I made the present experiment in order to learn the various phases of testicular damages and the functional changes caused by the damages.
1) The methods chosen for stimulating the testicle were…a) as physical stimuli, high temperature (by the electric iron, ultra short waves), low temperature (by dry ice), isotope (P³², Co⁶⁰), vasectomy, ischemia by ligation of blood vessels in spermatic cord…b) as chemical stimulants, maleic hydrazide, Trimeresurus venom…c) as hormonal stimulants, androgen, estrogen, bisteron, progesterone…d) as an allergic impediment to the testicle, Freund's adjuvants method.
2) In animal experiments, male adult guinea pigs were used, examining body weight, testicular weight, histological finding and also measuring the weight of accessory sexual glands, fructose of seminal vesicle secretion and acid phosphatase of prostate tissue, as an indicator of functional changes with histological investigation.
3) Among physical stimuli, ischemia, high and low temperature, isotope application caused prompt and severe impediments to testicle. Although the extent of damages depended upon the stimulating intensity and duration, in severer cases, necrosis was caused, Leydig cell as well as intratubular elements degenerating, while in milder cases, the chief damage observable was on intratubular elements only.
In the accessory sexual glands, the changes did not take place in a short time, but P³² application brought about functional decline in a comparatively short time, which fact may partly be attributed to the direct action of P³². In the case of vasectomy and temperature stimulus the inhibiting effect on the accessory glands was not produced even after a comparatively long time.
4) Trimeresurus venom which was poured directly into defferent duct seemed to act as poison to the blood vessel and cell, so that the damage on interstitial tissue as well as tubular elements was a characteristic result, accompanying hemorrhage, liquiating deterioration.
In the case of maleic hydrazide, the damage was observed chiefly on intratubular elements, only a little on Leydig cell, none on accessory sexual glands.
5) Testicular damage by steroid hormones was characteristic. The decrease of testicular weight and atrophy of seminiferous tubule after the treatment of a certain dosis of androgen and estrogen were remarkable, with corresponding changes in testicular tissue. Basement membrane thickened, Leydig and Sertoli cell lipid increased, while accessory sexual glands were remarkably inhibited by estrogen. Bisteron and progenin both exerted the effect similar to androgen on the testicle.
6) Singular, too, was the allergic damage on the testicle by Freund's adjuvants method. Its impediment was found only on tubular elements, Leydig cell showing no change, and so no change on accessory sexual glands either.
7) There was a remarkable difference between the resistence against stimulus of tubular elemets and that of Leydig cell, the former being more sensitive, especially germ cell which was advanced in differentiation was labile.
8) In the present experiment, I could name many factors causative of sterility, their reaction being of great variety in quality and quantity.
9) Although the administration of estrogen caused a remarkable inhibition on accessory glands, it was of interest to know that various physico-chemical stimuli and allergic stimulus as well as androgen caused little impediment on hormonal secretion and accessory sexual glands, in spite of the fact that they brought about testicular damage.

View full abstract

Recently, the relationship between renal insufficiency and bone changes has attracted the urologist's interest, because there is a striking tendency to stone formation and calcification of renal parenchyma in some osseous diseases.
A man, 45 year old, was admitted to our hospital, complaining of spontaneous fractures. X-ray examinations revealed fractures of ribs, clavicle, scapula, pelvis and four extremities and bilateral renal calcifications of high grade. Biochemical analyses of the blood and urine demonstrated tubular insufficiency to excrete acid urine, which has led to acidosis and hypercalcuria. Diagnosis is osteomalacia with nephrocalcinosis due to primary renal acidosis. Osteomalacia is a distinct clinical entity readily differentiated from other generalized osseous diseases by physicochemical examinations.

View full abstract