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Biomedical subjects

M Tatsuta

Publications and source records attributed to M Tatsuta.

At least 199 records · Page 11Linked to original sources
PubMed1990

Effect of ornithine decarboxylase inhibitor on tetragastrin treatment of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of combined administration of tetragastrin and the ornithine decarboxylase inhibitor 1,3-diaminopropane (DAP) on the incidence and number of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and the BUdR labelling indices of the fundic and antral mucosae, were investigated in inbred Wistar rats. Rats were given drinking water containing 2.5 g/l of DAP ad libitum and received alternate-day injections of 1 mg/kg body weight of tetragastrin in depot form after 25 weeks of oral treatment with MNNG. At week 52, prolonged administration of tetragastrin alone resulted in a significant reduction in the incidence and number of gastric cancers and a significant increase or decrease in the labelling indices of the fundic and antral mucosae, respectively. Concomitant administration of tetragastrin and DAP had no effect on the inhibition by tetragastrin of gastric carcinogenesis. With this treatment, the labelling index was significantly reduced in the fundic mucosa but not in the antral mucosa. These results suggest that ODC inhibitor does not attenuate tetragastrin inhibition of gastric carcinogenesis, and that anti-trophic action of tetragastrin on antral mucosa may be related to tetragastrin inhibition of gastric carcinogenesis.

Animals↗
PubMed1990

Diagnosis of hepatic cavernous hemangioma by fine needle aspiration biopsy under ultrasonic guidance.

Percutaneous aspiration biopsy of the liver using a heparinized 22-gauge needle was performed under ultrasonic guidance in 11 patients with hepatic cavernous hemangioma. Ten (91%) of 11 biopsy specimens obtained were cytologically diagnostic for hemangioma. No indications of malignancy were found. There was no relation between the cytological diagnosis and the location, size, or ultrasonographic findings. No complications were encountered. These findings indicate that cytological examination of the liver by fine needle aspiration biopsy is useful in diagnosing hepatic cavernous hemangioma of any size and in any location, provided optimal route to the lesions is chosen.

Aged↗
PubMed1990

Enhancement of mucus accumulation in a human gastric scirrhous carcinoma cell line (KATO-III) by fibroblast-tumor cell interaction.

Human fibroblasts (WI-38 cells) were found to enhance mucus accumulation by human scirrhous carcinoma cells (KATO-III cells). Coculture of KATO-III with WI-38 cells resulted in enlargement of the KATO-III cells and increases in the proportions of PAS- and colloidal iron-positive KATO-III cells. These morphological alterations were reversed when the KATO-III cells were again cultured without WI-38 cells. Conditioned media from cultures of WI-38 cells or cocultures of KATO-III and WI-38 cells induced the same morphological alterations in KATO-III cells, suggesting that WI-38 cells produce a factor or factors that enhance mucus accumulation in KATO-III cells. This factor seemed to be a protein with a molecular weight of more than 10,000 daltons.

Adenocarcinoma, Scirrhous↗
PubMed1990

Protection by oral phenylalanine against gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effect of oral administration of L-phenylalanine on the incidence and histology of gastric adenocarcinomas induced by N-methyl-N'-nitro-N-nitrosoguanidine was investigated in inbred Wistar rats. Oral administration of 6% phenylalanine after 25 weeks of treatment with the carcinogen significantly reduced the incidence and number of adenocarcinomas of the glandular stomach at experimental week 52. Oral administration of high dose phenylalanine significantly increased the basal serum gastrin level and significantly decreased the norepinephrine concentration in the antral portion of the gastric wall, as well as the labelling indices of antral mucosa. These findings indicate that orally administered phenylalanine inhibits the development of gastric cancers.

Adenocarcinoma↗
PubMed1990

Activity of cefixime against Helicobacter pylori and affinities for the penicillin-binding proteins.

Cefixime induced the formation of rounded cells from the spiral bacillary form of Helicobacter pylori at the MIC or less. Three main penicillin-binding proteins, called A, B and C, were separated from H. pylori. Cefixime had the strongest affinity to penicillin-binding protein B. The binding of cefixime to this protein may induce the formation of rounded H. pylori cells.

