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Biomedical subjects

K Noma

Publications and source records attributed to K Noma.

At least 91 records · Page 5Linked to original sources
PubMed1980

Effect of molybdate on activation and stabilization of steroid receptors.

The effects of molybdate on activation and stability of glucocorticoid, androgen, and estrogen receptors were studied. The activation of steroid receptors by heating or dialysis was inhibited by molydate, but molybdate had no effect on the nuclear binding of previously activated steroid-receptor complexes. The inhibitory effect of molybdate on activation was concentration dependent and was reversed when molybdate was removed by dialysis or gel filtration on Sephadex G-25. The steroid-binding capacities of the unoccupied glucocorticoid and androgen receptors were markedly reduced by removal of a small molecular weight factor(s) from the cytosol by dialysis or gel filtration on Sephadex G-25, even at 0 C. Molybdate blocked both this loss of steroid-binding ability on dialysis and also the heat-induced destabilization of the receptors. The dialysate of rat liver cytosol and molybdate had synergistic effects in increasing the stability of the glucocorticoid receptor in the cytosol after gel filtration at 25 C. These findings suggest that activation and destabilization have a common mechanism which involves a small molecular weight component(s) and that molybdate has a specific inhibitory effect on this mechanism.

Animals↗
PubMed1980

Relative potency in acute and chronic suppressive effects of prednisolone and betamethasone on the hypothalamic-pituitary-adrenal axis in man.

The relative potency in the hypothalamic-pituitary-adrenal (HPA) suppression of both prednisolone and betamethasone was examined in an acute study with normal volunteers and in a chronic study with glucocorticoid-treated patients. Circadian rhythm of plasma cortisol was studied after a single dose administration of 5 to 30 mg prednisolone or 0.5 to 3.0 mg betamethasone at 8:00 hr. Morning-rise of plasma cortisol occurred on the morning after the administration of 30 mg or less prednisolone but no morning rise was noted after the administration of 1.0 mg or more betamethasone. Plasma ACTH was slightly elevated on the morning after 30 mg prednisolone administration but showed low levels throughout the night after 3.0 mg betamethasone administration. Plasma cortisol responsiveness to ACTH was examined in patients before and during therapy with either prednisolone or betamethasone. The basal cortisol level was not suppressed and the responsiveness to ACTH remained nearly normal during long-term 5 mg prednisolone therapy, but these were completely suppressed during long-term 5 mg betamethasone therapy. The responsiveness to ACTH was nearly normal in patients receiving alternate-day therapy with prednisolone in such large doses as 50 or 60 mg every other day, but was completely suppressed in patients receiving 1.0 mg betamethasone every other day. The relative potency of betamethasone in acute and chronic suppressive effects on the HPA system seems to be much stronger than that of prednisolone in equivalent doses with comparable anti-inflammatory effects. It is also suggested that the alternate-day therapy with such long-acting steroids as betamethasone are useless in preventing HPA suppression.

Adrenocorticotropic Hormone↗
PubMed1978

Increased serum oestrone and oestradiol following spironolactone administration in hypertensive men.

The present study was undertaken to evaluate long-term effects of spironolactone on basal serum oestrone, oestradiol, testosterone, LH and prolactin concentrations in hypertensive male patients. Serum prolactin response to TRH was also evaluated. Patients were divided into two groups: a conventional-dosage group, consisting of six males with essential hypertension who took 75 to 150 mg of spironolactone daily for 12 weeks, and a high-dosage group, consisting of two males with idiopathic hyperaldosteronism who took 300 mg of spironolactone daily for more than 40 weeks. In the conventional-dosage group, serum oestrone concentrations significantly increased (P less than 0.01) at 12 weeks, serum oestradiol concentrations gradually increased throughout the study period, however, the increments were not statistically significant (P less than 0.2). Basal serum testosterone, LH and prolactin concentrations were not significantly changed throughout the study period. Enhancement of serum prolactin response to TRH was not found in any of the patients in the conventional-dosage group. In the high-dosage group, serum oestrone maintained high levels from the beginning of this study, and serum oestradiol concentrations increased with the development of gynaecomastia. Serum testosterone, LH and prolactin concentrations did not show any definite change throughout the study period. Thus, long-term spironolactone treatment increased the serum levels of oestrone and oestradiol in hypertensive men followed by the development of gynaecomastia. The elevation in circulating oestrogens could well explain the oestrogenic side-effects of spironolactone treatment.

Adult↗
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↗
PubMed1977

[Effect of biogenic amines on rat anterior pituitary cyclic AMP].

The effects of biogenic amines on the formation of adenosine-3',5' monophosphate (cAMP) in the anterior pituitary of rats were investigated. Pituitary halves were preincubated in a Krebs-Ringer bicarbonate buffer (pH 7.4) containing theophylline (10(-2)M) at 37 degrees C for 30 minutes and incubated in a fresh buffer for 15 minutes after the addition of test substances. Noradrenaline at 4 X 10(-4)M and serotonin at 3.3 X 10(-4)M were effective in elevating cAMP, but dopamine at 2 X 20(-4)M was ineffective. The beta adrenergic blocking agent, propranolol, effectively antagonized the cAMP response to noradrenaline, but the alpha adrenergic blocking agent, phentolamine, did not. The serotonin antagonist, methysergide, remarkably antagonized the cAMP response to serotonin, but the alpha and beta adrenergic agents did not.

Animals↗
PubMed1976

Macromolecular lactate dehydrogenase linked to serum IgG of a patient with liver cirrhosis.

An anomalous zymogram of lactate dehydrogenase (LDH) in the serum from a patient with liver cirrhosis was reported. Agar-gel electrophoresis of serum showed an extra LDH band close to the anodic side of LDH5 and a wide band of LDH5. Gel filtration of patient's serum in Sephadex G-200 demonstrated an abnormal LDH fraction eluted between immunoglobulin G (IgG) and macroglobulin in addition to a normal LDH component. Chromatographically abnormal LDH was demonstrated on agar gel as extra and wide LDH5 bands and resembled closely human hepatic LDH in various physico-chemical properties such as inhibition by urea or substrate, stability against heat, and Michaelis-Menten's constant. Immunological analyses demonstrated that abnormal LDH could be in the state combined with IgG. Molecular weight of the complex estimated by gel filtration was approximately 300,000. Mixtures of the heated patient's serum with normal or patient's hepatic LDH showed abnormal LDH fraction by gel filtration, whereas abnormal fraction was not demonstrated when heated normal serum was mixed with normal or the patient's hepatic LDH. These results strongly suggest that the occurrence of anomalous LDH zymogram in patient's serum is due to a formation of LDH-IgG complex, which is based on the binding of essentially normal hepatic LDH and abnormal IgG.

Adult↗