Thyroid glands of chick embryos from 7 to 20 days of incubation were studied with the electron microscope. In 7, 8 or 9 day-old embryos in which a colloid is not yet formed, the vacuole systems are not well developed in the epithelial cell. A few mitochondria, PALADE's particles and small GOLGI fields without large vacuoles are distributed throughout the whole cytoplasm of the secretory cell.
At 9-10 days when colloid-containing follicles and intracellular droplets of low density appear in the epithelial cell cords, the rough-and smooth-surfaced endoplasmic reticulum also becomes distinct. Sometimes the limiting membrane of this droplet continues with the rough-surfaced endoplasmic reticulum. This suggests that the granule of low density is produced in the rough-surfaced endoplasmic reticulum. Mitochondria observed near the outer surface of this reticulum might have also same function in manufacturing this droplet. On the other hand, the granule of high density is produced in the GOLGI vesicles. A typical apocrine secretory process is not observed in the embryonic thyroid of the chick.
Some of the colloid-containing follicles are produced by fusing of the intracellular colloid of one cell and that of an adjacent cell, while others are originated from the intercellular space.
A typical pericapillary structure consisting of two layers of basement membranes and pericapillary space between them is not distinct before 15 days of incubation.

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The adrenocortical activity of male Wistar rats during and following the administration of glucocorticoid was studied and compared wtih that of hypophysectomized rats. An experiment was also undertaken to determine whether or not glucocorticoid has any effect on the steroidogenesis at the adrenal level.
1) The subcutaneous administration of prednisolone produced a rapid reduction in plasma corticosterone, a less rapid reduction in adrenal corticosterone, and a gradual decrease in adrenal weight. Following a 20-day treatment, the adrenocortical activity became almost normal 7 days after withdrawal. The response of plasma and adrenal corticosterone to ACTH was suppressed significantly after a 2-day treatment, while the base-line level was still within normal range, but recovered to normal 7 days after the cessation of the treatment.
2) In hypophysectomized rats, the reduction in plasma and adrenal corticosterone and in adrenal weight was more rapid than in prednisolone treated rats. Although there were many resemblances in the adrenal histology of these two conditions, a distinct difference was observed. The lipid granules in the zona fasciculata were abundant until 30 days after hypophysectomy, while they were reduced soon after the beginning of prednisolone treatment.
3) The administration of prednisolone in hypophysectomized rats did not significantly affect the adrenal histology, nor the plasma and adrenal corticosterone. On the other hand, nor-androstenolone phenylpropionate, a potent androgen, caused a partial repair of the atrophied adrenal cortex after hypophysectomy, although it had no effect on the plasma and adrenal corticosterone. These findings led to the conclusion that the main difference in the adrenal histology of hypophysectomized rats and prednisolone treated rats could not be attributed to the direct action of prednisolone on the adrenal cortex.
4) The administration of prednisolone failed to affect the plasma and adrenal corticosterone and their response to ACTH in hypophysectomized rats. It may be concluded that glucocorticoids do not significantly inhibit the steroidogenesis at the adrenal level insofar as the usual dosage is concerned.
The comparative effects of cortisone, prednisolone, triamcinolone, dexamethasone and DOCA on the adrenal cortex and other organs of albino rats were studied.
1) Every glucocorticoid used produced a marked reduction in plasma and adrenal corticosterone as well as in adrenal weight. Histological examination of the adrenal gland revealed that the zona fasciculata had atrophied and was depleted in lipid content, while the zona glomerulosa had broadened and was rich in lipid granules. In the pituitary gland, glucocorticoids caused degranulation in basophils, a slight increase in the percentage of basophils and a slight decrease in acidophils.
Involution of the thymus, atrophy of the lymph follicles in the spleen, fatty degeneration of the liver and hyperplasia of the Langerhans' islets were observed in all glucocorticoid treated rats. Degeneration of the thyroid epithelium and hypoplasia of the prostate were seen in some of the rats treated with prednisolone and dexamethasone.
DOCA caused a slight but significant reduction in plasma corticosterone and adrenal weight. Histologically, the zona glomerulosa had atrophied and was diminished in lipid content, while the zona fascieulata appeared to be normal.
2) The relative potencies of cortisone, prednisolone, triamcinolone and dexamethasone to deposit liver glycogen, to inhibit granuloma formation and to suppress adrenocortical activity were studied. The ability of a given glucocorticoid to suppress adrenocortical activity does not parallel its liver glycogen deposition activity, but seems to parallel its anti-inflammatory activity.

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The effects of administration of T₄ on the levels of TSH and L.A.T.S. were studied in 4 hypothyroid and 3 hyperthyroid patients.
The activities of TSH and L.A.T.S. in the serum were determined by our modification of the method of McKenzie.
In all hypothyroid cases, the TSH activities were reduced significantly with an increase of PBI concentration, following intramuscular administration of 1mg of T₄ daily for two days. On the contrary the L.A.T.S. activities did not decrease at all despite of a rise of PBI level. Particularly the fact is noteworthy that not only the 12 hours' activity of L.A.T.S. but also the 2 hours' were not suppressed significantly.
In the immunological demonstration too, we found that anti-TSH serum was capable of neutralizing neither the 2 hours' activity of L.A.T.S. nor the 12 hours'.

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Adrenocortical activation after the single dosis of sodium, potassium and magnesium aspartates was determined by estimating the adrenal ascorbic acid concentration in the rat. Each salts were given intraperitoneally, orally or subcutaneously in the amounts of 100mg per body weight, while intravenously in the amounts of 20mg per body weight. All salts of aspartic acid tested caused a significant decrease of adrenal ascorbic acid, but the depletion was more definite and intense after potassium and magnesium salts than after sodium salt. As regards the mode of administration, an oral use was least effective for the adrenocortical activation. These depletions of adrenal ascorbic acid were inhibited by the administration of the large doses of cortisol acetate. It is suggested that this adrenocortical activation, induced through ACTH release from anterior pituitary, may be necessary and responsible for the metabolism of aspartates and its favorable effects on metabolic fatigue.

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