1. Effect of serotonin on blood lactate level of rats were examined.
2. Serotonin, administered intravenously, subcutaneously or intraperitoneally, caused a rise of blood lactate.
3. Effectiveness of serotonin in causing hyperlactacidemia was far more than that of epinephrine if considered on the basis of physiological concentration in circulation.
4. Serotonin had no effect on blood glycolysis both in vivo and in vitro.
5. The possibility that serotonin may act primarily on carbohydrate metabolism in peripheral and/or hepatic tissues are discussed.

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1. From the results now presented, serotonin-induced hyperlactacidemia occurs without participation of other endocrine factors.
2. Serotonin directly reduced the lactate utilization of perfused liver.
3. Eviscerated rats developed hyperlactacidemia in response to minute dose of serotonin.
4. It may be concluded that an increase of blood lactate caused by serotonin is due to both enhancement of extrahepatic production of lactate and retardation of hepatic utilization.

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Glycogenetic effect of 1mg of subcutaneous serotonin was demonstrated in diaphragm of glucose fed adrenodemedullated rats. The effect was shown to be additive to the action of 0.02 I. U. of glucagon-free insulin given intravenously. Failure of subcutaneous serotonin to increase cardiac glycogen was also noted, while insulin significantly increased it. The difference of serotonin effect by administration route and possible interrelations between serotonin and insulin were briefly discussed on peripheral utilization of glycogenic substance.

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On the metal complex formation of sex hormones and related substances in an ethanol solution by the ultraviolet absorption method, following results were obtained.
Diethylstilbestrol was observed to form the complexes with copper, cobalt, nickel, manganese, zinc, ferrous and ferric in a ethanol solution by spectrophotometry and other hormones were observed: estradiol; copper, cobalt: estradiol benzoate; copper, cobalt, nickel, manganese, zinc, ferric: estriol; copper, ferric: estrone; copper, manganese: testosterone; copper, ferrous, ferric: androsterone; copper: testosterone propionate; copper, nickel: phenylthiourea; copper, cobalt cholesterol; copper, ferric: lecithin; ferric
The formation was not observed with methyltestosterone and phenol in ethanol solution.

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1. The influence of estradiol-17β on cortisol metabolism was studied in vitro using the rat liver homogenate and microsome fraction.
2. It was found in the experiments using homogenates that β⁴-3-ketone reduction of cortisol was considerably increased following the addition of a given amount of estradiol-17β to the medium and this effect of estradiol-17β became more pronounced under an anaerobic condition or in the presence of potassium cyanide.
3. The stimulatory action of estradiol-17β on cortisol metabolism and its relation to TPNH-generating system were investigated in the purified enzyme system (24, 000×g supernatant fraction). It was found that estradiol-17β was able to replace glucose-6-phosphate system and no effect of estradiol-17β was observed in the presence of TPNH. Similar stimulatory effect of estradiol-17β was noted on aldosterone metabolism.
4. Experiments on estrogen metabolism in microsome fraction of the rat liver showed evidence that the addition of cortisol with TPN increased the production of estrone from estradiol-17β.
5. The results obtained suggest that estradiol-17β acts as a hydrogen donor to TPN to increase the reduction of A-ring of cortisol.

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The proteolytic action on α-uroparotin was rather mild for the cleavage of peptide bond except St. griceus protease. Of the biological activities, Ca-activity was unstable against enzymes except B. subtilis proteinase, while L-activity was stable except St. griceus protease. Carbohydrate component of α-uroparotin was distributed into a few polypeptide fragments produced by the enzymatic digestion. Thus, the responsible location for the occurrence of 2 activities was considered to be separated. On the other hand, an active polypeptide may be separated from the digested mixture of α-uroparotin and B. subtilis proteinase.

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(1) After the intramuscular injection of T₃, T₄ was increased in the anterior hypothalamus, and T3 in the hypophysis.
(2) Two hrs. after the intramuscular injection of T₄, 2 fold increase of T₄ and 3 fold of T₃ were seen in the anterior hypothalamus, while in the hypophysis, T₄ increased 3 times, and T₃ 4 times. No change was observed in the medial and the posterior hypothalamus.
(3) T₃ and T₄ are considered to constitute feedback type mechanism with TRF and TSH, respectively.

