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B Sato

Publications and source records attributed to B Sato.

162 records · Page 9Linked to original sources
PubMed1978

Serum prolactin levels in eighty patients with sarcoidosis.

Serum prolactin levels were measured by radioimmunoassay in eighty patients (thirty-four males, forty-six females) with sarcoidosis before treatment. In twelve patients (15%) serum prolactin levels were more than two standard deviations above the mean of normal subjects. Hyperprolactinaemia was found most frequently (22%) in patients with radiological stage II; however, 14% of patients with stage I also had elevated serum prolactin levels. In most cases serum prolactin levels fell to within the normal range after treatment with corticosteroid in parallel with improvement of intrathoracic lesions. These findings suggest that hyperprolactinaemia may be due to hypothalamic involvement by sarcoid granulomata. We conclude that the measurement of basal serum prolactin levels using radioimmunoassay is a sensitive and practical method for screening patients with sarcoidosis for hypothalmic lesions.

Adolescent↗
PubMed1978

Electron spin resonance studies of erythrocytes from patients with Duchenne muscular dystrophy.

The membrane organization of the erythrocytes from patients with Duchenne muscular dystrophy was studied by means of electron spin resonance. The fluidity of the membrane near the polar region of Duchenne muscular dystrophy erythrocytes was similar to that of normal erythrocytes. The membrane environment in the nonpolar region, however, was quite different from that of normal erythrocytes, judged by the spectra with 2-(14-carboxytetradecyl) - 2 - ethyl - 4,4 - dimethyl - 3 - oxazolidinyloxyl as probe. The temperature dependence of the ratio of the line height of central field to that at the low field showed two inflection points in normal erythrocytes at pH 7.4 (13.5 degrees -16.5 degrees and 37.5 degrees -40.5 degrees C, respectively) but the inflection point in the lower temperature range was not detected in Duchenne muscular dystrophy erythrocytes. When pH was varied, an abrupt decrease in the ratio was observed at pH 5.9-5.6 in normal erythrocytes whereas there was a gradual decrease over the range of pH from 6.6 to 5.0 in Duchenne muscular dystrophy erythrocytes. The rate of reduction of the radical 2-(3-carboxypropyl)-4,4-dimethyl-2-tridecyl-3-oxazolidinyloxyl by ascorbate in normal erythrocytes was faster than that in Duchenne muscular dystrophy erythrocytes. Treatment of both erythrocytes with phloretin markedly reduced the rate of reduction by ascorbate and eliminated the difference in the two types of erythrocyte. These results indicate that in Duchenne muscular dystrophy the erythrocyte membrane is involved as well as the muscle cell.

Adolescent↗
PubMed1978

Evidence of a small molecule in mouse Leydig cell tumors which inhibits the conversion of estrogen receptor from 4S to 5S.

The activation process of cytosol estrogen receptor (RE) from mouse Leydig cell tumors was investigated. When RE from tumors which were affected in their growth by estrogen was heated at 25 C for 30 min in high ionic strength buffer it was converted from native 4.0S to a transformed (5.3S) state. Dialysis of the cytosol from these tumors at 0-4 C in either the presence or absence of estradiol also resulted in conversion to 5.3S when estradiol was added before the sample was applied to the sucrose density gradient. When the dialyzed cytosol was applied to a sucrose density gradient without estradiol, the peak of estrogen binding capacity tested by adding E2 to the fractions from the gradient, occurred at approximately 4S. The dialysate of cytosol had an inhibitory effect on activation by warming. Dialysis of cytosol in the presence of estradiol enhanced the translocation of estradiol-receptor complex to nuclei. Molecular weight (approximately 128,000) and frictional coefficient (f/f0 1.62) of the estrogen-receptor complex dialyzed in the presence of high salt concentration were identical with those of warmed RE complex, but quite different from the native RE (approximately 73,000 daltons, frictional coefficient 1.48). This evidence indicates the presence in the cytosol of one or more small molecules which, when noncovalently bound to RE, inhibit the conversion of the native cytosol RE to the transformed state R'E2RE, having an additional protein unit.

Animals↗
PubMed1978

The possible roles of membrane organization in the activity of androgen biosynthetic enzymes associated with normal or tumorous mouse Leydig cell microsomes.

