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Biomedical subjects

H Taniguchi

Publications and source records attributed to H Taniguchi.

At least 703 records · Page 39Linked to original sources
PubMed1983

Effect of prolonged administration of gastrin on experimental carcinogenesis in rat colon induced by intrarectal instillation of N-methyl-N'-nitro-N-nitrosoguanidine.

The effect of tetragastrin on the incidence and histology of colonic tumors induced by intrarectal instillation of N-methyl-N'-nitro-N-nitrosoguanidine was investigated in Wistar rats. Prolonged administration of tetragastrin in depot form during and after treatment with N-methyl-N'-nitro-N-nitrosoguanidine resulted in a significant reduction in the incidence of colonic tumors in Experimental Week 35. Histological examinations showed that, unlike the well-differentiated adenocarcinomas with a typical glandular pattern in control groups, the adenocarcinomas that developed in rats treated with tetragastrin had high mucin-producing activity.

Adenocarcinoma↗
PubMed1983

[Extension modes in Borrmann-4 stomach carcinoma estimated by macroscopic appearances].

The clinico-pathologic findings on 91 patients with Borrmann-4 gastric carcinoma were studied. Based on macroscopic appearance of the gastric lesions, Borrmann-4 carcinoma was classified into 4 subtypes; (1) giant rugae type, (2) IIc surface type, (3) erosion type and (4) stricture type. According to the clinico-pathological characteristics of each subtype, these main modes of cancerous extension are suggested: Carcinoma of the giant rugae type develops from a small lesion at the gastric body into peritoneal sclerosing infiltration, cancer of the stricture type originates from the gastric antrum and progresses to peritoneal sclerosing infiltration, cancer of the IIc surface type and erosion type develops from large erosive lesions into lymphangitis carcinomatosa.

Female↗
PubMed1983

[Effects of sex hormones on carcinogenesis of the stomach].

Influences of sex-hormones on gastric cancer development induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in Wistar rats were studied. Well-differentiated adenocarcinoma developed in glandular stomach of 81% of male rats given 50 micrograms/ml of MNNG in drinking water for 4 months and sacrificed on the 12th month of the experiment. No gastric cancer was found in female rats given MNNG. In the additional estradiol-treated or castrated male rats, and the additional testosterone-treated or oophorectomized female rats, the incidence of carcinoma was 68% and 29%, and 33% and 5%, respectively. In the latter 3 groups, gastric erosion of the early stage was also low incidence. Histologically, poorly-differentiated adenocarcinoma was observed more frequently in these groups than in the alone MNNG-treated male group. These results have sagg-suggested that female-sex-hormone may inhibit and male-sex-hormone may accelerate the gastric carcinogenesis.

Adenocarcinoma↗
PubMed1982

Endoscopic diagnosis of early gastric cancer by the endoscopic Congo red-methylene blue test.

The endoscopic Congo red test combined with dyeing with methylene blue was performed in 85 patients with early gastric cancer (94 lesions). Results revealed that gastric cancer bleached the Congo red and methylene blue sprayed over their surface and this appeared in sharp contrast to the red-colored mucosa of unaffected areas. Grossly, polypoid and flat types, and histologically differentiated adenocarcinomas bleached the dyes more frequently and more intensely than depressed and undifferentiated adenocarcinomas. Thus the spread of cancerous growth could be judged rather accurately and so the target area could be reached by biopsy in cases where there were few if any visual signs of abnormality.

Adenocarcinoma↗
PubMed1982

Presence of insulin-like immunoreactivity and its biosynthesis in rat and human parotid gland.

Extracts from homogenates of rat and human parotid glands contained insulin-like immunoreactivity. The values were 5.6 +/- 2.8 ng/g wet tissue in six groups of rat parotid glands and 23.8 and 39.7 ng/g wet tissue in two human extracts. Upon gel filtration immunoreactive insulin of rat origin was eluted in a peak corresponding to the elution volume of isotopically labelled insulin. The material obtained from the two peak fractions showed an immunoassay dilution curve identical with that of rat insulin. Furthermore, biosynthesis of insulin-like immunoreactivity in rat and human parotid glands was confirmed in vitro by a specific separation method using anti-insulin antibody. These findings suggest that the parotid gland may be a further extrapancreatic source of insulin, and that insulin biosynthesis does occur in extrapancreatic tissues.

Animals↗
PubMed1982

Effect of sex hormones on the experimental induction of cancer in rat stomach - a preliminary study.

The effects of sex hormones on the induction of gastric carcinoma by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in Wistar rats. Well-differentiated adenocarcinomas developed with high frequency (88%) on the glandular stomach of male rats given MNNG in drinking water (50 micrograms/ml) for 4 months and sacrificed on the 12th month of the experiment. In female rats given MNNG, no gastric cancer was observed. In the castrated or estradiol-treated male rats, the incidence of carcinoma was lower (29 and 68%, respectively) than in the nontreated male rats. Histologically, poorly differentiated adenocarcinomas were observed more frequently in these groups than in the nontreated male group. In MNNG carcinogenesis, female, castrated male and estrogen-treated male rats had a lower incidence of gastric cancer with lower histological differentiation than did nontreated male rats.

