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R Oyasu

Publications and source records attributed to R Oyasu.

At least 127 records · Page 7Linked to original sources
PubMed1983

A minimal dose of N-methyl-N-nitrosourea carcinogenic to heterotopically transplanted rat urinary bladder.

The present investigation was conducted to determine a single dose of the carcinogen N-methyl-N-nitrosourea (MNU) which remains subcarcinogenic in a heterotopically transplanted rat urinary bladder with a communicating reservoir (HTB) either in a urine-free or urine-existing environment. A single dose of MNU, either 0.1 mg or 0.025 mg, was instilled directly into the HTB, and was followed by weekly instillation of normal rat urine or 2.1% NaCl solution (equiosmolar to the urine) for up to 52 weeks. Bladder tumors observed were divided into 2 categories depending upon their location. Those arising at the hyperplastic foci which were induced by mechanical irritation by the connector tip were referred to as inflammatory polyp (IP)-related tumors and those arising in the region free from the IP changes were referred to as IP-unrelated tumors. The results indicated that both carcinogen levels fail to induce IP-related or IP-unrelated tumors in the urine-free environment. In the presence of urine, however, the high MNU dose (0.1 mg) was tumorigenic at both IP-related and IP-unrelated sites, whereas, the low MNU dose exhibited tumorigenicity only at the IP-related site. Physical irritation by the connector enhanced MNU-initiated tumorigenesis at the connector tip only in the presence of urine in bladder lumen. Physical irritation per se induced tumors at the connector tip even without prior carcinogen treatment provided urine was present in the HTBs.

Animals↗
PubMed1983

Acute hemorrhagic obstructive uropathy as a complication of experimental autoimmune encephalomyelitis.

During studies related to immunoregulation in experimental allergic encephalomyelitis (EAE) in rats, acute hemorrhagic obstructive uropathy developed as an unexpected complication. The urinary retention was attributed to mucous plugs tightly impacted into the bladder neck. Although mucous plugs commonly are detected in the bladders of healthy adult rats, they could create a serious complication when impacted into the outflow tract as the result of malfunctioning sphincter actions by EAE-induced spinal cord injury.

Acute Disease↗
PubMed1981

Development of sarcomas in heterotopically transplanted rat urinary bladder unit exposed to glucuronic acid conjugate of N-hydroxy-4-aminobiphenyl.

The glucuronic acid conjugate of N-hydroxy-4-aminobiphenyl was tested for carcinogenicity using a heterotopically transplanted rat urinary bladder (HTB) diverted from urine flow. A low-grade transitional cell carcinoma developed in 1 of 16 HTB and sarcoma surrounding the Ommaya reservoir connected to HTB in 8 of 16 rats. This unexpected high incidence of sarcomas, not previously observed in HTB-carcinogenesis model, suggested that the glucuronide conjugate of N-hydroxy-4-aminobiphenyl is a locally active carcinogen to mesenchymal cells.

Aminobiphenyl Compounds↗
PubMed1981

Pure seminoma.

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Adolescent↗
PubMed1981

Carcinogenesis in heterotopically-transplanted urinary bladder by N-methyl-N-nitrosourea: a model for initiation and promotion.

The present investigation was conducted to establish a working model to evaluate the role of potential modifiers (promoters and inhibitors) of urinary bladder carcinogenesis. A single dose (0.25 mg) of the carcinogen N-methyl-N-nitrosourea (MNU) when instilled directly into heterotopically transplanted urinary bladder (HTB) induced a 9% (2 of 22) incidence of urinary bladder tumors by 30 weeks in the urine free HTB environment, whereas repeated instillation of urine into the HTB after MNU treatment resulted in a 61% (14 of 23) incidence of these tumors. Three doses of MNU (0.25 mg/dose once a week for 3 weeks) induced 33% (6 of 18) and 89% (16 of 18) incidence of tumors, respectively, in the absence and presence of urine in the HTB. These data confirm our previous observation that normal urine enhances urinary bladder carcinogenesis, and are consistent with the notion that normal urine exerts a tumor promoting effect.

Animals↗
PubMed1981

Induction of hepatic ornithine decarboxylase by hypolipidemic drugs with hepatic peroxisome proliferative activity.

