Biomedical subjects
Publications and source records attributed to J Kumazawa.
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Beta-D-glucan is an essential component of the cell wall of fungi. We measured its concentration in the urine of patients with funguria using the chromogenic endotoxin assay kits, Toxicolor and Endospecy. These assay systems use the same Limulus coagulation enzymes. Since the Endospecy test detects endotoxin but not factor G, which is activated by beta-D-glucan, the beta-D-glucan concentration can be calculated by subtracting the Endospecy value from the Toxicolor value. Concentrations of beta-D-glucan were found to be significantly higher in urine samples from patients with funguria (> or = 10(3) colony-forming units/ml) than in non-infected samples.
We report a rare case of obstructing sodium urate stones occurring in the form of extensive deposition on the wall of isolated ileum for replacement of the entire ureter. The stones were disintegrated and removed with a rigid ureteroscope and an electrohydraulic lithotriptor. Hyperuriaciduria, excessive alkalization of urine and urinary stagnation due to reflux, mucous retention, and prostatic hyperplasia were considered as the etiologic factors in the stone formation.
Male Sprague-Dawley rats were intravenously injected with 6.5 mg/kg of cisplatin combined with a subcutaneous methylprednisolone (MP) injection to study the prophylactic effects of steroid hormone on cisplatin-induced nephrotoxicity. In Expt. 1, the rats were injected twice with either 10, 20 or 50 mg/kg of MP4 and 0 h prior to the cisplatin injection and in Expt. 2, they were given a single injection of 100 mg/kg of MP either 24, 4, 2 or 0 h prior to the cisplatin injection. In Expt. 1, elevations of the BUN and serum creatinine levels caused by the cisplatin were dose-dependently inhibited by the administration of MP. In the second experiment, BUN and serum creatinine levels in rats which were pretreated with MP 4 or 2 h prior to the cisplatin injection were significantly lower than those in rats which received cisplatin alone. Our preliminary results suggest that pretreatment with MP is an effective means of protection against cisplatin-induced nephrotoxicity.
The distribution of any involved prostatic urethra, ducts and acini by urothelial carcinoma was studied to determine an adequate sampling method for detecting prostatic involvement using the maps of 38 cystoprostatectomy specimens. A total of 31 patients had prostatic duct and acini involvement, while 7 had prostatic urethral involvement alone. However, the distribution of the involved prostatic urethra, ducts and acini varied. In 29 of the 31 patients (93.5%) with prostatic duct and acini involvement, urethral carcinoma in situ and/or superficial gland involvement (an involvement of the afferent ducts within a few millimeters of the urethral mucosa) at the 5 and/or 7 o'clock position of the verumontanum portion was identified. In 7 patients with prostatic urethral involvement alone 2 had carcinoma foci at the 5 and/or 7 o'clock position of the verumontanum portion. Furthermore, the frequency of deeper gland involvement (an involvement of true prostatic acini except for superficial glands) was higher in patients with superficial gland involvement at the 5 and/or 7 o'clock position of the verumontanum portion (57.7%) than in patients without such involvement (20.0%). Therefore, this study emphasizes that a transurethral resection biopsy containing prostatic tissue at the 5 and/or 7 o'clock position of the verumontanum portion substantially improves the detection of prostatic duct and acini involvement in bladder cancer patients. Moreover, if the prostatic superficial glands are involved at the 5 and/or 7 o'clock position of the verumontanum portion, the potential involvement of the deeper glands should also be suspected.
Hyperosmolarity in the renal medulla inhibits host defenses against bacterial pyelonephritis. Urea and NaCl contribute most to high osmolarity in the renal medulla. We therefore examined the inhibitory mechanism of urea on superoxide generation by human polymorphonuclear leukocytes. Superoxide production was inhibited by high concentration of urea. This inhibition was found to be direct and immediate. In addition, direct inactivation of NADPH oxidase, the key enzyme complex of superoxide generation, was shown by an NADPH oxidase activity assay using cell lysates of polymorphonuclear leukocytes stimulated by phorbol myristate acetate. The inhibitory effect of urea on NADPH oxidase was reversed by washing urea out of the assay system of cell lysates. Kinetic analysis of the inhibition of NADPH oxidase activity by urea showed decreased Vmax and Km, suggesting uncompetitive inhibition. These findings suggested that urea inactivated polymorphonuclear leukocyte superoxide production through a direct and uncompetitive inhibition of NADPH oxidase.
