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Biomedical subjects

T Onaya

Publications and source records attributed to T Onaya.

At least 181 records · Page 10Linked to original sources
PubMed1985

Parvalbumin in rat cerebrum, cerebellum and retina during postnatal development.

Radioimmunoassay and immunohistochemical studies were performed on the occurrence and distribution of parvalbumin-like immunoreactivity (PA-LI) in developing rat cerebrum, cerebellum and retina. No PA-LI was detected in the nervous tissues of the newborn animals. In the cerebrum, the PA-LI appeared in non-pyramidal neurons at the 2nd postnatal week and increased linearly until the 8th week. In the cerebellum, a rapid increase in the PA-LI took place at the 2nd week, with an enrichment of the antigen to Purkinje neurons. In the retina, amacrine cells contained PA-LI, the levels of which increased from the 2nd to 4th week. Regulation of intracellular Ca2+ concentration may be one of the important factors for the maturation of the central nervous system.

Animals↗
PubMed1985

The effects of thyroxine and methimazole treatment on the synthesis of prostacyclin (PGI2) in the rat.

The effects of thyroxine (T4) and methimazole administration on plasma prostacyclin (PGI2) levels in vivo and on PGI2 release by aortic rings incubated in vitro were investigated in rats. Male rats were given single injection of T4 (200 micrograms/100 g body wt) ip every 24 h for either 3, 7 or 14 days for hyperthyroid rats. For hypothyroid rats, a group of rats were given methimazole (0.01 % in drinking water) for 14 days. PGI2 concentrations were determined in plasma and also in the medium in which aortic rings were incubated. PGI2 was measured as 6-keto-PGF1 alpha by RIA. Plasma PGI2 levels in T4-treated groups were found to be significantly higher than those of control animals. Aortic rings obtained from rats given single injection of T4 for 7 and 14 days showed significant increases in release of PGI2 into the incubation medium. In contrast, rats given methimazole for 14 days showed a significant decrease in the production of PGI2 by aortic rings without any significant changes in plasma levels. Direct addition of T4 into the incubation medium did not cause any significant changes in PGI2 release by aortic rings obtained from control rats. These results suggest the regulatory role of thyroid hormone in PGI2 synthesis in vivo.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Parvalbumin exists in rat endocrine glands.

Simple and rapid purification procedures for parvalbumin, one of the Ca2+-binding proteins (extracted from rat skeletal muscle), were developed, and its antiserum was produced in rabbits to measure the parvalbumin content of various rat tissues by RIA. The heat treatment, ammonium sulfate fractionation, and trichloroacetic acid precipitation of soluble fraction from rat skeletal muscle followed by single diethylaminoethyl Sephadex A-50 column chromatography yielded a pure 120 mg protein from 150 g skeletal muscle. Amino acid analysis, together with electrophoretic mobility, indicated that the protein was identical to parvalbumin. The antisera to this rat skeletal muscle parvalbumin (raised in rabbits) did not cross-react with calmodulin or S-100 proteins. The RIA for parvalbumin using this antisera and [125I]parvalbumin revealed that skeletal muscle and brain contained high levels of the antigen; the values of which were 69,486 +/- 4,933.1 and 881 +/- 165.6 ng/mg protein, respectively. However, the parvalbumin antigen in the heart, lung, liver, and spleen could not be detected. On the other hand, the contents of the antigen in the endocrine glands (in nanograms per mg protein) were as follows: pituitary (125 +/- 46.6), thyroid (108 +/- 50.0), adrenal (341 +/- 64.3), testes (227 +/- 37.2), and ovaries (218 +/- 10.1). All of these values were comparable to levels of antigen found in the brain sample. These results suggest an important role for parvalbumin in endocrine glands.

Adrenal Glands↗
PubMed1985

Iodide modulation of Ca2+ efflux from mouse thyroid.

In a preceding report, we showed evidence that thyrotropin (TSH) stimulates Ca2+ efflux from mouse thyroid gland and that TSH stimulation of Ca2+ efflux is inhibited by acute administration of excess iodide to mice fed a low iodine diet (Hashizume et al., 1984). The observations suggested that iodide inhibits Ca2+ efflux through an inhibition of TSH-sensitive adenylate cyclase activity. We found further, that iodide inhibits dibutyryl cyclic AMP (DBC)-stimulated Ca2+ efflux. The results suggested that iodide influences the step subsequent to the generation of cyclic AMP. In this report, we studied whether iodide can inhibit Ca2+ efflux by a mechanism which is distinct from adenylate cyclase inhibition. The acute administration of excess iodide to mice fed a regular diet did not decrease the basal Ca2+ efflux rate in the thyroid. TSH-induced stimulation of Ca2+ efflux in thyroids obtained from regular diet-treated mice was not modified by iodide administration. Iodide injection to mice fed a low iodide diet, however, decreased the basal Ca2+ efflux rate though the content of cyclic AMP in the thyroids was not altered by this treatment. The decreased-Ca2+ efflux rate induced by iodide in the low iodine diet-treated thyroids was not modified by TSH in vitro. The results indicate that an acute administration of excess iodide in thyroid inhibits Ca2+ efflux not only by an inhibition of adenylate cyclase but also by an inhibitory action which is distinct from the adenylate cyclase inhibiting action of iodide.

