Female rats were irradiated with 190R of X-rays at 10days of age and ovarian ultrastructures were studied 4 and 7 months after irradiation.
Ultrastructural changes were found in germinal epithelial cells, broblasts in the tunica albuginea and interstitial cells. The germinal epithelial cells exhibited various sings of degeneration but no sign of proliferation. Electron density of their basal part was reduced considerably. Their mitochondria became swollen and free ribosomes decreased in number. The nuclei often protruded from the free surface of these cells. These cells frequently fragmented and, finally, the complete desquamation occurred. The basement membrane became unevently thickened. Nuclei of enlarged broblasts in the tunica albuginea became irregular ellipsoid in shape, and the nuclear envelope was occasionally invaginated. Various cytoplasmic organelles of the broblasts were well-developed. Some abnormal invasion of cytoplasm into the nucleus was found in the interstitial cells showing the ultrastructural characteristics of steroid hormone synthesis. Various cytoplasmic organelles and inclusions invaded into the nucleus of these cells and the nuclear envelope sometimes disappeared locally. These interstitial cells contained a large number of irregular-shaped electron dense mitochondria with vesicular cristae, and numerous dilated vesicles of smooth-surfaced endoplasmic reticulum (SER).
The cells of anovular follicles in the irradiated ovaries resembled, in ne structure, the granulosa cells in normal primary follicles of the non-irradiated ovaries. These cells seem to be less aected by early postnatal irradiation

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The effect of temperature during preparation of rat adrenal quarters or isolated adrenal cell suspension on their response to ACTH was examined through a comparison of amounts of corticosterone produced after their incubation.
The response to ACTH added in vitro was considerably higher when adrenal quarters and isolated adrenal cell suspension were prepared at room temperature (25°C) than when prepared at ice-cold. Endogenous steroidogenesis was not affected by the temperature.
It seemed unlikely that this higher response to ACTH of adrenal quarters or isolated adrenal cell suspension prepared at room temperature was due to an activation of the cells. A possibility was discussed that cooling adrenal quarters or isolated adrenal cell suspension during the prepara

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The total and specific activity of thyroid homogenate of normal rat was 0.95×10-3 GU (guaiacol unit) per rat and 0.61×10^-3 GU per mg protein. These were increased 3.4 fold and 1.6 fold by chronic administration of thyroid stimulating hormone (TSH) and 5.1 fold and 2.5 fold by treatment with methylthiouracil (MTU), respectively. However, the soluble fractions, which were obtained by centrifugation at 105, 000×g for 120min from the homogenates, manifested only 2-3% of the activity of the original homogenates, and the specific activity was scarcely affected by the administration of TSH and MTU. Moreover, even the low activity of the soluble fraction might be due to contaminated microsomes. None of the results obtained favors the view that the peroxidase is released from the cell to the colloid lumen. The number of peroxidase molecule per cell of thyroid was roughly estimated to be 1.5×10⁵ for normal and 3.9×10⁵ for MTU-treated rat.

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A kindred with deficiency of thyroxine binding globulin (TBG) was presented. The propositus, a 1-year old female also had congenital hypothyroidism with ectopic (sublingual) thyroid. Decrease in TBG-binding capacity (TBG values ranging from 2.1-10.2μg/ 100 ml) was detected in the seven relatives on the maternal side. Of these subject 2 were male and 5 female; the males had the lowest binding capacities. But six members of paternal relatives were entirely normal in this respect. The mode of inheritance of the abnormality in this family was compatible with the presumption of Nikolai et al. and Shishiba et al., indicating that the inheritance was an X-linked semi-dominant trait. The kinetics of thyroxine (T₄) was investigated in a case of partial TBG deficiency with congenital hypothroidism (propositus). The half-life of T₄ was shortened, turnover rate increased, extrathyroidal organic iodine and degradation rate of T₄ decreased compared to normal values.

