Search PubMed⌕ Search

Biomedical subjects

M Hirose

Publications and source records attributed to M Hirose.

At least 523 records · Page 29Linked to original sources
PubMed1989

Antagonistic effect of diethylmaleate on the promotion of forestomach carcinogenesis by butylated hydroxyanisole (BHA) in rats pretreated with N-methyl-N'-nitro-N-nitrosoguanidine.

The effects of diethylmaleate (DEM), previously demonstrated to inhibit butylated hydroxyanisole (BHA)-induced forestomach hyperplasia, on BHA promotion of forestomach carcinogenesis in rats pretreated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were examined. Groups of male 6-week-old F344 animals were given a single i.g. administration of 150 mg/kg body weight MNNG and starting 1 week later administered powdered diet containing 1% BHA plus 0.2% DEM, 1% BHA, 0.2% DEM or basal diet alone for 51 weeks. Further groups of rats were treated with 1% BHA plus 0.2% DEM, 1% BHA, 0.2% DEM or basal diet alone without MNNG pretreatment. Histopathological assessment of lesions at week 52 revealed enhancement of MNNG-initiated papilloma (100 versus 50%) and squamous cell carcinoma (100 versus 0%) development by BHA as compared to controls. Additional treatment with DEM, however, significantly reduced the relative incidences of carcinoma in situ (0 versus 35.7%) and squamous cell carcinoma (35.7 versus 100%), as well as BHA-induced forestomach hyperplasia with or without prior MNNG treatment. The results thus clearly demonstrate that DEM acts as a potent antagonist to BHA-promotion of rat forestomach carcinogenesis.

Animals↗
PubMed1989

Modifying effects of simultaneous treatment with butylated hydroxyanisole (BHA) on rat tumor induction by 3,2'-dimethyl-4-aminobiphenyl, 2,2'-dihydroxy-di-n-propylnitrosamine and N-methylnitrosourea.

The modifying effects of concurrent treatment with high or low doses of butylated hydroxyanisole (BHA) on wide-spectrum carcinogen-induced carcinogenesis were studied in male F344 rats. Groups of 20 animals were treated with 2 or 0.04% BHA for 24 weeks. Starting 2 weeks after the commencement of BHA treatment, they were given s.c. injection of 50 mg/kg body weight 3,2'-dimethyl-4-aminobiphenyl (DMAB) once a week, i.g. administrations of 200 mg/kg body weight 2,2'-dihydroxy-di-n-propylnitrosamine (DHPN) once every 2 weeks, or i.p. injection of 15 mg/kg body weight N-methylnitrosourea (MNU) once every 2 weeks for 22 weeks. Further groups of rats were treated with DMAB, DHPN, MNU, or 2 or 0.04% BHA alone. All surviving animals were killed 24 weeks after the beginning of the experiment and the target organs examined histopathologically. The BHA treatment dose-dependently decreased the incidence of DMAB-induced liver preneoplastic lesions but was associated with significant tumor induction in the forestomach (papillomas, 40%, P less than 0.01) and urinary bladder (papillomas, 53%, P less than 0.001; carcinomas, 80%, P less than 0.001), where no lesions were observed in the group given only DMAB. Concurrent administration of 2% BHA also significantly inhibited the development of alveolar hyperplasia (P less than 0.001) of the lung in DHPN-treated animals, while enhancing induction of forestomach papillomas (P less than 0.05) and simple hyperplasia in the urinary bladder. Neither MNU nor 2% BHA alone induced forestomach carcinoma or papillary or nodular hyperplasia (PN hyperplasia) in the urinary bladder. However, these lesions were observed in 100% (P less than 0.001) and 55% (P less than 0.001) of animals respectively, receiving the two compounds in combination. These results demonstrated that concurrent treatment with BHA not only inhibits but can also strongly enhance carcinogenesis depending on the organ, irrespective of whether the carcinogens act directly or require metabolism. The finding that BHA potently modified carcinogenesis at 0.04% in diet, 1/50 of the carcinogenic dose, suggests that actual dietary levels close to the human situation might play a significant role in tumor development in man.

