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Biomedical subjects

H Iishi

Publications and source records attributed to H Iishi.

At least 163 records · Page 9Linked to original sources
PubMed1989

Inhibition by cysteamine of hepatocarcinogenesis induced by N-nitrosomorpholine in Sprague-Dawley rats.

The effect of cysteamine (2-aminoethanethiol hydrochloride) on hepatocarcinogenesis induced by N-nitrosomorpholine (NNM) was investigated in male Sprague-Dawley rats. Rats received alternate-day s.c. injections of cysteamine, and beginning in experimental week 3 were given drinking water containing NNM for 8 weeks. Pre-neoplastic and neoplastic lesions staining positive for gamma-glutamyl transpeptidase (GGT) or glucose-6-phosphate dehydrogenase (G6PD) were examined by histochemical techniques. In week 18, quantitative histological analysis showed that prolonged administration of cysteamine resulted in a significant reduction in the number of GGT-positive and G6PD-positive hepatic lesions. Histologically, hepatocellular carcinomas were significantly fewer and smaller in GGT-positive and G6PD-positive lesions in rats treated with cysteamine than in untreated rats. Administration of cysteamine also caused a significant decrease in the liver norepinephrine concentration and in the labelling indices of pre-neoplastic lesions and the surrounding liver. Our findings indicate that cysteamine inhibits hepatocarcinogenesis; this may be related to its reducing effect on norepinephrine concentration in the liver and its subsequent inhibition of cell proliferation in neoplastic lesions and surrounding hepatocytes.

Animals↗
PubMed1989

Effect of 6-hydroxydopamine on gastric carcinogenesis and tetragastrin inhibition of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of 6-hydroxydopamine (6-OHDA) on gastric carcinogenesis, on inhibition by tetragastrin of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine, and on the tissue catecholamine concentrations of the gastric wall and the labeling index of the gastric mucosa were investigated in inbred Wistar rats. Rats received s.c. injections of tetragastrin (1 mg/kg of body weight every other day) in depot form, i.p. injections of 6-OHDA (42 mg/kg twice within 24 h and 105 mg/kg every 2 wk), or injections of both compounds after 25 wk of p.o. treatment with N-methyl-N'-nitro-N-nitrosoguanidine (100 micrograms/ml). At Wk 52, prolonged administration of tetragastrin or 6-OHDA had significantly reduced the incidence and the number of adenocarcinomas. Combined administration of tetragastrin and 6-OHDA significantly enhanced the inhibitory effects of tetragastrin or 6-OHDA on gastric carcinogenesis. Administration of 6-OHDA but not tetragastrin, caused a significant decrease in norepinephrine concentrations in the antral portion of the gastric wall. Rats treated with tetragastrin or 6-OHDA had a significantly lower labelling index of the antral mucosa, and this index was significantly decreased by combined administration of tetragastrin and 6-OHDA, as compared with labeling indices observed after treatment with tetragastrin or 6-OHDA alone. These findings indicate that 6-OHDA exerts a protective effect against gastric carcinogenesis and enhances the inhibitory effect of tetragastrin on gastric carcinogenesis. This effect of 6-OHDA may be related to its ability to inhibit cell proliferation of the antral mucosa.

Animals↗
PubMed1989

Role of glucose-6-phosphate dehydrogenase on enhanced proliferation of pre-neoplastic and neoplastic cells in rat liver induced by N-nitrosomorpholine.

The relationship between G6PD and the number and size of pre-neoplastic and neoplastic lesions in rat liver was examined. Male Sprague-Dawley rats were given drinking water containing 250 mg/l of NNM for 8 weeks. Pre-neoplastic and neoplastic lesions with positive staining of GT were classified histochemically into G6PD-positive and G6PD-negative lesions. At week 24, quantitative analysis showed that the incidence and number of G6PD-positive lesions were significantly higher than those of G6PD-negative lesions. Histologically, hepatocellular carcinomas were more frequent and larger in G6PD-positive lesions than in G6PD-negative ones. Statistical analysis of the quantitative data also showed that the number and volume of G6PD-positive hepatocellular carcinomas were significantly higher than in G6PD-negative carcinomas. The G6PD-positive pre-neoplastic lesions had a significantly higher labelling index than G6PD-negative ones. These findings revealed a considerable difference in the growth of these 2 populations of the lesions, and indicate that G6PD activity may be closely related to proliferation of the pre-neoplastic and neoplastic cells in the liver.

