Kinetics of the proliferation and the maturation of germ cell, Sertoli cell and Leydig cell of the rat testis, with special reference to the influences of gonadotropic hormones, was investigated by the auto-radiographic method of intratesticular injection of tritiated thymidine in the following experimental conditions; (1) normal rat (Wistar) group reared from birth to maturation (2) immature rat group administered with gonadotropic hormones (FSH-NIH, LH-NIH, HCG, PMS): (3) adolescent rat group administered with gonadotropic hormones: (4) hypophysectomized mature rat group.
(a) Germ cell
The gonocyte proliferates by mitosis and differentiates to the spermatogonium A and B, successively 10 days and 12 days after birth. The seminiferous tubule in 50 percent contains spermatogonium which has incorporated tritiated thymidine. This percentage remains unchanged throughout the period of the testicular maturation. Differentiation of the spermatogonium to the primary spermatocyte by meiosis begins on the 14th day after birth. The number of the seminiferous tubules which contain the primary spermatocytes with intranuclear incorporation of tritiated thymidine shows a transient increase, but from the 25th day decreases again gradually to the figure of 5 percent which remains also unchanged throughout the maturation period. During differentiation of the primary spermatocyte to the secondary spermatocyte, and to spermatid and spermatozoa, incorporation of tritiated thymidine in these cells is autoradiographi-cally not demonstrated. This indicates that DNA synthesis in the nucleus of the germ cell takes place in the process of differentiation of gonocyte to the spermatogonium and the primary spermatocyte, but not after the differentiation of the secondary spermatocyte to the spermatozoa.
Any one of gonadotropic hormones does not stimulate the process of the proliferation from the gonocyte to the spermatogonium and the primary spermatocyte, whereas the process of the differentiation from the primary spermatocyte to the secondary spermatocyte and the maturation of spermatid to the spermatozoa is promoted mainly by follicle stimulating hormone (FSH). Luteinizing hormone (LH) alone does not show this action, but the possibility of the synergism with FSH can not be denied.
(b) Sertoli cell
DNA-synthesis in the nucleus of Sertoli cell can be observed in the new-born rat testis, with increasing activity to the 8th day after birth. But with gradual decrease after 13th day tritiated thymidine incorporated Sertoli cell can not be demonstrated in any seminiferous tubule. Gonadotropic hormones have not any influences on the process of cellular proliferation.
(c) Leydig cell
Leydig cell shows the intranuclear incorperation of tritiated thymidine at birth in about 10 percent. But this figure decreases gradually down to 2-3 percent at the maturation, which remains equal throughout the reproductive age. This result can be thought to indicate that in the mature rat testis Leydig cell is being constantly replaced at a rate of 2-3 percent. Proliferation and maturation of Leydig cell is stimulated by luteinizing hormone, but the finding that human chorionic gonadotropin (HCG) reveals more effectiveness than pure luteinizing hormone in the process of proliferation may indicate the possibility of synergistic action of luteinizing hormone and follicle stimulating hormone.

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The values of urinary free and total hydroxyproline (HOP) were measured by the method of Prockop and Udenfriend in 10 patients without any active disease that could be considered to affect the collagen metabolism as well as in 56 patients with urolithiasis.
The results were as follows:
A significantly high excretion of urinary HOP was observed in 8 patients with urolithiasis and 6 of them were suspected of primary hyperparathyroidism by other biochemical examinations. Moreover, of 48 patients with urolithiasis showing the normal value of urinary HOP, 5 were suspected of primary hyperparathyroidism by other examinations. The urinary excretion of free HOP was 3 to 4% of the total HOP in most patients, but the patients, who had been confined to bed, showed an increase of free HOP.
Nine patients without urolithiasis and 55 patients with urolithiasis were subjected to the calcium in-fusion test, which was described by Howard et al. While no alteration of free HOP could be observed in either group, the total HOP showed a noticeable decrease on the day of infusion, but on the day after infusion, both groups showed a significant increase in total HOP; but the urolithiasis group still remained below the original level.
Furthermore, when parathyroid extract was administrated to 2 non-urolithic patients and 2 patients with urolithiasis, no influence upon the total HOP was observed.

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The deoxyribonucleic acid (DNA) content in cell nuclei was determined by miciospectrophotometry in the epithelium of the normal prostate, hypertrophic prostate and prostatic carcinoma.
In the normal prostate, the DNA content was similar to that of the renal tubule which was employed as a control. The mean amount of DNA was within the diploid range and its histogram showed the normal distribution.
In the prostatic hypertrophy, no significant difference from the normal prostate was demonstrated. Hormonal treatment induced, it present at all, only slight changes in the pattern of DNA values.
The nuclear content of DNA in twelve cases of untreated prostatic carcinoma was demonstrated to be hyperdiploid in five cases and hypodiploid in one case. In the remaining six cases the DNA content was shown to be within the diploid range, but with a broader distribution than in case of normal prostate or prostatic hypertrophy. These findings in prostatic carcinoma differ considerably from those in carcinoma of organs other than the prostate. The hormonal treatment (estrogens and/or castration), especially administration of synthetic estrogen in retalively small doses (total dosis ranging 1.0-5.0g, 30-50mg per day), had a tendency to causeatransient scattering of the distribution of DNA content. In the majority of cases, the larger the estrogen-dosis, the more narrow was the distribution of the DNA content. In these cases the growth of the carcinoma was clinically observed to be inhibited.

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