Aminobiphenyl Compounds↗
PubMed1989

Effects of anion binding on the conformations of the two domains of ovotransferrin.

A previous paper (Harris (1985) Biochemistry 24, 7412-7418) reported the occurrence of two classes of anion binding sites in transferrin. To evaluate the locations of the two anion binding sites in relation to the two major domains of transferrin we determined the binding constants of whole ovotransferrin and its two half-molecules by means of the difference UV spectroscopic technique. Anions induced strong negative absorbance at 245 nm in the order: citrate greater than phosphate greater than bicarbonate for whole ovotransferrin and the N-terminal half-molecule; and: phosphate greater than citrate greater than bicarbonate for the C-terminal half-molecule. The anion dissociation constants of the N-terminal half-molecule were consistent with lower dissociation constants, and those of the C-terminal half-molecule, with higher dissociation constants of whole ovotransferrin, indicating that the two classes of anion binding sites correspond to the binding sites in individual structural domains. Anion binding markedly protected the N-terminal half-molecule, but not the C-terminal half-molecule from digestion with trypsin and disulfide reduction with dithiothreitol. As to the far and near ultraviolet CD spectra data, however, there was no significant difference between in the presence and absence of an anion. Therefore, the binding of an anion would induce some conformational changes which were not reflected by the CD spectrum.

Anions↗
PubMed1989

Potentiation of growth-inhibitory activity of 9-beta-D-arabinofuranosyladenine by 2'-deoxycoformycin in human cultured cell lines derived from leukemias and lymphomas.

Growth-inhibitory activity of 2'-deoxycoformycin (DCF) and 9-beta-D-arabinofuranosyladenine (Ara-A) used either singly or in combination was assessed in 30 human cultured cell lines (seven T-cell, nine B-cell, five non-T,non-B and nine myeloid cell lines) derived from leukemias and lymphomas. DCF had little activity even at 100 microM on any of the cell lines, while Ara-A had an obvious inhibitory effect on them, especially on non-T,non-B cell lines at 10 microM or less. Lymphoid cell lines were apparently more sensitive to the combined use of Ara-A and DCF than myeloid cell lines. DCF potentiated the antiproliferative activity of Ara-A not only in T-cell lines with high adenosine deaminase (ADA) activity, but also in some other cell lines with low ADA activity. DCF was stable in the culture medium, but Ara-A in the medium containing cultured cells was rapidly inactivated. DCF completely inhibited the inactivation of Ara-A in the medium containing P12/ICH or NALM-6, but not in the medium containing Daudi. This suggests that there is some unknown mechanism(s) of inactivation of Ara-A other than ADA in Daudi, which was insensitive to Ara-A in the presence of 1 microM DCF. The capacity of DCF to inhibit degradation of Ara-A in the medium containing these cultured cells correlated with the level of Ara-A sensitivity potentiated by DCF. In all seven T-cell lines, seven of the nine B-cell lines, all five non-T,non-B cell lines, and only three of nine myeloid cell lines, the IC50 value for Ara-A decreased to 5 microM or less in the presence of 1 microM DCF. These results suggest that the combination of DCF and Ara-A may be effective against various types of lymphoid malignancies and some myeloid leukemias.

Adenosine Deaminase↗
PubMed1989

[Changes in temperature and humidity at different layers inside clothing during rest, exercise, and recovery].

This paper presents the results of experiments in which we measured humidity and temperature changes that took place in different layers inside and on clothing. The experiments were conducted during rest, exercise, and recovery. During each experiment, subjects wore one of three kinds of outerwear made of three different materials, respectively. These materials were nylon taffeta (N), nylon taffeta-Goretex-nylon tricot laminated fabric (G), and polyvinylchloride-coated plain cotton fabric (V). The subjects wore an undershirt and a T-shirt under the outerwear. The humidity and the temperature were measured in the following parts of each subjects' back: (1) the layer between the subject's skin and the undershirt (first layer), (2) the layer between the undershirt and the T-shirt (second layer), (3) the layer between the T-shirt and the outerwear (third layer), and (4) the surface of the outerwear (fourth layer). We also measured the sensation of comfort, the skin temperature, the oral temperature and the degree of sweating of the subjects. The experiments were conducted in a climatic chamber under conditions of 20.7 +/- 0.4 degrees C, 61.2 +/- 3.6% RH and 2.5 +/- 0.5 cm/sec. The results we obtained were as follows: 1) While the subjects kept still, little change of humidity was observed with time in all the four layers. When the subjects were in motion, humidity increased as they started sweating. After the exercise ended, the humidity reached its maximum and then gradually decreased. 2) When subjects kept still, there was no difference in humidity in all the four layers of the outerwear.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[A case of Henoch-Schoenlein purpura with extremely low OKT4 positive T lymphocytes].

