TSH bioassays were experimentally carried out in view of the possibility of their clinical application, both in vivo and in vitro.
The results were as follows :
1) In the method using ³²P uptake with the thyroid gland of chick, the best dose-response curves were obtained (with the mean λ of 0.44 and the sensitivity of 25mJSu.) by measuring the total thyroidal radioactivity 6 hours after the simultaneous intraperitoneal administration of TSH and ³²P.
2) In the method using the release of ¹³¹I-labeled thyroid hormone after the administration of TSH in mouse, the precision of the dose-response curve was improved by the administration of TSH 24 hours after L-thyroxine and ¹³¹I were injected. The mean λ value was 0.24, and the detectable range of TSH, 1-16mJSu.
3) In the method based on the release of inorganic radioiodine with bovine thyroid tissue slices in vitro, a positive correlation between the thyroidal¹³¹I uptake rate (U) in the uptake phase and the thyroidal accumulation rate [U' (=100-release rate)] in the release phase was observed ; and using U'/U as a new index of this method, augmentation of the precision was obtained with a mean λ of 0.33, being better than that obtained by using the ¹³¹I release rate. The detectable range of TSH was 0.1-10.0mJSu.
4) By the modified assay technique for TSH based on the release of ¹³¹I with bovine thyroid tissue slices (in vitro) and the release of ¹³¹I-labelled thyroid hormone in mouse (in vivo), correlation between the dose-response relation of Standard (Pig) and Human (Pituitary) TSH, and the assay value of hypophyseal TSH, measured by the two method, were investigated.
A approximate parallel relationship between the dose-response curve of standard and human TSH, and between the in vitro and in vivo TSH value per pituitary was observed.

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I studied the mechanism of Phenethyldiguanide (PEDG) with the following results :
1) PEDG showed the hypoglycemic effect in the normal rat, alloxan rat and adrenalectomized rat. PEDG also showed the inhibition of hyperglycemia after glucose loading in the alloxan rat.
2) The glycogen content in the liver of normal rat on fasting and glucose loading was less in the PEDG group than in the control group. The decrease of glycogen in the liver, as mentioned above, was restored slightly with pantothenic acid.
3) PEDG enhanced the glucose uptake of diaphragm in the normal rat.
4) In the normal rat PEDG inhibited acetylation, which was restored with pantothenic acid and Vitamin B₆, but not with Vitamin B1. Also the decrease of CoA in the liver was noted on this occasion.
5) PEDG had no effect on the activity of hexokinase and glucose-6-phosphatase in the liver homogenate of the normal rat.
6) PEDG inhibited the activity of various enzymes which are related to TCA cycle.
7) PEDG inhibited oxydative phosphorylation in the mitochondria of liver in the normal rat. The inhibition of oxygen consumption was also noted, but this inhibition was restored slightly with the excess addition of ATP or cytochrome C.
8) PEDG had no effect on ATPase and d-amino acid oxydase in the liver of the normal rat.
9) In diabetic patients, PEDG had no effects on the basal metabolic rate and urinary 17-Keto-steroids. Serum cholesterol decreased slightly. No definite changes were found in plasma non-esterified fatty acid 6 hours after the oral administration of PEDG.

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Parathyroid hormone-like substance was extracted from rabbit and human plasma by the aqueous-phenol and acid acetone method and assayed by ³²P excretion in parathyroidectomized rats. Recovery of the extracting procedure was 68, 88, and 87% in aqueous phenol method and 75% in acid acetone method. In rabbits with experimental hypertension due to renal artery constriction, 5cc plasma showed a marked parathyroid hormone-like activity whereas the same amount of normal plasma did not contain a detectable activity. Parathyroid hormone-like activity was detectable in 80cc of human plasma in 4 of 6 normal subjects.

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