Previously, Tabayashi and Midorikawa in their studies on urethral stricture found degenerative changes of the walls of the arterioles located in the periurethral connective tissues showing proliferative or sclerocicatricial transformation. Since these changes are seen in all instances of uretheal stricture resulting from such causes as gonorrhea, trauma, tuberculosis or even by unknown etiology, these investigators regard such changes of the vascular wall to be common to all histologic characteristics of urethral stricture. Among the stricture due to unknown etiology, there are cases of habitual urticaria and of operations on duodenol stricture. There seems to be a relationship between the connective tissue changes and the degeneration of the vascular walls, and, from the standpoint of collagen diseases, Tabayashi and Yamamoto made pathologic observations on the finer artetioles and their tissue beds. The results disclosed that the cases showing proliferative or degenerative changes of the walls of peripheral vessels, or so-called vasculitis type, comprised 62.5%, those demonstrating sclerotic transformation 12.5%, and those with hypertropic changes 15.0%.
The pathologic findings in the vasculitis type are characterized by centripetal, marginal or obstructive changes of the lumen, although asthenic or patent forms may occasionally be seen. The intima shows often a marked hypertrophy due to fibrotic or proliferative changes as well as to cicatirization, resulting in luminal narrowing. The changes of the media are usually those of degeneration in varying degrees. Cellular infiltrations are chiefly of small round cell type, either aggregated around the vessles or widely scattered. On the basis of the above findings, which these authors interpreted to consist basically of so-called fibrinoid transformation, the condition was included in the category of collagenosis.
Many reports are already found in the literature on the experimental investigations on allergic and rheumatic changes. The author, following the experimental method of Prof, Otaka, has undertaken animal experiments for the purpose of ascertaining whether or not these changes really belong to the category of collagen diseases. It must be emphasized that it is of utmost importance to determine if the pathogenesis of urethral stricture is related in any way to allergy.
The experimental method consisted of producing urethral stricture by making stricture-inducing injectioes in animals repeatedly sensitized with stated amounts of horse serum, egg albumin and γ-globulin. The animals were then sacrificed at varying intervals of time and histological sections were prepared from the tissues corresponding to the pars membranacea bulbi of the human. Observations were made by staining the sections by the same method employed by Tabayashi-Yamamoto.
The results of observation may be summarized as follows:
1. So-called fibrinoid changes in the tissue beds consist of the swelling and loosening of connective tissue, the disruption, irregular arrangement and poor H·E, stainbility of fibrils, accompanied by cellular infiltrations.
2. The proliferative and degenerative changes of the walls of small vessels are particularly remarkable.
3. The changes of the vessel intima consist chiefly of proliferative hypertrophy, but occasionally of expansive swelling. As a result, the lumen is either narrowed or obstructed in varying manners and stagnation of erythrocytes and plasma may be seen.
4. The smooth muscle fibers of the media are often swollen and separated or their arrangement may be distorted, and when these changes are extreme partial lysis or even total disappearance may occur.
5. The specimens vary as to the extent of cellular infiltrations, the two most usual types being aggregation and diffusion, which may be either compact or loose.
These findings in animals present certain points of close resemblance to those seen in man, although there are

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In order to establish the proper method of administration and adequate dosage of androgen, in cases of primary male hypogonadism, male castrate or male sterility, experimental and clinical investigations were performed.
By the animal experiment using rats, it was proved that inhibitory effect of androgen on the pituitary gonadotropin is very weak. Clinically, alteration of the urinary gonadotropin following respective administration of androgen depot (testosterone heptanate), testosterone propionate, or methyltestosterone was examined and androgenic activity was evaluated at the same time by biochemical procedures.
The results obtained were:
1) By administration of androgen depot 100-250mg per month, the secretion of pituitary gonadotropin was not influenced. But the massive dose (over 400mg) inhibited the secretion.
2) By the use of testosterone propionate 150mg per week, the secretion of pituitary gonadotropin was inhibited, but on cessation it increased more than the level prior to the administration.
3) The continuous administration of methyltestosterone less than 25mg per day which had shown clinical improvement did not cause inhibition of the pituitary gonadotropin secretion.
From the above-mentioned findings the following conclusions were considered.
1) Androgen replacement therapy with adequate dosage for the senescence male complaining of so-called male climacteric symtoms are effective.
2) Androgenic treatment for male sterility applying rebound phenomenon is effective only when the secretion of pituitary gonadotropin is inhibited.
3) Androgen may be effective for the prostatic cancer if an enough dosage to cause inhibition of the secretion of pituitary gonadotropin is given.

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Sperma invasion may sefely be said to be a reactive granuloma which develops as a result of the invasion of sperma into the interstitial tissue of the testis, epididymis and vas deferens. However, the mechanism underlying the invasion of sperma into the interstitial tissue has not yet been established. For the purpose of studying that mechanism, the authors, using rabbits, performed vasectomy, activated sperma in epididymis and induced epididymitis separately or simultaneously,
As a result, it was demonstrated that this disease is caused by activation of sperma secondary to inflammation. The authors came to the conclusin that this inflammation would finally change into fibrosis.

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