We present a patient with Henoch-Schoenlein purpura who had extremely low number of OKT4 positive T lymphocytes. However his lymphocytes responded normally to Leu3a and Coulter T4, which are also monoclonal antibodies that react with CD4 epitope. In vitro lymphocyte function tests revealed that helper-inducer T cell functions were normal. From these findings, we concluded that this patient had an abnormality in the epitope of CD4 positive cells. Since expression of OKT4 antigens in his mother was also low, we considered the possibility of hereditary factors although no relationship with HLA was found.

Antibodies, Monoclonal↗
PubMed1989

[The accuracy of CT and tumor markers in the detection of a recurrent ovarian carcinoma].

Twenty-three patients previously diagnosed as having ovarian cancer were examined with both serum tumor markers (CA 125, CA 19-9, TPA, IAP, AFP) and a pelvic CT scan. The tumor markers predict the clinical outcome more accurately than the CT scan. Further, the tumor markers showed a clear correlation with the clinical course. But in one case, however, the tumor markers were seen to reduce below the normal level from chemotherapy, while the CT scan showed a tumor mass. Thus, both, a CT scan and tumor marker assays are felt to be indispensable for detecting the recurrence of an ovarian cancer.

Adenocarcinoma, Mucinous↗
PubMed1989

[Prostaglandin E1, as a vasodilator therapy, for low output syndrome after cardiac surgery].

Prostaglandin E1 (PGE1) has a direct vasodilating effect to smooth muscles of resistant vessel much more than that of capacitance one. In afterload mismatch, vasodilator which acts on resistant vessel mainly should be selected. We used PGE1 for vasodilator therapy to two patients with low cardiac output syndrome (LOS) in intensive care unit. One patient undergoing coronary artery bypass grafting developed LOS and disseminated intravascular coagulation which derived from post-transfusional anaphylactoid reaction. Another patient undergoing mitral valve replacement, tricuspid valve annuloplasty and coronary artery bypass grafting also developed LOS with massive thrombosis caused by cold agglutinin during cardio-pulmonary bypass. In both patients, PGE1 decreased systemic vascular resistance index and pulmonary arterial resistance index, and increased cardiac output. PGE1 inhibits release of lysosomal enzymes from polymorphonuclear leukocytes and increases splanchnic blood flow. These effects lead to inhibit production of myocardial depressant factor and might relate to the improvement of LOS partially. We suggest that PGE1 was effective for LOS after cardiac surgery, especially in afterload mismatch.

Aged↗
PubMed1989

[The use of PGE1 in an elderly patient with mitral valve regurgitation during general anesthesia].

PGE1 has a beneficial effect on cardiac failure with mitral valve regurgitation by decreasing the "after load". An 82-year-old female had a total cystectomy of a bladder tumor. The preoperative standard 12 lead electrocardiogram showed atrial fibrillation and incomplete right bundle branch block. The preoperative echocardiogram showed regurgitation of both mitral valve and tricuspid valve. Under heavy premedication, we intubated with fentanyl and pancuronium bromide, maintained anesthesia with enflurane. After incision, both pulmonary artery pressure and pulmonary capillary wedge pressure increased, and cardiac index decreased. Continuous injection of 100ng.kg-1.min-1 PGE1 made pulmonary artery pressure and pulmonary capillary wedge pressure to decrease, and cardiac index to increase. PaO2, however, decreased apparently. PGE1 was effective for cardiac failure with mitral valve regurgitation associated with pulmonary hypertension. But attention must be given to the decrease in PaO2.