Animals↗
PubMed1989

Prospective evaluation of diagnostic accuracy of gastrofiberscopic biopsy in diagnosis of gastric cancer.

The accuracy of gastrofiberscopic biopsy in diagnosis of gastric malignancies has been evaluated by studying operative and postmorten findings and clinical follow-up data in linkages at Osaka Cancer Registry, Japan, after an average of 7.7 years. Satisfactory data were obtained in follow-ups of all 1331 patients examined. There were only 31 (3.7%) false-negative diagnoses of malignancy among 858 patients diagnosed as having benign lesions, and only three (0.6%) false-positive diagnoses among 473 patients diagnosed as having malignant tumors. The false-negative diagnoses were most frequent in cases of elevated types of early cancer, advanced cancer of type 4 and leiomyosarcoma, or in cases located in the posterior wall and in the antrum. The three benign lesions that were diagnosed as malignant by biopsy were all associated with active ulceration, indicating that care is necessary in taking biopsy specimens of ulcerated lesions. From these findings the sensitivity and specificity of the gastrofiberscopic biopsy method for detection of gastric malignancies were calculated to be 93.8% and 99.6%, respectively, and the overall accuracy for all the patients was 97.4%. These results reconfirm that gastrofiberscopic biopsy is very useful for diagnosis of gastric malignancies.

Adenocarcinoma↗
PubMed1989

Effects of propranolol and cimetidine on cysteamine inhibition of gastric carcinogenesis induced in Wistar rats by N-methyl-N'-nitro-N-nitrosoguanidine.

The effects of propranolol and cimetidine on inhibition by cysteamine (2-aminoethanethiol hydrochloride) of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and on gastric acid secretion, serum gastrin level, and labelling index of the gastric mucosa were investigated in inbred Wistar rats. Rats received alternate-day injections of cysteamine (25 mg/kg body weight) with or without propranolol (dl-propranolol hydrochloride) (2 mg/kg bw) or cimetidine (50 mg/kg bw) in depot form after 25 weeks of oral treatment with MNNG. Prolonged administration of cysteamine significantly reduced the incidence of adenocarcinoma of the glandular stomach. A combination of cysteamine and propranolol significantly accelerated the inhibitory effect of cysteamine on gastric carcinogenesis. However, with concomitant administration of cysteamine and cimetidine, the incidence of adenocarcinoma was slightly but not significantly increased as compared to that after treatment with cysteamine alone. Administration of cysteamine caused a significant increase in gastric acid secretion and serum gastrin level, and a significant decrease in the labelling index of the antral mucosa. A combination of cysteamine and propranolol significantly increased gastric acid secretion by cysteamine alone and significantly decreased the labelling index of the antral mucosa. With this treatment, the serum gastrin level was significantly higher than the basal level, but the stimulated serum gastrin level was significantly lower than observed that after administration of cysteamine alone. In contrast, concomitant administration of cysteamine and cimetidine caused a significant decrease in gastric acid secretion and significant increase in the serum gastrin level as compared to the levels seen after treatment with cysteamine alone, but had no influence on the labelling index of the antral mucosa. These findings indicate that hypersecretion of acid, but not hypergastrinemia associated with hyposecretion of acid or achlorhydria, exerts a protective effect against gastric carcinogenesis, and that this effect may be related to its activity in decreasing proliferation of the antral mucosa.

Adenocarcinoma↗
PubMed1989

Enhancement of experimental gastric carcinogenesis induced in spontaneously hypertensive rats by N-methyl-N'-nitro-N-nitrosoguanidine.

