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Biomedical subjects

J Shimazaki

Publications and source records attributed to J Shimazaki.

At least 451 records · Page 25Linked to original sources
PubMed1981

Measurement of androgen receptor in cytosols from normal, benign hypertrophic and cancerous human prostates.

The binding of R 1881 in cytosols from the normal, benign hypertrophic and cancerous human prostates was examined in the presence of molybdate and triamcinolone acetonide. The addition of 10 mM Na2MoO4 resulted in an increase in the stability of the binder without any change in Kd. Triamcinolone acetonide added to the incubation of cytosol with R 1881 modified the inhibition pattern by other steroids, and the binding in the presence of triamcinolone acetonide exhibited the characteristics of androgen receptor. The complex of cytosol and R 1881 formed in the incubation in the presence of triamcinolone acetonide was sedimented at 8.5S. Kd of the binding to R 1881 of the normal and pathological prostates was almost identical, but maximum binding sites of the androgen receptor were larger in benign hypertrophic and cancerous prostates than in normal tissues. For the assay of binding capacity in needle biopsy specimens, one point determinations were performed using 2.5 nM R 1881 as the ligand. The number of binding sites obtained by this method were well correlated with those obtained by the Scatchard plot in various prostatic tissues.

Cytosol↗
PubMed1981

Histochemical observation of F 1881 binding protein in human benign prostatic hypertrophy.

A 3-carboxymethyloxime conjugate of R 1881 was conjugated with bovine serum albumin and reacted with fluorescein isothiocyanate. Tissue sections from patients with benign prostatic hypertrophy were incubated with this compound. Fluorescence was observed in the cytoplasm of gland cells, although both positive and negative cells were distributed evenly in some areas. Neither the stroma nor the nuclei of epithelial cells were fluorescent. Preincubation with a 20 fold molar excess of R 1881-carboxymethyloxime-bovine serum albumin, 1 microM of R 1881, or 1 microM of triamcinolone acetonide diminished fluorescence of the section. Bovine serum albumin conjugated with fluorescein isothiocyanate did not stain the section. Therefore, the fluorescence observed in the sections seems to be attributable to the high affinity binding of R 1881. The intensity and number of fluorescent cells and the R 1881 binding estimated by a biochemical method were well correlated.

Androgen-Binding Protein↗
PubMed1980

Binding to R 1881 (methyltrienolone) of proteins from human benign prostatic hypertrophy.

Cytosol of human benign prostatic hypertrophy bound to R 1881 in a high affinity manner. Most of the protein which bound to R 1881 was recovered in the precipitate of a 0-30% saturation of ammonium sulfate, and was eluted in the void volume on a Sephadex G-200 column. The binding of cytosol to R 1881 was more inhibited by progestins than by dihydrotestosterone and estradiol-17 beta. The binder therefore seemed to be different from dihydrotestosterone-binding protein. The R 1881-binding component extracted from the nuclei by 0.4M KCl bound also to dihydrotestosterone in a high affinity manner. Cytosol prelabeled with R 1881 was bound to the nuclei in a nonsaturable process, and the extraction pattern of R 1881 by 0.4M KCl from the nuclei was almost identical to that in the case of dihydrotestosterone as the ligand. These results suggested that a part of the cytosolic protein which bound to R 1881 entered the nuclei where it bound to nuclear such components as dihydrotestosterone-binding protein.

Cell Extracts↗
PubMed1980

Binding of chlormadinone acetate to cytosol from human benign prostatic hypertrophy.

Chlormadinone acetate was bound to cytosol from the human benign prostatic hypertrophy in a high affinity fashion. The kd and number of maximum binding site of the binding were 5.4 +/- 0.7 X 10(-9) M and 67.9 +/- 5.8 fmol/mg protein, respectively. When compared with the binding to dihydrotestosterone, the Kd for chlormadinone acetate was greater. The number of maximum binding site for chlormadinone acetate was observed to be smaller than that for dihydrotestosterone, but these two values were not different statistically. The binding of chlormadinone acetate was inhibited significantly by the addition of R 1881 or cyproterone acetate. However, dihydrotestosterone revealed itself to be a weak inhibitor of the binding. The cytosol prelabelled with chlormadinone acetate was not bound to the nuclei of the human prostate.

Androgen Antagonists↗
PubMed1980

Cell kinetic studies on androgen-dependent mouse mammary tumor and subline with altered dependency.

Cell kinetic study was performed using labeled mitosis method to compare growth characteristics of androgen-dependent mouse mammary tumor (SC115), which grows only in males, and its subline (Chiba subline No. 1), which has partially lost its dependency during passages through males and grows also in females, although at a slower rate. The subline, compared to the original tumor, showed higher growth fraction irrespective of whether inoculated into a male or a female. The cell cycle of the subline was faster in males than in femlaes due to acceleration of Gl phase and this trend was reflected in the cell production rate and overall rate of growth. The slower growth in females was restored by the administration of testosterone. However, growth fraction was rather in the inverse relationship with the cell production rate and this fact suggested that androgen-deprived conditions do not support survival of non-cycling cells. Primary effect of androgenic environment on this subline was considered to be the reduced length of Gl phase.

Androgens↗
PubMed1979

Suppression of 3H-lysine incorporation into the vascular non-collagenous protein in rats treated with estradiol-17 beta.

The in vivo incorporation of 3H-lysine into non-collagenous protein of the heart, aorta and mesenteric arteries was measured in castrated or non-castrated male young rats given hormone treatment once daily for 14 consecutive days. In rats given estradiol-17 beta (50 micrograms), a significant reduction of blood pressure was noted at 7 and 8 weeks of age. The lysine incorporation into non-collagenous protein was markedly decreased in mesenteric arteries and to a lesser extent in the aorta of rats treated with estradiol-17 beta (50 micrograms). The decline in blood pressure concomitant with the reduction of lysine incorporation into non-collagenous protein of the same vessels was of similar magnitude in castrated, testosterone (50 micrograms) plus estradiol-17 beta (50 micrograms)-treated rats as compared with that in castrated testosterone-treated (50 micrograms) animals. Despite the variety of hormone treatments, the incorporation of 3H-lysine into non-collagenous protein of heart was similar for all the rats examined. It is suggested that the suppressive effect of estradiol-17 beta on biosynthesis of vascular non-collagenous protein, especially in small arteries, plays an important role in lowering the blood pressure of young male rats.

Animals↗