Rat kidney cells were transformed in culture by one time of treatment with 3.3×10^-6M of 4-nitroqui-noline-1-oxide (4NQO) at 37°C for 30min. The cells were derived from 17-day-old female rats of the JAR-2 line and treated after 3 days of primary culture. In 56 days after the treatment, a colony of transformed cells was detected in the culture, followed by the formation of other two colonies within two weeks. The transformed cells showed an epithelial appearance and grew vigorously, piling up on each other. In the control cultures, however, no rapid cell growth was detected.
The 4NQO-transformed cells were found, on analysis of chromosomes 160 days after the treatment, to have the modes of hypertriploid number, i. e. 67 chromosomes for one cell line and 66 for another. On backtransplantation into hamster pouches 102 days after the 4 NQO-treatment, the transformed cells produced small nodules within 2 weeks which regressed in 4 weeks. The cells were inoculated into rats subcutaneously as well as intraperitoneally 112 days after the treatment. The results are now under observation.

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In 1898, Tigerstedt and Bergman detected a thermolabile, nondialyzable substance capable of increasing blood pressure in the extract of the rabbit kidney. Since then, the presence of this substance has been confirmed by a number of investigators. The name “renin” was given to this substance which integrated the humoral and neural elements of the renin-angiotensin system. However, its chemical structure is not clear even today. In 1934, Goldblatt and his associates succeeded in producing a persistent hypertension in dogs by constricting the main renal arteries. Their study was followed by others, in which the methods were modified to yield more reproducing results. In 1939, Page and Braun-Menendez independently discovered that renin itself had no activity to elevate blood pressure, but angiotensin possessed such an action. In 1953, Simpson & Reichstein isolated aldosterone as crystal. In 1955, Conn reported the presence of primary aldosteronism. Since then, attention has been paid to several features of aldosterone, such as enhancement of sodium transport, effection circulating blood volume and elevation of blood pressure. In 1960, Davis and his collaborators clarified that aldosterone-stimulating hormone (ASH), secreted from the kidney, might be identical with renin. Biron and his associates as well as Laragh and his collaborators discussed about the parallelism between the aggravation of hypertension and the increase of aldosterone secretion. After that, Marx confirmed from his experiments with unilaterally nephrectomized rats, that renin or angiotensin was related to the occurrence of hypertension. Cubbin obtained the same results. Observations on the adrenals in patients with hypertension secondary to renal or adrenal disorders suggested that these glands might play some role in the pathogenesis of hypertension. Therefore, it is considered that the responses to the reninangiotensin-aldosterone system might be occurred even in normotensive subjects. On the contrary, De Champlain could never find any increase in renin or angiotensin even in the case of renal hypertension. In short, it is a recent tendency to stress the role of renin as an aldosterone-stimulating factor rather than as a factor to participate in blood pressure elevation. Yet no definite conclusions have been drawn on the significance of the renin-angiotensin-aldosterone system in hypertension. The adrenal function has not completely been clarified morphologically by postmortem autopsy. Since adrenal biopsy is difficult on account of its locality, no sufficient investigation has been made on the adrenal function. To elucidate the function of the human adrenal cortex, histopathological as well as histochemical studies were carried out. In addition, vascular lesions of the kidneys and its relation to hypertension were discussed with the urinary aldosterone excretion.

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It has been shown by Kumar and his associates that infusion of aldosterone (0.5g/48hr, or 1.0g/24hr.) elevates blood pressure in rats. By Gornall (1960), similar increases of blood pressure in responses to aldosterone (0.4-0.5g/100g body weight) were reported in the same animal. It was opposed, however, by Gaint and Gross, who failed to induce experimental hypertension in rats in spite of long-term administration of aldosterone. At that period, numerous attempts were made to elucidate the mechanisms responsible for this experimental hypertension. However, thus far, direct evidence concerning the role of aldosterone in controlling blood pressure remained obscure. But a few groups, such as Gross and his collaborators, led to the same conclusion that, with the very small dosage of aldosterone, there was no increase: in mean arterial pressure, although further progressive rise could be maintained by administration of a large amount of aldosterone (0.2mg/day). Besides, it was demonstrated that the hypertensogenic action of aldosterone in large doses was not so remarkable as that induced by infusion of deoxycorticosterone. On the other hand, persistent hypertension has been produced in animals by constricting the main renal arteries. This experimental hypertension, produced by Goldblatt (1934), reduces the blood flow to the functioning components of the kidneys. The nature of the effective substances responsible for inducing the hypertension has been studied and has subsequently been ascribed primarily to humoral factors from the affected kidneys. But recent observations suggested that the Goldblatt's hypertension might be associated with disturbances of adrenals. From the experiments of several reserchers, such as Page and associates and Freed and collaborators, an adrenal mechanism was involved in the experimental hypertension at least under certain circumstances. For instance, definite elevation of blood pressure due to renal ischemia was, never occured in the bilaterally adrenalectomized animal without substitution treatment. But if these animals had been administered adrenocortical extracts or predonisolone, arterial pressure levels were strikingly elevated in the majority of the animals. The results of these experiments did indicate that adrenocortical function might, in some way, play an important part in initiating some degree of hypertension. Another approach that might offer means of diagnosing functionally significant hypertensive disorders wass the assay of angiotensin in blood, and the attempt by Skeggs to extract the pressor substance was successfully done in horses. The mechanisms controlling the secretion of aldosterone have been incompletely understood, although the immediate stimulus to the adrenal gland was probably angiotension II, at least in certain circumstances. Whatever the possible stimuli for aldosterone secretion might be, the experimental results indicate that renin-angiotensin-aldosterone system seems to play an important role in the maintenance of a certain type of hypertensive disorders. During a study of the effect of adrenal treatment, Skelton (1955) presented a simple technic for the production of the adrenal regeneration hypertension, which could be produced by unilateral adrenalectomy with contralateral adrenal enucleation, unilateral nephrectomy and salt loading. The regenerating adrenal cortices were suggested to be the predominant place of mineral corticoid secretion. Especially, endogenuous aldosterone has been suspected of playing a role in the genesis of hypertension. But the possibility that aldosterone fully sustains hypertension has not been proved yet. As for the adrenal, there have been many morphological researches previously described. However, there appeared to be only fragmentary observations on the adrenocortical function. Therefore, studies about the adrenocortical functions of hypertensive rats have been made and the results have been discussed.

