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Biomedical subjects

M Tatsuta

Publications and source records attributed to M Tatsuta.

At least 73 records · Page 4Linked to original sources

Inhibition by galanin of experimental carcinogenesis induced by azaserine in rat pancreas.

The effects of galanin on pancreatic carcinogenesis induced by azaserine and on the norepinephrine concentration in the pancreas were investigated in male Wistar rats. Rats were given weekly injections of 10 mg/kg body weight of azaserine for 25 weeks and 8 microg/kg body weight of galanin in depot form every other day for 62 weeks. Azaserine-induced pancreatic lesions were examined with hematoxylin and eosin and histochemical techniques. In week 62, quantitative histological examination showed that prolonged administration of galanin significantly reduced the number and size (as percent of parenchyma) of adenosine triphosphatase-positive pancreatic lesions, which are correlated closely with the ultimate development of pancreatic cancer. The number of pancreatic adenocarcinomas in rats treated with galanin was significantly less than in controls. Galanin also significantly decreased the bromodeoxyuridine-labeling index of azaserine-induced pancreatic lesions and the norepinephrine concentration in the pancreas. Our findings indicate that galanin inhibits pancreatic carcinogenesis and that such inhibition may be related to the suppression of sympathetic nervous system activity and subsequently to the inhibition of cell proliferation in neoplastic lesions of the pancreas.

Animals↗

Promotion by the alpha-adrenoceptor agonist phenylephrine, but not by the beta-adrenoceptor agonist isoproterenol, of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of prolonged administration of the alpha-adrenoceptor agonist phenylephrine and the beta-adrenoceptor agonist isoproterenol on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine and on the labeling index of gastric mucosa were compared in Wistar rats. Rats received subcutaneous injections of 3 or 6 mg/kg body weight of phenylephrine or 0.1 or 0.2 mg/kg body weight of isoproterenol every other day after 25 weeks of oral treatment with the carcinogen. Long-term administration of phenylephrine at a high dose, but not at a low dose, significantly increased the incidence of gastric cancers and the labeling index of antral epithelial cells at the end of the experiment in week 52. However, administration of isoproterenol at either dosage had no significant effect on the incidence of gastric cancers and the labeling index of antral epithelial cells. These findings indicate that increased activity of the sympathetic nervous system enhances gastric carcinogenesis through alpha-adrenoceptors.

Adrenergic alpha-Agonists↗

Effectiveness of premedication with pronase for improving visibility during gastroendoscopy: a randomized controlled trial.

BACKGROUND: Minute early gastric cancers can be removed with endoscopic mucosal resection techniques. However, early detection of these minute cancers with endoscopy is still difficult. For this purpose, use of a dye is helpful. To increase visibility further, gastric mucus should be removed before endoscopic examination. In this study, the effectiveness of premedication with pronase for improving visibility during gastroendoscopy was investigated. METHODS: From January through July 1996, outpatients scheduled for gastroendoscopy were randomly assigned to oral premedication with the antifoam agent dimethylpolysiloxane alone (n=34), with dimethylpolysiloxane plus sodium bicarbonate (n=32), or with dimethylpolysiloxane, sodium bicarbonate, and pronase (n=34). All were given about 10 minutes before the start of endoscopy. After inserting the endoscope, the endoscopist gave visibility scores at conventional endoscopy and after methylene blue spraying. RESULTS: Premedication with pronase significantly improved visibility before and after methylene blue spraying as compared with the two other groups pretreated without pronase. Pronase also significantly shortened the times for chromoendoscopic examination. Pronase had no significant effect on the culture of Helicobacter pylori. CONCLUSION: Premedication with pronase improved endoscopic visualization during conventional endoscopy and chromoendoscopy. Its routine use at gastroendoscopy is therefore recommended.

Adult↗

Myoepithelioma of the lung: report of two cases and review of the literature.

Myoepithelial tumors occur mainly in the salivary glands, the sweat glands or the breast, but uncommonly in the lung. Herein, we describe two cases of myoepithelioma of the lung. Both patients were 58-year-old men, in whom the tumors were located in the right-upper bronchus and in the left-upper bronchus, respectively, with endobronchial growth pattern. Surgery was performed, but metastasis occurred into the forearm and hip muscles in the former case, and into the liver in the latter. Histologically, the tumor in the former was a spindle-plasmacytoid type, and that in the latter was a plasmacytoid type in part with squamous differentiation. Based on histochemical, immunohistochemical and ultrastructural analyses, both were compatible with myoepithelioma. The clinicopathological uniqueness of this neoplasm is discussed, together with a review of reports of this disease in the literature.

