Kaoru Niki

Studies on corticoid action on the toad tadpole tail in vitro

The effect of adrenal corticoids on the shrinkage of tail segments from Bufo bufo japonicus tadpoles was studied in vitro. Deoxycorticosterone acetate (DCA) was effective in accelerating the shrinkage of tail segments if thyroxine (T4) or triiodothyronine (T3) was present in the medium. The shrinkage caused by DCA was dose dependent. In the absence of thyroid hormone, DCA did not induce tail resorption. Shrinkage of tail segments induced by DCA and T4 was blocked by prolactin. Among the steroid hormones testes in vitro, aldosterone and corticosterone exhibited a potent activity in accelerating shrinkage of tail segments in the presence of T4. The nature of the corticoid action is discussed.

Epidermal tissue requirement for tadpole tail regression induced by thyroid hormone

Abstract In this paper we report on the requirement of the epidermal tissue for thyroid hormone-induced tadpole tail regression. The epidermis was removed by two different methods, i.e., surgically or chemically. Chemical removal included EDTA and trypsin treatment. Epidermis-free tail fin blocks were cultured in vitro according to A. Derby, 1968 , J. Exp. Zool. 168, 147–156. and the effect of 3,3′,5-tri-iodo- l -thyronine (T3) was followed up for 4 days. No tissue breakdown was observed at the concentration of 10−8 M T3, which was enough to induce tissue resorption of the epidermis-containing normal tissue blocks. Tail muscle cubes with epidermis regressed in the T3-containing culture medium. However, the epidermis-deprived tail muscle cubes did not respond to the hormone. The tail fin mesenchymal connective tissue block deprived of the epidermis was cultured with epidermal tissues which had been removed surgically from the tail. The presence of T3 in this reconstituted culture induced the regression of the mesenchymal connective tissue blocks. These experiments clearly show that epidermal tissue plays a critical role in T3-induced tissue degradation.

Inhibition by hydroxy-N-methyl elliptinium of precancerous mammary hyperplastic alveolar nodule formation in mice

Daily subcutaneous injections of 5 micrograms hydroxy-N-methyl elliptinium for 4 weeks in a high mammary tumor strain of SHN virgin mice was found to decrease the number of precancerous mammary hyperplastic alveolar nodules (HAN) associated with the increase in the number of ghosts, the remnants of regressed HAN. On the other hand, the treatment had little influence on the normal mammary lobulo-alveolar system, serum prolactin level, estrous cycle and endocrine organ weights. The results have demonstrated that elliptinium can inhibit the formation of HAN and induce their regression with no modulation of endogenous conditions of mammotropic hormones.

Interrelationship between Pituitary and Ovarian Hormones in Normal and Neoplastic Growth of Mammary Glands of Micea

While prolactin is a key hormone for normal and neoplastic mammary gland growth, the participation of ovarian estrogen and progesterone is essential for these processes under the normal physiological conditions. Prolactin exerts its influence directly to the glands and indirectly through its luteotropic effects by stimulation of ovarian progesterone secretion. Furthermore, the action of prolactin, whether in promoting normal growth and function or enhancing the progression of neoplastic foci, depends upon the circulating levels of other mammotropic hormones as well as the level of prolactin itself. Presence of estrogen and prolactin is essential for manifestation of progesterone effects on mammary gland growth. Estrogen acts on the mammary glands directly by modulating mammary cell responsiveness to prolactin and indirectly by stimulating pituitary prolactin secretion. While data have been accumulated on the effects of growth hormone on mammary gland growth, the significance of these findings is still unknown. Neoplastic potential of mammary cells is largely dependent upon the susceptibility of the cells to mammotropic hormones.