In an attempt to clarify autoimmune nature of Graves' disease and Hashimoto's thyroiditis, thyroidal autoantibodies have been studied on 86 cases of Graves' disease, 54 cases of Hashimoto's thyroiditis, 31 cases of simple goiter, 11 cases of primary hypothyroidism and 22 cases of thyroid neoplasia as well as on 364 healthy subjects. Two kinds of tanned red cell hemagglutination tests were carried out on each case. One method using refined human thyroglobulin for sensitization of sheep red cells has been found to be specific for anti-thyroglobulin antibody and to be frequently positive in Hashimoto patients. However, in another method using human thyroidal microsomes (purified by ultracentrifugation) as sensitizing antigen, some heterogenous antibodies including anti-thyroglobulin antibody might be detected together with the antibody against the antigen proper to thyroidal microsome (HF antigen) which is derived from hyperfunctioning thyroidal follicular cells of Graves patients. Anti-HF antibody is frequently detected both in Hashimoto and Graves patients. In other thyroid diseases the titers of both thyroidal autoantibodies were generally. low, though higher than in healthy subjects. The effect of aging on thyroidal autoantibodies in healthy subjects was clearly observed in females but not in males. From the results of these two tests, it is possible to speculate that high-columnar and hyperfunctioning thyroidal follicular cells might exist focally in most cases of Hashimoto's thyroiditis.

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To investigate hypothalamic-pituitary functions and the primary site of the lesion in idiopathic pituitary dwarfism, various pituitary function tests, especially the pituitary hormone responses to the hypophysiotropic hormones were studied in 23 patients with idiopathic pituitary dwarfism. A few cases showed slight responses of GH to GH stimulation tests. Gonadotropin deficiencies were most frequently noted among pituitary hormones. The basal levels and the responses of plasma LH and FSH to LH-RH test were diminished markedly in all of the cases except in 5 cases with isolated GH deficiency. Responses of LH and FSH to LH-RH improved markedly after a long term administration of LH-RH for a period of one month in 2 patients with gonadotropin deficiency. As to TSH axis, half of the cases accompanied hypothyroidism.However, the responses of TSH to TRH were normal in all of the cases regardless of the thyroid function. The basal levels and the responses of plasma cortisol and 11-deoxycortisol to the rapid metopirone test were also impaired in about half of the cases. Basal levels of plasma prolactin were normal in all of the cases and the responses of prolactin to TRH were normal in cases with normal thyroid function, but slightly delayed in cases with hypothyroidism. It is concluded from the above observations that the incidences of various pituitary hormone deficiencies were quite high in this disorder and hypophysiotropic hormone deficiencies may cause pituitary hormone deficiencies. Therefore, it is suggested that the primary site of the lesion in this disorder might be at the hypothalamus.

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In intact urethane-anesthetized rats, plasma growth hormone (GH) levels were low but increased significantly following intravenous injection of chlorpromazine. Plasma GH levels were significantly elevated in rats with hypothalamic cuts such as complete deafferentation, anterior cut and antero-lateral cut, whereas plasma GH levels in rats with posterior cut or postero-lateral cut were not significantly different from those in rats with sham-operation. Intravenous injection of chlorpromazine caused an increase of plasma GH in rats with any type of hypothalamic cut. However, the maximum increments of plasma GH following chlorpromazine were larger in rats with antero-lateral cut and smaller in rats with posterior cut than in rats with sham-operation. These results suggest that extrahypothalamic inhibiting and stimulating neurons influence the regulatory mechanism of rat GH secretion through anterior and posterior routes to the hypothalamus respectively.