The incidence, number, and histological types of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine and the tissue norepinephrine concentration of the gastric wall were investigated in spontaneously hypertensive rats and in control Wistar Kyoto rats and Wistar rats. All rats were given drinking water containing 25 micrograms/ml of N-methyl-N'-nitro-N-nitrosoguanidine for 25 weeks. During Week 52, the incidence and number per rat of gastric cancers were significantly greater in spontaneously hypertensive rats than in Wistar Kyoto and Wistar rats. All tumors induced in the glandular stomach were adenocarcinomas, but no significant difference was found in the histological types of adenocarcinoma in the three strains of rats. At Weeks 15, 30, and 52, norepinephrine concentrations in the fundic and antral portion of the gastric walls and labeling indices in the antral and fundic mucosa were significantly higher in spontaneously hypertensive rats than in Wistar Kyoto and/or Wistar rats. These findings indicate that increased sympathetic nervous system activity enhances the development of gastric cancers, but immunological dysfunction in spontaneously hypertensive rats may contribute to the increased susceptibility to gastric cancer.

Adenocarcinoma↗
PubMed1989

Promotion by neurotensin of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of neurotensin on the incidence and histology of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine were investigated in Wistar rats. Rats were given 100 or 200 micrograms per kg of body weight of neurotensin s.c. every other day in depot form after 25 wk of p.o. treatment with the carcinogen. Prolonged alternate-day administration of neurotensin at 200 micrograms per kg of body weight resulted in a significant increase in the incidence of gastric cancers of the glandular stomach by Wk 52. However, it did not influence the histological appearance of the gastric cancers. Furthermore, it caused a significant increase in the labeling indices of the epithelial cells of the antrum and of gastric cancers. In contrast, the administration of neurotensin at 100 micrograms per kg of body weight had a slight, but not significant, influence on the development of gastric cancers. These findings indicate that neurotensin promotes gastric carcinogenesis, and that this effect may be related to its effect in increasing proliferation of epithelial cells in the antral mucosa and in gastric cancers.

Animals↗
PubMed1989

Diagnosis of gastric cancers with fluorescein-labeled monoclonal antibodies to carcinoembryonic antigen.

Forty gastric adenocarcinomas in 30 resected stomachs were examined by an endoscopic immunofluorescent technique using fluorescein isothiocyanate (FITC)-labeled antibodies to carcinoembryonic antigen (CEA). Fluorescence images of the tumors were obtained with a newly developed endoscopic television system for detecting faint fluorescence. Computer-assisted processing was used to enhance the detection and localization of the tumors visualized by the immunofluorescent technique. Twenty seven (90%) of 30 tumors showed positive fluorescence after treatment with FITC-labeled antibodies for 60 minutes, whereas only two (40%) of five cancers could be detected by the immunofluorescent technique after treatment with antibodies for less than 60 minutes. There was no significant relationship between positive fluorescence and the gross and histological types or the stages of the tumors. In contrast, no positive fluorescence could be demonstrated in cases of benign gastric lesions or after pretreatment with FITC-labeled alpha-fetoprotein. This study therefore suggests that the immunofluorescent technique using FITC-labeled anti-CEA antibodies can be useful in detecting the early stages of gastric cancer.

Adenocarcinoma↗
PubMed1989

Clinicopathological features and natural history of gastric hamartomatous polyps.

The clinicopathological features, chromoendoscopic findings, and natural history of hamartomatous polyps of the stomach were compared with those of gastric hyperplastic polyps. Hamartomatous polyps were found significantly more frequently in adult females than adult males, and all were found significantly more frequently in adult females than adult males, and all were located in the gastric body or the fundus. In general, the number of polyps per patient was less in older patients. Histologically, all these polyps were formed of cystically dilated oxyntic glands and irregularly deformed oxyntic glands. Chromoendoscopic examinations using Congo red showed that the polyps were associated with extensive acid-secreting areas, were all located in acid-secreting areas, and had an acid-secreting function. Colonoscopy and/or radiologic examinations showed that one or a few polyps were frequently also present in the colons of these patients, but none of the families of the patients had a history of gastrointestinal polyposis. One to 11 years after the initial endoscopy, in seven (50.0%) of 14 patients with hamartomatous polyps followed up, the number of polyps decreased significantly.

