The localization of the fibrinolytic activity in the kidney tissue and the origin of the urokinase are not fully understood.
The purpose of the present report is to study the localization of the tissue fibrinolytic activity and the changes of the fibrinolytic activity in various diseases of human kidney.
Examinations were made of kidneys in 53 autopsy cases and 49 operation cases with the 2M KSCN extraction method (Astrup's method) using human fibrinogen and with fibrinolytis autographs (Todd's method) using human fibrinogen.
The results were as follows.
1. A larger amount of tissue activator was extracted from the medulla than from the cortex of the kidney.
2. Lower activity was found in children and young adults than in adults.
3. No difference of the fibrinolytic activity was found between the saline perfused kidneys and the nonperfused kidneys by the 2M KSCN extraction method.
4. The fibrinolytic activity in the kidney was found in the wall of the intrarenal vessels by Todd' method. The activity seemed to be localized in the endothelium. The intensity of the activator activity of the vessels was roughly in the following order, 1) vasa recta and arcuate veins, 2) interlobular veins, venulae adjacent to glomerulus and subcapsular venulae, 3) glomerular capillaries. In addition to these vessels, fibrinolytic activity was found in the wall of arterioles, interlobular arteries, and arcuate arteries. In the glomerulus, fibrinolytic activity was found to be high in the vascular pole.
Fibrinolytic activity was not found in tubular epithelium, juxtaglomerular cells or epithelium of macula densa.
5. In cortical peritubular capillaries, fibrinolytic activity was not found, except for those around tubules adjacent to juxtamedullary glomeruli.
6. Very little fibrinolytic activity was found in a case of ischemic renal infarction which had completely lost the renal functions.
7. The relation between the degree of renal function disturbance and the degree of fibrinolytic activity was not always parallel.
8. In 9 cases of renal carcinoma (so-called Grawitz's tumor), fibrinolytic activity was not found in cancer cells, but in stromal capillaries.
9. Antifibrinolytic activity of the kidney tissue seemed to be higher in the cortex than in the medulla, and was considered to be the antiactivator activity.

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Reports on experimental tumor in the prostate date back to 1937, when Moore et al. artificially made a squamous cell carcinoma in the prostate of rats with 1:2-Benzpyrene. Since then many reports have been published on this subject in the United States and European countries. In contrast, in Japan, only Takenaka published a report in 1964 with reference to this theme. No report has so far been made on the experimental tumor of prostate induced with 4-nitroquinoline 1-oxide (4 NQO).
In the present study, the tumorogenic action of 4 NQO on the prostate of rats was evaluated on male Wistar strain rats. Particular attention was paid to the following 3 points: 1) presence of tumorogenic action, 2) observation on tumorogenic action with time course, and 3) influences of sexual hormones upon the tumorogenicity.
The experimental method consisted in the insertion of beenswaxbased pellets containing 10% of 4NQO into the ventral lobe of prostate of male Wistar strain rats in their age of 2-3 months.
1) Presence of tumorogenic action:
a) Formation of the first tumor could be detected in a rat 230 days after insertion of the pellet. Four other rats developed tumor on the 251st, 253rd. 267th, and 281st days, respectively. Eventually, 5 out of 9 rats developed tumor, which survived for more than 200 days, The occurrence rate of tumor was 55.6%. It was concluded on the basis of the above results that 4NQO has tumorogenicity on the prostate of rats.
b) Histological findings upon autopsy of the 5 rats turned out 3 cases affected with squamous cell carcinoma, 1 case with liomyosarcoma, and 1 case with anaplastic carcinoma. No adenocarcinoma was found induced.
2) Observation on tumorogenic action with time course: The groups I, II, III, IV, V, VI, VII, VIII, and IX were killed on the 130th, 150th, 170th, 190th, 200th, 210th, 220th, 230th, and 240th days. respectively, after the pellet insertion, in order to examine their tumorogenic conditions with time course.
a) Occurrence rate of tumor:
Tumor was induced in 13 out of 27 rate which survived for the period of 130 to 170 days and the occurrence rate was 48.1%, while the rate was 59.3% and 70.8% in the rats which survived for 190 to 210 days and 220 to 240 days respectively. In other words, it was observed that the tumorogenicity tended to be higher as the survival days of the rats became longer. The overall occurrence rate of the tumor was 57.7%, 45 out of 75 animals.
b) Histological finding:
Squamous cell type was detected in most of the tumors upon histological examination. Of these tumors, those which developed strong keratinization among those of the squamous cell type with no malignant patterns were classified as the hyperkeratotic type to be distinguished from carcinoma. The share of squamous cell carcinoma in all type of tumors was 53.8% in the groups of I-III, 60.0% in IV-VI, and 76.5% in VII-IX, showing an increasing tendency as the survival days became longer. On the other hand, it was observed with the hyperkeratotic type that share decreased as the survival days became longer in contrast to the squamous cell carcinoma. In addition to the squamous cell carcinoma and the hyperkeratotic type, one case with papilloma and two cases with sarcoma were observed.
c) In view of the above results, it may be claimed that the tumorogenic action of 4NQO on the prostate of rats and the subsequent malignant changes of the tumor are intensified as the 4NQO acts upon the prostate longer.
3) Effects of sexual hormones upon the tumorogenicity: The rats given 4NQO pellets through intra-prostatic insertion were divided into the castrated group, estrogen-administered group, and androgen administered group. They were killed 200 days after the insertion for the evaluation of the effects sexual hormones upon the tumorogenicity.
a) Occurrence rate of tumor:
The occurrence rate was 70.0%, 64.7% and 41.2% in the castrated group, the estrogen-administered group and the an