Fatal Outcome↗

Inhibition of experimental gastric carcinogenesis, induced by N-methyl-N'-nitro-N-nitrosoguanidine in rats, by sodium nitroprusside, a nitric oxide generator.

The effects of prolonged administration of sodium nitroprusside (SNP), a generator of nitric oxide (NO), on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and the labelling index of the gastric mucosa were investigated in male Wistar rats. The rats received intra-peritoneal injections of 2 or 4 mg/kg body weight of SNP every other day after 25 weeks' oral treatment with the carcinogen. Prolonged administration of SNP at 4 mg/kg body weight, but not at 2 mg/kg body weight, significantly decreased the incidence of gastric cancers in experimental week 52. However, it did not affect the histological types or depths of involvement of gastric cancers. SNP at 4 mg/kg body weight, but not at 2 mg/kg body weight, also significantly decreased the bromodeoxyuridine labelling index of the antral epithelial cells. These findings indicate that SNP inhibits gastric carcinogenesis and suggest that this effect may be related to the suppression of proliferation of the antral epithelial cells.

Animals↗

Low prevalence of Helicobacter pylori infection in patients with hamartomatous fundic polyps.

Helicobacter pylori infection of the gastric mucosal surface was investigated in patients with hamartomatous fundic polyps or hyperplastic polyps and in patients without endoscopic evidence of disease (healthy subjects). Presence of H. pylori infection was determined by culture, histologic examination, and the endoscopic phenol red test. Adherence of H. pylori was evaluated with scanning electron microscopic examination of antral biopsy specimens. Both prevalence of H. pylori infection (P < 0.001) and H. pylori adherence (P < 0.05) were less in patients with hamartomatous fundic polyps than in healthy subjects and patients with hyperplastic polyps. However, the percentages of plasma cells in gastric mucosa that contained IgA and of gastric epithelial cells that expressed Lewis b did not differ significantly among the three groups. These findings suggest that defense mechanisms against the attachment of H. pylori other than IgA or Lewis b antigen are present in patients with hamartomarous fundic polyps.

Biopsy↗

Inhibition by transforming growth factor (34-43)-alpha, a TGF-alpha antagonist, of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effect of prolonged administration of transforming growth factor (34-43)-alpha, an antagonist of TGF-alpha, on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and on the labelling and apoptotic indices and TGF-alpha immunoreactivity of gastric mucosa and gastric cancers was examined in Wistar rats. The rats received intraperitoneal injections of 10 or 20 microg kg(-1) body weight of TGF(34-43)-alpha every other day after oral treatment with MNNG for 25 weeks. Long-term administration of TGF(34-43)-alpha at both doses significantly reduced the incidence of gastric cancers at the end of the experiment in week 52. However, TGF(34-43)-alpha had no significant effect on the number, histological type or depth of involvement of gastric cancers. Administration of TGF(34-43)-alpha also significantly decreased the bromodeoxyuridine labelling index and TGF-alpha immunoreactivity, and significantly increased the apoptotic index of antral mucosa and gastric cancers. These findings indicate that TGF(34-43)-alpha inhibits gastric carcinogenesis, and that its effects are mediated through decreased cell proliferation and TGF-alpha immunoreactivity and increased apoptosis induction in the gastric cancers.

Adenocarcinoma↗

Suppression by pravastatin, an inhibitor of p21ras isoprenylation, of hepatocarcinogenesis induced by N-nitrosomorpholine in Sprague-Dawley rats.

The effect of pravastatin, an inhibitor of p21ras isoprenylation, on hepatocarcinogenesis induced by N-nitrosomorpholine and on p21ras isoprenylation were investigated in male Sprague-Dawley rats. Rats received i.p. injections of pravastatin (10 and 20 mg kg(-1) body weight) every other day and, from the beginning of the experiment, were given drinking water containing N-nitrosomorpholine for 8 weeks. Visible white nodules and hepatic lesions staining positively for gamma-glutamyl transpeptidase or glutathione-S-transferase, placental type, were examined macroscopically or histochemically. In week 15, pravastatin at both dosages significantly reduced the incidence, number and volume of visible white nodules. Quantitative histological analysis also showed that prolonged administration of pravastatin at both dosages resulted in significant reductions in the number and percentage area of hepatic lesions positive for gamma-glutamyl transpeptidase and glutathione-S-transferase, placental type. Administration of pravastatin also significantly decreased the amount of membrane-associated p21ras in the tumour and the labelling index of neoplastic nodules and increased the apoptoic indices of neoplastic nodules. These findings indicate that pravastatin suppresses hepatocarcinogenesis and suggest that this effect might be related to pravastatin's inhibition of p21ras isoprenylation and its subsequent inhibition of cell proliferation and induction of apoptosis in neoplastic lesions.