The enzymes involved in conversion of pregnenolone to testosterone in Leydig cell tumors showed a wide distribution among smooth endoplasmic reticulum (SER), rough endoplasmic reticulum (RER), and cytosol, while these enzymatic activities in normal testes were associated primarily with smooth endoplasmic reticulum. Progesterone, used as a substrate in the presence of an NADPH-generating system, was metabolized to androstenedione and finally to testosterone by microsomes from some strains of tumor which did not form testosterone from exogenous labeled androstenedione. Treatment of microsomal membranes from normal testes with 0.1 M Ca++ and Mg++ caused a marked decrease in 17 beta-dehydrogenase activity, measured as conversion of exogenous [3H]androstenedione to [3H]-testosterone, without serious effects on activities of 3 beta-ol-dehydrogenase or 17 alpha-hydroxylase. Studies of initial velocity kinetics showed that treatment with magnesium ion resulted in a marked reduction in affinity of androstenedione for 17 beta-dehydrogenase while the maximum velocity was the same as in untreated microsomes. Also, experiments using [14C]progesterone and [3H]androstenedione simultaneously as substrates demonstrated that treatment with Mg++ ion made it more difficult for exogenous [3H]androstenedione to reach the active site of 17 beta-ol-dehydrogenase than [14C]androstenedione formed in the microsomal membrane from [14C]progesterone. Microsomal proteins were more easily solubilized and 3 beta-ol-dehydrogenase was more severely influenced by Mg++ ion in tumor membranes than in normal microsomes.

17-Hydroxysteroid Dehydrogenases↗
PubMedDate not supplied

Stimulation by estrogen and progesterone of the in vivo growth of transformed murine Leydig cells only at the limited early phase of growth.

B-1 F is a cell line established from estrogen-responsive murine Leydig cell tumor and maintained in vitro. We investigated the effects of steroid hormones on the growth of tumors produced by the inoculation of B-1 F cells into mice. When tumor tissues were transplanted into castrated male mice, injections of estradiol-17 beta (E2) or progesterone shortened the period before tumors became palpable, but did not affect the growth rates of tumors after tumors became palpable. Injections of E2 or progesterone from the time when tumors became palpable did not affect the growth of tumors, and the discontinuation of injections of E2 or progesterone during the middle growth phase showed no effect on the growth of tumors. E2 or progesterone also did not increase the mitotic indices of tumors after they became palpable. E2 and progesterone did not stimulate the proliferation of dispersed tumor cells in vitro. The present results suggested that steroid hormones might exert their actions only at the limited early phase of growth of transplanted steroid hormone-responsive tumors in vivo.

Animals↗
PubMedDate not supplied

Regulatory role of arachidonic acid-derived metabolites for proliferation of transformed murine Leydig cell in serum-free culture condition.

The growth-regulatory ability of eicosanoids from arachidonic acid is poorly understood. To investigate their role in cell growth, we cultured transformed murine Leydig cells (B-1 or B-1 F) in serum-free medium supplemented with various compounds modulating arachidonic acid metabolism. The addition of 5-lipoxygenase inhibitors (AA 861, NDGA and quercetin) showed a growth-stimulative effect. On the other hand, their growth was remarkably inhibited by arachidonic acid added into the culture medium. This growth-inhibiting ability of arachidonic acid was almost completely reversed by a simultaneous exposure of B-1 cells to lipoxygenase inhibitor. Exogenously added 5-HETE inhibited cell proliferation in a dose-dependent manner. These results suggest that 5-lipoxygenase-catalyzed products from arachidonic acid have the ability to suppress the proliferation of some transformed cells.

Acetophenones↗
PubMedDate not supplied

Effects of androgen, fibroblast growth factors or other various growth factors on growth of Shionogi carcinoma cells in a protein-free medium.

Shionogi carcinoma 115 (SC115) has been accepted for 20 years as an androgen-responsive mouse mammary tumor. We have recently established an androgen-dependent cloned cell line (SC-3) from a SC115 tumor. We found in the present study that the growth of SC-3 cells can be stimulated by 10(-8) M testosterone (up to 100-fold) even in a protein-free medium beginning from plating [Ham's F-12: Eagle's minimum essential medium (1:1, v/v)]. In the protein-free culture, the proliferation of SC-3 cells was also found to be stimulated by acidic or basic fibroblast growth factor (FGF) alone (up to 50-fold) among various growth factors examined such as FGFs, insulin, insulin-like growth factor (IGF)-I, IGF-II, nerve growth factor, platelet-derived growth factor, epidermal growth factor, transforming growth factor (TGF)-alpha and TGF-beta. The testosterone (10(-8) M)- or FGF (10 ng/ml)-induced growth of SC-3 cells was abolished only by TGF-beta (greater than or equal to 1 ng/ml) among various growth factors examined. We show for the first time in this study an androgen-dependent growth of cancer cells (SC-3) in a protein-free medium. In the protein-free medium, growth of SC-3 cells is also stimulated by FGFs, and the androgen- or FGF-induced growth is inhibited only by TGF-beta.