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In order to clarify the physiological relationship between the prostate and liver, an animal experimentwas conducted: prostatic tumors were induced with 20-methylcholanthrene and hepatic injuries with carbon tetrachloride. Histological studies of the prostate of autopsied patients with cirrhosis or cancer of the liver were also undertaken.
In the animal experiment, histological changes in the prostate and incidence of prostatic tumor in rats with hepatic injury were investigated. In the first group, 0.1ml of Tween-80, containing 3 per cent 20-methylcholanthrene, was injected into an anterior lobe of the prostate. In the second group, 0.1ml of olive oil, containing the same volume of purified carbon tetrachloride, per 100g of body weight, was subcutaneously injected into the back twice a week. In the third group, the 20-methylcholanthrene solution (M.C.T.) was injected in the same way as mentioned above, following which this group was divided into 4 subgroups. These subgroups then received a subdermal injection of the carbon tetrachloride solutiln (C.T.C.) 1, 2 (early administration), 3 and 4 months (late administration) later, respectively. All the rats died within 200 days after the injection of M.C.T. The prostate was removed and fixed and sections were studied microscopically. The results obtained were as follows:
1. In the first group, the incidence of tumor was 25.4 per cent (16 of 63 rats), and histological examination revealed squamous cell carcinoma in 15 of the 16 tumors, adenocarcinoma in 1. The development of squamous metaplasia was observed in 7 of 63 rats (11.1 per cent).
2. In the second group (18 rats), severe, moderate and slight hepatic injuries were observed in 12, 2 and 4 rats, respectively. In rats with severe hepatic injury, the prostate was characterized by a prominent augmentation of interlobular connective tissue with a remarkable atrophy of epithelial cells.
3. In the third group, the incidence of squamous cell carcinoma was 30.2 per cent (26 of 86 rats). The development of squamous metaplasia was observed in 13 of 86 rats (15.1 per cent). The contralateral anterior lobe, except for the group injected with M.C.T. as a control, showed almost the same histological findings as in the second group. Among the rats with severe hepatic injury, the animals subjected to late administration of C.T.C. showed a significant increase of the incidence. Concerning the development of squamous metaplasia, both administered groups showed an equally marked increase. In rats with moderate hepatic injury, there was no influence upon the incidence of the tumor, whereas the development of squamous metaplasia increased, which was especially prominent in the late administration group. In rats showing slight hepatic injury, the tumor had a tendency to occur at an early stage after the injection of M.C.T. In a clinical study, the liver function of 30 patients with prostatic cancer was investigated. Six of these had various degrees of hepatic impairment, and 1 of the 6 patients already had a slight hepatic impairment before the onset of the anti-androgenic therapy. The 6 patients received the anti-androgenic therapy for a sufficient time without any deterioration of liver function. In 27 autopsied patients with cirrhosis or cancer of the liver, the relationship between histological findings on the prostate and results of the liver function test was investigated. In the case of severe hepatic impairment, the prostate was characterized by a prominent increase of connective tissue with a remarkable atrophy of epithelial cells.
The above results suggest that the prostate may be influenced by any condition causing a hyperestrogenism, including hepatic impairment and treatment with exogeneous estrogen. Concerning the experimentally induced prostatic carcinoma in rats, however, the hepatic injury exerted only an equivocal effect upon the tumor incidence. Possible relationships between prostatic cancer and hepatic impairme

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Erection and ejaculation were caused in male mongrel dogs by manual stimulation to the penis using a procedure of masturbation. The pressure alterations in the posterior urethra was recorded from the onset of the stimulation to the end of ejaculation. As a result, it was noted that the time course of the pressure change in the present experiment was the same as the posterior urethrogram in the former report, and that rhythmic alterations in the posterior urethrogram were identical with the pressure change in the posterior urethra during real ejaculation.