Adult↗
PubMed1989

Protective effect of oral cysteamine against induction of gastric cancer by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effect of oral administration of cysteamine (2-aminoethanethiol hydrochloride) on the incidence and histology of gastric adenocarcinomas induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) was investigated in inbred Wistar rats. Oral administration of 0.4% cysteamine in food after treatment with MNNG for 25 weeks significantly reduced the incidence and number of adenocarcinomas of the glandular stomach in experimental Week 52. Histological examination showed that adenocarcinomas that did develop in rats fed on cysteamine had high mucin-producing activity. Furthermore, oral administration of cysteamine caused a significant increase in serum gastrin level and significant decreases in the antral mucosal pH and the labeling indices of the antral mucosa. These findings indicate that cysteamine inhibits the development of gastric adenocarcinomas when given orally. This effect may be related to its ability to decrease proliferation of antral mucosal cells.

Adenocarcinoma↗
PubMed1989

Promotion by ethanol of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of ethanol (EtOH) on the incidence and histology of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in Wistar rats. The animals received alternate-day i.p. injections of 2.5 ml kg-1 body weight of 20% EtOH in 0.9% NaCl solution after 20 weeks of oral treatment with MNNG. Prolonged administration of EtOH resulted in a significant increase in the incidence and number of gastric cancers of the glandular stomach in week 52. However, it had no influence on the histological types of the gastric cancers. Furthermore, it caused a significant increase in the labelling index of the epithelial cells of the antrum in week 52. These findings indicate that EtOH promotes gastric carcinogenesis, and that this effect may be related to its effect in increasing proliferation of the antral epithelial cells.

Adenocarcinoma↗
PubMed1989

Effectiveness of discriminant analysis of serum CA 19-9 and elastase 1 in diagnosis of pancreatic carcinoma.

The accuracies of assays of serum CA 19-9 and elastase 1 in the diagnosis of pancreatic carcinoma were investigated by the cutoff method and discriminant analysis of data on 98 patients with pancreatitis, 65 patients with pancreatic carcinoma, 107 patients with benign diseases of other organs, and 108 patients with cancer of other organs. Comparison of the diagnostic accuracies of the cutoff method and multivariate analysis of CA 19-9 and elastase 1 showed that the latter was better for diagnosis in terms of its specificity. The performance of multivariate analysis was validated on independent data consisting of 52 patients with pancreatitis, 27 patients with pancreatic carcinoma, 79 patients with benign diseases of other organs, and 29 patients with cancer of other organs. Multivariate analysis of CA 19-9 and elastase 1 was very useful for differentiation of patients with and without pancreatic carcinoma: 24 (88.9%) of 27 patients with pancreatic carcinoma were correctly classified. Moreover, by this method, all patients with pancreatic carcinoma of less than 2 cm in longest diameter and 81.3% of those without jaundice were correctly classified.

Adult↗
PubMed1989

Promotion by nialamide of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of nialamide, a monoamine oxidase inhibitor, on the incidence, number, and histology of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in male Wistar rats. Rats were given subcutaneously 50 mg/kg body weight of nialamide in depot form every other day after 25 weeks of oral treatment with MNNG. Prolonged alternate-day administration of nialamide caused a significant increase in the incidence and number of gastric cancers of the glandular stomach in week 52. However, it did not affect the histology of the cancers. Nialamide also caused a significant increase in tissue norepinephrine concentrations in the gastric wall and in the labeling indices of the gastric mucosae. However, nialamide had no influence on serum gastrin levels in the fasting state and after re-feeding. These findings indicate that nialamide promotes gastric carcinogenesis and that this may be related to its effects in increasing norepinephrine in the gastric wall and stimulating proliferation of gastric epithelial cells.

Adenocarcinoma↗
PubMed1989

Enhancement by tetragastrin of experimental induction of gastric epithelium in the duodenum.