Animals↗

Prevention of gastric ulcer recurrence with tetraprenylacetone.

BACKGROUND: The role of cytoprotective agents in the treatment of ulcers remains unclear. In the present study we investigated the effect of tetraprenylacetone (TAP), a cytoprotective agent, on healing and recurrence of gastric ulcers infected with Helicobacter pylori and on the mucosal microvascular architecture of healed gastric ulcers. PATIENTS: Ninety-five gastric ulcer patients with H. pylori infection were studied. METHODS: Gastric ulcer patients with H. pylori infection received 20 mg omeprazole (44 patients) or 20 mg omeprazole and 150 mg TAP (46 patients) in random fashion. Ulcer healing was assessed with endoscopy 12 weeks after the start of treatment. The patients with healed ulcer were followed up for another 12 months without further therapy. During endoscopic examination at week 12, biopsy specimens were obtained from healed gastric ulcers, and the gastric mucosal microvascular architecture of the biopsy specimens was observed by means of the alkaline phosphatase staining method. RESULTS: The rate of ulcer healing at week 12 was similar in patients treated with omeprazole with and without TAP. However, at or within 12 months of the start of follow-up observation, ulcers recurred significantly less frequently in patients treated with both omeprazole and TAP than in those treated with omeprazole alone. Alkaline phosphatase staining methods showed that the mucosal microvascular architecture improved significantly more frequently in healed gastric ulcers that had been treated with both omeprazole and TAP than in those treated with omeprazole alone. CONCLUSIONS: Treatment with TAP plus omeprazole significantly decreases ulcer recurrence through TAP's improved mucosal restoration.

Adult↗

Helicobacter pylori infection in patients with early gastric cancer by the endoscopic phenol red test.

BACKGROUND: An endoscopic procedure that uses a pH indicator called phenol red to assess Helicobacter pylori infected gastric mucosa has recently been developed. This test makes it possible to take biopsy specimens from H pylori infected areas. AIM: This test was applied to patients with early gastric cancers to clarify the role of H pylori in gastric carcinogenesis. SUBJECTS: Sixty five patients with early gastric cancer (50 with differentiated adenocarcinoma and 15 with undifferentiated adenocarcinoma). METHODS: Patients with early gastric cancer underwent the endoscopic phenol red test before their operation. In this test, areas infected with H pylori can be observed as "coloured" areas where phenol red was turned from yellow to red. RESULTS: H pylori infection was significantly (p < 0.001) more frequent in patients with differentiated adenocarcinomas than in those with undifferentiated adenocarcinomas. Differentiated adenocarcinomas were usually located in areas of mucosa infected with H pylori, but undifferentiated adenocarcinomas were frequently located in non-infected areas. CONCLUSION: H pylori may be a strong risk factor for differentiated early gastric cancer.

Adenocarcinoma↗

[Neoadjuvant intraarterial chemotherapy for ten cases of inflammatory breast cancer by Seldinger's methods].

The conventional methods (CM) of intraarterial (IA) chemotherapy for inflammatory breast cancer were catheterizations from superior epigastric and brachial artery under general anesthesia. Since 1997, we selected the Seldinger's methods (SM) for ten cases of the disease to control local effects and simplify the technique. Complications of the SM were slight, and side effects were equal to those with CM. The postoperative pathological findings of the SM showed the direct effects of chemotherapy to tumor cells (degenerative and necrotic changes) as compared with the embolism-like effects of CM. But the overall histological effects of chemotherapy by SM were almost equal to those for CM. The strong points of the SM were as follows: 1) More selective IA chemotherapy is available, 2) one can find the passage of the aim vessels and no trouble related to catheter, 3) general anesthesia is not necessary, and the techniques are simple, 4) the wounds are not remarkable. The disadvantages are as follows: 1) Patients must rest the day of IA chemotherapy, 2) in 20% of the procedures, one can not search the vessels, and 3) in 4 cases complications of stiffness of Mj or Mn pectral muscles were found. In future, we expect more effective results by dose escalation or combination chemotherapy.

Adenocarcinoma↗

[Microwave tissue coagulation therapy with mini-laparotomy for hepatocellular carcinoma].