Animals↗
PubMed1985

A case of Cushing's syndrome associated with possible adrenomedullary hyperplasia.

A 57-year-old male, who had been suffered from hypertension and diabetes mellitus for 10 years, was admitted to the hospital because of thirst, lassitude and muscle wasting. On admission, his urinary excretion of 17-OHCS and plasma cortisol levels were elevated without diurnal variations. Plasma ACTH levels were found to be very low with repeated determinations. Dexamethasone suppression test, 2 mg 4 times a day orally for 2 days, showed no changes in plasma cortisol levels and only a mild reduction in urinary 17-OHCS excretion. Estimation of urinary catecholamines showed an increase only in norepinephrine. Abdominal computerized tomography and radionuclide scanning of adrenal glands with 131I-adosterol demonstrated a well-defined adrenal mass in the left side without apparent changes in the right side. 131I-metaiodobenzylguanidine scintigraphy was negative. At surgery, his left adrenal medulla was found to be hypertrophic in addition to the cortical tumor. The left adrenal gland was also removed. After surgery, excretion of urinary catecholamines fell to nearly the normal range and he was discharged without insulin and antihypertensive drugs. Microscopically, the cortical tumor is an adenoma consisting of lipid laden cells and eosinophilic compact cells. Medullary cells were distinctly hyperplastic in appearance and many of the cells were extensively vacuolated, suggesting an active functional status. The present report describes a patient with Cushing's syndrome who showed increased urinary catecholamine excretion due to the possible coexistence of adrenal medullary hyperplasia. As far as we know, this is the first case of Cushing's syndrome with this abnormality.

Adrenal Medulla↗
PubMed1984

Thyrotropin-induced acceleration of calcium efflux from mouse thyroid: evidence for inhibition by excess iodide.

We investigated the effect of TSH on calcium transport in mouse thyroid, as well as the influence of iodide thereupon. Thyroid lobes were incubated in Krebs-Ringer bicarbonate buffer containing [45Ca2+] and the time-dependent uptake of [45Ca2+] by the lobes was observed. In the presence of 0.5 mU/ml TSH, the uptake of [45Ca2+] was significantly depressed at early phases of incubation (from 20 to 40 min). Similarly, (Bu)2cAMP (DBC) depressed the [45Ca2+] uptake. The efflux of calcium was also studied by using thyroid lobes preloaded with [45Ca2+]. In the presence of 0.5 mU/ml TSH, [45Ca2+] release from the lobes was doubled in comparison with the control lobes incubated without TSH. DBC similarly accelerated [45Ca2+] release from the lobes. The acute administration of excess iodide to mice fed a low iodine diet inhibits the TSH-induced adenylate cyclase activation in thyroids. The acceleration of calcium efflux induced by TSH was completely abolished by the acute administration of excess iodide in thyroids obtained from animals fed a low iodine diet. Similarly, DBC-induced acceleration of calcium efflux was inhibited by pretreatment with excess iodide. However, the inhibitory effect of iodide on TSH- or DBC-induced acceleration of calcium efflux was not observed in thyroids obtained from mice fed a regular diet. Inhibition of TSH-induced acceleration of calcium efflux by iodide was diminished by treatment of mice with methimazole before iodide. These results suggest that 1) TSH accelerates calcium efflux from the thyroid as a result of accumulation of cAMP in the thyroid, and that 2) iodide inhibits calcium efflux by inhibition of TSH-induced adenylate cyclase activation and by inhibition of the mechanism(s) which is (are) activated by cAMP.

Animals↗
PubMed1984

Transient thyrotoxicosis after unilateral adrenalectomy in two patients with Cushing's syndrome.