Aged↗
PubMed1989

[Afterload reduction therapy with prostaglandin E1 (PGE1)].

Increases in afterload cause marked decreases in cardiac output and left ventricular stroke volume in patients with congestive heart failure. We studied the effects of afterload reduction therapy with prostaglandin E1 in three patients with intraoperative heart failure and two patients with low output syndrome after coronary artery bypass grafting. After 120 minutes, mean pulmonary arterial pressure decreased from 25.6 to 17.4 mmHg, pulmonary wedge pressure from 20.0 to 10.2 mmHg and right atrial pressure from 10.2 to 6.8 mmHg. Cardiac index increased from 1.73 to 2.80 l.min-1.m-2. The improvement of peripheral circulatory failure was remarkable and all patients recovered from heart failure. This study suggests that PGE1 is effective for afterload reduction therapy.

Aged↗
PubMed1989

[Anesthetic management of thrombotic thrombocytopenic purpura].

A 46-year-old man, with TTP and renal failure, received splenectomy because complete remission was not achieved after the treatments such as plasma exchange, antiplatelet agents and corticosteroid. After the administration of methylprednisolone, anesthesia was induced with thiamylal and succinylcholine chloride and maintained with nitrous oxide, enflurane, fentanyl and vecuronium. Total blood loss was 1710 gram. Four units of packed red cell and 9 units of fresh frozen plasma were infused. The anesthetic course was uneventful. TTP is a rare and usually fatal disease and its etiology is unknown. Careless infusion of platelet or fresh blood may accelerate the disease process and multiorgan dysfunction may present other anesthetic problems. In this report, problems of anesthetic management for TTP were discussed.

Anesthesia, Inhalation↗
PubMed1988

Metabolism of 2- and 3-tert-butyl-4-hydroxyanisole in the rat (III): Metabolites in the urine and feces.

The urinary and fecal metabolites of orally administered 2-tert-butyl-4-hydroxyanisole (2-BHA) and 3-tert-butyl-4-hydroxyanisole (3-BHA) in rats were identified. Samples of 2-day pooled urine and feces of rats given a single intragastric dose of 1 g/kg body wt of tert[butyl-14C]3-BHA (*Bu-3-BHA). tert[butyl-14C]2-BHA (*Bu-2-BHA), [methyl-14C]3-BHA (*Me-3-BHA) or [methyl-14C]-2-BHA (*Me-2-BHA) were analyzed by comparing thin-layer chromatography (TLC) retentions with authentic standards. Conjugated metabolites were identified after enzymatic hydrolysis. Proton magnetic resonance spectroscopy and electron impact mass spectrometry were used for confirmation of the authentic standards. In rats given 3-BHA, a major metabolite in the urine was 3-BHA-glucuronide with a smaller amount of tert-butylhydroquinone (TBHQ)-sulfate, while unchanged 3-BHA and 3-BHA-glucuronide were detected in the feces. In rats given 2-BHA, the main metabolites were the sulfate conjugates of 2-BHA, 4-tert-butyl-5-methoxy-1,2-benzoquinone (2-TBOQ) and the glucuronide of 2-BHA in the urine, while unchanged 2-BHA was found in the feces.

Administration, Oral↗
PubMed1988

Modifying effects of concomitant treatment with butylated hydroxyanisole or butylated hydroxytoluene on N,N-dibutylnitrosamine-induced liver, forestomach and urinary bladder carcinogenesis in F344 male rats.