Renal scarring is considered to develop in the later stages of chronic pyelonephritis. In our experimental model of pyelonephritis, bacteria with mannose-sensitive (MS) pili on their surface promoted renal scarring following inoculation into the renal parenchyma. The administration of cyclophosphamide to induce leukopenia and of superoxide dismutase to inactivate superoxide released from polymorphonuclear leukocytes (PMN) at the infection site suppressed any renal scarring following the infection. Conversely, the administration of phorbol myristate acetate at an early stage of infection significantly enhanced the renal scarring. These findings suggest that the PMNs which infiltrate the infection site and the superoxide they release play an important role in any renal scarring following infection with MS-piliated bacteria.
Polymorphonuclear neutrophils (PMN) represent an important defense mechanism against bacterial infection. Superoxide is one of the most important factors released by PMN following various stimulations including bacteria. Augmentation of chemiluminescence response of PMN stimulated by phorbol myristate acetate was observed following the addition of 25-200 micrograms/ml of ofloxacin, a new quinolone antimicrobial agent. In addition, the effects of two inhibitors of protein kinase C, staurosporine and H-7, were examined. The augmented superoxide production was inhibited by 1 or 2 microM of staurosporine or 50 or 100 microM of H-7. These results suggest that ofloxacin augments superoxide production of PMN and that this augmentation is probably due to the enhancement of leukocyte protein kinase C.
Chemotaxis is one of the most important functions of the polymorphonuclear leukocyte (PMN). In the host defense against pyelonephritis, the renal medulla is a site of interaction between bacteria and PMNs. At this site the osmotic pressure is elevated due to a high concentration of NaCl and urea. We evaluated the in vitro chemotactic activity of PMNs under the hyperosmolar conditions created by high concentrations of NaCl and urea. This activity was suppressed by the stimulation of opsonized zymosan and formyl-methionyl-leucyl-phenylalanine. The inhibition of chemotaxis was partially preserved by phosphoenolpyruvic acid (PEP), a precursor of adenosine triphosphate (ATP), in hyperosmolar NaCl but not in urea. The intracellular content of ATP was increased by supplementing the hyperosmolar NaCl with PEP. These observations suggest that inhibition of the chemotactic activity of PMNs is due to differing mechanisms for each NaCl and urea, and that PEP may protect the PMNs against hyperosmolar NaCl by maintaining ATP content.
To evaluate the effects of repeated administration of cisplatin on kidney platinum (Pt) accumulation and renal function, Pt content in the kidney was determined in 31 autopsy cases and changes in creatinine clearance (CCr) were retrospectively assessed in 26 of 31 autopsy cases. There was no significant correlation between the cumulative dose of cisplatin and Pt content in the kidney. However, the kidney Pt level was correlated with the dose of cisplatin injected within a 7-month period prior to the patient's death. We suggest that the dose of cisplatin injected during a relatively short period before a patient's death affects Pt content in the kidney. Neither the total dose of cisplatin nor the Pt content in the kidney was significantly correlated with the decrease in CCr following chemotherapy with cisplatin.
The expression of the multidrug-resistance gene product, P-glycoprotein was examined immunohistochemically in 31 untreated human renal cell carcinomas. In 17 of these, chemosensitivity to Adriamycin and vinblastine was also assessed by a microtiter succinate dehydrogenase inhibition test and the correlation between the expression of P-glycoprotein and intrinsic multidrug resistance was investigated. P-glycoprotein was detected in 16 (51.6%) of the 31 carcinomas. In the chemosensitivity test, 14 (82.4%) of the 17 carcinomas were estimated to be resistant to both drugs (multidrug resistant; MDR). Eight (72.7%) of the 11 carcinomas with a positive expression of P-glycoprotein were MDR, and none of them were sensitive of both drugs. On the other hand, MDR carcinomas were not necessarily associated with the expression of P-glycoprotein. Eight (61.5%) of the 13 MDR carcinomas showed a positive expression of P-glycoprotein while the remaining 5 (38.5%) were negative. These results suggest that the expression of P-glycoprotein is an important factor responsible for the intrinsic MDR phenotype of renal cell carcinoma, however, there are probably other factors involved as well which have yet to be fully elucidated.
