Biomedical subjects
M Hirose
Publications and source records attributed to M Hirose.
[Chronological effect of histamine H2 receptor antagonist ranitidine as serum gastrin response in gastric ulcer patients].
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[Statistical analysis of the healing rate in peptic ulcer].
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[Two cases of pulmonary artery aneurysm associated with patent ductus arteriosus].
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[Effects of concomitant drugs on the blood concentration of a histamine H2 antagonist (1st report). Oral administration of ranitidine together with high doses of neutralizing antacid and sucralfate].
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[Effects of concomitant drugs on the blood concentration of a histamine H2 antagonist (the 2nd report)--concomitant or time lag oral administration of ranitidine and sucralfate].
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[Combination chemotherapy with MOPP and intrathecal methotrexate in children with brain tumors].
Five children with brain tumors, who had had no prior chemotherapy, were treated with combination chemotherapy including nitrogen mustard, vincristine sulfate, procarbazine, prednisolone (MOPP) and intrathecal methotrexate. Four had progressive tumor or metastatic deposits, (one medulloblastoma, one malignant choroid plexus papilloma, and two were not explored) but responded to chemotherapy. One child with medulloblastoma underwent resection, which was considered to be macroscopically radical, and demonstrated objective improvement of neurological findings after chemotherapy. Toxicities were not severe enough to require termination of the chemotherapy.
[A case of traumatic tricuspid regurgitation].
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Promoting effects of phenobarbital and 3'-methyl-4-dimethylaminoazobenzene on the appearance of gamma-glutamyltranspeptidase positive foci in rat liver pretreated with varying doses of diethylnitrosamine.
The promotion potential of phenobarbital (PB) and 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) on liver carcinogenesis after initiation with various doses of diethylnitrosamine (DEN) was assessed using an in vivo short term system. Male F344 rats were pretreated with a single intraperitoneal injection of varying doses of DEN (0, 6, 12, 25, 50, 100 or 200 mg/kg body wt), and 2 weeks later were treated with 0.05% PB or 0.06% 3'-Me-DAB for 6 weeks. All animals were subjected to partial hepatectomy 3 weeks after the DEN treatment. Quantitation of gamma-glutamyltranspeptidase-positive (gamma-GT+) foci revealed a DEN dose-dependent response. Magnitude of promotion by PB and more pronounced by 3'-Me-DAB was, in contrast, strongest at the lower doses of DEN. The results suggest that quantitative differences with regard to initiation level may exist, influencing the promotability of initiated cells.
Modification by five antioxidants of 1,2-dimethylhydrazine-initiated colon carcinogenesis in F344 rats.
The effects of antioxidants given in the post initiation phase of colon tumor development were investigated in male F344 rats treated with 1,2-dimethylhydrazine (DMH). Animals (20/group) were given s.c. injections of DMH at a dose of 20 mg/kg once a week for four consecutive weeks. One week after the last injection, rats were fed diet containing 5% sodium L-ascorbate (SA), 0.5% butylated hydroxyanisole (BHA), 0.8% ethoxyquin (EQ), 1.0% propyl gallate or 0.5% butylated hydroxytoluene (BHT) for 36 weeks. A control group was fed the basal diet not containing antioxidants. The experiment was terminated 40 weeks after the first injection of DMH and all intestinal tumors were confirmed histologically. SA significantly increased the incidence of adenomas and the number of tumors per rat of the colon (especially of the distal colon). Although EQ and BHT did not affect the number of rats with colon tumors, the number of tumors per rat occurring in the distal colon was significantly increased by EQ while being decreased by BHT. No modification of tumor development was observed with BHA or PG. Thus, modification of tumor development by SA, EQ and BHT was apparent, mainly in the distal colon.
Correlation between nuclear histone acetylation and casein messenger RNA induction in the mammary gland.
Sodium butyrate prevented the accumulation of casein mRNA induced by the combined action of prolactin and glucocorticoid in the presence of insulin in the cultured mammary gland. This inhibition was reversible and dose-dependent. In addition to the inhibition of the mRNA induction, both nuclear histone acetylase and deacetylase activities were inhibited by the incubation of the glands with butyrate, whereas these enzyme activities were stimulated by glucocorticoid and prolactin, or by glucocorticoid alone, in the presence of insulin. These data strongly suggest that the increased metabolism of histone acetyl groups is involved in the hormone-mediated casein mRNA induction and that glucocorticoid plays a preferential role on this increased metabolism.
[Portosystemic A-V fistula and portal hypertension associated with islet-cell tumor of the pancreas].
