Biomedical subjects

Seiji Tsunada

Publications and source records attributed to Seiji Tsunada.

27 records · Page 2Linked to original sources

PubMed2003

Endoscopic closure of perforations caused by EMR in the stomach by application of metallic clips.

BACKGROUND: The number of complications associated with use of EMR for early-stage gastric cancer, including perforation, has increased with the increasing use of this procedure. Endoscopic clip application was performed in patients who sustained a perforation as a result of EMR for gastric neoplasm. PATIENTS AND METHODS: Seven patients who underwent endoscopic application of metallic clips to close perforations were studied. The omental patch method was applied in one case with a large perforation. OBSERVATIONS: In all patients, endoscopic clip application successfully closed the perforation of the stomach, which occurred after EMR. No patient required laparotomy. CONCLUSIONS: The technique of endoscopic clip application might be useful for treatment of patients who sustain a perforation caused by EMR.

Aged↗

PubMed2003

Chronic exposure to subtoxic levels of peroxidized lipids suppresses mucosal cell turnover in rat small intestine and reversal by glutathione.

Oxidative challenge can compromise intestinal growth and death responses. This studyexamines the effect of chronic consumption of subtoxic levels of peroxidized lipids on intestinal redox balance and turnover and the effect of glutathione (GSH) supplementation. Male Sprague-Dawley rats were fed standard rat chow or 4% peroxidized menhaden oil chow (2-8 weeks). Intestinal GSH and glutathione disulfide (GSSG), GSH synthetic and redox enzymes as well as proliferative (ornithine decarboxylase, ODC) and apoptotic activities were evaluated. Chronic peroxide intake did not affect overall animal growth, but decreased intestinal GSH/GSSG ratio that directly correlated with decreased GSH and increased GSSG, and suppressed peak circadian ODC activities and post-prandial mucosal apoptosis. Supplementation with GSH restored the mucosal GSH/GSSG ratio and abrogated the peroxide-induced suppression of intestinal cell turnover. Collectively, the results show that chronic lipid peroxide consumption induces intestinal GSH redox imbalance that interferes with regulation of enterocyte death and proliferation in vivo. These disruptive effects of lipid peroxides were reversed by GSH supplementation in accordance with the normalization of tissue GSH/GSSG redox balance.

Animals↗

PubMed2003

Chronic lipid hydroperoxide stress suppresses mucosal proliferation in rat intestine: potentiation of ornithine decarboxylase activity by epidermal growth factor.

We recently demonstrated that chronic exposure of rat intestine to sublethal levels of peroxidized lipids suppresses ornithine decarboxylase (ODC) activity, consistent with attenuated intestinal proliferation. The current study was designed to better understand the influence of exogenous epidermal growth factor (EGF) on intestinal proliferation in normal intestine and intestine that was challenged by oxidative stress induced by dietary consumption of peroxidized lipids. Male Sprague-Dawley rats (250-300 g) were fed standard chow (control) or peroxidized lipid chow for 4 weeks. EGF was injected intraperitoneally at a dose of 40 microg/kg. Intestinal proliferation was evaluated by ODC activity in fed or fasted states and at specified times during the circadian phase. Chronic peroxide consumption significantly attenuated ODC activities in association with increased tissue peroxide content. The suppressed ODC activities were restored to control values by EGF in the small intestine; in the colon, EGF increased ODC activity threefold over control rats given EGF. This elevated colonic ODC activity was correlated with decreased tissue GSSG and an increased GSH/GSSG ratio. These results show that EGF administration reverses the suppression of intestinal ODC activities induced by chronic peroxidized lipid intake. In contrast, EGF significantly elevates proliferative activity in the peroxide-stressed colon. This exaggerated proliferation may contribute to a better understanding of colonic susceptibility to oxidant-induced malignant transformation.

Animals↗

PubMed2003

Evaluation of endoscopic hemostasis with metallic hemoclips for bleeding gastric ulcer: comparison with endoscopic injection of absolute ethanol in a prospective, randomized study.

OBJECTIVE: Although metallic hemoclips have been used for hemostasis of bleeding ulcer, there have been few prospective trials to evaluate their efficacy. In this study, a prospective, randomized trial was performed to evaluate endoscopic hemoclipping for bleeding gastric ulcer in comparison with endoscopic injection of absolute ethanol. METHODS: During the period 1995-1998, 126 gastric ulcer patients with bleeding or nonbleeding visible vessel were considered for entry. They were randomly assigned to one of three groups: endoscopic hemostasis performed with injection of absolute ethanol (group I, n = 42), hemoclipping (group II, n = 42), and a combination of the two methods (group III, n = 42). RESULTS: The permanent hemostatic rate was 85.7% in group I, 90.5% in group II, and 92.9% in group III. The mean volume of blood transfusion was 313 +/- 77 ml in group I, 274 +/- 54 ml in group II, and 163 +/- 42 ml in group III, which was significantly less than in groups I or II (p < 0.05). No patients required emergency surgery. Five patients died within a month after initial hemostasis as a result of unrelated conditions. CONCLUSIONS: Endoscopic hemostasis with hemoclips for bleeding gastric ulcer was as effective and safe as that with injection of absolute ethanol, and a combination of ethanol injection and hemoclips did not result in a great advantage over the two individual procedures.

Equipment Design↗

PubMed2003

Intracerebroventricular administration of leptin-induced apoptosis in the rat small intestinal mucosa.

The localization of leptin and leptin receptors in the stomach and small intestine has been reported. Their function is still unknown, although leptin is a hormone that regulates appetite and fat-related metabolism. The small intestine is one of the important organs for regulating metabolism. The purpose of the present study was to investigate whether leptin regulates apoptosis in the small intestinal mucosa. Intestinal apoptosis was evaluated by percent fragmented DNA, electrophoresis, TUNEL staining, and western blotting analysis of caspase-3. Mucosal apoptosis in the rat jejunum and ileum was evaluated at 0, 3, 6, 12, and 24 hrs after injection. Rats were tested after ad libitum feeding and 24-hr fasting to exclude the anorectic effect of leptin. Leptin was injected intraperitoneally (ip) at a dose of 200 microg/rat and infused into the rat third cerebroventricle (icv) at a dose of 8 microg/rat. Leptin at a dose of 8 microg/rat significantly induced intestinal apoptosis in the small intestine at 3 and 6 hrs after icv administration in both ad libitum feeding and 24-hr fasted rats. This increase in apoptosis was not attenuated by vagotomy. Intestinal apoptosis increased 12 and 24 hrs after ip injection of leptin at a dose of 200 microg/rat. The peak of the increase in apoptosis in icv rats appeared earlier than that in ip rats. Leptin induced jejunal and ileal mucosal apoptosis in the rat, indicating that leptin might control intestinal function through the regulation of intestinal apoptosis.

Animals↗

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

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↗