papilla formation, by day 10. On day 14, the ulcer base was covered with thickened regenerated mucosa, with a decrease in the number of BrdU-labeled cells. Marked proliferative activity of the regenerated mucosa and thickening of the esophageal mucosa, with papilla formation, were observed during the healing process.

Thickness of Brunner’s glands and its clinical significance in peptic ulcer diseases

SummaryThe thickness of Brunner’s glands was measured using an ocular micrometer in 297 cases of surgically resected peptic ulcer and in 120 autopsy cases (control group). The mean maximum thickness of Brunner’s glands in the control group was 1.55±0.37mm (mean±SD) and no difference in thickness was noted for each decade of age. The mean maximum thickness of Brunner’s glands in patients with gastric ulcer, duodenal ulcer and gastroduodenal ulcer was 2.34±1.06, 3.18±1.07 and 3.24±1.05mm, respectively. When an ulcer is within the duodenum, Brunner’s glands near the ulcer were thicker than those contralateral to it. In patients with gastric ulcer, Brunner’s glands were the thickest in the pyloric ulcer group and negative correlation was noted between the thickness of Brunner’s glands and the distance to the ulcer from the pyloric ring. Since gastric acidity is supposed to be lower when an ulcer is located more proximally, these results suggest that Brunner’s glands become hyperplastic not only with the presence of an ulcer in the duodenum but also by acid hypersecretion of the stomach.

A case report of juvenile polyposis with adenomatous change and a review of 34 cases reported in Japan

SummaryIt has recently come to be thought that cases of juvenile polyposis have a natural tendency to develop adenoma and/or carcinoma. Here we present a case of juvenile polyposis coli with adenomatous change in a 21-year-old male, with a review of 34 cases of juvenile polyposis in the Japanese literature, and discuss the pathogenetic development of the polyps and their malignant potential. In this case, focal or entire adenomatous areas were found in large part of the polyps in the resected sigmoid colon and rectum, though these findings had not been recognized in 23 polypectomy specimens from the rectum 10 months prior to the operation. It was suggested that adenomatous change developed quickly in a very short time.

Possible Mechanisms of Diethyldithiocarbamate-Induced Gastro-Duodenal Mucosal Damage in Rats

A single s.c. injection of diethyldithiocarbamate (DDC, 1 g/kg) induced not only gastric but also duodenal mucosal damage in rats. DDC induced marked decreases in gastric acid output, gastro-duodenal mucosal blood flow and transmucosal potential difference prior to the development of mucosal lesions. Superoxide dismutase activity in the gastro-duodenal mucosa was also inhibited, while catalase and glutathione peroxidase activities gradually increased after the administration of DDC. These results suggest that a decrease in mucosal defensive mechanisms plays an important role in the development of DDC-induced gastro-duodenal mucosal damage and that oxygen-derived free radicals may also participate in the development of this mucosal damage.