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Biomedical subjects

K Miyaji

Publications and source records attributed to K Miyaji.

At least 19 recordsLinked to original sources
PubMed1995

Effects of protein kinase C modulators on multidrug resistance in human glioma cells.

To identify the role of protein kinase C (PKC) in multidrug resistance, the effects of phorbol-12-myristate-13-acetate (PMA), a PKC activator, or calphostin C, a PKC inhibitor, on intracellular vincristine accumulation and expression of P-glycoprotein phosphorylation were studied in one multidrug-resistant and three multidrug-sensitive human glioma cell lines. Basal PKC activities and immunoreactivities of PKC-alpha and -zeta were higher in multidrug-resistant cells than in multidrug-sensitive cells. There was no significant difference in the immunoreactivity of PKC-delta between multidrug-resistant and -sensitive cells, and immunoreactive PKC-beta, -gamma, and -epsilon were not detected in either multidrug-resistant or -sensitive cells. The treatment of multidrug-resistant cells with 100 nM PMA for 2 hours resulted in the activation not of PKC-zeta but of PKC-alpha, with concomitant decrease in vincristine accumulation and increase in P-glycoprotein phosphorylation. The exposure of multidrug-resistant cells to 100 nM PMA for 24 hours induced down-regulation not of PKC-zeta but of PKC-alpha, with concurrent decrease in vincristine accumulation, and reduced but still increased P-glycoprotein phosphorylation. The treatment of multidrug-resistant cells with 100 nM calphostin C for 2 hours decreased immunoreactive PKC-zeta and not immunoreactive PKC-alpha, inducing increase in vincristine accumulation, with concomitant decrease in P-glycoprotein phosphorylation. There was no evidence of significant change in vincristine accumulation in multidrug-sensitive cells treated with PMA or calphostin C. This may suggest that at least two isozymes of PKC, PKC-alpha and -zeta, are involved in P-glycoprotein phosphorylation and that vincristine efflux function in multidrug-resistant human glioma cells is closely associated with P-glycoprotein phosphorylation and is decreased by PKC inhibitor.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1995

Development of intestinal flora of human-flora-associated (HFA) mice in the intestine of their offspring.

Development of intestinal flora in newborn human-flora-associated (HFA) mice was compared with that in newborn conventional (CV) mice. Facultative anaerobes were detected from the first day after birth in both CV and HFA mice but anaerobes were not detected in the first week. Anaerobes rapidly increased from the 2nd week after birth and became predominant in newborn intestine. Most of the intestinal bacteria in adult CV and HFA mice were colonized in the intestine of CV and HFA mice, respectively, within 3 weeks after birth. The human intestinal flora established in the intestine of HFA mice finally reproduced without any remarkable change in composition in the intestine of newborn HFA mice. The development of intestinal flora in HFA mice was similar to that in CV mice but not that in human infants. These results indicated that human flora associated in HFA mice could be transferred from mothers to their offspring although HFA mice could not simulate the development of intestinal flora of the human infant.

Adult↗
PubMed1995

Inhibition by 5'-methylthioadenosine of cell growth and tyrosine kinase activity stimulated by fibroblast growth factor receptor in human gliomas.

Stimulation of three human glioma cell lines with basic fibroblast growth factor (bFGF) led to the enhancement of cell growth and the rapid tyrosine phosphorylation of cellular proteins, including major substrates of 90 kD. A methyltransferase inhibitor, 5'-methylthioadenosine (MTA), inhibited dose dependently the bFGF-stimulated cell growth and protein tyrosine phosphorylation in glioma cells by blocking both receptor autophosphorylation and substrate phosphorylation, as shown by immunoblotting with antiphosphotyrosine antibodies and cross-linking bFGF to receptors. The antiproliferative activity of MTA correlated quantitatively with its potency as an inhibitor of bFGF-stimulated protein tyrosine kinase activity. The methyltransferase inhibitor MTA had no effect on either epidermal growth factor- or platelet-derived growth factor-stimulated protein tyrosine phosphorylation in glioma cells, but inhibited specifically bFGF-stimulated protein tyrosine kinase activity. The concentration of MTA required for inhibition of protein methylation correlated well with the concentration required for inhibition of bFGF-stimulated cell growth and protein tyrosine phosphorylation. Because MTA had no effect on numbers and dissociation constants of high- and low-affinity bFGF receptors, the inhibition of bFGF-stimulated bFGF receptor tyrosine kinase activity is not likely to be the result of a reduction in bFGF receptor and bFGF binding capacity. In fact, MTA delayed and reduced the internalization and nuclear translocation of bFGF, and the internalized bFGF was submitted to a limited proteolysis that converted it to lower molecular peptides whose presence remained for at least 22 hours. The effect of MTA on bFGF-stimulated tyrosine phosphorylation was immediate and readily reversible.

