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Biomedical subjects

M Tatsuta

Publications and source records attributed to M Tatsuta.

At least 145 records · Page 8Linked to original sources
PubMed1993

Fundal atrophic gastritis as a risk factor for gastric cancer.

The role of atrophic gastritis of the gastric corpus (fundal atrophic gastritis) as a high-risk factor was investigated by studying operative findings and follow-up data on 690 patients with benign gastric diseases recorded at the Osaka Cancer Registry. The extent of fundal atrophic gastritis was determined by the endoscopic Congo red test. The patients were followed-up from the time of endoscopic examination (1968 to 1976) to December 31, 1987. The vital status of 654 patients (94.8%) at the end of the observation period was determined. During the follow-up period, 22 patients were found to have gastric cancer. The extent of fundal atrophic gastritis was shown to be closely related with the risk of developing gastric cancer. Patients who had been diagnosed as having severe fundal atrophic gastritis showed significantly higher risk of gastric cancer than patients who had been diagnosed as having little or no fundal atrophic gastritis (5.76-fold, calculated with adjustments for age, sex and the follow-up period). A positive linear relationship was found between the risk of developing gastric cancer and the extent of fundal atrophic gastritis. The observed number of gastric cancers was compared with the expected number calculated from the incidence in Osaka Prefecture. Analysis of the results showed that the observed and expected numbers of gastric cancers in patients with severe fundal atrophic gastritis were 11 and 4.8, respectively, the ratio of observed to expected numbers being 2.3 (p < 0.05). These findings indicate that severe fundal atrophic gastritis is a major risk factor for gastric cancer.

Adult↗
PubMed1993

Hookwire localizer as an aid for ultrasonic detection of small liver nodules.

We applied a V-shaped localizer and evaluated its clinical usefulness in nine patients with small hepatic nodules less than 2 cm in diameter. A small hepatic nodule was punctured with a 21-gauge localization needle under ultrasonic guidance, and the V-shaped localizer was pushed into the nodule with a wire. The localizer could be observed as a strong echo line by ultrasonography and as a high-density bar by computed tomography (CT). By this method, it was possible to precisely localize the nodule. Intraoperative ultrasonography became less time-consuming, and resection of the nodules could be confirmed with low-kilovoltage radiography.

Aged↗
PubMed1993

Clinicopathological features and endoscopic diagnosis of superficial early adenocarcinomas of the large intestine.

From October 1987 to March 1991, 21 (8%) superficial early cancers were found among 256 early colorectal cancers (Dukes A and B1). Superficial early cancers were defined as early cancers less than 3 mm in height. These tumors were found scattered throughout the large intestine and were often observed as reddish spots, which were easily overlooked without careful observation. Histologically, 19 (90%) of them were well-differentiated adenocarcinomas, and five (24%) of them reached the submucosal layer. Eighteen (86%) of them were not associated with adenoma.

Adenocarcinoma↗
PubMed1993

Suppressive effect of estrogen on hepatocellular tumorigenesis induced in mice by 3'-methyl-4-dimethylaminoazobenzene.

Treatment of female C57BL/6 x DS-F1 mice with 3'-methyl-4- dimethylaminoazobenzene (3'-Me-DAB) neonatally resulted in the development of hepatocellular adenomatous nodules. Ovariectomy at 1 month of age greatly hastened the time of appearance of these nodules and significantly increased their incidence. The incidence of adenomatous nodules in females ovariectomized at 1 month of age was about 70% at 12 months of age, and was decreased to 4% by implantation of a pellet containing estradiol-17 beta (E2 pellet) at 1 month of age (at the time of ovariectomy). The incidence of adenomatous nodules at 12 months of age was not decreased significantly when the implanted E2 pellet was removed at 4 or 6 months of age, but was decreased significantly when it was removed at 8 or 10 months of age. Implantation of E2 pellets into ovariectomized females at 4 and 6 months of age decreased the incidence of adenomatous nodules as effectively as their implantation at 1 month of age. The implantation of E2 pellets into ovariectomized females at 8 or 10 months of age resulted in significantly lower incidences of adenomatous nodules at 12 months of age, than that in females ovariectomized at 1 month of age. The present results suggest that the ovarian hormone, estrogen suppresses the development of hepatocellular tumors induced by 3'-Me-DAB, exerting its effect from about 6 months of age.