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Effect of parotin on serum citric acid was investigated. Serum citric acid was found to be significantly decreased 24hrs. after the injection of parotin. However, the authors'conclusion is that the well known action of parotin to decrease serum calcium is not secondary to its action on serum citric acid.

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The effect of pregnancy on the established lactation was examined with simultaneously pregnant and lactating mice. The measurements of respiratory activity of mammary tissue slices, nucleic acids content in mammary glands and litters'growth rate were taken as indices of lactational functions. There was no significant differences in oxygen consumption and R. Q. between non-pregnantlactating and pregnant-lactating groups either at the 14th or 19th day of lactation. Total DNA content was significantly higher in mammary glands of pregnantlactating animals than non-pregnant-lactating animals. Total RNA content was also higher in pregnant-lactating group but there was no significant difference in RNA/DNA ratio between 2 groups. The litter gain and rate of growth over the periods of the 7th to 14th and of the 12th to 19th day of lactation were not significantly different between 2 groups. These results may indicate that advancing pregnancy did not exert an inhibitory effect on lactation and that the hormonal condition suitable for mammary growth can coexist with that for lactation and vice versa, at least in mice under the present experimental condition.
The author is indebted to Prof. M. Naito for his advice and interest in this experiment.

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The effects of pituitary growth hormone on the development of 9-day chick embryo femora were studied in tissue culture. Pair-mate bones were cultivated by the roller-tube culture method without plasma, in which one of each pair was grown in the medium consisting of chick embryo extract, horse serum and saline solution and another in the plus-growth hormone medium.
In a high concentration, 100μg/ml, the radiosulfate uptake of the bones was markedly retarded and both elongation and dry weight of the treated bones were considerably less than those of the control. With decreasing concentration, however, the reduced uptake of 35S-sulfate and the inhibited longitudinal growth were restored. And in a low concentration, 6.25μg/ml, the incorporation of labeled sulfate into the treated bones significantly increased over that of the control and a significant enhancement was found also in the elongation, And, from a consideration that a concentration of 6.25μg growth hormone per ml of the medium would be regarded as within the physiologic level of concentration, it was suggested that growth hormone acts directly on the development of skeletal tissues in living organisms. As to the dry weight of the bones, however, a slight decrease was observed in all the concentrations used.

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Both the calcium activity and the leukocyte activity of parotin in aqueous solution (pH 8.0) were relatively stable against the incubation at 37°C. The calcium activity of parotin is labile in strong acid solution (pH 1.4), but is remarkably stable in strong alkaline solution (pH 12.6). In contrast to the calcium activity, the leukocyte activity of parotin is very stable in acid solution and extremely unstable in alkaline solution. The ultraviolet absorption maximum remained at 277mμ after incubation, and the extinction coefficient at that wave length showed slight increase in both solutions of pH 1.0 and pH 11.0 after incubation. No degradation or splitting of the molecule of parotin was demonstrated by paper partition chromatography, paper electrophoresis, or ultracentrifugation.

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Three types of the related compounds of IPTD were examined of their hypoglycemic action and of the influence on the glucagon content of the pancreas.
It was shown that the treatment with sulfonamides resulted in an increase of pancreatic glucagon content after 24 hrs.

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Magnesium silicate-water system of paper chromatography, modified one of water system, proved to achieve a good separation of individual corticosteroids, especially the separation of aldosterone from hydrocortisone and cortisone. The technique of this system is reasonably simple and corticosteroids can run sufficientlyin a short time.

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The formalin-filterpaper-pellet method has been standardized as a quantitative anti-inflammatory assay. This is based on the inhibition of granuloma produced by the subcutaneous implantation of the formalin-soaked filterpaper pellets into the adrenalectomized rats. The ideal concentration of formalin is 7%, and the optimal duration for the pellet implantation till autopsy is 6 days. Bilateroventral regions are recommendable as the implantation sites of the pellet for good development of granuloma.
This method is superior in accuracy and simplicity, to the cotton ball method based on the similar principle. Reproducibility of the tests for hydrocortisone acetate is satisfiable in terms of dose-response regressions.
Comparative assays of prednisolone and dexamethasone, using hydrocortisone acetate as a standard, indicate a potency ratio to the standard of 3 (range 1.8 to 5.3) for prednisolone and of 32 (range 24.8 to 41.2) for dexamethasone, suggesting the usefulness of this method as a standard assay procedure.

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