We found transient hyperthyroidism in the course of hydrocortisone withdrawal in two patients who had undergone unilateral adrenalectomy to resect cortisol-hypersecreting adenoma. A 38-yr-old woman showed clinical thyrotoxicosis 3 months after the operation. Serum T4, T3 and TBG levels were 11.9 micrograms/dl, 310 ng/dl and 16.5 micrograms/ml, respectively. She was given methimazole (MMI) 15 mg/day for 4 weeks. After the cessation of MMI treatment, she eventually recovered to the euthyroid state. The other patient, a 34-yr-old man showed very mild clinical symptoms of hyperthyroidism 2 months after the operation. Serum T4, T3 and TBG levels were 10.4 micrograms/dl, 240 ng/dl and 14.5 micrograms/ml, respectively. In this case, no antithyroid drug was given. Two to three months after the onset of hyperthyroidism, he returned to the euthyroid state spontaneously. We carefully eliminated the possibility of factitious thyrotoxicosis in both cases. They had neither neck pain nor fever. Both had low radioactive iodine uptake by the thyroid. Therefore, we diagnosed them as painless thyroiditis induced after the resection of hypersecreting adrenal adenoma.

Adrenalectomy↗
PubMed1984

A case of hypokalemic myopathy associated with transient hypothyroidism.

A case of transient hypothyroidism in the course of hypokalemic myopathy is reported. A 69-year-old woman had severe muscle weakness and marked potassium deficiency associated with alkalosis during treatment with thiazide diuretics. The cause of muscle weakness proved to be hypokalemic myopathy confirmed by clinical findings and muscle biopsy. After the episode of hypokalemic myopathy, serum levels of thyroid hormone were lowered (T4; 3.8 micrograms/dl, T3; 54 ng/dl) and that of TSH was elevated (25.1 microU/ml). Antithyroid microsomal antibody was positive (1:25600) and anti-thyroglobulin antibody was negative. About one month after potassium supplement, her thyroid functions returned to normal, along with normalization of serum potassium level. This is the first documented case report of hypokalemic myopathy accompanied by transient hypothyroidism in a patient with autoimmune thyroiditis. We suggest that this transient hypothyroidism might be induced by hypokalemia during the course of autoimmune thyroiditis.

Aged↗
PubMed1978

The biphasic stimulatory and inhibitory effects of concanavalin A on thyroid activation induced by thyrotropin.

Concanavalin A (Con A) was tested for its ability to affect thyroid activation induced by TSH in mouse thyroid lobes. Pretreatment of thyroid lobes with Con A at concentrations from 1.55--400 microgram/ml was found to have biphasic stimulatory and inhibitory effects of the TSH-induced accumulation of cAMP and formation of colloid droplets. Low concentrations of Con A potentiated TSH activation of thyroidal formation of cAMP and endocytosis. In contrast, higher concentrations of Con A markedly inhibited these TSH effects. The inhibitory effects observed after preincubation with Con A were abolished by the addition of alpha-methyl-D-glucoside to the incubation medium. A high concentration of Con A also inhibited cAMP formation induced either by prostaglandin E2 or the long-acting thyroid stimulator. However, the basal and TSH-stimulated glucose oxidation in mouse thyroid lobes was not depressed by a high concentration of Con A. Uptake of 125 I-labeled Con A by thyroid tissues increased with time up to 1 h and was directly proportional to tissue weight. These findings suggest that the specific interaction between Con A and its receptors may lead to conformational changes in the structure of the membranes of the thyroid follicular cells which facilitate TSH-induced thyroid hormone secretion via the adenylate cyclase-cAMP system.

Animals↗
PubMed1978

Evidence for activation by beta2-adrenergic receptors of adenosine 3',5'-monophosphate formation in Ehrlich ascites tumor cells.

The existence of aminergic receptors in mouse Ehrlich ascites tumor cells was studied. L-Isoproterenol in vitro stimulated the formation of cAMP in isolated Ehrlich ascites tumor cells. Stimulation by isoproterenol of cAMP formation was not significantly inhibited by practolol, a beta1-adrenoceptor antagonist-Salbutamol, a beta2-adrenoceptor agonist, markedly stimulated the formation of cAMP in Ehrlich ascites tumor cells at concentrations from 10(-8)-10(-3) M. After the addition of salbutamol, cAMP levels reached a maximum in 10 min and declined to about 2-fold of the basal level to 30 min. The stimulation by salbutamol of cAMP formation was markedly inhibited by butoxamine, a beta2-adrenoceptor antagonist, but not by practolol. Furthermore, the effect of a maximal dose of salbutamol was additive to that of prostaglandin E2. Histamine and 4-methylhistamine, a histamine H2 receptor agonist, had no significant effects. Therefore, it is suggested that a beta2-adrenergic receptor exists in the membranes of Ehrlich ascites tumor cells in terms of the adenylate cyclase-cAMP system.

Albuterol↗
PubMed1978

Altered responsiveness to thyrotropin in thyroid slices of Graves' disease preoperatively treated with excess iodide.