Anti-Infective Agents, Urinary↗
PubMed1990

Gastric emptying in patients with fundal gastritis and gastric cancer.

Gastric emptying was compared in patients with gastric cancers and fundal gastritis to determine its value in identifying patients at high risk of gastric cancer. Gastric emptying was measured by the acetaminophen absorption method, and the extent of fundal gastritis was determined by the endoscopic Congo red test. The results showed that gastric emptying was significantly slower in patients with severe fundal gastritis than in those without. Gastric emptying in patients with differentiated adenocarcinomas was significantly slower than in those with undifferentiated adenocarcinoma, its value being similar to that in patients with severe fundal gastritis. The Congo red test showed that the incidence of severe fundal gastritis was significantly greater in patients with differentiated adenocarcinomas than in those with undifferentiated cancers. These findings suggest that delayed gastric emptying may allow prolonged contact between dietary carcinogens and the stomach.

Adenocarcinoma↗
PubMed1990

Reduction of gastric ulcer recurrence after suppression of Helicobacter pylori by cefixime.

The effect on the recurrence of gastric ulcers after suppression of Helicobacter pylori by combined treatment with cimetidine and the antimicrobial drug cefixime was investigated. Twenty one of 43 patients with endoscopically proved gastric ulcer and H pylori infection were randomly assigned to receive cimetidine 800 mg daily for 12 weeks; the remaining 22 patients received cimetidine 800 mg daily for 12 weeks plus cefixime 100 mg daily for the last two weeks. After treatment, 88% of 17 patients on cimetidine only remained H pylori positive, whereas combined administration of cimetidine and cefixime had suppressed H pylori in 78% of 18 patients (p less than 0.05). Seventeen patients in the former group whose ulcers healed but who remained H pylori positive and 18 patients in the latter group whose ulcers healed and who were no longer infected with H pylori continued to be followed after treatment. These patients underwent endoscopy to detect ulcer recurrence if symptomatic, or at 12 and 24 weeks if asymptomatic. At 12 weeks, recurrence was observed in seven of 15 (47%) patients in whom H pylori persisted, but in only one of 14 (7%) patients in whom H pylori had been suppressed (p less than 0.05). At 24 weeks, however, recurrence rates were similar between the two groups. These findings indicate that H pylori infection may be closely related to early ulcer recurrence.

Cefixime↗
PubMed1990

[Problems concerning the diagnosis and treatment of multiple primary carcinoma of the lung].

Data on 44 patients with multiple primary carcinoma of the lung are presented. Twenty had metachronous tumors, and 24 had synchronous tumors. Twenty-one patients had undergone complete resection for both tumors, and 14 had undergone resection for only one of two tumors. The remaining 9 patients underwent no operation and were treated with photodynamic, radiation and/or chemotherapy. Long-term survival of more than 3 years was achieved for 11 patients, nine of whom had synchronous lesions. Furthermore, they included 3 patients who underwent nonsurgical therapy for both lesions. On the other hand, the prognosis after resection of the second tumor in patients with metachronous lesions was poor. This was thought to be the result of failure to diagnose the second lesion due to incomplete long-term follow-up. We conclude that careful attention to the operative indications is necessary for patients with multiple lesions, particularly lesions such as early squamous cell carcinomas.

Adenocarcinoma↗
PubMed1989

Tissue norepinephrine depletion as a mechanism for cysteamine inhibition of colon carcinogenesis induced by azoxymethane in Wistar rats.

The effects of cysteamine (2-aminoethanethiol hydrochloride) on the incidence, number and histology of colon tumors induced by azoxymethane (AOM), and on the norepinephrine concentration in the colon wall tissue and the labelling indices of colon mucosa and colon cancers were investigated in Wistar rats. Rats received 10 weekly injections of 7.4 mg/kg body weight of AOM and alternate-day subcutaneous injections of 25 mg/kg of cysteamine in 0.9% NaCl solution until the end of the experiment. At week 40, prolonged administration of cysteamine significantly reduced the incidence and number of colon tumors. Histologically, the adenocarcinomas that did develop in rats treated with cysteamine exhibited high mucin-producing activity. Administration of cysteamine caused significant decreases in the norepinephrine concentration in colon tissue and in the labelling indices of colon mucosa and cancers. Our findings indicate that cysteamine inhibits the development of colon tumors. This action may be related to its effect in decreasing norepinephrine concentration in the colon wall tissues and subsequently in decreasing proliferation of colon cancer cells.

