Biomedical subjects

T Kusakabe

Publications and source records attributed to T Kusakabe.

At least 181 records · Page 10Linked to original sources

PubMed1982

The glomus cell of the carotid labyrinth of Xenopus laevis.

The ultrastructure of the glomus cells of the carotid labyrinth was investigated in the anuran, Xenopus laevis. These cells show many catecholamine containing granules. About 50 cells in groups of 3-5 are located near the sinusoids. Morphologically, their organelles are similar to those previously reported in Bufo vulgaris. Striking features are (1) intimate appostion of the glomus cell to smooth muscle (g-s connection), (2) gap junctions between adjacent glomus cells, (3) exocytotic figures. Based on these findings a possible function of the glomus cell is discussed.

Animals↗

PubMed1978

An increase of plasma triiodothyronine and thyroxine after administration of dexamethasone to hypothyroid patients with Hashimoto's thyroiditis.

In an attempt to study the effect of adrenal steroids on plasma thyroid hormone concentration in patients with Hashimoto's thyroiditis, 2 mg dexamethasone was administered for 2-4 weeks to 9 patients with normal plasma TSH, 3 patients with compensatory increase of plasma TSH, and 10 patients with a marked elevation of plasma TSH. Dexamethasone depressed plasma T4, T3, and TSH and reduced thyroid size in nine euthyroid patients, whereas a similar treatment did not affect plasma T3 and T4, but reduced plasma TSH and thyroid size in three patients with compensatory increase of plasma TSH. In contrast, dexamethasone elevated plasma T3 and T4 in 10 hypothyroid patients with a marked elevation of plasma TSH. The increase of T3 was more than that of T4, suggesting preferential secretion of T3. Plasma TSH was reduced, but was still above normal after administration of dexamethasone. It is suggested that the intrathyroidal autoimmune processes inhibiting thyroid hormone synthesis are significant in patients with more severe Hashimoto's thyroiditis, and that dexamethasone stimulated hormone synthesis by depressing the autoimmune processes.

Adolescent↗

PubMed1976

Thyrotoxic periodic paralysis: a peculiar case with unusual dystonic behavior and variable relations of paralysis to serum potassium levels.

This report describes a male patient, aged 49, with tyrotoxic periodic paralysis. The patient had had episodes of main d'accoucheur for eight years. Since thyrotoxicosis had affected the patient last year, he had had attacks of flaccid paralysis of the limbs associated with main d'accoucheur. While the spontaneous attack was normokalemic and responded favorably to potassium, attacks similar to the spontaneous one were provoked not only by glucose infusion, carbohydrate feeding, and NaCl infusion, but also by oral KCl administration. Transition from hypokalemic to hyperkalemic type of paralysis occurred during potassium treatment of a sodium-induced attack, and that from hyperkalemic to hypokalemic type of paralysis occurred after glucose infusion given during a potassium-induced attack. Intra-arterial epinephrine injection caused prompt paralysis of the perfused hand. A main d'accoucheur was induced in one hand by cooling it in chilled water. The spontaneous attacks of flaccid paralysis disappeared after the patient returned to the euthyroid state, but reappeared when he was treated with high doses of desiccated thyroid. Even when the patient was relieved from thyrotoxicosis, he still experienced stiffness in his hands. The administration of glucose, insulin, and KCl also provoked attacks of paralysis with main d'accoucheur or main d'accoucheur. The disease could be of the normokalemic variety of periodic paralysis with fluctations in the potassium levels depending on the provocative tests employed. It seems that the unusual dystonic behavior of this patient is due not to myotonia, but to muscle spasm resulting from metabolic abnormalities. It could also be suggested that excess thyroid hormones have adverse effects on the development and syndrome of periodic paralysis by abetting a latent hereditary abnormality.

Blood Glucose↗

PubMed1975

Deficient cytochrome b5 reductase activity in nontoxic goiter with iodide organification defect.

A 37-yr-old woman with nontoxic goiter is presented. The thyroid 131I uptake at 3 and 24 hr were, respectively, 77.1% and 81.4% dose. Thiocyanate discharged 65.5% of the accumulated 131I in 30 min. In vitro organification of iodine in the thyroid homogenate from the patient was impaired and it was restored to normal by the addition of H2O2, glucose, and glucose oxidase system, FAD, or reduced cytochrome b5. Riboflavin, FMN, oxidized cytochrome b5, oxidized or reduced cytochrome c, NAD(H), and NADP(H) were ineffective in the reaction. The microsomal NADH-cytochrome b5 reductase activity was definitely low in the patient's thyroid. It was augmented to a normal level by incubation of the microsomes with FAD for 30 min or more. The activities of thyroid peroxidase, G6-PD, 6-PGD, catalase, protease, and NADPH-cytochrome c reductase were within normal limits. The major thyroid protein was normal thyroglobulin which could be readily iodinated in the presence of H2O2 and horse radish peroxidase. These findings suggest the correlation of an iodide organification defect with a cytochrome b5 reductase deficiency. Administration of high doses of FAD led to the restoration of thyroidal iodide organification mechanism associated with an increased thyroid hormone production and to a marked decrease of the goiter. Riboflavin was given without effect even at a high dosage level. Consequently, it seems likely that the deficient cytochrome b5 reductase activity in this patient is due to a defect in the biosynthesis of FAD, the coenzyme of the reductase, from riboflavin.

Adult↗

PubMed1975