Animals↗
PubMedDate not supplied

Effects of estrogen and tamoxifen on secretory glycoprotein synthesis in mouse Leydig cell tumor in vivo.

Effects of estrogen and tamoxifen on the synthesis of secretory proteins were examined using estrogen-responsive mouse Leydig tumor. Estrogenization of host mice bearing the tumor (T 124958-R) resulted in the appearance of the secretory glycoprotein with a molecular weight of 34,000 which was detected by incubation of dispersed cells or minced tissues with [35S]methionine. The discontinuation of in vivo estrogenization decreased the growth rate of the tumor with the simultaneous disappearance of this secretory protein. Transplantation of tumor grown in non-estrogenized mice showed reacquisition of estrogen dependency in terms of tumor growth as well as secretory glycoprotein synthesis. Furthermore, tamoxifen administration to mice enhanced the tumor growth with simultaneous induction of this secretory protein. These results suggest that this secretory glycoprotein can be used as a marker for estrogen- or tamoxifen-dependent growth in vivo.

Animals↗
PubMedDate not supplied

Androgen receptor system in androgen-independent mouse tumor developed from androgen-dependent Shionogi carcinoma 115.

An androgen-independent spindle-shaped cell tumor (NHD) formed from androgen-dependent medullary Shionogi carcinoma (SC115) in DS mice was examined. Although NHD tumors transplanted in female or male mice exhibited almost the same growth speed, the cytosol of this tumor was found to contain an androgen receptor which was similar in binding characteristics to SC115 tumor. Although significant amounts of specific binding sites for testosterone and 5 alpha-dihydrotestosterone were found in the SC115 nuclei as well as in the NHD nuclei shortly after the injection of 3H-testosterone, the androgens in the NHD nuclei disappeared rapidly. The androgen-independency of this tumor may be attributed to a rapid dissociation of the androgen-receptor complexes from NHD nuclei.

Animals↗
PubMedDate not supplied

Analysis of factors affecting the graft oxygenation state in living related liver transplantation.

BACKGROUND/AIMS: In liver transplantation, graft dysoxia after reperfusion may lead to graft failure. The aim of this study is to investigate the relationship between the factors, which were supposed to affect the oxygen supply to the graft, and the oxygenation state of the graft in order to determine which factor is important to prevent the graft from dysoxia. MATERIALS AND METHODS: The relationship between oxygen supply and oxygenation state of the graft was investigated in 56 successful cases of living related liver transplantation. Factors affecting the oxygen supply to the graft were considered as follows; portal venous flow (PVF), mean velocity of the hepatic artery (HA-Vm), hemoglobin concentration in the peripheral blood (Hb), size of the graft liver relative to the recipient body weight (G/R ratio), partial oxygen pressure in the arterial blood (PaO2), and rate-pressure product (BP*PR). Oxygenation state of the graft was estimated by oxygen saturation of hemoglobin in the graft tissue (graft SO2) as measured by tissue near infrared spectroscopy. RESULTS: 1) Graft SO2 was rather independent of PVF and HA-Vm probably due to compensatory interrelation between the portal venous flow and hepatic arterial flow. 2) Significant correlation between G/R ratio and graft SO2 was observed after portal reflow (p < 0.01), but the correlation diminished after hepatic arterial reflow. Positive correlation between G/R ratio and AKBR after portal reflow suggested that the graft with large G/R ratio is likely to suffer dysoxia early after reperfusion. 3) Graft SO2 was positively correlated with Hb (p < 0.05), while there was no significant correlation between graft SO2 and PaO2 or BP*PR. CONCLUSION: This study clarified the contribution of the factors which were supposed to affect the oxygen supply to the graft and the oxygenation state of the graft, and which factor is important to prevent the graft from dysoxia.

Adolescent↗