Antibodies↗
PubMed1994

Stimulation of protein-tyrosine phosphorylation in gerbil hippocampus after global forebrain ischemia.

Tyrosine phosphorylation in the gerbil hippocampus after a transient ischemia was analyzed by immunoblotting and immunohistochemistry. In control hippocampus, the phosphotyrosine was detected in many proteins of 165 to 10 kDa and the immunostain showed a distinct distribution. The ischemic insult induced various alterations of the phosphotyrosine immunoreactivities in both ischemia-resistant and -vulnerable neurons which were associated with alterations in the expression of 165 to 19 kDa-immunoreactive bands. These results suggest that tyrosine phosphorylation is involved in the ischemic hippocampus to play a role in the development of early and delayed neuronal deaths in CA4 and CA1 neurons, respectively.

Animals↗
PubMed1992

[Clinical evaluation of the intraluminal ultrasonography].

Although for the diagnosis of rectal diseases barium-enema and colonoscopy have been commonly carried out, by the methods neither information on the layer structure of the intestinal wall nor swelling of the regional lymphnodes can be provided. Therefore we tried intraluminal ultrasonography (IUS) for further evaluation of the rectum and peri-rectal lesion, and the usefulness of IUS in the rectal disease was described. In 46 cases of rectal cancer, the following results were obtained. Five layer structures were distinguished in the normal rectal wall by the IUS. Intraluminal invasion showed destruction of the layer structures of the colonic wall. The swelling of the regional lymphnodes was revealed as low echoic round mass. In 43 cases with benign diseases, characteristic variations of the layer structures in the colonic wall can be distinguished by the IUS. In conclusion, the IUS was of great use to observe the variation of the layer structure of colonic wall and to provide valuable information on metastasis into the regional lymphnodes.

Adult↗
PubMed1991

Interspecies comparison of c-myc gene in human and rat glioma cell lines.

Interspecies difference in expression of the c-myc gene between two human and three rat glioma cell lines was studied with use of a human c-myc probe. The c-myc deoxyribonucleic acid (DNA) fragments detected at higher stringency in Southern blotting, showed a difference in size and gene copy number between human and rat glioma cells. The c-myc transcript was detected at both higher and lower stringencies in Northern blotting in human glioma cells, whereas it was demonstrated only at lower stringency in rat glioma cells, and the c-myc transcript was seen in cytoplasms of both glioma cells by in situ hybridization. The c-myc protein, if examined with anti-human c-myc protein monoclonal antibody, was observed as two separate components in Western blotting and localized immunocytochemically in nuclei in human glioma cells, whereas it was detected as three separate forms in Western blotting and shown in both nuclei and cytoplasm in rat glioma cells. The above discrepancy in manifestation of c-myc DNA fragments, transcript and protein could be due to the difference in nucleotide sequence of c-myc gene between human and rat glioma cells.

Animals↗
PubMed1991

Residual neutron-induced radionuclides in samples exposed to the nuclear explosion over Hiroshima: comparison of the measured values with calculated values.

Residual radionuclides induced by neutrons from the Hiroshima atomic bomb have been measured at Kanazawa University for 14 years. The results of 152Eu, 154Eu and 60Co are reviewed in this paper. Where appropriate, an attempt is made to provide our new data with the aim of reinterpreting our published data. From the comparison of the measured values with the calculated values by DS86 methodology, we may point out here: (1) that close agreement was found between measured and calculated values for the specific radioactivity of 152Eu in the samples exposed at ground ranges between 320 m and 720 m; (2) that the calculated/measured ratios for the specific radioactivity of 152Eu were, however, larger than unity in the vicinity of ground zero and smaller than unity at locations more than 1000 m apart from ground zero; (3) that, in the vicinity of ground zero, epithermal neutron fluence evaluated from a set of measured specific radioactivities of 152Eu, 154Eu and 60Co showed a close agreement with the calculated result, whereas thermal neutron fluence evaluated in the same way was different from the calculated result; and (4) that the depth distribution of the specific radioactivity of 152Eu in a wall sample which was exposed at the location 320m from ground zero approximately agreed with the calculated result.

Humans↗
PubMed1990

Application of the Karhunen-Loeve expansion to evaluate regional cardiac excitation in body surface potential maps.

The authors investigated the usefulness of the Karhunen-Loeve technique applied to body surface maps to study regional cardiac excitation. Eigenvectors were derived from the body surface potential maps of 120 healthy adults using the Karhunen-Loeve expansion theory. Then, in the maps of various types of ventricular hypertrophy, each eigenvector coefficient was calculated for a statistical comparison. The first eigenvector coefficient in early QRS and the second in mid QRS were larger in patients with asymmetrical septal hypertrophy and in patients with left ventricular hypertrophy, respectively. The third was larger in patients with right ventricular hypertrophy. In the maps of patients with previous anteroseptal myocardial infarction, the second eigenvector coefficient decreased with asynergy of the anterior to apical wall, and the first decreased with the asynergy of the interventricular septum. They conclude that some eigenvector components and coefficients at particular times in the QRS are sensitive to changes in regional cardiac excitation and that they may facilitate the detection of local excitation changes such as occur in hypertrophy or infarction.

