The method for the separation of DNP-amino acids by paper chromatography was investigated. The resolution of the mixture of 20 kinds of DNP-amino acid was achieved by the following solvent systems: toluene-ethyl acetate-ethanol-1.5 N ammonia (1:1:1:1), toluene-acetic acid-water (2:1:1), toluene-chloroform-5% acetic acid (1:1:2), chloroform-n-butanol-1% acetic acid (4:1:5) and toluene-1% acetic acid (1:1).
The method was applied to the determination of the N-terminal amino acids of parotin, and it was found that 3 free α-amino groups are present in the molecule of parotin, which are located on alanine, aspartic acid and glycine residues.

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The thyroidectomized tadpoles of Rana temporaria ornativentris were kept in a 0.004% solution of PHP, and the influence of this treatment on the hypophysis and gonad was observed.
By the application of PHP, the secretory function in the anterior lobe of the hypophysis was depressed, and the acceleration of gonadal development produced by thyroidectomy was perfectly inhibited, and the remarkable excess of females resulted.

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Comparison of the effects of MTU and T₄ withdrawal on different thyroid parameters has been made in the rat. After the withdrawal of chronic MTU treatment, marked rebound in thyroidal ¹³¹I uptake and conversion ratio was produced but not in thyroid weight, while no rebound was produced in any of thyroid parameters after a single injection of MTU. After a single injection of T₄, however, pronounced rebound was produced in thyroidal ¹³¹I uptake, conversion ratio and thyroid weight.
A similar type of rebound of neurosecretory substance was also produced after the withdrawal of chronic MTU treatment.
It is postulated that the difference in the response of thyroid weight might be related to different pattern of circulating TSH. Possible participation of hypothalamic neurosecretory system for the production of rebound phenomena is discussed.

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The effect of the extirpation of the salivary glands upon uroparotin excretion in rabbits was investigated over a prolonged period of time. Thus, excretion of uroparotin stopped within about 15 weeks after the removal of both parotid and submaxillary glands together and the excretion also remarkably decreased after the removal of either one. The stopped or decreased excretion of uroparotin, however, was found to be completely restored to a normal level in all experiments over a prolonged period of time after the operation. Furthermore, the uroparotin was excreted temporarily after the administration of a considerable amount of parotin into rabbits in which salivary glands had been extirpated.

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The biochemical and histochemical investigations presented in this paper confirm that progesterone administered into the estrogen-primed immature female rabbit produces marked increase of carbonic anhydrase in the endometrium.
It is clearly demonstrated that the increases of carbonic anhydrase induced by progesterone takes place in the glandular portion of uterine mucosa and the precipitation of manganese granules resulting from the enzyme reaction are concentrated in the epithelial cells.
Acetazoleamide administered intravenously 30 mins. before autopsy causes marked reduction of endometrial carbonic anhydrase activity and poor stainning of the uterine section prepared by the Hausler's (1958) cobalt sulfate method for carbonic anhydrase.
Comparing the enzyme activity of one horn perfused with saline before the enzyme extraction with that of the other horn without perfusion on the same uterus, the activities derived from the blood contaminated in the extracts are investigated for a series of control and progesterone-treated groups. The data demonstrate that the rate of enzyme activity resulted from blood contamination in the extract of progesterone-treated group is rather smaller than that in the control group.
It is, therefore, concluded that the increase of endometrial carbonic anhydrase in the Clauberg rabbit treated with progesterone is probably due to the new biosynthesis of the enzyme in the epithelial cells of uterine mucosa.

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Several steroids, norethisterone, norethynodrel, estradiol, progesterone, testosterone propionate and 2α-hydroxymethylene-17α-methyl-dihydrotestosterone were injected subcutaneously once daily for 12 days into hypophysectomized immature female rats to demonstrate their direct effects on the gonadal morphology. The effects of 2 19-norsteroids, norethisterone and norethynodrel, are either quantitatively or qualitatively different from each other and from those of the naturally occurring sexagens such as estradiol, progesterone and testosterone.
The characteristic changes produced by norethisterone are the fluid retention under ovarian capsule, the appearance of many primary follicles in the ovaries and the typical secretory changes in uterine endometrium with glandular proliferation. However, norethisterone does not alter the reactivity of ovaries to gonadotrophins which increase the ovarian weights and produce superovulation in hypophysectomized immature female rats.
It is, therefore, difficult to support the assumption that norethisterone, one of the ovulation inhibiting agents, might have a property to depress the ovarian function, degenerate the ovarian follicles or decrease the ovarian reactivity to gonadotrophins and thus act as an anti-fertility agent. It is, therefore, concluded that the ovulation-inhibiting or anti-fertility effect of norethisterone is most likely due to the inhibition of pituitary gonadotrophin secretion.

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Intravenous injection of serotonin into intact rats caused 2 stages of glycemic response, i. e., initial hypoglycemia followed by marked hyperglycemia. Hyperglycemia was found to be due to the release of epinephrine from adrenal medulla since adrenodemedullated rats showed virtually no hyperglycemic response. Adrenodemedullation as well as anesthesia with sodium pentobarbital sensitized rats to hypoglycemic action of serotonin. Hypoglycemic response was roughly proportional to the dosage, and as low as 50μg per rat resulted in significant hypoglycemia. Subcutaneous and intraperitoneal serotonin showed comparable but less effect. Hypoglycemic effect of serotonin was additive to that of insulin and inhibited epinephrine induced hyperglycemia. Diaphragm of rats injected with serotonin prior to the sacrifice showed increased glucose uptake when incubated in vitro. Glucose as well as inulin tolerance test showed characteristic pattern of concentration curves. Chronically serotonin-treated rats showed increased insulin sensitivity and a little improved glucose tolerance than the control littermates. Possible role of serotonin in carbohydrate metabolism was discussed in conjunction with several reports by other investigators.

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Intravenous injection of serotonin resulted in decrease of hepatic and diaphragmatic, as well as significant increase of cardiac glycogen 10 mins. after the injection into adrenodemedullated rats. Change of hepatic glycogen was still demonstrable 2 hrs. after the administration when the responses of cardiac and diaphragmatic glycogen were not observed. Dosage as low as 50μg failed to affect cardiac and diaphragmatic glycogen, while hepatic glycogen showed still significant reduction. Inhibition of hepatic gluconeogenesis by serotonin was demonstrated in the reduction of urinary nitrogen excretion, blood urea accumulation and hepatic glycogen content after D, L-alanine administration. The possibility that the reduction of hepatic blood flow and the resultant glycogenolysis might play some role in the change of hepatic glycogen was suggested by the result of isolated rat liver perfusion experiments. Diaphragmatic glycogen content tended to increase after subcutaneous doses of serotonin. Comparable increment of cardiac glycogen was obtained by lactate administration, and the possible participation of blood lactate increment in the effect of serotonin on cardiac glycogen was postulated.

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A simplified technique for perfusion of isolated rat liver was presented. Modifications of apparatus along with the usage of diluted rabbit blood instead of rat blood as perfusing fluid was proposed, and the utility of the latter was confirmed in several experiments with epinephrine, glucagon and insulin. By the present method reduction of pyruvate production after addition of 4mg of serotonin into perfusing fluid was demonstrated.

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