Adenoma, Liver Cell↗
PubMed1993

Inhibition by amiloride of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of amiloride on the incidence and histological types of gastric cancers in Wistar rats induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and on the labelling index and proliferative fraction of gastric mucosa were investigated. After oral treatment with MNNG for 25 weeks, rats received s.c. injections of amiloride (0.25 mg kg-1 or 5.0 mg kg-1 body weight) in depot form every other day until the end of the experiment. Prolonged administration of 5.0 mg kg-1, but not 2.5 mg kg-1 of amiloride significantly decreased the incidence of gastric cancers in Week 52. However, it did not influence the histological features of the gastric cancers. It also significantly decreased the labelling index and proliferative fraction of the antral mucosa. These findings indicate that amiloride inhibits the development of gastric cancers, and that its effect may be related to its effect in decreasing cell proliferation of the antral mucosa.

Adenocarcinoma↗
PubMed1993

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

The effect of verapamil on hepatocarcinogenesis induced by N-nitrosomorpholine (NNM) was investigated in male Sprague-Dawley rats. Rats were given drinking water containing NNM for 8 weeks and received i.p. injections of verapamil or vehicle every other day for 16 weeks from the start of the experiment. Pre-neoplastic and neoplastic lesions staining positive for gamma-glutamyl transpeptidase (GGT) or the placental type of glutathione-S-transferase (GST-P) were examined histochemically at week 16. Prolonged administration of verapamil resulted in a significant decrease in the number of GGT-positive and GST-P-positive lesions. The incidence and volume as a percentage of parenchyma of hepatocellular carcinomas were also significantly less in rats treated with verapamil than in controls. Administration of verapamil significantly decreased the labelling indices of pre-neoplastic lesions and adjacent liver. These findings indicate that verapamil inhibits hepatocarcinogenesis and that this may be related to its inhibitory effect on cell proliferation in neoplastic lesions and surrounding hepatocytes.

Animals↗
PubMed1993

Suppression by oestrogen of hepatocellular tumourigenesis induced in mice by 3'-methyl-4-dimethylaminoazobenzene.

Treatment of female C57BL/6 x DS-F1 mice with 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) neonatally resulted in the development of adenomatous nodules and glucose-6-phosphatase (G-6-Pase) deficient foci at 8 and 6 months of age, respectively. Ovariectomy of these mice at 1 month of age hastened the development and increased the incidences of these lesions. Subcutaneous implantation of estradiol-17 beta (E2) with ovariectomy at 1 month of age markedly decreased the incidences of adenomatous nodules and G-6-Pase deficient foci at 10 or 12 months of age, but subcutaneous implantation of progesterone did not reduce their incidences. Subcutaneous implantation of E2 into ovariectomised mice at 6 months of age resulted in significant decreases in the incidences of adenomatous nodules and G-6-Pase deficient foci at 10 months of age, but implantation of E2 into the spleen of ovariectomised mice of the same age had no effect on their incidences. The present results suggest that E2 suppresses the development of adenomatous nodules and G-6-Pase deficient foci induced in the mouse liver by 3'-Me-DAB by actions on tissues other than the liver.

Adenoma↗
PubMed1993

Enhancement by thyroxine of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The affects of L-thyroxine (T4) on the incidence and histology of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and on the labelling index of gastric mucosal epithelial cells were investigated in Wistar rats. After oral treatment with MNNG for 25 weeks, the rats received s.c. injections of T4 (0.2 microgram kg-1) in depot form every other day until the end of the experiment in Week 52. This long-term treatment with T4 significantly increased the incidence of gastric cancers in Week 52. However, it did not influence the histological type of the gastric cancers. It also caused significant increases in the labelling indices of the fundic and antral epithelial cells. These findings indicate that T4 enhances the development of gastric cancers, and that its effect may be related to its effect in increasing proliferation of gastric epithelial cells.

Administration, Oral↗
PubMed1993

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

The effect of somatostatin on hepatocarcinogenesis induced by N-nitrosomorpholine (NNM) was investigated in male Sprague-Dawley rats. Rats were given drinking water containing NNM for 8 weeks and s.c. injections of 200 micrograms/kg body wt of somatostatin every other day from the beginning of the experiment until the end of week 16. Pre-neoplastic and neoplastic lesions staining for gamma-glutamyl transpeptidase (GGT) or placental type glutathione-S-transferase (GST-P) were examined histochemically. Administration of somatostatin for 16 weeks resulted in significant reduction in the percentage volume of GGT-positive and GST-P-positive lesions. The incidence, number and size of hepatocellular carcinomas were significantly less in rats treated with somatostatin than in untreated rats. Administration of somatostatin significantly decreased the labeling indices of pre-neoplastic lesions and adjacent liver. These findings indicate that somatostatin inhibits hepatocarcinogenesis and that this effect may be related to its effect in decreasing cell proliferation in pre-neoplastic lesions.