A 50-year-old woman was admitted on Feb. 25, 1983, complaining of hematemesis and melena. Endoscopic examination revealed the rupture of the esophageal varices. At first she was treated with pressure hemostasis using a S-B tube, but it was failed. Then she underwent esophageal transection under emergency thoracotomy. After the operation, she developed ascites and watery diarrhea, though there was no episode of hematemesis and melena. A bruit was audible at the epigastric region. Abdominal angiograms demonstrated a fist-sized portosystemic A-V fistula (PAVF) locating at the pancreas head, and suggested concomitant existence of portal hypertension. On May 16, 1983, laparotomy was carried out in order to reduce portal pressure, but it was not successful. She died 3 weeks after the second operation. Autopsy and pathological findings revealed that PAVF associated with a hen-egg-sized islet-cell tumor of the pancreas head. Etiology and clinical features of this rare entity may be characterized by the nature of the islet-cell tumor having rich and rapidly growing vascular supply.
[Effect of saliva on fluorapatite formation on tooth surfaces using a silica gel method].
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Significance of L-ascorbic acid and urinary electrolytes in promotion of rat bladder carcinogenesis.
The present studies report on the significance of L-ascorbic acid (AA) and urinary electrolytes for promotion of rat urinary bladder carcinogenesis. Male F344 rats were given an oral administration of 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) as an initiator for 4 weeks, and were then subjected to treatment with dietary supplements of test chemicals for 32 weeks. Administration of 5% sodium L-ascorbate (SA), the sodium ion form of AA significantly promoted urinary bladder carcinogenesis, whereas administration of 5% AA did not. The urine of rats given SA but not AA was characterized by an apparent elevation of pH, an increase of sodium ion concentration, and increases in the urinary content of total AA and its metabolite, dehydroascorbic acid. Administration of 3% NaHCO3, which induced elevation of pH and increase of sodium ion concentration in the urine, promoted BBN bladder carcinogenesis. When rats were given 5% AA plus 3% NaHCO3, AA enhanced the promoting activity of NaHCO3. Lowering of pH by 1% NH4Cl clearly reduced the promoting activity of 5% SA when these two compounds were given concurrently. Treatment with 5% AA plus 3% K2CO3 promoted BBN bladder carcinogenesis in rats, whereas addition of 5% CaCO3 or 5% MgCO3 to AA did not. These results strongly indicate the important role of urinary sodium or potassium ion concentration and pH in modulating urinary bladder carcinogenesis by AA.
[Ultrasonic patterns of the gallbladder in patients with acute liver damage].
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Short-term screening of promoters of bladder carcinogenesis in N-butyl-N-(4-hydroxybutyl)nitrosamine-initiated, unilaterally ureter-ligated rats.
The modifying effects of 17 environmental chemicals on the development of lesions in the urinary bladder of rats with unilateral ureteric ligation were investigated. Lesions were initiated by treatment of the animals with 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) for 2 weeks, and then test chemicals were given for 22 weeks. The lesions of the urinary bladder found were preneoplastic papillary or nodular hyperplasias (PN hyperplasias) and papillomas. Additions of sodium saccharin (5%), sodium o-phenylphenate (2%), butylated hydroxyanisole (2%), and sodium L-ascorbate (5%) to the diet had significant promoting effects on the incidences and numbers of PN hyperplasias and papillomas per 10 cm of basement membrane of the urinary bladder in this system. Sodium erythorbate (5%), ethoxyquin (0.8%) and carbazole (0.6%) significantly increased the incidence of PN hyperplasias. N-Nitrosopyrrolidine (0.02%) did not affect the incidence or number of PN hyperplasias but increased those of papillomas. Sodium o-phenylphenate also induced PN hyperplasias in rats without BBN-initiation. Ascorbic acid, ascorbic stearate, three dihydroxyphenols, methylhydroquinone, pyrogallol, quinoline, and uric acid did not show promoting activity in this test system. Thus, 8 of 17 chemicals tested had various promoting effects on urinary bladder carcinogenesis. These results show that this test system of BBN-initiated, unilaterally ureter-ligated rats should be useful for the detection of new bladder carcinogens and promoters.
[24 cases of May-Hegglin anomaly in one family].
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Dose-response study of urinary bladder carcinogenesis in rats by N-butyl-N-(4-hydroxybutyl)nitrosamine.
A dose-response study was carried out in male F344 rats with a specific urinary bladder carcinogen, N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN), which was administered as a solution in drinking water for up to 112 weeks. BBN was given in four different concentrations, 50, 10, 5, and 1 ppm, to groups of 30 rats. The highest dose induced urinary bladder cancer in all rats treated by week 91, decreasing yields being associated with lower dose levels: an incidence of 76.7% was observed with 10 ppm, followed by 20.0% with 5 ppm. The lowest dose (1 ppm) only induced two cases of papilloma (6.9%).