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The present study was designed to elucidate the feedback relationship between the release of pituitary gonadotropins and sex steroid hormones in Turner's syndrome and Klinefelter's syndrome. LH-RH stimulation test was employed to evaluate the effects of sex steroids on the release of gonadotropins. The release of gonadotropins in response to LH-RH as well as in baseline level was suppressed after the treatment with estrogen (mestranol 0.08mg/day) for 10 days, followed by the treatment of the same period with estrogen (mestranol 0.08mg/day) and progesterone (chlormadinone acetate 2.0mg/day) in combination in both syndromes. The inhibitory effect of the combined treatment was greater than that of the treatment with estrogen alone. Administration of testosterone propionate (25mg/day) for 3 days resulted in suppression of the release of both gonadotropins in baseline level and in response to LH-RH in both syndromes, but the suppressive effect appeared to be less complete as compared with that of estrogen or estrogen-progesterone.
It was thus verified that the feedback interaction between the pituitary gonadotropin release and sex steroids such as estrogen, estrogen-progesterone or testosterone was operative in the same fashion in the patients with Turner's syndrome and Klinefelter's syndrome.

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Human chorionic somatomammotropin extracted and purified from placenta at term was proved to have a lipolytic action in the epididymal fat pad of rats.
The following mechanism appears to be involved in the lipolytic action of the hormone; human chorionic somatomammotropin activates adenyl cyclase, thereby increasing the concentration of cyclic AMP in the tissue, which, in turn, activates protein kinase to lead to the activation of hormone sensitive lipase.

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The ovulation-inducing and LH, FSH and prolactin releasing activities of prostaglandin F_2α (PG F_2α) were investigated, using the female rats which had ovulation blocked by chlorpromazine (CPZ). Serum LH, FSH and prolactin concentrations were measured with NIAMD-rat-radioimmunoassay kits. The number of ova present in the fallopian tubes was investigated microscopically. Subcutaneous injection of 0.4-1.6mg of PG F_2α at 3:00 p.m. to CPZ-blocked proestrous rats induced ovulation in 80% of the animals during presumptive estrus. However, the percentage of ovulating rats was reduced in 40-60% of the animals when the same doses of P F_2α were injected intravenously. All control animals receiving the vehicle alone did not ovulated. The number of ova was not related to the dose of PG F_2α, but the percentage of ovulating rats was.
The serum LH peak was observed 10min after the intravenous injection and 60-180min after the subcutaneous injection of PG F_2α. The peak in serum FSH and prolactin occurred simultaneously 180min after both subcutaneous and intravenous injection of PG F_2α.
It is concluded from these data that PG F_2α, at dose levels used, may directly affect the hypothalamo-pituitary axis and consequently induce ovulation. These results further support the conception that the prostaglandins (PGs) have a central effect stimulating LH, FSH and prolactin release from the anterior pituitary.

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The effects of cyclic AMP, theophylline, angiotensin II and electrolytes upon renin release were examined by incubation of rat kidney slices.
Angiotensin inhibited renin release with increasing concentrations. On the other hand, cyclic AMP and theophylline stimulated it. Calcium also seemed to play an important role in the control of renin release from kidney slices. However, the direct effects of sodium and potassium upon renin release were not conspicuous.

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An unusual case of transient hypothyroidism during the course of chronic thyroiditis was reported. A 25 years old female noticed the remarkable enlargement of thyroid gland 3 months after parturition and was developed to be hypothyroidism with decreased blood thyroid hormone and increased serum TSH. The patient recovered to be euthyroid spontaneously in associatiation with the decrement of goiter size. Anti-thyroid microsomal antibody increased concomitantly with hypothyroid period and decreased parallel with the recovery of thyroid function. The ratio of TSH potency estimated by bioassay to that by immunoassay changed during the course. Possible etiologic factors of this transient changes were discussed.

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Gonadectomized male rats of Wistar strain were administered ³H-progesterone. Various brain tissues and anterior pituitary were analyzed for retention of radioactivity, using a liquid scintillation technique. Radioactivity, in all tissues, was highest at 20 min after steroid treatment, and thereafter dropped nearly in the same pattern as each other. Among the tissues examined median eminence and anterior pituitary retained more radioactivity for a longer time than did the other tissues. The results suggest that there is long-term retention of progesteronein the median eminence and anterior pituitary of male rats.