The present investigation was conducted to determine (1) if hepatomegalic and mitogenic effects of selected hypolipidemic peroxisome proliferators are associated with an elevation of hepatic ornithine decarboxylase (ODC) levels and (2) if induction of ODC is a specific event associated with the development of preneoplastic hepatocellular foci and the eventual formation of hepatomas. Following a single i.p. dose of Wy-14,643 (Wy), the hepatic ODC activity in rats rose sharply, reaching a peak at 8 h, and returned to the normal level by 24 h. Other peroxisome proliferators tested (methyl clofenapate, BR-931 and nafenopin) also increased the hepatic ODC activities significantly 8 h after i.p.. administration of a single dose. Continuous dietary administration of Wy, whether or not these animals were previously initiated with the carcinogen diethylnitrosamine (DEN), resulted in a sustained elevation of hepatic ODC activity. Although Wy exerted an enhancing effect on DEN-initiated tumorigenesis, there was no additional increase of ODC activity. There was no correlation between the level of ODC induction and the presence or absence of altered liver cell foci. These results suggest that induction of ODC by peroxisome proliferators is not a specific event associated with the development of preneoplastic foci and hepatocarcinogenesis, but is an event associated with the sustained maintenance of hepatomegaly and and increased liver cell proliferation.

Animals↗
PubMed1981

In vitro induction of ornithine decarboxylase in urinary bladder carcinoma cells.

The induction of ornithine decarboxylase by normal rat urine in bladder cancer cell cultures was tested in view of recent observations that urine acts as a tumor promoter. Addition of urine up to 15% in final concentration to culture medium resulted in a 10-fold increase in ornithine decarboxylase activity over the control. The stimulatory factor(s) contained in urine appears heat stable and may be multiple. 12-O-Tetradecanoylphorbol-13-acetate, a potent promoter in mouse skin carcinogenesis, induced a 39-fold increase in ornithine decarboxylase activity, the best response among the various substances tested. This suggests that it may act as a promoter of bladder cancer.

Animals↗
PubMed1981

Enhancement by urine of urinary bladder carcinogenesis.

The role of urine as a tumor-enhancing agent in urinary bladder carcinogenesis was investigated by using the heterotopically transplanted rat urinary bladder. Bladders removed from rats initiated with the carcinogen N-butyl-N-(4-hydroxybutyl)nitrosamine in drinking water for 4 or 10 weeks were heterotransplanted to syngeneic rats. These heterotopically transplanted bladders receiving repeated instillations of normal rat urine subsequent to transplantation had a higher incidence of carcinoma than did those receiving 0.9% NaCl solution. These results suggest that normal urine may contain tumor promoter(s).

Animals↗
PubMed1980

The effect of normal rat urine on mucosal regeneration in heterotopic urinary bladder.

A heterotopically transplanted urinary bladder (HTB) of the rat with a communicating Ommaya reservoir was developed in our laboratory as a model to elevate potential bladder carcinogens and the role of urine on the carcinogenesis. Following transplantation the mucosa undergoes ischemic necrosis, but regeneration ensues rapidly within 2 weeks. The present investigation evaluated the effect of two variants on the natural history of the HTB mucosa immediately following its transplantation: (1) presence of normal rat urine, and (2) the effect of alteration of intraluminal osmolality. The results indicate that alteration of osmolality had no effect on the regenerative process, and the epithelium returned to normal in a few weeks. Weekly administration of pooled sterile rat urine into HTB, however, induced simple hyperplasia which persisted throughout the 20-week study period. The HTBs maintained with pooled rat urine did not attain the normal ultrastructural surface characteristics even at 20 weeks posttransplantation. It is concluded that urine exerts a stimulatory effect on the bladder epithelium when first administered to HTB during the active regenerating phase and as long as urinary contact continues.

Animals↗
PubMed1980

Effects of urine and continued exposure to carcinogen on progression of early neoplastic urinary bladder lesions.

Based on reports of regression of superficial bladder tumors after urinary diversion, a study was designed to measure the effects of urine and continued exposure to carcinogen on the incidence of progression of N-[4-(5-nitro-2-furyl)-2-thiazolyl]-formamide-induced early urinary bladder lesions to invasive tumor. After being fed 0.2% N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide diet for 14 weeks, one-half of the male Fischer rats had urinary diversion by ureterosigmoidostomy, and the remainder were sham operated. One-half of each of these two groups was continued on the N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide diet while the remaining animals were fed regular chow postoperatively. One-half of each of the four groups was sacrificed at 3 months, and the remainder were sacrificed at 6 months after ureterosigmoidostomy or sham-operation. The incidence and mean number of tumors as well as the incidence of invasive tumor were tabulated. The combined 3- and 6-month data indicate that excreted carcinogen in the urine influences progression of the preinvasive lesions more than urine alone or systemic carcinogen alone. However, urine alone had a significant effect (p < 0.025) on tumor incidence (8 of 19 sham-operated animals with tumor versus 1 of 18 diverted animals with tumor). Urine acts as a promoter in this experimental system. These findings may have clinical applications in the treatment of early transitional cell carcinoma.

Animals↗