Adenocarcinoma↗
PubMed1982

Modulation of somatostatin release by endogenous glucagon and insulin: physiological relationship between A, B and D cells in rat pancreatic islets.

In order to understand the physiological role of endogenous insulin or glucagon in somatostatin release, isolated rat pancreatic islets were treated with antiinsulin or antiglucagon antiserum in the presence of physiological amounts of glucose. The release of somatostatin was unchanged by treatment with antiinsulin antiserum which neutralized insulin released by 3.3, 8.3 and 16.7 mM of glucose. However, somatostatin release after treatment with antiglucagon antiserum was much reduced at all concentrations of glucose when compared with the release from control serum. Exogenous rat insulin (0.11, 1.11 micrograms/ml) had no effect, but exogenous glucagon (1, 5 micrograms/ml) resulted in a significant increase. Somatostatin release was stimulated by glucose, but the effect was insignificant. These results clearly indicate the physiological role of endogenous glucagon in the modulation of somatostatin release from the islets of Langerhans. Furthermore, the physiological relationship between A, B and D cells may be mediated through the paracrine mechanism.

Animals↗
PubMed1982

Protection by nicotinamide against streptozotocin-induced reduction in pancreatic TRH.

The concentration of thyrotrophin-releasing hormone (TRH) immunoreactivity was determined in pancreatic islets and acini in the rat. In addition, time-course changes in TRH in response to an iv injection of streptozotocin (65 mg/kg body weight) with or without nicotinamide (500 mg/kg body weight) were examined in the whole pancreas. Furthermore, pancreatic TRH was measured in diabetic rats treated with insulin for 3 weeks. The TRH concentration in rat islets was 42-fold higher than in exocrine glands, indicating that the majority of pancreatic TRH is of islet origin. The mean concentration of pancreatic TRH decreased to 60 and 65% of the respective control values at 4 and 7 h after administration of streptozotocin, respectively. AT 24 h, it fell to 10% of control values without significant changes in TRH levels in the hypothalamus and gastrointestinal tract. In contrast, no significant change in pancreatic TRH was noted in rats given combined treatment with streptozotocin and nicotinamide. The injection of streptozotocin alone resulted in severe hypoglycaemia at 7 h and hyperglycaemia at 24 h, whereas neither resulted from the combined treatment. Insulin therapy had no influence on the decreased TRH concentrations in the diabetic pancreas. These results suggest that TRH may be localized to the B cells of pancreatic islets, and that the marked reduction in TRH in diabetic pancreases is not a metabolic consequence of insulin deficiency.

Animals↗
PubMed1982

Gastrin protection against chemically induced gastric adenocarcinomas in Wistar rats: histopathology of the glandular stomach and incidence of gastric adenocarcinoma.

The effects of gastrin on the histopathology of the glandular stomach and on the incidence of gastric carcinoma induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in inbred Wistar (W) rats. Prolonged administration of gastrin after treatment with MNNG significantly reduced the incidence of adenocarcinomas of the glandular stomach. In addition, atypical glandular proliferations were significantly less frequent and were smaller, and the incidence of marked mucosal atrophy was significantly reduced in both the antral and oxyntic gland mucosae. Both atypical glandular hyperplasia and mucosal atrophy are precursors of gastric cancers; prolonged administration of gastrin to rats after treatment with MNNG suppressed development of precursors of gastric cancer and so prevented development of gastric cancers.

Adenocarcinoma↗
PubMed1982

Effect of sex hormones on carcinogenesis in the stomachs of rats.

We have been investigating possible effects of sex hormones on the carcinogenesis of stomach cancer in Wistar rats that were given N-methyl-N'-nitro-N-nitrosoguanidine in drinking water (50 micrograms/ml) for 4 months. The incidences of stomach cancer in intact male, intact female, castrated male, and castrated female rats at Month 4 of the experiment were 5, 0, 0, and 0% respectively; and those at Month 8 were 40, 10, 0, and 0% respectively; indicating that the incidence in intact males was much higher than in the other groups. The difference in the incidence became more evident when the animals were sacrificed at Month 12 of the experiment (81, 0, 29, and 5%, respectively). Hypertrophy and dissociation of the lamina muscularis mucosae which are considered to occur in the carcinogenic process were observed only in the male rats at the earlier months, but not in female nor in castrated rats. In N-methyl-N'-nitro-N-nitrosoguanidine carcinogenesis, female and castrated rats had a lower incidence of gastric cancers with less change in the lamina muscularis mucosae than did the nontreated male rats. These findings, therefore, suggest that, in addition to the suppressive action of female hormones, male hormones facilitate carcinogenesis.

Animals↗