We observed a significant association between AGE levels and nocturia score > 1. Further research is necessary to clarify a possible causal relationship between oxidative stress and nocturia.

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Objectives To evaluate the effect of pretreatment C‐reactive protein/albumin ratio and modified Glasgow prognostic score on the prognosis in patients with metastatic renal cell carcinoma. Methods A retrospective study was carried out in 176 patients with metastatic renal cell carcinoma who received first‐line tyrosine kinase inhibitors. The effect of adding inflammatory prognostic scores to the International Metastatic Renal Cell Carcinoma Database Consortium model (International Metastatic Renal Cell Carcinoma Database Consortium‐C‐reactive protein/albumin ratio and International Metastatic Renal Cell Carcinoma Database Consortium‐Glasgow prognostic score models) on overall survival was evaluated using receiver operating characteristic curves. The prognostic value of inflammatory prognostic scores (C‐reactive protein/albumin ratio‐modified Glasgow prognostic score) was tested using the Kaplan–Meier method and Cox proportional regression models. Results Patients were stratified into two groups using the cut‐off value of 0.05: C‐reactive protein/albumin ratio‐low (<0.05) and C‐reactive protein/albumin ratio‐high (≥0.05). The area under the curve was significantly higher in the International Metastatic Renal Cell Carcinoma Database Consortium‐C‐reactive protein/albumin ratio model (0.720) than that of the International Metastatic Renal Cell Carcinoma Database Consortium model (0.689) and the International Metastatic Renal Cell Carcinoma Database Consortium‐modified Glasgow prognostic score model (0.703). Significant differences were observed in overall survival stratified by the number of risk factors in the International Metastatic Renal Cell Carcinoma Database Consortium‐C‐reactive protein/albumin ratio risk model between one or two and three or four factors (P < 0.001), and three or four and five or more factors (P = 0.001). For the patients in the International Metastatic Renal Cell Carcinoma Database Consortium intermediate‐risk group, overall survival was significantly different between the C‐reactive protein/albumin ratio‐low and ‐high groups (P = 0.001), whereas it was not significantly different between the patients with one and two International Metastatic Renal Cell Carcinoma Database Consortium risk factors (P = 0.106). Conclusion The C‐reactive protein/albumin ratio is a simple and independent predictor of overall survival in patients with metastatic renal cell carcinoma. The predictive activity was significantly improved in the International Metastatic Renal Cell Carcinoma Database Consortium‐C‐reactive protein/albumin ratio model compared with the International Metastatic Renal Cell Carcinoma Database Consortium/International Metastatic Renal Cell Carcinoma Database Consortium‐modified Glasgow prognostic score models.

Selenium is an essential trace element found in vegetables as selenomethionine (SeMet) and methylselenocysteine (MeSeCys). In the present study, we used stable isotopes of Se to investigate differences between how SeMet and MeSeCys are metabolized, using methylseleninic acid (MSA) as a reference methylselenol source. A mixture containing (76)Se-SeMet, (77)Se-MeSeCys, and (82)Se-MSA (each 25 microg Se/kg b.w.) was orally administered to rats, and then, speciation analyses of Se in urine and exhaled gas were conducted using HPLC-inductively coupled plasma (ICP)-MS and GC-ICP-MS, respectively. The proportions of (76)Se-, (77)Se-, and (82)Se-selenosugar (Se-sugar) to total urinary Se metabolites originating from each tracer were very similar, while the proportion of (77)Se-tirmethylselenonium (TMSe) was much less than that of(76)Se- and (82)Se-TMSe in urine, suggesting that(77)Se-SeMet is less efficiently metabolized to TMSe. Similarly, there was significantly less (77)Se-dimethylselenide (DMSe) originating from (77)Se-SeMet than(76)Se- and (82)Se-DMSe originating from (76)Se-MeSeCys and (82)Se-MSA in exhaled gas. It is generally accepted that DMSe and TMSe are metabolites of methylselenol, a putative metabolic intermediate in Se metabolism. Methylselenol is believed to be responsible for the cancer chemoprevention effects of Se. These results suggest that MeSeCys is converted to methylselenol more efficiently than is SeMet and that urinary TMSe and exhaled DMSe might be useful biomarkers for the generation of cancer chemopreventive forms of Se.