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Kazuma Fujimoto

Publications and source records attributed to Kazuma Fujimoto.

44 records · Page 3Linked to original sources
PubMed2003

Characteristics of gastroesophageal reflux disease in Japan: increased prevalence in elderly women.

The aim of this study was to examine the characteristics of gastroesophageal reflux disease in Japan. We evaluated the correlation between clinical symptoms and endoscopic findings in an age- and sex-specific manner. This study included 6010 Japanese subjects who had not received medication or undergone laparotomy for gastrointestinal disease. All subjects were questioned in regard to clinical symptoms by paramedical personnel before endoscopic examination. Esophageal mucosal breaks were evaluated according to the Los Angeles Classification of Esophagitis. The ratio of subjects with each complaint to all subjects is as follows: heartburn, 27.0%; dysphagia, 16.9%; odynophagia, 19.2%; acid regurgitation, 7.1%. The proportion of each grade was grade A, 9.6%; grade B, 4.6%; and grade C + D, 2.0%. The most common related symptom for endoscopic esophagitis among these four symptoms was heartburn (odds ration, 2.5), although about 40% of subjects with severe esophagitis of grade C or D did not complain of heartburn. Regarding odynophagia, acid regurgitation, and dysphagia, odds ratios were about 1.0. The age-related ratio of esophagitis and severe disease with grades C and D increased in women over 60 years of age. An age-related slouched position was related to the increased esophagitis in these elderly women. Male subjects whose body mass index was more than 25 tended to show a greater prevalence in the age group 30-50 years. The prevalence of hiatal herniation increased in an age-related manner. These data indicate the characteristics of esophagitis in Japan are as follows: (1) the prevalence of reflux esophagitis is about 15% and most of these cases are grade A or B; and (2) the prevalence of severe esophagitis increases in older women, who do not always complain of clinical symptoms.

Adult↗
PubMed2002

iNOS enhances rat intestinal apoptosis after ischemia-reperfusion.

The aim of this study was to demonstrate (i) the role of iNOS (inducible nitric oxide synthase) on apoptosis in the rat intestinal mucosa after ischemia-reperfusion, and (ii) the effect of iNOS on the release of cytochrome c from mitochondria. The superior mesenteric artery was occluded for 60 min and was followed by a 60 min reperfusion. Rats were pretreated with an intraperitoneal injection of the following iNOS inhibitors: N-nitro-L-arginine methyl ester, aminoguanidine, and (1S,5S,6R,7R)-7- chloro-3-imino-5-methyl-2-azabicyclo [4. 1. 0] heptane hydrochloride (ONO-1714). Apoptosis was evaluated and NO(X) in the portal vein was assayed. The amount of iNOS, caspase-3, and cytochrome c were determined by a Western blot analysis. Intestinal mucosal epithelial mitochondrial dehydrogenase activity was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoilium bromide. Ischemia-reperfusion increased intestinal mucosal apoptosis, NO(X) production in the portal vein, the amount of iNOS protein, and the release of cytochrome c, but not caspase-3. Inhibitors of iNOS significantly attenuated the induction of apoptosis, increased NO(X) production, and release of cytochrome c. Mitochondrial dysfunction was induced by ischemia-reperfusion, which was ameliorated by iNOS inhibitors. Our results indicate that iNOS is related to increased mucosal apoptosis in the rat small intestine after ischemia-reperfusion, which is partly explained by the release of cytochrome c from mitochondria to cytosols following mitochondrial dysfunction.

Animals↗
PubMed2002

Homeostasis in the small intestinal mucosa balanced between cell proliferation and apoptosis is regulated partly by the central nervous system.

The aim of this study was to investigate whether the central nervous system regulates mucosal cell growth and apoptosis in the rat small intestine. Ornithine decarboxylase is a key enzyme for polyamine synthesis, which plays an important role in intestinal mucosal growth. The increase in ornithine decarboxylase activity in the duodenum just before a dark period was abolished by truncal vagotomy. An infusion of 2-deoxy-D-glucose into the third cerebroventricle activated the enzyme activity in the small intestine. Epithelial homeostasis is balanced by the regulation of cell proliferation and cell death. Intestinal mucosal apoptosis decreased in rats with ventromedial hypothalamus lesions, which induced hyperphagia and obesity. In contrast, sustained anorexia induced by 1-deoxy-D-glucosamine increased intestinal apoptosis. These results indicate that the central nervous system, in addition to local factors, is related to the regulation of mucosal homeostasis in the intestinal mucosa.

Animals↗
PubMed2002

Lipid peroxide-induced redox imbalance differentially mediates CaCo-2 cell proliferation and growth arrest.

Dietary oxidants like lipid hydroperoxides (LOOH) can perturb cellular glutathione/glutathione disulphide (GSH/GSSG) status and disrupt mucosal turnover. This study examines the effect of LOOH on GSH/GSSG balance and phase transitions in the human colon cancer CaCo-2 cell. LOOH at 1 or 5 micro m were noncytotoxic, but disrupted cellular GSH/GSSG and stimulated proliferative activity at 6 h that paralleled increases in ornithine decarboxylase activity, thymidine incorporation, expression of cyclin D1/cyclin-dependent kinase 4, phosphorylation of retinoblastoma protein, and cell progression from G0/G1 to S. At 24 h, LOOH-induced sustained GSH/GSSG imbalance mediated growth arrest at G0/G1 that correlated with suppression of proliferative activity and enhanced oxidative DNA damage. LOOH-induced cell transitions were effectively blocked by N-acetylcysteine. Collectively, the study shows that subtoxic LOOH levels induce CaCo-2 GSH/GSSG imbalance that elicits time-dependent cell proliferation followed by growth arrest. These results provide insights into the mechanism of hydroperoxide-induced disruption of mucosal turnover with implications for understanding oxidant-mediated genesis of gut pathology.

Acetylcysteine↗
PubMed2002

Normalization of phospholipids concentration of the gastric mucosa was observed in patients with peptic ulcer after eradication of Helicobacter pylori.

BACKGROUND: Phospholipids concentration in the gastric mucosa decreased in patients with Helicobacter pylori infection. The aim of this study is to examine the effects of eradication of H. pylori on decreasing the phospholipids concentration in the gastric mucosa in patients with gastric or duodenal ulcer. MATERIALS AND METHODS: Phospholipids (phosphatidylcholine, phosphatidylethanolamine, and sphingonomyeline) were measured in biopsy specimens from the antrum and corpus using thin-layer chromatography. In H. pylori positive patients with gastric ulcer (n = 26) and duodenal ulcer (n = 13), and H. pylori negative controls (n = 20), the biopsy specimens were obtained before and 3 months after eradication. Eradication was performed using lansoprazole, amoxycillin, and clarithromycin. RESULTS: Compared with the H. pylori negative control group, the concentrations of phosphatidylcholine and phosphatidylethanolamine decreased significantly in the gastric ulcer group in both antrum and corpus mucosa, and in the duodenal ulcer group in antrum mucosa. This decrease returned to the control level after eradication. CONCLUSIONS: This study demonstrates that the eradication of H. pylori in patients with peptic ulcer normalized the decrease of phosphatidylcholine and phosphatidylethanolamine in the gastric mucosa.

2-Pyridinylmethylsulfinylbenzimidazoles↗