The modifying effects of concomitant antioxidant treatment on N,N-dibutylnitrosamine (DBN)-induced carcinogenesis were investigated. Male F344 rats were given 0.05% DBN in their drinking water for 16 weeks, and simultaneously administered powder diet containing 2.0% butylated hydroxyanisole (BHA) or 0.7% butylated hydroxytoluene (BHT) for 16 weeks. Control animals received drinking water containing 0.05% DBN without antioxidant treatment. The final incidences of hepatocellular carcinomas were 100, 100 and 40% in the DBN plus BHA, DBN plus BHT and DBN treated groups, respectively, the difference being significant (P less than 0.001). Lung metastases were only observed in the DBN plus BHT group and DBN plus BHA group (50%, P less than 0.001; 7%, respectively). The incidence of papillary or nodular hyperplasia of the urinary bladder in the DBN plus BHA group was significantly higher than that of the control (P less than 0.05). Furthermore, esophageal carcinomas and papillomas were observed in all DBN treated groups, with no inter-group significant variation in yield. On the other hand, combination of DBN treatment with BHA or BHT significantly reduced the resultant incidences of forestomach hyperplasia. The results clearly demonstrated that concomitant administration of antioxidants, and in particular BHT, can modify DBN carcinogenesis.

Animals↗
PubMed1988

Modification of N-methyl-N'-nitro-N-nitrosoguanidine-induced forestomach and glandular stomach carcinogenesis by phenolic antioxidants in rats.

The modifying effects of five phenolic antioxidants on N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-initiated forestomach and glandular stomach carcinogenesis were investigated in male F344 rats. Groups of 20 rats were given an intragastric dose of 150 mg/kg body weight MNNG, and starting from 1 week later received diet supplemented with 0.8% catechol (CC), 1.0% 2-tert-butyl-4-methylphenol, 1.5% p-tert-butyl-phenol, 1.5% methylhydroquinone, 1.5% 4-methoxyphenol (4MP), or basal diet alone for 51 weeks. Further groups of 10-15 rats were maintained as controls without prior treatment with MNNG. The incidences of squamous cell carcinoma of the forestomach in MNNG-treated animals were significantly elevated by the diets containing CC (P less than 0.001), 2-tert-butyl-4-methylphenol (P less than 0.001), or p-tert-butylphenol (P less than 0.01), while the development of carcinoma in situ was inhibited by 4MP (P less than 0.01). Treatment with CC, 2-tert-butyl-4-methylphenol, p-tert-butylphenol, or 4MP alone induced forestomach hyperplasia at incidences of 86.7, 40, 93.3, and 100%, respectively. In the pyloric region of the glandular stomach, the development of adenomatous hyperplasia and adenocarcinoma after MNNG treatment was significantly enhanced by diet containing CC (P less than 0.001). Moreover, treatment with CC alone induced 100% adenomatous hyperplasia and induced adenocarcinoma in 20% of animals. These results clearly demonstrated that while antioxidants causing proliferation in forestomach epithelium can markedly enhance carcinogenesis in this tissue, others displaying the same or greater potential for generating a hyperplastic response, like 4MP, can exert an inhibitory effect. In addition, it was shown that CC, which is widely present in our environment, is an unequivocal glandular stomach carcinogen also possessing strong enhancing activity for MNNG-induced lesion development.

Animals↗
PubMed1988

Analyses of intramolecular disulfide bonds in proteins by polyacrylamide gel electrophoresis following two-step alkylation.

A method that makes use of polyacrylamide gel electrophoresis was developed for the analysis of intramolecular disulfide bonds in proteins. Proteins with different numbers of cleaved disulfide bonds are alkylated with iodoacetic acid or iodoacetamide as the first step. The disulfide bonds remaining were reduced by excess dithiothreitol, and the newly generated free sulfhydryl groups were alkylated with the reagent not yet used (iodoacetamide, iodoacetic acid, or vinyl-pyridine) as the second step. This treatment made it possible for lysozyme (Mr, 14,000; 4 disulfides), the N-terminal half-molecule of conalbumin (Mr, 36,000; 6 disulfides), the C-terminal half-molecule of conalbumin (Mr, 40,000; 9 disulfides), and whole conalbumin (Mr, 78,000; 15 disulfides) to be separated by acid-urea polyacrylamide gel electrophoresis into distinct bands depending on the number of disulfide bonds cleaved. The method allowed us to determine the total number of disulfide bonds in native proteins and to assess the cleaved levels of disulfide bonds in partially reduced proteins. Two-step alkylation used in combination with radioautography was especially useful for the analysis of disulfide bonds in proteins synthesized in complex biological systems.

Alkylation↗