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Highly purified bovine parathyroid hormone (b-PTH 1-84) and its synthetic N-terminal peptide (b-PTH 1-34) were labelled with ¹²⁵I and incubated with rat kidney homogenate at 37°C for 1 hour to assess the degree of hydrolysis of the iodinated peptides through measurement of the increase of trichloroacetic acid soluble 125I fraction. Rat kidney homogenate rapidly hydrolyzed b-PTH 1-84 but was scarcely effective in hydrolyzing b-PTH 1-34. When ¹²⁵I labelled b-PTH 1-84 and b-PTH 1-34 were injected intravenously in rats, hydrolysis in vivo of the former appeared to be much more rapid than that of the latter, as showh by the faster disappearance from plasma of trichloroacetic acid precipitable fraction. Incubation of b-PTH (1-84) with rat kidney homogenate caused a shift of ¹²⁵I PTH peak almost to the position of salt peak, while the position of ¹²⁵I b-PTH (1-34) was almost unchanged by incubation with rat kidney homogenate. N-terminal peptide of bovine parathyroid hormone thus appears to be less susceptible to hydrolytic degradetion by rat tissue than the intact hormone, with resultant longer retention in the blood stream.

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The fornix was sectioned in the frontal plane by means of a razor blade knife, and acute and chronic effects of this section on gonadotropin secretion were estimated.
The 5-day cyclic rat which received the section of fornix under ether anesthesia at 12:00 on the day of diestrus II showed advancement of the proestrous and estrous vaginal smears and as well as ovulatory gonadotropin release by one day. It was revealed that the primary effect was the inducement of FSH release on the day of section.
The 4-day cyclic rat bearing the fornix section chronically resumed vaginal cyclicity after elapsing the diestrous period for 18 to 25 days. The rat ovulated normally and mean number of ova in oviducts was not different from that in the intact rat. However, the sectioned rat had an higher concentrations of pituitary and serum FSH on the day of diestrus II than that in the intact rat, and had an higher concentration of serum LH on the day of estrus.
These results indicate that the hippocampus exerts the inhibitory influence on LH and FSH release and if this is eliminated the facilitatory influence dominates the brain mechanism controlling gonadotropin release, resulting in the advancement of estrous cycle (the acute effect) or the increase of gonadotropin release (the chronic effect).

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Chronic administration of ouabain (3mg/Kg body weight, subcutaneously, once daily for consecutive 15 days) definitely inhibited epinephrine-induced increase of adrenal corticosterone secretion. The inhibition rate increased along with frequency of ouabain administration. Increase in adrenal corticosterone synthesis and secretion by ACTH (20-50mU/rat) administration was partially suppressed by pretreatment with chronic ouabain administration. A slight but significant increase of adrenal corticosterone secretion caused by epinephirine administration in hypophysectomized rats was also inhibited by pretreatment with ouabain administration. Chronic administration of neither phentolamine (1mg/rat, intraperitoneally, once daily for consecutive 15 days) nor propranolol (3mg/Kg body weight, subcutaneously, once daily for consecutive 15 days) caused significant changes in adrenal corticosterone secretion in response to ACTH as well as to epinephrine.
Chronic administration of ouabain in rats causes not only elevated secretion of ACTH from anterior pituitary but also functional change in adrenals leading to suppression of corticosterone secretion in response to ACTH or epinephrine administration.

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T₃ or iodide, at the concentration of 10^-3M, inhibits TSH-or dibutyryl-cyclic AMP-induced thyroidal intracellular colloid droplet formation, while leaving the TSH-induced increase in cyclic AMP levels intact. The effect of T₃ appeared not to be mediated through the iodide derived from deiodination of T₃. Those results clearly demonstrate that T₃ or iodide acts at the point beyond cyclic AMP generation and prior to the formation of intracellular colloid droplets. This is also the site at which microtubule active reagents exert their influence. Whether T₃ or iodide fits this category or acts in as yet undetermined manner remains to be established.