Adenocarcinoma↗
PubMed1989

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

The effects of somatostatin on the incidence, number, and histological type of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine were investigated in Wistar rats. Rats received alternate-day s.c. injections of 100 or 200 micrograms/kg body weight of somatostatin in depot form after 25 weeks of p.o. treatment with the carcinogen. Prolonged administration of somatostatin at both dosages significantly increased the incidence and number of gastric cancers of the glandular stomach in Week 52. Furthermore, somatostatin at 200 micrograms/kg caused a significant increase in the incidence of gastric cancers penetrating the muscle layer or deeper layers. However, somatostatin at both dosages did not influence their histological appearance. Histologically, somatostatin at both dosages significantly elevated the labeling index of gastric cancers but not of the antral mucosa and significantly reduced the gastrin levels. These findings indicate that somatostatin enhances gastric carcinogenesis after N-methyl-N'-nitro-N-nitrosoguanidine treatment and that this effect may be related to its effect in increasing proliferation of gastric cancers and decreasing serum gastrin level.

Animals↗
PubMed1989

Development of postoperative intrathoracic chemo-thermotherapy for lung cancer with objective of improving local cure.

From April 1985 through March 1988, 24 lung cancer patients with carcinomatous pleuritis were treated with a new combined treatment modality consisting of pulmonary resection and postoperative intrathoracic chemo-thermotherapy (PICT). They consisted of 15 male patients and nine female patients. A majority of the patients (79%%) had adenocarcinoma. The PICT was started 10 to 14 days after the operation. Immediately after a bolus intrathoracic injection of cisplatin (CDDP) 50-100 mg, thermotherapy was carried out using 13.56-MHz or 8.00-MHz radiofrequency waves for 60 minutes. The peripleural temperature was precisely monitored in 20 patients. The temperature was successfully maintained above 42 degrees C for 40 minutes in each of two or three treatment courses in 13 patients, with no complications. However, in the other seven patients the therapy resulted in incomplete treatment because of development of a side effect. Cytologic examination of the pleural effusion, which was performed after the completion of PICT, gave a negative result in 16 of 20 patients examined. The median follow-up period was 16 months. Local relapse was recognized in only three cases who received incomplete treatment or in whom no temperature measurement was performed. The overall survival of the treated patients (n = 24) was significantly prolonged in comparison with a historical control group treated by surgery only (n = 17) or exploratory thoracotomy (n = 11). Of those 17 patients treated by surgery only, ten patients (59%) died of local relapse. These results suggest that this new treatment modality consisting of pulmonary resection and PICT is useful for the treatment of lung cancer patients with carcinomatous pleuritis, especially in the light of improved local control.

Adenocarcinoma↗
PubMed1989

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

The effects of bombesin on the incidence, number, histological type, and depth of involvement of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in male Wistar rats. Rats received alternate-day s.c. administration of 20 or 40 micrograms/kg body weight of bombesin in depot form after p.o. treatment with the carcinogen for 25 weeks. Prolonged administration of bombesin at 40 micrograms/kg led to a significant increase in the incidence and number per rat of gastric cancers of the glandular stomach at Week 52. In rats that had received alternate-day injections of 20 micrograms/kg of bombesin, the number of gastric cancers per rat, but not the incidence of cancer, was significantly more than in untreated rats. However, bombesin at both dosages did not affect the histological appearance of the lesions or their depth of involvement. At Weeks 30 and 52, norepinephrine concentrations in the fundic and antral portion of the gastric walls and labeling indices in the antral and fundic mucosae were significantly higher in rats treated with bombesin at both dosages than in untreated rats. These findings indicate that bombesin enhances gastric carcinogenesis after administration of N-methyl-N'-nitro-N-nitrosoguanidine is stopped and that this effect may be related to its effects in increasing tissue norepinephrine concentrations in the stomach wall and increasing cell proliferation in the gastric mucosa.

Animals↗
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↗