Nagoya Journal of Medical Science

In female DDY mice, the incidence of 3-methylcholanthreneinduced skin tumors was increased in the hypothyroid state produced by the administration of Endojodin or l-methyl-2-mercaptoimidazole (p < 0.01) and decreased in the hyperthyroid state produced by L-thyroxine administration (p < 0.05) compared with controls. The calorigenic effect or the direct action of thyroid hormones may correlate with tumor induction in mice.

An experiment was performed on the delay effect and flap survival in the rat. When the flap was delayed with a teflon sheet, there was greater improvement of vascularity and flap survival than in the group that was delayed without the use of a teflon sheet.

To a further understanding of the role of steroid hormones in adrenal disorders, we have prepared free cell system of adrenal cells, using adrenal tissues that had been removed by operation from (i) cases of Cushing's syndrome due to adrenocortical adenoma or adrenocortical hyperplasia, (ii) a case of primary aldosteronism, and (iii) a patient with virilizing adrenal tumor. Twelve important steroid hormones were measured, such as pregnenolone, cortisol and aldosterone, which were produced by these cells. Adrenal glands removed from the cases of advanced breast cancer were used for the measurement of steroids as a control. No organic lesions were confirmed in these adrenal glands. An investigation as to what characteristics the adrenal cells with various disorders show, had been carried out by examining the patterns of their steroid hormone production. The results were as follows: It was not the case that adenoma cells of each disorder produced just one of three types of steroid hormones, that is, glucocorticoids, mineralocorticoids, and androgens. In fact, it is interesting enough that each adenoma produced all steroid hormones. But, the quantitative pattern of each steroid hormone production differed characteristically from one disorder to the other. It was discovered that the symptom varies depending on the amount of the more predominantly produced hormone among these steroid hormones. Consequently, adrenal disorders can be classified into the three types before-mentioned. It seems that symptoms of these disorders were also modified by other steroid hormones being produced simultaneously. Cells of adenoma in the cases of Cushing's syndrome produced a fair amount of mineralocorticoids as well as cortisol. That is why hypokalemic alkalosis and hypertension in this disorders developed. In the case of Cushing's disease due to adrenal hyperplasia, steroid hormone production pattern was similar to that in the control. In the case of virilizing adrenal tumor, androgens were predominantly produced, with the increased production of cortisol. In fact, the latter finding was consisted with the patient's Cushingoid appearance. It was also discovered that the quantitative proportion of the various steroid hormones produced by isolated adrenal cells, varied depending on the cells which were placed on the different conditions. In the case of Cushing's syndrome due to adrenocortical adenoma, for example, the quantitative proportion of mineralocorticoids was higher where no ACTH was added to the medium, compared to that where ACTH was added. These results appear to correspond with the clinical findings of the above-mentioned disorders. And, it can be said that these data are convincing for explaining the clinical symptoms.

An experiment was performed on the effeet of solcoseryl on the skin flap survival. When the flap threared with solcoseryl showed slight improvement.

This paper examined the availability of a method for calculating the "mean elastic constant" of tissue and its practical applicability. The error analysis for the elastic constant of tissue was obtained by theoretical and experimental methods. Its error depends on measured lengths from Computerized Tomograms (CT), Ultrasonograms (US), CT-values and their deviations. This method can be accurately applied to soft tissue and organs of 4 cm or more with an error of less than 20% in vivo with the exception of bone, lungs, and gas filled organs. The procedure we employed for obtaining the "mean elastic constant" by combining CT with US is presented.

This paper describes a method for calculating the elastic constant of tissue. Length measurements obtained from Ultrasonograms (US) are different from the results obtained from Computerized Tomograms (CT) when the velocity of sound is compared to standardized water measurements. The density of tissue PI can be approximated by the equation. ρ_t = 1-N_c/N_air where N_cand N_air are the CT-values of tissue and air respectively. The elastic constant (bulk modulus) K_t, sound velocity V, and density ρ_t are related through the following equation, V= (K_t/ρ_t)^0.5. The elastic constant K_t is then calculated by, K_t = K_w (L_c/L_u)²• (1 - N_c/N_air.), where K_w is the bulk modulus of water, and L_c and L_u are the measured distances from CT and US images respectively.