Recently microwave tissue coagulation therapy (MCT) has been established as a therapeutic procedure for hepatocellular carcinoma (HCC). The route of approach to penetrate the tumor is two-fold: By the percutaneous route (PMCT) or by conventional laparotomy. PMCT has the advantage of less invasive therapy, however, it is not applicable to a tumor that cannot be detected by ultrasonography. Therefore, we tried MCT with mini-laparotomy. The patient was a 57-year old man with HCC located in the S6 subsegment. The operation was performed at the semi-right side up position, and laparotomy was done by skin incision of 12 cm in the right hypochondral area. MCT was performed about 30 times, with an output of 60 watts for 45 seconds at a time. Abdominal CT image showed a low-density area of 7 x 4 cm on the 18th postoperative day. Slight damage to the liver and no obvious complications were observed. We concluded that a much wider range-coagulation than PMCT was able to be obtained by MCT with mini-laparotomy, and postoperative quality of life was better than MCT with conventional laparotomy.

Carcinoma, Hepatocellular↗

Ornithine decarboxylase inhibitor lessens the rat gastric carcinogenesis enhancement caused by tyrosine methyl ester.

The effects of combined administration of a catecholamine precursor, tyrosine methyl ester (TME), and an ornithine decarboxylase (ODC) inhibitor, 1,3-diaminopropane (DAP), on the incidence of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), the norepinephrine (NE) concentration and ODC activity of the gastric wall, and the labeling index of the gastric mucosa were investigated in inbred Wistar rats. Rats received s.c. injections of TME, 512 mg/kg body weight, every other day and drinking water with or without 2.5 g/l of DAP after 25 weeks of oral administration of MNNG. At week 52, administration of TME resulted in significant increases in the incidence of gastric cancers, in the NE concentration and the ODC activity of the antral portion of the gastric wall, and in the labeling index of antral epithelial cells. Administration of both TME and DAP significantly reduced the enhancements by TME of gastric carcinogenesis, NE concentration and ODC activity of the antral wall, and the labeling index of the antral mucosa. Our results suggest that ODC inhibition lessens enhancement by TME of gastric carcinogenesis and that the enhancement by TME of gastric carcinogenesis is mediated in part by polyamine biosynthesis.

Animals↗

Ha-ras mutations in N-nitrosomorpholine-induced lesions and inhibition of hepatocarcinogenesis by antisense sequences in rat liver.

To evaluate the application of Ha-ras mRNA antisense oligonucleotide therapy for liver tumors, we examined the frequency and types of mutation in codon 61 of the Ha-ras oncogene in preneoplastic lesions and hepatocellular carcinomas induced by N-nitrosomorpholine (NNM) in rats. Thirty-seven percent of preneoplastic lesions and 50% of hepatocellular carcinomas contained mutations, mostly CAA-CTA and CAA-AAA transversions. We also investigated the effects on NNM-induced lesions of an antisense oligonucleotide directed against a point mutation (CAA-CTA) in codon 61 of Ha-ras mRNA. In this experiment, Sprague-Dawley rats were given free access to water containing NNM for 8 weeks and received twice-weekly i.p. injections of a mutated Ha-ras antisense oligonucleotide with a 5' phosphorothioate linkage or a sense oligonucleotide in oligonucleotide-liposome complexes. At week 16, rats that had received the mutated Ha-ras antisense oligonucleotides had significantly fewer and smaller preneoplastic lesions positive for glutathione-S-transferase, placental type, and had smaller hepatocellular carcinomas than rats that had received the sense oligonucleotide. Mean cellular fluorescence in the liver was found to increase with higher doses of mutated, fluorescein-isothiocyanate-labeled antisense or sense oligonucleotides. Moreover, mutated Ha-ras antisense oligonucleotide decreased the expression of mutated Ha-ras mRNA (CAA-CTA). Our findings indicate that mutated Ha-ras antisense oligonucleotide significantly inhibits hepatocarcinogenesis in rats and could be an effective therapy against liver tumors.

Animals↗

d-Limonene inhibits N-nitrosobis(2-oxopropyl)amine induced hamster pancreatic carcinogenesis.