The effects of tetragastrin and truncal vagotomy on the incidence of gastric type epithelium in the duodenum by intraduodenal instillation of 5% NaOH solution were investigated in Wistar rats. Prolonged administration of 1 mg tetragastrin/kg body weight in depot form starting one week after NaOH treatment resulted in a significant increase in gastric acid secretion and the incidence and number of villi with gastric epithelium in the duodenum in experimental week 10. Villi with gastric epithelium were found in five (23%) of 22 rats in control group, whereas abnormal villi were found in 13 (59%) of 22 rats in the tetragastrin treated group (p less than 0.05). The average number of villi with gastric epithelium rose from 0.6 (0.4) per 100 villi in control rats to 2.4 (0.6) per 100 villi in tetragastrin treated rats (p less than 0.01). On histological examination, gastric type epithelium was most often found on stunted or flattened villi, and was always within the boundaries of the area of Brunner's glands. These mucosal changes reverted toward normal with time. In week 35, the incidence of gastric epithelium was significantly less than at week 10 (p less than 0.05). In contrast, no villi with gastric epithelium were found in vagotomised rats in week 10 (p less than 0.05). Vagotomy also caused a significant decrease in gastric acid secretion. These results show that exposure of the duodenal mucosa to high levels of gastric acid enhance the induction of gastric eithelium in the duodenum.

Animals↗
PubMed1989

Gastric emptying and gastrointestinal symptoms in patients with atrophic gastritis and the effects of domperidone.

The relationship of gastric emptying of liquid to the extent of fundal gastritis and gastrointestinal symptoms was investigated in a total of 37 subjects comprising healthy controls with no gastrointestinal symptoms and patients with constant gastrointestinal symptoms for at least 1 year. Gastric emptying was measured by the acetaminophen absorption method, and the extent of fundal gastritis was determined by the endoscopic Congo-red test developed at this hospital. Gastric emptying was significantly slower in patients with gastrointestinal symptoms than in healthy subjects. It was also significantly slower in patients with than in those without severe fundal gastritis. Gastrointestinal symptoms were significantly more frequent in patients with delayed gastric emptying. The acute effect of oral administration of domperidone on gastric emptying was examined. A single dose of domperidone (20 mg) significantly increased the rate of gastric emptying.

Adult↗
PubMed1988

Enhancement by prolonged administration of caerulein of experimental carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in rat stomach.

The effect of caerulein on the incidence and histology of gastric adenocarcinomas induced by N-methyl-N'-nitro-N-nitrosoguanidine was investigated in inbred Wistar rats. Prolonged alternate-day administration of caerulein at 10 micrograms/kg body weight after treatment with the carcinogen for 20 weeks significantly increased the incidence and number of adenocarcinomas of the glandular stomach. Histological examination showed that treatment with caerulein had no influence on the histology of induced adenocarcinomas. Furthermore, administration of caerulein resulted in a significant increase in the bromodeoxyuridine-labeling indices of the antral mucosa but did not influence the bromodeoxyuridine-labeling indices of the fundic mucosa and the carcinomas. These findings indicate that caerulein enhances gastric carcinogenesis and that the effect may be related to the promoting effect of caerulein on cell proliferation in the antral mucosa.

Animals↗
PubMed1988

Effects of bilateral and unilateral vagotomy on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

After administration of N-methyl-N'-nitro-N-nitrosoguanidine for 15 weeks, the effects of bilateral, anterior and posterior vagotomy on the incidence, number and location of gastric adenocarcinomas, gastric acid secretion and cell proliferation of the gastric mucosa were investigated in inbred Wistar rats. Bilateral or anterior vagotomy, but not posterior vagotomy, significantly increased the incidence and number of adenocarcinomas at experimental week 52. In sham-operated control rats and rats subjected to bilateral vagotomy, there was no significant difference between the incidence or number of gastric tumors in the anterior and posterior walls. After anterior and posterior vagal denervation, however, there were significantly more gastric cancers on the denervated side than on the other. Bilateral and unilateral vagotomy resulted in significantly reduced gastric acid secretion by experimental weeks 25 and 52. Bilateral vagotomy significantly increased the labelling indices of both the fundic and antral mucosa at both times, but did not cause any significant difference between those of the anterior and posterior wall. Anterior or posterior vagotomy resulted in a significant increase in the labelling indices of both the fundic and antral mucosa on the denervated side. These findings indicate that the vagal nerve exerts a trophic action on the gastric mucosa, and that the promoting effect of vagotomy on gastric carcinogenesis may be related to its effect in increasing proliferation of cells in the antral mucosa.

Animals↗