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Effects of electrical stimulation of the lateral amygdaloid areas on ovulatory gonadotropin release were examined in adult Wistar female rats. Electrical stimulation was applied in rats in proestrus under ether aneshtesia with square wave pulses of 0.5ms duration and 100Hz frequency for 30min (30 sec on and off).
Stimulation of the lateral amygdala blocked ovulation in 50% of animals when it was applied between 13: 30 and 14: 30 with a current of 300 μA. Stimulation of the medial amygdala under the same experimental condition was absolutely ineffective to block ovulation. Sham stimulation was also ineffective. In determining the gonadotropin concentration in serum, the stimulation into the lateral amygdala was observed to inhibit the ovulatory release of LH, FSH and prolactin.
It may be said that the lateral amygdaloid area participates in the control of gonadotropin rerease in an inhibitory manner.

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In order to know the pituitary reserves of ACTH, GH, LH, FSH, TSH and prolactin in patients with Cushing's syndrome, the responses of these hormones to hydrocortisone, lysine-8-vasopressin (LVP), insulin-induced hypoglycemia, luteinizing hormon-releasing hormone (LH-RH) and thyrotropin releasing hormone (TRH) were examined before and after treatment. Fourteen patients with Cushing's disease (adrenal hyperplasia), 3 patients with adrenal adenoma and one patient with adrenal carcinoma were investigated. Before treatment, sufficient response of plasma ACTH to LVP was observed in patients with Cushing's disease, while no response was observed in 3 patients with adrenal adenoma. There was no significant difference in the responses of other pituitary hormones between the patients with Cushing's disease. and the patients with adrenal adenoma. The response of plasma GH to insulin-induced hypoglycemia was impaired in most these patients. The response of plasma TSH to TRH was impaired in 6 of 8 patients tested. The response of plasma LH and FSH to LH-RH were preserved in 6 and 5 of 8 patients, respectively. The response of plasma prolactin to TRH was normal in most patients tested. After treatment, the improvements of the impaired responses of GH, TSH, LH and FSH were observed. Therefore, the impaired reserve observed in these patients before treatment seemed to be due to the hypercortisolemia. If the difference of the suppressibility of these pituitary hormones by cortisol may be judged simply from our observation, the order of the suppressibility is supposed to be ACTH, GH, TSH, LH and FSH, and then prolactin.

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When rats ovariectomized at 3 days of age and given a single injection of 1.25mg testosterone propionate on the next day became 60 days old, they were given 3 daily injections of 0.2μg estradiol-17β followed by 7 daily combined injections of 2mg progesterone and 0.2μg estradiol. Incidence of deciduomata in reaction to uterine trauma applied on the 4th day of the progesterone-estradiol injections was almost as high as that in neonatally ovariectomized, non-androgenized rats, but the response was significantly smaller in size in androgenized rats than in non-androgenized animals. If females similarly operated on were given injections of 0.1μg estradiol for 30 days prior to 7 daily injections of progesterone-estradiol, deciduoma formation in androgenized rats was markedly reduced in both incidence and size of the response. In non-androgenized group, deciduoma formation was not significantly affected by chronic administration of estradiol. Accordingly, it is likely that, although androgen injected during neonatal life is responsible for the reduction of uterine responsiveness in androgen-sterilized rats (Takewaki and Ohta, 1974), continued exposure of the uterus to estrogen may play a co-operative role in the event.

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Serum FSH and LH levels were estimated by radioimmunoassay following single subcutaneous administration, and repeated subcutaneous administration at various intervals in immature male rats. Single injection of LH-RH induced slight increase in FSH levels in comparison with considerable increase in LH. By two successive injections, the release of FSH was markedly stimulated when the time intervals were 15, 30, and 60 minutes, and rapidly elicited to release after the second injection. The greatest response was observed by two injections at 60 minutes interval. Moreover, the elevation of serum FSH level after the third injection was particularly remarkable, and the response was much stronger than that to the second injection. On the other hand, serum LH levels following the repeated injections were quite similar to that of FSH. And both FSH and LH were linearly responded to doses of LH-RH repeatedly administered.
These results indicated that the repeated quick administrations of LH-RH under appropriate intervals caused the acute high release of FSH, which was quite similar to LH release, and that these acute release of FSH and LH showed the dose-response relationship.

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