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A needle “indwelling” electrode was devised for electro-ureterography through a cystoscope in order to improve the “U-loop” collar electrode reported by Tsuchida and Kimura. Its structure and usability as compared with those of the “U-loop” electrode are reported in this paper.

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Nephrostomy was performed for the purpose of leading electroureterograms free from any influence of changes in the flow of urine. At the same time, the renal artery and vein were ligated, only the renal vein was ligated, or isoproterenol was injected when the renal vein alone had been ligated. Then electro ureterograms were led and recorded. The results obtained are as follows.
1. When nephrostomy was performed, the influence of changes in the amount of urine could be excluded at the time of oliguria, but not at the time of polyuria.
2. When the renal artery and vein were ligated, the discharge interval of the action potential was extended.
3. When only the renal vein was ligated, the influence of ligation was hardly observed on the electro ureterogram.
4. When the renal vein alone was ligated and isoproterenol administered by the intra-arterial route, the action potential ceased transitionally.

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Nephrostomy or ureterostomy has been widely accepted as a fairly effective method of urine diversion. Many uremic patients with carcinomas originating from intrapelvic organs such as the urogenital tract or the colon showed a favorable response to this procedure, although some died postoperatively.
Correlation between the preoperative clinical examinations and their postoperative courses in our 96 cases was analysed in detail. Nephrostomy or ureterostomy brought a succesful result even in patients under poor conditions. However, the procedure should not be recommended in cases with BUN elevated over 150mg/dl, serum potassium over 8.0mEq/l, RBC over 5×10⁶ or under 2×10⁶ and WBC over 3×10⁴ or under 2×10³. For such cases, other procedures such as artificial dialysis must be tried first of all.

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Previously Oka, our director, published many papers on the indication of the kidney conservative surgery for clinical hydronephrosis. This is one of the supplemental studies.
The results obtained were as follows:
1) The total number of hydronephrosis of degrees higher than C treated in our department during the past 21 years from 1947 to 1967 amounted 296 sides, of which 56 (19%) were markedly infected.
2) The percentage of marked infection for each degree of hydronephrosis was 13% in C, 22% in D, 37% in E and 50% in F. In short, it was found that the higher the degree of hydronephrosis, the more marked the infection.
3) Most of the high-degree hydronephrosis with marked infection were found to be caused by aquired diseases (83%). In the latter, there were calculi of the upper urinary tract in 65%. Strictures of UPJ and VUJ were identified in 80% of congenital cases.
4) As to the results of functional improvement of high-degree hydronephrosis with marked infection after conservative surgery, in congenital cases, considerable improvement was guaranteed. Only slight improvement, on the other hand, was noted in aquired cases. Especially, in those with renal calculi, the results were poor.
5) For the prevention of infection introduced by nephrostomized tube as well as for the treatment of infection before surgery, the author has devised an indwelling wash method of renal pelvis with excellent results.
6) Principally the advantage of kidney conservative surgery in high-degree hydronephrosis with marked infection is the same as that for not infected cases. In infected cases with renal calculi, a more cautious postoperative care is advisalle than in not infected cases.

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The author have examined testicular biopsy specimens obtained from 25 infertile men (8 cases of azospermia and 17 cases of oligospermia) and 2 normal men to explore chromosomal aberrations in spermatogonium and primary spermatocytes. Slide-preparations were made by the modified method of Sasaki & Makino (1965). Eighteen specimens from 27 cases examined provided a considerable number of deviding cells for investigation.
The results obtained are summarised as follows:
1) In 2 specimens from normal men, the chromosome number of spermatogonium was 46 and spermatocytic meiotic figures were also normal.
2) In 16 specimens from infertile subjects, cellularity in the preparations proved a close relation to the histological grading of spermatogenesis. In the spermatogonial metaphase, 15 specimens showed 46 chromosome numbers. The remaining one showed 46/47 mosaicism. This case, however, had no abnormality in the primary spermatocytic diakinesis and metaphase. A few aneuploid cells had chromosome numbers ranging 45, 47 and 48 and, in a majority of specimens, tetraploidy was recognized.
3) In spermatocytic analysis in 14 specimens of infertile cases, the ratio of XY bivalent cases to XY univalent cases was 79% to 21%. Chiasma formation in the XY bivalent was not exactly demonstrated, but at least the X chromosome seemed to be associated with its short arm at the distal end of the Y chromosome. Minor aberrations in spermatocytes, which showed the numerical abnormality of the autosome and the sex chromosome, were detected in 2 cases of oligospermia (1 case: multivalent spermatocyte, 1 case: 20-21 numbers of the autosome and the XY bivalent associated with one presumably extra X chromosome).

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