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M Ota

Publications and source records attributed to M Ota.

At least 343 records · Page 19Linked to original sources

Binding of [3H]methyltrienolone to androgen receptor in rat liver.

The synthetic androgen methyltrienolone is superior to testosterone and androstenedione for the measurement of androgen receptor in tissues where the native ligands are metabolized into inactive derivatives. [3H]Methyltrienolone binds with a high affinity to androgen receptor in cytosol prepared from male rat livers, as the Scatchard analysis revealed that the Kd value was 3.3 X 10(-8) M and the number of binding sites was 35.5 fmol/mg protein. Since methyltrienolone also binds glucocorticoid receptor which exists in rat liver, the apparent binding of androgen receptor is faulty when measured in the presence of glucocorticoid receptor. The binding of methyltrienolone to glucocorticoid receptor can be blocked by the presence of a 100-fold molar excess of unlabeled synthetic glucocorticoid, triamcinolone acetonide, without interfering in its binding to androgen receptor, because triamcinolone does not bind to androgen receptor. Triamcinolone-blocked cytosol exhibited that the Kd value was 2.5 X 10(-8) M and the number of binding sites was 26.3 fmol/mg protein, indicating a reduction to 3/4 of that in the untreated cytosol. The profile of glycerol gradient centrifugation indicated that [3H]methyltrienolone-bound receptor migrated in the 8-9 S region in both untreated and triamcinolone-blocked cytosols, but the 8-9 S peak in triamcinolone-blocked cytosol was reduced to about 3/4 of that of untreated cytosol.

Animals↗

Activation of the rat liver androgen-receptor complex.

Activation of androgen receptor in rat liver cytosol was studied in vitro. The state of activation was judged by binding of [3H] R1881-receptor complex to chromatin. High ionic strength (0.4 M KCl as a final concentration) provoked the binding of [3H] R1881-receptor complex to chromatin at 0 degrees C. At low ionic strength, activation was very slow at 0 degrees C, but was very rapid at 25 degrees C and reached the maximum at 15 min of heating.

Animals↗

Binding of cytoplasmic testosterone-receptor complex to nucleic from male rat livers.

A crude cytoplasmic androgen receptor preparation of rat livers or its partially purified one by a 30% ammonium sulfate precipitation was prelabeled with [3H] testosterone ([3H]T) and then incubated with nuclei from rat livers at 30 degrees C for 30 min. The formations of the [3H]T-cytosol receptor complex and its nuclear bound complex were determined. The formation of testosterone-cytosol receptor complex was a prerequisite for the nuclear binding of testosterone. Nuclear fraction, when incubated with the prelabeled crude cytosol, bound [3H]T-receptor complex as much as when incubated with the prelabeled partially purified cytosol. The addition of unlabeled crude cytosol to the prelabeled partially purified cytosol increased the nuclear binding of the receptor. The presence of a thermostable, low molecular inhibitor and a thermolabile, macromolecular activator in the crude cytosol preparation was suggested by dialysis, heating and gel chromatography.

Animals↗

Interaction of hepatic chromatin with androgen-receptor complex.

When the chromatin prepared from male rat livers interacted with [3H] testosterone-receptor complex prepared from male rat livers, the binding was much higher than when interacted with free [3H] testosterone, indicating that the formation of testosterone-receptor complex is prerequisite for interaction with chromatin. When the [3H] testosterone-receptor complex was interacted with the chromatin and the bound chromatin proteins were extracted into three fractions based on their extractability or solubility in salt solutions, higher radioactivities were found in the 0.35 M NaCl-extract and 2.0 M NaCl residual fraction. Chromatin was fractionated into 0.35 M NaCl-soluble, 2.0 M NaCl-soluble and insoluble fractions, and interaction of free [3H] testosterone or [3H] testosterone-receptor complex with chromosomal fractions was studied. The binding of the chromosomal fractions with free [3H] testosterone was negligible compared with that of [3H] testosterone-receptor complex. The binding of 0.35 M NaCl-soluble fraction with [3H] testosterone-receptor complex was higher than that of 2.0 M NaCl-soluble fraction. The binding ability of 2.0 M NaCl-insoluble fraction with [3H] testosterone-receptor complex was twice as much as that of the intact chromatin. This observation indicated that salt-soluble fractions of chromatin contributes only partly to the binding of chromatin with [3H] testosterone-receptor complex and that other components in 2.0 M NaCl-insoluble fraction may participate in the binding.

Animals↗

[Phonocardiographic findings of atypical patent ductus arteriosus with pulmonary hypertension].

Among 71 patients with proved patent ductus arteriosus (PDA) as a sole anomaly, 13 were diagnosed as having "atypical PDA" because of a lack of a continuous murmur. Of these, 10 had find-pulmonary hypertension and were the materials of the present study, in which the phonocardiographic findings were correlated with the findings by other techniques including pulsed Doppler echocardiography. Six cases with equal pulmonary arterial and aortic pressures showed a diastolic murmur alone. The murmur started with the pulmonic component of the second heart sound and continued throughout diastole. All cases showed inspiratory augmentation or presystolic accentuation of the diastolic murmur. Pulsed Doppler echocardiograms disclosed that the murmur was produced by pulmonary regurgitation in five of six cases and by a left-to-right shunt via the ductus plus pulmonary regurgitation in one case. A to-and-fro murmur was observed in three cases. Pulmonary artery pressure was significantly lower than that of the systemic artery in two of three cases. These hemodynamic findings and pulsed Doppler echocardiograms indicated that the murmur of the two cases was produced by both a left-to-right shunt through the ductus and pulmonary regurgitation. A systolic murmur only was seen in one case and the cause of this murmur was not clear. In four of five cases with grade IV and V murmur, division or plugging of the ductus was performed with uneventful clinical course in three and sudden death in one. On the other hand, four of five cases with grade II and III murmur showed Eisenmenger reaction and the surgery was not attempted. The second heart sound showed normal splitting in eight cases, abnormally wide splitting in one case and was single in one case.

Adolescent↗

Characterization of testosterone binding protein of rat liver cytosol.

Testosterone binding protein from rat liver cytosol, which had been incubated with [3H]testosterone followed by treatment with dextran-coated charcoal, was analyzed by DEAE-cellulose and phosphocellulose chromatography. On DEAE-cellulose chromatography, two distinct peaks of radioactivity were eluted at 0.07 M and 0.19 M KCl, both sedimented in 4 S regions. Phosphocellulose chromatography resulted in a broad peak at 0.08 M KCl, with a shoulder at 0.04 M KCl, both sedimented at 4 S. These findings indicated that testosterone binding protein consists of two types of components each with 4 S.

Androgen-Binding Protein↗

[Effects of adriamycin and daunomycin on cardiac functions].

The effects of adriamycin and daunomycin on cardiac function were studied in 33 patients with acute leukemia (16 cases), neuroblastoma (5 cases), osteosarcoma (4 cases), malignant lymphoma (3 cases), rhabdomyosarcoma (3 cases) and malignant histiocytosis (2 cases). The left ventricular function was evaluated by serial echocardiographic assessment. Ejection fraction (E.F.) and shortening fraction (S.F.) of left ventricule were calculated from echocardiographic measurements. Seven of 33 cases (21.2%) revealed the decrease of E.F. and S.F. There was the significant correlation between total doses of daunomycin and E.F. Three patients died of severe congestive heart failure probably due to daunomycin administration. Usually, cardiac dysfunction caused by these drugs has improved within 3 months after the discontinuation.

Acute Disease↗