Animals↗
PubMed1993

Enhancement by the tricyclic antidepressant, desipramine, of experimental carcinogenesis in rat colon induced by azoxymethane.

The effects of the tricyclic antidepressant drug desipramine on the incidence, number and histology of colon tumors induced by azoxymethane (AOM), and on the serum norepinephrine (NE) concentration and the labeling index of colon mucosa were investigated in Wistar rats. Rats were treated s.c. with 7.4 mg AOM/kg body wt once a week for 10 weeks, and also s.c. with 10 mg desipramine hydrochloride (desipramine)/kg body weight until the end of the experiment. Treatment with desipramine significantly increased the incidence, but not the number, of colon tumors in week 35. However, it did not influence the location and the histological appearance of the colon tumors or the histological types of colon adenocarcinomas. Furthermore, it significantly increased the serum NE level and the labeling index of colon mucosa during and after AOM treatment. These findings indicate that desipramine enhanced the development of colon tumors and that its effect may be related to its effect in increasing proliferation of colon epithelial cells.

Animals↗
PubMed1993

Enhancing effects of calcium-deficient diet on gastric carcinogenesis by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of ad libitum feeding of calcium-deficient diet on the incidence, number and histological types of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in male Wistar rats. Rats were fed standard pellet diet containing 0.5% (normal-calcium diet) or 0.01% calcium (calcium-deficient diet) after oral treatment with MNNG for 25 weeks. Oral administration of the calcium-deficient diet resulted in a significant increase in the incidence, but not the number, of gastric cancers in experimental Week 52. However, it did not affect the histological types of cancer. The calcium-deficient diet also caused a significant increase in tissue norepinephrine concentration of the antral portion of the gastric wall and in the labeling index of the antral epithelial cells. These findings indicate that the calcium-deficient diet enhanced gastric carcinogenesis and suggest that its effect may be related to increase in norepinephrine in the gastric wall and consequent stimulation of proliferation of antral epithelial cells.

Adenocarcinoma↗
PubMed1993

Effect of treatment with liu-jun-zi-tang (TJ-43) on gastric emptying and gastrointestinal symptoms in dyspeptic patients.

The effects of treatment with the Chinese herbal medicine Liu-Jun-Zi-Tang (TJ-43) on gastric emptying and gastrointestinal symptoms were investigated in 42 patients with chronic idiopathic dyspepsia. By random allocation, 22 patients received oral treatment with 2.5 g TJ-43 three times daily, and 20 patients received placebo. Gastric emptying was measured by the acetaminophen absorption method. After 7 days of treatment, gastric emptying was significantly accelerated and gastrointestinal symptoms were significantly reduced in patients treated with TJ-43. Placebo treatment produced no significant effects. These findings indicate that TJ-43 had a prokinetic action on gastric emptying and that it was useful in treating chronic dyspepsia.

Adult↗
PubMed1993

[A case of bronchogenic cyst in the posterior mediastinum with high level of serum SCC antigen].

A 78-year-old man was picked up by chest X-ray findings. His CT scan film showed a posterior mediasinal tumor shadow. Serum level of SCC antigen was high and thoracotomy revealed bronchogenic cyst with high production of SCC antigen. After resection of the cyst, his serum level of SCC was within normal range. It is proposed that the elevated serum level of SCC is due to chronic inflammation or structural feature of the cystic wall.

Aged↗
PubMed1992

Protection by muscimol against gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in spontaneously hypertensive rats.

The effects of prolonged administration of the gamma-aminobutyric acid receptor agonist muscimol on enhanced induction of gastric carcinogenesis by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in spontaneously hypertensive rats (SHR), and on the norepinephrine concentration in the gastric wall and the labeling index of gastric mucosa were investigated. SHR and normotensive Wistar Kyoto (WKY) rats as controls were given a solution of MNNG (25 micrograms/ml) for 25 weeks and then i.p. injections of 0.5 mg/kg body weight of muscimol every other day. In control WKY rats, gastric cancers were found in 1 (7%) of 14 rats examined at week 52. In SHR treated with NaCl solution only, the incidence of gastric cancers was significantly increased to 50% compared with that in control WKY rats. However, treatment of SHR with muscimol significantly increased its incidence to 12% compared with the value in SHR treated with NaCl solution only. The norepinephrine concentration in the gastric wall and the labeling index of the gastric mucosa were significantly greater in SHR than in WKY rats. Prolonged administration of muscimol to SHR significantly reduced the norepinephrine concentration in the antral portion of the gastric wall or the labeling index of the antral epithelial cells. These findings indicate that long-term treatment of SHR with muscimol attenuated the enhancement of gastric carcinogenesis in SHR.

