Electron microscopic observation of the peritubular wall of the seminiferous tubules was made on 15 clinical cases, including one normal adult, one infant, 11 of hypospermatogenesis (oligospermia 7; azoospermia 3; hematospermia 1), 2 of Klinefelter's syndrome. The conclusion was as follows:
1) The peritubular wall of the seminiferous tubules in the normal adult and infant showed the three main layers: (1) the basement membrane; (2) the non-cellular layer, containing mainly collagen fibers and very fine filaments; (3) the cellular layer, consisting of myofibroblast like cells and a few collagen fibers. The last two layers were composed of the so-called tunica propria.
2) The basement membrane of the seminiferous tubules in hypospermatogenesis revealed the various changes such as “Infolding”, “Lamellation”, “Thickening”, and “Pleat”. These changes were essentially similar to the changes due to X-irradiation, local heat, inflammation, chemical stimulation and hypophysectomy in rat and mouse testis.
3) The protrusion of the basement membrane into seminiferous epithelium has been called “Infolding”. The infoldings showed a spherical and columnar shape, and in part irregular projections. Two types of the infolding were recognized.
Type 1: The basement membrane protruded into the intercellular clefts between the spermatogonias or between the spermatogonia and Sertoli cell. This type of the infolding which was variously crooked showed a columnar, club like or sometimes labyrynthic shape. Its surface was irregularly uneven and showed in part projections. The size ranged from about 1-2μ to about 6-10μ. In some cases, the top of the giant infolding reached as far as the height of the spermatogonia. This type was recognized mainly in hypospermatogenesis.
Type 2: The basement membrane protruded directly into the cytoplasma of the Sertoli cell and occasionally spermatogonia. The shape appeared spherical and oval, and the size was about 1-2μ. This type was recognized mainly in Sertoli tubules.
4) The findings of the basement membrane was classified into four major types. (Cf. Fig. 21)
Type A: The basement membrane was thin, about 0.1μ in thickness, and was seen to be a monoor di-lamellar structure. Small infoldings (almost Type 1) were rarely present. This type was recognized in normal and in mild hypospermatogenesis.
Type B: The basement membrane showed a polylamellar structure. The infoldings, which were mainly Type 2, were frequently present. The pleats of the basement membrane were regularly seen. This type was recognized in mild, moderate, severe hypospermatogenesis.
Type C: The infoldings, lamellation, and pleats were frequently observed. Type of the infolding was almost Type 2. This type C was recognized in Sertoli tubules.
Type D: The basement membrane became thick, but the lamellar structure was obscure. Type of the infolding was almost Type 2. The pleats were not observed. This Type D was recognized in Sertoli tubules.
Moreover, the basement membrane-like structure could not been observed in the hyalinized seminiferous tubules, and the hyalinized space was occupied by a great number of collagen fibers. By electron microscope, the basement membrane of Sertoli tubules were divided into two different types, that is Type C and Type D, although light microscope could not distinguish between both typse.
5) The striking change of the tunica propria was a marked increase of collagen fibers in hypospermatogenesis. In such a case, collagen fibers were increased not only in the non-cellular layer, but also between peritubular cells in the cellular layer.
6) The degree of the changes in the basement membrane and tunica propria was almost proportional to the histological classification of spermatogenic failure. The more testicular damage, the more marked the changes of infolding, lamellation, thickening, pleat in basement membrane.

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Using the lanthanum-tracer and freeze-etching method, electron microscopic investigation on the ultrastructure of the blood-testis barrier was made in human testis, clinically obtained from 5 infertile patients by biopsy. The author revealed the existence of tight junction of the Sertoli cell junction as the blood-testis barrier in human testis. The findings were as follows:
(A) The permeation of lanthanum into seminiferous tubules
1) The tracer lanthanum penetrated to the tunica propria via the intercellular junction (about 70-150 angstrom) between the peritubular cells. There were no special junctions between the peritubular cells which blocked permeation of lanthanum.
2) The lanthanum easily permeated into the basement membrane of seminiferous tubule, even into a large enfolding. And then it deeply permeated to intercellular cleft between the Sertoli cell and spermatogonia.
3) The lanthanum abruptly stopped at a short distance in the Sertoli cell junction. This finding revealed that there was some protecting mechanism to the lanthanum permeation from the basal compartment into the adluminal compartment. In some of materials, however it was recognized that the lanthanum sporadically permeated into the surroundings of the primary spermatocyte through the Sertoli cell junction. Whether these findings indicate an increased permeability or physiological transient break of the blood testis barrier is difficult to decide now.
(B) Ultrastructure of tight junction in the Sertoli cell junction
1) The intercellular space of the Sertoli cell junction was about 50-150 angstrom in width. And there were many “punctata membrane fusion” in this junction. Subsurface cisternae of endoplasmic reticulum were found at a distance about 500 angstrom from plasma membrane, which coursed parallel to cell surface. In the lanthanum-filled preparation the constitution of tight junction was more clearly revealed as a pentalaminar fusion of adjoining cell membrane. The lanthanum-filled tight junction appeared as a rosary like shape with constriction at the point of membrane fusion.
2) In the en face section of the lanthanum-filled tight junction, electron-lucent lines and electrondense bands arrayed alternately. The electron-lucent lines were considered to correspond to membrane fusion, and the electron-dense bands were lanthanum in the intercellular space between membrane fusion. The electron-lucent lines ran parallel and in some part curved They also had several branchings and made anastomosing network. However some branchings had blind ends, and then they made a communication withr neighboring compartments, in some part just like labyrinth. These findings indicate the possibility of lanthanum permeation into the Sertoli cell junction in some part.
3) In a replica of the freeze-etched tight junction, there were thirty or more strands at the fracture face, which ran in parallel array linearly or curved. These strands made the anastomosing network which had some break in net, just like or more close-upped than the findings of the lanthanum-filled preparation.
4) The strands were seen as ridges on A fracture face and as grooves on B fracture face. The ridges on A fracture face appeared as linear aggregation of particles. These strands may correspond to electronlucent lines that were seen in the lanthanum-filled tight junction.
5) No special junctions between the Sertoli cell and spermatogonia or the peritubular cells could be found by the lanthanum-tracer and freeze-etching method.

