Search

We recently reported fleroxacin significantly affected cell proliferation in a dose-dependent manner in transitional cell carcinoma cell lines. In this study, we investigated the effect of fleroxacin on mouse bladder carcinogenesis with N-butyl-N-(4-hydroxybutyl) nitrosamine (BHBN). Five-week-old C57BL/6 female mice were divided into three groups. The forced oral administrations of fleroxacin (10 or 50 mg/kg/day) were done for 1 week, then the 0.05% BHBN was given for 8 or 12 weeks. Fleroxacin treatments were continued until sacrifice. The mice were sacrificed at 4 weeks or 8 weeks latent period after BHBN administration, and the histological changes in the bladder were examined. Our study suggested that fleroxacin tended to suppress the development of bladder carcinoma or the malignant changes induced by a shorter period of BHBN administration (8 weeks) in mice. However, in the group of the BHBN administration for 12 weeks, there were no significant effects on the prevention of bladder carcinoma in both of the treatment groups with fleroxacin (10 or 50 mg/kg/day). This study did not make it clear that oral administration of fleroxacin suppressed the development of bladder carcinoma induced by BHBN in mice. However, it is very preliminary data and further experiments need to be done with a much higher dose of the fleroxacin or with other kinds of fluoroquinolone antibiotics.

Adhesion and/or endocytosis of calcium oxalate crystals to the three kinds of tubular cells (Madin-Darby canine kidney (MDCK) cells, rat and human kidney) were demonstrated morphologically to presume the initial formation of kidney stone. After removal of the nonadhesion crystals, the cells were subsequently recultured in the vertical position. At various times thereafter, the interactions between COM crystals and MDCK cells were evaluated morphologically by SEM. COM crystals adhered to the surface of MDCK cells immediately, and the crystals were then endocytosed. The microvilli of the cells appeared to play an important role in these processes. At later times, some complexes that consist of aggregated calcium oxalate crystals and cell debris were observed sporadically. Kidney tissues were obtained from male Sprague-Dawley rats which were injected with sodium oxalate intraperitoneally. Experimentally induced calcium oxalate crystals were evaluated histologically using polarized light microscopy. Some crystals in the cortical portion were attached to the tubular epithelium or internalized into the luminal membrane. Whereas in the papilla, the aggregated crystals were observed lying free from the degenerated tubular lumen along with the cell debris. Human kidney tissues were obtained from 38 patients with calcium oxalate nephrolithiasis who underwent nephrolithotomy or partial nephrectomy before the era of ESWL. The specimens were examined for calcium crystals within the tubular lumen, attached to the tubular walls or internalized into the tubular cells, by polarized light microscopy. Approximately 50% of the specimens observed crystals attached to the tubular cell epithelium and some of them were seen inside the tubular cells. In conclusion, crystal-cell interaction resulted in movement of crystals from the lumen into the cells by an action of microvilli from the results of MDCK cells. However, it was not clear from the results in rats or human kidney tissue that crystal adhesion and/or endocytosis might be vital in the crystal growth in the kidney.

Thirty-seven patients who had undergone radical cystectomy and pelvic node dissection for pathologic stage pT2-4 and/or N+ disease received adjuvant chemotherapy involving the injection of cis-platinum alone or in its combination from June 1982 to April 1989. Adjuvant chemotherapy was performed using the following three protocols. Protocol 1 entails the administration of cis-platinum alone. Protocol 2, involving the administration of a combination of cis-platinum, adriamycin and 5-fluorouracil (CAF), was used for deeply invasive bladder cancer. Protocol 3, consisting of cis-platinum, vp-16 and adriamycin (CVA), was employed in patients with deeply invasive bladder cancer instead of protocol 2 from July 1987. Of the 37 patients, 27 were alive with no evidence of disease for an average of 42 months. One patient died as a result of factors unrelated to cancer. Local recurrence and/or distant metastases occurred in 9 patients and all died of cancer progression. The survival rate for all 37 patients at 87 months was 64.4%. The rates were 75% in pT2, 80% in pT3a, 50.8% in pT3b, and 44.4% in pT4. Although adjuvant chemotherapy combined with radical cystectomy seemed to be effective in cases with pathological stage pT3a or less, more intensive chemotherapy is needed in an attempt to improve poor prognosis in cases with pathological stages pT3b-4 or node involvement.

We report a case of retroperitoneal Castleman's disease of the hyaline vascular type. The tumor was excised with the left kidney because of tenacious adhesion to the renal pedicle. We suggest that knowledge of Castleman's disease in the retroperitoneal area would help to avoid an unnecessarily extensive operation.

Oral administration of ethylene glycol to rats, and the resultant intratubular depositions of microcrystals of calcium oxalate were studied investigating the influences of dietary calcium or magnesium and assessing the protective efficacies against the crystallizations by treatment with phytin and sodium citrate. With increase of calcium intake and consequent increase of urinary calcium excretion there was a marked increase in the amount of tubular deposit of calcium oxalate crystal and in the calcium content of renal tissue. Although magnesium deficiency accelerated renal tubular calcium oxalate deposition, the protection against the crystal formation was not observed with excessive dietary magnesium. When rats were fed a high-calcium diet supplemented with phytin, a significant inhibition of the intratubular crystallization was observed. It appeared obvious that a hypocalciuric action of phytin was attributed to the effect of the prevention. There was vigorous protection of crystal formation by treatment with sodium citrate, which correlated with the level of citrate concentration in the drinking water.