Analysis of Variance↗
PubMed1992

Cytologic examination of pure pancreatic juice in the diagnosis of pancreatic carcinoma. The endoscopic retrograde intraductal catheter aspiration cytologic technique.

BACKGROUND: Although cytologic examination of pure pancreatic juice obtained with a duodenofiberscope has been useful for the diagnosis of pancreatic carcinoma, the rate of false-negative results is reported to be high. To eliminate these false-negative results, the authors developed a new technique, endoscopic retrograde intraductal catheter aspiration cytology, especially for an accurate cytologic diagnosis of carcinoma of the body or tail of the pancreas. METHODS: The accuracy of conventional cytologic examination of pure pancreatic juice was assessed in 25 patients with pancreatic carcinoma, 29 patients with pancreatitis, and 52 control subjects. Pure pancreatic juice was collected from the pancreatic duct by endoscopic cannulation using a videoimaging duodenoscope after intravenous administration of secretin. The new endoscopic retrograde intraductal catheter aspiration technique was used in four patients with carcinoma of the body or tail of the pancreas and five patients with localized pancreatitis in whom a correct diagnosis was not made by previous cytologic examination of pure pancreatic juice. RESULTS: Positive cytologic findings were obtained in 76% of the patients with pancreatic carcinoma. Positive cytologic results were more frequent in patients with carcinoma of the head of the pancreas than in those with carcinoma of the body or tail. By the new technique, positive cytologic results were obtained in all of the patients with pancreatic carcinoma. This technique caused no severe complications. CONCLUSIONS: This procedure of endoscopic retrograde intraductal catheter aspiration cytology seems useful for diagnosis of pancreatic carcinoma.

Catheterization↗
PubMed1992

Inhibition by 6-hydroxydopamine of enhanced gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in spontaneously hypertensive rats.

The effects of chemical sympathectomy induced by 6-hydroxydopamine (6-OHDA) on the enhanced induction of gastric carcinogenesis by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in spontaneously hypertensive rats (SHR), and the norepinephrine (NE) concentrations in their gastric wall and the labeling index of gastric epithelial cells were investigated. SHR rats and normotensive Wistar Kyoto rats (WKY) as controls were given MNNG (25 micrograms/ml) in their drinking water for 25 weeks and then i.p. injections of 6-OHDA (42 mg/kg twice within 24 hr, and then 105 mg/kg every 2 weeks from 1 week later). In control group (WKY rat + NaCl), gastric cancers were found in 2 (11%) of 18 rats examined in week 52. In SHR rats treated with NaCl solution only, the incidence of gastric cancers significantly increased, to 53% compared with that in control WKY rats. Treatment of SHR rats with 6-OHDA significantly decreased its incidence to 12% compared with the value in SHR rats treated with NaCl solution only. Prolonged administration of 6-OHDA to SHR rats significantly reduced the NE concentration in the antral portion of the gastric wall and the labeling index of antral epithelial cells. These findings indicate that prolonged i.p. treatment with 6-OHDA attenuated the normally higher incidence of MNNG-induced gastric cancer in SHR rats.

Animals↗
PubMed1992

Inhibitions by 6-hydroxydopamine and neostigmine singly or together of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of chemical sympathectomy induced by 6-hydroxydopamine (6-OHDA) and administration of the acetylcholinesterase inhibitor neostigmine, singly or together, on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and on the tissue catecholamine concentration of the gastric wall and the labeling index of the gastric mucosa, were investigated in inbred Wistar rats. Rats received s.c. injections of neostigmine (0.075 mg/kg), and/or i.p. injections of 6-OHDA (42 mg/kg twice within 24 hr, and then 105 mg/kg every 2 weeks from 1 week later) 25 weeks after oral treatment with MNNG. Prolonged administration of 6-OHDA or neostigmine significantly reduced the incidence of gastric cancers by week 52, and in combination they had a significantly greater inhibitory effect. 6-OHDA and/or neostigmine had no influence on the histology of gastric cancers. Administration of 6-OHDA, but not neostigmine, significantly decreased the norepinephrine concentration in the antral portion of the gastric wall. The labeling index of the antral mucosa was decreased significantly by treatment with 6-OHDA or neostigmine, and decreased even more significantly by 6-OHDA plus neostigmine. Our findings indicate that 6-OHDA and neostigmine have protective effects against gastric carcinogenesis and that in combination their effects are additive. These results imply that the activities of the sympathetic and parasympathetic autonomic systems together influence gastric carcinogenesis.

Animals↗