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Studies were performed experimentally and clinically to confirm the significance of the closed drainage system.
The experiment indicated that contamination of drainage bag might lead to infection of the bladder. It seemed that a high degree of protection to the urinary tract, in the type having discharge tube, would be afforded by adding the drip chamber to the discharge tube of the drainage bag.
Clinical evaluation of our model of the closed drainage system was conducted. Risk of infection up to 7 days, 10 days and 15 days were 0%, 5% and 13%, respectively.
Some discussions were done on the closed drainage system.

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1. Ten cases of cystine calculi (8 male and 2 female) experienced in our clinic between 1963 and 1973 were reported. Their age were distributed from 14 to 64.
2. Their first episodes with urinary stone were seen at the age of 4 to 26, at 18 as a mean. All of them had had one or more episodes of stone discharge, or had been performed surgical operations once to 4 times until the admission to our clinic. One of them had experienced a stone discharge every year for the preceding 20 years.
3. Diagnosis of cystinuria was made by analysis of exstirpated stones in 6 cases and by examination of urine sediment in which cystine crystal was found in 4 cases.
4. Seven of the ten cases had hyperuricemia. It is suspected that it may have some relation with the formation of stone.
5. The statures of male patients were 146-169cm, which were below those of the general populations.
6. D-Penicillamine was administered for 4 patients. It was effective for all of them in the sense that there was no recurrent stone, but rash and fever were seen in one case.
7. α-Mercatopropionylglycine (Thiora^®) was administered in 9 cases, which prevented stone to recur or grow, except in one case, for 5 to 26 months. In addition, dissolution of stones was seen in two cases. Rash on limbs and trunk occurred in one case as a toxic effect.
8. The dose of Thiora required depends on the urinary excretion of cystine. We aim to keep this below 250mg/L for prevention of recurrent stones and below 100mg/L for dissolution of stones.
9. Studies of pedigree were done for 6 cases and one or more cystinurics were found in every case. None of them without a sister of case 2 had any episode of urinary tract calculus.

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1) A patient with renal cell carcinoma who visited our hospital due to varicocele alone is reported.
This 38-year-old man came to hospital with a chief complaint of indolent swelling in the left scrotum. Neither triad of symptoms (hematuria, pain and tumor) nor systemic symptoms were recognized. No abnormalities were found except the irregular values of total bilirubin (1.1mg/dl), GOT (38 units/ml) and GPT (63 units/ml). His illness was diagnosed as the renal cell carcinoma of the left kidney by excretory pyelography, nephrotomography and renal angiography, and so the nephrectomy was carried out.
The involvement of the tumor into the renal vein was not observed. The varicocele proved to have appeared, because the tumor which had generated in the lower pole of the kidney compressed the internal spermatic vein. After the nephrectomy, the varicocele disappeared.
2) Of 79 cases with renal cell carcinoma encountered for 22 years and 3 months from January 1953 to March 1975, 7 cases (8.9%) had varicocele. Of the 7 cases, 5 cases who had the left renal cell carcinoma developed varicocele in the left side and the remaining 2 cases who had the right renal cell carcinoma developed varicocele in the right side. The mechanisms of occurrence of varicocele were discussed from the findings in operations and from renal venograms, and it was proved that these renal cell carcinomas had been caused by the tumor thrombus of the renal vein in 2 cases and had been caused by the pressure of the tumor on the internal spermatic vein in 5 cases.
3) From the fact that 6 of the 7 cases were complicated by the hepatic dysfunction, it was considered that there is a common factor between the occurrence mechanisms of varicocele and that of the hepatic dysfunction.
4) In older man, when varicocele suddenly developed, when the varicocele doesn't disappear even at a supine position or when the varicocele appears in the right side, the varicocele may have the relation with renal cell carcinoma. These findings are considered to be very useful for diagnosis of renal cell carcinoma.

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