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The metabolism of pregnenolone-7α-³H and progesterone-4-¹⁴C by human corpora lutea tissue of menstrual cycles and pregnancy was studied. In the incubations, equimolar mixtures of pregnenolone-7α-³H and progesterone-4-¹⁴C were used as substrates. Three corpora lutea of cycles were used as minced tissue. From those corpora lutea progesterone, 17-hydroxyprogesterone and androstenedione were formed, although no estrogens were formed. One corpus luteum of cycle and one corpus luteum of pregnancy were used as homogenated tissue, and those formed estrone and estradiol as well as the same three Δ⁴-metabolites. The corpus luteum of cycle also formed testosterone. All metabolites including estrogens showed the lower ³H to ¹⁴C ratio than the starting ratio. 17-hydroxypregnenolone in only one corpus luteum, and no Δ⁵-metabolites in the other four corpus luteum were identified. It is therefore proposed that the major pathway for estrogen formation in human corpus luteum is pregnenolone →progesterone→17-hydroxyprogesterone→androstenedione (or testosterone)→estrone and estradiol.

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Partially purified bovine parathyroid hormone (PTH) produced two kinds of antisera, GP-100 reacting with ¹²⁵I-labeled bovine PTH (b-PTH 1-84) alone and GP-M reacting with ¹²⁵I-labeled synthetic N-terminal portion of bovine PTH (b-PTH 1-34) as well as b-PTH 1-84. Rat serum PTH reacted with the latter but not the former, suggesting a similarity to b-PTH 1-34. Rat serum PTH became undetectable after parathyroidectomy, and increased after Na₂-EDTA injection and following renal injury with sodium sulfacetylthiazole.

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Two cases of Liddle's syndrome were found in a brother and sister. Both showed typical hypokalemic hypertension without hyperaldosteronism. These cases showed similar responses in various pharmacological tests and their symptoms of hypokalemia and hypertention were relieved by triamterene. And in a family survey, the father appeared to be affected. This seems to be the first report on this syndrome in Japan.

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A case of Turner's syndrome with short stature and 45, XO/46, XXr mosaicism in chromosome study was presented. With special emphasis on endocrinological study, the size of the breasts was normal in contrast to the poor development of the breasts in most of types of Turner's syndrome. She showed normal thyroid function, slightly low level of urinary 17-OHCS, decreased 17-KS, poor response in metopirone test and poor response of HGH to insulin.

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We have presented here a case of atypical insulinoma. Despite the recurrent episodes of hypoglycemic symptoms, the plasma level of insulin has never been excessive at fasting or by regular provocative tests. Detailed examination had demonstrated qualitative rather than quantitative abnormality of insulin secretion. Hyposuppressibility of insulin secretion by hypoglycemia, borderline diabetic curveof glucose tolerance test, blunted response of insulin to glucagon and leucine were the principal characteristics of these abnormalities. After removal of adenoma, insulin response to glucose, glucagon and leucine was improved. Only secretin provoked a high level of insulin and this abnormal elevation was no longer seen after the removal of adenoma. A removed insulinoma contained 25 U of immunoreactive insulin per gram tissue, but was negative for aldehyde-fuchsin staining. On electronmicroscopy, only atypical β-cell granules were seen.

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This report deals with a detailed course of one patient with acromegaly who had a pituitary apoplexy. The pituitary apoplexy occurred suddenly 5 days after administration of a oral hypoglycemic agent, buformin, during hospitalization. Immediately after the attack changes of the concentrations of several hormones such as serum growth-hormone, serum thyroid hormone and urinary 17-hydroxycorticoids were followed until the development to hypopituitary state. Simultaneously with the decrease of the concentrations of the above-mentioned hormones, a regression of the physical manifestations of acromegaly and a complete amelioration of diabeteszmellitus were observed.

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