In a previous paper, we demonstrated that the acute administration of excess iodide inhibits the adenylate cyclase-cAMP system in mouse thyroid lobes. In the present study, we examined whether presurgical therapy with stable iodide reduces the responsiveness to TSH in thyroid tissues from patients with Graves' disease. Eight patients with Graves' disease were presurgically treated with methimazole and stable iodide and six were given methimazole alone. Normal tissues from five patients with thyroid nodules were also tested. We have found that stimulation by TSH (5 and 50 mU/ml) of cAMP formation in thyroid slices from patients preoperatively treated with methimazole and iodide is significantly less than in slices from patients treated with methimazole alone. Similar observations were also made with other thyroid stimulators, such as prostaglandin E2 and 4-methylhistamine. Furthermore, thyroid slices from patients treated with methimazole alone responded to TSH to the same degree as slices of normal tissues. The data suggest that one of the reasons for the hyporesponsiveness to TSH in thyroids from patients with Graves' disease is preoperative treatment with stable iodide.

Cyclic AMP↗
PubMed1977

Evidence for the existence of a histamine H2-receptor in the mouse thyroid.

The existence of a histamine H2-receptor in the thyroid was investigated. Histamine in vitro stimulated the formation of cyclic AMP and colloid droplet formation in mouse thyroid lobes. Stimulation by histamine of cyclic AMP formation in mouse thyroid lobes was significantly inhibited by metiamide, a histamine H2-receptor antagonist. 4-Methylhistamine, a histamine H2-receptor agonist, markedly stimulated cyclic AMP formation, whereas 2-methylhistamine, a histamine H1-receptor agonist, was ineffective. The stimulation by 4-methylhistamine of cyclic AMP formation was markedly inhibited by metiamide, but not by chlorpheniramine, a histamine H1-receptor antagonist. In contrast, metiamide did not affect cyclic AMP formation induced either by TSH or by the long-acting thyroid stimulator. Therefore, it is suggested that there exists a histamine H2-receptor in the membranes of the thyroid follicular cells which facilitate thyroid hormone secretion via the adenylate cyclase-cyclic AMP system.

Animals↗
PubMed1977

Effects of biogenic amines on the formation of adenosine 3',5'-monophosphate in human thyroid slices.

The effects of various concentrations of biogenic amines on the formation of adenosine-3', 5'-monophosphate (cyclic AMP) and their interactions with other thyroid stimulators were investigated in human thyroid slices from normal and Graves' disease. Most of biogenic amines were found to have the stimulatory effects to some extent. Among the biogenic amines tested, histamine was the most potent thyroid stimulator, norepinephrine and serotonin, the intermediate in terms of cyclic AMP formation. The effect of histamine was almost as potent as TSH in thyroid slices from Graves' disease. This stimulatory effect of histamine was blocked by metiamide, a histamine H2-receptor antagonist, but not by chlorpheniramine, a histamine H1-receptor antagonist. The effect of norepinephrine was completely inhibited by propranolol, but not by phentolamine. Polyphloretin phosphate did not inhibit norepinephrine- or histamine-induced cyclic AMP formation, while it significantly depressed cyclic AMP formation induced by prostaglandin E2. The maximal effect of histamine was additive to that of TSH. It is suggested that biogenic amines, histamine and norepinephrine, in particular, have the thyroid receptors different from that of TSH or prostaglandin E2 and could play an important role in thyroid physiology.

Catecholamines↗
PubMed1976

[Studies on the thyrotropin receptor in the thyroid: positive cooperativity of Concanavalin A binding and its biphasic effects on thyroid activation induced by thyrotropin (author's transl)].

Concanavalin A (Con A) was tested for its ability to affect thyroid activation induced by the thyroid stimulators in mouse thyroid tissues. Con A was found to have the biphasic stimulatory and inhibitory effects of thyrotropin (TSH)-induced cyclic AMP formation and endocytosis, a step in thyroid hormone secretion, in mouse thyroid tissues. Low concentrations of Con A potentiated TSH-stimulated cyclic AMP formation and endocytosis. In contrast, high concentrations of Con A markedly inhibited TSH stimulations. These effects were reversed by the addition of methyl-alpha-D-glucoside to the second preincubation medium (without Con A) prior to TSH. A high concentration of Con A alone did not depress the basal levels of cyclic AMP or basal glucose oxidation in thyroid tissues. A high concentration of Con A also inhibited cyclic AMP formation induced by prostaglandin E2 and the long-acting thyroid stimulator (LATS). Binding of 125I-labeled Con A to thyroid tissues increased with time up to 75 min and was very slowly reversible after attainment of equilibrium. Binding was directly proportional to tissue weight. Scatchard plot analysis on the binding of 125I-labeled Con A to thyroid tissues indicated a positive cooperativity which seemed to be well correlated to the biphasic effects.

Animals↗