No abstract

Bladder cancer (BC) is one of the most common malignancies worldwide. Several biomarkers related to the prognosis of patients with BC have previously been identified. However, these prognostic models use only one gene and are thus not reliable or accurate enough. The purpose of our study was to develop an innovative gene signature that has greater prognostic value in BC. So, in this study, we performed mRNA expression profiling of glycolysis-related genes in BC (n = 407) cohorts by mining data from The Cancer Genome Atlas (TCGA) database. The glycolysis-related gene sets were confirmed using the Gene Set Enrichment Analysis (GSEA). Using Cox regression analysis, a risk score staging model was built based on the genes that were determined to be significantly associated with BC outcome. Eventually, the system of risk score was structured to predict a patient's survival, and we identified four genes (CHPF, AK3, GALK1, and NUP188) that were associated with the outcomes of BC patients. According to the above-mentioned gene signature, patients were divided into two risk subgroups. The analysis showed that our constructed risk model was independent of clinical features and that the risk score was a highly powerful tool for predicting the overall survival (OS) of BC patients. Taking together, we identified a gene signature associated with glycolysis that could effectively predict the prognosis of BC patients. Our findings offer a new perspective for the clinical research and treatment of BC.

This study analyzed the ciprofloxacin (CIP) degradation in real reclaimed water through UV/chlorine and UV/persulfate (UV/PS) advanced oxidation processes. The influence of oxidant dosage, pH, inorganic anions, and humic acid (HA) on the oxidation capacity and performances of various UV‐based processes was investigated. The results revealed that the CIP degradation rate constants in the UV/chlorine and UV/PS processes were higher than that in UV/H2O2, direct‐UV, NaClO, and K2S2O8 processes. The removal rate peaked at 0.1 mM oxidant dosage for 1 μM CIP, while the rate constant was highest at pH 5 (UV/chlorine) and pH 7 (UV/PS). The presence of Cl−, HCO3−, and HA inhibited CIP removal in both processes. The degradation rate observed in reclaimed water was high, but still lower than that in laboratory water by 9.2 (UV/chlorine) and 9 (UV/PS) times. The UV/chlorine and UV/PS processes were found to be more cost‐effective and hence more feasible in removing refractory compounds in reclaimed water. Practitioner points The addition of oxidant and UV irradiation together had a pronounced promotion in the degradation of CIP. Cl· and SO4·− had potential importance for enhancing CIP degradation in UV/chlorine and UV/PS process, respectively. UV/chlorine and UV/PS processes exhibited effective removal capability to CIP in real reclaimed water.

Current research suggests that synovial phagocytic cells remove excessive amounts of free oxygen radicals (reactive oxygen species [ROS]), thereby preventing damage to synovial tissues. Moreover, ROS may affect the expression of growth arrest and DNA damage inducible α (GADD45A), thus further promoting the activation of synovial fibroblasts. Male adult rats were assessed for progression of collagen‐induced arthritis (CIA) using a macroscopic arthritis scoring system of the hind paws and by measuring the changes in the rat's body weight, and activity level before and after diagnosis of CIA. Rats were intraperitoneally injected twice daily with edaravone at doses of 3, 6, and 9 mL/kg. Samples were taken at 2, 4, and 6 weeks, respectively. Edaravone was found to significantly reduce macroscopic arthritis and microscopic pathology scores in CIA rats. The concentration of endothelial nitric oxide synthase‐6, glutathione, and heme oxygenase‐1 in the serum of rats decreased, as was the production of ROS around the synovium and inflammatory factors. Moreover, ROS‐1 increased the expression of the nuclear factor‐κB (NF‐κB) p65 protein by altering the expression level of GADD45A, causing aggravation of tissue damage. Edaravone also significantly improved the physiological condition of CIA rats, including appetite, weight changes, and loss of fur, as well as limb mobility. We believe that edaravone acts to reduce the expression of NF‐ĸB p65 by clearing ROS, which causes reduced expression of GADD45A, and subsequently reduces the level of apoptosis and inflammatory response proteins, thereby reducing the symptoms of CIA. We, therefore, propose that edaravone is an effective option for clinical treatment of rheumatic arthritis.