The effect of d-limonene on pancreatic carcinogenesis induced by N-nitrosobis(2-oxopropyl)amine (BOP) was investigated in Syrian golden hamsters. During and after 5 weekly injections of BOP, each hamster was fed diet containing d-limonene. In week 26, quantitative histological analysis showed that prolonged treatment with d-limonene significantly reduced the number of pancreatic carcinomas. Administration of d-limonene did not cause a significant increase in the apoptotic index, but caused a significant decrease in the BrdU labeling index of carcinoma. These findings indicate that d-limonene inhibits the development of pancreatic carcinoma not by enhancing tumor cell loss through apoptosis, but rather by inhibiting cell proliferation.

Animals↗

Reduction in NaCl-enhanced gastric carcinogenesis in rats fed a high-protein diet.

The effect of a purified, high protein diet on enhanced gastric carcinogenesis induced by oral administration of NaCl was investigated in Wistar rats. Rats were fed on a purified diet with an equalized caloric content, containing 8% NaCl and 25% casein (normal protein diet), or 50% casein (high protein diet) after oral treatment with N-methyl-N'-nitro-N-nitrosoguanidine for 25 weeks. In week 52, oral administration of NaCl had significantly increased the incidence and size of gastric cancer in rats fed a normal protein diet. However, NaCl had no significant effect on gastric carcinogenesis in rats fed a high protein diet. Oral administration of NaCl also caused a significant increase in tissue norepinephrine concentrations in the antral portion of the gastric wall, and increased the labeling indices of the antral epithelial cells of rats fed on a normal protein diet. However, in rats fed a high protein diet, administration of NaCl had no significant influence on these two parameters. These findings indicate that a high protein diet attenuates enhanced gastric carcinogenesis induced by the administration of NaCl, and that this effect may be related to its ability to decrease norepinephrine concentrations in the gastric wall, which subsequently decreases the proliferation of antral epithelial cells.

Animals↗

Enhancement by ethyl alcohol of experimental hepatocarcinogenesis induced by N-nitrosomorpholine.

The effects of ethyl alcohol (EtOH) during or after treatment with N-nitrosomorpholine (NNM) on hepatocarcinogenesis, ornithine decarboxylase (ODC) activity and the labeling index of the liver were investigated in male Sprague-Dawley rats. Rats were given drinking water containing NNM for 8 weeks and received i.p. injections of 1 g EtOH/kg body weight every other day during or after treatment with NNM. Pre-neoplastic and neoplastic lesions staining positively for glutathione-S-transferase, placental type (GST-P), were examined immunohistochemically. At the end of experiment at week 16, administration of EtOH after NNM treatment had no significant effect on the number and size of GST-P-positive hepatic lesions, whereas administration of EtOH during NNM treatment significantly increased the number and percentage area but not the mean area of GST-P-positive hepatic lesions. EtOH caused significant increases in the ODC activity of the liver and in the labeling indices of enzyme-altered lesions and the adjacent hepatocytes after the cessation of EtOH administration but not during EtOH treatment. Our findings indicate that EtOH enhances hepatocarcinogenesis and suggest that this effect may be closely related to the increases in ODC activity and cell proliferation in enzyme-altered lesions and the adjacent liver after EtOH treatment.

Animals↗

Diagnosis of carcinoma in situ of the pancreas by peroral pancreatoscopy and pancreatoscopic cytology.

BACKGROUND: Most pancreatic carcinomas are unresectable at the time of diagnosis, but recently the diagnosis of carcinoma in situ of the pancreas has become possible. This diagnosis can be made by the detection of cancer cells in pancreatic juice and the radiographically demonstrated lack of a mass lesion. It has greatly improved the effectiveness of surgery. Carcinoma in situ remains within the pancreatic ductal epithelium and has not yet invaded the parenchyma. However, it has often been difficult to locate carcinoma in situ by conventional diagnostic methods, such as ultrasonography, endoscopic ultrasonography, computed tomography, and endoscopic retrograde pancreatography. METHODS: Peroral pancreatoscopy and a new method of cytodiagnosis, pancreatoscopic cytology, were used to analyze 11 patients with carcinoma in situ of the pancreas, 10 with disease in the main duct of the pancreas and 1 with disease in the branch ducts. The results of pancreatoscopic cytology were compared with those of conventional pancreatic juice cytology. RESULTS: Under peroral pancreatoscopy, carcinoma in situ of the pancreas in the main duct appeared as papillary mucosa, irregular mucosa, or nodular mucosa. Using pancreatoscopic cytology, cancer cells were obtained from all the lesions, allowing a more thorough analysis than pancreatic juice cytology. CONCLUSIONS: Peroral pancreatoscopy and pancreatoscopic cytology are useful for locating and diagnosing carcinoma in situ of the pancreas.

Aged↗