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The nervous pathways controlling the two phenomena, seminal emission and closure of the internal urethral orifice were studied experimentally, using male mongrel dogs.
Methods: The nerves examined in this study were the nerve fibers entering the lower mesenteric plexus, the splanchnic nerves and the lumbar nerves. The peripheral cut end of these nerves was electrically stimulated continuously with pulses of 0.5-5V in amplitude, 0.5-2msec in duration and 1-40cps in frequency.
For seminal emission and ejaculation, posterior urethrogram was recorded by the method described in a previous report. For measurement of contraction of the internal urethral orifice, a latex balloon fitted at the tip of a No. 6 polyethylene tube was inserted into the internal urethral orifice and alteration of the pressure in the balloon was recorded.
The results obtained were as follows:
1) Selective Stimulation on the Nerve Fivers enterining the lower Mesenteric Plexus.
In this study the nerve fibers descending on the anterior wall of the aorta into the plexus were tentatively nominated as the central branch of the lower mesenteric plexus and the fibers entering from the lateral portion into the plexus as the lateral branch of the plexus.
When the central branch was stimulated, seminal emission occurred and contraction of the internal urethral orifice was not noted. On the other hand, when the lateral branch was stimulated, emission did not occur but the marked contraction in the internal urethral orifice was observed.
2) Stimulation of the Splanchnic Nerves.
Seminal emission was caused by stimulation of the greater splanchnic and the third lesser splanchnic nerves. The degree of emission was more remarkable on stimulation of the latter nerve. In regard to contraction of the internal urethral orifice, it was observed that when the 4th-6th lesser splanchnic nerves were stimulated the internal orifice contracted. In particular, contraction was most marked when the 5th lesser splanchnic nerve was stimulated. Accordingly, it was thought that seminal emission and contraction of the internal urethral orifice during ejaculation were controlled by the different nerve pathways upper the lower mesenteric plexus.
3) Stimulation of the Lumbar Nerves.
In this study, seminal emission was examined alone.
Slight emission was observed when the anterior roots of the 1st and 2nd lumbar nerves were stimulated. A remarkable emission was found to occur when the anterior root of the 3rd lumbar nerve was stimulated. Emission was not observed on stimulation of the other lumbar nerves and the posterior roots of the lumbar nerves.

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We successfully conducted the cystoplasty by regeneration on 2 cases of tuberculous contracted bladder by means of a Novectane-sprayed gelatin sponge bladder which was devised and developed by Tsuji, Orikasa, and other collaborators. Through the follow-up examination we observed that the gelatin sponge broke into small pieces, fell off, and at the same time stuck to the granulation bladder wall. The stuck gelatin sponges might result in inflammation and calculi, bringing disadvantageous factors for regeneration of the bladder. Furthermore, the fragility of the gelatin sponge itself made the delicate process of operation difficult.
In our view, an ideal material for regeneration of the bladder is that which makes easy operation possible, does not absorb or stick to the granulation bladder, and falls off completely from the granulation wall after a certain period following the completion of the bladder.
As shown in Figs. 1, A) and B), we have made artificial bladders with Novectane-sprayed thin papers (Japanese paper or tissue paper). As thin paper is used, any form of a paper bladder can be made by cutting and sticking together according to the operator's intension. A Novectane bladder with a core of thin paper is prepared by repeated spraying Novectane on this thin paper and drying. This artificial bladder is very stout with high elasticity due to the property of Novectane. We carried out the cystoplasty by regeneration to a 29 years old female with this artificial bladder. The details of cystoplasty by regeneration are illustrated in Figs. 3 and 4: The contracted bladder was subjected to a crucial incision, sharp and expansive. A No. 15 porous Nelaton catheter was inserted from the urethra into the bladder and the artificial bladder was sutured with the original incised one with a margin of 1cm using 00 cutgut (Fig. 4). All the procedures were performed outside the peritoneum. The artificial bladder fell off completely in the bladder, following the completion of the granulation bladder as shown in Fig. 5, in about 4 weeks after the cystoplasty. The fallen artificial bladder was extirpated transurethially. It was taken out, as shown in Fig. 1 C), in an utterly unchanged state.
Afterwards, as in Fig. 6, clear discrimination could be made between the original bladder wall and the granulation one inside the bladder. No foreign body that might cause calculi and inflammation was found to stick to the granulation bladder wall. The rapid regeneration of mucous membrane and vessels occurred from the original bladder over this granulation wall. And it was about 6 months until the whole granulation bladder wall was covered up. The progress of this regeneration of mucous membrane is shown in Figs. 7, 8, 9, and 10.
Clinical observations by cystogram are given in Figs. 2, (1), (2), (3), (4), (5), and (6). The capacity of the bladder was 50-60cc and the daily frequency of urination was 45-60 times before the operation. Following the cystoplasty the bladder capacity increased up to 350-400cc, being about 5-7 times as much as the value before the cystoplasty. The frequency of urination reduced to within 10 times daily.
As shown in Fig. 2, (5), the almost normal pattern of cystogram was observed about 4 months after the cystoplasty and residual urine also decreased to less than 10cc in 6 months after the cystoplasty.
Cystometrogram of 8 months after the cystoplasty is shown in Fig. 11. According to this cystometrogram, the first desire to void was at 270cc when the inner pressure was 13mmHg. On the other hand, the urgency was at 350-360cc when the inner pressure was 25-31mmHg. This was improved gradually with the regeneration of mucous membrane and an almost normal state was recovered in 8 months.
The patient was allowed to walk after about 2 weeks and to urinate by herself after about 3-4 weeks. At present, she is healthy and manages normally her household.
Following this

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