Adult↗
PubMed1987

[Eigenvector analysis in body surface potential maps for evaluating right ventricular hypertrophy in primary pulmonary hypertension].

This study related the eigenvectors derived from the QRS complex in body surface isopotential maps of normal subjects to regional myocardial excitation, with special emphasis on the right ventricle. The subjects consisted of 120 normal healthy adults and eight patients with primary pulmonary hypertension and right ventricular hypertrophy (PPH). According to the Karhunen-Loève theory, eigenvectors were derived from the normal group and the eigenvector coefficient of each subject was obtained against time for the first three components. The cumulative proportion of the first three eigenvectors was 90.3% in normals and 80.2% in PPH. The first eigenvector had a peak of eigenvector coefficients early in the QRS and had a bottom late in the QRS. The peak of the second was in the middle of the QRS. The coefficients of the third eigenvector were low compared to the former two eigenvectors, and had no characteristic time pattern. PPH had a similar time pattern of coefficients in the first eigenvector, reduced coefficients in the second, and a definite peak in the mid-QRS in the third. The average eigenvector coefficient of the third eigenvector in PPH was significantly higher than those in normal subjects (p less than 0.01). We conclude that the third eignevector derived from normal subjects strongly reflects right ventricular excitation.

Adult↗
PubMed1982

Gastric acid secretion, serum gastrin and parietal cell histology in hyperthyroidism.

A decrease in MAO by gastrin stimulation was observed in 13 of 20 hyperthyroid patients. Five of these 13 cases had achlorhydria. The decrease in gastric acid secretion had no relation to the duration of symptoms, serum T3 and T4 levels, serum antithyroglobulin antibody levels and serum antithyroid microsomal antibody levels. Gastroscopy with biopsy was performed in 17 cases. In patients with achlorhydria, macroscopic and histological atrophy was not observed in the body, and parietal cells were present and their succinic dehydrogenase activity was normal. Electron microscopy of the parietal cells of patients with achlorhydria showed that their cells were similar to those in the resting state of healthy subjects with the ability to secrete normal amounts of gastric acid. These findings demonstrate that the decrease in gastric acid secretion in hyperthyroidism is not caused by any structural changes in the gastric mucosa but by functional suppression. In the present experiment, this suppression was found resistant to gastrin. A rise in serum gastrin level was observed in 8 cases. Either achlorhydria or marked hypoacidity was found in 6 cases with the level more than 400 pg/ml. The HCl administration temporarily lowered elevated gastrin levels, and feedback inhibition by HCl was found to be maintained. A rise in gastric pH was considered to be one of the prerequisites for an increase in serum gastrin level.

Adolescent↗
PubMed1982

Gastric acid secretion, serum gastrin and parietal cell histology in rat hyperthyroidism.

Experimental hyperthyroidism was produced in rats by thyroxin injection, and changes in gastric acid secretion and serum gastrin level were determined to analyze the relation between these changes and hyperthyroidism. Administration of thyroxin to two groups of rats-20 micrograms per 100 g of body weight for 20 days and 75 micrograms for 7 days-brought about significant increases in serum T3 level, gastric pH and serum gastrin level. An increase in gastric pH took place later than that in serum T3 level; this time lag implies that a decrease in acid secretion was not caused by an direct effect of thyroxin on the parietal cell but by its secondary effect. In the T4-injected rats with decreased gastric acid secretion, the parietal cell remained normal in form and succinic dehydrogenase activity was also normal. The electron microscopical observations showed nothing abnormal in the parietal cells. These findings suggest that a decrease in acid secretion was not due to any structural changes in the gastric mucosa but to functional suppression. The serum gastrin level rose in correlation with an increase in gastric pH and fell by HCl administration to the stomach. Feedback inhibition by pH remained in the G cell.

Animals↗
PubMed1979

Plasma dopamine-beta-hydroxylase activity and thyroid suppressibility in Graves' disease.

Plasma dopamine-beta-hydroxylase (DBH) activity, serum T4, T3, T3U, and the 24-hr thyroid uptake before triiodothyronine suppression testing were studied in 34 patients with treated Graves' disease. Although all of them were in the euthyroid state, there was a statistically significant difference in presuppression plasma DBH activity between those patients who showed suppression of their RAI uptake with triidothyronine and those who did not. This suggests a relationship between plasma DBH activity and thyroid suppressibility.

Dopamine beta-Hydroxylase↗