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Biomedical subjects

E Ogata

Publications and source records attributed to E Ogata.

At least 361 records · Page 20Linked to original sources
PubMed1979

Failure to demonstrate stimulatory effect of prolactin on vitamin D metabolism in vitamin-D-deficient rats.

The effect of administration of bovine prolactin in vivo on renal 1 alpha-hydroxylase (1 alpha-OHase) activity was investigated using thyroparathyroidectomized and sham-operated vitamin-D-deficient male rats. A high dose (1.5 IU/hr) and a low dose (0.3 IU/hr) of bovine prolactin was constantly infused into the cannulated femoral vein for 6 hr or 30 hr. The accumulation of 1 alpha, 25-hydroxyvitamin D3 [1 alpha, 25-(OH)2-D3] in plasma produced from 25-hydroxy-vitamin D3 (25-OH-D3) was calculated from the 6-hr conversion of intravenously injected [3H]-25-OH-D3 to [3H]-1 alpha, 25-(OH)2-D3. Both high dose and low dose of prolactin administration caused no significant stimulatory effect on 1 alpha-OHase activity in TPTX animals. Also, in sham-operated rats the prolactin treatment produced no significant change in the 1 alpha-OHase activity. Plasma calcium concentrations showed a tendency to increase slightly. These results suggest that prolactin has no direct stimulatory role on renal 1 alpha-OHase activity in rats. Its effect on calcium metabolism may be mediated by a different mechanism(s).

Animals↗
PubMed1979

Ca2+-induced activation of succinate dehydrogenase and the regulation of mitochondrial oxidative reactions.

1. In rat liver mitochondria in vitro, an activation of succinate dehydrogenase [succinate: (2,6-dichloroindophenol)oxido-reductase], an inner membrane enzyme, was induced by Ca2+ at extramitochondrial concentrations (about 1.3 micron) close to those estimated in the cytosol. 2. The activation required both substrate (succinate) and ATP, and occurred whether mitochondria were coupled (Ca2+ could be accumulated) or uncoupled (Ca2+ could not be accumulated) by classical uncouplers. 3. The activation by Ca2+ of the uncoupled mitochondria was accompanied by a modest but significant change in the mitochondrial morphology as judged from light scattering measurements and electron microscopy. 4. In the uncoupled mitochondria, oxaloacetate added externally diminished the activation by Ca2+. In addition, the amount of oxaloacetate produced endogenously from succinate via malate fell after Ca2+ and ATP addition. However, the extent of the fall in mitochondrial oxaloacetate did not correlate with the degree of activation of succinate dehydrogenase. 5. The activation by Ca2+ of the uncoupled mitochondria was accompanied by a reductive shift of pyridine nucleotide and coenzyme Q, and an oxidative shift of flavoproteins and cytochromes b, c, and a-a3. 6. In the situation where the Ca2+-induced activation of succinate dehydrogenase (and consequently succinate oxidation) took place in the uncoupled mitochondria, oxidations of 3-hydroxybutyrate and pyruvate were markedly suppressed. 7. From the above findings, it is concluded that Ca2+ action on the mitochondrial inner membrane activates mitochondrial succinate dehydrogenase, and this action produces an inhibition of electron transport between NAD and flavoprotein. In view of the location of these reactions in the inner membrane, a conformation change of the membrane is suggested as a common cause.

Animals↗
PubMed1979

A case of multiple extra-adrenal pheochromocytomas.

A 22 year old man with two extra-adrenal pheochromocytomas located in the mediastinum and in the pelvis is presented. We believe this is the first report in Japan of extra-adrenal multiple pheochromocytomas in adult located in the two distant places.

Adult↗
PubMed1978

An estimation of the parathyroid hormone secretion rate in vitamin D deficient rats.