Renal scars have been thought to occur only in later stages of chronic pyelonephritis. In our experimental pyelonephritis model, bacteria with mannose-sensitive (MS) pili on its surface promoted renal scarring when inoculated into renal parenchyma. Pretreatment with recombinant human granulocyte-colony-stimulating factor (rhGCSF) inhibited the renal scarring which followed inoculation with MS-piliated bacteria, whereas posttreatment at an early stage of infection had no effect on renal scarring. These findings suggest that rhGCSF may be useful for the prevention of infection without increasing the tissue damage to the renal parenchyma which leads to the renal scarring. Even when rhGCSF is used for treatment of kidney infection, it does not promote increased renal scarring through the increased invasion of leukocytes at the inflammatory site.
To determine the mechanism of easy infectability of uremic patients, we studied the effect of sera from uremic patients who were undergoing chronic hemodialysis on the chemiluminescence (CL) response of polymorphonuclear leukocytes (PMN). The luminol-dependent CL response was examined following stimulation with phorbol myristate acetate (PMA) and N-formyl-methionyl-leucyl-phenylalanine (FMLP). The patient's sera suppressed the CL response following stimulation by PMA, but not by FMLP. These findings suggest that sera from uremic patients undergoing hemodialysis contain a suppressive substance that suppresses the activation of PMNs by PMA.
Renal scarring is considered a criterion of reflux nephropathy and the end stage of pyelonephritis. Prednisolone, a strong anti-inflammatory drug, at doses of 1 or 2 mg/kg prevented renal scarring in rats following infection with Serratia marcescens. Four or 8 mg/kg of prednisolone, however, did not inhibit renal scar formation. In a time course experiment, renal scarring was prevented when 4-day treatment with prednisolone was initiated 2, 5, or 13 days after infection. These results show that prednisolone is effective in preventing such scarring and suggest the clinical use of this drug for preventing renal scar formation after pyelonephritis and reflux nephropathy.
We analyzed the current status and problems of a screening for prostatic cancer (PCa) through a health examination in 12 hospitals in Fukuoka prefecture. From 1987 to 1991, a total of 16,126 subjects received this. The number of subjects who received this increased every year. In 5 hospitals in which such a screening is optional, however, only about 20% of subjects through a health examination received it each year. Furthermore, most of the subjects were in their 50s or 40s. Those in their 70s or more who are at higher risk for PCa rarely received such screening. PCa was detected in 6 subjects (0.04%) (well differentiated adenocarcinoma: 3, moderate differentiated adenocarcinoma: 3) in 5 years. Five were in stage B and treated with radical prostatectomy and one was in stage C and hormonal therapy was performed. The mean age of the 6 patients was 57.7 year old ranging from 51 to 66. The incidence of PCa detected by a screening in dock increased with age. Prostate specific antigen (PSA) was considered to be more useful for detecting prostate cancer in dock as compared with digital examination (DRE), transrectal ultrasonography or prostatic acid phosphatase because of its relatively high sensitivity (83.3%) and specificity (84.8%). The incidence of PCa detected with combination of DRE and determination of PSA was 0.15% and significantly higher than that detected with DRE alone, 0.01%. These results suggest the need for enlightenment on PCa and the significance of a screening with combination of DRE and determination of PSA through a health examination for detecting early stage of PCa.
Platinum (Pt) concentrations in the kidney and liver were determined in 12 autopsied cases following cisplatin treatment. The Pt level in the liver was generally higher than that in the kidney. Pt concentration in the liver showed a significant correlation with the total dose of cisplatin. However, no dose-dependent Pt accumulation was observed in the kidney. Kidney Pt levels were correlated with the doses of cisplatin injected within a 6-month period prior to the patient's death. It is suggested that the dose of cisplatin injected during a relatively short period before the patient's death affected the Pt concentration in the kidney.
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