In an attempt to define the rate of endogenous secretion of parathyroid hormone in vitamin D deficiency, graded amounts of hormone were infused constantly into vitamin D deficient and vitamin D fed acutely thyroparathyroidectomized rats in a perfusion balance study. The dose of hormone needed to compensate for acute thyroparathyroidectomy was estimated. Serum levels of calcium and phosphorus, renal clearances of phosphorus and urinary excretion of cyclic AMP, each determined 16 hr after the surgery, were employed as parameters of the hormone effect. It was concluded that, in the condition of the perfusion balance study, the secretion rate of parathyroid hormone was 5.1-8.6 USP u/hr in the vitamin D deficient animals compared with 0.81-0.84 USP u/hr in the control.

Animals↗
PubMed1978

Report on a case of functioning thyroid carcinoma provoking thyrotoxicosis with review of literature.

A 57-year old woman with thyroid carcinoma manifesting overt thyrotoxicosis is presented. After the patient had been made euthyroid with propylthiouracil, right lobectomy and lymph node dissection were performed. Permanent paraffin sections revealed follicular adenocarcinoma with capsular and vascular invasion. Metastases to the right humerus, both femurs, the skull and pleural cavity became prominent with the recurrence of thyrotoxicosis and the patient died 2 years and 3 months after operation. The clinical evidence indicates that thyrotoxicosis in the present case is caused by the excessive secretion of thyroid hormone by both the original carcinoma and the secondary deposits. Twenty three similar cases reported in the English and Japanese literatures are summarized.

Adenocarcinoma↗
PubMed1978

A case of Turner's syndrome with hyperthyroidism.

A female patient with classical gonadal dysgenesis associated with Graves' disease is reported. The karyotype was mosaicism of 45,X/46,X,i(Xq). The relationship among Graves' disease, Hashimoto's thyroiditis and Turner's syndrome is discussed along with a review of the reported cases.

Adult↗
PubMed1978

Thyroid hormone formation in ectopic thyroid gland. A case study.

Several steps of thyroid hormogenesis were studied on a subhyoid ectopic thyroid tissue in a case of compensated hypothyroidism with simultaneous sublingual and subhyoid ectopic thyroid. The patient, a 19-year-old girl, had normal values for serum T4, T3U and T3, and an elevated serum TSH level. The thyroidal 131I uptake was elevated both at 3 h and 24 h after oral 131I intake. No significant discharge of radioiodine was observed after perchlorate load. On the thyroid biopsy specimen, peroxidase activity was shown to be normal by both assays of guaiacol oxidizing and iodinating activity. Thyroglobulin was 19S and was normally iodinated in vitro with peroxidase. Iodine content of thyroglobulin was within the normal range. The mean percentage distribution of 131I administered 7 days prior to the biopsy showed no significant difference from the normal pattern. From these studies, no specific defects in thyroid hormogenesis could be detected in this case. It is suggested that abnormalities in thyroid function in this case are mainly due to insufficient functioning mass in the ectopic thyroid.

Adult↗
PubMed1977

Oxidative response to aldosterone of pyridine nucleotide in rat kidney in situ.

In an attempt to elucidate early biochemical events in the action of aldosterone on rat kidney in situ, the response of the pyridine nucleotide oxidation-reduction state of surface cells was directly and continuously recorded with an organ-fluorometer. Intravenous administration of aldosterone induced a rapid (maximum response in 10 min) and dose-related (2.5-25 microng/100 g rat) oxidative response that was specific to aldosterone and to the kidney. The oxidative response was 1) detectable with minute dise (approximately 0.2 microng/100 g rat) of hormone: 2) reproduced by other mineralocorticoids; 3) enhanced by a maneuver for expanding the extracellular fluid compartment or by adrenalectomy; and 4) prevented by spironolactone, progesterone, actinomycin D, and cycloheximide. All of these data argue that the redox response is related to the subsequent changes in aldosteronemediated ion transport. Experiments with an uncoupler and with redox substrates showed that mitochondrial NADH was the major nucleotide pool responding to hormone. The oxidation was not accompanied by changes in the adenylate energy charge level of the whole organ. These observations support the view that aldosterone acts on energy metabolism of tubular cells before developing apparent cation transport effects.

Adenine Nucleotides↗